Sopor and coma
Last reviewed: 23.04.2024
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Sopor and coma - impaired consciousness due to dysfunction of both hemispheres of the brain or the ascending activating reticular system. Sopor is a state of areactivity from which the patient can only be withdrawn for a short time by intense restimulation. Coma is a state of areactivity from which the patient cannot be removed by stimulation. Causes may be local organic and functional cerebral (often metabolic). Diagnosis is based on clinical data; laboratory tests and neuroimaging are required to determine the cause. Treatment is an emergency stabilization of the condition and a targeted effect on the cause. With prolonged stupor or coma, supportive therapy includes passive movements in the range of motion in all joints, enteral nutrition, and prevention of bedsores. The forecast depends on the cause.
The wakefulness state requires full-fledged work of the cerebral hemispheres and the mechanisms of the ascending activating reticular system (VARS) - a wide network of nuclear connections in the upper part of the bridge, midbrain and posterior divisions of the interstitial brain.
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What causes spoor and to whom?
Various organic and functional disturbances in the work of the central nervous system result in sopor or coma. Depression of consciousness occurs due to dysfunction of VARS or both hemispheres of the brain; the defeat of one brain hemisphere leads to the development of severe neurological deficit, but not coma. With the deterioration of the lesion, the coma turns into a coma, and the coma leads to brain death. Among other forms of disturbance of consciousness are delirium (often characterized by agitation rather than inhibition), syncope and convulsive seizures; in the last two cases, the loss of consciousness is short-lived.
Organic lesions lead to the development of podor or coma by direct mechanical destruction of VARS or indirectly through the mass effect (compression, displacement) and / or edema. Unilateral massive focal lesion of the hemisphere (for example, cerebral infarction in the basin of the left middle cerebral artery) does not disturb consciousness, if the opposite hemisphere is not compromised or swells. Heart attacks of the upper part of the trunk in accordance with the volume of the lesion give varying degrees of stupor or coma.
Common Causes of Sopor and Coma
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The reasons |
Examples |
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Structural Violations |
Aneurysm rupture and subarachnoid hemorrhage Brain abscess brain tumor Traumatic brain injury (bruises, tears, crush of brain substance, epidural or subdural hematoma) Hydrocephalus (acute) Infarction or hemorrhage in the upper sections of the brain stem |
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Diffuse disturbances |
Vasculitis with CNS involvement Preparations and toxins (for example, barbiturates, carbon monoxide, ethyl alcohol, methyl alcohol, opioids) Hypothermia Infections (meningitis, encephalitis, sepsis) Metabolic disorders (for example, diabetic ketoacidosis, hepatic coma, hypoglycemia, hyponatremia, hypoxia, uremia) |
Hypoxia and cerebral ischemia are often included in the pathogenesis of sopor and coma. Mental disorders (for example, mutism) can mimic disorders of consciousness, but they are usually differentiated from true stupor or coma during physical and neurological examination.
Syndromes wedges. After infancy, the skull is hard, so that intracranial mass formations or brain edema lead to an increase in intracranial pressure, which is fraught with a protrusion of brain tissue through the natural openings of the bones of the skull or dura.
With a transtentorial insertion (involving the para-hippocampal gyrus hook), the temporal lobe bulges beyond the edge of the cerebellum tent (a tent-like structure on which the temporal lobe normally rests). The hook - the medial edge of the protruding lobe - presses on the diencephalon and the upper part of the trunk, causing ischemia and infarction of the tissues that are part of VARS. The insertion of both temporal lobes (central insertion) is usually associated with bilateral volumetric masses or diffuse edema and causes symmetric compression of the midbrain and trunk.
The involvement of the cerebellar tonsils is associated with infra-or supratentorial (less commonly) volumetric formations. The tonsils of the cerebellum, when inserted into the large occipital foramen, squeeze the brain stem and block the current of the cerebrospinal fluid, causing acute hydrocephalus. Vklineniya and under the parade, and in the large occipital opening threaten the patient's life.
In lateral dislocation, the cingulate gyrus penetrates under the large sickle of the brain.
Diagnosis of coma and stupor
Diagnosis and stabilization should be carried out simultaneously. First of all, it is necessary to ensure the airway patency, normalize the function of respiration and blood circulation. With rare respiratory movements or low O 2 saturation (according to the criteria of pulse oximetry or arterial blood gas composition), intubation is indicated. Correction of hypotension is necessary. Determine the glucose content in peripheral blood. With a low glucose level, 100 mg of thiamine is injected intramuscularly (to prevent the development of Wernicke's encephalopathy) and 50 ml of 50% glucose. If an opiate overdose is suspected, 2 mg of naloxone is administered intravenously. With signs of injury to radiographic exclusion of a fracture, the neck is stabilized with a rigid orthopedic collar.
The medial part of the temporal lobe is inserted through the cerebellar lip. The usual reason is ipsilateral surround education. The ipsilateral nerve of the third pair (unilateral expansion and fixation of the pupil, paresis of the eye muscles), the posterior cerebral artery (homonymous hemianopsia) and the contralateral pedicle of the brain (ipsilateral hemiparesis) are primarily compressed. Then a picture of squeezing of the midbrain and trunk develops, manifested by impaired consciousness, pathological breathing, pupil fixation in the central position, loss of oculocephalic and ocular-vestibular reflexes (the eyes do not shift when the head is rotated and the caloric test), the development of symmetrical paresis with decerebration rigor orchem., Cushing's reflex appears (arterial hypertension, especially systolic and bradycardia). The displacement of both temporal lobes (central incision) is usually associated with bilateral volumetric formation and leads to symmetric compression of the midbrain and trunk with the symptoms already described.
The involvement of the cerebellar tonsils is a consequence of infra-or supratentorial (less commonly) bulky structures. Entering into the large occipital foramen, the tonsils of the cerebellum squeeze the brain stem and block the CSF current with the development of acute hydrocephalus. Symptoms include: lethargy, drowsiness, headache, vomiting, meningism, uncomfortable eye movements, sudden respiratory arrest and heart function.
Anamnesis. Medical identification bracelets, the contents of a handbag or wallet may contain useful information (for example, documents, drugs). Relatives, SMP personnel, the police should be interviewed about the circumstances of the incident (for example, convulsions, headache, vomiting, head injury, medication or drugs), to find out the situation in which the patient was found; food packaging, alcohol, drugs, narcotic and toxic substances should be inspected and stored for chemical analysis and as possible material evidence. Relatives should be interviewed for recent patient infections, mental problems, and medical history. It is advisable to see the medical records.
Objective examination. Medical examination should be focused and effective. Among the signs of traumatic brain injury are paraorbital hematomas ("raccoon eyes", synonymous with "symptom of glasses"), bruises behind the ears (Battlel sign), hematotympanum, upper jaw mobility, nasal and / or otolikvoreya. Bruises of the soft tissues of the head and small entrance bullet holes are often subtle. It is necessary to examine the fundus of the eye for edema of the disks of the optic nerves, hemorrhages and exudate. With passive flexion of the neck (if it is proven that there is no injury!), Stiffness may be determined, indicating subarachnoid hemorrhage or meningitis. Until a fracture has been ruled out (according to anamnesis, physical examination, and X-rays), the cervical spine should be immobilized.
Increased body temperature or petechial rash suggest the presence of CNS infection. Traces of injections raise the question of overdose of drugs (for example, opioids or insulin). Bite tongue indicates a convulsive fit. A peculiar odor may indicate alcohol intoxication.
Neurological examination. A neurological examination determines whether the brain stem is damaged or not and where the lesion is located in the CNS. The state of consciousness, pupils, eye movements, respiration and motor activity help determine the level of CNS dysfunction.
Attempts are made to wake the patient first with verbal commands, then with slight irritation and, finally, with painful stimuli (for example, pressing on the eyebrow, nail bed or sternum). On the Glasgow Coma scale, responses to stimuli are rated by the number of points. Opening of the eyes, grimaces and purposeful withdrawal of the limbs in response to a painful stimulus indicate a relatively mild degree of impairment of consciousness. Asymmetric locomotor activity in response to pain irritation indicates focal lesions of the cerebral hemispheres.
When a sopor goes into a coma, pain stimuli cause only the formation of stereotypical reflex postures. The decortication posture (flexion and adduction of the arms, stretching of the legs) indicates damage to the cerebral hemispheres, including corticospinal tracts, while maintaining the brainstem. Decerebral rigidity (neck, back, limbs unbent, jaws clenched) implies the defeat of the upper sections of the brain stem. Sluggish paralysis without any movement is a manifestation of a severe lesion along the entire nervous axis; this is the worst variant of impaired motility. Asterixis (fluttering tremor) and multifocal myoclonus accompany metabolic disorders, such as uremia, liver failure, hypoxia and drug intoxication. In the case of mutism, the motor response is absent, but muscle tone and reflexes are preserved.
When the tentorial insertion of the temporal lobe displacement in the first place, squeezes the ipsilateral nerve of the third pair (unilateral expansion and fixation of the pupil, paresis of the eye muscles); posterior cerebral artery (homonymous hemianopsia) and the opposite leg of the brain (ipsilateral hemiparesis). Then develops a picture of compression of the midbrain and trunk, manifested by impaired consciousness, abnormal breathing, pupil fixation in the central position, loss of oculocephalic and oculovestibular reflexes (the eyes do not move when the head is rotated and caloric test), the development of bilateral paresis with decerebration rigor orchemia. Cushing reflex (arterial hypertension, especially systolic, and bradycardia). Symptoms of squeezing of the midbrain are also manifested with central implantation.
When the cerebellar tonsils are inserted, symptoms include lethargy, headache, vomiting, meningism, non-conjugated eye movements, sudden respiratory arrest and cardiac activity.
Ophthalmological examination provides information on the work of the brain stem. The study includes pupillary reflexes, analysis of eye movements, ophthalmoscopy (for edema of the discs of the optic nerves and hemorrhages), evaluation of other neuro-ophthalmologic signs. Immobility of the pupils is an early manifestation of an organic lesion, and with metabolic coma the pupillary reflexes remain intact for a long time.
If there are no eye movements, check the oculocephalic reflex using the “eye of the doll” technique: observe eye movements during passive turns of the patient's head from side to side. Normally, a person in the consciousness of the movement of the eyes follows the movements of the head. In case of injury, this technique cannot be performed until a fracture of the cervical spine is ruled out. If the consciousness is depressed and the brain stem is not damaged, then when turning the head, the gaze seems fixed on the ceiling. With the defeat of the brain stem, the eyes shift with the head, as if they are fixed in the sockets.
In the absence of an oculocephalic reflex, an oculo-vestibular reflex is investigated (cold caloric study). After confirming the integrity of the tympanic membrane, it is irrigated for 30 s through the external auditory canal with ice water in an amount of 10-40 ml, using a syringe and a soft catheter. In response to a patient who is conscious (for example, in a psychogenic coma), the eyeballs are deflected to the side where the water is injected, and the nystagmus beats in the opposite direction. In a coma, while preserving the functions of the trunk, both eyes also bow to the side of irritation, but without nystagmus. With organic lesion of the trunk or deep metabolic coma, there is no reaction or it is unfriendly.
The nature of breathing. Dysfunction of both hemispheres or diencephalon is manifested by periodic cyclical breathing (Cheyne-Stokes or Bio); dysfunction of the midbrain or upper parts of the bridge is accompanied by central neurogenic hyperventilation with a respiratory rate of more than 40 in 1 min. Damage to the pons or medulla oblongata usually leads to long deep breaths (apneastic breathing), often turning into apnea.
Research. Begin with pulse oximetry, analysis of peripheral blood for glucose and monitoring of cardiac activity. They take a clinical blood test with the definition of leukocyte formula and platelets, samples for biochemistry, electrolytes, clotting and urea nitrogen. Determine the gas composition of arterial blood and, if the diagnosis is unclear, check the level of carboxyhemoglobin, sulfhemoglobin and methemoglobin.
Blood and urine smears should be stained Gram, take crops, conduct standard toxicological screening, determine the level of alcohol. Often, more than one drug is taken at the same time, so if you suspect drug poisoning, usually several drugs are determined at once (for example, salicylates, paracetamol, tri-cyclic antidepressants). It is necessary to remove the ECG in 12 leads.
When the cause is not clear, emergency CT scan of the brain without contrasting is indicated to exclude volume formation, hemorrhage, edema, and hydrocephalus. If questions remain, add contrasting, after which a CT scan or MRI can reveal a subdural hematoma in the isosensual phase, multiple metastases, thrombosis of the sagittal sinus, herpetic encephalitis, and other possible causes that are not detected by conventional CT scanning. Radiography of the chest is also shown.
If an infectious disease is suspected, a lumbar puncture is performed to assess the pressure of the CSF. In CSF, cell types and their quantity, protein, glucose, are sown, Gram-stained, special indications are performed (for example, cryptococcal antigen, VDRL for syphilis, PCR to detect herpes simplex virus). In unconscious patients before performing lumbar puncture, CT is required to exclude extensive intracranial formation or occlusive hydrocephalus, since in such cases a sharp decrease in the pressure of the cerebrospinal fluid during lumbar puncture is fraught with the danger of a lethal accident.
If the diagnosis is unclear, EEG can help: in rare cases, sharp waves or peak complexes - a slow wave indicate that the patient is in the epistatus, although there are no external cramps. But in most cases, nonspecific slow low-amplitude waves, common for metabolic encephalopathy, are seen in a coma on EEG.
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What do need to examine?
How to examine?
Prognosis and treatment of coma and stupor
The prognosis for sopor or coma depends on the cause, duration and degree of depression of consciousness. A score of 3-5 on the Glasgow coma scale after injury indicates fatal brain damage, especially if the pupils are fixed or not with ocular vestibular reflexes. If, 3 days after the cardiac arrest, the reaction of the pupils did not appear, the motor responses to painful stimuli, the patient has virtually no chance of a favorable prognosis in neurological terms. When coma is associated with an overdose of barbiturates or a reversible metabolic disorder, even in cases where all stem reflexes have disappeared and there are no motor reactions, the possibility of complete recovery is preserved.
In parallel with the diagnostic process, it is necessary in the emergency mode to stabilize the state and maintain vital functions. In most cases of stupor and coma, hospitalization in the intensive care unit is necessary to ensure mechanical ventilation and monitor neurological status. The specific treatment depends on the cause of the condition.
Intravenous administration of 25-100 grams of mannitol, endotracheal intubation and mechanical ventilation, providing PC0 2 in arterial blood of 25-30 mm Hg, are shown at the insertion. When a tumor is associated with a brain tumor, glucocorticoid injection is necessary (for example, 16 mg of dexamethasone intravenously, then 4 mg orally or intravenously every 6 hours). Surgical decompression in a mass should be performed as soon as possible.
Patients in sopor and coma need careful and long-term care. The use of stimulants and opiates should be avoided. Feeding begins with taking action against possible aspiration (for example, raising the headboard); if necessary, impose eynostoma. For the prevention of pressure sores, attention should be paid to the integrity of the skin in places of high pressure on the skin from the very beginning of the disease. For the prevention of drying of the conjunctiva used topical preparations. To prevent contractures of the limbs, perform passive movements within the capabilities of the joints.
Prognosis of coma and sopor
Prognosis with sopor or coma depends on the cause, duration and degree of depression of consciousness. 3-5 points on Glasgow coma scale after injury indicate fatal brain damage, especially if pupils are fixed or there are no oculo - vestibular reflexes. If there were no reaction of pupils, motor responses to painful stimuli after 3 days after cardiac arrest, patient has virtually no chance of favorable prognosis in neurological terms. When coma is associated with overdose of barbiturates or reversible metabolic disorders, even in cases, when all stem reflexes disappeared and there are no motor reactions, possibility of full recovery is maintained.