Intraoperative Blood Pressure Discrepancy Between Arms During Prone Position!
Cervicothoracic scoliosis associated thoracic outlet syndrome (TOS) even though infrequent can present with significant anesthetic challenges. TOS is a disorder resulting from compression of neurovascular structures crossing the thoracic outlet. TOS in children with congenital thoracic scoliosis may be due to the natural history of curve progression and constriction of the lung by the rib cage.1 Neurological complications occur in 95% of cases.2 However, in the first 2 decades of life, it is the vascular TOS which predominates.3
We report a case of a 13-year-old girl (25 kg, 128 cms) who was diagnosed with Diastematomyelia (type 1) with Tethered cord syndrome and was scheduled for surgical excision of bony spur and detethering of the cord. She had associated congenital thoracic scoliosis which gradually progressed over years (Fig. 1). Preoperatively, spirometry revealed mild restrictive lung disease even though it did not manifest clinically. All other investigations including echocardiography were within normal limits. In the operating room (OR), standard monitors, that is electrocardiogram, pulse oximeter (SpO2), and noninvasive blood pressure (NIBP) were attached. Baseline BP, heart rate, and SpO2 were 102/64 mm Hg (right arm), 108 beats/min (sinus rhythm) and 99% (room air), respectively. General anesthesia was induced with fentanyl 50 mcg and propofol 50 mg followed by facilitation of tracheal intubation with rocuronium 30 mg. Additional monitoring aids included end-tidal carbon dioxide and invasive BP (IBP) monitoring through a 22-G cannula inserted in the left radial artery. Anesthesia was maintained with sevoflurane in oxygen and nitrous oxide mixture (40:60) along with intermittent boluses of fentanyl 1 mcg/kg and rocuronium 0.2 mg/kg as and when required. The patient was positioned prone, and eyes and all other pressure points were protected. Both upper limbs were placed parallel to the trunk, and head was placed in neutral position. Once the patient was positioned prone and surgery started, a fall in BP to 50/36 mm Hg was observed in IBP recording. The arterial line was flushed with normal saline to rule out any effect of dampening on the waveform. Immediately, a bolus of ephedrine 2 mg was administered which also failed to improve IBP. Simultaneously, NIBP measured in right arm was 98/52 mm Hg which further increased to 107/62 mm Hg after administration of ephedrine. We continued NIBP monitoring (right arm) as obtaining additional arterial access was difficult due to prone position and sterile drapes. All mechanical causes of dampening of the arterial waveform including the compression of the left upper limb or pressure on inferior vena cava (causing low cardiac output) were excluded. There was no temporal relationship with the different stages of ongoing surgery. Possible causes of hypotension such as hypovolemia, blood loss, anaphylaxis, and effect of anesthetics were excluded. Surprisingly, when the patient was turned supine following completion of the surgery, the invasive arterial waveform spontaneously resumed its normal pattern and BP recordings were now similar to NIBP (right arm). Subsequently, reversal of anesthesia and tracheal extubation were uneventful. The vitals remained stable during the postoperative period.
One of the cause of discrepancy in interarm BP readings is TOS; other causes being aortic dissection, atherosclerosis,4 and hemiparetic stroke.5 Physiologically, this discrepancy is minimal and does not affect clinical management. In an already stretched concave side of scoliotic spine with fused upper ribs, prone position may have possibly aggravated impinging of ipsilateral subclavian artery. This in turn manifested as dampened arterial waveform, falsely low BP and poorly palpable pulse on the concave side. In the supine position, this pressure effect was not sustained, and thus, the pulsation and the normal waveform returned spontaneously.