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Respiratory Distress

Syndrome
Prof.Kamani Samarasinghe

Severe life threatening form of


progressive respiratory insufficiency
which involve pulmonary tissue
diffusely

Two forms
Neonatal RDS
Adult RDS
Both have common morphological change
formation of hyaline membrane in alveoli
Hyaline membrane disease

Neonatal respiratory distress


syndrome
This is a common complication in
preterm infants. Also seen in
- Babies of diabetic mothers
- Babies delivered by caesarean
section

Birth asphyxia
Inhalation of amniotic fluid
Various congenital abnormalities.
Excessive sedation of mother
2nd as compared with the 1st of twins.

Mortality rate is very high. 20-40%


If birth weight is <1000g-50%
Male>Female

RDS develop within a few minutes or


hours of birth characterized by
rapid respiratory rate.
Increased respiratory difficulty
cyanosis despite high concentration
of inhaled O2.

Chest X-ray shows


Opacities(Reticulo-nodular shadows)
Major etiological factor is the
immaturity of the lung.
The basic defect is deficient
surfactant production by type II
pneumocytes.

Surfactant normally reaches


adequate levels after 35 weeks of
gestation.
RDS occurs in
- 60 % born before
28/52
-40 % 28-32 weeks
-20 % 32 36 weeks
-< 3 % after 36
weeks

Surfactant reduces surface tension


Reduce the amount of pressure
required to open the alveoli.
In the intermediate neonatal period
surfactant is important in maintaining
expansion of the lung after first few
breaths
In surfactant deficiency the alveoli
collapse after initial expansion

-Failure of oxygenation
-Hypoxaemia
-Alveolar damage
-Protein exudation
- Alveolar haemorrhage

Hyaline
membrane

Babies who survive first few days recover


completely. Minority develop chronic lung
disease with fibrosis-Bronchopulmonary
dysplasia.
Amniocentesis can evaluate lung maturity
by testing for lecithin:Sphingomyelin ratio
(L:S) in amniotic fluid.
Early pregnancy Sphingomyelin exceeds
Lecithin. With lung maturity Lecithin
increases
2:1-Risk is minimal
<1:1-Risk is very high

Adult respiratory distress


syndrome(ARDS)-shock lung

A syndrome caused by diffuse alveolar


capillary damage and characterized
clinically by the rapid onset of severe life
threatening respiratory insufficiency,
cyanosis and severe arterial hypoxaemia
that is refractory to O2 therapy.
And frequently progresses to multi organ
failure.
Caused by variety of aetiological factors
Mortality rate is about 50%.

Causes of ARDS

Severe hypovolaemic shock


Septic shock. Gram ve
Inhalation of toxic gases- No,SO2
Severe burns,inhalation of hot smokes
Drugs-Chemotherapeutic agents
Ingested toxic agentsParaquat,Kerosone
Aspiration pneumonia especially gastric
contents

Radiation
Acute pancreatitis
Cardiopulmonary bypass
DIC
Air embolism/fat embolism
Near drowning
Narcotic overdose

Pathogenesis
The mechanisms by which ARDS
occurs are complex and varied.
1)
In hypovolaemic shock
Prolonged vasoconstriction

Ischemic injury to alveolar epithelium

2)Gram ve septicaemia
Endotoxins
Activate alveolar macrophages
TNF
Alveolar damage

3)Acute pancreatitis
Enzyme liberation
Alveolar injury
4)Toxic gas
Direct injury

Damage to capillary endothelium


or/& alveolar alveolar epithelium
Activate alveolar Activated neutrophils
macrophages
Fibronectin
Cytokines
PDGF, TGF

Release proteases,
PAF, Oxygen free
Release cytokines
radicals and
IL-8, IL 1 & TNF
leukotrienes

Proliferation of fibroblasts
and collagen
Stiff lung

Local alveolar damage


Intra alveolar oedema
Surfactant inactivation
Hyaline membrane

Pathology
Macro-Lungs are heavy , beefy,
oedematous, solid. Sink in water
Cut surface shows haemorrhages and
fluid exudate.

Micro-ARDS is characterized by
diffuse alveolar damage with loss of
type I pneumocytes.
-Endothelial damage- Fluid exudate
Early stage-Intra alveolar oedema
RBC Extravasation

Hyaline membrane is not specific to


RDS
Can be seen in any type of acute
alveolar damage
Eg- acute viral, allergic , chemical
pneumonia

Later-Diffuse alveolar damage


Intra alveolar haemorrhage
Alveoli collapse
Eosinophilic hyaline membrane in
the distended respiratory
bronchiolsand damaged alveoli
Hyaline membrane coagulated protein
lining admixed with necrotic epithelial
cells

Consequences
Death
Resolution-mild cases
Neonatal RDS-bronchopulmonary
dysplasia
Desquamated interstitial pneumonia
due to pneumocyte proliferation
supervened with inflammation
Widespread intestinal fibrosis(Hamman
Rich syndrome)

Clinical features
Patients are often very ill with some
other disease.
Rapidly increasing dyspnoea,
hypoxaemia, cyanosis
This usually occurs within 1-2 days of
the traumatic episode
CXR-Early- Normal

Diffuse interstitial oedema

Totally opaque lung field

Outcome
Therapy is difficult
Frequently fatal
Only minority recover with resorption
of oedema fluid & reexpansion of
atelectatic areas.

PULMONARY
HYPERTENTION

P.H.T.
Normal BP in pulmonary arterial
circulation is much lower (1/8 of
systemic BP)
Does not exceed 30/15 mmHg even
during exercise.
BP in pulmonary vein is 3-8 mmHg
PHT Systolic BP in the pulmonary
arterial circulation >30mmHg (1/4 of
systemic level)

P.H.T.
Two types
(1) primary / idopathic P.H.T.
(2) secodary P.H.T.
primary pulmonary hypertension
- uncommon
- unknown aetiology
- diagnosed after excluding secondary
P.H.T.
- young females 20 40 years of age

Contd..
Aetiopathogenesis unknown
? A neurohumoral vasoconstrictor
mechanism
? Unrecognized thromboemboli or
amniotic fluid emboli
? A form of collagen vascular disease
? Pulmonary veno occlusive disease
? Ingestion of substances Bush tea ,
O.C.P., Appetite depressant
? Familial

Secondary pulmonary
hypertension
- More common
- Secondary to recognized lesion in the
heart or lung
- Can occur in any age
- More frequently > 50 years

Aetiopathogenesis 3 groups
(1) passive P.H.T
- the commonest type.
- Caused by diseases raising pressure
in pulmonary veins , eg- Mitral
stenosis
-Chronic left
ventricular failure HT , aortic
stenosis , myocardial fibrosis.

(2) Hyperkinetic P.H.T.


- Blood enters the pulmonary arteries in greater volume or at a
higher pressure eg; PDA , ASD, VSD.
(3) vaso-occlusive P.H.T.
- 3 types (a) obstructive type block in the
circulation eg; multiple emboli or thrombi

pulmonary

(b) oblitrative type decrease in pulmonary vascular bed


eg; COAD, TB, pneumoconiosis
(c vasoconstrictive type-wide spread & sustained hypoxic
vasoconstriction eg; high altitude , pathologic obesity, severe
kyphoscoliosis, neuromuscular disease, upper airway disease
tonsillar hypertrophy

Pathological changes
Irrespective from the type of P.H.T. chronic
cases invariably lead to cor pulmonale
Pathological changes are in right side of the
heart & pulmonary arterial tree in the lungs
Hypertrophy of the right ventricle & the
right atrium
Vascular changes are not always specific &
frequently overlap between primary &
secondary P.H.T. & involve entire arterial
tree from the main pulmonary arteries down
to the arterioles

Arterioles & small pulmonary


arteries
(1) medial hypertrophy
(2) thickening & reduplication of elastic
laminae
(3) plexogenic pulmonary arteriopathy
intraluminal tuff of capillary formation
in dilated thin walled arterial branchescommonly seen in primary P.H.T.

Medium size pulmonary arteries


(1) medial hypertrophy not marked
in primary P.H.T.
(2) concentric intimal thickening
(3) advetitial fibrosis
(4) thickening & reduplication of
elastic laminae
Large pulmonary arteries
(1) atheromatous deposits