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Endocrine Emergencies PowerPoint Presentation

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Description : Check out this medical presentation on Hypoglycemia, which is titled "Endocrine Emergencies", to know about the Endocrine Emergencies including Adrenal (Addisonian Crisis and Pheochromocytoma), Thyroid (Thyroid Storm and Myxedema Coma), and Miscellaneous (Hypoglycemia and Diabetes Insipidus).

Tags : Hypoglycemia, Endocrine Emergencies

Published on : Jul 01, 2021 | Views : 3800 | Downloads : 7

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Slide 1-

ENDOCRINE EMERGENCIES Jim Holliman, M.D., F.A.C.E.P. Professor of Military and Emergency Medicine Uniformed Services University of the Health Sciences Clinical Professor of Emergency Medicine George Washington University Bethesda, Maryland, U.S.A.
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Endocrine Emergencies Adrenal Addisonian Crisis Pheochromocytoma Thyroid Thyroid Storm Myxedema Coma Miscellaneous Hypoglycemia Diabetes Insipidus
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General Mechanisms of Endocrine Pathophysiology Deficient hormone action Excess hormone production or action Neoplasia
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Mechanisms of Endocrine Pathophysiology 1. Deficient hormone action Primary glandular failure Congenital Acquired (atrophy, surgery, tumor, drug-induced, autoimmune, infectious) Secondary glandular failure Disordered hormone release or activation Accelerated hormone metabolism Target tissue resistance
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Mechanisms of Endocrine Pathophysiology (cont.) 2. Excess hormone production or action Gland autonomy (neoplasia, hyperplasia) Abnormal stimulation Ectopic hormone production Altered hormone metabolism Target tissue increased sensitivity to hormone action
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Mechanisms of Endocrine Pathophysiology (cont.) 3. Neoplasia Benign vs. malignant Functional vs. nonfunctional Ectopic hormone production Sporadic vs. familial syndromes
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Multiple Endocrine Neoplasia (MEN) Syndromes MEN I (Wermer) Hyperparathyroid, pituitary adenoma, pancreatic cancer MEN IIa (Sipple) Hyperparathyroid, thyroid medullary ca, pheochromocytoma MEN IIb (or III) Medullary thyroid ca, pheochromocytoma, mucosal neuromas, Marfinoid habitus
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Polyendocrine Failure Syndromes Type I Hypoparathyroidism Hypoadrenalism Mucocutaneous candidiasis Other (hypogonadism,autoimmune thyroid disease, JODM) Type II Adrenal insufficiency Autoimmune thyroid disease Other (JODM, primary or secondary gonadal failure)
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Diseases of the Adrenals Adrenocortical insufficiency Addison's Hypopituitarism Iatrogenic ACTH deficiency Cushing's Syndrome Cushing's Disease (cortical hyperplasia) Pituitary tumor Adrenal adenoma or carcinoma Ectopic ACTH syndrome (from tumors) Virilization Adrenal adenoma or carcinoma Congenital adrenal hyperplasia (CAH) Adrenal-mediated hypertension syndromes Primary hyperaldosteronism (adenoma vs. hyperplasia), Cushing's syndrome, Pheochromocytomas
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Etiologies of Primary Adrenal Insufficiency Iatrogenic suppression Autoimmune adrenalitis (idiopathic) Infections (mycobacteria, fungal, CMV, HIV) Sarcoidosis Hemorrhage (anticoagulants, meningococcemia, trauma, toxemia, emboli) Collagen vascular disease Amyloidosis Hemochromatosis Metastatic malignancy Congenital (hypoplasia, adrenogenital syndrome, adrenoleucodystrophy)
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CT scan showing bilateral adrenal hemorrhages in a 57 year old female with breast cancer
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Etiologies of Secondary Adrenal Insufficiency Pituitary insufficiency Congenital, tumor, infarction, sarcoid, autoimmune Hypothalamic dysfunction Tumor Vascular malformation
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Symptoms of Adrenal Insufficiency Weakness, fatigue, lethargy Nausea, vomiting +/- diarrhea Anorexia, weight loss Mental sluggishness +/- syncope Addisonian Crisis: Shock Cardiovascular collapse
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Signs of Adrenal Insufficiency Hypotension Other signs of dehydration Hyperpigmentation / vitiligo Skin atrophy Muscle wasting Loss of axillary & pubic hair +/- fever
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Lab Findings in Adrenal Insufficiency Hyponatremia Hyperkalemia Hypoglycemia Azotemia (prerenal) +/- eosinophilia +/- anemia
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Precipitating Factors for Addisonian Crisis Acute infection, esp. pneumonia Acute MI Pulmonary embolus Trauma / burns Surgery Heat exposure Vomiting / diarrhea Dehydration Blood loss Rapid cessation or reduction of chronic steroid therapy
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Acute Adrenal Crisis Caveats Suspect this dx when: Sudden hypotension in response to procedure or stress, and does not correct with initial IV fluids +/- raising legs Patients previously maintained on chronic glucocorticoid Rx may not exhibit severe dehydration or hypotension until preterminal since mineralocorticoid function is usually maintained
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Addisonian Crisis Rx High flow oxygen Aggressive fluid / electrolyte replacement Initially NS - usually need 4 to 6 liters Switch to LR when K+ decreases IV hydrocortisone 100 to 250 mg IV bolus 10 to 20 mg per hr. IV infusion +/- cortisone acetate 50 mg IM (in case infusion stops) Search for precipitating cause
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Further Rx of Addisonian Crisis Once the patient's condition improves: Decrease hydrocortisone to 100 mg bid Halve dose daily till maintenance dose achieved (usually 20 mg hydrocortisone per day) Add fludrocortisone 0.1 mg per day when dose of cortisone < 100 mg / day
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Prevention of Acute Adrenal Crisis For patients on chronic steroid Rx: Double their normal daily dose before and for at least 2 - 3 days after a stressful procedure or when an active infection is present For severe stress: Consider tripling steroid dose
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Dosing Comparisons for Adrenocortical Steroids STEROID t1/2 (hrs.) Relative potency Equivalent dose Cortisone 8 - 12 0.8 25 Cortisol 8 - 12 1.0 20 Prednisone 12 - 36 4.0 5 Methylpred- nisolone 12 - 36 5.0 4 Dexameth- asone 36 - 72 25 0.75
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Pheochromocytoma Tumor of chromaffin cells Chromaffin cells produce, store, & secrete catecholamines Clinical features of these tumors are due to excessive catechol release ( not usually due to direct tissue extension effects of tumor) Cause only 0.1% of cases of hypertension but represent a curable cause of hypertension
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Excised pheochromocytoma (left slice chromium stained)
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Excised pheochromocytoma
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High power microscopy view of stained pheochromocytoma cells
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Familial Syndromes Associated with Pheochromocytomas Most are autosomal dominant (variable penetration) MEN II (Sipple Syndrome) Pheos in > 75 % of cases MEN III (mucosal neuroma syndrome) Pheos in > 75 % Von Recklinghausen's neurofibromatosis Pheos in 1 % Von Hippel - Lindau Disease Pheos in 5 to 10 %
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Pheochromocytoma Locations Adrenal medulla : 90 % Abdomen : 8 % Neck or thorax : 2 % Multiple sites : 10 % Malignant : 10 % Associated with familial syndromes : 5 %
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Pheochromocytoma Catechol Secretion Most secrete both norepi and epi (generally norepi > epi) Most extrarenal tumors secrete only norepi Malignant tumors secrete more dopamine and HVA Predominant catechol secreted cannot be predicted by clinical presentation
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Most Common Symptoms of Pheochromocytoma Hypertension > 90 % Sustained 30 % Sustained with crises 30 % Paroxysmal 30 % Headache 80 % Sweating 70 % Palpitations 65 %
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Additional Symptoms of Pheochromocytoma Pallor 45 % Nausea +/- emesis 40 % Nervousness 35 % Fundoscopic changes 30 % Weight loss 25 % Epigastric or chest pain 20 %
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Indications to Screen Patients for Pheos Hypertension with: Grade 3 or 4 retinopathy of uncertain cause Weight loss Hyperglycemia Hypermetabolism with nl. thyroid profile Cardiomyopathy Resistance to 2 or 3 drug Rx Orthostatic hypotension (not due to drug Rx) Unexplained fever Marked hyperlability of BP Recurrent attacks of sx of pheos
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More Indications to Screen Patients for Pheos Severe pressor response during or induced by: Anesthesia or intubation Surgery Angiography Parturition Unexplained circulatory shock during: Anesthesia Pregnancy, delivery, or puerperium Surgery (or after surgery) Use of phenothiazines Family history of pheos Hyperlabile BP or severe hypertension with pregnancy X ray evidence of suprarenal mass
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Conditions Causing Increased Urinary Catechol Levels Hypoglycemia Surgery CHF Acute MI Circulatory shock Sepsis Acidosis Increased ICP Spinal cord injury Trauma / burns Parturition Delerium tremens Strenuous exercise
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Conditions Causing Decreased Urinary Catechol Levels Renal insufficiency (oliguria) Malnutrition Quadriplegia Orthostatic hypotension due to adrenergic insufficiency
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Localization Techniques for Pheos Abdominal CT : most useful Cannot confirm tissue dx Iodine 131 metaiodobenzylguanidine nuclear medicine scanning Helpful for non-abdominal tumors and to confirm function Angiography Requires medication prep for safety
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Bilateral pheochromocytomas (the one on the left has a small area of central hemorrhage)
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6 cm cystic pheo in the right adrenal of a 29 year old female
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Pheochromocytoma at the level of the 7th rib
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Intramyocardial pheo in a patient (who died of CHF from effects of the pheo) known to have a pheo but who never underwent radionuclide scanning to localize it
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Meds for Acute Symptom Control for Pheos (also for pre-angio or preop prep) Phentolamine 2 to 5 mg IV (alpha block) Then propranolol 1 to 2 mg IV (beta block) or labetolol 20 to 40 mg IV (alpha & beta block) Use nitroprusside or phentolamine infusion for hypertensive crisis (50 to 100 mg in 250 cc D5W) For hypotension : norepi infusion For arrhythmias : lidocaine bolus & infusion
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Meds for Nonemergent or Chronic Sx Control for Pheos Phenoxybenzamine 10 to 20 mg tid-qid (alpha block) Prazosin 1 to 5 mg bid Propranolol 10 to 40 mg qid or labetolol 200 to 600 mg bid (beta block) Alpha-methyl-p-tyrosine (metyrosine) 250 mg to 1 gram bid (synthesis inhibitor)
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Workup scheme for pheos
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Thyroid Storm Definitions "Exaggerated or florid state of thyrotoxicosis" Life threatening, sudden onset of thyroid hyperactivity" May represent end stage of the continuum: hyperthyroidism to thyrotoxicosis to thyrotoxic crisis to thyroid storm "Probably reflects the addition of adrenergic hyperactivity, induced by a nonspecific stress, into the setting of untreated or undertreated hyperthyroidism"
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Thyroid Storm Epidemiology Most cases secondary to toxic diffuse goiter (Grave's Disease) Mostly in women in 3rd to 4th decades Some cases due to toxic multinodular goiter Mostly in women in 4th to 7th decades Very rarely due to : Factitious Thyroiditis Malignancies Very rare in children
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51 year old male with Graves Disease who presented with urine retention
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Pretibial myxedema and square toes in the same patient on the prior slide
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Lag ophthalmos in a patient with Graves Disease
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Another patient with Graves Disease
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Thyroid scan of patient with Graves Disease Scan of patient with toxic multinodular goiter with hot nodule
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Thyroid Storm Prognosis Old references quote almost 100% mortality untreated and 20% mortality treated ( but before beta blockers) Current mortality ? < 5 % treated (although not well studied or reported due to rarity of cases)
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Thyroid Storm Clinical Presentation Most important: Fever Abnormal mental status (agitation confusion, coma) Tachycardia Vomiting / diarrhea +/- jaundice +/- goiter +/- exopthalmos
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Thyroid Storm CNS Manifestations With increasing severity of storm: Hyperkinesis Restlessness Emotional lability Confusion Psychosis Apathy Somnolence Obtundation Coma
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Thyroid Storm Cardiovascular Manifestations Increased heart rate Sinus tach or atrial fib Increased irritability First degree AV block, PVC's, PAC's Wide pulse pressure Apical systolic murmur Loud S1, S2 May develop CHF
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"Apathetic" or "Nonactivated" Thyrotoxicosis Represents dangerous hyperthyroidism masked by preexistent sx Usually age > 70 Recent weight loss > 40 lbs. May present as seemingly isolated sx: CHF Atrial fib CNS sx Somnolence, apathy, coma
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Thyroid Storm Precipitating Factors Infection, esp. pneumonia CVA CHF Pulmonary embolus DKA Parturition / toxemia Trauma Surgery I 131 Rx Iodinated contrast agents Withdrawl of antithyroid drugs
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Thyroid Storm Initial Lab Studies Needed CBC, lytes, BUN, glucose T4, T3, T3 RU, TSH U/A ABG +/- LFT's +/- serum cortisol
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Thyroid Storm Usual Lab Results Lab studies do NOT distinguish thyrotoxicosis from thyroid storm Usually T4 & T3 elevated, but may be only increased T3 Usually plasma cortisol low for degree of physiologic stress present Hyperglycemia common
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Thyroid Storm Emergent Rx High flow O2 Rapid cooling if markedly hyperthermic Ice packs, cooling blanket, mist / fans, NG lavage, acetominophen (ASA contraindicated) IV +/- IV fluid bolus if dehydrated May need inotropes if already have CHF) Propranolol 1 to 2 mg IV & repeat or labetolol 20 to 40 mg IV & repeat prn +/- digoxin, Ca channel blockers for rate control for atrial fib; +/- diuretics for CHF Find & treat precipitating cause
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Thyroid Storm Further Rx IV hydrocortisone 100 mg PTU 600 to 900 mg PO or NG, then 200 to 300 mg qid Iodine (> 1 hour after PTU): 1 to 2 gm sodium iodide IV drip, then 500 mg q 12 hr; or 20 gtts SSKI PO tid +/- Li CO3 600 mg PO then 300 mg tid +/- Colestipol (binds T4 in gut) 10 grams PO tid
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Myxedema Coma Represents end stage of improperly treated, neglected, or undiagnosed primary hypothyroidism Occurs in 0.1% or less of cases of hypothyroidism Very rare under age 50 50% of cases become evident after hospital admission Mortality 100% untreated, 30 to 60% treated Most cases present in the winter
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General Causes of Thyroid Failure Diseases of the: Thyroid (primary hypothyroidism) : 95 % Pituitary (secondary hypothyroidism) : 4 % Pituitary tumor or sarcoid infiltration Hypothalamus (tertiary hypothyroidism) : < 1 %
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Etiologies of Primary Hypothyroidism Autoimmune : most common Post thyroidectomy External radiation I 131 Rx Severe prolonged iodine deficiency Antithyroid drugs (including lithium) Inherited enzymatic defect Idiopathic
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Symptoms of Hypothyroidism Cold intolerance Dyspnea Anorexia Constipation Menorrhagia or amenorrhea Arthralgias / myalgias Fatigue Depression Irritability Decreased attention +/- memory Paresthesias
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Signs Related to Hypothyroidism Dry, yellow (carotenemic) skin Weight gain (41% of cases) Thinning, coarse hair "Myxedema signs“ : Puffy eyelids Hoarse voice Dependent edema Carpal tunnel syndrome Anemia
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Patient with myxedema coma
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Hypothyroidism and Myxedema Coma Cardiac Signs Hypotension Bradycardia Pericardial effusion Low voltage EKG Prolonged QT Inverted or flattened T waves
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EKG findings in a hypothyroid patient
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Myxedema Coma Typical Presentation Usual signs & sx of hypothyroidism plus: Hypothermia (80 % of cases) If temp. normal, consider infection present Hypotension / bradycardia Hypoventilation / resp. failure Ileus Depressed mental status / coma
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Lab Studies to Order for Suspected Myxedema Coma CBC Lytes, BUN, glucose, calcium T3, T4, TSH Serum cortisol ABG LFT's +/- drug levels
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Precipitants of Myxedema Coma Cold exposure Infection Pneumonia UTI Trauma CNS depressants Narcotics Barbiturates Tranquilizers General anesthetics CVA CHF
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Contributing Factors to Coma in Myxedema Coma Hypothyroidism itself Hypercapnia Hypoxia Hypothermia Hypotension Hypoglycemia Hyponatremia Drug (sedative) side effect +/- sepsis
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Emergency Treatment of Myxedema Coma O2 +/- intubation / ventilation (if resp. failure) Rapid blood glucose check +/- IV D50 +/- Naloxone Hydrocortisone 100 to 250 mg IVP Cautious slow rewarming (warm O2, scalp/groin/axilla warm packs, NG lavage) Thyroxine (T4) 500 micrograms IV, then 50 mcg qd IV Add 25 mcg triiodothyronine (T3) PO or by NG q 12h if T4 to T3 peripheral conversion possibly impaired Careful IV fluid rehydration ; watch for CHF Follow TSH levels ; should decrease in 24 hrs. & normalize in 7 days of Rx
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60 year old male with severe hypothyroid-ism
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Same patient as on prior slide 6 months after Rx with T4
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Causes of Hypoglycemia Fasting Insulinoma or extrapancreatic tumors Extensive hepatic dysfunction Starvation Sepsis Chronic renal failure Glycogen storage diseases Diseases with antibodies to insulin or receptor Hormonal deficiency (steroids, growth hormone, epi) Drugs (on next slide) Postprandial (Alimentary, Reactive, Genetic - galactosemia or fructose intolerance) Artifactual (leukemia, polycythemia)
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Drugs Causing Hypoglycemia Insulin Oral hypoglycemics Ethanol Salicylates Beta blockers Pentamidine Diisopyramide Quinine Isoniazid MAO inhibitors Various drugs causing decreased liver metabolism of oral hypoglycemic agents
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Symptoms and Signs of Hypoglycemia Symptoms Diaphoresis Palpitations Headache Hunger Trembling Faintness Signs Hypothermia Confusion Amnesia Seizures Coma ANY FOCAL CNS SIGN
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Diagnostic Approach to Fasting Hypoglycemia Prove that hypoglycemia is directly responsible for sx during attacks by showing: typical sx plasma glucose < 50 mg% prompt relief of sx by glucose ingestion or IV Consider checking: Serum insulin level Insulin antibodies Sulfonylurea levels C-peptide levels Proinsulin levels
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Causes of Polyuria UTI Osmotic diuresis (e.g., diabetes mellitus) Primary (psychogenic) polydipsia (Compulsive water drinking) Nephrogenic diabetes insipidus Central diabetes insipidus
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Causes of Diabetes Insipidus Central Head trauma Craniopharyngioma Infiltrative (sarcoid) Post neurosurgery Familial Vascular Infectious Idiopathic Nephrogenic Drugs Demeclocycline Lithium carbonate Acquired Sickle cell anemia K+ deficiency Hypercalcemia Amyloidosis Sjogren Syndrome Multiple myeloma Familial
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Hormone Preparations for Rx of Diabetes Insipidus Medication Duration of Action (hrs.) Dose Route Aqueous vasopressin 2 to 6 5 to 10 u SQ or IV Lysine vasopressin 2 to 6 2 to 4 u Nasal Pitressin in oil 24 to 48 5 u IM Desmo- pressin 12 to 24 10 to 20 mcg Nasal HCTZ (for nephrogenic) 12 to 24 50 to 100 mg PO
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