Patient management following extremity fasciotomy
- J Gregory Modrall, MD
J Gregory Modrall, MD
- Professor of Surgery
- University of Texas Southwestern Medical Center
- Section Editors
- Joseph L Mills, Sr, MD
Joseph L Mills, Sr, MD
- Section Editor — Vascular and Endovascular Surgery
- Professor and Chief
- Division of Vascular Surgery and Endovascular Therapy
- Baylor College of Medicine
- John F Eidt, MD
John F Eidt, MD
- Section Editor — Vascular and Endovascular Surgery
- Professor of Surgery, Texas A&M Health Science Center
- Vice Chair of Vascular Surgical Services, Baylor Heart and Vascular Hospital at Dallas
Extremity fasciotomy is the only recognized treatment for acute compartment syndrome and may be limb saving. Reperfusion following fasciotomy causes local and systemic effects that can be life-threatening and can complicate wound management.
The management of the patient following extremity fasciotomy, including management of reperfusion, wound care, and methods and timing of fasciotomy wound closure, will be reviewed here. Preoperative management and the indications, diagnosis, and techniques used to perform fasciotomy are discussed elsewhere. (See "Acute compartment syndrome of the extremities" and "Lower extremity fasciotomy techniques".)
Local and systemic consequences of ischemia-reperfusion occur after fasciotomy. Increased blood flow in the muscle following restoration of normal tissue pressure usually causes muscle edema. The extent of extremity swelling depends upon the duration and severity of ischemia, the predominant muscle cell type within a muscle, the location and mass of ischemic muscle, and the status of the venous circulation.
Animal studies show that cellular damage starts approximately three hours after a complete ischemic insult and is nearly complete by six hours . In humans, the level of tolerance to an ischemic insult varies and not all ischemic insults are complete. Patients with underlying peripheral artery disease may exhibit less than expected swelling due to the protective effects of pre-existing arterial collaterals that lessen the severity of ischemia . There is also evidence from animal studies that ischemic preconditioning in skeletal muscle may mitigate the severity of muscle injury, remote organ injury, and mortality after major ischemic events [3,4].
Swelling may be limited if there is incomplete reperfusion due to microvascular thrombosis. With prolonged ischemia, a "no reflow phenomenon" occurs that is characterized by capillary occlusion from endothelial swelling, plugging of capillaries with red and white blood cells, and increased interstitial pressure [5,6]. Reperfusion may occur at the macrovascular level, but there is no tissue perfusion. Clinically, this manifests as myonecrosis with minimal extremity swelling.
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