168
Pulmonary Diseases by: Eddie K. Lam M.D.
Pulmonary Diseases
by:
Eddie K. Lam M.D.
RESPIRTORY DISEASESCOUGHCOPDASTHMACHRONIC BRONCHITISEMPHYSEMATUBERCULOSISPULMONARY NODULESALPHA 1 ANTITRYPSIN DEFICIENCYPLEURISYPLEURAL EFFUSIONPNEUMOTHORAXVENOUS THROMBOLISM
COUGHAcute cough ( last < 3 weeks)Subacute (3 to 8 weeks)Chronic ( longer than 8 weeks)
Acute coughMost commonly associated with common coldDifferentiate between serious condition such as pulmonary embolism, CHF, pneumonia, asthma, COPD, Antihistamine or decongestant should be prescribed
Subacute coughIs the cough follow a respiratory infectionCough began with URI and lingered indicate postinfectious coughPostnasal drip, upper airway irritation, mucus accumulation, airway spasm
Chronic coughSmokingMedicationsAsthmaGERDUpper airway cough syndromeNonasthmatic eosinophilic bronchitisCancerAtypical infection
History and physicalLams criteria for cough
Smoking Throat irritationUps or downsProductiveItching DurationNasal drip, congestionEatingPositionHemoptysisEWeight loss
Physical examHEENTChest, heartLymph nodesSkins/fingers
Chest x rayReasonable as baseline if cough persists more than 3 weeksSuspect pneumoniaWeight lossHemoptysisNightsweats
Treatment of coughURI- 1st generation antihistamine + decongestantUpper airway- inhaled nasal steroidsBacterial- appropriate antibiotics + suppressantsCodeine Vs DMBrochospasm- Anticholinergic agentsDrug induced- Discontinue ACE inhibitors
treatment cont.Inhaled corticosteroidsOral corticosteroids
If all treatment failedNo waySuspect noncomplianceSuspect other causes: GERD, swallowing disorderConsider bronchoprovocation test? CTRefer to specialist
COPD
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Chronic obstructive pulmonary diseaseDefinition: an inflammatory respiratory disease, mostly by tobacco smokeExposure to cigarette smoking, airway inflammation, airflow obstruction that is not fully reversible
COPDChronic bronchitis and emphysema are no longer included in the definition of COPD, though still used clinicallyAsthma is the most often confused with COPD
Risk factorsCigarette smokingPersons who smoke, 12-13 times likely to die from COPD2nd hand smokeAdvancing ageEnvironmental or occupational pollutantsAlpha 1 antitrypsin deficiencyFamily history of COPD
Occupational exposuresMineral dust: coal mining, tunnel work, concrete, silica exposureOrganic dust: Cotton, flax, Noxious gas: Sulfur dioxide, isocyanates, heavy metal, welding fumes
pathophysiologyChronic airway irritationMucus production > decreased mucociliary functionPulmonary scarring/airway scarringLeads to hallmark of COPD Sx.> coughing and sputum production >Progressive airway obstruction and dyspnea
COPD is more common and fatal in women than menLung sizeMore hyperresponsive to irritants
Clinical historyHallmark SymptomsCough, increased sputum production, dyspnea (good predictor of mortality)Less common : edema, chest tightness, weight loss, nocturnal awakenings
Differential diagnosis??????????
Differential diagnosisAsthmaCHFBronchiectasisLung cancerInterstitial lung disease/fibrosisTB
Clinical historyPatient and family historyHistory of tobacco usePack years = number of packs smoked per day multiplied by number of years smokedOccupational historyJob activities
Family history of Alpha 1 antitrypsin deficiency, genetic anomaly of chromosome 14 leads to premature hepatic and pulmonary diseaseIncrease tissue damage from neutrophil elastase> alveolar damage> loss of elastic recoil> airway obstruction
Alpha 1 antitrypsin deficiciency59,000 Americans have Sx. COPD caused by alpha 1 antitrypsin deficiencyScreening in symptomatic adults with persistent obstruction on pulmonary function test
Physical examNot sensitive initiallyLung hyperinflationWidened A-P chest diameterHyperresonance on percussionCor pulmonale- peripheral edema, JVD, hepatomegalyCyanosis, cachexiaClubbing (rare), looking for cancer,fibrosis, brochectasis
Diagnostic testingSPIROMETRYShould perform in all smokers 45years or olderKey features: FEV1 FVC ( forced vital capacity)
FEV1 the volume of air patient can expire in one second following full inspirationFVC -- total maximum volume of air patient can exhale after a full inspiration
Diagnosis of COPDPostbronchodilator 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 testSpirometry is the key testCXRCT chestEKGCBCPulse oximetry
pharmacotherapyBronchodilatorBronchodilatorBronchodilatorBronchodilatorBronchodilatorbronchodilator
Short acting beta 2 agonistsBeta 2 agonists: stimulate beta 2 receptors, increase cyclic AMP, increase smooth muscle relaxation, lung emptying and air trappingShort acting: Proventil, Ventolin, Proair, XopenexSide effects: Tachycardia, cardiac disturbance, tremors
Long acting beta 2 agonistsMaintenance therapyLonger lasting improvementSalmeterol (Serevent Diskus)Formoterl (Foradil)
Short acting Anticholinergic agentsSmooth muscle relaxation of airwaysAntagonism of acetycholine at M3 receptors on airwaySlower onset of action than beta 2 but longer durationSide effects: Caution w/ glaucoma, BPHIpratropium (Atrovent)
Long acting Anticholinergic agentsSustained action over 24 hoursTiotropium (Spiriva) 24% lower of number exacerbation than Ipratropium
CorticosteroidsAct at multiple points in inflammatory processIncrease FEV1NOT APPROVED FOR SINGLE USE AGENT IN COPDRecommend as addition to maintenance therapySide effects: bruising, candidiasis, voice alteration
Combination therapiesBeta 2 + anticholinergic agent (Combivent)Corticosteroid + long acting Beta 2 (Advair) (Symbicort)
Acute exacerbation of COPDSustained worsening of patients 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 agents80% gram positive and gram negative bacteriaNosocomial30% viruses5-10% atypical bacteria
Treatment other than bronchodilatorsAntibioticsSmoking cessationPulmonary RehabilitationOxygen therapy: PaO2 < 55mmHg or O2 sat < 88%Long term use increase survival
ASTHMA
ASTHMAUnderlying cause of 40% young adults being evaluated for dyspneaPulmonary testing plays a major role
Common risk factors for asthma host factorsGeneticFemale sexLow birth weightObesityAtopy/allergieseczema
Environmental factorsPrenatal and childhood exposure to tobacco smokeLack of breast feedingSevere respiratory infections in 1st year of lifeIndoor allergens and outdoor pollutantsOccupational exposures
Clinical presentationWaxing and waning symptoms of dyspnea, cough, wheezing and chest tightnessExacerbation of symptoms usually gradual in onset and cessation
TriggersExposure to common allergensCold weatherViral infectionsPhysical exercise
Physical examFrequently normalStigmata of allergic rhinitisEczemaAirflow obstruction/wheezing (poor predictor value)
Laboratory testsCXRPulse oximetryCBC
SpiromeryNAEPP (National Asthma Education and Preventive Program) recommends using spirometry for initial diagnosis and long term follow up of AsthmaPerform at initial assessmentAfter treatment initiatedStabilized and during period of prolonged loss of asthma control and at least every 1 to 2 yrs
Peak expiratory flowNot equivalent to SpirometryEffective screening tool More variableGood to know the baselineGood to monitor for symptoms
Peak expiratory flowPersonal 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 monitoringMeasure upon awakening and between noon and 2pmMeasure before and after take beta agonistsMonitor for symptoms control
Peak flow zone system Green zone- 80% of personal best signal good controlYellow zone- 50-80%, must take short acting inhaled beta 2 agonists right away. See MDRed zone- below 50% of personal best, take agonists and see MD or ER
Reversible airwaySpirometry performed before and after bronchodilatorReversible airway obstruction- an increase of at least 12% and 200ml in either FVC or FEV1 after administration of a short acting bronchodilator
Methacholine challengebronchoprovocation challengeConsidered only when spirometric findings are normal in whom asthma is still suspectedMethacholine (acetyl beta methylcholine chloride) is the cholinergic agent
MethacholineInhalation of up to 5 or 10 sequentially increasing concentrations and the measurement of FEV1 and symptoms of each doseFall in FEV1 of more than 20% from baselineEvidence of airway hyperresponsiveness
PharmacotherapiesBrochodilatorsBeta 2 agonists short actingRegular use should alarm physician that patient is poorly controlled
Pharmacotherapies cont.CorticosteroidsICS mainstay of therapy in difficult control asthmaShould be give to all patients firstMost effectiveOral prednisone (1-5mg) for difficult patients
Cont.Long acting beta 2 agonists (LABAs)Indicated for use as corticosteroid sparing agents Adjunct on ICSPreferred add-on therapy to ICS
Cont.Leukotriene inhibitors (Montelukast) (Zafirlukast)Blocking inflammatory effects of leukotrienesMethylxanthines (theophylline, Aminophylline) outdated
CHRONIC BRONCHITIS
CHRONIC BROCHITISsmoke related diseasesChronic mucus hypersecretion syndromeDefined as production of sputum for 3 or more months per year for 2 consecutive yearsWith obstructive ventilatory defect
Pathophysiology of C.B.Hyperplasia of airway mucous glands and goblet cellsMucous plugging, thickening, tortuosity and fibrosis of airways
Clinical presentationHistory of cough and sputum production for yearsCough in winter monthsExertional dyspneaPeripheral edema secondary to right ventricular failure
Physical exam of C.B.Overweight and cyanoticChest percussion is normal resonantCoarse rhonchi and wheezes, change in location and intensitySustained heave at LLSB for RVH
Blue bloaters-chronic bronchitisAlveolar hypoxia, acidemia and hypercapniaPulmonary hypertension by pulmonary vasocostrictionHypoxiaLower O2 desaturate HemoglobinDesaturation and erythrocytosis combine to produce cyanosisAccentuates right-sided heart failure
Chest X ray of CBHyperinflationPeribronchial markings at lung basesThickening of airway wallsRight ventricle enlargement
Acute exacerbations of Chronic BronchitisPart of the clinical spectrumViral or Bacterial causesH.influenzae esp. in smokers, M.catarrhalis, S.pneumoniae, Pseudomonas
Diagnosis of AECBClinical presentationsCXR, ABG
Treatment of AECBBronchodilatorsCorticosteroidsAntibiotics MucolyticsOxygen
EMPHYSEMA
EMPHYSEMAsmoke related diseasesDefinition based on anatomyProgressive destruction of alveolar septa and capillariesAirspace enlargement and macroscopic bullae
Pathophysiology of EmphysemaReduced elastic recoil of lung (increased compliance)Slowing of max. expiratory airflow (decreased FEV1)HyperinflationDecreased alveolar gas exchange
CXR for EmphysemaFlattening of diaphragmHyperinflationEnlargement of central pulm arteriesBullae
Clinical presentation of EmphysemaExertional dyspnea with minimal coughAsthenic body with evidence of weight lossAccessory muscle of respirationProlonged expiration with grunting soundPatients lean forward, extending arm to brace themselves
Physical exam of EmphysemaIncreased A-P diameter of thorax- barrel chestPercussion note is hyperresonantBreath sounds are diminishedFaint high pitched rhonchi heard at end of expiration
Pink puffers-EmphysemaArterial O2 in mid 70s and Pco2 is low to normalAble to maintain arterial O2 sufficient to nearly saturate hemoglobin
TUBERCULOSIS
TUBERCULOSIS11 million persons in U.S. latently infected with Mycobacterium TBMost cases occur in foreign born persons from endemic countriesEconomically disadvantagedImmunosuppressive conditions (11% HIV)13,293 active cases in 2007
Diagnostic testTuberculin skin test (TST)Referred as Mantoux or Purified protein derivative test (PPD)Positive test: look for INDURATION, not redness
5 mm TST5mm positive:HIVRecent TB exposureCXR c/w old TBOrgan transplant15mg/day of prednisone > 1month
15 mm TSTIf you live in:
BOISE, IDAHO
False positive testNontuberculosis M.TBBacille Calmette-Guerin (BCG) vaccineSubjective interpretation
U.S. guidelines do not include BCG vaccination history in TST interpretation
Diagnosis of M. TBThorough history and physicalCXRSputum SmearSputum antigen-specific interferon gamma release assayNucleic acid amplificationSputum or other tissue cultureTissue biopsy
Latent Tuberculosis11 million persons in U.S.Lifetime risk reactivation 5-10%Isoniazid monotherapy X 9 months diminishes rate of reactivationEffectiveness 90% for compliant patients4 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 reactivationYoung childrenUntreated or suboptimal treated TBImmunosuppressedPatients taking TNF-alpha inhibitors (Rheumatoid patients)
Active Tuberculosis
COMBINATION THERAPY IS THE CORNER STONE
Two stages treatment of M.TBIntensive 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 TBExtensive replication of up to 10 to the 8th fold tubercles in some cavitary lesions produce primary drug resistanceInappropriate drug therapy, (too few drugs, subtherapeutic drug concentrations, inappropriate drug selection and modification)Poor patient complianceAverage 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, AmikacinRequires 18 to 24 months therapy
Case study82 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 caseANSWER:
PULMONARY NODULES
PULMONARY NODULESDefined as single pulmonary lesion with normal surrounding lung parenchymaNodule < 3cmMass > 3cmCan be malignant or benignUp to 51% of people screened with CT found to have at least one lung nodule
Pulmonary nodulesMost small, incidental nodules are benignNeed to be addressed once foundFollow up with serial CT imaging recommended
Common causes of solitary pulmonary nodulesBenign- infection (granuloma, abscess), inflammation, AV malformation, cyst, mucoid impactionMalignant- carcinoma, metastasis, lymphoma, carcinoid, sarcoma
Follow up depends on size, risk factorsNodules 4 mm or smaller
Very low risk of malignancyPatients with risk factors (hx of smoking or cancer) should have another CT 12 monthsBiopsy if increased in size
4 mm to 6 mm nodulesLow risk of malignancy (0.9%)Low risk patients, follow up CT 12 monthsRisk factors patients, follow up 6 to 12months, again at 18 to 24months
6 mm to 8 mm nodulesIntermediate risk of malignancy (6%)Low risk patients, 6-12 months, again at 18-24 monthsRisk factors patients, 3-6 months, again 9 to 12 months, again in 24 months if no change in sizeAny increased in size warrants biopsy
> 8 mm nodulesWorrisome (18% malignancy)Follow aggressively in 3 months or sent for biopsyRegardless of risk factorsConsider PET or biopsy
Clues to diagnosis malignancyCT appearance- calcification, edge characteristics, growth rate, popcorn appearanceEnhanced CT and positron-emission tomographyBiopsy
Lung Cancer ScreeningNo guidelines recommend in favor of routine CT screening for lung cancerScreening may not reduce deaths from lung cancerNo decline in number of advanced cases diagnosed or deaths from lung cancerNo relationship between tumor size and survival
Take-home pointsCT screening will uncover many benign nodules likely to receive intensive follow upLung nodules 8 mm in diameter or smaller are likely benignTraditional nodule characteristics predict malignancy are less useful with very small nodules
Take-home pointsSurveillance with serial chest CT is recommended once they are foundNo guidelines from any professional organization recommend in favor of routine CT screening for lung cancer
ALPHA 1 ANTITRYPSIN DEFICIENCY
Alpha-1 antitrypsin deficiencyAutosomal codominant conditionPredisposes to emphysema and liver disease100,000 Americans are severely deficient
Alleles antitrypsin activityM-normalS-intermediateZ-marked decreaseNull-absent (rare)
Phenotypes of antitrypsin deficiencyMM, MS, MZ, no increased riskSZ, mild increased riskZZ, 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 phenotypeAssociated with emphysema and 10% of chronic liver diseasesLiver 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 presentationsNo different than COPD or cirrhosisOn set of airflow obstruction before 50Family history of liver or lung diseaseEmphysema occurring in nonsmoker or very light smokerPersistent or worsening Sx despite treatmentBasilar hyperlucency >> than apical
Testing for alpha-1 antitrypsin deficiencyVery inexpensiveSerum alpha- antitrypsin levelIf below 100mg/dl, phenotyping
Why is it important?Mean duration between first symptom and initial diagnosis was 8.4 yearsMean number of physicians seen between first Sx and diagnosis was 4 physicians
Treatment Smoking cessationGenetic counselingAugmentation therapy with recombinant alpha-1 antitrypsin inhibitors
PLEURISY AND PLEURAL EFFUSION
PLEURISY
PleurisyInflammation of the parietal pleura that results in characteristic pleuritc pain with variety of causesPleuritic pain is the key feature
Pathophysiology of pleurisyVisceral pleura has no nociceptors or pain receptorsParietal pleura innervated by somatic nerves that sense painInflammation extend to pleural space involve parietal pleura, thus resulting pain
PathophysiologyParietal pleurae of the outer rib cage and lateral aspect of each hemidiaphragm innnervated by intercostal nervesPhrenic nerve innervate central part of each hemidiaphragmWhen 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 embolismPneumothoraxPericarditisPneumoniaMI
Once ruled out PPPPMcommon causes of pleurisyViruses (most common): influenza, parainfluenza, coxsakieviruses, RSV viruses mumps, EBVBacterial, TBRenal: CRF, Rheumatologic: Lupus, RA, SjogrenCardiac: post cardiac injury, post MI (dresslers), post pericadiotomyAsbestosisMalignancy, sickle cell
Presentation of pleurisyPleuritic pain localized to area of inflammation or referred pathwayExacerbates with breathing, talking, coughing or sneezingSharp pain worsened with movementLimits motion
Evaluation of pleurisyHistory and physical examChest X rayIf abnormal >>Pneumonia? Pnemothorx? Cardiomegaly? P.E. ?
Evaluation of pleurisyIf CXR is normal >> MI, Pulm embolism?EKG abnormal >> MI, PE, PericarditisEKG normal, no suggestion of PE, MI, look for other causes, Viral
Physical exam of pleurisyFriction rub with inspiration or expirationDue to surfaces between parietal and visceral pleurae rub against one another with inflammationDecreased breath sounds, ralesNormal physical with serious conditionHigh index of suspicion
Diagnostic testsChest X ray for pleural effusion, pneumonia, pulmonary embolism, pneumothoraxEKG for MI, pulmonary embolism, pericarditis
Treatment of PleurisyControl pleuritic chest painTreat underlying conditionNSAIDS do not suppress respiratory efforts or cough reflexLimited to IndomethacinSteroids are controversial
PLEURAL EFFUSIONSMost common causes are:Congestive heart failurePneumoniaMalignancyPulmonary embolism
Pathophysiology of Pleural effusionsPleural fluid originates in capillaries of parietal pleura and drained by lymphaticsMore fluid formed > absorbedPleural fluid can originate from interstitial lung spaces, lymphatics and peritoneal cavity
Pathophysiology of pleural effusionsCongestive heart failure
Nephrotic syndrome
Malignancy
Parapneumonic effusion
Hepatic hydrothorax
Increased hydrostatic pressure of vessels
Decreased oncotic pressureObstruction of lymphaticsIncreased capillary permeability
Increased peritoneal fluid
Subpulmonic effusionsWhen fluid becomes loculated between lower aspect of lung and diaphragm
Parapneumonic effusionsPleural effusions associated with bacterial pneumonia
EmpyemaPleural effusions associated with lung abscessCarry higher mortality than pneumonia and abscess without effusions
Clinical presentationDiffer according to etiologyAsymptomaticDyspnea, pleuritc chest painNonproductive coughFever
Physical examDullness on percussionDecreased or absent breath soundsDecreased tactile fremitus
Diagnosis and evaluationChest X ray- PA and lateralBlunting of posterior costophrenic angleElevated hemidiaphragm- suspect subpulmonic effusionUltrasound useful to identify loculated fluidCT scanThoracentesis
THORACENTESISEXUDATEParapneumonicEmpyemaTBMalignancyRA / lupusChylothoraxTRANSUDATECHFCirrhosisAtelectesisNephrotic syndromePE
EXUDATE TRANSUDATEProtein/ LDHWBC > 1000/ differentialNeutrophils= bacterialLymphocytes = TB,CAGram stainsGlucose < 60ANAAmylaseTriglycerides
WBC 2/3 of serum LDH
TreatmentTreat underlying conditionsTherapeutic thoracentesisChest tube drainageThoractomy with decorticationPleurodesis (fusion of visceral and parietal pleural to prevent recurrence of effusion)
PNEUMOTHORAXIntroduction of air into pleural spaceSpontaneous or trauma or iatrogenic
Spontaneous pneumothoraxNo clinically apparent diseasesMen > womenTall, thin male under 40 smokes or notRadiographically inapparent subpleural bullaeMay be associated physical activities
Secondary spontaneous pneumothoraxAsthma, COPDInterstitial lung diseasesPneumocystis carinii pneumoniaMarfans syndrome
Clinical presentation of spontaneous pneumothoraxIpsilateral pleuritc chest painDyspneaTachycardiaShift of trachea by examHyperresonance to percussionDecrease breath soundsHypotension
Diagnosis PeumothoraxChest X rayChest CT for bullae
Treatment of pneumothoraxCatheterChest tubeSurgerypleurodesis
VENOUS THROMBOEMBOLIC DISEASES
VENOUS THROMBOEMBOLIC DISEASEDeep Vein ThrombosisPulmonary Embolism
Deep venous thrombosis (DVT)Venous stasis from immobilityVirchows triadVenous stasisVessel wall damageIncreased blood coagulability
Clinical risk factorsRecent surgeryMajor traumaPrevious DVTIncreasing agePregnancy, postpartumOral contraception/smokeImmobilityConnective tissue disease
Familial thrombophilic diseaseActivated protein C resistance (factor V leiden),defect in factor VProthrombin 20210A, gene defect with increased prothrombin and thrombinProtein C and S deficiencyAntithrombin III deficiency
Clinical presentationLeg pain and swellingHomans sign, less than 40%Calf to thigh swelling and tendernessMost are asymptomaticBE ALERT
Complication of DVTPulmonary EmbolismThigh/Proximal DVT associated with PE70-90% of patients with symptomatic PE have silent thigh DVT
Diagnosis Clinical prediction rulesWELLS PREDICTION RULESEstablish the pretest probability of VTEEstimate the probability of DVT and PE before performing and interpreting other diagnostic testsBest applied to younger patient without other comorbidities
D-Dimer AssayMost often ordered by ER physiciansEnzyme linked immunosorbent assay (ELISA)Negative D-Dimer in younger patients whose pretest probability is low excludes VTEIn older patients with comorbidities and long duration of Sx, D-Dimer not enough
UltrasonographyHigh Specificity and sensitivity for diagnosing proximal DVT of LE for those who are symptomaticRecommended for patients who are at intermediate and high risk for DVTShould be repeated if suspected case where initial test is negativeContrast venography is the definite test
Helical computed tomography (CT)Higher specificity and sensitivity compared with pulm arteriography for PEVQ scan for those with high pretest probability
Wells prediction rule for DVTAlternative diagnosis as likely as DVT -2Active cancer 1Calf swelling 3cm > asymptomatic side 1Collateral superficial vein 1 Paralysis, paresis or recent plaster cast 1Pitting edema on symptomatic leg 1 Recent bedridden >3days/major surgery within 12 weeks 1 Swollen leg 1
Wells prediction rule for DVTClinical probability of DVT is Low if score 0 or lessIntermediate 1 or 2High if 3 or more
Wells prediction rule for PECancer1Hemoptysis1HR > 100bpm 1.5Previous PE or DVT1.5Recent surgery/immobil1.5Alternative Dx less likely3Clinical signs of DVT3
Wells prediction of PEProbability of PE if score 0-1 low
2-6 intermediate
7> high
Management of VTELow-molecular-weight Heparin (LMWH)Superior than unfractionated heparin for DVTFor PE, either LMWH or heparinLess risk of major bleeding Recommended for initial inpatient and outpatient management of VTE
Oral anticoagulationCoumadin (Warfarin)Maintained for three to six months for patients with VTE due to transient risk factorsFor recurrent DVT, 12 months therapyLMWH for those with difficult to control INR (international normalized ratio)
Complication of DVTPost thrombotic syndromeChronic postural dependent pain and edema or localized discomfort, in the context of a history of DVT
Complication of DVTPOST-THROMBOTIC SYNDROMEWear over the counter or custom-fit compression stockingsInitiated within one month of DVTUse at least one year
THE END
************************************************************************************************************************************************************************
