Dear Friends.. ARDS is an important clinical condition which needs discussions.. ARDS (Acute respiratory distress syndrome) It is an Acute onset of rapidly progressive dyspnea, tachypnea, and hypoxemia. DIAGNOSTIC CRITERIA for ARDS: (1)acute onset (2)PaO2/FiO2 of 200 or less regardless of PEEP (3)bilateral infiltrates seen on frontal chest radiograph and (4)no clinical evidence of left atrial hypertension(pulmonary artery wedge pressure of 18 mm Hg or less if measured) ARDS is believed to occur when a pulmonary or extrapulmonary insult causes the release of inflammatory mediators which causes damage to the vascular endothelium and alveolar epithelium… leading to pulmonary edema, hyaline membrane formation, decreased lung compliance, and poor air exchange. ARDS has to be differentiated from congestive heart failure, which usually has signs of fluid overload, and from pneumonia. I have attached tables to help you differentiate.. TREATMENT It is largely supportive and includes… (1)mechanical ventilation with a strategy of Low tidal volume & high positive end-expiratory pressure. (2)prophylaxis for stress ulcers and venous thromboembolism (3)nutritional support (4)treatment of the underlying injury. (5)conservative fluid therapy Applying above strategy of treatment improves outcomes. A spontaneous breathing trial is indicated as the patient improves and the underlying illness resolves. Most cases of ARDS in adults are associated with pulmonary sepsis or nonpulmonary sepsis. Risk factors include those causing (1)Direct lung injury (e.g., pneumonia, inhalation injury, pulmonary contusion) (2)Indirect lung injury (e.g., nonpulmonary sepsis, burns, transfusion-related acute lung injury). Risk factors in children are similar to those in adults, with the addition of age-specific disorders such as … Respiratory syncytial virus infection and near drowning aspiration injury. Pharmacologic options for the treatment of ARDS are limited. Although surfactant therapy may be helpful in children with ARDS, The use of corticosteroids is controversial. Randomized controlled trials and cohort studies tend to support early use of corticosteroids However, no consistent mortality benefit has been shown with this therapy. Mortality is between 34 and 55 percent in different recent trials and most deaths are due to multi-organ failure. Thanks Dr K N Poddar
Wonderful post from dear Poddar again. Nice topic, but tough too, made easy by Dr Poddar. Starting from Diagnostic criteria Treatment. As usual Poddar mark of teaching, unparalleled. None other than Dr Poddar can do this so understandable. Thanks again dear Poddar for your continuous teachings on Pulmonary Medicine. Pulmonary Medicine made easy. Author Dr K.N.Poddar Calcutta.
Again a wonderful post from Dr Poddar sir ARDS is an emergency which needs prompt attention and treatment . Very clear and simple way to differentiate between ARDS, Heart failure, and Pneumonia. Thanks for sharing the evidence based post sir
very useful post . thanks for poating important topic . hope you will keep educaring us the same way as you are Sir
poddar sir what is your view regarding prone ventilltion as far as I am concern it improves oxygenation but not modifies mortality
very nice , made easy atleast for other specialists other than pulmonologist , I appreciate and remain obliged Thanx
Nice post sir
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Respiratory Failure Definition: Clinically respiratory failure is defined as PaO2 <60 mmHg while breathing air, or a PaCO2 >50 mmHg. Type 1 respiratory failure - low PaO2 & low or normal PaCO2. -Type 2 respiratory failure -low PaO2 & raised PaCO2 _TYPES OF RF:_ 1. Acute hypoxia without hypercapnia - acute type 1. 2. Chronic hypoxia without hypercapnia - chronic type 1. 3. Acute hypoxia with hypercapnia - acute type 2. 4. Chronic hypoxia with hypercapnia -chronic type 2. Clinical Features: -Cyanosis -Unoxygenated hemoglobin 50 mg/L -Dyspnea: secondary to hypercapnia and hypoxemia -Paradoxical breathing -Confusion, somnolence and coma -Convulsions -Circulatory changes: tachycardia, hypertension, hypotension -Polycythemia: chronic hypoxemia-erythropoietin synthesis -Pulmonary hypertension: Cor-pulmonale or right ventricular failure. ACUTE TYPE 1 RF: _Causes_: -pneumonia. -pulmonary edema. -acute respiratory distress syndrome. -pulmonary embolism. - pneumothorax. _Management:_ -Treat underlying condition. -High conc of oxygen. -Artificial ventilation. CHRONIC TYPE 1 FAILURE: _Causes:_ -diseases associated with pulmonary fibrosis. -chronic chest wall or neuromuscular diseases. -chronic pulmomary edema pulmonary thromboembolism. _Management:_ -Treat underlying cause. -Oxygen therapy. -Artificial ventilation. -Venesection to reduce haematocrit for polycythemic. -Diuretics to reduce peripheral edema. ACUTE TYPE 2 RF: -Causes:_ -depressant drugs like diazepam, opiates & alcohol. -brainstem damage from stroke & trauma. -disorders of nerves & neuromuscular transmission like GBS. -Disorders of muscles like acute polymyositis. -severe airflow obstruction. -chest injuries resulting in tension pneumothorax-flial chest. _Management:_ -treat underlying condition. -oxygen therapy 24% oxygen. -removal of secretions by coughing or emergency bronchoscopic aspirations. -bronchodilators. -assisted ventilation. CHRONIC TYPE 2 PF: _Causes:_ -COPD. -Chestwall abnormalities like gross kyphoscoliosis. -central hypoventilation. _Management:_ -treat underlying cause. -oxygen therapy carries the risk of rise in PaCO2 resulting in confusion, drowsiness. -measure ABG levels before oxygen therapy. -do not give more than 24% oxygen. -give oxygen continously not intermittently at a rate of 1-2 litre/min. -stimulant drugs advocated like doxapram hydrochloride. -mechanical ventilation reserved for non respondant. -supportive treat includes antibiotics, nebulisers,clearing secretions by coughing, suction. Mechanical Ventilation (MV): -Non invasive with a mask. -Invasive with an endobronchial tube. -MV can be volume or pressure cycled -For hypercapnia: •MV increases alveolar ventilation and lowers PaCO2, corrects pH. •Rests fatigues respiratory muscles. -For hypoxemia: •O2 therapy alone does not correct hypoxemia caused by shunt. •Most common cause of shunt is fluid filled or collapsed alveoli (Pulmonary edema). Positive End Expiratory Pressure: -PEEP increases the end expiratory lung volume (FRC). -PEEP recruits collapsed alveoli and prevents recollapse. -FRC increases, therefore lung becomes more compliant. -Reversal of atelectasis diminishes intrapulmonary shunt. -Excessive PEEP has adverse effects •decreased cardiac output •barotrauma (pneumothorax, pneumomediastinum) •increased physiologic dead space •increased work of breathing
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