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may demonstrate a spectrum from peaked T waves, PR and QRS prolongation, loss of P-wave and T-wave flattening, and finally a sine wave. Hypocalcemia causes a prolonged QT

 


CHAPTER 70

hypocalcemia. These electrolyte and metabolic disturbances

can progress to clinical toxic effects, including renal insufficiency, cardiac arrhythmias, seizures, and death due to organ

failure. It is most common in cancers with high cell turnover

(leukemia and lymphoma).

One of the most common hematologic emergencies is

neutropenic fever, which is the presence of a fever >38°C

with an absolute neutrophil count of <500/!lL. Febrile neutropenia is a result of bone marrow suppression, a common

side effect of chemotherapy. Patients with neutropenia are

susceptible to life-threatening bacterial infections. Older

age has been shown to be an independent risk factor for the

development of neutropenia and febrile neutropenia. A history of previous chemotherapy-induced neutropenia predicts recurrent neutropenia and neutropenic fever.

CLINICAL PRESENTATION

..... History

Pain is the presenting symptom of spinal cord compression

in 90-95% of patients. The pain is usually constant and

close to the site of the lesion. Patients complain of a band

or girdle of pain/tightness radiating from back to front,

exacerbated by recumbency, movement, coughing and

sneezing. Symptoms may include numbness and tingling,

which usually precedes weakness. Weakness often presents

with "stiffness," dragging of a limb, or unsteadiness.

Facial edema is the most common symptom of SVC

syndrome with patients often describing feeling bloated.

Other symptoms include dyspnea, cough, chest and shoulder pain, and hoarseness. Dyspnea may be worse when

leaning forward or lying down. Arm swelling and lymphedema are other common symptoms of SVC syndrome.

In both acute and chronic hypercalcemia of malignancy, the major manifestations affect gastrointestinal,

renal, and neuromuscular function. Patients with acute

hypercalcemia commonly present with anorexia, nausea,

vomiting, polyuria, polydipsia, dehydration, weakness, and

confusion. Patients with tumor lysis syndrome may have

similar symptoms often related to acute renal failure.

Neutropenic patients, usually on chemotherapy, often

present to the ED with fever and no clear source of infection. Tachycardia and hypotension may accompany fever

and may indicate severe sepsis or septic shock. Weakness

and dehydration are usually present.

..... Physical Examination

Patients with cancer who present to the ED require a thorough physical examination to identify potential life threats

associated with malignancy. Vital signs and general assessment including mental status will often reveal whether an

acute medical emergency such as neutropenic sepsis or

arrhythmia exists. A thorough head-to-toe examination

should follow. Head, eyes, ears, nose, and throat examination should assess for a patent airway, oropharyngeal

infection, facial plethora, and cranial neuropathies. Neck

examination should assess for cervical spine tenderness and

dilated neck veins. Cardiovascular and respiratory exams

should assess breath sounds and cardiac rhythm. Decreased

breath sounds or distant heart sounds may indicate pleural

or pericardia! effusions. Abdominal exam should assess for

masses and possible source of occult infection. Back exam

should assess for any localized tenderness or masses, and

neurologic exam should identify any focal neurologic deficits. Extremities and skin should be assessed for hydration

status and edema, possibly related to acute renal failure.

DIAGNOSTIC STUDIES

..... Electrocardiogram

An electrocardiogram should be performed in all patients

with suspected electrolyte abnormalities. Patients with hypercalcemia may have a shortened QT interval due to the

increased rate of cardiac repolarization. Arrhythmias such as

bradycardia and first -degree atrioventricular b lock may occur.

Tumor lysis syndrome may result in multiple electrolyte

abnormalities that may manifest as arrhythmias. Hyperkalemia

may demonstrate a spectrum from peaked T waves, PR and

QRS prolongation, loss of P-wave and T-wave flattening, and

finally a sine wave. Hypocalcemia causes a prolonged QT

and may result in ventricular arrhythmias.

..... Laboratory

Serum basic metabolic panel (BMP) with calcium, magne ­

sium, and phosphorous should be assessed on all patients

with vague complaints, vomiting, or dehydration. BMP

should also be ordered for those at risk for hypercalcemia

(bony metastasis) and tumor lysis syndrome (recent cancer

treatment). Patients with tumor lysis syndrome present

with acute renal failure in the presence of hyperuricemia

(> 15 mg/dL), hyperphosphatemia (>8 mg/dL), hyperkale ­

mia, and hypocalcemia. A complete blood count should be

obtained on all patients to assess for neutropenia (absolute

neutrophil count <500/!lL), anemia, and thrombocytopenia. The absolute neutrophil count is determined by mul ­

tiplying the total white blood cell count times the

percentage of neutrophils plus bands. Multiple sets of

blood cultures and a urine culture should be collected in

all febrile neutropenic patients in the ED.

..... Imaging

Patients with signs or symptoms suggestive of spinal cord

metastasis should have their spine imaged. Plain radiographs may identify bony metastasis or pathologic fractures

but are not sufficiently sensitive to rule out the presence of

spinal disease. Computed tomography ( CT) scan of the

spine is more sensitive than plain films; however, magnetic

resonance imaging of the spine is the test of choice to

assess for spinal metastasis and cord involvement. Similarly,

chest radiograph may be used as an initial test for patients

with suspected SVC syndrome, but CT chest with contrast

is the test of choice for identification.

ONCOLOGIC EMERGENCIES

MEDICAL DECISION MAKING

Identification of common emergencies associated with

malignant disease is key to the expeditious ED care of the

cancer patient. Patients with acute shortness of breath

should be assessed for malignant pleural or pericardia! effusions or pulmonary embolus. Generalized weakness may be

from dehydration, electrolyte abnormalities associated with

tumor lysis syndrome or renal failure, or an occult infection

owing to immunosuppression from chemotherapy. Brain

or spinal cord metastasis should be considered for any focal

neurologic sign or symptom, and appropriate imaging

should be performed in the ED (Figure 70-1).

TREATMENT

For patients with acute spinal cord compression from spinal

metastasis, IV corticosteroids relieve pain, reduce edema,

and may improve neurologic function. They may also ternporarily prevent the onset of cord ischemia. Radiation

therapy provides more definitive treatment in most patients.

Indications for radiation therapy include known radiosensitive tumor with no spinal instability and palliative therapy

in patients who present with paraplegia.

SVC syndrome is treated in the ED with IV steroids

(dexamethasone 10 mg IV) and furosemide IV in an

attempt to reduce venous pressures. Patients with cardiac

or respiratory compromise or central nervous system

dysfunction may require emergent endotracheal intubation or radiation therapy. Vascular surgery should be consulted for possible SVC stenting.

Hypercalcemia is treated in the ED with IV fluid

administration. Levels > 13 mg/ dL usually require

treatment. An initial bolus of 1-2 L of normal saline (NS)

aware of the common complications associated with malignancies and available treatments. These complications can be broadly divided into those created by local tumor effects, complications from hematologic derange ­

 


Tintinalli's Emergency Medicine: A Comprehensive Study

Guide. 7th ed. New York, NY: McGraw-Hill, 20 l l,pp. l453-1456.

Peacy SR, Guo CY, Robinson AM, et al. Glucocorticoid replace ­

ment therapy: are patients over treated and does it matter? Clin

Endocrinol (Oxf). 1 997;46:255.

Stewart PM, Krone NP. The adrenal cortex. In: Kronnenberg H,

Melmed S, Polonsky K, Larson PR, eds. Williams Textbook

of Endocrinology. 1 2th ed. Philadelphia, PA: Saunders

Elsevier, 20 11, Pages 479-544.

Oncologic Emergencies

Biswadev Mitra, MD

Key Points

• Spinal cord compression should be considered in any

patient presenting to the emergency department with a

neurologic complaint and a history of malignancy.

• Electrolyte abnormal ities should be considered in all

patients with malignancy and nonspecific symptoms.

INTRODUCTION

Improvements in the management of cancer have lead to

an aging population presenting to emergency departments

(EDs) with complications related to malignant disease.

Oncologic emergencies occur in patients with recurrence

of a previously diagnosed malignancy, complications of

cancer treatment, or signs and symptoms that may lead to

a new diagnosis of cancer. Emergency clinicians must be

aware of the common complications associated with

malignancies and available treatments. These complications can be broadly divided into those created by local

tumor effects, complications from hematologic derange ­

ments and biochemical abnormalities, and complications

related to cancer treatment. When caring for patients with

oncologic related emergencies in the ED, consideration

should always be given to the nature of medical therapy

warranted in view of progression of the disease. Early

consultation with family members and stakeholders is

advised.

Emergencies related to local tumor invasion include

spinal cord compression and superior vena cava (SVC)

syndrome. Both are oncologic emergencies that require

prompt intervention. The most common primary tumors

that metastasize to the spine are lung (29%), prostate (19%),

and breast (13%). The thoracic spine is the most common

site involved (77%). The lumbar spine is affected 29% of

• Patients undergoing chemotherapy who present with

fever should be considered neutropenic until proven

otherwise.

the time with the cervical ( 12%) and sacral (7%) regions

being affected least often.

SVC syndrome is defined as obstruction of flow through

the superior vena cava due to tumor-related compression.

Lung cancer and non-Hodgkin lymphoma together cause

about 95% of cancer-related SVC syndrome. The incidence

of SVC syndrome in patients with lung cancer and nonHodgkin lymphoma is 2-4%. Thrombosis related to central

venous catheters can also cause SVC syndrome in patients

with cancer as a result of their prothrombotic state.

Emergencies related to biochemical derangements in

the cancer patient include hypercalcemia and tumor lysis

syndrome. Hypercalcemia has been reported to occur in

20-30% of patients with cancer at some time during the

course of their disease. It occurs most commonly in cancers associated with bone (multiple myeloma), bony

metastasis (breast, lung, prostate, renal), or cancers that

secrete parathyroid-like substance (lung) or osteoclastic

factors (lymphomas). The detection of hypercalcemia in a

patient with cancer signifies a very poor prognosis, with

death often occurring within months.

Tumor lysis syndrome is the most common diseaserelated emergency encountered in patients with hematologic

cancers. The syndrome occurs when tumor cells release their

contents into the bloodstream, either spontaneously or in

response to therapy, leading to the characteristic findings of

hyperuricemia, hyperkalemia, hyperphosphatemia, and

295

metabolic alkalosis is present in some patients with increased ACTH production. A random serum cortisol is not useful due to wide diurnal ranges.

 



In Cushing syndrome, hyperglycemia is commonly

present and is due to insulin resistance. Hypokalemic

metabolic alkalosis is present in some patients with

increased ACTH production. A random serum cortisol is

not useful due to wide diurnal ranges.

The rapid ACTH stimulation test is infrequently

performed in the ED, but may be used to test the

responsiveness of the adrenal glands. A baseline sample

of blood is drawn at time 0 for a cortisol level, then

0.25 mg of cosyntropin (synthetic ACTH) is given

intravenously (IV). Plasma cortisol levels are checked at

30 minutes and 1 hour. Dexamethasone should be given

empirically even without waiting for the results. In normal subjects, baseline cortisol (time 0) levels exceed 5

mcg/dL. Post-rapid ACTH stimulation test, plasma cortisol levels should rise at least? meg/ dL and peak at > 18

mcg/dL, which marks a normal response and rules out

primary disorders of the adrenal glands. Subsequent

measurement of the plasma ACTH level determines

whether adrenal insufficiency is primary (Addison disease) or secondary. Elevated ACTH levels indicate primary adrenal insufficiency, whereas normal or low levels

indicate secondary adrenal insufficiency.

� Imaging

Imaging studies are not routinely indicated in

adrenal insufficiency or Cushing syndrome. Chest x-ray,

electrocardiogram, or head computed tomography may

be useful depending on the clinical presentation (ie,

altered mental status, suspected pneumonia or cardiac

ischemia) .

MEDICAL DECISION MAKING

The differential diagnoses for adrenal insufficiency

include shock (cardiovascular, septic), dehydration, or

influenza infection. Consider adrenal crisis in any patient

who presents in shock, especially if they have a history of

adrenal insufficiency, withdrawal of chronic steroids,

characteristic electrolyte abnormalities (low Na, high K),

or hypoglycemia (Figure 69- 1). Acute adrenal insufficiency is usually precipitated by an underlying illness

(eg, sepsis), and it is important for the clinician to identify and treat both disorders. Polycystic ovary disease,

depression, diabetes mellitus, and hypothyroidism are

the most common differential diagnoses for Cushing

syndrome.

TREATMENT

IV 0.9 NS should be given to treat hypotension. Persistent

hypotension may require vasopressors. Dextrose is administered in the setting of hypoglycemia. An ampule of D50

is given initially and is repeated as needed. Dexamethasone

4-6 mg IV is given every 6 hours or hydrocortisone 1 00 mg

IV every 8 hours. Dexamethasone is preferred because,

unlike hydrocortisone, it does not interfere with cortisol

response to ACTH or the cortisol assay. If hydrocortisone

is given, results of the ACTH ( cosyntropin) stimulation

test will be difficult to interpret. Mineralocorticoids in the

form of fludrocortisone acetate (Florine£) 0.05-0.2 mg are

administered. Search and treat precipitating causes ( eg,

sepsis).

It is not the role of the emergency physician to make the

definitive diagnosis of Cushing syndrome but to suspect

the condition, treat the underlying cause, and refer the

patient for further testing or treatment.

CHAPTER 69

Suspect adrenal insufficiency

(history & exam)

Acute adrenal i nsufficiency

(adrenal crisis)

Emergent resuscitation and

administration of

glucocorticoids

Admission to ICU

Chronic ill ness (eg, fatigue,

hyperpigmentation, weight loss)

with normal vital signs and

electrolytes and glucose

Chron ic adrenal insufficiency

(primary or secondary adrenal

insufficiency)

If patient appears well,

discharge with fol low-up for

outpatient work-up

• Figure 69-1. Adrenal emergencies diag nostic algorithm. AMS, altered

mental status; ICU, intensive care unit.

DISPOSITION

� Admission

All patients with acute adrenal insufficiency require

hospital admission. Most patients will require an intensive

care unit setting.

� Discharge

Patients with chronic symptoms of either adrenal insufficiency or Cushing syndrome may be discharged with

close follow-up with a primary physician and

endocrinologist.

SUGGESTED READING

Idrose AM. Adrenal insufficiency and adrenal crisis. In: Tintinalli JE,

Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD.

Prolonged steroid administration is a risk factor for exogenous Cushing syndrome. Endogenous (Cushing disease) is more common in women aged 20-40 and in the

 



 Risk factors for primary adrenal insufficiency

include human immunodeficiency virus (HN) infection,

metastatic cancer (lung, breast, leukemia), infection (bac ­

terial, fungal, viral, tuberculosis), sarcoidosis, or sepsis.

HIV infection results in adrenal insufficiency at a much

higher rate than in the general population. Up to 25o/o of

patients with HIV have inadequate adrenal reserves.

Contributing factors in HIV patients include the human

immunodeficiency virus itself, opportunistic infections,

and medications.

Secondary adrenal insufficiency is due to inadequate

production of ACTH from the pituitary gland. Cortisol

production is decreased; however, aldosterone secretion is

usually intact because its production is stimulated to a

• Adrenal crisis should be considered in the presence of

refractory hypotension.

• The preferred steroid for adrenal insufficiency is

dexamethasone because it does not interfere with the

cosyntropin stimulation test.

much greater extent by angiotensin. Suppression of the

hypothalamic-pituitary-adrenal axis by exogenous steroid

administration is the most common cause of adrenal

insufficiency. It is based on the dose and duration of

treatment. Administrations of steroids for <2 weeks or doses

<5 mg per day are unlikely to result in adrenal insufficiency.

Steroid administration (withdrawal), pituitary tumors, and

trauma place patients at risk for secondary adrenal

insufficiency.

Acute adrenal insufficiency (Addison or adrenal crisis)

is an emergent condition that occurs in a person who has

underlying adrenal suppression who undergoes an acute

stress or illness. Some patients have a history of chronic

adrenal insufficiency; for others, adrenal crisis is the initial

presentation.

Cushing syndrome refers to a situation in which there

is a symptomatic excess of glucocorticoids. Prolonged

exogenous administration of steroids is the most c ommon

cause of Cushing syndrome. Cushing disease is present

when Cushing syndrome is due to excessive ACTH

secretion from the pituitary gland. Endogenous Cushing

syndrome (Cushing disease) is much less common and

occurs in 13 per 1 million persons.

In addition to exogenous steroid administration,

Cushing syndrome is due to an ACTH-producing tumor

of the pituitary gland (70%), adrenal gland (15%), or

other (15%). Other tumors producing ACTH include

292

ADRENAL EMERGENCIES

pancreatic cancer, small-cell lung carcinoma, and carcinoid tumors.

Prolonged steroid administration is a risk factor for

exogenous Cushing syndrome. Endogenous (Cushing

disease) is more common in women aged 20-40 and in the

presence of malignancy (lung, pancreatic).

CLINICAL PRESENTATION

� History

Patients with adrenal insufficiency r eport complaints of

fatigue, nausea, vomiting, abdominal pain, lighthead ­

edness, or diarrhea, whereas those with Cushing syndrome report fatigue, weakness, and menstrual

irregularities.

� Physical Examination

Patients with primary adrenal insufficiency will present

with hyperpigmentation of the skin due to increased levels

of circulating ACTH. This finding is present in 98% of

these patients. Acute adrenal insufficiency is characterized

by mental status changes, hypotension, and tachycardia.

Hypothermia may be present, but fever can be seen in the

setting of concurrent infection.

Physical findings in Cushing syndrome may include

truncal obesity, moon facies, buffalo hump, hirsutism, and

skin striae. Hypertension is a common finding.

DIAGNOSTIC STUDIES

� Laboratory

Laboratory studies in patients with suspected adrenal

insufficiency or Cushing syndrome should include complete

blood count, electrolytes with glucose, cortisol, and ACTH

level. In primary adrenal insufficiency, hyponatremia is

present in 90% of patients, hyperkalemia in 64%, and

hypercalcemia in 6-33%. In secondary adrenal insufficiency,

electrolyte abnormalities are less likely because aldosterone

production is not impaired. Anemia is present in 40% of

patients, and an elevated white blood cell count suggests

infection. Hypoglycemia is present in two thirds of patients.

A random serum cortisol level <15 mcg/dL in an

acutely ill patient is diagnostic of adrenal insufficiency in

most cases and can be performed in the emergency department (ED). An ACTH level can be drawn, but results are

rarely available in the ED.

CHF, congestive heart failure; ICU, intensive care unit; T 4, thyroxine; TSH, thyroid-stimu lating hormone. pranolol, radioactive iodine, subtotal thyroidectomy, and

 


treat and admit to ICU

Figure 68-2. Thyroid emergencies diag nostic algorithm.

CHF, congestive heart failure; ICU, intensive care unit; T 4,

thyroxine; TSH, thyroid-stimu lating hormone.

pranolol, radioactive iodine, subtotal thyroidectomy, and

occasionally steroids.

Prompt initiation of supportive treatment for patients

presenting in myxedema coma is very important and

includes IV fluids, passive rewarming, and possibly pressors and mechanical ventilation. TH should be replaced by

IV administration of T4 (levothyroxine) or free T3 (liothyronine or triiodothyronine). In severe myxedema coma,

T 3 should be given, either combined with T 4 or alone

(caution is necessary in patients with myocardial compromise). Administration of IV steroids is routinely recom ­

mended. A baseline cortisol level before initiating steroid

therapy should be obtained.

Uncomplicated hypothyroid patients can be treated

with oral replacement therapy using levothyroxine.

DISPOSITION

� Admission

Admit patients with concomitant illness such as CHF or

dysrhythmia. An ICU setting is indicated for patients with

thyroid storm or myxedema coma.

� Discharge

Discharge patients with uncomplicated thyrotoxicosis or

hypothyroidism, with proper instructions, timely referral,

and the initiation of treatment.

SUGGESTED READING

American Thyroid Association. Professional Guidelines. http:/ I

thyroidguidelines.net/

Idrose AM. Thyroid disorders: Hypothyroidism and myxedema

crisis. In: Tintinalli JE et al., Tintinalli's Emergency Medicine: A

Comprehensive Study Guide. 7th ed. New York, NY: McGrawflill, 201l, pp. 1 444-1447.

Idrose AM. Thyroid disorders: Hyperthyroidism and thyroid

storm. In: Tintinalli JE et al., Tintinalli's Emergency Medicine:

A Comprehensive Study Guide. 7th ed. New York, NY:

McGraw-fUll, 201 1, pp. 1447-1453.

McKeown NJ, Tews MC, et al. Hyperthyroidism. Emerg Med Clin

North Am. 2005;23:669.

Pimentel L, Hansen K. Thyroid disease in the emergency department: A clinical and laboratory review.! Emerg Med. 2005;28:20 1.

Tews MC, Shah SM, et al. Hypothyroidism: Mimicker of com ­

mon complaints. Emerg Med Clin North Am. 2005;23:649.

Adrenal Emergencies

lsam F. Nasr, MD

Key Points

• Adrenal crisis is a medical emergency and must be

recognized and treated promptly.

• Admin istration of steroids, saline, and vasopressors (as

needed) should be instituted when adrenal crisis is

suspected.

INTRODUCTION

Cortisol secretion is regulated by adrenocorticotropic

hormone (ACTH), which, in turn, is regulated by

corticotrophin-releasing hormone (CRH) from the hypothalamus. Aldosterone secretion is regulated by the reninangiotensin system.

Adrenal insufficiency is the failure of the adrenal cortex

to produce adequate amounts of cortisol, aldosterone, or

both. Primary adrenal insufficiency (Addison disease)

refers to failure of the adrenal gland as a result of tissue

destruction, most frequently from an autoimmune process

(70o/o of cases). It is uncommon, affecting 100 per 1 million

persons.

'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,

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