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Calcification of a ventriculoperitoneal shunt tube
156
Surg Neurol 1988;30:156-8
Calcification of a Ventriculoperitoneal Shunt T u b e Case Report Katsumi Shimotake, M.D., Akinori Kondo, M.D., Ikuhiro Aoyama, M.D., Kiyoshi Nin, M.D., Yuzuru Tashiro, M.D., and Tatsuya Nishioka, M.D. Department of Neurosurgery, Kitano Medical Research Institute and Hospital, Osaka, Japan
Shimotake K, Kondo A, Aoyama I, Nin K, Tashiro Y, Nishioka T. Calcification of a ventriculoperitoneal shunt tube. Case report. Surg Neurol 1988;30:156-8.
A 16-year-old boy who had undergone a ventriculoperitoneal (VP) shunt because of hydrocephalus at 8 years of age complained of pain around the right neck and chest. He concomitantly had a slight fever of unknown etiology, which had been lasting for several years. Skull and chest roentgenograms revealed an unusual calcified shadow around the shunt tube. After removal of the shunt apparatus, his pain and fever disappeared. Silicone tubes used in a VP shunt apparatus may induce fibrous connective tissue proliferation around the tubes in both children and adults, but no reports of radiologically verified calcification of a VP shunt tube are found in the literature, to the best of our knowledge. The possible mechanism of calcification of the VP shunt tube is discussed.
Case R e p o r t The patient was a 16-year-old, overweight boy (85 kg and 167 cm tall) who had undergone a right temporal craniotomy in 1976, when he was 8 years of age, to relieve an otogenic intracerebral abscess; a VP shunt (Pudenz's silastic tube, Heyer-Schulte, Inc., Goleta, Calif.) had been inserted because of the subsequent hydrocephalus. Thereafter, the patient was well and active especially in judo. A continuous low-grade fever began to appear in 1982, 6 years after the VP shunt operation, but the cause of fever remained unclear in spite of medical examinations at another hospital. In July 1984, he noticed pain in the right lateral neck and upper chest wall when he elevated his right arm. He was admitted to the Department of Neurosurgery of Kitano Medical Research Institute and Hospital on September 29, 1984 for an examination.
KEY WORDS: Calcification; Ventriculoperitoneal shunt; Silicone; Human adjuvant disease
Examination
Silicone implantation has become increasingly common in neurosurgical practice because silicone material is considered to be relatively inert in biological systems. Silicone, however, is sometimes encapsulated by fibrous tissue as foreign matter [6], and another of the unwelcome complications of the implant is calcification of silicone surface [5, 7, 11]. We report on a rare case of a 16-year-old boy whose plain roentgenograms of the neck and chest demonstrated calcification of a ventriculoperitoneal (VP) shunt tube. He had also had a continuous low-grade fever. To date there have been no reports of radiologicaUy verified calcification of a VP shunt tube and hence this case may be sufficiently interesting to be reported.
Address reprint requests to: Katsumi Shimotake, M.D., Department of Neurosurgery, Kitano Medical Research Institute and Hospital, 13-3, Kamiyama-cho, Kita-ku, Osaka, 530 Japan. Received March 30, 1987; accepted January 29, 1988.
© 1988 by ElsevierSciencePublishing Co., Inc.
There were no neurological abnormalities except for hearing loss of the conductive type in the right ear due to previous otitis media. Continuous low-grade fever (37.0°C in the morning and 37.2°C in the evening) was recorded. In laboratory tests, the erythrocyte sedimentation rate (ESR) was increased moderately (22 mm/hr), but C-reactive protein (CRP) was found to be negative. Serum calcium concentration was within the normal range, but the serum triglyceride titer was over the upper limit (178 mg/dL). A plain roentgenogram showed a linear calcified shadow along the VP shunt tube, starting from just below the shunt valve to the lower chest (Figure 1). Study of the shunt functioning disclosed complete obstruction of the abdominal tube. We considered his neck and chest pain to be stimulated by the calcified shunt tube.
Operation Under general anesthesia, the shunt tube distal to the cranial valve was totally removed together with the 0090-3019/88/$3.50
Calcification of a Ventriculoperitoneal Shunt Tube
Figure 1. Plain cervical and chest roentgenograms (anteroposterior projections). Arrows show the abnormal linear calcification along a VP shunt tube.
surrounding fibrous tissue. The tube had almost completely degenerated so that it could be torn off easily and many small sandlike, calcified particles, yellowishbrown, were discovered in the surface of silicone tube. A postoperative roentgenogram showed no abnormal calcified track in the neck and chest. About 10 days after the operation, his body temperature steadied below 37.0°C (36.6°C in the morning and 36.8°C in the evening), and ESR was normalized to 6 mm/h. Pathologic Examination
Calcification was found in the surface of the shunt tube by hematoxilin-eosin staining. Another important as well as interesting histologic finding of the peritubular connective tissue was a foreign body reaction with appearance of giant cells that had engulfed the silicone particles (Figure 2).
Surg Neurol 1988;30:156-8
157
Discussion It is well known that silicone is not biologically inactive despite its chemical inactivity and is considered to be a possible cause of adjuvant disease [10]. Despite findings of negative CRP, the patient's ESR was modestly increased, and the histopathologic findings in the peritubular fibrous sheath, such as the foreign body reaction and giant cells, indicated that a long-standing fever in this patient was probably associated with a siliconerelated immune response, one of the silicone-induced human adjuvant diseases. Calcification of implanted silicone is not uncommon. Koide [7] reported radiographically evident calcification in 10 of 32 cases (31%) of augmentation mammoplasty, and there have also been reports of calcification of silicone rubber joint implants [2] and of artificial heart valves [12]. There have, however, been no reports of radiologically verified calcification of VP shunt tubes. Carmen and Kahn [4] documented an interesting phenomenon by which silicone rubber heart poppets demonstrated lipid-sorptive phenomena in contact with blood, and his laboratory data of the lipid
158
Surg Neurol 1988;30:156-8
Shimotake et al
cal stress caused by judo [5]. T h e r e may be other possible mechanisms, e.g., the following pathologic mechanisms: repeated mechanical stress around the shunt tube induces a chronic inflammatory response o f the connective tissue, resulting in atrophy and necrosis o f fibrous tissue and deposition o f insoluble intracellular calcium and phosphate. This is the so-called dystrophic calcification [ 1]. W e think that calcification o f the silicone surface is never a p h e n o m e n o n limited to products of low quality but one that may take place universally in all silicone products as a response o f silicone to the bioenvironment.
Figure 2. Photomicrograph showing the silicone surface of a shunt tube. The white arrow indicates a calcified body of silicone surface and the black arrow i7~icates the multinucleated giant cell which has engulfed a ~rticle (hematoxilin and eosin staining, x I00).
sorbability o f silicone showed that the lipid contents of the balls were in the range of 0 . 1 - 5 . 5 weight percent. It was concluded that silicone implants in direct contact with blood, such as artificial heart valves, may pick up much higher concentrations o f lipids than joint implants which are bathed in synovial fluids [3]. In clinical cases, Meester and Swanson [8] verified in silicone rubber joint implants that the lipid absorption rate was between 0.18 and 2.55 weight percent, and among many absorbed lipids, cholesterol and triglyceride levels accounted for about 4 0 % o f the total lipid measured. Therefore, as a cause o f calcification o f silicone products, O w e n and Z o n e [9] hypothesized that absorbed lipids f o r m a negatively charged interface and this might lead to a higher surface concentration of Ca ++ on a p o l y m e r surface. T h e surface calcification of silicone tubing in our case may have involved the following factors: (a) an adolescent patient with increased calcium metabolism [5], (b) an obese boy with an elevated level o f serum triglyceride, and (c) increased blood volumes in the lateral neck and chest due to continuous mechani-
References 1. Anderson WAD. Pathology. 6th ed. St. Louis: CV Mosby, 1971:77-86. 2. Beck E. Silastikprothese zum Ersatz des resezierten Speichenk6pfchens bei Trfimmerbriichen. Arch Orthop Unfall-Chir 1974;80:143-52. 3. Bole GG. Synovial fluid lipids in normal individuals and patients with rheumatoid arthritis. Arthritis Rheum 1962;5:589-601. 4. Carmen R, Kahn P. In vitro testing of silicone rubber joint implants for lipid absorption. J Biomed Mater ges 1968;2:457-64. 5. Echizenya K, Sato M, Murai H, Ueno H, Abe H, Komai T. Mineralization and biodegradation of CSF shunting systems. J Neurosurg 1987;67:584-91. 6. Irving IM, Castilla P, Hall EG, Rickham PP. Tissue reaction to pure and impregnated silastic. J Pediatr Surg 1971;6:724-9. 7. Koide T. Roentgenographic appearance of augmentation mamaplasty with emphasis on the relationship between implanted materials and calcification. Nippon Acta Radiol 1981;41:511-26. 8. Meester WD, Swanson AB. In vivo testing of silicone rubber joint implants for lipid absorption. J Biomed Mater Res 1972;6:193-9. 9. Owen DR, Zone RM. Analysis of a possible mechanism of surface calcification on a biomedical elastomer. Trans Am Soc Artif Intern Organs 1981;27:528-31. 10. Pernis B, Paronetto F. Adjuvant effect of silica (tridymite) on antibody production. Proc Soc Exp Biol Med 1962;110:390-2. 11. Redfern AB, Ryan JJ, Su CT. Calcification of the fibrous capsule about mammary implants. Plast Reconstr Surg 1977;59:249-5 I. 12. Schoen FJ, Goodenough SH, Ionescu MI, Braunwald NS. Implications of late morphology of Braunwald-Cutter mitral heart valve prostheses. J Thorac Cardiovasc Surg 1984;88:208-16.
Surg Neurol 1988;30:156-8
Calcification of a Ventriculoperitoneal Shunt T u b e Case Report Katsumi Shimotake, M.D., Akinori Kondo, M.D., Ikuhiro Aoyama, M.D., Kiyoshi Nin, M.D., Yuzuru Tashiro, M.D., and Tatsuya Nishioka, M.D. Department of Neurosurgery, Kitano Medical Research Institute and Hospital, Osaka, Japan
Shimotake K, Kondo A, Aoyama I, Nin K, Tashiro Y, Nishioka T. Calcification of a ventriculoperitoneal shunt tube. Case report. Surg Neurol 1988;30:156-8.
A 16-year-old boy who had undergone a ventriculoperitoneal (VP) shunt because of hydrocephalus at 8 years of age complained of pain around the right neck and chest. He concomitantly had a slight fever of unknown etiology, which had been lasting for several years. Skull and chest roentgenograms revealed an unusual calcified shadow around the shunt tube. After removal of the shunt apparatus, his pain and fever disappeared. Silicone tubes used in a VP shunt apparatus may induce fibrous connective tissue proliferation around the tubes in both children and adults, but no reports of radiologically verified calcification of a VP shunt tube are found in the literature, to the best of our knowledge. The possible mechanism of calcification of the VP shunt tube is discussed.
Case R e p o r t The patient was a 16-year-old, overweight boy (85 kg and 167 cm tall) who had undergone a right temporal craniotomy in 1976, when he was 8 years of age, to relieve an otogenic intracerebral abscess; a VP shunt (Pudenz's silastic tube, Heyer-Schulte, Inc., Goleta, Calif.) had been inserted because of the subsequent hydrocephalus. Thereafter, the patient was well and active especially in judo. A continuous low-grade fever began to appear in 1982, 6 years after the VP shunt operation, but the cause of fever remained unclear in spite of medical examinations at another hospital. In July 1984, he noticed pain in the right lateral neck and upper chest wall when he elevated his right arm. He was admitted to the Department of Neurosurgery of Kitano Medical Research Institute and Hospital on September 29, 1984 for an examination.
KEY WORDS: Calcification; Ventriculoperitoneal shunt; Silicone; Human adjuvant disease
Examination
Silicone implantation has become increasingly common in neurosurgical practice because silicone material is considered to be relatively inert in biological systems. Silicone, however, is sometimes encapsulated by fibrous tissue as foreign matter [6], and another of the unwelcome complications of the implant is calcification of silicone surface [5, 7, 11]. We report on a rare case of a 16-year-old boy whose plain roentgenograms of the neck and chest demonstrated calcification of a ventriculoperitoneal (VP) shunt tube. He had also had a continuous low-grade fever. To date there have been no reports of radiologicaUy verified calcification of a VP shunt tube and hence this case may be sufficiently interesting to be reported.
Address reprint requests to: Katsumi Shimotake, M.D., Department of Neurosurgery, Kitano Medical Research Institute and Hospital, 13-3, Kamiyama-cho, Kita-ku, Osaka, 530 Japan. Received March 30, 1987; accepted January 29, 1988.
© 1988 by ElsevierSciencePublishing Co., Inc.
There were no neurological abnormalities except for hearing loss of the conductive type in the right ear due to previous otitis media. Continuous low-grade fever (37.0°C in the morning and 37.2°C in the evening) was recorded. In laboratory tests, the erythrocyte sedimentation rate (ESR) was increased moderately (22 mm/hr), but C-reactive protein (CRP) was found to be negative. Serum calcium concentration was within the normal range, but the serum triglyceride titer was over the upper limit (178 mg/dL). A plain roentgenogram showed a linear calcified shadow along the VP shunt tube, starting from just below the shunt valve to the lower chest (Figure 1). Study of the shunt functioning disclosed complete obstruction of the abdominal tube. We considered his neck and chest pain to be stimulated by the calcified shunt tube.
Operation Under general anesthesia, the shunt tube distal to the cranial valve was totally removed together with the 0090-3019/88/$3.50
Calcification of a Ventriculoperitoneal Shunt Tube
Figure 1. Plain cervical and chest roentgenograms (anteroposterior projections). Arrows show the abnormal linear calcification along a VP shunt tube.
surrounding fibrous tissue. The tube had almost completely degenerated so that it could be torn off easily and many small sandlike, calcified particles, yellowishbrown, were discovered in the surface of silicone tube. A postoperative roentgenogram showed no abnormal calcified track in the neck and chest. About 10 days after the operation, his body temperature steadied below 37.0°C (36.6°C in the morning and 36.8°C in the evening), and ESR was normalized to 6 mm/h. Pathologic Examination
Calcification was found in the surface of the shunt tube by hematoxilin-eosin staining. Another important as well as interesting histologic finding of the peritubular connective tissue was a foreign body reaction with appearance of giant cells that had engulfed the silicone particles (Figure 2).
Surg Neurol 1988;30:156-8
157
Discussion It is well known that silicone is not biologically inactive despite its chemical inactivity and is considered to be a possible cause of adjuvant disease [10]. Despite findings of negative CRP, the patient's ESR was modestly increased, and the histopathologic findings in the peritubular fibrous sheath, such as the foreign body reaction and giant cells, indicated that a long-standing fever in this patient was probably associated with a siliconerelated immune response, one of the silicone-induced human adjuvant diseases. Calcification of implanted silicone is not uncommon. Koide [7] reported radiographically evident calcification in 10 of 32 cases (31%) of augmentation mammoplasty, and there have also been reports of calcification of silicone rubber joint implants [2] and of artificial heart valves [12]. There have, however, been no reports of radiologically verified calcification of VP shunt tubes. Carmen and Kahn [4] documented an interesting phenomenon by which silicone rubber heart poppets demonstrated lipid-sorptive phenomena in contact with blood, and his laboratory data of the lipid
158
Surg Neurol 1988;30:156-8
Shimotake et al
cal stress caused by judo [5]. T h e r e may be other possible mechanisms, e.g., the following pathologic mechanisms: repeated mechanical stress around the shunt tube induces a chronic inflammatory response o f the connective tissue, resulting in atrophy and necrosis o f fibrous tissue and deposition o f insoluble intracellular calcium and phosphate. This is the so-called dystrophic calcification [ 1]. W e think that calcification o f the silicone surface is never a p h e n o m e n o n limited to products of low quality but one that may take place universally in all silicone products as a response o f silicone to the bioenvironment.
Figure 2. Photomicrograph showing the silicone surface of a shunt tube. The white arrow indicates a calcified body of silicone surface and the black arrow i7~icates the multinucleated giant cell which has engulfed a ~rticle (hematoxilin and eosin staining, x I00).
sorbability o f silicone showed that the lipid contents of the balls were in the range of 0 . 1 - 5 . 5 weight percent. It was concluded that silicone implants in direct contact with blood, such as artificial heart valves, may pick up much higher concentrations o f lipids than joint implants which are bathed in synovial fluids [3]. In clinical cases, Meester and Swanson [8] verified in silicone rubber joint implants that the lipid absorption rate was between 0.18 and 2.55 weight percent, and among many absorbed lipids, cholesterol and triglyceride levels accounted for about 4 0 % o f the total lipid measured. Therefore, as a cause o f calcification o f silicone products, O w e n and Z o n e [9] hypothesized that absorbed lipids f o r m a negatively charged interface and this might lead to a higher surface concentration of Ca ++ on a p o l y m e r surface. T h e surface calcification of silicone tubing in our case may have involved the following factors: (a) an adolescent patient with increased calcium metabolism [5], (b) an obese boy with an elevated level o f serum triglyceride, and (c) increased blood volumes in the lateral neck and chest due to continuous mechani-
References 1. Anderson WAD. Pathology. 6th ed. St. Louis: CV Mosby, 1971:77-86. 2. Beck E. Silastikprothese zum Ersatz des resezierten Speichenk6pfchens bei Trfimmerbriichen. Arch Orthop Unfall-Chir 1974;80:143-52. 3. Bole GG. Synovial fluid lipids in normal individuals and patients with rheumatoid arthritis. Arthritis Rheum 1962;5:589-601. 4. Carmen R, Kahn P. In vitro testing of silicone rubber joint implants for lipid absorption. J Biomed Mater ges 1968;2:457-64. 5. Echizenya K, Sato M, Murai H, Ueno H, Abe H, Komai T. Mineralization and biodegradation of CSF shunting systems. J Neurosurg 1987;67:584-91. 6. Irving IM, Castilla P, Hall EG, Rickham PP. Tissue reaction to pure and impregnated silastic. J Pediatr Surg 1971;6:724-9. 7. Koide T. Roentgenographic appearance of augmentation mamaplasty with emphasis on the relationship between implanted materials and calcification. Nippon Acta Radiol 1981;41:511-26. 8. Meester WD, Swanson AB. In vivo testing of silicone rubber joint implants for lipid absorption. J Biomed Mater Res 1972;6:193-9. 9. Owen DR, Zone RM. Analysis of a possible mechanism of surface calcification on a biomedical elastomer. Trans Am Soc Artif Intern Organs 1981;27:528-31. 10. Pernis B, Paronetto F. Adjuvant effect of silica (tridymite) on antibody production. Proc Soc Exp Biol Med 1962;110:390-2. 11. Redfern AB, Ryan JJ, Su CT. Calcification of the fibrous capsule about mammary implants. Plast Reconstr Surg 1977;59:249-5 I. 12. Schoen FJ, Goodenough SH, Ionescu MI, Braunwald NS. Implications of late morphology of Braunwald-Cutter mitral heart valve prostheses. J Thorac Cardiovasc Surg 1984;88:208-16.