Acute Respiratory Distress Syndrome

1
Acute Respiratory Distress Syndrome

• Dr. Vanya Chugh

University College of Medical Sciences GTB
Hospital, Delhi
2
Timeline

• In 1967 Ashbaugh, Bigelow, Petty, Levine -
  described Acute Respiratory Distress Syndrome in
  adults
• In 1971, Petty and Ashbaugh modified its name
  from acute to adult Respiratory Distress
  Syndrome to differentiate it from its newborn
  counterpart
• In 1974, Webb and Tierney confirmed the existence
  of ventilator associated lung injury
• In 1990, Hickling et al introduced the concept of
  permissive hypercapnia

3
Timeline

• In 1992, American European Consensus Conference
  (AECC) gave standardized definition for ARDS
• In 1997, Tremblay et al introduced the concept of
  biotrauma
• In 1998, Amato et al, conducted RCT - decrease in
  mortality using low tidal volume ventilation and
  high PEEP (open lung strategy)
• In 2000, ARDS network trial demonstrated the
  benefits of low tidal volume and PEEP ventilation

4
Definitions of ARDS

• Ashbaugh and colleagues, 1967
• Severe dyspnea
• Tachypnea
• Cyanosis refractory to oxygen therapy
• Decreased pulmonary compliance
• Diffuse alveolar infiltrates on chest radiograph.
• Loosely defined criteria
• Definition of hypoxemia inconsistent

5
Murray Mathay Lung Injury Score(1988)

• Chest Radiology findings
  Score
• No alveolar consolidation
  0
• One quadrant 1
• Two quadrant 2
• Three quadrant 3
• Four quadrant 4
• Oxygenation status (Hypoxemia Score)
• PaO2 / FiO2
• gt 300 mmHg 0
• 225-299 mmHg 1
• 175-224 mmHg 2
• 100-174 mmHg 3
• lt 100 mmHg 4

6
Pulmonary compliance
Score Compliance (ml/cmH2O)
gt 80 0 60-79 1 40-59 2 20-39 3 lt
19 4 PEEP settings (when ventilated) PEEP
(cmH2O) lt 5 0 6-8 1 9-11 2 12-14 3 gt
15 4 Acute lung injuries assessed by dividing sum
by 4 0 points No pulmonary injury 0.1-2.5
points Mild to moderate gt 2.5 points Severe
(ARDS)
7
Murray Mathay Lung Injury Score

• Advantages
• Ventilatory settings included
• Disadvantage
• Complex
• Lacks prospective validity

8
Bernard and colleagues, 1992 (American European
Consensus conference definition)

• A three-criteria system including chest
  radiograph, oxygenation score, and exclusion of
  cardiogenic causes
• Acute onset, bilateral infiltrates on chest
  radiography,
• Acute lung injury PaO2/FIO2 300
• ARDS subset PaO2/FIO2 200
• Pulmonary-artery wedge pressure of lt18 mm Hg or
  the absence of clinical evidence of left atrial
  hypertension

9
Bernard and colleagues, 1992 (American European
Consensus conference definition)

• Problems
• Acute onset arbitrary lt1 week
• Bilateral infiltrates inter observer variation,
  b/l pneumonia, atelectasis, cardiogenic pulmonary
  edema
• PAOP of lt18 mm Hg /absence of clinical evidence
  of left atrial hypertension PAOP poor estimate
  of PVH, falsely raised with high airway pressures
• Acute lung injury present if PaO2/FIO2 is 300
  new and arbitrary value

10
Delphi definition (2005) of ARDS

• Diagnosis 1- 4 present with 5a and/or
  5b1. PaO2/FiO2 ratio 200 on PEEP
  10.2. Bilateral airspace disease 2
  quadrants, frontal chest X-ray 3. Onset within
  72 hours.4. No clinical evidence/subjective
  finding of CHF
• (including use of PA catheter and/or echo if
  clinically indicated)
• 5a. Static respiratory compliance lt 50ml/cm H2O
• (patient sedated, TV 8ml/kg, PEEP 10.5b.
  Presence of direct or indirect risk factor
  associated with lung injury.

11
Delphi definition of ARDS contd.

• Airspace disease presence of one or more of the
  following-
• Air brochogram
• Acinar shadows
• Coalescence of acinar shadows
• Silhoutte sign
• Specificity delphi LIS gt AECC
• Sensitivity delphi LIS AECC
• Delphi criteria provisional, need further testing

12
Synonyms of ARDS

• Shock lung
• Pump lung
• Traumatic wet lung
• Post traumatic atelectasis
• Adult hyaline membrane disease
• Progressive respiratory distress
• Acute respiratory insufficiency syndrome
• Haemorrhagic atelectasis
• Hypoxic hyperventilation

• Postperfusion lung
• Oxygen toxicity lung
• Wet lung
• White lung
• Transplant lung
• Da Nang lung
• Diffuse alveolar injury
• Acute diffuse lung injury
• Noncardiogenic pulmonary edema.
• Progressive pulmonary consolidation

13
Epidemiology of ARDS

• Difficult to estimate
• Lack of standardization of the definition
• Difference in methodology
• KCLIP study (1999-2000) done on ARDS patients as
  per AECC criteria estimated -
• - incidence of ALI 78.9/lakh
  person years
• - mortality rate 38.5- 41.1

14
Precipitating Factors

• Direct Lung Injury
• Pneumonia
• Aspiration of gastric contents
• Pulmonary contusion
• Near-drowning
• Toxic inhalation injury

• Indirect Lung Injury
• Sepsis
• Severe trauma
• Multiple bone fractures
• Flail chest
• Head trauma
• Burns
• Multiple transfusions
• Drug overdose
• Pancreatitis
• Post-cardiopulmonary bypass

15
Differential risk factors

• Chronic alcohol abuse
• Absence of DM
• Age
• Gender
• Severity of illness APACHE score
• Excessive blood transfusion
• Cigarette smoking

16
Pathophysiology in ARDS

• Based on the histological appearance -
• Exudative phase (0-4 days)
• Alveolar and interstitial edema
• Capillary congestion
• Destruction of type I alveolar cells
• Early hyaline membrane formation
• Proliferative Phase (3-10 days)
• Increased type II alveolar cells
• Cellular infiltration of alveolar septum
• Organisation of hyaline membranes
• Fibrotic Phase (gt10 days)
• Fibrosis of hyaline membranes and alveolar septum
• Alveolar duct fibrosis

17
Pathology in ARDS

• Mechanisms in early phase -
• Release of inflammatory cytokines TNF alpha,
  IL- 1,6,8
• Failure of alveolar edema clearance, epithelial
  and endothelial damage
• Increased permeability of alveolo capillary
  membrane
• Neutrophil migration and oxidative stress
• Procoagulant shift fibrin deposition
• Surfactant dysfunction
• Mechanism in late (repair) phase
• Fibroproliferation -TGF beta, MMPs,
  thombospondin, plasmin, ROS
• Remodelling - matrix and cell surface
  proteoglycans, MMP, imbalance of coagulation and
  fibrinolysis.

18
Pathophysiology of ARDS
19
D/D Hydrostatic pulmonary edema

• PCWP 18 mmHg
• Causes
• Cardiogenic LVF (eg. MI, myocarditis)
• cardiac valvular
  disease (aortic, mitral)
• Vascular systemic HTN, pulmonary embolism
• Volume overload - excessive iv fluids, renal
  failure

20
Cardiogenic vs Non-cardiogenic edema
Cardiogenic
Non-cardiogenic
1. Prior h/o cardiac disease
Absence of heart disease
2.Third heart sound
No third heart sound
3. Cardiomegaly
Normal sized heart
4. Infiltrates Central distribution
Peripheral distribution
5. Widening of vascular pedicle No
widening of vascular pedicle
( ? width of mediastinum)
6. PA wedge pressure
N or ? PA wedge pressure
7. Positive fluid balance
Negative fluid balance
21
Management

• Treatment of the precipitating cause
• Mechanical ventilation
• Core ventilator management - protective lung
  ventilation strategy
• 
  - role of open lung approach
• Adjuncts to core ventilation -
• Fluid restriction
• Permissive hypercapnia
• Prone positioning
• Recruitment maneuvers

22
Management contd.

• Non conventional/Salvage interventions
• High frequency ventilation
• Airway pressure release ventilation
• Tracheal gas insufflation
• Inverse ratio ventilation
• Inhaled nitric oxide
• Inhaled prostacyclin
• Corticosteroids
• Surfactant administration
• Liquid ventilation
• Extracorporeal membrane oxygenation
• Supportive therapy nutrition, prevention of
  infection

23
Concept of VALI

• Mechanical ventilation - Basic care in
  critically ill ICU patients
• May cause or worsen lung injury ventilator
  induced/associated lung injury
• Components
• Barotrauma
• Volutrauma
• Atelectrauma
• Biotrauma

24
VALI and MODS
25
Concept of baby lung

• Put forward by Gattinoni and colleagues first in
  1987
• Lung injury in ARDS - non homogenous, basal
• Edema and consolidation gt dependent lung regions
  - ? density of dorsal regions
• Aerated ventral regions baby lung
  (300-500gms) high compliance
• Ventilation of baby lung with normal tidal
  volumes and pressures alveolar over distension
  injury to functional lung tissue

26
Management

• Lung protective ventilation ARDS network
  protocol
• Goals
• Oxygenation PaO2 55-80 mmHg, or SpO2 88 94
  (excluding pregnancy, intracranial hypertension
  or stroke where SaO2 goalgt94)
• Ventilation
• Tidal volume 4-6 ml/kg ideal body weight
• Plateau pressure lt30cmH2O
• Ph 7.25-7.35
• IE ratio of 11 13

27
Management contd.

• Oxygenation
• Initially high Fio2 given (1.0) to correct
  hypoxia
• Fio2 and PEEP adjusted to the lowest level
  compatible with the oxygenation goals
• Fio2 and PEEP adjusted in the following fixed
  combinations fio2/PEEP(mmHg)

FIO2
PEEP
28
Management contd

• Initial ventilator set up and adjustments
• STEP 1- Calculation of ideal body
  weight(IBW)
• For males, IBW(kg) 502.3height(inch) 60
• Or IBW(kg)50 0.91height(cm)152.4
• For females, IBW(kg) 45.52.3height(inch) 60
• Or IBW(kg)45.5 0.91height(cm)152.4

29
Management contd

• STEP 2 - Volume assist control selected as
  ventilator mode
• Initial tidal volume (TV) set at 8ml/kg IBW
• TV reduced by 1ml/kg IBW 2 hourly until TV
  6ml/kg IBW
• Initial ventilator rate set to maintain baseline
  minute ventilation( not gt35/min)
• TV and respiratory rate adjusted to achieve the
  pH and plateau pressure goals
• Inspiratory flow rate set above patients demand
  (usually gt80L/min)

30
Open Lung Approach

• Introduced by Amato et al in 1998 use of low
  tidal volume high PEEP recruitment (Open lung
  strategy) reduce mortality in ARDS
• Maintaining inflation deflation between 2
  inflection points during entire respiratory cycle
  
• Ventilatory settings - PEEP gtPflex TV reduced
  so that Pplat lt UIP
• Advantages- avoids repetitive opening and
  closing of alveoli (VALI)
• - minimizes shear injury

31
Open Lung ApproachPressure-Volume Curve
32
Management

• Treatment of the precipitating cause
• Mechanical ventilation
• Core ventilator management protective lung
  ventilation strategy
• 
  role of open lung approach
• Adjuncts to core ventilation
• Fluid restriction
• Permissive hypercapnia
• Prone positioning
• Recruitment maneuvers

33
Fluid restriction in ARDS

• Rationale alveolar flooding depends on
• Capillary hydrostatic pressure
• Oncotic pressure
• Alveolarcapillary permeability
• Capillary permeability increased in ARDS
• ? hydrostatic pressure and ? oncotic pressure
  may help.

34
Fluid therapy in ARDS

• Recommended
• Central venous pressure guided therapy 10-14
  mmHg ( ARDS Network Trial
  2003)
• Restricted fluid intake
• Increased urine output Diuretics or RRT
• Not recommended
• Vasodilators
• Albumin

35
Management

• Treatment of the precipitating cause
• Mechanical ventilation
• Core ventilator management - protective lung
  ventilation strategy
• 
  - role of open lung approach
• 
  
• Adjuncts to core ventilation
• Fluid restriction
• Permissive hypercapnia
• Prone positioning
• Recruitment maneuvers

36
Permissive Hypercapnia

• Hickling and colleagues 1990
• Degree of hypercapnia permitted in patients
  subjected to lower tidal volumes
• Upper limit not defined gt100 mmHg avoided
• Advantages
• Increased surfactant secretion (animal models)
  improved V/Q match, oxygenation (improved
  compliance)
• Increased cardiac output and oxygen delivery
  (sympathoadrenal effects predominate over
  cardiodepressant effects)
• Increased cerebral blood flow and tissue
  oxygenation

37
Permissive Hypercapnia

• Concerns
• Increase in pulmonary vascular resistance
• Impaired diaphragmatic function (impairs afferent
  transmission)
• Decrease in cardiac contractility
• Raised intracranial tension
• Individualize and treat

38
Management

• Treatment of the precipitating cause
• Mechanical ventilation
• Core ventilator management - protective lung
  ventilation strategy
• 
  - role of open lung approach
• Adjuncts to core ventilation
• Fluid restriction
• Permissive hypercapnia
• Prone positioning
• Recruitment maneuvers

39
Prone Position Ventilation

• First suggested by Piehl and Brown in 1976
• Offers improved oxygenation by
• Increased FRC
• Change in regional diaphragm motion
• Distribution of perfusion
• Better clearance of secretions

40
Prone Position Ventilation

• Sud and colleagues conducted meta-analysis of
  13 RCTs (1559 patients) on supine and prone
  position ventilation in ARDS/ALI patients
• Median MV of 12 hours ( 4-24hrs) for 4 days( 1-10
  days)
• Conclusion -cannot be recommended for routine
  Mx
• -no evidence of
  improved survival
• Gattinoni et al suggested no overall reduction in
  mortality except in very sick patients ( SAPS II
  Score gt50)
• No decrease in ventilator associated pneumonia

41
Problems of prone position

• Facial edema
• Airway obstruction
• Difficulties with enteral feeding
• Transitory decrease in oxygen saturation
• Hypotension Arrhythmias
• Vascular and nerve compression
• Loss of venous accesses and probes
• Loss of chest drain and catheters
• Accidental extubation
• Apical atelectasis d/t incorrect positioning of
  the tracheal tube
• Increased need for sedation

42
Management

• Treatment of the precipitating cause
• Mechanical ventilation
• Core ventilator management - protective lung
  ventilation strategy
• 
  - role of open lung approach
• Adjuncts to core ventilation
• Fluid restriction
• Permissive hypercapnia
• Prone positioning
• Recruitment maneuvers

43
Recruitment maneuvers

• High pressure inflation maneuver aimed at
  temporarily raising the transpulmonary pressure
  above levels typically obtained with mechanical
  ventilation
• Types Elevated sustained pressures 40 cm H2O
  for 40 seconds
• Sigh breaths ? tidal volume / PEEP for one
  or several breaths
• Extended sigh breath VCV with PEEP well
  above LIP for a longer time
• More effective in early ALI and those with more
  homogenous disease atelectasis gt consolidation.

44
Recruitment maneuvers

• Adverse effects
• Hypotension
• Barotrauma
• Raised ICP
• Haemodynamic instability

45
Management contd.

• Non conventional/Salvage interventions
• High frequency ventilation
• Airway pressure release ventilation
• Tracheal gas insufflation
• Inverse ratio ventilation
• Inhaled nitric oxide
• Inhaled prostacyclin
• Corticosteroids
• Surfactant administration
• Liquid ventilation
• Extracorporeal membrane oxygenation
• Supportive therapy nutrition, prevention of
  infection

46
High Frequency Ventilation

• Mechanical ventilatory support using higher than
  normal breathing frequencies
• Smaller tidal pressure swings (within inflection
  points) along with apt mpaw
• Smaller tidal volumes and higher mean pressure
  utilized for lung protection
• Special ventilators required
• Types - High Frequency Jet Ventilation (HFJV)
• High Frequency Oscillatory
  Ventilation (HFOV)

47
HFV

• HFJV
• A nozzle/injector creates high velocity jet of
  gas directed into the lung
• Injectors 1-3mm diameter
• Expiration is passive
• Frequencies available upto 600 breaths/min
• Available for neonatal and paediatric use only
• HFOV
• Characterized by rapid oscillations of a
  diaphragm (at 3 to 10 hertz i.e 180 to 160
  breaths/min) driven by a piston pump
• Frequencies available 300-3000 breaths/min
• Expiration is also active risk of air trapping
  minimal

48
HFV contd

• Advantages
• Better oxygenation and ventilation
• Aids lung recruitment (high mpaw)
• Reduces oxygen toxicity (high mpaw)
• Minimizes VILI
• Disadvantages
• Delivered tidal volumes difficult to monitor
• Deep sedation and/or paralysis required
• Inadequate humidification
• Direct physical airway damage

49
Airway Pressure Release Ventilation

• Alternative mode of ventilation that applies a
  form of CPAP that is released periodically,
  augmenting CO2 release.
• Pressure limited, time cycled mode
• Permits spontaneous ventilation throughout the
  respiratory cycle
• Based on the open lung concept maximize and
  maintain recruitment throughout the respiratory
  cycle

50
APRV contd

• Uses 2 airway pressures P high and P low 2 set
  time periods T high and T low, usually T
  highgtT low
• P high is set above the closing pressure of
  recruitable alveoli (lower inflection point)
• Set T high maintains the P high for several
  seconds
• T low helps remove CO2

51
APRV contd

• Potential benefits
• ? V/Q match
• ? diaphragmatic atrophy during critical illness
• ? cardiac output and oxygen delivery
• ? splanchnic perfusion
• ? renal and hepatic function
• Fewer days on mechanical ventilation
• Fewer days in ICU

52
Tracheal Gas Insufflation

• Normal ventilatory cycle - bronchi and trachea
  filled with alveolar gas at end expiration
• In the next inspiration, CO2 laden gas forced
  back into alveoli.
• TGI - stream of fresh gas (at 4-8L/min)
  insufflated through a small catheter/channels in
  the wall of endotracheal tube into the lower
  trachea
• CO2 laden gas flushed out of the trachea before
  next inspiration

53
Tracheal Gas Insufflation contd.

• Disadvantages
• Dessication of secretions
• Inadequate humidification
• Airway mucosal injury
• Accumulation of secretions in the TGI catheter
• Creation of auto PEEP from expiratory flow and
  resistance of the ventilator-exhalation tubes and
  valve

54
Inverse Ratio Ventilation

• Alternative mode of ventilation
• Entails use of prolonged inspiratory times
  (IEgt1) using volume or pressure cycled mode of
  mechanical ventilation
• Proposed mechanism of action alveolar
  recruitment at lower airway pressures, optimal
  distribution of ventilation
• Concerns generation of auto PEEP
• reduced cardiac output (
  ? MAP)

55
Inhaled Nitric Oxide

• NO endogenous vasodilator, from endothelium
• Vasodilatation of alveolar circulation reduces
  shunt and pulmonary hypertension
• Problems
• toxic nitrogen compounds
• methemoglobinemia
• pulmonary edema, acute RHF (interrupted flow)
• rebound pulmonary hypertension
• expensive
• Routine use not recommended

56
Inhaled Prostacyclin

• Cause vasodilation, inhibit platelet aggregation,
  reduction of neutrophil adhesion and activation,
  ? pulmonary hypertension, improved oxygenation
• Minimal systemic effects, harmless metabolites,
  no requirements for monitoring
• Both positive and negative results obtained in
  various trials
• Presently not recommended

57
Corticosteroids

• Established ARDS characterized by alveolar
  fibrosis
• Anti-inflammatory and antifibrotic properties of
  steroids probable role in ARDS
• No role in preventing but may help in treating
  ARDS

58
Surfactant Therapy

• Reduces alveolar surface tension
• Prevents alveolar collapse
• Anti inflammatory properties
• Anti microbial properties
• Exogenous surfactant successful in neonatal
  respiratory distress syndrome (reduced surfactant
  production)
• ARDS in adults increased surfactant removal,
  altered composition, reduced efficacy, reduced
  production
• Surfactant therapy not recommended in adults

59
Liquid Ventilation

• Involves filling the lung with liquid
• Removes the air liquid interface and supports
  alveoli, prevents collapse
• Perfluorocarbons have low surface tension,
  dissolve oxygen and carbon dioxide readily, non
  toxic, minimally absorbed, eliminated by
  evaporation though lungs
• Lowered surface tension may improve alveolar
  recruitment, arterial oxygenation, increased lung
  compliance
• Can recruit dependent alveoli (advantage over
  PEEP)

60
Liquid Ventilation contd.

• Types
• Total filling the entire lung with liquid,
  ventilated with a special ventilator
• - Expensive
• Partial - filling the lung to FRC with liquid,
  ventilated with conventional ventilator
• - Appropriate dose of PFC still to be
  determined
• - ? chances of pneumothoraces, hypoxic
  episodes, hypotensive episodes
• PFC radiodense impossible to detect infection
  or follow the progress of healing in a chest
  radiograph
• Liquid ventilation is not FDA approved

61
Extracorporeal Membrane Oxygenation

• Invasive, complex form of cardiopulmonary bypass
• Provides temporary gas exchange and blood
  circulation outside the body
• Severe but potentially reversible respiratory
  failure
• Such periods of lung rest allow the lungs to
  recover
• Used when conventional strategies fail
• No good evidence available over conventional
  management

62
ECMO contd.

• Types
• Veno - arterial a catheter placed in both vein
  and artery. Provides support both for heart and
  lungs
• Veno - venous single double lumen catheter
  placed in the vein. Provides support only for
  lungs
• ECMO allows ventilator pressures and volumes to
  be decreased to prevent further VILI
• Reduction in intra - thoracic pressure allows
  fluid removal from lungs with less risk of
  cardiovascular instability

63
ECMO contd

• Complications
• Haemorrhage
• Renal failure
• Haemolysis
• Hypotension/ hypertension
• Pneumothorax
• Infections

64
Management contd.

• Salvage interventions
• High frequency oscillatory ventilation
• Airway pressure release ventilation
• Tracheal gas insufflation
• Inverse ratio ventilation
• Inhaled nitric oxide
• Inhaled prostacyclin
• Corticosteroids
• Surfactant administration
• Liquid ventilation
• Extracorporeal membrane oxygenation
• Supportive therapy nutrition, prevention of
  infection

65
Nutrition

• Enteral over parenteral
• High fat low carbohydrate diet advocated - ?
  CO2
• Immuno modulatory nutrients
• -amino acids - arginine and glutamine
• -ribonucleotides
• -omega-3 fatty acids
• Diet rich in fish oil, ?-linolenic acid, and
  antioxidants
• Standard nutritional formulations recommended 

66
Antibiotics

• Infection - present initially nonpulmonary
  sepsis
• Develop later - nosocomial infections pneumonia
  and catheter-related sepsis.
• Aim identify, treat, and prevent infections.
• Most pneumonia gt 7 days
• Prompt initiation of appropriate empiric therapy.
• Hand washing by medical personnel
• New areas
• - continuous suctioning of subglottic
  secretions to prevent their aspiration
• -development of new endotracheal tubes -
  resist formation of bacterial biofilm that can be
  embolized distally with suctioning.

67
Management

• Treatment of the precipitating cause
• Mechanical ventilation
• Core ventilator management - protective lung
  ventilation strategy
• 
  - role of open lung approach
• Adjuncts to core ventilation -
• Fluid restriction
• Permissive hypercapnia
• Prone positioning
• Recruitment maneuvers

68
Management contd.

• Non conventional/Salvage interventions
• High frequency ventilation
• Airway pressure release ventilation
• Tracheal gas insufflation
• Inverse ratio ventilation
• Inhaled nitric oxide
• Inhaled prostacyclin
• Corticosteroids
• Surfactant administration
• Liquid ventilation
• Extracorporeal membrane oxygenation
• Supportive therapy nutrition, prevention of
  infection

69
Complications associated with ARDS

• Pulmonary barotrauma ,volutrauma, pulmonary
  embolism, pulmonary fibrosis, ventilator-associate
  d pneumonia (VAP), Oxygen toxicity
• Gastrointestinal haemorrhage (ulcer),
  dysmotility, pneumoperitoneum, bacterial
  translocation
• Cardiac Arrhythmias, myocardial dysfunction
• Renal acute renal failure (ARF), fluid retention
• Mechanical vascular injury, tracheal
  injury/stenosis (result of intubation and/or
  irritation by endotracheal tube)
• Nutritional malnutrition, anaemia, electrolyte
  deficiency

70
Long term sequelae of ARDS

• Pulmonary function mild impairment, improves
  over 1 year
• Neurocognitive dysfunction
• Post traumatic stress disorder
• Physical debilitation

71
Infantile Respiratory Distress Syndrome

• Hyaline membrane disease
• Deficiency of surfactant insufficient
  production in immature lungs, immature babies
• Genetic mutation in one of the surfactant
  proteins, SP-B rare, full term babies
• Prevention avoidance of premature birth,
  corticosteroids
• Treatment surfactant replacement

72
References

• Harrisons Principle of Internal Medicine, 16th
  ed.
• Christie JD, Lanken PN. Acute lung injury and the
  acute respiratory distress syndrome. Critical
  Care Hall
• Foner BJ, Norwood SH, Taylor RW. Acute
  respiratory distress syndrome. Critical Care, 3rd
  ed. Civetta
• Wiener-Kronish JP, et al. The adult respiratory
  distress syndrome definition and prognosis,
  pathogenesis and treatment. BJA 1990 65
  107-129.
• Clinical Anaesthesia. Barash, 6th ed.
• Egans Respiratory Care, 7th e

73
References

• Acute respiratory distress syndrome network.
  Ventilation with lower tidal volumes as compared
  with traditional tidal volumes for acute lung
  injury and the acute respiratory distress
  syndrome. N Engl J Med. 20002421301-1308
• Brower RG, Morris A, MacIntyre N, et al. Effects
  of recruitment maneuvers in patients with acute
  lung injury and acute respiratiry distress
  syndrome ventilated with high positive end
  expiratory pressure. Crit Care Med.2003312592-25
  97
• Hickling KG, Henderson SJ, Jackson R. Low
  mortality associated with low volume pressure
  limited ventilationwith permissive hypercapnia in
  severe adult respiratory distress syndrome.
  Intensive care med. 199016372-377
• Hickling KG, Walsh J,Henderson S, Jackson R. Low
  mortality rate in acute respiratiry distress
  syndrome using low volume pressure limited
  ventilation with permissive hypercapnia a
  prospective study. Crit Care Med.1994221568-1578