Endocrine Emergencies

Endocrine Emergencies - Endocrine Emergencies Bobby Oakes...

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Unformatted text preview: Endocrine Emergencies Bobby Oakes SICU R3 Endocrine Emergencies Endocrine Emergencies Diabetic Ketoacidosis Thyroid Storm Adrenal Insufficiency Diabetic Ketoacidosis (DKA) Diabetic Ketoacidosis Diabetic Ketoacidosis Physiology Hyperglycemia – – – Increased hepatic production of glucose. Diminished glucose uptake by peripheral tissues Insulinopenia/hyperglucagonemia Ketoacidemia Fluid and Electrolyte Depletion Diabetic Ketoacidosis Diabetic Ketoacidosis Physiology Hyperglycemia Ketoacidemia – The ketoacid is acetoacetic acid. Byproduct is acetone. The non­keto acid is beta­ hydroxybutyric acid – Increased lipolysis and hepatic ketogenesis – Reduced ketolysis by insulin­deficient peripheral tissues Fluid and Electrolyte Depletion Diabetic Ketoacidosis Diabetic Ketoacidosis Physiology Hyperglycemia Ketoacidemia Fluid and Electrolyte Depletion – Osmotic diuresis and dehydration due to hyperglycemia – On average, water deficit is about 5L, sodium 500mmol, potassium 400mmol, chloride 400mmol. Diabetic Ketoacidosis Diabetic Ketoacidosis General Considerations Initial presentation of Type 1 Diabetes (Can also occur in type 2 diabetics) Increased insulin requirements in Type 1 diabetics (Infection, trauma, myocaridial infarction, surgery) Mortality 5% in patients under 40. Up to 20% in elderly. Estimates of 5­8 episodes per 1000 at risk diabetics annually. One of the more common serious complications of insulin pump users – occurring 1 per 80 months of treatment. Typically due to unrecognized pump failure. Charfen MA, Fernandez­FrackeltonM. Diabetic Ketoacidosis. Emerg Med Clin North Am 2005;23:609­628 Diabetic Ketoacidosis Diabetic Ketoacidosis Essentials of Diagnosis – – – – Acidosis with blood pH <7.3 Serum bicarbonate < 15mEq/L Serum positive for ketones Elevated anion gap Variable, may occur without gap. – Hyperglycemia > 250 No correlation between severity of hyperglycemia and severity of ketoacidosis Gamblin GT, Ashburn RW, Kemp DG et al. Diabetic ketoacidosis presenting with a normal anion gap. Am J Med 1986;80:756­760 Brandt KR, Miles JM. Relationship between severity of hyperglycemia a nd metabolic acidosis in diabetic ketoacidosis. Mayo Clin Proc 1988;63:1071­1074 Diabetic Ketoacidosis Diabetic Ketoacidosis Clinical Findings Symptoms: – Early: polyuria, polydipsia, fatigue, N/V – Late: stupor – Coma Signs: – Rapid, Deep Breathing – Fruity breath odor of acetone – Tachycardia, Hypotension, mild hypothermia – Abdominal Pain and Tenderness Charfen MA, Fernandez­FrackeltonM. Diabetic Ketoacidosis. Emerg Med Clin North Am 2005;23:609­628 Diabetic Ketoacidosis Diabetic Ketoacidosis Laboratory Findings Glycosuria 4+, Ketonuria Hyperglycemia, ketonemia, low arterial blood pH, low plasma bicarb. Elevated serum potassium (despite total body potassium depletion) Elevated serum amylase (not specific for pancreatitis in this setting, use lipase) Leukocytosis If hyperthermic, likely due to infection since pts with DKA are hypothermic if uninfected. Diabetic Ketoacidosis Diabetic Ketoacidosis Treatment Insulin Replacement – – – – – 10­30mEq/hr replacememt to be started during second or third hour of treatment – – Clinical benefit has not been demonstrated. Use to correct pH to greater than 7.1. – Typical deficit is 4­5L. Initially, NS 1L/hr x 2hrs. Then 300­400mL/hr. Switch to 1/2NS if serum NA >150. Add D5 p glucose falls below 250 to maintain serum glucose 250­300mg/dL to prevent hypoglycemia and cerebral edema. Intensive insulin therapy is continued until ketoacidosis is corrected. – – Regular Insulin IV bolus 0.15 units/kg to ‘prime’ insulin receptors Regular Insulin gtt at 0.1 units/kg/hr Replete hypophosphatemia of <1.0mg/dL. Replete slowly (3­4mmol/hr) to aviod hypocalcemic tetany. Fluid Replacement Sodium Bicarbonate Potassium Phosphate Treatment of Associated Infection – Antibiotics as indicated – Cholecystitis and pyelonephritis may be particularly severe in these patients Diabetic Ketoacidosis Diabetic Ketoacidosis Treatment Insulin Replacement – – – – – 10­30mEq/hr replacememt to be started during second or third hour of treatment – – Clinical benefit has not been demonstrated. Use to correct pH to greater than 7.1. – Typical deficit is 4­5L. Initially, NS 1L/hr x 2hrs. Then 300­400mL/hr. Switch to 1/2NS if serum NA >150. Add D5 p glucose falls below 250 to maintain serum glucose 250­300mg/dL to prevent hypoglycemia and cerebral edema. Intensive insulin therapy is continued until ketoacidosis is corrected. – – Regular Insulin IV bolus 0.15 units/kg to ‘prime’ insulin receptors Regular Insulin gtt at 0.1 units/kg/hr Replete hypophosphatemia of <1.0mg/dL. Replete slowly (3­4mmol/hr) to aviod hypocalcemic tetany. Fluid Replacement Sodium Bicarbonate Potassium Phosphate Treatment of Associated Infection – Antibiotics as indicated – Cholecystitis and pyelonephritis may be particularly severe in these patients Diabetic Ketoacidosis Diabetic Ketoacidosis Treatment Insulin Replacement – – – – – 10­30mEq/hr replacememt to be started during second or third hour of treatment – – Clinical benefit has not been demonstrated. Use to correct pH to greater than 7.1. – Typical deficit is 4­5L. Initially, NS 1L/hr x 2hrs. Then 300­400mL/hr. Switch to 1/2NS if serum NA >150. Add D5 p glucose falls below 250 to maintain serum glucose 250­300mg/dL to prevent hypoglycemia and cerebral edema. Intensive insulin therapy is continued until ketoacidosis is corrected. – – Regular Insulin IV bolus 0.15 units/kg to ‘prime’ insulin receptors Regular Insulin gtt at 0.1 units/kg/hr Replete hypophosphatemia of <1.0mg/dL. Replete slowly (3­4mmol/hr) to aviod hypocalcemic tetany. Fluid Replacement Sodium Bicarbonate Potassium Phosphate Treatment of Associated Infection – Antibiotics as indicated – Cholecystitis and pyelonephritis may be particularly severe in these patients Diabetic Ketoacidosis Diabetic Ketoacidosis Treatment Insulin Replacement – – – – – 10­30mEq/hr replacememt to be started during second or third hour of treatment – – Clinical benefit has not been demonstrated. Use to correct pH to greater than 7.1. – Typical deficit is 4­5L. Initially, NS 1L/hr x 2hrs. Then 300­400mL/hr. Switch to 1/2NS if serum NA >150. Add D5 p glucose falls below 250 to maintain serum glucose 250­300mg/dL to prevent hypoglycemia and cerebral edema. Intensive insulin therapy is continued until ketoacidosis is corrected. – – Regular Insulin IV bolus 0.15 units/kg to ‘prime’ insulin receptors Regular Insulin gtt at 0.1 units/kg/hr Replete hypophosphatemia of <1.0mg/dL. Replete slowly (3­4mmol/hr) to aviod hypocalcemic tetany. Fluid Replacement Sodium Bicarbonate Potassium Phosphate Treatment of Associated Infection – Antibiotics as indicated – Cholecystitis and pyelonephritis may be particularly severe in these patients Diabetic Ketoacidosis Diabetic Ketoacidosis Treatment Insulin Replacement – – – – – 10­30mEq/hr replacememt to be started during second or third hour of treatment – – Clinical benefit has not been demonstrated. Use to correct pH to greater than 7.1. – Typical deficit is 4­5L. Initially, NS 1L/hr x 2hrs. Then 300­400mL/hr. Switch to 1/2NS if serum NA >150. Add D5 p glucose falls below 250 to maintain serum glucose 250­300mg/dL to prevent hypoglycemia and cerebral edema. Intensive insulin therapy is continued until ketoacidosis is corrected. – – Regular Insulin IV bolus 0.15 units/kg to ‘prime’ insulin receptors Regular Insulin gtt at 0.1 units/kg/hr Replete hypophosphatemia of <1.0mg/dL. Replete slowly (3­4mmol/hr) to aviod hypocalcemic tetany. Fluid Replacement Sodium Bicarbonate Potassium Phosphate Treatment of Associated Infection – Antibiotics as indicated – Cholecystitis and pyelonephritis may be particularly severe in these patients Diabetic Ketoacidosis Diabetic Ketoacidosis Treatment Insulin Replacement – – – – – 10­30mEq/hr replacememt to be started during second or third hour of treatment – – Clinical benefit has not been demonstrated. Use to correct pH to greater than 7.1. If used at all. – Typical deficit is 4­5L. Initially, NS 1L/hr x 2hrs. Then 300­400mL/hr. Switch to 1/2NS if serum NA >150. Add D5 p glucose falls below 250 to maintain serum glucose 250­300mg/dL to prevent hypoglycemia and cerebral edema. Intensive insulin therapy is continued until ketoacidosis is corrected. – – Regular Insulin IV bolus 0.15 units/kg to ‘prime’ insulin receptors Regular Insulin gtt at 0.1 units/kg/hr Replete hypophosphatemia of <1.0mg/dL. Replete slowly (3­4mmol/hr) to aviod hypocalcemic tetany. Fluid Replacement Sodium Bicarbonate Potassium Phosphate Treatment of Associated Infection – Antibiotics as indicated – Cholecystitis and pyelonephritis may be particularly severe in these patients DKA vs HHS DKA vs HHS Diabetic Ketoacidosis – Hyperglycemia >250 mg/dL – Acidosis; pH<7.3 – Serum bicarb <15 – Serum Ketones Hyperglycemic Hyperosmolar State – – – – – Hyperglycemia >600mg/dL Serum Osmolality >310 No Acidosis; pH>7.3 Serum Bicarb >15 Normal anion gap <14 Thyroid Storm Thyroid Storm Thyroid Storm Extreme form of thyrotoxicosis. Occurs with stressful illness, thyroid surgery. Manifested by marked delirium, severe tachycardia, vomiting, diarrhea, dehydration, and very high fever. Mortality rate is high. Franklyn JA. The management of hyperthyroidism. N Engl J Med 1994:330:1731­ 1738 Thyroid Storm Thyroid Storm Treatment Beta­Receptor Antagonists – Propanolol IV (1mg q 5min until desired effect) – Propanolol PO (20­120mg q 6hrs until antithyroid drug therapy effective Antithyroid Drugs – Methimazole 10­30mg daily – Propylthiouracil 75­100mg tid Iodine – Iodide (as Lugol’s solution 4gtts q 12hrs) Migneco A, Ojeti V, Testa A, et al. Management of thyrotoxic crisis. Eur Rev Med Pharmacol Sci 2005;9:69­74 Acute Adrenal Insufficiency Acute Adrenal Insufficiency Acute Adrenal Insufficiency General Presentations Following Stress (trauma, surgery, infection, or prolonged fasting) in patient with latent insufficiency. Following sudden withdrawal of adrenocortical hormone in a patient with chronic insufficiency Following bilateral adrenalectomy or a functioning adrenal tumor that had suppressed the other adrenal Following sudden destruction of the pituitary gland (pituitary necrosis) or when thyroid hormone is given to a pt with hypoadrenalism Following injury to both adrenals by trauma, hemorrhage, anticoagulant therapy, thrombosis, infection, or metastatic carcinoma. Cooper MS, Stewart PM. Corticosteroid insufficiency in acutely ill patients. N Engl J Med 2003;348:727­734 Adrenal Insufficiency Adrenal Insufficiency Diagnosis Weakness, abdominal pain, fever, confusion, nausea, vomiting, diarrhea Hypotension, dehydration, hyperpigmentation Hyperkalemia, Hyponatremia, Azotemia Cosyntropin (ACTH) test Note: More than 90% of serum cortisol is protein bound. Pts with serum albumin <2.5g/dL have low serum total cortisol levels but normal serum free cortisol levels and normal adrenal function. Serum FREE cortisol levels should be used in critically ill patients. Hamrahian AH, Oseni TS, Arafah BM. Measurements of serum free cortisol in critically ill patients. N Engl J Med 2004;350:1629 Adrenal Insufficiency Adrenal Insufficiency Diagnosis Rapid ACTH Stimulation Test – Not influenced by diurnal variations in cortisol secretion. – Baseline cortisol sample. ACTH 250mcg. Post­ ACTH plasma cortisol at 30min and 60min p injection. – Baseline above 34 is normal and less than 15 is evidence of insufficiency. When between the two, the incriment increase with ACTH should be greater than 9mcg/dL. Adrenal Insufficiency Adrenal Insufficiency Treatment In patients with high suspicion of insufficiency, dexamethasone (2mg) can be started immediately. Does not interfere with ACTH assay. After ACTH test is completed, Hydrocortisone can be started at 50mg IV q6hrs until test results return If test normal, hydrocortisone can be abruptly discontinued without a taper. If test reveals adrenal insufficiency, continue hydrocortisone 50mg IV q6hrs until no longer in a stressed condition. Taper to 20mg IV q6hrs or oral equivalent. Cooper MS, Stewart PM. Corticosteroid insufficiency in acutely ill patients. N Engl J Med 2003;348:727­734 ...
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This note was uploaded on 12/21/2011 for the course STEP 1 taught by Professor Dr.aslam during the Fall '11 term at Montgomery College.

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