Wandering around the hospital on a Friday afternoon (because I’m too much of a keeno to go home), looking for something to do because all the patients on the Care of the Elderly ward nap after lunch, I ended up in A&E. I love A&E!
The doctors in A&E are all super nice and they let you do things because there is lots to do, and the floor is so nice and the little bay compartments with their individual otoscopes hanging on the walls are so cute and- yeah, I really liked A&E.
I, along with my placement partner, spent most of the time with a young woman called Rosa (not real name). It was also really nice to see a young person after weeks with the elderly.
My partner took this history from her:
PC: 1 day history of chest tightness upon inhalation during exercise, SOBOE, light headed
HPC: Recent flight from Spain, cold symptoms prior to flight
PMHx: tonsilitis, gastroenteritis 4 months ago
DHx: just started on a new oral contraceptive (progestogen only pill)
FHx: father has asthma, maternal and paternal grandmothers had breast cancer, grandfather has Parkinson’s
SHx: non-smoker, 10 units of alcohol/week
Given the symptoms, one of the most important things to rule out was a pulmonary embolism (PE), which has the potential to be fatal.
I performed an ECG on her- my first ECG on a real patient! There was T wave inversion in lead III but otherwise normal.
Then, I did a peak flow- 370L/min (which is okay, probably a bit low considering I got 400 and she’s taller than me. Although, she probably wasn’t trying as hard as I was…)
I almost took some bloods after almost putting a cannula in. I was so close. I took too long hyping myself up and preparing the equipment and by the time I pushed in, the cannula was broken…so close. The doctors ended up doing it, much faster than I would have, and did an arterial blood gas (ABG) whilst they were at it. Blood tests sent off, included a D-dimer, which if low, make PE unlikely. The ABG was normal.
I really need to put a cannula in. I have a greater mental block with cannulas than I ever did with venepuncture. I’ve had a few opportunities but I’m terrified of doing it. Maybe this week.
On clinical examination, her chest was clear.
She also went for a chest X-ray, which showed a bit of whispy white consolidation in the right lung.
So, Rosa most likely did not have a PE and when we left, the doctor said it was probably a viral respiratory tract infection and they were waiting for bloods to come back. I’m afraid we’re going to have to stay in suspense over this one, because I’m only a keeno from 9 to 5.
Definition: occlusion of pulmonary vessels, most commonly by a thrombus that has travelled to the vascular system from another site
-emboli usually arise from thrombi in the iliofemoral veins (deep vein thrombosis*)
-rarely PE results from clot formation in the right heart (in AF patients or post-MI), or septic emboli from right-sided infective endocarditis
–other rare causes: fat, air or amniotic fluid embolism, neoplastic cells, parasites
-Risk factors for PE are the same as for deep vein thrombosis.
Major RFs: recent surgery, late pregnancy, C-section, post-partum, varicose veins, malignancy, > 1 wk immobility (e.g. hospitalisation), previous DVT/PE, family history of DVT/PE
Minor RFs: hypertension, oral contraceptive, HRT, COPD, serious infection, long-distance sedentary travel (so, not Spain), thrombophilian (e.g. antiphospholipid syndrome), polycythaemia, thrombocythaemia, obesity, cardiac failure, recent MI etc.
Epidemiology: relatively common condition, occurs in 10-20% of those with confirmed proximal DVT.
Mortality rate in England & Wales = 30,000-40,000/yr
–Small PEs: may be asymptomatic
–Moderate PEs: sudden onset dyspnoea (may be only symptom), pleuritic chest pain (sharp chest pain exacerbated by forceful breathing), cough, haemoptysis (if there is pulmonary infarction)
–Massive PEs (medical emergency): as with moderate + severe central pleuritic chest pain, shock, pale, sweaty, dizziness, collapse –> acute right heart failure or sudden death
→Always suspect PE in sudden collapse 1-2 wks after surgery.
–Small PEs: often no clinical signs, earliest sign is tachypnoea or tachycardia
–Moderate PEs: tachypnoea, tachycardia, pleural rub, low O2 saturation
–Massive PEs (medical emergency): shock/hypotension, central cyanosis, elevated JVP, right ventricular heave, accentuation of second heart sound, gallop rhythm, AF
–Multiple recurrent PEs: chest pain, fatigue, dyspnoea, syncope, right ventricular heave, loud pulmonary second sound, right heart failure in advanced disease. (i.e. signs and symptoms of pulmonary hypertension, developing over weeks to months)
-PE can cause atelectasis (partial collapse or incomplete inflation) which can result in a dull percussion note and a pleural effusion which is exudative in nature, causing a ‘stony dull’ percussion note.
-Signs of DVT- unilateral leg swelling
-Assessment of clinical probability of PE is essential in the interpretation of tests. Clinically assessment tools such as the Wells’ Criteria and PERC rule are used.
–Plasma D-dimer– a negative tests excluded PE in those with low clinical probability (highly sensitive, low specificity). It’s used to rule out rather than rule in because lots of things can raise your D-dimer, including, infection, inflammation and malignancy.
–CT pulmonary angiography (CTPA)-sensitive and specific in determining if emboli are in pulmonary arteries = FIRST LINE DIAGNOSTIC TEST
–Radionuclide lung scan (V/Q scan)- demonstrates ventilation-perfusion defects. PE excluded in those with normal scan. Results may be in inconclusive in those with cardiopulmonary disease. Perform if CTPA contra-indicated e.g. because of pregnancy, or unavailable.
–MRI/Magnetic Resonance Angiography– if CT contraindicated
–Pulmonary angiography- sometimes undertaken if surgery is considered in acute massive embolism or if V/Q scan unequivocal (invasive, rarely necessary)
–Doppler Ultrasound– clots in pelvic or iliofemoral veins
–Chest X-ray– often normal with small/medium emboli but good to exclude differentials, may show decreased vascular markings (oligaemia) and raised hemidiaphragm (loss of lung volume), dilated pulmonary artery, linear atelectasis (minimal degree of collapse as not taking deep breaths due to pleuritic chest pain); a late feature of pulmonary infarction is a wedge-shaped opacity next to pleural edge, sometimes with a pleural effusion
–ECG– may be normal with small/medium emboli, commonest finding is sinus tachycardia, features of acute right heart strain may be seen- right axis deviation, tall peaked P waves in lead II (P pulmonale– right atrial enlargement), inverted T waves in V1 to V4, and right bundle branch block. Classic SI,QIII,TIII pattern- deep S wave in lead I, Q wave in III, inverted T wave in III (classic in exams, not so classic in real life). May see AF.
–ABG– may be normal with small/medium emboli, may show hypoxaemia and hypocapnia: RESPIRATORY ALKALOSIS
–Echocardiogram- diagnostic in massive PE, shows proximal thrombus and right ventricular dilation
Prevention: graduated pressure stockings (TEDs) and prophylactic heparin (e.g. Dalteparin, Enoxaparin) prophylaxis, early mobilisation and adequate hydration post-surgery.
It is important to assess all patient’s risk of developing DVT/PE and give LMWH if risk high
Stop HRT or OCP pre-op if possible
Test for thrombophilia in young people with recurrent PEs or with a family history of PE/DVT
Inferior vena caval filter insertion may be necessary if recurrent emboli despite anti-coagulation
Management depends on clinical probability of a PE, assessed using clinical scoring systems such as the Wells’ Criteria.
Wells’ Criteria for PE:
PE is the most likely diagnosis = 3
Clinical signs and symptoms of DVT = 3
> 3 days immobilisation or surgery < 4wks ago = 1.5
HR > 100 bpm = 1.5
Previous diagnosis of DVT or PE =1.5
Haemoptysis = 1
Malignancy diagnosed in last 6M = 1
If the Well’s score is < 4 this indicates low clinical probability of PE. A D-dimer should be performed and if negative, you can be happy that it is extremely unlikely the patient has a PE. If it is positive, you should start them on Low Molecular Weight Heparin (LMWH) and request a CTPA to image the pulmonary arteries and if this is positive for a PE, start them on anti-coagulation such as warfarin or rivaroxaban. If the CTPA is negative, look for another diagnosis.
If the Well’s score is ≥ 4this indicates high clinical probability of PE. You should start them on LMWH and request a CTPA to image the pulmonary arteries and if this is positive for a PE, start on them anti-coagulation such as warfarin or rivaroxaban. If the CTPA is negative, look for another diagnosis.
-Patients diagnosed with PE be taken off LMWH when INR > 2 and should remain on warfarin, aiming for INR 2-3. They may stay 6wks on warfarin if obvious remedial cause, otherwise ≥ 3-6 months, long term if recurrent emboli or underlying malignancy.
Management of Large PE (haemodynamically unstable patient):
–Oxygen if hypoxic (10-15L/min)
-IV Morphine (5-10mg) + antiemetic if pained or very distressed
-Considere thrombolysis with Alteplase if critically ill with massive PE
-IV heparin (LMWH or unfractionated)
-If haemodynamically unstable (SBP < 90 mmHg):
In order, moving on to next if SBP not improving-
1- IV fluids/colloid
2- IV dobutamine (inotrope)
3- IV noradrenaline
4- Consider thrombolysis if not already given
-If/ when patient haemodynamically stable (SBP > 90 mmHg), start on warfarin.
-Confirm diagnosis (probably didn’t have time to do a CTPA whilst all this was going on).
-Syncope and death may rapidly follow a massive PE
-Pulmonary infarction, pulmonary hypertension
-Right heart failure
-untreated = 30% mortality
-most PE death occur within 1 hr.
-treated = 8% mortality
-patients have increased risk of future thromboembolic events
*Deep Vein Thrombosis- coming soon to a blog near you