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Diagnosis of Pulmonary Embolism

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Diagnosis of Pulmonary Embolism This material is protected by U.S. copyright law. Unauthorized reproduction is prohibited. To purchase quantity reprints, please e-mail [email protected] or to request permission to reproduce multiple copies, please e-mail [email protected]. DIAGNOSTIC REASONING CATHERINE C. BURKE, MS, APRN, BC, ANP, AOCN®—ASSOCIATE EDITOR Diagnosis of Pulmonary Embolism Lynn M. Cloutier, RN, MSN, ACNP, AOCN® Case 1: A 77-year-old Caucasian woman with a probable diagnosis of ovarian cancer developed an acute onset of short- ness of breath two days after being discharged for a workup of symptomatic ascites. Her medical history was signifi cant for hypertension and atrial fi brillation, and she was taking therapeutic doses of coumadin. She presented to the emergency department; was found to have a large, left pleural effusion; and was admitted to the hospital. A thoracentesis removed 2.1 L of fl uid. The patient’s respiratory distress improved; however, she experienced a second episode of sudden onset shortness of breath prior to her anticipated discharge. She was afebrile, with a room air pulse oximetry of 80%, pulse of 121 beats per minute, and respiratory rate of 28. A chest x-ray (CXR) showed only a small pleural effusion remaining on the left. An electrocardiogram (EKG) showed atrial fi brillation. A chest computed tomography (CT) was performed and showed bilateral pulmonary emboli. Case 2: A 57-year-old, obese, African patient’s hospitalization, she developed a abdomen and pelvis was performed to American woman with newly diagnosed rapid heart rate of 139 beats per minute. delineate the extent of the abscess and endometrial cancer presented to clin- An EKG showed sinus tachycardia, and a to reassess the initial abscess. The CT ic with a palpable left supraclavicular CXR revealed atelectasis and diminished showed an incidental fi nding of a pul- lymph node. A CXR revealed mediastinal lung volumes. Laboratory evaluation re- monary embolus in the right lower lobe, adenopathy, and a chest CT was per- vealed leukocytosis with a white blood which was confi rmed by chest CT. The formed to further delineate the size of cell count of 21.5/mm3, and a cardiac patient was completely asymptomatic. the mass and evaluate for metastases. The panel was negative. Her room air pulse She never displayed shortness of breath, CT revealed a Hampton’s hump and also oximetry was 100%. Following a diagno- she did not require oxygen, and her pulse was positive for pulmonary embolism sis of pneumonia, the patient developed rate was normal. (PE). The patient’s vital signs were nor- respiratory distress, was intubated, and These patients all have a diagnosis of mal, and she did not have any respiratory was transported to the intensive care cancer or an anticipated diagnosis of symptoms. An ultrasound of her lower unit. Continued workup with a chest CT cancer and a diagnosis of PE. Their cases extremities was negative for deep vein revealed bilateral pulmonary emboli and are more different than similar, which thrombosis (DVT). pulmonary metastases. illustrates how the presentation of PE Case 3: A 31-year-old Caucasian wom- Case 4: A 58-year-old Caucasian is sometimes unusual, often varied, and an receiving chemoradiation for cervical woman with a history of cervical cancer usually found incidentally. cancer was admitted to the hospital with underwent surgical debulking after an diffuse abdominal pain that occurred two aborted pelvic exenteration. She devel- days after completion of brachytherapy oped a wound dehiscence and pelvic Discussion and Analysis with after-loading tandem and ovoids, a abscesses postoperatively. A pelvic drain PE is an extremely common and highly treatment requiring complete bed rest was placed, and she was admitted to the lethal condition that is a leading cause for 48 hours. On admission, further re- hospital for IV antibiotic therapy. Dur- of death in all age groups and the fi rst- view of systems was negative; however, ing her hospitalization, she developed a or second-most common cause of un- the patient mentioned that she lived in second surface abscess and a CT of the expected death in most age groups. a two-story house and had shortness of breath after climbing stairs—a symptom she attributed to her body habitus and Lynn M. Cloutier, RN, MSN, ACNP, AOCN®, is a nurse practitioner at the University of Texas M.D. anemia. Her height was 162.5 cm, and Anderson Cancer Center in Houston. her weight was 135.9 kg. During the Digital Object Identifi er: 10.1188/07.CJON.343-348 Clinical Journal of Oncology Nursing • Volume 11, Number 3 • Diagnostic Reasoning 343 PE is the most serious complication of In approximately 25% of patients with pose a patient for PE, and most patients venous thrombosis and the third-most PE, the initial clinical manifestation is who develop PE are immobilized for less common cardiovascular problem after sudden death (Heit, 2006). than two weeks (Stein & Firth, 2003). coronary artery disease and stroke (Stein Virchow described PE in the mid- & Firth, 2003). More than 400,000 cases 1800s, when he showed how venous are undiagnosed in the United States blood clots travel to the pulmonary ar- Pathophysiology annually, resulting in 100,000 patient tery and form emboli. He noted that PE may result from the blockage of an deaths (Feied, 2002). PE is associated the clinical manifestation of PE was as- artery in the lungs by fat, air, a tumor, or with 300,000–600,000 hospitalizations phyxiation, caused by blockage of the a blood clot. This discussion will focus on each year (Garg, 2005). main trunks of the pulmonary artery. He blood clots. Normally, microscopic clots Prompt diagnosis and treatment of PE proposed that all primary thromboembo- are formed and destroyed constantly can dramatically reduce morbidity and lism resulted from three factors known in venous circulation, allowing for lo- mortality; therefore, a workup should be as Virchow’s triad—stasis of blood fl ow, cal hemostasis in response to an injury initiated as soon as any suspicion exists. injury to the vein, and hypercoagulability without enabling a clot to form. When Unfortunately, the condition is undiag- (Cardin & Marinelli, 2004; Dalen, 2002; the system is disrupted, microthrombi es- nosed far more often than it is diagnosed Riedel, 2004). At least one component cape the normal fi brinolytic system. Most because patients with PE often present of the triad is present in all categories of clots originate in the lower extremities; with vague and nonspecifi c complaints risk factors. the clots may build in the venous system, (Feied, 2002; Kline & Runyon, 2006) break loose, and travel in the venous sys- and classic symptoms are not present tem through the vena cava and into the in many cases (Goldhaber, 2004). PE Risk Factors right side of the heart, causing blockage is not an isolated disease of the chest, The assessment of PE begins with a of the pulmonary blood vessels (Feied, but a complication of DVT (see Figure careful physical examination and deter- 2002; Kline & Runyon, 2006). 1). DVT and PE are part of the same mination of risk factors (see Figure 2) venous thromboembolism process (Rie- (Ramzi & Leeper, 2004). Most patients del, 2004). Although as many as 90% of with PE have a combination of risk factors Presentation pulmonary emboli arise from the veins (Dalen, 2002; Desai, 2002). Immobility, The presentation of patients with PE of the lower extremities, many patients irrespective of the cause, is the most fre- can vary greatly (see Table 1). Young, with PE have no signs or symptoms of quent predisposing factor. Immobiliza- previously healthy patients with excel- DVT (Desai, 2002; Stein & Firth, 2003). tion for even one or two days may predis- lent cardiac reserve may have subtle signs and symptoms. PE tends to mimic other illnesses (Goldhaber, 2004). The classic triad of symptoms, which occur in fewer than 20% of patients, are dyspnea, often with accompanying tachypnea ( > 20 per minute); hemoptysis; and chest pain (pleuritic or substernal) (Riedel, 2004). PE is so lethal that the diagnosis should be sought actively in every patient who presents with any chest symptom that cannot be proven to have another cause (see Figure 3). Clinical Evaluation Prior to the development of diagnostic imaging techniques, the diagnosis of PE was based on dyspnea, hemoptysis, and chest pain (Colp & Stein, 2001). Currently, the diagnosis can be made through a combined approach of physical examination, assessment of risk factors, and imaging studies. Clinicians should assign a pretest prob- ability for PE before proceeding with Figure 1. Deep Vein Thrombosis Caused By Venous Stasis, Resulting objective testing (Hyers, 2000). Wells et in Pulmonary Embolism al.’s (2001) clinical decision rule is based on a seven-feature assessment, assigning Note. Copyright by Kevin A. Somerville/Phototake. All rights reserved. Reprinted with permission. points based on physical examination and 344 June 2007 • Volume 11, Number 3 • Clinical Journal of Oncology Nursing Air travel—greatest risk at distances Lower-extremity paralysis Arterial Blood Gas > 5,000 km or 3,100 miles Lupus anticoagulant Arterial blood gas should be performed Atrial fi brillation Major trauma to help establish a PE diagnosis. Charac- Burns Myocardial infarction teristic changes associated with PE in- Nephrotic syndrome Cancer clude a reduced arterial oxygen pressure Cardiomyopathy Obesity and an arterial carbon dioxide pressure Childbirth Oral contraceptive use that is normal or reduced because of hy- Disseminated intravascular coagulation Pregnancy Estrogen or hormone replacement therapy Personal history of deep vein thrombosis or perventilation. Arterial oxygen pressure Family history of deep vein thrombosis or pulmonary embolism may be normal in patients with a minor pulmonary embolism Prolonged bed rest or inactivity pulmonary embolus but is almost never Fracture of the hip or femur Prosthetic cardiac valves normal in patients with massive pulmo- Genetic or acquired hematologic disorders Recent surgery, especially for cancer nary emboli when more than 50% of the Cardiac surgery Reduced cardiac output pulmonary circulation is obstructed sud- Immobilization Sickle cell anemia denly.
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