Cardiac Arrest, Coma, and Cerebral Death


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.


Bold refers to most common causes within that category



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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Sep 24, 2016 | Posted by in NEUROLOGY | Comments Off on Cardiac Arrest, Coma, and Cerebral Death

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