A case of pulmonary embolism medical students experiences


Published on

1 Like
  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

A case of pulmonary embolism medical students experiences

  1. 1. A Case of Pulmonary Embolism; Medical Student’s Experience By: Muhamad Na’im B. Ab Razak Medical student of University Science of Malaysia Case Summary 53 Years Old Malay Lady who was recently findings and A-a gradient. Therefore, CT discharge from ward with problem list of Angiography was done and showed feature morbid obesity, uncontrolled diabetes of extensive pulmonary embolism. mellitus, hyperlipidaemia and hypertension presented to emergency department with the IV streptokinase 250 000 unit stat was chief complaint of sudden onset severe commenced and followed with shortness of breath associated with central Streptokinase IV infusion 500 000 unit in 50 pleuritic chest pain and diffuse sweating. ml normal saline and patient was transferred to Cardiology Care Unit for further She was alert and oriented to the time, place management. and person. Her blood pressure was 180/88 mmHg, heart rate was 120 b.p.m and respiratory rate was 20 breath per minute. Full blood count, Renal Function Test were inconclusive. Cardiac biomarkers were not elevated, D Dimer was >5000 ng/ml. ECG shows classical feature of Pulmonary embolism which are tachycardia, Deep S wave in lead I, Deep Q wave in lead III and inverted T wave in lead III (S1Q3T3) ABG under high flow mask of 100% oxygen, 10 L/min showed pH of 7.4, PCO2 28.6 mmHg, PO2 131 mmHg,HCO3- 19.6 mmol/L. Calculated Alveolar-arterial gradient (A-a gradient) was 190 which Fig 1: Urgent CTA of thorax shows good suggestive of V/Q mismatch. opacification of pulmonary trunk but inhomogenous opacification of bilateral right and left main pulmonary artery with filling A diagnosis of Pulmonary embolism was defect seeing within. Radiological diagnosis of made based on high index of suspiciousness pulmonary embolism was made by radiologist. in risk factor, clinical presentation, ECG
  2. 2. Fig 2: ECG shows Tachycardia, Deep S wave in lead I, Deep Q wave in lead III and inverted T in wave in lead III (S1Q3T3) Discussion. Pulmonary embolism (PE) is not a disease this non perfused lung will no longer per se but often a complication of other secretes surfactant and cause alveolar al vascular problem particularly deep vein collapse which exacerbates the hypoxemia. thrombosis. The devastating consequence of ing The non perfused lung tissue however this disease is mainly resulting from the seldom become infarcted because of difficulty in establishing the diagnosis due to continuous oxygen supply by bronchial nonspecific signs and symptoms. . circulation and airways. Mortality in untreated PE is approximately The European Society of Cardiology has 30%, but with adequate (anticoagulant) classified PE into two main groups which treatment, this can be reduced to 2 2–8%. [A. are massive and non-massive. Massive PE massive. M Torbicki et al] consists of shock and/or hypotension (defined as a systolic blood pressure <90 PE occurs when when one or more mmHg or a pressure drop of 40 mmHg for pulmonary artery being blocked by blood >15 min if not caused by new-onset new clots that dislodged from peripheral vein If vein. arrhythmia, hypovolumia or sepsis). volumia the blockage occurs at the bifurcation of the Otherwise non-massive PE can be massive main pulmonary artery, then it is called diagnosed. saddle pulmonary embolism In other words, massive PE also defined as The blockake cause V/Q mismatch in which embolus causing sufficient obstruction to the lung tissue is ventilated but not perfused. pulmonary flow to result in hemodynamic This will give rise to intrapulmonary dead instability, right ventricular failure, and space and impair gas exchange. After hours, hypoxemia [Paul Maggio et al]
  3. 3. Virchow’s triad consist of stasis of the blood, hypercoagulable state and endothelial Wells score for Probability of PE damage has been attributed to the deep vein Criteria Points thrombosis and PE. This condition can be Clinical signs of DVT +3 due to blood and blood vessel disorder, Alternative diagnosis less +3 probable than PE prolong immobilization, prolong surgery, Heart rate > 100 b.p.m +1.5 pregnancy, oral contraceptive and estrogen Immobilization or surgery < +1.5 replacement, and malignancy. 4 Weeks ago Previous DVT or PE +1.5 Even though the signs and symptoms for PE Haemoptysis +1 are not specific, Prospective Investigation of Cancer +1 Pulmonary Embolism Diagnosis (PIOPED) Table 1: Total score: <2 indicates a low probability of PE; study found out that the most common 2–6 indicates a moderate probability of PE; >6 indicates a presentation are dyspnea (73%), pleuritic high probability of PE chest pain (66%), cough (37%), and hemoptysis (13%) [Nader Kamangar]. ECG is a poor diagnostic tool for PE and it Other atypical symptoms include seizure, is rather being used to rule out other syncope, abdominal pain, fever, productive potential life threatening diagnosis such as cough, wheezing, altered sensorium, new myocardial infarction. [Chan TC et al]. The onset atrial fibrillation, and flank pain. ECG is often abnormal in PE however, the findings are not sensitive and not specific. In a time without or not readily accessible [Chan TC et al]. T-wave inversion in the CT angiography, few scoring system has precordial leads is the most common been develop to predict the possibility of PE abnormality (68%), and represents the ECG with the famous scoring system being sign best correlated to the severity of the Geneva score and Wells score. However, PE.[Emile Ferrari et al]. In the same study, both of this scoring system has not been Emile Ferrari et al found out that Anterior T validated and derived from selected wave inversions had a sensitivity of 85% population. and specificity of 81% for massive PE. The so called classical ECG manifestation of PE Therefore, diagnosis of PE should be made which is the SI Q3 T3 pattern was described based on high level of suspiciousness in the by McGinn and White in the year of 1935. presence of risk factor and clinical However, it is not a pattern that characterize manifestation. the pulmonary embolism alone but rather sign of acute cor pulmonale. Therefore, Chest X Ray is not really help in detecting other causes giving rise to cor pulmonale PE but it may show Westermark sign, such as acute bronchospasm and Hamptom Hump and pulmonary effusion. pneumothorax may as well give this ECG However, it is good to rule out other causes pattern. Apart from that, ECG findings often of dyspnoe. shows tachycardia.
  4. 4. D Dimer is a degradation product of pulmonary arterial pressure. A typical crosslinked fibrin. Previously, it is being echocardiographic picture of used as one of the main screening haemodynamically significant PE includes investigation for PE. However, it has less dilated, hypokinetic RV, an increased positive prediction value in diagnosing PE. RV/LV ratio caused by interventricular A level of D- Dimer below than 500 µg . l-1 septal bulging into the LV, dilated proximal is a cut off point to safely excludes PE. pulmonary arteries, increased velocity of the jet of tricuspid regurgitation (usually in the There is a practice among the clinician to range of 3–3·5 m s-1), and disturbed flow calculate alveolar-arterial gradient in order velocity pattern in the RV outflow tract. to establish the diagnosis of PE. This value, Furthermore, the inferior vena cava is can be calculated based on ABG result using usually dilated and does not collapse on the below formula. Normal adult A-a inspiration. [A. Torbicki et al] gradient is 20. However, Marc A. Rodger et al found out that none of the ABG data or The gold standard for diagnosing pulmonary prediction rules had sufficient negative embolism is CT Angiography. CT has predictive value, specificity, or likelihood become the first-line modality for imaging ratios to be useful in the management of in patients suspected of having PE. CT is patients with suspected PE. Therefore, they now an attractive means for establishing a conclude that ABG data alone or in safe, highly accurate, and cost-effective combination with other clinical data are not diagnosis of PE. [U.J Schoepf & P. useful in the assessment of suspected PE. Costello]. However, according to cohort study by M. J. L. Van Strijen et al, the sensitivity of spiral CT was 86% for A-a gradient = PAO2 − PaO2 segmental or larger PE and 21% in the group of patients with subsegmental PE. [FiO2*(Patm-PH2O)-(PaCO2/0.8) ] - PaO2 Therefore, they draw a conclusion that in patients with clinically suspected PE and an PAO2 = alveolar PO2 (calculated from the abnormal perfusion scintigraphy, single- alveolar gas equation) slice detector spiral CT is not sensitive PaO2 = arterial PO2 (measured in arterial enough to be used as the sole test to exclude blood A-a gradient) PE. = ( 760 - 47 ) x FiO2 - PaCO2 /0.8 (or 1) Doppler ultrasound is both 95% sensitive and specific in detecting deep venous thrombosis above the knee if DVT is Table 2 A-a gradient suspected as causes of PE. Echocardiography may suggest or reinforce clinical suspicion of PE if right ventricular (RV) overload and dysfunction is found in the presence of Doppler signs of increased
  5. 5. In the recent guidelines of the American Besides thrombolytic therapy, other College of Chest Physicians, either LMWH management includes, high flow oxygen or UFH is recommended for the initial supply, continuous vital sign monitoring treatment of venous thromboembolism. In particularly SPO2, heart rate and BP, patients with advanced renal insufficiency, measures to prevent or control the effect of the recommendation is to use UFH rather acute circulatory failure like infusion of the LMWH. [GF Pineo& RD Hull]. Dobutamine and dopamine. The usefulness of fluid challenge is controversial and Vitamin K antagonists (VKAs) are the should not exceed 500 ml. as it may agents of choice for long-term treatment and deteriorate the condition of the patient. secondary prophylaxis of pulmonary embolism (PE), as they were shown to be Acute pulmonary thrombectomy has a effective in preventing recurrence of the limited role in massive, life-threatening PE. disease [G Agnelli & C Becattini] Reference 1) A. Torbicki, E. J. R. van Beek , B. Charbonnier et al, "Guidelines on diagnosis and management of acute pulmonary embolism", European Heart Journal (2000) 21, 1301–1336 2) Chan TC, Vilke GM, et al. Electrocardiographic manifestations: pulmonary embolism. J Emerg Med. 2001; 21(3):263-70. 3) Emile Ferrari, Alain Imbert, Thierry Chevalier, et al, "The ECG in Pulmonary Embolism : Predictive Value of Negative T Waves in Precordial Leads--80 Case Reports", Chest 1997;111;537-543 4) Marc A. Rodger, Marc Carrier, Gwynne N. Jones et al, " Diagnostic Value of Arterial Blood Gas Measurement in Suspected Pulmonary Embolism ", Am. J. Respir. Crit. Care Med., Volume 162, Number 6, December 2000, 2105-2108 5) M. J. L. Van Strijen, W. De Monye, G. J. Kieft et al, "Accuracy of single-detector spiral CT in the diagnosis of pulmonary embolism: a prospective multicenter cohort study of consecutive patients with abnormal perfusion scintigraphy", Jour of Thromb and Haem, Vol 3, Issue 1, pages 17-25, International Society on Thrombosis and Haemostasis, 2010 6) Nader Kamangar, "Pulmonary Embolism", http://emedicine.medscape.com/article/300901 7) Sara F Sutherland, "Pulmonary Embolism", http://emedicine.medscape.com/article/759765 8) Stavros V. Konstantinides,"Management Of Acute Pulmonary Embolism", Humana Press Inc, New Jersey, 2007 9) Stephen Iles, Lutz Beckert, Martin Than and Ian Town, "Making a diagnosis of pulmonary embolism – new methods and clinical issues", Journal of the New Zealand Medical Association, 11-July-2003, Vol 116 No 1177 10) U. Joseph Schoepf & Philip Costello, " CT Angiography for Diagnosis of Pulmonary Embolism: State of the Art", Radiology, Volume 230, Number 2, 2004