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Diabetic ketoacidosis (DKA) is the main hyperglycemic complication in type 1 Diabetes Mellitus (DM1). The basic principles in treatment have to be followed carefully. The patient with DKA has a very deep volume depletion. To restore the circulatory capacity is the first step. From this point on, the restoration of the lost fluids is slow, around 1% per hour, aiming at the correction of the metabolic disturbance already on and avoiding great fluctuations in osmolality, which increases the risk of having complications. Attention to the development of cerebral edema, which, once suspected, deserves an urgent treatment plan, trying to avoid neurologic sequelae or even death. Subcutaneous ultra-rapid insulin has been demonstrated to be efficient and easier to use. As the perfusion gets improved and the levels of insulin increase, the lipolysis is blocked, as well as the generation of ketones and so the acidemia tends to be solved. DKA is still a high-mortality condition. And to be in a hurry frequently leads to neurologic sequelae and even to a fatal outcome.

The results of the study involving 123 patients suffering from hyperglycemic diabetic coma lead to the conclusion on ineffectiveness of high-dose insulin. Treatment of hyperglycemic coma by low-dose insulin is more preferable as warranting continuous decrease of glycemia without its transformation into hypoglycemia, ++post-hypoglycemia hyperglycemia, brain edema.

Hypoglycaemia remains a serious and much feared complication of insulin therapy. In this study, patients attending an accident and emergency department in hypoglycaemic coma were randomized to treatment with either intravenous dextrose (25g) or intramuscular glucagon (1mg), administered into the right thigh. Restoration of normal conscious level was slower after glucagon than dextrose (9.0 vs 3.0 min, P less than 0.01), although the average duration of hypoglycaemic coma was 120 min. Two patients in the glucagon-treated group, who failed to show satisfactory recovery after 15 min, required additional treatment with intravenous dextrose. On questioning following recovery, all except two patients reported loss of awareness of the onset of hypoglycaemia Intramuscular glucagon is valuable in the treatment of severe hypoglycaemia outwith hospital and, although the slightly slower and less predictable recovery may appear to make it a less attractive option than intravenous dextrose in the accident and emergency department, this must be balanced against the advantages of ease of administration and a lower incidence of serious adverse effects.

A 12 year old female patient presenting non ketotic hyperosmolar hyperglycemic coma as initial sign of diabetes mellitus is presented. She was successfully treated with continuous infusion of low dose of insulin and saline and glycosaline isotonic sera. Potassium was precociously added to the hydrating solutions. During convalescence she suffered a left iliofemoral thrombophlebitis which remitted with appropriate treatment. In coma stage, C-peptide was close to normal, indicating active insulin production by the pancreas.

We report the case of a boy aged 9 1/2 years with hyperosmolar, nonketotic diabetic coma. He was not known to be diabetic prior to the onset of coma. Pathogenetic aspects of this rare manifestation of juvenile diabetes are discussed. It is dangerous to decrease osmolarity too rapidly during infusion of very hypotonic solutions. Treatment with continuous low-dose insulin infusion may cautiously be tried.