Pulmonary embolism ms


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Pulmonary embolism ms

  2. 2. 2MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVTPulmonary embolism (PE) is a common and potentially lethal condition. Most patientswho succumb to pulmonary embolism do so within the first few hours of the event. Inpatients who survive, recurrent embolism and death can be prevented with promptdiagnosis and therapy. Unfortunately, the diagnosis is often missed because patientswith pulmonary embolism present with nonspecific signs and symptoms. If leftuntreated, approximately one third of patients who survive an initial pulmonary embolismdie from a subsequent embolic episode.The most important conceptual advance regarding pulmonary embolism over the lastseveral decades has been the realization that pulmonary embolism is not a disease;rather, pulmonary embolism is a complication of venous thromboembolism, mostcommonly deep venous thrombosis (DVT). Virtually every physician who is involved inpatient care (eg, internist, family physician, orthopedic surgeon, gynecologic surgeon,urologic surgeon, pulmonary subspecialist, cardiologist) encounters patients who are atrisk for venous thromboembolism, and therefore at risk for pulmonary embolism.DEFINITION:PE is the obstruction of the pulmonary artery or one of its branches by athrombus (or thrombi) that originates somewhere in the venous system or inthe right side of the heart .Definition for Massive PEAcute PE with with at least 1 of the following:1. Sustained hypotensionSBP <90 mmHg for at least 15 minutes or requiring inotropic support, notdue to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or LVdysfunction, drugs,etc.2. Pulselessness3. Persistent profound bradycardiaHeart rate <40 bpm with signs or symptoms of shockDefinition for Submassive PEAcute PE without systemic hypotension (SBP >90 mm Hg) but with either RVdysfunction or myocardial necrosis.
  3. 3. 3MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVT• RV dysfunction means the presence of at least 1 of the following:– Echo: RV dilation (apical 4-chamber RV diameter divided by LVdiameter >0.9), or RV systolic dysfunction•– CT: RV dilation (4-chamber RV diameter divided by LV diameter >0.9)– BNP > 90 pg/mL or N-terminal pro-BNP > 500 pg/mL– ECG changes: New complete or incomplete RBBB, anteroseptal STelevation or depression, or anteroseptal T-wave inversion• Myocardial necrosis is defined as either of the following:– Troponin I > 0.4 ng/mL, or Troponin T > 0.1 ng/mLDefinition for Low-Risk PEAcute PE and the absence of the clinical markers of adverse prognosis thatdefine massive or submassive PE.
  4. 4. 4MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVTPREVALENCEPE is estimated to cause 200,000 deaths each year in the United States .The 2ndleading cause of death among hospitalized patients, unexpected,nontraumatic death.Most cases are not recognized antemortem, and LESS THAN 10% ofpatients with fatal emboli have received specific treatment for thecondition.Management demands a vigilant systematic approach to diagnosis and anunderstanding of risk factors so that appropriate preventive therapy canbe given.The incidence of PE in USA is 650-900,000 per year.AETIOLOGYMany substances can embolize to the pulmonary circulation, including1. AIR (during neurosurgery, from central venous catheters)2. AMNIOTIC FLUID(during active labor), fat (long bone fractures)3. FOREIGN BODIES (talc in injection drug users)4. PARASITE EGGS (schistosomiasis)5. SEPTIC EMBOLI (acute infectious endocarditis)6. TUMOR CELLS(renal cell carcinoma).7. RED EMBOLUS (DVT, atrial fibrillation)The most common embolus is thrombus, which may arise anywhere in thevenous circulation or heart but most often originates in the deep veins of thelower extremities. Thrombi confined to the calf rarely embolize to thepulmonary circulation. However, about 20% of calf vein thrombi propagateproximally to the popliteal and ileofemoral veins, at which point they may breakoff and embolize to the pulmonary circulation.((50%asymptomatic DVT)).Pulmonary emboli will develop in 50–60% of patients with proximal deepvenous thrombosis (DVT); half of these embolic events will be asymptomatic.DEEP VEIN THROMBOSIS:50% of all patients with venous thrombosis of the lower extremities have nosymptoms. Approximately 50–70% of patients who have symptomaticpulmonary emboli will have lower extremity DVT when evaluated.
  5. 5. 5MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVTObstruction of the deep veins of the legs produces edema and swelling of theextremity because the outflow of venous blood is inhibited. The amount ofswelling can be determined by measuring extremity circumference at variouslevels with a tape measure. The skin over the affected leg may become warmer,and superficial veins may become more prominent. Tenderness, which usuallyoccurs later, is produced by inflammation of the vein wall and can be detected bygentle palpation by the extremity. Homan’s Signs, pain in the calf after sharpdorsiflexion of the foot, is not specific for deep venous thrombosis because it canbe elicited in any painful condition of the calf. In some cases, signs of apulmonary embolus are the first indication of a deep venous thrombosis. -Thrombosis of superficial veins produces pain or tenderness, redness, andwarmth of the involved area. The risk of dislodgment and embolization ofsuperficial venous thrombi is very low because the majority of them undergospontaneous lysis; thus, condition can be treated at home with rest, extremityelevation, analgesics, and possibly anti-inflammatory agents.CAUSES:1. Thrombus 2. Embolism3. Trauma 4. Surgery5. Hypercoaguability 6. Heart failure7. Pregnancy (increase coaguability of BLOOD)8. Older than 50 years 9. Arial fibrillationRISK FACTORS:PE and DVT are twomanifestations ofthe same disease.((DVT))► It commonlyaffects theleg veins,such as thefemoral veinor thepopliteal veinor the deepveins of thepelvis.
  6. 6. 6MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVTSIGNS AND SYMPTOMSPain,SwellingRedness ofthe leg anddilatation ofthe surfaceveinsShinning skinwith rednessHotness andtendernessPedal edemamay occur.Pathogenesis:The risk factors for PE are the risk factors for thrombus formation within thevenous circulation.
  7. 7. 7MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVT1. Venous stasis OR turbulence(Venous flow disturbance):o Immobility leads to local venous stasis by accumulation of clottingfactors and fibrin, resulting in thrombus formation.o The risk of pulmonary embolism increases with prolonged bed restor immobilization of a limb in a cast.o Paralysis increases the risk of DVT.o V. stasis leads to accumulation of platelets and thrombin in veinsBed rest—especially postoperative, Hip replacement, knee replacement,caesarian operation, post delivery, comatose patient in ICU, Fracture oflong bones, sitting for hours in work or long trip by car or airplane or buswith out activity, CCU admission, obesity, stroke, comatose patient).Intra-pelvic or intra-abdominal mass impairing venous return from thelower limbs ( ovarian mass, cervix cancer , uterine tumors , prostatecancer , sigmoid cancer).2. Hypercoagulable state(hyperviscosity)a. The complex and delicate balance between coagulation andanticoagulation is altered by many diseases, by obesity, aftersurgery, or by trauma.b. Concomitant hypercoagulability may be present in disease stateswhere prolonged venous stasis or injury to veins occurs.
  8. 8. 8MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVTCongenital –((inherited gene defects-Protein defects)) Factor (V) Leiden ( 20-40%)G to A mutation at base pair 1691 results in amino acid 506,Glu instead of Arg Prothrombin 20210 (6%)(G to A) Defect or deficiency of protein C (4%) (outozomal dominant) Defect or deficiency of Protein S (3-4%) ( outozomal dominant)pregnancy and estrogens reduced protein S Dysfibrinogenemia ( 3% ) Antithrombin deficiency ( 1% ) (outozomal dominant ) acquired deficiencyof it happened in sever obesity , liver disease , chronic renal failer , usingoral contraceptive ,immature neonates Dysplasminogenemia ( <1% ) Reduced Heparin cofactor II Elevation of PAI-1 Elevation of Coagulation factors VII,VIII,IX,X,XI and II Reduction of protein ZAcquired— Hematologic diseases : DIC(disseminated intravascular thrombocytopenia),thrombocytosis HIT(heparin induced thrombocytopenia), leukemia Anti phospholipid syndrome TTP(thrombocytopenic thrombotic purpura) HUS(hemolytic uremic syndrome)Thrombocytosis, leukemia , nephrotic syndrome, Oral contraceptives andestrogen replacement, antiphospholipid syndrome, Homocysteinemia .o Malignancy has been identified in 17% of patients with venousthromboembolism.o The neoplasms most commonly associated with pulmonaryembolism, in descending order of frequency, are pancreaticcarcinoma; bronchogenic carcinoma; and carcinomas of thegenitourinary tract, colon, stomach, and breast.
  9. 9. 9MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVT3. Endothelial injuryINJURY TO ENDOTHELIUM CAN BE CAUSED BY1. ATHEROSCLEROSIS2. HYPERTENSION3. HYPERCHOLESTEROLEMIA4. RADIATION INJURY5. SMOKING6. Thrombophlebitis -Vascular disease7. -Foreign bodies (IV/central venous catheters)Risk factors for venous thrombosis Age Prolonged immobility Obesity Neurological disease Cardiac disease Pregnancy Oral contraceptive (ocp) if the patient hasthe factor ( V ) leiden mutation the risk isincreased 28-fold Surgery MalignancyPathophysiology When a thrombus completely or partially obstructs a pulmonaryartery(massive embolus) or its branches in diseased lung or heart, The alveolar dead space is increased. The area, although continuing to beventilated, receives little or no blood flow. Thus, gas exchange is impairedor absent in this area. Regional blood vessels and bronchioles constrict.
  10. 10. 10MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVT More than 50% of the vascular bed has to be occluded before PAPbecomes substantially elevated In patients without cardiopulmonary disease, occlusion of 25-30 % of thevascular bed . Causes an increase in pulmonary vascular resistance. Impaired gasexchangeA . Ventilation/perfusion mismatchB. Release of inflammatory mediators leads to surfactant dysfunction,atelectasis, alveolar hemorrhage ,Intrapulmonary shunting PVR from 1. The regional vasoconstriction2. Reduced size of the pulmonary vascular bed. An increase in pulmonary arterial pressure An increase in right ventricular work to maintain pulmonary blood flow. When obstruction approaches 75%, the RV must generate systolicpressure in excess of 50mmHg to preserve pulmonary circulation. When the work requirements of the right ventricle exceed its capacity,right ventricular failure occurs, leading to a decrease in cardiac outputfollowed by a decrease in systemic blood pressure and the developmentof shock.(fatigue , syncopy, dizziness).
  11. 11. 11MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVTSYMPTOMOLOGY:Clinical clues cannot make the diagnosis of PE; their main value lies insuggesting the diagnosis.The symptoms are quite variable according to the heart and lung situationwhether they are healthy or diseased and degree of damage.Most of the cases are missed as no specific symptom that the symptomscan be explained by other diagnosis by most of doctors which can lead tolose of the patients.Signs and symptoms are highly variable, non- specific, and common inpatients without PE. Fatal PE typically leads to death within one to two hours of the event. Small PE in healthy pt= asymptomatic. Dyspnea (80%) – usuallyacute onset Pleuritic chest pain (44%) Calf pain/swelling (41-44%) Orthopnea (28%) Wheezing (21%) Cough (20%) Syncope (14%) Hemoptysis (7%) 1.Dyspnea is the most frequent symptom; all of a SUDDEN in high riskpatients , while in bed or moving from resting state, NEVER GRADUAL,The duration and intensity of the dyspnea depend on the extent ofembolization ,heart and lung status.
  12. 12. 12MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVT 2. Chest pain is common and is usually sudden and pleuritic. It may besubsternal and misdiagnosed with angina pectoris or a myocardialinfarction. It is severe from the first minute in high risk patient. 3. All chest symptoms may occur and all of sudden onset in absence ofother possibilities(( acute pneumothorax , acute left ventricular failure,acute dissection of ascending aorta)). 97% with PE have at least one of the following:1. Dyspnea2. Tachypnea3. Pleuritic pain Presence of DVT should trigger initial suspicion.OTHERS may present with low cardiac out put symptoms such as dizziness,syncopy, profuse sweating, sudden fatigability in suspected high risk patientwith dyspnea mimicking vasovagal attacks.OTHERS may present with sudden vomiting with epigastric pain anddiarrhea with fatigue and right hypochondrial discomfort or heaviness dueto right side congestion in massive/submassive P.E. WITH HYPOTENSION.Other symptoms include anxiety, fever, tachycardia, apprehension, cough,diaphoresis, hemoptysis, unexplained fatigue or palpitation/shivering.SIGNS: Tachypnea (53%) Tachycardia (24%) Rales (18%) Decreased breath sounds (17%) Accentuated P2 (15%) JV distension (14%) Signs of DVT
  13. 13. 13MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVTPhysical examination findings are quite variable in pulmonary embolism and, forconvenience, may be grouped into 4 categories as follows:Massive pulmonary embolismo The patient in SHOCK. (( systemic hypotension, poor perfusion ofthe extremities, tachycardia, and tachypnea , drowzy)).o Additionally, signs of pulmonary hypertension such as palpable P2second left intercostal space, loud P2, right ventricular S3 gallop,and (tricuspid regurgitation) may be present.Acute pulmonary infarctiono These patients have decreased excursion of the involvedhemithorax, palpable or audible pleural friction rub, and evenlocalized tenderness.o Signs of pleural effusion, such as dullness to percussion anddiminished breath sounds, may be present.Acute embolism without infarctiono These patients have nonspecific physical signs that may easily besecondary to another disease process.o Tachypnea and tachycardia frequently are detected, pleuritic painsometimes may be present, crackles may be heard in the area ofembolization, and local wheeze may be heard rarely.Multiple pulmonary emboli or thrombio Physical signs of pulmonary hypertension and cor pulmonale.o Patients may have elevated jugular venous pressure, rightventricular heave, palpable P2 , right ventricular S3 gallop, TR,hepatomegaly, ascites, and dependent pitting edema.o These findings are not specific for pulmonary embolism and requirea high index of suspicion for pursuing appropriate diagnosticstudies.LUNG EXAMINATION- collapse, consolidation where there is 2rypneumonia which may delay the diagnosis, elevation of diaphragm,cavitating lung cavity with missed diagnosis mimicking lung abscess,pleural effusion , pleural rub , localized wheezing ,basal inspiratory finecrepiataion .
  14. 14. 14MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVTAssessment and Diagnostic Findings: No single noninvasive test is sufficiently sensitive or specific to diagnoseor exclude PE in all patients. No single test can reliably rule out PE. Yep, that includes CT Angio (right?)THEY ARE HELPFUL IN MASSIVE /SUBMASSIVE PE NOT SMALL . The clinical priorities in the investigation of patients with suspected PEinclude:1. Diagnosis of extensive PE2. Diagnosis of PE in patients with severe symptoms and/or poorcardiopulmonary reserve3. Diagnosis of any PE when associated with symptomatic orasymptomatic proximal DVT4. Diagnosis in patients presenting with possible recurrent PE1.ABG-arterial blood gases: pO2 pCO2 Increased A-a gradient
  15. 15. 15MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVT2.D-dimer: This blood screening test relies on the principle that most patients withPE have ongoing endogenous fibrinolysis that is not effective enough toprevent PE but that does break down some of the fibrin clot to d-dimers . Although elevated plasma concentrations of d-dimers are sensitive for thepresence of PE, they are not specific. patients with a low clinical probability of PE who had negative d-dimerresults, additional diagnostic testing was not necessary Different assays have different sensitivities PE in low-risk patients with a negative D-dimer…o Thrombus formation >72 hrs before blood draw (circulating dimert1/2 = 8 hrs)o Subsegmental PE False-positives = age >70, pregnancy, active malignancy, recent surgery,liver disease, RA, infections, trauma False-negatives = Coumadin use, symptoms >5days, small clots orinfarction, isolated calf vein thrombosis. Therefore, the plasma d-dimer assay is ideally suited for outpatients oremergency department patients who have suspected PE but no coexistingacute systemic illness OR history of venous thromboembolism and whosesymptoms are of short duration. This test is generally not useful for acutely ill hospitalized inpatientsbecause their D-dimer levels are usually elevated. A normal d-dimer assayappears to be as diagnostically useful as a normal lung scan to exclude PE. D-dimer test should not be used when the clinical probability ofpulmonary embolism is high, because the test has low negative predictivevalue in such cases.
  16. 16. 16MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVT3.Electrocardiographic Signs:Sinus tachycardia( THE COMMENEST )Incomplete or complete right bundle branch blockRight-axis deviationT wave inversions in leads III and aVF or in leads V1-V4S wave in lead I and a Q wave and T wave inversion in lead III (S1Q3T3)QRS axis greater than 90 degrees or an indeterminate axisAtrial fibrillation or atrial flutter
  17. 17. 17MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVT4.Chest Radiography:A near-normal radiograph in the setting of severe respiratory compromiseis highly suggestive of massive PE.(AHA)Major chest radiographic abnormalities are uncommon.Focal oligemia (Westermark sign) indicates massive central embolicocclusion.A peripheral wedge-shaped density above the diaphragm (Hamptonhump) usually indicates pulmonary infarction.Subtle abnormalities suggestive of PE include enlargement of thedescending right pulmonary artery, elevated diaphragm,collapse.The vessel often tapers rapidly after the enlarged portion. PE.
  18. 18. 18MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVT5.Echocardiographic Signs: Right ventricular enlargement or hypokinesis, especially free wallhypokinesis, with sparing of the apex (the McConnell sign).Interventricular septal flattening and paradoxical motion toward the leftventricle, resulting in a D-shaped left ventricle in cross section. Tricuspidregurgitation. Pulmonaryhypertension with atricuspid regurgitantjet velocity>2.6 m/sec. Loss of respiratory-phasic collapse of theinferior vena cavawith inspiration. Dilated inferior venacava withoutphysiologicinspiratory collapse. Direct visualization of thrombus (more likely with transesophagealechocardiography)Overview of Imaging Modalities for Pulmonary Embolism: Lower extremity venous ultrasonography Multidetector helical CT pulmonary angiography MRI Ventilation-perfusion scintigraphy (V/Q scan)
  19. 19. 19MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVT6. Computed Tomography1. Size, location, and extent of thrombus2. Other diagnoses that may coexist with PE or explain PE symptoms:Pneumonia, Atelectasis, Pericardial effusion, Pneumothorax, abscess,Left ventricular enlargement3. Pulmonary artery enlargement === pulmonary hypertensionAge of thrombus: acute, subacute, chronic4. Location of thrombus: pulmonary arteries , deep leg veins,5.Right ventricular enlargement6.Contour of the interventricular septum: whether it bulges towardthe left ventricle, thus indicating right ventricular pressure overload7.Incidental masses or nodules in lung
  20. 20. 20MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVT7. CT pulmonary AngiographyCT angiography (CTA) is the initial imaging modality of choice for stablepatients with suspected pulmonary embolism(low risk).Sensitivity/Specificity ~90%withholding anticoagulation after negative pulmonary CTA resultsappears to be safe.CTPA use increased 10-fold from 1998-2006Incidence increased 81% from 1998-2006 (112/100,000) with only 3%mortality reductiono Increased in-hospital antigcoagulation complications during thatsame time period8. Spiral CT- can visualize main, lobar, and segmental pulmonary emboliwith a reported sensitivity of greater than 90%.Spiral CT scanning can help detect emboli as small as 2 mm that areaffecting up to the seventh border division of the pulmonary artery.A further benefit of spiral CT scanning is that the results may suggestan alternative diagnosis in up to 57% of patients.A significant limitation of spiral CT scanning is that small subsegmentalemboli may not be detected.o The technique is as follows: Spiral CT examination is performed immediately after infusionof 150-200 mL of 30% contrast material. Scanning is performed from the level of the aortic arch toapproximately 2 cm below the level of the inferior pulmonaryvein while the patient is holding his or her breath at fullinspiration. If the patient is not able to hold his or her breath for 20-30seconds, scanning may be performed during gentle breathing.Positive findings on CT imaging include a central intravascular fillingdefect within the vessel lumen, eccentric tracking of contrast materialaround a filling defect, and complete vascular occlusion. Smooth filling
  21. 21. 21MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVTdefects making an obtuse angle with a vessel wall may representchronic thrombi or recent recanalization. In the lung parenchyma, signsof pulmonary embolism include oligemia, pulmonary hemorrhage(ground-glass attenuation), and pulmonary infarction (peripheralwedge-shaped pleural-based opacification.9. Ventilation-perfusion (V/Q) scanning of the lungs:This is an important diagnostic modality for establishing the diagnosis ofpulmonary embolism.However, V/Q scanning should be used only 1.when CT scanning is notavailable or 2. If the patient has a contraindication to CT scanning orintravenous contrast material.New criteria for V/Q scanning diagnosis of pulmonary embolism, from theProspective Investigation of Pulmonary Embolism Diagnosis (PIOPED) IItrial:High probability criteria are as follows:Two large (>75% of a segment) segmental perfusion defectswithout corresponding ventilation or chest x ray defects.One large segmental perfusion defect and 2 moderate (25-75% of a segment) segmental perfusion defects withoutcorresponding ventilation or radiographic abnormalities.Four moderate segmental perfusion defects withoutcorresponding ventilation or chest radiographic abnormalities
  22. 22. 22MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVTIntermediate probability criteria are as follows:One moderate to fewer than 2 large segmental perfusiondefects without corresponding ventilation or chestradiographic abnormalitiesCorresponding V/Q defects and radiographic parenchymalopacity in lower lung zoneSingle moderate matched V/Q defects with normal chestradiographic findingsCorresponding V/Q and chest radiography small pleuraleffusionDifficult to categorize as normal, low, or high probabilityLow probability criteria are as follows:Multiple matched V/Q defects, regardless of size, withnormal chest radiographic findingsCorresponding V/Q defects and radiographic parenchymalopacity in upper or middle lung zoneCorresponding V/Q defects and large pleural effusionAny perfusion defects with substantially larger radiographicabnormalityDefects surrounded by normally perfused lung (stripe sign)More than 3 small (<25% of a segment) segmental perfusiondefects with normal chest radiographic findingsNonsegmental perfusion defects (cardiomegaly, aorticimpression, enlarged hila)Very low criterion is 3 small (<25% of a segment) segmentalperfusion defects with normal chest radiograph findings.
  23. 23. 23MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVTAdvantage1. a normal V/Q scan rules out PE>99% negative predictive value2. the radiation dose is low3. iodine-based contrast is not usedother investigations:1.MRI2.PULMONARY ANGIOGRAPHY3. Multidetector helical CT pulmonary angiography
  24. 24. 24MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVTSimplified Revised GenevaScore Age >65 Previous history of PE or DVT Sx or Fx within 1 month Active malignancy HR 75-94 HR >95 Unilateral leg edema Unilateral leg pain HemoptysisPoints111112111Risk factorsClinicalsignsSymptomsWicki J, Perneger TV, Junod AF, et al. Assessing clinical probability of pulmonary embolism in the emergency ward.Arch Intern Med. 2001;161:92-97.0-2 = PE unlikely , 3-7 = PE likelyPrevention Prevent deep venous thrombosis.1. Active leg exercises2. The intermittent pneumatic leg compression device ( venous stasis).3. Use of elastic compression stockings4. Anticoagulant therapyMedical Management• General measures to improve respiratory and vascular status• Anticoagulation therapy• Thrombolytic therapy• Surgical intervention
  25. 25. 25MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVTGENERAL MANAGEMENTOxygen therapy is administered to correct the hypoxemia, relieve thepulmonary vascular vasoconstriction, and reduce the pulmonaryhypertension.Thrombolytics Evidence of circulatory/respiratory insufficiency Hypotension (SBP <90) Hypoxia (SpO2 <95%) Evidence of RV dysfunction RV dilation/hypokinesis Elevated troponin-I (>0.4) or proBNP (>900) EKG changesFDA-recommended dose: Alteplase 100mg over 2hrsFibrinolysis ContraindicationsRelative Age > 75 Current anticoagulation use Pregnancy Noncompressible vascular punctures Traumatic or prolonged CPR >10 min Recent surgery/bleeding w/in 2-4 wks Poorly controlled HTN >180/110 Dementia Recent Ischemic CVA > 3 monthsAbsolute Prior ICH Known intracranial CV disease (AVM) Malignant intracranial neoplasm CVA within 3 months Suspected aortic dissection Active bleeding Recent surgery of spinal cord/brain Recent closed-head trauma with braininjury
  26. 26. 26MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVT Therapeutic anticoagulation with subcutaneous LMWH, intravenous orsubcutaneous UFH with monitoring, unmonitored weight-basedsubcutaneous UFH, should be given to patients with objectivelyconfirmed PE and no contraindications to anticoagulation. UFH=Weight-based dosing (nomogram)IV bolus – 80mg/kg IV bolus, then 18mg/kg/hrMonitor PTT (1.5-2.0 x), CBCContinue 4-5d and therapeutic on Warfarin for 2d (INR>2.0)LMWH Alternative regimen Lovenox – 1mg/kg SC q12h Better bioavailability, longer half-life, more predictable effect No monitoring of PTT (follow CBC) Contraindications: renal failure (CrCl<30), weight extremesWarfarin Start when therapeutic on Heparin Monitor INR daily Goal: INR 2.0-3.0 for 3-6 months Identified precipitant 3 mos First idiopathic episode 6 mos Prolonged/indefinite: 2 thrombotic episodes 1 spont. life-threatening episode Anti-phospholipid antibody syndrome, ATIII deficiency
  27. 27. 27MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVT Catheter embolectomy Surgical embolectomy Reasonable for… Massive PE if still unstable after fibrinolysis Massive/Submassive PE if fibrinolysis is contra-indicated or there isevidence of adverse prognosiso Three General Categories of Percutaneous InterventionAspiration thrombectomyThrombus fragmentationRheolytic thrombectomy
  28. 28. 28MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVTProbabilityof PE above treatmentthresholdSubmassive withoutRVStrain(Low risk PE)Submassive withRV strain(Abnormal echo orbiomarkers)Systolicblood pressure<90 mmHgfor >15 minHeparinAnticoagulationAssess forevidence ofincreased severity that suggestspotential forbenefitof fibrinolysis1. EVIDENCEOF SHOCK ORRESPIRATORY FAILURE:• Any hypotension (SBP<90 mm Hg) OR• Shock index >1.0 OR• Respiratory distress (SaO2 <95% with Borg score >8,oraltered mental status, or appearance of suffering)2. EVIDENCEOF MODERATE TO SEVERERV STRAIN:• RVdysfunction (RV hypokinesis or estimated RVSP> 40mmHg) OR• Clearly elevated biomarker values (e.g., troponin aboveborderline value, BNP >100 pg/mL or pro-BNP >900 pg/mL)NocontraindicationstofibrinolysisAlteplase 100 mg over 2 h IVHeparinAnticoagulation HeparinAnticoagulation