Coma - Causes and Symptoms

Definition

Coma is a protracted loss of consciousness: the patient is in a state of non-responsiveness to common stimuli, from which he cannot be awakened. This condition depends on dysfunction of both cerebral hemispheres or damage to the ascending reticular formation (also known as the ascending activating reticular system, it is a complex of neurons specialized in the control of the waking state and the circadian rhythm). Coma is not a sign of brain death, that is, of irreversible cessation of all brain functions, but may evolve in this condition.

The coma can have different causes, structural (eg increased intracranial pressure and cerebral ischemia) and non (eg toxic disorders or metabolic imbalances). Furthermore, the state of unconsciousness may result from conditions that produce widespread effects (such as hypoglycemia, hypoxia, uremia and overdose) or focal conditions (a more rare occurrence; a unilateral focal hemispheric lesion can alter the consciousness, if the contralateral hemisphere is already compromised) . Based on the general characteristics, a calm coma (diabetic or intoxicated) or agitated (hypoglycemic, hepatic and uremic) is distinguished.

Coma calm

Calm coma is a protracted loss of consciousness characterized by the patient's immobility. It can be found as a complication of diabetes and some forms of intoxication (barbiturates, opiates, sedatives and other CNS depressants, carbon monoxide, cyanides, hydrogen sulphide and petroleum derivatives).

Diabetic coma is a slow and progressive onset condition, in which the loss of consciousness is associated with global dehydration (in particular, the eyes appear hollow and the mucous membranes dry), ketotic breath (similar to the smell of apples), elevated blood sugar and glycosuria.

Coma agitated

In agitated coma, the patient appears to be prey to psychomotor agitation and fine tremors or shocks. This form represents a medical emergency, as it puts the subject's life at risk and requires prompt hospitalization.

The agitated coma can manifest itself in hepatic and renal insufficiency of any origin. Intoxications from alcohol, strychnine, cocaine and amphetamines can cause a loss of consciousness associated with convulsions and clonic spasms.

In the hypoglycemic coma, the patient is agitated and disoriented, he writhes and manifests primitive movements (suctions, reeling and grimacing); moreover, profuse sweating, tachycardia and convulsions may occur, sometimes with mouth foaming.

Coma from focal lesions

In the brain, the structural alterations that can lead to coma include abscesses, neoplasms, traumas (eg concussion, lacerations or cerebral contusions, epidural or subdural hematoma), acute hydrocephalus, ischemia and hemorrhages. Prolonged unconsciousness can also result from convulsions and post-ictal state after an epileptic seizure.

Coma from widespread injuries

Coma can result from diabetic ketoacidosis, hepatic encephalopathy and hypoxia. Other metabolic causes include uremia, hypoglycemia, hypercalcaemia, hypercarbia, hyponatremia and Wernicke's encephalopathy.

Coma can also be a consequence of infections (encephalitis, meningitis and sepsis), hypertensive encephalopathy, diffuse axonal damage, hyperthermia or hypothermia.

Coma with neurological signs

Depending on the cause, the state of unconsciousness can be associated with other symptoms, such as ocular anomalies (miosis, hemianopia and loss of the oculo-cephalic reflex), ataxia, hemiparesis and respiratory dysfunction.

The neurological signs associated with coma also include stiffness of the neck (due to bacterial or viral meningitis or subarachnoid hemorrhage) and paralysis (apoplexy).

The apoplectic coma is characterized by the abrupt onset of a profound loss of consciousness, with lack of reflexes; the patient lies motionless and often presents a facial asymmetry. Apoplexy is caused by thrombosis, hemorrhage and cerebral embolism and head injury.