CT Angiography and Pulmonary Embolism - Dissertation Example

?CT Angiography and Pulmonary Embolism Clinical History 55 year old James, a known patient of hypertension and diabetes mellitus, presented with complaints of chest pain, diaphoresis and breathlessness. On examination, he was alert and cooperative but tired. He was tachycardic (100 per minute), tachypneic (40 per minute) and hypertensive (150/100 mmHg). Saturations in room air were 86 percent. Examination of the systems was normal. ECG was normal. The patient was suspected to have pulmonary embolism and CT angiography was immediately ordered. Pulmonary embolism Pulmonary embolism is the second most common cause of sudden death. Death occurs within few hours of onset of the condition and in many situations, death occurs much before the diagnosis is made. In those who survive, recurrent embolism and mortality can be prevented by prompt diagnosis and management. However, diagnosis is often missed because of signs and symptoms that are nonspecific. Untreated individuals, who have survived the initial episode, are likely to die due to repeat embolism. Pulmonary embolism can be acute or chronic. Acute embolism occurs when the embolus is situated in the central portion of the vascular lumen or if the embolus occludes the lumen. Chronic embolism occurs when the embolus is eccentric, being contiguous with the wall of the vessel, decreases the diameter of the involved artery by atleast 50 percent and there is evidence of recanalisation or arterial web. Acute embolism distends the the vessel (Ouellette, 2011). Figure 1: Mechanism of pulmonary embolism (medicalook.com) Pulmonary embolism can be peripheral or central based on the branch of the artery located. Main pulmonary artery and its branches, the right and left pulmonary arteries and their subsequent main branches,the anterior trunk, the right and left interlobar arteries, right and left lower lobe arteries, right middle lobe artery and left upper lobe trunk are considered to be central zones. Other branches are peripheral zones (Ouellette, 2011). Pulmonary embolism can be massive or non-massive. Massive embolism occurs when hemodynamic compromise occurs (Ouellette, 2011). The clinical presentation of the condition is highly variable and hence provides scope for missed diagnosis. Classic presentation includes sudden onset of shortness of breath, pleuritic chest pain and hypoxia (Ouellette, 2011). Pulmonary embolism is considered to be a complication of venous thromboembolism like deep vein thrombosis, rather than just a disease. Thus, every individual who is at risk of venous thromboembolism is at risk of developing pulmonary embolism (Ouellette, 2011). In normal individuals, microthrombi, which are nothing but aggregates of platelets, lysed red blood cells and fibrin, are formed and subsequently lysed continuously in the venous system. Through such a mechanism, local hemostasis is possible in response to injury, thus preventing uncontrolled propagation of clot (Ouellette, 2011). In view of nonspecific clinical presentation, every individual with unexplained chest pain, tachypnea or dyspnea must undergo specific diagnostic tests to rule out the disease. Non-specific routine tests ar not helpful in establishing or giving clue for diagnosis. The criterion standard for diagnosis of pulmonary embolism is pulmonary angiography. However, this is rarely performed now and is replaced by computed tomography angiography or CT angiography which is more sensitive and specific (Ouellette, 2011). Famous personality who died of pulmonary embolism One of the famous personalities who died of pulmonary embolism is David Bloom, a noted TV journalist (DPSinfo, 2004). Anatomy The key for accurate interpretation of CT angiography is based on the understanding of bronchovascular anatomy (Refer to Figures 2 and 3). It is very important to adopt systematic approach of identifying vessels (Ouellette, 2011). Figure-2: Branches of pulmonary artery (imaios.com) Figure-3: Bronchopulmonary segments (imaios.com). Pathology Both hemodynamic and respiratory consequences arise due to pulmonary embolism. Acute respiratory consequences include increase in alveolar dead space, hyperventilation, hypoxemia, pulmonary infarction and regional loss of surfactant. Hypoxemia results due to ventilation-perfusion mismatch, decreased cardiac output, intrapulmonary shunts and intracardiac shunt through foramen ovale. Pulmonary infarction occurs because of bronchial arterial collateral circulation. Hemodynamic consequences mainly arise due to increased right ventricular afterload. This is because; pulmonary embolism results in decreased cross-sectional area of pulmonary vascular bed leading to increased pulmonary vascular resistance, which in turn can lead to right ventricular failure. In addition to this mechanism, reflex and humoral mechanisms also contribute to right sided failure (Ouellette, 2011). An individual is predisposed to pulmonary embolism due to 3 influences, which are grouped under Virchow's triad and they are hypercoagulability, changes in blood flow, either stasis or turbulence, and endothelial injury. The thrombosis usually begins as a platelet nidus on one of the valves in the veins, more often than not in the lower limbs. This nidus further grows due to accretion of fibrin and platelets, forming a red fibrin thrombus, which breaks and embolises. This undergoes partial dissolution and eventually gets incorporated into the wall of the vessel (Fedullo and Tapson, 2008). The most common site of origin of pulmonary embolism is thrombosis of lower limb veins. However, the embolism can arise from any vein in the body like renal veins, pelvic veins, veins in the upper extremity or even from the right heart chambers. The thrombi travel to the lung and they can get lodged at the pulmonary artery bifurcation or any of the lobar branches (Ouellette, 2011). Pulmonary embolism is multifactorial and risk factors include hypercoagulability, venous stasis, surgery, trauma, immobilization, pregnancy, malignancy, oral contraception, hereditary factors and acute medical illness (Ouellette, 2011). Differential diagnosis Differential diagnosis includes pericarditis, pleuritis, musculoskeletal pain, salicylate intoxication, lung trauma, acute mediastinitis, hyperventilation and silicone pulmonary embolism (Ouellette, 2011). CT angiography As of now, CT angiography is the diagnostic modality of choice in stable patients with a suspected diagnosis of pulmonary embolism. According to the American College of Radiology, chest CT angiography is the current standard of diagnosis for pulmonary embolism. It has the advantage of pulmonary angiography because it shows the emboli directly. Also, it is a non-invasive test and is cheaper than pulmonary angiography. It is also widely available. A major advantage of CT angiography is that it is useful in providing additional information for evaluation of alternate diagnosis (Roggenland et al, 2008). Both acute and chronic pulmonary embolism cause complete and partial intraluminal filling defects. The defects have sharp interface with the intravascular contrast material. In complete arterial occlusion due to acute pulmonary embolism, the artery that is affected may be enlarged. Partially filling defects that manifest in acute embolism are often centrally located. However, when eccentrically located, they form angles typically with the walls of the vessel. In chronic pulmonary embolism, complete occlusion of the disease in vessels that are smaller than the patent vessels in the adjacent area can occur. Other findings suggestive of chronic pulmonary embolism include webs, recanalization, flaps and partial filling defects with obtuse angles with the walls of the vessels (Wittram et al, 2004). Several factors contribute to the misdiagnosis of pulmonary embolism and they can be technical, patient related, pathologic and anatomic (Wittram et al, 2004). A test to exclude pulmonary embolism in bedside is d-dimer test. The test, though non-specific is highly sensitive and is useful only to rule out pulmonary embolism. Imaging is necessary to establish a diagnosis of pulmonary embolism (Ouellette, 2011). Though pulmonary angiography continues to be the gold standard for pulmonary embolism, it is performed infrequently because it is an invasive procedure and requires skilled labour. It is associated with some complications and has some limitations in diagnosing isolated peripheral emboli (Wittram et al, 2004). Nuclear imaging was also in vogue and was a popular method of diagnosing pulmonary embolism. But its use is declining because of increased evidence pointing to poor interobserver correlation. Contrast material–enhanced magnetic resonance (MR) angiography has also been employed by some clinicians. However, due to lack of sufficient spatial resolution for reliable assessment of pulmonary arteries in the peripheral region, this test is not popular. Also, this test cannot be employed in acutely ill patients because of difficulties encountered in patient monitoring, long examination times and lack of general availability (Wittram et al, 2004). Figure-5: CT angiography of pulmonary embolism (Kitagawa et al, 2009) Figure-5: CT angiogram of pulmonary embolism (Kitagawa et al, 2009) Thus, CT angiography is the most practical test, one for ease of testing, and other because even mediastinal and parenchymal structures can be evaluated, third, direct visualisation of the thrombus can be done (Sood et al, 2006). Two thirds of patients with suspected pulmonary embolism receive another clinical diagnosis and CT angiography is thus the best test for diagnosis because it helps in evaluation of other structural areas (Kitagawa et al, 2009). As far as interobserver congruency is concerned, it is better than in scintigraphic imaging. Also, the diagnostic algorithm for CT angiography is much cheaper than that for other imaging modalities like scintigraphy, ultrasonography and pulmonary angiography. Another major advantage with CT angiography is that it is not only useful in evaluating the anatomy of the thorax, it is also useful in ascertaining the physiology (Kitagawa et al, 2009). The main disadvantage with CT angiography is the inaccuracy in detecting small peripheral emboli. The modality can detect emboli only at segmental level and subsegmental level and not at peripheral level (Kitagawa et al, 2009). Image construction Current generation scanners of 4-, 8- and 16- detector row CT scanners allow coverage of the entire chest with high resolution of as much as 1mm or even less than that resolution within a breath hold of less than 10 seconds. CT angiography also covers substantial quantity of anatomic volumes with high levels of in-plane and through-plane spatial resolution and this is associated with several advantages. The currently used high-spatial-resolution multi– detector row CT helps in 2 and 3 dimensional visualization. This is useful in delivering important information to clinicians about the extent and location of the embolus. Even small peripheral emboli can be depicted. Single row CT with sections less than 3mm can provide excellent demonstration of segmental and subsegmental pulmonary arteries. In high spatial resolution of less than 1mm, evaluation of pulmonary vessels of even 6th order is possible and this eventually increases the rate of detection of segmental and subsegmental emboli. Such accurate detection has been possible due to reduced averaging of volume and accurate analysis of smaller vessels by using thinner sections. The best results pertaining to pulmonary embolism are obtained when using multidetector computed tomography (MDCT) scanners (Fedullo et al, 2003). Scanning protocol 50- 150 ml of radiocontrast is administered intravenously through an intravenous cannula. The rate of injection is 4ml per second through a syringe driver. In most centers, scanning is commenced soon after the contrast is detected first at the proximal pulmonary arteries. this is known as bolus tracking. CT machines which are state of art can complete the scan within 5 seconds. sections are performed at 1-3mm intervals with slices of 1-3mm. Pulmonary vessels filled with contrast appear white (Fleischmann, 2006). Embolus and other mass filling defects make the arteries appear dark. The scan must be completed before the contrast reaches the left side of aorta and heart, otherwise, artifacts can occur. The contrast agent used can be iodine based contrast agent, In those who are allergic to iodine, gadolinium based contrast agents can be used (Remy-Jardin et al, 2006). Patient preparation Before the procedure, the patient is asked not to eat anything and drink only water. All metal objects need to be removed from the body of the patient. Allergy test must be performed for the contrast material. An intravenous line is placed and the patient is shifted near the CT scanner. The contrast agent is then administered into the the IV line (Fedullo et al, 2003). Patient aftercare and treatment Other tests which need to be done to ascertain the cause of pulmonary embolism include hypercoagulation workup and screening for conditions like protein C deficiency, protein S deficiency, antithrombin III deficiency, lupus anticoagulant, connective tissue disorders and occult neoplasm. Along with these tests tests like d-dimer tests, complete blood picture, serum albumin levels, arterial blood gas analysis, electrocardiography and brain natriuretic peptide levels may be necessary to evaluate overall condition of the patient (Ouellette, 2011). Immediate therapeutic anticoagulation therapy must be initiated soon after the diagnosis is made. There is evidence that anticoagulation therapy with heparin decreases the mortality rates from 30 percent to 10 percent. Antithrombotic and thrombolytic therapy depends on the risk stratification and comorbid conditions. According to recent guidelines, all patients with a diagnosis of pulmonary embolism must be started on unfractionated heparin (UFH), low–molecular weight heparin (LMWH), or fondaparinux, along with oral anticoagulant like warfarin at the time of diagnosis. UFH, LMWH, or fondaparinux must be discontinued only after INR has reached 2 for atleast 24 hours, but no sooner than 5 days after warfarin therapy has been started. In those with hemodynamic compromise or right ventricular dysfunction, thrombolytic therapy must be initiated except in cases when major contraindications exists due to risk of bleeding (Ouellette, 2011). In those with massive pulmonary embolism, whenever concerns exist about renal failure or subcutaneous absorption or if thrombolytic therapy is considered, UFH is the recommended anticoagulation therapy in the intravenous form. The efficacy of the treatment is based on the critical therapeutic level of heparin within the first 24 hours of initiation of treatment. This is 1.5 times the upper limit of normal range for activated partial thromboplastin time. In those with acute non-massive pulmonary embolism, LMWH is the preferred choice because of greater bioavailability, subcutaneous route and longer duration of action. Also laboratory testing with aPTT is not essential. It also be given in an outpatient setting. Even UFH is as useful as LMW heparin (Ouellette, 2011). Other than the above treatments, patients must also receive supportive care in the form of fluid and electrolyte management, true gradient compression stockings, antibiotics and others (Ouellette, 2011). Reduction of radiation exposure to the patient CT angiography is associated with some risk of exposure to radiation and this increases the risk of developing cancer or skin allergy. According to FDA (2010), radiation exposure may be reduced by the usage of equipments that record, display and report radiation dose and alerts when the dose exceeds diagnostic reference levels and peak skin threshold levels. Other strategies include incorporating key quality assurance practices into participation and accreditation for imaging hospitals and facilities. and administering only that dose that is safe for the patient must be delivered. Brenner (2007) advised 3 ways to reduce overall radiation exposure to the patient due to computed tomography. The first strategy is to reduce the dose related to CT scanner in individual patients. This can be addressed by using scanners which have automatic exposure control option. The next option suggested by him was to replace CT scan as far as possible with other diagnostic modalities like ultrasonography. However, in patients with suspected pulmonary embolism, CT angiography is the diagnostic tool of choice. The third strategy described is reduction in the number of CT studies prescribed. Prognosis Prognosis depends on the underlying health condition of the patient, the cause and size of the embolus and the treatment initiated. Often, diagnosis is not made on time and this also influences the diagnosis. In those in whom diagnosis is made, the mortality is less than 20 percent. The mortality is higher in those who are older, have underlying morbidity and have delayed diagnosis. References Brenner, D.J. (2007). Computed Tomography — An Increasing Source of Radiation Exposure. N Engl J Med., 57, 2277-2284. DPSinfo. (2004). Celebrities and Notable People Who Died in the Year 2003. Retrieved from http://dpsinfo.com/dps/2003.html FDA. (2010). White . Paper: Initiative to Reduce Unnecessary Radiation Exposure from Medical Imaging. Retrieved from http://www.fda.gov/Radiation-EmittingProducts/RadiationSafety/RadiationDoseReduction/ucm199994.htm Fedullo, P.F., Tapson, V.F. (2003). Clinical practice. The evaluation of suspected pulmonary embolism. N. Engl. J. Med., 349 (13), 1247–56. Fleischmann, D. (2006). Contrast medium injection protocols for CT angiography. C212, 4(2), Retrieved from http://www.c2i2.org/vol_iv_issue_2/Contrast_medium_injection.asp Kitagawa, K., Lardo, A.C., Lima, J.A.C., and George, R.T. (2009). Prospective ECG-gated 320 row detector computed tomography: implications for CT angiography and perfusion imaging. Int J Cardiovasc Imaging, 15, 22-29. Ouellette, D.R. (2011). Pulmonary embolism. Medscape reference. Retrieved from www.medscape/300901-overview.htm Roggenland, D., Peters, S.A., Lemburg, S.P., et al. (2008). CT Angiography in Suspected Pulmonary Embolism: Impact of Patient Characteristics and Different Venous Lines on Vessel Enhancement and Image Quality. AJR, 190, W351-W359. Remy-Jardin, M., Bahepar, J., Lafitte, J. , et al. (2006). Multi–Detector Row CT Angiography of Pulmonary Circulation with Gadolinium-based Contrast Agents: Prospective Evaluation in 60 Patients. Radiology, 238, 1022-1035. Schoepf, U.J., and Costello, P. (2004). CT Angiography for Diagnosis of Pulmonary Embolism: State of the Art. Radiology, 230, 329–337. Sood, S., Negi, A., Dhiman, D.S., Sood, R.G., Negi, P.C., and Sharma, S. (2006). Role of CT angiography in pulmonary embolism and its comparative evaluation with conventional pulmonary angiography. Chest Radiology, 16(2), 215- 219. Wittram, C., Maher, M.M., Yoo, A.J., et al. (2004). CT Angiography of Pulmonary Embolism: Diagnostic Criteria and Causes of Misdiagnosis. Radiographics, 24, 1219-1238. Read More