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Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
Respiratory emmergencies 20 may 10
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Respiratory emmergencies 20 may 10

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  • 1. RESPIRATORY EMERGENCIES DR.SUHAS KULKARNI
  • 2. Objectives To enumerate most common respiratory emergencies To classify them according to etiology Prompt identification of the cause Emergency assessment of the patient (clinical evaluation) Appropriate investigations and management
  • 3. Classification Medical – 1) Massive hemoptysis 2) Pneumothorax 3) Aspiration syndromes 4) Large airway obstruction 5) Pulmonary embolism 6)Neuromuscular and infective eme. Traumatic- 1) Penetrating trauma 2) Blunt trauma Other - 1) Toxic gas inhalation 2) Drowning
  • 4. General Impression of Patient Position Color Mental Status Ability to Speak Respiratory Effort
  • 5. Initial Assessment Airway – open, no noises Breathing – 12-20 times per minute Circulation – warm, pink, dry, strong pulses Disability – mental status clear Vital Signs
  • 6. Focused History How long has this been going on? Start gradual or abrupt Better or worse with position Cough  Productive of sputum  Color of sputum– white? Yellow? Red? green? brown?
  • 7. Additional Symptoms Chest pain Fever/chills Wheezing Smoking history Trauma
  • 8. Medications Currently Taking Antibiotics Oxygen Steroids  Emphysema  Asthma Inhalers/nebulizers  Emphysema  Asthma Cardiac drugs
  • 9. Respiratory Emergencies For each, consider  Cause/Pathology  Signs and symptoms  Management
  • 10. HEMOPTYSIS Expectoration of blood from the respiratory tract, a spectrum that varies from blood streaking of sputum to coughing up of large amount of blood Can be mild , moderate or massive
  • 11. CausesA.Infections Tuberculosis Mycetoma Lung abscess Fungal infection Parasitic infectionsB. Neoplasms Bronchogenic carcinoma Bronchial adenoma Carcinoid Tumor Hematological malignancies
  • 12. Metastatic cancers Melanoma Carcinoma breast Carcinoma colon Renal cell carcinoma Chorio carcinoma Papillary thyroid Osteogenic sarcomaC. Chronic airway inflammation Bronchiectasis Cystic fibrosis Bronchitis Broncholithiasis Foreign body
  • 13. D.Pulmonary vascular disorders Congenital AV malformations E.g.. Osler weber rendu syndrome Heriditary hemorrhagic telangectasia Pulmonary artery aneurysms E.g.. Behcets disease Takayasu`s arteritis Pulmonary thromboembolism Pulmonary hypertensionE. Cardiac causes Mitral stenosis Pulmonary edema Congenital heart disease Tricuspid endocarditis
  • 14. Wegener`s granulomatosis F. Immunological disorders SLE Good pasture`s syndrome Systemic narcotizing vasculitis Idiopathic pulmonary hemosiderosisG.Iatrogenic causes Bronchoscopy with biopsy Transthoracic lung biopsy Pulmonary artery catheterizationH.Miscellaneous causes Chest trauma Coagulation disorders Drugs ( Anticoagulants , Pencillamine ) Endometriosis Pulmonary amyloidosis Cryptogenic
  • 15. Approach to the patientHistory Hemoptysis- rarely solitary event R/O pseudohemoptysis Differentiate from hematemesis
  • 16. Hemoptysis Hematemesis•Bright red and frothy •Coffee ground,mixed with food•Coughing & tickling in •Vomitingthroat •Abd.pain, vomiting,indigestion,•Cough expectoration,fever •Tarry stools•Rusty sputum •Acidic•Alkaline
  • 17. InvestigationsChest radiograph: Mass lesion Bronchiectasis Aspergilloma Pneumonitis Diffuse parenchymal pathology Evidence of old koch`sCT scan / MRI scan
  • 18. Blood investigations: CBP Grouping & typing Coagulation profile Renal profile
  • 19. Sputum : AFB Grams stain & C/S Malignant cells Fungal stains
  • 20. BronchoscopyFibre Optic : Useful for localizing site of bleed TamponadeRigid : Preferred in massive bleed Better airway management Greater suction capability
  • 21. ManagementMild : Less than 100 ml per dayModerate : 100 - 150 ml per dayMassive : more than 600 ml per day more than 150 ml per hour more than 150 ml for 3 consecutive days * Any hemoptysis that is life threatening can be termed massive *
  • 22. ManagementImmediate priorities : 1.Airway management •Intubation •Proper suctioning •Adequate oxygenation 2. Hemodynamic stability •Volume load with colloids / crytolloids •Restore hemoglobin
  • 23. 3. General measures •Nurse the patient with affected lung in dependent position •Suppress anxiety with mild sedation •Suppress Cough • ? Hemostyptics
  • 24. 3. Therapeutic measures to stop bleeding •Bronchoscopy •Topical therapy •Bronchial irrigation •Balloon tamponade •Laser photo therapy •Electro cautery •Unilateral lung ventilation •Bronchial artery embolisation •Surgery
  • 25. Bronchoscopy•Topical therapy •Thrombin & fibrinogen thrombin solution •Epinephrine •Bronchial irrigation •Repeated endo-bronchial irrigation with iced saline •Presumably acts by vaso-constriction. •An average of 500 ml fluid is required for each patient , in increments of 50ml.
  • 26. Pneumothotax Air in the pleural space i.e between lung and chest wall
  • 27. Classification[based on the cause]  Spontaneous Primary - Healthy , no lung disease & no precipitating event Secondary - Lung disease & no precipitating event  Traumatic Direct,Indirect,Iatrogenic
  • 28. Classification[based on the pathology] Open Closed Tension
  • 29. Primary spontaneous pneumothorax Etiology- Rupture of subpleural blebs Cause of subpleural blebs unclear in healthy Risk factors - Smoking [healthy smoking men=12%, non smoking=0.1%] -Tall individuals -Familial & genetic -High altitude & deep water diving
  • 30. Secondary spontaneous pneumothorax Complication of chronic lung diseases  COPD  Asthma  Pulmonary tuberculosis  Suppurative diseases of the lung rupturing into the pleura  Diffuse fibrosing pulmonary diseases  PCP in AIDS  Bullous lung diseases  CF
  • 31. Imaging Expiratory CXR not recommended for the routine diagnosis. [B] A lateral chest or lateral decubitus radiograph should be performed if the clinical suspicion is high, but a PA radiograph is normal. [B] CT scan-- differentiating a pthx from complex bullous lung disease, aberrant tube placement is suspected, and when the plain CXR is obscured by surgical emphysema. [C]
  • 32. Observation•TOC - small closed pthx without significant breathlessness. [B]•Pts with small (<2 cm) primary pneumothoraces not a/cbreathlessness --- discharge with early outpatient review. Ptsshould receive clear written advice to return in the event ofworsening breathlessness. [B]•Patient with a pthx if admitted overnight for observation, highflow (10 L/min) oxygen should be administered, withappropriate caution in patients with COPD [B]•Breathless patients --- intervention regardless of the size of thepneumothorax on a CXR [C]
  • 33. Simple aspiration•Primary pneumothoraces requiring intervention. Simpleaspiration is recommended as first line treatment for all[A]• Secondary pneumothoraces recommended only as aninitial treatment in small (<2 cm) pneumothoraces inminimally breathless patients < 50 years. [B]•Patients with secondary pneumothoraces treatedsuccessfully with simple aspiration should be admitted tohospital and observed for 24hrs [C]
  • 34. Repeat aspiration Primary pneumothorax - first aspiration unsuccessful (i.e. patient still symptomatic) and a vol of >2.5 l has been aspirated on the first attempt. [B]Catheter aspiration of simple pneumothorax •Catheter aspiration of pneumothorax (CASP)[8F] can be used where the equipment and experience is available. [B] •Catheter aspiration kits with an integral one way valve system reduce the need for repeat aspiration. [C]
  • 35. Intercostal tube drainage•Simple aspiration or catheter aspiration of pthx isunsuccessful in controlling symptoms [B]•Secondary pthx _except in pts who are not dyspneicand have a very small (<1 cm or apical) pthx. [B]
  • 36. Pulmonary ThromboembolismThe designation refers to migration of aclot (or clots) from systemic veins to thepulmonary vascular bed.
  • 37. Source of Emboli90 % from deep veins of legsBegins behind a valve in deep veinsUncommon but important source in women PelvicveinsMay be septic or bland
  • 38. Source of EmboliAmniotic Fluid embolismRare but catastrophic complication of pregnancyGain access to uterine veins while vigorouscontractionsThrough tears or surgical incisions in myometrium
  • 39. Source of EmboliAir embolismIntravenous injectionsHemodyalysisPlacement of central venous catheterArtificially pneumothorax or pneumoperitoniumAfter chest injury
  • 40. Pathophysiology and clinical presentation 1.Acute massive occlusion Clinical picture is of shock Pt. is pale, weak, listless to point of apathy, sweaty, nauseated Oliguric with impaired mentation Tachypnoea & tachycardia most striking Poor prognosis in most cases Autopsy discloses large embolus in major pulmonary artery Systemic hypo tension is consistent
  • 41. Diagnostic MeasuresLab DataCell counts & serum enzymes little valueTRIAD : ↑LDH ↑ Bilirubin ↓ TransaminaseOnce believed to be suggestive is now proved non – specific.D – dimer Suffer from uniformity in reagents & standards false positive in many conditions limit use Negative D – dimer test can be used to rule outthrombosis
  • 42. Diagnostic MeasuresArterial blood gases Both PaO2 & PaCO2 are somewhat low Normal ABG do not exclude PE But unexplained hypoxemia should raise suspicion of PEChest Radiograph May be normal May show infiltrate, effusion, atelectasis, Similar findings may occur in pneumonia, pleuritis & CCF Peripheral wedge shaped infarct (Hampton`s hump)
  • 43. Ventilation perfusion scans Ventilation defect as large as perfusion defectIn PE, perfusion defect unaccompanied by ventilation defectScans are classified into 4 categories Normal High probability Intermediate probability Low probability
  • 44. ElectrocardiographyECG changes are usually non-specificIn minor cases no haemodynamic stress - only sinustachycardia.In acute / subacute massive cases, evidence of right heartstrain may be seen (rightward shift of the QRS axis, transientright bundle branch block, T wave inversion in leads V1-3, Ppulmonale),Classic S1Q3T3 pattern occurs in only a few cases.The main value is in excluding other diagnoses - MI /Pericarditis.
  • 45. Pulmonary angiographyMost accurate diagnostic studyTwo angiographic findings Filling defect ( Most common & reliable) Cut off of radio – opaque streamEven though has low morbidity & mortality in experiencedhandsLimited by : Right heart catheterization, IV contrast material,Can detect clots as small as 0.5 mmException: Incomplete occlusionFLAWS : Invasive, Expensive, Complex, Limited availability
  • 46. Spiral or electron beam CTx Emerging as a non-invasive testing modality tocomplement or replace the standard lung scintigraphyx Can directly visualise intravascular thrombus, butsmaller, subsegmental emboli can be overlookedx Greater sensitivity and specificity for pulmonaryembolism than lung scintigraphy. Agreement amongreaders of CT better than among readers of scintigrams
  • 47. Spiral or electron beam CTx CT scans, like angiograms, are either positive ornegative for pulmonary embolism in the majority ofcases. Only 10% of CT scans are non-diagnostic(compared to 70% non-diagnostic scintigrams)x Can diagnose alternative causes of dyspnoeax Because of significant both false negative and falsepositive examinations, CT cannot yet be regarded as agold standard alternative to angiography.
  • 48. ManagementProphylaxis ( All hospitalized patient who are at risk ofDVT) Elevation of Foot Leg exercises Frequent position change Gradient elastic stocking Intermittent external pneumatic compressions.Any of the above or a combination of these can be used.
  • 49. NEJM 1996Volume 335 Number 24
  • 50. Thrombolytic therapyUsed in treating life-threatening casesEmboli causing hemodynamic instabilityLarge pulmonary emboli with Right heart dilatation even in the absence of significant cardiopulmonarycompromise Less certain in submassive & Large thrombi in proximal deepveins.After Thrombolysis anticoagulation with heparin followed byoral warfarin / sc heparin must to prevent recurrence
  • 51. Thrombolytic therapy Plasma Fibrin Load Hourl RecomAgent clearen binding dose y dose duration t½ min 250,000 IU PE 24 hrsSK 18 – 25 Minimal over 30 100,000 IU/h min DVT 48 – 72 hUK 4400 PE 12 hrs 13 – 20 Low 4400 IU/Kg/ IU/Kg over h DVT not 10 min approt – PA 2–6 PE 2 hrs Moderate None 50 mg / h DVT not appro
  • 52. Chest Trauma Blunt – motor vehicle accidents falls and beatings Penetrating – Stab or gun shot wounds
  • 53. Chest Trauma Blunt Thoracic Trauma:  Airway injuries  Pneumothorax  Hemothorax  Cardiac Tamponade
  • 54. Airway Injuries Tracheal disruption transverse, longitudinal or in combined direction within 2.5 cm of the carina Pre Tracheal Fascia preserves integrity of airway Disruption of main airway stem bronchus (sudden deceleration of motor vehicle accident) Often associated injuries of adjacent structures – descending thoracic aorta, esophagus, manubrium, mandible, cervical spine
  • 55. Clinical Presentation S/C Emphysema Respiratory distress Change in voice Pneumothorax Hemothorax Deep cervical or Mediastinal air
  • 56. Management Establish a reliable airway Intubation of the trachea beyond the injury under direct bronchoscopic vision Debridement of devitalised tissue Repaired or reanastomosed Rarely – Pulmonary resection, Pneumonectomy
  • 57. Tension Pneumothorax More likely after penetrating trauma Likelihood increases in blunt trauma with severity of injury to chest wall Signs – hypotension, absent breath sounds tympany on percussion, tracheal deviation to opposite side Immediate inervention – large bore needle in 2 nd intercostal space Placement of chest tube – Rx of choice
  • 58. Hemothorax If hemodynamically unstable – immediate exploration of chest after volume replacement If due to lung parenchyma chest tube drainage after blood volume replacement If blood drains at 200 ml/ hour for 2-3 hours – surgical exploration
  • 59. Simple Rib Fracture Fracture of lower ribs – look for injury to liver or spleen Pulmonary complications – Retained secretions atelectasis, ventilatory failure (sp. in COPD patients) and empyema Mm- Adequate analgesia, may require narcotics and inter costal nerve blocks
  • 60. Flail Chest Section of chest wall becomes unstable because of multiple rib fractures Ventilatory abnormalities partly due to paradoxical chest wall motion or lung contusion Earlier management strategies – external stabilization with sandbags, internal fixation of flail segment, internal pneumatic stabilization with mechanical ventilation
  • 61. Flail Chest Current treatment – CPAP, analgesia (continuous epidural analgesia excellent adjunct Operative fixation for severe flail
  • 62. ARDS Seen with associated factors – Sepsis syndrome, pulmonary contusion, aspiration of gastric contents, multiple blood transfusions and multiple major fractures 18% with one factor, 85% with 3 or more factors Mechanical ventilation, HFV, ECMO Single Lung ventilation – unilateral pulmonary contusion
  • 63. Acute Respiratory Failure A syndrome in which the respiratory system fails in one or both of its gas exchange functions:  oxygenation  carbon dioxide elimination. a PaO2 < 60 mm Hg @ room air PaCO2 > 50 mm Hg.
  • 64. Causes Depressed drive Drug over dose , Head injury Encephalitis, Hypothyroidism
  • 65. ♦Neuromuscular diseases Acute poliomyelitis G-B syndrome, Tetanus Myasthenia gravis Spinal cord lesions Phrenic nerve injury NM blockers, Snakebite
  • 66.  Airway diseases Bronchospasm Airway edema Secretions Tracheal or subglottic stenosis Epiglotitis Foreign body aspiration OSA
  • 67.  Increased production of CO2 High fever Hyper metabolic illness Frequent seizures Uncontrolled tetanus Respiratory muscle fatigue Hyper alimentation with increased caloric intake
  • 68.  Obstructive airway disease COPD,Asthma Restrictive lung disease Pulmonary edema Pneumonia , ARDS Atelectasis Interstitial lung diseases Pulmonary Thromboembolism
  • 69. Hypoxia  Cyanosis  Restlessness , Anxiety  Tachycardia , Hypertension  Rhythm disturbances  Bradycardia,Hypotension,Circulatory failure
  • 70. Hypercapnia  Flushing,Warmth,Sweating,Bounding Pulse  Headache  Flapping tremors  Drowsiness,Confusion,Coma  Muscle twitch,Seizures,Papilloedema
  • 71. Clinical Assessment Detailed History Physical examination Routine investigation  ABG  CBC  Biochemistry  X-ray Special investigation  Monitor CVP,CO,PAP,Shunt fraction
  • 72. Principles  Maintain clear airway  Use of Oxygen  Maintain Adequate Ventilation  Treat Cause
  • 73. Maintain clear airway  Liquefy the secretions  Proper hydration  Humidification  Mucolytics  Promotion of cough  Suction  Endotracheal intubation
  • 74. Use of oxygen ∀ ↑ PAO2 there by ↑ PaO2 • Life saving ∀ ↓ work of breathing ∀ ↓ Myocardial work • Improved cell function
  • 75. Maintain Adequate Ventilation  Respiratory Stimulants  NIPPV  Mechanical ventilation

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