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![Complications
leg swelling(edema),
abdominal swelling(ascites),
Pleural effusion,
Congestion & swelling of liver,
acute heart attack (myocardial infarction [MI]),
cardiogenic shock,
arrhythmias,
electrolyte disturbances,
mesenteric insufficiency,
protein enteropathy,
respiratory arrest, and death.](https://image.slidesharecdn.com/pulmonaryedema-141228063437-conversion-gate01/85/Pulmonary-edema-32-320.jpg)
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Pulmonary edema
- 1. Pulmonary EdemaDR. HARSHPANDYA R1 UNDER GUIDANCE OF DR.NIPA NAYAK M.D. ASSO. PROF
- 2. Outline Definition Epidemiology Pathophysiology Classifications & causes Pathogenesis Staging Clinical manifestations Complications Differential diagnosis Treatment
- 3. Definition Pulmonary Edema ;is a condition characterized by fluid accumulation in the lungs caused by extravasation of fluid from pulmonary vasculature in to the interstitium and alveoli of the lungs
- 4. The extent towhich fluid accumulates in the interstitium of the lung depends on the balance of hydrostatic and oncotic forces within the pulmonary capillaries and in the surrounding tissue. Hydrostatic pressure -favors movement of fluid from the capillary into the interstitium Oncotic pressure -favors movement of fluid into the vessel Maintenance -lymphatic in the tissue carry away the small amounts of protein that may leak out -tight junction of endothelium are impermeable to protein
- 5. Epidemiology Pulmonary edemaoccurs in about 1% to 2% of the general population. Between the ages of 40 and 75 years, males are affected more than females. After the age of 75 years, males and females are affected equally. The incidence of pulmonary edema increases with age and may affect about 10% of the population over the age of 75 years.
- 6. Pathophysiology imbalance ofstarling force -increase pulmonary capillary pressure -decrease plasma oncotic pressure -increase negative interstitial pressure damage to alveolar- capillary barrier lymphatic obstruction Disruption of endothelial barrier allow protein to escape capillary bed and enhance movement of fluid in to the tissue of the lung idiopathic or unknown
- 7. Classification based oninciting mechanism 1. Imbalance of Starling force A. Increased pulmonary capillary pressure -left ventricular failure -Volume overload B. Decreased plasma oncotic pressure - Hypoalbuminemia due to different cause C. Increased negativity of interstitial pressure -Rapid removal of pneumothorax with large applied negative pressures (unilateral)
- 8. Classification Based on incitingagent….. 2. Altered alveolar-capillary membrane permeability o Infectious pneumonia o Inhaled toxins o Circulating foreign substances o Aspiration o Endogenous vasoactive substances o Disseminated intravascular coagulation o Immunologic—hypersensitivity pneumonitis, drugs o Shock lung in association with non-thoracic trauma o Acute hemorrhagic pancreatitis
- 9. Classification Based oninciting agent…. 3. Lymphatic insufficiency -After lung transplant - Lymphangitic carcinomatosis -Fibrosing lymphangitis 4. Unknown or incompletely understood - High-altitude pulmonary edema - Neurogenic pulmonary edema - Narcotic overdose - Pulmonary embolism - Eclampsia -After anesthesia - After cardiopulmonary bypass
- 10. Classification Base on underliningcause o Cardiogenic pulmonary edema o Non-cardiogenic pulmonary edema
- 11. Cardiogenic pulmonary edema Is Pulmonaryedema due to increased pressure in the pulmonary capillaries because of cardiac abnormalities that lead to an increase in pulmonary venous pressure. o Hydrostatic pressure is increased and fluid exit capillary at increased rate
- 12. Cardiogenic PE Basicpathophysiology: A rise in pulmonary venous and pulmonary capillary pressures pushes fluid into the pulmonary alveoli and interstitium. CXR: B/L perihilar bat’s wing appearance,symmetric opacification of lung fields
- 13. Pathogenesis of CPE Leftsided heart failure Decrease pumping ability to the systemic circulation Congestion & accumulation of blood in the pulmonary area Fluid leaks out of the intravascular space to the interstitium Accumulation of fluid Pulmonary edema `
- 14. Risk Factors Varyby cause -Leading risk factor is clearly underlying cardiac disease.
- 15. Causes of CardiogenicPE LV failure is the most common cause. Dysrhythmia LV hypertrophy and cardiomyopathy LV volume over load Myocardia infarction left ventricular outflow obstruction
- 16. Non cardiogenic pulmonary edema Itis defined as the evidence of alveolar fluid accumulation with out hemodynamic evidence that suggest a cardiogenic etiology. Hydrostatic pressure is normal Leakage of protein and other molecule in to the tissue
- 17. Non cardiogenic PE oAssociated with dysfunction of surfactant lining the alveoli, increased surface force and a propensity for the alveoli to collapse at low volume. o Characterized by intra pulmonary shunt with hypoxemia and decrease lung compliance
- 18. Non cardiogenic pulmonary edema Mechanisminclude: Increased alveolar–capillary membrane permeability Decreased plasma oncotic pressure Increased negativity of pulmonary interstitial pressure Lymphatic insufficiency or obstruction
- 19. Non- cardiogenic PE cause I. Direct injury to the lung II. Hematogenous injury to the lung III. possible lung injury plus elevated hydrostatic pressure
- 21. Staging of PE Threestages of PE can be distinguished based on the degree of fluid accumulation: Stage-1 : all excess fluid can still be cleared by lymphatic drainage. Stage-2 : characterized by the presence of interstitial edema. Stage-3 : characterized by alveolar edema due to altered alveolor- capillary permeability
- 22. Mild: Only engorgementof pulmonary vasculature is seen. Moderate: There is extravasation of fluid into the interstitial space due to changes in oncotic pressure. Severe: Alveolar filling occurs.
- 23. Unusual type pulmonary edema Neurogenic pulmonary edema Patients with central nervous system disorders and without apparent preexisting LV dysfunction Re-expansion pulmonary edema Develops after removal of air or fluid that has been in pleural space for some time, post- thoracentesis Patients may develop hypotension or oliguria resulting from rapid fluid shifts into lung.
- 24. Unusual type pulmonary edema High altitude pulmonary edema occurs in young people who have quickly ascended to altitudes above2700m and who then engage in strenuous physical exercise at that altitude, before they have become acclimatized. Reversible (in less than 48 hours)
- 25. Pathophysiology on ascendingto high altitude, falling level of Po2 trigger hypoxic pulmonary vasoconstriction This directs blood flow away from hypoxic areas of lung towards area that are well oxygenated This results in a rise in mean pulmonary artery pressure & a heterogeneous blood flow to different parts of the lung
- 26. Cont… In areasthat receive high blood flow the capillary trans-mural pressure rises & walls of the capillary &alveolus are exposed to stress failure Extensive damage to alveolar capillary membrane Edema which is rich in high molecular weight proteins & RBCs to pass freely in to the alveoli & impair oxygenation. patient present with Headache, Insomnia, Fluid retention, Cough,Shortness of breath
- 27. Symptom of pulmonary edema ACUTE Shortness of breath A Feeling of suffocating Anxiety ,restlessness Cough-frothy sputum that may be tinged with blood excessive sweating pale skin chest pain if PE is cause by cardiac abnormality palpitation
- 28. Symptom…… Long term(chronic) Paraxosomalnocturnal dyspnea orthopnea Rapid weight gain Loss of appetite fatigue ankle and leg swelling
- 29. Signs Tachycardia Tachypnea Confusion Agitation Anxious Diaphoric Hypertension Cool extremities Rales Wheezing CVS findings ; S3 ,accentuation of pulmonic component of S2, jugular venous distention…..
- 30. Special considerations Unilateralpulmonary edema after rapid evacuation of large pneumothorax Findings may be apparent only by radiography. Occasionally, dyspnea with physical findings localized to edematous lung
- 31. Special consideration Lymphaticblockade secondary to fibrotic and inflammatory diseases or lymphangitic carcinomatosis Both clinical and radiographic manifestations are dominated by the underlying disease process. Neurogenic pulmonary edema Symptoms usually occur within minutes to hours of the injury
- 32. Complications leg swelling(edema), abdominal swelling(ascites), Pleural effusion, Congestion & swelling of liver, acute heart attack (myocardial infarction [MI]), cardiogenic shock, arrhythmias, electrolyte disturbances, mesenteric insufficiency, protein enteropathy, respiratory arrest, and death.
- 33. Differential diagnosis Pneumothorax Bronchitis Cardiac tamponed COPD Pericarditis Pneumonia (bacterial ,viral , PCP) Pulmonary embolism Shocks (cardiogenic ,septic ,anaphylactic) Venous air embolism
- 34. Distinguishing Cardiogenic from Non-cardiogenicPulmonary Edema Finding suggesting cardiogenic edema -S3 gallop -elevated JVP -Peripheral edema Findings suggesting non-cardiogenic edema -Pulmonary findings may be relatively normal in the early stages -.
- 35. Distinguishing ….. Chestradiography A cardiogenic cause is favored with Cardiomegaly Kerley B lines and loss of distinct vascular margins Cephalization: engorgement of vasculature to the apices Perihilar alveolar infiltrate Pleural effusion Non cardiogenic cause -Heart size is normal -Uniform alveolar infiltrate -pleural effusion is uncommon -lack of cephalization
- 36. Distinguishing….. Hypoxemia Cardiogenic -due to ventilation perfusion miss match -respond to administration of oxygen Non cardiogenic -due to intrapulmonary shunting -persist despite oxygen supplimentation
- 37. Exertional Dyspnea Orthopnea Aspiration of food or foreign body Direct Chest injuries Walking High altitude Chest Pain(right or left) Leg pain or swelling(Pulmonary Embolism) A cough that produces frothy sputum that may be tinged with blood(cardiogenic) History Taking Approach a Patient with Pulm.Edema
- 38. Cont… Palpitations Excessivesweating Skin color change-Pale skin Chest pain(if it is Cardiogenic) Rapid weight gain(cardiogenic) Fatigue Loss of appetite Smoking History
- 39. Past Medical History COPD, heart failure, HIV risk factors (pulmonary Kaposi’s sarcoma). Prior chest X-rays, CT scans, tuberculin testing (PPD).
- 40. Medications Anticoagulants Aspirin NSAIDs Narcotic Heroin Morphine Methadone and Dextropropoxyphene
- 41. INVESTIGATIONS CXR-PA view: unilateralor bilateral involvement,cardiogenic pattern or non cardiognic pattern(air bronchogram signs, fluffy opacities, asymmetrical inhomogenous involvement),lobar involvement in post infectious PE. ABG analysis: hypoxia and hypocapnia initially with respi. alkalois hypercapnea in later stage with respi and metabolic acidosis Hemodynamic measurement with Swan-Ganz catheter Blood work up and septic screen
- 42. Management stretagy Treatunderlying cause : Sepsis,heart failure,high altitude hypoxia,obstruction,fluid overload,hypoproteinemia etc. Respi support: NIV vs Intubation f/b venti support Indication for intubation f/b venti support Refractive hypoxia Excessive work of breathing : rate > 35/min , MV>12L/min Hemodynamic instability Inability to protect airway Anticipated rapid clinical deterioration
- 43. Management stretagy….. NIVsupport:CPAP Reasonable initial venti settings are EPAP 7 cmH2O and IPAP of around 15 cm H2O with adjustment according to patient tolerance and maintaining SaO2>90% Decreases work of breathing,FRC is increased,collapse of alveoli due to edema fluid is prevented and helps in opening up of already collapsed alveoli Good response is generally observed in 30 minutes,if not so or worsening is seen, consider elective intubation f/b venti support
- 44. Management stretagy… Principlesof mechanical ventilation Two fundamental principles 1. Prevention of overdistension of alveoli-limiting tidal volume or inspiratory pressure 2. Choose the level of PEEP sufficiently high to prevent derecruitment of alveoli at end of expiration
- 45. 1. Limiting tidalvolume High TV 12-15 ml per kg are dangerous in patient with PE Can lead to VOLUTRAUMA Tidal volume kept at 6-8 ml per kg to start with in patient of PE Then adjusted to keep the plateau pressure below 30 cm of H2O
- 46. 2. Use ofPEEP Recruits collapsed alveoli,prevents collapse,improves V/Q mismatch,decreases shunt and venous admixture,increases FRC,reduces pathological dead space Can allow adequate oxygenation at lower FiO2,protects from oxygen toxicity Most patients with ARDS will need PEEP of more than 10 cm H2O at FiO2<0.6 If high level of PEEP causes hemodynamic instability, use of pressure controlled – inverse ratio ventilation , prone posture can be beneficial Inverse ratio venti:changes inspiration-expiration ratio,lower peak pressure can be achieved,auto- PEEP develops,higher mean alveolar pressure with low peak pressure
- 47. Treatment in special conditions High altitude pulmonary edema Slow ascent ,prophylactically tab.nifedipine 20mg sustained release 8hrly, or tab dexamethasone 8 mg 12hrly,or inhaled salmeterol Descent and supplemental O2 are definitive Rx If descent not possible and O2 not available,start pharmacotherapy to reduce pulmonary artery pressure Tab nifedipine 10mg sublingual f/b 20 mg SR tab 6hrly Also hydralazine,inhaled nitrous oxide acetazolamide are helpful
- 48. Post Aspiration PE Preop gastric emptying by physical means(ryle’s tube aspiration) or pharmacological means(perinorm,atropine,glocopyrolate) Anti ematics ondensatron,granisatron injectable Induction in lateral position Head low position Bronchoscopic removal of particulate aspirate material NO BRONCHO-ALVEOLAR LAVAGE-removes surfactant and promotes collapse Supportive sterids PEEP and mechanical venti till edema clears
- 49.