HistoryThis section has been translated automatically.
Ashbaugh et al.
DefinitionThis section has been translated automatically.
Acute respiratory failure (chest X-ray or CT thorax: evidence of bilateral diffuse infiltrates, basally reinforced) in previously lung healthy patients is acute respiratory insufficiency (acute onset within one week) caused by various damaging factors, regardless of whether the resulting pulmonary inflammatory mechanisms are primarily pulmonary or systemically triggered. Acute respiratory failure must have an identifiable, non-cardiac cause (exclusion of cardiac pulmonary edema or overhydration).
AECC definition of ARDS (1994 clarification of the definition used since 1967):
- Diffuse lung infiltrates in the x-ray
- acute onset
- bilateral infiltrates in posterior-anterior chest X-ray
- Pulmonary capillary occlusion pressure (PCWP, wedge pressure) < 18 mmHg or lack of clinical evidence of increased left atrial pressure or echocardiographic exclusion of left heart failure
- PaO2 (oxygen partial pressure in arterial blood) / FiO2 (oxygen content of the breathing air) ≤ 200 mmHg (Horovitz quotient)
The current S3 guideline of 12/2017 "Invasive ventilation and use of extracorporeal procedures in acute respiratory failure" refers to this definition and has replaced the Berlin definition (Nanchal RS et al. 2018):
- Timeline: occurrence within one week,
- Respiratory failure is not explained by heart failure or hypervolemia,
- Classification; the new definition distinguishes three degrees of severity of ARDS depending on the severity of hypoxemia:
- mild: PaO2/FIO2 (Horovitz quotient)= 201-300 mmHg with PEEP ≥5 cm H2O
- moderate: PaO2/FIO2 (Horovitz quotient) = 101-200 mmHg for PEEP ≥5 cm H2O and
- heavy: PaO2/FIO2 (Horovitz quotient) ≤ 100 mmHg with PEEP ≥5 cm H2O
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Occurrence/EpidemiologyThis section has been translated automatically.
Incidence not known with certainty; it varies between (2-50/100,000 per year)
EtiopathogenesisThis section has been translated automatically.
Acute respiratory insufficiency in acute lung failure is caused by severe diffuse damage to the lung parenchyma. The damage to the lung parenchyma can be direct or indirect:
Direct damage to the lung parenchyma:
- Pneumonia (most common cause; Shah RD et al. 2017)
- Inhalation of toxic gases such as smoke gas (inhalation trauma, toxic pulmonary oedema), aspiration of stomach contents
- Lung transplantation: A transfusion-associated acute lung failure (TRALI) is clinically indistinguishable from ARDS, but is distinguished from ARDS because the prognosis is significantly better with TRALI.
- Lung contusion
- Aspiration of salt or fresh water (near drowning)
- Fat embolism
- Amniotic fluid embolism
- Inhalation of hyperbaric oxygen.
- Intoxication by paraquat, narcotics, drugs
Indirect damage to the lung parenchyma:
- severe trauma (especially polytrauma) with shock ("shock lung")
- Fat embolism
- Acute (necrotizing) pancreatitis
- severe course of malaria tropica,
- Drugs and immunosuppression (for example after bone marrow/stem cell transplantation).
- Hypersensitivity reactions e.g. after biologicals
Note: Other secondary factors such as chronic alcohol abuse, chronic lung disease and low serum pH increase the risk of developing ARDS.
The consequence of local lung damage and the inflammatory processes triggered by it is an impairment of the Euler-Liljestrand reflex. This leads to a lack of vasoconstriction in lung areas with reduced alveolar ventilation. Depending on the extent, a relevant shunt volume is created, which can be more than 30% of the cardiac output. Activation of the intravascular coagulation cascade can lead to microthrombolization of the pulmonary capillaries. This results in ventilated but not perfused lung areas. This leads to an increase in dead space. Due to the permeability edema, an increase in lung weight by three times the normal weight is possible. The consequence is a decrease in lung compliance. Hypoxia-related pulmonary vasoconstriction can lead to increased pulmonary arterial pressure and cause right heart strain (risk of acute cor pulmonale). Ultimately, ARDS leads to a differently pronounced inhomogeneous pattern of lung damage. In addition to ventilated parenchyma areas, there are also edematous, collapsed and consolidated lung areas.
Clinical featuresThis section has been translated automatically.
A few days after a triggering damaging event, the following clinical symptoms occur:
- hypothermia) or hyperthermia
The ARDS is organised in three phases:
- Exudative phase (increased capillary permeability and interstitial pulmonary edema); clinically this stage is characterized by hypoxemia+hyperventilation with respiratory alkalosis.
- Early proliferative phase (death of type II pneumocytes; reduced formation of surfactant factor, fluid transfer into the alveoli, formation of hyaline membranes, formation of intrapulmonary shunts, hypoxia); clinically this stage is characterized by increasing shortness of breath, incipient radiological changes (diffuse infiltrates, especially in the dependent parts)
- Late proliferative phase (development of pulmonary fibrosis and endothelial proliferation of the alveolar capillaries, perfusion and diffusion deterioration = irreversible stage); clinically this stage is characterized by respiratory global insufficiency (hypoxaemia+hypercapnia), respiratory acidosis, increasing radiologically detectable bilateral shadows of the lung.
ImagingThis section has been translated automatically.
X-ray/CT Thoracic: Follow ups. Bilateral diffuse infiltrates, especially of the dependent parts in the x-ray of the lung or in the computer tomography without other reasonable explanation.
Differential diagnosisThis section has been translated automatically.
Cardiac pulmonary edema-echocardiographic exclusion of left heart failure
Fluid lung (J81) in renal failure (increased renal parameters)
Pulmonary embolism (evidence of a possible phlebothrombosis, right heart strain, lung perfusion scintigram)
Diffuse alveolar haemorrhagic syndromes (caused by severe diffuse permeability disturbance of the pulmonary capillaries, e.g. by vasculitis with consecutive extravasation of blood into the alveolar space)
Hematooncological diseases such as lymphomas, leukemias or solid tumors
Pulmonary sequelae of non-protective invasive ventilation (Ventilator-induced lung injury)
Infectious exacerbated bronchial asthma
TherapyThis section has been translated automatically.
Intensive care: Positioning with raised upper body (450) and lung protective ventilation. As mechanical ventilation itself has a lung damaging effect (barotrauma), the following criteria must be observed: small breathing volumes, avoidance of high pressures (<30mbar), sufficiently high PEEP (= positive pressure at the end of exhalation, so-called expiratory pressure: 9-12mbar) and higher breathing frequencies. As soon as the patient breathes spontaneously, assisted spontaneous breathing methods (such as BIPAP or APRV) are used.
The patient must be fed enteral.
Accompanying low-dose heparinization due to the increased risk of thrombosis during immobilization
Enteral feeding via probe, or parenteral feeding via a central venous catheter. The parallel use of both forms of nutrition may be necessary.
Supportive kinetic therapy measures (rotorest therapy or intermittent prone position of the patient): Intermittent prone position for prophylaxis of dorsal atelectasis: In severe cases of ARDS, treatment with kinetic therapy is supported (rotorest therapy or intermittent prone position of the patient). The prone position is the method of choice in severe ARDS and should be performed early, as it significantly improves the chances of survival. The patient remains in the prone position for 16 hours before being turned on his back again. Only if the prone position is not possible without risk, for example due to instability of the spinal column or injuries to the abdomen or brain, continuous lateral rotation therapy can be performed as a less effective alternative. This positioning therapy ensures that the breathing gas is distributed homogeneously in the lungs under protective, controlled ventilation. Prone positioning can be performed in 135° and 180° body position.
Elimination of the triggering cause (causal therapy, e.g. infection).
Machine ventilation: To reduce additional lung damage caused by artificial ventilation, gentle ventilation modes are recommended: low breathing volumes: The ventilator should be set to a maximum breathing volume of 6 ml/kg ideal body weight. These low breathing volumes reduce the regular overstretching and subsequent collapse of the alveoli.
ECMO (acronym for "extracorporeal membrane oxygenation"). This is an intensive care medical procedure in which the blood is oxygenated and CO2 is eliminated by means of a membrane system via an extracorporeal circuit. ECMO is used as a temporary lung replacement (<4 weeks). Its benefit has been sufficiently proven by scientific studies. Remark: Due to the risks of the procedure, it should only be used in severe cases in which, despite optimized ventilation and storage measures, sufficient oxygen saturation of the blood cannot be achieved (AWMF S3 guideline 2017).
Drug therapy: There is no well-established drug therapy for acute lung failure. In practice, corticosteroids are often used to reduce tissue damage caused by inflammatory processes. However, there is no reliable data on this.
Beta-2 sympathomimetics: without proven success in ARDS
Surfactants: without proven success in ARDS (Bosman KJ et al. 2010)
Progression/forecastThis section has been translated automatically.
The mortality rate has decreased significantly in recent decades due to progress in supportive therapy:
- Mild ARDS: lethality 25%
- Moderate ARDS: lethality about 30%
- Severe ARDS: lethality around 45 percent (Derwall M et al 2018).
Pre-existing diseases and chronic alcohol consumption worsen the prognosis!
LiteratureThis section has been translated automatically.
- Ashbaugh D et al (1967) Acute respiratory distress in adults. The Lancet 7511: 319-323.
- ARDS Definition Task Force et al. (2012) Acute respiratory distress syndrome: the Berlin Definition. JAMA 307:2526-33
- AWMF S3 Guideline Invasive ventilation and use of extracorporeal procedures in acute respiratory failure Status/2017:11.
- AWMF S2e-Guideline: Positioning therapy and early mobilization for the prophylaxis or therapy of pulmonary dysfunction, Status 04/2015: 10-29.
- AWMF S3 guideline Invasive ventilation and use of extracorporeal procedures in acute respiratory failure, status 12/2017: 163-165.
- Bosma KJ et al (2010) Pharmacotherapy for prevention and treatment of acute respiratory distress syndrome: current and experimental approaches. Drugs. 70:1255-1282
Derwall M et al (2018) The acute respiratory distress syndrome: pathophysiology, current clinical practice, and emerging therapies. Expert Rev Respir Med 12:1021-1029.
- Nanchal RS et al (2018) Recent advances in understanding and treating acute respiratory distress syndrome. F1000Res 20: F1000 Faculty Rev-1322.
- Needham DM et al (2012) Lung protective mechanical ventilation and two year survival in patients with acute lung injury: prospective cohort study. BMJ 344: e2124-e2124
- Ranieri M et al (2012) Acute Respiratory Distress Syndrome - The Berlin Definition. JAMA 307: 2526-2533Shah RD et al. (2017) Viral Pneumonia and Acute Respiratory Distress Syndrome. Clin Chest Med 38:113-125.
- Ware LB et al. (2000) The Acute Respiratory Distress Syndrome. NEJM 342: 1334-1349.
- Yadav H et al. (2017) Fifty Years of Research in ARDS. Is Acute Respiratory Distress Syndrome a Preventable Disease? On J Respir Crit Care Med 195:725-736.
Outgoing links (4)Bronchial asthma (overview); Cor pulmonale, acute; Fluid lung; Pneumonia, atypical;
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