Acute Respiratory Distress Syndrome
Acute Respiratory Distress Syndrome, also known as adult respiratory distress syndome (ARDS), is a parenchymal lung injury which is diffuse resulting in severe respiratory distress and hypoxemic respiratory failure.
The pulmonary edema is non-cardiogenic in origin. The diagnosis is mainly made on clinical grounds. The American-European Consensus Conference has set forth the following criteria to make a clinical diagnosis of ARDS (Conrad, 2005):
1. Acute onset
2. Bilateral infiltrates
3. Pulmonary artery wedge pressure less than 19 mm Hg (or no clinical signs of congestive heart failure)
4. PaO2/FIO2 ratio less than 200 (ARDS) or less than 300 (acute lung injury [ALI]): ALI is a milder clinical expression of the injury of ARDS that may or may not progress to ARDS (Conrad, 2005).
There are many predisposing conditions leading to ARDS. These include:
1. Infections. Pneumonia of any etiology can predispose to the condition. Viral pneumonia is the commonest type of pneumonia leading to ARDS. Gram negative systemic sepsis also can predispose to ARDS (Conrad, 2005).
2. Septic and traumatic shock can predispose to ARDS. Infact, any type of shock can lead to this condition.
3. Aspiration of either gastric contents or water during drowning can lead to ARDS.
4. Toxic inhalation of fumes or smoke can predispose to ARDS
5. Direct injury to pulmonary parenchyma, contusion, fat embolisation and multiple trauma.
6. Drug ingestion overdose- heroin, methadone, barbiturates and salicylates.
7. Therapeutic- postcardiopulmonary bypass, massive blood transfusion, drug ingestion
8. Systemic inflammatory response syndrome, pancreatitis and multiple organ dysfunction.
The hallmark pathology in this condition is diffuse alveolar damage. There is also damage to the lung capillary endothelium (Harman, & Walia, 2006). This leads to loss of integrity of the alveolar-capillary barrier. There is transudation of protein-rich fluid across the barrier resulting in pulmonary edema. Intrapulmonary shunting occurs leading to hypoxemia (Conrad, 2005).
The pathogenesis of ARDS can be described in 3 phases:
1. Exudative phase: This is the initial phase in which there is injury to the endothelium and epithelium leading to inflammation and fluid exudation.
2. Fibroproliferative phase: In this phase which follows the initial phase, there is influx and proliferation of fibroblasts and other cellular elements. The patient may recover or worsen in this stage. In sepsis, the main focus of injury is in the vascular endothelium. In aspiration of gastric contents, the focus of injury is in the alveolar epithelium (Harman, & Walia, 2006). Neutrophils play an important role in the pathogenesis of ARDS (Harman, & Walia, 2006). The neutrophils trigger release of cytokines, such as tumor necrosis factor (TNF), leukotrienes and macrophage inhibitory factor. Platelet sequestration and activation is also noted (Harman, & Walia, 2006).
3. Fibrosis: This phase occurs in those who have survived ARDS. There is resolution of inflammation and development of pulmonary fibrosis (Conrad, 2005).
The obvious clinical symptom in ARDS is dysnoea. The patients present with labored breathing, tachypnea, incresed work of breathing and hyperventilation. Due to hypoxemia there may be cyanosi, agitation and eventually obtundation. Tachycardia is usually present. Auscultation of lungs reveals scattered crackles due to diffuse alveolar damage (Conrad, 2005).
The most important test in a patient with ARDS is arterial blood gas analysis (ABG). This test reveals hypoxemia and hypocapnia. As the ventilatory finding progresses, hypercapnia ensues. PaO2 will be less than 50 mm Hg with an FIO2 more than 0.6 (Conrad, 2005).
X-ray chest reveals findings only in later stages. There will be diffuse alveolar-interstitial infiltrates in all lung fields. X-ray in early stages may also be useful in detecting the predisposing factor like pneumonia. Other investigations like CT Scan and MRI are not of much value. When in doubt, ECHO may be helpful in ruling out cardiogenic cause of edema (Conrad, 2005). Hemodynamic monitoring with the Swan-Ganz catheter is often helpful in separating cardiogenic from noncardiogenic pulmonary edema (Harman, & Walia, 2006).
Blood culture, complete blood picture, sputum culture and broncho-alveolar lavage culture may be done as required to decide upon the cause and choice of antibiotics.
A patient with ARDS must be immediately admitted to the intensive care unit and an ABG done immediately to assess the severity of the condition and to decide upon intubation and mechanical ventilation. Basics of emergency like airway, breathing and circulation must be taken care of. The patient must be put on continuous pulse oximetry and cardiac monitoring. ABG must be done at regular intervals. In refractory hypoxemia or marked respiratory distress, endotracheal intubation and ventilation must be started. Mechanical ventilation must be done with positive end-expiratory pressure (PEEP) of 5-10 cm H2O. This is because high PEEP reduces intrapulmonary shunting and improves oxygenation (Conrad, 2005).
The aim of saturations should be 92-94%. To achieve this ventilation should be initiated with a FIO2 of 1 and then gradually decreased. The ideal tidal volume would be 8-10 mL/kg and respiratory rate of 10/minute. Pressure controlled ventilation is the preferred mode of ventilation. When hypercapnia is detected, increase in the ventilatory settings should be instituted only if the pH is less that 7.1 (Conrad, 2005).
Good intravenous access is mandatory. Monitoring of vital signs, if necessary even continuous arterial BP monitoring must be done.
Fluid overload must be avoided in ARDS because of already present pulmonary edema.
Irrespective of the etiology, broad spectrum antibiotics must be started in all cases of ARDS. The antibiotics must be changed according to the culture reports.
Course of the disease:
ARDS is potentially fatal disease. Mortality rate averages to 60% (Conrad, 2005). Many complications can occur during the course of the disease. These include multiple organ failure, superinfection with bacteria, permanent lung disease like pulmonary fibrosis or restrictie lung disease, and even death. Complications due to treatment like oxygen toxicity and barotrauma can also occur. Most of the patients succumb to sepsis or multiple organ failure.
Conrad, S.A. (2005). Respiratory Distress Syndrome, Adult. Emedicine from WebMD. Retrieved April 29, 2008 http://www.emedicine.com/emerg/topic503.htm
Harman, E.M. & Walia, R. (2006). Acute Respiratory Distress Syndrome. Emedicine from WebMD. Retrieved April 29, 2008 http://www.emedicine.com/med/TOPIC70.HTM
Cite this Acute Respiratory Distress Syndrome
Acute Respiratory Distress Syndrome. (2016, Jul 10). Retrieved from https://graduateway.com/acute-respiratory-distress-syndrome/