Gluteal compartment syndrome after lumbar laminectomy

Abstract

Gluteal compartment syndrome may, in its severe form, have serious consequences. It may result in severe rhabdomyolysis, and if left untreated it can result in acute renal collapse, multiorgan failure and even death. The present report concerns a patient who developed a gluteal compartment syndrome after lumbar surgery. The syndrome was complicated by acute renal failure with high concentrations of serum creatinine kinase, myoglobin, and potassium, requiring acute haemodialysis before surgical release. The operation revealed increased intracompartmental pressure with weak or absent reaction of muscles to electric stimulation. To prevent the development of gluteal compartment syndrome during operative procedures, it is important to avoid harmful pressure to the gluteal regions on the operating table. It is also important to optimise muscle circulation by adequate hydration therapy and avoidance of nephrotoxic stimuli. If gluteal compartment syndrome develops, immediate diagnosis and surgical decompression are mandatory .

Background

Pain in the legs and the gluteal regions may among a number of diseases which indicate muscle compartment syndromes. Compartment syndrome in the legs is well known^1–3 with a number of publications focusing on it, and with clinical awareness of the syndrome.^4,5 However, it has been argued that the diagnosis of the more elusive compartment syndrome of the gluteal region is more difficult than that of the legs.^6–9 Only seven articles about the disease were found in a recent literature search for description of the syndrome according to a number of criteria.¹⁰ A significant rhabdomyolysis may be induced during a gluteal compartment syndrome, and the large gluteal muscles may subsequently contribute to renal failure, multiorgan failure and even death.^9,11 The pathogenesis of renal failure secondary to rhabdomyolysis is acute tubular necrosis (ATN). The myoglobin released from muscle tissues are initially filtered in the kidneys. At some stage it may cause obstruction of the tubulus with intratubular haem pigment casts. The haem core of myoglobin and free cheletable iron mediates proximal tubular cell injury.¹² Concurrent volume depletion, renal ischaemia or hypoperfusion will aggravate the damage.¹³ Both rhabdomyolysis and acute renal failure can be averted by careful positioning of the patient and adequate hydration perioperatively.^14,15 Awareness of gluteal compartment syndrome, early detection and adequate treatment are crucial to prevent serious consequences.

Case presentation

A 65-year-old man, obese with a body mass index of 38 kg/m², underwent surgery with a lumbar laminectomy because of spinal stenosis characterised by radiating pain to both extremities, especially the left. No motor or sensory pathology was found preoperatively. The patient had poorly regulated type 2 diabetes mellitus, since 1987, complicated by retinopathy, neuropathy and diabetic nephropathy with renal disease stage III (estimated glomerular filtration rate (GFR) 59 ml/min/1.73 m²). He had a well regulated hypertension and was taking statins. The operation was performed under inhalational anaesthesia and in the elbow–knee position with side and buttock support. The operation lasted 4 h without observed complications, except for prolonged hypotension. Blood pressure at the start of the operation was 148/88 mm Hg. For 3 of these 4 h he had a systolic blood pressure between 80–100 mm Hg and a diastolic blood pressure between 40–60 mm Hg (mean arterial pressure (MAP) 65–70 mm Hg). He had adequate oxygen saturation above 95% at all times. Perioperatively cephalotin was administered as a prophylactic antibiotic. Bleeding was estimated to be around 400 ml. The perioperative diuresis was 375 ml and the patient was oliguric when he arrived in the postoperative unit. Postoperatively he developed quite severe respiratory acidosis with pH 7.13 (pCO₂ up to 9.66 kPa) attributed to opioid analgesia induced hypoventilation.

Investigations

Eleven hours postoperatively the senior house officer observed very sparingly, dark, red urine and the suspicion of rhabdomyolysis was raised. Analysis of the urine showed red supernatant, haematuria and pigmented granular casts. Immediate blood tests showed a very high concentration of creatine kinase (CK) of 75 858 U/l (normal range (NR) 40–280), myoglobin 99 423 µg/l (<60), creatinine 186 µmol/l (NR 60–100), carbamide 20.5 mmol/l (NR 3.5–8.5) and potassium 6.7 mmol/l (NR 3.5–4.4). The patient was normotensive but with respiratory distress. Chest x-ray showed increasing congestion. Fluid balance was estimated to be in excess of 4 litres. Because of this, intravenous fluids were stopped, and he was treated with intravenous diuretics alone . Despite the treatment he remained oliguric and the urine output was calcul ated to be 10–20 ml/h. The respiratory acidosis was treated with non-invasive respiratory support. The diagnosis of acute oliguric renal failure due to rhabdomyolysis was likely, but in spite of repeated clinical assessment no anatomic substrate for the pathology was found during the first 18 h.

During a clinical examination approximately 20 h postoperatively the patient reported increasing pain in both gluteal regions, especially on the left side. The pain did not respond to analgesic treatment. At palpation both gluteal regions, and especially the left one, were felt abnormally firm and painful. Both feet had decreased capillary filling and felt cold. Palpable pulsation was found in the arteria dorsalis pedis (ADP) and arteria tibialis posterior (ATP), verified by Doppler ultrasound. The patient reported a faint pain in the middle part of the left leg, but no abnormal neurological findings were noted. Based on these findings an acute gluteal compartment syndrome requiring surgery was diagnosed.

Differential diagnosis

Among relevant differential diagnoses, malignant hyperthermia must be suspected in a patient who experiences a rapid increase in CK peri- or postoperatively. Our patient had no muscle rigidity and a normal temperature, and the hyperthermia syndrome is rare. Other mechanisms of rhabdomyolysis, such as statin induced, immunologic or virally precipitated mechanisms, are all less likely in this setting. It is also mandatory to exclude myocardial infarction. In our case the CK was the MM-isoenzyme, and CK-MB and troponin T were at normal concentrations.

Treatment

Because of persistent oliguric acute renal failure with signs of increasing respiratory distress and rapidly increasing potassium, acute haemodialysis was initiated, 22 h after the first operation. Therefore it took 27 hours after the initial operation before a surgical decompression of the left gluteal compartment, which had been clearly pathological at examination, was performed by a posterior approach. Perioperatively increased intracompartmental pressure was found. The reaction of the gluteus medius and maximus muscles to electric stimulation was weak or absent (fig 1). However, there was no clear necrotic appearance of those muscles and therefore only minimal revision was done initially. The wound was left open for later revisions. Vacuum assisted closure was applied after the first revision and afterwards during two following revisions the necrotic parts of the gluteus medius and maximus muscle were removed (fig 2).

Figure 1.

Perioperative photograph demonstrating the muscle oedema under initial surgical decompression.

Figure 2.

Perioperative photograph demonstrating the muscle necrosis under first revision 3 days after initial surgical decompression.

Outcome and follow-up

Despite the minimal muscle revision initially, the CK values decreased dramatically after the decompression of the compartment, and steadily decreased further. The patient was discharged from hospital with nearly normal values of CK and myoglobin 12 days after the initial lumbar operation (fig 3). At that time he was increasingly polyuric and dialysis was not required any more.

Figure 3.

Creatine kinase (CK) and myoglobin values before and after surgical decompression of the gluteal compartment.

Discussion

Gluteal compartment syndrome seems to be a rather rare medical condition as few reports exist in the English literature.^8,9,16–19 Hayden, in her c case report from 2006, summarised 40 published cases from 1972 to 2001. Most of the reported cases were caused by surgical positioning (12 cases) or by prolonged recumbence associated with drug abuse (16 cases).⁸ In 2007 Kumar described four cases of obese patients with postoperative gluteal compartment syndrome, all of whom were treated with epidural analgesia after the primary operation. A reasonable degree of sensation and motor activity may be beneficial in order to distribute load bearing of the tissues around the hip during a postoperative phase. Kumar argued that an epidural anaesthesia may prevent the normal, spontaneous changes in a patient’s posture, and thereby increase the load on the gluteal regions.¹⁸ The observation of gluteal compartment syndrome after drug abuse may have been caused by a similar mechanism.

It is a challenge to diagnose gluteal compartment syndrome sufficiently early so that effective treatment can be instituted.^9,16,20 The most prevalent symptom is an excessive pain which does not respond to analgesia. Other symptoms tend to occur later when the intracompartment pressure is so elevated that it compromises the arterial perfusion and causes ischaemic damage to muscles, nerves and vessels.^5,6 In many cases some pain is expected after trauma or surgery, and it is a challenge to identify the cases where a compartment syndrome contributes to the pain. Clinical experience is needed to differentiate between such cases. Also, when evaluating the firmness and tenderness when palpating the gluteal regions, experience is crucial for detecting those cases where a compartment syndrome is developing.

In the present case the diagnosis of rhabdomyolysis was readily established following urine analysis due to the classical triad¹³ of pigmented granular casts, dark red urine supernatant, and excessively elevated CK. There are no well established thresholds for CK before renal damage develops, but with substantially elevated CK values, as in this case, >50% of patients will experience renal failure.²¹ As it typically takes between 2–4 h after injury for CK and myoglobin to leak out of damaged myocytes, additional factors may have contributed to the renal damage. Our patient had a moderate diabetic nephropathy preoperatively, which made him more susceptible to acute tubular necrosis. The perioperative hypotension is probably also an important contributing factor. It reduces the GFR and urinary production, and thereby reduces the washout of myoglobin.¹³ In addition the patient was obese. It has been suggested that these patients are more susceptible to perioperative rhabdomyolysis,²² and that they have a more rapid increase in the retention parameters than patients of normal weight.²³ Even if the compartment syndrome was actively searched for, the diagnosis of gluteal compartment syndrome was delayed.

During the clinical examination approximately 20 h after the initial surgery, the patient complained of increasing pain especially in the left gluteal region. Pallor of the foot, weak pulsation in the ATP and ADP, and decreased capillary filling could signify impaired arterial circulation to both lower extremities. Despite no serious neurological symptoms, the blood tests revealed advanced muscle ischaemia. As soon as the gluteal compartment was surgically decompressed CK fell dramatically. A rapid fall in CK values is an important measure for the effectiveness of the surgical decompression. Even if CK was steadily decreasing until the patient was finally discharged from hospital, the measured half-life was approximately 24 h (fig 3). This is almost twice the expected half-life of CK. It is the authors’ experience that CK has a longer half-life in this setting. It may reflect continuing muscular damage or, more likely, a washout phenomenon from the damaged muscle.

Compartment pressure monitoring might be helpful for the early diagnosis of gluteal compartment syndrome. Intracompartment pressure monitoring has been described by Whitesides,²⁰ and several techniques and catheter types have been developed.^24,25 Catheters that allow continuous pressure monitoring have been in use.^5,26 However, the accurate pressure threshold for performing fasciotomy has not been precisely described. Most authors suggest the threshold to be between 30–45 mm Hg,^5,24 but most of the data are based on the leg and forearm, and corresponding data for the gluteal region have not been determined.^8,27 Therefore, clinical judgment remains crucial for diagnosing gluteal compartment syndrome, and for deciding when to operate.

The present case strengthens the postulate of Kumar that overweight patients are at risk of developing gluteal compartment syndrome following surgery due to their positioning during the operation which increases load on the gluteal regions. Thus one way to protect patients against this syndrome is to position them during the operation in such a way as to avoid any harmful pressure. Our case also shows that very serious complications, caused by severe rhabdomyolysis and subsequent acute renal failure with life threatening serum potassium values, may be the result of gluteal compartment syndrome. Aggressive volume repletion and forced diuresis can ameliorate the course of renal damage merely by washing out the obstructing material and toxic substances. The role of alkalisation of the urine is under dispute and beyond the scope of this case report. Nephroprotective measures include adequate perioperative hydration, avoidance of hypotension, ischaemia and other nephrotoxic stimuli. Early diagnosis and rapid operation with surgical decompression of the affected muscle compartment is crucial for the treatment of gluteal compartment syndrome.

Learning points

• Identify patients at risk of gluteal compartment syndrome.

• Position the patient during surgery so that harmful pressure on the gluteal region is avoided.

• Nephroprotective measures include adequate perioperative hydration, avoidance of hypotension, ischaemia and other nephrotoxic stimuli.

• Aggressive volume repletion and forced diuresis can ameliorate the course of renal damage.

• Early diagnosis and rapid surgical decompression is essential.