Diabetic ketoacidosis (DKA) is typically associated with type 1 diabetes but can also occur in type 2 diabetes under extreme stress. DKA results from a lack of insulin and excess glucagon and catecholamines, leading to fat breakdown, ketone production, and high blood sugar. Symptoms include nausea, vomiting, fruity breath, and signs of dehydration. DKA is diagnosed based on hyperglycemia, ketonemia, and metabolic acidosis.

1. Diabetic Ketoacidosis (DKA)
Epidemiology
Diabetic ketoacidosis (DKA) is typically associated with type 1 diabetes. It also occurs in type 2 diabetes
under conditions of extreme stress such as serious infection, trauma, cardiovascular or other emergencies,
and, less often, as a manifestation of type 2 diabetes, a disorder called ketosis-prone diabetes mellitus.
DKA is more common in young (<65 years) patients. The National Diabetes Surveillance Program of the
Centers for Disease Control (CDC) estimated that there were 140,000 hospital discharges for DKA in 2009 in
the United States, compared to 80,000 in 1988. The mortality rate for hyperglycemic crisis declined from 54%
to 18% between 1980 and 2009. Mortality in hyperglycemic crisis is primarily due to the underlying
precipitating illness and only rarely to the metabolic complications of hyperglycemia or ketoacidosis. The
prognosis of hyperglycemic crisis is substantially worse at the extremes of age and in the presence of coma
and hypotension.
Pathogenesis
a) Metabolic Abnormalities
· Insulin deficiency and/or resistance à impairs glucose utilization in peripheral tissues & skeletal
muscle, increases the delivery of gluconeogenic precursors to the liver (such as glycerol from fat and alanine
from muscle), activates multiple enzymes in the gluconeogenic metabolic pathway, and increases glucagon
secretion by removing its (insulin) inhibitory effect, elevates potassium levels because insulin normally
promotes potassium cellular uptake
· Glucagon hormone excess à Increased hepatic/renal gluconeogenesis and glycogenolysis
· Increased secretion of catecholamines, cortisol, and growth hormone à opposes the actions of
insulin, and contributes to the increases in glucose and ketones production
b) Sources of Energy
· Decreased Glucose Utilization à Decreased cell entry of blood glucose as the body’s normal
source of energy
· Enhanced Lipolysis à As an alternative source, the body begins to use and transfer fatty acids from
peripheral fat stores to hepatocytes to produce ketones as a water soluble energy source
Etiology
· Infection (pneumonia, UTIs)
· Discontinuation or inadequate insulin therapy
· Severe dehydration (compromised water intake due to comorbid diseases requiring volume
restriction)
· Acute major illness (myocardial infarction, cerebrovascular accident, sepsis, pancreatitis)
· New onset type 1 diabetes
· Drugs that decrease carbohydrate metabolism (glucocorticoids, high-dose thiazide diuretics (HCTZ,
chlorthalidone), sympathomimetics (dobutamine, terbutaline), and 2nd generation “atypical” antipsychotics
(aripiprazole, clozapine, lurasidone, olanzapine, paliperidone, quetiapine, risperidone, ziprasidone)
· SGLT2 inhibitors (empaglifozin, canaglifozin, dapaglifozin)
· Cocaine use

2. · Psychological issues (eating disorders, intentional insulin nonadherence particularly in young patients
with type 1 diabetes due to fear of weight gain, hypoglycemia, rebellion from authority, and the stress from
chronic disease
Clinical Presentation
· Nausea, vomiting, abdominal pain frequent urination, hyperglycemia, lethargy, dyspnea with
hyperventilation (Kussmaul respirations), fruity odor on breath (due to exhaled acetone, similar to scent of
nail polish remover),
· Signs of dehydration: decreased skin turgor or dry skin, dry mouth or thirst, hypotension, tachycardia
Diagnostic Evaluation
https://www.aafp.org/afp/2013/0301/p337.html
http://care.diabetesjournals.org/content/32/7/1335
http://www.diabetes.org/living-with-diabetes/complications/ketoacidosis-dka.html
https://www-uptodate-com.jerome.stjohns.edu/contents/diabetic-ketoacidosis-and-hyperosmolar-
hyperglycemic-state-in-adults-clinical-features-evaluation-and-
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https://www-uptodate-com.jerome.stjohns.edu/contents/diabetic-ketoacidosis-and-hyperosmolar-
hyperglycemic-state-in-adults-
treatment?search=diabetic%20ketoacidosis&source=search_result&selectedTitle=1~150&usage_typ
e=default&display_rank=1#H1
http://spectrum.diabetesjournals.org/content/15/1/28#T1