persistent coma

Introduction

Introduction to prolonged coma Prolonged coma refers to a long-term coma after a patient's injury (for more than 3 months), and the loss of normal response to the outside world, which may be manifested as decortical syndrome, apathic mutism or plant survival, as this is a Very special coma, more people call it "syndromeinsearchofaname". basic knowledge The proportion of illness: 0.003% Susceptible people: no specific population Mode of infection: non-infectious Complications: hemorrhoids primary brain stem injury brain contusion

Cause

Cause of persistent coma

(1) Causes of the disease

Prolonged coma is due to primary or secondary brain stem injury, sustained increased intracranial pressure causes severe cerebral cortical ischemia, hypoxia, extensive and heavier brain contusion, axonal injury, brain resuscitation Caused in time.

(two) pathogenesis

1. Cortical cell damage occurs extensively irreversible degeneration and necrosis, in a state of inhibition, while the lower function of the subcortical central and brain stem damage has been restored, the patient may have a cortical state, and both functions are not restored. Cortical rigidity.

2. The reticular activation system of the upper part of the brain stem and the thalamus is damaged, and the cerebral hemisphere and its conduction pathway are not damaged when there is a motionless mutism, also known as blink coma.

3. Under the cortex and the cortex, when the brain stem is seriously damaged, the patient is brain dead or living in a plant.

According to Jennett (1976), in patients with severe brain trauma and deep coma, if the eyeball is still swimming, about 31% will eventually become vegetative or die; if the eye activity is reduced, 64% of them will be vegetative or die; It is as high as 95% for the complete disappearance of eye movements. It is also found that about 63% of these patients die or are in a vegetative state if they have only a retractive response to painful stimuli; if there is only an extension reaction or complete relaxation of the limbs, it is as high as 83%. .

Prevention

Protracted coma prevention

Should pay attention to the initial treatment of craniocerebral injury, timely cardiopulmonary resuscitation, reduce intracranial pressure, prevent brain edema, rescue cerebral palsy, improve microcirculation is expected to reduce the incidence of persistent coma.

Complication

Prolonged coma Complications, acne, primary brain stem injury, brain contusion

Due to prolonged bed rest, it is easy to have pulmonary infection, hemorrhoids, etc., and can also be complicated by primary or secondary brain stem injury, extensive and heavier brain contusion, and axonal injury.

Symptom

Prolonged coma symptoms Common symptoms Awakening state loss of sedation, anaesthetic coma, coma, coma, deep coma

Most patients are persistently unconscious after severe brain injury, or due to excessive damage to the primary brain stem; or intracranial hemorrhage, secondary brain stem damage caused by cerebral palsy; or severe cerebral ischemia caused by persistent intracranial hypertension Oxygen deficiency; even after a respiratory arrest and resuscitation, after the rescue, although the condition gradually stabilized, the intracranial pressure returned to normal, but the consciousness was in a long-term coma. After the injury, the patient was deeply comatose and painful. When the extremities are stretched and straightened, the cortex is straightened. After 1 to 2 months, the pain is stimulated, and the blinking action gradually appears. Then there may be instinctive spontaneous blinking, or a purposeless eye movement. However, they can't follow the activity and have no reaction to the language. At the same time, the original cortical rigidity disappears, and there is a slow limb retraction response to pain stimulation, and the muscle tension is still strong, and often has a strong grip. , sucking, grinding and chewing, etc., the patient has obvious wake and sleep rhythm, indifferent to the external environment, sometimes the eye can follow the movement of people or things, but lacks purposeful action, can not automatically adjust In the prone position, do not take the initiative to eat, check the muscle tension of the limbs, the upper limbs are mostly flexed, the passive stretch can have painful expression, occasionally paralyzed, both lower extremities internal rotation, adduction, placed in the extension or bend Position, bilateral paw flexion, shallow reflex examination, abdominal wall reflex disappeared, but often cremaster reflex still exists, corneal reflex, pupil photoreaction, swallowing and cough reflex.

Examine

Protracted coma

EEG

The EEG is obviously abnormal, showing diffuse high-slow wave activity or a low-amplitude 89Hz -wave, which is obvious in the forehead and central area, and has no response to external stimuli such as sound, light, pain, passive blinking, etc. Wave coma.

2.CT, MRI

There may be a whole cerebral hemisphere, basal ganglia and cerebellar white matter area with broad low density or long T1 long T2 signal. The midbrain, pons may have hemorrhage, softening the foci, and the medulla is often intact. Finally, with the development of brain atrophy, sulcus may appear. , pool widening, ventricular enlargement and other changes.

Diagnosis

Diagnosis of persistent coma

diagnosis

Diagnosis relies on typical clinical manifestations, longer than 3 months of coma and EEG and CT, MRI changes.

The diagnosis of persistent coma depends mainly on its unique clinical signs. At the same time, it should be combined with injury, coma time and auxiliary examination to confirm the diagnosis. EEG examination of such patients is often severe abnormality. CT and MRI also help diagnosis. .

Differential diagnosis

Atresia syndrome

Also known as the efferent state, because the head and neck injury involving the brain stem or vertebral-basal artery, also known as false coma or pons ventral syndrome, the patient's consciousness is clear, can communicate with the outside world through eye movements, can The language responds and can follow the movement of the eye, while the patients in the vegetative state are unconscious, unable to communicate with others, not to blink, close the eyes, sometimes in the acute phase after trauma, if the patient is still in a coma due to brain stem injury In the state, the two are more difficult to distinguish; however, when the condition gradually improves, the recovery process is always conscious, that is, although the consciousness has recovered but can not move, the mouth is lost, the swallowing and crying activities are silent, and the limbs are Soft state.

2. Hydrocephalus after trauma

Sustained coma after injury, hydrocephalus after traumatic brain injury was accompanied by significant increase in intracranial pressure. After ventricle puncture drainage or ventricular drainage and shunt, the condition improved rapidly. CT scan showed ventricular enlargement but cerebral sulcus and cerebral pool did not increase. It is wide and there is an interstitial edema around the ventricle, which can be distinguished.

3. Brain death

Patients with brain death have no response to all external stimuli, no spontaneous breathing, muscle relaxation, decreased body temperature, bilateral pupil dilation, fixation, photoreaction and corneal reflex disappear, EEG is a resting potential, which can be identified.

Usually the determination of brain death must include the following four points:

(1) At least 6 hours after continuous response to various stimuli.

(2) No spontaneous breathing and exercise for more than 1h.

(3) Both sides of the pupil dilated, fixed, photoreaction and corneal reflex disappeared.

(4) EEG tracing for more than 4 minutes, gain of 5V/mm or more, showing a flat wave EEG.

Of course, under special circumstances, cerebral angiography, nuclear angiography, CT-enhanced scanning and transcranial Doppler cerebrovascular scanning can be used to verify whether the cerebral blood circulation is interrupted, and the minimum observation time limit for determining brain death is not yet available. Uniform criteria, generally begin to detect brain death after artificial respiration for more than 12h after respiratory arrest, two clinical examinations are required at the time of diagnosis, with 6h or 12h in between.

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