Hyperglycemic hyperosmolar state (HHS) occurs when severe elevation of plasma glucose leads to hyperosmolarity and altered mental status.
HHS patients tend to be much older than DKA patients as HHS typically occurs in patients with type 2 diabetes mellitus.
Patients may live in institutional settings and not have free access to water.
In addition to altered mental status, they may exhibit neurological findings mimicking stroke that resolve with treatment of hyperosmolarity. Volume depletion is severe (0.1–0.2 L/kg), and signs such as tachycardia, hypotension, dry mucous membranes, and poor skin turgor are usually present on examination. Patients with poorly controlled hypertension may exhibit normotensive blood pressures that are an unusual change from baseline. Cardiopulmonary emergencies are well-known precipitants of HHS, and patients should be examined carefully for signs of coronary ischemia, heart failure, or chronic obstructive pulmonary disease (COPD) exacerbations.
Infections also commonly trigger HHS, and patients require prompt evaluation for urinary tract infections and pneumonia.
Glucocorticoids, thiazide diuretics, and beta-blockers may worsen preexisting diabetes or hyperglycemia.
Insulinopenia leads to impaired glucose uptake by skeletal muscle and inappropriate gluconeogenesis in liver, resulting in hyperglycemia that in turn induces osmotic diuresis and prerenal azotemia, further worsening hyperglycemia by limiting glucosuria.
(What causes insulinopenia)
Attenuated thirst response, as a consequence of either aging or central nervous system injury, also plays a role. There is sufficient insulin to suppress lipolysis and ketogenesis, distinguishing HHS from DKA.
Risk factors for HHS are listed in Figure 22-1. HHS patients tend to be much older than DKA patients as HHS typically occurs in patients with type 2 diabetes mellitus. Patients may live in institutional settings and not have free access to water. In addition to altered mental status, they may exhibit neurological findings mimicking stroke that resolve with treatment of hyperosmolarity. Volume depletion is severe (0.1–0.2 L/kg), and signs such as tachycardia, hypotension, dry mucous membranes, and poor skin turgor are usually present on examination. Patients with poorly controlled hypertension may exhibit normotensive blood pressures that are an unusual change from baseline. Cardiopulmonary emergencies are well-known precipitants of HHS, and patients should be examined carefully for signs of coronary ischemia, heart failure, or chronic obstructive pulmonary disease (COPD) exacerbations. Infections also commonly trigger HHS, and patients require prompt evaluation for urinary tract infections and pneumonia. Glucocorticoids, thiazide diuretics, and beta-blockers may worsen preexisting diabetes or hyperglycemia, and medications should be carefully reviewed.
Initial evaluation of patients with presumptive HHS is similar to workup of patients with DKA.
Key laboratories include electrolytes,
markers of renal and hepatic function, CBC, and amylase or lipase. Urinalysis and cultures of blood and urine should be obtained. Given the high risk of cardiopulmonary disease, EKG, chest films, and cardiac enzymes should also be screened.
The mortality rate for patients with HHS is as high as 10% to 15%. In a large study of nearly 500 patients presenting with HHS, age, severity of altered mental status on presentation, degree of hyperosmolarity, and renal function were independent predictors of mortality risk. Goals of therapy are to correct volume deficits and hyperglycemia with parenteral fluids and insulin, respectively, and in turn correct hyperosmolarity. Patients are also total body potassium depleted and require careful monitoring of potassium levels and therapy with supplemental potassium in intravenous fluids. Inciting events (eg, infection, coronary ischemia) also need to be identified and treated promptly.
Fluids, insulin, and supplemental potassium are initiated and managed mostly as discussed in management of DKA and summarized in Table 22-1. However, when plasma glucose falls below 300 mg/dL, dextrose is added to intravenous fluids and insulin rate is reduced (0.02–0.05 U/kg/h) to maintain plasma glucose in the range of 200 to 300 mg/dL until patients recover to baseline mental status as a protection against possible cerebral edema. Capillary glucose is monitored hourly and electrolytes every 2 hours while patients are managed with intravenous insulin. Patients require subcutaneous insulin to prevent recurrence of severe hyperglycemia, and intravenous insulin is overlapped 1 to 2 hours with the first dose of subcutaneous insulin.
A 62-year-old man presents with an asymptomatic abdominal aortic aneurysm (AAA) measuring 4.8 cm in diameter. The patient’s past medical history is significant for hypertension and stable angina. He has a 40-pack-year smoking history. His current medications include aspirin, a beta-blocker, and nitrates. The patient describes himself as an active man who just retired and plays 18-holes of golf two times a week. On examination, the carotid pulses and upper extremity pulses are normal. The abdomen is nontender with a prominent aortic pulse. Pulses in the femoral and popliteal regions are readily palpable and appear more prominent than usual.
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