Endocrine Emergencies - Illinois College of Emergency ... · Endocrine Emergencies Page 2 no...

Endocrine Emergencies

Carl Ferraro, MD, FACEP

Education Director, Department of Emergency Medicine, Mercy Hospital and Medical Center, Chicago; Clinical Associate Professor, University of Illinois at Chicago

Notes

Endocrine Emergencies Page 1

ENDOCRINE EMERGENCIES

(with a taste of vitamin disorders) I. DIABETIC EMERGENCIES

A. Diabetic Ketoacidosis

1. Definition of DKA: Hyperglycemia, ketonemia, and acidosis a. Blood sugar over 300 mg/dl b. Positive serum ketones (acetone) greater than 1:2 c. pH less than 7.30 or a low serum bicarbonate (<15 meq/L) d. High anion gap

2. Presentation a. May be the initial presentation of a diabetic in 10% of

cases b. Usually preceded by polydipsia, polyphagia, and polyuria c. Greater than 80% of cases will have an identifiable

precipitating factor d. Altered mental status

i. May range from subtle personality changes to lethargy to coma

3. Evaluation a. Immediate

i. Serum glucose reagent strip with monitor ii. Urine dip for glucose and ketones iii. ABGs iv. EKG - looking for changes due to hyperkalemia

b. Rapid i. Serum glucose ii. Electrolytes iii. Serum ketones (acetone) iv. Urinalysis

c. Others i. Based on presentation looking for underlying or

precipitating process 4. Management

a. ABCs b. Fluids

i. Resuscitation ii. Must replace/restore intravascular volume

• On-going losses- Due to hyperosmolar state and osmotic diuresis

c. Electrolytes i. Potassium ii. Usually high due to acidosis iii. Will fall due to therapy and must be replaced iv. Give as soon as urine output is established and there are

Notes


no hyperkalemic EKG changes v. Monitor every 1-2 hours and replace

d. Sodium i. Pseudo-hyponatremia due to hyperglycemia:

• For every 100 mg/dL above 100 mg/dL of glucose, the serum sodium level falls 1.6 meq/L due to osmotic dilution

ii. Normal saline as initial replacement fluid e. Phosphate

i. Will be low ii. Will correct without specific replacement as therapy

proceeds f. Flow sheet g. Insulin

i. Amount/Route- 0.1 U/kg per hour IV infusion ii. Timing iii. As soon as glucose level has been determined and volume

replacement is underway (usually at 1-2 hours) h. Acid-base status i. Metabolic j. Ketone bodies from lipolysis k. Lactate from hypoperfusion l. Respiratory m. Usually respiratory alkalosis (compensation). n. Hypoventilation implies fatigue or central dépression

5. Bicarbonate therapy a. Most authors recommend withholding bicarb unless severe

acidosis is present (pH < 7.0 or bicarb < 9) b. DO NOT PUSH; give 1-2 meq/kg over 2 hours

6. Disposition a. Admission

i. ICU: • Cardiovascular instability • Depressed level of consciousness • Significant underlying/precipitating illness, eg,

sepsis, MI, GI bleed ii. Floor: stable but require continued IV therapy

b. Discharge i. Alert, can tolerate PO fluids, and are stable

B. Hyperosmolar Hyperglycemic Nonketotic Coma

1. Definition - in a patient with depressed consciousness

a. Osmolarity greater than 350 mOsm b. Glucose greater than 600mg/dl c. Lack of ketosis, however: may have mild ketosis and normal

mental status 2. Manifestations

Notes


a. Insufficient fluid intake, polyuria b. Decreasing polydipsia c. Depressed mentation d. Evolution over days to weeks

3. Treatment priorities a. First priority - replace volume deficits saline b. Correct hyperosmolarity c. Insulin may not be necessary d. Blood glucose levels may decrease by 25% with fluid

replacement alone i. If used, begin slowly (infuse at 0.05 U/kg/hr)

e. Manage underlying illnesses

C. Hypoglycemia

1. Prevalence a. The most common endocrine emergency b. Majority of diabetics have experienced at least one episode c. Frequency may be increasing with the advent of very tight

control therapy (DCCT) 2. Definition / recognition

a. Whipple's Triad i. Typical symptoms ii. Low blood sugar iii. Response to administration of glucose

b. Adrenergic symptoms i. Tachycardia and palpitations, sweating, anxiety, tremor,

pallor, hunger c. Neuroglycopenic symptoms

i. Headache, visual disturbances, confusion, aberrant behavior, coma, psychiatric disturbance, seizures, focal findings

d. How low is low? i. Variable response to absolute blood glucose levels and

rate of fall ii. Most authors/studies agree on a level of 50mg/dL

3. Management a. Glucose

i. Simple glucose solutions orally or parenterally- D50 1 to 3 amps IV

ii. Complex carbohydrates after improvement b. Glucagon

i. Use when there is no IV access ii. Dose: 1mg IM iii. Dependent on adequate glycogen stores

c. Others i. Corticosteroids: if adrenal insufficiency suspected ii. Diazoxide

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iii. Surgery/chemotherapy for insulinoma d. Identification of cause

i. Need to prevent recurrences ii. Directs disposition

e. Disposition i. Discharge ii. Etiology clear and patient is improved iii. Admit iv. Unclear etiology v. Persistent neurologic deficit vi. Serious underlying illness vii. Intentional overdose

II. THYROID DISORDERS

A. Thyroid storm

1. Spectrum of disease: A variety of conditions have been described relating to thyroid hyperfunction. Although no clear definitions exist, hyperthyroidism and thyrotoxicosis refer to milder disease whereas thyrotoxic crisis and thyroid storm designate life-threats.

2. Clinical manifestations / differential diagnosis a. Fever

i. Common; sometimes > 106o ii. Heat intolerance by history

b. Cardiovascular i. Symptoms: palpitations, dyspnea, chest pain ii. Signs: systolic hypertension, (sinus) tachycardia, CHF

c. Neurological i. Anxiety, agitation, restlessness, mood swings, tremor-

may progress to delirium, psychosis, stupor, coma d. Eye findings

i. Upper lid retraction, staring, lid lag, exophthalmos, extraocular muscle palsies

e. Gastrointestinal i. Weight loss by history ii. Nausea, vomiting, diarrhea (enhanced intestinal transport) iii. Transaminase elevation and jaundice (hepatocellular dysfunction)

Notes


f. Diagnostic scoring system:

Findings Score Findings ScoreTemperature Tachycardia 99 - 99.9 5 90 - 109 5 100 - 100.9 10 110 - 119 10 101 - 101.9 15 120 - 129 15 102 - 102.9 20 130 - 139 20 103 - 103.9 25 > 140 25 > 104.0 30 CNS Effects Congestive Heart Failure Absent 0 Absent 0 Mild (agitation) 10 Mild (pedal edema) 5 Moderate (delirium, 20 Moderate (bibasilar rales) 10 psychosis, extreme Severe (pulmonary edema) 15 lethargy) Severe (seizure, coma) 30 Atrial Fibrillation Absent 0 Present 10 GI-Hepatic Dysfunction Absent 0 Precipitant History Moderate (diarrhea, 10 Negative 0 nausea/vomiting, Positive 10 abdominal pain) Severe 20 (unexplained jaundice) Interpretation: <25 unlikely 25-44 suggestive of impending storm >45 highly suggestive of thyroid storm

Adapted from Burch HB and Wartofsky L, "Life-Threatening Thyrotoxicosis: Thyroid Storm," Endocrinology and Metabolism Clinics of North America, 22(2)263-277, June 1993.

g. Differential diagnosis i. Sepsis, heat stroke, anticholinergic OD, adrenergic OD

(cocaine and amphetamines), hypoglycemia, withdrawal syndromes, psychiatric illness

3. Laboratory studies NOTE: None of the studies used to confirm the diagnosis of thyroid storm are available on an immediate basis in the ED. a. Thyroid Function Tests

i. T4 ii. T3

Notes


iii. TSH iv. TBG

b. "Routine" labs i. Multiple, mild abnormalities ii. Non-specific

4. Management A five-pronged approach must be utilized to halt thyroid dysfunction and its effects and to lessen morbidity/mortality from precipitating/underlying disease.

a. Block hormone synthesis i. Propylthiouracil (PTU)

• Dose: ranges from 100mg up to 600-1000mg load • Route: must be given PO or per NG • Also inhibits peripheral conversion (see [c] below) • Stops production within one hour

ii. Methimazole (MMI) • Longer half-life- 20mg PO every 4 hours

b. Inhibit hormone release i. Inorganic iodine

• Recommended dose range 0.2 - 2g/day PO ii. Potassium iodide (SSKI)-5 drops PO every 6-8 hours iii. Lugol's solution- 8 drops to 1ml PO every 8 hours iv. Sodium iodide- 1gm IV every 8 hours v. Ipodate (OragrafinR) - Inhibits release, peripheral

conversion, and antagonize receptor binding- 1-3gm daily vi. Lithium carbonate - 300mg every 6 hours

c. Inhibition of T4 to T3 conversion- PTU (as above) i. Glucocorticoids

• Dexamethasone 2mg IV every 6 hours • Hydrocortisone 100mg IV every 8 hours • Ipodate (as above)

ii. Propranolol (modest - through membrane stabilization) d. Adrenergic blockade

i. β-Blockade Propranolol • Bolus: 1-2mg slow IV every 15 minutes infusion:

5-10mg/hr • Oral: 60-80mg PO every 4 hours

Esmolol • Load: 250-500μg/kg • Infusion: 50-100μg/kg/min

ii. Others –If β-blockade is contraindicated by CHF, DM, pregnancy, or asthma/COPD: • Reserpine - 2.5-5mg IM every 4 hours • Guanethidine - 30-40mg PO every 6 hours

e. Systemic decompensation i. Identify precipitating event - 25-43% never found

Notes


ii. Hyperthermia • Acetaminophen (avoid ASA as it displaces hormone

from serum binding sites) • Cooling techniques

iii. Dehydration/nutritional deficits • Fluid and electrolytes (3-5 liters/day) • Glucose (depleted glycogen stores)

iv. Cardiovascular complications • Dysrhythmias and CHF treated with conventional

means • Consider Swan-Ganz monitoring

v. Supportive therapy • Steroids have been related to improved survival • Etiology-dependent

B. Myxedema coma

1. Importance

a. Although extremely rare (only 200-300 true cases in the literature), mortality despite treatment approaches 50-60%.

2. Presentation a. Diagnostic features: altered mental status, defective

thermoregulation, precipitating illness/event, age b. Precipitating event - cold exposure, stroke, CHF, infections,

drugs, anesthetics, GI bleed, trauma, metabolic disturbances c. Common signs and symptoms

i. Neuropsychiatric • Lethargy, slowed mentation, poor memory, cognitive

dysfunction, depression, psychosis, focal or generalized seizures

ii. Hypothermia • In virtually all cases • May be profound (<80oF) • Degree correlates to survival (worst if <90oF)

iii. Cardiovascular • Nonspecific EKG changes, cardiomegaly,

bradycardia, reduced contractility, hypotension iv. Respiratory

• Respiratory depression due to reduced hypoxic drive and decreased response to hypercapnia, impaired respiratory muscle function, and obesity

• Leads to alveolar hypoventilation / progressive hypoxemia, CO2 narcosis and coma

v. Gastrointestinal • Anorexia, nausea, abdominal pain, constipation / fecal

retention • Distended, quiet abdomen; paralytic ileus / megacolon

Notes


• Neurogenic oropharyngeal dysphagia vi. Infections

• “Normal” temperature – think underlying infection • Diaphoresis and tachycardia absent • Pneumonia worsens hypoventilation

d. Labs i. A low T4 and a high TSH are virtually diagnostic

3. Management a. Thyroid hormone therapy

i. Form: L-thyroxine (T4) [safest - controversial] ii. Dosage: 500μg IV bolus/infusion followed by 50-100μg

per day b. Treatment of precipitating factors

i. Common precipitating factors: infection, trauma, surgery, drugs, CHF, stroke, cold exposure, CO2 narcosis

c. Reversal of metabolic abnormalities i. Hypoventilation: hypoxemia and CO2 retention ii. Hypoglycemia: D50 iii. Hypothermia: passive rewarming iv. Hypotension: fluids (poor pressor response)

d. General supportive care i. Fluids and ventilatory support ii. Regulation of temperature iii. Corticosteroids: hydrocortisone 100mg every 8 hours

III. PARATHYROID DISORDERS

A. Hyperparathyroidism

1. Etiology a. Adenomatous gland 80% b. Hyperplasia 15-20% C. Carcinoma 0.5%

2. Findings a. Hypercalcemia

i. Hypercalcemia in the setting of an elevated PTH is diagnostic of primary hyperparathyroidism

ii. Frequently an incidental finding on routine screening iii. Signs and symptoms are related to rate of rise and

absolute levels iv. Common findings involve neurologic, cardiac, GI, renal,

and skeletal systems b. Parathyroid Hormone (PTH) - elevated

3. Management a. Acute

i. Management of hypercalcemia • Correct dehydration • Replace electrolytes

Notes


• Saline diuresis • Mithramycin and calcitonin • Dialysis

b. Supportive therapy c. Definitive

i. Symptomatic - surgery ii. Asymptomatic - follow guidelines

B. Hypoparathyroidism

1. Presentation

a. Symptomatic hypocalcemia i. Paresthesias ii. Muscle cramps iii. Carpopedal spasm iv. Hyperreflexia v. Stridor, tetany, seizures vi. Altered mental status

b. Rate of fall may dictate symptom c. Low serum PTH

2. Management a. If symptomatic - IV calcium b. Severity and degree of symptoms determines rapidity of

replacement c. If life-threat: 10% calcium gluconate 10 ml over 5-10

minutes d. No life-threat: 15 mg/kg over 4-10 hours e. Asymptomatic - Treat with PO calcium preparations

IV. ADRENAL DISORDERS

A. Acute adrenal insufficiency

1. Presentation a. Patients with chronic adrenal insufficiency, an identifiable

stress, and classic abnormalities are relatively simple. b. More typically, making the diagnosis is more difficult;

symptoms are nonspecific in someone without a prior history of adrenal disease.

c. Signs and symptoms i. Nausea & vomiting, fever, hypotension, vascular

collapse ii. Weakness, fatigue, weight loss iii. Hyperpigmentation

d. Labs i. Commonly: hyponatremia, hyperkalemia, azotemia ii. Rare: anemia, lymphocytosis, hypoglycemia,

hypercalcemia, eosinophilia

Notes


2. Management a. Do not wait for documentation of the diagnosis: if

suspected, draw levels (cortisol and ACTH) and institute therapy

b. Hydrocortisone 100mg IV every 6 hours c. Fluids: replace water and sodium deficits with saline

(possibly with dextrose) d. Investigate for underlying disease and treat appropriately

B. Pheochromocytoma

1. Etiology

a. Pheochromocytomas are rare catecholamine-secreting tumors b. Of neural crest origin, usually in the adrenal

2. Presentation a. Hypertension

i. Either continuous or paroxysmal ii. May present as hypertensive crisis

b. Symptoms i. Triad: sweating attacks, tachycardia, headache ii. Five Ps: pressure (hypertension) perspiration, palpitations,

pallor, pain (chest, abdominal, headache) 3. Management

a. Hypertensive crisis i. Labetalol IV/ infusion ii. Nitroprusside IV iii. Phentolamine (α-blocker): 1-5mg bolus followed by

infusion b. Chronic therapy with α-blockers c. Definitive therapy - surgery

V. NUTRITIONAL EMERGENCIES

A. Vitamins

There are two general classes of vitamins - the water soluble (B complex and C) and the fat soluble (A, D, E, and K). Any vitamin may be deficient; however, usually only fat soluble vitamins cause dysfunction in excess.

1. Deficiency syndromes

a. Thiamin (B1) i. Seen in alcoholics, un-enriched cereal grains as staples,

raw fish diet (thiaminase) ii. Early stage: anorexia, indigestion, constipation, malaise,

heaviness of legs, calf tenderness, skin anesthesia, palpitations

iii. Wet beriberi: edema of legs, face, trunk, and serous

Notes


cavities; fast pulse, distended neck veins, high blood pressure, decreased urine volume

iv. Dry beriberi: worsening of polyneuritis, difficulty walking, Wernicke- Korsakoff syndrome/encephalopathy

b. Riboflavin (B2) i. Mouth: soreness/burning of lips, mouth, and tongue,

cheilosis, angular stomatitis, glossitis, purple swollen tongue [similar to other B deficiencies]

ii. Eyes: photophobia, lacrimation, burning/itching of eyes, loss of visual acuity, corneal ulcers and superficial vascularization

iii. Skin: seborrheic dermatitis of nasolabial folds, vestibule of nose, ears, eyelids, scrotum/vulva

c. Niacin (B3) i. Occurs where corn is mainstay of diet ii. Early stages: muscular weakness, anorexia, indigestion,

skin eruptions iii. Pallagra: dermatitis, dementia, diarrhea ("3 Ds"), tremors,

sore tongue d. Pyridoxine (B6) peripheral neuritis e. Cobalamin (B12) megaloblastic and pernicious anemias,

glossitis, hypospermia, GI disorders f. Folic acid megaloblastic anemia, glossitis, GI disturbances g. Ascorbic acid (C) - cofactor in collagen synthesis scurvy:

follicular hyperkeratosis, swollen/inflamed gums, loosening of teeth, loss of hair, dry/itchy skin, impaired wound healing

h. Vitamin A i. Night blindness - inability to adapt from bright light or

glare to darkness (night driving) or difficulty seeing in dim light

ii. Xerophthalmia - usually in developing countries; associated with atrophy of periocular glands, conjunctival hyperkeratosis, and corneal involvement

iii. Infection - increased host susceptibility through loss of mucous membrane integrity; increased mortality in developing countries from respiratory disease and diarrhea

2. Cutaneous changes - follicular hyperkeratosis a. Vitamin D

i. Rickets (children) - malformation of bones due to deficient mineralization. Symptoms: initially profuse sweating and restlessness, then bowlegs when child walks; also potbelly, rachitic rosary (ribs), knock-knees, pigeon breast, frontal bossing

ii. Osteomalacia (adults) - pronounced softening of the bones similar to osteoporosis. Symptoms: rheumatic type pain, general weakness, waddling gait

Notes


b. Vitamin E

i. Neurologic disorders / peripheral neuropathy, anemia c. Vitamin K

i. Bleeding from depletion of dependent clotting factors; also hemorrhagic disease of the newborn from poor placental transfer and failure to establish K-producing intestinal flora

3. Hypervitaminoses a. Vitamin A

i. Dose: 200mg (660,000 IU) [polar bear liver: 10 million IU/lb]

ii. Symptoms: nausea, vomiting, fatigue, weakness, headache, anorexia, and (severe) exfoliation

b. Vitamin D i. Hypercalcemia leading to excessive calcification of

bones, kidney stones, soft tissue calcifications (kidney and lung)

Notes


ENDOCRINE EMERGENCIES

PEARLS 1. Hypoglycemia: glucose < 40 usually. 2. Etiology - hypoglycemia: reactive (post gastric surgery, DM, hyperal), fasting (underproduction or over-utilization), drug-induced (ASA, sulfonylureas, insulin, alcohol, haloperidol, propranolol). 3. Sx - hypoglycemia: tachycardia, paresthesias, HA, irritability, blurred vision, seizures, sweating, coma. 4. Treatment - hypoglycemia: D50W IV bolus or (if IV not available) glucagon 1.0 mg SQ/IM: dextrose infusion, meal, recheck glucose. May need continued treatment if induced by long-acting oral agent. 5. DKA may be induced by absolute insulin deficiency, stress, infection, MI. 6. Sx - DKA include NN, thirst, abdominal pain, polydipsia/polyuria. 7. Signs - DKA: AMS, hypo/hyperthermia, dehydration, acetone breath, Kussmaul respirations. 8. Lab findings - DKA: glucose > 300, serum ketones, acidosis, lo Na, lo Cl (vomiting), early elevated K (shift), followed by decrease K (depletion), elevated BUN/cr, urinary glucose, ketones. 9. Treatment - DKA: rehydration, insulin, correction of electrolyte and acid base balance, treatment of precipitating cause. 10. Rehydration: first liter NS over 30 minutes; may require several liters in first few hours; add dextrose when blood glucose < 250. Average fluid deficit 4-6 L. 11. Insulin in DKA: prime IV tubing with IO uR; IV drip 0. I uR insulin/kg/hour. 12. Electrolytes: add 20-40 meq K to each liter after renal function evaluated; phosphorous shifts intracellularly as DKA treated. 13. Bicarb only for severe acidosis < 6.9.

Notes


14. M + M of DKA: pulmonary edema, hypokalemia, CSF acidosis (due to bicarb administration), hypoglycemia, underlying cause, prolonged coma, older age. 15. Hyperglycemic, hyperosmolar nonketotic coma (HHNC): severe hyperglycemia and dehydration without significant ketosis, usually in the older diabetes patient. 16. Etiology of HHNC: infection, MI, CVA, GI bleed, underlying cardiovascular or renal disease, drugs. 17. Clinical HHNC: thirst, sx and signs CVA, fever, tachycardia, volume depletion, vascular collapse. 18. Labs in HHNC: glucose often > 800, serum osm > 350, negative ketones, lo or hi Na + K, elevated BUN/cr, +/- metabolic acidosis. Search for ppt cause: CBC, UA, U C+S, CXR, EKG, BC, LP, sputum C+S. 19. Treatment - HHNC: rehydration, reduction of glucose, electrolyte correction, tx of ppt cause. 20. Rehydration of HHNC: average fluid deficit 8-12 L. Replace 1/2 water first 12 hours; replace remainder next 24 hours. 21. Electrolyte replacement: Na deficit 500 meq (as in DKA). Add 10-20 meq KCI/hour after normal renal function confirmed. 22. Insulin as in DKA. 23. Mortality HHNC 50% due to age, underlying disease (especially renal

disease), cerebral edema, pulmonary edema, hypoglycemia. 24. Adrenal insufficiency. Alt Cortisol (regulated by hypothal-pit-adrenal axis) maintains glucose; Aldosterone (regulated by volume-K feedback loops) maintains Na, extracellular fluid balance. 25. Adrenal crisis: overwhelming intensification of chronic insufficiency, acute adrenal hemorrhage, rapid steroid withdrawal, stress. 26. Sx - adrenal insufficiency: cortisol-related anorexia, NN, lethargy, abdominal pain, malaise, myalgias; aldosterone-related dehydration (not seen in secondary Al). 27. Signs - adrenal insufficiency: Na depletion, orthostatic hypotension, shock, hyperkalemia, AMS, tachycardia, hyperpigmentation, vitiligo, muscle wasting, fever.

Notes


28. Labs in Al: lo Na, hyperkalemia, hypoglycemia, elevated BLJN, eosinophilia, EKG changes, narrow cardiac silhouette on CXR, hypercalcemia. Search for ppt cause. 29. Treatment Al: includes volume rehydration (D5NS IV), pressors ineffective, correction hypoglycemia, glucocorticoid replacement (200 mg hydrocortisone IVP or 4 mg dexamethasone plus 0. I mg fludrocortisone IVP). ACTH stim test: .25mg cosyntropin followed by serial cortisol levels. 30. Sx - hypothyroidism: AMS, constipation, paresthesias, cold intolerance, weight gain, myalgias, menorrhagia, sluggishness. 31. Signs - hypothyroidism: puffy face, dry skin, hoarse voice, myxedema, bradycardia, galactorrhea, HTN, yellow-tinged skin, absent lateral 1/3 eyebrows, prolonged relaxation phase DTR'S, pericardial, pleural, peritoneal effusion. 32. Labs - hypothyroidism: lo TFT'S, high cholesterol, SGOT, LDH, CPK, lo H/H. 33. Tx - hypothyroidism: thyroxine 50ug/day. Referral to primary care. 34. Myxedema - due to medication noncompliance, infection, MI, CHF, CVA, GI bleed, trauma, narcotics, sedatives, anesthetics. 35. Presentation - myxedema: coma, hypothermia, hypoventilation, hypotension, edema. 36. Labs - myxedema: decreased TFT'S, lo glucose, Cl, Na, Hb; hypoventilation/hypoxemia. 37. Tx - myxedema: supportive care with airway, correction hypothermia, \electrolyte imbalance, and glucose; replace thyroid (L-thyroxine 300 500 ug IV); treat possible Al (hydrocortisone I 00 mg IVP); avoid fluid overload. 38. Primary hyperthydroidism: Graves', nodular toxic goiter, thyroid CA, thyroiditis, apathetic hyperthyroidism. 39. Secondary hyperthyroidism: pituitary adenoma, struma ovarii, HCG tumors, factitious. 40. Thyroid storm induced by stress, infection, hypoglycemia, ketoacidosis, CVA, PE, thyroxine OD, anti-thyroid withdrawal, vigorous palpation of gland.

Notes


41. Sx - thyroid storm: hyperpyrexia with disproportionate tachycardia; dehydration, sweating, restlessness, psychosis, seizures, muscle weakness, coma, hi-output CHF, atrial fib, edema, N/V/D, abdominal pain. 42. Dx - thyroid storm is clinical. 43. Tx - hyperthyroidism: Graves'- PTU 300-600 mg/day or methimazole 30 60 mg/day, RAI, propranolol, surgery. 44. Tx - thyroid storm: id and tx ppt cause, cool, (block thyroid hormone peripheral effects [propranolol 2 mg IV]), block thyroid hormone synthesis (PTU or methimazole), block thyroid hormone release (Nal or Lugols' solution or SSKI), block conversion of T 4 to T3 (dexamethasone).

Notes


REFERENCES 1. Wolfson AB, ed, "Endocrine and Metabolic Emergencies," Emergency Medicine Clinics of North America, 7(4) November 1989. 2. Ober KP, ed, "Endocrine Crises," Endocrinology and Metabolism Clinics of North America, 22(2) June 1993. 3. Kecskes SA, "Diabetic Ketoacidosis," Pediatric Clinic North Am. 40(2)355-363, 1993. 4. Nayak B and Burman K, “Thyrotoxicosis and Thyroid Storm,” Endocrinology and Metabolism Clinics of North America, 35 (2006) 663-686. 5. Sarlis NJ and Gourgiotis L, “Thyroid Emergencies,” Reviews in Endocrine and Metabolic Disorders, 4 (2003) 129-136. 6. Wartofsky L, “Myxedema Coma,” Endocrinology and Metabolism Clinics of North America, 35 (2006) 687-698. 7. Fliers E and Wiersinga WM, “Myxedema Coma,” Reviews in

Endocrine and Metabolic Disorders, 4 (2003) 137-141. 8. Wolfson AB, "Update in Diabetic Ketoacidosis," Emerg Med Reports, 12(10)89-96, 1991. 9. Pheochromocytoma Bravo EL and Gifford RW, "Pheochromocytoma: Diagnosis, Localization and Management," NEJM, 311(20)1298-1303, November 15, 1984. 10. Vitamins Mayes PA, Chapter 53 "Structure and Function of the Water Soluble Vitamins," and Chapter 54 "Structure and Function of the Lipid-Soluble Vitamins," 547-570, in Harper's Biochemistry, Murray RK et al, eds, Appleton & Lange, East Norwalk, Connecticut, 1990. 11. Mahan LK and Arlin MT, eds, Chapter 6 "Vitamins," 71-105, i Krause's Food, Nutrition, and Diet Therapy, WB Saunders Co, Philadelphia, 1992. 8/10

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