By Dr Tahir Javed Assistant Professor of Pediatrics King Edward Medical University LAHORE HISTORY Ashbaugh 1967 adult respiratory distress syndrome AmericanEuropean Consensus Conference AECC ID: 775280
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Slide1
ACUTE RESPIRATORY DISTRESS SYNDROME
By
Dr Tahir Javed
Assistant Professor of Pediatrics,
King Edward Medical University
LAHORE
Slide2HISTORY
Ashbaugh: 1967
,
“
adult respiratory distress
syndrome
”
American-European
Consensus Conference (AECC)
: 1994 “ Acute substituted for ADULT”
B/L Lung infiltrates & severe hypoxemia without cardiogenic pulmonary edema
The
Berlin
Definition:
2012-The PaO
2
/FiO
2
mild
ARDS
:
201
- 300 mmHg (≤ 39.9
kPa
)
moderate ARDS: 101 - 200 mmHg (≤ 26.6
kPa
)
severe
ARDS
: ≤ 100 mmHg (≤ 13.3
kPa
)
Slide3The Respiratory System: Gross Anatomy
The AirwayExtra thoracicSupraglotticGlottic Conduction of AirInfraglottic IntrathoracicThe LungsLobes Conduction of Air + gas ExchangeSegmentsThe PleuraBlood Supply
Slide4The
extrathoracic
airway is
1-Pleura
2-Supraglottic
3-Lobe of the lung
4-Chest wall muscle
Slide5Slide6The Trachea
Extent
The length
The AP diameter
The layers: Mucosa,
Submucosa
,
Cartilage/ Muscle, Adventitia
The Bronchi
The blood supply
Inferior Thyroid
Intercostal
Bronchial
Slide7Question
Length of trachea at birth is
a-7cm
b-3cm
c-10cm
d-14cm
Slide8Answer
B
Slide9The Trachea: Histology
Slide10The Bronchial Epithelium
Slide11The Lungs
Slide12The Lungs
Functional unit of the lung is called
1-Lobe
2-Segment
3-Alveoli
4-Bronchus
Slide13The Pleura
Slide14The Pulmonary Vasculature
Slide15The Respiratory Zone
Slide16Mechanics of Breathing
Inspiration
Expiration
Compliance
Resistance
Slide17The Gas Exchange
Slide18Lung Volumes
Slide19The Protective Mechanisms
The Nose
The Cough
The Mucociliary Escalator
The Alveolar Macrophages
Slide20A C U T E
R E S P I R A T O R Y
D I S T R E S
S
S Y N D R O M E
Slide21ARDS
Disease of Alveoli: ↓ Gas Exchange
Diffuse Alveolar damage
Lung capillary endothelial Injury
Early Phase: Exudative
Late Phase: Fibro-proliferative
Slide22Pathophysiology
↑capillary permeability: fluid accumulation
Type 1 cell damage:
↓clearance
from
alveolar
spaces
Type 2 cell damage:
↓Surfactant
→
↓Compliance
ALVEOLAR COLLAPSE
Role of Neutrophils: Reactive rather than
causative
Role of
cytokines
Slide23Question
Type-II cell damage is caused by
1-Surfactant deficiency
2-Oxygen inhalation
3-Sepsis
4-Barotrauma
Slide24Answer
1
Slide25Pathophysiology
Barotrauma: Pneumothorax & Interstitial leaks
Volutrauma: Further damage
Intra
pulmonary
shunting
High FiO2:
DAD
(diffuse alveolar damage)
Hyaline
membrane formation
and
fibrosis
Pulmonary
Hypertension
Pulmonary fibrosis: ↑PCP-III: High mortality
Slide26Causes
No risk factors in 20% cases
Advanced age, female gender, alcoholism and smoking increase the risk of ARDS
Sepsis is the most common cause
Other causes include Pneumonia, fractures, trauma, burns, drug overdose, Aspiration, near drowning, post perfusion injury, pancreatitis and fat embolism
Slide27Epidemiology
Incidence: 75/100,000 population in USA
Incidence increases with
age
15-19
Yrs-16
cases /100,000 person Yrs
75-84 Yrs-306 cases/100,000 person Yrs
Gender: Incidence slightly more in females when cause is Trauma
190,600 new cases every year with 74,500 deaths
Slide28Prognosis
MORTALITY
40-70% mortality in 1990
30-40 % recently
Better understanding of Sepsis
Use of mechanical ventilation
MORBIDITY
long hospital Stays
High risk of Nosocomial infections
Muscle wasting
Functional impairment
Slide29History
Dyspnea
1
st
at exertion and soon at rest
Anxiety & agitation
Increasing need for higher O2 concentrations
Onset
: 12-48 Hrs but may take several days
Patients are critically ill, may be already admitted with multi-organ failure & may not furnish Hx
Slide30Examination
Tachypnea
Dyspnea
Cyanosis
Hypotension: ↑CRT, cold extremities, weak thready pulses
Rales in the chest
Absent breath sounds if pneumothorax
Agitation, Somnolence
Slide31Investigations
Hematologic: TLC, Platelet count esp. with DIC
B:N
Renal: deranged function tests when ATN
Hepatic: Disturbed functions
ABGs: Respiratory alkalosis later metabolic acidosis as CO2 rises
PaO2/FiO2<200
High IL-1, IL-6, IL-8
Normal Echocardiogram. May help diagnose Pulmonary Hypertension
Slide32What is pneumothorax?
Slide33Question
Pneumothorax is suggested by
1-Absent breath sound
2-Stony dull percussion
3-Bronchial breathing
4-Vesicular breathing
Slide34Radiology
Slide35Radiology
Slide36Radiology
Slide37CT Chest
More sensitive to detect
Pulmonary interstitial Emphysema
Pneumothorax
pneumomediastinum
Pleural effusion
Cavitation
Mediastinal
lymphadenopathy
Slide38SEQ
A 6 hours old neonate born at 28 weeks of gestation, to Para5 mother via emergency C-section, weighing 0.9 kg. He has developed respiratory distress
at
2 hours of birth. There is nasal flaring and intercostal and subcostal recessions. Baby is
cyanosed & grunting.
Chest
X-ray
shows
ground glass appearance
with air bronchogram throughout the lungs. His condition
is
worsening.
1-What is diagnosis?
2-What further investigations you will do?
3-What is treatment option?
Slide39Answer
Hyaline membrane disease
ABGs
Mechanical ventilation
Slide40Complications
Barotrauma: high PEEP, CPAP & mean AWP
leading to leak pathologies
Accidental extubation & right mainstem intubation
Prolonged ventilation requiring tracheostomy will
eventually lead to sub-
glottic
stenosis
Nosocomial infections: VAP, Line sepsis, UTI, Sinusitis, Clostridium difficile colitis, MRSA,VRE.
Renal failure esp. When cause of ARDS is sepsis,
Stress gastritis, Anemia
PCM and difficult rehabilitation
Slide41