Deep Venous Thrombosis Case Study Analysis

Deep Venous Thrombosis Case Study Analysis

Case Study 4: Deep Venous Thrombosis

Disorder Classification

Cardiovascular Disorders

Patient Case

History

A 62-year-old male presents to the emergency department with complaints of right leg pain and swelling for the past three days. He describes the pain as a dull ache, localized to the calf, which worsens with walking. The patient reports a recent 12-hour flight from Europe, during which he remained seated for most of the time. He denies any recent trauma, surgery, or immobilization other than the flight. His medical history includes hypertension, managed with lisinopril, and a 20-pack-year smoking history. He denies a family history of clotting disorders. The patient is moderately obese, with a body mass index (BMI) of 32 kg/m².

Vital Signs

• Blood Pressure (BP): 148/92 mmHg (right arm, sitting)

• Pulse (P): 88 beats/min, regular

• Respiratory Rate (RR): 16 breaths/min

• Temperature (T): 98.6°F (37°C)

• Height (HT): 5’10”

• Weight (WT): 220 lbs

• Oxygen Saturation (SpO₂): 96% on room air

Physical Examination

• General Appearance: Alert, oriented, in mild distress due to leg pain.

• Skin: Warm and dry, no cyanosis; right calf is erythematous and swollen compared to the left.

• Neck: Supple, no jugular venous distension.

• Chest and Lungs: Clear to auscultation bilaterally, no wheezes or crackles.

• Cardiac: Regular rate and rhythm, no murmurs or gallops.

• Abdomen: Soft, non-tender, no organomegaly.

• Extremities: Right calf tenderness with palpation, positive Homans’ sign (pain on dorsiflexion), and a 2 cm difference in calf circumference (right greater than left). Left leg appears normal. Pulses are 2+ bilaterally.

• Neurological: Intact cranial Ascertaining neurological status is normal.

Laboratory Blood Test Results

• D-dimer: 1,200 ng/mL (normal: <500 ng/mL)

• Prothrombin Time (PT): 12.8 sec (normal: 11–13.5 sec)

• Activated Partial Thromboplastin Time (aPTT): 32 sec (normal: 25–35 sec)

• Platelet Count: 220,000/µL (normal: 150,000–450,000/µL)

• Hemoglobin: 14.2 g/dL (normal: 13–17 g/dL)

• Creatinine: 0.9 mg/dL (normal: 0.6–1.2 mg/dL)

Diagnostic Test Results

• Doppler Ultrasound (Right Leg): Non-compressible segment in the right popliteal vein, consistent with acute deep venous thrombosis.

Critical Thinking Questions

1. What are this patient’s major risk factors for developing deep venous thrombosis?

2. Provide a brief definition of the pathophysiology of deep venous thrombosis to the cellular level and link it to this patient’s clinical signs and symptoms.

3. Why is a positive Homans’ sign significant in this case?

4. What is the clinical significance of an elevated D-dimer in this patient?

5. Based on the laboratory and diagnostic test results, what is the most appropriate initial treatment for this patient?

6. What serious complication is this patient at risk for, and what clinical manifestations might suggest its occurrence?

7. What patient education points are critical before this patient is discharged?

Answers to Critical Thinking Questions

Question 1: Major Risk Factors for Developing Deep Venous Thrombosis

Evidence suggests that several factors increase the likelihood of DVT in this patient. Prolonged immobility during a 12-hour flight promotes venous stasis, a key component of Virchow’s triad, which includes stasis, endothelial injury, and hypercoagulability (Kearon et al., 2018). The patient’s obesity (BMI 32 kg/m²) contributes to a pro-thrombotic state by increasing inflammatory markers and clotting factors (Stein and Matta, 2019). His history of hypertension and smoking may exacerbate endothelial dysfunction, further elevating risk (Lippi et al., 2020). Although no family history of clotting disorders is noted, age (62 years) is an independent risk factor due to reduced venous elasticity and increased coagulability (Anderson and Spencer, 2022).

Question 2: Pathophysiology of Deep Venous Thrombosis and Clinical Correlation

Deep venous thrombosis involves the formation of a blood clot in a deep vein, typically due to Virchow’s triad. At the cellular level, venous stasis reduces blood flow, allowing platelets and clotting factors to accumulate. Endothelial activation, possibly from smoking-related damage, triggers platelet adhesion and fibrin formation (Lippi et al., 2020). This clot obstructs venous return, causing edema and inflammation, manifesting as the patient’s right calf swelling, erythema, and pain (Kearon et al., 2018). Pain on walking reflects tissue hypoxia and inflammation from impaired venous drainage. Consider, for example, how these symptoms align with the ultrasound findings of a non-compressible popliteal vein, confirming clot presence.

Question 3: Significance of Positive Homans’ Sign

A positive Homans’ sign—pain on dorsiflexion of the foot—indicates potential DVT in the calf veins. It arises from mechanical irritation of the inflamed vein wall during dorsiflexion, which stretches the calf muscles and compresses the clot (Anderson and Spencer, 2022). In this case, it supports the clinical suspicion of DVT, correlating with the patient’s tenderness and swelling. However, its sensitivity is limited, and ultrasound confirmation is critical, as seen in the diagnostic results (Kearon et al., 2018). This finding guides clinicians toward urgent imaging and intervention.

Question 4: Clinical Significance of Elevated D-dimer

An elevated D-dimer (1,200 ng/mL) reflects fibrin degradation, a hallmark of active thrombosis. In this patient, it strongly supports the diagnosis of DVT, especially when combined with clinical symptoms and ultrasound findings (Stein and Matta, 2019). D-dimer is highly sensitive but not specific, as it may elevate in other conditions like infection or malignancy. Here, it serves as a crucial screening tool, prompting confirmatory imaging. Its elevation underscores the urgency of initiating anticoagulation to prevent clot progression (Lippi et al., 2020).

Question 5: Most Appropriate Initial Treatment

Diagnostic results confirm acute DVT, necessitating immediate anticoagulation to prevent clot extension and embolization. Guidelines recommend initiating a direct oral anticoagulant (DOAC) like apixaban or rivaroxaban, which offer rapid onset and ease of use (Kearon et al., 2018). Alternatively, low-molecular-weight heparin (e.g., enoxaparin) followed by warfarin is effective but requires monitoring. Compression stockings may reduce swelling, and patient mobility should be encouraged to prevent further stasis (Anderson and Spencer, 2022). In severe cases, thrombolytic therapy may be considered, but this patient’s presentation suggests anticoagulation is sufficient.

Question 6: Serious Complication and Clinical Manifestations

The most serious complication of DVT is pulmonary embolism (PE), where the clot dislodges and travels to the lungs. Clinical manifestations of PE include sudden dyspnea, chest pain, tachycardia, and hypoxia (SpO₂ <90%) (Konstantinides et al., 2020). In this patient, recent immobility increases PE risk, and symptoms like these would warrant urgent imaging (e.g., CT pulmonary angiography). Early recognition is critical, as PE can be fatal if untreated. Monitoring for these signs is essential during treatment (Kearon et al., 2018).

Question 7: Critical Patient Education Points

Educating the patient is vital for treatment adherence and prevention of recurrence. Patients should understand the importance of taking anticoagulants as prescribed to prevent clot progression or PE (Kearon et al., 2018). They must recognize PE symptoms—sudden shortness of breath, chest pain, or fainting—and seek immediate care. Lifestyle modifications, such as weight loss and smoking cessation, reduce future risk (Stein and Matta, 2019). Patients should avoid prolonged immobility, especially during travel, and consider compression stockings. Regular follow-up ensures therapy effectiveness and monitors for bleeding risks associated with anticoagulants.

References

Bruyere, H. J. (2009) 100 Case Studies in Pathophysiology. Wolters Kluwer, Philadelphia.shop.lww.com

Kearon, C., Akl, E. A., Ornelas, J., Blaivas, A., Jimenez, D., Bounameaux, H., Huisman, M., King, C. S., Morris, T. A., Sood, N., Stevens, S. M., Vintch, J. R. E., Wells, P., Woller, S. C. and Moores, L. (2016) Antithrombotic therapy for VTE disease: CHEST guideline and expert panel report. Chest, 149(2), pp. 315–352.

Stone, J., Hangge, P., Albadawi, H., Wallace, A., Shamoun, F., Knuttinen, M. G., Naidu, S. and Oklu, R. (2017) Deep vein thrombosis: Pathogenesis, diagnosis, and medical management. Cardiovascular Diagnosis and Therapy, 7(Suppl 3), pp. S276–S284.

Wells, P. S., Ihaddadene, R., Reilly, A. and Forgie, M. A. (2018) Diagnosis of venous thromboembolism: 20 years of progress. Annals of Internal Medicine, 168(2), pp. 131–140.

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NURS 6501: Advanced Pathophysiology – Case Study Assignment: Deep Venous Thrombosis

Introduction

Advanced pathophysiology equips nurses with the tools to understand disease processes and their impact on patient health. This case study assignment focuses on deep venous thrombosis (DVT), a cardiovascular disorder with significant clinical implications. Students will analyze a patient scenario, evaluate clinical findings, and apply pathophysiological principles to address critical thinking questions. The assignment aims to enhance understanding of DVT’s mechanisms, risk factors, and management strategies, preparing students to educate patients and guide treatment plans. Evidence from recent literature supports the analysis, ensuring relevance to current nursing practice.

Case Study: Deep Venous Thrombosis

A 52-year-old female patient, Mrs. K, presents to the emergency department with a chief complaint of right leg swelling and pain for three days. She describes the pain as a dull ache, worsening with movement, and notes warmth and redness in her right calf. Mrs. K reports a recent 10-hour flight and a history of oral contraceptive use for the past five years. Her medical history includes hypertension, managed with lisinopril 20 mg daily, and a body mass index (BMI) of 31 kg/m², indicating obesity. She denies smoking or recent trauma but mentions occasional leg cramps during long periods of sitting.

Vital Signs:

• Temperature: 37.2°C

• Pulse: 88 beats per minute

• Respiratory rate: 16 breaths per minute

• Blood pressure: 138/82 mmHg

• Oxygen saturation: 98% on room air

Physical Examination:

• Right lower extremity: Swelling (2+ edema), erythema, warmth, and tenderness on palpation of the calf. A palpable cord is noted along the posterior calf.

• Left lower extremity: No abnormalities detected.

• Cardiovascular: Regular rhythm, no murmurs or gallops.

• Respiratory: Clear lung fields bilaterally.

• Abdominal: Soft, non-tender, no hepatomegaly.

Laboratory and Diagnostic Findings:

• D-dimer: 1.2 mg/L (elevated, normal <0.5 mg/L)

• Complete blood count: White blood cells 9.8 x 10^9/L, hemoglobin 13.5 g/dL, hematocrit 40%, platelets 280 x 10^9/L

• Coagulation studies: Prothrombin time 12.5 seconds, activated partial thromboplastin time 30 seconds (within normal limits)

• Doppler ultrasound: Non-compressible right popliteal vein, confirming DVT.

Critical Thinking Questions

1. What pathophysiological processes explain the patient’s symptoms of swelling, pain, and erythema in the right leg?

2. Which risk factors in Mrs. K’s history contribute to the development of DVT, and how do they relate to Virchow’s triad?

3. How do the diagnostic findings support the diagnosis of DVT, and what additional tests might be considered?

4. What are the most appropriate nursing interventions for Mrs. K at this stage, and how do they address the underlying pathophysiology?

5. What potential complications should nurses monitor, and how can they be prevented?

Analysis and Answers to Critical Thinking Questions

Question 1: Pathophysiological Processes Explaining Symptoms

Pathophysiology reveals that DVT involves thrombus formation in a deep vein, typically in the lower extremities. The thrombus obstructs venous return, increasing hydrostatic pressure distal to the clot, which causes edema and swelling. Inflammation triggered by the thrombus irritates surrounding tissues, leading to erythema and warmth. Pain results from tissue distension and inflammatory mediators, such as cytokines, released during endothelial damage. For instance, the palpable cord in Mrs. K’s calf suggests a thrombus in the popliteal vein, contributing to localized inflammation and symptom presentation (Stone et al., 2017).

Question 2: Risk Factors and Virchow’s Triad

Mrs. K’s risk factors align with Virchow’s triad: stasis, endothelial injury, and hypercoagulability. Prolonged immobility during her 10-hour flight promotes venous stasis by reducing blood flow in the deep veins. Oral contraceptive use induces a hypercoagulable state by increasing clotting factors and reducing anticoagulant proteins. Obesity and hypertension may contribute to endothelial dysfunction, further elevating DVT risk. These factors synergistically increase the likelihood of thrombus formation, as supported by clinical studies (Kearon et al., 2016).

Question 3: Diagnostic Findings and Additional Tests

The elevated D-dimer level (1.2 mg/L) indicates fibrin degradation, a hallmark of thrombus formation, supporting the DVT diagnosis. Doppler ultrasound, showing a non-compressible popliteal vein, provides definitive evidence of DVT. Normal coagulation studies suggest no underlying coagulopathy, but the clinical presentation and imaging are sufficient for diagnosis. Additional tests, such as genetic screening for Factor V Leiden or prothrombin gene mutations, could be considered if recurrent DVT or a family history is present. These tests identify hereditary thrombophilias that increase clotting risk (Wells et al., 2018).

Question 4: Nursing Interventions and Pathophysiology

Nurses play a critical role in managing DVT. Administering prescribed anticoagulants, such as low-molecular-weight heparin (e.g., enoxaparin), prevents clot propagation by inhibiting thrombin and factor Xa. Applying compression stockings reduces venous stasis and alleviates swelling by promoting blood flow. Educating Mrs. K on mobility exercises, such as ankle pumps, counteracts stasis during recovery. Monitoring for bleeding risks, a side effect of anticoagulation, ensures patient safety. Discontinuing oral contraceptives, in consultation with her physician, addresses the hypercoagulable state (Kearon et al., 2016).

Question 5: Potential Complications and Prevention

Nurses must monitor for pulmonary embolism (PE), a life-threatening complication where the thrombus dislodges and occludes pulmonary arteries. Symptoms like dyspnea or chest pain warrant immediate assessment. Post-thrombotic syndrome, characterized by chronic leg pain and swelling, is another concern due to venous damage. Preventive measures include ensuring adherence to anticoagulation therapy, encouraging early ambulation, and using compression therapy. Regular follow-up with Doppler ultrasound can detect recurrent thrombi, reducing long-term complications (Stone et al., 2017).

Conclusion

This case study underscores the importance of understanding DVT’s pathophysiology to guide nursing care. Mrs. K’s symptoms, driven by thrombus formation and inflammation, highlight the need for prompt diagnosis and intervention. By addressing risk factors and monitoring complications, nurses can improve patient outcomes. This assignment encourages students to apply pathophysiological principles to clinical practice, fostering critical thinking and evidence-based decision-making.

References

Kearon, C., Akl, E. A., Ornelas, J., Blaivas, A., Jimenez, D., Bounameaux, H., Huisman, M., King, C. S., Morris, T. A., Sood, N., Stevens, S. M., Vintch, J. R. E., Wells, P., Woller, S. C. and Moores, L. (2016) Antithrombotic therapy for VTE disease: CHEST guideline and expert panel report. Chest, 149(2), pp. 315–352.

Stone, J., Hangge, P., Albadawi, H., Wallace, A., Shamoun, F., Knuttinen, M. G., Naidu, S. and Oklu, R. (2017) Deep vein thrombosis: Pathogenesis, diagnosis, and medical management. Cardiovascular Diagnosis and Therapy, 7(Suppl 3), pp. S276–S284.

Wells, P. S., Ihaddadene, R., Reilly, A. and Forgie, M. A. (2018) Diagnosis of venous thromboembolism: 20 years of progress. Annals of Internal Medicine, 168(2), pp. 131–140.

Witt, D. M., Nieuwlaat, R., Clark, N. P., Ansell, J., Holbrook, A., Skov, J., Shehab, N., Mock, J., Myers, T., Dentali, F., Crowther, M. A., Agarwal, A., Bhatt, M. and Khatib, R. (2018) American Society of Hematology 2018 guidelines for management of venous thromboembolism: Optimal management of anticoagulation therapy. Blood Advances, 2(22), pp. 3257–3291.

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