PULMONARYPULMONARY EMBOLISMEMBOLISM --EDHEDH-- SEPTEMBERSEPTEMBER 20072007 DRDR SS CC COKACOKA CASECASE PRESENTATIONPRESENTATION Mrs.Mrs. N.N. MkhizeMkhize 5151 yryr oldold presentedpresented with:with: -- ShortnessShortness ofof breathbreath forfor oneone daysdays durationduration RiskRisk factors:factors: -- RaisedRaised BMIBMI -- StrongStrong familyfamily hxhx ofof MIMI-- fatherfather andand sistersister bothboth dieddied ofof MIMI inin theirtheir 5050’’ss NoNo otherother traditionaltraditional riskrisk factorsfactors OnOn EnquiryEnquiry:: -- GradeGrade 33 dyspnoeadyspnoea (NYHAC)(NYHAC) associatedassociated chestchest painpain underunder leftleft breastbreast radiatingradiating toto thethe backback describeddescribed asas stabbingstabbing inin naturenature NoNo nausea,nausea, vomittingvomitting nornor sweating.sweating. painpain waswas ofof suddensudden onsetonset atat restrest notnot relatedrelated toto mealsmeals nono identifiableidentifiable relievingrelieving nornor exacerbatingexacerbating factorsfactors --NoNo historyhistory ofof orthopnea/orthopnea/ PND/pedalPND/pedal oedemaoedema --NoNo historyhistory ofof coughcough nornor haempotysishaempotysis PMHPMH:: NoneNone ofof notenote PSH:PSH: varicosevaricose veinvein strippingstripping inin leftleft legleg inin 19931993 PreviousPrevious C/SC/S inin 19851985 SHSH:: SheShe isis ofof sobersober habitshabits FH:FH: FatherFather dieddied ofof MIMI atat ageage 56,56, sistersister alsoalso dieddied ofof MIMI atat ageage 5454 andand brotherbrother hashas unstableunstable anginaangina PHYSICALPHYSICAL EXAMINATIONEXAMINATION:: GeneralGeneral Exam:Exam: PatientPatient waswas stablestable withwith goodgood generalgeneral conditioncondition IncreasedIncreased BMIBMI waswas notednoted ApyrexialApyrexial Hgt=6Hgt=6 mmoles/lmmoles/l BPBP 139/98139/98 P82P82 b/mb/m-- normalnormal volumevolume andand character,character, allall presentpresent andand =.=. RR=20RR=20 NoNo pedalpedal oedemaoedema NoNo signssigns ofof hyperlipidaemiahyperlipidaemia NoNo thyroidthyroid massmass BilateralBilateral varicosevaricose veinsveins werewere notednoted RespiratoryRespiratory system:system: NotNot inin respiratoryrespiratory failurefailure ChestChest movementsmovements werewere symmetricalsymmetrical ChestChest expansionexpansion waswas normalnormal PercussionPercussion notenote waswas normalnormal BreathBreath soundssounds == bilaterallybilaterally NoNo pleuralpleural rubrub CardiovascularCardiovascular system:system: NotNot inin heartheart failurefailure NoNo signssigns ofof pulmonarypulmonary hypertensionhypertension S1S1 S2S2 normalnormal NoNo murmursmurmurs oror addedadded soundssounds AbdominalAbdominal System:System: SNTSNT NoNo visceromegalyvisceromegaly NoNo pelvicpelvic massesmasses NoNo ascitesascites BSBS presentpresent CentralCentral nervousnervous system:system: FullyFully orientatedorientated NoNo meningismmeningism NoNo focalfocal signssigns Assessment:Assessment: 5151 yearyear oldold Mrs.Mrs. MkhizeMkhize withwith aa strongstrong familyfamily historyhistory ofof ischaemicischaemic heartheart disease,disease, varicosevaricose veinsveins andand increasedincreased BMIBMI presentedpresented withwith acuteacute dyspnoeadyspnoea andand chestchest painpain withwith nono signssigns ofof heartheart failurefailure nornor respiratoryrespiratory abnormality.abnormality. DifferentialDifferential Diagnosis:Diagnosis: 1.1. AcuteAcute coronarycoronary syndromesyndrome -- ?? UnstableUnstable anginaangina 2.2. PulmonaryPulmonary embolusembolus Investigations:Investigations: 1.1. ECGECG 2. Blood Investigations FBC: Hb : 15.0 Plt 208 WCC 13.27 U + E: Normal LFT: Normal INR: 1.2 LDH 876 Bloodgas: PH 7.39 CO2 4.8 kPa O2 18.9 kPa HCOз 21.8 mmol/l SO2 99% Cardiac enzymes: Myoglobin 40.2 Trop. I 0,02 D-dimers: › 20000mg ChestChest XX--rayray CTCT Angiogram:Angiogram: PulmonaryPulmonary EmbolismEmbolism Incidence Common, potentially lethal disease Diagnosis often missed as most patients present with non specific signs and symptoms. In US: PE is present in 60-80% of patients with DVT, even though more than half are asymptomatic. Third most common cause of death in hospitalised patients. ± 650 000 cases annually. Autopsy studies have shown ± 60% of patients who died in hospital had PE and diagnosis was missed in 70% of cases. Mortality/Morbidity Massive PE is second only to sudden cardiac death as cause of unexpected death. ± 10% of patients with PE die within first hour and 30% die from recurrent embolism. Anticoagulant treatment decreases mortality rate to less than 5%. SexSex:: RiskRisk ofof PEPE isis increasedincreased inin pregnancypregnancy andand duringduring postpartumpostpartum period;period; otherwiseotherwise sexsex isis notnot aa significantsignificant riskrisk factorfactor ofof PE.PE. AgeAge:: InIn hospitalisedhospitalised elderlyelderly patientspatients PEPE isis commonlycommonly missedmissed andand oftenoften isis thethe causecause ofof death.death. PathophysiologyPathophysiology 1.1. NaturalNatural historyhistory ofof pulmonarypulmonary embolismembolism ¾ Usually arise from thrombi in deep venous system of lower extremities, however rarely from pelvic, renal or upper extremity veins and right heart chambers. ¾ In the lung thrombi lodge at bifurcation of main pulmonary artery or lobar branches and cause haemodynamic compromise. ¾ Smaller thrombi travel distally, occluding a smaller vessel in the lung periphery. This produces an inflammatory response adjacent to the parietal pleura. ¾ Most emboli are multiple and lower lobes are commonly involved. 2.2. RespiratoryRespiratory consequencesconsequences ¾ IncreasedIncreased alveolaralveolar deaddead space,space, pneumoconstriction,pneumoconstriction, hypoxaemiahypoxaemia andand hyperventilation.hyperventilation. ¾ LaterLater regionalregional lossloss ofof surfactantsurfactant andand pulmonarypulmonary infarction.infarction. ¾ TheThe mechanismsmechanisms ofof hypoxaemiahypoxaemia includeinclude ventilationventilation –– perfusion,perfusion, mismatch,mismatch, intrapulmonaryintrapulmonary shunts,shunts, reducedreduced cardiaccardiac outputoutput andand intracardiacintracardiac shuntshunt viavia patentpatent foramenforamen ovale.ovale. ¾ InfarctionInfarction isis uncommonuncommon becausebecause ofof thethe bronchialbronchial collateralcollateral arterialarterial circulation.circulation. 3.3. HaemodynamicHaemodynamic consequencesconsequences ¾ Reduction of cross-sectional area of pulmonary vascular bed, resulting in increased pulmonary vascular resistance, which in turn increases the right ventricular after load. This may result in right ventricular failure. ¾ Humoral and reflex mechanisms can contribute to the pulmonary arterial constriction. ¾ Prior poor cardiopulmonary status in an important factor leading to haemodynamic collapse. ¾ Anticoagulant therapy decreases these consequences. Causes: Are multifactorial and not readily apparent in many cases. The following have been described in literature: 1. Venous stasis ¾ Leads to accumulation of platelets and thrombin veins. ¾ Increased viscosity may occur due to polycythemia and dehydration, immobility, raised venous pressure in cardiac failure or compression of vein by tumour. 2. Hypercoagulable states ¾ May be acquired or congenital. Factor V Leiden mutation causing resistance to activated protein C is the most common risk factor. Factor V mutation is present in up to 5% of the normal population is the most common cause of familial thromboembolism. ¾ Protein C, S, and antithrombin III deficiencies are other risk factors. Accounts for 10% of thrombosis in younger people. 3. Immobilisation ¾ Leads to local venous stasis by accumulation of clotting factors and fibrin, and thrombus is formed. ¾ Increase risk of PE occurs with prolonged bed rest or immobilisation of a limb. ¾ Paralysis increases the risk. 4. Surgery and Trauma ¾ Fractures of femur and tibia are associated with highest risk followed by pelvic and spinal fractures. ¾ Severe burns carry a higher risk of DVT and PE. ¾ Study by Greets in 1994 indicated major trauma was associated with 58% incidence of DVT. ¾ PE may account for 15% of all postoperative deaths. Leg amputations and hip, pelvic and spinal surgery have highest risks. 5. Pregnancy ¾ Risk is 1 in 200 deliveries to 1 in 1400 deliveries. ¾ Fatal cases may occur in 1 – 2 cases per 100 000 pregnancies. 6. Oral contraceptives and Eostrogen replacement ¾ Increased risk which is proportional to eostrogen content in HRT. ¾ Relative risk in threefold, but absolute risk is 20-30 cases per 100 000 per year. 7.7. MalignancyMalignancy ¾ IdentifiedIdentified inin 17%17% ofof patientspatients withwith thromboembolism.thromboembolism. ¾ CommonestCommonest withwith pancreaticpancreatic carcinomacarcinoma 8.8. OthersOthers ¾ StrokeStroke ¾ ObesityObesity ¾ VaricoseVaricose veinsveins ¾ PreviousPrevious historyhistory ofof thrombosisthrombosis ¾ CongestiveCongestive cardiaccardiac failurefailure ¾ InflammatoryInflammatory bowelbowel diseasedisease ¾ IndwellingIndwelling venousvenous catheterscatheters Clinical Presentation Presentation can be categorised in to 4 classes based on the acuity and severity of pulmonary arterial occlusion. 1. Massive pulmonary embolism ¾ Produce circulatory collapse and shock. ¾ Patient has hypotension, appears pale, weak, sweaty and oliguric and develops impaired mentation. 2. Acute pulmonary infarction ¾ Patients present with acute onset of pleuritic chest pain, beathlessness and haemoptysis. ¾ Chest pain may be indistinguishable from ischaemic myocardial