Supratentorial structural (20 % of total)
Infratentorial structural (15 % of total)
Metabolic and diffuse brain dysfunction (65 % of total)
Head trauma
Contusion with brain swelling
Subdural/epidural hematoma
Cerebrovascular disease
Brainstem ischemic stroke
Brainstem hemorrhage
Cerebellar ischemic stroke
Cerebellar hemorrhage
Drugs
Sedatives
Opioids
Tranquilizers and antidepressants
Anticonvulsants
Anesthetics
Cortical brain tumor
Primary or metastatic
Tumor
Brainstem
Cerebellar
Hypoxia
Cardiac or respiratory arrest
Severe anemia
Toxins (carbon monoxide)
Ischemic strokes
Massive stroke with brain herniation
Infectious
Brainstem abscess
Cerebellar abscess
Blood glucose abnormalities
Hypoglycemic coma from excess insulin
Hyperglycemic coma from diabetes mellitus
Brain hemorrhages
Intracerebral hypertensive hemorrhage
Arteriovenous malformation hemorrhage
Paraneoplastic syndrome
Brainstem encephalitis
Abnormal ionic CNS environment
Hypo/hyper blood sodium, potassium, calcium, magnesium, acidosis
Infectious or paraneoplastic syndrome
Encephalitis
Brain or epidural abscess
Limbic encephalitis
Organ diseases
Liver (hepatic coma)
Kidney (uremic coma)
Lungs (CO2 narcosis, respiratory failure)
Thyroid (myxedema coma)
Hypothermia (< 30 °C)
Diffuse intrinsic brain disorders
Subarachnoid hemorrhage
Status epilepticus or non-convulsive status
Brain co-factor deficiency
Thiamine (B1)
Cyanocobalamine (B12)
Pyridoxine (B6)
Poor cerebral perfusion
Hypertensive encephalopathy
Obstructive hydrocephalus
Bleeding with low blood volume
Decreased cardiac output (myocardial infarction, cardiac arrhythmia)
Toxins
Ethanol
Methanol
Ethylene glycol
Cyanide, etc.
Supratentorial structurally caused coma usually begins as a unilateral hemispheric mass that progressively expands to produce brain herniation (see Chap. 14 on brain tumors). As the herniation progresses across the tentorium, the upper brainstem pushes downward often rupturing and penetrating brainstem veins (Duret hemorrhages), producing fatal brainstem hemorrhages, and ischemia. Coma from infratentorial destruction can be from ischemic brainstem stroke or mass (hemorrhage or tumor) involving the brainstem or cerebellum, which directly damages or compresses the reticular formation.
Metabolic-caused coma primarily affects reticular formation neurons in the upper brainstem and thalamus but usually the entire brain is also affected. The mechanisms causing neuronal dysfunction vary widely from hypoxia, hypoglycemia, hypothermia, exogenous drugs or toxins, endogenous toxic molecules, acidosis, etc.
Major Clinical and Laboratory Features
There are three critical questions to be answered about a comatose patient. Where is the lesion? What is the cause? Is the coma stable, improving, or worsening? Generally, the physician first determines whether the etiologic category is supratentorial, infratentorial, or metabolic. The next step is to determine the cause within the etiologic category. Obtaining a history, including drug use, from a friend or relative is extremely helpful in placing the patient into an accurate category.
Table 16.2 gives the major clinical features found in each coma category. An elevated temperature and blood white count usually implies an infection (sepsis, pneumonia, or CNS) and a low temperature usually implies patient has been comatose in a cold environment for some period of time. Rapid regular breathing often denotes a metabolic acidosis from a metabolic cause. During the physical examination, attention should be paid to find signs of trauma (especially head or neck trauma), bleeding (external or internal), organ dysfunction (especially lungs, heart, kidney, thyroid), and sepsis. Since mentation, fine sensation, and coordination cannot be tested in a comatose patient, the neurologic exam focuses on spontaneous or pain-induced limb movements, breathing patterns, ocular findings, and cranial nerve function (Tables 16.2 and 16.3).
Table 16.2
Coma characteristics excluding that caused by head trauma
Characteristic | Supratentorial structural | Infratentorial structural | Metabolic |
---|---|---|---|
Early history | Signs suggesting dysfunction of the hemisphere (hemiparesis, hemisensory defect, aphasia, visual defect). Headaches common | Signs of cranial nerve dysfunction. Headaches and stiff neck may be present | Rapid onset (anoxia) or subacute progression (drugs, uremia, etc.). Patient looks asleep. Headaches uncommon. Fever may be present if sepsis or pneumonia present |
Breathing | Normal or Cheyne–Stokes (periodic cycles of rapid breathing followed by period of apnea) | Apneustic (deep inspiration, long pause, and prolonged exhalation at a rate about 5/sec) or ataxic (irregular, ineffective breathing that is often shallow) | Normal or rapid due to metabolic acidosis |
Early eye findings (See Fig. 16.1) | Pupillary light reflexes are present but pupil size may be small or unilaterally dilated. Papilledema may be seen. Vestibulo-ocular reflexes may be present or impaired | Pupil size often unequal and may be unresponsive to light (fixed). Eyes may not be parallel and vestibulo-ocular reflex is sluggish or absent. Papilledema is absent | Normal size and reaction to light, normal vestibulo-ocular reflexes, and no papilledema |
Motor (See Fig. 16.2) | Asymmetric spontaneous or pain-induced limb movements. Decorticate posturing (flexion of the arm and extension of the leg on the involved side) to pain may occur | Bilateral limb weakness or quadraparesis may be present. Decerebrate posturing (unilateral or bilateral extension of arms and legs) to pain seen in midbrain lesions | Symmetric spontaneous or pain-induced limb movements |
Reflexes | Often hyperactive with Babinski sign on contralateral side | Often normal or hyperactive. Babinski signs may appear | Normal or depressed. No Babinski signs |
Neuroimaging | Hemispheric mass (tumor, hemorrhage, abscess, stroke), shift of midline structures, brain herniation. Occasional obstructive hydrocephalus | Mass (tumor, hemorrhage, infarction) in brainstem or cerebellum, occasional cerebellar tonsillar herniation through foramen magnum | Normal |
Table 16.3
Bedside examination of cranial nerves in a comatose patient
Test | Cranial nerves tested | Testing method | Brainstem location tested |
---|---|---|---|
Papillary light reflex | 2, 3 | Normal: Bright light shined into one eye causes both pupils promptly to reduce in size. Large pupil that is fixed to ipsilateral and bilateral light implies damage to CN 3 | Midbrain |
Corneal reflex
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