Letters to Editor liver toxicity caused by D‑penicillamine treatment of rheumatoid arthritis. Ann Rheum Dis 1989;48:609‑10. 3. Habib GS, Saliba W, Nashashibi M, Armali Z. Penicillamine and nephrotic syndrome. Eur J Intern Med 2006;17:343‑8. 4. Blanusa M, Varnai VM, Piasek M, Kostial K. Chelators as antidotes of metal toxicity: Therapeutic and experimental aspects. Curr Med Chem 2005;12:2771‑94. 5. Alhamad T, Rooney J, Nwosu A, Maccombs J, Kim YS, Shukla V. Lessons learned from a fatal case of mercury intoxication. Int Urol Nephrol 2012;44:647‑51. 6. Alhamad T, Rooney J. A heavy heart. Am J Respir Crit Care Med 2012;185:785. 7. Clarkson TW. The pharmacology of mercury compounds. Annu Rev Pharmacol 1972;12:375‑406. 8. Woods JS, Echeverria D, Heyer NJ, Simmonds PL, Wilkerson J, Farin FM. The association between genetic polymorphisms of coproporphyrinogen oxidase and an atypical porphyrinogenic response to mercury exposure in humans. Toxicol Appl Pharmacol 2005;206:113‑20. Access this article online Quick Response Code:
Website: www.indianjnephrol.org
DOI: 10.4103/0971-4065.120353
Guidewire fragmentation complicating hemodialysis catheter insertion Sir, A 49‑year‑old (96 kg) female renal transplant recipient patient presented with the chronic graft rejection and imminent sepsis and was posted for hemodialysis. She was restless, had a short neck and had a platelet count of 47 × 103/μl. Two blind anatomical landmark attempts were under taken by the nephrologists in the right and left internal jugular veins (one on each side), but they were unable to pass the guidewire due to the difficult anatomy and patient’s restlessness. The procedure was abandoned and intensivist assistance was sought. Under ultrasonography (USG) guidance, the femoral vein was localized and punctured and the guide wire used in the previous two attempts was passed in the vessel. The double lumen Hemo Dialysis Catheter (MAHURKARTM, Mansfield, USA) was railroaded over the guide wire into the vessel. During removal of the guide wire mild resistance was felt, but upon application of traction, the guide wire 468
November 2013 / Vol 23 / Issue 6
Figure 1: Deformed smaller fragment guide wire stuck in to dialysis catheter tip
could be pulled out. When aspiration of the port of HDC was carried out, it was found that the venous blood backflow was absent. The position of the HDC was again confirmed with USG and it was found to be inside the vessel. Finding no cause for absent flow, the HDC was removed under USG guidance. Upon removal, it was observed that a portion of the distal end of the guide wire was attached to the distal opening of the catheter [Figure 1] blocking it. Close examination of the guide wire revealed that the guide wire had fragmented cleanly in two pieces. A new HDC set was taken and the USG guided procedure was repeated and this time, the HDC could be placed uneventfully. Though previous reports of the guide wire fracture have been attributed to faulty design (material weakness or fatigue)[1] or introducer needle injury,[2] in our case the two previous attempts of passing the guide wire may have injured and weakened its core as well as outer coil wire and during its forceful retrieval, it had got sheared off. However, the broken and deformed end had remained attached with the catheter thus, preventing disastrous complications such as embolism, perforation, sepsis, endocarditis, and cardiac arrest. [3] Smaller broken end lost its J shaped due to forward migration of the corewire. In this case guidewire (J tip) may have anchored into tributaries of the femoral vein leading to resistance during the retrieval. Intact guidewire is usually not damaged by relatively small traction during catheter insertion. Core and outer layer of the guide wire fragmented near the J tip in our case, which suggested of it’s material weakness, fatigue or manufacturing defects. Through this correspondence, we would like to emphasize that whenever unusual resistance is encountered during the guide wire removal, application of force should be avoided. Both the guide wire as well as the catheter should be pulled out together to minimize the risk of the guide wire shearing off and migration. If USG or fluoroscopy is available stuck guidewire should be removed under radiological guidance. R. Haldar, S. Samanta1, S. Samanta2 Departments of Anesthesiology, and 1Critical Care Medicine, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Luckow, Uttar Pradesh, 2Anesthesia and Intensive Care, Post Graduate Institute of Medical Education and Research, Chandigarh, India Indian Journal of Nephrology
Letters to Editor Address for correspondence: Dr. Sukhen Samanta, New PG Hostel, Room No. 218, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow ‑ 226 014, Uttar Pradesh, India. E‑mail: [email protected]
References 1.
Monaca E, Trojan S, Lynch J, Doehn M, Wappler F. Broken guide wire – A fault of design? Can J Anaesth 2005;52:801‑4. 2. Park SK, Yi IK, Lee JH, Kim DH, Lee SY. Fracture of J‑tipped guidewire during central venous catheterization and its successful removal under fluoroscopic guidance: A case report. Korean J Anesthesiol 2012;63:457‑60. 3. Fisher RG, Ferreyro R. Evaluation of current techniques for nonsurgical removal of intravascular iatrogenic foreign bodies. AJR Am J Roentgenol 1978;130:541‑8. Access this article online Quick Response Code:
Website: www.indianjnephrol.org DOI: 10.4103/0971-4065.120354
Is bullous skin lesion a risk factor for renal amyloidosis in patients with familial mediterranean fever? Sir, Familial Mediterranean fever (FMF) is an autosomal recessive disorder characterized by inflammation of the serous membranes. Clinical signs include fever, abdominal pain, arthritis, erysipelas‑like erythema, and chest pain. The most important and feared complication of the disease is amyloidosis. Colchicine is useful to prevent attacks and amyloidosis.[1] A 60‑year‑old male patient presented with chest pain, swelling of the feet, and recurrent fever or 15 days and his medical history was unremarkable except for hyperlipidemia, asthma treated with the theophylline 400 mg/day, atorvastatin 20 mg/day, and montelukast 4 mg/day. On physical examination, he had +2 pretibial edema bilaterally and 4‑5 bullous skin lesions measuring 1 cm × 1.5 cm on his back. Investigations showed hemoglobin 12.2 g/dl, leukocyte Indian Journal of Nephrology
count 10.620/mm 3, alanine transaminase, 7 U/L, gamma glutamyl transferase 14 U/L, total bilirubin 0.7 mg/dl, albumin 2.3 g/dl, globulin 2.4 g/dl, creatinine 1.24 mg/dl, urea 30 mg/dl, C‑reactive protein 44.76 mg/L, and 2840 mg/day proteinuria. Kidney biopsy was suggestive of amyloid, and immunohistochemical staining was positive for amyloid A, suggesting secondary amyloidosis. Genetic analysis revealed the presence of homozygous R202Q mutation in MEFV gene. He was started on colchicine, which led to regression of skin lesions. However, the serum creatinine level progressed to 5.39 mg/dl within 3 months, and he was started on hemodialysis. The patient is still follow‑up in our clinic. The MEFV gene is responsible for FMF. The mutations of the gene may be responsible for fever, skin lesions, and other additional clinical findings. The presence of homozygous M694V mutations, sex, intermarriage, arthritis, and resistant microalbuminuria are risk factors for amyloidosis.[2] The most characteristic cutaneous manifestation of FMF is erysipelas‑like erythema. Other skin manifestations are urticaria, non‑specific purpura, psoriasis, and erythema nodosum.[3] Bullous skin lesions may appear as a rare skin lesion.[4] Histopathological findings of the peritoneal cavity and synovial biopsy specimens are similar with the dermis during attacks. The association between other skin lesions except for erysipelas‑like erythema and presence of homozygous M694V mutations is still controversial.[2] In the literature, a patient with FMF who was stable since more than 14 years reported that the patient progressed to renal failure with the skin lesions.[5] The incidence of renal amyloidosis is 20‑25% in patients with untreated FMF. Although the presence of gene mutations are common in amyloidosis and skin findings, bullous lesions may accelerate amyloid deposition. G. Sargin, A. Alp1, H. Akdam1, H. Akar1, Y. Yenicerioglu1 Department of Internal Medicine, 1Division of Nephrology, Adnan Menderes University Medical Faculty, Aydin, Turkey Address for correspondence: Dr. Gokhan Sargin, Department of Internal Medicine, Adnan Menderes University Medical Faculty, 09000, Aydin, Turkey. E‑mail: [email protected]
References 1. Onen F. Familial Mediterranean fever. Rheumatol Int 2006;26:489‑96. 2. Medlej‑Hashim M, Delague V, Chouery E, Salem N, Rawashdeh M, Lefranc G, et al. Amyloidosis in familial Mediterranean fever patients: Correlation with MEFV genotype and SAA1 and MICA polymorphisms effects. BMC Med Genet 2004;5:4. November 2013 / Vol 23 / Issue 6
469
Copyright of Indian Journal of Nephrology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
Website: www.indianjnephrol.org
DOI: 10.4103/0971-4065.120353
Guidewire fragmentation complicating hemodialysis catheter insertion Sir, A 49‑year‑old (96 kg) female renal transplant recipient patient presented with the chronic graft rejection and imminent sepsis and was posted for hemodialysis. She was restless, had a short neck and had a platelet count of 47 × 103/μl. Two blind anatomical landmark attempts were under taken by the nephrologists in the right and left internal jugular veins (one on each side), but they were unable to pass the guidewire due to the difficult anatomy and patient’s restlessness. The procedure was abandoned and intensivist assistance was sought. Under ultrasonography (USG) guidance, the femoral vein was localized and punctured and the guide wire used in the previous two attempts was passed in the vessel. The double lumen Hemo Dialysis Catheter (MAHURKARTM, Mansfield, USA) was railroaded over the guide wire into the vessel. During removal of the guide wire mild resistance was felt, but upon application of traction, the guide wire 468
November 2013 / Vol 23 / Issue 6
Figure 1: Deformed smaller fragment guide wire stuck in to dialysis catheter tip
could be pulled out. When aspiration of the port of HDC was carried out, it was found that the venous blood backflow was absent. The position of the HDC was again confirmed with USG and it was found to be inside the vessel. Finding no cause for absent flow, the HDC was removed under USG guidance. Upon removal, it was observed that a portion of the distal end of the guide wire was attached to the distal opening of the catheter [Figure 1] blocking it. Close examination of the guide wire revealed that the guide wire had fragmented cleanly in two pieces. A new HDC set was taken and the USG guided procedure was repeated and this time, the HDC could be placed uneventfully. Though previous reports of the guide wire fracture have been attributed to faulty design (material weakness or fatigue)[1] or introducer needle injury,[2] in our case the two previous attempts of passing the guide wire may have injured and weakened its core as well as outer coil wire and during its forceful retrieval, it had got sheared off. However, the broken and deformed end had remained attached with the catheter thus, preventing disastrous complications such as embolism, perforation, sepsis, endocarditis, and cardiac arrest. [3] Smaller broken end lost its J shaped due to forward migration of the corewire. In this case guidewire (J tip) may have anchored into tributaries of the femoral vein leading to resistance during the retrieval. Intact guidewire is usually not damaged by relatively small traction during catheter insertion. Core and outer layer of the guide wire fragmented near the J tip in our case, which suggested of it’s material weakness, fatigue or manufacturing defects. Through this correspondence, we would like to emphasize that whenever unusual resistance is encountered during the guide wire removal, application of force should be avoided. Both the guide wire as well as the catheter should be pulled out together to minimize the risk of the guide wire shearing off and migration. If USG or fluoroscopy is available stuck guidewire should be removed under radiological guidance. R. Haldar, S. Samanta1, S. Samanta2 Departments of Anesthesiology, and 1Critical Care Medicine, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Luckow, Uttar Pradesh, 2Anesthesia and Intensive Care, Post Graduate Institute of Medical Education and Research, Chandigarh, India Indian Journal of Nephrology
Letters to Editor Address for correspondence: Dr. Sukhen Samanta, New PG Hostel, Room No. 218, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow ‑ 226 014, Uttar Pradesh, India. E‑mail: [email protected]
References 1.
Monaca E, Trojan S, Lynch J, Doehn M, Wappler F. Broken guide wire – A fault of design? Can J Anaesth 2005;52:801‑4. 2. Park SK, Yi IK, Lee JH, Kim DH, Lee SY. Fracture of J‑tipped guidewire during central venous catheterization and its successful removal under fluoroscopic guidance: A case report. Korean J Anesthesiol 2012;63:457‑60. 3. Fisher RG, Ferreyro R. Evaluation of current techniques for nonsurgical removal of intravascular iatrogenic foreign bodies. AJR Am J Roentgenol 1978;130:541‑8. Access this article online Quick Response Code:
Website: www.indianjnephrol.org DOI: 10.4103/0971-4065.120354
Is bullous skin lesion a risk factor for renal amyloidosis in patients with familial mediterranean fever? Sir, Familial Mediterranean fever (FMF) is an autosomal recessive disorder characterized by inflammation of the serous membranes. Clinical signs include fever, abdominal pain, arthritis, erysipelas‑like erythema, and chest pain. The most important and feared complication of the disease is amyloidosis. Colchicine is useful to prevent attacks and amyloidosis.[1] A 60‑year‑old male patient presented with chest pain, swelling of the feet, and recurrent fever or 15 days and his medical history was unremarkable except for hyperlipidemia, asthma treated with the theophylline 400 mg/day, atorvastatin 20 mg/day, and montelukast 4 mg/day. On physical examination, he had +2 pretibial edema bilaterally and 4‑5 bullous skin lesions measuring 1 cm × 1.5 cm on his back. Investigations showed hemoglobin 12.2 g/dl, leukocyte Indian Journal of Nephrology
count 10.620/mm 3, alanine transaminase, 7 U/L, gamma glutamyl transferase 14 U/L, total bilirubin 0.7 mg/dl, albumin 2.3 g/dl, globulin 2.4 g/dl, creatinine 1.24 mg/dl, urea 30 mg/dl, C‑reactive protein 44.76 mg/L, and 2840 mg/day proteinuria. Kidney biopsy was suggestive of amyloid, and immunohistochemical staining was positive for amyloid A, suggesting secondary amyloidosis. Genetic analysis revealed the presence of homozygous R202Q mutation in MEFV gene. He was started on colchicine, which led to regression of skin lesions. However, the serum creatinine level progressed to 5.39 mg/dl within 3 months, and he was started on hemodialysis. The patient is still follow‑up in our clinic. The MEFV gene is responsible for FMF. The mutations of the gene may be responsible for fever, skin lesions, and other additional clinical findings. The presence of homozygous M694V mutations, sex, intermarriage, arthritis, and resistant microalbuminuria are risk factors for amyloidosis.[2] The most characteristic cutaneous manifestation of FMF is erysipelas‑like erythema. Other skin manifestations are urticaria, non‑specific purpura, psoriasis, and erythema nodosum.[3] Bullous skin lesions may appear as a rare skin lesion.[4] Histopathological findings of the peritoneal cavity and synovial biopsy specimens are similar with the dermis during attacks. The association between other skin lesions except for erysipelas‑like erythema and presence of homozygous M694V mutations is still controversial.[2] In the literature, a patient with FMF who was stable since more than 14 years reported that the patient progressed to renal failure with the skin lesions.[5] The incidence of renal amyloidosis is 20‑25% in patients with untreated FMF. Although the presence of gene mutations are common in amyloidosis and skin findings, bullous lesions may accelerate amyloid deposition. G. Sargin, A. Alp1, H. Akdam1, H. Akar1, Y. Yenicerioglu1 Department of Internal Medicine, 1Division of Nephrology, Adnan Menderes University Medical Faculty, Aydin, Turkey Address for correspondence: Dr. Gokhan Sargin, Department of Internal Medicine, Adnan Menderes University Medical Faculty, 09000, Aydin, Turkey. E‑mail: [email protected]
References 1. Onen F. Familial Mediterranean fever. Rheumatol Int 2006;26:489‑96. 2. Medlej‑Hashim M, Delague V, Chouery E, Salem N, Rawashdeh M, Lefranc G, et al. Amyloidosis in familial Mediterranean fever patients: Correlation with MEFV genotype and SAA1 and MICA polymorphisms effects. BMC Med Genet 2004;5:4. November 2013 / Vol 23 / Issue 6
469
Copyright of Indian Journal of Nephrology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
