ACCN 5551 Case Study – Pulmonary Embolism Review The following paper relates to the case study of Angela

ACCN 5551 Case Study – Pulmonary Embolism Review
The following paper relates to the case study of Angela, a previously healthy 25-year-old female who presents to the Emergency Department with a history of chest pain and shortness of breath that began the day prior. The patient has a suspected pulmonary embolus (PE), which can be a life-threatening event if left untreated (Alberta Health Services AHS, 2017). According to Thrombosis Canada (2016b), “up to 10% of symptomatic pulmonary emboli are fatal within the first hour of symptom onset”. Statistics provided by Alberta Health Services show that 5773 visits to Emergency Departments across the province were related to pulmonary emboli from 2012 – 2014, and of those visits, half of the patients required admission to the hospital (AHS, 2017). This paper aims to explore the pathophysiology of pulmonary emboli and discuss the subsequent functional alterations and treatment relating to the condition.
Pathophysiology
The majority of pulmonary emboli result from detached thrombi that form in the deep veins of the lower limbs (Carter-Snell, Bray, & McLellan, 2016d; Huether & McCance, 2012). Other possible, though less likely causes of PE include fat, air, or amniotic fluid emboli (Carter-Snell et al., 2016d). Many conditions and disorders increase the risk of deep vein thrombosis (DVT) formation, including pregnancy, hormone replacement therapy, prolonged immobility, recent surgery, trauma, and cancer, among others (Carter-Snell et al., 2016d; Huether & McCance, 2012). According to Thrombosis Canada (2016a), approximately 45,000 patients will develop DVT per year in Canada alone. Virchow’s triad summarizes the main predisposing factors contributing to development of a DVT, which are as follows: venous stasis, a hypercoagulable state, and vessel wall injury (Carter-Snell et al., 2016e). Injury to the vessel wall triggers the body’s inflammatory response. As part of this response, platelets are activated and accumulate around the damaged endothelium, resulting in thrombus formation (Carter-Snell et al., 2016a). The clotting cascade, activated by chemical mediators released from tissues that are damaged, results in fibrin formation, which then deposits on the thrombus and forms a stable clot (Carter-Snell et al., 2016a). The body is usually able to dissolve the majority of thrombi without medical intervention; however, thrombi that cannot be broken down by the body’s natural processes have a high risk of embolizing to the lungs (Huether ; McCance, 2012). The patient in the case study has several risk factors for DVT, including oral contraceptive use, childbirth, and a history of cigarette smoking, which may have contributed to the development of a PE (Carter-Snell et al., 2016e; Huether ; McCance, 2012). In particular, concurrent use of oral contraceptives and cigarettes has been shown to significantly increase the risk of developing venous thromboemboli in women (Pomp, Rosendaal, ; Doggen, 2008).
Thrombi that embolize from the lower limbs are then carried to the pulmonary circulation where they can become lodged and obstruct pulmonary blood flow, resulting in a PE (Carter-Snell et al., 2016d; Huether ; McCance, 2012). This obstruction, if significant enough, can lead to a ventilation-perfusion (V/Q) mismatch, in which the area of the lung affected by the clot is being adequately ventilated but not perfused, resulting in an increased V/Q ratio (Carter-Snell et al., 2016d). The normal V/Q ratio is about 0.8, as the lung bases are usually better perfused than they are ventilated; any condition that alters either blood-flow or airflow will result in a change to the V/Q ratio (Carter-Snell et al., 2016b). The V/Q mismatch and subsequent hypoxemia caused by a PE is further worsened by the sequelae of a clot, which includes platelet aggregation and the activation of the inflammatory process; recruitment of vasoactive substances such as histamine, thromboxane, and serotonin causes vasoconstriction in unaffected areas of the lungs as well as bronchoconstriction (Carter-Snell et al., 2016a; Carter-Snell et al., 2016d). Vasoconstriction to surrounding vessels occurs in an attempt to isolate the area of injury and prevent further damage (Carter-Snell et al., 2016d; Tarbox ; Swaroop, 2013). These processes result in increased pulmonary vascular pressure, which in turn leads to increased right ventricular pressure and dilation of the right ventricle as blood begins to back up in the right side of the heart, eventually causing right-sided heart failure (Tarbox ; Swaroop, 2013). The consequent decrease in cardiac output activates a sympathetic nervous system response, producing the characteristic symptoms of tachycardia and hyperventilation often seen with pulmonary emboli (Carter-Snell et al., 2016f).
D-dimer and Pulmonary Emboli
One of the common laboratory tests ordered in the work-up of a patient with suspected pulmonary embolus is a d-dimer. D-dimer is a fibrin degradation product, produced during fibrinolysis, which is the process in which a clot is broken down by the body (Koschel, 2004; Weitz, Fredenburgh, ; Eikelboom, 2017). The presence of an elevated serum d-dimer indicates that coagulation and subsequent fibrinolysis have occurred, and so a patient with a PE would likely have an elevated, or positive, d-dimer result (Weitz, Fredenburgh, ; Eikelboom, 2017). Though sensitive, an elevated d-dimer is not specific, as it may be caused by several conditions, such as cancer or pregnancy (Garland ; Severn, 2017). As such, it is usually only used to rule out a PE when the results are negative, as opposed to confirming the diagnosis if positive. When a patient presents to the Emergency Department with suspected PE, most physicians will use a pre-test probability-scoring tool, such as the Wells’ Criteria for Pulmonary Embolism, to determine the likelihood of a pulmonary embolus (AHS, 2017). Based on this pathway, it is suggested that patients with low or intermediate probability results have a d-dimer level drawn, as a negative result can rule out a PE and prevent unnecessary and invasive diagnostic testing such as Computed Tomography (CT) pulmonary angiogram that would be used to confirm the diagnosis (Weitz, Fredenburgh, & Eikelboom, 2017). If the d-dimer result is positive, further testing is indicated for a definitive diagnosis (Weitz, Fredenburgh, & Eikelboom, 2017).
Functional Alterations
The functional alteration of highest priority for this patient would be altered oxygenation related to the alveolar dead space created by the embolus. The embolus results in a lack of gas exchange in the affected area of the lung, contributing to a low partial pressure of oxygen (PO2) in the blood (Carter-Snell et al., 2016b). As described previously, a PE can also contribute to the development of heart failure, which would diminish oxygen delivery to the tissues of the body.
Another priority functional alteration for this patient would be altered ventilation related to her breathing pattern. As noted in the case study, the patient is short of breath and has a respiratory rate of 30 breaths per minute, with shallow respirations and decreased chest expansion. The patient is possibly hyperventilating in an effort to increase her oxygen intake to counteract the hypoxemia caused by the embolus. Effective ventilation could also be compromised by cytokine-mediated bronchoconstriction, as discussed previously in this paper.
Finally, a PE may also cause altered transport and altered perfusion. Blood is unable to move past the obstruction, and thus there is decreased perfusion to the tissues at the site of and beyond the embolus.
Interventions and Immediate Therapy
The initial goal relating to altered oxygenation and ventilation would be to manage the patient’s airway and breathing, as with any other patient presenting to the Emergency Department. As long as the patient is able to maintain her own airway, the primary focus should be on correcting the hypoxemia that has developed to help correct the patient’s shallow and rapid breathing pattern. Oxygen administration should be initiated and titrated to maintain adequate oxygen saturation (Koschel, 2004). Within Alberta Health Services, the recommendation is to maintain oxygen saturation above 92% (AHS, 2017). If pulmonary function is severely compromised by the PE, the patient is at risk of developing acute respiratory failure (Carter-Snell et al., 2016c). If that were the case, then the patient may require an advanced airway and ventilatory support. Additionally, proper pain control, with opioid medication if the pain is severe, and comfort measures should be implemented to help relieve the patient’s symptoms of anxiety, which may assist in improving the patient’s respiratory rate and ventilation (AHS, 2017;Carter-Snell et al., 2016d).
Restoring adequate perfusion is one of the priorities in treatment of a PE, and will assist with correcting the functional alterations of altered transport and perfusion. The extent of treatment will depend on the patient’s status and the severity of the clot. A massive saddle embolus, in which the clot sits at the bifurcation of the pulmonary artery, generally leads to hemodynamic instability and other adverse events, and would thus require more aggressive treatment than a smaller PE (Kwak et al., 2013). Hemodynamically unstable patients will require fluid resuscitation, generally with a bolus or rapid infusion of normal saline or lactated ringer’s, depending on physician preference (AHS, 2017).
The mainstay in treatment of a pulmonary embolus is anticoagulant therapy with either low-molecular weight heparin (LMWH) or a vitamin K antagonist such as warfarin (AHS, 2017; Carter-Snell et al., 2016d; Thrombosis Canada, 2016b). These medications are used to prevent further thrombus formation while the body breaks down the existing clot (Koschel, 2004). Thrombolytics are suggested for use in patients that are unstable or are unlikely to be able to break down the clot themselves, and those confirmed to have a massive PE (AHS, 2017; Koschel, 2004). According to the Alberta Health Services Provincial Clinical Knowledge Topic on Pulmonary Embolism in Adult Emergency (2017), a 10mg bolus of Alteplase is recommended for such patients, followed by an infusion of 90mg of Alteplase over two hours. Risk of bleeding will need to be weighed against the potential benefits of thrombolytic therapy. A heparin infusion may also be initiated for patients with a massive or sub-massive PE (AHS, 2017). The final, and most invasive approach that can be used to restore perfusion is a surgical embolectomy, in which the clot is physically retrieved from the blood vessel that it is occluding; this approach is generally reserved for patients with significant right heart failure caused by the PE that has been unresponsive to other treatments (Carter-Snell et al., 2016d)
Patients diagnosed with a PE will be sent home on anticoagulant medications, and should expect to continue these treatments for at least three months (Thrombosis Canada, 2016b). Options for anticoagulation include a LMWH alone, LMWH used as a bridging medication in conjunction with warfarin administration, or a direct oral anticoagulant such as rivaroxaban or apixaban (AHS, 2017; Thrombosis Canada, 2016b). Warfarin should not be used alone, as it will require several days to reach a therapeutic INR of 2.0-3.0 (Thrombosis Canada, 2016b).
Patient Teaching
Up to one third of patients diagnosed with a DVT will develop another DVT or PE within 10 years, and so the patient in the case study should be educated on signs and symptoms of a DVT as well as PE (Thrombosis Canada, 2016a). Symptoms of a DVT often include unilateral leg swelling, redness, and pain (Huether & McCance, 2012). Symptoms of a pulmonary embolus include chest pain, shortness of breath or difficulty breathing, a rapid heart rate, and possibly blood-tinged sputum (Carter-Snell et al., 2016d). If the patient experiences any of these symptoms, she should return to the Emergency Department.
The patient should also be counselled on risk factors for developing additional thrombi, and ways in which she can prevent it from occurring. For example, risk factors that apply to the patient include prolonged sitting, cigarette smoking, and oral contraceptives. The patient works as a computer programmer, which has the potential to be a sedentary job. Prevention strategies that she can implement at work include getting up and walking frequently throughout the day as well as performing leg exercises while sitting (Healthwise, 2017). She could also discuss the use of compression stockings as another prevention strategy with her family doctor. The patient should also be given information regarding smoking cessation and provided with resources to help her with quitting. Many such resources can be found on the Alberta Quits website (www.albertaquits.ca).
As the patient will likely be discharged on anticoagulant medications, she should be provided with information specific to the medication prescribed and reminded to maintain strict adherence to the medication regime. For instance, if prescribed a LMWH, she may require teaching and demonstrations on proper self-administration of injections. If on warfarin, she should be told that she will require frequent blood-work to assess her INR levels and may need to adjust dosing based on this. Side effects of anticoagulant therapies should also be discussed with the patient, including increased risk for bleeding and easy bruising; she may mitigate some of these effects by using a soft-bristle toothbrush and avoiding using razors for hair removal. Finally, the patient will need to follow up with her primary care provider after discharge and continue to do so frequently while on anticoagulant medication.