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Revista Brasileira de Anestesiologia

Print version ISSN 0034-7094

Rev. Bras. Anestesiol. vol.56 no.4 Campinas Set./Aug. 2006

http://dx.doi.org/10.1590/S0034-70942006000400009 

CLINICAL INFORMATION

 

Rhabdomyolysis secondary to gluteal compartment syndrome after bariatric surgery. Case report*

 

Rabdomiolisis por síndrome compartimental glúteo después de cirugía bariátrica. Relato de caso

 

 

Márcio Luiz Benevides, TSAI; Rubens Jardin Nochi JúniorII

IAnestesiologista do Hospital Universitário Júlio Muller da FCM-UFMT. Título de Especialista em Terapia Intensiva, AMIB
IIME2 do CET/SBA Hospital Universitário Júlio Muller da FCM-UFMT

Correspondence to

 

 


SUMMARY

BACKGROUND AND OBJECTIVES: Bariatric surgery has become a common procedure and several complications have been reported. The objective of this report is to present a case of gluteal compartment syndrome that evolved to acute renal failure after bariatric surgery and to discuss the diagnosis, and the prophylactic and therapeutic measures.
CASE REPORT: A 42 years old male patient, white, with a body mass index (BMI) of 43, physical status ASA II, who underwent bariatric surgery of the duodenal switch type, under general anesthesia associated with epidural anesthesia. There were no complications during the procedure. The anesthetic-surgical procedure lasted 3 hours and 30 minutes. On postoperative day one the patient developed lumbosacral and gluteal pain, besides paresthesia in the lower limbs in the distribution of the sciatic nerve. On physical exam, the buttocks were slightly pale, tight, swollen, and painful to palpation and to movement. A diagnosis of gluteal compartment syndrome was made; it evolved to rhabdomyolysis and acute renal failure. The renal function improved and the patient did not present any motor or sensitive deficits.
CONCLUSIONS: Patients with morbid obesity undergoing bariatric surgery may present gluteal compartment syndrome as a complication. When it is not diagnosed and treated promptly, it may evolve to rhabdomyolysis and acute renal failure, which represents a serious life-threatening situation.

Key Words: COMPLICATIONS: gluteal compartimental syndrome, rabdomiolisis, renal insufficiency; DISEASES, Morbidity obesity, SURGERY, Bariatric.


RESUMEN

JUSTIFICATIVA Y OBJETIVOS: La cirugía bariátrica se convirtió en rutina y en algo muy complicado para ser relatada. El objetivo de este relato fue el de presentar un caso de síndrome compartimental glútea que evolucionó para la insuficiencia renal aguda después de la cirugía bariátrica y discutir aspectos del diagnóstico y conductas profiláctica y terapéutica.
RELATO DEL CASO: Paciente del sexo masculino, 42 años, blanco, índice de masa corporal (IMC) 43, estado físico ASA II, sometido a cirugía bariátrica tipo duodenal switch, bajo anestesia general asociada a la anestesia peridural. El procedimiento se dio sin incidencias. El tiempo anestésico quirúrgico fue de 3 horas y 30 minutos. El primer día del postoperatorio el paciente presentó dolor en la región lombosacral y en las nalgas, además de parestesia en los miembros inferiores en la distribución del nervio ciático. Durante el examen, las nalgas presentaban una discreta palidez, tensas, con edemas, dolían cuando eran tocadas y cuando se movían. Fue diagnosticado el síndrome compartimental glúteo que evolucionó con rabdomiolisis e insuficiencia renal aguda. Hubo una recuperación de la función renal y ninguna secuela motora o sensitiva se detectó.
CONCLUSIONES: Los pacientes obesos mórbidos sometidos a la cirugía bariátrica pueden presentar síndrome compartimental glúteo. Cuando no se diagnostica y se trata precozmente, puede evolucionar con rabdomiolisis e insuficiencia renal aguda representando una seria amenaza para la vida.


 

 

INTRODUCTION

The gluteal compartment syndrome classically occurs in a space anatomically confined by non-distensible structures. The gluteal compartment encloses the muscles gluteus maximus, medius and minimus surrounded by the fascia lata, posteriorly, and by the tensor fascia lata, anteriorly. The initial lesion is the prolonged direct compression of the muscles, which may lead to edema, increased pressure in the compartment, ischemia, anaerobic glycolysis, production of lactate and H+ ions, release of inflammatory mediators, release of free radicals, muscle necrosis, hypovolemia due to the sequestration of large amounts of fluid, release of myoglobin, production of uric acid, increased levels of creatinophosphokinase (CPK), myoglobinuria, and acute renal failure1,2.

The objective of this report is to present a case of gluteal compartment syndrome that evolved to acute renal failure after bariatric surgery and to discuss the diagnosis, and the prophylactic and therapeutic measures.

 

CASE REPORT

A 42 years old male patient, white, with a body mass index (BMI) of 43, with hypertension treated with enalapril maleate (10 mg.d-1), was submitted to bariatric surgery of the duodenal switch type3 under general anesthesia associated with lumbar epidural anesthesia at the L1-L2 level without a catheter. The anesthetic-surgical procedure lasted 3 hours and 30 minutes, without any complications. The patient received 3,500 mL of Ringer's lactate and presented a urine output of 450 mL, which was light yellow. Fifteen minutes after the surgery the patient was extubated, remaining in observation in the operating room for another 20 minutes. Afterwards he was removed to the intensive care unit (ICU) with a modified Aldrete score 9 and motor blockade 1 by the Bromage scale. In the ICU he received 2,000 mL of glucose 5% in water, with 20% NaCl (10 mL) and 19.1% KCl (3 mL) in each 500 mL of the solution. His urine output was 1,300 mL. He was discharge to the regular ward after 18 hours. At that moment, arterial blood gases with O2 per nasal canula (3 L.min-1) showed pH 7.35, pO2 88.9 mmHg, pCO2 43.9 mmHg, HCO3 23.7 mmol.L-1, BE 2, SaO2 96%. BUN and creatinine were not measured. On the 1st postoperative day the patient complained of lumbosacral pain, severe pain in the buttocks, and paresthesia in the lower limbs in the distribution of the sciatic nerve. On physical exam, the buttocks were slightly pale, tight, edematous, and painful to palpation and movement. There was no motor deficit in the lower limbs, and peripheral pulses were present and symmetric. The patient was treated with intravenous hydration (an average of 2,500 mL.d-1 PO in the first three days with the same glucose solution), non-steroidal anti-inflammatory (cetoprophen 200 mg.d-1), dipyrone and tramadol, change of decubitus, and local cold packs, with improvement of the symptoms. The patient was discharged from the hospital on the 4st postoperative day.

Two days after discharge, the patient was admitted to the ICU with malaise, asthenia, nausea, vomiting, oliguria, metabolic acidosis, hypercalcemia, elevated BUN and creatinine levels, which were as high as 352 mg% and 26.6 mg%, respectively. On the third hospital day CT scans of the thorax and abdomen were done. They showed atelectasis in the base of the left lung and decreased contrast, with reduced elimination by both kidneys. On two occasions Doppler ultrasound of the lower limbs were normal. CPK reached 11,980 U/L (reference level up to 190 U/L) on that day. The urine was dark and the urianalysis was positive for myoglobin. On the 4th hospital day the CPK was reduced to 6,607 U/L. The patient did not undergo dialysis. Prophylactic doses of low weight heparin were administered during the hospital stay. On the 7th hospital day the patient presented upper GI bleeding. Upper endoscopy showed an ulcer in the body of the stomach, in the area of the anastomosis, that had recently bled, requiring blood transfusion. The renal function improved and the patient did not develop any motor or sensitive deficits. The patient remained in the ICU for five days, being discharged from the hospital on the 21st day.

 

DISCUSSION

The gluteal compartment syndrome has been described in unconscious patients as a result of alcohol abuse and illicit drug use4, after trauma5, hip, knee and ankle surgeries, after postoperative analgesia through a epidural catheter with severe motor blockade6-8, and in urologic surgeries8,9, the majority of the cases are caused by remaining in the same position for a long period of time, frequently associated with obesity. More recently, cases of rhabdomyolysis have been reported in patients with morbid obesity that underwent bariatric surgery10-12.

Our patient presented signs and symptoms typical of gluteal compartment syndrome in the first postoperative day; however, they were not taken seriously. Initially, possible complications of the epidural blockade were ruled out. Since the signs and symptoms improved with conservative measures, the patient was discharged on the 4th postoperative day. The patient was admitted again 48 hours after discharge with acute renal failure.

The prolonged muscular compression caused an increase in the volume and pressure of the compartment, which could be monitored and help diagnose and guide the treatment. Fasciotomy is recommended when the pressure within the compartment exceeds 50 mmHg or if it remains between 30 and 50 mmHg and does not show a tendency to decrease after a period no longer than 6 hours2. According to some investigators, fasciotomy should be reserved for those cases with increasingly worse neurovascular function in both limbs due to the high risk of infection13. The aim of fasciotomy is to stop the progression of ischemia and rhabdomyolysis, therefore decreasing the damage to the kidneys.

Myoglobinuria will only be detected if serum myoglobin is above 1.5 mg.dL-1 2. Myoglobin gives the urine a typical brownish-red color (similar to Port wine)2. The urinalysis with a dipstick is neither specific, since it cannot differentiate hemoglobinuria from myoglobinuria, nor sensitive, being positive only in 50% of the cases1.

Elevated serum levels of CPK is enough to diagnose rhabdomyolysis, characterized by an increase greater than five times normal values1,10. Peak concentration is achieved in the first 24 h in 70% of the cases15. A serum myoglobin level greater than 30 mg.mL-1 is equally diagnostic of rhabdomyolysis1.

Renal lesion is seen in up to 50% of the cases of rhabdomyolysis10; there are several mechanisms involved, such as hypovolemia, tubular obstruction by precipitated myoglobin and uric acid, direct myoglobin toxicity, renal ischemia secondary to the release of vasoconstrictors by the muscular lesion, production of free radicals, and by metabolic acidosis1,2,15.

Rhabdomyolysis can be complicate by disseminated intravascular coagulation resulting from the activation of the coagulation cascade by substances released by the muscular lesion2.

The main treatment goal is to prevent the factors that cause renal failure, i.e., volume depletion, tubular obstruction, and release of free radicals.

The early infusion of liberal amounts of fluid is recommended, using several types of solutions, i.e., sodium - containing fluids (isotonic, ½), glucose 5% solution, with the addition of 50 to 100 mmol.L-1 of sodium bicarbonate. Mannitol, at a dose of 1.5 to 10 g.h-1 1,2,12,13 can be added to that combination. However, some authors question whether alkalization of the urine and the use of mannitol15,16 have a role in the treatment of this condition. Ten liters or more of fluid may be infused; urine output should be greater than 200 mL.h-1 1,16.

Allopurinol may be useful because it reduces the production of uric acid (release of purines secondary to cellular breakdown) and acts as a free radical scavenger1.

Damage to the sciatic nerve and the muscles itself may result in permanent or long lasting deficits, such as pain7-9, paresthesia5-7, foot drop, discomfort on sitting down4,6,7, and complex regional pain syndrome of the lower limb4.

In the case reported here, renal function improved without dialysis and, after a 12-month follow-up, the patient did not present neurological deficits.

Since it is a severe complication, it is important to identify inherent risks, such as obesity, diabetes mellitus, hypertension, use of medication for hyperlipedemia, prolonged surgical procedure10-12, postoperative epidural analgesia with motor blockade, and to have a strong suspicion on patients complaining of lumbosacral pain, pain in the buttocks and hips, with or without edema, and tightness of the region. We have to keep in mind that the diagnosis of compartment syndrome based in symptoms and clinical signs is frequently very difficult in the patient with morbid obesity17. Lumbar rhabdomyolysis may also be associated with that originated in the gluteal muscles18.

The use of soft mattresses, pillows under the buttocks, maintenance of the hemodynamic balance in the perioperative period, limiting the duration of the surgery, and the frequent change of decubitus, every 2 hours, in the perioperative, are prophylactic measures that should be routinely done10-12.

After this case, the use of foam mattresses, density 30, became routine in all patients undergoing bariatric surgery.

Bastanjian et al.11 recommend that CPK levels should be routinely checked in very obese patients, starting immediately after the surgical procedure and continued daily until levels show a clear tendency to be normal. If the CPK goes above 5,000 UI.L-1, aggressive hydration, administration of sodium bicarbonate and mannitol should be institute as prophylactic measures.

 

REFERENCES

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02. Vanholder R, Sever MS, Erek E et al – Rhabdomyolysis. J Am Soc Nephrol, 2000;11:1553-1561.        [ Links ]

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07. Pacheco RJ, Buckley S, Oxborrow NJ et al – Gluteal compartment syndrome after total knee arthroplasty with epidural postoperative analgesia. J Bone Joint Surg Br, 2001;83:739-740.        [ Links ]

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09. Rommel FM, Kabler RL, Mowad JJ – The crush syndrome: a complication of urological surgery. J Urol, 1986;135:809-11.        [ Links ]

10. Torres-Villalobos G, Kimura E, Mosqueda JL et al – Pressure-induced rhabdomyolysis after bariatric surgery. Obes Surg, 2003;13:297-301.        [ Links ]

11. Bostanjian D, Anthone GJ, Hamoui N et al – Rhabdomyolysis of gluteal muscles leading to renal failure: a potentially fatal complication of surgery in the morbidly obese. Obes Surg. 2003;13:302-305.        [ Links ]

12. Khurana RN, Baudendistel TE, Morgan EF et al – Postoperative rhabdomyolysis following laparoscopic gastric bypass in the morbidly obese. Arch Surg, 2004;139:73-76.        [ Links ]

13. Gunal AI, Celiker H, Dogukan A et al – Early and vigorous fluid resuscitation prevents acute renal failure in the crush victims of catastrophic earthquakes. J Am Soc Nephrol, 2004;15:1862-1867.        [ Links ]

14. Gabow PA, Kaehny WD, Kelleher SP – The spectrum of rhabdomyolysis. Medicine (Baltimore), 1982;61:141-152.        [ Links ]

15. Holt SG, Moore KP – Pathogenesis and treatment of renal dysfunction in rhabdomyolysis. Intensive Care Med, 2001;27:803-811.        [ Links ]

16. Lane R, Phillips M – Rhabdomyolysis. BMJ, 2003;327:115-116.        [ Links ]

17. Collier B, Goreja MA, Duke BE 3rd – Postoperative rhabdomyolysis with bariatric surgery. Obes Surg, 2003;13:941-943.        [ Links ]

18. Mognol P, Vignes S, Chosidow D et al – Rhabdomyolysis after laparoscopic bariatric surgery. Obes Surg, 2004;14:91-94.        [ Links ]

 

 

Correspondence to:
Dr. Rubens Jardin Nochi Júnior
Av. Marechal Deodoro, 615/502
Bairro Araés
s 78005-505 Cuiabá, MT
E-mail: rjnochi@terra.com.br

Submitted for publication 15 de agosto de 2005
Accepted for publication 13 de abril de 2005

 

 

* Received from Departamento de Anestesiologia, CET/SBA do Hospital Universitário Júlio Muller da Faculdade de Ciências Médicas da Universidade Federal de Mato Grosso (FCM-UFMT), Cuiabá, MT.