LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES

Respiratory Arrest and Cervical Infarction Following Lumbar Puncture in

MARGARET G. NORMAN

SUMMARY: A 6-year-old child with men­ Spinal cord damage is a rare com­ to painful stimuli by opening her eyes. ingitis had a respiratory arrest 20 minutes plication of bacterial meningitis. This When her mouth and pharynx were after a lumbar puncture. Thereafter she re­ case is being reported to draw attention suctioned, she blinked. Her corneal quired maintenance on a ventilator, had a to the fact that infarction of the cervical reflexes were sluggish, her gag reflex flaccid quadriplegia, and died 12 days was present, and her facial movements later. Necropsy showed infarction of the spinal cord can occur after respiratory central portion of the cord at the level of the arrest following lumbar puncture in were symmetrical. Intracranial pres­ decussation of the pyramids. The suggested meningitis. sure (ICP) monitoring was begun. The mechanism of damage is compression of first recorded pressures were 18, 20 the arterial supply to the cord at the level of CASE REPORT torr and subsequently remained at less the foramen magnum by herniated cerebel­ This six year old girl was well until than 10 torr so barbiturates and ICP lar tonsils; concomitant hypotension may the night prior to admission when she monitoring were discontinued on the have contributed to production of the developed and fever. The 5th day. CSF cultures grew H. in­ damage. Four similar cases, who survived next day she vomited and was noted to fluenza sensitive to ampicillin so with residual deficit, have also been chloramphenicol was discontinued. reported. Other separate mechanisms by be confused. By the time she was seen which the cord can be damaged in in her local hospital she was unrespon­ On the fifth day she was still meningitis are vasculitis, thrombosis and sive and had a stiff neck. A lumbar quadriplegic and required mechanical arachnoiditis. puncture showed turbid cerebrospinal ventilation. On command she would fluid. The CSF contained 21,400 open her mouth and eyes. She seemed RESUME: Un enfant de 6 ans soujfrant de leukocytes per cubic mm. and a smear more aware of her surroundings. Her meningite fut victime d'un arret respira- showed gram negative rods. Treatment corneal reflexes were brisk, and her gag toire 20 minutes apres une ponction lom- was commenced with ampicillin and reflex was present but depressed. On baire. Le tout fut suivi d'une quadriplegie chloramphenicol. Twenty minutes fol­ the eighth day her facial movements flasque necessitant un respirateur, mais lowing the lumbar puncture she had a were weak and swallowing was im­ I'enfant mourut 12 jours plus tard. L'au- respiratory arrest. She was intubated paired. On painful stimulation she topsie montra un infarcissement de la por­ tion centrale de la moelle au niveau de la and ventilated. Blood gases at this time withdrew her right foot slightly to pain, decussation des pyramides. Le mecanisme were as follows: 7.37 pH, pC02 35 but could not withdraw her foot when pathogenique semble etre une compression mm.Hg, p02 136 mm. Hg. asked to do so. de I'apport arteriel a la moelle au niveau du Three and one-half hours later, she She was afebrile for the first six foramen magnum par des amygdales was examined at the Vancouver hospital days. On the seventh day her cerebelleuses herniees; une hypotension temperature started to rise and reached concomittante peut avoir contribue a la General Hospital. At that time she was production de la lesion. Qualre ces unresponsive to painful stimuli. Her 40.9°C on the 10th day. On the ninth semblables ayant survecu, mais avec un de­ fundi was normal. Her eyes diverged day a chest roentgenogram showed ficit residuel, furent rapportes. D'autres and the pupils reacted sluggishly to the bilateral pneumonia. On lumbar punc­ mecanismes existent qui pourraient expli- light. Muscle tone was flaccid in all ture the opening pressure was 13 cm. quer une telle lesion de la moelle dans la four extremities, deep tendon reflexes The CSF was clear and colourless, and meningite; ce sont les vasculites, les throm­ were absent and plantar responses were contained 52 red blood cells per cu. boses et les arachnoidites. flexor. Blood pressure was 80/60, pulse mm., 9 leukocytes per cu. mm., protein rate 80 per minute. The right ear drum 30 mg/dl and glucose 90 mg/dl. Her was slightly red. Peripheral blood peripheral blood contained 24,500 leukocyte count was 10,000 per cu. leukocytes per cu. mm. on day 10. On mm. with 75% stab cells. She was the eleventh day her abdomen became treated with and man- distended, tense, silent and tympanitic. From the Department of Pathology, Vancouver nitol. Pentobarbital was administered Abdominal roentgenogram showed gas General Hospital and University of British Columbia, as an initial bolus of 10 mg. per kg. and throughout the bowel, with multiple air Vancouver, B.C. continued at a rate of 2 mg. per kg. per fluid levels, and air in the bowel wall Requests for Reprints to: Dr. M.G. Norman, Children's Hospital, 4480 Oak Street, Vancouver, hour. suggesting a diagnosis of necrotizing B.C. V6H3V4. Examination two and one-half hours enterocolitis. Air was also present in Presented in part at the Diagnostic Slide Session, the portal venous system. Her course American Association of Neuropathology, Philadel- after admission showed that she did not phia.June 12, 1982. respond to commands. She responded thereafter was one of continued

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deterioration. She died on the twelfth with macrophages replacing parenchy­ tion was seen, but the cerebellar tonsils day of her illness, 33 hours after the ma. These were similar to the infarcts were infarcted. During the 12 days the onset of abdominal distention. in the cord. Sections of the brain and of patient lived after her respiratory ar­ the cord, including levels T4-7 and LI rest, the gross herniation probably had Pathological Findings showed no infarction, residual time to recede, leaving the infarcted Post mortem examination showed meningitis, arteritis, or thrombosis. tonsils as a marker of previous hernia­ slight cerebral . Herniation of General necropsy revealed that the tion. The herniated cerebellar tonsils cerebellar tonsils was not seen on gross immediate cause of death was necrotiz­ produced sufficient compression of examination. Microscopic examination ing gastroenteritis. The cause of this structures in the foramen magnum to of serial sections of lower brain stem was unknown, though treatment with obstruct caudal flow in the vertebral and spinal cord showed discrete areas antibiotics, ischemia, and intragastric artery branches which give rise to the of infarction in the brainstem. The nutrition with a hyperosmolar solution anterior spinal artery and thus caused largest consisted of almost symmetrical were all considered theoretical pos­ infarction of the upper cervical cord areas of infarction throughout the first sibilities. Bilateral bronchopneumonia (Fig. 2). Since the infarctions were cervical segment (Ci), involving the was present. bilateral, either both arteries were com­ pyramidal decussation (Fig. 1). The in­ pressed before they united to form a farcts appeared to be of the same age. DISCUSSION single anterior spinal artery, or perhaps Most of the infarcted tissue had been The blood supply to the cervical the central arteries, branches of the removed by foamy macrophages, spinal cord comes from the anterior anterior spinal artery which supply the which replaced the parenchyma. A few spinal artery which arises as a midline central portion of the cord (Turnbull, neuroaxonal swellings were present at union of a branch from each vertebral 1971), were compressed rather than the the periphery of the infarct. Occasional artery. There is general agreement that anterior spinal artery. The small dis­ hypertrophied astrocytes were present the upper portion of the cervical cord is crete infarcts in the dorsal half of the in viable tissue surrounding the infarct. supplied from above, the lower portion cord may have resulted from compres­ Just below the frank infarction, at the from below (Fortuna et al, 1971). In sion of the pial arterial plexus. C2 and C3 levels, there were bilateral this patient, signs and symptoms of in­ Hypotension with resultant failure of neuroaxonal swellings at the subpial creased were al­ perfusion of the cord may also have surface of the cord, these being ready present, and the lumbar puncture contributed to production of the in­ damaged corticospinal axons which probably precipitated a cerebellar pres­ farct. The levels of cord usually in­ run on the surface between C2 and C4 sure cone, indicated in life by the farcted due to hypotension and is­ (Crosbie et al. 1962). Sections of respiratory arrest. At postmortem ex­ chemia are T4 (T4-7) and LI (Lazor- cerebellar tonsils showed infarction amination no gross cerebellar hernia­ thes 1972), which were not involved in

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Figure 1 — Distribution of infarcts in brain stem and upper cervical cord. Figure 2 — Proposed mechanism for infarction. Cerebellar tonsils Black areas denote infarction, which involves chiefly the corticospinal protrude down through foramen magnum and compress cord and tracts as they decussate. Ventral surface of brainstem and cervical cord descending branches of the vertebral arteries against the bony edges of is depicted on left, cross sectional area of infarct in the centre drawings, the foramen magnum. Arrows denote direction of flow. indicates and the longitudinal extent of the infarct on the right. region of abolished arterial blood flow to C1 segment. (Illustration adapted from Lazorthes 1972)

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this case . Experimental work in dogs consciousness. All four had a lumbar 'puncture. All were maintained on a indicates that perfusion of the spinal puncture, which confirmed the diagno­ ventilator, and all had small areas of cord is maintained with increased sis of bacterial meningitis. Within hours necrosis in the cervical spinal cord pressure at arterial of admission, presumably after the LP which the authors attributed to com­ perfusion pressures of greater than 50 was performed, each had a respiratory pression of the vascular supply by large mm. Hg (Griffiths et al, 1978). Perfu­ arrest, developed quadriplegia and re­ amounts of herniated cerebellar tissue sion is maintained when the cord is quired mechanical ventilation. In case 4 which were found around the spinal compressed directly until perfusion it is stated that there was "no hypoten­ cord at necropsy. In these cases it is pressure drops below 65-70 mm. Hg sion" during the period of respiratory probably vessels of the pial arterial (Griffiths et al, 1979). In this case com­ arrest; in cases 2 and 3 the arrest is plexus which were compressed. The pression and failure of perfusion may described as "cardiorespiratory". blood pressures in these patients at the have combined to produce the infarct, These four cases are probably similar time of the respiratory arrest were not although the blood pressure during the to the present case - that is, meningitis, stated. respiratory arrest is not known. some early increase in intracranial Table 3 describes three cases, all of Four patients have been described pressure, coning, and compression of whom had meningitis, a lumbar punc­ who survived following an episode of the small arteries at the foramen ture, no respiratory arrest, and damage respiratory arrest after lumbar punc­ magnum by herniated cerebellar tissue. to the spinal cord at levels below Tl. ture performed early during the course The four cases summarized in Table The mechanism damaging the cord is of bacterial meningitis (De Sousa et al, 2 are also similar in some respects, but probably either a vasculitis or arach­ 1978; Tal et al, 1980; Swart and Pye, did not have meningitis. All had noiditis. Case 10 and 11 are probably 1980; see Table I). All patients had cerebral pathology, all but one (Case 6) similar to the two "acute poliomyeli- headache, vomiting and some degree of had lumbar puncture, one (Case 8) had tic" cases described by Turner (1948), lethargy or decrease in their level of a respiratory arrest prior to lumbar in which there was sudden onset of a

TABLE 1 Reported cases of following lumbar puncture on children with meningitis

Age - Sex Time of Time on Clinical Features Postulated mechanism Case Reference (yrs.) Organism respiratory arrest respirator and Outcome of damage to cord

1 Present 6 F H. influenza 20 min after LP 12 days Level at decussation Infarct of cervical report of pyramids. cord. Compression of Flaccid quadriplegia. anterior spinal artery Death. by herniated cerebellum + hypotension 2 Tal et al 3 + 1/3 M H. influenza 8 hrs. after 6 mon. Flaccid of (1980) admission arms, spastic legs. Case 1 Recovery, residual Ischemia due to deficit. cardiac arrest 3 Tal et al 3+1/2 F N. meningi­ 3 hr. after NS Cranial nerve signs. Ischemia due to (1980) tidis admission Flaccid quadriplegia. cardiac arrest Case 2 Sensory level below C1. Recovery, residual deficit. 4 Swart & 15 M N. meningi­ 7 and 12 hr. after 2wk. Cranial nerve signs. "Vasculitis" Pye tidis admission Quadriplegia below (1980) cervico-medullary junction. Recovery, residual deficit. 5 De Sousa 3 F H. influenza "shortly after" 9wk. Cortically blind. "Vascular injury" etal transfer to Flaccid quadriplegia. (1978) referral centre Recovery, residual deficit.

NS — Not stated

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TABLE 2 Reported necropsy cases of cervical cord infarction attributed to compression of vascular supply to cord by herniated cerebellar tissue

Age - Sex Underlying Interval between LP Time on Lesion found Case Reference (yrs.) Disease and respiratory arrest respirator at necropsy

6 Herrick & 12 F less than 24 hours 96 hr. Pencil shaped Agamanolis with fatty necrosis posterior (1975) liver (Reye's columns cervical cord Case 3 syndrome) 7 Herrick & 4 F Encephalopathy ? less than 12 hours 61 hr. Necrosis posterior Agamanolis with fatty cervical & (1975) liver (Reye's thoracic cord Case 5 syndrome)

8 Herrick & 17 F End stage renal No LP 53'/2hr. Necrosis cervical cord Agamanolis disease dorsal and dorsolateral (1975) white Case 6 9 Herrick & 18 M R. subdural Prior 56 hr. Necrosis cervical cord Agamanolis empyema to LP (1975) Case 8

TABLE 3 Reported cases of damage to the spinal cord due to thrombosis, vasculitis or arachnoiditis in bacterial meningitis

Age - Sex Lesion. Postulated mechanism Case Reference (yrs.) Organism Clinical Features of damage of the cord

10 Tal et al 3 days M E. coli Asymptomatic. Softening of grey matter thoracic cord (1980) Death. and all of lumbo-sacral cord. Case 3 Thrombosis of anterior spinal artery. 11 Gottshall 20 M N. meningitis Original level "Vasculitis". No pathological verification. (1972) midlumbar. Recovery, residual deficit at S3-5.

12 Haupt 5'/2 M D. pneumoniae Flaccid paraplegia. Dense fibrous leptomeningeal adhesions etal Sensory level T2. at laminectomy. (1981) Recovery, residual deficit.

flaccid monoplegia during the course of loss and gliosis in the spinal cords of widespread neuronal loss and gliosis meningitis. These cases likely resulted six children following a cardiac arrest. most marked in the sacral region, from either thrombosis, as found in In all cases the damage was most decreasing rostrally. These six cases Case 10, or vasculitis. Turner's last two marked in, or limited to the lumbar are different from the one here cases and Case 12 are examples of cord. In four of these cases no LP was reported. Frank infarction of the cord damage to the cord resulting from a mentioned. One child had a cardiac ar­ was absent. Damage was caudal, not chronic arachnoiditis following rest the day following LP and another high in the cervical cord. These cases meningitis. (case 4) had a cardiorespiratory arrest represent a mechanism of damage to Gilles and Nag (1971) described during lumbar puncture and at the cord caused by failure of perfusion anoxic neuronal change or neuronal necropsy was found to have alone, without any element of compres-

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sion of vessels to the cord as postulated admission, and there were no instances GRIFFITHS, I.R., PITTS, L.H., CRAW­ in this case. of herniation before lumbar puncture. FORD, R.A., TRENCH, J.G. (1978). Spinal cord compression and blood flow: I. It is interesting that there are so few Apart from the occurrence of headache The effect of raised cerebrospinal fluid pres­ reports of cases of the type represented in 3 - 30% of patients after lumbar sure on spinal cord blood flow. Neurology in Table 1. There is considerable puncture, it is difficult to determine the 28: 1145-1151. variability in the blood supply to the exact incidence of complications of LP. GRIFFITHS, I.R., TRENCH, J.G., CRAW­ spinal cord and possibly some rare and The probable reason for this is that FORD, R.A. (1979). Spinal cord blood flow unique arrangement of vessels to the Ci serious complications are rare and de­ and conduction during experimental cord segment in these patients accounts for pend on factors related to the primary compression in normotensive and hypoten­ the spinal cord infarction at this level. disease for which the LP is performed, sive dogs. J. Neurosurg. 50: 353-360. Another factor may be that death particularly on whether or not there is HAUPT, H.M., KURLINSKI, J.P., BAR- usually occurs so quickly after coning increased ICP. Also, it is not always NETT, N.K., EPSTEIN, M. (1981). Infarc­ that clinical and morphological signs of possible to determine whether the com­ tion of the spinal cord as a complication of pneumococcal meningitis. J. Neurosurg. 55: cord infarction do not develop unless plication is directly due to the LP or to 121-123. patients are kept alive by mechanical the primary disease. HERRICK, M.K. and AGAMANOLIS, D.P. ventilation for a period of time. Of the (1975). Displacement of cerebellar tissue eight cases reported by Herrick et al ACKNOWLEDGEMENT into spinal canal: a component of respirator (1975), only those four maintained for I wish to thank Dr. T. Pantzar, who per­ brain syndrome. Arch. Pathol. 99: 565-571. the longest time on the respirator (a formed the autopsy, Drs. B.S. MacLean and F.A. Durity, who cared for the child, and Drs. HOROWITZ, S.J., BOXERBAUM, B., minimum of 5Vli hours) showed K. Berry and H. Dunn for helpful editorial sug­ O'BELL, J. (1980). Cerebral herniation in necrosis of the spinal cord at necropsy gestions. bacterial meningitis in childhood. Ann. Neurol. 7: 524-528. (Table II). REFERENCES Infarction of the spinal cord occurr­ LAZORTHES, G. (1972). Pathology, clas­ CROSBIE, E.C., HUMPHREY, T., LAUER, ing as a complication of L.P. has not sification and clinical aspects of vascular E.W. (1962). Correlative Anatomy of the diseases of the spinal cord. Edit. P.J. Vinken, been described previously. The extent . New York, MacMillian G.W. Bruyn. Handbook of Clinical Neurol­ to which the cervical cord damage in Co., p. 96. ogy, Amsterdam, North Holland Vol. 12, the present case is directly due to the DE SOUSA, A.L., KLEIMAN, M.B., pp. 492-506. LP is not clear. occurs MEALEY, J., Jr. (1978). Quadriplegia and SWART, S.S. and PYE, I.F. (1980). Spinal cord in meningitis and perhaps any time cortical blindness in Hemophilus influenzae ischemia complicating meningococcal there is a cerebellar pressure cone for meningitis. J. Pediatr. 93: 253-254. meningitis. Postgrad. Med. J. 56: 661-662. whatever reason, the situation is such FORTUNA, J.A., LA TORRE, E., OC- TAL, Y., CRICHTON, J.U., DUNN, H.G., that vascular compression and cord CHIPINTI, E. (1971). The direction of DOLMAN, C.L. (1980). Spinal cord blood flow in the cervical cord: an damage: a rare complication of purulent damage can occur. The LP may con­ angiographic study of infants and children. tribute by producing a more rapid meningitis. Acta Pedatr. Scand. 69: 471- Eur. Neurol. 5: 335-342. 474. change in pressure which precipitates GILLES, F.H., NAG, D. (1971). Vulnerability coning. Horowitz et al (1980) found TURNBULL, I.M. (1971). Microvasculature of of human spinal cord to transient cardiac ar­ the human spinal cord. J. Neurosurg. 35: that the incidence of cerebral herniation rest. Neurology 21: 833-839. 141-147. of all types was 6% in a clinical study GOTTSHALL, R.A. (1972). Conus medullaris of childhood bacterial meningitis. The TURNER, J.W.A. (1948). Spinal cord lesions in syndrome after meningococcal meningitis. cerebrospinal fever. Lancet I: 398-401. herniations occurred within 8 hours of New Engl. J. Med. 286: 881-883.

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