DVT and Pulmonary Embolism

Pulmonary Embolism & DVT

By Prof. Dr. Abdul Hameed AI Qaseer

Definition

It indicates occlusion of pulmonary artery by exogenous or endogenous material that travels to the lung through the pulmonary circulation , causing potential spectrum of consequences,

Introduction

Pathophysiology Risk Factors Symptoms Lab Findings Radiology Findings Treatment Prevention

Risk Factors for PE and DVT

Immobilization Surgery within the last 3 months Stroke History of venous thromboembolism Malignancy Preexisting respiratory disease Chronic Heart Disease Age >60 Surgery requiring >30mins of anesthesia
Recent travel (past 2weeks, >4 hours) Varicose veins Superficial vein thrombosis Central VV catheter/port/pacemaker Additional RF in Women: Obesity BMI >/=29 Heavy smoking (>25cigs/day) Hypertension Pregnancy

Pathophysiology

Dislodgement of a blood clot: Lower Extremities: 65% to 90% Pelvic venous system Renal venous system Upper Extremity Right Heart

Symptoms of P.E.

Dyspnea(~ 73%) Pleuritic pain ( 66%) Cough ( 37%) Hemoptysis (blood tinged/streaked/ pure blood) (~ 13%) From PIOPED study .


Signs of P.E.
Tachypnea ( 70%) Rales(51%) Tachycardia ( 30%) Hypoxia S4 (24%) Accentuated pulmonic component of S2 (23%) Fever: T <102 F (39C) (14%) Chest wall tenderness may be the only sign

Signs in Massive P.E.

“Massive PE”: hemodynamic instability with SBP <90 or a drop in baseline SBP by >/=40mmHgSigns as before PLUS:Acute right heart failureElevated J.V.P.Right-sided S3Parasternal lift

P.E. & Leg Symptoms

Most patients with P.E. do not have leg symptoms at time of diagnosis Patients with leg symptoms may have asymptomatic P.E.

Chronic PE

Acute minor PE
Acute massive PE
Chronic occlusion of pulmonary microvasculature ,RHF
Occlusion of segmental pulmonary artery--> infarction & sometimes pleural effusion
Major homodynamic effects ,reduction in cardiac output ,acute RHF
Pathophisology
Exertional dyspnea .Late symptoms of pulmonary hypertension or RHF .
Pleuritic chest pain ,restricted breathing ,haemoptysis
Faintness or collapse ,central chest pain ,apprehension ,severe dyspnea
Symptoms
May be minimal early in disease .Later RV heave ,loud split P2 . Terminal RHF
Tachycardia ,pleural rub ,raised hemidiaphram ,crackles ,effusion ,low-grade fever
Major circulatory collapse ,tachycardia ,hypotension. high JVP ,RV gallop rhythm ,split P2 .Severe cyanosis ,low UO
Signs
Enlarged pulmonary artery trunk ,enlarged heart ,prominent RV
Pleuropulmonary opacities ,pleural effusion ,linear shadows ,raised hemidiaphragm
Usually normal .May be subtle oligaemia .
Chest x-ray
RV hypertrophy and strain
Sinus tachycardia ,right axis deviation
S1Q3T3 ,anterior T wave inversion ,RBBB
ECG
Exertional reduction in PaO2 or desaturation
May be normal or reduced PaCO2
Low PaO2 & low PaCO2 ,Metabolic acidosis
Arterial blood gases
Other causes of pulmonary hypertension
Pneumonia ,pneumothorax ,musculoskeletal chest pain
MI ,pericardial tamponade ,aortic dissection
Differential diagnosis


Differential Diagnosis

WELL`S Clinical prediction rule for  Likelihood of PE

Lab & Radiologic Findings in P.E.
ABG BNP Cardiac Enzymes: Troponin D-dimer ECG Echocardiography CXR Ultrasound with colour Doppler study of leg veins V/Q Scan Spiral CT scanning Angiography

Lab Findings in P.E.(ABG)

ABG: Hypoxemia Hypocapnia (low CO2) Respiratory Alkalosis Massive PE: hypercapnia, mix resp and metabolic acidosis (inc lactic acid) Patients with RA pulse ox readings <95% are at increased risk of in-hospital complications, resp failure, cardiogenic shock, death

Lab Findings in P.E. (BNP)

BNP (brain natriuretic peptide)Insensitive test{ sensitivity(60%) & specifity (62%)}Patient’s with PE have higher levels than pts without, but not ALL patients with PE have high BNP Prognostic value measure: if BNP >90 pg| ml associated with adverse clinical outcomes (death, CPR, mechanical vent, pressure support, thrombolysis, embolectomy),One meta analysis revealed that BNP > 100 pg\ml or NT- proBNP > 600 pg\l increased mortality rate 6-16- fold .

Lab Findings in P.E. (Troponin)

Troponin High in 30-50% of pts with large PE

Lab Findings in P.E. (D- dimer)

D- dimer: Degredation product of fibrin >500 is abnormal Sensitivity: High, 95% of PE pts will be positive Specificity: Low

Lab Findings in P.E. (cont’d) ECG 2 Most Common finding on ECG: Nonspecific ST-segment and T-wave changes Sinus Tachycardia Historical abnormality suggestive of PE S1Q3T3 Right ventricular strain New incomplete RBBB

PE ECG

PE ECG

Classic ECG S1,Q3,T3

S1Q3T3!!!

RAD Right Atrial Enlargement

Radiologic Findings in P.E.


Radiology Findings in P.E. (cont’d) CXR: Normal Atelectasis and/or pulmonary parenchymal abnormality Pleural Effusion Cardiomegally

The CXR is read as “ normal” in up to 30% of pats. With angiographically proven PE (Mayo. 2008). In some series , an elevated hemidiaphragm is the most common finding with acute PE .


Chest Radiography

What’s This??? Hampton’s Hump

How About This???
Westermark's Sign: an abrupt tapering of a vessel caused by pulmonary thromboembolic obstruction. This CXR shows enlargement of the left hilum accompanied by left lung hyperlucency, indicating oligemia (Westermark's sign).

PE Chest x-ray

Radiology Findings in P.E. (cont’d) Lower Extremity Ultrasounds If DVT found then treatment is same if patient has a P.E. Disadvantage: If negative, patients with PE may be missed If false positive (3%), unnecessary intervention

Radiology Findings in P.E. (cont’d) CT Pulmonary Angiography (CT-PA) Widely used Institution dependent Sensitivity (83%) Specificity (96%): if negative, very low likelihood that pt has P.E.


Figure 19.58 CT pulmonary angiogram. The arrow points to a saddle embolism in the bifurcation of the pulmonary artery.
Downloaded from: StudentConsult (on 18 November 2006 08:58 AM)

Radiology Findings in P.E. (cont’d) Pulmonary Angiogram Gold Standard Not easily accessible Radiologist dependent

Pulmonary Angiography

Radiology Findings in P.E. (cont’d) EchocardiogramIncreased Right Ventricle SizeDecreased Right Ventricular FunctionTricuspid RegurgitationRarely:RV thrombusRegional wall motion abnormalities that spare the right ventricle apex (McConnell’s Sign)

Deep Vein Thrombosis

Diagnosis Compression ultrasonography of femoral & popliteal veins, sensitive for proximal vein thrombosis but less sensitive for calf vein thrombosis Impedance plethysmography Contrast venography Radionuclide venography

Contrast Venography Showing Ilio-femoral DVT

Right leg
Left leg

Radionuclide venography showing chronic iliofemoral DVT

Inter-iliac collaterals

Treatment of P.E.

Respiratory Support: Oxygen, intubation Hemodynamic Support: IVF, vasopressors Anticoagulation Thrombolysis IVC Filter


Anticoagulation
Start during resuscitation phase itself If suspicion high, start emperic anticoagulation Evaluate patient for absolute contraindication (i.e.: active bleeding)

Anticoagulation-1

Bed rest is not recommended for DVT unless substantial pain & swelling PE diagnosed, in patient therapy with initial bed rest for 24 to 48 hrs : often recommended

Anticoagulation-2

APE (+):IV anticoagulation with LMW heparin , or standard, UF heparin should be initiated unless contraindicated Not thrombolytic, but decreasing the thromboembolic burden If the suspicion of PE is high, parenteral anticoagulation should be considered even before imaging

Anticoagulation-3

Warfarin can be initiated on day 1 of therapy SC LMWH or weight-based UFH IV should be administered for at least 5 days until INR=2.0 to 3.0 for 2 consecutive days With standard heparin, a PTT checked Q6h until it is =1.5 to 2.5 X control Achieving a therapeutic a PTT within 24 hours ,reduce the risk of recurrence

Anticoagulation-4

VTE require long-term anticoagulation to prevent extension & recurrence Documented VTE with transient risk factors should treat 3 to 6 months, but more extended treatment is appropriate when significant risk factors persist, idiopathic or previous episodes of VTE D-dimer levels may help guide decisions about the duration of therapy

Management

LMWH Prepared by depolymerization of unfractionated heparin MW 100-10,000 (Mean 1,500-5,000) Better bioavailability S/C once or twice daily dose Longer half-life More predictable dose response Less risk of adverse bleeding events



Complications of heparin / LMWHMajor bleeding - 5% (less with LMWH)Osteoporosis – heparin > 1 month during pregnancyThrombocytopenia - 3% ( platelet count < 100,000 cells/ mm3) Management

Management

Oral vitamin K antagonist (Warfarin) – started within 24 hours of heparin therapyINR maintained between 2.0-3.0Heparin is discontinued when warfarin has been given for 4 days and INR is > 2.0 for two consecutive daysOral anticoagulants are continued for 3 months or longer

Thrombolysis

Considered once P.E. diagnosed If chosen, hold anticoagulation during thrombolysis infusion, then resumed Associated with higher incidence of major hemorrhage Indications: persistent hypotension, severe hypoxemia, large perfusion defects, right ventricular dysfunction, free floating right ventricular thrombus, paten foramen ovale Activase or streptokinase

Complications of Thrombolytic Therapy

The most devastating complication :ICH retroperitoneal & GI bleeding & bleeding from surgical wounds or sites of recent invasive procedures Contraindications : intracranial, spinal, or ocular surgery or disease, recent major surgery or other invasive procedures, active or recent major bleeding, pregnancy, & clinically obvious risks of bleeding

IVC Filter

Indication: Absolute contraindication to anticoagulation (i.e. active bleeding)Recurrent PE during adequate anticoagulationComplication of anticoagulation (severe bleeding)Also: Pts with poor cardiopulmonary reserveRecurrent P.E. will be fatalPatient’s who have had embolectomyProphylaxis against P.E. in select patients (malignancy)

ManagementIVC Filter

Simon Nitinol IVC Filter, Nickle & Titanium - MRI compatible

Embolectomy

Surgical or catheter Indication: Those who present severe enough to warrant thrombolysis In those where thrombolysis is contraindicated or fails