Intended learning outcomes
Describe the pathophysiological mechanisms linking postoperative ileus, intra-abdominal hypertension and acute kidney injury following radical cystectomy.
Recognise postoperative ileus as a potential cause of intra-abdominal hypertension, contributing to renal dysfunction in the postoperative setting.
Identify perioperative risk factors and modifiable strategies that may reduce the incidence and severity of postoperative ileus and related complications.
Apply a physiology-driven approach during the perioperative period to mitigate the risk of intra-abdominal hypertension and acute kidney injury.
Introduction
Bladder cancer ranks as the 11th most common malignancy in the United Kingdom [1], and radical cystectomy remains a cornerstone treatment for muscle-invasive or high-risk disease, with approximately 2100 cystectomies performed annually [2]. Despite advances in perioperative care, cystectomy continues to be associated with significant postoperative morbidity.
Among the most frequent complications after bladder cancer surgery are postoperative ileus (POI) and acute kidney injury (AKI), both considered independent predictors of worse long-term outcomes. While AKI has traditionally been attributed to factors such as preoperative kidney impairment, fluid management and perioperative haemodynamic instability, the potential contribution of gastrointestinal dysfunction has received less attention.
POI is a syndrome characterised by the impairment of gastrointestinal motility, causing progressive abdominal distension, which leads to an increase in intra-abdominal pressure (IAP). This has proven effects on renal perfusion and glomerular filtration. In this narrative article, we explore the pathophysiological link between POI, IAP and the development of AKI following bladder cancer surgery.
Report
A 69-year-old man with a diagnosis of muscle-invasive bladder cancer underwent a radical cystectomy with neobladder reconstruction after completion of neoadjuvant chemotherapy. The surgery was reported to be uneventful. The patient was admitted electively to an enhanced recovery unit for monitoring and implementation of the enhanced recovery pathway.
During the first 48 h after surgery, the progress in oral intake was limited by persistent nausea requiring the administration of antiemetics. Clinical assessment revealed the absence of bowel sounds, failure to pass flatus or stools, and progressive abdominal distension.
By postoperative day 3, the reduction in urinary output was significant; additionally, an increase in creatinine was noted, meeting criteria for AKI. At this stage, common contributors to renal dysfunction were considered; however, the evolving abdominal findings raised concerns regarding the potential role of gastrointestinal dysfunction in the development of renal impairment.
Question to be answered
Can POI after cystectomy surgery be one of the factors leading to AKI in the postoperative period?
Discussion
Epidemiology
Despite widespread adoption of enhanced recovery after surgery (ERAS) protocols, POI remains prevalent after cystectomy, with incidences reaching 51% [3]. Predictors include advanced age, fluid disturbances, opioid use, bowel manipulation and inflammation [4, 5].
AKI is similarly frequent, reaching up to 50% in high-risk cohorts. Risk factors include advanced age, diabetes, chronic kidney disease, exposure to nephrotoxics and hemodynamic instability. Despite this, the contribution of intra-abdominal hypertension (IAH), particularly in the context of POI, remains uncredited in perioperative practice [5].
Physiological mechanisms linking POI and IAH
POI is a multifactorial condition. Its pathophysiology reflects interaction between neural reflex inhibition, inflammatory response, pharmacological effects and direct surgical trauma (Figure 1). These mechanisms are further amplified in cystectomies by the extent of bowel handling, dissection and urinary diversion construction.
Reduced peristalsis produces an accumulation of intraluminal gas and fluid, causing progressive bowel distension, increasing the intra-abdominal volume within a relatively fixed compartment, contributing to a rise in IAP. The World Society of the Abdominal Compartment Syndrome defines IAH as a sustained IAP > 12 mmHg, while abdominal compartment syndrome is an IAP > 20 mmHg in the presence of new organ dysfunction [5].
Physiological mechanisms linking IAH and AKI
The relationship between IAH and AKI is primarily mediated by impaired renal perfusion. An increase in IAP causes compression of the renal vasculature, reducing the arterial inflow and increasing venous pressure. Consequently, the renal perfusion pressure – the difference between mean arterial pressure (MAP) and IAP – progressively declines as the IAP rises, resulting in glomerular filtration rate reduction. Simultaneously, compression of the renal parenchyma and venous system contributes to interstitial oedema, increasing intracapsular pressure, further compromising filtration.
These effects can be interpreted through the filtration gradient (FG) concept, which represents the net mechanical pressure driving glomerular filtration. In the setting of IAH, elevated IAP is transmitted to the renal veins and to Bowman’s capsule, creating a dual impediment to filtration. This can be expressed as: FG = MAP – (2 × IAP). As IAP increases – consequence of bowel distension – the FG decreases disproportionately compared with MAP or abdominal perfusion pressure (APP). These mechanisms explain why significant reductions in urine output and glomerular filtration may occur despite apparently adequate MAP. This model highlights how empiric fluid administration in response to oliguria may be ineffective or even harmful, by exacerbating bowel oedema and IAH, intensifying the reduction in FG [6].
Elevated IAP also exerts systemic effects. It reduces venous return, leading to decreased cardiac preload and cardiac output, precipitating hypotension, further compromising renal perfusion. Additionally, diaphragmatic elevation secondary to raised IAP increases the intrathoracic pressure, adversely affecting ventilation and oxygen delivery, exacerbating renal hypoxia.
Taken together, POI, IAH and AKI may represent interlinked sequential components of a shared pathophysiological process, highlighting the importance of earlier recognition and intervention [5].
Urinary diversion and its influence on developing POI
Following radical cystectomy, all patients require a urinary diversion. The lowest risk approach is formation of cutaneous urostomies, reserved for patients with significant comorbidity in whom the bowel manipulation should be minimised. More complex reconstructions, such as a neobladder, rely on the use of bowel segments. The ileal conduit is the most commonly performed urinary diversion, as it typically requires shorter bowel segments, less extensive bowel manipulation and reduced operative time [7]. These characteristics may be associated with a lower risk of POI; however, the type of urinary diversion represents only one of several factors.
Challenges to measure IAP in this population
The pressure measurement via a catheter placed inside the bladder is considered the gold standard for IAP measurement. As the bladder is removed during radical cystectomy, alternative methods, less validated in patients following cystectomy, must be considered.
Diversion route
In patients with neobladder reconstruction, the reservoir is fashioned from detubularised bowel. This tissue has different compliance and ‘stretching’ properties compared with the native bladder, which may lead to inaccurate pressure readings. For patients receiving an ileal conduit, the urinary diversion is non-continent and open to an external bag, making it impossible to maintain the closed system necessary for traditional pressure monitoring.
Alternative surrogate measurements
Intragastric pressure measurement is a reliable surrogate for IAP. This method requires a specialised nasogastric tube equipped with a pressure transducer, limiting its use [8]. The measurement of inferior vena cava pressure via a transfemoral venous catheter may indirectly reflect IAP. However, it is only considered a reliable surrogate when IAP > 20 mmHg. Another alternative is the direct measurement of IAP by connecting an external digital transducer to a peritoneal drain. However, this technique depends on the presence or placement of a peritoneal drain, entailing the risks associated with accessing the peritoneal cavity [8].
Perioperative mitigation strategies
Surgical planning and technique
Animal models have demonstrated that surgical manipulation of the bowel alone reliably induces ileus [9]. Visceral handling and traction activate nociceptive afferents within the splanchnic nerves, triggering increased sympathetic outflow and decreased parasympathetic activity, resulting in inhibition of gastrointestinal motility [10].
Even gentle bowel handling activates immune cells, provoking smooth muscle contractility inhibition, contributing to the development and persistence of POI [9]; its severity correlates with the amount of manipulation [9]. Therefore, patient-specific factors requiring increased bowel handling, such as previous abdominal surgery, radiotherapy or underlying bowel pathology, should be identified during preoperative planning.
While the choice of urinary diversion between ileal conduit and neobladder formation has not been consistently shown to reduce rates of POI [11, 12], a surgical approach warrants consideration. Minimally invasive techniques, such as laparoscopic or robotic cystectomy, have been associated with earlier return of gastrointestinal function [13]. The surgical aspects of a cystectomy represent a convergence of multiple ileus-promoting factors; thus, careful preoperative planning becomes critical [14].
Judicious administration of intravenous fluids
Intravenous fluids are pharmacological agents for which both underdosing and overdosing have deleterious consequences. Excessive fluid administration causes bowel wall oedema, impaired gastrointestinal motility and delayed return of normal bowel function, increasing the risk of POI [15]. Conversely, inadequate intravascular volume and untreated hypovolaemia are contributors to organ hypoperfusion, contributing to AKI.
Perioperative haemodynamic disturbances should prompt cause-directed management. Vasodilatory hypotension requires vasoactive agents, whereas hypovolaemia necessitates timely volume resuscitation with the right fluid. Continuous reassessment of volume status and renal function is essential to balance the competing risks of fluid overload, POI and AKI.
Adequate APP and filtration rate
APP is the difference between the MAP and IAP. While a MAP > 65 mmHg is generally considered adequate, this threshold may be insufficient in the presence of IAH. An increase in IAP at a constant MAP results in a proportional reduction in APP, compromising abdominal organ perfusion and reducing the FG. Hence, in patients with suspected IAH, MAP targets should be individualised to preserve APP and FG.
Analgesia
Effective postoperative analgesia is essential to facilitate engagement with ERAS pathways, as inadequate pain control can hinder mobilisation, prolong ileus and delay recovery. Opioids are contributors to gastrointestinal dysmotility, making analgesic management challenging. Many patients receive preoperative opioids to treat cancer-related pain, requiring higher doses during the postoperative period, and others may have pre-existing renal impairment, limiting the safe use of opioid-sparing medications, such as non-steroidal anti-inflammatory medications.
A balanced, multimodal analgesic strategy is recommended. Regional analgesic techniques, when feasible, can significantly reduce systemic opioid requirements. In this context, rectus sheath catheter analgesia has demonstrated efficacy following cystectomy, providing adequate pain control with reduced opioid consumption and fewer side effects compared with neuraxial analgesia [16].
Enhanced recovery pathways
ERAS pathways have been adopted to improve outcomes following surgery. Core components, including early mobilisation, early return to oral intake and optimised analgesia, are directly relevant to reducing the incidence and severity of POI. However, successful implementation requires continuous evaluation and local adaptation.
Postoperative nasogastric tubes (NGTs) are not recommended as a routine for cystectomy. Evidence shows that its omission or early removal does not increase POI incidence [17, 18]. Nevertheless, while prophylactic NGT use is not supported, gastrointestinal decompression has a role in POI. Further work is required to evaluate whether selective NGT use in patients with significant bowel distention could mitigate rising IAP and reduce downstream organ dysfunction.
Failure to meet ERAS milestones should prompt proactive investigation and intervention to prevent progression from POI to IAH and AKI.
Future directions and research gaps
Although links between POI, IAH and AKI are biologically plausible, important gaps limit perioperative strategies. Prospective studies integrating routine IAP monitoring, gastrointestinal outcomes and renal biomarkers are needed to clarify causality and identify early therapeutic thresholds.
Peripheral μ-opioid receptor antagonists, such as alvimopan and N-methylnaltrexone, have shown promise in accelerating gastrointestinal recovery after abdominal surgery; however, their role in cystectomy requires further investigation.
Finally, emerging evidence suggests that alterations in the gut microbiome may influence postoperative gastrointestinal recovery and inflammatory responses, raising the possibility of targeted microbiome-modulating strategies as future preventive interventions [19].
Conclusion
Radical cystectomy remains a high-risk surgical procedure. Postoperative complications following cystectomy should not be considered in isolation. The same pathophysiological mechanisms by which ileus contributes to IAH and renal dysfunction may also predispose patients to other complications, including impaired ventilation, atelectasis, hospital-acquired pneumonia and delayed mobilisation. Recognising the interdependence of these complications underscores the need for a holistic perioperative perspective, in which gastrointestinal dysfunction is viewed as a potential driver of multisystem impairment rather than a self-limiting abdominal issue.
Declarations and conflicts of interest
Research ethics statement
Not applicable to this article.
Consent for publication statement
This narrative article is based on a fictional clinical vignette and does not describe a real patient or clinical encounter, so consent for publication is not necessary. Images are used solely for illustrative purposes and are not related to the vignette. When real patient images are included, the authors confirm that written informed consent for publication has been obtained for this purpose in accordance with the journal’s patient consent requirements.
Conflicts of interest statement
The authors declare no conflicts of interest with this article.
Artificial Intelligence declaration
The authors acknowledge the use of Grammarly and ChatGPT-4 tools to improve language clarity, sentence structure, assist with grammar checking and help organise the references. The authors maintain that they, Nora Cruz Rodriguez, Rosalyn Hawkins and John Whittle, are the sole authors of this article and take full responsibility for the content therein.
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