This document provides an overview of pulmonary edema in children, including definitions, classifications, pathogenesis, clinical manifestations, diagnosis, management, and prognosis. Pulmonary edema can be cardiogenic, caused by elevated pressures in the heart, or non-cardiogenic (ARDS). Common causes in children include pneumonia, sepsis, and congestive heart failure. Symptoms include fast breathing and cough. Chest x-rays and BNP levels help diagnose the type. Treatment focuses on oxygen, ventilation if needed, and addressing the underlying cause such as using diuretics, vasodilators, and inotropes for cardiogenic edema. Outcomes depend on the severity of the primary condition but ARDS mortality can be over 50% without treatment.

1. Update on pulmonary Edema in Children
Dr. Sabona Lemessa (Assistant professor in pediatrics and child health, JUMC)
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2. Outline
 Definition
 Classification
 Pathogenesis
 Clinical manifestation
 Diagnosis
 Management
 Prognosis
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3. Definition
 Pulmonary edema is an abnormal fluid collection in the interstitium and
air spaces of the lung
resulting in oxygen desaturation
decreased lung compliance and
respiratory distress
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4. Classification
 Divided into two-
1. Cardiogenic and
2. Noncardiogenic or ARDS
 distinction between them is not always possible
 since the clinical syndrome may represent a combination of several
different disorders.
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5. Cardiogenic pulmonary edema (CPE)
 CPE due to:-
 Increased capillary hydrostatic pressure
 secondary to elevated pulmonary venous pressure
 Increase of net flux of fluid from the vasculature into the
interstitial space
 acute rise in pulmonary arterial capillary pressure (ie, to >18
mm Hg)
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6. Noncardiogenic PE
 Caused by injury to the lung parenchyma or vasculature
 Simplified concensus definition of ALI
Acute onset (<7 days)
Severe hypoxemia (Pao2/Fio2 < 300 for ALI or <200 for ARDS)
 Diffuse bilateral pulmonary infiltrates
 Absence of left atrial hypertension (pulmonary artery wedge
pressure <18 mm Hg if measured)
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7. Cont…
 From a total of 12,018 admissions,105(1.44%) patients developed ARDS and 64
(61.0%) died. Median time from PICU admission to the onset of ARDS was 16 h, and
in 63%24 h. Pneumonia (55.2%) and sepsis (22.9%) were the major predisposing
factors for ARDS.
 These were respectively 14 and 5 times as high a death rate as those of the
severely ill patients without ARDS.
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8. Cont…
Cardiogenic pulmonary edema Non cardiogenic pulmonary edema
(ARDS ) other name of NCPE
 Cardiac disorders
 Atrial outflow obstruction
 LV systolic dysfunction
 LV diastolic dysfunction
 Dysrhythmias
 LV hypertrophy and
 cardiomyopathies
 LV volume overload
 Myocardial infarction
 LV outflow obstruction
 Direct injury to lung
 chest trauma
 Pneumonia
 Pulmonary embolism
 Indirect injury to lung
 Sepsis
 Multiple transfusions
 Cardiopulmonary bypass
 Lung injury plus increased hydrostatic
pressure
 Neurogenic pulmonary edema
 High altitude pulmonary edema
 Reexpansion pulmonary edema
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9. Pathogenesis
 Toxin injury
 Pneumonia
 Inhalational injury
 HAPE
 Sepsis
 UAO
 Left to right shunt lesion
 Pulmonary venous obst
lesion
 MR
 LVF
 Cardiomyopathy
 HTN
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10. Clinical manifestation
 Have manifestation of underlying cause
 Fast breathing, grunting, SOB, Fever, Cough
 Peripheral edema
 Bilateral crepitation, wheezing
 S3 gallop, Hepatomegaly
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11. Diagnosis
 Clinical assessment may give clue
 Chest radiography-ABCD
Alveolar oedema
Bats wing hilar shadowing and Kerley B lines
Cardiomegaly
Diversion to the upper lobes (distension of upper pulm. veins)
Effusions: blunting of the costophrenic angles
 Brain natriuretic peptide
Differentiate cardiac PE from lung PE
BNP>500pg/ml- Cardiac, <100pg/ml- pulmonary
 Echo, OFT, ABG analysis, routine CBC
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12. Cont…
 Stage of pulmonary Edema
Stage 1: Distension of small pulmonary
capillaries due to increased left atrial
pressure
Stage 2: Interstitial edema
Stage 3: Flooding of alveolar space
causing hypoxia
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14. Management of CPE
 Conclusion CPAP produces a more rapid clinical and symptomatic
improvement in patients with acute PE particularly within the first hour.
 CPAP is a useful adjunctive treatment in the early management of acute
heart failure.
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15. Cont…
 ABCs of resuscitation, sitting position, low salt diet
 Supine if associated with Cardiogenic shock
 Oxygen therapy to keep Spo2> 90%.
 Noninvasive pressure-support ventilation
Face mask, CPAP and BiPAP
Recruiting alveoli, splinting airways
reducing the work of breathing
Preload reduction effect
 Mechanical ventilation if
persistent hypoxemia, acidosis, or altered mental status.
IRF or when patients are hemodynamically unstable
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16. Cont…
 Medical treatment of CPE focuses on 3 main goals:
Preload reduction
Afterload reduction
Inotropic support
 Preload Reduction
pulmonary capillary hydrostatic pressure and reduces fluid
transudation into the pulmonary interstitium and alveoli.
Nitroglycerin : oral or I/v 10 -100 mcg/min
Furosemide- (0.5-1mg/kg/dose)
Morphine sulfate-vasodilation and sedation
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17. Afterload Reduction
 Increases COP and improves renal perfusion
 allows for diuresis in the patient with fluid overload.
ACEI, ARB
Nitroprusside for 3-4mcg/kg/min IV infusion:
 Inotropic agents
Dobutamine
Dopamine
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18. 8/12/2022 18

19. Treatment of Noncardiogenic Pulmonary Edema
 Supportive measures
Oxygen therapy
Nutritional therapy
Fluid restriction
Mechanical ventilation
 Antiobiotics if suspicion of Infection
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20. Cont…
 High Altitude Pulmonary Edema due to
Inc sympathetic outflow
Inc pulmonary vascular pressures and
hypoxia-induced increases in capillary permeability
Occur when quickly ascended to altitudes above 2700m
 Treatment
Includes rest
administration of oxygen and
descent to a lower altitude.
If dxed early, recovery is rapid with a descent of only 500-1000 m.
Nifedipine, by reducing pulmonary arterial pressure, may be
effective
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21. Cont…
 Neurogenic Pulmonary Edema Treatment
sympathetic over reactivity with massive catecholamine surges
shifts blood from the systemic to the pulmonary circulation with
secondary elevations of left atrial and pulmonary capillary
pressures
Supplemental oxygen
Mechanical ventilation may be necessary
Usually occurs within 4 hours of the neurological event), and
the majority of cases resolve within 48 to 72 hours.
The outcome is determined by the course of the primary
neurologic insult
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22. Treatment of Reexpansion pulmonary edema
 rare but serious complication of thoracentesis.
 usually occurs unilaterally
 after rapid reexpansion of a collapsed lung
 typically present soon after the inciting event
 May be delayed for up to 24 hours in some cases.
 isolated radiographic changes to complete cardiopulmonary collapse.
 mortality rate as high as 20%
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24. Prognosis and Outcomes
 ARDS is associated with appreciable mortality, with estimates ranging
from 26 to 58%.
 CPE In a high-acuity setting, in-hospital death rates are as high as 15-20%.
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25. Reference
 Brandon T. Woods, Robert L. Mazor, Respitatory disease, 21st edition.
 Muhammad Ahmad Syammakh, International Journal of Research in
Medical Sciences, case report 2018
 Hugh O'Brodovich MD, pediatric pulmonology, 9th Edition.
 Stephen S Gottlieb, MD, pulmonary edema, uptodate 21.6
 Sherif Assaad,MD, Journal of Cardiothoracic and Vascular Anesthesia ,
Assessment of Pulmonary Edema , August 2017.
 Khosro Barkhordari, Respiratory Management of Acute Cardiogenic
Pulmonary Edema , Department of Anesthesiology and Critical Care, 2019.
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26. Thank you!
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