Acute Respiratory Distress Syndrome: Indian guidelines

Acute respiratory distress syndrome (ARDS) is the most severe form of acute lung injury resulting in extensive bilateral pulmonary infiltrates, severe refractory arterial hypoxemia and stiff lungs. Of the numerous clinical conditions identified to cause ARDS, sepsis syndrome, polytrauma, obstetric complications, and surgery, among others appear to be the most common causes.

The site of injury may be focused on either the vascular endothelium (eg. sepsis) or the alveolar epithelium (eg. aspiration of gastric contents). Injury to the endothelium results in increased capillary permeability and the influx of protein-rich fluid into the alveolar space. Injury to the alveolar lining cells also leads to pulmonary edema. In tropical countries, malaria, leptospirosis, tuberculosis (including miliary), enteric fever, and dengue haemorrhagic fever, organophosporus and paraquat poisoning; scorpion sting; inhalation of toxic fumes (e.g.chlorine); and heat stroke are important causes of ARDS.

Other known risk factors are bacteremia, sepsis, trauma with or without pulmonary contusion, fractures, particularly multiple fractures and long bone fractures, burns, massive transfusion, pneumonia, aspiration, drowning, postperfusion injury after cardiopulmonary bypass and acute pancreatitis.

Ministry of Health and Family Welfare has come out with the Standard Treatment Guidelines for Medicine (Respiratory Diseases). Following are its major recommendations for Acute respiratory distress syndrome.

Case definition

Acute onset

PaO2/FIO2 < 300*

SpO2/FIO2 < 315*

Bilateral infiltrates on the chest radiograph

PCWP < 18 mm Hg, or no clinical evidence of left atrial hypertension

Acute respiratory distress syndrome

Acute onset

PaO2/FIO2 < 200*

SpO2/FIO2 < 235

Bilateral infiltrates on the chest radiograph

PCWP < 18 mm Hg, or no clinical evidence of left atrial hypertension

The severity of hypoxemia is necessary to make the diagnosis of ARDS. The cardiogenic pulmonary edema must be excluded either by clinical criteria or by a pulmonary capillary wedge pressure (PCWP) lower than 18 mmHg in patients with a Swan-Ganz catheter in place.

Incidence of the condition in our Country

Global estimates suggest that ARDS occurs in 1.5 to 75 cases / 100,000 population. No systematic studies have been carried out till date to define the incidence of ARDS in India and reliable epidemiological data are not available.

Differential Diagnosis

1. Cardiogenic pulmonary oedema


2. Other considerations

Pneumonia

• Diffuse alveolar haemorrhage


• Idiopathic acute eosinophilic pneumonia


• Cryptogenic organizing pneumonia


• Acute interstitial pneumonia (Hamman-Rich syndrome)


• Metastatic malignancy


• Near drowning


• Drug reaction

Noncardiogenic pulmonary edema

• Acute hypersensitivity pneumonitis


• Transfusion-related acute lung injury (TRALI)


• Leukemic infiltration


• Fat embolism syndrome

Prevention and Counseling

No form of therapy is known to prevent the occurrence of ARDS

Optimal Diagnostic Criteria, Investigations, Treatment and Referral Criteria

At Secondary Hospital:

Clinical Diagnosis

Symptoms: The onset of ARDS is acute. The acute, or exudative, phase is characterised by rapid onset of dyspnoea, dry cough, respiratory failure, disorientation and agitation that usually develop 24 to 72 hours after the inciting event. The patient may be febrile or hypothermic.

Signs: Tachypnoea, tachycardia, cyanosis, crepitations and rhonchi may be present. Arterial hypoxaemia that is refractory to high concentrations of supplemental oxygen therapy is a hall mark of ARDS. Chest auscultation may reveal bilateral rales and rales may be absent despite diffuse involvement. In intubated and mechanically ventilated patient decreased breath sounds over one lung may indicate a pneumothorax or endotracheal tube down the opposite main bronchus. Careful physical examination to look for potential causes of sepsis including signs of lung consolidation or findings consistent with an acute abdomen, sites of intravascular lines, surgical wounds, drain sites, and decubitus ulcers for evidence of infection are needed. The cardiogenic pulmonary edema should be differentiated from ARDS, by carefully looking for signs of congestive heart failure or intravascular volume overload, including jugular venous distention, cardiac murmurs and gallops, hepatomegaly, and edema.

Investigations:

1. Pulse oximetry: Pulse oximetry reveals SpO2/FIO2 ratio less than or equal to 235. Severe refractory hypoxaemia in spite of supplemental oxygen therapy is evident.

2. Chest radiograph: The radiographic changes become evident by about 12 hours after the clinical onset of respiratory failure. Initially, patchy, illdefined opacities may become apparent throughout the lungs.

3. Echocardiography: Echocardiography is useful in differentiating ARDS from cardiogenic pulmonary oedema.

4. Arterial blood gas (ABG) analysis: ABG analysis usually reveals severe refractory hypoxemia, hypocapnia and alkalosis if the patient is breathing spontaneously. Hypercapnia usually does not occur unless chronic lung disease is co-existent.

Treatment:

Standard Operating procedure

In Patient

General therapeutic measures

• SpO2 monitoring by pulse oximetry


• Ensure adequate circulation and blood pressure using volume infusion and/or vasopressors


• Treatment of the aetiologcal cause of ARDS (e.g., appropriate antibiotic therapy for patients with sepsis syndrome)

Supplemental oxygen therapy: Initially, spontaneous ventilation using a face mask with a high flow gas delivery system can be used to deliver a FIO2 of up to 0.5 to 0.6.

Out Patient

Not applicable. ARDS is managed in an intensive care (ICU) unit setting

Referral criteria:

• 1. Diagnosis not clear 7


• 2. Response to therapy not optimal. Hypoxaemia (SpO2 ≤ 90) persists in spite of supplemental oxygen therapy


• 3. Haemodynamic instability

At Tertiary hospital

Clinical Diagnosis:

Symptoms: The onset of ARDS is acute. The acute, or exudative, phase is characterised by rapid onset of dyspnoea, dry cough, respiratory failure, disorientation and agitation that usually develop 24 to 72 hours after the inciting event. The patient may be febrile or hypothermic.

Signs: Tachypnoea, tachycardia, cyanosis, crepitations and rhonchi may be present. Arterial hypoxaemia that is refractory to high concentrations of supplemental oxygen therapy is a hall mark of ARDS. Chest auscultation may reveal bilateral rales and rales may be absent despite diffuse involvement. In intubated and mechanically ventilated patient decreased breath sounds over one lung may indicate a pneumothorax or endotracheal tube down the opposite main bronchus. Careful physical examination to look for potential causes of sepsis including signs of lung consolidation or findings consistent with an acute abdomen, sites of intravascular lines, surgical wounds, drain sites, and decubitus ulcers for evidence of infection are needed. The cardiogenic pulmonary edema should be differentiated from ARDS, by carefully looking for signs of congestive heart failure or intravascular volume overload, including jugular venous distention, cardiac murmurs and gallops, hepatomegaly, and edema.

Investigations

Computed tomography of the chest: Early in the exudative phase, computed tomography (CT) of the chest reveals diffusely distributed non-uniform ground glass opacification or consolidation which may not conform to the gravity distribution. Later in the exudative phase, the consolidation becomes more homogeneous and gravity dependent. In the proliferative and fibrotic stages, there is a decrease in the overall lung density and the appearance of an interstitial reticular pattern. CT also facilitates identification of underlying pulmonary causes of ARDS (e.g., pneumonia and lung abscess) and complications of ARDS, such as, pneumothorax, pneumomediastinum and interstitial emphysema may also be evident.

Swan-Ganz catheterization: The pulmonary capillary wedge pressure (PCWP) is less than 18 mm Hg and the cardiac index is more than 2.1 L/min.

Bronchoscopic procedures: Bronchoscopic procedures are helpful to exclude infectious causes of ARDS.

Treatment:

Standard Operating procedure

In Patient

General therapeutic measures

• SpO2 monitoring by pulse oximetry


• Ensure adequate circulation and blood pressure using volume infusion and/or vasopressors


• Treatment of the aetiologcal cause of ARDS (e.g., appropriate antibiotic therapy for patients with sepsis syndrome)

Supplemental oxygen therapy: Initially, spontaneous ventilation using a face mask with a high flow gas delivery system can be used to deliver a FIO2 of up to 0.5 to 0.6.

General therapeutic measures

• Haemodynamic stabilization. Pulmonary and systemic arterial lines are inserted for hemodynamic monitoring and rational fluid replacement therapy. Adequate circulation and blood pressure is ensured using volume infusion (crystalloids) and/or vasopressors, taking the CVP/PCWP as the guideline. The intravascular volume is maintained as low as possible while maintaining an adequate cardiac index, mean arterial pressure, at the same time ensuring adequate organ perfusion. In anaemic patients, transfusion of packed red cells can help improving oxygenation.


• Adequate nutrition should be ensured through the use of enteral feeding.


• Efforts should also be directed to prevent gastrointestinal bleeding and pulmonary thromboembolism

Supplemental oxygen therapy

• Spontaneous breathing using a face mask with a high flow gas delivery system can be used to deliver a FIO2 of up to 0.5 to 0.6. Continuous positive airway pressure (CPAP) may be added to improve PaO2 without increasing FIO2. If a FIO2 of more than 0.6 and CPAP of more than 10 cm H2O are needed to achieve PaO2 of more than 60 mm Hg, tracheal intubation and assisted mechanical ventilation are required.

Ventilatory support

• Aim of mechanical ventilation is to maintain gas exchange with minimal complications. Tidal volume should be set in the region of 6 ml/kg (“lung protective ventilation”) rather than the conventional 10 to 12 ml/kg and the plateau pressure should be limited to 30 to 35 cm H2O to prevent alveolar overdistension. PEEP and FIO2 settings are set as per ARDSnet protocol.


• Other alternative approaches, such as, prone positioning of the patient, high frequency jet ventilation (HFJV), high frequency oscillatory ventilation (HFOV), and liquid ventilation among others can also been tried in selected patients. The relative merits of these alternative methods of mechanical ventilation must be critically weighed against the potential side effects in every setting.

Corticosteroids and ARDS

• It is now conclusively established that corticosteroids have no useful role before the onset of ARDS or early in its course. When patients with ARDS have severe disease, and, do not show signs of improvement 7 to 14 days after the onset of ARDS (late ARDS), a one to two week trial with corticosteroids (prednisolone 2-4 mg/kg/day or equivalent) can be tried.

ARDS in the tropics

• Infectious causes such as pulmonary and miliary tuberculosis, falciparum malaria, enteric fever, and leptospirosis are rare but treatable causes of ARDS. When recognized to be the aetiological cause of ARDS, appropriate specific treatment must be instituted for primary conditions.

Out Patient

Not applicable. ARDS is managed in an intensive care (ICU) unit setting

Who Does What? And Timelines

Doctor: Diagnosis and Management including counseling

Nurse: Implementation of orders, monitoring of patients and counseling

Technician: Investigations

Respiratory physiotherapist: For administering supportive care to patients admitted in ICU

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