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ARDS
 

ARDS

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  • Mucus plug: asthma, chronic bronchitis, bronchiectasis
  • Hemodynamic edema Increased hydrostatic pressure. Left sided heart failure Volume overload Pulmonary vein obstructionDecreased oncotic pressureHypoalbuminemiaNephrotic syndrome Liver disease Protein losing enteropathiesEdema due to microvascular injury Infections Inhaled gases: oxygen, smoke Liquid aspiration: gastric content, near drowning Drugs and chemicals: chemotherapeutic agents (bleomycin) other medications (amphotericin B), heroin, kerosene, paraquat. Shock, trauma Radiation Transfusion related
  • There are two types of pulmonary edema, non cardiogenic and cardiogenic. Pulmonary edema is caused by damage to lung tissues or poor health or functioning of the heart or cardiovascular system. Non-cardiogenic pulmonary edema can be caused by the following  Severe infection  Upper airway obstruction  Ascent to high altitude occasionally causes high altitude pulmonary edema (HAPE)  Aspiration, e.g. gastric fluid or in case of drowning  Multiple blood transfusions  Inhalation of toxic gases  Pulmonary contusion, i.e. high-energy trauma  Multitrauma as in a severe car accident  Neurogenic such as subarachnoid hemorrhage  Certain types of medication  Reexpansion: post-pneumonectomy or large volume thoracentesis Reperfusion injury such as postpulmonarythromboendartectomy or lung transplantation Cardiogenic pulmonary edema can be caused by one of the following or a combination: Severe heart attack  Congestive heart failure  Pericardial effusion  Fluid overload as in the case of kidney failure  Tachycardia – fast heart beat  Bradycardia – slow heart beat

ARDS ARDS Presentation Transcript

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  • Congenital anomalies1- Agenesis or hypoplasia2- Tracheal & bronchial anomalies (atresia, stenosis, tracheoesophageal fistula)3- vascular anomalies.4- foregut cysts (abnormal detachment of primitive foregut) ,depending on wallstructure ,it classified into bronchogenic (most common), esophageal or entericcystBronchogenic cyst, 1-4cm in diameter, rarely connected to the tracheobronchialtree microscopically lined by respiratory epithelium with sq.metaplasia.5- pulmonary sequestration.presence of a discrete mass of lung tissue without any normal connection tothe airway system & with separate blood supply (not from pulmonary arteries butfrom aorta or its branches).- extralobar---- external to the lung anywhere in the thorax or mediastiunum.- intralobar---- within lung substance & usually associated with recurrentlocalized infection4
  • Atelectasis (collapse)Incomplete expansion of thelungs(neonatal) or to the collapse ofpreviously inflated lung (acquired oradult), producing relatively airlesspulmonary parenchymaTypes:1- Obstructive (resorption)2- Compression3- Contraction4- Patchy5
  • • Resorption (reversible)– Secretions (mucus plug)– Aspiration of foreign bodies– Tumors– Mediastinum: toward• Compression (reversible)– Hydrothorax (pl.effusion)– Pneumothorax– Hemothorax– Exudate in pleural cavity– Tumor– Mediastinum : awayContractionirreversible
  • Pulmonary edemaNormalHydrostatic pressure Oncotic pressureHydrostatic pressure Oncotic pressureCauses:- Heart failure- Mitral stenosisHydrostatic pressure Oncotic pressureCauses:- Nephroticsyndrome- Liver diseasesMicrovascular injuryCauses:- Infections- Aspiration- Drugs- RadiationcardiogenicNon-cardiogenic
  • Pulmonary Edema
  • Acute respiratory distress syndrome (ARDS)Diffuse alveolar damage, shock lungIs a clinical syndrome caused by diffuse alveolar capillarydamageClinicallyrapid onset of severe life-threatening respiratoryinsufficiency& severe arterial hypoxemia that is refractory tooxygen therapy & may progress to extrapulmonarymultisystem organ failure9
  • Etiology:-1)pulmonary ARDS" (caused by direct lunginjury)2)"extra-pulmonary ARDS" (a remote effect ofinjury elsewhere).By:-* Infection (viral), sepsis* gas inhalation or liquid(gastric)aspiration.* drugs, chemicals, radiation.* trauma (head injury), sepsis.10
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  • 12Basic lesion is injury to alveolar type I pneumocytes& capillary endothelial cellsBy:-* O2 free radicals.* activated macrophages & neutrophils.loss of surfactant.
  • Pathology1st /acute (exudative) stageWhen the alveolar+/or endothelialcells are injured fluid leaks into theinterstitial spaces and alveolar airspaces -- this is Non-CardiogenicPULMONARY EDEMA.Later, with cell necrosis, FIBRIN isreleased into the alveoli, producingHYALINE MEMBRANES. Of coursethere is LOSS OF SURFACTANT, somany alveoli COLLAPSE.During this early stage, the patient isvery tachypneic and dyspneic13
  • 2nd /Proliferative or organizing stageAs type I pneumocytes are destroyed,TYPE II PNEUMOCYTES DIVIDE toreplace them (regenerative epithelial hyperplasia" ).FIBROSIS ensues as the intra-alveolar hyaline membranesand the interstitial exudate organize14