following - jnnp.bmj.com · journal of neurology, neurosurgery, and psychiatry, 1980, 43, 489-494...

Journal of Neurology, Neurosurgery, and Psychiatry, 1980, 43, 489-494

Ischaemic neuropathy of the lumbosacral plexusfollowing intragluteal injectionM 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-arterialinjection of vasotoxic drugs into one of the gluteal arteries. Symptoms and follow-up ofthree cases arereported. The neuropathy is attributed to a toxic endarteritis with retrograde propagation of spasmand 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 syndromein fully developed cases and makes possible a correct diagnosis.

The obstruction of a main artery by embolism,thrombosis or following trauma may lead toischaemic neuropathy. The neurological syn-drome, predominantly sensory impairment and(more rarely) paralysis, or in milder cases painand paraesthesia, depends upon the duration ofischaemia and collateral blood supply.1-3 If theischaemia is of short duration a rapid and com-plete recovery of nerve functions will occur inmost cases, but ischaemia of a longer durationcan lead to permanent structural damage.2 4Since the oxygen turn-over of the peripheralnerve is rather low and blood supply is abundant,ischaemic neuropathies will rarely occur if onlyone of the main arteries or only some, but notall of the distal branches of the nerve vesselsare obstructed. However, partial or total seg-mental necrosis of nerves regularly occurs ifmicroembolism, microthrombosis or spasmsobstruct large portions of the epineural and peri-neural plexus.' 5 This mechanism is responsiblefor cases of neuropathies after intra-arterial in-jection of angiotoxic substances, for exampleinto the brachial artery,6 7 the inferior glutealartery8-'0 and the umbilical artery of the new-born."' 12An inadvertent injection of vasotoxic drugs

into one of the gluteal arteries may also resultin a toxic angiopathy with ischaemic damageof the sciatic or gluteal nerves. With the retro-

Address for reprint requests: Manfred Stohr, MD Lieber-meisterstr 18-20, Neurologische Universititsklinik, D-7400Tubingen-1, West Germany.

Accepted 13 March 1980

grade propagation of angiospasms and throm-bosis, the homolateral lumbosacral plexus cansuffer ischaemic damage, as observed in threecases.

CASE REPORTSCase I (BF, a 42 year old male): an injectionof about 45 ml Ultrademoplas (500 mg Phenyl-butazon-Natrium, 500 mg Aminophenazon, 45 mgLidocain-HCl, 4-5 mg Dexamethason, 9 mgPrednisolon and 2-8 mg Cyanocobalamin) wasgiven into the left buttock because of lower-back pain. Immediately a severe local pain wasfelt, lasting for about 30 s. Ten to fifteen minuteslater, the patient noticed numbness in the leftfoot which crept gradually upwards. Half anhour after the injection, standing and walkingwere no longer possible because of a severepain as well as a weakness in the left lowerlimb. The neurological examination revealed anearly complete paralysis of the left leg, includ-ing the hip-flexors and the gluteal muscles; deeptendon reflexes were absent. There was severesensory impairment in the territories of thefemoral, lateral femoral cutaneous and commonperoneal nerves, with less marked sensory dis-turbances in the other areas of the left lowerlimb. There was painful swelling and bluish dis-coloration of the left buttock. Additional swell-ing at the left paravertebral region above thepelvis ("Embolia cutis medicamentosa," fig 1)occurred and was followed by a deep gangrenewithin a few days. The left foot appeared colderand livid. A few days later, the persistent painin the left leg was intensified by paroxysms. On

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M Stdhr, J Dichgans, and D Dorstelmann

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<,;..;..X.b ....Fig 1 Swelling and bluish discoloration of the buttock (a); area of black necrotic skin, 11 cm above thepelvic rim and 6 cm laterally of the lumbar spine (b).

the fifth day, the intermittently slightly improvedweakness deteriorated again with one severeparoxysm of pain. In addition, micturition wasintermittently disturbed and painful. The patientwas not incontinent and defaecation was normal.The electromyographic examination revealedcomplete denervation of the quadriceps muscleand partial denervation of the other muscle-groups of the lower left limb, as well as of theparavertebral muscles at the L4/L5 level. Theninhydrine-test indicated a hypohidrosis of theleft foot.General examination and blood-tests revealed

no signs of diabetes mellitus or general vasculardisease. Myelography was normal. The CSF pro-tein was increased to 70 mg/dl; further CSFexaminations were normal.One year later, pain had considerably

decreased, but was still present, mainly in theanterior aspect of the thigh, and was aggravatedby walking. Neurological examination revealedsevere paresis of the extensors of the knee, footand toes, moderate paresis of the hip flexors andslight paresis of the other muscle-groups (includ-ing the gluteal muscles). There was moderatehypaesthesia combined with hyperpathia withinthe territories of the femoral, lateral femoralcutaneus and common peroneal nerves. Arterialpulses of the femoral and popliteal arteries were

slightly weaker on the left side. The skin tem-perature of the left foot was reduced by 1 °C.The oscillogram showed signs of a compensatedarterial obstruction. Diagnosis: Ischaemic neu-ropathy of the left lumbosacral plexus withelectromyographical signs of root involvement.Case 2 (WH, a 38 year old male): One ampouleDelphimix (600 mg Phenylbutazon-Natrium, 6mg Cinchocain, 40 mg Triamcinolon-diacetat, 1mg Cyanocobalamin) was injected into the leftbuttock, because of lower back pain. Five to sixhours later the patient awoke from sleep becauseof a numbness in the left leg. Another six hourslater he experienced severe waxing and waningpain predominantly at the anterior aspect of thethigh and he was no longer able to stand. Thepatient was admitted to the hospital, where apainful swelling and bluish discoloration of theskin were observed at the upper part of the but-tock. There was a severe paresis of the flexorsand adductors of the hip and of the extensorsof the knee, as well as marked hypaesthesia andhyperpathia anteromedially at the thigh werefound. For several weeks pain was almost totallyresistant to analgesic drugs. Pain disappearedonly slowly in the course of the next two years.General examination and blood tests werenormal.A follow-up examination two years later

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Ischaemic neurdpathy of the lumbo;acral plexus Jbllowing intragluteal injection

revealed slight residual paresis of the abovementioned muscle groups as well as markedhypaesthesia on the medial aspect of the knee.Knee-jerk was diminished and adductor reflexwas absent. The electromyographical investiga-tion showed signs of partial denervation of theiliopsoas, adductor longus and rectus femorismuscles. No abnormalities were found in theparavertebral muscles (L3 /L4). Diagnosis:Ischaemic neuropathy of the left lumbar plexus.Case 3 (BA, a 13 month old male): An injec-tion of penicillin into the left buttock wasfollowed by a painful local swelling, and a flaccidparalysis of the left lower limb. The neurologicalexamination 4-5 months later revealed a stillcomplete paresis of the whole leg, except for aweak residual innervation of the toe-flexors(fig 2). Deep tendon reflexes were absent in theleft, but were present in the right leg. There wasno reaction to painful stimuli in the left foot andlower leg.EMG examination and electrical nerve stimu-

lation showed nearly complete denervation ofthe long and short flexors of the toes, as well ascomplete denervation of the gluteal, quadriceps,

}....{. ~~~~~~~~~~~~~~~~~~..........

Fig 2 Case 3, 4 5 months after the injection.Nearly complete paresis of the left lower limb.

tibialis anterior and soleus muscles. There wereno signs of denervation in the paraspinal muscles(L3-L5). General examination, blood tests, CSFand X-rays of the pelvis and the spine were foundto be normal. Diagnosis: Ischaemic neuropathyof the left lumbosacral plexus.

Discussion

Lesions of the lumbosacral plexus following anintragluteal drug injection cannot be explainedby a direct mechanism, such as toxic neuropathyof the sciatic and gluteal nerves. The damage,because of its distance from the site of injection,suggests the importance of a vascular factor. Aninadvertent injection of vasotoxic or crystallinedrugs into the inferior gluteal artery, whichsupplies the proximal segment of the sciatic nerve,is known occasionally to result in a sciatic nervelesion.8 913 The underlying cause is most likely tobe either embolic obstruction by crystals14 or atoxic endarteritis with spasms and thrombosis,which spread to the epineural and perineuralblood vessels and cause segmental infarction.

Since the skin of the buttock is largely suppliedby the same artery, it is not surprising that theseparticular lesions of the sciatic nerve are invari-ably associated with a painful swelling and abluish discoloration of the buttock, which is thensometimes followed by gangrene ("embolia cutismedicamentosa").8 10 13 14A similar mechanism could be responsible for

lumbosacral plexus lesions, if a retrograde propa-gation of spasm and thrombosis occurs. Someobservations are in favour of such a possibility.Homolateral gangrene of rectum, bladder, penis,scrotum and vagina have been described followingan intragluteal injection8 13 15 and suggest a circu-latory disturbance within the distribution of theinternal iliac artery as their possible cause. Pro-vided that a still more extensive retrogradepropagation of the toxic angiopathy occurs, theexternal iliac artery may be occluded in addition,with subsequent ischaemia of the lower limb.'6 17Since the lumbosacral plexus receives its bloodsupply from branches of the iliac arteries (fig 3)it is reasonable to assume that lumbosacral plexuslesions may be another consequence of such awide-spread toxic angiopathy. In one of our cases(BF) a deep gangrene of the skin above the pelvis(fig 1) developed within the distribution of thefourth lumbar artery. This artery anastomiseswith the iliolumbal artery. The circulatory dis-turbance even in this proximal branch of theinternal iliac artery suggests a widespread retro-grade propagation of the toxic angiopathy.

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Fig 3 Blood supply of the lumbosacral plexus bybranches of the iliac arteries. (From St6hr, M.:latrogene Nervenliasionen. G. Thieme, Stuttgart,1980.)

Some cases reported earlier in the literaturemay be explained by the assumption of the samemechanism. A flaccid monoplegia of the ipsi-lateral lower limb after an intragluteal injectionwas first described by Dereux and Ernst,'8 a sixyear old child. Vasilescu and Stamatoiul' reportedfour cases of "femoral nerve palsy." In one casethe femoral nerve palsy was combined with an

M Stohr, J Dichgans, and D Ddrstelmann

obturator nerve palsy. Paresis invariably followedan injection into the ipsilateral buttock and wasaccompanied by immediate severe pain, discolora-tion of the buttock and a circulatory disturbancein the leg.

Regarding the distribution of the neurologicalsigns in these and our own cases we can differen-tiate three patterns of plexus damage, involving(1) the lumbar plexus or its femoral branch, or(2) the lumbar and sacral plexus, or (3) the lumbo-sacral plexus including some lumbosacral nerveroots (table). In very rare instances, the toxicangiopathy following an intraarterial injection ingluteal arteries can spread to the aortic bifurca-tion and result in a flaccid paraplegia.'9 20

Table Various neurological syndromes following aninadvertent drug injection into one of the glutealarteries

Distribution of Involved nervous Neurological Authorthe toxic structure syndronmeangiopathy

Inferior gluteal Sciatic nerve Sciatic or Gammel (1928)artery peroneal nerve Kimberley (1937)

palsy Duperrat et al(1952)

Ipsilateral iliac (a) Lumbar Femoral-, or Vasilescu andarteries plexus femoral and Stamatoiu (1965)

obturator nerve Stohr et alpalsies (Case 2)

(b) Lumbar Flaccid Dereux andand sacral paralysis of the Ernst (1951)plexus ipsilateral leg Stohr et al

(Case 3)(c) Lumbosacral Flaccid Stohr et alplexus with root paralysis of the (Case I)involvement ipsilateral leg

Aortic Spinal cord Flaccid Heckenrothbifurcation paraplegia (1955)

Merling (1959)

The ischaemic plexopathies following intra-arterial injection in gluteal arteries exhibit strikingsimilarities with a syndrome in newborns, whichresults from an injection of vasotoxic drugs intothe umbilical artery. The umbilical artery is abranch of the internal iliac artery, as are thegluteal arteries (fig 3). In this case the injectionmay result in a discoloration and sometimes gan-grene of the buttock and in a sciatic nerve palsy.Occasionally a femoral nerve palsy and agangrene of intrapelvic structures are asso-ciated." 12 21 22 As in lumbosacral plexopathiesfollowing an intragluteal injection, the develop-ment of the neurological signs may be delayedin newborns.2' 24 There is, however, one strikingdifference in the pattern of nerve damage follow-ing intragluteal and intraumbilical injections.When there is a drug injection into the umbilicalartery of the newborn, there is a predominantinvolvement of the sciatic nerve. This is probably



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Ischaemic neuropathy of the lumbosacral plexus following intragluteal injection

due to the greater functional importance of theinferior gluteal artery at this age. Plexus lesionsfollowing an injection into the buttock howevercase lesions of the lumbosacrel plexus, especiallyconcerning its femoral nerve portion.'6 The samepattern has frequently been observed in post-operative plexus-lesions, where the stretching ofnerves and nerve vessels appears to be the mostdamaging factor.26 The possibility of successfultherapy of vascular occlusion due to intra-arterialinjection is greater when quickly diagnosed.Intra-arterial injection may be suspected if thepatient immediately complains about severe localpain and may be ascertained by aspiration ofarterial blood before retracting the needle. In thissituation, 5 to 10 ml of Procaine 1% (withoutSuprarenin) and antispasmodic drugs such asPapaverine (40-80 mg in 10-20 ml isotonic salinesolution) may prevent the arterial spasms.7 27 Inorder to secure the retrograde propagation ofthese drugs the pressure of injection should behigh. Most frequently the correct diagnosis willnot be reached before the retraction of the needle.In these cases Papaverin should be given intra-venously. In addition, antithrombotic therapywith heparin and sympathetic blockade arerecommended.

Intra-arterial injection into one of the glutealarteries is more likely and if it happens morehazardous if the injection is performed on themedial aspect of the buttock, near the exit of thegluteal arteries from the pelvis. Therefore aninjection into the upper and outer part of thebuttock is recommended not only to prevent adirect sciatic nerve lesion, but also to diminishthe possibility of an intra-arterial injection. More-over, an aspiration test is mandatory prior toevery injection into the buttock. Lumbosacralplexus lesions following an injection into thebuttock within a few hours are a rather typicalsyndrome which can hardly be confused with anyother syndrome. A coincidence of intraglutealinjection and lumbosacral plexus lesion withoutcausal relation seems already very unlikely,especially unlikely when the rarity of the non-traumatic plexus lesions is considered. Moreover,there should be some evidence for another cause,which occasionally leads to an acute plexopathy,like diabetes mellitus, viral infections, haemo-philia or anticoagulation therapy. Other signs ofa widespread toxic angiopathy such as painfulswelling and discoloration of the buttock, ipsi-lateral gangrene of intrapelvic structures andischaemia of the lower limb support an ischaemicplexus-lesion following an intra-arterial druginjection.

References

1 Roberts JT. The effect of occlusive arterialdiseases of the extremities on the blood supplyof nerves. Experimental and clinical studies onthe role of the vasa nervorum. A mer Heart J1948; 35:369-92.

2 Richards RL. Ischaemic lesions of peripheralnerves: A review. J Neurol Neurosurg Psychiat1951; 14:76-87.

3 Schrader EA. Die Klinik der arteriellen Throm-bosen im Beckenbereich. Springer: Berlin, 1955.

4 Haimovici H. Peripheral arterial embolism: astudy of 330 unselected cases of embolism ofthe extremities. Angiology 1950; 1:20-45.

5 Asbury AK. Ischemic disorders of peripheralnerve. In: Vinken PJ, Bruyn GW (eds). Hand-book of clinical neurology 1970; vol. 8,2. NorthHolland Publ. Co. Amsterdam.

6 Cohen SM. Accidental intra-arterial injectionof drugs. Lancet 1948; 255/2:409-17.

7 Chase RA. Surgery of the hand. New Eng JMed 1972; 287:1227-34.

8 Gammel JA. Local accidents following the intra-muscular administration of salts of the heavymetals: Report of two cases of embolia cutismedicamentosa. Arch Derm 1928; 18:210-223.

9 Duperrat B, Behaque P, Koff. Dermite livedoidede Nicolau, nevralgie sciatique et ischemie dumembre inferieur apres une injection fessiere debismuth huileux. Sem Hop 1952; 28:660-1.

10 Santler R, Ebner H, Mischer P. Embolia cutismedicamentosa. Hautarzt 1972; 23:530-4.

11 Mills WG. A new neonatal syndrome. Brit MedJ 1949; 2:464-6.

12 Hudson FP, McCandless A, O'Malley AG.Sciatic paralysis in newborn infants. Brit Med J1950; 1:223-5.

13 Kimberley LW. Accidental intra-arterial injectionof bismuth by X-ray in the arterioles of thepenis. Amer J Syph 1937; 22:364-7.

14 Freudenthal W. Lokales embolisches Bismogenol-Exanthem. Arch Derm Syph 1924; 147:155-60.

15 Hochstetter A. Ober Probleme und Technik derintra-glutaalen Injektion. Schweiz Med Wschr1955; 85:1138-44.

16 Vasilescu N, Stamatoiu J. Le syndrome livedoido-paralytique. Presse Med 1965; 73:1685-8.

17 Deutsch J. Schwere lokale Reaktion nachBenzathin-Penicillin. Deutsch Gesundh 1966; 2:2433-7.

18 Dereux J, Ernst J. Monoplegie flasque dumembre inferieur gauche apparue brusquementapres une injection intra-fessiere d'un produitarsenical. Rev Neurol 1951; 84:335-7.

19 Heckenroth J. Les paraplegies consecutives auxinjections intra-musculaires fessieres. These,Marseille 1955.

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21 Shaw NE. Neonatal sciatic palsy from injectioninto the umbilical cord. J Bone Joint Surg 1960;42 B:736-41.

22 Heyer R, Giffels G. Ober die Gefahren beiInjektionen in die Nabelarterie des asphyktischenNeugeborenen. Archiv Kinderheilk 1971; 183:43-50.

23 Fahrni WH. Neonatal sciatic palsy. J Bone JointSurg 1950; 32 B:42-9.

24 San Agustin, Nitowsky HM, Borden JN. Neo-natal sciatic palsy after umbilical vessel injection.

M Stohr, J Dichgans, and D DorstelmannJ Pediat 1962; 60:408-13.

25 Biemond A. Femoral neuropathy. Vinken PJ,Bruyn GW, eds. In: Handbook of clinical neur-ology. Volume 8,2. North Holland PublishingCo., Amsterdam 1970.

26 Stohr M. Traumatic and postoperative lesions ofthe lumbosacral plexus. Arch Neurol 1978; 35:757-60.

27 Goethlin J, Olin T. Traumatic arterial spasm.An angiographic study in rabbits. Acta Radiol1970; 10:257-70.



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