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EM Board Review Pulmonary & Critical Care...Carrie Clark

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EM Board Review Pulmonary & Critical Care...Carrie Clark

  1. 1. + Board Review: Pulm and Critical Care Carrie Clark DO
  2. 2. + Respiratory Physiology  A-a gradient  =PAO2-PaO2  PAO2 value from alveolar gas equation   Alveolar gas equation: PAO2=150-(1.25xPaCO2) (at sea level and room air) PaO2 obtained from ABG
  3. 3. + Hypoxemia  Defined as PaO2<60mmHg  Etiology   V/Q mismatch  Airspace not being perfused OR perfused areas not being ventilated  Etiologies: asthma, COPD, PE, interstitial lung disease  Management: oxygen and treat underlying cause Shunting  Decreased diffusion of oxygen  Etiologies: alveolar collapseARDS, also from alveolar filling (pneumonia, pulmonary edema)  Management: does NOT respond well to oxygen responds better to PEEP
  4. 4. + Hypoxemia  Decreased diffusion    Etiologies: thickening of alveolar/capillary interface (commonly interstitial lung disease) Management: responds to O2 Hypoventilation    Lack of respiratory effort resulting in low PaO2 and high PaCO2, commonly from drug overdose Normal A-a gradient High Altitude  Decrease in partial pressure of available O2  Normal A-a gradient
  5. 5. + Critical Care: ARDS  Acute onset of alveoli edema caused by capillary membranes injury and increased permeability  Sepsis, acute pulmonary infection, DIC, shock lung, freebase cocaine smoking  You will see bilateral infiltrates on chest x-ray  Ratio of PaO2/FiO2<200mmHg  Symptoms: respiratory distress, hypoxemia unresponsive to increasing supplemental O2  Onset is often within the first 2 hours of inciting event, but it can be delayed as long as 1-3 days
  6. 6. + Critical Care: ARDS  Management  35-50% mortality  Treat underlying disease  Mechanical ventilation with PEEP  Use low tidal volumes to prevent barotrauma Steroids NOT shown to be beneficial
  7. 7. + Disorders of Pleura, Mediastinum and Chest Wall  Mediastinitis  Pneumomediastinum  Pleural Effusion  Pneumothorax
  8. 8. + Mediastinitus  Inflammation of the mediastinum  Etiology    Mixed organisms but most commonly Streptococcus and Bacteroides Esophageal rupture most common cause (foreign body ingestion or stuck fish bone may accompany history or esophageal inj) Risk Factors   Immunocompromise and diabetes, drug abuse Symptoms  Fever, dyspnea, pleuritic, retrosternal chest pain, sub-q emphysema of neck and chest
  9. 9. + Mediastinitis  Diagnosis   Soft tissue x-ray of the neck may show precervical or retropharyngeal air/edema   A CXR may show a widened mediastinum CT should be performed to further evaluate soft tissue spaces Management  Broad-spectrum antibiotic therapy  ENT and cardiothoracic consult
  10. 10. + Pneumomediastinum  Etiology  Spontaneousextremely rare, blunt chest trauma, endoscopy, obstructive lung disease  Considerer Boerhaave syndrom if h/o vomiting  Valsalva maneuver (foreceful cough against a closed glottis, consitpation)   Observed in crack cocaine users Symptoms  Chest pain and dyspnea  Signs: sub-q emphysema and Hamman sign (crunching, rasping sound, synchronous with heartbeat)  Decreased cardiac output if tension pneumomediastinum is present
  11. 11. + Pneumomediastinum  Diagnosis   Esophagogramperform in right lateral decubitus position, use a water-soluble contrast, if clinical suspicions remain high and the initial study is negative, repeat study with oral barium contrast  Esophagoscopyfor suspected esophageal rupture in acute traumatic rupture   CXRreveals free air within the mediastinum, air posterior to sternum and posterior to the heart on lateral film Bronchoscopyfor suspected bronchotracheal tree rupture Management  Should be admitted and observed for signs of serious complications  Broad-spectrum antibiotics for suspected esophageal rupture
  12. 12. + Pleural Effusion  Collection of fluid within pleural space  Epidemiology    CHF is the most common cause followed by malignancy, bacterial pneumonia, and PE TB is the most common etiology of pleural effusion in developing countries Etiology  TransudativeCHF, cirrhosis with ascites, nephrotic syndrome, PE  ExudativeCancer, infectious (pneumonia, empyema, abscess, TB), inflammatory (SLE, pancreatitis, RA, and PE
  13. 13. + Pleural Effusion  Symptoms   Dyspnea and pleuritic chest pain, decreased breath sounds on auscultation, dullness to percussion Diagnosis    CXR: AP XR demonstrates effusion when pleural fluid volume approaches 150cc CT or US most sensitive Thoracentesis necessary when etiology is unclear  Light criteriaa single positive criterion is enough to classify the fluid as an exudate  Glucoselow pleural fluid levels (<25)=RA, TB, empyema, and malignancies  pHlow pH=inflammatory and infiltrative processes (empyema, malignancies, TB, esophageal rupture)  Amylasehigh amylase (>200) pancreatitis, malignancy, rupture
  14. 14. + Pleural Effusion  Light Criteria Transudate Exudate Pleural and serum Protein <0.5 >0.5 Pleural and serum LDH <0.6 >0.6 Pleural LDH <200 >200
  15. 15. + Pleural Effusion  Management  Treat underlying cause  Therapeutic thoracentesis for patients dyspneic at rest  Thoracotomy tube placement for empyema
  16. 16. + Pneumothorax  Etiology    Spontaneousno underlying lung disease  Male:female 6:1  Young, tall, thin  Smoking 20:1  Valsalva  Ruptured bleb  Many recur (20-50%) Secondary-caused by underlying lung disease  Asthma, COPD, neoplasm  Marfan, Ehlers Danlos, Cystic fibrosis  Penumonia, especially with abscess or cavitation  HIV-PCP Tension pneumo
  17. 17. + Pneumothorax  Symptoms      Dyspnea and pleuritic chest pain Decreased breath sounds and hyperresonace to percussion JVD and hypotension Tracheal deviation away from affected side Diagnosis   Pneumothorax  CXR for simple pneumothorax (end expiratory for highest sensitivity)  CT test of choice for supine trauma patient Tension pneumo  Clinical diagnosis  Tracheal deviation away from affected lung  Hypotension  Do NOT wait for x-rays before treating
  18. 18. + Pneumothorax  Management  Small, stable ptx (<10%)   Reabsorb 5-7% per day   100% O2 Stable patient with a small ptx can be discharged with next day follow up after 6 hours observation and stable x-ray Large ptx    100% O2 Tube thoracostomy Tension ptx  Immediate decompression followed by chest tube
  19. 19. + Noncardiogenic Pulm Edema  Definition: radiographic evidence of alveolar fluid accumulation without hemodynamic evidence of a cardiogenic etiology (ie pulmonary capillary wedge pressure <18mmHg)  Etiology  ARDS  High-altitude pulmonary edema  Reexpansion pulmonary edema    Large volume thoracentesis (>1L) Rapid lung re-expansion of ptx, especially when it has been collapsed for >3 days Drug induced (meprobamate, opiates, naloxone, PCP, Salicylate)
  20. 20. + Obstructive Lung Disease  Asthma and reactive airway disease  COPD  Cystic Fibrosis
  21. 21. + Asthma and reactive airway disease  Chronic inflammatory disorder of the small airways characterized by reversible obstruction  Etiology and patho      Airway inflammation/bronchial wall edema leading to decreased airway diameter Airway hyperreactivity, smooth muscle contraction Secretions forming mucous plugs Chronic inflammation leads to lung remodeling Symptoms    Dyspnea with or without cough Prolonged expiratory phase with predominantly exp wheezing Severe exacerbations may present with absence of wheezing, inability to speak, pulses paradoxus and hypoxia
  22. 22. + Asthma and reactive airway disease  History associated with higher mortality  >2 hospitalizations during past year  >3 ED visits during past year  Prior intubation or ICU admission  Use of 2 or more adrenergic canisters per month  Current use of systemic steroids or recent withdrawal  Low socioeconomic class
  23. 23. + Asthma and reactive airway disease  Diagnosis   Bedside spirometrypeak flow to monitor response to beta-agonist treatment  Peak flow <50% indicates severe exacerbation Treatment     Oxygen to keep O2>88% Beta agonistsrelaxation of bronchial smooth muscle Epinephrine (1:1000)reserved for severe exacerbations, is administered sub-q 0.3 q20-30 minutes up to three doses Terbutaline reserved for severe exacerbations given SC 0.25mg every 20-30 min up to three doses  Longer duration of action than epinephrine
  24. 24. + Treatment cont.  Corticosteriodsused in both acute and chronic setting to prevent late phase inflammatory response  Oral dosing as effective as IV administration  Magnesiumbenefit in severe exacerbation  Mechanical ventilation  Avoid air-trapping or auto-peep  Smaller tidal volumes  Keep rate low  Consider increasing peak inspiratory flowlonger expiratory time
  25. 25. + Treatment cont  When treating pregnant asthmatics…  Fetus more susceptible to hypoxia than mother  No contraindications to use of beta agonists, corticosteroids and anticholinergics  Chronic steroids may result in lower birth weights  Epinephrine is teratogenic during first trimester and associated with preterm delivery
  26. 26. + COPD  Progressive partially reversible limitation of airflow  Caused by two processeschronic bronchitis and emphysema, which occur together in most patients  Epidemiology   The single most important risk factor for COPD is smoking Etiology  80% of acute COPD exacerbations are of infectious origin  Streptococcus pneumoniae, Haemophilus influenzae, or moraxella catarrhalis
  27. 27. + COPD  Signs and symptoms    Dyspnea on exertion, tachypnea, cyanosis, agitation, apprehension, and hypertension are indicative of hypoxia Wheezing, rales, rhonci, prolonged expiratory phase, pursed-lip breathing and clubbing of digits Diagnosis     Elevated hematocrit 2/2 chronic hypoxia ABG: mild to moderate hypoxemia without hypercapnea in early stages CXRhyperinflation, flattened diaphragm, long narrow heart shadow EKGa-fib, multifocal atrial tachycardia, cor-pulmonale (tall pwaves), right axis deviation and right ventricle hypertrophy
  28. 28. + COPD  Management  Supplemental oxygen reduces mortality in patients with advanced COPD with room air O2 saturaion <88%  Nebulized anticholinergics  Bronchodilators  Antibiotics  First line choices include amoxicillin, cefaclor, fluoroquinolones, or bactrim  Gram-negative infections more likely in those with frequent exacerbation and need a third-generaltion cephalosporin  corticosteroid
  29. 29. + Cystic Fibrosis  Most common in Europeans and Ashkenazi Jews  Autosomal recessive mutation    Abnormalities in chloride transport in exocrine tissues leads to multiorgan involvement Thick, viscous secretions in lungs, intestine, pancreas, and reproductive tract Symptoms and signs  Respiratory manifestationsmost common, exacerbations characterized by increased cough, sputum production, decreased lung function
  30. 30. + CF symptoms and signs cont.  Undiagnosed patients may present with failure to thrive chronic cough, repeated pulmonary or sinus infections, chronic diarrhea from pancreatic insufficiency  Alternative presentations  Increased salt content in sweat gland secretion  Meconium ileus in neonates  Steatorrhea from pancreatic enzyme insufficiency  Intestinal obstruction  Spontaneous pneumo  Chronic pancreatitis  Hepatobiliary disease
  31. 31. + CF diagnosis  Electrolytes   Hyponatremia and alkalosis CXR  Bronchiolar thickening, hyperinflation, and patchy, diffuse infiltrates  Newborn screening  Chloride sweat testing or genetic testing
  32. 32. + CF Management  Broad-spectrum antibiotics  Cover Staph aureus, H. flu, and double cover Pseudomonas  Chronic colonization with pathologic bacteria and chronic antibiotic use leads to resistant organisms requiring intravenous vanco, tobramycin, meropenem, cipro, and piperacillin  Mucolytics  Bronchodilators  Aggressive chest physiotherapy  Provide O2  Consult Pulm
  33. 33. + Restrictive Lung disease  Loss of lung compliance resulting in volumes loss  Interstitial Lung Disease   Idiopathic pulmonary fibrosis Sarcoidosis
  34. 34. + ILD  ILD   Restrictive pulmonary dysfunctions with the common end-point of interstitial collagen deposits and scarring Idiopathic pulmonary fibrosis  50% of ILDs  Likely autoimmune  Symptoms and signsdyspnea, cough, fine dry crackles, clubbing of fingers  DiagnosisCXR has honeycombed lungs, CTground glass opacity  Management corticosteroids, immune modulators, lung transplant
  35. 35. + Sarcoidosis  Epidemiology    African americans>caucasians females>males Etiologytypical finding includes non-caseating granuloma, which is composed of T-helper cells and other inflammatory cells
  36. 36. + Sarcoidosis  Symptoms and Signs  Most patients are asymptomatic  Disease is fatal in 10% of patients because of extensive organ involvement  Constitutional symptomsfever, fatigue, weight loss, polyarthritis, myositis  Pulm symptomscough, hemoptysis, shortness of breath with exertion  Neurobells palsy, seizures  Skin lesionsplaques, subcutaneous nodules, erythema nodosum  Cardiacarrhythmias, CHF  Lympthadenopathy  Ophthalmologicuveitis, or conjunctivitis
  37. 37. + Sarcoidosis  Diagnosis  CXR   Stage 1hilar adenopathy  Stage 2Hilar adenopathy and parenchymal involvement  Stage 3parenchymal involvement without adenopathy   Stage 0no findings Stage 4pulmonary fibrosis Lab studies  Leukocytosis, elevated ESR or serum ACE, hypercalcemia or hyperphosphatemia, elevated CK and CK-MB with cardiac involvement  Gallium 67used to detect extrapulmonary sarcoidosis  Biopsy of involved organ is most useful for diagnosis
  38. 38. + Sarcoidosis  Management  Cardiac monitoring  Consider steroids or cytotoxic medications  Lung transplantation for patients with severe refractory disease
  39. 39. + Thromboembolic Disease  DVT  PE
  40. 40. + DVT  Risk factors  Previous thrombosis  Vascular endothelial damage   Trauma, sugery (especially ortho), smoking Hypercoagulability   Factor V Leiden (most common hereditary hypercoagulability  Antithrombin III deficiency   Protein C or S deficiency Oral contraceptives or 3rd trimester pregnancy Immobilization or low cardiac output  Long periods of sitting, CHF
  41. 41. + DVT  Signs and Symptoms  Pain, warmth and edema  Discoloration of affected extremity  Palpable cord of a thrombosed vein
  42. 42. + DVT  Diagnosis  CT angiography  Doppler ultrasonography   Limitationsoperator dependent, cannot distinguish between old and new clot, not accurate in detecting DVT in the pelvis or the small vessels of the calf Management  Anticoagulationunfractionated low-molecular weight heparin or warfarin therapy  Filter placement for patients with failure of anticoagulation or contraindication to anticoagulation
  43. 43. + Pulmonary Embolus  Risk factor are the same as for DVT 60% of patients with a DVT have a PE  Symptoms and signs  Sudden-onset dyspnea, tachypnea, tachycardia, pleuritic pain, hemoptysis, syncope, cough, and wheeze
  44. 44. + PE diagnosis  ECG   Nonspecific ST-T wave changes and/or sinus tach are most common, S1Q3T3, precordial flipped T waves CXR    Findings are abnormal but nonspecific, pleural effusion, elevated hemidiaphragm secondary to atelectasis and noninfectious infiltrates Westermark signabrupt cut-off of vascular markings Hamptom humppleural based wedge-shaped infarct  CT pulm angiography  VQ scanuseful in severe contrast allergies  A normal scan is sufficient to exclude PE in patient with low pretest probability  Echomay reveal evidence of right heart strain  Pulmonary angiographythe gold standard for diagnosing PE (used infrequently because of noninvasive CT scans
  45. 45. + PE management  Supplemental O2  Hemodynamic support  Anticoagulation  Thrombolytic  Indicated in patients with associated hemodynamic instability  Surgical Embolectomy  IVC filter for anticoagulation failure or contraindication
  46. 46. + Pulmonary Infections  Pneumonia    Bacterial viral Tuberculosis
  47. 47. + Bacterial Pneumonia  Etiology  Typical Pneumonia   S. pneumoniae, H. influenzae, and Staph (S. Pneumo most common) Atypical Pneumonia  Influenza virus, mycoplasma, chlamydia, legionella, and adenovirus  IV drug usersS. aureus  Alcoholism, diabetes, and COPDK, Pneumoniae  AsthmaticsH. Flu  Hospital acquired pneumoniapseudomonas aeruginosa
  48. 48. + Bacterial Pneumonia  Symptoms and signs  Chest pain  Productive cough  Klebsiellacurrant jelly  S. Pneumoniaebloody or rusty colored  Aspirationfoul-smelling sputum  Chlamydiastaccato cough  Rigorsparticularly associated with S. Pneumonia  Diarrhea and GI upset with Legionella  Bullous myringitis with Mycoplasma pneumoniae  Pleural rubs
  49. 49. + Bacterial Pneumonia  DiagnosisChest radiography  Bilateral diffuse infiltrates consistent with atypical infections (M. Pneumoniae, P. Carinii, C. Psittaci)  Abscess and bulging lung fissures are indicative of infections caused by Klebsiella and S. aureus  Pleural effusions and empyema associated with cavitary lesions are seen with s. aureus and M. tuberculosis  Upper lung fieldsK. Pneumoniae  Lower lung fieldsL. Pneumoniae  Miliary patternM. Tuberculosis
  50. 50. + Bacterial Pneumonia  Laboratory studies  Hyponatremia and hypophosphatemia associated with L. Pneumophila  Sputum samples for gram stain and culture are accurate about 50% of the time  Adequate sputum contains <10 epithelial cells, >25 WBC per low power field and remain uncontaminated from oral flora  Mycoplasma and Chlamydia immunoglobulin M antibodies a rise in antibody titer of 1:128 confirms the diagnosis
  51. 51. + Bacterial Pneumonia  Management  Community-acquired pneumonia    Pneumonia severity index score helps determine risk Admit if total score >90 points and consider ICU for >130 Hospital-acquired pneumonia    Double-drug coverage for Pseudomonas Optimal combinations include cefipime plus levofloxacin, aztreonam, meropenem, or aminoglycoside Aspiration pneumonia  Intubation should be considered in any patient who is unable to protect airway, add anaerobic coverage
  52. 52. + Types of Bacterial Pneumonia  Bordetella Pertussis (whopping cough)   Summer and fall months, neither active disease nor vaccination provides lifelong immunity Symptoms and signs3 stages, each lasting about 2 weeks  Catarrhal   Paroxysmal   Most infectious during this time, symptoms indistinguishable from a URI Coughing episodes followed by an inspiratory “whoop” , posttussive exhaustion and emesis Convalescent  Chronic cough that can last several months  Complications include mucous plug, secondary bacterial infection, ruptured diaphragm, hernia, and rectal prolapse
  53. 53. + Pertussis  Diagnosis    Degree of lymphocytosis correlates with severity of disease Definitive diagnosis is made via nasopharyngeal culture Treatment  Erythromycin x14 days  Consider prophylaxis with erythromycin for close contacs  Consider hospitalization for infants <6 months, premature infants, and those with significant comorbitites
  54. 54. + Mycoplasma Pneumonia  Most common atypical  14-day incubation period  More common in young adults  CXR may show interstitial pattern or patchy infiltrate  Treat with macrolide antibiotic  Associations     Bullous myringitis Meningitis and encephalitis Erythema multiforme Guillain-Barre
  55. 55. + Chlamydia Pneumonia  Obligate intracellular parasite  Infants      Acquired at birth 50% conjunctivitis Tachypnea May be afebrile CXR shows hyperinflation and diffuse infiltrates  Common in young adults complaining of hoarseness, cough, and persistent malaise  Staccato cough  Treat with macrolide
  56. 56. + Legionella Pneumonia  Airborne and associated with water sources  Classically associated with recent air travel  No person to person transmission  Symtpoms and signs   Pleuritic chest pain, relative bradycardia, GI symtpoms Diagnosis  Labs may reveal hyponatremia and hypophosphatemia  Chest x-ray may show alveloar infiltrates or consolidation that my progress to hilar adenopathy and pleural effusion  Treat with erythromycin for 3 weeks
  57. 57. + Tuberculosis  Leading cause of death worldwide  Humans are sole reservoir  TB can remain dormant for years in granulomas  Risk factors  Immunocompromised (HIV, malignancy, DM, extremes of age)  Close contacts or occupational exposure  Medically underserved, low-income populations
  58. 58. + TB symptoms and signs  Primary TB  Only 10% of exposed individuals develop primary TB  Constitutional symptoms  Coughmost common symptoms of pulmonary TB  Initially nonproductive or nonspecific sputum  Hemoptysis may be presenting complaint  Pleuritic chest pain  Night sweats  “classic” presentation is uncommon
  59. 59. + TB  Postprimary TB (reactivation TB)  Lifetime risk in immunocompetent individual is 10% to 15%  In HIV-positive patients  37% with disease in 6 months  10% incidence of disease per year  Signs and symptoms similar to primary TB
  60. 60. + TB extrapulmonary  Lymphadenitis (scrofula)   Pleural effusion   Pott’s disease (spinal)spinal cord injury possible, lumbar infection may lead to psoas abscess acute disseminated   Small and unilateral, diagnosis through pleurocentesis Bone and joint infection   Most common EPTB, enlarging, painless, erythematous firm mass near cervical nodes, do NOT I and D Generalized systemic illness, typically in elderly and HIV patients, fever, weight loss, anorexia, weakness, SIADH is common, often associated with meningitis CNS   6% of cases, peak in newborn to 4 years, SIADH, tuberculosis meningitis CSF analysislowest glucose CSF levels of any meningitis
  61. 61. + TB diagnosis  TB skin testingread 48-72 hours later, induration not erythema  15mm in low-risk, immunocompetent patients  10mm in high-risk immunocopetent patients  5mm in HIV, Close contacts infectious TB, abnormal CXR, immunocompromised from steroids
  62. 62. + TB medical therapy  Latent TBinfections without active disease, chemoprophylaxis with isoniazid for 9 months  Active TBtreated for 6 months, 4 drugs until resistance pattern determined, after 2 months may discontinue pyrazinamide if TB isolates do not demonstrate resistance  Extrapulmonary TB->treat for 6 months  CNS infection (tuberculous meningitis) is the exception, requires 912 months of treatment  Consider steroids for CNS and pericardial TB
  63. 63. + Treatment of TBdrugs  First line agents  Isoniazid (INH)    8% resistance rate Prevent INH-related seizures: supplement with pyridoxine (B6) Rifampin    Orange discoloration of bodily fluids Oral contraception failure Pyrazinamide (PZA)   Hepatotoxicity, polyarthralgias Ethambutol (ETH)  Prevents emergence of RIF resistance  Retrobulbar neuritisdecreased visual acuity or red/green color blindness
  64. 64. + Treatment cont.  Noncompliant patients   Court-ordered directly observed therapy (DOT)   Uncooperative and potentially infectious patients may be compelled to comply Incarceration as last resort In pregnancy  INH, RIF, ETH cross placenta and are safe
  65. 65. + Viral Pneumonia  Influenza  Varicella  Cytomegalovirus  hantavirus
  66. 66. + influenza  Often associated with bacterial superinfection (s. aureus)  Diagnosis: nasopharyngeal swab culture for influenza aid diagnosis  CXR shows diffuse bilateral infiltrates
  67. 67. + Varicella  Symptoms and signs: pneumonia may present with chest pain and hemoptysis preceded by a rash  More severe in adults  Managementmandates admission for treatment with acyclovir
  68. 68. + cytomegalovirus  Most common in solid organ transplant and bone marrow transplant recipients  Often presents simultaneously with pneumocystis pneumonia  Management   IV ganciclovir or foscarnet plus immunoglobulin therapy CXR  Bilateral interstitial pattern
  69. 69. + Hantavirus  Aerosolized contaminated material from rodent feces or urine  Southwest US  Symptoms and signsflu-like symtpoms that progress to respiratory distress and shock  DiagnosisCXR reveals bilateral infiltrates
  70. 70. + Fungal Pneumonia  Histoplasma capsulatum, blastomyces dermatitides and coccidioides present in the soil in various geographic areas of the US  Histoplasma capsulatum in the mississippi and Ohio River valleys  Coccidioides immitis in desert areas of the Southwest  Symptoms and signs vary from acute or chronic pneumoina to asymptomatic granulomas on CXR  Diagnosishilar adenopathy

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