Massive PE Secondary to Physiotherapy....

Physiotherapy? That's not one of the major risk factors for PE I hear you cry...

But that's how this scenario played out on a recent shift on the floor...

Scenario

30 something previously well female presents acutely to the ED via ambulance, after a syncopal episode in the street whilst walking home after an appointment with her physiotherapist. She had been receiving treatment for a "calf sprain" that she had complained of, with ongoing pain in her right calf for the preceding 2 weeks. Bystanders called for an ambulance, and on arrival to the ED, she was found to have a systolic BP of around 70mmHg, hypoxic with saturation of 80% on air, and tachycardic with a rate of 150 bpm. She denied having any chest pain. She was immediately transferred to a resuscitation bay, and rapidly assessed.

Assessment

A - Patent and protected airway, despite being in extremis, she was able to speak, and was orientated, and coherent.

B - Tachypnoeic  with a rate > 30 breaths per minute, but moving air, sats of > 90% on 15L O2 via non re-breather mask.

C - Hypotensive at 90/60, HR of 140. Cool peripheries

Her ECG showed a sinus tachycardia, with S1Q3T3 pattern, right axis deviation, and right ventricular strain pattern. 

Basic bedside echo demonstrated a large right ventricle. 

At this stage massive PE was suspected, though, meanwhile her BP had improved somewhat to 110 systolic, her heart rate had come down to 120 bpm, and she was no longer hypoxic on high flow O2. 

The decision was made to obtain a CTPA which demonstrated bilateral PEs, with a large clot sitting and occluding her right main pulmonary artery, with a dilated RV confirmed on CT. 

She was subsequently thrombolysed with 100mg of Alteplase, and heparinised, and transferred to ICU where she stabilised. She was found to have an elevated troponin, and BNP.

I thought I would take this opportunity to look at massive and submassive PE in a bit more detail

Massive PE

PE causing cardiogenic shock with persistent hypotension with a systolic BP < 90mmHg for more than 15 minutes.

Submassive PE

PE without hypotension, but with evidence of right ventricular dysfunction or strain (with elevated troponin in the absence of ECG changes of STEMI)

RV strain indicators

- ECG - RBBB, right axis deviation, dominant R waves in anterior chest leads, S1Q3T3 pattern, anteroseptal T inversion

- Echo - Dysfunction of RV +/- pulmonary hypertension

- CTPA - Dilation of RV - diameter RV/LV greater than 0.9

Biochemical Indicators

- Elevated troponin i > 0.4ng/ml indicating myocardial necrosis

- Elevated BNP (brain natriuretic peptide) > 500pg/ml

Management

Massive PE

- Thrombolysis if not contraindicated, with 100mg recombinant tPA given via peripheral IV over 2 hours

- Heparin - 5000 iu intravenous bolus with the first 10mg of rtPA, and infusion after thrombolytic administered.

- Transfer to ICU/HDU setting for post thrombolytic monitoring 

Submassive PE

- The jury is still out on this, though if evidence of RV strain, it may be reasonable to proceed with thrombolysis if not contraindicated. 

Options when thrombolysis contraindicated or ongoing instability

- Catheter embolectomy / fragmentation

- Surgical embolectomy

Suggested Exclusion Criteria for tPA

Absolute

- Prior ICH

- known malignant intracranial neoplasm

- ischaemic stroke within 3 months

- suspected aortic dissection

- active bleeding or bleeding diathesis

- recent surgery

- recent significant closed head / facial trauma

Relative

- Age > 75

- Current anticoagulation use

- Pregnancy

- Non-compressible vascular puncture

- Traumatic / prolonged CPR (> 10 mins)

- Severe or uncontrolled hypertension (> 180mmHg systolic, or > 110mmHg diastolic)

- recent internal bleeding

- dementia

- major surgery within 3 weeks.

Suggested AHA Algorithm 

Further Reading

AHA Scientific Statement on Management of Massive and Submassive PE

ECG in PE - LITFL