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Original articles

Surfactant administration in premature infants with RDS 

Ismeta Kalkan, Suada Heljić, Amra Čengić, Verica Mišanović, Duško Anić, Fedžat Jonuzi, Hajrija Maksić 

SIGNA VITAE 2007; 2(1): 21 - 24 61 Kb 

Introduction Respiratory distress syndrome, (RDS, hyaline membrane disease, hyposurfactosis) is the most common disturbance in preterm

infants, appearing in approximately 60% of infants born before 30 weeks gestation. The main cause of the disease is inadequate

amounts of lung surfactant. Surfactant replacement reduces mortality and morbidity rates in premature infants, reduces duration of

ventilatory support, number of complications and medical costs. Surfactant therapy is not a substitute for an attempt to increase lung

maturity by delaying premature delivery or by using antenatal corticosteroids with the aim of preventing RDS (1-5).

Many studies of different regimes of surfactant therapy, related to time of application, have been undertaken during the 80s and 90s

(6,7,8).

Prophylactic surfactant replacement is given to preterm neonates at high risk of developing acute RDS in the delivery room, shortly

after resuscitation, as they start to breathe. Rescue therapy refers to treatment given after the diagnosis is established, 2 to 24

hours after birth (3,9-11). Most centers use rescue therapy as the mode of treatment. Each regime increases oxygenation of

ventilated preterm babies and reduces mortality and morbidity rates. This correlates with a significant reduction of medical costs

(12,13,14).

The aim of this study was to find an optimal regime of surfactant therapy, early vs. late treatment, and also to test the efficacy of

multiple doses vs. a single dose.

Patients and methods The investigation included 78 preterm infants with RDS, between 25 and 35 weeks gestation, treated with surfactant. All children

were hospitalized in the neonatal intensiv care unit (NICU) of the Pediatric Clinic, Clinical Centre Sarajevo during 2004 and 2005.

Surfactant was given to infants with radiological and clinical signs of RDS (tachypnea, cyanosis on room air) who required more

then 40% O2 in inhaled air. Surfactant was given after intubation, radiological confirmation of correct tube placement and

stabilization of vital functions. We used bovine surfactant - Survanta, 4ml/kg, which was administered according to standard

procedures. The following parameters were chosen on the ventilator: PIP (Positive Inspiratory Pressure) needed for the rising of the

chest but without overdistension; pressure at the end of expiration (PEEP) of 4 cm H2O; inspiratory time (IT) of 0,5 sec., frequency

of 30/min, start FiO2 1,0. Surfactant was given in one or more doses, in sterile conditions. The second dose was given 12 hours

after the first dose. Each dose was administered over 30s into each lung quadrant. If saturation fell below 85% we stopped with theinstillation. Treatment was continued after O2 saturation improved upon previous values. Effects of surfactant therapy were

assessed based on O2 saturation (determinated by pulse oximetry), gas analyses in arterial and capillary blood, the clinical

condition of the child and chest X-ray.

The group of investigated children was divided into subgroups, depending on the number of doses received, time of treatment

(early, late) and O2 requirement. Early treatment was related to patients who received the first dose within 6 hours of birth and late

treatment - six or more hours after birth. In regard to O2 requirements, our study group was divided into those who needed <

60%O2 in inhaled air and those who needed 60% O2 or more.

Results Comparing the results of early treatment (giving Surfactant within 6 hours of birth) and late treatment (six or more hours after birth)

we found that there is a significant difference between treated groups (p=0,005). In the study group which received surfactant within

6 hours of birth, 34 (out of 43) children survived, compared with 17 (out of 35) children who received surfactant 6 hours after birth or

later (table 1).

From the table 2, it can be seen that 53 (out of 78) children received one dose of surfactant comparable with 25 who received two

doses. 38 (out of 53) children, who received one dose survived, whereas, only 13 (out of 25) children who received two doses

survived. There is no significant difference between these two groups (p=0,088), although the mortality rate in children who received

two doses of surfactant was lower in comparison with the group which received one dose.

There is a significant difference (p= 0,015) between groups related to O2 requirement. In the group of children requiring O2

concentration less then 60% (n=22), as many as 19 (out of 22) survived in comparison with the group who required 60% or more

oxygen, at the time of surfactant replacement, where 32 (out of 56) children survived (table 3). Early treatment with surfactant at

lower O2 concentrations is associated with a lower mortality rate.

Table 1. Outcome of illness in relation to time of first surfactant dose

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Hours 

Survived  Died 

Total (%)  c2  p 

No (%)  No (%) 

0- 6  34 (79)  9 (21)  43 (100) 

7,9  0,005 More then 6  17 (49)  18 (51)  35 (100) 

Total  51  27  78 (100) 

Table 2. Outcome of illness in relation to no. of doses

Number of doses 

Survived  Died 

Total (%)  c2  p 

No (%)  No (%) 

1 dose  38 (72)  15 (28)  53 (100) 

2,9  0,088 2 doses  13 (52)  12 (48)  25 (100) 

Total  51  27  78 (100) 

Table 3. Outcome of illness dependent upon O2 requirement

O2 concentration 

Survived  Died 

Total (%)  c2  p 

No (%)  No (%) 

<0,6  19 (86)  3 (14)  22 (100) 

6,0  0,015 0,6 or more  32 (57)  24 (43)  56 (100) 

Total  51  27  78 (100) 

Discussion Many clinical trials, carried out during the 80s and 90s, showed that surfactant use in preterm infants significantly reduces mortality

rate and complications within 28 days of birth (9,12). Our study, conducted on 78 preterm babies, showed that the overall

percentage of survival in children treated with surfactant was 65,38%.

Generally, surfactant is being given 6-24 hours after birth, as rescue therapy, when diagnosis of severe respiratory distress

syndrome is established. On the other hand, treatment in the delivery room is considered optimal, only if it's given after establishing

breathing and ventilation by positive pressure. In most of the studies, treatment of RDS with surfactant started between 2-4 hours

after birth or in the delivery room after stabilization of the baby, within 15 minutes of birth. In relation to timing of the first dose, two

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strategies are used (7,15,16).

In our study, the first dose of surfactant was given as soon as diagnosis of severe respiratory distress syndrome was established:

within 6 hours from birth (early treatment) and after 6 hours (late treatment). In the study group which received surfactant within 6

hours of birth, 34 (out of 43) children survived, compared with 17 (out of 35) children who received surfactant 6 hours after birth or

later (p<0,005). Our results confirm the advantages of early treatment vs. late treatment. So, a reasonable recommendation is to

treat the infants as soon as clinical signs of developing respiratory distress appear. Waiting for the complete clinical picture to

develop before commencing treatment will minimize the effect of surfactant therapy (17,18). The treatment in the delivery room

should be reserved for the smallest infants with the highest risk for developing acute RDS and should be given by a person

experienced in neonatal resuscitation and surfactant administration (19).

In most cases, multiple doses of surfactant are being given, with the intent of avoiding functional inactivation of surfactant. Multiple

doses are believed to be useful because the effect of one dose is considered transient (10,20). When comparing multiple doses with

single doses, authors (7, 9,21) have found a reduction in the frequency of pneumothorax and mortality rate (within 28 days) with

multiple doses. It is not clear whether all sick infants benefit from multiple doses. Most children respond to treatment or re-treatment,

but some of them show little or no response. These infants can have other illnesses like pneumonia, pulmonary hypoplasia or

congenital heart disease. Structural immaturity of the lungs and birth asphyxia can reduce the response to surfactant therapy

(23,22).

In our study, there was no significant difference between groups treated with one and two or more doses (p<0,088), although the

mortality rate in children who received two doses of surfactant was lower compared with the group which received one dose. The

necessity for more doses should be individualized and considered based on clinical circumstances, such as in infants with residual

lung disease, so that the risk of complications like pneumothorax or prolonged ventilatory support can be avoided (24,25).

It seems that early surfactant treatment, when O2 requirement is lower, reduces the need for later treatment, O2 requirement andmechanical ventilation. Surfactant given early is more effective. The optimal time for administration is not defined. The current

recommendation is that a preterm baby with RDS needs surfactant replacement if he/she needs endotracheal intubation and if O2

requirement in inhaled air is more than 40% (26,27). In our study there is a significant difference (p<0,05) between groups related to

O2 requirement. In the group of children which required O2 concentrations less than 60% (n=22), as many as 19 (out of 22)

survived compared with 32 (out of 56) who required 60% or more oxygen concentration in inhaled air at the time of surfactant

replacement. Early treatment of surfactant with lower O2 requirements is associated with a lower mortality rate.

Our study confirmed the benefits of surfactant use in preterm babies with respiratory distress syndrome. We confirmed the

advantages of early treatment vs. late treatment, which is also connected with O2 requirement. In this study we could not confirm

the advantage of multiple over single doses. Therefore a reasonable recommendation is to treat infants as soon as clinical signs of

developing respiratory distress appear with individualized dosaging for each infant.

References 1. Jobe AH. Lung Development. In: Martin RJ, Fanaroff AA, eds. Neonatal-perinatal Medicine, Diseases of the Fetus and Infant. St

Louis: Mosby; 1997, pp 1019-1040.

2. Honrubia D, Stark AR. Respiratory Disorders. In: Cloherty JP, Eichenwald EC, Strak AR, eds. Manuale of Neonatal Care.

Philadelphia: Lippincott, Williams&Wilkins; 1997, pp 341-378.

3. Gomella TL, Gleason BL. Hyalin Membrane Disease. In: Gomella TL, eds. Neonatology. Appleton and Lange; 1988/89, pp 381-

385.

4. Katz R. Function and Physiology of the Respiratory System. In: Furhman BP, Zimmerman JJ, eds. Pediatric critical care. St Louis:

Mosby; 1992, pp 386-399.

5. Fackler JC, Arnold JH, Nickols DG, Rogers MC. Acute Respiratory Distress Syndrome. In: Rogers MC, eds. Textbook of Pediatric

Intensive Care, Baltimore: Williams and Wilkins; 1996, pp 197-225.

6. Leahy A. Respiratory distress. In: Southall D, Coulter B, Ronald Ch, Nicholson S, Parke S, eds. International Child Health Care.

London: BMJ; 2002, pp 129-131.

7. Jobe AH. Pulmonary surfactant therapy. New England Journal of Medicine 1993; 328:861-8.

8. Enhoring G, Shennan A, Possmazer F. Prevention of neonatal respiratory distress syndrome by tracheal instillation of surfactant.

Pediatrics 1985;76:145-53.

9. Schwartz RM, Luby AM, Scanlon JW, Kellogg RJ. Effect of surfactant on morbidity, mortality, and resource use in newborn infants

weighting 500 to 1500 g. New England Journal of Medicine 1944;330:1476-80.

10. Gortner LA. Multicenter randomized controlled trial of bovine surfactant for prevention of respiratory of distress syndrome. Lung

1990;168: 864-91.

11. Stevens TP, Blennov M, Soll RF. Early surfactant administration with brief ventilation vs. selective surfactant and continued

mechanical ventilation for preterm infants with or at risk for RDS. Cochrane Database Syst Rev 2002;CD003063.

12. Jeffrey A, Timothy E. Hydrophobic Surfactant Proteins in Lung Function and Disease. New England Journal of Medicine

2002;347:2141-2148.

13. Soll RF, Blanco F. Natural surfactant extract versus synthetic surfactant for neonatal respiratory distress syndrome. Cochran

Database Syst Rev 2001;CD000144.

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14. Hafner D, Germann PG, Hauschke D. Comparison of rST-C surfactant with natural and synthetic surfactants after late treatment

in a rat model of the acute respiratory distress syndrome. New England Journal of Medicine 1998;124(6):1083-90.

15. Soll RF. Appropriate surfactant usage in 1996. Eur J Pediatr 1996;2:S8-13.

16. Ehitelaw A. Controversies: synthetic or natural surfactant treatment for respiratory distress syndrome/The case for synthetic

surfactant. J Perinatal Med 1996;24(5):427-35.

17. Gortner L.A. Multicenter randomized controlled trial of bovine surfactant for prevention of respiratory of distress syndrome. Lung

1990;168:864-91.

18. Jobe A.H. Pulmonary surfactant therapy. New England Journal of Medicine 1993;328:861-8.

19. Speer CP, Halliday HL. Surfactant therapy in the newborn. Current Paediatrics 1994; 4:5-9.

20. Halliday HL. Where we are now with the prenatal steroids and postnatal surfactant. Biol Neonate 1996:69:186-7.

21. Mathay MA. The Acute Respiratory Distress Syndrome. New England Journal of Medicine 1996;334:1469-147.

22. Jobe AH. Pulmonary Surfactant Therapy. New England Medical Journal 1993;328:861-868.

23. Bard H, Belanger S, Fouron JC. Comparison of effects of 95% and 90% oxygen saturation in RDS. Prenatal and Neonatal

Medicine 2001;75 F94-6.

24. Ramanathan R, Rasmussen MR, Gerstmann DR, Finer N, Sekar K. A Randomized, Multicenter Masked Comparison Trial of

Poractant Alfa (Curosurf) versus Beractant (Survanta) in the Treatment of Respiratory Distress Syndrome in Preterm Infants.

American Journal of Perinatology 2004;21:3.

25. Vermont-Oxford Neonatal Network. A multicenter, randomized trial comparing synthetic surfactant with modified bovine

surfactant extract in the treatment of neonatal respiratory distress syndrome. Pediatrics 1996;97:1.

26. Ainsworth SB, Beresford MW, Milligan DWA. Pumactant and Poractant alfa for treatment of respiratory distress syndrome in

neonates born at 25 to 29 weeks gestation. Lancet 2000;355:1387-139.27. Ramanathan R, Rasmussen MR. Curosurf and Survanta in the treatment of respiratory distress syndrome in pre term infants.

Biol Neonate 2002;81:36.

"ARDS" redirects here. For other uses, see  ARD (disambiguation). 

Adult respiratory distress syndrome

Classification and external resources 

Chest x-ray of patient with ARDS

ICD-10  J80. 

ICD-9  518.5, 518.82 

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DiseasesDB 892 

MedlinePlus   000103 

eMedicine  med/70 

MeSH D012128 

Acute respiratory distress syndrome (ARDS), also known as respiratory distress syndrome (RDS) or adult

respiratory distress syndrome (in contrast with IRDS) is a serious reaction to various forms of injuries to thelung. 

ARDS is a severe lung disease caused by a variety of direct and indirect issues. It is characterized byinflammation of the

lung parenchyma leading to impaired gas exchange with concomitant systemic release ofinflammatory

mediators causing inflammation, hypoxemia and frequently resulting in multiple organ failure. This condition is often fatal,

usually requiring mechanical ventilation and admission to an intensive care unit. A less severe form is called acute lung

injury (ALI).

ARDS formerly most commonly signified adult respiratory distress syndrome to differentiate it from infant respiratory distress

syndrome in premature infants. However, as this type of pulmonary edema also occurs in children, ARDS has gradually

shifted to mean acute rather than adult . The differences with the typical infant syndrome remain.

Definition

[edit]Historical background

Acute respiratory distress syndrome was first described in 1967 by Ashbaugh et al .[1][2] Initially there was no definition,

resulting in controversy over incidenceand mortality. In 1988 an expanded definition was proposed which quantified

physiologic respiratory impairment.

In 1994 a new definition was recommended by the American-European Consensus Conference Committee.[1][3] It had two

advantages: first, it recognizes that severity of pulmonary injury varies, and secondly, it is simple to use.[4] 

ARDS was defined as the ratio of arterial partial oxygen tension (PaO2) as fraction of inspired oxygen (FiO2) below 200

mmHg in the presence of bilateralinfiltrates on the chest x-ray. These infiltrates may appear similar to those of left ventricularfailure, but the cardiac silhouette appears normal in ARDS. Also, the pulmonary capillary wedge pressure is normal (less

than 18 mmHg) in ARDS, but raised in left ventricular failure.

A PaO2 /FiO2 ratio less than 300 mmHg with bilateral infiltrates indicates acute lung injury (ALI). Although formally considered

different from ARDS, ALI is usually just a precursor to ARDS.

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Signs and symptoms

ARDS patients usually present with shortness of breath, tachypnea and occasionally with confusion resulting from low

oxygen levels.

ARDS can occur within 24 to 48 hours of an injury (trauma, burns, aspiration, massive blood transfusion, drug/alcohol

abuse) or an acute illness (infectious pneumonia, sepsis, acute pancreatitis).

[edit]Diagnosis

An arterial blood gas analysis and chest X-ray allow formal diagnosis by the aforementioned criteria. Although severe

hypoxemia is generally included, the appropriate threshold defining abnormal PaO2 has never been systematically studied.

Note though, that a severe oxygenation defect is not synonymous with ventilatory support. Any PaO2 below 100 (generally

saturation less than 100%) on a supplemental oxygen fraction of 50% meets criteria for ARDS. This can easily be achieved

by high flow oxygen supplementation without ventilatory support.

Any cardiogenic cause of pulmonary edema should be excluded. This can be done by placing a  pulmonary artery

catheter for measuring the pulmonary artery wedge pressure. However, this is not necessary and is now rarely done as

abundant evidence has emerged demonstrating that the use of pulmonary artery catheters does not lead to improved patient

outcomes in critical illness including ARDS.

Plain chest X-rays are sufficient to document bilateral alveolar infiltrates in the majority of cases. While CT scanning leads to

more accurate images of the pulmonary parenchyma in ARDS, it has little utility in the clinical management of patients with

ARDS, and remains largely a research tool.

[edit]Pathophysiology

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In sepsis or trauma-induced ARDS, infiltrates are usually more patchy and diffuse. The posterior and basal segments are

always more affected, but the distribution is even less homogeneous.

Loss of aeration also causes important changes in lung mechanical properties. These alterations are fundamental in the

process of inflammation amplification and progression to ARDS in mechanically ventilated patients.

Progression

If the underlying disease or injurious factor is not removed, the amount of inflammatory mediators released by the lungs in

ARDS may result in a systemic inflammatory response syndrome (or sepsis if there is lung infection).[1] The evolution

towards shock and/or multiple organ failure follows paths analogous to the pathophysiology of sepsis.

This adds up to the impaired oxygenation which is the central problem of ARDS, as well as to respiratory acidosis, which is

often caused by ventilation techniques such as permissive hypercapnia which attempt to limit ventilator-induced lung injury

in ARDS.

The result is a critical illness in which the 'endothelial disease' of severe sepsis / SIRS is worsened by the pulmonary

dysfunction, which further impairs oxygen delivery.

[edit]Treatment

[edit]General

Acute respiratory distress syndrome is usually treated with mechanical ventilation in the Intensive Care Unit. Ventilation is

usually delivered through oro-tracheal intubation, or tracheostomy whenever prolonged ventilation (≥2 weeks) is deemed

inevitable.

The possibilities of non-invasive ventilation are limited to the very early period of the disease or, better, to prevention in

individuals at risk for the development of the disease (atypical pneumonias, pulmonary contusion, major surgery patients).

Treatment of the underlying cause is imperative, as it tends to maintain the ARDS picture.

Appropriate antibiotic therapy must be administered as soon as microbiological culture results are

available. Empirical therapy may be appropriate if local microbiological surveillance is efficient. More than 60% ARDS

patients experience a (nosocomial) pulmonary infection either before or after the onset of lung injury.

The origin of infection, when surgically treatable, must be operated on. When sepsis is diagnosed, appropriate

local protocols should be enacted.

Commonly used supportive therapy includes particular techniques of mechanical ventilation and pharmacological agents

whose effectiveness with respect to the outcome has not yet been proven. It is now debated whether mechanical ventilation

is to be considered mere supportive therapy or actual treatment, since it may substantially affect survival.

Mechanical ventilation

Further information:  Pressure Regulated Volume Control  

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The overall goal is to maintain acceptable gas exchange and to minimize adverse effects in its application. Three

parameters are used: PEEP (positive end-expiratory pressure, to maintain maximal recruitment of alveolar units), mean

airway pressure (to promote recruitment and predictor of hemodynamic effects) and plateau pressure (best predictor of

alveolar overdistention).[9] 

Conventional therapy aimed at tidal volumes (V t) of 12-15 ml/kg. Recent studies have shown that high tidal volumes can

overstretch alveoli resulting involutrauma (secondary lung injury). The ARDS Clinical Network, or ARDSNet, completed a

landmark trial that showed improved mortality when ventilated with a tidal volume of 6 ml/kg compared to the traditional 12

ml/kg. Low tidal volumes (V t) may cause hypercapnia and atelectasis[1] due to their inherent tendency to increase dead

space. 

Low tidal volume ventilation was the primary independent variable associated with reduced mortality in the NIH-sponsored

ARDSnet trial of tidal volume in ARDS. Plateau pressure less than 30 cm H2O was a secondary goal, and subsequent

analyses of the data from the ARDSnet trial (as well as other experimental data) demonstrate that there appears to be NO

safe upper limit to plateau pressure; that is, regardless of plateau pressure, patients fare better with low tidal volumes (see

Hager et al., American Journal of Respiratory and Critical Care Medicine, 2005).

[edit]APRV (Airway Pressure Release Ventilation) and ARDS / ALI

It is often said that no particular ventilator mode is known to improve mortality in ARDS. The landmark ARDSNet trial used a

volume controlled mode comparing delivered tidal volumes of 6 ml/kg with 12 ml/kg and showed decrease mortality with

smaller volumes and typically higher set rates. However, other modes of ventilation, like airway pressure release ventilation

(APRV), have not been directly compared to volume controlled ventilation.

Some practitioners favor APRV when treating ARDS. Well documented advantages to APRV ventilation include: decreased

airway pressures, decreased minute ventilation, decreased dead-space ventilation, promotion of spontaneous breathing,

almost 24 hour a day alveolar recruitment, decreased use of sedation, near elimination of neuromuscular blockade,

optimized arterial blood gas results, mechanical restoration of FRC (functional residual capacity), a positive effect on cardiac

output (due to the negative inflection from the elevated baseline with each spontaneous breath), increased organ and tissue

perfusion and potential for increased urine output secondary to increased renal perfusion.

A patient with ARDS, on average, spends between 8 and 11 days on a mechanical ventilator; APRV may reduce this time

significantly and conserve valuable resources.

  A study is needed to evaluate whether APRV will reduce patient mortality when compared to the ARDSNet protocol.

There seems to be little political will, within the medical community, to address the need for this study, in spite of the

clinical successes seen with APRV.

Positive end-expiratory pressure

Positive end-expiratory pressure (PEEP) is used in mechanically-ventilated patients with ARDS to improve oxygenation. In

ARDS, three populations of alveoli can be distinguished. There are normal alveoli which are always inflated and engaging in

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gas exchange, flooded alveoli which can never, under any ventilatory regime, be used for gas exchange, and atelectatic or

partially flooded alveoli that can be "recruited" to participate in gas exchange under certain ventilatory regimens. The

recruitable aveoli represent a continuous population, some of which can be recruited with minimal PEEP, and others which

can only be recruited with high levels of PEEP. An additional complication is that some or perhaps most alveoli can only be

opened with higher airway pressures than are needed to keep them open. Hence the justification for maneuvers where

PEEP is increased to very high levels for seconds to minutes before dropping the PEEP to a lower level. Finally, PEEP can

be harmful. High PEEP necessarily increases mean airway pressure and alveolar pressure. This in turn can damage normal

alveoli by overdistension resulting in DAD.

The 'best PEEP' used to be defined as 'some' cmH2O above the lower inflection point (LIP) in the sigmoidal pressure-volume

relationship curve of the lung. Recent research has shown that the LIP-point pressure is no better than any pressure above

it, as recruitment of collapsed alveoli, and more importantly the overdistension of aerated units, occur throughout the whole

inflation. Despite the awkwardness of most procedures used to trace the pressure-volume curve, it is still used by some to

define the minimum PEEP to be applied to their patients. Some of the newest ventilators have the ability to automatically

plot a pressure-volume curve. The possibility of having an 'instantaneous' tracing trigger might produce renewed interest in

this analysis.

PEEP may also be set empirically. Some authors suggest performing a 'recruiting maneuver' (i.e., a short time at a very high

continuous positive airway pressure, such as 50 cmH2O (4.9 kPa), to recruit, or open, collapsed units with a high distending

pressure) before restoring previous ventilation. The final PEEP level should be the one just before the drop in

PaO2 (or peripheral blood oxygen saturation) during a step-down trial.

Intrinsic PEEP (iPEEP), or auto-PEEP, first described by John Marini of St. Paul Regions Hospital, is a potentially

unrecognized contributor to PEEP in patients. When ventilating at high frequencies, its contribution can be substantial,

particularly in patients with obstructive lung disease. iPEEP has been measured in very few formal studies on ventilation in

ARDS patients, and its contribution is largely unknown. Its measurement is recommended in the treatment of ARDS

patients, especially when using high-frequency (oscillatory/jet) ventilation. 

A compromise between the beneficial and adverse effects of PEEP is inevitable.

[edit]Prone position

Distribution of lung infiltrates in acute respiratory distress syndrome is non-uniform. Repositioning into the prone position

(face down) might improve oxygenation by relieving atelectasis and improving perfusion. However, although the hypoxemia

is overcome there seems to be no effect on overall survival.[1][10] 

[edit]Fluid management

Several studies have shown that pulmonary function and outcome are better in patients that lost weight or pulmonary wedge

pressure was lowered by diuresisor fluid restriction.[1] 

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Corticosteroids

A Meduri et al. study has found significant improvement in ARDS using modest doses of corticosteroids. The initial regimen

consists of methylprednisolone2 mg/kg daily. After 3 –5 days a response must be apparent. In 1 –2 weeks the dose can be

tapered to methylprednisolone 0.5-1.0 mg daily. Patients with ARDS do not benefit from high-dose corticosteroids.[1][11] This

was a study involving a small number of patients in one center. A recent NIH-sponsored multicenter ARDSnet LAZARUS

study of corticosteroids for ARDS demonstrated that they are not efficacious in ARDS.

[edit]Nitric oxide

Inhaled nitric oxide (NO) potentially acts as selective pulmonary vasodilator. Rapid binding to hemoglobin prevents systemic

effects. It should increase perfusion of better ventilated areas. There are no large studies demonstrating positive results.

Therefore its use must be considered individually.

Almitrine bismesylate stimulates chemoreceptors in carotic and aortic bodies. It has been used to potentiate the effect of

NO, presumably by potentiating hypoxia-induced pulmonary vasoconstriction. In case of ARDS it is not known whether this

combination is useful.[1] 

[edit]Surfactant therapy

To date no prospective controlled clinical trial has shown a significant mortality benefit of exogenous surfactant in adult

ARDS.[1] 

[edit]Complications

Since ARDS is an extremely serious condition which requires invasive forms of therapy it is not without risk. Complications

to be considered are:[1] 

  Pulmonary: barotrauma (volutrauma), pulmonary embolism (PE), pulmonary fibrosis, ventilator-associated

pneumonia (VAP).

  Gastrointestinal: hemorrhage (ulcer), dysmotility, pneumoperitoneum, bacterial translocation.

  Cardiac: arrhythmias, myocardial dysfunction.

  Renal: acute renal failure (ARF), positive fluid balance.

  Mechanical: vascular injury, pneumothorax (by placing pulmonary artery catheter), tracheal injury/stenosis (result of

intubation and/or irritation by endotracheal tube.

  Nutritional: malnutrition (catabolic state), electrolyte deficiency.

Epidemiology

The annual incidence of ARDS is 1.5 –13.5 people per 100,000 in the general

population.[citation needed ] Its incidence in the intensive care unit (ICU),mechanically

ventilated population is much higher. Brun-Buisson et al. (2004) reported a

prevalence of acute lung injury (ALI) (see below) of 16.1% percent in ventilated

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patients admitted for more than 4 hours. More than half these patients may develop

ARDS.

Mechanical

ventilation, sepsis, pneumonia, shock, aspiration, trauma (especially pulmonary

contusion), major surgery, massive transfusions, smoke inhalation, drug reaction

or overdose, fat emboli and reperfusion pulmonary edema after lung

transplantation or pulmonary embolectomy may all trigger ARDS. Pneumonia and

sepsis are the most common triggers, and pneumonia is present in up to 60% of

patients. Pneumonia and sepsis may be either causes or complications of ARDS.

Elevated abdominal pressure of any cause is also probably a risk factor for the

development of ARDS, particularly during mechanical ventilation.

The mortality rate varies from 30% to 85%.

[citation needed ]

Usually, randomizedcontrolled trials in the literature show lower death rates, both in control and

treatment patients. This is thought to be due to stricter enrollment criteria.

Observational studies generally report 50% –60% mortality.[citation needed ] 

[edit]