Discussion
The present study included 314 patients with posterior fossa tumors, of whom 231 underwent surgery in the sitting position and 83 in the park-bench position. The patients were observed over 6 years, offering the opportunity to highlight the cardiovascular and respiratory implications in relation to intraoperative positioning. Both the sitting and park-bench positions show cardiorespiratory changes dependent on VAE, as well as changes independent of its occurrence. For both positions in question, we analyzed the major monitoring parameters, including both hemodynamic and respiratory variables.Patients in the sitting position had a significantly greater incidence of anesthetic complications and hypotension. Hypoxemia and death occurred more frequently in the park-bench group.
The most common causes of hemodynamic and respiratory instability during posterior fossa surgery are anesthesia induction, patient positioning, brainstem and cranial nerve manipulation, VAE, and rapid and severe bleeding. The response to these changes translates into hypertension, hypotension, tachycardia, bradycardia [
8], hypercapnia, hypocapnia and hypoxia.
In both the sitting position and the park-bench position, blood pressure may increase for various reasons related to anesthesia and positioning, as well as for each individual, depending on associated comorbidities. Various studies have shown that changing a patient’s position is associated with numerous cardiovascular changes [
9,
10].
Hypertension occurrence is one of the variables analyzed in the present study. The percentages varied from one position to another: in the sitting position, 51.95% of patients had hypertension, whereas in the park-bench position, 39.76% had hypertension. The variability of above-normal blood pressure values was observed, particularly during positioning, as well as after positioning. In both positions, hypertension episodes may lead to worsening of cerebral edema and increase the risk of intraoperative bleeding. In our study, pain and stress were associated with increased blood pressure in both the sitting and park-bench positions. Pain occurs following cranial clamping, incisions, and dura mater opening and has stimulatory effects that may lead to hypertension and tachycardia. Anesthetic management is used to suppress the pain response both by injecting local anesthetic at the insertion site of the fixation device and by supplementing intravenous analgesia. Other causes leading to increased blood pressure were associated with each patient’s individual pathology, such as chronic arterial hypertension, certain drugs used in neurosurgery (corticosteroids), and secondary complications such as infections or cerebrospinal fluid (CSF) disturbances that may trigger a systemic response and lead to intraoperative hypertension.
In our study, arterial hypotension was considered if there was a decrease of more than 20% in the systolic blood pressure of the patient. In the sitting position, more than half of the patients had arterial hypotension (61.9%), while the percentage was significantly lower (16.87%) for the park-bench position. Hemodynamic instability does not always occur with the use of the sitting position. Rath et al. demonstrated similar hemodynamic instability between patients in the prone and sitting positions [
11].
Compared with another study published by Sonari Kore et al. in 2016 [
12], where the occurrence of arterial hypotension was also observed during positioning, in our study, in both the sitting and park-bench positions, arterial hypotension was observed after anesthetic induction and until approximately 60 min after patient positioning. Blood pressure returned to normal afterward. In another study, Lindroos et al. reported brief periods of arterial hypotension in 38% of patients in the sitting position [
13]. An important aspect to consider and one frequently encountered in our practice is transient arterial hypotension, which is encountered later during neurosurgical intervention without a specific clinical cause; these findings were reported by the Helsinki team [
14] and by F. Dallier and C Di Roio [
15]. Other predictive factors for the occurrence of orthostatic hypotension are as follows: antihypertensive medication and beta-blocker treatment, Parkinson’s disease status, diabetes mellitus status [
16,
17,
18,
19,
20], and degree of dehydration.
In addition to the fluids administered for maintenance and observed losses, the patients in whom arterial hypotension was not transient required a combination of colloid and vasopressor treatment. In the sitting position, colloids were necessary in 25.54% of patients, and vasopressor support was necessary in 36.8% of patients, whereas in the park-bench position, the need for colloids occurred in 42.17% of patients, and the need for vasopressor treatment was much lower—18.07%. The difference in percentages between the two positions and the decision to administer colloid vs. vasopressor as first-line treatment for hypotension were determined by the anesthesiologist and varied depending on the patient’s response.
Heart rate variability depends on humoral mechanisms, cranial nerve manipulation and the postural stress response [
21].
In our study, tachycardia was present in 13.85% of the sitting position cases and 21.69% of the park-bench position cases. The presence of tachycardia was not only associated with pain-induced hypertension and VAE incidence but also with cranial nerve manipulation.
Bradycardia occurred in 38.1% of the cases in the sitting position and in 15.66% of the cases in the park-bench position. Bradycardia was associated with cranial nerve manipulation and was resolved in many cases after the surgeon was alerted and stopped the maneuver. Some of the patients also required atropine: 25.11% of those in the sitting group and 8.43% in the park-bench group.
In the case of the sitting position results, both tachycardia and bradycardia following tumor and cranial nerve manipulation were comparable with the results of a study published in 1976 by M.S. Albin et al., in which tachycardia occurred in 23% of patients (13.85% in the present study), and bradycardia occurred in 25% of patients (38.1% in the present study)[
7].
A frequently encountered complication in the sitting position is VAE. In our study, documented VAE occurred in 10.39% of the patients. VAE occurrence is frequently encountered when a negative gradient is created between atmospheric pressure and venous blood or when the cephalic extremity is located more than 20° above the heart [
22]. Subatmospheric pressure in noncollapsing cerebral veins facilitates the entry of air; thus, VAE can induce right ventricular failure, pulmonary edema, and acute respiratory distress syndrome [
23].
A wide range of VAE occurrence incidents (1.6% to 76%) are reported in the literature, and the majority of reported VAEs appear to be clinically irrelevant [
24].
Because of the risk of VAE occurrence, it is vital to exclude patent foramen ovale in patients with an additional risk of paradoxical gas embolism due to a right‒to-left shunt in the systemic circulation [
25,
26].
In this study, we used capnography to detect VAE by continuous monitoring of EtCO2 in parallel with hemodynamic parameters. Compared with a study published in 2011 by Ozlem Korkmaz Dilmen et al. [
27], VAE diagnosed via EtCO2 had a 20.4% incidence in the adult population, a higher percentage than that in our study, where VAE was present in only 10.39% of cases. The results where VAE is detected through EtCO2 also appear in studies published by Muley (17.2%) and Bithal (22%) [
28,
29]. Although capnography is a less sensitive method for diagnosing VAE than transesophageal echocardiography and precordial Doppler ultrasound are, the use of capnography combined with the experience of the anesthesiologists and neurosurgeons was demonstrated to be useful for detecting VAE, making it an effective diagnostic tool with a low complication rate.
VAE without prompt initiation of treatment could be fatal for patients. Prompt treatment of VAE requires good communication between the anesthesiologist and the neurosurgeon. In our practice, when a drop of more than 2 mmHg of EtCO2 is observed on the monitor, in parallel with a drop in blood pressure and tachycardia onset, the surgeon is alerted and takes action by covering the operating field with saline-soaked compresses. Simultaneously, 100% oxygen is immediately administered, jugular vein compression is performed, air is suctioned through the central venous catheter, arrhythmias are treated, volemic resuscitation is performed, and vasopressor support is offered.
In the sitting position, 3 deaths occurred(1.3%), whereas in the park-bench position, 5 deaths occurred (6.02%). In the sitting position, the deaths were not VAE related. A previous study reported a 1% mortality rate due to VAE [
30].
EtCO2 values and capnography are useful tools in VAE diagnosis, as they are convenient and practical methods, albeit relatively insensitive compared with other monitoring techniques. Although these markers aid in VAE diagnosis, CO2 analysis from a single breath provides real-time information on CO2 production and elimination, metabolism, circulation and ventilation [
31]. Manipulating CO2 levels can help reduce cerebral blood flow and intracranial pressure. Moreover, it plays an important role in autoregulation and recovery from brain injuries [
32].
In our group, EtCO2 was monitored at both positions. EtCO2 decreases of more than 2 mmHg occurred in 35.06% of patients in the sitting position and in 15.66% of patients in the park-bench position. Independent of VAE, fluctuations in EtCO2 levels occurred in both positions during patient mobilization for positioning, both before and at the end of surgery.
In the present study, VAE was not documented in the park-bench group, but given the fluctuating EtCO2 drops and episodes of hemodynamic instability, transient VAE episodes were suspected. In one study, Black et al. reported a 12% incidence of VAE in the horizontal position in 74 adults monitored via precordial Doppler [
33].
In our sitting group, 4 patients had hypoxia (1.73%), whereas in the park-bench group, hypoxia was present in 7 patients (8.43%). Decreased arterial SpO2 could be used to confirm VAE but may not occur despite the onset of VAE if high concentrations of inspired oxygen are used. A shunt increase occurs early during VAE; therefore, inspired oxygen should be increased early in VAE management [
34]. Desaturation episodes in both positions have been associated with the occurrence of severe arterial hypotension before vasopressor correction. In the park-bench position, hypoxia episodes are caused by atelectasis and an altered ventilation/perfusion ratio, requiring an increased fraction of inspired oxygen and alveolar recruitment maneuvers during the procedure.
One reason why the sitting position is preferred over the horizontal position is that it reduces intraoperative bleeding. A retrospective review of 579 posterior fossa craniectomies at the Mayo Clinic [
35,
36] over 3 years revealed that the transfusion requirements were more than 2 units of blood in 13% of patients who underwent operation in the horizontal position and only 3% of patients with who underwent operation in the sitting position. In the present study, transfusions were given to 2.6% of the patients in the sitting group and 8.43% of those in the park-bench group.
Patient positioning has an impact on cerebral hemodynamics and, implicitly, on intracranial pressure, particularly in the sitting and park-bench positions. Regardless of the mechanism by which supratentorial pneumocephalus and ventricular air accumulation occur in the sitting position, whether due to the pressure difference between atmospheric air and the skull structures after dura mater incision, during tumor resection through tumor volume reduction or excessive CSF drainage, the cephalic extremity above the heart is the culprit. In the park-bench position, pneumocephalus is less common — the mechanisms of its occurrence are the same, but the difference is that the cephalic extremity is not located more than 20° above the heart and the intracranial air volume is reduced. The severity of the complication is affected by the intracranial air volume. The supratentorial pneumocephalus diagnosis is performed via postoperative brain computed tomography (CT), with the presence of the characteristic Mount Fiji sign [
37]. T. Sloan et al. described supratentorial pneumocephalus occurrence in 42.1% of patients who underwent operation in the sitting position; these patients had an air volume between 6–280 cm
3, with potential somatosensory impairment due to cerebral ischemia, when the intracranial air volume exceeded 90 cm
3 [
38]. In the present study, only 12 (5.19%) of the patients who underwent surgery in the sitting position and 3 (3.61%) of the patients who underwent surgery in the park-bench position had supratentorial pneumocephalus. None of the patients required a twisted-drill procedure for evacuation or insertion of an external ventricular drain. Treatment consisted of oxygen therapy (2 l O
2/min for 4–6 hours/day) and chest and cephalic extremity elevation to 40° until complete resorption. Air absorption occurred gradually, starting on the second postoperative day, with dynamic monitoring via native brain CT.
Both cerebral venous pressure decrease, which involves reducing intraoperative hemorrhage and venous clotting time, and postoperative increases in cerebral venous pressure, which are part of the treatment for VAE, increase the risk of postoperative hematoma in patients who undergo operation in the sitting position. In the park-bench position, postoperative hematoma may occur as a result of increased venous pressure in the cerebral hemisphere near the floor plane due to gravity or uneven venous drainage when the venous sinus tears. Regardless of patient position, an important role is played by individual factors, such as associated pathology, preexisting coagulopathy, fluctuating blood pressure values and tumor vascularization. In the literature, postoperative hematoma is described as having a low risk of occurrence; however, it has devastating effects [
39,
40,
41,
42]. The present study revealed the presence of postoperative hematoma in the tumor bed of 10 (4.33%) patients who underwent operation in the sitting position and in 6 (7.23%) patients who underwent operation in the park-bench position. Treatment consisted of hematoma evacuation. General preventive measures include careful blood pressure monitoring, rigorous hemostasis and correct positioning of the patient before and after surgery [
43,
44].
The influence of neurosurgical patient positioning on hydrocephalus development has rarely been studied. In the sitting position, CSF aspiration contributes to good visibility of the operative field, but prolonged suction may lead to decreased uptake of CSF by the arachnoid villi due to temporary inactivity, resulting in hydrocephalus [
45]. Obstruction of the aqueduct of Sylvius following resection of pineal region tumors or midbrain tectal tumors is another cause of hydrocephalus, either intraoperatively or postoperatively [
46]. Another triggering factor for hydrocephalus is postoperative mixed CSF cellularity, which may block absorption by the villi, resulting in communicating hydrocephalus [
47]. Very rarely, hydrocephalus is caused by ventriculitis due to CSF flow obstruction [
48].
In the park-bench position, increased venous pressure in the cerebral hemisphere near the operating table predisposes patients to venous infarction and associated cerebral edema [
49,
50] and hemodynamic changes with an impact on altering CSF dynamics, resulting in hydrocephalus. Surgical handling of the anatomical structures of the posterior fossa to obtain easy access may alter the free CSF flow. The general factors specific to both neurosurgical positions are the obstruction of CSF flow resulting from tumor debris [
51], postoperative hematoma [
52] or postoperative scar sites [
53]. Preexisting hydrocephalus may be a cause of postoperative hydrocephalus development. Duraplasty or insertion of an external ventricular or ventriculoperitoneal shunt may influence hydrocephalus development either by overdrainage [
54] or insufficient drainage [
55]. In our study, 7 (3.03%) patients developed hydrocephalus in the sitting position, and 4 (4.82%) developed hydrocephalus in the park-bench position. The treatment used was ventriculocisternostomy (VCS) in 3 (27.27%) patients and ventriculoperitoneal drainage (VPD) in 8 (72.73%) patients. The recommended preventive measures are avoiding excessive CSF drainage, careful dissection of posterior fossa structures and, last but not least, intraoperative imaging of CSF flow to exclude or eliminate obstructive sites. Postoperative imaging follow-up is essential in the management of early hydrocephalus signs.
Cranial nerve injury during neurosurgical procedures may occur due to several factors, and patient positioning may also influence the risk of injury. In the sitting position, cranial nerve injury most commonly occurs through prolonged traction and compression [
56]. The facial nerve and trigeminal nerve are frequently affected in posterior fossa surgery [
57]. By decreasing cerebral perfusion pressure, which is induced by the sitting position due to gravity, cranial nerves become more susceptible to ischemia during prolonged neurosurgical interventions [
58]. In the park-bench position, the accessory and hypoglossal cranial nerves are most frequently affected [
59], either due to cephalic extremity hyperextension during positioning or compression of the surgical instruments, given the limited operating field, as gravity does not influence CSF or hemorrhage drainage. The duration of surgery and preexisting cranial nerve damage influence the degree of intraoperative injury and thus the postoperative prognosis [
60]. Absent or inadequate intraoperative neurophysiological monitoring may increase the risk of cranial nerve injury, as early nerve damage signs go unnoticed [
61]. In the present study, only 7 (3.03%) patients presented House-Brackmann grade VI facial paralysis: 4 patients who underwent operation in the sitting position, and 3 patients who underwent operation in the park-bench position. Facial paralysis recovery grades of III and IV occurred in 2 (28.57%) and 5 (71.43%) patients, respectively. To minimize cranial nerve injury risk, it is necessary to pay special attention to patient positioning, use a surgical technique that allows the surgeon a level of intraoperative comfort, avoid excessive traction or compression, ensure adequate cerebral perfusion and use neurophysiological monitoring.
In the sitting position, VAE causes hypotension and decreased cerebral perfusion [
62], thus increasing the risk of ischemia in the brainstem and cerebellar hemisphere [
63]. Decreased central venous pressure may reduce cerebral perfusion and increase cerebellar susceptibility to ischemia, especially when the self-regulatory mechanism is insufficient [
64]. Changes in intracranial pressure, either due to hypotension or excessive CSF drainage, compromise blood flow to posterior fossa structures, leading to potential posterior fossa ischemia. In the park-bench position, lateral rotation of the cephalic extremity may cause compression of the posterior inferior cerebellar artery, with the development of ischemia in the cerebellar hemisphere [
65]. Because of gravity, the park-bench position can cause a difference in cerebral blood flow and venous return between the two cerebral hemispheres [
66], an alteration that predisposes individuals to cerebral perfusion imbalance by compromising cerebellar circulation, especially in the case of increased pressure in the posterior fossa, accelerating the onset of ischemic lesions at this level. Both hypercapnia, caused by respiratory changes following park-bench positioning [
67], and hypotension [
49], as part of blood pressure fluctuations, can reduce cranial pressure, both of which increase the risk of posterior fossa ischemia. However, general factors specific to both positions should not be overlooked either. These include long surgery durations [
66], surgical manipulation, inadequate blood pressure management and, last but not least, preexisting vascular conditions. In our study, 2 (0.87%) patients who underwent surgery in the sitting position and 1 (1.2%) patient who underwent surgery in the park-bench position experienced posterior fossa ischemia. All three patients required decompressive craniectomy, but they unfortunately died. In total, 8 deaths occurred: 3 (1.3%) patients who underwent operation in the sitting position and 5 (6.03%) patients who underwent operation in the park-bench position. The other patient who underwent operation in the sitting position and the other four patients who underwent operation in the park-bench position died due to postoperative hematoma.
Early extubation may have negative repercussions on a patient’s neurological and respiratory recovery. Therefore, depending on the events that occurred intraoperatively, the time of extubation is decided between the anesthesiologist and neurosurgeon.Delayed postoperative extubation, prolonged duration of anesthesia and surgery and the need for prolonged intensive care unit stay lead to an unfavorable prognosis, with the occurrence of respiratory complications that may have a negative impact on neurological status and delay recovery [
68,
69]. In our study, immediate postoperative extubation was performed in 215 (93.07%) patients who underwent operation in the sitting position and 72 (86.75%) patients who underwent operation in the park-bench position. Postoperative ventilation was required for 16 (6.93%) patients who underwent operation in the sitting position and 11 (13.25%) patients who underwent operation in the park-bench position. Prolonged postoperative ventilation hinders neurologic evaluation, diagnosis and therapeutic decision-making, and imaging remains the only available diagnostic method. In both positions, the time spent under anesthesia was approximately the same.
Correct patient positioning, careful intraoperative monitoring, maintenance of hemodynamic stabilization and careful surgical resection are recommended to prevent the development of posterior fossa ischemia. By understanding the specific risks associated with both the neurosurgical position and the implementation of strategic preventive measures, the possibility of posterior fossa complications can be significantly reduced.