Stoelting Thyroid Sstorm

Thyroid storm is a life-threatening exacerbation of hyperthyroidism precipitated by trauma,

infection, medical illness, or surgery. It is a clinical diagnosis. Thyroid function tests may not
help in differentiating thyroid storm from symptomatic hyperthyroidism. Surprisingly, thyroid
hormone levels may not be significantly higher than uncomplicated hyperthyroidism. It may be
the acute, rapid increase in the plasma level that triggers the event. It most often occurs in the
postoperative period in untreated or inadequately treated patients for emergency surgery. Patients
present with extreme anxiety, fever, tachycardia, cardiovascular instability, and altered
consciousness. The etiology is probably a shift from protein-bound thyroid hormone to free
hormone secondary to circulating inhibitors to binding. Treatment includes rapid alleviation of
thyrotoxicosis and general supportive care. Dehydration is managed with intravenous glucose
containing crystalloid solutions, and cooling measures (e.g., cooling blanket, ice packs, cool
humidified oxygen) are used to counter the fever. Necessary medications include propranolol,
labetalol, or esmolol titrated to decrease heart rate to less than 90 bpm, and dexamethasone 2 mg
every 6 hours or cortisol 100 to 200 mg every 8 hours. Antithyroid drugs (PTU 200400 mg
every 8 hours) may be administered through a nasogastric tube, orally, or rectally. If circulatory
shock is present, an intravenous direct vasopressor (phenylephrine) is indicated. A -adrenergic
blocker or digitalis is recommended for atrial fibrillation accompanied by a fast ventricular
response. Serum thyroid hormone levels generally return to normal within 24 to 48 hours and
recovery occurs within 1 week. Unfortunately, the mortality rate for thyroid storm remains
surprisingly high at approximately 20%.
Thyroid storm and malignant hyperthermia can present with similar intraoperative and
postoperative signs and symptoms (i.e., hyperpyrexia, tachycardia, hypermetabolism).
Differentiation between the two may be extremely difficult. The preoperative detection of
thyrotoxicosis (tremors, diaphoresis, fatigue, tachypnea, tachycardia, fever, an enlarged thyroid)
is very important. Although thyrotoxicosis is an uncommon adult endocrine disorder, it is very
rare in children. Regardless, thyrotoxicosis should be considered in the differential diagnosis of
malignant hyperthermia in any age group.
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Iodine: 5 drop of 10% KI PO tid
by IVdrip over 24 h
Propylthiouracil: 600 mg PO given before iodine,then 400 mgq6h
Propranolol:40 mg PO qid;or 1 mg
slowly IVq4h under close monitoring;do not
exceed 1
mg/min; repeat 1-mg dose maybe givenafter 2 min;or esmolol
infusion
IVdextrose solutions
Correction of dehydration
& electrolyte imbalance
Cooling blanketfor hyperthermia
Antiarrhythmicdrugs (e.g.,Ca channel blockers,adenosine,
l3-blockers) if
necessary for atrial
fibrillation
Treatment of underlying dz,such as infection
Corticosteroids: Hydrocortisone 100 mg IVq8h or dexamethasone 8 mg IVqd

POSTOPERATIVE MORGAN
The most serious threat to hyperthyroid patients in the postoperative period is
thyroid storm, which is characterized by hyperpyrexia, tachycardia, altered consciousness
(eg, agitation, delirium, coma), and hypotension. The onset is usually 624 h after surgery

but can occur intraoperatively, mimicking malignant hyperthermia. Unlike malignant

hyperthermia, however, thyroid storm is not associated with muscle rigidity, elevated
creatine kinase, or a marked degree of metabolic (lactic) and respiratory acidosis.
Treatment includes hydration and cooling, an esmolol infusion or intravenous propranolol
(0.5-mg increments until the heart rate is < 100/min), propylthiouracil (250500 mg every
6 h orally or by nasogastric tube) followed by sodium iodide (1 g intravenously over 12 h),
and correction of any precipitating cause (eg, infection). Cortisol (100200 mg every 8 h) is
recommended to prevent complications from coexisting adrenal gland suppression. Thyroid
storm is a medical emergency that requires aggressive management and monitoring (see
Case Discussion, Chapter 48).
Thyroid storm (crisis) is a medical emergency that carries a 1050% mortality rate.
It is usually encountered in patients with poorly controlled or undiagnosed Graves disease.
Precipitating factors include (1) the stress of surgery and anesthesia, (2) labor and delivery,
(3) severe infection, and, rarely, (4) thyroiditis 12 weeks following administration of
radioactive iodine. Manifestations usually include mental status changes (irritability,
delirium, or coma), fever, tachycardia, and hypotension. Both atrial and ventricular
arrhythmias are common, particularly atrial fibrillation. Congestive heart failure develops in
25% of patients. Hypertension that often precedes hypotension, heat intolerance with
profuse sweating, nausea and vomiting, and diarrhea may be prominent initially.
Hypokalemia is present in up to 50% of patients. Levels of thyroid hormones are high in
plasma but correlate poorly with the severity of the crisis. The sudden exacerbation of
thyrotoxicosis may represent a rapid shift of the hormone from the protein-bound to the
free state or increased responsiveness to thyroid hormones at the cellular level.
Treatment is directed toward reversing the crisis as well as its complications. Large
doses of corticosteroids (dexamethasone intravenously, 10 mg followed by 2 mg every 6 h)
inhibit the synthesis, release, and peripheral conversion of thyroxine (T 4) to triiodothyronine
(T3).

Corticosteroids

also

prevent

relative

adrenal

insufficiency

secondary

to

the

hypermetabolic state. Propylthiouracil, 600 mg, followed by 200 mg every 2 h, is used to

inhibit synthesis of thyroid hormone. Although methimazole inhibits thyroid hormone
production and has a longer half-life, propylthiouracil is preferred because it also inhibits
peripheral conversion of T4. Intravenous preparations are not available for either agent, so
they must be administered orally or via nasogastric tube. Iodide is given to inhibit release of
thyroid hormones from the gland. The iodide may be given intravenously as sodium iodide,
1 g over 24 h, or enterally as potassium iodide, 100200 mg every 8 h; the X-ray contrast
agent sodium ipodate 1 g/d can alternatively be used. Propranolol not only antagonizes the
peripheral effects of the thyrotoxicosis but may also inhibit peripheral conversion of T 4.
Combined

- and

-blockade is preferable to selective

metoprolol) because excessive

2

-antagonism (esmolol or

-receptor activity is responsible for the metabolic effects.

-Receptor blockade also reduces muscle blood flow and may decrease heat production.

Supportive measures include surface cooling (cooling blanket), acetaminophen (aspirin is

not recommended because it may displace thyroid hormone from plasma carrier proteins),
and generous intravenous fluid replacement. Vasopressors are often necessary to support
arterial blood pressure. Digoxin is indicated in patients with atrial fibrillation to control the
ventricular rate (see Chapter 19) and those with congestive heart failure. A pulmonary
artery catheter greatly facilitates management in patients with signs of congestive heart
failure or persistent hypotension by allowing measurements of cardiac output and indices of
ventricular filling pressures.

-Adrenergic blockade is contraindicated in patients with low

cardiac output.
Propranolol, dexamethasone, propylthiouracil, and sodium iodide are given; the
patient is admitted to the ICU, where treatment is continued. Over the next 3 days, his
mental status markedly improves. The T3 and total thyroxine levels on the day of surgery
were both elevated to 250 ng/dL and 18.5 mg/dL, respectively. He was discharged home 6
days later on a regimen of propranolol and propylthiouracil with a blood pressure of 124/80
mm Hg, a pulse of 92 beats/min, and an oral temperature of 37.3C.
Miller Hyperthyroidism

Although hyperthyroidism is usually caused by the multinodular diffuse enlargement in Graves

disease (also associated with disorders of the skin or eyes, or both), it can also occur with
pregnancy, thyroiditis (with or without neck pain), thyroid adenoma, choriocarcinoma, or TSHsecreting pituitary adenoma. Five percent of women have thyrotoxic effects 3 to 6 months
postpartum and tend to have recurrences with subsequent pregnancies. Major manifestations of
hyperthyroidism are weight loss, diarrhea, warm moist skin, weakness of large muscle groups,
menstrual abnormalities, osteopenia, nervousness, jitteriness, intolerance to heat, tachycardia,
cardiac arrhythmias, mitral valve prolapse, and heart failure. When the thyroid is functioning
abnormally, the entity most threatened is the cardiovascular system. When diarrhea is severe,
dehydration should be corrected preoperatively. Mild anemia, thrombocytopenia, increased
serum alkaline phosphatase, hypercalcemia, muscle wasting, and bone loss frequently occur in
hyperthyroidism. Muscle disease usually involves the proximal muscle groups; it has not been
reported to cause respiratory muscle paralysis. In the apathetic form of hyperthyroidism (seen
most commonly in persons older than 60 years), cardiac effects dominate the clinical picture.
Signs and symptoms include weight loss, anorexia, and cardiac effects such as tachycardia,
irregular heart rhythm, atrial fibrillation (in 10%), heart failure, and occasionally, papillary
muscle dysfunction.
Although -adrenergic receptor blockade can control the heart rate, its use is fraught with hazard
in a patient already experiencing CHF. However, a decreasing heart rate may improve heartpumping function. Thus, hyperthyroid patients who have fast ventricular rates, who are in CHF,
and who require emergency surgery are given esmolol guided by changes in pulmonary artery
wedge pressure and their condition. If slowing the heart rate with a small dose of esmolol
(50 g/kg) does not aggravate the heart failure, we administer more esmolol. We believe that we
should aim to avoid imposing surgery on any patient whose thyroid function is clinically
abnormal. Therefore, we believe that only life or death emergency surgery should preclude

making the patient pharmacologically euthyroid, a process that can take 2 to 6 weeks. Evaluation
of hyperthyroidism is also covered in Chapter 34 . Antithyroid medications include
propylthiouracil and methimazole, both of which decrease the synthesis of T4 and may enhance
remission by reducing TSH receptor antibody levels (the primary pathologic mechanism in
Grave's disease). Propylthiouracil also decreases the conversion of T4 to the more potent T3.
However, the literature indicates a trend toward preoperative preparation with propranolol and
iodides alone.[77] This approach is quicker (i.e., 7 to 14 days versus 2 to 6 weeks); it shrinks the
thyroid gland, as does the more traditional approach; it decreases conversion of the prohormone
T4 into the more potent T3; and it treats symptoms but may not correct abnormalities in left
ventricular function. Regardless of the approach, antithyroid drugs should be administered
chronically and on the morning of surgery. If emergency surgery is necessary before the
euthyroid state is achieved, if subclinical hyperthyroidism progresses without adequate
treatment, or if hyperthyroidism gets out of control during surgery, intravenous administration of
esmolol, 50 to 500 g/kg, could be titrated to restore a normal heart rate (assuming the absence
of CHF) (see earlier). In addition, intravascular fluid volume and electrolyte balance should be
restored. However, administering propranolol or esmolol does not invariably prevent thyroid
storm.
No controlled study has demonstrated clinical advantages of any anesthetic drug over another for
surgical patients who are hyperthyroid. A review of cases performed at the University of
California, San Francisco, from 1968 to 1982 revealed that virtually all anesthetic drugs and
techniques[78] have been used without adverse effects even remotely being attributable to the drug
or technique. Furthermore, although some investigators have recommended that anticholinergic
drugs (especially atropine) be avoided inasmuch as they interfere with the sweating mechanism
and cause tachycardia, atropine has been given as a test for the adequacy of antithyroid
treatment. Because patients are now subjected to operative procedures only (or almost only)
when euthyroid, the traditional steal of a heavily premedicated hyperthyroid patient (so
commonly found in the iodine-deficient locales surrounding the Lahey, Mayo, and Cleveland
clinics) in the operating room has vanished.
A patient with a large goiter and an obstructed airway can be handled in the same way as any
other patient with problematic airway management. Preoperative medication should avoid
excessive sedation, and an airway should be established, often with the patient awake. A firm
armored endotracheal tube is preferable and should be passed beyond the point of extrinsic
compression. It is most useful to examine CT scans of the neck preoperatively to determine the
extent of compression. Maintenance of anesthesia usually presents little difficulty.
Postoperatively, extubation should be performed under optimal circumstances for reintubation in
the event that the tracheal rings have been weakened and the trachea collapses.
Of the many possible postoperative complications (nerve injury, bleeding, and metabolic
abnormalities), thyroid storm (discussed later), bilateral recurrent nerve trauma, and
hypocalcemic tetany are the most feared. Bilateral recurrent laryngeal nerve injury (secondary to
trauma or edema) causes stridor and laryngeal obstruction as a result of unopposed adduction of
the vocal cords and closure of the glottic aperture. Immediate endotracheal intubation is required,
usually followed by tracheostomy to ensure an adequate airway. This rare complication occurred
only once in more than 30,000 thyroid operations at the Lahey Clinic. Unilateral recurrent nerve

injury often goes unnoticed because of compensatory overadduction of the uninvolved cord.
However, we often test vocal cord function before and after this surgery by asking the patient to
say e or moon. Unilateral nerve injury is characterized by hoarseness and bilateral nerve
injury by aphonia. Selective injury to the adductor fibers of both recurrent laryngeal nerves
leaves the abductor muscles relatively unopposed, and pulmonary aspiration is a risk. Selective
injury to the abductor fibers leaves the adductor muscles relatively unopposed, and airway
obstruction can occur. Bullous glottic edema, an additional cause of postoperative respiratory
compromise, has no specific cause or known preventive measure.
The intimate involvement of the parathyroid gland with the thyroid gland can result in
inadvertent hypocalcemia during surgery for thyroid disease. Complications related to
hypocalcemia are discussed in the later section Hypocalcemia.
Because postoperative hematoma can compromise the airway, neck and wound dressings are
placed in a crossing fashion (rather than vertically or horizontally) and should be examined for
evidence of bleeding before a patient is discharged from the recovery room.
Thyroid Storm

Thyroid storm is the name for the clinical diagnosis of a life-threatening illness in a patient
whose hyperthyroidism has been severely exacerbated by illness or surgery. Thyroid storm is
characterized by hyperpyrexia, tachycardia, and striking alterations in consciousness. It can thus
be manifested very similarly to malignant hyperthermia, pheochromocytoma, or neuroleptic
malignant syndrome. No laboratory tests are diagnostic of thyroid storm, and the precipitating
(nonthyroidal) cause is the major determinant of survival. Therapy can include blocking the
synthesis of thyroid hormones by administering antithyroid drugs, blocking the release of
preformed hormone with iodine, meticulous attention to hydration and supportive therapy, and
correcting the precipitating cause. Blocking the sympathetic nervous system with reserpine, and -receptor antagonists, or 2-agents may be exceedingly hazardous and requires skillful
management and constant monitoring of the critically ill patient.
Thyroid dysfunction, either hyperthyroidism or hypothyroidism, develops in more than 10% of
patients treated with the antiarrhythmic agent amiodarone.[79] Approximately 35% of the drug's
weight is iodine, and a 200-mg tablet releases about 20 times the optimal daily dose of iodine.
This iodine can lead to reduced synthesis of T4 or increased synthesis. In addition, amiodarone
inhibits the conversion of T4 to the more potent T3.
Patients receiving amiodarone might be considered to be in need of special attention
preoperatively and may even require special attention to anesthesia, not just because of the
arrhythmia that led to such therapy but also to ensure that no perioperative dysfunction or
surprises occur because of unsuspected thyroid hyperfunction or hypofunction.[80] Many patients
with amiodarone-induced thyrotoxicosis receive steroids for a period, another area of questioning
that might be triggered by the use of amiodarone in a preoperative patient.
Msthst XIII.

Thyroid storm

A. The clinical syndrome and diagnostic criteria. Thyroid storm is a syndrome of severe
hyperthyroidism with exaggerated symptoms and signs, usually occurring as an acute
exacerbating of pre-existing hyperthyroidism. Because the diagnosis is a matter of degree (once
biochemical hyperthyroidism is established), diagnostic criteria include calculation of a score,
with more points for increasing degrees of hyperpyrexia, tachycardia, severity of congestive
heart failure, presence of atrial fibrillation, altered mental status (with higher scores for seizure or
coma), and GI symptoms (including diarrhea, vomiting, abdominal pain, and jaundice). Points
are also given for history of an event that may have precipitated the thyroid storm, such as an
iodine load (from medications or IV contrast), thyroid surgery, trauma, infection, or any other
severe stress including nonthyroidal surgery.
B. Treatment consists of supportive therapy and medications targeted specifically at the
excessive action, production, and release of thyroid hormone. Initial therapy should include an
IV &bgr;-blocker titrated to control tachycardia. Stress-dose glucocorticoids (100 mg
hydrocortisone IV every 8 hours) are administered to reduce T4 to T3 conversion by deiodinase
and to ensure thyroid storm is not complicated by adrenal insufficiency due to rapid
glucocorticoid metabolism. The use of thionamide medications such as methimazole and
propylthiouracil to reduce the production of thyroid hormone, followed by iodine to inhibit
thyroid hormone release, is similar to the treatment of less severe hypothyroidism, except that the
doses are larger. Supportive care includes aggressive treatment of hyperpyrexia,
P.417
fluid resuscitation, ventricular rate control in atrial fibrillation, and diagnosis and treatment of
any precipitating conditions

Table 6.4. Treatment of thyroid storm

Block Sympathetic Response
Propranolol
12 mg IV (repeat as needed) or
4080 mg orally every 6 hours
Verapamil
510 mg IV (repeat as needed)
Esmolol
50100 g/kg/min IV
Block Thyroid Hormone Synthesis (Thionamides)
PTU
200 mg orally every 46 hours
Methimazole
20 mg orally or per rectum every 4 hours
Block Thyroid Hormone Release
Iopanoic acida
500 mg orally twice a day
Dexamethasone
2 mg orally every 6 hours
Block T4 to T3 Conversion
Propranolol, PTU, Iopanoic acid,
Steroids (Hydrocortisone 100 mg orally/IV every 8 hours or
dexamethasone 2 mg orally/IV every 6 hours)
Supportive Therapy
Fluids, cooling (with meperidine to block shivering), electrolyte

replacement, antipyretics (no aspirin), treatment of precipitating

illness and congestive heart failure, oxygen, nutrition, consider
plasmapheresis and airway support
a
Give iopanoic acid >1 hour after PTU or methimazole to avoid a hormone surge
Thyroid Storm longnecker

At the other end of the spectrum from

subclinical hyperthyroidism is thyroid
21
19
6,18,20
21
4
6

storm. Thyroid storm is an acute lifethreatening

form of hyperthyroidism
with
a significant mortality rate of
>20%.
23,24

The diagnosis of thyroid

storm is a clinical one, because serum
levels of thyroid hormones are about
the same as encountered in hyperthyroidism.
Four clinical features are required
for the diagnosis of thyroid
storm:
23,24

(a) Temperature elevation

with diaphoresis. Temperatures above
106F have been reported. (b) A
marked tachycardia that is disproportionate
to the temperature elevation.
This
may manifest as sinus tachycardia,
atrial fibrillation, or other supraventricular
or ventricular tachycardia.
(c) Cerebral dysfunction, which
may
range from agitation, restlessness,
and emotional lability to confusion, psychosis, seizures, and coma.
(d) Gastrointestinal disturbance ranging
from nausea, vomiting, and diarrhea
to intestinal obstruction or acute
abdomen.
The presence of jaundice is
a
poor prognostic sign.
23,24

The precipitating
event varies and may include
(most
commonly) infection; surgery;
treatment
with radioactive iodine, or
the
administration of iodinated contrast
dyes; cessation of antithyroid
medication;
amiodarone; exogenous

administration
of thyroid hormone;
diabetic
ketoacidosis; hypoglycemia;
congestive
heart failure; pulmonary
embolism,
cerebrovascular accident
(CVA);
bowel infarction; any acute
trauma;
toxemia of pregnancy, parturition,
and the postpartum state; dental
extraction; and even vigorous palpation
of the thyroid.

Treatment
23,24

The approach to treatment of thyroid

storm is 4-fold
20,2325

:
1. Decrease production and secretion
of thyroid hormone.
2. Block the peripheral effects of thyroid hormones.
3. Maintain supportive care. Aggressive treatment of fever, temperature
elevation, acidbase abnormalities,
along with respiratory and
cardiovascular
support.
4. Determine the underlying cause.
Chapter 69 provides a more det

Barash Treatment and Anesthetic Considerations

The most important goal in managing the hyperthyroid patient is to make the patient euthyroid
before any surgery, if possible. The drugs propylthiouracil and methimazole are thiourea
derivatives that inhibit organification of iodide and the synthesis of thyroid hormone.5
Propylthiouracil also decreases the peripheral conversion of T4 to T3. Normal thyroid glands
usually contain a store of hormone that is large enough to maintain a euthyroid state for several
months, even if synthesis is abolished. Therefore, hyperthyroid patients are unlikely to be
regulated to a euthyroid state with antithyroid drugs alone in <6 to 8 weeks. Toxic reactions from
these drugs are uncommon but include skin rash, nausea, fever, agranulocytosis, hepatitis, and
arthralgias.
Inorganic iodide inhibits iodide organification and thyroid hormone releasethe Wolff-Chaikoff
effect. Iodide is also effective in reducing the size of the hyperplastic gland and has a role in the
preparation of the patient for emergency thyroid surgery. Antithyroid drugs should be started
before iodide treatment because of the possibility of worsening the thyrotoxicosis.
-Adrenergic antagonists are effective in attenuating the manifestations of excessive sympathetic
activity and should be used in all hyperthyroid patients unless contraindicated. -Adrenergic
blockade alone does not inhibit hormone synthesis, but specifically propranolol does impair the
peripheral conversion of T4 to T3 over 1 to 2 weeks. Propranolol given over 12 to 24 hours
decreases tachycardia, heat intolerance, anxiety, and tremor. Any beta-blocker may be used, and

long-acting agents may be more convenient. The combination of propranolol (in doses titrated to
effect) plus potassium iodide (two to five drops every 8 hours) is frequently used before surgery
to ameliorate cardiovascular symptoms and reduce circulating concentrations of T4 and T3.
Preoperative preparation usually requires 7 to 14 days. Heart failure secondary to poorly
controlled paroxysmal atrial fibrillation may improve with slowing of the ventricular rate, but
abnormalities of left ventricular function secondary to hyperthyroidism may not be corrected
with the use of -antagonists. If a hyperthyroid patient with clinically apparent disease requires
emergency surgery, -adrenergic blockade should be administered to achieve a heart rate <90
beats per minute. Beta-blockers do not prevent thyroid storm. Glucocorticoids such as
dexamethasone (8 to 12 mg/day) are used in the management of severe thyrotoxicosis because
they reduce thyroid hormone secretion and the peripheral conversion of T4 to T3.
Iopanoic acid, a radiographic contrast agent that decreases peripheral conversion of T4 and
releases iodine that inhibits synthesis, is useful for emergency preparation.
Radioactive iodine therapy is an effective treatment for some patients with thyrotoxicosis.6
However, it should not be administered to patients who are pregnant because it crosses the
placenta and may destroy the fetal thyroid. A side effect of RIA therapy is hypothyroidism; 10 to
60% of cases occur in the first year of therapy, and an additional 2% occur per year thereafter.
A variety of anesthetic techniques and drugs have been used for hyperthyroid patients
undergoing surgery. All antithyroid medications are continued through the morning of surgery.
The goal of intraoperative management in the hyperthyroid patient is to achieve a depth of
anesthesia that prevents an exaggerated sympathetic response to surgical stimulation while
avoiding the administration of medication that stimulates the sympathetic nervous system.
Pancuronium should be avoided. It is best to avoid using ketamine, even when a patient is
clinically euthyroid. Hypotension that occurs during surgery is best treated with direct-acting
vasopressors rather than a medication that provokes the release of catecholamines. The incidence
of myasthenia gravis is increased in hyperthyroid patients; thus, the initial dose of muscle
relaxant should be reduced and a twitch monitor should be used to titrate subsequent doses.
Regional anesthesia is an excellent alternative when appropriate; however, epinephrinecontaining solutions should be avoided.
Thyroid storm is a life-threatening exacerbation of hyperthyroidism that most commonly
develops in the undiagnosed or untreated hyperthyroid patient because of the stress of surgery or
nonthyroid illness.7 Operating on an acutely hyperthyroid gland may provoke thyroid storm,
although this is probably not due to mechanical release of hormone.8 Its manifestations include
hyperthermia, tachycardia, dysrhythmias, myocardial ischemia, congestive heart failure,
agitation, and confusion. It must be distinguished from, or considered with, pheochromocytoma,
malignant hyperthermia, and light anesthesia. Although free T4 levels are often markedly
elevated, no laboratory test is diagnostic. Treatment involves large doses of propylthiouracil and
supportive measures to control fever and restore intravascular volume. Hemodynamic
monitoring (pulmonary artery catheter, arterial catheter) is especially useful in guiding the
treatment of patients with significant left ventricular dysfunction (Table 49-3). Again, it is
essential to remove or treat the precipitating event.
Anesthesia for Thyroid Surgery
Subtotal thyroidectomy as an alternative to prolonged medical therapy is used less frequently
now than in the past. Indications
P.1283

include failed medical therapy, underlying cancer, and symptomatic goiter. It is usually
performed under general endotracheal anesthesia, although the use of the laryngeal mask airway
is increasing.9 Use of a laryngeal mask airway allows real-time visualization of vocal cord
function because the patient is allowed to breathe spontaneously. Limited thyroidectomy may
also be performed under bilateral superficial cervical plexus block. The anesthesiologist must be
prepared to manage an unexpected difficult intubation because the incidence of difficult
intubation during goiter surgery is 5 to 8%.10 Thyroid cancer increases the risk, but the size of the
goiter is not predictive. Airway obstruction is a potential problem in the patient with a large
substernal goiter, although rarely a problem with goiters exclusively in the neck. Evidence of
significant airway obstruction or tracheal deviation or narrowing may warrant inhalation
induction or awake fiberoptic intubation. The complications after subtotal thyroidectomy include
recurrent laryngeal nerve damage, tracheal compression secondary to hematoma or
tracheomalacia, and hypoparathyroidism. Hypoparathyroidism secondary to the inadvertent
surgical removal of parathyroid glands is most frequently seen after total thyroidectomy. The
symptoms of hypocalcemia develop within the first 24 to 96 hours after surgery11 (see Chapter
14). Laryngeal stridor progressing to laryngospasm may be one of the first indications of
hypocalcemic tetany. The intravenous administration of calcium chloride or calcium gluconate is
warranted in this situation. Magnesium levels should also be monitored and corrected if low.
Bilateral recurrent laryngeal nerve injury is an extremely rare injury and necessitates
reintubation. Unilateral nerve injury is more common and is often transient.12 Unilateral damage
to the recurrent laryngeal nerve is characterized by hoarseness and a paralyzed vocal cord,
whereas bilateral injury causes aphonia (see Chapter 29). It is wise to evaluate vocal cord
function before and after surgery by laryngoscopy or by asking the patient to phonate by saying
the letter e. Routine postoperative visualization of the vocal cords is not warranted.
Postoperative extubation of the trachea should be performed under optimal conditions.
Intraoperative laryngeal nerve injury or collapse of the tracheal rings from previous weakening
may mandate emergency reintubation.
Table 49-3 Management of Thyroid Storm
Administer IV fluids.
Administer sodium iodide, 250 mg PO or IV q6h.
Administer propylthiouracil, 200400 mg PO or via NGT q6h.
Administer hydrocortisone, 50100 mg IV q6h.
Administer propranolol, 1040 mg PO q46h, or esmolol infusion to treat hyperadrenergic signs.
Cooling blankets and acetaminophen and meperidine (2550 mg) IV q46h may be used to
prevent shivering.
Use digoxin for heart failure especially in the presence of atrial fibrillation with rapid ventricular
response.
IV, intravenous(ly); PO, oral(ly); NGT, nasogastric tube.