Download - Non Traumatic Coma

8/4/2019 Non Traumatic Coma

1/8

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


2/8

Arun Bansal et al

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).


3/8

Non Traumatic Coma


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%)


4/8

Arun Bansal et al


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)


5/8

Non Traumatic Coma


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 =


6/8

Arun Bansal et al


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.


7/8

Non Traumatic Coma


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.

REFERENCES

1. Seshia SS, Seshia MMK, Sachdeva RK. Coma in childhood .Dev

Med Child Neurol 1977; 19 : 614-628.

2. Sofiah A, Hussain HM. Childhood non-traumatic coma inKuala Lumpu r, Malaysia.Ann Trop Pediatr1997; 17 : 327-331.

3. Nayan a Prabha PC, Nalini P, Serane VT. Role of Glasgow

Coma Scale in ped iatric nontrau matic coma. Indian Pediatr

2003; 40 : 620-625.

4. Ahuja GK, Mohan KK, Prasad K, Behari M. Diagnostic criteria

for tuberculous meningitis and th eir validation. Tuber Lung Dis

1994; 75 : 149-152.

5. Kirkham FJ. Non-traumatic coma in children.Arch Dis Child

2001; 85 : 303312.

6. Plum F, Posner JB. The Diagnosis of Stupor an d Coma. 3rd edn.

Philadelphia; FA Davis CC; 1980.

7. Vijayakum ar K, Knight R, Prabhakar P, Murphy PJ, Sharples

PM. Neurological outcome in children with n on-traumatic

coma ad mitted to a regional paediatric intensive care unit.

Arch Dis Child2003; 88: A30-32.

8. Ogunm ekan AO. Non-traumatic coma in childhood: etiology,clinical findings, morb idity, prognosis and mortality.J Trop

Pediatr1983; 29: 230 232.

9. Matuja WB, Matekere NJ. Causes and early prognosis of non-

traumatic coma in Tanzania. Muhimbili Medical Centre

experience. Trop Geogr Med1987; 39: 330-335.

10. Bates D, Caronn a JJ, Cartlidge NE, Knill Jones RP, Levy DE,

Shaw DA, Plum F. A prospective study of nontraum atic coma:

methods and results in 310patients.Ann Neurol 1977; 2 : 211

220.

11. Johnston B, Seshia SS. Prediction of outcome in non-traum atic

coma in childhood.Acta Neurol Scand1984; 69 : 417427.

12. Tasker RC, Matthew JD, Helms P, Dinwid die R, Boyd S.

Monitoring in non-traum atic coma. Part I: invasive intracranial

measurements.Arch Dis Child1988; 63 : 888-894.

13. Ishikawa T, Asano Y, Morishima T, Nagashima M, Sobue G,

Watana be K, Yama guchi H. Epidem iology of acute childhoodenceph alitis. Aichi Prefecture, Japan, 1984-90.Brain Dev 1993;

15 : 192-197.

14. Holbrook PR, Fields IA. Drowning and near d rowning. In

Holbrook PR, ed. Textbook of Pediatric Critical Care. WB

Saunders Co., Philadelphia, PA, 1993; 91-93.


8/8

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)


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

Download - Non Traumatic Coma

Top Related