Case
A 32-year-old Hispanic man presented to the ED with complications associated with diabetes mellitus (DM), the symptoms of which started approximately 3 days prior to arrival. The patient reported feelings of fatigue, dry mouth, increased thirst, and frequent urination. He denied sweating, nausea, chest pain, shortness of breath, diarrhea, or blood in his urine; he also denied blurry vision or dizziness.
During history intake, the patient informed the emergency physician (EP) that he had been diagnosed with DM and hyperglycemia earlier that day by his primary care physician, who had immediately referred the patient to the ED for urgent management. The patient’s own medical history was noncontributory; however, his father’s history was notable for DM and chronic renal failure. The patient further stated that he was not on any medications. Regarding his social history, he denied cigarette smoking and noted only occasional alcohol consumption.
The patient’s vital signs on presentation were: blood pressure (BP), 116/74 mm Hg; heart rate, 113 beats/minute; respiratory rate, 26 breaths/minute; and temperature, 97.8°F. Oxygen saturation was 97% on room air. On physical examination, the patient was severely anxious, with tachycardia and respiratory distress. He was obese, with a body mass index of 30.9 kg/m2 (height, 5 feet, 4 inches; weight, 180 lb).
The patient was started on an intravenous (IV) bolus of 0.9% normal saline (2 L at 20 mL/kg). After a consultation with endocrinology, he was then given a maintenance dose of normal saline IV at 250 cc/h and an IV insulin drip at 0.1 U/kg/h following a bolus of 8 units of insulin IV. His glucose levels were carefully monitored via hourly finger-stick glucose testing.
Although the patient’s condition stabilized, he collapsed while walking to the bathroom. He had agonal respirations and no pulse. Resuscitation efforts were started with bag-valve-mask ventilation, along with emergent advanced cardiac life support (ACLS) treatment, the protocol of which included epinephrine administration (x2) IV push 5 minutes apart, 2 ampules of sodium bicarbonate (50 mEq each) IV push, and calcium gluconate 10% (x1) 10 mL (1 g) IV push. A pulse was re-established, and the patient was intubated.
The patient was diagnosed with diabetic ketoacidosis (DKA) and admitted to the intensive care unit where repeat laboratory evaluation was ordered. Additional pharmacological management included IV administration of dopamine, norepinephrine, phenylephrine, vasopressin, antibiotics (azithromycin, meropenem, and vancomycin), pantoprazole, and subcutaneous heparin.
During treatment, the patient coded a second time and was revived according to ACLS protocols. Shortly thereafter, he coded a third time, but resuscitation efforts failed. Pathology reported no biological cause of death, and the coroner closed the case as death due to DM-related complications.
Diabetic Ketoacidosis
Diabetic ketoacidosis is a major complication of DM.4 Although the condition usually occurs in type 1 DM, it can also develop in type 2 DM. Diabetic ketoacidosis may be an inciting event leading to the eventual diagnosis of DM, but can also develop during a concurrent illness such as a urinary tract infection or an eating disorder.5 Risk factors for DKA include patients with type 1 or type 2 DM, a family history of DM, obesity, and nonwhite patients whose ethnic background places them at increased risk.6 Hispanic, black, and African American patients are at a greater risk of developing DKA and are more likely to develop “ketosis-prone” type 2 DM.7
Patients who do not fit into the definitive categories of type 1 or 2 DM can be classified under ketosis-prone DM.7,8 Diabetic ketoacidosis acts as the inciting event for the disease and evolves into severe β-cell dysfunction, hence blurring the lines between the archetypal DM categories. Fifty percent of ketosis-prone DM patients are A-β+ (absent autoantibodies, present β-cell function), which indicates that the dysfunction can be partially reversed. Reversal of the condition is largely based on long-term β-cell reserves, which are dependent on tight glycemic control and insulin dependence. Higher incidences of the A-β+ variant of ketosis-prone diabetes are seen in the male population and are often unprovoked.9-11
Etiology
Diabetic ketoacidosis is the result of either a decrease or absence of insulin in the body (Table 2).4 Without insulin modulating exogenous glucose intake and endogenous glucose production (via glucagon, glycogenolysis, and gluconeogenesis), high levels of glucose are found in the circulation, leading to prominent hyperglycemia (>250 mg/dL or >13.8 mmol/L).6 This environment causes the body to switch from carbohydrate metabolism to fatty acid metabolism. As a result, acidic ketone bodies such β-hydroxybutyrate and acetoacetate are produced. These physiological changes in the body cause the signs and symptoms typically found in DKA.