12 twelvemonth old female kid occupant of Nepal, presented with cough, progressive shortness of breath, loss of appetite, two episodes of haemoptysis and low class intermittent febrility of five old ages continuance and abdominal distention with swelling of pess since one twelvemonth. Child had non been immunized boulder clay day of the month. There was history of taking ATT for 3 months one twelvemonth back. There was no history of thorax hurting, faint, palpitation, icterus, chronic diarrhoea, joint puffinesss, ocular perturbation, skin roseola, unwritten ulcers or exposure to industrial pollutants. There was no history of contact with a instance of TB.
What are the causes of persistent or chronic cough in kids?
Respiratory: Bronchial Asthma, Pertussis, Tuberculosis, FB aspiration, Interstitial lung disease, Fungal infection, Cystic fibrosis, Bronchiectasis and Hyperimmunoglobin E syndrome ( Job syndrome )
Cardiac: Congenital acyanotic bosom disease ( L a†’ R Shunt ) , CCF
Congenital: Tracheo-oesophageal fistulous withers, Broncho-pulmonary disease, Immobile cilia syndrome, Intralobar bronchopulmonary segregation
Assorted: GERD, Otitis media, Sinusitis, Histiocytosis, HIV, Psychogenic – Tourette syndrome
What are the causes of haemoptysis in kids?
Respiratory: Bronchiectasis, Idiopathic Pulmonary haemosiderosis, Cystic fibrosis, Lung Abscess, GpA-BHS pneumonia, Pertussis, Tuberculosis, Foreign organic structure in Laryngo-tracheal bronchial tree
Cardiac: Mitral stricture, Pulmonary intercalation
Assorted: Hemorrhagic upsets, Goodpasture ‘s Syndrome, SLE, Wegner ‘s granulomatosis
In newborn: Hypoxic LBW babes
Define an Un-immunized kid?
A kid, who is non, immunized as per UIP guidelines for immunisation i.e. non immunized for BCG, DPT, Measles and Polio.
What is the importance of BCG inoculation?
BCG has to be given to all kids under five old ages of age since it protects against terrible signifiers of TB and Neurotuberculosis.
What are the IAP recommendations for inoculations in this age?
This kid should be immunized with diphtheria, noncellular whooping cough, lockjaw, hepatitis A, hepatitis B and German measles vaccinum.
What is contact history?
Any kid who lives in a family with an grownup enduring from TB, or has taken ATT in the last 2 old ages.
What are the possible derived function diagnosings based on history so far?
Respiratory: Tuberculosis, Interstitial Lung Disease, Asthma, Sarcoidosis
Cardiac: Acquired bosom disease – Arthritic, Cor pulmonale, Cardiomyopathy
On scrutiny she had a BMI of 14.5 Kg M2, BP of 80/60 millimeter of Hg, pulse rate of 80/min and was afebrile. She had pulsus paradoxus, raised JVP, positive Kussmaul mark, lividness, cervical and alar lymphadenopathy. On respiratory scrutiny: she had barrel shaped thorax ; air entry was bilaterally equal, cracklings were present bilaterally with few wheeze. Per venters revealed monolithic ascites with fluid bang. On cardiovascular scrutiny apex round was non seeable, bosom sounds were weak and no mutter was heard. Other systems were basically normal.
Define Pulsus paradoxus and how do we mensurate it?
It is an hyperbole or accentuation of normal bead in systolic BP seen during inspiration and measured by sphygmomanometer by entering systolic BP at the terminal of termination and so during full inspiration. A difference in the systolic blood force per unit area of more than 10 mm Hg is defined as pulsus paradoxus. It is seen in conditions like pericardiac gush, terrible asthma or emphysema, restricted myocardiopathies, pneumothorax, mediastinal mass, tracheal obstructor and pneumonic intercalation. It is a misnomer and there is nil self-contradictory about it.
What is the pathophysiology behind pulsus paradoxus?
There are few mechanisms suggested for pulsus paradoxus:
Dilatation of Pulmonary venas during inspiration causes pooling of blood in lungs taking to decreased left atrial filling.
During inspiration there is increased intra-pericardial force per unit area as a consequence of grip from its fond regard on environing constructions, this impairs venous return to bosom ensuing in reduced shot volume.
Entire Heart volume is fixed. In the competition between two ventricles for a fixed entire diastolic volume, increased RV make fulling on inspiration causes impaired filling of left bosom ensuing in a†“ LV stroke volume.
What is Kussmaul mark?
It is an addition in the jugular venous force per unit area instead than normal lessening during inspiration. Neck veins go more outstanding with inspiration. It is seen in conditions like constricting pericarditis, cardiac tamponage, severe right sided failure and right ventricular infarct.
What are the differential diagnosings based on history and scrutiny?
Constricting pericarditis ( ? Tubercular )
Interstitial Lung Disease / Childhood Asthma ( ? Cor pulmonale )
Hb – 13.6, ESR-18 millimeter, LFT, RFT, Electrolytes-normal, HIV- Non reactor, phlegm for AFB -ve, Mantoux trial -ve, Chest X-ray – patchy consolidation RUZ & A ; LLZ, pleural gush right, Ascitic fluid: Entire protein- 2.3 g/dl with albumen of 1.4 g/dl [ high SAAG ascitis ] , WBC 70/cmm with prevailing lymph cells, LDH-143 ( Transudate ) , DNA PCR for mycobacteria TB and ADA – negative. QuantiFERON-TB Gold trial was negative. 2D ECHO showed burbling constricting Pericarditis with EF & gt ; 65 % . HRCT thorax: bilateral pleural & A ; pericardiac gush, right upper lobe alveolar opacities cardiomegaly, pericardiac calcification. Bronchoscopy showed coarseness of tracheo-bronchial mucous membrane with widened Carina. Right cervical lymph node biopsy showed a reactive image. Bone marrow aspirate and biopsy showed normal cellularity with increased eosinophilic precursors. Repeat CT scan after 3 months of ATT showed declaration of consolidation.
What is Quanti FERON-TB Gold trial? What is its sensitiveness and specificity?
It is an ELISA trial that measures the interferon-gamma secreted by T cells in response to tubercular antigens which is a cell-mediated immune response in TB-infected persons. It is an nonsubjective, extremely consistent trial that yields a “ positive ” or “ negative ” reply with no demand for reading. Besides because it is a blood trial, it has no inauspicious reactions. It has a sensitiveness of 87 % and specificity of 97-99 % .
How childhood TB is different from grownup TB?
Reactivation or Re-infection
Primary Infection occurs for the first clip
Lowering of unsusceptibility leads to reactivation and locally progressive disease
T cell response dissemination in immuno-compromised
Well marked lymphadenopathy
Hematogenous spread is uncommon
Lymphatic and hematogenous spread more common – miliary / disseminated TB
Cavitory lesion common
Multi bacillary and extremely infective
Paucibacillary and noninfectious
Main cause of decease and disablement is pneumonic Terbium
Main cause of decease and disablement is non pneumonic Terbium
Mending of lesion is chiefly by fibrosis
Calcification is more common, fibrosis is unusual
What are the indicants of steroids in TB?
CNS TB – TBM
Renal piece of land TB
Massive lymph node expansion
How make you categorise and handle paediatric TB as per RNTCP?
New phlegm positive
Seriously sick smear negative
Seriously sick excess pulmonary
AFB +ve, PPD, Pleural gush, CNS, Pericardial, genito-urinary and osteo articular
Sputum smear positive backsliding
Sputum smear negative
Extra pneumonic non earnestly ill
Primary composite, Lymph node, one-sided Pleural gush, Skin TB
What is the difference between restrictive myocardiopathy and constricting pericarditis?
Equal Rt & A ; Lt side filling force per unit areas
Lt 3-5 millimeter Hg & gt ; Rt
Ventricular wall thickness
Pulm Arterial systolic force per unit area & gt ; 60 mmHg
Course in infirmary
Started on antibiotics, Diuretics, Bronchodilators and supportive therapy
In position of occupant of Nepal, diagnostic with chronic cough and non-resolving consolidation, constricting pericarditis and irregular intervention with ATT in yesteryear, she was started on ATT ( SEHRZ ) along with Prednisolone 2mg / Kg
After six hebdomads she became symptomless, shortness of breath decreased, could walk about 1 Km, with no orthopnea or PND and started go toing school
After 6 months of ATT, she was taken up for pericardiectomy and had uneventful recovery.
Concluding diagnosing: Constricting Pericarditis with Calcification
( Possible etiology – Consumptive )
Constricting pericarditis in kids is a diagnostic challenge because of its rare happening and uncharacteristic clinical image. Common etiologies are morbific, chiefly tubercular, collagenosis, uraemia, neoplasias, radiation, injury and granulomatous diseases. Constrictive pericarditis is non common in kids. In 235 pericarditis patients treated at the Toronto Hospital for Sick Children over about 30 old ages, merely two developed pericardiac thickener and bottleneck.
Clinical manifestations of constricting pericarditis consequence chiefly from decreased ventricular filling and impaired myocardial contractility, although systolic map can besides be altered to a varying grade. The clinical status in general restricted to systemic and pneumonic congestion. In approximately 75 % of instances, Beck ‘s three is found, dwelling of small diagnostic grounds of cardiac disfunction, increased venous force per unit area and ascites, non relative to the normally distinct or non evident hydrops. Hepatomegaly is intense and non-pulsatile. This fact, coupled with the possible presence of hypoproteinemia, mimics chronic hepatic disease and sometimes primary malnutrition. Pericardial calcification is detected in about 50 % of instances. Electrocardiographic features are restricted to low electromotive force of QRS composites and nonspecific changes in ventricular repolarization. Echocardiography does non let an accurate rating of the grade of bottleneck.
The definite intervention to be considered is surgery, to be performed every bit shortly as possible after handling the implicit in upset. As in instances of cardiac outflow obstructor, the usage of digitalin, water pills and vasodilatives are contraindicated, because tachycardia, increased venous force per unit area and peripheral vasoconstriction are compensatory hemodynamic responses.
WHO guidelines for National Tuberculosis programme on the direction of Tuberculosis in Childhood.2006.
RNTCP preparation faculty for medical practicians. Central TB Division, Directorate General of Health Services, Ministry of Health and Family Welfare, New Delhi 2006.
Consensus statement on childhood Tuberculosis. IAP working group: Indian Pediatr 2010 ; 47:41-55.
Daniel Bernstein. Diseases of Myocardium and Pericardium. In: Kliegman, Behrman, Jenson editors. 18th erectile dysfunction. Nelson text edition of Pediatric s, Vol 2, 2008 ; 1963-75.
Demmler GJ: Infectious pericarditis in kids ‘ Pediatt Infect Dis J 2006:25:165-166.
6. Keith JD. Constrictive pericarditis. In: Rowe RD, Vlad P. Heart Disease in Infancy and Childhood. 2nd erectile dysfunction. New York: The McMillan Co. , 1978: 255-8.