This document summarizes key endocrine emergencies including thyroid storm, adrenal crisis, and hypoglycemia. Thyroid storm is a life-threatening complication of hyperthyroidism caused by Graves' disease or toxic multinodular goiter in 1-2% of cases, with a mortality rate of 20% without treatment. Adrenal crisis can occur due to primary or secondary adrenal insufficiency and presents with low blood pressure. Hypoglycemia is most commonly caused by insulin therapy in diabetic patients but can occur in non-diabetics, defined as a blood glucose below 50-60 mg/dL.

1. Endocrine emergencies

2. Thyroid crisis Adrenal crisis Hypoglycemia

3. Thyroid crisis

4. Introduction Thyroid crisis or thyroid storm -> life threatening manifestations of thyroid hyperactivity. Hyperthyroidism , thyrotoxicosis ↑ thyroid hormone levels -> in blood. Graves’ disease, toxic multinodular goiter the most common cause -> 1 – 2 % thyroid storm With treatment 20% mortality rate

5. CAUSES OF THYROTOXICOSIS Graves’ disease (toxic diffuse goiter) Toxic multinodular goiter Toxic adenoma (single hot nodule) Factitious thyrotoxicosis Thyrotoxicosis associated with thyroiditis Hashimoto's thyroiditis Subacute (de Quervain's) thyroiditis Postpartum thyroiditis Sporadic thyroiditis Amiodarone thyroiditis Iodine-induced hyperthyroidism (areas of iodine deficiency) Amiodarone Radiocontrast media Metastatic follicular thyroid carcinoma hCG-mediated thyrotoxicosis Hydatidiform mole Metastatic choriocarcinoma Hyperemesis gravidarum TSH-producing pituitary tumors Struma ovarii

6. Pathophysiology ↑ catecholamine-binding sites ↑ response to adrenergic stimuli ↑ free T4 , T3 Stress precipitating thyroid storm Not sudden release of hormones

7. PRECIPITANTS OF THYROID STORM Medical Infection/sepsis Cerebral vascular accident Myocardial infarction Congestive heart failure Pulmonary embolism Visceral infarction Emotional stress Acute manic crisis

8. Trauma Thyroid surgery Nonthyroid surgery Blunt and penetrating trauma to the thyroid gland Vigorous palpation of the thyroid gland Burns

9. Endocrine Hypoglycemia Diabetic ketoacidosis Hyperosmolar nonketotic coma

10. Drug-Related Iodine-131 therapy Premature withdrawal of antithyroid therapy Ingestion of thyroid hormone Iodinated contrast agents Amiodarone therapy Iodine ingestion Anesthesia induction Miscellaneous drugs (chemotherapy, pseudoephedrine, organophosphates, aspirin)

11. Pregnancy-Related Toxemia of pregnancy Hyperemesis gravidarum Parturition and the immediate postpartum period

13. Diagnostic Strategies Best screening TSH definitive diagnosis T4 , T3

15. Differential Considerations sympathomimetic anticholinergic intoxication withdrawal syndrome ( fever & altered mental status ) heatstroke, neuroleptic malignant syndrome, serotonin syndrome, bacterial meningitis

16. Management Avoid precipitants - iodinated contrast media - amiodarone - NSAID - sympathomimetic ( salbutamol , ketamine )

18. After 1 h of PTU

19.  B non-selective &  conversion T4 to T3

22. Plasmapharesis or dialysis

25. Aggressive management resolve fever , tachycardia and alter mental status in 24 hs. Dispose :ICU Avoid interruption : reoccurrence and death

26. Acute Adrenal Insufficiency

27. Physiology BP

28. Acute Adrenal Insufficiency Primary ( adrenal gland ) Secondary ( pituitary or hypothalamus )

29. Pathophysiology

30. Pathophysiology

31. Clinical manifestation

32. Causes of 2 nd adrenal insufficiency A. HPA suppression with long term steroids B. Pituitary - infarction - hemorrhage - tumor - infiltrative disease e.g sarcoidosis C. Hypothalamic insufficiency D. Head trauma

33. Precipitants

34. Diagnosis Clinical ACTH stimulation test (adrenal response to exogenous ACTH)

35. Management Glucocorticoids replacement Correction of electrolytes, metabolic abnormalities & ↓ BP Treat precipitant

36. Glucocorticoids replacement Unconfirmed diagnosis - dexamethasone 4 mg iv q6 – 8 h Confirmed diagnosis - hydrocortisone 100 mg iv q6-8h

37. Supportive care ↓ BP : aggressive volume(NS+D5W) + steroid replacement ↓ glucose : iv glucose ( 50 – 100 ml of D50W) Electrolytes : - corrected with rehydration - treat ↑ K+

38. Find & Treat precipitant

39. Hypoglycemia

40. Introduction DM pt therapy -> hypoglycemia Most common cause of coma in DM pt . Non DM -> Diagnosis

41. Definition Symptomatic hypoglycemia ( 40 – 50 mg/dL ) ( 2.2 – 2.7 mmol/L ) DM 3.5 mmol/L Factors - rate of ↓ - age - size - gender - previous hypoglycemia

42. Response to hypoglycemia

45. Clinical featrues Symptoms Adrenergic tremor Palpitations anxiety/arousal Cholinergic Sweating hunger paresthesias autonomic

46. Clinical featrues Symptoms neuroglycopenic - cognitive impairment behavioral changes - seizure and coma

47. Clinical featrues Signs Diaphoresis Pallor Tachycardia Raised BP

48. Somogyi phenomenon Common with DM-I ↑ insulin dosage -> unrecognized hypoglycemic episode morning pt sleeping. rebound hyperglycemia pt awakens ↑ insulin dose

49. PRECIPITANTS OF HYPOGLYCEMIA IN DIABETIC PATIENTS Insulin Oral hypoglycemics Recent change of dose or type of insulin or oral hypoglycemic Sepsis Malnutrition Old age Worsening renal insufficiency Ethanol Factitious hypoglycemia Hepatic impairment Some antibacterial sulfonylureas Hyperthyroidism Hypothyroidism

50. Treatment of hypoglycemia in DM 1. Check serum glucose; obtain sample before treatment. If clinical suggestion of hypoglycemia is strong, proceed before laboratory results are available. 2. Correct serum glucose. If patient is awake and cooperative, administer sugar-containing food or beverage PO. If patient is unable to take PO: 25–75 g glucose as D 50 W (1–3 ampules) IV Children: 0.5–1 g/kg glucose as D 25 W IV (2–4 mL/kg) Neonates: 0.5–1 g/kg glucose (1–2 mL/kg) as D 10 W If unable to obtain IV access: 1–2 mg glucagon IM or SC ; may repeat q20min Children: 0.025–0.1 mg/kg SC or IM ; may repeat q20min

51. OHA induced hypoglycemia

52. Ann Emerg Med. 2008 Apr;51(4):400-6. Epub 2007 Aug 30. Comparison of octreotide and standard therapy versus standard therapy alone for the treatment of sulfonylurea-induced hypoglycemia . Fasano CJ , O'Malley G , Dominici P , Aguilera E , Latta DR . Department of Emergency Medicine, Albert Einstein Medical Center, Philadelphia, PA 19141, USA. fasanoc@einstein.edu Comment in: Ann Emerg Med. 2008 Jun;51(6):795-6; author reply 796-7. Abstract STUDY OBJECTIVE: This study is designed to test the hypothesis that the administration of octreotide acetate (Sandostatin; Novartis Pharmaceuticals) in addition to standard therapy will increase serum glucose level measured at serial intervals in patients presenting to the emergency department (ED) with sulfonylurea-induced hypoglycemia compared with standard therapy alone. METHODS: This study was a prospective, double-blind, placebo-controlled trial . All adult patients who presented to the ED with hypoglycemia (serum glucose level < or = 60 mg/dL) and were found to be taking a sulfonylurea or a combination of insulin and sulfonylurea were screened for participation in the study. Study participants were randomized to receive standard treatment (1 ampule of 50% dextrose intravenously and carbohydrates orally) and placebo (1 mL of 0.9% normal saline solution subcutaneously) or standard treatment plus 1 dose of octreotide 75 microg subcutaneously. Subsequent treatment interventions were at the discretion of the inpatient internal medicine service. RESULTS: A total of 40 patients (18 placebo; 22 octreotide) were enrolled. The mean serum glucose measurement at presentation was placebo 35 mg/dL and octreotide 39 mg/dL. The mean glucose values for octreotide patients compared with placebo were consistently higher during the first 8 hours but showed no difference in subsequent hours. Mean glucose differences approached statistical significance from 1 to 3 hours and were significant from 4 to 8 hours after octreotide or placebo administration. CONCLUSION : The addition of octreotide to standard therapy in hypoglycemic patients receiving treatment with a sulfonylurea increased serum glucose values for the first 8 hours after administration in our patients. Recurrent hypoglycemic episodes occurred less frequently in patients who received octreotide compared with those who received placebo. PMID: 17764782 [PubMed - indexed for MEDLINE]

53. Non- DM pt Whipple's triad 1- hypoglycemia symptoms 2- low blood glucose with the symptoms 3- symptoms relieved by glucose

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