Sciatic nerve injury following intramuscular injection: a case report and review of the literature.
Subject: Sciatic nerve (Injuries)
Sciatic nerve (Research)
Injections, Intramuscular (Research)
Authors: Ramtahal, Jason
Ramlakhan, Shammi
Singh, Khaimraj
Pub Date: 08/01/2006
Publication: Name: Journal of Neuroscience Nursing Publisher: American Association of Neuroscience Nurses Audience: Professional Format: Magazine/Journal Subject: Health care industry Copyright: COPYRIGHT 2006 American Association of Neuroscience Nurses ISSN: 0888-0395
Issue: Date: August, 2006 Source Volume: 38 Source Issue: 4
Topic: Event Code: 310 Science & research
Accession Number: 150366885
Full Text: Abstract: A 25-year-old male patient presented with foot drop indicative of a sciatic nerve injury following gluteal intramuscular (IM) injections. Blood tests and magnetic resonance imaging of his spine were within normal limits, but electrophysiological studies confirmed a partial sciatic nerve lesion. The course of the sciatic nerve in the gluteal region places it at risk for injury from IM injections. Proper technique minimizes the risk of injury.


Intramuscular (IM) injection is an important means of administering medication. Sound knowledge of the anatomy of the area to be injected is essential. This article describes a case of sciatic nerve injury after gluteal IM injections. Related literature is reviewed with the goal of improving practice.

Case Report

A 25-year-old male migrated to the United Kingdom from the Congo after an imprisonment of 2 years. While in prison, he had received several left gluteal IM injections (the indications and drugs are unknown). Approximately 12 months before presenting, he developed a painful, swollen left leg that improved during several weeks. He then noticed that his left leg "started to shrink." He provided no history of polio infection and did not have any weakness in other limbs or associated sensory disturbance.

He was currently being treated for pulmonary tuberculosis that was diagnosed after migration. He was taking isoniazid, rifampicin, ethambutol, and pyridoxine. He was hepatitis-C positive but had tested negative for HIM. He had no significant surgical, social, or family history.

Neurological examination data were normal, apart from positive findings in his left lower limb. Inspection of his lower leg revealed marked muscle wasting with prominent fasciculations in the L4-S1 distribution. Power was markedly reduced to grade I out of 5 for dorsiflexion, inversion, and eversion. He had an absent left ankle jerk, although his sensory examination was normal. He had the typical high-steppage gait indicating left foot drop.

Blood tests revealed normal full blood count, urea and electrolytes, liver function, C-reactive protein and erythrocyte sedimentation rate, thyroid function, and vitamin B12 and folate levels. Polio and Coxsackie serology were negative. Two separate stool samples were also negative for the polio virus. Spinal magnetic resonance imaging excluded any structural cause, including disseminated tuberculosis (Pott's disease).

Electrophysiological studies revealed an absent left superficial peroneal sensory potential. The left sural sensory potential was at the lower limit of normal. There were absent compound muscle action potentials from the left extensor digitorum brevis and tibialis anterior as well as electromyographic evidence of complete denervation in the left tibialis anterior, with no sign of reinnervation. Other sampled muscles were normal. The findings were consistent with a partial sciatic nerve injury, most likely secondary to the injections. The prognosis for improvement was poor, because there had been no recovery during the past 12 months. Our goal was to exclude every possible cause of foot drop.


When giving gluteal injections, it is safest to use the upper outer quadrant. The choice of site for injection must be based on good clinical judgment, using the best evidence available and individualized client assessment. There is wide agreement in the literature that the ventrogluteal site is preferable (Small, 2004). Review of the literature on relevant injection procedure found that injury to the sciatic nerve is associated with use of the dorsogluteal site for injection, because the sciatic nerve commonly courses this site (Fig. 1).


Ndiaye, Sakho, Fall, Dia, and Sow (2004) performed sciatic nerve gluteal dissection on 10 fresh adult African cadavers, on both sides. The nerve pathway was 19 times out of 20 in the subpiriformis canal. In all cases the pathway was identical, with an oblique and vertical portion running down through the ischio-trochanteric channel. The cutaneous projection of the sciatic nerve was distant from the upper lateral quadrant of the buttock.

The site of injection is the crucial factor in determining the degree of nerve fiber injury. The degree of injury varies significantly, depending upon the specific agent injected. The most severe injuries have been associated with widespread axonal and myelin degeneration (Gentili, Hudson, and Hunter, 1980a). Pathological alterations in the nerve were evident as early as 30 minutes following injection injury (Gentili et al., 1980b).

Although postinjection injury can occur in both adults and children, children appear to be at higher risk (Krasnikova, 1986). Fatunde and Familusi (2001) did a retrospective study of all children with a diagnosis of sciatic nerve injury during a 12-year period. They examined 27 children, 5 months-12 years of age, with a diagnosis of postinjection sciatic nerve injury. The drugs administered to 17 patients included chloroquine, novalgin, paraldehyde, procaine penicillin, and sulfadoxine-pyrimethamine. However, the most neurotoxic agents tested in a previous study appear to be penicillin G, diazepam, and chlorpromazine (Yaffe, Pri-Chen, Lin, Engel, & Modan, 1986). The postulated mechanisms of injury include direct needle trauma, secondary constriction by scar, and direct nerve fiber damage, due to both axon and Schwann cell, with a breakdown in the blood-nerve barrier by neurotoxic chemicals in the injected agent (Gentili et al., 1980b; Villarejo & Pascual, 1993)

Neurological sequelae can range from minor transient sensory disturbance to severe sensory disturbance and paralysis, with poor recovery (Villarejo & Pascual, 1993). In one study, seven patients (26%) presenting with foot drop had had recent IM injections in the buttock. An additional 20 patients (74%) presented much later (Fatunde & Familusi, 2001). In fact, gluteal IM injection that led to sciatic nerve injury most often presented as paralytic drop foot (Mayer & Romain, 2001; Sobel, Huang, & Wieting, 1997).

Children who present with drop foot may later develop gluteal fibrosis (diagnosed 5.1 years after the injections). In contrast, sciatic nerve palsy, presenting as equinovarus or equinus deformity, was diagnosed on average 3.8 months after the intragluteal injections (Napiontek & Ruszkowski, 1993). Cavovarus and calcaneocavus foot deformities have also been reported (Bigos & Coleman, 1984).

Medical treatments including administration of vitamins and alphachymotrypsine have been tried with varying results, depending on the extent of the lesion. Early (within 2 months) physiotherapy may provide a better chance of recovery (Bourrel & Souvestre, 1982). Our patient presented 12 months after nerve injury and, thus, his chances of recovery were small.

The recommended treatment rang es from a conservative approach to immediate operative exposure and irrigation and has included early neurolysis or delayed exploration with neurolysis or resection and anastomosis (Villarejo & Pascual, 1993). Of 190 patients with gluteal sciatic nerve injuries in one retrospective study, the injuries were caused by injection in 164 patients (86.32%). Fifteen were treated by conservative means, and the other 175 had surgical intervention. Neurolysis was performed in 160 cases, epineural neurorrhaphy in 12 cases, nerve grafting in 2 cases, and nerve exploration but no repair in I case. Late-stage functional reconstruction of the foot and ankle was performed in 23 cases. Follow-up of 151 patients for an average 8.5 years revealed excellent to good nerve recovery (i.e., 57% and 78% in the early and late stage, respectively). We believe that neurolysis should be performed as soon as possible in cases of injection injury (Huang, Yan, & Lei, 2000).

Epineural neurorrhaphy should be performed in cases of nerve rupture. Functional reconstruction of the foot and ankle should be carried out in the late stage for the improvement of the limb function, if a surgical team is available for this purpose (Huang et al., 2000). If performed within 24 hours after injury, neurolysis may prevent the occurrence of paralysis (Mayer & Romain 2001; Yaffe et al., 1986). Our patient was offered physiotherapy rather than surgical treatment because of his late presentation. To date, his improvement has been minimal.

The implications for nurses include the need to learn and practice safe injection technique. Nurses must also assess for complications (both immediate and long term), and educate patients.


Post-IM injection sciatic nerve injury can be avoided. Proper training and an anatomical understanding of the sciatic nerve course are essential. We recommend that the superolateral gluteal area between the crest of the ilium and the greater trochanter be properly defined as the preferred site for IM injection (Bigos & Coleman, 1984). Children are at higher risk of injury as opposed to adults. Sciatic nerve injury presents most commonly as foot drop. Treatment should include early surgical exploration and physiotherapy to minimize long-term sequelae.


Bigos, S. J, & Coleman, S. S. (1984). Foot deformities secondary to gluteal injection in infancy. Journal of Pediatric Orthopedics, 4, 560-563.

Bourrel, P., & Souvestre, R. (1982). A particular nervous traumatology: Lesions of sciatic nerve by quinine intragluteal injections. Medecine Tropicale: Revue du Corps de Sante Colonial, 42(2), 209-213.

Fatunde, O.J., & Familusi, J. B. (2001). Injection-induced sciatic nerve injury in Nigerian children. Central African Journal of Medicine, 47(2), 35-38.

Gentili, F., Hudson, A. R., & Hunter, D. (1980a). Clinical and experimental aspects of injection injuries of peripheral nerves. Canadian Journal of Neurological Sciences, 7(2), 143-151.

Gentili, F., Hudson, A. R., Kline, D., & Hunter, D. (1980b). Early changes following injection injury of peripheral nerves. Canadian Journal of Surgery, 23(2), 177-182.

Huang, Y., Yan, Q., & Lei, W. (2000). Gluteal sciatic nerve injury and its treatment. Chinese Journal of Reparative and Reconstructive Surgery, 14(2), 83-86.

Krasnikova, E. (1986). Post-injection neuritis of the sciatic nerve. Zhurnal nevropatologii i psikhiatrii imeni S.S. Korsakova, 86, 499-501.

Mayer, M., & Romain, O. (2001). Sciatic paralysis after a buttock intramuscular injection in children: An ongoing risk factor. Archives of Pediatrics, 8, 321-323.

Napiontek, M., & Ruszkowski, K. (1993). Paralytic drop foot and gluteal fibrosis after intramuscular injections. Journal of Bone and Joint Surgery, 75(1), 83-85.

Ndiaye, A., Sakho, Y., Fall, F., Dia, A., & Sow, M. L. (2004). Sciatic nerve in gluteal portion: Application of sciatic nerve post injection lesion. Morphologie, 88(282), 135-138.

Small, S. P. (2004). Preventing sciatic nerve injury from intramuscular injections: Literature review. Journal of Advanced Nursing, 47, 287-296.

Sobel, E., Huang, E. Y., & Wieting, C. B. (1997). Drop foot as a complication of acupuncture injury and intragluteal injection. Journal of the American Podiatric Medical Association, 87(2), 52-59.

Villarejo, F. J., & Pascual, A. M. (1993). Injection injury of the sciatic nerve (370 cases). Child's Nervous System, 9, 229-232.

Yaffe, B., Pri-Chen, S., Lin, E., Engel, J., & Modan, M. (1986). Peripheral nerve injection injury: An experimental pilot study of treatment modallties. Journal of Reconstructive Microsurgery, 3(1), 33-37.

Questions or comments about this article may be directed to Jason Ramtahal, MBBS PGCTLCP MA MRCP, at j.ramtahal@liverpool. He is a clinical lecturer in neurology at the University of Liverpool and Walton Centre for Neurology and Neurosurgery, Liverpool, England.

Shammi Ramlakhan, MBBS MRCS, is an emergency medicine registrar at Barnsley Hospital National Health Service Trust, Barnsley, England.

Khaimraj Singh, MBBS MRCS, is a family physician at Woodside Green Medical Centre, Telford, England.
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