Relative insulin deficiency and inadequate fluid intake are the underlying causes of HHS. Hyperglycemia induces an osmotic diuresis that leads to profound intravascular volume depletion. HHS is often precipitated by a serious, concurrent illness such as myocardial infarction or sepsis and is compounded by conditions that impede access to water.
Presenting symptoms include polyuria, thirst, and altered mental state, ranging from lethargy to coma. Notably absent are symptoms of nausea, vomiting, and abdominal pain and the Kussmaul respirations characteristic of DKA. The prototypical pt is an elderly individual with a history of polyuria, weight loss, and diminished oral intake. The laboratory features are summarized in Table 25-1 Laboratory Values in DKA and HHS (Representative Ranges at Presentation). In contrast to DKA, acidosis and ketonemia are usually not found; however, a small anion gap may be due to lactic acidosis, and moderate ketonuria may occur from starvation. Prerenal azotemia is typically present. Although the measured serum sodium may be normal or slightly low, the corrected serum sodium is usually increased (add 1.6 meq to measured sodium for each 5.6-mmol/L [100-mg/dL] rise in the serum glucose). HHS, even when adequately treated, has a significant mortality rate (up to 15%), which is in part explained by comorbidities and pt age.
| TREATMENT | ||
Hyperglycemic Hyperosmolar StateThe precipitating problem should be sought and treated. Sufficient IV fluids (1-3 L of 0.9% normal saline over the first 2-3 h) should be given to stabilize the hemodynamic status. The calculated free water deficit (usually 9-10 L) should be reversed over the next 1-2 days, using 0.45% saline initially then 5% dextrose in water. Overly rapid fluid replacement should be avoided to prevent worsening of neurologic status. Potassium repletion is usually necessary. The plasma glucose may drop precipitously with hydration alone, though insulin therapy with an IV bolus of 0.1 units/kg followed by a constant infusion rate (0.1 units/kg per hour) is usually required. If the serum glucose does not fall, the insulin infusion rate should be doubled. Glucose should be added to IV fluid when the plasma glucose falls to 11.1-13.9 mmol/L (200-250 mg/dL), and the insulin infusion rate should be decreased to 0.02-0.1 unit/kg per hour. The insulin infusion should be continued until the pt has resumed eating and can be transitioned to a subcutaneous insulin regimen. |