Overview.
Hyperosmolar nonketotic diabetic coma (HNDC). Hyperosmolar nonketotic diabetic coma (HNDC) is a clinical syndrome characterized by severe hyperglycemia due to a relative shortage of insulin in the body and an increase in insulin counter-regulatory hormones and the release of hepatic glucose, which leads to plasma hyperosmolar dehydration and progressive impairment of consciousness. It is seen in middle-aged and elderly patients with or without a history of diabetes mellitus and has a high mortality rate.
Etiology
The disease is most common in the elderly, those with mild diabetes mellitus or impaired glucose tolerance, and is easily induced in the presence of the following factors: severe stress such as acute infections, acute cardiac infarction, cerebrovascular disease, acute pancreatitis, uremia, burns, and cranio-cerebral surgery. Hypertonicity may be exacerbated by thiazides, mannitol, sorbitol, hypertonic sugar and sodium-containing fluids, and peritoneal dialysis. Glucocorticoids, beta-blockers, phenytoin sodium, diazoxide, cimetidine, etc. may lead to insulin resistance and induce it.
Symptoms
1. Triggers
All kinds of acute infections, severe vomiting and diarrhea, acute myocardial infarction, cerebrovascular disease, acute pancreatitis, traumatic brain injury, burns, cranio-cerebral surgery, as well as diuretics, peritoneal dialysis, and the input of excessive glucose solution.
2. Slow and gradual onset
Early thirst, polyuria, fatigue, appetite loss aggravated, gradually appear obvious thirst, polyuria, dehydration signs.
3. Hypertonic dehydration symptoms
Thirsty, dry and cracked lips and tongue, dry skin, poor elasticity, sunken eyes, low urine output, urinary closure, insufficient blood volume, rapid heartbeat, low blood pressure and even shock.
4. Neuropsychiatric symptoms
There are different degrees of consciousness disorders, such as slow reaction and indifferent expression in mild cases, and hallucinations, aphasia, blurred consciousness, drowsiness and even coma in severe cases. There may be coarse tremor of upper limbs, limited seizures, transient hemiparesis, hyperreflexia or disappearance of knee reflexes, and the cone beam sign may be positive.
Examination
1. Blood glucose
Often >33.6mmol/L (600mg/dl), urine sugar is strongly positive.
2. Blood ketone bodies
Normal or mildly elevated, urine ketone negative or weakly positive.
3. Electrolytes
Blood sodium > 150mmol/L, blood potassium: normal or decreased.
4. Plasma osmolality
>330 mOsm/L. Effective plasma osmolality can be calculated by the formula: effective plasma osmolality (mOsm/L) = 2[blood sodium + blood potassium (mmol/L)] + blood glucose (mmol/L).
5. Blood pH or carbon dioxide binding capacity
Normal or low, significantly lower in those with acidosis.
6. Blood urea nitrogen, creatinine
May be increased by dehydration and shock.
7. White blood cell count
Increase due to infection or dehydration, and increase in hematocrit.
8. Electrocardiogram
Electrolyte disorders (especially hypokalemia) and myocardial ischemia or arrhythmic changes may be present.
Diagnosis
Any middle-aged or elderly patient, with or without a history of diabetes mellitus, who develops unexplained progressive impaired consciousness with obvious signs of dehydration should be considered as a possible cause of the disease, and should be examined promptly for blood glucose, urinary glucose and ketone bodies, and blood electrolytes. If the diagnosis of diabetes mellitus has been made, especially middle-aged and elderly patients with type 2 diabetes mellitus, without dietary control and formal treatment, with the above triggers in the recent past, the sudden worsening of polydrinking, polyuria symptoms, depression, sleepiness, in addition to considering ketoacidosis, should also be vigilant for the occurrence of this disease.
Laboratory diagnostic reference criteria for hyperosmolar non-ketotic diabetic coma are: ① blood glucose ≥33.3mmol/L; ② effective plasma osmolality ≥320mOsm/L; ③ serum bicarbonate ≥15mmol/L, or arterial blood pH ≥7.30; ④ urine glucose is strongly positive, while urine ketone is negative or weakly positive. The diagnosis is established if there are clinical signs of impaired consciousness and significant dehydration while blood glucose exceeds 33.3 mmol/L, urine glucose is strongly positive (those with altered renal thresholds can be incompatible with blood glucose), and plasma effective osmolality exceeds 330 mOsm/L, and if urine ketone bodies are negative or weakly positive on examination.
Treatment
1. Immediately send to intensive care unit
Open the vein, check blood sugar, electrolytes, blood gas analysis, blood and urine routine, urine ketone, electrocardiogram, as well as chest radiographs and brain CT, etc. urgently.
2. Rehydration
Infusion volume is estimated at 12% of body weight: if there is no cardiac or renal dysfunction, saline can be rapidly replenished with 1000-2000 ml in the first 1-2 hours, followed by 500-1000 ml of IV drip in 2-4 hours, until blood pressure rebounds and urine output increases. As most patients are very seriously dehydrated, the speed of intravenous rehydration is limited, gastric tube rehydration can quickly correct the dehydration state, while reducing the burden on the heart and kidneys, gastric tube rehydration need to pay attention to each gastric tube should not be too much water, so as not to cause aspiration. Elderly, cardiac and renal insufficiency, need to use central venous pressure monitoring, in order to prevent the infusion of fluids too quickly lead to heart failure and pulmonary edema, those who can not tolerate can be replenished from the gastric tube. When blood glucose drops to 13.9mmol/L (250mg/dl) and plasma osmolality drops to less than 320mOsm/L, switch to 5% dextrose solution.
3. Insulin therapy
The method is the same as the treatment of diabetic ketoacidosis, with a small dose of insulin continuous intravenous drip at 0.1-0.15 U/kg/h, blood glucose down to 13.9mmol/L, switch to 5% dextrose or 5% glucose saline. Blood glucose should be kept at 11.1mmol/L to prevent osmotic pressure from dropping too fast causing cerebral edema.
4. Potassium supplementation
The principle is the same as diabetic ketoacidosis.
5. Others
Generally, alkali supplementation is not needed, and blood glucose should not fall too fast, so that the drop of 5.6mmol/L (100mg/dl) per hour is appropriate. After the disease is stabilized, insulin can be changed to subcutaneous injection.
Other treatments: ①Remove the causative factors: apply antibiotics for infected people. ② Correct shock: if shock is not corrected after rehydration, plasma can be transfused. ③ Because of hypertonicity, blood viscosity increases, arterial and venous thrombosis and disseminated intravascular coagulation (DIC) should be prevented and treated with appropriate anticoagulation. ④Prevent the complication of cerebral edema in the course of treatment.