PARAPLEGIA AND INTRACRANIAL HYPERTENSION FOLLOWING EPIDURAL ANESTHESIA

REPORT OF FOUR CASES

FREDERICO A . D . K L I E M A N N

There are, now, many reported cases of irreversible neurologic syndrome caused by spinal (subarachnoid) anesthesia Vd> 2 ,> 2 2 - 2 5 > ; i 2 and some about the perhaps less frequent complications of epidural anesthesia 3- i> 5 . 2 S .

A very complete revision of 32 verified cases of arachnoiditis post spinal anesthesia was made by Schwartz and B e v i l a c q u a 2 5 . Neurologic complica­tions were present in 17 of 11.574 spinal anesthesia 1 9 in 84 cases of 1 0 . 4 4 0 2 3

and in 37 of 10.098 anesthesias 7 in three different series, but only the last two series of patients were followed up. Severe, irreversible situations, ho­wever, are much less frequent and occurred in no patient of these three series.

Hel lmann 1 0 reports no neurologic complication in 26 .127 cases of epidural anesthesia in his obstetrical series, and two cases of severe neurological complications in his surgical series; again, follow-up of patients is not spe­cified. Bonica et a l . 2 describe one case of serious neurologic complication among 3.637 peridural blocks.

Even in more recent papers, the pathogenesis of neurologic sequellae of both epidural and subarachnoid anesthesias is discussed and not c l e a r 2 7 .

Chemical contaminants were experimentally shown 1 2 to be able to produce severe arachnoiditis and clinical paraplegia in monkeys and could be the causal agent in some clinical situations. Increased concentration of the anes­thetic agent was also demonstrated to produce, in experimental animals, neurologic syndromes similar to the observed in clinical situations 1 6 > 1 7 . Treat­ment of neurologic sequellae is usually unsuccessful and most cases are irreversible.

F r o m t h e D e p a r t m e n t or I n t e r n a l Medicine. Divis ion of Neuro logy , F a c u l t y of Medic ine of P o r t o Alegre , F e d e r a l Un ive r s i ty of Rio G r a n d e do Sul, a n d I n s t i t u t o de N e u r o c i r u r g i a , P o r t o Alegre , Bras i l .

Acknowledgments — T h e a u t h o r wishes to exp re s s h i s t a n k s to Dr. Fe l i zbe r to F e r r e i r a for h i s s u p p o r t a n d e n c o u r a g e m e n t a n d to t h e anes thes io log i s t s whose k ind a n d prec ise i n f o r m a t i o n s w e r e of g r e a t v a l u e .

During the last four years, six patients with severe neurologic disabilities following epidural anesthesia were seen at the Institute of Neurosurgery, Porto Alegre. The present report concerns four of these patients in whom good information was obtained about the anesthetic procedure and close observation about evolution was possible.

REPORT OF FOUR CASES

CASE 1 — F.Z. , white , male, age 63, w a s in good hea l th unti l July 24, 1970, when operated on for inguinal hernia, under epidural anesthesia. He w a s pre-medieated wi th Val ium 10 m g and put in the left lateral position. Puncture w a s made in L2-L3, by the resident, under supervision of the anesthesiologist , wi th T-16 needle. Ascerta inment of epidural space w a s reported to be difficult, but no arachnoid perforation w a s reported. Epidural tray was cleaned in water and autoclaved. The anesthet ic agent w a s Lidocaine 2%, 400 mg, wi th adrenaline, 1:160.000. The operation w a s uneventful and no hypotension occurred during surgery. Immediate ly after surgery, the pat ient felt tired and slept, just to awake, 2 or 3 hours later, w i t h very severe pains in both legs. He required several analgesic injections during the next 10 hours and nex t morning he complained of numbness in both legs and chiefly in saddle area, retention of urine, constipa­tion and weakness in both lower limbs.

At this time, neurologic examinat ion showed reduction of all kinds of sensation from L3 to L5 and anest thes ia from L5 down to S5, bi lateral ly absent ankle jerks, extensor plantar responses; motor s trength w a s reduced in extensors of toes and feet and external rotation of feet. No fasciculat ions and no pains. Lumbar puncture revealed colourless fluid under normal pressure, containing 120 cel ls per ml, and 300 m g of protein per 100 ml. Bacteriologic examinat ion w a s ne­gat ive . On the assumption this was an aseptic spinal cord inf lammation secondary to epidural anesthesia, oral corticoid treatment w a s started wi th Decadron 12 m g a day, progressively reducing dose until December 1970. In August , 7, 1970, cerebrospinal fluid (CSF) examinat ion showed: protein 149 m g per 100 CU. MM., 15 cells per ml, increased a lbumin/g lobul in relat ion in Cellogel proteinogram. The patient's s i tuat ion improved s lowly during the next four months: on the begin­ning of September the urethral catheter could be taken off and he w a s able to pass urine w i t h some difficulty, by abdominal compression. His gai t improved and he w a s able to drive his car. Sensation w a s normal to pinprick to L5, and reduced from L5 to S5. Vibration w a s reduced at the ankles and proprioception showed some errors at the toes.

In December, 1970, CSF contained 5 cel ls per CU. MM. and 120 m g procein per 100 ml. CSF culture w a s negat ive , E.S.R. 8, normal hemogram and serum proteinogram; irrelevant lumbar and sacral spine X-Ray. Urine infection w a s pre­sent since August and not yet cured. As his s i tuation w a s stat ionary the patient decided to see another neurologist, by w h o m Pantopaque myelography was indicated and done, and later said to have shown "cord atrophy".

Comment: acute lumbo-sacral myelopathy wi th inf lamatory findings in CSF, occurring immediate ly after epidural anesthesia . Part ial improvement during next four months.

CASE 2 — M . B . R . , 27 years old, whi te female, w a s in good hea l th unti l September 1970 w h e n she had epidural anesthes ia for her second vag ina l delivery. Pregnancy w a s normal. Puncture made by anesthesiologist , in lateral position, L3-4, first tap, 10-T needle, epidural space ascertained by Dogl iott i technique. During puncture, pat ient reported sensat ion "like shock in the whole spine", but

no blood or CSF came. Epidural tray prepared by autoc lavat ion , including Li-docaine. Syringes and needles previously washed and cleaned wi th detergent and then washed in water. Lidocaine 1.5%, 300 mg, wi th adrenaline 1:320.000 injected in 5 minutes . Immediate ly on being turned to supine position, patient w a s unable to move legs and trunk, and felt numbness up to upper limbs. She also reported difficulty in swal lowing and got extremel ly anxious. Blood pressure 90 x 60, no respiratory depression. Three to four hours after anesthesia, she complained of pricking and t ingl ing sensations, from head down to lower limbs, immediate ly followed by very intense pains in both legs and trunk, during the next 6 hours.

Some days later her legs seemed to be weak and she fell frequently. By November, she started noticing numbness in her feet, which increased very slowly during the next four months. In February, 1971, she had ankle c lonus and difficulty in pass ing urine.

She w a s first seen in March, 10, 1971. Neurologic examinat ion showed: marked reduction in f lexion and extension of the toes and internal rotation of the feet. Sl ight reduction of external rotation and dorsal f lexion of both feet. Bilateral extensor plantar responses and ankle clonus and + + + symmetrical knee jerks. Upper superficial abdominal ref lexes present and lower abdominals absent. Pin­prick sensat ion markedly reduced from T10 to L4 but spared in L5 and perineum. Vibration reduced in both knees and ankles and proprioception absent in the toes.

The situation was indicative of a myelopathy wi th upper level in T10, but sparing of pain sensation from L5 drown suggested a central cord lesion, possibly related to anterior spinal artery obstruction. A lumbar puncture w a s performed but no fluid obtained. A myelography wi th posit ive contrast w a s done by sub­occipital route and showed a partial stop in T9 and complete stop in T10. Sub­occipital CSF w a s normal. Chiefly in v iew of the posibility of a preexist ing central cord tumor, a laminectomy w a s performed in March, 1971, and disclosed an intense proliferative arachnoiditis, containing some whit ish cysts of fluid; cord w a s narrowed, pale, and completely impossible to be liberated from the arachnoid. Both cord and roots were enmeshed by a thick, fibrous tissue. After surgery, patient's neurologic s i tuat ion continued to deteriorate, s lowly but progressively. She w a s g iven oral Prednisone, s tart ing w i t h 60 m g a day and reduced s lowly to 10 m g in June.

In August 1971, she w a s taken to Boston (U.S.A.) and seen at the Mass. Seneral Hospital . At this t ime she presented a complete spastic paraplegl ia wi th bilateral ankle and knee clonus, extensor plants and paralysis from the lower abdominals down; sensory anesthes ia wi th level in T10 for al l modalit ies of sen­sation. She w a s still able to control bladder and bowels . Suboccipital fluid showed normal chemical and cytologic examinat ions . In v i ew of the progressively wor­sening situation, methyl prednisolone acetate (Depo-Medrol) 40 mg, w a s injected at the suboccipital level in August 27, 30 and September 3. At that date, only 1 cc of faintly turbid CSF could be aspirated and there w a s a question of loculation wi th adhesions at that point. It w a s felt that further inst i l lat ions of Depo-Medrol were not l ikely to be of value .

After complet ing paraplegia with sensory and motor leve l in T10 the pa­tient's s i tuat ion stabilized and is much the same after 2 and 1/2 years. She is stil l able to control urine. She developed urinary infection, controlled with diffi­culty during last year.

Comment: s lowly progressive thoraco- lumbar arachnoidit is and consequent mye-lomalat ia , w i th level in T10, stabilized after complete paraplegia; insidiously de-velopped after epidural anesthes ia in which probable total spinal anesthesia occurred.

CASE 3 — L.M.M. , 25 years old, white female, w a s in perfect hea l th unti l December 1972, w h e n received epidural anesthes ia for cesarean delivery. This w a s uneventful . Premedicated with Val ium 10 mg. Puncture in L3-L4, wi th number 10 Crawford needle. Pat ient seated. Identif ication of epidural space by loss of resistance. No back flow of fluid when needle turned to the four angles . Epidural tray prepared by autoc lavat ion; syringes and needles previously washed wi th de­tergent and then wi th water. Lidocaine 2%, 360 mg, wi th adrenaline 1:160.000, w a s s lowly injected. On being turned to supine position, pat ient reported numbness in both lower limbs. A s hypotension w a s observed, she w-as put in Trendelemburg position and treated wi th Metaraminol and oxygen. A few hours after cesarean, she had intense pains in both legs and low back, which al leviated only after the third analges ic injection.

She w a s wel l for about thirty days, when she started feeling pins and needles, and then numbness in both feet, which gradual ly involved her legs and thighs. In beginning of March she started w i t h daily, intense headaches, accompanied by sweat ing and dizziness. At about the same t ime she noticed gait disturbances and loss of power in both lower limbs. No bowel or bladder disturbance. For 10 days before admission, headache episodes were also accompanied by transitory bilateral blindness last ing 1 to 3 minutes .

She was admited to the Department of Internal Medicine, Hospital de Cli­nicas, Porto Alegre, on March, 27, 1973. She had no systemic complaints or disturbances; we ight 73 kg. Neurologic examinat ion: slow, horizontal nys tagmus to both directions; isochoric pupils react ing normally. Hypoesthesia for pain and temperature in the region of the right maxi l lary nerve. Power markedly reduced in both lower limbs, chiefly on the right, where there w a s complete paralysis of extension of toes and foot and of external rotat ion of the foot; loss of power w a s less marked in the same groups on the left; f lexion of both legs and th ighs w a s bi lateral ly reduced whereas extension w a s normal. Sensation w a s reduced for touch and pain from T4, and absent from T6 down; vibration absent from T4. Deep ref lexes in the upper and lower l imbs + + + bilaterally; extensor plantar reflexes bilaterally. Intense bilateral papi loedema w a s present.

Evidently, this w a s a gradual ly progressing myelopathy, w i th a more severe lesion in T4. The history m a d e clear tha t it w a s an ascending lesion, and she had signs of invo lvement of intracranial s tructures and intracranial hypertension as wel l . The s i tuat ion w a s very sugges t ive ly related to epidural anesthes ia and ascending arachnoidit is w a s an obvious diagnosis . Lumbar puncture w a s performed but no fluid obtained. Cysternal puncture w a s then made, w i th pat ient in seated position, and clear, colourless fluid showed normal cytological and chemical findings. Other laboratory examinat ions : hemogram, E.S.R., serum proteinogram, were normal. V.D.R.L. and tuberculin test negat ive .

The decision w a s taken to g ive her both oral and intra-thecal steroids. Oral Prednisone w a s started wi th 60 m g a day, and 40 m g of methyl-prednisolone ace ta te injected suboccipital on the third day in Hospital . Headache stopped imme­diately after the first injection, and so the episodes of transitory blindness; the nystagmus, and p a p i l l e d e m a were absent by the end of the first week, but there w a s no change in the motor and sensory findigs. By the end of the second week, headache and transitory blindness reappeared and a second injection w a s made of 40 m g methyl-prednisolone: the symptoms cleraed now for only three days. A third injection w a s made but useless . Her s i tuat ion deteriorated rapidly during the fourth week and in April 23 she w a s transferred to the Neurosurgery Inst i tute . At this t ime she presented a complete paraplegia wi th sensory level in T5 and bilateral p a p i l l e d e m a wi th mult iple hemorrhages in both dysks and retinas. Epi­sodes of bi lateral blindness recurred several t imes a day, last ing somet imes for more than 5 minutes; fundi examinat ion showed no additional abnormality in

these occasions. A carotid angiography w a s done and showed symmetrical hy­drocephalus.

A ventriculo-peritoneal shunt w a s placed in April 27, with a medium pressure Raimondi catheter, coupled to a Portnoy ventricular catheter. Headache disappeared the same day and she had no more episodes of blindness so far. Ophtalmoscopic examinat ion in May 16, showed "almost complete reabsorption of retinal haemorrha­ges and marked reduction o£ protrusion of the dysks". Normal fundi in June 6.

In May 5, she started wi th movements in left foot; intensive physiotherapy w a s started after ventriculo-peritoneal shunt was placed. By Augus t 4, she had f lexion and extension of both legs and thighs. In October 19 she w a s able to walk wi th Canadian canes and long braces in both lower limbs, and in December 26 she w a s able to walk 10 steps wi thout canes and braces. Motor power, by this time, w a s only reduced bi lateral ly in extension of the toes and in dorsal f lexion and external rotation of the feet. Vibration w a s felt normal ly in both legs, but pain sensation was stil l reduced, a l though present, from T6 down. Ankle clonus w a s now absent. She stopped oral Prednisone in October. In April 23, 1974, pat ient is wa lk ing alone, wi thout canes, and motor power 3s practical ly normal.

Comment: s lowly progressive ascending myelopathy wi th chief level in T4; increased intracranial pressure and episodes of transitory blindness. Ascending spinal and intracranial arachnoidit is s tart ing one month after "epidural anesthesia". Short las t ing improvement after intra-cysternal methyl-prednisolone injection, fol lo­wed by deterioration unti l complete paraplegia and bilateral choked dysks wi th hemorrhagic foci. Immediate disappearance of intracranial hypertension and epi­sodes of transitory blindness after ventriculo-peritoneal shunt. Steady, marked progressive recovery from paraplegia during next 12 months after ventriculo-pe­ritoneal shunt.

CASE 4 — H.M.M. , 25 years old, whi te female, w a s in perfect hea l th unti l October 21, 1973, when received epidural anesthes ia for vag ina l delivery. This w a s her first pregnancy and first experience wi th epidural anesthesia . Del ivery w a s uneventful . Puncture w a s done in L3-L4 interspace, w i th a T-16 needle, by a midline approach. Epidural space has been located after one attempt, and confirmed by Gutierrez method. Xylocaine 1.2% wi th adrenaline 1:200.000 20 ml has been injected, after nega t ive aspiration for fluid. About 8 min. later the patient was markedly dyspneic and felt lower l imbs paresthesias . She received oxygen, there w a s no need for vasopressors and the del ivery w a s uneventful w i th a newborn in exce l lent conditions.

Less than one hour after delivery, pat ient started fee l ing pins and needles in both lower limbs, and then very intense pains irradiating from the pelvic girdle to lower l imbs. The pains were only al leviated by the third injection of Propoxiphene, about 8 hours after delivery. Influenced by the knowledge of other cases, the anesthesiologist decided to cal l a neurologist at th is t ime. Fourteen hours after epidural injection, the pat ient w a s well and neurologic examinat ion w a s normal, showing not even meningea l signs. Lumbar puncture showed a faintly turbid fluid under normal pressure.

In v i ew of the turbid aspect of the fluid, this w a s a l lowed to drop unti l 75 ml were taken out, stopped by patient's headache; 40 m g of methyl-prednisolone were dissolved in 10 additional ml of fluid and reinjected slowly.

N e x t s ix days she w a s submitted to 5 lumbar punctures, unti l normal fluid w a s obtained. Apart from transitory hypotension headache during punctures, pa­t ient w a s wel l and had no symptoms. Two additional injections of Depo-Medrol were done during this week (Table 1) .

The pat ient w a s sent home in October 29 and w a s wel l unt i l November 27, when started wi th headache, chiefly occipital, somet imes accompanied by dizziness. Neurologic examinat ion w a s normal and so were ocular fundi. Two days later, headache was strong and incipient bi lateral p a p i l l e d e m a was seen. Lumbar punc­ture showed clear fluid under pressure of 30 cm water . Methyl-prednisolone was again injected two times, 40 m g each, unti l normal fluid came. Both headache and p a p i l l e d e m a cleared immediately. She w a s kept under oral Dexamethasone 4.5 mg a day, unti l December 21, w h e n she stopped Decadron.

She w a s admitted to our Service as an urgency, on December 29, after being treated at home, by another physician, for some days. During this time, headache reappeared and w a s then accompanied by vomiting, lassitude, numbness and weakness in both legs, trunk, and, in rapid progression, urinary retention, paraple­gia, tremors in both hands, diplopia, respiratory difficulty and clouding of cons­ciousness. On examinat ion, she had bilateral s ixth nerve and unilateral right, complete third nerve paralysis, wi th mydriasis and ptosis; clouded consciousness, diaphragmatic breathing and complete flacid paraplegia wi th sensory level probably in T2. Severe bilateral p a p i l l e d e m a wi th numerous, large, hemorrhagic foci.

A ventriculo-peritoneal shunt w a s urgent ly placed, the same day, wi th medium pressure Raimondi catheter coupled to a Portnoy ventricular catheter.

From next day she had no more headache and w a s in perfect s tate of cons­ciousness. P a p i l l e d e m a disappeared during next two weeks. In January 28, ocular movements and pupils were normal, and she w a s able to feel pinprick down to L2 and to localize tact i le st imuli in both legs and feet. In February 23 she had flexion and extension of both feet and toes, but proximal muscles of lower limbs were still paralysed. In April 20, power was s l ightly reduced in flexion and extension of both feet, and moderately reduced in flexion and extension of both legs. Sensation was normal. In Sept. 13, patient wa lks alone, wi thout canes.

Comment: acute aseptic meningit is immediate ly fol lowing "epidural anesthesia". Treatment wi th repeated lumbar punctures and intra-thecal injections of Me­thyl-prednisolone acetate unti l normal fluid obtained. Increased intracranial pressu­re, one month later, normalized after a second series of lumbar punctures and intra-thecal Methyl-prednisolone. Acute increased intracranial pressure, oculomotor disturbances and complete paraplegia in T2 one month later. Complete norma­lization of intracranial pressure and partial recovery of paraplegia after ven­triculo-peritoneal shunt.

DISCUSSION

In probably three of our patients (cases 2, 3 4) the high level of anesthesia obtained is indicative of spinal (subarachnoid) anes thes ia 2 . The rapid onset of neuromuscular weakness and sensory level to a very high dermatome could be interpreted as possible misplacement of the anesthetic solution into the subdural s p a c e 2 6 . This could not be excluded as no fluid was obtained in these instances, but would be hard to demonstrate.

The immediate neurologic deficit in case 1 is suggestive of radicular — cauda equina — lesion, but the presence of unequivocal extensor plantar responses made it clear that a cord lesion was also present, in L3.

Ischaemic lesions of the cord are a likely cause of some of the neurologic problems occurring after epidural anesthesia. In some cases 5 . 2 8 it is sugges-

ted that the combined vasoconstrictive effect of the adrenaline and the hypotension produced by the epidural blockade, by occluding the radicular vessels to the spinal cord, are sufficient to deprive the cord of an adequate blood supply. Cord ischaemia is certainly involved in many other cases and possibly in most cases of myelopathy secondary to spinal (subarachnoid) anesthesia. Vascular changes in radicular and anterior spinal artery were present in most cases whose pathologic material was reported 2 5 . Intrathecal adrenaline was demonstrated to cause paraplegia in dogs, but in doses corres­ponding to 2,5 m g per k g 4 . It is possible that the immediate myelopathy observed in case 1 was caused by cord ischaemia. A vascular — anterior spinal artery — syndrome, was also present in our case 2.

CSF cytology was normal in the case reported by U r q u h a r t - H a y 2 8 and not reported in the patients of Davies and S o l o m o n 5 , Braham and S a i a 3

and Bonica et a l . 2 . CSF examination in our cases 1 and 4 (the two who were examined in the first 24 hours after epidural anesthesia) are cha­racteristic of an acute inflammatory reaction, a chemical meningitis.

Many of the reported cases of arachnoiditis post spinal (subarachnoid) anesthesia are atributed to the presence of contaminants in the spinal anes­thetics 1 8 - 2 2 > 3 0 . Contaminants were p r o v e d 1 2 to be able to cause severe arachnoiditis in experimental monkeys and the lesions and conditions of anes­thesia were very similar to those in human cases pathologically studied.

Among the contaminants possibly responsible for such reactions, there are some detergents commonly used in many Hospitals for cleaning of surgical and anesthetic material. As long ago as in 1954, Paddison and A l p e r s 2 2

emphasized that caution should be exercised in the use of detergent cleaned apparatus for intrathecal injections and that detergent materials should not be employed in the preparation of those items used in mixing and injecting spinal anesthetic agents. In two of our patients (cases 2 and 3) detergents were certainly used in preparation of the peridural tray. They were probably not used in case 1. If detergents were the responsible agent of chemical meningitis and arachnoiditis after spinal anesthesia, they would certainly be able to cause the same reactions after introduction of a larger amount, even in epidural space. Much of the anesthetic material is diffused, through the arachnoid villi, to the subarachnoid s p a c e 2 6 . In fact, there is not an experimental study to demonstrate diffusion of detergents through arachnoid villi. Actually, at these times, detergents should never be used for prepa­ration of anesthetic trays and disposable syringes and needles should be used whenever possible.

In our case 4 w e are sure that no detergent or any other possible contaminant was used in the preparation of the anesthetic material.

Bonica et a l . 2 report that in 19 cases of epidural anesthesia a subarach­noid block was produced unintentionally, but in 17 of these cases the spinal block resulted from the test dose and was recognized before the full amount

of solution was injected. In one patient in whom massive subarachnoid block occurred, serious neurologic sequelae developed; soon after the injection, the patient began to complain of severe lancinating pain.

Tissue reactions have been observed for the usual local anesthetics in concentrations only somewhat higher than those recommended for anesthe­s i a 1 3 . 2 4 . Experimentally, paraplegia was provoked in animals by increased concentrations of anesthetic agents 1 6 . 1 7 .

There would be strong evidence that increased amount of anesthetic in the subarachnoid space is the cause of cord lesion in our case 4. Even if we cannot rule out the action of detergents in cases 2 and 3, the similarity of our four cases suggests that they were possibly caused by the intra­thecal (subarachnoid or subdural) injection of large amounts of Lidocaine.

Dural perforation is not so rare on epidural anesthesia, and this would still leave the possibility for an hiperergic reaction to Lidocaine in the patients where the reaction occurs. All four anesthesias were done by res­pectful, experienced anesthesiologists, and in no case was CSF obtained before injection of the anesthetic.

Even if the test dose is injected, the possibility of neurologic compli­cations to develop still remains, and its early detection would be desirable if therapeutic measures were able to change the course of the disease.

All four patients had very intense pains, that must be interpreted as radicular, in the first 8 to 10 hours after anesthesia, and these ceased with analgesics, not to return. In both patients — cases 1 and 4 — who had a lumbar puncture performed during the first 24 hours, CSF was typical of an aseptic meningitis. It could be supposed that the radicular syndrome of the other two patients was also the expression of an aseptic meningitis.

In at least one patient (case 4) and, with all probability, also in cases 2 and 3, the disease run a three stages course: aseptic meningitis, followed by an asymptomatic period, and then the adhesive, fibrous, thickening of the arachnoid, causing obstruction to CSF flow and compression of cord vessels.

Intracranial subarachnoid obstruction occurred in two of our cases. It is very much rarer than the spinal lesions. Thickening of the leptomeninges of the base of the brain was demonstrated in some cases 15> 22> 3 0 after spinal anesthesia. Because of the severity of intracranial hypertension, carotid angiography instead of pneumoencephalography was made in case 3 and symmetrical hydrocephalus was shown. No radiologic demonstration of hy­drocephalus was considered necessary in case 4 in view of the urgency to reduce intracranial pressure and of the obvious clinical diagnosis. In both cases, immediate reduction of intracranial hypertension syndrome by ventri­culo-peritoneal shunt was demonstrative that it was caused by hydrocephalus.

Howland at a t . 1 1 studied the effect of intrathecal corticosteroids in preventing the development of paraplegia and arachnoiditis after experi­mental injection of Pantopaque and blood in subarachnoid space. Even if the study was made with a limited number of animals, neurologic sequellae were less conspicuouis in the treated group. Davis et a l . 6 suggested the addition of methyl-prednisolone to the contrast medium Conray (meglumine iothalamate) to minimize the risk of arachnoiditis. Positive evidence of the benefit of this procedure is still l ack ing . 1 . Intrathecal methyl-prednisolone was demonstrated by Lehrer et a l . 1 4 to achieve markedly increased con­centrations of the steroid in nervous structures close to the injection when compared to administration by systemic route. They propose that more effec­tive local soluble steroid levels within the central nervous system can be obtained with intrathecal than with systemic administration.

Intrathecal injections of Depo-Medrol were administered to cases 2, 3 and 4. In case 2 their effect cannot be judged because they were made after parapleglia was complete. Both in cases 3 and 4 a remarkable impro­vement of the intracranial hypertension was observed after some Depo-Medrol injections. Improvement lasted for three and four weeks, respectively, and was very brief after a second injection in case 3.

Nicholson and E v e r s o l e 2 1 advised irrigation of the subarachoid space with isotonic saline solution when a cauda equina syndrome was observed after spinal anesthesia. Removal of large amounts of CSF was made in several consecutive days in our case 4 and this proved to be unsatisfactory. It may still be possible that energic washing of subarachnoid space or con­tinuous drainage of CSF, coupled or not with more intensive intrathecal corticosteroid therapy would be effective in preventing the ulterior deve­lopment of arachnoiditis when the initial meningo-radicular syndrome is present and disclosed. Lumbar puncture should be performed whenever radicular pains are very severe after peridural anesthesia.

Surgical liberation of arachnoid adhesions is a difficult task and usually unefective, although rare reports of good results in chronic arachnoiditis justify a trial in more localized l e s i o n s 8 . 2 9 . Neurologic deficit, however, is some times relieved only temporarily and then, subsequently, progress to complete paraglegia 3 1 .

The time relation of development of paraplegia and unexpected recovery after placement of ventriculo-peritoneal shunt, in cases 3 and 4, suggest a causal relation. Recovery would not be atributed to intra-thecal Depo-Me­drol, for neurologic deterioration continued after the injections and no other therapeutic measure was used at this time.

Nelson et al. 2 0 reported 2 cases of adhesive arachnoiditis occurring as suposed complication of intrathecal methyl-prednisolone therapy for multiple sclerosis. However, one patient received 23 injections of Depo-Medrol and the other had a myelogram before intrathecal steroid was started. An

increase in protein was the only significant change noted in spinal fluid in their cases. CSF protein decreased in successive examinations in our cases, transiently during and after methyl-prednisolone injections.

SUMMARY

F o u r pa t i en t s w h o received ep idura l anes thes ia p resen ted sus t a ined m y e ­lopa thy; t h r e e of t h e m h a d comple te pa rap leg ia and one a lumbo-sacra l mye lopa thy w i t h u r i n a r y re ten t ion . All four pa t i en t s compla ined of ve ry in tense r ad i cu l a r pains immedia te ly a f te r the analges ic effect of Lidocaine w a s over. T w o pa t i en t s in w h o m l u m b a r p u n c t u r e was done in t h e f i rs t 24 h o u r s p resen ted an asep t i c meningi t ic r eac t ion in C S F . P a r a p l e g i a comple ted in t w o to t en m o n t h s in t h r e e pa t i en t s and in two of t h e m severe i n t r ac r an i a l hyper tens ion developped a t th is t ime . I t is proposed t h a t t h e disease r u n s a two-s t ages course, a t l eas t in some cases, cha rac t e r i zed by a n asept ic m e ­ningit is , followed, a f t e r a s i lent per iod of some mon ths , by signs of adhesive spinal and i n t r a c r a n i a l a rachnoid i t i s . I n t r a c r a n i a l hyper tens ion w a s con­t ro l led by vent r icu lo-per i tonea l s h u n t ; in two pa t i en t s a t r ans i to ry effect of i n t r a t h e c a l injections of methyl -predniso lone a c e t a t e was observed. T w o pa­t i en t s recovered a l m o s t complete ly f rom parapleg ia .

RESUMO

Paraplegia e hipertensão craniana após anestesia epidural. Relato de 4 casos.

Q u a t r o pac ien tes que r e c e b e r a m anes tes ia ep idura l a p r e s e n t a r a m mielopa¬ t i a de longa evolução; e m t r ê s ocor reu pa rap leg ia comple ta e u m apresen­tou u m a s índrome m e d u l a r lombo-sacra com r e t e n ç ã o u r ina r i a . Todos os pac ientes se q u e i x a r a m de in tensas dores r ad icu la res i m e d i a t a m e n t e após a cessação do efeito analgésico da l idocaína. Dois pac ien tes a p r e s e n t a r a m u m a r e a ç ã o mening í t i ca assépt ica no líquido ce fa lo r raqueano nas p r ime i ra s 24 horas . A parap leg ia tornou-se comple ta e m 2 a 10 meses após a anes t e s i a ; dois pac ien tes t i v e r a m h ipe r t ensão c r a n i a n a severa . E m a lguns casos, senão e m todos, e s t a afecção a p r e s e n t a u m a evolução e m duas e t apas , c a r a c t e r i z a d a s por men ing i t e assép t ica imedia ta , seguida, depois de u m período silencioso de poucos meses , de sinais de a racnoid i te ades iva espinal e i n t r a c r a n i a n a . A h ipe r t ensão i n t r a c r a n i a n a foi con t ro lada por der ivação ven t r icu lo-per i tonea l ; e m 2 pac ien tes houve m e l h o r a t r ans i t ó r i a pela admin i s t r a ção de met i l -p redn i¬ solona in t r a t eca l . E m dois pac ien tes houve r ecupe ração quase comple ta da paraplegia .

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