Is Central Venous Access Fruitful in VAE: Role Beyond Aspiration

Sir, A 19-year-old 53 kg male presented with headache and seizures, diagnosed as a pineal region mass (3 × 3 cm), was scheduled for midline suboccipital craniotomy and excision in the sitting position. Preoperative evaluation, including clinical and blood investigations, was unremarkable. On the day of surgery, after standard intubation, the patient was mechanically ventilated in volume control mode with tidal volume – 480 mL, respiratory rate – 15 bpm, and positive end-expiratory pressure – 5 cmH2O to maintain end-tidal carbon dioxide (EtCO2) – 30–35 mmHg. Anesthesia was maintained with oxygen, air (40:60), sevoflurane, and fentanyl-rocuronium infusion. Post-intubation, large-bore peripheral cannulas, an invasive arterial line, and 7F triple-lumen right subclavian central line were established. Intermittent pneumatic compression pumps were applied to both lower limbs. A Mayfield 3-pin head holder was fixed, and after fluid administration, patient was gradually positioned for sitting while maintaining stable hemodynamics. The arterial and central venous pressure (CVP) transducers were leveled at the external auditory canal and nipple, respectively. The EtCO2 was 31 mmHg, and CVP was 4 mmHg. During muscle dissection, sudden drop in EtCO2 from 31 to 17 mmHg was observed, accompanied by a rise in CVP from 4 to 9 mmHg, with normal blood pressure and heart rate [Figure 1], airway pressure was between 14–15 cmH2O, and the oxygen saturation was 99–100%. The surgical team was alerted to the potential for venous air embolism (VAE). Saline was used to flood the surgical field, 100% oxygen was administered, and some air was aspirated from the CVP line. Gradually, the EtCO2 level increased, and CVP returned to baseline. Patient remained hemodynamically stable, allowing the surgery to continue without further complications. After reversing the neuromuscular blockade, the patient achieved a Glasgow coma scale – E4VTM6 with no deficit, and the trachea was extubated.Figure 1: (a) Vital trends (11:30–11:36) showing (yellow box) continuous fall in EtCO2 31 to 17 mmhg and increase in CVP 4 to 9 mmhg during VAE episode, (b) Vital trends (11:38–11:44) showing (yellow box) gradual rise in EtCO2 to 31 mmhg and return of CVP to 2 mmhg during VAE recovery, (c) graphical representation of CVP time and EtCO2 time graph during and recovery from VAE, (d) aspiration of some air (black arrow) from the CVP distal lineThe incidence of VAE in neurosurgical procedures performed in sitting ranges 10–76%.[1,2] This variation is influenced by the monitoring techniques used. Commonly used monitors for detection of VAE are transesophageal echocardiogram, EtCO2, precordial Doppler, and pulmonary arterial catheter.[3–5] In our patient, we observed a significant increase in CVP corresponding with the fall in the EtCO2. The CVP rise persisted till the period when EtCO2 remained low and came back to normal with air aspiration and improvement of the EtCO2. The other causes of the rise in CVP were excluded by the absence of hypervolemia, change in patient and transducer position, and change in ventilatory parameters. The CVP is elevated in VAE due to the obstruction caused by air bubbles in the vena cava, leading to a decreased venous return to the heart and increased pressure within the venous system. One reported case of a decrease in EtCO2 with an increase in CVP but without any real-time pictorial evidence of their concurrent change in trend; findings very useful for VAE detection as an adjunct to EtCO2.[6] However, if this fall in EtCO2 associated with acute hypotension may confuse the diagnosis of hypovolemic (acute blood loss) vs obstructive (VAE) shock. CVP can guide us in differentiating between these two critical scenarios when a transesophageal echocardiogram is not available or feasible. EtCO2 and CVP would fall in hypovolemic shock, but in VAE, CVP would rise with a decrease in EtCO2. CVP is commonly inserted in high-risk patients for VAE for air aspiration, though air aspiration is feasible only in 10% of cases.[7] It also helpful for inotropes and vasopressor administration in case of hemodynamic instability. The depicted rise followed by fall in CVP exhibited a useful information for diagnosing VAE also. It can be used to differentiate VAE from acute hypovolemia, where both causing fall in EtCO2, but CVP will decrease in acute hypovolemia. In conclusion, our case emphasizes the vital role of CVP monitoring in the complex arena of diagnosing VAE and hypovolemic shock. A sudden fall in EtCO2 with a significant drop in blood pressure, but simultaneously, an increase in CVP can be a key indicator of VAE. As an adjunctive tool, CVP provides essential information to enhance timely and accurate patient care, highlighting its significance in modern clinical practice. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.