374.4 📋 章末速蚘 Summary

374.4.1 🔑 䞀句話瞜結

Coma = pathological unconsciousness — eyes closed + unaware + unarousable + no purposeful movement; consciousness requires arousal (brainstem RAS) + awareness (cerebral cortex); spectrum alert → confused → drowsy → stuporous → coma; persistent disorders — vegetative state (UWS — unresponsive wakefulness syndrome, eyes open + sleep-wake + no awareness, persistent 1 mo → permanent 3 mo non-traumatic/12 mo traumatic) vs minimally conscious state (MCS — inconsistent awareness, better prognosis) vs locked-in syndrome (ventral pontine lesion often basilar artery occlusion — quadriplegic + anarthric + AWAKE/AWARE + preserved vertical eye movements + blinking); two anatomic causes — (1) bilateral cerebral hemispheric dysfunction (most common — toxic/metabolic >> structural) including drugs (opioids/BZDs/alcohol/sedatives), hypoglycemia, hyperglycemia (HHS, DKA), hyponatremia/hypernatremia/Ca/Mg, hypothyroid (myxedema)/thyroid storm, adrenal insufficiency, hepatic encephalopathy (asterixis + triphasic EEG), uremia, hypoxia, hypercapnia (CO2 narcosis), hypothermia/hyperthermia, sepsis, Wernicke (thiamine), post-anoxic, meningitis/encephalitis, seizure/post-ictal, bilateral structural (large strokes, SAH, DAI, PRES); (2) brainstem RAS dysfunction at midbrain/pons/upper medulla — pontine hemorrhage + basilar artery infarct + brainstem tumor + central pontine myelinolysis + posterior fossa mass compression; Glasgow Coma Scale (GCS) = E (1-4) + V (1-5) + M (1-6) = 3-15, GCS ≀ 8 consider intubation; pupils critical — bilateral pinpoint reactive = pontine hemorrhage OR opioids OR organophosphate, mid-position fixed = midbrain, bilateral fixed dilated = anoxia/atropine/brain death/late herniation, unilateral fixed dilated = CN III compression (uncal herniation, PCA aneurysm), metabolic mostly preserved reactivity; eye movements — oculocephalic (doll’s eyes) present in coma = intact brainstem (DO NOT perform if cervical injury); oculovestibular (cold calorics) more sensitive — eyes deviate TOWARD cold ear in coma; motor response — localizes (cortex intact) > withdraws > decorticate flexor (above red nucleus) > decerebrate extensor (below red nucleus — worse) > none; breathing patterns — Cheyne-Stokes (cerebral/HF) + central neurogenic hyperventilation (midbrain) + apneustic (lower pons) + ataxic/Biot (medullary pre-arrest); brain herniation syndromes — uncal (CN III compression unilateral dilated pupil + decerebrate) + central (bilateral progression alert→drowsy→diencephalic→midbrain→medullary) + tonsillar (cerebellar tonsils through foramen magnum → apnea/sudden death) + subfalcine (cingulate under falx → ACA compression); workup — glucose immediate + ABG + electrolytes + Ca/Mg + LFTs + ammonia + TFTs + cortisol + CBC + coag + toxicology + alcohol + salicylates + acetaminophen + cultures + pregnancy + CK + lactate + CT head EMERGENT (rule out hemorrhage/herniation) + MRI if negative + LP after imaging + EEG (NCSE, encephalopathy patterns, prognosis post-arrest); empiric therapy — thiamine 100 mg IV BEFORE glucose (Wernicke prevention) + D50W if low/unmeasured + naloxone if opioid suspected + flumazenil controversial (seizure risk); specific causes — opioid OD (pinpoint + hypoventilation + naloxone), hypoglycemia (can mimic stroke focal), hepatic encephalopathy (asterixis + triphasic waves + lactulose/rifaximin), uremic (myoclonus + asterixis + dialysis), Wernicke triad ophthalmoplegia + confusion + ataxia (only 16% all 3) + thiamine before glucose, post-anoxic coma (prognostication at 72 hr off sedation normothermic — NSE/EEG/SSEP/MRI multimodal), septic encephalopathy, CO2 narcosis (COPD + O2 → BiPAP), CO poisoning (cherry red rare, co-oximetry, 100% O2, hyperbaric)。

374.4.2 💊 治療粟芁

  • empiric in unknown comathiamine 100-500 mg IV BEFORE glucose (Wernicke prevention) + glucose D50W 50 mL if low or unmeasured + naloxone 0.4-2 mg IV/IM/IN if opioid suspected + flumazenil controversial (seizure risk if BZD-dependent or co-ingestion)
  • Wernicke encephalopathythiamine 500 mg IV TID × 3 days → 250 mg IV daily × 5 days → 100 mg PO daily ongoing + alcohol use disorder + treat underlying
  • hepatic encephalopathylactulose titrate to 2-3 soft stools/day + rifaximin 550 mg BID + treat precipitant (infection, GI bleed, electrolytes) + protein NOT routinely restricted
  • uremic encephalopathydialysis (hemodialysis or CRRT) + correct underlying
  • opioid ODnaloxone 0.04-2 mg IV/IM/IN (short T1/2 — monitor for re-narcotization, continuous infusion if needed)
  • CO2 narcosis (COPD + O2 overshoot)BiPAP + cautious O2 titration to SpO2 88-92%
  • CO poisoning100% O2 via non-rebreather + hyperbaric O2 for severe (LOC, neurologic deficit, COHb > 25%, pregnancy with COHb > 15%); co-oximetry (SpO2 misleading)
  • anti-NMDA-R encephalitistumor search (ovarian teratoma + others) + IVIG 2 g/kg + methylprednisolone pulse + rituximab + cyclophosphamide + plasmapheresis
  • brain herniation imminenthead elevation 30° + osmotherapy (mannitol 0.5-1 g/kg, 3% hypertonic saline target Na 145-150) + hyperventilation (acutely, PaCO2 30-35) + sedation + surgical decompression (craniectomy) if applicable
  • status epilepticus → comatreat as SE Ch372

374.4.3 🎯 盧醫垫的考前提醒

  1. Consciousness components: arousal (brainstem RAS) + awareness (cerebral cortex) — both required; coma vs UWS (eyes open + sleep-wake but no awareness) vs MCS (inconsistent awareness) vs locked-in (awake + aware + preserved vertical gaze, ventral pontine lesion)
  2. Two anatomic causes of coma: (1) bilateral cerebral hemispheric (toxic-metabolic >> structural — most common) vs (2) brainstem RAS dysfunction (midbrain/pons/upper medulla); unilateral hemispheric usually doesn’t cause coma UNLESS mass effect → herniation
  3. GCS (memorize): E (1-4) + V (1-5) + M (1-6) = 3-15; GCS ≀ 8 → consider intubation; confounded by intubation, sedation, intoxication
  4. Pupils critical for localization: bilateral pinpoint reactive = pontine hemorrhage OR opioids OR organophosphate + mid-position fixed = midbrain + bilateral fixed dilated = anoxia/atropine/brain death + unilateral fixed dilated = CN III compression (uncal herniation OR PCA aneurysm — EMERGENCY) + metabolic mostly preserves reactivity
  5. Eye movements: oculocephalic (doll’s eyes) present in coma = intact brainstem (DO NOT perform if C-spine concern); oculovestibular (cold calorics) more sensitive — eyes deviate TOWARD cold ear in coma (only slow phase)
  6. Motor response gradient: localizes > withdraws > decorticate flexor (above red nucleus) > decerebrate extensor (below red nucleus — worse prognosis) > none
  7. Breathing patterns: Cheyne-Stokes (cerebral, HF) + central neurogenic hyperventilation (midbrain) + apneustic (lower pons) + ataxic/Biot (medullary — PRE-ARREST!)
  8. Empiric therapy unknown coma (memorize sequence): thiamine 100 mg IV BEFORE glucose (Wernicke prevention!) → D50W if low/unmeasured → naloxone if opioid suspected; Wernicke triad ophthalmoplegia + confusion + ataxia (only 16% have all 3 — treat empirically in any suspicious case)
  9. Brain herniation syndromes: uncal (medial temporal → CN III → unilateral fixed dilated pupil + contralateral hemiparesis) + central (progressive: alert → drowsy → diencephalic → midbrain → medullary) + tonsillar (cerebellar tonsils through foramen magnum → apnea/sudden death) + subfalcine (cingulate under falx → ACA compression → contralateral leg weakness)
  10. Hepatic encephalopathy clues: asterixis + triphasic waves on EEG + variable ammonia → lactulose + rifaximin + treat precipitant (infection, GI bleed, electrolytes, dehydration, constipation); CO2 narcosis (COPD + O2) → BiPAP; post-anoxic coma prognostication at 72 hr off sedation/normothermic — multimodal NSE + EEG + SSEP + MRI