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bin by regenerating 2,3-diphosphoglycerate However, three randomized studies in which phosphate was replaced in only half of a group of patients with diabetic ketoacidosis did not show any apparent clinical benefit from phosphate administration Moreover, attempts to use the phosphate salt of potassium as the sole means of replacing potassium have led to a number of reported cases of severe hypocalcemia with tetany To minimize the risk of inducing tetany from toorapid replacement of phosphate, the average deficit of 40 50 mmol of phosphate should be replaced intravenously at a rate no greater than 3 4 mmol/h in a 60 70-kg person A stock solution (Abbott) provides a mixture of 112 g KH2PO4 and 118 g K2HPO4 in a 5-mL single-dose vial (this equals 22 mmol of potassium and 15 mmol of phosphate) One-half of this vial (25 mL) should be added to 1 L of either 045% saline or 5% dextrose in water Two liters of this solution, infused at a rate of 400 mL/h, will correct the phosphate deficit at the optimal rate of 3 mmol/h while providing 44 mEq of potassium per hour (Additional potassium should be administered as potassium chloride to provide a total of 10 30 mEq of potassium per hour, as noted above) If the serum phosphate remains below 25 mg/dL after this infusion, a repeat 5-hour infusion can be given 7 Hyperchloremic acidosis during therapy Because of the considerable loss of keto acids in the urine during the initial phase of therapy, substrate for subsequent regeneration of bicarbonate is lost and correction of the total bicarbonate deficit is hampered A portion of the bicarbonate deficit is replaced with chloride ions infused in large amounts as saline to correct the dehydration In most patients, as the ketoacidosis clears during insulin replacement, a hyperchloremic, lowbicarbonate pattern emerges with a normal anion gap This is a relatively benign condition that reverses itself over the subsequent 12 24 hours once intravenous saline is no longer being administered 8 Treatment of associated infection Antibiotics are prescribed as indicated Cholecystitis and pyelonephritis may be particularly severe in these patients
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The frequency of deaths due to diabetic ketoacidosis has been dramatically reduced by improved therapy of young diabetics, but this complication remains a significant risk in the aged and in patients in profound coma in whom treatment has been delayed Acute myocardial infarction and infarction of the bowel following prolonged hypotension worsen the outlook A serious prognostic sign is renal failure, and prior kidney dysfunction worsens the prognosis considerably because the kidney plays a key role in compensating for massive pH and electrolyte abnormalities Cerebral edema has been reported to occur rarely as metabolic deficits return to normal This is best prevented by avoiding sudden reversal of marked hyperglycemia Maintaining glycemic levels of 200 300 mg/dL for the initial 24 hours after correction of severe hyperglycemia reduces this risk
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Kitabchi AE et al Management of hyperglycemic crises in patients with diabetes Diabetes Care 2001 Jan;24(1):131 53 [PMID: 11194218]
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ketoacidosis may retard recognition of the syndrome and delay therapy until dehydration becomes more profound than in ketoacidosis Reduced intake of fluid is not an uncommon historical feature, due to either inappropriate lack of thirst, nausea, or inaccessibility of fluids to elderly, bedridden patients Lethargy and confusion develop, progressing to convulsions and deep coma Physical examination confirms the presence of profound dehydration in a lethargic or comatose patient without Kussmaul respirations
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Hyperglycemia > 600 mg/dL Serum osmolality > 310 mosm/kg No acidosis; blood pH above 73 Serum bicarbonate > 15 mEq/L Normal anion gap (< 14 mEq/L)
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B Laboratory Findings
(Table 27 12) Severe hyperglycemia is present, with blood glucose values ranging from 600 mg/dL to 2400 mg/dL In mild cases, where dehydration is less severe, dilutional hyponatremia as well as urinary sodium losses may reduce serum sodium to 120 125 mEq/L, which protects to some extent against extreme hyperosmolality However, as dehydration progresses, serum sodium can exceed 140 mEq/L, producing serum osmolality readings of 330 440 mosm/kg Ketosis and acidosis are usually absent or mild Prerenal azotemia is the rule, with serum urea nitrogen elevations over 100 mg/dL being typical
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