Thyroid crisis

Grand Round

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
1.Glucocorticoids replacement
2.Correction of electrolytes, metabolic
abnormalities & ↓ BP
3.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. [email protected]
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