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ICU Endocrine Emergencies Bradley J. Phillips, MD Burn-Trauma-ICU Adults & Pediatrics ICU - Endocrine Disorders Glucose metabolism Thyroid dysfunction Adrenal disorders Pituitary disorder Unusual – Carcinoid crisis – Hyperparathyroidism ICU - Glucose Metabolism Hyperglycemia Hypoglycemia Diabetic Ketoacidosis (DKA) Hyperglycemic Hyperosmolar Syndrome Diabetes in the ICU Diagnosis – Fasting glucose > 126 – Random glucose > 200 x 2 Complications – – – – – Diuresis and dehydration Acidosis Hyponatremia Hypocalcemia Immune dysfunction DKA Presentation – – – – – – – Anorexia, nausea, emesis, polyuria Kussmaul breathing “Fruity” breath Deterioration mental status Hypotension Progressive acidosis Chest and/or abdominal pain 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%) DKA Tests – – – – – – Hyperglycemia (> 250) Ketonemia (ß-hydroxybutyrate) Glycosuria and ketonuria Acidosis (pH < 7.3) with anion gap Low serum bicarbonate (< 15) Moderate hyperosmolality 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 DKA Management – Fluid resuscitation Normal saline 500-1000 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 DKA Management – Potassium K< 3.5 add 40 meq/l K > 3.5 and < 5.5 20 meq/l check q 2 hrs – Replete hypophosphatemia – Give bicarbonate if pH < 7.1 – Treat underlying cause DKA Complications – – – – – Hypotension and shock Thrombosis Cerebral edema Renal failure Hypoglycemia 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 ICU - Thyroid Dysfunction Hypothyroidism Myxedema coma Thyrotoxicosis – Thyrotoxic crisis 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 Myxedema Coma Acute exacerbation of hypothyroidism Highly lethal = 50% Precipitating factors – – – – – – – CVA CHF drugs (narcotics, diuretics, sedative) surgery/trauma GI hemorrhage bowel obstruction hypoadrenalism Myxedema coma Non-pitting edema “doughy” Severe sensorial depression Airway obstruction Respiratory muscle weakness Severe hypoventilation Thyrotoxicosis Etiology – – – – Graves toxic goiter thyroiditis drugs amiodarone iodine thyroxine (particularly IV) – Pituitary adenoma – Molar pregnancy Thyrotoxicosis Thyroid crisis / “storm” – life-threatening 10-20% mortality – precipitation factors Infection Thyroid manipulation (operation, palpation) Metabolic disorders (DKA) Trauma MI PE Pregnancy Thyrotoxicosis Vs “Storm” Neuro – emotional lability – tremors – weakness CV – tachycardia – systolic HTN – afib – delirium – seizures – coma GI – diarrhea CV – CHF – arrhythmias Thermo – fevers Thermo – heat intolerance Neuro GI – emesis – diarrhea – jaundice Thyroid - Diagnostic Tests TSH Free T4 ( or FTI) T3 –RIA (Radioimmune Assay) 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, antipsychotics) differeriate with history/clinical exa, – If low, check T3 to r/o T3 toxicosis Radioactive iodine uptake test Therapy - Hyperthyroidism Uncomplicated hyperthyroidism – – – – outpatient methimazole or PTU B-blockers for adrenergic +/- I31 ablation Severe hyperthyroidism – possible hospitalization restricted activity compliance with medications education 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 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 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 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 Therapy - Hypothyroidism Uncomplicated – outpatient treatment – full dose 1.7 ug/kg – age dependent young 50-100 ug/d old 12.5 to 25 ug/d – check TSH at 4-6 weeks – change doses 12.5 to 25 ug increments 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 Therapy - Hypothyroidism Thyroxine replacement – loading dose 300-500 uq IV no CV complications in critically ill ? Higher mortality in high T3 toxicosis – maintenance 50-100 ug/d 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 Adrenal disorders Adrenal insufficiency Pheochromocytoma and “ crisis” Aldosterone deficiency Adrenal Insufficiency Incidence – General population 40-60/million – ICU 1-20% SICU 0.66% – SICU trauma – SICU nontrauma 0.23% 0.98% SICU – > 14 days – age > 55 – > 14 days and age > 55 – Blunt adrenal injury 5% 6% 1.7% 11% 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 Presentation of AI Non-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 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 “Clues” to AI History – other endocrine abnormalities – family h/o endocrine abnormalities Eosinophilia AI Differential Diagnosis Sepsis Neurogenic shock Overdose of vasodilator Severe anemia AV shunt Thyrotoxicosis Beriberi Pregnancy Adrenal Insufficiency - AI Primary Central Relative 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 Primary AI Pathological process within adrenal gland – 90% o f gland destruction Etiology – Autoimmune - 65-80% – Infectious - 35% – Hemorrhagic Risk factors (Rao et al , Ann Intern Med, 1989) – coagulopathy – thromboembolic disease – postoperative state Central AI Central dysfunction – 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 Steroid and Potency Glucocorticoid vs Mineralocorticoid Steroid Hydrocortisone Prednisolone Dexamethasone Aldosterone Fludrocortisone Glucocorticoid Mineralocorticoid 1 4 40 0.1 10 1 0.7 2 400 400 Potential for HPA Suppression Higher risk for suppression – – – – – higher glucocorticoid potency short frequency of dosing evening dosing systemic therapy duration > 1 week 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 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 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 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 HPA Axis Assessment - Test Summary Treatment Hemodynamically unstable – – – – – 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 Treatment - Steroids Hydrocortisone – provides glucocorticoid and mineralocorticoid – physiological doses max 300 mg/day – normal daily adrenal output AM 25 mg /PM 12..5 mg Dexamethasone – not cross-reactive with cortisol assays – no mineralocorticoid activity – useful while diagnostic testing being completed Fludrocortisone (Florinef) – uncommonly required for mineralocorticoid activity Outcome Untreated = 100% mortality Treated in critically ill = 50% mortality Cortisol level – positively correlated to severity of illness – negatively correlated to survival ICU Endocrine Emergencies Questions…? Bradley J. Phillips, MD Burn-ICU SBH-UTMB