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Patients with severe hyperglycemia should immediately undergo assessment and stabilization of their airway and hemodynamic status. Naloxone, to reverse potential opiate overdose, should be considered for all patients with altered mentation. Thiamine, for acute treatment of Wernicke's encephalopathy, should be considered in all patients with signs of malnutrition. In cases requiring intubation, the paralytic succinylcholine should not be used if hyperkalemia is suspected; it may acutely further elevate potassium.

Immediate assessment also includes placing patients on a cardiac monitor and oxygen as well as obtaining vital signs, a fingerstick glucose, intravenous (IV) access, and an electrocardiogram to evaluate for arrhythmias and signs of hyper- and hypokalemia.

The differential diagnosis for hyperglycemic crisis includes the "Five I's": infection, infarction, infant (pregnancy), indiscretion (including cocaine ingestion), and insulin lack (nonadherence or inappropriate dosing). In addition to clinical history and physical examination, diagnostic tests should include a venous blood gas,complete blood count, basic metabolic panel, and urinalysis; a urine pregnancy test must be sent for all women with childbearing potential.

Critically ill patients should undergo additional testing as clinically indicated, including a complete metabolic panel, serum osmolality, phosphate, lactate, and cardiac markers for older patients. A urine drug screen, blood alcohol level, and aspirin and acetaminophen levels should be sent for any patient with unexplained DKA and all patients with HHS. Evaluation for infection or injury should be guided by history and the physical examination. Effective serum osmolality should be calculated. The corrected serum sodium is estimated by decreasing measured serum sodium by 1.6 mEq/L for every 100 mg/dl increase in blood glucose over a baseline of 100 mg/dl; for every 100 mg/dl increment increase in blood glucose >: 400 mg/dl, measured serum sodium is decreased by an additional 4 mEq/L.

Intravenous Fluid

Critically ill patients with severe hyperglycemia resulting from DKA or HHS should be treated immediately with a bolus of normal saline. The average fluid deficit for patients with DKA is 3-5 liters; fluid resuscitation in young, otherwise healthy patients should begin with a rapid bolus of 1 liter of normal saline followed by an infusion of normal saline at 500 ml/hour for several hours.

Patients with HHS are often severely dehydrated, with cumulative fluid deficits of 10 liters or more. However, because they tend to be older and sicker, they require careful resuscitation. Expert opinion advocates for a rapid bolus of 250 ml of normal saline repeated as needed until the patient is well perfused. Fluid therapy is then continued at a rate of 150-250 ml/hour based on cardiopulmonary status and serum osmolality.

The choice and rate of IV fluid for patients with DKA who are not critically ill should be based on their corrected serum sodium and overall fluid status. While awaiting laboratory study results, most of these patients may be given a bolus of 500 ml of normal saline. Patients with mild to moderate DKA should be given normal saline at 250 ml/hour; those with an elevated corrected serum sodium should be given half-normal saline at 250 ml/hour.

Insulin therapy

Critically ill patients with DKA should be given a loading dose of regular insulin at 0.1 units/kg body weight to a maximum of 10 units followed by an infusion of regular insulin at 0.1 units/kg body weight/hour, to a maximum of 10 units/hour. Other doses and routes of insulin administration have been studied, but these have not been evaluated outside of the research setting or in critically ill patients.

Less seriously ill patients with DKA should be given an infusion of regular insulin at 0.1 units/kg body weight/hour without a loading dose to minimize the risk of hypoglycemia. Insulin should not be started until hypovolemia has been addressed and serum potassium has been confirmed to be > 3.5 mEq/L. Giving insulin to patients with a serum potassium level < 3.5 mEq/L may precipitate life-threatening arrhythmias.

Expert opinion regarding the use of insulin for patients with HHS is mixed. Because some patients with HHS achieve euglycemia with fluid resuscitation alone,30 and given the theoretical risks of precipitating oliguric renal failure or cerebral edema in inadequately fluid-resuscitated patients, insulin should not be given as part of initial therapy. However, if the patient's serum glucose does not decrease by 50-70 mg/dl per hour despite appropriate fluid management, a bolus of IV regular insulin at 0.1 units/kg body weight to a maximum of 10 units may be given.

Electrolyte replacement

Patients with DKA or HHS experience rapid shifts in potassium during resuscitation that may trigger life-threatening arrhythmias. Death during initial resuscitation of patients with DKA is usually caused by hyperkalemia, whereas hypokalemia is the most common cause of death after treatment has been initiated. Therefore, serum potassium should be checked every 2 hours until it has stabilized in all patients with hyperglycemic crisis, and these patients should remain on a cardiac monitor. Guidelines for the treatment of hyperkalemia and hypokalemia in patients with hyperglycemic crisis based on expert opinion and our clinical experience are found in Table 2.

Many critically ill patients with DKA manifest hypophosphatemia during resuscitation. To avoid potential cardiac and skeletal muscle weakness and respiratory depression from hypophosphatemia, a serum phosphate of < 1.5 mg/dl should be repleted with K2PO4 at 0.5 ml/hour. No studies have evaluated replacement of phosphate in HHS, but critically ill patients with HHS should have their phosphate monitored and replaced appropriately.

Bicarbonate should not be used routinely in the treatment of DKA or HSS. Expert opinion suggests that it may be used in patients with DKA and severe acidosis (pH < 6.9) or in patients with severe hyperglycemia who present with a wide-complex or disorganized cardiac rhythm thought to be caused by hyperkalemia. Several small studies have shown no improvement in mortality when bicarbonate is used in patients with a pH > 6.9. Additionally, bicarbonate may prolong hypokalemia, has been associated with longer hospitalizations, and is thought to cause paradoxical acidosis of the cerebral spinal fluid and decrease oxygen tissue delivery. In children, its use has been associated with increased risk of cerebral edema.