Hyperosmolar nonketotic diabetic coma

Hyperosmotic non-ketotic diabetic coma Hyperosmolar ketosis (hyperosmolarnonketoticdiabeticcoma, referred to as hyperosmolar coma) is another clinical type of acute metabolic disorder of diabetes, caused by elevated blood osmotic pressure caused by hyperglycemia, severe dehydration and progressive disturbance of consciousness, no significant Ketoacidosis, often accompanied by clinical syndromes with varying degrees of neurological manifestations. More common in elderly type 2 diabetes patients, the age of good hair is 50 to 70 years old, about 2 / 3 patients have no history of diabetes before the onset, or only mild symptoms. The mortality rate of this disease is very high, the early report is as high as 40% to 70%, and the reported mortality rate in China is about 50% to 69.2%. Therefore, early detection and timely rescue are the most important. basic knowledge Sickness ratio: 0.0001% Susceptible people: no specific population Mode of infection: non-infectious Complications: disseminated intravascular coagulation thrombosis

Hyperosmotic nonketotic diabetic coma

(1) Causes of the disease

1. Stress and infection: such as cerebrovascular accident, acute myocardial infarction, acute pancreatitis, gastrointestinal bleeding, trauma, surgery, heatstroke or hypothermia, infection, especially upper respiratory tract infection, urinary tract infection, etc. Induced.

2. Insufficient water intake: the sensitivity of the elderly thirst center is reduced, bedridden patients, mentally disordered or comatose patients, and young children who cannot take the initiative to take water.

3. Excessive water loss and dehydration: such as severe vomiting, diarrhea, large area burn patients, intraneuropathy, surgical dehydration treatment, dialysis treatment, etc.

4. High sugar intake and input: such as large intake of sugary drinks, high-sugar foods, intravenous injection of large amounts of glucose solution when diagnosis is missed, complete intravenous high nutrition, and hemodialysis or peritoneal dialysis using sugary solutions Such conditions, especially in some patients with endocrine diseases complicated with glucose metabolism disorders, such as hyperthyroidism, acromegaly, hypercortisolism, pheochromocytoma, etc. are more likely to be induced.

5. Drugs: Many drugs can be an inducement, such as a large number of glucocorticoids, thiazides or furosemide (furosemide) and other diuretics, propranolol, phenytoin, chlorpromazine, cimetidine, Glycerin, azathioprine and other immunosuppressive agents can cause or aggravate the body's insulin resistance and increase blood sugar, dehydration is aggravated, and some drugs such as thiazide diuretics also inhibit insulin secretion and reduce insulin sensitivity. Thus, HNDC can be induced.

6. Others: such as acute, chronic renal failure, diabetic nephropathy, etc., due to decreased glomerular filtration rate, the removal of blood sugar also decreased, can also be a cause.

In short, almost all patients with HNDC in the clinic have obvious causes of the disease. Animal experiments also indicate the occurrence of hyperosmolar coma. In addition to the original diabetes, there are obvious triggering factors, which should be inquired and removed.

(two) pathogenesis

The basis of HNDC is that patients have different degrees of glucose metabolism disorders. The basic causes are insulin deficiency and dehydration. Under certain incentives, the original glucose metabolism disorder is aggravated, the islet response to sugar stimulation is reduced, and insulin secretion is reduced. Hepatic glycogen decomposition increases, blood sugar is significantly increased, severe hyperglycemia and diabetes cause osmotic diuresis, resulting in a large loss of water and electrolytes from the kidneys. Because patients have active water intake disorders and varying degrees of renal dysfunction, Hyperglycemia, dehydration and high plasma osmotic pressure gradually increase, eventually leading to hypertonicity, that is, HNDC state, normal plasma osmotic pressure is maintained at 280 ~ 300mmol / L, which is mainly provided by blood Na +, but also cause plasma when blood sugar is significantly increased The osmotic pressure is increased.

In HNDC, hyperglycemia and high urine sugar cause osmotic diuresis. About 50% of urinary osmotic pressure is maintained by glucose in urine. Therefore, patients often lose water more than electrolytes, and patients often take active water to maintain body water. Decreased balance and renal insufficiency, resulting in more severe hyperglycemia and dehydration, the latter often accompanied by hypokalemia, one can cause increased secretion of cortisol, catecholamines and glucagon; and further inhibit insulin secretion, Continue to increase hyperglycemia, forming a vicious circle that eventually leads to HNDC.

HNDC is different from DKA, mainly with no or only mild ketoacidosis; more common in middle-aged and elderly people; hyperglycemia, dehydration and high plasma osmotic pressure are more serious than DKA, and the mechanism of this difference has not been fully elucidated. Currently considered:

1. HNDC patients have relatively high insulin secretion, which is sufficient to inhibit the decomposition of fat and the formation of ketone bodies, but it can not prevent the increase of blood glucose caused by other incentives. Some people think that there is no significant difference between them. Some patients with HNDC have plasma insulin levels. Low unpredictable.

2. Patients with plasma growth hormone and catecholamine levels are lower than ketoacidosis, and both hormones have a strong role in promoting fat breakdown and ketone body formation, but it has also been reported that these two hormones are not between the two. Significant differences.

3. The patient has severe dehydration, and severe dehydration is not conducive to the formation of ketone bodies. The body's water reserve is lower than that of young patients, and there is often a decrease in thirst central sensitivity and renal insufficiency. Severe acidosis, fatty acid -oxidation and the formation of ketone bodies require the participation of water, so severe dehydration can affect the production of ketone bodies. In addition, severe dehydration can cause blood concentration, renal glucose disorders, and cause more severe hyperglycemia.

4. The patient's liver ketogenic dysfunction, the kidney's ability to release sugar, resulting in high blood sugar and ketosis is very light, some people found that some patients with plasma non-esterified fatty acid levels without ketones, support liver ketone function barriers, normal people In the state of hyperglycemia, 20 g of glucose can be excreted from the urine per hour, so the blood sugar of normal renal function generally does not exceed 27.8 mmol / L (500 mg / dl), about 90% of patients with this disease with kidney disease, sugar discharge function Obstacles cause a serious increase in blood sugar.

5. Severe hyperglycemia may have mutual antagonism between ketone body formation. Some people try to explain that patients with severe hyperglycemia have no obvious ketoacidosis, and patients with ketoacidosis have significant ketoacidosis. The relatively low blood sugar level, the injection of glucose in the dog with the pancreas can inhibit the formation of ketone bodies in the body; and the oxidation of a large number of fatty acids can reduce the proportion of plasma NAD/NADH in patients, which is necessary for gluconeogenesis. The level of alanine is reduced, thereby inhibiting hepatic gluconeogenesis.

Clinical data show that HNDC and DKA are not two distinct symptoms. There are various intermediate types between them, forming a continuous pathological spectrum. The two are the extremes of this continuous disease spectrum. It can be seen that many patients with HNDC have ketosis or ketoacidosis at the same time, and many patients with ketoacidosis have significantly increased plasma osmotic pressure. As reported in foreign countries, 275 hyperglycemic diabetes emergencies, only HONK accounts for 32%. Another 18% have significant ketoacidosis in hypertonic fashion. In typical ketoacidosis, 26% have hyperosmotic state at the same time. It can be seen that there may be overlap between NHDC and DKA. Overlap syndrome, such as HNDC with DKA overlap syndrome, or DKA with HNDC overlap syndrome, typical ketoacidosis, can not negate the diagnosis of HNDC; severe hyperglycemia, hypertonic state, sometimes seen in ketoacid For poisoned patients, this should be taken seriously in clinical work.

Hyperosmotic nonketotic diabetic coma prevention

1. Strengthen the education and health check of diabetes knowledge, early detection of early treatment, elderly people over 50 years of age should regularly check blood sugar, patients diagnosed with diabetes, should take regular medication, control diet, strengthen exercise, and strictly control blood sugar levels.

2. Control various predisposing factors, actively treat various infections, treat hemodialysis, peritoneal dialysis, mannitol dehydration, etc., should pay attention to whether there is dehydration, timely monitoring of blood sugar, urine sugar.

3. Pay attention to the induction of drug applications, such as diuretics, cortisol, propranolol (propranolol) and so on.

Hyperosmolar nonketotic diabetic coma complications Complications, disseminated intravascular coagulation and thrombosis

1. Regarding the prevention and treatment of thrombotic diseases: In HNDC, it is considered that there is a higher risk of thrombosis in the course of treatment. Therefore, if there is a possibility of thrombotic disease in patients, there is no contraindication, especially in the elderly. Patients, some people advocate heparin treatment, generally given heparin 5000U, subcutaneous injection, 1 time / 8h, but should pay attention to the blind use of heparin has the risk of gastroparesis, gastrointestinal bleeding.

2. About cerebral edema: In patients with HNDC, when the plasma osmotic pressure is significantly increased, several intraosseous granules are produced in a compensatory manner. When the osmotic pressure of the extracellular fluid drops sharply, the free water enters a large amount. In the hypertonic state of the cells, causing cerebral edema, especially in the course of treatment, whether a large amount of hypotonic solution will cause brain edema, is a clinically worthy of attention, close observation during treatment, early detection, timely treatment.

Clinically, the mortality rate of cerebral edema in patients with HNDC is not high, and it is not as fatal cerebral edema in DKA in young type 1 diabetes. The death of most patients is caused by insufficient treatment, rather than the treatment is too urgent. There is no evidence yet. Slowing down the rate of correcting hypertonic conditions can reduce the incidence of cerebral edema, pulmonary edema and heart failure.

3. About disseminated intravascular coagulation: It is a serious complication of patients with HNDC. Early detection and timely treatment are essential. Once found, it is an indication for timely use of heparin therapy.

4. About anti-infection: HNDC patients, especially infections, are often the main cause of late death (about 2/3) of patients. They must be given a large dose from the beginning of treatment, effective combination antibiotic treatment, and treatment according to refractory infection.

Hyperosmolar non-ketotic diabetic coma symptoms Common symptoms Polyuria, fatigue, polydipsia, loss of water, appetite, dehydration, circulatory failure, consciousness, confusion, confusion

History

Most of the elderly, mostly in the 50 to 70 years old, the prevalence of men and women is about the same, about half are known to have diabetes, about 30% have a history of heart disease; about 90% have kidney disease.

Diabetes type: mostly type 2 diabetes; a small number can be type 1 diabetes, and more often with DKA; occasionally can occur in patients with diabetes such as hypercortisolism, acromegaly.

2. The way of onset

Slower, patients from days to weeks before the onset of the disease, often have clinical symptoms of increased symptoms of diabetes, including polydipsia, polydipsia, fatigue, dizziness, loss of appetite and vomiting.

3. Dehydration and peripheral circulatory failure

Patients often have severe dehydration signs, dry skin and decreased elasticity, eyeball depression, dry tongue and longitudinal cracks. When the patient has peripheral circulatory failure, the pulse is fast and weak, the jugular vein is incomplete in the lying position, and the erectility is low. Blood pressure, the systolic pressure drop after standing is 1.3kPa (10mmHg) lower than that in the supine position. Many patients are in shock state at the time of treatment. However, due to severe dehydration, there is no cold sweat found during physical examination. Some patients have severe dehydration, but some patients have serious dehydration. The hypertonic state of the plasma causes the intracellular fluid to go out, supplementing the blood volume, which may mask the severity of the water loss and keep the blood pressure still normal.

4. Neurological symptoms and signs

About half of the patients were confused and 1/3 were in a coma. Some patients were misdiagnosed as cerebrovascular accidents, and even misplaced with hypertonic glucose solution or dehydrating agent, which caused the disease to worsen. The main obstacle of HNDC patients' consciousness disorder and its degree The degree and speed of plasma osmotic pressure increase have a certain relationship with the level of blood sugar, but have little to do with the degree of acidosis. It has been found in foreign countries that when the patient's plasma osmotic pressure exceeds 320mmol/L, psychiatric symptoms can occur. Such as apathy, lethargy, etc.; more than 350mmol / L, 40% of patients may have confusion or coma, but some patients have a steady increase in plasma osmotic pressure, although the patient has exceeded 400mmol / L, the patient is still awake status.

Signs of the nervous system: such as epileptic seizures, transient hemiplegia, muscle relaxation or involuntary contractions, aphasia, ipsilateral hemianopia, visual impairment, nystagmus, hallucinations, half-length sensation, Babinski sign positive and central Fever, etc. These signs suggest that the patient may be associated with cerebral cortical or subcortical damage caused by dehydration, blood concentration or vascular embolism. These changes may be reversed or returned to normal after effective treatment, and a few are corrected within a period of time after HNDC correction. Some nerves, symptoms of mental disorders can still be left behind.

5. Symptoms and signs associated with the disease

Patients may have hypertension, kidney disease, coronary heart disease and other original disease manifestations; pneumonia, urinary tract infections, pancreatitis and other induced disease manifestations; and cerebral edema, thrombosis, vascular embolism and other complications, the patient's body temperature is normal or Mild elevation, such as decreased body temperature, suggests that it may be accompanied by acidosis and/or sepsis, which should be given enough attention.

Examination of hyperosmolar nonketotic diabetic coma

1. Blood sugar and urine sugar: This disease is characterized by high blood sugar and high urine sugar. The blood sugar is more than 33mmol/L (600mg/dl). The urine sugar is strong positive. Patients such as dehydration or kidney function damage make kidney sugar. When the threshold is raised, urine sugar may not be strongly positive, but urine glucose-negative is rare.

2. Blood electrolyte: Under normal circumstances, normal or elevated blood sodium can also be reduced; normal or decreased blood potassium can also be elevated; overall sodium and potassium are reduced, patients may also have calcium, magnesium, phosphorus loss The level of blood sodium and potassium in patients depends on the amount of loss and distribution in and out of the cell, as well as the degree of water loss. In HNDC, most patients lose 300-500 mmol/L of sodium and potassium loss. The total sodium, potassium and chlorine loss of the patient were 5-10 mmol/kg, 5-15 mmol/kg and 5-7 mmol/kg body weight, respectively.

In patients with HNDC, when hyperosmolar diuresis occurs, renal tubular reabsorption of sodium is inhibited, and intracellular water is transferred to the outside of the cell, which tends to lower blood sodium. It has been found that blood glucose rises by 5.6 mmol/L (100 mg/ Dl), blood sodium will drop by about 1.7mmol / L, in addition, polydipsia can reduce blood sodium levels, increased plasma chylomicrons, can also cause a false reduction in blood sodium, contrary to the above factors that cause elevated blood sodium, Hypertonic diuresis loses more water than sodium, and the decrease in blood volume can stimulate the secretion of aldosterone and cause sodium retention and potassium excretion. These factors determine the level of blood sodium to varying degrees. Similarly, hyperosmotic diuresis, Loss of appetite and increased secretion of adrenocortical hormone can reduce blood potassium, blood volume expansion after treatment, blood sugar drop and blood potassium transfer to the cells, can also cause further decline of blood potassium; and dehydration, blood concentration and kidney Functional failure can increase blood potassium levels, so untreated HONK patients may have different levels of serum sodium and potassium.

3. Blood urea nitrogen and creatinine: often significantly increased, the degree reflects severe dehydration and renal insufficiency, urea nitrogen (BUN) can reach 21 ~ 36mmol / L (60 ~ 100mg / dl), creatinine (Cr) up to 163 ~600mmol / L (1.7 ~ 7.5mg / dl), BUN / Cr ratio of up to 30:1 or more (normal people are more than 10:1 ~ 20:1), patients with progressively elevated BUN and Cr have a poor prognosis, After effective treatment, there was a significant decrease in blood BUN and Cr, and some patients still failed to return to the normal range, indicating that they had renal insufficiency before HNDC.

4. Plasma osmotic pressure: Significant elevation is an important feature and diagnostic basis of HNDC. Plasma osmotic pressure can be directly determined, but the following formula is commonly used in clinical practice:

Plasma osmotic pressure (mmol/L) = 2 ([Na+] [K+]) (blood glucose mg/dl) / 18 (BUNmg/dl) / 2.8

In the formula, the unit of sodium and potassium ions is mmol/L, and the blood glucose and BUN units are mg/dl. Since the molecular weight of glucose is 180, the BUN molecule contains two nitrogen atoms, and the sum of the nitrogen atoms is 28, so the mg/dl is To be mmol/L, the blood glucose and BUN values should be divided by 18 and 2.8 respectively. Blood sugar and BUN can also be directly calculated by mmol/L. The normal human plasma osmotic pressure is 280-300mmol/L, such as more than 350mmol/L. Can be diagnosed as hypertonic.

Since BUN can freely pass through the cell membrane and cannot constitute the effective osmotic pressure of the extracellular fluid, most authors advocate that the BUN is omitted in the calculation, and the plasma osmotic pressure is calculated. The calculation formula is as follows:

Plasma osmotic pressure (mmol/L) = 2 ([Na+] [K+]) Blood glucose (mmol/L)

The effective osmotic pressure is higher than 320mmol/L, which is hyperosmotic. The effective plasma osmotic pressure of HNDC patients is higher than 320mmol/L.

5. Acid-base imbalance: about half of patients have mild or moderate metabolic, high anion gap acidosis, anion gap increased by about 1 times, blood [HCO3-] is higher than 15mmol / L, pH value is higher than 7.3, The increased anions are mainly organic acid radicals such as lactic acid and keto acid, and also contain a small amount of sulfuric acid and phosphate.

The calculation formula for the anion gap is as follows:

Anion gap = [Na+] [K+]-[CI-]-[HCO3-]

In the formula, the unit is mmol/L. If the [HCO3-] term is expressed by CO2CP (vol/dl), the value can be divided by 2.24 and converted to mmol/L, because under standard conditions, the volume of any gas of 1 mmol is 22.4. L, the normal human anion gap is 12 to 16 mmol / L.

6. Blood ketone and urinary ketone: The blood ketone is normal or slightly elevated, and the quantitative determination is no more than 50mg/dl. When measured by the dilution method, there is very little blood plasma diluted to above 1:4, still positive, urinary ketone Negative or weakly positive.

7. Others: The blood white blood cell count of patients with HNDC is often increased to 50×109/L; the hematocrit is increased, reflecting dehydration and blood concentration.

According to the condition, urine culture, chest X-ray film and electrocardiogram were selected.

Diagnosis and diagnosis of hyperosmolar nonketotic diabetic coma

Diagnostic criteria

1. Suspected indications

The diagnosis of HNDC is not difficult. The key is that all clinicians should improve their vigilance and understanding of this disease. Especially for middle-aged and elderly patients, the following clinical conditions, regardless of the history of diabetes, may have HNDC, and should be immediately tested. Room inspection.

(1) Patients with progressive disturbance of consciousness and severe dehydration without significant deep breathing.

(2) There are central nervous system symptoms and signs, such as epileptiform convulsions and pathological reflexes.

(3) Those who have polyuria under stress conditions such as co-infection, myocardial infarction, and surgery.

(4) In the case of a large amount of sugar, intravenous sugar or hormones, phenytoin, propranolol and other drugs that can cause high blood sugar, polyuria and consciousness changes.

(5) There are insufficient water intake, water loss and diuretics, dehydration treatment and dialysis treatment.

2. Laboratory diagnostic criteria

(1) Blood glucose 33 mmol / L (600 mg / dl).

(2) The effective osmotic pressure of plasma is 320mmol/L.

(3) Serum [HCO3-] 15mmol / L or arterial blood gas test showed pH value 7.30.

(4) Strong positive urine sugar, negative or weakly positive for ketone body.

The first three items above can be used as the necessary diagnosis basis, and the fourth item may vary according to clinical conditions. It is worth noting that HNDC has the possibility of concurrent DKA or lactic acidosis. The hyperosmotic state of individual cases is mainly caused by hypernatremia. Because of high blood sugar, therefore, urine ketone body positive, acidosis is obvious or blood glucose is lower than 33mmol / L, and can not be used as a basis for negating HNDC diagnosis, but HNDC patients have obvious hyperosmotic state without exception, such as In patients with coma, the plasma osmotic pressure is lower than 320mmol/L, and other diseases that can cause coma should be considered. Some patients have high blood sugar, but the blood sulphur is low, and the effective osmotic pressure does not reach 320mmol/L. Although not diagnosed as HNDC, it should still be treated as HNDC.

3. Prognosis of poor prognosis Once the diagnosis of HNDC is critically ill, the following clinical manifestations should be considered as indicators of poor prognosis:

(1) The coma persisted for 48 hours and has not recovered.

(2) High plasma osmotic pressure could not be corrected within 48 hours.

(3) coma with epileptiform convulsions and pathological reflex positive.

(4) Patients with severe or refractory infections.

(5) Overlapping with DKA and/or lactic acidosis.

Differential diagnosis

1. Different from non-diabetic cerebrovascular accident patients, this patient's blood sugar is not high, or mild stress blood sugar is increased, but it is impossible to >33.3mmol/L, HbA1c is normal.

2. Some people think that HNDC and diabetic patients with poor diabetes and non-urinary renal failure for differential diagnosis are clinically important. Both can have severe hyperglycemia and elevated blood BUN and Cr levels, but the treatment is completely Different, the former requires a lot of fluid supplement and appropriate amount of insulin; for the latter, insulin alone can lower blood sugar, reduce blood volume and relieve heart failure, and a large number of infusions are very dangerous, but diabetic patients with renal failure often have anemia. Instead of blood concentration, there may be hyponatremia, hyperkalemia, increased blood volume and congestive heart failure, so the identification of the two is not difficult.

3. For comatose patients with a history of diabetes, it should also be identified as HNDC, ketoacidosis, lactic acidosis or hypoglycemia coma.

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