Occulsion of the fistula in a dialysis patient – is it always a common reason?

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NDT Plus (2008) 2: 117–119 doi: 10.1093/ndtplus/sfm021

Advance Access publication 17 January 2008

Nephroquiz

(Section Editor: M. G. Zeier)

Occlusion of the fistula in a dialysis patient—is it always a common

reason?

Yi-Lung Lin, His-Hsien Chen and Tzen-Wen Chen

Division of Nephrology, Department of Internal Medicine, Taipei Medical University and Hospital, Taipei, Taiwan

Keywords: diffuse intravascular coagulation; prostate cancer; trousseau’s syndrome

A 67-year-old man with chronic glomerulonephritis and end-stage renal disease (ESRD), on maintenance haemodialysis for 1 year, had a history for failure of a right radiocephalic fistula, a right radiocephalic graft, a right sub-clavian permanent catheter and a left radiocephalic fistula due to refratory thrombosis. He presented to our hospi-tal with intermittent gross haematuria for 9 months and swelling over the right arm and left hand for 1 month. On further questioning, he also reported a history of deep ve-nous thrombosis over bilateral lower legs, 3 months earlier. He had no local cutaneous erythema and heat, fever or flank pain.

His blood pressure was 130/70 mmHg. Physical exam-ination identified pale appearance and swelling over right arm and left hand. On admission, pre-dialytic blood cre-atinine was 7.2 mg/dL, urea nitrogen 75.4 mg/dL, albu-min 3.5 g/dL, haemoglobin 9.0 g/dL, platelet 100 k/µL, cholesterol 68 mg/dL, triglycerate 98 mg/dL, sodium 138 mmol/L, potassium 4.3 mmol/L, calcium 10.0 mg/dL and phosphate 5.1 mg/dL. Pro-thrombin time was 11.6 s (normal 10.7–13 s, control 12.15 s), INR 1.1 and activated partial thromboplastin time 25 s (normal 20–36 s, control 31.1 s). Fibrinogen was 800 mg/dL (200–400), fibrino-gen degradation products>20 µg/mL (<10) and D-dimer

>1 µg/mL (<0.5). Lupus anticoagulants, anti-thrombin III,

protein C, S and other plasma coagulation factors were negative or within normal limits. Urinalysis showed macro-scopic haematuria 40–60 per high power field. Prostate sonography (Figure 1) displayed a prostate tumour. Prostate specific antigen (PSA) was 38.94 ng/mL. Transurethral radical prostatectomy was done, and the pathology re-ported prostate adenocarcinoma without local invasion. Correspondence and offprint requests to: Tzen-Wen Chen,

Divi-sion of Nephrology, Department of Internal Medicine, Taipei Med-ical University and Hospital, 252 Wu-Hsing Street, Taipei 110,

Taiwan. Tel: +886-2-27372181 ext 3330; Fax: +886-2-27363051;

E-mail: yilunglin@ntu.edu.tw

Venography for right arm (Figure 2a) and left hand (Figure 3) was performed, for further workup.

What abnormalities are seen on the venography of

right superior vena cava (SVC) and left upper

limb?

What is the clinical diagnosis?

THE DIAGNOSIS: prostate adenocarcinoma with chronic diffuse intravascular coagulation and recurrent thrombosis of vascular access (trousseau’s syndrome).

Right SVC venography showed near-total occlusion of SVC lumen (Figure 2a, white arrow). There were patent basilic, median, medial cubital and axillary veins at left forearm and arm. However, cephalic vein was poorly vi-sualized (Figure 3a). There were also patent ulnar, radial, distal basilic and median veins at left forearm. Poor flow over distal cephalic vein due to thrombosis was disclosed (Figure 3b). After surgical thrombectomy with pathological proof of fibrin thrombi, patency of SVC was demonstrated (Figure 2b, white arrow).

PSA declined to 0.06 ng/mL 6 months after prostatec-tomy. With low molecular weight heparin and then a shift to coumadin to keep INR 1.5–2X, the newly created brachio-basilic graft functioned well. Swelling of upper limbs also disappeared in several weeks.

Trousseau’s syndrome was first reported over 100 years ago, whereby cancer patients have an increased incidence of venous thromboembolism (VTE) in patients with a wide variety of tumours such as bladder, breast, lung, stomach and colon tumours, although pancreatic cancer accounts for 50% of all cases [1]. Paraneoplastic syndrome of prostate cancer (trousseau’s syndrome), such as in our case, was also reported in a few earlier cases [2–3]. VTE is increased fourfold in patients with cancer, and underlying malignancy accounts for 10% to 20% of causes of VTE. Indeed, the presence of an unexplained and recurrent vascular or shunt thrombosis can be clinical reason enough to screen for oc-cult malignancy in patients on maintenance haemodialysis [1].

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at Taipei Medical University Lib. on May 14, 2011

ndtplus.oxfordjournals.org

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118 Y.-L. Lin et al.

Fig. 1. Prostate sonography showed lobulated prostate mass with intra-vesical protruding.

Fig. 2. (a) Left: right SVC venography showed near-total occlusion of SVC lumen (white arrow). (b) Right: after surgical thrombectomy with pathological proof of fibrin thrombi, patency of SVC was demonstrated (white arrow).

Along with a comprehensive medical history and physi-cal examination, numerous conventional diagnostic testing and imaging including blood tests, tumour markers, chest radiography, venography, endoscopy, computed tomogra-phy and magnetic resonance imaging of the chest, abdomen and pelvis can be used to successfully diagnose VTE with a primary malignancy in approximately 85% to 95% of pa-tients. These clinical findings have been supported by labo-ratory studies, which have identified altered levels of blood clotting factors in the serum of cancer patients, including elevated fibrinogen, FDP, 3P test, D-dimer as well as de-clined or normal PT, PTT and PLT count [4]. These changes susceptible to coagulation are also risk factor for vascular access failure in haemodialysis patients. Currently, vascu-lar access problems are the most common complication

en-countered in patients undergoing long-term haemodialysis, as well as thrombosis, which is a leading cause of vascular access failure, usually resulting from occlusion or stenosis caused by progressive thrombosis in the venous outflow system. In addition to endothelial injury following a shunt operation, excessive intra-luminal pressure, turbulent flow and frequent needle insertion during haemodialysis, hy-percoagulability like paraneoplastic syndrome, trousseau’s syndrome and DIC are also common aetiologies of shunt failure [5].

Proposed mechanisms include changes in anti-thrombotic and pro-anti-thrombotic proteins, tumour-cell-induced thrombosis responsive to hypoxia and dysregulated angiogenesis, hypoxia-induced pro-coagulant gene expres-sion, cytokine activation, endothelial dysfunction, and

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Occlusion of the fistula in a dialysis patient 119

Fig. 3. (a) Left: there were patent basilic, median, medial cubital and axillary veins at left forearm and arm. Cephalic vein was poorly visualized. (b) Right: there were patent ulnar, radial, distal basilic and median veins at left forearm. Poor flow over distal cephalic vein due to thrombosis was disclosed.

conditions that can lead to chronic disseminated intravas-cular coagulation [6].

The cornerstone of management is the treatment of the underlying cancer, anticoagulants and adequate prophylaxis in patients with high risk for VTE [4].

Conflict of interest statement. None declared. References

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2. Miyake H, Hara I, Yamanaka K et al. Elevation of urokinase-type plasminogen activator and its receptor densities as new predictors of disease progression and prognosis in men with prostate cancer. Int J

Oncol 1999; 14: 535–541

3. Lwaleed BA, Francis JL, Chisholm M. Monocyte tissue factor levels in patients with urological tumours: an association between tumour presence and progression. BJU Int 1999; 83: 476–482

4. Levi M, ten Cate Hugo. Disseminated intravascular coagulation N Engl

J Med 1999; 341: 586–592

5. Song IS, Yang WS, Kim SB et al. Association of plasma fibrinogen con-centration with vascular access failure in hemodialysis patients Nephrol

Dial Transplant 1999; 14: 137–141

6. Denko NC, Giaccia AJ. Tumor hypoxia, the physiological link between trousseau’s syndrome (Carcinoma-induced coagulopathy) and metasta-sis Cancer Res 2001; 61: 795–798

Received for publication: 4.10.07 Accepted in revised form: 6.11.07