Transcript Thyroid storm

Thyroid storm
DR KH. ELMIZADEH
GYNE-ONCOLOGIST
Thyroid storm is a rare, life-threatening condition
characterized by severe clinical manifestations of
thyrotoxicosis
incidence of thyroid storm in hospitalized patients was 0.20
per 100,000 per year
the mortality rate of thyroid storm is substantial (10 to
30 percent)
RISK FACTORS
Although thyroid storm can develop in patients with long-standing
untreated hyperthyroidism (Graves’ disease, toxic multinodular goiter,
solitary toxic adenoma), it is often precipitated by an acute event such as
thyroid or nonthyroidal surgery, trauma, infection, or parturition.
In addition, irregular use or discontinuation of antithyroid drugs is a
commonly reported precipitant of thyroid storm
The advent of appropriate preoperative preparation of hyperthyroid
patients undergoing surgery for hyperthyroidism has led to a dramatic
reduction in the prevalence of surgically-induced thyroid storm.
Why certain factors result in the development of thyroid
storm.
Hypotheses include :
-A rapid increase in serum thyroid hormone levels
-Increased responsiveness to catecholamines
-Enhanced cellular responses to thyroid hormone .
-The degree of thyroid hormone excess elevation of T4 and T3 and
suppression of TSH typically is not more profound than that seen in
patients with uncomplicated thyrotoxicosis. However, one study found
that while the total T4 and T3 levels were similar, the free T4 and free T3
concentrations were higher in patients with thyroid storm
CLINICAL FEATURES
Patients with severe and life-threatening thyrotoxicosis typically have an exaggeration of the
usual symptoms of hyperthyroidism.
Cardiovascular symptoms in many patients include tachycardia to rates that can exceed 140
beats/minute and congestive heart failure. Hypotension, cardiac arrhythmia, and death from
cardiovascular collapse may occur.
Hyperpyrexia to 104 to 106°F is common.
CNS symptoms :Agitation, anxiety, delirium, psychosis, or coma are also common and are
considered by many to be essential to the diagnosis.
GI symptoms: Severe nausea, vomiting, diarrhea, abdominal pain, or hepatic failure with
jaundice can also occur.
Physical examination :
may reveal goiter, ophthalmopathy ,lid lag, hand
tremor, and warm and moist skin.
Laboratory findings
All patients have low TSH and high free T4 and/or T3 concentrations.
The degree of thyroid hormone excess typically is not more profound
than that seen in patients with uncomplicated thyrotoxicosis.
Other nonspecific laboratory findings may include mild
hyperglycemia, mild hypercalcemia, abnormal liver function tests,
leukocytosis, or leukopenia.
Diagnosis
The diagnosis of thyroid storm is based upon the presence of severe and lifethreatening symptoms (hyperpyrexia, cardiovascular dysfunction, altered
mentation) in a patient with biochemical evidence of hyperthyroidism (elevation
of free thyroxine [T4] and/or [T3] and suppression of [TSH]).
There are no universally accepted criteria or validated clinical tools for
diagnosing thyroid storm.
This system is probably best used as a clinical guideline rather than a
strict formula to include or exclude thyroid storm as a diagnosis.
Thermoregulatory
Temp. (°F) Points
99-100
5
100-101
10
101-102
15
102-103
20
103-104
25
>104
30
CNS
Alteration
mild (agitation)
Congestive Heart Failure
Points
10
moderate
(delirium, psychois) 20
Symptom
Points
mild (pedal edema)
5
Moderate
(bibasilar rales)
10
Severe
(pulmonary edema)
Atrial fibrillation
15
10
Gastrointestinal
Symptom
Precipitant History
Points
Moderate
(n/v/d, abd pain)
severe (jaundice)
absent 0
10
20
present 10
•Scores greater than 45 are indicative of
thyroid storm
• Scores 25-45 suggest thyroid storm
• Scores less than 25 are unlikely to be
thyroid storm.
Thyroid function tests (TSH) should be assessed in all patients in
whom there is a clinical suspicion of thyroid storm.
If the TSH is below normal, free T4 and T3 should be measured.
The degree of hyperthyroidism is not a criterion for diagnosing
thyroid storm.
Radioiodine uptake is not necessary for the diagnosis of thyroid storm,
and treatment should not be delayed for scanning in patients with
clinical manifestations of thyroid storm.
TREATMENT
The therapeutic options for thyroid storm are expanded from those
used for uncomplicated hyperthyroidism, with additional drugs often
used such as glucocorticoids and an iodine solution.
The standard drugs are given in higher doses and with more
frequent dosing. In addition, full support of the patient in ICU is
essential, since the mortality rate of thyroid storm is substantial.
The principles of treatment outlined below are based upon
clinical experience and case studies, since there are no
prospective studies. They are frequently also applied to
patients with severe hyperthyroidism who do not fully meet
the criteria for thyroid storm.
The therapeutic regimen typically consists of multiple
medications, each of which has a different mechanism of
action.
●A beta blocker to control the symptoms and signs induced by increased adrenergic tone
●A thionamide to block new hormone synthesis
●An iodine solution to block the release of thyroid hormone
●An iodinated radiocontrast agent (if available) to inhibit the peripheral conversion of (T4) to
(T3)
●Glucocorticoids to reduce T4-to-T3 conversion, promote vasomotor stability, and possibly treat
an associated relative adrenal insufficiency
●Bile acid to decrease enterohepatic recycling of thyroid hormones
For patients with clinical features of thyroid storm or with severe thyrotoxicosis
who do not fully meet the criteria for thyroid storm), we begin immediate
treatment with a beta blocker (propranolol in a dose to achieve adequate
control of heart rate, typically 60 to 80 mg orally every four to six hours, with
appropriate adjustment for heart rate and blood pressure)
and either propylthiouracil (PTU) 200 mg every four hours or methimazole (20
mg orally every four to six hours).
PTU is favored over methimazole because of PTU’s effect to decrease
T4 to T3 conversion.
However, for severe but not life-threatening hyperthyroidism,
methimazole (20 mg every six hours) may be preferred because of its
longer half life, lower risk of hepatic toxicity, and because it ultimately
restores euthyroidism more quickly than PTU. Patients initially
treated with PTU should be transitioned to methimazole before
discharge from the hospital.
One hour after the first dose of thionamide is taken, we
administer iodine (saturated solution of potassium iodide
[SSKI], five drops orally every six hours, or Lugol's solution,
10 drops every eight hours).
The administration of iodine should be delayed for at least
one hour after thionamide administration to prevent the
iodine from being used as substrate for new hormone
synthesis.
For patients with clinical features of thyroid storm, we also
administer glucocorticoids (hydrocortisone, 100 mg intravenously
every eight hours) and cholestyramine (4 g orally four times daily) to
reduce enterohepatic circulation of thyroid hormone.
In addition, supportive therapy and recognition and treatment of any
precipitating factors (eg, infection), in addition to specific therapy
directed against the thyroid, may be critical to the final outcome.
Many patients require substantial amounts of fluid, while others may
require diuresis because of congestive heart failure. Digoxin and beta
blocker requirements may be quite high because of increased drug
metabolism as a result of hyperthyroidism. Infection needs to be
identified and treated, and hyperpyrexia should be aggressively
corrected. Acetaminophen should be used instead of aspirin, since
the latter can increase serum free T4 and T3 concentrations by
interfering with their protein binding.
●After
the clinical manifestations of thyroid storm are improved, longterm therapy is required to prevent a recurrence of severe
thyrotoxicosis. For definitive therapy of patients with
hyperthyroidism secondary to Graves’ disease, toxic multinodular
goiter, or toxic adenoma, we suggest radioiodine therapy as our first
choice, given its lower cost and lower complication rate than surgery
(Grade 2B). Surgery is an option for patients with hyperthyroidism
due to a very large or obstructive goiter.
THANKS FOR YOUR
ATTENTION