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Thyroid crisis
 

Thyroid crisis

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    Thyroid crisis Thyroid crisis Presentation Transcript

    • Endocrine emergencies
      • Thyroid crisis
      • Adrenal crisis
      • Hypoglycemia
    • Thyroid crisis
    • 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
    • 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
    • Pathophysiology
      • ↑ catecholamine-binding sites
      • ↑ response to adrenergic stimuli
      • ↑ free T4 , T3
      • Stress precipitating thyroid storm
      • Not sudden release of hormones
    • PRECIPITANTS OF THYROID STORM
      • Medical
      •    Infection/sepsis    Cerebral vascular accident    Myocardial infarction    Congestive heart failure    Pulmonary embolism    Visceral infarction    Emotional stress    Acute manic crisis
      • Trauma
      •    Thyroid surgery    Nonthyroid surgery    Blunt and penetrating trauma to the thyroid gland    Vigorous palpation of the thyroid gland    Burns
      • Endocrine
      •    Hypoglycemia    Diabetic ketoacidosis    Hyperosmolar nonketotic coma
      • 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)
      • Pregnancy-Related
      •    Toxemia of pregnancy    Hyperemesis gravidarum    Parturition and the immediate postpartum period
    •  
    • Diagnostic Strategies
      • Best screening TSH
      • definitive diagnosis T4 , T3
    •  
    • Differential Considerations
      • sympathomimetic
      • anticholinergic intoxication
      • withdrawal syndrome
      • ( fever & altered mental status )
      • heatstroke, neuroleptic malignant syndrome, serotonin syndrome, bacterial meningitis
    • Management
      • Avoid precipitants
      • - iodinated contrast media
      • - amiodarone
      • - NSAID
      • - sympathomimetic ( salbutamol , ketamine )
    •  
    • After 1 h of PTU
    •  B non-selective &  conversion T4 to T3
    •  
    •  
    • Plasmapharesis or dialysis
    •  
    •  
      • Aggressive management resolve fever , tachycardia and alter mental status in 24 hs.
      • Dispose :ICU
      • Avoid interruption : reoccurrence and death
    • Acute Adrenal Insufficiency
    • Physiology BP
    • Acute Adrenal Insufficiency
      • Primary ( adrenal gland )
      • Secondary ( pituitary or hypothalamus )
    • Pathophysiology
    • Pathophysiology
    • Clinical manifestation
    • 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
    • Precipitants
    • Diagnosis
      • Clinical
      • ACTH stimulation test (adrenal response to exogenous ACTH)
    • Management
      • Glucocorticoids replacement
      • Correction of electrolytes, metabolic abnormalities & ↓ BP
      • Treat precipitant
    • Glucocorticoids replacement
      • Unconfirmed diagnosis
      • - dexamethasone 4 mg iv q6 – 8 h
      • Confirmed diagnosis
      • - hydrocortisone 100 mg iv q6-8h
    • Supportive care
      • ↓ BP :
      • aggressive volume(NS+D5W) + steroid replacement
      • ↓ glucose :
      • iv glucose ( 50 – 100 ml of D50W)
      • Electrolytes :
      • - corrected with rehydration
      • - treat ↑ K+
    • Find & Treat precipitant
    • Hypoglycemia
    • Introduction
      • DM pt therapy -> hypoglycemia
      • Most common cause of coma in DM pt .
      • Non DM -> Diagnosis
    • 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
    • Response to hypoglycemia
    •  
    •  
    • Clinical featrues Symptoms
      • Adrenergic
      • tremor
      • Palpitations
      • anxiety/arousal
      • Cholinergic
      • Sweating
      • hunger
      • paresthesias
      autonomic
    • Clinical featrues
      • Symptoms
      • neuroglycopenic
      • - cognitive impairment
      • behavioral changes
      • - seizure and coma
    • Clinical featrues
      • Signs
      • Diaphoresis
      • Pallor
      • Tachycardia
      • Raised BP
    • Somogyi phenomenon
      • Common with DM-I
      • ↑ insulin dosage -> unrecognized hypoglycemic episode morning pt sleeping.
      • rebound hyperglycemia pt awakens
      • ↑ insulin dose
    • 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   
    • 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
    • OHA induced hypoglycemia
      • 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]
    • Non- DM pt
      • Whipple's triad 
      • 1- hypoglycemia symptoms
      • 2- low blood glucose with the symptoms
      • 3- symptoms relieved by glucose
    • Thank you