Outline the pathophysiology, complications and treatment of hyper-osmolar non-ketotic coma.
Pathophysiology: insulin deficiency (and/or resistance) impairs peripheral glucose utilisation in skeletal muscle, increases fat and muscle breakdown and promotes hepatic gluconeogenesis; glucagon excess also promotes hepatic gluconeogenesis. Other stressors may precipitate (e.g. infection, myocardial infarction, and surgery), partially by increasing cortisol and catecholamine release; omission of normal treatment may also be responsible. Osmotic diuresis results in significant fluid depletion (e.g. 8 to 10 litres), with associated deficits of potassium and phosphate (despite variable plasma levels).
Complications: CNS depression/coma, hypovolaemia, hyperosmolality, metabolic acidosis, potassium and phosphate depletion, and thromboembolism. Cerebral oedema if glucose lowering or fluid shifts too rapid.
Treatment: of underlying precipitants (sepsis, myocardial infarction), replace fluid deficit (± invasive monitoring) without rapidly dropping osmolality, insulin therapy (eg. infusion), careful monitoring and replacement of electrolytes (esp. potassium, phosphate), prevention of pulmonary thromboembolism.
In brief, one would have to say that HONK results from uncontrolled hyperglycaemia in a patient with some residual insulin secretion. Like the DKA patient, these people usually have some sort of precipinant, be it myocardial infarction, stroke, sepsis, or what have you- anything that causes a stress response and decreases peripheral insulin sensitivity. However, unlike the type 1 diabetic who would switch to ketone production and become acidotic, the HONK patient suffers few symptoms initially. Their decreased insulin sensitivity ensures that the hyperosomolar hyperglycaemic state is maintained, and the residual insulin secretion ensures that hepatic metabolism resists conversion into ketone production.
The resulting hyperglycaemia results in an osmotic diuresis, gradually dehydrating the patient and producing a hyperosmolar state.
The complications of HONK are also asked about in Question 18.1 from the second paper of 2008. In brief summary, they are as follows:
The stereotypical approach to management is listed below:
Key issues of "specific therapy:
Hyperglycemic Comas by P. VERNON VAN HEERDEN from Vincent, Jean-Louis, et al. Textbook of Critical Care: Expert Consult Premium. Elsevier Health Sciences, 2011.
Oh's Intensive Care manual: Chapter 58 (pp. 629) Diabetic emergencies by Richard Keays
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