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Pathophysiology of Diabetic Ketoacidosis

Diabetic ketoacidosis is a common complication of diabetes mellitus. It commonly arises

due to absolute insulin deficiency, missed insulin dosage, or increased insulin requirements. This

complication usually presents with polydipsia, Kussmaul breathing, polyphagia, and

dehydration.

High serum osmolarity results in osmotic diuresis. Due to either absolute deficiency of

insulin or insulin receptors' resistance, entry of glucose into the cells will be impaired. Serum

glucose thus increases to levels beyond the renal reabsorption threshold, which is usually at

10mmol/l in most people but differs with age and sex. The affected persons, therefore, lose water

through the kidneys resulting in increased urinary frequency and volume. Besides, the effective

circulating volume will reduce, thus causing severe dehydration and sometimes hypovolemic

shock.

Increased serum ketone levels cause metabolic acidosis, resulting in Kussmaul breathing

and abdominal pain. Decreased entry of glucose into the cells triggers the release of

catecholamines, corticosteroids, and glucagon. These hormones stimulate the breakdown of fatty

acids, proteins, and glycogen as alternative pathways for energy generation by the body resulting

in the formation of ketones, alanine, and glucose (Gosmanov & Kitabchi). Glucose further

worsens hyperglycemia, polydipsia, and dehydration, while alanine is used in gluconeogenesis.

Ketones are released into the bloodstream to be used by the cells to generate adenosine
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triphosphate (Seth, Kaur & Kaur, 3). Since the individual lacks insulin, these products will not

enter the cell and cause metabolic acidosis. Patients hyperventilate to compensate for metabolic

acidosis by mopping out carbon dioxide in the blood. Corticosteroids and hypotension contribute

to the formation of gastric ulcers leading to abdominal pain in a subset of patients with DKA.

Reduced glucose entry into the cells due to absolute insulin deficiency or increased

insulin demands results in hyperglycemia and ketonemia. Hyperglycemia causes osmotic

diuresis and hypovolemia. Ketonemia causes metabolic acidosis leading to Kussmaul breathing

and abdominal pain.

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Works Cited

Gosmanov, Adair R., and Abbas E. Kitabchi. "Diabetic ketoacidosis." (2015).

Seth, Pankaj, Harpreet Kaur, and Maneet Kaur. "Clinical profile of diabetic ketoacidosis: a

prospective study in a tertiary care hospital." Journal of clinical and diagnostic research:

JCDR 9.6 (2015): OC01.