From Alice Springs ICU 2009
Definition: In the appropriate clinical condition, (sepsis, trauma, pneumonia-commonly in Central Australia) the onset of an acute presentation and persistent symptoms of bilateral symmetric opacities radiologically consistent with pulmonary oedema and no clinical/hemodynamic evidence of raised left atrial pressure and PAO2/FiO2 less than 200(300 for ALI).
Note: The evolution of ARDS can be rapid (within 12 hrs) and the documentation of ongoing hypoxia warrants repeat Chest X rays.
Disease associations: Pneumonia, aspiration, trauma with massive transfusion, burns/inhalation injury, pancreatitis, pulmonary contusions are diseases commonly seen locally which can dispose to the development of ARDS.
Chronic liver disease, alcoholism is associated with greater severity of ARDS. Glutathione depletion has been postulated as the causal agent in alcohol abusers who develop ARDS.
ARDS imitators: In the absence of an infectious aetiology and common disease association’s, illicit or therapeutic drug history, immunological disease and environmental history should be obtained. Imitators include AIP (acute interstitial pneumonia), eosinophilic pneumonia, and diffuse alveolar haemorrhage syndromes. Timing of BAL for diagnosis and the role of steroids have to be actively considered when ARDS imitators are suspected.
Management: General principles-
1) ARDS is not a disease entity in isolation and the application of standard ventilatory protocols by itself will not produce an optimum result. ARDS nearly always occurs in the background of severe sepsis or alternatively in pts with SIRS who additionally may develop infectious complications. The procedures and protocols used in sepsis-source control, early goal oriented resuscitation, tight control of glucose, activated protein C, and steroids for septic shock, saline for resuscitation will nearly always be used either singly or in multiple combinations.
2) Assess the patient and decide whether the ARDS is primary (focus in lung eg –pneumonia) or secondary to systemic sepsis with an extrapulmonary focus. Primary ARDS may not have as much recruitable potential (Pts in Alice often have chronic lung disease and may not tolerate recruitment manoeuvres).
3) Frequent assessment of the patient to see if the goals of therapy-oxygenation, cardiovascular stability and patient comfort and safety are being attained are probably more important than rigid adherence to set protocols. The frequent assessments should be coupled with therapeutic challenges to assess the pts volume and recruitment status. ARDS is a dynamic process and therapy should be dynamic and adaptive.
4) The lung is impacted by other organs, and intra-abdominal pressures will affect ventilatory parameters and measurement of intra-abdominal pressure is necessary when intra-abdominal pathology has caused ARDS. Similarly chest wall disease can impact on lung mechanics. The performance of the heart has to be assessed by available haemodynamic measurements (Picco/Swan). A mixed venous saturation of more than 70% and a difference of less than 25 between arterial and venous saturation can be assumed to denote a satisfactory cardiac output (>2.5 L/min/m2).
5) Monitoring of the lung mechanics need to be done in the volume control mode. The ARDS net protocol recommends assist control mode the same objectives can be achieved using pressure limited modes (the strength of evidence is however not as high).
Non-Ventilatory management of ARDS:
1) Fluid management: ARDS by definition should have a PaoP of less than 18 mmHg. However a significant proportion of ARDS pts will have pressures in excess of this at some stage during their illness. These patients have not had compromises of cardiac function, which goes to suggest that there is an element of fluid overload. Such patients will have a worse outcome and there is limited evidence that limiting the volume of fluids without compromising tissue perfusion will improve the outcome. Till the trials studying fluid restriction in ARDS are completed, fluid management in ARDS will have to be empirical and be guided with invasive haemodynamic monitoring.
2) Nitric oxide:- Inhaled NO is theoretically attractive in that it is delivered only to the ventilated alveoli and improves perfusion. Oxygenation can be improved with doses as small as 5 ppm but no advantage has been shown in giving doses more than 40 ppm. Whilst oxygenation has been shown to improve no significant long term improvement in mortality and morbidity has been shown. In addition NO is expensive and may be technically difficult to administer. The short term use of NO results in the improvement of oxygenation and helps in tiding over a difficult period when oxygen requirements may be very high.
3) Inhaled Prostacyclin: Prostacyclin is easier to administer and cheaper than NO and has a similar action. The therapeutic actions are more pronounced in extra-pulmonary ARDS and pulmonary vasodilatation can decrease the increases in pulmonary hypertension that have been described in ARDS. However the level of evidence showing a decrease in mortality and morbidity with prostacyclin is low.
4) Neuro muscular blocking agents: Normal respiratory muscle oxygen requirements are less than 5% of total oxygen requirements, and in ARDS the requirements can be as much as 25% of the total requirements. Relaxants are theoretically attractive in that they can decrease work of breathing, improve chest wall compliance and decrease peak airway pressures. However the use of relaxants has not been studied extensively and the dangers of prolonged use have been well described. The use of intermittent rather than continuous infusions will promote better monitoring, and the use of agents like atracurium which are metabolized may be better as renal failure is quite a common finding in patients with ARDS.
5) Steroids: The use of steroids in ARDS is controversial. Studies have not shown any use in early ARDS. The use of steroids after 1 week has shown benefit but the studies have been criticised methodologically. Steroids can be considered after 1 week of therapy when there are no signs of infection with a view to prevent the development of pulmonary fibrosis. Results of a large trial are awaited from the ARDS network group.
6) Alternative pharmacological therapy: Cytokine inhibitors. Phosphatidic inhibitors, Immunonutritionals, anti-inflammatory agents and a host of other therapies have been tried in ARDS without convincing evidence from large scale trials
The ARDSNET protocol has been described which has been shown in a large trial to reduce mortality significantly. The trial excluded patients under the age of 18, and pts with severe lung or liver disease. Diseases in which hypercapnoea could be harmful will preclude use of the protocol.
1) Calculate the pts ideal body weight (IBW) :
a. Females-45.5+0.91(Ht in cm-152.4)
b. Males-50+0.91(Ht in cm-152.4)
2) Set the ventilator in volume controlled mode(A/C)
3) Set the TV to 8 ml/kg and the flow rate to 80L/min(more than peak demand)
4) Set the rate to approx pts rate but not to exceed 35/min.
5) Reduce TV by 1 ml/kg approximately every 2 hours or less till a tidal volume of 6 ml/kg is reached and pH and plateau pressure goals are reached.
6) Plateau goals: Plateau <= 30 cm water
a. The plateau must be less than 30 cm water and checked every 4 hours with a pause of 0.5 seconds, and check after every adjustment of Peep and oxygen.
b. If the plateau is more than 30 the Tv is decreased in steps of 1ml/kg till a TV of 4ml/kg or a plateau of less than 30 is reached.
c. If the plateau is less than 25 and the TV is less than 6ml/kg the TV is increased till the plateau reaches 25 or the TV reaches 6ml/kg.
d. If breath stacking occurs TV can be increased to a maximum of 8ml/kg.
7) Ph goals: 7.30-7.45
a) If pH between 7.15-7.30-Increase RR till pH.7.3 or more or pCO2<25. Maximum RR is 35, if RR is 35 and pCO2<25 and pH not controlled consider NaHCO3.
b) If bicarb has been used and ph goal not achieved can increase TV by 1ml/kg (plateau of 30 can be overridden)
c) If pH>7. 45 decrease RR.
8) Oxygenation goal: Sats 88-95% or PaO2 55-80 mmHg Permissible Peep/oxygen combinations:
USE PEEP more than 16-18 with caution in ALICE (high incidence of bronchiectasis/stiff lungs)
9) Keep I/E ratios 1 to 1 is to 3, IE ratios can be kept 1:1 if fIO2 is 1 and use flow rates to modify I/E ratios
a. Initiate CPAP trial if Peep<=8, FIO2<=0.5, acceptable respiratory efforts, systolic>-90 without inotropes.
b. Set CPAP=5 and FIO2 0.5 and if RR<35 for 5 minutes proceed to PSV weaning.
c. If RR>35 within 5 minutes repeat trial after suction, analgesia, if still not tolerated A/c for 24 hrs more.
11) PSV weaning:
a. If CPAP rate <25 set PS to 5 cm water and assess for 2 hours and more for ability to extubate/Swedish nose trial the patient.
b. If CPAP RR 25-35, set PS 20 cm the reduce PS gradually till 5 and follow step a above (the protocol recommends reduction 5 min intervals but in ASH more gradual reduction would be practical)
c. Non toleration of PSV weaning would indicate return to A/C settings.
12) Failure to tolerate Swedish nose would be an indication to continue PSV.
13) The same principle can be used to manage a patient with Pressure controlled mode of ventilation by limiting pressures to 35-40 cm water and then measuring mechanics in a volume controlled mode every 4 to 6 hours.
14) Recruitment: If standard therapy does not improve oxygenation attempts at recruitment can be made (cautiously!) by applying PeeP at 40 cm water for 40 seconds. Paralyze patient and put in CPAP mode and at 10-15 second intervals increase Peep to 40 hold it for 40 seconds and gradually bring the Peep down in steps of 5 to pre-existing Peep over 60 seconds.
15) Proning: Proning will improve oxygenation on the short term but this can only be tried when staffs are familiar with the technique. At present in ASH ICU proning is non-standard therapy.