On the death of Infants

The recent controversy and allegations over the infant death in the BC Roy Post-Graduate Institute of Paediatric Sciences demands that we examine the issue critically. Every death is lamentable but we should also recognize that every death is not preventable unless action is taken in a timely manner. Only by examining what went wrong we can begin to rectify them.

Image Courtesy : Rana2030

Various reports from the media state that initially 12 infants died within a period of 48 hours and later 3 more deaths occurred in the third day taking the toll to 17 infants in 3 days (1, 2).

The role of the media here calls for criticism. What the media is trying to report is the rate of infant death but it is meaningless unless we know how many infants were admitted in the hospital in these days. The media failed to mention the prevailing infant mortality rate in the hospital. Was the death rate in these 3 days significantly higher than the prevailing death rate? Without this crucial information any reporting of the incident only helps in polarizing and sensationalizing the issue and is of no real help.

Let us look at some data. I couldn’t find data specifically for the hospital in question but data was available for another hospital in the city (3). Although it is not ideal, we can use it as a proxy for the absent data from the hospital in question. A total of 1216 infants were admitted to a tertiary care hospital in a year. 286 died, making the infant mortality rate 23.52%/year which is pretty high. Consider this, if 20 infants were admitted everyday for 3 days, we can expect that a total of 14 would have died. This example of course has several limitations. For starters we don’t know how many infants were actually admitted to the hospital in question. We don’t know the prevailing infant mortality in the hospital. It may so happen babies who were very sick and couldn’t be managed elsewhere were referred to the BC Roy hospital as it is a specialized hospital. What I want to say with this example is that we can’t draw any meaningful conclusion from what the media reported though it is a sensitive issue on which we should have an informed opinion.

The knee-jerk response of the government is also unfortunate. The solution that the government proposes is opening of more Sick Newborn Care Units all across the state. This is commendable but we should realize that this constitutes what the public health doctors term as secondary prevention, meaning taking early action after the disease/event has already occurred. A better way is primary prevention which aims at preventing the disease/event from happening at the first place. Primary prevention demands long term commitment from the all the parties involved. Let us look at the common causes of hospitalized infant deaths in the city – septicemia, birth asphyxia, prematurity, acute respiratory tract infections, meningitis, congenital anomalies, congenital heart defects etc (3).

If we examine the risk factors for the causes of infant death, we can see that many of them are preventable. For example higher paternal education significantly decreases the risk of birth asphyxia. Low birth weight is an established risk factor for birth asphyxia and chronic mater malnutrition is one of the major causes of low birth and prematurity. Poor prenatal care, low socioeconomic status, low birth weight and birth asphyxia itself are causes of septicemia in infants (4, 5, 6).

There are few factors which if controlled will lead to a decreased incidence of the diseases affecting neonates and by extension a reduction in the infant deaths. Maternal nutrition, proper antenatal checkups, improvement in the socioeconomic and living standards of the mothers, proper education of the parents are some of the areas where improvement will lead to a better outcome. This, in conjunction with improved secondary prevention strategies will hopefully prevent further occurrences of such incidences in future.

Conflict of interest – I had attended few lectures of Dr. DK Paul, Superintendent of BC Roy Post-Graduate Institute of Paediatric Sciences when he was posted at my college.

References:

1. MARCUS DAM. Four more crib deaths in Kolkata hospital, 12 in Bardhaman hospital. The Hindu. October 29, 2011
2. Infant deaths in B C Roy hospital again. The Telegraph. 26th October, 2011.
3. Roy, RabindraNath. (2008) Mortality pattern of hospitalized children in a tertiary care hospital of Kolkata. Indian Journal of Community Medicine, 33(3), 187
4. Lee, A. CC. (2008-05-01) Risk Factors for Neonatal Mortality Due to Birth Asphyxia in Southern Nepal: A Prospective, Community-Based Cohort Study. PEDIATRICS, 121(5), e1381-e1390.
5. Anderson-Berry AL. Neonatal Sepsis. Medscape Reference.
6. Paul VK, Singh M, Sundaram KR, & Deorari AK. (1997) Correlates of mortality among hospital-born neonates with birth asphyxia. The National medical journal of India, 10(2), 54-7.

Outbreak of viral encephalitis in Bihar, India

An outbreak of viral encephalitis is ravaging the childrenof Magadh division in Bihar India. This is the second wave of encephalitis that has hit the state after the rainy season with 383 children affected and 82 lives lost. The local health authorities are ill equipped to handle such an epidemic and Bihar being one of the poorest states of India does not help much. Conveniently the local media has given it scant or no coverage.

Image courtesy: The Hindu

 Suspected causative agents

It appears that more than one microorganism is responsible for the outbreak with the Japanese encephalitis virus (JEV) being the prime suspect. It is estimated that at least one third of the cases are caused by JEV which is endemic in the region. JEV, a flavivirus, consists of eight virus species and two subtype viruses. Japanese encephalitis is a zoonotic disease with the zoonotic cycle affecting mosquitoes and pigs and/or water birds. Humans are dead end hosts and become infected accidentally. The major vector implicated in transmission to humans is the mosquito Culex tritaeniorhynchus, breeding mainly in rice paddies. Both rice paddies and pigs are abundant in rural Bihar, perpetuating the epidemic.

JEV has an incubation period of 5 to 15 days with the average incubation period being 6-8 days. There is usually a prodromal period at the onset characterized by nausea, vomiting, diarrhea, fever and headache. The prodromal period, which can last for several days, is followed by higher mental functional abnormalities ranging from mild confusion to coma. Seizures are common in children. Tremors and other movement disorders may occur. Acute flaccid paralysis resembling poliomyelitis may also occur. The fever generally disappears by the second week of the disease followed by the onset of extrapyramidal symptoms like chorea.

On examination, hypertonia and hyperreflexia may be present. There may be cranial nerve involvement like facial palsy etc. Parkinson like extrapyramidal features may be present. Mortality in resource poor settings is about 35%.

In ProMED-mail, an internet based outbreak reporting system of the International Society for Infectious Diseases, enterovirus infection has also been suggested as a plausible etiologic agent. However there is no evidence available at present for an enteroviral cause.

Failure of Policy?

Following an outbreak of JE in 2009 in the Bodh Gaya division of Bihar, a massive vaccination campaign was launched in that division and no further cases of JE were reported. Inexplicably such vaccination campaigns were not organized in other divisions of the state. Result – fresh outbreak in another division (Magadh).

The local hospital is also in shambles with water and power shortages and the only ventilator lying useless.

Mackenzie, J., Gubler, D., & Petersen, L. (2004). Emerging flaviviruses: the spread and resurgence of Japanese encephalitis, West Nile and dengue viruses Nature Medicine, 10 (12s) DOI: 10.1038/nm1144

Hepatosplenomegaly with fever in a child

Yesterday I got into a discussion with one of my friends about a case. He had examined a 7 year old male child who presented with fever for the last 7 days. The fever was of mild grade, continuous in type. The fever was not associated with any chills, rigor or sweating. There were no complaints of headache, vomiting, visual disturbance or convulsions. There was no history suggestive of any upper respiratory tract infection , urinary tract infection or any rash. The child complained of dark colored stool but on further inquiry it was not judged to be melaena. There was a history of mild abdominal pain, non colicky and possibly dull aching in nature (one can only get so much out of a child).

On examination the vitals were normal. There was mild, soft tender hepatomegaly and mild splenomegaly. There were no visible veins over abdomen. There was no lymphadenopathy. There was no jaundice. Rest of the examination findings were within normal limits.

Hepatomegaly - from NIH

Based on the history and examination findings the differential diagnosis consisted of

·        Acute viral hepatitis

·        Acute leukemia

·        Malaria

·        Acute hemolysis

·        Enteric fever

·        Lymphoma

·        Disseminated tuberculosis

My friend was of the opinion that the child had malaria. I disagreed.  My argument was that for a child to have malaria with hepatosplenomegaly, the duration needs to be pretty long. More over there is a correlation between jaundice and hepatomegaly in patients of malaria (1). Here the child did not have jaundice. I thought that enteric fever or acute leukaemia fits better. Mind you, neither of us had any test results at that point.

The test results came back positive for malaria and the child was started on chloroquine therapy. However, I still think based on the clinical picture, it would have been inappropriate to come to a provisional diagnosis of malaria, as there was no jaundice, the rapid course of the disease and mild grade of the fever, though certainly it was in the differential.

Interestingly, jaundice and hepatomegaly is associated with increased risk of acute renal failure in children suffering from malaria (1) but not an increase in the risk of cerebral malaria. However, in this case there was clinical finding of any abnormal renal function and the test results were within normal limits. There were also no features of CNS involvement (no headache, vomiting, visual disturbance, irritability or sleepiness), CSF examination was within normal limits.

1.  Nacher M, Treeprasertsuk S, Singhasivanon P, Silachamroon U, Vannaphan S, Gay F, Looareesuwan S, & Wilairatana P (2001). Association of hepatomegaly and jaundice with acute renal failure but not with cerebral malaria in severe falciparum malaria in Thailand. The American journal of tropical medicine and hygiene, 65 (6), 828-33 PMID: 11791981

Case of bilateral congenital ectropion

Recently I came across a case report published in the journal Indian Pediatrics by Surana I and Surana S. about bilateral congenital ectropion of the upper eyelids in a six month old infant. The child also had features of Down’s syndrome, a genetic disorder characterized by chromosomal abnormality of trisomy 21. Congenital ectropion is frequently associated with a condition called blepharophimosis, a condition in which there is bilateral shortening of the eyelid openings, both horizontally and vertically.

Ectropion of the lower lid - from NHS

Ectropion is a condition in which the eyelids are everted or turned away from the globe or the eyeball. It is characterized by epiphora or overflow of the tears. This happens because the lacrimal punctum, the opening through which the tear drains form the eye is situated on the lid margin. As the lid is turned away, the tears are no longer able to flow through their normal path. Instead they accumulate and subsequently overflow. It is interesting to note that in this case, epiphora would not be a prominent symptom. Why is it so? It is because  most of the tear is drained by the punctum of the lower eyelid as tears naturally tend to gravitate downwards. Only a small amount of tear is drained by the upper punctum and without the involvement of the lower punctum the drainage remains sufficient. Ectropion may also lead to keratitis (inflammation of the cornea) and corneal ulcer. This happens because the eye is continuously exposed to the environment; hence it is also termed as exposure keratitis.

Ectropion is subdivided according to its causes-

• Involutional or senile
• Cicatricial
• Paralytic
• Congenital
• Mechanical

Let us examine the rationale behind the diagnosis. Involutional ectropion is ruled out as the patient is an infant. Cicatricial and mechanical ectropion is also ruled out as there is not history of scar formation, injury or space occupying lesion. Paralytic ectropion follows the paralysis of orbicularis oculi, the muscle that closes the lid. It is supplied by the temporal and zygomatic branches of the facial nerve. So paralysis of the facial nerve may cause ectropion. In this case, facial nerve paralysis was ruled out. Hence we get the diagnosis of congenital ectropion.

Ectropion is one of the rarest ocular symptoms of Down’s syndrome. In this case, although there were features of Down’s syndrome, the diagnosis was not established. The management of ectropion usually aims at prevention of keratitis and corneal ulcer formation. This can be achieved initially by application of artificial tears and local antibiotics. In severe cases, surgical management is necessary to correct the defect. In this case, the condition of the patient was stable on treatment with artificial tears, hence surgery was not undertaken.

Links:

• Congenital Ectropion - Indian pediatrics

Otitis Media in winter: Acute Otitis Media or Otitis Media with Effusion?

Winter is at our doorstep and with it the incidence of viral respiratory tract infections and allergic conditions of the upper respiratory tract is on the rise. Both these conditions give rise to otitis media by blocking the Eustachian tube and impairing middle ear cavity drainage. This results in fluid accumulation which may  become infected causing acute otitis media. The incidence of otitis media with effusion is very common; almost 90% of children suffer from otitis media with effusion before school age.

Eustachian Tube

Otitis media with effusion may immediately precede an attack of acute otitis media or may follow an attack of acute otitis media. These two conditions need to be differentiated because antibiotic treatment is not always necessary in otitis media with effusion. Unnecessary antibiotic treatment may cause treatment failure and subsequent drug resistance.

Signs and Symptoms	Otitis media with effusion	Acute otitis media
Hearing Loss	Mild-to-moderate	Mild-to-moderate
Earache	Absent	Moderate-to-severe
Tenderness	Absent	Absent
Purulent drainage from ear	Absent	Only after perforation of tympanic membrane
Bacterial infection	Absent	Present
Systemic symptoms  ( fever, malaise)	Present	Present

Otitis media with effusion generally presents with mild to moderate hearing loss, conductive in type and is not associated any pain or fever. It is diagnosed by pneumatic otoscopy in which the tympanic membrane is immobilized. Tympanometry is also a useful investigation. On examination of the infected ear, the tympanic membrane is retracted. Fluid is present behind the tympanic membrane, presence of air bubbles or air-fluid level is pathognomonic. It generally resolves without treatment.

Retracted tympanic membrane

Acute Otitis media is sudden in onset, associated with pain in the affected ear and hearing loss, conductive in type is present. System symptoms such as fever are present. On examination, the tympanic membrane is red and bulged; rupture of the tympanic membrane provides relief to the symptoms.

Red, bulged tymanic membrane in AOM

 More information:

• http://www.aap.org/healthtopics/earinfections.cfm 
• http://cme.medscape.com/viewarticle/730698