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By Dr Emma Batistich and Prof Peter Jones

Dr Emma Batistich and Prof Peter Jones are Emergency Medicine Specialists at Auckland Emergency Department. Both Emma and Peter completed the EGLS course 3 months prior to this case and stated they would not have been able to do it if they had not attended the course!


74 year old man usually well with a background of dual chamber pacemaker for symptomatic AV block, no other significant comorbidities, nil regular medications, lives independently with this wife.

The pacemaker had been implanted in December 2010 and required reburial of the leads 2 years later for threatened lead erosion. On a recent pacemaker check there had been evidence that the RV lead was non-functioning. 2 days prior to presentation he underwent a procedure where the device and leads were extracted with reimplantation. This was completed without complication. Fig 1 shows his post procedure xray with normal placement of the RV leads.

Fig 1 – CXR performed immediately after the lead extraction/replacement showing RV leads in the correct position

Three days after the procedure he presented in the evening to the ED after he developed severe (10/10) central chest pain after rolling over in bed. He described the pain as sharp and pleuritic with some radiation to lateral aspect of chest but not back. He had pain with breathing in deeply but did not feel short of breath. The pain was constantly present with occasional sharp exacerbations.

On exam he was alert, appeared uncomfortable and intermittently in distress with more severe pain.

Observations: HR 65, BP 157/104, RR 18, SpO2 95% on air, afebrile.

JVP was not elevated, HS dual + no murmur, no leg oedema and calves were soft and non-tender.

Chest clear with equal air entry.

Pacemaker pocket not red, no exudate, not particularly tender, wound healthy.

Fig. 2 ECG on arrival to the Emergency Department. SR 63/min, normal axis, nil acute changes

The initial concern with the presentation was of migration of the RV leads through the ventricular wall with potential pericardial effusion/tamponade development.

Other differentials for this presentation were acute coronary syndrome, aortic dissection, PE and pneumothorax. These were all thought to be less likely than a complication of the recent procedure.

A bedside echo was performed which revealed no significant pericardial effusion (fig 3)

Fig 3 – PLAX view with no effusion

A CXR was performed (Fig 4) – which showed that the RV wire appeared to have migrated to the lateral wall of the ventricle, of note the cardiac size remained stable.

Fig 4. CXR: Migration of the RV wire.

The pacemaker technician interrogated the device and confirmed wire migration with concern for perforation through the RV wall.

Cardiology was consulted and a formal bedside echo was performed by an echo technician, who confirmed that the wires had perforated through the RV, with no significant pericardial effusion.

He was treated with IV fentanyl which significantly improved his pain. As he was stable, the plan was to admit him to CCU with a plan to operate the following day.

Around 15 minutes after the formal echo had been performed the patient suddenly developed worsening chest pain. He was extremely distressed, clutching his chest, said the pain felt a lot different, now radiating to his throat. He complained of feeling very dizzy and presyncopal. Shortly after his change in condition he lost consciousness and suffered a PEA arrest. After a brief period of CPR he gained ROSC but remained critically unwell with a systolic BP of 50 with a HR of 60 and a decreased level of consciousness.

Repeat bedside USS by an emergency physician showed a new large pericardial effusion with echocardiological signs of tamponade (fig 5 and 6).

Fig 5 – PSLX showing new effusion

Fig 6 – apical view showing new effusion

An ultrasound guided pericardiocentesis was performed using a long 22G LP needle initially utilising an apical approach. Two clinicians were involved – one holding the echo probe and another controlling the needle. USS confirmed correct placement of the needle but minimal blood was aspirated. This was thought to be due to clotting of the blood preventing aspiration through a small bore needle.

A decision was made to place a larger bore pericardial pig-tail drain. This was performed under ultrasound guidance using a seldinger technique again in the apical approach with two clinicians. Interestingly again, aspiration of the pericardial fluid with the needle yielded little blood but on placement of the drain 120ml was aspirated immediately with radiological decrease in tamponade and of the patient clinically. Around 10 minutes after the procedure was performed, the patient had normal haemodynamics and had regained consciousness.

The patient was taken to the OR that night and had the leads replaced. The drain remained insitu and was removed the following day after echo evidence that the effusion had resolved.

He made a full recovery and was discharged 2 days later.

This case is an excellent example of the utility of bedside ultrasound to rapidly diagnose and treat an imminently life threatening condition.


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