'lid lag is tested by having a patient look straight and placing an object in the midline of their vision slightly a bove the eye level.

 

'lid lag is tested by having a patient look straight and placing an

object in the midline of their vision slightly a bove the eye level.

Move the target down and ask patient to follow it with his or her

eyes. Observe the upper lid in relation to the iris during the movement. Lag is present if the lid does not fol low the iris immed iately

and white sclera is visible between the lid and the l imbus.

,,.·,change in deep tendon reflexes is described as Woltman sign.

This sign consists of brief u pstroke and slow relaxation.

the thyroid gland. Because of the negative feedback

mechanism by TH, low ISH will indicate hyperthyroid ­

ism, and high ISH will suggest primary hypothyroidism

(Table 68-2). If ISH is abnormal, free T4 level should be

ordered (FT4

). In special circumstances, for example, in

severely ill patients with high suspicion of thyroid dysfunction, it is appropriate to order ISH and FT 4 ± free T 3

at the same time.

It is not useful to order total T 3 or T 4 levels from the

emergency department (ED). Although only free TH is

clinically active, more than 99% of both T 3 and T 4 are

protein bound in the serum. Measuring the total level of

the hormones does not reliably provide information about

the clinical thyroid status.

Very frequently, the onset of thyroid storm or myxedema coma is triggered by non-thyroid-related illness,

CHAPTER 68

.A. Figure 68-1. Goiter.

such as infection, myocardial infarction, stroke, diabetic

ketoacidosis, etc. Other tests should be devoted to determining the etiology of the precipitating event.

Depending on the clinical presentation, those tests

include complete blood count, chemistry, cardiac

enzymes, electrocardiogram, urinalysis and blood, and

urine cultures.

� Imaging

Imaging studies ordered from the ED will be more useful

in identifying a precipitating event (for example, chest

Table 68-2. Changes in laboratory measurements

of TSH and free T4 (FT4) in thyroid disorders.

Thyroid Disorder TSH Level Free T 4 Level

Primary hyperthyroidism Low High

Primary hypothyroidism High Low

Secondary hyperthyroidism High High

Secondary hyperthyroidism Low Low

Primary disorders (intact hypothalamus and pitu itary function,

thyroid gland dysfunction) constitute a sign ificant majority of

cases. In those cases, low TSH and high FT 4 suggest thyrotoxicosis,

and high TSH and low FT 4 suggest hypothyroidism. In a small

percentage of cases, malfunction of pituitary gland affects the

downstream function of thyroid gland (secondary hyper-or hypo ­

thyroid). For example, pitu itary adenoma overprod ucing TSH will

result in high TSH levels and subsequently high FT 4 levels.

Panhypopitu itarism resulting from tumors, hemorrhage, or infiltrative disease wou ld cause low TSH and subsequently low FT 4.

x-ray) than in evaluation of thyroid dysfunction. Of note,

use of computed tomography with iodinated contrast

should be avoided whenever possible in patients with

thyrotoxicosis because administration of iodinated contrast may precipitate thyroid storm. In addition, iodinated contrast diminishes the effectiveness of nuclear

thyroid imaging that is used for both diagnostic and

treatment purposes. This effect persists for several weeks

after an iodine load.

MEDICAL DECISION MAKING

Differential diagnosis for patients presenting with severe

symptoms of thyrotoxicosis includes other life-threatening

conditions such as sepsis, pheochromocytoma, sympathomimetic overdose (cocaine or amphetamine), or

neuroleptic malignant syndrome. Similarly, patients in

myxedema coma may appear similar to patients in sepsis

or adrenal crisis. If the patient has a history of thyroid

problems, it should raise the index of suspicion for thyroid disorder. Of note, it is not uncommon for patients

with a history of treated hyperthyroidism ( eg, Graves

disease treated with thyroidectomy or radioactive iodine)

to present with symptoms of hypothyroidism at later

stages of the disease.

A diagnostic algorithm for patients with thyroid disease

is provided in Figure 68-2.

TREATMENT

Initial treatment of acutely ill patients with thyroid

storm is stabilization, airway protection in cases of

altered mental status, monitoring, IV fluids, and cooling

blankets. Further treatment targets de novo synthesis of

TH, release of TH, and adrenergic hyperactivity. There

are 2 main medications that block de novo synthesis of

TH: propythiouracil (PTU) and methimazole. Neither of

them can be administered IV; they need to be given

orally, through a nasogastric tube, or rectally. PTU also

has an added advantage of blocking the peripherial conversion of T4 to T3

• To block the release of stored TH,

iodine or lithium carbonate can be used, but should be

administered at least 1 hour after the initiation of blockade of de novo synthesis. Adrenergic blockers are used

for symptomatic treatment, propranolol being the medication of choice. Alternative medications include esmolol, and for patients with contraindications to

beta-blockers, guanethidine or reserpine. As a part of

supportive treatment, IV steroids are used (hydrocortisone or dexamethasone) and acetaminophen for fever. If

the patient presents in congestive heart failure, they may

need diuretics and digoxin for arrhythmia control.

Salicylates should not be used, because they increase the

free T4 level. As mentioned before, the precipitating

cause should be treated.

Outpatient treatment of hyperthyroid patients varies

with the cause and may include PTU or methimazole, pro-

THYROID EMERGENCIES

Clinical suspicion of

thyroid disease

• If uncompl icated thyroid

dysfunction, refer ± in itiate

treatment

• If elderly and evidence of endorgan insufficiency (eg, CHF),

admit

• If thyroid storm/myxedema coma,