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Encephalopathy and Coma
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Encephalopathy and Coma Neurologic Emergencies July 17, 2007
Case Presentation 35 year-old man who, after 2 months of increasingly severe left-sided headaches, became rapidly lethargic and then stuporous.
Unconsciousness vs. unresponsiveness
Unconsciousness Loss of consciousness requires: Disruption of ascending reticular activating system OR Bihemispheric cerebral dysfunction
Unconsciousness Loss of consciousness requires: Disruption of ascending reticular activating system OR Bihemispheric cerebral dysfunction Often transient
Unconsciousness Loss of consciousness requires: Disruption of ascending reticular activating system OR Bihemispheric cerebral dysfunction Often transient OR Dominant hemisphere lesions
Unresponsiveness Ability to respond requires: Consciousness Language Subcortical and cortical motor system integrity Descending pyramidal tracts Etc..
Coma A state of “unarousable unresponsiveness”
Approach to unresponsive patient This is an emergency! Immediate evaluation should include: Airway Breathing Circulation Glucose Electrolytes, ABG, liver and thyroid function tests, CBC, toxicology screen, ECG
Approach to unresponsive patient Empiric treatments when indicated Supplemental oxygen Intubation if needed Intravenous fluids Thiamine 100mg IV If there is a malnourished appearance or if there is a known history of alcoholism Before glucose!! Glucose
Approach to unresponsive patient Empiric treatments when indicated Lower the intracranial pressure Mannitol 0.25 to 2.0 grams/kg IV (15-25% solution) over 60 minutes Hyperventilation (target pCO2 25-30 mmHg) Remember concept of rebound Naloxone/flumazenil Treat seizures Empiric treatment for acute CNS infection
Examining the unresponsive patient Outline of examination Observation Respiratory pattern Verbal responses Eye opening Pupillary reactions Spontaneous eye movements Oculocephalic responses = Oculovestibular responses Corneal responses Motor responses Tendon reflexes Muscle tone Elicit meningismus
Examining the unresponsive patient Reproducibility is key Observation before stimuli Stepwise approach to stimuli Verbal stimulation – call pt’s name loudly Gentle tactile stimulation – shake/hold pt’s hand Noxious tactile stimulation – shoulder pinch Noxious stimuli on each limb – nailbed pressure Important part of motor and sensory exam Record each behavior (or lack thereof) sequentially
Examining the unresponsive patient Reproducibility is key Give simple verbal instructions Ask for a motor response from each limb Eye and eyelid movements Record each behavior (or lack thereof) sequentially
Example “The patient lay motionless in bed unless called loudly by name, when he opened his eyes only briefly and looked only to the left. He failed to respond verbally to questions. He did not follow any instructions. He withdrew from nailbed pressure with his left arm and leg vigorously, but not with his right arm/leg.”
Examining the unresponsive patient Always assume the patient can hear you. Introduce yourself and explain your exam. Do not forget to look for vertical eye and eyelid movements. Develop a routine for examining and recording.
Case Presentation Examination also shows: The left pupil is dilated and unreactive. The left eye fails to adduct during oculovestibular testing. There is left-sided hemiplegia.
Your diagnosis? Empiric treatment?
Approach to an unresponsive patient Identification of syndrome Localization Differential diagnosis Evaluation Treatment Prognosis
Findings with Localizing Value The pupils Respiratory patterns Eye movements Motor activity of body and limbs
Pupillary responses Pupillary pathways are most resistent to metabolic insults Excellent localizing value Helpful differentiating metabolic from structural causes of coma The unilateral dilated and unreactive pupil Oculomotor nerve compression Posterior communicating artery aneurysm Uncal herniation
Pupillary responses REMEMBER: 8 – 18% of population has a physiologic anisocoria of at least 0.5mm Probably should assume that this represents pathology in an emergency situation
Pupillary responses Ciliospinal reflex Pinch skin of face or neck and watch for bilateral pupil dilation (1-2mm) Tests integrity of: Trigeminal nerve/spinal dorsal horn Brainstem autonomic centers C8-T2 levels (ciliospinal center of Budge) Ascending autonomic fibers
Cheyne-Stokes respirations Forebrain/diencephalic lesions Central neurogenic hyperventilation Mibrain/pons lesions Apneustic breathing Bilateral pontine tegmentum lesions Cluster breathing Lesions near pontomedullary junction Apnea Bilateral ventrolateral medullary lesions
Decerebrate rigidity/posture The arms are held in adduction and extension with the wrists fully pronated. Extension, internal rotation, and plantar flexion in the lower extremities.
Decerebrate rigidity/posture Experimentally produced by transection at the collicular level between the red nuclei and vestibular nuclei In theory: disinhibited vestibular tone increases extensor tone in limbs Think: Metabolic disorders (anoxia, others) Midbrain/upper pons lesions (infarcts) Downward transtentorial herniation Space-occupying lesions in posterior fossa
Decerebrate rigidity/posture Sometimes accompanied by opisthotonus, an arching of the trunk usually with clenched teeth and tonic neck and arm posturing.
Decorticate rigidity/posture Flexion of the arms, wrists, and fingers. Adduction of upper extremities. Extension, internal rotation, and plantar flexion in the lower extremities.
Decorticate rigidity/posture Experimentally produced by bilateral lesions from forebrain down to the level of the rostral midbrain. If unilateral, the rigidity will be contralateral to the involved cerebral hemisphere. Less specific in terms of localization and etiology.
Syndromes of Unresponsiveness Encephalopathy and coma Acute confusional state/delirium Locked-in syndrome Akinetic mutism Catatonia Psychogenic unresponsiveness Persistent vegetative state
Akinetic mutism The patient is seemingly awake but remains silent and motionless. Failure to gain patient’s attention and interest. Eyes often fix on examiner and will follow moving objects. They may also follow auditory stimuli. May have frontal release signs or signs of corticospinal tract involvement. May also exhibit stereotyped limb movements.
Akinetic mutism Some may try to speak spontaneously Can be difficult to distinguish from psychogenic and/or catatonic unresponsiveness. EEG will show generalized slowing.
Akinetic mutism This syndrome does have localizing value Causative lesions can be: Bilateral frontal regions, especially the anterior cingulate gyri The diencephalo-mesencephalic reticular formation The globus pallidus The hypothalamus NOTE: this is NOT a psychiatric diagnosis
Akinetic mutism More common causative conditions: Anoxia Head trauma Cerebral infarction Severe acute hydrocephalus Compression by tumor
Locked-In Syndrome Unresponsiveness except for vertical eye and eyelid movements. These patients are often awake, alert, and completely conscious. Lesion of ventral pons (basis pontis) Causes: Basilar artery thrombosis Pontine hemorrhage/tumor Central pontine myelinolysis
Delirium Or “acute confusional state” Acute cognitive impairment Disorientation Attentional abnormalities Increased or decreased psychomotor activity (“agitated” or “quiet” delirium) Disorder of the sleep/wake cycle
Delirium Testing attention: Counting, serial 7s, spelling “world” backwards
Delirium Common! 10-15% of medical/surgical ward pts Even higher prevalence in elderly 32% prevalence in pts after cardiac surgery 45-55% prevalence in pts after hip fracture surgery 70% prevalence in pts with bacteremia
Case 2 65 year-old man suddenly collapsed. EMS intubated him. On exam the patient is comatose. He has pinpoint pupils and ocular bobbing. There is spontaneous decerebrate posturing. He has bilateral extensor toe signs.
Case 2 Hyperdense basilar artery sign Presumed basilar artery thrombosis/embolism Treatment?
Case 2 Hyperdense basilar artery sign Presumed basilar artery thrombosis/embolism Treatment? Intra-arterial tPA MERCI retrieval/thrombectomy
Added On : 8 Years ago.
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