Infection-induced coma

Introduction Acute coma is common in people with infection. These infectious diseases include: 1 viral infections: such as epidemic encephalitis, forest encephalitis, meningoencephalitis, enteroviral encephalitis, epidemic hemorrhagic fever, encephalitis-type influenza, etc.; Infection; 3 parasitic infections: such as cerebral malaria, acute cerebral schistosomiasis, diffuse cerebral cysticercosis, etc.; 4 infectious toxic encephalopathy: such as toxic pneumonia, toxic dysentery, sepsis, etc.; 5 spirochete infection.

Cause

First, the medical history question

1. Focus on understanding the urgency and onset of coma. Acute onset is common in trauma, infection, poisoning, cerebrovascular disease and shock.

2, to understand whether coma is the first symptom, if it occurs in the course of the disease, you should know what is the disease before coma. For example, diabetic patients may have hyperosmolar coma and hypoglycemia coma, liver cirrhosis patients may have hepatic coma, hyperthyroidism patients may have hyperthyroidism crisis.

3. Whether there is a history of trauma.

4, with or without pesticides, gas, sleeping pills, poisonous plants and other poisoning.

5, whether there are medical diseases that can cause coma, such as diabetes, kidney disease, liver disease, severe heart and lung disease.

6, for patients with transient coma, should pay attention to epilepsy or syncope and other diseases.

Second, physical examination found

1, should carefully observe body temperature, breathing, blood pressure, pulse, skin and head and neck. High fever should pay attention to severe infection, heat stroke, pons bleeding, atropine poisoning, etc., people with hypothermia should pay attention to shock, mucous edema, hypoglycemia, sedative poisoning, frostbite, etc.; pulse slowness should pay attention to intracranial hypertension, atrioventricular block or Myocardial infarction, heart rate is too fast, common in cardiac ectopic rhythm, fever and heart failure; respiratory rhythm changes type can help determine the brain lesions, pay attention to respiratory odor (diabetic acidosis has fruit odor, uremia has urine Stinky, hepatic coma with rancid smell, alcoholism with alcohol, organic phosphorus poisoning with garlic odor; high blood pressure can be seen in cerebral hemorrhage, hypertensive encephalopathy and intracranial hypertension, hypotension is common in shock, myocardial infarction, Sleeping medicine poisoning, etc.; skin is cherry red for CO poisoning, skin sputum is seen in sepsis, epidemic meningitis, anti-cholinergic drug poisoning or heatstroke when the skin is dry, skin is wet and sweaty during shock; attention to ear, nose, conjunctiva No evidence of trauma such as bleeding or discharge.

2, nervous system examination should pay attention to the presence or absence of focal neurological signs, pupil and fundus conditions, heavy pressure on the upper edge of the sputum with or without defense response and expression response, re-scratch the foot with or without limb escape response, pay attention to eye position, tendon reflex Symmetry and pathological reflex; patients with intracranial hypertension and subarachnoid hemorrhage often have optic edema and hemorrhage; bilateral dilated pupils are found in cerebral hypoxia, atropine poisoning, and severe midbrain lesions. Bilateral pupillary needle-like narrowing is seen in the pons of the pons, hemorrhage, organophosphate and morphine poisoning. One side of the pupil dilated is seen in the ipsilateral brain hook back; one side is narrowed to the early stage of the Horner's sign or the ipsilateral brain hook.

3, pay attention to the presence or absence of meningeal irritation, common in central nervous system infections and intracranial hemorrhagic diseases.

Third, the coma classification

The conscious state of the coma patient is lost, and the clinical manifestation is that the patient's awakening-sleep cycle disappears and is in a continuous "deep sleep" and cannot be awakened. Many psychological activities such as patient perception, attention, thinking, emotion, orientation, judgment, and memory are lost. No understanding of themselves and the external environment, no response to external stimuli. Cannot be executed for simple commands. Gives a strong painful stimulus, except for sometimes a painful expression or a sputum, a completely unconscious reaction.

According to the state of awakening, the content of consciousness and the progression of physical loss and the extent and extent of impaired brain function, clinical coma is usually divided into four stages.

Shallow coma

Clinical manifestations of blinking reaction disappeared or occasionally semi-closed state, language loss, spontaneous movement is rare, all kinds of stimulation and internal needs of the outside, completely unconscious and reaction. However, strong painful stimuli can be seen in patients with painful expressions, paralyzed or limb defenses and increased breathing. Brainstem reflexes such as swallowing reflexes, cough reflexes, corneal reflexes, and pupils are still present for light reflections, and ocular brain reflexes may also be present. There is no significant change in breathing, pulse, and blood pressure. Defecation or incontinence.

2. Moderate coma

The patient's blink, language, and spontaneous movement have been lost, and they have no response to various external stimuli, and may have defensive reflexes for strong pain stimuli. There is no movement in the eyeball, the corneal reflex is weakened, the pupil is slow to reflect light, and the breathing is slowed or increased. Central respiratory disorder such as periodic breathing and central neuron hyperventilation can be seen. Pulse and blood pressure have also changed. With or without limb tonic extension and angulation (de-cortical rigidity). Defecation or incontinence.

3. Deep coma

Muscle relaxation throughout the body, and strong pain stimulation can not lead to escape response and cortical rigidity. The eyeball was fixed, the pupil was significantly enlarged, and the pupil was completely lost to light reflection, corneal reflex, anterior chamber reflex, swallowing reflex, cough reflex, and sacral reflex. Irregular breathing, blood pressure may drop, incontinence, and even detention.

4. Brain death

It manifested as an unresponsive deep coma, spontaneous breathing stopped, the pupil was enlarged and fixed, and the brainstem reflex disappeared, accompanied by a decrease in body temperature and blood pressure. EEG is silent, and cerebral angiography is not developed. At this time, even if the heartbeat is still maintained, the whole brain function will never recover, and the heartbeat will stop in a certain period of time.

In 1959, French scholars first proposed the concept of brain death. After nearly half a century of exploration and practice, the standard of brain death has become more and more perfect, and has gradually replaced the standard of cardiac death as the gold standard for death judgment. Currently, about 80 countries or regions around the world have issued adult brain death standards. China's brain death research started very late, and there are still many problems to be solved.

The diagnostic criteria and steps for brain death proposed by Shanghai Huashan Hospital are as follows:

(1) Prerequisites for the diagnosis of brain death, ie, the subject of brain death diagnosis.

1 primary brain organic disease, such as craniocerebral injury, stroke, intracranial space-occupying lesions or intracranial infectious diseases.

2 Deep coma, spontaneous breathing disappeared, and a respirator has been used to maintain respiratory function.

3 The primary disease has been clarified, and reasonable treatment has been carried out, which causes irreversible damage to brain tissue due to the nature of the lesion.

(2) Excluding reversible coma, it cannot be used as a target for brain death.

Children under the age of 16.

2 acute drug poisoning.

3 rectal body temperature below 32 ° C.

4 metabolic, endocrine system disorders, hepatic encephalopathy, uremia or hyperosmolar coma.

5 The cause is unknown.

(3) Start with a respirator, observe at least 12h, and the patient is in a deep coma within 12h without spontaneous breathing.

1 primary brain tissue damage, need to be observed for 12h.

2 primary brain tissue damage, and sedative drug poisoning may be observed after the drug half-life (about 24h) for another 12h. If the type of drug is unknown, at least 72 hours should be observed.

(4) The brainstem function test should first meet the above preconditions 1, 2, and 3.

1 The first inspection: First need to meet the following 6 brain stem reflexes:

A. Head and eye reflexes (disappearance).

B. The pupil reflects light (disappears).

C. Corneal reflex (disappearance).

D. Vestibular reflex (disappearance).

E. For painful stimulation of any part of the body, whether there is any reaction (no reaction) in the distribution of brain nerves.

F. Use a catheter to suck in the trachea to see if there is vomiting or coughing reflex (without any reflection).

2 followed by a non-breathing test:

A. Supply 100% oxygen by artificial respirator for 10 min, then add 95% oxygen plus 5% carbon dioxide mixture, or slow down the respiration rate of the respirator so that PaCO2>5.33 kPa (40 mmHg).

B. The respirator is disengaged from the patient, and the oxygen inhalation catheter is inserted into the tracheal carina, supplied with 100% oxygen 6 L/min, and then observed for 10 min. If the patient does not breathe spontaneously, PaCO2>8kPa (60mmHg), it can be proved that the patient has no spontaneous breathing.

C. If the patient does not breathe spontaneously, then the respirator is connected.

D. If the patient is obviously cyanotic and the blood pressure drops significantly, the test should be stopped.

3 The second inspection: After the first brainstem function and respiratory examination, the artificial respirator should be connected to artificial respiration for 4 hours, and then the second inspection should be carried out. The procedure is the same as the first examination.

an examination

Related inspection

Brain CT examination of granulocyte to red blood cell ratio

Laboratory inspection:

Serious infections: pneumonia, typhoid fever, malaria, Huafu syndrome, etc., cerebrospinal fluid or leukocytosis, often without focal symptoms.

Differential diagnosis

The diagnosis should be differentiated from the following symptoms:

Hyperosmolar coma

Hyperosmolar non-ketotic diabetic coma, referred to as hyperosmolar coma, is a rare and serious acute diabetic complication. Its main clinical features are severe hyperglycemia, dehydration, and elevated plasma osmotic pressure without obvious Ketoacidosis.

2. Sedation, anesthesia caused by coma

Patients with anterior pituitary hypofunction crisis are very sensitive to sedation and anesthesia. The commonly used amount can cause the patient to fall into a long period of slumber and even coma.

3. Central nervous system inhibitors induce coma

Central nervous system inhibitor-induced coma is one of the types of pituitary crisis and pituitary stroke crisis, that is, when the anterior pituitary dysfunction, the adrenal cortex hormone and thyroid hormone deficiency, the body's stress ability declines, in infection, vomiting, diarrhea, dehydration Crisis is induced by the use of sleeping pills or anesthetics in cold, hunger, etc. Pituitary tumor sudden intratumoral hemorrhage, infarction, necrosis, tumor expansion, causing acute neuroendocrine lesions called pituitary apoplexy.

4. Nearly forced coma

Hepatoencephalopathy (hepatoencephalopathy) used to be called hepatic coma. It is a comprehensive symptom of central nervous system dysfunction caused by severe liver disease and is caused by metabolic disorders. It is one of the manifestations of severe liver cell function failure. The main symptoms are conscious disturbance, behavioral disorder and coma, while subclinical or recessive hepatic encephalopathy has no obvious clinical manifestations and biochemical abnormalities. Only a fine intelligence test and/or electrophysiological test can be used to make a diagnosis. Portal shunt encephalopathy is the most common, the main mechanism of occurrence is portal hypertension, there is a collateral circulation between the portal vein and the vena cava, so that a large number of portal vein blood bypasses the liver and the human body circulates.

5. Deep coma

Deep coma: All consciousness is lost, no response to various external stimuli, various reflexes disappear, and the whole body muscles are relaxed.

In patients with deep coma, the clinical manifestations are no response to any stimulation, no spontaneous activity, loose muscles, fixed eyeballs, dilated pupils, various reflexes disappear, vital signs of vital signs, such as irregular breathing, heart rhythm disorders, blood pressure Fluctuation, etc.

6. Light coma

Light coma: Conscious activity and mental activity disappear, but strong pain stimuli (such as pressing the upper arm) can show expression or motor response, can not be awakened; pupils reflect light normal, deep and shallow reflections exist.

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