ARDS Presentation FY1 Teaching

Acute Respiratory Distress Syndrome (ARDS)

Kartik Kumar

- Case Study

- What is ARDS?

- Risk factors and epidemiology

- Identification

- Treatment

Case Study:Mr A. Ramsdale

Case Study: Mr Ramsdale

Mr Ramsdale (55 Male) presents to A&E with a 3/7 hx of productive cough, fever and chills. PMH: HTN, T2DM. No previous Hospital / ICU admissions Drug hx: Candesartan 8mg OD, Metformin 500mg OD NKDA OE: coarse crackles to Rt base, tachypnoeic, clammy skin. Obs: BP 122/73, HR 102 sinus tachycardia, RR 28, SpO2 94% on RA, Temp 38.6 1) What are your impressions? 2) Anything else you would like to find out from his history? 3) Initial investigations and management?

Case Study: Investigations

Bloods: Raised CRP, raised WCC (predominantly neutrophils) COVID -ve, Influenza A -ve CXR and ABG are as shown:

ABG results:

• pH: 7.36 (7.35-7.45)
• pO2: 9.8 (10–14)
• pCO2: 5.0 (4.5–6.0)
• HCO3: 22 (22-26)
• BE: -2 (-2 to +2)

Case study: 2 days later

You are on a medical on call shift when you are called to review Mr Ramsdale. The Nurse looking after him sounds very worried.

• He is now feeling worse, Increasing O2 demand and now on 5L FM with sats of 92%
• OE: Bilateral coarse crackles with expiratory wheeze
• Obs: Sats 92% on 5L FM, BP 100/66, HR 116 ST, RR 30, Temp 38.8
• What can we do?!

ABG:

• pH 7.3 (7.35-7.45)
• pO2 8.0 (10-13) on 5L FM
• pCO2 8.8 (4.9-6.1)
• HCO3 26 (22-28)

Case Study: Investigations 2

He is escalated on 15L NRB and the ABG is repeated:ABG:

• pH 7.28 (7.35-7.45)
• pO2 8.1 (10-13) on 15L NRB
• pCO2 9.0 (4.9-6.1)
• HCO3 26 (22-28)

...Big yikes! I think we need some help

Escalating to Critical Care

Mr Ramsdale has ARDS and needs escalation above ward level Oxygen (High flow, CPAP continuous /BIPAP Bi-level, invasive ventilation) Critical Care is where patients can receive organ support - ventilation, vasopressors, RRT etc. Referral in hours: Critical Care Outreach Nurses (Bleep 1107) / ICU reg. Referral OOH: ICU Reg: (Bleep 7403)

Investigations and Ceiling of Care

Know the History Well

What is their BACKGROUND

• What tx have they had so far?
• What investigations?
• Do they have a ceiling of care? DNACPR?
• Has the patient been asked?

• Exercise tolerance (flat, stairs)
• ADLs, Home O2?
• Are they going to be able to survive an ICU admission?

• What have they presented with?
• PMH, any previous admissions?
• Previous ICU admissions

Mr Ramsdale is currently in single organ failure. He is escalated to ICU where he has 1/7 of BIPAP before eventually being intubated and ventilated due to clinical deterioration.

ARDS: The Basics

Definition:

An acute inflammatory syndrome manifesting as diffuse pulmonary oedema and respiratory failure that cannot be explained by, but may co-exist with, left-sided heart failure – AECC 1994 Definition updated to include 3 grades of severity depending on degree of hypoxaemia - Berlin 2012

Basic Overview:

Due to severe inflammation (infection or injury) causes fluid from blood vessels to leak into alveoli.

Symptoms / Features:

• Bilateral presentation
• Acute Onset
• Refractory Hypoxaemia

• Severe SOB
• Rapid, shallow breathing
• Tired, drowsy or confused
• Feeling faint

Patho-Physiology

Inflammation of Alveoli

Inflammation of alveolar-capillary membrane (gas exchange surface) – Increased permeability resulting in inflammatory exudate – resulting pulmonary oedema

Inactivation of Surfactant

Inflammatory exudate inactivates surfactant – causes collapse and consolidation of distal air spaces – progressive loss of gas exchange area

Lack of Hypoxic Vasoconstriction

Usually would be compensated by hypoxic pulmonary vasoconstriction, but this is hampered by inflammation – resulting VQ mismatch

Refractory Hypoxaemia

de-oxyengated blood going to unventilated parts of lung – profound hypoxaemia and eventually T2RF due to tiring

Causes

Risk Factors

Advanced age -History of tobacco use - History of alcoholism - Chronic lung disease - High risk surgery -

Pulmonary:

• Pneumonia / COVID
• Aspiration
• Smoke / Toxin Inhalation
• Near Drowning

Non- Pulmonary:

• Sepsis
• Acute pancreatitis
• Transfusion related (TRALI)

2012 Retrospective Cohort Study - Mortality

24% Mortality

In Moderate ARDS

48% Mortality

In Most Severe Forms of ARDS

Outcomes

• The mortality stats are worrying. Most deaths are usually attributed to the causes of ARDS. ARDS itself is more of a symptom which is a poor prognostic factor for disease survival as opposed to a disease itself.

• Disease process usually lasts >15 days
• Long term respiratory failure is uncommon
• Other long term outcomes though - commonly muscle weakness and neuropsychiatric problems
• <50% return to work within 12 months of DC from ICU
• Patients still suffering after leaving – physically, socially and financially

Diagnosis - P/F Ratio and LIPS score

P/F ratio is the ratio of PaO2 to FiO2. Partial pressures for a given inspired O2. P/F Ratio of <300mmHg = ARDS Grouped into mild (300-200), moderate (200-100) and severe (<100) LIPS clinical score - mostly used for studies. Score of >3 is threshold for ECMO referral When used 4-7 days from initial symptoms score of >2.5 is a poor prognostic factor

Mr Ramsdale had severe ARDS

Diagnosis - Imaging (CXR)

Exudative Phase (1-7 days)

Proliferative Phase (8-14 days)

Latent / Fibrotic Phase (>15 days)

Similar appearance to phase 1 with bilateral diffuse opacities. This is very important - any change may be superadded infection. Consider repeat CXR in acute deterioration of ARDS patient.

CXR often normal at first except in pulmonary ARDS. Deterioration takes 1-2 days leading to an appearance of bilateral and symmetrical interstitial opacities - ddx is heart failure driven pulmonary oedema - absence of cardiomegaly, septal lines and pleural fluid - although can co-exist

Usually regression back to usual appearance. Sometimes some fibrotic changes are seen but CT is more accurate at identifying these.

CT in Diagnosis and Guiding Treatment

To scan or not to scan?

Classical ARDS picture

Long Term Changes?

CT is good for both aiding with diagnosis and prognostication. Can differentiate between pulmonary/non-pulmonary ARDS which helps guide treatment. Have to balance this with the risks of taking an intubated and sedated patient down to scan.

Opacification with an anterior to posterior density gradient along with widespread ground glass opacification. Also some dilatation of terminal bronchioles. Density gradient improves with proning.

Sometimes CT is done for FU. Can sometimes identify pulmonary cysts / bullae (likely due to prolonged ventilation.) Masclans et al found that 76% of patients in their study had abnormalities on high res CT at 6 months FU.

Treatment - Principles

Where is the magic pill to treat ARDS?

It is very hard to develop drug treatments - ARDS is not a disease but a 'syndrome describing acute respiratory failure as a result of a wide variety of conditions' - therefore very few drug targets

1. Identify early - Scoring systems (PF ratio and LIPS) utilising imaging modalities - identify deterioration
2. Exclude differentials - Left sided HF, major PE, ILD (especially acute interstitial pneumonia) and pulmonary vasculitides - although less acute
3. Treat underlying causes - antibiotics for sepsis, ECRP for pancreatitis
4. Deploy supportive measures - early escalation, lung-protective ventilation
5. Minimise iatrogenic injury - prevent fluid overload, ventilator associated lung injury
6. PREVENTION

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Faculty of ICM and intensive care society (FICM and ICS) guidelines 2018

• 54 page, peer reviewed guideline that collated data from several different studies to make treatment recommendations.
• Evaluated the following treatment options
• Good to note that most act by reducing ventilator associated lung injury (except conservative fluid management, proning and corticosteroids) - not actually to treat the ARDS

Ventilatory Strategies

Neuromuscular Blockade

Inhaled Vasodilators

Lower Tidal Volumes

lack of mortality benefit and increased risk of renal dysfunction.

Very good outcomes - aim to reduce barotrauma from ventilation

good if used early on in mod/severe - risk of ICU acquired weakness

Higher PEEP (peak end expiratory pressure)

High frequency Oscillation (HFOV)

multiple RCTs demonstrate no benefit and one demonstrated an increase in mortality - risks of barotrauma, hypotension and oxygenation failure

Improves 'recruitment' (number of previously collapsed alveoli inflated for a given pressure) - Better in non-pulmonary ARDS as lung is more compliant - risks of barotrauma

ECMO and ECCO2R

• ECMO (Extracorporeal Membrane Oxygenation) and ECCO2R (Extracorporeal CO2 Removal) - basically temporary heart/lung bypass machines.
• Allows for very controlled and light ventilation of lung for protective ventilation.
• ECMO is recommended in severe ARDS whereas more evidence is needed for ECCO2R
• Problems associated e.g. anticoagulation, line associated complications, access to an ECMO centre

Non-Ventilatory Strategies

Corticosteroids

Prone Positioning

12h per day with mod/severe ARDS - ET tube displacement, pressure sores, loss of IV access - can be mitigated with training - signficantly reduced mortality

potential reduction in hospital day of 4.8 days although evidence weak - potential harms e.g. excess HA infections, neuromyopathy, delirium - large multi-centre study in the works

Conservative Fluid Management

5 RCTs between 2002-2014 – 29-1000 participants - suggests using conservative fluid management strategy utilising fluid restriction, diuretics and possibly hypotonic albumin to avoid positive fluid balance - Risks: AKI, requirement for RRT, cognitive dysfunction.

Prevention - Better Than a Cure?

Many Iatrogenic factors leading to the development of ARDS - therefore lots of room for preventative measures:

1. Avoid excessive fluid therapy
2. Preventative measures to reduce rates of HAP's
3. Reduce aspiration in hospitals - SALT assessments
4. Reduce inappropriate and excessive transfusion (TRALI is worse in plasma containing fluids)

Summary Points!

Diagnostic Methods

What is ARDS?

Escalate!

A P/F ratio of <300 mmHg indicates ARDS, as well as bilateral and symmetrical interstitial opacities on CXR and ground glass lesions with an AP density gradient in CT. Changes to imaging appearances may be due to superadded infection.

When escalating to critical care for organ support consider patient functional status, ceilings of care and relevant history/interventions.

ARDS is an inflammatory response to either pulmonary (pneumonia, aspiration) or non-pulmonary (Sepsis, pancreatitis) triggers, resulting in severe, refractory hypoxaemia which often requires escalation.

Protect the Lungs

Treatment Methods

Lung protective ventilation and proning are proven treatments. Preventative measures are a vital aspect of ARDS management.

Most important aspects of treatment involve early identification, escalation and deployment of supportive measures, as well as the minimisation of iatrogenic injury.

References

• https://www.nhs.uk/conditions/acute-respiratory-distress-syndrome/#:~:text=Acute%20respiratory%20distress%20syndrome%20(ARDS)%20is%20a%20life%2Dthreatening,the%20time%20they%20develop%20ARDS.

• https://www.lung.org/lung-health-diseases/lung-disease-lookup/ards/learn-about-ards

• https://www.ficm.ac.uk/sites/ficm/files/documents/2021-10/Guidelines_on_the_Management_of_Acute_Respiratory_Distress_Syndrome.pdf

• http://rc.rcjournal.com/content/57/4/607

• https://nursing.com/lesson/04-38-ards-case-study-60-min/

• https://effectiveness.lahc.edu/academic_affairs/healthsci/nursing/current/345/Unit%20IV/Lecture%20Slides/Student%20ARDS%209.19.19.pdf

Thanks for Listening :)