ARDS / ALI

Question 1

What are the five diagnostic criteria for ARDS/ALI?

Answer 1

1. Acute onset of respiratory distress
2. Known risk factor must be present
3. Evidence of pulmonary capillary leak not associated with increased capillary pressures
4. Evidence of inefficient gas exchange
5. Evidence of inflammation

Question 2

Pathophysiology of ARDS/ALI

Answer 2

• not well understood
• Crazy inflammatory response: cytokines and other inflammatory mediators cause neutrophils and T-lymphocytes
• Four overlapping stages:
  1. Exudative:
• occurs within hours and can last for days
• Type I pneumocytes becomes damaged and type II stops producing surfactant
• results in alveolar damage and vascular endothelial damage
• causes non-cardiogenic pulmonary oedema
• high mortality rate
  2. Proliferative:
• Type II multiply rapidly in an effort to repair damaged areas
• causes clogging due to over production of interstitial fibroblast
  3. Fibrotic:
• results in even more fibroblast proliferation that leads to more deposits of collagen
• lungs become cobblestone and severe fibrosis occurs
  4. Recovery
• rarely documented in veterinary patients
• most will die

Question 3

What are the differences between ARDS and AIL?

Answer 3

• Major difference is the degree of hypoxia (PaO2 levels)
• Must obtain arterial blood gas
• Calculate ratio of arterial oxygen pressure (PaO2) to fractional inspired oxygen
• If ratio is less than 300 = ALI
• if ratio is less than 200 = ARDS

Question 4

PaO2

Answer 4

Is NOT the measurement of how much oxygen is in the blood but is the pressure exerted by the dissolved oxygen molecules!

Normal PaO2 is between 80-100mmHg at sea level
Hypoxemia: PaO2 is less than 80mmHg
Severe hypoxemia:PaO2 is than 60mmHg

*As a rule, PaO2 should be 5X the FiO2
E.g. if FiO2 is 100% then PaO2 should be 500mmHg

**Normal PaO2/FiO2 ratio is 476 (100/0.21)
*To calculate ratios:
If PaO2 is 59mmHg on room air, the PaO2/FiO2 ration is 59/0.21=280 = AIL level!

Question 5

What would u see on a radiograph of an ARDS patient?

Answer 5

• Evidence of capillary leakage not associated with increased capillary pressures
• Bilateral alveolar infiltrates will be seen in most cases (but can be due to other disease processes as well so accurate history is super important)

Question 6

What are the risk factors for ARDS/ALI?

Answer 6

Can be pulmonary or extrapulmonary

1. Pulmonary:
   - direct trauma to the lungs
   - pneumonia
   - noncardiogenic pulmonary edema (electrocution, head trauma)
2. Extrapulmonary:
   - sepsis
   - systemic inflammatory response syndrome
   - viral infection (parvo)
   - smoke inhalation
   - multiple blood transfusion: TRALI
   - peritonitis
   - pancreatitis

Question 7

Signs and symptoms of ARDS/ALI

Answer 7

Severe respiratory distress
Severely lethargic
Collapsed
Poor perfusion
Crackles
Orthopnea
Non-cardiogenic pulmonary edema (due to pulmonary capillary leakage)
Pulmonary hypertension (from vasoconstriction) - this could lead to right ventricular dysfunction of the heart.
Multi Organ failure (MODS) due to severe hypoxemia
In dogs: High rate of bacterial pneumonia, aspiration pneumonia or sepsis
DIC (due to severe changes to othe vascular system)

Question 8

Tx for ARDS/ALI

Answer 8

1. Oxygen therapy-Minimise stress and restraints -ideally mechanical ventilation -Monitor o2 stats-Aretrial blood gas if possible-Venous blood gas from jugular vein or vena cava as more accurate :normal PVO2 is above 40mmHg :below 30mmHg requires intervention :below 20mmHg is an emergency -Pulse Oximetry
   : oxygen sat in hemoglobin
   :Spo2 of 96% = PaO2 of 80mmHg
   : SpO2 of 91% = PaO2 of 60mmHg
2. Intravenous fluids
   -Crystalloids
   -Consider colloids
   -Watch for fluid overload : chemosis, increase in RR, nasal discharge
3. Antibiotics
   -high chance of secondary infection hence used
   -Look for signs of sepsis or infection: pyrexia, increase in WBC, decreases in blood glucose, increases in heart rate and respiratory rate
4. Steroids
   -use is controversial
   -possible improvement from suppression of ongoing inflammation in the proliferative stage
5. Blood pressure
   -use of vasopressors and vasodilators are controversial
6. Nutritional support
   -increase in resting energy expenditure and an increase consumption of protein
   -early provision of nutrition for these patients is essential
7. Mechanical ventilation
   -primary treatment but costly
   -higher chance of developing pneumonia or a pneumothorax
   -consider ventilating at a lower tidal volume and higher PEEP pressure
8. Additional care
   -TPRs ever 2 hourly
   -constant ECG, BP and CVPs monitored
   -Central line and urinary catheter and arterial line
   -rotate patient to prevent fluid buildup on one side
   -capnograph
   -lubricate eyes
   -Endotracheal tube changes and repositioning
   -moisten oral mucous membranes