h;d/~nft. Pe~tr. 44 :' 65, 1977
PURULENT
MENINGITIS
IN INFANCY
AND
CHILDHOOD
K. KALRA AND R . S . DAYAL
Agla Pyogenie meningitis does not spare any age in paediatric practice. The extent of the subarachnoid space and the weak bacteriotidal power of C.S.F. makes it an inevitably serious disease. Once the ordinary defence mechanism of the body is overcome and the virulent pyogenic organism gains access to the C.S.F., rapid generalized infection of the subarachnoid space may occur. Prior to effective chemotherapy, such an infection was almost invariably fatal. I f the meningeal inflammation is recognised and the causative o~ganism identified early, a dramatic improvement is observed with an optimal therapeutic regimen. Nevertheless, a significant proportion of patients of all ages still continue to die and have serious residual complications if the therapy is started late. Material
and Method
One hundred and ninety-six cases with pm-ulent meningitis treated at the S.N. Hospital, Agra (1966-69) were studied. The parents were asked for a past history of upper respiratory tract infection, otitis media, injury, small pox vaccination or any other septic focus. History regarding duration of illness and therapy administered prior to host, italization was also taken. *From the Department of Paediauics. S.N. Medical College, Agra Papez'read at 36th U.P. State Conle;'ence of Indian Medical Association, Ahgarh, 1971. Received June 10, 1976.
The clinical examination included general examination, signs of meningitis, bulging of the anterior fontanelle and neurological examination. L u m b a r puncture was also done in all the cases and the C.S.F. was examined. Observations
The children belonged to various economic groups. There were 134 males and 62 females. The youngest patient in our series was one m o n t h old and the oldest was 12 years (Table I). The clinical pictnre was quite diverse and non-specific. History of high fever of short duration was present in all except two cases. Refiasal to accept feeds, vomiting, convulsions, headache, irritability, diarrhoea, altered consciousness and pain in the neck were common presenting features. The duration of illness ranged from one to 30 days. 82% of cases presented with an acute onset (]'able 2.) Past history ol gastrointestinal symptoms and fever were present in 64 and 25 cases respectively. History of respiratory intection was present in 18, ear discharge in 12, head injury in 2 cases and repeated lumbar puncture in 4 cases. On clinical examination
all the cases
had marked toxaemia. Definite neck rigidity and positive Kernig's sign were detected in 116 cases. Bulging of the anterior fontanelle was observed in children below 2 years of age. Signs of upper
66
XNmANJOURNAL OF PEDIATRICS
respiratory tract infection were present in 68, p u l m o n a r y congestion in 22, altered consciousness in 65, otitis m e d i a in 8 and skin intection in 4 cases respectively. Fundus changes were observed in 13 cases (dilatation of retinal vessels in 7, pallor of optic disc and papilloedema in 3 cases each.) Deep tendon reflexes were exaggerated in 7, involuntary movements in 2 and hemiparesis in I case. Leucocytosis in the peripheral blood smear was present in 60~o, and polymorphonuclear leucocytosis in 77% cases (Table 3). C.S F. was under increased pressure in 176 and normal in 12 cases. T h e tension was low in 8 cases, because of thick pus in 3 and a subarachnoid block was suspected in 5 cases. T h e fluid was turbid and cloudy in 184, clear in 5, haemorrhagic in 4 and thick pus was present in 3 eases. T h e cell count of C.S.F. ranged from 2 0 0 - 8 , 0 0 0 cells/cu.mm, and 8 0 - 9 0 % of cells were polymorphs. T h e protein content was raised in 160 cases and 1 3 0 o u t o f t h e m had more than 100 rag.%. The sugar level was low in 176 and the chlorides were altered in 67 cases. S m e a r examination and culture were done in 127 cases and an organism could be identified in 70 cases. I n our series, the c o m m o n organisms were pneumococci, staphylococci, meningococci and streptococci (Tables 4, 5 & 6). O u t of 4 cases who had recurrent attacks of septic meningitis, two of them had associated hypogammaglobulinaemia. One case had a brain abscess and another developed a mastoid abscess.
Therapy Acute bacterial meningitis is a medical emergency. T r e a t m e n t must be prompt, vigorous and effe.ctive regardless of the species of organisms. All the infants and
VOL. 44, No. 350 children in this series were treated by a fairly uniform therapeutic regimen as follows: Crystalline penicillin 25,000--50,000 I.U./kg. I.M. Sulphadiazine 0.12--0.15 G./kg. (I.M., I.V. or oral) Chloramphenicol 1 0 0 m g / k g . (I.M. or oral). All the three drugs were given simultaneously. An intrathecal injection of crys. penicillin 5000-10000 I.U. diluted in 2 c.c. of distilled water was administered. T h e basic treatment was continued till the child recovered completely and the C.S.F. became clear. T h e period of therapy varied from 10-15 days. Fluid balance and nutritional requirements were adequately maintained. Sedatives were used whenever indicated. Steroids had to be given in I0 patients who were very toxic (? with low B.P.). We lost 22 cases in the present series. Seventeen of these were admitted with one to two days' acute illness before their death. (Table 7)
Discussion Meningitis is still a relatively c o m m o n disease with a high mortality. I n our series 19~/o of the cases were below the age of 3 years. A higher incidence in this age group has been reported by Achar (1953), Paul (1960), Athavale (1967) and Vashi r al. (1968). The pathogenesis of purulent meningitis has been well described by Achar (1954), Haggerty et al. (1960), Groover et al. (1961) and Hervig et al. (1963). T h e common source of infection was the pharynx, nasopharynx paranasal sinuses, p u l m o n a r y infections and p y a e m i e abscesses (skin and brain). Similar observations have been recorded by I n s a f (1964), Craigg and Bennet (1959) and Benson et al. (1960).
67
KALRAAND D A Y A L - - P U R U L E N T MENINEITI$ IN INFANCY AND CHILDHOOD
Age and sex incidence.
Table 1. Age
Male
Female
Total
0-1 Yr.
10
5
15
I-3 Yrs.
13
8
21
3-6 Yrs.
45
21
66
6-9 Yrs.
33
9
42
9-12 Yrs.
33
19
52
Table 2. Signs
Clinical signs.
No. of cases
Percentage
Pyrexia
194
99.0
Kernig's sign
116
59.2
Neck rigidity
116
59.2
Upper respiratory tract infection
68
34.7
Pulmonary congestion
22
11.2
Convulsions
37
18.8
Altered consciousness
29
14,9
Otitis
8
4.1
Pyoderma
5
2.5
10
5.1
Deep jerks exaggerated
7
3.5
Optic nerve (papilledema)
6
3.1
Hemiparesis
1
0.5
Plantar extensor response
"[able 3. Total leucocyte count
No. of cases
Haematological values. Differentia] count
No. of cases
Above 15000/cu,mm.
76
Polymorphs above 80%
86
12000-- t 5000/cu.mm. 9000-- 12000/cu.mm.
59 42
60--80% 40--60%
79 24
19
elow 40%
8
Below 9000/cu.m
68
v~7OL. 44, No. 350
INDIAN JOURNAL Or PEDIATRICS
T a b l e 4.
Cerebrospinal fluid findings. No. of cases
Feature
Tension Raised + +
40 136
Raised -tNormal
Colour
12
Low
8
Clear
5 184
Turbid Purulent
3
Traumatic
4
Leucocyte count 200-- 1000/cu. ram.
44
1000--4000/cu. ram.
73 76
Above 4000/cu. ram. Pus
3
T a b l e 5.
Biochemicalchanges in C.S.F. No. of cases
Proteins Below I00 m g . %
22
1 0 0 - - 200 mg.%
110
Above 300 rag.%
64
S~gar Below I0 mg.~o
122
10 - - 4 0 r a g . %
54
40 -- 80 mg.~
20
CMorides 6e0 -- 650 m g . %
129
650 -- 750 mg.%
(37
KALRA
AND
DAYAL--PURULENT
M E N I N G I T I S IN I N F A N C Y
T a b l e 6.
AND
69
CHILDHOOD
C.S.F. bacterial culture. No. of eases
Culture
(Total 127 cases)
a) Sterile
57
b) Positive
70
Pneumococci
19
Staphylococci
17
Meningococci
10
Streptococci
8
E. Coli.
3 13
Mixed bacterial infection
T a b l e 7. Duration of illness (days) I,ess than 3 4 - 7 8 -
15
16 -- 30
Duration of illness and therapeutic response. No. of
Cure
38
21
17
120
116
4
32
31
1
6
6
cases
The clinical picture is variable. The child m a y present with a febrile illness, generalized constitutional symptoms, headache, anorexia, vomiting, drowsiness, convulsions and septicaemia. The infants usually present with refilsal to accept feeds. Convulsions, neck rigidity, bulging of the anterior fontanelle and altered consciousness were noticed in 14.9O/o . A similar clinical picture has been observed by Chaudhuri (1958), Udani (1963), Haycock and Noble (1964), Jasper (1965) and Vashi et al. (1968).
Mortal;t,,
--
T h e aetiological agents of purulent meningitis m a y vary in different regionsand populations. I n 55% of cases the organisms could be obtained on smear or culture studies. In our series, the c o m m o n organisms were pneumococci (19), staphylococci (17) and meningococei (10). Heycock and Noble (1964) found that the causative organisms could not be isolated in 47% of cases even with the best laboratory facilities. Similarly, 42% bacteriologically negative cases were reported by Achar
70
VOL. 43, N o . 3 4 6
INDIAN JOURNAL OF PEDIATRICS
(1964). I n their series, the antibiotics had not been administered prior to hospitalization. Yu a n d G r a u a n g ( 1 9 6 3 ) r e p o r t e d that m a t e r n a l b a c t e r a e m i a led to neonatal, septicaemia a n d the organisms responsibl6 were E. coli, staphylococci, p n e u m o c o c c i , streptococci a n d IIaemophilus influenzae. Zia and H a g g a r t y (1958), Yelvin et. al. (1956) and Vahlquist (1960) also n o t i c e d the same type o f organisms in their series a n d they also reported that g a m m a g l o b u l i n levels were low in some children. A c h a r et al. (1964) found that H. influenzae was the c o m m o n e s t organism, while Paul (1960), W e b b (1961), Athavale ( 1 9 6 7 ) a n d Vashi (1968) observed m e n i n g o c o c c i as the most frequent offending agents. et al.
T h e high mortality and serious sequelae r e m a i n a continuing challenge. Despite a striking i m p r o v e m e n t in therapy a n d good prognosis with appropriate a n t i m i c r o b i a l agents, 8.6% of cases die (I-Ieycoek and Noble (1964). I n our series the mortality was 11. 2%. W e observed that a m o n g the
cases w h o reported with acute illness and m a r k e d toxaemia, especially in the younger age group, the m o r t a l i t y was high (17 out of 38). Despite some complications, viz. h y d r o c e p h a l u s and m a s t o i d abscess in one case each, the final recovery was good in all the cases.
Summary 196 cases o f purulent meningitis were studied. T h e history of aetiological factors was taken. Most of the cases presented with high fever and a classical picture o f meningitis. C.S.F. was u n d e r tension in 176 cases a n d frank pus was observed in three cases. P o l y m o r p h o n u c l e a r leucocytosis was detected in all the C.S.F. specimens. Bacterial culture was d o n e in 127 cases and organisms could be d e t e c t e d in 70. Despite some complications, viz. brain abscess, mastoid abscess and hydrocephalus, final r e c o v e r y was good. T h e mortality was high in those cases who were a d m i t t e d with acute illness a n d m a r k e d toxaemia.
Refor@naes
Achar, S.T. and Thambia. (1954). Indian ,7. Chld. Hlth 3, 218. Athavale, V.B. (1968). personal communication. Benson, P., Nyhan, W.E., Shlmisu, H. (1960). The r)rognosls of subdural effusion complicating pyogenic meningitis. 07 Pediatr. 57, 670. Craig, J. and Bennette, E.F. (1959). Menin~ococeal meningitis. Lanra, 1,248. Chaudhari, B.K. (1953). Meningitis in childhood. Indian ,7. Pediatr. 20, 15. Grover, R.V., Sutherland, J.M. and Landing, B.H. (1961). Purulent meningitis in newborn infants. New. Eng..7. Med 268, 1115. Herwig, J.C., Neal, M.K. and Jartman, (1963). Simultaneous mixed bacterial meningitis in children. ~. Pediatr. 63, 76. Haggerty. R.J. and Ziai, M. (1965). Acute bacterial meningitis. Advances in Pediatrics by Levin, S. Vol. III. P. 129. Heyeock, J.B. and Noble, J.C. (1964). Pyogenic meningitis in infancy and childhood. Br. Med a~. 1, 658.
Insaf, H.A. (196t). Clinicotherapeutic evaluation of pyogenic meningitis. LA.M.A. 53, 2')9. Jasper. P.L. and Merrill, R.E. (1965). Hydro-
cephalous and myelo-meningocoele. Am. J. Dis. Child. 10, 652. Paul, S.S. (1.q60). Pyogenic meningitis in children. Indian J. Chld. Hlth. 9 533. Pohowalla, J.M. (1956). Paper presented at VII All India Paediatric Conference, lndore 1956. Udanl, p.M. (1962). Morbidity and mortality2 Indian 7. Chld. Ilhh. I1,243. Vahlquist, B. (1960). Neonatal immunity. Am. aT. Dis. Child. 99, 729. Vashi, N. and Joshi, A. (1968). A changing pattern of purulent meningitis. Indian Pediatr. 5, 444. Walker, S.H. a~,d Colhn, C.C. (1968). Features of cephaloridine in haemophitlc influenzae meningitis. Am..7. Dis. Chdd. 116, 285. Webb, J.K. and Ahmed, I. (1961). Pyogenic meningitis infancy and childhood. Paper read a t All Asian Paed. Conf. at Delhi 1961. Yu, J S. and Grauang, M. (1963). Purulent meningitis in the neonatal period. Arch. Dis. Child. 33, 3.ql. Ziai, M. and Haggerty, R.J. (1958). Neonatal purulent met/ingitis. New Engl. J,. Med. 259,314. Veivin, R., Salzberger, M. and Olitzki, A.L. (1956). Meningitis in cHldren. Pidiatricsl8, 19.
PURULENT
MENINGITIS
IN INFANCY
AND
CHILDHOOD
K. KALRA AND R . S . DAYAL
Agla Pyogenie meningitis does not spare any age in paediatric practice. The extent of the subarachnoid space and the weak bacteriotidal power of C.S.F. makes it an inevitably serious disease. Once the ordinary defence mechanism of the body is overcome and the virulent pyogenic organism gains access to the C.S.F., rapid generalized infection of the subarachnoid space may occur. Prior to effective chemotherapy, such an infection was almost invariably fatal. I f the meningeal inflammation is recognised and the causative o~ganism identified early, a dramatic improvement is observed with an optimal therapeutic regimen. Nevertheless, a significant proportion of patients of all ages still continue to die and have serious residual complications if the therapy is started late. Material
and Method
One hundred and ninety-six cases with pm-ulent meningitis treated at the S.N. Hospital, Agra (1966-69) were studied. The parents were asked for a past history of upper respiratory tract infection, otitis media, injury, small pox vaccination or any other septic focus. History regarding duration of illness and therapy administered prior to host, italization was also taken. *From the Department of Paediauics. S.N. Medical College, Agra Papez'read at 36th U.P. State Conle;'ence of Indian Medical Association, Ahgarh, 1971. Received June 10, 1976.
The clinical examination included general examination, signs of meningitis, bulging of the anterior fontanelle and neurological examination. L u m b a r puncture was also done in all the cases and the C.S.F. was examined. Observations
The children belonged to various economic groups. There were 134 males and 62 females. The youngest patient in our series was one m o n t h old and the oldest was 12 years (Table I). The clinical pictnre was quite diverse and non-specific. History of high fever of short duration was present in all except two cases. Refiasal to accept feeds, vomiting, convulsions, headache, irritability, diarrhoea, altered consciousness and pain in the neck were common presenting features. The duration of illness ranged from one to 30 days. 82% of cases presented with an acute onset (]'able 2.) Past history ol gastrointestinal symptoms and fever were present in 64 and 25 cases respectively. History of respiratory intection was present in 18, ear discharge in 12, head injury in 2 cases and repeated lumbar puncture in 4 cases. On clinical examination
all the cases
had marked toxaemia. Definite neck rigidity and positive Kernig's sign were detected in 116 cases. Bulging of the anterior fontanelle was observed in children below 2 years of age. Signs of upper
66
XNmANJOURNAL OF PEDIATRICS
respiratory tract infection were present in 68, p u l m o n a r y congestion in 22, altered consciousness in 65, otitis m e d i a in 8 and skin intection in 4 cases respectively. Fundus changes were observed in 13 cases (dilatation of retinal vessels in 7, pallor of optic disc and papilloedema in 3 cases each.) Deep tendon reflexes were exaggerated in 7, involuntary movements in 2 and hemiparesis in I case. Leucocytosis in the peripheral blood smear was present in 60~o, and polymorphonuclear leucocytosis in 77% cases (Table 3). C.S F. was under increased pressure in 176 and normal in 12 cases. T h e tension was low in 8 cases, because of thick pus in 3 and a subarachnoid block was suspected in 5 cases. T h e fluid was turbid and cloudy in 184, clear in 5, haemorrhagic in 4 and thick pus was present in 3 eases. T h e cell count of C.S.F. ranged from 2 0 0 - 8 , 0 0 0 cells/cu.mm, and 8 0 - 9 0 % of cells were polymorphs. T h e protein content was raised in 160 cases and 1 3 0 o u t o f t h e m had more than 100 rag.%. The sugar level was low in 176 and the chlorides were altered in 67 cases. S m e a r examination and culture were done in 127 cases and an organism could be identified in 70 cases. I n our series, the c o m m o n organisms were pneumococci, staphylococci, meningococci and streptococci (Tables 4, 5 & 6). O u t of 4 cases who had recurrent attacks of septic meningitis, two of them had associated hypogammaglobulinaemia. One case had a brain abscess and another developed a mastoid abscess.
Therapy Acute bacterial meningitis is a medical emergency. T r e a t m e n t must be prompt, vigorous and effe.ctive regardless of the species of organisms. All the infants and
VOL. 44, No. 350 children in this series were treated by a fairly uniform therapeutic regimen as follows: Crystalline penicillin 25,000--50,000 I.U./kg. I.M. Sulphadiazine 0.12--0.15 G./kg. (I.M., I.V. or oral) Chloramphenicol 1 0 0 m g / k g . (I.M. or oral). All the three drugs were given simultaneously. An intrathecal injection of crys. penicillin 5000-10000 I.U. diluted in 2 c.c. of distilled water was administered. T h e basic treatment was continued till the child recovered completely and the C.S.F. became clear. T h e period of therapy varied from 10-15 days. Fluid balance and nutritional requirements were adequately maintained. Sedatives were used whenever indicated. Steroids had to be given in I0 patients who were very toxic (? with low B.P.). We lost 22 cases in the present series. Seventeen of these were admitted with one to two days' acute illness before their death. (Table 7)
Discussion Meningitis is still a relatively c o m m o n disease with a high mortality. I n our series 19~/o of the cases were below the age of 3 years. A higher incidence in this age group has been reported by Achar (1953), Paul (1960), Athavale (1967) and Vashi r al. (1968). The pathogenesis of purulent meningitis has been well described by Achar (1954), Haggerty et al. (1960), Groover et al. (1961) and Hervig et al. (1963). T h e common source of infection was the pharynx, nasopharynx paranasal sinuses, p u l m o n a r y infections and p y a e m i e abscesses (skin and brain). Similar observations have been recorded by I n s a f (1964), Craigg and Bennet (1959) and Benson et al. (1960).
67
KALRAAND D A Y A L - - P U R U L E N T MENINEITI$ IN INFANCY AND CHILDHOOD
Age and sex incidence.
Table 1. Age
Male
Female
Total
0-1 Yr.
10
5
15
I-3 Yrs.
13
8
21
3-6 Yrs.
45
21
66
6-9 Yrs.
33
9
42
9-12 Yrs.
33
19
52
Table 2. Signs
Clinical signs.
No. of cases
Percentage
Pyrexia
194
99.0
Kernig's sign
116
59.2
Neck rigidity
116
59.2
Upper respiratory tract infection
68
34.7
Pulmonary congestion
22
11.2
Convulsions
37
18.8
Altered consciousness
29
14,9
Otitis
8
4.1
Pyoderma
5
2.5
10
5.1
Deep jerks exaggerated
7
3.5
Optic nerve (papilledema)
6
3.1
Hemiparesis
1
0.5
Plantar extensor response
"[able 3. Total leucocyte count
No. of cases
Haematological values. Differentia] count
No. of cases
Above 15000/cu,mm.
76
Polymorphs above 80%
86
12000-- t 5000/cu.mm. 9000-- 12000/cu.mm.
59 42
60--80% 40--60%
79 24
19
elow 40%
8
Below 9000/cu.m
68
v~7OL. 44, No. 350
INDIAN JOURNAL Or PEDIATRICS
T a b l e 4.
Cerebrospinal fluid findings. No. of cases
Feature
Tension Raised + +
40 136
Raised -tNormal
Colour
12
Low
8
Clear
5 184
Turbid Purulent
3
Traumatic
4
Leucocyte count 200-- 1000/cu. ram.
44
1000--4000/cu. ram.
73 76
Above 4000/cu. ram. Pus
3
T a b l e 5.
Biochemicalchanges in C.S.F. No. of cases
Proteins Below I00 m g . %
22
1 0 0 - - 200 mg.%
110
Above 300 rag.%
64
S~gar Below I0 mg.~o
122
10 - - 4 0 r a g . %
54
40 -- 80 mg.~
20
CMorides 6e0 -- 650 m g . %
129
650 -- 750 mg.%
(37
KALRA
AND
DAYAL--PURULENT
M E N I N G I T I S IN I N F A N C Y
T a b l e 6.
AND
69
CHILDHOOD
C.S.F. bacterial culture. No. of eases
Culture
(Total 127 cases)
a) Sterile
57
b) Positive
70
Pneumococci
19
Staphylococci
17
Meningococci
10
Streptococci
8
E. Coli.
3 13
Mixed bacterial infection
T a b l e 7. Duration of illness (days) I,ess than 3 4 - 7 8 -
15
16 -- 30
Duration of illness and therapeutic response. No. of
Cure
38
21
17
120
116
4
32
31
1
6
6
cases
The clinical picture is variable. The child m a y present with a febrile illness, generalized constitutional symptoms, headache, anorexia, vomiting, drowsiness, convulsions and septicaemia. The infants usually present with refilsal to accept feeds. Convulsions, neck rigidity, bulging of the anterior fontanelle and altered consciousness were noticed in 14.9O/o . A similar clinical picture has been observed by Chaudhuri (1958), Udani (1963), Haycock and Noble (1964), Jasper (1965) and Vashi et al. (1968).
Mortal;t,,
--
T h e aetiological agents of purulent meningitis m a y vary in different regionsand populations. I n 55% of cases the organisms could be obtained on smear or culture studies. In our series, the c o m m o n organisms were pneumococci (19), staphylococci (17) and meningococei (10). Heycock and Noble (1964) found that the causative organisms could not be isolated in 47% of cases even with the best laboratory facilities. Similarly, 42% bacteriologically negative cases were reported by Achar
70
VOL. 43, N o . 3 4 6
INDIAN JOURNAL OF PEDIATRICS
(1964). I n their series, the antibiotics had not been administered prior to hospitalization. Yu a n d G r a u a n g ( 1 9 6 3 ) r e p o r t e d that m a t e r n a l b a c t e r a e m i a led to neonatal, septicaemia a n d the organisms responsibl6 were E. coli, staphylococci, p n e u m o c o c c i , streptococci a n d IIaemophilus influenzae. Zia and H a g g a r t y (1958), Yelvin et. al. (1956) and Vahlquist (1960) also n o t i c e d the same type o f organisms in their series a n d they also reported that g a m m a g l o b u l i n levels were low in some children. A c h a r et al. (1964) found that H. influenzae was the c o m m o n e s t organism, while Paul (1960), W e b b (1961), Athavale ( 1 9 6 7 ) a n d Vashi (1968) observed m e n i n g o c o c c i as the most frequent offending agents. et al.
T h e high mortality and serious sequelae r e m a i n a continuing challenge. Despite a striking i m p r o v e m e n t in therapy a n d good prognosis with appropriate a n t i m i c r o b i a l agents, 8.6% of cases die (I-Ieycoek and Noble (1964). I n our series the mortality was 11. 2%. W e observed that a m o n g the
cases w h o reported with acute illness and m a r k e d toxaemia, especially in the younger age group, the m o r t a l i t y was high (17 out of 38). Despite some complications, viz. h y d r o c e p h a l u s and m a s t o i d abscess in one case each, the final recovery was good in all the cases.
Summary 196 cases o f purulent meningitis were studied. T h e history of aetiological factors was taken. Most of the cases presented with high fever and a classical picture o f meningitis. C.S.F. was u n d e r tension in 176 cases a n d frank pus was observed in three cases. P o l y m o r p h o n u c l e a r leucocytosis was detected in all the C.S.F. specimens. Bacterial culture was d o n e in 127 cases and organisms could be d e t e c t e d in 70. Despite some complications, viz. brain abscess, mastoid abscess and hydrocephalus, final r e c o v e r y was good. T h e mortality was high in those cases who were a d m i t t e d with acute illness a n d m a r k e d toxaemia.
Refor@naes
Achar, S.T. and Thambia. (1954). Indian ,7. Chld. Hlth 3, 218. Athavale, V.B. (1968). personal communication. Benson, P., Nyhan, W.E., Shlmisu, H. (1960). The r)rognosls of subdural effusion complicating pyogenic meningitis. 07 Pediatr. 57, 670. Craig, J. and Bennette, E.F. (1959). Menin~ococeal meningitis. Lanra, 1,248. Chaudhari, B.K. (1953). Meningitis in childhood. Indian ,7. Pediatr. 20, 15. Grover, R.V., Sutherland, J.M. and Landing, B.H. (1961). Purulent meningitis in newborn infants. New. Eng..7. Med 268, 1115. Herwig, J.C., Neal, M.K. and Jartman, (1963). Simultaneous mixed bacterial meningitis in children. ~. Pediatr. 63, 76. Haggerty. R.J. and Ziai, M. (1965). Acute bacterial meningitis. Advances in Pediatrics by Levin, S. Vol. III. P. 129. Heyeock, J.B. and Noble, J.C. (1964). Pyogenic meningitis in infancy and childhood. Br. Med a~. 1, 658.
Insaf, H.A. (196t). Clinicotherapeutic evaluation of pyogenic meningitis. LA.M.A. 53, 2')9. Jasper. P.L. and Merrill, R.E. (1965). Hydro-
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