Idiopathic eosinophilic pneumonia (PowerPoint) by ert554898

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									Idiopathic Eosinophilic Pneumonia


        Dr. Hadil Alotair
             KKUH
                History

A 18 Y/O saudi lady living in Riyadh. she is a
 student

– C/O
   •Fever                    8 days
   •productive cough         8 days
   •Chest pain               2 days
   •Dizziness+syncope        2 days
– She was seen in a private hospital and was given
  Augmentin and azithromycin for five days
  without any improvement.

Past H/O
– BA
– Eczema
– Allergic rhinitis
– WPW
        Drug Hx

•Budesonide
•Flexinase
•Ventolin
•Singulare
                Examination
• looked sick.
• Pulse 125/minute, BP 108/67 mm Hg.
• Temperature 37. 8c.
• Respiratory rate 22/minute.
• No lymphadenopathy.
• 02 saturation was 88% on room air.
• Chest
  – Decreased chest expansion on the right side
  – Dull ness
  – Bronchial breathing
                            Rt. Infrascapular
  – Coarse crepitations
  – Pleural rub

• Other systemic examination- NAD
                    Investigations
• CBC:
   –   WBC 29,000
   –   RBC 4.5
   –   Hb 137
   –   Plt 327
   –   ESR 14.


• Differential: neut 51, lymph 14,mono 5, eos 30%
• Urea and electrolytes: Normal
• LFT – Normal.
• ABG:
   – pH              7.43
   – PC02            36
   – Po2             51.9
   – HC03            23.2
   – 02 saturation   87.9 on RA
                    Hospital course
• The patient was admitted initially with the impression of
    - CAP
• on the following day
   – increasing SOB , cough
   -- Desaturated.
• she was transferred to the MICU
                              MICU
• In MICU
  -- Ceftriaxone increased (2 g iv BD)
   – CIarithromycin
   – along with 02 10 lt
   – active nebulization with Ventolin, Atrovent and Pulmicort,
• ABG on 10 l o2 via NRBM

   – PH 7.39     Pco2 41      Po2 88 HCo3 24

• She was put on non invasive ventilation BIPAP 60% O2
   IPAP-10       EPAP-4
• Her blood culture - Streptococcus pneumoniae

• Meropenem and levoftoxacin

• she was not responding to BiPAP


• hemodynamically unstable – inotropes


• She was Intubated
• Her ventilator mode was
  – ACMV ,PEEP 10, FIO2 60%, Vt 350, RR 22

  pH – 7.49 PCO2- 42 PO2- 85 HCO3 – 31 %O2Sat-97

  – CT scan showed
     •Large pneumonic consolidation of the right lung with para
      pneumonic effusion
     •Dense opacification in the apical segment of left lower lobe
     •Early ARDS.
• At this stage the DDx was:
  – CAP
  – ABPA
  – Churg Strauss Syndrome
  – Pulmonary eosinophilic syndrome such as
      •Loffler’s syndrome
      •Acute eosinophillic pneumonia
      •Hyper eosinophilic syndrome
  – Drug induced
                 Investigation results
• PLF
   – Negative for malignant cells
      •
   – Inflammatory infiltrate consists mainly of neutrophil
     mixed with moderate no. of eosinophil & few plasma
     cells & lymphocytes
Bronchial lavage :
Eosinophils – 35%
Negative for malignant cells.
  Negative for fungal element and gram
  staining and AFB
• Endobronchial biopsy:

  Marked eosinophilic infiltration in bronchial mucosa.
•Skin biopsy:

     Drug related dermatitis.
  Methylprednisolone 40 mg iv
   q8h

• Improved

• Extubated - 5 days
    Results of pending investigations

• Serum Aspergillus antibodies: Negative for all
  variants.
• Serum anti-mycoplasma IgM: Negative
• ANA, Anti DNA – Negative
• ANCA – Negative
                Etiology
• Acute hypersensitivity reaction to inhaled
  antigen in a previously healthy Individual
• Enviromental factors
• Cigarette smoking
• World trade centre
• Military personnel in Iraq
• HIV
Clinical presentation
 •   Cough
 •   Dyspnea
 •   Pleuritic chest pain
 •   Myalgia
 •   Night sweats
             Physical exam
•   Fever
•   Tachypnea
•   Tachycardia
•   Bibasilar crackers
•   rhonchi
           Complication

• Hypoxemic respiratory failure
• 14 of 22 patients(63%) required MV
• Hyper dynamic Shock
                   Lab
•   Neutrophilia
•   Eosinophilia
•   IgE
•   ESR
                      CXR
•   Reticular infiltrate
•   Kerly B line
•   Bil.diffuse alveolar &reticular opacities
•   Isolated reticular or alveolar
•   Small bil effusion)Eosinophilic)
                  HRCT
• Bil.patchy ground glass or reticular
  opacities
• Effusion
                   BAL
•   Eosinophilia >25%(mean 37%)
•   IL-5
•   GM-CSF
•   IL-1ra
•   VEGF
                Pathology
• Acute &organising diffuse alveolar
  damage
• Interstitial&alveolar &bronchiolar infiltration
  of eosinophil
• Hyaline membranes and interstitial
  widening
• Organising intra alveolar fibrinous exudate
                 Treatment
•   Spontaneous improvement rare
•   Resp. failure (50-60%)
•   Steroids
•   Clinical response 12-48 hrs
•   Continue steroids for 2-4 wks after plain X-
    ray normalises (2-6wks)
           ACR – Classification Critera:
   Asthma

   Eosinophilia of > 10%

   Mono or poly-neuropathy

   Migratory or transient pulmonary opacities

   Para-nasal sinus abnormalities

   Biopsy containing blood vessel –extra vascular eosinophils

								
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