After prolonged insulin deficiency the patient can present with four acute problems: hyperglycemia, dehydration, electrolyte depletion, and metabolic acidosis (Figure 37-2). Stress causes release of counterregulatory hormones, which can lead to gluconeogenesis. Severe hyperglycemia increases serum osmolality and leads to osmotic diuresis, resulting in significant dehydration. Osmotic diuresis leads to urinary losses of water, sodium, potassium, magnesium, calcium, and phosphorus. The typical total body water loss in DKA is 6 L in adult patients.

It is thought that the hyperosmolarity further impairs insulin secretion and promotes insulin resistance. Without insulin, the newly liberated glucose cannot be used, further increasing serum blood glucose levels, urine glucose concentrations, and osmotic diuresis. ³ Fats and muscle proteins are metabolized for energy. The ensuing lipolysis causes a buildup of fatty acids, which overcomes the body’s natural buffering system and leads to ketoacidosis.

DKA develops over a relatively short time, usually 2 to 3 days. The condition occurs most often in young adults and can result from infection, illness, stress, substance abuse, or failure to adhere to an insulin regimen. The patient describes a steady progression of symptoms, including polydipsia, polyuria, fatigue, and weakness. Patients with new-onset diabetes report recent weight loss. As ketoacidosis worsens, nausea, vomiting, decreased appetite, and abdominal cramping occur. The patient appears in moderate to severe distress with possible alteration in level of consciousness, confusion about recent events, or slow response to questions. Lethargy can progress to coma, and hyperthermia may be present.

Rapid, deep, Kussmaul respirations are present, and a fruity odor is usually noted on the breath. This acetone smell indicates worsening ketoacidosis. The cause of Kussmaul breathing is a respiratory compensation for a metabolic acidosis. Blood gas values from a patient with Kussmaul breathing will show a decreased PCO ₂ level because of a forced increased respiration (blowing off the CO ₂). The patient feels an involuntary urge to breathe rapidly and deeply. The skin is usually hot and dry, skin turgor is diminished, and mucous membranes are dry. Hypotension can result from severe dehydration. The most frequently seen cardiac rhythm is sinus tachycardia, but dysrhythmias related to electrolyte disturbances also occur. This is a grave situation in the pregnant woman because of deleterious effects on the fetus. Early identification and aggressive interventions are critical to minimize effects on the fetus and the mother.

Initial laboratory studies should be obtained early and fluid therapy started on arrival to the ED. A serum glucose level higher than 300 mg/dL and normal or elevated potassium levels are usually present. Creatinine and blood urea nitrogen (BUN) levels may be elevated as a result of dehydration. Serum osmolality is greater than 310 mOsm/kg, and serum acetone titrations are positive. Serum ketone testing based on the measurement of β-hydroxybutyrate (BOHB or β-OHB, the main ketoacid causing acidosis) is recommended for diagnosis and monitoring. Mean BOHB levels in DKA are about 7 mmol/L, but can range from 4 to 42 mmol/L. ³ Urinalysis results include elevated levels of ketones and glucose. Blood gas results typically demonstrate normal arterial oxygen pressure (PaO ₂), respiratory alkalosis, and metabolic acidosis. Infection can precipitate DKA, so blood cultures and a urine culture should be obtained when infection is suspected. After cultures are obtained, antibiotic therapy should begin. Radiographs may also be required to determine the primary site of infection.

Management in the ED should be aggressive. Treatment focuses on correction of hyperglycemia, dehydration, electrolyte imbalances, and metabolic acidosis. Close monitoring with frequent reassessment is essential to prevent complications. Serum glucose and potassium levels should be monitored every 1 to 2 hours, and pH should be monitored every 2 to 4 hours. ³ Oxygen therapy should be initiated for any signs of hemodynamic compromise or altered mental status.

Intravenous fluid replacement should start immediately with 1 to 2 L of normal saline over the first 1 to 2 hours of treatment for adults. In children the initial fluid bolus is weight based (5 to 20 mL/kg, dependent on the child’s perfusion status); volume replacement is carefully titrated because of the high risk for cerebral edema in the pediatric population. The adult patient may require up to 8 to 10 L of fluid. Volume is gradually replaced after the initial fluid bolus because rapid infusion of a large volume increases the risk for development of cerebral edema. Close observation of intake and output is essential; placement of a urinary catheter ensures accurate output assessment. A continuous infusion of regular insulin is administered at 0.1 units/kg/hr to stop ketogenesis and achieve a steady decrease in serum glucose level of 50 to 75 mg/dL/hr; an initial intravenous (IV) bolus of 0.15 units/kg of regular insulin may be administered. The short duration of action for regular insulin allows better control of serum glucose levels. After serum glucose level reaches 250 to 300 mg/dL, fluids should be converted to 5% dextrose in normal saline (D ₅NS) to provide fuel until the patient is able to eat. Resolution of a hyperglycemic emergency occurs when the serum glucose level is less than 200 mg/dL, serum bicarbonate level is greater than or equal to 18 mEq/L, and in DKA, the venous pH is greater than 7.3. ³

Fluid replacement dilutes serum potassium and promotes diuresis. In addition, total body hypokalemia is exacerbated by metabolic acidosis, so potassium replacement should begin after the initial liter of IV fluids is infused, even when initial values are normal. Potassium levels frequently drop precipitously in the first few hours after treatment has been initiated because potassium moves back to the intracellular space along with the insulin and existing glucose. Serum potassium levels must be repeated every 1 to 2 hours during initial management. Cardiac monitoring is essential because dysrhythmias can develop with significant hypokalemia.

Acidosis generally corrects with insulin therapy. Insulin allows the cells to use available glucose for energy, leading to decreased proteinolysis and lipolysis, and the ketoacidosis resolves. Insulin infusion should be continued until the pH or serum bicarbonate level has normalized; IV fluids should be converted to D ₅NS once the serum glucose level reaches 250 to 300 mg/dL to prevent hypoglycemia. Acidosis in DKA is not routinely treated with sodium bicarbonate because sodium bicarbonate administration can cause rebound alkalosis, which can worsen hypokalemia and increases the risk for development of cerebral edema.

Controlling nausea and vomiting not only improves patient comfort but prevents worsening dehydration. The patient may require analgesia to relieve abdominal pain, headaches, or other somatic complaints. Providing a quiet, calm environment can improve patient comfort. Stress reduction plays an important part in patient recovery. Thorough explanation of treatment, medications, and plan of care can alleviate stress related to hospitalization.

Potential complications include hypoglycemia, hypokalemia, dysrhythmias, and cerebral edema. Monitor capillary/serum glucose levels, electrocardiogram (ECG), laboratory values, vital signs, intake and output, and neurologic status carefully. If the serum glucose level falls rapidly, the resulting fluid shift can lead to cerebral edema, which is associated with a higher mortality rate. Cerebral edema remains the leading cause of death for children presenting in DKA.

Hyperosmolar hyperglycemic state (HHS), also known as hyperosmolar hyperglycemic nonketotic coma (HHNC), is a life-threatening emergency characterized by marked elevation of blood glucose level, hyperosmolarity, and little or no ketosis. HHS threatens type 2 (non–insulin-dependent) diabetic patients with mortality rates as high as 10% to 50%, although true mortality data are difficult to interpret due to the high incidence of comorbidities. ¹⁹ Delayed diagnosis in undiagnosed type 2 diabetes, alcoholics, and dialysis patients place these groups at the greatest risk.

With the increase in the prevalence of type 2 diabetes and the aging population, this condition is likely to be encountered more frequently in the future. The precipitating causes are numerous, with underlying infections, acute myocardial infarction, and stroke being the most common. Other causes include certain medications, medication and treatment noncompliance, undiagnosed diabetes, substance abuse, and coexisting disease. Physical findings include those associated with profound dehydration and various neurologic symptoms such as coma.

Typically, patients presenting with HHS are over 50 years of age and have undiagnosed diabetes or type 2 diabetes managed by diet and/or oral medications. In addition, they frequently are on medications that aggravate the problem, such as diuretics that cause mild dehydration. ¹⁹ Type 2 diabetic patients over 50 years typically present with other contributing health problems, so it is necessary to search for other underlying illness. When stressed with illness, surgery, or injury, the body responds with increased glucose levels. Type 2 diabetic patients produce enough insulin to avoid ketoacidosis but not enough to prevent profound hyperglycemia.

Increased serum glucose levels act as osmotic diuretics, leading to severe dehydration. Patients are unable to replace lost fluids, so their condition progressively worsens. Lack of sufficient circulating insulin causes the body to metabolize fat and muscle tissues, which increases circulating fatty acid and amino acid levels. The resulting hepatic gluconeogenesis compounds existing hyperglycemia. Underlying renal disease or decreased intravascular volume will decrease the glomerular filtration rate and cause the glucose level to increase. The loss of more water than sodium leads to hyperosmolarity. Insulin is present, but it is not sufficient to reduce blood glucose levels, particularly in the presence of insulin resistance. ¹⁹Figure 37-3 illustrates the pathophysiology of HHS.

Onset of symptoms in HHS is much more insidious than with DKA, developing over days or even weeks. Subtlety of symptoms may account for delay in seeking treatment. The patient may notice vague abdominal pain, decreased appetite, polydipsia, and polyuria. As the disease progresses, neurologic symptoms such as headaches, blurred vision, and confusion develop. Changes in level of consciousness, seizures, or coma also occur. Tachycardia, dysrhythmias, and hypotension may also be present. Respirations may be increased but do not have the fruity smell associated with DKA. It is the decrease in mental status that usually brings the patient to the hospital.

Laboratory analysis includes complete blood count (CBC), electrolytes, urinalysis, and arterial blood gases. Typical laboratory findings in HHS include blood glucose levels greater than 600 mg/dL (33.3 mmol/L), serum osmolality greater than 320 mOsm/kg, pH levels greater than 7.30, and mild or absent ketonemia. Elevated white blood cell (WBC) count is present with infection. Serum sodium and potassium levels may be normal or elevated depending on the level of dehydration.