Introduction
The sitting position, anatomically and physiologically, has several advantages such
as good surgical access, less bleeding, and better ventilation. However, it could
be associated with potentially devastating complications, such as venous air embolism
(VAE), cerebral ischemia due to hemodynamics compromise, quadriplegia, tension pneumocephalus,
and compressive neuropathy.[1] Historically, any kind of surgical intervention in the posterior fossa of the brain
was avoided since it was believed that any type of manipulation in this area could
lead to loss of respiration, sudden deterioration, and even death.[2] In 1906, Sir Victor Horsley performed the first posterior fossa surgery in the lateral
oblique position.[3] The first neurosurgical procedure in the sitting position was performed by De Martel
in 1913, for a posterior fossa tumor under local anesthesia.[4] In 1928 in the United States, Frazier and Gardner used this position for surgery
on the Gasserian ganglion to treat trigeminal neuralgia.[5] Slbin et al in 1976 published their experience of 180 neurosurgical patients in
this position.[6] Since this position has numerous possible complications, many neurosurgeons may
prefer the prone position. However, the advantages of sitting or semisitting position
over prone are many. In the sitting position, there is improved access to the tracheal
tube, face, chest wall, and arms. Once the patient is positioned prone, the access
to the airway is very difficult, not to mention that the endotracheal tube is vulnerable
to movement and tube position needs to be rechecked clinically repeatedly, to rule
out endobronchial intubation or accidental extubation. Pressure exerted on the abdomen
and raised intra-abdominal pressure may decrease thoracic compliance and increase
airway pressure, which in turn can increase intracranial pressure (ICP). Numerous
potential pressure ulcer areas in the prone patient include the face, breasts, genitalia,
and bony prominences. Postoperative facial edema, visual loss, and retinal ischemia
as a result of direct pressure on the eye has also been reported following prone surgery.[7]
Preoperative Optimization
To ensure patient safety and a successful outcome, a thorough preoperative anesthetic
evaluation to decide if the sitting position is suitable for the patient is essential.
As in any neurosurgical case, all patients need to be evaluated preoperatively for
physical and neurological status, as well as blood and other pertinent investigations
to formulate an appropriate anesthetic plan. Cardiovascular assessment (electrocardiogram
[ECG], echocardiogram) is important because there may be perioperative blood pressure
fluctuations, ECG changes, arrhythmias, and myocardial ischemia or failure, which
occur due to central neurogenic effects on the myocardium and the autonomic nervous
system or concurrently associated medical conditions. Any signs such as dysphagia,
loss of gag reflex, and altered state of consciousness should be noted preoperatively
as these are important for assessment at emergence and to plan postoperative care.
Documented preoperative ability of the patient to move the neck without neurological
symptoms such as paraesthesia, pain, or dizziness should be ascertained. This precludes
the use of the sitting position in affected patients, so as to prevent unnecessary
or excessive movement of the neck and any further impairment of function that may
occur due to positioning during surgery.
Contraindications
In the sitting position, the risk of venous air embolism (VAE) is high. It may have
cardiovascular, pulmonary, and neurological sequelae. After analysis of 28 studies
conducted from 1972 to 2007, Fathi et al found the incidence VAE to be 0 to 76% in
sitting position as compared to 0 to 12% in the horizontal position.[9] The presence of a patent foramen ovale (PFO), which is about 25% in the normal population,
is a contraindication to performing any surgery in the sitting position as it can
lead to paradoxical air embolism (PAE) with resultant ischemia or infarction in the
heart or brain through the right-to-left shunt. In the above meta-analysis by Fathi
et al, the incidence of paradoxical embolism in neurosurgical procedures in the semisitting
position was between 0 and 14%.[9] In 2018, Klein et al in their systematic review analyzed four observational studies
with a total of 977 patients who underwent surgery of the posterior fossa or cervical
spine in the semisitting position, of whom 82 had a PFO, and observed an incidence
of VAE in 33 of these 82 patients (40.2%) and found no incidence of paradoxical embolism.
They also surmised that if the PFO is large or if there is a permanent right-to-left
shunt with history of PAE, closure of PFO, usually transcutaneously, should be preferably
done prior to surgery. PFO can be detected preoperatively by two main methods: Transesophageal
echocardiography (TEE) allows for direct visualization of the interatrial septum and
PFO, whereas a transcranial Doppler (TCD) is a highly sensitive indirect method relying
on microbubbles detected in a cerebral artery (middle cerebral artery [MCA]) after
the intravenous injection of air in the presence of a PFO.[10] Thus, a mandatory contrast echo/bubble test done preoperatively could help rule
out a PFO, if the sitting position is to be used.
Other relative contraindications for neurosurgery in the sitting position include
atherosclerotic cardiovascular disease, hemodynamic instability, and severe cervical
canal stenosis.[11]
Anesthesia Technique and Monitoring
Neuroanesthesia requires a good understanding of neurophysiology to maintain adequate
cerebral hemodynamics while providing optimum operating conditions. Induction with
intravenous agents such as propofol, opioids, and nondepolarizing muscle relaxants
attenuates the hypertensive response to laryngoscopy and intubation, with minimal
effects on intracerebral hemodynamics. For neurosurgery in the sitting position, reinforced
endotracheal tubes are preferred to prevent intraoperative kinking, which may lead
to increase in the airway pressure and ICP. The endotracheal tube should also be carefully
secured ensuring that there is no obstruction of cerebral venous drainage.[12] Although there are no consensus recommendations, total intravenous anesthesia (TIVA)
is usually preferred. In a meta-analysis by Chui et al, both propofol and volatile
anesthesia had similar brain relaxation scores; however, mean ICP values were lower
and CPP values higher with propofol.[13] Bastola et al in their study of 75 patients concluded that propofol, sevoflurane,
and desflurane had comparable clinical profiles when used for craniotomies.[14]
Nitrous oxide, however, should be avoided as it causes cerebral vasodilation and increase
in cerebral blood flow (CBF) and ICP. Since it has a high blood:gas partition coefficient
(0.47), the use of nitrous oxide could worsen intraoperative VAE, if it occurs, and
any existing postoperative pneumocephalus. Losasso et al in their study have repudiated
this finding and found that 50% nitrous oxide did not increase the risk of VAE.[15] In another study by Losasso et al, the use of nitrous oxide helped reduce opioid
and inhalational agent requirement, facilitating early recovery and neurologic assessment.[16]
The use of PEEP (positive end-expiratory pressure) during neurosurgical procedures
performed in the sitting position is another controversy. Physiological PEEP of 4
to 5 cm H2O helps decrease the venous gradient as the increase in the transthoracic pressure
is transmitted to the central veins, which increases the CVP. This helps decrease
the amount of air entrained during VAE. Voorhies et al recommended PEEP for both prevention
and treatment of VAE,[17] whereas Giebler et al concluded that PEEP in this position should be abandoned as
it does not decrease the incidence of VAE but is associated with significant adverse
cardiovascular effects.[18] Dilmen et al used PEEP at physiological levels (5–10 cm H2O) to prevent VAE.[19]
In addition to the routine monitoring of the neurosurgical patient, specific monitoring
is required to screen for known complications such as VAE. Capnography (end-tidal
CO2 [ETCO2]) is used as a standard of care monitor for all cases of general anesthesia, and
a sudden drop of 2 mm Hg or more in the ETCO2 is highly suggestive of air embolism. Historically, the esophageal stethoscope was
used to confirm a Mill-Wheel murmur that is classically associated with large intracardiac
air emboli and described as a “characteristic splashing auscultatory sound.” However,
the sensitivity of the esophageal stethoscope is very low. The change in the heart
sounds are not detected until the rate of infusion of air is more than 1.7 mL/kg/min.[20] Precordial Doppler is highly sensitive as compared to capnography for the diagnosis
of VAE. However, it is a subjective, nonquantitative method, and the anesthesiologist
needs to be familiar with it use.[21] TEE has the advantage of making a precise diagnosis and is very sensitive. TEE allows
for the detection of small air volumes in the heart, even 0.01 mL/kg of air. Its use
is essential for diagnosing the patent foramen.[9] Feigl et al evaluated the risk of PAE in patients with PFO, and concluded that with
standardized anesthesia, TEE, and capnometry monitoring for VAE, these patients can
be safely operated in the semisitting position.[22] Pandia et al, in a trial with 140 patients undergoing surgery of the posterior fossa,
made a comparison between using ETCO2 and TEE for the diagnosis of air embolism and concluded that in the presence of a
diagnosis of air embolism using TEE with no associated changes in capnography, it
is unlikely for the air embolism to cause any hemodynamic imbalances.[23]
Another monitor that has recently emerged to further ensure patient safety in the
sitting position is regional cerebral oximetry (rSO2). Heroabadi et al in 2017 found that there was a statistically significant reduction
in mean arterial pressure (MAP) and rSO2, 15 minutes after establishment of sitting position, but this was not clinically
significant and may not increase the risk of cerebral hypoxia in elective neurosurgery
in the sitting position.[24] Schramm et al in 2016 studied cerebral oxygen saturation in supine and sitting positions
at predetermined endpoints. They found that rSO2 values increased after sitting position, and therefore it was safe to use this position
for cerebral oxygen saturation.[25]
Technique of Positioning
Positioning of the neurosurgical patient in the sitting position is challenging. It
is the responsibility of both the surgeon and anesthesiologist. Patient positioning
is done after induction of general anesthesia and placement of arterial and venous
lines, and requires adequate anesthesia depth and maintenance of hemodynamic stability.[26]
The sitting or Fowler’s position is a standard patient position in which the patient
is seated in an upright sitting position (45–60 degrees) and may have knees either
bent or straight. In the semisitting position, the head elevation is less, about 30
to 45 degrees, and the foot of the bed is raised at the knee to bend the legs. In
the modified sitting position, the table is positioned in a steep Trendelenburg position,
the back end is elevated, and the Mayfield clamp is fixed at the back section of the
table. In case of VAE, by lowering the back section of the table, it can be returned
to the horizontal position. The lower extremities are semiflexed with legs resting
on pillows, thus reducing flexion and kinking of blood vessels of the lower extremities
and therefore improving venous return and decreasing the risk of thromboembolism.[27]
Complications
In this position, the incidence of hypotension varies from 5% to 32%. This is due
to pooling of blood in the lower limbs, decreasing the venous return, stroke volume,
and cardiac output. The resultant hypotension decreases cerebral perfusion pressure
(CPP) and can result in cerebral hypoxia.[28] Anesthetic agents, both inhalational and intravenous such as propofol, have vasodilator
properties and depress cardiac contractility that may also contribute to the hemodynamic
instability. Preoperative intravascular status and positive-pressure ventilation further
aggravate the hypotension. Therefore, the patient should be preloaded with adequate
intravenous fluids and the sitting position gradually given over a period of 5 to
10 minutes with continuous monitoring of blood pressure, to check whether the patient
tolerates the same. Ranjith et al, in their prospective observational trial of 20
patients, preloaded the patients with a volume of 20 mL/kg of crystalloid before positioning
them from supine to sitting position. This maintained hemodynamic stability and avoided
any vasopressor requirement.[29]
Dohn and Gardner in 1956 devised a “G” suit that consisted of inflatable leggings
and an abdominal binder, which, by constricting the lower part of the body, prevented
pooling of blood and increased the venous return, and thus reduced hypotension in
anesthetized patients in this position.[30] Meyer et al studied the use of antishock trousers (MAST suit) and PEEP 8 to 10 cm
H2O in children undergoing neurosurgical procedures in the sitting position. After the
sitting position was given, inflation of the MAST suit induced a dramatic increase
in right atrial pressure (RAP) and jugular bulb venous pressure (JBVP), reinforced
by addition of PEEP.[31] However, ventilation and hypoperfusion of intra-abdominal organs need to be borne
in mind. Intermittent pneumatic compression stockings for the lower limbs should therefore
be mandatorily used for all patients who are operated in the sitting position. However,
as noted by Martin, these have minimal value as prophylaxis against air embolism.[32] Correct positioning of the patient with flexion of the hips and elevation of the
knees to the level of the heart will also minimize the hypotension; modified sitting
position is therefore advocated.[3] Dilmen et al found the incidence of hypotension with positioning to be 37.6% in
adults and 18.6% in children, as well as a correlation between high ASA (American
Society of Anesthesiologists) physical status and hypotension with positioning.[19]
Extreme flexion of the head and neck may obstruct the jugular venous and lymphatic
drainage, which increases the cerebral venous pressure and may cause postoperative
face, tongue, soft palate, and posterior pharyngeal wall edema. This can lead to postoperative
airway obstruction, hypoxemia, and need for reintubation and prolonged ventilation.
Use of oral airways and long duration of surgery are also associated with this condition.[3]
[33] Rath et al noted that infants are at a higher risk of edema because of a small tracheal
diameter and relatively large tongue.[34]
Cervical spine ischemia with neck and head hyperflexion, especially compounded by
hypotension, can lead to quadriplegia. The risk increases with age and vascular and
structural cervical spine pathology. It is recommended to keep a sufficient distance
of at least two to three fingerbreadths between the chin and nearest bone, usually
the clavicle.[3] Somatosensory evoked potential monitoring has been proposed as an indicator of the
adequacy of regional spinal cord perfusion in these cases. Buchheit et al in their
study in 1998 concluded that SSEPs may help identify, and thus prevent, midcervical
flexion myelopathy secondary to placement of a patient in the semisitting or sitting
position.[35]
Incidence of peripheral nerve injuries is less than 1%. As per the “Summary of Task
Force Consensus on the Prevention of Perioperative Peripheral Neuropathies Relevant
to Positioning for Neurosurgery,” padding at the elbow decreases the risk of upper
extremity neuropathy. Specific padding is used to prevent pressure of a hard surface
against the peroneal nerve at the fibular head to decrease the risk of peroneal neuropathy.[36]
The main concerns in the sitting position are the complications that can occur and
their sequelae as noted previously. VAE is a potentially serious complication that
occurs since the site of surgery is above the level of the heart, which causes a negative
pressure or subatmospheric gradient between the right atrium and the cranial venous
sinuses, and allows the air to entrain into the venous system. Pathophysiology and
clinical manifestations of VAE depend on amount and rate of air entrainment.[37] The lethal amount of air entrained for adults is 3 to 5 mL/kg. Once the air gets
into the circulation, it passes through the right atrium into the pulmonary circulation
and impedes gas exchange that causes the drop in ETCO2. When the amount of air is small, the pulmonary capillaries can filter it, but when
the air volume is larger, there may be significant right ventricular outflow obstruction
with decrease in cardiac output, hypotension, and myocardial and cerebral ischemia.
Modest amounts of air entrainment into the pulmonary circulation may lead to pulmonary
vasoconstriction, release of inflammatory mediators, bronchoconstriction, and an increase
in ventilation-perfusion mismatch. If the embolism is large (> 5 mL/kg), a gas airlock
scenario can lead to right-sided heart failure and immediate cardiovascular collapse.[21] The true incidence of VAE depends on the method of detection used. Ganslandt et
al in 2013 in their study of 600 cases had an overall 19% incidence of VAE. The incidence
of VAE differed depending on the monitoring technique used for detection of VAE. The
incidence was 25.6% of the cases in which TEE was used, and 9.4% of the patients monitored
with Doppler ultrasound.38 Fathi et al found that the incidence of VAE ranged from
25% to 50% as documented through precordial Doppler and up to 76% with TEE.[9] Mammoto et al studied 21 patients undergoing neurosurgery in the sitting position
and monitored those patients with TEE and capnography. During VAE, microbubbles detected
on TEE in the right atrium were noted, and the severity was graded as follows: grade
0 (0 microbubble), grade 1 (< 5 microbubbles per frame), grade 2 (10–12 microbubbles
per frame), and grade 3 (too many microbubbles to be counted per frame). A fall in
ETCO2 greater than 3 to 4 mm Hg occurred with every episode of grades 2 and 3 air embolus.[39] Feigl et al used the Tubingen scale to grade VAE: grade 0 (no air bubbles visible,
no air embolism); grade I (air bubbles on TEE); grade II (air bubbles on TEE with
decrease of ETCO2 ≤3 mm Hg); grade III (air bubbles on TEE with decrease of ETCO2
> 3 mm Hg; grade IV (air bubbles on TEE with decrease of ETCO2 > 3 mm Hg and decrease
of mean arterial pressure ≥20% or increase of heart rate ≥40% (or both); and grade
V (VAE causing arrhythmia with hemodynamic instability requiring cardiopulmonary resuscitation).[22] Harrison et al noted that VAE can occur at any time during the surgery and noted
an incidence of VAE of 9.3% (38 of 407 of pediatric neurosurgery cases). These occurred
during opening of the dura, tumor dissection, and on closure of the dura.[40] The treatment for VAE is aimed at stopping further entrainment of air into the circulation
and managing any complications. If VAE is suspected either by fall in ETCO2 or microbubbles on TEE, the neurosurgeon is immediately informed and the surgical
field should be irrigated or covered with saline soaked swabs, ventilated with 100%
oxygen and intravenous fluids, and, if necessary, vasopressors started to support
the circulation.[21]
[37]
[40] Transient bilateral compression of the jugular veins is a technique described to
reduce the inflow of air through the exposed sinuses, as well as identify the source
of air entrainment. In neurosurgical procedures performed in the sitting position,
when VAE occurs, transient manual jugular venous compression limits further air entry
into the circulation. As per the study by Eckle et al, an intrajugular balloon was
placed into bilateral jugular vessels and inflated during VAE, as an alternative technique
aimed at reducing the risk of air embolism. Additionally, accumulated air could be
aspirated from an orifice of the catheter. These findings may help in further development
of intrajugular balloon catheters designed to reduce the risk of air embolism. However,
two central venous lines would have to be placed, and temporary inflation and compression
of both veins could damage the intimal layer of the vessel. Additional risks include
accidental arterial puncture or cannulation, nerve injury, and pneumothorax.[41]
Longatti et al in their preliminary study of 10 cases suggested that a CO2-enriched surgical field decreased the hemodynamic effects of VAE, since CO2 emboli are more soluble and therefore better tolerated than air emboli.[42]
Matjasko et al reported a significantly higher incidence of VAE in children (62%)
compared with adults (23%); however, a retrospective comparison between adults and
children undergoing suboccipital craniotomy in the sitting position by Cucchiara et
al showed a lower incidence of VAE in children (16 of 48) than in adult controls (22
of 48).[43]
[44] Bithal et al similarly reported the incidence as 22% in children and 28% in adults
out of a total of 430 patients (96 children and 334 adults) who underwent posterior
fossa surgery in the sitting position.[45] As per Gupta et al, since the sagittal sinus pressure remains positive in children
even in the sitting position up to the age of 9 years, VAE was compared in children
between the age range of above 2 years and below 9 years and in those above 9 years
of age, but the incidence of VAE was found to be comparable (p = 0.7) in the two groups.[46]
Gupta et al noted in their study of complications related to the sitting position
during pediatric neurosurgery that intraoperative hemodynamic instability can occur
unrelated to VAE. These were mainly bradycardia, tachycardia, and occasional ventricular
premature beats, associated with hypotension or hypertension, due to tumor manipulation
near the brainstem, and they resolved spontaneously after cessation of surgical stimulation.[46]
One of the advantages of the sitting position is decreased blood loss due to drainage
of cerebral venous blood away from the operating site. Black et al reported that in
adult patients, intraoperative blood loss and volume of blood transfused were significantly
less in patients undergoing posterior fossa craniectomy in sitting position as compared
with those operated in the horizontal position.[47] Orliaquet et al compared perioperative complications in children undergoing posterior
fossa surgery in sitting and prone positions and concluded that the volume of intraoperative
blood transfusion was significantly larger in the prone position as compared with
the sitting position.[48]
Schäfer et al analyzed the records of 799 patients between 1990 and 2009 and found
that VAE tends to activate platelets, evoke thrombocytopenia, and platelet dysfunction.
In patients who had VAE in this study, there was a significant decrease in mean platelet
count, whereas in age-matched controls without VAE, the mean platelet count did not
change.[49]
Rath et al, in their study of complications related to positioning in posterior fossa
craniectomy, found that prolonged postoperative mechanical ventilation was seen more
in the sitting position, probably due to brainstem handling. However, lower cranial
nerve functions were preserved better in the sitting position (p < 0.05).[34]
Postoperative pneumocephalus develops in the sitting position, and the incidence may
reach 100%. It is due to the intraoperative drainage of CSF, commonly via the subarachnoid
drainage and the gravitational effect of sitting position, or residual air during
closure of the dura. It has been attributed to the diminution of brain volume secondary
to mannitol administration, hyperventilation, removal of the space-occupying mass,
and contraction of intravascular blood volume due to intraoperative hemorrhage.[26]
[45]
[47] Nitrous oxide, if used, should be discontinued 20 to 30 minutes before completion
of the procedure; however, pneumocephalus can develop even without the use of nitrous
oxide and may persist for weeks after surgery.[26]
[50] Drainage of CSF during the surgery creates a negative ICP that entrains air. Lunsford
et al in 1979 described this as a phenomenon analogous to the entry of air into an
inverted pop bottle in which as the fluid pours out, air bubbles to the top. If the
patient has coexisting hydrocephalus, the risk of pneumocephalus is increased.[51] Tension pneumocephalus, though rare, is a life-threatening emergency and should
be considered whenever a patient fails to recover as expected following posterior
fossa surgery. Sachkova et al, in their study of predictors of ventricular tension
pneumocephalus after posterior fossa surgery in the sitting position, found an incidence
of 3.9% of tension pneumocephalus cases, which produced severe neurological deterioration
and required an external ventricular drain (EVD) insertion.[52] Presenting symptoms include delayed recovery, severe restlessness, deterioration
of consciousness, and seizures. Management of tension pneumocephalus involves the
urgent relief of the ICP. This is achieved with urgent neurosurgical interventions
such as craniotomy, drilling of burr holes, needle aspiration, ventriculostomy placement,
and closure of the dural defects.
Other complications include subdural, epidural, and remote intraparenchymal hematomas.[53] Neck flexion and head tilt in the sitting position may cause acute parotitis.[54] Piriformis syndrome may occur due to compression of sciatic nerve. Recurrent laryngeal
nerve palsy and tension pneumoventricle are also associated with sitting position.[55]
