Respiratory

• A.R.D.S.

• Acute Respiratory Distress Syndrome)
• It is also called "Shock Lung“
• Definition: It is a syndrome in which there is pulmonary oedema without increment in the pulmonary capillary venous pressure or non cardiac pulmonary oedema

• Unlike the Lt.sided heart failure , in which there is pulmonary oedema due to increment in the Lt. atrial pressure which causes increment in the pulmonary venous pressure → oozing of fluids to the lung tissue → cardiiac pulmonary oedema.
• While in ARDS, the pulmonary oedema is due to oozing of fluids through the capillaries without increment in pulmonary venous pressure which means that the defect in the respiratory membrane.

How to understand ARDS & Acute lung injury (ALI)

Acute lung injury (ALI) :-
It is any form of lung damage and less severe form of the condition is called It could progress to ARDS

• This syndrome is caused by a variety of causes that are either directly or indirectly cause damage to the lung tissue.
• Directly : bullet injury, blast, embolus, infections,…etc. Indirectly : haemolytic anaemia, multiple fractures, head injury,..etc.

Causes

There are many processes that precipitate ARDS.


The following are well known causes

:
• 1) Pulmonary infection:
• Viral, e.g. H1N1 influenza, SARS,…
• Mycoplasmal, ..
• Bacterial,
• Tuberculosis

2) Injuries : either directly by bullet or blast …etc. or indirectly by fractures or haemolytic anaemia.. etc.
• 3) Fractures
4) Head injury
• 5) Surgery – if prolonged- cause ARDS
6) Septicemia & septic shock, in fact all shock states can cause ARDS, that is why ARDS is called "Shock lung"

7) Acute pancreatitis

8) Burn
• 9) Embolization : either fatty embolus, pulmonary thrombo-embolus, air embolus, & amniotic fluid embolus..
** usually, embolization is due to small ambolus that blocks small tributary of pulmonary artery; but the patient may develop ARDS (unknown cause) or by big embolus → massive pulmonary embolizaion → ARDS
• 10) Direct damage to the lung by acids (due to vomiting or regurgitation) → ARDS


11) Drowing : water is detrimental to the lung & can initiates ARDS
12) Hanging : either suicidal or execution , if the patient –for example- survive after hanging himself → develop ARDS
13) Inhalation of chemicals & toxic materials : as in the wars, which cause ARDS & serious respiratory problems to the soldiers, or it can happen to the workers (who works in water refinery system)where chlorine is used for water cleaning, but chlorine is very irritant to the lung & cause damage to the lung tissue →ARDS also happen in housewives who use detergent in large conc.
• 14) In cardio pulmonary bypass in cardiac surgery
• 15) Multiple blood transfusion
• 16) Gastric aspiration

• 17. Toxic gases that cause this syndrome One of which is O2 . Though O2 is used in the treatment of this syndrome, it is an irritant gas if given in high conc. So it is mandated not to give high conc. for more than 24 hours, & this could happen in mechanical ventilators, if you breath into close circuit & getting pure O2 (100% conc.), so if you need O2, you should not use pure O2 over 24hs because it may lead to this syndrome.

Pathophysiology

Regardless of the cause of ARDS, it will lead to destruction of the lung tissue & this tissue contains endothelium of the blood vessels & the epithelium in the alveoli which constitute the respiratory membrane.

Hence, the process will lead to damage to both epithelium & the endothelium or to any one of them, & once the capillaries get damaged it will lead to oozing of oedema fluid to the alveolar spaces, this is actually a pulmonary oedema, (such thing can occur in left sided heart failure) & there will be oozing of fluid from the capillaries to the air-spaces of the lung tissue.

Hence, damage to the epithelial & endothelial layers due to inflammatory process of ARDS will lead to stiffness of the lung.

• Severe ALIB/L radiographic infiltratesPaO2/FiO2 <200mmHg (ALI 201-300mmHg)Severe ALIB/L radiographic infiltratesPaO2/FiO2 <200Severe ALIB/L radiographic infiltratesPaO2/FiO2 <200mmHg (ALI 201-300mmHg)No e/o L Atrial P; PCWP<18mmHg (ALI 201-300mmHg)No e/o L Atrial P; PCWP<18No e/o L Atrial P; PCWP<18

Severe ALI

B/L radiographic infiltrates
PaO2/FiO2 <200mmHg (ALI 201-300mmHg)
No e/o L Atrial P; PCWP<18


Acute Phase:
Pulmonary oedema with normal vascular pedicle
Associated with no cardiomegaly or upper lobe blood diversion
When pulmonary vessels can be distinguished they are often constricted
Septal lines usually absent because capillary leak occurs directly into alveolar spaces (cardiogenic pulmonary oedema)
Progressive lung destruction and transition from alveolar to interstitial opacities

Chronic phase

fibrosis
focal emphysema

Inflammatory Alveolar Injury

Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells
Increased permeability of alveolar capillary membrane
Influx of protein rich edema fluid and inflammatory cells into air spaces
Dysfunction of surfactant





• Inflammatory Alveolar Injury
• Fluid in interstitium and alveoli
• Impaired gas exchange
•  Compliance
•  PAP
• Pro-inflmm cytokines (TNF, IL1,6,8)
• Neutrophils - ROIs and proteases damage capillary endothelium and alveolar epithelium

• Severe ALIB/L radiographic infiltratesPaO2/FiO2 <200mmHg (ALI 201-300mmHg)Severe ALIB/L radiographic infiltratesPaO2/FiO2 <200Severe ALIB/L radiographic infiltratesPaO2/FiO2 <200mmHg (ALI 201-300mmHg)No e/o L Atrial P; PCWP<18mmHg (ALI 201-300mmHg)No e/o L Atrial P; PCWP<18No e/o L Atrial P; PCWP<18

Clinical Features

Any patient having severe medical or surgical problem & the patient developed severe RF within the first 1 or 2 days, you should think about ARDS.
Again you find the features of the cause of the ARDS.

• Complications

_ Bacterial super infection, because oedema fluid is a good medium for infection by many M.O.
_ Multiple organ faailure, because there will be septicemia which can leads to liver, kidney, heart, or brain failure that is why the mortality rate is high even in the best centers. Mortality rate in the best centers is about 50%, here in our country the mortality rate is about 90% !! because of lack of sophisticated equipment, the average mortality rate is about 70%.
_ If the patient survive the acute phase then the patient will end up into pulmonary Fibrosis.


• Summery of finding
1) Progressive SOB (1-2 days) following any medical or surgical problem.
2) Central cyanosis (resistant to treatment).
3) Hypoxia & hypocapnoea.
4) Wide-spread shadowing (bilateral) on chest X-ray.
5) On right sided cardiac catheterization to check the pulmonary venous pressure, it will be normal (i.e. there is normal pulmonary wedge pressure, yet there is pulmonary oedema.
6) Pulmonary fibrosis.
7) Fine crepitation, due to pulmonary edema

Treatment

The patient should be cared in an "Intensive Care Unit" ICU, with facility for mechanical ventilator & Rx is directed toward:
A: cause (medical or surgical)
B: General measures

General Measures

These include the following
1 * O2 therapy: it is general Rx or therapy for all causes; but not pure O2 because it is irritant to the lung tissue
2 * Mechanical ventilation: in ARDS, there is damage to type -II pneumatocyte → decrease amount of surfactant, so you need always a +ve pressure to keep the lung inflated & push the fluids away from the airspaces

There are 2 types of assisted ventilation to keep this +ve pressure :

1) IPPV “intermittent positive pressure ventilation"
2) PEEP "positive end expiratory pressure"


Other general measures that include
• Dealing with infection.
• IV nutrition may be needed in ICU
• Cleanliness
• Prevent bed sore
• Electrolyte balance must be carefully controlled.
• Use of Steroids