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REA LORRAINE FLORESSTUDENT RT
JAN.2010
RSV and Sepsis
Baby X
4 mo female Admitted in the PICU on Jan. 27th
Diagnosed with sepsis and RSV pneumonia Intubated and ventilated, fluid-resuscitated Clinical course was complicated by difficulties to
ventilate and oxygenate Conventional HFO (late Jan. 28th) NO
(Jan.31st)
Objectives
Pathophysiology Normal physiology PathologyTreatment strategies
Pathophysiology
Pneumonia in Infants
Pneumonia, a leading cause of morbidity and mortality in the paediatric population
Mostly affects children under 2 years of age Nearly 80% have a viral aetiology e.g. RSV (most
common), parainfluenza 1, 2 and 3, and adenovirus RSV often causes bronchiolitis, but pneumonia can
develop
RSV Infections
Rates of illness are highest among infants 1-6 mos of age Seasonal: winter (rarely in spring and summer) Attack rates approaches 100% in areas such as day-care
centres By age 2, nearly all children will have been infected by
RSV. RSV accounts for 20-25% of hospital admissions for
pneumonia, while up to 75% for bronchiolitis Older children and adults can be infected by RSV, but
milder (can progress to a severe illness if immunocompromised)
Mode of Transmission of RSV
Contact (direct and indirect) Droplet
*Incubation period: about 4-6 days *Viral shedding > 2 weeks
Pathogenesis of RSV
Cell-mediated immunity is a more important mechanism of host defence against RSV compared to antibody-mediated
Infections can be severe even in infants who have moderate levels of serum antibody from their mothers
Reinfections can occur
Pediatric A & P
Large upper airway structures Small-diameter airways High chest wall compliance Major muscle of breathing – diaphragm High basal metabolic rate Less muscle glycogen stores – fatigue Decreased elasticity – air trapping High proportion of extracellular fluid – prone to
dehydration
Pathophysiology of RSV
Reaches the respiratory tract by cell-to-cell transfer
Forms a syncytium (neighbouring cells merged together)
Triggers the inflammatory processes In the bronchioles: (edema, mucus, cellular debris) - partially obstructed (“ball-valve”-> air trapping) - completely obstructed (atelectasis)
Bronchiolitis
Increased WOB
Due to:A. Changes in mechanics of breathing Raw lung compliance B. Active infectionEdemaConsolidation O2 consumption
Sepsis
A systemic response to infection or tissue injuryPro-inflammatory exceeds anti-inflammatory
substancesShock: imbalance between the supply of nutrients
and O2 to the tissues and the metabolic demand of the tissues
Compensatory mechanisms: cardiac output ( HR)Anaerobic metabolism...Cardiorespiratory failure
Treatment Strategies
Intubation and ventilation Fluid resuscitation and inotropes Conventional and HFO NO therapy
Clinical Course
Pre-Admission
Clinic: presented with...o 1-wk hx of cough/ URTI symptomso diarrheao poor feedingNearby ER...olethargico decreased muscle toneounable to get a BPoO2 saturation in the 40sInterventions: O2, intubate & ventilate, fluid resuscitationTransferred to HSC
PICU Admission
On arrival... Secured ETT in situ Persistent desaturations Poor perfusion Interventions: Sedation Fluids (N/S, albumin) Vasopressor (Dopamine) Antibiotics Diagnostics: blood and sputum cultures, CXR
Re-intubated with a 3.5 ETT, nasally secured @ 15 cm
ETT position (nasal)= [(Age + 2) + 12] + 3
Servoi SIMV PC + PS
Vent Day 2MODE SIMV PC + PS SIMV PC +PSFiO2 0.70 0.70RR set 25 18PIP 28 25PEEP 10 10PS 15 15Vt 41 28pH 7.31 7.26
PCO2 52 61
PaO2 76 62
HCO3 26 26
BE 0 0
RR total 35 34HR 110-130BP 86/44SpO2 92-95%Fluid Balance
-74.4
Vent Day 2MODE SIMV PC + PS HFOFiO2 1.0 1.0RR set 25 f 12PIP 27 P-P 60PEEP 12 MAP 20.6PS 17 Bias flow 30Vt 34pH 7.24 7.41PCO2 65 51PaO2 65 51HCO3 27 32BE 0 +6RR total 35HR 180 118BP 81/38 99/40SpO2 Mid 70-low 80s 92-96%Fluid Balance
+300.8
Vent Day 4MODE HFO SIMV PC + PSFiO2 1.0 1.0 .85RR set f 12 15PIP P-P 60 29PEEP MAP 22 10PS Bias flow 35 22Vt
pH 6.87 7.26PCO2 207 74PaO2 61 56HCO3 36 32BE -5 +4RR total 15HR 160-185 118BP 120/52 (mean 94) 83/42 (mean 58)SpO2 81-84% 90-91%Fluid Balance
+275.7
Article 1
Curley M., Hibberd, P. & Fineman, L. (2005). Effect of Prone Positioning on Clinical Outcomes in Children With Acute Lung Injury: A Randomized Controlled Trial. JAMA, 294 (2): 229-237.
Found no significant difference in duration of mech vent and mortality, time to recovery and organ-failure free days
Suggested an increase in oxygenation with no decrease in vent support days
Article 2
Duval, E. & van Vught A. (2000). Status asthmaticus treated by high-frequency oscillatory ventilation. Pediatric Pulmonology, 30(4):350-3.
Case report on 2 yo girl with severe asthmaHFOV in obstructive disease:
Stent open the airway by sufficient MAPLower FPermissive hypercapniaLong Te
References
1. Czervinske, M. & Barnhart, S. Perinatal and Pediatric Respiratory Care. 2nd ed. Elsevier: 2003.
2. Des Jardins, T. & Burns, G. Clinical Manifestations and Assessment of Respiratory Disease. 5th ed. Mosby: 2006.
3. Fauci, A. Harrison's manual of medicine. McGraw-Hill: 2009.
4. Huether, S. Pathophysiology: the biologic basis for disease in adults & children. Mosby: 2002.