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Compartment Syndrome after Compression Sclerotherapy
Compartment Syndrome after Compression Sclerotherapy Yong Pil Cho, MD,1 Eugene Kim, MD,2 Soo-Jung Choi, MD,3 Myoung Sik Han, MD,1 Young Jun Choi, MD,2 Hyuk Jai Jang, MD,1 Yong Ho Kim, MD,1 and Sung Gyu Lee, MD,4 Gangneung and Seoul, Republic of Korea
Acute limb compartment syndrome is a condition in which raised pressure within a closed fascial space reduces capillary perfusion below a level necessary for tissue viability. Although it is a rare but potentially disastrous complication of orthopedic injury to the extremities, it may occur spontaneously without a history of trauma, and any insult that tends to increase resistance to flow in the capillary bed in any anatomical situation may result in a compartment syndrome. We report an extremely rare case of compartment syndrome following compression sclerotherapy.
Acute compartment syndrome is a rare but potentially disastrous complication of orthopedic injury to the extremities.1 However, although the exact mechanism remains obscure in most cases, compartment syndrome may be related to several injected agents in uninjured extremities.2 Stab avulsion and compression sclerotherapy are usually simple and safe techniques for the treatment of varicose veins. We report a case of compartment syndrome following compression sclerotherapy.
CASE REPORT A 34-year-old woman suffering from small, dilated veins on her left calf was admitted to the hospital. She complained of cosmetic handicap. On physical examination, varicose veins were seen as usually dilated, tortuous superficial veins in the distribution of the tributaries of the lesser saphenous vein (C2AEPAS4P).3 Past and family 1 Department of Surgery, Gangneung Asan Hospital, Gangneung, Republic of Korea. 2 Department of Orthopedic Surgery, Gangneung Asan Hospital, Gangneung, Republic of Korea. 3 Department of Diagnostic Radiology, Gangneung Asan Hospital, Gangneung, Republic of Korea. 4 Department of Surgery, Seoul Asan Hospital, Seoul, Republic of Korea. Correspondence to: Yong Pil Cho, MD, Department of Surgery, University of Ulsan College of Medicine, Gangneung Asan Hospital, 415 Bangdong-ri, Sacheon-myeon, Gangneung-si, Gangwon-do, Republic of Korea, 210-711, E-mail: [email protected]
Ann Vasc Surg 2005; 19: 1-3 DOI: 10.1007/s10016-005-0021-5 Ó Annals of Vascular Surgery Inc. Published online: j
histories were unremarkable. Venous Doppler showed no evidence of incompetence of the saphenofemoral or saphenopopliteal junctions or of perforating veins. Stab avulsion of varicosities was carried out under spinal anesthesia. After stab avulsion, injection of a sclerosing agent (sodium tetradecyl sulfate, 3%) for the removal of residual varicosities was performed on the upper calf area. Gentle injection of low volumes (0.3 mL/injection site, total volume <1.0 mL) of a sclerosing agent produced a small blanch. During sclerotherapy, there was no evidence of extravasation or intraarterial injection of a sclerosing agent. A compression bandage was applied from the ankle to above the uppermost injection site. Following stab avulsion and compression sclerotherapy, the patient was transferred to the recovery room and subsequently to the general ward. Six hours after sclerotherapy, the patient complained of severe cramping in the left lower leg. Pulses of the posterior tibial and dorsal foot arteries were palpable. After 3 hr of observation, we cut away both edges of the bandage to release the compression. However, because she continued to complain of severe cramping of the affected leg, the entire bandage was removed 2 hr later. Over the course of the following 2 days, she had a swollen and tense left lower leg with inability to move the foot or toes. Clinical studies indicated ischemic neuromuscular damage of the posterior tibial nerve. Compartment syndrome was suspected, and we measured intracompartmental pressure using the side-ported needle method described by Awbrey et al.4 The side-ported needle was a 1-gauge stainless-steel needle with a 1.0 mm port, 1.5 mm from the tip on the short side of the beveled opening. It was introduced directly into the muscular compartment, at a right angle to the surface of the compartment. It was connected to a mercury manometer. Intracompartmental pressure from the pos1
2 Case reports
Fig. 1. MRI shows diffuse muscular swelling in the posterior compartment of left calf (white arrows). Linear fluid collection along muscle fascia is also shown in the posterior compartment. Note that muscular venous and arterial signal intensities are normal (black arrows). R, right; L, left. terior compartment was 37 mm Hg. Magnetic resonance imaging (MRI) revealed diffuse muscular swelling in the posterior compartment of the left calf (Fig. 1). Decompression fasciotomies were not performed because she refused fasciotomy, and follow-up measurement of intracompartmental pressure decreased to 29 mm Hg. She was treated conservatively, resulting in gradual improvement. Upon discharge from the hospital, she suffered from residual neurological sequelae but could walk with a limp without a foot brace.
DISCUSSION Acute limb compartment syndrome is a condition in which raised pressure within a closed fascial space reduces capillary perfusion below a level necessary for tissue viability.1 It is a serious life- and limbthreatening complication of extremity trauma. Fractures, crush injuries, burns, and vascular injuries all can result in an acute compartment syndrome. It may occur spontaneously without a history of trauma, and any insult that tends to increase resistance to flow in the capillary bed in any anatomical situation may result in a compartment syndrome.5,6 Rarely, several injected agents may cause a compartment syndrome in uninjured extremities. Intravenous administration of blood products, hypertonic saline, and diazepam have led to or been postulated to cause compartment syndrome.2 Intraarterial injection of phenobarbital has also led to compartment syndrome. In these rare cases related to injected agents, the postulated mechanisms include direct vessel injury leading to thrombosis or vasospasm or increased osmotic activity leading to intravascular volume expansion.2
Annals of Vascular Surgery
For the treatment of varicose veins, injection of a sclerosing agent results in an injury to the endothelium, followed by sloughing and a transmural injury. The vessel reacts with spasm, inflammatory changes, and thrombosis acutely, followed by chronic thickening and fibrosis leading to permanent occlusion of the varix. For sclerotherapy to be effective without recanalization of the thrombotic vessel, the endothelial damage and resulting vascular necrosis must be extensive enough to destroy the entire blood vessel wall.7 Compression is important in minimizing the incidence of complications after sclerotherapy or surgery for varicose veins such as hemorrhage, recanalization, pigmentation, and thrombophlebitis and in reducing edema formation and enhancing wound healing. Multiple factors are responsible for swelling of a treated area after compression sclerotherapy.8 These factors include changes in the pressure differential between the intravascular and perivascular spaces and changes in endothelial permeability. The extent of edema is also related to the strength of the sclerosing agents used. This result apparently correlates with the degree of perivascular inflammation produced by the sclerosing agent. The byproducts of inflammation, including release of histamine and various mediators, increase endothelial permeability. In addition to the degree of inflammation induced by sclerotherapy itself, the innate sensitivity of a patientÕs perivascular mast cells, concomitant medications that may promote or inhibit mast cell degranulation, and previous exposure sensitivity to the sclerosing agent may all contribute to edema. Stab avulsion and compression sclerotherapy are usually simple and safe techniques for the treatment of varicose veins. Every sclerosing agent may have undesirable reactions. The most common complications and side effects of sclerotherapy are the following: pigmentation, transient edema and swelling, ecchymosis, pain, tenderness, discomfort, thrombophlebitis, skin necrosis, deep venous thrombosis, anaphylactic reaction, and matting. Although three cases with compartment syndrome after varicose vein stripping have been reported, no previous study has reported acute compartment syndrome following stab avulsion and compression sclerotherapy of varicose veins.9 Compartment syndrome has been described in many clinical situations. It may be caused by either an increase in volume within a compartment raising the pressure or externally applied pressure compressing a compartment. A tight external compression such as a cast or nonelastic bandages may be one of the etiologies of compartment syndrome. However, in
Vol. 19, No. 3, 2005
this case, we believe that it may be related to a sclerosing agent because (1) we applied a shortstretch bandage for compression after cotton wool and pads were fixed to the leg with a light, absorbent dressing; (2) MRI revealed diffuse muscular swelling only in the posterior compartment, a treated area by compression sclerotherapy; and (3) no other related problems were identified. Although the exact etiology remains obscure, injection of a sclerosing agent leading to thrombosis and vasospasm followed by increased osmotic activity leading to intravascular volume expansion may be an explanation for this rare case of compartment syndrome. We report an extremely rare case of compartment syndrome following compression sclerotherapy. REFERENCES 1. Mubarak SJ, Hargens AR. Acute compartment syndromes. Surg Clin North Am 1983;63:539-565.
Case reports 3
2. Ananthanarayan C, Castro C, McKee N, Sakotic G. Compartment syndrome following intravenous regional anesthesia. Can J Anaesth 2000;47:1094-1098. 3. Porter JM, Moneta GL. International Consensus Committee on Chronic Venous Disease. Reporting standards in venous disease: an update. J Vasc Surg 1995;21:635-645. 4. Awbrey BJ, Sienkiewicz PS, Mankin HJ. Chronic exerciseinduced compartment pressure elevation measured with a miniaturized fluid pressure monitor. A laboratory and clinical study. Am J Sports Med 1988;16:610-615. 5. Mars M, Hadley GP. Raised intracompartmental pressure and compartment syndrome. Injury 1998;29:403-411. 6. Vahedi MH, Ayuyao A, Parsa MH, Freeman HP. Pneumatic antishock garment-associated compartment syndrome in uninjured lower extremities. J Trauma 1995;38: 616-618. 7. Green D. Compression sclerotherapy techniques. Dermatol Clin 1989;7:137-146. 8. Goldman MP. Complications and adverse sequelae of sclerotherapy In: Goldman, MP, ed. Sclerotherapy. Treatment of Varicose and Telangiectatic Leg Veins. St. Louis: Mosby, 1995, pp 280-349. 9. Widmer MK, Hakki H, Reber PU, Kniemeyer HW. Rare, but severe complication of varicose vein surgery. Compartment syndrome. Zentralbl Chir 2000;125:543-546.
Acute limb compartment syndrome is a condition in which raised pressure within a closed fascial space reduces capillary perfusion below a level necessary for tissue viability. Although it is a rare but potentially disastrous complication of orthopedic injury to the extremities, it may occur spontaneously without a history of trauma, and any insult that tends to increase resistance to flow in the capillary bed in any anatomical situation may result in a compartment syndrome. We report an extremely rare case of compartment syndrome following compression sclerotherapy.
Acute compartment syndrome is a rare but potentially disastrous complication of orthopedic injury to the extremities.1 However, although the exact mechanism remains obscure in most cases, compartment syndrome may be related to several injected agents in uninjured extremities.2 Stab avulsion and compression sclerotherapy are usually simple and safe techniques for the treatment of varicose veins. We report a case of compartment syndrome following compression sclerotherapy.
CASE REPORT A 34-year-old woman suffering from small, dilated veins on her left calf was admitted to the hospital. She complained of cosmetic handicap. On physical examination, varicose veins were seen as usually dilated, tortuous superficial veins in the distribution of the tributaries of the lesser saphenous vein (C2AEPAS4P).3 Past and family 1 Department of Surgery, Gangneung Asan Hospital, Gangneung, Republic of Korea. 2 Department of Orthopedic Surgery, Gangneung Asan Hospital, Gangneung, Republic of Korea. 3 Department of Diagnostic Radiology, Gangneung Asan Hospital, Gangneung, Republic of Korea. 4 Department of Surgery, Seoul Asan Hospital, Seoul, Republic of Korea. Correspondence to: Yong Pil Cho, MD, Department of Surgery, University of Ulsan College of Medicine, Gangneung Asan Hospital, 415 Bangdong-ri, Sacheon-myeon, Gangneung-si, Gangwon-do, Republic of Korea, 210-711, E-mail: [email protected]
Ann Vasc Surg 2005; 19: 1-3 DOI: 10.1007/s10016-005-0021-5 Ó Annals of Vascular Surgery Inc. Published online: j
histories were unremarkable. Venous Doppler showed no evidence of incompetence of the saphenofemoral or saphenopopliteal junctions or of perforating veins. Stab avulsion of varicosities was carried out under spinal anesthesia. After stab avulsion, injection of a sclerosing agent (sodium tetradecyl sulfate, 3%) for the removal of residual varicosities was performed on the upper calf area. Gentle injection of low volumes (0.3 mL/injection site, total volume <1.0 mL) of a sclerosing agent produced a small blanch. During sclerotherapy, there was no evidence of extravasation or intraarterial injection of a sclerosing agent. A compression bandage was applied from the ankle to above the uppermost injection site. Following stab avulsion and compression sclerotherapy, the patient was transferred to the recovery room and subsequently to the general ward. Six hours after sclerotherapy, the patient complained of severe cramping in the left lower leg. Pulses of the posterior tibial and dorsal foot arteries were palpable. After 3 hr of observation, we cut away both edges of the bandage to release the compression. However, because she continued to complain of severe cramping of the affected leg, the entire bandage was removed 2 hr later. Over the course of the following 2 days, she had a swollen and tense left lower leg with inability to move the foot or toes. Clinical studies indicated ischemic neuromuscular damage of the posterior tibial nerve. Compartment syndrome was suspected, and we measured intracompartmental pressure using the side-ported needle method described by Awbrey et al.4 The side-ported needle was a 1-gauge stainless-steel needle with a 1.0 mm port, 1.5 mm from the tip on the short side of the beveled opening. It was introduced directly into the muscular compartment, at a right angle to the surface of the compartment. It was connected to a mercury manometer. Intracompartmental pressure from the pos1
2 Case reports
Fig. 1. MRI shows diffuse muscular swelling in the posterior compartment of left calf (white arrows). Linear fluid collection along muscle fascia is also shown in the posterior compartment. Note that muscular venous and arterial signal intensities are normal (black arrows). R, right; L, left. terior compartment was 37 mm Hg. Magnetic resonance imaging (MRI) revealed diffuse muscular swelling in the posterior compartment of the left calf (Fig. 1). Decompression fasciotomies were not performed because she refused fasciotomy, and follow-up measurement of intracompartmental pressure decreased to 29 mm Hg. She was treated conservatively, resulting in gradual improvement. Upon discharge from the hospital, she suffered from residual neurological sequelae but could walk with a limp without a foot brace.
DISCUSSION Acute limb compartment syndrome is a condition in which raised pressure within a closed fascial space reduces capillary perfusion below a level necessary for tissue viability.1 It is a serious life- and limbthreatening complication of extremity trauma. Fractures, crush injuries, burns, and vascular injuries all can result in an acute compartment syndrome. It may occur spontaneously without a history of trauma, and any insult that tends to increase resistance to flow in the capillary bed in any anatomical situation may result in a compartment syndrome.5,6 Rarely, several injected agents may cause a compartment syndrome in uninjured extremities. Intravenous administration of blood products, hypertonic saline, and diazepam have led to or been postulated to cause compartment syndrome.2 Intraarterial injection of phenobarbital has also led to compartment syndrome. In these rare cases related to injected agents, the postulated mechanisms include direct vessel injury leading to thrombosis or vasospasm or increased osmotic activity leading to intravascular volume expansion.2
Annals of Vascular Surgery
For the treatment of varicose veins, injection of a sclerosing agent results in an injury to the endothelium, followed by sloughing and a transmural injury. The vessel reacts with spasm, inflammatory changes, and thrombosis acutely, followed by chronic thickening and fibrosis leading to permanent occlusion of the varix. For sclerotherapy to be effective without recanalization of the thrombotic vessel, the endothelial damage and resulting vascular necrosis must be extensive enough to destroy the entire blood vessel wall.7 Compression is important in minimizing the incidence of complications after sclerotherapy or surgery for varicose veins such as hemorrhage, recanalization, pigmentation, and thrombophlebitis and in reducing edema formation and enhancing wound healing. Multiple factors are responsible for swelling of a treated area after compression sclerotherapy.8 These factors include changes in the pressure differential between the intravascular and perivascular spaces and changes in endothelial permeability. The extent of edema is also related to the strength of the sclerosing agents used. This result apparently correlates with the degree of perivascular inflammation produced by the sclerosing agent. The byproducts of inflammation, including release of histamine and various mediators, increase endothelial permeability. In addition to the degree of inflammation induced by sclerotherapy itself, the innate sensitivity of a patientÕs perivascular mast cells, concomitant medications that may promote or inhibit mast cell degranulation, and previous exposure sensitivity to the sclerosing agent may all contribute to edema. Stab avulsion and compression sclerotherapy are usually simple and safe techniques for the treatment of varicose veins. Every sclerosing agent may have undesirable reactions. The most common complications and side effects of sclerotherapy are the following: pigmentation, transient edema and swelling, ecchymosis, pain, tenderness, discomfort, thrombophlebitis, skin necrosis, deep venous thrombosis, anaphylactic reaction, and matting. Although three cases with compartment syndrome after varicose vein stripping have been reported, no previous study has reported acute compartment syndrome following stab avulsion and compression sclerotherapy of varicose veins.9 Compartment syndrome has been described in many clinical situations. It may be caused by either an increase in volume within a compartment raising the pressure or externally applied pressure compressing a compartment. A tight external compression such as a cast or nonelastic bandages may be one of the etiologies of compartment syndrome. However, in
Vol. 19, No. 3, 2005
this case, we believe that it may be related to a sclerosing agent because (1) we applied a shortstretch bandage for compression after cotton wool and pads were fixed to the leg with a light, absorbent dressing; (2) MRI revealed diffuse muscular swelling only in the posterior compartment, a treated area by compression sclerotherapy; and (3) no other related problems were identified. Although the exact etiology remains obscure, injection of a sclerosing agent leading to thrombosis and vasospasm followed by increased osmotic activity leading to intravascular volume expansion may be an explanation for this rare case of compartment syndrome. We report an extremely rare case of compartment syndrome following compression sclerotherapy. REFERENCES 1. Mubarak SJ, Hargens AR. Acute compartment syndromes. Surg Clin North Am 1983;63:539-565.
Case reports 3
2. Ananthanarayan C, Castro C, McKee N, Sakotic G. Compartment syndrome following intravenous regional anesthesia. Can J Anaesth 2000;47:1094-1098. 3. Porter JM, Moneta GL. International Consensus Committee on Chronic Venous Disease. Reporting standards in venous disease: an update. J Vasc Surg 1995;21:635-645. 4. Awbrey BJ, Sienkiewicz PS, Mankin HJ. Chronic exerciseinduced compartment pressure elevation measured with a miniaturized fluid pressure monitor. A laboratory and clinical study. Am J Sports Med 1988;16:610-615. 5. Mars M, Hadley GP. Raised intracompartmental pressure and compartment syndrome. Injury 1998;29:403-411. 6. Vahedi MH, Ayuyao A, Parsa MH, Freeman HP. Pneumatic antishock garment-associated compartment syndrome in uninjured lower extremities. J Trauma 1995;38: 616-618. 7. Green D. Compression sclerotherapy techniques. Dermatol Clin 1989;7:137-146. 8. Goldman MP. Complications and adverse sequelae of sclerotherapy In: Goldman, MP, ed. Sclerotherapy. Treatment of Varicose and Telangiectatic Leg Veins. St. Louis: Mosby, 1995, pp 280-349. 9. Widmer MK, Hakki H, Reber PU, Kniemeyer HW. Rare, but severe complication of varicose vein surgery. Compartment syndrome. Zentralbl Chir 2000;125:543-546.