PULMONARY PULMONARY EMBOLISM EMBOLISM EDHSEPTEMBER 2007SEPTEMBER 200 - PDF document

1 PULMONARY PULMONARY EMBOLISM EMBOLISM -E
PULMONARY PULMONARY EMBOLISM EMBOLISM -EDH-SEPTEMBER 2007SEPTEMBER 2007DR S C COKADR S C COKA CASE PRESENTATIONCASE PRESENTATION Mrs. N. Mkhize 51 yr old presented with:Mrs. N. Mkhize 51 yr old presented with:--Shortness of breath for one days durationShortness of breath for one days durationRisk factors:Risk factors: --Raised BMIRaised BMI--Strong family hx of MIStrong family hx of MI--father and sister father and sister both died of MI in their 50both died of MI in their 50’’ssNo other traditional risk fa

2 ctorsNo other traditional risk factors O
ctorsNo other traditional risk factors On EnquiryOn Enquiry ::--Grade 3 dyspnoea (NYHAC)Grade 3 dyspnoea (NYHAC)associated chest pain under left breastassociated chest pain under left breastradiating to the back described as stabbing in radiating to the back described as stabbing in naturenatureNo nausea, vomitting nor sweating.No nausea, vomitting nor sweating.pain was of sudden onset at rest pain was of sudden onset at rest not related to meals

3 not related
not related to meals no identifiable relieving nor exacerbating factorsno identifiable relieving nor exacerbating factors--No history of orthopnea/ PND/pedal oedemaNo history of orthopnea/ PND/pedal oedema--No history of cough nor haempotysis PMHPMH : None of note: None of notePSH:PSH: varicose vein stripping in left leg in varicose vein stripping in left leg in 19931993Previous C/S in 1985Previous C/S in 1985SHSH : She is of sober hab

4 its: She is of sober habitsFH:FH: Fath
its: She is of sober habitsFH:FH: Father died of MI at age 56, sister also died Father died of MI at age 56, sister also died of MI at age 54 and brother has unstable of MI at age 54 and brother has unstable anginaangina PHYSICAL EXAMINATIONPHYSICAL EXAMINATION : : General Exam:General Exam: Patient was stable with good general condition Patient was stable with good general condition Increased BMI was notedIncreased BMI was notedApyrexialApyrexialHgt=6 mmoles/l BP 139/98 P82 b/mHgt=6 mmoles/l BP 13

5 9/98 P82 b/m--normal volume normal volu
9/98 P82 b/m--normal volume normal volume and character, all present and =. RR=20and character, all present and =. RR=20No pedal oedemaNo pedal oedemaNo signs of hyperlipidaemiaNo signs of hyperlipidaemiaNo thyroid massNo thyroid massBilateral varicose veins were notedBilateral varicose veins were noted Respiratory system:Respiratory system: Not in respiratory failure Not in respiratory failure Chest movements were symmetrical Chest movements were symmetrical Chest expansion was normal Chest expansion wa

6 s normal Percussion note was normal Perc
s normal Percussion note was normal Percussion note was normal Breath sounds = bilaterally Breath sounds = bilaterally No pleural rub No pleural rub Cardiovascular system: Cardiovascular system: Not in heart failure Not in heart failure No signs of pulmonary hypertension No signs of pulmonary hypertension S1 S2 normal S1 S2 normal No murmurs or added sounds No murmurs or added sounds Abdominal System: Abdominal System: SNT No visceromegaly No pelvic masses No pelvic masses No ascites No ascites BS presen

7 t BS present Central nervous system:Cent
t BS present Central nervous system:Central nervous system: Fully orientated Fully orientated No meningismNo meningismNo focal signs No focal signs Assessment:Assessment: 51 year old Mrs. Mkhize with a strong family 51 year old Mrs. Mkhize with a strong family history of ischaemic heart disease, history of ischaemic heart disease, varicose veins and increased BMI varicose veins and increased BMI presented with acute dyspnoea and chest pain with no signs of heart failure chest pain with no signs of heart fa

8 ilure nor respiratory abnormality. Diffe
ilure nor respiratory abnormality. Differential Diagnosis:Differential Diagnosis: 1.Acute coronary syndrome Acute coronary syndrome --? Unstable ? Unstable anginaangina2.2.Pulmonary embolus Pulmonary embolus Investigations:Investigations: 1.ECG 2. 2. Blood Investigations Blood Investigations FBC : Hb : 15.0Hb : 15.0Plt 208 Plt 208 WCC 13.27WCC 13.27U + EU + E LFT: Normal LFT: Normal : 1.2 : 1.2 LDH 876 LDH 876 Bloodgas: PH 7.39PH 7.39CO2 4.8 kPa CO2 4.8 kPa O2 18.9 kPaO2 18.9 kPaHCOHCO21.8 mmol/l21.8

9 mmol/lSO2 99%Cardiac enzymes: Cardiac en
mmol/lSO2 99%Cardiac enzymes: Cardiac enzymes: MyoglobinMyoglobin40.2Trop. I Trop. I 0,02 0,02 DD--dimersdimers:: ›20000mg 20000mg Chest XChest X--ray CT Angiogram: CT Angiogram: Pulmonary EmbolismPulmonary Embolism Incidence Incidence Common, potentially lethal disease Common, potentially lethal disease Diagnosis often missed as most patients present with non specifiDiagnosis often missed as most patients present with non specific signs and symptoms.symptoms.In US: PE is present in 60In US: PE is prese

10 nt in 60--80% of patients with DVT, even
nt in 60--80% of patients with DVT, even though more 80% of patients with DVT, even though more than half are asymptomatic.than half are asymptomatic.Third most common cause of death in hospitalised patients. Third most common cause of death in hospitalised patients. ±±650 000 650 000 cases annually. cases annually. Autopsy studies have shown Autopsy studies have shown ±±60% of patients who died in hospital had PE 60% of patients who died in hospital had PE and diagnosis was missed in 70% of cases. and diag

11 nosis was missed in 70% of cases. Mortal
nosis was missed in 70% of cases. Mortality/Morbidity Mortality/Morbidity Massive PE is second only to sudden cardiac death as cause of unMassive PE is second only to sudden cardiac death as cause of unexpected expected death.±±10% of patients with PE die within first hour and 30% die from10% of patients with PE die within first hour and 30% die fromrecurrent recurrent embolism. Anticoagulant treatment decreases mortality rate to leembolism. Anticoagulant treatment decreases mortality rate to less than s

12 s than 5%.5%. SexSex : Risk of PE is inc
s than 5%.5%. SexSex : Risk of PE is increased in pregnancy and Risk of PE is increased in pregnancy and during postpartum period; otherwise sex is during postpartum period; otherwise sex is not a significant risk factor of PE.not a significant risk factor of PE.AgeAge :In hospitalisedIn hospitalisedelderly patients PE is elderly patients PE is commonly missed and often is the cause commonly missed and often is the cause of death.of death. PathophysiologyPathophysiology 1.Natural history of pulmonary emboli

13 sm Natural history of pulmonary embolism
sm Natural history of pulmonary embolism Usually arise from thrombi in deep venous system Usually arise from thrombi in deep venous system of lower extremities, however rarely from pelvic, of lower extremities, however rarely from pelvic, renal or upper extremity veins and right heart renal or upper extremity veins and right heart chambers.chambers.In the lung thrombi lodge at bifurcation of main In the lung thrombi lodge at bifurcation of main pulmonary artery or lobar branches and cause pulmonary artery o

14 r lobar branches and cause haemodynamich
r lobar branches and cause haemodynamichaemodynamiccompromise.Smaller thrombi travel distally, occluding a smaller Smaller thrombi travel distally, occluding a smaller vessel in the lung periphery. This produces an vessel in the lung periphery. This produces an inflammatory response adjacent to the parietal inflammatory response adjacent to the parietal pleura.pleura.Most emboli are multiple and lower lobes are Most emboli are multiple and lower lobes are commonly involved. commonly involved. 2.2.Respi

15 ratory consequencesRespiratory consequen
ratory consequencesRespiratory consequencesIncreased alveolar dead space, Increased alveolar dead space, pneumoconstriction, hypoxaemia and pneumoconstriction, hypoxaemia and hyperventilation.hyperventilation.Later regional loss of surfactant and Later regional loss of surfactant and pulmonary infarction.pulmonary infarction.The mechanisms of hypoxaemia include The mechanisms of hypoxaemia include ventilation ventilation –perfusion, mismatch, perfusion, mismatch, intrapulmonary shunts, reduced cardiac intra

16 pulmonary shunts, reduced cardiac output
pulmonary shunts, reduced cardiac output and intracardiac shunt via patent output and intracardiac shunt via patent foramen ovale.foramen ovale.Infarction is uncommon because of the Infarction is uncommon because of the bronchial collateral arterial circulation. bronchial collateral arterial circulation. 3.3.Haemodynamicconsequences Reduction of crossReduction of cross--sectional area of pulmonary sectional area of pulmonary vascular bed, resulting in increased pulmonary vascular bed, resulting in increase

17 d pulmonary vascular resistance, which i
d pulmonary vascular resistance, which in turn increases the vascular resistance, which in turn increases the right ventricular after load. This may result in right right ventricular after load. This may result in right ventricular failure.ventricular failure.Humoraland reflex mechanisms can contribute to and reflex mechanisms can contribute to the pulmonary arterial constriction.the pulmonary arterial constriction.Prior poor cardiopulmonary status in an important Prior poor cardiopulmonary status in an imp

18 ortant factor leading to factor leading
ortant factor leading to factor leading to haemodynamichaemodynamiccollapse.Anticoagulant therapy decreases these Anticoagulant therapy decreases these consequences. consequences. Causes:Causes: Venous stasis Venous stasis Surgery and TraumaSurgery and Trauma 7.7.Malignancy Identified in 17% of patients with Identified in 17% of patients with thromboembolism.thromboembolism.Commonest with pancreatic carcinoma Commonest with pancreatic carcinoma 8.8.Others Stroke Obesity Varicose veins Varicose veins Previ

19 ous history of thrombosis Previous histo
ous history of thrombosis Previous history of thrombosis Congestive cardiac failure Congestive cardiac failure Inflammatory bowel diseaseIndwelling venous catheters Indwelling venous catheters and develops impaired mentation. and develops impaired mentation. Pulmonary Embolism Diagnosis (PIOPED) study were:Pulmonary Embolism Diagnosis (PIOPED) study were:New onset atrial fibrillation New onset atrial fibrillation Investigations Investigations 1.Lab studies Lab studies a) Arterial a) Arterial bloodgasbl

20 oodgasMay reveal hypoxaemia, May reveal
oodgasMay reveal hypoxaemia, May reveal hypoxaemia, hypocapniahypocapniaand respiratory alkalosis, and respiratory alkalosis, however predictive value of hypoxaemia is low.however predictive value of hypoxaemia is low.Low PaO2 in conjunction with dyspnoea in high risk settings may Low PaO2 in conjunction with dyspnoea in high risk settings may have a strong predictive value.have a strong predictive value.b) Db) D--dimerDegradation product produced by Degradation product produced by plasminplasmin–mediated p

21 roteases mediated proteases is measured
roteases mediated proteases is measured via ELISA or latex agglutination tests. Latex is measured via ELISA or latex agglutination tests. Latex agglutination is unreliable and has a sensitivity of 50agglutination is unreliable and has a sensitivity of 50--60%. ELISA 60%. ELISA is more sensitive but does not carry a highly negative predictivis more sensitive but does not carry a highly negative predictive e value.value.DD--dimertest misses 10% of patients with PE while only 30% of test misses 10% of patients

22 with PE while only 30% of patients with
with PE while only 30% of patients with positive Dpatients with positive D--dimerhave a confirmatory diagnosis of have a confirmatory diagnosis of PE. PE. Test alone is not recommended for definitive diagnosis or Test alone is not recommended for definitive diagnosis or initiating treatment. initiating treatment. 2.2.Imaging Studies Imaging Studies a) Chest radiographa) Chest radiographMay initially be normal In later stages may show In later stages may show WestermarkWestermarksign (dilatation of pulmo

23 nary vessels and a sharp (dilatation of
nary vessels and a sharp (dilatation of pulmonary vessels and a sharp cutoff), cutoff), atelectasis, a small pleural effusion, and , a small pleural effusion, and an elevated diaphragm.an elevated diaphragm.b) Ventilation b) Ventilation ––perfusion scan (V/Q)perfusion scan (V/Q)Important diagnostic tool.Important diagnostic tool.Scans should be interpreted either as having a Scans should be interpreted either as having a diagnostic or non diagnostic pattern, indicating diagnostic or non diagnostic pattern,

24 indicating whether the patient has a hig
indicating whether the patient has a high likelihood or does whether the patient has a high likelihood or does not have a high likelihood of having PE. not have a high likelihood of having PE. Diagnostic pattern:Diagnostic pattern:I.I.Normal V/Q scan indicates an absence of any perfusion defects. 4% of these of any perfusion defects. 4% of these patients may still have a PE.patients may still have a PE.II.II.High probability scan findings are 2 or High probability scan findings are 2 or more segmental or 1

25 larger perfusion defects in the presenc
larger perfusion defects in the presence of normal chest radiography findings and ventilation scan findings. ±±87% of these patients 87% of these patients were found to have PE.were found to have PE. High probability perfusion High probability perfusion lung scan showing lung scan showing segmental perfusion segmental perfusion defects in right upper lobe defects in right upper lobe and sub segmental and sub segmental perfusion defects in right perfusion defects in right lower lobe. lower lobe. 3.3.Pulmon

26 ary angiography Pulmonary angiography Go
ary angiography Pulmonary angiography Gold standard Gold standard Safe procedure Safe procedure Negative pulmonary Negative pulmonary angiogram findings even angiogram findings even if false negative exclude if false negative exclude clinically relevant PE.clinically relevant PE. Angiogram showing abrupt termination of ascending branch of right upper lobe Pulmonary embolism 4.4.ECGMost common findings are tachycardia and Most common findings are tachycardia and non specific STnon specific ST--T wave abnorma

27 lities.T wave abnormalities.Classic find
lities.T wave abnormalities.Classic finding of right heart strain Classic finding of right heart strain demonstrated by an S1Q3T3 pattern is demonstrated by an S1Q3T3 pattern is observed in only 20% of patients with observed in only 20% of patients with proven PE.proven PE.5.5.Doppler ultra sound Doppler ultra sound Used in assessing DVTUsed in assessing DVT6.6.Other Other Spiral CT Spiral CT MRI Treatment Treatment Immediate full anticoagulation is Immediate full anticoagulation is mandatory.mandatory.Dia

28 gnostic investigations should not delay
gnostic investigations should not delay Diagnostic investigations should not delay anticoagulant therapy.anticoagulant therapy.Initial anticoagulation is performed with Initial anticoagulation is performed with heparin to slow or prevent progression of heparin to slow or prevent progression of embolus. Patient should be started embolus. Patient should be started simultaneously on oral warfarin. simultaneously on oral warfarin. After a therapeutic dose of warfarin is After a therapeutic dose of warfarin is e

29 stablished, heparin is discontinued and
stablished, heparin is discontinued and established, heparin is discontinued and warfarin is continued.warfarin is continued. Therapy Therapy Should be considered for patients who are Should be considered for patients who are metalasemetalaseLMWH should be initiated at first suspicion of PE.LMWH should be initiated at first suspicion of PE.embolisationembolisation 3.3.Surgical Treatment Surgical Treatment IVC interruption by insertion of an IVC filter IVC interruption by insertion of an IVC filter (Greenfie

30 ld) is indicated in the following:(Green
ld) is indicated in the following:(Greenfield) is indicated in the following:a)a)Those patients who have an absolute contra indication to anticoagulant therapy indication to anticoagulant therapy b)b)Patients with massive PE who survived but in Patients with massive PE who survived but in whom recurrent embolism would be fatal.whom recurrent embolism would be fatal.c)c)Patients who have objectively documented Patients who have objectively documented recurrent thromboembolism adequate recurrent thromboemboli

31 sm adequate anticoagulant therapy not wi
sm adequate anticoagulant therapy not with standing. anticoagulant therapy not with standing. Complications Complications 1.Sudden cardiac deathSudden cardiac death2.2.Obstructive shockObstructive shock3.3.Pulselesselectrical activity electrical activity 4.4.Atrial or ventricular arrhythmias Atrial or ventricular arrhythmias 5.5.Secondary pulmonary arterial hypertension Secondary pulmonary arterial hypertension 6.6.Corpulmonale7.Right to left intra cardiac shunt Right to left intra cardiac shunt 8.8.Lung

32 infarction 9.Pleural effusion Pleural e
infarction 9.Pleural effusion Pleural effusion 10.10.Paradoxical embolism Paradoxical embolism Prognosis Prognosis Depends on two factors:(1) underlying disease Depends on two factors:(1) underlying disease and (2) appropriate diagnosis and treatment and (2) appropriate diagnosis and treatment At 5 days of therapy, 36% of lung scan defects At 5 days of therapy, 36% of lung scan defects resolved, at 2 weeks 52% are resolved, at 3 resolved, at 2 weeks 52% are resolved, at 3 months 73% resolved.months 73% re

33 solved.The mortality rate in patient wit
solved.The mortality rate in patient with undiagnosed The mortality rate in patient with undiagnosed PE is 30%.PE is 30%.In the PIOPED study the 1 year mortality rate In the PIOPED study the 1 year mortality rate was 24%. Deaths occurred due to cardiac was 24%. Deaths occurred due to cardiac diseases, recurrent PE, infection and cancer.diseases, recurrent PE, infection and cancer.Risk of recurrence of PE due to recurrence of Risk of recurrence of PE due to recurrence of proximal venous thrombosis is proxima