RAH Intensive Care Unit Manual 2012

Royal Adelaide Hospital
Intensive Care Unit
Medical Manual
2012 Edition
Welcome to Intensive Care.
This manual has been written to facilitate the daily running of the RAH Intensive Care
Unit. It is by no means the definitive answer to all intensive care protocols and
procedures, nor is it designed to be a textbook.
A standardised approach to management is desirable for optimal patient care and safety,
improving communication and understanding between members of the ICU team and
associated specialties. This approach provides a common platform for staff who come
from different countries and training backgrounds.
The manual outlines various Protocols, which represent a standard approach to practice
within the Unit. These have been derived from the available literature, clinical
experience and where appropriate, cost-effectiveness. Guidelines designed to assist in
clinical management are included but patient management will ultimately depend upon
the clinical situation. Consultants may modify these guidelines on consideration of the
nuances of a particular clinical case. Registrars wishing to go outside the guidelines
should discuss this with the Duty Consultant before proceeding.
Assistance is always available from the Duty Consultant and senior nursing staff. Use
your time in the Unit to get the most out of the large clinical caseload. Ask questions
about clinical problems, equipment and procedures with which you are unfamiliar.
There are numerous textbooks, journals and references available in the Unit.
This manual has undergone numerous changes, with contributions from many of the ICU
staff and from other specialty services within the hospital. The contents of this manual
are produced from the consensus views of the senior medical staff. We aim to make the
information in this manual as accurate and consistent with the available evidence as
possible at the time of publication. However no guarantee can be provided that errors do
not exist – please notify the Duty Consultant if you identify any errors of fact.
A/Prof Robert Young
12th Edition
FOREWORD ....................................................................................................................... 2
CONTENTS......................................................................................................................... 3
PART 1 - ADMINISTRATION .............................................................................................. 6
A. Staffing - Royal Adelaide Hospital ICU ............................................................... 6
B. Rostering and Job Descriptions ............................................................................. 8
Table: Team Duties .............................................................................................. 8
Table: Registrar Shifts ....................................................................................... 10
C. Orientation .......................................................................................................... 11
D. Weekly Programme............................................................................................. 12
Table: Weekly Unit Programme ........................................................................ 12
E. Admission and Discharge Policies ...................................................................... 13
F. Care for Patients Discharged from ICU for Terminal Care. ............................... 15
G. Clinical Duties in the ICU ................................................................................... 16
H. Documentation .................................................................................................... 19
I. Consent in ICU ................................................................................................... 21
J. ICU Ward Rounds ............................................................................................... 22
K. Clinical Duties Outside of the Intensive Care Unit ............................................. 23
L. Hospital Emergencies ......................................................................................... 28
M. Research in ICU .................................................................................................. 29
N. Information Technology in ICU .......................................................................... 30
PART 2 - CLINICAL PROCEDURES .................................................................................. 31
A. Introduction ......................................................................................................... 31
B. Procedures ........................................................................................................... 31
C. Peripheral IV Catheters ....................................................................................... 32
D. Arterial Cannulation ............................................................................................ 33
E. Central Venous Catheters .................................................................................... 34
F. Urinary Catheters ................................................................................................ 36
G. Epidural Catheters ............................................................................................... 37
H. PICCO Catheters ................................................................................................. 37
Table: PiCCO Values and Decision Tree ........................................................... 38
I. Pulmonary Artery Catheters ................................................................................ 39
Table: Standard Haemodynamic Variables ........................................................ 41
J. Pleural Drainage .................................................................................................. 42
K. Endotracheal Intubation ...................................................................................... 44
L. Weaning Guidelines ............................................................................................ 49
Flowchart: Ventilation Weaning Protocol .......................................................... 50
M. Extubation ........................................................................................................... 50
N. Emergency Surgical Airway Access ................................................................... 52
O. Fibreoptic Bronchoscopy .................................................................................... 53
P. Tracheostomy ...................................................................................................... 54
Q. Cardiac Pacing .................................................................................................... 57
R. Pericardiocentesis................................................................................................ 60
S. Intra-Aortic Balloon Counterpulsation................................................................ 61
T. Gastric / Oesophageal Tamponade Tubes ........................................................... 64
U. Extracorporeal Membrane Oxygenation.............................................................. 65
PART 3 - DRUGS AND INFUSIONS.....................................................................................66
A. Policy ................................................................................................................... 66
B. Principles of Drug Prescription in Intensive Care ............................................... 67
C. Cardiovascular Drugs .......................................................................................... 67
Table: Cardiovascular Effects of Catecholamines .............................................. 68
Table: Inotropic Agents Used in ICU ................................................................. 69
Table: Vasopressors............................................................................................ 70
Table: Antihypertensive & Vasodilator Agents .................................................. 71
Table: Antiarrhythmic Agents ............................................................................ 74
Table: Thrombolytics ......................................................................................... 77
Table: Antiplatelet Agents .................................................................................. 78
D. Respiratory Drugs ................................................................................................ 79
Table: Bronchodilators ....................................................................................... 80
E. Sedation, Analgesia and Delirium ....................................................................... 81
Table: Nurse Controlled Sedation Protocol ........................................................ 82
Table: Modified Richmond Agitation Sedation Scale (RASS) .......................... 82
Table: Drugs Associated with Increased Delirium ............................................. 84
Flowchart: Confusion Assessment Method for ICU (CAM-ICU) ..................... 85
Table: Sedatives / Analgesics ............................................................................. 86
F. Muscle relaxants .................................................................................................. 88
Table: Muscle Relaxants .................................................................................... 88
G. Anticoagulation ................................................................................................... 89
Table: HITS Probability Score – ‘4T Score’ ...................................................... 92
Table: Anticoagulants ......................................................................................... 93
Table: Heparin Infusion Protocol ........................................................................ 94
Table: Lepirudin Infusion Protocol ..................................................................... 94
H. Endocrine Drugs .................................................................................................. 96
Flowchart: Blood Glucose Management in ICU ................................................ 97
Table: Insulin Infusion Protocol ......................................................................... 97
Table: Steroid Doses / Relative Potencies .......................................................... 99
I. Renal Drugs - Diuretics ................................................................................... 100
Table: Diuretics ................................................................................................ 101
J. Gastrointestinal Drugs ....................................................................................... 102
Table: GI Drugs ................................................................................................ 103
K. Antibiotics ......................................................................................................... 104
Table: Vancomycin Dosing Schedule .............................................................. 106
Table: Antibiotic Infusion Schedules ............................................................... 107
Table: Peri-operative Antibiotic Prophylaxis ................................................... 109
Table: Perioperative Endocarditis Prophylaxis ................................................. 110
Table: Empiric Antibiotics ............................................................................... 111
Table: Antibiotics for Specific Organisms ....................................................... 113
PART 4 - FLUIDS AND ELECTROLYTES.........................................................................114
A. Principles of Fluid Management in Intensive Care............................................ 114
Table: Common IV Solutions ........................................................................... 115
B. Nutrition ............................................................................................................ 116
Flowchart: Nutritional Therapy Protocol ......................................................... 117
Table: Average Daily Requirements ................................................................ 120
Table: Baxter TPN Solution Options ............................................................... 121
C. Blood Component Therapy ............................................................................... 122
Table: Critical Bleeding (Massive Transfusion) .............................................. 124
Table: Guidelines for the Management of an Elevated INR ............................ 128
Table: Pre-operative Dabigatran Management................................................. 131
Flowchart: Management of Bleeding Patient on Dabigatran ........................... 132
Table: Blood Transfusion Reactions ................................................................ 135
D. Guidelines for the Management of Electrolytes ................................................ 136
Table: Classification of Lactic Acidosis .......................................................... 144
PART 5 - CLINICAL MANAGEMENT .............................................................................. 147
A. Cardiopulmonary Resuscitation ........................................................................ 148
Flowchart: Basic Life Support ......................................................................... 148
Flowchart: Advanced Life Support .................................................................. 149
Flowchart: Paediatric Cardiorespiratory Arrest ............................................... 150
Induced Hypothermia Post Cardiac Arrest ........................................................ 151
B. Failed Intubation Drill ....................................................................................... 152
Flowchart: Failed Intubation Drill.................................................................... 153
C. Respiratory Therapy .......................................................................................... 154
Table: Oxygen Delivery Devices ...................................................................... 154
Table: Oxygen Delivery Percentage - Nasal High Flow .................................. 156
D. Management of Cardiothoracic Patients ........................................................... 166
Flowchart: Arrest Post Cardiac Surgery ........................................................... 168
Flowchart: Bleeding Post Cardiac Surgery ...................................................... 169
Table: Antibiotic Prophylaxis for Cardiac Surgery .......................................... 170
E. Renal Failure ..................................................................................................... 171
Table: Haemodialysis Solutions ....................................................................... 179
Prismaflex – ST 150 Circuit .............................................................................. 184
Form: Dialysis Data for Drug Overdose .......................................................... 185
F. Neurosurgical protocols .................................................................................... 186
Flowchart: Cerebral Perfusion Pressure Algorithm .......................................... 189
Table: World Federation of Neurosurgeons Classification .............................. 190
G. Microbiology Protocols..................................................................................... 195
Flowchart: Antifungal Treatment in Immunosuppressed Patients ................... 201
H. Drug Overdose .................................................................................................. 204
Flowchart: The Unconscious, Undetermined Overdose .................................... 207
Graph: Modified Rumack-Matthew Nomogram .............................................. 209
Flowchart: Acute Paracetamol OD - Known Time of Ingestion ...................... 210
Flowchart: Repeated Supratherapeutic Paracetamol Ingestion ........................ 211
Table: N-Acetylcysteine Administration ......................................................... 211
I. Bites and Envenomation ................................................................................... 220
J. Limitation of Therapy ....................................................................................... 221
K. Brain Death and Organ Donation ...................................................................... 221
L. Donation After Cardiac Death (DCD) .............................................................. 226
Table: Contact Phone Numbers ....................................................................... 229
Consultant Medical Staff
- Royal Adelaide Hospital ICU
Deputy Director
A/Prof Rob Young
Dr Peter Sharley
Director of Research
A/Prof Marianne Chapman
Supervisor of Training
Dr Nick Edwards
Dr Mike Anderson
Dr Stuart Baker
Dr David Clayton
Dr Adam Deane
Dr David Evans
Dr Mark Finnis
A/Prof Arthas Flabouris
Dr Ken Lee
Dr Matt Maiden
Dr Stuart Moodie
Dr Richard Newman
Dr Ben Reddi
Dr Richard Strickland
Dr Krishnaswamy Sundararajan
A/Prof Mary White
Dr Alex Wurm
Senior Nursing Staff
Nursing Director:
Mr Ian Blight
Clinical Services Coordinators:
Ms Deb Herewane
Ms Ros Acott
Ms Tracey Cramey
Mr Michael Schwarz
Mr Steve Wills
Nurse Managers:
Ms Ali Coventry
Ms Heather Pile
Administrative Staff
Administrative Manager
Ms Melissa Filleti
Resource Accountant
Ms Tammy Moffat
Team Leader / Roster Manager
Ms Sherridan Clark
Unit Secretary
Ms Kristina Gabell
Ward Clerks
Ms Ali Fraser
Ms Lisa Migliaccio
Mr Gavin Sain
a) Three levels of registrars are rostered in the unit:
i) Senior Registrars (SR):
 Advanced trainees in the College of Intensive Care Medicine (CICM)
(or equivalent training program)
 Have completed or near completed specialist training.
 Take “first on-call” at night and experience responsibility at a
consultant level.
 The SRs help manage the registrar roster, coordinate registrar
presentations, simulator training and contribute to teaching activities.
ii) Senior Trainees:
 Usually CICM trainees (or equivalent)
 Rostered according to seniority and experience.
iii) Junior Trainees/RMOs:
 Vocational trainees, trainees in other specialist programs
e.g. surgical, physician training, etc
 Residents in general rotations.
b) Portfolios are determined by experience and rostering requirements.
c) All registrars, except SRs, will rotate through Units A, B and C.
d) Training positions at Royal Adelaide Hospital:
i) Intensive Care Positions
 The College of Intensive Care Medicine has accredited the RAH as a
C24 Unit for training for the fellowship in intensive care (FCICM).
 Registered CICM trainees may undertake their full 24 months of core
ICU training at the RAH.
 Non-CICM-trainee registrars wishing to gain further postgraduate
experience in intensive care may apply for these positions.
 Applications including a current c.v. should be forwarded to:
Dr Alex Wurm. ([email protected])
 Trainees in formal training programs are given appointment priority.
Positions for non-intensive care trainees
 Rotations of registrars in these positions are made from the respective
specialty based training programs at the RAH.
 Anaesthesia trainees:
1 position (3 or 6 month term).
 Physician trainees:
1 position (3 or 6 month term).
 Surgical trainees:
1 position (3 or 6 month term).
 Emergency Medicine trainees:
2 positions (3 or 6 month term).
iii) Supervisors of Training at Royal Adelaide Hospital:
 Intensive Care:
Drs Nick Edwards
& Peter Sharley
 Medicine:
Dr S M Guha
 Anaesthesia:
Dr I Banks
 Surgery:
Mr P G Devitt
 Emergency Medicine:
Dr R Dunn
Rostering and Job Descriptions
Table: Team Duties
0800 - 1900
ICU Team A
Beds 1-12
ICU Team B
Beds 12-24
ICU Team C
Beds 25-34
Consultant Team A
Manages Unit A
Senior Registrar A
Manages Unit A, TPN
Registrar A1 (D1)
Beds 1-6.
Registrar A2 (D2)
Beds 7-12.
Consultant Team B
Manages Unit B
Senior Registrar B
Manages Unit B
Registrar B1 (D3)
Beds 13-18
Registrar B2 (D4)
Beds 19-24
Consultant Team C
Manages Unit C
Registrar C1 (D5)
Registrar C2 (D6)
Unit C, Beds 25-34.
Duty Intensivist
Speed Dial 1650
Bed management, Ward consults
CICU Consultant
Cardiothoracic ICU Consultant
Teaching Consultant
Undergraduate and postgraduate teaching
D7 registrar
Consults, Code blue, TPN
1830 - 0830
ICU 1st On-Call
Consultant / Senior Registrar
Attends evening handover round.
On-call for any problems overnight.
ICU 2nd On-Call Consultant
Backs-up ICU 1st on-call when required.
Night Registrar 1 (N1)
Beds 1-12
Night Registrar 2 (N2)
Beds 13-24
Night Registrar 3 (N3)
Beds 25-34
Night Senior (NS)
Consults, Code blue calls.
Oversees beds 1-34, allocates workload
Senior Registrar 1
First Consultant call Wednesday and Saturday
Senior Registrar 2
First Consultant call Thursday and Sunday
NB: The allocation of responsibilities overnight is at the discretion of the registrars present and
should be established by mutual agreement between the registrars and consultant on call. It is
assumed that all registrars will maintain an awareness of all patients in ICU and will provide
assistance in other areas of the ICU if required. Hence the workload should be spread evenly and
all registrars should be allowed to have their required (and reasonable) rest periods.
1. Roster Guidelines
a) Rosters are primarily designed to meet training and patient care requirements,
taking into account overall staff numbers and skill-mix.
b) In addition, award requirements, occupational health & safety considerations,
and individuals’ preferences and requests are taken into account.
c) The system is not infallible – if there is a problem with any aspect of the roster,
please notify the ICU secretary as soon as possible.
d) Each roster covers a 4 week period, with the working week commencing on a
e) Rosters are usually posted two weeks in advance.
f) Where possible you will be rostered two or more days-off following night duty.
g) When rostered to night duty, you are not expected to attend weekly teaching
sessions, as this would result in unsafe work hours.
h) The rostering system utilises a wide variety of different codes as set out in the
following table:
Table: Registrar Shifts
Shift Description
Times & Meal Breaks
Senior Registrar
Day shift: report to DI
1x 30min meal break
Day shift Unit A
Day shift Unit B
Day shift Unit C
1x 30min meal break
Day shift: consults & Code blue
Night shift Unit A
Night shift Unit B
Night shift Unit C
2x 30min meal breaks
Night shift: consults & Code blue
Annual, Study, Exam, Conference leave
2. Requesting Shifts
a) Particular shifts or days-off can be entered on a ‘request roster sheet’ that is
posted on the pin-up board opposite the medical staff pigeon holes.
b) The request sheet is collected on the date indicated on the top of the sheet.
c) Requests should also be discussed with the ICU secretary.
(Ph: 8222 5325 or email: [email protected]).
d) Factors to consider when requesting shifts:
i) Requests can significantly complicate the roster and you should therefore
exercise some restraint and not request your entire roster.
ii) If you need to request several shifts please indicate in red, which two are
the most important and priority will be given to these requests.
iii) Requests cannot be granted if they disadvantage other staff, compromise
skill-mix, or overall staffing numbers necessary for the shift.
3. Changing/Swapping Shifts
a) If you wish to change a shift after the roster has been posted, you may do so
with the following guidelines:
i) Once the roster is posted, the onus is on the individual to arrange any shift
swaps and these must occur within the same roster period.
ii) You should first endeavour to swap the shift with someone in the same
skill group so that the skill-mix is maintained for the shift.
iii) You must speak to the ICU Secretary for approval (T: 8222 5325 or email:
[email protected]) and then note changes on the rosters
posted in the ward and on the medical pin-up board.
4. Annual Leave
a) Annual leave for medical staff is on a “first come - first served” basis, so book
leave as soon as possible.
b) Only 3 registrars can be on leave at any one time, so before filling in an
application form check that leave is available with the ICU secretary.
c) Please contact the ICU Secretary if you have any questions or concerns about
your roster at anytime.
d) Leave is in accordance with the SA Salaried Medical Officers’ Award (5 weeks
annual and 1 week study leave) and registrars are required to forward a signed
copy of leave requests to the Senior Registrar for rostering purposes.
5. Sick Leave
a) If you are sick and unable to attend work, please contact both:
i) The Duty Intensivist by day, or
Senior Registrar at night (SD: 1650), and
ii) The Roster Manager - Mon-Fri (09:00-16:00)
b) If you can, predict an expected day or night of return to work.
c) Annotate your pay sheet as “sick leave” accordingly.
1. Registrars commencing duty within the unit at the main RMO changeover dates will
undergo a half-day orientation program.
2. This will include sessions from:
a) The Director of ICU (or delegate)
b) The Director of Research
c) Infectious Diseases / Clinical Microbiology
d) The Acute Pain Service
Weekly Programme
Table: Weekly Unit Programme
Handover round
Handover round
Handover round
Handover round
Handover round
Bedside round
Bedside round
Bedside round
Bedside round
Bedside round
ICU Grand Round
ICU Grand Round
ICU X-ray meeting
Consultant meeting
Bedside round
Simulator Training
Simulator Training
Journal Club
Registrar tutorial
Primary Exam
(1 trainees)
Clinical Teaching
Trainee Tutorial
BICMed Course
junior registrar
Handover round
Handover round
(all registrars)
Handover round
Handover round
Handover round
Admission and Discharge Policies
1. Admissions Policy
a) Patients are managed by the ICU staff during their stay in ICU.
b) Admission is reserved for patients with actual or potential vital organ system
failures, which appear reversible with the provision of ICU support.
c) All admissions, including transfers and retrievals, must be approved by the
Duty Intensivist (SD: 1650).
d) Resuscitation or admission must not be delayed in imminently life threatening
cases, unless specific advanced directives exist and are clearly documented.
e) Such admissions should be discussed with the Duty Intensivist ASAP.
f) Patients are admitted to ICU under the ‘bed-card’ of the original or taking clinic.
g) MedStar Retrievals
i) Require admission under a parent clinic, who should be aware prior to patient
transfer and notified of the patient’s arrival in the ICU.
ii) Must be discussed with the Consultant when the SR is on 1st call.
h) Clinics requesting elective postoperative surgical beds should book the bed at least
one day in advance and must confirm bed availability with the Duty Intensivist on
the day of surgery, prior to anaesthesia commencing.
i) Admission disputes must be referred to the Duty Intensivist.
2. Discharge Policy:
a) All discharges should be:
i) Approved by the responsible ICU consultant.
ii) Discussed with the parent clinic prior to patient transfer
 including discussion of any ongoing or potential problems.
iii) Transferred “In hours”
 i.e. prior to 18:00 - unless specifically approved by a consultant.
b) A discharge summary must be completed and a copy filed in the case-notes.
c) All patients on insulin protocols should be referred to the Endocrine Unit prior to
discharge (preferably the day before)
d) Patients discharged on TPN must be entered in the TPN folder in Unit A.
e) Notify the Acute Pain Service of patients discharged under their care.
f) Withdrawal or limitation of therapy is a consultant responsibility.
g) Treatment limitation/non-escalation directives must be discussed with the patient
or patient’s family, the parent clinic and clearly documented prior to discharge.
h) Referral to the Palliative Care should occur pre-discharge where indicated.
3. Deaths Policy:
a) The duty ICU consultant must be informed of all unexpected deaths.
b) The duty ICU registrar must ensure:
i) A death certificate is completed or the Coroner notified
ii) The parent clinic or duty intern is notified
iii) Referring doctors (i.e. GP’s, other specialists / hospitals) are notified.
c) Where indicated, consent for a post-mortem should be obtained from relatives as
soon as possible.
d) The Coroner must be notified in all cases where death is:
i) A death in custody, e.g. police, corrections, mental health detention.
ii) A death by unusual, unexpected, unnatural, violent or unknown cause.
iii) A death during, as a result of or within 24 hours of a surgical, invasive or
diagnostic procedure, including the administration of an anaesthetic for the
carrying out of the procedure.
iv) The term ‘anaesthetic’ means a local or general anaesthetic and includes a
sedative or analgesic. The following procedures are excluded:
 The giving of an intravenous injection
 The giving of an intramuscular injection
 Intravenous therapy
 The insertion of a line or cannula
 Artificial ventilation
 Cardio-pulmonary resuscitation
 Urethral catheterisation
 The insertion of a naso-gastric tube
 Intra-arterial blood gas collection
 Venipuncture for blood collection for testing
 Subcutaneous injection or infusion
v) A death within 24 hours of being discharged from a hospital or having
sought emergency treatment at a hospital.
vi) A death of a person under a ‘protected person’ order under the Aged or
Infirm Persons’ Property Act 1940 or the Guardianship and
Administration act 1993.
vii) A death in the course or as a result or within 24 hours of a person receiving
medical treatment to which consent for that treatment has been given under
Part 5 of the Guardianship and Administration act, 1993.
viii) A death of a child subject to a custody or guardianship order under the
Children’s Protection Act 1993.
ix) A death on an aircraft or vessel with a place in South Australia as its place
of disembarkation.
x) A patient death in an approved treatment centre under the Mental Health
Act 1993.
xi) Death of a resident of some (but not all) supported residential facilities
licensed under the Supported Residential Facilities Act. A list of the
relevant facilities is provided in the “Coroner’s Folder” in the nursing bay
xii) A death in a hospital or treatment facility for the treatment for a drug
xiii) If no certificate as to the cause of death has been given to the Registrar of
Births, Deaths and Marriages.
Care for Patients Discharged from ICU for Terminal Care.
1. Preparation for discharge.
a) For the families of dying patients, moving from a familiar environment will add
a level of anxiety and uncertainty, even if it will be to a quieter setting.
b) Handover to the ward treating team should be as comprehensive as possible,
including a social as well as medical history.
c) Families should be supported to accept that there may still be uncertainty about
the patient’s course and the timing of death.
d) Families should be reassured that the focus will be on maintaining comfort.
e) Levels of ongoing active support for the patient, e.g. IV or subcutaneous fluids
should be clarified between ICU staff, the Ward team and family members.
2. Symptom management in terminal care.
a) Physical symptoms that should be considered in planning ongoing care are:
i) Pain – either spontaneous or on movement
ii) Agitation, restlessness
iii) Respiratory tract secretions
iv) In a conscious patient there may be other symptoms
e.g. nausea and vomiting, dyspnoea
v) Prevention of seizures may be a relevant issue
b) If the patient is requiring either analgesia or sedation in ICU, these should be
continued on discharge to the ward.
i) Opioid infusions can be continued as subcutaneous infusions via a pump
(e.g. Graseby® or equivalent)
ii) If sedation is required, midazolam can be administered via subcutaneous
route as a continuous infusion, with an opioid if already in use.
c) If the patient has not required regular opioid or sedation in ICU, the following
PRN orders should be in place prior to discharge:
i) For pain:
 Opioid naïve patient
- e.g. morphine 2.5-5mg s.c. 2 hrly prn
 Opioid tolerant
- dose guided by background usage
ii) For agitation, restlessness:
 Midazolam 2.5mg - 5mg s.c. 1 hrly prn
iii) For management of secretions:
 Hyoscine hydrobromide 400 µg s.c. 3-4 hourly prn
 Atropine 600 µg s.c. 3-4 hourly prn
3. Where appropriate, formal consult and involvement of the Palliative Care Service is
G. Clinical Duties in the ICU
1. Infection Control in ICU
a) Prevention and containment of nosocomial infection is a fundamental principle of
effective medical practice.
b) The critically ill patient is highly vulnerable to nosocomial infection, which results
in significant morbidity, prolonged length of hospital stay, increased cost and
attributable mortality.
c) It is the responsibility of every member of the health care team to ensure
compliance with Hospital and Unit infection control policies. This may include
reminding senior colleagues or visiting teams to conform to basic issues such as
hand-washing or additional precautions.
d) Hand-hygiene remains an established method of effective infection control and
must be strictly performed by all members of the health care team:
i) Aqium hand gel must be used by all staff:
 Every time they enter or exit a patient’s cubicle
(defined as the line of the door or curtain of bed space.)
 Before wearing gloves
 Before and after patient contact
 Before and after contact with a patient’s environment
ii) Hand wash with soap where:
 Contact with blood or body fluids
 Hands are visibly soiled
 After removing gloves
iii) Hand wash with chlorhexidine:
 Prior to clinical procedures
 After contact with patients with multi-resistant organisms
e) Gloves
i) Disposable gloves must be worn for all contact with patient’s bodily fluids,
dressings and wounds.
ii) Gloves must be disposed of within the patient cubicle on leaving
f) Plastic aprons are to be worn:
i) With gross physical contact with the patient (e.g. patient turns)
ii) For “additional precautions” (see below)
g) Additional precautions:
i) The following patients require additional precautions:
 Infection or colonisation with:
a. Methicillin Resistant Staph. Aureus
b. Vancomycin Resistant Enterococcus
c. Multiresistant gram negatives
d. Clostridium difficile
 Burns
 Febrile neutropenia
 Immunosuppressed patients as directed by Infection Control
ii) These patients will normally be managed in either Units A or B.
iii) An “Additional Precautions” sign is placed outside cubicles of patients
identified as infective risks:
 Red sign
= patient has multi-resistant organism
 Blue sign
= patient is immunocompromised
iv) New disposable gowns and gloves must be used for each person entering
the cubicle and disposed of within the cubicle upon leaving.
v) Consumable stock within the cubicle should be kept to a minimum.
vi) Notify appropriate staff if patients are transported to theatre, for diagnostic
procedures, or for ambulance transport.
vii) Once the patient has been transferred or discharged, the area should remain
vacant until “terminally cleaned” in accordance with RAH policy.
viii) Environmental swabbing in Intensive Care is conducted as required by
Infection Control staff.
h) Aseptic technique
i) Aseptic technique is to be used for all patients undergoing major invasive
procedures (refer to procedures section).
ii) This includes:
 Hand disinfection: surgical scrub with chlorhexidine for >1 minute
 Sterile barrier: full gown, mask, hat, gloves and sterile drapes.
 Skin preparation with chlorhexidine 2% in 70% alcohol.
i) Sharps disposal
i) The person performing the procedure is responsible for disposal of all
sharps (needles, blades) using the sharp disposal containers.
ii) The nursing staff are not responsible for sharps disposal.
j) “Traffic control”
i) Movement of people through the unit should be kept to a minimum.
ii) This applies equally to visiting clinics and large numbers of relatives.
iii) All visitors are expected to conform to the above infection control
measures and should be tactfully reminded or instructed when necessary.
k) Nominated isolation/quarantine rooms for highly contagious patients:
i) Rooms 3, 4, 5 & 6
- shared air-conditioning
ii) Rooms 21 & 22
- sealed, independent, negative pressure A/C units.
2. Guidelines for admission of a new patient to ICU
a) Handover from the referring doctor. Obtain as much information as possible.
b) Primary survey:
i) Ensure adequate airway, breathing and place the patient on a FiO2 = 1.0 until
a blood gas is done.
ii) Check circulation and venous access.
c) Notify the duty consultant.
d) Secondary survey: fully examine the patient.
e) Document essential orders:
i) Ventilation
ii) Sedation / analgesia
iii) Drugs, infusions
iv) Fluids
f) Outline the management plan to the nursing staff.
g) Secure appropriate basic monitoring/procedures:
i) SpO2
ii) ECG
iii) Arterial line
iv) IDC, nasogastric tube
v) CVC for the majority
h) Basic investigations as indicated:
i) Routine biochemistry, blood picture and coagulation studies
ii) Group and screen.
iii) Septic screen / microbiology.
iv) Arterial blood gas
v) ECG
vi) CXR (after placement of appropriate lines)
i) Advanced investigations: CT, angiography, MRI, etc
j) Advanced monitoring where indicated: e.g. PA catheter, ICP, PiCCO.
k) Document in case notes. (See below)
l) Notify the parent clinics of patients admitted directly to ICU
NB: this applies particularly to patients who have been retrieved.
m) Clinic Interns and RMOs should clerk hospital admissions direct to ICU.
n) Inform and counsel relatives.
3. Daily management in ICU.
a) Daily investigations:
i) Routine blood tests (U&E, LFT, Mg, Hb, WCC, Plts, ABG) are ordered on
the daily flow chart and signed for on the 11:00 am fluid round.
ii) Coagulation studies, drug levels or other tests are requested as required and
may also be requested on the daily flow chart.
iii) The night duty nurses take the bloods at 06:00 and complete the request form,
which must be signed by the night registrar.
iv) Registrars are responsible for taking blood specimens:
 When nursing staff request assistance.
 For blood transfusion - the requesting MO must ensure that the labelling
of the request form and specimen matches the patient’s wristband.
Chest x-rays are ordered after the morning handover round via OACIS.
 Routine daily chest x-rays are not performed in ICU
 Chest x-rays are performed
a. On admission to ICU (beds 1-24)
b. Following invasive procedures:
i. Endotracheal intubation
ii. Complicated percutaneous tracheostomy
iii. CVC placement (subclavian or jugular)
iv. Nasogastric or IABP placement
c. Suspected pneumothorax
d. At the discretion of the attending doctor
b) Handover ward rounds are at 08:00 and 18:30. These are brief business rounds to
handover essential information to the next team (either day or night) and are
attended by the duty consultant, team registrars and senior nursing staff.
c) Liaison with parent clinics is essential to ensure continuity of management.
Clinics must be informed of significant changes in a patient’s condition or the
requirement for specialist investigations or interventions.
d) Complex investigations (e.g. CT, MRI scans) and procedures should be authorised
by the duty consultant and discussed with the parent clinic where appropriate.
H. Documentation
The following guidelines are designed to facilitate the recording of clear, relevant
information that is essential for continuity of care, audit and medico-legal review.
Entries should establish a balance, being concise but still accurately recording all
relevant information and events.
Specific documentation expected from ICU registrars includes:
Admission note for all patients admitted to ICU (Units A, B & C)
Daily entry in case notes during admission.
Handover summary
Discharge summary
Death certificates.
1. Admission Notes
a) All patients admitted to Units A & B must have a detailed admission summary.
i) The admitting clinic must be notified by the admitting registrar and invited
to record an admission summary for patients admitted directly to ICU.
This is to ensure that clinics are aware when a patient has been admitted
under their bedcard.
ii) The admission note should incorporate all relevant aspects of the patient’s
medical history, clinical examination and investigation results.
b) Complicated Unit C patients require the same detail as Unit A & B patients.
c) Routine postoperative, short stay patients in Unit C do not need detailed
admission notes. In these patients record:
i) Relevant operative & anaesthetic details
ii) Significant comorbidities and history
iii) Anticipated problems
iv) Procedures e.g. epidural, invasive monitoring, TPN
2. Daily case-note entries
a) A daily entry must be made in the case notes.
i) Notes are most efficiently recorded after the 11:00 ward round so that
current results and management plans are recorded
b) Additional notes must be made for the following:
i) Significant changes in physical condition necessitating changes in
management, e.g. renal failure requiring dialysis.
ii) Invasive procedures, e.g. laparotomy, tracheostomy, PAC/CVC insertion
iii) Results of specific investigations or tests, e.g. CT scans, endocrine tests
iv) Changes in policy, e.g. non-escalation of treatment, advance directives.
3. Handover summary
a) Due to the large number of complex patients, an ongoing handover summary
should be established for each patient
b) This facilitates ease of handover between day and night resident staff and for the
duty consultant staff.
c) This is not a formal casenote, nor does it take the place of a thorough review of
each patient and their casenotes. This is meant to be an aide-mémoire to be
updated each shift.
d) This is stored in a specific ICU database available on the PCs in the ICU.
4. Discharge summary
a) All patients transferred from ICU (Units A/B/C) require a Medical Transfer
Summary (MR 42) form completed.
b) This is a single page document outlining all relevant transfer information.
c) The original should be filed in the case notes and a photocopy placed in the
marked box in the Unit B station for filing by the secretary.
d) The duty registrar on the day of transfer is responsible for completing the form.
e) Incomplete or missing summaries will be forwarded to the responsible registrar
for completion.
f) Short term Unit C patients do not require detailed discharge summaries, only
pertinent information relating to their stay.
5. Death certificates
a) The following forms need to be completed:
i) RAH Notification and Certification of Death (MR 150.2)
 all patients including those reported to the Coroner
ii) Death Certificate ("the yellow form")
 do not complete this for deaths reported to the Coroner
iii) First Medical Certificate
 do not complete this for deaths reported to the Coroner
b) Deaths notifiable to the Coroner:
i) Contact the Coroner’s office and provide preliminary demographic details
of the deceased.
ii) The Coroner’s office will then fax the Medical Practitioner’s Deposition
form for you to complete and return by fax.
iii) File the original deposition in the patient’s case-notes.
Consent in ICU
1. Competent patients:
a) All competent patients undergoing invasive procedures should have a standard
RAH consent form (MR: 60.16) completed and signed by the patient.
2. Incompetent patients (sedation, coma or encephalopathy):
a) Third party consent is not necessary for routine ICU procedures:
i) endotracheal intubation
ii) arterial lines
iii) central venous lines
iv) pulmonary artery catheters
v) transvenous pacing wires
vi) underwater seal drains
vii) jugular bulb catheters
viii) intra-aortic balloon counterpulsation
ix) oesophageal tamponade tubes
x) bronchoscopy
b) However, relatives should be informed prior to the procedure if present.
c) The indications, conduct and complications of the procedure should be
documented in the casenotes.
d) Major invasive procedures such as percutaneous tracheostomy, coronary
angiography, permanent pacemaker insertion or major surgical procedures
require completion of a consent form:
i) Emergency procedures signed by two doctors
ii) Non-urgent procedures by third party consent (next-of-kin).
e) Responsibility for consent lies with the operator performing the procedure.
ICU staff are not responsible for consent for procedures performed outside of
ICU, e.g. surgical tracheostomy, or PICC lines placed in radiology
g) A person, not necessarily next-of-kin, who has been nominated by the patient as
a medical power of attorney may sign or refuse consent on behalf of the patient.
h) Relatives should always be informed of any non-routine procedures and the
consent issue explained, irrespective of the presence or absence of a medical or
legal power of attorney.
i) If relatives cannot be contacted, emergency life saving treatment should
proceed immediately, with discussion with the Duty Consultant.
ICU Ward Rounds
1. Grand rounds
a) Held on Mondays and Fridays are an integral feature of the running of the unit.
b) These are open, multi-disciplinary meetings to discuss management issues and are
a valuable teaching forum.
c) Current x-rays and investigation results are displayed via computer projection.
d) The ward round is attended by:
i) Team A, B, C and Duty ICU consultants and all floor registrars
ii) An infectious diseases consultant
iii) Senior nursing staff
iv) Physiotherapists
v) A pharmacist
vi) A dietician
vii) Invited clinics when appropriate
viii) Medical students
e) Registrars are expected to present their allocated patients and to actively participate
in management discussion.
f) Presentations should be of a standard suitable for a fellowship examination:
i) Should take no more than 5-8 minutes.
ii) Emphasise the relevant and pertinent issues only:
 Patient details and demographics.
 State day of ICU admission (e.g. Day 6 ICU).
 Diagnosis or major problems.
 Relevant pre-morbid history pertinent to this admission.
 Relevant progress and events in ICU
(deterioration/improvement, procedures, investigations).
 Current clinical status (system by system).
 Outline features on daily pathology and radiology.
 Current plan of management:
a. Medications
b. Further investigations / procedures
c. Discharge planning & prognosis
2. Bedside patient rounds
a) Are held daily, including grand-round days.
b) Team consultants and registrars review each patient’s condition.
c) Unit A&B flowcharts are re-written daily and include orders for ventilation,
procedures, medications, infusions and fluid therapy.
i) To ensure all aspects of patient care have been considered, the
“FATDOGS” algorithm should be considered in all patients:
 F - Feeding & fluids
 A - Analgesia & sedation
 T - Thromboprophylaxis
 D - Drugs – therapeutic & usual
 O - Oxygen & ventilation
 G - Glucose control
 S - Sit out of bed
ii) You need to either write up each one of these each day or have a reason
why you have not.
d) Printed stickers should be used for routine medications and infusions.
e) All orders must be signed by a doctor.
f) Requests for routine blood tests are made on the chart.
g) Patients transferred to the general ward or Unit C
i) Should have the hospital “blue folder” completed.
ii) All medication orders should be re-written
iii) Fluid or nutrition orders for the next 24 hours are prescribed.
iv) Patients started on TPN should have their details entered in the “TPN
folder” kept in Unit A.
h) Similarly, Unit C patients have their charts reviewed, however all medications
and fluids are recorded on the hospital blue treatment folders.
K. Clinical Duties Outside of the Intensive Care Unit
1. Policy regarding outside consults:
a) NB: The Unit must not be left unattended at any time to attend outside calls.
(i.e. at least one registrar must remain on the floor)
b) The consults and code-blue/trauma pagers are carried by the Consults Registrar
(D7) during the day and Night Senior overnight (this may be modified at the
discretion of the 1st on-call consultant / senior registrar).
c) All consults should be addressed as soon as possible.
d) If the ICU workload is heavy, refer ward consults to the DI, who will delegate
e) Notify the senior nurse and fellow registrar(s) when leaving the floor.
f) The following duties accompany the Consults pager (pager no #89 22888*):
i) Ward consults
ii) Requests for Total Parenteral Nutrition (refer to Team A SR)
iii) Requests for retrieval (refer to MedStar)
g) The following duties accompany the Emergency pager (#33)
i) Code blue calls
ii) Escalated MET calls
| *see (4) below.
iii) Trauma (P1) resuscitation
 Trauma pages are subdivided into levels
 Attendance by the ICU registrar is only required for Level 1 calls.
h) All consults/MET calls potentially requiring admission to ICU must be
discussed with the Duty Intensivist (DI).
2. Ward Calls
a) Consults regarding potential admissions from the general wards, theatre or ED.
b) Pre-operative consults for potential or booked surgical patients.
c) Advice regarding fluid and electrolyte management, oxygen therapy, sedation and
analgesia (usually referred to APS).
d) Review as requested patients in the:
i) Spinal Injuries Unit with potential respiratory failure.
ii) Burns Unit for airway / breathing assessment, IV access or resuscitation.
e) Requests for venous access:
i) Requests must come from registrar level or above and after reasonable
attempts have been made to obtain IV access.
ii) Radiology provide a PICC line service in working hours.
iii) CVCs are not to be inserted on ward patients.
iv) Should be attended to in a timeframe appropriate to the patient’s condition.
f) Requests for TPN.
3. Total Parenteral Nutrition (TPN)
a) ICU provides a TPN service for the hospital.
b) Requests for TPN are elective (i.e. Mon to Fri: 0800-1800) and should be made
according to recommended indications.
c) Requests are made via the DI or consults registrar.
d) The ‘TPN Folder’ is kept in the Unit A ward station.
e) The Team A Senior Registrar and Consultant will manage:
i) Initial consultation with the requesting clinic.
ii) Recording TPN patients in the “TPN Folder”.
iii) Insertion of a PICC catheter.
iv) Daily:
 Review of electrolytes and fluid balance,
 Review of the central venous catheter/PICC,
 Prescription of TPN orders ± vitamins / trace elements,
 Issue a request form for serum electrolytes.
 Use pink labels from ICU & leave a spare for labelling of specimen tubes
- this ensures priority in the lab
f) Refer to the section on nutrition in the clinical protocols for indications &
4. Code Blue & MET Calls
a) The RAH medical emergency code is “33#”.
i) Upon dialling 33#, switchboard automatically page the following people:
 ICU registrar
 ICU equipment nurse
 Medical registrar
b) These calls are divided into:
i) Code Blue
*all calls must be attended immediately
 Cardiac &/or respiratory arrest (actual or impending)
 Threatened airway
 Major haemorrhage
ii) MET calls
 Significant clinical deterioration (see MET criteria)
 MET calls are not routinely attended by ICU Registrars.
 The ICU Registrar should remain immediately available if a MET call
has been activated, so that assistance can be provided to the MET team if
required (e.g. avoid starting procedures such as CVC insertions if the
MET pager has activated).
c) When “33” is displayed on the pager:
i) Dial “33#” on an internal phone.
ii) Switchboard will then state the location of the arrest.
iii) Clearly state who you are (i.e. ICU registrar) and go to the location.
d) Ensure that the ICU staff know where you are going and that the Unit is not left
e) At the emergency:
i) This hospital follows the Australian Resuscitation Council guidelines for
cardiopulmonary resuscitation.
ii) The ICU/resuscitation registrar is responsible for initial assessment, securing
the airway and establishing effective ventilation.
iii) Basic life support is done by attending nursing and medical staff and may be
directed by either ICU or medical registrar.
iv) Advanced life support is directed by the more senior registrar present. This is
usually the ICU registrar.
v) Depending on the outcome of the Code Blue, the patient may be admitted to
ICU, CCU or remain on the ward according to standard admission policies.
vi) As a general rule, it is better to admit a patient if previous details are not
immediately available than to prematurely abandon resuscitation.
vii) Document your involvement with the resuscitation in the casenotes.
viii) The home team should be involved or at least informed of their patient’s
condition, including when resuscitation is unsuccessful.
5. Trauma Calls
a) As in cardiac arrest, a “33#” call is activated for trauma patients who meet
specified trauma criteria. (Refer to trauma directives.)
b) Trauma pages will appear as 2 Levels:
i) Level 1: major trauma requiring immediate attendance / airway support
ii) Level 2: trauma requiring full assessment in ED/Resus.
c) The following people are paged and the level response detailed on the pager:
i) ICU/resuscitation registrar
ii) Trauma Service registrar
iii) Accident and emergency registrar
d) On receiving a Level 1 call the ICU registrar should proceed directly to Resus in
the Emergency Department (ED)
e) Ensure that ICU staff know where you are going and that the Unit is not left
f) At the trauma resuscitation:
i) This hospital follows the Early Management of Severe Trauma (RACS)
ii) The team leader is designated by the current Trauma Service Directive (found
on the wall in Resus).
iii) Role of the ICU registrar:
 Primarily as a backup for acute life threatening situations in the event that
sufficiently experienced personnel are not available in Resus.
 If anaesthetic staff are present in Resus, there is no requirement for ICU
registrars to attend the resuscitation unless specifically requested by these
personnel or the Trauma Director.
 If anaesthetic staff are not immediately available, the following role is
indicated until appropriate personnel arrive:
a. Initial airway assessment and management.
b. Establishing effective ventilation
c. Assistance with vascular access and restoration of circulation.
d. Other acute interventions (e.g. UWSD) as required
 Once anaesthetic & trauma team members are present and the situation is
under control, return to ICU - do not leave ICU unattended for lengthy
periods of time.
 If prolonged resuscitation is anticipated, call in the ICU or Trauma
Consultant and/or delegate to the anaesthetic/resuscitation registrars.
 Transportation of trauma patients to CT scan, angiography etc. is the
responsibility of the emergency anaesthetic staff.
 ICU registrars must not do prolonged intra-hospital transports for trauma
patients without approval by the duty ICU consultant.
iv) General principles:
 Document your involvement with the resuscitation in the casenotes
 Once the primary survey is completed, proceed to the secondary survey
and order appropriate investigations as per the Trauma team leader.
 In critically ill patients, ensure that a suitably qualified person (in terms of
resuscitative skills) remains with the patient at all times. This is
mandatory if the patient is transported from Resus (e.g. to radiology,
ICU, theatre).
 Notify ICU staff of pending admissions.
 Demarcation disputes are referred to the duty Trauma Consultant.
6. Retrieval Requests
a) Requests for consultation may originate from a number of sources. Namely,
i) The DI phone (SD: 1650)
ii) Other ICU telephones
iii) ICU registrar pager
iv) Other clinics who have been consulted by outside medical officers.
b) All retrieval requests should be referred immediately to the state retrieval
service, MedStar on 82224222.
c) All requests from MedStar for the transfer of patients to the RAH must be
referred to the on-call ICU consultant.
7. Intrahospital transportation of Intensive Care patients
All transports must be authorised by the duty ICU consultant.
The transport/investigation must be considered in the best interests of the patient.
All ventilated and potentially unstable transports need a medical escort.
Stable, self-ventilating patients may be transported by an ICU RN
If ICU nursing staff are concerned, then a medical escort is required.
At no stage must the unit be left uncovered.
If the Unit is busy, or transports clash with ward rounds, other personnel may be
deployed to do the transport. This is coordinated by the duty ICU consultant.
h) As a general rule, ICU staff are responsible for transportation of ICU patients.
i) Anaesthesia is responsible for transport of the following ICU patients:
i) Trauma resuscitation patients
ii) Patients to and from theatre
iii) Patients to and from hyperbaric medicine.
j) The transport of patients undergoing prolonged investigations or treatments, (e.g.
MRI, angiographic embolisation, invasive radiological procedures, TIPS) should
be discussed with the Duty ICU consultant and Duty Anaesthetist (SD 1175)
k) Guidelines
i) Registrars must familiarise themselves with transport monitors, portable
ventilators and infusion pumps.
ii) Inform and discuss the transport with the nursing staff as soon as possible.
iii) Patients must be appropriately monitored during the transport and
observations recorded on the flow chart.
iv) Document any problems which may occur during transport.
v) Ensure that the results of investigations performed (e.g. CT scans etc) are
recorded in the case notes by the appropriate person.
Hospital Emergencies
1. The emergency number is 33# : state the nature and location of emergency
2. Fire
a) A copy of the hospital emergency procedures (fire, smoke, bomb-threat) is kept in
the P4A and P4C nursing stations.
b) The chief fire and emergency officer is the overall controller during a fire or smoke
emergency (Code Red).
c) Become familiar with the location of fire exits, extinguishers and blankets in ICU
i) Unless small and easily contained do not attempt to fight a fire yourself.
ii) Remove yourself from the immediate vicinity of the fire, alerting other staff
members as indicated, and position yourself behind the automatic fire doors.
iii) The MFS has a 3 minute response time to the RAH.
iv) Wait for the arrival of the Fire Chief and assist in any patient
movement/evacuation only as indicated by the Fire Chief.
d) Role of medical staff:
i) There is no place for “heroic” action - ensure your own safety first!
ii) Wait for the arrival of the MFS.
iii) Assist in patient assessment/management under the coordination of the Fire
iv) In the event of a significant fire / smoke hazard, staff will only re-enter the
danger zone in the immediate company of a MFS fire-fighter, with
appropriate breathing apparatus.
M. Research in ICU
1. Background:
There is a prolific research programme at the RAH ICU. This research is world
leading in the areas of gastrointestinal motility, nutrient absorption and incretin
hormones in the critically ill.
2. Personnel:
a) Director of Research
b) Research Fellow
c) Research Manager
d) Research Nurses
e) Research Scientists
- A/Prof. Marianne Chapman
- Dr Adam Deane
- Ms Stephanie O’Connor
- Ms Justine Rivett
- Mr Luke Chester
- Ms. Alison Ankor
- Mr Matthew Summers
- Mr Antony Zaknic
3. There are students studying toward their higher degrees frequently working in the
ICU. These students are strongly supported by the ICU Research Unit. Trainees
interested in undertaking a higher degree are always well received.
4. There are broadly 3 types of research studies occurring in the unit:
a) Locally initiated studies
b) Drug company sponsored studies
c) Studies performed with the ANZICS Clinical Trials Group (see below).
5. Medical and nursing staff are encouraged to become involved in research:
a) Registrars are expected to assist in obtaining consent for ongoing studies.
b) Knowledge of these studies can be obtained from any of the research staff.
c) Further involvement is encouraged and there are supports within the unit to
facilitate research to occur.
d) Because the ICU is a world-leader in several areas, it is advised to leverage on
the expertise and availability of sophisticated methodologies within the group.
However, independent projects, driven by highly committed individuals, will
always be supported.
6. The CICM formal project takes, at a minimum, 12 months to complete.
a) Trainees interested in undertaking a study for their formal project are advised to
approach potential supervisors with sufficient time to complete their project.
b) Potential projects (and initial contact persons) are:
i) Retrospective observational studies (A/Prof Flabouris and Dr Finnis)
ii) Prospective observational studies (Dr Sundarajarajan)
iii) Experimental work using a sheep model (Dr Maiden)
iv) Laboratory based work (Dr Reddi) and
v) Prospective clinical research (A/Prof Chapman and Dr Deane).
7. Most projects require prior RAH Research Ethics Committee approval. Your
supervisor will be able to provide details.
8. Completed research projects should be presented at either a local or interstate
scientific meeting.
a) Partial funding is available for staff who present work at approved meetings.
b) Applications should be made to the Coordinator of Research.
c) Eligible meetings include, but are not limited to:
i) ANZICS / ACCCN Annual Scientific Meeting - October.
ii) CICM Annual Scientific Meeting – May/June.
iii) ACCCN (Institute of Continuing Education), Conference. Annual – May.
9. ANZICS Clinical Trials Group (CTG).
a) A national clinical trials group to facilitate multicentre trials in Australia & NZ.
b) World-leading in critical care research and is open to all interested parties.
c) CTG meetings are held once per season, with the main meeting in March.
d) Resource person: A/Prof. Marianne Chapman.
10. If you are unsure of what to do about a patient enrolled in a study, please contact the
relevant staff member regardless of the time of day.
a) Queries about drug company sponsored studies should be directed to the ICU
Research Nurse on-call (SD 1520)
b) Queries relating to a local investigator studies should be directed to the primary
Information Technology in ICU
a) All consultant and registrar offices and the Registrar Teaching Room are
equipped with PCs, connected to the RAH local area network (LAN).
b) Facilities available through the LAN include:
i) Intranet e-mail accounts
ii) WWW browsing facilities (available on application).
iii) Intranet resources, which are being continuously expanded:
 UpToDate®, eMIMS, Medline, Toxnet, etc.
 An extensive range of electronic text books
 ICU Handover Database
iv) On application registrars will be allocated a username, which will carry
with it an ‘Internet’ e-mail account for the duration of their stay.
c) In addition, many of the consultants have access to the University of Adelaide,
including Barr-Smith Library resources.
d) The Unit has an internet presence at http://www.icuadelaide.com.au/
e) NB: Use of hospital computers to access inappropriate material is not tolerated.
RAH guidelines detail appropriate use.
1. Registrars are encouraged to become proficient in all Intensive Care procedures.
2. Invasive procedures should be authorised by a senior registrar or the duty ICU
3. Adequate familiarisation and supervision with unfamiliar procedures is essential:
there is always someone available to help.
4. The relative risk vs. benefit of all procedures must be carefully considered.
5. Do not persist if you are having difficulty with the procedure - call for help.
6. Consent for procedures:
*refer to Administration / Consent
a) Competent patients undergoing invasive procedures should have a standard
RAH Consent Form (MR:60.16) completed and signed by the patient
b) Third party consent is not necessary for incompetent patients undergoing
routine ICU procedures.
c) Major ICU procedures, such as percutaneous tracheostomy or
enterogastrostomy, require third party or two-doctor consent.
7. The indications, conduct and any complications of the procedure should be clearly
documented in the case notes, in addition to a consent form if this is completed.
8. Discuss the planned procedure with the nursing staff and allow sufficient time for
setting up of trays and equipment.
9. Remember: the nursing staff have extensive experience with these procedures.
10. It is the responsibility of the operator to discard all sharps used in the procedure and
to ensure that they are placed in a sharps disposal container.
1. Registrars are expected to become proficient in all routine procedures.
2. Where appropriate trainees are expected to learn to place lines both
a) Via surface anatomical landmark, and
b) With ultrasound guidance
3. Whilst ultrasound may aid in delineating the relevant anatomy:
a) Trainees will find themselves in environments where U/S is unavailable
b) The time delay involved in the use of U/S may be clinically deleterious, and
c) There are insufficient data that the use of U/S actually reduces complications.
4. Specialised procedures are done either by the Duty Consultant or strictly under
consultant supervision.
5. Guidelines for the listed routine and specialised procedures are outlined in the
following sections.
Routine ICU procedures
Endotracheal intubation
Peripheral venous catheterisation
Arterial cannulation
Central venous catheterisation / PICC line insertion
Urinary catheterisation
Lumbar puncture
Epidural catheterisation
PiCCO Catheter
Pulmonary artery catheterisation
Pleural Drainage
Underwater seal drain insertion
Nasogastric tube insertion
Specialised ICU procedures
Fibreoptic bronchoscopy
Percutaneous tracheostomy
Cardiac (transvenous) pacing
Intra-aortic balloon counterpulsation
Oesophageal tamponade tube insertion
Extracorporeal Membrane Oxygenation
Peripheral IV Catheters
1. Indications:
a) First line IV access for resuscitation, especially blood transfusion
b) Stable patients where a CVC is no longer necessary
2. Management protocol:
a) Remove/replace all resuscitation lines inserted in unsterile conditions.
b) Generally avoid peripheral IV use in ICU patients and remove if not in use.
c) Use local anaesthesia in awake patients.
d) Aseptic technique:
i) Handwash with AVAGARD® (chlorhexidine 2%) or
MEDISPONGE® (chlorhexidine 4%) + gloves
ii) Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol)
iii) Dressing:
Opsite® or equivalent occlusive dressing
e) Change / remove all peripheral lines after 48 hours.
f) Avoid lower-limb placement in patients with vascular disease.
3. Complications
a) Infection
- local and systemic
b) Thrombosis
c) Extravasation in tissues
Arterial Cannulation
1. Indications:
a) Routine measurement of systemic blood pressure in ICU
b) Multiple blood gas and laboratory analysis
c) Measurement of BP during transport of patients in hostile environments
2. Management protocol:
a) Remove and replace lines inserted in unsterile conditions as soon as possible.
b) Brachial and femoral arterial lines should be changed as soon as radial or
dorsalis pedis arteries are available.
c) Aseptic technique:
i) Handwash with
AVAGARD® (chlorhexidine 2%) or
MEDISPONGE® (chlorhexidine 4%) + sterile gloves
ii) Skin prep. with
SOLU-IV (chlorhexidine 2% / 70% alcohol)
d) Local anaesthesia in awake patients.
e) Cannulae:
i) Arrow® radial or femoral kits (Seldinger technique).
ii) 20G Insyte®.
iii) Single lumen 20G CVC (paediatric) for femoral arterial lines.
f) Insertion sites – in order of preference:
radial > dorsalis pedis > femoral > brachial
g) The femoral artery may be the sole option in the acutely shocked patient.
h) Secure with a StatLock® device.
i) There is no optimal time for an arterial line to be removed or changed.
j) IA cannulae are changed/removed in the following settings:
i) Invasive IA line is no longer necessary.
ii) Distal ischaemia
iii) Mechanical failure (overdamped waveform, inability to aspirate blood)
iv) Evidence of local or unexplained systemic infection
k) Measurement of pressure:
i) Transducers should be ‘zeroed’ each nursing shift
ii) Zero reference = the mid-axillary line, 5th intercostal space
l) Maintenance of lumen patency
i) Continuous pressurised (Intraflo®) saline flush at 3ml/hr.
3. Complications
a) Infection
b) Thrombosis / digital ischaemia
c) Vessel damage / aneurysm
d) Haemorrhage / disconnection
Central Venous Catheters
NB: Registrars should be familiar with the interpretation and limitations of
haemodynamic variables derived from central catheters (CVC, PICCO and PAC) in
critically ill patients.
1. Indications:
a) Standard IV access in ICU patients:
i) Vasoactive infusions
ii) Fluid administration (including elective transfusion)
iii) Hypertonic solutions (TPN, amiodarone, nimodipine, etc.)
b) Monitoring of right atrial pressure (CVP)
c) Venous access for:
i) Pulmonary artery catheterisation (PAC)
ii) Continuous renal replacement therapy (CVVHDF)
iii) Plasmapheresis.
iv) Transvenous pacing.
v) Jugular bulb oximetry.
d) Resuscitation
i) Large bore peripheral IV line(s) are 1st line.
ii) Standard lumen CVCs are not appropriate for acute volume resuscitation.
iii) Consider using a PAC sheath or Vascath if central access is required and
adequate peripheral access is unobtainable.
2. Management protocol: (applies to all types of CVC):
a) Types:
i) The default CVC for all ICU patients is a Cook antimicrobial
impregnated (rifampicin/minocycline) 7F 15 or 20cm 3-lumen catheter.
ii) Non-impregnated catheters inserted outside the ICU should be changed to
an impregnated catheter according to clinical indication.
iii) Dolphin Protect® catheters are used for CVVHDF and plasmapheresis
iv) Pulmonary artery catheter sheath (part of the PAC kit)
v) Dress non-impregnated catheters with a BioPatch®
b) Sites:
i) Preferred site for routine stable patients → SCV > IJV.
ii) Femoral v. access is preferable where:
 Dolphin Protect® / CVVHDF
 Limited IV access (burns, multiple previous CVC’s),
 A thoracic approach is considered hazardous with:
a. Severe respiratory failure from any cause (PaO 2/FiO2 < 150)
b. Hyper-expanded lung fields (severe asthma, bullous disease)
c. Coagulopathy (see below)
 Inexperienced staff requiring urgent access, where supervision is not
immediately available.
c) Coagulopathic patients:
i) INR > 2.0 or APTT > 50s
correct with FFP and/or
ii) INR 1.5-2.0 or APTT 40-50s 
correct with FFP, or
use IJ or femoral approach
iii) Platelets < 50,000
transfuse 1 pack (5U) platelets
 Failure to increment
femoral approach or PICC
iv) Uncontrolled coagulopathy
femoral approach or PICC
 Including recent therapy with Dabigatran
v) Insertion under ultrasound guidance may be preferred.
d) Technique policy
i) Use local anaesthesia in awake patients.
ii) Strict aseptic technique at insertion:
 Handwash with
AVAGARD® (chlorhexidine 2%) or
MEDISPONGE® (chlorhexidine 4%)
 Sterile barrier:
gown, sterile gloves, mask, hat
sterile drapes (CVC - Patient Cover)
 Skin prep. with
SOLU-IV (chlorhexidine 2% / 70% alcohol)
iii) Seldinger technique or ultrasound guided insertion – Sonosite®
iv) U/sound guided insertion may be preferred where:
 There is an increased complication risk (e.g. bleeding, pneumothorax)
 Large bore catheter insertion.
 Distorted patient anatomy.
v) CVC Catheter lengths:
 15cm - right subclavian or internal jugular
 20cm - left subclavian or internal jugular, either side femoral
vi) Secure all lines with a StatLock® device or securely suture
vii) Dressing: non-occlusive dressing
viii) Flush all lumens with saline.
ix) Transduce pressure ASAP post-insertion to exclude arterial placement.
x) Check CXR prior to use (SCV, IJV), except in urgent circumstances
e) Maintenance
i) Routine IV administration set change at 7 days.
ii) Daily assessment for infection irrespective of insertion duration.
iii) Catheters remain as long as clinically indicated and are changed when:
 Evidence of systemic infection
a. New, unexplained fever or WCC
b. Deterioration in organ function
c. Positive blood culture by venipuncture with likely organisms
(S. epidermidis, candida spp.), and/or
 Evidence of local infection - inflammation or pus at insertion site.
iv) Guidewire exchanges are actively discouraged. They may be indicated in
the following situations, only after discussion with a consultant:
 Mechanical problems in a new catheter (leaks or kinks)
 Difficult or limited central access (e.g. burns).
Maintenance of lumen patency
 Central venous catheters (pre-printed on the patient flowsheet)
a. Flush unused lumens with 1ml normal saline 8 hourly
 Vascath: into each lumen 8 hourly (printed sticker)
a. Withdraw 2ml and discard.
b. Flush with 2ml normal saline.
c. Flush 1.5ml solution (5000U heparin/3ml = 2500U/lumen).
d. NB: Each lumen has it’s internal volume printed on it.
3. Complications:
a) At insertion
i) Arterial puncture – haematoma, thrombosis, embolism
ii) Pneumothorax, haemothorax, chylothorax
iii) Neural injury (phrenic, brachial plexus, femoral nn.)
b) Passage of wire/catheter
i) Arrhythmias
ii) Wire embolism
*if this occurs, notify senior staff immediately
iii) Perforation of SVC / RA - tamponade
c) Presence of catheter
i) Catheter infection: rates increase under the following conditions:
 Size of catheter - thicker catheters (PAC, Vascaths)
 Site of catheter - femoral > internal jugular > subclavian sites
 Number of lumens
 Nature of fluid through catheters - TPN or dextrose solutions
ii) Thrombosis, HITS secondary to heparin
iii) Catheter / Air embolism
iv) Knotting of catheters (esp. PAC)
v) Pulmonary infarct / arterial rupture (PAC)
NB: Where CVC insertion presents a “significant risk” in a non-urgent
situation, consider insertion of a PICC line as an alternative.
Urinary Catheters
1. Standard in all ICU patients
2. Management protocol:
a) Aseptic technique at insertion.
i) Hand disinfection: surgical scrub with chlorhexidine for >1 minute
ii) Sterile barrier: gloves and sterile drapes.
iii) Skin prep: chlorhexidene 1%
b) Local anaesthesic gel in all patients.
c) Only BiocathTM catheters should be inserted in ICU & changed 6 weekly.
d) Standard Foley catheters should be changed to a BiocathTM after 14 days.
e) Silastic catheters should be changed after 1 month.
f) Remove catheters in anuric patients and perform intermittent catheterisation
weekly, or as indicated.
G. Epidural Catheters
1. Indications
a) Post-operative pain relief (usually placed in theatre)
b) Analgesia in chest trauma.
2. Management protocol:
a) Notify the Acute Pain Service of any epidural placed in ICU.
b) Epidural cocktails should follow the Acute Pain Service protocols
c) Strict aseptic technique at insertion.
d) Daily inspection of the insertion site. The catheter should not be routinely
redressed, except under the advice of the APS.
e) Leave in for a maximum of 5 days and then remove.
f) Remove if:
i) Not in use for > 24 hours, or
ii) Clinical evidence of unexplained sepsis, or
iii) Positive blood culture by venipuncture with likely organisms
(S. epidermidis, candida).
iv) Heparin/Warfarin Protocol
*also see ‘Acute Pain Service Guidelines for Anaesthetists’
3. Complications
a) Hypotension from sympathetic blockade / relative hypovolaemia
i) This usually responds to adequate intravascular volume replacement
ii) Occasionally, a low-dose vasopressor infusion is required
iii) If this is considered, occult bleeding must be excluded.
b) Pruritis, nausea & vomiting, or urinary retention (opioid effects)
c) Post-dural puncture headache
d) Infection: epidural abscess
e) Pneumothorax (rarely)
4. NB: Further guidelines for the management of epidural catheters can be obtained
from “The Acute Pain Service Guidelines for Anaesthetists”. Manuals are stored in
each ICU station.
H. PICCO Catheters
1. Introduction
a) PiCCO uses a combination of thermodilution and pulse waveform analysis to
provide an estimate of cardiovascular status.
b) Trainees should become familiar with the theory of insertion, indications,
interpretation and complications of PiCCO catheters.
c) Indicated in the assessment & response to therapy in shock states.
2. Technique
a) A normal CVC line can be used.
b) The peripheral arterial catheter is inserted into a femoral, brachial or axillary
artery using an aseptic Seldinger technique.
c) The pulse waveform analysis of continuous cardiac output is calibrated by
thermodilution according to the device instructions.
d) Calibration should be repeated once per nursing shift and as indicated.
e) Additional measurements of Global End-diastolic Volume Index (GEDI) and
Extravascular Lung Water Index (ELWI) can be made via thermodilution.
3. Below are the normal values and a suggested decision tree from the manufacturer
which should be used as a guide only:
Table: PiCCO Values and Decision Tree
Cardiac Index
Global End-diastolic Blood Volume Index
Intrathoracic Blood Volume Index
Stroke Volume Variation
 10
Extravascular Lung Water Index*
Pulmonary Artery Catheters
1. Policy
a) Insertion of PA catheters must be authorised by the duty consultant.
b) Trainees should become familiar with the theory of insertion, indications,
interpretation and complications of PACs.
c) Insertion of a PAC must never delay resuscitation of a shocked patient.
d) Allow sufficient time for nursing staff to set up insertion trays and transducers.
e) Remove catheters once they are not being routinely used.
f) They may be left in situ for up to 7 days.
2. Indications:
a) Haemodynamic measurements
i) Aid to diagnosis and response to therapy of shock states,
e.g. cardiogenic, septic or hypovolaemic
b) Measurement of right heart pressures (RAP, PAP):
i) Acute pulmonary hypertension
ii) Pulmonary embolism
iii) Cardiac tamponade
c) Estimation of preload / left heart filling (PAOP)
i) Intravascular volume status & response to fluid loading
ii) LVF
d) Measurement of intracardiac shunt: (Acute VSD)
e) Derivation of oxygen delivery & utilization variables (VO2, DO2)
3. Management protocol:
a) Insertion protocol as per CVC, with the following features:
i) Sheath introducer (8.5Fr) with side port, haemostatic valve and plastic
contamination shield.
ii) Shared transducer for RAP (proximal) and PAP (distal) lumens
iii) Check competence of balloon and concentric position
iv) Ensure all lumens are flushed with heparinised-saline prior to insertion.
v) Ensure the system is zeroed and an appropriate scale (0-40mmHg) on the
monitor prior to insertion.
vi) Insert the catheter observing changing waveforms (RARVPA) on the
monitor, with the balloon inflated and locked, until catheter displays
pulmonary artery occlusion tracing
 Subclavian and left IJ ~ 50cm
 Right IJ
~ 40cm
vii) Deflate the balloon and ensure an adequate PA trace reappears.
viii) Adjust the catheter depth until a PAOP trace appears consistently
with 1-1.5ml balloon inflation.
ix) Suture introducer and attach the contamination shield to the hub.
x) Apply a BioPatch® and non-occlusive dressing.
b) Ensure an adequate PA tracing is on the monitor at all times
c) “Wedged” tracings must be corrected as soon as possible:
i) Flush distal lumen with 2ml N.Saline
ii) Withdraw the catheter until a PA trace is visible
d) Measurement of pressures:
i) Reference pressures to the mid-axillary line
ii) Measure at end-expiration of the respiratory cycle
iii) Do not disconnect ventilated patients to measure pressures.
iv) Measurement of PAOP:
 End expiration: lowest point in ventilated patients, highest point in
spontaneously ventilating patients
 Use the “electronic cursor” on monitors after 2-3 respiratory cycles.
 Do not use the electronic average of the wedge tracing.
e) Haemodynamic measurements
i) These are routinely performed by the nursing staff, however registrars
should become familiar with the procedure.
ii) Record all measurements in the flow chart in the results folder.
iii) Cardiac outputs:
 Injectate: 10ml 5% dextrose @ room temperature
 Inject at random times in the respiratory cycle
 Take > 3 measurements and ignore values > 10% from average.
iv) Derived variables:
 CO/CI and SVR are routinely charted (8 hrly or as indicated).
 Other variables including PVR(I), SV(I), L(R)VSWI are recorded in
the haemodynamics flowsheet.
 Mixed venous oxygen levels should be measured on a sample taken
from the distal (yellow) port.
 Oxygen saturation should be directly measured with co-oximetry.
 Derived haemodynamic variables (see table), should be used in
conjunction with clinical assessment.
4. Complications
a) Related to CVC cannulation (see CVC section)
b) Related to insertion/use of a PAC
i) Cardiac perforation
ii) Thromboembolism
iii) Pulmonary infarction
~ 0-1.4%
iv) Pulmonary artery rupture
~ 0.06-0.2%
v) Catheter related sepsis
vi) Endocarditis
vii) Pulmonary valve insufficiency
viii) Catheter knotting
ix) Balloon fragmentation / embolism
x) Tachyarrhythmias
xi) RBBB
(2 persistent wedging)
(mortality 50%)
Table: Standard Haemodynamic Variables
Normal range
Cardiac index
2.5-5 l/min/m2
Systemic vascular
Systemic vascular
resistance index
 79.9
Pulmonary vascular
resistance index
 79.9
Stroke volume index
LV stroke work index
LVSWI  MAP PAOP  SVI  0.0136
50-120 g/m2 / beat
RV stroke work index
RVSWI  mPAP  PAOP  SVI  0.0136
25-55 g/m2 / beat
Arterial oxygen content
CaO2   Hb  134
.  SaO2    PaO2  0.003
17-20 ml/100ml
Venous oxygen content
CvO 2  Hb  134
.  SvO 2  PvO 2  0.003
12-15 ml/100ml
Oxygen delivery index
DO2 I  CI  CaO2  10
550-750 ml/min/m2
Oxygen consumption
VO2 I  CI  CaO2  CvO2  10
Oxygen extraction ratio
O 2 ER 
Shunt equation
Qs CcO 2  CaO 2
Qt CcO 2  CvO 2
End capillary oxygen
CcO 2  Hb  1.34  1.0  PAO2  0.003
80-100 ml/100ml
Alveolar gas equation
PAO2  FiO2  760  47   PaCO2  125
. 
100-650 mmHg
 79.9
33- 47 ml/beat/m2
 
VO 2 I
DO 2 I
115-160 ml/min/m2
Pleural Drainage
1. Indications:
a) Pneumothorax
b) Tension pneumothorax may require urgent needle thoracostomy
c) Haemothorax
d) Large symptomatic pleural effusion
2. Management protocol:
a) Needle thoracostomy (tension pneumothorax):
i) 14 or 16G cannula placed in mid-clavicular line, 2nd intercostal space
ii) Always place an UWSD following this procedure
b) Pleurocentesis: (pleural effusion)
i) Prior to commencement, ultrasound the chest to confirm the presence of
fluid and indentify/mark an appropriate insertion site.
ii) Strict aseptic technique at insertion:
 Handwash with
AVAGARD® (chlorhexidine 2%) or
MEDISPONGE® (chlorhexidine 4%)
 Sterile barrier:
gown, sterile gloves, mask, hat & drape(s)
 Skin prep. with
SOLU-IV (chlorhexidine 2% / 70% alcohol)
iii) Local anaesthesia in conscious patients.
iv) Seldinger technique:
 Pigtail catheter or ThalQuick® 12F kit.
 Insert guidewire through needle into pleural space
 Insert catheter into pleural space over the wire
 Aspirate intermittently with closed system or attach to an UWSD.
v) Record volume removed and send for MC&S, cytology & biochemistry.
vi) Check CXR post-procedure.
c) Underwater seal drainage:
i) Local anaesthesia in awake patients.
ii) Aseptic insertion technique - as above.
iii) Site:
 Mid-axillary line, 3-5th intercostal space
 Mid-clavicular line, 2nd intercostal space ( air only)
 Do not insert drains through old wounds
iv) ICU patients need large drains: 28F catheter or larger
v) Use soft Mallinkrodt tubes in preference to the stiffer Argyle tubes
vi) Remove the trochar from catheter: do not use the trochar for insertion
vii) For the usual lateral ICD, go for the anterior or mid-axillary lines, avoid
the posterior sites as the chest wall is too thick, and there is a danger to
neurovascular structures
viii) Make a 2-3cm skin incision parallel to the ribs (#10 or #15 scalpel)
ix) Instruments & technique:
 Blunt dissect using short artery forceps, avoid long forceps.
 Do not “plunge” into the chest with either instrument.
 Access to the intercostal space is by careful blunt dissection of the
intercostal muscles above the rib below.
 The chest wall hole must be 2-3 cm wide in order that a finger can be
inserted into the pleural space to identify possible adhesions.
 The soft tube should be guided by the intrapleural finger so that the
tube goes in between the finger and chest wall
x) Connect to an underwater seal drain apparatus
xi) Insert 2 purse string sutures:
 1 to fasten the tube
 1 (‘Z’ or purse-string) to close the skin incision on drain removal.
xii) Insert additional sutures as required to close the external wound.
xiii) Dressing: occlusive dressing (Hypafix)
xiv) Check CXR.
xv) Maintenance
 Remove or replace drains inserted in unsterile conditions ASAP.
 Leave the drain in situ until:
a. Radiological resolution of pleural collection (air/fluid)
b. No ongoing air-leak
(no drain bubbling)
c. Minimal drainage
(< 150 ml/24 hrs).
 In ventilated patients, consider clamping the drain for 4 hours prior to
removal, providing the patient remains stable and/or post CXR.
 Surgically placed drains are the responsibility of the surgeon and
should only be removed in consultation.
3. Complications
a) NB: minimised using the blunt technique
b) Incorrect placement
- extrapleural, intrapulmonary, subdiaphragmatic
c) Pulmonary laceration
- haemorrhage, fistula
d) Pneumothorax
e) Bleeding
i) local incision, intercostal vessels
ii) lung
iii) IMA (with anterior placement)
iv) Great vessels (rare)
f) Infection
i) Soft tissue
ii) Empyema
g) Mechanical (kinking, luminal obstruction)
K. Endotracheal Intubation
1. Policy:
a) Endotracheal intubation in ICU patients is a high risk but vital procedure:
i) Usually an emergency procedure, with limited time.
ii) Usually indicated for acute respiratory failure, or associated with limited
respiratory reserve
iii) Patients may have cardiovascular instability and significant co-morbidities
iv) Patients may have cervical spine or oropharyngeal trauma / surgery
v) Patients are at risk of vomiting and aspirating
vi) Positioning is difficult.
b) Familiarisation with the intubation trolleys, equipment and drugs is essential.
c) Intubation should ideally not be done as a sole operator procedure.
Skilled assistance should always be sought.
d) If you are alone (i.e. after hours):
call for help!
i) Expertise in intubation is always available.
ii) Remember emergency anaesthesia staff.
e) The majority of ICU patients mandate rapid sequence induction.
2. Indications
a) Institution of mechanical ventilation
b) To maintain an airway
i) Upper airway obstruction
 Potential e.g. early burns
 Real
e.g. epiglottitis, trauma
ii) Patient transportation
c) To protect an airway
i) Patients at risk of aspiration
ii) Altered conscious state
iii) Loss of glottic reflexes
d) Tracheal toilet
3. Techniques
a) Orotracheal intubation is the standard method of intubation in this unit.
b) Nasotracheal intubation may be indicated where:
i) Patients require short-term ventilation and are intolerant of oral ET tubes.
ii) Nasal Fibreoptic intubation may be indicated for:
 Oro-maxillary surgery and pathology
 Inability to open the mouth:
e.g. intermaxillary fixation, TMJ trauma, rheumatoid arthritis.
 Upper airway obstruction and nasal route preferred
iii) Contraindicated in base of skull & LeForte facial fractures
c) Methods:
i) Direct laryngoscopy, C-MAC after rapid sequence induction
ii) Fibreoptic bronchoscopic awake intubation (oral or nasal)
iii) Intubating laryngeal mask – LMA – Fastrac®
4. Endotracheal Tubes
a) Standard tube:
i) Low pressure, high volume cuff.
ii) Males:
8-9 mm secure at 21-23cm to incisors
iii) Females: 7-8 mm secure at 19-21cm to incisors
iv) Do not cut tubes to less than 26 cm length
b) Double lumen tubes:
*rarely indicated in ICU:
i) Lung isolation for broncho-pulmonary fistula, abscess or haemorrhage
ii) Inserted as a temporary manoeuvre prior to definitive therapy
iii) Allow differential lung ventilation
iv) Males:
Left 41F
v) Females: Left 39F
vi) NB: right bronchial tubes are harder to correctly site.
vii) Position should be checked with bronchoscope.
c) Intubated patients from theatre may have the following tubes that are not
recommended for prolonged intubation. These tubes must be changed if intubation
is anticipated > 48 hrs and exchange is safe and feasible.
i) Plain PVC tubes
- no above cuff suction port
ii) Armoured tubes
- risk kinking & obstruction
iii) RAE tubes
- difficulty with suction & malposition
5. Protocol for endotracheal intubation in ICU
a) Personnel:
i) Intubation is a 3-4 person procedure - skilled assistance is mandatory
ii) The “top end” intubator coordinates the procedure
iii) One person to administer drugs
iv) One person to apply cricoid pressure (CP) post-induction:
 This is routine for all emergency intubations
 CP is considered safe in the presence of suspected spinal injury.
 CP must be correctly applied - distortion of the larynx and difficulty in
intubation may occur if poorly applied.
v) One person to provide in-line cervical spine immobilisation (trauma and
spinal patients only).
b) Secure adequate IV access
c) Equipment (kept in difficult airway & intubation trolleys in P4-A,B&C).
Ensure the following equipment is available and functional:
i) Adequate light
ii) Oropharyngeal airways
iii) Working suction with a rigid (Yankauer) sucker
iv) Self-inflating hand ventilating assembly and mask
v) 100% oxygen, i.e. working flowmeter at 15 l/min
vi) 2 working laryngoscopes (standard & long blades)
vii) Magill forceps
viii) Malleable introducer and gum-elastic bougie
ix) 2 Endotracheal tubes
 Normal size + 1 size smaller
 Check cuff competence
x) Access to difficult intubation equipment and be aware of the difficult
airway trolley location and its contents.
 Be aware of the Failed Intubation Drill.
 Airtrach, C-MAC, Heine Flex tip
 Intubating Fastrach LMA
 Cricothyroidotomy equipment
a. Percutaneous kit or
b. #15 scalpel & #6.0 cuffed ETT
d) Monitoring (on all patients) :
i) SpO2, ETCO2, ECG
ii) Invasive BP
*desirable but not essential and must not delay intubation
if urgent
e) Drugs
i) Induction agent
- propofol, fentanyl, ketamine, midazolam
ii) Suxamethonium
- 1-2mg/kg is the muscle relaxant of choice.
 Contraindicated in:
a. Burns > 3 days
b. Chronic spinal injuries (i.e. spastic plegia)
c. Chronic neuromuscular disease (e.g. GBS, motor neurone disease)
d. Hyperkalaemic states. (K+ > 5.5)
 Consider Rocuronium (1-2 mg/kg) if Sux. contraindicated
iii) Atropine
- 0.6-1.2mg available
iv) Adrenaline
- 10ml 1:10000 solution available
Procedure: Rapid sequence induction and orotracheal intubation
i) Pre-oxygenate with 100% oxygen for 3-4 minutes.
ii) For patients on mask CPAP/NIV, pre-O2 with the NIV mask
iii) Preload with 250-500ml IV crystalloid
iv) Inotropes may be necessary after induction/intubation
v) Induction agent + suxamethonium
 Induction doses in the critically ill must be modified from routine
doses used in general anaesthesia
vi) Cricoid pressure applied (ensure correct positioning)
vii) Direct visualisation of vocal cords and tracheal intubation
viii) Inflation of cuff until airway sealed
ix) Confirmation of ETCO2
x) Chest and gastric auscultation with manual ventilation
xi) Cricoid pressure released
xii) Secure tube at correct length
xiii) Connect patient to ventilator (see default ventilator parameters)
xiv) Ensure adequate sedation ± muscle relaxant
xv) Consider insertion of a naso/oro-gastric tube.
 Required by the majority of ICU patients.
 Insertion will avoid repeating the CXR.
xvi) Chest X-ray
xvii) Confirm blood gas analysis and adjust FIO2 accordingly.
g) Sedation post-intubation:
i) None if comatose or haemodynamically unstable
ii) Propofol ± fentanyl infusions as clinically indicated.
6. Maintenance of endotracheal tubes
a) Securing to face
i) Secure ETT with white tape after insertion.
ii) Ensure that the loop of tape is snug around back of neck but not too tight to
occlude venous drainage  should allow 2 fingers under tape.
iii) Re-secure with adhesive tape once CXR check done.
b) Cuff checks
i) Volumetric tests are done following insertion and whenever a leak is
detected: sufficient air to obtain a seal + 1ml
ii) Seal is assessed by auscultation over trachea during normal ventilation.
iii) Manometric tests are inaccurate and do not correlate with mucosal
pressure. These are an adjunct only if cuff malfunction is suspected.
c) Persistent cuff leaks
i) Tubes requiring more than 8ml of air to obtain a seal or if there is a
persistent cuff leak must be examined by direct laryngoscopy as soon as
 Even if taped at the correct distance at the teeth.
 Ensure that the cuff has not herniated above the cords
 Tube has not ballooned inside the oral cavity and “pulled’ the cuff
above the cords.
ii) Patients at high risk for cuff leaks:
 Nasal RAE’s
- prone to outward migration
 Cut tubes
- do not cut tubes < 26 cm
 Facial swelling
- burns, facial trauma
 Patients requiring high airway pressures during ventilation
7. Endotracheal tube change protocol
a) Ensure adequate skilled assistance, equipment, drugs and monitoring as for de
novo intubation.
b) Procedure
i) Set the FIO2 = 1.0 and change SV modes to SIMV.
ii) Ensure sufficient anaesthesia and muscle relaxation (fentanyl / propofol +
neuromuscular blockade)
iii) Perform laryngoscopy and carefully identify:
 Patency of upper airway after suction
 Anatomy of larynx
 Degree of laryngeal exposure and swelling.
iv) IF clear view of larynx and no or minimal laryngeal swelling:
 Application of cricoid pressure by assistant and careful, graded
extubation under direct laryngoscopic vision.
 Maintain laryngoscopy and replace tube under direct vision.
IF impaired visualisation of larynx:
 Re-evaluate the need to change ETT
 Use gum elastic or ventilating bougie
 Place bougie through tube under direct vision and insert to a length
that would be just distal to the end of the ETT (approximately 30cm
from end of tube)
 Have an assistant control the bougie so that it does not move during
movement of the endotracheal tube
 Application of cricoid pressure by assistant and careful, graded
 Maintain laryngoscopy and ensure bougie is through the cords on
 Replace tube over bougie and guide through larynx under available
 Inflate cuff, check ETCO2, auscultation and expired tidal volume
 Release cricoid pressure.
 Secure tube with tape.
Weaning Guidelines
1. Commencement of weaning is a medical decision.
2. Weaning is contraindicated with any of the following:
a) Unstable ICP (abort weaning if ICP increases)
b) Need for heavy sedation (e.g. upper airway obstruction)
c) Haemodynamic instability
d) Significant bronchospasm
e) High work of breathing.
3. Trial pressure support daily if the patient meets both the following criteria:
a) PaO2/FiO2 ratio > 150
b) Patient can take spontaneous breaths if SIMV resp-rate reduced.
4. Weaning protocol:
a) See the flow diagram following page.
b) Set initial pressure support to maintain adequate VT
i) Start at 10 cmH2O and adjust to:
 VT ≤ 6 ml/kg IBW for patients recovering from ARDS.
 VT ≤ 8 ml/kg IBW for all others.
 IBW Males
= 0.91 × (height [cm] – 152.4) + 50
 IBW Females = 0.91 × (height [cm] – 152.4) + 45.5
ii) Alternatively, use target VT = 80-100% of set SIMV VT
iii) Allowable PS range = 5-25 cmH2O
 If VT cannot be achieved with 25cmH2O, cease trial
c) Assess at 15 and 30 minutes for “weaning success criteria”
d) Assess each hour for suitability to wean PS
e) Once PS has reached minimum (5cmH2O) then wean PEEP to 5cmH2O
f) If PS & PEEP = 5cmH2O then assess for extubation.
5. Weaning Success Criteria:
i) RR
< 30/min
ii) SpO2 > 90%
 May be set lower with COPD, e.g. >86-88%
iii) FIO2 ≤ 0.5
iv) No respiratory distress as shown by 2 or more of the following:
 HR > 120% baseline
 Accessory muscle use
 Diaphoresis
 Paradoxical abdominal movements
 Marked dyspnoea
Flowchart: Ventilation Weaning Protocol
NO Weaning Contraindication:
PaO2/FiO2 > 150
PEEP < 10 cmH2O
“Start Weaning” Settings:
 Reduce patient sedation
 Reduce SIMV-Rate to 8bpm
 Adjust initial PS to target VT
8ml/kg IBW, or
6ml/kg IBW if ARDS
 Allowed PS range (5-25 cmH2O)
 PEEP remains on previous setting.
Unstable ICP
Need for heavy sedation
Haemodynamic instability
Significant bronchospasm.
Check each 15 minutes Weaning Success Criteria:
< 30/min
SpO2 > 90% (*lower in COPD)
≤ 0.5
No respiratory distress as shown
by 2 or more of the following:
HR > 120% baseline
Accessory muscle use
Paradoxical muscle movements
Marked dyspnoea
Weaning Failure:
 IF post PS decrease 
return to previous settings
*note change to PS decrease rate
 IF post return to settings 
set PS to max = 25 cmH2O
 IF on maximum PS 
return to SIMV settings
 IF PSMax or SIMV, patient should
be reviewed by SR or Consultant
Weaning Complete:
 If PS = 5 & PEEP = 5 cmH2O
 Check ABG
 Assess for Extubation – see over.
Assess After Each Hour Set Pressure Support Level:
 If weaning successful after 1st
 cease SIMV
 If successful on subsequent hours
 decrease PS, as per …
 If no previous weaning failure
 decrease PS by 4 cmH2O
 If previous episode of failure
 decrease PS 1-2 cmH2O
 If at minimum PS = 5 cmH2O
 decrease PEEP by 1-2 cmH2O
M. Extubation
1. The decision to extubate is made by medical staff, in consultation with either the
senior registrar, fellow or duty consultant.
2. Extubation is to be performed by medical or senior nursing staff, with airway
competent medical staff immediately available.
3. Criteria to predict successful extubation are helpful, however, ongoing success
should never be assumed:
a) FiO2
< 0.5 with PEEP ≤ 5 cmH2O
b) PaO2
> 70
** lower values may be appropriate in
> 90%
chronically hypoxaemic patients
c) RR
< 30
with PS ≤ 5cmH2O (Dräger)
d) pH
> 7.2
e) No respiratory distress (see over)
f) Patient able to obey commands
g) Patient able to protect airway and cough
h) Patient able to cope with amount of secretions
i) Reason for intubation resolved.
*this may include checking for an air leak with the cuff deflated
4. Early extubation to NIV may be considered for some patients who present with
hypercapnic exacerbation of COPD or pulmonary oedema:
a) Performed with close supervision by senior medical staff.
b) If no improvement after 1-2 hrs, the patient should be considered for
5. Extubation protocol:
a) Ensure equipment, monitoring and adequate assistance is available, as for
b) Plastic surgical and ENT patients with intermaxillary fixation/wiring require
consultation with the Parent Clinic.
i) A wire cutter must be present in the room at all times.
ii) The parent clinic should be given opportunity to be present during extubation
if the jaws are wired.
c) All patients should receive supplemental oxygen pre/post-extubation.
Emergency Surgical Airway Access
1. Policy
a) Call for skilled assistance then proceed without delay.
b) Difficult airway & failed intubation trolleys are in areas A, B & C
c) Cricothyroidotomy, percutaneous or surgical, is the recommended procedure for
urgent surgical airway access and emergency oxygenation.
d) Standard percutaneous tracheostomy is not an emergency procedure.
e) Cricothyroidotomy is a temporary airway - arrange a definitive surgical airway
(ENT surgeons) as soon as possible.
2. Indications:
a) Refer to the failed intubation drill in the clinical protocols section.
b) Inability to establish an effective airway following failed laryngoscopy despite:
i) Basic manoeuvres
- jaw thrust / chin lift / oral-nasal airways
ii) Attempted LMA insertion
c) Inability to ventilate.
3. Cricothyroidotomy
a) Percutaneous technique
i) Equipment
 Cook Melker Emergency Cricothyrotomy Catheter kit (cuffed)
ii) Procedure
 Palpate cricothyroid membrane with neck well extended
 1cm horizontal incision through skin
 Locate tracheal lumen with fluid-filled syringe & needle/cannula
 Insert wire through cannula, then remove the cannula over the wire.
 Insert dilator/introducer & tube assembly over wire in single motion
 Remove wire & introducer leaving the cuffed tube.
 Inflate cuff & suction prior to ventilation.
 Confirm endotracheal placement with ETCO2 & CXR.
b) Surgical technique
i) Equipment
 Size 15 scalpel + handle
 Size 6.0 cuffed endotracheal tube
 Straight forceps
 Oxygen delivery circuit: Laerdal bag
ii) Procedure
 Palpate cricothyroid membrane.
 2cm horizontal incision through skin and cricothyroid membrane
 Insert forceps into wound and open to enlarge the wound
 Consider insertion of long blue ventilating bougie into trachea
 Insert endotracheal tube, directly into the trachea or over bougie
 Remove bougie and connect oxygen circuit
 Confirm placement with ETCO2, auscultation and CXR
 Perform catheter suction ASAP after adequate oxygenation
O. Fibreoptic Bronchoscopy
1. Policy:
a) This is only to be used by skilled personnel and authorised by the duty consultant.
b) Under no circumstances may the bronchoscope be loaned to other clinics.
c) Expertise with bronchoscopy takes time. Registrars are encouraged to approach
the Department of Thoracic Medicine to attend bronchoscopy clinics to become
familiar with the anatomy of the tracheobronchial tree and use of the flexible
2. Indications:
a) Semi-elective difficult intubation: not used as an aid to failed intubation
b) Luminal obstruction
i) Sputum retention - persistent collapse refractory to physiotherapy
ii) Foreign bodies
iii) Luminal pathology - diagnostic
c) Diagnostic bronchoalveolar lavage (BAL)
3. Protocol for fibreoptic intubation
a) Indication as per endotracheal intubation
b) Procedure
i) All equipment, drugs and monitoring c.f. routine endotracheal intubation
ii) Supplemental oxygen must be given
 Routinely via a mask – this may need to be cut to facilitate intubation
 May also be given via the suction channel of the bronchoscope
iii) Can be via oral (with bite protection mandatory) or via nasal route
iv) Local anaesthesia / preparation of the airway:
 Nasal mucosa
- topical 10% lignocaine or 2% amethocaine spray.
 Pharynx
- viscous lignocaine gargle
 Larynx
- choice according to operator experience
a. Transtracheal injection and/or direct application through the scope
b. Nebulised
- 5 mls 4% lignocaine
c. Superior laryngeal nerve blockade (2-3ml 1-2% lignocaine).
v) Check ET tube cuff
vi) Place a warmed appropriately sized ETT (7mm tube for either sex) into
posterior nasal space.
vii) Insert the scope through the tube under direct vision.
viii) Identify the vocal cords and advance the scope into the trachea.
ix) Advance the ETT over scope into trachea, maintaining view of the tracheal
rings or carina, then remove the scope.
x) Confirm ETT placement by ETCO2, auscultation and CXR.
xi) Administer additional sedation/analgesia to the patient as required.
xii) NB: Suction at least 500ml water through scope immediately following use
and notify the equipment nurse for cleaning ASAP.
4. Protocol for BAL
a) Diagnosis of nosocomial pneumonia (colonization vs. infection)
b) Other indications – alveolar proteinosis, eosinophilic lung disease, etc.
c) Sufficient reserve to tolerate procedure:
i) Ideally PaO2 > 70 and FiO2 < 0.7
ii) BAL will commonly result in a 10% reduction in PaO2 for up to 24 hours
after procedure
d) Procedure
i) Ensure sufficient sedation & place patient on 100% oxygen
ii) Select lobe to be lavaged from recent CXR
iii) Local anaesthetic gel is contra-indicated (interferes with culture media)
iv) If possible, do not suction through scope prior to lavage (upper airway
bacterial contamination)
v) Pass the scope directly into the selected lobe
vi) Wedge the scope as far as possible – ideally to 3rd generation bronchi
vii) Lavage with 4-6 x 20-40 ml aliquots of sterile normal saline
viii) Aspirate between aliquots and label aliquots accordingly
ix) Send aspirates for quantitative culture and atypical pneumonia screen.
 NB: label specimens “Immunocompromised protocol” as indicated.
1. Policy:
a) Percutaneous tracheostomy (PCT) is the preferred procedure in suitable patients.
b) To be performed only by consultant staff or advanced ICU trainees.
c) Patients must have the option of surgical tracheostomy cleared by the parent
clinic (either medical or surgical). This is a courtesy.
d) The decision to perform a PCT is at the discretion of the ICU consultant.
e) PCT is an elective procedure and has no place in urgent airway access.
2. Indications :
a) The indications for PCT are the same as surgical tracheostomy:
b) Airway maintenance
i) Prolonged intubation, e.g. > 10 days
ii) Laryngeal pathology – this may also be a contraindication to PCT
c) Airway protection
i) Delayed return of glottic reflexes
ii) Tracheal toilet
3. Relative Contraindications to PCT
a) Lack of consent - absolute
b) Coagulopathy
i) Platelets:
< 100,000
ii) APTT:
> 40
iii) INR:
> 1.5
Difficult anatomy - e.g. previous neck surgery, short fat neck
Unstable cervical spine injury
Grade III or IV intubation (relative – consider use of Glidescope / C-MAC)
FIO2  0.6 / PEEP  10cmH2O
4. Procedure:
a) Ensure consent has been obtained and documented.
b) Equipment, monitoring and drugs as per endotracheal intubation
c) Coagulation screen prior to procedure.
d) Bedside procedure light essential.
e) General anaesthesia - the airway operator must be appropriately experienced.
f) Ventilate the patient on 100% oxygen.
g) Tracheostomy equipment:
i) Standard technique: modified Cook Ciaglia kit using the “Blue Rhino”
ii) Tracheostomy tubes
 EVAC® aspirating tubes are standard for all tracheostomies.
a. Includes patients having surgical tracheostomies
b. Ensure that an EVAC tube goes with the patient to theatre.
 Patients who have non-aspirating tracheostomy tubes in place (e.g.
from CTSU or other hospitals) must have these tubes changed to an
EVAC tube as soon as safe and feasible. This is usually 4-5 days posttracheostomy.
 Other tubes:
a. Foam cuffed tubes - patients with tracheomalacia or persistent air
b. Uncuffed tube (usually #6.0) used in weaning
c. Fenestrated tube: these are either cuffed or un-cuffed with a
fenestration to allow patients to talk.
d. XLT – extended length tubes: useful for patients with marked
neck or soft tissue swelling.
h) Insertion technique:
i) Aseptic technique.
ii) Goggles are essential for both the operator and anaesthetist
iii) Local anaesthetic infiltration (2% lignocaine + 1:200000 adrenaline) over
the pretracheal rings.
iv) Check the tube cuff, lubricate and insert the dilator into the tube.
v) 1.5-2cm horizontal incision over 1st or 2nd tracheal ring
vi) Pretracheal tissue blunt dissection down to fascia
*look for anterior jugular vein and ligate if identified.
vii) Insert a 14G IV cannula mounted on a syringe with saline into trachea and
aspirate through saline/water to confirm intratracheal placement.
viii) Removal the stylet and reconfirm intratracheal placement by aspirating air
via the IV cannula
ix) Insert the guide-wire through the IV cannula and remove the cannula.
Insert the small pre-dilator over the wire into the trachea and make a hole
large enough to accommodate the main dilating instrument.
xi) Blue Rhino® graduated 1-step dilator:
 Lubricate with water, not gel
 Place the dilator and guide cannula (white) over the wire, noting:
a. The black marker on the guide at the proximal end of the Rhino
b. The silver marker on the wire at the proximal end of the guide
 Slowly insert to the required ETT size, ensuring that both markers
(wire and guide) remain in alignment at the proximal end.
xii) Remove the dilator leaving the white guide cannula on the wire and insert
the tracheostomy tube & dilator over the wire/guide into the trachea
xiii) Remove the dilator and wire, inflate the cuff and suction the trachea
xiv) Ventilate and confirm ETCO2 - self-inflating bag or ventilator
xv) Secure tracheostomy tube with tapes.
xvi) Obtain a CXR post procedure.
xvii) Document the procedure in the case notes and complete a separate
operation note.
5. Complications (of tracheostomy)
a) Loss of the airway *immediately re-intubate the patient orally
b) Bleeding
c) False passage
d) Pneumothorax
e) Cricoid cartilage fracture
f) Laryngeal dysfunction
g) Tracheal stenosis
h) Infection
6. Prolonged care of tracheostomy
a) Cuff checks
i) Volumetric (sufficient air to obtain a seal) tests are done following
insertion and whenever a leak is detected with a manual hyperinflation
once per nursing shift.
ii) Manometric tests are inaccurate and do not correlate with mucosal
pressure. These are an adjunct only if cuff malfunction is suspected.
b) Tube changes - routine change at 28 days.
c) Aspirate EVAC tube 2 hourly or more frequently if > 10ml supraglottic
secretion per hour.
Q. Cardiac Pacing
1. Policy:
a) If inserted by ICU staff, the procedure is only to be performed by consultant
staff or advanced vocational trainees under supervision.
b) Become familiar with the theory of insertion, indications, interpretation and
complications of TVP.
2. Indications:
a) Medical pacing with adrenaline or transthoracic pacing may be adequate to treat
some symptomatic bradycardias and has obviated the need for prophylactic
pacing in high-risk patients. NB: particularly for retrievals.
b) Any sustained symptomatic bradycardia which does not respond to medical
treatment, or predisposes to a malignant ventricular arrhythmia.
Note: pacing is indicated by the haemodynamic consequences of the rhythm,
not the arrhythmia per se.
c) Ventricular tachycardias (especially polyphasic) may respond to overdrive
suppression pacing.
d) Following cardiac surgery in high-risk patients (epicardial leads):
i) Valve replacement / repair (especially mitral).
ii) VSD repair / papillary muscle rupture.
iii) Acute myocardial infarction.
3. Types:
a) Semi-rigid, bipolar pacing lead (VVI) inserted under image intensification
(standard TVP at RAH)
b) Epicardial leads
i) Placed during cardiac surgery in high risk patients
ii) Usually unipolar ventricular, but may be bipolar, atrial or ventricular:
check the operative note and liaise with the surgeon.
c) Balloon flotation leads
- ECG or pressure guided catheters
d) Paceport PA catheters
4. Paceport PA protocol
a) VVI mode only
b) Ensure a ventricular demand pacemaker box is available
c) Insert the Paceport PA catheter using standard technique (see PAC section)
d) A pressure transducer should be attached to the RV as well as the distal port
e) The RV port should be 1-2cm distal to the tricuspid valve
i) In some patients the catheter may wedge before the RV port is in the RV in
these cases an alternate technique should be used
f) Attach the adapter to the RV port
g) Insert probe to the reference mark
h) Connect distal electrode to V lead of ECG and advance until ST elevation
indicates contact with the endocardium (usually 4-5cm)
i) Secure the probe and connect side port to a saline flush
j) Commence pacing
k) Check adequate capture and sensing (see next section)
5. Semi-rigid Wire protocol: (VVI lead)
a) Strict aseptic technique
b) Image intensification
c) Local anaesthesia where appropriate
d) Insertion protocol:
i) 6F peel away sheath or PAC introducer
ii) Right IJ vein is the preferred route, then left subclavian.
NB: if permanent pacing is likely then avoid subclavian placement.
iii) Under I-I control, feed the wire until the tip just stops on the RV wall
iv) Connect to the control box (switched off)
v) Set output and sense to their minimum value, and rate 20bpm faster than
the patient's own rate (or 70bpm, whichever is greater).
vi) Turn the generator on and gradually increase the output while watching the
ECG for capture.
vii) If there is no capture or a high output is required:
 Place on demand mode
 Turn output right down, advance or reposition the wire slightly
 Try to capture again. An ideal capture setting is ~ 2 mA
 Ensure wires are not exposed and tape both sides
viii) Suture the wire and apply an occlusive dressing
ix) Arrange a post-insertion CXR.
x) Always be aware of the risk of tamponade even when pacing has been
e) Daily check:
i) Battery strength
ii) Capture: set the output  2x higher than threshold for safety.
6. Flotation Catheter Insertion
a) These may be inserted either “blind”, under ECG guidance (standard
recommendation), or via pressure guidance for catheters having an infusion
lumen (c.f. PA catheter insertion).
b) Aseptic technique & local anaesthesia where appropriate
c) Insertion protocol:
i) 6F peel away sheath, do not use a PAC introducer as these will leak
ii) Attach V5 lead of an ECG to the distal electrode of catheter & monitor
iii) Note P then QRS wave-form changes as the catheter advances to the RV
iv) Advance catheter another 2cm, deflate the balloon & advance 1cm
v) Connect to the pulse generator (switched off)
vi) Set output and sense to their minimum value, and rate 20 bpm faster than
the patient's own rate.
vii) Turn the generator on and gradually increase output while watching the
ECG for capture.
viii) If there is no capture or a high output is required - see (5.d.vii) above
ix) Suture the wire and apply an occlusive dressing
x) Arrange a post-insertion CXR.
1. Policy
a) This procedure must be authorised by an ICU consultant and performed by
consultant staff, trainees under supervision, or cardiology.
b) Confirmation of pericardial effusion or tamponade with echocardiography is
required prior to the procedure, except in peri-arrest situations.
c) Liaison with cardiology is essential.
2. Indications
a) Symptomatic pericardial effusion (tamponade).
b) Although advocated in EMST (ATLS), this procedure has limited utility in
traumatic pericardial tamponade.
3. Procedure
a) Strict aseptic technique.
b) Local anaesthetic infiltration in an awake patient.
c) This procedure should be performed under ultrasound guidance.
d) Technique: Seldinger technique and insertion of a pigtail catheter
i) Insert needle on syringe at 45° from the horizontal axis and aim for tip of
left shoulder
ii) Advance slowly and aspirate until confirmation by aspirating blood or serous
iii) Insert catheter using Seldinger technique over guidewire.
iv) Confirm placement by aspiration and/or echocardiography
v) Check CXR (pneumothorax)
vi) Suture and occlusive dressing if leaving for > 24 hours.
4. Complications
a) Cardiac tamponade!
b) Arrhythmias
c) Myocardial laceration
d) Pneumothorax, pneumopericardium
e) Liver laceration
Intra-Aortic Balloon Counterpulsation
1. Policy:
a) The ICU consultant should be involved in the decision to insert an IABP
b) Only to be performed by a consultant or advanced vocational trainee under
c) Become familiar with the theory of insertion, indications, interpretation and
complications of IABP.
2. Indications :
a) As a mechanical bridge prior to, and/or following myocardial revascularization
or transplantation:
b) Ischaemic heart disease
i) Low cardiac output states following cardiac surgery
ii) Cardiogenic shock: in association with angiography and revascularization
(PTCA, stent or CAVG)
iii) Acute mitral incompetence (papillary muscle rupture) or VSD following
AMI pending operative repair.
c) Myocardial disease
i) Severe myocardial contusion
ii) Severe myocarditis
iii) Cardiomyopathy
iv) Severe -blocker overdose.
3. Contra-indications:
a) Aortic regurgitation
b) Aortic dissection
c) Severe peripheral vascular disease
d) Tachyarrhythmias (relative)
e) Coagulopathy (relative)
4. Procedure protocol
a) Strict aseptic technique
b) Check IABP function prior to insertion:
i) Adequate helium cylinder volume
ii) Arterial pressure manifold: referenced & zeroed to mid-axillary line
iii) Dedicated 5 lead ECG connected to IABP
iv) Turn on and leave in standby mode
v) Initial settings:
 ECG sense:
1:3 ratio
 Augmentation:
minimum (pre-insertion only)
 Inflate and deflate times:
c) Insertion procedure:
i) Local anaesthesia in awake patients
ii) Scrubbed assistant recommended
iii) Select size (by patient’s height)
 < 152cm
25ml balloon
 152 – 162cm
34ml balloon
 162 – 183cm
40ml balloon
 >183cm
50ml balloon
iv) Femoral artery insertion of a 12F introducer, Seldinger technique.
v) Check the length for balloon catheter insertion, using the angle of Louis
(level of T4) as the surface landmark, prior to insertion.
vi) Insert the balloon to the level of T 4.
 The double black marker on the balloon catheter must be visible
 This indicates that the balloon has fully exited the sheath.
vii) Connect to pressure transducer and pump.
viii) Press the [IAB Fill] button to fill the balloon & wait for completion.
ix) Press the [Assist/Standby] button to start the pump.
x) Start on minimal augmentation and increase to maximum.
NB: subsequent augmentation should not be set below 50%
xi) Suture in place and cover with an occlusive dressing.
xii) Set timing:
 Check balloon inflation against pressure wave:
 set to peak of dicrotic notch.
 Check balloon deflation against ECG:
 prior to QRS complex and
observe decrease in end diastolic pressure.
 Check diastolic augmentation on pressure wave.
 Select augmentation ratio: *standard = 1:1
d) Maintenance
i) Check CXR post insertion:
tip of IABP below T 4 (carina) & origin of the left subclavian artery
ii) Neurovascular obs of insertion site, lower limbs and left arm hourly.
iii) Nurse at < 30° elevation.
iv) Document pump timing (ratio) and adequacy of augmentation.
v) Assess haemodynamic response: CI, MAP, SVR, filling pressures, CXR.
vi) Ensure clear balloon tubing is exposed:
 Monitor condensation (due to rapid helium shuttling), or
 Blood in tubing (balloon rupture).
e) Timing during arrhythmias
i) Ectopics: keep on ECG trigger, system will automatically deflate on
ii) Tachycardia > 160/min :
 Reduce augmentation (equal to patient systole)
 Decrease ratio to 1:2 if reducing augmentation is not adequate
iii) Atrial fibrillation: move deflate slide to extreme right to deflate on R wave
(not required on newer pumps)
iv) VT or VF: defibrillate or cardiovert as required, the IABP is isolated
v) Cardiac arrest (no output)
 start ECM
 Effective output: set on pressure trigger to synchronise balloon
inflation with ECM
 No output: set internal mode for a fixed rate of 40 bpm + 20ml
f) Weaning:
i) Commence when patient’s haemodynamics have improved.
ii) Methods:
 Reducing ratio from 1:1 to 1:2 to 1:3 and / or
 Reduce augmentation. NB: minimum balloon inflation 50%
g) Removal of catheter
i) Notify cardiac / vascular surgeons
ii) Cease heparin infusion 3 hours prior to removal
iii) Disconnect IABP tubing: do not aspirate the balloon
iv) Withdraw balloon up to (but not into) the introducer sheath. Even empty
the used balloon will not fit into the sheath, and may rupture if attempted.
v) Remove the sheath and balloon as single unit, applying pressure
vi) Use Femostop® local pressure during catheter removal:
 Remove IABP catheter with Femostop at 60-80mmHg
 Inflate dome to 20mmHg above systolic as catheter is fully withdrawn
 Reduce pressure by 15mmHg at 10-15 min intervals
 If bleeding occurs, reinflate the Femostop to the previously effective
pressure and recommence cyclic pressure reduction
 Remove Femostop and apply a firm dressing
vii) 10-20% may require surgical repair to the artery.
5. Complications:
a) Limb ischaemia – thrombotic or embolic
b) Bleeding at the insertion site or systemically
c) Infection
d) Aortic dissection
e) Occlusion of origins of aortic arch vessels if too high
f) Occlusion of renal/splanchnic vessels if too low
g) Thrombocytopaenia
h) Balloon rupture: gas embolism
i) Femoral artery aneurysm
Gastric / Oesophageal Tamponade Tubes
1. Policy:
a) Ensure the Gastroenterology Unit are informed.
b) The ICU consultant must be involved in the decision to insert an oesophageal
tamponade tube.
c) All patients should be intubated prior to insertion and managed in ICU.
i) High risk  torrential regurgitation of blood into the airway
ii) Should only be undertaken by an experienced operator.
d) Major complications following insertion of tamponade tubes have been reported
to occur in 15%, particularly if inserted by inexperienced clinicians.
2. Indications:
a) Upper gastro-intenstinal variceal haemorrhage.
i) Temporising measure while awaiting endoscopy, TIPSS and / or surgery.
ii) The tamponade tubes are used in conjunction with an octreotide infusion.
3. Types of tubes:
a) Minnesota:
b) Sengstaken:
c) Linton:
oesophageal and gastric balloons and 2x aspirating ports
oesophageal and gastric balloons and gastric aspirating port
gastric balloon and aspirating port
4. Procedure:
a) Preferably use a bulk & frame bed to allow application of traction.
b) Prior to insertion:
i) Check both balloons for leaks.
ii) Inflate the gastric balloon with 300ml of air and record pressure reading
with a manometer.
iii) Deflate all balloons completely and lubricate the tube.
c) Estimate insertion length = bridge of nose to earlobe + nose to xiphoid process.
d) Insert via nose or mouth, under direct vision using a laryngoscope.
e) Must ensure gastric balloon is not in the oesophagus.
i) Perform urgent x-ray to tube is adequately in the stomach.
ii) NB: inflating the gastric balloon in the oesophagus is virtually 100% fatal!
f) Inflate the gastric balloon in 50ml increments up to 300ml while monitoring the
balloon pressure.
i) If the balloon pressure ≥ 5mmHg above the pre-insertion pressure then
incorrect (oesophageal) placement is probable
ii) This mandates deflation of the balloon and reinsertion of the tube.
g) Pull back until resistance is felt as the balloon rests against the gastric fundus.
h) Note the measurement at the lips and apply gentle traction with 500ml bag of
fluid on a rope and pulley system.
Inflation of the oesophageal balloon is usually not required.
i) If bleeding continues despite adequate placement of the gastric balloon and
optimizing medical therapy, consider inflating oesophageal balloon.
ii) It should only be inflated after discussion with the ICU consultant.
iii) Inflate oesophageal balloon to 40 mmHg and reduce pressure by 5mmHg
once bleeding is controlled.
j) Recheck position on x-ray once balloons inflated and traction applied.
k) After 12-24 hours, the balloons should be deflated to check for ongoing
Extracorporeal Membrane Oxygenation
1. Extra Corporeal Membrane Oxygenation (ECMO) is a method of oxygenating
blood in cases of overwhelming respiratory failure (veno-venous ECMO) or
temporary circulatory support in reversible cases of refractory cardio-respiratory
failure (veno-arterial ECMO).
2. ECMO policies and protocols are a separate document to this ICU manual and can
be accessed on the RAH ICU website (www.icuadelaide.com.au).
3. Any requests for ECMO support must be immediately directed to the ICU
4. ECMO circuit and equipment must not be altered without ICU consultant and/or
perfusionist supervision.
1. Patients admitted to the ICU must have a complete drug history documented:
a) Premorbid and current medications
*see pharmacy’s drug listing within the patient’s medical records.
b) Previous adverse drug reactions and allergies
*if known the basis for that allergy.
c) Note potential drug interactions.
2. Charting of drugs and infusions is to be done by ICU medical staff.
a) Parent clinics must not write on the ICU flowchart.
b) Therapeutic changes suggested by the home team must be communicated to the
appropriate ICU medical staff for consideration prior to charting.
3. All changes to drug and fluid orders must be written and signed for on the flowchart.
a) Nursing staff must be notified of such changes.
b) Verbal orders alone are neither sufficient nor legal.
4. All drugs, infusions and fluids are reviewed and transcribed at least daily.
5. Printed labels for commonly used infusions and drugs should be used where possible.
6. Standardisation of infusion concentrations is essential for the prevention of drug
errors. Infusion concentrations should not be changed (e.g. ‘double strength’) from
the protocols outlined below.
7. Vasoactive or hypertonic infusions (e.g. TPN) must be administered through a
dedicated lumen of a CVC or PICC.
8. Vasoactive infusions must not be used in the general wards, other than for patients en
route to ICU and who are being continuously monitored.
9. All antibiotics written on the ICU flowchart must also have an indication of either:
a) Date started and due date for review/completion, or
b) Duration and position in course, e.g. “Day 4/7”.
10. Patients cleared for discharge from ICU must have all appropriate drugs, infusions and
fluids prescribed on the standard hospital forms, prior to discharge. Where
appropriate, old drug charts should be re-written.
11. Patients discharged on TPN must have their details entered in the TPN folder (stored
in the Unit A office area).
12. Any changes to acute pain drug regimens in patients under the care of the Acute Pain
Service should be done in consultation with the Acute Pain Service.
13. Any proposed changes to specialty type drugs, e.g. immunosuppressives,
anticoagulants, antiplatelet agents, etc should be discussed with home teams.
Principles of Drug Prescription in Intensive Care
1. Drugs should be prescribed according to Unit protocols and guidelines.
2. Critically ill patients have altered pharmacokinetics and pharmacodynamics, with the
potential for toxicity and drug interactions.
3. Where possible:
a) Use drugs that can be titrated or prescribed to an easily measured endpoint.
b) Use drugs that can be measured to monitor therapeutic drug levels.
c) Avoid drugs with narrow therapeutic indices (e.g. digoxin, theophylline),
particularly in patients with associated hepatic or renal dysfunction.
d) Cease a drug if there is no apparent benefit.
e) If two drugs are of equal efficacy, choose the cheaper drug as the cost of drugs in
ICU is significant.
4. Prescribe using generic drug names only.
5. When there is a medication change (e.g. replacing an antibiotic for another, alteration
in drug dose, ceasing a drug) then some indication as to the reason behind doing so
should be made within the patient’s medical records or drug chart.
6. A Clinical Pharmacist conducts a daily review (Mon-Fri) of ICU drug charting,
attends grand ward-rounds and is available for consultation. This is an invaluable
service and should be utilized accordingly.
Cardiovascular Drugs
1. Inotropes
Inotropes (specifically catecholamines) are frequently used in ICU. There are varied
prescription practices and preferences for these drugs, mostly based upon the reported
pharmacological effects of the different agents.
a) General principles:
i) Defence of BP in the critically ill forms the basis of haemodynamic
resuscitation and organ perfusion.
 Must be interpreted in the context of the patient’s pre-morbid BP
 Particularly in renovascular hypertension or cerebrovascular disease.
ii) Hypovolaemia is the most common cause of hypotension and low cardiac
output in ICU and must be assiduously monitored and corrected.
iii) The main indications for the use of inotropes are to increase myocardial
contractility, heart rate and/or vascular tone.
iv) The use of inotropes requires regular haemodynamic monitoring:
 Arterial line and CVC are mandatory
 Where indicated - PAC, PiCCO, Vigileo CO or ultrasound.
v) No single inotrope (or mixture) has been shown to be superior to another.
vi) There is marked inter-individual variation in the response to inotropes:
 Pre-existing chronic illness, genetic variation
 Co-administration of other drugs
 Qualitative and quantitative changes in adrenergic receptor kinetics.
vii) Prolonged exposure to catecholamine infusions can produce adrenergic
receptor down-regulation and tachyphylaxis.
b) Catecholamines
i) Receptor effects may be unpredictable, however, in general:
 -adrenergic effects predominate at low doses, and
 -adrenergic effects at higher doses.
ii) It is impossible to predict the dose range for an individual patient.
iii) Prescription on a body weight basis (µg/kg/min) is of little clinical utility.
iv) Infusions should be started at a low rate (3-5 µg/min) and titrated to a set
clinical response, e.g. MAP (not systolic)
v) There is no well established maximal dose.
vi) Regular assessment should be made of both global (pH, lactate) and
regional effects (urine output/creatinine clearance, limb perfusion).
c) Phosphodiesterase inhibitors (milrinone)
i) Inhibition of PDE3 increases intracellular cAMP and calcium, causing:
 an increase in myocardial contractility
 systemic and pulmonary vasodilatation, and
 improved diastolic relaxation (lusitropy)
ii) Any resultant hypotension (due to systemic vasodilatation) usually
responds with the addition of a vasopressor (e.g. noradrenaline).
iii) Phosphodiesterase inhibitors have longer half-lives than catecholamines,
are less titratable and their half-life is prolonged with renal failure.
Table: Cardiovascular Effects of Catecholamines
1 effects
 Chronotropy
 Dromotropy
 Inotropy
2 effects
 Inotropy
 glucose/lactate
 effects predominate at low dose
1 effects
2 effects
 Inotropy
 Inotropy
 effects predominate at high dose
+ = strong effect
(+) mild effect
- = no effect
Table: Inotropic Agents Used in ICU
Standard Infusion
6 mg / 100 ml 5% dextrose
First line drug in septic shock
Maintenance of blood pressure
6 mg / 100 ml 5% dextrose
Cardiopulmonary resuscitation
Acute severe asthma
Cardiogenic shock
Maintenance of blood pressure
Medical pacing
500 mg / 100 ml 5% dextrose
Primarily a vasodilator, weak inotropic action
Traditionally used in cardiogenic shock or low
output, high afterload states or when filling
pressures high
Often used in combination with noradrenaline
(ml/hr = µg/min)
(ml/hr = µg/min)
(ml/hr approx µg/kg/min)
400 mg / 100ml 5% dextrose
(ml/hr approx µg/kg/min)
Maintenance of blood pressure
No advantage over adrenaline/noradrenaline
“Renal dose” dopamine is not used
Endocrine side effects
6 mg / 100 ml 5% dextrose
Vasodilator, chronotrope (rarely used)
Symptomatic bradycardia
12.5 mg / 250 mL 5% dextrose
Loading dose: 6-12µg/kg/10min
Infusion: 0.05-0.2 µg/kg/min
NB: Loading dose may cause
marked hypotension, may be
omitted or reduced.
Calcium sensitizer
Increases myocardial contractility in an oxygen
efficient manner and dilates coronary and systemic
Role in Intensive Care not established
10mg / 100 ml 5% dextrose
Loading dose: 50µg/kg/20 min
Infusion: 0.5 µg/kg/min*
(ml/hr = µg/min)
*Standard milrinone prescription for 70 kg patient:
Cardiogenic shock due to diastolic failure
Pulmonary hypertension following valve
Catecholamine induced down regulation
Loading dose: 3500 µg = 35 ml over 20 minutes
Maintenance: 2100 µg/hr = 20 ml/hr.
2. Vasopressor agents
a) General principles
i) Vasopressors usually act directly on the peripheral vasculature and are
primarily used to acutely elevate BP
ii) The most common cause of hypotension in ICU patients is hypovolaemia.
iii) Pressor agents should not be used as an alternative to fluid resuscitation.
b) Indications (in ICU)
i) Tissue infiltration with local anaesthesia
ii) Topically prior to nasal intubation
iii) Hypotension following sympathetic block (e.g. epidural anaesthesia)
iv) Hypotension refractory to large doses of catecholamines (vasoplegia):
 Consider relative hypoadrenalism
 Consider use of vasopressin
c) Complications
i) Rebound hypertension
ii) Vagal reflex bradycardia
iii) Tachyphylaxis
Table: Vasopressors
Standard Infusion / Dose
10mg / 10ml 5% dex: titrate
 Potent short acting vasoconstrictor
30mg / 10ml 5% dex: titrate
 Synthetic indirect sympathomimetic.
 Commonly used in anaesthesia, little
benefit over adrenaline.
20units/20ml 5%dex:
1.8mls/hrs (0.03u/min)
 Noradrenaline resistant hypotension.
 May be useful in septic shock and post
cardiac bypass for catecholamine
resistant hypotension
3. Antihypertensive agents
a) General principles
i) The most common cause of hypertension in ICU patients is sympathetic
drive due to pain, agitation, drug withdrawal or delirium. These should be
treated with adequate sedation, anxiolytics and/or analgesia.
ii) Patients in the recovery phase of acute renal failure are often hypertensive.
This usually represents the resetting of endogenous neurohumoral
mechanisms and as such does not routinely require treatment.
iii) Hypertension following an intracranial event (haemorrhagic or ischaemic)
is common and the underlying mechanism dictates therapy. A high BP
may be tolerated in ischaemic stroke, c.f. the setting of SAH with an
unclipped aneurysm, where treatment would be paramount.
iv) Target therapy should be titrated against the patient’s premorbid BP.
v) In the absence of adverse effects, the maximal therapeutic dose of a
selected agent should be used prior to commencing a second or third agent.
b) Indications
i) Acute
 Perioperative control of BP in “at risk” patients.
 Hypertensive crisis (malignant hypertension)
 Pre-eclampsia / eclampsia
 Phaeochromocytoma
 Untreated aneurysm or vascular injury,
e.g. intracranial aneurysm, ruptured/dissected aorta
ii) Other indications for vasodilators
 Reduction of afterload in CCF or valvular disease
 Adjunct to passive warming in hypothermia
iii) Chronic
 Sustained essential hypertension
 Ischaemic heart disease
 Cerebrovascular disease
c) Complications – are many, but in relation to ICU patients:
i) Hypotension
 First-dose effect / especially in hypovolaemia
ii) Reflex tachycardia
iii) Tachyphylaxis
iv) Pulmonary vasodilatation  shunt and hypoxaemia
v) Cyanide toxicity (SNP)
vi) Angioedema – especially ACEI
vii) Deterioration in renal function
viii) Electrolyte disturbances
Table: Antihypertensive & Vasodilator Agents
Infusion & Dose
trinitrate (GTN)
30mg / 100ml 5%D
(non PVC bottle and giving set)
Range 2-25 ml/hr
First line drug in RAH ICU
Can be given topically.
Mainly venodilation:
Useful in cardiac ischaemia
Less predictable control of BP than SNP
Tachyphylaxis develops within 24-48hr
will need additional agents for persistent BP
50mg / 250 ml 5%D
Range 3-40 ml/hr
Rapid control of hypertensive crises.
Tachyphylaxis and metabolic acidosis may imply
cyanide toxicity (total dose > 1.5mg/kg/24 hrs)
10mg / 10ml 5%D: titrate
Pure -blockade, short acting antihypertensive
5-10 mg as bolus
20-40 mg 6-8 hourly
Short to medium term IV agent.
Often use with -blockers to control reflex tachycardia
Useful in renovascular hypertension
5-10mg oral bd
Long acting oral Ca++ antagonist.
Caution in renal impairment
Start low dose ~ 5-6.25mg
 up to 50mg orally 8 hrly
Syrup: 5mg/ml or tablets
Acute hypertension: 5-25mg
sublingually prn
Treatment of hypertension
Left ventricular dysfunction, esp post-MI
Left ventricular failure
Diabetic nephropathy
Caution in renovascular disease and renal failure
Start 2.5mg daily
 up to 10mg daily orally
Oral : 10mg/day and increase
until postural hypotension
IV : 1mg/kg/day
dilute to 200-500ml
1/3 dose over 1/24
2/3 dose over 1/24
Long acting, non-competitive -blocker
Preoperative preparation of phaeochromcytoma
Idiosyncratic hypotension may occur
Start with 0.5mg, and
increase up to 5mg tds orally
Potent antihypertensive agent
Prominent first dose effect
Oral: 25-100mg bd
IV: 1-2mg bolus every 2-3
minutes up to 10 mg.
High sympathetic drive states: neurogenic BP
All grades of hypertension, inc renovascular
Cardiac ischaemia
Control of reflex tachycardia with vasodilators
Thyroid crisis
Caution in poor LV function, asthma
Mainly eliminated by hepatic metabolism
Loading dose 0.5 mg/kg
Infuse 100mg/10ml and titrate
Ultra-short acting -blocker
Useful as trial for patients with poor LV function.
Adjunct to vasodilators post cardiac surgery
25µg boluses of up to
Oral: 75µg bd
 up to 150-300µg tds.
Acute, centrally mediated hypertension
Useful post cardiac surgery
Withdrawal states
Care with hepatic or renal dysfunction
Rebound hypertension with chronic use
Sedation, especially 1st dose
400 µg in 40mls
load 1µg/kg over 20min
infuse 1-5ml/hr
Selective alpha-2-agonist
Acute, centrally mediated hypertension
Not a first line drug.
Selected use by senior medical staff only
5-10 mmol loading
Infuse at 4-12 mmol/hr
Target plasma [Mg] ~ 1.5-2
Pre-eclampsia / eclampsia
Sympathetic overdrive in tetanus
Portal hypertension
4. Antiarrhythmics
a) General principles
i) Prior to administration of antiarrhythmic agents, optimise correction of the
 Hypovolaemia
 Metabolic abnormalities
a. K+, Mg++, Ca++, HPO4=
b. Hypoxaemia, hypo/hyper-carbia, alkalosis/acidosis
 Myocardial ischaemia or cardiac failure (especially post-cardiac
 Pain and agitation.
ii) All antiarrhythmic drugs are potentially arrhythmogenic.
iii) Virtually all depress myocardial contractility.
iv) Antiarrhythmics drugs are indicated with:
 Actual or potential haemodynamic compromise, or
 Susceptible patients with myocardial ischaemia.
v) Consider anticoagulation if AF > 48 hours
vi) More than one antiarrythmic may be required
b) Indications
i) Termination of an acute arrhythmia
ii) Prophylaxis against recurrence
iii) Rate control
iv) Enhance efficacy of cardioversion
Table: Antiarrhythmic Agents
Infusion & Dose
Acute use:
900mg / 250ml 5%D:
Load 100ml / 1 hr (5mg/kg)
Infuse 10 ml/h for 24-48 hrs
Bolus Dose 150-300mg
200-400 mg IV/oral daily
Rapid AF / flutter or MAT
Monomorphic ventricular tachycardia
Generally does not suppress contractility
Can cause acute hypotension if given too rapidly
Less proarrhythmic than most other drugs
Causes QTc, but rarely Torsade de pointes
Renal excretion is minimal – no need to change dose
in renal failure
Long term side-effects rare in short-term use.
Interference with digoxin kinetics and assay.
Interference with thyroid function tests.
5-10 mmol IV slow bolus
Infuse at 2-5 mmol/hr. 2.4g MgSO4
= 10 mmol Mg++
Acts principally as a calcium blocker
Useful in SVT and Torsade de pointes
5-10 mg IV slow bolus
Conversion atrial flutter  SR
Loading dose: 0.5-1 mg IV.
Maintenance: 62.5-250 µg IV/day
Ventricular rate control in rapid AF (usually 2nd line to
amiodarone in critically ill)
Narrow therapeutic index esp in renal failure and
metabolic abnormalities ( K+, Mg, PO4, alkalosis)
Proarrhythmic potential high in critically ill patients
Minimal inotropic effect in critically ill patients
Hypokalaemia potentiates effects
Levels: 0.6–1.0 mmol/l
1-2 mg IV bolus (up to 10 mg)
25-100 mg oral bd
10-80 mg IV slow bolus
(10-15 min)
Used in high sympathetic drive states : neurogenic
hypertension, hyperthyroidism
Control of reflex tachycardia with vasodilators
Caution in poor LV function, asthma
Mainly hepatic metabolism
Class III and -blocking actions
Supraventricular tachyarrhythmias
Conversion AF/flutter  SR
Low pro-arrhythmic potential
6-12 mg IV push
Diagnosis / conversion of SVT
0.4% solution = 4mg/ml :
60 ml/hr (4mg/min) for 1-2 hrs
45 ml/hr for 2-4 hrs
30 ml/hr for 2-4 hrs
2nd line drug after amiodarone
Sustained, recurrent VT
No longer routinely used for prophylaxis for VT
VF resistant to defibrillation (now questioned)
Potent negative inotrope, pro-convulsant
1 mg/kg slow IV push
100 mg oral BD (max of 300
AV nodal re-entrant tachycardia
Ventricular dysrythmias
15 mg/kg loading / 1 hr
300 mg/day
(level 40-80 mmol/l)
Digoxin toxicity
Tricyclic induced malignant arrhythmias
5. Thrombolytic Therapy
a) All patients with acute MI are potential candidates for primary angioplasty:
i) Cardiology must be notified as early as possible.
ii) The duty cardiologist will decide between primary angioplasty,
thrombolysis and medical management.
b) Indications
i) Acute myocardial infarction
 Thrombolysis is standard in the management of AMI unless primary
angioplasty is performed.
a. No specific age limit
b. Onset within 12hrs (potentially 24hrs) of presentation
i. Benefit is inversely proportional to delay in thrombolysis,
 therapy should be considered a “medical emergency”
ii. Late therapy may be inappropriate for “small” infarcts.
c. ECG evidence of acute infarction:
i.  ST segment  2mm in  2 adjacent chest leads, or
ii.  ST segment  1mm in  2 adjacent limb leads, or
iii. New LBBB
iv. Posterior infarction (R in V1 + ST in V2)
d. No benefit has been demonstrated for patients with ST-depression,
T-wave inversion, or a normal ECG.
 The patient should be advised of the potential risks and benefits.
ii) Haemodynamically unstable pulmonary embolism.
 An unequivocal diagnosis is necessary (spiral CT or angiogram).
 Tenecteplase is preferred in life threatening pulmonary embolism.
iii) Ischaemic Cerebrovascular Accident
 Within 4.5 hrs of onset of symptoms
 CT head: confirming CVA and excluding intracranial haemorrhage
 Oedema on initial CT head is associated with a higher incidence of
 In consultation with a neurologist according to RAH protocol.
c) Contraindications:
i) Absolute:
 Active internal bleeding or bleeding diathesis.
 Recent head/facial trauma, major trauma or surgery within 3 months.
 Previous intracerebral haemorrhage.
 Known structural cerebral vascular lesion or malignant intracranial
 CVA within 3 months.
 Lack of verbal informed consent.
 Prolonged CPR (> 10 mins) and/or traumatic resuscitation
 History of poorly controlled hypertension
 Uncontrolled hypertension at presentation: systolic >180mmHg
diastolic >110mmHg
 CVA greater than 3 months
 Other intracranial disease, including dementia
 Diabetic proliferative retinopathy.
 For streptokinase or anistreplase - a prior exposure (>5 days
previously) or allergic reaction to these drugs
 Major Surgery within 3 weeks.
 Active peptic ulceration or other GI bleeding within 2-4 weeks
 Non-compressible vascular puncture/injury.
 Pregnancy.
d) Complications
i) Reperfusion arrhythmias
ii) Bleeding (cerebral haemorrhage  0.5%)
iii) Anaphylaxis/anaphylactoid reactions: hypotension, rash, bronchospasm
e) Routine follow-up
i) ECG at 1 and 4 hours post TNK
ii) Cardiac enzymes 6, 12 and 24 hours post infusion
iii) If ST-elevation persists ≥ 1 hr post-TNK,
contact cardiology regarding “rescue angioplasty”.
Table: Thrombolytics
Single dose:
1. 0.5 mg/kg over 10 sec
2. non-glucose containing line
3. flush line with N.Sal pre & post
 Aspirin 150mg pre-Rx, then daily
 Enoxaparin 30mg IV prior to TNK
 Enoxaparin 1mg/kg sc bd
(if renal function normal)
 If renal impairment consider heparin IV
instead of enoxaparin.
Maximum dose = 50mg (=10,000U)
Bolus Dose = 15 mg.
Infusion (1) = 0.75 mg/kg over 30 min
(max of 50mg), then
Infusion (2) = 0.5 mg/kg over 60 min
(max of 35mg)
Therapeutic Heparin Infusion
- per RAH protocol.
 Observe vital signs and neurological
observations every 30 minutes for the first
6 hours post infusion then hourly for the
next 16 hours
 Repeat BP more frequently if elevated
 Keep BP <180/105
Alteplase in
0.9 mg/kg intravenously (max 90mg)
10% as a bolus, then
remainder over 60 min
 Heparin 5000U IV pre-TNK
 Heparin infusion: APTT > 50-80 secs
Fibrinogen level
Euglobulin clot lysis time
Apply local pressure (if possible)
Reverse heparin with protamine
Cryoprecipitate 10 units + FFP 2 units
Defibrination or intracranial bleed:
tranexamic acid 10 mg/kg over 20
minutes then 1mg/kg/hr infusion
6. Antiplatelet Agents
Table: Antiplatelet Agents
Usual dose
75-150 mg
 Post acute coronary syndrome
 Other thrombotic cardiac event
 Post TIA / stroke
75mg orally daily
 Irreversibly modifies platelet ADP receptor,
inhibiting aggregation
 Uses: prevention of vascular ischaemic events
e.g. MI, CVA, PTCA
300mg oral loading dose pre-PTCA
(then 75mg daily)
Bolus: 0.25mg/kg IV over 1 min,
10mins before PTCA
0.125µg/kg/min IV for 12hrs.
(max rate = 10µg/min)
0.4 µg/kg/min
for 30 mins
0.1 µg /kg/min
for at least 48hrs
NB: reduce doses by 50% with
severe renal insuff. (e.g. creat
clearance <30ml/min)
 Only to be ordered by Cardiology
 Binds to platelet glycoprotein IIb/IIIa receptor,
inhibiting platelet aggregation and thrombus
 Primarily used with PTCA
 Used with aspirin and heparin
(target ACT >200sec)
 Increased risk of major bleeding and
Only to be ordered by Cardiology
Blocks glycoprotein IIb/IIIa receptor
Short half-life (1.4-1.8 hrs)
Uses: unstable angina, non-Q wave MI
Use with heparin and aspirin
Continue through angiography, and for 12-24hrs
 Check platelet count 6hrs post-bolus, then at
least daily. If <90,000 cease and contact
 SEs: bleeding (major 1.4%), thrombocytopenia,
Respiratory Drugs
1. Inhaled bronchodilators
a) General Principles:
i) Relieve bronchoconstriction.
ii) They are not routinely used in all ventilated patients.
iii) Not all wheeze is bronchoconstriction – consider other pathology such as
upper airway obstruction, pulmonary oedema, consolidation.
iv) Regularly review:
 Patients symptoms.
 Work of breathing (i.e. respiratory rate, accessory muscle use).
 Wheeze.
 Airway pressures.
 End-tidal CO2.
 Blood gases.
b) Indications:
i) Asthma.
ii) Chronic obstructive pulmonary disease (COPD).
iii) Bronchospasm 2° to infection, aspiration or during mechanical ventilation,
not primarily due to airway secretions.
iv) For the treatment of hyperkalaemia (nebulised salbutamol only).
c) Metered dose inhalers:
i) MDIs are the default therapy for ICU patients.
ii) Can be administered via a MDI adaptor on the ventilator circuit.
d) Nebulised medication:
i) Nebulsied medications are best avoided due to the risk of aerosolising airway
secretions and suboptimal delivery of drug to smaller airways.
ii) Nebulisers are used only if inadequate response to 10 puffs of MDI.
iii) Continuous nebulised bronchodilators can be administered in status
2. Parenteral therapy
a) Indications:
i) Adjunctive therapy for patients with acute severe asthma or COPD not
responding to maximum dose inhaled bronchodilators.
b) Complications
i) Tachyarrhythmias.
ii) Hypokalaemia.
iii) Hyperglycaemia.
iv) Lactic acidosis.
Table: Bronchodilators
Infusion / dose
Clinical uses
Salbutamol MDI
Usual Dose - 2 puffs 4 hrly.
Max Dose - 10 puffs every 15
 First line bronchodilator.
 Default method of administration.
Salbutamol (nebulised)
Usual Dose - 5mg every 1-4 hours.
Max Dose - 20mg every hour
(i.e. continuous nebs).
 Bronchospasm refractory to MDI.
 Severe hyperkalaemia.
Ipratropium MDI
Usual Dose – 2 puffs 6hrly
Max Dose - 4 puffs hrly as required.
 Acute Asthma.
 Chronic obstructive pulmonary disease.
 Bronchorrhoea.
Usual Dose - 500ug 8 hrly.
Max Dose - 500ug hrly as required.
Adrenaline (nebulised)
Max Dose – 1mg every 15 minutes.
 Severe bronchospasm unresponsive to
continuous salbutamol nebs.
Salbutamol (IV)
6 mg / 100 ml 5%D
(ml/hr = µg/min)
Load = 200ug over 1 minute.
Infusion = 5-20ug/min
 Acute severe asthma
 Acute severe asthma unresponsive to
continuous inhaled bronchodilators + systemic
Adrenaline (IV)
6 mg / 100 ml 5%D
(ml/hr = µg/min)
Infusion = 1-20 ug/min
 Acute severe asthma unresponsive to
continuous inhaled bronchodilators + systemic
 Titrate until blood pressure rises..
1000mg / 100ml 5%D
Loading 5-7mg/kg,
Infuse 2-4ml/hr (1gm/day)
Levels: 55-110 mol/l
 Unproven efficacy in acute asthma / COAD.
 Narrow therapeutic index.
Sedation, Analgesia and Delirium
1. Sedation and Analgesia
a) Adequate analgesia and anxiolysis are primary management goals in ICU.
b) Pain and anxiety are associated with significant adverse effects:
i) Hypertension, tachycardia
ii) Increased myocardial and cerebral oxygen consumption
iii) Gastric erosions
iv) Intracranial hypertension
v) Increased catabolism
vi) Delirium
c) Sedatives and analgesics are also associated with adverse effects:
i) Respiratory depression
ii) Prolonged ventilation and complications (e.g. nosocomial infections)
iii) Delirium
iv) Hypotension
v) Gastroparesis, ileus and resultant feed intolerance
vi) Increased cost & ventilator days
d) Sedation protocol for ICU patients:
i) Important to obtain a reasonable balance between the awake, distressed
patient and the patient that is oversedated.
ii) Sedation should be given by infusion ± boluses to maintain  constant levels
rather than peaks and troughs
iii) Titrate infusions to clinical effect: there is marked inter-individual variability
and absolute doses are of little value
iv) Sequential increases in infusion rate, without the use of a bolus dose,
increases the risk of over-sedation as steady-state is reached (5 half-lives)
v) The half-life for fentanyl increases with the duration of infusion (contextsensitive half-time), so time to steady-state may be greatly prolonged.
vi) Grimacing alone is not a reliable sign and may only indicate awareness or
reflex activity.
vii) Patients with an encephalopathy, renal or hepatic impairment are likely to
require significantly less or no sedation.
viii) Prescribe the desired sedation level (RASS = 0 to -5) in the box on the ICU
flow chart.
ix) In the absence of a contraindication, sedation should be held daily from 0800
for all patients, except those prescribed a sedation score of - 4 or -5.
e) PCA or epidurals are considered when the patients are awake, in cooirdination
with the Acute Pain Service.
Table: Nurse Controlled Sedation Protocol
 Hold the infusion until the patient reaches the prescribed level
 If ongoing sedation is required, recommence at half the previous
infusion rate.
 Use a bolus of sedation/analgesia and increase rate according to
dose range prescribed.
 If insufficient repeat until a satisfactory sedation level is attained.
 Infusions should not be titrated to responses during high-intensity stimuli, e.g. suction.
 In these situations, bolus sedation should be provided.
Table: Modified Richmond Agitation Sedation Scale (RASS)
Term Description
Overtly combative / violent
Immediate danger to staff
Very agitated, pulls or removes tube(s) or catheter(s)
Agitated, frequent non-purposeful movement
Fights ventilator
Restless, anxious
Movements not aggressive or vigorous
Alert and calm
Eyes open spontaneously
Not fully alert but responds easily to voice or light touch.
Sustained awakening & eye contact >10 seconds
Responds easily to voice or light touch.
Difficulty staying awake & eye contact <10 seconds
Difficult to rouse, responds to voice or touch with movement or brief eye opening
No eye contact
No response to voice or touch.
Movement or eye opening to physical stimulation (discomfort / tracheal suction)
No response to voice or physical stimulation
Weak or absent cough on tracheal suction
2. Delirium
a) Delirium: “an acute, reversible organic mental syndrome with disorders of
attention and cognitive function, increased or decreased psychomotor activity and
a disordered sleep wake cycle”.
b) An independent predictor of longer ICU stay and increased mortality.
c) Three forms characterised:
i) Hyperactive - agitated, paranoid
ii) Hypoactive - withdrawn, quiet, paranoid
iii) Mixed
- combination of above
d) Hypoactive delirium is under recognised, especially without specific screening.
e) Patients with a modified RASS score ≥ -3 will be screened for delirium by
nursing staff using the CAM-ICU (see below):
i) Adaptation of the ‘Confusion Assessment Method’ for non-verbal patients.
ii) Sensitive and specific tool and if positive the patient likely has delirium.
iii) Should be assessed and a management plan formulated daily.
f) Prevention:
i) Provide appropriate analgesia and anxiolysis, avoiding oversedation
ii) Hold sedation daily until the patient wakes  RASS > -1,
unless contraindicated, i.e. patients prescribed RASS  -4 / -5
iii) When possible correct physiological disturbances
 Hypoxia, acidosis, electrolyte imbalance
 Drug withdrawal (nicotine, alcohol, opiates, benzodiazepines)
iv) After prolonged infusion opiates may require weaning rather than abrupt
v) Provide psychological support and orientation
 Encourage patient participation in treatment
 Repeatedly orientate the patient in time, place and person
 Involve relatives in reassuring patient if possible
 Consider papers, television etc. to help orientate patient during the day
vi) Provide an unambiguous environment
vii) Allow an environment for sleep (minimal noise, light etc. at night)
 If possible do not performing invasive procedures at night
 Minimise nocturnal interventions when clinically safe.
 Perform RASS concurrent with GCS assessment.
 Use nocturnal sedation as a last resort
viii) Maintain competence
 Maintain activity levels and promote early mobilisation
 Make sure glasses, hearing aids etc. available for use
 Consider interpreters for non English speaking patient
ix) Minimise use of drugs associated with delirium. (see table below)
 If appropriate consider sedation with a central α-2 agonist
g) Management of Delirium
i) Identify and treat predisposing factors:
 Pain
 Metabolic and haemodynamic instability
 Infection
 Drug interactions and withdrawal
 CNS disorders (stroke, abscesses, seizures, tumours)
 Renal, cardiac, hepatic, GI failure
 Myocardial ischaemia
 Ventilator dysynchrony
 Immobilisation
 Frustration / Anxiety
Minimise use of drugs associated with delirium:
Table: Drugs Associated with Increased Delirium
iii) Pharmacotherapy
 Limited evidence pharmacotherapy shortens duration of established
delirium however may be necessary for behavioural control
 Drug choice should be individualized and therapy short term.
 Recommended agents (see table below) include:
a. Haloperidol
b. Olanzapine
c. Dexmedetomidine /clonidine
d. Quetiapine, Chlorpromazine
 Benzodiazepines are best avoided unless indicated for rapid sedation or
treatment of GABA withdrawal syndromes, e.g. delirium tremens.
 One agent should be titrated to maximal safe dose (or onset of adverse
effect) before introduction of a second agent.
iv) Physical Restraint – see following.
3. Physical Restraint – for emergency medical treatment
a) The use of restraints can be humane and effective while facilitating diagnosis and
treatment and preventing injury to the patient and medical staff.
b) Restraint may be indicated when a professional and proper approach, including
verbal techniques are unsuccessful.
c) Patients may be restrained under either:
i) The Mental Health Act (1993): when a patient requires immediate treatment
for a mental illness including drug and alcohol induced delirium
ii) The Consent to Medical Treatment and Palliative Care Act (1995): when a
patient over 16 years of age requires treatment for an immediate risk to life
or health and is incapable of giving consent
d) The process requires:
i) Examination by two doctors (when available) to confirm the patient is
incapable of giving consent. A person can be deemed incapable when they
are unable to comprehend, retain and judge information relating to the
consequences of having or not having treatment
ii) This can be demonstrated by positive CAM-ICU
iii) Documentation in the case-notes of the patient’s incapability and a treatment
plan for the condition, detailing the need for temporary restraint.
e) Identification and treatment of the illness precipitating the mental incapability
f) The doctor to be acting in good faith and in accordance with professional
standards in order to preserve or improve quality of life
g) Regular reassessment of the need for physical restrain is required and restraints
must be removed if a patient regains mental competence (ie the delirium resolves,
which may be evidenced by a negative CAM-ICU)
h) If the patient has a guardian they should be notified of the need for restraint as
soon as possible.
i) A Form 1 need only be completed if the patient is detained under The Mental
Health Act (1993). In this instance it is necessary to inform the Psychiatry team.
j) A patient with the capacity to make reasonable decisions and who poses no threat
to himself or others cannot be confined or restrained without their permission.
Doing so is illegal. If patient deemed to be competent poses a significant threat
security and the police should be called
k) On ICU discharge ensure a plan regards cessation of agents used to manage
delirium is documented and communicated verbally to the home team.
Flowchart: Confusion Assessment Method for ICU (CAM-ICU)
Table: Sedatives / Analgesics
Clinical uses
10mg/ml (neat solution)
Initial rate 3-5ml/hr
Titrate against effect
 First line sedation in combination with fentanyl
 Anaesthesia for minor procedures where prompt return of
consciousness is required (e.g. tracheostomy, CVC)
 Potent myocardial depressant/vasodilator
 No analgesic effect.
Maximum 4mg/kg*/hr
(*estimate lean weight)
100-200 µg IV bolus
Infusion: 20-200 µg/hr
(neat solution)
 First line analgesic
 Potent medium acting narcotic with relative
haemodynamic stability
 Combined with propofol for sedation
 Useful for ICU procedures.
Morphine and
morphine 60mg +
midazolam 30mg
per 50ml 5% dextrose
Rate: 1-10 ml/hr
 Second line sedation - consider if propofol
contraindicated or causing adverse effects (eg
 Review rate/sedation at least daily
 Effects prolonged in renal failure
1-5 mg IV, sc prn, or
PCA per protocol
 Alternative analgesic to fentanyl
 Caution in renal failure
IV: 2-10 mg prn
Orally: 5-20mg bd-qid*
 First line in acute alcohol or benzodiazepine withdrawal
 Larger doses may be required esp. delirium tremens
 Avoid in delirium not related to alcohol/benzo withdrawal
Epidural cocktail
(APS protocol)
Fentanyl 5µg/ml and
Bupivacaine 0.1% or
400 µg in 40mls
load 1µg/kg over 20min
infuse 0.2-0.7 ug/kg/hr
 Selective central alpha-2-agonist
 Short term sedation / weaning from ventilation / delirium /
withdrawal states
 Selected use by senior medical staff only
Standard epidural analgesic regimen
Plain bupivacaine may be used (0.25%)
Maximal duration 4 days unless indicated
Rate: age related doses (per APS)
Agents Primarily Used in Agitation/Delirium
0.5-2.5 mg IV prn
Max dose: 10mg
First line major tranquilliser
Delirium, agitation
Esp. in opioid / benzodiazepine withdrawal.
 blocker : may cause hypotension
QTc, seizures, extrapyramidal ettects
2.5-5 mg IV prn
 2nd / 3rd line agent for delirium
 More sedating, unpredictable & longer acting
 Vasodilator
5-10mg SL or orally
(2.5-5mg in the elderly)
Maximum dose 10mg BD
50-100mg enterally BD
 QTc prolongation
 Reduced seizure threshold.
  Metabolism (CYP-3A4) with fluconazole, erythromycin
Increase delirium (central cholinergic effect)
QTc prolongation
Reduced seizure threshold
Extrapyramidal effects
Metabolism (CYP-1A2) is reduced by Ciprofloxacin
4. Analgesia in Awake Patients – See APS Intranet Guidelines
Age (yrs)
SC morphine/oxycodone
Oral oxycodone*
15 – 39
7.5 – 12.5
15.0 – 25.0
40 – 59
5.0 – 10.0
10.0 – 20.0
60 – 69
2.5 – 7.5
5.0 – 15.0
70 – 85
2.5 – 5.0
5.0 – 10.0
> 85
2.0 – 3.0
2.5 – 5.0
Recommended dose interval: 2 hourly prn
* ↓ if pain not severe
Acute Pain Service (APS) contact numbers
Mon-Fri: 0830-1730
pager 22556
After 1730 hrs
SD 1175
W/E & Pub Hol
via Switch
▪ Suggest start in middle of dose range; upper limit of dose range can be increased if
analgesia is inadequate, sedation score is less than -2 and resp rate > 8 /min (first
check that doses are correct/ have been given as ordered)
▪ Sedation score - 2 = responds easily to voice or light touch but difficulty staying
awake, eye contact maintained < 10 seconds
Dose equiv.
SC (mg)
Oral (mg)
150 microgram
400 microgram (patch)
800 microgram (SL)
Simple analgesia:
▪ Unless contraindicated, paracetamol is best ordered for all patients and on a regular
rather than prn basis
Muscle relaxants
1. General principles
a) These agents have a limited role in ICU and must not be used unless the patient is
adequately sedated (modified RASS -4 / -5).
b) Non-depolarising agents (except rocuronium) should not be used for emergency
(rapid sequence induction) endotracheal intubation.
2. Indications
a) Depolarising: suxamethonium
i) First line agent for emergency endotracheal intubation
b) Non-depolarising: rocuronium, vecuronium, atracurium
i) Acute control of ventilation post-intubation
ii) Patient transport / retrieval on Oxylog ventilator who cannot be managed
by other means
iii) Selected patients with poor lung compliance who are difficult to ventilate
following “heavy” sedation
iv) With anaesthesia for procedures: tracheostomy, bronchoscopy
3. Complications
a) Hyperkalaemia, bradycardia (suxamethonium)
b) Sympathetic overdrive, particularly in under-sedated patients
c) Adverse outcome in head injury when used as a measure to control ICP
d) Use of non-depolarising relaxants may be associated with increased risk of critical
illness polyneuropathy, especially with concomitant use of steroids.
Table: Muscle Relaxants
100-200 mg or
1-2 mg/kg
 1st line agent in Rapid Sequence Induction (RSI)
 Consider pre-treatment with atropine (0.6-1.2mg) if
potential bradycardia
 Contraindicated in burns (>3 days), chronic spinal and
neuromuscular disease, hyperkalaemic states (K+ > 5.5)
 Caution in any patient with any central or peripheral
muscle weakness including critical illness related
0.6 mg/kg
1.0 mg/kg
for RSI
4-10mg IV prn
First line non-depolarising agent in ICU
Rapid onset (60secs)
2nd line agent in RSI = alternative to suxamethonium
Duration of action : 30-40 minutes
 2nd line non-depolarising agent in ICU
 Duration similar to rocuronium
 Cardiostable, low incidence of allergy
G. Anticoagulation
1. General principles
a) All patients on systemic anticoagulation must have an APTT, INR and CBP
performed daily.
2. Indications
a) Acute systemic anticoagulation:
i) As a general rule, heparin infusions are used in critically ill patients:
 Allows monitoring/titration to a therapeutic APTT.
 Provision for reversal if indicated (e.g. procedures, bleeding).
ii) Enoxaparin is effective but more difficult to use in critically ill patients:
 Inability to monitor activity
 Dose variation in renal disease and
 Inability to reverse effect.
iii) Indications:
 Proven venous or arterial thromboembolism
 Acute coronary syndromes
 Prosthetic heart valves:
a. Prior to commencement of oral anticoagulants
b. During an acute illness, where oral anticoagulation is relatively
 AF in patients complicated by emboli < 70 years.
 AF for more than 48 hours, in which cardioversion is being considered
 Extracorporeal circuits e.g. CVVHDF, ECMO
iv) RAH Heparin Protocol – see below
b) Partial anticoagulation
i) low dose IV heparin (500 u/hr)
ii) IV prostacyclin
c) Warfarin
i) The kinetics of warfarin are highly variable in the critically ill.
ii) Normally only used in stable long term patients
iii) Prosthetic valves (mitral > aortic valves)
iv) Previous thromboembolism
v) Maintenance of thromboprophylaxis in high risk patients (# pelvis)
3. Protocol for DVT/VTE prophylaxis
All patients must have a documented plan for DVT prophylaxis
a) Mechanical prophylaxis
i) TED stockings
 All patients except those with:
a. Significant PVD
b. Significant lower limb trauma, cellulitis, dermatitis or oedema
c. Peripheral venous or arterial access on lower limb(s)
d. For most of the above patients, a single TED should be used on
the unaffected limb
 TED stockings can be used in patients with proven DVT to decrease
the incidence of post DVT thrombophlebitis
 Continue until the patient can mobilise effectively
ii) Sequential calf compression devices
 SCCD’s have an additive effect to other forms of DVT prophylaxis.
 Patients unable to use chemoprophylaxis or at high risk are given
 In patients without DVT prophylaxis > 24 hrs  consider a lower
limb ultrasound to exclude DVT prior to application of SCCD’s
b) Chemoprophylaxis
i) Enoxaparin or heparin should be charted for all patients unless
contraindicated and continued throughout their ICU stay
ii) For patients with a high risk of bleeding, communication with the relevant
surgical teams (neurosurgery, spinal, ophthalmology, etc) is essential.
iii) Enoxaparin 40 mg s/c daily is the default agent.
 Start on day 1 or as early as possible especially in high risk patients.
 Potential accumulation in renal failure
 Not routinely monitored (anti-Xa level).
iv) Unfractionated (UF) Heparin 5000U s/c b.d.-t.d.s
 Used in patients with a high risk of bleeding or renal failure
 Shorter duration of action and ease of reversal.
v) Enoxaparin 60 mg s/c daily
(20mg mane + 40mg nocte)
 Considered for high risk patients:
a. Pelvic or long bone fractures
b. Significant spinal injury or paralysis
c. Previous PTE/DVT
 Routine monitoring is not necessary.
vi) No other DVT protocols are to be used except post-pelvic surgery 
 Adjusted dose heparin protocol may be used
 See “VTE Prophylaxis in Orthopaedics” on the RAH Intranet
vii) Cease prophylaxis for significant bleeding or suspected HITS - see below
viii) Absolute and relative contraindications for heparins:
 Significant active haemorrhage
 High risk of bleeding
a. Coagulopathy - DIC, thrombocytopenia, liver failure, etc.
b. Post-surgical
- neuro, spinal, eyes
c. Major trauma - TBI with parenchymal lesions, liver/spleen
 Known or suspected adverse reaction to heparin
a. Documented or suspected HITS, known heparin allergy
 Patients already on therapeutic anticoagulation
c) IVC filter
i) In high risk patients with ongoing contraindications to chemoprophylaxis,
an IVC filter can be considered.
4. Perioperative anticoagulation in patients on Warfarin
a) Heparin infusion
i) First choice in ICU
ii) Effect is more readily monitored and reversed.
b) Where heparin is contraindicated, consider danaparoid or consult haematology.
5. Protocol for Heparin Induced Thrombocytopaenia Syndrome (HITS)
a) General principles
i) HITS is a prothrombotic disorder caused by platelet-activating antibodies
ii) An intense hypercoagulable state often complicated by venous and arterial
iii) Risk factors
 Duration of therapy *see 4T table
 Type of Heparin
 Type of patient
postsurgical > medical > pregnancy
b) Diagnosis
i) The 4T Score  ‘pre-test probability’ of HITS
 Points - 0, 1, or 2 for each of 4 categories (see table)
 Maximum possible score = 8
a. High risk
6-8 points
b. Intermediate risk
4-5 points
c. Low risk
0-3 points
 If probability is intermediate or high do a HIT screen for antibodies.
 If high probability cease heparin immediately pending test results
ii) HIT Screen
 ELISA detects antibodies against heparin and PF4.
 Also detects other non-HIT heparin-Ab, therefore lower specificity
 If ELISA positive then test further with a "functional assay",
serotonin release assay (SRA)
iii) Lower limb doppler U/S
Table: HITS Probability Score – ‘4T Score’
Risk Factor
2 Points
1 Point
0 Points
Platelet fall >50%
Nadir >20
Platelet fall 30-50%
or >50% fall due to surgery
or nadir 10-19
Platelet fall <30%
Nadir <10
Timing of onset of
platelet fall (or other
sequelae of HITS)
Day 5-10
Day 1 with heparin
in last 30 days
> Day 10 or timing unclear
< Day 1 with heparin
in last 31-100 days
< Day 4
No recent heparin
Thrombosis or
other sequelae
Proven new thrombosis,
skin necrosis
Anaphylactoid reaction after
IV heparin bolus
Progressive or recurrent
erythematous skin lesions,
suspected thrombosis,
asymptomatic upper limb DVT
OTher cause
of platelet fall
Pre-test probability score: High (6-8) | Intermediate (4-5) | Low (0-3)
a) Treatment principles
i) Two Do’s
 Do stop all heparin (including flushes, LMWH, etc )
 Do start an alternative non-heparin anticoagulant in therapeutic doses.
a. Lepirudin
- difficult to use, or
b. Danaproid - may cross react
c. Discuss with haematology
ii) Two Don’ts
 Don’t administer warfarin acutely and if warfarin has already been
administered, give vitamin K
 Don’t give prophylactic platelet transfusions
iii) Two Diagnostics
 Test for HIT antibodies
 Investigate for lower limb DVT
Table: Anticoagulants
Infusion / Dose
Variable dose  Daily INR
See age-adjusted Warfarin loading protocol on the RAH intranet.
NB. This is meant only as a guide, and was developed for noncritically ill patients, whose pharmacodynamics may differ
significantly from the intensive care population.
Heparin (infusion)
25000u/50ml = 500u/ml
See below: titrate against APTT:
Cease 4-6 hours prior to surgical procedures
Heparin (subcut)
5000 u subcut bd
<70 kg
5000 u subcut 8 hrly >70 kg or high risk DVT
40mg subcut daily
20mg subcut daily if Creat clearance < 30ml/min
“High risk” 20mg mane 40mg nocte
1mg/kg subcut bd - lean body mass
1mg/kg subcut once daily if CrCl < 30ml/min
Enoxaparin (Clexane®)
Prostacyclin (infusion)
Dose: 0.2-0.6 µg/kg/hr
500µg (+10ml diluent): add to 40ml NSal = 10µg/ml solution
Start at 2ml/hr and monitor platelet count
May cause hypotension
IV loading dose:
< 60kg
1500 U
60-75 kg
2250 U
75-90 kg
3000 U
> 90 kg
3750 U
Infusion: 2250U of danaparoid in 250ml 5% dextrose:
44 ml/hr (400 U/hr) x 4 hours
33 ml/hr (300 U/hr) x 4 hours
22 ml/hr (200 U/hr)
Adjust dose to anti-Xa levels (target 0.5-0.8 anti-Xa U/ml)
Long half life (25 hrs): cease early if changing to oral anticoagulants
Danaparoid (subcut)
750 U 8-12 hourly
Complex see below
See below
Danaparoid sodium
Table: Heparin Infusion Protocol
Infusion adjustment
IV bolus
< 37
5,000 units
Stop Infusion
Rate Change
Repeat APTT
 400u/hr
6 hrs
 200u/hr
6 hrs
No change
 50u/hr
6 hrs
30 min
 100u/hr
6 hrs
60 min
 150u/hr
6 hrs
120 min or
APTT <150
 200u/hr
2 hrs
> 150
Infusion: 25,000 units in 50ml syringe = 500U/ml
Check first APTT 6 hrs after bolus dose
Table: Lepirudin Infusion Protocol
CrCl (ml/min)
Bolus Dose
> 60
% original dose
0.4 mg/kg
(max 44mg)
0.1 (max 11mg/hr)
0.2 mg/kg
< 15
Maintenance Infusion
7. Lepirudin
a) Recombinant direct thrombin inhibitor
b) Dose range varies by a factor of 20x
i) Care must be used in determining the precise dose
ii) Renally excreted and must be carefully monitored in the critically ill
c) NB: a bolus dose is only used if patient has life threatening thrombus
8. Dabigatran
a) Competitive direct thrombin inhibitor.
b) Used as an oral alternative to warfarin.
c) Current indications include:
i) Atrial fibrillation
ii) VTE prophylaxis following major orthopaedic surgery.
d) Renally cleared with a half-life  12-14 hrs.
e) Monitoring
i) INR cannot be used to monitor efficacy or toxicity.
ii) APTT provides an approximate indication of the level of anticoagulation
iii) A normal APTT suggests that drug is unlikely to be present in significant
iv) APTT of > 80 seconds suggests that drug is present in excess.
f) No specific antidote is available to reverse effect.
i) For severe bleeding, supportive strategies are recommended, including
transfusion of fresh whole blood, or fresh frozen plasma.
ii) Dialysis may be indicated in patients with prolonged APTT particularly if
renal function is impaired.
iii) The role of prothrombinex and rFVIIa is unclear.
iv) For advice under these circumstances contact the on-call Haemostasis
Service through Transfusion on 8222 5430 or 8222 5431.
H. Endocrine Drugs
1. Insulin
a) Indications:
i) Diabetic emergencies – DKA and hyperosmolar coma
ii) Treatment of hyperkalaemia
 50% dextrose 50ml, plus Actrapid 10U
iii) Perioperative diabetic patients (both insulin and non-insulin dependent)
iv) General ICU patients
 Hyperglycaemia  10 mmol/l or glycosuria in acute illness:
a. Maintaining BGL 6-10mmol/l is recommended for all critically ill
b. Majority of ICU patients will require insulin using this protocol.
c. NB: This protocol is not designed for patients with diabetic
ketoacidosis and is a guideline only.
d. Some patients will require individual manipulation of dose.
 Subcutaneous sliding scale insulin:
a. Is inadequate for most critically ill patients and should be avoided.
b. May be used in a small number of less critically ill patients, who
have a limited requirement for exogenous insulin.
c. A regular dose of subcutaneous intermediate/long-acting insulin,
adjusted according to BGL may be suitable in some ICU patients.
b) ICU Insulin Protocol – see following page.
i) Target BGL = 6-10mmol/l.
ii) Blood for testing should ideally be:
 Sampled from the arterial line rather than capillary (finger prick), as the
former is more accurate in the critically ill.
 Measured via the blood gas analyser, c.f. bedside glucometer.
iii) Protocol Precautions:
 If insulin rate ≥ 8 U/hr and the BGL remains high, measurement may
be erroneous  take a sample from another site and measure in the
blood gas analyser.
 Consider holding the infusion if feed or glucose infusions are stopped.
 Potassium level
a. Administration of insulin reduces K+ levels.
b. Check K+ on ABG specimen at least twice daily and more often if
the insulin infusion rate is high or changing acutely.
c. If [K+] < 3.5 mmol/l
 KCl ~ 30 mmol over 1h via a pump.
Flowchart: Blood Glucose Management in ICU
Target BGL = 6-10mmol/l
Perform BGL on Admission
BGL = 6-10mmol/l
BGL > 10 mmol/l
Commence Protocol
Perform BGL 4hrly
Table: Insulin Infusion Protocol
Subsequent infusion
Repeat BGL
Units IV
Increase by 1
Increase by 1
If BGL dropping continue current rate.
If static or rising increase by 0.5
Continue current rate
If BGL dropping for 2 consecutive hrs
decrease rate by 0.5.
1 (2hrly if
BGL stable
for 6 hrs)
1 (4hrly if off
Call MO
c) Discharge Management:
i) Pre-discharge, cease insulin infusion for at least 4 hours and check BGL
ii) Order BGL to be checked 8 hourly on the ward
iii) Refer to the RAH intranet documents:
 Insulin Protocol for Patients Discharged from ICU.
 Diabetes Management Guidelines.
iv) Liaise with Endocrinology as indicated.
2. Diabetes insipidus: protocol for DDAVP
a) Diabetes insipidus may occur in the following situations:
i) Post ablative pituitary surgery
ii) Severe head injury, esp. anterior cranial fossa #, trauma
iii) Evolving brain death
iv) Lithium administration
b) Indications for DDAVP
i) Acute perioperative management (24-48hrs) of DI following pituitary
surgery is usually fluid based – the use of DDAVP is rarely indicated.
ii) Persistent polyuria in the absence of diuretics > 300ml/hr for > 3hrs
iii) Altered conscious state, inability to detect thirst or take oral fluids
iv) Low urine osmolality in the presence of high plasma osmolality
v) Pre-existing hyperosmolar state or predisposition to pre-renal failure where
persistent polyuria may exacerbate this.
c) DDAVP Prescription
i) Dose 1-2µg s.c. bd as required. (4µg is excessive)
ii) Adjust maintenance fluids according to the response
d) Maintenance fluids should be prescribed in the usual manner, according to
volume status, renal function and osmolality.
e) Presumptive or proven brain death:
i) DI should be treated early (i.e. as soon as polyuria occurs)
ii) Delayed administration of DDAVP can result in significant electrolyte
abnormalities, which may influence the organ donation process.
3. Steroids
a) Indications
i) Pre-existing steroid therapy:
 Wide variety of indications, doses and durations of therapy.
 The need to continue steroids, with or without dose adjustment, should
be assessed.
ii) ICU conditions where steroid therapy may be beneficial. :
 Addisonian crisis
 Anaphylaxis
 Asthma, Chronic obstructive pulmonary disease
 Bacterial meningitis - esp. pneumococcal prior to antibiotics
 Croup, post-extubation laryngeal oedema
 Fulminant vasculitis
 Hypercalcaemia
 Idiopathic thrombocytopenic purpura
 Myasthenic crisis
 Myxoedema coma / Thyroid storm.
 Organ transplantation
 Pneumocystis jurovecii pneumonia
iii) Conditions where supporting data are variable and the decision to administer
steroids should be made on a case-by-case basis
 Sepsis
b) Contra-indications / non-indications
 Active infection
 Acute head injury
 Guillain-Barré syndrome
 Fat embolism syndrome
c) Relative drug potencies
Table: Steroid Doses / Relative Potencies
dose (mg)
Cortisone acetate
d) Limitations of a random cortisol
i) Marked fluctuation in plasma cortisol in the critically ill.
ii) The ‘normal’ range in critical illness is not defined.
iii) There is no consensus ‘cut-off’ value below which insufficiency is present.
e) Limitations of total cortisol
i) Free cortisol is the bioactive fraction of cortisol
ii) Large variation in total cortisol assay results when the same specimen is
tested in different laboratories and using different assays
iii) Peripheral tissue-specific glucocorticoid resistance is not tested
f) Conventional (high-dose) short synacthen test (HDSST)
i) Synacthen concentrations are supraphysiological
ii) Published data likely overestimate the incidence of adrenal insufficiency,
as most studies did not excluded patients on etomidate.
iii) The low-dose SST may be more a better predictor of outcome.
iv) Insufficient data to support the routine use in patients with septic shock.
v) Should only be performed if there is suspicion of hypoadrenalism
 Hyperkalaemia/hyponatraemia
 Hypoglycaemia
 Refractory acidosis
 Catecholamine resistance
Renal Drugs - Diuretics
1. General principles
a) Oliguria in acutely ill patients is frequently a manifestation of:
i) Hypovolaemia – relative or absolute
ii) Decreased cardiac output
iii) Direct renal toxicity, or
iv) A combination of these factors.
b) Therapy should be directed toward causative factors and not maintenance of urine
output by the administration of a diuretic agent.
c) Urine output, in the absence of diuretic use, represents one of the best markers of
end-organ perfusion and is a useful guide to clinical management.
d) Diuretics should never be used to treat oligo/anuria, they are only a treatment for
fluid overload
2. Indications
a) Symptomatic fluid overload
i) Pulmonary oedema / CCF
ii) Cor pulmonale
b) Hyperaldosterone states: ascites
c) Chronic renal failure
3. Contraindications
a) Hypovolaemic and/or Na+-depleted states
b) Known drug hypersensitivity (esp. sulphonamide group)
4. Complications
a) Hypovolaemia
b) Hyperosmolar states
c) Potentiation of renal failure - 2° to hypovolaemia
d) Electrolyte disturbance especially  K+, Mg, PO4, metabolic alkalosis
e) Natriuresis and kaliuresis will alter urine electrolytes and osmolality for 24-48
hrs post dose.
Table: Diuretics
Clinical uses
40-250 mg/day
IV / oral
First line, potent loop diuretic
Doses may be increased in diuretic dependence
 K+, Mg, PO4, metabolic alkalosis common
250-500 mg IV tds
Carbonic anhydrase inhibitor
Alkaline diuresis with HCO3- excretion
Used for severe metabolic alkalosis after
correction of hypovolaemia:  K+, Mg++, PO4=
Post-hypercapnic alkalosis
25-100 mg oral bd
20% solution /
200 mg/ml
Dose 100 ml prn
(0.5g/kg is
too much!!)
Potassium sparring diuretic
Often given with loop and thiazide diuretics
Indicated as part of a chronic treatment regimen
for left ventricular failure
Use in acute LVF is less certain
May be of use in patients with ascites, particularly
if secondary hyperaldosteronism is a feature.
Careful administration is required in patients with
impaired renal function.
Potent osmotic diuretic
May cause
- initial hypervolaemia
- late hypovolaemia
- hyperosmolal state
- osmolal gap.
Maintain measured osmolality < 300 mosmol/l
Limited role in suspected acute life-threatening
intracranial hypertension as a bridge to definitive
surgical therapy.
Limited (unproven) roles in rhabdomyolysis,
transfusion reactions, myoglobinuria for renal
Gastrointestinal Drugs
1. Stress ulcer prophylaxis
a) Routine ‘stress ulcer prophylaxis’ is not indicated:
i) Low prevalence of clinically significant bleeding due to stress ulceration
ii) No evidence of survival benefit with use of stress ulcer prophylaxis
iii) Possible increased incidence of VAP and/or clostridium difficile infection
b) Pantoprazole may be considered in patients at high risk.
c) Patients on pre-existing therapy (with PPIs or H2-blockers) should be continued
d) Patients with clinically suspected GI bleeding should commence on a PPI
e) Enteral feeding should be commenced as soon as possible.
2. Acute GI bleeding
a) Definition
i) Overt bleeding
 Blood in the NGT
 Haematemesis or malaena
ii) Plus either:
  MAP > 20 mmHg
  Hb  20 g/L in 24 hours
 Required  2 units blood transfusion in 24 hrs
iii) Blood in the NG tube is frequently due to local erosion and by itself does not
constitute clinically significant GI bleeding.
b) Management
i) Resuscitation - ABC
ii) Correct coagulopathy
iii) Cease heparin / anticoagulants
iv) Commence PPI - pantoprazole 40 mg bd/tds.
v) Endoscopy  sclerotherapy
vi) If the source is not identified and with ongoing bleeding, consider:
 Labelled red cell scan
 Angiography (+/-embolisation), or
 Colonoscopy.
3. GI drugs
Table: GI Drugs
Clinical uses
10 mg IV 6 hrly, prn
Persistent vomiting, nausea
Large gastric aspirates
(in combination with erythromycin)
100-200 mg IV bd
Large gastric aspirates
(in combination with metoclopramide)
0.625 mg IV prn
Potent, effective antiemetic
Minimal side effects
2 mg IV / oral daily
Use if anticholinergic side effects are to be
4 mg IV prn / 12 hrly
Second line, antiemetic
(not available at RAH)
50 mg 8hrly IV
150-300 mg daily po
Stress ulcer prophylaxis
Peptic ulcer disease
Does not prevent acute rebleeding
Reduce dose in renal failure.
Acute RX:
40 mg IV bd/tds
Maint. RX:
40 mg daily
First line RX for peptic ulceration
Refractory peptic ulcer, ulcerative oesophagitis
Z-E syndrome
Upper GI bleeding
Bolus: 50 g IV
Varices: 50 g / hr
Fistulae: 100-200 g
sc 8-hrly
Variceal bleeding
(as effective as sclerotherapy)
Enteric, pancreatic fistulae
Sulphonylurea overdose
Severe secretory diarrhoea, e.g. post-chemo
K. Antibiotics
1. Policy
a) Prescription of antibiotics must conform to RAH guidelines.
b) The over-prescription and irrational use of antibiotics is associated with the
development of bacterial resistance, nosocomial infection and drug related
c) All antibiotics must be reviewed daily and where appropriate, discussed with
Infectious Diseases or Clinical Microbiology.
d) Record the day and expected course of antibiotics in the left-hand margin of the
drug chart, e.g. ‘D4/7’ = day 4 of a 7 day course.
e) Record date, test and results (including sensitivities) in the “results folder”.
2. Principles of antibiotic prescription
a) The treatment of infection consists of (in order of priority)
i) Adequate resuscitation
ii) Source control  drainage of infected collections, etc.
iii) Relevant samples for microbiological and/or histological analysis
iv) Routine cultures:
 Blood - 2 sets at different times from venous stabs
 Urine
 Sputum
 Any other suspicious site
v) Prompt administration of
 Rational empiric antibiotics
 Culture-directed antibiotics
 NB: time to effective ABx treatment affects outcome.
b) General indications for antibiotics:
i) Prophylaxis for invasive procedures and operations
 Proven indications
a. Abdominal surgery which involves a breach of the colonic mucosa
(traumatic or elective), or draining an infected cavity
b. Selected obstetrical and gynaecological procedures:
i. Caesarean section with ruptured foetal membranes
ii. Vaginal hysterectomy
c. Insertion of a prosthetic device
d. Compound fractures
e. Amputation of gangrenous limb
 Unproven but recommended
a. Lacerations penetrating into periosteum or into joint cavities
b. Crush injuries
c. Insertion of a neurosurgical shunt
d. Cardiac valve replacement
e. Arterial prosthesis
Empirical antibiotics
 Obtain as many cultures as possible before antibiotics commenced.
 Should be commenced early in critically ill patients
 Should be rationalised according to gram stain & culture results.
iii) Specific infections where the organisms is known
c) Complications of antibiotics
i) Antibiotic effect related
 Bacterial resistance
 Nosocomial infection
 Pseudomembranous colitis
ii) Systemic reactions
 Skin rashes
 Anaphylactoid / anaphylactic reactions
iii) Specific organ toxicities, e.g.
 Interstitial nephritis, ATN
 Seizures
 Marrow suppression, thrombocytopaenia
 QT prolongation
iv) Cost
d) Gentamicin / Tobramycin
i) Where possible, the aminoglycosides should be used for a limited duration
and therapy changed to a suitable alternative when possible.
ii) Pharmacodynamic properties
 Concentration-dependent killing  peak:MIC ~ 10:1
 Significant post-antibiotic effect
iii) Toxicity
 Nephrotoxicity
- non-oliguric renal failure
 Ototoxicity
- permanent, vestibular or auditory
iv) Dosing
 All dosing is by estimated Lean Body Weight (LBW):
a. Male:
kg  50 + 0.9×(height - 150cm)
b. Female: kg  45 + 0.9×(height - 150cm)
 Initial Dose: 5-7 mg/kg *irrespective of renal function
a. Measure level 6-10 hrs post-dose
b. Liaise with ICU Pharmacist (Pg: 22916), or
Drug Information (Ext: 25546) re further dose requirements.
c. Do not use the standard dosing normogram in ICU patients.
 Synergistic gentamicin, e.g. tds dosing in endocarditis
a. Measure pre-dose trough levels
b. Aim for < 1.0 mg/L to avoid toxicity.
e) Vancomycin
i) Pharmacology
 Time-dependent killing  max 24h-AUC:MIC ratio
 Moderate post-antibiotic effect
 Renally cleared
 Plasma t½  4-6 hrs
ii) Toxicity
 Ototoxicity
< 2%
 Nephrotoxicity
- very rare (20 case reports 1956-84)
*probably non-existent with current preparations
 ‘Red-man’ synd.
 rate of IV administration.
iii) Preference in ICU is for continuous infusion, c.f. interval dosing.
 More constant plasma levels & efficacy
 Reduced ‘red-man’ syndrome
 Irritant to veins, dilute to 250ml
 Daily drug levels until stable
*assessment of CrCl in critical illness is sub-optimal.
iv) For patients on CRRT or CrCl < 20ml/min
 Intermittent Dose = 1.0g slow IV when levels < 15mg/l
v) For patients transferring to the ward, see RAH intranet guidelines.
Table: Vancomycin Dosing Schedule
> 60 ml/min
Initial Dosing
Renal Function
Loading dose IV
Infusion Rate
2.0-4.0g / 24 hrs
1.0g / 24 hrs
 Dose 1.0g/day§
 Dose 0.5g/day§
 Dose 500mg/day
 Dose 250mg/day
Target Level = 20-25mg/L  Cont Current Infusion Rate
Not indicated
*Daily levels until stable
< 15mg/L§
> 30mg/L
CrCl < 20 ml/min
25 mg/kg (max 2.0g) | Slow infusion (1/24)
in All Patients
Vanc Level
Infusion Dose Adjustment
Hold 12 hrs
Recheck Level
Hold 12 hrs
Recheck Level
critically unwell patients with low levels, consider giving a
further bolus dose 0.5-1.0g in addition to increasing the rate.
Not indicated
Table: Antibiotic Infusion Schedules
Standard Infusion Dose (per 24 hrs)  Renal Function
IV Loading
All Patients
Max Hrs
Penicillin G
CrCl > 60 ml/min
CrCl ~ 20-60ml/min
CrCl < 20 ml/min
1.0-4.0g/day – Per Levels
Not indicated
1 Standard
Infusion Orders:
(per Max Hrs Stability)
24 Hrs
Dose in 100ml {N.Saline | 5%Dext.}
@ 4ml/hr
12 Hrs
(Dose / 2) in 100ml {N.Saline | 5%Dext.} @ 8ml/hr
8 Hrs
(Dose / 3) in 100ml {N.Saline | 5%Dext.} @ 12ml/hr
6 Hrs
(Dose / 4) in 100ml {N.Saline | 5%Dext.} @ 16ml/hr
2 Vancomycin should be diluted into 250mls if given via a peripheral line. Loading dose over at least 60 mins, or 10mg/min.
*NB: Add the reconstituted solutions to a 100mL bag of compatible fluid, having first removed an equivalent volume of solution,
i.e. so the final total volume of the bag remains 100ml, then administer over the required interval.
3. Ventilator associated pneumonia (VAP)
a) Significant cause of mortality and morbidity in ICU
b) Clinical diagnosis based upon the presence of a number of the following:
i) New CXR infiltrates (hard to see in patients with ARDS)
ii) New clinical chest signs
iii) Increasing oxygen requirement
iv) Increased purulent sputum
v) Indications of systemic sepsis:
 Increased/decreased WCC
 Fever
 Hypotension
c) Treatment
i) Sputum culture
ii) Commence antibiotics immediately
 Tazocin 13.5g/24hrs &
Gentamicin 5mg/kg on day 1, then as per levels
 If gentamicin contraindicated, ciprofloxacin 200-400mg b.d.
 In patients with known MRSA or ICU stay > 5days
a. Add vancomycin
b. Stop if no gram positive organisms seen on micro
iii) Review sputum culture
 If no organism and not on ABx consider another diagnosis
 De-escalate to narrow spectrum therapy ASAP
 Normal treatment 5-7 days except pseudomonas sp. then 10-14 days
4. Antibiotic prophylaxis
a) Peri-operative (Table)
i) Ongoing prophylactic therapy is required for selected post-operative
patients in ICU.
ii) Refer to individual protocols for recommendations on pre-operative
antibiotic prophylaxis.
Table: Peri-operative Antibiotic Prophylaxis
 Elective cases
 Cefazolin 1g IV 8h x 3 doses
 Traumatic wounds
 Involving bone or joint
 Cefazolin 1g IV 8h x 2 days
compound fractures
Abdominal Surgery
 + severe tissue damage
 + myonecrosis
 + vascular injury
 Cefazolin 1g IV 8h x 2 days
 Colorectal
 Cefazolin 1 gm ± gentamicin 3 mg/kg
+ Gentamicin 5 mg/kg IV daily x 2 days
+ Benzyl pen. 3 g IV stat, 1.2 g IV 6h x 2 days
+ Metronidazole 500mg IV single doses
 Biliary surgery
 Gentamicin 3 mg/kg x 1 dose, or
cefazolin 1g x 1 dose
Vascular surgery
 Elective cases
 + severe bowel injury
 + myonecrosis or
vascular injury
 Amputation
 Cefazolin 1g IV 8h x 3 doses
 + Gentamicin 5 mg/kg LBW IV daily x 2 days
+ Metronidazole 500 mg IV bd x 2 days
+ Benzyl pen. 3 g IV stat, 1.2 g IV 6h x 2 days
 Cefazolin 1g IV 8h x 3 doses
+ Metronidazole 500 mg IV bd x 2 doses
 CSF leak / # Skull base
 None: treat only if signs of meningitis
 Craniotomy / ICP insertion
 Cefazolin 1g IV at induction
Head & neck,
 Craniofacial with breach of
 Cefazolin 1g IV 8h x 3 doses
Cardiac Surgery
 See Section “Management of Cardiothoracic Patients”
nasal or oral mucosa
+ Metronidazole 500 mg IV bd x 2 doses
Table: Perioperative Endocarditis Prophylaxis
Table: Empiric Antibiotics
Type / Comment
 Community acquired
 Immunocompetent
 Admitted to ICU / HDU
(i.e. respiratory failure)
 Azithromycin 500mg IV daily, plus
*Ceftriaxone 1 IV daily
 For treatment failure, consider Moxifloxacin
400mg IV daily ± Flucloxacillin 1g 6h
(if high suspicion of S.aureus)
 *Default ICU therapy differs from the RAH standard protocol (penicillin + gentamicin) due to
the wide variability in renal function in ICU patients and the inability to use baseline creatinine
as a marker of renal function.
 Ventilator associated
 Hospital acquired
 Tazocin 4.5g IV 8 hrly or 13.5g/day
+ Gentamicin 5 mg/kg IV daily
 Consider Vancomycin 1g b.d. IV
 See above
 Immunocompromised host
 Contact ID
 No antibiotics without evidence of proven infection.
 With proven infection
 Benzyl penicillin 1.2g IV 6 hrly, plus
metronidazole 500 mg IV 12 hrly
Exacerbation of
 No clinical signs of pneumonia
 Treat as community acquired pneumonia
 Usually H. influenzae
 Ceftriaxone 1 g IV daily
 Suspected bacterial
 Usually:
pneumococcus, or
H. influenzae
 Ceftriaxone 2g IV 12 hrly, plus
Penicillin 1.8g to 2.4g IV 4 hrly
 Dexamethazone 10mg IV
before or with the first dose of antibiotic
then 6hrly for 4 days
 Not definitely bacterial
 Consider Acyclovir 10mg/kg IV 8hrly
 Without systemic sepsis in patients
with a urinary catheter
 No treatment.
 Remove / change catheter
 With systemic sepsis
 Amoxycillin 2g IV 6 hrly, plus
gentamicin 5mg/kg IV daily, or
 Ceftriaxone 1gm IV daily
if unable to tolerate gentamicin
 Faecal peritonitis
 Perforated viscus
 Amoxycillin 2 gm IV 6 hrly
+ Gentamicin 5 mg/kg IV daily
+ Metronidazole 500 mg IV bd x 7 days
 Recurring intra-abdominal sepsis or
failed Rx with above
 Consult ID/Clinical Microbiology
 No CT evidence of necrosis
 No antibiotics
 Significant CT necrosis
 Tazocin 4.5g IV 8 hrly
 Acute cholecystitis
 Amoxycillin 1 g IV 6 h
+ Gentamicin 5 mg/kg/d IV x 7 days
 Amoxycillin 2 gm IV 6 h
+ Gentamicin 5 mg/kg/d IV
Urinary tract
Biliary sepsis
 Ascending cholangitis
 Previous biliary tract surgery or
known biliary obstruction
 add Metronidazole 500mg IV BD x 7 days
 Septicaemia secondary to PID
 Amoxycillin 2g IV 6 h
+ Gentamicin 5 mg/kg IV dly
+ Metronidazole 500 mg IV bd x 5 days
 Suspected S. aureus infection
 Lincomycin 1.2g IV bd
+ Gentamicin 5 mg/kg IV dly x 7 days
 Community acquired
 Benzyl penicillin 1.8 g IV 4 h
+ Gentamicin 1 mg/kg IV tds
± Flucloxacillin 2g IV qid
 Hospital acquired
 Prosthetic valve, or
 Penicillin allergic
 Vancomycin 1g IV bd
+ Gentamicin 1 mg/kg IV tds
Gynae sepsis
Suspected Bacterial
 3 sets of blood cultures, and review at 48 hrs
 Manage pre-dose trough levels for gentamicin <1 mg/L to avoid toxicity
 Suspected candidiasis
 Amphotericin 0.5-1 mg/kg/day, or
 Fluconazole 400 mg IV daily
(in non-neutropaenic patients)
 Suspected aspergillosis
 Voriconazole IV/oral 6mg/kg BD loading for 24
hours, then 4mg/kg BD
 Caspofungin 70mg IV daily loading for 24
hours, then 50mg daily
Consult ID for all proven fungaemias
Remove all potential sources of infection (lines, catheters, etc)
Monitor renal / hepatic function during the course of antifungal therapy.
Adjust the amphotericin dose in renal insufficiency, or consider the use of fluconazole if
Voriconazole levels can be monitored for toxicity and clinical responses.
IV voriconazole is contraindicated in patients with CrCl < 30mL/min due to accumulation
of the excipient
No antibiotics without evidence of bacterial infection
 Wound infection
+ signs of systemic sepsis
 Benzylpenicillin 1.8 g IV 4 h
+ Flucloxacillin 1-2 g IV 6 h or
 Cefazolin 1g IV 8h
 Synergistic gangrene
 Necrotising fasciitis
 Meropenem
 Lincomycin 600 mg IV 8 hrly, or
Clindamycin 600 mg IV 8 hrly
 Consider IV-Ig 2.0g/kg total dose (3 days)
 In addition to surgery
± hyperbaric oxygen
 Severe oral infections
 Penicillin 1.2 g IV 4-6 hourly
+ Metronidazole 500 mg IV bd
 Patient not overtly septic
 Remove unnecessary, old or clinically suspect
lines & send for culture.
 Blood cultures by venipuncture
 No antibiotics
 Patient overtly septic
 Prosthetic valve / arterial graft
 High risk patient
 Vancomycin 1 g IV BD until blood culture
results available
Line sepsis
Table: Antibiotics for Specific Organisms
1st choice
2nd choice
Benzyl penicillin 1.2g IV 4-6 h
Ceftriaxone 1 IV dly
Staphylococcus aureus
Flucloxacillin 2 gm IV 6 h
Vancomycin 1gm IV bd or
Cefazolin 1-2g IV 8h
Benzyl penicillin 1.2g IV 4-6 h
Ceftriaxone 1g IV dly
Meningococcus contacts
Ciprofloxacin 500mg po x 1dose
Rifampicin 600mg po bd x 2 days
Vancomycin 1g IV bd
Consult ID
Amoxycillin 1-2 g IV 6 h
(+ Gentamicin 5 mg/kg if SBE)
Vancomycin 1g IV dly
(+ Gentamicin 5mg/kg if SBE)
Gp A Strep.
With Shock
Benzylpenicillin 1.8g 4 hrly IV
+ Lincomycin 1.2g IV bd
+ Intragam 2.0g/kg total dose (3 days)
Consult ID
Haemophilus influenzae
Ceftriaxone 1g IV daily
Amoxycillin 1-2 g IV 6 h
(if sensitive)
H. influenzae contacts
Rifampicin 600 mg oral bd x 4 days
Ceftriaxone 1g IM dly x 2 doses
E. Coli
Gentamicin 5 mg/kg IV dly
Ceftriaxone 1g IV dly
Gentamicin 5 mg/kg IV dly
Meropenem 500mg IV 8h
Gentamicin 5 mg/kg IV dly
Ceftriaxone 1g IV dly
Pseudomonas aeruginosa
Piperacillin 4 g IV 8 hrly
+ Gentamicin 5-7 mg/kg IV dly
Choice based on sensitivity results:
Ceftazidime 2g IV 8hrly
Tazocin 4.5g IV 8hrly
Gentamicin 5-7 mg/kg IV daily or
Ciprofloxacin 400mg IV bd
Legionella spp.
Moxifloxacin 400mg IV daily
Azithromycin 500mg IV daily
Mycoplasma pneumoniae
Erythromycin 1g IV 6h
Pneumocystis jurovecii
Co-trimoxazole 15-20 ml IV 6 h
+ methylpred 40mg bd x 5d,
methylpred 40mg die x 5d,
methylpred 20mg die x 11d,
Pentamidine isethionate
4 mg/kg/day IV
+ methylprednisolone
40mg 6 hrly x 7days
Clostridium difficile:
1. Mild / moderate
Cease antibiotics
1. Metronidazole 400 mg o tds
(or 500mg IV if npo)
x 7-10 days
2. Repeat above
Consult ID or Clinical Micro.
Treatment options are:
Bacitracin 25,000U 6hrly 7-10d
Vancomycin 125mg po 6hrly 7-10d
Benzylpenicillin 1.8g IV 4 hrly
+ Gentamicin 5 mg/kg IV dly
+ Metronidazole 500 mg IV bd
+ surgical debridement
 hyperbaric oxygen
Lincomycin 600 mg IV 8 hrly
+ Gentamicin 5 mg/kg IV daily
Severe, or relapse post RX
Clostridial infection
(Polymicrobial Infection)
Cease IG when pt. improves
Principles of Fluid Management in Intensive Care
1. All fluids, infusions are reviewed daily and rewritten:
a) On the ICU flowchart (Units A & B), or
b) In the IV Fluid chart in the ward folder (Unit C).
2. Assessment of volume status and fluid balance:
a) Clinical markers
i) Skin turgor, mucous membranes, capillary refill, peripheral perfusion
ii) HR, BP, Urine output
iii) CVP, PAOP
iv) PiCCO catheter - GEDI, ELWI, stroke volume variability.
v) CXR, interstitial oedema
vi) Echo – IVC distensibility index, LVOT-VTI variability
b) Biochemical markers
i) Serum Na+, Cl-, osmolality
ii) Urea / creatinine (± ratio)
iii) Bicarbonate
iv) Haematocrit
c) Charted fluid balance (notoriously inaccurate!)
i) Total intake including drug & infusion volumes
ii) Total output including urine output, drains, NG losses, blood loss
iii) Insensible losses due to pyrexia, transcellular shifts, etc.
(NB: usually impossible to quantify accurately)
3. Fluids should be considered in two components:
a) Maintenance fluids
i) Usually crystalloids - 5% dextrose, 4% dextrose + 1/5 N.Saline
- N.Saline
- Hartmann’s, CSL
ii) Usual volumes: 25-30 ml/kg/day  80-120 ml/hr
iii) TPN (refer to guidelines)
b) Replacement / resuscitation fluids
i) N.saline should be used for most fluid resuscitation.
 Equivalent to 4% albumin for resuscitation
 Better for patients with head trauma.
ii) Colloid
- 4% albumin, gelofusine
 May be considered for fluid resuscitation in selected patients.
 Greater cost, no demonstrable advantage.
 Should be avoided in patients with traumatic brain injury.
iii) Blood and components as indicated according to NH&MRC guidelines.
iv) Crystalloid replacement is usually used for excessive renal, enteric and
burns losses (see below).
v) Hyperchloraemia may be harmful so consider the use of fluids with other
anions, e.g. Hartmann’s.
4. Composition of commonly used fluids (1000ml solution):
Table: Common IV Solutions
N Saline
N/2 Saline
N/5 Sal. + 4% Dex.
5% Dextrose
Gelofusine (500ml)
Albumex 4% (500ml)
40 g
50 g
5. Fluid management in burns patients
a) The RAH Burns Unit uses the modified Parkland regimen.
b) This is a guide - other clinical markers such as urine output, heart rate, blood
pressure, CVP, serum sodium and osmolality, and haematocrit must be taken
into account.
c) As a result, both solution composition and administration rate may have to be
modified in order to maintain the above parameters within normal ranges.
d) Protocol:
i) Assess the patient’s % burn surface area (%BSA) using an accurate chart.
ii) Assess patient weight (kg).
iii) Formula:
 First 24 hours
= total fluid (as Hartmann’s solution):
Wt. x %BSA burn x 4.0 ml
a. give ½ the total fluid during first 8 hours post-burn
b. give ½ the total during the subsequent 16 hours
 Second 24 hours fluid is given as Albumex 4%
Wt x %BSA burn x 0.5 ml
 Other maintenance fluid is given according to the above physiological
 The primary endpoint of fluid resuscitation is generally accepted to be
a urine output  0.5-1 ml/kg/hr
 Catecholamines:
a. Should be commenced only when adequate volume replacement is
unable to maintain a satisfactory urine output, or there is
associated myocardial failure.
b. The duty consultant or SR should be consulted prior to use.
iv) Commence enteral feeding as soon as possible.
1. Enteral nutrition
a) Enteric feeding is the preferred mode of nutritional support and should be
considered in all patients as soon as possible after admission.
b) Advantages
i) Early EN in trauma patients has been associated with improved outcome.
ii) Use of the gut decreases mucosal atrophy, which may reduce bacterial
translocation thereby reducing the incidence and duration of sepsis.
iii) The incidence and severity of gastric erosions and stress ulceration may be
iv) Cheaper than TPN
v) CVC complications (especially infection) are reduced or avoided.
c) Disadvantages
i) Regurgitation / aspiration
ii) Nosocomial pneumonia
iii) Diarrhoea (other causes are more likely than enteral feeding)
d) Indications
i) As soon as possible in all intubated / tracheostomised patients, where
admission and duration of intubation is expected to be > 24-48 hours.
ii) Patients with an operative jejunostomy may commence feeding within 6
hours of placement.
e) Contraindications
i) Gastrointestinal (including oesophageal) perforation, gastrointestinal
fistulae, bowel obstruction, ileus.
ii) Recent bowel anastomosis is not a contraindication – however, discussion
with the surgical team is essential.
iii) Absent bowel sounds are not a contraindication.
f) Protocol (see feeding protocol at bedside)
i) Liaise with the dietician (who will order feeds) during the fluid round.
ii) Outline any problems: e.g. hyperkalaemia, renal failure, osmolality
iii) Place a 12F or larger nasogastric tube (to allow reliable aspiration)
iv) Use orogastric tubes in patients with anterior and middle cranial fossa #
v) Check the position of the feeding tube with x-ray prior to use.
 Attach label to NG tube, and
 Document in notes that the position of the tube has been checked.
vi) Nurse the patient at 30-45° head up.
vii) Commence feed at 80 ml/hr continuously according to the protocol.
viii) Aspirate all NG and PEG tubes 6 hrly
ix) Do not aspirate jejunostomies, naso-duodenal/jejunal tubes or PEJs
Flush jejunostomy/gastrostomy tubes with 20ml N.saline 6hrly.
 Aspirate < 250 ml:
a. Return aspirate to stomach
b. If {rate < max} then increase rate by 20 ml/hr
c. Repeat aspiration at 6hrs and
If {aspirate < 250 ml} then  rate to max (usually 80-100 ml/hr)
 Aspirate > 250 ml:
a. Return 250 ml
b. Halve the feed rate (not less than 20 ml/hr)
c. Continue to aspirate 6 hrly
d. Consider prokinetics:
i. Metoclopramide 10 mg IV 6 hrly, plus
Erythromycin 100-200 mg IV bd
ii. Continue until tolerating feed for > 72hrs,
then cease and observe
iii. Recommence as needed
e. Reduce narcotic administration if possible.
 Aspirates > 250 ml while receiving prokinetics, consider:
a. Post-pyloric feeding tube
i. Using the Cortrak® device, or
ii. Endoscopically placed by the GI Unit
b. Feeding jejunostomy
c. Nasogastric naloxone 4-8mg tds
d. TPN.
Consider a PEG, PEJ or feeding jejunostomy in long term patients
e.g. Guillain Barré or severe head injury
Cease feeds 4 hrs prior to extubation, tracheostomy, ET tube change.
There is no requirement to cease feeds until immediately prior to going to
theatre, unless:
 Surgical procedure on the GIT
 Planned for tracheostomy or ETT change.
Remember to modify insulin dose when feeds are reduced or ceased.
2. Enteral Protocol - See over page.
Flowchart: Nutritional Therapy Protocol
Patients expected to be mechanically ventilated for > 48h should have
enteral nutrition (EN) commenced within 24 h of admission to ICU
Pts unsuitable
for EN should
be considered
for TPN if EN
unlikely for > 5
days. Include;
short gut, GI
to placing NET,
GIT perforation.
feeds should
commence at
rate of 1 ml/kg/h
or as
by Dietitian and
flushed 20 ml N
saline QID.
Insert NET, confirm position by XR and confirm
suitability for commencement of feeds
Commence feeds Osmolite 1 ml/kg/h
(1 kcal/ml @ max 80 ml/h)
(unless pt fluid restricted)
Refer Pt to Dietitian for Nutritional Ax
Check Gastric residual volume (GRV) every 6 h
for ALL gastric tubes, document on chart.
Do NOT aspirate post pyloric tubes.
GRV < 250 ml
return aspirate,
continue feed
regimen (if not at
goal increase rate
by 20 ml/h)
GRV ≥ 250 ml
return 250 ml,
halve feed rate,
Feeding interruptions
• Do not hold feeds for
routine nursing care,
bedside procedures
or diagnostic tests
unless specified.
• No need to fast prior
to surgery unless
ETT to be removed,
i/o tracheostomy,
tracheostomy change
or GIT surgery.
• If fasting for theatre,
commence fast when
pt called to theatre.
Or fast for 4 hr prior
to r/o ETT, i/o
tracheostomy change
or surgery on gut
• EN and insulin to
cease during time in
OT and restart at
same rate as when
• Cease feeds 4hr prior
to planned
Do NOT aspirate post pyloric feeding tubes.
Monitor pt for signs of intolerance including abdominal distension, constipation,
diarrhoea or vomiting. Notify physician of concerns.
If GRV remains high (i.e. 2
aspirates ≥ 250 ml within
12 h) consider post-pyloric
Both Metoclopramide 10mg QID IV and Erythromycin 100 - 200mg BD IV
Metoclopramide not recommended for use in head injury pts.
Consider TPN if unable to
place post pyloric tube
Referral to Dietitian for Nutritional Ax
Weekdays - ICU Dietitian will review ICU / SDU pts daily and chart max recommended feeding rate on daily obs chart.
Contact ICU Dietitian on Pg 1342 if any concerns / queries.
Weekends - Nursing T/L should be advised of new NET / changes to existing regimens. On call Dietitian should be
contacted (SD 1156 / 0401711460) and advised of - new ICU / SDU NET feeds; changes to existing regimens; pt
Cover (when ICU Dietitian on leave) - Clinical Dietetics should be contacted (Pg 1342) and advised of all NEW ICU /
SDU NET feeds and changes to existing regimens.
3. Post-pyloric feeding protocol:
a) Commence feed at 1ml/kg/hr, up to a maximum 80 ml/h.
b) No need to cease feed for any procedures, other than GI surgery.
c) Consider placement of a NG tube to aspirate and ensure an empty stomach.
4. Parenteral Nutrition
a) General principles
i) TPN may be harmful in critically ill patients.
ii) Enteral nutrition is preferred and TPN should only be considered for patients
in whom this is not possible.
iii) Supplementing EN with TPN is not beneficial and should be avoided.
iv) Refer to ‘Clinical Duties Outside ICU’, regarding the responsibilities and
management of ward patients receiving TPN.
v) TPN is usually ordered by the Unit A Senior Registrar, under the supervision
of Dr Adam Deane.
vi) IV access may be via a CVC or PICC line, with the latter being preferred.
vii) TPN for ICU patients is prescribed during the midday fluid round.
viii) Patient being discharged from ICU on TPN must be entered into the TPN
folder in Unit A.
b) Indications for TPN in the patient who cannot be fed enterally are:
i) GIT Failure > 7-10 days and expected duration of support > 5-7 days.
 Prolonged post-operative ileus
 Enteric fistulae
ii) Short GIT syndrome following major intestinal resection.
c) Complications of TPN:
i) Depression of immune function, esp. in cancer patients
ii) Intestinal villous atrophy
iii) Metabolic imbalance
 Electrolyte disturbances ( K+, HPO4=, Mg++)
 Glucose intolerance: hyperglycaemia and glycosuria
 Hyperosmolar dehydration syndrome
 Rebound hypoglycaemia on cessation of TPN
 Hyperbilirubinaemia
 CO2 production, esp. in COPD patients
iv) Central venous access complications
d) Protocol
i) On commencement:
 Add the following orders to the patient's drug folder:
a. Cernevit MV 1 ampoule IV daily.
b. Trace elements 1 ampoule daily
c. Vitamin K 10 mg IV weekly
d. Commence insulin:
i. Initial dose = 5U s.c. qid
*hold if BGL < 10
ii. Check BGL qid
iii. Adjust the dose on subsequent days guided by BGLs
iv. “Sliding Scale” regimens are no longer used.
 Commence TPN solution at a lower rate (40ml/hr) in “starved” patients
a. Potential movement of K+ / HPO4= into cells with re-feeding
b. May cause acute severe hypokalemia and hypophosphataemia.
 Slowly increase to desired rate, usually 60-80 ml/hr.
 Dietician will provide a calculated energy requirement as a guide
ii) Daily:
 Review the patient, CVC site, biochem, BGL chart and fluid balance.
 Prescribe TPN selecting the most appropriate “option” from the table
 These bags are pre-prepared and must not be altered, i.e. no further
additives. Patients requiring K+, PO4 and fluids etc. above the quantities
provided must receive these in a separate line/infusion.
iii) Intralipid
 Commence TPN with lipid-free solutions (#3, #4)
 Lipid is indicated if the period of malnutrition > 4 weeks or if the patient
is hyperglycaemic.
Table: Average Daily Requirements
0.5-2.0 g/kg/day
1.0 mmol/kg/day
1.0 mmol/kg/day
Dependent on renal function
0.2 mmol/kg/day
Dependent on renal function
B groups daily
B12, Folate, A, D, E, K weekly
1. Urine
2. Nasogastric/ileostomy
3. Pancreatic/biliary fistulae
1. Glucose: 2g/kg/day @ 4.1 kcal/g
2. Fat:
2g/kg/day @ 9 kcal/g
1. 2:5 essential:total amino acids
2. 150:1 kcal:g N2 (non-nitrogen kcal)
Trace elements as required.
1. ½ Normal saline ± KCl 10 ml/L
2. ½ Normal saline ± KCl 10 ml/L
3. Hartmann’s solution
Table: Baxter TPN Solution Options
Baxter Option 1
With Lipid
With Potassium
Baxter Option 2
With Lipid
No Potassium
Baxter Option 3
No lipid
With Potassium
Baxter Option 4
No Lipid
No Potassium
Total Volume
Solution shelf life
12 mths room T
6 mths room T
12 mths room T
6 mths room T
Lipid source is Clinoleic 20% which comprises olive oil 80% and soya oil 20%.
Multivitamin and trace elements to be given separately from TPN.
Nothing may be added to TPN bags.
All solutions come in triple phase bag and have light protection cover.
NB: Specialised prescription TPN can be ordered via pharmacy, e.g. when large daily potassium requirements are not feasibly
administered by 10mmol/100ml bags and the standard 60mmol/2L TPN.
Blood Component Therapy
1. Indications
a) Blood component therapy should only be given if benefit outweighs the risk
b) The decision to transfuse should be based on clinical assessment, disease course
and response to previous transfusion as well as [Hb] levels.
c) Potential risks including
i) Mis-identification / acute transfusion reaction
ii) Bacterial / viral infection
iii) Transfusion associated acute lung injury (TRALI)
iv) Transfusion associated circulatory overload (TACO)
v) Immune modulation (this and TRALI are probably the most significant)
d) The best way to reduce the risk of blood component therapy is to reduce
i) Minimise unnecessary blood sampling
ii) Minimise blood loss during procedures
iii) Consider nutritional and iron stores state
2. Red Blood Cells
a) Elective
*as per NHMRC / ASBT guidelines.
i) Use of RBCs at Hb > 100g/L is likely to be inappropriate
ii) Use of RBCs at Hb < 70g/L is likely to be appropriate but in some
asymptomatic patients a lower threshold may be acceptable
iii) At Hb 70-100g/L clinical assessment of risk versus benefit is required.
iv) The following criteria may indicate RBC transfusion is indicated
 Significant ongoing bleeding present or anticipated.
 Clinical signs of impaired oxygen transport such as dyspnoea,
tiredness/weakness, angina, syncope.
 Cardiac ischaemia or cardiac failure due to anaemia.
v) Order as “Red cells” or RBCs on the ICU or ward fluid chart
vi) “Type & Screen” specimens are held for 10 days for compatibility testing.
vii) For transfusion, a new specimen is needed for cross-match every 72 hours.
b) Resuscitation
i) Abnormal bleeding is usually surgical and requires urgent surgical and/or
radiological intervention.
ii) A full cross-match takes 30 minutes if marked urgent (not including the
time for transfer of blood); this should be performed if possible while
volume is replaced with crystalloid or colloid.
iii) If blood is required faster than this, the request “Time Required” box
should be marked:
 “Desperate”
*group O Rh(D)-ve blood is issued immediately
(see massive transfusion protocol)
 “10 minutes”
*group-specific (ABO/Rh-D) but without full
compatibility testing
 “30 minutes”
urgently processed, fully crossmatched blood
NB: The requesting MO accepts full responsibility for these (*)
iv) Blood replacement should start immediately in the setting of:
 Rapid blood loss leading to hypovolaemia and shock.
 Blood loss estimated or anticipated to exceed 20-25% of blood
volume, i.e. 1000-1500 ml in a normal adult.
3. Massive Transfusion Protocol
a) Definition:
i) Loss of one blood volume within a 24 hr period.
ii) Alternative, more practical definitions:
 ≥ 50% blood volume loss within 3 hr, or
 ≥ 150 ml/min rate of loss.
b) The RAH massive transfusion protocol should be activated as soon as the need
is identified
c) Correction of critical bleeding requires simultaneous approach to:
i) Control the source of bleeding
ii) Contact key personnel required for haemorrhage control
iii) Maintain blood volume
iv) Prevent hypothermia and acidosis
d) Principles
i) Trauma patients with critical bleeding are coagulopathic on presentation
ii) Prevention of further coagulopathy with aggressive management is much
more effective than delayed treatment
iii) Acidosis and hypothermia worsen coagulopathy
e) On identification:
i) Take blood and place in red bags for:
 CBE, Group and match
 Extended Coags
ii) Notify transfusion medicine on 47*
iii) Dispatch blood samples ASAP
iv) Transfusion will provide products in “Massive Transfusion Packs”
v) Notify transfusion when bleeding controlled
f) Tranexamic acid
i) Routinely used in trauma only as per CRASH2
ii) Triggers modified for local use (see Chart)
iii) Dose 1g over 10 minutes then 1g over 8 hours
iv) Delivered with first MTP pack
Table: Critical Bleeding (Massive Transfusion)
 Samples to Blood Bank for T&S
 CBE, INR, APTT, fibrinogen
 Biochemical profile, blood gases etc.
 Take samples at earliest opportunity as
results may be affected by colloid
 Mis-identification is commonest
transfusion risk.
 May need to give components before
results available.
 Use “Massive Transfusion–Priority
Processing” labels with ‘Red bag’ to alert
lab for speedy processing.
 Repeat CBE, INR, APTT, Fib
after blood component infusion, or
every 4 hrs until stable.
Suitable RBC
 Un-crossmatched group O Rh(D)
negative in extreme emergency until
blood group known, then group-specific.
 Then fully crossmatched blood when
time permits.
 To prevent hypothermia by the use of
blood warmer and/or rapid infusion
 Employ intra-op blood salvage if
available and appropriate.
 Rh(D) positive is acceptable if patient is
male or post-menopausal female.
 Laboratory will complete compatibility
testing after issue.
 Further compatibility test not required
after replacement of 1 blood volume (8–
10 units).
 Blood-warmer indicated if flow rate >50
ml/kg/hr in adult.
 Salvage contraindicated if wound heavily
 Anticipate platelet count <50x109/L after
2 x blood volume replacement.
 Target platelet count: >100x109/L for
multiple/CNS trauma or if platelet
function abnormal.
 Target >50x109/L for other situations.
(10-15 ml/kg – 1 litre
or 4 units for an adult)
 Aim for INR <1.5 and APTT <40 secs.
 Allow for 30 min thawing time.
 Consider extended life plasma
 INR >1.5 and APTT >40 secs correlates
with increased surgical bleeding.
 Keep Ca++>1.13mmol/L
(2-4 units)
 Replace fibrinogen.
 Aim for fibrinogen >1.0 g/L.
 Allow for 30 min thawing time.
 Fibrinogen <0.5 strongly associated with
microvascular bleeding.
Fresh whole blood
 Request hospital Blood Bank to contact
ARCBS on-call MO.
 Anticipated major blood loss in elective
patients with platelet or coagulation
abnormalities. Continued significant
bleeding even after use of conventional
component therapy. Role in haemostasis
Recombinant FVIIa
 Obtain approval from consultation with
senior Surgeons / Anaesthetists /
Intensivists and Haematologists /
ARCBS on-call MO.
 May be considered when the patient’s
condition continues to deteriorate to
likely haemorrhagic death
 Usually as a desperate effort after other
measures fail.
Dose ~ 90 μg/Kg
See Massive Transfusion Protocol
4. Platelets
a) Standard dose is “Platelets - 1 Adult Pack”
b) Prophylactic transfusion before surgery or other “at risk” procedures:
i) Platelet count
< 50 × 109/L
ii) Platelet count
> 50 × 109/L
with evidence of inherited or acquired (drug-induced) platelet dysfunction
c) Prophylactic transfusion in marrow failure:
i) Platelet count
< 10 × 109/L, or
ii) Higher levels with clinical evidence of bleeding or other risk factor
d) Therapeutic transfusion for uncontrolled haemorrhage:
i) As per the massive transfusion protocol
ii) Platelet count
< 50 × 109/L
iii) Platelet count
< 100 × 109/L with microvascular bleeding
iv) Irrespective of platelet count with evidence of platelet dysfunction.
e) Platelet dysfunction can contribute to bleeding with a normal platelet count
f) ITP: Only if life-threatening bleeding is present.
5. Fresh Frozen Plasma (FFP)
a) Prophylactic transfusion before surgery or other invasive procedure that could
result in significant bleeding:
i) Urgent correction of prolonged INR or APTT in warfarin overdose or
vitamin K deficiency (see below)
ii) Correction of prolonged INR or APTT in liver disease
iii) Correction of inherited coagulation factor deficiencies where specific
coagulation factor concentrates are not available
b) Therapeutic transfusion for uncontrolled haemorrhage in:
i) Warfarin overdose
ii) Liver disease
iii) Vitamin K deficiency
iv) Inherited coagulation factor deficiencies where specific coagulation factor
concentrates are not available
v) DIC
c) Plasma exchange in TTP & related syndromes
d) As per the massive transfusion protocol
e) Post massive transfusion with coagulopathy:
i) INR > 1.5, or
ii) APTT > 40 seconds
6. Extended Life Plasma
a) Recent regulatory changes allow transfusion laboratories to used thawed FFP
for up to 5 days.
b) By using thawed FFP the product can now be provided immediately, c.f. the
standard 20-30 minute delay normally involved in thawing.
c) Five day thawed FFP will be labelled ‘Extended Life Plasma’
Table: Guidelines for the Management of an Elevated INR
Clinical Setting
INR < 5.0
Bleeding absent
 Lower the dose or omit the next dose of warfarin.
 Resume therapy at a lower dose when the INR approaches therapeutic range.
 If the INR is only minimally above therapeutic range (up to 10%), dose reduction
may not be necessary.
INR ~ 5.0–9.0*
Bleeding absent
 Cease warfarin; consider reasons for  INR and patient-specific factors.
 If bleeding risk is high, give vitamin K1 (1.0–2.0mg orally or 0.5–1.0mg IV) †.
 Measure INR within 24 hrs, resume warfarin at a reduced dose once INR is in
therapeutic range.
INR > 9.0
Bleeding absent
Any clinically
bleeding where
warfarin induced
coagulopathy is
considered a
contributing factor
 Cease warfarin therapy, give 5.0–10.0mg vitamin K1 intravenously, as well as
Prothrombinex-HT (25–50 IU/kg) and fresh frozen plasma (150–300mL), assess
patient continuously until INR < 5.0, and bleeding stops.§
 If fresh frozen plasma is unavailable, cease warfarin therapy, give 5.0–10.0mg
vitamin K1 intravenously, and Prothrombinex-HT (25–50 IU/kg), assess patient
continuously until INR < 5.0, and bleeding stops.§
 If Prothrombinex-HT is unavailable, cease warfarin therapy, give 5.0–10.0mg
vitamin K1 intravenously, and 10–15mL/kg of fresh frozen plasma, assess
patient continuously until INR < 5.0, and bleeding stops.§
Where there is a low risk of bleeding
Cease warfarin, give 2.5–5.0mg vitamin K1 orally or 1.0mg IV
Measure INR in 6-12 hrs & resume warfarin at a reduced dose once INR < 5.0.
Where there is high risk of bleeding‡
Cease warfarin, give 1.0mg vitamin K1 IV.
Consider Prothrombinex-HT (25–50 IU/kg) and FFP (150–300mL)
Measure INR in 6-12 hrs, resume warfarin at a reduced dose once INR < 5.0.
* Bleeding risk increases exponentially from INR 5 to 9,  INR ≥ 6 should be monitored closely.
† Vitamin K effect on INR can be expected within 6-12 hours.
‡ Examples of patients with a high bleeding risk:
active gastrointestinal disorders (such as peptic ulcer or inflammatory bowel disease)
those receiving concomitant antiplatelet therapy
those who underwent a major surgical procedure within the preceding two weeks, and
those with a low platelet count.
§ In all situations carefully reassess the need for ongoing warfarin therapy.
From consensus guidelines Australian Society of Thrombosis and Haemostasis 2004
7. Cryoprecipitate
a) Bleeding and fibrinogen < 1.0 g/L in:
i) DIC.
ii) Massive transfusion.
iii) Hereditary hypofibrinogenaemia.
b) 10U of cryoprecipitate will  plasma fibrinogen by ~ 1.0g/l
c) Standard dose = 8U for hypofibrinogenaemia.
a) Standard dose = 0.3-0.4µg/kg intravenously over 30 mins
b) Increases factors VIII:C, VIII:vWF and platelet adhesion.
c) Indications: actual, or significant risk of bleeding with,
i) Haemophilia A
ii) type I von Willebrand's disease
iii) Post cardio-pulmonary bypass (check with surgeon)
iv) Clinical scenarios where platelet dysfunction is likely
 Uraemia
 Drugs
- aspirin, clopidogrel
9. Recombinant activated factor VII (rFVIIa, NovoSeven)
a) TGA approved indications
i) Haemophilia patients with antibodies to factor VIII
ii) Glanzmann's thrombasthenia with antibodies to GPIIb-IIIa and/or HLA,
and who have past or present refractoriness to platelet transfusions
iii) Patients with congenital factor VII deficiency
b) Effective in improving coagulopathies associated with trauma, major surgery,
and organ transplantation = ‘off-label’ indications.
c) No risk of virus transmission and contains no human protein
d) Binds to tissue factor (TF) activating both factors IX and X.
i) High doses activate factor X on the surface of activated platelets
ii) Has both TF-dependent and TF-independent effects
e) Recommended dose for the treatment of a severe coagulopathy  90µg/kg
f) Acts within a few minutes and has a half-life of about 2.5 hours.
g) Requires consultant/haematology approval because of high cost and absence of
current TGA approval for these indications.
10. Dabigatran Clinical Guidelines
a) General Information
i) Dabigatran etexilate (Pradaxa) is a pro-drug of dabigatran
ii) Reversible direct thrombin inhibitor
iii) Onset of anticoagulant effect within 30 minutes after oral administration
iv) Peak plasma concentration and effect within 2-3hrs.
v) Usual half-life: 12-14 hrs
vi) Renally cleared, ClCr < 30 ml/min  t½ > 24 hrs.
b) Effect on Laboratory Coagulation Parameters
i) Monitoring is not routinely required
ii) No direct relationship between coagulation tests and therapeutic effect.
iii) Thrombin time (TT)
 Particularly sensitive to dabigatran 
 A normal TT excludes clinically significant dabigatran levels.
iv) Activated partial thromboplastin time (APTT)
 Shows best correlation with plasma levels
 Increasing APTT occurs with dabigatran concentration.
a. Usual peak concentration APTT
~ 2x control
b. Trough levels (12 hrs post dose)
~ 1.5x
 A normal APTT suggests that minimal drug is present
 A significantly prolonged APTT suggests drug excess:
a. APTT > 65s at trough (12 hrs post-dose) or
b. APTT > 80s at any time.
v) Prothrombin time (PT)
 At therapeutic concentrations (50-200 ug/L) dabigatran has little effect
on PT and therefore INR.
 INR results therefore do not reflect anticoagulant activity.
 At supra-therapeutic concentrations the INR may be  2.0.
c) Dabigatran Assay
i) Haemoclot dabigatran assay has been established by SA Pathology
ii) A “dabigatran level” should be requested on the pathology form and the
timing of the last dabigatran dose given.
iii) A single citrate tube is required. For further information ring 8222 3918.
d) Dabigatran and other anticoagulants
i) When converting patients from warfarin do not commence dabigatran
until the INR is < 2.0.
ii) For patients on dabigatran commencing parenteral anticoagulation, wait
 12 hours (CrCl ≥ 30 mL/min) or
 24 hours (CrCl < 30 mL/min) after the last dose.
iii) For patients receiving a parenteral anticoagulant commencing dabigatran
 LMWH (b.d.) commence dabigatran 0-2 hours before the next dose of
LMWH was to have been administered
 Heparin infusion - commence dabigatran on cessation of infusion.
e) Peri-operative dabigatran management
i) The requirement to cease anticoagulation should be assessed
ii) If cessation is required, the timing will be dependent upon renal function
and the bleeding risk associated with the procedure.
Table: Pre-operative Dabigatran Management
Renal Function
(CrCl ml/min)
dabigatran (hrs)
> 80
> 50 to  80
> 30 to  50
 30*
Timing of discontinuation prior to surgery
Standard bleeding risk
High bleeding risk
24 hrs
2-4 days
24 hrs
2-4 days
At least 2 days
4 days
2-5 days
> 5 days
NB: *Ongoing treatment with dabigatran should be reviewed as use in patients with a CrCl <
30ml/min is contra-indicated.
Bridging therapy with parenteral anticoagulation
i) Pre-operative bridging is not required in the majority of patients.
ii) Post-operative bridging
 The onset of therapeutic anticoagulation after administration of
dabigatran is rapid (within 1-2 hrs)
 Caution should be exercised in restarting within 48-72 hrs following
high bleeding risk procedures
 Alternative parenteral prophylactic anticoagulation may be warranted
(eg subcutaneous enoxaparin) in the time period prior to resuming
dabigatran, depending on the procedure performed.
g) Epidural and other regional anaesthesia/analgesia and dabigatran
i) LP, spinal, epidural and some forms of major regional block should not be
performed within 24 hrs post-dabigatran, longer with renal dysfunction.
ii) Dabigatran should not be administered to patients with an epidural catheter
in-situ (and some regional analgesia catheters – discuss with anaesthetist).
iii) Dabigatran should be delayed  4 hrs following performance of an
epidural, spinal, LP, regional block or after catheter removal.
h) Emergency procedures
i) Surgery or invasive procedures should be delayed at least 12 hrs post-dose
ii) An urgent APTT +/- dabigatran level can be requested and bleeding risks
are small providing:
 normal APTT or
 dabigatran level < 50 ug/L.
iii) See guideline for management of bleeding in patients receiving dabigatran
for details regarding the treatment of surgical bleeding.
Flowchart: Management of Bleeding Patient on Dabigatran
Bleeding Patient on Dabigatran
Initiate Standard Resuscitation Procedures as Required
Urgent bloods:
FBC, APTT, PT, TT and dabigatran level*
E, C&U, Creatinine
*2 x citrate tubes + time of last dose of dabigatran.
Severe Bleeding
Mild Bleeding
- Local haemostatic measures.
- Delay next dose of dabigatran
or discontinue if felt
appropriate by prescribing
Moderate Bleeding
- Consult critical bleeding on-call
- Consult critical bleeding on-call
haematologist via transfusion. (25430/25431)
haematologist via transfusion.
- Consider oral charcoal administration if
dabigatran ingestion < 2 hrs prior.
- Consult ICU or if necessary other
appropriate facility.
- Local haemostatic measures
- Institute measures as for moderate to
severe bleeding.
o Mechanical compression
o Consider seeking an opinion regarding
surgical intervention
- Administer rVIIa 90 ug /kg
- Maintain adequate hydration to aid drug
consider repeat dose at 30
- Transfusion support
- Consider dialysis particularly indicated if
high drug level as indicated by excessively
o Packed cell transfusion as indicated by Hb
and ongoing bleeding
(rounded up to nearest mg), and
minutes, if no response.*
prolonged aPTT > 80 secs or
o Consider platelet transfusion if platelets <
70 x 109/L or if taking antiplatelet therapy.
dabigatran level > 200 ug/L and/or impaired
renal function.
o Consider 25U/kg prothrombinex if INR >
Consider dose of rVIIa immediately prior to
vascular access if significantly prolonged aPTT.
o If ongoing bleeding resulting in clinical
instability despite above measures consider
4 hrs of haemodialysis will reduce
rVIIa* +/- dialysis as described as for severe
drug level by approx. 60%.
- Neither rVIIa nor dialysis is likely to improve
outcome in patients with a normal aPTT or a
dabigatran level of < 50 ug/L
Moderate bleeding – reduction in Hb ≥ 20g/L, transfusion of ≥ 2 units of red cells
Severe bleeding – bleeding in critical area or organ (intraocular, intracranial, intraspinal, compartment
syndrome, retroperitoneal or pericardial), hypotension not responding to resuscitation.
* This is an off license use of rVIIa (NovoSeven) and the risk of thrombotic complications when rVIIa is
used for this indication is unclear. The use of rVIIa is supported by laboratory data however clinical
evidence supporting an improvement in clinical outcomes is still lacking.
11. Disseminated intravascular coagulation (DIC)
a) Definition
i) DIC occurs when the balance of the haemostatic and fibrinolytic systems
becomes disordered. It occurs in response to severe pathophysiological
stimuli and is a part of multisystem organ dysfunction (often associated
with ARDS and acute renal failure). It is characterised by:
 Microthrombi formation causing microvascular obstruction
 Consumption of platelets and clotting factors
 Abnormal fibrinolysis
b) DIC screen:
i) Complete blood picture
 microangiopathic haemolytic anaemia with red cell fragmentation
 haemolysis
 thrombocytopenia
ii) Extended coagulation screen:
 prolongation of TCT, APTT, PT
 hypofibrinogenaemia
 low factor VIII
 excess fibrinolysis with elevated FDPs
iii) Liver and renal function tests
c) Treatment
i) Treatment of the underlying cause
ii) Replacement of blood components in the bleeding patient
- based on INR/APTT
 cryoprecipitate - for marked fibrinogen deficiency
iii) Controversial therapies (following consultant approval only)
 heparin, fibrinolytics (tPA)
 anti-fibrinolytics (EACA)
11. Blood transfusion reaction protocol
a) Plasma can cause reactions ranging from mild pruritus, erythema and urticaria
through to severe flushing, hypotension, fever, angioedema, bronchospasm and
fulminant anaphylaxis.
b) Suspected Reaction Protocol
i) Stop the transfusion immediately – do not disconnect the IV line.
ii) Recheck the patient identification on the blood product pack label against
the patient’s wristband and verbally with the patient if possible.
iii) If there is an unexplained discrepancy, discontinue the transfusion and
treat as per (iv, v below)
iv) Mild Reactions
  Temp. < 1.5º C
 Mild or no hives or rash.
 Action - slow the rate and continue transfusing the same unit of blood.
Severe Reactions
 Severe hives and/or a rash.
  Temp. > 1.5°C and is the only clinical sign or symptom
 Action
a. Consider an antihistamine and antipyretic
b. Cease and then restart transfusing the same unit of blood after
approximately 20 minutes.
 If there are further signs & symptoms of a reaction
 discontinue & order a transfusion reaction investigation
 If there is a sudden and acute change in the patient’s condition, e.g.
cyanosis, bad headache, backache, or significant change in pulse or
blood pressure for no apparent clinical reason
 discontinue & order a transfusion reaction investigation
vi) Investigation of a transfusion reaction:
 A transfusion reaction investigation form (IMVS 224) should be
completed and sent to Transfusion Medical Unit (TMU) with:
a. A description of the relevant clinical findings and vital signs
b. A post-reaction 10ml EDTA blood specimen, preferably from a
vein other than that used for transfusion
c. Any used or unused blood packs and the attached IV set(s).
 If there is a major reaction, it is also recommended that the first urine
specimen voided after reaction is saved, and patient’s urine output
over the next few hours is recorded.
 Further blood samples for biochemical assays, coagulation tests, and
cultures will be needed.
 Administration of incompatible blood constitutes a Sentinel Event.
vii) Haemovigilance
 The IMVS and RAH are participating in the ‘Blood Safe’
haemovigilance scheme, an adverse incident reporting system aimed at
the quality and safety improvement of transfusion practices.
 Contact the Transfusion Safety RN (Pager: 1575, Tel: 22975)
Table: Blood Transfusion Reactions
Signs & Symptoms
Febrile non-haemolytic
transfusion reaction
Pyrexia (> 1°C rise)
Withhold transfusion.
Mild fever without other
symptoms may be treated
by slowing infusion.
An antipyretic may be
Investigate as for
suspected HTR if the
reaction is significant.
Consider use of
leucodepleted red cells or
platelets if a recurrent
Circulatory Overload
Distended cervical veins.
Pulmonary oedema
Dyspnoea. Headache.
Heaviness in limbs.
Institute treatment for fluid
e.g. diuretic
Give all fluids slowly to
patients with compromised
cardiac or renal status.
Use red cell concentrates.
If anticipated, give diuretic.
Urticaria, itchy hives
Facial oedema
Slow rate of flow.
Consider anti-histamine.
Watch for laryngeal
oedema and development
of anaphylaxis.
When anticipated,
use prophylactic
Dyspnoea from laryngeal
oedema or bronchospasm,
sometimes cyanosis and
Discontinue transfusion
Institute treatment for
e.g. Adrenalin, steroids
Use of Medi-Alert
wristband in proven
IgA deficient patients.
Acute Haemolytic
Transfusion Reaction
Lumbar pain
Pain along vein
Oliguria – later uraemia
Discontinue transfusion
Get expert advice
Save all used packs, blood
Save all urine.
Collect fresh blood
Extreme care in
collecting the correct
blood sample for T&S.
Careful compatibility
testing by laboratory.
Careful method for storing
& labelling blood.
Careful identification
of the correct recipient.
Infected blood
Bacterial sepsis with
Pain in limb & chest
Burning pain along vein
Low blood pressure
Rapid pulse
Profound collapse & shock
Discontinue transfusion
Acute medical emergency
– get advice immediately.
Save used packs, all blood
samples, with labels.
Save all urine.
Anti-shock treatment and
Storage at correct temp.
Do not remove from
refrigerator until
immediately before
pulmonary oedema.
Transfusion related acute
lung injury (TRALI): rare
ARDS picture within 6
hours after transfusion.
Maintain blood pressure &
cardiac output with fluid
support. May require
ventilatory support.
Difficult, usually in the
setting of multiparous blood
donor with anti-recipientWBC antibodies.
NB: See RAH Intranet, Transfusion Medicine (http://rahadm05v.had.sa.gov.au/)
Guidelines for the Management of Electrolytes
1. General principles
a) Total body water (60% total body weight):
i) intracellular fluid : predominant ions : K+, PO42ii) extracellular fluid:
 75% interstitial fluid: predominant ions : Na +, Cl 25% plasma volume (PV)
b) Osmotic equilibrium is maintained by Na+/K+ pump
i) ECF ions therefore reflect total osmolality:
Calculated osmolality  2×Na+ + urea + glucose
ii) Magnesium is a cofactor for this pump
c) Most electrolyte disturbances in critically ill patients relate to changes in the
distribution and concentrations of the predominant ECF and ICF ions.
d) As a general rule, changes in one ion will be reflected in the associated cation or
e) Electrolyte disturbances should be considered in terms of the following groups:
i) Erroneous results
 Lab error
 Bloods taken from a drip arm
 Haemolysed specimen
- traumatic (old IA lines), delayed samples
 Osmolar agents
ii) Decreased or increased losses: usually
 Renal
 Extra renal: GIT, skin losses
iii) Transcellular shifts.
iv) Decreased or increased intake
f) Treatment should be directed at the underlying cause.
g) Rapid correction of electrolyte disturbances may be deleterious.
h) One electrolyte disturbance may be predictive of another electrolyte disturbance
e.g. K+ often associated with Mg+
i) The following paragraphs outline the common electrolyte disturbances.
2. Hyponatraemia:
Na < 130 mmol/l
a) Aetiology / classification
i) Misleading result
 Isotonic
- Hyperlipidaemia
- Hyperproteinaemia
 Hypertonic
- Hyperglcaemia
- Mannitol, glycerol, glycine or sorbitol excess
ii) Water Retention
 Renal Failure
 Hepatic Failure
 Cardiac Failure
 Drugs
 Psychogenic polydipsia
iii) Water retention / Salt depletion
 Post-operative, post-trauma
 Patients with excess fluid losses given inappropriate replacement
 Cerebral salt-wasting syndrome
 Adrenocortical failure
 Diuretic excess
b) Diagnosis & Management:
i) Factitious: ignore and manage underlying condition then recheck Na+
ii) Misleading:
 Hyperglycaemia:  BGL  10 mmol/l   [Na+]  3 mmol/l
a. Hyponatraemia per se is real, but treatment is directed at the
underlying cause, where correction of the hyperglycaemia will
correct the plasma [Na+]
b. NB: Total body Na+ deficit may co-exist with diuresis in DKA
 Mannitol:
a. [Na+] early, then diuresis & late [Na+] are more problematic
b. Maintain adequate plasma volume with N.saline initially
 Alcohols: permeate solutes,  [Na+] less problematic
iii) Hypovolaemic states:
 Restore volume with colloid or normal saline according to clinical
markers: urine output, plasma [Na+], RAP
 Aim for slow Na+ correction:  2 mmol/l/hr, unless seizures.
 Urine Na+ is uninterpretable after diuretics or catecholamines for 24hrs
iv) Hypervolaemic states: *most common clinically
 Fluid restriction < 15 ml/kg/day
a. “Water Excess” ~ (140 - Na+ )/140 × (Wt × 0.6)
e.g., 70kg patient with plasma [Na+] = 120 mmol/l:
= (140 - 120)/140 × (70kg × 0.6)
= 6 litres
b. Will slowly correct excess
- ADH group & “reset osmostat”
c. Treat the underlying cause
- CCF, nephrotic synd., ascites
 Causes
a. Ectopic ADH production by tumours
e.g. small cell bronchogenic tumour
b. CNS disorders
e.g. tumour, abscess, trauma, SAH etc
c. Pulmonary diseases
e.g. TB, pneumonia, abscess etc
 Diagnosis
a. Hypo-osmolar hyponatraemia
b. Urine osmo > plasma osmo
c. Urine Na+ > 40 mosm/l
d. Normal endocrine, renal, hepatic, cardiac function
e. No diuretics or drugs affecting ADH secretion
f. Corrected by water restriction alone
 Management: fluid restriction
vi) Severe Symptomatic Hyponatraemia : fitting, or decreased consciousness
 Resuscitation / ABC
 Consider anticonvulsants - phenytoin, benzodiazepines
 Hypertonic saline (3%) may be indicated
a. Always discuss use with the Duty Consultant
b. Correct [Na+] rapidly only to ~ 120mmol/l
 Thereafter, slow correction with N.saline over 24-36hrs ( 2 mmol/l/hr)
 Treat the underlying cause.
3. Hypernatraemia:
Na+ > 145 mmol/l
a) Hypernatraemia is always a hyperosmolar state
b) Most body fluids have a [Na ] < plasma  net water loss
c) Aetiology / classification:
i) Water depletion / inadequate replacement
 Renal
a. Diuretics, glycosuria
b. ARF/CRF, partial obstruction
c. Central diabetes insipidus
i. Post traumatic head injury or surgery
ii. CNS infection, tumour, granulomatous disease, GBS
d. Nephrogenic diabetes insipidus:
i. 1° : congenital renal resistance to ADH
ii. 2° : hypokalaemia, hypercalcaemia, lithium, multiple
myeloma, sickle cell anaemia, nephrocalcinosis, amyloid
 GIT losses - diarrhoea, vomiting, fistulae, SBO
 Respiratory - IPPV with dry gases
 Skin losses
a. Fever, high ambient temperature
b. Vasodilatory states
c. Exfoliative skin disorders, burns
d. Thyrotoxicosis
 Unconsciousness
 “Reset osmostat”
ii) Salt gain
- Na+ gain > H2O gain
 Iatrogenic
a. Most common cause
b. Excess “normal saline”
~ 150 mmol/l [Na+]
c. NaHCO3, feeding formulae, TPN
 Mineralocorticoid excess:
a. Conn's, Cushing's syndromes
b. Steroid excess
d) Management
i) Hypovolaemic states
 Restore volume according to clinical markers:
BP, HR, urine output, RAP
a. Hartmann’s solution - slightly hypo-osmolar
b. Colloid: initial resuscitation, severe hypovolaemic states
ii) Slow Na+ correction:  2 mmol/l/hr
 Water deficit:
~ (Na+ - 140)/140 × (B.Wt × 0.6)
70 kg patient, with plasma [Na+] = 160 mmol/l
~ (160-140)/140 × (70 × 0.6)
~ 6.0 litres
1 litre water replacement will reduce [Na+] ~ 3-4 mmol/l
 In addition to basal fluid requirements & ongoing losses
 Replace over a 24-48 hr period with 5% dextrose
 Monitor [Na+] regularly
 Manage aetiological causes
 Cease causal drugs and inappropriate IVT
 DDAVP for central DI only ~ 1-2 µg s.c.
4. Hypokalaemia:
K < 3.0 mmol/l plasma
K+ < 3.5 mmol/l serum
a) Aetiology / classification:
i) Compartmental / transcellular shift
 Alkalaemia
 pH ~ 0.1   [K+]pl ~ 0.5 mmol/l
 Catecholamines / salbutamol
 Insulin / anabolism
- refeeding effect
 Hypomagnesaemia
- ICF K+ depletion
 Toxic / poisoning
- barium, toluene
 Familial periodic paralysis
 Hypothermia
ii) Reduced intake
- urine [K+] < 20 mmol/L
 Starvation
iii) Increased clearance/losses
 Renal
- urine [K+] > 20 mmol/L
a. Diuretics 
 distal tubular flow
i. Loop agents
- frusemide, bumetanide
ii. PT agents
- acetazolamide, mannitol
iii. Early DT
- thiazides
b. Steroids / Mineralocorticoid excess
i. Conn’s, Cushing’s, Bartter’s syndrome
ii. Ectopic ACTH - Small cell Ca lung
- Pancreatic, thymus carcinoma
iii. Exogenous steroids
c. Drugs
i. Anionic drugs
- antibiotics (penicillins, amphotericin)
ii. High dose gentamicin
iii. Lithium
d. Hypomagnesaemia, Hypocalcaemia
e. RTA I, II
 GIT losses
a. Villous adenoma
b. Ureterosigmoidostomy
c. Fistulae, malabsorption syndromes
d. Diarrhoea, Laxatives
 Skin losses
b) Management:
i) Treat underlying cause
ii) Correct hypovolaemia: volume contraction will potentiate both alkalosis
and hypokalaemia
iii) Always add Mg++
 normomagnesaemia is essential for correction of hypokalaemia
iv) Look for and treat concurrent hypophosphataemia
Potassium preparations
 KCl:
10 ml = 10 mmol/l
 KH2PO4: 10 ml = 10 mmol/l
 K-acetate: 5 ml at 5 mmol/ml
25 mmol K+ + 25 mmol acetate (bicarbonate)
5. Hyperkalaemia:
K+ > 5.0 mmol/l serum
K+ > 4.5 mmol/l plasma
a) Aetiology / classification:
i) Artefactual
 Drip arm specimen
 Tourniquet / Haemolysed specimen (extravascular)
 Thrombocytosis > 750,000
> 50,000
ii) Compartmental / transcellular shift
 Acidosis
 pH ~ 0.1  [K+] ~ 0.5 mmol/l
 Insulin deficiency:
NB: normo- or hypo-kalaemia in the presence of severe DKA is
associated with a marked total body K+ deficit, which must be
addressed prior to correction of the acidaemia.
 Familial periodic paralysis
 Suxamethonium
 Digoxin, -blocker overdose
 Fluoride poisoning
  ECF tonicity
a. Water moves from cells → [K+]ICF and passive diffusion
b. Seen with large doses of mannitol given rapidly (1.5-2.0 g/kg)
c. Hyperkalaemia of DKA is due to this in addition to the acidaemia
& insulin deficiency
iii) Cellular disruption / death
 Tissue breakdown
 Rhabdomyolysis, haemolysis (intravascular), ischaemia / reperfusion
 Severe burns
 Tumour lysis syndrome, leukaemia
iv) Increased intake
- rarely a problem unless impaired renal function
 Massive transfusion
 Direct IV/oral
 Drugs (penicillins)
Reduced clearance
 Acute renal failure
a. Any cause for  distal tubular flow, or  distal NaCl delivery
b. Hypoaldosteronism
i. Mineralocorticoid deficiency, Addison’s
ii. K+ is multifactorial - K+ICF  K+ECF
- distal tubular flow
- DT aldosterone effect
 Type IV RTA
 ACE Inhibitors
 Potassium sparing diuretics
a. aldosterone antagonists
- spironolactone
b. distal Na+ channel inhibitors - amiloride, triamterene
b) Management:
i) The clinical scenario will dictate treatment
ii) Acute K+ > 6.0 mmol/l is a medical emergency
iii) Associated with acute ECG changes, or haemodynamic compromise:
In following order (not mixed together),
 CaCl2
10 ml IV stat
 NaHCO3
50-100 ml IV stat
 Glucose 50% 50g + Insulin 20 units
 Salbutamol nebs continuously
iv) Refractory or persistent:
 intermittent dialysis
v) Chronic  K+ or slow rate of rise or no ECG changes:
Resonium 30g oral / PR 8 hourly
vi) Address aetiological factors
vii) Normalise renal function / volume status
6. Acid base disturbances
a) Acid base disturbances in ICU are frequently mixed disorders
b) Correction of these should be directed at the underlying cause and maintenance
of cardiopulmonary homeostasis.
c) Primary correction of an acid base disturbance with acid or alkali is seldom
7. “Rules of thumb”
*these are approximations only
a) Primary metabolic disturbances: last 2 digits of pH will reflect PaCO2
i) Met Acid to min 7.10
e.g. pH 7.25  PaCO2 25 mmHg
ii) Met alkalosis to max 7.60
e.g. pH 7.57  PaCO2 57 mmHg
b) Primary respiratory acidosis:
i) HCO3 ~ 1mmol/l per 10mmHg PaCO2 above 40 to max 30
c) Primary respiratory alkalosis
i) HCO3 ~ 2.5mmol/l per 10mmHg PaCO2 below 40 to min 18
d) Chronic respiratory acidosis
i) HCO3 ~ 4mmol/l per 10mmHg PaCO2 above 40 to max 36
8. Metabolic acidosis
a) Assessment of metabolic acidosis must include the anion gap:
Anion Gap = [Na+ + K+] - [Cl- + HCO3-] ~ 12-17 mmol/l
Unmeasured cations
~ 1.2
~ 2.2
~ 7.0
Unmeasured anions
~ 15
~ 23
b) This allows sub-classification of metabolic acidosis into raised or normal anion
gap acidoses.
i) Beware a low [Alb] in critically ill lowering the measured AG
ii) Measurement of chloride in the lab is highly variable
iii) Assessment of the AG must be viewed within the clinical context.
c) Aetiology of raised anion gap:
i) Renal failure
- H2PO4- , HSO4- (rarely AG > 23)
ii) Lactic acidosis
- types A&B
* normal AG does not exclude a lactic acidosis
iii) Ketoacids
- -OH-butyrate, acetoacetate
- diabetes mellitus, starvation, alcohol
iv) Rhabdomyolysis
- organic acids
v) Drugs / poisons:
 Aspirin
- salicylate, lactate, ketones
 Paracetamol
- lactate, pyroglutamate
 Ethanol
- acetoacetate, lactate
 Methanol
- formate (formaldehyde), lactate
 Paraldehyde
- formate, acetate, lactate, pyruvate
 Ethylene glycol - oxalate
 Xylitol, Sorbitol - lactate
 Fructose
- lactate
Table: Classification of Lactic Acidosis
Type A
Type B
Drug induced
Severe exercise
Cardiac arrest
Thiamine deficiency
Hepatic failure
Renal failure
Leukaemia, lymphoma
Short bowel syndrome
IV fructose
G6PD deficiency
d) Aetiology of low or normal anion gap:
i) Hyperchloraemic metabolic acidosis
 Resolving renal failure
 Resolving DKA
 Renal tubular acidosis / carbonic anhydrase inhibitors
 Mineralocorticoid deficiency
 Pancreatic, enteric fistulae
 Ureterosigmoidostomy
 IV HCl, NH4Cl, Arginine
ii) Metabolic alkalosis due to HCO3- gain
iii) Hypoalbuminaemia
iv) Myeloma
- IgG has positive charge,  's AG
v) Increased Mg++ or Ca++ (rarely)
vi) Artefactually elevated Clvii) ? Hyperlipidaemia
e) Management
i) High anion gap
 Treat the underlying cause
 No indication for NaHCO3
ii) Normal anion gap
 Treat the underlying cause.
 Replace HCO3  serum level and losses
a. Approx. deficit = (24 - [HCO3]) × (Wt. × 0.6) mmol/l
e.g. for a 70kg patient with a [HCO3] = 4 mmol/l
= (24 - 4) × (70 × 0.6)
= 840 mmol (= ml of standard bicarb solution)
b. Replace 1/3-1/2 of this amount then remeasure blood gases.
9. Metabolic alkalosis
a) Aetiology / classification
i) Common causes:
 Diuretics
 Vomiting
 Post-hypercapnia > 48 hours
 Commonly associated with hypovolaemia and/or hypokalaemia
however, actual causation by these is debated
ii) Increased proton losses: acid loss is either renal or GIT
 Renal
a.  Na+ reabsorption (hypovolaemia, dehydration, etc.)
b. Cushing's syndrome, exogenous steroids
c. Hyperaldosteronism 1° / 2°
d. Bartter's syndrome
(JGA hyperplasia)
e. Liddle's syndrome
f. Hypercalcaemia / hypomagnesaemia  nephrogenic DI
g. Drugs: steroids, diuretics, carbenoxolone
a. N/G suctioning, protracted vomiting
b. Diarrhoea
iii) Increased bases
 Administration of NaHCO3
 Metabolism of exogenous acid anions - citrate, lactate, acetate
 Milk/alkali syndrome
 Renal conservation of HCO3- acidosis, hypercarbia
iv) Factors tending to maintain an alkalosis
 Any fluid loss replaced with insufficient Na +  ↑ H+ excretion
(contraction alkalosis)
 Hypovolaemia
 Hypokalaemia, hypochloraemia, hypomagnesaemia
 Chronic hypercapnia
 Mild chronic renal failure
b) Management
i) Correct hypovolaemia
*normal ECF volume is essential for the correction of alkalosis
ii) Inotropic support of cardiac output and GFR
iii) Correct  K+, Mg++, HPO4=
iv) Consider acetazolamide if the alkalosis is persistent - provided the above
are corrected.
10. Respiratory acidosis
a) Aetiology
i) Any cause of hypoventilation  respiratory failure (see diag.)
 A. Respiratory centre / CNS
 B. Upper motor neuron / spinal cord
 C. Anterior horn cell
 D. Lower motor neuron
 E. Neuro-muscular junction
 F. Respiratory muscles
 G. Elasticity/compliance of lungs/chest wall
 H. Structural integrity of chest wall & pleural cavity
 I.
Increased airways resistance – intra/extrathoracic
ii) May be acute or chronic
i) Restore ventilation / manage underlying cause(s)
ii) No indication for HCO3
Respiratory alkalosis
b) Aetiology
i) Early hypoxia, shock or hypotension
ii) Anxiety, hysteria, neurogenic hyperventilation
iii) PTE
iv) Hepatic failure
v) Prescribed hyperventilation (rarely indicated)
c) Management
i) Treat underlying cause
ii) Neurogenic hyperventilation is a marker of severity of head injury
The following protocols are designed to facilitate clinical management of patients in the
Intensive Care.
These protocols may vary from other ICUs and do not represent the sole approach to
patient management. However, they do represent a standardised approach which has
evolved in this ICU over the years.
Each clinical scenario is managed according to the particular situation and individual
patient - it is neither practical nor appropriate to apply rigid policies to clinical
situations. However, as clinical medicine is at times more art than a science, these
protocols are designed to assist in areas that are unfamiliar and to standardise
approaches by all staff members of the Unit.
The following protocols are outlined.
A. Cardiopulmonary resuscitation
B. Failed intubation drill
C. Respiratory therapy
D. Management of cardiothoracic patients
E. Renal failure
F. Neurosurgical protocols
G. Microbiology protocols
H. Drug overdose
Bites and Envenomation
Withdrawal of therapy
K. Organ donation and brain death
A. Cardiopulmonary Resuscitation
Flowchart: Basic Life Support
Flowchart: Advanced Life Support
Flowchart: Paediatric Cardiorespiratory Arrest
Induced Hypothermia Post Cardiac Arrest
1. Aim: To improve CNS outcome by actively cooling to a TCore  32-34°C
2. Inclusion Criteria
a) Non-traumatic cardiac arrest with return of spontaneous circulation
a) Unconscious, intubated and ventilated
b) Absence of an immediately correctable cause for coma
c) TC > 34.5°C
4. Exclusion Criteria
a) Cardiac arrest related to trauma or intracranial injury
b) Ongoing CPR and/or persistent cardiovascular instability
c) Cardiology consultation  need for acute intervention
d) Criteria that preclude 40mls/kg of cold Hartmann’s solution,
e.g. acute pulmonary oedema, T C < 34.5°C
e) Time from cardiac arrest to ED > 12 hrs
f) Pregnancy – relative C/I
5. Procedure - Initial Treatment Protocol
a) ECG and routine blood tests as indicated
b) Record core temperature (TC):
rectal, oesophageal or bladder catheter
c) Ensure adequate IV access (1x 16G)
d) Document neurological function, specifically:
i) Pupillary responses to light
ii) Response to painful stimuli (all limbs), vocalization
iii) Reflexes – gag, conjunctival, lash, tendon & plantar
e) Hartmann’s (Temp.  4°C) / Bolus  40mls/kg. / Infuse @ 100ml/min.
f) Maintain MAP  80-100mmHg
(relative to premorbid BP)
g) Maintain K+  4-5mmol/L and Mg++  0.8-1.2mmol/L
h) If TC > 35°C after 1 hour, add surface cooling (cooling blanket / packs)
i) If patient is shivering and/or goal T C not achieved:
i) Midazolam (0.05mg/kg bolus, repeat every 5 min as required)
ii) Midazolam (1-5mg/hr) or Propofol infusion as clinically indicated.
iii) If sedation ineffective, consider a non-depolarizing muscle relaxant
6. Observations
a) Maintain TC  32-34°C for 12-24 hrs from the time of achieving goal temp.
b) To increase temp. (T < 31.5°C), use heated air blanket until 33°C
c) To decrease temp. (T > 34.5°C), use cold packs, cooling blanket, sedation and
then consider using non-depolarizing muscle relaxants
7. Complications
a) Arrythmia
b) Reduced cardiac index / increased peripheral resistance.
c) Ongoing cardiac instability may necessitate stopping the hypothermia protocol.
d) Hyperglycaemia
8. Aftercare
a) At 24 hrs cease all active cooling and allow passive rewarming.
b) If temp increases < 1°C per 4 hours then rewarm actively to temp > 36°C
c) Once TC > 35°C, cease sedation and muscle relaxants
Failed Intubation Drill
1. Following rapid sequence induction in ICU we are generally committed to securing
the airway by some means. Allowing the patient to wake-up in the event of a failed
intubation is rarely practical.
2. Risk of failed intubation in ICU is higher than in the operating theatre.
3. Before intubating, you MUST have a contingency plan for a difficult airway/failed
4. After hours, remember the anaesthesic staff may be available to assist.
5. Ensure all equipment is working and that the ETCO2 monitor provides a reliable
6. Ensure adequate IV access with running intravenous fluids.
7. Ensure ready access to vasopressors and resuscitation drugs.
8. Always have the difficult intubation trolley at hand.
9. Visually confirm that each individual piece of airway equipment is immediately
available and operational.
10. ICU patients have limited O2 reserves and desaturate quickly.
a) If initial intubation attempts fail, or the patient desaturates significantly, ensure
you can manually ventilate the patient.
b) Failure to achieve manual ventilation is an absolute emergency
“can’t intubate + can’t ventilate”
11. If an intubation technique fails, move on quickly to an alternative.
12. There are a range of airway devices available to help secure the airway.
a) Guedel airway / Nasopharyngeal airway
b) Bougie
c) C-Mac
d) Laryngeal Mask / Intubating Laryngeal Mask
e) Cricothyroidotomy
f) Jet insufflation
g) Bronchoscopy (for anticipated difficult intubations)
13. You must be familiar with the devices you plan to use in the case of a failed
14. Airway equipment and intubating manikins are available for practice in the
registrar’s room.
Flowchart: Failed Intubation Drill
Committed to
 McCoy / Flextip
 Airtraq
Best Attempt
Failure or
SpO2 < 88%
Call for help
ILMA +/Bronchoscope
Failure to
Respiratory Therapy
1. Respiratory Failure
a) Definition = failure of efficient gaseous exchange and/or effective ventilation.
i) Type 1 Respiratory Failure
 Hypoxaemia, PaO2:FiO2 < 300 mmHg
 i.e. failure to oxygenate
ii) Type 2 Respiratory Failure
 Hypercapnoea, PaCO2 > 50 mmHg, with a pH < 7.35
 i.e. failure to ventilate
2. Oxygen Delivery Capacity
Table: Oxygen Delivery Devices
Oxygen Flow (l/min)
Approx. FIO2 (%)
24 - 50
30-50 l/min
21 - 95
6 - 15
FiO2 = 21% + 4% per l/min
Closed Circuits
e.g. IPPV, NIV
21 - 100
Oxylog 1000 and 2000
Oxylog 3000
Airmix : 60
No airmix : 100
40 - 100
Nasal catheters
Semi - rigid masks
(e.g. Hudson, CIG)
Venturi type mask
(e.g. Ventimask, Accurox)
Nasal High Flow
(humidified circuit)
Reservoir plastic masks
(Non-rebreathing mask)
a) The FiO2 delivered to the patient by an “open circuit” will depend on the
patient’s peak inspiratory flow rate (PIFR).
b) The higher the PIFR, the higher the O2 flow required to provide a given FiO2.
3. Humidification
a) All ventilated patients must have adequate humidification of inspired gases for
optimal mucociliary function and conservation of temperature.
b) Optimal humidification requires:
i) Delivery of gas to the trachea at a constant temperature (32-36ºC).
ii) Relative humidity 75-100%.
iii) No increase in circuit resistance.
iv) No increase in circuit dead space.
v) Applicable to spontaneous and controlled ventilation.
vi) Sterile inspired gas
c) Types of humidifiers available
i) Heat/moisture exchangers (HME)
 First line humidification.
 Effective for most patients.
 Incorporates a bacterial and viral filter.
 Cannot be used with nebulised drugs.
 Secretions increase resistance and reduce HME efficacy. Change to
wet circuit (FP) in patients with bronchorrhoea or mucous inspissation.
 Single use & change every 48 hrs, or as required.
ii) Fisher Paykel (FP) evaporative humidifier (wet circuit)
 Bronchorrhoea or mucous inspissation.
 Hypothermic or heat-loss susceptible patients (e.g. burns).
 Ventilation anticipated for more than 48 hrs.
 Set chamber to 40°C.
iii) Inspiron (aerosolised T-piece).
 Relatively inefficient humidification.
 Allows variable FiO2 : 0.21-0.7
4. Nasal High-Flow Oxygen
a) NHF delivers high gas flows through a unique Optiflow™ nasal cannula.
b) Critical to NHF is the delivery of optimal humidity to allow delivery of high
flows directly into the nares.
c) This provides greater patient comfort while optimising mucociliary clearance.
d) Main benefits of NHF:
i) Delivery of up to 100% oxygen.
 Actual FiO2 will depend upon the patient’s breathing pattern
ii) Anatomical dead space flushed.
iii) Positive airway pressure (2-5cmH2O) throughout the respiratory cycle.
iv) Improved mucociliary clearance.
Table: Oxygen Delivery Percentage - Nasal High Flow
O2 %
30 LPM
40 LPM
50 LPM
5. Mechanical Ventilation
a) Mechanical ventilation is one of the mainstays of intensive care medicine.
b) There are 2 main types of mechanical ventilation:
i) Non-invasive ventilation.
ii) Invasive ventilation.
c) An understanding of the types of mechanical ventilation, indications,
complications, practical aspects of mechanical ventilators and their use in
respiratory failure is essential.
d) Registrars should familiarise themselves with the ventilators, understand the
default settings and common modes of ventilation.
e) All changes to ventilation orders must be recorded on the flowchart and
conveyed to the bedside nurse.
f) All ventilator alarms must be addressed immediately.
g) Any changes to alarm settings must be relayed to the bed-side nurse.
6. Non-Invasive Ventilation
a) Definition: Mechanical positive pressure respiratory support in the absence of
tracheal intubation (e.g. via a face mask, nasal mask, head piece/box)
b) Modes
i) Continuous positive airway pressure (CPAP)
ii) Bi-level positive airway pressure (BiPAP).
c) Indications
i) As an adjunct to weaning from ventilation (e.g. extubation to NIV).
ii) Acute exacerbation of COAD.
iii) Cardiogenic pulmonary oedema.
iv) Obstructive sleep apnoea / obesity hypoventilation syndrome.
v) Post-extubation hypoxia due to pulmonary oedema or atelectasis.
vi) Febrile neutropaenia with pulmonary infiltrates.
d) Prerequisites
i) Adequate glottic reflexes should be present to protect from aspiration moribund patients require intubation where appropriate.
ii) Patients receiving CPAP or BiPAP are generally managed in Units A&B.
iii) Selected patients may be managed in Unit C.
e) Complications
i) Inadequate ventilation.
ii) Mask leaks.
iii) Aerophagia, gastric distension, vomiting, aspiration.
iv) Claustrophobia and mask intolerance.
v) Pressure necrosis of nasal bridge.
vi) Dry secretions.
vii) Barotrauma.
viii) Reduced preload and hypotension.
ix) Raised intracranial and intraocular pressure.
7. Non-Invasive Ventilators
a) BiPAP® Vision
i) Microprocessor controlled.
ii) Nasal, face & full head masks can be used.
iii) IPAP = Inspiratory positive airway pressure.
iv) EPAP = Expiratory positive airway pressure (PEEP).
v) Pressure support = IPAP - EPA
vi) Monitors machine pressure against proximal airway (mask pressure) to
ensure effective delivery of pressure despite circuit leaks.
vii) Need to calibrate for tubing and mask.
viii) Uses internal algorithm for respiratory cycling and leak adjustment.
ix) Liquid crystal displays:
 IPAP, EPAP, Rate, FiO2.
 VT, Vmin, PIP, Insp. time/total cycle time.
 Leak (patient & total), % patient triggered breaths.
 Graphical display of pressure, volume & flow.
x) Operation:
 Machine starts up in mode previously used.
 Press [Mode] hard key to display CPAP or S/T mode
 Press [Activate New Mode] soft key to select the new mode.
 Select soft key parameters displayed & turn adjustment knob
 CPAP Mode - Default settings
a. CPAP 5cmH2O, FiO2 1.0
 S/T Mode - Default settings
a. IPAP 15cmH2O, EPAP 5cmH2O
b. FiO2 1.0, Rate 12, TInsp 1 sec, IPAP rise time 0.1 sec
b) CPAP via Dräger EVITA
i) Operation:
 Select “Non-Invasive” Mode
 Default settings:
a. Pressure support
10 cmH2O (above PEEP)
5 cmH2O
c. Inspiratory time
4 sec
d. Trigger
5 L/min
 Adjust Press Support and Rise Time to provide the assisted breaths.
8. Indications for Invasive Ventilation
a) Respiratory Failure.
b) Intubated for airway protection.
c) Severe metabolic disturbance with altered conscious state.
9. When to institute invasive ventilation
a) Clinical assessment is the most sensitive assessment of respiratory failure.
b) Do not delay the initiation of ventilatory support pending results, blood gases or
mechanical measurements in the following settings:
i) Threatened airway.
ii) Fatigue / exhaustion.
iii) Failure of secretion clearance.
iv) Overt respiratory failure.
v) Speech impairment due to dyspnoea.
vi) Reduced GCS in the absence of other causes.
c) Objective measurements are adjuncts to clinical assessment:
i) RR
> 35 bpm
ii) VC
< 15 ml/kg
iii) SpO2 < 90% on 15L O2
iv) PaCO2 > 60 mmHg (with pH < 7.2)
10. Modes of Ventilation in ICU
a) Synchronised intermittent mandatory ventilation (SIMV).
i) Default ventilation setting at RAH.
ii) Prescribed tidal volume.
iii) Airway pressure is variable.
b) Pressure control ventilation (PCV).
i) Prescribed peak pressure.
ii) Tidal volume is variable.
iii) High sedation requirements, occasional use of muscle relaxants.
c) Pressure Support Ventilation (PSV) + PEEP
i) Spontaneous ventilation mode for patients with adequate respiratory drive,
respiratory mechanics and strength.
ii) Commonly used when weaning from ventilation.
iii) Requires patient effort to initiate ventilatory assistance.
11. Optimising Ventilation
a) Optimise oxygenation:
i) Use the lowest FiO2 to achieve an ‘adequate’ SpO2 or PaO2.
e.g. SpO2 > 95% and/or PaO2 > 80 mmHg.
ii) Lower values may be appropriate with chronic lung disease.
b) Optimise PaCO2:
i) Adjust relative to pre-morbid PaCO2.
ii) Consider permissive hypercapnia in patients with poor lung compliance.
c) Optimise patient-ventilator interface:
i) Reduce work of breathing through the ETT and ventilator circuit.
ii) Pressure support.
iii) Automatic Tube Compensation (ATC).
iv) Appropriate trigger threshold.
v) Adequate expiratory time.
vi) Prevent gas trapping: measurement and manipulation of auto-PEEP
vii) Patient positioning.
d) Optimise sedation and analgesia.
i) Review the need for sedation daily.
ii) Calculate the RASS score for each patient daily.
iii) Order depth of sedation on the ICU obs chart.
iv) Always assess suitability for ceasing sedation.
e) Minimise volutrauma (barotrauma)
12. Complications of Mechanical Ventilation
a) Haemodynamic.
i) Reduced preload.
ii) Increased RV afterload  unmasked hypovolaemia.
b) Respiratory.
i) Ventilator Associated Pneumonia (VAP).
ii) Volutrauma / Barotrauma  Ventilator associated lung injury.
iii) Patient ventilator dys-synchrony.
c) Metabolic.
i) Post-hypercapnoeic metabolic alkalosis.
ii) SIADH.
d) Raised intracranial and intraocular pressure.
e) Need for sedation
i) Reduced patient mobility  DVT, pressure sores, weakness
ii) Reduced joint movement.
f) Local pressure effects from intubation, tracheostomy or face masks.
13. Drager EVITA 2 Ventilator
a) The Evita 2 are the default ventilator at the RAH.
b) Modes: SIMV, PCV, Pressure Support, CPAP, APRV.
c) Non-invasive ventilation modes are also available.
d) Specific features:
i) Auto flow: automated adjusted inspiratory flow according to lung
mechanics during controlled ventilation.
ii) Rise time: manual adjustment in all modes.
iii) 100% O2 suction button: delivers 100% oxygen for 3 minutes.
iv) Programmable default parameters.
v) Flow and Pressure-Volume loops.
vi) Preset emergency and apnoea ventilation parameters.
vii) Automatic tube compensation to assist weaning.
viii) Automated respiratory mechanics:
 Static and dynamic compliance.
 Automated estimation of auto-PEEP and occlusion pressure (P 0.1).
 Inspiratory airway resistance.
 Negative inspiratory pressure.
 Vital capacity.
i) Default settings:
SIMV: 600×12, PS = 5 / PEEP = 5, FiO2 = 1.0
ii) Select mode: SIMV.
iii) FiO2
= 1.0
iv) VT
= 0.6 L
v) Rate
= 12 bpm
vi) PS
= 5 cmH2O
vii) PEEP
= 5 cmH2O
viii) Rise time = 0.2 secs
ix) Adjust TInsp  I:E ratio  1:2 (default 1.7 secs)
x) “Extra settings” mode
 Flow trigger = 5 l/min
 Backup ventilation (CMV) : Off
f) PC (Pressure control)
i) Default settings
PInsp = 30×12, PEEP = 5, FiO2 = 1.0, I:E=1:2
ii) Select mode: PCV+
iii) Select total inspired level of pressure (PInsp) = 30 cmH2O
iv) Rate
= 12
v) Rise time = 0.2 secs
vi) PS
= 5 cmH2O
vii) PEEP
= 5 cmH2O
viii) FiO2
= 1.0
ix) Adjust TInsp  I:E ratio  1:2 (default 1.7 secs)
x) Do not exceed total inspired pressure > 40 cmH2O
xi) Tidal volume is determined by respiratory compliance.
g) Pressure Support (PS) + PEEP
i) Total inspiratory pressure, when using PS on the Evita, is the dialed value
plus dialled PEEP value
ii) Mode
iii) Rise time = 0.2 secs
iv) PS
= 10 cmH2O
= 5 cmH2O
vi) FiO2
= 1.0
h) I:E Ratio
i) Alteration of the I:E ratio is potentially hazardous and should only be done
following discussion with the duty consultant.
i) Measurement of auto-PEEP
i) Not accurate if patient effort, patients should be well sedated / paralysed.
ii) Measurement of intrinsic PEEP at end expiration + closed airway.
iii) Press the [Special Procedure] button & select [PEEPi].
iv) Press [Start] to begin the automatic 7sec manoeuvre.
v) Read off the PEEPi and trapped gas volume (V Trap)
vi) The value displayed includes applied PEEP, so:
vii) auto-PEEP = PEEPi - applied PEEP
j) Measurement of occlusion pressure (P 0.1)
i) Measurement of the negative airway pressure generated in the first
100msec of inspiration against an occluded airway.
ii) Reflects diaphragmatic effort and neuromuscular drive.
iii) Normal value  3-4 mbar.
iv) Press [Special Procedure] button.
v) Select P0.1 and press [Start] to measure value.
k) Always examine the flow, pressure and volume vs time loops
i) Upper/lower airway obstruction.
ii) Recruitable lung.
iii) Increased airway resistance.
iv) Dynamic hyperinflation
e.g. flow does not return to baseline before the next breath
v) Sudden reversal of flow / pressure which does not trigger a breath may
indicate wasted patient effort.
14. RAH – ARDS Ventilation
a) Initial Ventilator Set-up and Adjustments (Dräger)
i) Mode:
ii) Resp. Rate:
18 bpm
iii) Insp. Flow Rate: Autoflow
iv) Tidal Volume:
6 ml/kg IBW
b) Tidal Volume Settings are determined by calculated Ideal Body Weight
i) Males = 0.91 × (height [cm] – 152.4) + 50
ii) Females = 0.91 × (height [cm] – 152.4) + 45.5
iii) Calculate IBW and VT = 6 x IBW
c) Adjust RR to achieve the pH goals according to ABG’s.
i) After any RR change, check the I:E ratio and T Insp.
ii) Target I:E Ratio  1:1 – 1:3
iii) Maintain TInsp  0.8 sec.
d) Adjust VT according to inspiratory plateau pressure (P Plat) goals.
i) Target PPlat < 30cmH2O
ii) Check PPlat with a 2 sec inspiratory pause every 4 hrs and after each change
in PEEP or VT.
iii) Method (Dräger): [Measurements] + press [Insp Hold] for 0.5sec
 PPlat will appear on the screen for 1 sec.
iv) PPlat > 30cmH2O
  VT by 1 ml/kg IBW steps (min VT = 4ml/kg IBW).
v) PPlat < 25cmH2O and VT < 6ml/kg IBW
  VT by 1ml/kg IBW.
vi) NB: Observe spontaneous tidal volumes and adjust PS downwards if
volumes generated are higher than the calculated goal VT.
e) Adjust FiO2 & PEEP according to SpO2 and PaO2.
i) Goal
PaO2 = 55-80mmHg
SpO2 = 88-95%.
ii) Use the table (right) to adjust FiO2 / PEEP combinations
for the target PaO2 range required, e.g.
 If FiO2 = 0.4 / PEEP = 5 and the PaO2 = 54,
  PEEP to 8 cmH2O
 If FiO2 = 0.9 / PEEP = 14 and the SpO2 = 99%
  FiO2 to 0.8
Other therapies that may improve oxygenation.
i) Recruitment Manoeuvres
ii) Prone Ventilation
iii) Nitric Oxide / Nebulised prostacylcin.
iv) ECMO
None proven – see over.
15. Recruitment Manoeuvres
a) Recruitment of under-ventilated alveoli may be achieved by prolonged
inspiration with higher inspiratory pressures and higher PEEP.
b) There are a variety of strategies employed.
c) These should only be performed following discussion with the consultant.
d) Contraindications to a LRM include the following:
i) Mean BP < 60mmHg despite fluids/vasopressors
ii) Active air leak through thoracostomy tube, i.e. broncho-pleural fistula
iii) Pneumatoceles, subpleural cysts, or pericardial or mediastinal emphysema
iv) Subcutaneous emphysema not related to trauma, surgical or ICU
e) Early termination of a LRM is mandatory if any of the following develop:
i) SpO2 < 85%
ii) HR < 60 or > 140
iii) New arrhythmia - except isolated supraventricular extrasystoles
iv) New air leak through thoracostomy tube
v) Fall in mean BP < 60 mmHg
16. Prone Ventilation.
a) May improve oxygenation
b) Has never been shown to improve ICU survival from ARDS
c) Risky and labour intensive intervention.
d) Should only be considered and undertaken under direct consultant supervision.
17. Nitric Oxide / Nebulised Prostacylcin.
a) Both can improve oxygenation but do not improve survival from ARDS
b) Nitric Oxide is not currently provided in ICU at RAH
c) Nebulized prostacylcin should only be commenced per the duty consultant.
18. Extra-Corporeal Membrane Oxygenation (ECMO)
a) ECMO can be used to provide either:
i) Oxygenation in cases of overwhelming respiratory failure (veno-venous
ii) Circulatory support in reversible cases of refractory overwhelming cardiorespiratory failure (veno-arterial ECMO).
b) ECMO services commenced at the RAH in 2009, and continue to evolve.
c) Any cases for potential ECMO support will be discussed in detail prior to
initiation, and will be supervised closely by duty ICU consultant.
d) The ECMO circuit and equipment must not be altered without ICU consultant
and/or perfusionist supervision.
e) The policies, protocols and procedures for ECMO are contained in a manual
that is attached to the ECMO machine and available online.
19. Weaning From Ventilation
a) General principles
i) No mode of weaning has been demonstrated to be superior to another.
ii) Short-term patients with acute resolution of respiratory failure (e.g. postoperative, drug overdose, trauma) may be rapidly weaned and extubated.
iii) Long-term patients with multiple intercurrent problems take longer and
effectively “go at their own pace”.
iv) See – Flowchart: Ventilation Weaning Protocol (p50)
b) Clinically important determinants for weaning from ventilation
i) Resolution of the process requiring ventilation.
ii) No new CXR abnormality.
iii) Completion of therapeutic options that require ventilation
e.g. debridements, operations.
iv) Appropriate conscious state - cooperative patient.
v) Appropriate peripheral motor function.
vi) Adequate analgesia.
vii) Haemodynamic stability.
viii) Metabolic, acid-base stability.
c) Methods
i) Spontaneous effort is required for the patient to be weaned.
ii) SIMV with reducing RR and VT in conjunction with PSV and PEEP.
iii) Use PSV + PEEP alone once the patient’s spontaneous rate is sufficient to
prevent a respiratory acidosis.
iv) T-piece weaning: intermittent T-piece and positive pressure support.
v) Non-invasive bi-level ventilation.
d) “Objective” measurements
i) Adjuncts to the assessment of weaning success.
ii) Respiratory rate and tidal volume are the most sensitive:
 Rate ( f ) < 30/min
 VT
> 5 ml/kg
 f /VT
< 100 (rapid shallow breathing index)
 PaO2/FiO2 > 200 and PEEP < 10 cmH2O
 PaCO2
< 60 mmHg
 pH
> 7.3
20. Extubation Protocol
a) The duty consultant or SR must be involved in all decisions to extubate.
b) In case of urgent re-intubation, ensure equipment, monitoring and adequate
assistance is immediately available.
c) Extubation is preferentially done during daytime working hours and is a
medical responsibility.
d) Extubation criteria:
i) Return of adequate conscious state to maintain adequate protective
laryngeal reflexes and secretion clearance.
ii) Adequate pulmonary reserve.
iii) Adequate cuff leak if upper airway surgery or airway swelling.
iv) Ability to be re-intubated.
v) Resolution of reason why patient was intubated.
e) Beware of patients with inter-maxillary fixation and wiring.
i) Home team must be aware of planned extubation.
ii) Wire cutters must be present during extubation.
f) All patients must receive supplemental oxygen post extubation.
Management of Cardiothoracic Patients
1. General Principles
a) The following guidelines apply to elective post-cardiac surgical patients.
b) These are only guidelines and each individual consultant will manage the
patients as is clinically indicated.
2. Respiratory:
a) Following surgery use the following default ventilator settings:
i) FIO2 =1.0
ii) SIMV 12 × 600, PS 10cmH2O, PEEP 5cmH2O.
b) After the first ABG, adjust the FIO2 to maintain a PaO2 > 80mmHg
c) Wean from ventilation according to past history, surgery performed and current
clinical status
d) Suggested extubation criteria:
i) Temperature > 36C
ii) Awake, able to obey commands
iii) Adequate analgesia
iv) Cardiovascular stability on minimal inotropes
(< 10µg/min noradrenaline or adrenaline)
v) Adequate gaseous exchange:
 PaO2 > 80 mmHg on FIO2  0.5, PEEP 5cm
vi) Bleeding: drain losses < 100 ml/hr
e) Respiratory failure post-extubation secondary to collapse / consolidation is
i) Ensure good analgesia and frequent, effective physiotherapy
ii) CPAP may be required in the first 48 hours.
f) Patients with poor LV function / recurrent acute pulmonary oedema are prone to
extubation failure and may benefit from the use of ACE inhibitors or inodilators
prior to extubation.
3. Post-operative bloods:
a) Check CBE, U&E, Mg, ACT, APPT, INR and ABGs on all patients.
b) Maintain [K+] > 4.0 mmol/l
4. Hypotension
± increasing inotrope requirements may occur for a variety of reasons:
a) Hypovolaemia
i) Return any remaining pump blood as soon as possible.
ii) Correct fluid/blood losses as appropriate
iii) Check ECG
b) Low cardiac output states
i) Noradrenaline is the first choice vasopressor.
ii) Low dose dobutamine (to improve regional blood flow to splanchnic/renal
vascular beds), may also be considered.
iii) Adrenaline can be used for severely impaired ventricles.
iv) If required vasoactive agent > 20µg/min and increasing, and the patient is
euvolaemic, consider:
 Echo to exclude tamponade, AMI, papillary muscle rupture, or VSD.
 PA catheter insertion or pulse contour CO measurement, e.g. Vigileo.
v) Consider pacing (either epicardial or transvenous) if hypotension is rate
related (HR < 60). A-V sequential pacing is the ideal mode (DDD)
vi) Consider IABP if hypotension persists despite inotropes.
vii) Consider milrinone or dobutamine for patients with predominantly
diastolic cardiac failure or pulmonary hypertension.
c) Tamponade
i) This is a medical emergency.
ii) If suspected, the cardiothoracic surgeon must be notified immediately.
iii) Diagnosis:
 Refractory hypotension despite adequate volume replacement and
inotropic support
 Cessation / reduction of blood coming from drains
 Perform urgent CXR if time available. Globular heart shadow on CXR
and muffled heart sounds may be present but are unreliable signs
 Diastolic equalisation of right-sided pressures on PA catheter insertion
 Echocardiographic evidence of tamponade.
iv) Treatment
 Support MAP with aggressive volume and inotropic support.
 Ensure sufficient blood is cross-matched ( 6 units)
 If stable, reopening in theatre is the preferred treatment
 In emergency situations the chest may need to be opened in ICU.
d) Tension pneumothorax
i) This is a medical emergency.
ii) If a pleural drain is already present, quickly exclude obstruction/kinking.
iii) Otherwise, needle decompression followed by insertion of an underwater
seal drain.
e) Cardiac arrest
i) This is a medical emergency.
ii) The resuscitation guidelines are different from standard BLS/ALS.
iii) A major and important difference is that in patients who arrest following
cardiac surgery, chest compressions should only be commenced if the
sternotomy cannot be performed within 3 minutes.
iv) See guidelines below.
Flowchart: Arrest Post Cardiac Surgery
Resuscitation of a Patient Who Arrests Post Cardiac Surgery
Assess rhythm Hand ventilate
(Administer FiO2 100% with Bag mask/ETT turn OFF PEEP. Auscultate chest to exclude tension pneumothorax)
Ventricular Fibrillation
Ventricular Tachycardia
Profound Bradycardia
HR < 30
Pulsless Electrical
Commence Advanced Life Support
If an IABP in situ change to pressure trigger
No CPR or Precordial thump
DC shock
(3 attempts)
+/- Amiodarone
Atropine 3 mg IV
Pace : Invasively (If Wires Present)
If paced turn OFF to exclude
Ventricular Fibrillation
Activate 4 Key Roles in Emergency Resternotomy
CPR if Resternotomy expected to take longer than 3 minutes
Perform Resternotomy
- Internal Defibrillation
- Internal Cardiac Massage
- Relieve Tamponade (If Present)
- Internal Cardiac Massage
- Relieve Tamponade (If present)
- Internal Cardiac Massage
- Relieve Tamponade (If present)
Adapted From: Dunning J, et al. Guideline for resuscitation in cardiac arrest after cardiac surgery. European Journal of Cardiothoracic Surgery, 2009
5. Hypertension
a) MAP should be kept at approximately 70 mmHg for the first 24-36 hrs.
b) This may vary according to the patient’s pre-morbid BP.
c) Management:
i) Ensure adequate analgesia
ii) Nitroprusside or GTN: titrate to maintain MAP ~ 70 mmHg.
iii) If nitroprusside infusion > 40-50 ml/hr (2 µg/kg/min), consider:
 Metoprolol:
1-2 mg IV, (if no contraindication)
 Clonidine:
25-50 µg IV (up to 300µg/24 hrs)
 Hydralazine: 10-20 mg IV
 Captopril:
6.25-12.5mg 2 hourly PRN (up to 150mg/24 hrs)
6. Management of Bleeding
Flowchart: Bleeding Post Cardiac Surgery
Excessive bleeding post-op:
> 200 mL/hr for 3-4 hrs, or
> 1500 mL total loss
Or, as per Surgeon’s advice
ACT = 145-159s
ACT > 160s
 25mg protamine once only
 50mg protamine once only
Transfuse RC to maintain Hb > 80g/L
INR > 1.5 or APTT > 45 sec
 give 3-4 units FFP
Fib < 1.0g/L
 give 5 bags (apheresed) of cryoprecipitate
Platelet <100 x 109/L or prolonged by pass time
or pre-op clopidogrel
 give 1 bag of platelet (pooled/apheresed)
Treat acidosis, hypocalcaemia, hypothermia
Resend CBP/coag screen
IF Bleeding Continues +
Discuss with haematologist or activate MTP
Consider DDAVP (0.3 mcg/kg) but must discuss with surgeon
7. Sedation/Analgesia:
a) Propofol if required
b) Fentanyl IV boluses PRN while on ventilator
c) Morphine or fentanyl subcutaneously post-extubation
d) Paracetamol IV or po 4/24 PRN for first day then 6/24 if no contraindication
e) Oxycodone po 4/24 PRN in appropriate dose from second post-op day
8. Anticoagulation / DVT prophylaxis:
a) Heparin 5000U s/c 8 hrly - all patients.
i) Start 6-12 hours post-op in the absence of excessive bleeding.
b) Aspirin 300mg daily
- following coronary artery grafts.
i) Start at the same time as the heparin.
ii) Give via NG/OGT or S/L if the patient remains intubated.
c) Commence patients with mechanical valve replacements on warfarin (5mg
nocte) from the second post-operative day if extubated.
d) Discuss anticoagulation requirements for tissue valves with the surgeon.
e) Patients with a mitral valve replacement ventilated > 48hrs may require
heparinisation as will patients in AF for > 48hrs.
9. Antibiotic prophylaxis:
Table: Antibiotic Prophylaxis for Cardiac Surgery
 Non-allergic, or
 Type 3 Penicllin allergy –
delayed rash only
 Penicillin allergy – Type 1
Cardiac valve surgery
 Cefazolin 2g IV
+ Gentamicin 240mg 30min pre-incision, then
 Cefazolin 1g IV post-onset-bypass, then
 Cefazolin 1g IV 8 hourly for 24 hours
 Gentamicin 240mg day 1 post-op
(omit if CrCl < 60 ml/min)
 Vancomycin 1g (1.5g > 80kg)
+ Gentamicin 240mg 30min pre-incision, then
 Vancomycin 500mg, 6hrs post bypass
 Gentamicin 240mg day 1 post-op
(omit if CrCl < 60 ml/min)
 Vancomycin 1g (1.5g > 80kg)
+ Gentamicin 240mg 30min pre-incision, then
 Vancomycin 500mg, 6hrs post bypass
 Gentamicin 240mg day 1 post-op
(omit if CrCl < 60 ml/min)
10. Other Drugs
a) Calcium Channel Blockers. Following radial artery grafts, diltiazem (30mg po
tds) may be required from first postoperative day. Discuss with surgeon.
b) Stress ulcer prophylaxis not routinely indicated unless the patient has preexisting peptic ulcer disease.
c) Insulin is managed as per the general ICU protocol.
11. Minimally Invasive Mitral Valve Repairs
a) These are performed through a right sided mini-thoracotomy with the patient
on femoro-femoral bypass
b) Patients may have a “pain buster” placed perioperatively for analgesia
c) Management is as for other cardiothoracic patients.
d) Clarify with surgeon if warfarin is to be given postop. This may vary with
exact type of repair, use of annuloplasty ring, heart rhythm etc.
Renal Failure
1. Background
a) The mortality from acute renal failure remains high:
i)  8% in isolation
ii) ≤ 70% when associated with other organ or system failures.
b) Patients who die with acute renal failure, usually die from the underlying cause
rather than ARF itself.
c) There is a spectrum of renal dysfunction with variable definitions of what
constitutes “Renal Failure”.
d) Bellomo has proposed the following definitions:
UO / d
Acute Renal Impairment
> 120
> +60
> +4
Acute Renal Failure
> 240
> +120
> 12
> +8
e) Approx. 30% of ICU patients have pre-existing renal impairment.
f) Patients at high risk of developing ARF are those with:
i) Pre-existing renal impairment (creatinine > 120).
ii) Severe sepsis
iii) Hypertension
iv) Diabetes
v) Arteriovascular disease
vi) Heart failure
vii) Large contrast media loads
g) The minimum urine output required to excrete the
obligatory solute load  0.5 ml/kg/hr.
h) ARF can be “oliguric” or “non-oliguric”.
i) Non-oliguric renal failure has a better prognosis.
j) Duration of ARF is variable and depends upon resolution of the underlying
injury, severity of the injury and pre-morbid renal function.
k) Consequences of ARF:
i) Fluid overload.
ii) Uraemia – encephalopathy, platelet dysfunction, pericardial effusions.
iii) Acidaemia.
iv) Electrolyte derangements – K+, PO4=, HCO3v) Accumulation of pro-inflammatory cytokines (theoretical)
2. Pathogenesis – ARF in critically ill patients is usually multifactorial.
a) Pre-Renal
i) The most common cause of renal failure in ICU.
ii) Aetiologies:
 Low cardiac output states
 Hypovolaemia.
 Vasodilation
- sepsis, vasodilators
 Renal vasoconstriction
 Renal artery obstruction
- stenosis, embolus, post-surgical
iii) Reduced renal blood flow 
  GFR and renal function
  angiotensin-II and glomerular efferent arteriolar constriction
  blood flow to the renal medulla
 If maintained, then ischaemic renal injury occurs (e.g. ATN).
b) Renal
i) Acute Tubular Necrosis.
 Ischaemic
- see above
 Nephrotoxic
- drugs, contrast, myoglobin, sepsis
ii) Interstitial Nephritis - infections, drugs
iii) Vascular disease
- renal vein occlusion, HUS, vasculitis
iv) Glomerulonephritis
c) Post-Renal
i) Obstruction of the renal collecting system leads to GFR.
ii) Must be considered in unexplained renal failure.
iii) Cannot be reliably ruled out clinically and hence requires imaging.
iv) Ensure a bladder catheter is inserted and draining freely.
v) Aetiologies:
 Drugs - opiates, anticholinergics
 Pelvic neoplasms.
 Retroperitoneal collections (e.g. blood, pus, fibrosis).
 Pregnancy.
 Prostatic Obstruction
 Renal calculi
d) Specific Renal Failure Syndromes
i) Increased intra-abdominal pressure (IAP)
 Effects at all levels
- pre-renal, renal and post-renal
 May consider decompression when IAP > 20 mmHg with ARF.
ii) Hepato-Renal Syndrome
- predominantly pre-renal
  albumin, vasodilatation, splanchnic shunting
 diuretics for oedema, lactulose, diarrhoea, intra-abdo pressure
iii) Rhabdomyolysis
- pre-renal, renal and post-renal
iv) Ineffective plasma volume
 e.g. nephrotic syndrome, liver failure, cardiac failure.
3. Renal Investigations
a) Blood tests
i) Creatinine
 Logarithmic (inverse) relationship with GFR.
 Can lose up to 60% renal function and maintain a “normal” creatinine.
 Conversely in severe renal failure, a small decrease in renal function
can cause large rises in serum creatinine.
 Lags behind the evolution of renal injury.
 Insensitive where muscle mass is low – elderly, wasting diseases
ii) Creatinine clearance (ClCr)
 ClCr slightly overestimates GFR due to tubular secretion
 Estimated on IMVS biochemistry (eGFR) from single specimen
creatinine, thus has same inaccuracies as creatinine
 Measured ClCr requires min 8 hour urine collection
iii) Urea
 Less accurate indicator of GFR than creatinine
 Modified by diet, catabolic state, GIT blood, liver disease
iv) Electrolytes
- Na+, K+, HPO4=, ABGs.
v) GN screen
- ESR, C3, C4, ANA, RhF, ANCA, anti-GBM.
vi) Haemolysis screen
- RBC frags, LDH, haptoglobins, bilirubinaemia.
b) Urine
i) M, C&S
- infection must always be excluded
ii) Myoglobin
iii) Urinary electrolytes
 impossible to interpret with diuretic or natriuretic agents (CAs).
iv) Urinary sediment
 Epithelial cell casts - ATN
 RBC / WBC casts
- GN
 Eosinophils
- interstitial nephritis
 Crystals
- oxalate (e.g. ethylene glycol)
- urate (e.g. tumour lysis)
c) Imaging
i) Ultrasound
 Exclude urinary tract obstruction.
 Doppler studies can assess renal artery and venous flows
ii) CT Renal Tract (non-contrast) – highlights renal stones and masses.
iii) IVP
- rarely required given availability of U/S and CT.
iv) DMSA scan - a static radionuclide scan to reveal kidney structure.
v) MAG3 scan - a dynamic radionuclide scan
- renal function, collecting system obstruction, ATN.
d) Biopsy
i) Glomerulonephritis
ii) Interstitial nephritis
iii) Infiltration
4. Renal protection
a) Established renal protection strategies
i) Fluid resuscitation to maintain circulating blood volume.
ii) Haemodynamic support of MAP and CO using inotropes
 adrenaline, noradrenaline, dobutamine
iii) Exclusion of post-renal obstruction
 check IDUC, renal tract U/S, nephrostomy
iv) Avoidance / close monitoring of nephrotoxic drugs
 aminoglycosides, amphotericin
 contrast agents
 ACE inhibitors
v) Prompt detection & treatment of urinary infection.
b) Unproven strategies for renal protection
i) N-acetyl cysteine
ii) Frusemide infusion / high dose
iii) Mannitol infusion / intermittent
iv) HCO3- for rhabdomyolysis.
v) Aminophylline infusion
vi) Calcium channel blockers
vii) Clonidine
c) Contrast Prophylaxis
i) Best evidence is to use HCO3ii) Add 150ml 8.4% NaHCO3 to 850ml 5% Dextrose.
iii) Run at 3ml/kg the hour prior to contrast administration,
then continue at 1ml/kg/hr for 6 hours
d) Low Dose Dopamine
i) May temporarily increase urine output
ii) Does not reduce the incidence of dialysis dependent renal failure or
mortality. (ANZICS CTG).
5. Indications for renal replacement therapy
a) Symptomatic or refractory:
i) Acidosis
ii) Hyperkalaemia
iii) Fluid overload
- e.g. pulmonary oedema
iv) Uraemia
- urea > 35 mmol/l or symptomatic
b) Severe sepsis / developing oliguric renal failure
c) Diuretic resistant pulmonary oedema.
d) Drug removal (see Dialysis in Overdose)
e) The decision to commence RRT should be discussed with the duty consultant.
f) RRT is generally initiated early before serious complications develop.
g) The choice of RRT modality depends on patient’s type and severity of illness,
equipment availability and local expertise.
h) The renal unit should be notified “early” of patients who are potential long-term
dialysis candidates.
6. Renal Replacement Therapy Principles
a) Haemofiltration.
i) Convective solute and fluid removal down a hydrostatic pressure gradient
to form an ultrafiltrate (UF).
ii) Clears middle molecules (> 500D) and fluid.
iii) UF formation is dependent on the pressure gradient and membrane
characteristics (effective pore size & surface area).
iv) Predilution replacement of ultrafiltrate with balanced salt solution
increases the availability of urea for convective transfer by favouring its
movement from red cells.
b) Haemodialysis.
i) Diffusion of solute down a concentration gradient across a semi-permeable
membrane, running dialysate fluid counter-current to blood flow
ii) Clears urea, creatinine, electrolytes (i.e. small molecules).
iii) Solute clearance is adjusted by changing the dialysate fluid solute
concentration, blood and dialysate flow rates.
iv) Intermittent HD (IHD)
 Utilised if the patient is stable and requires longer-term dialysis.
 Takes 3-5 hours using higher blood flows of 300 ml/min
 Fluid removal occurs quickly, not tolerated in unstable patients.
 Performed by the Renal Unit.
v) Sustained Low Efficiency Dialysis (SLED)
 Similar to standard IHD but occurs over 8-12 hours
 Lower blood and dialysate flow rates.
 Well tolerated by the critically ill.
 Used in some ICUs (not the RAH) for nursing and cost reasons.
 Although better tolerated than IHD in the critically ill, there is little
evidence to confirm equipoise with CVVHD/F in terms of outcomes.
c) Continuous veno-venous haemodiafiltration (CVVHDF).
i) Standard form of continuous renal replacement therapy in this Unit.
ii) The combination of ultrafiltration and dialysis improves solute clearance.
iii) Advantages of CVVHDF over conventional intermittent haemodialysis:
 Effective and more flexible control over fluid balance.
 Greater cardiovascular stability.
 Does not require attendance of Renal Unit staff.
 May have a role in modification of the septic response.
 Some trials suggest improved patient mortality (not proven).
 Allows patients to receive continuous protein rich diet.
7. Complications of CVVHDF
a) Hypothermia.
b) Prolonged exposure to heparin:  incidence of HITS, bleeding
c) Prolonged venous access: infection, thrombosis, vascular injury
d) Prolonged exposure to extracorporeal membrane: thrombocytopenia
e) Air embolism.
f) Increased nursing workload.
g) Electrolyte imbalance: hypomagnasemia, hypophosphataemia
Diagram: CVVHDF Circuit
To Patient
8. CVVHDF Equipment
a) Dialysis catheters
i) Priority of site placement and optimal catheter length:
ii) Use Dolphin Protect® high flow catheter guided as above
iii) Heparin lock all catheter lumens 8 hourly when not in use
 5000U in 3 mls, divided equally into both lumens.
b) Filters
i) Older filters were made from cellulose and would often initiate an
inflammatory response (i.e. “membrane reaction”).
ii) Membranes are now synthetic (polycarbonate, polyacrylonitrile)
iii) These are more permeable and biocompatible
iv) Standard filter = Prisma® AN69:
 Membrane
= acrylonitrile
 Membrane thickness
= 50m.
 Surface area
= 1m2 /1.5m2 (RT-150)
(larger filters 1.2–2m allow blood flow and clearance)
 Blood volume in set
= 150ml
c) Dialysis machine settings
i) The PrismaFlex® is the standard dialysis machine at the RAH
ii) Older “Prisma” machines are still in use but are being phased out.
d) For patients on ECMO
i) CVVHDF can be performed via the ECMO circuit without additional VasCath placement.
ii) Must be discussed with ICU consultant supervising ECMO
9. Prescribing CVVHDF
a) Orders for the PrismaFlex or Prisma® should be written on a standard sticker.
b) The following variables require assessment/prescription for CVVHDF.
c) Haemofiltration solution (“replacement”).
i) Standard solution = Gambro Phoxilium.
ii) Hemosol B-Zero will remain available when required for:
 A [K+] < 4 mmol/l (e.g. severe hyperkalaemia), or
 A phosphate free solution (e.g. tumour lysis syndrome)
Table: Haemodialysis Solutions
Haemosol B-zero
iii) Flow rate  1000-2000 ml/hr (higher rates in catabolic patients)
iv) Ultrafiltration rate target  25 ml/kg/hr (averaged over 24hrs)
v) Standard is to deliver replacement pre-filter (termed pre-blood pump
fluid), but may be given post-filter if required (e.g: some toxidromes)
vi) When given pre-filter on the PrismaFlex®, still require at least 100ml/hr
replacement post-filter for the deaeration chamber to function properly.
d) Dialysis solution
i) Gambro® Phoxilium (or Hemosol B-zero if indicated)
ii) Rate = 500-2000 ml/hr (higher rates if marked electrolyte abnormalities)
e) Blood flow rate
i) On commencing CVVHDF, gradually increase blood flow as tolerated by
patient haemodynamics
ii) Target rate: 250ml/min
*limited by machine/access pressures.
f) Anticoagulation
i) Blood passing through the filter activates the clotting cascade.
ii) Anticoagulation is often required to prolong “filter life”
iii) Circuit is primed with heparin 5,000U
iv) No ongoing anticoagulation is required for patients with coagulopathy
v) Systemic anticoagulation (if no contra-indications exist)
 Heparin 5000 units stat, then continue at 500-1000 units/hr
 Heparin is infused into the circuit pre-filter
 Check APTT after 6 hrs and then daily if stable
 End-point is “filter life” rather than a therapeutic APTT (i.e. if filter is
working and APTT < 45sec, there is no need to increase heparin dose)
vi) Regional anticoagulation
 Citrate (see citrate protocol)
 Heparin
a. Utilised when:
 Maintenance of filter life is problematic.
 Systemic anticoagulation and citrate are contraindicated
 No contraindication to heparin administration.
b. The circuit still needs to be primed with heparin
c. Heparin is administered pre-filter as above
d. Protamine 5-10 mg/hr post-filter
e. Check APTT 6 hourly after any dose changes.
vii) For patients with heparin induced thrombocytopenia (HIT) consider
 Danaparoid or lepirudin (systemically, not into circuit – see protocol)
 Prostacyclin 5 ng/kg/min (see protocol)
g) Fluid removal
i) Determine how much fluid should be removed from the patient.
ii) Consider its effects on patient haemodynamics
iii) The amount of fluid removed is the difference between the effluent and the
dialysate plus replacement fluid volumes
h) Potassium
i) Gambro® Phoxilium contains 4 mmol/l potassium and will not require
additional potassium
ii) Haemosol B-zero solution contains no potassium.
 Supplementary K+:
a. Required for all patients, except in the initial management phase
of marked hyperkalaemia
b. Should to be added to both the replacement & dialysate bags
 Plasma K+ < 4.0 mmol/l
= 20 mmol / bag
 Plasma K 4.1 – 4.8 mmol/l = 15 mmol / bag
 Plasma K+ 4.9 - 5.5 mmol/l = 10 mmol / bag
 Plasma K+ 5.5 – 6.0mmol/l = 5 mmol / bag
 Plasma K+ > 6.0
= 0 mmol / bag
c. K-Acetate can be used in severe acidosis:
 Acetate is effectively metabolised to HCO3- via the liver
 Vial = 25mmol/5ml, dose = 3-4mls per 5L bag
iii) Target plasma [K+] = 3-4mmol/L
i) Drug prescription
i) Consult Antibiotic Guidelines / Pharmacy regarding antibiotic dosing
 e.g. meropenem, ciprofloxacin, fluconazole
ii) Monitor drugs that are renally cleared and potentially toxic
 e.g. gentamicin, vancomycin, digoxin
10. Citrate Anticoagulation for Renal Replacement Therapy
a) Rationale:
i) Anticoagulation of the extracorporeal circuit improves life of dialysis
filters resulting in improved ‘dose’ of dialysis, less patient blood loss and
probable cost efficiency.
ii) When systemic anticoagulants are contraindicated it is possible to use
citrate to provide regional anticoagulation of the dialysis circuit without
altering patients coagulation
b) Indication:
i) CRRT is indicated
ii) Systemic anticoagulation is contraindicated and filter life is inadequate
c) Requirements
i) Appropriate high flow vascular access
ii) Gambro Prismaflex dialysis machine
iii) Gambro dialysis fluids
 Dialysate: Prism0cal
 PBP fluid: Prismocitrate 10/2
 Post filter replacement: 0.9% saline
iv) Dedicated central access for calcium infusion
(not required if using Prismaflex software v6.1 – see below)
d) Process
i) Prior to priming the mode of anticoagulation is set to Citrate.
ii) The Prismaflex software will display the steps necessary to prime the
 Pre-blood pump (PBP) fluid (coded white) is Prismocitrate 10/2
 Dialysate (coded green) is Prism0cal, a zero calcium, zero potassium,
bicarbonate (32mmol/l) buffered dialysate.
 Post filter replacement (coded purple) is normal saline, a 1 liter bag
can be hung on the central hook
iii) At completion of the priming process the Prismaflex displays:
 Flow rates:
a. Reduce dialysate to 1000ml/hr
b. Reduce replacement to 100ml/hr
c. Confirm “post replacement” is set
 The commencement citrate concentration should be set at 2.5mmol/l
(current default 3.0mmol/l)
 Confirm final prescription and dialysis dose
iv) Commence calcium infusion and dialysis simultaneously
Ionized calcium should be checked 30 min post-commencement, both
 Post-filter (blue port)
a. Target ionized calcium:
b. If > 0.5mmol/l   [citrate] by 0.3-0.5mmol/l
c. If < 0.3mmol/l   [citrate] by 0.3-0.5mmol/l
d. The usual citrate concentration range is 1.5-4.0mmol/l
 Arterial
a. Target ionized calcium:
0.9-1.1 mmol/l.
b. Calcium replacement should be commenced with dialysis.
c. If [Ca2+] < 0.9 or there is a strong downward trend
 commence infusion via CVC: CaCl 10%  4ml/hr.
d. After calcium is commenced arterial levels should be checked
hourly until stable.
e. Infusion rates should be adjusted by 1ml/hr until arterial calcium
is in the target range
f. If dialysis is ceased the calcium infusion should be stopped.
g. The Prismaflex will display an alert to this effect
(software v6.1 will automatically cease calcium infusion)
vi) Post-filter and arterial calcium should be monitored 2 hourly until stable
then checked 8 hourly
vii) With Prismaflex software v6.1 (due 2012)
 Calcium replacement occurs via the ‘heparin syringe’ on the
Prismaflex using a Gambro algorithm.
 Separate replacement is unlikely to be necessary.
 Check Ca2+ via arterial analysis 8 hourly.
e) Complications
i) Hypocalcaemia:
 Calcium is removed via:
a. Clearance of citrate:Ca2+ complexes during haemofiltration
b. Dialysis against calcium free dialysate
 In the presence of citrate bound calcium fraction falls and may be as
low as 20%.
 The systemic binding of calcium to citrate contributes to a small
degree, however this component reverts as citrate is metabolised.
 Unless using Prismaflex software v6.1, separate replacement of
calcium via a CVC is recommended – see above.
ii) Hypercalcaemia:
 May occur due to excess calcium replacement.
 Corrected by monitoring and appropriate titration of CaCl.
iii) Acidosis:
 Possible in advanced liver failure due to accumulation of citric acid.
 Citrate anticoagulation is relatively contraindicated in liver disease.
iv) Alkalosis:
 Citrate enters the citric acid cycle and end products of metabolism are
CO2 and bicarbonate.
 A small increase in bicarbonate and pH is expected over days.
 Citrate overdose may result in metabolic alkalosis.
 Estimated 40-70% of citrate is cleared via a high flux dialyser, hence
does not enter the systemic circulation.
 Significant alkalosis requires a reduction in citrate dose or cessation of
citrate. This is uncommon.
v) Hypophosphataemia
 Prolonged filter life and high pre-dilution flow rates may result in a
high dose of dialysis being delivered.
 Associated with an increased risk of hypophosphataemia.
 Phosphate should be checked twice daily and replaced appropriately.
 Once stable daily monitoring is acceptable.
vi) Hypomagnasaemia
 Mg2+ may be chelated by citrate and hypomagnasaemia is common.
 Mg2+ should be checked twice daily (with phosphate) and replaced
11. Dialysis in Overdose
a) Institution of dialysis for a life-threatening overdose is a consultant decision.
All cases are to be discussed with the ICU Consultant on call
b) There are a number of drugs effectively cleared by extracorporeal techniques
i) These agents are generally small, hydrophillic molecules with low protein
binding and volume of distribution
ii) The kinetics of many agents change in overdose (eg valproate) and
therefore discussion with the ICU Consultant and Toxicologist is required
iii) Common agents cleared by dialysis include:
 Lithium
 Toxic alcohols
 Sodium Valproate
 Carbamazepine
 Atenolol / Sotalolol
 Salicylates
iv) There are a number of other less common agents potentially amenable to
clearance via dialysis but requiring special consideration
 eg. paraquat, procanamide, methotrexate, chloral hydrate
c) Institution of dialysis is more likely to be effective in the absorption phase when
a drug is concentrated in plasma than after distribution to tissue.
d) Standard ICU dialysis guidelines (ie. dialysis stickers) are designed for gradual
clearance of uraemic toxins and are not ideal for use in overdose
e) The aim of diafiltration in overdose is to optimize clearance by maximizing
extracorporeal blood flow, dialysate gradient and occasionally transmembrane
pressure gradient.
i) For this reason all patients should be treated with the Prismaflex,
not the older Prisma machines, with an ST-150 circuit
ii) An appropriate size femoral dialysis catheter should be inserted to allow
blood flow rates > 250ml/min (ideally  300ml/min)
f) Diafiltration of life threatening overdose should commence as follows:
Prismaflex – ST 150 Circuit
Blood Flow Rate
*increase as tolerated
300 ml/min
Phoxilium or Hemosol BO
4000 ml/hr
Pre-blood pump Replacement
Phoxilium or Hemosol BO
100 ml/h
Post Filter Replacement
Phoxilium or Hemosol BO
2000 ml/hr
Heparin 500u/ml
1-2 ml/hr
g) Potassium should be added to both dialysate and replacement when using
Hemosol BO unless overdose is associated with severe hyperkalaemia.
h) At high dialysis doses it must be remembered that
i) Hypomagnasaemia and hypophosphataemia (if using Hemosol BO) are
common and occur rapidly. Levels should be checked twice daily and
replaced as indicated
ii) Clearance of many therapeutic drugs is increased and dose adjustment may
be necessary
iii) Levels of other antidotes may be altered (e.g. ethanol) and where possible
need regular monitoring
i) Conventional intermittent haemodialysis may be preferable:
i) Dialysate flow rates and early clearance of small molecules are greater.
ii) If not readily available, institution of CVVHDF is indicated even though
extraction ratios are generally lower, total body clearance is often greater
j) Data on clearance of toxins using CVVHDF and modern membranes is sparse.
For this reason samples should be taken for drug levels as per the form below:
Form: Dialysis Data for Drug Overdose
Estimated Time of Overdose:
Drug/s & Estimated Dose:
Blood Flow Rate:
Dialysis Flow Rate:
Replacement Flow Rate:
Fluid Balance:
0 hrs
2 hours
4 hours
8 hours
12 hours
Neurosurgical protocols
1. Neurotrauma in ICU
a) Close liaison and communication with the neurosurgeons is essential for the
coordinated management of acute head injuries.
b) ICU management of the neurotrauma patient includes:
i) Acute trauma resuscitation
ii) Liaison and coordination with other clinics in the multi-trauma patient.
iii) Cardiopulmonary / renal / metabolic homeostasis.
iv) Maintenance of cerebral homeostasis – see CPP algorithm
v) Transport for imaging
c) Principles of ICU management:
i) Ventilation
 Maintain normoxia:
PaO2 > 80 mmHg
 Ventilation to normocapnia:
PaCO2  35-40 mmHg
ii) Haemodynamics:
 Fluid maintenance
a. Maintain euvolaemia
b. Crystalloid depending upon Na+ and measured osmolality
c. Avoid dehydration if patients become polyuric (DI / mannitol)
 Maintain cerebral perfusion pressure:
a. CPP  60–70 mmHg
i. A lower threshold may be tolerable in some patients
ii. Must be discussed with the ICU Consultant
b. MAP  80 mmHg in the absence of ICP measurement
c. NB: use inotropes if required once euvolaemic
 Avoid interference with cerebral venous return
a. Nurse patients at 30° head-up elevation
b. Neutral head position
c. Avoid circumferential ETT ties, etc.
iii) Osmotherapy
 Should be discussed with the ICU Consultant
 Indications for osmotherapy prior to ICP monitoring are:
a. Unequivocal signs of intracranial hypertension prior to imaging or
evacuation of an intracranial mass lesion
b. Threatened transtentorial/brainstem herniation, or
c. Progressive CNS deterioration not due to systemic pathology.
 Hypertonic saline
a. Fewer complications c.f. mannitol.
b. Standard dose:
20ml of 20%NaCl
c. Slow IV push through a CVC
d. Osmolality should not exceed 320mosmol/l
 Mannitol
a. Patient must be euvolaemic and normotensive (relative to premorbid BP) before the administration of mannitol
b. Osmolality (measured) should not exceed 320mosmol/l
i. Mannitol and alcohol cause an osmolal gap
ii.  calculated  measured osmolality
c. Standard dose = 0.25g/kg
i. 1.25ml/kg of 20% mannitol
ii. Duration of action is variable (90min – 6hrs)
d. A urinary catheter is essential.
Seizure prophylaxis - indications:
 Closed head injury with structural damage
(intracerebral or paraxial haematomas)
 Penetrating head injuries
 Depressed skull fracture
 Pre-existing epilepsy
 Phenytoin prescription:
a. 15 mg/kg loading over 30 minutes
b. 300 mg iv daily or 400mg NG x 7 days only
c. Monitor levels: therapeutic 40-80mol/l
Antibiotics - indications:
 Insertion of ICP monitoring catheters: cefazolin 1g stat
 Base of skull fractures: antibiotics are not indicated in the absence of
signs of meningitis
 Nosocomial infections: as per infectious diseases guidelines.
 Consider the use of propofol in patients where regular review of CNS
status is required (majority of patients)
 Control large sympathetic swings with fentanyl (100-200µg IV)
 Many opioids have been demonstrated to increase ICP and should not
be used as sole therapy to control intracranial hypertension.
 The use of muscle relaxants is relatively contraindicated and must be
discussed with the ICU Consultant.
 Consider -blockade or clonidine in labile neurogenic hypertension.
 Establish enteral feeding as soon as feasible
 Maintain BGL in the normal range by insulin infusions if necessary.
 Hyperglycaemia is common in the acute phase and may precipitate a
hyperosmolar state with resultant polyuria.
Stress ulcer prophylaxis is not routinely indicated (see protocol)
ix) Thromboprophylaxis:
 All patients should have TED stockings and SCCDs applied within
8hrs of admission unless contra-indicated.
 Pharmacological thromboprophylaxis is relatively contraindicated in
the first 72 hrs after injury or surgery or if there is ongoing bleeding.
 Thromboprophylaxis may be commenced when indicated following
discussion with Neurosurgery
 In patients at high risk of VTE or with contra-indications to
mechanical prophylaxis, consideration should be given to early
insertion of a caval filter
x) Avoid hyperthermia.
d) Monitoring of head injured patients:
i) Cardiorespiratory:
 In addition to routine ICU monitoring ETCO2 is recommended
a. Interpret with caution & calibrate with PaCO2 when,
i. Change in ventilation
ii. Sudden rise in ICP
b. Adjust ETCO2 to PaCO2  35-40 mmHg
ii) Neurological:
 ICP monitoring
a. At the RAH ICP monitors are inserted by neurosurgeons
b. Indications:
i. Severe CHI (GCS < 8) and an abnormal CT scan, or
ii. GCS < 8 and two of
 Age > 40 yrs
 Focal motor signs
 Hypotension after volume resuscitation
iii. Brain swelling following evacuation of intracranial
iv. Intracerebral haematomas where the decision to operate will
depend on ICP
v. Polytrauma patients in whom cerebral status cannot be
adequately assessed (e.g. patients requiring ventilation)
vi. Rarely in non-traumatic raised ICP
 Meningitis / encephalitis
 Hepatic failure.
 Ventricular drain and external pressure monitor:
a. Closed system
b. CSF for M,C&S as clinically indicated
c. Set height for drainage according to neurosurgical consultation.
d. Preferred for ICP monitoring in CHI
Flowchart: Cerebral Perfusion Pressure Algorithm
Initial Therapy to Optimise CPP
Maintain euvolaemia with IV fluids
Ensure appropriate sedation
Commence inotropes to maintain CPP  60-70 mmHg (MAP-ICP)
Maintain normocarbia, PaCO2 35-40 mmHg
ICP > 20 mmHg for > 10min or CPP < 60 mmHg
Ensure accurate MAP, ICP and where relevant, SjO 2 readings
Immediately correct hypovolaemia and hypoxia
Ensure normocarbia: PaCO2  35-40 mmHg
Ensure adequate sedation
Consider drainage 2-5ml CSF if intraventricular catheter in situ
Exclude contributing factors
Neck position / venous obstruction
30º head-up position
Fever, Seizures
Commence osmotherapy with hypertonic saline or mannitol and notify ICU
Consider short-term hyperventilation whilst arranging urgent CT
Consider neuromuscular blockade
Notify neurosurgeon on-call
CT Head
Surgical Lesion
Immediate Neurosurgical
Non-Surgical Lesion
Attempt to maintain CPP > 60 mmHg with fluids / inotropes
Consider additional therapies after discussion with Duty ICU Consultant:
Propofol / barbiturate coma
Neurosurgical referral for decompressive crainectomy
Aneurysmal Subarachnoid Haemorrhage
Table: World Federation of Neurosurgeons Classification
Motor Deficit
Present or absent
Present or absent
a) Principles of ICU management:
i) Priorities:
 Monitoring of airway and adequacy of ventilation
 Maintenance of adequate cerebral perfusion
 maintain appropriate MAP (relative to premorbid BP)
 Monitoring of conscious state (GCS)
 Early diagnosis and treatment of causes of reduced GCS
a. Rebleed from aneurysm
(notify neurosurgeon)
b. Hydrocephalus
(notify neurosurgeon)
c. Vasospasm
d. Seizure
ii) Monitoring:
 ECG, SpO2, Invasive BP
 ICP in patients with a ventricular drain in situ:
a. May be set at a level (usually 10 cm) above head and/or
b. Connected to monitor transducer
c. CSF culture as clinically indicated
b) Anticonvulsants: as clinically indicated
c) Angiographic Coiling
i) Prefered approach for selected, amenable aneurysms:
 Less invasive procedure
 Better outcomes at 12 months c.f. clipping
ii) Performed in radiology under sedation (provided by anaesthesia)
iii) May still require insertion of an EVD for hydrocephalus.
iv) Post-procedure management in P4-C as for operative patients.
d) Operative therapy:
i) Early (within 48 hrs): usual practice at RAH
 Advantages (proposed): prevention of rebleeding, reduction of
vasospasm, prevention of ischaemia
 Disadvantages: high risk of rupture, difficult dissection
ii) Late (after 11 days)
 Advantages: easier procedure, opportunity to monitor.
 Disadvantages: re-rupture, prolonged risk of vasospasm
e) Prevention and treatment of vasospasm
i) Specific drug therapy:
 Nimodipine:
a. Indications
i. CT proven SAH
ii. IV preferably through central line (2 mg/hr)
*may be given through a peripheral IV
iii. Change to oral as soon as possible (60mg 4hrly)
b. Complications: hypotension (may require cessation of nimodipine)
 Statins (simvastatin 80mg daily) may reduce the incidence of
radiological vasospasm and improve outcomes following SAH.
ii) Triple H therapy (hypertension / hypervolaemia / haemodilution):
 Has no role in the prevention of vasospasm
 prophylactic HHH therapy may be harmful
 It is imperative to avoid hypotension and hypovolaemia.
 Patients should have fluid therapy targeted at maintaining euvolaemia.
iii) Euvolaemic hypertension
 May be indicated in selected patients with proven vasospasm postaneurysmal clipping / coiling.
 Induced hypertension must be titrated to a mean arterial pressure:
systolic BP is not an accurate indicator of cerebral perfusion pressure.
 Principles:
a. Discuss with ICU consultant prior to initiating therapy
b. Intra-arterial pressure monitoring is mandatory
c. Maintain IV volume
i. Continue IV filling until clinically euvolaemic
ii. Avoid volume overload (pulmonary congestion/oedema)
iii. Monitor electrolytes 8 hrly  normal osmolality and [K+].
d. Commence noradrenaline titrated to:
i. MAP > 90mmHg, or
ii. MAP > 10mmHg above premorbid baseline
(for known hypertensive patients), or
iii. MAP  5-10mmHg > “defined MAP”
 On occasions there may be neurological improvement at a
certain MAP  titrate therapy 5-10mmHg above this
iv. Reset target MAP if high doses (> 10g/min) are required, or
if polyuria, arrhythmias or other complications ensue.
 Complications:
a. Pulmonary oedema, hypoxia
b. Cardiac arrhythmias, myocardial ischaemia
c. Polyuria, electrolyte disturbances
iv) Chemical (papaverine / verapamil) or balloon angioplasty
 Limited role in angiographically proven vasospasm
 Requires transport for angiography and may be performed on
consecutive days.
2. Status epilepticus
a) Definition:
i) Continuous seizure activity > 30 minutes duration, or
ii) Sequential seizures (≥ 2) without recovery of consciousness.
b) Principles of ICU management
i) Assessment of airway and adequacy of ventilation
 Intubate and ventilate if appropriate
 Avoid muscle relaxants after intubation
ii) IV access
iii) Control of seizures:
 Midazolam:
1-10 mg/hr via infusion, or
10-20 mg IV prn
 Phenytoin:
18 mg/kg load, then 300 mg daily
check for previous administration
therapeutic levels 40-80mol/l
 If refractory, liaise with neurologists and consider:
a. Clonazepam 1-2 mg IV prn or by infusion 0.5-2 mg/hr
b. Valproate 200-500mg NG/IV 8 hrly
c. Levetiracetam (Kepra) 500mg NG 8 hrly
d. Thiopentone infusion
i. Loading dose:
5mg/kg of 25mg/ml solution
(2500mg / 100ml N.sal)
ii. Infusion:
1-3 mg/kg/hr
(~ 150 mg/hr or 6 ml/hr)
e. Obtain EEG and consider EEG monitoring
iv) Look for a cause and treat appropriately:
 CT scan with contrast if unclear
 Previous epilepsy / poor compliance
 Intracranial pathology:
a. Vascular (haemorrhage, thrombosis), spasm
b. Infection (consider LP if no evidence of raised ICP on CT)
c. Tumour
 Extracranial pathology:
a. Check electrolytes: especially Na+, Ca++, Mg++, K+, PO4=
b. Metabolic: exclude hypoglycaemia, thiamine deficiency
c. Toxic ingestion.
 Infection
 Severe hypertension
c) Maintenance of homeostasis / seek and treat complications
i) Ensure adequate hydration: maintenance fluids according to
creatinine/urea, Na+ and osmolality
ii) Ensure adequate urine output: prolonged seizures may be associated with
iii) Evaluate for joint dislocations and occult fractures
4. Exclusion of Traumatic Cervical Spinal Injury
a) Safe practices are vital to prevent secondary damage to the cord
b) Spinal immobilisation should be practiced in all patients with;
i) significant distracting injury or injury above the clavicles
ii) altered conscious state for any reason (head injury, alcohol, drugs etc)
iii) neck pain or tenderness
iv) abnormal neurological signs or symptoms
v) NB:
 Hard collars allow up to 73% of normal flexion and extension – and so
still need appropriate spinal care even if in place.
 Soft collars do not provide effective C-spine immobilisation.
c) Clinically clearing the C-spine requires all of the following criteria to be
i) normal conscious state, with no drugs or alcohol onboard
ii) no neck pain or tenderness
iii) no abnormal neurological signs or symptoms
iv) no significant distracting injury, or significant injury above the clavicles
and then,
v) normal head control (unassisted)
vi) pain-free movement
d) If all of these are confirmed, the hard-collar can be removed, and the C-spine
e) If the C-spine cannot be clinically cleared for any reason, radiology needs to be
performed (the majority of patients seen in Trauma Resus)
f) Virtually all patients presenting to Trauma Resus require a trauma series of
adequate AP, lateral, and odontoid C-spine plain views
g) A complete series of 3 plain views will still miss up to 7% of C-spine injuries –
hence the importance of clinically clearing (if possible) the C-spine even if the
Xrays appear normal.
h) If the C-spine cannot be clinically cleared following normal plain films,
maintain spinal precautions and liaise with the Trauma Registrar.
i) Clearing the C-spine in the patient with altered conscious state:
i) If drugs, alcohol or minor closed head injury are the problem, they are
often resolved within 12 hours – maintain spinal precautions until that
stage, and then assess clinically
ii) If the patient is unlikely to become clinically assessable and clearable
within 12-24 hours (most intubated ICU patients):
 Perform a complete plain Xray series in ED, and:
 Perform a limited CT;
a. C0-2 in all, during first visit to scanner
b. CT any suspicious areas on the plain films
c. CT may be required to visualise cervicothoracic junction
d. CT entire cervical spine with 3-D reconstructions (the current
 If these films are all documented normal, the collar may be removed
and the C-spine cleared ‘as per RAH protocol’.
 Any ongoing concerns are referred to the Trauma and/or Spinal
Flexion-extension views of the C-spine must not be performed, unless ordered
by the Spinal Unit, with the Spinal Fellow in attendance
As with the C-spine, the thoracolumbar spine should be imaged in all patients in
whom it can not be clinically assessed. This should be done prior to arriving in
ICU. If CT chest and abdomen have been performed, these images can be used
to assess and clear the thoracic and lumbar spines.
25% with a spinal injury at one level will have a second non-contiguous injury.
Therefore, if a fracture is found anywhere in the spine, the entire spine should
be Xrayed
Spinal Xrays should ideally be performed in an Xray area (Trauma Resus Room
or Xray Dept) prior to ICU admission.
The quality of spinal Xrays performed in ICU is usually very poor
The Trauma Registrar must document the status of spinal clearance on the
Trauma Form
Steroid use in acute spinal cord injury is not currently recommended by the
Spinal Injuries Unit.
The RAH Trauma Service Procedures, Practices and Guidelines (TSPPG) on
‘Acute Spinal Injury Management’ is available on the RAH Intranet and
contains more detail.
G. Microbiology Protocols
1. Policy
a) Sepsis is the most common cause of death in critically ill patients.
b) The prompt diagnosis and treatment of infection in critically ill patients is both
important and difficult.
c) Sepaia must be aggressively sought and promptly treated with source control
(where indicated) and appropriate antibiotics.
d) Simple preventative measures are the most important factors in the containment
of nosocomial infection and minimisation of bacterial resistance:
i) Compulsory hand washing and/or use of alcohol hand-gel by all staff
ii) Attention to aseptic technique for invasive procedures
iii) Attention to invasive procedure protocols as outlined in this manual
iv) Avoidance of over-prescription of antibiotics
e) Regular routine microbiological examination in critical care patients is not cost
effective. Investigations should only be ordered on specific indications.
f) Septic screens must follow the guidelines below.
2. Definitions
a) Systemic Inflammatory Response Syndrome (SIRS)
i) Describes the inflammatory process that occurs in response to a variety of
clinical insults resulting in a clinical picture suggestive of “sepsis”
ii) The syndrome includes at least 2 of the following:
 temperature
> 38° or < 36° C
 heart rate
> 90 bpm
 respiratory rate > 20 bpm, or
< 32 mmHg
> 12,000/mm3, or
< 4,000/mm3, or
> 10% immature (banded) neutrophils
iii) SIRS is non-specific and may be due to non-infectious causes:
 Trauma, Post-operatively after major surgery
 Haemorrhagic shock, post blood transfusion
 Pancreatitis
 Burns
 Drug reactions
 Intracranial pathology, esp. intraventricular or thalamic blood
b) Sepsis:
the presence of SIRS 2° to infection
c) Septic shock: decreased vital organ perfusion/function 2° to sepsis
d) Nosocomial infection is defined as infection that occurs during hospitalisation
that was neither present, nor incubating on admission.
e) Colonisation is defined as the presence of microorganisms that do not elicit an
inflammatory response.
3. Septic screen
a) Routine, performed only on the clinical suspicion of sepsis:
i) New pyrexia
ii)  WCC, WCC, or  Platelets
iii) Deterioration in gaseous exchange or pH
iv) Cardiovascular instability
 Hypotension / relative hypovolaemia
 Increased or new inotrope requirement
v) Oliguria or increased creatinine
b) Screen:
i) Urine
- C&S
ii) Tracheal aspirate
- urgent gram stain, C&S
iii) Blood culture x2
iv) Any other drainage fluid as indicated, e.g. wound, pleural etc.
c) Other
i) Fungal cultures
ii) Pleural fluid, CSF
iii) Sinus x-rays
iv) Bronchoscopy specimens (BAL)
d) Urine:
i) UTI in a catheterised patient is defined as:
 > 105 bacteria + positive culture of organisms, plus
 > 500 WBC/HPF.
ii) Bacteria and white cells are a normal finding in a catheterised patient
iii) Treatment with antibiotics will not result in clearance of colonisation and
is only indicated for systemic involvement.
iv) The only effective treatment is catheter removal.
v) Bladder wash-out may reduce bacterial load / infective risk.
e) Tracheal aspirate:
i) Cultures often grow mixed colonising oral flora:
 Gram positive cocci
- S. aureus and S. pnuemoniae
 Gram negative bacilli
- H. influenzae
 Yeast
- Candida sp.
ii) Antibiotics will not result in a clearance of colonisation and are only
indicated for invasive (local or systemic) infection.
f) Blood cultures:
i) Esily contaminated by skin organisms,  careful technique required:
 Clean the skin with an alcohol or betadine swab
 Clean the top of culture medium bottle with an alcohol swab and
allow to completely dry before injecting.
 Use a sterile needle and aseptic technique during venipuncture
 Inject blood immediately into bottle with same needle - do not touch
the needle.
ii) Blood cultures are best taken by clean venipuncture.
iii) Skin organisms grown from a single bottle are usually a contaminant but
must be interpreted in the context of the patient.
4. Investigation of pneumonia
a) Community acquired pneumonia:
i) Usual organisms: S. pneumoniae, H. influenzae
ii) Less commonly:
 Bacterial:
Legionella sp., Gram neg bacilli, S. aureus
 Viral:
Influenza A, B, Parainfluenza, Adenovirus, RSV
 Other :
Mycoplasma pneumoniae,
Chlamydia psittaci (birds),
Coxiella burnetti (sheep or cattle),
TB, Chlamydia pneumoniae
iii) Investigations
 Haematology - High (> 15000) or Low (< 3000) WCC
- coagulopathy
 Biochemistry - note renal function and LFTs
 ABGs
 Microbiology:
* prior to antibiotic Rx where possible
a. Blood cultures x 2
b. Endotracheal aspirate
i. M,C&S + urgent gram stain
ii. Legionella culture
iii. Respiratory viral Ag (PCR) & culture
NB: If not intubated, then collect a nasopharyngeal aspirate
for respiratory viruses
c. Urine
- L. pneumoniae 1 Ag
* only where high index of suspicion or outbreak
d. Pleural fluid - M,C&S
b) Healthcare associated pneumonia – Immunosuppressed Host:
i) Possible organisms
 As above plus
a. Bacterial:
b. Viral:
CMV, HSV, varicella zoster
c. Fungal:
candida, cryptococcus, aspergillus
d. Protozoal:
pneumocystis jirovecii (PCP)
 Consider non-infective causes of a similar picture e.g. ARDS
ii) Investigations:
* As per above, plus
 Label request “Immunosuppressed Protocol”
 Sputum or tracheal aspirate of limited value
 Consider BAL if initial cultures negative
 HIV serology
iii) Treatment prior to microbiological diagnosis: refer to antibiotic guidelines
& discuss with ID.
c) Nosocomial pneumonia in ICU
i) Principles:
 Accurate diagnosis and treatment are important but difficult.
 Incidence: 20% of all ICU patients
70% of patients with ARDS
major cause of death in patients with ARDS
 Clinically indistinguishable from pulmonary fibrosis, alveolar
haemorrhage, atelectasis and other causes of lung infiltrates
 Clinical diagnosis, including use of tracheal aspirate, has poor
sensitivity and specificity
 Appropriate antibiotics do improve outcome
 Empiric broad-spectrum antibiotics are potentially harmful.
ii) Consider nosocomial pneumonia when:
 New and persistent CXR changes
 Tachycardia, tachypnoea
 Fever or hypothermia
- temperature >37.5 or <35.5
 Leucocytosis or leucopaenia
- WCC: >10 or < 4 x 109/l
 Purulent sputum
 Deterioration in lung function
iii) Confirmation of pulmonary infection:
 Tracheal aspirate → MC&S
 Preliminary results to direct therapy may be obtained on gram stain
 Consideration should be given to obtaining pulmonary samples by
bronchoalveolar lavage (or open lung biopsy) for patients with:
a. Persistent signs of pneumonia
b. Inadequate response to antibiotics
c. Inabililty to obtain adequate tracheal aspirates, or
d. To exclude non-infectious causes of respiratory failure
e.g. interstitial fibrosis or alveolar haemorrhage
 Septic screen including blood cultures should also be performed.
5. Vascular catheter sepsis
a) Refer to the invasive procedures section
b) Suspect line sepsis when:
i) Evidence of systemic infection
 New, unexplained fever
 Unexplained  or  in WCC
 Deterioration in organ function
 Positive blood culture by venipuncture with likely organisms
(coagulase negative staph, candida), and/or
ii) Evidence of local infection - inflammation or pus at the insertion site
iii) The following patients are more susceptible to line infections:
 Prolonged vascular access (> 7-10 days)
→ exponential increase in line infection after 4 days.
 Endovascular infection (SBE, prosthetic graft infection)
 Cutaneous infection
 Burns
 Severe intra-abdominal infection (pancreatitis)
 Deep-seated infections (empyema / abscess)
iv) The incidence of line sepsis with the antibiotic impregnated lines is around
1% and most of these are due to Candida spp.
c) Protocol
i) Take blood cultures from a peripheral vein
ii) Positive blood cultures from the line may only indicate colonisation so
blood culture bottles must be carefully labelled as to site of sampling
 Common organisms in line sepsis are normal skin flora
e.g. Staph spp., C. albicans
 In ICU gram negative organisms can also be involved
iii) On suspicion of line sepsis the line should be removed
iv) The tip of the catheter should be sent for culture
 Avoid contamination of the catheter tip with skin organisms
 Skin should be cleaned thoroughly with alcohol, allowing at least one
minute drying time, before removing the catheter
v) Catheter related bloodstream infection is defined as infection where the
same organism is grown from the blood and from the catheter tip
d) Treatment
i) Removal of the line will usually clear low-virulence organism
bacteraemias, e.g. S. epidermidis
ii) Antibiotics are indicated, even if blood culture negative, when:
 The patient is high risk
- e.g. joint or endovascular prosthesis
 Infection with a virulent organism, e.g. S. aureus
 Signs of sepsis continue after catheter removal
iii) If ongoing sepsis occurs, additional blood cultures should be taken prior to
starting antibiotics
iv) Refer to antibiotic guidelines.
e) Further venous access:
i) Reassess the need for ongoing central access, consider PICC line
ii) Whenever possible:
 Wait 24 hours before reinsertion
 Select a different insertion site
iii) Guidewire exchanges are not performed unless:
 Mechanical problems in a new catheter (leaks/kink & < 4 days old)
 Difficult or limited central access (e.g. burns)
6. Bacterial Meningitis
a) Steroids should be started before antibiotics in all patients with a high
probability of bacterial meningitis.
i) No demonstrated benefit given post-antibiotics.
ii) Should occur in A&E / pre-retrieval - check on admission
b) Dose: dexamethasone 10mg 6 hrly for 4 days
c) Antibiotics are as per ID guidelines
7. Fungal infections
a) General principles
i) The incidence of systemic fungal infections in ICU patients has increased:
 Increased numbers of immunosuppressed patients admitted to ICU
 The use of broad-spectrum antibiotics, and
 Prolonged use of intravascular catheters
ii) Fungaemia is an indication to commence antifungal therapy.
iii) Whilst candidaemia is associated with significant mortality, systemic
infections can occur with negative blood cultures.
b) Risk factors for candidaemia and disseminated candidiasis:
i) Neutopaenia
ii) Long term CVC use
iii) Candida colonization
iv) Broad spectrum antibiotics
v) Haemodialysis
vi) Immunosuppressants
c) Antifungal prophylaxis
i) Systemic prophylaxis is not recommended for general ICU patients
ii) Solid organ transplant patients do not require prophylaxis
iii) Posaconazole prophylaxis is effective and tolerated in bone marrow
transplant and neutropaenic cancer patients
d) Prophylaxis and treatment are as per the RAH guidelines – see flowchart in
following page, or RAH intranet
Flowchart: Antifungal Treatment in Immunosuppressed Patients
8. Necrotising soft tissue infections
a) General principles
i) This is a generic group of patients with life threatening infections
involving combinations of mucocutaneous, fascial and myofascial planes
ii) These infections represent a medical emergency: patients may present with
severe septic shock and rapidly developing multiple organ failure
iii) In rapidly progressive infections, local signs of inflammation may
underestimate the degree of underlying tissue necrosis
iv) Usually due to one or more of the following organisms:
 Anaerobes
- clostridium spp, bacteroides
 Gram positives
- group A streptococcus, staphylococcus
 Gram negatives
- enteric organisms
b) Management protocol:
i) Appropriately trained personnel, familiar with the severity of the patient's
condition and with appropriate resuscitative equipment, must accompany
these patients during all phases of their management
ii) The hallmarks of management involve a detailed multidisciplinary
approach coordinated by the duty Intensive Care consultant and involving
the following:
 The duty ID consultant must be notified as soon as possible.
 Prompt and effective resuscitation, restoration of vital organ perfusion
and control of metabolic emergencies (e.g. hyperkalaemia,
hypoglycaemia, coagulopathy). This is coordinated by the Intensive
Care team and must not significantly delay surgery.
 Early, aggressive and repeated surgical debridement.
a. Patients with necrotising soft tissue infections must be reviewed
by a plastic surgical consultant (not trainee) ASAP.
b. The Duty Anaesthetist must be notified as soon as surgery is
 Prompt identification of organisms with early prescription of
appropriate empirical, then specific antibiotics as required (refer
empirical and specific antibiotics section).
 Immune Globulin (IV-Ig)
a. Clearest evidence in Gp A Strep infections.
b. Should be used in conjunction with clindamycin
c. Liaise with ID in all cases & confirm if to be used
d. Standard regimen over 3 days:
i. 1.0g/kg Day1
ii. 0.5g/kg Days 2&3
e. “Rescue Therapy”
i. May be considered in cases where surgery would prove
devastating, or where surgery is unduly delayed
ii. Dose: 2.0g/kg as single bolus over 3-6hrs.
NB: This may be > 3000ml IV-Ig
 Hyperbaric oxygen is an adjunctive therapy in selected patients:
a. HBO must not delay debridement and resuscitation must be
maintained during treatments.
b. Indications for hyperbaric oxygen:
i. Progressive bacterial (clostridial) gas gangrene.
ii. Selected patients with severe multisystemic disease not
responding to resuscitation, antibiotics and surgery.
c. The number of HBO treatments on a given day will depend on the
stability of the patient, availability of staff and timing of surgery.
d. As a general rule, patients undergoing surgical debridement will
return to ICU following surgery for stabilisation and assessment
prior to subsequent transfers for HBO. This will be co-ordinated
by the duty Intensive Care and hyperbaric medicine consultants.
H. Drug Overdose
1. General principles
a) The majority of drug overdoses are poly-pharmaceutical and respond to general
supportive measures.
b) Overall, early mortality is low and usually relates to cardiorespiratory arrest.
c) Following admission, morbidity relates primarily to aspiration pneumonitis, or a
delay in definitive respiratory care.
d) There is a poor correlation between depth of coma and preservation of glottic
reflexes. Accordingly, if there is any doubt the patient should be intubated.
e) Antidotes such as naloxone or flumazenil:
i) Should generally not be used as alternatives to supportive measures
ii) Are not to be used to facilitate gastric lavage or charcoal administration
iii) The main utility is in aiding diagnosis of the underlying cause of coma
- small doses only are required
iv) Usefulness in treatment is limited by their short half-lives
v) Continuous infusion is required where ongoing therapy is contemplated
vi) Both agents may initiate a withdrawal syndrome or unmask to the toxicity
of co-ingestants.
vii) In the case of flumazenil these effects may be life threatening.
f) ICU/HDU admission criteria following an overdose may include:
i) Intubated patients
ii) Reduced GCS with potential airway compromise
iii) Uncontrolled seizures
iv) Persistent hypotension
v) ECG criteria:
 Ventricular or supraventricular tachyarrhythmias
 Sinus tachycardia > 140/min with tricyclics or thyroxine
 AV block
2nd or 3rd degree
 QTC interval > 0.5s
 QRS interval  0.12s
 Acute RBBB
vi) Metabolic disturbance requiring HDU-level of care
vii) Requirement for extracorporeal elimination
2. Gastrointestinal Decontamination
a) A variety of approaches have been used historically in an attempt to reduce the
dose absorbed following an oral ingestion.
b) There is minimal evidence for improved survival or shortened duration of
toxicity, particularly when applied to unselected patients.
c) The decision to use decontamination requires individual patient risk-benefit
analysis. Appropriate patients and modalities should be selected, and
gastrointestinal decontamination should never proceed to the detriment of
resuscitative and supportive care.
d) Gastric lavage
i) Largely historical
ii) Formal lavage (large bore tube placement, water instillation and aspiration)
should not be performed.
iii) For intubated patients, an orogastric or nasogastric tube of appropriate
(standard) size should be inserted, and any gastric content aspirated
iv) No additional fluid should be instilled via the tube.
e) Charcoal
i) Charcoal aspiration has a high morbidity and mortality:
 Adequate airway reflexes must be present, or
 If there is any doubt the patient should be intubated
ii) For appropriate ingestions administer:
 1g/kg body weight (to a maximum of 100g) stat
 25g 4 hourly x 3 doses
- slow release medications
- drugs with enterohepatic circulation
 Cease administration should an ileus develop.
iii) Indications:
 Presentation < 1hr from ingestion
a. Compound bound by charcoal
b. Ingestion expected to cause significant morbidity or mortality.
 Presentation > 1hr, consider administration for:
a. Salicylates
b. Slow release or enteric coated preparations
c. Agents which delay gastric emptying, and
d. Drugs with enterohepatic circulation.
iv) Charcoal is ineffective for:
 Elemental metals and their salts
 Hydrocarbons and alcohols
 Acids or alkalis
v) With multiple dose charcoal administration, constipation is likely and the
addition of sorbitol may be considered. (NB. Sorbitol may interfere with
the adsorptive capacity of charcoal.)
f) Whole bowel irrigation
i) Use of polyethylene glycol solution to decontaminate the bowel.
ii) Use restricted to life threatening overdoses where:
 The agent is a slow release or enteric coated preparation
 The agent is not expected to be bound by charcoal.
 A good outcome is not expected with supportive care and antidote
administration alone.
 The patient presents before the advent of severe toxicity
iii) May be potentially useful following:
 Iron overdose > 60mg/kg
 Slow release potassium chloride > 2.5mmol/kg
 Major slow release verapamil or diltiazem ingestion
 Symptomatic arsenic trioxide ingestion
 Lead ingestion
 Body packers (heroine)
iv) Contraindications
 Good outcome expected with standard care
 Uncooperative patient
 Uncontrollable vomiting
 Reduced GCS or seizures expected in subsequent 4 hours
 Ileus or bowel obstruction
 Intubated patients (relative)
v) Technique
 Polyethylene glycol solution (standard endoscopy bowel prep.)
 Administer via correctly placed nasogastric tube at 2L/hour
(25ml/kg/hr in children)
 To minimize vomiting start at a slower rate & titrate up as tolerated
 Administer metoclopramide to enhance gastric emptying
 Be prepared for explosive diarrhoea
- sit on commode or place effluent tube for example
 Continue until rectal effluent is clear or an ileus/abdominal distension
3. Osmolal Gap
OG = Measured – calculated osmolality
Calculated Osmo = 2×[Na + K] + Gluc + Urea + ethanol
Baseline osmolar gaps are highly variable in the normal population.
Evaluation of potential toxic alcohol ingestion requires serial assessments over
time looking for a characteristic pattern with worsening acidaemia, increasing
anion gap and decreasing osmolar gap.
e) Single measurements may confirm an ingestion but are not reliable in excluding
Flowchart: The Unconscious, Undetermined Overdose
Don’t Ever Forget Glucose
Glucose 50%
1. Patient
2. Relatives
3. SAAS Crew
1. Clinical toxidromes
2. Trauma
3. Nerve palsies
4. Pressure areas
5. Preganacy?
Urine drug
screens rarely
management and
should be used
Drug levels:
Others as
NO Metabolic Acidosis
1. Sedatives
2. Hypnotics
3. Paracetamol
4. Theoplylline
5. Anticholinergics
6. Antihistamines
7. Antipsychotics
8. Antidepressants
9. Anticonvulsants
10. Lithium
11. Organophosphates
Arterial Blood Gas
Metabolic Acidosis
Normal Anion Gap
1. Acid ingestion
2. Toluene sniffing
3. Bicarbonate loss
Raised Anion Gap
Osmolal Gap§
OG < 10
Carbon monoxide
Lactic acidosis
OG > 10
Other alcohols
4. Specific therapies / protocols
a) Paracetamol: Acute overdose
i) Defined as a single ingestion, or staggered ingestion occurring over 8
hours or less.
ii) If the time of ingestion can be defined risk assessment and the decision to
treat may be based upon the modified Rumack-Matthew nomogram (use
the initial ingestion time as the assumed total ingestion time when plotting
staggered ingestions occurring over < 8hrs).
iii) Potentially hepatotoxic dose in a fit adult is > 200 mg/kg (or > 10g)
iv) Markedly less in high risk individuals:
 Chronic alcoholics and the malnourished
 Pre-existing liver disease
 Those taking cytochrome P450 inducing medications
v) The risk of hepatic injury without NAC (N-acetylcysteine) is predicted by
plotting a level taken 4-15 post ingestion on the Rumack-Matthew
vi) The probability, with a 4hr drug level, is:
 1-2% < 1320 µmol/L
 30%
~ 1320-1980 µmol/L
 90%
> 1980 µmol/L
(> 300mg/L)
vii) The risk of hepatic impairment with NAC is determined primarily by the
time from overdose to commencement of NAC:
 Survival is 100% where NAC is commenced within 8 hours
 Benefit is reduced if NAC commenced at 8-24 hours
 Benefit is not confirmed if commenced beyond 24 hours, except in the
setting of hepatic failure.
viii) The administration of NAC is indicated in the following settings (refer to
flowcharts on following pages):
 Patients who present within 8 hours of ingestion and have a 4-8 hour
level falling above the treatment line
 All patients presenting 8-24 hours post-ingestion
*may be ceased if the subsequent level is non-toxic and transaminases
are normal
 Patients presenting beyond 24 hours post-ingestion with detectable
paracetamol and elevated transaminases
 Unknown time of ingestion (follow the >8 hour scenario in Box 3)
 Late presenters with clinical or biochemical evidence of hepatic injury
ix) For repeated supra-therapeutic ingestions see “Flowchart: Repeated
Supratherapeutic Paracetamol Ingestion” for management guidelines.
For sustained released paracetamol preparations:
 Start NAC if > 200mg/kg or 10gm (whichever is less) ingested.
 Use paracetamol levels to determine the need for NAC.
a. Check serum levels at 4 hours and repeated 4 hours later.
b. If either level > nomogram line, continue or commence NAC.
c. NAC may be discontinued if both levels < nomogram line
NAC may be ceased in the following settings:
 Patients in whom NAC was commenced < 8 hrs post-ingestion who
are clinically well and without hepatic tenderness at the completion of
the 20 hour infusion (no further investigation required)
 Patients in whom NAC was commenced > 8 hrs post-ingestion who
are clinically well and have normal transaminases at the completion of
the 20 hour infusion. Those whose transaminases are abnormal at this
time should continue an infusion at 100mg/kg/16 hrs until
transaminases and INR (tested 12-24 hourly) are falling.
Consultation with liver transplant services (FMC) for consideration of
transplant should commence with any of the following high risk criteria:
 INR > 3.0 at 48 hours or > 4.5 at any time
 Oliguria or creatinine > 200 µmol/L
 Acidosis with pH < 7.3 after resuscitation
 Ongoing hypotension with systolic BP < 80mmHg
 Hypoglycaemia
 Severe thrombocytopenia
 Encephalopathy (any degree)
The default position, if in doubt, should be to treat with NAC.
Toxicological advice should be sought if there are any uncertainties.
Graph: Modified Rumack-Matthew Nomogram
Flowchart: Acute Paracetamol OD - Known Time of Ingestion
*from Daly FFS, Fountain JS, Murray L, Graudins A, Buckley NA. Guidelines for the management of
paracetamol poisoning in Australia and New Zealand – explanation and elaboration (Consensus Statement).
MJA 2008; 188: 296-301.
Flowchart: Repeated Supratherapeutic Paracetamol Ingestion
Table: N-Acetylcysteine Administration
 NAC 150mg/kg in 200mls of 5% dextrose over 30 minutes
 NAC 50 mg/kg in 500mls of 5% dextrose over 4 hours
 NAC 100mg/kg in 100mls of 5% dextrose over 16 hours
b) Lithium - Acute overdose
i) Generally produces significant GIT symptoms with nausea, vomiting,
abdominal pain and diarrhoea.
ii) Ingestion < 25g in the setting of normal renal function is benign
iii) Ingestion > 25g may cause more significant GIT toxicity
iv) Neurotoxicity is rare with good supportive care and hydration
v) Renal impairment, dehydration and sodium depletion cause a reduction in
renal lithium excretion and increase the risk of delayed neurotoxicity
vi) Patients presenting late with established neurotoxicity should be managed
as for chronic toxicity, and have similar long term morbidity
vii) Lithium levels > 5mmol/L 4-8 hrs post ingestion are not uncommon
viii) Treatment
 Normal saline rehydration
 Maintenance of urine output > 1ml/kg/hr
ix) Haemodialysis is reserved for:
 Those with established or worsening renal failure, and
 Those presenting late with established neurotoxicity
c) Lithium - Chronic poisoning:
i) The clinical features of chronic toxicity are primarily neurological
ii) Develops when renal lithium excretion is impaired for any reason
iii) Serum lithium levels correlate poorly with clinical toxicity
iv) Neurotoxicity may persist well after lithium levels return to normal.
v) The Hansen-Amdisen classification may be used to grade severity:
 Grade 1 (mild):
tremor, weakness, ataxia, hyperreflexia
 Grade 2 (moderate): stupor, rigidity, hypertonia, hypotension
 Grade 3 (severe):
myoclonus, convulsions, coma
vi) Cardiac effects can occur in late toxicity following the establishment of
neurological features, which includes rhythm disturbances, A-V delay,
heart block and non-specific ST segment and T wave abnormalities
vii) Lithium levels
 Confirm a diagnosis but should not be used to grade severity
 Are useful serially to monitor response to therapy
viii) Principles of therapy
 Careful correction of fluid and sodium balance
 Cease lithium and any medications that may impair excretion
 Monitor urine output, renal function, electrolytes and lithium levels
ix) Indications for haemodialysis
 Neurotoxicity and a serum level > 2.5 mmol/L
 Grade 3 neurotoxicity regardless of level
 Pre-existing renal or cardiac disease preventing the achievement of an
adequate urine output with hydration alone
 Repeated haemodialysis treatments may be required
d) Opioids
i) Produce CNS and respiratory depression, often just above analgesic doses
ii) Death is usually due to respiratory failure, either primary effect or
compounded by aspiration, and good supportive care ensures survival
iii) Some opioids may possess additional cardiac and neurologic toxicity
- e.g. dextropropoxyphene, tramadol, pethidine
iv) Controlled release preparations may cause delayed and prolonged toxicity
v) Treatment is generally supportive
vi) Naloxone (50 to 100µg IV repeated as needed)
 Useful for diagnostic purposes
 Can assist in the management of airway and breathing
 May result in a withdrawal syndrome
vii) If repeated naloxone boluses are required to ensure a protected airway,
intubation is the preferred method of ongoing management
viii) If a naloxone infusion is established:
 Initial hourly requirement is generally half the effective dose used over
the preceding hour, i.e. that required to achieve airway protection and
adequate tidal volumes
 Infusions require constant observation/assessment
 Hospital deaths have occurred due to inadequate observation
e) Carbon monoxide
i) CO is a common cause of poisoning death
ii) Most deaths occur pre-hospital.
iii) Acute effects are due to tissue hypoxia
iv) Those that arrive at hospital alive should survive.
v) In-hospital management involves supportive care and identification of
those at risk of long term neuropsychiatric sequelae
vi) Delayed neurological effects are secondary to unrelated and incompletely
understood mechanisms
vii) HbF binds CO more avidly than HbA, and the foetus is at particular risk
viii) Self poisonings involve high concentration, short term exposures, and are
associated with fewer long-term sequelae than industrial and domestic
exposures (low concentration, prolonged exposures)
ix) High risk features for delayed neurological sequelae:
 Loss of consciousness or coma
 Persisting neurological deficit (e.g. confusion)
 Cerebellar signs
 Metabolic acidosis
 Myocardial ischaemia
 Age > 55yrs
Treatment options
 Normobaric oxygen at high flow via non rebreather mask
a. Continue until all symptoms resolve
b. Pregnant women to continue for 24 hours with concomitant foetal
 Hyperbaric oxygen
a. May be indicated in patients with 1 or more high risk factors
b. Indications and effectiveness are controversial
i) Acute cyanide poisoning is rare, dramatic and lethal
ii) Removal from the source of exposure, good resuscitative care and selective
antidote use provide the best chances of survival
iii) Most deaths will occur pre-hospital, and those who arrive alive in hospital
post-inhalational exposure are likely to survive with supportive care.
iv) Risks to those involved in care delivery are negligible.
v) Decontamination should involve removal of clothes and washing of skin
with soap and water.
vi) Cyanide levels are not available in a timely manner and do not aid
vii) Serum lactate levels parallel cyanide levels and may be used as a proxy
marker of exposure
viii) A lactate level > 10 mmol/L correlates with a toxic cyanide level
(in the absence of an alternative cause for elevation)
ix) Management should proceed along normal resuscitative lines with the
delivery of 100% oxygen
x) Consider using an antidote in the following settings:
 Altered mental state
 Seizures
 Hypotension
 Significant and persisting metabolic acidosis (lactic)
xi) Antidote choice and administration
 100% oxygen in all cases
 Hydroxocobalamin (1st line)
a. 5g in 200mls of 5% dextrose over 30 minutes
b. Repeat in 15 minutes if no improvement
 Sodium thiosulphate (adjunct to Hydroxocobalamin, or 2 nd line)
a. 12.5g IV
b. Repeat dose at 30 minutes if acidosis persists
 Sodium nitrite
a. 300mg IV over 3 minutes
b. Follow immediately with sodium thiosulphate
c. Half dose may be repeated in 30 minutes if required
d. Monitor methaemoglobin (must not exceed 40%)
g) Toxic alcohols
i) A variety of alcohols (methanol, ethylene and diethylene glycol etc) are
used as industrial solvents, cleaning agents and reactants.
ii) Accidental ingestions are rarely of sufficient volume to cause toxicity
iii) Deliberate ingestion is associated with severe metabolic acidosis,
multiorgan dysfunction and potentially death.
iv) Cause an initial “ethanol like” intoxication followed by a progressive
metabolic acidosis and compound specific end-organ toxicities, e.g.
 Retinal toxicity/blindness (methanol)
 Acute renal failure (multiple agents)
 Seizures (multiple agents)
 Refractory hypotension (multiple agents)
 Delayed neurological sequelae (diethylene glycol)
v) Diagnosis is based upon a history suggestive of ingestion and a
characteristic evolution of metabolic acidosis
 Initially:  osmolar gap (OG) + normal pH and anion gap (AG)
 Evolution of acidosis with pH, OG and AG
 Variability in osmolar gap amongst the normal population is such that
a single assessment of acid-base, AG and OG is insufficient to
exclude significant exposure (although it may confirm it)
vi) Specific treatment
 Ethanol
a. Commence ASAP, regardless of symptomatology, in all with:
i. Acidosis, or
ii. An elevated OG (with or without acidosis),
b. Check baseline BAL, if > 0.1g/dl a loading dose is not required
c. Titrate to BAL  0.1-0.2g/dL while on dialysis
d. May be given orally (via NGT) or by IV infusion
e. Oral protocol
*avoid in ICU if possible
i. Loading dose of 1.8ml/kg of 43% ethanol
(4 x 30ml vodka shots for a 70 kg adult)
ii. Maintenance infusion of 0.2-0.4 ml/kg/hr
(1 x 40ml vodka shot per hour)
f. Intravenous protocol
i. Loading dose:
8ml/kg of 10% ethanol
ii. Maintenance:
1-2ml/kg/hr of 10% ethanol
g. Actual requirements vary widely between individuals, and serial
blood alcohol assessments are required to ensure a level within the
target range
h. If on CVVHDF, then safer to dialyse against desired [ETOH]
i. 0.1g/dl = 5ml ETOH / 5l Bag (inc. replacement)
ii. first bag may be run at 0.2g/dl = 10ml ETOH / 5l bag
 Haemodialysis (HD)
a. Significantly more efficient at clearing alcohols than CVVHD
b. Indications
i. Serum pH
< 7.3
ii. Serum bicarb
< 20 mEq/L
iii. Worsening acidosis or vital signs despite supportive care and
ethanol infusion
 Folate 50mg IV QID or folinic acid
 Thiamine 300mg IV daily
& pyridoxine 50mg QID for ethylene glycol poisoning
 Correct hypocalcaemia (if symptomatic) & hypomagnesaemia
h) Organophosphorous agents
i) Includes the organophosphates (OP) and carbamates (CM)
ii) Similar initial presentation
iii) Most deaths occur as a consequence of respiratory failure
iv) OPs as a group have greater lethality
 Form a covalent bond with serine esterase enzymes
 In contrast to the competitive bond formed by CM.
v) There is great variability amongst the OPs in terms of enzyme aging,
toxicity profiles, and pralidoxime responsiveness
vi) High quality supportive care and aggressive use of antidotes is necessary to
ensure survival.
vii) The diagnosis is essentially clinical:
 Muscarinic features
- diarrhoea, emesis, urination
- miosis, lacrimation, salivation
- bronchorrhoea, bronchospasm
- bradycardia, hypotension
 Nicotinic features
- fasciculation, tremor, weakness
- respiratory muscle paralysis
- tachycardia, hypertension
 CNS features
- agitation, seizures, coma
- delayed neuropsychiatric effects
viii) Cholinesterase levels:
 Plasma cholinesterase levels fall more rapidly and recover more
quickly than RBC cholinesterase levels, they are useful in confirming
exposure but do not correlate with toxicity.
 RBC cholinesterase levels correlate better with toxicity and response
to therapy, but take longer to perform (limiting their clinical utility)
ix) Decontamination
 Resuscitation must not be delayed by external decontamination
 These agents do not vapourise at atmospheric pressure
 There is no risk to care providers from inhalational exposure
 The characteristic odour is due to a hydrocarbon solvent, which may
cause headaches & eye irritation, but is otherwise harmless
 Staff should wear impermeable gowns, gloves, glasses and facemasks
 Care should be delivered in a well ventilated setting
 The patient’s clothing should be removed and the skin washed with
soap and water
 Ventilatory and CVS support as indicated
 Atropine
a. Reverses muscarinic effects only – it will not reverse paralysis!
b. Titrate 1.2 mg at 5 min intervals (doubling the dose every 5 min)
until signs of successful atropinisation are noted 
i. Drying of secretions
ii. Resolution of bradycardia
iii. Clear chest
c. Over 10-20mg, or infusions of up to 5 mg/hr may be required in
severe poisoning.
d. Typically commenced at 10-20% of loading dose per hour.
e. NB: HR and pupil size are not useful for clinical monitoring after
nerve agent exposure
 Diazepam IV
a. Treatment of seizures
b. Reduces the incidence of neuropsychiatric sequelae
c. Regular dosing is recommended.
 Pralidoxime Iodide
a. Efficacy is unclear and is likely to be compound specific
b. Default is to give ASAP
c. Not required for documented carbamate ingestion (although not
i. 1g IV over 30 minutes
ii. 500 mg/hr for 24 hours
iii. May be ceased at 24 hours in the absence of nicotinic or
muscarinic features. The benefit of continuing beyond 24
hours is unclear and warrants specialist consultation.
Calcium Channel Blockers
i) Of the common slow release formulations, verapamil and diltiazem
frequently cause profound CVS collapse 4-16 hrs post-ingestion.
ii) Other agents within the class rarely cause major toxicity
iii) Onset of toxicity may be delayed:
 Up to 2 hours post-ingestion of the standard preparation, and
 Up to 16 hours after ingestion of the SR formulation
iv) Ingestion of >10 tablets of verapamil SR or diltiazem SR may cause
serious toxicity
The key issues in management are:
 Identification of patients at risk
 Judicious use of the pre-toxicity window of stability
 Consideration of GIT decontamination options
(including whole bowel irrigation), and
 A graduated approach to developing or established toxicity
vi) Risk of serious toxicity is significantly increased by:
 Co-ingestion of other cardiac medications, and
 Underlying cardiac disease or advancing age
vii) Graduated response to hypotension: failure to achieve stability at each step
should prompt immediate initiation of the next
 Fluid load with 10-20 ml/kg isotonic crystalloid (avoid overload)
 Calcium load
a. Calcium gluconate
- 60ml of 10% solution, or
b. Calcium chloride
- 20ml of 10% solution
c. Commence an infusion to keep calcium levels > 2.0mEq/L
 Atropine to a total of 1.8mg
 Catecholamine infusion effects are variable in terms of:
a. Central
- negative inotropic & chrontropic effects
- Adrenaline is an appropriate 1st line agent
b. Peripheral - reduced vascular tone
-Noradrenaline 1st line agent
c. Do not persist with escalating inotrope doses in the setting of
continued instability
 High dose insulin & dextrose / euglycaemia
a. Most effective when used early.
b. Glucose
i. Bolus
 25g (50 mL of 50% solution)
 unless hyperglycaemia (BGL > 22 mmol/L) present
ii. Infusion  25 g/h IV titrated to maintain euglycaemia
c. Actrapid insulin
i. 1 IU/kg bolus
ii. Infusion  0.5 IU/kg/h
 titrated every 30 min to a maximum of 5-10 IU/kg/h
d. Monitor:
i. Glucose
- every 20 min for first hour, then every 1 h
ii. Potassium - replace only if < 2.5 mmol/L and there is a
source of potassium loss
e. Therapeutic end points:
i. BP > 90mmHg, HR > 60, resolution of acidaemia
ii. Adequate urine output (1-2 mL/kg/h)
iii. QRS interval < 120 ms
iv. Improved mentation
viii) Seek guidance from Clinical Toxicologist (via switchboard or Poisons
Information Centre) or ICU consultant staff regarding protocol
ix) Cardiopulmonary bypass, ECMO, cardiac pacing and intra-aortic balloon
pumps have been used successfully as extraordinary manoeuvres
Beta Blockers
i) Usually minimal toxicity and require only simple supportive care.
ii) By contrast overdoses of sotalol or propranolol may be life threatening
iii) In addition to class 1 and 2 effects (bradycardia, conduction blocks and
 Propranolol
a. Na+ channel blocking effects  wide complex arrhythmias
b. Highly lipid soluble  enters the CNS (coma and seizures)
 Sotalol
a. Blocks cardiac K+-channels
b. Causing QT prolongation and torsades de pointes
iv) The clinical response to overdose is highly variable, but the threshold for
severe toxicity from propranolol may be as low as 1g
v) With the exception of sotalol and slow release preparations, toxicity is
usually apparent within a few hours post-ingestion
vi) PR prolongation in the absence of bradycardia is an early marker of
vii) Approach to immediate life threatening symptoms:
 Bradycardia and hypotension
a. Atropine
b. Adrenaline
c. Noradrenaline
d. Glucagon 5-10mg bolus & 1-5mg/hr infusion (cumbersome), or
e. High dose insulin dextrose euglycaemia
(targeting impaired contractility)
 Wide QRS
a. Sodium bicarbonate bolus 1-2 mEq/kg
b. Repeat as required
c. Intubate and hyperventilate targeting serum pH  7.5 to 7.55
 Torsades de pointes
a. Isoprenaline
b. Magnesium
c. Overdrive pacing
k) Tricyclic Antidepressants (TCAs)
i) Tricyclic antidepressant use has escalated after an initial reduction
secondary to SSRI introduction
ii) TCAs remain a significant cause of toxicological morbidity and mortality
iii) Poisoning  rapid onset CNS and CVS toxicity
peak between 4-6 hrs post ingestion
 Dose > 10mg/kg is potentially life threatening
 Dose > 30mg/kg is expected to cause severe cardiotoxicity and coma.
 Prompt intubation, hyperventilation and sodium bicarb administration
at the onset of major toxicity is life saving.
iv) The investigation of choice is the 12 lead ECG, with diagnostic and
prognostic features including:
 Prolongation of the PR and QRS intervals
 Terminal R wave in aVR
 Increased R/S ratio (>0.7) in aVR
 QRS > 100 ms is predictive of seizures
 QRS > 160 ms is predictive of ventricular tachycardia
v) The approach to resuscitative management includes the following:
 Prompt intubation and hyperventilation (to serum pH 7.5-7.55) at the
onset of CNS depression
 Ventricular arrhythmias are unlikely to respond to defibrillation:
a. NaHCO3 ~ 2 mmol/kg IV every 2 minutes until perfusing rhythm
restored. (Most effective when used in combination with
b. Lignocaine is a 2nd line agent if arrhythmias persist despite pH.
 Hypotension is managed with crystalloid and alkalinisation followed
by noradrenaline
 Seizures are managed with benzodiazepines (*avoid phenytoin)
Bites and Envenomation
1. Up to date and detailed information on envenomation may be found at the
toxinology website http://www.toxinology.com/ managed by the Women’s &
Children’s Hospital
2. Medical advice for doctors can be sought by contacting the clinical toxinologist,
A/Prof Julian White via the WCH switchboard (Ph: 81617000)
3. Emergency cases are seen through the Emergency Departments of major hospitals,
while less urgent cases are seen after discussion with the treating doctor.
Limitation of Therapy
a) Limitation may involve either withholding and/or withdrawal of life supporting
b) There is no ethical or legal distinction between these processes.
c) Limitation may involve challenging ethical and legal issues; however, in patients
with no realistic chance of meaningful recovery, decisions to limit life-sustaining
therapies are both clinically and ethically indicated.
d) Assisted suicide and euthanasia are medically and ethically distinct from limitation
of therapy, are illegal in SA and should never occur.
e) The administration of medication to relieve the suffering of a dying patient is
imperative, even though a side-effect may be to hasten the onset of the patient’s
death. Such therapy is legally distinct from euthanasia.
f) Approximately 70% of all RAH-ICU deaths involve some limitation of therapy.
g) Absolute requirements for limitation of therapy are:
i) Medical consensus, including the treating ICU and admitting clinical teams
ii) Clear and open discussion with the patient, family or next of kin regarding
this consensus medical opinion; and, an ‘absence of objection’ to this
proposed management direction.
iii) Clear documentation in the patient’s medical record, along with a description
of the process by which the decision was made.
h) Counselling patients and families in limitation of therapy requires clarity and
sensitivity to ensure that all parties understand and accept the plan of management.
i) The concerns and wishes of the patient and family are important considerations.
j) The overriding goal is to provide the best care possible for the patient. This may be
to concentrate on palliation, rather than life sustaining therapies.
k) The decision to limit treatment is a consultant responsibility.
l) Refer to the CICM Policy Document IC-14
K. Brain Death and Organ Donation
1. Reference: ANZICS Statement on Death and Organ Donation
2. For further information, trainees should liaise with the ‘Organ Donation Hospital
Medical Directors’:
a) Dr David Evans
b) Dr Stewart Moodie
c) Dr Peter Sharley
d) Dr Alex Wurm
3. Declaration of brain death
a) This is an absolute requirement prior to ‘beating-heart’ organ donation
b) Declaration must be made by two members of the ICU staff:
i) The Duty ICU consultant, and
ii) Another ICU doctor (more than 5yrs qualified with appropriate experience).
c) The declaration of brain death may be by either clinical or imaging certification.
4. Clinical certification of brain death
a) The procedure is completed on a Certification of Brain Death form (MR150.0) and
documented in the case notes.
b) Record the time of onset of coma
i) Last time the patient showed response such as breathing, pupil reaction or
coughed on suction.
ii) This can be determined from the nursing observations
c) Pre-conditions:
i) A recognised irreversible cause of coma must be identified.
ii) Potentially reversible causes of coma have been excluded:
 Hypotension
 Hypothermia
*core temp must be > 35ºC
 Drugs or poisons.
 Neuromuscular blocking drugs
 Metabolic or endocrine disturbance including:
a. Deranged renal or hepatic function
b. Hyperglycaemia, hypoglycaemia, thyroid function
c. Electrolyte disturbances
iii) Ability to perform examination of:
 Cranial nerves
 Apnoea testing (e.g. not severely hypoxaemia or high cervical injury)
d) Clinical confirmation of absent brain stem function
i) Performed separately by 2 doctors, with the first test at least 4 hours after the
onset of coma (longer in the case of hypoxaemic/ischaemic injuries).
ii) Absent pupillary responses to light, both direct and consensual
iii) Absent corneal reflexes
iv) Absent vestibulo-ocular reflex
 No nystagmus on injection of 20ml iced water into the ear
 Check tympanic membranes prior to this procedure
 Occulo-cephalic reflexes are often tested, but are not formally required
v) Absent gag / cough reflex.
vi) Absent response to pain in the cranial nerve distribution.
vii) Apnoea following disconnection from the ventilator:
 Pre-oxygenate patient with 100% oxygen
 Disconnect ventilator and connect to bag with 100% O2 at 1-2 l/min
 Confirm PaCO2 > 60mmHg and pH < 7.30 (with PaO2 > 60mmHg)
 Continuously look for apnoea clinically
e) The following are compatible with Brain Death
i) Spinal reflexes
ii) Sweating, blushing and tachycardia
iii) Normal BP without pharmacological support
iv) Absence of Diabetes Insipidus
f) The 2 practitioners may choose to be present at each examination, however,
each must perform and be responsible for one of the 2 examinations
g) From the onset of coma until the second set of testing, there should be a
continuous period of observation by nursing staff
h) Families may benefit from witnessing the clinical testing for brain death
i) The time of death is the time when certification of brain death is completed – i.e.
on completion of the second examination and documentation in the case notes.
j) There is no legal requirement for certification of persons not considered for
organ donation, however this is encouraged as it can assist in counselling
relatives and the subsequent cessation of inappropriate medical intervention.
5. Imaging (Non-clinical) certification of brain death
a) Consider when clinical examination is “consistent with” brain death, however, the
preconditions (2c) for clinical certification cannot be met.
b) Demonstrated absence of cerebral blood flow is therefore required.
c) Ideally there should be a period of observation of 4 hours to increase the likelihood
that no flow will be demonstrated.
d) Absence of cerebral blood flow may be established by either:
i) Radionuclide cerebral perfusion scan (Tc99 HMPAO).
ii) 4 vessel cerebral angiography (rarely performed at the RAH)
e) Certification of brain death is by 2 clinicians, (not including the doctor who
performed the imaging investigation) who have considered the onset and cause of
coma, the clinical examination and the results of the investigation performed.
6. Organ donation
a) General principles
i) Any patient who is, or may become brain dead is a potential donor. There are
no automatic exclusion criteria.
ii) All potential donors should be offered the opportunity to donate
iii) Notify the Donor Coordinator from Donate Life, SA (Ph: 82077117) when a
potential donor is identified.
b) Criteria for brain dead organ donation
i) The patient has been declared brain dead
*for donation after cardiac death see below.
ii) Usually, no patient history of:
 HIV, untreated bacterial, fungal or viral infection.
 IV drug abuse
 Malignancies other than primary brain tumours and minor skin lesions.
 Treatment with hormones of human pituitary origin.
 Dementia (or family history of dementia).
 Disease of the donor organ
iii) All brain dead patients should be discussed with the Donor Coordinator,
regardless of relative contraindications.
c) Procedure:
i) Organ donation should not be discussed with the family until brain death has
been certified and the family informed.
ii) Family approaches regarding donation prior to the patients death should be
referred to the consultant
iii) Counselling families with regard to brain death and organ donation requires
considerable compassion, knowledge, skill and time. While this is primarily a
consultant responsibility, advanced trainees are encouraged to participate in
the process under supervision.
iv) The wishes of the patient and family are paramount.
v) A “donor kit” is kept in the cupboard in P4A which contains a check-list, plus
all the forms and specimen bottles required.
vi) Following consent for organ donation, blood should be sent for:
 HTLV-1, HIV 1 + 2
 HBsAg, HBsAb, HBcAb, HCV
 Group and X-match
 Tissue typing – volume of blood varies according to blood group
 Mark the request forms: “Urgent – Organ Donor, cc: Donate Life”
vii) Coronial approval will be sought by the Donor Coordinator where required.
viii) The RAH Designated Officer may give permission for donation if all efforts
to find relatives have failed.
ix) It is the responsibility of ICU medical staff to provide either a death certificate
or report to the coroner. Time of death is the time of second certification.
x) Notification of the recipient and procuring teams (which may come from
interstate) and coordination of operating theatre time, collation of results and
investigations are dealt with by the Donor Coordinator(s)
xi) Donor coordinators may seek assistance from ICU staff with ordering
xii) The following investigations are normally required:
 Recent ECG
 Recent CXR
 Echocardiography
d) Management of the organ donor:
i) The situation is time critical as it is not possible to stabilise a brain dead
patient indefinitely.
ii) Aim to ensure perfusion and protection of all organs for donation to achieve
the optimal outcome for all recipients
iii) Avoid focused management strategies aimed at single organ systems
iv) Ventilation:
 Adequate oxygenation:
PaO2 > 60 mmHg | FIO2 < 0.5
 Adequate ventilation:
PaCO2  35-45 mmHg
 Prevention of atelectasis and lung recruitment is important.
v) Cardiovascular instability:
 Common around the time of cerebral herniation (coning).
 Hypertensive episodes should be treated with short acting agents.
 Maintain MAP > 70 mmHg:
a. Adequate volume loading prior to using inotropes.
b. If CVC present:
CVP  8-14mmHg
c. High dose inotropic support may reduce organ viability.
vi) Aim for a urine output > 0.5ml/kg/hr
vii) Maintain normothermia:
 Established hypothermia can be difficult to manage.
 Prevention is preferred, using active warming devices if necessary.
viii) Check biochemistry and maintain normal electrolytes.
ix) Diabetes insipidus
 Common but not universal in the setting of brain death
 Treatment should commence on clinical suspicion and not be delayed for
confirmatory results.
 Hypernatraemia adversely affects liver transplant outcomes.
 DDAVP  1-2 µg IV bd
x) Evidence for hormonal resuscitation is conflicting. Steroids and vasopressin
should be considered if hypotension is refractory.
xi) Consider non-depolarising muscle relaxants if spinal reflexes persist, as these
may be disconcerting for relatives and attending carers.
7. Tissue Donation
a) All patients who die in the ICU may become tissue donors.
b) Tissues donated include:
i) Corneas
ii) Heart valves
iii) Bones
Donation After Cardiac Death (DCD)
1. Introduction
a) DCD provides an option where there is a strong desire for organ/tissue donation;
however, the patient is unlikely to progress to brain death.
b) In all circumstances, the decision to withdraw life sustaining therapy is made
independent & prior to any consideration of organ donation.
c) DCD may be considered when:
i) A patient is planned for withdrawal of active therapy.
ii) The patient and/or their representative(s) support organ/tissue donation.
iii) Preferably age ≤ 65 (c.f. donation after brain death)
iv) Cardiac standstill is probable within 90 minutes of withdrawal:
 Liver and Pancreas
30 minutes
 Kidneys
60 minutes
 Lungs
90 minutes.
v) There is good underlying organ function
vi) Normal contraindications to donation are absent
e.g. malignancy, active infection etc. (consult donor coordinator)
d) If a patient is likely to progress to brain death - this is preferred to DCD.
2. Determining the patient’s wishes
a) As for all organ donations, the pre-morbid wishes of the patient are paramount.
b) The Australian Organ Donor Register may assist with decision making.
c) DCD can be difficult for families, relevant issues include but are not limited to:
i) The discussion of donation prior to patient death
ii) Families may change their mind at any time without reason or question.
iii) Logistic requirements which inevitably delay the withdrawal process.
iv) Reasonable escalation of supports may occur, however if the patient becomes
too unstable donation may not occur.
v) The requirement for ante-mortem testing and interventions.
vi) Consent should be sought and rationale provided for ante mortem therapies
intended solely to aid donation.
vii) The immediate transfer of the deceased following death for organ
procurement and effective “removal” from the family.
viii) Difficulty in predicting the time of death.
ix) A significant risk of donation not proceeding, depending upon timing.
x) If the patient does not die within the organ suitability times, then palliative
care will continue in ICU and possibly the ward.
xi) There may be unknown medical reasons why donation cannot occur.
d) Under some circumstances (such as complex difficult decisions to withdraw
therapy) it may not be appropriate to include discussion about DCD.
e) A plain language statement on DCD is available from the Donate Life website.
3. Process of DCD
a) The process will be governed by the duty ICU consultant, in conjunction with the
Organ and Tissue Donor Coordinator (OTDC - pager 83781671) and Organ
Donation Hospital Medical Director as required.
b) If “reportable” under the Coroner’s Act:
i) The treating ICU team should complete the required documentation.
ii) The OTDC will seek “in principle” approval for donation and notify the
Coroner’s representative between death and donation.
c) Withdrawal is best done as planned event in working hours.
d) The organ retrieval teams must not be involved in direct patient care before death.
4. Ante-Mortem Interventions
a) Ongoing supportive care prior to donation is rational and accepted.
b) Escalation of care, for the sole purpose of facilitating donation, is less clear.
c) The following may be considered excessive in most circumstances:
i) CPR
ii) Massive use of blood products
iii) Escalating organ support in the setting of deteriorating physiology
d) For invasive interventions, such as bronchoscopy or biopsy, discussion/consensus
with the next of kin is recommended .
e) Interventions directly aimed at the organ donation process i.e. of benefit to the
recipient but not the patient, may be considered when unlikely to cause harm
e.g. antibiotics or steroids.
f) High dose heparin with intra-cerebral pathology or ante-mortem cannulation for
organ perfusion are not considered acceptable.
g) Advice can be sought from the Organ Donation Hospital Medical Director
5. Care of the dying patient
a) Use of sedative and analgesic drugs should be in accordance with the standard
practice of good palliative care.
b) Locality
i) There is no suitable location in the current theatre suite so withdrawal should
occur in ICU with transport to theatre after death.
ii) An appropriate route should be pre-identified and kept clear.
iii) Normally there will be an OTDC with both the theatre and ICU teams.
iv) Withdrawal should not occur until there is direct communication from the
ODTC that theatre is ready.
c) Monitoring
i) HR, BP (IA), SpO2 and respiratory rate
ii) Alarms should be disabled.
iii) Remote monitoring may be preferable.
iv) Warm ischaemic time is considered to be from when SBP ≤ 50 mmHg.
v) All timing is recorded by the OTDC in the ICU.
d) Determination of Death
i) Death is considered “irreversible” in the context of DCD when 5 minutes
have passed since circulation ceased.
 Best determined by loss of a pulsatile waveform on IABP.
 ECG monitoring may be used along with clinical signs.
ii) A note including the time of death should be documented in the patient’s case
notes declaring death prior to organ procurement surgery.
iii) Should death not occur in the required time the family and organ retrieval
teams should be informed and standard comfort care continued.
iv) The family may wish to view their relative following organ procurement; this
can be facilitated by the OTDC.
See the 2010 Organ and Tissue Donation and Transplant Authority (AOTDTA)
Table: Contact Phone Numbers
ICU Secretary
Ph: 8222 5325
Ph: 8222 4222
Organ Donor Coord
T: 8207 7117
F: 8222 2826
Duty Intensivist
SD: 1650
Pg: 8378 1671
M: 0434 605 903
Transfusion IMVS
Consults Pager
Pg: #89 22888
Pg: #33
Duty Anaesthetist
SD: 1175
Pg: #89 22556
ICU Research RN
SD: 1520
SD: 1156
ICU Dietician
M: 0401 711 460
Pg: 1342
Transfusion RN
Ext: 25430 / 25431
Pg: #89 1575
Ext: 22975
Massive Transfusion
WCH Toxicology
T: 8161 7000