FURTHER EVIDENCE R E G A R D I N G T H E SPINAL CORD P A R A L Y S E S FOLLOWING S P I N A L ANESTHESIA
F O S T E R K E N N E D Y A B R A H A M S . E F F R O N
Doctor Foster Kennedy is deeply sorry that he could not be here to address you on the subject of spinal cord paralyses following spinal anes-thesia. This subject is very close to his mind and deep to his conscience. Only the most definite opinions of his physicians, who forbid him to make the journey, could persuade him against presenting such a serious problem to this fine audience, and especially to the surgeons, obstetricians and anesthetists who may be present.
During the past 5 years, detailed accounts of various types of spastic spinal paralyses brought on by the use of spinal anesthesia were published by Doctor Kennedy and his colleagues 1 1 2
at Bellevue Hospital. It is im-portant at the outset to note that these sequelae of surgical and obstetrical procedures are not generally observed while the patient is in hospital, but are usually seen independently by the neurologist weeks or months after the patient has been discharged from hospital. The early complaints include numbness, weakness of feet and legs, sphincter loss and sensory loss often over periods of months. In the majority of cases symptoms are mild im-mediately after spinal anesthesia, and only proceed to a paralytic stage weeks or months later. Thus, the surgeons and anesthetists employing spinal anesthesia do not become aware of the grave results often emerg-ing from their procedures.
For a period of a few weeks after the publication of our article about the grave spinal cord paralyses caused by spinal anesthesia in October 1 9 5 02
, we received 70 letters from people who became paralyzed
follow-F r o m the N e u r o l o g i c a l Service of B e l l e v u e H o s p i t a l , N e w Y o r k , U . S . A .
Nota da Redação — E s t e trabalho, o último escrito pelo D r . F o s t e r K e n n e d y e p r e p a r a d o p a r a u m a apresentação p e r a n t e congresso m é d i c o , foi enviado ao D r . L . B a r r a q u e r B o r d a s pela viúva daquele p r a n t e a d o neurologista, a c o m p a n h a -d o -das seguintes palavras que e m p r e s t a m g r a n -d e valor à sua publicação nesta
revista: " A s you p r o b a b l y know b y now m y dear husband, F o s t e r K e n n e d y , w a s called a w a y f r o m us on the 7th of J a n u a r y of this year. I n g o i n g through the correspondence which he had to leave unanswered, I f o u n d a letter from y o u asking that he should submit an original p a p e r for the June issue of the A R Q U I V O S
ing spinal anesthesia. All of them had been assured the operation o r anesthetic was blameless. Some sought help and relief from their affliction, and others were hopeful as one patient who wrote, "Perhaps now it won't happen to others".
Many of these patients presented early symptoms which were most often thought to be due to "post-operative weakness", and in the present general poverty of neurological knowledge, the subsequent paralysis in many of our 70 paralyzed people was called "multiple sclerosis", while in a smaller number they were referred to as "psychosomatic" complaints. These diagnostic errors and the lack of subsequent examinations once a post-operative patient has been discharged are responsible for the diversity of statistics which exist in medical literature concerning the complications of spinal anesthesia.
We are told in those cases where serious neurological complications followed spinal anesthesia, the etiological factor was not the spinal anes-thetic but resulted from "previously undiagnosed neurological disease". However, if the anesthetists and surgeons who put forth this theory really believe it to be so, why do not all pre-operative patients have a careful and complete neurological examination? Do they soothe their consciences by believing that the patient was not paralyzed by their procedure, but that it would have happened anyhow? W e do not deny that an occasional case may have pre-existing disease o f the central nervous system. Yet, in spite of this, the use of spinal anesthesia has come to be so routine a procedure for some men that the administration of this type of anesthetic is not withheld even for such a case. If this so-called pre-existing disease of the central nervous system is latent and cannot be determined even after examination, are we right to take the risk o f introducing an anesthetic agent into the intrathecal space? This is not even a calculated risk, for we have no means of testing the patient and weighing the risk.
We will briefly review some of the facts from the literature as previous-ly reported by us, and then add additional clinical and pathological evidence. Animal experiments by independent investigators have resulted in agree-ment that the anesthetic substance is the etiological agent responsible for central nervous system complications produced by spinal anesthesia. The damage i s2
These are essentially the same pathological changes seen at operation or post-mortem in patients who have had complications after spinal anes-thesia. The lesion of chronic progressive arachnoiditis compressing the spinal cord has been verified by both touch and vision. In none of our cases has there been any improvement as a result of operation. In most cases a manometric spinal fluid block occurred, and all of those reported had sustained severe pyramidal tract lesions, most times accompanied by a sensory spinal level below which sensation is either lost or inadequate, together with paralyzing of sphincters and, in men, loss of potency. The progressive paralysis is due, of course, to the progressive tightening of arachnoid adhesions around the spinal cord.
D . M . * , a 19 year old w o m a n , had an uneventful p e r i o d of p r e g n a n c y . She
received a saddle block anesthesia with 5 m g of nupercaine a t the level of the third l u m b a r interspace. S h o r t l y thereafter a sensory level could be d e m o n s t r a t
-ed a t the 7th thoracic segment. T w o hours later the patient went into v a s o m o t o r collapse, with a r e s p i r a t o r y rate of 5-6 per minute. L u m b a r p u n c t u r e f o u r hours
a f t e r the administration of the anesthetic a g e n t revealed clear cerebrospinal fluid with a pressure of 140 m m . of w a t e r . O n examination the next d a y , she w a s
in coma. T h e lower limbs were p a r a l y s e d and flaccid. T h e spinal fluid pressure w a s 470 m m . of w a t e r a n d the fluid contained 3 1 1 4 R . B . C . and 741 W . B . C . of
which 8 1 % were p o l y m o r p h s . T h e patient's condition remained essentially un-changed, except for the demarcation of a sensory level a t the 5th thoracic spinal
s e g m e n t on the left, a n d 2 n d thoracic spinal s e g m e n t on the right. O n the 19th d a y repeated a t t e m p t s at l u m b a r p u n c t u r e w e r e unsuccessful. A ventriculogram
the next d a y showed a s y m m e t r i c a l dilation of the ventricles, with an especial dilation of the 4th ventricle. T h e s e air studies were interpreted as indicating
the presence of internal hydrocephalus, a n d a shunting operation to relieve the o b s t r u c t e d ventricles w a s decided upon. A l e f t v e n t r i c u l o m a s t o i d o s t o m y w a s p e r
-f o r m e d , without remedy. O u r clinical diagnosis w a s meningo-myeloencephalitis s e c o n d a r y t o the spinal anesthesia. T h e p a t i e n t died on the 86th d a y a f t e r the
anesthetic had been administered.
A description of the spinal cord at p o s t - m o r t e m reads as f o l l o w s : 'The dural envelope is not readily r e m o v e d ; in extensive regions there is obliteration
of the s u b d u r a l space with fibrous adhesions. T h e s e adhesions are s e p a r a t e d with considerable difficulty. T h e spinal c o r d then presents an arachnoidal s u r f a c e
which is of diminished lustre and shows splotchy yellow and brown discolorations, this change being m o s t m a r k e d in the thoracic region. T h e r e is obvious
thicken-ing of the arachnoid. Cross sections of the lower cervical spinal cord reveal n o r m a l l a n d m a r k s . H o w e v e r , in cross sections through the thoracic c o r d , the
m a r k i n g s are seen to be c o m p l e t e l y obscured and the substance of the cord is generally peculiarly yellow and o p a q u e in these r e g i o n s ; in certain sites, b r o w n
discoloration is n o t e d ; in other areas, the cord a p p e a r s as though h o n e y - c o m b e d with small cavities. I n the region of the arachnoid cisterns, the arachnoid is
thickened a n d of diminished t r a n s p a r e n c y ; adhesions of arachnoid to pia are en-countered, this change being m o s t m a r k e d in the region of the cisterna m a g n a .
T h e arteries a t the base of the brain are e m b e d d e d in thickened arachnoid m e m b r a n e . T h e dominant pathological process is a severe chronic reactive l e p t o
-meningitis t h r o u g h o u t the spinal cord and brain stem. T h e destructive changes
in the cord and brain stem are of a n o n - i n f l a m m a t o r y nature and are r e g a r d e d
as the result of progressive ischemic necrosis. T h e distribution of the necrotic lesions in the brain stem are directly related to the arteries affected".
A n a b s t r a c t f r o m the pathological r e p o r t of one of our earlier cases r e a d s :
"The spinal cord g r o s s l y w a s reduced to a ribbon-like structure". M i c r o s c o p i c examination disclosed w i d e s p r e a d and m a r k e d alterations in the n a t u r e of a
dif-fuse a n d , in places, of a p a t c h y demyelinating and rarifying process. I n the opinion of the neuropathologist, the disease process w a s a "degenerative
dis-integrating disease due p r e d o m i n a n t l y to s o m e toxic agent".
I n addition, we can relate the neurological sequelae of two y o u n g w o m e n
patients w h o received saddle block anesthesia during labor. O n e b e g a n to c o m -plain of n u m b n e s s of her legs five w e e k s p o s t - p a r t u m , and several weeks later
p r e s e n t e d a clinical picture of c o m p l e t e transverse myelitis at the level of D?. The second patient w a s a s y m p t o m a t i c until 9 months a f t e r delivery. I n both
patients there w a s a complete subarachnoid block. O n l a m i n e c t o m y they showed a t y p i c a l adherent arachnoiditis with a v e r y sharp demarcation between the
in-volved and the n o r m a l portion of the cord.
W e w o u l d also like to c o m m e n t on a patient w h o complained of lack of sensation in the feet some months a f t e r a Caesarian operation u n d e r spinal
anesthesia. T h i s sensory loss w a s slowly progressive over a period of months. N o spinal fluid could be obtained with r e p e a t e d l u m b a r puncture. M y e l o g r a m
revealed m a r k e d arachnoidal thickening. T h e patient b e c a m e p r e g n a n t again d u r -ing the next year. D u r i n g this p r e g n a n c y her condition was noted to improve
r e m a r k a b l y . T h e vascular changes occasioned b y the second p r e g n a n c y , as f a r as w e can determine, could not have been sufficiently definite to be the agent
responsible f o r the recovery f r o m the existing arachnoiditis. T h e r e f o r e , w e sug-gest that it m i g h t be of interest in cases of post-spinal arachnoiditis to a t t e m p t
to dissolve the arachnoidal adhesions by reproducing the hormone conditions f o u n d in p r e g n a n c y . Since the adrenal cortex experiences g r e a t stimulation during
p r e g n a n c y , the use o f A C T H and Cortisone might well be e x p e r i m e n t a l l y evaluated.
COMMENT
"The neurological complications of spinal anesthesia occur in those regions of the central nervous system or its membranes most closely situated to the site of injection of the anesthetic compound. This is attested by the reported cases, together with operative and post-operative observation. These sequelae are rarely due to direct injury since such accidents are not found after lumbar puncture. In rare cases, marked symptoms occur in patients who complain of severe pain during the injection of the anes-thetic". On introduction of the effective agent into the subarachnoid space dilution and diffusion occur, but not before considerable absorption and fixation have taken place near the site of injection where the membranes and nerves are in contact with the full concentration of the anesthetic drug" 2
.
The anesthetic drug is the toxic agent in these cases. MacDonald and Watkins 3
con-tributory cause may be the possibility of alcohol or other sterilizing fluid seeping into the anesthetic vials either by defective sealing or minute breaks, or perhaps by bacterial contamination. If this should prove true, then certainly the only way to avoid this complication is by the administration of other methods of anesthesia rather than spinal.
We are then asked whether general anesthesia is any "safer" than spinal anesthesia. It is not easy to obtain reliable figures on this subject because of the frequent time lag in insiduous paralysis. It is our impres-sion that the lethal statistics as regards spinal and general anesthetics are about the same, but that spinal paralyses occur sufficiently often after spinal anethesia to become highly noticeable in neurological wards of a general hospital. Those cases in which the spinal anethesia has been un-successful and has to be followed by volatile anesthesia should not be too lightly forgotten. There is no such thing as conservative choice of spinal anethesia because we cannot know beforehand whether the patient will be-come one of the paralyzed. Certainly paralysis of the lower limbs, and a tied-in catheter should not be a possible complication of a simple hernio-tomy, appendechernio-tomy, or a delivery. From the neurological point of view, we repeat the opinion that spinal anesthesia should be rigidly reserved for those patients unable to accept a local or general anesthetic. One of the most distinguished surgeons in the country informs us that he has given up spinal anesthesia since these paralyses cases were published and "that morning he had done two sigmoidectomies under perfect operative conditions with pentothal and curare". Anesthetists and obstetricians should not employ this method of anethesia if any other be available. T o do so shows a lack of reverence for tissue; spastic paraplegia is altogether too high a price to ask a patient to pay in order that the anesthetist should have a simple anesthetic administration, and the surgeon a clear field of relaxation in which to employ his skill.
Neurological Service of Bellevue Hospital, New York, U.S.A.
BIBLIOGRAPHY
1 . K e n n e d y , F . , S o m b e r g , H . M . a n d G o l d b e r g , B. R . — A r a c h n o i d i t i s a n d p a r a l y s i s f o l l o w i n g s p i n a l a n e s t h e s i a . J . A . M . A . , 1 2 9 : 6 6 4 , 1 9 4 5 .
2 . K e n n e d y , F . , E f f r o n , A . S. a n d P e r r y , G . — T h e g r a v e s p i n a l c o r d p a r a l y s e s c a u s e d b y s p i n a l a n e s t h e s i a . S u r g . , G y n e c . a. O b s t . , 9 1 : 1 , 1 9 5 0 .
