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ARDS
- 1. A L OK H R I D A Y M I S H R A 7 A 1 ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
- 2. TOPIC TO COVER INTRODUCTION PATHOPHYSIOLOGY PHASES CAUSES SIGN AND SYMPTOM DIAGNOSIS TREATMENT
- 3. INTRODUCTION AS THE NAMESUGGEST, ITS AN ACUTE DISORDER OF RESPIRATORY SYSTEM WHICH LEADS TO WIDESPREAD INFLAMMATION OF LUNG LEADING TO RESPIRATOY FAILURE. ARDS IS ALSO CALLED AS NCPE(NON CARDIOGENIC PULMONARY EDEMA) IT IS A CONDIITON IN WHICH INTERSTIUM OF LUNG FILLED BY FLUID (PRIMARILY). BECAUSE OF CAPILLARY LEAK DUE TO ENDOTHELIAL DAMAGE. DIFFUSE ALVEOLAR DAMAGE OCCUR DAMAGE CAUSES CAN BE DIRECT OR INDIRECT. IT IS ONE OF THE MAJOR DISORDER WORLDWIDE WITH MORTALITY RATE AS HIGH AS 32% TO 52% IT AFEFCTS PEOPLE OF ALL AGES
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- 5. DETAIL:- 1. INTRODUCE CAUSATIVEAGENT 2. RELEASE OF CYTOKINE AND CHEMOKINE 3. DAMAGE OF ENDOTHELIAL 4. ENDOTHELIAL EXRESS CAM 5. RECRUITMENT OF NEUTROPHIL 6. RELEASE OF MORE PROTEASE + ROS + CYTOKINE BY WBCS 7. PNEUMOCYTE GETS DAMAGES (BOTH TYPE) 8. ATELECTASIS MAY OCCUR 9. EXUDATE FILL WITH NECROTIC CELL 10. FORMATION OF HYALINE LIKE MEMBRANE 11. VENTILATION PERFUSION RATE DECREASES 12. HYPOXEMIA CENTRAL CYANOSIS 13. RESPIRATORY FAILURE
- 6. PHASES ARDS IS DIVIDEDINTO THREE MAIN PHASES: 1. EXUDATIVE PHASE:- START FROM 24 Hr. FROM THE ONSET LAST UPTO 7 DAYS FORMATION OF HYALINE MEMBRANE ALVEOLAR EDEMA HYPOXEMIA TACHYPNEA PROGRESSIVE DYSPNEA LATE INSPIRATION CRACKLE CAN BE HEARD BY AUSCALTATION RESPIRATOY FAILURE OCCUR.
- 7. 2. PROLIFERATIVE PHASE:- DAY 7-12 DAMAGED PNEUMOCYTE PROLIFEFRATE BY BRONCHAL STEM CELLS. NO HYALINE FURTHER FORM ALVEOLAR MACROHAGE DIGEST REMNANT OF HYALINE MOST PATIENT RECOVER BUT SOME MAY SHOW PULMONARY FIBROSIS. 3. FIBROTIC PHASE:- 3-4 WEEK OF INITIAL ULMONARY INJURY PROGRESSIVE FIBROSIS PATIENT MAY NEED SUPPLEMENTAL O2
- 9. CAUSES AND RISKFACTOR 1. INFECTION:- (SEPSIS, DIFFUSE PULMONARY INFECTION, GASTRIC ASPIRATION, PNEUMONIA) 2. PHYSCIAL INJURY:- (TRAUMA, BURN, IONIZING RADIATION, PULMONARY CONTUSION) 3. INHALED IRRITANT:- (OXYGEN TOXICITY, SMOKE, IRRITANT GAS AND CHEMICAL) 4. CHEMICAL INJURY:- (HEROIN OVERDOSE, ACETYSALICYLIC ACID OVERDOSE, BARBITURATE OVERDOSE) 5. HEMATOLOGIC CONDITION:- (DIC, TRANSFUSION ASSOCIATED INJURY) 6. LIVER INJURY 7. PANCREATITIS 8. HYPERSENSITIVITY REACTION
- 10. NOTE:- ALL OFTHE FOLLOWING CAUSE ARE CATEGORIZED AS DIRECT OR INDIRECT CAUSES, DEPENDING UPON WHETHER THE CAUSATIVE AGENT DIRECTLY OR INDIRECTLY AFFECT LUNG. Although ARDS CAN TARGET ANY AGE GROUP IRRESECTIVE OF THEIR LIFE STYLE AND OTHER FACTOR, SEPSIS INCREASE THE RISK BY 40% GASTRIC ASPIRATION BY 30% SHOCK BY 20% FOLLOWED UP BY INFECTION
- 11. SIGN AND SYMPTOM INCREASED RESPIRATORY RATE INCREASES HEART RATE DECREASE BLOOD PRESSURE DYSPNEA TACHYPNEA HYPOXIA CYANOSIS FEVER
- 12. DIAGNOSIS THERE ARE FOURMAIN CRITERIA FOR ARDS:- 1. ACUTE ONSET 2. DIFFUSE BILATERAL PULMONARY INFILTRATE 3. PaO2/FiO2 <200 mmHg 4. ABSENCE OF ELEVATED LEFT ATRAIL PRESSURE (PULMONARY ARTERY WEDGE PRESSURE <18mmHG) CXR (BILATERAL DIFFUSE OPACITY) ARTERIAL BLOOD GAS (ABG) CBC LFT KFT PFT TO EXCLUDE OTHER CAUSES NOTE:- FOR CONDITION TO BE ATELECTASIS paO2/fiO2 < 300 , (500 is normal) its 300 then its acute lung injury Less than 200 fall under the spectrum of ARDS
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- 14. TREATMENT 1. ANTIBIOTIC 2. USEOF VENTILATOR OR PEEP(POSITIVE END EXIRATORY PRESSURE) TIDAL VOLUME (4-6 mL/Kg) NOTE:- PEEP VALUE CAN HIGH AS 10 (MAX) AND PEEP PROVIDED DEPENDS UON THE SEVERITY OF PATIENT 3. DECREASING FiO2 4. PUT PATIENT IN PRONE POSITION RATHER THAN SUPINE POSITION 5. PROVIDE ADEQUATE NUTRITION
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