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© 2002 American Society for Clinical Oncology
Some Unusual Complications of MalignanciesCase 2. Marantic Endocarditis in Advanced CancerMayo Clinic, Rochester, MN A 33-year-old woman with grade 3/4 primary peritoneal mucinous adenocarcinoma with hepatic metastases was not responsive to two cycles of paclitaxel. While sitting in the waiting room, she experienced sudden, sharp, excruciating left flank pain accompanied by diaphoresis and emesis. She denied chills, dysuria, hematuria, or a history of nephrolithiasis. She reported that the pain was markedly different from that experienced during a past episode of pyelonephritis. She had no history of cardiac disease or deep venous thrombosis. Her family history was negative for hypercoagulability. Two weeks earlier, the patient had experienced the acute development of right facial droop and slurred speech, which she regarded as side effects from a fentanyl patch. The slurred speech resolved within 24 hours, but the facial droop remained. She was evaluated at a local hospital and 1 week later by a neurologist. On the basis of magnetic resonance imaging findings, treatment with oral dexamethasone was begun. An axial T2-weighted magnetic resonance imaging scan (Fig 1) revealed multiple foci of increased T2 signal within both cerebral hemispheres with mild gadolinium enhancement and smaller foci of abnormal signal in the left frontal and parietal lobes (arrows). Magnetic resonance angiography of the intracranial circulation (Fig 2) revealed occlusion of the left middle cerebral artery distal to the M-1 segment (arrows), with abnormal caliber of the anterior temporal branches bilaterally, more marked on the left. Diffusion-weighted and gadolinium-enhanced scans (not shown) supported a diagnosis of embolic disease rather than metastatic lesions.
The patient was admitted to the oncology service, where, on initial physical examination, she was tachypneic but normotensive and afebrile. Results of cardiac and pulmonary examinations were within normal limits. The abdominal examination was significant for hepatomegaly 3 cm below the right costal margin, a fixed right-lower-quadrant mass 4 cm above the pelvic brim, and marked left-sided costovertebral tenderness. Neurologic examination revealed slightly pale ocular discs bilaterally with normal acuity, a mild lower facial droop, and diffuse hyperreflexia with flexor plantar responses. Examination of the extremities revealed splinter hemorrhages (Fig 3) in the nailbeds of the hands bilaterally.
Hematologic studies showed a WBC count of 14.4 x 109/L (normal, 3.5 to 10.5 x 109/L), a platelet count of 82 x 109/L (normal, 150 to 450 x 109/L), normal prothrombin and partial thromboplastin times, a fibrinogen level of 127 mg/dL (normal, 200 to 440 mg/dL), and a D-dimer level of 2,000 ng/mL (normal, < 250 ng/mL). Soluble fibrin monomers were negative, suggesting a consumptive coagulopathy. There was no evidence of an underlying hypercoagulable state, with antithrombin III, protein C, and homocysteine levels in the normal range; protein S was measured at 57% (normal, 60% to 120%), anticardiolipin antibodies were negative, and there was no evidence of prothrombin 20210 or factor V Leiden mutation. Liver function testing revealed elevations of alkaline phosphatase to 484 U/L (normal, 81 to 213 U/L), AST to 240 U/L (normal, 12 to 31 U/L), and ALT to 148 U/L (normal, 9 to 29 U/L). Bilirubin levels were normal. Urine and blood cultures were negative. CSF from a lumbar puncture revealed normal protein and glucose with normal cell counts and no organism growth. Chest radiograph was normal. Computed tomography scanning of the abdomen and pelvis (Fig 4) revealed multiple low-attenuation lesions in the liver consistent with metastases and smaller, wedge-shaped defects in the midportion of the right kidney and spleen, findings that are consistent with arterial occlusion. The large left renal infarcts undoubtedly were responsible for the patient’s left flank pain.
During her hospital course, the patient was treated with subcutaneous heparin and warfarin. Dexamethasone was continued as treatment for cerebral edema. Her pain was controlled with morphine. A transesophageal echocardiogram was offered; however, because of her overall poor clinical prognosis, the patient declined. The patient’s medical history, presentation, examination findings, and imaging studies were all consistent with the diagnosis of marantic endocarditis. When she was dismissed to home, to be under the care of her local physicians, she was receiving anticoagulants and had good pain control. Nonbacterial thrombotic endocarditis (NBTE) was first described by Ziegler1 in 1888. The pathologic event was thought to be the deposition of fibrin on cardiac valves that were normal or superficially degenerated. It was not until 1923 that Libman2 termed it a "terminal type," or marantic endocarditis. Cancer ranks high on the differential diagnosis of causes of marantic endocarditis. Neoplasms are thought to cause NBTE through the initiation of a hypercoagulable state, therefore fulfilling the criteria for Trousseau syndrome.3 Studies have found the incidence of NBTE to be as high as 9% in patients coming to autopsy, with an average of 1.2%.4 The most frequently associated malignancies are those of the breast, lung, prostate, and colon. The neoplasm is usually far advanced by the time of diagnosis. Echocardiographic studies have not prospectively evaluated cancer patients for NBTE.5 The presenting symptom of NBTE is usually systemic or pulmonary embolization. The most common sites are the cerebral, coronary, renal, and mesenteric arteries. However, little is known about NBTE from cases in which it was diagnosed while patients were alive. Pathologic findings indicate that NBTE most commonly involves the aortic and mitral valves, with multiple vegetations smaller than 3 mm in diameter. Transesophageal echocardiography is recommended for diagnosis because case studies have noted the failure of transthoracic echocardiography to detect valvular lesions that were later viewed on autopsy.6 Treatment for NBTE is based on the principle of treating it as an underlying thrombotic disorder complicating cancer as part of Trousseau syndrome.7 For this reason, anticoagulant therapy with heparin is generally thought to be the initial treatment of choice. However, it is unknown whether this treatment has a significant effect on mortality. Surgical replacement of affected valves is rarely undertaken because these patients generally have advanced metastatic disease. Patients with an overall poor prognosis often choose, as ours did, to forgo treatment and opt for palliative care.
NOTES Copyright © 2002 American Society of Clinical Oncology REFERENCES 1. Ziegler E: Ueber den Bau und die Entstehung der endocarditischen Efflorescenzen. Verh Kong Inn Med 7: 339-343, 1888
2. Libman E: Characterization of various forms of endocarditis. JAMA 80: 813-818, 1923 3. Trousseau A: Phlegmatia alba dolens: Clinique Médicale de l’Hôtel-Dieu de Paris. London, N Syndenham Soc 3: 94, 1865 4. Lopez JA, Ross RS, Fishbein MC, et al: Nonbacterial thrombotic endocarditis: A review. Am Heart J 113: 773-784, 1987[CrossRef][Medline] 5. Joffe II, Jacobs LE, Owen AN, et al: Noninfective valvular masses: Review of the literature with an emphasis on imaging techniques and management. Am Heart J 131: 1175-1183, 1996[CrossRef][Medline]
6. Shuaib A: Stroke from other etiologies masquerading as migraine-stroke. Stroke 22: 1068-1074, 1991 7. Bell WR, Starksen NF, Tong S, et al: Trousseau’s syndrome: Devastating coagulopathy in the absence of heparin. Am J Med 79: 423-430, 1985[CrossRef][Medline]
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Copyright © 2002 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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