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Ann Thorac Surg 2007;83:1869-1870
© 2007 The Society of Thoracic Surgeons
Ponce Plastic Surgery, Mercedita, Puerto Rico
Accepted for publication December 5, 2006.
* Address correspondence to Dr Chattar-Cora, Ponce Plastic Surgery, PO Box 388, Mercedita, Puerto Rico 00715 (Email: deowallchattar{at}yahoo.com).
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Introduction |
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Given the patency rates of radial artery grafts, it is now commonly used for CABG [2, 3]. The reported morbidity associated with the donor site has been predominantly minor wound problems and parasthesias [4]. This is a case report of forearm extensor compartment necrosis after radial artery harvesting for CABG.
A 56-year-old man who was right hand dominant was scheduled for CABG using the left internal mammary artery, and radial artery grating from the left arm. Preoperative Allen’s testing was normal. During the radial artery harvesting the artery was clamped both proximally and distally with adequate palmar circulation demonstrated with a pencil Doppler. After ligating the distal radial artery there was good back bleeding seen from the distal stump. The rest of the intraoperative course was uneventful.
The patient had no arrhythmias perioperatively and was able to extubate without difficulty. On postoperative day 1 he complained of left forearm pain. His examination demonstrated some pitting edema of the left hand and forearm, good capillary refill, and intact palmar Doppler signals. Because of edema the patient was given several doses of diuretics. The edema decreased, but the patient continued to complain of forearm pain, and on postoperative day 6 the patient had wrist drop develop and was unable to extend his fingers. An orthopedic surgeon was consulted, and a diagnosis of radial neurapraxia was suspected due to retraction or possibly a hematoma, or both. A splint was ordered, and plastic surgery consultation was obtained for nerve exploration and possibly decompression of any hematoma. An evaluation of the patient found that he lacked sensation in the radial nerve distribution and suffered from loss of extensor function in his left wrist and hand.
The patient underwent operative exploration and was found to have forearm extensor and supinator muscle necrosis. There was no hematoma or signs of a hemorrhage found. The extensor and supinator muscles were debrided and the posterior interosseous branch of the radial nerve was identified in anticipation of an innervated muscle transfer. Of note there was no iatrogenic injury to the brachial, ulnar, or radial recurrent arteries, and a 1-cm proximal radial artery stump was visualized. The patient subsequently underwent two operative debridements. An upper extremity angiogram was performed that demonstrated a patent ulnar artery and its branch, the posterior inter-osseous artery.
On postoperative day 22 after CABG, the patient underwent an innervated gracilis free muscle transfer and tendon transfers. The patient had metacarpal-phalangeal joint stiffness develop, and 7 months after the muscle transfer he underwent intraoperative joint manipulation. Nine months after the gracilis transfer he had return of sensation in the radial nerve distribution, had the ability to extend his wrist, and was regaining some ability to extend his metacarpal phalangeal joints. On last follow-up the patient still has stiffness of his metacarpal phalangeal joints and the transferred muscle is still gaining function.
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Compartment Syndrome After CABG
Acute compartment syndrome occurs when the pressure within a contained fascial space exceeds capillary blood perfusion. If untreated, irreversible muscle damage with subsequent fibrosis and contracture occur. Compartment syndrome of the extremity is a recognized clinical condition associated with necrosis of the muscles and nerves within the involved compartment, which has significant morbidity. Although treatment options are available, reconstructive techniques are complex, not readily available at all centers, and functional return is never normal. Thus early diagnosis is important. It has long been taught that pulselessness, pallor, and paralysis led to the diagnosis; however, use of these clinical parameters can be misleading because loss of pulses and capillary refill and paralysis are late findings and they can be present in a patient with compartment syndrome [5]. During the early phase of the syndrome a palpable pulse may be present because the patient’s systolic pressure may be greater than 30 mm Hg, which is an intra-compartmental pressure commonly associated with compartment syndrome [6].
In reliable patients, pain out of proportion to the injury, pain on stretching the involved compartment, paralysis, and paresthesia, hypoesthesia, or anesthesia can be reliable clinical findings suggestive of the diagnosis. If needed, measurement of the intra-compartment pressure can help with the diagnosis. In obtunded patients or in patients that are unreliable, measurement of compartment pressures can help diagnose the condition. The exact pressure that necessitates fasciotomy is presently being debated; thus a high index of clinical suspicion is important in the diagnosis.
Compartment syndrome after CABG has been previously reported in the lower extremity. The cause of lower extremity compartment syndrome after CABG involves vascular cannulation of the lower extremity. However, compartment syndrome of the upper extremity after coronary bypass surgery has been rare. Poullis and colleagues [7] reported one case of upper extremity compartment syndrome; however the cause was not stated.
Our patient had forearm pain and swelling during the immediate postoperative period. He subsequently went on to have anesthesia and paralysis in the radial nerve distribution develop, suggesting that he may have had an undiagnosed compartment syndrome. Postoperative pain medication and diuretics, which helped mask the pain and decrease compartment edema led to a delayed diagnosis. Because the normal circulation and collateral circulation were detectable on angiographic study, possible causes for this compartment syndrome include ischemia reperfusion injury, aberrant circulation to the dorsal forearm musculature, or generalized tissue trauma in the forearm leading to significant forearm muscle edema; because the volar compartment fascia was released with arterial harvesting, this compartment was spared. The posterior compartments were not entered, and thus these were not decompressed. However the definitive cause for the compartment syndrome in this patient is not known.
To prevent this complication in patients undergoing CABG with radial artery harvesting, close clinical vigilance is required with urgent compartment decompression as indicated.
In conclusion, coronary artery bypass surgery is an effective modality for treating coronary ischemia. The use of radial artery grafts for CABG has increased. Although compartment syndrome after CABG has been rare, vigilance is required because early diagnosis is critical in preventing significant morbidity.
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