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Monitoring and Supporting an Edematous brain. Perry Chau 23/10/2009 ICU, Pamela Youde Nethersole Eastern Hospital, Hong Kong. Cerebral edema . Frequently in critically ill patients with acute brain injury from diverse origins Lethal consequences

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monitoring and supporting an edematous brain

Monitoring and Supporting an Edematous brain

Perry Chau


ICU, Pamela Youde Nethersole Eastern Hospital, Hong Kong

cerebral edema
Cerebral edema
  • Frequently in critically ill patients with acute brain injury from diverse origins
  • Lethal 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 edema1
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)
cerebral edema2
Cerebral edema
  • 3 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
Cytotoxic cerebral edema
  • Swelling of the cellular elements (neurons, glia, and endothelial cells)
  • Cellular metabolism dysfunction, inadequate functioning of Na pump
  • Retention of Na and water intracellularly
  • Affect both grey and white matter
  • Resistant to any known medical treatment
vasogenic cerebral edema
Vasogenic cerebral edema
  • Increase in extracellular fluid volume
  • Breakdown of tight-junction the BBB
  • Increased vascular permeability
  • Commonly encountered in TBI, neoplasms, and inflammatory conditions
  • Predominantly affects white matter
  • Responsive to steroid (esp. neoplasm) and osmotherapy
interstitial cerebral edema
Interstitial cerebral edema
  • Impaired absorption of CSF
  • CSF penetrate brain and spread into extracellular space
  • Acute hydrocephalus
  • Not responsive to steroid administration
  • Response to osmotherapy debatable
pathophysiology of cerebral edema
Pathophysiology of cerebral edema
  • Potentially increase intracranial pressure (ICP)
  • Compromise cerebral perfusion pressure (CPP)


  • ICP able to be maintained at initial stage of cerebral edema (Monro-Kellie hypothesis)
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 icp1
Cerebral edema & ICP
  • Global ICP may not be raised in some focal cerebral edema
  • Focal cerebral ischemia
  • Intracranial compartmental shifts due to pressure gradients intracranially
  • Herniation
monitoring of cerebral edema
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 edema1
Monitoring of cerebral edema
  • Decorticate posture - fisted hands, arms flexed on the chest, extended legs with internally rotated feet
monitoring of cerebral edema2
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 monitoring
ICP monitoring
  • Helpful 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 monitoring1
ICP monitoring
  • Ideally measured by intraventricular catheter (EVD)
  • Accurate, simple and allow therapeatic drainage of CSF in some causes of ICP
  • Risk of infection and haemorrhage
  • Technically difficult for small ventricle
  • Other methods: Intraparenchymal, epidural and subarachnoid
management of cerebral edema
Management of Cerebral edema
  • General measures
  • Specific therapies
    • Medical
    • Surgical
general measures
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 positions
Head and Neck Positions
  • To optimize venous drainage from the cranium
  • 30º elevation of the head to lower ICP
  • may compromise cerebral perfusion
  • Avoid the use of restricting devices and garments around the neck
  • avoiding jugular compression
ventilation and oxygenation
Ventilation and Oxygenation
  • Intubated if GCS =< 8 or poor upper airway reflex for airway protection
  • Avoid hypoxia or hypercapnia (cerebral vasodilators) in cerebral edema
  • PEEP may increase ICP by elevations in central venous pressures and impedance of cerebral venous drainage
fluid management
Fluid management
  • Maintenance of CPP using adequate fluid
  • Avoid dehydration and use of hypotonic fluids
  • Isotonic fluids (e.g 0.9% saline)
  • Monitoring daily fluid balance, body weight, and serum electrolyte
blood pressure
Blood pressure
  • Vasopressor may be needed for adequate CPP


  • Aim CPP > 60mmHg
  • Hypertension - 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 prophylaxis
Seizure Prophylaxis
  • Seizures can increase metabolic demands and oxygen consumption of brain
  • Benefits 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
  • Fever increase oxygen demand of brain
  • Numerous studies demonstrated the deleterious effects of fever on outcome following brain injury
  • Paracetamol
  • Surface cooling devices
  • Rule out and treat other causes of fever
  • Hyperglycemia 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
  • Prompt institution and maintenance of nutritional support is important
  • Enteral 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 sedation
Analgesia and Sedation
  • Pain 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 therapy
Specific Therapy
  • Specific medical therapy
    • Control hyperventilation
    • Osmotherapy
    • Steroid
    • Pharmacological Coma / Paralysis
    • Therapeutic hypothermia
  • Specific surgical therapy
controlled hyperventilation
Controlled Hyperventilation
  • Hypocapnia induced vasoconstriction
  • Thus decreases in CBF and CBV in the intracranial vault, resulting in prompt ICP reduction
  • Common practical target PaCO2 ~30-35mmHg
  • Overaggressive hyperventilation may result in cerebral ischemia
  • Rebound cerebral vasodilatation
  • Slowly reversing hyperventilation over 6 to 24 hours to avoid cerebral hyperemia
  • Resuscitative measure for short duration until more definitive therapies are instituted
  • Create an osmotic gradient to cause water withdraw from the brain compartment into the vasculature, thereby cerebral edema
  • Serum osmolality: Na, Glucose, Urea
  • Normal serum osmolality 285-295 mOsm/L
  • Osmotherapy: serum osmolality 300-320 mOsm/L
  • Mannitol
    • 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
  • Possible complication:
    • Pulmonary edema
    • Hypotension
    • Hemolysis
    • Hyperkalemia
    • Renal impairment
    • Myelinolysis
loop diuretics
Loop Diuretics
  • Controversial use for the treatment of cerebral edema when using alone
  • Lasix may combine with mannitol or hypertonic saline to enhance diuresis
  • Risk of serious volume depletion
  • Useful in vasogenic edema associated with tumor
  • Decrease tight-junction permeability and stabilize the disrupted BBB
  • Glucocorticoids (e.g dexamethasone) are preferred
  • Failed to show any substantial benefit in TBI or stroke
  • S/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 coma
Pharmacological Coma
  • Barbiturates
    • 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
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 easily
  • Nondepolarizing agents e.g Rocuronium
  • May mask seizures and have other harmful effects
therapeutic hypothermia
Therapeutic Hypothermia
  • External cooling devices such as air-circulating cooling blankets, iced gastric lavage, and surface ice packs
  • Two 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 hypothermia1
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 interventions
Surgical Interventions
  • Craniotomy
    • 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
  • Monitoring
    • Clinical signs and symptoms of ICP
    • ICP monitoring
    • Neuroimaging
  • Supporting
    • General measures
    • Specific medical therapies
    • Specific surgical therapies
  • Alberti 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, 2000
  • Alvarez B, Ferrer-Sueta G, Radi R: Slowing of peroxynitrite decomposition in the presence of mannitol and ethanol. Free Radic Biol Med 24:1331–1337, 1998
  • Angelini G, Ketzler JT, Coursin DB: Use of propofol and other nonbenzodiazepine sedatives in the intensive care unit. Crit Care Clin 17:863–880, 2001
  • Apuzzo 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, 1977
  • Battison 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, 2005
  • Berger 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, 1995
  • Bhardwaj A, Ulatowski JA: Cerebral edema: hypertonic saline solutions. Curr Treat Options Neurol 1:179–188, 1999
the end

The End

Thank you