Acute Respiratory Distress Syndrome (ARDS)

Title of Guideline (must include the word Guideline (not

protocol, policy, procedure etc)

Guideline for the management of

Acute Respiratory Distress
Syndrome (ARDS) Protocol

Contact Name and Job Title (author)

Dr Megan Smith (Consultant paediatric

Intensivist)
Directorate & Speciality

Family Health; PICU

Date of submission

January 2005
Date on which guideline must be reviewed (this should be one
to three years)
Explicit definition of patient group to which it applies (e.g.
inclusion and exclusion criteria, diagnosis)

Abstract

March 2014

Patients with Acute Respiratory

Distress Syndrome (ARDS) in
PICU
This guideline describes the
management of patients with
acute respiratory distress
syndrome (ARDS) in PICU

Key Words

PICU; ARDS; Respiratory Distress

Statement of the evidence base of the guideline has the
guideline been peer reviewed by colleagues?
Evidence base: (1-5)

5: recommended best practise based

on the clinical experience of the
guideline developer

Consultation Process

PICU Staff
Target audience

PICU Staff

This guideline has been registered with the Nottingham University Hospital Trust.
However, clinical guidelines are guidelines only. The interpretation and application of
clinical guidelines will remain the responsibility of the individual clinician. If in doubt
contact a senior colleague or expert. Caution is advised when using guidelines after the
review date.

Definition
. Acute lung injury is defined as a syndrome of acute and persistent lung
inflammation with increased vascular permeability It is characterised by1,2:
Widespread bilateral radiographic infiltrates
PaO2/FiO2 < 40 kPa (300mmHg). This is regardless of PEEP.
No clinical evidence of elevated left atrial pressure (i.e. left heart failure). If
measured, the pulmonary wedge pressure is less than 18mmHg.
The distinction between ARDS and acute lung injury is somewhat arbitrary as the
degree of hypoxia does not correlate well with survival3. Nevertheless, ARDS
refers to the severe end of the spectrum of acute lung injury and a Pa02/FiO2
ratio < 27 kPa is characteristic.
ARDS typically develops over 4 to 48 hours and persists days or weeks4. ARDS
is frequently accompanied by acute injury to other organ systems but can occur
in isolation (e.g. massive air embolism or chlorine gas inhalation).
Diagnostic difficulties
1) Clinically and radiographically, ARDS closely resembles left heart failure
Indeed, as many as 20% of patients with ARDS have concomitant left
ventricular dysfunction. ECHOCARDIOGRAPHY IS THEREFORE
INDICATED IN ALL ARDS PATIENTS. Pulmonary wedge pressures can
help but may not be elevated in cases of transient left ventricular
dysfunction (e.g. myocardial ischaemia) or partially corrected fluid
overload.
2) The distinction between left heart failure and ARDS is often apparent from
the clinical circumstances leading to the respiratory distress. Pulmonary
wedge pressures may help.
3) Diffuse alveolar haemorrhage (e.g. pulmonary vasculitis or pulmonary
haemosiderosis) is a rare but important differential. It should always be
considered if there is an unexplained drop in Hb. Bronchoscopy may help
this diagnosis.
4) Lymphoma or Acute Leukaemia may occasionally cause a similar picture
5) Miliary Tuberculosis

Causes of ARDS
Sepsis leading cause, ARDS often occurs after high fluid resuscitation for
sepsis.
Aspiration of gastric contents
Infectious Pneumonia (e.g. Pneumococcal, Viral, PCP, Pseudomonas, Staph
Aureus, Legionella, Gram negatives)
Surface Burns
Trauma (including lung contusions, massive traumatic tissue injury, fat emboli)
Massive Blood Transfusion
Following relief of upper airways obstruction by intubation or tracheostomy
Lung and bone marrow transplantation
Transfusion Reaction (blood bank can conirm this by testing a sample of the
transfused plasma for antibodies directed against white blood cells in a sample of
the recipients blood)
Drugs (e.g. protamine, nitrofurantoin, and cytotoxics) (also in overdose: aspirin,
cocaine, opioids, phenothiazines and tricyclic antidepressants)
Neurogenic Pulmonary Oedema (intraerebral bleeds / seizures)
Near Drowning
Acute Pancreatitis
Opioid withdrawal
Investigations

Routine investigations as dictated by clinical condition

Consider repeat CXR daily
Daily Creatnine Kinase levels (especially in paralysed patients)
Monitor inflammatory markers (CRP, WCC etc) closely in all ARDS
patients
ECHO and 12 lead ECG

Consider bronchoscopy for inspection and bronchoalveolar lavage (for

microscopy, culture, culture for mycobacteia / PCP / legionella / viruses &
cytology)
Consider Swan-Ganz catheter in older children
Management

General Management
1. Treatment of the underlying cause.
2. Empirical treatment of sepsis when indicated and of secondary nosocomial
infections. The development of nosocomial infections occurs in 60% of ARDS
patients5.
3. Good nutritional support. Feeding should be introduced as soon as it is safe
medically/surgically to do so. Early feeding is an important therapeutic tool.
4. Effective ventilation strategies aimed at reducing ventilator associated lung
injury to a minimum.
5. General supportive care.
Ventilation
Appropriate use of the ventilator is important in the treatment of these patients
and to minimise ventilator associated lung injury. Important therapeutic
approaches include:
Low tidal volume ventilation
Permissive hypercapnia
Use of PEEP to improve hypoxia and limit tidal atelectasis
Prone Ventilation
Suggestions in ARDS:
1. Use the lowest level of PEEP that is capable of producing an adequate
arterial PaO2 on FiO2 less than 0.6
2. Aim for a tidal volume of 6 ml/kg
3. Note that when a patient requiring high PEEP is disconnected from the
ventilator for even a single breath, alveolar de-recruitment will occur.
Consider the use of in-line suctioning devices.
4. Try to keep Plateau Pressure less than cm H20
5. Early in the course of ventilation, fully supported modes of ventilation are
preferred.
6. Prolonging inspiratory time may improve oxygenation. Inverse Ratio
Ventilation is a possible manoeuvre to improve oxygenation (i.e. longer
inspiratory time than expiratory) but should be used with care to avoid
barotraumas.
7. Aim to keep plateau pressure less than 30cm H2O
8. When weaning, wean FiO2 in preference to PEEP until FiO2< 50%.
9. Echocardiography is indicated in all ARDS patients.

Oxygenation
Aim to keep FiO2 less than or at 60% if at all possible. This can primarily be
achieved by using adequate PEEP. The following points may also be useful in
minimising FiO2:

During the peri-intubation period 100% oxygen is used. However, rapidly

titrate Fi02 downwards to the lowest fraction necessary to maintain an
Sa02 >90%.
Other than the peri-intubation period, 100% oxygen should be avoided as
this may cause absorptive atelectasis6. Once established, absorptive
atelectasis is not rapidly reversed by reducing Fi02.
ARDS patients are likely to develop pulmonary oedema, regardless of
volume status. Hence, a trial of diuresis to improve oxygenation is
reasonable as long as hypotension and organ hypoperfusion are
avoided.
Consider prone-positioning
Oxygen consumption can be assessed by measuring mixed venous
saturation. Oxygen consumption may be decreased by treating fever,
providing adequate analgesia and providing heavy sedation. Paralysis
does reduce oxygen consumption but should rarely be necessary as
neuromuscular sequelae can be severe in these patients.
Oxygen delivery is dependent on Haemoglobin concentrations but
increasing Hb above 9 g/dl is unlikely to increase benefit7. Most patients
will benefit from a conservative policy keeping Hb between 7 and 9 g/dl7.
Similarly, use of inotropes solely to increase oxygen delivery, in the face
of a high oxygen index, should be avoided as this policy may
paradoxically increase mortality.

Refractory Hypoxaemia
Possible strategies in the face of continued hypoxia include:
High Frequency Oscillation
Pulmonary vasodilators e.g. nitric oxide(for neonates with pulmonary
hypertension)
ECMO
Permissive Hypercapnia
Hypoventilating these patients when using mechanical ventilation minimises
ventilator associated lung injury11. Lower rates and tidal volumes can be used to

achieve permissive hypercapnia. PaCO2 up to 12 kPa have been allowed as long

as the rise is not too rapid and the pH > 7.1
Contraindications to permissive hypercapnia include:
1.
2.
3.
4.

Raised Intracranial Pressure or known seizure disorder.

Poor myocardial function
Significant Metabolic acidosis
Possible pregnancy

Note:
Heavy sedation is usually required so that patient will tolerate hypercapnia
A rise in FIO2 is to be expected when utilising permissive hypercapnia
PaCO2 should be allowed to rise slowly in increments of 1kPa every 2 to 3
hours
pH should be maintained above 7.1
Sodium Bicarbonate is seldom indicated in these patients

Prone-Ventilation
Prone ventilation improves gas exchange in the majority of patients. It may also
reduce ventilator induced ling injury.
Avoid if:

Open anterior surgical wounds

Facial fractures
Haemodynamic and cardiac rhythm disturbances are strong relative
contraindications, since immediate access for cardiopulmonary
resuscitation is limited
Spinal instability is the major absolute contraindication to prone positioning

Clinical use of prone ventilation

1. Prone positioning should be tried early in the course of ARDS in patients with
an Fi02> 60% or PEEP> 11kPa.
2. An improvement will be seen within 30 mins of prone positioning. Failure to
see any improvement in PaO2 at 30 mins often implies the patient is a nonresponder to prone positioning.
3. There is no agreed time limit to the duration of maintaining the prone position.
The prone position can be continued for as long as effective prior to the onset
of attempted weaning, with position changes only as necessary for routine
nursing care. However some authors recommend repeated cycles of
proning10 (eg. 48 hours prone, 12 hours supine). After this, placing the patient

supine again for 12 hours (minimum 4 hours) will be beneficial. After this, the
patient may be placed prone again9.

Weaning

As a generalisation, wean FiO2 in preference to PEEP (or Mean Airway

Pressure) until Fi02 is less than 50%.
When weaning, it is important to minimise patient ventilator asynchrony as
this will increase agitation and gas trapping. This can be achieved either by
adequate sedation or, at this stage, by reducing the rate of ventilator breaths
and allowing more patient-synchronised pressure supported breaths.
ReferencesNottingham Children's Hospital Guideline
1. Bernard et al. The American-European consensus conference on
2. ARDS: Definitions, mechanisms, relevant outcomes, and clinical trial
coordination. Am J Respir Crit Care Med 1999; 159:1849
3. Artigas et al. The American-European consensus conference on ARDS,
part 2. Ventilatory, pharmacologic, supportive therapy, study design
strategies, and issues related to recovery and remodelling Am. J Respir
Crit Care Med 1994; 157: 1332
4. Doyle et al. Identification of patients with acute lung injury. Predictors of
mortality. Am J Resp Crit Care Med 1995; 152:1818
5. Pepe et al. Clinical predictors of the adult respiratory distress syndrome.
Crit Care Med 1995; 152: 1818
6. Delclaux et al. Lower tract respiratory colonization and infection during
severe acute respiratory distress syndrome. Am J Resp Crit Care Med
1997; 156: 1092
7. Wagner et al. Continuous distributions of ventilation-perfusion ratios in
normal subjects breathing air and 100% oxygen. J Vlin Invest 1974; 54: 54
8. Hebert et al. A multicenter, randomized, controlled clinical trial of
transfusion requirements in critical care. N Engl J Med 1999; 340: 409
9. Curley, MA. Prone positioning of patients with acute respiratory distress
syndrome: a systematic review. Am J Crit Care 1999; 8:397
10. Fridrich, P, Krafft, P, Hochleuthner, H, Mauritz, W. The effects of longterm prone positioning in patients with trauma-induced adult respiratory
distress syndrome. Anesth Analg 1996; 83:1206.
11. The Acute Respiratory Distress Syndrome Network. Ventilation with lower
tidal volumes as compared with traditional tidal volumes for acute lung
injury and the acute respiratory distress syndrome. New England Journal
of Medicine May 4 2000, 342:18 1301-1308