Case Pres. - Winning Over TB in Children,,,A Lost Cause[1]

8/3/2019 Case Pres. - Winning Over TB in Children,,,A Lost Cause[1]

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General Data:J.C.N., 12-year-old male,

Filipino, Catholic, presently residing

at Manatra Buli, Muntinlupa City,

was admitted at MCGH for the firsttime on May 6, 2010.


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Chief Complaint:cough and abdominal pain


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History of Present Illness:9 months PTA fever

cough

Consult: Health CenterMeds:Paracetamol

Salbutamol

Follow-up twice

Med: Paracetamol


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7 months PTA fever, cough, coldsvomiting, dizzinesshypogastric painbilateral flank paindysuria, nocturiadark yellow urinepolyuria, oliguria

feeling of bladdernot fully emptied

Consult: Health Center

Dx: TonsillitisMeds: ParacetamolSalbutamol?med. for vomiting

Amoxicillin


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5 months PTA persistence of symptoms

abdominal pain(epigastric, RUQ)

Consult: PGH

CXR: PneumoniaMed: AmoxicillinPTB consideredAdvised ff-up


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3 months PTA condition unimproved

urinary symptoms notedgradual abdominal enlargementweight lossnight sweats

Consult: PGHDx: UTIMed: Cotrimoxazole

Ff-up at PGH

Med: Cefaclor


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2 months PTA condition persisted

Consult: Ospital ng

MuntinlupaWhole Abdomen Ultrasound:

Hepatomegaly with liver parenchymal disease process notruled out

Bilateral renal parenchymal disease considered.

Pre-aortic possibly mesenteric lymphadenopathy.

Ultrasonically normal gallbladder, bile ducts, pancreas,spleen and aorta

Advised consult atHealth Center fortreatment of Tuberculosis


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Few hours PTA persistence of condition

Consult: PGHImpression: t/c Disseminated TB

(Pulmo, GI, lymph nodes)

Referred to SLH

CXR requested

Admitted


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Family History: (+) PTB Father, not compliant to medications

- paternal grandmother died of PTB

(+) Asthma paternal side

(+) Hypertension maternal grandfather

(-) Diabetes Mellitus

(-) Cancer


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Immunization History:No Vaccinations

Personal & Social History/Environment:Patients parents separated since he was 5 mos. old.

He presently lives along railways in a congested area withhis mother. There are 5 household members, including thepatient, who occupies a small room. He is the youngest

among 4 siblings. He is an incoming grade 4 student.


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Review of Systems:- no irritability, no changes in sensoriumno convulsion

- no head lesions; no eye, nasal nor auraldischarge; no throat pain

- with shortness of breath

- with easy fatigability

- no cyanosis

- no diarrhea nor constipation

- no hematuria

- no muscle nor joint pains


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Physical Examination : conscious, coherent, weak-looking, in mild cardio-

respiratory distress

CR = 122 RR = 25 T = 37.6oC

pink palpebral conjunctivae, anicteric sclerae, mattedcervical lymphadenopathy, pale skin

symmetrical chest expansion, tachypneic, no retractions,harsh breath sounds with occasional rales

adynamic precordium, tachycardic, no murmur

globular abdomen, normoactive bowel sounds, directtenderness on RUQ, hepatomegaly, visible abdominalveins, (+) Kidney Punch Test

full and equal pulses


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Admitting Diagnosis at the Ward:Disseminated TB (Hepatic, lymph nodes)

Pneumonia

UTI

Severe Malnutrition


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Admission:IVF : D5 0.3 NaCl

Labs: CBC w/ platelet count., urinalysis,serum Na, K, Cl, SGOT, SGPT,Alkaline Phosphatase, BUN,

Creatinine, sputum AFB smear x 3days

PPD

Chest x-ray- negative

UTZ of whole abdomen

Meds: Paracetamol (10 mg/kg/dose)

Penicillin G Na (200,000 u/kg/day)


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1st Hospital day:Subjective

Afebrile * Productive cough no dyspnea * hypogastric pain bilateral flank pain * dysuria, nocturia dark yellow urine * polyuria, oliguria * feeling of bladder not fully emptied

Objective

weak-looking * pallor matted CLAD * prominent rib cage liver edge 6cm below right subcostal margin

iManagement

Continue present management I and O strictly monitored


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2nd Hospital day:Subjective

Afebrile no dyspnea No abdominal pain

Objective

weak-looking * pallor matted CLAD * prominent rib cage liver edge 9cm below right subcostal margin * grade 3/6 systolic murmur at 2nd ICS MCL

Diagnostics

PT,PTT * Abdominal CT Scan w/ contrast Urine CS with ARD * 2D Echo

Blood CS with ARD * ECG

Management

Pen. G shifted to Cefuroxime (100mkd)

Referral to Gastro. & Cardio


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5/8/10

PT

Patient = 13.8

Control = 15.2

% Activity = 86.5%

INR = 1.08

5/8/10

APPT

Patient = 31.6

Control = 36.2


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5th Hospital day:Subjective

Afebrile pallor Good oral intake

Objective

weak-looking * pallor

matted CLAD * prominent rib cage liver edge 9cm below right subcostal margin * grade 3/6 systolic murmur at 2nd ICS MCL

Diagnostics

CBC with platelet * Blood typing Peripheral Blood smear * Serum Electrolytes

Scour film of the abdomen

Management

INH (9mkd) * Abdominal CT Scan deferred Rifampicin (15mkd) PZA (20mkd) Streptomycin (25mkd)


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5/11/1 CBC/ platelet

Hgb 9.53

Hct 29.82

WBC 8.4

Neu. 73.80

Lym 16.40

Plt. 288

Blood Type: O+

5/11/1 Peripheral Blood SmearThe smears show microcytic

hypochromic red blood cellswith anisocytosis andpoikilocytosis. The white bloodcells are adequate in numberwith predominance ofneutrophils. Likewise seen aremany lymphocytes, raremonocytes, and eosinophils,there are no immature bloodcells, or inclusions noted.Platelets are adequate with nomorphological abnormalitiesnoted.

5/11/1 Scout Film of theAbdomen There are normalbowel gas pattern.

The liver andsplenic shadows areenlarged. The psoasand flanks stripes

are intact. Irregularcalcifications areseen in the leftlumbar arealevel of L4 to S1.The osseousstructures areunremarkable.


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Febrile

Objective Harsh Breath sounds, right

Diagnostics

Repeat CBC with platelet Chest Xray

Blood culture and sensitivity

Management

Cefuroxime shifted to Ceftriaxone (100mkd)

Pleural Effusion considered


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febrile,

no oliguria

Management

Urine AFB for 3 days

Anti-Kochs meds. continued


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Whole Abdomen Ultrasound

Enlarged liver with parenchymal disease

TB of the liver not ruled out

Slightly enlarged spleen

Enlarged left kidney with parenchymal disease

Normal gallbladder, right kidney and urinary bladder


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12th HD

febrile night sweats

vomiting, 1 episode harsh BS

occasional rhonchi

13th HD

febrile, no dyspnea

repeat urinalysis

Medications continued


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5/18-20/10

Urine AFB

acid-fast bacilli present 1+

5/19/10 Urinalysis Dark red, turbid

sp. gr. 1.027 pH 5.5

Sugar negative

protein 50 mg/dL RBC >20/hpf WBC >50/hpf Bilirubin 1.0 mg/dL+++ Nitrite 0.1 mg/dL+ hyaline cast many (+4) RBC cast many (+4)


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Afebrile * no dyspnea no cyanosis * urinary symptoms

Objective (+)murmur grade 1 -2

Diagnostics Urine AFB result

Management

Dibencozide * Multivitamins Vitamin B Complex * Quadruple anti-Kochs meds.

continued


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Afebrile * no dyspnea no abdominal pain * no polyuria (+) complete bladder emptying

Objective pallor

Diagnostics

repeat CBC with platelet count

CXR result

Management

Meds. continued


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5/2/1

Chest x-ray

Normal ChestFindings

CBC w/ platelet Hgb 9.87

Hct 30.65

WBC 8.29

Neu. 80.3

Lym. 10.2

Plt. 386


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25th Hospital day:

afebrile,comfortable.

No urinarysymptoms

Home meds:

* INH (10mkd)

* Rifampicin (15mkd)

* PZA (20mkd)

* Streptomycin(21mkd)

* Vit. B Complex

* Dibencozide

* Discharged

improved

* Follow- up @OPD Pedia


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Final Diagnosis:

Disseminated TB (Hepatic, Renal, Lymph nodes)

Anemia secondary to Chronic Infection

Severe Malnutrition


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a common and often deadly infectious

disease caused by various strains ofmycobacteria, usually Mycobacteriumtuberculosis in humans

attacks the lungs but can also affect otherparts of the body

most infections in humans result in anasymptomatic, latent infection

one in ten latent infections eventuallyprogresses to active disease which, if leftuntreated, kills more than 50% of its victims


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EpidemiologyOne third of the worlds population is

infected with Mycobacterium tuberculosis

Each year, about 9 million people developTB, of whom about 2 million die.

Of the 9 million annual TB cases, about 1million (11%) occur in children (


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Causes

Mycobacterium tuberculosis

- a small aerobic non-motile bacillus

- high lipid content

- divides every 16 to 20 hours- classified as a Gram-positive bacterium

- can withstand weak disinfectants & survive in a drystate for weeks

- can grow only within the cells of a host organism, butcan be cultured in vitro


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Transmission

people suffering from active PTB

cough, sneeze, speak, or spit

infectious aerosol droplets (0.5 to 5 um)

transmit the disease


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Transmission

- people with prolonged, frequent, or intense contact: highrisk of becoming infected (22% infection rate)

- people with active but untreated TB can infect 10 15

other people per year

- can only occur from people with active not latent TB

- depends upon the number of infectious droplets expelled

by a carrier, effectiveness of ventilation, duration ofexposure, & virulence of M. TB strain


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Pathogenesis

- Mycobacteria reach the pulmonary alveoli, where theyinvade & replicate within the endosomes of alveolarmacrophages

- primary site of infection in the lungs: Ghon focus

- bacteria are picked up by dendritic cells (can transportthe bacilli to local/mediastinal lymph nodes)

- further spread through bloodstream to other tissues &organs where secondary TB lesions can develop in

other parts of the lung, peripheral lymph nodes,kidneys, brain, & bone


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Risk of TB infection in children

Depends on contact with an adult who has

active TB disease

- extent and duration of exposure

Susceptibility to infection -very young (


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Risk of progression from infection to active

disease: (often within 12 months of infection)

- more common among children


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Primary TB infection in children

Asymptomatic in 80-90%

- 5-10% may develop disease

Extra Pulmonary TB is common

Transmission of TB- source of infection

mostly adults

Children represent about 5-15% of all TBcases


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Young children with TB differ from Adult

Presentation

Infectiousness- generally not infectious

Progression to disease- faster, more often,

more extrapulmonary

Response to treatment Side effect profile


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o Often difficult!- Children rarely cough up sputum

- gastric aspiration not always possible

- Under 2 years of age- other infection/s may mask TB, e.g.,

pneumonia

R d d A h


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Recommended Approach

Careful history identify index case

Clinical examination

TB Skin Test

Bacteriology whenever possible

Investigations relevant to the suspected

type of TB

H t di g TB i hildr


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How to diagnose TB in children

Diagnosis depends on:

History of contact with a smear positive adult

Chronic symptoms

Clinical picture suggestive symptoms

Positive tuberculin skin test

Chest X-ray suggestive of TB


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Clinical signs and symptoms

General most common clues are:

Failure to gain weight/ failure to thrive

Loss of appetite without obvious cause

Chronic cough for 2 weeks or more, not

responding to a course of antibiotics

Painless swelling of the lymph nodes

An audible wheeze due to airway compression

Unexplained fever


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Tools to help with the diagnosis

Chest X Ray

Tuberculin Skin Test (TST) or

Mantoux Test/PurifiedProtein Derivative (PPD)

- intra-dermal injection- read 48-72 hours later

- It measures the bodys immuneresponse to TB

- Infected not necessarily activeTB disease


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Clinical Manifestations

25% of active cases occurs more commonly in immunosuppressed

persons & young children

sites:

- pleura in tuberculosis pleurisy

- CNS in meningitis

- lymphatic system in scrofula of the neck

- genitourinary system in urogenital TB

- bones & joints in Potts disease of the spine


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Tuberculosis of the Cervical Lymph Nodes (Scrofula)

the most common form of extrapulmonary TB in

children

through direct extension from a primary pulmonaryinfection

the cervical chain of nodes becomes the mostcommonly affected

often unilateral; bilateral involvement may occur

cervical nodes may also be involved from other

tuberculous foci: nasopharynx, middle ear ortonsils

diagnosis:(+) tuberculin test, excisional biopsy &culture & fine needle aspiration cytology


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Genitourinary Tuberculosis

2nd most common site for tuberculous infection afterthe lungs

almost always affects the kidneys during the primaryexposure to infection but does not present clinically

true incidence of renal TB may be underestimated:

- radiologic findings may be absent

- diagnosis made by urine culture

Genital TB- usually secondary to renal tuberculous

infection

Renal TB-an uncommon complication of primaryTB occurring very late, up to 15 20 years afterprimary infection


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Renal Tuberculosis

can be unilateral or bilateral

can spread caudad to involve the bladder

can be insidious in onset

75% of patients would present with symptomsrelated to urinary tract inflammation- dysuria,

hematuria, sterile pyuria, flank pain

suspected in the presence of destructive PTB with

persistent, painless, sterile pyuria with associated

albuminuria & hematuria


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Diagnosis of GUTB

GUTB: very uncommon in children

symptoms of renal TB do not appear for 3 to 10 ormore years after the primary infection

frequent painless micturition

urgency uncommon unless there is extensive bladderinvolvement

urine normally sterile, contains leukocytes in high

proportion of patients overt hematuria: 10% of patients; microscopic

hematuria: up to 50%

renal & suprapubic pain: rare presenting symptom

Diagnosis of GUTB


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secondary TB with vague symptoms; often long-

standing urinary symptoms with no obvious cause

latent period of 20 years or more between infection

with the tubercle bacillus & the expression of GUTB

characterized with pyuria, albuminuria, hematuria

75% of patients- abnormal chest X-ray on admission

88% (+) skin tests

63%: abnormal excretory urography

16%: renal calcification

Renal TB:accompanied by manifestations of the urinarysyndrome in 70.4% of cases & by thepresence of Mycobacteria TB in 100%


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Diagnosis of GUTB

most important step:patient history

- history of voiding problems & chronicurgency non-responding to antibacterialdrug regimens: indicative of GUTB

- other symptoms: back, flank, & suprapubicpain, hematuria, frequency, & nocturia

- renal colic: uncommon

- constitutional symptoms: unusual

- symptoms are intermittent & have beenpresent for some time before the patientseeks medical advice


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Diagnosis of GUTB

microbiologic diagnosis of TB- isolation of the

causative organism from urine or biopsymaterial on conventional solid media or byan automated system (radiometry)

positive culture or histological analysis of biopsyspecimens possibly combined with PCR- definitediagnosis

detection of AFB from urine samples by microscopy

(Ziehl-Neelsen acid fast stain)- not reliable

(bec. of the possible presence of M. smegmatis)


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Diagnosis of GUTB

- made based on culture studies

-at least 3, but preferably 5, consecutive early morningspecimens of urine should be cultured, each onto 2slants:

(1) a plain Lowenstein-Jensen culture medium toisolate M. TB, BCG, & the occasionalnontuberculous mycobacteria

(2) a pyruvic egg medium containing penicillin toidentify M. bovis

Diagnosis of GUTB


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Diagnosis of GUTB

Radiography:

Plain X-ray films of the urinary tract:

- may show calcification in the renal areas & in thelower GUT

Intravenous urography:

- distortion of a calyx (fibrosed & completelyoccluded, multiple small calyceal deformities, orsevere calyceal & parenchymal destruction)

Ultrasonography:- may reveal renal calyceal dilation & more overtevidence of obstruction

Computed tomography & nuclear magnetic imaging


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Treatment of GUTB

6-month regimens for the treatment of uncomplicatedGUTB

Intensive phase Continuation phase

3 months

INH, RMP, EMB (or SM)

daily

3 months

INH, RMP

Twice or thrice per week

2 months

INH, RMP, PZA, EMBdaily

4 months

INH, RMPTwice or thrice per week


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Case Pres. - Winning Over TB in Children,,,A Lost Cause[1]

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