Presented by Michael Fernandes, MD
Chief Complaint: “I’m having trouble breathing.”
History of Present Illness:
This is a 46 year-old female presents to the emergency department as a medical code. Her primary complaint is severe shortness of breath. She is fully alert, complaining that her breathing has been getting progressively worse, as well as feeling her heart beating inside her chest. She has also been experiencing progressive swelling of her extremities and abdomen, and significant weakness and fatigue causing her to have difficulty “getting around”. The duration of these symptoms has been for the past 4-5 months with progressive worsening; today being the worst that she has felt. She had her family call the ambulence to bring her to the emergency department. In the ED, she denies any chest pain or chills. She does admit to having a nonproductive cough with no hemoptysis, and state she is feeling warm, but with no distinct fever. She has no other acute complaints at this time.
Past Medical History: Negative for hypertension, diabetes, or coronar artery disease
Past Surgical History: Laparoscopic cholecystectomy in 2002
Social History: She denies any drug use. She does admit to smoking ½ pack of cigarettes every 2 days, and consumes alcohol socially.
OB/GYN History: G3P3003. Her last menstrual period was 4/22/09.
Family History: Significant for unspecified heart disease; however, she is not aware of any MI, strokes, or diabetes.
Vital Signs: BP: 161/94, P: 192, RR: 32, T 38.3, SpO2: 93% on RA
General: Pt appears her stated age. She is propped up on the stretcher in moderate respiratory distress
HEENT: Head is Normocephalic, atraumatic.
Eyes: Appear to be slightly proptotic, PERRLA, EOMI, sclerae is anicteric, no conjunctival pallor.
Ears: TM are clear, no hemotympanum bilaterally.
Nose: MMM, no erythema, no swollen turbinates, no rhinorrhea or discharge.
Mouth and Throat: MMM, no erythema, no tonsillar exudates, no intraoral lesions.
Neck: Supple, no lymphadenopathy, trachea is midline, carotids are 2+, however, there is significant JVD with the patient sitting upright with the head of the bed at an angle of approximately 85 degrees.
Lungs: Decreased breath sounds on the right, clear on the left. No wheezing, rhonchi, or rales. She had significant use of her accessory muscles. She appears to be acutely dyspneic, however, no cyanosis, no diaphoresis. She also has dullness to percussion on the right lung base posteriorly.
Cardiovascular: Irregularly, irregular rhythm with a tachycardic rate, unable to appreciate any murmurs, rubs or gallops due to the rapid rate, peripheral pulses are 2+ and symmetric in all 4 extremities.
Abdomen: Firm, markedly proturberant. Normoactive bowel sounds. Non-tender, with shifting dullness. No discernable organomegaly, guarding, or rebound.
Extremities: FROM, strength is 5/5 proximately and distally in both upper and lower extremities. She has marked dependent pitting edema bilaterally in her lower extremities.
u Feels warm and moist to the touch. No rashes, no lesions.
Neurological: AAO x3, normal speech and hearing, face is symmetrical. Sensation is equal and intact throughout. She has no gross focal motor deficits.
Lytes: Na:142 K:4.2 Cl:101 CO2:26 BUN:18 Cr:0.8 Glu:123
Ca:9.1 Mg:2.1 Phos:3.5
CBC: WBC:13,200 Hgb:13.9 Plt:372,000
Coags: PT:11.6 INR:1.04 PTT:24.2
LFTs: WNL Albumin:2.8
ABG: pH:7.46 PCO2:34 PO2:61 O2 sat:87.2%
Tropnin I: <0.02
1. What is the primary medical problem with this patient?
a. cardiac tamponade
b. congestive heart failure
c. hypertensive crisis
d. pulmonary embolism
2. Which agent will block the release of stored thyroid hormone?
d. propylthiouracil (PTU)
e. saturated solution of potassium iodide (SSKI)
3. Which of the following groupings of medications represents the proper treatment sequence?
a. propanolol, PTU or methimazole, SSKI
b. propanolol, PTU, SSKI, methimazole
c. propanolol, SSKI, PTU, methimazole
d. propanolol, SSKI, PTU or methimazole
e. SSKI, PTU or methimazole, propanolol
1. E Thyrotoxicosis
As previously stated, thyrotoxicosis refers to a hypermetabolic clinical syndrome resulting from elevation in serum thyroid hormone, specifically free (T4), (T3), or both. Hyperthyroidism is one form of thyrotoxicosis where accelerated thyroid hormone biosynthesis and secretion by the thyroid gland produce the clinical syndrome of thyrotoxicosis. The presence of clinical features such as, tachycardia, tremor, eyelid lag, and warm moist skin in a patient with weight loss, difficulty climbing stairs (fatigue and dyspnea), palpitations, and intolerance of warm temperature are all symptoms pathognomonic for thyrotoxicosis.
2. E saturated solution of potassium iodide (SSKI)
Saturated solution of potassium iodide (SSKI), is necessary to block the release of stored thyroid hormone. Administration of iodide causes temporary inhibition of iodide organification. High intrathyroidal iodide concentration is the crucial factor inducing this response. Thyrotoxic patients are especially sensitive to this effect. The thyroid uptake of 131I is acutely depressed in thyrotoxic patients by administration of 2 mg potassium iodide, whereas more than 5 mg is needed to depress uptake in normal subjects. Concentrations of serum iodide above 5 µg/dl block binding in the thyrotoxic gland. It should be administered 1 hour after PTU to ensure that exogenous iodide is not taken up and used to make more thyroid hormone.
3. A Propanolol, PTU or methimazole, SSKI
Propanalol blocks the activity of the nerves which form the sympathetic nervous system. Overactivity of the sympathetic nervous system is responsible for many of the symptoms of thyrotoxicosis which are “dampened down” by treatment with Propranolol. These include rapidly beating heart (palpitations), shakiness (tremor), intolerance to heat and sweating, diarrhoea, muscle aches and mental symptoms. PTU, exerts its actions by decreasing thyroid hormone synthesis, and by blocking the conversion of thyroxine (T4) to triiodothyronine (T3). While methimazole works, as does PTU, to reduce the levels of thyroid hormone by decreasing thyroid hormone synthesis. In contrast to PTU, methimazole does not significantly inhibit T4 to T3 conversion. Iodide, although it is taken up by the thyroid and used to make thyroid hormone, it can paradoxically suppress release of thyroid hormones from the thyroid gland for several days. Thus, in some patients with severe hyperthyroidism, iodide may be administered to try and shut off stored thyroid hormone release after PTU or methimazole has been started.
Thyrotoxicosis refers to a hypermetabolic clinical syndrome resulting from elevation in serum thyroid hormone levels, specifically free thyroxine (T4), triiodothyronine (T3), or both. Hyperthyroidism is one form of thyrotoxicosis where accelerated thyroid hormone biosynthesis and secretion by the thyroid gland produce the clinical syndrome of thyrotoxicosis. However, hyperthyroidism and thyrotoxicosis are not synonymous. In some patients thyrotoxicosis is caused by hyperthyroidism, but other patients may have thyrotoxicosis caused by inflammation of the thyroid gland, which can cause release of stored thyroid hormone (not accelerated synthesis), or by the ingestion of exogenous thyroid hormone. Differentiating between thyrotoxicosis caused by hyperthyroidism versus other etiology is important because disease management and therapy differs. Thyroid imaging and radiolabeled tracer thyroid uptake measurements combined with serologic data enable specific diagnosis and appropriate patient treatment.
The clinical features of thyrotoxicosis are mostly independent of its cause. The presence of tachycardia, tremor, eyelid lag, and warm moist skin in a patient with weight loss, difficulty climbing stairs (fatigue and dyspnea), palpitations, and intolerance of warm temperature are clinical signs and symptoms pathognomonic for thyrotoxicosis. Elderly patients may have fewer symptoms and limited signs of disease; presenting only with atrial fibrillation, lethargy, or weight loss. The acute presentation or exacerbation of these signs or symptoms may indicate the onset of thyroid storm, a potentially fatal condition that requires immediate recognition and treatment.
The thyroid gland actively transports iodide from circulating blood into the thyroid follicular cells. Subsequently, iodide is organified into tyrosyl residues of thyroglobulin and stored within the thyroid follicles. When required, thyroglobulin undergoes proteolysis with the release of T3 and T4 as the principle active forms of thyroid hormone. In extrathyroidal tissues, some of the T4 is deiodinated to the more metabolically potent T3 hormone.
The process of synthesis, storage, and release of T3 and T4 by the thyroid is normally controlled by the pituitary gland through its release of thyroid stimulating hormone (TSH), also known as thyrotropin. This process involves a negative feedback loop wherein increasing blood levels of T3 and/or T4, inhibit release of thyrotropin-releasing hormone (TRH) from the hypothalamus and TSH (thyrotropin) from the pituitary.
Management includes five components:
Supportive care, blockade of peripheral effects, inhibition of thyroid hormone synthesis, slowing of thyroid hormone release, and treatment of the precipitating cause.
1. Supportive care includes the ABCs, treatment of fever, and, if necessary, treatment of arrhythmias (e.g., atrial fibrillation) with antidysrhythimic agents. A diuretic such as furosemide may be required for the treatment of pulmonary edema.
2. Blockade of the peripheral effects of thyroid hormone is crucial in the treatment of thyroid storm. Propranolol is recommended at an adult dose of 1 to 2 mg IV q5 minutes until control of clinical symptoms is achieved. For patients with conditions such as COPD, asthma, or CHF, a shorter acting and more easily titratable beta-blocker may be preferred, such as esmolol or metoprolol.
3. Inhibition of thyroid hormone synthesis is achieved with a class of drugs known as thionamides, that include propylthiouracil (PTU) or methimazole. These drugs prevent hormone sythesis by interfering with the iodination of tyrosine within the colloid of the thyroid follicle. However, they do not prevent the release of stored thyroid hormone. The onset of action is within 1 hourr and the full therapeutic effect may take several hours.
4. Iodide, in the form of saturated solution of potassium iodide (SSKI) or Lugol’s solution, is necessary to block the release of stored thyroid hormone. It should be administered 1 hour after PTU to ensure that exogenous iodide is not taken up and used to make more thyroid hormone. Lithium can be an alternative in patient with allergy to iodide.
5. Glucocorticoids reduce T4-to-T3 conversion, and may have a direct effect on the underlying autoimmune process when the etiology is Graves’ disease. Their use for the treatment of thyroid storm appears to have improved outcome in at least one study series. It is acceptable to administer hydrocortisone 100 mg IV every eight hours in patients with thyroid storm; in contrast, glucocorticoids are not routinely used in patients with symptomatic, but not life-threatening, hyperthyroidism.
In patients in whom clinical deterioration occurs despite appropriate therapy, removal of thyroid hormone may be attempted through an exchange transfusion, plasmapheresis, or charcoal hemoperfusion.
• Recognition of the symptoms of thyrotoxicosis as a medical emergency
• Labs to order, TSH, free T3, T4
• Beta-blocker (propranolol preferred), if (COPD, asthma, CHF use esmolol or metoprolol); PTU or methimazole; 1 hour after thionamide – Iodide (SSKI or Lugol’s 7% solution)
• Treat precipitants or underlying causes, DKA, MI, infection, trauma
• If patient is allergic to Iodide (SSKI or Lugol’s 7% solution) use Lithium
Conclusion of the case:
The patient’s ABG showed some evidence of hypoxemia with a mild respiratory alkalosis, she was placed on 3 L of oxygen by nasal cannula. The patient’s ECG showed she was in atrial fibrillation with rapid ventricular rate, she was initially started on diltiazem, which did bring down her heart rate, however, only temporarily. Clinically, it was felt that she was thyrotoxic (TSH < 0.002 with clinical presentation), the diltiazem was discontinued and propanolol was started 2 mg IV times 3 doses for a total of 6 mg. PTU 800 mg was given by mouth, and approximately 1 hour later she received 5 drops of Lugol’s 7% solution. MICU was contacted to admit the patient. The patient also received 100 mg of hydrocotisone IV. At the time the patient left the ED, her heart rate was 130 bpm and her BP came down into the 110/70 range. Her condition remained guarded.
The patient was hospitalized for 20 days. Echocardiogram showed a dilated RV, mild LVH, and severe systolic dysfunction with an estimated EF of 20-25%. Treatment of atrial fibrillation and CHF included furosemide, metoprolol, diltiazem, digoxin, and coumadin (thromboembolic prophylaxis). Her hyperthyroidism was treated with PTU 150 mg. three times daily (methimazole may have been a better choice due to its once a day dosing). Her hospital stay was complicated by a pneumothorax requiring chest tube placement following a diagnostic and therapeutic thoracentesis. The patient was readmitted in July 2008 for respiratory failure and unfortunately died.
This case discussion presented by Michael Fernandes, MD
Filed under: Intern Report |