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Cerebral edema Definition: excessive accumulation of water in the intracellular or extracellular spaces of the brain tissue Response to a primary brain insult Traumatic brain injury (TBI), ischemic stroke, SAH, ICH, brain tumor, meningitis, cerebral abscess, and encephalitis, and severe toxic- metabolic derangements (hyponatremia and fulminant hepatic encephalopathy)
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Monitoring and Supporting an Edematous brain
Perry Chau23/10/2009
ICU, Pamela Youde Nethersole Eastern Hospital, Hong Kong
Cerebral edema Frequently in critically ill patients with acute brain injury from diverse originsLethal consequences Cerebral ischemia from compromised regional or global
cerebral blood flow (CBF) Intracranial compartmental shifts due to intracranial
pressure gradients => compression of vital brain structures
Rx Goal - maintain CBF to meet the metabolic requirements of the brain and prevent secondary neuronal injury from cerebral ischemia
Cerebral edema Definition: excessive accumulation of water in the intracellular or extracellular spaces of the brain tissueResponse to a primary brain insultTraumatic brain injury (TBI), ischemic stroke, SAH, ICH, brain tumor, meningitis, cerebral abscess, and encephalitis, and severe toxic-metabolic derangements (hyponatremia and fulminant hepatic encephalopathy)
Cerebral edema3 major subtypes: Cytotoxic, Vasogenic, Interstitial
Over simplistic Usually combination of subtypes with one predominate depending on the type and duration of brain injury Valuable as a simple therapeutic guide
Cytotoxic cerebral edema
Swelling of the cellular elements (neurons, glia, and endothelial cells)Cellular metabolism dysfunction, inadequate functioning of Na pumpRetention of Na and water intracellularlyAffect both grey and white matterResistant to any known medical treatment
Vasogenic cerebral edema
Increase in extracellular fluid volumeBreakdown of tight-junction the BBBIncreased vascular permeabilityCommonly encountered in TBI, neoplasms, and inflammatory conditions Predominantly affects white matter Responsive to steroid (esp. neoplasm) and osmotherapy
Interstitial cerebral edema
Impaired absorption of CSFCSF penetrate brain and spread into extracellular spaceAcute hydrocephalusNot responsive to steroid administrationResponse to osmotherapy debatable
Pathophysiology of cerebral edema
Potentially increase intracranial pressure (ICP)Compromise cerebral perfusion pressure (CPP)
CPP = MAP – ICP
ICP able to be maintained at initial stage of cerebral edema (Monro-Kellie hypothesis)
Monro-Kellie hypothesis
Principle: “The total volume of intracranial contents must remain constant.” Any increase in volume of one of the cranial constituents (brain, blood, CSF) must be compensated by a decrease in volume of another Otherwise, ICP raises
Cerebral edema & ICP
Cerebral edema & ICPGlobal ICP may not be raised in some focal cerebral edemaFocal cerebral ischemiaIntracranial compartmental shifts due to pressure gradients intracranially Herniation
Brain Herniation
Monitoring of cerebral edema
Serial and close bedside monitoring Level of consciousness (GCS)New or worsening focal neurological deficits ICP: headache, nausea, vomiting, ocular palsies, back pain and papilledema Cushing's triad:
Hypertension, bradycardia, respiratory depression Herniation: low GCS, fixed and dilated pupils, decorticate posture
Monitoring of cerebral edema
Decorticate posture - fisted hands, arms flexed on the chest, extended legs with internally rotated feet
Monitoring of cerebral edema
Serial neuroimaging (CT or MRI brain)Exacerbation of cerebral edema (sulcal effacement and obliteration of basal cisterns)Intracranial compartmental shifts (midline shift, ventricular compression, herniation)
ICP monitoringHelpful if neurological status is difficult to ascertain serially (e.g sedated and paralyzed)Brain Trauma Foundation guidelines for TBI GCS =< 8 & abnormal CT brain GCS =< 8 & normal CT brain + 2 of followings:
Age >40 years Unilateral or bilateral motor posturing Systolic blood pressure (SBP) <90 mmHg
No guideline for other types of brain injury
ICP monitoringIdeally measured by intraventricular catheter (EVD)Accurate, simple and allow therapeatic drainage of CSF in some causes of ICPRisk of infection and haemorrhageTechnically difficult for small ventricle Other methods: Intraparenchymal, epidural and subarachnoid
Management of Cerebral edema
General measures
Specific therapiesMedicalSurgical
General Measures
Goals: optimize cerebral perfusion and
oxygenation improve cerebral venous drainage minimize cerebral metabolic demands avoid disturbance of ionic or osmolar
gradient between the brain and the vascular compartment
Head and Neck PositionsTo optimize venous drainage from the cranium 30º elevation of the head to lower ICPmay compromise cerebral perfusion Avoid the use of restricting devices and garments around the neck avoiding jugular compression
Ventilation and Oxygenation
Intubated if GCS =< 8 or poor upper airway reflex for airway protectionAvoid hypoxia or hypercapnia (cerebral vasodilators) in cerebral edemaPEEP may increase ICP by elevations in central venous pressures and impedance of cerebral venous drainage
Fluid managementMaintenance of CPP using adequate fluid Avoid dehydration and use of hypotonic fluidsIsotonic fluids (e.g 0.9% saline) Monitoring daily fluid balance, body weight, and serum electrolyte
Blood pressureVasopressor may be needed for adequate CPP
CPP = MAP – ICPAim CPP > 60mmHgHypertension - do not normally interfere with it The maximum blood pressure tolerated in different clinical situations of brain injury is variable Cautious use of antihypertensives (e.g labetalol) is recommended in treating hypertension Avoid potent vasodilators (nitroglycerine, nitroprusside)
Seizure ProphylaxisSeizures can increase metabolic demands and oxygen consumption of brainBenefits of prophylactic anticonvulsants in most causes leading to brain edema remain unproven Reduce seizures in TBI by prophylactic phenytoin for 1 or 2 weeks without a significant increase in drug-related side effects Prophylactic anticonvulsants in ICH can be justified, as subclinical seizure activity may cause progression of shift and worsen outcome in patients with ICH
FeverFever increase oxygen demand of brainNumerous studies demonstrated the deleterious effects of fever on outcome following brain injury Paracetamol Surface cooling devices Rule out and treat other causes of fever
HyperglycemiaHyperglycemia can exacerbate brain injury and cerebral edema Clinical studies in patients with ischemic stroke, SAH, and TBI suggests a strong correlation between hyperglycemia and worse clinical outcomes Rigorous glycemic control may be beneficial in all patients with brain injury
NutritionPrompt institution and maintenance of nutritional support is importantEnteral route of nutrition is preferred Attention to the osmotic content of formulations, to avoid free water intake that may result in a hypo-osmolar state and worsen cerebral edema
Analgesia and SedationPain and agitation can worsen cerebral edema and raise ICP significantly Analgesia and sedation are used to reduce agitation and metabolic needs of the brain morphine and benzodiazepine
Specific TherapySpecific medical therapyControl hyperventilationOsmotherapySteroidPharmacological Coma / ParalysisTherapeutic hypothermia
Specific surgical therapy
Controlled Hyperventilation
Hypocapnia induced vasoconstriction Thus decreases in CBF and CBV in the intracranial vault, resulting in prompt ICP reduction Common practical target PaCO2 ~30-35mmHgOveraggressive hyperventilation may result in cerebral ischemia Rebound cerebral vasodilatationSlowly reversing hyperventilation over 6 to 24 hours to avoid cerebral hyperemia Resuscitative measure for short duration until more definitive therapies are instituted
OsmotherapyCreate an osmotic gradient to cause water withdraw from the brain compartment into the vasculature, thereby cerebral edemaSerum osmolality: Na, Glucose, UreaNormal serum osmolality 285-295 mOsm/L Osmotherapy: serum osmolality 300-320 mOsm/L
OsmotherapyMannitol An alcohol derivative of simple sugar mannose 0.25 to 1.5 g/kg IV bolus, Q6H and guided by serum osmolality (target
approximately 320 mOsm/L) Maximal ICP lowering effect 20-40min after administration
Hypertonic saline 2, 3, 7.5, 10, and 23% 1–2 ml/kg/hr via CVC Target serum Na 145-155 mEq/L Rapid withdrawal of therapy may cause rebound hyponatremia leading to
exacerbation of cerebral edema
OsmotherapyPossible complication:Pulmonary edema HypotensionHemolysisHyperkalemiaRenal impairmentMyelinolysis
Loop DiureticsControversial use for the treatment of cerebral edema when using aloneLasix may combine with mannitol or hypertonic saline to enhance diuresisRisk of serious volume depletion
Steroid Useful in vasogenic edema associated with tumorDecrease tight-junction permeability and stabilize the disrupted BBBGlucocorticoids (e.g dexamethasone) are preferredFailed to show any substantial benefit in TBI or strokeS/E: peptic ulcers, hyperglycemia, impairment of wound healing, psychosis, and immunosuppression caution is advised in the use of steroids for cerebral edema unless absolutely indicated
Pharmacological ComaBarbiturates reduce cerebral metabolic activity, thus reduce CBV
and ICP cerebral edema associated with intractable elevations
in ICP and refractory to other therapies effective in reducing ICP in TBI but no improvement in
clinical outcome limited evidence in tumor, ICH and ischemic stroke S/E: vasodepressor, cardiodepression,
immunosuppression and systemic hypothermia inability to track subtle changes of neurological status,
which necessitates frequent serial neuroimaging
Pharmacological Paralysis Neuromuscular blockade can be used as an adjunct to other measures when controlling refractory ICP Paralysis allows the cerebral veins to drain more easilyNondepolarizing agents e.g Rocuronium May mask seizures and have other harmful effects
Therapeutic HypothermiaExternal cooling devices such as air-circulating cooling blankets, iced gastric lavage, and surface ice packsTwo recent trials of therapeutic mild hypothermia (32°C) following out-of-hospital cardiac arrest, accomplished within 8 hours and maintained for 12 to 24 hours, improved mortality and functional outcomes A few small clinical series of patients with hypothermia in ischemic stroke are encouraging
Therapeutic Hypothermia
No consensus exists regarding the duration, the method to be used (active versus passive), or the duration over which rewarming is to be employed The adverse side effects of induced hypothermia are substantial and require close monitoring; these include an increased incidence of systemic infection, coagulopathy, and electrolyte derangements
Surgical InterventionsCraniotomy part of skull being removed in order to access the brain the amount depends on the type of surgery being performed most small holes can heal with no difficulty large bone flap will usually be retained and replaced immediately
after surgery
Craniectomy A large part of the skull is removed and not replaced immediately
to allow the brain to swell without crushing it or causing herniation
ConclusionMonitoring Clinical signs and symptoms of ICP ICP monitoringNeuroimaging
SupportingGeneral measuresSpecific medical therapiesSpecific surgical therapies
ReferencesAlberti O, Becker R, Benes L, Wallenfang T, Bertalanffy H: In itial hyperglycemia as an indicator of severity of the ictus in poor-grade patients with spontaneous subarachnoid hemorrhage. Clin Neurol Neurosurg 102:78–83, 2000Alvarez B, Ferrer-Sueta G, Radi R: Slowing of peroxynitrite decomposition in the presence of mannitol and ethanol. Free Radic Biol Med 24:1331–1337, 1998Angelini G, Ketzler JT, Coursin DB: Use of propofol and other nonbenzodiazepine sedatives in the intensive care unit. Crit Care Clin 17:863–880, 2001Apuzzo JL, Weiss MH, Petersons V, Small RB, Kurze T, Heiden JS: Effect of positive end expiratory pressure ventilation on intracranial pressure in man. J Neurosurg 46:227–232, 1977Battison C, Andrews PJ, Graham C, Petty T: Randomized, controlled trial on the effect of a 20% mannitol solution and a 7.5% saline/6% dextran solution on increased intracranial pressure after brain injury. Crit Care Med 33:196–202, 2005Berger S, Schurer L, Hartl R, Messmer K, Baethmann A: Re duction of post-traumatic intracranial hypertension by hypertonic/hyperoncotic saline/dextran and hypertonic mannitol. Neurosurgery 37:98–107, 1995Bhardwaj A, Ulatowski JA: Cerebral edema: hypertonic saline solutions. Curr Treat Options Neurol 1:179–188, 1999
The End
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