Intraoperative propofol-induced desaturation in lateral position during posterior fossa surgery

Sir,

A 35-year-old man, weighing 70 kg, was posted for left retromastoid suboccipital craniotomy and excision of left cerebello-pontine angle tumor. He had pulmonary tuberculosis 20 years ago and right upper lung-zone fibrosis on chest X-ray. Rest of the examination and investigations were unremarkable.

Anesthesia was induced with intravenous fentanyl 150 μg, propofol 120 mg, and rocuronium 70 mg. Trachea was intubated with 8.5 mm orotracheal flexometallic tube. Right subclavian central venous and right radial artery catheters were placed. Anesthesia was maintained with O₂–air–isoflurane with intermittent vecuronium and fentanyl. The patient was positioned right lateral with right arm hanging beyond the cephalic edge of the table. Intraoperatively, brain relaxation was inadequate despite mannitol 1 g/kg. So, propofol was started at 10 mg/kg/h after 50 mg bolus and isoflurane was switched off. Within 2 min, oxygen saturation (SpO₂) decreased to 76%. Heart rate increased to 90/min from 75/min and blood pressure decreased to 84/50 from 110/70 mmHg. Airway pressure and capnography were normal. Lung fields were clear on auscultation and bilateral air-entry was equal. EtCO₂ decreased slightly from 33 to 31 mmHg. Sample for arterial blood gas (ABG) was sent immediately; 100% O₂ was started and ephedrine 6 mg was injected intravenously. Propofol infusion was stopped. SpO₂ increased to 90% over 5 min and reached 98% after 15 min. FiO₂ was decreased to 0.5 and another sample for ABG sent. Serial ABG reports are shown as Table 1. Blood pressure increased to 110/65 mmHg over 10 min. Propofol infusion was restarted at 6 mg/kg/h. Brain relaxation was adequate subsequently and surgery was completed uneventfully. Trachea was extubated and the patient was shifted to ICU for overnight observation.

Table 1.

Arterial blood gases at points of time

Propofol bolus can cause hypotension, but intraoperative desaturation is rare. The possible causes of desaturation can be an increase in ventilation–perfusion mismatch, pulmonary embolism or allergic reaction. An episode of pulmonary embolism would have caused significant fall in EtCO₂ and persistent desaturation even after normalization of blood pressure. An allergic reaction is unlikely to get relieved without any anti-inflammatory drugs.

In anesthetized–paralyzed patient, change of position from supine to lateral has been shown to increase V/Q mismatch (pulmonary shunt increases from 5% in supine position to 10%–15% in lateral position), decrease in PaO₂ and increase in areas of atelectasis in the dependent lung in CT scan.[1,2] Furthermore, regional V/Q distribution becomes significantly less uniform as fractional blood flow through the atelectatic areas increase with anesthesia–paralysis in the right lateral position.[3,4] This increase in V/Q mismatch is reflected as an increase in P(A – a)O₂ gradient.

The patient had right upper lung-zone fibrosis and therefore V/Q mismatch, which was increased under anesthesia in the right lateral position. During the phase of propofol-induced acute hypotension, gravitational force may have significantly decreased the perfusion of the nondependent lung, and presence of residual isoflurane (0.8%) in the circuit reduced the pulmonary vascular tone of the dependent lung and reduced pulmonary blood flow of the nondependent lung.[5] Both the factors further increased V/Q mismatch, widening the (A – a) gradient, which lead to desaturation.

In conclusion, intraoperative propofol bolus can lead to significant desaturation in lateral position, particularly if it is associated with hypotension and pathological dependent lung.