REPERFUSION EDEMA: THE DEVIL IN THE MOISTURE. POST ACUTE TREATMENT AND REHABILITATION Sergio De Marchi
Division of Vascular Rehabilitation, University of Verona, Azienda Ospedaliera Universitaria Integrata di Verona - Italy
Reperfusion edema inducing acute compartmental syndrome is a severe condition that may cause extended damage of muscles, nerve lesions and tissue damage. Post-ischemic compartment syndrome is a consequence of a biphasic ischemia-reperfusion injury: the ischemic phase causes an important damage and complex metabolic changes, reperfusion of oxygenated blood adds new damage. The ischemia-reperfusion injury is caused by the interaction of oxygen-derived free radicals, endothelial factors, inflammatory molecules, platelets and leukocyte activation. Oxygen-derived free radicals peroxidate cellular membrane lipids with damage. The consequence is the loss of microcirculatory regulation and increased capillary permeability. Another source of damage is the ischemic depletion of high-energy phosphate forms with further ischemic muscle injury. In the ischemic leg, microcirculatory unit is hypoperfused and is characterized by vasodilation and extensive loss in vasomotion; reperfusion causes an overflow that suddenly increases transmural pressure, that with reduced vessel permeability increases tissue edema. Acidosis and increased protein content of interstitial space amplifies the phenomenon. Edema and consequent swelling leads to reduced venous outflow with increased pressures and reduction in microculatory perfusions. Microvascular thrombosis may reduce swelling but it is a sign of extensive severe damage. Fasciotomy is the standard treatment and sometimes is used as a prophylactic therapy. Reperfusion edema may have severe systemic consequences such as hyperkalemia, metabolic acidosis and acute kidney injury due to myoglobinuria. The leg should be evaluated for the extension of wounds created from the fasciotomy (examine for infection and necrosis), presence of ischemic lesions in other sites, neurological damage, venous thrombosis, ankylosis and muscle loss. Patient should be also checked for arterial patency. The goals of wound management include identifying and debriding nonviable muscle and avoiding further muscle injury from wound desiccation. In complicated wound, negative pressure wound therapy or hyperbaric therapy can be associated. Reduction of edema can be obtained in post acute phase, with limph drainage in particular at proximal segments and bandage with low compression and frequent change. Neurological improvement can be obtained with reduction of edema and stimulation with specific exercise of proprioception, active and passive mobilization. The relief of muscular pump has pivotal role, so ankle mobilization is a crucial step of the therapy; also activation and passive mobilization of the foot is very important and effective involving plantar sole and venous backflow.
The follow up of these patients is intensive in the first year then it will be periodical, every 3-6 months for checking arterial patency and the chronic edema that often can be observed.
Reperfusion edema is a complex and sometimes severe syndrome that requires multidisciplinary approach with intensive rehabilitative care and accurate followup.
References
1. Menger MD, Rücker M, Vollmar B. Capillary dysfunction in striated muscle ischemia/reperfusion: on the mechanisms of capillary "no-reflow". Shock 1997; 8:2. 2. Steinau, H-U. Major Limb Replantation and Postischemia Syndrome: Investigation of
Acute Ischemia-Induced Myopathy and Reperfusion Injury, Springer Verlag, New York 1988.
3. Blaisdell FW. The pathophysiology of skeletal muscle ischemia and the reperfusion syndrome: a review. Cardiovasc Surg 2002; 10:620.
4. Zannis J, Angobaldo J, Marks M, et al. Comparison of fasciotomy wound closures using traditional dressing changes and the vacuum-assisted closure device. Ann Plast Surg 2009; 62:407.
5. Ojike NI, Roberts CS, Giannoudis PV. Compartment syndrome of the thigh: a systematic review. Injury 2010; 41:133.
6. Rush DS, Frame SB, Bell RM, et al. Does open fasciotomy contribute to morbidity and mortality after acute lower extremity ischemia and revascularization? J Vasc Surg 1989; 10:343.
7. Heemskerk J, Kitslaar P. Acute compartment syndrome of the lower leg: retrospective study on prevalence, technique, and outcome of fasciotomies. World J Surg 2003; 27:744.
8. Fitzgerald AM, Gaston P, Wilson Y, et al. Long-term sequelae of fasciotomy wounds. Br J Plast Surg 2000; 53:690.
9. Bermudez K, Knudson MM, Morabito D, Kessel O. Fasciotomy, chronic venous insufficiency, and the calf muscle pump. Arch Surg 1998; 133:1356
10.Ritenour AE, Dorlac WC, Fang R, et al. Complications after fasciotomy revision and delayed compartment release in combat patients. J Trauma 2008; 64:S153.
