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A 46-year-old man is evaluated in the emergency department with a one-day history of progressive dyspnea and nonproductive cough. He does not have hemoptysis, chest pain, or leg discomfort and has no personal or family history of cancer or clotting episodes. He had outpatient ophthalmologic surgery under local anesthesia last week. His medical history includes mild asthma and impaired glucose tolerance, which is controlled by diet. His only medication is a topical optic analgesic.
On physical examination, he is dyspneic and appears anxious; the temperature is 37.6°C (99.8°F), blood pressure is 150/89 mm Hg, heart rate is 110 beats/minute, and respiration rate is 24 breaths/minute. Cardiac examination discloses tachycardia without murmurs or gallops or evidence of jugular venous distention. Examination of the lungs discloses faint bilateral expiratory wheezes, without rhonchi or rales; the hemi-diaphragms descend normally during inhalation. The abdomen is normal. Extremities are not swollen and are nonedematous, nontender, and not cyanotic.
Chest radiograph is normal; an electrocardiogram shows tachycardia. Measurement of arterial blood gases with the patient breathing room air show a Po2 of 93 mm Hg, a Pco2 of 36 mm Hg, and a pH of 7.45. The D-dimer level is 200 mg/dL (normal
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A 46-year-old man is evaluated in the emergency department with a one-day history of progressive dyspnea and nonproductive cough. He does not have hemoptysis, chest pain, or leg discomfort and has no personal or family history of cancer or clotting episodes. He had outpatient ophthalmologic surgery under local anesthesia last week. His medical history includes mild asthma and impaired glucose tolerance, which is controlled by diet. His only medication is a topical optic analgesic.
On physical examination, he is dyspneic and appears anxious; the temperature is 37.6°C (99.8°F), blood pressure is 150/89 mm Hg, heart rate is 110 beats/minute, and respiration rate is 24 breaths/minute. Cardiac examination discloses tachycardia without murmurs or gallops or evidence of jugular venous distention. Examination of the lungs discloses faint bilateral expiratory wheezes, without rhonchi or rales; the hemi-diaphragms descend normally during inhalation. The abdomen is normal. Extremities are not swollen and are nonedematous, nontender, and not cyanotic.
Chest radiograph is normal; an electrocardiogram shows tachycardia. Measurement of arterial blood gases with the patient breathing room air show a Po2 of 93 mm Hg, a Pco2 of 36 mm Hg, and a pH of 7.45. The D-dimer level is 200 mg/dL (normal less then250 mg/dL).
Which of the following would most effectively determine the clinical likelihood of this patient's having a pulmonary embolism?
A. Obtaining the report of the patient's ophthalmologic surgery
B. Measuring hemoglobin A1c
C. Determining the effect of bronchodilators on the patient's signs and symptoms
D. Repeating D-dimer after one therapeutic dose of low-molecular-weight heparin
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dont know indeed
might be C
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Correct answer: C. Determining the effect of bronchodilators on the patient's signs and symptoms.
The likelihood of pulmonary embolism after a negative CT scan is determined by the negative likelihood ratio of the scan as well as the pretest likelihood of pulmonary embolism. This patient with dyspnea has no specific symptoms, family history, or physical examination findings that suggest pulmonary embolism.
The patient has expiratory wheezing on examination and a history of asthma; therefore, resolution of the dyspnea and physical findings after administration of bronchodilators would provide strong evidence of an asthma exacerbation as the cause of his symptoms and thereby decrease the likelihood of his having pulmonary embolism.
The extent of the patient's recent ophthalmologic surgery may affect the risk/benefit relationship of anticoagulation. However, there is no evidence that a more extensive surgery (done under local anesthesia for a relatively brief time) would substantially influence the probability for pulmonary embolism. An elevated hemoglobin A1c may reflect recent episodes of hyperglycemia due to the patient's diabetes, but wouldn't indicate an elevated risk for venous thromboembolism.
The D-dimer fragment is shed into the blood when cross-linked fibrin, present within thrombi and within many areas of inflammation, is digested by fibrinolytic enzymes. D-dimer reflects the presence of thrombosis (or inflammation), but does not reflect the activity of thrombosis and would not decrease acutely in response to anticoagulation.
Key point
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D-dimer reflects the presence of thrombosis (or inflammation), but does not reflect the activity of thrombosis.
