Neuraxial anaesthesia-induced hypotension during Caesarean section

Learning objectives.

By reading this article, you should be able to:

• •Describe the risk factors and predictors for spinal anaesthesia-mediated hypotension (SAMH) during Caesarean section.
• •Discuss recent advances in the detection of hypotension by non-invasive measures.
• •Review the risks and benefits of different pharmacological options to treat SAMH.

Key points.

• •Non-invasive haemodynamic measurements can guide the management of spinal anaesthesia-mediated hypotension (SAMH).
• •Although giving colloid and crystalloid fluids can decrease the severity of SAMH, vasopressor infusions are the mainstay of management.
• •Left uterine displacement should be continued in high-risk maternal or fetal conditions.
• •Noradrenaline (norepinephrine) is safe and effective but requires careful preparation and vigilance.
• •Phenylephrine remains the first-line vasopressor for the management of SAMH.

Neuraxial anaesthesia is commonly used for Caesarean section because it avoids airway instrumentation and exposure of the fetus to anaesthetic drugs, provides superior postoperative analgesia and decreases blood loss compared with general anaesthesia. Despite its popularity, neuraxial anaesthesia, especially spinal anaesthesia, often leads to profound hypotension caused by blockade of preganglionic sympathetic nerve fibres resulting in arterial vasodilation, venodilation and increased peripheral blood pooling.¹ This has been defined as spinal anaesthesia-mediated hypotension (SAMH). Hypotension is further exacerbated by the supine position with the gravid uterus resting on the inferior vena cava (IVC), reducing venous return and cardiac output. Consequences of untreated hypotension range from minor (nausea and dizziness) to more serious adverse outcomes (compromised uteroplacental blood flow with fetal acidaemia, loss of consciousness and cardiac arrest). It is therefore important to minimise the incidence and severity of hypotension; and vasopressors are the mainstay in this regard.² By increasing systemic vascular resistance (SVR), vasopressors counteract the effect of acute sympathetic blockade from neuraxial anaesthesia to sustain maternal blood pressure. The past two decades have provided extensive new data on the choice and dose of vasopressors and their impact on fetal status. The goal of this review is to provide a state-of-the-art overview of maternal hypotension after spinal anaesthesia and its management with vasopressors.

Risk factors and predictors

Criteria for SAMH are not well defined. Klöhr and colleagues found 15 different definitions of hypotension during Caesarean section and high variation in the incidence of intraoperative hypotension when applying these various definitions.³ Furthermore, inconsistencies regarding the frequency and timing of blood pressure measurement, and differences in the definitions of other maternal haemodynamic variables such as bradycardia and hypertension, are broadly prevalent within research studies and limit the general application of their findings. Given this, we advocate readers to exercise due diligence when interpreting and comparing studies on this subject area. We also highlight guidance provided by an international consensus recommending that systolic blood pressure is maintained at > 90% of baseline measured before spinal anaesthesia, and avoiding a reduction to < 80% of baseline.²

The identification of risk factors for SAMH can optimise clinical care by guiding the initiation and titration of prophylactic measures. Although such guidance could be less useful now given the widespread prevalence of prophylactic phenylephrine infusions, a more nuanced understanding of the predicted haemodynamic trajectory may be particularly useful in high-risk cases with uteroplacental compromise. Patients with a higher pretest probability of SAMH may benefit from more aggressive management, including additional preloading and coloading with fluids, and higher starting doses of a prophylactic vasopressor agent. In a meta-analysis of 38 studies involving 3086 patients, Yu and colleagues analysed over 30 potential clinical predictors across seven domains and identified only weak correlations for most of these; higher BMI, weight gain during pregnancy, gravidity >3, a history of hypotension, higher baseline heart rate, lower systolic blood pressure and altered sympathetic/vagal balance appeared to be modestly correlated with increased SAMH, although the results were inconsistent across studies.⁴

The advent of non-invasive continuous blood pressure monitoring devices has significantly enhanced our understanding of maternal hypotension, and provide valuable insights on how best to address it. These devices provide information on haemodynamic variables such as stroke volume (SV), stroke volume variation (SVV), heart rate variability and SVR. In a prospective study of women undergoing elective Caesarean section under spinal anaesthesia with a crystalloid coload and prophylactic phenylephrine infusion, an SVV cutoff of 7% to predict hypotension corresponded to a sensitivity and specificity of 84% and 83%, respectively. The SVV induced by a passive leg raise predicted hypotension with a sensitivity and specificity of 70% and 69%, respectively.⁵ These findings suggest that patients with a higher SVV may benefit from a more aggressive resuscitation strategy, although approximately 17% of patients still have inconclusive results that constitute a diagnostic grey zone. Similarly, the plethysmography waveform obtained from standard pulse oximeters can be used to reliably assess peripheral vascular tone through calculation of a perfusion index (PI), which is a ratio of the pulsatile signal to the non-pulsatile signal expressed as a percentage from 0.02% to 20%. A lower PI indicates stronger peripheral tone, and a higher PI correlates with vasodilation and the onset of spinal anaesthesia. Patients with higher resting PI, therefore, may require more vasopressor than patients with lower resting PI to prevent hypotension.⁶ The combination of an increasing heart rate, as a marker of peripheral vasodilation, with a decrease in regional cerebral oxygen saturation has also been suggested as a potential early indicator of hypotension.⁷

Finally, point-of-care ultrasound is another promising tool that may improve intraoperative haemodynamic management during Caesarean section. Transthoracic echocardiography and measurement of subaortic variation in the velocity time integral before and after passive leg raising effectively predicts hypotension with high specificity and sensitivity.⁸ Ultrasonographic evaluation of the IVC and the internal jugular vein (IJV), and measurement of the dynamic variation in diameter facilitates calculation of a collapsibility index (CI) to predict the hypotensive response to spinal anaesthesia. Both IVC-CI and IJV-CI are reliable markers with a sensitivity and specificity greater than 80% for predicting SAMH.⁹ Similarly, ultrasonographic measurement of the transverse diameter of the right common femoral vein, more superficial and easily measured with a high-frequency ultrasound probe than the IVC, is also associated with SAMH.¹⁰ Further prospective validation of these ultrasonographic measurements is needed to characterise their usefulness in clinical practice.

Non-pharmacological management of hypotension

Fluids

Giving crystalloid fluids before spinal anaesthesia is an important strategy for mitigating hypotensive effects. Withholding a fluid bolus, for example, significantly exacerbates hypotension after induction of spinal anaesthesia.¹¹ Both the type of fluid (crystalloid or colloid) and timing (before or simultaneous to the onset of spinal anaesthesia) have been studied. Colloid preloading appears to be superior to crystalloid preloading, and colloid ‘coloading’ seems to be equally efficacious as crystalloid coloading.¹² A recently published study by Theodoraki and colleagues compared a preload with colloid to a ‘coload’ with colloid during spinal anaesthesia, both groups also receiving an infusion of noradrenaline (norepinephrine).¹³ They found that the incidence of hypotension was comparable between both strategies, and the authors advocated either fluid loading technique during spinal anaesthesia for Caesarean section. Park and colleagues revealed no benefit of giving colloids over crystalloids during elective Caesarean section in the presence of a prophylactic infusion of phenylephrine.¹⁴ A recent network meta-analysis examining a subset of only randomised double-blind trials from a pool of 49 studies and 4317 patients concluded that the greatest chance of success in preventing hypotension was observed with colloid preload (79%), colloid coload (78%), crystalloid coload (37%) and crystalloid preload (6%).¹² However, these results should be interpreted cautiously as it is unclear whether the differences between interventions have effect sizes that are meaningful in clinical practice. Indeed, trial sequential analysis (TSA) revealed insufficient data to identify any one fluid strategy as being superior to another. Interestingly, a recent investigation into the differential impact of colloid and crystalloid coloads during spinal anaesthesia for Caesarean section showed a 30% reduction in the prophylactic noradrenaline infusion dose in women who received colloid coload.¹⁵ More research is required to ascertain the impact of escalating doses of vasoactive drug infusion, which is known to reduce the incidence of hypotension, on the volume of fluid required. Until then, institutional fluid algorithms are likely to be determined by product availability and cost.

Positioning

The influence of the sitting compared with the lateral position during placement of spinal anaesthesia can affect the severity of SAMH. In a recent comparative study of the two positions, a significantly greater proportion of women experienced hypotension in the sitting position at both 6 and 8 min after spinal anaesthesia using hyperbaric bupivacaine and sufentanil.¹⁶ This finding is consistent with a previous study in which there was a greater incidence of sensory block above the T4 dermatome in the sitting position after induction of spinal anaesthesia with plain bupivacaine.¹⁷ However, these results are in contrast to those of an older study in which the lateral position was associated with faster progression of block height and increased requirement for ephedrine in the first 10 min after starting spinal anaesthesia with hyperbaric bupivacaine.¹⁸ Differences between studies may be attributable to variations in practice including the time between induction of spinal anaesthesia and positioning, degree of left lateral tilt, the choice, dose and baricity of local anaesthetic. Furthermore, standard prophylactic vasopressor infusions are needed to define the effect of positioning during spinal anaesthesia more clearly.

The assumption of the supine position after spinal anaesthesia leads to significantly reduced venous return. In an MRI study of pregnant women in their third trimester, the supine position resulted in a 16.4% decrease in cardiac output compared with the left lateral position and a 32% reduction of blood flow through the abdominal aorta at the level of its bifurcation.¹⁹ To minimise the consequences of supine hypotension, the introduction of a left lateral tilt is routine clinical practice during Caesarean section, but the extent of necessary tilt is unclear. Evaluation of women who were at term and tilted at 15°, 30° and 45° revealed that significant relief of IVC compression shown by MRI was not achieved with 15° lateral tilt.²⁰ However, tilting more than 15° is impractical. A subsequent ultrasonographic study determined that 15° of lateral tilt significantly reduces the IVC CI and the incidence of hypotension during Caesarean section.²¹ Lee and colleagues examined the impact of a 15° lateral tilt in the presence of a crystalloid coload and phenylephrine infusion during spinal anaesthesia for elective Caesarean section and found no difference in umbilical arterial base excess between the supine vs lateral position.²² Importantly, cardiac output and systolic blood pressure were lower in the first 15 min after anaesthetic induction in the supine group, and the influence of this critical time period is unclear in the compromised fetus during non-elective Caesarean section. More research with standardised study designs is required to clarify the impact of left uterine displacement on placental perfusion. Until then, use of this manoeuvre during Caesarean section, especially for non-elective Caesarean section where the uteroplacental vasculature is potentially compromised, seems prudent.

Pharmacological management

Vasopressor agents are critical for both prevention and treatment of SAMH. Though vasopressors were historically given as intermittent boluses, the lag time between the oscillometric blood pressure measurement and triggered treatment response often led to significant under- or over-treatment of hypotension with harmful consequences. These concerns necessitated the introduction of continuous vasopressor administration using titratable infusion pumps with significantly improved response time and patient outcomes.

Ephedrine

Ephedrine is an indirect and non-specific sympathomimetic adrenergic agonist with primarily β-agonist activity. It leads to the presynaptic release of noradrenaline, resulting in an increased cardiac output with less impact on SVR. Given its slow onset and long duration of action, titration of ephedrine for SAMH is challenging. After the publication of several important studies describing the comparatively negative impact of ephedrine on fetal acid–base status during Caesarean section, phenylephrine became widely regarded as the vasopressor of choice for SAMH.^23,24 The adverse fetal metabolic profile associated with ephedrine is likely to stem from its lipophilicity and transplacental transfer, leading to increased fetal metabolism and resultant catecholamine, glucose and lactate production.²⁴ The unfavourable metabolic profiles of neonates exposed to ephedrine have not been reproduced in non-elective Caesarean section, and a meta-analysis and TSA concluded that inadequate evidence exists to conclusively determine the superiority of ephedrine or phenylephrine for high-risk Caesarean section.²⁵ Despite a paucity of evidence clearly correlating its use with adverse neurobehavioral outcomes, ephedrine use has substantially decreased globally in favour of phenylephrine.

Phenylephrine

Phenylephrine is a potent, rapidly-acting vasopressor with a short duration of action. It is an α-agonist with no significant β-agonist activity at clinical concentrations and doses. Phenylephrine increases SVR by binding to α-receptors in the vasculature and causing arteriolar vasoconstriction. Phenylephrine use has become prevalent worldwide given its easy titratability via an infusion pump, familiarity with its use for non-obstetric surgery and minimal impact on fetal acid–base status.²⁴ In non-obstetric patients, phenylephrine increases venous return through constriction of capacitance vessels unless venous resistance is already increased. In women randomly assigned to receive a phenylephrine infusion targeted to either 100%, 90% or 80% of maternal systolic blood pressure, those assigned to the strictest control experienced less nausea and their neonates were born with higher umbilical arterial pH.²⁶ Phenylephrine is commonly associated with a baroreceptor-mediated reflex bradycardia that can result in decreased cardiac output, reduced placental blood flow, and a negative effect on fetal wellbeing. Despite these concerns, even large doses of phenylephrine have not been shown to cause adverse neonatal outcomes in low-risk Caesarean deliveries.^11,24 These results may be partially explained by the pressure dependence of the uteroplacental vasculature. Although cardiac output has been suggested as a more reliable surrogate for placental blood flow than blood pressure, its comparative influence on regional blood flow at the uteroplacental interface is unclear, especially in patients with pre-existing uteroplacental compromise.

Noradrenaline

In 2018, an international consensus statement suggested that vasopressors with β-agonist activity possess the best pharmacological profile for treating hypotension during Caesarean section because of their capacity to minimise reflex bradycardia and reduced cardiac output.² Noradrenaline is a potent α-agonist that also has some desirable β-agonist effects, attenuating the bradycardia typically associated with high doses of α-agonism through binding of β₁ receptors on the myocardium. Direct positive chronotropic and indirect negative chronotropic effects result in an overall neutral effect on heart rate. Noradrenaline is the preferred first-line agent in intensive care as it is associated with improved organ perfusion compared with pure α-agonists.²⁷ In contrast to phenylephrine, noradrenaline can increase venous return without increased venous resistance owing to the presence of β-adrenergic receptors in veins. As a promising alternative to phenylephrine with a less negative influence on maternal heart rate, noradrenaline has been the subject of significant investigation over the last decade. Several randomised controlled trials have demonstrated the efficacy and safety of noradrenaline infusions during spinal anaesthesia and Caesarean section.28, 29, 30 When given as a prophylactic infusion during Caesarean section, noradrenaline is approximately six times more potent than phenylephrine.³¹ The effective dose of weight-adjusted and fixed-rate noradrenaline infusions for preventing hypotension during Caesarean section, defined as a decrease in systolic arterial pressure ≥ 20% below baseline or to ≤ 90 mmHg before fetal delivery, was calculated by Fu and colleagues³² to be 0.029 and 0.080 μg kg⁻¹min⁻¹ in 50% and 90% (ED₉₀) of women, respectively.

The perceived safety risks associated with peripheral noradrenaline infusions, specifically extravasation leading to tissue ischaemia and necrosis, have prevented its widespread use for Caesarean section. However, this concern is not based on evidence. In the emergency department setting, peripheral noradrenaline infusions in hypotensive patients for an average of 32 h at a maximum rate of 30 mg min⁻¹ were well tolerated without adverse effects.³³ In intensive care, noradrenaline concentrations up to 32 μg ml⁻¹ used through peripheral venous cannulae resulted in local tissue complications in less than 2% of patients.³⁴ In a large multicentre study of 14,385 non-obstetric surgical patients, no significant associations between peripheral noradrenaline infusion at 20 μg ml⁻¹ and adverse events were reported.³⁵

Although the use of noradrenaline has been well established, it is uncertain as to whether clinical outcomes are substantially better than using phenylephrine. A recent randomised controlled trial compared low-dose infusions of both noradrenaline at a rate of 2.5 μg min⁻¹ and phenylephrine at a rate of 50 μg min⁻¹ and found the umbilical artery pH and Apgar scores to be comparable.³⁶ These findings are consistent with those of an earlier study by Ngan Kee and colleagues that compared a computer-controlled infusion of noradrenaline 5 μg ml⁻¹ with phenylephrine 100 μg ml⁻¹ in 104 patients undergoing Caesarean section.³⁷ Both infusions were similarly efficacious in controlling blood pressure, but noradrenaline resulted in a greater heart rate and cardiac output and lower SVR. The incidence of bradycardia, defined as a heart rate less than 60 beats min⁻¹, occurred in 18.4% and 55.8% of the noradrenaline and phenylephrine groups, respectively. Umbilical plasma catecholamine concentrations were lower and umbilical vein pH and oxygen content were higher in the noradrenaline group than in the phenylephrine group, suggesting improved placental perfusion with noradrenaline. However, these differences were small and of unclear clinical significance. In a recent randomised study of fetal outcome involving 668 patients, noradrenaline was shown to be non-inferior to phenylephrine as evaluated by umbilical arterial pH, with subgroup analysis confirming this result for elective cases but not for non-elective cases.³⁸

Adrenaline (epinephrine)

Few studies have evaluated adrenaline as a vasopressor for SAMH. This is likely because of its perceived and actual potency, and strong β-adrenergic receptor agonism that has largely relegated its clinical use to crisis situations. When given as an infusion at a rate of 0.1 μg kg⁻¹min⁻¹ and titrated to maintain a systolic blood pressure between 90% and 120% of baseline at the induction of spinal anaesthesia, adrenaline leads to a smaller reduction of heart rate and cardiac output compared with a phenylephrine infusion at a rate of 1 μg kg⁻¹ min⁻¹ without causing tachycardia, defined as heart rate greater than 140 beats min⁻¹.³⁹ Interestingly, the umbilical artery pH was superior in those who received adrenaline, suggesting improved uteroplacental perfusion compared with phenylephrine, but without subsequent significant differences in fetal acidosis or Apgar scores at 1 and 5 min. In a recently published randomised controlled dose-finding trial that included 271 patients undergoing elective Caesarean section under spinal anaesthesia, women were randomised to receive prophylactic adrenaline infusions at either 0.01, 0.02 or 0.03 μg kg⁻¹ min⁻¹.⁴⁰ The authors found that a dose of 0.03 μg kg⁻¹ min⁻¹ was associated with the least hypotension and rescue ephedrine use with comparable incidences of excessive tachycardia, hypertension and neonatal outcomes.

Comparisons of vasopressor agents

In 2020, a meta-analysis by Heesen and colleagues examined 13 studies and 2002 patients that compared noradrenaline with phenylephrine infusions.⁴¹ They found considerable heterogeneity across studies and only four studies were assessed to be at low risk of bias for the primary outcomes of maternal hypotension and fetal acidosis. In two of these studies, there were no cases of fetal acidosis, one study reported a non-significantly higher incidence of fetal acidosis with noradrenaline, and one found similar numbers in both groups. The authors concluded that no meaningful conclusion was able to be drawn from the current literature, and maternal hypotension, hypertension and tachycardia did not differ between noradrenaline and phenylephrine. In the most comprehensive synthesis of evidence on this subject to date, a network meta-analysis by Singh and colleagues examined 52 randomised controlled trials and 4216 patients and established a probability rank order of vasopressors least likely to cause fetal acidosis.⁴² Their results suggested noradrenaline was the superior vasopressor, followed by mephentermine, metaraminol, phenylephrine and ephedrine. Although limited by the number of indirect comparisons in the network, this systematic review nonetheless contributed substantially to the growing body of evidence supporting the clinical role of noradrenaline. The relevant pharmacology of vasopressors for Caesarean section under spinal anaesthesia is summarised in Table 1.

Table 1.

Comparison of vasopressor agents that may be used for spinal anaesthesia-mediated hypotension during Caesarean delivery with recommended doses.

Vasopressor	Receptor	Mechanism	Onset (min)	Duration of action (min)	Effect on heart rate	Bolus dose	Infusion rate
Phenylephrine	α1	Direct	1	5–10		100 μg	25–50 μg min−1
Ephedrine	α1, α2, β1, β2	Indirect	2–5	60		5–10 mg	Not recommended
Noradrenaline	α1, α2, β1	Direct	1	5–10		6 μg	0.02–0.08 μg kg−1 min−1
Adrenaline	α1, α2, β1, β2	Direct	1	5–10		Not recommended	0.01–0.03 μg kg−1 min−1

Special circumstances

Pre-eclampsia

Patients who have pre-eclampsia are more likely to have an abnormal uteroplacental blood flow and be more sensitive to the effects of exogenous vasopressors compared with women are who normotensive. This may be caused by higher circulating levels of endogenous vasoactive mediators such as endothelin and thromboxane, and further influenced by the fact that women with pre-eclampsia are also more likely to be delivered at lower gestational ages with smaller birth weights and therefore less aortocaval compression in the supine position.

In a recent dose–response study by Hu and colleagues, the ED₉₀ (95% confidence interval) of phenylephrine given as a bolus for the primary treatment of the first episode of SAMH in patients with normotension and severe pre-eclampsia were 107 μg (95.9–128.6) and 70.7 μg (62.9–86.7), respectively, revealing a 34% decrease in the dose needed for patients who have severe pre-eclampsia.⁴³ Furthermore, bolus doses of either phenylephrine 50 μg or noradrenaline 4 μg have been found to be equally effective in patients who have pre-eclampsia for treating SAMH with comparable neonatal and maternal outcomes.⁴⁴ Interestingly, the number of boluses required in the phenylephrine group was significantly higher than that required in the noradrenaline group, whereas the incidence of hypotension in the noradrenaline group was increased, resulting in a similar overall requirement for vasopressors in both groups. Fetal acid–base measures were also comparable except for reduced venous oxygen partial pressure and venous oxygen saturation in the phenylephrine group. These findings reflect the results by Ngan Kee and colleagues in normotensive women, and is thought to result from dose-dependent and phenylephrine-mediated vasoconstriction of the arteries that perfuse the uterus with subsequently reduced uteroplacental blood flow, although no adverse neonatal outcomes owing to this mechanism have been described.³⁷

The prophylactic use of vasopressors in patients who have pre-eclampsia has also been evaluated. In a recent study by Guo and colleagues, prophylactic noradrenaline and phenylephrine infusions were compared in 69 patients.⁴⁵ Bradycardia was defined as a heart rate less than 60 beats min⁻¹ and hypotension as a systolic blood pressure less than 80% of baseline. The incidence of hypotension was 15.9% and 14.5% in the noradrenaline and phenylephrine groups, respectively, which is lower than the reported incidence of greater than 30% in healthy patients.³² Phenylephrine infusion was associated with greater incidence of bradycardia, whereas no differences were reported in the incidence of maternal hypotension or neonatal outcomes between both groups. Guidelines with regard to use of vasopressor agents during Caesarean section for patients with and without pre-eclampsia with severe features are detailed in Figure 1.

Fig 1.

Flowchart depicting suggested perioperative algorithm for vasopressor administration during Caesarean section. Dosing recommendations assume concomitant colloid preload or crystalloid colloid and 15° left lateral tilt. Ephedrine is omitted from this algorithm given its association with fetal acidosis but may be considered after delivery in lieu of glycopyrrolate for hypotensive patients with heart rate < 60 beats min⁻¹. Should vasopressor infusion doses exceed phenylephrine 100 μg min⁻¹ or noradrenaline 0.2 μg kg⁻¹min⁻¹, evaluate infusion tubing, i.v. catheter insertion site and blood pressure cuff. If phenylephrine infusion dose exceeds 100 μg min⁻¹, consider switching to noradrenaline. SBP, systolic blood pressure.

Summary of recommendations

The validation of non-invasive continuous haemodynamic monitoring in patients undergoing Caesarean section has paved the way for more nuanced intraoperative management and sophisticated research objectives. Although this technology is still nascent in clinical practice and the costs may be prohibitive, it can provide real-time information on clinical variables such as SVV and SVR and represents a major opportunity for tailored perioperative decision-making with respect to fluids vasopressors. Clinicians' interventions are only as effective as the data upon which they are based, and such tools therefore offer the greatest chance of providing individualised care in this setting. Extensive research over the past two decades conclusively identifies noradrenaline as a physiologically superior choice for both mother and baby during spinal anaesthesia for Caesarean section. However, the use of noradrenaline as the vasopressor of choice during Caesarean section requires close oversight of drug preparation, dilution and dosing. Close monitoring of vital signs and regular inspection of the i.v. cannula used for infusion are essential. Until such preventive mechanisms are in place, we recommend the routine use of prophylactic phenylephrine infusions.

Declaration of interests

The authors declare that they have no conflicts of interest.

MCQs

The associated MCQs (to support CME/CPD activity) will be accessible at www.bjaed.org/cme/home by subscribers to BJA Education.

Biographies

Adithya Devadas Bhat MD is an obstetric anaesthesiologist at Northwestern University Feinberg School of Medicine with special interests in quality of care in obstetric anaesthesia, medical simulation and curriculum development.

Preet Mohinder Singh MD is an obstetric anaesthesiologist at Washington University School of Medicine in St. Louis. His professional focus revolves around epidemiological and outcomes research within the realm of anaesthesiology.

Arvind Palanisamy MD FRCA is the division chief of obstetric anesthesiology at Washington University School of Medicine in St. Louis. He is an active researcher covering the entire spectrum from basic sciences to clinical and epidemiological research in maternal and neonatal health.

Matrix codes: 1A02, 2G04, 3B00