PULMONARY EMBOLISM – PERMANENT DIAGNOSTIC AND THERAPEUTICAL CHALLENGE
Received for publication: 18th of July, 2013
Revised: 25th of July, 2013
SUMMARY: (Hide the summary)
Pulmonary embolism (PE) is a common problem often hard to diagnose especially when the clinical findings are atypical. We present the case of a 54 years old male patient recently diagnosed with systemic hypertension who experienced a dramatic abdominal and thoracic atypical pain syndrome and supported several episodes of hospitalization in different specialized medical units. The diagnosis of PE needed substantial investigational efforts and individualized therapeutical approach with positive denouement. The challenges for physicians involved in this case consisted in discrepancy between severe clinical manifestations and mild cardiac changes, non-correlation between the total absence of electrocardiographical signs for PE and echocardiographical aspects, the domination of abdominal symptoms, the recurrency of PE and the suprainfection of PE. Despite the remarkable progress of all technical methods with great deal in diagnostic approach we must remind over and over again the major importance of detailed anamnesis for providing valuable informations for adequate diagnosis and therapy.
Pulmonary embolism, abdominal pain, pneumonia, deep vein thrombosis.
Pulmonary embolism (PE) is a common problem often hard to diagnose1 and when the clinical findings are atypical or another pathological symptomatology superimpose the clinical manifestation of PE the diagnostic challenge is more powerful1. Considered one of the “three great cardiovascular killers” along myocardial infarction and stroke1,2 PE positive and differential diagnosis benefits by modern imagistic techniques, especially thoracic computer scan angio-tomography3. However the main problem of present times became excessive use of irradiation imagistic technology4 and decrease of importance of anamnesis, physical exam and clinical judgement5. The consequences of this trend might be low accurate diagnosis, delayed therapeutical measures and evitable repetitive and prolonged hospitalization.
A 54 years old male non-smoker with recent diagnosis of high blood pressure values and history of gastric ulcer in his youth was admitted in Clinical Hospital with gastroenterological profile acusing pain in the right upper and lateral part of the abdomen, associated with nausea, headache and fever (37,80C). The X-ray chest examination shown no abnormalities of the intrathoracic structures (Fig.1), so the physician concentrated on abdominal findings, including abdominal utrasonography, complete endoscopic gastric and colonic vizualization.
Obtained data excluded gastric or colonic disease (including appendicitis or neoplasia), while the laboratory findings revealed the existence of inferior urinary infection, with not specificated etiological agent. The patient was discharged at home with Angiotensin converting enzyme inhibitor (ACEI) and antibiotic therapy recommendation (Zofenopril 30 mg/day, respectively Ciprofloxacinum 500 mg bid for total time of 10 days). But after 2-3 days of stable health condition the previous symptoms reoccurred with amplified severity associated with dyspnea, non-productive cough and fever (380C). The right upper part of abdominal pain extended on right posterior base of thorax and in lower right quadrant of the abdomen. In the Emergency Department the ECG recording was quite normal (Fig.2), chest X-ray exposure, abdominal and urological ultrasonography were performed showing no evidence for acute abdominal disease, but the thoracic image (Fig.3) revealed right hemidiafragm ascension, a few bilateral bazal atelectatic stripes and an increase diffuse reticular network, while the laboratory findings indicated high level of WBC. Therefore the patient was related to Pneumological Clinic under suspicion of interstitial pneumonia. During the presence in this clinic the patient started mucopurulent and haemoptoic cough and he performed angiographic CT scan of the chest. This investigation showed (Fig.4) left and right lateral bazal periferic PE with associated nearby undergoing pulmonary microinfarction, without pleural or pericardic effusion. The diagnostic conclusion was bilateral bazal PE and the patient was transfered in our Cardiological Clinic.
Fig. 1 . Chest X-ray image – Gatroenterological Medical Clinic.
Fig.2. Electrocardiography recorded in Emergency Department; (absence of significant abnormalities)
Fig. 3. Chest X-ray image in Emergency Department : left ventricular hypertrophy, right hemidiafragm ascension, a few bilateral bazal atelectatic stripes and an increase diffuse reticular network.
Fig. 4. Chest CT scan angiography in Pneumological Clinic: left and right lateral bazal periferic PE with associated nearby undergoing pulmonary microinfarction, without pleural or pericardic effusion.
Fig. 5. Transthoracic echocardiography : -Right ventricle (RV)=29 mm, right atrium (RA)=25 mm, Pulmonary artery systolic pressure (PASP)=63 mmHg, second degree mitral regurgitation, normal sized left ventricle (LV) and left atrium (LA), LVEF=52%
Clinical exam on admission revealed severe altered physical condition, fever (38,90C), dyspnea, mucopurulent and haemoptoic cough, severe right bazal thoracic pain with respiratory movement exacerbation and antalgic immobilization of right side of the body, nausea, diaphoresis and fatigue. Objective physical findings consisted of tachycardia (112 beats/min.), absent vesicular murmur in right bazal side of thorax, right hypochondrium abdominal pain with upper extension and respiratory exacerbation. Laboratory findings showed elevated WBC with granulocytes, high level of blood fibrinogen, while the ECG aspect was unchainged (no electrical signs for right cavities overload) as previously recorded in Emergency Department and Pneumological Clinic. Transthoracic echocardiography (Fig.5) confirmed a moderate pulmonary hypertension with normal sized right cavities, mild degenerative mitral regurgitation, vegetation free valvular structures and preserved left ventricular ejection fraction (LVEF). In this moment the diagnostic problems were: bilateral PE complicated with right bazal pulmonary infarction, sepsis of unknown etiology. The next step was to perform more bacteriological investigations (blood cultures, urine culture, sputum culture). We discovered Escherichia coli in respiratory tract, but it’s presence did not explain in that moment the severity of digestive symptoms. Therefore we reconsidered abdominal ultrasonography and X-ray and concluded with surgery specialist exam, but all these procedures did not find a local cause for abdominal symptoms.
Fig. 6. Chest X-ray in Cardiological Clinic : modified aspect of the right lung suggesting the presence of pneumonia, associated with right basal pleurisy and right upper hemidiaphragm ascension
A new X-ray chest exposure (Fig.6) revealed modified aspect of the right lung suggesting the presence of pneumonia, associated with right basal pleurisy and right upper hemidiaphragm ascension. This new image conducted us to conclusion of an existing right bazal pulmonary infective process, with material incetive of right hemifiaphragm and consecutive upper right abdominal pain reaction.
Fig. 7. Transthoracic echocardiography : RV=39 mm, RA=34 mm, PASP=55 mmHg, second degree mitral regurgitation, normal sized LV and LA, LVEF=49%
Fig. 8. Left lower limb popliteal venous ultrasonography : dilated and compressible left popliteal vein, containing "sludge" blood
We began medical therapy : oral hydration (2-2,5 litres/day) with gastric protective food, anticoagulation (unfraction heparin in continous venous perfusion 1000-1200 IU/hour, maintaining APTT between 50-75 seconds and continued with Acenocoumarol once a day dose after 5 days association with heparin, maintaining INR~2), wide spectrum intravenous antibiotherapy (Cefuroxime 4,5 g/day, according to sputum culture antibiogram) and expectorant (oral N-Acetyl-cysteine 600 mg/day).
The 3rd day after admission the patient developed a brutal right bazal thoracic and upper abdominal pain syndrome associated with severe general condition, high fever (39,60C), reactive hyperalgesia and rigidity of right body contracted musculature in antalgic position, periferic cyanosis and severe dyspnea. In absence of any new ECG disturbances the transthoracic echocardiography (Fig.7) showed acute right cavities dilatation, with the same moderate pulmonary hypertension and preserved LVEF, suggesting a new episode of PE. Searching for the “guilty” we return to the anamnestic patient account and he remembered that during the first hospitalization he has had a not mentioned short episode of painful left lower limb oedema and he has done self intensive local massage with consecutive mild improvement of local discomfort. So we performed lower limb venous ultrasonography (Fig.8) and we confirmed the suspicion of left deep popliteal venous thrombosis. Probably this was the “primum movens” event for developing PE from the beginning of all symptoms.
The concluded diagnosis was : acute bazal bilateral pulmonary embolism complicated with right bazal recurrent pulmonary infarction, moderate pulmonary hypertension, acute vascular cor pulmonale, acute right bazal pneumonia with E. coli, mild degenerative mitral insufficiency, 2nd degree systemic hypertension high added risk, NYHA II class preserved ejection fraction heart failure, recent left lower limb profound venous thrombosis.
The patient evolution was favourable with improvement of general condition, cough, fever and dyspnea disappearance, echocardiographic parameters normalization (Fig.9) and no more pathological findings at X-ray chest control before discharging (Fig.10). The patient was discharged to home with ACEI and oral anticoagulant therapy for at least 6 months, controlling INR each month (therapeutical target ~2) and cardiac reevaluation at the end of this period.
Related case is a fine example for polymorphic clinical picture of PE especially when it is associated with extrapulmonary symptoms. In this particular situation we noted the debut with lack of pulmonary symptoms for PE and the predominance of abdominal manifestations, culminating with suspicion of acute appendicitis and/or proliferative colonic process. That explains investigational efforts concentration (digestive endoscopy, ultrasonography and X-ray exposure) to find out the underlying cause. After admission in our Cardiological Clinic the added sepsis to PE rised a great challenge to determine the source of persistent infection in a patient previously treated with antibiotics: acute associated pneumonia, infected pulmonary infarction, infective endocarditis, insufficient/incomplete treated urinary infection, all covered by acute abdominal syndrome with uncertain etiology. In this point of clinical judgement bacteriological confirmation of pneumonia was very helpful and gave us the possibility to administrate targeted-antibiotherapy for best results. The origin and the persistence of incriminated bacteria Escherichia coli for suprainfection of PE made us consider it as the probable consequence of inadequate antibiotherapy of something what was first diagnosed as urinary infection without specified agent.
Fig. 9. Transthoracic echocardiography before discharging at home : RV=23 mm, RA=22 mm, PASP=31 mmHg, second degree mitral regurgitation, normal sized LV and LA, LVEF=53%
Fig. 10. Final chest X-ray image : no active pleuro-pulmonary lesions
In the same time we consider significant the discrepancy between the absence of electrocardiographical disturbances together with mild echocardiographical changes and the severe clinical manifestations during repetitive hospitalization. Transient right cavities dilatation with moderate pulmonary hypertension were the only remarkable abnormalities demonstrated by echocardiography, in contrast with no electrocardiographic signs for right cavities overload, far away from classical aspect described as S1Q1T3 waveform pattern in PE.
The most critical moment during hospitalization was the reurrency of PE associated with worsening of patient condition, situation that required answers for more questions : if it was a new episode of PE when were the first etiological conditions for appearance, the source for PE remained the same and which factors favourized recurrency. The new discussion in anamnestic approach discovered a small but significant detail : short episode of left lower limb thrombosis culminating with self local massage, manoeuvre that might be responsible for mobilization of local thrombi and producing PE. The lower limb venous ultrasonography confirmed the existence of deep popliteal vein thrombosis still significant source for PE. Sepsis is known as favourable condition for pro-thrombotic coagulation status 6 and so we reconstructed the coexistent circumstances for PE recurrency.
At last but not least we strongly reaffirm the major importance of detailed anamnesis for obtaining personal pathological history in which every information may count and can offer valuable data conducting to better diagnosis and therapy.
- Torbicki A., Perrier A, Konstantinides S, et al : Guidelines on the diagnosis and management of acute pulmonary embolism : The Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC), Eur Heart J 29 : 2276, 2008
- Anderson FA Jr, Zayaruzny M, Heit JA et al : Estimated annual numbers of US acute-care hospital patients and risk for venous thromboembolism. Am J Hematol 82 : 777, 2007
- Stein PD, Kayali F, Olson RE : Trends in the use of diagnostic imaging in patients hospitalized with acute pulmonary embolism. Am J Cardiol 93 : 1316, 2004
- Schoepf UJ, Goldhaber SZ, Costello P : Spiral computed tomography for acute pulmonary embolism. N Engl J Med 354 : 2317, 2006
- van Belle A, Buller HR, Huisman MV, et al : Effectiveness of managing suspected pulmonary embolism using an algorithm combining clinical probability, D-dimer testing and computed tomography, JAMA 295 : 172, 2006
- Zhu T, Martinez I, Emmerich J : Venous thromboembolism : Risk factors for recurrence. Arterioscler Thromb Vasc Biol 29 : 298, 2009