J Orthop Sci (2015) 20:444–448 DOI 10.1007/s00776-013-0484-0
CASE REPORT
Acute compartment syndrome after extracorporeal membrane oxygenation Ji Hyun Yeo • Ki Hyuk Sung • Chin Youb Chung • Kyoung Min Lee • Young Choi • Tae Gyun Kim • Soon-Sun Kwon • Seung Yeol Lee • Moon Seok Park
Received: 19 May 2013 / Accepted: 6 October 2013 / Published online: 16 November 2013 Ó The Japanese Orthopaedic Association 2013
Introduction Acute compartment syndrome is a surgical emergency caused by increased pressure within an anatomical compartment, resulting in ischemia and necrosis [1, 2]. Most cases occurring in the lower leg are associated with trauma, prolonged compression, and vascular injury. Extracorporeal membrane oxygenation (ECMO) has recently been used as a final option for resuscitation in patients undergoing cardiopulmonary resuscitation [3]. ECMO support in children with intractable cardiac arrest can yield favorable outcomes in 30 % of patients [4]. From the theoretical viewpoint, during ECMO, acute compartment syndrome can develop because of limb ischemia or reperfusion. However, few reports have described cases of acute compartment syndrome in the lower leg caused by ECMO [5]. Moreover, case reports on the development of acute compartment syndrome in pediatric patients who received ECMO support are extremely rare. A previous study [6]
J. H. Yeo and K. H. Sung contributed equally to the writing of this article. J. H. Yeo C. Y. Chung K. M. Lee Y. Choi T. G. Kim S. Y. Lee (&) M. S. Park Department of Orthopaedic Surgery, Seoul National University Bundang Hospital, 300 Gumi-Dong, Bundang-Gu, Sungnam, Kyungki 463-707, Korea e-mail: [email protected] K. H. Sung Department of Orthopaedic Surgery, Kwandong University Myongji Hospital, Goyang, Kyungki, Korea S.-S. Kwon Biomedical Research Institute, Seoul National University Bundang Hospital, Sungnam, Kyungki, Korea
123
indicated that [50 % of pediatric patients who received ECMO management experienced ischemic changes in the limbs. Therefore, a greater number of case reports are required to evaluate the causes of acute compartment syndrome following ECMO support and thus prevent the development of this condition. We describe a case of a 12-year-old girl with acute compartment syndrome after ECMO who needed surgical treatment. The study was exempted from institutional review board review because it was a single, retrospective case report. Informed consent was obtained from the patient.
Case report A 12-year-old girl with allergic rhinitis who was scheduled to undergo coblation tonsillectomy sustained a sudden in-hospital cardiac arrest immediately after lidocaine injection in the tonsil. Cardiopulmonary resuscitation was started immediately with intubation, and two cardioversions were attempted. Approximately 43 min elapsed before restoration of spontaneous circulation was achieved after the last cardioversion. The patient was then transferred to a surgical intensive care unit. Her systemic blood pressure was *40 mmHg. On electrocardiography, she had a wide QRS tachycardia that converted to wide QRS bradycardia. Because her cardiac function was refractory to all medical treatment (epinephrine, atropine, etc.), femoral venoarterial ECMO was initiated approximately 1.5 h after the cardiac arrest. An arterial cannula (16 F) and a venous cannula (17 F) were percutaneously inserted into her right femoral artery and vein using the Seldinger technique. The ECMO pump flow was maintained between 2.6 and 2.7 L/min. Fraction of inspired oxygen (FiO2) was set at 0.7. Her vital signs stabilized, and her O2 saturation was maintained[98 %.
Compartment syndrome after ECMO
Four hours after ECMO insertion, the dorsalis pedis pulse disappeared and could not be detected even on Doppler examination. Her mid-thigh circumference increased by 2 cm, and her lower leg became cold. Because the ischemia in her right lower extremity worsened, a distal perfusion line was inserted, and the dorsalis pedis pulse was immediately restored. However, 5 h after insertion of the distal perfusion catheter, the dorsalis pedis pulse disappeared again, and the lower leg became more tense. Physical examination showed severe tension in the anterior and lateral compartment. Measurement of intracompartmental pressure revealed a significantly elevated pressure of 80 mmHg in the anterior compartment; consequently, the patient was diagnosed with acute compartment syndrome. At the time of this diagnosis, the level of creatine kinase (CK) was 16,339 IU/L (normal range 20–270 IU/L), and the CK muscle–brain (CK-MB) subunit was also elevated to 609.5 ng/ml (normal range 0–2.8 ng/ml). A double-incision, four-compartment fasciotomy was performed immediately under local anesthesia. The muscles in the superficial and deep posterior compartment appeared partially viable––they were pink, bleeding, and responded to electrical stimulation. However, the muscles in the anterior and lateral compartments were pale without bleeding and did not respond to electrical stimulation. After fasciotomy, sterile wet dressing was maintained (Fig. 1). The day after fasciotomy, the patient’s vital signs stabilized, and echocardiography showed nearly-normal ventricular function and a visual ejection fraction of 50–60 %. Although the ejection fraction decreased to 40 % upon
445
clamping, both ventricular functions were tolerable. Therefore, ECMO was removed. By day 12 after the fasciotomy, swelling of the affected lower leg had decreased sufficiently and primary wound closure was performed. At the time of closure, more than half of the tibialis anterior, extensor hallucis, and extensor digitorum were necrosed, so extensive debridement was performed. Primary wound closure was possible in the lateral fasciotomy site. In addition to the tissue necrosis, the patient also experienced medical complications immediately after the acute compartment syndrome. Her myoglobin increased to 25,620 ng/ml (normal range 0–100 ng/ml), and urine output decreased to 10 ml/h. Her serum creatinine increased to 2.40 mg/dl (normal range 0.7–1.4 mg/dl). The pediatrician diagnosed acute renal failure. Hydration, urine alkalization with sodium bicarbonate (NaHCO3), and diuresis with furosemide were initiated. Four days after fasciotomy, urine output and serum creatinine had normalized. Renal ultrasonography showed a normal renal parenchymal echo without focal lesion. At the time of discharge, there was no contracture of the ankle joint, and passive range of motion of all toes was fully possible. However, active dorsiflexion of the ankle and toes had not recovered, and the power remained at Grade I. To prevent foot drop and contracture of the ankle joint, an ankle–foot orthosis brace was applied, and the patient was educated about passive and assisted active range of motion exercises. One year after the fasciotomy, the muscle power of her extensor hallucis longus and ankle evertor were Grade I and II, respectively. The ankle showed varus tendency (Fig. 2). Passive dorsiflexion of the
Fig. 1 Muscles of the posterior compartment. a Compared with muscles of the lateral compartment, the medial fasciotomy site was relatively viable. b Lateral fasciotomy site. The images were obtained 9 days after fasciotomy
Fig. 2 Ankle showing varus tendency 1 year after the fasciotomy
123
446
ankle was limited to the neutral position. Therefore, we performed tibialis posterior split transfer to the peroneal brevis and tendo-Achilles lengthening. Although the tibialis anterior was also contracted, we did not transfer it to prevent foot drop.
Discussion ECMO has evolved markedly over recent years and is now used widely. The ECMO system removes deoxygenated blood from the patient’s venous system, circulates it through an artificial lung with a pump, and then returns the oxygenated blood back to the patient [3]. ECMO provides oxygenation of blood outside the patient’s body and can therefore provide artificial support for patients with cardiac or respiratory failure. ECMO is indicated for the management of life-threatening pulmonary or cardiac failure when no other form of treatment has been, or is likely to be, successful [7]. An ECMO system consists of two vascular cannulas to access and return the blood, a pump, a membrane oxygenator, and a heat exchanger that maintains blood temperature via the oxygenator [8] (Fig. 3). Drained blood from the access cannula is passed through a pump to the membrane oxygenator. There, the deoxygenated blood is oxygenated and transferred to the heat exchanger before being returned to the body via a second cannula. The manner in which an ECMO circuit interacts with the patient’s circulation defines it as either venoarterial (VA) or venovenous (VV) (Fig. 4). VA ECMO involves oxygenation of blood drawn from the venous system and returned into the arterial circulation, providing cardiac support in addition to gas exchange. The VA mode can be Fig. 3 Extracorporeal membrane oxygenation (ECMO) system consists of two vascular cannulas to access and return blood, a pump, a membrane oxygenator, and a heat exchanger that maintains blood temperature via the oxygenator. Blood from the venous cannula is passed through a pump to a membrane oxygenator. Then, deoxygenated blood becomes oxygenated; it is then transferred to the heat exchanger and is finally returned to the body via the arterial cannula
123
J. H. Yeo et al.
achieved by either peripheral (femoral vessel) or central cannulation. In central cannulation, blood is directly removed from the right atrium and returned to the proximal ascending aorta. In peripheral cannulation, both the drainage and returning catheter are inserted in the femoral vein and artery [8]. In VV ECMO, blood is drained from the venous system and returned to the venous system. This technique provides oxygenation and is used for respiratory failure when cardiac output is sufficient [7]. Femoral VA ECMO provides effective cardiopulmonary support for critically ill patients. However, distal leg ischemia is a significant complication after femoral artery cannulation. To prevent limb ischemia, a bidirectional arterial cannula or a special right-angle, high-flow, arterial cannula can be used [9, 10]. Furthermore, a distal perfusion catheter can also be inserted in patients at risk for ischemia, depending on the blood pressure in the superficial femoral artery [10] (Fig. 5). Previous reports show that ECMO plays an important role in patients with respiratory or cardiac failure, but it also increases the risk of vascular injury, limb ischemia, and compartment syndrome [6, 11]. One study reported that limb ischemia occurred in as many as 18 % of ECMO cases [11]. During ECMO, femoral arterial cannulation usually completely or partially occludes the distal arterial lumen, thereby causing distal limb ischemia [5]. In femoral VA ECMO, the arterial cannula is relatively large and fits tightly in the femoral artery. This allows for delivery of large amounts of oxygenated blood to the proximal aorta, but it also can cause a significant reduction in arterial blood flow to the involved lower extremity. In addition, the VA ECMO cannula can increase the venous pressure in the lower extremity. The combination of decreased arterial flow and increased venous pressure causes a reduction in
Compartment syndrome after ECMO
Fig. 4 a Venoarterial (VA) extracorporeal membrane oxygenation (ECMO) system is used after failure of cardiac function. The arterial cannula (red) is located in the femoral artery, and the venous cannula (blue) is located in the femoral vein. Oxygenated blood from the ECMO system is returned to the body through the arterial cannula, and deoxygenated blood from the body is drained from the venous
Fig. 5 To prevent limb ischemia during extracorporeal membrane oxygenation (ECMO), a distal perfusion catheter can be used. An arterial catheter enters the common femoral artery, with the side branch providing flow into the distal perfusion catheter down the superficial femoral artery
perfusion pressure. If the perfusion pressure decreases significantly, the compartmental tissue undergoes ischemic changes. Tissue ischemia results in interstitial edema, which increases compartmental pressure and further decreases perfusion pressure [5]. This vicious cycle closes lymphatic vessels and small venules, resulting in compartment syndrome [5, 12–14]. To prevent limb ischemia, a number of techniques have been attempted [9, 10].
447
cannula. b Venovenous (VV) ECMO is used when respiratory function fails but cardiac function remains sufficient. Both arterial and venous cannulas are located in the femoral vein. Oxygenated blood from the ECMO system is returned to the body via the venous cannula, and deoxygenated blood from the body is also drained from the venous cannula
In the case reported here, signs of limb ischemia developed 4 h after the initiation of ECMO, but a distal perfusion line was inserted immediately, resulting in an immediate return of the dorsalis pedis pulse. However, revascularization also can cause compartment syndrome. One study reported that any procedure used for revascularization of the limb can result in a muscle compartment syndrome, with an incidence ranging between 0 % and 21 % [15]. During reperfusion, a complex mechanism eventually leads to vascular leakage. Factors such as leukotrienes, tumor necrosis factor alpha, and free radicals play a role in this mechanism [15, 16]. In our case, because limb ischemia progressed after ECMO, a distal perfusion catheter was inserted, after which edema and tenseness of the lower leg worsened, and CK level increased. This finding suggests that reperfusion injury further increases the pressure in the lower leg. We believe that a distal perfusion catheter should be inserted at the time of initiation of ECMO to prevent limb ischemia and acute compartment syndrome. To our knowledge, no study has yet assessed the risk factors for acute compartment syndrome during ECMO. One study compared ECMO-related variables among children with and without limb ischemia after ECMO [6]. That study revealed no significant difference in age, sex, weight, height, or cannula site between the two groups. Additionally, neither body surface area (BSA) nor BSA-to-
123
448
cannula ratio was significantly different between groups. Thus, no variable was predictive of the development of limb ischemia. Only younger age is known as a risk factor of acute compartment syndrome because of the tighter and stronger fascia and muscle fillings in these patients [14, 17]. Pain is the main clinical symptom of a developing acute compartment syndrome [14]. However, in our case, the patient was unconsciousness and unable to provide feedback about her pain. High pressure of the lower leg was recognized after it began developing pulselessness and pallor. At an intracompartmental pressure of 30–33 mmHg, the fascial membranes reach their maximum stretching tolerance, which limits compliance of the compartment [14]. A previous study advocated fasciotomy for absolute compartment pressure reaching 30–45 mmHg [18]. Therefore, we believe that regular measurement of intracompartmental pressure during ECMO can help earlier detection of acute compartment syndrome in unconscious patients. Acute compartment syndrome can cause significant sequelae if it is not detected early and adequate treatment is not provided. As described above, during ECMO, severe limb ischemia can occur and may lead to acute compartment syndrome. Therefore, insertion of a distal perfusion catheter at the time of ECMO initiation may prevent limb ischemia and acute compartment syndrome. In addition, cardiac surgeons, orthopedic surgeons, and nurses in intensive care units need to have a high index of suspicion for the possibility of acute limb compartment syndrome during ECMO. Furthermore, because patients receiving ECMO usually have several conditions that may potentially delay the diagnosis of compartment syndrome, routine surveillance with Doppler or continuous monitoring of compartment pressure should be performed. Conflict of interest No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article.
References 1. Khan RJ, Fick DP, Guier CA, Menolascino MJ, Neal MC. Acute paraspinal compartment syndrome. A case report. J B Jt Surg Am. 2005;87:1126–8. 2. Khan SK, Thati S, Gozzard C. Spontaneous thigh compartment syndrome. West J Emerg Med. 2011;12:134–8.
123
J. H. Yeo et al. 3. Schuerer DJ, Kolovos NS, Boyd KV, Coopersmith CM. Extracorporeal membrane oxygenation: current clinical practice, coding, and reimbursement. Chest. 2008;134:179–84. 4. Alsoufi B, Al-Radi OO, Nazer RI, Gruenwald C, Foreman C, Williams WG, Coles JG, Caldarone CA, Bohn DG, Van Arsdell GS. Survival outcomes after rescue extracorporeal cardiopulmonary resuscitation in pediatric patients with refractory cardiac arrest. J Thorac Cardiovasc Surg. 2007;134(4):952.e2–959.e2. 5. Wall CJ, Santamaria J. Extracorporeal membrane oxygenation: an unusual cause of acute limb compartment syndrome. Anaesth Intens Care. 2010;38:560–2. 6. Gander JW, Fisher JC, Reichstein AR, Gross ER, Aspelund G, Middlesworth W, Stolar CJ. Limb ischemia after common femoral artery cannulation for venoarterial extracorporeal membrane oxygenation: an unresolved problem. J Pediatr Surg. 2010;45:2136–40. 7. Marasco SF, Lukas G, McDonald M, McMillan J, Ihle B. Review of ECMO (extra corporeal membrane oxygenation) support in critically ill adult patients. Heart Lung Circ. 2008;17(Suppl 4):S41–7. 8. Lindstrom SJ, Pellegrino VA, Butt WW. Extracorporeal membrane oxygenation. Med J Aust. 2009;191:178–82. 9. Huang SC, Yu HY, Ko WJ, Chen YS. Pressure criterion for placement of distal perfusion catheter to prevent limb ischemia during adult extracorporeal life support. J Thorac Cardiovasc Surg. 2004;128:776–7. 10. Greason KL, Hemp JR, Maxwell JM, Fetter JE, Moreno-Cabral RJ. Prevention of distal limb ischemia during cardiopulmonary support via femoral cannulation. Ann Thorac Surg. 1995;60:209–10. 11. Smedira NG, Moazami N, Golding CM, McCarthy PM, Apperson-Hansen C, Blackstone EH, Cosgrove DM 3rd. Clinical experience with 202 adults receiving extracorporeal membrane oxygenation for cardiac failure: survival at 5 years. J Thorac Cardiovasc Surg. 2001;122:92–102. 12. Elliott KG, Johnstone AJ. Diagnosing acute compartment syndrome. J B Jt Surg Br. 2003;85:625–32. 13. Mars M, Hadley GP. Raised intra-compartmental pressure and compartment syndromes. Injury. 1998;29:403–11. 14. Shadgan B, Menon M, Sanders D, Berry G, Martin C Jr, Duffy P, Stephen D, O’Brien PJ. Current thinking about acute compartment syndrome of the lower extremity. Can J Surg. 2010;53:329–34. 15. Kostler W, Strohm PC, Sudkamp NP. Acute compartment syndrome of the limb. Injury. 2005;36:992–8. 16. Duran WN, Takenaka H, Hobson RW 2nd. Microvascular pathophysiology of skeletal muscle ischemia-reperfusion. Semin Vasc Surg. 1998;11:203–14. 17. Frink M, Hildebrand F, Krettek C, Brand J, Hankemeier S. Compartment syndrome of the lower leg and foot. Clin Orthop Relat Res. 2010;468:940–50. 18. White TO, Howell GE, Will EM, Court-Brown CM, McQueen MM. Elevated intramuscular compartment pressures do not influence outcome after tibial fracture. J Trauma. 2003;55:1133–8.
CASE REPORT
Acute compartment syndrome after extracorporeal membrane oxygenation Ji Hyun Yeo • Ki Hyuk Sung • Chin Youb Chung • Kyoung Min Lee • Young Choi • Tae Gyun Kim • Soon-Sun Kwon • Seung Yeol Lee • Moon Seok Park
Received: 19 May 2013 / Accepted: 6 October 2013 / Published online: 16 November 2013 Ó The Japanese Orthopaedic Association 2013
Introduction Acute compartment syndrome is a surgical emergency caused by increased pressure within an anatomical compartment, resulting in ischemia and necrosis [1, 2]. Most cases occurring in the lower leg are associated with trauma, prolonged compression, and vascular injury. Extracorporeal membrane oxygenation (ECMO) has recently been used as a final option for resuscitation in patients undergoing cardiopulmonary resuscitation [3]. ECMO support in children with intractable cardiac arrest can yield favorable outcomes in 30 % of patients [4]. From the theoretical viewpoint, during ECMO, acute compartment syndrome can develop because of limb ischemia or reperfusion. However, few reports have described cases of acute compartment syndrome in the lower leg caused by ECMO [5]. Moreover, case reports on the development of acute compartment syndrome in pediatric patients who received ECMO support are extremely rare. A previous study [6]
J. H. Yeo and K. H. Sung contributed equally to the writing of this article. J. H. Yeo C. Y. Chung K. M. Lee Y. Choi T. G. Kim S. Y. Lee (&) M. S. Park Department of Orthopaedic Surgery, Seoul National University Bundang Hospital, 300 Gumi-Dong, Bundang-Gu, Sungnam, Kyungki 463-707, Korea e-mail: [email protected] K. H. Sung Department of Orthopaedic Surgery, Kwandong University Myongji Hospital, Goyang, Kyungki, Korea S.-S. Kwon Biomedical Research Institute, Seoul National University Bundang Hospital, Sungnam, Kyungki, Korea
123
indicated that [50 % of pediatric patients who received ECMO management experienced ischemic changes in the limbs. Therefore, a greater number of case reports are required to evaluate the causes of acute compartment syndrome following ECMO support and thus prevent the development of this condition. We describe a case of a 12-year-old girl with acute compartment syndrome after ECMO who needed surgical treatment. The study was exempted from institutional review board review because it was a single, retrospective case report. Informed consent was obtained from the patient.
Case report A 12-year-old girl with allergic rhinitis who was scheduled to undergo coblation tonsillectomy sustained a sudden in-hospital cardiac arrest immediately after lidocaine injection in the tonsil. Cardiopulmonary resuscitation was started immediately with intubation, and two cardioversions were attempted. Approximately 43 min elapsed before restoration of spontaneous circulation was achieved after the last cardioversion. The patient was then transferred to a surgical intensive care unit. Her systemic blood pressure was *40 mmHg. On electrocardiography, she had a wide QRS tachycardia that converted to wide QRS bradycardia. Because her cardiac function was refractory to all medical treatment (epinephrine, atropine, etc.), femoral venoarterial ECMO was initiated approximately 1.5 h after the cardiac arrest. An arterial cannula (16 F) and a venous cannula (17 F) were percutaneously inserted into her right femoral artery and vein using the Seldinger technique. The ECMO pump flow was maintained between 2.6 and 2.7 L/min. Fraction of inspired oxygen (FiO2) was set at 0.7. Her vital signs stabilized, and her O2 saturation was maintained[98 %.
Compartment syndrome after ECMO
Four hours after ECMO insertion, the dorsalis pedis pulse disappeared and could not be detected even on Doppler examination. Her mid-thigh circumference increased by 2 cm, and her lower leg became cold. Because the ischemia in her right lower extremity worsened, a distal perfusion line was inserted, and the dorsalis pedis pulse was immediately restored. However, 5 h after insertion of the distal perfusion catheter, the dorsalis pedis pulse disappeared again, and the lower leg became more tense. Physical examination showed severe tension in the anterior and lateral compartment. Measurement of intracompartmental pressure revealed a significantly elevated pressure of 80 mmHg in the anterior compartment; consequently, the patient was diagnosed with acute compartment syndrome. At the time of this diagnosis, the level of creatine kinase (CK) was 16,339 IU/L (normal range 20–270 IU/L), and the CK muscle–brain (CK-MB) subunit was also elevated to 609.5 ng/ml (normal range 0–2.8 ng/ml). A double-incision, four-compartment fasciotomy was performed immediately under local anesthesia. The muscles in the superficial and deep posterior compartment appeared partially viable––they were pink, bleeding, and responded to electrical stimulation. However, the muscles in the anterior and lateral compartments were pale without bleeding and did not respond to electrical stimulation. After fasciotomy, sterile wet dressing was maintained (Fig. 1). The day after fasciotomy, the patient’s vital signs stabilized, and echocardiography showed nearly-normal ventricular function and a visual ejection fraction of 50–60 %. Although the ejection fraction decreased to 40 % upon
445
clamping, both ventricular functions were tolerable. Therefore, ECMO was removed. By day 12 after the fasciotomy, swelling of the affected lower leg had decreased sufficiently and primary wound closure was performed. At the time of closure, more than half of the tibialis anterior, extensor hallucis, and extensor digitorum were necrosed, so extensive debridement was performed. Primary wound closure was possible in the lateral fasciotomy site. In addition to the tissue necrosis, the patient also experienced medical complications immediately after the acute compartment syndrome. Her myoglobin increased to 25,620 ng/ml (normal range 0–100 ng/ml), and urine output decreased to 10 ml/h. Her serum creatinine increased to 2.40 mg/dl (normal range 0.7–1.4 mg/dl). The pediatrician diagnosed acute renal failure. Hydration, urine alkalization with sodium bicarbonate (NaHCO3), and diuresis with furosemide were initiated. Four days after fasciotomy, urine output and serum creatinine had normalized. Renal ultrasonography showed a normal renal parenchymal echo without focal lesion. At the time of discharge, there was no contracture of the ankle joint, and passive range of motion of all toes was fully possible. However, active dorsiflexion of the ankle and toes had not recovered, and the power remained at Grade I. To prevent foot drop and contracture of the ankle joint, an ankle–foot orthosis brace was applied, and the patient was educated about passive and assisted active range of motion exercises. One year after the fasciotomy, the muscle power of her extensor hallucis longus and ankle evertor were Grade I and II, respectively. The ankle showed varus tendency (Fig. 2). Passive dorsiflexion of the
Fig. 1 Muscles of the posterior compartment. a Compared with muscles of the lateral compartment, the medial fasciotomy site was relatively viable. b Lateral fasciotomy site. The images were obtained 9 days after fasciotomy
Fig. 2 Ankle showing varus tendency 1 year after the fasciotomy
123
446
ankle was limited to the neutral position. Therefore, we performed tibialis posterior split transfer to the peroneal brevis and tendo-Achilles lengthening. Although the tibialis anterior was also contracted, we did not transfer it to prevent foot drop.
Discussion ECMO has evolved markedly over recent years and is now used widely. The ECMO system removes deoxygenated blood from the patient’s venous system, circulates it through an artificial lung with a pump, and then returns the oxygenated blood back to the patient [3]. ECMO provides oxygenation of blood outside the patient’s body and can therefore provide artificial support for patients with cardiac or respiratory failure. ECMO is indicated for the management of life-threatening pulmonary or cardiac failure when no other form of treatment has been, or is likely to be, successful [7]. An ECMO system consists of two vascular cannulas to access and return the blood, a pump, a membrane oxygenator, and a heat exchanger that maintains blood temperature via the oxygenator [8] (Fig. 3). Drained blood from the access cannula is passed through a pump to the membrane oxygenator. There, the deoxygenated blood is oxygenated and transferred to the heat exchanger before being returned to the body via a second cannula. The manner in which an ECMO circuit interacts with the patient’s circulation defines it as either venoarterial (VA) or venovenous (VV) (Fig. 4). VA ECMO involves oxygenation of blood drawn from the venous system and returned into the arterial circulation, providing cardiac support in addition to gas exchange. The VA mode can be Fig. 3 Extracorporeal membrane oxygenation (ECMO) system consists of two vascular cannulas to access and return blood, a pump, a membrane oxygenator, and a heat exchanger that maintains blood temperature via the oxygenator. Blood from the venous cannula is passed through a pump to a membrane oxygenator. Then, deoxygenated blood becomes oxygenated; it is then transferred to the heat exchanger and is finally returned to the body via the arterial cannula
123
J. H. Yeo et al.
achieved by either peripheral (femoral vessel) or central cannulation. In central cannulation, blood is directly removed from the right atrium and returned to the proximal ascending aorta. In peripheral cannulation, both the drainage and returning catheter are inserted in the femoral vein and artery [8]. In VV ECMO, blood is drained from the venous system and returned to the venous system. This technique provides oxygenation and is used for respiratory failure when cardiac output is sufficient [7]. Femoral VA ECMO provides effective cardiopulmonary support for critically ill patients. However, distal leg ischemia is a significant complication after femoral artery cannulation. To prevent limb ischemia, a bidirectional arterial cannula or a special right-angle, high-flow, arterial cannula can be used [9, 10]. Furthermore, a distal perfusion catheter can also be inserted in patients at risk for ischemia, depending on the blood pressure in the superficial femoral artery [10] (Fig. 5). Previous reports show that ECMO plays an important role in patients with respiratory or cardiac failure, but it also increases the risk of vascular injury, limb ischemia, and compartment syndrome [6, 11]. One study reported that limb ischemia occurred in as many as 18 % of ECMO cases [11]. During ECMO, femoral arterial cannulation usually completely or partially occludes the distal arterial lumen, thereby causing distal limb ischemia [5]. In femoral VA ECMO, the arterial cannula is relatively large and fits tightly in the femoral artery. This allows for delivery of large amounts of oxygenated blood to the proximal aorta, but it also can cause a significant reduction in arterial blood flow to the involved lower extremity. In addition, the VA ECMO cannula can increase the venous pressure in the lower extremity. The combination of decreased arterial flow and increased venous pressure causes a reduction in
Compartment syndrome after ECMO
Fig. 4 a Venoarterial (VA) extracorporeal membrane oxygenation (ECMO) system is used after failure of cardiac function. The arterial cannula (red) is located in the femoral artery, and the venous cannula (blue) is located in the femoral vein. Oxygenated blood from the ECMO system is returned to the body through the arterial cannula, and deoxygenated blood from the body is drained from the venous
Fig. 5 To prevent limb ischemia during extracorporeal membrane oxygenation (ECMO), a distal perfusion catheter can be used. An arterial catheter enters the common femoral artery, with the side branch providing flow into the distal perfusion catheter down the superficial femoral artery
perfusion pressure. If the perfusion pressure decreases significantly, the compartmental tissue undergoes ischemic changes. Tissue ischemia results in interstitial edema, which increases compartmental pressure and further decreases perfusion pressure [5]. This vicious cycle closes lymphatic vessels and small venules, resulting in compartment syndrome [5, 12–14]. To prevent limb ischemia, a number of techniques have been attempted [9, 10].
447
cannula. b Venovenous (VV) ECMO is used when respiratory function fails but cardiac function remains sufficient. Both arterial and venous cannulas are located in the femoral vein. Oxygenated blood from the ECMO system is returned to the body via the venous cannula, and deoxygenated blood from the body is also drained from the venous cannula
In the case reported here, signs of limb ischemia developed 4 h after the initiation of ECMO, but a distal perfusion line was inserted immediately, resulting in an immediate return of the dorsalis pedis pulse. However, revascularization also can cause compartment syndrome. One study reported that any procedure used for revascularization of the limb can result in a muscle compartment syndrome, with an incidence ranging between 0 % and 21 % [15]. During reperfusion, a complex mechanism eventually leads to vascular leakage. Factors such as leukotrienes, tumor necrosis factor alpha, and free radicals play a role in this mechanism [15, 16]. In our case, because limb ischemia progressed after ECMO, a distal perfusion catheter was inserted, after which edema and tenseness of the lower leg worsened, and CK level increased. This finding suggests that reperfusion injury further increases the pressure in the lower leg. We believe that a distal perfusion catheter should be inserted at the time of initiation of ECMO to prevent limb ischemia and acute compartment syndrome. To our knowledge, no study has yet assessed the risk factors for acute compartment syndrome during ECMO. One study compared ECMO-related variables among children with and without limb ischemia after ECMO [6]. That study revealed no significant difference in age, sex, weight, height, or cannula site between the two groups. Additionally, neither body surface area (BSA) nor BSA-to-
123
448
cannula ratio was significantly different between groups. Thus, no variable was predictive of the development of limb ischemia. Only younger age is known as a risk factor of acute compartment syndrome because of the tighter and stronger fascia and muscle fillings in these patients [14, 17]. Pain is the main clinical symptom of a developing acute compartment syndrome [14]. However, in our case, the patient was unconsciousness and unable to provide feedback about her pain. High pressure of the lower leg was recognized after it began developing pulselessness and pallor. At an intracompartmental pressure of 30–33 mmHg, the fascial membranes reach their maximum stretching tolerance, which limits compliance of the compartment [14]. A previous study advocated fasciotomy for absolute compartment pressure reaching 30–45 mmHg [18]. Therefore, we believe that regular measurement of intracompartmental pressure during ECMO can help earlier detection of acute compartment syndrome in unconscious patients. Acute compartment syndrome can cause significant sequelae if it is not detected early and adequate treatment is not provided. As described above, during ECMO, severe limb ischemia can occur and may lead to acute compartment syndrome. Therefore, insertion of a distal perfusion catheter at the time of ECMO initiation may prevent limb ischemia and acute compartment syndrome. In addition, cardiac surgeons, orthopedic surgeons, and nurses in intensive care units need to have a high index of suspicion for the possibility of acute limb compartment syndrome during ECMO. Furthermore, because patients receiving ECMO usually have several conditions that may potentially delay the diagnosis of compartment syndrome, routine surveillance with Doppler or continuous monitoring of compartment pressure should be performed. Conflict of interest No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article.
References 1. Khan RJ, Fick DP, Guier CA, Menolascino MJ, Neal MC. Acute paraspinal compartment syndrome. A case report. J B Jt Surg Am. 2005;87:1126–8. 2. Khan SK, Thati S, Gozzard C. Spontaneous thigh compartment syndrome. West J Emerg Med. 2011;12:134–8.
123
J. H. Yeo et al. 3. Schuerer DJ, Kolovos NS, Boyd KV, Coopersmith CM. Extracorporeal membrane oxygenation: current clinical practice, coding, and reimbursement. Chest. 2008;134:179–84. 4. Alsoufi B, Al-Radi OO, Nazer RI, Gruenwald C, Foreman C, Williams WG, Coles JG, Caldarone CA, Bohn DG, Van Arsdell GS. Survival outcomes after rescue extracorporeal cardiopulmonary resuscitation in pediatric patients with refractory cardiac arrest. J Thorac Cardiovasc Surg. 2007;134(4):952.e2–959.e2. 5. Wall CJ, Santamaria J. Extracorporeal membrane oxygenation: an unusual cause of acute limb compartment syndrome. Anaesth Intens Care. 2010;38:560–2. 6. Gander JW, Fisher JC, Reichstein AR, Gross ER, Aspelund G, Middlesworth W, Stolar CJ. Limb ischemia after common femoral artery cannulation for venoarterial extracorporeal membrane oxygenation: an unresolved problem. J Pediatr Surg. 2010;45:2136–40. 7. Marasco SF, Lukas G, McDonald M, McMillan J, Ihle B. Review of ECMO (extra corporeal membrane oxygenation) support in critically ill adult patients. Heart Lung Circ. 2008;17(Suppl 4):S41–7. 8. Lindstrom SJ, Pellegrino VA, Butt WW. Extracorporeal membrane oxygenation. Med J Aust. 2009;191:178–82. 9. Huang SC, Yu HY, Ko WJ, Chen YS. Pressure criterion for placement of distal perfusion catheter to prevent limb ischemia during adult extracorporeal life support. J Thorac Cardiovasc Surg. 2004;128:776–7. 10. Greason KL, Hemp JR, Maxwell JM, Fetter JE, Moreno-Cabral RJ. Prevention of distal limb ischemia during cardiopulmonary support via femoral cannulation. Ann Thorac Surg. 1995;60:209–10. 11. Smedira NG, Moazami N, Golding CM, McCarthy PM, Apperson-Hansen C, Blackstone EH, Cosgrove DM 3rd. Clinical experience with 202 adults receiving extracorporeal membrane oxygenation for cardiac failure: survival at 5 years. J Thorac Cardiovasc Surg. 2001;122:92–102. 12. Elliott KG, Johnstone AJ. Diagnosing acute compartment syndrome. J B Jt Surg Br. 2003;85:625–32. 13. Mars M, Hadley GP. Raised intra-compartmental pressure and compartment syndromes. Injury. 1998;29:403–11. 14. Shadgan B, Menon M, Sanders D, Berry G, Martin C Jr, Duffy P, Stephen D, O’Brien PJ. Current thinking about acute compartment syndrome of the lower extremity. Can J Surg. 2010;53:329–34. 15. Kostler W, Strohm PC, Sudkamp NP. Acute compartment syndrome of the limb. Injury. 2005;36:992–8. 16. Duran WN, Takenaka H, Hobson RW 2nd. Microvascular pathophysiology of skeletal muscle ischemia-reperfusion. Semin Vasc Surg. 1998;11:203–14. 17. Frink M, Hildebrand F, Krettek C, Brand J, Hankemeier S. Compartment syndrome of the lower leg and foot. Clin Orthop Relat Res. 2010;468:940–50. 18. White TO, Howell GE, Will EM, Court-Brown CM, McQueen MM. Elevated intramuscular compartment pressures do not influence outcome after tibial fracture. J Trauma. 2003;55:1133–8.
