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.
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 +.
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
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 }
11.
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)
13.
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
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
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
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 )
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)
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
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.
Exudation of protein-rich fluid into alveolar spaces follows with decrease in aerated lung and lung compliance. Injury to type II pneumocytes decreases alveolar fluid clearance, impairs surfactant production and turnover. Inactivation of surfactant by alveolar fluid and inflammatory mediators exacerbates alveolar instability.
