Services on Demand
Print version ISSN 0034-7094
Rev. Bras. Anestesiol. vol.56 no.6 Campinas Nov./Dec. 2006
Lumbar plexopathy after abdominal hysterectomy. Case report*
Plexopatía lumbar después de la histerectomía abdominal. Relato de caso
Elizabeth Vaz da Silva, TSAI; Marco Antonio Cardoso de Resende, TSAII; Alberto Pantoja, TSAIII; Adriana Barrozo Ribeiro Furuguem CarvalhoIV; Alexandre Barbosa da SilvaV, Fabrício Azevedo CardosoVI
pelo CET HUAP/UFF; Professora Adjunta do Departamento de Cirurgia Geral e Especializada
IIInstrutor do CET/SBA do HUAP/UFF
IIIAnestesiologista do HUAP/UFF
IVEx-Membro do Serviço de Anestesiologia do HUAP/UFF Anestesiologista do Hospital Geral de Bonsucesso
VME2 da CNRM do HUAP/UFF
VIME3 da CNRM do HUAP/UFF
CASE REPORT: A woman patient, 38 years old, 58 kg, 1.63 m, physical status ASA I, was admitted to undergo a total abdominal hysterectomy for treatment of uterine leiomyomatosis. Initial monitoring included pulse oxymetry, non-invasive blood pressure, electrocardioscope, and urine output. After venous cannulation in the left upper limb with an 18G catheter, cefazoline (2 g), dypirone (2 g), dexamethasone (10 mg), and metochlopramide (10 mg) were administered. With the patient in left lateral decubitus, a 16G Tuohy needle was inserted in the L3-L4 space, in the median line, for the epidural block. Fifteen milliliters of 0.75% ropivacaine and 2 mg of morphine were administered, followed by placement of the catheter for postoperative analgesia. The surgery was uneventful, and the patient's cardiovascular parameters were stable. Eight hours after the procedure, at the postanesthetic follow-up, the patient could not walk and presented monoparesis in the left lower limb. The hypothesis of radicular syndrome was ruled out after clinical and radiological evaluation. Since symptoms did not resolve, an electroneuromyography was done 30 days later, and was compatible with lumbar plexopathy, which was possibly caused by trauma.
CONCLUSIONS: The anesthesiologist must be aware of the postoperative neurological complications and should be part of the efforts to diagnose their causes, of the treatment, and its evolution.
RELATO DEL CASO: Paciente del sexo femenino, 38 años, 58 kg, 1,63 m de altura, estado físico ASA I, internada para tratamiento de leiomiomatosis uterina, con indicación de histerectomía total abdominal. La monitorización inicial incluyó oxímetro de pulso, presión arterial no invasiva, electrocardioscopio y diuresis. Después de la punción venosa en el miembro superior izquierdo con catéter 18G, fueron administrados, por vía venosa, cefazolina (2 g), dipirona (2 g), dexametasona (10 mg) y metoclopramida (10 mg). La anestesia peridural fue realizada con aguja Tuohy 16G, en el espacio L3-L4, en la línea mediana con la paciente en decúbito lateral izquierdo. Fueron administrados 15 mL de ropivacaína a 0,75% y 2 mg de morfina, a continuación posicionado catéter para analgesia postoperatoria. La intervención quirúrgica no tuvo intercurrencia, manteniendo a la paciente estable bajo el punto de vista cardiovascular. En la visita posanestésica, 8 horas después del procedimiento, la paciente no deambulaba y presentaba monoparesia en el miembro inferior izquierdo. Después de las investigaciones clínicas y radiológicas fue descartada la hipótesis diagnóstica de síndrome radicular. Al no haber regresión del cuadro, 30 días después fue realizada una electroneuromiografía que quedo compatible con plexopatía lumbar de posible origen traumática.
CONCLUSIONES: El anestesiólogo debe estar atento a las complicaciones neurológicas que puedan surgir en el postoperatorio, participando de la elucidación de las causas, del tratamiento y de su evolución.
Severe neurological complications have been described after regional block. Postoperative neuropathies are frequently attributed to the anesthesia; however, it may also be secondary to the surgery itself.
Plexopathies and neuropathies are secondary to anesthetic blocks, and can be caused by intraneural injection 1, hematoma 2,3, mispositioning 4 and local neuritis.
Lesions in the femoral, lateral femoral cutaneous, and obturator nerves, although rare, do occur after pelvic surgeries, and trauma is the most frequent mechanism. Femoral nerve lesion is reported in the literature associated with several surgical procedures, such as inguinal herniorrhaphy, total hip arthroplasty, gynecological surgeries, and intra-abdominal vascular surgeries, and, less often, with appendectomy, lumbar sympathectomy, and laparoscopies 5. The objective of this report was to present the case of a patient who underwent total abdominal hysterectomy and went on to develop plexopathy, and to discuss the probable causes.
A woman patient, 38 years old, 58 kg, 1.63 m, physical status ASA I, was admitted to the hospital for a total abdominal hysterectomy for uterine leiomyomata.
Premedication included midazolam 7.5 mg PO at 10 p.m., the night before the surgery, and at 7 a.m., i.e., one hour before the surgery.
Monitoring included pulse oxymetry, non-invasive blood pressure, electrocardioscope in the DII derivation, and urine output. Ringer's lactate was administered after venous cannulation with an 18G catheter in the left upper limb.
The patient was placed on left lateral decubitus and epidural puncture was done with a 16G Tuohy needle in the median line in the L3-L4 space. The epidural space was identified by the loss of resistance technique. After making sure there was no blood or cerebrospinal fluid return, a test dose of 3 mL of 2% lidocaine (60 mg) with adrenaline 1:200.000 followed by 15 mL of 0.75% ropivacaine with 2 mg morphine were administered. A catheter for postoperative analgesia was then placed. Twenty minutes after the epidural block, the maximum sensitive blockade obtained was in T4.
Cefazoline (2 g), dypirone (2 g), dexamethasone (10 mg), and metochlopramide (10 mg) were administered in the beginning of the procedure, and ephedrine (2 mg) 15 minutes after the block, when there was a 30% drop in blood pressure.
There were no complications during the surgery, which lasted 160 minutes, and the patient was transferred to the posthanestetic recovery unit.
Eight hours after the procedure, the patient could not ambulate and developed monoparesis in the left lower limb.
She was evaluated by the Neurology service, being diagnosed with a probable radicular syndrome. On physical exam, she presented paresthesia in the upper left thigh, lateral and anterior aspect of the left thigh, patellar reflex absent on the left, Achilles reflex present and equal bilaterally.
X-rays of the lumbosacral spine and abdomen did not show any abnormalities; CT scan of the lumbosacral spine was normal.
The patient's signs and symptoms remained the same and, 30 days after the surgery, an electroneuromyography was done. It showed a normal nervous conduction, the needle exam showed positive waves and fibrillation of the left quadriceps and left adductor muscles, suggesting the diagnosis of lumbar plexopathy.
The lumbar plexus is formed by the nervous roots of T12 to L4 6,7. The femoral, lateral femoral cutaneous, and obturator nerves are formed by the superior roots of L2-L3-L4, being responsible for the sensitive-motor innervation of the thigh 8. In the pelvis, the femoral nerve emerges from the major psoas muscle, descending deep within the iliac fascia. The femoral nerve ends 4 cm below the inguinal ligament; behind this ligament, the anterior branch gives rise to the medial cutaneous nerve of the thigh and the intermediate cutaneous nerve that innervate the anteromedial aspect of the thigh down to the knee. The posterior branch of the femoral nerve innervates the quadriceps femoris and sartorius muscles. The saphenous nerve represents the terminal branch that innervates the skin of the medial aspect of the leg down to the medial portion of the foot 7. The femoral cutaneous nerve migrates laterally, running under the inguinal ligament close to the anterosuperior iliac spine. The obturator nerve, the third branch of the lumbar plexus, runs medially and posteriorly in the pelvis; when it emerges from the obturator foramen, it provides sensitive-motor fibers to the medial portion of the thigh and medial aspect of the knee 8.
The neurophysiological study has interpretative limitations in radiculopaties. It might be difficult to differentiate, for example, L2-L3 or L4 radiculopathy from lumbar plexopathy or femoral neuropathy because the innervation of the thigh muscles by these three nerve roots overlaps 9. In 1933, Pollock 10 stated that the paralysis of the femoral nerve is rarely caused by gynecological disease and that such lesion would happen after gynecological surgeries, resulting from trauma and adhesions. Until that publication only four cases of paresis of the femoral nerve associated with gynecological surgeries had been reported.
In 1958, Winkelman and Johnson 11,12 reported paresis of the femoral nerve, isolated or combined with paresis of the obturator nerve, in surgical procedures with rotation, abduction and internal flexion of the lower limbs. The neuritis affecting isolated nerves after surgeries would be caused by ischemia or a mechanical factor, such as compression, stretching, or direct trauma 13. Four degrees of lesions were described: (1) no effects; (2) paralysis with fast recovery due to release of pressure; (3) paralysis with slow recovery without degeneration; and (4) anatomical lesion with degeneration 14.
A prospective study by Kvist-Poulsen and Borel 15 showed that the lesion of the femoral nerve after abdominal hysterectomy is much more frequent than indicated in the literature, with an incidence between 7.45% and 11.6%. This high incidence suggests that many cases of milder lesion of the femoral nerve might not be diagnosed due to the short duration of the symptoms or lack of knowledge about this complication. Fifteen of 17 patients studied had spontaneous recovery and only two had residual sensitive disturbances, without more serious changes.
Most cases reported in the literature had spontaneous recovery within one to six months, but one case had loss of sensitivity and motor dysfunction 13.
As a rule, there are sensitivity changes in cases of neuropathy of the obturator nerve, but there might be motor dysfunction of the adductor muscles of the thigh. The neuropathy of the lateral femoral cutaneous nerve is usually temporary since, unlike the other two nerves, it is only sensitive 16.
A British prospective study with 100 patients who underwent total abdominal hysterectomy tried to analyze the disparity between the reported incidence by Kvist-Poulsen and Borel and the real incidence, since there was only one case in the United Kingdom. Seven patients presented clinical evidence of nerve lesion, and the investigation demonstrated there was a lesion of the lateral femoral cutaneous nerve, at the level of the Balfour retractor, in six patients as a complication of the surgery 17.
Static retractors, by exerting continuous pressure on the ileopsoas muscle, stretch the femoral nerve, making it ischemic by occlusion of the external iliac artery or compressing blood vessels closely related to the nerve when going through the muscle. The obturator nerve can be stretched or squeezed by retractors placed deeply in the pelvic floor. Excessive abduction of the thigh can stretch the obturator nerve. There can also be direct pressure over the lateral femoral cutaneous nerve, since its trajectory varies. Small branches of this nerve can puncture the inguinal ligament, and the hyperflexion of the thigh over the abdomen can increase the pressure on the ligament 16.
There are three predisposing factors for the lesion: Plannenstiel incision, slender build, and the need to apply greater pressure on the retractors used to better expose the surgical field, causing direct nerve compression 7,13,17,18. The neuromuscular blockade and inadequate positioning of the patient also contribute to the pathogenesis 4,16. However, some studies indicate that the following factors cannot be considered specific pathogenic factors: surgical technique, pelvic disease, type of incision, and the surgeon's technical ability 15,18.
Most neuropathies of the lower limbs are symptomatic shortly after regression of the anesthesia. The opposite is seen in the upper limbs, where the symptoms of lesion of the ulnar nerve, the most frequent, have a late beginning in 62% of the cases 20.
Peripheral nerve lesion related to epidural anesthesia has a prevalence of 0.1%, for the transitory lesion, and 0.02%, for the permanent lesion, and is usually associated with diluents and addictives in the solution of the local anesthetic 18,21-23.
Although a peripheral nerve lesion is often attributed to the anesthesia, it can have other causes, such as mechanical trauma associated with the surgical instruments. It is important to emphasize the importance of the postanesthetic follow-up as well as of the diagnosis of this unusual complication of pelvic surgeries. Nowadays, this follow-up is an integral part of the anesthesiologists' defense in face of possible medical-legal suits.
01. Schafhalter-Zoppoth I, Zeitz ID, Gray AT Inadvertent femoral nerve impalement and intraneural injection visualized by ultrasound. Anesth Analg, 2004;99:627-628. [ Links ]
02. Klein SM, D'Ercole F, Greengrass RA et al Enoxaparin associated with psoas hematoma and lumbar plexopathy after lumbar plexus block. Anesthesiology, 1997;87:1576-1579. [ Links ]
03. Aveline C, Bonnet F Delayed retroperitoneal haematoma after failed lumbar plexus block. Br J Anaesth, 2004;93:589-591. [ Links ]
04. American Society of Anesthesiologists, Task Force on the Prevention of Perioperative Neuropathies. Practice guidelines for the prevention of perioperative neuropathies. Anesthesiology, 2000;92:1168-1182. [ Links ]
05. Kim DH, Kline DG Surgical outcome for intra- and extrapelvic femoral nerve lesions. J Neurosur, 1995;83:783-790. [ Links ]
06. Amaral JLG, Rodrigues RC Anestesia de membro inferior. Rev Bras Anestesiol 1995;45:(Supl20):134-142. [ Links ]
07. Barbosa JS, Rabello RP, Saraiva RA et al Lesão de nervo periférico nem sempre é complicação da anestesia regional. Rev Bras Anestesiol ,1992;42:239-242. [ Links ]
08. Mulroy MF Bloqueio de Nervos Periféricos, em: Barash PG, Cullen BF, Stoelting RK Anestesia Clínica, 1ª ed., São Paulo, Manole, 2004;715-742. [ Links ]
09. http://www.emglab.com.br/html/emg_-_limitacoes.html. Acesso em: 10 out. 2005; 21:30:25.
10. Pollok LJ Curtis Obstetrics and Gynecology. Philadelphia, W.B. Saunders, 1933. [ Links ]
11. Winlkelman NW Femoral nerve complications after pelvic surgery; a report f six cases. Am J Obstet Gynecol, 1958; 75:1063. [ Links ]
12. Johnson DA, Montgomery RR Femoral neuropathy in abdominopelvic surgery. Med Ann Dist Columbia. 1958;27:513-514. [ Links ]
13. Vosburgh LF, Finn WF Femoral nerve impairment subsequent to hysterectomy. Am J Obstet Gynecol, 1961;82:931- 937. [ Links ]
14. Slocum HC, O'Neal KC, Allen CR Neurovascular complications from malposition on the operating table. Surg Gynecol Obst, 1948;86:729. [ Links ]
15. Kvist-Poulsen H, Borel J Iatrogenic femoral neuropathy subsequent to abdominal hysterectomy: incidence and prevention. Obstet Gynecol, 1982;60:516-520. [ Links ]
16. Warner MA Perioperative Neuropathies in the Lower Extremities, em: Faust, RJ Anesthesiology Review, 3rd ed., Philadelphia, Churchill Livingstone, 2002;569-570. [ Links ]
17. Morgan K, Thomas EJ Nerve injury at abdominal hysterectomy. Br J Obstet Gynaecol, 1995;102:665-666. [ Links ]
18. Georgy FM Femoral neuropathy following abdominal hysterectomy. Am J Obstet Gynecol, 1975;123: 819-822. [ Links ]
19. Rosenblum J, Schwarz GA, Bendler E Femoral neuropathy a neurological complication of hysterectomy. JAMA, 1966; 195:409-414. [ Links ]
20. Cheney FW, Domino KB, Caplan RA et al Nerve injury associated with anesthesia: a closed claims analysis. Anesthesiology, 1999;90:1062-1069. [ Links ]
21. Zugliani JA Dano ao sistema nervoso periférico de natureza mecânica relacionado à anestesia. Tese de livre Docência. Niterói UFF, 1976. [ Links ]
22. Bromage P Analgesia Epidural. São Paulo, Manole, 1980; 667-675. [ Links ]
23. Usubiaga JE Neurological complications following epidural anaesthesia. Int Anesthesiol Clin, 1975;13:1-153. [ Links ]
Dr. Marco Antonio Cardoso de Resende
Av. 7 de Setembro, 91/1501 Icaraí
24230-250 Niterói, RJ
Submitted for publication
31 de janeiro de 2006
Accepted for publication 25 de julho de 2006
* Received from Serviço de Anestesiologia do Hospital Universitário Antônio Pedro da Universidade Federal Fluminense (HUAP/UFF), Niterói, RJ