Page 1418 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 103: Thyroid Disease 991

delirium, stupor, coma, and convulsions may be related to the direct
action of thyroid hormone on the brain. Thyroid hormone can affect TABLE 103-6 Laboratory Findings in Thyroid Storm
40
the concentrations and distributions of various neurotransmitters. Elevated levels of T and free T 4
41
4
Hematologic manifestations of thyrotoxicosis are rarely life threatening. Elevated T level
42
3
It is useful for the intensivist to be aware that hyperthyroidism can cause Hyperglycemia
slight anemia. Anemia may be secondary to hemodilution caused by
increased blood volume, but true reduction of red blood cell mass may be Leukocytosis with left shift
caused by reduced iron absorption and vitamin B deficiency associated Anemia
12
with autoimmune reduction of gastric acidity and intrinsic factor. Hypercalcemia
Minimal thrombocytopenia, with rare instances of idiopathic throm-
bocytopenic purpura, has been reported. Moderate eosinophilia may Hypokalemia
43
occur and has been attributed to relative or absolute hypoadrenalism. Abnormal liver function test findings
A variable relative or absolute lymphocytosis may be associated with Hypercortisolemia
hyperthyroidism. These manifestations may cloud the picture of a
critically ill patient who may have other hematologic perturbations for
different reasons.
Hypercalcemia is the most common life-threatening electrolyte abnor- TREATMENT
mality seen in thyrotoxicosis. Severe hypercalcemia (11.8-19.2 mg/dL) To prevent irreversible cardiovascular collapse, the treatment of thyroid
42
has been reported in several patients with thyrotoxicosis. 44 storm should take a four-pronged approach: (1) therapy to reduce the
The most notable effect of thyrotoxicosis on the gastrointestinal system serum thyroid hormone levels, (2) therapy to reduce the action of
is hypermotility with malabsorption. The myopathy of hyperthyroidism the thyroid hormones on peripheral tissues, (3) therapy to prevent car-
45
may cause weakness of the striated muscles of the pharynx and, perhaps, diovascular decompensation and to maintain normal homeostasis, and
the smooth muscle of the esophagus. Such patients could have dysphagia (4) treatment of the precipitating event(s).
and then could aspirate and develop pneumonia. Patients with hyper- Therapy to Reduce Thyroid Hormone Levels: An antithyroid drug, either
46
thyroidism appear to have a higher incidence of gastritis. This associa-
47
tion is consistent with the hypergastrinemia seen in thyrotoxic patients. PTU or methimazole (MMI), is given to prevent further synthesis of
48
thyroid hormone. These drugs are not available in parenteral form; they
Treatment with H blockers or proton-pump inhibitors is indicated.
2
Rarely, fulminant hepatic necrosis or less severe hepatic injury occurs. can only be given orally or by nasogastric tube. Instances may arise
Although thyroid hormone has no direct toxic effect on the liver, hyper- in which these drugs cannot be given even by nasogastric tube—such
thermia can result in hepatic failure. In patients receiving propylthiouracil as, for example, in patients with infarcted bowel (see below). PTU
offers a slight advantage over MMI in that, in addition to its inhibitory
(PTU), drug toxicity is more likely the cause of fulminant hepatic necro-
sis. Any thyrotoxic patient who presents with jaundice or other signs of effect on hormone synthesis, it decreases the conversion of T to T in
3
49
4
peripheral tissue. PTU should be given in a dose of 200 to 250 mg every
hepatic injury should have a thorough evaluation for possible alternative
causes of liver damage. 6 hours, and MMI should be given in a dose of 25 mg every 6 hours.
Some authors recommend giving an initial PTU loading dose of 600
to 1000 mg, but this strategy has not been proved to be advantageous.
THYROID STORM In patients in whom oral or nasogastric administration is not possible
one 600-mg loading dose of PTU (12 tablets suspended in 90 mL of
Thyroid storm, or thyrotoxic crisis, is a life-threatening though rare water) is given as a retention enema, followed by 250 mg of PTU every
complication of severe thyrotoxicosis. The diagnosis is clinical, bearing 4 hours plus potassium iodide, 1 g diluted in 60 mL of water, given
no direct relation to the absolute levels of thyroid hormones in serum. after the second PTU dose. PTU has an immediate onset of action for
53
The cardinal features of thyroid storm are marked tachycardia, hyper-
tension, and widened pulse pressure; hyperpyrexia (usually greater than
38.5°C [101°F]); and altered mental status. In extreme cases, cardio-
vascular collapse and shock may be seen. Some investigators contend TABLE 103-7 Factors Precipitating Thyroid Storm
that abnormal mentation is the most important diagnostic component Surgery
of thyroid storm. Of course, these clinical features can occur with a Infection
29
multitude of illnesses in the absence of thyrotoxicosis. Some authors
propose a “point system” for determining whether a patient’s condi- Acute psychiatric illness
tion represents true storm or severe thyrotoxicosis, but the distinction Congestive heart failure
between these two entities is not useful clinically. The key to treatment Diabetic ketoacidosis
47
of this condition is to recognize severe thyrotoxicosis or storm and treat
immediately. Recent studies have shown a 10% mortality rate in patients Pulmonary embolism
with “storm.” A blood sample for measurement of the levels of T or Bowel infarction
50
4
free T , or the free T index (FT I), and TSH, by a sensitive method, Parturition
4
4
4
should be obtained immediately in all individuals suspected of having
this disorder. Empirical treatment then should begin. It is prudent to Trauma
obtain a blood sample for cortisol determination before “stress doses” Vigorous palpation of thyroid gland
of steroids are administered for use later in deciding later whether long- Withdrawal of antithyroid medication
term therapy is necessary. Laboratory findings in thyroid storm are Drugs
listed in Table 103-6.
■ PRECIPITATING FACTORS Sympathomimetic drugs such as pseudoephedrine
Amiodarone
Patients who develop thyroid storm usually have poorly controlled Radioactive iodide therapy
thyrotoxicosis; often there is an identifiable precipitating factor 51,52 Iodine-containing contrast agents
(Table 103-7). In many cases, it is difficult to determine whether the
intercurrent illness is the cause or the consequence of the thyroid storm. “Health food” preparations containing seaweed or kelp
section08.indd 991 1/14/2015 8:28:36 AM