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Interesting Case presentations

  1. 1. Case Studies Gamal Rabie Agmy, MD, FCCP Professor of chest Diseases, Assiut university
  2. 2. Second Session SIX CASES
  3. 3. Case No. 1
  4. 4. • A 45-year-old nonsmoking woman was referred for an opinion regarding management of recurrent pneumothorax. • She was well until age 27 when she had a right- sided spontaneous pneumothorax. • Two years later, she had another right-sided pneumothorax and underwent thoracotomy and stapling of the right lung apex. She has had no further episodes since that time. • She is seeing a dermatologist for multiple facial papules, but otherwise, her general health is excellent. She denies any respiratory symptoms.
  5. 5. • Results of a physical examination are normal other than multiple skin colored papules over the central face and nose.
  6. 6. • Results of a chest radiograph demonstrated right apical pleural thickening but were otherwise normal. The C-T scan
  7. 7. The most likely diagnosis of this condition is: A. Langerhans cell histiocytosis. B. Lymphangioleiomyomatosis (LAM). C. Sarcoidosis. D. Birt-Hogg-Dubé syndrome (BHDS).
  8. 8. • The CT scan reveals several cysts in the left lung and scarring at the right apex related to the previous surgery.
  9. 9. • A history of recurrent pneumothorax, lung cysts, and skin lesions (fibrofolliculomas) with normal lung function is consistent with the diagnosis of Birt-Hogg-Dubé syndrome (BHDS) (choice D is correct).
  10. 10. • Langerhans cell histiocytosis is characterized by diffuse cystic disease of the lung, spontaneous pneumothorax, and airway obstruction related to cigarette smoking. These findings are not present in this patient (choice A is incorrect). • Similarly, airflow obstruction, recurrent pleural effusions, and diffuse pulmonary disease are characteristic of LAM, features that also are not found in this patient (choice B is incorrect).
  11. 11. • Sarcoidosis is a granulomatous inflammatory lung disease characterized by diff use parenchymal opacities, airflow obstruction, and possibly, skin lesions. • Lupus pernio, one of the skin manifestations of sarcoidosis, appears as purple nodules on the nose, cheeks, and ears, and none of these features is present in this patient (choice C is incorrect).
  12. 12. • BHDS is an autosomal dominantly inherited genodermatosis that predisposes a person to the development of cutaneous hamartomas (fi brofolliculomas), kidney neoplasms, lung cysts, and spontaneous pneumothorax. • The BHD locus has been mapped to the short arm of chromosome 17(17p11.2). BHD is composed of 14 exons, and more than 40 unique mutations in BHD have been reported. • Most BHD germline mutations are frameshift or nonsense mutations that are predicted to truncate the BHD protein, folliculin.
  13. 13. • Patients exhibit multiple 1- to 5-mm white- colored or skin-coloured papules distributed over the face, neck, and/or upper trunk, which histologically, are fibrofolliculomas.
  14. 14. • BHDS is associated with a unique histologic spectrum of bilateral and multifocal kidney tumors ranging from hybrid oncocytic (67%) to chromophobe renal carcinoma (23%) to oncocytic renal carcinoma (3%). • Clear cell renal cell carcinoma (3%) has also been reported in a few patients with BHDS. Pulmonary manifestations are a major feature of BHDS. • Most patients who are affected (89%) have multiple pulmonary cysts. The number of lung cysts is clearly related to the risk of pneumothorax. • Approximately one-quarter of patients with BHDS have a history of one or more pneumothoraces. Smoking does not appear to be a risk factor for pneumothorax in this population
  15. 15. Lung Cysts By Gamal Rabie Agmy , MD , FCCP Professor of Chest Diseases ,Assiut University
  16. 16. Lung Cysts Differential Diagnosis Pulmonary fibrosis (Honeycombing) Lymphangliomyomatosis Langerhans cell histiocytosis Lymphocytic Interstitial Pneumonia (LIP) Birt-Hogg-Dubé syndrome (BHDS)
  17. 17. Rough Reticular Fine Reticular Traction Bronchiectasis and Interface sign Honey combing UIP UIP or NSIP
  18. 18. Usual Interstitial Pneumonia UIP HRCT Findings Reticular opacities, thickened intra- and interlobular septa Irregular interfaces Honey combing and parenchymal distorsion Ground glass opacities (never prominent) Basal and subpleural predominance
  19. 19. Basal and subpleural distribution UIP
  20. 20. The Many ‘HRCT Faces’ of NSIP Honeycombing not a prominent feature !!!!
  21. 21. Lymphangioleiomyomatosis (LAM) HRCT Morphology Thin-walled cysts (2mm - 5cm) Uniform in size / rarely confluent Homogeneous distribution Chylous pleural effusion Lymphadenopathy in young women
  22. 22. Lymphangioleiomyomatosis (LAM)
  23. 23. Tuberous Sclerosis (young man)
  24. 24. Langerhans Cell Histiocytosis HRCT Findings Small peribronchiolar nodules (1-5mm) Thin-walled cysts (< 1cm), Bizarre and confluent Ground glass opacities Late signs: irreversible / parenchymal fibrosis Honey comb lung, septal thickening, bronchiectasis
  25. 25. 1 year later Peribronchiolar Nodules Cavitating nodules and cysts Langerhans Cell Histiocytosis
  26. 26. Langerhans Cell Histiocytosis
  27. 27. Langerhans Cell Histiozytosis Key Features Upper lobe predominance Combination of cysts and noduli Characteristic stages Increased Lung volume Sparing of costophrenic angle S M O K I N G
  28. 28. Langerhans Cell Histiocytosis
  29. 29. Langerhans Cell Histiocytosis Differential Diagnosis Only small nodules Sarcoidosis, Silicosis Only cysts idiopathic Fibrosis LAM Destructive emphysema
  30. 30. .......after cessation of smoki
  31. 31. Benign lymphoproliferative disorder Diffuse interstitial infiltration of mononuclear cells Not limited to the air ways as in follicular Bronchiolitis LIP = Lymphocytic Interstitial Pneumonia
  32. 32. Sjögren: LIP
  33. 33. LIP = Lymphocytic Interstitial Pneumonia Rarely idiopathic In association with: Sjögren’s syndrome Immune deficiency syndromes, AIDS Primary biliary cirrhosis Multicentric Castlemean’s disease
  34. 34. Sjoegren disease Dry eye and dry mouth Fibrosis, bronchitis and bronchiolitis LIP Overlap Sarcoid, DM/PM, MXCT SLE, RA (pleural effusion) Up to 40 x increased risk for lymphoma (mediastinal adenopathy) and 2 x times increased risk for neoplasma
  35. 35. Young woman Dry mouth Smoker LAM LIP Histiocytosis
  36. 36. Wegener‘s disease
  37. 37. Rheumatoid Arthritis
  38. 38. History of recurrent pneumothorax, lung cysts, and skin lesions (fibrofolliculomas) with normal lung function is consistent with the diagnosis of Birt-Hogg-Dubé syndrome Birt-Hogg-Dubé syndrome
  39. 39. • BHDS is an autosomal dominantly inherited genodermatosis that predisposes a person to the development of cutaneous hamartomas (fi brofolliculomas), kidney neoplasms, lung cysts, and spontaneous pneumothorax. • The BHD locus has been mapped to the short arm of chromosome 17(17p11.2). BHD is composed of 14 exons, and more than 40 unique mutations in BHD have been reported. • Most BHD germline mutations are frameshift or nonsense mutations that are predicted to truncate the BHD protein, folliculin.
  40. 40. Centrilobular Emphysema
  41. 41. Panlobular Emphysema
  42. 42. Mosaic pattern and its differential
  43. 43. Where is the pathology ??????? in the areas with increased density meaning there is ground glass in the areas with decreased density meaning there is air trapping
  44. 44. Pathology in black areas Airtrapping: Airway Disease Bronchiolitis obliterans (constrictive bronchiolitis) idiopathic, connective tissue diseases, drug reaction, after transplantation, after infection Hypersensitivity pneumonitis granulomatous inflammation of bronchiolar wall Sarcoidosis granulomatous inflammation of bronchiolar wall Asthma / Bronchiectasis / Airway diseases
  45. 45. Airway Disease what you see…… In inspiration sharply demarcated areas of seemingly increased density (normal) and decreased density demarcation by interlobular septa In expiration ‘black’ areas remain in volume and density ‘white’ areas decrease in volume and increase in density INCREASE IN CONTRAST DIFFERENCES AIRTRAPPING
  46. 46. Bronchiolitis obliterans
  47. 47. Early Sarcoidosis
  48. 48. Chronic EAA
  49. 49. Hypersensitivity pneumonitis Extr. Allerg. Alveolitis (EAA)HRCT Morphology chronic: fibrosis Intra- / interlobular septal thickening Irregular interfaces Traction bronchiectasis acute - subacute acinar (centrilobular) unsharp densities ground glass (patchy - diffuse)
  50. 50. Pathology in white Areas Alveolitis / Pneumonitis Ground glass desquamative intertitial pneumoinia (DIP) nonspecific interstitial pneumonia (NSIP) organizing pneumonia In expiration both areas (white and black) decrease in volume and increase in density DECREASE IN CONTRAST DIFFERENCES
  51. 51. DI P
  52. 52. Cellular NSIP
  53. 53. Mosaic Perfusion Chronic pulmonary embolism LOOK FOR Pulmonary hypertension idiopathic, cardiac disease, pulmonary disease
  54. 54. CTEPH = Chronic thrombembolic pulmonary hypertension
  55. 55. Case No. 2
  56. 56. • A 34-year-old woman is admitted with cough, fever, shortness of breath, and malaise. • She has no past medical history and was well until 5 days prior to admission when she developed a sore throat, low-grade fever, and non-productive cough. • After 3 days, she used acetaminophen and pseudoephedrine for increasing sputum and develops some anterior chest wall pain and increased cough.
  57. 57. • On the day of admission, she begins to have increasing shortness of breath, fatigue, and malaise. • She denies contact with sick individuals or travel, and she works as an administrative assistant in a law office • Her temperature is 39.2C, BP is 90/55 mm Hg, heart rate is 132/min, and respiratory rate is 34/min. • Her oxygen saturations are 84% on room air.
  58. 58. • She is using accessory muscles of respiration and is in moderate respiratory distress. • Fine inspiratory crackles are heard in all lung fields, with decreased breath sounds at the left lung base.
  59. 59. • Her WBC count is 15,400/L (15.4 × 109/L), hematocrit concentration is 41% (0.41), and platelet count is 185 × 103/L (185 × 109/L). • Her BUN level is 11 mg/dL (3.93 mmol/L). • Creatinine level is 0.9 mg/dL (79.6 mol/L) • Arterial blood gas analysis reveals a pH of 7.55, Pco2 of 20 mm Hg, and a Po2 of 48 mm Hg.
  60. 60. • Chest radiograph are shown
  61. 61. • CT scan image
  62. 62. • Due to increasing respiratory fatigue and hypoxemia, she is intubated. • Her sputum Gram stain shows 2 WBCs, 5 to 10 squamous epithelial cells, 2 gram-positive cocci, 1 gram-positive rods, and 1 gram-negative bacilli. • A multiplex diagnostic polymerase chain reaction (PCR) of her nasal lavage fluid performed in the ED shows a positive result for rhinovirus.
  63. 63. Which is the next best step? A. Start ceftriaxone and azithromycin therapy. B. Start methylprednisolone therapy. C. Start amantadine therapy. D. Start trimethoprim/sulfamethoxazole therapy
  64. 64. • This patient has a fever, leukocytosis, diffuse alveolar opacities, and respiratory failure, along with multiple organisms seen on Gram stain of the sputum and rhinovirus detected on nasal lavage results. • Thus, community-acquired pneumonia (CAP) is of high causative probability, and appropriate antibiotic administration must be rapid in order to improve survival. • Therefore, ceftriaxone and azithromycin should be administered immediately (choice A is correct).
  65. 65. • The use of rapid viral testing is becoming more common, especially with multiplex PCR. In these instances, a virus respiratory panel can be applied to a nasal or bronchial lavage. • The most common panel includes rhinovirus, coronavirus, infl uenza, parainfl uenza, respiratory syncytial virus (RSV), adenovirus, and metapneumovirus. • Thus, the rapid detection of these viruses in cases of suspected CAP is becoming more common. However, a sole viral cause for CAP occurs in 10% to 30% of cases, depending on method of testing.
  66. 66. • In a prospective study of 105 adults with suspected CAP evaluated by conventional microbiologic techniques and multiplex real-time PCR, respiratory viral infections were detected in 15 patients (14%) and 59 patients (56%) by conventional methods and PCR, respectively. • Rhinovirus occurred in 31% of patients, coronavirus and infl uenza in 23%, and band parainfl uenza in 13%. In the patients in whom rhinovirus or coronavirus were implicated, another pathogen was identified 93% of the time, most often bacterial.
  67. 67. • Thus, rhinovirus or coronavirus are likely not the cause of pneumonia but, rather, impair upper airway defenses, leading to lower airway disease from a bacterial agent. • In patients with RSV and influenza, a second organism was found in a minority of patients, and thus, treatment focused on these viruses is warranted.
  68. 68. • Another study detected at least one virus by PCR in 32% of patients with CAP (lobar pneumonia), 5% of control subjects, and a surprising 55% of patients with diff use lower respiratory opacities. • Adenovirus, rhinovirus, and RSV were most commonly associated with CAP, while influenza was the most common agent seen in diff use lower respiratory opacities. • Therefore, in many patients with CAP, viral isolation does not preclude the use of antibiotics until other causes have been eliminated. It should also not delay the early administration of antibiotics in patients with CAP
  69. 69. • The use of methylprednisolone may be indicated, but in the absence of an etiology of this patient’s opacities, it is not warranted and could be harmful (choice B is incorrect). • Although influenza can cause a similar picture, amantadine is not the treatment of choice for severe influenza due to resistance (oseltamivir is preferred) (choice C is incorrect). • Trimethoprim/sulfamethoxazole is not an appropriate antibiotic for severe CAP (choice D is incorrect). This patient’s sputum culture grew Streptococcus pneumoniae, and she recovered after antibiotic administration
  70. 70. Antibiotic Strategy in CAP Gamal Rabie Agmy, MD,FCCP Professor of Chest Diseases, Assiut university
  71. 71. 79 Pneumonias – Classification • Community AcquiredCAP • Health Care AssociatedHCAP • Hospital AcquiredHAP • ICU AcquiredICUAP • VentilatorAcquiredVAP Nosocomial Pneumonias
  72. 72. *HCAP: diagnosis made < 48h after admission with any of the following risk factors: (1)hospitalized in an acute care hospital for > 48h within 90d of the diagnosis; (2) resided in a nursing home or long-term care facility; (3) received recent IV antibiotic therapy, chemotherapy, or wound care within the 30d preceding the current diagnosis; and (4) attended a hospital or hemodialysis clinic HCAP
  73. 73. Infection of the lung parenchyma in a person who is not hospitalized or living in a long-term care facility for ≥ 2 weeks. This pneumonia develops in the outpatient setting or within 48 hours of admission to a hospital. Definition of CAP
  74. 74. Symptoms: • Respiratory: Cough dry or productive, mucopurulent sputum , sometimes rusty, dyspnea, sometimes pleuritic chest pain • Non-respiratory: Fever, body aches, altered mental state, vomiting or diarrhea. The clinical diagnosis of CAP
  75. 75. Signs: Generally: Fever, sometimes hypothermia, tachycardia, tachypnea. Local: signs of consolidation The clinical diagnosis of CAP
  76. 76. 84 CAP – The Two Types of Presentations Classical • Sudden onset of CAP • High fever, shaking chills • Pleuritic chest pain, SOB • Productive cough • Rusty sputum, blood tinge • Poor general condition • High mortality up to 20% in patients with bacteremia • S.pneumoniae causative • Gradual & insidious onset • Low grade fever • Dry cough, No blood tinge • Good GC – Walking CAP • Low mortality 1-2%; except in cases of Legionellosis • Mycoplasma, Chlamydiae, Legionella, Ricketessiae, Viruses are causative Atypical
  77. 77. Sputum Gram stain: is a rapid and inexpensive test that can help a lot: • Differentiate Gm –ve from Gm +ve bacteria. • Excess pus cells without organism suspect atypical infection. The Bacteriological Diagnosis of CAP
  78. 78. Cultures to identify the causative organism: Sputum cultures are not recommended in cases of CAP except in certain occasions: • Patients admitted in hospital or ICU. • Patients who do not respond to empirical antibiotic therapy. • Suspection of resistant strains of S.pneumoniae. The Bacteriological Diagnosis of CAP
  79. 79. Blood Culture: Recommended for all patients with moderate and high severity CAP, preferably before antibiotic therapy is commenced. Examination of sputum for Mycobacterium TB The Bacteriological Diagnosis of CAP
  80. 80. 88 CAP – Pathogenesis Inhalation Aspiration Hematogenous
  81. 81. 90 PORT Scoring – PSI Clinical Parameter Scoring Age in years Example For Men (Age in yrs) 50 For Women (Age -10) (50-10) NH Resident 10 points Co-morbid Illnesses Neoplasia 30 points Liver Disease 20 points CHF 10 points CVD 10 points Renal Disease (CKD) 10 points Clinical Parameter Scoring Clinical Findings Altered Sensorium 20 points Respiratory Rate > 30 20 points SBP < 90 mm 20 points Temp < 350 C or > 400 C 15 points Pulse > 125 per min 10 points Investigation Findings Arterial pH < 7.35 30 points BUN > 30 20 points Serum Na < 130 20 points Hematocrit < 30% 10 points Blood Glucose > 250 10 points Pa O2 10 points X Ray e/o Pleural Effusion 10 points Pneumonia Patient Outcomes Research Team (PORT)
  82. 82. 91 Classification of Severity - PORT Predictors Absent Class I  70 Class II 71 – 90 Class III 91 - 130 Class IV > 130 Class V
  83. 83. 92 CAP – Management based on PSI Score PORT Class PSI Score Mortality % Treatment Strategy Class I No RF 0.1 – 0.4 Out patient Class II  70 0.6 – 0.7 Out patient Class III 71 - 90 0.9 – 2.8 Brief hospitalization Class IV 91 - 130 8.5 – 9.3 Inpatient Class V > 130 27 – 31.1 IP - ICU
  84. 84. 93 CURB 65 Rule – Management of CAP CURB 65 Confusion BUN > 30 RR > 30 BP SBP <90 DBP <60 Age > 65 CURB 0 or 1 Home Rx CURB 2 Short Hosp CURB 3 Medical Ward CURB 4 or 5 ICU care
  85. 85. 95 CAP – Criteria for ICU Admission Major criteria  Invasive mechanical ventilation required  Septic shock with the need of vasopressors Minor criteria (least 3)  Confusion/disorientation  Blood urea nitrogen ≥ 20 mg%  Respiratory rate ≥ 30 / min;  Core temperature < 36ºC  Severe hypotension;  PaO2/FiO2 ratio ≤ 250  Multi-lobar infiltrates  WBC < 4000 cells;  Platelets <100,000
  86. 86. The Radiological Diagnosis of CAP
  87. 87. 97 CAP – Value of Chest Radiograph • Usually needed to establish diagnosis • It is a prognostic indicator • To rule out other disorders • May help in etiological diagnosis J Chr Dis 1984;37:215-25
  88. 88. 98 Infiltrate Patterns and Pathogens CXR Pattern Possible Pathogens Lobar S.pneumo, Kleb, H. influ, Gram Neg Patchy Atypicals, Viral, Legionella Interstitial Viral, PCP, Legionella Cavitatory Anerobes, Kleb, TB, S.aureus, Fungi Large effusion Staph, Anaerobes, Klebsiella
  89. 89. 99 Normal CXR & Pneumonic Consolidation
  90. 90. 100 Lobar Pneumonia – S.pneumoniae
  91. 91. 101 CXR – PA and Lateral Views
  92. 92. 102 Lobar versus Segmental - Right Side
  93. 93. 103 Lobar Pneumonia
  94. 94. 104 Special forms of Consolidation
  95. 95. 105 Round Pneumonic Consolidation
  96. 96. 106 Special Forms of Pneumonia
  97. 97. 107 Special Forms of Pneumonia
  98. 98. 108 Complications of Pneumonia
  99. 99. 109 Empyema
  100. 100. 110 Mycoplasma Pneumonia
  101. 101. 111 Mycoplasma Pneumonia
  102. 102. 112 Chlamydia Trachomatis
  103. 103. 113 Rare Types of Pneumonia
  104. 104. 114
  105. 105. Pneumonia Posterior intercostal scan shows a hypoechoic consolidated area that contains multiple echogenic lines that represent an air bronchogram.
  106. 106. Post-stenotic pneumonia Posterior intercostal scan shows a hypoechoic consolidated area that contains anechoic, branched tubular structures in the bronchial tree (fluid bronchogram).
  107. 107. Contrast-enhanced ultrasonography of pneumonia A: Baseline scan shows a hypoechoic consolidated area B: Seven seconds after iv bolus of contrast agent, the lesion shows marked and homogeneous enhancement C: The lesion remains substantially unmodified after 90 s.
  108. 108. The Treatment of CAP
  110. 110. MECHANISMS OF ACTION OF ANTIBACTERIAL DRUGS  Mechanism of action include:  Inhibition of cell wall synthesis  Inhibition of protein synthesis  Inhibition of nucleic acid synthesis  Inhibition of metabolic pathways  Interference with cell membrane integrity
  111. 111. EFFECTS OF COMBINATIONS OF DRUGS  Sometimes the chemotherapeutic effects of two drugs given simultaneously is greater than the effect of either given alone.  This is called synergism. For example, penicillin and streptomycin in the treatment of bacterial endocarditis. Damage to bacterial cell walls by penicillin makes it easier for streptomycin to enter.
  112. 112. EFFECTS OF COMBINATIONS OF DRUGS  Other combinations of drugs can be antagonistic.  For example, the simultaneous use of penicillin and tetracycline is often less effective than when wither drugs is used alone. By stopping the growth of the bacteria, the bacteriostatic drug tetracycline interferes with the action of penicillin, which requires bacterial growth.
  113. 113. EFFECTS OF COMBINATIONS OF DRUGS  Combinations of antimicrobial drugs should be used only for: 1. To prevent or minimize the emergence of resistant strains. 2. To take advantage of the synergistic effect. 3. To lessen the toxicity of individual drugs.
  114. 114. Patterns of Microbial Killing Concentration dependent – Higher concentration greater killing Aminoglycosides, Flouroquinolones, Ketolides, metronidazole, Ampho B. Time-dependent killing – Minimal concentration-dependent killing (4x MIC) – More exposure more killing Beta lactams, glycopeptides, clindamycin, macrolides, tetracyclines, bactrim
  115. 115. The Ideal Drug* 1. Selective toxicity: against target pathogen but not against host  LD50 (high) vs. MIC and/or MBC (low) 2. Bactericidal vs. bacteriostatic 3. Favorable pharmacokinetics: reach target site in body with effective concentration 4. Spectrum of activity: broad vs. narrow 5. Lack of “side effects”  Therapeutic index: effective to toxic dose ratio 6. Little resistance development
  116. 116. Resistance Physiological Mechanisms 1. Lack of entry – tet, fosfomycin 2. Greater exit  efflux pumps  tet (R factors) 3. Enzymatic inactivation  bla (penase) – hydrolysis  CAT – chloramphenicol acetyl transferase  Aminogylcosides transferases REVIEW
  117. 117. Resistance Physiological Mechanisms 4. Altered target  RIF – altered RNA polymerase (mutants)  NAL – altered DNA gyrase  STR – altered ribosomal proteins  ERY – methylation of 23S rRNA 5. Synthesis of resistant pathway  TMPr plasmid has gene for DHF reductase; insensitive to TMP (cont’d) REVIEW
  118. 118. Empirical Treatment is the recommended strategy in treatment of CAP and shouldn’t be delayed.
  119. 119. 132 CAP – Special Features – Pathogen wise Typical – S.pneumoniae, H.influenza, M.catarrhalis Blood tinged sputum - Pneumococcal, Klebsiella, Legionella H.influenzae CAP has associated of pleural effusion:S.Pneumoniae – commonest – penicillin resistance problem S.aureus, K.pneumoniae, P.aeruginosa S.aureus causes CAP in post-viral influenza; Serious CAP K.pneumoniae primarily in patients of chronic alcoholism P.Aeruginosa causes CAP in pts with CSLD or CF, Nosocom Aspiration CAP only is caused by multiple pathogens Extra pulmonary manifestations only in Atypical CAP
  120. 120. Outpatient treatment: Oral Respiratory Fluroquinolones OR Oral B-Lactam/ B-Lactamase + Oral New Macrolide OR IM 3rd Generation Cefalosporines + New Macrolide Recommendations for the Empirical Treatment:
  121. 121. In-patient treatment: Non-ICU: Intravenous ( IV )Respiratory fluoro- quinolone OR IV B-Lactam/ B-Lactamase + IV New Macrolide OR IV 3rd Generation Cephalosporin + IV New Macrolide Recommendations for the Empirical Treatment:
  122. 122. In-patient treatment: ICU: No Monotherapy. IV Respiratory fluoroquinolone + 3rd or 4th generation cephalosporin OR IV Imipenem + IV New Macrolide Recommendations for the Empirical Treatment:
  123. 123. In-patient treatment: ICU: No Monotherapy. IV Respiratory fluoroquinolone + 3rd or 4th generation cephalosporin OR IV Imipenem + IV New Macrolide Recommendations for the Empirical Treatment:
  124. 124. Special entities in ICU: Aspiration: As Before + i.v. Clindamycin OR Metronidazole Risk of Pseudomonas Infection: Antipseudomonal beta-lactam (3rd or 4th generation cephalosporin OR Piperacillin-tazobactam OR carbapenem) Plus (aminoglycoside OR antipseudomonal fluoroquinolone) For community-acquired methicillin-resistant Staphylococcus aureus infection (MRSA): Add Teicoplanin OR linezolid Alternative: Vancomycin (considering its renal side effects) Recommendations for the Empirical Treatment:
  125. 125. 138 Duration of Therapy • Minimum of 5 days • Afebrile for at least 48 to 72 h • No > 1 CAP-associated sign of clinical instability • Longer duration of therapy If initial therapy was not active against the identified pathogen or complicated by extra pulmonary infection
  126. 126. 139 Strategies for Prevention of CAP • Cessation smoking • Influenza Vaccine It offers 90% protection and reduces mortality by 80% • Pneumococcal Vaccine (Pneumonia shot) It protects against 23 types of Pneumococci 70% of us have Pneumococci in our RT It is not 100% protective but reduces mortality Age 19-64 with co morbidity of high for pneumonia Above 65 all must get it even without high risk • Starting first dose of antibiotic within 4 h & O2 status
  127. 127. 140 Switch to Oral Therapy  Four criteria  Improvement in cough, dyspnea & clinical signs  Afebrile on two occasions 8 h apart  WBC decreasing towards normal  Functioning GI tract with adequate oral intake  If overall clinical picture is otherwise favorable, hemodynamically stable; can switch to oral therapy while still febrile.
  128. 128. 141 Management of Poor Responders  Consider non-infectious illnesses  Consider less common pathogens  Consider serologic testing  Broaden antibiotic therapy  Consider bronchoscopy
  129. 129. 142 CAP – Complications  Hypotension and septic shock  3-5% Pleural effusion; Clear fluid + pus cells  1% Empyema thoracis pus in the pleural space  Lung abscess – destruction of lung - CSLD  Single (aspiration) anaerobes, Pseudomonas  Multiple (metastatic) Staphylococcus aureus  Septicemia – Brain abscess, Liver Abscess  Multiple Pyemic Abscesses
  130. 130. 143 CAP – So How Best to Win the War?  Early antibiotic administration within 4-6 hours  Empiric antibiotic Rx. as per guidelines (IDSA / ATS)  PORT – PSI scoring and Classification of cases  Early hospitalization in Class IV and V  Change Abx. as per pathogen & sensitivity pattern  Decrease smoking cessation - advice / counseling  Arterial oxygenation assessment in the first 24 h  Blood culture collection in the first 24 h prior to Abx.  Pneumococcal & Influenza vaccination; Smoking cessation
  131. 131. Case No. 3
  132. 132. • A 63-year-old man who is 15 months postoperative from a right single-lung transplant for idiopathic pulmonary fibrosis is seen in follow-up. • His initial postoperative course was unremarkable. • He was cytomegalovirus (CMV)-positive prior to transplant and received a graft from a CMV- positive donor.
  133. 133. • The patient reports that he has noted some mild dyspnea on exertion with an occasional dry cough and intermittent wheezing. • He has had subjective fevers but denies chills or weight loss. • His medications include tacrolimus, mycophenolate mofetil, and prednisone. Valganciclovir and trimethoprim- sulfamethoxazole were discontinued at 12 months.
  134. 134. • His last polymerase chain reaction test results were negative for CMV. • On physical examination, he is afebrile. • The right lung examination reveals scattered expiratory wheezes, and the left native lung reveals crackles. • The remainder of the examination results are unremarkable. Laboratory studies are within normal limits. • His tacrolimus level is 8 ng/mL. • His FEV1 has decreased by 5% since his last visit 2 months ago
  135. 135. His chest CT revealed
  136. 136. A histologic specimen obtained via bronchoscopy with transbronchial biopsy from the right upper lobe is shown.
  137. 137. The next best step in this patient’s management is which of the following? A. Administer a corticosteroid bolus and increase the tacrolimus dose. B. Begin evaluation for retransplantation. C. Continue current immunosuppression and begin IV ganciclovir. D. Decrease current immunosuppression and begin rituximab.
  138. 138. • This patient has developed a posttransplant lymphoproliferative disorder (PTLD) as seen in the pathology specimen showing numerous small lymphocytes and a reduction in immunosuppression and initiation of rituximab are indicated (choice D is correct). • PTLDs are reported more frequently following lung transplantation than following other types of solid-organ transplantation, with an incidence reported to range between 1.8% and 9.4%.
  139. 139. • The PTLDs are composed of a heterogeneous group of lymphoid proliferations of variable clonality. • B-cell non-Hodgkin lymphoma is the most frequent form of PTLD and have been associated with Epstein-Barr virus (EBV) activity, either serologically or by identification of viral DNA in tissue.
  140. 140. • Most PTLDs in solid organ transplant recipients are of recipient origin. There is no clear correlation between episodes of rejection, specific immunosuppressive drugs, and the development of PTLD. • Those patients who have negative serologic findings for EBV prior to transplantation and receive an organ from a donor who is EBV- positive, resulting in seroconversion, are at a significantly higher risk for developing PTLD. • Children are at higher risk due to their frequent EBV-negative status.
  141. 141. • The clinical features of PTLD in lung transplant recipients include development in the first or second posttransplant year, involvement of the allograft, and radiographic findings of solitary or multiple pulmonary nodules, mediastinal adenopathy, and/or nodular opacities, with multiple nodules in the right transplanted lung and fibrosis in the left native lung. • Extrapulmonary involvement of the skin, CNS, and GI tract has been described.
  142. 142. • Treatment for PTLD includes the anti-CD20 monoclonal antibody rituximab and a reduction in immunosuppression. • Case series using rituximab report complete remissions in the majority of patients, with minimal side effects. • In a series of B-cell patients with PTLD treated with rituximab and a decrease in immunosuppression, median relapse-free survival was 34 months as assessed by conventional imaging and PET scans.
  143. 143. • The most common reported side effect with rituximab is a transient infusion reaction. Pulmonary toxicity including interstitial pneumonitis, organizing pneumonia, pulmonary edema, and diffuse alveolar hemorrhage has been described. Adjunctive treatment of PTLD with antiviral therapy can be considered. Radiation, chemotherapy, and/or surgery are second-line treatment choices if the patient does not respond to rituximab.
  144. 144. • Throughout treatment, there must be a careful attempt to balance treatment of the PTLD and rejection. • With high-grade PTLD, as staged by standard lymphoma staging systems, mortality may be significant. An increased incidence of other nonlymphomatous malignancies, most commonly skin cancers, has been reported in the lung transplant population, and careful screening is recommended
  145. 145. • An increase in immunosuppression, not indicated for PTLD (choice A is incorrect) would be indicated for acute rejection, which usually occurs in the first year following lung transplantation and is characterized histologically by a lymphocytic vasculitis. • An increase would also be indicated for chronic rejection, characterized by a decline in pulmonary function, with pathologic findings showing obliterative bronchiolitis or a nondiagnostic bronchoscopy in the setting of a reduction in pulmonary function tests, the bronchiolitis obliterans syndrome.
  146. 146. • Retransplantation might be considered for refractory chronic rejection but would never be considered for PTLD (choice B is incorrect). • Ganciclovir and a reduction in immunosuppression might be indicated for the treatment of cytomegalovirus infection, also not present in this patient (choice C is incorrect)
  147. 147. MALIGNANT LYMPHOPROLIFRATIVE DISORDERS What is the difference between a leukemia and a lymphoma?  In leukemias the neoplastic cell originates in the bone marrow and the neoplastic cells are found predominantly in the bone marrow and peripheral blood.  In lymphomas, the neoplastic cell originates in the lymph nodes or spleen and causes the development of a solid tumor.  Some lymphomas have a “leukemic phase” where the neoplastic cells are found in the peripheral blood. They may be difficult to differentiate from a leukemia.
  148. 148. MALIGNANT LYMPHOPROLIFRATIVE DISORDERS Lymphomas  Lymphomas are divided into 2 major categories: Hodgkins lymphoma and non-Hodgkins lymphoma Hodgkins lymphoma:  Can occur at any age with peak incidences at 20-30 and over 50.  Patients present to the doctor with symptoms of lymphadenopathy and may have fever, night sweats, weight loss and malaise  Diagnosis depends upon finding the Reed- Sternberg (RS) cell (something a pathologist must identify)  Are divided into 2 basic types based on the histopathology of the involved lymph nodes
  149. 149. MALIGNANT LYMPHOPROLIFRATIVE DISORDERS  Nodular lymphocyte predominance – occasional or rare RS cell seen; rare, but has a good prognosis  Classic Hodgkins lymphoma which is further subdivided into: Nodular sclerosis - bands of collagen are seen in the lymph nodes. There are mature appearing lymphocytes (T helper cells) associated with varying numbers of granulocytes, macrophages and eosinophils. Numerous RS cells are seen. This is the most common form of the disease. Mixed cellularity – the lymph nodes contain proliferating lymphocytes, histiocytes, plasma cells, and eosinophils. There are a moderate number of RS cells Lymphocyte depleted – there are few lymphocytes and a predominance of RS cells Lymphocyte rich – there are numerous small T lymphocytes and occasional RS cells
  150. 150. MALIGNANT LYMPHOPROLIFRATIVE DISORDERS Extranodal Hodgkins lymphoma – involves tumors in bone marrow, liver, or spleen  Lab features – normochromic, normocytic anemia with transitory increase in lymphocytes, monocytes, eosinophils, and sometimes platlets  Prognosis depends upon  The clinical stage of the disease (see next slide)  The histiologic type of the disease – in general, the prognosis is better the higher the number of lymphocytes and the lower the number of RS cells  Treatment  Combination chemotherapy  Radiation  A combination of chemotherapy and radiation  Cure rates are 80% or more, particularly if diagnosis occurs in an early stage of the disease.
  152. 152. MALIGNANT LYMPHOPROLIFRATIVE DISORDERS Non-Hodgkins lymphoma (malignant lymphoma) Many are associated with specific chromosomal translocations Can be grouped morphologically by cell size into  Small  Intermediate  Large Can be grouped functionally into  B cell  T cell  Null cell
  153. 153. MALIGNANT LYMPHOPROLIFRATIVE DISORDERS Can be grouped based on cell maturity into  Well differentiated  Poorly differentiated Can be grouped based on how aggressive the disease is into  Low grade  Intermediate grade  High grade
  155. 155. MALIGNANT LYMPHOPROLIFRATIVE DISORDERS Prognosis –  Prognosis worsens generally with increased cell size  Prognosis worsens with decreased differentiation of the malignant cell  Low grade lymphomas have a better prognosis than high grade lymphomas
  156. 156. MALIGNANT LYMPHOPROLIFRATIVE DISORDERS Multiple myeloma (plasma cell myeloma)  This is usually seen in older adults  When the patient is first diagnosed the following are usually seen: Multiple bone lesions with bone marrow infiltration of malignant cells Monoclonal gamopathy (usually IgG or IgA) Generalized hypogammaglobulinemia Bence Jones proteinuria  What does this all mean? A single immunoglobulin(antibody) is produced in excess = monoclonal gamopathy
  157. 157. MALIGNANT LYMPHOPROLIFRATIVE DISORDERS Synthesis of normal immunoglobulins is suppressed = generalized hypogammaglobulinemia There is an overproduction of light chains resulting in light chains being found in the urine = Bence Jones proteinuria  A common complication is renal impairment  On a peripheral smear, rouleaux is the hallmark of the disease and occasional circulating plasma cells may be seen
  158. 158. MALIGNANT LYMPHOPROLIFRATIVE DISORDERS  Waldenstrom’s macroglobulinemia  This is a plasma cell dyscrasia (abnormality) in which a monoclonal IgM is secreted.  Soft tissue involvement rather than bone marrow involvement is seen  Patients have problems with hyperviscosity of the blood.
  159. 159. MALIGNANT LYMPHOPROLIFRATIVE DISORDERS Heavy chain disease  This results from an overproduction of abnormal heavy chains.  Clinically the patients present with symptoms typical of malignant lymphoma.
  160. 160. Case No. 4
  161. 161. • A 66-year-old man complains of increasing shortness of breath at rest and with exertion accompanied by cough productive of purulent sputum for the last 5 days. • He notes he had upper respiratory symptoms 1 week ago consisting of a dry cough, nasal congestion, and an intermittent fever up to 38.3C, and his fever still persists. • His past medical history is significant for coronary artery disease.
  162. 162. • Physical examination: Moderately short of breath Temperature of 38.3C, Respiratory rate of 24/min Decreased breath sounds in the left mid chest laterally Cardiac examination without a murmur or S3.
  163. 163. • Laboratory findings: WBC count of 14,300/L (14.3 × 109/L) with a left shift Hematocrit concentration of 42% (0.42).
  164. 164. Chest radiograph
  165. 165. CT scan of the chest
  166. 166. Ultrasound of the left chest are obtained
  167. 167. • Thoracentesis is performed, showing:  Cloudy pleural fluid  Protein level of 3.9 g/dL (39 g/L), Lactate dehydrogenase level of 1,213 U/L (20.3 kat/L) (serum: 214 U/L, 3.6 kat/L), Glucose level of 32 mg/dL (1.8 mmol/L), and pH of 7.15. Gram stain is positive for Gram-positive diplococci
  168. 168. Which is the most appropriate next therapeutic step for this patient in addition to starting antibiotics? A. Image-guided large-bore chest tube (32F) placement, streptokinase. B. Image-guided small-bore chest tube (14F) placement. C. Continue antibiotics with no additional intervention. D. Decortication.
  169. 169. • This patient has a complicated parapneumonic effusion evidenced by a loculated pleural effusion seen on chest radiograph (moving up the lateral chest wall and not obeying the law of gravity), chest CT scan (with similarly gravity defying fluid), and ultrasound showing multiple septations (loculations). • The low pleural fluid pH and low pleural fluid glucose indicate the need for small-bore chest tube drainage, ideally placed under image guidance, in addition to antibiotic therapy (choice B is correct).
  170. 170. • At a minimum, antibiotic therapy is required, but drainage must also occur (choice C is incorrect), with a pH 7.20 being the most powerful predictor of the need for chest tube drainage. • Purulent, turbid, cloudy, or loculated fluid, in addition to organisms on fluid Gram stain, are also all indications for tube placement in a parapneumonic effusion. Complicated parapneumonic effusions and empyema occupy a continuum of disease, with the distinction often blurred, as many confine the term empyema to the presence of frank pus.
  171. 171. • The failure of the C-reactive protein level to fall by 50% in a patient with community-acquired pneumonia is associated with increased incidence of empyema and an adverse outcome. Antibiotics must be selected, recognizing a distinct difference in the organisms causing community-acquired vs hospital-acquired pleural space infections. • Community-acquired pleural space infections have a greater proportion of Streptococcus species and anaerobes. • Hospital-acquired empyemas have a greater predominance of Staphylococci, including methicillin-resistant Staphylococcus aureus and Enterobacteriaceae
  172. 172. • A small-bore chest tube (10-14 F) is adequate for most pleural infections and is the recommendation of the 2010 British Thoracic Society pleural diseases guidelines. Regular flushing of these small-bore catheters to prevent blockage is recommended. Ideally, chest tube insertion should be performed under image guidance.
  173. 173. • However, successful drainage of infected pleural fluid is central to management, regardless of the chest tube size chosen. • Most importantly, the addition of streptokinase does not improve survival or reduce hospital time, regardless of the chest tube size chosen (choice A is incorrect).
  174. 174. • Currently, there is no indication for the routine use of intrapleural fibrinolytics in pleural infection. Only patients with persistent pleural-related sepsis and/or a residual pleural fluid collection should be referred for evaluation for surgical intervention (choice D is incorrect). • This patient has not had an attempt at pleural drainage and antibiotic therapy. The exact timing and indications for surgical intervention in complicated parapneumonic effusions and empyema remain controversial.
  175. 175. Pleural Ultrasound By Gamal Rabie Agmy , MD , FCCP Professor of Chest Diseases ,Assiut University
  176. 176. the "seashore sign" (Fig.3).
  177. 177. Absent lung sliding Exaggerated horizontal artifacts Loss of comet-tail artifacts Broadening of the pleural line to a band Lung point Loss of lung impulse The key sonographic signs of Pneumothorax
  178. 178. Case No. 5
  179. 179. • A 57-year-old man was in good health until 2 months ago when he noted some difficulty walking. At first, he felt some fatigue when walking from the parking lot to his office at work. • However, he then noted his feet catching on the edge of stairs, and he had to use his arms to rise up from a chair. • Over the subsequent weeks, he began to notice difficulty lifting objects over his head, and at this time, his wife noted his eyes were “droopy.”
  180. 180. • He was referred by his primary care physician to a neurologist who documented a neurologic examination with normal cognitive function and memory. • He was slightly dysarthric. • His pupils were round and reactive to light, and extraocular movements were normal, but there was bilateral ptosis
  181. 181. • Muscle bulk and tone were normal and there were no fasciculations. Muscle strength was 3- 4/5 in the proximal lower extremities but normal elsewhere. His deep tendon reflexes were diminished at all sites. There was no ataxia of the upper limbs. • His gait was slow, and he had difficulty lifting his legs, as well as difficulty getting from a sitting to a standing position
  182. 182. • The patient has been treated for hypertension and type 2 diabetes for a number of years. He works as a lab technician in a steel mill. He has smoked 1 pack of cigarettes a day for 25 years. • A neurologic evaluation is initiated, and as part of his routine testing, • The patient is referred to your clinic for evaluation of his thoracic abnormalities
  183. 183. Chest X-ray
  184. 184. C-T scan chest
  185. 185. Which of the following findings gathered with additional testing would be consistent with this patient’s presentation and underlying problem? A. Aortography demonstrating an aortic dissection involving the spinal arteries at a thoracic level. B. CT-guided biopsy of the thoracic abnormalities revealing squamous cell carcinoma. C. Serum antibodies directed against the acetylcholine receptor. D. Increased tendon reflexes and strength after maximal isometric contraction of a muscle group
  186. 186. • This patient has Lambert-Eaton myasthenic syndrome (LEMS), a neuromuscular disorder similar in some respects to myasthenia gravis and strongly associated with lung cancer. • This patient’s chest imaging reveals a large mass in the aortopulmonary window and a peripheral lung nodule on the left. • CT-guided biopsy of the peripheral nodule revealed small cell lung cancer (SCLC). • One clinical feature of LEMS that is distinct and different from myasthenia is postexercise or postactivation facilitation, which can sometimes lead to improved deep tendon reflexes or improvement in weakness by examining the patient before and after maximal isometric contraction (choice D is correct).
  187. 187. • This phenomenon can also be demonstrated at the time of electromyography, when repetitive nerve stimulation leads to an increase in the compound muscle action potential amplitude, a means of distinguishing LEMS from myasthenia gravis electrophysiologically. • The radiologic abnormalities do not suggest an aortic dissection, and aortic dissection with spinal cord involvement would not explain the full range of this patient’s neurologic symptoms and findings (choice A is incorrect)
  188. 188. • LEMS has been shown to result from a disordered release of acetylcholine from the motor neuron, not an abnormality of the acetylcholine receptor and not from blocking antibodies against the receptor, as have been described in myasthenia gravis (choice C is incorrect). • Instead, antibodies directed against the voltage- gated calcium channel (VGCC) have been shown to play a central role in LEMS, creating a mechanism by which acetylcholine release may be impaired. Antibodies to VGCC were identified in this patient
  189. 189. • LEMS is rare and likely much less common than myasthenia gravis. Approximately one- half of LEMS cases are associated with malignancy, primarily SCLC (choice B is incorrect). • The incidence of LEMS in patients with SCLC is estimated to be approximately 3%. • Other tumors that have been associated with LEMS include atypical carcinoid, malignant thymoma, and Hodgkin lymphoma
  190. 190. • Initial symmetric limb weakness is a presenting symptom in the vast majority of patients with LEMS and is somewhat unusual as the predominant early symptom for myasthenia gravis, a disorder with very prominent early ocular symptoms. • However, ptosis is common in LEMS. Muscle weakness can be profound in LEMS, and this disorder should be included in the differential diagnosis of patients who have undiagnosed neuromuscular respiratory failure.
  191. 191. • Signs of autonomic dysfunction are also common in LEMS, with sluggish pupillary light reflexes and reduced salivation being most common. The diagnosis of LEMS rests on the clinical presentation, with confirmation by detection of VGCC antibodies and a typical electrodiagnostic study
  192. 192. • Treatment of LEMS includes treatment of the underlying malignancy, if present. Additional therapies, including plasmapheresis and immunosuppression, are often required, as well
  193. 193. Case No. 6
  194. 194. • You are asked to evaluate a 62-year-old man for an abnormal chest CT. • The patient reports that he was in his usual state of health until 2 months ago when he began to notice the onset of dyspnea when performing his usual activities. He reports a dry cough without hemoptysis. • Review of systems is notable for a 20-lb (9-kg) unintentional weight loss and some blurry and double vision.
  195. 195. • For the past 2 weeks he has had several episodes of dizziness, a sensation of the “room spinning,” and an unsteady feeling when he walks. • He has recently lost his balance on two occasions. A friend said he has been slurring his speech. • He is a 100 pack-year smoker. On physical examination, the patient is in no distress. • Lung examination is clear
  196. 196. • Neurologic examination reveals: Diplopia Ataxic gait difficulty with finger-to-nose testing. He has a mild tremor. There is nystagmus. There are no focal motor or sensory abnormalities. • The remainder of the physical examination results are unremarkable.
  197. 197. His chest CT scan is shown.
  198. 198. A contrasted head CT scan is unremarkable.
  199. 199. Which of the following is true about the likely disease process? A. Squamous cell carcinoma is the likely cell type. B. A common pathogenic mechanism is production of anti-Hu antibodies. C. Nerve conduction studies show augmentation of the action potential with repeated stimulation. D. Th e syndrome is likely to resolve with treatment of the underlying cause.
  200. 200. • This patient with a history of tobacco use has a chest CT that reveals a right hilar lung mass, mediastinal adenopathy, and postobstructive pneumonia. This patient also has a clinical picture of a paraneoplastic neurologic syndrome; in this case, paraneoplastic cerebellar degeneration (PCD). • The pathophysiology in PCD, and in most paraneoplastic neurologic syndromes, is an autoimmune process. • In PCD, it is most commonly (44% of cases) due to tumor production of Hu antigen, which stimulates production of type 1 antineuronal nuclear antibodies (ANNA-1), also known as anti-Hu-antibodies, directed against like cellular proteins in the cerebellum (choice B is correct).
  201. 201. • The Hu antigen is found in neurons, but in the normal host, these antigens are protected from exposure to the circulation due to the blood-brain barrier. • Small cell cancers express Hu antigen and stimulate self anti-Hu antibody formation. Up to 20% of patients with small cell lung cancer can have detectable levels of circulating anti- Hu antibody.
  202. 202. • The anti-Hu antibody reacts with 35- to 42-kD proteins present in nuclei and cytoplasm of virtually all neurons. Autopsy specimens may reveal lymphocytic opacities in the corresponding aff ected areas of the nervous system. • Anti-Hu (ANNA-1) antibodies are also associated with other paraneoplastic neurologic syndromes associated with small-cell carcinoma of the lung, such as encephalomyelitis and paraneoplastic sensory neuropathy
  203. 203. • Patients with PCD usually have the subacute acute onset of nausea and vomiting, dizziness, vertigo, ataxia, blurry vision, double vision, dysarthria, and tremor. Physical examination reveals fi ndings seen in patients with cerebellar disease
  204. 204. • Up to 80% of patients with PCD have associated lung cancer, and this is nearly always small cell carcinoma, which was the diagnosis in this patient (choice A is incorrect). • PCD can occur in up to 1% of patients with a small cell lung cancer. The remainder of cases is associated with other malignancies, including several types of sarcoma and prostate carcinoma and neuroblastomas, also via an anti-Hu mechanism.
  205. 205. • The neurologic findings may precede the lung cancer on plain chest radiograph, in some patients, by as long as 2 years. Unlike other paraneoplastic neurologic symptoms, such as Lambert-Eaton myasthenic syndrome (LEMS), cerebellar dysfunction typically does not respond to treatment of the tumor (choice D is incorrect). • The nerve conduction findings described in choice C are characteristic of LEMS, not PCD (choice C is incorrect).
  206. 206. THANK YOU