MED 7721: Neurologic Exam of Comatose Patients

• The presented material is part of MED 7721 Clinical Neurology
• It is about approaching a patient with a neurologic issue, specifically neurologic examination of unconscious or comatose patients and evaluation for brain death
• The presentation is given by Reynaldo B. Sta. Mina, Jr., M.D.

Learning Objectives

• How to perform a neurologic examination on an unconscious or comatose patient
• How to evaluate a comatose patient for “brain death”

Examination of the Unconscious or Comatose Patient

• General physical and neurologic exams, looking for signs of trauma, blood pressure and temperature abnormalities, meningeal irritation, and optic fundi

General Physical Examination

• Inspection of head to reveal signs of trauma of basilar skull fracture
• Palpation of the head to demonstrate a depressed skull fracture or soft tissue swelling at the site of trauma
• Evaluation of Blood Pressure - elevated for long-standing hypertension, or as a consequence of the process causing the coma
• Evaluate Temperature:
  • Hypothermia may be caused by ethanol or sedative drug intoxication, hypoglycemia, Wernicke encephalopathy, hepatic encephalopathy, myxedema and exposure
  • Hyperthermia may be seen in heat stroke, status epilepticus, malignant hyperthermia , anticholinergic drug intoxication, pontine hemorrhage, and hypothalamic lesions.
• Signs of meningeal irritation such as such neck stiffness, may suggest meningitis or subarachnoid hemorrhage, but these signs are lost in deep coma

Neurologic Examination

• Pupils evaluation to determine etiology diagnosis in comatose patients
• Normal pupils are typically 3 to 4 mm and equal in size
• Constrict briskly and symmetrically in response to light, characteristic of a metabolic cause
• Thalamic pupils are slightly smaller (~2 mm) reactive pupils present early in thalamic compression
• Thought to be due to interruption of the descending sympathetic pathways
• Fixed, dilated pupils are pupils greater than 7 mm in diameter and fixed - usually result from compression of the oculomotor (III) cranial nerve or drug intoxication
• The common cause is transtentorial herniation of the medial temporal lobe from a supratentorial mass
• Fixed, midsized pupils are fixed at approximately 5 mm due to brainstem damage in the midbrain
• Pinpoint pupils are pupils (1-1.5 mm)
  • Usually indicate opioid overdose or a focal pontine lesion
  • Can also be caused by organophosphate poisoning, miotic eye drops, or neurosyphilis (Argyll-Robertson pupils).
• Asymmetric pupils are pupillary size asymmetry (anisocoria)
  • A difference of 1 mm or less in diameter is a normal finding that occurs in 20% of the population

Eye Movements Testing

• Begins at the pontomedullary junction (vestibular [VIII] nerve and nucleus), synapses in the caudal pons (horizontal gaze center, VI nerve nucleus), up through the brainstem reticular activating system (medial longitudinal fasciculus), arrives to the contralateral midbrain (oculomotor [III] nucleus and nerve).
• Stimulating the semicircular canals of the middle ear helps test comatose patients’ eye movements by passive head rotation (oculocephalic reflex) or ice-water irrigation (oculovestibular reflex)
• The eyes should move in the direction opposite to that of head rotation
• A more potent stimulus includes irrigating one tympanic membrane with ice water
  • It is contraindicated is the tympanic membrane is perforated

Motor Response to Pain

• Assessed by strongly applying pressure on the supraorbital ridge, sternum, or nail beds
• Response can indicate whether the condition affecting symmetrical parts of the brain (typical of metabolic and diffuse disorders) versus asymmetrically (unilateral structural lesions)
• The motor response to pain may help localize cerebral dysfunction or guide the depth of coma
  • Localization by reaching may occur with moderate severity dysfunction
  • Movements involving limb abduction almost never represent reflex movements
• Decorticate response involves flexion of the arm at the elbow, adduction at the shoulder, and extension/internal rotation of the leg and ankle
  • Classically associated with lesions that involve the thalamus or large hemispheric masses compress the thalamus
• Decerebrate response is extension at the elbow, internal rotation at the shoulder and forearm, and leg extension
  • Tends to occur when brain dysfunction is at the midbrain level
  • Indicates more severe brain dysfunction than decorticate posturing

Glasgow Coma Scale

• Using a numerical scale it is easy to notice changes in the examination over time and compared between different examiners, including pupillary, eye movement, and motor responses

Findings Associated with Specific Lesions

• Supratentorial, Infratentorial, metabolic, or diffuse lesions produce characteristic symptoms that can aid in diagnosis
• Supratentorial structural lesions can cause coma if they are acute or cause significant lateral brain displacement
  • Transtentorial herniation includes downward brain displacement/brainstem dysfunction which interrupts the activate system - respirations may progress, and decorticate posturing may progress to decerebrate and then unresponsiveness
  • Unilateral oculomotor palsy may change to complete eventually with circulatory collapse and death
• Lesions may include trauma, stroke, infection and neoplasm
• Infratentorial structural lesions can cause downward herniation through the foramen magnum with compression of the medulla, apnea, and circulatory collapse
  • Suggested on the basis of crossed cranial nerve and long-tract signs, miosis, dysconjugate gaze, ophthalmoplegia, or ataxic breathing.
• Metabolic, diffuse, or multifocal encephalopathy, mental and respiratory abnormalities tend to occur early
  • May include tremor, asterixis, or multifocal myoclonus.
  • Except in poisoning or brain damage, the pupils are not reactive

Brain Death Evaluation

• Absence of clinically detectable brain functions when the immediate cause is irreparable
• The absence of potentially confounding factors
  • Neuromuscular blocking agents and deep sedation
  • Severe metabolic disturbances
  • Hypothermia
• Etiology includes severe injury to the brain, including the brainstem and both cerebral hemispheres, that leads to irreversible whole brain destruction
• Including trauma, hypoxic-ischemic injury, stroke and intracranial infection

Clinical Features

• Coma without cerebral motor response to pain below and above the neck
• No oculocephalic and oculovestibular reflexes
• Pupils don't response to light
• Apnea

Apnea Testing

• Must be confirmed by a formal testing:
• Core temperature needs to be >=36°C; systolic blood pressure >=100 mmHg; normal SpO2; PCO2 >35 mmHg
• Connect a pulse oximeter and pre-oxygenate with 100% O2 for at least 10 minutes, then discontinue ventilator support
  • Visually monitor for chest wall movement
• Draw arterial blood gas after approximately 8–15 minutes and reconnect the ventilator
• If respiratory movements are absent and arterial PCO2 is >60 mmHg, it supports the diagnosis of neurologic death
  • If <60 mmHg or <20 mmHg over baseline PCO2, the result is inconclusive
• Terminate immediately if spontaneous respiratory movements, hemodynamic instability i.e. hypotension, hypoxemia, arrhythmia are observed

Signs of brainstem function absent and not misinterpreted

• Spinal extremity movements, shoulder elevation and adduction, back arching
• Autonomic responses such as sweating, tachycardia
• Up-going plantar responses

Diagnosis

• Protocol for determining brain death may vary by country and by institution
  • Made on the basis of repeated assessments after an interval of no less than 6 hours in adults
  • Inability to exclude reliably potentially confounding conditions requires confirmation by an ancillary test

Established Ancillary Tests for Brain Death Confirmation

• Conventional catheter-based cerebral angiography show absent intracranial flow above the skull base
• Radionuclide brain imaging shows absent brain blood flow
• Transcranial Doppler ultrasound shows oscillating flow or short systolic spikes in both hemispheres/foramen magnum
• EEG shows electrocerebral silence

YouTube Video Link

• Neurologic Examination of the Unconscious Patient available on YouTube