This document describes the case of an 11-month-old male child presenting with cough and fast breathing for 10 days. Initial assessments found decreased oxygen saturation, clubbing, and skin rashes. Investigations revealed bilateral lung infiltrates, developmental delays, and urine testing positive for cytomegalovirus (CMV). The child was diagnosed with disseminated CMV infection and severe pneumonia, and treated with ganciclovir. Though initially suspected to have acute respiratory distress syndrome (ARDS), the presentation and test results were found to be more consistent with CMV pneumonia masquerading as ARDS.

1. CMV PNEUMONIA
MASQUERADING AS ARDS
Dr.MANOJ PRABHAKAR
Resident , Dept. of Paediatrics

2. HISTORY OF PRESENT ILLNESS:
• 11 months old male child brought to the casualty
with c/o fast breathing since 10 days. Cough +. No
post tussive vomiting.
• Fever low grade (subsides on giving paracetamol.
Irritability and poor appetite since 4 days.
• No vomiting/loose stools. Exclusively breast fed
till 6 months of age and now on complimentary
feeds. No bad child rearing practices.

3. • H/O aspiration of feeds
• Occasionally h/o regurgitation of feeds
• No h/o suck rest suck cycle
• No h/o cyanosis
• Antenatal history : No h/o fever with rash
• Family history: 2nd born child to a 3rd degree
CM married couple

4. Past History
• NICU admission soon after birth for 7 days in view of
skin rash. Treated the child as sepsis. Given IV
antibiotics.
• At 4 months of age child was observed to have
nystagmus. Worked up in Aravind eye hospital and said
to have vision defects. Mother later observed that child
was unable to follow light or objects.
• Admitted in Panrutti GH for 8 days as a case of
bronchopneumonia and treated with IV antibiotics.
• Vaccinated till date.
• Global developmental delay +.

5. @ ER
• Initial assessment
• Primary assessment:
• Secondary assessment

6. GENERAL EXAMINATION:
• Child was conscious .Pallor & cyanosis +.
Saturation 56% on room air.Increased work of
breathing observed.
• Pandigital Clubbing +. Hyperpigmented skin
rash present on the lower limbs. No
neurocutaneous markers.
• Anthropometry:
W/A <-3SD (severly under wt)
L/A <-3Sd (severly stunted)
HC :43 cm

7. S/E
• RS: B/l air entry equal. SCR +, ICR+, Crepts +.
• CNS: Nystagmus +. Brisk reflexes, well
sustained clonus.
• CVS: S1+S2, no murmur
• PA: Soft, no organomegaly

8. Provisional diagnosis
• Severe Pneumonia
• Failure to thrive
• Developmental Delay

9. Course..
• Day 1-3: Child was admitted in PICU and kept on nasal
prongs with 2 lt of O2. Routine investigations were done.
• CXR: B/l Diffuse infiltrates with air bronchogram.
• ECHO: Normal. Started on maintainance IV fluids & IV Abx
(Cefaperazone + sulbactam )
• Child not maintaining saturation with 4 lt of O2 via nasal
prongs, Bubble CPAP and NIV were tried.
• IVO of worsening distress causing impending failure child
was intubated and connected to mechanical ventilator.
(SIMV /PC mode+PS )
• IVO of worsening respiratory failure ,vancomycin was
added & Azithromycin also added .

10. Contd..
• Venti Settings :
Fio2 : 65%
PEEP : 8
Delta P : 16
V- rate 35/min
--- No shock like features { no inotropes }

12. Contd..
• CT thorax was planned for interstitial lung
disease.
• Gene Xpert for TB. (Tracheal aspirate : neg)
• Ophthalmic examination: Pale optic disc.
Traction bands. Ghost vessels (possibility of
past CMV retinitis)
• Planned to workup for congenital CMV
infection as clinical picture correlates (FTT,
Developmental Delay, Pneumonitis, Skin rash)

14. Contd..
Day 4-12: Urine CMV PCR –positive in high titres . Hence for CMV
Pneumonitis Inj.Ganciclovir was started.
• CT Brain: Globe Calcification.
• CD4 count sent.{NORMAL }
• Mantoux negative.
• HIV ( NEGATIVE )
• Trial of CPAP given and child tolerating well. Hence extubated
and put on NIV. Later changed to O2 via prongs.
• Received Vancomycin for 7 days and Cefoperazone + Sulbactam
for 10 days.

15. GANCICLOVIR
5mg/kg/dose – 2 doses/day
CMV Pneumonia – 14 days
For Disseminated infection/occular
• Valganciclovir = iv Ganciclovir
• 6weeks – 6 months
-- S/e : Leukopenia , thrombocytopenia

16. Final Diagnosis
• Severe Pneumonia
• Disseminated CMV infection
• Developmental Delay / Failure to thrive

17. ARDS

18. Berlin Definition for ARDS
• ARDS is an acute diffuse, inflammatory lung
injury, leading to
- Increased pulmonary vascular permeability
- Increased lung weight
- Loss of aerated lung tissue

19. ASHBAUGH (1960)
FiO2/PaO2
• ALI < 300
• ARDS < 200

20. The Pediatric Acute Lung Injury
Consensus Conference Group

22. Key Components
• Acute meaning onset over 1 week or less
• Radiographic Criteria : B/l infiltrates
• Oxygenation Citeria :
paO2/FiO2 ratio < 300mmhg
• Exclusion Criteria : Clinical evidence of left
atrial HTN.

23. Severity
ARDS paO2/FiO2
MILD 200-300
MODERATE 100-200
SEVERE <100

24. CAUSES
Pulmonary/Local Insult
(Primary )
Systemic Insult
( Secondary )
Pneumonia Burns
Aspiration event Sepsis, Shock
Inhalational injury Major trauma
Fat / Air / Amniotic embolism Pancreatitis
Radiation injury Poisoning
Pulmonary contusion Cardiopulmonary bypass
Drowning TRALI

25. PATHOGENESIS
Decrease in aerated lung and lung compliance
Exudation of protein-rich fluid into alveolar spaces
Injury to type II pneumocytes
Inactivation of surfactant
Alveolar instability

26. Phases of the disease
• Acute - Exudative, inflammatory
(0 - 3 days)
• Subacute - Proliferative
(4 - 10 days)
• Chronic - Fibrosing Alveolitis
( > 10 days)

27. Clinical Features
- Increased work of breathing
- Tachypnea
- Hypoxemia
- Hypocarbia ( Due to tachypnea )
- Hypercarbia (Due to fatigue )

28. Imaging Studies
1) Chest X-ray :
• Small volume lungs with diffuse alveolar
infiltrates.
• Air bronchogram +/- pleural effusion
• Widespread atelectasis
• Prominent reticular opacities ( Areas of lung
injury evolving into fibrosis )

29. Imaging Studies
2) Computed Tomography :
• Heterogenous distribution of the
opacification.
• Increased lung densities
• Overdistended non-dependent ventral regions
( due to well aeration )

30. THERAPEUTIC STRATEGIES
• Cotrol of causative factors ( Sepsis,Shock etc)
• Mechanical Ventilation
• Careful Fluid Management
• Careful I/O charting
• Positioning ( Prone)
• Supportive therapies
• Drug based therapies

31. MECHANICAL VENTILATION
• The goal of mechanical ventilation should be
to maintain adequate gas exchange
• Minimizing lung injury
• Adequate oxygen delivery

32. Lung Protective Ventilatory Strategies:
•Controlled O2 exposure
•Low tidal volume ventilation
(will limit harmful airway pressures)
•Permissive hypercapnia
( low VT = hypercapnia & hypoxemia)
•Optimal PEEP
(results in best oxygenation,least
hemodynamic compromise & best
compliance)

33. SUPPORTIVE MEASURES
•Fluid Management
•Sedation & Analgesia
•Nutrition
•NIV
•HFOV
•Prone positioning

34. PRONE POSITIONING
Is turning the ARDS patient
“prone” to be helpful?

35. Contd..
• Theory: let gravity improve matching
perfusion to better ventilated areas
• Improvement immediate
• Uncertain effect on outcome
• May be considered in the patient with severe
ARDS and refractory hypoxemia

36. Drug Based Therapies
• Nitric Oxide
• Corticosteroids
• Surfactant
• ECMO

37. Take home message
• ARDS results from a variety of pulmonary and
non-pulmonary insults.
• The therapy of ARDS is supportive. Low tidal
volume is the only therapy that has
consistently shown a mortality benefit and
should be implemented in all cases.
• Mechanical ventilation should be titrated very
carefully in order to avoid VILI, and potential
multi-organ dysfunction syndrome.

38. THANKYOU