Diabetic ketoacidosis/ketoacidemia (DKA) is an absolute or relative insulin deficiency resulting in ketone body production and decreased serum total CO2 concentration. This potentially life-threatening metabolic disturbance occurs most commonly in type 1 diabetics, but may also occur in type 2 diabetics.
Absolute or relative insulin deficiency results in hyperglycemia, glycosuria, and intracellular starvation, leading to release of counterregulatory hormones (glucagon, epinephrine, cortisol, and growth hormone). This results in lipolysis, proteolysis, glycogenolysis, gluconeogenesis, and insulin resistance. Glycogenolysis and gluconeogenesis exacerbate the already-present hyperglycemia. A negative cycle of progressive ketoacidemia and insulin resistance, associated with a surge of counterregulatory hormones, leads to increasing insulin resistance, hyperglycemia, dehydration, electrolyte losses, potential brain swelling, and may result in metabolic death.
Figure 14.1 ▪ Diffuse Brain Swelling; Diabetic Ketoacidosis.
A noncontrast head computed tomographic scan shows obliteration of all cerebrospinal fluid spaces including ventricles and basal cisterns with blurring of the margins of gray and white matter, typical for diffuse cerebral edema and herniation around the brainstem. These findings were seen in a patient with new-onset diabetes who initially presented with a normal mental status, severe ketoacidemia without shock, and received isotonic saline 60 mL/kg over 2 hours. Progressively diminished arousability and hypertension were unrecognized signs of raised intracranial pressure until irregular respirations and a decrease in heart rate ensued. (Photo contributor: Geetha Chari, MD.)
Figure 14.2 ▪ Brain Swelling Seen at Autopsy; Diabetic Ketoacidosis (DKA).
A dorsal view of the brain shows severe brain swelling with flattened gyri and effaced sulci. Evidence of brain swelling with herniation was seen on the brain’s ventral surface. Pretreatment brain herniation is rare, but brain swelling prior to treatment (incompletely understood cause[s]) appears common among pediatric patients with DKA. This 17-year-old known diabetes patient collapsed at home and developed hypertension, bradycardia, and agonal respirations on arrival of first responders. Such patients underscore the need for careful volume resuscitation, fluid and electrolyte management, and timely administration of insulin in those with DKA, because they likely present with some degree of brain swelling even before treatment begins. (Photo contributor: M.G.F. Gilliland, MD.)
Key findings include polyuria, nocturia, polydipsia, no change in appetite, polyphagia or decreased appetite, varying degrees of dehydration, weight loss, abdominal pain, vomiting, hyperventilation, Kussmaul breathing (which is clinically visible and may be confused with respiratory distress from primary respiratory diseases such as pneumonia), subnormal body temperature (in severe DKA; may also occur in sepsis), altered mental status (which may be caused by shock, profound ketoacidemia or raised intracranial pressure [ICP]), the fruity odor of ketones on the breath, and Candida infections (eg, vaginitis or perineal yeast). Typical laboratory findings include hyperglycemia (may only be modest with serum glucose <300 mg/dL), glycosuria, ketonemia, ketonuria, metabolic acidosis/acidemia, and compensatory hypocarbia. Enuresis, urinary incontinence, apparent or actual hyponatremia, hypernatremia, hypokalemia, hypophosphatemia, hypomagnesemia, increased serum urea nitrogen, increased serum creatinine, hypertriglyceridemia, and increased serum amylase may also be present. Increased lipase in the absence of pancreatitis may occur. Initially, potassium, magnesium, and phosphorus may be increased or normal; however, close monitoring is required because serum concentrations of these ions may decrease significantly with treatment as they move intracellularly, and total body depletion of one or more of these ions becomes manifest.
Figure 14.3 ▪ Candidiasis as a Presenting Sign of Diabetes.