Thyroid crisis

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

PhysiologyBP

Acute Adrenal Insufficiency

• Primary ( adrenal gland )

• Secondary ( pituitary or hypothalamus )

Pathophysiology

Pathophysiology

Clinical manifestation

Causes of 2nd 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

1. Glucocorticoids replacement 2. Correction of electrolytes, metabolic

abnormalities & ↓ BP3. 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 featruesSymptoms

• 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 D50W (1–3 ampules) IV Children: 0.5–1 g/kg glucose as D25W IV (2–4 mL/kg)

Neonates: 0.5–1 g/kg glucose (1–2 mL/kg) as D10W 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. [email protected] in :Ann Emerg Med. 2008 Jun;51(6):795-6; author reply 796-7 .

AbstractSTUDY 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