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)

http://www.biomedcentral.com/1471-2369/5/9/figure/F1

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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