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Ischaemic Neuropathy of the Lumbosacral Plexus Following Intragluteal Injection

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Ischaemic Neuropathy of the Lumbosacral Plexus Following Intragluteal Injection J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.43.6.489 on 1 June 1980. Downloaded from Journal of Neurology, Neurosurgery, and Psychiatry, 1980, 43, 489-494 Ischaemic neuropathy of the lumbosacral plexus following intragluteal injection M STOHR, J DICHGANS, AND D DORSTELMANN From the Department of Neurology, University of Tubingen and the Municipal Hospital of Pforzheim, West Germany SUMMARY A lesion of the lumbo sacral plexus may result from an inadvertent intra-arterial injection of vasotoxic drugs into one ofthe gluteal arteries. Symptoms and follow-up ofthree cases are reported. The neuropathy is attributed to a toxic endarteritis with retrograde propagation of spasm and thrombosis. Swelling and bluish discoloration of the buttocks ("embolia cutis medicamentosa") as well as an impaired circulation in the homolateral leg are associated withthe neurological syndrome in fully developed cases and makes possible a correct diagnosis. The obstruction of a main artery by embolism, grade propagation of angiospasms and throm- thrombosis or following trauma may lead to bosis, the homolateral lumbosacral plexus can ischaemic neuropathy. The neurological syn- suffer ischaemic damage, as observed in three Protected by copyright. drome, predominantly sensory impairment and cases. (more rarely) paralysis, or in milder cases pain and paraesthesia, depends upon the duration of CASE REPORTS ischaemia and collateral blood supply.1-3 If the Case I (BF, a 42 year old male): an injection ischaemia is of short duration a rapid and com- of about 45 ml Ultrademoplas (500 mg Phenyl- plete recovery of nerve functions will occur in butazon-Natrium, 500 mg Aminophenazon, 45 mg most cases, but ischaemia of a longer duration Lidocain-HCl, 4-5 mg Dexamethason, 9 mg can lead to permanent structural damage.2 4 Prednisolon and 2-8 mg Cyanocobalamin) was Since the oxygen turn-over of the peripheral given into the left buttock because of lower- nerve is rather low and blood supply is abundant, back pain. Immediately a severe local pain was ischaemic neuropathies will rarely occur if only felt, lasting for about 30 s. Ten to fifteen minutes one of the main arteries or only some, but not later, the patient noticed numbness in the left all of the distal branches of the nerve vessels foot which crept gradually upwards. Half an are obstructed. However, partial or total seg- hour after the injection, standing and walking mental necrosis were no of nerves regularly occurs if longer possible because of a severe http://jnnp.bmj.com/ microembolism, microthrombosis or spasms pain as well as a weakness in the left lower obstruct large portions of the epineural and peri- limb. The neurological examination revealed a neural plexus.' 5 This mechanism is responsible nearly complete paralysis of the left leg, includ- for cases of neuropathies after intra-arterial in- ing the hip-flexors and the gluteal muscles; deep jection of angiotoxic substances, for example tendon reflexes were absent. There was severe into the brachial artery,6 7 the inferior gluteal sensory impairment in the territories of the artery8-'0 and the umbilical artery of the new- femoral, lateral femoral cutaneous and common 12 born."' peroneal nerves, with less marked sensory dis- on September 27, 2021 by guest. An inadvertent injection of vasotoxic drugs turbances in the other areas of the left lower into one of the gluteal arteries may also result limb. There was painful swelling and bluish dis- in a toxic angiopathy with ischaemic damage coloration of the left buttock. Additional swell- of the sciatic or gluteal nerves. With the retro- ing at the left paravertebral region above the pelvis ("Embolia cutis medicamentosa," fig 1) Address for reprint requests: Manfred Stohr, MD Lieber- occurred and was followed by a deep gangrene meisterstr 18-20, Neurologische Universititsklinik, D-7400 within a few days. The left foot appeared colder Tubingen-1, West Germany. and livid. A few days later, the persistent pain Accepted 13 March 1980 in the left leg was intensified by paroxysms. On 489 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.43.6.489 on 1 June 1980. Downloaded from 409 M Stdhr, J Dichgans, and D Dorstelmann D.fm;. ..,~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~.. .. Protected by copyright. <,;..;..X.b .... Fig 1 Swelling and bluish discoloration of the buttock (a); area of black necrotic skin, 11 cm above the pelvic rim and 6 cm laterally of the lumbar spine (b). the fifth day, the intermittently slightly improved slightly weaker on the left side. The skin weakness deteriorated tem- again with one severe perature of the left foot was reduced by 1 °C. paroxysm of pain. In addition, micturition was The showed intermittently oscillogram signs of a compensated disturbed and painful. The patient arterial obstruction. Diagnosis: Ischaemic neu- was not incontinent and defaecation was normal. ropathy of the left lumbosacral plexus with The electromyographic examination revealed electromyographical signs of root involvement. complete denervation of the quadriceps muscle Case 2 a 38 old and (WH, year male): One ampoule partial denervation of the other muscle- Delphimix (600 mg Phenylbutazon-Natrium, 6 groups of the lower left limb, as well as of the 40 paravertebral mg Cinchocain, mg Triamcinolon-diacetat, 1 muscles at the L4/L5 level. The mg Cyanocobalamin) was injected into the left ninhydrine-test indicated a hypohidrosis of the buttock, because of lower back Five to six pain. http://jnnp.bmj.com/ left foot. hours later the patient awoke from sleep because General examination and blood-tests revealed of a numbness in the left Another no signs of diabetes leg. six hours mellitus or general vascular later he experienced severe waxing and waning disease. Myelography was normal. The CSF pro- at the tein pain predominantly anterior aspect of the was increased to 70 mg/dl; further CSF thigh and he was no able to examinations were longer stand. The normal. patient was admitted to the hospital, where a One year later, pain had considerably painful swelling and bluish discoloration of the decreased, but was still present, mainly in the skin were observed at the of upper part the but- on September 27, 2021 by guest. anterior aspect of the thigh, and was aggravated tock. There was a by severe paresis of the flexors walking. Neurological examination revealed and adductors of the hip and of the extensors severe paresis of the extensors of the knee, foot of the as well as marked and toes, knee, hypaesthesia and moderate paresis of the hip flexors and hyperpathia at the were slight paresis of the other anteromedially thigh muscle-groups (includ- found. For several weeks pain was almost totally ing the gluteal muscles). There was moderate resistant to analgesic drugs. Pain disappeared hypaesthesia combined with hyperpathia within in the course the only slowly of the next two years. territories of the femoral, lateral femoral General examination and blood tests were cutaneus and common peroneal nerves. Arterial normal. pulses of the femoral and popliteal arteries were A follow-up examination two years later J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.43.6.489 on 1 June 1980. Downloaded from Ischaemic neurdpathy of the lumbo;acral plexus Jbllowing intragluteal injection 491 revealed slight residual paresis of the above tibialis anterior and soleus muscles. There were mentioned muscle groups as well as marked no signs of denervation in the paraspinal muscles hypaesthesia on the medial aspect of the knee. (L3-L5). General examination, blood tests, CSF Knee-jerk was diminished and adductor reflex and X-rays of the pelvis and the spine were found was absent. The electromyographical investiga- to be normal. Diagnosis: Ischaemic neuropathy tion showed signs of partial denervation of the of the left lumbosacral plexus. iliopsoas, adductor longus and rectus femoris muscles. No abnormalities were found in the Discussion paravertebral muscles (L3 /L4). Diagnosis: Ischaemic neuropathy of the left lumbar plexus. Lesions of the lumbosacral plexus following an Case 3 (BA, a 13 month old male): An injec- intragluteal drug injection cannot be explained tion of penicillin into the left buttock was by a direct mechanism, such as toxic neuropathy followed by a painful local swelling, and a flaccid of the sciatic and gluteal nerves. The damage, paralysis of the left lower limb. The neurological because of its distance from the site of injection, examination 4-5 months later revealed a still suggests the importance of a vascular factor. An complete paresis of the whole leg, except for a inadvertent injection of vasotoxic or crystalline weak residual innervation of the toe-flexors drugs into the inferior gluteal artery, which (fig 2). Deep tendon reflexes were absent in the supplies the proximal segment of the sciatic nerve, left, but were present in the right leg. There was is known occasionally to result in a sciatic nerve no reaction to painful stimuli in the left foot and lesion.8 913 The underlying cause is most likely to lower leg. be either embolic obstruction by crystals14 or a EMG examination and electrical nerve stimu- toxic endarteritis with spasms and thrombosis, lation showed nearly complete denervation of which spread to the epineural and perineural Protected by copyright. the long and short flexors of the toes, as well as blood vessels and cause segmental infarction. complete denervation of the gluteal, quadriceps, Since the skin of the buttock is largely supplied by the same artery, it is not surprising that these particular lesions of the sciatic nerve are invari- ably associated with a painful swelling and a bluish discoloration of the buttock, which is then sometimes followed by gangrene ("embolia cutis medicamentosa").8 10 13 14 A similar mechanism could be responsible for lumbosacral plexus lesions, if a retrograde propa- gation of spasm and thrombosis occurs. Some observations are in favour of such a possibility.
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