Clinical presentation

An 82-year-old woman was admitted electively for surgical stabilisation of a persistently painful osteoporotic fracture of T12 vertebra She had a history of kyphosis with two previous osteoporotic fractures at T8 and T9 treated by kyphoplasty. She was noted to be persistently hypoxic with saturations of 80% on room air. She required 4 L/min of oxygen to maintain her saturations at >94%. There was no platypneoa-orthodeoxia. She had no history of significant cardiorespiratory disease, was an ex-20 pack year smoker and denied breathlessness. Cardiorespiratory examination was normal apart from moderate kyphosis.

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Figure 1

Colour flow doppler revealing shunt from right to left atria across a patent foramen ovale (white arrow); Left atrium= LA, Right atrium= RA and interatrial septum= IAS

Chest radiograph was normal as was spirometry with a forced expiratory volume (FEV₁) of 132% predicted, forced vital capacity (FVC) of 145% predicted with an FEV₁/FVC ratio of 71%. Age-adjusted d-dimer was not elevated and arterial blood gas on room air confirmed type 1 respiratory failure with a PO₂ of 7.1 kPa, a PCO₂ of 4.4 kPa and a large alveolar-arterial oxygen gradient of 8.2 kPa. CT scan of thorax revealed normal lung parenchyma. Echocardiography and trans-oesophageal echocardiography were performed which revealed an abnormality (figure 1).

The patient underwent surgical stabilisation with posterior pedicle fixation of T10/11 and L1/2 under general anaesthesia. FiO₂ requirement decreased during the operation from 0.5 to 0.3 and within 3 days of surgery saturations were 98% on room air (figure 2).

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Figure 2

Radiography revealing change in thoracic anatomy pre and post operatively

Question

What was the cause of hypoxia in this patient?

Answer

As illustrated, echocardiograph confirmed a shunt from right to left across the interatrial septum which on trans-oesophageal echocardiography was further characterised as a large patent foramen ovale (PFO) (see online supplementary videos 1 and 2). Right and left heart catheterisation was performed preoperatively and was normal apart from aortic oxygen saturation of 91%. The mean pulmonary artery pressure and right atrial pressures were normal at 20 mm Hg and 7 mm Hg, respectively.

We believe she developed an acute right-to-left shunt temporally related to a change in her thoracic anatomy as a result of her vertebral fracture, potentially causing stretching of her previously undiagnosed PFO. This anatomical change may have altered the direction of the jet of venous return to the right atrium resulting in increased flow through a pre-existing large PFO. This postulated mechanism has been previously described by Fukuoka et al 1 in a case of platypneoa orthodexia syndrome due to a vertebral fracture post a car accident.

Shunting in relation to kyphosis has been rarely described before in patients with platypneoa orthodexia syndrome.2 PFOs occur in 25% of the normal population3 and may become pathological in the form of a right-to-left shunt if there is pulmonary hypertension. Previously documented acquired anatomic causes, other than kyphosis,1 include lung resection,4 aortic dilatation5 and spinal cord injury.6 In lung resection, the problem can be due to an altered mediastinal anatomy displacing the interatrial septum in relation to a fixed inferior vena cava.4 Alternatively, postoperatively an elevated right hemidiaphragm can compress the right ventricle with resultant pressure increase in the right atrium and subsequent shunting through a PFO.4

In pathological interatrial shunting, the mainstay of treatment usually consists of closure of the septal defect. This can be achieved by surgical or percutaneous means with the latter the preferred option.2 Some cases of postlung resection cases have been successfully treated by plication of the right hemidiaphragm thus decompressing the right ventricle.2 4

The aim of surgery in our patient was to reduce pain and prevent further kyphosis of the spine. Fortuitously, there was redirection of flow away from the PFO due to a change in thoracic anatomy (figure 2) and the patients’ normal oxygenation was re-established.