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1 Acute Complications of Diabetes. 2 Diabetic Ketoacidosis

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Text of 1 Acute Complications of Diabetes. 2 Diabetic Ketoacidosis

  • Slide 1
  • 1 Acute Complications of Diabetes
  • Slide 2
  • 2 Diabetic Ketoacidosis
  • Slide 3
  • Introduction 3 DKA is an acute life threatening complication of DM of hospital admissions for DM Occurs predominantly in type I though may occur in II Incidence of DKA in diabetics 15 per 1000 patients 20-30% of cases occur in new-onset diabetes Mortality less than 5% Mortality higher in elderly due to underlying renal disease or coexisting infection
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  • Definition 4 Exact definition is variable Most consistent is: Blood glucose level greater than 250 mg/dL Bicarbonate less than 15 mEq/L Arterial pH less than 7.3 Moderate ketonemia
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  • Pathophysiology 5 Bodys response to cellular starvation Brought on by relative insulin deficiency and counter regulatory or catabolic hormone excess Insulin is responsible for metabolism and storage of carbohydrates, fat and protein Lack of insulin and excess counter regulatory hormones (glucagon, catecholamines, cortisol and growth hormone) results in: Hyperglycemia (due to excess production and underutilization of glucose) Osmotic diuresis Prerenal azotemia Ketone formation Wide anion-gap metabolic acidosis Clinical manifestations related to hyperglycemia, volume depletion and acidosis
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  • Pathophysiology 6 Free fatty acids released in the periphery are bound to albumin and transported to the liver where they undergo conversion to ketone bodies The metabolic acidosis in DKA is due to -hydroxybutyric acid and acetoacetic acid which are in equilibrium Acetoacetic acid is metabolized to acetone, another major ketone body Depletion of baseline hepatic glycogen stores tends to favor ketogenesis Low insulin levels decrease the ability of the brain and cardiac and skeletal muscle to use ketones as an energy source, also increasing ketonemia Persistently elevated serum glucose levels eventually causes an osmotic diuresis Resulting volume depletion worsens hyperglycemia and ketonemia
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  • Electrolytes 7 Renal potassium losses already occurring from osmotic diuresis worsen due to renin-angiotensin- aldosterone system activation by volume depletion In the kidney, chloride is retained in exchange for the ketoanions being excreted Loss of ketoanions represents a loss of potential bicarbonate In face of marked ketonuria, a superimposed hyperchloremic acidosis is also present Presence of concurrent hyperchloremic metabolic acidosis can be detected by noting a bicarbonate level lower than explainable by the amount the anion gap has increased As adipose tissue is broken down, prostaglandins PGI 2 and PGE 2 are produced This accounts for the paradoxical vasodilation that occurs despite the profound levels of volume depletion
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  • DKA in Pregnancy 8 Physiologic changes in pregnancy makes more prone to DKA Maternal fasting serum glucose levels are normally lower Leads to relative insulin deficiency and an increase in baseline free fatty acid levels in the blood Pregnant patients normally have increased levels of counter regulatory hormones Chronic respiratory alkalosis Seen in pregnancy Leads to decreased bicarbonate levels due to a compensatory renal response Results in a decrease in buffering capacity
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  • DKA in Pregnancy 9 Pregnant patients have increased incidence of vomiting and infections which may precipitate DKA Maternal acidosis: Causes fetal acidosis Decreases uterine blood flow and fetal oxygenation Shifts the oxygen-hemoglobin dissociation curve to the right Maternal shifts can lead to fetal dysrhythmia and death
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  • Causes of DKA 10 25% have no precipitating causes found Errors in insulin use, especially in younger population Omission of daily insulin injections Stressful events: Infection Stroke MI Trauma Pregnancy Hyperthyroidism Pancreatitis Pulmonary embolism Surgery Steroid use
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  • Clinical Features 11 Hyperglycemia Increased osmotic load Movement of intracellular water into the vascular compartment Ensuing osmotic diuresis gradually leads to volume loss and renal loss of sodium, chloride, potassium, phosphorus, calcium and magnesium Patients initially compensate by increasing their fluid intake Initially polyuria and polydipsia are only symptoms until ketonemia and acidosis develop
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  • Clinical Features 12 As acidosis progresses Patient develops a compensatory augmented ventilatory response Increased ventilation is stimulated physiologically by acidemia to diminish PCO 2 and counter the metabolic acidosis Peripheral vasodilation develops from prostaglandins and acidosis Prostaglandins may contribute to unexplained nausea, vomiting and abdominal pain Vomiting exacerbates the potassium losses and contributes to volume depletion, weakness and weight loss
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  • Clinical Features 13 Mental confusion or coma may occur with serum osmolarity greater than 340 mosm/L Abnormal vital signs may be the only significant finding at presentation Tachycardia with orthostasis or hypotension are usually present Poor skin turgor Kussmaul respirations with severe acidemia
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  • Clinical Features 14 Acetone presents with odor in some patients Absence of fever does not exclude infection as a source of the ketoacidosis Hypothermia may occur due to peripheral vasodilatation Abdominal pain and tenderness may occur with gastric distension, ileus or pancreatitis Abdominal pain and elevated amylase in those with DKA or pancreatitis may make differentiation difficult Lipase is more specific to pancreatitis
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  • Clinical Suspicion 15 If suspect DKA, want immediately: Acucheck Urine dip ECG Venous blood gas Normal Saline IV drip Almost all patients with DKA have glucose greater than 300 mg/dL
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  • Acidosis 16 Elevated serum -hydroxybutyrate and acetoacetate cause acidosis and ketonuria Elevated serum ketones may lead to a wide-anion gap metabolic acidosis Metabolic acidosis may occur due to vomiting, osmotic diuresis and concomitant diuretic use Some with DKA may present with normal bicarbonate concentration or alkalemia if other alkalotic processes are severe enough to mask acidosis In which case the elevated anion gap may be the only clue to the presence of an underlying metabolic acidosis
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  • ABGs 17 Help determine precise acid-base status in order to direct treatment Venous pH is just as helpful Studies have shown strong correlation between arterial and venous pH in patients with DKA Venous pH obtained during routine blood draws can be used to avoid ABGs Decreased PCO 2 reflects respiratory compensation for metabolic acidosis Widening of anion gap is superior to pH or bicarbonate concentration alone Widening is independent of potentially masking effects concurrent with acid base disturbances
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  • Potassium 18 Total body potassium is depleted by renal losses Measured levels usually normal or elevated
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  • Sodium 19 Osmotic diuresis leads to excessive renal losses of NaCl in urine Hyperglycemia artificially lowers the serum sodium levels Two corrections: Standard-1.6 mEq added to sodium loss for every 100 mg of glucose over 100 mg/dL True-2.4 mEq added for blood glucose levels greater than 400 mg/dL
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  • Electrolyte Loss: 20 Osmotic diuresis contributes to urinary losses and total body depletion of: Phosphorus Calcium Magnesium
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  • Other values elevated: 21 Creatinine Some elevation expected due to prerenal azotemia May be factitiously elevated if laboratory assays for Cr and Acetoacetate interfere LFTs Due to fatty infiltration of the liver which gradually corrects as acidosis is treated CPK Due to volume depletion Amylase WBCs Leukocytosis often present due to hemoconcentration and stress response Absolute band count of 10,000 microL or more reliably predicts infection in this population
  • Slide 22
  • ECG changes 22 Underlying rhythm is sinus tachycardia Changes of hypo/hyperkalemia Transient changes due to rapidly changing metabolic status Evaluate for ischemia because MI may precipitate DKA
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  • Differential Diagnosis 23 Any entity that causes a high-anion-gap metabolic acidosis Alcoholic or starvation ketoacidosis Uremia Lactic acidosis Ingestions (methanol, ethylene glycol, aspirin) If ingestion cannot be excluded, serum osmolarity or drug-level testing is required Patients with hyperosmolar non-ketotic coma tend to: Be older Have more prolonged course and have prominent mental status changes Serum glucose levels are generally much higher (>600 mg/dL) Have little to no anion-gap metabolic acidosis
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  • Studies 24 Diagnosis should be suspected at triage Aggressive fluid therapy initiated prior to receiving lab results Place on monitor and have one large bore IV with NS running Rapid acucheck, urine dip and ECG CBC Electrolytes, phosphorus, magnesium, calcium Blood cultures ABG optional and required only for monitoring and diagnosis of critically ill Venous pH (0.03 lower than arterial pH) may be used for critically ill
  • Slide 25
  • Treatment Goals: 25 Volume repletion Reversal of metabolic consequences of insulin insufficiency Correction of electrolyte and acid-base imbalances Recognition and treatment of precipitat

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