Internal medicine review for national license examination 2

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

Asthma
COPD
Pneumonia
Tuberculosis
Sepsis and septic shock
Pleural eﬀusion

Airway Diseases: Asthma and COPD

General Steps of Approach of Airway Diseases
Typical
symptoms of  
airway disease
Detailed
history/examination
Diagnostic tests

Typical Clinical Features in Airway Diseases
Mucociliary
clearance
Bronchospasm
Coughing
Sneezing
Chronic cough Sputum  
production
Wheezing  
Dyspnea/shortness of breath
Chest tightness

Spirometry with Bronchodilator Response Test
Airflow limitation: Reduced FEV1/FVC (Normal 0.75-0.80)
Reversibility: FEV1 increases >12% and 200 mL

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

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

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)

Pathogenesis of Allergic Asthma

Airway Abnormalities in Asthma
Normal bronchiole Asthmatic bronchiole
1
2
3
4
Smooth muscle  
hypertrophy
Vascular proliferation  
Capillary leakage
Submucosal gland
hypertrophy
Mucous  
hypersecretion

Physiologic Change in Asthma
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Airway Resistance
Airway narrowing
➡ 
Increased resistance
➡
Increased work of breathing
➡
Dyspnea, muscle fatigue
➡
Respiratory failure

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

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

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

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%

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

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

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

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

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

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

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

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

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

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

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

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)

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

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

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

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

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

IMPORTANT!!
Acute exacerbation of asthma = uncontrolled asthma
Review and modify treatment to prevent another exacerbation
BEFORE send them home

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

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

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

Causes and Pathogenesis of COPD
สาเหตุและกลไกการเกิดโรคปอดอุดกั้นเรื้อรัง

Physiologic and Health Effects of COPD
Expiratory airflow limitation
Air trapping
Hyperinflation
Inactivity
Deconditioning Activity limitation Poor quality of life
Dyspnea
Exacerbations

Diagnosis
การวินิจฉัยโรคปอดอุดกั้นเรื้อรัง

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

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

B CA D
Less symptoms
Low risk
MORE symptoms
Low risk
Less symptoms
HIGH risk
MORE symptoms
HIGH risk

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 ☐

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

Exacerbations and Progression of COPD
การกำเริบเฉียบพลันกับการดำเนินโรค
FEV1
อายุ
ไมมีการกำเริบ
เสียชีวิต
เริ่มมีอาการ
เกิดการกำเริบเฉียบพลัน
ยิ่งมีการกำเริบของโรคบอย และมาก ยิ่งทำใหเสียชีวิตเร็วยิ่งขึ้นMORE exacerbations HIGHER mortality

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%%

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.

Components of COPD Management
Component 2:
Symptom & Risk Management
Component 1:
Identify &
Control risk factors
Component 3:
Rehabilitation & Health promotion

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

Component 1:
Identify and Control Risk Factors

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.

Immunization for COPD Patientsการใหวัคซีนแกผูปวยโรคปอดอุดกั้นเรื้อรัง
Influenza vaccine Pneumococcal vaccine
ควรพิจารณาใหกับผูปวยทุกรายหากเปนไปได
ทั้งนี้ขึ้นกับแนวปฏิบัติบริการในประเทศนั้น ๆ

Component 2:
Symptom and Risk Management

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

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

Component 3:
Rehabilitation and Health Promotion

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

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

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.

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.

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].

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

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

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.

Radiographic Patterns of Tuberculosis
Reticulonodular
infiltration
Miliary pattern
lymphatic/interstitial spread
Cavitation
Bronchiectatic
change
Bronchoalveolar pattern
bronchial-alveolar spread

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
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

Diagnostic Algorithm: Radiographically-suggestive
Asymptomatic patient with 
radiographically suggestive tuberculosis
Sputum examination for acid-fast bacilli
Review previous chest radiograph
AFB - positive
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

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

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”

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

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

“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)

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

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

Antituberculosis Drug Side Effects: Major
Isoniazid Rifampin Pyrazinamide Ethambutol Streptomycin
Skin rash ☑ ☑ ☑ ☑ ☑
Confusion ☑ ☑ ☑ ☑
Hepatitis/Jaundice ☑ ☑ ☑
Renal dysfunction ☑ ☑
Thrombocytopenia ☑
Nystagmus/vertigo ☑
Visual disturbance ☑

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

Treatment After Interruption
Interruption occurred during
intensive phase of treatment
Duration of interruption
Duration of interruption
≥80%
Continue
treatment
until
complete
yes no
Total treatment received
<80%
<14 days ≥14 days
Continue
treatment
until
complete
Start over
<3 months≥3 months

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

The Disease Triangle
Host Pathogen
Environment

Airway-Lung Defense Mechanisms
Mucociliary
clearance
Bronchospasm
Cellular/
chemical
immunity
Coughing
Sneezing
Mechanical
barriers

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

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

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.

Host Defense-modifying Conditions
Diabetes
Gram negative bacilli
Melioidosis
Mucormycosis
Aspergillus spp.
Candida spp.
Alcoholics
Liver disease
Anaerobes
Chronic lung disease
P. aeruginosa
Nocardia spp.
Aspergillus spp.
AIDS
Pneumocystis jirovecii
Toxoplasma spp.
Rhodococcus spp.
Histoplasma spp.
C. neoformans
Penicillium marneﬃi

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

Pathologic-Radiographic Patterns
Inter- and intralobular
septal thickening
Alveolar space filling
with preserved air in bronchi
“Interstitial “Alveolar

Radiographic Patterns
Alveolar filling pattern Interstitial pattern

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

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.

Diagnostic Workups
Microbiology
workups
Clinical Status
workups
Sputum
Gram stain
Culture for bacteria
Blood
Hemoculture
BUN, CrCBC Arterial Blood Gas

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

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.

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.

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

Treatment Modification in Host Defense Abnormalities
Diabetes
Melioidosis
Mucormycosis
Aspergillus spp.
Candida spp.
Alcoholics
Liver disease
Anaerobes
Chronic lung disease
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

Complications of Pneumonia
Acute respiratory failure
ARDS
Pleural eﬀusion
Empyema
Lung abscess Sepsis
Septic shock

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)

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)

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”

Diagnosis of Pleural Effusion: Ultrasonography
Eﬀusion without fibrin formation Eﬀusion with fibrin formation

Diagnosis of Pleural Effusion: CT scan
Eﬀusion without loculation Eﬀusion with loculation

Pleural Fluid Analysis
Specific
biochemical tests
Additional test(s)
Initial biochemical
tests
Protein
LDH
Glucose
ADA
Cholesterol
Triglyceride
pH
Cytology
Pathology
Tumor/inflammatory markers

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

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

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

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

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

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

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

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

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

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

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

Component 1:
Diagnosis &
Severity assessment
Management
of
Sepsis

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

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

Assessment of Severity: APACHE II Score

Component 2:
Resuscitation &
Hemodynamic monitoring
Management
of
Sepsis

Early Goal-Directed Therapy (EGDT) for Septic Shock

Central Venous Pressure Measurement: Noninvasive
Phlebostatic axis

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

Fluid Resuscitation: Types of Solution
Crystalloid ColloidCrystalloid ColloidCrystalloid Colloid

Importance of Fluid Resuscitation
ภาวะปกติ ภาวะติดเชื้อรุนแรง ภาวะติดเชื้อรุนแรง
Normal Severe Infection
Vasodilatation
Decreased vascular tension
Fluid  
resuscitation
Restoration
of vascular tension

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

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

Vasopressor Therapy in Patients with Sepsis
Dopamine
5-20 µg/kg/min
Norepinephrine
0.1 µg/min
Dopamine
+
Norepinephrine
+
Epinephrine

Resuscitation of Microcirculation Level: Rationale
O2
CO2
Delivery
Consumption

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

Maximizing Oxygen Delivery to Tissues: Oxygen & Lungs
Oxygen Therapy
Mechanical
Ventilatory
Support
Oxygen Therapy
Mechanical
Ventilatory
Support
Oxygen therapy
Mechanical  
ventilatory support

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

Maximizing Oxygen Delivery to Tissues: Blood Content
Inotropic drugs
Red cell transfusion
increase Hb-O2 binding capacity
Keep Hct 30%

Component 3:
Sepsis workup &
Sepsis control
Management
of
Sepsis

Microbiological Studies in Sepsis Workup
Direct identification Culture system
Gram stain AFB stain Fluid/secretion Blood

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

Septic Workup Procedures and Specimen Collection
Lumbar puncture Thoracentesis Paracentesis ArthrocentesisLumbar puncture Thoracentesis Paracentesis Arthrocentesis

Blood Collection for Hemoculture
Catheter/device Peripheral veinCatheter/device Peripheral vein

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

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

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.

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.

“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

Surgical Control of Infection
Drainage Remove

Component 4:
Respiratory &
Metabolic support
Management
of
Sepsis

Mechanical
ventilatory
support
Sedation
Analgesia
Stress ulcer
prophylaxis
Transfusion
therapy
DVT
prophylaxis
Renal  
replacement
Glucose  
control

Internal medicine review for national license examination 2

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