الفهرس 
Pathophysiology and Complications of Diabetes MellitusOnly 14 pages are availabe for public view
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Abstract
This condition is characterised by hyperglycaemia and high plasma osmolalility with ketoacidosis being absent or less marked. This most commonly occurs in type 2 diabetes and is typically of gradual onset. This is a partial misnomer as patients presenting with this are rarely in a coma due to diabetes. There is usually an underlying medical condition that has exacerbated the (often undiagnosed) type 2 diabetes.
The blood glucose rises slowly, but inexorably, over a number of days and the patient becomes progressively more unwell. In most cases there is enough circulating insulin to prevent ketone formation, and therefore there is no acidosis due to ketonaemia; however, if they are very ill lactic acidosis may supervene. The serum osmolality is very high, usually greater than 340 mosm/kg with a blood glucose often in excess of 50 mmol/l.
Serum osmolality is estimated as 2([Na] + [K]) + [Glucose]. Some authorities also add the serum urea, but this contributes little to tonicity in vivo and may be omitted. Serum osmolality can be measured by the laboratory and if the difference between measured osmolality and estimated osmolality is significant, that is 20 mosm/kg, it suggests the presence of another solute, for example alcohol, which can be a precipitant for both DKA and HONK.
Traditionally the vast majority of patients with HONK are elderly, but there is an awareness that this may occasionally occur in children as the prevalence of type 2 diabetes is rising rapidly in this group. Treatment is essentially the same as for DKA, but with some modifications, in particular one can use 0.45% saline as the initial replacement fluid if the serum sodium is greater than 155 mmol/l. Insulin replacement is required initially at a maximum of 6 U/hour, but with volume replacement the blood glucose levels fall rapidly and after recovery not all patients require insulin treatment.
Mortality was 17% in one study, but is associated with preexisting comorbidity. While thromboembolic disease risk is increased it accounts for few deaths; it is unclear whether this is due to prophylactic treatment with subcutaneous heparin, or that the risk has been exaggerated. Shocked patients require catheterisation and measurement of hourly urinary output, but is not necessary in the great majority of patients. Nevertheless, it should be considered if patients have not passed urine after two hours, even if not shocked.
Patients’ conscious level may be reduced. If they do not respond to commands, nasogastric tube insertion and aspiration should be considered. The white cell count may be markedly raised from DKA alone, therefore only give antibiotics if there is clinical evidence of infection.
Silent acute myocardial infarction is not uncommon and an electrocardiogram (ECG) is mandatory in those over 30 years of age with DKA and HONK. However, in severe DKA the ECG may be abnormal and can be mistakenly interpreted as indicating a myocardial infarction. Repeat ECGs may be required and note that serum troponin levels may be mildly raised in DKA, as in many severe illnesses, thus these should be interpreted with care; if necessary cardiology input may be requested.