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Myelophthisis as a Solitary Manifestation of Failure From Rectal Carcinoma A Batson Phenomenon?

The well-recognized routes of spread of colorectal carcinoma are lymphatic, intramural, portal venous, implantation, and direct extension. The patterns of failure from rectal carcinoma that reflect these include lymph nodes metastases, suture line recurrences in low-anterior resections, pelvic recurrences, peritoneal metastases, and liver, lung, and bony metastases. It is unusual to find systemic failure in the absence of liver metastases,[1] although the portosystemic shunting that exists at the anorectal junction does permit hematogenous spread outside the portal circulation to the internal iliac vessels and the cava. Lung metastases in the absence of liver metastases are usually explained by this mechanism. Symptomatic bony metastases are uncommon in rectal carcinoma, and reviews of patterns of failure in more than 4000 patients with colorectal cancer[1,2] have suggested that the incidence of bony metastases in colorectal carcinomas is small, generally less than 10%. In contrast to the right colon, sigmoid and rectal carcinomas appear to be associated with a higher incidence of osseous metastases, favoring the pelvis and lumbosacral spine.[1,3] Early studies on the patterns of failure from resected rectal carcinomas have suggested an osseous pattern of spread that favors sacrum, coccyx, pelvis, and lumbar vertebrae in descending order of frequency.[4] These observations have delineated the possibility that a unique route of metastasis may play a role in the spread of rectal carcinomas (ie., the Batson vertebral venous plexus).[1,5]

Myelophthisic anemia secondary to rectal carcinoma is unprecedented in our experience and consistent with previous observations that bony metastases are rare.[1,2] The finding of a myelophthisic process in a patient undergoing radical resection for localized rectal carcinoma may, therefore, direct consideration toward a primary hematologic malignant neoplasm or a second malignant neoplasm metastatic to the bone marrow. We report a case in which myelophthisis in the setting of apparently localized rectal carcinoma was confirmed to be secondary to spread from rectal primary and consider the implications of this observation.


A 49-year-old white woman presented with symptoms of pelvic pain and change in bowel habit. Endoscopy revealed a mass at the level of the dentate line. The biopsy specimen showed a grade 3 mucin-producing adenocarcinoma. The patient underwent external beam radiation therapy with concurrent infusional 5-fluorouracil for 6 weeks, with minimal complications. Postradiation digital examination revealed an anterior rectal mass, which was mobile and extended inferiorly to the external sphincter muscle. There was no adenopathy, results of a chest x-ray examination were normal and abdominal computed tomographic scan showed a very low-lying rectal carcinoma, with no evidence of metastatic disease. On repeat anoscopy, an ulcerated polypoid mass measuring 1 cm, involving the distal rectum at the 9 o'clock position with extension into the squamocolumnar junction, was seen. Endoscopic ultrasound findings included thickening of the distal rectal wall with invasion of the rectal muscular wall by tumor. The patient subsequently underwent abdominoperineal resection without complications. At surgery, no evidence of metastatic disease was found on the peritoneum or the liver surface. A gross total resection of the tumor was performed, although fibrotic adherence to the vagina required resection of part of the vaginal wall. Pathologic analysis revealed an invasive mucinous carcinoma that measured 2.5 cm with transmural invasion into the subserosa. Resection margins, including the vaginal radial margin, were negative for disease. Four pericolic nodules were identified, which were judged to represent regional lymph nodes effaced with metastatic tumor.

One month postoperatively, the patient was readmitted with complaints of hip and pelvic pain radiating down her leg and subjective patchy numbness of the thigh, recurrent anemia, and transfusion dependence. Examination showed generalized weakness, a tender lumbosacral spine, hyperreflexia, and clonus in both lower extremities without objective sensory loss. A second computed tomographic scan of the abdomen and pelvis showed no sign of tumor recurrence. The blood cell count showed anemia and thrombocytopenia with the following indexes: hemoglobin, 8.7 g/dL; platelets, 23 x [10.sup.9]/L; white blood cells, 6.7 x [10.sup.9]/L; white blood cell differential: segmented neutrophils, 40%; bands, 34%; lymphocytes, 8%; monocytes, 8%; metamyelocytes, 3%; myelocytes, 3%; and nucleated red blood cells, 4%. Reticulocyte count was 8%. Coagulation profile showed the following: fibrinogen, 159 mg/dL (reference range, 127-409 mg/dL); D-dimer, more than 1 (reference value, [is less than] 0.5); prothrombin time, 13.3 s (reference range, 11.5-14.0 s); and activated partial thromboplastin time, 28 s (reference range, 21-36 s). Blood chemistry results included the following values: lactate dehydrogenase, 3259 U/L (reference range, 300-600 U/L); haptoglobin, less than 6 mg/dL (reference range, 16-200 mg/dL); total bilirubin, 3.1 mg/dL (reference range, 0.1-1.1 mg/dL); alkaline phosphatase, 134 U/L (reference range, 34-122 U/L); aspartate aminotransferase, 94 U/L (reference range, 13-40 U/L); and alanine aminotransferase, 43 U/L (reference range, 9-51 U/L). Urinalysis showed the following values: pH 6.0; specific gravity, 1.013; protein, 100 mg/dL; bilirubin, small; blood, large; urobilinogen, 1.0 mg/dL; red blood cells, 9 per high-power field; white blood cells, 20 per high-power field; squamous epithelial cells, less than 1 per high-power field; blood urea nitrogen, 20 mg/dL (reference range, 7-23 mg/dL); creatinine, 0.74 mg/dL (reference range, 0.7-1.7 mg/dL); and calcium, 9.9 mg/dL (reference range, 8.6-10.6 mg/dL). Bone scan showed multiple areas of bony metastases involving the spine, ribs, and proximal long bones. Magnetic resonance imaging of the lumbosacral spine showed marrow replacement with enhancing tumor in all lumbar vertebrae and the entire pelvis. No cord compression or meningeal enhancement was noted.

Peripheral blood smear confirmed a leukoerythroblastic picture with evidence of microangiopathic hemolysis (Figure 1). A pelvic bone biopsy was performed, which showed replacement of the bone marrow by pools of mucin and scattered groups of malignant epithelial cells with intracellular mucin, consistent with the rectal primary (Figure 2).



Atypical patterns of metastasis may be explained by several mechanisms: intrinsic biological heterogeneity in the metastatic phenotype so that a cancer may evolve through its genetic instability with variant adhesion molecules, local extension of tumor beyond the host organ anatomic limits, alterations in the natural pathways of spread by distortion of lymphatic or venous drainage by prior trauma, or modulation of tumor biology by effective adjuvant therapy. The Batson venous plexus was first suggested to play an unrecognized role in vertebral metastases from prostatic carcinoma.[6] A rich network of vertebral veins was believed to interconnect with the prostatic venous plexus. Dye injection studies in cadavers and experimental animals confirmed this hypothesis. Since the veins are valveless, the Batson plexus is thought to allow migration of tumor cells into the vertebral plexus when the intra-abdominal pressure is increased, even in physiologic situations such as moving from the supine to the sitting and standing positions.[7] The vertebral venous complex forms innumerable anastomoses with the sinusoidal structure of the vertebral bone marrow and the epidural venous channels. Experimental injections of labeled human prostate cells in nude mice under concomitant vena cava clamping have confirmed metastatic competence to the vertebral venous channels and the bone marrow of the lumbosacral vertebrae.[8] Based on clinical evidence of the pattern and frequency of osseous metastases in colorectal cancers, Vider et al[5] and Welch and Donaldson[1] have suggested that the Batson plexus plays a role in the spread of rectal carcinomas.

In the patient described in this report, the symptomatic evidence of lumbosacral metastases within a month after the completion of therapy suggests that these metastases were well established and undetected at diagnosis. The radiologic findings of extensive marrow replacement in lumbosacral spine and the presence of myelophthisic anemia suggest that a heavy burden of metastatic disease was already present throughout the bone marrow. The absence of clinically detectable metastases in the classic landing sites for rectal carcinoma strongly suggests that spread to the pelvis, lumbar vertebrae, and beyond occurred via the Batson plexus to the vertebral venous plexus.

Lindemann et al[9] studied the frequency of micrometastases

in the bone marrow of patients undergoing radical resection for localized colorectal cancers. Interestingly, a higher incidence of micrometastases in rectal cancers (15/36 or 42%) than in colon cancers (13/52 or 25%) was found (univariate P = .08). The presence of micrometastases was found to have prognostic significance for relapse, independent of tumor penetration, lymph node status, and grade of differentiation. It is unclear if the Batson plexus plays a role in generating these micrometastases. Myelophthisis as a solitary manifestation of failure in rectal cancer may be an extreme and rare example of the Batson phenomenon in rectal cancer metastases, but it draws renewed attention to the experimentally established validity and clinical implications of this mode of spread in pelvic neoplasms.[10] A better understanding of the role of the Batson plexus in rectal cancer and the implications of bone marrow micrometastases could influence the approach to staging and therapy in these patients.


[1.] Welch JP, Donaldson GA. The clinical correlation of an autopsy study of recurrent colorectal cancer. Ann Surg. 1979;189:496-502.

[2.] August DA, Ottow RT, Sugarbaker PH. Clinical perspective of human colorectal cancer metastasis. Cancer Metastasis Rev. 1984;3:303-324.

[3.] Antoniades J, Croll MN, Walner RJ, Brady LW. Bone scanning in carcinomas of the colon and rectum. Dis Colon Rectum. 1976;19:139-143.

[4.] Bacon HE, Gilbert PD. Sites of metastases from carcinoma of the anus, rectum and sigmoid colon. JAMA. 1938;111:219-221.

[5.] Vider M, Maruyama Y, Narvaez R. Significance of the vertebral venous (Batson's) plexus in metastatic spread in colorectal carcinoma. Cancer. 1977;40:67-71.

[6.] Batson OV. The function of the vertebral veins and their role in the spread of metastases. Ann Surg. 1940;112:138-149.

[7.] Suzuki T, Kurokawa K, Jimbo H, et al. The role of intraabdominal pressure in venous blood drainage from the prostate into the vertebral vein system. Jpn J Physiol. 1993;43:697-708.

[8.] Harada M, Shimizu A, Nakamura Y, Nemoto R. Role of vertebral venous system in metastatic spread of cancer cells to the bone. In: Karr JP, Yamanaka H. Prostate Cancer and Bone Metastasis. New York, NY: Plenum Press; 1992:83-92.

[9.] Lindemann F, Schlimok G, Dirschedl P, Witte J, Riethmuller G. Prognostic significance of micrometastic tumour cells in bone marrow of colorectal cancer patients. Lancet. 1992;340:685-689.

[10.] Geldof AA. Models for cancer skeletal metastasis: a reappraisal of Batson's plexus. Anticancer Res. 1997;17:1535-1539.
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Author:Mathew, Paul; Fleming, Declan; Adegboyega, Patrick A.
Publication:Archives of Pathology & Laboratory Medicine
Article Type:Brief Article
Geographic Code:1USA
Date:Aug 1, 2000
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