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Moderator : Dr S.S. Gupta(HOD & Associate Professor)
Dr Abhishek Agarwal (Assistant Professor)
Dept. of Pulmonary Medicine, ELMCH
Pulkit Agarwal
3RD Year Resident
Pulmonary Medicine
An Interesting Case of Bronchial
Asthma with Fleeting Opacities
CASE HISTORY
 SHAKEELA
 40/F
 NONSMOKER
 EXPOSED TO DOMESTIC SMOKE FOR 30 YRS
 HOUSEWIFE
 LIVED IN KACCHA HOUSE
 WITH HER HUSBAND & 2 CHILDREN
PRESENTING COMPLAINTS
 BREATHLESSNESS FOR 20 YRS
 PRODUCTIVE COUGH FOR 5 YRS
 FEVER ON & OFF FOR 5 YRS
PRESENTING COMPLAINTS
 BREATHLESSNESS FOR 20 YRS
 PRODUCTIVE COUGH FOR 5 YRS
 FEVER ON & OFF FOR 5 YRS
ASTHMA LIKE
EXAMINATION
 Clubbing Grade II
 B/l coarse crepts with Rhochi
CHEST XRAYS
CHEST XRAYS
12/03/10 25/03/10
INVESTIGATIONS
INVESTIGATIONS
X-RAY ON ADMISSION
X-RAY ON ADMISSION
SPUTUM EXAMINATION
D/ds
 Allergic Broncho Pulmonary Aspergillosis
 Cystic Bronchiectasis cause ? Infective
D/ds
 Allergic Broncho Pulmonary Aspergillosis
 Cystic Bronchiectasis cause ? Infective
HRCT THORAX
HRCT FINDING
The patient
was put &
started on
Corticosteroids
SPIROMETRY
SPIROMETRY
SPIROMETRY
OBSTRUCTION
SPIROMETRY
OBSTRUCTION
GOOD BDR
CHEST X-RAY --- After 3 Months
Definition
 ABPA is an allergic pulmonary disorder
caused by hypersensitivity to Aspergillus
fumigatus clinically manifesting as chronic
asthma, recurrent pulmonary infiltrates, and
bronchiectasis
 Occurs in asthma or cystic fibrosis2
 result of immune response to Aspergillus
colonization of airway and poor clearance of
mucus secretions
 subsequent bronchiectasis, pulmonary
fibrosis, and compromise of pulmonary
function
 first described by Hinson et al in 1952 in UK
1.CHEST 2009; 135:805–826.
2. Middleton’s Allergy, Principle&Practice 7th edition.
Clinical feature
 Symptom
 occasionally be asymptomatic
 low-grade fever, wheezing, bronchial
hyperreactivity,
 hemoptysis, or productive cough
 Expectoration of brownish black mucus plugs (31 to
69%)
 Physical examination
 wheeze
 Clubbing (16% )
 coarse crackles (15%)
 localized findings of consolidation and atelectasis
during exacerbation
CHEST 2009; 135:805–826.
Definition
 ABPA is an allergic pulmonary disorder
caused by hypersensitivity to Aspergillus
fumigatus clinically manifesting as chronic
asthma, recurrent pulmonary infiltrates, and
bronchiectasis
 Occurs in asthma or cystic fibrosis2
 result of immune response to Aspergillus
colonization of airway and poor clearance of
mucus secretions
 subsequent bronchiectasis, pulmonary
fibrosis, and compromise of pulmonary
function
 first described by Hinson et al in 1952 in UK
1.CHEST 2009; 135:805–826.
2. Middleton’s Allergy, Principle&Practice 7th edition.
Radiologic Investigations
 Chest radiographic findings
 Transient changes
 Patchy areas of
consolidation
 Radiologic infiltrates:
toothpaste and gloved finger
shadows due to mucoid
impaction in dilated bronchi
 Collapse: lobar or
segmental
 Permanent changes
 Parallel-line shadows
representing bronchial
widening
 Ring-shadows 1–2 cm in
diameter representing
dilated bronchi en face
 Pulmonary fibrosis: fibrotic
scarred upper lobes with
cavitation
 HRCT findings
 Central bronchiectasis
 Mucus plugging with
bronchoceles
 Consolidation
 Centrilobular nodules
with tree-in-bud
opacities
 Bronchial wall
thickening
 Areas of atelectasis
 Mosaic perfusion with
air trapping on
expiration
CHEST 2009; 135:805–826
Diagnosis and Diagnostic Criteria
 Rosenberg-Patterson criteria
 Major criteria ( ARTEPICS )
 A = Asthma
 R = Roentgenographic
fleeting pulmonary opacities
 T = Skin test positive for
Aspergillus (type I)
 E = Eosinophilia
 P = Precipitating Abs (IgG) in
serum
 I = IgE in serum elevated ( >
1,000 IU/mL)
 C = Central bronchiectasis
 S = Serums A fumigatus-
specific IgG and IgE (more
than twice the value of
pooled serum samples from
patients with asthma who
have Aspergillus
hypersensitivity)
 Minor criteria
 Presence of Aspergillus in
sputum
 Expectoration of brownish
black mucus plugs
 Delayed skin reaction to
Aspergillus Ag (type III )
 presence of 6 of 8 major
criteria makes diagnosis
almost certain; disease is
further classified as ABPA-
S or ABPA-CB
CHEST 2009; 135:805–826
Complication
 recurrent asthma exacerbations
 development of bronchiectasis
 subsequent pulmonary hypertension
 Respiratory failure
CHEST 2009; 135:805–826
Management
 Systemic Glucocorticoid Therapy
 treatment of choice for ABPA
 Suppress immune hyperfunction & antiinflammatory
 Long term therapy not recommended
 Regimen 2 (steroid dependence 13.5%)
 Prednisolone, 0.75 mg/kg/d, for 6 wk, 0.5 mg/kg for
6 wk, then tapered by 5 mg every 6 wk to continue
for total duration of at least 6 to 12 mo.
 total IgE levels are repeated every 6 to 8 wk for 1 yr
to determine baseline IgE
CHEST 2009; 135:805–826
Management
 Follow-up and monitoring
 Hx and PE , chest radiograph, and total IgE every 6
wk to demonstrate decline in IgE levels and clearing
of chest radiograph
 35% decline in IgE level signifies satisfactory
response to therapy
 Doubling of baseline IgE : silent ABPA exacerbation
 If cannot be tapered off prednisolone, disease has
evolved into stage IV. Management should be
attempted with alternate-day prednisone with least
possible dose
 Monitor for adverse effects (eg, HT, secondary DM)
 Prophylaxis for osteoporosis: oral calcium and
CHEST 2009; 135:805–826
Management
 Oral itraconazole
 Dose: 200 mg bid for 16 wk then once a day for 16
wk
 Indication: First relapse of ABPA or glucocorticoid-
dependent ABPA
 Follow-up and monitoring
 Monitor for adverse effects (eg, nausea, vomiting,
diarrhea,and elevated liver enzymes)
 Monitor for drug–drug interactions
 Monitor clinical response based on clinical
course,radiography, and total IgE levels
CHEST 2009; 135:805–826
Treatment with itraconazole
 reduces immune activation in ABPA
 improves short-term symptoms
 Reduces frequency of exacerbations that require
use of oral corticosteroids
 Not shown improvement in lung function
 may exacerbate adrenal suppression seen with
regular corticosteroid use
Respiratory Medicine (2004) 98, 915–923
THANK
YOU

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A CASE OF ABPA (1).pptx

  • 1. Moderator : Dr S.S. Gupta(HOD & Associate Professor) Dr Abhishek Agarwal (Assistant Professor) Dept. of Pulmonary Medicine, ELMCH Pulkit Agarwal 3RD Year Resident Pulmonary Medicine An Interesting Case of Bronchial Asthma with Fleeting Opacities
  • 2. CASE HISTORY  SHAKEELA  40/F  NONSMOKER  EXPOSED TO DOMESTIC SMOKE FOR 30 YRS  HOUSEWIFE  LIVED IN KACCHA HOUSE  WITH HER HUSBAND & 2 CHILDREN
  • 3. PRESENTING COMPLAINTS  BREATHLESSNESS FOR 20 YRS  PRODUCTIVE COUGH FOR 5 YRS  FEVER ON & OFF FOR 5 YRS
  • 4. PRESENTING COMPLAINTS  BREATHLESSNESS FOR 20 YRS  PRODUCTIVE COUGH FOR 5 YRS  FEVER ON & OFF FOR 5 YRS ASTHMA LIKE
  • 5. EXAMINATION  Clubbing Grade II  B/l coarse crepts with Rhochi
  • 13. D/ds  Allergic Broncho Pulmonary Aspergillosis  Cystic Bronchiectasis cause ? Infective
  • 14. D/ds  Allergic Broncho Pulmonary Aspergillosis  Cystic Bronchiectasis cause ? Infective HRCT THORAX
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  • 18. The patient was put & started on Corticosteroids
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  • 25. CHEST X-RAY --- After 3 Months
  • 26. Definition  ABPA is an allergic pulmonary disorder caused by hypersensitivity to Aspergillus fumigatus clinically manifesting as chronic asthma, recurrent pulmonary infiltrates, and bronchiectasis  Occurs in asthma or cystic fibrosis2  result of immune response to Aspergillus colonization of airway and poor clearance of mucus secretions  subsequent bronchiectasis, pulmonary fibrosis, and compromise of pulmonary function  first described by Hinson et al in 1952 in UK 1.CHEST 2009; 135:805–826. 2. Middleton’s Allergy, Principle&Practice 7th edition.
  • 27. Clinical feature  Symptom  occasionally be asymptomatic  low-grade fever, wheezing, bronchial hyperreactivity,  hemoptysis, or productive cough  Expectoration of brownish black mucus plugs (31 to 69%)  Physical examination  wheeze  Clubbing (16% )  coarse crackles (15%)  localized findings of consolidation and atelectasis during exacerbation CHEST 2009; 135:805–826.
  • 28. Definition  ABPA is an allergic pulmonary disorder caused by hypersensitivity to Aspergillus fumigatus clinically manifesting as chronic asthma, recurrent pulmonary infiltrates, and bronchiectasis  Occurs in asthma or cystic fibrosis2  result of immune response to Aspergillus colonization of airway and poor clearance of mucus secretions  subsequent bronchiectasis, pulmonary fibrosis, and compromise of pulmonary function  first described by Hinson et al in 1952 in UK 1.CHEST 2009; 135:805–826. 2. Middleton’s Allergy, Principle&Practice 7th edition.
  • 29. Radiologic Investigations  Chest radiographic findings  Transient changes  Patchy areas of consolidation  Radiologic infiltrates: toothpaste and gloved finger shadows due to mucoid impaction in dilated bronchi  Collapse: lobar or segmental  Permanent changes  Parallel-line shadows representing bronchial widening  Ring-shadows 1–2 cm in diameter representing dilated bronchi en face  Pulmonary fibrosis: fibrotic scarred upper lobes with cavitation  HRCT findings  Central bronchiectasis  Mucus plugging with bronchoceles  Consolidation  Centrilobular nodules with tree-in-bud opacities  Bronchial wall thickening  Areas of atelectasis  Mosaic perfusion with air trapping on expiration CHEST 2009; 135:805–826
  • 30. Diagnosis and Diagnostic Criteria  Rosenberg-Patterson criteria  Major criteria ( ARTEPICS )  A = Asthma  R = Roentgenographic fleeting pulmonary opacities  T = Skin test positive for Aspergillus (type I)  E = Eosinophilia  P = Precipitating Abs (IgG) in serum  I = IgE in serum elevated ( > 1,000 IU/mL)  C = Central bronchiectasis  S = Serums A fumigatus- specific IgG and IgE (more than twice the value of pooled serum samples from patients with asthma who have Aspergillus hypersensitivity)  Minor criteria  Presence of Aspergillus in sputum  Expectoration of brownish black mucus plugs  Delayed skin reaction to Aspergillus Ag (type III )  presence of 6 of 8 major criteria makes diagnosis almost certain; disease is further classified as ABPA- S or ABPA-CB CHEST 2009; 135:805–826
  • 31. Complication  recurrent asthma exacerbations  development of bronchiectasis  subsequent pulmonary hypertension  Respiratory failure CHEST 2009; 135:805–826
  • 32. Management  Systemic Glucocorticoid Therapy  treatment of choice for ABPA  Suppress immune hyperfunction & antiinflammatory  Long term therapy not recommended  Regimen 2 (steroid dependence 13.5%)  Prednisolone, 0.75 mg/kg/d, for 6 wk, 0.5 mg/kg for 6 wk, then tapered by 5 mg every 6 wk to continue for total duration of at least 6 to 12 mo.  total IgE levels are repeated every 6 to 8 wk for 1 yr to determine baseline IgE CHEST 2009; 135:805–826
  • 33. Management  Follow-up and monitoring  Hx and PE , chest radiograph, and total IgE every 6 wk to demonstrate decline in IgE levels and clearing of chest radiograph  35% decline in IgE level signifies satisfactory response to therapy  Doubling of baseline IgE : silent ABPA exacerbation  If cannot be tapered off prednisolone, disease has evolved into stage IV. Management should be attempted with alternate-day prednisone with least possible dose  Monitor for adverse effects (eg, HT, secondary DM)  Prophylaxis for osteoporosis: oral calcium and CHEST 2009; 135:805–826
  • 34. Management  Oral itraconazole  Dose: 200 mg bid for 16 wk then once a day for 16 wk  Indication: First relapse of ABPA or glucocorticoid- dependent ABPA  Follow-up and monitoring  Monitor for adverse effects (eg, nausea, vomiting, diarrhea,and elevated liver enzymes)  Monitor for drug–drug interactions  Monitor clinical response based on clinical course,radiography, and total IgE levels CHEST 2009; 135:805–826
  • 35. Treatment with itraconazole  reduces immune activation in ABPA  improves short-term symptoms  Reduces frequency of exacerbations that require use of oral corticosteroids  Not shown improvement in lung function  may exacerbate adrenal suppression seen with regular corticosteroid use Respiratory Medicine (2004) 98, 915–923