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Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001.

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ARDS

, M.D.

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The term ARDS (Adult Respiratory Distress Syndrome; the word “adult” has been replaced nowadays by “acute”) was introduced in 1967 by Ashbaugh. Similarities to the hyaline membrane disease or infant respiratory distress syndrome (IRDS) prompted to coin this entity. Acute respiratory distress syndrome is the endpoint of an acute lung injury (ALI). All patients with ARDS have an acute lung injury, but not all patients with ALI develop an ARDS (1). Because of the varying etiologies, although inducing a generally uniform inflammatory reaction and increased permeability, the prognosis in ARDS is diverse. Therefore, every ARDS case is not just the same as the other.

Definition

Acute lung injury is defined as “a syndrome of inflammation and increasing permeability that is associated with the constellation of clinical, radiological and physiologic abnormalities that cannot be explained by, but must not exist with, left atrial or pulmonary capillary hypertension” (1).

Table I shows the currently accepted criteria for ALI and ARDS. These criteria, particularly those for ALI, describe a static picture of the syndrome. A pulmonary injury can also exist at PaO2/FiO2 values higher than 300 mmHg and may require the same management as for ALI and ARDS. Furthermore, the time factor is vaguely formulated, which is probably due to the fact that the onset of the triggering event cannot be exactly defined.

Table I. Criteria for acute lung injury (ALI) and ARDS.

Table I

Criteria for acute lung injury (ALI) and ARDS.

From patho-anatomical and pathophysiological viewpoint, ALI is “any significant deterioration in lung function due to characteristic pathologic abnormalities in the lungs' normal underlying structure or architecture” (2) and ARDS is “a specific form of injury with diverse causes, characterized pathologically by diffuse alveolar damage, and pathophysiologically by a breakdown in both the barrier and gas exchange functions of the lung, resulting in proteinaceous alveolar edema and hypoxemia” (2).

Common causes of ALI and ARDS are summarized in table II. From therapeutic and prognostic viewpoint, it seems reasonable to differentiate between primary (direct damage of the lung parenchyma via the airways) and secondary ARDS (indirect damage of the lung from the capillary side, the prototype being sepsis-associated) (1).

Table II. Causes of primary and secondary ARDS.

Table II

Causes of primary and secondary ARDS.

Pathogenesis

Endothelial damage, inflammatory infiltrate, destruction of the alveolar epithelium, protein-rich interstitial and alveolar edema as well as atelectasis due to functional damage to the alveolar surfactant constitute the morphological changes in ARDS. The course of the inflammatory reaction at the site of gas exchange between the endothelium, interstitium and epithelium is most probably uniform, regardless of whether the trigger mechanism is primary (transbronchial) or secondary (systemic). This exudative early phase can subside or progress into a proliferative fibrotic late phase.

Transbronchial pulmonary affections, such as following aspiration or inhalation of toxic substances, induce release of chemokines and other chemotactic factors from the alveolar epithelium and macrophages, which in turn result in an accumulation and activation of neutrophil granulocytes.

The systemic triggering of ARDS involves the release of products of activated cascades, toxins, cytokines and inflammatory cells into the pulmonary vasculature, followed by activation of the endothelium, neutrophil sequestration and increased permeability. After migration of active inflammatory cells into the interstitium, diverse mechanisms are initiated along the site of gas exchange, which amplify the inflammatory reaction. In this process, not only pro- and anti-inflammatory cytokines but also other products of cellular and cascade activation (proteases, oxidants and lipid mediators) play a crucial role, which interact with cells, extracellular matrix as well as with one another (36).

Although the alveolar cell is more resistant to destruction of the alveolo-capillary integrity than the endothelial side (7), the surfactant production finally declines, resulting in widespread atelectasis. This dysfunction of pulmonary integrity renders the lung susceptible to bacterial colonization and super-infection.

Accumulation of neutrophil granulocytes in ARDS differs from that in pneumonia due to its nonspecific and uncontrolled nature (3).

Epidemiology and prognosis

The population incidence of ARDS is estimated to be about 2–8 cases per 100,000 people per year (8). Data for ALI are not available. The incidence of ARDS varies depending on the underlying disease. Sepsis with an ARDS incidence of 25–37%, severe multiple trauma with 25–44%, severe pancreatitis, overtransfusion and aspiration of gastric content represent high risk groups.

Mortality due to ARDS also varies considerably depending on the underlying cause (table III).

Table III. ARDS - etiology and mortality.

Table III

ARDS - etiology and mortality.

Independent predictors of mortality for ALI and ARDS are multiple organ failure, liver cirrhosis, sepsis, HIV infection, malignant tumors, organ transplantation, patient age > 65 years and the APACHE-III score (810).

In contrast, there is no correlation between mortality and the lung injury score (11).

Sepsis is the most common cause of ARDS. During the course of sepsis, ARDS may manifest early (12) as a one-organ failure with a low mortality, which rises as the number of organ failures increases (13).

Diagnosis

The diagnosis of ALI and ARDS is based on the criteria laid by the Consensus Conference (table I (1)). Increased intrapulmonary shunt and reduced static lung compliance are also commonly observed. The pulmonary artery pressure increases due to the high pulmonary vascular resistance as a result of hypoxic pulmonary vasoconstriction (8). Ensuing right ventricular sequels can be identified by echocardiography.

For severity classification, the lung injury score (LIS) introduced by Murray or simply the oxygenation or PaO2/FiO2 index measured at FiO2 of 1.0 are used. In a multivariate analysis, it could be shown that LIS does not have any predictive value (9). Nevertheless, the oxygenation index can be applied to quantify the efficacy of therapeutic measures.

Our experience with the measurement of extravascular lung water by means of the double indicator dilution technique is that it is elevated in sepsis-related ARDS, while this is not always the case in other forms.

Further diagnostic measures are related to the underlying cause and its dynamics. It is crucial to look for an infectious or septic cause which has a prognostic and therapeutic relevance. Procalcitonin, in addition to SIRS criteria, CRP and other inflammatory markers, seems useful to identify bacterial infections (14). Initial and persistently high plasma levels of TNF-α, IL-1 β , IL-6 and IL-8 are found to be signs of poor prognosis . Early markers of the development of ARDS in risk groups are considered to be IL-8, procoagulatory activity, D-dimer as well as matrix metalloproteinases in the bronchoalveolar lavage (4, 6).

Management

Due to the etiologic diversity in ARDS there is no therapeutic “magic bullet”. Simultaneous to the causal treatment of the underlying disease, symptomatic management of ALI and ARDS should be started with the aim of eliminating the hypoxia. This includes:

  • fluid restriction
  • kinetic therapy
  • alveolar recruitment
  • drugs
  • surfactant instillation
  • inhalation of NO and aerosolized prostanoides
  • extracorporeal membrane oxygenation
  • partial liquid ventilation

Fluid restriction

Interstitial and alveolar edema is a sign of fluid maldistribution. The filtration volume VF is dependent on the filtration coefficient KF and the gradient of the filtration pressure (PC-PIS) and the oncotic pressure (COPPL-COPIS), as shown by the equation:

Image ch110e1.jpg

where PC is capillary hydrostatic pressure, PIS interstitial hydrostatic pressure, COPPL plasma colloid osmotic pressure, and COPIS interstitial colloid osmotic pressure. Under normal colloid osmotic pressure and standard KF the filtration volume is dependent mainly on PC and PIS, the latter being influenced by a positive end-expiratory pressure (PEEP).

Therefore, fluid restriction, diuretics and, in some cases, hemofiltration are basic therapeutic measures to lower the PC and keep the patient “dry”.

Fluid restriction should be maintained as long as it is hemodynamically tolerated. The goal is to achieve a sufficient cardiac output with the lowest possible pulmonary capillary wedge pressure (PCWP) (2). On the other hand, hypovolemia and the necessity of high doses of noradrenalin should be avoided. Higher intravascular volume may be necessary to maintain hemodynamic stability under high PEEP.

Theoretically and practically, hydroxyethyl starch (HES) is an appropriate solution for volume substitution (HES 10% has a molecular weight of 200 kDa and a substitution degree of 0.6). The reasons are the balanced water binding, titrable increment in PCWP and COP and the higher molecular weight compared to electrolytes and albumin. However, there is no study which documented the superiority of any of the available solutions.

Kinetic therapy

Gattinoni (15) has shown the advantage of prone positioning and introduced it in the treatment of ARDS. The following mechanisms influence oxygenation during prone positioning of the patient:

  • elimination of the ventilation/perfusion mismatch in the dorsal dependent lung areas;
  • better reabsorption of edema fluid as a result of the redistribution in better ventilated areas (16);
  • amplifying the effect of PEEP by increasing lung volume and recruitment of new lung areas (16);
  • easing the weight of the congested lung and heart as well as reduction of the intraabdominal pressure on the previously dependent areas (17);
  • better drainage of bronchial secretion.

Clinical studies have shown the positive effects of this maneuver on gas exchange and pulmonary shunt volume without a negative influence on hemodynamics (1619). The prone position can be maintained as long as PaO2 values are higher than those in the supine position. The responder rate is 50% to 80%. Generally, position change should be carried out after 12 hours.

In conclusion, kinetic therapy is today one of the basic principles in the treatment concept of ARDS.

Alveolar recruitment

The current strategy of mechanical ventilation in ARDS includes lower tidal volume (6–8 ml/kg body weight), pressure limitation (peak inspiratory pressure < 35 cm H2O), high PEEP (above the lower inflection point), inverse ratio ventilation, and tolerating permissive hypercapnia. This results in a certain degree of alveolar recruitment and keeps the alveoli open. It is also protective because lower tidal volumes are applied and the shear forces between ventilated and non-ventilated alveoli are reduced. Additionally, pressure controlled ventilation has been shown to be an important basic principle within the concept of protective ventilation because through pressure limitation and decelerating flow a limited volume is administered depending on the pressure decrease as a result of alveolar recruitment. Therefore, volume trauma to the ventilated alveoli is avoided.

The concept of protective ventilation was compared with the conventional procedure in a prospective randomized study by Amato (20), which showed a significant reduction of the 28-day mortality in the first group (grade A).

The results of ARDS network trial impressively confirmed the benefit of low fidal volumes. Comparing different volumes it has been shown a signigicant less mortality using tidal volumes of 6 ml/kg versus 12 ml/kg BW (21).

Low-volume, pressure controlled, inverse ratio, high PEEP ventilation is currently considered as the state of the art in the ventilatory management of ARDS.

A common problem with this form of ventilation is the permissive hypercapnia. Although the effect of the degree and duration of the resultant respiratory acidosis is not yet fully elucidated, there are findings that this may have a negative effect on organ function (22).

Other forms of mechanical ventilation also aim at alveolar recruitment: keeping the lung open by means of intrinsic PEEP using higher respiratory rate and inverse ratio ventilation; biphasic positive airway pressure (BIPAP) and airway pressure release ventilation (APRV); rapid alveolar recruitment by means of a brief reopening maneuver followed by the principle of “keeping the lung open” (“complete” open lung concept, (23); and administration of very low tidal volumes using very high respiratory rate (high frequency ventilation).

Drugs

There is no confirmatory evidence on the advantage of the treatment of ARDS with N-acetylcysteine, ambroxol, steroids, liposomal prostaglandin E1, ketoconazole or almitrine.

N-acetylcysteine, an antioxidant and a precursor of glutathione synthesis, has been found to inhibit the production of proinflammatory cytokines. Although studies in patients with ARDS and septic shock did not show any significant reduction in mortality, a rise in plasma and erythrocyte glutathione content, improvement in chest x-ray findings, a rise in systemic vascular resistance, increases in oxygen delivery and consumption, improved oxygenation and a reduction of the duration of mechanical ventilation were observed with this drug (grade B). Recommended dose is 150mg/kg body weight as a bolus, followed by 12.5 mg/kg/hr as a maintenance dose (2426).

Ambroxol is also an antioxidant found to stimulate surfactant production. Clinical efficacy was observed in patients with bronchopulmonary complications following upper abdominal surgery (27) and in case reports on its prophylactic administration to prevent postoperative atelectasis, and as a therapy in pulmonary aspiration of gastric content (grade B). Recommended dose is 300mg/day as a continuous intravenous infusion, to be reduced over 5 to 6 days.

Randomized placebo controlled studies did not show any reduction in sepsis mortality with steroids (28, 29). High dose methylprednisolone did not influence outcome in sepsis-related ARDS, following aspiration, and in some other forms of secondary ARDS (grade B). Therefore, this group of drugs is not indicated in the early exudative phase of ARDS. Fat emboli with resultant ARDS, pneumocystis carini pneumonia and the late proliferative phase of ARDS are considered as indications for steroid treatment (30).

Liposomal prostaglandin E1 (PGE1) resulted in an improvement in PaO2 and lung compliance and shorter duration of mechanical ventilation. Results of a multicenter study are expected (31).

The administration of ketoconazole in preventive studies has shown a positive trend in mortality reduction due to ARDS. The recommended dose is 400 mg on the first day(32) (grade B).

The effect of almitrine in combination with nitric oxide inhalation (NO) (5–10 ppm) has been prospectively compared with the application of NO alone. The combination resulted in a better reduction in pulmonary artery pressure and a rise in the oxygenation index than NO alone (33) (grade B).

Surfactant instillation

Surfactant application is considered as a pathophysiologically defined treatment option. However, a significant reduction in mortality could not be achieved (34, 35) (grade B).

Therefore, currently there are no reliable data to recommend the use of surfactant in the treatment of ARDS (36).

Surfactant application may be beneficial in isolated cases, such as therapy refractory lobar or segmental atelectasis. The recommended dose (local bronchoscopic instillation) is 1–2 g/lung segment up to 300 mg/kg body weight on the first day; repeat application at a dose of 150–300 mg/kg body weight on the next day may be required. Tracheobronchial suction or any disruption of the closed ventilatory system should be avoided during treatment.

Inhalation of nitric oxide and vasoactive prostanoides

NO inhalation results in selective intrapulmonary vasodilatation followed by a reduction in pulmonary artery pressure and a rise in oxygenation due to a decrease in the intrapulmonary shunt. Reasons for nonresponse are presumed to be a normal pulmonary vascular tension or a preexisting fixed pulmonary hypertension (37). The recommended dose for ARDS is usually less than 10 ppm. The initially high expectations of improved oxygenation with NO application sunk following clinical experience and published studies (38, 39) (grade B) which showed that survival and ventilator weaning are not significantly influenced. Reports of increased mortality and higher incidence of dialysis under NO inhalation (38) are doubtful.

A possible indication for NO inhalation may be in the treatment of severe ARDS, when complex treatment measures may have been ineffective.

Although aerosolized prostanoides (PGI2) are found to induce a selective intrapulmonary vasodilatation, controlled studies are not yet available.

Extracorporeal membrane oxygenation (ECMO)

ECMO is not an alternative to the conventional mechanical ventilation; it is rather an additional option in the overall treatment strategy.

It not only improves oxygenation, but also leads to further relief to the injured lung through protective ventilation. Available studies (40, 41) (grade C and B), however, did not show any significant improvement in survival. Two German clinical prospective studies (42, 43) reported improvement in mortality using ECMO compared to conventional therapy (grade C). However, the patient groups are not comparable. Commonly accepted criteria of “fast” and “slow” entry are listed in table IV.

Table IV. “Fast” entry and “slow” entry criteria for ECMO.

Table IV

“Fast” entry and “slow” entry criteria for ECMO.

As long as there are no randomized controlled studies comparing ECMO with conventional treatment, it remains just an option in the management of ARDS, particularly when conventional treatment cannot be fully implemented (e.g. due to pneumothorax) or turns to be ineffective in a patient, in whom the underlying cause could potentially be eliminated or improved (44).

Partial liquid ventilation (PLV)

PLV includes the partial filling of the airways with perfluorocarbon, which is biologically inert and reduces the surface tension, combined with conventional mechanical ventilation. Although an improvement in alveolar recruitment and gas exchange as well as reduction in ventilator - associated lung injury (45) were reported, other clinical studies (46, 47) (grade B and C) did not show any significant reduction in mortality.

Recommended dose (47) for newborns: initial volume of 15 ± 4 ml perfluorocarbon/kg body weight, substitution of loss with 3.3 ± 0.9 ml/kg; duration of treatment 24–72 hours.

This method is still in its experimental phase, but it seems not to have any short- or long-term adverse effects.

Conclusion

ARDS is still a big challenge in intensive care. It represents a common pathway of diverse events and disease entities, which account for the varying outcome. Sepsis is a leading cause of ARDS. Besides the standard treatment, which consists of therapy of the underlying cause, fluid restriction, kinetic therapy and protective mechanical ventilation combined with adjuvant drug treatment, the “complete” open lung concept which allows a rapid alveolar recruitment may be a useful addition that still requires widespread clinical evaluation. Surfactant instillation, NO inhalation and ECMO remain restricted for use in special cases. Partial liquid ventilation is yet in its infancy.

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