non traumatic coma
TRANSCRIPT
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Indian Journal of Pediatrics, Volume 72June, 2005 467
Original Article
Correspondence and Reprint requests : Dr. Sunit Singhi, Professor
& Head , Pediatric Emergency and Intensive Care Units, Advanced
Pediatrics Center, PGIMER. Chandigarh 160012. Fax No. +91-172-
2744401, 2745078
Abstract.Objective:To study the etiology and clinical profile of non-traumatic coma in children and to determine the clinicalsigns predictive of outcome. Methods:100 consecutive cases of non- traumatic coma between 2 months to 12 years. Clinical
signs studied were temperature, pulse, heart rate, blood pressure, coma severity by Glasgow coma scale (GCS), respiratorypattern, pupillary and corneal reflex, extra ocular movements, motor patterns, seizure types and fundus picture. These were
recoded at admission and after 48 hours of hospital stay. Etiology of coma was determined on basis of clinical history,
examination and relevant laboratory investigations by the treating physician. The outcome was recorded as survived or died,and among those who survived as normal, mild, moderate, or severe disability. Chi-square test and logistic regression analysis
were done to determine predictors of outcome. Results:Etiology of coma in 60% cases was CNS infection (tubercularmeningitis- 19, encephalitis- 18, bacterial meningitis- 16, others- 7); other causes were toxic-metabolic conditions (19%), status
epilepticus (10%), intracranial bleed (7%), and miscellaneous (4%). 65 children survived, 11 were normal, 14 had mild disability,
21 had moderate disability and 14 were severely disabled and dependent. Survival was significantly better in patients with CNSinfection (63%) as compared to those with toxic-metabolic causes (27%) and intracranial bleed (43%, P < 0.05). On bivariate
analysis age 3 years, poor pulse volume, abnormal respiratory pattern and apnoea, abnormal pupillary size and reaction,abnormal extra ocular movements, absent corneal reflex, abnormal motor muscle tone at admission or 48 hours correlated
significantly with mortality. Survival was better with increasing GCS (Spearman rho = .32, P < 0.001). On logistic regressionage < 3 years, poor pulse volume, absent extraocular movements and papilloedema at admission and 48 hours after admission
were independent significant predictors of death. Conclusion:CNS infections were the most common cause of non-traumatic
coma in childhood. Simple clinical signs were good predictors of outcome. [Indian J Pediatr 2005; 72 (6) : 467-473]E-mail : [email protected], [email protected]
Key words :Non-traumatic coma;Outcome variables; Glasgow coma scale
Non Traumatic Coma
Arun Bansal, Sunit C. Singhi, Pratibha D . Singhi, N . Khandelwal1 and S. Ramesh
Departments of Pediatrics and1Radiodiagnosis, Advanced Pediatrics Center, Post Graduate Institute of Medical
Education and Research Center, Chandigarh.
Non- t r auma t i c coma in ch ildhood i s an impor tant
ped iatric emergency. It can result from a wide ran ge ofpr imary et iologies. Neurologic outcome is of ten of
foremost concern to paren ts and p hysicians. It may ran ge
from absence of impa irment to severe disability or death.
Et iology of coma and clinical statu s at the t ime o f
presentation are likely predictors of outcome. A better
understan ding of causes and outcome is essential to help
improve the approach and to plan rational management
of non-trauma tic coma.
Literature on ped iatric non-trau matic coma is rather
inconclusive, as there are few system atic stud ies, and most
of these are retr ospective. Very l i t t le informa tion is
available particularly so from developing countries
includ ing India.1-3 In a prospective study the au thors have
therefore examined the et iology, clinical signs an d
severity of non-trauma tic coma in children, w ith a view to
define pred ictors of outcome.
MATERIALS AND METHODS
This prospective observational stud y was cond ucted inthe p ediatric emergency un it of a tertiary care teaching
and referral hosp ital over a p eriod of 10 mon ths. The
stud y was ap proved by Institutional Ethics committee.
Informed written consent was obtained from th e parents
/ guardian of the subjects.
Inclusion and exclusion criteria:All the children between
2 months to 12 years of age, presenting with coma were
eligible for inclusion in the study . Those w ith history of
trauma w ere exclud ed.
Demographic and c lin i ca l da ta w as r ecorded a t
adm ission. Patients were re-examined at 48 hours to
record cl inical data and at discharge to record the
outcome. The clinical variables recorded were h eart rate,respiratory rate and p attern, blood p ressure (average of
three recordings, using mercury sphygm omanometer, by
auscultatory m ethod), temperatu re, coma severity (using
mod ified Glasgow Coma Scale) , pupi l lary size and
response to light, extra ocular movem ents, corneal reflex,
postu re, motor pattern (recorded su bjectively by assessing
the passive tone) , seizure i f any, type of seizure,
involuntary movements and fundu s picture.
The etiology of coma w as determined on the basis of
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468 Indian Journal of Pediatrics, Volume 72June, 2005
history, clinical examination and relevant laboratory
invest igat ions. The invest igat ions, such as lum bar
pu ncture, CT scan an d m etabolic work-up, dep ended on
the clinical presentation and were determined by the
consul tan t in-charge. Et iology w as classi fied into
infectious, toxic-metabolic, includ ing hyp oxic-ischemic,
post -status epi lept icus, int racranial bleed and
miscellaneous.
Bacterial meningitis wa s defined as acute febrile
encephalopathy with identification of microorganisms
from the CSF cultu re or latex agglutin ins, or presence of 3
or m ore of the following abn orm alit ies in CSF (i)
polymorphonuclear leucocytosis 100 cells/ mm 3 (ii)
glucose ~ 40 mg / dl or 50% of blood su gar (iii) elevated
proteins > 40 mg/ dl (iv) micro-organisms seen by Gram
staining. Diagnosis of tuberculou s meningitis was based
on the criteria by Ahu ja et al.4 Encephalitis was d efined as
acute febrile encephalopathy with CSF pleocytosis with
lymphocyte predom inance (>5 cells/ mm 3) and absence of
bacter ia on di rect microscopy, cul ture or latex
agglutination and w here no other alternative diagnosiswas identif iable. Hypertensive encephalopathy was
diagnosed w hen coma of acute onset was associated w ith
blood p ressure more than 95th percentile for age and sex,
wi th or w i thout r e t ina l changes . When there was
metabolic derangem ent commensu rating with the clinical
picture or toxic ingestion w as confirmed, a label of toxic-
metabolic coma w as used . Coma following hyp oxic
cerebral injury such as af ter cardio-respi ratory
compromise or shock was considered to be hyp oxic-
ischem ic. Children with coma w ith evidence of bleed on
radio imaging of head were labeled as having intracranial
bleed.
Clinical variables that were found significant on chi-
square test were considered for logist ic regression
analysis. Etiology was not includ ed becau se a definitive
diagnosis was not often made at the initial examination.
Definitions of study variables w ere as follow s
Coma : A state of unresponsiveness wi thout evidence of
awareness of self or environment, a state from w hich the patient
cannot be aroused by vocal or sensory stimuli.
Tachycardia: Heart rate above the u pper limit for that age.
Bradycardia : Heart rate less than sixty per m inute.
Hypertension: Blood pressure more than 95 th centile for age
and sex.
Hypotension:Blood pressu re below 5th centile for the age an d sex.
Hyperthermia : Axillary temperature above 380C.
Hypothermia: Temperature below 350C.
Coma severity : Based on score obtained on the mod if iedGlasgow coma scale5.
Pupils: (i) normal both pu pils equal in size, 2-3 mm in diam eter
and reactive to light, (ii) abnor mal-pu pils small (= 1mm ), or dilated
(= 4 mm), unequal or non reactive to light.
Extra ocular mo vements (EOM): (i) normal - no impairment of
movem ent in any d irection, (ii) abnormal - if lateral, med ial, upw ard,
down ward or all movements of eyeballs were absent.
Corneal reflex: absent or present.
Motor patternswere recorded as norm al pattern or abnormal if
there w as diffuse decrea se in tone (flaccidity), increase in tone
(hypertonia) or decerbrate or decorticate posture6
Respiratory patt ern was said to be abnorma l if the breathing was
central neurogenic hyperventilation, apneustic, ataxic or apnoeic.6
Outcome variables:Outcome was recorded as survived and
died. Among those who survived it was further graded as norm al, or
those having mild, moderate or severe disability, defined as:
Normal: no motor deficit , ataxia, cranial nerve palsy, and
functional level back to pr e-illness state.
Mild disabili ty : minimal al terat ions of tone/ deep tendon
reflexes, isolated cranial nerve palsy and weakness of grade 4 orataxia.
Moderate disability: mod erate weakn ess (grade 3) or ataxia,
behaviour disturbance and mu ltiple cranial nerve involvement.
Severe disabil i ty: severe w eakness (grad e 3) or ataxia and
quadriplegia.
Statist ical Analysis:Descriptive statistics (frequ ency,
percentages) were calculated. The stud y variables were
analyzed for thei r associat ion w i th the ou tcome by
applying the Chi-square test, and calculation of Odds
ratio and relative risk (RR) with 95% confidence interval
(95% CI). Clinical variables that were found significant on
Chi-squa re test were further an alysed u sing logistic
regression ana lysis. SPSS 10.0 and Epinfo 1.1 statisticalpackage were used.
RESULTS
A total of 100 comatose children (65 boys, 35 girls) were
includ ed in the stud y. Fifteen patients were below the age
of 1 yr, 25 were 1-3 yr, 34 were 4-5 yr an d 26 were 6 to 12
ys old.
Central nervous system (CNS) infections accounted for
60% of the cases (Table 1). Am ong the 19 childr en
classified a s toxic-metabolic, 6 fulfilled the C enter for
Disease Controls criteria for Reyes synd rome, three gave
history of toxic ingestion and four children had hypoxic
ischaemic encephalopath y (HIE) secondary to shock
caused by sepsis (n-2) or acute diarrhoea (n-2). Seven
children had intracranial bleed because of non -acciden tal
injury, wh ich w as not susp ected at the time of adm ission.
Outcome:Thirty-five pa tients died an d 65 survived . Of
the 65 survivors, 5 left against med ical advice before the
recovery from primary illness, 10 were normal (without
any deficit), 13 had m ild disab ility, 22 wer e mod erately
disabled and 15 were severely disabled and depend ent
(Table 3)
Mortality rate was 48 % (7 of 15) amon g infants, 44%
(11 of 25) among tod dlers 1-3 years old, 74% (8 of 34)
among p reschool children, and 27.7% among children 6
12 years. None of the infants had a norm al outcome,
wh ereas 10% of toddlers, 12% of preschool an d 16% ofschool age children had no deficits at discharge. Mortality
was similar between the tw o sexes. Severe d isability was
high er in m ale children (10 of 33, 30%) comp ared to
female (5 of 27, 18.5%) whereas intermediate level of
disability w as more in female children.
Mortality with var ious CN S infections w as similar
(Table 1) but as a grou p CNS infections had significantly
better surv ival rate as compared to toxic- metabolic group
(RR = 0.5; 95% CI 0.3 to 0.9; P = 0.04).
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Indian Journal of Pediatrics, Volume 72June, 2005 469
TABLE 1.Etiology of Coma in the S tudy Population and N eurological Outcome in Relation to Etiology Amon g the S urvivors
Diagnosis Frequency No. Died No. Survived Disability
(n=100) (n=35) (n=65) Normal Mild Moderate Severe
CNS Infections: Total 60 16 (26.7%) 44 (73.3%)
Tubercular meningitis 19 5 (26.3%) 14 0 6 4 4
Encephalitis 18 5 (27.7%) 13 1 3 7 2
Bacterial meningitis 16 4 (25.0%) 12 1 2 7 2Herpes encephalitis 3 1 (33.3%) 2 0 0 0 2
Cerebral malaria 2 0 2 2 0 0 0
Rabies 1 1 (100%) 0 0 0 0 0
Multiple Neurocysticercosis 1 0 1 1 0 0 0
Toxic-metabolic 19 12 (63.2%) 7 (36.8%)
Reyes syndrome 6 5 (83.3%) 1 0 1 0 0
Hepatic coma 4 2 (50%) 2 2 0 0 0
Hypoxic encephalopathy 4 2 (50%) 2 1 0 1 0
(Secondar y to shock)
Poisoning 3 2 (66.7%) 1 0 0 0 1
Snake bite 1 1 (100%) 0 0 0 0 0
Diabetic Ketoacidosis 1 0 0 0 0 0 1
Post status epilepticus 10 2 (20%) 8 (80%) 3 1 2 2
Intra cranial bleed 7 4 (57.1%) 3 (42.9%) 0 0 2 1
Others (CNS malformations, 4 1 (25%) 3 (75%) 2 1 0 0medulloblastoma,
hypertensive
encephalopathy)
P value by chi - square amongst the patients who died= 0.025
P value by Fisher's Exact amongst th e main etiological causes lead ing to disability among
survivor s = 0.100
P value by Fisher's Exact am ongst the v arious cau ses of infections leading to disability
amon g surv ivors = 0.511
TABLE 2. Clinical Signs at Admission and at 48 Hours and Their Association w ith Survival
Variables At admission At 48 hours
Total Survived Died Odds ratio p value Total Survived Died Odds ratio p value
(95% CI) (95% CI)
Age
3 years 48 26 22 (46%)
Sex
Male 52 37 15 (29%)
Female 48 28 20 (42%)
Temperature
Normal 63 45 18 (29%) 0.125 68 51 17 (25%) 1.1 (0.3-0.9) 1.000
Abnormal 37 20 17 (46%) 15 11 4 (27%)
Hyperthermia 33 19 14 (42%) 0.315 13 11 2 - 0.057
Hypothermia 4 1 3 (75%) 2 0 2
Heart rate
Normal 33 25 8 (24%) 0.176 45 39 6 (13%) 9.5 (2.5-35.7) 0.002
Abnormal 67 40 27 (40%) 0.176 38 23 15 (40%)
Tachycardia 60 39 21 (35%) 0.015 38 24 15 (40%)
Bradycardia 7 1 6 (86%) 0 0 0
Pulse volume
Good 67 53 14 (21%)
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470 Indian Journal of Pediatrics, Volume 72June, 2005
TABLE 2. Continued
Variables At admission At 48 hours
Total Survived Died Odds ratio p value Total Survived Died Odds ratio p value
(95% CI) (95% CI)
GCSa
13 0 0 0 2 2 0 -12 0 0 0 0 0 0
11 0 0 0 2 2 0
10 0 0 0 15 13 2
9 0 0 0 2.4 (0.9-6.2) 0.034 9 9 0
8 15 13 2 13 13 0
7 24 17 7 5 3 2
6 21 16 5 5 5 0
5 13 7 6 0 0 0
4 10 6 4 0 0 0
3 17 6 11 0 0 0
Respiratory
patterns
Normal 48 41 7 (15%) 3.8 (1.31.2) 0.000 51 47 4 (8%) 13.3 (3.945.8)
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Predictors of outcome at admission
On bivariate analysis younger age ( 3 years), poor p ulse
volume, brady cardia, hypotension, modified GCS 5,
abnormal respiratory pattern and apnoea, non-reactive
pu pi l , impaired or absent ext ra ocular movements,
absence of corneal reflex and abnorm al motor mu scle tone
at ad mission correlated significantly w ith m ortality.Hyp othermia / hyperthermia did not show significant
associat ion (Table 2) . Brad ycardia had signif icant
correlation w ith m ortality (odd s rat io 13.2; 95% CI 1.6
305, P = 0.0037) as also the hyp otension (odd s ratio 5.1,
95% CI 1.5 17.7; P = 0.002). Poor p ulse v olum e w as
associated w ith death in 63.6% (21 of 33) pa tients (RR 2.2;
95% C.I. 1.4 3.5, P = 0.00003) w hile 79% (19 of 25)
children wh o had non-reacting p up il died (Table 2).
Significantly increased risk of m ortality was seen in 25
patients who had non-reactive pupils as compared to 75
patients with reactive pupils (odds ratio 11.7, 95% CI 3.6
39.7, P = 0.000008). Absen t corneal reflex and ap noea
each was associated w ith death in 9 of 10 patients with the
sign (RR 7.1; 95% C.I. 1.1 to 45.9; P = 0.0005). Survival
rate and Glasgow coma scores at admission were d irectly
proportional (Table 2) and had a significant correlation.
(Spearm an rho = 0.32, P < 0.001).
On logistic regression age < 3 years, low pu lse volume,
absent oculocephalic reflex and presence of papilloedema
at presenta t ion were the s igni f i cant independent
pred ictors of death (Table 3).
Predictors o f outcome at 48 hours
Of 35 dea ths, 21 occurred after 48 hou rs of adm ission. The
significant p redictors of death after 48 hou rs stay in
hospi tal on bivar iate analysis were simi lar to the
predictors at adm ission. These were p oor pu lse volum e,
abnormal respiratory pattern / apnoea, nonreactive
pu pil , abnorm al extra ocular movem ents, absence of
corneal reflex, and abnorm al motor tone. In add ition,
tachycardia and presence of papilloedema correlated
significantly w ith m ortality at 48 hou rs (Table 2). The
assessment of GCS at 48 hours of admission was
confound ed by various factors. Several children were
und er sedat ion and some were a l so para lyzed for
mechan ical ventilation. Use of diazepam infusion for
status epilepticus ha d also mad e assessment of GCS
dif f icul t . GCS score could be obtained at 48 hrs of
adm ission in only 51 patients.
Of 16 patients with p oor pu lse volume at 48 hours 14
(87%) died ; this accounted for two-third of all dea ths after
48 hou rs (RR 7.2; 95% CI 2.0 to 26; P =
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3). Poor pulse volume at admission was associated with
mortality in abou t two third of patients; and of those who
survived, 81.8% had mod erate or severe d isabil ity.
Neurodef i c i t s amongst surv ivor s had s igni f i cant
correlation w ith low GCS, both at ad mission (OR 0.554,
95% CI 0.355 0.864, P = 0.009) and at 48 hou rs (OR
0.742, 95% CI 0.583 0.945, P = 0.016).
DISCUSSION
Pediatric coma has been for long an enigma w ith only few
stud ies and inconclusive informa tion. This stud y fills in
the gap of a prospective observational study from India.
In add ition to d emograp hic variables and etiology, two
sets of clinical signs as prognostic indicators of coma w ere
studied. First set includ ed v ital signs and second set
consisted of sp ecific neu rological signs that a ssessed
integrity of cerebral hemispheres and bra in stem.
In comatose patients, evidence of widespread dam age
of brain stem or cerebral hemispheres at onset usually
pred icts death or severe d isability. Therefore clinical signsthat reflect extent and severity of dysfunction of cerebral
hemispheres and/ or brain stem w ere studied. Glasgow
Coma Scale (GCS) Score reflects the integrity of cerebral
functions. Eye movements (in response to vestibular
stimulation), pu pillary responses, and corneal responses
primarily express functions regulated by the brain stem.
Breathing pattern and signs of abnormal tone of limbs
and postu ring indicate the extent and severity of cerebral
hemisphere as well as brain stem d amage.
I t was observed tha t CNS infec t ions were the
common est cause of non-traum atic coma. This is also
supp orted by other studies,7, 8 wh erein infections of the
CNS were found to be the l eading causes of non-traum atic coma in children (Table 4). How ever, the type
of infection seems to vary in different regions. Cerebral
malar ia was common in Afr ica 9, whereas dengue
haemorrh agic fever was an importan t cause of coma in
South-East Asia.2 The imp ortance of infective etiologies in
children is in sharp contrast to adu lt-hospital based series
where degenerative and cerebrovascular p athologies
predominate.10 Among the non-infectious causes, toxic-
metabolic causes were the commonest and were also
compar able in frequency w ith other stu dies (Table 1). In
series from U.K.7 and Nigeria8 status epilepticus was th e
second commonest cause contributing to m ore than on e
fourth of cases of non-traum atic coma; in contrast, it was
seen in only 10% of cases in the p resent stud y.Th e overall mortality of 35% was slightly h igher as
compared to other pediatric hosp ital based series, (26.7%)
from Nigeria8 and Canada.1 This was possibly due to
presentat ion later in the n atural history of disease.
How ever, mortality was considerably lower than th at
reported in adu lts; their mortality rates being 60% and
neu rological intact sur vival rates 10%.9
Mor ta l ity r a t e among chi ldren un der 3 yr s was
significantly higher in th e present stu dy. It was related to
higher frequency of toxic-metabolic causes, intracranial
bleed and higher mortality with CNS infections. The
inciden ce and ou tcome of coma was not associated w ith
gend er. Seshia and Seshia1 also did not observe any
significant difference in the incidence of coma between
the tw o sexes. Earlier studies11 had show n a greater mor-
tality in male (42%) compared to female children (20%).
CNS infection grou p fared significantly better than the
toxic/ metabolic group. In the stud y by Seshia et al,11 these
two group s had a similar outcome with four deaths.
Amon g survivors of CNS infections in the p resent stud y,
only one third h ad a norm al outcome or mild disability.
Severe d isability was seen in about 23% of patients. This
is in contrast to other pu blished studies wh ere 59% and
74% of the infec t ious grou p had a good outcome
compared wi th 36% and 47% respect ively in the
metabolic group.12, 13
It is believed that prognosis in coma depends on its
severity but there is rather inconclusive data on the use of
GCS score and i ts predictive value in ped iatric non-
traum atic coma. In the p resent study th e mod ified GCSrecorded at adm ission had significant association with
outcome; mortality rates progressively increased with
decreasing GCS.
Contrary to comm on belief,fever at admission or its
continuing p resence at 48 hours after hosp italization was
not associated with high er r isk of mortali ty or poor
neurological outcome. On the other hand hypothermia
spelled poor pr ognosis, but the nu mber w as too small for
any m eaningful conclusion. In the series by Johnson and
Seshia,11 al l t he 13 hypothermic ch i ldren d ied .
Hyp othermia, regardless of etiology causes diminished
cerebral metabolism and very low temperature may
result in an isoelectric electroencepha logram.14
All the signs ofcirculatory instability pred icted higher
mortality and p oor neurological outcome. Poor pulse
volume at admission and at 48 hours p redicted two-thirds
of all dea ths. Further, 81% of 11 survivors w ho had a p oor
pu lse at adm ission had mod erate or severe neurod eficits.
Bradycardia had a very high association with mortality;
six of seven pa tients with bradycard ia at admission died.
Tachycardia was also associated with increased risk of
death and poor neurological outcome wh en compared
wi th a normal hear t r a t e . No s tudy r epor t ing on
pred ictive value of heart rate in the p rognosis of a non-
traum atic coma in children .
Hypotension was a poor prognostic sign; two-third of 18
chi ldren w ho were hyp otensive at adm ission died.Further, all the survivors of hypotension except one, had
mod erate or severe neu rological deficit. This is similar to
the stud y by Johnston and Seshia11, wherein 14 of 15
hyp otensive children died . Interestingly, the r isk of
mor tal i ty and n eurological def ici t s was simi lar in
hyp er tensive and norm otensive pat ients. This data
supports the view that acute hypertension in comatose
pat ients may be neuro p rotect ive and should not be
brought down.
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Indian Journal of Pediatrics, Volume 72June, 2005 473
Various abnormalities in respiratory pattern may be seen
in coma depending on the region of brain involved. It was
therefore expected that an abnormal breathing p attern
would predict a poorer outcome. The p rognosis was best
wi th a norma l r esp i r a tory pa t t e rn wh i le apnea a t
adm ission had highest risk of mortality. This is similar to
a study f rom Canada 11 in which about 60% of apneic
children d ied. Abnorm al breathing pattern including
apneust ic, ataxic, Cheyne-Stokes respi rat ion or
neurogenic hypervent i lat ion, also had signif icant
association with increased mortality and m oderate to
severe neurological disability.
Pupillary signs were very good p redictors of survival
and neurologic outcome. Non- reac t ive pupi l s a t
adm ission as w ell as at 48 hours were strong p redictors of
a fatal outcome. In th e stud y by Seshia et al 68% of
children w ith f ixed d ilated p up ils for more than 2 hr
died1. Ogunm ekan m ade similar observations in a large
retrospective stud y from Nigeria.8 How ever, it should be
app reciated that abou t one-fourth of children with non -
reactive pupils may survive.Neu rological outcome an d d isability also correlated
with abnormality of pupillary size. Severe deficits were
seen in 28% of those with u nequal reacting p up ils, and in
18% of those with equ al reacting bu t dilated pup ils.
Presence of the corneal reflex indicates functional
interconnections in the pons. Absent corneal reflexes in
children w ith deep coma prognosticated a poor outcome.
Presence of dolls eye m ovemen ts sug gests intact
interconnections between cranial nerve n uclei III, IV and
VI via the medial longitudinal fasciculus and intact
vestibular inp ut to this system. Asymmetrical or p artial
absence of eye movemen ts therefore, generally indicates
asymm etrical brain stem lesion in mid brain or pons while
complete absence of dolls eye movem ents sug gests
bilateral structural brainstem abn ormality or severe
metabolic-toxic enceph alopathies.
In the presen t stud y, 80% of children , with preserved
EOM at presenta tion, survived wh ereas, 54% of childr en
wi th absent EOM died . Non e of the ch ildren w i th
impai r ed eye movement s had normal neurologica l
outcomes; all of them had mod erate to severe disability
and were n ot capable of self-care. This goes with the
earlier stud ies that suggest absent or impaired EOM as a
sensi t ive index for prognost icat ing the outcome.
Preserved EOM have been associated w ith favourable
outcome in previous studies.8, 10 Seshia et al11 observed that
67% of children who had normal EOM recovered and 16%died; in contrast, all those with absent EOM died and
needed assisted ventilation.
In the present study, abnormality of motor pattern was
pred ictive of higher risk of death . Interestingly, it was
f laccidi ty that was associated wi th higher r i sk as
compared to hyp ertonia. This was similar to findings of
Seshia et al1who observed that 84% of those with a normal
motor pattern had a normal ou tcome w hereas 82% of
those who were flaccid died .
The present study shows clinical signs such as poor
pu lse volum e, absent EOM or non-reactive pup ils were
strong pred ictors of death or severe hand icap following
severe non-traum atic coma. The stud y also reaffirms that
clinical variables and GCS score rema in the m ost read ily
available tools for assessmen t of non-traum atic coma, to
identify those who are likely to die and those having the
greatest potential for recovery. This is particularly help ful
in resou rce-limited countries for d irecting th e limited
resources for maximal benefit.
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SYMPOSIA SCHEDULE FOR 2005
Title Guest Editor(s)
Fest-Schrift for Late Dr. P.M. Ud ani (Apr) V. Udan i (India)
Common Pediatric Surgical Problems-II (May) D.K. Mitra (India)
Pediatric Cardiology-I (June) Anita Saxena (India) and P.S. Rao (USA)Pediatric Cardiology-II (July) Anita Saxena (India) and P.S. Rao (USA)
Nephrology Arvind Bagga (India)
Newer Diagnostics A. Sibal (India) and I.C. Verma (India)
New Drugs Antibiotics Arvind Taneja (India) and Ashir Kumar (USA)
Gastroenterology & Hepatology N.K. Arora (India) and Anil Dhawan (USA)
Developmental and Behavioral Disorders Nand ini Mundkur (India) and D.R. Patel (USA)
474 Indian Journal of Pediatrics, Volume 72June, 2005
ARTICLES APPEARING IN FORTHCOMING ISSUES
Cost of Pediatric Services in Public Sector Setting in India :A. Krishan, N.K. Arora, C.S. Pandav et al
Patterns of Development in Young Children w ith Autism : P. Malhi and P. Singhi
Hepatitis B Vaccine in the EPI Schedule :A.K. Jain, S.K. Mittal, S. Ramji and A. Chakravarti
Blue Babies : Whom to Intervene? :Savitri Srivastava
Fetal Echocardiography : Where are We? :Anita Saxena and N . Reeni
Supraventricular Tachycardia :Michael J. Kantoch
Current Perspectives on Kawasaki Disease :Monesha Gupta-Malhotra and P. Syamasunder Rao
Pituitary Adenoma in Childhood : S.K. Singh and R. Aggarwal
Neural Tube Defects in a Tertiary Care Hospital :B. Mahadevan and B. Vishnu Bhat
Helicobacter pylori and Recurrent Pain Abdomen :Niranjan Biswal, Vikram Kate, P. N alini et al
Quality of Life in Children with Sickle Cell Hemoglobinopathy :Archna B. Patel
Physical Grow th and Nutritional Status of School Going Girls of Pauri, Garhw al :R.N. Vasishat et al