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What is causing this patient's low back pain?

Umar, Mohamad DSc, EMPA-C; Benish, Trisha DSc, EMPA-C; Camacho, Lance DSc, EMPA-C

Journal of the American Academy of PAs: September 2019 - Volume 32 - Issue 9 - p 53–56
doi: 10.1097/01.JAA.0000578800.23040.2d
A Difficult Diagnosis
Free

Mohamad Umar is a director and assistant professor of the US Army/Baylor University Emergency Medicine PA Residency Program at San Antonio (Tex.) Military Medical Center and practices in emergency medicine at San Antonio Military Medical Center. Trisha Benish is a recent graduate of the US Army/Baylor University Emergency Medicine PA Residency Program and practices in emergency medicine at 673rd Medical Group in Joint Base Elmendorf-Richardson, Ala. Lance Camacho is an assistant director and assistant professor of the US Army/Baylor University Emergency Medicine PA Residency Program and practices in emergency medicine at San Antonio Military Medical Center. The authors have disclosed no potential conflicts of interest, financial or otherwise.

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CASE

Figure

Figure

A 47-year-old man presented to the ED with a 9-day history of gradual onset acute lower back pain. He described the pain as a constant and dull tightness across the lumbar spine and rated it a 9 out of 10 on a pain intensity rating scale.

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History

The patient had a history of lower back pain but had not previously had bilateral gluteal tightness. He denied bladder or bowel incontinence, loss of motor or sensory function, venous claudication, fall, or other trauma. The patient was unable to identify aggravating factors, such as movement. He said no interventions helped the pain, including the diclofenac prescribed by his primary care physician a week earlier. His past medical history was significant for migraine headaches, gout, post-traumatic stress disorder, and obstructive sleep apnea, colorectal cancer, and previous surgeries. He was diagnosed with stage IIA colorectal cancer 5 years ago and had a partial colon resection 4 years ago. Additional surgery included a sacral nerve stimulator placement 3 years ago to help with stool incontinence. He had no personal or family history of cardiac dysrhythmia, pulmonary embolus, or deep vein thrombosis. He takes sertraline, bupropion, hydroxyzine, diclofenac, and rizatriptan. He denied tobacco and illicit drug use and said he consumed alcohol rarely.

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Physical examination

The patient was well appearing with a typical nonantalgic gait. His vital signs were within normal limits. Spinal examination was significant for mild decreased forward flexion. Tenderness to palpation was observed diffusely across the lumbar paraspinal muscles, sparing the spinous processes, but without palpable spasms or gross deformity. Rectal tone was preserved. Lower extremities were free of overt signs of involvement, demonstrating an intact neuromuscular examination with normal sensation, straight leg raise, and deep tendon reflexes. He had benign skin, neck, lung, heart, abdomen, and genitalia examinations.

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Diagnostic testing and initial management

Peripheral access was obtained, and he was given morphine 4 mg IV and a bolus of 500 mL 0.9% sodium chloride solution. Lumbar spine radiograph was ordered and revealed degenerative joint disease without evidence of acute osseous defects. Complete blood cell count, basic metabolic panel, and urinalysis were within normal limits, except for mild elevations in the blood urea nitrogen, 24.4 mg/dL (normal range, 8 to 23 mg/dL); creatinine, 1.28 mg/dL (normal range, 0.67 to 1.17 mg/dL); and anion gap, 14.7 mmol/L (normal range, 5 to 14 mmol/L).

During the clinical course, the patient began to express signs of rapid decline, including bilateral lower extremity cyanosis, loss of sensation, and the absence of distal pulses (including with Doppler examination). In light of the marked clinical progression, an emergency IV contrast CT of the chest, abdomen, and pelvis with venous runoff to the bilateral lower extremities was promptly arranged.

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DIFFERENTIAL DIAGNOSIS

  • metastatic spinal cord compression
  • cauda equina syndrome
  • ruptured abdominal aortic aneurysm
  • abdominal aortic dissection
  • inferior vena cava (IVC) thrombosis
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OUTCOME

The CT revealed bilateral femoral artery occlusion (Figure 1), an IVC interruption with azygous continuation (Figure 2), and a subsegmental pulmonary embolism. This vascular occlusion put the patient at risk for ischemic injury. The vascular surgeon was consulted and anticoagulation initiated with 5,000 units of heparin as an IV bolus, followed by an infusion of 13 units/kg/h.

FIGURE 1

FIGURE 1

FIGURE 2

FIGURE 2

The patient was immediately taken to the OR with the diagnosis of bilateral lower extremity arterial ischemia. Intraoperatively, the surgeon noted significant bilateral femoral vein engorgement, but no arterial thromboembolism. Venography demonstrated a cutoff of contrast entering the IVC and obstruction of venous return from the lower extremities, with no signs of extravasation. A superior vena cavagram revealed an IVC occlusion and a large azygous vein. Bilateral saphenous veins and vena cava pressures were greater than 90 mm Hg. These findings represented an IVC acute thrombosis with venous congestion.

Bilateral lower extremity fasciotomies, IVC recanalization, and stenting were performed (Figure 3) and a fibrinolytic was administered to evacuate the thrombus. In the ensuing days, the patient was taken to the OR repeatedly for washouts and debridement. About 3 weeks after his initial ED presentation, the patient developed muscle necrosis and required a through-the-knee amputation of the right lower leg. After a 35-day hospital course, he was discharged on rivaroxaban for indefinite anticoagulation and sent to long-term rehabilitation.

FIGURE 3

FIGURE 3

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DISCUSSION

IVC thrombosis is a rare condition occurring in 1 in 10,000 people.1 Between 2.6% and 4% of all patients with confirmed lower extremity deep vein thrombosis (DVT) will also have an IVC clot.2 Patients with IVC thrombosis have a 30% risk of developing venous thromboembolism (VTE) and pulmonary embolus.1 Amputation, although rare, may be needed secondary to compromised arterial blood flow to the limbs.2 Other acute complications include renal vein thrombosis leading to acute renal failure, post-thrombotic syndrome, and chronic venous insufficiency.1,2 Early recognition and treatment is vital to reducing the acute complication as well as preventing long-term complications.

Congenital IVC anomalies have been reported as a potential risk for the development of IVC thrombosis, occurring in 0.3% to 0.6% of the general population, but with a contributing prevalence of 60% to 80% of reported cases.2-4 Normal IVCs are categorized into three anatomic segments—infrarenal, renal, and suprarenal/infrahepatic.5 This patient had an IVC interruption characterized by absence of the suprarenal segment, which is more common in men and typically asymptomatic.1,5 This embryologic anomaly results from failure of the hepatic and the infrarenal segments to fuse, which then causes shunting of distal venous blood back to the heart via the azygous vein.5,6

In the absence of these congenital phenomenon, a spontaneous IVC thrombosis in patients with a normal IVC is uncommon, and usually is caused by external compression or the development of a hypercoagulable state.2 Intra-abdominal mass such as abdominal aortic aneurysm and polycystic kidney disease have been reported to compress the IVC, interfering with normal blood flow and facilitating clot formation.7 Additionally, any disease that disrupts the coagulation system can lead to venous thromboembolism. Malignancy is a well-documented cause of hypercoagulable state and risk for IVC thrombosis.8 Colorectal cancer is a particular concern because of its tendency to produce mass compressive effects on the blood vessels in addition to its upregulation of the clotting system.8 Surgical resection and chemotherapy for colorectal cancer further increase clot risk secondary to extensive endothelial damage.8 The case patient had a history of colorectal cancer and surgical resection. At the time of presentation, he had been cancer-free for 26 months as confirmed by CT surveillance.

IVC thrombosis manifesting as low back pain is a challenging diagnosis because the clinical presentation is often ambiguous, lacking specific findings of the disease. Patients commonly complain of nonspecific lower back and abdominal pain that is followed by leg heaviness, limb swelling, and cramping.1,2 The diagnosis of IVC thrombosis often is considered only when signs and symptoms of clot migration and/or venous hypertension become apparent.2 On rare occasions, in chronic IVC occlusion, the dilated veins of the large paraspinal collateral channels compress the spinal cord and other peripheral nerves, resulting in lumbar radicular pain, sciatica, and even cauda equina syndrome.2

Though contrast venography is regarded as the gold standard for diagnosing IVC thrombosis, it is rarely performed because of its invasive nature.1 Instead, duplex ultrasound is the preferred initial study, as it is noninvasive, low-risk, and readily available.7 CT and MRI also can be used to detect thrombosis with more specificity and with the added advantage of evaluating a wider differential in the abdomen, pelvis, and retroperitoneal region.1 Laboratory results are not helpful in diagnosing IVC thrombosis.7

The treatment of IVC thrombosis requires eliminating the thrombus and addressing long-term complications, clot migration, and recurrence. No guidelines exclusively deal with anticoagulation management of patients with IVC thrombosis.2 However, practice favors the American College of Chest Physicians (ACCP) guidelines for anticoagulant therapy for patients with VTE, which recommend 3 to 6 months of oral anticoagulants for provoked VTE brought on by temporary risks such as trauma or surgery, and 12 months for unprovoked VTE.2,9 Although no shared consensus about treatment duration exists in the literature, most authors advocate indefinite anticoagulation, especially in patients with irreversible thrombotic risk due to caval anomaly.1

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CONCLUSION

IVC thrombosis manifesting as low back pain is a rare occurrence associated with significant morbidity. Clinicians must be aware of this condition and its associated risk factors, and maintain a high index of suspicion. Understanding the most appropriate imaging modalities for timely recognition and treatment is critical to preventing acute and chronic complications.

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REFERENCES

1. McAree BJ, O'Donnell ME, Fitzmaurice GJ, et al Inferior vena cava thrombosis: a review of current practice. Vasc Med. 2013;18(1):32–43.
2. Alkhouli M, Morad M, Narins CR, et al Inferior vena cava thrombosis. JACC Cardiovasc Interv. 2016;9(7):629–643.
3. Sitwala PS, Ladia VM, Brahmbhatt PB, et al Inferior vena cava anomaly: a risk for deep vein thrombosis. N Am J Med Sci. 2014;6(11):601–603.
4. Halparin J, Monagle P, Newall F. Congenital abnormalities of the inferior vena cava presenting clinically in adolescent males. Thromb Res. 2015;135(4):648–651.
5. Aaditya A, Neelam D, Nageswar Rao J, Deepak G. Congenital anomalies of inferior vena cava, review of embryogenesis, presentation, associated congenital anomalies and surgical importance. Cardiovasc Thorac Surg. 2018;3(2):1–6.
6. Piciucchi S, Barone D, Sanna S, et al The azygos vein pathway: an overview from anatomical variations to pathological changes. Insights Imaging. 2014;5(5):619–628.
7. Fernandez LG. Inferior vena cava thrombosis. https://emedicine.medscape.com/article/1933035. Accessed June 18, 2019.
8. Rees PA, Clouston HW, Duff S, Kirwan CC. Colorectal cancer and thrombosis. Int J Colorectal Dis. 2018;33(1):105–108.
9. Kearon C, Akl EA, Ornelas J, et al Antithrombotic therapy for VTE disease: CHEST Guideline and Expert Panel Report. Chest. 2016;149(2):315–352.
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