An Interesting Case of Treatment Resistant Asthma

An Interesting case of Treatment
resistant Asthma
Unit – III
Prof.Dr.V.Ushapadmini M.D.
Dr.Rajamahendran M.D.
Dr.Ranjith M.D.
Dr.V.R.Bhuvaneswari,Post graduate
CASE SUMMARY
 Mrs.Chellamani,42 /F , agricultural labourer,
 Chief complaints
 Breathlessness on and off past 7 years, aggravated for past 1 year,
aggravated in early morning, aggravated in cold climate.
 Cough with expectoration – past 1 year,more so past 2 weeks.
H/O blood stained sputum +
 Chest pain-pleuritic type of pain right side past 2 weeks

 H/o loss of weight +
 N/o H/o evening rise of temperature or night sweats
 No H/o Loss of appetite.
 No H/o chest pain, palpitation, syncope.
 No H/o swelling of legs or abdominal pain or distension.
Past history
 Patient is a K/C/O bronchial asthma on treatment for past 7
years – with courses of short term steroids and Inhalers

 Since the pt was poorly responding to treatment she was suspected to have
PTB and started on ATT in December 2016 But subjectively no
improvement
 No H/O contact with TB or H/O HT,DM.CAD
 Occupational history-Agricultural labourer with exposure to environmental

fungi
Personal history
 Mixed diet consumer.
 No specific addictions.
Family history
 No similar complaints in family members.
On examination
 Patient was conscious
 Oriented
 Afebrile
 Ill built, emaciated
 Pallor +
 No clubbing
Vitals
Temperature-97.4 F
 PR – 92/min
 BP – 110/70 mm Hg
 RR – 26/min
Respiratory system
Inspection
 Trachea midline
 chest is symmetrical
 Movements equal on both sides
Palpation
 Trachea in midline
 Ap diameter – 18 cm
 Transverse diameter – 30 cm
 Chest expansion equal on both sides
 VF – normal
 No tactile fremitus
Percussion
 All lung fields are resonant
Auscultation
 Normal vescicular breath sounds
 Coarse leathery crepitations heard in all lung fields
 VR – normal
 Other systems - normal
Provisional diagnosis
 PT sequelae, Bronchiectasis .
 HB- 8.5, TC- 8800, DC – P 58%, L20%,E-12%%, ESR – 35
MM in 1 hr, RBC – 2.6,PCV – 26%, Plt – 1.9 L.
 Urea – 36, sugar – 128, creat – 1.2.
 ECG – within normal limits.
 Peripheral smear – normocytic hypochromic anemia.
 Sputum AFB – negative. Sputum CB NAAT – negative
 Sputum shows atypical organisms-Chlamydia/Mycoplasma
 HIV - negative
. AEC – 126/cu.mm.
 Patient was treated with i.v. Antibiotics, i.v. Bronchodilators and
Nebulisation.
 There was no improvement.
 Further evaluation done to find out the cause.

 Final diagnosis- Allergic bronchopulmonary aspergillosis.
 Expert opinion obtained and patient was started on T .
Itraconazole 200 mg bd, T.prednisolone – 30 mg OD
 Patient symptoms improved significantly.

DISCUSSION
INTRODUCTION
 ABPA - Idiopathic inflammatory disease of the lung – allergic
inflammatoryresponse to colonisation of airways by A.fumigatus

or other fungi.
 Allergic bronchopulmonary mycosis-Identical clinical syndrome
is also seen with

C.albicans,Helminthosporium,alternaria,curvilaria,saccharomyc
es,stemphylium.
 New entity – severe asthma with fungal sensitivity (SAFS).
 Complicates 7 – 14 % of cases of chronic steroid dependent
asthma.
 7 – 15 % of cases of cystic fibrosis.
 common in 3 – 5 decades of life.
 Familial cases – genetic factors play an important role.

Pathogenesis
 Conidia colonize airways – germinate into somatic hyphae –
chronic allergic inflammatory response – tissue injury.
 Gene mutations – CFTR, MHC Class II DR2/DR5-predispose,
DQ2 – protective. TLR 9, Chitotriosidase 1 exon mutation play a

role in pathogenesis.
 Type I hypersensitivity – elevated total and A.fumigatus specific
IgE.
 Type III hypersensitivity – A.fumigatus specific IgG antibodies,
circulating immune complexes.
 Type IV hypersensitivity – immediate and delayed skin
sensitivity.
 Helper T cells play a role in pathogenesis – increased airway T
helper cells,increased level of soluble interleukin 2 receptors in

the circulation.
 Lymphocytes , eosiniphils, basophils contribute to local airway
injury.
 Neutrophils play a role – IL 8,sputum neutrophilia, MMP levels.
 Aspergillus derived antigens and proteases with antibody
binding capacity may amplify the inflammatory response.

Clinical features
 Dyspnea
 Wheezing
 Poor asthma control
 Cough – productive of thick, brown mucus plugs.
 Malaise
 Low grade fever
 Occasionally hemoptysis.
 History of recurrent asthma exacerbations with pneumonias.
 Atopy
Clinical types
 ABPA – seropositive-ABPA(S)
 ABPA – central bronchiectasisABPA-(CB)

Severe asthma with fungal sensitivity
 Patients with poorly controlled asthma with response to
antifungals – with some criteria of ABPA.
 Milder allergic response
 Lack of exaggerated IgG response
 No radiographic abnormalities.
Differential diagnosis
 Steroid dependent asthma without  Chronic eosiniphilic pneumonia
ABPA  Lymphoma
 SAFS  Idiopathic hypereosinophilic
 COPD syndrome
 Chronic necrotizing aspergillosis  Auto immune disease
 Tuberculosis  Cocaine use
 Parasitic infections  Cystic fibrosis
 Hypersensitivity pneumonitis
 Churg-Strauss syndrome
 Acute eosinophilic pneumonia

Diagnostic studies
 BAL – eosinophilia, increased Aspergillus specific IgE and IgA
 Bronchoscopy – mucoid impaction, bronchial brushing shows
aggregates of eosinophils, fungal hyphae and charcot laden

crystals.
 Hyphae filled mucus plugs – pathognomonic of ABPA.
 PFT – obstructive ventilatory defect. Stage V – restrictive defect.

Imaging
 Typical manifestations – pulmonary infiltrates and Central
bronchiectasis.
 Infiltrates are irregular and transient(1-6 weeks) .Fleeting infiltrates
 Tramline shadows
 Toothpaste shadows
 Ring shadows
 Local consolidation
 Lobar collapse
Treatment
 Goals – controlling symptoms, preventing
exacerbations,preserving normal lung function.
 Systemic steroids are the mainstay.
 Stage I, III – prednisone 0.5 – 1 mg/kg a day – 2 weeks
 Followed by 0.5 mg/kg every other day – 6 – 8 wks.
 Subsequently tapered by 5-10 mg every 2 weeks.
 Low maintenance dose may be required (5 – 7.5 mg/day)

 Cortico steroid therapy – relief of symptoms, >35% decrease in
serum IgE., reduction in peripheral blood eosinophils, resolution

of pulmonary infiltrates.
 IgE levels –monitored every 2 months.
 Escalation of steroid therapy – if IgE levels rise more than 100%.

 Antifungals – Itraconazole 200 mg twice daily for 16 weeks.
 Reduction in steroid dosage
 Decreased IgE levels.
 Greater resolution of pulmonary infiltrates.
 Gains in exercise tolerance or pulmonary function.

THANK YOU

An Interesting Case of Treatment Resistant Asthma

Uploaded by

Copyright:

Available Formats

An Interesting Case of Treatment Resistant Asthma

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

An Interesting Case of Treatment Resistant Asthma

Uploaded by

Copyright:

Available Formats

An Interesting case of Treatment

 Breathlessness on and off past 7 years, aggravated for past 1 year,

aggravated in early morning, aggravated in cold climate.

 Cough with expectoration – past 1 year,more so past 2 weeks.

H/O blood stained sputum +

 Chest pain-pleuritic type of pain right side past 2 weeks

 N/o H/o evening rise of temperature or night sweats

 No H/o Loss of appetite.

 No H/o chest pain, palpitation, syncope.

 No H/o swelling of legs or abdominal pain or distension.

 Patient is a K/C/O bronchial asthma on treatment for past 7

years – with courses of short term steroids and Inhalers

 Occupational history-Agricultural labourer with exposure to environmental

 Patient was conscious

 Ill built, emaciated

 Movements equal on both sides

 Chest expansion equal on both sides

 All lung fields are resonant

 Normal vescicular breath sounds

 Coarse leathery crepitations heard in all lung fields

 Other systems - normal

MM in 1 hr, RBC – 2.6,PCV – 26%, Plt – 1.9 L.

 Urea – 36, sugar – 128, creat – 1.2.

 ECG – within normal limits.

 Peripheral smear – normocytic hypochromic anemia.

 Sputum AFB – negative. Sputum CB NAAT – negative

 Sputum shows atypical organisms-Chlamydia/Mycoplasma

 There was no improvement.

 Further evaluation done to find out the cause.

 Expert opinion obtained and patient was started on T .

Itraconazole 200 mg bd, T.prednisolone – 30 mg OD

 Patient symptoms improved significantly.

inflammatoryresponse to colonisation of airways by A.fumigatus

 Allergic bronchopulmonary mycosis-Identical clinical syndrome

is also seen with

 Complicates 7 – 14 % of cases of chronic steroid dependent

 7 – 15 % of cases of cystic fibrosis.

 common in 3 – 5 decades of life.

 Familial cases – genetic factors play an important role.

chronic allergic inflammatory response – tissue injury.

 Gene mutations – CFTR, MHC Class II DR2/DR5-predispose,

DQ2 – protective. TLR 9, Chitotriosidase 1 exon mutation play a

 Type III hypersensitivity – A.fumigatus specific IgG antibodies,

circulating immune complexes.

 Type IV hypersensitivity – immediate and delayed skin

 Helper T cells play a role in pathogenesis – increased airway T

helper cells,increased level of soluble interleukin 2 receptors in

 Neutrophils play a role – IL 8,sputum neutrophilia, MMP levels.

 Aspergillus derived antigens and proteases with antibody

binding capacity may amplify the inflammatory response.

 Poor asthma control

 Cough – productive of thick, brown mucus plugs.

 Low grade fever

 History of recurrent asthma exacerbations with pneumonias.

 ABPA – central bronchiectasisABPA-(CB)

antifungals – with some criteria of ABPA.

 Milder allergic response

 Lack of exaggerated IgG response

 SAFS  Idiopathic hypereosinophilic