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Internal medicine review for national license examination 2

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Internal Medicine review, with focus on pulmonary medicine and critical care medicine including pneumonia, asthma, COPD, tuberculosis, and sepsis & septic shock. Intended to be used for medical students.

Publicada em: Saúde e medicina
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Internal medicine review for national license examination 2

  1. 1. Internal Medicine Reviews for 
 National License Examination II S a n t i S i l a i r a t a n a , M D Division of Pulmonary Medicine, Department of Medicine, Faculty of Medicine Vajira Hospital Navamindradhiraj University Pulmonary Medicine and Critical Care
  2. 2. Asthma COPD Pneumonia Tuberculosis Sepsis and septic shock Pleural effusion
  3. 3. Airway Diseases: Asthma and COPD
  4. 4. General Steps of Approach of Airway Diseases Typical symptoms of 
 airway disease Detailed history/examination Diagnostic tests
  5. 5. Typical Clinical Features in Airway Diseases Mucociliary clearance Bronchospasm Coughing Sneezing Chronic cough Sputum 
 production Wheezing 
 Dyspnea/shortness of breath Chest tightness
  6. 6. Spirometry with Bronchodilator Response Test Airflow limitation: Reduced FEV1/FVC (Normal 0.75-0.80) Reversibility: FEV1 increases >12% and 200 mL
  7. 7. Asthma versus COPD Asthma COPD Age group Typically begins in childhood Patient typically >40 years of age Smoking No direct relationship Mainly smokers and ex-smokers Dyspnea Episodic attacks with exposures to allergen, irritant, or exercise Progressive shortness of breath, usually with exertion Cough Typically a dry cough at night Productive cough, typically in the morning
  8. 8. Asthma
  9. 9. Asthma 3 Episodic breathlessness, wheezing, chest tightness Associated with airway hyperresponsiveness2 1 Chronic inflammation of airways 5 Reversible either spontaneously or with treatment 4 Airflow limitation
  10. 10. Asthma Phenotypes Asthma with obesityAllergic asthma Late-onset asthmaNon-allergic asthma Exercise-induced asthma Occupational asthma Work-aggravated asthma Aspirin-induced asthma Asthma-COPD 
 overlap syndrome (ACOS)
  11. 11. Pathogenesis of Allergic Asthma
  12. 12. Airway Abnormalities in Asthma Normal bronchiole Asthmatic bronchiole 1 2 3 4 Smooth muscle 
 hypertrophy Vascular proliferation 
 Capillary leakage Submucosal gland hypertrophy Mucous 
 hypersecretion
  13. 13. Physiologic Change in Asthma http://www.google.co.th/url? sa=i&rct=j&q=&esrc=s&source=images&cd=&docid= Hk_PSlY10HFWQM&tbnid=YCHYLHpoyi8JSM:& ved=0CAUQjRw&url=http%3A%2F%2Fquizlet.com %2F17264799%2Frespiratory-mechanics-ii-flash- cards %2F&ei=cwdyU_iJD9WF8gWZzoGwAQ&bvm=bv. 66330100,d.c2E&psig=AFQjCNGA1cMV-5TviGGyZ TbCe-i4J2_l_g&ust=1400068322927498 Airway Resistance Airway narrowing ➡
 Increased resistance ➡ Increased work of breathing ➡ Dyspnea, muscle fatigue ➡ Respiratory failure
  14. 14. General Steps of Approach: Asthma Screening typical symptoms of asthma Detailed history/examination
 for asthma Diagnostic tests for asthma Evidence of variable respiratory symptoms Evidence of variable airflow limitation
  15. 15. Symptoms of Asthma Increased probability of asthma More than one symptoms of asthma,
 especially in adults Symptoms often worse at night or
 early morning Symptoms vary over time and in intensity Symptoms are triggered by viral infection,
 exercise, allergen exposure, changes in
 weather, laughter, or irritants Decreased probability of asthma Isolated cough with no other respiratory 
 symptoms Chronic production of sputum Shortness of breath associated dizziness,
 lightheadedness, paresthesia Chest pain Exercise-induced dyspnea with 
 noisy inspiration
  16. 16. Diagnostic Tests for Asthma Peak Expiratory Flow Broncho- provocation test Spirometry Exercise 
 challenge test Inflammatory markers FEV1/FVC Reversibility Methacholine Histamine Eucapnic hyperventilation Mannitol Variability Reversibility Exhaled nitric oxide (FENO) Allergy test Serum IgE level Sputum eosinophil
  17. 17. (Mini-Wright) Peak Flow Meter
  18. 18. Peak Flow Variability PEF max PEF min PEF variability = (PEF max - PEF min) 1/2 x (PEF max + PEF min) Diagnosis of asthma can be made when average daily diurnal PEF variability 
 >20%
  19. 19. Minimum Morning Pre-bronchodilator PEF PEF max PEF min Min%Max = PEF min PEF max Diagnosis of asthma can be made when Min%Max 
 <80% PreviousGuidelines
  20. 20. Methacholine Challenge Testing Baseline spirometry Repeat spirometry Repeat spirometry
 until FEV1 fall 20% or the dose 
 of 16 mg/mL 
 is reached Methacholine 0.031-0.625 mg/mL Methacholine 2x-4x of initial concentration Albuterol 
 2 puff Repeat spirometry
  21. 21. Diagnostic Algorithm for Asthma: Summary Clinical Features Shortness of breath, Chest tightness, Recurrent wheezing, and Cough Symptoms get worse during nighttime, early morning, seasonal, allergen exposure, or exercise Presence of allergic disease or a family history of allergy or asthma (not required) Reversibility Spirometry: FEV1/FVC <75% with FEV1 increase ≥12% AND 200 mL post bronchodilator Peak expiratory flow (PEF): Increase ≥20% or ≥60 L/min post bronchodilator Variability Test Average diurnal PEF variability: >10% Minimum morning PEF: <80% Bronchoprovocation Test Methacholine test: PC20 <8 mg/mL Exercise challenge test: FEV1 reduces >10% and 200 mL
  22. 22. Asthma & Asthma Symptoms: Tip of the Iceberg Airway inflammation Bronchial
 hyperresponsiveness Bronchospasm Airflow limitation Asthma symptoms Risk of asthma exacerbation Treatment for Asthma (symptom) control Treatment for Worsening/exacerbation risk
  23. 23. General Principles of Asthma Management Assessing disease severity Identify risk(s) Provide treatment and modify risk(s) Assessment of symptom and risk control Step treatment
 up or down to maintain control
  24. 24. Initiation of Treatment GINA 2014 Presenting symptoms Preferred initial controller Symptoms or SABA use <2/month No waking due to asthma symptom No risk factor No controller Infrequent symptoms Presence of ≥1 risk factors for exacerbation Low dose ICS Symptoms or SABA use >2/month but <2 /week Waking due to asthma ≥1/month Low dose ICS Symptoms or SABA use >2/week Low dose ICS LTRA or Theophylline Symptoms in most days Waking due to asthma >1/week Medium/high dose ICS Low dose ICS/LABA Severly symptomatic or acute exacerbation Short course of oral corticosteroids AND High dose ICS OR Moderate dose ICS/LABA Global Strategy for Asthma Management and Prevention. Revised 2014
  25. 25. Inhaled Corticosteroid Dosage ICS Low dose (µg) Medium dose (µg) High dose (µg) Beclometasone 200-500 500-1000 1000-2000 Budesonide 200-400 400-800 800-1600 Fluticasone propionate 100-250 250-500 500-1000 Ciclesonide 80-160 160-320 320-1280 Mometasone furoate 200-400 400-800 800-1200 แนวทางวินิจฉัยและรักษาโรคหืดในประเทศไทย V.5 สำหรับผู้ใหญ่และเด็ก พ.ศ. 2555
  26. 26. Level of Asthma Control Characteristics Controlled (All of the following) Partly Controlled (Any measure present 
 in any week) Uncontrolled Daytime symptoms None (twice or less/week) More than twice/week Three or more features of partly controlled asthma present in any week Limitations of activities None Any Nocturnal symptoms/awakening None Any Need for reliever/rescue treatment None (twice or less/week) More than twice/week Lung function (PEF or FEV1) Normal <80% predicted or personal best (if known) Exacerbations None One or more/year One in any week
  27. 27. Management Options CPU Uncontrolled Partly Controlled Controlled Step up treatment Maintain treatment and observe Step down treatment Step up treatment Maintain treatment and observe 3-6 Months
  28. 28. Stepwise Approach Step 5 Step 4 Refer for add-on treatment (e.g. anti-IgE) Step 3 Medium/high dose
 ICS/LABA Step 1 Step 2 Low dose
 ICS/LABAPreferred Low dose ICS Optional Consider 
 low dose ICS LTRA Theo Medium/high dose ICS Low dose ICS +LTRA Low dose ICS + Theo High dose ICS + LTRA
 High dose ICS + Theo Add low dose OCS As needed short-acting beta2 agonist (SABA) As needed short-acting beta2 agonist (SABA) or Low dose ICS/formoterol ICS = Inhaled corticosteroids LTRA = Leukotriene receptor antagonists LABA = Long-acting beta2 agonists Theo = Theophylline OCS = Oral corticosteroids Global Strategy for Asthma Management and Prevention. Revised 2014
  29. 29. Options for Stepping Down Treatment Current Step Current medication and dose Options for stepping down 5 High dose ICS/LABA plus OCS or other add-on agents Continue high dose ICS/LABA, reduce OCS dose Use sputum-guided approach to reduce OCS Alternate-day OCS treatment Replace OCS with high dose ICS 4 Moderate to high dose ICS/LABA maintenance treatment Continue combination ICS/LABA with 50% reduction in ICS component by using available combination Discontinuing LABA (more likely to lead to deterioration) Medium dose ICS/formoterol as maintenance and reliever Reduce maintenance ICS/formoterol to low dose, and continue as needed low dose ICS/formoterol reliever High dose ICS plus second controller Reduce ICS dose by 50% and continue second controller Global Strategy for Asthma Management and Prevention. Revised 2014
  30. 30. Options for Stepping Down Treatment Current Step Current medication and dose Options for stepping down 3 Low dose ICS/LABA maintenance Reduce ICS/LABA to once daily Discontinuing LABA (more likely to lead to deterioration) Low dose ICS/formoterol as maintenance and reliever Reduce maintenance ICS/formoterol to once daily, and continue as needed low dose ICS/formoterol reliever Moderate or high dose ICS Reduce ICS dose by 50% 2 Low dose ICS Once-daily dosing (budesonide, ciclesonide, mometasone) Low dose ICS or LTRA Stop controller treatment (when no symptoms for 6-12 months 
 and no risk factor) Complete cessation of ICS (increased risk of exacerbation in adults) Global Strategy for Asthma Management and Prevention. Revised 2014
  31. 31. Patient with Poor Symptom Control 1 3 42 Check inhaler technique Discuss adherence Confirm the diagnosis of asthma Remove potential
 risk factors Consider treatment step up Assess and manage comorbidities
  32. 32. Management of Asthma Exacerbation Initial assessment 2nd Assessment Intubation Unconscious Air hunger RR <12/min Unstable hemodynamics A Hx of intubation
 Hx of steroid use Admission in 1 year Rescue medication use 
 >1 canister/month B PR >130/min RR >30/min Wheezing C Incomplete sentence Accessory muscle used Abdominal paradox Unable to lie down D Ram athibodiaction plan
  33. 33. Short acting bronchodilators: 4 puffs of salbutamol (100 µg) via spacer q 15-20 min Salbutamol 1 NB via nebulizer q 15-20 min if Any of B or D Systemic corticosteroid: Dexamethasone 4-5 mg iv Oral prednisolone 40 mg p.o. PEF 3rd AssessmentA C D PEF Ram athibodiaction plan
  34. 34. Discharge 4th Assessment Iprotropium/fenoterol 4 puff via spacer 1 NB via nebulizer PEFR >70% PEFR >70% + any of C PEFR 50-70% + any of C PEFR 50-70% + any of A, D PEFR <50% PEFR >70% PEFR 50-70% + any of C Admit ward Admit ICU PEF Ram athibodiaction plan
  35. 35. Treatment in Acute Care Setting Recommended Oxygen: 
 to achieve arterial oxygen saturation of 93-95%
 low flow oxygen is preferred to high flow (100% O2) Inhaled short-acting beta2-agonist and Iprotropium bromide: The most cost-effective and efficient delivery: pMDI with a spacer When nebulization is used, initiate with continuous therapy, followed by intermittent on-demand therapy Iprotropium bromide - greater improvement in PEF and FEV1 Systemic corticosteroids: Oral administration = intravenous administration Dose: Prednisolone 50 mg/day or Hydrocortisone 200 mg/day Duration: 5-7 days
  36. 36. IMPORTANT!! Acute exacerbation of asthma = uncontrolled asthma Review and modify treatment to prevent another exacerbation BEFORE send them home
  37. 37. Discharge Management Medications Risk Reduction Uncontrolled asthma symptoms Excessive SABA use Inadequate ICS Low FEV1 (<60% predicted) Major psychological or socioeconomic problems Exposures: smoking, allergens Comorbidity: obesity, rhinosinusitis Self-management & Asthma action plan 
 Review inhaler technique Review PEF technique Provide written asthma 
 action plan Evaluate the patient’s response to the exacerbation Review the patient’s use of controller treatment Oral corticosteroids: At least 5-7 days of Prednisolone 1 mg/kg/day (max. 50 mg/day) Inhaled corticosteroids: Initiate (if not done) Step up treatment for 2-4 wks Remind adherence Reliever medications: Transfer back to as-needed use beta2-agonist is preferred
  38. 38. Chronic Obstructive Pulmonary Disease (COPD) นพ.สันติ สิลัยรัตน พบ. อายุรแพทย โรคระบบการหายใจและเวชบำบัดวิกฤตทางการหายใจ แผนกอายุรกรรม ศูนยแพทยศาสตรศึกษาชั้นคลินิก โรงพยาบาลอุดรธานี Holistic approach for COPD: Time to Treat Earlier to Prevent Future Risk ความรูเรื่องโรคปอดอุดกั้นเรื้อรัง
  39. 39. Definition 3 Characterized by persistent airflow limitation Associated with noxious particles and gases2 1 Chronic inflammation of airways 4 Exacerbation and comorbidities contribute to the overall severity 5 Preventable and treatable
  40. 40. Causes and Pathogenesis of COPD สาเหตุและกลไกการเกิดโรคปอดอุดกั้นเรื้อรัง
  41. 41. Physiologic and Health Effects of COPD Expiratory airflow limitation Air trapping Hyperinflation Inactivity Deconditioning Activity limitation Poor quality of life Dyspnea Exacerbations
  42. 42. Diagnosis การวินิจฉัยโรคปอดอุดกั้นเรื้อรัง
  43. 43. Grading of COPD Severity ระดับความรุนแรงของโรคปอดอุดกั้นเรื้อรัง ระดับความรุนแรง Mild Moderate Severe Very Severe FEV1/FVC <70%<70%<70%<70% FEV1 (% of predicted) >80 50-79 30-49 <30 หรือ <50 รวมกับมีภาวะ การหายใจลมเหลวเรื้อรัง หรือมี cor pulmonale
  44. 44. Combined Assessment for COPD C D A B Risk GOLD classification 
 of Airflow Limitation 1 2 3 4 ≥2 1 0 Risk Exacerbation history mMRC 0-1 CAT <10 mMRC ≥2 CAT >10
  45. 45. B CA D Less symptoms Low risk MORE symptoms Low risk Less symptoms HIGH risk MORE symptoms HIGH risk
  46. 46. Modified Medical Research Council Questionnaire สำหรับการประเมินระดับอาการเหนื่อยในผู้ป่วยโรคทางเดินหายใจ Modified Medical Research Council Questionnaire สำหรับการประเมินระดับอาการเหนื่อยในผูปวยโรคทางเดินหายใจ เลือกขอใดขอหนึ่งตอไปนี้ตามอาการที่ทานเห็นวาใกลเคียงกับความรูสึกของทานมากที่สุดเลือกขอใดขอหนึ่งตอไปนี้ตามอาการที่ทานเห็นวาใกลเคียงกับความรูสึกของทานมากที่สุดเลือกขอใดขอหนึ่งตอไปนี้ตามอาการที่ทานเห็นวาใกลเคียงกับความรูสึกของทานมากที่สุด Grade 0: รูสึกเหนื่อยเฉพาะเวลาที่ออกกำลังกายหนัก ๆ ☐ Grade 1: รูสึกเหนื่อยเวลาเดินขึ้นบันได หรือเดินขึ้นเนิน ☐ Grade 2: รูสึกเหนื่อยเมื่อเดินบนพื้นราบจนเดินไดชากวาคนทั่วไป หรือตองพักเมื่อตองเดินไกล ๆ ☐ Grade 3: รูสึกเหนื่อยจนเดินบนพื้นราบไดไมถึง 100 เมตร หรือเดินไดไมกี่นาที ☐ Grade 4: รูสึกเหนื่อยจนไมกลาออกจากบาน หรือเหนื่อยจากการทำกิจวัตรประจำวัน ☐
  47. 47. COPD Assessment Test 0 1 2 3 4 5 คะแนน ฉันไม่มีอาการไอเลย ⚪ ⚪ ⚪ ⚪ ⚪ ⚪ ฉันไอตลอดเวลา ฉันไม่มีเสมหะในปอดเลย ⚪ ⚪ ⚪ ⚪ ⚪ ⚪ ปอดของฉันเต็มไปด้วยเสมหะ ฉันไม่รู้สึกแน่นหน้าอกเลย ⚪ ⚪ ⚪ ⚪ ⚪ ⚪ ฉันรู้สึกแน่นหน้าอกมาก ฉันรู้สึกหายใจได้คล่องเมื่อต้องเดินขึ้นเนิน หรือขึ้นบันไดหนึ่งชั้น ⚪ ⚪ ⚪ ⚪ ⚪ ⚪ ฉันเหนื่อยหอบอย่างมากเมื่อต้องเดินขึ้นเนิน หรือขึ้นบันไดหนึ่งชั้น ฉันทำกิจกรรมต่าง ๆ ที่บ้านได้โดยไม่จำกัด ⚪ ⚪ ⚪ ⚪ ⚪ ⚪ ฉันทำกิจกรรมต่าง ๆ ที่บ้านได้อย่างจำกัดมาก ฉันมีความมั่นใจที่จะออกไปนอกบ้านได้ แม้ว่าปอดฉันยังมีปัญหา ⚪ ⚪ ⚪ ⚪ ⚪ ⚪ ฉันไม่มั่นใจเลยที่จะออกไปนอกบ้านเพราะ ปัญหาที่ปอด ฉันนอนหลับได้สนิท ⚪ ⚪ ⚪ ⚪ ⚪ ⚪ ฉันนอนหลับไม่สนิทเพราะปอดมีปัญหา ฉันรู้สึกกระฉับกระเฉงอย่างมาก ⚪ ⚪ ⚪ ⚪ ⚪ ⚪ ฉันรู้สึกอ่อนเพลียและเหนื่อยล้า
  48. 48. Exacerbations and Progression of COPD การกำเริบเฉียบพลันกับการดำเนินโรค FEV1 อายุ ไมมีการกำเริบ เสียชีวิต เริ่มมีอาการ เกิดการกำเริบเฉียบพลัน ยิ่งมีการกำเริบของโรคบอย และมาก ยิ่งทำใหเสียชีวิตเร็วยิ่งขึ้นMORE exacerbations HIGHER mortality
  49. 49. Severity Grading and Number of Exacerbationsจำนวนครั้งเฉลี่ยของการกำเริบเฉียบพลันตอปในผูปวย COPD 0" 5" 10" 15" 20" 25" zero" 0*1" 1*2" 2*3" 3*4" 4*6" 6*8" >8" %" pa3ents" Annualised"rate"of"exacerba3ons" GOLD%Stage%3,4% (FEV1%<%50%%pred)% Jones"et"al""Eur"Respir"J"2003;"21:"68–73"" 0" 5" 10" 15" 20" 25" 30" zero" 0*1" 1*2" 2*3" 3*4" 4*6" 6*8" >8" %" pa3ents" GOLD%Stage%2%% (FEV1%>%50%%pred)% >40%%
  50. 50. Combined Assessment for COPDอัตราการเกิดการกำเริบปานกลาง/รุนแรงภายหลังการใช ICS Calverley et al. NEJM 2007; 356:775-789. 0 0.3 0.5 0.8 1.0 1.3 1.5 Placebo Salmeterol Fluticasone Salmeterol/Fluticasone 0.85 0.930.97 1.13 25% reduction * * *✝ *p < 0.001 vs placebo; †p = 0.002 vs SALM; p = 0.024 vs FP*p < 0.001 vs placebo; †p = 0.002 vs SALM; ☨p = 0.024 vs FP Calverley et al. NEJM 2007; 356:775-789.
  51. 51. Combined Assessment for COPD C D A B Risk GOLD classification 
 of Airflow Limitation 1 2 3 4 ≥2 1 0 Risk Exacerbation history mMRC 0-1 CAT <10 mMRC ≥2 CAT >10
  52. 52. Components of COPD Management Component 2: Symptom & Risk Management Component 1: Identify & Control risk factors Component 3: Rehabilitation & Health promotion
  53. 53. Goals of COPD Management เพื่อคง เพื่อลด สภาพรางกายในปจจุบันใหดีที่สุด ความเสี่ยงที่จะเกิดขึ้นในอนาคต อาการ โครงสรางและ สมรรถภาพปอด ความถี่ของการใชยาขยาย หลอดลมตามอาการ โรคหรือภาวะรวม สถานะสุขภาพ กิจกรรมในแตละวัน การกำเริบของโรค ความเสื่อมสถานะ สุขภาพ ความเสี่อมของโครงสราง และสมรรถภาพปอด โรคหรือภาวะรวม ที่อาจเกิดขึ้นใหม ผลขางเคียงของยาที่ใช การเสียชีวิต แผนการรักษา COPD เพื่อคง เพื่อลด
  54. 54. Component 1: Identify and Control Risk Factors
  55. 55. Importance of Smoking Cessation in COPDผลของการหยุดบุหรี่กับการเปลี่ยนแปลงของสมรรถภาพปอด Fletcher C et al.The Natural History of Chronic Bronchitis and Emphysema. 1976. Scanlon PD et al. Am J Respir Crit Care Med 2000; 161: 381-390. Age25 ผูที่ยังคงสูบบุหรี่ ผูที่ไมสูบบุหรี่ 40 70 เริ่มมีอาการ 55 เสียชีวิต เลิกบุหรี่ FEV1 Fletcher C et al. The Natural History of Chronic Bronchitis and Emphysema. 1976. 
 Scanlon PD et al. Am J Respir Crit Care Med 2000; 161: 381-390.
  56. 56. Immunization for COPD Patientsการใหวัคซีนแกผูปวยโรคปอดอุดกั้นเรื้อรัง Influenza vaccine Pneumococcal vaccine ควรพิจารณาใหกับผูปวยทุกรายหากเปนไปได ทั้งนี้ขึ้นกับแนวปฏิบัติบริการในประเทศนั้น ๆ
  57. 57. Component 2: Symptom and Risk Management
  58. 58. Treatment Options for COPD Patient Group First Choice Second Choice Alternative Choice A SAMA prn SABA prn LAMA LABA SAMA + LABA Theophylline B LAMA LABA LAMA+LABA SAMA +SABA Theophylline C ICS + LABA LAMA LAMA + LABA iPDE4 SAMA + SABA Theophylline D ICS + LABA LAMA ICS + LAMA ICS + LAMA + LABA ICS + LABA + iPDE4 LAMA + LABA
 LAMA + iPDE4 Carbocysteine SAMA + SABA Theophylline SAMA = short-acting muscarinic antagonist (anticholinergic) SABA = short-acting beta-2 agonist ICS = inhaled corticosteroid iPDE2 = phosphodiesterase inhibito Non ICS ICS
  59. 59. สรุปหลักการใชยา สำหรับผูปวยโรคปอดอุดกั้นเรื้อรัง ประเมินความพรอมในการใชอุปกรณ (แรงสูดยา, ความสัมพันธระหวางการสูดกับการกดยา) เลือกอุปกรณที่เหมาะสมกับผูปวย ติดตามผลการรักษา (อาการหอบเหนื่อย, CAT, mMRC, การกำเริบของโรค) ปรับเพิ่มยาขยายหลอดลม เมื่อยังบรรเทาอาการหอบเหนื่อยไดไมเพียงพอ ปรับเพิ่มยา ICS เมื่อมีการกำเริบบอย หรือยังมีอาการหอบ
  60. 60. Component 3: Rehabilitation and Health Promotion
  61. 61. Rehabilitation for COPD Patientsการฟนฟูสมรรถภาพปอด เพิ่มความทนทาน ตอการออกกำลังกาย Pulmonary Rehabilitation ลดโอกาส การเสียชีวิต เสริมประสิทธิภาพของ การรักษาดวย ICS/LABA ทำใหสุขภาพจิตดีขึ้น คลายความกังวล ทำใหคุณภาพชีวิตดาน ภาวะสุขภาพดีขึ้นทำใหกำลังกลามเนื้อแขนขาดีขึ้น ลดจำนวนและวันใน การเขารักษาในโรงพยาบาล ฟนตัวจากอาการ กำเริบของโรคไดเร็วขึ้น
  62. 62. Tuberculosis
  63. 63. Tuberculosis IDENCE 88,043 34,066 27,047 62,819 60,767 78,392 51,685 41,537 36,885 95,207 94,627 60,688 44,942 37,260 10,319 06,201 89,351 86,130 85,015 84,546 79,656 . More people die from TB than from any WHO. Global tuberculosis control: surveillance, planning, financing: WHO report 2005. Geneva: WHO, 2005. Poverty Congregation HIV pandemic
  64. 64. Tuberculosis-HIV Coinfection Figure5 PREVALENT ADULT TB CASES COINFECTED WITH HIV, 2004 Source:reference3. Dye C, Watt CJ, Bleed DM et al. Journal of American Medical Association 2005; 293:2767-75.
  65. 65. The Gap between Estimated and Notified Cases Estimated TB cases 
 8.8 Million Health facility TB cases Diagnostic 
 tests Recorded & reported 4.1 Million cases 
 reported Detected but not notified private sector military prisons ⊕ ⊖ WHO. Global tuberculosis control: surveillance, planning, financing: WHO report 2005. Geneva: WHO, 2005.
  66. 66. Multidrug-resistant and Extensively drug-resistant TB Multidrug-resistant (MDR) TB Resistance against at least rifampicin and isoniazid Extensively drug-resistant (XDR) TB MDR-TB PLUS Resistance to any fluoroquinolones AND ≥1 injectable second-line agents O’Grady J, Maeurer M, Mwaba P et al. Current Opinion in Pulmonary Medicine 2011, 17; 134-141.(ethionamide, prothionamide, cycloserine, terizidone, para-aminosalicylic acid, clofazimine, amoxicillin-clavula- are those used directly on patient samples where a set of drug-containing and drug-free media is inoculated 136 Infectious diseases Figure 2 Estimated percentage of multiple drug resistant tuberculosis among new tuberculosis cases, 2008a , 0 to <3; , 3 to <6; , 6 to <12; , 12 to <18; , !18; ‘, no data available; , subnational data only. Reproduced with permission from [2].
  67. 67. AFB stain Myc Culture Drug susceptibility Chest radiography CT scan History Chronic productive cough* Sputum production* Prolonged low grade fever Night sweats Weight loss Physical examination Bronchial breath sound Crepitation Digital clubbing Establishing Tuberculosis: Pulmonary TB Imaging Additional test(s) Clinical features suggestive for tuberculosis Microbiology
  68. 68. Sputum Microscopy for Acid-fast Bacilli Friedrich Carl Adolf Neelsen (1854-1898) Franz Ziehl (1857-1926) Neelsen-Ziehl (Acid fast bacilli) Staining Acid-fast bacilli appear pink 
 in a contrasting methylene blue background
  69. 69. Light Emitting Diode (LED) Fluorescence Microscopy Same (or slightly more) sensitivity Cheaper and longer life duration of bulb (10,000 hr) Cheaper microscopy A dark room is not required WHO recommended to use LED fluorescence microscope as a standard technique WHO. Fluorescent light-emitting diode (LED) microscopy for diagnosis of tuberculosis: policy statement. Geneva: WHO 2011.
  70. 70. Radiographic Patterns of Tuberculosis Reticulonodular infiltration Miliary pattern lymphatic/interstitial spread Cavitation Bronchiectatic change Bronchoalveolar pattern bronchial-alveolar spread
  71. 71. Diagnostic Algorithm: Clinically-suggestive Patient with clinical features suggestive 
 for pulmonary tuberculosis Sputum examination for acid-fast bacilli Chest radiograph AFB - positive CXR - compatible with TB AFB - negative CXR - compatible with TB AFB - negative CXR - incompatible with TB Sputum culture and drug susceptibility testing for mycobacteria Treatment for pulmonary tuberculosis Look for alternative diagnosis แนวทางเวชปฏิบัติการรักษาวัณโรคในผู้ใหญ่ พ.ศ. 2556 (ฉบับร่าง). สำนักวัณโรค กรมควบคุมโรค สมาคมอุรเวชช์แห่งประเทศไทย
  72. 72. Diagnostic Algorithm: Radiographically-suggestive Asymptomatic patient with
 radiographically suggestive tuberculosis Sputum examination for acid-fast bacilli Review previous chest radiograph AFB - positive CXR - compatible with TB AFB - negative CXR - unavailable AFB - negative CXR - unchanged Sputum culture and drug susceptibility testing for mycobacteria Treatment for pulmonary tuberculosis Re-evaluation and repeat CXR in 3 months AFB - negative CXR - active TB AFB - negative CXR - old lesion แนวทางเวชปฏิบัติการรักษาวัณโรคในผู้ใหญ่ พ.ศ. 2556 (ฉบับร่าง). สำนักวัณโรค กรมควบคุมโรค สมาคมอุรเวชช์แห่งประเทศไทย
  73. 73. Mycobacterial Culture Minion J, et al. The Lancet Infectious Disease. 2010; 10 (10): 688-698. Richter E, et al. Exper Rev Resp Med. 2009; 3 (5): 497-510. Conventional TB culture 
 system Rapid colorimetric drug susceptibility test 20-30 days Liquid culture-based technique Mycobacterial growth indicator tube (MGIT) 7-10 days
  74. 74. Treatment Regimen for Pulmonary Tuberculosis 1 2 3 4 5 6 7 8 Isoniazid Rifampin Pyrazinamide Ethambutol Isoniazid Rifampin Isoniazid Rifampin Pyrazinamide Ethambutol Streptomycin Isoniazid Rifampin Pyrazinamide Ethambutol Isoniazid Rifampin Ethambutol Months of treatment “New case” “Retreatment”
  75. 75. Antituberculosis Drug: Dosage Isoniazid (4-8 mkd) Rifampin (8-12 mkd) Pyrazinamide (20-30 mkd) Ethambutol (15-20 mkd) Streptomycin (15 mkd) Body 
 weight
 (kg) 35-40 300 450 1000 600 500 41-50 300 450 1250 800 750 50-70 300 600 1500 1000 750-1000 mkd = mg/kg/day
  76. 76. 3 weeks 6 weeks Sputum AFB Chest x-ray Response Monitoring in New Case Pulmonary TB: M+ Start 1 2 3 4 5 6 Sputum AFB Sputum AFB Chest x-ray if positive Sputum culture for TB if positive Chest radiograph 2 months 2 months IRZE IR Chest radiograph if positive “failure” Sputum AFB Sputum Culture for TB* Chest radiograph
  77. 77. “High Risk” of Drug-resistance TB History of close contact to a patient with MDR-TB Return after default of >2 months Relapse pulmonary TB Treatment failure (smear positive at 5th month) Special population (immigrants, prisoners, 
 HIV infected persons)
  78. 78. Sputum AFB Chest radiograph Response Monitoring in New Case Pulmonary TB: M- Start 1 2 3 4 5 6 Re-evaluate Look for other cause Chest radiograph 2 months 2 months IRZE IR 4 weeks 5 weeks Chest radiograph if not improved/progressive
  79. 79. Antituberculosis Drug Side Effects: Minor Isoniazid Rifampin Pyrazinamide Ethambutol Streptomycin Nausea/vomiting/pain ☑ ☑ ☑ Joint pain ☑ ☑ Numbness ☑ Sedative ☑ Flu-like symptomps ☑ Anti TB drug can be continued; supportive treatment is usually adequate
  80. 80. Antituberculosis Drug Side Effects: Major Isoniazid Rifampin Pyrazinamide Ethambutol Streptomycin Skin rash ☑ ☑ ☑ ☑ ☑ Confusion ☑ ☑ ☑ ☑ Hepatitis/Jaundice ☑ ☑ ☑ Renal dysfunction ☑ ☑ Thrombocytopenia ☑ Nystagmus/vertigo ☑ Visual disturbance ☑
  81. 81. Antituberculosis Drug Side Effects: Minor Isoniazid Rifampin Pyrazinamide Ethambutol Streptomycin Nausea/vomiting/pain ☑ ☑ ☑ Joint pain ☑ ☑ Numbness ☑ Sedative ☑ Flu-like symptomps ☑ Anti TB drug can be continued; supportive treatment is usually adequate
  82. 82. Response Monitoring in Re-treatment Pulmonary TB 2 1 month Start 1 2 3 4 5 6 Sputum AFB Sputum AFB Chest x-ray Sputum culture for TB Sputum AFB Chest radiograph 2 months 2 months IRZES IRE Chest radiograph if positive “failure” Sputum AFB Sputum Culture for TB Chest radiograph 7 8 3 wks2 2 IRZE 1 month if positive Sputum culture for TB if positive
  83. 83. Treatment After Interruption Interruption occurred during intensive phase of treatment Duration of interruption Duration of interruption ≥80% Continue treatment until complete แนวทางเวชปฏิบัติการรักษาวัณโรคในผู้ใหญ่ พ.ศ. 2556 (ฉบับร่าง). สำนักวัณโรค กรมควบคุมโรค สมาคมอุรเวชช์แห่งประเทศไทย yes no Total treatment received <80% <14 days ≥14 days Continue treatment until complete Start over <3 months≥3 months
  84. 84. Treatment for Extrapulmonary Tuberculosis Treatment duration (months) Lymph node 6-9 Pleura 6 Pericardium 6 Meninges and tuberculoma ≥12 Bone and joint 9-12 Urinary tract 6 Disseminated depends on the organ(s) involved
  85. 85. Community-acquired Pneumonia
  86. 86. The Disease Triangle Host Pathogen Environment
  87. 87. Airway-Lung Defense Mechanisms Mucociliary clearance Bronchospasm Cellular/ chemical immunity Coughing Sneezing Mechanical barriers
  88. 88. Transmission and Pathogenesis 3 2 5 4 Inhalation of aerosols Aspiration of 
 oropharyngeal secretions Hematogenous spread Reactivation of latent infection Mycoplasma pneumoniae Chlamydophila pneumoniae Legionella pneumophila Chlamydophila psittaci Streptococcus pneumoniae Haemophilus influenzae Gram-negative bacilli Anaerobes Mycobacterium tuberculosis Pneumocystis jiroveci Staphylococcus aureus Extrapulmonary bacteremias 1 Direct contact & Droplets Rhinovirus Adenovirus Influenza virus
  89. 89. Community-acquired Pneumonia: Common Pathogens Bacteria Aerobic gram-positive cocci Aerobic gram-negative bacilli Anaerobic bacteria “Atypical”pathogen Mycoplasma pneumoniae Legionella pneumophila Chlamydophila pneumoniae Viruses RSV Adenovirus Influenza virus
  90. 90. Pathogen-related Severity Outpatients (Mild) Non-ICU inpatients ICU (Severe) S pneumoniae S pneumoniae S pneumonia M pneumoniae M pneumoniae Legionella spp. H influenzae C pneumoniae H influenzae C pneumoniae H influenzae Gram-negative bacilli Respiratory viruses Legionella spp. S aureus Aspiration respiratory viruses P aeruginosa File T M. Lancet 2003; 362:1991-2001.
  91. 91. Host Defense-modifying Conditions Diabetes Gram negative bacilli Melioidosis Mucormycosis Aspergillus spp. Candida spp. Alcoholics Liver disease Gram negative bacilli Anaerobes Chronic lung disease Gram negative bacilli P. aeruginosa Nocardia spp. Aspergillus spp. AIDS Pneumocystis jirovecii Toxoplasma spp. Rhodococcus spp. Histoplasma spp. C. neoformans Penicillium marneffii
  92. 92. Diagnosis of Pneumonia Clinical features of pneumonia Imaging History Fever Cough Dyspnea Chest pain Physical examination Decreased lung expansion Dullness on percussion Vocal resonance Crepitation Tachypnea Cyanosis New or Presumed new 
 opacity (infiltrates) on chest radiograph Host responses Tissue injuries Airspace filling/consolidation Interstitial/reticular opacity
  93. 93. Pathologic-Radiographic Patterns Inter- and intralobular septal thickening Alveolar space filling with preserved air in bronchi “Interstitial “Alveolar
  94. 94. Radiographic Patterns Alveolar filling pattern Interstitial pattern
  95. 95. C U R B - 65 Confusion BUN >7 mmol/L (20 mg/dL) Respiratory rate ≥30 bpm Blood pressure SBP <90 mmHg DBP ≤60 mmHg Age
  96. 96. CURB-65 Score and Mortality Mortality(%) 0 20 40 60 80 100 Total CURB-65 Scores 0 1 2 3 4 5 1 2 9 15 40 57 Total CURB scores:
 0-1 Outpatient setting 2 Inpatient setting ≥3 ICU management Lim WS, van der Eerden MM, Laing R, et al. Thorax 2003; 58:377–82.
  97. 97. Diagnostic Workups Microbiology workups Clinical Status workups Sputum Gram stain Culture for bacteria Blood Hemoculture BUN, CrCBC Arterial Blood Gas
  98. 98. Principles of Empirical Therapy Confirmation of infection Defining location of infection Common pathogen(s) Host 
 factors Environmental factors Infected or suspected organ(s) Bacteria Virus fungus Alternative diagnosis of noninfectious disease? AIDS Cirrhosis Diabetes CKD Alcoholics Community Hospital
  99. 99. Recommended Empirical Antibiotics: OPD Previously healthy; No previous ATB use within 3 months A Macrolide (Roxithromycin, Clarithromycin, Azithromycin) Doxycycline Presence of Comorbidities 
 (chronic heart, lung, renal or liver disease, DM, 
 alcoholism, malignancy, aplenia, immunosuppressed) Previous ATB use within 3 months A respiratory fluoroquinolone (Levofloxacin, Gemifloxacin, Moxifloxacin) A beta-lactam (Amoxicillin-clavulanate, Cefdinir, Cefspan) PLUS a macrolide Incidence of DRSP >25% A respiratory fluoroquinolone Mandell L A, Wunderink R G, Anzueto A, et al. CID 2007; 44:S27–72.
  100. 100. Recommended Empirical Antibiotics: IPD & ICU ICU treatment A beta-lactam (cefotaxime, ceftriaxone, or ampicillin-sulbactam) 
 PLUS azithromycin or a respiratory FQ Pseudomonas infection suspected An antipneumococcal, antipseudomonal beta-lactam 
 (piperacillin-tazobactam, cefipime, imipenem, meropenem) PLUS either Ciprofloxacin or Levofloxacin The above beta-lactam PLUS antipneumococcal fluoroquinolone PLUS an aminoglycoside MRSA suspected Add Vancomycin or linezolid Non-ICU treatment A respiratory floroquinolone IV A beta-lactam PLUS a macrolide IV Mandell L A, Wunderink R G, Anzueto A, et al. CID 2007; 44:S27–72.
  101. 101. Supportive Treatment Respiratory & Hemodynamic support Drainage & Airway clearance Chest physical therapy Postural drainage Coughing/huffing Symptomatic treatment 
 Mucolytic/expectorants Antipyrexia Bronchodilators Oxygen support: Oxygen cannula Oxygen mask Ventilatory support: Noninvasive Invasive Hemodynamic support: Noninvasive Invasive
  102. 102. Treatment Modification in Host Defense Abnormalities Diabetes Gram negative bacilli Melioidosis Mucormycosis Aspergillus spp. Candida spp. Alcoholics Liver disease Gram negative bacilli Anaerobes Chronic lung disease Gram negative bacilli P. aeruginosa Nocardia spp. Aspergillus spp. AIDS Pneumocystis jirovecii Toxoplasma spp. Rhodococcus spp. Histoplasma spp. C. neoformans Penicillium marneffii Ceftazidime Meropenem Amphotericin B Voriconazole Amoxicillin-clavulanate Ceftazidime Cotrimoxazole Cotrimoxazole Levofloxacin Amphotericin B Itraconazole
  103. 103. Complications of Pneumonia Acute respiratory failure ARDS Pleural effusion Empyema Lung abscess Sepsis Septic shock
  104. 104. Pleural Effusion
  105. 105. Pleural Cavity and Pleural Fluid History of close contact to a patient with MDR-TB Return after default of >2 months Relapse pulmonary TB Treatment failure (smear positive at 5th month) Special population (immigrants, prisoners, 
 HIV infected persons)
  106. 106. Pleural Effusion: Pathophysiology Increased pleural fluid production Decreased pleural fluid reabsorption High hydrostatic Congestive heart failure hepatic hydrothorax Low oncotic Cirrhosis Hypoalbuminemia Nephrotic syndrome Permeability/Leakage Pneumonia Inflammatory diseases Chylothorax Lymphatic obstruction Malignant Effusion Pleural Thickening Complicated parapneumonic effusion Asbestosis Trapped lung Rheumatoid pleurisy (late)
  107. 107. Diagnosis of Pleural Effusion: Chest Radiograph Upright film: blunt costophrenic angle fluid in fissures Decubitus film: fluid shift to dependent area of the lung Supine film: fluid distributed along posterior plane “Filter effect”
  108. 108. Diagnosis of Pleural Effusion: Ultrasonography Effusion without fibrin formation Effusion with fibrin formation
  109. 109. Diagnosis of Pleural Effusion: CT scan Effusion without loculation Effusion with loculation
  110. 110. Pleural Fluid Analysis Specific biochemical tests Additional test(s) Initial biochemical tests Protein LDH Glucose ADA Cholesterol Triglyceride pH Cytology Pathology Tumor/inflammatory markers
  111. 111. Pleural Fluid Analysis: Transudate VS Exudate Modified Light’s Criteria Exudate Transudate Fluid protein/ serum protein ratio >0.5 <0.5 Pleural fluid LDH >200 IU/L or >2/3 upper limit of normal <200 IU/L or <2/3 upper limit of normal Fluid LDH/ serum LDH ratio >0.6 <0.6 Additional Criteria Exudate Transudate Pleural fluid protein >3 g/dL <3 g/dL Pleural fluid cholesterol >45 mg/dL <45 mg/dL Fluid cholesterol/ serum cholesterol ratio >0.3 <0.3 Albumin gradient ≤1.2 g/dL >1.2 g/dL
  112. 112. Pleural Fluid Analysis: Cell Count and Differentials Neutrophil predominated exudates Acute bacterial pneumonia Acute pulmonary embolism Acute pancreatitis Rheumatoid pleurisy (acute) Tuberculous effusion (acute) Lymphocyte- predominated exudates Tuberculous effusion Chylothorax Lymphoma Rheumatoid pleurisy (chronic) Sarcoidosis Uremic pleuritis Post surgery Eosinophil- predominated exudates 
 Pneumothorax Hemothorax Benign asbestos Pulmonary embolism Parasitic disease Fungal disease Lymphoma Churg-Strauss syndrome
  113. 113. Pleural Fluid Analysis: Other Special Tests Diseases Diagnostic pleural fluid tests Empyema Present of microbial or positive culture Malignancy Positive cytology Lupus pleuritis Positive LE cells Tuberculous pleural effusion Positive AFB stain, ADA >40 IU/L Esophageal rupture Salivary amylase, pH <6.0 Chylothorax Triglyceride >110 mg/dL; positive chylomicrons Cholesterol effusion Cholesterol >300 mg/dL; Cholesterol/triglyceride ratio >1.0, cholesterol chrystals
  114. 114. Pleural Fluid Analysis: Other Special Tests Diseases Diagnostic pleural fluid tests Hemothorax Hematocrit of pleural effusion/blood ratio >0.5 Rheumatoid pleurisy Characteristic cytology; pH <7.0, glucose <30 mg/dL, LDH >1,000 IU/L Peritoneal dialysis Protein <1.0 g/dL, glucose >300 mg/dL Urinothorax Creatinine of pleural fluid/serum ratio >1.0
  115. 115. Parapneumonic Effusion
  116. 116. Clinico-pathological Stage in Pleural Effusion Exudative phase Fibropurulent phase Organizing stage Parenchymal inflammation with
 neutrophilic migration Release of IL-6, IL-8, TNF-α Increased vascular permeability Fluid moves into pleural space Secondary bacterial invasion
 into pleural space Depression of intrapleural fibrinolytic activity Fibrin formation and loculation of intrapleural fluid Release of platelet-derived growth factors (PDGF) and transforming growth factor (TGF-β) Proliferation of fibroblasts Pleural scarring
  117. 117. Pleural Fluid Characteristics Simple parapneumonic effusion Complicated parapneumonic effusion Empyema Appearance Maybe turbid Maybe cloudy Pus Biochemical Markers pH >7.30 LDH elevated (F/P >0.6) Protein elevated (F/P >0.5) Glucose >60 mg/dL pH <7.20 LDH >1000 IU/L Glucose <35-40 mg/dL n/a Cell differentials Neutrophil (usually <10,000/µL) Neutrophil (usually >10,000/µL n/a Gram stain negative negative positive Culture negative maybe positive maybe positive
  118. 118. Bacteriology of Pleural Fluid Cultures 6% 15% 16% 17%47%Streptococci Staphylococci Aerobic Gram negatives Anaerobes Others E. coli Klebsiella spp. P. aeruginosa Enterobacter spp. S. pneumoniae S. milleri S. pyogenes S. aureus MRSA
  119. 119. Management of Parapneumonic Effusion Confirmation of pleural effusion: Chest radiograph, ultrasonography or CT pH <7.20 LDH > 1,000 IU/L Glucose <35 mg/dL Positive Gram stain Positive culture Frank pus Thoracentesis: 
 for pH, LDH, glucose, Gram stain, culture Drainage pH >7.30 LDH <1,000 IU/L Glucose >60 mg/dL Negative microbiology Fluid amount >1/2 hemithorax Observe yes no
  120. 120. Sepsis and Septic Shock
  121. 121. Host–pathogeninteraction Proinflammatory response Excessive inflammation causing collateral damage (tissue injury) Antiinflammatory response Pathogen factors Host factors Environment Genetics Age Other illnesses Medications Load Virulence Pathogen-associated molecular patterns Immunosuppression with enhanced susceptibility to secondary infections Cytokines Proteases Reactive oxygen species Complement products Perpetuation of inflammation Coagulation proteases Damage-associated molecular patterns Leukocyte activation Neuroendocrine regulation Impaired function of immune cells Inhibition of proinflammatory gene transcription Complement activation Coagulation activation Necrotic cell death NLRs RLRs TLRs CLRs Vagus nerve Apoptosis of T, B, and dendritic cells Antiinflammatory cytokines Soluble cytokine receptors Negative regulators of TLR signaling Epigenetic regulation Brain Celiac ganglion Liver, intestine Norepinephrine Acetylcholine Spleen Adrenal gland Inhibition of proinflammatory cytokine production Catecholamines Cortisol Hypothalamic– pituitary– adrenal axis Expansion of regulatory T and myeloid suppressor cells Impaired phagocytosis Endosome Host cell
  122. 122. MicrocirculationTissue Release of mitochondrial contents Mitochondrial dysfunction Increased coagulation Decreased anticoagulation Monocyte Neutrophil NETs with trapped platelets Tissue factor ↓ Antithrombin Endothelial cell ↓Tissue factor pathway inhibitor ↓ TM ↓ Endothelial protein C receptor ↓ Protein C ↓ Activated protein C ↓ Activated protein C and ↑ thrombin ↓Fibrinolysis↑ PAI-1 Thrombosis Tissue hypoperfusion Loss of barrier function ↓Tissue oxygenation Organ failure ↑ PAR1 S1P3 S1P1 ↑ S1P3 and ↓ S1P1 ↑ Angiopoietin 2 ↓ VE cadherin and ↓Tight junctions Cell shrinkage and cell death Capillary leak and interstitial edema Vasodilatation ↓ Blood pressure ↓ Red-cell deformability Thrombus Tissue hypoperfusion Loss of barrier function
  123. 123. Management of Sepsis Component 2: Resuscitation & Hemodynamic monitoring Component 1: Diagnosis & Severity assessment Component 3: Sepsis workup & Sepsis control Component 4: Respiratory & Metabolic support Management of Sepsis
  124. 124. Component 1: Diagnosis & Severity assessment Management of Sepsis
  125. 125. Infectious VS Noninfectious Causes of Fever Causes of FeverCauses of Fever Infectious Noninfectious Central Nervous System Meningitis Encephalitis Cerebral infarction/hemorrhage Seizure Respiratory system Pneumonia Empyema Sinusitis Deep vein thrombosis Atelectasis Pulmonary embolism Gastrointestinal/Hepatobiliary system Intra-abdominal abscess Cholecystitis/cholangitis Peritonitis GI hemorrhage Pancreatitis Ischemic colitis Genitourinary system Cystitis Pyelonephritis Skin, soft tissue, bones and joints Cellulitis Wound infection Septic arthritis Thrombophlebitis Gout/pseudogout Vasculitis
  126. 126. Definition Infection Bacteremia Septicemia Sepsis Sepsis induced hypotension Severe sepsis Septic shock Presence of microbial invasion Presence of microbes or toxin in blood Infection PLUS SIRS SIRS PLUS hypotension, fluid responsive SIRS PLUS ≥2 organ dysfunction severe sepsis PLUS hypotension, fluid irresponsive
  127. 127. Assessment of Severity: APACHE II Score
  128. 128. Assessment of Severity: APACHE II Score
  129. 129. Component 2: Resuscitation & Hemodynamic monitoring Management of Sepsis
  130. 130. Early Goal-Directed Therapy (EGDT) for Septic Shock
  131. 131. Central Venous Pressure Measurement: Noninvasive Phlebostatic axis
  132. 132. Central Venous Pressure Measurement: Invasive Venesection “Cutdown” Internal Jugular vein cathether Subclavian vein catheter Pulmonary artery catheter “Swan-Ganz” Venesection “cutdown” Internal jugular vein catheter Subclavian vein catheter Pulmonary artery (Swan-Ganz) catheter
  133. 133. Fluid Resuscitation: Types of Solution Crystalloid ColloidCrystalloid ColloidCrystalloid Colloid
  134. 134. Importance of Fluid Resuscitation ภาวะปกติ ภาวะติดเชื้อรุนแรง ภาวะติดเชื้อรุนแรง Normal Severe Infection Vasodilatation Decreased vascular tension Fluid 
 resuscitation Restoration of vascular tension
  135. 135. Fluid Resuscitation: Fluid Challenge Testing Time CVP (cmH2O) Fluid challenge Initial reading <15 200 mL in 15 min ≥15 50-100 mL in 15 min During fluid challenge increase >5 cmH2O Stop and wait Following fluid challenge increase >3 cmH2O wait ≤3 cmH2O Repeat
  136. 136. Fluid Resuscitation: Target Central venous pressure (CVP) 12-15 cmH2O AND Mean arterial pressure (MAP) ≥65 mmHg Mean arterial pressure = [Systolic blood pressure (SBP) + 2 x Diastolic blood pressure] 3 Mean arterial pressure = [Systolic blood pressure (SBP) + 2 x (Diastolic blood pressure (DBP)] 3
  137. 137. Vasopressor Therapy in Patients with Sepsis Dopamine 5-20 µg/kg/min Norepinephrine 0.1 µg/min Dopamine + Norepinephrine + Epinephrine
  138. 138. Resuscitation of Microcirculation Level: Rationale O2 CO2 Delivery Consumption
  139. 139. Oxygen Delivery to Tissues Inspired oxygen Lung Heart pump Blood content Oxygen delivery = 10 x Cardiac output x [(1.39 x Hb x SaO2) + (PaO2 x 0.0031)] Pump Lung OxygenBlood content Lung Heart pump Blood 
 content Oxygen delivery = 10 x Cardiac output x [(1.39 x Hb x SaO2) + (PaO2 x 0.0031)] Pump Blood content Lung Oxygen
  140. 140. Maximizing Oxygen Delivery to Tissues: Oxygen & Lungs Oxygen Therapy Mechanical Ventilatory Support Oxygen Therapy Mechanical Ventilatory Support Oxygen therapy Mechanical 
 ventilatory support
  141. 141. Maximizing Oxygen Delivery to Tissues: Cardiac Output Inotropic drugs increase myocardial contractility Dopamine 5-20 µg/kg/min Dobutamine 5-15 µg/kg/min Inotropic drugs increase myocardial contractility Dopamine 5-20 µg/kg/min Dobutamine 5-15 µg/kg/min
  142. 142. Maximizing Oxygen Delivery to Tissues: Blood Content Inotropic drugs increase myocardial contractility Dopamine 5-20 µg/kg/min Dobutamine 5-15 µg/kg/min Red cell transfusion increase Hb-O2 binding capacity Keep Hct 30%
  143. 143. Component 3: Sepsis workup & Sepsis control Management of Sepsis
  144. 144. Microbiological Studies in Sepsis Workup Direct identification Culture system Gram stain AFB stain Fluid/secretion Blood
  145. 145. Primary Source of Infection Respiratory system Pneumonia Lung abscess Empyema thoracis Deep neck infection KUB system Acute pyelonephritis Acute cystitis GU system Tubo-ovarian abscess Pelvic infection Skin & Soft tissue Cellulitis Necrotizing fasciitis GI system Acute cholangitis Acute cholecystitis Peritonitis CNS system Acute meningitis Acute cerebritis Acute meningoencephalitis
  146. 146. Septic Workup Procedures and Specimen Collection Lumbar puncture Thoracentesis Paracentesis ArthrocentesisLumbar puncture Thoracentesis Paracentesis Arthrocentesis
  147. 147. Blood Collection for Hemoculture Catheter/device Peripheral veinCatheter/device Peripheral vein
  148. 148. Principles of Empirical Therapy Confirmation of infection Defining location of infection Common pathogen(s) Host 
 factors Environmental factors Infected or suspected organ(s) Bacteria Virus fungus Alternative diagnosis of noninfectious disease? AIDS Cirrhosis Diabetes CKD Alcoholics Community or Hospital
  149. 149. Recommended Antimicrobial Therapy: Community-acquired Infected/Suspected Organ Respiratory Intra-abdominal Skin & soft tissue Urinary tract CNS Common pathogens S. pneumoniae H. influenzae Legionella spp. C. pneumoniae E. coli B. fragilis S. pyogenes S. aureus Polymicrobials E. coli Klebsiella spp. Proteus spp. Enterococci S. pneumoniae N. meningitidis L. monocytogenes H. influenzae Recommended therapy Ceftriaxone or cefotaxime PLUS azithromycin Ceftriaxone PLUS metronidazole Cloxacillin/ Vancomycin OR Amoxicillin- Clavulanate Ciprofloxacin or Levofloxacin OR Amoxycillin- clavulanate Ceftrixone or cefipime PLUS Ampicillin Vancomycin
  150. 150. Recommended Antimicrobial Therapy: Hospital-acquired Infected/Suspected Organ Respiratory Intra-abdominal Skin & soft tissue Urinary tract CNS Common pathogens K. pneumoniae P. aeruginosa A. baumanii MRSA E. coli Klebsiella spp. P. aeruginosa Anaerobes Candida spp. S. pyogenes S. aureus Polymicrobials E. coli Klebsiella spp. Proteus spp. Enterococci S. pneumoniae N. meningitidis L. monocytogenes H. influenzae Recommended therapy Imipenem Meropenem PLUS colistin PLUS vancomycin Imipenem Meropenem PLUS aminoglycosides Imipenem Meropenem Cefipime PLUS vancomycin Imipenem Meropenem Cefipime PLUS vancomycin Cefipime PLUS vancomycin Adapted from: Simon D, Trenholme G. Crit Care Clin. 2000;16:215-230.
  151. 151. Host Defense-modifying Conditions Diabetes Gram negative bacilli Melioidosis Mucormycosis Aspergillus spp. Candida spp. Alcoholics Liver disease Gram negative bacilli Anaerobes Chronic lung disease Gram negative bacilli P. aeruginosa Nocardia spp. Aspergillus spp. AIDS Pneumocystis jirovecii Toxoplasma spp. Rhodococcus spp. Histoplasma spp. C. neoformans Penicillium marneffii
  152. 152. Speed is Life!
  153. 153. Antimicrobial Therapy Delay and Mortality Kumar A, Robers D, Wood K E, et al. Crit Care Med 2006; 34:1589-1596. 0 0.25 0.5 0.75 1 0 0.5 1 2 3 4 5 6 9 12 24 >36 Fraction of patients receiving therapy Fraction of surviving patients Time laps from recognition to the first dose of antimicrobials Fraction of Patients Kumar A, Robers D, Wood K E, et al. Crit Care Med 2006; 34:1589-1596.
  154. 154. “We recommend that intravenous antibiotic therapy be started as early as possible and within the first hour of recognition of septic shock and severe sepsis without septic shock.” Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008
  155. 155. Surgical Control of Infection Drainage Remove
  156. 156. Component 4: Respiratory & Metabolic support Management of Sepsis
  157. 157. Mechanical ventilatory support Sedation Analgesia Stress ulcer prophylaxis Transfusion therapy DVT prophylaxis Renal 
 replacement Glucose 
 control
  158. 158. Thank You

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