Acute Respiratory Distress Syndrome

Since World War I,

By definition:

an acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia in the absence of evidence for cardiogenic pulmonary edema.

ARDS is a clinical Dx
According to the AECC criteria, the severity of hypoxemia necessary to make the diagnosis of ARDS is defined by the ratio of the partial pressure of oxygen in the patient s arterial blood (PaO2) to the fraction of oxygen in the inspired air (FIO2). In ARDS, the PaO2/FIO2 ratio is less than 200, and in ALI, it is less than 300.

FIO2

Room air 0.21 (21%) Nasal canula @ 1 LPM 0.24 (24%) Simple face mask: up to 0.5 FMRB : upto 0.7

 . In addition, cardiogenic pulmonary odema must be excluded either by clinical criteria or by a pulmonary capillary wedge pressure (PCWP) lower than 18 mm Hg in patients with a pulmonary artery (Swan-Ganz) catheter in place

Etiology
Multiple risk factors In 20% no cause Most common risk factor ??????

SEPSIS

Risk Factors
Sepsis Trauma, with or without pulmonary contusion Fractures, particularly multiple fractures and long bone fractures Burns Massive transfusion Pneumonia Aspiration Drug overdose Near drowning Postperfusion injury after cardiopulmonary bypass Pancreatitis Fat embolism

Epidemiology
No sex variation except in trauma cases (F>M) Incidence increases with age (345 in every 10000 annually aged between 75 to 84) In USA 190,000 yearly with 74000 deaths Mortality : Before 1990s : up to 70% after : 30 to 40 % Also with a very serious mortalities: no numbers

History
characterized by the development of acute dyspnea and hypoxemia within hours to days of an inciting event, such as trauma, sepsis, drug overdose, massive transfusion, acute pancreatitis, or aspiration Patients developing ARDS are critically ill, often with multisystem organ failure

 Typically, the illness develops within 12-48 hours after the inciting event, although, in rare instances, it may take up to a few days With the onset of lung injury, patients initially note dyspnea with exertion. This rapidly progresses to severe dyspnea at rest, tachypnea, anxiety, agitation, and the need for increasingly high concentrations of inspired oxygen.

 tachypnea, tachycardia, and the need for a high fraction of inspired oxygen (FIO2) to maintain oxygen saturation The patient may be febrile or hypothermic in the context of sepsis, associated hypotension and peripheral vasoconstriction with cold extremities may be presen Cyanosis of the lips and nail beds

 Manifestations of the underlying cause Because cardiogenic pulmonary edema must be distinguished from ARDS, carefully look for signs of congestive heart failure or intravascular volume overload, including jugular venous distention, cardiac murmurs and gallops, hepatomegaly, and edema.

Workup
ARDS is a clinical diagnosis (ARDS) is defined by the acute onset of bilateral pulmonary infiltrates and severe hypoxemia in the absence of evidence of cardiogenic pulmonary edema

Workup
PaO2/FiO2 ratio & ABGs: < =200 in ARDS <300 ALI usually respiratory alkalosis, but e sepsis it may show metabolic acidosis e or eout resp compensation

But with progression of the condition it may go into a respiratory alkalosis

Workup
CBC: high or low WBCS , low platelets with low HCT RFT LFT Cytokines: high IL1 IL6 IL8

Workup (RADIOGRAPHY)

Anteroposterior portable chest radiograph in patient who had been in respiratory failure for 1 week with diagnosis of acute respiratory distress syndrome. Image shows endotracheal tube, left subclavian central venous catheter in superior vena cava, and bilateral patchy opacities in mostly middle and lower lung zones.

Workup (RADIOGRAPHY)

Workup (RADIOGRAPHY)

P. Odema

P. Odema

P. Odema

Workup (RADIOGRAPHY)
presence of bilateral pulmonary infiltrates may be diffuse and symmetric or asymmetric superimposed upon preexisting lung disease or if the insult causing ARDS was a pulmonary process, such as aspiration or lung contusion. evolve rapidly: first 3 days maximum ground glass changes or frank alveolar infiltrates (see the image below).

Workup (RADIOGRAPHY)
The correlation between radiographic findings and severity of hypoxemia is highly variable. In addition, diuresis tends to improve infiltrates and volume overload tends to worsen them, irrespective of improvement or worsening in underlying ARDS For patients who begin to improve and show signs of resolution, improvement in radiographic abnormalities generally occurs over 10-14 days; however, more protracted courses are common.

Workup (RADIOGRAPHY)
computed tomography (CT) scanning may be indicated in some situations. CT scanning is more sensitive than plain chest radiography in detecting pulmonary interstitial emphysema, pneumothoraces and pneumomediastinum, pleural effusions, cavitation, and mediastinal lymphadenopathy. The heterogeneity of alveolar involvement is often apparent on CT scan even in the presence of diffuse homogeneous infiltrates on routine chest radiograph. In some instances, the discovery of unexpected pulmonary pathology, such as a pneumothorax, may be lifesaving. However, this potential benefit must be weighed against the risk associated with transporting a critically ill patient on high-intensity mechanical ventilation out of the intensive care unit (ICU) to the CT scan equipment.

Workup (RADIOGRAPHY)
patients with ARDS should undergo 2dimensional echocardiography for the purpose of screening. If findings are suggestive of patent foramen ovale shunting, 2-dimensional echocardiography should be followed up with transesophageal echocardiography.[15]

Workup Invasive Hemodynamic Monitoring

hemodynamic monitoring with a pulmonary artery (Swan-Ganz) catheter may be helpful in selected cases for distinguishing cardiogenic from noncardiogenic pulmonary edema. Mixed venous oxygen saturation to allow the calculation of shunt and oxygen delivery is used by some to adjust ventilator parameters and vasoactive support. Mixed venous oxygen saturation is also used in goal-directed therapy for sepsis.

Workup Invasive Hemodynamic Monitoring

Study(by ARDS clinical trials network) showed no benefit of SG cath over CVP monitoring; with double complications
N Engl J Med. May 25 2006;354(21):2213-24

Thus, use of the pulmonary artery catheter past the time of initial resuscitation confers no survival benefit and possibly has an adverse effect on survival.

Workup Bronchoscopy
to evaluate the possibility of infection, alveolar hemorrhage, or acute eosinophilic pneumonia in patients acutely ill with bilateral pulmonary infiltrates Culture material (bronchoalveolar lavage)

Treatment
No drug has proved beneficial in the prevention or management of acute respiratory distress syndrome (ARDS).

So, major effort should be directed towards treating the primary cause(s)

Treatment
The use of stress-dose steroids in patients with septic shock did not change survival in a recently reported controlled trial N Engl J Med. Jan 10
2008;358(2):111-24

A recent study concluded that the early use of corticosteroids was also ineffective in patients with the pandemic H1N1 influenza A infection, resulting in an increased risk of superinfection
Intensive Care Med. Feb 2011;37(2):272-83)

Treatment
A randomized, clinical trial determined that simvastatin improved oxygenation and respiratory mechanics in patients with ALI.[27] Further studies are needed, but treatment with simvastatin appears safe and may be associated with improved organ dysfunction in patients with ALI. (The HARP Study). Am J Respir Crit Care Med. Mar 1
2011;183(5):620-6.

Treatment
Small sepsis trials suggest a potential role for antibody to tumor necrosis factor (TNF) and recombinant interleukin (IL)-1 receptor antagonist Inhaled nitric oxide(used with promise but till now it appears to be ineffective) N Engl J Med. Dec 22
2005;353(25):2683-95

Treatment
Activated protein C is now indicated for use in severe sepsis pts under supervision of an Intensivist, BUT the drug was drawn from markets 25-10-2011 when postmarketing studies showed higher mortality rate with its use (this area is causing the biggest controversy in critical care world now) Clin Ther. Feb 2003;25(2):396-421
(PROWESS)-SHOCK clinical trial

Treatment(FLUID MANAGEMENT)
Early aggressive resuscitation for associated circulatory shock and its associated remote organ injury are central aspects of initial management. However, several small trials have demonstrated improved outcome for ARDS in patients treated with diuretics or dialysis to promote a negative fluid balance in the first few days

Treatment(FLUID MANAGEMENT)
Thus, distinction between primary ARDS due to aspiration, pneumonia, or inhalational injury, which usually can be treated with fluid restriction, from secondary ARDS due to remote infection or inflammation that requires initial fluid and potential vasoactive drug therapy is central in directing initial treatments to stabilize the patient

Treatment(FLUID MANAGEMENT)
An ARDS Clinical Trials Network study of a fluidconservative strategy versus a fluid-liberal strategy in the management of patients with ARDS or acute lung injury (ALI) found no statistically significant difference in 60-day mortality between the 2 groups 72 hours after presentation with ARDS. However, patients treated with the fluid-conservative strategy had an improved oxygenation index and lung injury score and an increase in ventilator-free days, without an increase in nonpulmonary organ failures. N Engl J Med. Jun 15 2006;354(24):2564-75.

Treatment(FLUID MANAGEMENT)
Maintaining a low-normal intravascular volume may be facilitated by hemodynamic monitoring with a central venous or pulmonary artery (Swan-Ganz) catheter, aimed at achieving a central venous pressure (CVP) or pulmonary capillary wedge pressure (PCWP) at the lower end of normal.

Treatment(FLUID MANAGEMENT)
Closely monitor urine output and administer diuretics to facilitate a negative fluid balance. In oliguric patients, hemodialysis with ultrafiltration or continuous veno-venous hemofiltration/dialysis (CVVHD) may be required.

Treatment(Noninvasive Ventilation)
noninvasive positive-pressure ventilation (NIPPV) may be beneficial in patients with acute lung injury (ALI) because intubation and mechanical ventilation may be associated with an increased incidence of complications, such as barotrauma and nosocomial pneumonia This is usually given by full facemask

Treatment(Noninvasive Ventilation)
Sometimes continuous positive airway pressure (CPAP) ventilation alone may be sufficient to improve oxygenation. BUT BE CAREFUL: Patients who have a diminished level of consciousness, vomiting, upper GI bleeding, or other conditions that increase aspiration risk are not candidates for NIPPV

Treatment(Noninvasive Ventilation)
Other relative contraindications include hemodynamic instability, agitation, and inability to obtain good mask fit.

Treatment(Mechanical Ventilation)
The only treatment found to improve survival in ARDS is a mechanical ventilation strategy using low tidal volumes (6 mL/kg based upon ideal body weight). The goals of mechanical ventilation in ARDS are to maintain oxygenation while avoiding oxygen toxicity and the complications of mechanical ventilation

Treatment(Mechanical Ventilation)
maintaining oxygen saturation in the range of 85-90% aim for reducing the fraction of inspired oxygen (FIO2) to less than 65% within the first 24-48 hours moderate-to-high levels of positive endexpiratory pressure (PEEP).

Treatment(Mechanical Ventilation)
be careful, mechanical ventilation is one of the leading causes of acute lung injury This is avoided simply by using lung protective strategy TV 6 ml/kg(predicted) PEEP to maintain SPO2 >94%(5 to 10) FIO2 less than 50% Permissive hypercapnia what is this??

 When we are using low tidal volume ventilation we are causing and promoting respiratory acidosis due to decreased washout of CO2 at the expense of protecting the lung from high pressures generated by high tidal volume Recent guidance from the ARDS Network Study to do this and to correct the acidosis by increasing the RR and giving NaHCO3

Treatment(Mechanical Ventilation)
Great consideration for early weaning by daily interruption of sedation and paralytic agents and giving the chance for the pt to breath by him/her self

Treatment(Tracheostomy)
In patients requiring prolonged mechanical ventilation, tracheostomy allows the establishment of a more stable airway, which may allow for mobilization of the patient and, in some instances, may facilitate weaning from mechanical ventilation. Usually 2 weeks after intubation

Treatment(Nutritional Support)
after 48-72 hours of mechanical ventilation usually is recommended. Enteral support is preferred unless CI low-carbohydrate high-fat enteral formula TPN ( total parentral nutrition)

Treatment(Activity Restriction )
on bed rest Frequent position changes (RESP. thearpy) Elevation of the head of the bed 45 deg to avoid VAP

Treatment
Use of broad spectrum antibiotics DVT prophylaxis Skin care Removal of unnecessary tubes and cathters Early recognition of complications (e.g pneumothorax, GI bleeding)

Prevention
no successful preventive measures have been identified Careful fluid management in high-risk patients may be helpful prevent aspiration use of lower tidal volumes in all patients on mechanical ventilation

TAKE HOME MESSAGES

ARDS is very serious Do not forget the PRIMARY CAUSE DO NOT FORGET to peruse SEPTIC FOCI YOUNGE Pts have the best chance

TAKE HOME MESSAGES

Please do CHEST X-Ray to any critical Pt And do it early

TAKE HOME MESSAGES

Take a full detailed history and perform a thorough examination

TAKE HOME MESSAGES

Think of ARDS in every deteriorating septic or SIRS pt

TAKE HOME MESSAGES

Difficult to be treated

TAKE HOME MESSAGES

Treatment is all about supporting lungs

TAKE HOME MESSAGES

DO NOT cause ARDS and Acute Lung Injury

TAKE HOME MESSAGES

When ever you doubt P. odema think about ARDS

TAKE HOME MESSAGES

Treat sepsis very early and very effectively

TAKE HOME MESSAGES

Every time you will put a pt on IPPV or SIMV, try to use a LUNG PROTECTIVE STRATEGY

Almost all materials were adopted from emedicine.com & GOOGLE PICS