Hypoglycemic coma

Introduction Hypoglycemic coma: This type of coma is most common. When hypoglycemia occurs, the patient is weak, dizzy, dizzy, sweating, palpitation, pale, and may have headache, vomiting, and nausea. Blood pressure is generally low, and severe cases cannot be measured. It can be irritated or unresponsive, the pupils are reflected by light, and the sputum reflexes disappear after the initial sputum. The sputum test can be positive, and the muscle tension can be increased or convulsions, convulsions, and stuns in severe cases.

Cause

The reason may be spontaneous, that is, due to eating too little or not eating, especially when there is infection, or induced by insulin (for islet tolerance test or insulin treatment for loss of appetite), or because of high sugar diet Or after injection of a large amount of glucose, causing endogenous insulin secretion. In patients with this disease, due to insufficient cortisol, reduced glycogen storage, decreased growth hormone, increased sensitivity to insulin, and decreased thyroid function, the absorption of glucose in the intestine is reduced, so the fasting blood glucose is lower in normal times. In the above situation, it is easy to cause hypoglycemia and coma.

an examination

Related inspection

Glucose insulin

1. Blood sugar: Hypoglycemia is a critical condition. First, the patient's blood sugar must be measured quickly and accurately. Do not wait for biochemical analysis results for suspicious patients, and treatment should be performed immediately after the specimen is taken. Rapid determination and biochemical detection are performed simultaneously under conditions.

Normal human venous plasma glucose concentration, after fasting overnight, <3.3mmol / L (50mg / dl) suggests hypoglycemia. Because the individual difference in the diagnosis of hypoglycemia should be a range rather than a specific value, this range should be 2.5 ~ 3.3mmol / L (45 ~ 60mg / dl), and less than 2.5mmol / L, and repeated The test confirmed that there was a clear presence of hypoglycemia.

2. Other examinations: Other laboratory tests are not necessary for every patient with diabetes mellitus and hypoglycemia.

(1) Glycosylated hemoglobin (GHB): HBAc is the main product of hemoglobin binding to glucose, which reflects the average blood glucose level in the past two months. The normal value of HBAc is 4% to 6%. In patients with type 1 diabetes who have been intensively treated with insulin for a long time, the HBAc value is negatively correlated with the incidence of hypoglycemia <6%, and the incidence of hypoglycemia is significantly increased. Therefore, it is more suitable to maintain HBAc between 6% and 7%. Studies have shown that in patients with undetected hypoglycemia, relaxation of blood glucose control, maintaining HBAc at around 8.0% for 3 months, can partially reverse the anti-regulatory effects of impaired hypoglycemic hormone and reduce the incidence of undetected hypoglycemia. .

(2) Determination of liver and kidney function: Liver and kidney dysfunction can significantly increase the chance of hypoglycemia. For diabetic patients, it is necessary to fully understand liver and kidney function, choose reasonable treatment, reduce the incidence of hypoglycemia, and also contribute to the cause of hypoglycemia. analysis.

(3) Determination of blood ketone body, lactic acid and osmotic pressure: helpful for identification with DKA, HHC and lactic acidosis.

Related tests: Ammonia lactate, insulin, glucose hemoglobin.

Differential diagnosis

Differential diagnosis of hypoglycemic coma:

(1) pituitary apoplexy: rapid onset, headache, dizziness, vomiting, and then into coma, due to acute bleeding within the pituitary tumor, hypothalamic and other life centers are oppressed. The main cause of hypopituitarism is the metabolic disorder caused by a variety of hormone deficiency, and the body's ability to resist various stimuli is weak. The maintenance of consciousness depends on the integrity of some of the central functions of the cerebral cortex, thalamus, hypothalamus and midbrain reticular formation. If the neuronal metabolism of these conscious centers is impaired, confusion or loss of consciousness occurs. The maintenance of normal neuronal metabolism depends mainly on the oxidation of glucose and glutamate under the catalysis of some specific enzymes. Patients with hypopituitarism have biochemical changes, such as hypoglycemia, hyponatremia, and sometimes due to trauma, compression or edema, which impede the delivery of oxygen and nutrients to the above-mentioned nerve centers. Adrenal cortex hormones and thyroxine deficiency can cause neuron metabolism disorders. Coma is more common in patients with severe peripheral endocrine gland dysfunction, especially adrenal insufficiency. Adrenal cortical function can only barely cope with the patient's need for a very low metabolic condition. Once severe stimulation occurs, adrenal insufficiency occurs. Adrenal cortex hormones have a good effect on coma in patients with this disease. After the patient was treated with adrenal cortical hormone replacement therapy, the incidence of coma was significantly reduced.

(2) infection-induced coma: patients with this disease due to the lack of a variety of hormones, mainly lack of adrenocorticotropic hormone and cortisol, so the body's resistance is low, prone to infection. After concurrent infection and high fever, it is prone to unconsciousness, resulting in coma, hypotension and shock. The loss of consciousness caused by infection is mostly gradual. The body temperature can be as high as 39 to 40 ° C, and the pulse often does not increase correspondingly. The blood pressure is lowered, and the systolic blood pressure is usually below 80 to 90 mmHg. In severe cases, shock occurs.

(3) sedation, anaesthetic-induced coma: patients with this disease are very sensitive to sedation, anesthesia, the usual dose can make patients fall into a long period of slumber and even coma. Sodium pentobarbital or thiopental, morphine, phenobarbital and meperidine can cause coma. Long-term lethargy can also occur after receiving a general therapeutic dose of chlorpromazine (oral or intramuscular).

(4) sodium loss coma: sodium loss caused by gastrointestinal disorders, surgery, infection, etc., can promote a crisis like primary adrenal insufficiency. The peripheral circulatory failure of this type of crisis is particularly remarkable. It is worth noting that patients with this disease may have increased excretion of sodium during the first few days of starting corticosteroid use, possibly because the glomerular filtration rate is very low and is improved after treatment. Less than a week after treatment with cortisol, the patient entered a coma with a significant negative sodium balance. In addition, when thyroid preparations are used alone, especially when the dosage is too large, the body's need for adrenocortical hormone is increased due to an increase in metabolic rate, and the deficiency of adrenocortical hormone is more serious. On the other hand, thyroid preparations have a hypothyroidism. Promote solute excretion, causing loss of water and loss of sodium.

(5) Toxic coma in water: The patient has drainage disorder. When the water is too much, water retention can occur, and the extracellular fluid is diluted to cause hypotonic state. Then the water enters the cell, and the introduced water contains too much water and the cells are swollen. Cell metabolism and dysfunction. Excessive water in nerve cells can cause a series of neurological symptoms. The occurrence of this condition can be spontaneous or caused by water diuretic test, especially when the blood sodium concentration of the patient is very low. Therefore, blood sodium should be measured before the water test, and low blood sodium should not be suitable. Do this test. The clinical manifestations of water poisoning are weakness, lethargy, loss of appetite, vomiting, mental disorder, convulsions, and finally into a coma. This type of coma is different from the crisis caused by salt loss. The patient has no signs of dehydration, but may have edema and weight gain. If there is no obvious loss of sodium, the blood circulation remains normal. The blood cell volume is reduced, the serum sodium concentration is lowered, the blood potassium is normal or decreased, and generally no acidosis or azotemia.

(6) hypothermia coma: Some patients feel ambiguous in the winter, when exposed to cold, can induce coma, or make the coma that has occurred more prolonged. Such dangers often occur in the winter, the onset is slow, gradually into a coma, the body temperature is very low, the temperature is not measured by the ordinary thermometer, the temperature of the anus should be measured by the thermometer used in the laboratory, and the low temperature can be as low as 30. °C.

(7) coma after pituitary resection: after pituitary resection for pituitary tumors or metastatic breast cancer, severe diabetic retinopathy, etc., patients may develop coma. Those with pituitary dysfunction before surgery are more likely to occur. Coma after uterine resection can cause disturbance of consciousness due to local injury, or due to hypofunction of endocrine glands, especially preoperative adrenal insufficiency, can not tolerate severe irritation caused by surgery, or due to water before and after surgery Electrolyte metabolism disorder. The patient can't recover after surgery, and is in a state of lethargy or coma. It can last for several days or even months, incontinence, and it can still respond to pain stimulation, sometimes temporarily awakening. The grip reflection and the sucking reflex disappear, the pulse rate and blood pressure can be normal or slightly lower, and the body temperature can be high or low, or normal. Blood sugar and blood sodium can also be normal or slightly lower.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.