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Thyroid crisis

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Grand Round

Grand Round

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  • 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
  • 12.  
  • 13. Diagnostic Strategies
    • Best screening TSH
    • definitive diagnosis T4 , T3
  • 14.  
  • 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 )
  • 17.  
  • 18. After 1 h of PTU
  • 19.  B non-selective &  conversion T4 to T3
  • 20.  
  • 21.  
  • 22. Plasmapharesis or dialysis
  • 23.  
  • 24.  
  • 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
  • 43.  
  • 44.  
  • 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
  • 54. Thank you

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