Anesthesia for Robotic Pelvic Surgery: The Hidden Physiology of Steep Trendelenburg and Pneumoperitoneum

Key Points

• A high CVP during steep Trendelenburg may mainly reflect hydrostatic and intrathoracic pressure transmission, not effective preload.
• A stable EtCO2 can coexist with a rising PaCO2, especially in older patients and during prolonged positioning.
• High airway pressure partly reflects chest-wall and abdominal pressure; use plateau pressure, driving pressure, compliance, oxygenation, and hemodynamic response together.
• A normal or increased cerebral NIRS value does not exclude impaired venous drainage or increased intracranial-pressure surrogates.
• Facial or conjunctival edema is an airway warning, not merely a cosmetic finding.

Why This Physiology Is Easy to Underestimate

Robotic pelvic surgery creates a distinctive anesthetic problem: the two exposures that improve surgical access also change the meaning of the numbers used to judge cardiopulmonary stability. Pneumoperitoneum compresses the abdomen from below. Steep Trendelenburg shifts blood, abdominal contents, and fluid toward the chest and head. The result is not simply a larger preload plus a stiffer lung. It is a coupled pressure system in which intra-abdominal pressure, intrathoracic pressure, venous pressure, vascular resistance, airway pressure, and tissue edema change together. [1,2]

This distinction matters because pressure is not the same as flow. A higher arterial pressure does not guarantee adequate cardiac output. A higher central venous pressure does not guarantee useful ventricular filling. A normal pulse oximeter does not exclude dependent atelectasis or impaired ventilation. A rising cerebral oximeter value does not prove normal cerebral venous drainage. In a large systematic review, steep Trendelenburg was not associated with a clear excess of several major postoperative complications compared with alternative approaches. Still, the evidence was heterogeneous and does not erase patient-level physiologic vulnerability. [3]

For this review, steep Trendelenburg means approximately 25 to 45 degrees head-down. The exact angle, insufflation pressure, and duration vary by procedure, surgeon, platform, body habitus, and institutional practice. The highest-risk period begins when tilt and pneumoperitoneum coexist, and access becomes restricted after docking.

The Coupled Load: Pressure From Below, Fluid Shift Toward the Head

CO2 insufflation raises intra-abdominal pressure and pushes the diaphragm towards the head. Functional residual capacity and respiratory-system compliance fall, airway pressures rise, and dependent lung regions become more prone to collapse. At the same time, compression of abdominal vessels, neurohumoral responses, and absorbed CO2 can increase systemic vascular resistance. Trendelenburg increases hydrostatic pressure in thoracic and cephalad veins and promotes facial, conjunctival, pharyngeal, and cerebral venous engorgement. [1,2,4]

The combined response is time-dependent and patient-dependent. A patient with normal ventricular function may tolerate a higher afterload and a large increase in filling pressure without a fall in measured cardiac output. A patient with pulmonary hypertension, right-ventricular dysfunction, restrictive lung disease, obesity, COPD, impaired intracranial compliance, glaucoma, or chronic kidney disease may have much less reserve. The same monitor value can therefore mean different things in different patients and at different phases of the case.

Cardiovascular Physiology: Preload Is Not CVP

In 16 ASA I-II patients studied at 45 degrees, CVP rose almost three-fold, pulmonary artery and wedge pressures roughly doubled, and MAP rose about 35%. At the same time, stroke volume and cardiac output were unchanged. [2] In another Doppler study, Trendelenburg increased stroke volume, while adding pneumoperitoneum increased MAP and systemic vascular resistance and reduced aortic diameter without a significant change in cardiac output. [4] These findings are not contradictory. They show how a large pressure rise can coexist with stable flow in selected patients.

The practical error is to treat a high CVP as proof of intravascular volume adequacy or as a reason to withhold all fluid, and the opposite error is to treat low urine output or hypotension as proof that more crystalloid is required. Intrathoracic pressure transmission, head-down hydrostatic pressure, ventricular compliance, afterload, venous return, anesthetic depth, blood loss, and vasomotor tone all contribute. When instability occurs, ask whether the dominant problem is pressure, flow, rhythm, volume loss, ventricular interaction, or a mechanical event such as excessive insufflation pressure or impaired venous return.

A useful response sequence is to verify the surgical phase and insufflation pressure, inspect the arterial waveform and heart rate, check for bleeding or circuit problems, reassess ventilation and intrathoracic pressure, and use focused cardiac ultrasound or another flow-sensitive assessment when the diagnosis remains uncertain. Treating a number without identifying its mechanism can worsen venous congestion, pulmonary edema, or right-ventricular loading.

Respiratory Mechanics: The Airway Pressure Is Not All Alveolar Pressure

Pneumoperitoneum and Trendelenburg increase the elastic load imposed by the abdomen and chest wall. Peak pressure may rise because of resistance, reduced compliance, or both. Plateau pressure better reflects the static pressure required to distend the total respiratory system, but even plateau and driving pressure include the chest-wall component. A rise during insufflation therefore does not automatically mean that the same increase has occurred across the lung itself. Interpret the response alongside delivered tidal volume, compliance, oxygenation, capnography, hemodynamics, and the pre-insufflation baseline. [1,2,7]

Use a lung-protective tidal volume based on predicted body weight, then individualize PEEP after positioning and insufflation. Recruitment and PEEP can reopen dependent lung and improve distribution, but both can increase intrathoracic pressure and affect venous return. In a randomized study, recruitment followed by PEEP 15 cm H2O produced more homogeneous ventilation, better compliance, lower driving pressure, and better oxygenation than PEEP 5 cm H2O, but postoperative lung function did not improve. [5] A 2026 randomized trial used decremental titration to minimize driving pressure; the individualized group received a median PEEP of 8 cm H2O during Trendelenburg, had lower driving pressure and lung-ultrasound de-aeration scores, and had higher PaO2, but postoperative pulmonary complications and length of stay were unchanged. [6]

These trials support physiologic titration, not a universal high-PEEP prescription. Recruitment should be avoided or modified when hemodynamic tolerance is poor, and PEEP should be reconsidered after major changes in tilt, insufflation pressure, or surgical retraction. Ventilator mode is secondary to the physiology delivered. Randomized mode comparisons have found pressure differences without a consistent oxygenation advantage, so lower peak or mean pressure by itself should not be mistaken for proven lung protection. [8]

Before emergence, reassess after desufflation and return to neutral. Recent observational data show that some adverse respiratory mechanics and oxygenation indices can remain abnormal immediately after the combined exposure ends. [7] Confirm a normal-looking ventilator after undocking against the patient’s baseline, gas exchange, and clinical condition rather than assuming it.

CO2 Physiology: EtCO2 Can Understate PaCO2

CO2 is continuously absorbed from the peritoneum, so minute ventilation usually must increase. The harder problem is that the arterial-to-end-tidal gradient can widen as dead-space and ventilation-perfusion relationships change. In 92 patients, PaCO2 and the PaCO2-EtCO2 gradient rose progressively during pneumoperitoneum and steep Trendelenburg, with larger increases in patients older than 65 years, even though EtCO2 did not change significantly. [9]

An EtCO2 target therefore does not guarantee arterial CO2. Consider an arterial line or arterial blood gas when age, obesity, COPD, pulmonary vascular disease, long case duration, high insufflation pressure, unexplained acidosis, cerebral vulnerability, or a changing clinical picture makes the gradient consequential. Ventilation should be adjusted to an arterial CO2 goal appropriate to the patient, while avoiding unnecessary airway pressure or intrinsic PEEP from excessive respiratory rate.

Cerebral Physiology: Oxygenation and Venous Drainage Are Different Questions

Head-down positioning raises cerebral venous pressure, while hypercapnia can increase cerebral blood flow. Selected physiologic studies found that cerebral perfusion-related variables remained acceptable during prolonged robotic prostatectomy, and regional cerebral oxygen saturation often increased rather than decreased. [10,11] That is reassuring only within the limits of the populations and measurements studied.

A 2026 prospective study illustrates the hidden physiology. In 40 ASA I-III patients at 30 degrees, regional cerebral saturation and oxyhemoglobin increased during Trendelenburg. At the same time, deoxygenated hemoglobin increased later in the case and optic nerve sheath diameter enlarged progressively. The authors interpreted the coupled pattern as potentially consistent with cerebral venous congestion. [12] These are surrogate observations, not a validated treatment threshold, but they show why a normal or high NIRS number cannot exclude impaired venous drainage.

Keep the head and neck neutral, avoid tight straps or circuit forces that obstruct jugular drainage, control arterial CO2 deliberately, and maintain a patient-appropriate cerebral perfusion pressure. Consider cerebral oximetry or optic nerve sheath ultrasound in selected prolonged or high-risk cases. Still, no evidence supports routine use or shows that intervention based on these signals improves outcomes.

Ocular Physiology: IOP Rises With Time, but Outcome Evidence Is Limited

Intraocular pressure rises during steep Trendelenburg and tends to increase with duration. [13] Most patients do not develop a visual complication, but known glaucoma, optic neuropathy, prior retinal or optic-nerve disease, severe anemia, prolonged positioning, marked facial edema, and direct orbital pressure should heighten concern. Protect the eyes before docking, eliminate external pressure, and preserve access for reassessment whenever feasible.

Two small randomized studies suggest possible ways to reduce the IOP burden. Propofol-based anesthesia produced a smaller IOP increase than sevoflurane-based anesthesia, and a modified Z Trendelenburg strategy reduced IOP by a mean of about 4.6 mmHg compared with standard positioning. [14,15] Neither study proved prevention of visual injury. These are options for multidisciplinary consideration in selected ocular-risk patients, not universal mandates and not substitutes for avoiding direct pressure, excessive tilt, or unnecessary duration.

Renal Physiology: Oliguria Is Not a Simple Fluid Gauge

Pneumoperitoneum can reduce renal blood flow through direct parenchymal and vascular compression, renal venous congestion, and neurohormonal responses. A contemporary review concludes that intra-abdominal pressure above about 10 mmHg can produce transient oliguria, although the human evidence for specific preventive strategies remains limited. [16]

An isolated fall in urine output during a stable, insufflated, head-down case should not automatically trigger a fluid bolus. Reassess MAP and flow, blood loss, baseline renal risk, bladder-catheter patency, insufflation pressure, duration, acid-base status, and the rest of the hemodynamic picture. Persistent oliguria, hypotension, bleeding, obstruction, or postoperative creatinine change still requires investigation. The point is not to ignore urine output; it is to avoid treating a compression-and-congestion signal as if it were always pure hypovolemia.

Airway and Soft Tissue: Edema Becomes an Extubation Problem

Head-down hydrostatic pressure and fluid administration promote facial, conjunctival, lingual, and pharyngeal edema. In a study that included patients with and without COPD, postoperative upper-airway resistance increased after robotic prostatectomy, pulmonary-function changes lasted longer in COPD, and chemosis was associated with airway edema. [17] These findings make the face and conjunctiva clinically relevant airway monitors.

After major positioning or insufflation changes, reconfirm endotracheal tube depth, bilateral ventilation, circuit security, and airway pressure. Before extubation, return the patient to neutral, desufflate, allow time for redistribution, inspect facial and tongue swelling, reassess pulmonary mechanics and gas exchange, and verify complete quantitative neuromuscular recovery. Current ASA guidance supports quantitative monitoring at the adductor pollicis and a train-of-four ratio of at least 0.9 before extubation. [19] A cuff-leak assessment can help when edema is suspected, but it does not guarantee safe extubation. Delay extubation when airway patency, ventilation, oxygenation, hemodynamics, or access to rescue is uncertain.

A Phase-Based Anesthetic Approach

1. Preoperative Phenotype and Team Plan

Clarify the exact procedure, planned head-down angle, expected insufflation pressure, likely duration, port and robot configuration, degree of post-docking access, and emergency-undocking process. Identify the physiologic domain with the least reserve: ventricular function and pulmonary vascular load; obesity, restriction, COPD, or difficult ventilation; cerebrovascular or intracranial disease; glaucoma or optic neuropathy; chronic kidney disease; and difficult airway or limited neck mobility.

Standard ASA monitoring is the minimum floor, not the ceiling. [18] Consider continuous arterial pressure and blood gas access when disease burden, expected duration, CO2 uncertainty, or hemodynamic volatility makes intermittent noninvasive data inadequate. Cerebral oximetry is optional and most useful when you have a baseline and a plan for interpreting trends.

2. Before Docking

Secure the tracheal tube, breathing circuit, intravenous lines, arterial line when used, and monitoring cables so tilt and robotic movement cannot dislodge them. Protect both eyes without external pressure. Pad elbows, hands, fibular heads, and other pressure points; prevent sliding with broad surface support rather than focal shoulder loading; and keep the head and neck neutral. Positioning and access-related complications can occur remote from the operative field, so the final team check should include a rapid-undocking plan and a clear method to reach the airway. [20]

Record a useful baseline before insufflation: airway pressure, plateau pressure when obtainable, PEEP, compliance, delivered tidal volume, EtCO2, hemodynamics, and an arterial blood gas when indicated. A brief tolerance assessment during initial tilt, before final docking when feasible, can reveal severe hemodynamic or ventilation limitation while access is still easy.

3. After Insufflation and Final Positioning

Treat this as a new physiologic state, not a continuation of baseline. Recheck tube depth and breath sounds, calculate driving pressure, assess compliance and oxygenation, review the capnogram, and compare pressure with flow. Titrate PEEP and recruitment to the patient’s mechanics and hemodynamic tolerance. Increase minute ventilation as needed, then confirm PaCO2 when the gradient may matter. Ask the surgeon to use the least tilt and insufflation pressure that preserves an adequate field, recognizing that the feasible minimum is procedure-specific.

4. During the Prolonged Maintenance Phase

Trend the exposure itself: angle, insufflation pressure, and time. Reassess after every meaningful change. Avoid large empiric fluid loads based on CVP or urine output alone, but also avoid unrecognized hypovolemia and blood loss. Use vasoactive therapy, fluid, ventilation changes, reduction in insufflation pressure, or reduction in tilt according to the identified mechanism. When surgical pauses permit, a temporary decrease in tilt or pressure may reduce cumulative cephalad congestion, but coordinate feasibility with the surgeon.

5. Undocking, Emergence, and Recovery

After desufflation and neutral positioning, allow physiology to settle before deciding on extubation. Reassess hemodynamics, lung mechanics, gas exchange, airway edema, neuromuscular recovery, temperature, and mental status. Patients with persistent hypercapnia, edema, hypoxemia, hemodynamic instability, prolonged exposure, or low cardiopulmonary reserve may need extended post-anesthesia monitoring or planned postoperative ventilatory support.

Table 1. What a Reassuring Monitor Value May Conceal

Observation	Possible hidden physiology	Practical response
CVP or filling pressure rises	Hydrostatic and intrathoracic pressure transmission, venous congestion, or reduced ventricular compliance; not necessarily effective preload.	Judge pressure with MAP, flow, bleeding, ventricular function, ventilation, and surgical phase. Do not give or withhold fluid from CVP alone. [2,4]
EtCO2 is stable	PaCO2 may still rise as the arterial-to-end-tidal gradient widens, especially with age and duration.	Confirm arterial CO2 when the gradient is likely to change management. [9]
SpO2 remains normal	Dependent atelectasis, reduced FRC, impaired compliance, or high inspired oxygen may mask loss of aeration.	Use mechanics, plateau and driving pressure, oxygen requirement, and recruitment response, not SpO2 alone. [5-7]
Peak or plateau pressure rises	Increased chest-wall and abdominal load as well as possible lung stress.	Recheck tube and circuit, compare peak with plateau, calculate driving pressure, and assess compliance and hemodynamics. [1,2]
Cerebral rSO2 rises	Increased cerebral blood volume or oxygenated hemoglobin can coexist with deoxygenated hemoglobin accumulation and venous congestion.	Interpret the trend with PaCO2, MAP, head and neck position, and clinical risk; do not use rSO2 as an ICP monitor. [11,12]
Urine output falls	Renal compression, venous congestion, and neurohormonal effects may be present without simple volume depletion.	Check perfusion, bleeding, catheter patency, renal risk, insufflation pressure, and trend before reflex fluid loading. [16]
Facial or conjunctival edema appears	Cephalad soft-tissue and upper-airway edema may be developing.	Reassess airway risk, fluid balance, duration, and extubation readiness after neutral positioning. [17]

Table 2. Phase-Based Management Checklist

Phase	Priorities	Escalation triggers
Planning	Define angle, insufflation pressure, duration, docking constraints, undocking plan, and the patient’s least-reserve organ system.	Severe ventricular or pulmonary vascular disease, difficult ventilation or airway, intracranial or ocular disease, renal vulnerability, or expected prolonged exposure.
Before docking	Secure airway and lines; protect eyes and pressure points; prevent sliding without focal shoulder loading; document baseline mechanics and gas exchange.	Uncertain tube position, inadequate access, unstable hemodynamics, poor compliance, or inability to execute emergency undocking. [20]
After tilt and insufflation	Reconfirm tube, recalculate compliance and driving pressure, titrate PEEP, adjust ventilation, and review pressure versus flow.	Abrupt hypotension, high airway pressure, worsening oxygenation, severe hypercapnia, arrhythmia, or loss of signal after docking.
Prolonged maintenance	Trend angle, pressure, time, urine output, edema, PaCO2 when indicated, and cumulative fluid; coordinate the lowest feasible tilt and pressure.	Rising vasopressor need, widening CO2 concern, persistent oliguria, progressive edema, worsening mechanics, or neurologic or ocular concern.
Undocking and emergence	Desufflate, return neutral, reassess mechanics and gas exchange, inspect airway edema, and confirm quantitative train-of-four ratio at least 0.9.	Persistent hypercapnia, hypoxemia, edema, hemodynamic instability, inadequate neuromuscular recovery, or uncertain rescue access. [17,19]

What the Evidence Can and Cannot Establish

The evidence base is clinically useful but narrow. Much of it comes from robotic prostatectomy in men with ASA physical status I-II or otherwise selected risk profiles. Many studies measure pressures, oxygenation, compliance, NIRS, optic nerve sheath diameter, intraocular pressure, urine output, or lung-ultrasound aeration rather than patient-centered complications. The recent ventilation and cerebral-monitoring studies improve mechanistic understanding. Still, they do not validate a single safe angle, maximum duration, insufflation pressure, PEEP, NIRS threshold, IOP threshold, fluid strategy, or extubation test. [5,6,12]

The most defensible conclusion is therefore not that steep Trendelenburg is unsafe, or that it is harmless. It is that the exposure changes the meaning of routine monitors and narrows physiologic reserve. Safe care depends on recognizing those changes early, matching monitoring to patient vulnerability, and coordinating pressure, position, ventilation, fluid, and time with the surgical team.

 

References

1. Kalmar AF, Foubert L, Hendrickx JFA, Mottrie A, Absalom A, Mortier EP, Struys MMRF. Influence of steep Trendelenburg position and CO2 pneumoperitoneum on cardiovascular, cerebrovascular, and respiratory homeostasis during robotic prostatectomy. Br J Anaesth. 2010;104(4):433-439. https://doi.org/10.1093/bja/aeq018 PMID: 20167583.
2. Lestar M, Gunnarsson L, Lagerstrand L, Wiklund P, Odeberg-Wernerman S. Hemodynamic perturbations during robot-assisted laparoscopic radical prostatectomy in 45 degrees Trendelenburg position. Anesth Analg. 2011;113(5):1069-1075. https://doi.org/10.1213/ANE.0b013e3182075d1f PMID: 21233502.
3. Katayama S, Mori K, Pradere B, et al. Influence of steep Trendelenburg position on postoperative complications: a systematic review and meta-analysis. J Robot Surg. 2022;16:1233-1247. https://doi.org/10.1007/s11701-021-01361-x PMID: 34972981.
4. Falabella A, Moore-Jeffries E, Sullivan MJ, Nelson R, Lew M. Cardiac function during steep Trendelenburg position and CO2 pneumoperitoneum for robotic-assisted prostatectomy: a trans-oesophageal Doppler probe study. Int J Med Robot. 2007;3(4):312-315. https://doi.org/10.1002/rcs.165 PMID: 18200624.
5. Shono A, Katayama N, Fujihara T, Bohm SH, Waldmann AD, Ugata K, et al. Positive End-expiratory Pressure and Distribution of Ventilation in Pneumoperitoneum Combined with Steep Trendelenburg Position. Anesthesiology. 2020;132(3):476-490. https://doi.org/10.1097/ALN.0000000000003062 PMID: 31770148.
6. Cho S, Kim BR, Park SY, Yoon SH, Bahk JH, Yoon S. Driving pressure guided ventilation in robot-assisted laparoscopic surgery with steep Trendelenburg position: a randomized controlled study. Anesth Pain Med (Seoul). 2026;21(2):223-234. https://doi.org/10.17085/apm.25337 PMCID: PMC13175901. Accessed August 12, 2026.
7. Tontu F, Akca H, Berktas CK, Asar S, Ozcan FG. The impact of pneumoperitoneum and steep Trendelenburg positioning on novel oxygenation and saturation indices in robot-assisted laparoscopic prostatectomies: a prospective observational study. Saudi J Anaesth. 2025;19(3):271-276. https://doi.org/10.4103/sja.sja_600_24 PMID: 40642630. PMCID: PMC12240497.
8. Kim MS, Soh S, Kim SY, Song MS, Park JH. Comparisons of Pressure-controlled Ventilation with Volume Guarantee and Volume-controlled 1:1 Equal Ratio Ventilation on Oxygenation and Respiratory Mechanics during Robot-assisted Laparoscopic Radical Prostatectomy: a Randomized-controlled Trial. Int J Med Sci. 2018;15(13):1522-1529. https://doi.org/10.7150/ijms.28442 PMID: 30443174. PMCID: PMC6216054.
9. Choi DK, Lee IG, Hwang JH. Arterial to end-tidal carbon dioxide pressure gradient increases with age in the steep Trendelenburg position with pneumoperitoneum. Korean J Anesthesiol. 2012;63(3):209-215. https://doi.org/10.4097/kjae.2012.63.3.209 PMCID: PMC3460148.
10. Kalmar AF, Dewaele F, Foubert L, Hendrickx JF, Heeremans EH, Struys MMRF, Absalom A. Cerebral haemodynamic physiology during steep Trendelenburg position and CO2 pneumoperitoneum. Br J Anaesth. 2012;108(3):478-484. https://doi.org/10.1093/bja/aer448 PMID: 22258202.
11. Park EY, Koo BN, Min KT, Nam SH. The effect of pneumoperitoneum in the steep Trendelenburg position on cerebral oxygenation. Acta Anaesthesiol Scand. 2009;53(7):895-899. https://doi.org/10.1111/j.1399-6576.2009.01991.x PMID: 19426238.
12. Campiglia L, Matta B, Santoro Y, Becherucci F, Cappellini I, Pavoni V. NIRS monitoring during steep Trendelenburg in robotic prostatectomy. J Clin Monit Comput. 2026;40:875-886. https://doi.org/10.1007/s10877-026-01443-x PMID: 42189385. PMCID: PMC13391443. Accessed August 12, 2026.
13. Awad H, Santilli S, Ohr M, Roth A, Yan W, Fernandez S, Roth S, Patel V. The effects of steep Trendelenburg positioning on intraocular pressure during robotic radical prostatectomy. Anesth Analg. 2009;109(2):473-478.
14. https://doi.org/10.1213/ane.0b013e3181a9098f PMID: 19608821.
15. Yoo YC, Shin S, Choi EK, Kim CY, Choi YD, Bai SJ. Increase in intraocular pressure is less with propofol than with sevoflurane during laparoscopic surgery in the steep Trendelenburg position. Can J Anaesth. 2014;61(4):322-329. https://doi.org/10.1007/s12630-014-0112-2 PMID: 24500661.
16. Raz O, Boesel TW, Arianayagam M, Lau H, Vass J, Huynh CC, Graham SL, Varol C. The effect of the modified Z Trendelenburg position on intraocular pressure during robotic assisted laparoscopic radical prostatectomy: a randomized, controlled study. J Urol. 2015;193(4):1213-1219. https://doi.org/10.1016/j.juro.2014.10.094 PMID: 25444990.
17. Villa G, Fiorentino M, Cappellini E, Lassola S, De Rosa S. Renal implications of pneumoperitoneum in laparoscopic surgery: mechanisms, risk factors, and preventive strategies. Korean J Anesthesiol. 2024;77(6):575-586. https://doi.org/10.4097/kja.24011 PMID: 38664893. PMCID: PMC11637592.
18. Kilic OF, Borgers A, Kohne W, Musch M, Kropfl D, Groeben H. Effects of steep Trendelenburg position for robotic prostatectomies on intra- and extrathoracic airways in patients with or without chronic obstructive pulmonary disease. Br J Anaesth. 2015;114(1):70-76. https://doi.org/10.1093/bja/aeu322 PMID: 25236948.
19. American Society of Anesthesiologists. Standards for Basic Anesthetic Monitoring. Last amended October 15, 2025; original approval October 21, 1986. https://www.asahq.org/standards-and-practice-parameters/standards-for-basic-anesthetic-monitoring Accessed August 12, 2026.
20. Thilen SR, Weigel WA, Todd MM, Dutton RP, Lien CA, Grant SA, et al. 2023 American Society of Anesthesiologists Practice Guidelines for Monitoring and Antagonism of Neuromuscular Blockade. Anesthesiology. 2023;138(1):13-41. https://doi.org/10.1097/ALN.0000000000004379 PMID: 36520073.
21. Maerz DA, Beck LN, Sim AJ, Gainsburg DM. Complications of robotic-assisted laparoscopic surgery distant from the surgical site. Br J Anaesth. 2017;118(4):492-503. https://doi.org/10.1093/bja/aex003 PMID: 28403397.