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DIAGNOSTIC REASONING CATHERINE C. BURKE, MS, APRN, BC, ANP, AOCN®—ASSOCIATE EDITOR

Diagnosis of

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 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 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 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 . 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 ( > 20 per minute); ; and (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. Widening of the alveolar to arterial Increasing age Smoking gradient (> 20 mm/Hg) may be more sen- Stroke Indwelling venous catheters sitive than arterial oxygen pressure alone Large pelvic tumors (Dalen, 2002; Hyers, 2000; Riedel, 2004). Figure 2. Risk Factors for Pulmonary Embolism Although and respiratory alkalosis are nonspecifi c, they are the classic fi ndings on arterial blood gas. A normal arterial oxygen pressure is found history. The tool can be used to rapidly who require supplemental oxygen and in 15% of patients, and a normal alveolar assess the clinical probability of PE (see monitor patients who have a drop in to arterial gradient is found in 10%–15% Table 2). A diagnosis of PE is unlikely in oxygen saturation (Feied, 2002; Kline & of patients (Desai, 2002). patients given a score of four points or less Runyon, 2006). Room air pulse oximetry (van Belle et al., 2006). Within that group, will fall lower than 92% in most patients Electrocardiogram about 5% of patients will be diagnosed with PE. Patients with a room air pulse with PE. oximetry of 95% or more at diagnosis of and Chest X-Ray PE will have a signifi cantly lower prob- An EKG and CXR should be performed Physical Examination ability of in-hospital complications (Kline in all patients to support the clinical et al., 2003). suspicion of PE and exclude alternative Physical examination of patients with suspected PE should be performed in a systematic, thorough manner because Table 1. Prevalence of Presenting Signs and Symptoms the clinical picture varies widely. Some of Pulmonary Embolism patients may present only with a change in vital signs; others are dyspneic, SIGN OR SYMPTOM PRESENTATION (%) hypoxic, acutely ill, and unstable. If the presentation is not obvious, astute Sudden onset of shortness of breath at rest or with exertion; 73–84 dyspnea or worsening of chronic dyspnea clinicians will look for subtle changes in Tachypnea 70–96 patients’ conditions. Tachypnea, tachy- Chest pain under the breastbone or on one side 66–90 cardia, and a complaint of chest pain may • Pleuritic 66–74 be present. of the lungs may • Nonpleuritic 14 elicit a or . A Rales 51–58 Unexplained anxiety 50–65 with blood-tinged may Fever 43 be present (Stein & Firth, 2003). Clini- Cough of sudden onset 37–73 cians should examine patients for a posi- Third or fourth heart sound gallop 34 tive Homan’s sign and evidence of DVT, Signs and symptoms of thrombophlebitis 32 which includes extremity swelling, pain, Tachycardia (heart rate > 100 beats per minute) 30–50 Lower-extremity edema 24–28 redness, or a palpable cord of a throm- Cardiac murmur 23 bosed vein. Patients may exhibit anxiety 19 or cyanosis because of hypoxemia and Hemoptysis 13–30 have a low room-air pulse oximetry. Fur- Diaphoresis 11–36 ther evaluation with an arterial blood gas New onset of wheezing 9 Syncope 5–13 is recommended. Note. Other presenting symptoms have been reported, including decreased pulse oximetry less Pulse Oximetry than 92% on room air, splinting of ribs with , lightheadedness, dizziness, and new car- diac arrhythmia. Pulse oximetry is not helpful in the Note. Based on information from Desai, 2002; Feied, 2002; Stein & Firth, 2003. diagnosis of PE but will identify patients

Clinical Journal of Oncology Nursing • Volume 11, Number 3 • Diagnostic Reasoning 345 (Hyers, 2000). V/Q scanning does not Acute coronary syndrome D-Dimer require IV contrast and therefore is the Angina D-dimer is a fi nal product of fi brin imaging modality of choice for patients degradation. A positive serum D-dimer with major renal impairment, anaphylax- indicates that high levels of fi brin degra- is to IV contrast, and pregnancy (Piazza Carcinoma dation products are present in the blood. Chronic obstructive pulmonary disease & Goldhaber, 2006). Fibrin degradation products are released Congestive heart failure V/Q scanning is an indirect study of into the blood as a result of fi brinolysis, Myocardial infarction embolism because it shows perfusion which occurs with signifi cant clot for- or pleuritis abnormality. Defects in tracer uptake mation and degradation or because of Pneumonia when inhaled into the lungs are reported an endovascular thrombus (Neff, 2003). Pneumothorax as normal, near normal, or indicating The enzyme-linked immunosorbent as- low, moderate, or high probability for Figure 3. say method is the preferred testing pro- PE (Ramzi & Leeper, 2004). In 1990, the for Pulmonary Embolism cess. Almost all patients with a proven Prospective Investigation of Pulmonary pulmonary embolus will have a D-dimer Embolism Diagnosis ([PIOPED], 1990) level of more than 500 ng/ml (Desai, trial, a multi-institutional study of V/Q 2002). diagnoses (Riedel, 2004). EKG fi ndings scanning and pulmonary angiography, Measurement of D-dimer is an excel- are abnormal, but nonspecifi c, in as many assessed diagnostic specifi city and sen- lent test to rule out the diagnosis of PE. as 70% of patients with PE and may be sitivity of V/Q scans for the diagnosis of A negative test is sensitive in low-risk normal in young, previously healthy pa- PE. The study revealed that a V/Q scan patients, and the workup for PE can tients (Dalen, 2002; Piazza & Goldhaber, with normal fi ndings virtually excludes stop if the D-dimer level is normal. A 2006; Ramzi & Leeper, 2004). In patients PE because occlusive PE of all types normal D-dimer can exclude PE in more with a minor pulmonary embolus, the produces a defect of perfusion. A V/Q than 90% of cases (Martino et al., 2005); EKG may show only sinus tachycardia scan with high-probability findings is however, the test is nonspecifi c and can- or nonspecifi c ST-T wave. A normal EKG virtually diagnostic for PE and mandates not be used alone to establish the diag- is very unusual in patients with an acute treatment. nosis. An elevated D-dimer level may be pulmonary embolus. An EKG also can be Although V/Q scanning is sensitive seen in hospitalized patients, especially used to rule out other diagnoses, such enough to serve as a screening test, speci- patients with cancer and those who re- as myocardial infarction or pericarditis fi city is limited. A low or indeterminate cently had surgery. Elevated levels also (Desai, 2002; Goldhaber, 2004; Riedel, may be seen in patients with infl amma- 2004). Twenty-five percent of patients tory diseases, pneumonia, myocardial with a proven pulmonary embolus have Table 2. Pretesting Assessment infarction, sepsis, pregnancy, trauma, EKGs that are unchanged from baseline for Probability of Pulmonary and disseminated intravascular coagula- (Feied, 2002). tion (Riedel, 2004; Schoepf, Goldhaber, Embolism A CXR often is the fi rst imaging pro- & Costello, 2004). Further confi rmatory cedure that is obtained when patients POINTS POSITIVE FEATURES testing is required in the setting of a present with dyspnea. A normal film positive D-dimer test (Ebell, 2004; Rath- 3 Clinical signs and symptoms in patients with severe, acute dyspnea bun, Whitsett, & Raskob, 2004). of deep vein thrombosis without wheezing is very suspicious for PE. The CXR is more helpful in excluding 3 Alternative diagnosis less like- other conditions that mimic PE, such as Diagnostic Imaging ly than pulmonary embolism pneumothorax, pneumonia, left-sided The confi rmation or exclusion of PE 1.5 Heart rate greater than 100 heart failure, tumor, rib fracture, mas- may be achieved through multiple diag- beats per minute sive pleural effusion, and lobar collapse nostic mechanisms and imaging studies (Riedel, 2004). 1.5 Immobility or surgery in the (see Figure 4). The diagnostic tool most Three rare fi ndings indicative of PE previous four weeks appropriate for a particular case should (i.e., , Hampton’s hump, be determined by patients’ medical his- 1.5 Previous venous thromboem- and Palla’s sign) may be present on CXR tories, allergy profi les, and conditions. bolism (Piazza & Goldhaber, 2006). Westermark sign is the focal area of decreased pul- 1 Hemoptysis monary vasculature, which commonly Ventilation and Perfusion Scan 1 Malignancy (currently receiv- occurs when large emboli affect a lobe or The ventilation and perfusion (V/Q) ing treatment, including pallia- entire lung or in patients with pulmonary scan consists of two sequential tests. The tive therapy; patient received embolus complicated by infarction of the perfusion scan shows the distribution of treatment in the past six lung (Dalen, 2002). Hampton’s hump is a microvascular blood fl ow in the lungs months.) peripheral wedge-shaped, pleural-based after IV injection of a radionuclide, and Note. Based on information from Neff, 2003; density with apex pointing to the hilum. the ventilation scan shows distribution Ramzi & Leeper, 2004; van Belle et al., 2006; Palla’s sign is the presence of an enlarged, of ventilation in the small airways after Wells et al., 2001. right, descending pulmonary artery. inhalation of a radioactive gas or aerosol

346 June 2007 • Volume 11, Number 3 • Clinical Journal of Oncology Nursing study does not rule out a diagnosis of PE, PE is absent (Ramzi & Leeper, 2004). Pulmonary embolism is excluded by and further evaluation should be under- CT angiography can resolve increas- • Normal pulmonary angiogram taken (Ramzi & Leeper, 2004; Riedel, ingly smaller diameter subsegmental • Normal perfusion scan 2004). A V/Q scan often is not diagnostic pulmonary vessels without the need • Normal thin collimation (multidetector) in patients with chronic pulmonary dis- for invasive pulmonary artery catheters • CTPA [computed tomography pulmo- ease or pleural effusion (Ebell, 2004). (Garg, 2005). PIOPED II studied pa- nary angiogram] tients with suspected PE and concluded • Low probability perfusion scan and low Pulmonary Angiogram that CT angiography was as accurate clinical probability • Normal D-dimer level (assay with high Pulmonary angiogram is considered as invasive pulmonary angiography for sensitivity) and low clinical probability the gold standard for the diagnosis of PE the diagnosis of acute PE (Quiroz et al., 2005). Scans that are positive or nega- • Normal single detector spiral CTPA and to which sensitivity and specifi city of all compression ultrasonography (or com- tive to the level of subsegmental arter- other radiographic methods for diagnosis puted tomography venography) ies are considered diagnostic, and no of PE have been compared. Pulmonary • Nondiagnostic lung scan and normal angiography is an invasive imaging pro- other imaging is necessary. A pulmonary results on serial leg testing cedure of the body’s blood vessels and is angiogram is recommended for patients unavailable in many clinical settings. It who have a normal scan and no evi- Pulmonary embolism is confi rmed by requires placement of a catheter from a dence of lower extremity DVT (Martino • Intraluminal fi lling defect on pulmonary peripheral vein, either in the arm or the et al., 2005; Neff, 2003; Riedel, 2004; angiogram • Intraluminal fi lling defect on spiral CTPA groin, which is threaded through the Schoepf et al., 2004; Wittram, Maher, • High probability scan and moderate or vascular system to the right-sided cardiac Halpern, & Shepard, 2005). Iodinated high clinical probability structures and into the main pulmonary contrast agents are needed; therefore, CT angiography is contraindicated in pa- • Apparative evidence of acute DVT [deep artery. Contrast dye is injected through vein thrombosis] with nondiagnostic tients with renal impairment and severe the catheter, allowing the multiple ves- scan or spiral CTPA sels of the pulmonary system to be visible allergy to the contrast material. on x-ray. Figure 4. Test Results That Pulmonary angiography should be Conclusion Effectively Exclude or Confi rm considered only if all other imaging Pulmonary Embolism studies are inconclusive. Passage of the PE often is asymptomatic, has varied presentations, may masquerade as other Note. From “Diagnosing Pulmonary Em- catheter through the right ventricle Postgraduate diseases, and may cause sudden death. bolism,” by M. Riedel, 2004, may provoke nonsustained ventricu- Medical Journal, 80, p. 315. Copyright 2004 Ruling out PE should be a priority to lar tachycardia. Patients feel hot and by the British Medical Journal Publishing Ltd. clinicians who believe it is the cause of flushed when the contrast media is Reprinted with permission. injected and also may experience tran- patients’ shortness of breath or tachy- sient hypotension and coughing spasms cardia. If PE is not immediately fatal, the diagnosis should be made quickly (Goldhaber, 2005). A negative test es- for clinical events and death (Hyers, and appropriate treatment initiated. sentially excludes the diagnosis of PE 2000). In a disease state that often is Reducing the mortality rate from pul- (Desai, 2002). Pulmonary angiography deadly, prevention is paramount. is contraindicated in patients who are monary embolus is connected to the prevention of and prophylaxis against pregnant and those who have a signifi - Author Contact: Lynn M. Cloutier, RN, MSN, venous thromboembolism. Preventive cant bleeding risk, renal insuffi ciency, ACNP, AOCN®, can be reached at lcloutier@ mechanisms include early mobility and or a known right-sided heart thrombus mdanderson.org, with copy to editor at ambulation after surgery, leg exercises (Riedel, 2004). [email protected]. while in bed and sitting for long peri- Spiral Computed Tomography ods of time, compression stockings, References and sequential compression devices. Angiography and Chest Compression stockings must provide a Cardin, T., & Marinelli, A. (2004). Pulmo- Computed Tomography Angiogram gradient of 30–40 mm/Hg or more to nary embolism. Critical Care Nursing High-resolution helical (spiral) CT be effective. These stockings provide Quarterly, 27, 310–322. Cobelli, R., Zompatori, M., De Luca, G., angiography is gaining wide acceptance the highest level of pressure at the toes Chiari, G., Bresciani, P., & Marcato, C. as fi rst-line imaging for the detection and gradually decrease in pressure up (2005). Clinical usefulness of computed of PE. The sensitivity and specifi city of to the level of the thigh (Feied, 2002). tomography study without contrast injec- the test may be as high as 100% (Cobe- Prophylaxis can be obtained with frac- tion in the evaluation of acute pulmonary lli et al., 2005). Following the injection tionated or unfractionated heparin in embolism. Journal of Computer Assisted of contrast, the entire chest can be individuals who must be confi ned to bed Tomography, 29, 6–12. scanned for abnormalities. Intraluminal for long periods of time. Studies show Colp, C., & Stein, M. (2001). Re-emergence fi lling defects are identifi ed in segmental that combinations of drug therapy and of an “orphan test” for pulmonary embo- or pulmonary arteries, and scanning compression methods are more effective lism. Chest, 120, 5–6. may diagnose other abnormalities in than either approach alone. Preventive Dalen, J.E. (2002). Pulmonary embolism: as many as two-thirds of patients when therapy provides tenfold risk reduction What have we learned since Virchow?

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348 June 2007 • Volume 11, Number 3 • Clinical Journal of Oncology Nursing