Gluteal Compartment Syndrome Following Abdominal Aortic Aneurysm Repair: A Case Report

Gluteal Compartment Syndrome Following Abdominal Aortic Aneurysm Repair: A Case Report M.H. Chew, G.G. Xu, P.W. Ho, and C.W. Lee, Singapore, Republic of Singapore

Compartment syndromes occur when the elevated tissue pressure within a confined limb’s myofascial compartment exceeds capillary pressure, with subsequent neurovascular compromise. In order to reduce disability and the consequences of ensuring ischemia, it is essential for early recognition and intervention. This is more commonly recognized in the calf. We report an unusual case of gluteal compartment syndrome after abdominal aortic aneurysm (AAA) repair.

INTRODUCTION Compartment syndromes occur when the elevated tissue pressure within a confined limb’s myofascial compartment exceeds capillary pressure, with subsequent neurovascular compromise. To reduce disability and the consequences of ensuring ischemia, early recognition and intervention are essential. This is more commonly recognized in the calf. We report an unusual case of gluteal compartment syndrome (GCS) after abdominal aortic aneurysm repair.

CASE REPORT A 64-year-old Chinese male smoker presented with a known history of hypertension. He was previously diagnosed with an incidental asymptomatic 4.4-cm infrarenal abdominal aortic aneurysm (AAA) after computed tomography (CT) of the abdomen and has been on conservative management. The patient presented to the emergency department 1 year later with an 8-hour history of sudden onset of bilateral lower limb weakness and mild abdominal pain with

Department of General Surgery, Tan Tock Seng Hospital, Singapore, Republic of Singapore. Correspondence to Dr. Chee-Wei Lee, Department of General Surgery, Tan Tock Seng Hospital, 11 Jalan Tan Tock Seng, Singapore 308433, Republic of Singapore, E-mail: [email protected] Ann Vasc Surg 2009; 23: 535.e15-535.e20 DOI: 10.1016/j.avsg.2008.08.019 Ó Annals of Vascular Surgery Inc. Published online: October 1, 2008

radiation to the back. The patient’s blood pressure was elevated at 190/100 mm Hg and in sinus tachycardia with a heart rate of 100 beats/min. Abdominal examination revealed a nontender pulsatile AAA on palpation. Lower limb examination revealed absent femoral pulses bilaterally and was cool up to both mid thighs. Power was reduced bilaterally with the left lower limb weaker than the right. Anal tone was mildly lax, but there was no saddle anesthesia. No other neurological deficits were noted in the clinical examination. Urgent CT aortogram revealed a 4.4  3.6-cm infrarenal AAA and bilateral common iliac aneurysms with extensive mural thrombus in the sac extending down both common iliac vessels. Duplex of the lower limbs revealed various degrees of stenosis (35%-75%) along the arteries, but otherwise trickle flow was noted on the distal vessels bilaterally. Magnetic resonance imaging of the brain and spine did not reveal any concurrent cerebrovascular ischemia or spinal cord pathology. An aortobifemoral bypass was performed about 18 hours after the first onset of symptoms. Intraoperatively, the AAA was noted to have acute-on-chronic thrombus extending down to common iliac arteries. There was also a small posterolateral pseudoaneurysm around the second lumbar spine, suggestive of a contained leak. A 16  8-mm Dacron trouser graft was anastomosed to the infrarenal aorta and bilateral common femoral arteries. Infrarenal clamp time was less than 1 hour, and external iliac, superficial femoral, and profunda arteries were trawled for clots using a size 4 Fogarty catheter. Good backflow was noted, and a biphasic Doppler signal was noted in both dorsalis pedis pulses postoperatively. The patient was kept intubated postoperatively. Blood investigations revealed the development of acute renal failure and rhabdomyolysis. Serum creatine kinase was noted to climb from 979 U/L (normal, 30-350 U/L) to

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535.e16 Gluteal compartment syndrome following AAA repair

Fig. 1. Incision after fasciotomy of calf demonstrating ischemic lateral group (peroneii brevis and longus).

Annals of Vascular Surgery

Fig. 3. Fasciotomy of the gluteus performed with curvilinear incision following the iliac crest. Ischemic gluteal maximus muscle at the iliac crest origin. longus) were noted to be ischemic but was otherwise viable (Fig. 1). Creatine kinase level continued to climb to 148,300 U/L, however, and the development of bruising and tense swelling over the left buttocks was noted about 16 hours later (Fig. 2). Left gluteal compartment pressure was measured to be 115 mm Hg compared with the right gluteal compartment pressure of 25 mm Hg. Surgical decompression and debridement of the left gluteal compartments were performed using a curvilinear incision following the iliac crest, taking care to avoid the sciatic nerve (Fig. 3). Splitting of the gluteus maximus revealed localized ischemic gluteal maximus muscle at the iliac crest origin. The gluteus medius, minimus, and tensor fasciae latae were initially noted to be viable. Postoperatively, the patient required hemodialysis. A dramatic decrease in serum creatine kinase values and gradual improvements in kidney function were noted. Repeated surgical debridements followed by complete excision of the gluteal maximus, medius, and minimus were necessary due to the progression of necrosis. This was followed by subsequent split-thickness skin grafting. The wounds healed uneventfully but the patient was unable to restore normal gait.

DISCUSSION

Fig. 2. Development of bruising and tense swelling over the left buttocks 16 hours post AAA repair.

9381 U/L and subsequently 63,573 U/L 12 hours postoperatively, and the left calf was noted to be tenser than the right. Clinical impression was that of compartment syndrome, and the patient underwent a four-compartment fasciotomy and debridement of the calf muscles. The lateral compartment group of muscles (peroneii brevis and

GCS is uncommon. Our literature review has revealed 65 known cases including 5 reported cases of bilateral GCS (Table I). The most common etiology is that of excessive pressure or an extended period of compression to the gluteus. This is a result of prolonged immobility from substance abuse or epidural analgesia, or secondary to improper positioning during surgery. The surgical procedures at risk reported occur in bariatric surgery for the morbidly obese as well as urological operations.1-23 Other etiologies include traumatic injury to the gluteus or its

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Gluteal compartment syndrome following AAA repair 535.e17

Table I. Summary of all reported cases of gluteal compartment syndrome Etiology

Prolonged immobilization/ improper positioning

Trauma/injections/post procedure

Authors (year)

Kumar V, et al. (2007)

1

No. of cases

Remarks

4

Kao CL, et al. (2006)2 Heyn J, et al. (2006)3 Somayaji HS, et al. (2005)4

1 1 1 (Bilateral)

Reisiger KE, et al. (2005)5

2

Rodriguez Uranga JJ, et al. (2005)6 Chua HC, et al. (2003)7 Bostanjian D, et al. (2003)8

1

Krysa J, et al. (2002)9

1

Pacheco RJ, et al. (2001)10

2

Hill SL and Bianchi J (1997)11 Bleicher RJ, et al. (1997)12 Hynes JE and Jackson A (1994)13 Yoshioka H (1992)14 Schmalzried TP, et al. (1992)15 Barnes MR, et al. (1992)16 Bosch U and Tscherne H (1992)17 Rommel FM, et al. (1986)18

1 1 (Bilateral) 1

Post joint arthroplasty under epidural anaesthesia Sedative drug overdose Post prolonged surgery Post hip arthroplasty under epidural anesthesia Post prolonged laparoscopic renal surgery Post bariatric surgery in morbid obese Sedative drug overdose Post bariatric surgery in morbid obese Post arthroscopic posterior cruciate ligament repair Post knee arthroplasty under epidural anesthesia Sedative overdose Sedative overdose Sedative overdose

4 2

Sedative overdose Sedative overdose

1 4

Drug overdose Sedative overdose

1

Lementhal I, et al. (1985)19

1

Goldberg M, et al. (1980)20

1

Owen CA, et al. (1978)21

3

Evanski RM and Waugh TR (1977)22 Klock JC and Sexton MR (1973)23 Hayden G, et al. (2006)24

1

Post prolong urological operation Exaggerated dorsal lithotomy position Exaggerated dorsal lithotomy position Post prolonged immobilization Sedative overdose

1

Sedative overdose

1

Vikram D, et al. (2005)25 Roth JS and Newman EC (2002)26 Kuhle JW and Swoboda B (1999)27 Pai VS (1996)28

1 (Bilateral) 1

Rupture of superior gluteal artery post trauma Fall from height Post bone marrow biopsy

1

Post IM gluteal injection

1

Prynn WL, et al. (1994)29 Yoshioka H (1992)14 Lund N and Jensen KH (1990)30

1 1 1

Post total hip arthroplasty, damage to medial circumflex femoral artery Trauma Trauma Post IM gluteal injection

1 6

(Continued)

535.e18 Gluteal compartment syndrome following AAA repair

Annals of Vascular Surgery

Table I. Continued Etiology

Medical

Vascular

Authors (year)

No. of cases

Remarks

Brumback RJ (1990)31

1

Petrik ME, et al. (1988)32 Ferrie R and Loveland RC (2000)33 Kuklo TR, et al. (2000)34 Klockgether T, et al. (1997)35

1 1 (Bilateral)

Rupture of superior gluteal artery post trauma Trauma Post ecstasy hyperpyrexia

Schmalzried TP, et al. (1992)15

1

Bosch U and Tscherne H (1992)16 Kaufman G and Choi B (1972)36 Pua BB, et al. (2005)37 Maldonado TS, et al. (2004)38 Ishibashi H, et al. (2004)39 Su WT, et al. (2004)40

2

Over exertion Rhabdomyolysis after heroin abuse Spontaneous gluteal artery rupture in Ehlers-Danlos syndrome Necrotizing fasciitis of gluteus

1

Sickle cell anemia

1 (Bilateral) 2 1 1

Post open AAA repair Post endovascular AAA repair Post open AAA repair Post internal iliac artery embolization before endovascular AAA repair

vessels, as well as procedures such as injections or bone marrow aspirates.14,24-32 Uncommon etiologies include case reports from ecstasy consumption,33 heroin abuse,34 overexertion after a physical fitness test,35 spontaneous superior gluteal artery rupture in Ehlers-Danlos syndrome,15 necrotizing fascitis of the gluteus,16 and sickle cell-induced infarction involving the gluteus.36 GCSs occurring after AAA repairs are, however extremely rare, with only five cases reported to date.37-40 In three cases, GCS developed after endovascular AAA repair due to elective occlusion of one or both internal iliac arteries. This was necessary as a result of aneurysmal involvement of the common and internal iliac arteries.38,40 In the two open AAA repair cases, common and internal iliac aneurysms were similarly present.37,39 Postulated mechanism of the occurrence of GCS in open AAA repair was due to an extended period of ischemia to the gluteal muscles during crossclamping of the iliac arteries while performing anastomosis. Our case report is the sixth known case to occur after AAA repair, and the third after open repair. In our patient, GCS occurred likely as a result of severe and prolonged occlusion of blood supply to the gluteal muscles due to total aortic and common iliac occlusion from an acuteon-chronic thrombus formation. This was likely contributed by a delay in presentation as well as in arriving at a diagnosis. Revascularization was thus performed only about 18 hours after

1 1

symptoms. Despite attempts at revascularization, there was likely the presence of ischemic necrosis to the gluteal compartments, which were further aggravated by subsequent reperfusion injury. The development of unilateral rather than bilateral GCS is possibly due to the presence of better collaterals on the contralateral side and thus subsequent less initial ischemic damage. The gluteal compartment is a nondistensible osseofascial compartment that is continuous with the fascia lata of the thigh. Owen et al.21 demonstrated in cadaveric studies the presence of three separate compartments: the gluteus maximus, gluteus medius/minimus, and the tensor fasciae latae. The fascia lata overlies the gluteus medius and minimus, forming one compartment. The fascia lata splits into two layers to encompass the gluteus maximus posteriorly and the tensor fascia lata anteriorly, forming the other two compartments. The sciatic nerve lies under the gluteus maximus and emerges from the inferior border of the piriformis. While not enclosed in a fascial compartment, the sciatic nerve is susceptible to compression from adjacent muscles due to its proximity. Because of the large muscle mass involved, manifestations of crush syndrome and rhabdomyolysis usually occur. The diagnosis of GCS is often difficult to make. The presence of pain on passive flexion and adduction of the hip21 may not be easily differentiated from those resulting from trauma. Or, as in our case, when the patient is intubated, or in other

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patients who are unconscious as a result from overdose of sedatives, clinical features of a tense swelling and bruising of the buttocks may be the only suggestive feature of a compartment syndrome. These signs were evident in our patient and we were thus able to arrive at the diagnosis of GCS and intervene. The measurement of compartment pressures would be a useful adjunct and should be performed in suspected cases. Pressures of 30 mm Hg or greater are considered to be indicative of a compartment syndrome necessitating a fasciotomy.21 Caution has to be taken to avoid superior gluteal nerve and vessels during needle placement. Vikram et al.25 recommended the following needle placement techniques on the basis of cadaveric studies: the needle in the gluteus maximus should be positioned perpendicularly in the proximal and inner quadrant of the buttocks, over the posterior quarter of the iliac wing; the needle in the gluteus medius and minimus should be placed 2 cm inferior to the iliac crest, over the middle third of the iliac wing; and the needle in the tensor fasciae latae should be placed 2 cm anterior to and 3 cm distal to the tip of the greater trochanter, which would penetrate the deep fascia before lying in the belly of the tensor fasciae latae. These methods would thus measure the pressures of each compartment without causing damage to vital neurovascular bundles. Debridement of the gluteal muscles and tensor fasciae latae should be performed early in all three compartments described once diagnosis is achieved. The sciatic nerve must be identified and preserved and injury to the superior and inferior gluteal vessels and nerves should be avoided. It has been suggested that in compartment syndromes recognized late, as functional recovery in the limb is unlikely, approach may be used. 41 For GCS, we are of the opinion that decompression and debridement of muscles are necessary even in cases where diagnosis is recognized late. This is because gluteal compartments possess a large muscle bulk and the large amount of necrotic muscle removed would reduce the myoglobin load, thus preventing further damage to the kidneys. It may also facilitate better recovery of the lower limb function.

CONCLUSION GCS after AAA repair remains an uncommon complication and is likely as a result of delayed revascularization or prolonged immobility during AAA

Gluteal compartment syndrome following AAA repair 535.e19

repair. It is associated with high incidence of morbidity such as rhabdomyolysis, renal failure requiring hemodialysis, loss of lower limb function due to sciatic nerve palsy or muscle necrosis, and possibly death. Early recognition and diagnosis are necessary to avoid such sequelae.

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Annals of Vascular Surgery

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