pe
Table of Contents
pulmonary embolism (PE)
see also: EMedicine.com - PE
Epidemiology:
- deep venous thrombosis (DVT) & PE are much more common than is usually realised
- without anticoagulant prophylaxis, acute DVT's are found in (50% of these will have PE):
- 10-13% of all general medical pts admitted for bedrest > 1wk
- 29-33% of medical ICU pts
- 20-26% of pulm. disease pts kept in bed >= 3 days
- 27-33% of CCU pts post-AMI
- 48% of asymptomatic pts post-CAG surgery
- prophylactic heparin given to medical pts admitted via ED reduced overall mortality by 31%
- having an autopsy tends to double the likelihood that PE will be listed on death certificate
- PE was found in 18.5% of consecutive autopsies & were responsible for 11% of all deaths
- PE is 2nd only to AMI as a cause of sudden unexpected natural death at any age & the Dx is especially likely to be missed in older pts:
- in pts dying of massive PE, correct Dx made in 30% overall, but only 10% in those aged > 70yrs
- PE is the single most common unsuspected cause of death in pts who die while on ventilator
- Bedell found a major missed diagnosis in 14% of pts who die in hospital & had autopsy after CPR:
- 90% of these major missed diagnoses were PE's or bowel ischaemia
- at autopsy of pts clinically diagnosed with primary pulm. HT, 57% will have chronic pulm. thromboembolism rather than primary pulm. HT (the Mx is different for each of these diseases!!)
- The bad news about thromboembolism:
- most DVTs are asymptomatic
- most DVTs produce PE
- most PEs are asymptomatic
- many PEs are not detectable by current imaging techniques
- many DVTs are not detectable by current imaging techniques
- many non-detectable DVTs & PEs will progress, with recurrences that can cause sudden death and chronic morbidity
Clinical presentations
cardiac arrest
crashing massive PE
- systolic BP < 90mmHg or less than 40mmHg below usual BP for more than 15 minutes requiring high dose vasopressor support, or,
- persistent bradycardia HR < 40 with clinical features of shock, or,
- patient in extremis (diaphoretic, mottled, confused, sensation of dying)
non-crashing massive PE
- systolic BP < 90mmHg or less than 40mmHg below usual BP for more than 15 minutes but not requiring high dose vasopressor support, or,
- persistent bradycardia HR < 40
high risk sub-massive PE
- no features of massive but either:
- raised troponin,
- RV dysfunction on echo,
- large clot seen in RV,
- raised lactate,
- diaphoresis, mottled, severe tachypnoea, or,
- shock index (HR/SBP) > 1, or,
- Neutrophil to lymphocyte ratio >9.2 in patients with no other cause for a raised neutrophil count (suggests high mortality risk of around ~26%)
low risk sub-massive PE
- no features of higher severity as above, but:
- large clot burden on CT scan, and,
- definite RV dilatation, and,
- euvolaemic (no other cause for any haemodynamic instability such as dehydration or blood loss)
PE Severity Index (PESI) for 30 day mortality risk
- not really useful in an ED setting as we need more acute mortality risk scoring, and those with high-risk submassive PE may have a low PESI score
points | |
---|---|
age | age in yrs |
male | +10 |
cancer | +30 |
heart failure | +10 |
Ch lung disease | +10 |
HR ≥ 110 | +20 |
Syst BP < 100mmHg | +30 |
RR ≥ 30 | +20 |
Temp < 36 | +20 |
Altered mental status | +60 |
SaO2 < 90% | +20 |
- interpretation:
- ≤ 65 = class I (very low risk)
- 66-85 = class II (low risk)
- 86-105 = class III (intermediate risk)
- 106-125 = class IV (high risk)
- ≥ 126 = class V (very high risk)
Prognosis:
- 10% of pts with acute PE will die in 1st 60min
- presence of shock increases mortality 3-7x, with most deaths occurring within 1hr presentation1)
- mortality rates in the 1st 3 days following diagnosis depends upon severity of presentation2):
- cardiac arrest on arrival = ~95%
- requiring mechanical ventilation or CPR = ~80%
- syncope = ~40%
- haemodynamically stable patients who have echocardiographic evidence of right ventricular dysfunction = 15% (and a further 8% mortality within 1 yr if survive to discharge from hospital)3)
- all “stable” patients who had CT-PA or V/Q = 1-2%
- massive PE
- 90 day mortality: 58% (International Cooperative Pulmonary Embolism Registry (ICOPER) )
- sub-massive PE with abnormal RV function and raised troponin levels:
- hemodynamically stable PE, with an RV/LV transverse ratio on CTPA ≥ 0.9 was associated with increased death or clinical deterioration (HR 3.8, 95% CI 1.3–10.9, p = 0.007) 4)
- elevated troponins were associated with increased short-term death (OR 5.24; 95% CI 3.28–8.38) 5)
- raised high-sensitive cardiac troponin T (hsTnT) also showed increased death (OR 3.80, 95% CI 2.74–5.27) 6)
- in normotensive PE patients, hsTnT levels ≥ 14 pg/mL had a PPV and NPV for adverse 30 day outcomes of 8% and 100%, respectively 7)
- ? 5% mortality in 1st 48hrs with early anticoagulation
- 30 day mortality with anticoagulation: PEITHO study: 1.2% Becattini et al study: 7.7% I-COPER registry: 16% 8)
- 90 day mortality of all “sub-massive” cases: 15% (International Cooperative Pulmonary Embolism Registry (ICOPER) )
- of those patients who do not present with massive PE:
- 1/3rd will be eventually diagnosed & Rx:
- of these 1 in 12 will die from massive PE or complications of PE
- 2/3rds will remain undiagnosed (ie. 400,000 cases /yr in USA):
- of these, 1/3rd will die
- survivors will be at risk of:
- recurrent PE's
- risk is dependent upon:
- persisting underlying cause for thrombosis (eg. cancer, thrombophilia)
- “unprovoked” PE
- elevated D-Dimer after cessation of anticoagulant Rx
- compliance with anticoagulation Rx
- chronic thromboembolic pulmonary hypertension (CTEPH)
- 4% of treated patients by 2 yrs after PE
- risk depends upon:
- more than one episode of PE (odds ratio, 19.0)
- younger age (odds ratio, 1.79 per decade)
- a larger perfusion defect (odds ratio, 2.22 per decile decrement in perfusion)
- idiopathic pulmonary embolism at presentation (odds ratio, 5.70)9)
Pathophysiology:
aetiology:
thromboembolism:
- apart from gynae. surgery pts & major trauma pts, lower extremity venous thrombosis virtually always starts in the calf veins, and propagates above the knee in 87% of cases with symptomatic DVT
- in pts with PE, 70% have DVT evident on venograms (?50% on US) although up to 90% of all PEs arise from pelvic or lower DVTs
- risk of embolisation from DVTs:
- ileofemoral: ~100%
- popliteal-femoral: 60-80% (half of these PEs will be asymptomatic) - degree of proximity not important
- calf veins: 33-46%
- 35% of pts with PE
- 25% of lethal PEs
- 33% of “serious” PEs (NB. all PE's are clinically significant as minor ones may just be sentinal events!)
non-thrombotic PEs:
- amniotic fluid embolism:
- most commonly occurs near end of 1st stage of labour, but also in abortion or immediate post-partum period
- Mx:
- empty the uterus
- Rx DIC which contributes to the 80% mortality rate
- fat embolism:
- most commonly occur after fractures of long bones
- fat globules pass through pulm. circulation to enter systemic circulation where end-organs are affected via obstruction of end-capillaries causing petechiae, CNS symptoms (headache, irritability, convulsions, coma), ARDS, thrombocytopenia
- Mx:
- high-dose steroid Rx
- heparin is C/I as theoretical risk of increasing production of toxic fatty acids in the lungs.
- air embolism:
- generally iatrogenic, but may be from pressurised underwater breathing apparatus, air-powered drills, vaginal insufflation (in orogenital sex, esp. in pregnancy)
- often venous (causing circulatory collapse) and arterial (causing CNS impairment)
- clinical syndrome:
- loud churning murmur over precordium
- air bubbles within heart may be seen on echo
- circulatory collapse may result from as little as 5ml/kg of air forming an air lock in RV or pulm. circulation
- Mx:
- left lateral position in an attempt to trap air within RA
- other embolism:
- bile:
- post-percutaneous transhepatic drainage for Ca pancreas
- tumour:
- ~20% of embolism deaths in pts with solid cancers
- bone marrow:
- assoc. with # long bones or sternum/ribs in CPR
- IV drug preparations
- broken catheters
- parasites
- bullets
- cardiac vegetations
effects of PE:
- blockage of one portion of pulm. vasculature causes increased pulm. vasc. resistance
- ⇒ increased pulm. arterial pressures (if > 25% pulm. vasculature blocked)
- ⇒ increased RV pressures
- ⇒ if > 50% blocked then:
- signif. pulm. HT results with cor pulmonale
- in extreme cases, with PABP > 40mmHg, TI results
- haemodynamic collapse may occur ⇒ death
- ⇒ V/Q mismatches ⇒ nonperfused lung converted into physiologic dead space
- ⇒ increased minute ventilation (~1% increase per 1% decrease in perfused alveoli)
- eg. 15% increase via RR 14to16/min or 150ml increase in tidal volume ⇒ subtle!
- pain/anxiety ⇒ further hyperventilation
- after 24hrs, localised alveolar oedema may occur ⇒ rales
- release of neurohumoral factors may ⇒ pulm. vasoconstriction & bronchoconstriction ⇒ rhonchi
- small recurrent PE's:
- pulm. arterial endothelium is relatively incapable of lysing thrombus so most emboli remain there permanently!!
- V/Q & angio. abn. often resolve but this is by organisation & recanalisation
- decreased pulm. vascular distensibility, thus any attempt to increase cardiac output results in increased pulm. vasc. resistance
- ⇒ cardiac output can only increase if PABP increases enough to overcome this additional resistance
- ⇒ pulmonary HT ⇒ chronic cor pulmonale
Clinical features of thromboembolic PE:
Predisposing factors
- clinically apparent factor(s) present in 90% of pts with PEs:
- past DVT/PE - single strongest risk factor for recurrence (RR 15-30x)
- immobilisation
- malignancy
- stroke
- recent surgery
- pregnancy & post partum:
- recognised thromboembolism occurs in 3-4/1000 births
- accounts for 20-50% of maternal mortality
- 75% of clinically recognised PEs occur antepartum, > 50% in 1st 15wks gestation, HOWEVER, it is likely that incidence is equal in each of the trimesters, it just gets harder to diagnose later in pregnancy
- gradient compression stockings are strongly recommended for all pregnant pts
- NB. post-partum endometritis:
- risk of septic pelvic vein thrombophlebitis ⇒ septic pulmonary emboli in 40% if untreated
- thus consider anticoagulant Rx in pts with significant post-partum endometritis
- NB. ovarian vein thrombosis:
- diagnosis is rarely clinically apparent & usually made laparoscopically or at C.S. or on CT
- thrombus may extend into vena cava in which case a vena caval filter is indicated
- cardiac failure, AMI
- haematological factors (usually not clinically apparent)
- obesity (> 20% more than ideal)
- see also: haemostasis pathophysiology
Clinical presentations:
- PE is known as “the great masquerader”
- pleuritic chest pain
- “pneumonia”
- “asthma”
- “All that wheezes is not asthma” (Chevallier Jackson). PE may appear as asthma when diffuse wheezing results from the release of vasoactive and bronchoactive mediators. 10-20% of PE patients present with wheezing.
- “pleurisy”
- “angina” (4-30% present & misdiagnosed as angina)
- “AMI” (PE is 10% of deaths in pts Dx with AMI)
- conversely, AMI is the most common cause of death when clinical Dx of PE is incorrect!
- paradoxical embolism (usually from calf DVTs which tend have smaller emboli):
- 27% adults have patent foramen ovale
- pulmonary infarction mimicking “bronchogenic carcinoma” or if cavitates, a “lung abscess” on CXR or V/Q
- “psychosomatic hyperventilation” or “anxiety disorder”
- collapse, cardiac arrest with PEA and death - within 2 hrs of onset of massive PE
Historical features:
- dyspnoea (73%)
- pleuritic pain (66%)
- cough (37%)
- leg oedema (28%)
- leg pain (26%)
- haemoptysis (13%)
- palpitations (10%)
- wheeze (9%)
Examination features:
- tachypnoea (70%)
- rales (51%)
- tachycardia (30-44%)
- elevated neck veins (31%)
- S4 (24%)
- loud S2 (23%)
- cyanosis (11%)
- sweating (11%)
- rhonchi (5%)
- pleural rub (3%)
non-specific investigations:
ABG's:
- increased A-a gradient (75-90%):
- see under hypoxia
- normal A-a gradient:
- in air:
- < 10mmHg in young adults
- < 20mmHg in elderly
- < 4+ age/4 on air (Skorodin)
- < 10% pIO2
- A-a gradient = alveolar pO2 - arterial pO2
- alveolar pO2 = (760-47)xFiO2 - arterial PCO2/R, where R usually = 0.8
- may be normal in 23% of pts with PE
- if abnormal, is more likely to be due to other pulmonary pathology rather than PE
- thus although better than pO2 or pCO2, it has poor predictive value
- pO2:
- has zero predictive value (as does SaO2)
- 20% have pO2 > 80mmHg in air & 5% have pO2 > 100mmHg in air
- in pts with suspected PE (ie. probability of PE ~50%):
- the incidence of PE is higher in the group with pO2 higher rather than lower than an arbitrary pO2 cutoff value (whether 65, 70 or 80mmHg)
- low pCO2:
- poor marker - 35% PE's vs 33% no PE!
ECG:
- abnormal in 70% but non-specific abnormalities due to right heart strain:
- acute PE:
- ST/T changes (esp. III, V1-2) (49%)
- sinus tachycardia (44%)
- RBBB (15%)
- S1Q3T3 (12%)
- P pulmonale (6%)
- atrial arrhythmias (2%)
- chronic PE:
- RAH (7%)
- RVH (6%)
- T wave inversion (esp. III, V1-2) (40%) - if T inv. in both ant. & inf. leads this is highly specific for PE (75%) - Marriott
- pseudoinfarction (11%)
CXR:
- usually abnormal (84%) but mostly subtle abnormalities:
- atelectasis or parenchymal abnormality (68%) - may take 3 days to develop
- pleural effusion (48%)
- pleural based opacity (35%)
- eg. Hampton's hump (rare):
- pleural based density/lung consolidation with a rounded border pointing to hilum
- elevated hemidiaphragm (30%)
- reduced pulmonary vasculature (21%)
- prominent central pulmonary arteries (14%)
- Westermark's sign (7%)
- dilated pulmonary outflow tract on side of embolism with area of decreased perfusion distal to it
- pulmonary oedema (4%, BUT 13% pts without PE had it!!)
- useful in diagnosis of other conditions (eg. pneumonia, APO, pneumothorax)
- if “normal” in setting of hypoxaemia then suggestive of PE
lung scans for Dx of PE
V/Q scan
CT-PA
- PIOPED II study: sens 83% and spec 96% for PE thus positive likelihood ratio (LR) = 0.83/(1-0.96) = 21
pe.txt · Last modified: 2022/04/26 06:23 by gary1