Keywords
gluteal compartment syndrome - type A aortic dissection repair - aortic dissection
complication
Introduction
A muscular compartment as hard as a rock is a cause for concern. The gluteal compartment
or “buttock” is no exception. Gluteal compartment syndrome (GCS) is rarely reported.
Failure to recognize this condition may lead to dramatic consequences. We report the
case of a patient developing a GCS after type A aortic dissection repair. Prompt diagnosis
and treatment led to a successful outcome. The surgical approach to the gluteal compartment
is described. Permission to report this case was obtained from the institutional review
board.
Case Presentation
A 41-year-old man, working in a furniture confection plant, experienced severe “tearing”
chest pain upon heavy lifting. On presentation in another health facility, a chest
computed tomography (CT) scan, with incomplete imaging of the iliofemoral axis, revealed
a type A aortic dissection (DeBakey type I). Following transfer to our center, physical
examination showed a pulseless left femoral artery, while no sign of acute limb ischemia
was present. The patient underwent a mechanical Bentall procedure with hemiarch replacement
under circulatory arrest for a total procedure time of 7 hours, 45 minutes. The immediate
postoperative course was uneventful. The femoral pulses were symmetrical and well
palpable once the patient rewarmed. Thirty-six hours after surgery, the patient was
extubated and complained of severe pain to his left buttock. The lower limb pulses
were present and no sensory or strength deficit was found. The left limb was normal,
while the buttock was tense and painful especially upon flexion and adduction of the
hip. A GCS was suspected. A CT angiography scan of the pelvis showed a dissection
flap ending proximal to the iliac bifurcation without direct involvement of the iliac
arteries. The false lumen was thrombosed and preferentially oriented toward the common
left iliac artery. The opacification of the left internal and external iliac arteries
was good. Preoperative CT angiography showed left gluteus muscle swelling ([Fig. 1]). This was likely related to a malperfusion following thrombotic or embolic occlusion
([Fig. 2]). The patient was diagnosed with GCS, further supported by a peak creatine kinase
of 91 865 U/L.
Fig. 1 Computed tomography scan prefasciotomy showing net asymmetry of the gluteal muscles,
especially the large left buttock measuring 77.4 mm (▪) versus 54.3 mm on the contralateral
side (*).
Fig. 2 Computed tomography angiography prefasciotomy of maximum intensity projection. (A–D) and three-dimensional (E) reformatted images of the pelvis: (A) Axial: Dissection of bilateral common iliac arteries with thrombosed false lumen
in the left common iliac artery; (B) Axial: Thrombosed false lumen in the left common iliac artery and patent left inferior
gluteal artery; (C) Axial: Minimally decreased contrast opacification and minimally dilated left inferior
gluteal artery compared with contralateral side; (D) Sagittal: Reformatted image showing dissection of the abdominal aorta extending
in the left common iliac artery with poor opacification of the false lumen in the
left common iliac artery. The false lumen is oriented toward the ostium of the left
internal iliac artery, but the dissection is not extending into the left internal
and external iliac arteries. The left internal iliac artery and its branches, the
left superior and inferior gluteal arteries, are well opacified; (E) Dissection of the abdominal aorta with an intimal flap extending into bilateral
common iliac artery. The false lumen is thrombosed within the left common iliac artery
leading to a smaller size than the right. The left internal and external iliac arteries
are well opacified.
A Kocher-Langenbeck procedure ([Fig. 3]) was performed under general anesthesia with the patient placed in a right lateral
decubitus position, with his legs bent at a 30° to 40° angle. An incision was made
from the posterior superior iliac crest up to 5 cm of the greater trochanter and then
to the lateral aspect of the femoral shaft. The tensor fascia latæ was fully opened
longitudinally. The superficial and deep fascia of the gluteus maximus muscle and
the fascia of the tractus iliotibialis were incised, revealing the heavily compressed
muscles. The muscle bulged out of the incision. Muscles were then split along their
fibers allowing opening of the fascia of the medius gluteus muscle where necrotic
fibers were retracted anteriorly. The gluteus minimus muscle exhibited normal color.
The left buttock was left open for 4 days, after which the skin was closed primarily,
leaving the fascia open. Frequent dressing change was required as the edema was heavily
seeping out of the wound. After 4 days, the muscle had significantly decreased in
size and closing only the skin allowed the muscle to be completely tension free. The
patient was discharged home on postoperative day 13. After 17 weeks, the patient returned
to work and noticed intermittent claudication. Peripheral vascular impedance plethysmography
and contrast-enhanced CT confirmed a 50% stenosis of the left iliac arterial axis.
The patient was treated conservatively and is doing well without residual claudication
2 years thereafter.
Fig. 3 Kocher-Langenbeck approach: (A) Right lateral decubitus position; (B) Planned skin incision from the posterior superior iliac spine up to 5 cm of the
greater trochanter and then to the lateral aspect of the femoral shaft; (C) Incision showing the gluteus maximus with fascia and iliotibial tract; (D) Gluteus maximus and iliotibial tract incision showing underlying structures with
tensor fascia lata incised; (E) Anterior retraction of the gluteus medius muscle showing the gluteus minimus muscle.
Discussion
Gluteal compartment syndrome is seldom reported. To date, one case has been reported
before an endovascular abdominal aortic aneurysm repair[1] and four cases after acute abdominal aortic occlusion.[2] No case has been reported after thoracic aortic surgery.
The mechanism of GCS in our patient is most likely related to a temporary dynamic
malperfusion of the left iliac artery axis in relation to an overpressurized false
lumen. The reason why the gluteus maximus muscle was preferentially implicated is
likely related to an isolated external iliac hypoperfusion brought by the dorsal decubitus
positioning of the patient during the surgery. Regardless of the underlying mechanism,
not recognizing this complication might have led to serious consequences such as myonecrosis,
rhabdomyolysis, sepsis, severe acute renal insufficiency, multiorgan failure, and
even death.[1]
Diagnosis of GCS resides on a high index of suspicion since classic symptoms and signs,
such as pain on passive movement, pallor, paresthesia, paralysis, poikilothermia,
and pulselessness, are oftentimes not present in the buttock region.[3] In our patient, diagnosis was guided by the patient's symptoms of buttock pain.
In addition, CT imaging depicted a thickened gluteal compartment.
Once identified, the GCS must be surgically addressed, in which case urgent decompression
is the cornerstone of the treatment. The gluteal region is composed of the tensor
fascia lata compartment and the gluteal compartments (maximus, medius, and minimus),
all of which must be decompressed by fasciotomy (Fig. 3).[4] The buttock skin needs to remain open until edema resolves and primary closure without
tension is allowed (4–10 days). If edema is still an issue on the 10th to 12th day,
a skin graft may be necessary.
Herein, we report a case of GCS after type A aortic dissection repair. The patient
was managed successfully with a fasciotomy of the left buttock. This complication
may have been a result of a temporary occlusion of the left iliac axis with subsequent
reperfusion of the femoral and gluteal regions. Prompt identification and surgical
treatment of this syndrome led to a successful outcome.
