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Monitoring and Supporting an Edematous brain

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

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  1. Monitoring and Supporting an Edematous brain Perry Chau 23/10/2009 ICU, Pamela Youde Nethersole Eastern Hospital, Hong Kong

  2. 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

  3. 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)

  4. 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

  5. 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

  6. 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

  7. 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

  8. 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)

  9. 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

  10. Cerebral edema & ICP

  11. 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

  12. Brain Herniation

  13. 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

  14. Monitoring of cerebral edema • Decorticate posture - fisted hands, arms flexed on the chest, extended legs with internally rotated feet

  15. 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)

  16. 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

  17. 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

  18. Management of Cerebral edema • General measures • Specific therapies • Medical • Surgical

  19. 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

  20. 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

  21. 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

  22. 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

  23. Blood pressure • Vasopressor may be needed for adequate CPP CPP = MAP – ICP • 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)

  24. 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

  25. Fever • 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

  26. Hyperglycemia • 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

  27. Nutrition • 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

  28. 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

  29. Specific Therapy • Specific medical therapy • Control hyperventilation • Osmotherapy • Steroid • Pharmacological Coma / Paralysis • Therapeutic hypothermia • Specific surgical therapy

  30. 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

  31. Osmotherapy • 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

  32. Osmotherapy • 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

  33. Osmotherapy • Possible complication: • Pulmonary edema • Hypotension • Hemolysis • Hyperkalemia • Renal impairment • Myelinolysis

  34. 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

  35. Steroid • 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

  36. 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

  37. 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

  38. 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

  39. 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

  40. 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

  41. Conclusion • Monitoring • Clinical signs and symptoms of ICP • ICP monitoring • Neuroimaging • Supporting • General measures • Specific medical therapies • Specific surgical therapies

  42. References • 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

  43. The End Thank you

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