The<unk>  (HHS) is a life-threatening and acute complication in patients with poorly treated diabetes mellitus (chronic high blood sugar or<unk> . HHS is more common in type II diabetics, and in individuals greater than 65 years of age. However, it has also been reported in children, younger adults and in type I diabetics. The basic pathogenesis is relative insulin deficiency and excess of counter-regulatory stress hormones which leads to<unk>  and<unk> ity. Osmotic diuresis due to<unk>  causes dehydration, prerenal azotemia and furthers aggravates plasma osmolality. The common precipitating factor for<unk>  include infections (mostly GI and genitourinary), myocardial infarctions, stroke, aggravation of already existing chronic kidney disease and poorly controlled diabetes. The initial symptoms are due to<unk>  and dehydration which include lethargy, extreme fatigue, polyuria, excessive thirst and leg cramps. The neurological symptoms develop with increased plasma osmolality greater than 320 mOsm/kg and include confusion, seizures and eventually coma. Patients with the<unk>  may also appear dehydrated, lethargic, disoriented and in shock. Physical examination of patients with the<unk>  is usually remarkable for hypothermia, hypotension, tachycardia, tachypnea, nausea, vomiting and seizures or other focal neurological signs. HHS must be differentiated from diabetic ketoacidosis and other conditions that can present with an altered mental<unk> s or focal neurological signs and symptoms such as CNS infections and stroke. All these conditions may be differentiated on the basis of history findings, clinical features, and laboratory abnormalities. The symptoms of<unk>  (HHS) develop slowly over a period of days to weeks as compared to diabetic ketoacidosis which presents within hours of inciting event. If left untreated, patients may develop multiorgan failure and eventually death. Common complications are renal failure, thrombotic events, and cardiovascular complications. The prognosis of the<unk>  (HHS) depends on the hemodynamic<unk> s, comorbidities, and age at presentation. Laboratory findings consistent with the diagnosis of<unk>  (HHS) as outlined by the American Diabetes Association include plasma glucose > 600 mg/dl, serum osmolarity > 320 mOsm/kg, blood pH > 7.3, serum bicarbonate > 18 mEq/L and negative or trace positive urine or serum ketones. The mortality rate ranges from a low of less than 5000 per 100,000 individuals to a high of 20,000 per 100,000 individuals which is ten times higher than diabetic ketoacidosis. The mainstay of therapy for HHS is medical therapy including intravenous insulin, fluids, and potassium replacement therapy. The basic principles guiding therapy include rapid restoration of adequate circulation and perfusion, correction of<unk> ity, electrolytes balance,<unk> , identifying and treating the underlying precipitating cause and close monitoring to prevent and treat complications if they develop. The complications due to treatment can be cerebral edema, pulmonary edema, and hypoglycemia. The management of HHS is mainly derived from studies on patients with diabetic ketoacidosis (DKA) and there is a need for prospective clinical trials, which focus on HHS as a separate clinical entity, for the optimum treatment options.
Hyperosmolar hyperglycemic state
Ketotic hypoglycemia
Diabetic ketoacidosis
Hyperglycemic crises
Diabetic Ketoacidosis
Hypokalemic sensory overstimulation
Dehydration
Psychogenic polydipsia