Paroxysmal hypertension secondary to increased ... - Springer Link

2 downloads 0 Views 173KB Size Report
We here report a case of a. ~ine month old infant, who had paroxysmal hypertension as a presenting feature of tuberculous meningitis. Possible mechanisms.
iMij mft. pedlaff. 46: 295, 379

IpARoXYSMAL ItYPERTENSION SECONDARY TO INCREASED I N T R A C R A N A I L PIIESSURE* R e p o r t o f m Came **SUNIT SINOHI AND * * * V . P . CHAUDHARY ,New Delhi

Acute episodic hypes tension in chndren can occur in several clinical condit;ons, such as glomerulonephritis, Henoch Schonlein purpura, hemolytic-ur,'mic sy**dr,me, Gullian-Barre syndrome, poliomyelitis, neurofibromatosis, prophyria, and in diseases associated with increased intracranial pressure (ICP). H o w e v e r , paroxysmal hypertension occurs very rarely in association with meningitis. W e here report a case of a ~ine month old infant, who had paroxysmal hypertension as a presenting feature of tuberculous meningitis. Possible mechanisms leading to systemic hypertension following increased I C P are discussed.

R e p o r t o f a Case J., 9 months old male, was admitted to the Pediatric Service of All I n d i a Institute of Medical Sciences Hospital for mild puffiness of face, pedal oedema, fever and nasal discharge of 2 days' duration. He weighed 10.2 kg and was moderately pale. His blood pressure was 100160 m m of Hg. On the evening of admission, his blood *From the Department of Paediatrics, All India Institute of Medical Sciences, New Delhi-I i0016. *~ address: Lecturer in Paediatrics, Department o~ Paediatric*, J.L.N. Medical College, Ajmer (Rajasthan). *e'Reprint requests to Dr. V.P. Chaudhary, Assistant PmfeaJorof Paediatrics, All India Institute of Medical Sclences, ,Item Delhi- 110018. Received on December 12, 1978.

pressure was recorded as 210/150 m m of Hg. This came down to 110/70 after parenteral administration of 1 mg reserpine. His hemoglobin was 7.7 gm/dl and total and differential leukocyte counts were normal. Sedimentation rate was 58 ram. Repeated urine analysis revealed only trace to one plus albumin. U r i n e cultures were sterile. Stool examination showed cysts ofgiard~a lambia. Tuberculin test was negative with I and 5 tuberculin u n i t s Skiagram of the chest revealed a parenchymal lesion in the right lower zone. Blood urea, blood sugar, serum electrol) tes, creatir,ine, cholesterol , and protein levels were within normal limits. Serum complement was 110% of normal. Twenty four-hour urinary albumin , sodium, and potassium excretion were within normal limits. The child was discharged on ampicillin, metronidazole and hematinics. Three days later, he was readmitted with recurrence of fever, vomiting, decreased a c t i v i t y a n d loss of interest in surroundings. The blood pressure was 110/60 m m of Hg. Detailed neurological examina.tion including fundus e x a m i n a u o n was normal. T w o hours later he developed an episode of'hypertension (BP 200]140 m m of Hg) which subsided on its own. The leukocyte counts, urine examination, blood urea, blood sugar, and serum electrolytes were within normal limits. Blood and urine cultures .were sterile. T w e n t y four hour

2"(;

.iNDIA;'q JOLIRNAL tglr I ' E D I A r R I G ~

urin~.ry catechoh, rrHne excretiun was 2.8 Hg As ti;e initial X-ray of the chest had .qLr,wn a parenchymal N:'sion, and the patient did r,,t show ;,n ndcqnate improvement, per, icillin and gent;,micin were started in piace of ampicillin. 'ihe blood pressure rec/#ded at regular intervals, was within norroal limit. On the fourth day of second admission, the child had a left focal convulsion, which was controlled by 2 mg of intravenous diazepam. The convulsion recurred a few rr~inutes later and the child lapsed lnto grade I l I coma. On examination, anterior fontanelle was bulging and blood pressure was 150190 m m of Hg. Over the next half an hour the blood pressure rose to 1 7 0 / l l S r n m of Hg. This was controlled after administration of 1 nag reserpine intramuscularly. A lumbar tap revealed turbid CSF under increased pressure wi'h 440 cf:lls/rnrnZ (all lymphocytes), q-he CSF sugar was 35 mg/dl, proteins were 416 mg/dl, and globulin levels was high. G r a m staining, arid Zeiht Neelson staining for a c i d f~st bacilli were non contributory. Bacteliological cul,nre of CSF ~zs sterile. In addition to cr.xstalline penicillin and gentamicin, the child was started on antitubercular t!~er~py, intravenous mannitol, dexameth~sone, ~nd dilantin. Over the next three days his condition did not improve. Subdural tap was negative axad ventricular t~p was within normal limits. A second spinal t*p on sixth hospital~ation day, reve,~led turbid CSF tinder increased pressure ~ith 1430 cells/ram 3 (all lymphocytes). "/-he CSF sugar was 58 mg/dl and p r o t e i n - w a s 132 mg/dl. C u l t u r e of CSF was sterile. The electroencephalogram revealed generalised low-voltage and slow-wave activity, suggestive of diffuse cerebral damage. Echoe~acephalo-

VoL. 46, Noo;~lm graphy did not show any shift of brain,:-~!! blood pressure continued tu fluctuate,,b"~ ween 90-160/50-90 mm of Hg., durlng t~il first eleven day,s of hospitalisation. Lat/~'~ stabilized around 120-130170 mm of::'.~ He was discharged on request after 20,~fl'~ of hospitalization. Discussion

The proxysmal hypertension in ~l~ infant was apparently secovd:~.ry to .,~l crea,zed intracranial tension due to m e n i r r j tis. However, other signs and sympt0im suggestive of meningitis were not pres~! initially. Episodes of severe hypertension due l l ~ increased intracranial pressure secondaryi~iB meningitis are rare. Among the five cases am systemic hypertension following increa/~j intracranial tet,sion reported by Eden a .~a]I (;977) none was secondary to meningiLI]l In many large studies on meningitill proxysmal systemic hypertension has n.li been documented eithar as the initial or ohm of the presenting menifestations (Lldani:;m al. 1974, Benkappa et al. 1975, Sehgai 1975J "/'he mechanisms of hypertension secondar~ to increased iutracranial tension are not weil understood. The clinical and experl~ mental evidences suggest the following possible mechanisms: 1. lschemia or hypoxia of medullary cen~ rers secondary to raised I.C.P., l e a d i ~ to heavy vasomotor discharge (Cushing~ 1901, Evans 1967). 2. Axial distortion of brain stem due tg pressure gradient between infratentoriaI and supratentorial compartment~ (Thompson and Malina 1959). 3. Unregulated activity of cerebral- barorr ceptors sensitive to cerebral perfusi0~ pressure (Robard and Saiki 1952).

|iblOHI AND t;JIAUI)IIARY --PARtlXYhMAI. |IY pI..'q?.'I'ENSIt)NSI~GONI)ARY 4,

Stimulation

(,f

central

neurone.s in the I)r;titt s t e m

symp,~thetic and

spi,al

cord ( R o w a n a h d .Johanst,,t~ {975} 5.

Increased

and

tmregttlated

a c t i v i t y of

o s m o r e c e p l o r s , t~:stxli;,,g its h y p t ' r v o l e t n l a ( E d e n et al. 1977). It is possible t h a t s y s t e m i c h y p r , ....... : , , , may be d u e to o n e o f these factors other r n e c h a l d s m s elucidated. Rise in

which

intracranial

occurrence

of

to be

pressure

quite f r e q u e n t l y i n c l i n i c a l p r a c t i c e associated

or s o m e

still n e e d

occurs yet

hypertensicm

the is

rarely d o c u m e n t e d , l ' a r o x y s m M n a t u r e o f h y p e r t e n s i o n m a y b e o n e e x p l a n a t i o n for this. W e suggest t h a t a c o n s t a n t v i g i l a n c e for liypertensive e p i s o d e s s h o u l d b* .,:n_.aint~ined in all the p a t i e n t w i t h i n c r e a s e d I . C . P . Referencel

Benkappa, D.G., Chandrasekhar, -r Chandra~ekhar, P., Kakkur, M., Bhargava, M K. (1'.,7.~), Tuberculous rnenil~gitis, review of 50 cases. Indian Paliatr. 12, 1161. Cushing, FI. (1901). quoted by Rowan, J.O. and Johanston, J.H. (1975). Eden, D.B., Sills, J.A., Brow,J,K. (1977) H~pertension in acute ~eurological diseases of child-hood. Dr Mtd. Child. Neurol. 19, 437. Evans, A. (1967). C.erebra] ischemia a~ a factor in vasomotor response to increased intracrat)ial pressure. Texas .~. Mad. 63, 84. Robard, b., Saiki, H. r Mechanism of pressure response to increased intracrm.ial pressure. Am..,3. Phjsioi. 168, 23~*.

297

Rowan, JO,,Johanston, l,H. (1975). Blood pressure rcspvnse to r,tised C~F pressure, 1, intracranial Pressure-It, i;dttu**--Lundbcr~, N , Po,ten. U. and Ihock, 1t. Sp~i~ger-Verlag. Berlin, p. 29g. S ',gal, tt, ~.972,~. A compata ire stndy of treatment of pyoget,ic rnet)ingitis with arJh:nicrobial therapy it, dttTereJit combination, India, I'r 9, 005. Thompson, R.K., Malina, ~. (1959). Dynamic axial r as mechanism explaining the cardiorespiratury cha~ges in increased intracranial pressure. J. Ncu~osu,g. 16, 664. Odani0 I'.M., Bhat (Parekh), U.S. (19"/4). Tul~erculosis of central nervous system-ll, Clinical a.pects, lizdian Ptdiatr. ll~ 7. Marrts, D.D.B. 0953). Recovery in partly paralysed mu.cles..]. [lone .~t. Surg. 358, t,50. Sodden, h J. (19r O, In discussion of the management of poliomye:itis: The convalescent stage. Polymyelitis, Papers anddiscuasions presented at the Filst International Poliomyelitis Conf. p. 187. Philadelphia. ~. B. L;p[;~.'c:*.. Sharrard, W.J.W. (1953}. Correlation between change in the spinal cord and mu~de paralysis in pollcmyehtis. Proc. R. Soc. Mid. 46, 346. Shatrard, W J . D..C. {1955). Muscle recovery in poliomyelitis. ~. Bo~e a,,dfft. Aurg 37. b3. Sharrard, ~,V.J.W. (J955). "Ihe distribution of the permanent paralysis in the lower hmb in poliomyelitis. .7. Bo,,r a.4d ~t. ~'urg. 37 B, 540. Sin. er, M , Roseinnes, P. (1963). The recovery from poliomyelitis. E. and S. l wingstan* Ltd.j Edinburgh, p 29. Skirlhoj, E. (1949). Some problems of acute anterior p(diomyelids and its sequelae. Copenhagen: Eiziar Mut&-gaard. Watkins, A.L. (l.q4.q). Progressive rehabilitation in po]iamyeiitis p. pets ar, d discus.'ior, at t]:.e First h.ternational Polls,myelitis Conference, p. 142, Philadelphia, ~.B. LipPincott Company.