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Neurotrauma: an ICU standpoint

Neurotrauma: an ICU standpoint. Bradley J. Phillips, M.D. Burn-Trauma-ICU Adults & Pediatrics. Incidence. Head injury is the leading cause of MORTALITY and MORBIDITY after trauma Hospitalized 350,000-500,000 per year Death = 50,000 (10%) Severe disability = 50,000 (10%). Primary

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Neurotrauma: an ICU standpoint

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  1. Neurotrauma: an ICU standpoint Bradley J. Phillips, M.D. Burn-Trauma-ICU Adults & Pediatrics

  2. Incidence • Head injury is the leading cause of MORTALITY and MORBIDITY after trauma • Hospitalized 350,000-500,000 per year • Death = 50,000 (10%) • Severe disability = 50,000 (10%)

  3. Primary Abrupt deceleration contusions/lacerations SDH contrecoup injury Rotational acceleration axonal disruption hemorrhage brain edema Mass lesions cerebral ischemia Secondary hyperglycemia hyperthermia Anemia Hypotension Hypoxia Types of Brain Injury **Double mortality** **Preventable**

  4. Arterial hypoxemia due to hypoventilation loss of consciousness airway obstruction pulmonary compromise flail chest pneumothorax hemothorax Hypotension SBP < 90 35% of severe injury, doubles mortality cerebral autoregulation is impaired cerebral blood flow directly related to MAP Secondary Injury

  5. Biochemical process Focal Ischemia Extracellular K Excitatory amino acids Cytokines Acetylcholine Catecholamines Oxygen free radicals Increased intracellular Ca Decreased intracellular Mg Toxicity Lactic acidosis Edema Oxygen free radicals Inflammation Increased sensitivity to ischemia Ischemia Edema, hyperemia Oxygen free radicals Increased Ca entry Mechanism of Secondary Brain Injury

  6. Associated Factors of Severe Injury • Skull fractures • marker for subset of patients at risk for CNS injury • linear fractures are most common • depressed fractures are more serious • rule of thumb - important if depression greater than thickness of skull • rule of thumb - 50 times more likely to have an intracranial lesion requiring operation • Operation if CSF leak, impingement by bone fragments, or cosmetic deformity

  7. Associated Factors of Severe Injury • Basilar skull fractures • often not well visualized • location • ethmoid bone • rhinorrhea • petrous bone • Battle’s sign • hematotympanum, otorrhea, carotid artery injury, and 7th/8th nerve injury • cribiform plate • Raccoon eyes

  8. Definitions • Concussion • transient loss of consciousness • little or no tissue damage on CT • PET scan shows metabolic lesions • Contusion • tissue injury with capillary damage and interstitial hemorrhage • Diffuse Axonal Injury (DAI) • involves corpus callosum and subcortical white matter

  9. Diffuse Axonal Injury Clinically Corpus/Cerebral Sympathetic overdrive Hyperthermia Hypertension Spasticity Brainstem Comatose Posturing (brainstem) Radiographically CT scan - normal MRI - punctuated lesions

  10. Intracranial Hematoma • Most frequent indication for craniotomy • 25% of severe head injuries • Most do not require operative intervention • Operative (general indications) • accessible • > 30 cc blood • midline shift > 5 mm • severely impaired or deteriorating neurologic status

  11. Subdural Hematomas • Relatively poor prognosis associated with acute SDH if underlying brain damage present • Types • acute - < 24 hrs • subacute - 24 hrs to 10 days • chronic - > 10 days

  12. Epidural Hematoma • 3% of patients with severe head injury • Associated with temporal bone fractures • Classic presentation initial unconsciousness with lucid period, and then several hours HA, LOC, and neurologic deterioration • lucid interval in a minority of patients • 1/3 never regain consciousness • 1/3 never loss consciousness

  13. Subdural vs. Epidural Hematoma

  14. Subarachnoid Hemorrhage • Higher incidence of increased ICP in patients with closed head injury and SAH • Higher hypoxia and hypotension • Longer ICU stay • Worse Glasgow scores at discharge

  15. Herniation • Supratentorial swelling or hematoma • Types • subfalcine herniation • agitation, rapid comatose • transtentorial herniation • midbrain compression -isilateral dilated and fixed pupil with contralateral hemiparesis • cerebellar herniation • compression of medulla - brady and respiratory distress • Herniation without craniotomy = poor outcome

  16. Brain Herniation Syndromes

  17. Cerebral Blood Flow • Normal 55 ml/100 g/min • EEG changes < 25 ml/100g/min • Infarction < 18 ml/100g/min • Regulation • PaCO2 • PaO2 • BP • cerebral vascular resistance

  18. Cerebral Blood Flow vs Blood Pressure

  19. Cerebral Blood Flow • PaCO2 • 1 mmHg PaCO2 = 2-3% decrease in flow • PaCO2 < 20-25 mm Hg results in 1/2 blood flow • Hypoxia little effect unless PaO2 < 50 mmHg • Numerous studies indicate injured brain tissue has reduced blood flow Cerebral perfusion pressure (CPP) = MAP - ICP

  20. Increase Intracranial Pressure • Cerebral edema • vasogenic • cytotoxic • Intracranial volume 1.6 -1.8 L • 80-90% brain • 5-10% blood • 5-10% CSF • Normal ICP 5-10 mm Hg ( > 20-25 should be treated) • Inability to reduce ICP < 20 , poor prognosis

  21. ICP Monitoring • Fundamentals • only as reliable as the system providing the information • only one aspect of the patient’s condition • little value without knowledge of the disease, clinical condition, and ICP dynamics • Indications • GCS 3 to 8 and abnormal CT scan • GCS 3-8, normal CT scan, but 2 of the following • age > 40 • unilateral or bilateral posturing • SBP < 90 mmHg • treatment to be taken for increased ICP • invasive operation

  22. ICP Monitoring • At a given BP, increases in ICP = decreases in CPP • CPP should be maintained = > 70 mmHg • Cushing response to increase ICP = increase BP • Severe HTN = brain swelling and increased ICP • increased capillary filtration pressures • increased transcapillary fluid movement

  23. ICP Monitoring Devices Ventriculostomy ICP Bolt

  24. Diagnosis of Head Injury • Physical Exam • Level of consciousness (particularly changes) • Associated injuries • 1 in 4 other body injury • cervical spine injury • 6% of head injuries • 26% of spine injuries have head injuries Assume all head injuries have cervical spine injury until proven otherwise

  25. Diagnosis of Head Injury • Neurologic evaluation • Glascow coma score (GCS) • Pupil examination • must reestablish perfusion and oxygenation for adequate exam • size, shape and reactivity • pearl - unilateral dilated but reactive pupil first sign of expanding mass in temporal lobe or epidural hematoma in middle fossa • Motor and sensory • purposeful movement - intact cortex down • flexor or extensor posturing - severe head injury

  26. Glasgow Coma Score

  27. Ventilatory Patterns • Significant deterioration in LOC is almost invariably associated with abnormal breathing • Cheyne-Stokes variant (mild injury) • hyperventilation/hypoventilation without apnea • True Cheyne-Stokes (severe injury) • regular pattern of hyperventilation with apnea secondary exaggerated response to increased PaCO2 • Ataxic (severe brainstem injury/terminal sign) • irregular inspiratory/expiratory phases with apnea

  28. Studies • Blood chemistry/hemoglobin/platelets • Coagulation factors • Alcohol/illicit drug screen • Radiographs • CT most accurate in localizing and quantifying • MRI - more sensitive than CT, useful for identifying aneurysms (MRA) and DAI • EEG • absence of somatosensory-evoked cortical potentials with first 24 hrs and GCS < 9, 95% death or major disability

  29. Management • Sine qua non • prevent secondary injury • avoid hypotension !!!! • avoid hypoxia !!!! • repetitive exams and timely interventions • Intubation • clinical respiratory distress • motor posturing or absence of motor response to pain • increasing or high ICP • airway protection • repeated convulsions (?)

  30. Management • Ventilatory support • maintain PO2 > 80 mm Hg • maintain PCO2 35-40 mm Hg • PEEP < 10 ok, no sig increase in ICP if HOB >30 degrees • sedation or neuromuscular blockade occasionally needed • Intubation drugs • rapid sequence with vecuronium or succinylcholine • fentanyl effective at blunting HR/BP • lidocaine prevents increase in ICP • barbiturates lower ICP, but lower BP

  31. Management • Fluid administration • Hypotension is BAD • Best treated with IVF, even if ICP is increased • Promising data using hypertonic saline (? dosing and timing) • Mannitol dehydrates the brain, not meant to reduce blood volume • Dopamine is needed to maintain MAP • Antibiotic for open depressed fractures or penetrating brain injuries • Avoid hyperthermia • Steroids do not offer beneficial effect

  32. Hypothermia • Definition • Moderate – core temperature 32-34 C • Deep – core temperature 25-30 C • Risks • Profound cardiac disturbance with CV collapse • Predisposition to infections and sepsis • Outcomes • Deep hypothermia – abandoned • Moderate hypothermia – “jury” still out

  33. Hypothermia and Trauma Clifton, G, et al. Lack of Effect of Induction of Hypothermia after Acute Brain Injury. NEJM, 2001, 344:556

  34. Hypothermia and Cardiac Arrest The Hypothermia After Cardiac Arrest Study Group. Mild Therapeutic Hypothermia To Improve The Neurologic Outcome After Cardiac Arrest. NEJM, 2002, 346:549

  35. Controlling ICP • Elevation head of bed • Diuretics • mannitol (0.5 to 1.0 g/kg) every 4-6 hours • ? Lasix • hyperventilation • transient effect only • use for impending herniation • maintain PCO2 about 35 mmHg • Dilantin • Any blood seen on CT or evidence of seizures • Continue 7 days and stop if no seizure activity • No benefit of prophylactic use to prevent late posttraumatic seizures

  36. Treating Uncontrolled IC Hypertension

  37. Barbiturate Coma • Best studied of uncontrolled IC HTN treatments • Effect • Reduce cerebral metabolism and blood flow • Induce burst suppression on EEG • Oxygen free-radical scavengers • Reduce ICP • Indication • Failed routine management for ICP control • ICP > 35 • Disadvantages • Cardiac depression • Hypotension • Most if not all require vasopressors and cardiostimulants

  38. Barbiturate Coma • Dosing • Loading: 10 mg/kg over 30 minutes • Maintenance: 1 mg/kg/h • Monitoring effectiveness • Follow ICP • ?Titrate for myocardial depression • Serum levels do not correlate with effect • Outcome • If lower ICP, mortality is less than non-responders

  39. Operative Management • Scalp lacerations • carefully explored, irrigated, and closed (galea should be closed in layers) • Skull fracture • nondisplaced with scalp laceration no intervention • if significantly depression should be considered for elevated • optic nerve or facial nerve compression should be decompressed • CSF leak • Antibiotics (controversial) • trend to avoid use to prevent more virulent CNS pathogens • HOB elevation > 60 degrees • > 3-4 days, trial of LP • > 7-10 days repair via dural patch

  40. Operative Management • Intracranial hematomas • required in 13% of patients with unconsciousness • decompression if mass lesion • increasing neurologic dysfunction • persistent ICP > 25 mmHg • more than 5 mm midline shift • “Sooner the better” • example SDH < 4 hrs to drainage 30% mortality > 4 hrs to drainage 90% mortality

  41. Sites of Emergency Trephine Openings

  42. Complications • Diabetes insipidus (basilar skull fx) • rule out excessive IVF, diuretics, or hyperglycemia • DDAVP, hypotonic saline • SIADH • treated best with dehydration • Malnutrition • severe hypermetabolic state last about 1 week • may exceed negative nitrogen balance of 30g/d • start nutritional support early • Coagulopathy • Pneumonia • risk ratio = 4x greater

  43. Complications • Neurogenic Pulmonary edema (NPE) • neurogenic increase in lung water • massive sympathetic discharge increases PVR • fluid overload increases tendency of NPE • ARDS • difficult to differentiate between NPE • Fat embolism • cause of hypoxemia and CNS changes in multiple extremity fx’s • 12-26 hrs after trauma • suspicion if platelet count lower than expected (???) • GI Bleeding • common, up 30 % of severe head injury • classic - Cushing ulcers

  44. Outcomes • GCS moderately predictive • Increased age = worse outcome • Significant cognitive defects for minor brain injury for 3-6 months post injury

  45. Inadequate attention to other injuries Delay in restoring BP and hypoxia Delay in intubating Little or no neuro defect in mild head injuries Focus on ICP not CPP Failure to promptly repeat CT for neurologic deterioration Inadequate frequency in exams, especially intoxicated patients Failure to act promptly to change in pupil size Failure to r/o spine injury Failure to monitor UOP Correcting hypertension without giving attention to cause Frequent Errors

  46. Case Study • 78 yom s/p fall (1 flight of stairs) • PMH: Afib, COPD, Depression • GCS on arrival 11 • CT scan - small R frontal SDH, R frontal contusion, posterior occipital contusion, no shift • Other injuries • R rib fractures, PTX (CT placed) • R iliac crest fracture

  47. Case Study • ICU admission • NPO/IVF (NS) • Dilantin started • Neurochecks • Pulmonary “toilet” • CT scan (24hrs later) - stable SDH, increased size of contusions, no shift • GCS 11

  48. Case Study • HD #2 - developed purulent sputum, infiltrate on CXR, started on Ceftriaxone • HD #3 - developed deteriorating mental status (GCS 7) • Repeat CT head no change • Required intubation • ? Etiology of MS changes

  49. Dilantin Toxicity • CNS - drowsiness, ataxia, confusion • GI - gingival hyperplasia, N/V, diarrhea • Derm - skin rashes • Heme - leukopenia, thrombocytopenia, pancytopenia, agranulocytosis, anemia • Hepatic - liver toxicity, toxic hepatitis • Misc - hyperglycemia, pulmonary fibrosis • CV - rare (associated with rapid IV admin.)

  50. Toxicity • Unbound phenytoin responsible for the therapeutic effect and toxicity • Serum phenytoin level measured is total concentration ( 10-20 ug/ml) • Usual unbound phenytoin is < 10% • Alterations in protein binding increase unbound phenytoin > 20%

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