Coma is defi ned by a profound altered state of consciousness, linked to dysfunction of the reticular activating the brain stem responsible for the physiological arousal.
Violations of consciousness may be more or less marked (confusion, stupor, coma), but respond to similar causes.
In coma stage ultimate, there is no communication or opening of the eyes, and the patient may be difficult or not awake.
A coma may be the end of the evolution of a chronic progressive disease with altered consciousness or enter the context of a severe polytrauma.
IMMEDIATE MANAGEMENT OF A COMATOSE PATIENT:
Coma is an emergency that can quickly become life-threatening. Its management requires prompt recourse to a hospital structure resuscitation via EMS (center 15).
Meanwhile the emergency healthcare, the patient should be managed as follows.
Audit and Evaluation of the depth of coma:
a spontaneous eye opening Wanted or on demand, achieving a simple verbal order and reaction to painful stimulation.
The Glasgow scale (3-15 points) is the most practiced and allows, for its good reproducibility, to assess the state of consciousness and track its evolution. A score of 15 points testifies to the absence of impaired consciousness. The motor response is listed after painful stimulation.
Resistance to eye opening towards a post-critical oppositional demonstration or simulation.
The persistence of eye opening and tracking movements of the eyeballs evokes a “locked-in syndrome” (bilateral ischemic injury of the foot of the projection).
Assessment and life support:
The altered state of consciousness sounds on ventilation and permeability of the upper airway. The airway maneuvers release and the maintenance of satisfactory oxygenation are required.
When the coma is deep, without other vital disorders (respiratory or hemodynamic) in the recovery position setting reduces the risk of flooding bronchial pending a doctor able to perform endotracheal intubation.
Hemodynamic constants should be maintained if necessary by means of a filling.
The establishment of an IV is needed as soon as possible.
Performing a blood glucose:
The injection of glucose 30% must be achieved in doubt hypoglycemia, or if there is a diabetic patient treated with insulin or hypoglycemic sulfonamides.
If opiate overdose:
If the context is suggestive of an overdose of opiate (miosis, injection, etc.) Injection of naloxone (1/2 IVL bulb [slow intravenous]) can be performed in case of respiratory pauses.
Anamnesis:
The collection from the entourage or data on witnesses coma installation manual (circumstances, speed of installation), the presence of inaugural symptoms (fever, headache, convulsions, vomiting, neurological deficit, etc.)medication, drugs or alcohol, and the existence of a chronic underlying disease (respiratory, liver or kidney failure) is particularly useful for the further management of the patient.
CARE HOSPITAL:
The assessment and life support outweigh the etiological investigation.
Neurological research review as soon as ventilation and hemodynamic are controlled:
– A head injury went unnoticed;
– A tongue biting;
– A challenge cit focused;
– Stiff neck.
General symptoms, such as fever, rash or breathing abnormalities, are sought.
If the coma is deep, ocular study allows a lesional approach, specifying the light reflex, corneal and eye movements:
– Review of the pupil light reflex and represent the first policy element:
– A little reactive mydriasis in pupil evokes an expansive intracranial process,
– 2 pupils in mydriasis aréactives evoke severe midbrain injury or acute intoxication with anticholinergic,
– A bilateral reactive miosis is observed in metabolic encephalopathies and poisoning to opiates and barbiturates;
– Spontaneous and induced eye movements must be analyzed in search of a brain stem injury.
Eye divergence is normal. The abduction of an eye associated with mydriasis evokes a disorder of cranial nerve III and adduction, a violation of the VI. The “skew deviation” (a lower eye than the other) shows cerebellar lesion or pontic. A horizontal deflection conjugated shows a hemispheric lesion on the side of the deflection or contralateral lesion of the trunk;
– Corneal reflex (stimulation of the cornea with a cotton) normally results in bilateral eyelid occlusion. Its abolition reflects a Pontic abolition connections between the V and VII two.
Blood samples allow for complete biochemical analysis (glucose, calcium, renal and hepatic function, acidosis, osmolarity, etc.) And toxicological research (alcohol, drugs, carboxyhemoglobin, etc.).
Imaging by CT or MRI will be performed as soon as possible (CT), possibly associated with anelectroencephalogram (EEG) and a lumbar puncture if the origin of the coma is unknown or suspect to be neurological.
Causes of Comas:
Toxic coma:
The hypothesis of a poisoning, the most common cause is suspected in any coma. Mark toxic in the blood and urine is systematic and can be supplemented by mass spectrometry.
Pharmacological comas are voluntary or associated with accidental overdose. Barbiturates are responsible for a peaceful coma, respiratory depression with hypotonic; tricyclic antidepressants cause a coma with mydriasis and risk of arrhythmias and seizures.
Exogenous causes to look for are: carbon monoxide poisoning, acute alcoholic, organophosphates, opiate overdoses (coma, miosis tight reactive, respiratory depression, pitting).
Metabolic coma:
Metabolic attacks generate vigilance disorders ranging from confusion to coma (rapid progression), with suggestive history:
– Respiratory encephalopathies (anoxic or hypercapnia), liver (hyperammonemia) and kidney (azotemia), where the vigilance disorders are associated with abnormal movements (asterixis, clonus, rigidity);
– The deficiency encephalopathy (Wernicke deficiency in vitamin B1) or accompanying endocrine disorders (severe hypothyroidism, adrenal crisis);
– Other metabolic abnormalities (severe hyponatremia, rapid changes in serum calcium, diabetic hyperosmolar coma, hypoglycemic coma, etc.).
Whatever the cause of a coma, metabolic factor can be superimposed.
Neurological Coma:
A sudden coma evokes meningeal bleeding, cerebral hematoma, or brain stem infarction; other intracranial causes give more readily vigilance disorders secondary to evolving a deep coma. Cerebral infarction is the cause of a disturbance of consciousness with that when massive cerebral edema and temporal commitment.
The prognosis is then very dark.
When the clinical examination finds the location of signs (focal deficits challenge), brain imaging (CT or MRI) to search for elements:
– A h cerebral émorragie;
– Vascular ischemic attack;
– Does a cerebral thrombophlebitis of the superior sagittal sinus or vein of Galen;
– Hypertensive encephalopathy or occupant process with intracranial hypertension (or secondary primary tumors Supratentorial or sub-tentorial, chronic subdural hematoma, brain abscess, etc.).
Meningeal involvement (stiff neck) should be systematically sought. But when the coma is deep, stiff neck may disappear. Lumbar puncture will make the diagnosis; it is carried out before all unexplained vigilance disorders.
Febrile patient with in the presence of purpura or if a scanner is carried out before the lumbar puncture (localizing sign), the first antibiotic injection is performed immediately.
Outside a febrile context, subarachnoid hemorrhage be sought by a brain scan (blood scanner in the subarachnoid spaces) supplemented by a lumbar puncture. The causes are mainly related to aneurysmal malformations of Willis.
A seizure, even in the absence of concept of tonic-clonic seizure is suspected in a loss of urine, tongue biting, a stertorous breathing.
The post-critical phase of a crisis of epilepsy rarely exceeds 20 to 30 minutes before returning to normal consciousness. In addition, consider a traumatic complication, vascular, tumor, infectious, toxic or metabolic.
In the absence of clinical convulsive phenomena, the hypothesis of a state of non-convulsive epilepticus justifies conducting an EEG (paroxysmal activity subclinical).
Differential diagnosis of coma:
A patient who keeps his eyes open but does not obey the orders is not in a coma.
If he is able to mobilize, it can be a global aphasia or a hallucinatory psychosis or challenge cit. If it does not move, we can evoke a “locked-in syndrome” or akinetic mutism (bilateral frontal damage).
The diagnosis of hysterical coma is more delicate.
The patient :
– do not talk ;
– not moving ;
– And keep your eyes closed.
Wanted phenomena opposition (resistance to lifting of eyelids, avoidance, background tone at the sudden mobilization contrasts with the lack of responsiveness to noxious stimuli, etc.).
TREATMENT:
Available treatments essentially depend on the etiology of coma associated with the prevention of superimposed lesions.
Hyperthermia, hypoglycemia, hypercalcemia, hypercapnia and hypoxia should be corrected as soon as possible.
Hemodynamics is maintained by fluid resuscitation and vasoactive drugs.
The correction of metabolic disorders is done case by case.
Mechanical ventilation with endotracheal intubation is systematic, due to the risk of inhalation when the Glasgow score ≤ 7. One can stay where rapid improvement is expected: antidote naloxone kind (NarcanR) for opiates and alcohol or flumazenil (AnexateR) for benzodiazepines, post-critical phase of a seizure.
Due to the poor prognosis of consciousness disorders associated with ischemic stroke, intubation should be discussed based on the neurological prognosis.
