Merge From Ofoct

Respiratory System Disease
The First Affliated Hospital of XinJiang Medical

University
Respiratory Centre
Bin Jia
Demand
• Be familiar with the anatomy and physiology of
respiratory system.
• To master the main symptoms, signs, laboratory

examination and diagnosis,differential diagnosis of
respiratory disease.
• To know the cause of respiratory disease and the

present situation,the progress of the frontier of the
respiratory diseases.
Pandect
• Common and Frequently-Occurring Disease.
• Accounted for the fourth place of city mortality in
China，the fourth place in countryside.(except lung
cancer,COPD,TB----2009,ministry health of China)
• High morbidity,high disability rate,high mortality.
• Lung cancer account for the first place of all
malignant tumor(liver cancer, Gastric cancer, breast
cancer,etc).
• Increasing trend of incidence rate.Health killer,
heavey burden on society.(SARS-2003!!!)
Anatomy and Physiology of Respiratory System
• The upper respiratory tract:Up from the nasal

cavity,to the throat(nasal and oral cavities,pharynx
咽,larynx 喉 and trachea)
{warm,moisten and filter the air}

Lower respiratory tract: below the cricoid 环状软骨
cartilage(main bronchi and lungs)
• Divided into right and left main bronchus at the
trachea carina,segmental and subsegmental branches
until the acinus is reached.
The Respiratory System Structure
The Respiratory System Structure
• Right main bronchus:divided into upper,middle and

lower lobes by oblique and horizontal fissure(10
sections).
• Left main bronchus:divided into uper and lower lobe
bronchi by oblique fissure(8 sections).
• Two groups of blood supply:pulmonary circulation
(gas exchange) and systemic circulation(nutrient
vessels).
• The lymph network drains into the thoracic duct.
The Relationship Between Structure and Disease
• Open system :the most frequently contact with the

outside world, liable be affected by kinds of harmful
factors(sensitinogen,pathogen,etc...).
• General breathing area of Adult about 100 square
meters.10 thousand liter gas exchanged per day.
• Low pressure,low resistance and high capacity system.
• The lymph and blood flow of the lung are interlinked

with the whole body organs.(thrombus, tumor
thrombus, bacterial embolus)
Major Related Influencing Factors
• The harm of air pollution and smoking
• Increased inhaled allergen
• The etiology characteristics of respiratory

System infection
• Aging Population.
Diagnosis of respiratory system disease
• Medical history
• Symptoms
• Signs
• Laboratory and other tests

Medical history
• Details of personal history, exposure history,

occupational history, medication history and family
history.
• Systemic rheumatic diseases;Risk factors for

AIDS;Drug use (immunosuppressive agents, cancer
chemotherapy, radiation therapy, amiodarone, ß-
blocking agents, angiotensin-converting enzyme
inhibitors (ACEI)
History of smoking
• The number of years of smoking
• The intensity (i.e., number of packs per day)
• The interval since smoking cessation
• A history of significant secondhand (passive)
exposure to smoke .
• COPD,Asthma, Neoplasia, Spontaneous pneumothorax,

Respiratory bronchiolitis-interstitial lung disease
Family factors
Genetic component:
• 1.Cystic fibrosis
• 2.α1-antitrypsin deficiency
• 3.Pulmonary hypertension
• 4.Asthma
Symptoms
Cough：
• Acute(bronchitis) or chronic(COPD)?
• Seasonal or associated with wheezing? (Asthma)
• Associated with chest pain(peumonia)
• Associated with fever or sputum?
• Irritation dry cough，persistence.(lung cancer)
• Any associated diseases or risk factors for disease
(e.g., cigarette smoking, risk factors for infection with HIV,
environmental exposures)?
Symptoms
Sputum:
• character, quantity and odour.
• Large amount of yellow phlegm---Bronchiectasis,
lung abscess .
• Iron-rust sputum---Streptococcus Pneumoniae.
• Fetor---combined with anaerobic bacteria infection.
• Thin pink froth sputum---Pulmonary edema patient.
• Coffee like phlegm---lung Amoebiasis 阿米巴--amoeba.
Symptoms
Hemoptysis:
• Originated from the airways: distinguish with
haematemesis[hɛmə'tɛməsɪs] or bleeding from the
nasopharynx[neɪzəʊ'færɪŋks].
→Bronchitis, Bronchiectasis, Cystic fibrosis, Bronchial
carcinoma 肺癌.(smokers)
• Originating from the pulmonary parenchyma:
→ Pneumonia, Lung abscess, Tuberculosis, Infection with
Aspergillus, Goodpasture’s syndrome,
• Originating from the vasculature:
→ Thromboembolic diseases, Arteriovenous malformations 畸形.
Symptoms
Chest pain：
• Related with breath and cough usually be
pleurisy.(sharp pain)
• Continuous and do not relieve may be lung
cancer.
• Company with high fever and chill may be
pneumonia.
• Rib fracture,herpes zoster—localised chest
wall tenderness.
Symptoms
Dyspnea:
Acute (over a period of hours to days):
1.Acute attack of Asthma
2.Acute pulmonary edema (coronary heart disease)
3.Bacterial pneumonia
4.Pneumothorax
5.Pulmonary embolus
Symptoms
Dyspnea:
Subacute (over days to weeks):
1. Asthma
2. Chronic bronchitis
3. Pleural effusion
4. Congestive heart failure
Symptoms
Dyspnea:
Chronic (over months to years):
• 1. COPD
• 2. Chronic interstitial lung disease
• 3. Chronic cardiac disease
Signs
• Pay attention to acropachia ,cyanosis
杵状指 [,saɪə'nəʊsɪs],
position of the trachea,breath sound and rales

of the lung.
• Signs of the lung does not parallel with the
severity of disease. Negative signs do not
mean no disease,but positive signs state the
lesion of lung.
Phisical examination:
• Inspection: The rate and pattern of breathing; The depth and
symmetry of lung expansion.
• Palpation:The symmetry of lung expansion confirming the
findings observed by inspection;Vibration produced by spoken
sounds.
• Percussion:The relative resonance or dullness of the tissue
underlying the chest wall.
• Auscultation:The quality and intensity of the breath sounds
and extra sounds[crackles (rales), rhonchi, pleural friction
rubs and stridor.
Laboratory examination
• Blood test:Indicate infection or allergy etc,
serological antibody test has diagnostic values in
Virus, Mycoplasma,Bacteria infection.
• Antigen Skin test: Allergen skin test positive of
Asthma help determine allergies and desensitization 脱
敏 treatment with antigen.
• Examination of sputum:pathological examination

can help find lung cancer,bacterial exam find
pathogenic bacterium.
• Pleural effusion exam：Identification of benign or
malignant. transudate or exudate.
Collection of Sputum
• Collected either by spontaneous expectoration or
after inhalation of an irritating aerosol 喷雾剂['eərəsɒl], such
as hypertonic saline.高渗生理盐水
• Qualified Sample: Squamous epithelial cells <10/HP,
WBC >25/HP or WBC/Squamous epithelial cells
>2.5.
X-ray
Good for image of lung tissue full of gas(postero-anteria)
X-ray
• Lateral radiogragh help localise an abnormality
CT scan
• show bronchus, mediastinum and lymph node.High
resolution CT can show interstitial tissue of the lung.
MRI
• sensitive to mediastinal and vascular disease.
PET
• Positron emission tomographic (PET)
scanning:increasingly being used to identify
malignant lesions in the lung based on their increased
uptake and metabolism of glucose.
• The technique involves injection of a radiolabeled
glucose analogue, 18F-fluoro-2-deoxyglucose
[di:,ɔksi'glu:kəus] (FDG), which is taken up by metabolically
active malignant cells.

Bronchial Arteriography and Embolization
• diagnosing and therapy of massive hemoptysis.

Bronchoscope:
• Passed through either the mouth or nose
Bronchoscope:
• Samples collection and suction:
1. Broncho-alveolar lavage (BAL) (particularly useful
for the recovery of organisms such as Pneumocystis.
carinii in patients with HIV infection) .
2. Transbronchial lung biopsy (TBLB) (complications:

pneumothorax, pulmonary hemorrhage).
3. Culture of secretions.brushing and washing for

microbiological diagnosis.
Blood Gas Analysis:
• has great importance for diagnosing of respiratory failure and
acid-base balance disorders and know about the effect.
Blood Gas Analysis:
• Type I respiratory failure:hypoxic
• Type II respiratory failure:hypoxic and

hypercapnia.
Lung Function Test:
• ventilation,gas-change test,airway stimulating test, movement
lung function inspection,has important significance to evaluate
the lung function before surgery.
Lung Function Test:
• Obstruction：chronic bronchitis,emphasema,asthma
FEV1(forced expiratory volume in one second
)↓FEV1/FVC↓(forced vital capacity)、RV↑、RV/TLC↑
• Restriction：pleurisy,chest deformity, pulmonary

fibrosis.
VC↓,TLC↓
Thoracoscopy
• Mainly used for the diagnosis of pleural diseases and treatment
of pulmonary disease with minimally invasive method.
• medical thoracoscopy and surgical thoracosocpy.
Coexistence
Respiratory
symptoms
Contribution Pulmonary
coorelation function
tests
Physical
examination Chest
radiography
Progress of Diagnosis and Therapy
• Respiratory diseases increased in these years,such
as:Obstructive Sleep Apnea Hypopnea
Syndrome(OSAHS).Interstitial Lung Diseases(ILD).
• Basic subject of diagnosing,like molecular biology
oncogene,anti-oncogene in early diagnosing of lung
cancer.
• Sleep monitor for OSAHS.
• PET-CT for identify the nature of enlarged lymph
nodes in mediastinal(Benign or malignant).
• Ultrasonic bronchoscope(EBUS)
Progress of Diagnosis and Therapy
• In therapy,we have formulated the guidelines for

COPD,HAP and Asthma,regulate the prevention and
control of disease.
• Progress of antibiotics and anti-tuberculosis drugs

improve the prognosis of infection disease.
• The use of kinds of Ventilators and monitors also

improve the prognosis of severe respiratory failure
patients.
Prevention
• Protect the environment, purify the air.
• To improve the way of life, encouraged to stop

smoking.
• To strengthen the management of infectious diseases.

Summary：
• The characteristics of respiratory system

disease,common presentation of
symptom,sign,laboraytory exam and
therapeutic Principle.
• The key point is master the clinical

significance of symptom and sign of
Respiratory system.
Clinical Diagnostics
He yuanbing
The First Affiliated Hospital of Xinjiang Medical University
Department of respiratory medicine1
What is Clinical Diagnostics?
• Fundamental theory（Pathology, anatomy,
immunology, etc.）
Techniques of diagnosing disease（laboratory
science，ultrasonic , etc. ）
Mode of clinical thinking
What is Clinical Diagnostics?
• Instruct a concise logical approach to recognize
the genius of the diseases
• A fundamental course of clinical medicine

Fundamental elements of
Diagnostics
Diagnosis
Identification Analysis
Diagnosis
☆ Derived from Greek words

distinguish or discern
☆ English term
Diagnostic
The distinguishing sign and symptoms with
which it gerenally begins, continues and goes
off…as it were, a history of the disease
\
In 18th century: Nosography

☆
Electrocardiogram, CT, blood test, rash and herpes zoster
nature of pain: Sharp pain, dull pain, knife cut pain, burning pain, colic pain
Persistent pain and paroxysmal pain
☆ In modern usage:
Identification of a disease by investigation of its

signs and symptoms
☆ Medical terminology:
Clinical diagnosis Laboratory diagnosis

X-ray diagnosis Electrocardiographic diagnosis
Gene diagnosis
Identification:
Inquiry
Physical examination
Laboratory tests/Special examination
Analysis:
Basic knowledge of medicine
Overall analysis
Scientific way of clinical thinking
Importance of Diagnostics
Essential
Basic courses
Bridge
Tools
Clinical medicine
Content of Clinical Diagnostics
Symptomatic diagnosis
Physical diagnosis
Laboratory tests or clinical ancillary tests

Medical record
Diagnostic processes and the way of
clinical thinking
Symptomatic Diagnosis
History taking--- Interview

Symptoms --- patient‘s complaints
Epidemic areas, infectious diseases

family history, genetic diseases
Symptom
Subjective sensation that patient describes,

such as headche, cough、dyspnea
Physiological & Pathological
functional Morphological
Fever Cough Rash Mass

Physical Diagnosis
Sign （Fever, tenderness mass and jaundice ）
Abnormality observed by the physician
Conducted with thoroughness , alertness to detect even
slight derivations from normal
Inspection
Palpation
Percussion
Auscultation
stethoscope
Laboratory test or ancillary tests
• Serum, Urine, Stool tests
• X-ray film
• EKG
• Endoscopy
• Ultrasonic imaging（ Abdomen ）
• CT
• MRI
• PET (Positron Emission Tomography)
Medical record
Medical record is a systematized way of
storing the required data, information and
other relevant documents
Specific requirement in terms of format

and content
Special terms in clinical
diagnosis
Impression
Tentative diagnosis
Differential diagnosis
Evidence based medicine
• Preliminary diagnosis/Tentative diagnosis
• Exclusion of other diseases
• Selecting a number of possibilities to explain the

clinical and laboratory findings in the case in question
• The way of exclusion is called Differential diagnosis

It is the conscientious, explicit and judicious
use of current best evidence in making
decisions about the care of the individual
patient
It means integrating individual clinical expertise

with the best available external clinical
evidence from systematic research
One need to:
• Be conscientious: it requires effort and thought.
• Be explicit: decisions will need to be backed up by good
evidence
• Relate to specific problems: it is not about a
hypothetical "average" case. Integrate individual clinical
experience: it does not denigrate clinical skills in history
taking, examination and diagnosis.
One need to:
• Look for current best evidence: the perfect study

may not yet have been published, written up or
even commenced. We may have to settle for
something less rigorous, but be on the look out for
new research that will supersede older studies.
Important aspects---
interrogation 问诊
• To get the history in detail of a patient’s illness

• The history is taken at initial contact between
physician and patient
• As some crucial points might be overlooked by the
patients, one will ask many searching questions to
make the history more informative and complete, who
must at the same time avoid suggesting answers
• Occasionally to interrogate his family member
Other important aspects
• The diagnostic process is very complex
• The number of facts that can be collected in a

detailed medical history and in thorough physical
examination are almost without limit
• The laboratory tests or specialized technical

procedures that can employed are numerous and
costly
• Questions for interrogation, maneuver in P.E.,
laboratory test should be thoughtfully selected
with the view to eliminate some of the possible
diagnosis and guide the search expeditiously to a
specific disease
• Method of approaching a diagnosis:

Analysis of symptoms
Recognition of the syndrome
Consideration of disease mechanisms
Important aspects
• Modern & advanced ancillary techniques:
have their limitations.
It can’t reduced the importance of certain parts
of the classic P. E
• It should be avoided to neglect fundamental
methods
Interrogation
Scientific clinical thinking
Approaches
Basic knowledge learning
Clinical practice
Bedside activity
Standardized patient
Developmental History of
clinical diagnostics
• Western Medicine: from ancient to modern
• Traditional Chinese Medicine

Contribution of ancient doctors---Western
Hippocrates
•Born on the island of Cos,

Greece (c. 460-377 BC)
•The Father of medicine

Hippocratic oath
Hippocratic corpus:
a collection of 70 works
Hippocratic oath
Galen
• c.130-c.200
• His work in
anatomy/physiology is notable
• Identified artery and vein
• Added greatly to knowledge of the
brain, spinal cord and pulse
Auenbrugger
•Born at the village of Graz, Austria (1722)

•Son of an innkeeper
•The working experiences helped him to find
Percussion
•Author of <Inventum Novum>(1761)
translated as ‘On Percussion of the chest’ in 1936
Laennec RTH
•A French physician
•Invented Auscultation and stethoscope
Laennec RTH
1816
Contribution of Western Physician
17th~19th century
Leenwenhock Microscopy (end of 17th century)
Fahrenheit Thermometer (1724)
Ludwig Hematomanometer (1847)
Welcher Hematinometer (1854)
20th century
X-ray film EKG Endoscopy CT PET
Ultrasonic imaging
CT imaging
MRI
PET
Traditional Chinese Medicine
Wood
Fire
Earth
Metal
Water
Contribution of ancient doctors---Chinese
Inspection
Interrogation
Smell
Pulse palpation
Pay attention to:
Good medical ethics
Attach importance to clinical practice
Unit theory with practice

Goals
• Inquiry:
Independent systemic inquiry
Comprehensive understanding of patient’s chief
complains, signs, symptoms and their interrelation
• Physical Examination:
Systemic/thorough
• Familiar with routine tests, EKG manipulation and figure
analysis
• Good case writing and propose the primary diagnosis
• Scientific clinical thinking
nDiseases of Biliary Tract
Department of General Surgery

First Teaching Hospital XJMU
n Anatomy and Pathophysiology
n Diagnostic techniques
n Stones of Biliary tract
n Infection of Biliary tract
n Biliary Tumors
Anatomy of biliary tract
Intrahepatic bile duct:
Biliary tract
Extrahepatic bile duct:

Left hepatic duct
Right hepatic duct
Common hepatic → common bile
duct
Gallbladder →cystic duct

Calot Trangle:
Liver : upper border
Common hepatic duct diameter =0.4-0.6cm
Cystic duct lower border length 3cm
The cystic artery runs in this triangle

Common Bile Duct
n Diameter 0.6-0.8cm > 1cm abnormal
n Length 7-9cm
n supraduodenal segment
n Retro duodenal segment
n Retro pancreatic segment
n Duodenal wall segment
The papilla of Vater
Pancreatic sphincter
The Sphincter Common sphincter

of Oddi
Biliary sphincter
Gallbladder
n Length:8-12cm
n width:3-5cm variable
n size:40-60ml
n shape: pearshaped
component:
fundus
body
the neck
The physiological function of
Gallbladder
n Store and concentrate hepatic bile

n Secretion of water and electrolytes
n Empty bile into the common bile duct
Bile secretion
n Hepatocytes secrete bile 800-1200ml

n Bile composition:
bile acids
bile pigments
cholesterol
phospholipids
inorganic electrolytes
water
Diagnostic techniques
Abdominal Ultrasonography
1.Untraumal
2.Low cost
3.Flexibicity
4.First choice
Abdominal Ultrasonography
n Diagnose biliary stone

n Identify the cause of jaundice
n PTCD by β-ultrasound guided
n Doppler blood flow
Percutaneous Transhepatic
Cholangiography
n Show the dilated bile

duct above obstruction
site
n Drainage of bile by
PTCD
n Traumatic methods
Complications of PTC
n Bile leakage
n Haemorrhage
n Sepsis
ERCP
(Endoscopic Retrograde Cholangiopancreatography)
n Directly observe papilla

lesion and biopsy
n Show the entire biliary
tract
n Show the biliary tract
proximal to obstruction
site
n Drain bile
Complications of ERCP
n Acute pancreatitis
n Postprocedure cholangitis
n Other complications
Operative and postoperative
direct cholangiography
n Show the entire biliary tract

n Display the stone and
stenosis
n Tube cholangiography done
before biliary drainge with
drawn
CT and MRI
n High resolution
n More accurate
n Expensive
n Show the stone ,tumor,
dilated duct
n MRCP show the entire
biliary tree
Plain Radiographs
n Show radio-opaque calcui

n Air in the biliary tree
n Calcification of the
gallbladder
Oral Cholecystography
Show the function of gallbladder

Show the stones polyps and tumor
Contraindications
n Sensitivity to iodine
n Liver and renal disease
n pregnancy
Choledochoscope
n Intraoperative use:
n Explore the CBD stone
n Tumor,stenosis
n Reduce retained stone rate
n Remove stone
n biopsy
Other examination
n Intravenous cholangiogram
n Angiography
n Isotopic studies
How to choose
1.Ultrasound
2.MRCP and CT
3.ERCP and PTC

Infections of biliary tract
1.Cholecystitis
2.Cholangitis
obstruction
stone infection
core
Acute cholecystitis
n Acute calculous
cholecystitis 95%
n Acute acalculous
cholecystitis 5%
Etiology
1.Cystic duct obstructed by a gallstone impacting in
Hartmann’s pouch
2.Bacteial infection of the stagnant bile
Aerobic enteric-derived organisms
Escherichia coli, klebsiella pneumoniae, streptococcus faecalis
gallstone impaction →mucosal damage
Lecithin → lysolecithin
↑
phospholipases
Pathology
Cystic duct obstruction →gallbladder →Edema
→suppurate → gangrene → pericholecystic abscess
→perforation
Cholecyst-enteric fitula Peritonitis
intestinal obstruction
Acute → chronic → atrophy

Clinical features
1.Sudden and severe pain mainly in the right
hypochondrium radiate to the right scapular region
Possible risk factor : fatty foods
2.Nausea and vomiting
3.Fever
4.Tenderness and rigidity in the right upper quadrant
5.Positive Murphy’s sign
6.Jaundice
7.A palpable gallbladder mass (1/4)
Mirrizzi’s Syndrome
The common hepatic is obstructed due to
stones impacted in or extruded from Hartman’s
pouch of the gallbldder or the cystic
duct.Cholecystobiliary or cholecystoenteric
fistulae are common complication.
Differential Diagnosis
n Perforated peptic ulcer

n Acute pancreatitis
n Retrocaecel appendicitis
n Right low lobe pneumonia
n Hepatic abscess
n Acute viral hepatitis
Laboratory Test
n Leukocytosis in the range of l0000-15000

n Serum bilirubin ↑or normal
n Alkaline phosphatase ↑or normal
n Transaminase ↑or normal
n Serum amylase ↑ or normal
Treatment
Conservative treatment
1.Intravenons fluid and electrolyte
replacement
2.Nasogastric suction
3.Systemic antibiotics
4.Parenteral analgesia
Surgical Treatment
1.Attack within 48-72 h of diagnosis

2.Deterioration in patient’s general condition
3.Complications are present
Perforation
Peritonitis
Acute obstructive suppurative cholangitis
Acute pancreatitis
Surgical methods
n Open cholecystectomy
n Laparoscopic cholecystectomy
Indication of Choledochotomy
Patients with known choledocholithiasis

①a history of jaundice
②a history of pancreatitis
③ recurrence of cholangitis
④stones in bile duct confirmed by Intraoperative cholangiography
⑤stones,tumor and ascarids confirmed by surgery
⑥Diameter of common bile duct >1cm
⑦a large cystic duct and small gallstones
⑧there are pus,blood and sandy Pigment stones in bile through
puncture of bileduct
Acalculous Cholecystitis
n Complications of major trauma, burns and
sepsis
n Complications of parenteral feeding
n Not easy to make a clear diagnosis
n Need prompt surgical intervention
n over 70% with atheroscclerotic cardiovascular
disease
n Biliary scintiscanning helpful for diagnosis
Acute cholangitis and acute
obstructive suppurative
cholangitis
Etiology
n Choledocholithiasis 80%
n Benign strictures
n Obstructed biliary anastomotic strictures
n Malignant obstruction
n Ascarid
Pathophysiology
Biliary obstruction →intraductal pressure

>20mH20→biliary stagnation
→bacteremia,bacteria proliferation→reflux
into hepatic veins and perihepatic
lymphatics→systemic signs of cholangitis
Clinical presentation
n Fever and chill
n Jaundice charcot’s triad)
n Right upper-quadrant pain
n Hypotension
n Mental obtundation
Reynold’s Syndromes
n Tenderness
n Abdominal guarding
n Swollen gallbladder
n Hepatomegaly
Laboratory Test
n Leukocytosis
n Hyperbilirubinemia
n Alkaline phosphatase ↑
n Aminotransferases ↑
n Leukopenia
n Profound gram-negative sepsis and
immunosuppression
n Serum amylase ↑
Radiological Evaluation
n Ultrasonography
n CT
n MRCP
n PTC
n ERCP
Treatment
General support
n Cessation of oral intake

n Antibiotics
n Keep liquid and electrolyte balance
n Intravenous fluids
Biliary decompression
n Percutanecus transhepatic biliary drainage

n Endoscopic drainage papillotomy and placement
of a nasobiliary tube
n Operative decompression
n CBD exploration and T tube drainage
Cholelithiasis
Classification of gallstone
Cholesterol stones: light brown, smooth or faceted,
single or multiple cross-section
laminated/crystalline appearance
Pigment stone: small, black or brown, irregular cross-
section a morphous/crystalline
Mixed stone
Location
n Gallbladder stones
n Common bile duct stone Extrahepatic
n Intrahepatic bile duct stone bile duct stone
Clinical presentation
n Dyspepsia
n Right upper quadrant abdominal pain in
association with or shortly after a heavy or fatty
meal
n A feeling of gaseous bloating
n Biliary colic
n Usually normal
n Chronic hydrops of gallbladder→mass
n Some times tenderness
Radiological Test
A plain abdominal roentgenogram
Oral cholecystography
Ultrasonography the initial diagnostic study
CT
MRI
Complications
n Acute cholecystitis
n Jaundice
n Cholangitis
n Pancreatitis
n Mtrizzi syndrome
n cancer
Surgical Indication
n Accelerating symptoms
n Poor visualization or non-visulization on
oral cholecystography
n Diabetas
n Porcelain gallbladder
n stone>2-3cm
Laparoscopic Cholecystectomy
n Indications:
Chronic, uncomplicated cholecystitis
Cholelithiasis
GB polyps
?
n Benefits:
Reducing hospitalization and associated costs
Decreasing pain
Improved cosmetic outcome
Reduced post-operative recovery
Other treatment
n Dietary therapy a low-fat diet, avoidance of
heavy meals
n Antispasmodic medication
n Chenodeoxycholic acid and ursodeoxycholic acid
n Extracorporeal shock wave lithotripsy
Carcinoma of Gallbladder
n Incidence
The most common form of biliary tract malignancy
the fifth gastrointestinal cancer
Encountered in 1-2% of cholecystectomy specimens
Predominantly occurs in elderly females
Over 90% of patients are were 50 years of age
The peak age of incidence is 70-75% years
A male to female ratio of 1:3
Etiology
n Cholelithiasis
n Benign adenoma
n Polypoid gallbladder lesions (polyp greater than
1cm)
n Anomalous pancreatiobiliary junction
n Chronic inflammatory bowel disease
Pathology
n Adenocarcinoma 80% carcinoid
tumours
n Undifferentiated carcinoma 6% sarcoma
n Squamous carcinoma 3%
melanoma
n Mixed tumor or acanthoma 1%
lymphoma
UICC
Ⅰ stage:mucosa and muscular
Ⅱ stage:total layer of the gallbladder
Ⅲ stage:invasion into liver <2cm or
regional lyphatic spread
Ⅳ A stage: invasion into liver >2cm
Ⅳ B stage: spread to distal organ and
lymph node
Clinical Features
n The diagnosis of gallbladder cancer is usually
made when the disease is well advanced. There
are no characteristic features at an early and
curative stage
Laboratory investigations
n Can’t provide diagnostic information

n Provide some helpful clues
n Anaemia
n Serum alkaline phosphatase ↑
n CEA↑
n CA19-9↑
n CA125 ↑
Radiological Diagnosis
n Plain abdominal radiography
n Oral cholecystography
n PTC
n ERCP
n CT
n MRI MRCP
Other Methods for Diagnosis
n FNAC
n ultrasound
Treatment
n UICC Ⅰ cholecystectomy
n UICC Ⅱ
Curative excision procednre
n UICC Ⅲ IVA
extended curative excision
n UICC ⅣB
Palliative procedures
Billiary or duodenal bypass
Prognosis
n Piehler and crichlow
Report of 6000 patients :
1 year survivial rate 11.8%
5 year survival rate 4.1%
Palliative procedure
1.Extra bile drainge
T tube
U tube
PTCD
2.Intra-drainge
Biliary-enteric bypass or intubation
Non-operative endoprosthetic insertion
Clinical Diagnostics
He yuanbing
Department of respiratory medicine
What is Clinical
Diagnostics?
• Fundamental theory（Pathology, anatomy,
immunology, etc.）
Techniques of diagnosing disease（laboratory
science，ultrasonic , etc. ）
Mode of clinical thinking

What is Clinical
Diagnostics?
• Instruct a concise logical approach to recognize
the genius of the diseases

• A fundamental course of clinical medicine

Fundamental elements of
Diagnostics
Diagnosis
Identification Analysis

Diagnosis
Derived from Greek words☆
distinguish or discern
☆ English term
Diagnostic
The distinguishing sign and symptoms with which
it gerenally begins, continues and goes off…as it
were, a history of the disease
\
In 18th century: Nosography
☆Electrocardiogram, CT, blood test, rash and herpes zoster
nature of pain: Sharp pain, dull pain, knife cut pain, burning pain, colic pain
Persistent pain and paroxysmal pain
☆ In modern usage:
Identification of a disease by investigation of its
signs and symptoms
☆ Medical terminology:
Clinical diagnosis Laboratory diagnosis
X-ray diagnosis Electrocardiographic diagnosis
Gene diagnosis
Identification:
Inquiry
Laboratory tests/Special examination
Analysis:
Basic knowledge of medicine
Overall analysis
Scientific way of clinical thinking
Importance of Diagnostics
Essential
Basic courses
Bridge
Tools
Clinical medicine
Content of Clinical Diagnostics
Symptomatic diagnosis
Physical diagnosis
Laboratory tests or clinical ancillary tests
Medical record
Diagnostic processes and the way of
clinical thinking
History taking--- Interview
Symptoms --- patient‘s complaints
Epidemic areas, infectious diseases
family history, genetic diseases
Symptom
Subjective sensation that patient describes
Physiological & Pathological
Morphological
functional
Fever Cough Rash Mass

Physical Diagnosis
Sign （Fever, tenderness mass and jaundice ）
Abnormality observed by the physician
Conducted with thoroughness , alertness to detect even
slight derivations from normal
Inspection
Palpation
Percussion
Auscultation
stethoscope
Laboratory test or ancillary tests
• Serum, Urine, Stool tests
• X-ray film
• EKG
• Endoscopy
• Ultrasonic imaging（ Abdomen ）
• CT
• MRI
• PET (Positron Emission Tomography)
Medical record
Medical record is a systematized way of
storing the required data, information and
other relevant documents
Specific requirement in terms of format
and content
Special terms in clinical
diagnosis
Impression
Tentative diagnosis
• Preliminary diagnosis/Tentative diagnosis

• Exclusion of other diseases
• Selecting a number of possibilities to explain the
clinical and laboratory findings in the case in question
• The way of exclusion is called Differential diagnosis

It is the conscientious, explicit and judicious use
of current best evidence in making decisions
about the care of the individual patient
It means integrating individual clinical expertise
with the best available external clinical evidence
from systematic research
One need to:
• Be conscientious: it requires effort and thought.
• Be explicit: decisions will need to be backed up by good
evidence
• Relate to specific problems: it is not about a
hypothetical "average" case. Integrate individual clinical
experience: it does not denigrate clinical skills in history
taking, examination and diagnosis.
One need to:
• Look for current best evidence: the perfect study
may not yet have been published, written up or even
commenced. We may have to settle for something
less rigorous, but be on the look out for new
research that will supersede older studies.
Important aspects---
interrogation 问诊
• To get the history in detail of a patient’s illness
• The history is taken at initial contact between
physician and patient
• As some crucial points might be overlooked by the
patients, one will ask many searching questions to
make the history more informative and complete, who
must at the same time avoid suggesting answers
• Occasionally to interrogate his family member
• The diagnostic process is very complex
• The number of facts that can be collected in a
detailed medical history and in thorough physical
examination are almost without limit
• The laboratory tests or specialized technical
procedures that can employed are numerous and
costly
• Questions for interrogation, maneuver in P.E.,
laboratory test should be thoughtfully selected
with the view to eliminate some of the possible
diagnosis and guide the search expeditiously to a
specific disease
• Method of approaching a diagnosis:
Analysis of symptoms
Recognition of the syndrome
Consideration of disease mechanisms
Important aspects
• Modern & advanced ancillary techniques:
have their limitations.
It can’t reduced the importance of certain parts
of the classic P. E
• It should be avoided to neglect fundamental
methods
Interrogation
Scientific clinical thinking
Approaches
Basic knowledge learning
Clinical practice
Bedside activity
Standardized patient
Developmental History of clinical
diagnostics
• Western Medicine: from ancient to modern
• Traditional Chinese Medicine
Hippocrates
•Born on the island of Cos,
Greece (c. 460-377 BC)
•The Father of medicine
Hippocratic oath
Hippocratic corpus:
a collection of 70 works
Hippocratic oath
Galen
• c.130-c.200
• His work in
anatomy/physiology is notable
• Identified artery and vein
• Added greatly to knowledge of the
brain, spinal cord and pulse
Auenbrugger
•Born at the village of Graz, Austria (1722)
•Son of an innkeeper
•The working experiences helped him to find
Percussion
•Author of <Inventum Novum>(1761)
translated as ‘On Percussion of the chest’ in 1936
Laennec RTH
•A French physician
•Invented Auscultation and stethoscope
Laennec RTH
1816
Contribution of Western Physician
17th~19th century
Leenwenhock Microscopy (end of 17th century)
Fahrenheit Thermometer (1724)
Ludwig Hematomanometer (1847)
Welcher Hematinometer (1854)

20th century
X-ray film EKG Endoscopy CT PET
Ultrasonic imaging
CT imaging
MRI
PET
Traditional Chinese Medicine
Wood
Fire
Earth
Metal
Water
Contribution of ancient doctors---Chinese
Inspection
Interrogation
Smell
Pulse palpation
Pay attention to:
Good medical ethics
Attach importance to clinical practice
Unit theory with practice
Goals
• Inquiry:
Independent systemic inquiry
Comprehensive understanding of patient’s chief
complains, signs, symptoms and their interrelation
• Physical Examination:
Systemic/thorough
• Familiar with routine tests, EKG manipulation and figure
analysis
• Good case writing and propose the primary diagnosis
• Scientific clinical thinking
InquiryInquiry
He yuanbing
Department of respiratory medicine
InquiryInquiry
l It is the method that physician obtain the clinic
data of patient, and further propose clinical
judgment by comprehensive analysis
l Inquiry is the major methods of history taking

l It is a fundamental skill that every physician
should know
BasicBasic principlesprinciples
l Good communication skills are the foundation of
excellent medical care
l It improves health outcomes by resolving symptoms and
reducing patients’ psychological distress and anxiety
l The quality of patient care depends greatly on the skills
of interviewing, because the relationship that a patient
with a physician is probably the most extraordinary
relationship between two human beings
l To gather all basic information pertinent to the
patient’s illness and the patient’s adaptation to
illness
l An experienced interviewer considers all the
aspects of the patient’s presentation and follows
the leads that appear to deserve the most attention
l The clinician must be keenly aware of all clues, subtle or
obvious
l Although body language is important, the spoken word
remains the central diagnostic tool in medicine
l The art of talking and listening continues to be the central
part of the doctor-patient interaction
l Once all the clues from the history have been gathered, the
assimilation of those clues into an ultimate diagnosis is
relatively easy
l Communication is the key to a successful
interviews
l It must be able to ask questions of the patient
freely
l These questions must always be easily understood
and keyed to the medical sophistication of the
patient
ContentContent ofof inquiryinquiry
l General data
l Chief complaint
l History of present illness
l Past history
l Review of systems
l Personal history
l Marital history
l Menstrual history
l Family history
GeneralGeneral datadata
Name Gender
Age birth place
Native place Nation
Marital status Mail address
Profession Data of admission
Data of record Source
Reliability

ChiefChief complaintcomplaint
l It is the patient’s brief statement explaining why
he or she sought medical attention
l It is the answer to the question
“What is the problem that brought you to the
hospital?”

l In the written history, it is frequently a quoted
statement of the patient
l It should be one or two sentences including the
time periods from onset to seeing the doctor
l Not the diagnostic term from the doctor
l Fractures、angina pectoris、 asthma
“Chest pain for the past 5 hours”
“Terrible nausea and vomiting for 2 days”
“Headache for the last week, on and off”
HistoryHistory ofof presentpresent illnessillness
l The history of the present illness refers to the recent
changes in health that led the patient to seek medical
attention at this time
l It describes the information relevant to the chief
complaint
l It should answer the questions what, when, how, where,
which, who, and why
l Chronology is the most practical frameworks for
organizing the history
l It enables the interviewer to comprehend the
sequential development of the underlying
pathologic process
l In this section the doctor gathers all the necessary
information, starting with the first symptoms of
the present illness and following its progression to
present day
l It is important to verify that the patient was
entirely well before the earliest symptom to
establish the beginning of the current illness
l The character of symptoms
location identity during intensity
relief or provoke factors
l Time during may be lasted for years, months, days
l It may also be of hours or minutes (in those with
acute onset)
l Causes and inducing factors
investigate the causes that related with onset of the
disease:
trauma intoxication infection
inducing factors: emotion diet environment
l Caution
the causes that recently occurred may be easily
recognized by the patient
hardly recognized by the patients if the causes are
complicated or if the courses lasted for years
l Progression
including the changes in predominant symptoms or
occurrence of new symptoms
cirrhotic patient manifested some neurological signs,
hepatic encephalopathy should be highly suspected；
chest pain lasted unusually and more severely than
previous episodes of angina, myocardial infarction should
be suspected
l Accompanying symptoms
it is useful in differential diagnosis
e.g. patient manifested nausea, vomiting and
fever,
accompanied with jaundice and/or shock, acute
biliary infection or acute pancreatitis should be
considered

l Course of diagnosis and treatment
The diagnosis and treatment the patient had received in
other medical institution may provide informative data
The diagnosis made by others could not replace one’s
diagnosis
l General condition during the course : diet、sleep、
weight stool urine etc
it may also provide some useful information
PastPast medicalmedical historyhistory
l The past medical history consists of the overall assessment of the
patient’s health before the present illness include a statement of
childhood and adult problems
l Parameters including:
general state of health past illness
injuries hospitalizations
surgery allergies
immunizations substance abuse
diet sleep patterns
current medications alternative therapies
PastPast medicalmedical historyhistory
l The patient should be asked about any prior injuries or accidents
The type of injury and the data are important
l All hospitalization must be indicated, including admissions for
medical, surgical, and psychiatric illness
l All surgical procedures should be specified. The type of procedure,
data, hospital
l All allergies should be described. These include environmental,
ingestible, and drug related
l It is important to determine the immunization history of all patients
Drug allergy
ReviewReview ofof systemssystems
l The review of systems summarizes in terms of
body systems all the symptoms that may have
been overlooked in the history of the present
illness or in the medical history
l By reviewing in an orderly manner the list of
possible symptoms, the interviewer can
specifically check each system and uncover
additional symptoms of “unrelated” illness not yet
discussed
l The review of systems is best organized from the head
down to the extremities
l Patients are told that they are going to be asked whether
they have ever had a particular symptom and should
answer “Yes” or “no”
l Joint pain, dry mouth, rash, shivering
l Respiratory system
cough: identity frequency
sputum production: quantity appearance
coughing up blood shortness of breath
l Cardiovascular system
chest pain shortness of breath with exertion
palpitations shortness of breath lying flat
sudden shortness of breath while sleeping
history of heart attack
l GI system
appetite excessive hunger excessive thirst
nausea constipation diarrhea
heartburn vomiting abdominal pain
change in stool color/caliber/consistency
frequency of bowel movements vomiting blood
rectal bleeding black tarry sto
ols
diabetes ， bowel cancer
l Urinary system
frequency urgency incontinence difficulty in the
starting the stream
excessive urination pain on urination
burning blood in the urine
bed-wetting waist pain history of retention
urine color urine odor
l Hematological system pallor yellow skin
hemolytic petechia purpura ecchymosis
hematoma

l Endocrinological system and metabolite
weakness profound sweating
abnormal appetite weight change

l Neurologic system
fainting dizziness mood changes
loss of memory speech disorders
general behavioral change disorientation
l Musculoskeletal system
weakness paralysis muscle stiffness
limitation of movement joint pain
joint stiffness arthritis gout deformities
l Review of systems may involved lots of clinical
diseases
l One has to understand the pathophysilogical meaning
of these signs and symptoms
l In each systems, it is practical to ask several symptoms
l The inquire may be intensified if there is positive
symptoms/signs is elicited
PersonalPersonal historyhistory
l Social experiences
birth place
living area and duration particularly those
epidemical areas Liver cirrhosis, schistosomiasis, infectious diseases
education living condition hobby
l Profession and working place/condition
l Habit smoking (amount and duration)
drinking anesthetic drug
UnhealthyUnhealthy sexualsexual historyhistory
l Unhealthy sexual history:
Sexually transmitted disease
MaritalMarital historyhistory
l Marital history:
single or married
age of marriage
health condition of spouse
MenstrualMenstrual historyhistory
l Menstrual history: only for women
age of menarche (first menstrual cycle)
cycles and flow lasting
amount of vaginal bleeding/discharges
menopause and age of menopause
l Format
flow lasting(day)
menarche last menopause
cycle(day)
FamilyFamily historyhistory
l It provides information about the health of the
entire family，living and dead
l Pay attention to possible genetic and
environmental aspects of disease that might have
implications for the patient
SkillSkill andand methodsmethods inin inquireinquire
l Getting started
l The narrative
l The closing
GettingGetting startedstarted
l The diagnostic process begins at the first moment of
meeting
l One should be dressed appropriately, wearing a white
coat with one’s name badge identifying one as a
physician
l One should make patient as comfortable as possible
l One should sit in a chair directly facing the patient in
order to make good eye contact
l The interviewer should sit in a relaxed position
without crossing arms across the chest
l The crossed-arms position is not appropriate, as
this body language projects an attitude of
superiority and may interfere with the progress of
the interview
l Making the patient feel that you are interested and concerned
l Once the introduction has been made, you may begin the
interview by asking a general ,open-ended question
“What medical problem has brought you to the hospital?”
l This type of opening remark allows the patient to speak first
l The interviewer can determine the patient’s chief complaint
or the problem that is regarded as paramount
l If the patient says “Haven’t you read my records?”
l It is correct to say “No, I’ve been asked to interview you
without any prior information”
or “I would like to hear your story in your words”
l Patients can determine very quickly if you are friendly
and personally interested in them
TheThe narrativenarrative
l Novice interviewers are often worried about
remembering the patient’s history
l It is poor form to write extensive notes during the
interview
l Attention should be focused more on what the
person is saying and less on the written word
l After the introductory story, the interviewer should
proceed to questions related to the chief complaint
l These should naturally evolve into questions related to the
other formal parts of the medical history, such as the
present illness,past illnesses, social and family history,
and review of body system
l Patients should largely be allowed to conduct the
narrative in their own way
l The interviewer must select certain aspects that
require further details and guard the patient toward
them
l Overdirection is to be avoided, because this stifles
the interview and prevents important points from
being clarified
l When patients use vague terms such as “often”,
“a little”, “sometimes”, the interviewer must
always for clarification, ask “What does
‘sometimes’ mean?” or “How often is ‘often’?”
l The interviewer should be alert for subtle clues
from the patient to guide the interview further
l There are a variety of technique to encourage and
sustain the narrative
TheThe closingclosing
l By the conclusion of the interview, the
interviewer should have a clear impression of the
reason why the patient sought medical help, the
history of the present illness, the patient’s past
medical history
l If any part of the history needs clarification, this
is the time to obtain it
TheThe closingclosing
l At the conclusion, it is polite to encourage the patient to
discuss any additional problems or to ask any questions
“Is there anything else you would like to tell me that I
have not already asked?”
l Thank the patient and tell him or her that you are ready
to begin the physical examination
BasicBasic interviewinginterviewing techniquestechniques
l Questioning
l Silence
l Facilitation
l Confrontation
l Interpretation
l Reflection
l Support
QuestioningQuestioning
Open ended questions
l They are used to ask the patient for general information
l It is most useful in opening up the interview or for
changing the topic to be discussed
l An open-ended question allows the patient to tell his
story spontaneously and does not presuppose a specific
answer
Open-endedOpen-ended questioningquestioning
What kind of medical problem are you having?
Can you describe your feelings when you get the pain?
Are you having stomach pain? Tell me about it
DirectDirect questioningquestioning
l After a period of open-ended questioning, the interviewer
should direct the attention to specific facts learned during
the open-ended question period
l This type of question gives the patient little room for
explanation
l A direct question can usually be answered in one word or
a brief sentence
Where does it hurt?
When do you get the burning
How do you compare this pain with your ulcer pain?
Notice: avoid asking direct questions in a manner that
might bias the response
l Symptoms are classically characterized into
several dimensions or elements, including bodily
location, quality, quantity, chronology, setting,
precipitating or palliating factors and associated
manifestations
l These elements may be used as a framework to
clarify the illness
l Bodily location
Can you tell me where you feel the pain?
Do you feel it anywhere else?
l Onset (chronology)
When did you first notice it?
How long did it last?
l Precipitating factors
What makes it worse?
What seems to bring on the pain?
l Palliating factors
What do you do to get more comfortable?
Does lying quietly in bed help you?
Does eating make it better?
l Quality
What does it feel like?
Can you describe the pain?（Blunt pain, acute pain,
knife cut pain, burning pain？）
l Radiation
When you get the pain in your chest, do you feel it in any
other part of your body?
When you experience your abdominal pain, do you have
pain in any other area of your body?
l Severity (quantity)
How many times did you vomit?
Can you fall asleep with the pain?
l Setting
Does it ever occur at rest?
Does the pain occur with your menstrual cycle?

l Associated manifestation
Do you ever have nausea with the pain?
Have you noticed other changes that happen when
you start to sweat?
O-P-Q-R-S-TO-P-Q-R-S-T
It stands for onset (chronology), precipitating
(palliative), quality, radiation, severity (setting),
and temporal, is useful to help you remember
these important dimensions of a symptom
QuestionQuestion typestypes toto avoidavoid
l Suggestive question
It may provide the answer to the question
“Do you feel the pain in your left arm when you
get it in your chest?” x
A better way to ask the same question would be:
“When you get the pain in your chest, do you
notice it anywhere else?” √
l Why question
It carries tones of accusation
This type of question almost always asks a patient to
account for his/her behavior and tends to put the person
on the defensive
Why did you stop taking the medication?
Why did you wait so long to call me?
Try rephrasing the “Why” questions to “What is the
reason…?”
l Multiple question
The patient can easily become confused and
respond incorrectly, answering no part of the
question adequately
“How many brothers and sisters do you have, and
has any one of them ever had asthma, heart
disease, pneumonia, or tuberculosis?”
l Medical jargon
“You seem to have a homonymous hemianopsia”
l Leading question or biased question
It carries a suggestion of the kind of response the
interviewer is looking for
Always ask questions in the positive, not the negative
“You don’t have diabetes, do you?”
it should be “Do you have diabetes?”
Thank you
Pneumonia
The First Affliated Hospital of XinJiang
Medical University
Respiratory Unite
Bin Jia
Aim and Demand
 Learn about the classification of pneumonia.
 Discuss diagnosis and management of CAP.
 Describe common pathogens, pathology, clinical
manifestation and treatment of Pneumococcal
pneumonia.
 Master the clinical feature,diagnostic criteria and
therapy of Pneumococcal pneumonia, Staphylococcal
Pneumonia, Klebsiellar pneumonia, Legionella
pneumonia and Mycoplasma pneumonia.
Definition
 Inflammation of the lung parenchyma,include
terminal airway, alveolar space and pulmonary
interstitium.
 Caused by varities of pathogens,Such
as:Bacteria,Virus,Fungus,etc.
 Come with fever, chills, cough, pleuritic chest pain,
sputum production, hyper- or hypothermia, increased
respiratory rate, dullness to percussion, bronchial
breathing, crackles, wheezes, pleural friction rub.
 Opacity on chest radiography.
Epidemiology
 Pneumonia is the sixth leading cause of death in the
United States;Among infectious causes of death,it
ranks number one.
 An estimated 4 million cases of CAP occur each year
in the United States.Approximately 20% of these
cases require hospitalization,and among these
patients,mortality average is 15%,compared to <1%
of patients who can be managed as outpatients.
 High incidence mortality and drug resistance rate.
Etiology
 Pathogenic microorganism
 Physical and chemical factors
 Immunologic injury
 Allergy
 Drugs
Pneumonia or not?
 There are two factors involved in the formation of
pneumonia.
☆ Pathogen:quantity and virulence.
☆ Host defenses:Respiratory defense and systemic
immunity.
 Host factors:age,socioeconomic status,smoking,prior
antibiotic use,underlying medical condition.(alcohol
abuse,COPD,DM,chronic liver disease,chronic renal
insufficiency,CHF,use of immunosuppressive drugs)
Route of infection
 Air suction.
 Blood dissemination.
 Spread by the near infection site.
 Aspirated the colonized bacteria of upper respiratory
tract and gastrointestinal.
 Invasive operation.
Etiological classification:
 Bacterial Pneumonia:Streptococcus pneumoniae,
Staphylococcus aureus. Klebsiella pneumoniae, Colibacillus,
Pseudomonas aeruginosa, Anaerobic bacteria. Legionella
pneumonia and Mycoplasma pneumonia.
 Virus pneumonia: Adenovirus,Respiratory Syncytial Virus,
Influenza virus.
 Fungal pneumonia: Candida albicans, aspergillus.
 Other pathogens: Chlamydia[klə'mɪdɪə] , Rickettsia,
衣原体
Pneumocystis carinii 卡氏肺孢子虫, parasite,etc.

Anatomy classification:
 Lobar Pneumonia
(segmental)
 Lobular Pneumonia
(bronchopneumonia)
 Interstitial pneumonia
Lobar Pneumonia
 Involvement of an entire lobe. Pathogens cause

inflammation in alveoli[æl'vɪəlaɪ] first, spread to other
alveoli through Cohn hole. Lead to partial or whole
segment,lobe inflammation.
 Most pathogens are Streptococcus Pneumoniae .

Lobar Pneumonia
Lobular Pneumonia
 Involvement of parts of lobe only,segmental or of
alveoli contiguous[kən'tɪgjʊəs] to bronchi.pathogens cause
inflammation of bronchiole['brɒŋkɪəʊl], terminal
bronchiole and Alveolus via bronchus.
 Pathogens can be Streptococcus Pneumoniae ,
Staphylococcus,Virus, Mycoplasma, Legionella[,li:dʒə'nelə].
Lobular Pneumonia
Interstitial pneumonia
 Inflammation give priority to pulmonary interstitial.
 caused by bacteria,virus or radiation and idiopathic
reason.
 Gas-exchange disorder.
Environmental classification
 Community-Acquired Pneumonia
 Hospital-Acquired Pneumonia
Community-Acquired Pneumonia
 Occure in community within 48 hours.S.pneumonia is
the most common CAP in elderly people.
 Incidence:5~10/1,000/year; 6th leading cause of
death in U.S; Number one among the infectious
diseases.Mortality vary between 6 to 20%.
 Pathogens:Streptococcus pneumoniae, Haemophilus
influenzae, M catarrhalis, Legionella species,
Mycoplasma pneumoniae,etc.
 Manifestations:sudden onset, shaking chill, Fever ,
nausea, vomiting, malaise[mæ'leɪz], and myalgias[maɪ'ældʒəs] .
pain with breathing on the affected side (pleurisy).
Cough, dyspnea, and sputum production.
 Signs:T: 38~ 40.5℃; tachycardia[,tækɪ'kɑːdɪə];
 Tachypnea(respirations accelerate to 20 to 45
breaths/min). lobar consolidation; crackles; pleural
effusion.
 General Lab Examinations:
Blood tests：leukocytosis with a shift to the left
hypoxemia ＋respiratory alkalosis.
Diagnosis
 Fever>380 C
 New cough, ± sputum, hemoptysis[hɪ'mɒptɪsɪs]+Pleuritic
chest pain.WBC>10×109 or <4×109
 Rales, rhonci, wheezing
 New or evolving infiltrate on chest radiograph
 High-resolution computed tomography (CT)
 Sputum stains and culture
 Lower respiratory secrets.
Hospital-Acquired Pneumonia
 Certain illness may predispose HAP because
of:impaired defenses,chronic illness,
coma,malnutrition,prolong hospitalization,
intervention and endotracheal intubation,etc
 Pathogens:S.aureus,Enterobacteriaceae
['entərəu,bæktəri'eisi,i:] ,Anaerobic bacteria,Aspergillus sp,Viral.
 Usually caused by Gram-negative organism.

Diagnosis
 Clinical
----fever; cough with purulent sputum……
 Radiographic
-------new or progressive infiltrates on CXR,
 Lab
-------leukocytosis[,ljuːkəʊsaɪ'təʊsɪs] or leukopenia
 Microbiologic
--------Suggestive gram stain and positive cultures of
sputum, tracheal aspirate, BAL, PSB, pleural fluid or
blood
Symptoms
 Cough/expectoration
 Dyspnea
 Pleuritic chest pain
 Fever
 Myalgias
 Chills/sweats
 Fatigue
 Headache/diarrhea
Pneumococcal Pneumonia
 Caused by streptococcus pneumoniae, more than half
of infection outside the hospital,may be pulmonary
segments or lobs consolidation.
 The disease onset is acute and can be
serious,accompanied by chills,fever,chest
pain,cough,Iron-rust sputum.
Etiology
 Streptococcus Pneumoniae is gram positive

bacteria,has capsule outside the body.
 Most occure in winter and early spring.healthy young
adult.have history of influenza,catch a
cold,drunkenness or General Anesthesia.defense
mechanism of respiratory is damaged.
Pathogenesis
 Bacteria was inhaled into lower respiratory

tract,cause congestion,edema, exudation of red blood
and white blood cell.Exudate diffuse to central of
alveola via Cohn hole,involve several segments or
lobs.
Pathology
 Congestive stage
 Red hepatization stage
 Gray hepatization stage
 Resolution stage
Pathology
 Lung tissue hyperaemia[haipə'ri:miə] oedema and infiltrated by

Red and white blood cells,macrophage swallow the bacteria.
 Fibrin Degradation Product dissolve, absorb,alveolar
inflates again.Lung tissue structure without damage after
resolution.
 Individual fibre not completely absorbed, lead to
cryptogenic organizing pneumonia,part of them complicated
with Pleurisy,Empyema.
Clinical manifestation
 Have a history of catch cold,be caught in the
rain,fatigue,drunkenness. Onset rapidly,chill,high
fever,continuous fever. 39℃～40℃,chest
pain ,cough,Iron-rust sputum.
Signs
 Acute sickly-look, cyanosis,dyspnea,chest movement
degree reduced,dullness of percussion sound,vocal
fremitus enhanced,bronchial breath sound can be
heard.
 Rales be heard in resolution period.Shock,ARDS,
blurred mind,delirium[dɪ'lɪrɪəm] and coma can be seen in
severe cases.
 In 5 to 10 days of disease course, tempreture
suddenly dropped.
High risk groups
 Smokers,dementia[dɪ'menʃə]痴呆,chronic bronchitis;
 bronchiectasis;
 cardiac failure;
 immunosuppressants users;
 the elderly,infants and young children.
Complications
 Septic shock:blood pressure decreased,cold
limbs,cyanosis of lips.
 Myocarditis:tachycardia,cardiac arrhythmia.
 ARDS(Acute respiratory distress syndrome)
 Pleurisy.
 Pulmonary Abscess.
 Organized pneumonia.
 Pleural effusion and empyema.
Laboratory Test
 Blood routine examination: WBC>10×109/L,can be

normal,but neutrophils must increased,>80% core
shift to left.
 Sputum smear and culture can clear the
pathogens.Blood or pleural effusion cuture.
 Blood gas analysis:PaO2 can be decreased,PaCO2
can be normal or decreased,metabolic acidosis.
Chest radiography
 Lobe or section distribution of flake infiltrating

shadows,air bronchogram can be seen in the shadow.
 Air-filled bronchi sign.
Diagnosis
 Preceding history of common cold or other URI.
 Symptoms:abrupt onset,high fever,cough with a rusty
sputum,chest pain,dyspnea,etc.
 Signs:remarkerble moist rale.
 Blood test:leukocytosis
 Radiologic study:lobar consolidation.
 A definitive diagnosis require demonstration of
pneumonia in sputum culture,blood ,lung tissue.
 1.Caseous Pneumonia：Often has low-grade
fever,fatigue,night sweat,TB be positive in sputum
smear.
 2.Acute lung abscess：A large amount of purulent
sputum,vomica and fluid levels can be seen in chest
X-ray.
 3.Lung cancer:the elderly,recurrent pneumonia ,
enlargement of lymph node inhilum of the lung,CT
scan and bronchoscope should perform for exclusion.
 4.Other diseases：Pleural effusion,should differential
with tuberculous pleurisy, pulmonary
infarction.abdominal pain differential with the
abdominal diseases.
Criteria of severe pneumonia
 Repiratory rate >30/min;
 Blood prussure <90/60mmHg;
 Blood gas:PaO2<60mmHg,
PaO2/FiO2<300mmHg;
 BUN>7.1mmol/L;
 Confusion;
 X-ray:two lobes are involved.
Therapy
 Antibiotics:Preferred PenicillinG 80 ten-thousand
U,intramuscular,BID in mild patients.400 ten-
thousand U iv.gtt Q6h in severe cases.
 Erythromycin,Lincomycin,the first or second
generation Cephalosporin ,respiratory
fluoroquinolone can be used in allergy
patients,duration is 5-7 days or after the patients
afebrile for 2-3 days.
Therapy
 Deal with the complications:The extraction liquid
drainage of pleura effusion.
 Supporting treatment:bed rest,analgesic,Fluid
infusion for fever patient,when atery oxegen pressure
less than 60 millimetermercury,oxygen uptake is
needed.Mechanical ventilation therapy in ARDS.
Therapy of septic shock
 Supplyment of blood volume:low molecular weight
dextran or balanced salt solution.
 Vasoactive agent:When the blood volume is
sufficient,Dopamine can be used to improve
Microcirculation,protect the kidney,increase oxygen
supply for organization.
Therapy of septic shock
 Infection control：High-dose Penicillin
iv.gtt,combined antibiotics can be used in severe
cases,add Cephalosporin.
 Glucocorticoid: Hydrocortisone100～200milligram
or Dexamethasone 5-10 milligram iv.gtt in severe
cases.
 Correct the unbalance of Acid-Bases and electrolyte.
 Symptomatic treatment.
Prevention
Following good hygiene habits:
----cough or sneeze into a tissue;
-----use separate drinking glass and eating utensils;
-----wash your hands frequently with warm soapy
water.
 Improve immunity:eat healthy,sleep well,aviod
smoking,exercise,reduce stress,do not drink alcohol

in excess.
Staphylococcus Pneumonia
 Mostly occure in Poor immune function patients.
 Such as:Diabetes Mellitus,Leukemia,hepatopathy etc.
 By inhalation or via Skin focal infection
(Furuncle['fjʊərʌŋk(ə)l],Folliculitis[fə,lɪkjə'laɪtɪs],infection,etc),enter
into the lung through blood circulation.
Clinical features
 Acutely onset,high fever,chill,chest
pain,cough,purulent sputum or bloody phlegm.
 White blood cell count and neutrophilin creased.
 Chest X-ray:lobularor pulmonary segments

filtration ,consolidation.
 May complicated with Empyema,Pyopneumothorax.

Therapy
 Infection in hospital:coagulase positive, the first
choice is Semisynthetic penicillins: Oxacillin 4-
8gram,iv.gtt;cefazolin4-8 gram.
 Methicillin-resistant Staphylococcus aureus can

choose Vancomycin,Rifampicin.
Klebiella pneumonia
1.More can be seen in the elderly,malnutrition,resistance
decreased patients.
2. More in the upper lobes, thick exudation.
3.The germ has capsule,grow in alveoli, cause lung
tissues liquefied necrotic,form lung abscess.
4. Acutely onset,high fever,purulent sputum,brick red
colour,gelatinous,can appear shock.Lobular
consolidation in chest X-ray.Multiple lung abscess.
Therapy
 The first choice is aminoglycosides:Amikacin,etc.
Legionella pneumonia
 Caused by Legionella pneumophila, can grow
in special medium.
 Can be found in hot water systems of all types.
 Middle-aged and aged people,smoking,chronic

heart, lung and kidney disease patients easy
occur.
Clinical manifestations
 Onset may present small outbreak.
 Systemic intoxication symptoms like:fatigue,

myalgia,headache,diarrhea,etc.
 Cough,bloody phlegm.chest pain,high fever,

psychosomatic manifestations in severe
patients.
Examinations
 Lung consolidation shadow in chest X-
ray,company with pleura effusion.
 Serum immunofluorescence antibody detection,
antibody of serum tube agglutination test
present four times growth or more higher can
be diagnosed.
 The urine may contain Legionella antigen in
some patients.
Therapy
 The first choice is Erythromycin1-2 gram

iv.gtt,may add Rifampicin.
 High –dose Ciprofloxacin is effecive

treatment,also other Quinolones.
Mycoplasma pneumonia
 More occure in autumn,often be seen in children and
the teenagers.
 Onset slowly,dry cough,fever,malaise
 Many forms infiltration of lung in chest X-
ray,segmental distribution,major in mesenchyme.
Mycoplasma pneumonia
 Fever is usually moderate.
 Red blood cell condensation test positive two weeks
after onset.More than 1:32 can diagnose.
 Mycoplasma antibody IgM positive can clear.
 Therapy:First choice is Erythromycin,can add
Tetracycline.
Thinking Case
 A 30 years old young man,with high
fever,chill,cough , yellow phlegm for five days.
 Physical examination:T:39centigrade,breath sound
decreased in lower right lung, can hear moist rales.
 Flake infiltration of lower right lung can be seen in
chest X-ray, little vomica inside it,small amount of
effusions in pleural cavity.WBC10×109/L.
 Question:What kind of pneumonia this patient belong
to?how to diagnose and cure next step?
Summary
 Common symptom,sign,laboratory
test ,diagnosis,differential diagnosis and principles of
antibiotics use of all kinds of pneumonia.
 Diagnosis and therapy of Severe pneumonia.
 Master the definition, classification, etiology,
pathophysiology and pathology of Pneumococcal
Pneumonia.
Inquiry
He yuanbing
Department of respiratory medicine1
Inquiry
 It is the method that physician obtain the clinic
data of patient, and further propose clinical
judgment by comprehensive analysis
 Inquiry is the major methods of history taking
 It is a fundamental skill that every physician

should know
Basic principles
 Good communication skills are the foundation of
excellent medical care
 It improves health outcomes by resolving symptoms and

reducing patients’ psychological distress and anxiety
 The quality of patient care depends greatly on the skills

of interviewing, because the relationship that a patient
with a physician is probably the most extraordinary
relationship between two human beings
Basic principles
 To gather all basic information pertinent to the
patient’s illness and the patient’s adaptation to
illness
 An experienced interviewer considers all the

aspects of the patient’s presentation and follows
the leads that appear to deserve the most attention
Basic principles
 The clinician must be keenly aware of all clues, subtle or
obvious
 Although body language is important, the spoken word
remains the central diagnostic tool in medicine
 The art of talking and listening continues to be the central
part of the doctor-patient interaction
 Once all the clues from the history have been gathered,
the assimilation of those clues into an ultimate diagnosis is
relatively easy
Basic principles
 Communication is the key to a successful
interviews
 It must be able to ask questions of the patient

freely
 These questions must always be easily understood
and keyed to the medical sophistication of the
patient
Content of inquiry
 General data
 Chief complaint
 History of present illness
 Past history
 Review of systems
 Personal history
 Marital history
 Menstrual history
 Family history
General data
Name Gender
Age birth place
Native place Nationality
Marital status Mail address
Profession Data of admission
Data of record Source
Reliability
Chief complaint
 It is the patient’s brief statement explaining why
he or she sought medical attention
 It is the answer to the question

“What is the problem that brought you to the
hospital?”
 In the written history, it is frequently a quoted

statement of the patient
Chief complaint
 It should be one or two sentences including the

time periods from onset to seeing the doctor
 Not the diagnostic term from the doctor

 Fractures、angina pectoris、 asthma
Chief complaint
“Chest pain for the past 5 hours”
“Terrible nausea and vomiting for 2 days”
“Headache for the last week, on and off”

History of present illness
 The history of the present illness refers to the recent

changes in health that led the patient to seek medical
attention at this time
 It describes the information in datail relevant to the chief

complaint . It is the most important part of the medical
record
 It should answer the questions what, when, how, where,

which, who, and why
 Chronology is the most practical frameworks for

organizing the history
 It enables the interviewer to comprehend the

sequential development of the underlying
pathologic process
 In this section the doctor gathers all the necessary
information, starting with the first symptoms of
the present illness and following its progression to
present day
 It is important to verify that the patient was

entirely well before the earliest symptom to
establish the beginning of the current illness
 The character of symptoms

“location identity time duration intensity
relief or provoke factors”
 Time duration may be lasted for years, months,
days
 It may also be of hours or minutes (in those with
acute onset)
 Causes and inducing factors
investigate the causes that related with onset of the
disease:
trauma intoxication infection
inducing factors: emotion diet environment
 Caution
the causes that recently occurred may be easily
recognized by the patient
hardly recognized by the patients if the causes are
complicated or if the courses lasted for a long time
 Progression
including the changes in predominant symptoms or
occurrence of new symptoms
cirrhotic patient manifested some neurological signs,
hepatic encephalopathy should be highly suspected；
chest pain lasted unusually and more severely than
previous episodes of angina, myocardial infarction should
be suspected
 Accompanying symptoms
it is useful in differential diagnosis
e.g. patient manifested nausea, vomiting and fever,
accompanied with jaundice and/or shock, acute
biliary infection or acute pancreatitis should be
considered
 Course of diagnosis and treatment

The diagnosis and treatment the patient had received in
other medical institution may provide informative data
The diagnosis made by others could not replace one’s
diagnosis
 General condition during the course : diet、sleep、
weight stool urine etc
it may also provide some useful information
Past medical history
 The past medical history consists of the overall assessment of the
patient’s health before the present illness include a statement of
childhood and adult problems
 Parameters including:
general state of health past illness
injuries hospitalizations
surgery allergies
immunizations substance abuse
diet sleep patterns
current medications alternative therapies
Past medical history
 The patient should be asked about any prior injuries or accidents

The type of injury and the data are important
 All hospitalization must be indicated, including admissions for

medical, surgical, and psychiatric illness
 All surgical procedures should be specified. The type of procedure,
data, hospital
 All allergies should be described. These include environmental,
ingestible, and drug related
 It is important to determine the immunization history of all patients
Drug allergy
Review of systems
 The review of systems summarizes in terms of
body systems all the symptoms that may have
been overlooked in the history of the present
illness or in the medical history
 By reviewing in an orderly manner the list of
possible symptoms, the interviewer can
specifically check each system and uncover
additional symptoms of “unrelated” illness not yet
discussed
Review of systems
 The review of systems is best organized from the head

down to the extremities
 Patients are told that they are going to be asked whether

they have ever had a particular symptom and should
answer “Yes” or “no”
 Joint pain, dry mouth, rash, shivering

Review of systems
 Respiratory system
cough: identity frequency
sputum production: quantity appearance
coughing up blood (hemoptysis) shortness of
breath
 Cardiovascular system
chest pain shortness of breath with exertion
palpitations shortness of breath lying flat
sudden shortness of breath while sleeping
history of heart attack
Review of systems
 GI system
appetite excessive hunger excessive thirst
nausea constipation diarrhea
heartburn vomiting abdominal pain
change in stool color/caliber/consistency
frequency of bowel movements vomiting
blood(haematemesis)
rectal bleeding (hematochezia) black tarry stools
diabetes ， bowel cancer
Review of systems
 Urinary system
frequency urgency incontinence difficulty in the
starting the stream
excessive urination pain on urination
burning blood in the urine (hematuria)
bed-wetting waist pain history of retention
urine color urine odor
Review of systems
 Hematological system pallor yellow skin
hemolytic petechia purpura ecchymosis
hematoma
 Endocrinological system and metabolite

weakness profound sweating
abnormal appetite weight change
Review of systems
 Neurologic system
fainting dizziness mood changes
loss of memory speech disorders
general behavioral change disorientation
 Musculoskeletal system
weakness paralysis muscle stiffness
limitation of movement joint pain
joint stiffness arthritis gout deformities
Review of systems
 Review of systems may involved lots of clinical
diseases
 One has to understand the pathophysilogical meaning

of these signs and symptoms
 In each systems, it is practical to ask several symptoms
 The inquire may be intensified if there is positive

symptoms/signs is elicited
Personal history
 Social experiences
birth place
living area and duration particularly those
epidemical areas Liver cirrhosis, schistosomiasis,
infectious diseases education living condition
hobby
 Profession and working place/condition
 Habit smoking (amount and duration)
drinking anesthetic drug
Unhealthy sexual history
 Unhealthy sexual history:

Sexually transmitted disease
Marital history
 Marital history:
single or married
age of marriage
health condition of spouse
Menstrual history
 Menstrual history: (only for women)
age of menarche (first menstrual cycle)
cycles and flow lasting
amount of vaginal bleeding/discharges
menopause and age of menopause
 Format
flow lasting(day)
menarche last menopause
cycle(day)
Family history
 It provides information about the health of the
entire family，living and dead
 Pay attention to possible genetic and

environmental aspects of disease that might have
implications for the patient
Skill and methods in inquiry
 Getting started
 The narrative
 The closing
Getting started
 The diagnostic process begins at the first moment of
meeting
 One should be dressed appropriately, wearing a white
coat with one’s name badge identifying one as a
physician
 One should make patient as comfortable as possible
 One should sit in a chair directly facing the patient in
order to make good eye contact
Getting started
 The interviewer should sit in a relaxed position

without crossing arms across the chest
 The crossed-arms position is not appropriate, as

this body language projects an attitude of
superiority and may interfere with the progress of
the interview
Getting started
 Making the patient feel that you are interested and concerned
with him
 Once the introduction has been made, you may begin the
interview by asking a general ,open-ended question
“What medical problem has brought you to the hospital?”
 This type of opening remark allows the patient to speak first
 The interviewer can determine the patient’s chief complaint

or the problem that is regarded as paramount
Getting started
 If the patient says “Haven’t you read my records?”
 It is correct to say “No, I’ve been asked to interview you

without any prior information”
or “I would like to hear your story in your words”
 Patients can determine very quickly if you are friendly

and personally interested in them
The narrative
 Novice interviewers are often worried about
remembering the patient’s history
 It is poor form to write extensive notes during the

interview
 Attention should be focused more on what the

person is saying and less on the written word
The narrative
 After the introductory story, the interviewer should

proceed to questions related to the chief complaint
 These should naturally evolve into questions related to the

other formal parts of the medical history, such as the
present illness,past illnesses, social and family history,
and review of body system
The narrative
 Patients should largely be allowed to conduct the

narrative in their own way
 The interviewer must select certain aspects that

require further details and guard the patient toward
them
The narrative
 Overdirection is to be avoided, because this

stifles the interview and prevents important points
from being clarified
 When patients use vague terms such as “often”,
“a little”, “sometimes”, the interviewer must
always for clarification, ask “What does
‘sometimes’ mean?” or “How often is ‘often’?”
The narrative
 The interviewer should be alert for subtle clues

from the patient to guide the interview further
 There are a variety of technique to encourage and

sustain the narrative
The closing
 By the conclusion of the interview, the
interviewer should have a clear impression of the
reason why the patient sought medical help, the
history of the present illness, the patient’s past
medical history
 If any part of the history needs clarification, this

is the time to obtain it
The closing
 At the conclusion, it is polite to encourage the patient to

discuss any additional problems or to ask any questions
“Is there anything else you would like to tell me that I

have not already asked?”
 Thank the patient and tell him or her that you are ready
to begin the physical examination
Basic interviewing techniques
 Questioning
 Silence
 Facilitation
 Confrontation
 Interpretation
 Reflection
 Support
Questioning
Open ended questions
 They are used to ask the patient for general information

 It is most useful in opening up the interview or for
changing the topic to be discussed
 An open-ended question allows the patient to tell his
story spontaneously and does not presuppose a specific
answer
Open-ended questioning
What kind of medical problem are you having?
Can you describe your feelings when you get the pain?
Are you having stomach pain? Tell me about it

Direct questioning
 After a period of open-ended questioning, the
interviewer should direct the attention to specific facts
learned during the open-ended question period
 This type of question gives the patient little room for

explanation
 A direct question can usually be answered in one word or

a brief sentence
Direct questioning
Where does it hurt?

When do you get the burning
How do you compare this pain with your ulcer pain?
Notice: avoid asking direct questions in a manner that

might bias the response
Direct questioning
 Symptoms are classically characterized into

several dimensions or elements, including bodily
location, quality, quantity, chronology, setting,
precipitating or palliating factors and associated
manifestations
 These elements may be used as a framework to
clarify the illness
Direct questioning
 Bodily location
Can you tell me where you feel the pain?
Do you feel it anywhere else?
 Onset (chronology)
When did you first notice it?
How long did it last?
Direct questioning
 Precipitating factors
What makes it worse?
What seems to bring on the pain?
 Palliating factors
What do you do to get more comfortable?
Does lying quietly in bed help you?
Does eating make it better?
Direct questioning
 Quality
What does it feel like?
Can you describe the pain?（Blunt pain, acute pain,
knife cut pain, burning pain？）
 Radiation
When you get the pain in your chest, do you feel it in any
other part of your body?
When you experience your abdominal pain, do you have
pain in any other area of your body?
Direct questioning
 Severity (quantity)
How many times did you vomit?
Can you fall asleep with the pain?

Setting
Does it ever occur at rest?
Does the pain occur with your menstrual cycle?
Direct questioning
 Associated manifestation
Do you ever have nausea with the pain?
Have you noticed other changes that happen when
you start to sweat?
O-P-Q-R-S-T
It stands for onset (chronology), precipitating
(palliative), quality, radiation, severity (setting),
and temporal, is useful to help you remember
these important dimensions of a symptom
Question types to avoid
Suggestive question
It may provide the answer to the question
“Do you feel the pain in your left arm when you
get it in your chest?” x
A better way to ask the same question would be:
“When you get the pain in your chest, do you
notice it anywhere else?” √
 Why question
It carries tones of accusation
This type of question almost always asks a patient to
account for his/her behavior and tends to put the person
on the defensive
Why did you stop taking the medication?

Why did you wait so long to call me?
Try rephrasing the “Why” questions to “What is the
reason…?”
 Multiple question
The patient can easily become confused and
respond incorrectly, answering no part of the
question adequately
“How many brothers and sisters do you have, and

has any one of them ever had asthma, heart
disease, pneumonia, or tuberculosis?”
 Medical jargon
“You seem to have a homonymous hemianopsia”
 Leading question or biased question

It carries a suggestion of the kind of response the
interviewer is looking for
Always ask questions in the positive, not the negative

“You don’t have diabetes, do you?”
it should be “Do you have diabetes?”
Thank you
Primary bronchogenic
carcinoma
Learning goal
§ To master:
§ The pathological type of lung cancer and the type of clinical
characteristics
§ Lung cancer clinical manifestations
§ staging of lung cancer treatment
§ To familiar :
§ Lung cancer definitions, etiology, pathogenesis.
What is lung cancer?
§ Lung cancer is the uncontrolled growth of abnormal cells in

the lung .
§ Tumors gradually form as these cells replicate.
§ It originates in the lungs but tends to spread uncontrollably to

other regions.
§ It’s malignant.
 accountsaccounts forfor >> 90%90% ofof allall

lunglung
tumorstumors ＜10%10%
••secondarysecondary tumorstumors
90%90% •• fromfrom liver,liver, breast,breast,
etc.etc.
••benignbenign lunglung tumorstumors
PrimaryPrimary •• adenoma(adenoma(腺瘤）
bronchogenicbronchogenic • Hamartoma(构瘤)
（脂肪瘤）
carcinomacarcinoma •• lipomalipoma
•• fibromafibroma（瘤）
••otherother malignantmalignant tumorstumors
ofof lunglung
•• sarcomasarcoma（肉瘤）
overover allall TumorsTumors ofof lunglung
epidemiology
§ Lung cancer is the most common cancer in both men and women.
§ It accounts for about 14% of all new cancers in both men and women.
§ Lung cancer mainly occurs in older people. peak incidence occur
between ages 55-65 years . there is a 3:1 male : female ratio.
§ For smokers the risk is much higher.
§ Lung cancer is the leading cause of cancer death among both men and
women.
§ Lung cancer accounts for about 1 in 4 cancer deaths each year.
§
Etiology
§ The etiology of lung cancer is not clear, but there are many
risk factors.
§ Risk factors are anything that can increase or decrease a
person’s chance of getting a disease, such as cancer.
§ There are many known risk factors for lung cancer.
Etiology
§ Smoking is the leading cause of lung cancer.

§ About 80% of lung cancer deaths are linked to smoking.
§ Many others are caused by exposure to secondhand smoke.
§ There are other known causes of lung cancer, but they are
much less common.
§ A small percentage of lung cancers occur in people with no
apparent risk factors.
Lung cancer risk factors
§ Tobacco smoke
§ Smoking is leading risk factor for lung
cancer.
§ Cigar smoking and pipe smoking also cause
lung cancer.
§ Secondhand smoke
§ Even if you don’t smoke, breathing in the
smoke from others( called secondhand
smoke or environmental tobacco
smoke[ETS]) can increase your risk of lung
cancer.
Risk factors
Tobacco (and passive ) smoking
ØMost important factor
ØResponsible for 80％～90％ of males’ lung cancer cases

ØAssociate with 20％～40％ of females’ lung cancer cases
whywhy SmokingSmoking isis thethe mostmost
importantimportant factor?factor?
highhigh mortality:mortality:9~109~10 timestimes higherhigher inin

smokersmoker
Pathologically,Pathologically, smokingsmoking cause cause pre-cancerouspre-

cancerous epitheliumepithelium
changeschanges
carcinogeniccarcinogenic substancesubstance :: benzopyrenebenzopyrene（苯并比）

Occupational exposure
If the workplace exposure to carcinogenic substance, to all
workmen, it is also a risk factor for lung cancer. especially
in smokers.
§ Asbestos
§ （石棉）
§ Arsenic（砷）
Air pollution
§ Pollution indoor：cook fumes

§ Pollution outdoor：air pollution
automobile exhaustion; smog
§ Especially from heavily traveled roads in cities → slightly increased risk
Radiation
Come from：
• medical exposure：X-ray
• Nuclear radiation：atomic bomb
• Nature radiation
§ A history of lung cancer yourself or lung cancer in a family

member
§ TB
§ Carcinoma can develop in scar regions from healed TB.
§ Risk is increased 5~10 times over general population
§ Most common cancer is adenocarcinoma in this patients.
§Nutrition
§ Lack of Vitamin-A and β-carotene
§ Deficiency of vegetables and fruits
§ Too much fat intake

Pathology and
classification
The anatomy of lungs
§ The trachea divides into 2

tubes called the bronchi
which divide into smaller
branches called
bronchioles.
§ At the end of the

bronchioles are tiny air
sacs known as alveoli.
Clinical classification
§ According to the anatomy

§ Central lung cancer
§ occurs from segmental
bronchus to main bronchus
§ It accounts About ¾ of lung
cancer
§ Mainly Squamous or Small
cell lung cancer
§ Peripheral lung cancer
§ Occurs below the segmental
bronchus
§ About ¼
§ adenocarcinoma
Clinical classification
Central lung cancer Peripheral lung cancer
Histological classification
SCLC:(10-15%)
including
Large cell carcinoma
(10%)
NSCLC Squamous cell carcinoma
(30-60%)
Adenocarcinoma(10-
30%)
Epidermiod [squamous]
carcinoma -35% :
§ occurs most frequently in men and old
people
§ It is strongly associated with smoking.
§ usually starts on one breathing tubes,
and cause obstructive pneumonia or
atelectasis.
§ tend to be localized in the chest longer
than other types of lung cancer.
§ does not tend to metastases early.
§ Tend to necrosis, and form cavity.
Adenocarcinnoma-30%:
§ most common cancer among women.
§ usually started near the outer edges of the lung.
§ Invasion of pleura and mediastinal lymph node is common.
§ may spread to other parts of the body.
§ can be seen in non smoker.
Large cell carcinoma – 15% :
§ less well – differentiated.
§ may occur at any part of the lung.
§ Tumors are large by the time they are diagnosed.
§ has greater possibility of spreading to brain and

mediastinum.
Small cell lung cancer:
§ small cell lung cancer also called oatcell because SCLC cells have oat
grain appearance.
§ It arises from endocrine cells [kulchitisky cells] where many hormones are
secreted.
§ spread to lymph nodes and other organs more quickly than NSCLC .
§ usually started in one larger breathing tube,
§ Tend to grow rapidly .
§ commonly has spread by the time diagnosis and is considered a systemic
disease.
§ It is the only one of the bronchial carcinomas that respond to chemotherapy
Clinical stage
Primary tumor classification
§ T3 separate tumor nodules

in the same lobe.
§ T4 Separate tumor nodules
in a different ipsilateral lobe
Regional Lymph nodes classification
Distant metastasis (M) classification
TNM and clinical stage
Stage 0 Tis Stage IIIa T1N2M0

Stage Ia T1N0M0 T2N2M0
Stage Ib T2N0M0 T3N1M0
Stage IIa T1N1M0 T3N2M0
Stage Iib T2N1M0 Stage IIIb T4N(0-3)M0
T3N0M0 T(0-4)N3M0
Stage IV T(0-4)N(0-3)M1
Clinical manifestation:
(5-15% no symptom)
ØSymptoms caused by tumor
ØSymptoms due to tumor expansion
ØSymptoms due to remote metastasis
ØExtra thoracic manifestations

1. Symptoms caused by tumor
⑴ Persistent cough:
⑵ hemoptysis :
⑶ wheezing:
⑷ chest distress and breathless :
⑸ weight loss：
⑹ fever:
Symptoms caused by tumor
1- cough ( in 80% of cases ) :

§ It is the most common early symptoms.
§ Stimulating cough, little sputum or dry cough, and persistent.
§ sputum is purulant if there is second infection.
§ Alveolar cell carcinoma can have a lot of mucus sputum.
§ A change in the character of the (regular cough) associated with
other new respiratory symptoms increase the possibility of B.C.
2- Haemoptysis ( in 70% of cases) :
- Repeated episodes of scanty cough hemoptysis or

blood –streaking of sputum in smokers are highly
suggestive of B.C and should be always investigated .
3- Dyspnea ( 60% of cases ):
- reflect obstruction of a large bronchus resulting in tumor

in airway or compression by large lymph nodes or
development of pleural effusion.
4- Pleural pain :
reflect malignant invasion of the pleura or reflect infection

distal to a tumor (which is recurrent and fail to resolve).
5. fever
cause by the necrosis of tumor tissue or obstructive
pneumonia.
6. Weight loss
emaciation, cachexia.
Symptoms due to tumor expansion
1. Chest pain
dull pain is common.
cause by the invasion of pleura or chest wall or

compression of intercostal nerve.
there is a tender point at ribs or spine if invasion of

bone.
2. Hoarseness
§ Cause by the compression of
recurrent laryngeal nerve because
of tumor or large lymph nodes.
§ causing unilateral vocal cord
paresis with hoarseness of voice.
3. dysphagia
Involvement of esophagus
4.Invassion of phrenic nerve ,
causing paralysis of the diaphragm.
5. Pleural effusion:
§10% of cases have pleural effusion
§Caused by invasion of pleura or blocking of pulmonary
lymphatic reflux.
6. Horner's syndrome: tumor at lung apex

(Pancoast tumor), compresses the
cervical sympathetic nerve (部交感神）
causes ipsilateraly :
ptosis of upper eyelid,
miosis （瞳孔小）
enophthalmos 眼( 球内陷）
anhidrosis （无汗症）
sometimes tumor pressing on the brachial plexus may causes
sustained pain of the arm.
7. superior vena cava obstruction :
Superior vena cava
obstruction causing early
morning headache, facial
congestion and edema
involving the upper limb,
distention of jugular vein
and veins of the chest.
Symptoms due to remote metastasis
⑴ to brain and central nerve system: intracranial pressure increase,

headache, nausea, vomit. Epileptic seizure. Hemiplegia, myasthenia.
⑵ to bone:
bone pain and pathological fracture.
⑶ to abdomen:
involvement of pancreas, digestive tract, adrenal gland
⑷ to lymph node:subclavian lymph nodes

ExtraExtra thoracicthoracic manifestationsmanifestations
⑴ hypertrophic pulmmonary
Osteoarthropathy
（肥大性肺性骨关病）
⑵ gynaecomastia
（男性乳房育）
large cell lung cancer
⑶ Cushing's syndrome:
§ Common in SCLC.
§ ACTH increase in tumor tissue or blood.
§ central obesity, muscle weakness, skin thinning,
hypertension,hairiness, etc.
⑷ syndrome of inappropriate anti-diuretic hormone secretion

(SIADHs)（抗利尿激素分泌异常综合征）
• Symptom of water intoxication: Anorexia, nausea, vomit,
• Hyponatremia (Na < 135 mmol/L)
• Hypotonic (serum osmolality < 280 mOsm/Kg)
⑸ neuromyopathic syndromes:
• Common in SCLC.
• Cortical degeneration(皮质变性), cerebellar degeneration（小脑变性）
, peripheral neuropathy, myasthenia gravis（重症肌无力）,
myopathy（肌病）
• Occur before the tumor or at the same time or after operation
• No associated with the position of tumor and metastasis.
⑹ hypercalcemia
• Common in squamous cell carcinoma.
• Sleepiness, Anorexia, nausea, vomit, weight loss
§ 7. carcinoid syndrome
§ episodic flushing or edema at face or upper extremities
or trunk; acceleration of gastrointestinal peristalsis;
diarrhea; tachycardia; wheeze.
§ Because of releases of 5-hydroxytryptamine, bradykinin,
catecholamine.
Auxiliary examination
1.X-ray
. chest x-ray:
common radiological presentation of bronchial
carcinoma.
1- unilateral hilar-enlargement.
2- peripheral pulmonary opacity.
3- lung, lobe or segmental collapse.
4- pleural effusion .
5- broadening of the mediastinum,
enlarged cardiac shadow, elevation
of hemidiaphram.
6- rib distruction.
肺癌
2. CT scan
2. CT scan
2. CT scan
2. CT scan
lymphagitis carcinomatosa
interlobular septal thickening

3. MRI( magnetic resonance imaging) : To detect the

relationship of blood vessel and tumor
§ Cytologic examination （胞学)of sputum : at least 3 - 4

times
§ Pleural fluid cytology in pleural effusion
Management
Investigation:
. Sputum cytology: high yield for
endobronchial tumors such as
squamous cell and small cell
carcinoma.
. Bronchoscopy : gives high yield in excess of

90% (allows biopsy and bronchial brush samples)
if fail precautious fine needle aspiration under CT.
5. Fiberoptic bronchoscopy:
euthyphoria, needle biopsy,brush biopsy, forceps biopsy,
sucking
Squamous Cell
Normal Trachea Normal Carina
Carcinoma, Trachea
Adenocarcinoma
Adenocarcinoma Extrinsic Pressure
Left Lingular Bronchus Right Truncal Intermedus Trachea
EBUS
Electromagnetic navigation
fine needle aspiration under
CT.
open lung biopsy :
only for highly suspected patient, if the general condition

permitted.
others:
Scanning with radioisotopes, tumor antigens (CEA) ,

serological tests, etc.
these have no definite proved value.
Diagnosis the metastasis
.CT thorax and upper abdomen.
.Head CT scan.
.Radio nuclide bone scanning.
.liver US.
.bone marrow biobsy.

Diagnosis
1、Case history、health examination and auxiliary

examination
2、 General investigation of high risk group

Diagnosis
§ Diagnosis procedure:
§ 1. X-ray film(-) and sputum for cytology (-)  FBC(-)

follow up once a month /year.
§ 2. X-ray film(+) and sputum for cytology (+)  （FBC ）

 therapy.
§ 3. X-ray film(-) and sputum for cytology (+)  ruling out

the tumor of upper respiratory tract first  FBC.
§ 4 X-ray film(+) and sputum for cytology (-)  FBC(-) 

lung biopsy.
Differential diagnosis:
1. Tuberculosis
⑴ Tuberculoma:核球
⑵ Hilar lymph node tuberculosis:
（肺淋巴核）
⑶ Miliary tuberculosis 粟粒性核
2. Pneumonia:
3. Lung abscess 肺
4. Tuberculous pleural effusion核性胸腔液
Treatment
1.Resection by operation: especially for NSCLC.
2.Radiotherapy radical: cure /alleviative treatment
3.Chemotherapy：especially for SCLC.
4. targeted therapy :especially for advanced stage

NSCLC.
5. immunotherapy
6.Traditional Chinese medicine therapy etc.
Treatment
NSCLC:
Ⅰ-Ⅲa operation.
Ⅲb Radiotherapy +others. Or targeted therapy
Ⅳ Chemotherapy +others Or targeted therapy
WHAT IS A “TARGETED” THERAPY?
• Drugs directed at the molecular or physiologic concomitants

of malignancy which are uniquely disrupted in cancer.
- Receptors
- Genes
- Angiogenesis
- Tumor pH
• Implications:
- “Biological Effective Dose” rather than “Maximal Tolerated
Dose”
-Patient Selection Possible by assaying some aspect of the
target
EGFR 信号通路
Chong CR, Jänne PA. Nat Med. 2013 Nov;19(11):1389-400

EGFR inhibitors
Iressa(gefitinib, ZD1839), Tarceva (Erlotinib), Erbitux (Cetuximab, EGFR

Monoclonal antibody)
To the advanced stage NSCLC patients with EGFR gene mutation,

TKI(Tyrosine Kinase Inhibitor) is recommended as the first-line treatment.
Treatment
SCLC:
chemotherapy
+
radiotherapy /chemotherapy.
prognosis
§ squamous carcinoma
>
adenocarcinoma
>SCLC
Depends on early diagnosis ,early treatment.

reviews
§ Etiology: smoking, occupational exposure

§ The pathological type of lung cancer and the type of clinical
characteristics
§ Squamous cell carcinoma
§ Adenocarcinoma
§ Large cell carcinoma
§ Small cell lung carcinoma
reviews
§ Lung cancer clinical manifestations

§ Symptoms caused by the original tumor
§ Symptoms caused by the tumor expansion
§ Symptoms caused by the tumor metastasis
§ Lung cancer diagnosis, differential diagnosis
§ staging of lung cancer treatment
§ surgery; chemotherapy; radiation therapy; targeted therapy
case
§ female, 79 years old

§ hemoptysis for 1 week.
Squamous cell carcinoma

EGFR 19del mutation
EGFR-TKI: Iressa
Thank you
The Physical
Examination
The physical examination
Necessary equipments for examination

Required Optional Required Optional
Stethoscope Nasal speculum Oto- Gauze pads
ophthalmoscope
hemomanomet Nasal Safety pins or Gloves

er illuminator straight pins
Tongue blades Tuning Tape measure Coated fabric

fork:128Hz,
512Hz
penlight Pocket visual +
acuity card
Reflex hammer Lubricant gel
Preparation for examination
 Wash your hands before examination
washing with soap and water is an effective way
to reduce the transmission of disease
 It is preferable to use daylight for illumination.
skin color changes may be masked by artificial
light.
 Become facile in each organ system examination.
the complete examination with the least amount
of movement of the patient is an excellent
manipulation.
Preparation for examination
 Stands to the right of the patient as the

patient lies in bed.
 Should expose only the areas that are
being examining.
The physical examination
 There are four principles:
Inspection
Palpation
Percussion
Auscultation
inspection
 Examiners can observe the following
aspects of the patient:
General appearance
State of nutrition
Body habitus
Complexion and emotion express
Posture and gait
Consciousness
Palpation
 Palpation is the use of the tactile

sense to determine the
characteristics of an organ system.
 Examiner can use it to check all over
the body, especially abdomen.
Palpation manipulation
 Light palpation
 Deep palpation
Light palpation
 Examiner put a palm on the examined site

lightly, gliding and feeling with the coherent
movement of finger and wrist.
 it is used for examining superficial position,
shallow artery, vein, and nerves,
articulation, soft tissue, bursa of testes, and
chorda spermatica, etc.
Deep palpation
 It is used for examining the

magnitude of abdominal organ,
and abnormal lumps.
Deep slipping palpation
Bimanual palpation
Deep press palpation
Ballottement
Deep slipping palpation
 Examiner gradually touches the
organ or lumps in abdomen with the
tips of forefinger, middle finger , and
fourth finger.
 It is used for examining the lumps in
deep belly and disorders of stomach
and intestine.
Bimanual palpation
 Examiner pushes the checked organ or

position to right with left hand which is on the
back of checked organ or lumps, and uses
right hand to touch.
 It is used for examining liver, spleen, kidney,
and lumps in abdomen,and can be used to
pelvic examination.In this technique,the
examined tissure is between two hands.
Deep press palpation
 Examiner gradually presses the thumb or
several fingers deeply on the abdomen.
 It is used for detecting the place of
abdominal deep disorders, or deciding the
abdominal tenderness point.
 When checking rebound tenderness,
examiner presses the position deeply, then
raises his or her hand quickly, observes
whether patients seem painful.
Ballottement
 Examiner moves 3~4 fingers together
with the angle of 70~90 degree, puts
them on the checked position, quickly and
heavily batters them several times, feels
the floating and sunken pulse of
abdominal organ.
 It is only used for checking liver and
spleen in patients with severe ascites.
Attention items
 Size
 Appearance
 Texture
 Surface
 Borderline
 tenderness
 Clear up the patients’ anxiety emotion
 Warm your hands before palpation,relax
muscles.
 Employ proper position
 Palpate lower abdomen,ask patient
urination.
肝触诊示意图
脾脏触诊示意图
颈前淋巴结检查
Percussion
 Percussion relates to the tactile
sensation and sound produced when
a sharp blow is struck to an area
being examined.
 This provides valuable information
about the structure of the underlying
organs or tissues.
Percussion
 Indirect percussion
 Direct percussion
Indirect percussion
 Examiner firmly sticks the left middle finger

on the surface of checked position, the palm
and other fingers hold off the position, lets
the right hand bend naturally, uses the tip of
right middle finger to strike left middle finger,
makes sure of the tip direction being vertical
to the surface.
Indirect percussion
 Examiner should mainly use the carpal

articulations and metacarpophalangeal
articulations, avoid using elbow joint and
scapulohumeral articulation.
 Examiner raise his or her right hand
immediately after percussion.
 Examiner should tap 2~3 times at on
position. If uncertain, he or she can strike
again.
 Only the left phalanx should touch the wall.
 To furnish blows of equal intensity ,the
right hand are held flexed and wrist is
loose.
 Neither elbow nor shoulders should be
moved.
Indirect percussion
This is the right way of indirect percussion

Indirect percussion
Indirect
percussion
Direct percussion
 Examiner use the right fingers’ palm to flap the

checked place.
 It is used for patients with extensive disorders of
chest or abdomen, such as patients with pleural
thickening, severe pleural effusion or ascites.
 Be careful to not strike the patient too firmly.
Percussion sound
 Resonance:
Can be heard when checking a normal
person’s chest.
 Tympany:
person’s abdomen and aerogastria.
Percussion sound
 Hyperresonance:
child’s chest.
In normal adult, there is no such
percussion sound. It can just be heard
in patients with emphysema.
Percussion sound
 Dullness
Can be heard when checking heart or
liver part covered by lung,ascites.
 Flatness
Can be heard when checking the
heart or liver part not be covered by
lung, or parenchyma organs.
Auscultation
 Auscultation involves listening to
sounds produced by internal organs.
 This technique gives information
about an organ’s pathophysiology.
Smell
 Breath
 Sputum
 Vomitus
 Feces
 Urine
 pus
PLEURAL EFFUSIONS
Anatomy of pleural membrane
and pleural space
 Pleural membrane consists of parietal

pleura and visceral pleura
 A space situated between parietal and
visceral pleura is called pleural space
 It is normally filled with 5 - 15 milliter
of fluid
Mechanism of formation
of pleural fluid
Parietal pleura Visceral pleura

Hydrostatic Pressure of pleural
pressure
→ space (5)
Oncotic
pressure
← Permeability of pleural
fluid (8)
Pressure for formating fluid

=Hydrostatic pressure — Oncotic pressure
 Transudative effusions
 (hydrostatic pressure &  plasma oncotic pressure)
 The cause is
 Heart failure
 Cirrhosis of liver with ascites
 Hypoalbuminemia (nephrotic syndrome)
 Exudative effusions
 ( capillary permeability  exudation of fluid, protein, cells )
 The cause may be
 Lung and pleural cancer
 TB pleuritis
 pneumonia
 pulmonary embolism
 viral infection
Two kinds of pleural effusions
Transudates and exudates
Transudate Exudate
 Cause non-inflammatory flammatory,tumor
 Apperance light yellow yellow, purulent
 Specific gravity <1.018 >1.018
 Coagulability unable able
 Revalta test negative positive
 Protein content <30g/L >30g/L
 LDH < 200 I U/ L > 200 I U / L
 Cell count < 100×10 6/ L > 500×10 6 / L
 Differential cell Lymphocyte Different
Haemorrhagic effusion
l. Trauma
2. Tumor
3. Pulmonary infarction
4. TB
5. Spontaneous pneumothorax
Empyema
l. TB
2. Pulmonary infection
3. Trauma
 T B ( Tuberculosis ) is the most
common cause of pleural effusion ,
especially in young people, the common
symptom include: fever 、chest pain expicially
during inspiction,chest tightness, night sweat,
fatigue, bad appitide , weight loss
 Malignant pleural effusion is frequently
met in aged people

 Pleural transudation is most commonly
caused by congestive heart failure

Pleurisy
 it may occur with or without pleural
effusion
Dry or fibrinous pleurisy :
without pleural effusion
Humid or exudative pleurisy :
with pleural effusion
 Dry pleurisy is often followed by humid pleurisy
Diagnostic procedures 12345
History(primary diseases)
clinical signs
physical examinations
clinical signs
 pleural pain,
 dyspnea,
 tachypnea,
 mild outward bulging of the intercostal
spaces,
 decreased tactile fremitus,
 dullness or flatness,
 decreased transmission of breath and vocal
sounds in the area of the effusion,
 and pleural friction sound in its
early stage (dry pleurisy)
Chest X-ray examination
Blunting of the normally sharp costophyrenic
angle, a concave shadow with its highest margin
along the pleural surface, shift of the tracheal and
mediastinum toward the normal side if pleural is
huge
Pleural effusion
B- Ultrasonic examination
To localize a small pleural effusion and
determine the correct site for performance
of a thoracentesis
Thoracentesis is importmant to
diagnosis the cause and alleviated the
sign
To aspirate the pleural effusion for laboratory
examination:
Appearance, Specific gravity, Protein content,
Cell counts, LDH lipid content, ADA
bacteria culture,
Cytologic examination, etc.
Pleural biopsy
To obtain a specimen for histologic
examination and culture usually
under B ultrasonic or CT guidance
Treatment
Treatment for many pleural effusions, whether

transudates or exudates is primarily for the
underlying pulmonary or systemic disease:
 aspiration of fluid is usually indicated
to establish the
diagnosis, aspirration of pleural fluid may be
necessary to relieve breathlessness. It is
inadvisable to remove more than 1 litre on
the first occasion because “re-expansion”
amountslly follows the aspiration of
pulmonary edama occasionally follow the
aspiration
Tuberculous pleural effusion
Patients with tuberculous effusions should always receive

antituberculosis chemotherapy. Aspiration is required initially if
the effusion is large and causing breathlessness. The addition of
prednisolone 20mg daily by mouth for 4-6 weeks will promote
rapid absorbtion of the fluid, obviate the need for further
aspiration and may prevent fibrosis.
Malignant effusions
Effusions caused by malignant infiltration of the pleural surfaces
re-accumulate rapidly. To avoid the distress of repeated aspiration,
an attempt should be made to drain all fluid via an intercostal tube
than obliterate the pleural space by the injection of substances
which produce an inflammatory reaction and extensive pleural
adhesions. The agents most frequently used are tetracycline,kaolin
and bleomycin
Pulmonary
Tuberculosis
He yuanbing
The first affiliated hospital of
Xinjiang medical
university,Respirarory
department
General consideration
• This disease, which is caused by bacteria of the
Mycobacterium tuberculosis comlex, usually
affects the lung, years ago was considered to be
almost under control, has once again become a
serious word –wide problem.
• Morbidity: 64.7/10000，tuberculosis smear
(+)18.9/10000
• Mortality: 2.1/10000. It is a serious public
healthy problem, expecially in the rural area and
underdeveloped country
• WHO estimated over 10400000 TB patient by
the year 2015, 1400000 patients died of TB
However, in developed countries
there is still a tendency for
tuberculosis to be overlooked, the
diagnosis being made late or only at
autopsy.
Multiple resistence TB(MR-TB) is
much sever than normal TB
Transmission of M.tuberculosis
• Mainly from the spread by droplet
nucleus from coughs,sneezes.expecilly
from tuberculosis smear positive patients
• Close contacts,eg: skin.
• From Blood .
• From the alimentary tract.
Etiology
Entry of the tubercle bacillus

(mycocobacterium tuberculosis complex
cause of most infection, Mycobacterium
bovis-endemic in cattle, spread by human
milk), into the body or the alimentary or
respiratory tract is not necessarily followed
by a clinical illness, the development of
which is dependent upon several other
factors.
Those at greatest risk of acquiring
tuberculosis
• Children,adolescents
• Contacts of patients with smear-positive
tuberculosis patients.
• People living in overcrowed conditions
• Immunocompromised individuals(e.g.AIDS
patient and those on immunosuppressive
therapy and corticosteroids druge usage)
• Pre-existing conditions-diabetes melllitus,
gastric surgery, silicosis, alcoholism.
mycobacterium tuberculosis
杆菌
不典型分支杆菌
Types of mycobacteria causing disease in
humans
• Mycobacterium cause most human’s

tuberculosis
• Mycobacterium M.bovis in cattle,spread to
humans by milk.
.
Pathology
• Basic pathologic process:

initial primary tuberculosis Infiltration,
necrosis, hyperplasia, .caseous lesions in
the regional lymph nodes, heal and calcify
tuberccle bacilli enter the blood
stream, ”haematogenous” lesions ,
dissemination throughout the body, cause
miliary tuberculosis, meningitis often
complicate, tuberculosis cavity formed
calcified nodule
calcified tuberculous nodule

Clinical Type
• Primary pulmonary tuberculosis
• Hematogenous (miliary) pulmonary
tuberculosis
• Post-primary pulmonary tuberculosis
• Tuberculous pleuritis
• Other extra-pulmonary tuberculosis
Primary pulmonary tuberculosis
• Usually occurs in children.

• Typical primary complex
(the primary infection and the associated lymph
node lesions, lymph tube which between
them).
primary tuberculosis
Post-primary pulmonary tuberculosis
• Infiltrative pulmonary tuberculosis
• Chronic fibro-cavitative pulmonary

tuberculosis
• Caseous pneumonitis pulmonary

tuberculosis
Miliary tuberculosis .
• Occurs chiefly in children and young
adults.
• Few bacilli spread into the vein and
produces acute dissemination .
• Chest radiograph: miliary mottling
symmetrically distributed throughout
both lung fields.
Post-primary pulmonary
tuberculosis
• Majority of the cases are middle-aged and elderly
ones.
• Lesions are most situated in the upper lobes,

distributed bilateral.
• Both infiltration, necrosis, hyperplasia ,

tuberculous cavity exit
Post-primary pulmonary
tuberculosis
----following reactivation of an
incompletely healed primary focus.
----may be the result of reinfection.
Post-primary pulmonary tuberculosis
• Infiltrative pulmonary tuberculosis
• Chronic fibro-cavitative pulmonary

tuberculosis
• Caseous pneumonitis pulmonary

tuberculosis
cavitation
Tuberculous pleurisy
• Pleurisy
• Exudate Pleural
effusion
Extra-pulmonary tuberculosis
• Tuberculosis can affect any organ and tissue of

the body.
• Gastrointestinal tuberculosis: tuberculosis of
peritoneum and intestine obstruction, ascites
• Pericardium: pericardial effusion, constrictive
pericarditis, tampponade
• Central nervous system tuberculosis:
tuberculous meningitis, cerebral brain
tuberculoma
Genitourinary TB: renal
tuberculosis
Bone and joint TB:
vertebral collapse, pyarthrosis,
osteomyelitis,” cold abscess
formation
Lymph node TB: lymph node
（especially cervical)
enlargement,usually
painless,fluctuant and sinus
formation is common
Eye: polyctenular
conjunctivitis,,Choroiditis
Adrenal: Addison’s disease
Bone marrow: Anaemia,

Thrombocytopenia
Skin: lupus vulgaris, Erythema

nodosum
Clinical features
• Symptoms and signs

• Persistent cough
• Hemoptysis, blood stained or huge
hymoptysis
• Pleural pain not associated with acute illness
• Spontaneous pneumothorax
• dyspnea
• Lethargy
• Weight loss
Other symptoms of active TB
disease:
• Chill
• Night sweating
• Bad appetite
• Weight loss
• Fever: usually low temparature
• Easy featigability
Diagnosis 1
• Medical history
• Physical examination
• Tuberculin skin test
• Chest radiography:
• Bacteriologic smear or culture or histo-
pathological exam
Old Tuberculin (OT) or PPD skin
test
• Read reaction 48-72 hours after injection
• Tuberculin
• Mearuse only induration
• Recored reaction in millimeters
• 1-4mm(-）
• 4-20mm
• >20mm（+-++）
• Babble and necrosis(+++-++++)
• False negative
• HIV—decreased or supressed cellular

immunity function
• Miliary tuberculosis+late stages of
tubeulosis meaningitis sever
tuberculosis
• Elderly patients
• Immunosuppressive drugs usage
Bacteriologic or histologic test
• If Consider TB in patients can be done
acid-fast bacilli test. (at least three
specimens of sputum should be included.)
• Microscopic examination of sputum smear
• by Ziehl-Neelson stained method
• Auramine-phenol fluorescent test
• Tuberculosis Culture of sputum
• PCR or NGS(next generation sequence)
• Drug sensitivity test
Molecular biology diagnosis of TB
PCR
TB DNA
NGS(next generation sequence)
Diagnosis2
• Radiological examination of the lungs.
Chest X rays, if not certain ,CT is more
accurate and sensitive
• Examination of the secretion of the

respiratory tract.
• Erythrocyte sedimentation rate
(ESR).raised
bronchoscopy
• Bronchoscopy with bronchial
brushings,washing, biopsy or
transbronchial biopsy of the lung lesion
tracheal bronchial
tuberclosis TBTB
EBTB
Management of TB
General principle of control and prevention
• Case finding, expicially tubercuolis
smear(+)patients
• BCG vaccination: conferring protection for up
to 7 years, readuces the incidence of TB by
80% and minimises the risk of serious
disseminaed TB disease
• TB patients expecially Tb smear(+)patient has
trasmited harmful to others ,so sputerm should
be disinfected and wear a mask, donot spit
sputum casualiy
Basic principles of treatment
• Provide safest,most effctive therapy in
shortest time
• Multiple drugs to which the organisim
susceptible
• Never add single drug
• Ensure adherence to therapy, usually 9
mounth-1year
Chemotherapy
First line treatment:
 rifampicin(RFP), 450mg(children 10-20mg/kg),

side effects: hypersensitivity hepatitis, vasculitis,
skin-flushing, nause and abdominal pain,
 isoniazid(INH),200-300mg(children10mg/kg),
side effects: hypersensitivity, polyneuropathy,
lack of mental concentration
pyrazinamide(PZA),20-35mg/kg, side
effects: hepatitis,gout,hypersensitivity
ethambutol(EMB):25mg/kg. side effects:

eye optic neuritis, hypersensitivity
Streptomycin sulphate: children 30mg/kg,

adult under 40 years old 1.0g, adult 40-60
y and weighing less than 45kg, 0.75g
side effects: vestibular disturbance,,
hypersensitivity, deafness(rare)
Rationale combination of
chemotherapy
• An initial phase using at least 3 drugs

• A continuation phase using 2 drugs
Chemotherapy
 2HRZE(S)/4HR
 2H3R3Z3E3(S)/4H3R3
 2H2R2Z2E2 (S)/4H2R2
 ciprofloxacin: have not been formally
assessed in clinical trials.
Other therapy to TB:
Surgical treatment
Interventional treatment to TB: from
bronchoscope, DSA pulmonary
blood embolism to huge
hymoptesis due to TB
• Thank you
C. Lung and pleura
When chest is examined, the patient is generally in
sitting or supine position with upper garment stripped
off for adequate exposure of the chest. The room should
be comfortably warm. Good lightening is quite
important. The examination of lung and pleura routinely
includes inspection, palpation, percussion, and
auscultation.
I . Inspection
1. Breath movement: The breath movement in healthy
subject at rest is steady and regular. This is controlled by the
breath center and regulated by the nerve reflex. Hypoxemia
can stimulate the carotid sinus and the aortic body chemo-
receptor, thus quicken the respiration. In condition of
metabolic acidosis, the blood PH drops, and respiration
become deeper and slower to remove CO2 out of the lung
compensately. In addition, pulmonary stretch reflex can also
change the rhythm of respiration, seen in conditions like
pneumonia or pulmonary congestion caused by heart failure,
thus breath becomes superficial and quick.
Respiration in healthy males and children tends to be
predominantly diaphragmatic, the lower part of thorax and
the upper abdomen move up and down substantially, and
form abdominal respiration. Whereas in female, the
respiration is mainly dependent on intercostal muscles, this
is thoracic respiration. Actually, both forms of respiration
exist simultaneously with different degrees. Some diseases
can change respiratory patterns.
In patients with partial obstruction of the upper
breathing tract, air flow into the lung is impedent,
thus the inspiratory muscle contraction may lead
to extremely high negative intrathoracic pressure
and cause the depression of supersternal fossa,
superclavical fossa and interspaces, termed
“ three depression sign”. On such occasions
inspiration is prolonged, hence called inspiratory
dyspnea. It usually occurs when trachea is
obstructed, by foreign body, for example.
inspiratory dyspnea
laryngeal foreign body

expiratory dyspnea
status asthmaticus
On the contrary, in patients with lower respiratory tract
is obstructed, because the airflow out of the lung is
impedent, exhalation with exertion may lead to bulging
of the interspaces. This is associated with prolonged
expiration, called expiratory dyspnea, it usually occurs
in asthma and obstructive emphysema.
1.Respiratory rate:
normal adult at rest, the respiratory rate is 10-20 per
minute.
The ratio of respiratory rate to pulse rate is 1:4. The
respiratory rate in newborn is about 44 per minute, and
decreases gradually upon growing up.
1) tachypnea: Indicates the increased respiratory rate that
over 24 per minute, usually seen in fever, pain, anemia,
hyperthyroidism and heart failure. Usually the respiratory
rate increases approximately four additional cycles per
minute for each 1°above the normal temperature.
2) bradypnea: Indicates the decreased respiratory rate
that less than 10 per minute. The respiration becomes
superficial, seen in over dose of anesthetics or sedatives
and elevated intracranial pressure.
3) Change of the breath depths:
Hypopnea could be seen in respiratory palsy, ascites
and fatness, etc. And also could be seen in pneumonia,
pleurisy, pleural effusion and pneumothorax.
Hyperpnea, could be found during strenuous
exercises, for increased body oxygen supply needs more
air exchange through the lung. It can also appear when
one is excited or nervous, because of over ventilation.
Decreased PaCO2 ensues and could induce respiratory
alkalosis.
Deep and slow breath could appear during serious
metabolic acidosis. This is because the HCO3 in the
extracellular fluid is not enough, and PH is lower, for
compensation, CO2 is eliminated by the lung to
maintain the acid-base balance. This kind of deep and
slow breath is also named as Kussmaul breath, seen
in diabetic ketoacidosis and uremic acidosis.
(3) Rhythm of the breath
Normal adult respiration is basically regular and smooth in
testing status. The rhythm of the breath usually changes in
diseases.
1. Tidal breathing Also called as cheyne-stokes respiration.
Respiration waxes and wanes cyclically so that periods of
deep breathing alternate with periods of apnea(no breathing).
The periods of the tidal breath can last from 30s to 2min. The
periods of apnea can persist 5-30s. So only through carefully
and long enough observation, the whole process could be
realized.
30 秒—2 分 5—30 秒
2. Ataxic breathing Also called Biot’s breahting.
Ataxic breathing is characterized by unpredictable
irregularity. Breaths may be shallow or deep, and stop
for short periods . Ataxic breathing is more severe than
the tidal breathing, the prognosis is worse, often
happening before demise. Aging people normally may
show tidal breathing in sleep, this is a sign of
cerebrovascular sclerosis.
3.Inhibitory breath
The inspiration is suspended while a severe pain in the
chest happened, the respiratory movement restrained
suddenly and momently. The expression of the patient is
suffering, breath become shallow and frequent. Causes
include acute pleurisy, tumor, costal fracture and severe
trauma of the thorax.
4. sighing respiration
Breathing punctuated by frequent sighs should alert you
to the possibility of hyperventilation syndrome – a
common cause of dyspnea and dizziness. Occasional
sighs are normal.
2. PALPATION
(1) Thoracic expansion
It is the movement range of the thorax during respiration.
Easy to obtain when examine the antero-inferior part of the
thorax, where the respiratory movement is much obvious.
Place your thumbs along each costal margin, and your hands
along the lateral rib cage. When the patient inhales deeply,
watch the divergence of your thumbs as the thorax expands,
and feel the range and symmetry of respiratory movement.
Causes of unilateral diminution of or delay in chest
expansion include huge pleural effusion, pneumothorax,
pleural thickening and atelectasis etc
(2) Vocal fremitus Also called tactile fremitus. Vocal
fremitus refers to the palpable vibrations transmitted through
the bronchopulmonary system to the chest wall when the
patient speaks. Ask the patient to repeat the words “yi—“. If
fremitus is faint, ask the patient to speak more loudly or in a
lower voice.
Palpate and compare symmetrical areas of the lungs using
either the ball of your hand (the bony part of the palm at the
base of the fingers) or the ulnar surface of your hand.
In either case you are using the vibratory sensitivity of
the bones in your hand to detect fremitus.
Identify, describe, and localize any area of increased or
decreased fremitus. Fremitus is typically more prominent
in the interscapular area than in the lower lung fields, and
is often more prominent on right side than on the left. It
disappears below the diaphragm.
Fremitus is decreased or absent when the voice is soft or
when the transmission of vibrations from the larynx to the
surface of the chest is impeded.
Causes include an obstructed bronchus, chronic
obstructive pulmonary disease, separation of the pleural
surfaces by fluid (pleural effusion), fibrosis ( pleural
thickening), air (pneumothorax) or an infiltrating tumor;
and also a very thick chest wall.
Fremitus is increased when transmission of sound is
increased, as through the consolidated lung of lobar
pneumonia.
(2) pleural friction fremitus
During acute pleurisy, the fibrin deposit between the
two layers of the pleura, the visceral pleura and the
parietal pleura rub with each other, this can be felt by the
examiner’s hand, so it is called pleural friction fremitus.
It can be palpated both in inspiration and expiration. It is
most obvious at the lower part of the thorax for the
movement range here is the greatest.
The other method of evaluating tactile
fremitus is to use the fingertips instead of
the ulnar side of the hand.
shown in figure 12-13
Table 12-5 lists some of the important
pathologic causes for changes in tactile
fremitus .
Percussion
In percussion of the chest, the examiner
places the middle finger of one hand firmly
against the patient’s chest wall parallel to
the ribs in an interspace, with the palm and
other fingers held off the chest.
The tip of the right middle finger of the
other hand strikes a quick, sharp blow to
the terminal phalanx of the left finger on
the chest wall.
The motion of the striking finger should
come from the wrist and not from the
elbow.
The technique of percussion is
diagrammed in Figure 12-14 and shown
in Figure 12-15.
1. Classification of the percussion notes
The sound heard and the tactile sensation
felt are dependent on the air-tissue ratio.
● Percussion over a solid organ, such as the
liver, produces a dull, low-amplitude, short-
duration note without resonance.
● Percussion over a structure containing air
within a tissue, such as the lung, produces a
resonant, higher- amplitude, lower-pitched note.
● Percussion over a hollow air-containing
structure, such as the stomach, produces
a tympanic, high-pitched, hollow-quality
note.
● Percussion over a large muscle mass,
such as the thigh, produces a flat, high-
pitched note.
● in the chest, dullness over the heart
and resonance over the lung
● pneumonia, resonance is replaced by
dullness.
●Hyperresonance: found in emphysema.
Hyperresonance is a low-pitched, hollow-
quality,sustained resonant note bordering
on tympany.
2. Percussion of the pulmonary boundary
(1)Upper pulmonary boundary
that is the width of the apics. The method is: percuss
from the middle trapezius muscle outwards to lateral side
little by little, when the sound turns from resonance to
dullness gradually, the lateral termination of the upper
border is identified.
And then, percuss from the same middle part to inner-

side, when the resonance turn to dullness again, the inner
termination of the border comes out.
The width of this resonant boundary is the
width of apics, 4-6 cm regularly, it is also
named as Kronig isthmus.
The width of right side is narrower than left,
for right apics is located lower and the muscle
of right shoulder girdle is stronger. The
boundary is narrowed or sounds dull when
tuberculosis infiltrates the apics and fibrosis
or atrophy is formed. The upper boundary
widened or changed to hyperresonance when
there is emphysema.
(2) The inferior pulmonary boundary
It is about the same of two sides, located at the 6th
intercostal space at the midclavicular line, 8th
interspace at the midaxillary line, 10th interspace at
the scapular line.
It is different in different body type. In fat person,
the boundary could be elevated about one
intercostal space and in thin person descended
about one interspace.
Pathologically, the boundary descends with
emphysema, celiac organ declined. It elevates with
atelectasis, celiac hypertension.
肺下界
inferior
Infer.(6th)
(8th)
(10th)
(3) The anterior pulmonary boundary
The heart normally produces an area of dullness to the
left of sternum. The right anterior pulmonary boundary is
at the sternal line,
the left one is at the parasternal line from 4th to 6th
interspace. It is influenced by the size of heart, pericardial
effusion, aortic aneurysm, enlarged lymph nodes of the
pulmonary portal and also by the emphysema.
Percuss the Posterior Chest
The sites are shown in Figure 12-16. The

bony scapulae are not percussed. The
examiner should start at the top and work
downward, proceeding from side to side,
comparing one side with the other.
Evaluate Diaphragmatic Movement
The patient is asked to take a deep breath and
hold it. Percussion at the right lung base
determines the lowest area of resonance. The
patient is then instructed to exhale as much as
possible, and the percussion is repeated. The
difference between the inspiration and
expiration levels represents diaphragmatic
motion, which is normally 4-5 cm.
● In patients with emphysema, the
motion is reduced. In patients with a
phrenic nerve palsy, diaphragmatic
motion is absent. This test is illustrated in
Figure 12-17.
Auscultation
The stethoscope usually has two heads:
the bell and the diaphragm. The bell is
used to detect low-pitched sounds, and
the diaphragm is better at detecting high-
pitched sounds. The bell must be applied
loosely to the skin. In contrast, the
diaphragm is applied firmly to the skin.
shown in Figure 12-18. It is never
acceptable to listen through clothing.
Types of Breath Sounds
four types of normal breath sounds.
*Tracheal *Bronchial
*Bronchovesicular * Vesicular
● Tracheal breath sounds are harsh,
loud, high pitched sounds heard over the
extrathoracic portion of the trachea. The
inspiratory and expiratory components are
approximately equal in length. Although
these sound are always heard when one
listens over the trachea, they are rarely
evaluated because they don’t represent
any clinical lung problem.
● Bronchial breath sounds are loud
and high pitched and sound like air

rushing through a tube. The expiratory
component is louder and longer than the
inspiratory component. These sounds are
normally heard when one listens over the
manubrium.
● Bronchovesicular breath sounds are
a mixture of bronchial and vesicular
sounds. The inspiratory and expiratory
components are equal in length. They are
normally heard only in the first and
second interspaces anteriorly and
between the scapulae posteriorly. This is
the area overlying the carina and main-
stem bronchi.
● Vesicular breath sounds are the soft,
low-pitched sounds heard over most of

the lung fields. The inspiratory
components is much longer than the
expiratory component, which is also much
softer and frequently inaudible.
The four types of breath sounds are
shown and summarized in Figure 12-19.
Auscultate the posterior Chest
Auscultation should be performed in a
quiet environment. The patient is asked
to breathe in and out through the mouth.
Very soft breath sound are referred to as
distant. Distant breath sounds are
commonly found in patients with
hyperinflated lungs, as in emphysema.
CorCor pulmonalypulmonaly
 Cor pulmonale is a condition that causes the right side
of the heart to fail. Long-term high blood pressure in
the arteries of the lung and right ventricle of the heart
can lead to cor pulmonale
 Causes
 High blood pressure in the arteries of the lungs is
called pulmonary hypertension. It is the most
common cause of cor pulmonale.
 In people who have pulmonary hypertension, changes
in the small blood vessels inside the lungs can lead to
increased blood pressure in the right side of the heart.
This makes it harder for the heart to pump blood to
the lungs. If this high pressure continues, it puts a
strain on the right side of the heart. That strain can
cause cor pulmonale.
Lung conditions that cause a low blood oxygen
level in the blood over a long time can also lead
to cor pulmonale. Some of these are:
Autoimmune diseases that damage the lungs,
such as scleroderma
Chronic obstructive pulmonary disease (COPD)
Chronic blood clots in the lungs
Cystic fibrosis (CF)
 Scarring of the lung tissue (interstitial lung disease)
 Severe curving of the upper part of the spine (kyphoscoliosis)
 Obstructive sleep apnea, which causes stops in breathing because of
airway inflammation
 Idiopathic (no specific cause) tightening (constriction) of the blood
vessels of the lungs
 Symptoms
 Shortness of breath or lightheadedness during activity is often the first
symptom of cor pulmonale. You may also have a fast heartbeat and
feel like your heart is pounding.
 Over time, symptoms occur with lighter activity or even while you are
at rest. Symptoms you may have are:
 Fainting spells during activity
 Chest discomfort, usually in the front of the chest
 Chest pain
 carring of the lung tissue (interstitial lung disease)
 Severe curving of the upper part of the spine
(kyphoscoliosis)
 Obstructive sleep apnea, which causes stops in
breathing because of airway inflammation
 Idiopathic (no specific cause) tightening
(constriction) of the blood vessels of the lungs
Symptoms
Shortness of breath or lightheadedness during
activity is often the first symptom of cor
pulmonale. You may also have a fast heartbeat
and feel like your heart is pounding.
Over time, symptoms occur with lighter activity
or even while you are at rest. Symptoms you may
have are:
Fainting spells during activity
Chest discomfort, usually in the front of the chest
Chest pain
Swelling of the feet or ankles
Symptoms of lung disorders, such as wheezing or
coughing or phlegm production
Bluish lips and fingers (cyanosis)
Exams and Tests
Your health care provider will perform a physical exam
and ask about your symptoms. The exam may find:
Fluid buildup in your belly
Abnormal heart sounds
Bluish skin
Liver swelling
Swelling of the neck veins, which is a sign of high
pressure in the right side of the heart
Ankle swelling
These tests may help diagnose cor pulmonale as well
as its cause:
Blood antibody tests
Blood test to check for a substance called brain
natriuretic peptide (BNP)
Chest x-ray
CT scan of the chest, with or without an injection of a
contrast fluid (dye)
Echocardiogram
ECG
Lung biopsy (rarely done)
Measurement of blood oxygen by checking
arterial blood gas (ABG)
Pulmonary (lung) function tests
Right heart catheterization
Ventilation and perfusion scan of the lungs (V/Q
scan)
Tests for autoimmune lung disease
Treatment
The goal of treatment is to control symptoms. It is
important to treat medical problems that cause
pulmonary hypertension, because they can lead to cor
pulmonale.
Many treatment options are available. In general, the
cause of your cor pulmonale will determine which
treatment you receive.
If your provider prescribes medicines, you may take
them by mouth (oral), receive them through a vein
(intravenous or IV), or breathe them in (inhaled). You
will be closely monitored during treatment to watch
for side effects and to see how well the medicine
works for you. Never stop taking your medicines
without first talking to your doctor.
Other treatments may include:
Blood thinners to reduce the risk of blood clots
Medicines to manage heart failure symptoms
•Oxygen therapy at home
•A lung or heart-lung transplant, if medicine does not
work
Important tips to follow:
•Avoid strenuous activities and heavy lifting.
•Avoid traveling to high altitudes.
•Get a yearly flu vaccine, as well as other vaccines,
such as the pneumonia vaccine.
•If you smoke, stop.
•Use oxygen if your doctor prescribes it.
•Women should not get pregnant.
Pulmonary hypertension

Pulmonary hypertension
is high blood pressure in the arteries of the
lungs. It makes the right side of the heart
work harder than normal
Causes
The right side of the heart pumps blood
through the lungs, where it picks up oxygen.
Blood returns to the left side of the heart,
where it is pumped to the rest of the body.
When the small arteries (blood vessels) of
the lungs become narrowed, they cannot
carry as much blood. When this happens,
pressure builds up. This is called pulmonary
hypertension.
The heart needs to work harder to
force the blood through the vessels
against this pressure. Over time, this
causes the right side of the heart to
become larger. This condition is called
right-sided heart failure, or cor
pulmonale.
Pulmonary hypertension may be caused by:
•Autoimmune diseases that damage the
lungs, such as scleroderma and rheumatoid
arthritis
•Birth defects of the heart
•Blood clots in the lung (pulmonary embolism)
•Heart failure
•Heart valve disease
•HIV infection
•Low oxygen levels in the blood for a long
time (chronic)
•Lung disease, such as COPD or pulmonary
fibrosis or any other severe chronic lung
condition
•Medicines (for example, certain diet
drugs)
•Obstructive sleep apnea
In rare cases, the cause of pulmonary
hypertension is unknown. In this case, the
condition is called idiopathic pulmonary
arterial hypertension (IPAH). Idiopathic
means the cause of a disease is not known.
IPAH affects more women than men.
If pulmonary hypertension is caused by a
known medicine or medical condition, it is
called secondary pulmonary hypertension.
Symptoms
Shortness of breath or lightheadedness during activity
is often the first symptom. Fast heart rate
(palpitations) may be present. Over time, symptoms
occur with lighter activity or even while at rest.
Other symptoms include:
•Ankle and leg swelling
•Bluish color of the lips or skin (cyanosis)
•Chest pain or pressure, usually in the front of the
chest
•Dizziness or fainting spells
•Fatigue
•Increased abdomen size
•Weakness
People with pulmonary hypertension often have symptoms
that come and go. They report good days and bad days.
Exams and Tests
Your health care provider will perform a physical exam and
ask about your symptoms. The exam may find:
•Abnormal heart sounds
•Feeling of a pulse over the breastbone
•Heart murmur on the right side of the heart
•Larger-than-normal veins in the neck
•Leg swelling
•Liver and spleen swelling
•Normal breath sounds if pulmonary hypertension is
idiopathic or due to congenital heart disease
•Abnormal breath sounds if pulmonary hypertension is from
other lung disease
In the early stages of the disease, the exam may be normal or
almost normal. The condition may take several months to
diagnose. Asthma and other diseases may cause similar
symptoms and must be ruled out.
Tests that may be ordered include:
•Blood tests
•Cardiac catheterization
•Chest x-ray
•CT scan of the chest
•Echocardiogram
•ECG
•Lung function tests
•Nuclear lung scan
•Pulmonary arteriogram
•6-minute walk test Sleep study Tests to check for
autoimmune problems
•
Treatment
There is no cure for pulmonary hypertension. The goal
of treatment is to control symptoms and prevent
more lung damage. It is important to treat medical
disorders that cause pulmonary hypertension, such as
obstructive sleep apnea, lung conditions, and heart
valve problems.
Many treatment options for pulmonary arterial
hypertension are available. If you are prescribed
medicines, they may be taken by mouth (oral),
received through the vein (intravenous, or IV), or
breathed in (inhaled).
Your provider will decide which medicine is
best for you. You will be closely monitored
during treatment to watch for side effects
and to see how well you are responding to
the medicine. DO NOT stop taking your
medicines without talking to your provider
Other treatments may include:
•Blood thinners to reduce the risk of blood clots,
especially if you have IPAH
•Oxygen therapy at home
•Lung, or in some cases, heart-lung transplant, if
medicines do not work
Other important tips to follow:
•Avoid pregnancy
•Avoid heavy physical activities and lifting
•Avoid traveling to high altitudes
•Get a yearly flu vaccine, as well as other vaccines such
as the pneumonia vaccine
•Stop smoking

Acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS) is
a life-threatening lung condition that prevents
enough oxygen from getting to the lungs and
into the blood. Infants can also have respiratory
distress syndrome
Causes
ARDS can be caused by any major direct or
indirect injury to the lung. Common causes
include:
•Breathing vomit into the lungs (aspiration)
•Inhaling chemicals
•Lung transplant
•Pneumonia
•Septic shock (infection throughout the body)
•Trauma
Depending on the amount of oxygen in the blood
and during breathing, the severity of ARDS is
classified as:
•Mild
•Moderate
•Severe
ARDS leads to a buildup of fluid in the air sacs
(alveoli). This fluid prevents enough oxygen from
passing into the bloodstream.
The fluid buildup also makes the lungs heavy and
stiff. This decreases the lungs' ability to expand.
The level of oxygen in the blood can stay
dangerously low, even if the person receives
oxygen from a breathing machine (ventilator)
through a breathing tube (endotracheal tube).
ARDS often occurs along with the failure of other
organ systems, such as the liver or kidneys.
Cigarette smoking and heavy alcohol use may be
risk factors for its development.
Symptoms
Symptoms usually develop within 24 to
48 hours of the injury or illness. Often,
people with ARDS are so sick they cannot
complain of symptoms. Symptoms can
include any of the following:
•Shortness of breath
•Fast heartbeat
•Low blood pressure and organ failure
•Rapid breathing
Exams and Tests
Listening to the chest with a stethoscope
(auscultation) reveals abnormal breath sounds,
such as crackles, which may be signs of fluid in
the lungs. Often, blood pressure is
low. Cyanosis (blue skin, lips, and nails caused by
lack of oxygen to the tissues) is often seen.
Tests used to diagnose ARDS include:
Tests used to diagnose ARDS include:
•Arterial blood gas
•Blood tests, including CBC (complete blood count)
and blood chemistries
•Blood and urine cultures
•Bronchoscopy in some people
•Chest x-ray or CT scan
•Sputum cultures and analysis
•Tests for possible infections
An echocardiogram may be needed to rule
out heart failure, which can look similar to
ARDS on a chest x-ray.
Treatment
ARDS often needs to be treated in an intensive
care unit (ICU).
The goal of treatment is to provide breathing
support and treat the cause of ARDS. This may
involve medicines to treat infections, reduce
inflammation, and remove fluid from the lungs.
A ventilator is used to deliver high doses of
oxygen and positive pressure to the damaged
lungs. People often need to be deeply sedated
with medicines. During treatment, health care
providers make every effort to protect the lungs
from further damage. Treatment is mainly
supportive until the lungs recover.
Sometimes, a treatment called
extracorporeal membrane oxygenation
(ECMO) is done. During ECMO, blood
is filtered through a machine to
provide oxygen and remove carbon
dioxide
Acute Respiratory Distress Syndrome And
Multiple Organ Dysfunction Syndrome
Professor Xu sicheng
contents
keys:
difinition
causes
clinical features
diagnosis and differential diagnosis
treatment
understanding:
pathogenesis and pathology
Variety of systemic or pulmonary insults can lead to injury of
multiple organs including the lungs, Severe injury can result in
acute lung injury (ALI) or acute respiratory distress syndrome (
ARDS ) and multiple organ dysfunction syndrome ( MODS) .
ALL/ARDS is usually the first presentation of MODS and plays
important role in determining the outcome of MODS. Proper
application of mechanical ventilation is important intervention
for ALL/ARDS.
ACUTE LUNG INJURY AND ACUTE RESPIRATORY
DISTRESS SYNDROMEDEFINITION
ARDS denotes acute hypoxemic respiratory failure following a
systemic or pulmonary insult without evidence of heart failure.
ARDS is the most severe form of acute lung injury and is
characterized by bilateral, widespread radiographic pulmonary
infiltrates,normal pulmonary capillary wedge pressure (≤18 mmHg)
and a PaO2/FiO2 ratio ≤200. ARDS may follow variety of severe
systemic or pulmonary insults, which can induce systemic
inflammatory response. Pro-inflammatory cytokines released from
stimulated inflammatory cells appear to be pivotal in lung injury.
Although the mechanism of lung injury varies with the
cause, damage to capillary endothelial cells and alveolar
epithelial cells is common to ARDS regardless of cause.
Damage to these cells causes increased vascular permeability
and decreased production and activity of surfactant; these
abnormalities lead to interstitial and alveolar pulmonary
edema, alveolar collapse, and hypoxemia.
ARDS first was described in 1967 as the abrupt onset of diffuse
lung injury characterized by severe hypoxemia and generalized
pulmonary infiltrates on the chest radiograph in the absence of overt
cardiac failure. In the early 1990s , the term acute lung injury
officially was introduced to include traditional ARDS and less
severe forms of lung injury. The definitions of ALI and ARDS
require bilateral pulmonary infiltrates compatible with pulmonary
edema in the absence of clinical heart failure(usually as determined
by no evidence of elevated left atrial pressures), but the two are
differentiated by the degree of abnormal oxygenation: Patients are
defined as having ALI if the PaO2 divided by the FiO2 ( PaO2/
FiO2) is less than or equal to 300 mmHg; when the PaO2/ FiO2 is
less than or equal to 200 mmHg, the patient meets criteria for
ARDS.
CAUSES AND PATHOGENESIS CAUSES
ARDS may follow a wide variety of clinical events (Table 1-14-
1). Common risk factors for ARDS include sepsis , aspiration of
gastric contents, shock , infection, lung contusion, nonthoracic
trauma, toxic inhalation , near-drowning , and multiple blood
transfusions. About one third of ARDS patients initially have
sepsis syndrome.
Systemic insults
Pulmonary insults
Sepsis
Aspiration of gastric contents
Shock Table 1-14-1 Selected disorders associated with ARDS Embolism

of thrombus, fat, air, or amniotic fluid
Trauma Miliary
tuberculosis
Pancreatitis Diffuse
pneumonia(e. g, SARS)
Multiple transfusions Acute

eosinophilic pneumonia
Disseminated intravascular coagulation

Cryptogenic organizing pneumonitis
Burns Free-
base cocaine smoking
Drugs and drug overdose, such as Opioids, Aspirin, Phenothiazines, Tricyclic Near-
drowning
antidepressants, Amiodarone , Chemotherapeutic agents, etc.
Thrombotic thrombocytopenic purpura Toxic

gas inhalation, such as Nitrogen dioxide , Chlorine, Sulfur dioxide,
Ammonia.
Smoke , etc.
CardiopulmonaryNote: SARS=severe bypass acute respiratory syndrome. Oxygen

toxicity
Head injury lung

contusion
Poisoning, such as Paraquat

Radiation exposure
High-
altitude exposure
Lung
reexpansion or reperfusion
PATHOGENESIS
Although the pathogenesis of ARDS is not fully understood yet
, ARDS occurs primarily as the result of inflammatory injury to
the alveoli producing diffuse alveolar damage, which is part of
systemic inflammatory response syndrome (SIRS) in response to
variety of insults . The lungs probably are particularly vulnerable
to inflammatory injury because mediators are released into the
bloodstream, and the lungs receive the entire cardiac output.
Pro-inflammatory cytokines such as tumor necrosis factor ,
interleukin 1, interleukin-6, and interleukin-8 are released in
response to any of a variety of precipitants . Neutrophils are
recruited to the lungs , become activated, and release toxic
mediate such as reactive oxygen species and proteases which
damage the capillary endothelium and alveolar epithelium.
Impaired neutrophil apoptosis in the early stages of ARDS may
amplify this phenomenon, and may result from increased
concentrations of G-CSF and GM-CSF within alveolar fluid.
As a result, the normal barriers to alveolar edema are lost.
Protein escapes from the vascular space, and the osmotic
gradient favoring resorption of fluid is lost. Fluid pours into the
interstitium and overwhelms the capacity of the lymphatics . Air
spaces fill with bloody, proteinaceous edema fluid and debris
from degenerating cells. Functional surfactant is lost , resulting
in alveolar collapse. The main physiologic derangements
responsible for clinical presentation of hypoxemia and
respiratory distress are as following:.
Impaired Gas EXchange
Ventilation-perfusion mismatching and physiologic shunting
are the major causes of hypoxemia.Increased physiologic dead
space may interfere with CO2 elimination. Although
hypercapnia is uncommon, the minute volume required to
maintain a normal PaCO2 rises significantly.
Impaired Compliance
Decreased pulmonary compliance is one of the hallmarks of
ARDS. The low compliance is due to the stiffness of poorly or
nonaerated lung rather than changes in the pressure-volume
characteristics of residual functioning lung units. Because only
the remaining portions of normally functioning lung
meaningfully participate in gas exchange, even small tidal
volumes may exceed the lung’s inspiratory capacity and cause a
dramatic rise in airway pressures .
Other Mechanisms
Other mechanisms may be involved in the development of
respiratory distress in ARDS. These include stimulation of J-
receptor adjacent to pulmonary capillary by pulmonary
hyperemia and edema, pulmonary hypertension and increased
airways resistance.
PATHOLOGY
The pathologic abnormalities in acute lung injury and ARDS
are nonspecific and are described as diffuse alveolar damage by
pathologists. Abnormalities of epithelial cells, particularly type I
alveolar cells, and pulmonary vascular endothelial cells are seen.
The initial process is inflammatory in nature,with neutrophils
usually predominating in the alveolar fluid. Hyaline membranes,
similar to those seen in premature infants with infant respiratory
distress syndrome, develop, presumably related to the presence
of large-molecular-weight proteins that have leaked into the
alveolar space. Alveolar flooding leads to impairment of
surfactant, which is abnormal in quantity and quality.
The result is microatelectasis , which may be associated with
an impairment of immune function. Cytokines and other
inflammatory mediators usually are markedly elevated , although
with different patterns over time in the bronchoalveolar lavage
and the systemic blood. Lung repair also is disturbed; there is
early evidence of profibrotic processes manifest by the
appearance of breakdown products of procollagen in the
bronchoalveolar lavage fluid, followed by subsequent scarring.
Because lung function improves over time in survivors of ARDS.
however, it has been assumed that this scarring is potentially
reversible.
The pathology of ARDS can be arbitrarily divided as
exudative, proliferative and fibrotic stages. These pathologies are
often overlapped..
CLINICAL FEATURES
ARDS is marked by the rapid onset of profound dyspnea and
hypoxemia that usually occurs within five days( mean time from
12-48 hours) from the onset of underline diseases process.
Respiratory distress presenting as labored breathing, tachypnea ,
intercostals retractions are often accompanied with cyanosis,
agitation, anxiety and diaphoresis ,which are refractory to
oxygen therapy. These abnormalities can not be explained by the
underline diseases and the possibility of cardiogenic pulmonary
edema could be excluded. Abnormal signs on physical
examination are not remarkable or fine crackles can be noted.
LABORATORY FINDINGS
CHEST X-RAY
Chest radiography shows diffuse or patchy bilateral infiltrates
that rapidly become confluent. Air
bronchograms occur in about 80% of cases. The abnormality on
chest X-
ray varies from interstitial infiltrate to bilateral generalized opaci
ties(white
lungs). Interstitial lung fibrosis can persist for several months in
patients recovering from ARDS.
ARTERIAL BLOOD GASES
Arterial blood gases usually show severe hypoxemia, acute res
piratory alkalosis, and elevated alveolar-
arterial oxygen gradient. Pa02/F102 is less than
or equal to 300 mmHg in ALI and less than or equal
to 200 mmHg in ARDS( PaO2 is measured in mmHg
and the FiO2 is expressed as a value between 0.21 and 1.00).
BEDSIDE MONITORING
Decreased compliance of lungs and increased Vo/Vt
ratio are common finding in ARDS, which is helpful
in severity assessment. Swan-
Ganz catheter is sometime necessary to measure the pulmonary c
apillary
wedge pressure(PCWP) in patient suspecting cardiac failure.A P
CWP≤18 mmHg will help to exclude the possibility of
cardiac fallure.
DIAGNOSIS
The diagnosis of ARDS should met all the five criteria in follo
wing：
a. Evidence of underline diseases( predisposing
factors) just as mentioned above.
b. Acute onset of tachypnea and respiratory distress.
C. Hypoxemia: Hypoxemia with PaO2,/FiO2, ratio≤200 mmH
g in ARDS and≤300 mmHg in ALI.
d. Bilateral infiltrates on radiography.
e. PCWP< 18 mmHg or without evidence of left
atrial hypertension or congestive heart failure.
DIFFERENTIAL DIAGNOSIS.
Since ARDS is a physiologic and radiographic syndrome rather
than a specific disease, the concept of differentialosis do diagnes
not strictly apply. Carbiogenic or hydrostatic pulmonary edema
must be excluded. Measurement of PCWP may be required in
selected patients with suspected cardiac dysfunctionbut routine
use of the Swan-Ganz catheter in ARDS is discouraged.
TREATMENT
Treatment of ARDS must include identification and specific
treatment of the underlying precipitating and secondary
conditions(e. g, sepsis). Meticulous supportive care must then be
provided to compensate for the severe dysfunction of the
respiratory system associated with ARDS and to prevent
complications.
OXYGEN THERAPY
Ensure adequate oxygenation is important for vital organs.
Oxygen therapy of high inspiratory oxyger concentration with
mask to maintain arterial hemoglobin saturation
of≥90%(PO2≥60mmHg)is ussually the first step of
management in ARDS, although the response to oxygen
therapy is generally poor and majority of the patients need
mechanical ventilation.
MECHANICAL VENTILATION
Treatment of the hypoxemia seen in ARDS usually requires
tracheal intubation and positive-pressure mechanical ventilation
although there have been some reports on the use of
noninvasive positive pressure ventilation in ALI or less severe
ARDS.The indications and criteria for initiating intubation are
not fully established yet.
The main purposes of mechanical ventilation are to improve
oxygenation and maintain adequate ventilation.A variety of
mechanical ventilation strategies are available,but there is no
universal standard for proper selection of ventilation
mode.Current recommendations for mechanical ventilation via
endotracheal intubation emphasize lower tidal volumes based
on a patient's predicted body weight(6-8mL/kg),limitation of
peak inspiratory pressure(30-35 cmH20),proper use of PEEP
and permissive hypercapnia.
PEEP remains a mainstay in the ventilatory strategy for
ARDS,although the method for determining the optimal level of
PEEP has not been convincingly established.PEEP can increase
end expiratory lung volume,maintain open of alveoli,improve
oxygenation and allow a lower FiO2.A“lung
protective"ventilation strategy in which patients underwent
ventilation with levels of PEEP above the lower inflection point
of a respiratory system pressure-volume curve,which was
intended to maintain patency and reduce cyclic opening and
closing of injured alveoli,a process that is thought to be a major
cause of ventilator-induced lung injury.
FLUID MANAGEMENT
Proper fluid management is important in the treatment of
ARDS.The goal of fluid management is to maintain pulmonary
capillary wedge pressure at the lowest level compatible with
adequate cardiac output and hemodynamic
stability.Administering fluids to increase intravascular volume
should be done only with great caution because increases in
pulmonary capillary pressure worsen pulmonary edema in the
presence of increased capillary permeability.
Management of serum total protein and oncotic pressure are
subject to controversy.Some recent studies suggested that
infusion of albumin and diuretics to achieve a proper colloid
pressure and negative fluid balance improve short-term
oxygenation,longer-term hemodynamic stability,and trends
toward reduction in mechanical ventilation days and length of
stay in the ICU,although no benefit in overall mortality was
observed.
GENERAL SUPPORTIE MEASURES
General supportive measures in ARDS include proper
nutritional support,prevention of nosocomial
infection,pulmonary thromboembolism and gastric stress
ulceration as well as careful nursing.
PHARMACOTHERAPIES
A number of pharmaceutical agents have been tried in
management of ARDS,which include systemic
corticosteroids,surfactant replacement therapy,inhaled nitric
oxide,etc.The efficacy and safety of these pharmaceutical
agents demand further investigation.
PROGNOSIS
The mortality rate associated with ARDS is 30%-
40%,depending on the underline diseases and severity.The
major causes of death are the primary illness and secondary
complications such as multiple organ system failure or
sepsis.Most survivors of ARDS are left with some pulmonary
symptoms(cough,dyspnea,sputum production)which tend to
improve over time.
ESTABLISHMENT AND MANAGEMENT OF
ARTIFICIAL AIRWAY
Artificial airway is important in maintaining air-way patency and
ensuring adequate ventilation and oxygenation,which is crucial in
the management of ARDS.
PURPOSES OF ARTIFICIAL AIR-WAY
ESTABLISHMENT
a. Ensure airway patency.b. Manage airway secretion.c. Protect
airway from aspiration.d. Connect ventilator for mechanical
ventilation.
METHODS OF ARTIFICIAL AIR-WAY
ESTABLISHMENT
Artificial airway can be established through oral
intubation,nasal intubation,or tracheotomy,depend on the
clinical situation and expertise of responsible doctor.Some
other airway devices(e.g.,laryngeal mask airway,esophageal
obturator airway,etc.)may be acceptable and useful in acute
emergent situation,although they do not provide the airway
control and protection afforded by an endotracheal tube.
MECHANICAL VENTILATION
Mechanical ventilation supplied through artificial
airway(e.g.,endotracheal intubation or tracheoto-my)is called
invasive mechanical ventilation.Non-invasive ventilation can be
provided by devices that apply intermittent negative
extrathoracic pressure or furnish intermittent positive pressure
through a tight-fitting nasal or face mask without an artificial
airway in place.In the following paragraph,only invasive
mechanical ventilation will be discussed.
INDICATIONS
Indications for invasive mechanical ventilation in-clude cardiac
respiratory arrest and severe respirato-ry failure due to variety of
underline diseases.The following crileria are general guides for
initiating invasive mechanical ventilation,although there are no
universal agreement yet.
a.Acute inerease in PaCO2 to >50 mmHg with a decrease in
pH to<7.30.b.Respiratory rate>35 breaths/min for prolonged
period.c.Tidal volume <5 ml/kg body weight.d.Ratio of
respiratory rate(breaths/min)to tidal volume(L)>105.e.Minute
ventilalion>10 L/min.f.Vital capacity <10 mL/kg body
weighi.g.Maximum inspiratory pressure between O and 20
cmH20.h.Dead space to tidal volume fraction 0.60 or
more.i.Acute hypoxemia(PaO2<60 mmHg or
Sa0,<90%,especially if inspired oxygen fraction is 0.4 or more,or
P(A-a)02>300 mmHg on inspired FiO2 of 1.0).j.Clinical
instability.
CONTRAINDICATION
There is no absolute contraindication for mechanical
ventilation.Obvious pneumothorax and pneumomediastinum
without adequate drainage are relative contraindication.
MODES OF MECHANICAL VENTILATION
As the progress of mechanical ventilation,variety of modes of
mechanical ventilation has been used in clinical practice.Basically
the modes of mechanical ventilation can be classified as controlled
or assisted mechanical ventilation,the former is mainly used in
patients with weak or no respiratory effort and the later is used in
patients with satisfactory level of respiratory effort.The commonly
used modes include volume controlled ventilation(CMV),pressure
controlled ventilation(PCV),synchronized intermittent mandatory
ventilation(SIMV),pressuresupport ventilation(PSV)and
continuous positive airway pressure(CPAP)or positive end-
expiratorypressure(PEEP).
COMPLICATIONS
The complications of mechanical ventilation inchude positive
ventilation induced and artificial airway induced
complications.The commonly encountered complications are
ventilator induced lung injury(VILI),cardiovascular system
compromise,ventilator associated pneumonia and tracheal
injury.
WEANING
Weaning is the process of discontinuing assisted mechanical
ventilation.Mechanical ventilatory support can generally be
discontinued when there is complete or near-complete
resolution of the patient's disease process.This process may be
accomplished by trial of connecting the endotracheal tube to a
piece of tubing(T-piece)with oxygen therapy,synchronized
intermittent mandatory ventilation,or pressure-support
ventilation.
III SYSTEMIC INFLAMMATORY RESPONSE
SYNDROME(SIRS)
SIRS is defined as the systemic inflammatory response to a wide
variety of severe clinical insults,manifested by two or more of
the following conditions:(1) temperature>38 C or <36 C;(2)heart
rate>90 beats/min;(3) respiratory rate>20 breaths/min or
PaCO2<32 mmHg；and (4)WBC count>12,000/mm3
or<4,000/mm3，or>10% immature(band)forms.
SEPSIS
SEPSIS is defined as the systemie inflammatory response to
infection.In association with infection,mainfestations of sepsis
are the same as those previously defined for SIRS.
SEVERE SEPSISSevere sepsis is defined as sepsis associated
with organ dysfunction,hypoperfusion,or hypotension.
SEPTIC SHOCK
Septic shock is a subset of severe sepsis and defined as sepsis-
induced hypotension despite adequate fluid resuscitation along
with the presence of perfusion abnormalities.Patients receiving
inotropic or vasopressor agents may no longer be hypotensive
by the time they manifest hypoperfusion abnormalities or
organ dysfunction,yet they would still be considered to have
septicshock
MULTIPLE ORGAN DYSFUNCTION
SYNDROME(MODS)
MODS is a frequent complication of an exaggerated
proinflammatory state in the setting of sepsis,SIRS,and
ARDS,which is defined as the development of organ system
dysfunction involving two or more organs such that normal
homeostasis cannot be maintained in the setting of a systemic
inflammatory response to a variety of insults.
thank you
CirrhosisCirrhosis
1
IntroductionIntroduction
CirrhosisCirrhosis isis aa chronicchronic degenerativedegenerative

diseasedisease ofof thethe liverliver inin whichwhich thethe organorgan
becomesbecomes fibroticfibrotic withwith changeschanges inin thethe
cellscells
andand connectiveconnective tissue.tissue.
TheThe resultresult isis aa lossloss ofof liverliver functionfunction
andand anan
increaseincrease inin resistanceresistance toto thethe flowflow ofof
bloodblood
throughthrough thethe liver.liver. SomeSome causescauses ofof
cirrhosiscirrhosis
includeinclude alcoholism,alcoholism, hepatitis,hepatitis,
cholestaticcholestatic
liverliver disease,disease, andand drug-induceddrug-induced liverliver
disease.disease.
2
DefinitionDefinition
CirrhosisCirrhosis representsrepresents thethe finalfinal commoncommon
histologichistologic
pathwaypathway forfor aa widewide varietyvariety ofof chronicchronic
liverliver diseases.diseases.
ManyMany formsforms ofof liverliver injuryinjury areare markedmarked byby
fibrosis.fibrosis.
ThisThis responseresponse toto liverliver injuryinjury potentiallypotentially
isis reversiblereversible..
InIn contrastcontrast,, inin mostmost patients,patients, cirrhosiscirrhosis
isis notnot aa
reversiblereversible process.process.
CirrhosisCirrhosis isis defineddefined histologicallyhistologically asas aa

diffusediffuse
hepatichepatic processprocess characterizedcharacterized byby fibrosisfibrosis
andand thethe
conversionconversion ofof normalnormal liverliver architecturearchitecture
intointo
structurallystructurally abnormalabnormal nodules.nodules. TheThe
progressionprogression ofof
liverliver injuryinjury toto cirrhosiscirrhosis maymay occuroccur overover
weeksweeks toto
years.years. Indeed,Indeed, patientspatients withwith hepatitishepatitis CC
maymay havehave
chronicchronic hepatitishepatitis forfor asas longlong asas 4040 yearsyears
beforebefore
progressingprogressing toto cirrhosis.cirrhosis.
3
4
5
6
7
8
9
DefinitionDefinition
OftenOften aa poorpoor correlationcorrelation existsexists betweenbetween
histologichistologic findingsfindings andand thethe clinicalclinical
picture.picture. SomeSome
patientspatients withwith cirrhosiscirrhosis areare completelycompletely
asymptomaticasymptomatic andand havehave aa reasonablyreasonably normalnormal
lifelife
expectancy.expectancy. OtherOther individualsindividuals havehave aa
multitudemultitude
ofof thethe mostmost severesevere symptomssymptoms ofof end-stageend-stage
liverliver
diseasedisease andand havehave aa limitedlimited chancechance forfor
survival.survival.
CommonCommon signssigns andand symptomssymptoms maymay stemstem fromfrom
decreaseddecreased hepatichepatic syntheticsynthetic functionfunction
,decreased,decreased
detoxificationdetoxification capabilitiescapabilities ofof thethe liverliver
(eg,(eg, hepatichepatic
encephalopathyencephalopathy),), oror portalportal hypertensionhypertension
(eg,(eg,
varicealvariceal bleeding).bleeding).
10
11
12
13
14
Normal liver
15
Liver cirrhosis
16
EpidemiologyEpidemiology
ChronicChronic liverliver diseasedisease andand cirrhosiscirrhosis isis

thethe
ninthninth leadingleading causecause ofof deathdeath inin thethe
UnitedUnited
States.States.
ManyMany patientspatients diedie fromfrom thethe diseasedisease inin
theirtheir
fifthfifth oror sixthsixth decadedecade ofof life.life.
17
MorbidityMorbidity
VaricealVariceal hemorrhagehemorrhage isis thethe mostmost commoncommon

complicationcomplication associatedassociated withwith portalportal
hypertensionhypertension causecause byby cirrhosis.cirrhosis.
AlmostAlmost 90%90% ofof patientspatients withwith cirrhosiscirrhosis
developdevelop varices,varices, andand approximatelyapproximately 30%30%
ofof varicesvarices bleed.bleed.
TheThe firstfirst episodeepisode ofof varicealvariceal hemorrhagehemorrhage
isis
estimatedestimated toto carrycarry aa mortalitymortality raterate ofof 30-
30-
50%.50%.
18
EtiologyEtiology
AlcoholicAlcoholic liverliver diseasedisease onceonce waswas

consideredconsidered
toto bebe thethe predominantpredominant causecause ofof cirrhosiscirrhosis
inin thethe
UnitedUnited States.States. HepatitisHepatitis CC hashas emergedemerged asas
thethe
nation'snation's leadingleading causecause ofof bothboth chronicchronic
hepatitishepatitis
andand cirrhosis.cirrhosis.
ManyMany casescases ofof cryptogeniccryptogenic cirrhosiscirrhosis
appearappear toto
havehave resultedresulted fromfrom nonalcoholicnonalcoholic fattyfatty
liverliver
diseasedisease (NAFLD).(NAFLD). WhenWhen casescases ofof
cryptogeniccryptogenic
cirrhosiscirrhosis areare reviewed,reviewed, manymany patientspatients
havehave oneone
oror moremore ofof thethe classicalclassical riskrisk factorsfactors forfor
NAFLD:NAFLD:
obesity,obesity, diabetes.diabetes.
19
EtiologyEtiology
UpUp toto oneone thirdthird ofof AmericansAmericans havehave

nonalcoholicnonalcoholic fattyfatty liverliver diseasedisease
(NAFLD).(NAFLD).
20
EtiologyEtiology
MostMost commoncommon causescauses ofof cirrhosiscirrhosis

HepatitisHepatitis B,B, CC
AlcoholicAlcoholic liverliver diseasedisease
CryptogenicCryptogenic causescauses
21
EtiologyEtiology
causescauses ofof chronicchronic liverliver diseasedisease andand
cirrhosiscirrhosis
ØØAutoimmuneAutoimmune hepatitishepatitis
ØØPrimaryPrimary biliarybiliary cirrhosiscirrhosis
ØØSecondarySecondary biliarybiliary cirrhosiscirrhosis
ØØPrimaryPrimary sclerosingsclerosing cholangitischolangitis
ØØWilsonWilson diseasedisease
ØØDrug-inducedDrug-induced liverliver diseasedisease
ØØVenousVenous outflowoutflow obstructionobstruction
ØØChronicChronic right-sidedright-sided heartheart failurefailure
22
23
PATHOPHYSIOLOGYPATHOPHYSIOLOGY
TheThe developmentdevelopment ofof hepatichepatic fibrosisfibrosis

reflectsreflects anan alterationalteration inin thethe normallynormally
balancedbalanced processesprocesses ofof extracellularextracellular
matrixmatrix
productionproduction andand degradation.degradation.
24
25
PATHOPHYSIOLOGYPATHOPHYSIOLOGY
FutureFuture drugdrug strategiesstrategies toto preventprevent

fibrosisfibrosis
maymay focusfocus onon reducingreducing hepatichepatic
inflammation,inflammation, inhibitinginhibiting stellatestellate cellcell
activation,activation, inhibitinginhibiting thethe fibrogenicfibrogenic
activitiesactivities ofof stellatestellate cells,cells, andand
stimulatingstimulating
matrixmatrix degradation.degradation.
26
PathologyPathology
AllAll chronicchronic liverliver diseasesdiseases thatthat progressprogress

toto
cirrhosiscirrhosis havehave inin commoncommon thethe histologichistologic
featuresfeatures ofof hepatichepatic fibrosisfibrosis andand nodularnodular
regeneration.regeneration.
27
hepatic fibrosis and nodular regeneration28
MANIFESTATIONSMANIFESTATIONS
fatigue,fatigue, anorexia,anorexia, weightweight loss,loss, musclemuscle
wasting,wasting, markedmarked ascites,ascites, andand severesevere
hepatichepatic encephalopathy,encephalopathy, withwith mildmild oror
deeplydeeply jaundicejaundice
spiderspider angiomata,angiomata, skinskin telangiectasiastelangiectasias ,,
palmarpalmar erythema,erythema, whitewhite nails,nails,

disappearancedisappearance ofof lunulae,lunulae, andand fingerfinger
clubbing,clubbing, especiallyespecially inin thethe settingsetting ofof
hepatopulmonaryhepatopulmonary syndrome.syndrome. MalesMales maymay
developdevelop gynecomastiagynecomastia andand impotenceimpotence ..
LossLoss ofof axillaryaxillary andand pubicpubic hairhair isis notednoted
inin
bothboth menmen andand women.women.
29
HematologicHematologic manifestationsmanifestations
AnemiaAnemia maymay resultresult fromfrom folatefolate

deficiency.deficiency. ThrombocytopeniaThrombocytopenia
usuallyusually isis secondarysecondary toto
hypersplenismhypersplenism ..
30
PulmonaryPulmonary andand cardiaccardiac
manifestationsmanifestations
PatientsPatients withwith cirrhosiscirrhosis maymay havehave impairedimpaired
pulmonarypulmonary function.function. PlePle uu ralral effusionseffusions

andand
thethe diadia phragphrag mama tictic elevationelevation causedcaused byby
massivemassive ascitesascites maymay alteralter ventilation-ventilation-
perfusionperfusion relations.relations.
31
qqManifestationManifestation relatedrelated toto
hepatocellularhepatocellular necrosisnecrosis andand chronicchronic
hepatichepatic dysfunctiondysfunction
PPascitesascites ,, jaundicejaundice
PPfatigue,dyspepsiafatigue,dyspepsia ,, palmarpalmar erythemaerythema
PPspiderspider angiomas,angiomas, bleedingbleeding problemsproblems
PPGynecomastiaGynecomastia (men),(men), menstrualmenstrual
irregularitiesirregularities (women)(women)
PPparotidparotid hypertrophyhypertrophy
PPtesticulartesticular atrophyatrophy
32
qqManifestationManifestation ofof portalportal
hypertensionhypertension
PPPortal-systemicPortal-systemic colcol lala tete

ralsrals(esophageal(esophageal
andand gastricgastric varices,varices, hemorrhoidhemorrhoid,, dilateddilated
abdominalabdominal wallwall oror umbilicalumbilical veinsveins (caput(caput
medusae)medusae)
PPascitesascites
PPSplenomegaly(mildSplenomegaly(mild toto moderatemoderate ))
33
Anatomy of
the portal
venous
system : the
portal vein
is formed by
the union of
the splenic
vein and
superior
mesenteric
veins
34
Endoscopy:Endoscopy:
A:esophageal varices B:gastric varices
35
36
37
38
39
40
CLINICALCLINICAL HistoryHistory
–– HistoryHistory ofof jaundicejaundice

–– HistoryHistory ofof bloodblood transfusions,transfusions,
intravenousintravenous
drugdrug useuse (hepatitis(hepatitis BB andand C)C)
PatientsPatients whowho areare knownknown toto havehave chronicchronic
viralviral
hepatitishepatitis BB oror CC havehave aa higherhigher
probabilityprobability ofof
havinghaving cirrhosiscirrhosis
–– FamilyFamily historyhistory ofof hereditaryhereditary liverliver
diseasedisease
–– HistoryHistory ofof alcoholalcohol abuseabuse
41
42
43
CLINICALCLINICAL HistoryHistory
DeterminingDetermining thethe presencepresence ofof thethe
complicationscomplications ofof
portalportal hypertensionhypertension involvesinvolves thethe
following:following:
–– HematemesisHematemesis oror melenamelena (gastroesophageal(gastroesophageal
varicealvariceal bleedingbleeding oror bleedingbleeding fromfrom

portalportal
gastropathy)gastropathy)
–– MentalMental statusstatus changeschanges increasedincreased
irritability,irritability, andand
alteredaltered sleepsleep patternspatterns (presence(presence ofof
portosystemicportosystemic encephalopathy)encephalopathy)
–– IncreasingIncreasing abdominalabdominal girthgirth (ascites(ascites
formation)formation)
–– AbdominalAbdominal painpain andand feverfever (spontaneous(spontaneous
bacterialbacterial peritonitisperitonitis [SBP],[SBP], whichwhich alsoalso
presentspresents
withoutwithout symptoms)symptoms)
–– HematocheziaHematochezia 44
CLINICALCLINICAL PhysicalPhysical
SignsSigns ofof liverliver diseasedisease includeinclude thethe
following:following:
–– AscitesAscites
–– JaundiceJaundice
–– SpiderSpider angiomasangiomas
–– PalmarPalmar erythemaerythema
–– TesticularTesticular atrophyatrophy
–– GynecomastiaGynecomastia
–– MuscleMuscle wastingwasting
–– SplenomegalySplenomegaly
45
Clinical
manifestations
of portal
hypertension
46
Spider angiomas palmar erythema
47
48
Jaundice Spider angiomas
49
gynecomastiagynecomastia
50
dilateddilated abdominalabdominal wallwall andand umbilicalumbilical
veinsveins51
52
53
54
ascitesascites andand umbilicalumbilical herniahernia 55
rupture of an umbilical hernia scrotal edema
56
scrotalscrotal edemaedema
57
58
59
60
61
62
63
64
ComplicationsComplications
11 SpontaneousSpontaneous bacterialbacterial peritonitisperitonitis

(SBP)(SBP)
22 BleedingBleeding fromfrom esophagealesophageal varicesvarices
33 HepaticHepatic encephalopathyencephalopathy
44 HepatocellularHepatocellular carcinomacarcinoma
55 HepatorenalHepatorenal syndromesyndrome
66 HepatopulmonaryHepatopulmonary syndromesyndrome
77 ElectrolyteElectrolyte disturbancesdisturbances
65
11 Spontaneous bacterial peritonitis
(SBP)
FluidFluid inin thethe abdominalabdominal cavitycavity (ascites)(ascites)
isis thethe
perfectperfect placeplace forfor bacteriabacteria toto grow.grow.
Normally,Normally, thethe
abdominalabdominal cavitycavity containscontains aa veryvery smallsmall
amountamount
ofof fluidfluid thatthat isis ableable toto resistresist
infectioninfection well,well, andand
bacteriabacteria thatthat enterenter thethe abdomenabdomen (usually(usually
fromfrom
thethe intestine)intestine) areare killedkilled oror findfind theirtheir
wayway intointo thethe
portalportal veinvein andand toto thethe liverliver wherewhere theythey
areare killed.killed.
InIn cirrhosis,cirrhosis, thethe fluidfluid thatthat collectscollects inin
thethe abdomenabdomen
isis unableunable toto resistresist infectioninfection normally.normally.
SBPSBP isis aa life-life- threateningthreatening complication.complication.
SomeSome
patientspatients withwith SBPSBP havehave nono symptoms,symptoms,
whilewhile
othersothers havehave fever,fever, chills,chills, abdominalabdominal
painpain andand
tenderness,tenderness, diarrhea,diarrhea, andand worseningworsening
ascites.ascites.
66
22 BleedingBleeding fromfrom esophagealesophageal
varicesvarices
InIn thethe cirrhoticcirrhotic liver,liver, thethe scarscar tissuetissue

blocksblocks
thethe flowflow ofof bloodblood returningreturning toto thethe heartheart
fromfrom thethe intestinesintestines andand raisesraises thethe

pressurepressure
inin thethe portalportal veinvein (portal(portal
hypertension).hypertension). TheThe
mostmost commoncommon veinsveins throughthrough whichwhich bloodblood
bypassesbypasses thethe liverliver areare thethe veinsveins lininglining
thethe
lowerlower partpart ofof thethe esophagusesophagus andand thethe
upperupper
partpart ofof thethe stomach.stomach.
67
BleedingBleeding fromfrom esophagealesophageal
varicesvarices
AsAs aa resultresult ofof thethe increasedincreased flowflow ofof
bloodblood andand
thethe resultingresulting increaseincrease inin pressure,pressure, thethe
veinsveins inin
thethe lowerlower esophagusesophagus andand upperupper stomachstomach
expandexpand andand thenthen areare referredreferred toto asas
esophagealesophageal andand gastricgastric varices;varices; thethe
higherhigher thethe
portalportal pressure,pressure, thethe largerlarger thethe varicesvarices
andand thethe
moremore likelylikely aa patientpatient isis toto bleedbleed fromfrom
thethe
varicesvarices intointo thethe esophagusesophagus oror stomach.stomach.
68
69
ComplicationsComplications BleedingBleeding
BleedingBleeding fromfrom varicesvarices usuallyusually isis
severesevere ,, withoutwithout
immediateimmediate treatment,treatment, cancan bebe fatal.fatal.
SymptomsSymptoms ofof
bleedingbleeding fromfrom varicesvarices includeinclude vomitingvomiting
bloodblood (the(the
vomitusvomitus cancan bebe redred bloodblood mixedmixed withwith
clotsclots oror
"coffee"coffee grounds"grounds" inin appearance,appearance, thethe
latterlatter duedue toto
thethe effecteffect ofof acidacid onon thethe blood),blood),
passingpassing stoolstool
thatthat isis blackblack asas itit passespasses throughthrough thethe
intestineintestine
(melena),(melena), andand orthoortho staticstatic dizzinessdizziness oror
faintingfainting
(caused(caused byby aa dropdrop inin bloodblood pressurepressure
especiallyespecially
whenwhen standingstanding upup fromfrom aa lyinglying position).position).
patientspatients hospitalizedhospitalized becausebecause ofof

activelyactively
bleedingbleeding esophagealesophageal varicesvarices havehave aa highhigh
riskrisk ofof
developingdeveloping spontaneousspontaneous bacterialbacterial

peritonitis.peritonitis. 70
ComplicationsComplications 33 Hepatic encephalopathy
SomeSome ofof thethe proteinprotein inin foodfood thatthat escapesescapes
digestiondigestion andand absorptionabsorption isis usedused byby

bacteriabacteria thatthat
areare normallynormally presentpresent inin thethe intestine.intestine.
WhileWhile usingusing
thethe proteinprotein forfor theirtheir ownown purposes,purposes, thethe
bacteriabacteria
makemake substancessubstances thatthat theythey releaserelease intointo
thethe
intestine.intestine. TheseThese substancessubstances thenthen cancan bebe
absorbedabsorbed intointo thethe body.body.
SomeSome ofof thesethese substances,substances, forfor example,example,
ammonia(NH3),ammonia(NH3), cancan havehave toxictoxic effectseffects onon
thethe
brain.brain. Ordinarily,Ordinarily, thesethese toxictoxic
substancessubstances areare
carriedcarried fromfrom thethe intestineintestine inin thethe portalportal
veinvein toto thethe
liverliver wherewhere theythey areare removedremoved fromfrom thethe
bloodblood andand
detoxified.detoxified.
71
HepaticHepatic
encephalopathyencephalopathy
TheThe toxictoxic substancessubstances alsoalso makemake thethe

brainsbrains ofof
patientspatients withwith cirrhosiscirrhosis veryvery sensitivesensitive
toto drugsdrugs
thatthat areare normallynormally filteredfiltered andand
detoxifieddetoxified byby thethe
liver.liver. DosesDoses ofof manymany drugsdrugs thatthat normallynormally
areare
detoxifieddetoxified byby thethe liverliver havehave toto bebe
reducedreduced toto
avoidavoid aa toxictoxic buildupbuildup inin cirrhosis,cirrhosis,
particularlyparticularly
sedativessedatives andand drugsdrugs thatthat areare usedused toto
promotepromote
sleep.sleep. AlternativelyAlternatively,, drugsdrugs maymay bebe usedused
thatthat dodo
notnot needneed toto bebe detoxifieddetoxified oror eliminatedeliminated
fromfrom thethe
bodybody byby thethe liver,liver, forfor example,example, drugsdrugs
thatthat areare
eliminatedeliminated byby thethe kidneys.kidneys.
72
ComplicationsComplications Hepatic encephalopathy
whenwhen cirrhosiscirrhosis isis present,present, liverliver cellscells

cannotcannot
functionfunction normallynormally eithereither becausebecause theythey
areare
damageddamaged oror becausebecause theythey havehave lostlost theirtheir
normalnormal relationshiprelationship withwith thethe blood.blood. InIn
addition,addition, somesome ofof thethe bloodblood inin thethe portalportal
veinvein bypassesbypasses thethe liverliver throughthrough otherother

veins.veins.
TheThe resultresult ofof thesethese abnormalitiesabnormalities isis thatthat
toxictoxic substancessubstances cannotcannot bebe removedremoved byby

thethe liverliver cells,cells, and,and, instead,instead, thethe toxictoxic
substancessubstances accumulateaccumulate inin thethe blood.blood.
73
ComplicationsComplications Hepatic encephalopathy
WhenWhen thethe toxictoxic substancessubstances accumulateaccumulate
sufficientlysufficiently inin thethe blood,blood, thethe functionfunction
ofof thethe
brainbrain isis impaired,impaired, aa conditioncondition calledcalled
hepatichepatic encephalopathy.encephalopathy.
SleepingSleeping duringduring thethe dayday ratherrather thanthan atat
nightnight ((reversalreversal ofof thethe normalnormal sleepsleep
pattern)pattern)
isis amongamong thethe earliestearliest symptomssymptoms ofof hepatichepatic
encephalopathy.encephalopathy.
SevereSevere hepatichepatic encephalopathyencephalopathy causescauses
comacoma andand death.death.
74
ComplicationsComplications 44 Hepatorenal syndrome
PatientsPatients withwith worseningworsening cirrhosiscirrhosis cancan
developdevelop thethe hepatorenalhepatorenal syndrome.syndrome. ThisThis
syndromesyndrome isis aa seriousserious complicationcomplication inin
whichwhich thethe functionfunction ofof thethe kidneyskidneys isis
reduced.reduced. ItIt isis aa functionalfunctional problemproblem inin
thethe
kidneys,kidneys, thatthat is,is, therethere isis nono physicalphysical
damagedamage toto thethe kidneys.kidneys. Instead,Instead, thethe
reducedreduced functionfunction isis duedue toto changeschanges inin thethe
wayway thethe bloodblood flowsflows throughthrough thethe kidneyskidneys

themselves.themselves.
75
ComplicationsComplications Hepatorenal syndrome
TheThe hepatorenalhepatorenal syndromesyndrome isis defineddefined asas
progressiveprogressive failurefailure ofof thethe kidneyskidneys toto
clearclear
substancessubstances fromfrom thethe bloodblood andand produceproduce
adequateadequate
amountsamounts ofof urineurine eveneven thoughthough somesome otherother
importantimportant functionsfunctions ofof thethe kidney,kidney, suchsuch
asas
retentionretention ofof salt,salt, areare maintained.maintained.
IfIf liverliver functionfunction improvesimproves oror aa healthyhealthy
liverliver isis
transplantedtransplanted intointo aa patientpatient withwith
hepatorenalhepatorenal
syndrome,syndrome, thethe kidneyskidneys usuallyusually beginbegin toto
workwork
normally.normally.
ThisThis suggestssuggests thatthat thethe reducedreduced functionfunction
ofof thethe
kidneyskidneys isis thethe resultresult ofof thethe accumulationaccumulation
ofof toxictoxic
substancessubstances inin thethe bloodblood whenwhen thethe liverliver
fails.fails. 76
55 Hepatopulmonary syndrome
Rarely,Rarely, somesome patientspatients withwith advancedadvanced
cirrhosiscirrhosis cancan developdevelop thethe hepatopulmonaryhepatopulmonary
syndrome.syndrome. TheseThese patientspatients cancan experienceexperience

difficultydifficulty breathingbreathing becausebecause certaincertain
hormoneshormones releasedreleased inin advancedadvanced cirrhosiscirrhosis
causecause thethe lungslungs toto functionfunction abnormally.abnormally.
BloodBlood flowingflowing throughthrough thethe lungslungs isis
shuntedshunted
aroundaround thethe alveolialveoli andand cannotcannot pickpick upup
enoughenough oxygenoxygen fromfrom thethe airair inin thethe
alveolialveoli..
AsAs aa resultresult thethe patientpatient experiencesexperiences
shortnessshortness ofof breath.breath.
77
ComplicationsComplications 66 hepatocellular carcinoma
CirrhosisCirrhosis duedue toto anyany causecause increasesincreases thethe
riskrisk ofof
primaryprimary liverliver cancercancer (hepatocellular(hepatocellular
carcinoma).carcinoma).
PrimaryPrimary refersrefers toto thethe factfact thatthat thethe
tumortumor
originatesoriginates inin thethe liver.liver. AA secondarysecondary
liverliver cancercancer isis
oneone thatthat originatesoriginates elsewhereelsewhere inin thethe
bodybody andand
spreadsspreads toto thethe liver.liver.
TheThe mostmost commoncommon symptomssymptoms andand signssigns ofof
primaryprimary liverliver cancercancer areare abdominalabdominal painpain
andand
swelling,swelling, anan enlargedenlarged liver,liver, weightweight
loss,loss, andand
fever.fever. InIn addition,addition, liverliver cancerscancers cancan
produceproduce andand
releaserelease aa numbernumber ofof substances,substances,
includingincluding onesones
thatthat causecause anan increasedincreased inin redred bloodblood
cellcell countcount
((erythrocytosiserythrocytosis),), lowlow bloodblood sugarsugar
((hypoglycemiahypoglycemia),), andand highhigh bloodblood calciumcalcium
(hypercalcemia(hypercalcemia).). 78
79
80
DiagnosisDiagnosis
TheThe singlesingle bestbest testtest forfor diagnosingdiagnosing
cirrhosiscirrhosis isis
biopsybiopsy ofof thethe liverliver.. LiverLiver biopsies,biopsies,
however,however, carrycarry
aa smallsmall riskrisk forfor seriousserious complications,complications,
and,and,
therefore,therefore, biopsybiopsy oftenoften isis reservedreserved forfor
thosethose
patientspatients inin whomwhom thethe diagnosisdiagnosis ofof thethe
typetype ofof
liverliver diseasedisease oror thethe presencepresence ofof
cirrhosiscirrhosis isis notnot
clear.clear.
TheThe possibilitypossibility ofof cirrhosiscirrhosis maymay bebe
suggestedsuggested byby
thethe history,history, physicalphysical examination,examination, oror
routineroutine
testing.testing. IfIf cirrhosiscirrhosis isis present,present, otherother
teststests cancan bebe
usedused toto determinedetermine thethe severityseverity ofof thethe
cirrhosiscirrhosis
andand thethe presencepresence ofof complications.complications.
TestsTests alsoalso maymay bebe usedused toto diagnosediagnose thethe
underlyingunderlying diseasedisease thatthat isis causingcausing thethe
cirrhosis.cirrhosis.
81
DiagnosisDiagnosis
InIn takingtaking aa patient'spatient's history,history, thethe
physicianphysician
maymay uncoveruncover aa historyhistory ofof hepatitishepatitis ,a,a
historyhistory ofof excessiveexcessive andand prolongedprolonged intakeintake
ofof alcohol,alcohol, oror aa historyhistory ofof intravenousintravenous

drugdrug
abuse.abuse. TheseThese piecespieces ofof informationinformation
suggestsuggest thethe possibilitypossibility ofof liverliver diseasedisease
andand
PatientsPatients whowho areare knownknown toto havehave chronicchronic
viralviral hepatitishepatitis BB oror CC havehave aa higherhigher
probabilityprobability ofof havinghaving cirrhosis.cirrhosis.
82
DiagnosisDiagnosis
SomeSome patientspatients withwith cirrhosiscirrhosis havehave
enlargedenlarged liverslivers
and/orand/or spleens.spleens. AA doctordoctor cancan oftenoften feelfeel
(palpate)(palpate)
thethe lowerlower edgeedge ofof anan enlargedenlarged liverliver belowbelow
thethe
rightright ribrib cagecage andand feelfeel thethe tiptip ofof thethe
enlargedenlarged
spleenspleen belowbelow thethe leftleft ribrib cage.cage. AA
cirrhoticcirrhotic liverliver
alsoalso feelsfeels firmerfirmer andand moremore irregularirregular thanthan
aa
normalnormal liver.liver.
havehave smallsmall redred spider-likespider-like markingsmarkings onon

thethe skinskin
(telangiectasias),(telangiectasias), particularlyparticularly onon thethe
chest,chest, thatthat
areare mademade upup ofof enlarged,enlarged, radiatingradiating bloodblood
vessels.vessels.
83
DiagnosisDiagnosis
SwellingSwelling ofof thethe abdomenabdomen (ascites)(ascites) and/orand/or

thethe lowerlower extremitiesextremities (edema)(edema) duedue toto
retentionretention ofof fluidfluid isis commoncommon amongamong
patientspatients withwith cirrhosis.cirrhosis.
EsophagealEsophageal varicesvarices maymay bebe foundfound
unexpectedlyunexpectedly duringduring upperupper endoscopyendoscopy
(EGD),(EGD), andand theythey stronglystrongly suggestingsuggesting
84
DiagnosisDiagnosis
Esophagea
l and
gastric
varices with
correspond
ing
endoscopic
views.
85
DiagnosisDiagnosis
ComputerizedComputerized TomographyTomography (CT(CT )) oror

magneticmagnetic resonanceresonance imagingimaging (MRI)(MRI)
scansscans andand ultrasoundultrasound examinationsexaminations ofof
thethe abdomenabdomen donedone forfor reasonsreasons otherother
thanthan evaluatingevaluating thethe possibilitypossibility ofof liverliver
diseasedisease maymay unexpectedlyunexpectedly detectdetect
enlargedenlarged livers,livers, abnormallyabnormally nodularnodular
livers,livers, enlargedenlarged spleens,spleens, andand fluidfluid inin
thethe abdomenabdomen thatthat suggestsuggest cirrhosis.cirrhosis.
86
87
88
DiagnosisDiagnosis
AdvancedAdvanced cirrhosiscirrhosis leadsleads toto aa reducedreduced
levellevel ofof albuminalbumin inin thethe bloodblood andand reducedreduced
bloodblood clottingclotting factorsfactors duedue toto thethe lossloss ofof

thethe
liver'sliver's abilityability toto produceproduce thesethese
proteins.proteins.
Thus,Thus, reducedreduced levelslevels ofof albuminalbumin inin thethe
bloodblood oror abnormalabnormal bleedingbleeding suggestsuggest
Auto-antibodiesAuto-antibodies (antinuclear(antinuclear antibody,antibody, anti-
anti-
smoothsmooth musclemuscle antibodyantibody andand anti-anti-
mitochondrialmitochondrial antibody)antibody) sometimessometimes areare
detecteddetected inin thethe bloodblood andand maymay bebe aa clueclue
toto
thethe presencepresence ofof autoimmuneautoimmune hepatitishepatitis oror
primaryprimary biliarybiliary cirrhosis,cirrhosis, bothboth ofof whichwhich
cancan
leadlead toto cirrhosis.cirrhosis. 89
DiagnosisDiagnosis
TheThe singlesingle bestbest testtest forfor diagnosingdiagnosing

cirrhosiscirrhosis isis biopsybiopsy ofof thethe liverliver
90
LabLab StudiesStudies
LabLab studiesstudies areare directeddirected towardstowards
investigatinginvestigating
etiologiesetiologies ofof cirrhosis,cirrhosis, whichwhich isis thethe
mostmost commoncommon
causecause ofof portalportal hypertension.hypertension. LabLab studiesstudies
includeinclude
thethe following:following:
– Liver function tests
– Prothrombin time
– Albumin
– Viral hepatitis serologies
– Platelet count
– Antinuclear antibody, anti-mitochondrial antibody
– Iron index
– Ceruloplasmin, 24-hour urinary copper - To be
considered only in individuals aged 3-40 years who
have unexplained hepatic, neurologic, or psychiatric
disease 91
ImagingImaging StudiesStudies
Duplex-DopplerDuplex-Doppler ultrasonographyultrasonography
–– UltrasoundUltrasound (US)(US) isis aa safe,safe, economical,economical,
andand effectiveeffective
methodmethod forfor screeningscreening forfor portalportal
hypertension.hypertension. ItIt alsoalso
cancan demonstratedemonstrate portalportal flowflow andand helpshelps inin
diagnosingdiagnosing
cavernouscavernous transformationtransformation ofof thethe portalportal
vein,vein, portalportal
veinvein thrombosisthrombosis,, oror splenicsplenic veinvein
thrombosis.thrombosis.
–– FeaturesFeatures suggestivesuggestive ofof hepatichepatic cirrhosiscirrhosis
withwith portalportal
hypertensionhypertension includeinclude thethe following:following:
–– NodularNodular liverliver surfacesurface isis suggestive.suggestive.
However,However, thisthis
findingfinding isis notnot specificspecific forfor cirrhosiscirrhosis
andand cancan bebe
observedobserved withwith congenitalcongenital hepatichepatic
fibrosisfibrosis andand
nodularnodular regenerativeregenerative hyperplasia.hyperplasia.
Splenomegaly is a suggestive finding.
Patients may demonstrate the presence of collateral
circulation. 92
ImagingImaging StudieStudie CTCT scanscan
CTCT scanscan isis aa usefuluseful qualitativequalitative studystudy
inin
casescases wherewhere sonographicsonographic evaluationsevaluations areare
inconclusive.inconclusive.
–– CTCT scanscan isis notnot affectedaffected byby patients'patients'
bodybody
habitushabitus oror thethe presencepresence ofof bowelbowel gas.gas.
–– WithWith improvementimprovement ofof spiralspiral CTCT scanscan andand 3-
3-
dimensionaldimensional angiographicangiographic reconstructivereconstructive
techniques,techniques, portalportal vasculaturevasculature maymay bebe
visualizedvisualized moremore accurately.accurately.
–– FindingsFindings suggestivesuggestive ofof portalportal
includeinclude thethe following:following:
–– CollateralsCollaterals arisingarising fromfrom thethe portalportal
systemsystem areare
suggestivesuggestive ofof portalportal hypertension.hypertension. 93
MagneticMagnetic resonanceresonance imagingimaging (MRI)(MRI)

–– MRIMRI providesprovides qualitativequalitative informationinformation
similarsimilar toto
CTCT scanscan whenwhen DopplerDoppler findingsfindings areare
inconclusive.inconclusive.
–– MRIMRI angiographyangiography detectsdetects thethe presencepresence ofof
portosystemicportosystemic collateralscollaterals andand

obstructionobstruction ofof
portalportal vasculature.vasculature.
–– MRIMRI alsoalso providesprovides quantitativequantitative datadata onon
portalportal
venousvenous andand bloodblood flow.flow.
94
Liver-spleenLiver-spleen scanscan
–– ThisThis isis describeddescribed forfor historicalhistorical
interestinterest only.only.
95
ProceduresProcedures
EndoscopyEndoscopy
–– PerformPerform upperupper endoscopy,endoscopy, asas appropriate,appropriate,
toto
screenscreen forfor varicesvarices inin everyevery patientpatient withwith
suggestivesuggestive findingsfindings ofof portalportal
hypertension.hypertension.
Additionally,Additionally, allall patientspatients withwith cirrhosiscirrhosis
shouldshould
bebe consideredconsidered forfor thethe presencepresence ofof varicesvarices
atat
thethe timetime ofof thethe initialinitial diagnosisdiagnosis ofof
96
GastroesophagealGastroesophageal varicesvarices confirmconfirm thethe
diagnosisdiagnosis ofof portalportal hypertension;hypertension;
however,however,
theirtheir absenceabsence doesdoes notnot rulerule itit out.out. AtAt
times,times,
gastroesophagealgastroesophageal varicesvarices areare incidentalincidental
findingsfindings inin patientspatients undergoingundergoing upperupper
endoscopyendoscopy forfor otherother reasonsreasons (eg,(eg,
dyspepsiadyspepsia refractoryrefractory toto medications,medications,
dysphagia,dysphagia, weightweight loss).loss). TheseThese patientspatients
shouldshould undergoundergo furtherfurther investigationsinvestigations forfor
etiologiesetiologies ofof portalportal hypertension.hypertension.
97
ProceduresProcedures
–– VariousVarious indirectindirect indices(index),indices(index), suchsuch asas
plateletplatelet
count,count, spleenspleen size,size, albumin,albumin, andand Child-PughChild-
Pugh
score,score, havehave beenbeen studiedstudied toto helphelp diagnosediagnose
varicesvarices withoutwithout endoscopy.endoscopy. AA recentrecent casecase

reviewreview
studystudy revealedrevealed somesome ofof thesethese predictorspredictors
asas
unreliable.unreliable. ForFor thethe timetime being,being, endoscopyendoscopy
remainsremains thethe criterioncriterion standardstandard forfor

screeningscreening
patientspatients withwith cirrhosiscirrhosis forfor varices.varices.
–– InIn compensatedcompensated patientspatients withoutwithout varices,varices,
repeatrepeat
endoscopyendoscopy atat 2-2- toto 3-year3-year intervalsintervals toto
evaluateevaluate forfor
thethe developmentdevelopment ofof varices.varices.
–– InIn compensatedcompensated patientspatients withwith smallsmall
varices,varices,
repeatrepeat endoscopyendoscopy atat 1-1- toto 2-year2-year
intervalsintervals toto
evaluateevaluate thethe progressionprogression ofof varices.varices. 98
DIFFERENTIALSDIFFERENTIALS
TricuspidTricuspid RegurgitationRegurgitation
TuberculosisTuberculosis
MyeloproliferativeMyeloproliferative DiseaseDisease
Pericarditis,Pericarditis, ConstrictiveConstrictive
99
TREATMENTTREATMENT
TreatmentTreatment ofof cirrhosiscirrhosis includesincludes

1)1) preventingpreventing furtherfurther damagedamage toto thethe liverliver
2)2) treatingtreating thethe complicationscomplications ofof cirrhosiscirrhosis
3)3) preventingpreventing liverliver cancercancer oror detectingdetecting itit
earlyearly
4)4) liverliver transplantation.transplantation.
100
TREATMENTTREATMENT
11、、PreventingPreventing furtherfurther damagedamage toto thethe liverliver
::
-Consume-Consume aa balancedbalanced dietdiet andand oneone
multivitaminmultivitamin daily.daily. PatientsPatients withwith
impairedimpaired
absorptionabsorption ofof fatfat solublesoluble vitaminsvitamins maymay
needneed additionaladditional vitaminsvitamins DD andand K.K.
-Avoid-Avoid drugsdrugs (including(including alcohol)alcohol) thatthat
causecause
liverliver damage.damage.
101
TREATMENTTREATMENT NutritionNutrition
ManyMany patientspatients gotgot anorexia,anorexia, whichwhich maymay bebe
compoundedcompounded byby thethe directdirect compressioncompression ofof
ascitesascites onon thethe GIGI tract.tract. CareCare shouldshould bebe
takentaken toto
ensureensure thatthat patientspatients receivereceive adequateadequate
caloriescalories
andand proteinprotein inin theirtheir diets.diets. PatientsPatients
frequentlyfrequently
benefitbenefit fromfrom thethe additionaddition ofof commonlycommonly
availableavailable
liquidliquid andand powderedpowdered nutritionalnutritional
supplementssupplements toto
thethe diet.diet.
OnlyOnly rarelyrarely cancan patientspatients notnot toleratetolerate
proteinsproteins inin
thethe formform ofof chicken,chicken, fish,fish, vegetables,vegetables,
andand
nutritionalnutritional supplements.supplements. InstitutionInstitution ofof aa
low-low-
proteinprotein dietdiet inin thethe fearfear thatthat hepatichepatic
encephalopathyencephalopathy mightmight developdevelop placesplaces thethe
patientpatient
atat riskrisk forfor thethe developmentdevelopment ofof profoundprofound
musclemuscle
wasting.wasting. 102
DosesDoses ofof manymany drugsdrugs thatthat normallynormally areare
detoxifieddetoxified byby thethe liverliver havehave toto bebe
reducedreduced
toto avoidavoid aa toxictoxic buildupbuildup inin cirrhosis,cirrhosis,
particularlyparticularly sedativessedatives andand drugsdrugs thatthat areare
usedused toto promotepromote sleep.sleep.

Alternatively,Alternatively, drugsdrugs maymay bebe usedused thatthat dodo
notnot needneed toto bebe detoxifieddetoxified oror eliminatedeliminated
fromfrom thethe bodybody byby thethe liver,liver, forfor example,example,
drugsdrugs thatthat areare eliminatedeliminated byby thethe kidneys.kidneys.
103
DrugDrug hepatotoxicityhepatotoxicity inin thethe patientpatient
withwith cirrhosiscirrhosis
TheThe institutioninstitution ofof anyany newnew medicalmedical
therapytherapy
warrantswarrants thethe performanceperformance ofof moremore frequentfrequent
liverliver chemistries.chemistries. Indeed,Indeed, patientspatients withwith

liverliver
diseasedisease cancan illill affordafford toto havehave drug-induceddrug-
induced
liverliver diseasedisease superimposedsuperimposed onon theirtheir
condition.condition. MedicationsMedications associatedassociated withwith
drug-induceddrug-induced liverliver diseasedisease includeinclude
NSAIDs,NSAIDs, isoniazidisoniazid,, erythromycin,erythromycin,
amoxicillin/amoxicillin/clavulanateclavulanate,, chlorpromazinechlorpromazine
andand ezetimibe.ezetimibe.
104
DrugDrug hepatotoxicityhepatotoxicity inin thethe patientpatient
withwith cirrhosiscirrhosis
CareCare shouldshould bebe takentaken toto avoidavoid
postpost
-operative-operative infection,infection, fluidfluid overload,overload,
unnecessaryunnecessary sedatives,sedatives, andand potentiallypotentially
hepatotoxichepatotoxic andand nephrotoxicnephrotoxic drugsdrugs
105
TREATMENTTREATMENT 下下次次
22、、TreatingTreating thethe complicationscomplications ofof
cirrhosis:cirrhosis:
1)1) EdemaEdema andand ascitesascites:: withwith aa low-sodiumlow-
sodium dietdiet
RetentionRetention ofof saltsalt andand waterwater cancan
leadlead toto swellingswelling
ofof thethe anklesankles andand legslegs (edema)(edema) oror
abdomenabdomen
(ascites)(ascites) inin patientspatients withwith cirrhosis.cirrhosis.
DoctorsDoctors oftenoften
adviseadvise patientspatients withwith cirrhosiscirrhosis toto
restrictrestrict dietarydietary saltsalt
(sodium)(sodium) andand fluidfluid toto decreasedecrease edemaedema andand
ascites.ascites.
TheThe amountamount ofof saltsalt inin thethe dietdiet
usuallyusually isis restrictedrestricted
toto 22 gramsgrams perper dayday andand fluidfluid toto 1.21.2
litersliters perper day.day.
InIn mostmost patientspatients withwith cirrhosis,cirrhosis,
however,however, saltsalt andand
fluidfluid restrictionrestriction isis notnot enough,enough, andand
diureticsdiuretics havehave toto
bebe added.added.
106
TreatingTreating thethe complicationscomplications ofof cirrhosis:cirrhosis:
DiureticsDiuretics areare medicationsmedications thatthat workwork inin

thethe
kidneyskidneys toto promotepromote thethe eliminationelimination ofof
saltsalt andand
waterwater intointo thethe urine.urine. AA combinationcombination ofof
thethe
diureticsdiuretics spironolactonespironolactone (Aldactone(Aldactone 安安体体舒舒通
通))
andand furosemidefurosemide （（呋呋塞塞米米））cancan reducereduce oror
eliminateeliminate thethe edemaedema andand ascitesascites inin mostmost
patients.patients.
DuringDuring treatmenttreatment withwith diuretics,diuretics, itit isis
importantimportant toto
monitormonitor thethe functionfunction ofof thethe kidneyskidneys byby
measuringmeasuring
bloodblood levelslevels ofof bloodblood ureaurea nitrogennitrogen (BUN)(BUN)
andand
creatininecreatinine toto determinedetermine ifif tootoo muchmuch
diureticdiuretic isis
beingbeing used.used. TooToo muchmuch diureticdiuretic cancan leadlead toto
kidneykidney dysfunctiondysfunction thatthat isis reflectedreflected inin

elevationselevations
ofof thethe BUNBUN andand creatininecreatinine levelslevels inin thethe

blood.blood. 107
Sometimes,Sometimes, whenwhen thethe diureticsdiuretics dodo notnot
work,work, aa
longlong needleneedle oror cathetercatheter isis usedused toto drawdraw
outout
thethe asciticascitic fluidfluid directlydirectly fromfrom thethe
abdomen,abdomen, aa
procedureprocedure calledcalled abdominalabdominal paracentesisparacentesis..
ItIt
isis commoncommon toto withdrawwithdraw largelarge amountsamounts (liters)
(liters)
ofof fluidfluid fromfrom thethe abdomenabdomen whenwhen thethe
ascitesascites isis
causingcausing painfulpainful abdominalabdominal distensiondistension
and/orand/or
difficultydifficulty breathingbreathing becausebecause itit limitslimits
thethe
movementsmovements ofof thethe diaphragms.diaphragms.
AnotherAnother treatmenttreatment forfor refractoryrefractory ascitesascites
isis aa
procedureprocedure calledcalled transjugulartransjugular intravenousintravenous
portosystemicportosystemic shuntingshunting (TIPS).(TIPS).

108
109
2)2) varicealvariceal bleedingbleeding

•• Balloon-tubeBalloon-tube tamponadetamponade shouldshould bebe usedused
onlyonly inin massivemassive bleedingbleeding asas aa measuremeasure
untiluntil definitivedefinitive treatmenttreatment cancan bebe
instituted.instituted.
•• PharmacologicPharmacologic therapytherapy isis directeddirected atat
treatingtreating acuteacute bleedingbleeding andand providingproviding
primaryprimary oror secondarysecondary prophylaxis.prophylaxis.
SomatostatinSomatostatin（（生生长长抑抑素素）） areare usedused toto
treattreat acuteacute bleeding.bleeding.
110
EndoscopicEndoscopic
therapytherapy
EndoscopicEndoscopic injectioninjection sclerosclero therapytherapy

involvesinvolves injectinginjecting aa sclerosantsclerosant solutionsolution
intointo
thethe bleedingbleeding varixvarix,, obliteratingobliterating thethe
lumenlumen
byby thrombosis,thrombosis, oror intointo thethe overlyingoverlying
submucosa,submucosa, producingproducing inflammationinflammation
followedfollowed byby fibrosis.fibrosis.
111
EndoscopicEndoscopic
therapytherapy
EndoscopicEndoscopic varicealvariceal ligationligation (EVL)(EVL) isis
achievedachieved byby aa bandingbanding devicedevice attachedattached toto
thethe tiptip ofof thethe endoscope.endoscope. TheThe varixvarix isis
aspiratedaspirated intointo thethe bandingbanding chamber,chamber, andand aa
triptrip wirewire dislodgesdislodges aa rubberrubber bandband carriedcarried
onon thethe bandingbanding chamber,chamber, ligatingligating thethe

varix.varix.
OneOne toto 33 bandsbands areare appliedapplied toto eacheach varix,varix,
resultingresulting inin thrombosis.thrombosis. EVLEVL isis lessless

proneprone
toto complicationscomplications thanthan injectioninjection
sclerotherapy.sclerotherapy.
112
SurgicalSurgical
CareCare
SurgicalSurgical carecare includesincludes decompressivedecompressive
shunts,shunts, devascularizationdevascularization procedures,procedures, andand
liverliver transplantation.transplantation.
DecompressiveDecompressive shunts:shunts: TheseThese includeinclude
totaltotal
portalportal systemicsystemic shunts,shunts, partialpartial portalportal
systemicsystemic shunts,shunts, andand otherother selectiveselective
shunts.shunts.
DevascularizationDevascularization procedures:procedures: TheseThese
includeinclude splensplen ectomyectomy,, gastroesophagealgastroesophageal
devascularization,devascularization, andand esophagealesophageal
transectiontransection .. 113
2)2) varicealvariceal bleedingbleeding TIPSTIPS
TransjugularTransjugular intrahepaticintrahepatic portosystemicportosystemic

shuntshunt (TIPS)(TIPS) isis aa non-surgicalnon-surgical procedureprocedure
toto
decreasedecrease thethe pressurepressure inin thethe portalportal
vein.vein. TIPSTIPS isis
performedperformed byby aa radiologistradiologist whowho insertsinserts aa
tubetube
throughthrough aa neckneck vein,vein, downdown thethe inferiorinferior
venavena cavacava
andand intointo thethe hepatichepatic veinvein withinwithin thethe
liver.liver. TheThe
tubetube thenthen isis placedplaced soso thatthat oneone endend isis
inin thethe highhigh
pressurepressure portalportal veinvein andand thethe otherother endend
isis inin thethe
lowlow pressurepressure hepatichepatic vein.vein. ThisThis tubetube
shuntsshunts
bloodblood aroundaround thethe liverliver andand byby soso doingdoing
lowerslowers
thethe pressurepressure inin thethe portalportal veinvein andand
varicesvarices andand
preventsprevents bleedingbleeding fromfrom thethe varices.varices.
114
3)3) SBPSBP
Most patients with spontaneous bacterial peritonitis are
hospitalized and treated with intravenous antibiotics such
as ampicillin, and one of the newer generation
cephalosporin. Patients usually treated with antibiotics
include:
Patients with blood, urine, and/or ascites fluid cultures
that contain bacteria.
Patients without bacteria in their blood, urine, and ascitic
fluid but who have elevated numbers of white blood cells.
Elevated neutrophil numbers in ascitic fluid often means
that there is bacterial infection. Doctors believe that the
lack of bacteria with culturing in some patients with
increased neutrophils is due either to a very small
number of bacteria or ineffective culturing techniques.
115
3)3) SBPSBP
PatientsPatients withwith cirrhosiscirrhosis whowho areare
hospitalizedhospitalized forfor
bleedingbleeding varicesvarices havehave aa highhigh riskrisk ofof
developingdeveloping
spontaneousspontaneous bacterialbacterial peritonitisperitonitis andand
shouldshould bebe
startedstarted onon antibioticsantibiotics earlyearly duringduring thethe
hospitalizationhospitalization toto preventprevent spontaneousspontaneous
bacterialbacterial
peritonitisperitonitis
PatientsPatients withwith lowlow proteinprotein levelslevels inin thethe

asciticascitic fluidfluid
(Ascitic(Ascitic fluidfluid withwith lowlow levelslevels ofof
proteinprotein isis moremore
likelylikely toto becomebecome infected.)infected.)
116
SurgicalSurgical CareCare
33、、LiverLiver transplantationtransplantation
CirrhosisCirrhosis isis irreversibleirreversible.. ManyMany
patients'patients'
liverliver functionfunction willwill graduallygradually worsenworsen
despitedespite
treatmenttreatment andand complicationscomplications ofof cirrhosiscirrhosis
willwill increaseincrease andand becomebecome difficultdifficult toto
treat.treat.
Therefore,Therefore, whenwhen cirrhosiscirrhosis isis farfar
advanced,advanced,
liverliver transplantationtransplantation oftenoften isis thethe onlyonly
optionoption
forfor treatment.treatment.
117
MonitoringMonitoring thethe patientpatient withwith cirrhosiscirrhosis
PatientsPatients withwith cirrhosiscirrhosis shouldshould undergoundergo

routineroutine follow-upfollow-up monitoringmonitoring ofof theirtheir
completecomplete bloodblood count,count, renalrenal andand liverliver
chemistries,chemistries, andand prothrombinprothrombin time.time. PolicyPolicy
isis toto monitormonitor stablestable patientspatients 3-43-4 timestimes
perper
year.year.
118
performsperforms routineroutine diagnosticdiagnostic endoscopyendoscopy toto

determinedetermine whetherwhether thethe patientpatient hashas
asymptomaticasymptomatic esophagealesophageal varices.varices.
Follow-upFollow-up endoscopyendoscopy isis performedperformed inin 22
yearsyears ifif varicesvarices areare notnot present.present. IfIf
varicesvarices
areare present,present, treatmenttreatment isis initiatedinitiated withwith
aa
nonselectivenonselective ((ββ)beta-blocker)beta-blocker ..
119
PatientsPatients intolerantintolerant ofof beta-blockersbeta-blockers

shouldshould
undergoundergo endoscopicendoscopic varicealvariceal ligation.ligation.
performperform abdominalabdominal ultrasonographyultrasonography andand
alpha-fetoproteinalpha-fetoprotein (AFP)testing(AFP)testing twicetwice
yearly,yearly,
120
chestchest andand abdominalabdominal CTCT scansscans andand byby
bonebone scanscan
PreventionPrevention andand earlyearly detectiondetection ofof liverliver
cancercancer：：mostmost patientspatients withwith cirrhosis,cirrhosis,
particularlyparticularly hepatitishepatitis BB andand C,C, areare
screenedscreened yearlyyearly oror everyevery sixsix monthsmonths withwith
ultrasoundultrasound examinationexamination ofof thethe liverliver andand
measurementsmeasurements ofof cancer-producedcancer-produced
proteinsproteins inin thethe blood,blood, e.g.e.g.
alphafetoproteinalphafetoprotein
(AFP(AFP levellevel ofof greatergreater thanthan 400400 ng/mLng/mL isis
believedbelieved toto havehave thethe samesame diagnosticdiagnostic
powerpower toto
guidedguided liverliver biopsy)biopsy) 121

PrognosisPrognosis
Clinical variable 1 point 2 points 3 points
Child- Encephalopathy None Stages 1-2 Stages 3-4

Turcotte-
Pugh
Scoring Ascites Absent Slight Moderate
System for
Cirrhosis Bilirubin (mg/dL) <2 2-3 >3
(Child
Class A=5- Bilirubin in PBC <4 4-10 10
6 points, or PSC (mg/dL)
Child Class Albumin (g/dL) >3.5 2.8-3.5 <2.8
B=7-9
points,
Child Class Prothrombin <4 s or 4-6 s or INR >6 s or INR
C=10-15 time(seconds INR <1.7 1.7-2.3 >2.3
points) prolonged or
INR)
122
reviewreview
11、、WhatWhat areare thethe symptomssymptoms andand signssigns ofof
cirrhosis?cirrhosis?
22、、WhatWhat areare thethe complicationscomplications ofof cirrhosis?
cirrhosis?
33、、WhatWhat areare thethe commoncommon causescauses ofof cirrhosis?
cirrhosis?
（Chronic viral hepatitis ，Alcohol Autoimmune
hepatitis， Primary biliary cirrhosis ， drugs ，
Nonalcoholic fatty liver disease (NAFLD) ， chronic
heart failure ）
44、、CommonCommon clinicalclinical manifestationsmanifestations ofof
portalportal
55、、HowHow isis cirrhosiscirrhosis diagnoseddiagnosed andand evaluated?
evaluated?
123
THANKTHANK YOUYOU
124
Respiratory Failure
Professor Xu sicheng
contents
keys:
difinition
causes
classification
acute respiratory failure
chronic repiratory failure
understanding:
pathophysiology
Respiratory Failure
Respiratory failure isdefined as a syndrome in which respiratory

dysfunction results in abnormalities oxygenation and/or ventilation
(CO2, elimination),leading to hypoxemia and hypercapnia and

associated physiological disturbance and clinical manifestation.
Arterial blood gas criteria for respiratory failure are a PO2, under
60 mmHg and/or a PCO2, over 50mmHg under the condition of room
air breathing during rest at sea level of altitude and exclusion of the
arterial blood gas abnormality due to cardiac shunt or low cardiac
output etc.
CAUSES
Respiratory failure may occur in a variety of pulmonary

and nonpulmonary disorders involving the chain of AIRWAY DISORDERS
breathing activities.
PARENCHYMAL LUNG DISORDERS
PULMONARY VASCULAR DISORDERS
CHEST WALL, DIAPHRAGM, ANDPLEURAL DISORDERS
NEUROMUSCULAR AND RELATED DISORDERS

AIRWAY DISORDERS
• Acute attack of asthma, acute exacerbation of chronic obstructive pulmonary
disease(COPD)
obstruction of pharynx, larynx, trachea, mainstem,bronchus, or lobar bronchus
by edema, mucus,mass, or foreign body, etc.
PARENCHYMAL LUNG DISORDERS

• Pneumonia, interstitial lung diseases, pulmonaryedema, diffuse alveolar
hemorrhage syndromes, aspiration, lung contusion, etc.
PULMONARY VASCULAR DISORDERS
• Thromboembolism, air embolism, amniotic fluid embolism and
pulmonary vasculitis, etc.
CHEST WALL, DIAPHRAGM, ANDPLEURAL DISORDERS

• Rib fracture flail chest, pneumothorax, pleuraleffusion, massive
ascites, kyphoscoliosis, severe abdominal distention. etc
NEUROMUSCULAR AND RELATED DISORDERS
• Cerebral vasculardisorders,brain trauma,tumor, central nervous
system infections, spinacord injury, myasthenia gravis,
polymyosItIs,overuse of sedative, organophosphates poisoning, etc.
CLASSIFICATION
• Hypoxemic(Type I)
RespiratoryFailure
ARTERIAL BLOOD GAS • Hypercapnic(Type
II)Respiratory
Failure
• Acute Respiratory Failure

SPEED OF DEVELOPMENT • Chronic Respiratory Failure
PATHOGENESIS
CLASSIFICATION BASED ON ARTERIAL BLOOD GAS
Hypoxemic(Type I) Respiratory Failure
• The characteristics of hypoxemic respiratory failure is PaO2＜60 mmHg with
reduced or normal PaCO2,. Hypoxemic respiratory failure is usually associated with
pathology leading to abnormal ventilation/perfusion ratio, diminished diffusion

capacity and pulmonary arterial-venous shunt, such as severe pneumonia,
interstitial lung disease, pulmonary embolism , etc.
Hypercapnic(Type II)Respiratory Failure
• The characteristics of hypercapnic respiratory failure is PaCO2,>50 mmHg and

PaO2<60 mmHg. Hypercapnic respiratory failure is due to hypoventilation,such as
severe COPD,etc.
CLASSIFICATION BASED ON SPEED OF DEVELOPMENT
Acute Respiratory Failure
• The term acute implies a relatively sudden onset (from hours to days)of the
underline disease and respiratory failure developed rapidly.Acute respiratory
failure is often associated with severe dyspnea and sometime life threatening as
there is not enough time for human body to compensate the abnormality.
Chronic Respiratory Failure
• Chronic refers to the gradual development of respiratory failure over period of
time and physiological and metabolic derangement is diminished through
compensation mechanisms.
• The acute or chronic respiratory failure is arbitrarily defined.In patients with
chronic respiratory failure,acute exacerbation of respiratory failure due to acute
deteriorating underline disease is commonly encountered clinical event,which

may lead to the physiological abnormality similar to acute respiratory failure.
CLASSIFICATION BASED ON PATH- OGENESIS
• Respiratory failure can result from inadequate ventilation(pump

failure)or abnormal gas exchange in the lung parenchyma(lung
failure).Pump failure usually presents as hypercapnic respiratory
failure and lung failure can present as hypercapnic or hypoxemic
respiratory failure.
PATHOPHYSIOLOGY
MECHANISMS OF HYPOXEMIA AND HYPERCAPNIA
SYSTEMIC EFFECTS OF HYPOXEMIA AND HYPERCAPNIA

A combination of the above mechanisms is often responsible for the

development of respiratory failure.
Hypoventilation
Diffusion Abnormality
Ventilation/Perfusion(V/Q)Mismatch
Shunt
•
Hypoventilation
Hypoventilation is the most common

mechanism in hypercapnic respiratory failure.
A decrease in alveolar ventilation can result
from a reduction in overall (minute)ventilation or an
increase in the proportion of dead space ventilation.
At a constant rate of carbon dioxide production,PaCO2 is determined
by the level of alveolar ventilation(Va),where VCO2 is ventilation of carbon
dioxide and K is a constant value(0.863).
PaCO2=(K x VCO2)/Va
Hypoventilation
Shunt
•
Diffusion abnormalities refer to the abnormality of gas exchange
between the alveoli and pulmonary capillary.
The diffusion capacity is determined by the partial pressure of
gas,diffusion coefficient and the characteristics of alveolar
membrane(area,thickness and permeability).
As the diffusion coefficient of oxygen is only one twentieth of
that of carbon dioxide,disease leading to abnormal diffusion,such as
acute respiratory distress syndrome,results in mainly hypoxemia rather
than hypercapnia.
Hypoventilation
Shunt
•
During ideal gas exchange,ventilation and blood flow match
each other perfectly with V/Q ratio of 0.8.V/Q mismatch is the most
common cause of hypoxemia.
(1)Low V/Q ratio: The low V/Qratio may occureither from a decrease in ventilation
secondary
toairway or interstitial lung disease(such as in pneumonia or atelectasis)or from
overperfusion in
thepresence of normal ventilation,Low V/Q ratio is also named as functional
shunt,as it results in
inadequately oxygenated blood returning to systemic circulation and hypoxemia.
(2)High V/Q ratio: HighV/Q ratio usually occurs when local blood decreases,which
wastes
ventilation and results in deadspace effect(also named as physiological
deadspace).So,high V/Q
ratio augments ventilatorydemand and work of breathing.
Hypoventilation
Shunt
•
Shunt
Shunt is defined as deoxygenated blood(mixed venous blood) by
passes the ventilated alveoli and mixes with oxygenated blood that has
flowed through the ventilated alveoli, consequently leading to a reduction in
arterial blood content.
Shunt can be distinguished from V/Q mismatch by the persistence of
hypoxemia despite 100% oxygen inhalation.
Anatomical shunt exists in normal lungs because of the direct return
of bronchial circulations to pulmonary vein, accounting for 2%-3% of shunt.
Increased shunt as a cause of hypoxemia is observed primarily in
pneumonia, atelectasis and severe pulmonary edema of either cardiac or
noncardiac origin.
SYSTEMIC EFFECTS OF HYPOXEMIA AND HYPERCAPNIA
Hypoxemia and hypercapnia have profound systemic effects, including metabolism,

multiple organ dysfunctions and structural changes.
Central Nervous System
Central nervous system is very sensitive to hypoxia. Mild hypoxemia
results in reduced attention and orientation abilities. Moderate to severe
hypoxemia results in anxiety, altered mental status,confusion or even coma.
Irreversible brain damage occurs if complete stop of oxygen supply for more
than 5 minutes.
Hypercapnia can inhibit the metabolism and activity of brain cells
through the elevation of H+ concentration . Mild hypercapnia will exert
incentive effects and result in restlessness , tremor , asterixis , slurrd
speech, diaphoresis and headache .Severe hypercapnia will lead to
somnolence , lethargy and Coma(carbon dioxide narcosis).
Circulatory System
Mild hypoxemia and hypercapnia can result in tachycardia ,

hypertension, increase of cardiac contractility and cardiac output through
reflex mechanism. However, severe hypoxemia and hypercapnia can lead to
hypotension , bradycardia and even cardiac arrest.
Respiratory System
Respiratory response to hypoxemia and hypercapnia depends on the
underline disease and acute or chronic respiratory failure.
Mild hypoxemia can stimulate respiratory center to increase
respiratory effort through the reflex of chemoreceptors of carotid and aortic
bodies. However,in severe hypoxemia suppression of respiration is more
prominent as the direct suppression effect of hypoxemia on respiratory
center supersedes the stimulation effect on peripheral chemoreceptors.
Respiratory System
Hypercapnia is much more potent respiratory stimulant than
hypoxemia.CO2 can directly stimulate respiratory center and increase

respiratory effort . However , adaptation to hypercapnia can develop in
chronic hypereapnia and the stimulation of respiratory center depends
mainly on hypoxemia . This might be the mechanism of respiratory
suppression and deterioration of hypercapnia after oxygen therapy in some
chronic hypercapnic patient.
Other Systemic Effects
Hypoxemia and hypercapnia have profound systemic effects including

renal function , digesting function , etc. The mechanisms are not fully
understood . Increased release of inflammatory mediators and cytokines ,
change of endocrine function and electrolytes and acid-base disturbance are
the main mechanisms for most of the systemic effects . In most of the cases ,
systemic organs dysfunction will disappear after the correction of hypoxemia
and hypercapnia.
Ⅰ. ACUTE RESPIRATORY FAILURE
CAUSES
As mentioned above,acute respiratory failure may occur in a variety of severe
pulmonary and nonpulmonary disorders involving the chain of breathing ac
tivities,leading to acute development of hypoxemia and/or hypercapnia.
CLINICAL FINDINGS
Symptoms and signs of acute respiratory failure are those of the underlying
disease combined
with those of hypoxemia or hypercapnia.
1.DYSPNEA
Dyspnea is the early and most common symptom of acute respiratory
failure.Signs associated
with dyspnea include tachypnea and activation of accessory respiratory
muscles.However,signs
of dyspnea can be complete absent in acute respiratory failure due to suppression
of central
nervous system,such as overuse of sedative medication.
2.CYANOSIS
Cyanosis is the typical presentation of hypoxia.It develops when oxygen
saturation drops
below 90%.However,cyanosis is affected by other factors,such as content of
hemoglobin in
blood,peripheral perfusion,cardiac output,etc.
3.PSYCHIATRIC AND NEURAL SYMPTOMS
These include headache,restlessness,anxiety,asterixis,impaired
consciousness,confusion and
delirium,Coma can occur in severe hypoxemia and hypercapnia.
4.CIRCULATORY PRESENTATION
Tachycardia is common.Peripheral and conjunctival hyperemia is often associated
with
hypercapnia.Severe hypoxemia and acidosis can result in myocardial
injury,hypertension,cardiac
dysrhythmias,bradycardia and cardiac arrest.
5.PRESENTATIONS OF DIGESTIVE AND URINARY SYSTEMS
Severe acute respiratory failure can result in multiple organs dysfunction.The
common
presentation of digestive system includes dyspepsia and elevated hepatic
enzymies.Upper
digestive track bleeding can occur in severe cases.The presentations of urinary
system include
decreased urine discharge,abnormal urine test and elevated BUN.
DIAGNOSIS
The diagnosis of acute respiratory failure is based on the history,physical

examination and laboratory testing As the clinical presentations are nonspecific
and may overlap with the underline disease,so the arterial blood gas analysis is
important in confirming the diagnosis.
TREATMENT
The principles of treatment of the patient with acute respiratory failure consist
of：
I.specific therapy directed toward the underlying disease;

2.maintenance of airway patency;
3.respiratory supportive care directed toward the maintenance of adequate gas
exchange;
4.general supportive care.
（1）MAINTENANCE OF AIRWAY PATENCY
Airway patency is important in ensuring adequate ventilation and reducing
airway
resistance,which is crucial for a successful management of respiratory
failure.Maintaining upper
airway open,clearing airway secretion and properly application of bronchodilators
in case of
bronchoconstriction are effective approaches in reducing airway
resistance.Artificial airway
establishment is necessary if above mentioned approaches fail to maintain adequate
airway
patency.
（2）OXYGEN THERAPY
The main therapeutic goal in acute hypoxemic respiratory failure is to ensure
adequate
oxygenation of vital organs.Oxygen therapy is the initial choice of treatment of
hypoxemia.
① Inspired O2 Concentration(FiO2)
Inspired oxygen concentration should be the lowest value that results in an
arterial hemoglobin
saturation>90%(PO2>60 mmHg).Higher arterial oxygen tensions are of no proven

benefit.
Restoration of normoxia may rarely cause hypoventilation in patients with chronic
hypercapnia ;
however,oxygen therapy should not be withheld for fear of causing progressive
respiratory
acidemia.Hypoxemia in patients with obstructive airway disease is usually easily
corrected by
administering low-flow oxygen by nasal cannula(1-3L/min) or Venturi mask(24%-
40%).Higher
concentrations of oxygen are necessary to correct hypoxemia in patients with
ARDS,pneumonia,and
other parenchymal lung diseases.
② O2 Delivery System
A.Nasal Prongs Or Nasal Cannula
Nasal prongs or nasal cannula is commonly used for low concentration of O2

therapy.The advantages
of nasal cannula are good tolerance and allow the patient to cough,speak,eat,and
drink while
receiving O2.The level of O2 can be adjusted by the flow rate to the nasal
prongs.The drawback of
nasal cannula is the limitation in providing higher FiO2.At flows of greater than 6
L/min,only a small
further augmentation in FiO2 can be achieved with maximal FiO2 of approximately
0.50.
B.Masks
Masks for oxygen therapy include nonrebreathing mask,Venturi mask and
nonrebreathing mask with
O2 reservoir.Oxygen therapy with mask can deliver 50% to 100% 02 depend on the type
of the mask.
Venturi Oxygen facemask has the advantages of able to regulate FiO 2.The drawback
of mask is
interfering cough and eating.
（3）AUGMENTATION OF VENTILATION
① Respiratory Stimulants
The overall usefulness of respiratory stimulants in management of
respiratory failure is
limited. The principle of administering respiratory stimulants is under the
condition of adequate
airway patency. Respiratory stimulant might be effective in hypoventilation due to
suppression
of central nervous system, but no effect in hypoxemic respiratory failure due to
abnormal gas
exchange in the lungs, such as pneumonia and pulmonary fibrosis. The commonly used
medications are nikethamide and lobeline, although the effectiveness is limited.
Doxapram is
new generation of respiratory stimulant, which is more effective than the old one.
② Mechanical Ventilation
Mechanical ventilation is very effective therapy in improving alveolar

ventilation and
oxygenation, decreasing work of breathing and enabling respiratory muscles rest.
Mechanical
ventilation can be provided through invasive (intubation or tracheotomy) or
noninvasive
methods.
Indications for invasive mechanical ventilation vary according to the underline

disease and
clinical situations. In general, indications include (1) apnea;(2) acute
hypercapnia that is not
quickly reversed by appropriate specific therapy;(3) severe hypoxemia;(4)
progressive patient
fatigue despite appropriate treatment.
Noninvasive mechanical ventilation may also be provided via a full face mask,
nasal mask,
nasal pillow or mouthpiece etc. It has become first-line therapy in COPD patients
with
hypercapnic respiratory failure who can protect and maintain the patency of their
airway, handle
their own secretions, and tolerate the mask apparatus.
Potential complications of mechanical ventilation are numerous, including

Barotrauma
(alternatively referred to as "volutrauma"), manifested by subcutaneous emphysema,
pneumomediastinum, subpleural air cysts, pneumothorax, or systemic gas embolism,
hypotension, ventilator-associated pneumonia and airway obstruction, etc.
（4）ACTIE MANAGEMENT OF UNDERLINE DISEASE

The proper management of underline disease is crucial for the recovery of
（5）GENERAL SUPPORTIVE MANAGEMENT
Proper management of electrolytes and acid-base derangement is necessary as
hypokalemia,
hypophosphatemia and acidosis may worsen hypoventilation due to respiratory muscle
weakness. Maintenance of adequate nutrition is vital, parenteral nutrition should
be used only
when conventional enteral feeding methods are not possible. Overfeeding, especially
with
carbohydrate-rich formulas, should be avoided, because it can increase CO2

production and may
potentially worsen or induce hypercapnia in patients with limited ventilatory
reserve. Proper
monitoring of fluid balance and systemic organs function are also important in
management
Ⅱ.CHRONIC RESPIRATORY FAILURE
CAUSES
Most of the causes of respiratory failure(as mentioned above) can lead to
chronic respiratory failure. In general, chronic respiratory failure results
usually
from chronic bronchial and pulmonary diseases, such as COPD, severe
tuberculosis, interstitial pulmonary fibrosis, pneumoconiosis, etc. Other severe
chronic thoraxic and neuromuscular disorders can also result in chronic respiratory
failure.
CLINICAL PRESENTATIONS
In general, the symptoms and signs of chronic respiratory failure are similar
lo
acute respiratory failure. However, there are also some differences in clinical
characteristics in the following aspects.
① DYSPNEA
Dyspnea may exist long before the occurrence of chronic respiratory failure. A
typical
presentation of mild chronic respiratory failure resulting from COPD is strenuous
breathing with
expiratory prolongation. As the severity of chronic respiratory failure progresses,
rapid shallow
breathing develops. Bradypnoea and Cheyne-Stokes respiration are life-threatening
presentation, usually as the result of rapid progress or severe hypercaprua.
②PSYCHIATRIC AND NEURAL SYMPTONS
As hypercapnia progresses from mild to severe, the presentations turn from
excitatory to
inhibitory symptoms. The excitatory symptoms include insomnia, agitation,
restlessness, sleepy
at daytime with insomnia at nighttime, etc. It is contraindicated to use sedative
medication in
this situation as it will lead to inhibition and deterioration of hypercapnia. In
severe hypercapnia,
pulmonary narcosis may occur, presenting as impaired consciousness, confusion,
delirium,
flapping tremor and coma. Abnormal central neural reflex can occur occasionally. A
differential
diagnosis from disorders of central neural system is necessary.
③CIRCULATORY PRESENTATION
Chronic hypercapnia can lead to dilatation of veins, with manifestation of
dilatation of
peripheral veins, hyperemia of skin, diaphoresis, hypertension and increased
cardiac output.
Tachycardia is common. Pulse headache can occur as the result of dilatation of
intracranial veins.
DIAGNOSIS
The diagnosis of chronic respiratory failure is similar to that of acute

respiratory
failure. As hypercapnic respiratory failure is more common in chronic respiratory
failure, it is common to have arterial blood gas results of PaO2>60 mmHg and
PaCO2>50 mmHg in patients after oxygen therapy.
TREATMENT
The principles of treatment of chronic respiratory failure are similar to
those of acute respiratory
failure.
Oxygen therapy for chronic respiratory failure is usually administered low
oxygen flow(1 to 3
L/min or FiO2 of 24% to 32%).High FiO2 might result in deterioration of hypercapnia

. Long term
home oxygen therapy can improve the symptoms and prolong survival.
Respiratory infection is the most common trigger for acute exacerbation of
chronic respiratory
failure. So, proper monitoring and management of respiratory infection is important
for successful
management of chronic respiratory failure.
Oral respiratory stimulant of Almitrine (50mg to 100mg , twice daily ) can
increase respiratory
drive through stimulating chemoreceptors of carotid and aortic bodies. Long term
administration of
Almitrine may be beneficial to some patients although the overall efficacy is not
established yet.
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Respiratory System Disease

The First Affliated Hospital of XinJiang Medical

• To master the main symptoms, signs, laboratory

• To know the cause of respiratory disease and the

• The upper respiratory tract:Up from the nasal

{warm,moisten and filter the air}

• Right main bronchus:divided into upper,middle and

• Open system :the most frequently contact with the

• Low pressure,low resistance and high capacity system.

• The lymph and blood flow of the lung are interlinked

• Increased inhaled allergen

• The etiology characteristics of respiratory

• Laboratory and other tests

• Details of personal history, exposure history,

• Systemic rheumatic diseases;Risk factors for

• COPD,Asthma, Neoplasia, Spontaneous pneumothorax,

position of the trachea,breath sound and rales

• Examination of sputum:pathological examination

active malignant cells.

• diagnosing and therapy of massive hemoptysis.

2. Transbronchial lung biopsy (TBLB) (complications:

3. Culture of secretions.brushing and washing for

• Type I respiratory failure:hypoxic

• Type II respiratory failure:hypoxic and

• Restriction：pleurisy,chest deformity, pulmonary

• In therapy,we have formulated the guidelines for

• Progress of antibiotics and anti-tuberculosis drugs

• The use of kinds of Ventilators and monitors also

• To improve the way of life, encouraged to stop

• To strengthen the management of infectious diseases.

• The characteristics of respiratory system

• The key point is master the clinical

• A fundamental course of clinical medicine

☆ Derived from Greek words

In 18th century: Nosography

Identification of a disease by investigation of its

Clinical diagnosis Laboratory diagnosis

Laboratory tests or clinical ancillary tests

History taking--- Interview

Epidemic areas, infectious diseases

Subjective sensation that patient describes,

Fever Cough Rash Mass

Specific requirement in terms of format

• Exclusion of other diseases

• Selecting a number of possibilities to explain the

• The way of exclusion is called Differential diagnosis

It means integrating individual clinical expertise

• Look for current best evidence: the perfect study

• To get the history in detail of a patient’s illness

• The number of facts that can be collected in a

• The laboratory tests or specialized technical

• Method of approaching a diagnosis:

Basic knowledge learning

• Western Medicine: from ancient to modern

• Traditional Chinese Medicine

•Born on the island of Cos,

•The Father of medicine

•Born at the village of Graz, Austria (1722)

Good medical ethics

Attach importance to clinical practice

Unit theory with practice

Department of General Surgery