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Coma

Chapter 30 | Part 2: Cardinal Manifestations and Presentation of Diseases · Part 2 – Cardinal Manifestations & Presentation · Chapter 30

Key Clinical Points

  1. Coma is defined as a deep sleep-like state with eyes closed from which the patient cannot be aroused.
  2. Eye movement direction provides localization: toward a hemispheral lesion and away from a brainstem lesion.
  3. Ocular bobbing (brisk downward and slow upward movements) is diagnostic of bilateral pontine damage.
  4. Alpha coma on EEG (widespread, variable 8- to 12-Hz activity) is associated with a poor prognosis.
  5. Pinpoint pupils (<1 mm) characterize opioid overdoses but also occur with extensive pontine hemorrhage.
  6. Posturing indicates lesion level: Decorticate (rostral to midbrain) vs. Decerebrate (caudal to midbrain).
  7. A normal CT scan does not exclude an anatomic lesion as the cause of coma (e.g., early bilateral hemisphere infarction, acute brainstem infarction).
  8. Hypothermia causes coma when the temperature is <31°C (87.8°F) regardless of the underlying etiology.
  9. The vegetative state prognosis for regaining meaningful mental faculties is poor after several months and almost nil after a year.
  10. Delirium prevention involves promoting wakefulness, sleep, and reducing tethers (nasal cannula, Foley catheter, telemetry, and CPO).

DEFINITION & OVERVIEW

• Coma: A deep sleep-like state with eyes closed, from which the patient cannot be aroused. • Stupor: A lower threshold for arousability; patient can be transiently awakened by vigorous stimuli, accompanied by motor behavior to avoid/withdraw from noxious stimuli. • Drowsiness: Simulates light sleep; characterized by easy arousal that may persist for brief periods. • Vegetative State: Awake-appearing but nonresponsive; eyelids open periodically; respiratory and autonomic functions retained; few/no meaningful responses to environment. Often associated with extensive damage in both cerebral hemispheres (e.g., decorticate or decerebrate posturing). • Minimally Conscious State: Patient displays rudimentary vocal or motor behaviors, often spontaneous, but sometimes in response to touch, visual stimuli, or command. • Locked-in State: Awake but paralyzed; no means of producing speech or voluntary limb movement; retains voluntary vertical eye movements. • Akinetic Mutism: Partially or fully awake state; patient remains virtually immobile and mute but can form impressions (damage to medial thalamic nuclei or frontal lobes). • Abulia: Milder form of akinetic mutism; mental and physical slowness and diminished ability to initiate activity (damage to medial frontal lobes). • Catatonia: Hypomobile and mute syndrome, usually part of a major psychiatric disorder. Features include waxy flexibility (catalepsy) and response to lorazepam.

EPIDEMIOLOGY

• Prevalence: Common neurologic emergency in general medicine; high volume of ED visits. • Safety Risk: Patients may pose a threat to themselves or staff, requiring acute management.

ETIOLOGY & PATHOPHYSIOLOGY

• Primary Mechanisms: 1. Widespread abnormalities of both cerebral hemispheres. 2. Reduced activity of the Reticular Activating System (RAS) (upper brainstem and thalamus). • Metabolic vs. Structural: Metabolic causes (hypoglycemia, anoxia, uremia, etc.) are far more common than structural injuries.

Anatomy and Physiology of Coma

• Herniation Dynamics: - Uncal: Displacement of the uncus into the tentorial opening; causes midbrain compression and ipsilateral CN III palsy (dilated pupil). - Central: Symmetric downward movement of thalamic structures through the tentorial opening; results in miotic pupils and drowsiness. - Foraminal: Displacement of cerebellar tonsils into the foramen magnum; leads to early medullary compression and respiratory arrest. • Metabolic Mechanisms: - Hypoxia/Ischemia: Depletes glucose (exhausted in ~2 min) and oxygen (exhausted in 8–10 s). - Hepatic Encephalopathy (HE): High ammonia → increased glutamine, astrocyte swelling, increased GABA. - Renal Failure: Multifactorial; includes neurotoxic substances (creatinine, guanidine), catecholamine depletion, and inflammation.

Cerebral Mass Lesions and Herniation Syndromes

• Uncal Herniation: Midbrain/CN III compression → ipsilateral pupil dilation; subsequent coma as brainstem is compressed. - Central Herniation: Symmetric thalamic movement → miotic pupils and drowsiness. - Foraminal Herniation: Medulla compression → early respiratory arrest.

Coma Due to Metabolic, Drug, and Toxic Disorders

• Metabolic Factors: - Hypothermia: <31°C (87.8°F) → coma regardless of etiology. - Hypoglycemia/Hyponatremia: Common causes of metabolic encephalopathy. • Toxicology: - Opioids: Produce pinpoint pupils (<1 mm). - Sedative Drugs: Can mimic brain death; must be excluded before declaring brain death. - Anticholinergics: (Not specified in source text, but noted as a common clinical consideration).

Coma Due to Widespread Structural Damage

• Hypoxia-Ischemia: Primary cause of large-scale structural damage. - Structural Causes: Trauma, stroke (basilar artery thrombosis), and intracranial hemorrhage.

CLINICAL FEATURES

• History: Timing/rapidity of onset; duration; presence of fever, seizure, or headache; drug/alcohol use. • Physical Examination: - Fever: Suggests infection, toxidrome, or heat stroke. - Hypotension: Suggests shock, alcohol/barbiturate toxicity, or sepsis. - Fundoscopy: Papilledema (ICP) or subhyaloid hemorrhage (SAH). - Skin: Petechiae (TTP, meningococcemia); Cyanosis (CO poisoning).

Neurologic Examination

• Movement Patterns: - Decorticate Posturing: Flexion of upper extremities; indicates damage rostral to the midbrain. - Decerebrate Posturing: Extension of upper extremities; indicates damage caudal to the midbrain. • Special Signs: - Ocular Bobbing: Brisk downward and slow upward movements; diagnostic of bilateral pontine damage. - Asterixis: Suggests metabolic encephalopathy or drug intoxication.

Level of Arousal

• Stimulus Response: - Mild Stimuli (e.g., tickling): Movement of head in all but deeply stuporous patients. - Stronger Stimuli (e.g., pinprick/pressure): Required for those with higher arousal thresholds. • Pupillary Findings: - <1 mm (Pinpoint): Opioid overdose or extensive pontine hemorrhage. - Dilated/Unreactive: Severe midbrain damage from supratentorial mass.

Brainstem Reflexes

• Pupillary Response: Tests midbrain and CN III function. - Corneal-Blink Reflex: Tests trigeminal (V) and facial (VII) nerve pathways. - Reflex Conjugate Eye Movements: Indicates integrity of pons and medial longitudinal fasciculus (MLF). - Respiratory/Pharyngeal Responses: Reflects medullary integrity.

DIFFERENTIAL DIAGNOSIS

• Table 30-1: Differential Diagnosis of Coma 1. Diseases with no focal brainstem or lateralizing signs (CT often normal): - Intoxications (alcohol, sedative drugs, opiates). - Metabolic disturbances (anoxia, hyponatremia, hypernatremia, hypercalcemia, diabetic acidosis, nonketotic hyperosmolar hyperglycemia, hypoglycemia, uremia, hepatic coma, hypercarbia, Addisonian crisis, hypo- and hyperthyroid states, profound nutritional deficiency). - Severe systemic infections (pneumonia, septicemia, typhoid fever, malaria, Waterhouse-Friderichsen syndrome). - Shock from any cause. - Status epilepticus, nonconvulsive status epilepticus, postictal states. - Hyperperfusion syndromes (hypertensive encephalopathy, eclampsia, PRES). - Severe hyperthermia, hypothermia. - Concussion; Acute hydrocephalus. 2. Diseases with focal brainstem or lateralizing cerebral signs (CT typically abnormal): - Hemispheral hemorrhage (basal ganglionic, thalamic) or infarction (large MCA territory). - Brainstem infarction (basilar artery thrombosis/embolism). - Brain abscess, subdural empyema. - Epidural and subdural hemorrhage, brain contusion. - Brain tumor with surrounding edema. - Cerebellar and pontine hemorrhage and infarction. - Widespread traumatic brain injury. 3. Diseases with meningeal irritation (with or without fever; high WBC/RBC in CSF): - Subarachnoid hemorrhage (SAH) from ruptured aneurysm, AVM, or trauma. - Infectious meningitis and meningoencephalitis. - Paraneoplastic and autoimmune encephalitis. - Carcinomatous and lymphomatous meningitis.

INVESTIGATIONS & DIAGNOSIS

• Laboratory Studies: Assess metabolic (glucose, electrolytes), toxic (alcohol, drugs), and infectious markers. • Imaging Studies: - CT Scan: Standard initial study; note that normal CT does not rule out early infarction or brainstem injury. - MRI: Detailed structural assessment of tumors, infarcts, or inflammation. • Electroencephalography (EEG): - Alpha Coma: Widespread, variable 8- to 12-Hz activity; associated with poor prognosis.

MANAGEMENT & TREATMENT

• General Management Principles: 1. Stabilize respiratory and cardiovascular status. 2. Determine severity/nature of coma to guide investigation. • Delirium Prevention Strategy: 1. Identify high-risk patients → initiate "ABC" protocols (A: Wakefulness, B: Sleep, C: Continuous Pulse Oximetry). 2. Reduce tethers: Remove nasal cannula, Foley catheter, and telemetry if not strictly necessary. 3. Environment: Use sitters or personal sitters instead of physical restraints. • Specific Toxicologic Reversal: 1. Identify specific toxins (e.g., opioids) → administer specific antidotes. 2. Antipsychotics: Reserved for patients with severe agitation and significant potential to harm self/staff; not used for general prevention. 3. Benzodiazepines: Avoid unless delirium is caused by alcohol or benzodiazepine withdrawal.

Delirium Management and Prevention Flowchart

  1. Initial Assessment: Identify high-risk patients → Implement non-pharmacological "ABC" (Wakefulness, Sleep, CPO).
  2. Safety Risk Assessment: Does patient pose threat to self/staff?
  3. No → Continue non-pharmacological management.
  4. Yes → Assess need for sitters or personal sitters.
  5. Escalation Path: If severe agitation persists despite sitters → Administer very-low-dose typical or atypical antipsychotics (as a last resort).
  6. Pharmacological Selection: Determine state (stupor/drowsiness) → Evaluate level of confusion → Use medications only for safety, not as primary treatment.

PROGNOSIS & COMPLICATIONS

• Vegetative State: Prognosis for meaningful mental faculties is poor after months; almost nil after one year. • Minimally Conscious State: Prognosis depends on the extent of brain damage. • Locked-in Syndrome: Patients are aware but paralyzed (except vertical eye movements).

KEY PEARLS & CLINICAL TRAPS

• Pupil Size Rule: <1 mm = Opioid/Pontine; larger/unreactive = Midbrain damage. • Hypothermia Rule: <31°C (87.8°F) → coma regardless of cause. • Posturing Rule: Decorticate (Rostral to midbrain) vs. Decerebrate (Caudal to midbrain). • Delirium Prevention: Non-pharmacological methods are primary; antipsychotics are for safety only. • Ocular Bobbing: Brisk down/slow up = bilateral pontine damage.

Reference Tables

TABLE 30-1 Differential Diagnosis of Coma 1. Diseases that cause no focal brainstem or lateralizing neurologic signs

Harrison's 22e, p.191

    1. Diseases that cause no focal brainstem or lateralizing neurologic signs
      (CT scan is often normal)
      a. Intoxications: alcohol, sedative drugs, opiates, etc.
      b. Metabolic disturbances: anoxia, hyponatremia, hypernatremia,
      hypercalcemia, diabetic acidosis, nonketotic hyperosmolar hyperglycemia,
      hypoglycemia, uremia, hepatic coma, hypercarbia, Addisonian crisis,
      hypo- and hyperthyroid states, profound nutritional deficiency
      c. Severe systemic infections: pneumonia, septicemia, typhoid fever, malaria,
      Waterhouse-Friderichsen syndrome
      d. Shock from any cause
      e. Status epilepticus, nonconvulsive status epilepticus, postictal states
      f. Hyperperfusion syndromes including hypertensive encephalopathy,
      eclampsia, posterior reversible encephalopathy syndrome (PRES)
      g. Severe hyperthermia, hypothermia
      h. Concussion
      i. Acute hydrocephalus
      2. Diseases that cause focal brainstem or lateralizing cerebral signs
      (CT scan is typically abnormal)
      a. Hemispheral hemorrhage (basal ganglionic, thalamic) or infarction (large
      middle cerebral artery territory) with secondary brainstem compression
      b. Brainstem infarction due to basilar artery thrombosis or embolism
      c. Brain abscess, subdural empyema
      d. Epidural and subdural hemorrhage, brain contusion
      e. Brain tumor with surrounding edema
      f. Cerebellar and pontine hemorrhage and infarction
      g. Widespread traumatic brain injury
      h. Metabolic coma (see above) in the setting of preexisting focal damage
      3. Diseases that cause meningeal irritation with or without fever, and with an
      excess of white blood cells or red blood cells in the CSF
      a. Subarachnoid hemorrhage from ruptured aneurysm, arteriovenous
      malformation, trauma
      b. Infectious meningitis and meningoencephalitis
      c. Paraneoplastic and autoimmune encephalitis
      d. Carcinomatous and lymphomatous meningitis