Hyperosmolar hyperglycemic syndrome differs from DKA in the more dramatic degree of dehydration, higher serum glucose, lack of acidosis, advanced patient age, and much higher mortality (Fig. 18.8).
Hyperosmolar hyperglycemic syndrome (HHS) connotes severe hyperglycemia without (or with mild) acidemia or ketoacidosis. The pathophysiologic assumption is that patients with HHS have a greater insulin reserve and, unlike patients with DKA, are able to inhibit lipolysis and avoid ketoacid formation. Typically, serum glucose is higher than in diabetic ketoacidosis, patients are remarkably more dehydrated, older, and with more prominent underlying illnesses.
The severe dehydration and hyperglycemia often results in effective serum osmolality (Table 18.2) greater than 320 mOsm/L, a level at which depression of consciousness or coma can be attributed to the hyperosmolar state. Patients commonly have type 2 diabetes mellitus, with poor antecedent glucose control. Thrombotic complications, which may occur in DKA, are a feared complication of HHS. Coronary arteries may clot, and arterial clots may propagate from the periphery to include the large central vessels. Presumably, the severe dehydration results in hemoconcentration and a hypercoagulable state. Because of the advanced patient age and the hypercoagulability and decreased perfusion accompanying severe dehydration, myocardial infarction must be specifically excluded as a precipitating or a complicating event [small doses of intravenous heparin (500–1000 units/h) are appropriate unless contraindicated].
Fig. 18.8 There is no clear separation of DKA and hyperglycemic hyperosmolar syndrome (HHS). The less extreme glucose elevations and more extreme acidosis can be labeled DKA. The more extreme glucose elevations with no or minimal acidosis can be labeled HHS. In between, there is overlap and the clinician tailors therapy accordingly
Abdominal pain in HHS should be evaluated as a medical emergency, with consideration of perforated viscus, acute cholecystitis, and ischemic bowel. Patients should be treated in an intensive care setting. Fluid management with aggressive rehydration is the critical aspect of treatment of hyperosmolar syndrome. An immediate fluid challenge should be given to guarantee continued renal perfusion and urine output. One or two liters of fluid in the first hour of therapy followed by 1 l/h for the next 4 h are commonly recommended. The water deficit can be calculated from the serum osmolality (the serum sodium can be substituted for osmolality in the equation). Half the water deficit should be replaced in the first 8–12 h. Exceptions include patients with renal or congestive heart failure, who require highly individualized fluid management. The “corrected” serum sodium (Table 18.2) indicates the degree of free water loss – the higher the corrected sodium, the greater the water loss. In spite of marked free water loss, initial fluid replacement is with isotonic solutions, usually normal saline (NS), to establish blood pressure and perfusion. Hypotonic fluids (1/2 NS) are then administered, followed again by isotonic fluids when the glucose falls significantly (for example, to levels of 300–500 mg/dL). The rationale is that hypotonic fluids distribute more evenly between the intravascular and the extravascular space, whereas isotonic fluids remain in the intravascular space. As hyperglycemia resolves, fluid leaves the intravascular space and moves intracellularly. The movement of fluid out of the intravascular space in a severely dehydrated patient may result in vascular “collapse” (hypotension and irreversible shock). Insulin plays only a minor role in the treatment of HHS, since these patients are not “ketosis prone,” are not acidotic, and do not require restraint of free fatty acid release. The glucose osmotic diuresis that occurs with fluid administration is the most important factor in lowering the blood glucose toward the renal threshold of 180 mg/dL. Small doses of insulin may be useful, but rapid blood lowering of the serum glucose with insulin is not desirable, because the osmotic pull of glucose helps to maintain intravascular volume and to prevent cerebral edema.
When it is over, the physician must educate the patient not to omit insulin at times of stress.
Patients with type 1 diabetes must always take insulin; patients with type 2 diabetes must understand when insulin doses need to be increased. Common misconceptions have to be corrected. The patient must take insulin even when not able to eat. Ordinarily, the diabetic patient will have long-acting depot insulin or continued pump therapy between meals and during overnight fasting. Patients get confused, however, when they are not eating because of illness, such as gastrointestinal “upset.” At these times, counter-regulatory hormones may rise and the patient must know that he or she needs to treat both the finger stick glucose and urine ketone elevations measured by “ketostik” or other convenient methods.
Conclusions
The next patient will be different . . . but the witnesses – glucose, free fatty acids, serum electrolytes and pH, ketoacids – will always tell their stories. The fingerprint of relative insulin deficiency permitting substrates (free fatty acids, amino acids and glycerol) to reach the liver and counter-regulatory excesses driving hepatic gluconeogenesis and ketogenesis will be clear to your experienced eye. The reversal of controlled storage and synthetic processes resulting in hyperglycemia, systemic acidosis, osmotic diuresis, and dehydration will be familiar. Therapy is straightforward, requiring insulin, fluid, and electrolyte administration. Key to a successful clinical outcome is careful monitoring of the patient, anticipation of responses, and investigation of potential precipitating factors.
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