Page 1421 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

994 PART 8: Renal and Metabolic Disorders

turnover rate, thyroxine has a half-life of at least 72 hours, and frequently Third, consider a 25-year-old 38-week primigravida who must
it takes more than 1 week to achieve a normal FT I—an unacceptable undergo emergent cesarean section for fetal distress. The patient is
4
wait, especially when the need for surgery is urgent. In such instances, known to have active Graves disease. She has not been compliant in
the preoperative therapeutic goal is to prevent the occurrence of thy- taking the prescribed PTU and is febrile, tachycardic, and hallucinating.
roid storm. Blocking the effect of thyroid hormone on the sympathetic Appropriate preparation for this patient prior to general anesthesia and
nervous system, particularly on the heart, is an alternative (if not an emergency cesarean section would be intravenous propranolol, 1.0 to
ideal) approach to therapy. An arbitrary goal of maintaining a heart 2.0 mg as a slow intravenous bolus. Then 10 to 15 mg propranolol can
70
rate below 90 beats per minute may not always be achieved in patients be added to 500 mL 5% dextrose and infused while the patient’s and
who have a pulse rate of 200 beats per minute at the outset. In fact, there fetus’s heart rates are monitored. Continuation of the propranolol after
are no strict criteria for the response to therapy prior to surgery. surgery would be indicated, as discussed earlier. The use of atropine
Propranolol is the most widely used drug 71-73 ; other parenteral prepara- to control bronchial secretions during surgery should be avoided in
tions are now available, but there is no clear evidence that any of them thyrotoxic patients because of possible exacerbation of the sympathomi-
has advantages over any other. Propranolol, however, has the added metic activity. There are reports of the use of plasma exchange in severe
effect of decreasing the conversion of T to T in peripheral tissues. This thyrotoxicosis of pregnancy. In summary, euthyroidism can be rapidly
54
4
3
effect may not be shared by other β-blockers, such as atenolol. By and accomplished with iopanoic acid and dexamethasone, β-blockers, and,
large, β-blockers have little effect on the serum concentration of T or on when possible, antithyroid drugs. 74,75
4
the metabolic status of the patient. The combined use of an antithyroid
drug (PTU or MMI) and iodide provides the most rapid means of reduc- AMIODARONE-INDUCED THYROTOXICOSIS
ing the serum level of thyroid hormone; the antithyroid drug blocks the
synthesis of the hormone, and iodide blocks its release. Although Amiodarone is an iodine-rich antiarrhythmic (37% of its weight is
the results of determinations of serum thyroid hormone concentrations organic iodine). Because of its efficacy, it has become widely used. This
may not be available on a stat basis, it is important to obtain a blood has resulted in a significant increase in side effects associated with the
sample before treatment is initiated. drug, such as thyrotoxicosis. Given the patient’s underlying cardiac
We would like to discuss three scenarios for the preoperative treat- problem that necessitated the use of this drug, the thyrotoxicosis,
ment of thyrotoxic patients. First, consider an ICU patient who is in a when it occurs, results in a worsening of the problem. The incidence of
septic condition with severe cholecystitis. The presence of thyrotoxicosis amiodarone-induced thyrotoxicosis (AIT) is thought to be higher in
has been confirmed by an FT I of 21 (normal range = 6-10.5) and a TSH individuals with low dietary iodine. Amiodarone can also cause hypo-
4
level below 0.01 mU/L. A cholecystectomy is planned as the definitive thyroidism but usually in populations with relatively high dietary iodine.
treatment, to take place in approximately 1 week. In this instance, the The mechanism of AIT is unknown but undoubtedly involves thyroid
physician has time to institute therapy aimed at reducing the thyroid iodine dysautoregulation and destruction and/or inflammation of the
hormone concentration and to follow serum hormone levels as guides thyroid gland. AIT is classified as types I and II. Type I occurs in struc-
of therapeutic response. Initiation of PTU, 200 mg every 8 hours given turally abnormal thyroid glands (such as a nodular goiter), and type II
orally or by nasogastric tube, followed by 1 or 2 drops of ssKI twice occurs in a structurally normal gland. Type I is caused by iodine-
76
daily, is the suggested treatment for this patient’s thyrotoxicosis. The induced thyroid hormone synthesis, and type II is believed to be due to
reason for starting PTU before iodide is to prevent the gland from being a destructive thyroiditis. Treatment of type I and type II AIT in critically
flooded with iodide, which has been shown to produce, on occasion, ill patients can be a challenge, and often the type of AIT is not apparent
a later exacerbation of thyrotoxicosis. A full discussion of these drugs at the time of presentation.
appears under “Thyroid Storm” above and in Table 103-4. Thyroid The diagnosis is made in a patient who presents with the typical labo-
function tests should be performed every 2 days. ratory findings of thyrotoxicosis and a history of being on or recently
Second, consider a 65-year-old woman admitted for semiemergent having been on amiodarone. Owing to accumulation of the drug in fat
aortic valvuloplasty for severe aortic stenosis due to rheumatic carditis. tissue, it has a long half-life in the body. Laboratory tests such as an ele-
She has been noted to be thyrotoxic; recent thyroid function tests revealed vated spot urinary iodine determination or an I uptake test (although
123
an FT I of 19 and a TSH level of less than 0.01 mU/L. The valvuloplasty is the latter is rarely practical in the ICU setting) can be helpful to confirm
4
scheduled for the next morning. While antithyroid drugs and ssKI should the diagnosis in a patient who is thyrotoxic and on amiodarone.
be given at the onset, in this case there is little chance for this treatment to The most appropriate treatment of AIT is still to be determined.
reduce the thyroid hormone levels in 24 hours. Propranolol can provide a All agree that amiodarone should be discontinued immediately in all
rapid and effective preparation for surgery. An initial oral dose of 40 mg patients, where possible. Two recent investigations have demonstrated
73
every 6 hours is appropriate, to be followed by increments of 20 mg every that treatment with prednisone or prednisolone was advantageous in
6 hours, depending on the response, as judged by the heart rate. Although resolution of the hyperthyroidism. 77,78 The mechanism of how steroids
the usual dose is approximately 40 mg every 6 hours, doses of up to help may be related to their anti-inflammatory effect during a destruc-
320 mg/d may be required. Symptoms of tachycardia, anxiety, and sweat- tive type II AIT or to the effect on reduction of conversion of T to T . A
3
4
ing should be relieved within 12 hours. Intraoperative propranolol may be protocol for the treatment of AIT in the ICU is outlined in Figure 103-2.
administered for tachycardia as needed. Propranolol treatment should be Briefly, the critically ill patient should be placed on prednisone 30 mg
resumed within 4 to 6 hours after surgery and maintained for 48 hours. daily, along with an antithyroid drug, PTU 200 mg three times daily or
If the patient is unable to take oral medications perioperatively, then MMI 20 mg twice daily, and potassium perchlorate, 500 mg twice daily.
propranolol can be administered as a 1.0- to 2.0-mg slow intravenous This regimen should continue for 2 weeks, at which time repeat serum
bolus. On postoperative day 3, the dose of propranolol can be halved; it can FT I and FT I and urine iodine level should be measured. If the FT I
3
4
4
be halved again on day 4, and the drug can be discontinued completely on and FT I both are normal, a rapid taper of the steroid and discontinu-
3
day 5, 6, or 7, depending on the symptoms and the response to continu- ation of the potassium perchlorate (because of its poor gastrointestinal
ing antithyroid drug therapy. Propranolol is not indicated in patients with tolerance) should be initiated, and management of the antithyroid drug
asthma, advanced grades of heart block, nor in patients taking quinidine should be as in anyone with hyperthyroidism. If the FT I and/or FT I
3
4
or psychotropic drugs that augment adrenergic activity. β-Blockers gener- are elevated, then the same course of medications should be contin-
ally are safe and effective in congestive heart failure, when administered ued for 2 more weeks, and then remeasurement of the serum thyroid
with caution, and are useful in correcting the high-output failure of thyro- hormone and urine iodine levels would be indicated. In circumstances
toxicosis. Three cases have been reported in which thyroid storm followed where medication is not an option and the severity of the thyrotoxico-
surgery for which the patient had been prepared with propranolol alone. 67-69 sis is causing cardiovascular collapse, patients should be stabilized as

section08.indd 994 1/14/2015 8:28:38 AM