REVIEW ARTICLE                      Management of Acute Intracranial Hypertension                                         ...
Latorre and Greer                                                                          The Neurologist • Volume 15, Nu...
The Neurologist • Volume 15, Number 4, July 2009                                                                Increased ...
Latorre and Greer                                                                       The Neurologist • Volume 15, Numbe...
The Neurologist • Volume 15, Number 4, July 2009                                                              Increased IC...
Latorre and Greer                                                                     The Neurologist • Volume 15, Number ...
The Neurologist • Volume 15, Number 4, July 2009                                                                Increased ...
Latorre and Greer                                                                     The Neurologist • Volume 15, Number ...
The Neurologist • Volume 15, Number 4, July 2009                                                       Increased ICP Manag...
Latorre and Greer                                                                    The Neurologist • Volume 15, Number 4...
The Neurologist • Volume 15, Number 4, July 2009                                                                          ...
Management of acute intracranial hypertension neurologist 2009
Management of acute intracranial hypertension neurologist 2009
Management of acute intracranial hypertension neurologist 2009
Management of acute intracranial hypertension neurologist 2009
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Management of acute intracranial hypertension neurologist 2009

  1. 1. REVIEW ARTICLE Management of Acute Intracranial Hypertension A Review Julius Gene S. Latorre, MD,* and David M. Greer, MD† Focal neurologic findings occur invariably, but are most commonlyBackground: Patients with acute brain injury from various etiologies com- due to horizontal tissue shifts28 that may not be associated withmonly develop increased intracranial pressure. Acute intracranial hyperten- increased ICP.29,30sion resulting from elevation of intracranial pressure is a medical emergency All patients at risk for AIH should have a head CT onrequiring prompt diagnosis and management. Appropriate and timely man- admission and repeat imaging within the first 24 hours, or moreagement strategies result in better patient outcome in an otherwise severely emergently if new symptoms or signs appear.31 Emergent braindebilitating or fatal disease process. imaging is critically important to evaluate the cause of the patient’sReview Summary: The clinical manifestation and principles of management change in examination. A noncontrast head CT is the preferredof acute intracranial hypertension are discussed and reviewed. Acute treat- imaging technique. When time permits, MRI may be useful toment protocols are presented in an algorithm-based format aimed at utilizing further define the brain pathology. If a mass lesion is identified,the current available management strategies and suggested therapeutic goals. neurosurgical consultation should be done emergently for possibleIndividualization of specific therapeutic modalities is emphasized to opti- evacuation or decompression.mize the clinical outcome. ICP monitoring is advocated for patients at high risk for AIH,Conclusions: Clinicians treating patients with acute brain injury should be especially for those with a worsening examination due to the poorfamiliar with the principles of management of increased intracranial pres- reliability of clinical signs and symptoms of AIH and the need forsure. Since acute intracranial hypertension is a potentially reversible condi- prompt recognition and timely intervention.32–34 ICP monitoringtion, high index of suspicion, and low threshold for diagnostic and thera- makes AIH management straightforward with clear goals of therapy,peutic strategies will improve patient care. enabling early identification of refractory cases for more aggressiveKey Words: intracranial pressure, intracranial hypertension, acute brain interventions. In addition, neurosurgical consultation is facilitatedinjury, neurocritical care and appropriate surgical intervention may be planned if specific(The Neurologist 2009;15: 193–207) medical endpoints (eg, poor response or lack of response to osmotic therapy, metabolic suppression, hypertonic saline, hypothermia, etc) MANAGEMENT OVERVIEW are met. Although no randomized trial has been done, retrospective studies and reviews on aggressive management of AIH with ICP monitoring have shown improved outcome in traumatic brain injury Acute intracranial hypertension (AIH) is a clinical condi- (TBI)11,13,35– 40 and intracranial hemorrhage (ICH).41 The role oftion defined as the persistent elevation of intracranial pressure ICP monitoring in malignant ischemic infarction and diffuse cere-(ICP) above 20 mm Hg1 for greater than 5 minutes in a patient bral edema due to metabolic encephalopathies, such as acute liverwho is not being stimulated.2 AIH occurs commonly in acute failure and central nervous system infection is not well defined.45 Anbrain injury related to trauma,3,4 ischemia,5 or hemorrhage,6 and external ventricular drain (EVD) is the preferred monitoring tech-is associated with poor outcome regardless of cause.7 It is a nique, as it also permits therapeutic cerebrospinal fluid (CSF)neurologic emergency that requires prompt diagnosis and treat- drainage for relief of increased ICP.46 When the ventricles are small,ment. Aggressive treatment of AIH is effective in reducing EVD placement may be more difficult, and an intraparenchymalmortality and improving outcome.8 –10 Because of potential side monitor may be used. The nondominant hemisphere is the preferredeffects of therapy and intensive ICP monitoring,11 identifying site of ICP monitor placement, unless the primary pathology affectspatients at risk for developing AIH (Table 1) is crucial in the nondominant hemisphere extensively, in which case the domi-preventing pathologic changes that may result in poor outcome nant side is used. The current intraparenchymal monitor systemsand increased mortality. The creation of standardized manage- have added capabilities to monitor brain tissue oxygenation, tem-ment protocols has reduced variations in ICP, decreased duration perature, and compliance and may be preferred in selected cases.of AIH,12 and improved outcome,9 and is the basis of this review. The monitor is usually positioned in the perilesional area or ipsilat- Clinical signs and symptoms of AIH (Table 2) are highly eral to the most damaged hemisphere.47variable and depend on the nature of the primary brain injury(ischemic, traumatic, or hemorrhagic), the extent of compartmental-ization, the presence and location of a mass lesion, and the rate ofincrease in ICP. The most common symptom of AIH is progressivedecline in mental status, eventually leading to a comatose state.27 ICP monitoring is advocated for patients at high risk for AIH, especially for those with a worseningFrom the *Department of Neurology, SUNY Upstate Medical University, Syra- examination. cuse, New York; and †Department of Neurology, Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts.Reprint: Julius Gene S. Latorre, MD, 7134UH, Department of Neurology, SUNY Upstate Medical University, 750 East Adams Street, Syracuse, NY 13210. E-mail: latorrej@upstate.edu. The management of AIH primarily revolves around reduc-Copyright © 2009 by Lippincott Williams & WilkinsISSN: 1074-7931/09/1504-0193 tion in volume of 1 of the 3 intracranial compartments: brain,DOI: 10.1097/NRL.0b013e31819f956a blood, and CSF. Treatment response is highly dependent onThe Neurologist • Volume 15, Number 4, July 2009 www.theneurologist.org | 193
  2. 2. Latorre and Greer The Neurologist • Volume 15, Number 4, July 2009 multiple factors, including the nature of primary brain injury, theTABLE 1. Patients at Risk For Developing AIH Who May extent of tissue shift, cerebral edema, mass effect, obstruction ofBenefit From ICP Monitoring CSF flow, and the status of the cerebrovascular autoregulatoryTraumatic brain injury (TBI): Up to 72% develop AIH with 92% reserve.48 –52 mortality vs. 18% without AIH13 Based on outcome studies, treatment thresholds (Table 3) Severe TBI (Glasgow Coma Scale 9)14 have been established to minimize poor outcome and therapeutic Mild to moderate TBI with abnormal admission head CT scan15 complications while improving mortality and good outcome. In Mild to moderate TBI with normal admission head CT scan and 2 of an ICP-based management, the primary goal is reduction of ICP the following: to 20 mm Hg using a number of therapeutic modalities as Age 40, SBP 90 mm Hg, Motor posturing16 outlined in the latter part of this review. On the other hand,Hemorrhage: proponents of cerebral perfusion pressure (CPP)-based therapy Subarachnoid Hemorrhage (SAH): up to 20% develop AIH, with 40% recommend withholding AIH treatment for ICP 20 if CPP can mortality17 be maintained 80.53 This is based on the fact that brain High grade (Hunt and Hess grade 2) SAH with radiologic evidence metabolism may be maintained in relatively normal state at CPP of hydrocephalus6 above 80 mm Hg and become abnormal below 60 mm Hg. To Patients with SAH requiring endovascular treatment for vasospasm date, no study has shown any advantage over ICP-based or Intraparenchymal hemorrhage (IPH): CPP-based management.54 Adjuncts to ICP or CPP monitoring Supratentorial IPH 50 mL with mass effect18 include assessment of global (jugular venous O2 saturation SjvO2 ) and regional (brain tissue O2 saturation PbtO2 ) oxy- Cerebellar Hemorrhage18 30 mm diameter genation, enabling individualized CPP and ICP thresholds,55–59 Subdural or Epidural hematoma with associated midline shift19,20 although this has not yet been shown consistently to improveIschemia: outcome.60 Hemispheric Infarction 50% middle cerebral artery (MCA) territory21Others: Refractory hypertensive encephalopathy22,23 Herpes virus or other viral encephalitides with stupor Acute hepatic encephalopathy,24 Hepatic encephalopathy Grade III or IV, or hepatic failure with arterial ammonia 150 micromol/L25 In an ICP-based management, the primary goal is Diabetic Ketoacidosis Encephalopathy26 Other Metabolic/Toxic Encephalopathy with radiologic evidence of reduction of ICP to 20 mm Hg. cerebral edema or hydrocephalusTABLE 2. Overt Sign of AIH—The Herniation Syndromes42Syndrome Mechanism Imaging Findings43 Clinical Manifestation44Transtentorial—Descending Medial temporal lobe pushes downward Contralateral temporal horn Ipsilateral pupil dilatation: earliest signUnilateral (Uncal) into the posterior fossa through the widening External ophthalmoplegia incisura Ipsilateral ambient cistern widening Contralateral hemiparesis Ipsilateral prepontine cistern Decerebrate posturing widening Variable impairment in consciousness Uncus extending into the suprasellar cisternTranstentorial-Descending Downward displacement of the cerebral Effacement of sulci Medium sized, fixed pupils Bilateral (Central) hemispheres and the basal nuclei Obliteration of the suprasellar Early coma compressing and displacing the cistern Decorticate posturing diencephalon and the midbrain Compression and posterior Cheyne-Stokes respiration rostrocaudally through the tentorial displacement of the quadrigeminal Diabetes insipidus notch cisternTranstentorial-Ascending Infratentorial mass effect protruding Spinning top appearance of midbrain Nausea/vomiting upward compressing the midbrain Narrowing of bilateral ambient Progressive stupor cisterns Filling of quadrigeminal cisternsSubfalcine-Cingulate Brain tissue extending under the falx in Attenuation of ipsilateral aspect of Small reactive pupils the supratentorial cerebrum frontal horn Headache Asymmetric anterior falx Contralateral leg paralysis Obliteration of ipsilateral atrium of lateral ventricle Septum pellucidum shiftTonsillar Cerebellar tonsils protruding below the Cerebellar tonsils at the level of the Hypertension-bradycardia-bradypnea foramen magnum compressing the dens on axial images Coma medulla and upper cervical cord Cerebellar tonsils on sagittal images Respiratory arrest 5 mm below foramen magnum (7 Bilateral arm dysesthesia mm in children)194 | www.theneurologist.org © 2009 Lippincott Williams & Wilkins
  3. 3. The Neurologist • Volume 15, Number 4, July 2009 Increased ICP Management Review The general neurologist taking care of patient has the responsi- bility of determining the risk of developing AIH (Table 1). Once the Adjuncts to ICP or CPP monitoring include patient is identified as high risk for AIH, general measures as outlined below should be instituted as soon as possible. The patient should be assessment of global and regional oxygenation, monitored and evaluated serially for presence of signs and symptoms of AIH (Table 2). This is ideally done in the intensive care unit. The patient enabling individualized CPP and ICP thresholds. should be referred to an intensivist and/or neurosurgeon for further evalu- ation and management. Table 4 outlines the appropriate therapeutic mea- sures for patients with overt sign of intracranial hypertension.TABLE 3. Goals of Therapy For AIH GENERAL MEASURES Therapeutic Meticulous multidisciplinary management of critically ill pa-Parameter Normal Value Treatment Threshold Target tients is paramount to the success of any intensive care unit. In patientsICP 0–15 mm Hg 20 mm Hg for 5 20 mm Hg who are at high risk for AIH but do not have overt signs of herniation, min61,62 the basic tenets of acute resuscitation should be kept in mind. TheCPP 60–150 mm Hg 50–60 mm Hg63 60 mm Hg airway should be secured early and immediately. Indications for endo- tracheal intubation are outlined in Table 5. Intubation should be donePBtO2 20–40 mm Hg 10–15 mm Hg55,64 20 mm Hg with full anesthesia support to avoid a sudden surge in ICP. Once the airway has been secured, ventilator settings should be adjusted to the optimal setting required to maintain an O2TABLE 4. Emergent Management of Patients With Overt saturation above 90%, a PaO2 between 80 to 120 mm Hg and aSign of AIH: No ICP Monitoring in Place PaCO2 within 35 to 40 mm Hg range.65– 67 The mode of ventilationPerform ABC’s while preparing patient for emergent non-contrast head should be selected based on patient response and comfort. Prophy- CT lactic hyperventilation is not advocated.67 A–Airway: Secure airway, call Anesthesia stat to do rapid sequence Maintenance of euvolemia is important for hemodynamic sta- intubation, maintain/induce sedation with propofol and/or fentanyl bility. Central venous pressure (CVP, normal: 4 to 8 mm Hg, with B–Breathing: Perform hyperventilation using ambu-bag while waiting additional 2 to 4 mm Hg during positive pressure ventilation68) roughly for Anesthesia/intubation, maintain PaCO2 26–30 mm Hg estimates intravascular volume. In hypovolemic patients, the goal of resus- C–Circulation: Assess for euvolemia, give 1L NS bolus if CVP 5 or citation includes CVP 8 to 12 mm Hg or pulmonary capillary wedge SBP 100 or MAP 70 prior to instituting osmotic therapy pressure 10 to 15 mm Hg.18,54 Colloids are not recommended in acuteOnce euvolemia is established, airway is secured, patient is sedated, HOB brain injury due to its adverse effect on survival69 except in acute ischemic elevated to 30 degrees, hyperventilation on-going, institute osmotic stroke.70,71 Normal saline is the preferred solution for fluid bolus/mainte- therapy on the way to CT scanner nance in the neurocritical care unit.72,73 Hypertonic saline (3%–7.5%) may Serum Na, K, BUN, Glu, Osmolality stat, and Q4–6 h thereafter be used to augment volume in the prehospital setting74 and in the ICU,75 Mannitol 1–2 g/kg IV bolus stat then 1 g/kg Q4–6 h especially for patients who are sensitive to volume overload, as long as Hold mannitol dose for Osm Gap 10 or Change in Osm Gap 10 serum sodium is maintained below 160 to 165 mEq/L and the patient is 23.4% NaCl 0.5–1 mL/kg IV bolus over 15–30 min if no significant not in renal failure. Prophylactic use of osmotic agents are not advo- ICP reduction within 1 hr of Mannitol administration, or if unable to cated due to their volume-depleting effect and questionable benefit.67 give Mannitol due to high baseline serum Osmolality, repeat in Avoidance of hypotension is paramount in early management of between Mannitol doses if ICP 20 acute brain injury.76 Systolic blood pressure (SBP) must be kept aboveOnce CT scan results are available, call neurosurgery stat as indicated, 90 mm Hg and/or mean arterial blood pressure (MAP) above 70 mm while continuing above maneuvers Hg77 (target SBP 120 mm Hg and MAP 90 mm Hg for severe Focal mass lesion with midline shift–refer for emergent decompressive TBI).77,78 When ICP monitoring is available, SBP and MAP should be craniectomy maintained to keep CPP 60 mm Hg.77,79 Norepinephrine is the Diffuse brain edema/swelling–refer for intraparenchymal bolt placement vasopressor of choice due to its favorable cerebral hemodynamic Hydrocephalus–refer for emergent EVD insertion and CSF drainage effects.80 – 82 It may cause reflex bradycardia. Combined inotropes orNote: Gradually wean hyperventilation with ETCO2/PaCO2 guidance to vasopressors such as dopamine, phenylephrine, or norepinephrine may no more than 1 mm Hg/h to avoid rebound ICP surge, post- be used especially in patients with marginal or poor cardiac status. operatively These agents may cause arrhythmia and telemetry monitoring is nec- Once ICP monitoring becomes available, switch mannitol dosing to 1 essary. Higher goals (CVP: 8 –12 mm Hg, SBP: 160 –200 mm Hg) may g/kg IV bolus Q4–6 h as needed for ICP 20 for 5 min, otherwise be necessary if there is an evidence of regional ischemia, such as in continue with repeated dosing and follow-up clinical exam and serial patients with vasospasm due to subarachnoid hemorrhage, acute isch- imaging emic stroke with large perfusion mismatch, or acute brain injury with perilesional ischemia. In these conditions, the use of albumin (5%) 250 to 500 mL IV bolus Q6 to 8 hours PRN to achieve the CVP goal mayTABLE 5. Indication for Endotracheal Intubation in the augment volume expansion.Neurocritical Care UnitGCS 9 with one or more risk factors for AIHPatients with signs of respiratory distress: Declining O2 saturation When ICP monitoring is available, SBP and MAP Increasing O2 requirement Labored breathing should be maintained to keep CPP 60 mm Hg.Patients unable to protect airway due to respiratory/oropharyngeal weakness© 2009 Lippincott Williams & Wilkins www.theneurologist.org | 195
  4. 4. Latorre and Greer The Neurologist • Volume 15, Number 4, July 2009 Strict glucose control is essential to the management ofacutely injured brain, as hyperglycemia has been correlated with TABLE 6. Acute Brain Injury and Risk of Seizurepoor outcome.83– 86 Intensive insulin therapy to keep the blood Pathology High Risk Condition Seizure Riskglucose level between 80 and 110 mg/dL is shown to improve Any acute brain injury Comatose 10%–34%110outcome and reduce mortality in medical and surgical intensive care TBI Moderate to severe TBI 4%–14%107,111,112units.87– 89 However, several experimental90 and clinical studies91have shown that intensive systemic glucose lowering reduces brain Abnormal CT scanglucose concentration, a risk factor for poor outcome. In a recent Subdural hematomastudy on subarachnoid hemorrhage, intensive insulin therapy Penetrating injuryshowed no significant effect on neurologic outcome and mortality.92 Depressed skull fractureCurrently, a less aggressive glucose target of 80 to 140 mg/dL is Ischemic stroke Large cortical 3%–6%113,114recommended for patients with acute brain injury. A continuous involvementinsulin infusion should be started if 2 subsequent random blood Primary Intracerebral Lobar location 6%–28%113-115glucoses within 6 hours show values above 140 mg/dL, as this level Hemorrhage (ICH) (temporoparietal)has been found to discriminate between good and bad outcome in Subcortical with corticalneurocritically ill patients;85 otherwise a regular insulin sliding scale extensionregimen may suffice. SAH Unprotected aneurysm 16%–20%116,117 Maintenance of normothermia at 36°C to 37°C augments ICP (pre-treatment)management93 and may be done using antipyretics and cooling Fisher group 3blankets. Care should be taken when giving paracetamol, as it may Post-operative Cerebral abscess Up to 14%118cause hypotension in selected individual, which may compromise Traumatic intracerebralcerebral perfusion.94 Special surface cooling devices and endovas- hematomascular cooling catheters may be used for refractory hyperthermia.95,96 SAH (MCA) clipping The use of sedation and analgesia is an important manage- AVMment strategy, especially in patients with AIH. Propofol is the Gliomapreferred agent for short-term sedation due to its short half-life, Parasaggitalmaking frequent clinical examination possible. It also has a favor- meningiomaable effect on cerebral hemodynamics, reducing ICP.97,98 A ceilingdose of 5 mg/kg/h is advocated to prevent complications related toprolonged propofol infusion.99 Fentanyl infusion may be added inseverely agitated patients who are not controlled adequately by high abdominal issues, parenterally and should be started as soon asdose propofol. Narcotic analgesics are routinely used as needed for possible within 72 hours after injury. Patients with non-TBIcomplimentary pain management. Short-acting benzodiazepines should be fed with 100% resting metabolic expenditure adjustedsuch as lorazepam or midazolam may be used for anxiety and for age, sex, and body surface area. Patients with TBI should berestlessness.100 given 140% resting metabolic expenditure with 15% protein.119 A summary of general measures outlined above is presented in Table 7. Propofol is the preferred agent for short-term EMERGENT MANAGEMENT OF PATIENTS WITH OVERT SIGN OF AIH: NO ICP MONITORING sedation due to its short half-life, making frequent IN PLACE clinical examination possible. Patients with overt signs of AIH need special attention and require synchronized evaluation of the primary etiology of AIH and control of elevated ICP (Table 4). Patients should have a noncontrast head CT emergently. Hyperventilation must be instituted immedi- Head of bed elevation to 30 degrees has been shown to ately and PaCO2 should be maintained to 26 to 30 mm Hg.32reduce ICP while maintaining an adequate CPP in brain-injured Although not effective and harmful for prolonged use,65,66,120 hyperventilation for acutely symptomatic patients may be lifesav-patients,101–104 except in patients with large ischemic stroke when it ing.121 Severe hypocapnea to PaCO2 less than 25 is not advocatedmay compromise flow through a stenosed proximal cerebral ves- as the risk of brain ischemia significantly increases with no furthersel.105 Maintenance of straight head position prevents kinking of the reduction in ICP.122,123 Patient must be intubated if the airway hasjugular venous system and facilitates venous drainage.106 not yet been secured with full anesthesia support using rapid se- A significant number of patients with acute brain injury are at quence intubation to avoid further increases in ICP. Propofol with orrisk for early seizures (Table 6). Seizures acutely increase the ICP without fentanyl IV infusion should be started to maintain adequateand amplify metabolic demand. Because of this, patients at risk for sedation. Head of bed elevation to 30 degrees above horizontal mayAIH should be given seizure prophylaxis with phenytoin107 (loading reduce ICP without compromising CPP. Euvolemia must be estab-dose of 20 mg/kg IV over 1 hour and maintenance of 100 mg Q8H lished prior to instituting osmotic therapy to avoid further reductiondaily) or levetiracetam108 (500 mg Q12H daily). The duration of in cerebral perfusion. Mannitol in 20% or 25% concentration shouldtherapy remains controversial. However for TBI, 7 days after trauma109 be given by IV bolus at 1 to 2 g/kg. Repeat doses may be done everyand 1 month after ICH18 is recommended, unless patients have 4 to 6 hours (as necessary if ICP monitoring has been started) untilexperienced spontaneous seizures. clinical response or stabilization of mass effect by serial imaging is Nutrition is an important part of management of acute achieved. Calculated (1.86 (Na K) Glu/18 BUN/2.8brain injury patients. Feeding may be done enterally (jenunal 10)124,125 and measured serum osmolality (normal value 270 –preferred over gastric) or if not possible due to concomitant 290 mOsm/L) and osmolar gap (measured– calculated osmolality:196 | www.theneurologist.org © 2009 Lippincott Williams & Wilkins
  5. 5. The Neurologist • Volume 15, Number 4, July 2009 Increased ICP Management ReviewTABLE 7. General Management of Neurocritical CarePatients With AIH Hyperventilation for acutely symptomatic patientsAirway. Secure early in the following patients: GCS 9 at high risk for AIH may be lifesaving. Patient with signs of respiratory distress Declining O2 saturation ( 90%) Increasing O2 requirement (FiO2 50%) Labored breathing EMERGENT MANAGEMENT OF PATIENTS WITH Rising pCO2 ( 45 mm Hg) in patients without COPD OVERT SIGN OF AIH: ICP MONITORING IN PLACE Patient unable to clear out secretions due to respiratory/oropharyngeal Patients in whom ICP is being monitored usually do not weakness suddenly show overt signs of AIH without corresponding changes in Patients with severe agitation requiring sedation that may compromise ICP. However, in the event that sudden deterioration occurs, a airway similar management response as in an unmonitored patient (Table 4)Breathing. Maintain PaO2 between 80–120 mm Hg, PaCO2 35–40 mm should be initiated. If EVD is in place, CSF drainage of 5 to 10 mL Hg, O2Sat 90% may be done for persistently elevated ICP. Osmotic therapy remainsCirculation the cornerstone of management (Table 8). The decision to consider Maintain Euvolemia with goal CVP 5 mm Hg second or third tier therapy for AIH (Table 9) must be individualized 0.9% NaCl at 1–3 mL/kg/h maintenance fluid depending on the patient’s primary condition and with full partici- 0.9% NaCl 0.5–1.0 L IV bolus prn pation of the family members/designated patient’s decision makers. Maintain MAP 70 mm Hg and/or SBP 90 mm Hg Phenylephrine infusion at 10–1000 mcg/min SPECIFIC MEASURES FOR MANAGEMENT OF AIH The goal of AIH management is to identify and prevent Norepinephrine infusion at 2–100 mcg/min secondary ischemic brain injury brought about by an excessively Dopamine infusion at 10–1000 mcg/min increased ICP with a compromised CPP, thereby maintaining cere- Epinephrine infusion at 1–12 mcg/min bral perfusion adequate for a given metabolic demand and conse-Head Position. HOB elevation, keep head at 30° (except in large ischemic quently improving outcome and reducing mortality. Available ther- stroke) apeutic options are outlined in Table 10.Temperature: Keep Temp below 38°C Acetaminophen 650 mg PO/PR Q4H Osmotherapy Cooling blanket Two osmotic agents are currently in use in most neurocritical Surface cooling care units: mannitol and hypertonic saline. Both are highly effective in reducing acutely elevated ICP in various clinical conditions, with Endovascular cooling almost immediate effect lasting for several hours. Mannitol is theGlucose control: Keep Blood Glucose (BG) between 80–140 mg/dL preferred osmotic agent due to its availability and physician’s Regular Insulin sliding scale familiarity of use. It has several mechanisms of action. An imme- Regular Insulin IV drip if BG 140 mg/dL 2 taken 6 h apart diate effect from bolus administration results from plasma expansionSedation/Analgesia: with reduction of blood viscosity,127 improvement in microvascular Propofol IV drip at 0.1–5 mg/kg/h Fentanyl IV drip at 50–200 g/h Morphine 2–4 mg IVP Q 2–4 h as needed TABLE 8. Emergent Management of Patients With Overt Ativan 1–2 mg IVP Q4–6 h as needed Sign of AIH: ICP Monitor in PlaceSeizure prophylaxis, for patients at high risk: Perform management maneuvers as in Table 7 Phenytoin (or Fosphenytoin) 1 g LD IV then 100 mg Q8H 7 d If EVD in place, drain 5–10 mL CSF stat and Q30–60 min as needed for Levetiracetam 500 mg PO BID 7 d ICP 20 mm HgNutrition: Keep EVD at 10–15 cm above external auditory meatus and open Enteral (jenunal preferred vs gastric) to be started within 72 h Note: Close EVD during patient transport to avoid overdrainage. In SAH Parenteral (if with contraindication to enteral, or unable to start patients with unsecured aneurysm, CSF drainage is not advocated and enteral feeding within 72 h) EVD should be clamped to prevent rebleed 100% RME for non-traumatic and patients on paralyzing agents If ICP 20 mm Hg despite sedation, controlled hyperventilation, 140% RME with 15% protein for TBI patients euvolemia, CSF drainage, institute osmotic therapy: Mannitol 1–2 g/kg IV bolus stat, then Q4–6 h as needed for ICP 20 mm Hg 23.4% NaCl given as 0.5–1 mL/kg IV over 15–30 min Q4–6 h asnormal value 0 –5) should be done at baseline and prior to each needed for ICP 20 mm Hg may be used in the following circumstances:mannitol dosing to avoid mannitol-induced renal insufficiency. Ameasured serum osmolality 320 mOsm/L126 especially in patients 1. In lieu of mannitol in patients with high baseline osmolar gap ( 15), high baseline serum osmolality ( 320 mOsm/L), or history ofwith history of hypertension and diabetes, osmolal gap 10 or chronic or acute renal insufficiency, diabetes and poorly controlledchange in osmolal gap from baseline 10 correlate with poor hypertensionmannitol clearance,125 and increased risk of renal toxicity. Neuro- 2. In sequence with mannitol infusion, in patients with partial responsesurgery consultation should be done at the onset of patient deterio- (ie post mannitol reduction 25% of pretreatment ICP but absoluteration in anticipation for emergent surgical management based on ICP value 20 mm Hg)imaging results.© 2009 Lippincott Williams & Wilkins www.theneurologist.org | 197
  6. 6. Latorre and Greer The Neurologist • Volume 15, Number 4, July 2009 osmotic gradient.158,159 Because of this phenomenon, osmoticTABLE 9. Therapeutic Failure Criteria: AIH Treatment Tier therapy must be tapered after 24 hours of continued use to avoidFirst Tier to Second Tier Criteria rebound AIH.160 Relative contraindications to osmotic therapy Failure to reduce ICP 20 mm Hg within 2 h of sequential mannitol/ include chronic or acute renal failure and symptomatic conges- hypertonic saline infusion. (Note: Return of ICP to pretreatment tive heart failure.144 value within 4 h before next dose of osmotic agent is a relative Other osmotically active agents have been evaluated clini- indication for switching to next AIH treatment tier, unless CPP can cally and experimentally for AIH. Glycerol, sorbitol, and urea were be maintained 60) found to be inferior to mannitol and associated with more severe Development of adverse effect (renal failure, congestive heart failure, rebound edema.141 rebound phenomenon, severe hypernatremia, poor mannitol clearance based on osmotic gap) barring continuation of osmotic agentsSecond Tier to Third Tier Criteria Metabolic Suppression Therapy Failure to reduce ICP by 25% of pretreatment value In patients with preserved flow-metabolism coupling, barbi- Persistent ICP elevation 20–25 mm Hg during metabolic suppression turate-induced cerebral metabolic suppression is an effective way of therapy despite burst suppression EEG pattern at 1–2 burst per reducing ICP refractory to osmotherapy.14,40,161–166 Barbiturates minute for 2 h reduce cerebral metabolism with concomitant reduction in cerebral Persistent ICP elevation 20–25 mm Hg during induced hypothermia blood flow thereby decreasing ICP.132 In addition, barbiturates have with target temperature of 32°–34° for 2 h neuroprotective properties including free radical scavenger func- Development of adverse effect (marked hypotension requiring 1 tion,167 apoptosis inhibition,168 and reduction in intracerebral pyru- vasopressor to keep MAP 70 or CPP 60; coagulation abnormality vate, and lactate production.165 Thiopental is a short-acting barbi- with increased bleeding risk; presence or development of severe turate with a short half-life in the range of 9 to 27 hours after infection/sepsis) barring use/continuation of hypometabolic agents prolonged infusion169 and may be more effective than pentobarbital in reducing ICP.170 Pentobarbital is given as IV infusion at a usual rate of 1 to 8cerebral blood flow,128 cerebral oxygenation,129 and CPP130 with mg/kg/h. A loading dose of 5 to 10 mg/kg repeated every 15 to 20reduction in cerebral blood volume,130,131 and ultimately lowering minutes as needed may be necessary if ICP does not respond.40of ICP. A slightly delayed effect, occurring within 15 to 30 minutes Thiopental may be given with a loading dose of up to 4 g over 1 toand lasting for up to 6 hours, results from a direct osmotic effect on 5 hours (300 –500 mg IV bolus every 30 minutes) until a positiveneural cells with reduction in total brain water.132 Additional pos- ICP response appears, followed by continuous infusion of 1 to 6sible mannitol effects include reduced CSF production,133 free mg/kg/h.169 Frequent small loading doses are advocated to preventradical scavenging,134 and inhibition of apoptosis.135 Doses ranging sudden hypotension and reduction of CPP. The duration of therapyfrom 0.2 to 2.0 g/kg as intermittent or continuous infusion have been depends on the ICP response. Continuous infusion is not advocatedstudied but 1 to 2 g/kg136 given as IV bolus137 as needed138 is if the loading dose does not show any ICP response. If the ICP dropsrecommended. Repeated doses of mannitol require ICP monitoring 25% with a loading dose, continuous infusion may be institutedsince the effect diminishes over time and a rebound phenomenon for 24 to 180 hours or until ICP is well controlled.has been noted after prolonged use in experimental models139,140 A minimum barbiturate dose required to control ICP 20 isalthough clinical studies have shown variable results.141–143 The advocated with frequent dose adjustment every 2 to 4 hours. Thereosmolar gap correlates better with the mannitol level and is the have been no consistent predictable relationships between cerebralpreferred monitoring parameter to prevent mannitol-induced re- metabolism and barbiturate blood levels, precluding its clinicalnal failure.144 use.171 Continuous EEG monitoring is recommended only to pre- vent overdosing as the maximum effect on metabolic suppression, CBF and ICP reduction is achieved with an EEG pattern showing 1 to 2 bursts per minute;172,173 any further increase in barbiturate dose increases the risk of cerebral ischemia due to further reduction of Two osmotic agents are currently in use in most systemic blood pressure and cardiac output without a further decre- ment in cerebral blood blow and ICP. In patients with impaired neurocritical care units: mannitol and hypertonic saline. cerebral autoregulation, concomitant monitoring of global (SjvO2) or regional (PbtO2) cerebral oxygenation may be used in com- bination with continuous EEG monitoring to maximize barbitu- rate-induced ICP reduction without inducing cerebral isch- Hypertonic saline use in neurocritical care is increasing due to emia.161 Gradual weaning after prolonged infusion (more than 24its favorable effect on systemic hemodynamics,145–147 ease of use, hours) is suggested due to potential development of barbiturateand proven efficacy.144,148 –151 In addition to its dehydrating effect, withdrawal seizures.it promotes rapid CSF absorption,152 increases cardiac output, and Despite its efficacy, barbiturate therapy has a variable effectexpands intravascular volume thereby augmenting the CPP with a on outcome163,174,175 and no benefit has been shown with prophy-positive inotropic effect,153 diminishing the inflammatory re- lactic administration.176 Systemic hypotension almost always occurssponse,154 and inducing glutamate reuptake.153 A number of prep- with barbiturate therapy, often requiring vasopressor therapy andarations have been studied clinically ranging from 1.5% to 30% meticulous fluid management. Barbiturate infusion should be dis-NaCl with variable results. For continuous infusion, 3% NaCl is continued if significant hypotension occurs that compromises CPPpreferred,155,156 whereas for bolus administration, 23.4% NaCl is despite vasopressor and fluid management. Other side effects ofused.149,150,157 Hypertonic saline has similar efficacy with mannitol barbiturate therapy include sepsis, electrolyte abnormalities, andand may be used interchangeably, especially in patients with a high hepatic and renal dysfunction.177 Because of significant potentialosmolar gap.144 adverse effects with no clear effect on long-term outcome, high dose Prolonged increase in osmolality induces the cerebral ho- barbiturate therapy is considered a second tier treatment strategy formeostatic mechanism to produce idiogenic osmoles to reduce the AIH intractable to osmotic agents.198 | www.theneurologist.org © 2009 Lippincott Williams & Wilkins
  7. 7. The Neurologist • Volume 15, Number 4, July 2009 Increased ICP Management ReviewTABLE 10. Specific Therapy for AIH MOA Dose/Administration Monitoring Adverse EffectEmergent Tx Transient Reduction of CO2 causing Ambubag/ventilator rate of 30–40 PaCO2 to keep at 26–30 mm Hg Cerebral ischemia hyperventilation cerebral vasoconstriction breaths per minute to increase ABG monitoring Q15 min to Rebound AIH if and reduction of CBV minute ventilation by 15–20L/ avoid overshoot stopped suddenly min, wean slowly over 12–24 h SjvO2 and/or PbtO2 monitoring to prevent rebound AIH Effective suggested only for a few hours Avoid prolonged ( 6 h) or prophylactic use Decompressive Expansion of cranial vault Wide craniectomy with duraplasty ICP monitoring recommended Death, ICH, Stroke, surgery releasing pressure and and evacuation of mass lesion, Brain imaging as clinically Bleeding, infection improvement in CBF done as soon as possible indicated Evacuation of mass effect External ventricular Drainage of CSF improving Usually inserted in the nondominant ICP monitoring CNS infection drainage cerebral compliance and frontal area Brain imaging as clinically Bleeding reducing ICP EVD at 10–15 cm above external indicated EVD malfunction auditory meatus and open 5–10 mL CSF drainage every 30–60 min as needed for ICP 20 mm HgFirst Tier Mannitol Reduces brain water 1–2 g/kg IV bolus every 4–6 h Serum Na, K, BUN, Glu, Osm, Renal failure Reduced RBC viscosity taper dose if continued use for 24 h Osm gap before each dose Electrolyte abnormality Increase CBF Alternate with 23.4% NaCl if with Hold for Osmolar gap 5 (using CHF Free radical scavenger partial response formula: 1.86 (Na K) Rebound effect Reduces CBV BUN/2.8 Glu/18 10) Reduced CSF production If baseline Osm Gap 5, hold for change in Osm Gap 5 Hypertonic saline Reduces brain water 23.4% NaCl IV bolus over 15–30 Serum Na, Osm Renal failure Reduced RBC viscosity min at 0.5–1 mL/kg/dose given Do not exceed Na rise 0.5 CHF Increase CBF, Improves every 4–6 h alternate with or in mEq/L per hr if with history Electrolyte abnormality CO between mannitol doses of chronic hyponatremia Rebound effect Increased CSF absorptionSecond Tier Barbiturate Reduction of metabolic Thiopental 1–5 g IV LD as 500 mg Continuous EEG Systemic hypotension, demand reduces CBF and IV bolus Q15–30 min over 1–5 h Keep CPP 60 using severe infection, ICP until ICP response vasopressors as necessary respiratory Free radical scavenger If complete response (ICP 20), SjvO2 or PbtO2 recommended complications, renal Anti-apoptotic return to first tier agents, or Blood culture Q24–48 h and hepatic Neuroprotective repeat bolus doses as necessary Serum lytes, CBC, coags, LFTs dysfunction If incomplete response (ICP 20 daily but reduction 25%), start IV infusion at 1–8 mg/kg and adjust dose every 30–60 min to ICP goal 20 or until burst suppression EEG pattern at 1–2 burst/min Duration of treatment between 12– 180 h with gradual weaning over 24 h Hypothermia Reduction of metabolic Target temperature of 32°C–34°C Bladder temperature Shivering activity reduces CBF and with surface or endovascular Surveillance culture Sepsis ICP cooling method Routine coagulation studies Hypotension and Reduces release of Duration of treatment between 24– electrolyte excitatory 72 h, followed by passive abnormality neurotransmitters rewarming over 12–24 hThird Tier Surgery Expansion of cranial vault Most effective if done in patients ICP monitoring by EVD or bolt Death, ICH, Stroke, releasing pressure and who failed medical AIH SjvO2 or PbtO2 recommended Bleeding, infection improvement in CBF management but does not have Evacuation of mass effect overt herniation syndrome yet© 2009 Lippincott Williams & Wilkins www.theneurologist.org | 199
  8. 8. Latorre and Greer The Neurologist • Volume 15, Number 4, July 2009 Other metabolic suppressive agents have been evaluated forICP reduction but side effects have limited their use. Prolonged use TABLE 11. Indication for Surgery in Patients With AIHof high dose propofol (more than 5 mg/kg/h) may cause “propofol Decompressive craniectomy, evacuation of mass lesion with or withoutinfusion syndrome” with rhabdomyolysis, pancreatitis, and meta- duraplastybolic acidosis.99,178,179 In addition, bolus administration of propofol Severe TBI, no mass lesion, refractory ICPcauses significant hypotension that may compromise CPP.180,181 Any TBI, mass lesion causing significant tissue shiftStudies on etomidate have shown variable results,182–187 with an Malignant MCA infarctionincreased incidence of adrenal suppression188 and renal failure.189 Infratentorial ICH 3 cm diameter with or without hydrocephalus Relative contraindications to metabolic suppression therapy in- Patients with diffuse brain edema from a number of causes who areclude active septicemia, coagulopathy, and unstable hemodynamic status. refractory to medical AIH management Minimally invasive surgery with or without thrombolysisHypothermia ICH with GCS 6–12 and deteriorating neurologic status Induced hypothermia is effective in reducing ICP from mul- ICH with clot volume 20–80 mL causing midline shift and raised ICPtiple causes190 –194 by suppressing all cerebral metabolic activities, External ventricular Drainthereby reducing CBF. It has been found to be cytoprotective in Ventricular obstruction causing hydrocephalusanimal models,195 reducing ischemia-induced release of gluta- Intraventricular hemorrhage or extension distortion of 4th ventricle withmate.196 The use of hypothermia for patients at high risk for AIH but effacement of ambient cisternsno overt sign of increased ICP have shown variable re- Need for ICP monitoringsults.191,192,197–203 The increased amount of resources associatedwith its use in addition to potential adverse effects make hypother-mia a second tier AIH therapy in refractory ICP. TABLE 12. Antishivering Strategies for Therapeutic Hypothermia Nonpharmacologic204 Induced hypothermia is effective in reducing ICP Boots and mittens heated to 46°C Application of warming blanket from multiple causes by suppressing all cerebral Neck and face air warming with humidified air (standard face tent with metabolic activities, thereby reducing CBF. 6–10 L/min of humidified air warmed to 32°C) Pharmacologic: For nonintubated patients Tramadol219 100–200 mg PO Q4–6H Mild (34°C–36°C) to moderate (32°C–34°C) hypothermia Clonidine220 0.1–0.2 mg PO Q12Hmay be induced by surface cooling200 or endovascular cooling Meperidine221,222 25–75 mg IV/PO Q2–4H0.4 mg/kg/h IV infusioncatheter.95 Surface cooling with a body vest is the preferred method Ondansetron222 8 mg IV/PO Q6–8 Hdue to its noninvasive nature and relative efficacy in achieving the Buspirone204 30 mg PO Q8Htemperature goal.204 The endovascular cooling catheter has the For intubated patients:advantage of faster time to target temperature but is associated with Dexmedetomidine223 0.05–0.7 mcg/kg/H IV infusionthe risk of infection, bleeding, and intravascular thrombosis.205 *Propofol224 1–5 mg/kg/H IV infusionOther side effects206,207 common to all techniques of hypother- *Alfentanyl225 50–75 mcg/kg IV LD then 0.5–3 mcg/kg/min IVmia include bleeding diathesis, respiratory infection, shivering, infusionand myocardial dysfunction especially with deep208 (less than *Require paralytic agent: Cisatracurium226 0.1– 0.2 mg/kg LD as IV bolus then31°C) hypothermia.209 Rebound cerebral edema occurs com- 0.01– 0.15 mg/kg/h.monly during rewarming.210 A target temperature between 32°C and 35°C achieved as fastas possible for maximum effect is advocated for ICP reduction vs. prolonged 72 hours),212 duration and rapidity of rewarming,therapy. Cold saline infusion (30 mL/kg of 0.9% NS at 4°C as an IV and control of shivering.218bolus over 30 minutes) is safe and shortens the time to targettemperature.211 Patients require an aggressive antishivering regimen Otherswith adequate sedation (mentioned in Table 11). Cooling is main- A number of agents for AIH management have been used intained for 24 –72 hours or longer depending on ICP response.212 the past but have not gained wide acceptance because of variablePassive rewarming over 24 hours is critical due to development of clinical results and lack of solid evidence on efficacy. These agentsrebound cerebral edema, hypotension, and electrolyte abnormali- may be used as a last resort while waiting for definitive management such as surgical decompression or prior to switching to second tierties.192,213,214 In addition, meticulous attention should be devoted to therapy in patients with relative contraindications to a specific agent.management of shivering (Table 12) to prevent a hypercatabolic Tris-hydroxymethyl-amino-methane or tromethamine is ef-state and rebound hyperthermia. Relative contraindications to hypo- fective in reducing refractory AIH,227–229 given as 0.3 M solution atthermia include active septicemia, coagulopathy, and unstable he- a dose of 1 mmol/kg (121 mg/kg or 4 mL/kg) over 1 hour, repeatedmodynamic status. every 12 hours, or followed by continuous infusion of 1 mL/kg/h for A significant number of issues215 remain unresolved, includ- up to 5 days. It acts as a cerebral buffer and induces metabolicing the ideal target temperature (mild, moderate, or deep hypother- alkalosis without increasing PCO2 and serum Na, resulting inmia), patient selection,190,216,217 mode of administration of cooling cerebral vasoconstriction, reduction in CBV and ICP. Patients need(surface vs. endovascular), timing of intervention (prophylactic, to be ventilated to avoid respiratory compensation. Side effectsearly vs. delayed or only with AIH), duration of treatment (24 hours include local tissue irritation and necrosis, respiratory depression,200 | www.theneurologist.org © 2009 Lippincott Williams & Wilkins
  9. 9. The Neurologist • Volume 15, Number 4, July 2009 Increased ICP Management Reviewand hypoglycemia. Renal failure is a relative contraindication to ischemia, but mild to moderate hypocapnea may be enough totromethamine use. cause regional ischemia due to regional differences in cerebral Indomethacin is a nonspecific cyclooxygenase inhibitor that autoregulatory dysfunction in the acutely injured brain (perile-has been found to have a vasoconstrictive effect in cerebral vessels, sional area being most affected).65,244 Prophylactic hyperventi-predominantly affecting the small resistance vessels, causing reduc- lation has been shown to adversely affect outcome. For thesetion in ICP by reducing CBV and CBF.230 –232 It is usually given as reasons, prophylactic, prolonged, and/or profound hyperventila-a 50 mg IV bolus repeated every 6 to 8 hours or followed by 10 to tion is highly discouraged.65– 67,245–24730 mg/h continuous infusion 24 – 48 hours.233 So far, its effect on Fluid limitation resulting in dehydration in acute brain injurylong-term outcome is unknown, and there is theoretical danger of has been advocated in the past in the hope of preventing cerebralinducing cerebral ischemia from vasoconstriction. In addition, re- edema but has been associated with an adverse outcome. Dehydra-bound AIH has been noted with use of indomethacin after sudden tion causes inadequate systemic and cerebral perfusion, increasesdiscontinuation.233–235 susceptibility to renal and drug toxicity, reduces responsiveness to osmotic therapy, and adversely affects blood viscosity. The currentIneffective or Harmful Therapy recommendation is for fast and adequate fluid resuscitation to There is ample evidence that corticosteroids do not improve maintain normovolemia and preserve CPP.67outcome in acute brain injury from trauma, ischemia, or hemorrhageand may actually be harmful due to increased adverse effects relatedto its use.123,236 –241 Surgery Hyperventilation beyond 6 hours looses its efficacy in Surgical decompression and early evacuation of a focal massreducing ICP due to rapid cerebral compensation.121,242,243 Pro- lesion is effective in reducing ICP but the efficacy on improvingfound hypocapnea (reduction of PaCO2 below 25 mm Hg) may functional outcome and mortality depends largely on timing andinduce severe cerebral vasoconstriction causing global cerebral selection of patients248 (Table 11). FIGURE 1. Algorithm for the Management of Acute Intracranial Hypertension.© 2009 Lippincott Williams & Wilkins www.theneurologist.org | 201
  10. 10. Latorre and Greer The Neurologist • Volume 15, Number 4, July 2009 Following initial resuscitation, early ( 24 hour) decompres- that future outcome studies may shed light in the efficacy of thesesive craniectomy and evacuation of a focal mass lesion is the single new treatment options.most important treatment in TBI, resulting in improved outcome.249 Decompressive craniectomy after massive hemispheric ACKNOWLEDGMENTSstrokes in selected patients with clinical and radiographic evidence The authors thank Guy Rordorf, MD, Jonathan Rosand, MD,of cerebral edema is effective in reducing ICP250 and improving Raul Nogueira, MD, Mary Guanci, RN, and Lee Schwamm, MD foroutcome.251–253 Predictors of poor outcome after decompresive their critical review and appraisal of the manuscript.craniectomy include age beyond 60,254 low preoperative GCS ( 8),preoperative anisocoria, early ( 72 hours from stroke onset) clinical REFERENCESdeterioration, and multiple territory infarction.255 1. 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