How is
venous air embolism (VAE) detected and treated?
VAE is a potentially life-threatening event
which must be detected and treated promptly. It is often associated with cases
performed in the sitting position but it can occur under certain physiologic
circumstances. In neurosurgical procedures, air may enter the venous system via
non-collapsible venous channels such as the dural sinuses and diploic veins.
When the head is elevated above the heart a pressure gradient can exist which
facilitates air entrainment. In the sitting position, the incidence of VAE is
almost 4 times higher than the incidence in other positions (45% vs. 12%). Air
can also be entrained from the pin sites during a stereotactic biopsy in the
semi-sitting position.
Monitoring for VAE generally includes a
precordial Doppler, capnometry, central venous pressure (CVP) catheter, pulse
oximeter, and esophageal stethoscope. When placed properly, as determined by
rapid bolus fluid injec-tion through a CVP catheter, a precordial Doppler can
detect 0.1 ml of air. Transesophageal echocardiography (TEE) is also sensitive
for detecting and recognizing intra-cardiac air but is not generally used in
this setting due to technical difficulty and cost. The CVP catheter is best
located at the junction of the superior vena cava and the right atrium, where
air collects after its entrainment into the venous system. It is a diagnostic
device for detection or confirmation of VAE, rarely a therapeutic measure. It
is of value when aspirating air from the right atrium in the rare instance of
massive VAE creating an air lock. Multiorifice catheters are more efficacious
for air aspiration than single-lumen catheters.
Pulmonary artery catheters may provide valuable
infor-mation because pulmonary artery pressures rise during VAE. Unfortunately,
pulmonary artery catheters are less efficient for air aspiration than CVP
catheters. Continuous end-tidal carbon dioxide (ETCO2) monitoring
demon-strates a rapid decline as VAE ensues. Arterial PaCO2 rises
simultaneously, increasing the gradients between these two measurements. The
difference rises as alveolar dead space increases. If minute ventilation
remains constant, the divergence between PaCO2 and ETCO2
may represent a useful marker for the severity of VAE. Classically, the “mill
wheel” murmur heard through an esophageal stethoscope is associated with
intracardiac air. Once detected, VAE requires rapid treatment.
Surgeons must be alerted immediately when VAE
is detected so that open sinuses may be identified and flooded with saline or
closed surgically to halt the entrainment of air. In the absence of an obvious
source of air entrainment, venous pressure in the head should be raised in an
attempt to force blood through the concealed opening. This is accom-plished by
lowering the head relative to the heart, manipulat-ing the table’s position, or
occluding venous outflow from the head with jugular compression. N2O
administration should cease immediately. Rapid diffusion of N2O into
air bubbles will expand their volume, creating mechanical obstruction to flow,
and hemodynamic compromise may ensue. Volume, inotropes, and vasopressor
administration contribute to hemodynamic support, churning large air pockets
into smaller ones to be carried out to the pul-monary blood vessels.
The application of PEEP in an attempt to
increase CVP and decrease the magnitude of VAE is controversial. High levels of
PEEP greatly increase the risk of hypotension in patients who are already
intravascularly depleted. Furthermore, right atrial pressure may be increased
in the face of lowered left atrial pressure, predisposing the patient to
paradoxical air embolism through a patent foramen ovale. Application of PEEP
should probably be limited to situations in which all other attempts at
preventing con-tinuous VAE have failed. Even moderate amounts of VAE may result
in decreased PaO2. Initial treatment should be supportive with
enhanced inspired oxygen concentrations guided by pulse oximetry and arterial
blood gas determina-tions. Postoperatively, patients may develop an
interstitial pulmonary process that usually resolves in 24–48 hours.
Related Topics
Privacy Policy, Terms and Conditions, DMCA Policy and Compliant
Copyright © 2018-2023 BrainKart.com; All Rights Reserved. Developed by Therithal info, Chennai.