Acute Respiratory Distress Syndrome (ARDS) is a serious respiratory condition of diffuse alveolar injury seen frequently in intensive care patients. It was first identified in 1967 by Ashbaugh, Bigelow, Petty and Levine as the acute onset of broad respiratory symptoms. This improved the clinical and pathological understanding of the condition. Small changes to therapeutic practice have developed, however despite these developments the morbidity and mortality in patients of all ages with ARDS remains significantly high (Fan, Needham, & Stewart, 2005).
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This topic has been chosen by the author as they have a personal interest in this type of patient after having recently cared for a critically ill ARDS patient in their ICU (Intensive Care Unit). The author has previously been involved in caring for ARDS patient’s at their place of work and over that period has observed changing practices and treatment. A further knowledge and understanding of this complex patient is their motivation for this topic. A case study relating to a case of ARDS is attached as Appendix 1 and will be referred to throughout this assignment.
The pathophysiology of this disease leading up to the presenting signs and symptoms of ARDS will be presented. Current literature and treatment trends will be discussed in conjunction with the medical and nursing practice observed within the ICU workplace. Treatment trends and recommended best practices will be identified and critically analysed. Recommendations will then be presented to encourage best practice within the ICU workplace.
First described in 1967 by Ashbaugh and colleagues as Adult Acute Respiratory Distress Syndrome, ARDS patients continue to have a high rate of mortality and morbidity (Fan, Needham, & Stewart, 2005). A definition was implemented in 1988 (MORE DETAILS>>>) and then a new simplified definition was recommended in 1994 by the American-European Consensus Conference (AECC) (Harman 2009). It acknowledged that the severity of lung injury varies, and it was a definition that was easy to apply in the clinical setting (Ware & Matthay, 2000). The new definition involved changing the name from “adult” to “acute” respiratory distress syndrome as it was observed that the syndrome occurs in adults and children. The AECC definition states that the patient must have an acute condition, characterised by bilateral pulmonary infiltrates and severe hypoxaemia in the absence of evidence of cardiogenic pulmonary oedema. Hypoxaemia is calculated as a ratio of PaO2/FiO2. In ARDS the ratio is less than 200. Cardiogenic pulmonary oedema is excluded either clinically or by pulmonary wedge pressure of less than 18mm Hg in patients with a Swan-Ganz catheter.
Despite this official and accepted definition there is still argument over the ability to accurately define ARDS when it is a syndrome and not an illness and because of this the presentation and pathway of the disease varies between patients (Zambon & Vincent, 2008). There has also been criticism over the simplicity of the AECC definition as it does not identify the underlying cause, nor does it require other systems affected to be assessed (Ware & Matthay, 2000). The major benefit of the universally accepted definition has been the ability for hospitals and investigators to begin the advancement of clinical trials into treatment of this syndrome (Ware & Matthay, 2000).
In patients diagnosed with ARDS 80% can have the cause related to either direct or indirect injuries. Direct injuries include pneumonia, aspiration, lung contusion, fat embolism, near-drowning, inhalation injury, and reperfusion injury. While indirect injuries include non-pulmonary sepsis, multiple trauma, massive transfusion, pancreatitis and cardiopulmonary bypass (Berten & Soni 2009).
This insult to the respiratory system is reflected in a variety of pathophysiological presentations leading to the patients presenting signs and symptoms. There are 3 identified stages of ARDS. The acute or exudative phase is seen in days 1-7. The sub-acute or proliferative stage is seen from around day 7, and the chronic or fibrotic phase is generally seen around 2-3 weeks after the initial onset (Marshall, Bellingan, & Laurent, 1998, Griffiths 2007).
The exudative phase leads to the disruption of the normal alveoli-capillary barrier which therefore disrupts ventilation and oxygenation. Inflammation occurs in the lungs and the body releases cytokines and inflammatory mediators from the epithelial and endothelial cells. Other cells (neutrophils and T-lymphocytes) move into the lungs and causing alveolar damage. The inflammation causes endothelial dysfunction, and increases the permeability of this barrier which allows fluid to escape from the capillaries and limits the draining of fluid out from the lungs. Small vessel thrombosis occurs as a result of pulmonary capillary and endothelial swelling Cell debris plugs the alveolus lumen leading to pulmonary oedema increasing the thickness in the alveolar-capillary space. Surfactant supply depletes and production becomes inactivated.
The exudative phase is seen in the ICU patient as increased shortness of breath, higher respiratory rate, productive cough, “wet” sounding chest, decreased oxygenation. These symptoms were all seen with the patient in Appendix A.
The Proliferative Phase is
and involves the initial stimulus causing the stimulation of the cascade effect. All ARDS patients will experience this stage. It leads to an increase in the permeability of the alveolar-capillary barrier leads to a rush of fluid into the alveoli. This injury allows pulmonary oedema to occur in patients with no known cardiogenic failure. This protein rich fluid engulfs the alveoli drawing in activated neutrophils and macrophages. This initiates the inflammatory cascade which releases interleukins, tumour necrosis factor and inflammatory mediators. Neutrophils release oxidants, leukotrienes and various proteases. The effect of this process is cell damage, with cell debris blocking alveolus lumen and the inactivation of surfactant.
As a result platelets combine, a procoagulant cascade may arise. Surfactant inactivation, alveolar filling, cellular debris all lead to an increase in respiration rate. Surfactant loss causes alveolar collapse due to increased surface tension and causes a decreased closing lung volume. This leads to less than normal functional residual capacity causing increased respiratory rate and reduced lung compliance. The alteration in the harmony between alveoli and vascular **************************************************
The proliferative stage is generally seen after day 7. It involves the proliferation of fibroblasts, hyperplasia of pneumocytes and ongoing inflammation.
The Fibrotic phase is seen 3 weeks after presentation and the patient is seen to have lung fibrosis, honeycombing and bronchiectesis. This leads to long-term chronic lung conditions.
Clinical management of ARDS is focused on promptly and appropriately treating the underlying cause, supporting lung function and preventing complications related to the medical treatment and the disease process. No treatment is definitive, but early anticipation of complications can reduce the length of stay.
Treatment is supportive
As previously noted mortality rates have barely reduced over the years. There has been much research into new ventilation strategies along with pharmacological and non-pharmacological techniques. So far few have improved survival. The most important and practice changing study was in 2000 when The Acute Respiratory Syndrome Network did a large (861 patients) multi-centred randomised trial comparing traditional tidal volumes with lower tidal volumes. At the time patients were being ventilated with tidal volumes (VT) of 10-15ml per kilogram of body weight with plateau pressures of 50, to achieve normocarbia and pH. The study was abandoned early as there was seen to be a 22% decrease in mortality of those patients with the lower range of TV. The high peak pressure and the high tidal volumes were found to be causing shearing injuries to the lungs and also causing a higher mortality. This study revolutionalised ventilation strategies of ARDS patients and demonstrated that lung protection techniques could improve survival (Levy, 2004). It is now common practice worldwide to ventilate patients on tidal volumes of around 6ml/kg and as low as 4ml/kg and to allow permissive hypercarbia. I
There continues to be research in to the benefit of PEEP in ARDS. There have been several studies conducted looking at the benefits but few have had conclusive results. Ashbaugh et al. (1967) identified patients that were mechanically ventilated with ARDS and had no PEEP became immediately severely hypoxaemic. Research has continued since then as to identify the optimal amount of PEEP. PEEP is important as it assists the severe ARDS patient by minimising alveolar collapse and improving gas exchange and lung compliance. Traditionally PEEP is set at 5-12cmH2O (Briel et al., 2010) but it is yet to be established what is the optimal level of PEEP ( Gattiononi, & Caironi, 2008, & Dellinger, Levy, Carlet et al, 2008). recent studies have been trying to identify if higher PEEP is better than lower, or traditional PEEPS. The problem has been what is low and what is high PEEP? A recent analysis by Briel et al. (2010) and supporting commentary by Rubenfeld (2010) has identified that the
it has also been found that PEEP can be dangerous in but it is not established how much is enough PEEP.
The author has identified medical and treatment seen within their place of work and will discuss this further. Oxygenation is optimised as seen in appendix A by Treatment includes optimising gas exchange by maintaining oxygenation, adequate tissue perfusion. Strict fluid balance. Ensuring nutritional requirements are met
Before 1990 ARDS was reported to have a mortality rate of 40-70% in the US (there were few studies outside the USA initially) (Harman, 2009). Since then several studies have been done around the world. New research has found the rate of mortality has deceased marginally in some studies, but still not significantly. A couple of studies in the US and the UK in the 1990’s have found mortality rates much lower in the 30-40% range (Davidson, Caldwell & Curtis, 1999, Davey-Quinn, Gedney & Whitely 1999). A 2002 Australian study identified mortality at 34% (Bersten, Edibam, Hunt, Moran, and the ANNZCCSCTG). A 2008 systematic analysis of ARDS statistics identified mortality still in the range of 15-61% in studies published after 2000 (Zambon & Vincent, 2008). It must be acknowledged that some of this data was from studies with very small groups of patients in the trials. Despite this it still identifies a high rate of mortality and very little improvement in survival over the years.
Improvements have been developed in the care due to ventilation strategies, improved intensive care… better understanding and treatment of sepsis, recent changes in the application mechanical ventilation, better overall supportive care of critically ill patients
Medical and nursing management within the authors
One of the biggest developments in the treatment of ARDS was a study done in 2000 which challenged the traditional ventilation of high
Treatment is supportive with the aim of maintaining adequate oxygenation to the tissues via
Mrs X is a 51 year old female who is normally fit and well. She has no past medical history. She does not take any regular medicines. She has no known allergies.
She lives with her husband and 3 adult children and works full time.
She returned from Melbourne 10 days prior to her presenting symptoms appearing.
Mrs X has been unwell for 7 days with lethargy, myalgia, and a slight cough.
She presents to her GP with a 72 hour of worsening headache, myalgia, and now a productive cough. Her GP prescribes antibiotics (Amoxycillin) and advises her to commence them the following day.
The following day Mrs X is taken to the local tertiary hospital (A) by her husband with further worsening symptoms and now respiratory distress. Her respiratory rate is 30; her SpO2 is 93% on room air. She is tachycardic (110), afebrile, normotensive and her chest x-ray shows right middle and right lower lobe pneumonia, early basal consolidation, and a small left pleural effusion.
Mrs X is admitted to the medical ward on CPAP
Presents at tertiary hospital (A) with worsening symptoms. Respiratory Rate 30. CXR shows RML + RLL pneumonia, early basal consolidation, and small L) pleural effusion.
Admitted to medical ward with CPAP, tiring over the evening with increasing PEEP and FiO2 requirements. Transferred to ICU on CPAP.
Intubated at 2130hrs due to worsening condition and tiring.
Continues to deteriorate over the next 12 hours, now with a vasopressor requirement.
Referred to tertiary hospital (B) for transfer. Swabs and cultures taken for multiple bacteria and to identify the source of pneumonia. Broad spectrum antibiotic cover commenced. (Screening included H1N1, mycoplasma serology, and urinary legonella-all eventually coming back as negative).
Managed in tertiary hospital (A) overnight with high PEEP (20) and Fio2 (90%) requirements. Spo2 and PaO2 remain low (85%/55). Recruitment manoeuvres attempted by consultant and found to bed unsuccessful.
Bloods show early coagulopathy, thrombocytopenia.
Worsening CXR: RUL, RML, RLL, LML, LLL consolidation. Discussion with family regarding possibility of ECMO in tertiary hospital (C) if continued deterioration. Tertiary hospital (B) arrives the following afternoon. Pt being managed “prone”.
Unproned and transferred to Tertiary Hospital (B).
Arterial blood gas on arrival=
Managed in hospital (B) with high respiratory support. Peaking with Fio2 1.0 PEEP of 24. Aiming for Pao2 >60, SpO2 >88%.
Condition further deteriorates on day 3 in hospital (B). Ventilation and oxygenation proving difficult. Any movement causing severe desaturation. Increasing PEEP (18) and decreasing FiO2 (0.6-0.7) found to be beneficial in this patient. ABG over the day
Time FiO2 pH pCO2 pO2
0908 0.6 7.35 53.5 59.7
1452 0.7 7.36 52.4 60.5
2001 0.6 7.35 53.6 62.6
2300 0.7 7.38 49.7 55.0
Initial arterial blood gas shows
Sedated on morphine and midazolam and propofol.
Strict fluid balance.
Commenced on regular IV steroids. IV frusemide. IV erythromycin and imipenem.
FASTHUG principle applied. Enteral feeding recommenced
Remained febrile despite antibiotic and line changes.
Chest drain insertion on day 3 in hospital (B)
Tracheostomy on day 9 as not respiratory or cardiovascularly stable enough earlier.
Remained on a FiO2 of an average of 0.60 and PEEP of 16-20 for the first 12 days.
De-sedated and a slow respiratory wean commenced on day 10.
Patient continues to be critically ill and have slow respiratory wean on day 18 when she is transferred back to her domicile hospital (Hospital A) to continue recovery and weaning
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