Acute Respiratory Distress syndromeSophy sony, BMCON
DEFINIION ARDS is a severe lung disease caused by avariety of direct and indirect issues. It is characterized by inflammation of the lung parenchyma leading to impaired gas exchange with concomitant systemic release of inflammatory mediators causing inflammation, inflammation, hypoxemia and frequently resulting in multiple organ failure. failure. This is often fatal, usually requiring mechanical ventilation and admission to an intensive care unit. A less severe form is called unit. acute lung injury (ALI). ALI).
Aiso known as. Noncardiogenic pulmonary edema;IncreasedIncreased-permeability pulmonary edema; Stiff lung; Shock lung; ARDS; Acute lung injur
Historical Background Since WWI physicians have recognized a syndrome ofrespiratory distress, diffuse lung infiltrates and respiratory failure in pt with various medical conditions including from battle trauma to severe sepsis, pancreatitis, massive transfusions etc
In 1967, Ashbaugh et al become the first to describe thesyndrome which they referred to as adult respiratory distress syndrome in 12 such patients (1)
Historical Background in 1971, Ashbaugh and Petty further defined thesyndrome in a form that summarized the clinical features well (but lacked specific criteria to identify pts systematically) (2)
- severe dyspnea - cyanosis refractory to O2 - decreased pulm compliance - diffuse alveolar infiltrates on CXR - atelectasis, vascular congestion, hemorrhage, pulm edema and hyaline membranes at autopsy
Historical Background in 1988, a more expanded definition was proposed thatquantified the physiologic respiratory impairment through the use of 4-point lung injury scoring system (3) 4- level of PEEP - P/F RATIO - static lung compliance - degree of infiltration on CXR - *also included nonpulm organ dysfunction This definition still had its shortcomings in that it specific criteria to r/o cardiogenic pulm edema and is not predictive of outcomes
Historical Background 1994 American - European Consensus ConferenceCommittee (AECC) came up with definition that became widely accepted syndrome from adult respiratory distress - Acute onset - bilateral infiltrates on CXR - PCWP =< 18 mmHg - P/F ratio =< 200 ( ALI if P/F ratio =< 300 )
also changed the name to acute respiratory distress defined it as a spectrum of ALI
Epidemiology the problem has always been how to identify the cases attempts at extrapolating incidences based on the variousdefinitions offered above have resulted in various numbers (1.5-8.3 (1.575/100,000) Scandinavia (reported incidence of 17.6/100,000 for ALI and 13.5/100,000 for ARDS (4) Washington 4/1999-7/2000) reported much higher numbers for age4/1999ageadjusted incidence (5) - ALI - 86.2/100,000 person-yrs (reaching 306 in ages 75-84) person75- estimated annually cases base on these stats 190,600 - mortality 74, 500/yr
the first study using the 1994 AECC definition was done in
More recently the ARDSNet study (done in King County,
Morbidity and Mortality prior to ARDSNet study - mortality rate for ARDS has been estimated at 40-70% 40ARDSNet found a much lower overall mortality rate 30-40% (6) 30notable that MR increases with age: 24 % ages 1515-19 and 60 % in > 85 yrs 2/2 co-morbid conditions coMortality is attributable to sepsis or multiorgan dysfunction
Morbidity and Mortality Morbidity- prolonged hospital course- nosocomial courseinfections especially VAP - wt loss - muscle weakness - functional impairment in months following
CausesDIRECT LUNG INJURY(primary lung injury)COMMON PNA Aspiration LESS COMMON Pulm contusion Fat emboli Near-drowning Near Inhalation injury Reperfusion pulmonary edema after CPbypass
INDIRECT LUNG INJURY(secondry) INJURY(secondry)COMMON Sepsis Severe trauma with shock and multiple transfusions LESS COMMON Cardiopulm bypass Acute pancreatitis Transfusions Drug overdose Anaphylaxis DIC Nonpulmonary sys.diseases Severe head injury
Pathophysiology Diffuse alveolar damage Lung capillary damage Inflammation/pulm edema* Resulting severe hypoxemia anddecreased lung compliance
Injury to the alv .cap.memb release of imflm. mediators imflm. Damaged type2 alv cell
Surfactant production alv. Cap.mem. alv. vascular permiability narrowing & Alv.compliance & recoil obsrtn BROCHOCOSTRICTION Atelectasis outward migration of bld.cells& fld bld.cells& hyaline mem. formation mem. from capillaries impairment in gas exchange ARDS pul.oedema
PathophysiologyOccurs in stages 1. Exudative ( Acute Phase) 2. Proliferative 3. Fibrotic 4. Recovery
Exudative phase (Acute Phase)(1Phase)(17days) Alveolar-capillary barrier is formed by Alveolarmicrovascular endothelium and alveolar epithelium Under normal conditions epithelial barrier is much less permeable than endothelium Epithelium is made up of type I and II cells Type I cells are injured easily and Type II cells are more resistant
Exudative Phase In ALI/ARDS damage to either oneoccurs,adherence of neutrophils to vas.endothelium--vas.endothelium--resulting in increased permeability of the barrier. Ie. Ie. Capilary permiability. Engorgement of perivascular permiability. & peribronchial interstitial space interstitial edema, fluid crosses the alv. Epithelium alv. Influx of proteinproteinrich edema fluid into the alveolar space intra pulmonary shunt as blood passing through them can not be O2nated. WOB, dyspnoea. dyspnoea. Injury of Type I cells results loss of epithelial integrity and fluid extravasation (edema) Injury of Type II cells then impairs the removal of the edema fluid
Exudative Phase Dysfunction of Type II cellsproduction and turnover of surfactant to alveolar collapse Widespred atelectasis lung complance, complance, compromised gas exchange, hypoxemia
If severe injury to epithelium occurs
disorganized/insufficient epithelial repair occurs ie, ie, hyaline membrane begins to line the alveoli resulting in fibrosis and atelectasis. atelectasis. In addition to inflammatory process, there is evidence that the coagulation system is also involved pul.microvascular occlusion PA bld flow to ventilated portions dead space, PulHTN
Proliferative Phase After acute phase, some pt will have uncomplicated course and rapid resolution. Still may have dyspnoea,tachypnoea, & hypoxemia. dyspnoea,tachypnoea, Histologically first sigs of resolution are -initiation of lung repair -organization of alveolar exudate -a shift from neutro to lympho predominant pul. pul. Infiltrate. -Proliferation of type-2 pneumocyte along alv. typealv. Basement memb. & syn. of new pul.surfactant memb. and differentiate into ty-1 pneumocytes. ty- pneumocytes.
With intervention (mechanical ventilation) there is clearance of alveolar fluid Soluble proteins are removed by diffusion between alveolar epithelial cells Influx of neutro., mono.,lympho., & fibroblasts neutro., mono.,lympho., proliferation as a part of the inflm. Response. inflm. Insoluble proteins are removed by endocytosis and transcytosis through epithelial cells and phagocytosis through macrophages Injured has immune regenerrative capacity after a/c lung injury.
Proliferative Phase Type II cells begin to differentiate into Type Icells and reepithelialize denuded alveolar epithelium. Further epithelialization leads to increased alveolar clearance This phase is complete when the diseased lung is characterised by -dense firouse tissue pul.VR & PHTN lung compliance(Bcos interstitial fibrosis) compliance(Bcos Hypoxemia(due to thick alv.mem diffusion limitation & shunting. *if repe. Phase persists repe. widespread firosis,if arrested.leasion firosis,if arrested.leasion resolves.
Fibrotic Phase (chronic/late) Intense inflammation leads to obliteration of the normal lung architecture Occurs about 2-3 wks after the initial injury. 2Alveolar space is filled with mesenchymal cells and their products Reepithelialization and new blood vessel formation occurs in disorganized manner Fibroblasts also proliferate, collagen is deposited resulting in thickening of interstitium Fibrosing alveolitis and cyst formation
Diffuse scaring & fibrosis
lung compliance + marked reduction in surface area bcos of int.fibrosis hypoxemia PHTN from pul.vas. desruction & fibrosis pul. pul. dead space . risk of pneumonia, morbidity
Consequences Impaired gas exhange leading to severehypoxemia - 2/2 ventilation-perfusion mismatch, ventilationincrease in physiologic deadspace Decreased lung compliance due to the stiffness of poorly or nonaerated lung Pulm HTN 25% of pts, due to hypoxic vasoconstriction, Vascular compression by positive airway compression, airway collapse and lung parenchymal destruction
Clinical Features Pts are critically ill develop rapidly worsening tachypnea, dyspnea, tachypnea, dyspnea,hypoxia requiring high conc of O2 Occurs within hours to days ( usually12-48 usually12hours) of inciting event Early clinical features reflects precipitants of ARDS Physical exam shows cyanosis, tachycardia, tachypnea and diffuse rales and other signs of inciting event
Clinical Features Initial presentation often insidious . Initially may not experience res.sympts. res.sympts. Or only cough,dyspnoea, tacypnoea, & restlessnes cough,dyspnoea, tacypnoea, Chest aus.may be N or reveal fine scatterd crackles
ABG- mild hypoxemia, & res.alkalosis caused by ABGhyperventilation.
Resp. alk. From hypoxemia&juxtra cap.recep