Abstract
Background
Although functional endoscopic sinus surgery (FESS) constitutes a standard treatment for the management of chronic rhinosinusitis, intraoperative bleeding poses a considerable challenge by impairing visibility and increasing complication risks. Controlled hypotension is a widely employed technique to mitigate bleeding; however, excessive blood pressure reduction may compromise systemic perfusion and predispose to organ ischemia.
Objectives
Due to the scarcity of literature evaluating the safety of controlled hypotension in FESS, we aimed to systematically review current evidence on the risks and potential complications of this technique, with an emphasis on systemic adverse events (hemodynamic instability, neurological impairment, and renal dysfunction).
Methods
The PubMed, Embase, and Cochrane databases were searched for English-language original articles published until October 1, 2025. Studies were considered eligible if they reported mean arterial pressure (MAP) values achieved and evaluated systemic complications associated with controlled hypotension during FESS.
Results
A total of 32 articles were found eligible and included in the further analysis. Most protocols aimed for a MAP of 50–70 mmHg, primarily using dexmedetomidine, propofol, and remifentanil. Only 8 of the 32 studies utilized advanced intraoperative monitoring (e.g., near-infrared spectroscopy [NIRS], transcranial Doppler [TCD], and non-invasive cardiac output monitoring [NICOM]). The most frequent minor complication was postoperative nausea and vomiting (in 2–62% of cases). Significant hemodynamic disturbances included intraoperative bradycardia and severe hypotension (MAP < 50 mmHg), requiring pharmacological intervention. While no permanent neurological deficits were reported, intraoperative cerebral desaturation was observed in 2 studies. The follow-up observation rarely extended beyond the post-anesthesia care unit and did not include a structured assessment of cerebral and renal function.
Conclusions
Subclinical complications of controlled hypotension during FESS may be overlooked without advanced intraoperative monitoring, postoperative biomarker surveillance, and a long-term follow-up period. The application of a uniform MAP target of 50–70 mmHg may be insufficient in high-risk patients. The development of personalized hemodynamic management strategies and enhanced perfusion-monitoring protocols is required to reduce the risk of occult organ ischemia and to define safe limits for controlled hypotension in FESS.
Supplementary Information
The online version contains supplementary material available at 10.1186/s12871-026-04021-5.
Keywords: Intranasal endoscopic surgery, Organ perfusion, Myocardial ischemia, Brain oxygenation, Cerebral hypoperfusion, Acute kidney injury, Intraoperative monitoring
Introduction
Functional endoscopic sinus surgery (FESS) is a widely used technique for the management of chronic rhinosinusitis, nasal polyposis, and other disorders of the nasal cavity and paranasal sinuses. The procedure involves the insertion of an endoscope and specialized micro-instruments into the nasal cavity to restore patency of the natural sinus ostia and remove pathological tissue [1]. FESS is considered minimally invasive, with major complication rates ranging from 0.3% to 3% [2]. Reported adverse events include injury to orbital structures, excessive lacrimation, cerebrospinal fluid leakage, and intracranial complications. Life-threatening events such as massive hemorrhage requiring transfusion or intraoperative mortality remain exceedingly rare.
Among all complications, intraoperative bleeding is the most frequent, accounting for approximately 23–40% of cases. Even relatively small volumes of blood might significantly impair endoscopic visibility, increasing the risk of iatrogenic injury or the need to discontinue the procedure [2, 3]. Controlled hypotension is therefore a widely applied anesthetic strategy in FESS, intended to reduce bleeding and improve surgical field clarity. While physical positioning (reverse Trendelenburg position or isolated head elevation) may assist in lowering blood pressure, pharmacological agents that reduce systolic blood pressure (SBP)/mean arterial pressure (MAP) – β-blockers, α2-agonists, nitrates, intravenous and inhalational anesthetics, and clonidine – remain the primary method [4, 5].
Although controlled hypotension improves visibility and shortens operative time, excessive blood pressure reduction (SBP to 80–90 mmHg or MAP to 50–70 mmHg) may compromise systemic perfusion and predispose to cerebral, renal, myocardial, splanchnic, or hepatic ischemia (Fig. 1) [3, 4]. Reported complications remain rare (approximately 0,6%), and perioperative mortality is negligible in several studies [6, 7]. Nevertheless, evidence evaluating the microcirculatory and systemic safety of controlled hypotension in FESS is limited, as most research focuses primarily on bleeding reduction and surgical field grading.
Fig. 1.

Hemodynamic impact of controlled hypotension. MAP – Mean Arterial Pressure; SBP – Systolic Blood Pressure; DBP - Diastolic Blood Pressure; AKI – Acute Kidney Injury
The aim of this systematic review is to synthesize current evidence on the risks and potential complications associated with controlled hypotension during FESS, with an emphasis on the systemic adverse events – hemodynamic instability, neurological impairment, and renal dysfunction.
Methods
Study guidance
The review was conducted in accordance with the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines [8].
Search strategy and criteria
The PubMed, Embase, and Cochrane databases were searched independently by three authors (R.K., W.SG., L.Z.) for English-language papers published from 1st January 2000 to 1st October 2025. The search strategy combined the following terms (“complications” OR “adverse effects” OR “silent myocardial infarction” OR “myocardial injury” OR “cardiac ischemia” OR “troponin” OR “regional cerebral oxygen saturation” OR “stroke” OR “cerebral ischemia” OR “cerebral oximetry” OR “ischemic injury” OR “cerebral perfusion” OR “acute kidney failure” OR “acute renal insufficiency” OR “acute renal injury” OR “creatinine”) AND (“controlled hypotension” OR “deliberate hypotension” OR “hypotensive anesthesia” OR “mean arterial pressure”) AND (“sinus surgery” OR “endoscopic sinus” OR “FESS” OR “ESS”). Generic isolated terms such as “hypotension” or “intraoperative hypotension” were not used as stand-alone intervention terms because the review question focused on intentional controlled hypotension rather than unplanned or incidental hypotensive episodes. Records retrieved under MAP and controlled/deliberate hypotension terminology were therefore screened specifically for intentional hypotensive protocols used during FESS.
After the removal of duplicates, two authors (R.K. and L.Z) independently screened the titles and abstracts of the remaining records to identify studies meeting the following inclusion criteria: (1) study design: clinical studies, clinical trials, and randomized controlled trials (RCTs); (2) population: patients aged 16 years and older; (3) articles published in English; (4) intervention: controlled hypotension during FESS induced by intravenous drug administration, and (5) outcome: reporting complications or adverse events (specifically, cerebral/renal ischemia and cardiovascular instability; with the exclusion of surgical field visibility/bleeding assessments).
Studies were excluded at this stage if they: (1) constituted reviews, meta-analyzes, case reports or case series (n < 5 patients); (2) included patients aged 15 years and younger; (3) were non-English articles; (4) were published before 1st January 2000; (5) described surgical procedures other than FESS (e.g., septoplasty, rhinoplasty, or non-endoscopic sinus surgery – from external approach); (6) did not describe the application of controlled hypotension or used exclusively inhalational or oral hypotensive protocols, and (7) did not report complications or adverse events associated with controlled hypotension.
Additionally, the reference lists in all preselected articles were screened for further relevant studies.
Eligibility criteria
Full-text articles were retrieved and assessed for eligibility by two authors (R.K. and W.GS.). The study was considered eligible if it: (1) utilized an intravenous controlled hypotension protocol during FESS; (2) specified target MAP levels; (3) reported the incidence rates of perioperative complications, and (4) described the intraoperative monitoring techniques and patient follow-up.
Any disagreements during the screening and selection phases were first resolved through discussion until a consensus was reached. If consensus could not be achieved, the final decision was adjudicated by a third reviewer (M.A.).
Data extraction
From the included studies, the following data were extracted: (1) hypotensive agent: a specific intravenous drug used for controlled hypotension; (2) hemodynamics: achieved mean arterial pressure (MAP) values and, where reported, heart rate targets or heart-rate-modifying agents; (3) complications: incidence rates of adverse; (4) intraoperative monitoring modalities (basic and advanced); and (5) duration and details of patient follow-up; and (6) when available, surgical duration and surgical field visibility/bleeding scores. Surgical field quality and operative duration were noted descriptively but were not incorporated into the primary safety synthesis, because the main objective of this review was to evaluate complications and monitoring rather than comparative efficacy.
Assessment of study quality and risk of bias in included studies
Three authors (M.A., R.K., and L.Z) independently assessed the risk of bias for each included article using the revised Cochrane Risk of Bias Tool for Randomized Trials (RoB 2) for RCTs, and the Risk of Bias in Non-randomized Studies of Interventions tool (ROBINS-I) for non-randomized studies. Any discrepancies were resolved through discussion until consensus was reached.
Results
Study selection
The initial database search identified 1228 records, including 286 from PubMed, 515 from Embase, and 427 from Cochrane. After removing 866 duplicates, 362 records were screened. One hundred ninety-two reviews, systematic reviews, or meta-analyses were excluded, and 99 articles on irrelevant topics were rejected, as well as 9 case reports, 6 non-English language, 5 articles with patients aged 15 and younger, and 2 case series (n < 5 patients). After the exclusion of 313 articles that did not meet the predefined criteria, the full text of 49 reports was sought for retrieval, of which 5 could not be obtained.
A total of 44 full-text articles were assessed for eligibility. Following detailed evaluation, 12 were excluded because 1 was published before 1st January 2000, 2 were non-English-language articles, and the remaining 9 were irrelevant to the research question. Additionally, 12 articles were identified through a manual backward citation chaining. Of these, 1 could not be retrieved, and the remaining 11 were excluded because 2 were duplicates, 2 were published before 1st January 2000, and 7 were reviews or systematic reviews.
A total of 32 articles were found eligible and included in the further analysis. Figure 2 shows the entire literature selection process.
Fig. 2.

PRISMA flowchart of the medical database search strategy
Study characteristics
The analysis of 32 included studies (15 evaluating single interventions [9–23] and 17 comparative studies [24–40]) rendered 2422 patients. Among the studies included in the systematic review, 4 were cohort studies [9–12] (evaluating a total of 328 patients), and 28 constituted randomized controlled trials [13–40] (enrolling a total of 2094 individuals). Complete study characteristics are presented in Table 1.
Table 1.
Characteristics of the included studies
| Author, year | Study design | Number of patients | Mean age (SD) (years) | Used drugs/ Compared drugs | Achieved MAP range (mmHg) |
|---|---|---|---|---|---|
| Cincikas et al.; 2003 [9] | Cohort study | 52 | 44.1 (11.2) | Nitroglycerin | 50–60 |
| Naik et al.; 2011 [10] | Cohort study | 213 | 16–67* | Propofol, Remifantanyl | 60–70 |
| Ha et al.; 2014 [11] | Cohort study | 32 | 48 | Propofol | 44–72 |
| Heller et al.; 2015 [12] | Cohort study | 31 | 54.3 (16.1) | Propofol, Remifentanyl, Nitrous Oxide | 57–83 |
| Goksu et al.; 2008 [13] | RCT | 62 | 38.46 (10.26) | Dexmedetomidine | 85–98 |
| Sartcaoglu et al.; 2005 [14] | RCT | 46 | 35 (10.3) | Nitroglycerine | 60–70 |
| Zhang et al.; 2021 [15] | RCT | 39 | 50.55 (14.34) | Nicardipine, Esmolol | 67–71 |
| Tirelli et al.; 2004 [16] | RCT | 64 | 48.07 (9.40) | Propofol, Remifentanyl | 60–70 |
| Li et al.; 2023 [22] | RCT | 110 | 44.5 (11.8) | Propofol, Remifentanyl | 65–75 |
| Jiwanmall et al.; 2017 [17] | RCT | 60 | 18–65* | Clonidine | 55–65 |
| Hassan et al.; 2024 [23] | RCT | 70 | 42.26 (11.44) | Dexmedetomidine | 55–65 |
| Gollapudy et al.; 2020 [18] | RCT | 70 | 41 (13) | Propofol vs. Desflurane | 60–70 |
| Neethirajan et al.; 2020 [19] | RCT | 92 | 35 (13.5) | Dexmedetomidine | - |
| Rehab et al.; 2023 [20] | RCT | 52 | 28.77 (6.95) | Aminophylline | 60–65 |
| Ankichetty et al.; 2011 [21] | RCT | 40 | 31.55 (11.54) | Propofol vs. Isoflurane | 60–70 |
| Skalias et al.; 2023 [24] | RCT | 72 | 50.4 (9.5) (B) | Bisoprolol vs. Nifedipine | 69–117 |
| 49.1 (12.9) (Nif) | |||||
| Alkan et al.; 2021 [25] | RCT | 60 | 36.5 (R) | Esmolol vs. Remifentanil vs. Nitroglycerin | 60–65 |
| 33.5 (E) | |||||
| 47.5 (Ntg) | |||||
| Bharathwaj et al.; 2019 [26] | RCT | 80 | 35.05 (10.91) (D) | Labetalol vs. Dexmedetomidine | 60–70 |
| 35.90 (13.41) (P) | |||||
| Bajwa et al.; 2016 [27] | RCT | 150 | 31.6 (5.2) (D) | Nitroglycerine vs. Esmolol vs. Dexmedetomidine | 60–70 |
| 36.4 (6.1) (Ntg) | |||||
| 34.3 (5.6) (E) | |||||
| Yun et al.; 2015 [28] | RCT | 28 | 30.5 (Ntp) | Nitroprusside vs. Remifentanil | 60–70 (30% decline from baseline) |
| 30.5 (R) | |||||
| Sajedi et al.; 2016 [29] | RCT | 62 | 36.36 (12.35) (R) | Remifentanil vs. Labetalol | 50–60 (20–30% decline from baseline) |
| 34.34 (10.91) (L) | |||||
| Sujatha et al.; 2023 [30] | RCT | 100 | 36.18 (2.54) (D) | Dexmedetomidine vs. Propofol | 60–70 |
| 38.30 (7.42) (P) | |||||
| Praveen et al.; 2024 [31] | RCT | 80 | 45.36 (10.01) (D) | Dexmedetomidine vs. Clonidine | 55–65 |
| 44.45 (9.91) (C) | |||||
| Bafna et al.; 2021 [32] | RCT | 70 | 27.23 (7.75) (D) | Dexmedetomidine vs. Clonidine | 65–70 |
| 27.49 (8.68) (C) | |||||
| Sharma et al.; 2025 [33] | RCT | 60 | 37.43 (5.21) (E) | Esmolol vs. Dexmedetomidine | 60–70 |
| 37.3 (7.32) (D) | |||||
| Escamilla et al.; 2019 [34] | RCT | 94 | 47.60 (11.0) (C) | Clonidine vs. Dexmedetomidine | 55–65 |
| 48.02 (10.51) (D) | |||||
| Eghbal et al.; 2018 [35] | RCT | 100 | 31.7 (9) (L) | Labetalol vs. Dexmedetomidine | 65–75 |
| 5.06 (9.64) (D) | |||||
| Moshiri et al.; 2017 [36] | RCT | 100 | 35.16 (8.2) (D) | Propofol vs. Dexmedetomidine | 65–75 |
| 36.90 (8.2) (P) | |||||
| Huh et al.; 2020 [37] | RCT | 140 | 46 (17) (D) | Dexmedetomidine vs. Remifentanil | 65–75 |
| 42 (17) (R) | |||||
| Karabayirli et al.; 2016 [38] | RCT | 47 | 36 (R) | Dexmedetomidine vs. Remifentanil | 55–65 |
| 37 (D) | |||||
| Mugabo et al.; 2024 [39] | RCT | 80 | 33.90 (6.85) (C) | Dexmedetomidine vs. Clonidine | 55–65 |
| 35.15 (6.62) (D) | |||||
| Lee et al.; 2013 [40] | RCT | 66 | 39.8 (17.4) (R) | Dexmedetomidine vs. Remifentanil | 65–75 |
| 45.5 (12.1) (D) |
*, age range, no data for the mean age was provided in the study
RCT Randomized Controlled Trial, MAP Mean Arterial Pressure, TIVA Total Intravenous Anesthesia, B Bisoprolol, Nif Nifedipine, R Remifentanil, E Esmolol, Ntg Nitroglycerin, D Dexmedetomidine, Ntp Nitroprusside, L Labetalol, C Clonidine, P Propofol
Risk of bias analysis
Fourteen of the 28 RCTs [13–15, 17, 21, 24, 26–31, 34, 39], assessed using RoB 2, were judged to have “some concerns” regarding the risk of bias, primarily related to outcome measurement and the selection of the reported results. One trial [16] was rated as posing a high risk of bias arising from the randomization process. Detailed results of the RoB2 assessment are presented in Figs. 3 and 4.
Fig. 3.

Results of the bias risk assessment using RoB 2 for randomized studies. RoB 2, revised cochrane risk of bias tool for randomized trials
Fig. 4.

Proportion of bias risk assessment results using RoB 2 for randomized studies. RoB 2, revised cochrane risk of bias tool for randomized trials
Among the non-randomized studies evaluated with the ROBINS-I tool, two studies [9, 10] were found to pose a high risk of bias, primarily due to confounding and outcome measurement. The detailed results of ROBINS-I analysis are presented in Figs. 5 and 6.
Fig. 5.

Results of the bias risk assessment using ROBINS-I for non-randomized studies. ROBINS-I, cochrane risk of bias tool for non-randomized studies - of interventions
Fig. 6.

Proportion of bias risk assessment results using ROBINS-I for non-randomized studies. ROBINS-I, cochrane risk of bias tool for non-randomized studies - of interventions
Hemodynamic impact and target MAP
The analysis of 32 included studies demonstrated that most protocols successfully achieved the intended MAP of 50–70 mmHg, generally accepted as the threshold balancing favorable operating conditions with maintained perfusion. In two studies [28, 29], the target was defined as a 20–30% reduction in MAP relative to baseline, yet the achieved absolute values remained within the same range. Only one study [19] reported a lack of complete numerical data on the course of MAP during surgery (Table 1).
In the analyzed material, the most frequently studied pharmacological agents used to induce and maintain controlled hypotension were: dexmedetomidine (16/32 studies [13, 19, 23, 26, 27, 30–40]), propofol (9/32 [10–12, 16, 18, 21, 22, 30, 36]), and remifentanil (9/32 [12, 16, 22, 25, 28, 29, 37, 38, 40]). The efficacy of substances such as nicardipine [15], aminophylline [20], bisoprolol [24], nifedipine [24], and sodium nitroprusside [28] was evaluated less frequently (one study for each drug). In the case of inhalation anesthetics (desflurane, isoflurane, nitrous oxide), they were mainly applied in control groups [18, 21] or were used only during anesthesia induction and therefore were not subject to the primary analysis of hypotensive efficacy in this review (Table 1).
Notably, significant variability in extreme pressure values was observed. In one study [11], MAP decrease to 44 mmHg was recorded, which exceeded the lower safety limit (50 mmHg) adopted in most protocols. In contrast, several other studies [12, 13, 24] recorded consistently higher-than-intended MAP (exceeding 70–80 mmHg), indicating challenges in achieving hypotensive targets with certain drug protocols (Table 1).
Perfusion monitoring and follow-up period
In all 32 studies analyzed, basic intraoperative monitoring included: blood pressure measurement (including MAP), peripheral oxygen saturation (SpO2), capnography (EtCO2), and ECG recording. In one study [9], this scope was extended to include intraoperative diuresis monitoring and postoperative assessment of laboratory parameters (activated partial thromboplastin time [APTT], hemoglobin [Hgb], hematocrit [Ht], uric acid, electrolytes) (Table 2).
Table 2.
Summary of the intraoperative monitoring methods and patient observation period in the included studies
| Studies on a specific drug | Studies comparing specific drugs | ||||
|---|---|---|---|---|---|
| Author; year | Intraoperative monitoring | Follow-up observation | Author; year | Intraoperative monitoring | Follow-up observation |
| Cincikas et al.; 2003 [9] | Basic + diuresis, APTT, Hgb, Ht, urea, electrolytes | Intraoperatively and in the PACU | Skalias et al.; 2023 [40] | Basic | Intraoperatively and in the PACU |
| Naik et al.; 2011 [10] | Basic | Intraoperatively and in the PACU | Alkan et al.; 2021 [39] | Basic + BIS | Intraoperatively |
| Ha et al.; 2014 [11] | Basic + TCD via MCA | Intraoperatively | Bharathwaj et al.; 2019 [37] | Basic | Intraoperatively |
| Heller et al.; 2015 [12] | Basic + NIRS | Intraoperatively and in the PACU | Bajwa et al.; 2016 [36] | Basic | Intraoperatively and in the PACU |
| Goksu et al.; 2008 [13] | Basic | Intraoperatively and in the PACU(2 h) | Yun et al.; 2015 [22] | Basic + NICOM | Intraoperatively and in the PACU |
| Sartcaoglu et al.; 2005 [14] | Basic + cognitive tests: MMSE and VADST in 2 h and 24 h | Intraoperatively, in the PACU, and 24 h after surgery | Sajedi et al.; 2016 [23] | Basic | Intraoperatively and in the PACU(2 h) |
| Zhang et al.; 2021 [15] | Basic + NIRS (rSO2); MMSE; BIS | Intraoperatively and in the PACU; MMSE 24 h after surgery | Sujatha et al.; 2023 [35] | Basic | Intraoperatively and in the PACU |
| Tirelli et al.; 2004 [16] | Basic | Intraoperatively and in the PACU | Praveen et al.; 2024 [34] | Basic | Intraoperatively, in the PACU, and 24 h after surgery |
| Li et al.; 2023 [38] | Basic | Intraoperatively, in the PACU, and 7 days after surgery | Bafna et al.; 2021 [33] | Basic | Intraoperatively and in the PACU(0,5 h) |
| Jiwanmall et al.; 2017 [17] | Basic | Intraoperatively and in the PACU(0,5–1 h) | Sharma et al.; 2025 [32] | Basic | Intraoperatively |
| Hassan et al.; 2024 [24] | Basic + BIS | Intraoperatively and in the PACU | Escamilla et al.; 2019 [31] | Basic | Intraoperatively, in the PACU, and 7 days after surgery |
| Gollapudy et al.; 2020 [18] | Basic + FloTrac (CO, CI, SVR, BP) | Intraoperatively and in the PACU | Eghbal et al.; 2018 [30] | Basic | Intraoperatively |
| Neethirajan et al.; 2020 [19] | Basic | Intraoperatively and in the PACU | Moshiri et al.; 2017 [29] | Basic | Intraoperatively and in the PACU |
| Rehab et al.; 2023 [20] | Basic | Intraoperatively and in the PACU | Huh et al.; 2020 [28] | Basic + BIS | Intraoperatively and in the PACU |
| Ankichetty et al.; 2011 [21] | Basic | Intraoperatively, in the PACU, and 48 h after surgery (only PONV and pain) | Karabayirli et al.; 2016 [27] | Basic | Intraoperatively, in the PACU, and 24 h after surgery |
| Mugabo et al.; 2024 [26] | Basic | Intraoperatively and in the PACU | |||
| Lee et al.; 2013 [25] | Basic | Intraoperatively and in the PACU | |||
Basic – MAP, HR, ECG, SpO2 and EtCO2
MAP Mean Arterial Pressure, HR Hear Rate, ECG Electrocardiography, SpO2 Peripheral Oxygen Saturation, EtCO2 End-Tidal Carbon Dioxide – Capnography, BIS Bispectral Index, NICOM Non-Invasive Cardiac Output Monitoring, TCD Transcranial Doppler, NIRS Near-Infrared Spectroscopy, rSO2 Regional Cerebral Oxygenation, MMSE Mini–Mental State Examination, VADST Visual Aural Digit Span Test, PACU Post-Anesthesia Care Unit, APTT Activated Partial Thromboplastin Time, Hgb hemoglobin, Ht hematocrit, PONV Postoperative Nausea And Vomiting
Advanced intraoperative monitoring was applied in a total of eight studies [11, 12, 15, 18, 23, 25, 28, 37]. The bispectral index (BIS) (in three studies [15, 25, 37]) and near-infrared spectroscopy (NIRS) (in 2 studies [12, 15]) were used most frequently. In individual cases, the following were used: transcranial Doppler (TCD) assessment of blood flow [11], non-invasive cardiac output monitoring (NICOM) [28], and the FloTrac haemodynamic monitoring system [18]. In two studies [14, 15], the postoperative assessment was supplemented with cognitive function tests: Mini-Mental State Examination (MMSE) and/or Visual Aural Digit Span Test (VADST) (Table 2).
In all reports, patients were continuously monitored intraoperatively, and in most cases, observation also included assessment of clinical status in the post-anesthesia care unit (PACU). Information on further monitoring of patients was not included in 5 studies [11, 25, 26, 32, 35]. The length of stay in the PACU, although rarely specified, ranged from 0.5 to 2 h. Descriptions of postoperative follow-up appeared sporadically and most often covered a period of 24 h [14, 15, 31, 38], 48 h [21] (concerned only pain and postoperative nausea and vomiting (PONV)) or 7 days [22, 34](Table 2). Structured neurological or renal follow-up was infrequent.
Minor and major complications
The safety analysis revealed a varied profile of complications. Among the 32 studies included in the analysis, 14 [9, 10, 14–16, 21, 24, 26, 28, 30, 32, 34, 36, 37] did not report any complications. In the remaining studies, complications were classified as minor or major/hemodynamic (Table 3).
Table 3.
The incidence of minor and major complications reported in the analyzed studies
| Studies on a specific drug | Studies comparing specific drugs | ||||||
|---|---|---|---|---|---|---|---|
| Author; year | Used drug | Complications | Author; year | Used drugs | Complications | ||
| Minor | Major | Minor | Major | ||||
| Cincikas et al.; 2003 [9] | Nitroglycerin | Not reported | Not reported | Skalias et al.; 2023 [40] | Bisoprolol vs. nifedipine | Not reported | Not reported |
| Naik et al.; 2011 [10] | Propofol TIVA | Not reported | Not reported | Alkan et al.; 2021 [39] | Esmolol vs. remifentanil vs. nitroglycerin | Not reported |
10% (REM) and 5% (ESM) of bronchospasm 15% (REM) of bradycardia (requiring atropine) |
| Ha et al.; 2014 [11] | Propofol TIVA | Not reported | Decrease in Vmca > 50% at MAP < 60 but without complications | Bharathwaj et al.; 2019 [37] | Labetalol vs. dexmedetomidine | Not reported | Not reported |
| Heller et al.; 2015 [12] | Propofol + remifentanyl + nitrous oxide | 11% of PONV in patients with lower SctO2, but not statistically significant | SctO2 <60% in 16% of patients resulted in a longer stay in the PACU | Bajwa et al.; 2016 [36] | Nitroglycerine vs. esmolol vs. dexmedetomidine |
6%(DEX), 14% (NIT), and 16% (ESM) of PONV 4% (DEX), 18% (NIT), and 8% (ESM) of shivering 26% (DEX), 8% (NIT), and 6% (ESM) of dry mouth |
Not reported |
| Goksu et al.; 2008 [13] | Dexmedetomidine | 13% of PONV | 6,7% of bradycardia (requiring treatment with atropine) | Yun et al.; 2015 [22] | Nitroprusside vs. remifentanil | Not reported | Not reported |
| Sartcaoglu et al.; 2005 [14] | Nitroglycerine | Not reported | Not reported | Sajedi et al.; 2016 [23] | Remifentanil vs. labetalol | 9,1% (REM) and 62,1% (LAB) of PONV |
3% (REM) and 17,2% (LAB) of hypotension requiring treatment 3% (REM) and 3,4% (LAB) of bradycardia 38% (LAB) of hypotension in PACU |
| Zhang et al.; 2021 [15] | Nicardipine + esmolol | Not reported | Not reported | Sujatha et al.; 2023 [35] | Dexmedetomidine vs. propofol | Not reported | Not reported |
| Tirelli et al.; 2004 [16] | Propofol + remifentanyl | Not reported | Not reported | Praveen et al.; 2024 [34] | Dexmedetomidine vs. clonidine | 10% (DEX) and 17,5% (CLO) of PONV |
15% (DEX) and 10% (CLO) of bradycardia 7,5% (DEX) and 15% (CLO) of hypotension |
| Li et al.; 2023 [38] | Propofol + remifentanyl |
5,5% (3/55) of sore throat; 2% (1/55) of PONV |
9,1% (5/55) of hypoxemia; | Bafna et al.; 2021 [33] | Dexmedetomidine vs. clonidine |
2,9% (DEX) and 11,4% (CLO) of PONV 11,4% (DEX) and 2,9% (CLO) of dry mouth |
8,6% (DEX) and 5,7% (CLO) of bradycardia 8,6% (DEX) and 5,7% (CLO) of hypotension |
| Jiwanmall et al.; 2017 [17] | Clonidine | 6,7% of prolonged sedation |
33% of hypotension episodes requiring treatment; 3,3% of bradycardia episodes requiring treatment |
Sharma et al.; 2025 [32] | Esmolol vs. dexmedetomidine | Not reported | Not reported |
| Hassan et al.; 2024 [24] | Dexmedetomidine | 5,7% of PONV | 3% of bradycardia requiring treatment with atropine | Escamilla et al.; 2019 [31] | Clonidine vs. dexmedetomidine | Not reported | Not reported |
| Gollapudy et al.; 2020 [18] | Propofol vs. desflurane |
8,6% of PONV 10% of prolonged sedation |
2,8% of ST changes 4,3% of hypotension |
Eghbal et al.; 2018 [30] | Labetalol vs. dexmedetomidine | 11% (LAB) of PONV | Not reported |
| Neethirajan et al.; 2020 [19] | Dexmedetomidine | Not reported |
8,7% of bradycardia required treatment with atropine; 13% of hypotension required treatment with ephedrine |
Moshiri et al.; 2017 [29] | Propofol vs. dexmedetomidine | Not reported | Not reported |
| Rehab et al.; 2023 [20] | Aminophylline |
11,5% of PONV 7,7% of headache and lightheadedness |
7,7% of hypotension 3,9% of bradycardia |
Huh et al.; 2020 [28] | Dexmedetomidine vs. remifentanil | Not reported | Not reported |
| Ankichetty et al.; 2011 [21] | Propofol vs. isoflurane | Not reported | Not reported | Karabayirli et al.; 2016 [27] | Dexmedetomidine vs. remifentanil |
21,7% (DEX) and 25% (REM) of PONV 4,2% (both groups) of shivering 13% (DEX) and 21% (REM) of pain required treatment |
Not reported |
| Mugabo et al.; 2024 [26] | Dexmedetomidine vs. clonidine | Not reported |
5% (DEX) of bradycardia required treatment with atropine 5% (DEX) of hypotension required treatment with ephedrine |
||||
| Lee et al.; 2013 [25] | Dexmedetomidine vs. remifentanil | Not reported |
62% (REM) and 34% (DEX) patients treated with ephedrine 41% (REM) and 25% (DEX) patients treated with atropine |
||||
TIVA Total Intravenous Anesthesia, PONV Postoperative Nausea And Vomiting, DEX Dexmedetomidine, REM Remifentanil, CLO Clonidine, LAB Labetalol, ESM Esmolol, NIT Nitroglycerine, SctO2 Cerebral Tissue Oxygenation, MAP Mean Arterial Pressure, Vmca Velocity in the Middle Cerebral Artery
Minor adverse events occurred in 13 studies [12, 13, 17, 18, 20, 22, 23, 27, 29, 31, 32, 35, 38]. The predominant problem was postoperative nausea and vomiting (PONV) reported in 12 studies [12, 13, 18, 20, 22, 23, 27, 29, 31, 32, 35, 38] with a wide range of incidence from 2% to 62%. Less frequently observed complications included prolonged sedation (6.7–10%) [17, 18], postoperative shivering (4–18%) [27, 38], and dry mouth (3–26%) [27, 32]. Individual reports concerned sore throat (5.5%) [22], headaches and dizziness (7.7%) [20], and increased postoperative pain requiring additional analgesia (13–21%) [38] (Table 3).
Significant hemodynamic disturbances and organ complications were reported in 15 studies [11–13, 17–20, 22, 23, 25, 29, 31, 32, 39, 40]. The most frequently reported events were intraoperative bradycardia (< 50–60 beats/min), noted in 10 studies (3–15%) [13, 17, 19, 20, 23, 25, 29, 31, 32, 39], and severe hypotension (defined as MAP < 50 mmHg or SBP < 90 mmHg), reported in 8 studies (4.3–33%) [17–20, 29, 31, 32, 39]. Most of these episodes required pharmacological intervention (e.g., ephedrine or atropine). In one study [29], 38% of patients experienced delayed hypotension in the PACU. Notably, the study by Lee et al. [40] reported high use of rescue medications (ephedrine in 32–64% of patients, atropine in 21–45% of patients), without specifying the corresponding incidence of hypotension or bradycardia (Table 3).
There were also a few clinically critical signs of organ and respiratory ischemia. These included hypoxemia (9.1%) [22], bronchospasm (10%) [25], and ST-segment changes on ECG suggesting myocardial ischemia (10%) [18].
Cerebral perfusion abnormalities included a decrease in cerebral saturation (rScO2) < 60% in 16% of patients (NIRS monitoring) in Heller et al. study (2014) [12], and middle cerebral artery (MCA) flow reduction > 50% with a decrease in MAP < 60 mmHg (TCD) in Ha et al. study [11]. No permanent neurological deficits were reported, although follow-up was insufficient to exclude subtle or delayed complications (Table 3).
Discussion
The available evidence supports the efficacy of controlled hypotension in improving intraoperative conditions during FESS. However, its safety profile remains insufficiently characterized, primarily due to the limited use of advanced monitoring, short and inconsistent postoperative follow-up, and the lack of systematic assessment of organ function (e.g., renal biomarkers, cognitive testing, troponin measurement). Importantly, few studies have directly evaluated the consequences of controlled hypotension or the incidence of complications associated with organ hypoperfusion. Numerous publications have focused on comparing pharmacological agents with respect to surgical field visibility and intraoperative bleeding, whereas safety aspects – particularly the risk of end-organ ischemia – are rarely analyzed in depth. Consequently, the heterogeneity and incompleteness of available data preclude definitive conclusions regarding the safety of controlled hypotension in FESS.
Although the present review was primarily designed to evaluate safety rather than operative efficacy, most of the included studies also reported measures of intraoperative bleeding or surgical field quality. These outcomes are most commonly assessed using the Fromme-Boezaart/Boezaart scale, which grades bleeding intensity and the frequency of suctioning required during endoscopic surgery, and the Wormald surgical field grading scale, a more detailed video-endoscopic instrument developed specifically for assessing bleeding during endoscopic sinus surgery [41, 42]. Operative duration was reported inconsistently across the included studies and, given the safety-focused scope of this review, was not amenable to quantitative synthesis. Overall, the available literature suggests that controlled hypotension may improve surgical field visualization; however, the magnitude and consistency of this benefit vary across studies and should be interpreted alongside the limited evidence regarding end-organ safety.
Furthermore, technique safety is determined not only by the achieved MAP reduction but also by the duration, depth, and frequency of hypotensive episodes. Many studies report average or target MAP values without quantifying hypotension exposure (e.g., time spent below a clinically meaningful threshold, the number of hypotensive events, the rapidity of pressure declines, or the need for rescue vasopressors). This limits the interpretability of the results, since the risk of end-organ ischemia is likely driven by the cumulative hypotension burden rather than by a single intraoperative MAP value. Standardized reporting of hypotension exposure metrics would substantially improve cross-study comparability and enable the identification of non-hazardous boundaries.
Advanced monitoring modalities such as NIRS, TCD, and NICOM remain underutilized, despite providing valuable real-time information on tissue perfusion and oxygenation [43]. Incorporation of such modalities – especially in high-risk individuals – could significantly improve patient safety. Specifically, intraoperative cerebral oximetry enables continuous evaluation of brain oxygenation and facilitates early detection of cerebral hypoperfusion [43]. However, the absence of reported neurological deficits in reviewed studies should not be interpreted as evidence of the absence of cerebral injury. Subclinical cognitive impairments may go undetected without postoperative neuropsychological testing, and the limited duration of follow-up in most studies precludes the identification of delayed neurological sequelae. Future studies should therefore include a structured neurological assessment, ideally consisting of a focused postoperative neurological examination in the PACU and at 24 h, supplemented in research settings by baseline and postoperative cognitive screening. Practical tools could include MMSE or Montreal Cognitive Assessment (MoCA) performed preoperatively and repeated at 24–48 h and, where feasible, at 7–30 days; more sensitive domain-specific tests may be considered when subtle postoperative cognitive dysfunction is a primary endpoint. In addition, in FESS, relatively minor differences in ventilation and EtCO2 may influence both cerebral perfusion and the surgical field. Hypocapnia can reduce cerebral blood flow through vasoconstriction and might affect cerebral oximetry (NIRS) or TCD-derived flow indices, while CO2-related changes in vascular tone might also modify bleeding intensity [44]. Therefore, future studies should report – and ideally standardize – ventilatory targets (including a defined EtCO2 range), as they constitute a plausible confounder for both perfusion monitoring outcomes and surgical field quality.
Regarding cardiac complications, continuous ECG monitoring remains essential; yet it is insufficient to detect all ischemic events. Myocardial Injury after Non-cardiac Surgery (MINS) – a form of prognostically significant myocardial ischemia – may develop without typical ECG changes or clinical symptoms and is often precipitated by intraoperative hypotension-induced oxygen supply-demand mismatch [45, 46]. Consequently, routine postoperative assessment of cardiac injury biomarkers, particularly high-sensitivity cardiac troponin T (hs-cTnT), should be considered in patients at increased cardiovascular risk or in those exposed to prolonged or profound hypotension [47]. This risk-stratified approach is consistent with contemporary perioperative guidelines, including the 2017 Canadian Cardiovascular Society recommendations and the 2022 European Society of Cardiology guidelines, which advocate troponin surveillance in patients at increased cardiovascular risk undergoing major non-cardiac surgical procedures [48, 49]. Importantly, MAP is only a surrogate for organ perfusion and does not directly reflect forward flow or oxygen delivery. Perfusion depends on cardiac output/cardiac index and systemic vascular resistance, so two hypotensive protocols achieving the same MAP may generate markedly different oxygen delivery (DO2) and, consequently, distinct risks of MINS or acute kidney injury (AKI) [50]. This supports the selective use of hemodynamic monitoring, including flow parameters (e.g., NICOM, FloTrac), particularly in patients with limited cardiovascular reserve.
Although none of the reviewed studies systematically assessed renal function, MAP below 65 mmHg is widely recognized as a significant predictor of AKI. The absence of postoperative creatinine follow-up in the analyzed studies represents a considerable knowledge gap, especially for vulnerable patients with pre-existing renal disease, dehydration, or treatment with angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs). These populations are particularly prone to hypoperfusion-related injury. From a pragmatic and cost-conscious perspective, routine advanced biomarker surveillance is unlikely to be justified in all low-risk FESS patients. However, serum creatinine assessment within 24–48 h is relatively inexpensive and should be considered in high-risk patients, after prolonged or deep hypotension, or when intraoperative rescue vasopressors are required. Future research should integrate perioperative measurements of renal biomarkers, such as Neutrophil Gelatinase-Associated Lipocalin (NGAL) and cystatin C, together with urine output assessment, to better define the renal safety margins of controlled hypotension [51].
Another critical limitation of the reviewed literature concerns the wide variability in pharmacological regimens applied to induce hypotension. The lack of standardized protocols across studies hinders direct comparison of safety profiles. Furthermore, essential perioperative variables – including preoperative hydration status, intraoperative fluid balance, and the continuation or withdrawal of ACEI-ARB therapy – were rarely reported. This omission is crucial, as both preoperative hypovolemia and the blunted renin-angiotensin response in ACEI/ARB-treated patients may potentiate drug-induced hypotension, leading to profound and resistant decrease in blood pressure. Ensuring adequate hydration and establishing standardized guidelines for perioperative management of antihypertensive therapy are therefore imperative steps toward reducing the risk of end-organ hypoperfusion.
Heart rate control constitutes an additional clinically relevant determinant of surgical field quality and systemic organ perfusion. Vasodilator-based hypotensive techniques may elicit baroreceptor-mediated reflex tachycardia and increased myocardial contractility, thereby maintaining or increasing cardiac output, enhancing peripheral vasodilatation, and potentially contributing to venous oozing within the operative field. Consequently, in routine anesthetic practice for FESS, optimal surgical conditions are often achieved not through MAP reduction alone, but through a combined strategy of moderate controlled hypotension and concomitant heart rate control, commonly with a target heart rate of approximately 60–70 beats/min, using beta-blockers such as esmolol or sympatholytic agents such as dexmedetomidine [25, 27, 42]. This interaction is clinically significant, as both arterial hypotension and pharmacological heart rate reduction may independently, and in combination, decrease oxygen delivery, particularly in patients with limited cardiovascular reserve. Future studies should therefore systematically report heart rate targets, use of beta-blockers and other negative chronotropic agents or sympatholytic agents, requirements for vasopressor rescue, and cardiac output or other flow-related parameters, rather than relying on MAP values alone.
Most authors have adopted a target MAP of 50–70 mmHg as the operational range for controlled hypotension during FESS. Although MAP values below 50 mmHg may approach or exceed the lower limits of cerebral and renal autoregulation, particularly in patients with hypertension or established vascular disease, MAP values above 70–80 mmHg may compromise surgical field visibility, prolong operative time, and potentially increase procedure-related risk [50]. Accordingly, controlled hypotension should be regarded as an individualized risk-benefit intervention, with hemodynamic targets adjusted accordingly to each patient’s baseline blood pressure, cardiovascular reserve, and comorbidity profile. We do not consider it appropriate to recommend a single universal percentage reduction from baseline for all patients undergoing FESS. A pragmatic approach would be to report both absolute MAP values and relative reductions from preoperative baseline, to avoid MAP values below 50 mmHg in all patients, to avoid sustained MAP values below 65 mmHg in higher-risk individuals, and, in general, to limit MAP reduction to no more than approximately 20–30% from baseline. In patients with chronic hypertension, diabetes mellitus, atherosclerosis, renal impairment, or other forms of vascular disease, even more conservative reductions may be warranted, as autoregulatory thresholds may be shifted toward higher perfusion pressures [52–54]. Reporting and interpreting relative hypotension in conjunction with absolute MAP thresholds may therefore provide a more physiologically appropriate framework and may facilitate the development of patient-specific, dynamically guided hypotensive protocols, as has been proposed in other surgical disciplines.
Furthermore, current research on optimal MAP targets in FESS is limited by small sample sizes, heterogeneous study designs, and inconsistent reporting of complications. The diversity of pharmacological agents and the lack of standardized definitions for adverse events impede robust cross-study comparisons. Few studies incorporate advanced perfusion monitoring, which limits the detection of organ-specific disturbances and restricts interpretation to MAP rather than actual tissue oxygen delivery. Moreover, many trials omit key parameters such as hypotensive duration, frequency of perfusion disturbances, or postoperative biomarker trends, rendering their conclusions potentially misleading.
Future research should aim to define both standardized and patient-individualized MAP targets for controlled hypotension in FESS. These studies should integrate multimodal monitoring beyond basic hemodynamic measures, combining MAP assessments with markers of cerebral, renal, and myocardial perfusion. In addition, protocols should quantify hypotension exposure (e.g., time below thresholds, number and depth of hypotensive episodes) and relate achieved pressures to baseline hemodynamics to clarify the role of relative hypotension in high-risk subgroups. Routine postoperative evaluation of serum troponin and creatinine levels, as well as cognitive function, would allow for a more comprehensive assessment of the physiological consequences and long-term safety of controlled hypotension. Only such an approach will enable the establishment of validated safety thresholds and the development of personalized hemodynamic management strategies in endoscopic sinus surgery (Fig. 7).
Fig. 7.

The primary issues and proposed solutions. MAP – Mean Arterial Pressure
Conclusions
Controlled hypotension markedly improves intraoperative conditions during FESS; however, its systemic safety, particularly with respect to organ perfusion, remains incompletely defined. Current evidence primarily addresses surgical visibility and bleeding reduction, while subclinical complications (cerebral desaturation, myocardial injury, AKI) may be overlooked without appropriate intraoperative monitoring and postoperative biomarker surveillance. The widespread application of a uniform MAP target of 50–70 mmHg may be insufficient, particularly in older individuals with cardiovascular or metabolic comorbidities. A paradigm shift toward individualized hemodynamic management, tailored to baseline blood pressure, heart rate, comorbidities, and overall risk profile, is required. Selective, risk-stratified use of perfusion-oriented monitoring (NIRS, NICOM, TCD) and routine postoperative renal/cardiac biomarker assessment, together with standardized complication reporting and longer follow-up (including neurological outcomes), is needed to define safe limits for controlled hypotension in FESS.
Supplementary Information
Acknowledgements
Not applicable.
Authors' contributions
Conceptualization: M.A, S.B. Methodology: M.A. Data Curation: R.K., L.Z., W.SG. Formal Analysis: M.A., J.D., R.K., L.Z., W.SG. Writing – Original Draft: M.A., R.K. Writing – Review & Editing: M.A., J.D., R.K., L.Z., W.SG. Visualization: L.Z., W.SG. Supervision: M.A., S.B. All authors have approved the final version of the manuscript.
Funding
No funding was received to assist with the preparation of this manuscript.
Data availability
The data generated during this study are available within the article. Datasets analyzed during the current study preparation are available from the corresponding author upon reasonable request.
Declarations
Ethics approval and consent to participate
Not applicable.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Citations
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Supplementary Materials
Data Availability Statement
The data generated during this study are available within the article. Datasets analyzed during the current study preparation are available from the corresponding author upon reasonable request.
