Encephalitis

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Encephalitis

• Encephalopathy plus CSF pleocytosis
• Pratibha Shirsat, M.D.

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• The progression to coma
• 1. Lethargy difficulty maintaining an aroused
  state.
• 2. Delirium confusion, loss of attention,
  delusions, disorientation may be agitated and/
  or violent.
• 3. Stupor arousal occurs only with repeated,
  vigorous stimulation.
• 4. Coma total absence of self and environmental
  awareness.

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• Caveat Lack of responsiveness may not equal
  lack of consciousness
• 1. Vegetative state eyes can open but cannot
  follow commands.
• 2. Locked in state selective
  deafferentation of motor pathways in the
  brainstem alert but cannot move RARE in
  children.
• 3. Infant botulism may be unable to open eyes
  although aware.

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Pathogenesis

• How does coma result?
• A. Bilateral cerebral hemisphere depression
• B. Localized abnormality of the switch (ARAS) in
  the brainstem
• 1. Ascending reticular activating system
  (ARAS)
• C. Global CNS dysfunction

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• D. Two Roads to Coma
• 1. The High Road neuronal excitability
• a. Restlessness ? confusion ? tremor ?
• hallucinations ? delirium ?myoclonic
• jerks ? seizures ? stupor ? coma
• 2. The Low Road decreased neuronal
  excitability
• a. Lethargy ? obtundation ? stupor ? coma

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Significant History

• 1. Delirium toxic or metabolic until proven
  otherwise.
• 2. Lethargy and coma suggest a more urgent
  neeed to diagnose due to risk of increased
  ICP.

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Physical Examination

• A. Modified Glascow Coma Scale
• B. Rapid, organized approach is crucial
• 1. Are VS normal?
• 2. Evidence of herniation?
• 3. Evidence for increased ICP?
• 4. Evidence for focal neurological disease?

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• C. Signs of Impending Doom
• 1. Abnormal respiratory pattern
• 2. Altered mental status
• 3. Hypothermia
• 4. Impending shock.
• D. Physical Exam Specifics
• 1. Respiratory pattern
• a. Hyperventilation Cheyne-Stokes, centra
  neurogenic
• b. Hypoventilation apneustic, ataxic

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• 2. Pupil size and reaction
• a. Miosis
• b. Mydriasis
• c. Light reflex /-
• 3. Extraocular movements
• a. Position at rest
• b. Spontaneous abnormal movements
• c. A CN III palsy is always ipsilateral

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• 4. Ocular response to labyrinthine
  stimulation (oculocephalics)
• 5. Motor posture and response to stimulation
• a. Posture
• i. Decorticate
• ii. Decerebrate

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• b. Spontaneious movements
• c. Muscle tone
• d. Response to noxious stimuli
• 6. Brainstem reflexes
• a. Pupil light reaction (CN II, III)
• b. Reflex eye movements (CN III, VI, VII,
  MLF)

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• c. Preservation suggest offending lesion is
  not primary in the brainstem but involves
  both cerebral hemispheres.
• 7. Note bene The mass is ipsilateral to the
  dilated, unresponsive pupil until proven
  otherwise.

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Etiology

• A. Structural
• 1. 20 - 30
• 2. Supratentorial
• 3. Subtentorial
• B. Toxic/metabolic
• 1. 70 80
• 2. Alterations of oxygen or glucose delivery
  to the brain

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• 3. Exogenous toxin poisons
• a. Alcohols
• b. Antihistamines
• c. Barbiturates
• d. Carbon monoxide
• e. Narcotics
• f. Salicylates
• g. Tricyclic antidepressants

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• h. Atropinics
• I. Anticonvulsants
• j. Organophosphates insecticides
• k. PCP
• l. Heavy metals (Pb)
• 4. Endogenous toxins infection,
  metabolic disorder.

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• 5. Epidural hemorrhage
• a. Dilated unresponsive pupil
• b. LOC may be gradual as usually
  venous origin in children
• 6. Subdural hemorrhage
• a. Usually with visible external
  trauma and immediate LOC

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• b. Often only one component of
  multiple injuries
• c. Shaken baby syndrome is the
  exception _ No external injuries
• 7. Nontraumatic supratentorial
• a. Rare
• b. CVA
• c. Subdural empyeme (complication of
  missed basilar skull fracture)
• d. Tumors

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• 8. Subtentorial
• a. Posterior fossa
• b. Destruction of ARAS or
  brainstem compression
• c. Coma often post hemorrhage
• 9 Metobolic
• a. Altered mental status earliest
  sign.
• b. Change in respiratory function
• c. Transient focal signs

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• d. Partial dysfunction at may
  levels
• e. Tremor, asterixis, multifocal
  myoclonus
• 10. Toxidromes
• a. Anticholinergics
• b. Opiates
• c. Cholinergics
• e. Sedative/hypnotics
• f. Phenothiazines

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Signs and symptoms of Elevated ICP

• A. Cushings Triad
• 1. Hypertension
• 2. Bradycardia
• 3. Pupil asymmetry
• B. Herniation
• 1. Central (rostrocaudal) usually
  orderly progression
• 2. Uncal less orderly deterioration may be
  unpredictable and sudden

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• C. The Equations
• 1. CPPSAP ICP
• 2. CBFCPP/CVR

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Emergent Treatment of increased ICP

• Therapy Mechanism of Action
• Elevate head 30 Decrease venous
  pressure
• Keep head midline Prevent jugular
  constriction
• Hyperventilation Decrease CBV
• Mannitol0.52.0gm/kg Osmotic Diuresis
• Lasix-1.0mg/kg Diuresis
• Decadron-1-2mg/kg ??????

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Treatment and Evaluation

• A. ABCs, C-spine stabilization, temperature
  support
• B. Trauma protocol if necessary
• C. Treat elevated ICP if necessary
• D. Treat infection if necessary
• E. Labs Chemistries, ABG, NH4,LFTs, renal
  function
• F. Give glucose, Narcan (thiamine?)

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• G. Foley Catheter
• H. Check for intoxication (?)
• I. CT, LP as indicated
• J. Admit ICU

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Significant History and Physical

• Signs and symptoms of elevated ICP
• symptoms signs
• Headache Papilledema
• Vomiting Cranial nerve palsies
• Stiff neck Stiff neck
• Double vision Retinal hemorrhage
• Episodic severe headache MacEwens sign
• Gait difficulties Obtundation
• Dulled intellect Unconsciousness
• Irritability Progressive hemiparesis

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Significant History and Physical

• Signs of Tentorial Herniationª
• Progressively server headache
• Decreasing level of consciousness
• Ipsilateral pupillary dilation
• Contralateral hemiparesis or posturing
• contralateral pupillary dilation
• Bilateral decerebration
• __________________________________________
• ªCheyne-Stokes respiration often accompanies the
  above signs and symptoms