Congenital Tuberculosis

Suryakant Khopkar, Asawari Setigiri,

Vilas Jadhav, Mukesh Agarwal

Edited By: Deepak Seth

Tuberculosis infection in a female of reproductive age-group is associated with profound consequences, ranging from infertility to the transmission of infection in her new born. Congenital tuberculosis is a well established clinical entity, though until pre-chemotherapeutic era the reorganization of congenital tuberculosis was mainly academic, as the condition was always fatal.

Case report

A three months old infant weighing 4.8 kg was admitted with complaints of fever, cough and breathlessness since 3 days. The baby was delivered vaginally with birth weight of 2.8 kg following an uneventful pregnancy and labor. There was no history suggestive of tuberculosis contact, including in the mother.

On examination, the baby had respiratory rate of 60/min with intercostals retractions. Air-entry was decreased and crepts were heard on both sides. Liver and spleen were palpable 2 cm each below costal margin routine haematogram revealed normal total and differential counts with ESR of 45 at the end of 1 hr and no definite evidence of septicemia. The initial X-ray of the chest showed bilateral diffuse mottling with left upper zone emphysematous bulla. Blood gas analysis showed pH 7.35, PO2- 42, PCO2-49, Sat. O2-72% and HCO3 - 15. Blood culture was sterile. Mantoux test was negative. Baby's and mother HIV were negative. Baby was started on IV Ceftriaxone and Amikacin considering staphylococcus bronchopneumonia but the baby continued to have respiratory distress and high grade fever.

Couple of day's later, gastric lavage examination revealed the acid fast bacilli with Ziehl-Neelson's staining and fluorescent microscopy. The baby was started on anti-tubercular therapy with INH (5-10 mg/kg/day), rifampicin (15-20 mg/kg/day) and Pyrazinamide (25 mg/kg/day) with prednisolone (2 mg/kg/day). After 7 days of treatment, baby developed recurrent left focal seizures with hemiparesis. CSF examination then revealed proteins 54 mg% and sugar 48 mg% and total cells 40/cumm with polymorphs 50%. CSF ADA level was raised 10 units/L (normal 10 units/ L). CSF culture was sterile and ELISA test in CSF for TB antibodies was positive. CT scan of brain showed right cortical infarct with no evidence of basal exudates or hydrocephalus.

Patient succumbed on 22^nd day of admission i.e. after 2 weeks of anti-tubercular therapy. The mother's X-ray showed old calcified tuberculosis lesion at right upper zone but she was clinically asymptomatic.

Discussion

Until pre-chemotherapeutic era, recognition of the congenital tuberculosis was academic as the condition was always fatal. There have been approximately 300 reported cases in the medical literature. Surprisingly, there are few case reports from India despite of high prevalence of tuberculosis.

Recognition of congenital tuberculosis requires high index of suspicion as the manifestation are different from the older children. The disease usually manifest during first weeks of life but our patient presented little later. The common presenting manifestations are fever, respiratory distress, hepatomegaly, splenomegaly, irritability, prematurity and lymphadenopathy; sometimes indistinguishable from other causes of intrauterine or postnatal infection. Jaundice, seizure and meningitis are not very common, through may develop during the course of the disease. Infection of the fetus can occur either by transplacental route or secondary to ingestion or/and aspiration of infected amniotic fluid, usually at the time of delivery. Mother may be asymptomatic, though in some of them a radiological underlying focus is detectable.

Criteria for diagnosis of congenital tuberculosis were established in 1935 by Beitzke, which are still valid

1. The tuberculosis nature of the lesion must be proved.

· A primary complex in the liver is proof of congenital (intrauterine) origin

2. If there is no primary focus in the liver the infection is then only accepted as congenital if lesions are found in-utero, at birth or a few days later. In cases which manifest relatively later, all extrauterine sources of infection must be eliminated with certainty.

In present case, age of the child, presence of focus the mother and absence of infection in other contacts on screening, points towards a congenital origin of the disease.

Gastric aspirate for acid fast bacilli by Ziehl-Neelsen's staining, fluorescent microscopy or culture is very useful diagnostic too through over all yield is less than 20-30% with best available techniques.

Once the diagnostic of congenital tuberculosis is confirmed, with early treatment survival rate is approximately 45%. Association of tubercular meningitis with congenital tuberculosis is unusual and has poor outcome. While considering the prognosis of tuberculosis meningitis age is an important prognostic factor, and it is inversely related to mortality.

Conclusion

To conclude, early diagnosis of congenital tuberculosis depends on high index of suspicion, especially in endemic and susceptible high risk population, as the clinical manifestations are usually vague and investigations are unrewarding.

Prolonged Diarrhea: Chronic/Persistent/Recurrent?

By: Dr. Deepak Seth
Contributed by: Dr. Neeraj Jain

We all know and keep on experiencing physiological increase in number of motions (should not 'fear' (!) of Diarrhea) Acute mild to severe and chronic Diarrhea. It may keep on recurring or is persistent and keeps on troubling parents as well as treating doctors AND UNFORTUNATELY some (or majority) of patients keep on getting different, un-required and harmful 'treatment' from different doctors.

IS IT NOT OUR DUTY THAT IN OUR TROPICAL COUNTRY, WHERE WE KNOW THAT THIS PROBLEM IS SO COMMON AND HOW MAJORITY OF 'POOR CHILDREN' ARE BEING TREATED WE MUST TAKE SERIOUS STEPSTO KNOW THE SUBJECT IN TRUTH AND REALITY.

Recurrent diarrhea: Here, a child gets current episodes of acute diarrhea, clearly separated by intervening non-diarrheal periods. Arbitrarily, more than 6 episodes per year or >3 episodes/6 months or more than 2 episodes in 3 months may be defined as recurrent diarrhea.

Persistent diarrhea: A diarrheal illness starting as acute watery diarrhea, persisting for 15 days or more, is called persistent diarrhea. This is usually seen in early infancy. The term intractable diarrhea is used to define those cases of protracted diarrhea where the cause is not easily discernible, and the response to treatment is extremely unsatisfactory, The term protracted diarrhea has been applied when weight loss accompanies persistent diarrhea.

Chronic diarrhea: The onset is insidious and the course is sub-acute or chronic, with the passage of large amounts of semisolid stools. The diarrhea is usually of more than 1 month duration, Intervening normal periods may occur. This may occur at any age but is seen more often in older infants and children.
Now taking the problem in short

RECURRENT ACUTE DIARRHEA
This type of clinical syndrome is caused by recurrence of factors that cause acute diarrhea; especially recurrent infections of the gut. Each episode of recurrent acute diarrhea should be analyzed like an episode of acute diarrhea and managed accordingly. The most common predisposing factor for recurrence is an unhygienic environment, especially a contaminated water supply from tube wells, hand pumps or wells. Proper treatment of the acute episode, together with advice regarding the boiling of water and feeding bottle, is usually enough the mother should be advised about the usefulness of continued feeding of infant during the diarrheal episode (to maintain normal nutritional status), as malnutrition is also an important predisposing factor in causing recurrent diarrhea.

Nutritional advice, regarding additional food appropriate-far-age, should also be given. The child should be kept under close supervision to ensure adequate weight gain and to prevent development of malnutrition.

HOW THE CHILD IS WHOSE ACUTE DIARRHEA FAILS TO SETTLE DOWN IN 5-7 DAYS MANAGED?
Although this is not yet persistent diarrhea, but the fact remains that most parents (and the physician) would be very concerned even when the diarrhea is of 7 days' duration. A review of literature indicates that most episodes are a part of the natural history of the disease, being in nature and require no active management. However, some children do have problems and our job is to identify these cases. We should do (i) through clinical examination to detect dehydration and any systemic infection. (ii) Recording weight and comparing with any' previous record. Also recording the weight daily during the episode. (iii) Stool examination for ova and cyst, pH and reducing substances.

If the clinical examination is normal, the child is well hydrated, is maintaining or gaining weight and has normal stool examination, then no active intervention is required. Increase in non-milk calories (like cereals, pulses, curd, and banana) and some decrease in milk, while maintaining adequate calorie intake,' is all that is generally required.

Even children with LACTOSEINTOLERANCE (pH <5.5>14 days duration.

PERSISTENT/PROTRACTED DIARRHEA
This is a common and often baffling clinical problem. It is estimated to occur following 10-14 percent of episodes of acute diarrhea. It is seen more often in young infants «6 months) especially those on top-feed. Also, it is more common in malnourished children. Various causes, that may be responsible for persistent diarrhea are: (i) Resistant infection (ii) Unsuspected parenteral infection (iii) Malnutrition (iv) Disaccharidase-deficiency, including lactose-intolerance (v) Cow's milk protein intolerance (vi) Antibiotic induced diarrhea (vii) Soya protein and other food allergies (viii) Immuno-deficiency syndromes. .

In persistent or protracted diarrhea syndrome, the underlying common pathology is a persistent intestinal mucosal injury, with inadequate or no regeneration. The factors mentioned above, individually or collectively; play an important role in perpetuating mucosal injury. The maintenance of normal nutritional intake during episodes of acute diarrhea is most important for the prevention of the persistent stage. The hallmark of children with
protracted diarrhea is failure to thrive.

This is a complex problem, with a high mortality rate and requires management at the hospital level. One need not wait for 15 days before referring the child. Once weight-loss has set in, the case should be immediately referred to a specialist. In the hospital, a child with persistent diarrhea should be thoroughly examined to look for any systemic infection. A detailed stool examination, including microscopic examination, pH and reducing substances, should also be obtained. Blood counts and blood culture may be done, to exclude any systemic infection. Urine cultures and x-ray chest should be obtained to detect any occult infection. While the results of these reports are awaited, it would be prudent to withdraw all antibiotics (unless the child is very sick or has obvious signs of infections) and milk feeds, for 2-3 days. The child may be given extra low-lactose foods instead and, perhaps, a lactobacillus preparation as well. Most children would respond to this regimen unless there is an associated systemic infection, which would then need appropriate management. However, if the child's weight does not improve, enteral/parenteral alimentation and further investigations, like jejunal biopsy and sigmoidoscopy may be required. For this the child is required to be referred to a hospital with a gastroenterology unit. '

CHRONIC DIARRHEA
Most of these cases occur in older infants and children. These cases are akin to the mal-absorption syndrome. Since there is significant mal-absorption of fat always, they may not have the typical large, fatty stools seen in mal-absorption syndrome. The diarrhea may occasionally be semi-liquid type and may resemble those of persistent diarrhea except for the absence of the acute phase. These children usually do not get dehydrated unless their condition is superimposed by acute diarrhea. This factor may often be the presenting complaint.

This type of diarrhea may be due to a variety of causes, like giardiasis, gluten enteropathy and pancreatic mal-absorption. However, in our experience, it is because of heavy contamination of the gut by non specific bacteria leading to mild mucosal damage. We like to label these children as TROPICAL ENTEROPATHY. This largely occurs in low socio-economic groups of children and most episodes tend to occur during the summer or monsoon months, when gut infections tend to be high.

In all these children, weight should be carefully recorded and followed up periodically. Also 2 - 3 stool examinations may be done to rule out giardiasis or associated worm infestation. If these children maintain a good rate of weight gain, have a good appetite and have no giardia in stools; then they require good dietary (appropriate or increased calorie intake for age) and hygiene maintenance advice.

They normally tend to outgrow their problem. Presence of giardia would warrant metronidazole therapy. However if the child is not thriving (not gaining or loosing weight) and there is no giardia in the stool, then these children would require complete investigations like D-xylose absorption, fat balance study and jejunal biopsy. Now-a-days satisfactory intestinal biopsies can be obtained through GI endoscopy and hence these children should be referred to a pediatric endoscopy unit for further investigations and management.

LACTOSE-INTOLERANCE
Lactose, the sugar present in milk, is broken down in the intestine into glucose and galactose by an enzyme lactase, which is present in the superficial layers of the intestinal villi. Acute gastroenteritis may often result in the shedding of superficial layers of intestinal villi, with resultant lactose deficiency. The lactose is thus not metabolized and absorbed by the body. The lactose within the lumen of the gut is fermented by bacterial action into lactic acid, carbon dioxide and water. Stools in such a child tend to become acidic, loose and explosive. The increased water content of the stools is due to the osmotic action of unabsorbed lactose in the intestinal lumen.

Although some degree of lactose-intolerance may occur in many children with acute gastroenteritis in the first 48 hours, it usually does not cause any therapeutic problem. Clinically significant lactose intolerance should be suspected when an infant's diarrhea is perpetuated by the ingestion of cow's milk. It occurs in only 3-5 percent of cases and usually does not occur before 5-7 days of diarrhea. The chance of developing lactose intolerance is higher in malnourished children and in children following acute watery diarrhea due to Rota virus. It is rare in invasive diarrhea (dysentery).

Clinically, lactose-intolerance may be suspected if after the reintroduction of milk, diarrhea relapses, or persists beyond 1 week or so, with the passage of watery stools containing much air and a characteristic sour smell. Due to the acidic nature of the stools and frequent cleaning of perianal area develop perianal redness and this is an important sign in diagnosing this condition. These infants usually have a good appetite, as opposed to infants with infective diarrhea.

Lactose-intolerance can be confirmed by examination of the stools for reducing substances, with the help of Benedict's reagent, which gives a orange or yellow reduction. The stool pH is usually below 5.5 in such cases. The stool pH and reducing substances, should be tested in freshly passed liquid stools (within 1/2 hour) collection on plastic nappies (better as water is not absorbed by them). Contamination with urine should be avoided. These investigations are sufficient for the routine diagnosis of lactose-intolerance. Other sophisticated tests like the estimation of lactose content of the intestinal mucosa and lactose-tolerance tests, are neither easily available nor generally required.

Lactose-intolerance is usually not total and thus most children will tolerate small amount of lactose (1-2 gm/kg/day) contained in 30-50 ml/kg cow or buffalo milk. Curd is also low in lactose. Thus, a small diet of milk and curd-khichri is a very effective. Milk-withdrawal is usually not necessary for longer than 3-5 days and it should be gradually reintroduced in the diet. If diarrhea recurs or is not controlled on lactose-restricted diet then the child would require intravenous fluids and complete elimination of milk from the diet for longer time (4 to 6 weeks).

Low Lactose Foods
Milk substitutes ............ Curd, soya milk
Cereal products .............Rice or wheat porridge, khichri
Vegetables or fruits.......mashed bananas, vegetable
Non vegetarian................freshly prepared chicken soup

A Child With Heart Murmur

By: Banani Poddar & Srikant Basu

Pediatricians often encounter children with heart murmurs, either as a part of ′well-baby′ examination or during assessment of intercurrent illnesses. The dilemma faced at such a time is to decide which child requires further evaluation and which child has an `innocent′ murmur. In this article, clinical differentiation between pathologic and innocent murmurs has been outlined so that parents of children with the latter can be re-assured and saved from further investigations and /or referral.

What is a Murmur?

Audible sound waves in the range of 20-2000 Hz emanating from the heart and vascular system constitute a cardiac murmur. It can also be said to be the auditory (auscultatory) consequence of turbulent blood flow from within the cardiovascular system.

How Important Are Murmurs?

A large number of children (including neonates) are detected to have a cardiac murmur, especially prior to school age.[1] Some murmurs in neonates, many in infants and most in childhood are ′benign′ or ′innocent′. However, a cardiac murmur may be the first sign of a serious structural cardiac disease, especially in the neonate. The latter not only carry a high morbidity (and if untreated, mortality) but also have enormous financial and psychological implications for the child and parents. Hence differentiation of one from the other is mandatory.

INNOCENT MURMURS

Those murmurs that occur in the absence of structural cardiac disease are said to be ′innocent′. They have been variously described as functional, benign, innocuous or physiologic murmurs.

Innocent Murmurs of Childhood

• Systolic murmurs
• Vibratory Still′s murmur
• Pulmonary flow murmur
• Peripheral pulmonary arterial stenosis murmur
• Supraclavicular or brachiocephalic systolic murmur
• Aortic systolic murmur
• Continuous murmurs
• Venous hum
• Mammary arterial soufflé

The Vibratory Still′s Murmur

This is the most common innocent murmur in children. First described by George F. Still in 1909 it presents most often between the ages of 2 and 6 years, though it may be present at extremes of age (adolescence and infancy). It is an early systolic, grade 1 to 3 (usually grade 2), low to medium pitched murmur, best heard at the lower left sternal edge and extending to the apex and loudest in the supine position. It changes on sitting or standing. It has a distinctive vibratory quality or a twanging sound, which gives it a musical character.

The origin of the murmur is not clear. This has been attributed to various causes including vibration of the pulmonary valves during systolic ejection, physiologic narrowing of the left ventricular outflow tract[8] and presence of ventricular false tendons.

The Pulmonary Flow Murmur

This may be heard in children, adolescents and young adults. It is an ejection systolic murmur, crescendo - decrescendo in character, of low intensity (Grade 2-3) and is heard at the left sternal border in the 2nd and 3rd intercostal spaces. It is rough in character and is thus distinct from the musical Still′s murmur. Best heard in the supine position, it is also exaggerated by a pectus excavatum, a straight back or kyphoscoliosis that results in compression or brings the right ventricular outflow tract closer to the chest wall. The murmur increases in intensity in expiration while inspiration and upright position decrease it.
The innocent pulmonary flow murmur should be distinguished from murmurs due to increased flow in an atrial septal defect and also from pulmonary valvar stenosis. The presence of a hyperdynamic right ventricular impulse; wide, fixed splitting of the S2 and a mid-diastolic flow murmur help in the distinction of the former, while in the latter, the presence of a systolic thrill, a longer and more harsh murmur and an ejection click would aid in the diagnosis.

Peripheral Pulmonary Arterial Stenosis Murmur

This is commonly heard in infants and neonates. It is of ejection systolic character, grade 1 to 2, low pitched and extends till or just beyond S2. These murmurs become more prominent with viral upper respiratory tract infections, especially in the recovery phase, and reactive airway disease. They are often best heard in the axillae or on the back.

The relative disparity in size between the main pulmonary artery trunk and its small branches at birth is thought to be the cause for this murmur. Further, the branches of the pulmonary artery arise at sharp angles, again resulting in turbulence. In older infants with respiratory tract infections, regional vascular reactivity and redistribution of blood flow may cause reappearance of the murmur. Differentiation from the murmur due to an anatomic narrowing of the pulmonary arterial branches is by the longer duration of the latter, the higher pitch and the older age group in whom the latter is heard.

The Supraclavicular /Brachiocephalic Systolic Murmur
This murmur, heard in children and young adults is a crescendo - decrescendo early systolic murmur best heard above the clavicles with radiation to the neck. It is low to medium pitched and brief. The murmur does not change with supine or sitting position but diminishes with hyperextension of the shoulders.[10] This murmur is thought to originate from the brachiocephalic vessels as they arise from the aorta.

The Aortic Systolic Murmur

This murmur is an innocent systolic flow murmur arising from the left ventricular outflow tract and associated with increased systemic cardiac output. It is ejection in character, systolic and is best heard in the aortic area. Common situations in children when these murmurs are heard include fever, anemia, anxiety, hyperthyroidism etc. Similar murmurs may be heard in trained athletes with slower heart rates and greater stroke volume.

The main differentiation is from hypertrophic obstructive cardiomyopathy (HOCM) and left ventricular outflow tract obstruction. In HOCM, increased venous return (as in rapid squatting) diminishes the murmur, while the Valsalva maneuver causes it to be louder. Also, the presence of a positive family history should alert the clinician in favour of HOCM.

The Venous Hum

This is the most common continuous murmur in children. Initially described by Potain in 1867,[11] it is most audible in the neck, anteriorly, just lateral to the sternocleidomastoid muscle often extending to the infraclavicular region of the chest wall. It is usually louder on the right side, better heard sitting than lying and is best elicited with the patient sitting up and looking away from the side of examination. It is widely variable in character and intensity, from faint to grade 6. Gentle compression over the jugular vein or turning the head towards the side of the murmur diminishes the murmur.

Turbulence at the confluence of flow from the internal jugular and subclavian veins as they enter the superior vena cava, or angulation of the internal jugular vein as it courses over the transverse process of the atlas, is thought to cause this venous hum.[12]

The Mammary Artery Soufflé

This murmur, well recognised in late pregnancy and lactation, can rarely occur in adolescence. This starts in systole but may extend into diastole and is heard on the anterior chest wall over the breast. It is high pitched, has a superficial character and firm pressure with the stethoscope may sometimes abolish the murmur. Thought to be arterial in origin, it occurs due to the enlarged vessels of the chest wall. Differentiation from a murmur due to patent ductus arteriosus or arterio-venous fistula is essential.

APPROACH TO A CHILD WITH A MURMUR

Having thus described the various innocent murmurs in childhood, let us now examine the approach to a child with a heart murmur.

History
The history should elicit the presence or absence of the cardinal cardiac symptoms. The symptoms of congestive heart failure in infants are very subtle and may be missed, if not specifically asked for. Past history to suggest rheumatic fever must be excluded. Family history of hypertrophic cardiomyopathy, congenital heart disease or unexplained childhood/early adulthood death is of importance. A perinatal history of premature birth, maternal diabetes, drug or toxin ingestion and intrauterine infection is relevant.

Examination
Apart from examination of the cardiovascular system, perhaps, the most important assessment is the evaluation for dysmorphism and the presence of other congenital anomalies. Presence of anomalies of other organ systems is associated with congenital heart disease in as many as 25% of cases. The assessment of the child’s growth and development is vital and may inform us about "failure to thrive". The child’s play capacity &/or ability to exercise should be sought for. A systematic cardiovascular examination including assessment of the arterial pulses and perfusion, measurement of blood pressure, the systemic venous assessment, precordial inspection, palpation and auscultation in the four different areas, are done. Step-by-step auscultation firstly for heart sounds and subsequently for murmurs, and for additional sounds, as also clicks is required. A crucial auscultatory assessment in children is to characterize the second heart sound and its components. Auscultation should also be carried out over the back, the axillae and the neck. Variations of murmurs and heart sounds with position (supine, sitting, standing) and various manouvres (respiration, Valsalva, exercise) further characterise the nature of these.

Investigations
The chest X-ray (CXR), electrocardiogram (ECG) and echocardiogram are invaluable tools to diagnose and assess the severity of a cardiac disease. However, they add little or no information in a child clinically assessed to have an `innocent murmur′. Hence, these investigations are not routinely recommended. The pitfalls associated with such investigations have been dealt with later.

A INNOCENT MURMUR- CLINICAL DIAGNOSIS

The diagnosis of an innocent murmur requires the absence of symptoms referable to the cardiovascular system, the absence of dysmorphism or characteristic cardiovascular signs and the recognition of the characteristic features of ′innocent′ murmurs.. To aid us to this end, several ′guidelines′ have been published.

We are aware of the `Nadas′ criteria′ for the diagnosis of congenital heart disease. In addition, several studies have addressed this issue as to whether clinicians can accurately classify murmurs as ′innocent′ or ′pathologic′ and several characteristic attributes of each murmur were found. In a study of 222 children being evaluated for a heart murmur by pediatric cardiologists, the following clinical signs were identified, the presence of any of which negates a diagnosis of an ′innocent murmur′. These include:

• Pansystolic Murmur
• Murmur Intensity ≥ grade 3
• Maximal intensity of murmur at left sternal border.
• Harsh quality murmur
• Presence of an early/midsystolic click.
• Presence of abnormal S2

In another such study, the characteristics of pathologic murmurs were found to be

• A systolic murmur with intensity of ³ grade 3
• A diastolic murmur
• An increase in murmur intensity with the patient standing.
  

Hence, the Nadas′ criteria, in addition to these above attributes of murmurs, clearly define ′red flags′ in the diagnosis of innocent murmurs.

Important Pitfalls of Diagnostic Tests

While an enlarged thymus on a CXR causes confusion about heart size in the infant, interpretation of an ECG requires a thorough knowledge of normal age-related changes in infancy and childhood.

In a study of asymptomatic infants and children with a cardiac murmur, a low reproducibility and accuracy was found of radiologic assessment of chest radiography by pediatric radiologists with respect to presence or absence of heart disease. Similarly, in a study on 120 infants and children being evaluated for a heart murmur, the ECG was found to be of no help in discrimination between heart disease and no heart disease. In this study mentioned above,[16] revision of the diagnosis after ECG and CXR was more often misleading than helpful. However, these modalities certainly enhance the diagnostic accuracy when heart lesions are present. While the ECG enhanced detection of an atrial septal defect and to a certain extent pulmonary stenosis, the X-ray enhanced detection of a hemodynamically significant ventricular septal defect. Hence, there are limitations of diagnostic utility of routine CXR and ECG, especially where the clinical diagnosis is that of an `innocent murmur′.

The gold standard for the diagnosis of a structural cardiac disease is an echocardiographic evaluation. However, there can be problems when performed in laboratories without expertise in pediatric heart disease. Normal physiological variations such as presence of a patent foramen ovale or PDA in a neonate may be misinterpreted as presence of heart disease. It has been amply demonstrated that a routine echocardiography is not required in all cases with a heart murmur. Moreover, these babies often require conscious sedation for the procedure, which may lead to problems.

Even in today’s hi-tech world, the best way to correctly classify a murmur as ′innocent′ or ′pathological′ is by clinical evaluation with special emphasis on a careful auscultation. Recently a technique for sending a recording of heart sounds (electronic stethoscope) via e-mail to a specialist, with a high sensitivity and specificity of correctly classifying the murmur. Has been described similarly, using an electronic stethoscope, heart sounds were recorded and fed into an artificial neural network (ANN) after processing The accuracy of classification into ′innocent′ and ′pathological′ was 100% using this ANN. In the absence of such sophistication available routinely, pediatricians can play a pivotal role in correctly classifying a heart murmur as ′innocent′ or ′pathological′. Thus all further investigations and/or referral in children with ′innocent′ murmurs may be avoided and the child kept on follow-up. In case of a clinical impression of a ′pathological′ murmur or the presence of the ′red flags′ as highlighted above, the child may be referred for further evaluation. The urgency with which such an evaluation is done depends on the age of the patient. It is usually within hours in neonates, days in infants and weeks in children.[1]

Hence, to conclude the only way to make a diagnosis of an innocent murmur is by auscultation and routine echocardiography is not indicated. The decision regarding referral for echocardiography and/or to a pediatric cardiologist depends on:

(a)The clinical impression (`innocent′ or pathologic murmur),

(b) The ′comfort′ factor i.e. the anxiety level of the parents,

(c) The confidence of the examining pediatrician and

(d) The availability of the child for follow-up.

This important and useful article is inspired by a special write-up by respected BANANI PODDAR & SRIKANT BASU, from the department of pediatrics, Govt. Medical College and Hospital, Chandigarh.

We have no words to express our thanks for helping all of us.

We invite all those who are interested to share their work and experience with the others by our means, to send us your articles. Thank you

DIAGNOSTIC APPROACH OF RECURRENT /PERSISTANT PNUEMONIA IN CHILDREN

I wish HAPPY NEW YEAR to Everyone.
This month we are going discuss something about the diagnostic approach in recurrent pneumonia in children.

In hospital practice recurrent and persistent pneumonia is a relatively common problem in children and there is very few literature available on this subject. Even though a number of conditions are known to cause recurrent and persistent pneumonia in children, little is known about these groups of cases. Recurrent pneumonia is defined as two episodes of pneumonia in one year, or more than three episodes at any time with radiographic clearance between two episodes. Persistent pneumonia is characterized by persistence of symptoms and roentgenographic abnormalities of more than a month. It is often difficult to determine whether pneumonia is persistent or recurrent, unless there has been a symptom-free interval during which chest radiographs have documented clearing of the pneumonia infiltrations. Bacterial pneumonia may appear to be a recurrent infection, if infection is persistent because therapy was inappropriate for the underlying pathogen; or else, because the duration was inadequate as a result of non-compliance. Even when chest radiographs are available, there may be problems in distinguishing between persistent and recurrent pneumonia. Variability in the technical quality and positioning of chest radiographs may result in misinterpretation of resolution of the pulmonary pathologic process. Reappearance of radiological densities in the same area on subsequent films may be attributed to recurrence, whereas the densities actually represent persistence of previous pulmonary lesions.

Clinical Evaluation:
A careful history, through physical examination and review of chest radiograph helps clinicians for further evaluation. The age of onset of pneumonia is important factor in the evaluation of underlying etiological agents. The possibility of associated congenital anomaly or hereditary disorder is greater soon after birth. Particular attention should be paid to the sequence of events leading to diagnosis of pneumonia, such as nature and pattern of cough, presence and duration of fever; physical finding is such as crackles or wheeze. Nature and pattern of cough is helpful in the evaluation. E.g., A brassy cough is suggestive of tracheal irritation; a croupy cough implies involvement of glottis or subglottis; Paroxysmal cough is associated with foreign body in the respiratory tract. The history of cough and its relationship to feeding or swallowing is important for detecting swallowing dysfunction or defects, GER or poor feeding techniques. It is important to inquire about any family history of asthma, allergic disease, cystic fibrosis, congenital anomalies or recurrent infection suggesting immunnological disorders. Infants below 1 year of age are vulnerable to persistent or recurrent pneumonia due to the bad child rearing practices like oil bath, blowing into the nose and throat clearing maneuvers by the attendants who are routinely giving bath to children. CBC and Mantoux test are done routinely in all cases. Leucocytosis with toxic granules in leucocytes is suggestive of bacterial pneumonia. A positive Montoux test should warrant further work up of tuberculosis. It is important to document specific area of pulmonary infiltrates on all chest radiography and classify the pulmonary infiltrates into those that are unilobar or involve multiple lobes.

Evaluation of recurrent / persistent unilobar / pneumonia:
The differential diagnosis of a child with persistent or recurrent pneumonia involving a single lobe of the lung may be due to intra-luminal obstruction, extra-luminal bronchial obstruction and structural malformation of the bronchus, the intraluminal obstruction being the commonest. In children, the most often cause of intraluminal obstruction is a foreign body. First step in diagnostic workup is the Flexible Fiber-optic Bronchoscopy (FFBS). It is useful both in diagnosis and therapy. Broncho Alveolar Lavage (BAL) or biopsy is performed in other cases of intralobar obstructions (I.e. bronchial adenoma or lipoma). A tracheal bronchus can be diagnosed by FFBS. If bronchoscopy is normal or not revealing any abnormality, CT scan is performed to identify the extraluminal cause of bronchial obstruction. When there is a space occupying lesion in CT Scan, a bronchogenic cyst or sequestered lobe is suspected; an aortogram will be helpful to confirm the diagnosis of sequestered lobe.

Evaluation of recurrent persistent pneumonia involving multiple lobes:
The diagnostic considerations for multilobar-infiltrates are broadly classified into aspiration syndromes, asthma, immunodeficiency states, mucociliary dysfunction, structural abnormalities, alpha-1 antitrypsin deficiency, hypersensitivity pneumonitis and pulmonary hemosideoris should be considered. When aspiration is suspected, a barium study or cineesophagogram is performed to study any defect in swallowing disorders or esophageal pathology. If gastro esophageal reflux is present, it is further confirmed by esophageal pH monitor, technetium milk scan, esophagoscopy and biopsy. If Gastro-Esophageal reflux is absent, FFBS is performed and the Broncho alveolar lavage (BAL) may yield lipid laden alveolar macrophages, which is suggestive of lipoid aspiration. A child presenting with wheeze and mutilobar pulmonary infiltrates often pose problem in the management. If there is PEFR variation of more than 20% with good response to the bronchodilator therapy - asthma is confirmed. The pulmonary infiltrates are secondary to the multiple atelectasis from mucus plugging. If there is a poor response to bronchodilator therapy, the other underlying conditions can be considered based on the following factors. To detect the structural abnormalities of tracheo-bronchial tree, a CT Scan and bronchogram will be done. A careful cardiac evaluation with an echocardiography can identify a congenital heart disease. Evaluation of immunodeficiency state includes quantitative estimation of immunoglobulins and for phagocyte disorder- total and differential white blood cell count are performed in addition to nitroblue tetrazolim (NBT), to evaluate mechanism of intracellular killing. Cystic fibrosis can be diagnosed by sweat chloride estimation be quantitative pilocarpineiontophoresis method. The ciliary dyskinesia can be identified by saccharin clearance, a simple test to assess the ciliary beat frequency. The simplest screening test to study ciliary defects is the measurement of the ciliary beat frequency by studying under electron microscopy the nasal brush biopsy or scrapping the nasal mucosa. By doing serum electrophoresis the absence of alpha globulin can be detected and further confirmation by gene analysis to confirm alpha-1 antitipsin deficiency.
The hypersensitivity pneumonitis can be diagnosed by doing lung biopsy. The patients will show gradual improvement in hospital atmosphere and relapse on return to home when exposed to the offending antigens in the environment. BAL is performed when a child presents with anemia and recurrent pneumonia, which may show alveolar macrophages filled with hemosiderin pigments which is suggestive of pulmonary hemosiderosis.

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