EXAMINATION OF THE COMATOSE PATIENT

OBJECTIVES:1.Understand the pathophysiologic mechanisms of

impaired consciousness. Distinguish between "structural" and "metabolic" causes/manifestations of coma.

2.Be aware of the differential diagnosis of coma.3.Be familiar with the basic clinical evaluation of

the comatose patient.4.Plan an algorithm to investigate and for the

management of a comatose patient.

CONSCIOUSNESS?

• WHAT IS IT?

CONSCIOUSNESS?

Consciousness represents the reciprocal interaction and successful functioning of two neural components:

1. The Ascending Reticular Activating System (ARAS)-- provides AROUSAL or A-WAKEFULNESS (ALERTNESS).

2. The cerebral cortex -- provides AWARENESS.Sufficient impairment of either of these two

"systems" (or both) produces coma.

COMA

Coma is characterized by the total absence of arousal and of awareness, must last 1 hr.

COMA 2 CATEGORIES

1.coma due to injury or compression of the ARAS = STRUCTURAL COMA

2.coma due to generalized impairment of cerebral cortex (+/- the brainstem) = METABOLIC COMA

In general, the former represents the more urgent emergency (more potentially life-threatening) than the latter.

CONSCIOUSNESS DISORDERS

• Patients in MCS have a severe alteration in consciousness but demonstrate wakefulness and cyclic arousal and intermittently demonstrate self or environmental awareness, such as following of commands, the ability to signal yes/no (regardless of accuracy), intelligible speech, or purposeful behavior.

Brain Death. Consciousness disorders must be distinguished from brain death, which is the irreversible loss of all brain and brainstem function, clinically diagnosed by demonstrating absence of consciousness, lack of motor response to noxious stimulus, and the disappearance of brainstem reflexes and respiratory drive (9).

• Coma is characterized by the total absence of arousal and of awareness.must

last 1 hr (10). • The vegetative state (VS) is notable for

preserved arousal mechanisms associated with a complete lack of self or environmental awareness Patients in a VS open their eyes spontaneously; however, there is no evidence of sustained visual pursuit (tracking) or visual fixation.

DISORDERS OF CONSCIOUNESS

COMA CAUSESBilateral or diffuse hemispheric disorders • Traumatic brain injury (contusions, diffuse axonal injury) CT HEAD• Ischemic (watershed, cardioembolism, vasculitis, hypercoagulable disorder) CT HEAD,HISTORY• Hemorrhagic (subarachnoid hemorrhage, intraventricular hemorrhage) CT HEAD• Hypoxic-ischemic encephalopathy CT HEAD• Cerebral venous thrombosis CT HEAD• Malignancy CT HEAD• Meningitis; encephalitis HSITORY CT HEAD LP• Generalized or complex partial seizures; status epilepticus (convulsive, nonconvulsive) HISTORY,EEG• Hypertensive encephalopathy HISTORY VITALS• Posterior reversible encephalopathy syndrome • Acute disseminated encephalomyelitis • Hydrocephalus HISTORY CT HEAD• Unilateral hemispheric disorders (with displacement of midline structures) CT HEAD• Traumatic (contusions, subdural hematoma, epidural hematoma) CT HEAD• Large hemispheric ischemic stroke CT HEAD• Primary intracerebral hemorrhage CT HEAD• Cerebral abscess CT HEAD HISTORY• Brain tumor CT HEAD• Brain stem disorders (pons, midbrain) MRI • Hemorrhage, infarction, tumor, trauma CT HEAD• Central pontine myelinolysis MRI• Compression from cerebellar infarct, hematoma, abscess, tumor MRI

COMA CAUSES

Systemic derangements causing comaToxic • Medication overdose/adverse effects (opioids,

benzodiazepines, barbiturates, tricyclics, neuroleptics, aspirin, selective serotonin reuptake inhibitors,acetaminophen, anticonvulsants) TOXICOLOGY SCREEN

• Drugs of abuse (opioids, alcohol, methanol, ethylene glycol, amphetamines, cocaine) HISTORY CLINICAL EXAM. ABG TOXICOLOGY SCREEN

• Exposures (carbon monoxide, heavy metals)

COMA CAUSES

Endocrine • Panhypopituitarism Acute hypopituitarism

(e.g., pituitary Apoplexy) - sudden headache, collapse, hypothermia, hypoglycaemia and hypotension - may be a life-threatening emergency.  Prompt steroid replacement.

• Adrenal insufficiency- ABG, Na, K, Glucose levels, serum ACTH,CORTISOL,ALDOSTERONE,RENIN

• Hypothyroidism; hyperthyroidism -TFT SCREEN

COMA CAUSESMetabolic• Systemic inflammatory response syndrome-sepsis HISTORY

CLINICAL EXAM. ABG • Hypoxia; hypercapnia ABG• Hypothermia HISTORY TEMPERATURE• Hypoglycemia; hyperglycemic crises (diabetic ketoacidosis,

nonketotic hyperosmolar hyperglycemic state) HISTORY BLOOD SUGAR URINE /SERUM KETONES

• Hyponatremia, hypernatremia ABG,U & E• Hypercalcemia ABG,Ca• Hepatic failure CLINICAL EXAMINATION,SERUM

AMMONIA,LFT, ABG,• Renal failure SERUM UREA CREATININE,ELECTROLYTES• Wernicke’s encephalopathy HISTORY,

HERNIATION

RAISED ICP

• This diagram shows four types of herniation.

• 1) The brain squeezes under the falx cerebri in cingulate herniation

• 2)The brainstem herniates caudally

• 3) The uncus and the hyppocampal gyrus herniate into the tentorial notch

• 4)The cerebellar tonsils herniate through the foramen magnum in tonsillar herniation.

Results of herniation

• The patient may become paralyzed on the same side as the lesion causing the pressure, or damage to parts of the brain caused by herniation may cause paralysis on the side opposite the lesion.

• Damage to the midbrain, which contains the ARAS network that regulates consciousness will result in coma.

• Damage to the VITAL centers in the medulla will cause respiratory and cardiac arrest.

1. What is the level of consciousness/coma? GCS

2. Is there evidence of impending herniation? PUPIL AND VITALS

3. Is brainstem function affected? VITALS4. Are there any focal findings that are helpful?

TONE, DEEP TENDON REFLEXES,GCS5. Clinical Patterns In general, the pattern of

brainstem/respiratory and motor findings can provide clues to the level or region of structural brain involvement

REFLEXES

PRIORITY

1. to promptly identify cases in which progressive herniation (rostrocaudal deterioration) will lead to further damage and death.

2. Similarly, early identification of toxic causes

separate metabolic from structural causes

1. toxic/metabolic comas are often of slower onset and may be preceeded by delirium.

2. respiratory impairment often occurs earlier in toxic/metabolic states.

3.pupillary responses and oculocephalic reflexes are more likely to be preserved in toxic/metabolic comas.

4. focal features are usually absent in toxic-metabolic comas.

5. tremor, asterixis and multifocal myoclonus usually limited to toxic-metabolic comas.

• REFERENCE Approach to the comatose patient Crit Care Med 2006 Vol. 34, No. 1