Transcript Pulmonary Diseases

Pulmonary Diseases
by:
Eddie K. Lam M.D.
RESPIRTORY DISEASES
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COUGH
COPD
ASTHMA
CHRONIC BRONCHITIS
EMPHYSEMA
TUBERCULOSIS
PULMONARY NODULES
ALPHA 1 ANTITRYPSIN DEFICIENCY
PLEURISY
PLEURAL EFFUSION
PNEUMOTHORAX
VENOUS THROMBOLISM
COUGH
• Acute cough ( last < 3 weeks)
• Subacute (3 to 8 weeks)
• Chronic ( longer than 8 weeks)
Acute cough
• Most commonly associated with common cold
• Differentiate between serious condition such
as pulmonary embolism, CHF, pneumonia,
asthma, COPD,
• Antihistamine or decongestant should be
prescribed
Subacute cough
• Is the cough follow a respiratory infection
• Cough began with URI and lingered indicate
postinfectious cough
• Postnasal drip, upper airway irritation, mucus
accumulation, airway spasm
Chronic cough
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Smoking
Medications
Asthma
GERD
Upper airway cough syndrome
Nonasthmatic eosinophilic bronchitis
Cancer
Atypical infection
History and physical
Lam’s criteria for cough
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Smoking
Throat irritation
Ups or downs
Productive
Itching
Duration
Nasal drip, congestion
Eating
Position
Hemoptysis
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Weight loss
Physical exam
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HEENT
Chest, heart
Lymph nodes
Skins/fingers
Chest x ray
• Reasonable as baseline if cough persists more
than 3 weeks
• Suspect pneumonia
• Weight loss
• Hemoptysis
• Nightsweats
Treatment of cough
• URI- 1st generation antihistamine +
decongestant
• Upper airway- inhaled nasal steroids
• Bacterial- appropriate antibiotics +
suppressants
• Codeine Vs DM
• Brochospasm- Anticholinergic agents
• Drug induced- Discontinue ACE inhibitors
treatment cont.
• Inhaled corticosteroids
• Oral corticosteroids
If all treatment failed
• No way
• Suspect noncompliance
• Suspect other causes: GERD, swallowing
disorder
• Consider bronchoprovocation test
• ? CT
• Refer to specialist
COPD
– CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Chronic obstructive pulmonary
disease
Definition: an inflammatory respiratory
disease, mostly by tobacco smoke
Exposure to cigarette smoking, airway
inflammation, airflow obstruction that
is not fully reversible
COPD
• Chronic bronchitis and emphysema are no
longer included in the definition of COPD,
though still used clinically
• Asthma is the most often confused with COPD
Risk factors
• Cigarette smoking
• Persons who smoke, 12-13 times likely to die from
COPD
• 2nd hand smoke
• Advancing age
• Environmental or occupational pollutants
• Alpha 1 antitrypsin deficiency
• Family history of COPD
Occupational exposures
• Mineral dust: coal mining, tunnel work,
concrete, silica exposure
• Organic dust: Cotton, flax,
• Noxious gas: Sulfur dioxide, isocyanates, heavy
metal, welding fumes
pathophysiology
• Chronic airway irritation
• Mucus production > decreased mucociliary
function
• Pulmonary scarring/airway scarring
• Leads to hallmark of COPD Sx.> coughing and
sputum production >
• Progressive airway obstruction and dyspnea
• COPD is more common and fatal in women
than men
• Lung size
• More hyperresponsive to irritants
Clinical history
• Hallmark Symptoms
• Cough, increased sputum production, dyspnea
(good predictor of mortality)
• Less common : edema, chest tightness, weight
loss, nocturnal awakenings
Differential diagnosis
??????????
Differential diagnosis
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Asthma
CHF
Bronchiectasis
Lung cancer
Interstitial lung disease/fibrosis
TB
Clinical history
• Patient and family history
• History of tobacco use
• Pack years = number of packs smoked per day
multiplied by number of years smoked
• Occupational history
• Job activities
• Family history of Alpha 1 antitrypsin
deficiency, genetic anomaly of chromosome
14 leads to premature hepatic and pulmonary
disease
• Increase tissue damage from neutrophil
elastase> alveolar damage> loss of elastic
recoil> airway obstruction
Alpha 1 antitrypsin deficiciency
• 59,000 Americans have Sx. COPD caused by
alpha 1 antitrypsin deficiency
• Screening in symptomatic adults with
persistent obstruction on pulmonary function
test
Physical exam
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Not sensitive initially
Lung hyperinflation
Widened A-P chest diameter
Hyperresonance on percussion
Cor pulmonale- peripheral edema, JVD,
hepatomegaly
• Cyanosis, cachexia
• Clubbing (rare), looking for cancer,fibrosis,
brochectasis
Diagnostic testing
• SPIROMETRY
• Should perform in all smokers 45years or older
• Key features: FEV1
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FVC ( forced vital capacity)
• FEV1 – the volume of air patient can expire in
one second following full inspiration
• FVC -- total maximum volume of air patient
can exhale after a full inspiration
Diagnosis of COPD
• Postbronchodilator FEV1/FVC ratio of less
than 0.7 associated with FEV1 less than 80%
of predicted value is diagnostic of airflow
limitation and confirms COPD
• Peak expiratory flow rates are not helpful in
diagnosis of COPD
Other diagnostic test
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Spirometry is the key test
CXR
CT chest
EKG
CBC
Pulse oximetry
pharmacotherapy
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Bronchodilator
Bronchodilator
Bronchodilator
Bronchodilator
Bronchodilator
bronchodilator
Short acting beta 2 agonists
• Beta 2 agonists: stimulate beta 2 receptors,
increase cyclic AMP, increase smooth muscle
relaxation, lung emptying and air trapping
• Short acting: Proventil, Ventolin, Proair,
Xopenex
• Side effects: Tachycardia, cardiac disturbance,
tremors
Long acting beta 2 agonists
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Maintenance therapy
Longer lasting improvement
Salmeterol (Serevent Diskus)
Formoterl (Foradil)
Short acting Anticholinergic agents
• Smooth muscle relaxation of airways
• Antagonism of acetycholine at M3 receptors
on airway
• Slower onset of action than beta 2 but longer
duration
• Side effects: Caution w/ glaucoma, BPH
• Ipratropium (Atrovent)
Long acting Anticholinergic agents
• Sustained action over 24 hours
• Tiotropium (Spiriva)
• 24% lower of number exacerbation than
Ipratropium
Corticosteroids
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Act at multiple points in inflammatory process
Increase FEV1
NOT APPROVED FOR SINGLE USE AGENT IN COPD
Recommend as addition to maintenance therapy
Side effects: bruising, candidiasis, voice alteration
Combination therapies
• Beta 2 + anticholinergic agent (Combivent)
• Corticosteroid + long acting Beta 2 (Advair)
(Symbicort)
Acute exacerbation of COPD
• Sustained worsening of patient’s condition
from stable state and beyond normal day to
day variations, that is acute in onset and
necessitates a change in regular medication in
a patient with underlying COPD
Infectious agents
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80% gram positive and gram negative bacteria
Nosocomial
30% viruses
5-10% atypical bacteria
Treatment other than bronchodilators
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Antibiotics
Smoking cessation
Pulmonary Rehabilitation
Oxygen therapy: PaO2 < 55mmHg or O2 sat <
88%
• Long term use increase survival
COPD
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AGE >40
10 pk yrs
Sputum often
Allergies infreq.
Progressive worse
Clinical Sx. Persistent
Airflow partial
reversible
ASTHMA
• <40
• Usually none/min
• Infrequent
• Often
• Nonprogressive
• Variable
• Complete reversible
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ASTHMA
ASTHMA
• Underlying cause of 40% young adults being
evaluated for dyspnea
• Pulmonary testing plays a major role
Common risk factors for asthma – host
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Genetic
Female sex
Low birth weight
Obesity
Atopy/allergies
eczema
Environmental factors
• Prenatal and childhood exposure to tobacco
smoke
• Lack of breast feeding
• Severe respiratory infections in 1st year of life
• Indoor allergens and outdoor pollutants
• Occupational exposures
Clinical presentation
• Waxing and waning symptoms of dyspnea,
cough, wheezing and chest tightness
• Exacerbation of symptoms usually gradual in
onset and cessation
Triggers
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Exposure to common allergens
Cold weather
Viral infections
Physical exercise
Physical exam
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Frequently normal
Stigmata of allergic rhinitis
Eczema
Airflow obstruction/wheezing (poor predictor
value)
Laboratory tests
• CXR
• Pulse oximetry
• CBC
Spiromery
• NAEPP (National Asthma Education and Preventive
Program) recommends using spirometry for initial
diagnosis and long term follow up of Asthma
• Perform at initial assessment
• After treatment initiated
• Stabilized and during period of prolonged loss of
asthma control and at least every 1 to 2 yrs
Interpretation of airflow obstruction
• FEV1/FVC <70%
• FEV6 is an option
Peak expiratory flow
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Not equivalent to Spirometry
Effective screening tool
More variable
Good to know the baseline
Good to monitor for symptoms
Peak expiratory flow
• Personal best peak flow is the highest PEF
number one can achieve over a 2 to 3 week
period when the asthma is under control
Peak expiratory flow monitoring
• Measure upon awakening and between noon
and 2pm
• Measure before and after take beta agonists
• Monitor for symptoms control
Peak flow zone system
• Green zone- 80% of personal best signal good
control
• Yellow zone- 50-80%, must take short acting
inhaled beta 2 agonists right away. See MD
• Red zone- below 50% of personal best, take
agonists and see MD or ER
Reversible airway
• Spirometry performed before and after
bronchodilator
• Reversible airway obstruction- an increase of
at least 12% and 200ml in either FVC or FEV1
after administration of a short acting
bronchodilator
Methacholine challenge
bronchoprovocation challenge
• Considered only when spirometric findings are
normal in whom asthma is still suspected
• Methacholine (acetyl beta methylcholine
chloride) is the cholinergic agent
Methacholine
• Inhalation of up to 5 or 10 sequentially
increasing concentrations and the
measurement of FEV1 and symptoms of each
dose
• Fall in FEV1 of more than 20% from baseline
• Evidence of airway hyperresponsiveness
Pharmacotherapies
• Brochodilators
• Beta 2 agonists short acting
• Regular use should alarm physician that
patient is poorly controlled
Pharmacotherapies cont.
• Corticosteroids
• ICS mainstay of therapy in difficult control
asthma
• Should be give to all patients first
• Most effective
• Oral prednisone (1-5mg) for difficult patients
Cont.
• Long acting beta 2 agonists (LABAs)
• Indicated for use as corticosteroid –sparing
agents
• Adjunct on ICS
• Preferred add-on therapy to ICS
Cont.
• Leukotriene inhibitors (Montelukast)
(Zafirlukast)
• Blocking inflammatory effects of leukotrienes
• Methylxanthines (theophylline,
Aminophylline) outdated
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CHRONIC BRONCHITIS
CHRONIC BROCHITIS
smoke related diseases
• Chronic mucus hypersecretion syndrome
• Defined as production of sputum for 3 or
more months per year for 2 consecutive years
• With obstructive ventilatory defect
Pathophysiology of C.B.
• Hyperplasia of airway mucous glands and
goblet cells
• Mucous plugging, thickening, tortuosity and
fibrosis of airways
Clinical presentation
History of cough and sputum production for
years
Cough in winter months
Exertional dyspnea
Peripheral edema secondary to right ventricular
failure
Physical exam of C.B.
• Overweight and cyanotic
• Chest percussion is normal resonant
• Coarse rhonchi and wheezes, change in
location and intensity
• Sustained heave at LLSB for RVH
Blue bloaters-chronic bronchitis
• Alveolar hypoxia, acidemia and hypercapnia
• Pulmonary hypertension by pulmonary
vasocostriction
• Hypoxia
• Lower O2 desaturate Hemoglobin
• Desaturation and erythrocytosis combine to produce
cyanosis
• Accentuates right-sided heart failure
Chest X ray of CB
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Hyperinflation
Peribronchial markings at lung bases
Thickening of airway walls
Right ventricle enlargement
Acute exacerbations of Chronic
Bronchitis
• Part of the clinical spectrum
• Viral or Bacterial causes
• H.influenzae esp. in smokers, M.catarrhalis,
S.pneumoniae, Pseudomonas
Diagnosis of AECB
• Clinical presentations
• CXR, ABG
Treatment of AECB
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Bronchodilators
Corticosteroids
Antibiotics
Mucolytics
Oxygen
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EMPHYSEMA
EMPHYSEMA
smoke related diseases
• Definition based on anatomy
• Progressive destruction of alveolar septa and
capillaries
• Airspace enlargement and macroscopic bullae
Pathophysiology of Emphysema
• Reduced elastic recoil of lung (increased
compliance)
• Slowing of max. expiratory airflow (decreased
FEV1)
• Hyperinflation
• Decreased alveolar gas exchange
CXR for Emphysema
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Flattening of diaphragm
Hyperinflation
Enlargement of central pulm arteries
Bullae
Clinical presentation of Emphysema
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Exertional dyspnea with minimal cough
Asthenic body with evidence of weight loss
Accessory muscle of respiration
Prolonged expiration with grunting sound
Patients lean forward, extending arm to brace themselves
Physical exam of Emphysema
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Increased A-P diameter of thorax- barrel chest
Percussion note is hyperresonant
Breath sounds are diminished
Faint high pitched rhonchi heard at end of
expiration
Pink puffers- Emphysema
• Arterial O2 in mid 70’s and Pco2 is low to
normal
• Able to maintain arterial O2 sufficient to
nearly saturate hemoglobin
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TUBERCULOSIS
TUBERCULOSIS
• 11 million persons in U.S. latently infected
with Mycobacterium TB
• Most cases occur in foreign born persons from
endemic countries
• Economically disadvantaged
• Immunosuppressive conditions (11% HIV)
• 13,293 active cases in 2007
Diagnostic test
• Tuberculin skin test (TST)
• Referred as Mantoux or Purified protein
derivative test (PPD)
• Positive test: look for INDURATION, not
redness
5 mm TST
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5mm positive:
HIV
Recent TB exposure
CXR c/w old TB
Organ transplant
15mg/day of prednisone > 1month
10 mm TST
• Recent ( <2 yrs.) skin test conversion
• IVDA, DM, Heme, Head and Neck CA,
Weight loss to 10% less than IBW
• Member of high incidence group:
• Immigrants from high-incidence area
• Underserved population and Long term
care facility
15 mm TST
• If you live in:
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BOISE, IDAHO
False positive test
• Nontuberculosis M.TB
• Bacille Calmette-Guerin (BCG) vaccine
• Subjective interpretation
• U.S. guidelines do not include BCG vaccination
history in TST interpretation
Diagnosis of M. TB
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Thorough history and physical
CXR
Sputum Smear
Sputum antigen-specific interferon gamma release
assay
• Nucleic acid amplification
• Sputum or other tissue culture
• Tissue biopsy
Latent Tuberculosis
• 11 million persons in U.S.
• Lifetime risk reactivation 5-10%
• Isoniazid monotherapy X 9 months diminishes
rate of reactivation
• Effectiveness 90% for compliant patients
• 4 months of rifampin alternative, less
hepatotoxity, but drug interaction and resist.
Latent TB, cont.
• Isoniazid-associated hepatotoxity is 0.1 to 1%
• Risk increases with chronic liver disease,
ETOH, Viral hepatitis and older age
Populations at risk of reactivation
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Young children
Untreated or suboptimal treated TB
Immunosuppressed
Patients taking TNF-alpha inhibitors
(Rheumatoid patients)
Active Tuberculosis
• COMBINATION THERAPY IS THE CORNER
STONE
Two stages
treatment
of M.TB
• Intensive phase:
• Four drugs: INH, Rifampin, Pyrazinamide (PZA)
and ethambutol (Myambutol)
• Duration: 2 months
cont.
• Continuation phase:
• INH, Rifamycin daily for 4 to 7 months
Drug resistance of TB
• Extensive replication of up to 10 to the 8th fold
tubercles in some cavitary lesions produce primary
drug resistance
• Inappropriate drug therapy, (too few drugs,
subtherapeutic drug concentrations, inappropriate
drug selection and modification)
• Poor patient compliance
• Average cost of treatment: $250,000
Definition of D. R.
• Strains resistant to INH and Rifampin, with
additional resistance to fluoroquinolones and
at least one injectable agent, Amikacin
• Requires 18 to 24 months therapy
Case study
• 82 year old male with COPD, Oxygen
dependent, presented with Cough, low grade
fever and hypoxia, O2 satuation at office was
85%. Patient was admitted.
Pearls of the case
• ANSWER:
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PULMONARY NODULES
PULMONARY NODULES
• Defined as single pulmonary lesion with normal
surrounding lung parenchyma
• Nodule < 3cm
• Mass > 3cm
• Can be malignant or benign
• Up to 51% of people screened with CT found to have
at least one lung nodule
Pulmonary nodules
• Most small, incidental nodules are benign
• Need to be addressed once found
• Follow up with serial CT imaging
recommended
Common causes of solitary pulmonary
nodules
• Benign- infection (granuloma, abscess),
inflammation, AV malformation, cyst, mucoid
impaction
• Malignant- carcinoma, metastasis, lymphoma,
carcinoid, sarcoma
Follow up depends on size, risk factors
Nodules 4 mm or smaller
• Very low risk of malignancy
• Patients with risk factors (hx of smoking or
cancer) should have another CT 12 months
• Biopsy if increased in size
4 mm to 6 mm nodules
• Low risk of malignancy (0.9%)
• Low risk patients, follow up CT 12 months
• Risk factors patients, follow up 6 to 12months,
again at 18 to 24months
6 mm to 8 mm nodules
• Intermediate risk of malignancy (6%)
• Low risk patients, 6-12 months, again at 18-24
months
• Risk factors patients, 3-6 months, again 9 to 12
months, again in 24 months if no change in size
• Any increased in size warrants biopsy
> 8 mm nodules
• Worrisome (18% malignancy)
• Follow aggressively in 3 months or sent for
biopsy
• Regardless of risk factors
• Consider PET or biopsy
Clues to diagnosis malignancy
• CT appearance- calcification, edge
characteristics, growth rate, popcorn
appearance
• Enhanced CT and positron-emission
tomography
• Biopsy
Lung Cancer Screening
• No guidelines recommend in favor of routine CT
screening for lung cancer
• Screening may not reduce deaths from lung cancer
• No decline in number of advanced cases diagnosed
or deaths from lung cancer
• No relationship between tumor size and survival
Take-home points
• CT screening will uncover many benign nodules likely
to receive intensive follow up
• Lung nodules 8 mm in diameter or smaller are likely
benign
• Traditional nodule characteristics predict malignancy
are less useful with very small nodules
Take-home points
• Surveillance with serial chest CT is
recommended once they are found
• No guidelines from any professional
organization recommend in favor of routine
CT screening for lung cancer
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ALPHA 1 ANTITRYPSIN
DEFICIENCY
Alpha-1 antitrypsin deficiency
• Autosomal codominant condition
• Predisposes to emphysema and liver disease
• 100,000 Americans are severely deficient
Alleles antitrypsin activity
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M-normal
S-intermediate
Z-marked decrease
Null-absent (rare)
Phenotypes of antitrypsin
deficiency
• MM, MS, MZ, no increased risk
• SZ, mild increased risk
• ZZ, most common severe deficient variant,
accounting more than 90% of people with
severe alpha-1 antitrypsin deficiency (single
amino acid substitution of the protein)
ZZ phenotype
• Associated with emphysema and 10% of chronic liver
diseases
• Liver disease (neonatal jaundice to cirrhosis to
hepatoma)
• Panniculitis (inflammatory disease of subcutaneous
tissue with ulcerating and painful skin lesions)
• Vasculitis positive for C-ANCA
Clinical presentations
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No different than COPD or cirrhosis
On set of airflow obstruction before 50
Family history of liver or lung disease
Emphysema occurring in nonsmoker or very light
smoker
• Persistent or worsening Sx despite treatment
• Basilar hyperlucency >> than apical
Testing for alpha-1 antitrypsin
deficiency
• Very inexpensive
• Serum alpha- antitrypsin level
• If below 100mg/dl, phenotyping
Why is it important?
• Mean duration between first symptom and
initial diagnosis was 8.4 years
• Mean number of physicians seen between
first Sx and diagnosis was 4 physicians
Treatment
• Smoking cessation
• Genetic counseling
• Augmentation therapy with recombinant
alpha-1 antitrypsin inhibitors
PLEURISY AND PLEURAL EFFUSION
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PLEURISY
Pleurisy
• Inflammation of the parietal pleura that
results in characteristic pleuritc pain with
variety of causes
• Pleuritic pain is the key feature
Pathophysiology of pleurisy
• Visceral pleura has no nociceptors or pain
receptors
• Parietal pleura innervated by somatic nerves
that sense pain
• Inflammation extend to pleural space involve
parietal pleura, thus resulting pain
Pathophysiology
• Parietal pleurae of the outer rib cage and lateral
aspect of each hemidiaphragm innnervated by
intercostal nerves
• Phrenic nerve innervate central part of each
hemidiaphragm
• When fibers are activated, sensation of pain is
referred to ipsilateral neck or shoulder
Differential diagnosis of pleurisy
(ppppm)
• Patient presented with pleuritc chest pain,
need to rule out:
• Pulmonary embolism
• Pneumothorax
• Pericarditis
• Pneumonia
• MI
Once ruled out PPPPM
common causes of pleurisy
• Viruses (most common): influenza, parainfluenza,
coxsakieviruses, RSV viruses mumps, EBV
• Bacterial, TB
• Renal: CRF,
• Rheumatologic: Lupus, RA, Sjogren
• Cardiac: post cardiac injury, post MI (dressler’s), post
pericadiotomy
• Asbestosis
• Malignancy, sickle cell
Presentation of pleurisy
• Pleuritic pain localized to area of inflammation
or referred pathway
• Exacerbates with breathing, talking, coughing
or sneezing
• Sharp pain worsened with movement
• Limits motion
Evaluation of pleurisy
• History and physical exam
• Chest X ray
• If abnormal >>Pneumonia?
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Pnemothorx?
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Cardiomegaly?
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P.E. ?
Evaluation of pleurisy
• If CXR is normal >> MI, Pulm embolism?
• EKG abnormal >> MI, PE, Pericarditis
• EKG normal, no suggestion of PE, MI, look for
other causes, Viral
Physical exam of pleurisy
• Friction rub with inspiration or expiration
• Due to surfaces between parietal and visceral
pleurae rub against one another with inflammation
• Decreased breath sounds, rales
• Normal physical with serious condition
• High index of suspicion
Diagnostic tests
• Chest X ray for pleural effusion, pneumonia,
pulmonary embolism, pneumothorax
• EKG for MI, pulmonary embolism, pericarditis
Treatment of Pleurisy
• Control pleuritic chest pain
• Treat underlying condition
• NSAIDS do not suppress respiratory efforts or
cough reflex
• Limited to Indomethacin
• Steroids are controversial
PLEURAL EFFUSIONS
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Most common causes are:
Congestive heart failure
Pneumonia
Malignancy
Pulmonary embolism
Pathophysiology of Pleural
effusions
• Pleural fluid originates in capillaries of parietal
pleura and drained by lymphatics
• More fluid formed > absorbed
• Pleural fluid can originate from interstitial lung
spaces, lymphatics and peritoneal cavity
Pathophysiology of pleural
effusions
• Congestive heart failure
• Nephrotic syndrome
• Increased hydrostatic pressure
of vessels
• Parapneumonic effusion
• Decreased oncotic pressure
• Obstruction of lymphatics
• Increased capillary
permeability
• Hepatic hydrothorax
• Increased peritoneal fluid
• Malignancy
Subpulmonic effusions
• When fluid becomes loculated between lower
aspect of lung and diaphragm
Parapneumonic effusions
• Pleural effusions associated with bacterial
pneumonia
Empyema
• Pleural effusions associated with lung abscess
• Carry higher mortality than pneumonia and
abscess without effusions
Clinical presentation
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Differ according to etiology
Asymptomatic
Dyspnea, pleuritc chest pain
Nonproductive cough
Fever
Physical exam
• Dullness on percussion
• Decreased or absent breath sounds
• Decreased tactile fremitus
Diagnosis and evaluation
• Chest X ray- PA and lateral
• Blunting of posterior costophrenic angle
• Elevated hemidiaphragm- suspect subpulmonic
effusion
• Ultrasound useful to identify loculated fluid
• CT scan
• Thoracentesis
THORACENTESIS
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EXUDATE
Parapneumonic
Empyema
TB
Malignancy
RA / lupus
Chylothorax
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TRANSUDATE
CHF
Cirrhosis
Atelectesis
Nephrotic syndrome
PE
EXUDATE TRANSUDATE
Protein/ LDH
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WBC > 1000/ differential
Neutrophils= bacterial
Lymphocytes = TB,CA
Gram stains
Glucose < 60
ANA
Amylase
Triglycerides
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WBC <100
Protein PF/SER < 0.5
LDH PF/SER < 0.6
LDH/PF > 2/3 of serum
LDH
Treatment
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Treat underlying conditions
Therapeutic thoracentesis
Chest tube drainage
Thoractomy with decortication
Pleurodesis (fusion of visceral and parietal
pleural to prevent recurrence of effusion)
PNEUMOTHORAX
• Introduction of air into pleural space
• Spontaneous or trauma or iatrogenic
Spontaneous pneumothorax
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No clinically apparent diseases
Men > women
Tall, thin male under 40 smokes or not
Radiographically inapparent subpleural bullae
May be associated physical activities
Secondary spontaneous
pneumothorax
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Asthma, COPD
Interstitial lung diseases
Pneumocystis carinii pneumonia
Marfan’s syndrome
Clinical presentation of spontaneous
pneumothorax
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Ipsilateral pleuritc chest pain
Dyspnea
Tachycardia
Shift of trachea by exam
Hyperresonance to percussion
Decrease breath sounds
Hypotension
Diagnosis Peumothorax
• Chest X ray
• Chest CT for bullae
Treatment of pneumothorax
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Catheter
Chest tube
Surgery
pleurodesis
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VENOUS THROMBOEMBOLIC
DISEASES
VENOUS THROMBOEMBOLIC
DISEASE
• Deep Vein Thrombosis
• Pulmonary Embolism
Deep venous thrombosis (DVT)
• Venous stasis from immobility
• Virchow’s triad
– Venous stasis
– Vessel wall damage
– Increased blood coagulability
Clinical risk factors
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Recent surgery
Major trauma
Previous DVT
Increasing age
Pregnancy, postpartum
Oral contraception/smoke
Immobility
Connective tissue disease
Familial thrombophilic disease
• Activated protein C resistance (factor V
leiden),defect in factor V
• Prothrombin 20210A, gene defect with
increased prothrombin and thrombin
• Protein C and S deficiency
• Antithrombin III deficiency
Clinical presentation
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Leg pain and swelling
Homan’s sign, less than 40%
Calf to thigh swelling and tenderness
Most are asymptomatic
BE ALERT
Complication of DVT
• Pulmonary Embolism
• Thigh/Proximal DVT associated with PE
• 70-90% of patients with symptomatic PE have
silent thigh DVT
Diagnosis
Clinical prediction rules
• WELLS PREDICTION RULES
• Establish the pretest probability of VTE
• Estimate the probability of DVT and PE before
performing and interpreting other diagnostic
tests
• Best applied to younger patient without other
comorbidities
D-Dimer Assay
• Most often ordered by ER physicians
• Enzyme linked immunosorbent assay (ELISA)
• Negative D-Dimer in younger patients whose
pretest probability is low excludes VTE
• In older patients with comorbidities and long
duration of Sx, D-Dimer not enough
Ultrasonography
• High Specificity and sensitivity for
diagnosing proximal DVT of LE for those
who are symptomatic
• Recommended for patients who are at
intermediate and high risk for DVT
• Should be repeated if suspected case
where initial test is negative
• Contrast venography is the definite test
Helical computed tomography (CT)
• Higher specificity and sensitivity compared
with pulm arteriography for PE
• VQ scan for those with high pretest probability
Wells prediction rule for DVT
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Alternative diagnosis as likely as DVT -2
Active cancer
1
Calf swelling 3cm > asymptomatic side 1
Collateral superficial vein
1
Paralysis, paresis or recent plaster cast 1
Pitting edema on symptomatic leg
1
Recent bedridden >3days/major surgery within 12 weeks
1
• Swollen leg
1
Wells prediction rule for DVT
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Clinical probability of DVT is
Low if score 0 or less
Intermediate 1 or 2
High if
3 or more
Wells prediction rule for PE
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Cancer
1
Hemoptysis
1
HR > 100bpm
1.5
Previous PE or DVT
1.5
Recent surgery/immobil 1.5
Alternative Dx less likely 3
Clinical signs of DVT 3
Wells prediction of PE
• Probability of PE if score
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• 0-1
low
• 2-6
intermediate
• 7>
high
Management of VTE
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Low-molecular-weight Heparin (LMWH)
Superior than unfractionated heparin for DVT
For PE, either LMWH or heparin
Less risk of major bleeding
Recommended for initial inpatient and
outpatient management of VTE
Oral anticoagulation
• Coumadin (Warfarin)
• Maintained for three to six months for
patients with VTE due to transient risk factors
• For recurrent DVT, 12 months therapy
• LMWH for those with difficult to control INR
(international normalized ratio)
Complication of DVT
Post thrombotic syndrome
• Chronic postural dependent pain and edema
or localized discomfort, in the context of a
history of DVT
Complication of DVT
• POST-THROMBOTIC SYNDROME
• Wear over the counter or custom-fit
compression stockings
• Initiated within one month of DVT
• Use at least one year
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THE END