Page 1417 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

990 PART 8: Renal and Metabolic Disorders

α-adrenergic agents should be avoided because patients are already T derived from blood is converted into the active hormone, T , by
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vasoconstricted. removal of a single iodine atom from the 5′ position in the outer ring
■ EFFICACY OF TREATMENT of the molecule. This reaction is mediated by a tissue-specific 5′-deio-
dinase. Removal of iodine from the inner ring yields the inactive form
Assuming that an accurate diagnosis has been made and that proper rT . Intracellular T binds to nuclear receptors, through which it exerts
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therapeutic measures have been carried out, how are the patient’s prog- its effects.
to treat the patient for several days or as long as the serum TSH con- ■ DIAGNOSIS IN THE ICU
ress and the efficacy of treatment followed? The physician is committed
centration remains elevated. Reduction of the TSH level is the earliest Thyrotoxicosis may be manifested by adverse changes in every organ
indicator of a response to thyroid hormone therapy. Irreversible damage system. Pyrexia, tachycardia, congestive heart failure, oxyhemoglobin
to the respiratory centers has been observed, with failure of spontane- desaturation, and hypertension are the hallmarks of thyrotoxic crisis.
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ous respiration, despite full repletion of thyroid hormone. No laboratory There may also be involvement of the CNS, ranging from tremulousness
measurements are helpful in assessing the peripheral tissue responses to seizures and coma, or involvement of the respiratory system, with
to thyroid hormone in the critical care setting. The ultimate gauge of tachypnea and respiratory muscle fatigue. Goiter and exophthalmos are
successful treatment is complete clinical recovery. as likely to be absent as present. Unfortunately, at the time of presentation
in the ICU, most patients with these characteristics have only modest
GOITER AND ACUTE AIRWAY OBSTRUCTION elevations of thyroid hormone concentration in serum (see above).
Failure to recognize these symptoms as manifestations of thyrotoxicosis
Large goiters, weighing 150 g or more, can cause some degree of tracheal may result in nonspecific treatment, with a resulting risk of morbidity
obstruction, especially if they are substernal in location. In a series of or even death. On the other hand, failure to treat pyrexia as a sign of
2908 goiters, only 58 (2.0%) caused tracheal obstruction at presentation. sepsis or tachycardia as a sign of ischemia or hypoxia could be equally
Tracheal compression obstructing up to 75% of the tracheal lumen devastating. Stat laboratory measurement of thyroid hormone levels is
often remains asymptomatic. Although dyspnea on exertion has been not always available to provide firm laboratory support for the diagno-
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attributed to goiter, the symptoms are often only nocturnal, manifesting sis. A 2-hour radioiodine uptake test conceivably could be done at the
as stridor or, when more severe, as sleep apnea. This problem can be bedside using a portable gamma counter probe, but it is not practical.
confirmed by x-ray and CT views of the trachea at rest and during a Therefore, the preliminary diagnosis of thyrotoxicosis usually is based
reverse Valsalva maneuver and by sleep studies. 32 on a careful history and physical examination. Useful findings are
Growth of the goiter would have to be extensive to cause direct (1) a previous diagnosis and treatment of thyrotoxicosis, (2) presence
tracheal compression. In Riedel struma, there is tracheal cartilage of exophthalmos, (3) goiter, (4) a history of thyroid hormone ingestion,
destruction by fibrous invasion, which can also cause bilateral vocal (5) evidence of previous thyroid surgery, including an anterior neck
cord paralysis. Several case reports have been published describing the surgical scar, and (6) recent use of iodine-containing radiologic contrast
acute presentation of tracheal obstruction associated with goiter. 33,34 agents. Such information only supports the possibility that suggestive
Management of these patients is somewhat difficult because emergency physical signs may be due to thyrotoxicosis.
tracheostomy may be difficult to perform owing to interference by the ■
thyroid gland. The use of small endotracheal tubes and immediate sub- PHYSIOLOGIC CONSEQUENCES
total thyroidectomy should reduce the need for tracheostomy. It should AND CARDIOVASCULAR COMPLICATIONS
be noted that subtotal thyroidectomy may not be successful in the pres- Thyroid hormone exerts its tissue effect both directly by interaction
ence of tracheomalacia, which may necessitate prosthetic supports. In with specific nuclear receptors and indirectly through activation of the
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some instances, a simple division of the thyroid isthmus may be suf- sympathoadrenal system. Each of these actions causes unique effects on
ficient to relieve the symptoms. Although not particularly useful in the various tissues. The physiologic basis of the sympathomimetic effect of
acute care setting, I therapy can be effective in the long term in elderly thyroid hormone is unknown. Table 103-5 summarizes the cardiopul-
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patients with large, compressive goiters. 36 monary complications of thyrotoxicosis.
Perhaps the most detrimental effect of thyrotoxicosis, which clearly is
THYROTOXICOSIS evident in the more severe state of thyroid storm (see below), is pyrexia.
Increased body temperature may be secondary to the increased basal
Thyrotoxicosis occurs when the supply of thyroid hormone exceeds metabolic rate or to actual resetting of hypothalamic thermoregulation.
the amount needed for normal tissue function. The source of thyroid Pyrexia further increases cardiovascular stress; therefore, reduction of
hormone may be (1) excessive synthesis and secretion of hormone body temperature is an important goal of therapy.
from the thyroid gland in response to either TSH or abnormal thyroid- Neurologic complications of severe thyrotoxicosis include neuromus-
stimulating substances (usually immunoglobulins), (2) autonomous cular disorders of myopathy (present in over 50% of all hyperthyroid
hormone hypersecretion or abnormal release of preformed hormone, patients and classified as severe in 4%), exophthalmic ophthalmoplegia,
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or (3) production of the hormone by an exogenous or ectopic source. aggravation of myasthenia gravis, and thyrotoxic periodic paralysis
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Manifestations can be mild or severe depending on the degree of hor- (primarily in Asian men). Except for irritability and tremulousness, the
mone excess and its duration, as well as the presence of intercurrent
illness. Aspects related to thyrotoxicosis in the severely ill patient will be
the focus of this section.
A few basic facts about thyroid physiology are important for under- TABLE 103-5 Cardiopulmonary Complications of Thyrotoxicosis
standing the therapeutic approach to thyroid disorders. Iodine is Increased metabolic demand with increased O consumption and CO production
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actively transported into the thyroid gland, where it is covalently bound Respiratory muscle weakness
to tyrosines within the thyroglobulin molecule. The iodinated tyrosines Increased work of breathing
are coupled to form mainly T as well as some T . It is in the form of
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thyroglobulin that the hormone is stored in the colloid of the thyroid Hyperdynamic circulation
follicles. In response to TSH or an abnormal stimulator, thyroglobulin Potential for high-output heart failure
is digested by proteolysis, and the liberated hormone—predominantly Potential for myocardial ischemia
T —is secreted into the circulation. In the blood, T is transported
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bound to specific serum proteins. In virtually all peripheral tissues, Arrhythmias

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