Endocrine Emergencies Flashcards
1
Q
endocrine emergencies
A
- Group of potentially life threatening conditions that are frequently over looked
- This results in delay in diagnosis and treatment
- This further contributes to already high mortality rates
- This discussion will highlight 5 of the most prevalent endocrine emergencies
2
Q
most prevalent edocrine emergencies
A
- Thyroid Storm
- Myxedema Coma - critical hyperthyroidism
- Diabetic Ketoacidosis
- Hyperosmolar Hyperglycemic State
- Adrenal Crisis
- Hyperosmolar and diabetic ketoacidosis are both types of hyperglycemia
3
Q
thyroid storm
A
- Hyperthyroidism or thyrotoxicosis refers to disorders that result from overproduction and release of hormone from the thyroid gland.
- This refers to any cause of excessive thyroid hormone.
- Malignant thyrotoxicosis or thyroid storm represents an extreme manifestation with resultant end-organ dysfunction.
- Grave’s disease (autoimmune hyperthyroidism is the most common cause of this)
- Thyrotoxicosis = overproduction or release of thyroid hormone. - hyperthy and thyrotox are the more benign types of too much thy
- End organ disease: this is where we see changes in the heart, etc.
- Graves disease is also MCC of hyperthyroidism
4
Q
thyroid storm description
A
- Malignant or critical thyrotoxicosis or thyroid storm is a life threatening medical emergency in which excessive concentrations of thyroid hormone produce organ dysfunction.
- It occurs in <10% of the patients hospitalized for hyperthyroidism.
- If untreated, there is an 80-90% mortality rate.
- Even with treatment the mortality rated exceeds 20%.
- Early recognition and management is critical.
5
Q
thyroid storm incidence
A
- Occurs in both men and women of any age
- More common in teenage or young adult woman
- Maybe initial manifestation of a thyroid condition
- Often precipitated by surgery, trauma, iodine ingestion or d/c of antithyroid medications
- Definitely from a thyroid perspective, women are more likely, but men still get them
6
Q
clinical manifestations of thyroid storm
A
- Marked hypermetabolism results in multiorgan dysfunction.
- Thermoregulatory dysfunction: high fever, warm moist skin, diaphoresis
- Neurologic manifestations: mental status change, seizure, coma, hyperreflexia, lid lag
- Cardiovascular dysregulation: atrial fibrillation, tachycardia, hypertension, CHF
- Respiratory distress: dyspnea, tachypnea
- Gastrointestinal Dysfunction: diarrhea, abdominal pain, nausea vomiting
- They feel hot and they are hot because they are constantly burning calories
- HYPERREFLEXIA
- Lid lag: people have the whites of their eye showing all the way around their iris
- Not necessarily diarrhea but they have VERY frequent bowel movements
7
Q
thyroid storm physical
A
- Eyes: Stare due to upper eyelid retraction and eyelid lag (both due sympathetic over-activity).
- Grave’s ophthalmopathy (periorbital edema, proptosis) is an autoimmune mediated inflammation and edema of extraocular muscles and intra-orbital connective tissue.
- Neck: Smooth, diffusely and symmetrical goiter. No palpable nodularity. Typically NTTP, may have bruit over a large vascular gland
- Cardiac: sinus tachycardia. Heart failure and arrhythmia (atrial fibrillation) more common in adults. High cardiac output produces bounding pulse, widened pulse pressure.
- Skin: Warm (cutaneous vasodilation) and moist (diaphoresis) Grave’s dermatopathology (bilateral non-pitting edema with associated thickening and induration of the skin) Typically seen over the ankles and feet. Rare in children
- Neuro: Altered mental status, hand tremor, agitation, psychosis, hyperreflexia
- Not everyone who has graves has a goiter
- Diffusely enlarged, smooth and symmetric – this is VERY indicative of Graves
- Paper test – will help someone tell if they have a hand tremor
8
Q
differential diagnosis for thyroid storm
A
- Endocrine: pheochromotcytoma
- Sepsis
- CNS infection
- Anticholinergic or adrenergic intoxication
- Acute psychiatric illness: Anxiety, panic attack
- Medication withdrawal: cocaine opiates
9
Q
biochemical abnormalities of thyroid storm
A
- TSH <0.01 with elevated Free T4 and T3 (because of increased T4 to T3 conversion the T3 elevation is typically more dramatic)
- Hypercalcemia (From osteoclast mediated bone remodeling)
- Elevated Alk phos (caused by bone remodeling)
- Hyperglycemia (secondary to enhanced glycogenolysis and increased catecholamines)
- Adrenal insufficiency (especially among Grave’s disease patients should be evaluated prior to the initiation of treatment)
10
Q
treatment of thyroid storm
A
- Supportive Care to minimize secondary effects of organ failure
- Respiratory and hemodynamic support and treatment of hyperthermia
- Antipyretics can be given but salicylates (eg. Aspirin) should be avoided as they are associated with displacement of thyroid hormone binding with TBG
- Identify and treat precipitating event if warranted
- You don’t want to give anything that will increase the amount of free hormone
- T3 is the more active hormone and T4 is the hormone more abundantly produced
- We want the conversion of T4 to T3 and block production of T4 and T3
- Most Critical (Thionamide) Block the release and effects of circulating thyroid hormone and inhibit peripheral conversion of T4 to T3.
- Propylthiouracil is preferred as it blocks the production and the peripheral conversion
- Loading dose 600-1000mg and 1200mg/d divided into dose Q4-5 hours
- Methimazole alternative but does not block T4 to T3 conversion
- Beta blockers can improve tachycardia and hypertension
- Propylthiouracil is preferred as it blocks the production and the peripheral conversion
- propranolol IV 1mg Q 10-15min
- Iodine therapy blocks the release of prestored hormone and decreases iodide transport and oxidation in follicular cells.
- Lugol solution can be given to stop thyroid hormone release.
- Thionamide therapy must be instituted first, and these drugs only given at least 1 h later.
- Lugol solution can be given three to four times to a total of 30–40 drops/day. Initial treatment may start with 8–10 drops. Lugol solution provides 8 mg iodide/drop.
11
Q
myxedema coma
A
- Uncommon presentation of Severe hypothyroidism
- Mortality rates exceeds 60%
- Better termed critical hypothyroidism as myxedema and coma are not diagnostic criteria or common at presentation
- Very rare because its easy to test for
- This would happen in pts in a care facility and the pt has some problem (i.e. stroke or heart attack) and they go to the hospital and the friend brings all the meds but doesn’t think about thyroid meds
12
Q
myxedema coma incidence
A
- Occurs most often in patients with long standing, pre existing hypothyroidism
- Hypothyroidism is 4 times more common in women than men and 80% of these cases occur in women.
- Almost always age > 60
- 300 cases reported in literature
- Most cases are during winter
13
Q
clinical manifestations of myxedema coma
A
- Can be precipitated by infections especially pneumonia or cardiac events or cerebral infarction
- Findings are similar to hypothyroidism but are more profound
- Hypothermia
- Hypotension
- Bradycardia
- Mental status depression
- May result in centrally mediated hypoventilation and hypercapnic respiratory failure
- Myxedema is generalized skin and soft tissue swelling, periorbital edema, ptosis, macroglossia and cool, dry skin.
14
Q
biochemical abnormalities of myxedema coma
A
- Clinical diagnosis confirmed with TFTs but do not wait for results to initiate treatment
- The degree of hypothyroidism does not distinguish hypothyroidism from myxedema coma the distinction is based on clinical findings
15
Q
treatment of myxedema coma
A
- Rapid replacement of thyroid hormone
- IV bolus of 300-500mcg followed by 50-100mcg daily depending on age and weight
- All patients need to be monitored continuously for hypertension and cardiac ischemia (Most common cause of death in these patients)
- Treatment of precipitating causes
- General supportive measures
- Ventilator support
- Passive external rewarming
- Correction of underlying electrolyte abnormalities