Senile coma
Introduction
Introduction to senile coma Coma is a pathological state in which brain function is highly inhibited. The main feature is severe disturbance of consciousness, and the patient does not respond to all stimuli in and out of the body. Consciousness disorders and coma account for about 3% of all emergency cases, especially in the elderly, and should be actively treated and rescued. basic knowledge The proportion of illness: 0.005% Susceptible people: the elderly Mode of infection: non-infectious Complications: cerebral palsy, arrhythmia, respiratory failure
Cause
Cause of senile coma
(1) Causes of the disease
There are many reasons for coma. In addition to the secondary brain dysfunction caused by metabolic and other extracranial diseases, the common causes of neurology are as follows:
Diffuse brain lesions
(1) Various central nervous system specific or non-specific infections, such as encephalitis, meningitis and the like.
(2) extensive craniocerebral trauma.
(3) Subarachnoid hemorrhage.
(4) Drug poisoning.
2. Focal brain lesions
(1) Various intracranial space-occupying lesions:
1 brain abscess, subdural empyema or effusion, meningitis, encephalitis.
2 traumatic acute, chronic subdural hematoma, epidural hematoma, intracerebral hematoma, brain contusion, brain edema.
3 various intracranial tumors or metastases; 4 hypertension cerebral arteriosclerotic cerebral hemorrhage.
(2) Cerebrovascular disease:
1 brain hemorrhage.
2 cerebral infarction or brain embolism.
3 hypertensive encephalopathy.
(3) Increased intracranial pressure syndrome.
(4) status epilepticus and the like.
(two) pathogenesis
The maintenance of consciousness is a functional effect of the brain stem-brain-cerebral cortex closely related to each other. When the upper reticular activation system above the upper part of the pons is damaged, the disturbance of consciousness may occur. There may be three mechanisms:
1. The reticular structure above the upper end of the pons is damaged, and it is difficult to release the impulse to maintain the arousal state of the cortex, thus causing disturbance of consciousness.
2. The midbrain reticular structure-thalamic-cerebral cortical circuit is destroyed, and the upward impulse to maintain cortical excitability is lost.
3. The gray matter in the posterior region of the hypothalamus and the central midbrain is damaged, destroying the loop formed between the excited network structures and causing disturbance of consciousness.
In addition, the body's metabolic disorders such as ischemia, hypoxia, the norepinephrine synthesis is reduced or stopped, so that the excitability of the brain tissue, especially the brain tissue of the ascending inflammatory system, is extremely reduced, causing disturbance of consciousness, Various types of acidosis, especially metabolic acidosis (pH 7.O ~ 6.5), can stop the synaptic transmission of many brain tissues including agonistic structures, resulting in loss of functional association between reticular agonistic structures and cerebral cortex. Thus, a disturbance of consciousness occurs, and a serious person falls into a coma, which may be one of the important factors leading to coma caused by uremia, diabetes or other types of acidosis.
Brain tissue itself has metabolic disorders (such as insufficient energy supply in brain tissue during hypoglycemia) and poisoning (such as organic phosphorus, anesthetics and sedatives) can affect or inhibit the function of the upstream reticular activation system, causing disturbance of consciousness, and coma in severe cases. .
In the case of coma, some special dysfunctions may be associated, such as respiratory rhythm regulation and ventilatory function disorders; pupil size and responsiveness, and changes in motor behavior, so in the disturbance of consciousness, changes in central nervous system functional activities are certain The extent can be reflected from the EEG.
Prevention
Senile coma prevention
1. Strengthen care to prevent complications.
2. Life support therapy, washing, grooming, skin cleansing, eye care, cold and warm clothes, and toilet treatment should be based on the situation, scientific management according to the disease.
Complication
Senile coma complications Complications, cerebral arrhythmia, respiratory failure
Common complications include infection, increased intracranial pressure, and even cerebral palsy, and myocardial hypoxia, cardiac arrhythmia, cardiac arrest and respiratory failure.
Symptom
Symptoms of senile coma, common symptoms, fainting, coma, cold, sweat, weakness, deep coma, senile tremor, convulsion, arrhythmia, increased intracranial pressure, disturbance of consciousness
1. Classification to determine the extent of disturbance of consciousness. In 1974, Teasdale and Jennelt developed the Glasgow's Coma Scale (GCS), which is still in use.
The highest score is 15 points, the lowest score is 3 points, the higher the score, the better the state of consciousness, the scale is simple and easy to use, more practical, but the elderly are slow to respond, often low scores.
2. Performance and grading Coma is a serious disturbance of consciousness. According to its degree, it is generally divided into 3 levels, namely, shallow coma, coma, and deep coma.
(1) State of light coma (or drowsiness): The patient's consciousness is not clear, and there is no active response to external stimuli. Only when the pain is stimulated, there is a defensive reaction, sometimes it is ambiguous, no purpose shouting, no Any thinking content, closed eyes like sleep all day, no change in reflection, cough, swallowing, sneezing, cornea and other brain stem reflexes exist.
(2) coma: serious consciousness is not clear, no response to external stimuli, pain stimulation can not cause defensive reaction, no thinking content, no shouting, swallowing and cough reflexes are slow, sputum reflexes are weakened, and pathological reflexes often appear.
(3) Deep coma: The most serious disturbance of consciousness, all reflexes including sputum reflexes and brainstem reflexes disappear, muscle tension is low, and sometimes pathological reflexes disappear. Individual patients have gone to the brain or cortex.
In addition, there are 2 special coma states:
1 Inactive mutism (winked coma): for the thalamus, hypothalamus, upper brain stem, cerebral cortex or corpus callosum injury, while oculomotor function preservation, patient's eyeball rotation from time to time, directional reflection of sound and The blinking reflection of visual stimuli exists, but the response to pain stimuli is very slow. It may only cause defensive reflexes of the limbs. It does not speak, does not move, can't exchange ideas, has a long time to fall asleep, has sweating and body temperature disorders, and has more urine. For a vegetative state.
2 cortical state: the patient's eyes are often squatting, the limbs are cortical tonic (two upper limb elbow joints, wrist and knuckle flexion, two lower limbs straight extension, internal rotation, bipedal flexion), corneal reflex, directional reflex to sound stimulation Swallowing reflexes, etc. still exist, facial expressions and evasive reflexes of pain sensation are normal, or even hyperthyroidism, and there is a sobering reaction to sleep, which is also a vegetative state, which is caused by extensive damage of bilateral cerebral cortex or diffuse degeneration of white matter.
Examine
Senile coma
Blood routine
(1) White blood cells: Increased inflammation, infection, dehydration and other stress conditions should be considered; reduction of blood disease or hypersplenism should be suspected.
(2) Hemoglobin: Anyone suspected of anemia, who has internal bleeding should check this item.
(3) Platelet count: reduction should consider the possibility of blood diseases.
(4) Others: Those suspected of carbon monoxide poisoning should be tested for carbon monoxide qualitative test.
2. Urine routine
(1) A large amount of urinary protein, accompanied by red, white blood cell casts should consider uremia.
(2) urinary tribilis: urinary bilirubin (+), urinary biliary > 1:20 (+), suggesting liver damage.
(3) urine sugar and ketone body detection to identify diabetes or hypoglycemia coma, with or without ketosis or acidosis.
3. Feces routine
(1) Microscopic examination: diarrhea or suspected toxic dysentery should be taken for sputum microscopy, if necessary, enema or anal finger examination, and stool specimens should be taken.
(2) occult blood test, suspected of black stool or internal bleeding may be used for fecal occult blood test.
4. Cerebrospinal fluid examination
Cerebrospinal fluid examination should be performed for those suspected of central nervous system diseases.
(1) Increased pressure indicates an increase in intracranial pressure.
(2) routine and biochemical (protein, sugar, sodium chloride) examination, macroscopic or microscopic blood cerebrospinal fluid, if it can exclude puncture trauma, should consider intracranial hemorrhage; cerebrospinal fluid examination is normal and clinical hemiplegia, should consider ischemia Cerebrovascular disease; cerebrospinal fluid pressure is high and conventional biochemical normal, may be toxic or metabolic encephalopathy; leukocytosis in cerebrospinal fluid, suggesting infectious or inflammatory disease; cerebrospinal fluid cells are normal and protein is increased, it may be intracranial tumor , demyelinating disease or infectious polyradiculitis.
(3) Other examinations: Considering the cerebrospinal fluid manifestation of purulent meningitis should be used for Gram staining smear to find bacteria and culture and to determine drug sensitivity. It is suspected that tuberculous meningitis should be used for film smear acid-fast staining or amplification. Method (PCR) to find Mycobacterium tuberculosis, suspected fungal meningitis, should be centrifuged to stain the smear with ink to find fungi, in addition, cerebrospinal fluid can be used for a variety of immune tests such as immunoglobulin, syphilis reaction and a variety of neurotransmitter examination Can also be used for cell examination.
5. Other selective checks
Those suspected of organophosphorus poisoning should check blood cholinesterase activity; suspected diabetic coma should check blood sugar, urea nitrogen, carbon dioxide binding, blood gas analysis and blood potassium, sodium and chloride; suspected uremia should be Check urea nitrogen, creatinine, carbon dioxide binding and blood potassium, sodium, calcium and chloride; suspected hepatic encephalopathy should be blood ammonia and liver function; suspected pulmonary encephalopathy should check blood gas analysis and check pH; Those with heart disease should have ECG, echocardiography or ECG oscillography.
6. X-ray film inspection
If the coma is suspicious, take a skull X-ray film to find a skull fracture, chest X-ray film can find blood, pneumothorax, lung inflammation or tumor; abdominal X-ray film can exclude axillary gas or intestinal obstruction.
7. Other
Various angiography (gas brain, ventricle, angiography), B-mode ultrasound and Doppler vascular ultrasound images, radionuclide scanning, cerebral blood flow map, CT, magnetic resonance imaging (MRI) and other auxiliary examinations can help to understand the lesion And nature, the help of differential diagnosis is greater.
Diagnosis
Diagnosis of senile coma
Diagnostic criteria
History
You must ask your family, accompanying staff, etc. for medical history and grasp the characteristics to understand the basis of the disease.
(1) Current medical history:
1 Incidence: understanding the rapid onset of the disease, acute complications caused by chronic diseases such as acute cerebrovascular disease caused by hypertensive arteriosclerosis, A-S syndrome caused by sick sinus node, brain caused by intracranial tumor Hey, you can also be a sudden coma caused by poisoning, poisoning, hypoglycemia, etc.
2 changes in the condition: gradually increased coma is more common in metabolic or toxic encephalopathy and central nervous system infections, etc. These patients are often accompanied by primary symptoms before coma, symptoms can be light and heavy, head trauma into a coma, After waking up and then coma, consider the possibility of epidural hematoma.
3 accompanying symptoms: Before coma, pay attention to whether there is fever, headache, vomiting, hematemesis, hemoptysis, jaundice, edema, blood pressure changes, abnormal urine, convulsions, and the order of these symptoms and disturbance of consciousness.
(2) Past history: Asking patients for chronic diseases such as heart, lung, liver, kidney and other organs, with or without diabetes, high blood pressure and similar coma history, should be aware of whether patients use sleeping, sedative or psychotropic drugs on weekdays. History, as well as the time and dose of medication; the dose and time of insulin injection in diabetic patients.
(3) Environmental and on-site characteristics:
1 season: carbon monoxide poisoning should be considered in winter, shock coma caused by lung infection; heatstroke, food poisoning, toxic dysentery, etc. should be thought of in summer.
2 In the morning, the discoverer should think of carbon monoxide poisoning, hypoglycemia and coma, and take poison.
3 coma patients found in public places should pay attention to cerebrovascular accidents, cardiac arrest, A-S syndrome, epilepsy and so on.
4 The physical object around the patient: collect the unfinished tablets, dichlorvos or pesticides, and pay attention to the smell of the vomit.
5 pre-onset conditions: pay attention to the possible incentives for emotional changes.
6 Whether there is trauma, especially the history of head trauma and the investigation of the site where head trauma may occur.
2. Physical examination
(1) The cause and extent of coma should be quickly determined.
(2) Vital signs:
1 body temperature: there is infection, body temperature rises when inflammation, too high may be heat stroke, pons, ventricular hemorrhage, atropine poisoning, etc.; too low suggestive of shock, third ventricle tumor, adrenal cortex, hypothyroidism, hypoglycemia, etc. It can also be a frostbite or a sedative overdose.
2 pulse: too fast may be heart failure, shock, high fever, infection or hyperthyroidism; slowness suggests increased intracranial pressure, A-S syndrome or drug poisoning; weak weakness or shock or internal bleeding; heart disease.
3 Breathing: Changes in respiratory rhythm suggest different plane damage to the brain.
Deep and rapid breathing is seen in diabetic acidosis, called Kussmaul breathing, shallow and rapid regular breathing is seen in shock, in addition, cardiopulmonary disease or sleeping pills poisoning can cause respiratory failure.
(3) Odor: The alcoholic taste is acute alcoholism, the garlic smell is dichlorvos poisoning, the rotten apple flavor is diabetic acidosis, the liver smell is hepatic encephalopathy, and the urine smell is uremia.
(4) skin mucosa: pay attention to the color of skin mucosa, flushing is seen in inflammation and alcoholism, pale can be seen in blood loss, collapse, shock, hypoglycemia, anemia; yellow staining suggests hepatic encephalopathy or drug poisoning, also need to pay attention to other livers, Biliary, pancreatic and blood diseases; hairpins are seen in the heart, lung disease; cherry red is carbon monoxide poisoning; cold sweat is hypoglycemia, shock; dry skin is diabetic coma, dehydration, central hyperthermia, etc.; lip mucosa, tongue bite The injured suggest epilepsy.
(5) Head and face: pay attention to skin ecchymosis or scalp hematoma in the hair covering area, nostril, external ear canal discharge or bleeding is common in skull base fracture, double pupil diminishing suggesting sleeping pills or organophosphate poisoning, double pupil dilated in deep coma, Also seen in atropine drug poisoning; double pupils are not equal, may have cerebral palsy, ocular edema of the fundus, for increased intracranial pressure.
(6) Chest: heart expansion, valve murmur, heart rate is common in heart failure, arrhythmia is common in atrial fibrillation, atrial flutter, A-S syndrome, etc., barrel chest, percussion response enhanced, lip cyanosis, lung Auscultation with a voice, such as severe emphysema and lung infection, may be associated with pulmonary encephalopathy.
(7) Abdomen: Liver splenomegaly with ascites is often hepatic encephalopathy, abdominal distension and tenderness may be internal bleeding or paralytic ileus.
(8) Limbs: Muscle tremor is seen in organophosphorus poisoning. Both hands are toxic or metabolic encephalopathy. The clubbing suggests chronic heart and lung disease. There are horizontal white lines in the nails, which may be severe anemia or heavy metal poisoning. Both lower extremities can be depressed edema, which may be heart, liver or kidney disease.
(9) Nervous system: focus on checking meningeal irritation signs and vertebral body tract signs, including neck stiffness, Kernig sign, Babinski sign, etc., fever with meningeal irritation often indicates central nervous system infection, no fever and meningeal irritation is seen in the cobweb Hemorrhage in the subarachnoid, hemiplegia is more common in cerebrovascular disease or intracranial tumors.
Differential diagnosis
Whether the patient is in a coma needs to be differentiated from a seemingly comatose state.
1. The state of mental depression is often caused by intense mental stimulation after trauma or snoring. It is characterized by lying dead, no response to stimuli, closed eyes, open eyes and seeing the eyeballs turn upwards. The patient has no abnormal nervous system signs, often Excessive breathing, psychotherapy may be effective.
2. Patients with tension and stiffness are silent, do not move, refuse to eat, do not urinate, and do not respond to strong stimuli. In fact, they can perceive the surrounding things without consciousness disorder, and the brain stem reflex is normal. It is more common in schizophrenia. Hysteria and reactive psychosis.
3. The atresia syndrome is mainly the ventral dysplasia of the pons. The basal artery occlusion is more common. In addition to some eye movements, the patient has quadriplegia, can't talk and swallow, lacks expression, but understands language and movement. It is indicated by closed eyes or vertical movement of the eyes, indicating that the consciousness is clear.
