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Acute Respiratory Distress
Syndrome
Presenter:
Dr. Priyam Dalmia
MBBS
Intern, 14th batch
Department of medicine
Content
• Introduction
• Epidemiology
• Causes
• Clinical course and pathophysiology
• Clinical features
• Diagnostic criteria
• Differential diagnosis
• Investigations
• Management
• Prognosis and recovery
Introduction
• ARDS is a clinical syndrome of dyspnea of rapid onset,hypoxemia and
diffuse pulmonary infiltrates leading to respiratory failure.
• ARDS is also referred with variety of terms like
Stiff Lung
Non cardiogenic pulmonary edema
Shock lung
Wet lung
Post traumatic lung
Adult respiratory distress syndrome
Adult hyaline membrane disease
Capillary leak syndrome &
Congestive atelectasis.
Epidemiology
• Annual incidence : 60 cases/ 1,00,000 population
• Approximately 10% of all intensive care unit (ICU) admissions involve
patients with ARDS
• The mortality rate was traditionally very high (50–70%), Changes in
patient care have led to mortality decline to 30%
Causes
• Clinical disorder associated with development of ARDS
• Direct Lung Injury:
Pneumonia
Aspiration of gastric contents
Pulmonary contusion
Near drowning
Inhalation injury
• Indirect lung injury
Sepsis
Severe trauma
Multiple bone fracture
Flail chest
Burns
Acute pancreatitis
Multiple transfusion (TRALI)
Clinical course and pathophysiology
Natural history of ARDS is marked by 3 distinct phases:
• Exudative (0-7 days)
• Proliferative ( 7-21 days)
• Fibrotic ( > 21 days)
Exudative (0-7 day)
• Capillary endothelial cells and alveolar epithelial cells are injured,
• Exudation and protein rich edema fluid accumulates in the interstitial and
alveolar spaces.
• Increased pro-inflammatory cytokines
• Recruitment of leukocytes (especially neutrophils) into the interstitium and
alveoli.
• Formation of hyaline membrane
• Alveolar edema in dependent portions of the lung
• Intrapulmonary shunting
• Hypoxemia
• Work of breathing increases, leading to dyspnea.
Proliferative phase
• This phase of ARDS usually lasts from day 7 to day 21
• Marked, with the initiation of lung repair
• Exudates cleared and a shift from neutrophil- to lymphocyte-
predominant pulmonary infiltrates.
• Type II pneumocytes regenerate along alveolar basement
membranes. These specialized epithelial cells synthesize new
pulmonary surfactant
• And differentiate into type I pneumocytes.
Fibrotic ( > 21 days)
• Most patients with ARDS recover
• Very few progresses into fibrotic phase
• There is extensive alveolar-duct and interstitial fibrosis.
• Marked disruption of acinar architecture leads to emphysema-like
changes, with large bullae.
• Intimal fibro proliferation in the pulmonary microcirculation causes
progressive vascular occlusion and pulmonary hypertension.
• The physiologic consequences include an increased risk of
pneumothorax, reductions in lung compliance, and increased
pulmonary dead space.
Clinical features
• Precipitating insult is usually evident
• Fever
• Cough
• Dyspnea
• Tachypnea
• Tachycardia
• Restlessness
• Due to worsening hypoxemia
Agitation, anxiety, confusion
• Cyanosis even with supplemental oxygen ( refractory hypoxemia)
Berlin Diagnostic criteria
1. Acute onset (within 7 days of a known clinical insult )
2. Chest x-ray:
• Bilateral opacities not fully explained by lobar collapse, mass or effusion
3. Absence of left atrial hypertension (no hydrostatic edema)
4. Severity:
Pao2/fio2 ≤ 300 mm of Hg , with a positive end-expiratory pressure (PEEP)
of at least 5 cm H2o
• Mild ARDS ( pao2/fio2 ≤ 300 mm of Hg )
• Moderate ARDS (pao2/fio2 ≤ 200 mm of Hg)
• Severe ARDS (pao2/fio2 ≤ 100 mm of Hg )
Differential Diagnosis
• Cardiogenic pulmonary edema
• Diffuse alveolar hemorrhage
• Acute pulmonary embolism
• TACO
Investigation
• CBC
• Chest x-ray
• ABG analysis
• CT chest
• Echo
• Pro-NBP level( less than 100
pg/mL )
• Na+, K+
• Blood urea
• S. creatinine
• Blood culture/sensitivity
• Procalcitonin
• LFT
• Anti nuclear, Anti mpo ,Anti
cytoplasmic, anti ds-dna
X-ray of ARDS
-Bilateral diffuse opacity over lung
field
-No Cardiomegaly
-No Pleural effusion
CT chest
Hyperdense shadow at
dependent part of lung
Dependent pulmonary edema
in ARDS
Cardiogenic pulmonary edema
Diffuse alveolar hemorrhage
Pulmonary Embolism
TRALI Vs TACO
• Fever No Fever
• Hypotension Hypertension
• JVP Unchanged JVP Raised
• EF- Normal Decreased
• Pulmonary Edema Fluid- Exudate Transudate
• Response To Diuretic- Minimal Significant
Management
1. TREATMENT of the cause
e.g. antibiotics for pneumonia, sepsis
2.Supportive therapy
Protective lung ventilation,
Fluid management
Prone positioning
3.Pharmacological treatment
Steroids, vasodilators, DVT prophylaxis & sedation.
Lung protective ventilation
Patients meeting clinical criteria for ARDS frequently become fatigued
from increased work of breathing and progressive hypoxemia, requiring
mechanical ventilation for support.
• Mechanical ventilation with low tidal volume (4-6 mL/kg ideal body
weight)
• PEEP of atleast 5cm of H2O
• P plateau <30 cm of H2O
• Alveolar over distension and cyclic atelectasis are the principal causes
of ventilator- associated lung injury(VALI)
Low tidal volumes
• Prevents from volutrauma and barotrauma by alveolar overdistention
• Because of the mortality benefit, the pCO2 of the patient is allowed to
rise. (known as permissive hypercapnia)
• For patients in ARDS, the pH is allowed to drift down to 7.30
• When pH< 7.2 then it needs to be buffered.
Advantages of PEEP:
• Minimize cyclic atelectasis
• It opens collapsed alveoli /
Reverse atelectasis - known as lung
Recruitment, and it increases the available surface area in the lungs for
gas exchange
• Increases arterial oxygenation at lower fio2 by decreasing
intrapulmoary shunting
Neuromuscular blockade
• In severe ARDS sedation alone is not beneficial for lung protective
ventilation but also adequate for ventilator patient synchrony.
• Early NMB is the preferred in severe ARDS for initial 48 hrs.
• This increase rate of survival and ventilator free days without
increasing ICU acquired paresis
Prone position
• A recent trial demonstrated a significant reduction in 28-day mortality
with prone positioning (32.8 to 16%) for patients with severe ARDS
• Possible mechanisms :
Recruitment of dependent lung zones,
Improved ventilation-perfusion matching
Relief of compression of the lung by the heart and mediastinal structures
• This maneuver requires a critical-care team that is experienced in
“proning,” as repositioning critically ill patients can be hazardous,
leading to accidental endotracheal extubation, loss of central venous
catheters, and orthopedic injury
Fluid management
• Primary cause is leakage of fluid and pulmonary edema, so negative
fluid balance should be done
• Fluid restriction and diuretics is an important aspect of ARDS
management, not causing hypotension or hypoperfusion of vital
organs(MAP>65 mm hg)
• Maintaining a low left atrial pressure minimizes pulmonary edema
and improves oxygenation and lung compliance.
Inhaled Nitric Oxide
• It is very short acting pulmonary vasodilator
• When delivered (5-10ppm) improves blood flows to well ventilated
areas, thus improving V/Q matching
• Effect lasts only for 48 hour and rebound effect can occur if
withdrawn
• No mortality benefit is shown in clinical trials
• Used as Rescue therapy , when other modality has failed
• Also in patients with PAH
Glucocorticoids use
• Many attempts have been made to treat both early and late ARDS
with glucocorticoids, with the goal of reducing potentially deleterious
pulmonary inflammation.
• Current evidence does not support the routine use of glucocorticoids
in the care of ARDS patients.
Extracorporeal membrane oxygenation (ECMO)
• There use is restricted to specialized centres.
• Controlled trials indicate improved survival in severe ards pts
• Veno-venous ECMO is designed to provide gas exchange
• ARDS associated with pneumonia (viral or bacterial) is the most
common cause of refractory hypoxemia that requires ECMO
Bundled Care For ICU Patients
• Venous thrombosis should be prevented with the use of sc low-molecular-
weight heparin
• To help prevent decubitus ulcers, frequent changes in body position and the
use of soft mattress overlays and air mattresses are employed.
• To prevent gi mucosal injury h2 –receptor antagonists, antacids, and
sucralfate have all been used
• Nutritional support by enteral feeding through either a nasogastric or an
orogastric tube should be initiated and maintained whenever possible.
• Delayed gastric emptying is common in critically ill patients taking sedative
medications but often responds to promotility agents such as
metoclopramide.
Decision To Wean From Mechanical Ventilation
Conditions as indicating amenability to weaning:
1. Lung injury is stable or resolving;
2. Gas exchange is adequate, with low PEEP<8 cm of H2O and FiO2<0.5
3. Hemodynamically stable , not on vasopressors
4. Able to initiate spontaneous breaths
If the patient passes the wean screen then can be tried for spontaneous breathing
trials (SBT)consist of breathing through the ET tube without ventilator support or
minimal pressure support (T-piece using 1–5 cmH2O CPAP or PSV from the
ventilator to offset resistance from the endotracheal tube) for period of 30-120
min.
The spontaneous breathing trial is declared a failure and stopped if any
of the following occur:
(1) respiratory rate >35/min for >5 min,
(2) O2 saturation <90%
(3) Pulse :20% increase or decrease from baseline
(4) systolic blood pressure >180 mmHg or <90 mm Hg
(5) increased anxiety or diaphoresis.
If, at the end of the spontaneous breathing trial, none of the above
events has occurred and the ratio of the respiratory rate and tidal
volume in liters (f/VT) is <105 , patient can be extubated
Prognosis
• Mortality declined from 50% to ~30% in past decade
• In the recent report from LUNG SAFE trial, hospital mortality
estimates for ARDS range from
34.9% for mild ARDS,
40.3% for moderate ARDS, and
46.1% with severe ARDS.
• Risk factors having higher mortality rates:
Advanced age>70yr
Non pulmonary cause of ards(sepsis)
Chronic medical illness
>60 yr and sepsis
Severe ARDS
Functional Recovery in ARDS Survivors
• It is a testament to the resolving powers of the lung that the majority
of patients who survive regain nearly normal lung function.
• Patients usually recover maximal lung function within 6 months.
• A year later, more than one-third of ARDS survivors have normal
spirometry values and diffusion capacity.
• Most of the remaining patients have only mild abnormalities in
pulmonary function.
Reference
• Harrison’s Principle Of Internal Medicine,20th Edition
• Davidson’s Principal And Practice Of Medicine,22nd Edition
Thank you …

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Acute respiratory distress syndrome

  • 1. Acute Respiratory Distress Syndrome Presenter: Dr. Priyam Dalmia MBBS Intern, 14th batch Department of medicine
  • 2. Content • Introduction • Epidemiology • Causes • Clinical course and pathophysiology • Clinical features • Diagnostic criteria • Differential diagnosis • Investigations • Management • Prognosis and recovery
  • 3. Introduction • ARDS is a clinical syndrome of dyspnea of rapid onset,hypoxemia and diffuse pulmonary infiltrates leading to respiratory failure. • ARDS is also referred with variety of terms like Stiff Lung Non cardiogenic pulmonary edema Shock lung Wet lung Post traumatic lung Adult respiratory distress syndrome Adult hyaline membrane disease Capillary leak syndrome & Congestive atelectasis.
  • 4. Epidemiology • Annual incidence : 60 cases/ 1,00,000 population • Approximately 10% of all intensive care unit (ICU) admissions involve patients with ARDS • The mortality rate was traditionally very high (50–70%), Changes in patient care have led to mortality decline to 30%
  • 5. Causes • Clinical disorder associated with development of ARDS • Direct Lung Injury: Pneumonia Aspiration of gastric contents Pulmonary contusion Near drowning Inhalation injury
  • 6. • Indirect lung injury Sepsis Severe trauma Multiple bone fracture Flail chest Burns Acute pancreatitis Multiple transfusion (TRALI)
  • 7. Clinical course and pathophysiology Natural history of ARDS is marked by 3 distinct phases: • Exudative (0-7 days) • Proliferative ( 7-21 days) • Fibrotic ( > 21 days)
  • 8.
  • 9. Exudative (0-7 day) • Capillary endothelial cells and alveolar epithelial cells are injured, • Exudation and protein rich edema fluid accumulates in the interstitial and alveolar spaces. • Increased pro-inflammatory cytokines • Recruitment of leukocytes (especially neutrophils) into the interstitium and alveoli. • Formation of hyaline membrane • Alveolar edema in dependent portions of the lung • Intrapulmonary shunting • Hypoxemia • Work of breathing increases, leading to dyspnea.
  • 10. Proliferative phase • This phase of ARDS usually lasts from day 7 to day 21 • Marked, with the initiation of lung repair • Exudates cleared and a shift from neutrophil- to lymphocyte- predominant pulmonary infiltrates. • Type II pneumocytes regenerate along alveolar basement membranes. These specialized epithelial cells synthesize new pulmonary surfactant • And differentiate into type I pneumocytes.
  • 11. Fibrotic ( > 21 days) • Most patients with ARDS recover • Very few progresses into fibrotic phase • There is extensive alveolar-duct and interstitial fibrosis. • Marked disruption of acinar architecture leads to emphysema-like changes, with large bullae. • Intimal fibro proliferation in the pulmonary microcirculation causes progressive vascular occlusion and pulmonary hypertension. • The physiologic consequences include an increased risk of pneumothorax, reductions in lung compliance, and increased pulmonary dead space.
  • 12.
  • 13. Clinical features • Precipitating insult is usually evident • Fever • Cough • Dyspnea • Tachypnea • Tachycardia • Restlessness • Due to worsening hypoxemia Agitation, anxiety, confusion • Cyanosis even with supplemental oxygen ( refractory hypoxemia)
  • 14. Berlin Diagnostic criteria 1. Acute onset (within 7 days of a known clinical insult ) 2. Chest x-ray: • Bilateral opacities not fully explained by lobar collapse, mass or effusion 3. Absence of left atrial hypertension (no hydrostatic edema) 4. Severity: Pao2/fio2 ≤ 300 mm of Hg , with a positive end-expiratory pressure (PEEP) of at least 5 cm H2o • Mild ARDS ( pao2/fio2 ≤ 300 mm of Hg ) • Moderate ARDS (pao2/fio2 ≤ 200 mm of Hg) • Severe ARDS (pao2/fio2 ≤ 100 mm of Hg )
  • 15. Differential Diagnosis • Cardiogenic pulmonary edema • Diffuse alveolar hemorrhage • Acute pulmonary embolism • TACO
  • 16. Investigation • CBC • Chest x-ray • ABG analysis • CT chest • Echo • Pro-NBP level( less than 100 pg/mL ) • Na+, K+ • Blood urea • S. creatinine • Blood culture/sensitivity • Procalcitonin • LFT • Anti nuclear, Anti mpo ,Anti cytoplasmic, anti ds-dna
  • 17. X-ray of ARDS -Bilateral diffuse opacity over lung field -No Cardiomegaly -No Pleural effusion
  • 18. CT chest Hyperdense shadow at dependent part of lung Dependent pulmonary edema in ARDS
  • 22. TRALI Vs TACO • Fever No Fever • Hypotension Hypertension • JVP Unchanged JVP Raised • EF- Normal Decreased • Pulmonary Edema Fluid- Exudate Transudate • Response To Diuretic- Minimal Significant
  • 23.
  • 24. Management 1. TREATMENT of the cause e.g. antibiotics for pneumonia, sepsis 2.Supportive therapy Protective lung ventilation, Fluid management Prone positioning 3.Pharmacological treatment Steroids, vasodilators, DVT prophylaxis & sedation.
  • 25. Lung protective ventilation Patients meeting clinical criteria for ARDS frequently become fatigued from increased work of breathing and progressive hypoxemia, requiring mechanical ventilation for support. • Mechanical ventilation with low tidal volume (4-6 mL/kg ideal body weight) • PEEP of atleast 5cm of H2O • P plateau <30 cm of H2O • Alveolar over distension and cyclic atelectasis are the principal causes of ventilator- associated lung injury(VALI)
  • 26.
  • 27. Low tidal volumes • Prevents from volutrauma and barotrauma by alveolar overdistention • Because of the mortality benefit, the pCO2 of the patient is allowed to rise. (known as permissive hypercapnia) • For patients in ARDS, the pH is allowed to drift down to 7.30 • When pH< 7.2 then it needs to be buffered.
  • 28. Advantages of PEEP: • Minimize cyclic atelectasis • It opens collapsed alveoli / Reverse atelectasis - known as lung Recruitment, and it increases the available surface area in the lungs for gas exchange • Increases arterial oxygenation at lower fio2 by decreasing intrapulmoary shunting
  • 29. Neuromuscular blockade • In severe ARDS sedation alone is not beneficial for lung protective ventilation but also adequate for ventilator patient synchrony. • Early NMB is the preferred in severe ARDS for initial 48 hrs. • This increase rate of survival and ventilator free days without increasing ICU acquired paresis
  • 30. Prone position • A recent trial demonstrated a significant reduction in 28-day mortality with prone positioning (32.8 to 16%) for patients with severe ARDS • Possible mechanisms : Recruitment of dependent lung zones, Improved ventilation-perfusion matching Relief of compression of the lung by the heart and mediastinal structures • This maneuver requires a critical-care team that is experienced in “proning,” as repositioning critically ill patients can be hazardous, leading to accidental endotracheal extubation, loss of central venous catheters, and orthopedic injury
  • 31.
  • 32. Fluid management • Primary cause is leakage of fluid and pulmonary edema, so negative fluid balance should be done • Fluid restriction and diuretics is an important aspect of ARDS management, not causing hypotension or hypoperfusion of vital organs(MAP>65 mm hg) • Maintaining a low left atrial pressure minimizes pulmonary edema and improves oxygenation and lung compliance.
  • 33. Inhaled Nitric Oxide • It is very short acting pulmonary vasodilator • When delivered (5-10ppm) improves blood flows to well ventilated areas, thus improving V/Q matching • Effect lasts only for 48 hour and rebound effect can occur if withdrawn • No mortality benefit is shown in clinical trials • Used as Rescue therapy , when other modality has failed • Also in patients with PAH
  • 34. Glucocorticoids use • Many attempts have been made to treat both early and late ARDS with glucocorticoids, with the goal of reducing potentially deleterious pulmonary inflammation. • Current evidence does not support the routine use of glucocorticoids in the care of ARDS patients.
  • 35. Extracorporeal membrane oxygenation (ECMO) • There use is restricted to specialized centres. • Controlled trials indicate improved survival in severe ards pts • Veno-venous ECMO is designed to provide gas exchange • ARDS associated with pneumonia (viral or bacterial) is the most common cause of refractory hypoxemia that requires ECMO
  • 36.
  • 37. Bundled Care For ICU Patients • Venous thrombosis should be prevented with the use of sc low-molecular- weight heparin • To help prevent decubitus ulcers, frequent changes in body position and the use of soft mattress overlays and air mattresses are employed. • To prevent gi mucosal injury h2 –receptor antagonists, antacids, and sucralfate have all been used • Nutritional support by enteral feeding through either a nasogastric or an orogastric tube should be initiated and maintained whenever possible. • Delayed gastric emptying is common in critically ill patients taking sedative medications but often responds to promotility agents such as metoclopramide.
  • 38.
  • 39. Decision To Wean From Mechanical Ventilation Conditions as indicating amenability to weaning: 1. Lung injury is stable or resolving; 2. Gas exchange is adequate, with low PEEP<8 cm of H2O and FiO2<0.5 3. Hemodynamically stable , not on vasopressors 4. Able to initiate spontaneous breaths If the patient passes the wean screen then can be tried for spontaneous breathing trials (SBT)consist of breathing through the ET tube without ventilator support or minimal pressure support (T-piece using 1–5 cmH2O CPAP or PSV from the ventilator to offset resistance from the endotracheal tube) for period of 30-120 min.
  • 40. The spontaneous breathing trial is declared a failure and stopped if any of the following occur: (1) respiratory rate >35/min for >5 min, (2) O2 saturation <90% (3) Pulse :20% increase or decrease from baseline (4) systolic blood pressure >180 mmHg or <90 mm Hg (5) increased anxiety or diaphoresis. If, at the end of the spontaneous breathing trial, none of the above events has occurred and the ratio of the respiratory rate and tidal volume in liters (f/VT) is <105 , patient can be extubated
  • 41. Prognosis • Mortality declined from 50% to ~30% in past decade • In the recent report from LUNG SAFE trial, hospital mortality estimates for ARDS range from 34.9% for mild ARDS, 40.3% for moderate ARDS, and 46.1% with severe ARDS. • Risk factors having higher mortality rates: Advanced age>70yr Non pulmonary cause of ards(sepsis) Chronic medical illness >60 yr and sepsis Severe ARDS
  • 42. Functional Recovery in ARDS Survivors • It is a testament to the resolving powers of the lung that the majority of patients who survive regain nearly normal lung function. • Patients usually recover maximal lung function within 6 months. • A year later, more than one-third of ARDS survivors have normal spirometry values and diffusion capacity. • Most of the remaining patients have only mild abnormalities in pulmonary function.
  • 43. Reference • Harrison’s Principle Of Internal Medicine,20th Edition • Davidson’s Principal And Practice Of Medicine,22nd Edition