A precipitating factor may be a coexisting acute infection such as pneumonia but Non ketotic hyperglycemic-hyperosmolar coma can also occur when patients with undiagnosed or neglected type II Diabetes receive drugs that impair glucose tolerance (eg, glucocorticoids) or increase fluid loss (diuretics). The consistent and diagnostic features of Non ketotic hyperglycemic-hyperosmolar coma are CNS alterations, extreme hyperglycemia, dehydration and hyperosmolarity, mild metabolic acidosis without marked hyperketonemia, and prerenal azotemia (or pre existing chronic renal failure). The state of consciousness at presentation varies from mental cloudiness to coma. In contrast to diabetic ketoacidosis , focal or generalized seizures may occur. The plasma glucose is usually much higher than in most cases of diabetic ketoacidosis (about 1000 mg/dL). Most of the clinical signs and symptoms are similar to that of diabetic ketoacidosis because of hyperosmolarity. (Wiggam et al 1998)
Hyperosmolarity is a condition in which the blood is much more concentrated with sodium, glucose, and other molecules which, in turn, attracts water into the blood stream. This creates a vicious cycle of increasing dehydration and increasing blood-glucose levels. Risk factors are older age; underlying kidney insufficiency; congestive heart failure; recent discontinuation of insulin or oral hypoglycemic agents; and a precipitating event such as infection, stroke, or recent surgery.
Hypoglycemia/insulin shock is very uncommon in people without diabetes. Low blood sugar is more common in people taking insulin than in those who are using pills to manage their diabetes. It rarely happens when diabetes is being treated by diet alone and without medications. Early symptoms are: shakiness, sweating ,hunger, dizziness, blurry vision and poor concentration if untreated, the patient may develop to headache, confusion mood changes and coma or seizure. Diagnosis is made by an abnormally low plasma glucose level is usually defined as lower than 50 mg/dL in men or lower than 45 mg/dL in woman. Blood samples may be used also to determine initial plasma insulin, proinsulin, and C-peptide levels or to perform a drug scan when necessary. Blood lactate and pH should be determined and the plasma checked for ketones. Treatment is either by oral ingestion of glucose or intravenous injection of 50 or 100 mL of 50% glucose followed by a continuous infusion of 10% glucose for severe symptoms or when a patient cannot take oral glucose. In order to make diagnosis clinical signs and symptoms must be taken into account. The symptoms of hyperglycaemic coma are polyuria, Polydipsia, weight loss, which may be dramatic due to breakdown of protein and fat stores, muscle pains and cramps, symptoms of acidosis and dehydration, abdominal pain that may be severe enough to present as a surgical emergency, shortness of breath that may be mistaken for primary respiratory distress, confusion and coma in the absence of recognized head injury. Other secondary symptoms include vomiting, signs of intercurrent infection (eg, in urinary, respiratory tracts), weakness and nonspecific malaise that may precede other symptoms of hyperglycemia. (Edge JA, Dunger DB 1994)
Clinical diagnosis is made by measuring a number of components such as blood and urea as well as imaging techniques. Plasma glucose levels range from 350 to 700mg/dl in Diabetic ketoacidosis and are higher again in Non ketotic hyperglycemic-hyperosmolar coma. Some creatinine assays can be affected by the presence of ketones, thus giving falsely elevated results. Under these circumstances, blood urea may be used to provide a better measure of dehydration. Potassium initial blood levels usually are normal or high, despite considerable deficits of total body potassium. This is because the acidosis encourages leakage of intracellular potassium. Insulin drives potassium back into the cells, and levels may drop very quickly with treatment. Bicarbonate levels are also measured (usually available from blood gas analysis) as reflects degree of acidosis. CT head scan is also common in coma patients. Chest x-ray are also sometimes performed. On undertaking of a full blood count WBC will usually be elevated, even in absence of infection
Once Diagnosis is made treatment consists of fluid replacement, insulin, electrolyte replacement and bicarbonate. (Wiggam et al 1998)
No randomized trials of fluid replacement have been conducted, and over the years a variety of regimes have been proposed. Often the best outcomes have been achieved by using normal or half-strength saline for first resuscitation and replacement. Slowly correcting the fluid deficit over 24-48 hours appears safer than rapid rehydration. The osmotic dieresis will continue while blood glucose levels remain above 300 mg/dL. This can cause greater urinary output than the rate of fluid replacement. Obviously, the patient can become more dehydrated and acidotic unless ongoing losses are replaced. Clinicians may need to calculate and replace losses on an hourly basis by measuring fluid losses and the weight of the patient.
In Hyperglycaemia patients are all ways treated with insulin to reduce the blood sugar levels and to have the inhibitory effect on the lipolytic action of cortisol and growth hormone. Continuous, low-dose intravenous insulin infusion generally is accepted as the safest and most effective method of insulin delivery for treating diabetic ketoacidosis. Low-dose intravenous insulin infusion is simple, provides more physiological serum levels of insulin, allows gradual correction of hyperglycemia, and reduces the likelihood of sudden hypoglycemia and hypokalemia. A normal starting rate is 0.1 U/kg/h for a newly diagnosed case, then the rate is adjusted according to its effect on blood glucose levels.In non ketotic hyperglycemic-hyperosmolar coma it is especially important that insulin dose is small as they are more sensitive to the action of insulin. (Wiggam et al 1998)
Patients with diabetic ketoacidosis always have a total body deficit of potassium. After initial resuscitation, and provided serum/plasma levels are below 5 mEq/L, or a good renal output has been maintained, add potassium to all replacement fluids. Potassium chloride most commonly is administered. This theoretically could make the acidosis worse, but no evidence exists that administration of other potassium salts such as phosphate or acetate is more effective. (Edge JA, Dunger DB 1994)
Although metabolic acidosis may be severe, no evidence supports administration of intravenous sodium bicarbonate to improve outcomes and has been shown to harm and delay recovery. The only justification for using intravenous bicarbonate is when the acidosis is sufficiently severe to compromise cardiac contractility. Although patients usually have an absolute deficit of phosphate and magnesium, no evidence exists of a need for replacement.
Constant monitoring of patients is required, capillary blood glucose samples analysed on a reflectance meter are acceptable for monitoring changes in blood glucose levels as treatment progresses, glucose levels must be measured at least hourly. Blood gases traditionally, arterial blood samples are used, but free-flowing capillary or venous samples are as reliable for monitoring acidosis and are much easier to collect. In moderate and severe diabetic ketoacidosis, pH will be less than 7.2. ECG is a useful adjunct to monitor potassium status characteristic changes appear with extremes of potassium status. Sodium values are likely to be low because of the dilutional effect of hyperglycemia but should rise with treatment. Failure of sodium levels to rise is associated with an increased risk of cerebral edema. Urinalysis checks all urine for glucose and ketones for at least 24 hours.
Factors that must be taken into account by the clinician are that extremely high triglyceride levels sometimes are present which can causes an artificial lowering of other blood values such as glucose, sodium, and potassium and that blood amylase levels often are elevated in diabetic ketoacidosis and can be misleading in the presence of abdominal pain. (Edge JA, Dunger DB 1994)
In cases in which diabetic ketoacidosis occurs as a new diagnosis of diabetes, the process of education and support by the diabetes team should begin when the patient recovers. In cases in which diabetic ketoacidosis occurs in a child with established diabetes, explore the cause of the episode and take steps to prevent a recurrence.
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