Documentation of an Examination of the Peripheral Vascular System
Subjective Data
The patient is a 76-year-old African American female admitted to the in-patient diabetic clinic with post-surgical complications after a right leg amputation. The patient complains of pain in the remaining left leg. The pain is a cramping pain emanating from the left calf. She reports that she started feeling the pain the previous day. The pain gets worse when she tries getting up and gets better when she applies some compression force on it. She also reports that the skin around where the pain is coming from is swollen. She denies having any shortness of breath or chest pains. The patient is a known diabetic who recently had a right knee amputation after developing a diabetic foot. She has been bedridden for the past five days.
The patient is currently on metformin, gliclazide, and insulin. She is also on clopidogrel and atorvastatin. She is allergic to aspirin and pollen. His family history is significant of diabetes and venous occlusive disorders. Her mother died from pulmonary embolism, while her older brother has been admitted twice for venous thromboembolic disorders.
Objective Data
The patient is alert and cooperative but appears to be in pain and anxious. She has an oral temperature of 37 degrees, a BP of 128/84mmHg, a PR of 78 beats per minute, and a respiratory rate of 17 breaths per minute. Pulse oximetry findings revealed a PO2 of 94%. No jugular venous distension was seen on inspecting the neck region. Inspection of the extremities revealed left leg oedema. There was also a notable swelling on the left calf. The calf was warm, tender, and reddened. There was no evidence of cyanosis on the fingers and toes. The patient had a capillary refill time of 3 seconds.
A prominent P2 component of the second heart sound was heard during cardiovascular auscultation. An S3 gallop sound was also heard. No mitral and tricuspid regurgitation murmurs were heard. No wheezing, lung rales, crackles, or pleuritic rub sounds were heard on lung examination. ABG analysis revealed no hypercapnia.
Risk Factors
The patient is at risk of developing pulmonary embolism, as evidenced by the presence of deep vein thrombosis. Deep vein thrombosis occurs when blood clots form in deep veins and get deposited in the venous walls to create a thrombus. This thrombus may break and get transported to pulmonary circulation. Deposition of this thrombus in the pulmonary circulation causes pulmonary embolisms with the resultant effects of reduced cardiac functionalities (Turetz et al., 2018. Up to 80% of all patients with proximal DVT proceed to develop pulmonary embolism. Another 10% of patients with superficial DVT will develop pulmonary embolism (Cordeanu et al., 2019). Pulmonary embolism is one of the leading causes of death for patients with venous occlusive disorders. The patient having symptoms of DVT and having other modifiable risks for pulmonary embolism has a higher chance of developing pulmonary embolism.
The patient is at risk for impaired cerebral perfusion, as evidenced by a thrombus in the systemic circulation. The clot formed in the deep veins may also dislodge and enter the cerebrovascular circulation. When this clot reaches the narrower vessels within the cerebrovascular circulation, it may cause occlude of these vessels, thus impairing cerebral perfusion. Cerebrovascular accidents, the leading cause of paralysis, result from venous occlusion from clots formed elsewhere and deposited in the cerebral circulation (Eswaradass et al., 2018). The resultant ischemia causes loss of cerebral functionalities, as seen in stroke.
References
Eswaradass, P., Dey, S., Singh, D., & Hill, M. (2018). Pulmonary Embolism in Ischemic Stroke. Canadian Journal Of Neurological Sciences / Journal Canadien Des Sciences Neurologiques, 45(3), 343-345. https://doi.org/10.1017/cjn.2017.288
Cordeanu, E., Lambach, H., Heitz, M., Di Cesare, J., Mirea, C., & Faller, A. et al. (2019). Pulmonary Embolism and Coexisting Deep Vein Thrombosis: A Detrimental Association. Journal Of Clinical Medicine, 8(6), 899. https://doi.org/10.3390/jcm8060899
Turetz, M., Sideris, A., Friedman, O., Triphathi, N., & Horowitz, J. (2018). Epidemiology, Pathophysiology, and Natural History of Pulmonary Embolism. Seminars In Interventional Radiology, 35(02), 92-98. https://doi.org/10.1055/s-0038-1642036
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