Indian J Pediatr (2010) 77:1409–1416 DOI 10.1007/s12098-010-0190-2 SYMPOSIUM ON PICU PROTOCOLS OF AIIMS Management of Raised Intracranial Pressure Naveen Sankhyan & K. N. Vykunta Raju & Suvasini Sharma & Sheffali Gulati Received: 3 August 2010 / Accepted: 18 August 2010 / Published online: 7 September 2010 # Dr. K C Chaudhuri Foundation 2010 Abstract Appropriate management of raised intracranial pressure begins with stabilization of the patient and simultaneous assessment of the level of sensorium and the cause of raised intracranial pressure. Stabilization is initiated with securing the airway, ventilation and circulatory function. The identification of surgically remediable conditions is a priority. Emergent use of external ventricular drain or ventriculo-peritoneal shunt may be lifesaving in selected patients. In children with severe coma, signs of herniation or acutely elevated intracranial pressure, treatment should be started prior to imaging or invasive monitoring. Emergent use of hyperventilation and mannitol are life saving in such situations. Medical management involves careful use of head elevation, osmotic agents, and avoiding hypotonic fluids. Appropriate care also includes avoidance of aggravating factors. For refractory intracranial hypertension, barbiturate coma, hypothermia, or decompressive craniectomy should be considered. either an increase in brain volume, cerebral blood flow, or cerebrospinal fluid (CSF) volume. Despite its high incidence, there are few systematically evaluated treatments of intracranial hypertension. Most management recommendations are based on clinical experience and research done in patients with traumatic brain injury. Intracranial Pressure: Normal Values Introduction Intracranial pressure is the total pressure exerted by the brain, blood and CSF in the intracranial vault. The MonroeKellie hypothesis states the sum of the intracranial volumes of brain (≈80%), blood(≈10%), and CSF(≈10%) is constant, and that an increase in any one of these must be offset by an equal decrease in another, or else pressure increases. The ICP varies with age and normative values for children are not well established. Normal values are less than 10 to 15 mm Hg for adults and older children, 3 to 7 mm Hg for young children, and 1.5 to 6 mm Hg for term infants . ICP values greater than 20 to 25 mm Hg require treatment in most circumstances. Sustained ICP values of greater than 40 mm Hg indicate severe, life-threatening intracranial hypertension . Raised intracranial pressure (ICP) is a common neurological complication in critically ill children. The cause may be Cerebral Pressure Dynamics N. Sankhyan : K. N. Vykunta Raju : S. Sharma : S. Gulati (*) Child Neurology Division, Department of Pediatrics, All India Institute of Medical Sciences, New Delhi 110029, India e-mail: [email protected] Cerebral perfusion pressure (CPP) is a major factor that affects cerebral blood flow to the brain. CPP measurement is expressed in millimeters of mercury and is determined by measuring the difference between the mean arterial pressure (MAP) and ICP (CPP = MAP – ICP). It is apparent from the formula that, CPP can reduce as a result of reduced MAP or raised ICP, or a combination of these two. CPP Keywords Coma . Critically ill child . Intracranial hypertension . Traumatic brain injury 1410 measurements aid in determining the amount of blood volume present in the intracranial space. It is used as an important clinical indicator of cerebral blood flow and hence adequate oxygenation. Normal CPP values for children are not clearly established, but the following values are generally accepted as the minimal pressure necessary to prevent ischemia: adults CPP>70 mm Hg; children CPP>50–60 mm Hg; infants/toddlers CPP>40– 50 mm Hg . Indian J Pediatr (2010) 77:1409–1416 Assessment and Monitoring Identify children at risk for raised ICP (Table 1). Those at greater risk are children with head trauma, suspected neuroinfections, or suspected intracranial mass lesions. Raised pressure usually manifests as headache, vomiting, irritability, squint, tonic posturing or worsening sensorium. However the symptoms depend on the age, cause, and evolution of the raised ICP. Initial Assessment Causes of Raised ICP The various causes of raised ICP (Table 1) can occur individually or in various combinations. Based on the Monroe-Kellie hypothesis, raised ICP can result from increase in volume of brain, blood, or CSF. Frequently it is a combination of these factors that result in raised ICP. The causes of raised ICP can also be divided into primary or secondary depending on the primary pathology. In primary causes of increased ICP, normalization of ICP depends on rapidly addressing the underlying brain disorder. In secondary causes of raised ICP the underlying systemic or extracranial cause has to be managed. Table 1 Causes of raised intracranial pressure Increased brain volume Intracranial space occupying lesions Brain tumors Brain abscess Intracranial hematoma Intracranial vascular malformation Cerebral edema Encephalitis (viral, inflammatory) Meningitis Hypoxic ischemic encephalopathy Traumatic brain injury Hepatic encephalopathy Reye’s syndrome Stroke Reye’s syndrome Increase in CSF volume Hydrocephalous Choroids plexus palpilloma Increased blood volume Vascular malformations Cerebral venous thrombosis Meningitis, encephalitis As with any sick child, one begins with assessment and maintenance of the airway, breathing and circulatory function. An immediate priority is to look for potentially life threatening signs of herniation (Table 2). If these signs are present then measures to decrease intracranial pressure should be rapidly instituted. Cushing’s triad (bradycardia, hypertension and irregular breathing) is a late sign of herniation. Neurological Assessment After the initial stabilization, a thorough history and clinical examination is performed to determine the possible etiology and further course of management. Pupillary abnormalities and abnormalities in ocular movements as determined by spontaneous, dolls eye or cold caloric testing are important clues to the localization of brainstem dysfunction. The examination of fundus is focused on detection of papilledema, keeping in mind that its absence does not rule out raised ICP. The motor system examination focuses on identifying posturing or flaccidity due to raised ICP or focal deficits. Findings on the general physical and systemic examination may provide clues to the underlying cause for raised ICP (e.g. jaundice/hepatomegaly in hepatic encephalopathy, rash in viral encephalitis etc.). Neuroimaging The imaging study of choice for the patient with raised intracranial pressure presenting to the emergency room is a computed tomography (CT) scan. A contrast study is helpful to identify features of infection (meningeal enhancement, brain abscess etc.) and tumors. If CT scan is normal, and the patient has clinical features of raised ICP, then an MRI with MR venogram must be obtained once the patient is stabilized. MRI can pick up early stroke, venous thromboses, posterior fossa tumors and demyelinating lesions which might be missed on CT. Invasive ICP Monitoring ICP monitoring is used mainly to guide therapy, such as in determining when to drain CSF or administer Indian J Pediatr (2010) 77:1409–1416 1411 Table 2 Clinical recognition of herniation syndromes Type of herniation Clinical manifestations Subfalcine herniation (medially, of the cingulate gyrus) Central transtentorial Impaired consciousness, monoparesis of the contralateral lower extremitya Impaired consciousness, abnormal respirations, symmetrical small reactivea or midposition fixed reactive pupils, decorticatea evolving to decerebrate posturing Impaired consciousness, abnormal respirations, third nerve palsya (unilateral dilated pupil, ptosis), hemiparesisa Prominent brainstem signs, downward gaze deviation, upgaze palsy, decerebrate posturing Impaired consciousness, neck rigidity, opisthotonus, decerebrate rigidity, vomiting, irregular respirations, apnea, bradycardia Lateral transtentorial (downward and medially of uncus and parahippocampal gyrus) Upward Transtentorial (upward of the cerebellar vermis and midbrain) Transforaminal (downward of cerebellar tonsils and medulla) a Clinical signs of potentially reversible brain herniation mannitol or sedation. In addition, invasive monitoring allows for observation of the shape, height, and trends of individual and consecutive ICP waveforms that may reflect intracranial compliance, cerebrovascular status and cerebral perfusion. Guidelines for ICP monitoring are available for traumatic brain injury . ICP monitoring is indicated for a patient with Glasgow Coma Scale (GCS) score of 3–8 (after resuscitation) with either an abnormal admission head CT or motor posturing and hypotension . The role and benefit of ICP monitoring in other conditions such as subarachnoid hemorrhage, hydrocephalus, intracranial infections, and Reyes syndrome remains unclear. Also, the availability of this modality is limited. In other brain injuries, such as hypoxic and ischemic injuries, monitoring ICP has not been shown to improve outcome . Management of Intracranial Hypertension The goal for patients presenting with raised ICP is to identify and address the underlying cause along with measures to reduce ICP (Fig. 1, Table 3). It is important not to delay treatment, in situations where identifying the underlying cause will take time. When elevated ICP is clinically evident, the situation is urgent and requires immediate reduction in ICP. Avoidance of factors aggravating or precipitating raised ICP is an important goal for all children with intracranial hypertension. The availability of ICP monitors is not universal and should not come in the way of emergent therapy. ABCs The assessment and management of the airway, breathing and circulation (ABCs) is the beginning point of management. Early endotracheal intubation should be considered for those children with GCS <8, evidence of herniation, apnea or have inability to maintain airway. Intubation should proceed with administration of medications to blunt the ICP during the procedure. Suggested medications are lidocaine, thiopental and a short-acting non depolarizing neuromuscular blockade agent (e.g.vecuronium, atracurium) . Appropriate oxygenation should be ensured. If there is evidence of circulatory failure, fluid bolus should be given. Samples should be drawn for investigations as suggested by history. Positioning Mild head elevation of 15–30° has been shown to reduce ICP with no significant detrimental effects on CPP or CBF . The child’s head is positioned midline with the head end of the bed elevated to 15–30° to encourage jugular venous drainage . Sharp head angulations and tight neck garments or taping should be avoided . One has to ensure that the child is euvolemic and not in shock prior to placing in this position . Hyperventilation Decreasing the PaCO2 to the range of 30–35 mm of Hg, is an effective and rapid means to reduce ICP [6, 9]. Hyperventilation acts by constriction of cerebral blood vessels and lowering of CBF. This vasoconstrictive effect on cerebral arterioles lasts only 11 to 20 h because the pH of the CSF rapidly equilibrates to the new PaCO2 level. Moreover, aggressive hyperventilation can dramatically decreases the CBF, causing or aggravating cerebral ischemia [10, 11]. Hence, the most effective use of hyperventilation is for acute, sharp increases in ICP or signs of impending herniation . 1412 Indian J Pediatr (2010) 77:1409–1416 Fig. 1 Algorithmic approach to a child with raised ICP Child with signs/symptoms of raised ICP Immediate Measures* . . Maintain airway and adequate ventilation and circulation Head end elevation-15- Ongoing care Sedation and analgesia Avoid noxious stimuli Control fever Prevention and treatment of seizures Hyperventilation: (target PCO2 : 30-35mm Hg ) To be used in emergent situations like herniation to bridge more definitive therapy. Not to be used for more than a few Surgical intervention Evacuation of hematoma Maintain euglycemia Neuroimaging : Suggestive of surgically remediable cause; hydrocephalous, large hematoma, etc No hyotonic fluid infusions Maintain Hb above 10gm% “Yes” CSF diversion Decompressive craniectomy “No” or delay Osmotherapy** BP Normal: Mannitol Hypotension, Hypovolemia Serum osmolality >320 mOsm/kg, Renal failure: Hypertonic Saline Other options;*** . . . Heavy sedation and paralysis Barbiturate coma Hypothermia Special situations . . Steroids: Intracranial tumors with perilesional edema, neurocysticercosis with high lesion load, ADEM, pyomeningitis,TBM, Abscess Acetazolamide: Hydrocephalus, Benign intracranial, high altitude illness (*- May be initiated immediately after brief evaluation if situation is urgent. Measures also used in children awaiting surgical/radiologial procedures, ** -Preferable to monitor ICP, ***- undertake only with ICP monitoring) Osmotherapy Mannitol Mannitol has been the cornerstone of osmotherapy in raised ICP. However, the optimal dosing of mannitol is not known. A reasonable approach is to use an initial bolus of 0.25–1 g/kg (the higher dose for more urgent reduction of ICP) followed by 0.25–0.5 g/kg boluses repeated every 2– 6 h as per requirement. Attention has to be paid to the fluid balance so as to avoid hypovolemia and shock. There is also a concern of possible leakage of mannitol into the damaged brain tissue potentially leading to “rebound” rises in ICP . For this reason, when it is time to stop mannitol, it should be tapered and its use should be limited to 48 to 72 h. Apart from hypotension, rebound rise in ICP, mannitol can also lead to hypokalemia, hemolysis and renal failure. Hypertonic Saline Hypertonic saline has a clear advantage over mannitol in children who are hypovolemic or hypotensive. Other situations where it may be preferred are renal failure or serum osmolality >320 mosmol/Kg. It has been found effective in patients with serum osmolality of up to Indian J Pediatr (2010) 77:1409–1416 Table 3 Summary of measures to reduce intracranial pressure 1 2 3 4 5 6 7 8 9 10 11 12 13 14 Assessment and management of ABC’s (airway, breathing, circulation) Early intubation if; GCS <8, Evidence of herniation, Apnea, Inability to maintain airway Mild head elevation of 15–30° (Ensure that the child is euvolemic) Hyperventilation: Target PaCO2: 30–35 mm Hg (suited for acute, sharp increases in ICP or signs of impending herniation) Mannitol: Initial bolus: 0.25–1 g/kg, then 0.25–0.5 g/kg, q 2–6 h as per requirement, up to 48 h Hypertonic Saline: Preferable in presence of Hypotension, Hypovolemia, Serum osmolality >320 mOsm/kg, Renal failure, Dose: 0.1–1 ml/kg/hr infusion, Target Na+−145–155 meq/L. Steroids: Intracranial tumors with perilesional edema, neurocysticerocosis with high lesion load, ADEM, pyomeningitis, TBM, Abscess Acetazolamide: Hydrocephalous, benign intracranial, high altitude illness Adequate sedation and analgesia Prevention and treatment of seizures: use Lorazepam or midazolam followed by phenytoin as initial choice. Avoid noxious stimuli: use lignocaine prior to ET suctioning [nebulized (4% lidocaine mixed in 0.9% saline) or intravenous (1–2 mg/kg as 1% solution) given 90 sec prior to suctioning] Control fever: antipyretics, cooling measures Maintenance IV Fluids: Only isotonic or hypertonic fluids (Ringer lactate, 0.9% Saline, 5% D in 0.9% NS), No Hypotonic fluids Maintain blood sugar: 80–120 mg/dL Refractory raised ICP: • Heavy sedation and paralysis • Barbiturate coma • Hypothermia • Decompressive craniectomy 360 mosmol/Kg . Concerns with its use are bleeding, rebound rise in ICP, hypokalemia, and hyperchloremic acidosis, central pontine myelinolysis, acute volume overload, renal failure, cardiac failure or pulmonary edema [15– 17]. Despite these concerns, current evidence suggests that hypertonic saline as currently used is safe and does not result in major adverse effects . In different studies the concentration of hypertonic saline used has varied from 1.7% to 30% . The method of administration has also varied and hence, evidence based recommendations are difficult. It would be reasonable to administer hypertonic saline as a continuous infusion at 0.1 to 1.0 mL/kg/hr, to target a serum sodium level of 145–155 meq/L [19, 20]. Serum sodium and neurological status needs to be closely monitored during therapy. When the hypertonic saline therapy is no longer required, serum sodium should be slowly corrected to normal values (hourly decline in serum sodium of not more than 0.5 meq/L) to avoid complications 1413 associated with fluid shifts . Monitoring of serum sodium and serum osmolality should be done every 2–4 h till target level is reached and then followed up with 12 hourly estimations. Under careful monitoring, hypertonic saline has been used for up to 7 days . Other Agents Acetazolamide (20–100 mg/kg/day, in 3 divided doses, max 2 g/day) is a carbonic anhydrase inhibitor that reduces the production of CSF. It is particularly useful in patients with hydrocephalous, high altitude illness and benign intracranial hypertension. Furosemide (1 mg/kg/day, q8hrly), a loop diuretic has sometimes been administered either alone or in combination with mannitol, with variable success [22, 23]. Glycerol is another alternative osmotic agent for treatment of raised ICP. It is used in the oral (1.5 g/kg/day, q4–6hrly) or intravenous forms. Given intravenously, it reduces ICP with effect lasting for about 70 min without any prolonged effect on serum osmolality . Glycerol readily moves across the blood brain barrier into the brain. Though not proven, there is concern of rebound rise in ICP with its use. Steroids Glucocorticoids are very effective in ameliorating the vasogenic edema that accompanies tumors, inflammatory conditions, infections and other disorders associated with increased permeability of blood brain barrier, including surgical manipulation . Dexamethasone is the preferred agent due to its very low mineralocorticoid activity (Dose: 0.4–1.5 mg/kg/day, q 6 hrly) . Steroids are not routinely indicated in individuals with traumatic brain injury . Steroids have not been found to be useful and may be detrimental in ischemic lesions, cerebral malaria and intracranial hemorrhage [26, 28, 29]. Sedation and Analgesia Raised ICP is worsened due to agitation, pain, and patientventilator asynchrony . Adequate analgesia, sedation and occasionally neuromuscular blockade are useful adjuvant in the management of raised ICP. Appropriate Analgesia and sedation is usually preferred over neuromuscular blockade, as it is quickly reversible and allows for neurological monitoring. For sedation it is preferable to use agents with minimal effect on blood pressure. Short acting benzodiazepines (e.g. midazolam) are useful for sedation in children. If the sedatives are not completely effective, then a neuromuscular blocking agent (e.g. Pancuronium, atracurium, vecuronium) may be required. 1414 Indian J Pediatr (2010) 77:1409–1416 Minimization of Stimulation Prevention and Treatment of Seizures Attempt must be made to reduce the number of elective interventions that are likely to be painful or excessively stimulating. Lidocaine instilled endotracheally has been shown to prevent the endotracheal suctioning-induced ICP increase and CPP reduction in adults with severe traumatic brain injury . It is recommended to instil lidocaine at body temperature, slowly, and through a fine tube advanced into the endotracheal tube within its length (avoid direct contact with the mucosa) . Lidocaine can be given in nebulized (usually 4% lidocaine mixed in 0.9% saline) or intravenous forms (1–2 mg/kg as 1% solution given 90 sec prior to suctioning) for the same purpose . Children with significant head injury and neuroinfections are at risk for seizures. Seizures can increase CBF and cerebral blood volume leading to increased ICP. They can also increase the metabolic needs of the brain and predispose to ischemia . Seizures, if clinically evident, must be treated. Given the lack of studies in children and in patients with non traumatic raised ICP, evidence based recommendation regarding prophylactic anti-epileptic therapy are not possible. But it is reasonable, and a common practice is to use prophylactic anticonvulsants for short term in children with raised ICP, unless indicated otherwise [6, 26]. If available, it is prudent to use continuous electroencephalography (EEG) to identify subclinical seizure activity in children with increased risk for seizures. Fluids Anemia The main goal of fluid therapy is to maintain euvolemia, normoglycemia and prevent hyponatremia. Children with raised ICP should receive fluids at a daily maintenance rate, as well as fluid boluses as indicated for hypovolemia, hypotension, or decreased urine output. Maintenance fluids usually consist of normal saline with daily requirements of potassium chloride based on body weight. All fluids administered must be isotonic or hypertonic (e.g. Ringer lactate, normal saline) and hypotonic fluids must be avoided (e.g. 0.18% saline in 5% dextrose, Isolyte P) . Hyponatremia is to be avoided and if it occurs, must be corrected slowly. Theoretically, anemia would increase CBF and secondarily raise ICP. There have been case reports of patients with severe anemia presenting with symptoms of raised ICP and papilledema . Though not rigorously studied, it is common practice to maintain hemoglobin above 10 g/dL in patients with traumatic brain injury and raised ICP. Blood Glucose Blood glucose must be maintained between 80–120 mg/dL in a child with raised ICP . Studies in children with traumatic brain injury have shown that hyperglycemia is associated with poor neurological outcome and increased mortality . On the other hand, hypoglycemia is known to induce a systemic stress response and cause disturbances in CBF, increasing the regional CBF by as much as 300% in severe hypoglycaemia. Hypoglycemia can also lead to neuronal injury and therefore, should be managed aggressively. Temperature Regulation Maintaining normothermia is important to prevent complications of temperature fluctuations. This is achieved by frequent measurements of body temperature and correcting any fluctuations using antipyretics, and assisted cooling or heating per needed. Surgical Therapy Cerebrospinal Fluid Drainage CSF drainage using a external ventricular drainage (EVD) or ventriculoperitoneal shunt provides for an immediately effective means to lower ICP. In addition EVD provides a method for continuously monitoring ICP. CSF drainage is particularly useful in the presence of hydrocephalus. But it may be considered even in children without hydrocephalus. Its effectiveness in lowering ICP has been shown to be comparable to intravenous mannitol or hyperventilation . However, it is of limited utility in diffuse brain edema with collapsed ventricles. Resection of Mass Lesions Surgery should be undertaken when a lesion amenable to surgical intervention is identified as the primary cause of raised ICP. Common situations where this neurosurgical intervention is preferentially employed are acute epidural or subdural hematomas, brain abscess, or brain tumors. Target of Therapy When facilities for ICP monitoring are available, the management is tailored to maintaining an adequate CPP Indian J Pediatr (2010) 77:1409–1416 (i.e. Children >50–60, infants/toddlers >40–50 mm Hg) and lower ICP to acceptable levels (i.e. <20 mm Hg for children older than 8 yrs, <18 for 1–8 yrs, and <15 mm for infants). Other Therapies for Refractory Raised ICP Barbiturates Use of barbiturates is generally reserved for cases with refractory raised ICP. Thiopentone can be used for this purpose and the dosing of the drug is adjusted to a target ICP as monitored on an ICP monitor. The drug is titrated to a 90% burst suppression (2–6 bursts per minute) using an EEG monitor. Monitoring a child in barbiturate coma should include EEG, ICP monitoring, invasive hemodynamic monitoring (arterial blood pressure, central venous pressure, SjvO2) and frequent assessment of oxygenation status. The complication rate of barbiturate therapy is high and includes hypotension, hypokalemia, respiratory complications, infections, hepatic dysfunction and renal dysfunction . 1415 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. Hypothermia Evidence from carefully conducted studies in adults and children does not show any improvement in the neurologic outcome in head injured patients with the use of therapeutic hypothermia [35, 36]. However, studies do suggest a lowered ICP during the hypothermia therapy in children [35, 37]. 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