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988 PART 8: Renal and Metabolic Disorders

concentrations of thyroid hormone without an appropriate increase in TABLE 103-2 Indications for Thyroid Hormone Treatment in Patients with Severe NTI
serum TSH level would, under normal conditions, raise the suspicion
of pituitary (secondary) or hypothalamic (tertiary) hypothyroidism. Increased serum TSH concentrations
However, in a critically ill patient, the diagnosis of primary hypothyroid- History of radioactive iodine treatment
ism with inadequate pituitary response needs consideration. A modest Hypothermia
elevation of serum TSH level without an increase in rT concentration is
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a strong indicator of primary hypothyroidism. Except in the presence of Macroglossia
renal failure, a decreased rT level raises the possibility of hypothyroid- Goiter
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ism and should prompt a search for the etiology. While these possible History of thyroid disease
diagnoses are being investigated, thyroid hormone replacement and
glucocorticoid treatment are indicated. Since results of rT measure- Treatment with thyroid hormone at any time prior to the current illness
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ment often are not obtained readily, this test is useful in retrospect for Hypercholesterolemia
ruling out primary endocrine dysfunction and adds little to the initial Hyporeflexia
management of patients. Since only severe primary hypothyroidism
requires emergency treatment, its recognition is usually simple because Unexplained pleural or pericardial effusions
of persistent TSH elevation, a prior history of thyroid disease, and physi- Increased serum creatine phosphokinase level
cal findings compatible with hypothyroidism.
■ TO TREAT OR NOT TO TREAT ■ WHAT TO TREAT WITH

Should patients with low serum levels of thyroid hormone in the If the decision is made to treat a sick patient who has reduced thyroid
face of catastrophic NTIS receive hormonal replacement? In order hormone levels, the logical choice is T . Administration of T does not
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to answer this question, several issues need to be determined: (1) Is change the serum T concentration significantly—it only increases the
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the serum TSH level an accurate reflection of the thyroid status of all level of the biologically inactive rT . The problem with T treatment is its
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body tissues, or does it only reflect the status of the pituitary? (2) Are potential cardiac “toxicity.” One possible problem is the proarrhythmogenic
the tissues of the body functionally hypothyroid? and (3) Is the low effect of T in anesthetized patients; another possible problem is that T
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serum T level an adaptive mechanism for conservation of energy may increase the oxygen demand of a myocardium with a fixed coronary
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during critical illness? Unfortunately, these questions remain relatively artery lesion. T is now available as the product Triostat™; however, the
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unanswered. In a randomized, prospective study to determine the cost of a single day’s treatment for myxedema would be in excess of $3500!
effect of T treatment in NTIS, 11 patients admitted to an ICU with Alternatively, a solution of T for intravenous use can be prepared by the
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reduced thyroid hormone levels were treated with intravenous T , and hospital pharmacist by dissolving l-T in 0.1 N NaOH, followed by a 10-fold
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12 served as controls. The study indicated an earlier mortality in the dilution in normal saline containing 2% albumin to a final concentration of
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treated group, although the number of survivors was not significantly 25 µg T per milliliter. The solution is sterilized by a single passage through
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different between the groups. It was concluded that T therapy was not a 0.22-µm Millipore filter and is stored, for no longer than 1 week, at 4°C,
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beneficial, and inhibition of TSH secretion by the administration of T protected from light. The materials for this preparation cost about $1.
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may be detrimental to the recovery of thyroid function. These results
have been confirmed in a similar study carried out in an ICU setting. MYXEDEMA COMA
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Nevertheless, many physicians understandably find it difficult to with-
hold treatment in a dying patient with virtually undetectable thyroid ■ DIAGNOSIS
hormone levels.
Not only are data on the benefit of thyroid hormone treatment limited, Myxedema coma is caused by marked and prolonged depletion of thyroid
but it is unlikely that an answer regarding the efficacy of this treatment hormone. The cardinal features of myxedema coma are (1) defective
will be forthcoming, given multiple-organ involvement in serious illness thermoregulation to the point of hypothermia, (2) altered mental status
and the difficulty of interpreting the effect of thyroid hormone replace- to the point of coma, (3) a history or sign (such as a neck scar) of ablative
ment in individuals receiving multiple drugs. Thus the argument centers thyroid treatment, and (4) an identifiable precipitating event. The condi-
not only on the question of whether such patients are truly hypothyroid tion is a medical emergency because it is fatal in approximately one-half
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(hence the bias of the term euthyroid sick) but also on whether this tem- of cases. This rare entity occurs typically in elderly women with long-
porary hypothyroidism may not, in fact, be beneficial. Inhibition of the standing hypothyroidism who develop an intercurrent illness and lapse
type I 5′-deiodinase is the principal mechanism that reduces the supply into coma or in hypothyroid persons exposed to cold or given sedatives,
of biologically active thyroid hormone, T , to peripheral tissues in the hypnotics or opiates, sufficient to push them to the brink of myxedema
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severely ill. Experimental work in a rat model indicates that peripheral coma. Table 103-3 lists events likely to precipitate myxedema coma. The
tissue hypothyroidism is maintained by an inhibition of the usual com- usual features of severe hypothyroidism (myxedema) include dry, coarse
pensatory increase in TSH level. This inhibition occurs because normal skin, scaly elbows and knees, yellowness in the skin without scleral icterus,
levels of T are generated in the pituitary gland, which uses a different coarse hair, thinning of the lateral aspect of eyebrows, macroglossia
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form of 5′-deiodinase, the type II enzyme, that is actually more active in and hoarseness, obtundation, delayed deep tendon reflexes, and hypo-
severe illness. 11,21 Teleologists argue that this mechanism to reduce the thermia. When a markedly reduced serum T level and an elevated TSH
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delivery of thyroid hormone to peripheral tissues is not accidental and, concentration accompany these signs, the diagnosis is obvious. However,
therefore, that reduced metabolic activity may be beneficial in the face as for thyrotoxic crisis, initiation of treatment should not be delayed until
of the increased catabolism characteristic of severe illness. The question the results of the thyroid function studies are available. Furthermore,
is: Does the physician or nature know best? At our institution there is no because of intercurrent illness, TSH values may not be elevated in pro-
consensus on this subject. portion to the severity of hypothyroidism. A high index of suspicion in a
Studies have shown decreased serum T concentrations in patients patient presenting as just described should prompt immediate treatment
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undergoing cardiopulmonary bypass surgery. T treatment can normal- after a blood sample is taken for laboratory confirmation of the diagnosis.
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ize the serum levels and may increase cardiac output and lower systemic ■
vascular resistance ; however, these effects may be negligible. 23 PULMONARY AND CARDIOVASCULAR COMPLICATIONS
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Table 103-2 may serve as a bedside guide to the intensivist for the Alveolar hypoventilation is known to occur in myxedema. It is thus
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selection of patients for thyroid hormone treatment. not surprising that patients with underlying lung pathology experience
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