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The Case Files

Fool Me Once

An Uncommon Presentation of PE

Irizarry-Delgado, Freddie; Kakaiya, Varoon; Raziuddin, Ahmed, MD

doi: 10.1097/01.EEM.0000549601.91022.7c
The Case Files

Mr. Irizarry-Delgadois a fourth-year medical student doing an emergency medicine elective clerkship andMr. Kakaiyaa third-year medical student doing an internal medicine core clerkship, both at Weiss Memorial Hospital, University of Medicine and Health Sciences. Dr. Raziuddinis a board-certified emergency physician and internist at Weiss Memorial Hospital, Gottlieb Memorial Hospital (Loyola University), and Westlake Hospital in Melrose Park, IL.

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An 86-year-old African-American woman was brought to the ED by her daughter after two days of nutritional neglect, abdominal pain, and altered mental status. Her daughter said her mother felt lightheaded, appeared dehydrated, and vomited nonbilious watery fluid once. The patient had a history of diabetes mellitus type 2, DVT/PE, dementia, and early signs of parkinsonism.

Her vital signs were remarkable only for tachypnea (24 bpm). Her troponin I was markedly elevated at 1.7 ng/mL. A D-dimer was ordered because of her history of unprovoked DVT/PE, and it showed significant elevation at 4,360. PA and lateral chest x-rays were notable for mild cardiomegaly without any focal consolidation or pulmonary edema. A 12-lead ECG showed a left axis deviation, incomplete right bundle branch block, prolonged QT interval, and poor R wave progression with T wave inversions in inferolateral leads (aVF, V2-V5).

She was admitted for an acute inferolateral NSTEMI, and empirically managed with aspirin 81 mg daily, metoprolol 12.5 mg twice daily, and atorvastatin 40 mg daily. Her troponin I showed a downward trend, and cardiology performed a coronary angiogram, which was unremarkable for clinically emergent coronary artery pathologies. The patient also had a bilateral lower extremity venous Doppler study evident for left lower extremity chronic DVT and right lower extremity subacute DVT.

Further study was recommended to rule out the concomitant finding of a potential subclinical PE. A V/Q lung scan was performed, and results showed normal perfusion throughout the lung parenchyma. These results were not able to ascertain the etiology of the notably increased D-dimer, requiring further testing. A CT angiogram had to be administered the following day to avoid IV dye load. It showed mild pericardial effusion and extensive acute bilateral pulmonary emboli extending from the main pulmonary arteries into the upper lobar, segmental, and subsegmental pulmonary arteries.

An enlarged main pulmonary artery suggestive of pulmonary hypertension secondary to pulmonary embolisms was also found. A transthoracic echocardiogram was performed to determine the extent of pathology caused by the pulmonary embolisms found. It uncovered a moderately to severely dilated right ventricle and atrium and an enlarged IVC diameter size with an increased PCWP indicating an elevated pulmonary arterial pressure.

The patient was started on apixaban 10 mg orally every 12 hours for 12 days and then switched to apixaban 5 mg to be given indefinitely to manage the pulmonary embolisms.

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No Signs or Symptoms

Pulmonary embolisms affect as many as 650,000 people each year in the United States with an estimated 60 percent of cases presenting as sudden death. (Arch Intern Med 2003;163[14]:1711; http://bit.ly/2PP3LHh.) The obstruction, usually a blood clot, of the pulmonary artery or one of its contributing vessels through the pathological lodging of material such as thrombus, fat, air pockets, and metastases released from hematologically-disseminated cancers. The challenge of determining the gravity of this disease based on clinical presentation alone has pushed clinicians to step out of structured workup flowcharts.

Although some pulmonary embolisms exhibit neither, signs and symptoms of pulmonary embolisms often include dyspnea at rest or exertion, tachypnea, tachycardia, and diaphoresis. Risk factors include prolonged immobility, tobacco use, obesity, and pregnancy. A pulmonary embolism can often be recognized from clinical symptoms, but a V/Q scan and CT angiogram are currently considered definitive. (Am J Med 2007;120[10]:871; http://bit.ly/2POCl4c.)

Patient populations most at risk for this type of disease process would be individuals who find themselves in hypercoagulable states such as pregnant women, patients with leukemia/lymphoma, recent trauma victims, bedridden terminally ill patients, and patients who have had recent orthopedic surgeries such as joint and hip replacements. (Mitchell RN, Kumar V. Hemodynamic disorders, thrombosis, and shock. In: Kumar V, et al., eds. Basic Pathology. 6th ed. Philadelphia: WB Saunders; 1997: 60-80).

Patients tend to have an altered ventilation/perfusion ratio because of the shunting of intrapulmonary blood flow caused by lung collapse, cardiovascular dysfunction from decreased cardiac output and stroke volume, and infarction from occlusion of pulmonary vessels meant to perfuse lung tissue.

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The majority of emboli make their way to the pulmonary arterial tree stem from the venous supply of the lower extremities and the pelvis. When determining the characteristics of a PE, we must first find out whether the etiology of this embolus comes from an acute development or a chronic process to decide on the clinical management to be undertaken. The difference between the two is determined based on the location of the embolus in relation to the blood vessel anatomy and whether it occludes the blood flow that is in transit. An acute PE will most likely be centrally placed, locate itself in the bifurcation of the main pulmonary artery, or progress to downstream pulmonary arteries and frankly occlude the vessel. A chronic PE will be eccentrically placed in relation to the intimal layer of the blood vessel; about half of the blood vessel diameter is reduced and collateral revascularization to supplement lack of proper blood flow takes place.

Current clinical guidelines advise using scoring systems, such as Well's or Geneva, to determine the tests needed and the future risk of a patient to develop PE during his life span. (N Engl J Med 2008;358[10]:1037.) Afterwards, if the scoring system favors the diagnosis, a plasma D-dimer is done. A high plasma D-dimer level requires a CTA to confirm the diagnosis and a V/Q perfusion scan if there is any contraindication to the CTA in the patient. (Ann Intern Med 2015;163[9]:701; http://bit.ly/2Pd62z8.)

The V/Q perfusion scan as an alternative for CTA to rule out PE is unreliable, even for a patient in whom a CTA is contraindicated. Some proponents also suggest that CTA alone is sometimes not enough to rule out a clinically significant PE. One study found that negative D-dimer values and a negative CTA were not sufficient to rule out this diagnosis in patients with a high pretest probability for PE. (West J Emerg Med 2018;19[3]:487; http://bit.ly/2JaSu1q.)

More aggressive strategies must be devised to screen these elusive patients. This patient was unique because the V/Q scan reading was normal despite bilateral pulmonary emboli.

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