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Lumbar Muscle Rhabdomyolysis After Abdominal Aortic Surgery

Bertrand, Michele MD; Godet, Gilles MD; Fleron, Marie-Helene MD; Bernard, Marguerite-Anne PharmD; Orcel, Philippe MD; Riou, Bruno MD, PhD; Kieffer, Edouard MD; Coriat, Pierre MD

Cardiovascular Anesthesia: Society of Cardiovascular Anesthesiologists

Lumbar muscle rhabdomyolysis has been very rarely reported after surgery.The aim of this study was to determine its incidence and main characteristics in a large population undergoing abdominal aortic surgery. Over a 21-mo period, 224 consecutive patients, 209 male and 15 female, mean age 65 +/- 10 yr, underwent abdominal aortic surgery (aortic aneurysm in 142 patients and occlusive aortic degenerative disease in 82 patients). Surgical incision was a midline incision with exaggerated hyperlordosis in 173 patients and a flank incision with a retroperitoneal approach in 51 patients. Postoperative rhabdomyolysis was diagnosed in 20 patients. In these patients, 9 (4%) experienced severe low back pain, and lumbar muscle rhabdomyolysis was confirmed by tomodensitometry (n = 6) or muscle biopsy (n = 3). The remaining 11 patients had lower limb muscle rhabdomyolysis. Rhabdomyolysis occurred after surgery of longer duration, which involved more frequent visceral artery reimplantation, with longer duration of aortic clamping and greater intraoperative bleeding. Lumbar rhabdomyolysis occurred in younger patients who were more frequently obese. On first postoperative day, the mean creatine kinase (CK) value was greater in lumbar rhabdomyolysis than in lower limb rhabdomyolysis (17,082 +/- 15,003 vs 3,313 +/- 3,120 IU/L, P < 0.05). Acute renal failure and postoperative death did not occur in patients with lumbar muscle rhabdomyolysis. Lumbar rhabdomyolysis was not a rare event after abdominal aortic surgery (4%). This syndrome was characterized by postoperative low back pain of unusual severity, which required analgesic therapy, and induced a very high increase in CK with typical findings at tomodensitometry or muscle biopsy but was not associated with postoperative renal failure.

(Anesth Analg 1997;85:11-5)

Departments of (Bertrand, Godet, Fleron, Riou, Coriat) Anesthesiology and Critical Care, (Bernard) Biochemistry, (Orcel) Rheumatology, and (Kieffer) Vascular Surgery, Groupe Hospitalier Pitie-Salpetriere, Paris VI University, Paris, France.

Accepted for publication March 27, 1997.

Address correspondence to Dr. Gilles Godet, Department of Anesthesiology and Critical Care, Groupe Hospitalier Pitie-Salpetriere, Paris VI University, 75013 Paris, France.

Rhabdomyolysis can occur after prolonged limb ischemia or traumatic compression, malignant hyperthermia, prolonged immobilization during coma, or drug overdose [1-2]. Postoperative rhabdomyolysis is a rare event, which occurs with various surgical positions, which may lead to prolonged muscle compression, muscle-compartment syndrome, and, thus, crush syndrome [3]. The knee-chest and lithotomy positions are most often associated with postoperative rhabdomyolysis [4-7]. Other surgical positions have been very rarely incriminated [8,9], except in patients with muscular diseases [10].

Abdominal aortic surgery is a relatively frequent surgical procedure requiring satisfactory exposure of the operative site, which can be achieved by placing the patient in a physiologically abnormal position. Only one case of lumbar muscle rhabdomyolysis after abdominal aortic surgery has been reported [8]. According to our previous experience, lumbar muscle rhabdomyolysis after abdominal aortic surgery is not a rare event. Therefore, we undertook a prospective study to better determine the incidence and main characteristics of this complication.

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After institutional approval, over a 21-mo period, all patients who underwent abdominal aortic surgical repair were included in this study. Patients operated emergently were excluded. This study was part of a larger prospective epidemiological evaluation of postoperative complications after abdominal aortic surgery. The following preoperative data were recorded by a staff anesthesiologist who performed a clinical examination: age, gender, weight, height, type of abdominal aortic disease (aneurysm or occlusive atheroma), presence of known coronary-artery disease, hypertension, chronic obstructive pulmonary disease, chronic renal failure (serum creatinine >200 micro mol/L), or diabetes mellitus. Obesity was defined as body weight greater than 20% of ideal weight, using Lorenz's formula (ideal weight = height in centimeters - 100 - [height - 150]/2.5 for male; = height in cm - 100 - (height - 150)/4 for female).

After premedication with midazolam (5 mg per os) and morphine chlorhydrate (10 mg subcutaneously [sc]) 1 h before induction, anesthesia was induced with sufentanil 0.5 micro g/kg and propofol 3 mg/kg intravenously (IV). Muscular relaxation was achieved with atracurium 0.6 mg/kg. Then, the trachea was intubated, and anesthesia was maintained with isoflurane and 50% nitrous oxide in oxygen. Mechanical ventilation was performed to obtain an end-tidal CO2 concentration within 30-36 mm Hg. Monitoring included electrocardiogram with ST segment analysis of V5, V6, and DII leads, invasive blood pressures using a radial artery catheter and a pulmonary artery balloon flotation catheter, and expired gas analysis. Postoperative analgesia was performed using paracetamol (8 g/day IV) and morphine chlorhydrate (40-80 mg/day sc).

Surgery was performed either in the supine position with a lumbar pad placed to obtain a hyperlordotic position or in the right lateral position with a lower thorax pad, according to the surgical incision required, i.e., midline incision or retroperitoneal approach, respectively. Heparin (50 UI/kg) was administered IV during surgery. The duration of surgery, intraoperative blood loss, type of aortic graft procedures including associated vascular procedures, type of aortic cross-clamping (supra- or infrarenal), and duration of clamping were recorded.

During the postoperative period, the following biological variables were measured daily over the first 3 days and on the 5th and 10th postoperative days: serum creatinine and creatine kinase (CK) and MB isoenzyme of CK using immunoenzymofluorimetric technique. In these assays, the reagents and protocols of the manufacturer were used. The upper limit of normal for total CK activity was 210 IU/L. Chest radiograph and electrocardiograph were also performed daily during the first 3 days, then on the 5th and 10th postoperative days. Postoperative complications were diagnosed as previously reported [10]. Follow-up ended at discharge.

Rhabdomyolysis was defined as a postoperative CK value more than 1750 UI/L, as previously reported [12]. This threshold corresponds to the mean value +/- 2 SD of maximum CK value observed after abdominal aortic surgery in our unit, which usually occurs during the first postoperative day [12].

All patients with rhabdomyolysis and severe lumbar pain that persisted despite postoperative analgesia were considered to potentially have lumbar rhabdomyolysis. These patients were examined by an internist physician and underwent either diagnostic tomodensitometry or lumbar muscle biopsy. Muscular scintigraphy was not available in our hospital [8].

Patients were retrospectively divided into three groups: control group of patients without rhabdomyolysis, patients with lumbar muscle rhabdomyolysis, and patients with lower limb rhabdomyolysis.

All patients with rhabdomyolysis received crystalloids and/or furosemide to maintain a diuresis greater than 100 mL/h. Hypovolemia was diagnosed using the pulmonary artery catheter and/or echocardiography and corrected using colloids.

All data were stored daily on a computer disk using database software (Access 2.0; Microsoft Corp., Seattle, WA). Data are expressed as mean +/- SD. Comparison of the groups was performed using Student's t-test or the Fisher's exact test with the Bonferroni correction. All comparisons were two-tailed, and a P value of less than 0.05 was considered significant.

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During the study period, 225 patients underwent abdominal aortic surgery. One patient died within 2 h after surgery and was excluded from the analysis. Of the 224 patients studied, 209 (93%) were male and 15 (7%) were female, with a mean age of 65 +/- 10 yr (Table 1). Aortic lesions were aortic aneurysm in 140 (63%) patients and occlusive aortic atheromatous disease in 84 (37%) patients. Surgical incision was a midline incision in 171 (77%) patients and a retroperitoneal approach in 53 (23%) patients (Table 2).

The following postoperative complications were recorded: myocardial infarction (n = 6), cardiac failure (n = 13), infectious pneumonia (n = 16), and acute renal failure (n = 15) requiring hemodialysis in three cases. Death occurred in 12 cases (pulmonary embolism = 1, stroke = 1, cardiac death = 3, acute respiratory disease = 3, surgical complication = 2, multiple organ failure = 2).

Postoperative rhabdomyolysis was diagnosed in 20 (9%) patients. Of these patients, nine experienced severe intractable lumbar pain and were considered for the diagnosis of lumbar muscle rhabdomyolysis. The diagnosis was confirmed by tomodensitometry (Figure 1) in six patients and lumbar muscle biopsy (Figure 2 and Figure 3) in the three remaining patients. Tomodensitometry of lumbar muscles showed typical images of lumbar muscle rhabdomyolysis with enlargement of muscle related to significant edema and multiple muscle hypodensities indicating necrosis. Biopsy showed microfoci of myocytic involvement (with swelling, heterogeneous or encroached appearances) and interstitial edema.

One patient underwent lumbar muscle surgical decompression to relieve very severe pain; lumbar muscle pressure measured intraoperatively was 130 mm Hg (with a control value of 50 mm Hg measured in deltoid muscle). He was a 50-yr-old patient who, after reoperation for aortic stenosis with a surgery duration of 7 h, experienced a large increase of CK (42,000 UI/L on Postoperative Day 1). His follow-up was uneventful.

In the 11 remaining patients without lumbar muscle pain, rhabdomyolysis was considered to be secondary to prolonged lower limb ischemia and/or cholesterol emboli.

Comparison of the preoperative characteristics of patients in the three groups is depicted in Table 1: lumbar rhabdomyolysis occurred in younger patients. Characteristics of surgery are shown in Table 2. Rhabdomyolysis occurred after surgery of longer duration, which involved more frequent visceral artery reimplantations, with longer duration of aortic clamping and greater intraoperative bleeding. All patients who were diagnosed with lumbar muscle rhabdomyolysis received midline incision (Table 2). In the control group, the mean CK value on Postoperative Day 1 was 365 +/- 356 IU/L (range 14-1750 IU/L). The mean CK value was greater in the lumbar muscle rhabdomyolysis group than in the lower limb rhabdomyolysis group (respectively, 17,082 +/- 15,003 vs 3,313 +/- 3,120 IU/L, P < 0.05). Acute renal failure and postoperative death did not occur in the lumbar muscle rhabdomyolysis group (Figure 4).

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In the present study, lumbar muscle rhabdomyolysis occurred in 4% of 224 consecutive patients undergoing elective abdominal aortic surgery, and we identified several risk factors: midline incision with hyperlordotic position, young age, obesity, and long duration of the surgical procedure.

Lumbar muscle rhabdomyolysis has been very rarely reported after surgery, mainly after lithotomy or genupectoral positions. As observed in these cases, lumbar muscle rhabdomyolysis observed after aortic surgery seems highly dependent on the posture required by surgery. One must note the possible additive role played by morbid obesity, which may increase muscle pressure during operation. Only a single case had been reported after aortic surgery, by Bukowski et al. [8]. In contrast with our patients, their patient was anesthetized with succinylcholine and suffered severe low back pain as well as postoperative renal failure. Bukowski et al. [8] pointed out the possible role of posture and of the long duration of surgery and clamping in the genesis of such a complication.

Some remarks must be included to assess the relevance of our study. First, since we did not perform tomodensitometry or muscle biopsy in patients without clinical signs of lumbar rhabdomyolysis, we cannot rule out that subclinical lumbar muscle rhabdomyolysis occurred in some of the 11 patients with obvious lower limb rhabdomyolysis. Nevertheless, the clinical impact of such a minor complication should be very limited. Second, even if we did not observe any renal failure after lumbar muscle rhabdomyolysis, this does not mean that our resuscitation protocol was optimal. Indeed, the prevention of renal failure in rhabdomyolysis is still a matter of debate, and the precise role of therapeutic agents such as mannitol and bicarbonate, as well as surgery, need to be determined.

In conclusion, lumbar muscle rhabdomyolysis is not a rare complication after abdominal aortic surgery. This syndrome should be suspected in patients operated in the hyperlordotic position who experience severe lumbar postoperative pain and great increase in CK activity. The diagnosis should be suspected in any patient with severe low back pain and rhabdomyolysis unrelated to lower limb ischemia. Tomodensitometry or biopsy appears to be a helpful diagnostic test to confirm this postoperative complication.

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