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DIABETIC KETOACIDOSIS BY: HOSAM M. TAHLAWI K.A.A.U. MADICAL SCHOOL Diabetic Ketoacidosis an acute, life threatening metabolic acidosis complicating IDDM and some cases of NIDDM with intercurrent illness (infection or surgery) usually coupled with an increase in glucagon concentration with two metabolic consequences: – 1) Maximal gluconeogenesis with impaired peripheral utilization of glucose – 2) activation of the ketogenic process and development of metabolic acidosis. Gluconeogenesis Maximal gluconeogenesis occurs as glucagon lowers the concentration of F2,6- bisphosphate which is the intermediate that activate glycolysis and inhibit gluconeogenesis. This results in hyperglycemia and osmotic diuresis with a resultant dehydration characteristic of DKA. Ketogenesis KETOGENESIS occurs as a results of high glucagon/insulin ratio: – 1) increased liberation of free fatty acids due to the loss of the inhibitory action of insulin on the hormone sensitive lipase. – 2) activation of the transport system (or reestrification to VLDL will occur and nothing will happen) this results in high levels of acetone, acetoacetate and -hydroxybutyrate . Clinical Presentation anorexia, N/V, along with polydepsia and polyuria for about 24 hrs. followed by stupor (or coma). Abdominal pain and tenderness could be present (remember DDx of acute abdomen). Kussmaul breathing with fruity odor “acetone” Sings of dehydration ( HR, postural BP, etc.) normal or low temperature: NB.: if fever is present it suggests infection while leukocytosis alone is not because DKA per se can cause fever. Initial lab result in DKA: (series) in mmol/l glucose: 26-41 sodium: 132 potassium: 4.8-6.0 bicarbonate: 6.0- 10 BUN: 9.0-15 acetoacetate: 4.8 -hydroxybutyrate: 13.7 free fatty acid: 2.1-2.3 lactate: 4.6 osmolality: 310-331 osmolality= 2([Na]+[K])+ [Glu]+ BUN Sources of acid include acetoacetate and BHB along with lactate, FFA, & PO4 Sodium is low due to dilutional effect of shifting of fluid to the ECF. Sodium leveld below 110 mmol/L suggest either: – vomiting and excessive water drinking – interference by hypertriglyceridemia Initial potassium could be normal or high but this is misleading since there is a huge total- body potassium deficit. Prerenal azotemia is a reflection of the volume depletion. Serum amylase might be elevated and frank pancreatitis can occur. Diagnosis of DKA in IDDM patient is not that difficult. The problem is pointing towards the cause of acidosis with anion gap in a person who is not known diabetic. Causes to consider: 1) lactic acidosis. 2) uremia. 3) alcoholic ketoaciosis (see later) 4) certain poisonings. The initial step in diagnostic approach is testing urine for glucose and ketones. Diagnostic criteria for DKA: – hyperglycemia (>250 mg/dl) – ketosis (ketonemia or ketonuria) – acidosis (pH<7.3, HCO3<15mEq/L) supporting features are volume depletion and Kussmaul’s breathing. Diabetic Vs. Alcoholic Ketoacidosis by definition AKA occurs in chronic alcoholism especially after a binge drinking!? always occurs with starvation. sever abdominal pain and tenderness and pancreatitis occur in 75%. 90% presents with glucose level <150 mg/dl rapidly reversed with IV glucose, but remember to give thiamin to avoid Beriberi Insulin: is a prerequisite for recovery – preferable way is to give 25-50U as an initial IV bolus (or IM) followed by infusion of 15-25U/hour till ketosis is reversed. – IGF-1 is used in insulin resistance IVF: the usual fluid deficit is 3-5L – on arrival the patient is given 1-2L of isotonic saline or ringer’s lactate followed by infusion rates dependent on fluid status and urine output. – when glucose reaches 300mg/dl add 5% glucose solution (? cerebral Edema) Potassium: replacement is always necessary – if value on arrival is high: delay replacement till reversal of ketosis – if values are low: give K early – if values are very low: hold insulin for 60-90 min. till 40- 50 mmol of K are given bicarbonate: – indicated in sever acidosis (pH 7.0 or below) or with hypotension (that can be caused by acidosis alone) – stop the infusion at pH 7.2 to avoid alkalosis upon reversal of ketosis. THERAPUTIC CONSIDERATIONS 1) Plasma glucose will invariably fall more rapidly than ketones. So, don’t stop insulin unless reversal of ketosis occur. 2) plasma ketones are not very helpful in assessing clinical response. So use the pH and anion gap instead. AG = (Na+K) - (Cl+HCO3) ALL patients should be followed with a flow sheet outlining amounts and timing of insulin and fluids together with record of vital signs, urine volume, and blood chemistries. Without such a record therapy tends to be chaotic. Patients are not doctors so we have to make sure that each patient receives intensive detailed instructions about how to avoid this potentially disastrous complication of diabetes mellitus. Complications of DKA and clues to their development Acute gastric dilatation or erosive gastritis – by vomiting blood or coffee-ground material Cerebral edema – obtundation or coma with or without neuro. Signs, especially if occurring with initial improvement. Hyperkalemia cardiac arrest hypokalemia cardiac arrythmias. Infection is known by fever hypoglycemia is considered when there is adrenergic or neuorologic signs or rebound ketosis. Insulin resistance: unremitting acidosis after 4-6 hrs of Rx MI: chest pain, appearance of HF, hypotension despite adequate fluids. Mucormycosis: facial pain, bloody nasal discharge, blurred vision, proptosis. ARDS: hypoxemia in absence of pneumonia, COPD, or HF Vascular thrombosis: stroke-like picture or signs of ischemia in nonnervous tissue.
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