UNPUBLISHED MEDICAL CONCEPT--2

CHILD'S BRAIN &MOTHER'S THYROXIN:
THE NEUROLOGICAL DEVELOPMENT IF HUMAN BRAIN GREATLY DEPENDS UPON THYROXIN HORMONE,IS AN ESTABLISHED FACT.THE DEVELOPING EMBRYO GETS ITS BLOOD SUPPLY,FROM MOTHER WHOSE THYROXIN LEVEL IN BLOOD SHOULD BE ADEQUATE THERE ARE MANY PREGNANT MOTHERS LIVING IN MANY VILLAGES,DRINK WATER WITH LESS IODINE, MAIN SOURCE OF WHICH IS WATER &SALT.AS A RESULT IF AN EMBRYO IS GROWING IN A BLOOD DEPRIVED OF IODINE WILL RESULT IN THE NEURAL TISSUE DEVELOPEMENT BEING QUALITATIVELY AFFECTED.UNLESS THE BLOOD LEVEL OF IODINE ARE MONITORED THRICE DURING PREGNANCY HYPOTHYROID STATE DEVELOPING BECOMES INEVITABLE.A BABY BELOW SUB CLINICAL LEVEL OF THYROXIN WILL NOT APPEAR LIKE A CRETIN,BUT WILL HAVE POOR ACADEMIC PERFORMANCE&ALSO EXHIBIT EVIDENCE OF LOWERED MENTAL MOTOR MILESTONES

ADHD-UNPUBLISHED CONCEPT

THE POSTULATED CAUSE IS METABOLIC DISORDER,IN A LOCALISED AREA OF THE BRAIN-THE PRE-FRONTAL CORTEX.BUT AT WHAT AGE(IMMEDIATE POSTNATAL?)IS NOT CLEARED BY INVESTIGATERS.ACTUALLY THIS IS A BEHAVIURAL DISORDER &THERE IS A NEURELOGICALLY DISORDERED MECHANISM SPREAD ALL OVER THE BRAIN,A CHILD'S DISORDERED BEHAVIUR IS NOT CONFINED TO ANY ONE CNS AREA DAMAGE..IT INVOLVES VISION HEARING ,MOTOR FUNCTION,SENSORY,CRANIAL NERVE FUNCTIONSWITH COORDINATION.SUCH WIDE SPREAD DISORDER IS POSSIBLE WITH MEASLES,.THIS CAN NOT BE PROOVED BY EEG ALSO.BUT ULTRAMICROSCOPIC CHANGES DUE TO BRAIN ENVIRONEMENTAL INTERFERENCE,BY VIRUS DRUGS ,INTRA,OR EXTRAUTERINE CAUSESCAN VERY WELL PRODUCE ADHD.THEREFORE IT IS POSSIBLE TO PREVENT THIS DISORDERBY IMMUNISATION,&NO MULTIPLE VACCINATION AT SINGLE SITTING,AS IT CAN CAUSE MICROSCOPIC INTRA-CRANIAL HEAMORRHAGES.BETTER NEONATAL RESUSITATIONIS NECESSARY,AS VERY MINIMALAPHYXIA NEONATORUMCAN ALSO CAUSE ADHD.

UNPUBLISHED MEDICAL CONCEPTS

1) YAWNING-A CLINICAL SIGNIFICANCE.
FROM FOETUS TO FATHER,ALL OF US YAWN MANY TIMES DURING OUR LIFE TIME .VARIOUS POSTULATIONS MADE .SOME ARE:1) OXYGEN LACK, 2) CARBONDIOXIDE ACCUMILATION IN THE BLOOD. 3)AN INVOLUNTARY ACT. 4)NEUROCHEMICAL TRANSMITTERS AFFECTING THE BRAIN TISSUE.5)ASSOCIATED WITH SEIZURE DISORDER LIKE EPILEPSY.6)AN EXPRESSION OF BOREDOM DUE TO PSYCHOLOGICAL DECOMPRESSION.7) A WAY TO REGULATE THE TEMPERATURE OF BLOOD CIRCULATING IN THE BRAIN8)EVEN COMPARED TO AN AIR COOLED ENGINE RADIATER AS IF AN YAWN IS ATHERMOREGULATER.

A U T H E R 'S C O N C E P T:

THOUGH THIS IS ALSO A CONCEPT, THIS CAN NOT BE DISMISSED UNLESS DISPROOVED
BY CERTAIN LAB STUDIES, SPECIALLY BACKED BY E.E.G. STUDIES, DURING WAKEFULNESS,DURING SLEEP, DURING YAWNING.FOLLOWING SCIENTIFICALLY PROOVEN FACTS CAN BE CONSIDERED TO UPHOLD THIS CONCEPT.
A) THIS IS A SLEEP RELATED PHYSICAL SIGN.B)A SIGN RELATED TO BRAIN STIMULATION BY VISION,HEARING,OR BOTH.C)A PREMONITARY SIGN PRIOR TO SEISURE DISORDER . IN ALL THE ABOVE,THERE IS DEFINITE CHANGE OF PATTERN OF E.E.G.,SPECIALLY THEETA WEAVES.

REFERENCES AVAILABLE TO THE EFFECT THAT THERE IS A 30% INCREASE IN THE HEART RATE AFTER YAWNING. BUT BEFORE &DURING YAWNING IT IS MOST LIKELY TO BE 30%LESS CONFIRMING,THAT THE ACT OF YAWNING ITSELF, IS NOTHING BUT A NEURALOGICAL MECHANISM THAT ARRESTS CIRCULATION FOR FEW SECONDS THEREBY PROOVING THAT THERE IS AN ELEMENT OF ELECTRICAL DYSRHYTHMIA
WHICH CAUSES YAWNING & IS AKIN TO A SEISURE DISORDER MOST OFTEN FOLLOWED OR PRECEDED BY SLEEP &CAN BE CONFIRME BY 24 HOUR E,E,G. YAWNING ITSELF IS CONSIDERED BY MANY CLINICIANS AS A VARAENT OF AN EPILEPTIC EQUIVALANT.YAWNING AS A PREMONITARY SIGN OF EPILESY IS WELL DOCUMENTED.

,

AIDS-CONTINUED

AIDS-- CONTINUATION ..


103) HIV LIVING ON THE EDGE OF EXTINCTION
BUT FOR ITS SPREAD TO CITIES IN PERFECTION
DISEASE PREVENTION MOST IMPORTANT
'REUTERS'&'NATURES' REPORT PROVES POTENT.


104)AIDS PANDEMIC RESEARCHERS SAY
DUE TO GENETIC SEQUENCE OF HIV-1 GROUP-M ASSAY
MUTATIONS ACCUMULATE IN HIV ORIGIN
FIRST BEGAN SPREADING FROM 1908TO CARRY ON GENE


105)AIDS ANCESTORS 100 YEARS OLD
SPREAD VIA CHIMPANZEE HUMAN BOLD
HIV INFECTED PEOPLE 33 MILLION
HIV-KILLED PEOPLE 25 MILLION


106)ZIDAVUDINE &ACYCLOVIR FIRST
ZIDAVUDIN&INTERFERON ALPHA NEXT
ZIDA& I V IMMUNOGLOBULIN BEST
DRUG COMBINATION ESTABLISHED JUST.


107)MONTHLY IVIG PROLONGED SURVIVAL
ALSO INCREASED INFECTION FREE REVIVAL
PNEUMOCYSTIS CARNI TRIMETHOPRIME TREATED
SULPHA METHOXAZOLE COMBINATION BEST SUITED.


108)HIGH PCP PROPHYLAXIS FOR CHILDREN UNDER SIX
DEPENDING UPON AGE&T4 CELL COUNT DOSE FIXED
NEBULISATION WITH AEOROSOLISED PENTAMIDINE IS ALTERNATIVE
DAPSONE +TMP CONSIDERED SUPERLATIVE

Case Report

Dr. P. Selvaraj

Consultant paediatrician,

S.R.M Speciality Hospital

RAMAPURAM.

Chennai – 89

TUBERCULOUS ACUTE ON CHRONIC LARYNGO TRACHEO BRONCHITIES

1. Abstract:-

A case of upper respiratory infection due to tuberculosis is presented. In children the usual manifestation is cough with ( or ) without fever and loss of appetite. This 12 year old child presented as whooping cough. Clinical, Radiological, Immnunological, findings along with family History, childs previous history, point towards tuberculous etiology.

2. Keywords

Primary complex, Mx Test, pertussoid cough, spasmodic cough, lymph node biopsy deseminated tuberculosis, TB Meningo encephalitis.

3. Introduction

In children primary complex is usually diagnosed by X- ray chest and Mantoux test along with clinical History of fever, cough and loss of appetite. This child presented as whooping cough, which is unusual in 12 year old child. The article aims at finding out etiopathologically, the causative agent with reasonable supportive findings.

4. Case Presentation

A 12 year old female child weighing (25 kg) looking very much with emaciated face and all four extremities. Presenting complaint was severe cough, spasmodic in nature, ending in the vomiting. Child used to get this 10-15 episodes perday. There was no other complaints, (or) positive physical findings during cough episodes except child’s supra sternal space indrawing was very unusually deep.

5. Previous History:-

Child had fever, cough, positive X- ray findings and treatment for primary complex with single drug regimen Rifamycin 3 years.

6. Family History:

Grand mother is having cough with productive sputum for last 10 years.

7. History of present illness:

Child was having cough and fever for 5 years since repeatedly. Diagnosed as primary complex and treated with Rifamycin. Cough subsided after 6 months. But the general condition went on deteriorating and now having pertussoide cough with frequent episodes in the last 6 months.

8. Clinical exam:

Thin looking individual. Throat NAD, Chest NAD, pertussoide cough still present and not amenable for conventional cough remedies. Has spasmodic cough suggestive of laryngo tracheo bronchitis. Chest clinically normal.

9. Investigations:

X- ray chest normal, mantaux test positive more than 25mm, TC – 8,000

DC

P- 42%

L-57%

E-1%

ESR – 1 hour 46mm

10. Discussion:-

Tuberculosis is still rampant in India, so the incidence of primary complex is also not reduced in the past 3 decades. Dr. P.M. udhani of Bombay was one person who has done maximum number of Histo pathological examination of tissues (lymphnodes mainly), from the paediatric patient’s of tuberculosis 4 decades back. He was only one in India who has made tissue pathological diagnosis in peadiatric tuberculosis to a maximum number. Primary complex can not only affect the pulmonary tissue but also lymphoid tissue in tonsils and the respiratory tract including soft palate, Vocal card, larynx, trachea, Bronchi, bronchioles and all regional lymphnodes and wherever there is increased lymphatic flow. Tuberculosis not only affect the respiratory system where it is known as primary complex in children. It also affect all other system in the body in peadiatric age group, most probably the central nervous system and the liver. In the yestear years disseminated tuberculous and tuberculous meningo encephalitis was often diagnosed. Now it is said to have reduced due to the use of B.C G vaccination. In the International scene India, Malaysia, Singapore, are practicing B.C .G Immunisation in the neonatal states.

1. The inability to eradicate tuberculosis in India is due to drug resistance type of organism (INH reistance)

2. B.C.G Vaccine in not prepared from INH resistant strains of AFB.

3. Pulmonary& tuberculosis with cavity, consolidation, atlectasis must be removed surgically & is being practiced only in the Armed forces India- (Lobectamy, segmental resection, plurectomy are all unheard in most Civil hospital practices) Children with laryngeal tuberculosis almost always have cavitary pulmonary diseases. ( Nelson) our case didn’t have cavitary lesion in lung.

Differential diagnosis:-

Any infection ( Virus/ Bacteria), growth, foreign body or any respiratory allergen, that causes branchial hyper reactivity (or) mucus membarane irritation anywhere is the larynx, trachea can cause this condition.

Bronchi & bronchioles can produce spasmodic pertussoid cough which may result in complete suffocation demanding emergency tracheostomy.

1. Diphtheria: Though the clinical picture is same in all the above pathological process this infection usually produces a membrane like picture over, Tonsils, cricoid, vocal cords, sometimes with haemorrhagic spots. If larynx is involved, tracheostomy often required.

2. H. Influenza Laryngitis: only throat swab can establish diagnosis

3. Viral: Usually acute in onset, preferably during epidemics with change of voice to brassy cough.

4. Pertussis: Age, history of non immunization & throat swab culture can clinch diagnosis. Typical cough in under 5 year child is often diagnostic.

Causative Viruses: Myxovirus, Para influenza

Type I: Measles Virus

Bacterial Agent: Strepto, Staphylo, H Influenza, Tubercle bacillus, : Except AFB all others generally produce acute symptoms. AFB can produce laryngo tracheal stenosis, causing repiratory stridar is a chronic disease with acute exacerbation now & then till disease is cured. When there is a scar in the trachea due to late treatment, symptoms may persist till surgical intervention which may cause further worsening.

Diagnosis:-

Following are positive findings towards diagnosis of this case.

1. Family History (grand mother) suffering from chronic pulmonary disease with productive cough even today since 10 years

2. Presently symptomatic with whooping cough like episode ending in vomiting

3. Clinically looks emaciated

4. Child’s chest X- ray & (primary complex – segmental collapse) taken 5 yrs back& treatment with Rifamycin for 3 yrs only with Rifamycin on & off is insufficient.

5. Mantaux test positive > 25mm now.

Case 2

50 yr old lady. In highly affluent society has cough on and off- 10 yrs, with more severity with expectorations – 5 yrs having spasmodic cough like whooping cough ending in vomiting after a repetitive succession of short coughs. Since – 1 month, not relieved by conventional therapy including steroids seen by well qualified super specialists. She was never investigated O/E Throat NAD looks healthy. Chest minimal wheeze x-ray chest : a) Rt interlobar effusion b) increased translucensy upper zones . c) completely opaque at lower zones sputum for AFB, Concentration method: AFB – positive 6n questioning father has PT being treated.

She was advised 1) inj SM – 45 2) ethambutol 600mg x OD 3. Rcin 600 x OD

The pertussoid cough is under control after 15 inj of SM + R cin + ET + Liv52

Discussion: Formerly all cases of haemoptysis were labelled as PT. Many inclined to see pertussoid cough as LTB of viral etiology & kock’s etiology often went unnoticed & unrecognized caseation is not noticed in our two cases. The author has not seen pertussoid cough in many cases of pulmonary caseation in military Hospital Aundh – Poona ( now military cardio – Thoracic center Golibar maiden Poona). Perhaps in the years to come, Acute on chronic LTB may be the order of the day for chronic Tuberculosis of Respiratory tract.

Treatment:

Being treated with following regimen

Inj. Streptomycin + Rifamycin + ethambutal + Pyrazinamide

↓

(45 Injection)

Prognosis: Child is almost

50%Asymptomatic after 2 weeks therapy

Conclusion

Two cases of Acute on chronic laryngo tracheo bronchitis diagnosed based on family history presenting symptom & supportive radiographic findings. This is an unusual presentation of TB as LTB

Summary

Two cases of Tuberculosis or respiratory system presenting as LTB reported. The unusual findings in pertussoid cough in both cases. But for this they may not have met the doctor, who must be highly kock’s Conscious. In the child, positive mantoax, old X-ray & family history of TB were enough. In the adult X-ray, sputum & family history of TB were positive & enough to clinch the diagnosis. It is this authors personal experience that Inj. Streptomycin should be added to all cases of TB including primary complex if we don’t want future complications. The lesson learnt from these two cases in cough suppressants can work only upto certain limits. When the roof cause is not eradicated, cough will continue & take a different “avatar” – the pertussoid cough demanding for efficacious treatment.

References:

1. Disease of the ear, nose throat:

Fourth editon, them ballentyne & Jhon Groves Bufferworths

2. Short practice of otolaryngology – 3^rd edition by prof KK Ramaligam et al ( page 276)
3. Waldo E Nelson 14^th edition 1992

Tips for practicing pediatricians

1)Be calm in a situation with a calamity.
2)patiently listen to parents version of ailment.
3)Do not jump into conclusions.
4)Take time to think.If required refer book quick..Give assurance that it can be cured
5) Also forget not to mention that it is God who makes final decision.
6)Tell your job is to "give medicine &bandage to the injury.It is God who heals the wound"
7)Some young kids may in an uncomfortable situation &end up in vomiting.
console the parents.SAY THIS MAY HABITUALLY RECUR.&NOT A CONCERN FOR WORRY.
8)In a sturdy 5 year old ,in an uncooperative child,venflon fixing may be extremely difficult..Try butter fly needle to give dose of diazapam ,i.v.to sedate,or wrap the child with a blanket to immobilise the lower extremities.Venesection may also be considered in a critical case like scorpion sting with peripheral circulatory failure.
There are many more tips.If required can consult me-mobile:9841354335.

PEDIATRIC-OPHTHALMOLOGY

PEDIATRIC – OPTHALMOLOGY

EYE SIGNS IN PEDIATRICS

DR. P.SELVARAJ MD. DCH.,
CONSULTANT PEDIATRITIAN
SRM GENERAL HOSPITAL
RAMAPURAM
CHENNAI – 600089 TAMILNADU

ABSTRACT:

In a busy general practioner’s office practice, inspection of eye can be often missed, unless the patient’s complaints point towards eyes. 19 clinical conditions can be diagnosed by inspection of eyes alone if one includes eyes also in the cursery exam. All conditions discussed briefly.

KEY WORD:

· Bitots Spots
· Keratomalasia
· Film star Eyelashes
· Cretinism
· Leukocoria
· Down’s syndrome
· Cataract
· Kayser – Fleischer ring
· Phlectan
· Hydrocephalus
· Naso lacrimal duct obstruction
Aim:
To focus important ‘Eye Signs’ on naked eye examination by inspection alone. Commonest conditions met in the day to day practice while dealing with the children is emphasized. Only external & surface manifestations on the eyeballs are considered. Internal, retinal, optic disc manifestations & ocular syndrome manifestations are not aimed at. It is hoped that this article may be found also useful for a paediatric post graduate/ undergraduate student both for exam point of view & practical usability.

Introduction:

“Eyes don’t see what the mind doesn’t. Therefore it is important that a clinician remembers to look into eyes of children whenever and wherever necessary as a routine examination. Many important diagnosis can be missed if eyes are not looked into. Eye is only a small part of the body reflecting great pathological – events taking place inside body as a whole sometimes very early and sometimes late. Though it is late its significance may be great. (Eye is said to be the window of the brain. This is mainly true with regard to fundus specially during seizure episodes to assess evidence of raised intra- cranial tension where there is a blurred disc margin on fundus examination by opthalmoscope.)

1.Clinical Conditions:

Nineteen important clinical signs pertaining to various clinical –Pathological states are discussed, in brief. Their significance is not only helpful for diagnosis and treatment, but can also alert a physician a possible and impending risky situations likely to be met by the practicing physician during busy hours leading to medico- legal implications.

Vitamin A deficiency – due to nutritional deficiency. The conjunctive of sclera are dull / brownish / silvery scales / plaques/ loose conjuctive with fissues / folds / furrows / Bitots spots / corneal ulceration with different colours and opacification / wrinkling / cloudiness of cornea ( Keratomalacia) & melting of cornea

Film Star Eye lashes:

Dense abnormally long & curved eye lashes on both upper & lower eye lids. Usually seen as a Vit A difficiency as an associated sign along with other signs of malnutrition with or without evidence of primary complex clinically or radiologically. In a well nourished child such a sign may be due to hyper vitaminosis A

Keratomalacia in AGE

Acute onset of keratitis leading to ulcer cornea and eventual blindness observed in most of the diarrhoeal states. During a diarrohoeal episode, inflammed intestinal mucosa can not absorb Vit A. If there is an associated lack of Vitamin A storage in liver, it leads to a sudden lowering of circulating serum vitamin A level which in turn predisposes to development of keratitis. Hence the convenient dictum in all diarrhoeal cases is to give vitamin A 7500 μg as a single stat dose IM Xeropthalmia is a permanent corneal lesion and can not be cured medically though corneal transplantation is the final answer. Medical treatment with injection Vitamin A 7500 μg daily once till healing takes place is recommended.

Exopthalmose:

Sign of hyper thyroidism when the eye is made to look downwards the upper eye lid lags behind. Impairment of convergence and retraction of upper eyelid and in frequent blinking may be present.

Confirm diagnosis by other signs & symptoms as in adults. Blood T3 T4 raised TSH suppressed.

Congenital hyperthyroidism

(Neonatal hyper thyroidism)
Eyes are widely opened and appear exophthalmic all other equivalent signs & symptoms of adults present. Associated jaundice plus or minus
T4 level markedly elevated
Can be due to maternal diseases

Cretinism ( genitically determined)

Narrow palpabral fissure. Very small portion of cornea seen. Confirm with associated signs & symptoms like a. prolongation of neonatal physiological jaundice b. no social smile c. No head control at age 6 months d. lack of alert appearance e. female sex preponderance f. Lithargic state g. Low T3 , T4 & high TSH

Difficult to describe in words. Has to be appreciated by photo or actual looks by visualization

The eye signs & facies are abnormal and is kept in exams for spotter – diagnosis

Treatment: Thyroxine – life long – mental retardation preventable

Diminished Visual acuity

Infant or young child, having poor Visual attention, inability to fixate on an object or reduced response to bright light may suggest diminished acuity of vision.
Nystafmus may be a sign of decreased vision.

Leukocoria: (white pupil) or cats’ eye appearance

Sign of unilateral retinoblastma in the age group of 1 -3 yrs. Strabismus occular misallignment is the first sign of ocular malignancy in 25% of cases. Typically diagnosed in the first year of life in the familial & bilateral cases where both pupils will appear white.

Down’s syndrome:

Distance between central points of both cornea will be greater than normal
Epicanthic folds present
Palpabral fissure tilted upwards and laterally & bilaterally (oblique)
Confirmed by
1. Associated flat nasal bridge
2. Single palmar crease
2. Protruding tongue
3. Mal formed ear lobes
4. Mental retardation
5. High arched palate
6. CHD (VSD)
7. Decreased acetabular / iliac angles (X- ray pelvis)
8. Trisomy 21 ( chromosomal analysis)

Anaemia ( Pallor):

Routinely inspected to see the inside of lower eye lid for presence of pallor. In a neonate it may be a congenital problem either in the bone marrow or red cell destruction due to various causes notably maternal malaria during pregnancy leading to congenital malaria . In Rh incompatibility the yellow colour seen in a pale background

10. Icterus:

Jaundice in a neonate on D1, D2, D3 could be due to blood group incompatibility specially Rh. It is a sign of Hepatitis and Hepato- biliary disease. Currently Leptospirosis and hepatitis A are predominent causes ( most children immunized with Hep-B Vaccine) still blood test for HBs – AG has to be done to rule out ‘Hep B’ or ‘Non- B’ jaundice on D3 and after in a neonate especially in a premature baby is often due to physiological jaundice

11. Phlectanular kerato conjunctivitis:

One or two isolated blood vessels running from angle of eye ending and merging in the lateral margin of cornea, usually unilaterally. It is a sign of Tuberculosis and hence requires confirmation by investigations. It is due to allergy to bacterial (AFB) Protein .

12. Measles conjunctivitis:

Like any other conjunctivitis there is florid inflammation of both conjunctivae Eyes & lower eye lids are deeply inflamed. Associated oral inflammation signs plus fever after D3 confirms. Often there is continuous cough day & night . Maculo – popular rash all over the body is pathagnamonic & diagnostic

13. Madras Eye/ Bombay Eye/ Acco

Purulent conjunctivitis of sudden onset. Often there is widespread diseases in the community as an epidemic. Prior to actual conjunctivitis, puritus, intense over both eyes are significant , conjunctivitis within 24 hrs of pruritis is important. Profusely purulant conjunctivitis within 24 hrs of birth may be due to Gonococcal infection. When conjunctivitis occurs sporadically with closure of eyelids due to purulent material the cause is bacterial often. Antibacterial eye drops recommended for both.

14. Naso Lacrimal duct obstruction

Usually seen in Neonates or young infants.Purulent secretions formed in either eye or both eyes at medial aspect. Gentle rubbing on the surface marking of Naso lacrimal duct 25 times x 2-3 times daily for 1-2 weeks with eyedrops improves condition. Usually reported to doctor after 1-2 weeks of eye drops alone not improving situation without physiotherapy of facial skin.

15. Dehydration:

Eye balls are sunken. Conjuctiva dry, cornea dry only in severe dehydration. Lacrimation less in a crying child. History of diarrhoea /vomiting confirms along with the other signs of clinical dehydration

15. Cataract : ( often Congenital)

May be unilateral or Bilateral may be obviously visible or by ophthalmic microscope usually due to congenital Rubella as a sole finding or with after associated findings like microcephaly , Hepatosplenomegaly CHD/VSD + CNS signs

17. Kayser – Fleis cher ring

Due to deposition of copper in Descemets membrane of over the iris muscle and appears as a fine golden ring around cornea, best appreciated by slit lamp. This is pathagnomonic & diagnostic of wilson’s diseases ( Hepto lenticular degeneration) Any liver disease above age 5 should be thought of and excluded wilson’s disease. Many wilson’s disease in children appear and mimic as an ordinary Hepatitis with jaundice whenever neurological symptoms occur with a liver dysfunction, serum ceruloplasmin level estimated and also urinary copper excretion done.

18. Hydrocephalus:

Eye sign is setting sun appearance on both eyes. Depending upon degree of intra - cranial pressure and CSF obstruction the eye balls are tilted forwards to down wards and the disappearance of significant portion of cornea underneath the lower eyelid is appreciable confirmation by measurement of head circumference 2 to 2-5 cm more than normal is significant. Otherwise serial CT scan brain & serial head circumference measurements are mendatory. This will rule out development of ventriculomegaly and fecilitate early surgical treatment for correction ( Ventriculoperitoneal shunt). This should be strongly suspected in all cases where corrective surgery for meningo – myeerocele’ already done as CSF obstructive signs and symptoms most likely to develope in such infants. Early VP shunt procedure lessens risk of neuronal degeneration of brain tissue.(Brain atrophy)

19. Impending Death

Corneal haziness in a case of very severe dehydration over 15 %, all vital parameter’s come down gradually for a stand still. If cornea is shining it is a sign of life. The lacrimal secretion stops when all after body function stops due to decreasing general blood circulation. It is a sign of end stage of any disease more so and earlier in dehydration .First there is cloudiness, haziness and dusty opacification of transparency of cornea leading to opacification. There is diminished eye ball movements. Puplis are dilating and sluggishly reacting to light gradually unfolding the impending death signs. The HR& RR are gradually coming down. Thus the signs of tissue death noticed earlier in eyes than in any other organs.


Conclusion

The basic rule of clinical medicine is inspection, palpation , percussion and auscultation we skip over occasionally during busy hours this important inspection aspect as we know the diagnosis through other sources many times. Jaundice, anaemia, cataract missed in infants. Like touching anterior fontenalle as routine in a neonatal exam or looking for meconium for anal patency at birth during neonatal resuscitation, looking at eyes routinely can give valuable information in all age groups, more so in pediatrics. One may not make exact diagnosis on inspection. But it will be helpful far further investigation & confirmation. Eye is not only the window of the brain but also the window of the practicing physicians mind. It is the physician’s choice to keep the window closed or open however.

References

Test book of pediatrics: Waldoo Nelson 14th edition 1992
Text book of principles of internal medicine by Harrisons 8th edition 1977
American Academy of ophthalmology 1999- 2000 ( Peadiatric ophthalmology)