Acute Gastrointestinal and Genitourinary Disorders

Acute Gastrointestinal
and
Genitourinary Disorders
Christiana E. Hall, MD MS
Division of Neurocritical Care
University of Texas Southwestern Medical Center
Dallas, Texas
Upper & Lower GI bleeding
UGIB CAUSES
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Peptic ulcer disease most common
Variceal hemorrhage most feared
Aortoenteric fistula deadly
Other causes: esophagitis, mallory-weiss
tear, Dieulafoy’s lesion, angiodysplasia,
tumors
Upper & Lower GI bleeding
LGIB CAUSES
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Diverticular Dz most common
Angiodysplasia second most common
Ischemic colitis most feared
Postpolypectomy bleeds most annoying
Other causes: (LGIB) Colitis, Dieulafoy’s
lesion, tumors, anorectal fissures/varices/
hemorrhoids.
• **Meckel’s diverticulum – rare, small
bowel, ALWAYS rule out in young people
Upper & Lower GI bleeding
Initial approach & management
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UGIB more likely hemodynamically unstable than LGIB
Adequate IV access ie 2 large bore IVs
Stat type & cross, CBC, coags, chemistry, LFT
Up to 2 liters crystalloid; consider O(-)
Transfuse as appropriate correct coagulopathy and
consider holding additional PRBC units
• NGT for room temp saline lavage unless clearly LGIB
• Consult GI endoscopist
• If massive, initiate massive bleeding transfusion protocol
to include FFP & Plts etc; rapid infuser/warmer to BSD
Upper & Lower GI bleeding
UGIB Non-variceal
UGIB Variceal
• Begin resuscitation Hgb > 7
• Arrange endoscopy for dx and tx
(w/in 24 hrs)
• Consider pre-endoscopy PPI;
definite PPI post treatment
• No promotility agents, no
somatostatin, no H2 antagonists
• Surgery or intravascular tx when
endoscopy fails
• F/U testing for H pylori
• Home on PPI
• antiplt or NSAID tx safer with PPI
• Prompt attn. Hgb ~ 8
• Urgent endoscopy for dx & tx
(w/in 12 hrs)
• Consider protective intubation
• Balloon Tamponade – temporize
(Sengstaken-Blakemore Tube)
• somatostatin immediately3-5 d
• *TIPS if endoscopy + pharmacotherapy unsuccessful
• Cirrhotics: I week SBP prophylaxis
w/ quinolone or Ceftriaxone
*TIPS – transjugular intrahepatic portosystemic Shunt
Ann Intern Med. 2010;152(2):101-13.
Ann Intern Med. 2003 Nov 18;139(10):843-57
Am J Gastroenterol. 2007 Sep;102(9):2086-102.
Upper & Lower GI bleeding
LGIB PEARLS
Acute & Fulminant Hepatic Failure
• Acute Liver Failure = onset
of hepatic encephalopathy
and coagulopathy (INR >
1.5) within 26 weeks of
initial jaundice in a patient
without preexisting liver dz:
– Fulminant = within 8 wks
– Subfulminant = > 8 < 26 wks
• Causes
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Acetaminophen
Drugs & toxins
Viral hepatitis
Malignancy/ Budd-Chiari
Wilson’s disease
Autoimmune
Pregnancy related
• HELLP syndrome
• Acute Fatty Liver of
pregnancy
Acute & Fulminant Hepatic Failure
Am J Dig Dis 1978;23:398- 406
Acute & Fulminant Hepatic Failure
Gastroenterology 1989;97:439–55
Gastroenterology 2003;124:91–6
Acute & Fulminant Hepatic Failure
Acute & Fulminant Hepatic Failure
Treatments
• Acetaminophen  N-acetylcysteine
– Oral NAC 140 mg/kg load  then 70 mg/kg q 4 hrs
– Oral NAC 150 mg/kg over 15-60 mins, then 12.5 mg/kg/hr x 4
hrs, then 6.25 mg/kg/hr
– Until clinical improvement***
• Amanita phalloides  penicillin
– PCN G 1 gm/kg daily IV plus NAC protocol as per APAP tx
• Herpes Simplex  acyclovir 30 mg/kg/day
• Autoimmune  methylprednisolone 60 mg/kg/day
• HBV  Lamivudine 100-150 mg/daily PO
Crit Care Med. 2007 Nov;35(11):2498-508
Acute & Fulminant Hepatic Failure
Approach to ALF pt in ICU
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Determine if pt is TPL candidate
If not can pt be salvaged without TPL
Goals of care
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2.
3.
Support and bridge TPL candidates to operation
Support survival candidates through non-op course
Provide comfort care to non-TPL candidates with
unsurvivable ALF
Crit Care Med. 2007 Nov;35(11):2498-508
Acute & Fulminant Hepatic Failure
• Ammonia
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gut nitrogen escapes liver metabolism & crosses BBB
detoxified by astrocytes  osmotically active moieties
Injures astrocytes  cytotoxic edema
If used, lactulose with precautions avoid neomycin
• Surveillance Cultures & empiric ABX tx (90% infex rate)
– Stage III/IV HE
-- Overt SIRS
– Refractory HypoTN
-- TPL waiting list
– Suggested  3rd gen cephalosporin; vanc for all catheter-related
infex; antifungal if no improvement
• Seizures
– Common subtle SZ in III/IV
– Prophylaxis not recommended, low threshold for EEG tx if sz
Crit Care Med. 2007 Nov;35(11):2498-508
Acute & Fulminant Hepatic Failure
• Coagulopathy
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Vit K
Targets for intervention/ active bleeding  plt 50K & INR 1.5
Avoid prophylactic FFP / do use GI prophylaxis  H2 or PPI
Hypfibrinogenemia  cryoprecipitate
oozing  aminocaproic acid
If rVIIa then low dose 40 mcg/kg & FFP for other fx
• Nutrition
– Adequate protein
-- Avoid hypoglycemia
• Circulatory
– SBP > 90
-- MAP > 65
– judicious hydration -- Norepinephrine preferred
– Hydrocortisone if adrenal insufficiency
Crit Care Med. 2007 Nov;35(11):2498-508
Acute & Fulminant Hepatic Failure
• Cerebral Edema ICP
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ICP montoring HE III/IV only (SA Bolt or IP fiberoptic)
ICP < 25
-- CPP 50 - 80
Mannitol 1st line
-- Hypertonic saline 2nd line
Hypothermia controversial
-- Barbiturate Coma
Indomethacin rescue 25 mg IV push  mech vasoconstriction
• Renal failure
– CRRT
-- Avoid prerenal azotemia  fluid challenges
• Pulmonary
– ARDS-NET approach
Crit Care Med. 2007 Nov;35(11):2498-508
Ileus & Toxic Megacolon
Ileus
• Common, multiple medical & surgical precipitants
• N&V, distension, absent stool & flatus
• Conservative management
– Bowel rest
– Suck and drip
-- Remove offending drugs
-- Ambulation where feasible
Ogilvie’s
• Massive colonic dilation without obstruction
• precipitants  trauma, infections, cardiac dz, pelvic
region surgery (hip and c-section)
• abdominal distension, pain, N&V. Flatus & stool passed.
• Illness severity, old age, ischemia or perforation
cecal diameter (> 12cm)
duration (>6 days)
Ileus & Toxic Megacolon
Ogilvie’s
Gastrointest Endosc 2002;
56:789–792.
Best Practice & Research
Clinical Gastroenterology
2007; 21:671–687.
Toxic Megacolon
• deadly form of colitis
• vicious cycle of inflammation in the colonic wall
with atony and dilation
• grave systemic illness
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Diarrhea
Constipation
abdominal pain
distension
-- bloody diarrhea,
-- obstipation,
-- tenderness,
-- decr bowel sounds.
– CT: dilated colon, bowel wall thickening, submucosal
edema, pericolic stranding, ascites, perforations,
abscesses, ascending pyelophlebitis
Toxic Megacolon
• Toxic Megacolon classically associated with
inflammatory colidites:
– ulcerative colitis
– Crohn’s disease
• frequently reported in association with infectious
diarrheas
– C. difficile
• Jalan’s Diagnostic Criteria:
– Fever > 101.5°F (38.6°C) + Heart rate > 120 bpm
+ WBC >10.5
OR
– Anemia + one of the following criteria: dehydration, mental
changes, electrolyte disturbances, or hypotension
Toxic Megacolon
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General Measures
Intravenous fluid support
Correct electrolyte
abnormalities
Complete bowel rest
Discontinue
anticholinergics and
narcotics
Rule out infectious etiology
Am J Gastroenterol 2003;98:2363–2371
Gastroenterology 1969;57:68–82
Decompressive therapies
• Rectal tube
• Nasogastric or long
nasointestinal tube
• Repositioning maneuvers
(prone, knee elbow)
• Endoscopic treatment is
NOT a usual intervention
Radiology
• Frequent assessment with
plain films
• Abdominal CT scanning
may aid in management
Toxic Megacolon
Medical Care
(7 day trial in non-worsening
patients may be “colon sparing”)
• Specific treatment for infections
– (i.e. metronidazole if C diff)
• Intravenous corticosteroids for
inflammatory bowel disease
– (e.g. hydrocortisone 100 mg
q 8 hr or methylprednisolone
15 mg q 6 h)
• Broad spectrum antibiotics
– consider empirically if only to
reduce mortality in case of
perforation)
Surgical intervention
(total or subtotal colectomy)
• Failed medical care
• Progressive toxicity or dilation
• Signs of perforation
Am J Gastroenterol 2003;98:2363–2371
Acute GI Tract Perforations
• Esophagus  rectum
• Many causes
• GI Spillage into sterile spaces
– inflammation, sirs, infection and sepsis.
• longer interval between perforation to diagnosis to
definitive treatment  the higher is the M&M
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Contamination: Colon >>>>stomach
Free Air: Stomach & colon >>>> small bowel
Rapid dx and operative cleansing & repair are key
Pts have acute abdomen, do not breathe with abdominal
muscles and lie motionless on stretcher
Acute GI Tract Perforations
• Esophagus
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CT surgery territory
Free air in mediastinum, neck st, prevertebral on plain film
Gastrographin swallow to localize tear
Risk life threatening mediastinitis
• Stomach
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Anterior wall and duodenal ulcers by far most common
Large free air “3 way of abdomen” plain films
Spillage has low bacterial content but causes severe SIRS (acid)
X-lap unless posterior and contained
• Small bowel
– Lesser gas, CT may be needed to see free air
– X-lap, run bowel, antibiotics
Acute GI Tract Perforations
• Colon
– Divertucular rupture – by far most common
– Walled off diverticular ruptures may respond to abx +
percutaneous drainage
– Free air and perfs due to other causes require operation
• Patients and risks
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Often older & sicker bringing in many medical comorbities
Third spacing and intravascular contraction
Bacteremia
Peritonitis, pancreatitis ARDs  MOF
Multiple Ors for washout, abd compartment syndrome
Exacerbations of CAD etc.
X-lap unless posterior and contained
Late comps: dehiscences, abscess formation, PE, DVT
Acute GI Tract Perforations
• Preop
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Fluid resuscitation
Correct electrolyte derangements
CVP monitoring for the critically ill
ABX: Ampicillin + Metronidazole + fluoroquinolone (alt.
aminoglycoside)
combination chosen represents the best empiric estimate to
cover the likely organisms depending on location.
goal of antibiotics is to minimize risks of postoperative infectious
complications.
Suck & drip
To OR urgently
Acute GI Tract Perforations
• Post-op
– Fluid management to maintain intravascular volume, CVP &
UOP
– Bowel rest  suck & drip until GI output minimal & flatus returns
– ABX continued as preop unless cultures dictate change
– All ABX by IV route
– maintain electrolytes
– Vigilance for compartment syndrome
– Adequate pain management
• Failure of clinical improvement (@ 2-3 days)
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inadequacy of initial operative procedure
secondary complications
superinfection at a remote site
antibiotic dosing is inadequate or spectrum of coverage is
insufficient
Acute Intestinal Vascular Disorders
& mesenteric infarction
• final common pathway for infarcted bowel is necrosis and
perforation
• By the time perforation occurs with its obvious symptoms,
irreversible tissue death has long since completed
• Infarction of long segments of small bowel such as is the
territory of the superior mesenteric artery (SMA) is
incompatible with life
• Goal: recognize gut ischemia early and rescue tissue at risk
before infarction occurs
• This is no easy task
Acute Intestinal Vascular Disorders
& mesenteric infarction
• Causes:
– trauma, obstruction with severe dilation or torsion, Atherosclerotic
vascular disease, low flow states as in shock, in vasospasm, with
prolonged procedures with clamping or on cardiac bypass or due to
thromboembolization. Iatragenic from IA Procedures!
• Classic neuroscience patient at risk is the vasculopath on
the stroke service
• patients may give an episodic history of intestinal angina
typically postprandial (increased blood flow demand)
• “Pain out of proportion to exam.” is the classical
presentation
– sudden in onset of severe abdominal pain but the exam
remains rather benign, not an acute abdomen
Acute Intestinal Vascular Disorders
& mesenteric infarction
• diagnosis:
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Classic exam, history, setting
Labs may include leukocytosis, lactic acidosis, elevated amylase
KUB may be mistaken for partial SBO leading to delays
Angiography is gold std
Some surgeons bypass angio and go straight to OR (time is gut)
Goals of operation are revascularization and resection of infarcted
bowel
– Second looks allow for gut sparing
– Compassionate care involves peak and shriek when extensive
completed infarction incompatible with life id found and return to ICU
for comfort care
• Angiographic tx
– Definate role for IA vasodilator therapy in vasospasm
– Possible role for embolectomy in very early partial obstructions where
infarction has not yet occurred (repersfion injury, endotoxin shock)
Acute Intestinal Vascular Disorders
& mesenteric infarction
•Don’t let this patient be yours :
• Eliminate drivers of shock
• Resuscitate adequately, avoid excessive pressors
Pancreatitis
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In pancreatic inflammation, pancreatic enzymes are
stimulated resulting in autodigestion and necrosis
This pancreatic parenchymal process may have far
reaching systemic effects
3 phase model
1. trypsin is prematurely activated within the acinar
cells and then in turn activates a cascade of
injurious pancreatic enzymes designed for digestive
processes in the gut lumen
2. intrapancreatic inflammation perpetuates through
numerous pathways
3. Extrapancreatic inflammation develops taking the
form of such entities as SIRS and ARDS
Pancreatitis
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leading causes of pancreatitis
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alcoholism and gall stones.
Other etiologies:
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trauma including the postoperative state
Hypercalcemia
drugs (classic examples are HCTZ and steroids.)
Diagnose when 2 of the following 3 factors are present:
1. abdominal pain characteristic of acute pancreatitis
a.
b.
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3.
classical pain is epigastric, continuous and often radiates to the back
Pain is usually severe and often attended by nausea and vomiting
amylase and/or lipase ≥3 times upper limit of normal
CT findings compatible with pancreatitis
Pancreatitis
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Initial laboratory evaluation
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CBC with diff, complete serum chemistry including calcium, liver
functions, lactate dehydrogenase, amylase, lipase and triglycerides.
Pancreatitis
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distribution of severity in acute pancreatitis
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85% Simple interstitial pancreatitis
15% of cases are necrotizing
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1/3 necrotizing cases develop infected necrosis
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Interstitial Pancreatitis
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only 1 in 10 will develop any organ failure, it tends to be reversible
necrotizing pancreatitis
– median prevalence for organ failure is about 50%
Overall mortality for pancreatitis is 5%
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range of 3% for interstitial to 17% for necrotizing.
In the absence of organ failure mortality is nil; 3% for single
organ failure & nearly 50% for MOF.
Am Coll of Gastroenterology. Practice Guidelines in Acute Pancreatitis. Am J Gastroenterol 2006; 101:2379-2400.
Pancreatitis
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Predicting who will have necrotizing course
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Older age, obesity
Increasing Apache II in first 48 hrs
Increasing Hemoconcentration in first 48 hours
Dynamic CT with contrast, best if delayed ~ 48 hrs
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Shows pancreatic necrosis where present
Work-up
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Urgent US of RUQ for stones
If obstruction ERCP for relief urgently if cholangitis and if
none, after 72 hrs if failure to improve
Delayed cholecystectomy when stones present
Am Coll of Gastroenterology. Practice Guidelines in Acute Pancreatitis. Am J Gastroenterol 2006; 101:2379-2400.
Pancreatitis
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management
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Fluid support up to 6 liters may be reguired in 3rd spacing
Hypovolemia perturbs necrosis via hypoperfusion
Pain control
Feeding tubes distal duodenum or jejunum
PPI to compensate for insufficient pancreatic bicarb
Prophylactic ABX not recommended, but empiric tx of suspected
sepsis or SIRS indistinguishable from sepsis during work up
Suspicion of infected pancreatic necrosis
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CT guided percutaneous aspiration, may repeat q week
GS = GNR  carbipenum + fluoroquinolone +
metronidazole
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GS = GPC  Vancomycin
Surgical debridement of infected necrosis urgently or after period of
organization
Sterile necrosis may or may not require delayed debridement
Am Coll of Gastroenterology. Practice Guidelines in Acute Pancreatitis. Am J Gastroenterol 2006; 101:2379-2400.
Pancreatitis
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There are 3 complication situations in which a
patient with sterile necrosis may require emergent
operation.
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development of abdominal compartment syndrome,
suspected secondary bowel obstruction, perforation or
ischemia,
for bleeding of a pseudoaneurysm where hemostasis
cannot be achieved endovascularly.
Delayed pancreatic abscesses respond well to
percutaneous drainage
Am Coll of Gastroenterology. Practice Guidelines in Acute Pancreatitis. Am J Gastroenterol 2006; 101:2379-2400.
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