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 physical Lam’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 ?????????? 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 • • • • • • • 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 • 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 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 • 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 • • • • 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 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 • • • • 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 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 • • 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 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? • 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 • 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 • • • • • 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 TRANSUDATE Protein/ 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 Clinical presentation • • • • • 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 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 • THE END