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Hyperosmolar Hyperglycemic State (HHS)

Hyperosmolar Hyperglycemic State (HHS). Hyperosmolar Hyperglycemic State (HHS) is a complication of non-insulin dependent (Type II) diabetes. It most commonly occurs in patients who have some

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Hyperosmolar Hyperglycemic State (HHS)

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  1. Hyperosmolar Hyperglycemic State (HHS)

  2. Hyperosmolar Hyperglycemic State (HHS) is a complication of non-insulin dependent (Type II) diabetes. It most commonly occurs in patients who have some illness that leads to reduced fluid intake.

  3. Infection is the most common preceding ailment. Most patients present with severe dehydration and focal or global neurologic deficits. HHS usually presents in older patients and carries a higher mortality rate than DKA.

  4. In 30-40% of cases, HHS is the patient’s initial presentation of diabetes. HHS usually develops over a course of days to weeks, unlike diabetic ketoacidosis (DKA), which develops more rapidly over the course of a few days.

  5. HHS may include the following • Plasma glucose level of 600 mg/dL or greater • Serum osmolality of 320 mOsm/kg or greater • Profound dehydration, up to an average of 9L • Serum pH greater than 7.30 • Bicarbonate concentration greater than 15 mEq/L • Small ketonuria and absent-to-low ketonemia • Some alteration in consciousness

  6. Insulin is necessary to transport glucose into cells to be used for energy and is secreted by the beta cells of the islets of Langerhans in the pancreas

  7. Glucagon stimulates the production of glucose in the liver and is secreted by the alpha cells of the islets of Langerhans in the pancreas.

  8. If the liver makes glucose the by-products include ketones. Overproduction of ketones by the liver leads to ketoacidosis

  9. However, Patients with HHS do not develop significant ketoacidosis. The reason for this is not fully known. One possible contributing factor is the availability of insulin in amounts sufficient to inhibit ketogenesis but insufficient to prevent hyperglycemia.

  10. Another possible factor is that the levels of Epinephrine,Glucagon, Cortisol andGrowth hormone are found to be lowerin patients with HHS than in those with DKA. When these levels are high they increase insulin resistance.

  11. Normally, all of the glucose filtered by the kidneys is reabsorbed. When glycemia reaches around 180 mg/dL, proximal tubular transport of glucose from the tubular lumen into the renal interstitium stops because the renal interstitium is saturated.

  12. The glucose that remains in the renal tubules continues to travel into the distal nephron and eventually the urine; carrying water and electrolytes with it. This osmotic diuresis causes a decrease in total body water.

  13. If the renal water loss is not compensated for by oral water intake, dehydration leads to hypovolemia, hypovolemia leads to hypotension and hypotension results in impaired tissue perfusion. When severe electrolyte disturbances occur with hypotension, neurologic changes are the end result.

  14. A wide variety of focal and global neurologic • changes may be present, including the following: • Drowsiness and lethargy • Delirium • Focal or generalized seizures • Visual changes or disturbances • Hemiparesis • Sensory deficits • Coma

  15. Intravenous fluid therapy is required for HHS. The usual fluid deficit may be as much as 9 liters. 1 to 2 liters of Isotonic saline or Ringer's lactate should be given rapidly IV on arrival in the emergency department.

  16. Although many patients with HHS respond to fluids alone, IV insulin in dosages similar to those used in DKA can facilitate correction of hyperglycemia. Insulin used without concomitant vigorous fluid replacement increases the risk of shock.

  17. Potassiumreplacement is important too because of the losses incurred during the osmotic diuresis triggered by the hyperglycemia. Hypokalemia predisposes the patient to cardiac arrhythmias. 

  18. Monitor ECG changes caused by low K+ • Increased amplitude and width of the P wave • Prolonged PR interval • T wave flattening and inversion • ST depression • Prominent U waves

  19. Cerebral edema is rare in HHS and is usually observed in patients younger than average age of 60. It may occur from rapid lowering of glucose levels and a rapid drop in plasma osmolarity. Brain cells preferentially absorb water and swell during rapid rehydration.

  20. Acute Respiratory Distress Syndrome (ARDS) should be considered if a drop in the partial pressure of alveolar oxygen is noted. PE, MI, or a worsening pneumonitis should also be considered.

  21. Vascular complications may occur because the severe dehydration of HHS leads to hypotension and hyperviscosity of the blood, both of which predispose patients to thromboembolic events of the coronary, cerebral, pulmonary and/or mesenteric beds.

  22. Summary • Severe dehydration • Focal or global neurologic deficits • Plasma glucose level of 600 mg/dL or greater • Develops over several days to weeks • Minimal or no ketosis • Replace fluids, K+ and Insulin as needed • Watch for complications

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