ards by dr muhammad akram khan qaim khani

05/02/2023DR. MUHAMMAD AKRAM KHAN QAIM KHANI 1

ARDS

BYDR MUHAMMAD AKRAM

MATERNITY AND CHILDREN HOSPITALMAUSADIA, JEDDAH

RESIDENT ICU

INTRODUCTION

In 1967 the investigators from university of Colorado presented the modern concept of ARDS.

A type of Acute Respiratory failure of noncardiac origin.


What is ARDS?

Definition formalized in 1992 American European Consensus Conference

1. Acute onset, bilateral infiltrates on CXR

2. PCWP ≤ 18 mmHg or no clinical evidence of left atrial hypertension

3. PaO2/FiO2 (P/F) Ratio ≤ 300 for ALI ≤ 200 for ARDS

Bernard et al. AJRCCM 1994;149:818-824

What is ARDS? – Berlin Definition

The ARDS Definition Task Force. JAMA 2012;307:2526-2533

CLINICAL FEATURES

The clinical features of ARDS usually appear within 6 to 72 hours of an inciting event and worsen rapidly

Patients typically present with dyspnea cyanosis (ie, hypoxemia) diffuse crackles.

Respiratory distress is usually evident, including tachypnea, tachycardia, diaphoresis, and use of accessory

muscles of respiration. A cough and chest pain may also exist.


CLINICAL FEATURES

Arterial blood gases reveal hypoxemia High concentrations of supplemental oxygen are generally

required to maintain adequate oxygenation. The initial chest radiograph typically has bilateral alveolar

infiltrates computed tomography (CT) usually reveals widespread

patchy or coalescent airspace opacities that are usually more apparent in the dependent lung zones.


EPIDEMIOLOGY

The incidence of ARDS in the United States . Within intensive care units,

approximately 10 to 15 percent of admitted patients and up to 20 percent of mechanically ventilated patients meet criteria for ARDS .

The incidence of ARDS may be somewhat higher in the United States than in other countries .


OUT COME

Mortality varies from 40 to 60%. Most die of non respiratory complication

during the supportive phase of ARDS rather then hypoxia


COMPLICATIONS

BarotraumaDeliriumNosocomial infection


PATHOPHYSIOLOGY

• Endothelial injury– Endothelin-1, VWF

• Epithelial injury • Neutrophil-mediated injury

– Near endothelium, retained, activated • Cytokines – TNF, IL-1, IL-8 • Oxidative injury • Ventilator-induced injury • Hypercoagulability • Fibrosis

Ware LB. Sem in Resp Crit Care Med 2006


Pathology

Like interstitial nephritis and acute hepatitis, the term ARDS encompasses many distinct disorders that share common clinical and pathophysiologic features.

The pathological features of ARDS are typically described as passing through three overlapping phases: exudative, proliferative and finally fibrotic phase.

PATHOLOIC FEATURES

Depend on the time of tissue sampling As the clinical disorder unfolds, there is

histologic evidence of diffuse alveolar damage

Features include Presence of microthrombi of platelets and

WBCs within capillary lumen, denudation of epithelial lining cells, swelling of the capillary endothelial cells, infiltration by polymorph nuclear leukocytes(PMNLs), and hyaline membrane formation within alveoli


Pathogenesis

Lung injury is primarily initiated by a specific insult (sepsis, trauma, VILI); with the initiation of inflammation there is rapid and increased recruitment of leucocytes, together with inflammatory mediators to the site of injury, several mechanisms had been involved in the pathogenesis of ARDS.

Pathogenesis

MANAGEMENT

Guidelines for ventilatory support of the patient with ARDS from the ACCP Consensus Conference on Mechanical Ventilation include the following: 1. Clinicians should choose a ventilatory mode that is

capable of supporting oxygenation and ventilation and one with which they are familiar.

2. Oxygenation target is arterial oxygen saturation of >90%.

3. End-inspiratory plateau pressures of >35 cm H2O are a concern for the development of alveolar overdistention. In this setting, clinicians ought to consider decreasing the tidal volume to values as low as 5 mL/kg.


MANAGEMENT

4. To meet target end-inspiratory pressure goal, the PaCO2 may be permitted to rise as long as there is no evidence of increased intracranial pressure or other contraindication to permissive hypercapnia.

5. Positive end-expiratory pressure (PEEP) is beneficial in supporting oxygenation; however, the level of PEEP support used should be minimized and continually evaluated.

6. The goal for FIO2 is to achieve adequate oxygenation with the least amount of supplemental oxygen. Attempts should be made to decrease the FIO2 to levels <0.55, if possible. The use of PEEP may assist with the reduction in oxygen support.

7. When oxygenation is inadequate, clinicians ought to consider the use of sedation, paralysis, or position changes and strategies to increase tissue oxygen delivery.


MANAGEMENT STEPS

Removal of precipitating/ underlying cause

Ventilatory support Oxygenation with min. ventilatory

trauma Low tidal volumes of 05 to 07 mls./ kg. Limit inspiratory pressure of <35

cmH2O Permissive hypercapnia ?? Permissive hypoxia pO2 55-65

mmHg


MANAGEMENT TECHNIQUES

Alveolar recruitment PEEP inc. Pa O2 with min. FiO2 (10-20

cm) Ventilatory facilitated recruitment

techniques Physiotherapy Ventilation strategies Inverse ratio / newer modes Nitric Oxide PRONE VENTILATION 05/02/2023DR. MUHAMMAD AKRAM KHAN QAIM KHANI 22

Adjuncts to Improve Survival

Daily spontaneous breathing trials Daily discontinuation of sedation Avoiding neuromuscular blocakde DVT prophylaxis HOB elevation Stress ulcer prophylaxis Enteral nutrition (when possible)


OTHER MANAGEMENT OPTION

Steroids Surfactant PDE inhibitors Extrapulmonary gas exchange:-

IVOX ( Intra Venacaval gas exchange) ECMO ( Extra Carporeal Membrane

Oxygenation) ECCO2- R ( Extra Carporeal CO2 Removal)

Ketoconazole Prostaglandin inhibitors.


PERMISSIVE HYPERCAPNIA

TV is reduced to allow ventilation at lower peak airway pressure and less risk of volutrauma

This approach may allow better oxygenation but leads to hypercapnia

Gradual elevation of PaCO2 about 2.5mmHg/hr is well tolerated

Acute elevation in PaCO2 leads to Increased Sympathetic activity Raised Cardiac Output High pulmonary vascular resistance Impaired skeletal and bronchomotor tone Dialated cerberal vessels Impaired CNS function


SURFACTANT THERAPY

It is produced by type 2 pneumocytes, decreases surface tension at the air-fluid interface of small airways and alveoli

Without surfactant the alveoli may collapse and resist opening, even high airway pressures

Plasma protein leak into the alveolar airspaces inactivate the existing surfactant

Resulting increasing surface tension leads to Atelactesis and decreased lung compliance

Newer preparation in current clinical trial


NITRIC OXIDE

A powerful endogenous vasodilator Because it is rapidly inactivated, its

effects are restricted to the blood vessels at the site of administration

Inhalation dilates pulmonary vessels perfusing aerated lung units, diverting blood flow from poorly ventilated or shunt regions

An ideal agent to treat Pulmonary Hypertension and ARDS


INVERSE RATIO VENTILATION

Inspiratory phase is prolonged and leads to an increase in inspiration-to-expiration ratio ( between 1:1 and 4:1 )

This approach increases the mean airway pressure maintaining acceptable peak airway pressure

Disadvantages of IRV include air trapping leading to auto PEEP. Therefore, requires heavy sedation and neuromuscular blocked


POSITIVE END-EXPIRATORY PRESSURE ( PEEP )

It is the pressure maintained in the lungs at the end of expiration

Prevents collapse of alveoli, thus increases the surface area of O2 transfer

High level causes over distension of the alveoli, poor lung compliance, increase in the airway pressures, and deleterious effect on cardiac out put

“BEST PEEP” is a balance between the advantages and disadvantages of PEEP

Recommendation are to start with PEEP of 5cm H2O and increase by 03 to 05 cm H2O to achieve Oxygen saturation >/=90%


TRACHEAL GAS INSUFFLATION

Physiologic dead space is elevated in ARDS, and small tidal volume ventilation causes hypercapnia and acute acidosis

With TGI, a stream of fresh gas ( approximately 04 to 08 L/min. ) is insufflated through a small catheter or through small channels in the wall of the ETT into lower trachea, flushing CO2- laden gas out prior to next inspiration

It can be used throughout respiratory cycle ( continuous flow catheter ) or only during a segment of it ( Phasic catheter flow )

Disadvantage include:- Auto PEEP Catheter may become nidus for infection Desiccation of secretions and airway mucosal injury


FLUOROCARBON LIQUID-ASSISTED VENTILATION

Surface tension can be eliminated by filling the lungs with a liquid such as fluorocarbon.

It can dissolve O2 17 times more O2 than water, has low surface tension and spreads quickly over the respiratory epithelium, and evaporates

Requires a liquid-gas exchange device to oxygenate liquid, deliver the tidal volume, and remove CO2


EXTRAPULMONARY GAS EXCHANGE

Reduces the requirement for ventilating pressure

Methods include ECMO ECCO2-R IVOX

There has been 50% mortality reported comparing to 90% in a control group by Gatinoni in 1986. Approximately same stands for study by Brunet while patients were treated with low-frequency positive-pressure ventilation ( LFPPV )


ECMO


GLUCOCORTICOID THERAPY

High dose of glucocorticoids do not prevent the development of ARDS in patients with sepsis

Serum complement level are not lowered in patients with sepsis induced ARDS

Patients with late- phase of ARDS have persistent inflammation, with cytokines release in the airspaces in lungs, glucocorticoids at this stage could facilitate recovery.

Increase the risk of nosocomial infection, which could diminish the chances of recovery


PROSTAGLANDIN AGONISTS/ INHIBITORS

Ketoconazole, a potent inhibitor of thromboxane and leukotriene synthesis, prevent the development of ARDS

Prostaglandin E1 is a vasodilator that blocks platelet aggregation and decreases neutrophil activation


PRONE POSITIONING FOR ARDS

Indications: Pulmonary dysfunction despite

escalating mechanical ventilatory support

Goals of Ventilation: SaO2 >92% PaO2/FiO2 ≥200 pH 7.25 – 7.40 Pplat <35 cm H2O



Criteria for Inclusion: CXR with diffuse bilateral infiltrates

consistent with ALI or ARDS Mechanical ventilation

FiO2 ≥ 0.6 for 48 hours PEEP ≥ 15 cm for 48 hours (includes PCIRV,

auto PEEP) Increasing respiratory dysfunction as

evidenced by: PaO2/FiO2 < 200



Exclusion Criteria: Closed head injury with ICH Unstable orthopedic fracture Spinal cord injury Hemodynamic instability Active intraabdominal process Pregnancy



Procedure: Order from Attending doctor ETCO2 monitor and arterial line in-place. Low air-loss mattress. Discontinue gastric feeding. Stomach to

be evacuated via NGT. Explanation of procedure to patient and

family Minimum of 3 RNs, Attending doctor, and

RT.



Reposition ECG leads to patient’s back. Anticipate the need for frequent ETT

suctioning. Obtain ABG 20 minutes after

repositioning. Duration of prone positioning is

dependent upon patient’s hemodynamic status


Transfusion-Related Acute Lung Injury


Respiratory distress, pulmonary edema, hypoxia,hypotension and fever• Within 2 hours of transfusion (6 at most)• Mechanism– Plasma in transfused product– HLA antibodies or granulocyte specific antibodies• 1/5000?• 5-10% mortality• Diagnosis:– Difficult to tease out– Isolation of antibodies

Popovsky et al. Guidelines for the management of TRALI. AABB 2003

Transfusion-Related Acute Lung Injury


Stop the transfusion• Treat pulmonary and cardiac dysfunction• Test the transfused units• Contact a reference lab for advice• Subsequent transfusions to that individualnot a problem

ards by dr muhammad akram khan qaim khani

Healthcare