Download - Pulmonary Diseases by: Eddie K. Lam M.D.. RESPIRTORY DISEASES COUGH COPD ASTHMA CHRONIC BRONCHITIS EMPHYSEMA TUBERCULOSIS PULMONARY NODULES ALPHA 1 ANTITRYPSIN.

Pulmonary Diseases

by:

Eddie K. Lam M.D.

RESPIRTORY DISEASES• 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

• Smoking• Medications• Asthma• GERD• Upper airway cough syndrome• Nonasthmatic eosinophilic bronchitis• Cancer• Atypical infection

History and physicalLam’s criteria for cough

• Smoking • Throat irritation• Ups or downs• Productive• Itching • Duration• Nasal drip, congestion• Eating• Position• Hemoptysis• E• Weight loss

Physical exam

• 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

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Differential diagnosis

• 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

• 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• 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

• Spirometry is the key test• CXR• CT chest• EKG• CBC• Pulse oximetry•

pharmacotherapy

• 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

• 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

• 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

• 80% gram positive and gram negative bacteria• Nosocomial• 30% viruses• 5-10% atypical bacteria

Treatment other than bronchodilators

• Antibiotics• Smoking cessation• Pulmonary Rehabilitation• Oxygen therapy: PaO2 < 55mmHg or O2 sat <

88%• Long term use increase survival

COPD ASTHMA

• AGE >40• 10 pk yrs• Sputum often• Allergies infreq.• Progressive worse• Clinical Sx. Persistent• Airflow partial reversible

• <40

• Usually none/min

• Infrequent

• Often

• Nonprogressive

• Variable

• Complete reversible

• ASTHMA

ASTHMA

• Underlying cause of 40% young adults being evaluated for dyspnea

• Pulmonary testing plays a major role

Common risk factors for asthma – host factors

• 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

• Exposure to common allergens• Cold weather• Viral infections• Physical exercise

Physical exam

• 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

• 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 challengebronchoprovocation 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

• CHRONIC BRONCHITIS

CHRONIC BROCHITISsmoke 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


History of cough and sputum production for years

Cough in winter monthsExertional dyspneaPeripheral 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

• 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

• Bronchodilators• Corticosteroids• Antibiotics • Mucolytics• Oxygen

• EMPHYSEMA

EMPHYSEMAsmoke 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

• Flattening of diaphragm• Hyperinflation• Enlargement of central pulm arteries• Bullae

Clinical presentation of Emphysema

• 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

• 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

• 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

• 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:

• 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

• 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

• 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:

• 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 factorsNodules 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

• 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

• 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• 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

• 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 PPPPMcommon 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?• Pnemothorx?• Cardiomegaly?• 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

• 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

• Malignancy

• Parapneumonic effusion

• Hepatic hydrothorax

• Increased hydrostatic pressure of vessels

• Decreased oncotic pressure• Obstruction of lymphatics• Increased capillary

permeability

• Increased peritoneal fluid

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


• 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

• EXUDATE• Parapneumonic• Empyema• TB• Malignancy• RA / lupus• Chylothorax

• TRANSUDATE• CHF• Cirrhosis• Atelectesis• Nephrotic

syndrome• PE

EXUDATE TRANSUDATEProtein/ LDH

• WBC > 1000/ differential• Neutrophils= bacterial• Lymphocytes = TB,CA• Gram stains• Glucose < 60• ANA• Amylase• Triglycerides

• WBC <100• Protein PF/SER < 0.5• LDH PF/SER < 0.6• LDH/PF > 2/3 of serum

LDH

Treatment

• 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

• 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

• Asthma, COPD• Interstitial lung diseases• Pneumocystis carinii pneumonia• Marfan’s syndrome

Clinical presentation of spontaneous pneumothorax

• 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

• Catheter• Chest tube• Surgery• pleurodesis

• 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

• 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


• 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• 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

• 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

• 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• • 0-1 low

• 2-6 intermediate

• 7> high

Management of VTE

• 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 DVTPost 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

• THE END