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ICU Endocrine Emergencies

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Presentation on theme: "ICU Endocrine Emergencies"— Presentation transcript:

1 ICU Endocrine Emergencies
Bradley J. Phillips, MD Burn-Trauma-ICU Adults & Pediatrics

2 ICU - Endocrine Disorders
Glucose metabolism Thyroid dysfunction Adrenal disorders Pituitary disorder Unusual Carcinoid crisis Hyperparathyroidism

3 ICU - Glucose Metabolism
Hyperglycemia Hypoglycemia Diabetic Ketoacidosis (DKA) Hyperglycemic Hyperosmolar Syndrome

4 Diabetes in the ICU Diagnosis Complications Fasting glucose > 126
Random glucose > 200 x 2 Complications Diuresis and dehydration Acidosis Hyponatremia Hypocalcemia Immune dysfunction

5 DKA Presentation Anorexia, nausea, emesis, polyuria Kussmaul breathing
“Fruity” breath Deterioration mental status Hypotension Progressive acidosis Chest and/or abdominal pain

6 DKA Occurs in absence or near-absence of insulin
NIDDM (type 2) at risk during catabolic stress More common in adults than children 40% over 40 20% over 55 Infectious cause most common Mortality 5-10% Increases with age ( > 65 = 20-40%)

7 DKA Tests Hyperglycemia (> 250) Ketonemia (ß-hydroxybutyrate)
Glycosuria and ketonuria Acidosis (pH < 7.3) with anion gap Low serum bicarbonate (< 15) Moderate hyperosmolality

8 DKA - Associated Abnormalities
Sodium variable fall by 1.6 for every 100 increase in glucose falsely low with hypertriglyceridemia Chloride hyper in ketoacidosis hypo associated with severe emesis Potassium high with acidosis at high risk for severe hypokalemia

9 DKA Management Fluid resuscitation Insulin
Normal saline cc/hr with bolus of 1L If UOP good and NA > 140, slow IVF and change to .45 NS Add D5 once BS < 300 Insulin 0.4u/kg with 1/2 IV and 1/2 SQ IV qtt or hourly IV injections continue until ketones in urine resolved change to SQ once BS< 200, pH > 7.3, Bicarb > 18

10 DKA Management Potassium Replete hypophosphatemia
K< 3.5 add 40 meq/l K > 3.5 and < meq/l check q 2 hrs Replete hypophosphatemia Give bicarbonate if pH < 7.1 Treat underlying cause

11 DKA Complications Hypotension and shock Thrombosis Cerebral edema
Renal failure Hypoglycemia

12 Hyperglycemic Hyperosmolar Syndrome
Present with severe hydration without ketosis and acidosis Glucose > 1000 Coma, seizures, tremors, hemiplegia Causes infection MI hemorrhage and trauma burns Treat the same as DKA

13 ICU - Thyroid Dysfunction
Hypothyroidism Myxedema coma Thyrotoxicosis Thyrotoxic crisis

14 Hypothyroidism cold intolerance hypothermia apathy
depressed mental status weight gain alopecia dry coarse skin arthralgia and myalgia hoarseness enlarged tongue goiter periorbital edema hyponatremia hypoventilation hypotension cardiac dysfunction bradycardia pericardial effusion

15 Myxedema Coma Acute exacerbation of hypothyroidism Highly lethal = 50%
Precipitating factors CVA CHF drugs (narcotics, diuretics, sedative) surgery/trauma GI hemorrhage bowel obstruction hypoadrenalism

16 Myxedema coma Non-pitting edema “doughy” Severe sensorial depression
Airway obstruction Respiratory muscle weakness Severe hypoventilation

17 Thyrotoxicosis Etiology Graves toxic goiter thyroiditis drugs
amiodarone iodine thyroxine (particularly IV) Pituitary adenoma Molar pregnancy

18 Thyrotoxicosis Thyroid crisis / “storm”
life-threatening 10-20% mortality precipitation factors Infection Thyroid manipulation (operation, palpation) Metabolic disorders (DKA) Trauma MI PE Pregnancy

19 Thyrotoxicosis Vs “Storm”
Neuro emotional lability tremors weakness CV tachycardia systolic HTN afib Thermo heat intolerance GI diarrhea Neuro delirium seizures coma CV CHF arrhythmias Thermo fevers GI emesis diarrhea jaundice

20 Thyroid - Diagnostic Tests
TSH Free T4 ( or FTI) T3 –RIA (Radioimmune Assay)

21 Thyrotoxicosis Differential Diagnosis
Check free T4 if high, r/o euthyroid hyperthyroxinemia etiology high TBG (pregnancy, estrogen) acute illness liver disease drug-induced (amiodarone, heparin, narcotics, anti-psychotics) differeriate with history/clinical exa, If low, check T3 to r/o T3 toxicosis Radioactive iodine uptake test

22 Therapy - Hyperthyroidism
Uncomplicated hyperthyroidism outpatient methimazole or PTU B-blockers for adrenergic +/- I31 ablation Severe hyperthyroidism possible hospitalization restricted activity compliance with medications education

23 Management of Thyroid “Storm”
Always ICU management Supportive Fever reduction decreases metabolic rate decreases percentage of free T4 tylenol avoid salicylates (alters protein binding) Aggressive fluid resuscitation large losses from sweating, emesis, diarrhea replete glucose and vitamins ? Hemodynamic monitoring rate control - first line digoxin avoid B-Blockers

24 Management of Thyroid “Storm”
Pharmacologic control Antithyroid drugs methimazole or PTU give po/NGT/rectally Inhibit release of T4 and T3 SSKI or Lugol’s solution initial of dose of antithyroid drug must be given consider lithium

25 Management of Thyroid “Storm”
Pharmacologic control Inhibit conversion of T4 to T3 consider steroids or PTU ipodate sodium (Oragrafin) highly effective caution long-term use (“escape” Reduction of hyperadrenergic state propranolol (historical) cautious of B-blockers in CHF Removal of T4 plasmaphresis or hemoperfusion emergent thyroidectomy

26 ICU Complications of Hyperthyroidism
Atrial arrthythmias most convert within 3 weeks of euthyroidism never after 4 months no prospective study on anticoagulation CVA age-dependent not atrial fib -dependent CHF Malnutrition/dehydration Metabolic failure Drug metabolism

27 Therapy - Hypothyroidism
Uncomplicated outpatient treatment full dose 1.7 ug/kg age dependent young ug/d old 12.5 to 25 ug/d check TSH at 4-6 weeks change doses 12.5 to 25 ug increments

28 Therapy - Hypothyroidism
Profound or myxedema coma endocrine emergency supportive care correct hypothermia blood volume restoration monitor electrolytes (free water clearance impaired) glucose replacement check for drug toxicity (digoxin etc) r/o underlying infection

29 Therapy - Hypothyroidism
Thyroxine replacement loading dose uq IV no CV complications in critically ill ? Higher mortality in high T3 toxicosis maintenance ug/d

30 Hypothyroidism in Surgical Patients
Historical complications peri-op more common Recent studies mild-moderate - little influence no increased cardiopulmonary difficulties, wound healing impairment, or infections Critically ill ? respiratory dysfunction and vent weaning T4 and T3 reduced, TSH high/low/normal Controlled studies of T4/T3 administration no benefit overall in trauma, burns ? Benefit in organ transplantation

31 Adrenal disorders Adrenal insufficiency Pheochromocytoma and “ crisis”
Aldosterone deficiency

32 Adrenal Insufficiency
Incidence General population 40-60/million ICU % SICU % SICU trauma 0.23% SICU nontrauma 0.98% SICU > 14 days 6% age > % > 14 days and age > 55 11% Blunt adrenal injury 5%

33 Risk Factors - AI Age > 55 Malnutrition
Prolonged hospital or ICU stay Chronic alcoholism High APACHE score Stress in form of trauma, surgery, infection, and dehydration

34 Presentation of AI Non-ICU ICU insidious
nonspecific (weakness, wt loss, lethargy, GI symptoms) ICU acute adrenal crisis altered by co-existing disease usually precipitated by physical stressor (trauma, surgery, infection, dehydration) other causes AIDS, TB, or pituitary tumor

35 ICU Clinical Presentation
Refractory hypotension High-output circulatory failure CI > 4 tachycardia low SVR with normal wedge Electrolytes disturbances high K , low Na, and low glucose Febrile (> 39C) Mental status changes Dehydration GI disturbances

36 “Clues” to AI History Eosinophilia other endocrine abnormalities
family h/o endocrine abnormalities Eosinophilia

37 AI Differential Diagnosis
Sepsis Neurogenic shock Overdose of vasodilator Severe anemia AV shunt Thyrotoxicosis Beriberi Pregnancy

38 Adrenal Insufficiency - AI
Primary Central Relative

39 Adrenal Insufficiency - AI
Primary autoimmune, infection, hemorrhage(bilateral), medications (ketaconazole, etc), metastatic carcinoma, lymphoma Central long-standing steroid use Relative increased degradation resistance increased demand

40 Primary AI Pathological process within adrenal gland Etiology
90% o f gland destruction Etiology Autoimmune % Infectious - 35% Hemorrhagic Risk factors (Rao et al , Ann Intern Med, 1989) coagulopathy thromboembolic disease postoperative state

41 Central AI Central dysfunction Etiology pituitary (secondary)
hypothalamus (teritary) Etiology  long-term glucocorticoid therapy uncommon post-partum pituitary necrosis (Sheehan’s syndrome) transient ACTH deficiency (alcoholics) pituitary radiation empty sella syndrome

42 Steroid and Potency

43 Glucocorticoid vs Mineralocorticoid
Steroid Glucocorticoid Mineralocorticoid Hydrocortisone Prednisolone Dexamethasone Aldosterone Fludrocortisone

44 Potential for HPA Suppression
Higher risk for suppression higher glucocorticoid potency short frequency of dosing evening dosing systemic therapy duration > 1 week

45 Relative AI Relative increased degradation of glucocorticoids
drugs that activate hepatic metabolism treatment of hypothyroidism resistance to glucocorticoid activity AIDS increased demand (stress response) numerous ICU studies

46 HPA Axis Assessment - Tests
H-P Axis and Adrenal Low-dose ACTH stimulation (1 ug) Adrenal only Short ACTH stimulation test (250 ug) H -P Axis only Insulin-induced hypoglycemia test Metyrapone CRH stimulation

47 Laboratory Assessment
Random cortisol level draw before steroids given draw between 6-8 am decadron generally consider not cross-reactive positive if < 10 in normal or < 15 in critically ill 10-20 indeterminant Cosyntropin testing Corticotropin-releasing hormone test (CRH) Plasma renin and aldosterone measurements

48 Cosyntropin stimulation test
Standard short baseline cortisol level 0.25 mg cosyntropin with level 60 minutes later peak > 20 or rise of 7 in critically ill Low-dose short ( more sensitive for central) more accurate and physiologic same as standard but only 1 ug dose Long differentiation of primary vs central replaced by ACTH measurement

49 HPA Axis Assessment - Test Summary

50 Treatment Hemodynamically unstable Hemodynamically stable
Baseline cortisol Treat with Hydrocortisone 100 IV bolus and q8 +/- cosyntropin testing Isotonic IVF with D5 treat underlying disease or precipitating factors Hemodynamically stable same as above cosyntropin testing

51 uncommonly required for mineralocorticoid activity
Treatment - Steroids Hydrocortisone provides glucocorticoid and mineralocorticoid physiological doses max 300 mg/day normal daily adrenal output AM 25 mg /PM mg Dexamethasone not cross-reactive with cortisol assays no mineralocorticoid activity useful while diagnostic testing being completed Fludrocortisone (Florinef) uncommonly required for mineralocorticoid activity

52 Outcome Untreated = 100% mortality
Treated in critically ill = 50% mortality Cortisol level positively correlated to severity of illness negatively correlated to survival

53 ICU Endocrine Emergencies
Questions…? Bradley J. Phillips, MD Burn-ICU SBH-UTMB

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