Abstract

The laryngeal mask airway (LMA) has gained popularity as an airway management device in the perioperative setting due to its ease of use, reduced invasiveness compared to endotracheal intubation, and lower incidence of complications. However, hiccups, though relatively uncommon, can pose a significant challenge during the perioperative period when an LMA is in place. Abrupt movement because of hiccups can lead to delay in surgery as well as interfere with surgical instrumentation. This discussion presents a case where perioperative hiccups occurred with LMA use and explores the management strategies employed.

Introduction

Hiccups or singultus are sudden, involuntary contractions of the diaphragm and external intercostal muscles, followed by the abrupt closure of the glottis, producing the distinctive “hic” sound [1]. In recent scenarios, the laryngeal mask airway (LMA) has gained popularity as an airway device for spontaneous and controlled ventilation, as it helps avoid complications associated with endotracheal intubation. Acute hiccup during sedation or general anesthesia after the use of LMA is a minor yet notable complication that can have several disruptive effects. It may disturb the surgical field, making it difficult for the surgeon to perform precise procedures. Additionally, it can interfere with lung ventilation, potentially compromising the patient’s oxygenation and ventilation status [2]. This condition can also hinder diagnostic procedures, particularly those requiring steady or controlled conditions, such as imaging or endoscopic examinations. While generally not severe, managing acute hiccups promptly is important to prevent these potential complications. This case suggests that using an LMA device may trigger hiccups, with the incidence of LMA-related hiccups being approximately 1%-14% [3].

Case Presentation

We hereby present a case of a 30-year-old female with a height of 160 cm and 55 kg weight, diagnosed with fibroadenoma in her right breast, scheduled for elective excision surgery under general anesthesia. Classic LMA was decided to be used as an airway adjunct. She had no other significant history, chronic medical conditions, prior surgeries, artificial dentures, or drug allergies.

She was physically fit, with a respiratory rate of 18 breaths/minute, pulse rate of 70 beats/minute, and blood pressure of 110/70 mmHg in the sitting position. On auscultation, breath sounds in both lung fields were normal, and no cardiac murmurs were present. Her airway assessment was Mallampati class I, and she was classified under the American Society of Anesthesiologists (ASA) physical status grade I.

All routine laboratory investigations, including complete blood count, renal function test, liver function test, prothrombin time, and international normalized ratio, were normal with normal ECG and chest X-ray. An informed and written consent was obtained from the patient. The patient was kept nil by mouth for 8 hours preoperatively.

All ASA standard monitors in the operating room were connected, showing a body temperature of 36.8°C, pulse rate of 80 beats/minute, noninvasive blood pressure of 110/70 mmHg, and pulse oximeter saturation of 100%. An intravenous cannula of 20G was taken from the left hand, and 500 mL of Ringer’s lactate solution was started.

Premedication with 0.2 mg intravenous glycopyrrolate, 1 mg midazolam, and 2 μg/kg of fentanyl intravenously was done. An oxygen mask was attached at a flow rate of 8 L/minute, and the patient was induced with 2 mg/kg of propofol. A classic LMA of size 3 was inserted, and 20 mL of air was used for inflating the cuff. Anesthesia was maintained with sevoflurane, nitrous oxide, and oxygen. The patient was kept on controlled ventilation, and intraoperative analgesia was achieved with intravenous paracetamol (1 g). The oxygen saturation and pulse rate were continuously monitored. Noninvasive blood pressure was recorded at five-minute intervals during the intraoperative period.

After 20 minutes of induction, the patient suddenly developed hiccups. They continued despite administering 40 mg of propofol in repeated 10 mg boluses. These hiccups disturbed the surgeon’s instrumentation during the procedure. Next injection, 0.5 mg atropine was given intravenously but was not effective. Subsequently, 50 μg of dexmedetomidine was administered intravenously over a 10-minute period, which successfully resolved the hiccups. Following the administration of dexmedetomidine, there was a noted decrease in both heart rate and blood pressure, though this did not exceed 20% of the patient’s baseline values. The surgery then proceeded without further complications for another 25 minutes.

At the end of surgery, a thorough oral suction was performed, and inhalational agents were discontinued. Once the patient was awake and all airway reflexes were restored, the cuff was deflated, and LMA was removed. She was transferred to the recovery room for further observation. Hiccups did not recur for the next three days while she stayed in the hospital.

Discussion

Hiccups can significantly disrupt surgery, so addressing them promptly is crucial. The hiccup reflex arc consists of two limbs: afferent and efferent limbs. The afferent limb consists of vagal, sympathetic chains from T6 to T12 and phrenic nerves that travel to the hiccup center located at the posterolateral part of the medulla oblongata. The efferent pathway is through the motor fibers of the phrenic nerve and the accessory nerve to the diaphragm. Any stimulation along the reflex pathway leads to a hiccup. It also increases the risk of aspiration by creating a pressure gradient across the lower esophageal sphincter, enabling reflux.

Various etiologies of intraoperative hiccups are excessive food and carbonated beverages preoperatively [2] and various anesthetic drugs and techniques used during general anesthesia like methohexital, thiopentone, midazolam, and opioids [4,5]. Propofol is also one of the causes of hiccups, which can be treated with intravenous lidocaine [6]. However, since propofol is usually given with lidocaine for ameliorating pain during injection, it is rarely found to be the causative agent (Table 1) [7].

Bag mask ventilation before induction has pros and cons. On the one hand, it leads to preoxygenation, and on the other, it leads to stomach insufflation, which can cause hiccups due to vagus nerve stimulation. Patients with preexisting conditions like gastroesophageal reflux disease (GERD) and central nervous disorders are also more prone to hiccups.

Patients induced with LMA cause hiccups due to the stimulation of mechanoreceptors. The distal end of a well-seated LMA lies over the proximal esophagus, and the sudden and rapid stretch of mechanoreceptors in the proximal esophagus leads to hiccups. The stimulus for hiccups in intraoperative settings can also be pain at the surgical site and decreased depth of anesthesia [9].

Treatment guidelines are unclear because the reflex arc is incompletely understood, and various possible etiologies exist. The main goal is to disrupt the reflex arc using pharmacological or nonpharmacological methods.

As a lighter plane of anesthesia is one reason for hiccups, we deepened the plane of anesthesia by giving boluses of propofol, but still, hiccups were present.

Acetylcholine is one of the neurotransmitters triggering the reflex arc. Therefore, giving anticholinergics like atropine 0.5 mg intravenously blocks the vagally mediated reflex from LMA insertion and abolishes the efferent arc from the hiccup center [2]. It additionally decreases intraesophageal pressure [3]. In our case, 0.5 mg atropine was unsuccessful in terminating the reflex arc.

In a study by Koteswara and Dubey, dexmedetomidine, a selective alpha-2 adrenergic receptor agonist, was found to abolish hiccups in a similar scenario, implying that sympatholytic drugs abolish intraoperative hiccups [10]. Since atropine was ineffective, we gave dexmedetomidine 1 μg/kg, and the hiccups ceased. There was a slight decrease in heart rate and blood pressure.

Various other modalities can be used in addition to these drugs. For anesthetic agent-induced hiccups, metoclopramide, through its dopamine antagonism and serotonin agonism, seems to be a potent agent for terminating hiccups [8].

Dexmedetomidine offers several advantages over metoclopramide in the management of hiccups. While metoclopramide was traditionally used for treating hiccups due to its dopamine antagonist properties, dexmedetomidine presents unique benefits that may make it preferable.

Sedative, analgesic, and anxiolytic properties

Stimulating presynaptic receptors in sympathetic nerve endings and central postsynaptic receptors inhibits sympathetic activity. Analgesia is achieved by stimulating α2 adrenoreceptors in the spinal cord. This inhibition of sympathetic activity (one of the pathways of the reflex arc in the hiccups pathway), along with analgesic and sedative properties, may have been the reason for suppressing intraoperative hiccups [10].

Reduced risk of adverse neurological effects

Metoclopramide is known to carry risks of extrapyramidal symptoms, especially in young adults who are at higher risk for developing dystonic reactions [11]. Dexmedetomidine, by contrast, lacks these dopamine-blocking effects, which is a significant advantage in younger patients who are more susceptible to these adverse reactions.

GERD patients are, in general, more prone to hiccups, which, in turn, leads to a higher risk of aspiration, so prophylactically proton pump inhibitors should be used. The only Food and Drug Administration-approved treatment is chlorpromazine (25-50 mg) intravenously [12].

Nonpharmacological stomach desiring and nasal airway lubrication with lidocaine lead to pharyngeal stimulation opposite to C2 C3 and terminate hiccups. Lung recruitment, application of 25-30 cm of H₂O continuous positive airway pressure [2], and suboccipital release technique all reduce pressure on the vagus and interrupt reflex arc [2]. Deliberate hypoventilation, where the end-tidal carbon dioxide is targeted at 48 mmHg, also halts hiccups [13]. Stellate ganglion block is a recent technique for intractable hiccups [14].

Conclusions

Intraoperative hiccups are a nuisance for both anesthetists and surgeons. Using classic LMA heightens the chance of aspiration, especially in the absence of a nasogastric tube. Hence, strategies to reduce gastric insufflation, early detection of the cause, and effective management using various drug modalities are the key points to prevent any complications.

Numerous interventions have been suggested for managing hiccups during anesthesia. However, perioperative treatment remains largely based on empirical evidence, with no approach being “evidence-based.” As a result, no definitive recommendations can be made to treat hiccups. In our case, conventional medications and techniques for multimodal management were ineffective, so dexmedetomidine was administered, successfully controlling the hiccups.

References

1. Musumeci A, Cristofori L, Bricolo A: Persistent hiccup as presenting symptom in medulla oblongata cavernoma: a case report and review of the literature. Clin Neurol Neurosurg. 2000, 102:13-7. 10.1016/s0303-8467(99)00058-x
2. Mathew J, Shen S, Liu H: Intraoperative laryngeal mask airway-related hiccup: an overview. Transl Perioper Pain Med. 2020, 7:145-51. 10.31480/2330-4871/103
3. Kanaya N, Nakayama M, Kanaya J, Namiki A: Atropine for the treatment of hiccup after laryngeal mask insertion. Anesth Analg. 2001, 93:791-2. 10.1097/00000539-200109000-00047
4. Marhofer P, Glaser C, Krenn CG, Grabner CM, Semsroth M: Incidence and therapy of midazolam induced hiccups in paediatric anaesthesia. Paediatr Anaesth. 1999, 9:295-8. 10.1046/j.1460-9592.1999.00378.x
5. Liu CC, Lu CY, Changchien CF, Liu PH, Perng DS: Sedation-associated hiccups in adults undergoing gastrointestinal endoscopy and colonoscopy. World J Gastroenterol. 2012, 18:3595-601. 10.3748/wjg.v18.i27.3595
6. Krishnakumar M, Srinivasaiah B, Naik SS, Goyal A: Propofol-induced hiccups in MRI suite treated with dexmedetomidine. Saudi J Anaesth. 2023, 17:450-1. 10.4103/sja.sja_816_22
7. Landers C, Turner D, Makin C, Zaglul H, Brown R: Propofol associated hiccups and treatment with lidocaine. Anesth Analg. 2008, 107:1757-8. 10.1213/ane.0b013e3181853605
8. Prakash S, Sitalakshmi N: Management of intraoperative hiccups with intravenous promethazine. J Anaesthesiol Clin Pharmacol. 2013, 29:561-2. 10.4103/0970-9185.119131
9. Nwagwu CC, Ebirim LN: Postoperative hiccup induced by LMA—a case report with literature review. Open J Anesthesiol. 2014, 4:236-9. 10.4236/ojanes.2014.410035
10. Koteswara CM, Dubey JK: Management of laryngeal mask airway induced hiccups using dexmedetomedine. Indian J Anaesth. 2013, 57:85. 10.4103/0019-5049.108583
11. Fink FM, Bognar M, Hengl P, Paulmichl M, Nofziger C: Case report: metoclopramide induced acute dystonic reaction in adolescent CYP2D6 poor metabolizers. Front Pharmacol. 2023, 14:1201566. 10.3389/fphar.2023.1201566
12. Polito NB, Fellows SE: Pharmacologic interventions for intractable and persistent hiccups: a systematic review. J Emerg Med. 2017, 53:540-9. 10.1016/j.jemermed.2017.05.033
13. Obuchi T, Shimamura S, Miyahara N, Fujimura N, Iwasaki A: CO(2) retention: the key to stopping hiccups. Clin Respir J. 2018, 12:2340-5. 10.1111/crj.12910
14. Lopez DJ, Kumar S: Stellate ganglion block for intractable hiccups secondary to a motor vehicle collision. Cureus. 2023, 15:e37030. 10.7759/cureus.37030

Background

Hypotension during spinal anesthesia occurs due to sympathetic nervous system blockade, resulting in decreased systemic vascular resistance and reduced cardiac output. Due to reduced sympathetic tone, peripheral arterial vasodilatation and blood pooling in lower limbs due to venodilatation occur, reducing preload to the heart and stroke volume. The elderly patients have reduced cardiovascular compensatory mechanisms, increasing the frequency and severity of hypotension due to sympathetic blockade after spinal anesthesia significantly. Vasopressors correct hypotension during the intraoperative period to maintain organ perfusion. Fluids can be administered, and if given excessively, can cause fluid overload and urinary retention. This study aimed to compare the effectiveness of vasopressors, phenylephrine, and ephedrine in maintaining hemodynamic stability intraoperatively through prophylactic infusion after spinal anesthesia in elderly patients for lower limb orthopedic surgeries.

Methodology

A total of 174 elderly patients aged 60 years and above with American Society of Anesthesiologists (ASA) Classification I and II, undergoing lower limb orthopedic surgeries, enrolled in a randomized comparative study, were allocated into three groups: Group P (phenylephrine, n=58) received 250 mcg phenylephrine in 30 ml normal saline using infusion syringe pump, Group E (ephedrine, n=58) received 30 mg ephedrine in 30 ml normal saline using infusion syringe pump, and Group C (control group, n=58) received mephentermine I/V (6 mg bolus) when the fall in blood pressure was below 30% of baseline without any placebo infusion. Hemodynamic parameters (systolic and diastolic blood pressure, mean arterial pressure (MAP), heart rate) at 15, 10, and 5-minute intervals before spinal anesthesia, and at 3, 6, 9, 12, 15, 20, 25, and 30-minute intervals after spinal anesthesia. The need for rescue doses to treat hypotension after spinal anesthesia was recorded.

Result

At all time intervals following spinal anesthesia, Group E reported heart rate and systolic blood pressure better than Groups P and C, significantly. At 3, 6, 9, 12, 15, and 25-minute intervals following spinal anesthesia, the diastolic blood pressure in Group E was enhanced significantly than Groups P and C. The MAP in Group E was substantially higher than in other groups at 3, 6, 15, and 20-minute intervals following spinal anesthesia, which was statistically significant. Compared to Groups P and C, Group E required lesser rescue doses to treat intraoperative fall in hypotension 30% below baseline and lesser events of bradycardia.

Conclusion

Following spinal anesthesia, the preload to the heart is to be maintained with intravenous (crystalloid or colloidal) solutions to maintain cardiac output adequately. Intraoperative use of phenylephrine and ephedrine as a low-dose prophylactic infusion can be used, as it increases both systemic vascular resistance and preload without cardiac stimulation along with intravenous solutions to maintain hemodynamic parameters such as systolic and diastolic blood pressure, MAP, heart rate effectively but preferably ephedrine in elderly patients.

Introduction

Hypotension is frequently observed after induction of spinal anesthesia which is a commonly used regional technique in elderly patients undergoing lower limb orthopedic procedures [1]. It occurs due to reduced cardiac output and peripheral vascular resistance, which raises the possibility of myocardial ischemia. Impaired cerebral auto-regulation during the perioperative period decreases middle cerebral artery velocity [2]. Reducing the spinal dose and the extent of anesthetic spread to the necessary dermatomes decreases the incidence of adverse effects [3]. As crystalloids are frequently ineffective in ameliorating blood pressure, their administration can soon result in circulatory overload and congestive cardiac failure [4].

The elderly are more likely to have comorbid diseases, which increases their risk of hypoperfusion, which is due to hypotension, the primary risk factor for which is hypovolemia [4,5]. Vasopressors such as phenylephrine and ephedrine can be immediately infused into elderly people to prevent hemodynamic abnormalities following spinal anesthesia [6]. More research is to be done to study the efficacy and minimal dose requirement of vasopressors as a prophylactic infusion to maintain hemodynamics in the elderly population.

The objective of this study was to determine the effectiveness of vasopressors such as phenylephrine and ephedrine as a low-dose prophylactic intravenous infusion to study hemodynamic variations in elderly patients immediately after spinal anesthesia and to prevent hypotension and the need for rescue doses to maintain vital parameters in patients aged 60 years and above undergoing lower limb orthopedic surgeries.

Materials & Methods

This study was registered at Clinical Trials Registry-India with link https://ctri.nic.in/Clinicaltrials/login.php under the CTRI/2023/04/051451 registration number. The study time was from May 2023 to August 2024. The study was conducted after receiving approval from the institutional ethical committee of Bijapur Lingayat District Education (BLDE) (Deemed to be University), Shri BM Patil Medical College, Hospital and Research Centre with ethical clearance number BLDE(DU)/IEC/787/2022-23. A total of 174 patients aged 60 years and above belonging to American Society of Anesthesiologists (ASA) grades I and II [7], scheduled for elective lower limb orthopedic surgical procedures under spinal anesthesia, were included in the study. The study excluded patients with infection at the site of injection, uncontrolled hypotension, allergic or hypersensitivity to vasoconstrictors, coagulopathies, sepsis, fixed cardiac output states, uncontrolled hypertension, hypothyroidism, uncontrolled diabetes, untreated or uncontrolled heart failure, pheochromocytoma, on monoamine oxidase inhibitors, tricyclic antidepressants, phenothiazine compounds, recent myocardial ischemia/infarction.

During the pre-anesthetic evaluation, a detailed history and general and systemic examinations were carried out the previous day. A history of any significant medical illness was elicited and medication history was taken. The airway, respiratory system, and cardiovascular system were assessed. Written informed consent was obtained. Routine investigations such as complete blood profile, bleeding time and clotting time, random blood sugar, serological tests, chest X-ray, and 2D echocardiography were performed.

On the day of the surgery, nil per oral status was confirmed. An 18G IV cannula was secured and preloading with Ringer lactate solution (15 ml/kg) was infused. On the operating table, vital monitors such as non-invasive blood pressure (NIBP), electrocardiography (ECG), and pulse oximetry were attached to record baseline heart rate, blood pressure, and SpO2. The patients were positioned in a sitting posture. Using a 25G Quincke spinal needle, a lumbar puncture was done at the L3-4 or L4-L5 interface following skin disinfection and 2% lignocaine infiltration. Premedication was given with midazolam 0.5 mg I/V to alleviate the anxiety of the patients. The groups were intrathecally administered with 0.5% hyperbaric bupivacaine 15 mg I/V. Subsequently, patients were supined and oxygen (5 L/min) was delivered with a face mask. Five minutes after intrathecal injection, sensory blockade of spinal anesthesia was assessed using ice cubes or pinpricks.

Patients were split randomly into three groups. Group P received a low-dose continuous infusion of 30 ml 0.9% normal saline with 250 mcg of phenylephrine for 30 minutes (8.3 mcg/min) immediately following spinal anesthesia using an infusion syringe pump. Group E received a continuous infusion of 30 ml 0.9% normal saline with 30 mg of low-dose ephedrine for 30 minutes (1 mg/min) immediately following spinal anesthesia using an infusion syringe pump. Group C (control) received a bolus of mephentermine 6 mg I/V after spinal anesthesia when required without any placebo infusion. The infusion of treatment medication in Group P and Group E was started immediately after spinal anesthesia at an infusion rate of 60 ml/hour, and infusion was stopped after 30 mins (study period) following induction of spinal anesthesia. NIBP, heart rate, ECG, and percentage of oxygen saturation (SpO2) were monitored. Incidence of hypotension and bradycardia were noted. Hemodynamic parameters were recorded at 15, 10, and 5 minutes prior to spinal anesthesia and for 0, 3, 6, 9, 12, 15, 20, 25 and 30-minute intervals after spinal anesthesia.

The rescue treatment protocol to treat intraoperative hypotension was followed. If the reduction in systolic blood pressure was greater than 30% below baseline, then a bolus dose of phenylephrine 50 mcg I/V or ephedrine 5 mg I/V was given in respective groups. Atropine 0.6 mg I/V was given if the heart rate was less than 50 beats per minute. In the case of hypertension, the ongoing infusion was stopped.

Statistical analysis

Using G*Power Version 3.1.9.4 (Heinrich-Heine-Universitat Dusseldorf, Dusseldorf, Germany) for sample size calculation, the mean arterial pressure (MAP) for control (mean=90, SD=12), phenylephrine (mean=85, SD=12), and ephedrine (mean=84, SD=9) were obtained. This study required a total sample size of 174 (for each group 58, assuming equal group sizes) to achieve a power of 80% for detecting a difference means [7].

The data was entered into a Microsoft Excel sheet and statistical analysis was performed using IBM SPSS Statistics for Windows, Version 20 (IBM Corporation, New York, US). The findings were evaluated using basic statistics, including mean and standard deviation of numerical variables and percentages for categorical variables. To compare categorical variables between the two groups, the chi-square test was used. For groups that were not normally distributed, the Kruskal-Wallis test was performed. All analyses were two-tailed, with a p-value of <0.05, which was considered to be statistically significant.

Results

In the present study, constituting 174 elderly patients aged 60 years and above, 58 in each group were posted for all elective lower limb orthopedic surgeries (such as open reduction and internal fixation of fractures, tendon repairs, soft tissue procedures, arthroplasty, arthroscopic knee surgeries, etc.) to assess the impact of phenylephrine or ephedrine infusion administered intravenously as a prophylactic measure to prevent hypotension and its effect on heart rate. The present study followed The Consolidated Standards of Reporting Trials (CONSORT) guidelines (Figure 1). There was no statistically significant difference in all groups with demographic characteristics such as age (p=0.496), sex (p=1), ASA grades (p=0.197), and body mass index (p=0.271).

Figure 1: CONSORT flow diagram

CONSORT: Consolidated Standards of Reporting Trials; n: Number of patients

The mean systolic blood pressure at different time intervals was plotted for each group (Figure 2). The mean systolic blood pressure at induction (0 mins) of spinal anesthesia was superior in Group P compared to Group E and the control group. It was enhanced in Group E when compared to other groups at 6 (p=0.001), 9 (p=0.001), 12 (p=0.01), 15 (p=0.02), 20 (p=0.001), 25 (p=0.001) and 30 (p=0.002) minute time intervals after spinal anesthesia, which was statistically significant (p<0.05).

Figure 2: Comparison of SBP before and after SA

SBP: Systolic blood pressure; SA: Spinal anesthesia

The mean diastolic blood pressure at different time intervals was plotted for each group (Figure 3). The mean diastolic blood pressure at induction (0 min) of spinal anesthesia was superior in Group P compared to Group E and the control group. It was enhanced in Group E with reference to other groups at 3 (p=0.002), 6 (p=0.002), 9 (p=0.001), 12 (p=0.02), 15 (p=0.001) and 25 (p=0.01) minute time intervals after spinal anesthesia, which was statistically significant (p<0.05).

Figure 3: Comparison of DBP before and after SA

DBP: Diastolic blood pressure; SA: Spinal anesthesia

The mean values of MAP at different time intervals were plotted and the mean MAP was superior in the control group compared to other groups (Figure 4). The mean MAP was enhanced in the ephedrine group in comparison to Group P at 3 (p=0.02), 6 (p=0.017), 15 (0.007), and 20 (0.006) minute time intervals after spinal anesthesia, which was statistically significant (p<0.05).

Figure 4: Comparison of MAP before and after SA

MAP: Mean arterial pressure; SA: Spinal anesthesia

The mean heart rate at different time intervals was plotted for each group (Figure 5). The mean heart rate was superior in Group E in comparison to other groups and was statistically significant (p<0.05) at 3 (p=0.013), 6 (p=0.014), 12 (p=0.001), 15 (p=0.001), 20 (p=0.001), 25 (p=0.001), and 30 (p=0.001) minute time intervals after spinal anesthesia.

Figure 5: Comparison of heart rate before and after SA

SA: Spinal anesthesia

The number and percentage of rescue doses of vasopressors to treat hypotension if it falls below 30% of baseline, given among all groups, were evaluated using the chi-square test and tabulated (Table 1). The obtained p-value of 0.297 was observed to be statistically insignificant.

The number and percentage of atropine I/V to treat bradycardia (heart rate less than 50 beats/min) given among all groups was tabulated and it was observed to be statistically insignificant (Table 2). The atropine I/V required to treat bradycardia was less in Group E than in Group P and the control group.

The present study observed the hemodynamic variations after spinal anesthesia. Results showed that the mean systolic blood pressure (Group E>Group P>Group C), diastolic blood pressure (Group E>Group P>Group C), MAP (Group E=Group P=Group C), and heart rate were better maintained in Group E compared to Groups P and C above baseline blood pressure before induction. Elderly patients with untreated sympathetic block after spinal anesthesia have lower systolic blood pressure, systemic vascular resistance, and mean venous pressure due to decompensated state. Restoring preload to the heart during spinal block should be accomplished by administering sufficient intravenous fluids (8-10 ml/kg). Adequate preloading precludes a decrease in cardiac output and unanticipated cardiac arrests, but excessive fluid administration can lead to fluid overload [8]. A vasopressor should be administered if the systolic blood pressure declines by 25 to 30% baseline value or less than 90 mmHg. Vasopressors are known to cause vasoconstriction by increasing systemic vascular resistance to prevent spinal-induced hypotension (SIH) eventually, thus they are a better choice for maintaining hemodynamics in elderly patients [9]. The alpha-adrenergic agonist phenylephrine is typically linked to reflex bradycardia [10]. It raises blood pressure due to venoconstriction and arterial vasoconstriction. It increases venous tone, venous return (preload), and systemic vascular resistance.

Ephedrine, a mixed-action (alpha and beta) adrenergic agonist, increases the cardiac output and prevents a decrease in heart rate as it causes greater venoconstriction than arteriolar constriction and results in increased venous return (preload) and enhances cardiac output, blood pressure, and heart rate [11].

As per the observed results in the present study, phenylephrine 250 mcg/30 ml and ephedrine 30 mg/30 ml, were both effective in maintaining hemodynamic stability after subarachnoid block. The systolic blood pressure was well maintained in Group E>Group P>Group C following induction of spinal block. The attenuation of systolic blood pressure due to sympathetic blockade was more pronounced within the initial 15 minutes after spinal anesthesia and well optimized by Group E compared to Groups P and C.

The diastolic blood pressure was enhanced in Group E>Group P>Group C. The MAP was observed to be equally maintained above and at baseline in all groups (Group P=Group E=Group C). However, the initial drop in MAP following the spinal block was better optimized in the ephedrine group. Zunic et al. reported the impact of phenylephrine or ephedrine infusion following spinal anesthesia on hemodynamics in elderly patients for orthopedic surgeries. They observed that cardiac index, MAP, and heart rate were better in Group E than in Groups P and C [7]. Conversely, Abbasivash et al. found that the MAP, systolic and diastolic blood pressures, and the frequency of hypotension were all considerably reduced in the phenylephrine group after spinal anesthesia, with no apparent difference in heart rate among phenylephrine and ephedrine groups. Less vasopressor use was observed in the phenylephrine group [12]. In this study, less vasopressor rescue dose was required to treat hypotension in Group E compared to Groups P and C. Mon et al. demonstrated that Groups P and E achieved good systolic blood pressure, but ephedrine increased cardiac output in comparison to phenylephrine in parturients [13]. Asokan et al. concluded that ephedrine 6 mg and phenylephrine 100 mcg did not differ in their effectiveness in treating hypotension during subarachnoid block for cesarean section. However, maternal bradycardia was more in the phenylephrine group, with equal incidence of fetal acidosis in the study groups [14]. In this study, both ephedrine and phenylephrine were effective in maintaining hemodynamics and considerably better in the ephedrine group. The incidence of bradycardia was also less in the ephedrine group compared to other groups.

The heart rate in the present study was maintained better in Group E>Group C>Group P. Four patients in the phenylephrine group were given atropine 0.6 mg I/V in response to bradycardia, whereas in the Ephedrine group, only two patients had bradycardia. The rescue doses (phenylephrine 50 mcg/ephedrine 5 mg) to maintain systolic blood pressure after a fall of more than 30% below baseline, were required more in the phenylephrine group than in the ephedrine group. Sinha et al. conducted a study and concluded that following subarachnoid block for cesarean delivery, the three vasopressors efficiently preserved arterial blood pressure. When compared to ephedrine and mephentermine, phenylephrine significantly lowered heart rate [15].

Limitations

A larger sample size is required and a multi-centric study is preferred. Invasive blood pressure (IBP) monitoring provides precise monitoring of blood pressure, which was not done in the present study. Cardiac output is not measured which is crucial in determining the effectiveness of vasopressors among the elderly population.

Conclusions

Hypotension following spinal anesthesia, caused by a reduction in stroke volume can be treated with crystalloid or colloidal solutions. Administration of vasopressor agents increases stroke volume and preload by increasing systemic vascular resistance without heart stimulation. Hence, both vasopressors (ephedrine and phenylephrine) can be used along with crystalloid solutions to correct hypotension post-subarachnoid block in elderly patients. Consequently, prophylactic low-dose infusion of ephedrine (0.4-0.5 mg/kg) could be a better vasopressor agent of choice than phenylephrine in maintaining hemodynamic stability in elderly patients aged 60 years and above for lower limb orthopedic surgeries under spinal anesthesia.

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5. Hartmann B, Junger A, Klasen J, et al.: The incidence and risk factors for hypotension after spinal anesthesia induction: an analysis with automated data collection. Anesth Analg. 2002, 94(6):1521-1529. 10.1213/00000539-200206000-00027
6. Minville V, Fourcade O, Grousset D, et al.: Spinal anesthesia using single injection small-dose bupivacaine versus continuous catheter injection techniques for surgical repair of hip fracture in elderly patients. Anesth Analg. 2006, 102:1559-63. 10.1213/01.ane.0000218421.18723.cf
7. Žunić M, Krčevski Škvarč N, Kamenik M: The influence of the infusion of ephedrine and phenylephrine on the hemodynamic stability after subarachnoid anesthesia in senior adults – a controlled randomized trial. BMC Anesthesiol. 2019, 19:207. 10.1186/s12871-019-0878-4
8. Critchley LA: Hypotension, subarachnoid block and the elderly patient. Anaesthesia. 1996, 51:1139-43. 10.1111/j.1365-2044.1996.tb15051.x
9. Biricik E, Ünlügenç H: Vasopressors for the treatment and prophylaxis of spinal induced hypotension during caesarean section. Turk J Anaesthesiol Reanim. 2021, 49:3-10. 10.5152/TJAR.2020.70
10. Rivera R, Antognini JF: Perioperative drug therapy in elderly patients. Anesthesiology. 2009, 110:1176-81. 10.1097/ALN.0b013e3181a10207
11. Becker DE: Basic and clinical pharmacology of autonomic drugs. Anesth Prog. 2012, 59:159-68. 10.2344/0003-3006-59.4.159
12. Abbasivash R, Sane S, Golmohammadi M, Shokuhi S, Toosi FD: Comparing prophylactic effect of phenylephrine and ephedrine on hypotension during spinal anesthesia for hip fracture surgery. Adv Biomed Res. 2016, 5:167. 10.4103/2277-9175.190943
13. Mon W, Stewart A, Fernando R, et al.: Cardiac output changes with phenylephrine and ephedrine infusions during spinal anesthesia for cesarean section: a randomized, double-blind trial. J Clin Anesth. 2017, 37:43-8. 10.1016/j.jclinane.2016.11.001
14. Asokan A, Muthalu A, Ananthy V, et al.: Comparison of intravenous bolus doses of phenylephrine vs ephedrine along with crystalloid co-loading in the prevention of hypotension during spinal anesthesia for caesarean section. Indian J Clin Anaesth. 2021, 8(4):537-542. 10.18231/j.ijca.2021.116
15. Sinha G, Hemalatha S, Gurudatt C L: Effectiveness of intravenous boluses of phenylephrine, ephedrine and mephentermine as vasopressors for management of perioperative hypotension in elective lower segment caesarean section under spinal anaesthesia – a prospective comparative study. Indian J Clin Anaesth. 2020, 7(1):46-53. 10.18231/j.ijca.2020.009

Abstract

This case report details the successful management of labor pain using epidural analgesia in a 22-year-old primigravid patient with a history of spina bifida and extensive surgical repair. Spina bifida, a congenital neural tube defect, presents unique challenges for neuraxial anesthesia due to altered spinal anatomy and potential neurological deficits. Despite these complexities, effective pain relief was achieved through careful patient counseling, comprehensive pre-procedural planning, and meticulous technique. Upon admission for labor induction due to preeclampsia, a physical examination revealed significant lumbar scarring with obscure anatomical landmarks. Despite these challenges, informed consent was obtained, and an epidural catheter was successfully placed using palpable bony prominences above the presumed T12-L1 interspace. A standard midline approach with saline loss of resistance technique was employed, epidural space was confirmed at a depth of 5 cm, and a catheter was placed. Continuous patient-controlled epidural analgesia (PCEA) comprising fentanyl and ropivacaine provided consistent pain relief throughout a 17-hour labor period, maintaining a dermatome level of T10. Post-delivery, neurosurgical evaluation confirmed successful catheter removal without complications, and the patient exhibited normal neurological function. This case underscores the importance of individualized pain management strategies in patients with spina bifida, necessitating thorough risk-benefit assessment, detailed patient education, and interdisciplinary collaboration for optimal outcomes. Despite the inherent challenges, epidural analgesia can be a viable option with careful planning and execution, contributing to improved maternal comfort and satisfaction during labor and delivery for patients with a history of spina bifida.

Introduction

This case report discusses the successful management of labor pain in a patient with a history of extensive surgical repair of spina bifida using epidural analgesia. Spina bifida is a congenital neural tube defect that can lead to various neurological and musculoskeletal complications. Effective neuraxial analgesia in such patients can be challenging due to altered anatomical and physiological considerations. In these circumstances, it is common that the spinous process of multiple vertebrae, which are classic landmarks for the guidance of placement of an epidural catheter, is significantly altered or absent. Even if these landmarks are patent, the underlying epidural space may be completely obliterated. This case highlights the importance of including the patient in pain management planning, taking a thorough patient history, and weighing the risks and benefits of treatment options to achieve optimal outcomes.

Spina bifida is characterized by congenital incomplete closure of the neural tube during embryonic development. This process can result in a wide range of abnormalities, including neurological and orthopedic problems such as motor deficits, musculoskeletal defects, and sensory disturbances. Neuraxial techniques for the management of labor pain in these patients pose a particular challenge due to a multitude of possible complicating factors, including altered internal spinal anatomy, missing anatomic landmarks, pre-existing neurologic deficits, and post-surgical changes, amongst others. Epidural analgesia is a well-established technique for providing adequate relief of typical labor pains. When patients with a prior diagnosis of spina bifida are identified, anesthesiologists must carefully assess whether this modality is appropriate or feasible and have a frank and truthful discussion with the parturient. Risks associated with this technique, including inadvertent dural puncture, no relief or “patchy” relief, as well as risks of worsening neurologic deficits, must be discussed. The totality of these factors, both from the standpoint of risks associated with difficult placement and possible failure, epidural analgesia, remains a controversial topic. Despite these challenges, this case demonstrates that a successful labor epidural without complications is possible using a cautious technique combined with a thorough discussion and an eager patient.

Case Presentation

A 22-year-old, G2, term 0, preterm 0, abortion 1, living 0, 97 kg female with a history of spina bifida, extensive surgical repair in infancy, and subsequent tethered cord syndrome requested epidural analgesia for labor analgesia. There was no prior history of neuraxial anesthesia. This term singleton pregnancy was complicated by preeclampsia leading to induction of labor; she was experiencing irregular contractions upon admission. Upon initial presentation, no imaging was available. A physical exam revealed extensive scarring with no palpable landmarks in the lumbar region. A bony process presumed to be a spinous process was palpable at an estimated T12 level. Neurological exam and history revealed no sensory or motor deficits.

The patient was counseled that epidural catheter placement carries a significantly greater risk for the spina bifida patient population. Additional or increased risks discussed were failure to access the epidural space, inadvertent dural picture with accompanying headache, incomplete or “patchy” pain relief, high epidural blockade, nerve damage, and increased length of time for placement. The patient acknowledged the risks, displayed full understanding, and elected to proceed.

After palpation of remaining anatomic landmarks, the decision was made to proceed with epidural catheter placement just above the level of the surgical scar and at the first palpable bony prominence, which was presumed to be the T12-L1 interspace. The patient was placed in the sitting position, and the procedure was performed with standard sterile precautions, a 17 g Tuohy needle, and a 19 g epidural catheter. From a midline approach, the loss of resistance to saline technique was utilized. The epidural space was accessed at a depth of 5 cm, and 3 cm of the catheter was left in the epidural space via the Touhy needle. A test dose was administered through the catheter of 3 mL of 1.5% lidocaine and 1:200,000 epinephrine. Following a negative test dose, patient-controlled epidural analgesia (PCEA) dosing was initiated using a solution containing fentanyl 2 mcg/mL and ropivacaine 0.125% at a basal rate of 8 mL/hour with a PCEA bolus of 3 mL and interval lockout of 15 minutes and a one-hour dose limit of 30 mL. No bolus was given due to the perceived risk of a high epidural. Patients, family members, and nursing staff received extensive education on the signs and symptoms of a high epidural blockade. The pain was well controlled with a dermatome level of T10 throughout labor, and vaginal delivery was completed after approximately 17 hours. The epidural catheter was removed with the tip intact without complications. A prior computed tomography scan of the abdomen was discovered after our procedure. Upon review, the epidural space appears to be completely scarred below the T12-L1 interspace. A small patent epidural space can be identified in Figures 1–2 at the T11-T12 interspace.

Figure 1: Sagittal computerized tomography scan of abdomen, arrow indicates possible epidural space

Figure 2: Transverse computerized tomography scan of abdomen, arrow indicates potential epidural space

Effective pain management was achieved throughout labor. On postpartum day 1, the patient was found to have normal neurologic function marked by normal ambulation and return of bowel and urinary function. The patient denied headaches or any signs and symptoms of secondary complications of epidural catheter placement.

Discussion

Spina bifida occulta may be present in up to 5-10% of the population [1,2]. Spina bifida patients are more likely to require a cesarean section, and traditionally, neuraxial techniques have been avoided due to concerns of secondary complications [3]. Additionally, previous spinal surgery has been considered a relative contraindication to the use of neuraxial anesthetic techniques. The anatomy of the epidural space at the level of the spinal lesion following surgical correction remains unclear. It has been described as “lobules of fat lying in the midline adherent to fascia and surrounding tissues or entirely obliterated” [4,5]. An attempt at epidural placement at the level of the defect significantly increases the risk of incidental dural puncture. A blood patch as a treatment for an inadvertent dural puncture presents similar technical difficulties and may be ineffective. Even if neuraxial needle placement is successful, then the spread of local anesthetic is rather unpredictable and may produce an incomplete block. Despite this, multiple case reports exist in the literature describing the successful use of epidural analgesia in patients with spina bifida both with and without corrective surgery [6,7]. There are no definitive guidelines in place for epidural analgesia in spina bifida patients after spine surgery.

Daley et al. [8] reviewed the experience of 18 patients for a total of 21 separate attempts at epidural analgesia for obstetric patients with previous spinal surgery. Continuous labor analgesia was established in 20 out of 21 cases reviewed. However, only 10 of them were placed easily on the first attempt, leaving the remaining 11 with higher requirements of local anesthetic and/or an incomplete block. Hubbert [9] attempted epidural analgesia in 17 laboring patients with a history of Harrington rod fusion and was successful in nine. It is noted that in only four (23%) was epidural analgesia easily obtained, two patients had inadvertent spinal anesthesia from a dural puncture, and 11 required multiple attempts at various levels. Tidmarsh [10] attempted 10 epidural catheter placements for labor analgesia in a parturient with known neural tube defects, of which four had prior corrective surgery. A similar approach was taken as in our case with a midline approach just above the level of defect at first palpable normal spinous process. Out of the 10 epidurals placed, six received normal symmetrical block at or below low thoracic dermatome levels. Of the four remaining, one block was asymmetric, one excessively high blockade, and two were inadequate analgesia below the level of spinal defect. Notably, of the four epidurals placed in patients with a history of corrective surgery, two received normal sensory blockade, one had an excessively high level (T3) of block, and one had inadequate analgesia at a level below the defect. Therefore, in this case series, 50% of those with corrective surgery had complications or inadequate labor analgesia.

It is worth discussing alternative techniques used to place epidural catheters, which include fluoroscopic and ultrasound-guided techniques. Fluoroscopic guided technique has been shown to have a “higher success rate than traditional landmark technique as it can accurately identify anatomical structures and epidural spaces using imaging devices” [11]. However, due to the difficulty of using fluoroscopy in daily practice and the burden of radiation exposure, the practical use is rather limited, especially in the obstetric population. The role of ultrasound guidance in placing epidural catheters is relatively new, but the evidence regarding its practical application and efficacy continues to grow. Chin et al. performed a thorough literature review regarding the benefits and limitations of ultrasound-guided thoracic and lumbar neuraxial blockades. They discovered the evidence suggests ultrasound guidance could improve neuraxial success rate, quality of epidural analgesia, ease of performance, identification of required needle depth, and identification of intervertebral levels [12]. However, the ultrasound-guided technique has displayed limitations in obese and elderly patients, and its use in those with prior spinal surgery remains unknown [12]. Also, extensive experience with ultrasound-guided techniques may be required before competence is attained [12]. In this case, an anesthesiologist with this experience was not readily available.

Our case is unique in that inadequate imaging was available prior to the placement of the epidural catheter and using a surgical scar as a landmark for a potentially patent epidural space proved to be a successful approach. Additionally, it is unusual given the extent of her post-surgical scarring that a continuous epidural space would retain the patency necessary for successful labor analgesia to be achieved.

Conclusions

Effective pain management for patients with a history of spina bifida requires a personalized approach due to their unique anatomic and physiologic factors. A clear discussion about the potential complications and the challenges of effective pain control even with safe epidural placement must be had with this patient population. Despite these challenges, epidural catheter placement can be a safe and effective means of achieving labor analgesia. Collaborating with specialists and considering various imaging modalities may enhance the precision of epidural placement and improve overall outcomes.

References

1. Eubanks JD, Cheruvu VK: Prevalence of sacral spina bifida occulta and its relationship to age, sex, race, and the sacral table angle: an anatomic, osteologic study of three thousand one hundred specimens. Spine (Phila Pa 1976). 2009, 34:1539-43. 10.1097/BRS.0b013e3181a98560
2. McGrady EM, Davis AG: Spina bifida occulta and epidural anaesthesia. Anaesthes. 1988, 43:867-9. 10.1111/j.1365-2044.1988.tb05602.x
3. O’Neal MA: A pregnant woman with spina bifida: need for a multidisciplinary labor plan. Front Med (Lausanne). 2017, 4:172. 10.3389/fmed.2017.00172
4. Bromage PR: Epidural Analgesia. WB Sanders Company, Philadelphia; 1978. 707-8.
5. Ingraham FD, Hamlin H: Spina bifida and cranium bifidum. N Engl J Med. 1948, 228:10.1056/NEJM194305202282001
6. Vaagenes P, Fjaerestad I: Epidural block during labour in a patient with spina bifida cystica. Anaesthes. 1981, 36:299-301. 10.1111/j.1365-2044.1981.tb10205.x
7. Bajaj P: Regional anaesthesia in the patient with pre-existing neurological dysfunction. Indian J Anaesth. 2009, 53:135-8.
8. Daley MD, Rolbin SH, Hew EM, Morningstar BA, Stewart JA: Epidural anesthesia for obstetrics after spinal surgery. Reg Anesth. 1990, 15:280-4.
9. Hubbert CH: Epidural anesthesia in patients with spinal fusion. Anesth Analg. 1985, 64:843.
10. Tidmarsh MD: Epidural anesthesia and neural tube defects. Int J Obstet Anesth. 1998, 7:111-14.
11. Parra MC, Washburn K, Brown JR, et al.: Fluoroscopic guidance increases the incidence of thoracic epidural catheter placement within the epidural space: a randomized trial. Reg Anesth Pain Med. 2017, 42:17-24. 10.1097/AAP.0000000000000519
12. Chin KJ, Karmakar MK, Peng P: Ultrasonography of the adult thoracic and lumbar spine for central neuraxial blockade. Anaesthes. 2011, 114:1459-85. 10.1097/ALN.0b013e318210f9f8

Abstract

Spinal anesthesia has many side effects, one of them being a drop in blood pressure (BP). Identifying predictive factors for this drop is a clear matter of concern. In this regard, the expiratory inferior vena cava/abdominal aorta (eIVC/Ao) index has already been spotted as such for doses of 0.5% hyperbaric bupivacaine greater than 12mg. Departing from the demonstrated correlation between this index and hypotension post-spinal anesthesia, our study aimed to (1) evaluate whether an eIVC/Ao index greater than 0.7, thus defining non-hypovolemic patients, can also predict minimal BP for doses inferior to 12mg and (2) identify other predictive factors for minimal BP post-spinal anesthesia. Lastly, we verified whether preoperative fasting induces hypovolemia.

This single-center prospective observational pilot study included 20 patients. The baseline measurements of BP, eIVC/Ao index, and fasting time were recorded at time T0′. Then spinal anesthesia was administered with 0.5% hyperbaric bupivacaine in doses inferior to 12 mg. The patients’ systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and metameric levels were each recorded at times T5′, T10′, T15′, and T20′.

The results indicated that baseline DBP was predictive of low DBP and minimum MAP, which reflect myocardial perfusion and systemic pressures, respectively. Therefore, it should trigger prophylaxis (spinal-lateralized, continuous, or lower dose) in patients with a low DBP baseline. Additionally, baseline SBP was predictive of minimum SBP, an independent risk factor for post-anesthetic hypotension if its baseline is less than 120 mmHg. Although female gender was linked to minimum SBP, other confounding factors (size, dose administered, and type of surgery related to gender) must also be considered. Moreover, a correlation was established between height and MAP in parturients. Hypotension was not recorded at local anesthetic (LA) doses between 8 and 12 mg and the doses administered were sufficient to achieve the metameric levels required for surgery (ether tests). Since 8 mg of 0.5% hyperbaric bupivacaine achieved the same level as 12 mg, lower doses of LA might prevent a significant drop in BP and its deleterious effects.

Therefore, in the current cohort, the eIVC/Ao index was not predictive of minimum BP during spinal anesthesia with doses less than 12 mg of 0.5% hyperbaric bupivacaine. However, predictive factors for minimum BP included gender and baseline SBP (for minimum SBP), height and baseline DBP (for minimum MAP), and baseline DBP (for minimum DBP). Lastly, preoperative fasting did not cause hypovolemia.

Introduction

Spinal anesthesia is associated with a significant drop in blood pressure (BP) to the point of hypotension (defined as systolic blood pressure (SBP) < 90 mmHg and/or diastolic blood pressure (DBP) < 60 mmHg [1]). Hypotension occurs in 15.3%-33% of cases [2] (particularly in pregnant women) and can interfere with tissue perfusion, leading to significant morbidity [3].

The index of the diameter of the inferior vena cava in exhalation compared to that of the abdominal aorta in systole (the expiratory IVC/Ao index) is a rapid, simple, non-invasive, and reliable method of determining the volume status of patients [4-6]. The pilot study by Salama et al. comprising 100 patients undergoing spinal anesthesia showed that the eIVC/Ao index is a predictive factor for the occurrence of post-spinal anesthesia arterial hypotension [7]. However, the doses of 0.5% hyperbaric bupivacaine were greater than 12 mg in the study.

The present study aimed to evaluate whether an eIVC/Ao index > 0.7 ± 0.09 [4] was predictive of minimal post-spinal anesthesia BP for < 12 mg of 0.5% hyperbaric bupivacaine in non-hypovolemic patients. In addition, we also determined whether there were other factors predictive of minimal post-spinal anesthesia BP and whether the duration of preoperative fasting-induced hypovolemia.

Materials & Methods

Herein, we conducted a single-center, prospective, observational pilot study at University Hospital Saint-Pierre, Brussels (Belgium) including 20 patients. The study was approved by the ethics committee (BE0762023231202).

The demographic characteristics recorded were sex, age, height, weight, body mass index (BMI), and American Society of Anesthesiologists (ASA) score.

The inclusion criteria were as follows: age between 18 and 65 years, ASA score I-II, and scheduled lower limb, urological, gynecological, or digestive surgery that could be performed under spinal anesthesia with 0.5% hyperbaric bupivacaine.

The exclusion criteria included patient refusals, contraindication to spinal anesthesia, lateralized spinal anesthesia, pediatric and geriatric populations, emergency surgery, patients with extremes of stature, i.e. too short (<160 cm) or too tall (>190 cm), use of sedatives, intrathecal adjuvant, preoperative volume replenishment, pregnant women, patients with poor echogenicity, those treated with beta-blockers and/or angiotensin-converting enzyme (ACE) inhibitors, and those assessed as hypovolemic using the according to the eIVC/Ao index or already suffering from arterial hypotension prior to spinal anesthesia.

Preoperative recording and evaluation

The duration of fasting was recorded when the patient arrived in the operating room. At T0′, the anesthetist recorded the baseline BP (SBP, DBP, and mean arterial pressure (MAP)). Then, the patient’s eIVC/Ao index was measured in the semi-seated position by ultrasound. In M mode (curvilinear low-frequency probe CA2-8AD, Siemens HS40 machine) in the subxiphoid window: measurement of the diameter of the inferior vena cava (eIVC) in the long axis 2 cm from the right atrial outlet. The anteroposterior systolic diameter of the aorta was estimated to be between 5 and 10 mm above the celiac trunk. Subsequently, the eIVC/Ao index was calculated as the ratio of the maximum diameter of the IVC during exhalation to the maximum diameter of the aorta during systole [6,7]. The image was recorded during three consecutive respiratory cycles in the inspiratory and expiratory phases by the same anesthetist (for the 20 cases) with a level 2 ultrasound experience and with a resident cardiologist reviewing and validating the images (Figure 1).

Figure 1: Ultrasound measurement point location for eIVC and aorta

A: Expiration IVC; B: Systole aorta

eIVC: Expiration Inferior Vena Cava

After ultrasound identification of the lumbar spine in the seating position, a 27-G Whitacre needle was inserted subarachnoidally at L3-L4. Then, a dose of < 12 mg of 0.5% hyperbaric bupivacaine was injected and adjusted according to the metameric level required for surgery. Each of the SBP, DBP, and MAP values was recorded at time points T5′, 10′, 15′ and 20′, and so were the metameric levels, by ether tests. Finally, arterial hypotension, if ever occurring, was planned to be treated using vasoactive agents and/or fluid challenge as appropriate.

Statistical analysis

Pearson’s correlation analysis was applied to compare the continuous data. The relationship between a continuous variable and a discrete variable was assessed using Student’s t-test when the underlying assumptions were met: 1) homogeneity of variances was evaluated using the Bartlett test and 2) normality of residuals was assessed using the Kolmogorov-Smirnov test. The results of the Student’s t-test were presented as the means and standard deviations per group. When the hypotheses underlying the t-test were not fulfilled, a Wilcoxon rank test was applied to the data, and the results were presented as medians and interquartile ranges. Finally, the data of several independent variables were analyzed using multiple linear regression models to predict the minimum BP level during the perioperative period. These data were entered into the multivariate regression analysis predicting minimum BP. For each of them, no multicollinearity was established (variance inflation factor (VIF) ≤ 5). In the case of multicollinearity, one of the two causative factors was removed from the regression model.

Next, we used a backward variable selection approach, sequentially removing the non-significant variables.

R software version 4.2.0 (R Core Team, 2021) was used to produce the statistical results [8].

Results

A total of 24 patients were recruited in the present study. Of these, three had poor echogenicity or structure detection was not feasible, and one patient withdrew consent. Consequently, 20 patients were included in the study. Among them, three (15%) had undergone orthopedic surgery, five (25%) had gynecological surgery, nine (45%) had urological surgery, and three (15%) patients had undergone proctological surgery. The cohort comprised 11 (55%) men and nine (45%) women, and their average age was 39.4 ± 12.35 years, average height 172.8 ± 7.52 cm, average weight 76.35 ± 9.84 kg, and average BMI 25.34 ± 2.80 kg/m². Moreover, 11 (55%) patients were ASA I vs. 9 (45%) ASA II.

The average duration of preoperative fasting was 13.9 ± 3.22 h for solids and 11.9 ± 4.53h for liquids. The average eIVC/Ao index was 1.07 ± 0.21.

No hypotensive episodes were observed in the perioperative period. The minimum recorded post-spinal anesthesia SBP, the minimum MAP, and the minimum DBP were 108, 78, and 60 mmHg, respectively (Tables 1, 2).

Independently of the BP studied (systolic, diastolic, and mean) at the cuff, the eIVC/Ao index was not predictive of the minimum BP in the study population (if p > 0.05) (Tables 3–11).

However, two variables, height and baseline SBP, were predictive of minimum SBP. These variables were included in a multivariate regression analysis. Although the VIF was 8 for baseline SBP, baseline SBP did not detect multicollinearity between the variables (VIF close to 1) in the final model, which explained 37.91% of the variance in minimum SBP. The only variable predicting minimum SBP in a multivariate regression model was baseline SBP (p = 0.0151). Additionally, once controlled for baseline SBP, height did not have a significant role in predicting minimum SBP (p = 0.1374) and was removed from the model (Table 2). On the other hand, a correlation was established between minimum SBP and female gender (p = 0.01564).

Furthermore, two variables predicted minimum DBP: baseline DBP and baseline MAP. These were included in a multivariate regression analysis, and no concern for multicollinearity was detected. Then, the variable not significantly associated with the dependent variable was removed: baseline MAP (p = 0.484). The final model contained baseline DBP, which explained 35.95% of the variance in the minimum DBP (Tables 6–8).

The independent variables significantly associated with the baseline MAP were entered in multivariate regression analysis. A significant VIF was detected for baseline SBP, which we removed from the analysis. We also removed the variable non-significantly associated with the dependent variable: baseline SBP (p = 0.2555). The final model contained baseline height and baseline DBP, which explained 35.2% of the variance in minimum MAP (Tables 9–11).

Discussion

In the present study, we did not find a correlation between the eIVC/Ao index and minimum BP during spinal anesthesia with 0.5% bupivacaine at doses < 12 mg. The pilot study by Salama et al. predicted the occurrence of arterial hypotension using the eIVC/Ao index during spinal anesthesia [7]. However, this study differs from our approach in several aspects: (1) Our study included only patients who were not hypovolemic according to the eIVC/Ao index; (2) A low dose of 0.5% hyperbaric bupivacaine injected (< 12 mg vs. 12-15 mg); (3) The average age of the patients was lower (39.4 years vs. 49.5 years).

Previous studies have identified the factors associated with a drop in BP following spinal anesthesia: the dose of the local anesthetic (LA) injected, the height of the T5′ block, and age of ≥ 40 years [3,9,10]. In our opinion, these methodological and demographic differences between our study and that of Salama et al. may explain the absence of a significant drop in BP in our cohort.

Another study comprising 172 patients demonstrated that the mean eIVC/Ao index in normovolemic patients was 1.2 ± 0.12, hypovolemic 0.7 ± 0.09, and hypovolemic 1.6 ± 0.05 [4]. These results were further confirmed with an eIVC/Ao index of 1.2 ± 2 for SD = 0.17, defining a normovolemic state [6]. These findings align with the results as the mean value of the eIVC/Ao index in our cohort (1.07 ± 0.21) is compatible with a state of non-hypovolemia, which may also be termed a state of “physiological dehydration” [6]. Another recent study by Rahman et al. suggested a cutoff of the eIVC/Ao index at 1.14 ± 2 with SD 0.18 to detect the early phase of hypovolemic shock [5]. These relative discrepancies suggested that the standardization of eIVC/Ao index values concerning different volemic statuses needs an in-depth investigation.

The lack of correlation between the eIVC/Ao index and minimum BP in our cohort could be explained by the small sample size or a minimal drop in the BP.

The average age of our cohort was 39.4 ± 12.35 years, representing a relatively young population. Thus, it is not surprising that age was not a predictive factor for minimal BP after spinal anesthesia in our population. Elderly patients (defined by the World Health Organization (WHO) as individuals > 60 years old; clinical studies use a cutoff of 65 years) are at greater risk of a drop in BP following spinal anesthesia due to “closure” of the holes of conjugation linked to bone deformations [11-14]. This phenomenon might hinder the diffusion of the LA outside the medullary sheath, causing significant diffusion of the anesthetic block and other cardiovascular performance factors [9,10,13].

Similarly, obesity (defined by a BMI > 30 kg/m² according to the WHO [15]) is a risk factor for post-spinal anesthetic pressure drop. Magnetic resonance imaging showed that obese people have up to 10 ml less cerebrospinal fluid than those with a normal BMI, which is a potential source of excessive spinal block for the same dose of LA, therefore causing a drop in BP [3,13]. The average BMI in our cohort was 25.34 ± 2.8 kg/m²; thus, our patients were below the risk profile.

In addition, some studies have shown that a high ASA score (> II) is a determining factor in arterial hypotension during general or spinal anesthesia; the older the patient, the greater the risk [16]. All our patients were considered to be at low risk of anesthesia (55% ASA I and 45% ASA II); therefore, our results were in line with the literature.

On the other hand, we also determined other factors predictive of minimal BP during spinal anesthesia with 0.5% bupivacaine at doses < 12 mg. Baseline DBP appeared to be a factor underlying DBP and minimal perioperative MAP. Since DBP and MAP are crucial in myocardial and systemic perfusion, respectively, patients with lower baseline DBP may be identified as requiring special monitoring during surgery [17].

Baseline SBP was predictive of minimal SBP post-spinal anesthesia with 0.5% bupivacaine. Hence, the anesthetic was termed an independent risk factor for the development of post-spinal arterial hypotension if the baseline SBP is < 120 mmHg [3].

A statistical relationship was established between minimum SBP and female gender (p = 0.01564). Also, confounding factors, such as height, dose administered, and type of surgery, could explain this result.

Finally, height also seemed to be a factor predicting minimum MAP; this relationship has been elaborated mainly in the literature on parturients [18].

In agreement with Muller et al. [19], we found that the recorded duration of fasting was not associated with preoperative hypovolemia. Instead, our patients had an eIVC/Ao index > 0.75, corresponding to a state of non-hypovolemia, despite fasting duration exceeding the current recommendations [20].

Furthermore, our study found no evidence of arterial hypotension (absolute minimum SBP: 108 mmHg and absolute minimum DBP: 60 mmHg) for doses of hyperbaric 0.5% bupivacaine ranging from 8 mg to 12 mg. Also, we did not observe any failure of spinal anesthesia regardless of the type of surgery considered, which was confirmed by the ether test of the metameric levels at time points T5′, T10′, T15′, and T20′. These findings suggested that we could consider doses of 0.5% hyperbaric bupivacaine in our daily practice to obtain a sufficient metameric level in certain surgeries. Although the same metameric level could be achieved for different doses of 0.5% hyperbaric bupivacaine (8 mg or 12 mg), the duration of the sensory-motor block is altered (39 min vs. 55 min) [14]. A lower dose of 0.5% hyperbaric bupivacaine might prevent arterial hypotension and its potentially deleterious effects. Thus, the baricity of the LA and the dose are two of the main determinants of LA distribution [13,14].

Methodology limitation

The primary limitation of this study is the small sample size, which results in insufficient statistical power. Thus, future studies with larger patient cohorts are recommended to confirm or refute our findings.

Conclusions

The eIVC/Ao index did not show any correlation with minimum BP during spinal anesthesia with hyperbaric 0.5% bupivacaine at doses less than 12 mg in non-hypovolemic patients. However, predictive factors for minimum blood pressure, under the set circumstances, were gender and baseline SBP (for minimum SBP), height and baseline DBP (for minimum MAP), and baseline DBP (for minimum DBP). Lastly, the duration of preoperative fasting in our cohort did not result in hypovolemia, according to the eIVC/Ao index.

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