Thyroid crisis


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Thyroid crisis

  1. 1. Endocrine emergencies
  2. 2. <ul><li>Thyroid crisis </li></ul><ul><li>Adrenal crisis </li></ul><ul><li>Hypoglycemia </li></ul>
  3. 3. Thyroid crisis
  4. 4. Introduction <ul><li>Thyroid crisis or thyroid storm </li></ul><ul><li>-> life threatening manifestations of thyroid hyperactivity. </li></ul><ul><li>Hyperthyroidism , thyrotoxicosis </li></ul><ul><li>↑ thyroid hormone levels -> in blood. </li></ul><ul><li>Graves’ disease, toxic multinodular goiter the most common cause -> 1 – 2 % thyroid storm </li></ul><ul><li>With treatment 20% mortality rate </li></ul>
  5. 5. CAUSES OF THYROTOXICOSIS <ul><li>Graves’ disease (toxic diffuse goiter)    Toxic multinodular goiter    Toxic adenoma (single hot nodule)    Factitious thyrotoxicosis    Thyrotoxicosis associated with thyroiditis    </li></ul><ul><li>Hashimoto's thyroiditis    Subacute (de Quervain's) thyroiditis     Postpartum thyroiditis    Sporadic thyroiditis     Amiodarone thyroiditis    Iodine-induced hyperthyroidism (areas of iodine deficiency)    </li></ul><ul><li>Amiodarone     Radiocontrast media    Metastatic </li></ul><ul><li>follicular thyroid carcinoma    hCG-mediated thyrotoxicosis    Hydatidiform mole    Metastatic choriocarcinoma    Hyperemesis gravidarum    TSH-producing pituitary tumors    Struma ovarii </li></ul>
  6. 6. Pathophysiology <ul><li>↑ catecholamine-binding sites </li></ul><ul><li>↑ response to adrenergic stimuli </li></ul><ul><li>↑ free T4 , T3 </li></ul><ul><li>Stress precipitating thyroid storm </li></ul><ul><li>Not sudden release of hormones </li></ul>
  7. 7. PRECIPITANTS OF THYROID STORM <ul><li>Medical </li></ul><ul><li>   Infection/sepsis    Cerebral vascular accident    Myocardial infarction    Congestive heart failure    Pulmonary embolism    Visceral infarction    Emotional stress    Acute manic crisis </li></ul>
  8. 8. <ul><li>Trauma </li></ul><ul><li>   Thyroid surgery    Nonthyroid surgery    Blunt and penetrating trauma to the thyroid gland    Vigorous palpation of the thyroid gland    Burns </li></ul>
  9. 9. <ul><li>Endocrine </li></ul><ul><li>   Hypoglycemia    Diabetic ketoacidosis    Hyperosmolar nonketotic coma </li></ul>
  10. 10. <ul><li>Drug-Related </li></ul><ul><li>   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) </li></ul>
  11. 11. <ul><li>Pregnancy-Related </li></ul><ul><li>   Toxemia of pregnancy    Hyperemesis gravidarum    Parturition and the immediate postpartum period </li></ul>
  12. 13. Diagnostic Strategies <ul><li>Best screening TSH </li></ul><ul><li>definitive diagnosis T4 , T3 </li></ul>
  13. 15. Differential Considerations <ul><li>sympathomimetic </li></ul><ul><li>anticholinergic intoxication </li></ul><ul><li>withdrawal syndrome </li></ul><ul><li>( fever & altered mental status ) </li></ul><ul><li>heatstroke, neuroleptic malignant syndrome, serotonin syndrome, bacterial meningitis </li></ul>
  14. 16. Management <ul><li>Avoid precipitants </li></ul><ul><li>- iodinated contrast media </li></ul><ul><li>- amiodarone </li></ul><ul><li>- NSAID </li></ul><ul><li>- sympathomimetic ( salbutamol , ketamine ) </li></ul>
  15. 18. After 1 h of PTU
  16. 19.  B non-selective &  conversion T4 to T3
  17. 22. Plasmapharesis or dialysis
  18. 25. <ul><li>Aggressive management resolve fever , tachycardia and alter mental status in 24 hs. </li></ul><ul><li>Dispose :ICU </li></ul><ul><li>Avoid interruption : reoccurrence and death </li></ul>
  19. 26. Acute Adrenal Insufficiency
  20. 27. Physiology BP
  21. 28. Acute Adrenal Insufficiency <ul><li>Primary ( adrenal gland ) </li></ul><ul><li>Secondary ( pituitary or hypothalamus ) </li></ul>
  22. 29. Pathophysiology
  23. 30. Pathophysiology
  24. 31. Clinical manifestation
  25. 32. Causes of 2 nd adrenal insufficiency <ul><li>A. HPA suppression with long term steroids </li></ul><ul><li>B. Pituitary - infarction </li></ul><ul><li>- hemorrhage </li></ul><ul><li>- tumor </li></ul><ul><li>- infiltrative disease e.g sarcoidosis </li></ul><ul><li>C. Hypothalamic insufficiency </li></ul><ul><li>D. Head trauma </li></ul>
  26. 33. Precipitants
  27. 34. Diagnosis <ul><li>Clinical </li></ul><ul><li>ACTH stimulation test (adrenal response to exogenous ACTH) </li></ul>
  28. 35. Management <ul><li>Glucocorticoids replacement </li></ul><ul><li>Correction of electrolytes, metabolic abnormalities & ↓ BP </li></ul><ul><li>Treat precipitant </li></ul>
  29. 36. Glucocorticoids replacement <ul><li>Unconfirmed diagnosis </li></ul><ul><li>- dexamethasone 4 mg iv q6 – 8 h </li></ul><ul><li>Confirmed diagnosis </li></ul><ul><li>- hydrocortisone 100 mg iv q6-8h </li></ul>
  30. 37. Supportive care <ul><li>↓ BP : </li></ul><ul><li>aggressive volume(NS+D5W) + steroid replacement </li></ul><ul><li>↓ glucose : </li></ul><ul><li>iv glucose ( 50 – 100 ml of D50W) </li></ul><ul><li>Electrolytes : </li></ul><ul><li>- corrected with rehydration </li></ul><ul><li>- treat ↑ K+ </li></ul>
  31. 38. Find & Treat precipitant
  32. 39. Hypoglycemia
  33. 40. Introduction <ul><li>DM pt therapy -> hypoglycemia </li></ul><ul><li>Most common cause of coma in DM pt . </li></ul><ul><li>Non DM -> Diagnosis </li></ul>
  34. 41. Definition <ul><li>Symptomatic hypoglycemia </li></ul><ul><li>( 40 – 50 mg/dL ) ( 2.2 – 2.7 mmol/L ) </li></ul><ul><li>DM 3.5 mmol/L </li></ul><ul><li>Factors </li></ul><ul><li>- rate of ↓ </li></ul><ul><li>- age </li></ul><ul><li>- size </li></ul><ul><li>- gender </li></ul><ul><li>- previous hypoglycemia </li></ul>
  35. 42. Response to hypoglycemia
  36. 45. Clinical featrues Symptoms <ul><li>Adrenergic </li></ul><ul><li>tremor </li></ul><ul><li>Palpitations </li></ul><ul><li>anxiety/arousal </li></ul><ul><li>Cholinergic </li></ul><ul><li>Sweating </li></ul><ul><li>hunger </li></ul><ul><li>paresthesias </li></ul>autonomic
  37. 46. Clinical featrues <ul><li>Symptoms </li></ul><ul><li>neuroglycopenic </li></ul><ul><li>- cognitive impairment </li></ul><ul><li>behavioral changes </li></ul><ul><li>- seizure and coma </li></ul>
  38. 47. Clinical featrues <ul><li>Signs </li></ul><ul><li>Diaphoresis </li></ul><ul><li>Pallor </li></ul><ul><li>Tachycardia </li></ul><ul><li>Raised BP </li></ul>
  39. 48. Somogyi phenomenon <ul><li>Common with DM-I </li></ul><ul><li>↑ insulin dosage -> unrecognized hypoglycemic episode morning pt sleeping. </li></ul><ul><li>rebound hyperglycemia pt awakens </li></ul><ul><li>↑ insulin dose </li></ul>
  40. 49. PRECIPITANTS OF HYPOGLYCEMIA IN DIABETIC PATIENTS <ul><li>Insulin </li></ul><ul><li>  Oral hypoglycemics </li></ul><ul><li>Recent change of dose or type of insulin or oral hypoglycemic </li></ul><ul><li>   Sepsis </li></ul><ul><li>  Malnutrition </li></ul><ul><li>  Old age </li></ul><ul><li>Worsening renal insufficiency </li></ul><ul><li>Ethanol </li></ul><ul><li>Factitious hypoglycemia </li></ul><ul><li>Hepatic impairment </li></ul><ul><li>Some antibacterial sulfonylureas </li></ul><ul><li>  Hyperthyroidism </li></ul><ul><li>Hypothyroidism    </li></ul>
  41. 50. Treatment of hypoglycemia in DM <ul><li>1.      Check serum glucose; obtain sample before treatment.    If clinical suggestion of hypoglycemia is strong, proceed before laboratory results are available. </li></ul><ul><li>  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 </li></ul>
  42. 51. OHA induced hypoglycemia
  43. 52. <ul><li>Ann Emerg Med. 2008 Apr;51(4):400-6. Epub 2007 Aug 30. </li></ul><ul><li>Comparison of octreotide and standard therapy versus standard therapy alone for the treatment of sulfonylurea-induced hypoglycemia . </li></ul><ul><li>Fasano CJ , O'Malley G , Dominici P , Aguilera E , Latta DR . </li></ul><ul><li>Department of Emergency Medicine, Albert Einstein Medical Center, Philadelphia, PA 19141, USA. </li></ul><ul><li>Comment in: </li></ul><ul><li>Ann Emerg Med. 2008 Jun;51(6):795-6; author reply 796-7. </li></ul><ul><li>Abstract </li></ul><ul><li>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. </li></ul><ul><li>PMID: 17764782 [PubMed - indexed for MEDLINE] </li></ul>
  44. 53. Non- DM pt <ul><li>Whipple's triad  </li></ul><ul><li>1- hypoglycemia symptoms </li></ul><ul><li>2- low blood glucose with the symptoms </li></ul><ul><li>3- symptoms relieved by glucose </li></ul>
  45. 54. Thank you