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Clinical case reports · 2026

Uremic Paralytic Ileus in a 70 Years Old Female: A Diagnostic Dilemma.

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Gohar A, Rehman A, Ilyas M, Rehman A, Bilal M, Iman H, Ali M, Ahmad MH

Аннотация

Uremia has been associated with slowed intestinal motility, resulting in loss of peristalsis and the development of paralytic ileus. We present a case of uremia-induced paralytic ileus in a 70-year-old woman. The patient was admitted with a 7-day history of abdominal pain, vomiting, and constipation. Initial evaluation revealed a soft non-tender abdomen with decreased bowel sounds. Urgent ultrasonography showed dilated gut loops and sluggish gut motility, while atrophic kidneys with hydronephrosis were also appreciated. Routine biochemistry labs revealed elevated creatinine and potassium levels, and an erect abdominal X-ray showed mild to moderate air-fluid levels. Notably, common risk factors for paralytic ileus, such as recent surgery or gastrointestinal procedures, immobility, hypokalemia, hypothyroidism, hypercalcaemia, hypocalcemia, hypomagnesemia, and diabetes mellitus, were ruled out. The patient also had no history of anticholinergic or opioid use. Given the absence of other causes, uremia was established as the underlying cause of paralytic ileus. After initial treatment for ileus, the patient underwent hemodialysis, which led to significant improvement in symptoms. This case highlights the importance of recognizing uremia as a potential cause of unexplained ileus, contributing to the limited literature on uremia-associated ileus.

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This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

Introduction

Paralytic ileus is a condition characterized by the temporary cessation of normal gastrointestinal (GI) motility in the absence of mechanical obstruction [ 1 ]. A specific subset, adynamic ileus, occurs due to impaired motor activity and is closely associated with metabolic conditions such as uraemia [ 2 ], a complication of renal failure that disrupts GI motility through toxin accumulation and electrolyte imbalances. Uraemia, a key contributor, exacerbates GI dysfunction through the accumulation of metabolic toxins, electrolyte imbalances, and systemic inflammation [ 3 ]. Additional factors, including vagus nerve dysfunction and bacterial endotoxins, further impair normal bowel movement [ 3 ]. Paralytic ileus is a significant clinical issue due to its impact on patient morbidity and healthcare utilization. It presents with symptoms like nausea, vomiting, abdominal distension, and constipation [ 2 ]. While most cases are self‐limiting, prolonged or severe cases may require medical intervention. Uremic ileus, which arises from metabolic disturbances related to renal failure, remains less explored but is likely underdiagnosed in this population [ 4 ].

The pathophysiology of paralytic ileus is multifactorial. It typically results from neuromuscular failure of the myenteric (Auerbach's) and submucosal (Meissner's) plexuses, leading to impaired peristaltic activity. Although the small intestine is most often affected, the stomach and colon may also be involved [ 2 ]. Other causes include postoperative factors such as surgical manipulation and inflammation, infections like peritonitis and medications such as opioids and anticholinergic [ 1 , 5 , 6 , 7 ]. Paralytic ileus is often categorized into postoperative, prolonged, drug‐induced, and uremic forms, each requiring tailored management strategies [ 3 ]. Diagnosis is primarily clinical, supported by imaging studies such as abdominal X‐rays or CT scans, which reveal dilated bowel loops and air‐fluid levels [ 1 , 2 , 7 ]. Laboratory tests help identify underlying causes, including renal dysfunction and metabolic derangements. Management involves correcting the underlying cause, supportive care with intravenous fluids, bowel rest, and nasogastric decompression [ 1 , 7 , 8 ]. Emerging pharmacological options, such as prokinetic agents [ 3 ], show promise but require further validation, especially in uremic cases.

This article explores the pathophysiology, diagnosis, and management of paralytic ileus, with a focus on uremic ileus, highlighting the need for a comprehensive, multidisciplinary approach to improve patient outcomes.

Case History and Examination

A 70 years old female, normotensive and non‐diabetic, presented in the surgery emergency department of a tertiary care hospital with presenting complaints of abdominal pain, vomiting, and constipation for 7 days. There was no history of trauma, previous surgery, medication, or recent infection. Her vitals were blood pressure: 130/90, heart rate: 76 beats per minute, respiratory rate: 16/min, temperature: 98.6°F, blood sugar: 95 mg/dL, and maintaining oxygen saturation of 98% at room air. Her abdomen was soft, non‐tender with decreased bowel sounds and no visceromegaly. Rest of the examination was unremarkable.

Methods (Differential Diagnosis, Investigations, and Treatment)

To rule out acute abdomen urgent ultrasound abdomen was done, which showed dilated gut loops up to 3 cm and sluggish peristalsis. Other findings on ultrasonography showed atrophic kidneys with hydronephrosis. X‐ray erect abdomen was done which showed mild to moderate air‐fluid levels (Figure 1 ). Chest X‐ray was normal while electrocardiogram showed hyperkalemic changes. Her laboratory investigations showed hemoglobin 10.7 g/dL, total leucocyte count 8.1 × 10 3 /μL, and platelets 239 × 10 3 /μL. On routine biochemistry potassium was 5.7 mEq/L and creatinine was 16 mg/dL. Serum sodium 136 mEq/L, calcium (8.7 mg/dL), phosphate (2.6 mg/dL), magnesium (2.1 mg/dL), and albumin 3.6 g/dL were in normal range. Glycosylated hemoglobin (HbA1c) was 5.2% and thyroid stimulating hormone (TSH) was 1.1 μU/mL (Normal 0.5–5 μU/mL). Viral serology for hepatitis B, C, and Human Immunodeficiency Virus (HIV) was negative. Laboratory investigations showed normal values for serum amylase (30 U/L, normal range: 25–125 U/L), lipase (20 U/L, normal range: 10–60 U/L), arterial blood gases (ABGs) showing pH (7.42, normal range: 7.35–7.45), bicarbonate (24 mmol/L, normal range: 22–28 mmol/L), and pCO2 (38 mmHg, normal range: 35–45 mmHg). The urine complete examination was also normal, with a pH of 6.0 (normal range: 4.6–8.0), specific gravity of 1.020 (normal range: 1.005–1.030), and negative results for protein, glucose, ketones, and blood. These results indicate no apparent pancreatic or renal abnormalities or acid–base disturbances.

FIGURE 1 X Ray(s) Erect Abdomen (a–c): Day 1, 6, and 14 showing air fluid levels respectively.
FIGURE 1 X Ray(s) Erect Abdomen (a–c): Day 1, 6, and 14 showing air fluid levels respectively.

As there was no mechanical cause of obstruction, surgery team came up with diagnosis of Uremic Ileus. Patient was resuscitated with intravenous fluids in emergency department. Nasogastric (NG) tube was passed for decompression of stomach. She was depotashed with calcium gluconate, dextrose water and insulin. Patient was admitted in high dependency unit (HDU). As per nephrologist consultation, hemodialysis was initiated and total 5 sessions of HD were done during 2 weeks hospital stay. Trend of creatinine and serum electrolytes during hospital stay was given in Table 1 .

TABLE 1
Routine biochemistry trend during hospital stay.

ParameterDay 1Day 2Day 3Day 4Day 5Day 6Day 7
Hemoglobin (g/dL)10.610.8111111.11111.2
Total leucocyte count× 10 3 /μL8.68.377777
Serum sodium (mmol/L)146140142140138137139
Serum potassium (mmol/L)5.75.454.74.44.13.8
Creatinine (mg/dL)161310742.31.7
Urea (mg/dL)1341149574553617

Results and Conclusions (Outcome and Follow‐up)

Patient symptoms were relieved, NG was removed and oral intake was encouraged. Patient was discharged after 17 days stay in hospital and asked to follow up in nephrology clinic.

Discussion

Diagnosing the exact cause of ileus can be challenging, as the condition may occur in association with diverse disorders or in the postoperative setting. Most studies have focused primarily on postoperative ileus, but this represents only one subset of the condition [ 1 ]. Various interventions have been explored to prevent or shorten the duration of ileus, yet randomized controlled trials (RCTs) have shown limited or inconsistent benefits. Consequently, paralytic ileus remains a burdensome problem, both economically and clinically, with significant distress to patients and healthcare providers. Importantly, there is insufficient epidemiological data on the prevalence and severity of paralytic ileus related to uremia secondary to chronic renal disease, making recognition and reporting of such cases important.

In our case clinical and imaging findings were consistent with the paralytic ileus. The usual risk factors—recent surgery, medication use, or electrolyte imbalance—were systematically excluded, in line with the approach described by Shantanu et al. [ 1 ]. Normal leukocyte count ruled out the possibility of infection. The key to reaching the correct diagnosis was the ultrasonographic evidence of atrophic kidneys with hydronephrosis, combined with biochemical evidence of severe renal dysfunction—markedly elevated creatinine and potassium levels. The resolution of ileus following hemodialysis further confirmed uremia as the underlying cause.

In this case, Ogilvie syndrome—also known as acute colonic pseudo‐obstruction—was an important differential diagnosis. Previous reports by Carissa et al. [ 4 ] and Costantino et al. [ 7 ] described patients presenting predominantly with colonic dilatation and marked abdominal distension, confirmed by CT imaging. In contrast, our patient's imaging showed dilatation restricted to the small intestine, with no colonic involvement. Moreover, the concurrent findings of atrophic kidneys and biochemical evidence of uremia strongly supported a systemic cause, rather than a localized pseudo‐obstructive process. This distinction was crucial, as the management pathways for the two conditions differ significantly. Ogilvie syndrome is generally managed conservatively with bowel rest, fluid resuscitation, and in refractory cases, pharmacological or surgical intervention [ 4 , 7 ]. By contrast, uremic ileus requires correction of the underlying metabolic disturbance, with prompt initiation of hemodialysis serving as the definitive therapy.

Several clinical reports reinforce that paralytic ileus can be triggered by systemic illness, not just surgical insult. Carraro et al. described cases in pediatric onco‐hematology patients' post‐chemotherapy, while Yusrie et al. reported ileus associated with pneumonia—both illustrating non‐surgical precipitants [ 9 , 10 ]. Metabolic causes have also been documented: hypercalcemic crises from multiple myeloma [ 11 ] and severe hypothyroidism complicated by acute kidney injury [ 12 ] both led to paralytic ileus, which resolved after correcting the metabolic derangement. In all these instances, bowel function recovered once the metabolic abnormality was corrected—mirroring our patient's improvement following dialysis. This shows that ileus is not a purely mechanical disorder but also reflects complex neuro‐immune interactions, which may similarly operate in uremic states [ 13 ].

This case therefore highlights the importance of considering uremia as an underrecognized cause of paralytic ileus, particularly in patients without recent surgery, medication exposure, or infection. Clinicians should remain alert to this possibility, as timely recognition and treatment with hemodialysis can lead to rapid symptom resolution and prevent unnecessary invasive interventions.

Conclusion

The imperative to consider uremic paralytic ileus in patients presenting with abdominal pain, vomiting, and constipation stems from the recognition that this condition constitutes a rare yet potentially life‐threatening complication of untreated uremia. This case report's proof of the temporal association between the start of hemodialysis and the ensuing improvement of symptoms emphasizes how crucial early detection and treatment are. If other diagnoses are not ruled out, therapy may be delayed or insufficient, which may increase patient morbidity and death.

Author Contributions

Muhammad Husnain Ahmad: conceptualization, data curation, writing – original draft, writing – review and editing. Ali Gohar: conceptualization, data curation, writing – original draft. Abdur Rehman: conceptualization, data curation, writing – original draft, writing – review and editing. Abdul Rehman: conceptualization, data curation. Maryam Ilyas: conceptualization, data curation, writing – original draft. Muhammad Bilal: conceptualization, data curation, writing – original draft, writing – review and editing. Hafiza Iman: conceptualization, data curation, writing – original draft, writing – review and editing. Masab Ali: conceptualization, visualization.

Funding

The authors have nothing to report.

Ethics Statement

The authors have nothing to report.

Consent

A written informed consent was obtained from the patient based on the journal's policies.

Conflicts of Interest

The authors declare no conflicts of interest.

Acknowledgments

We would like to thank the team of clinicians who helped manage this case.

Gohar A., Rehman A., Ilyas M., et al., “Uremic Paralytic Ileus in a 70 Years Old Female: A Diagnostic Dilemma,” Clinical Case Reports 14, no. 2 (2026): e72018, 10.1002/ccr3.72018.

Data Availability Statement

Data and materials available upon request from corresponding author.

References

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4. Du C., Iftikhar N., Ganti L., and Smith‐Gonzalez A., “Acute Colonic Pseudo‐Obstruction: A Case of Ogilvie Syndrome,” Cureus 16, no. 2 (2024): e66038, 10.7759/cureus.66038.

5. Schwarz N. T., Beer‐Stolz D., Simmons R. L., and Bauer A. J., “Pathogenesis of Paralytic Ileus: Intestinal Manipulation Opens a Transient Pathway Between the Intestinal Lumen and the Leukocytic Infiltrate of the Jejunal Muscularis,” Annals of Surgery 235, no. 1 (2002): 31–40, 10.1097/00000658-200201000-00005.

6. Feinberg M., “The Problems of Anticholinergic Adverse Effects in Older Patients,” Drugs & Aging 3, no. 4 (1993): 335–348, 10.2165/00002512-199303040-00004.

7. Caroselli C., Soardi G. A., Zaccaria E., and Bruno G., “Acute Colonic Pseudo‐Obstruction: A Syndrome due to Many Causes,” Internal and Emergency Medicine 16, no. 1 (2021): 161–165, 10.1007/s11739-019-02190-5.

8. Piao X., Ying G. W., Chaney M. J., Samuel S., Sharko A., and Zahra F., “Chronic Idiopathic Intestinal Pseudo‐Obstruction,” Cureus 13, no. 22 (2021): e16563, 10.7759/cureus.16563.

9. Carraro F., Rivetti E., Romano E., and Fagioli F., “Two Cases of Paralitic Ileus in Onco‐Hematologic Patients,” Pediatric Reports 4, no. 2 (2012): e3, 10.4081/pr.2012.e3.

10. Yusrie K. U., “Paralytic Ileus in a Vegetarian With Pneumonia Infection,” Indonesian Journal of Gastroenterology, Hepatology and Digestive Endoscopy 5, no. 3 (2004): 109–114.

11. Guo Y., He L., Liu Y., and Cao X., “A Rare Case Report of Multiple Myeloma Presenting With Paralytic Ileus and Type II Respiratory Failure due to Hypercalcemic Crisis,” Medicine 96, no. 52 (2017): e9215.

12. Rodrigo C., Gamakaranage C. S., Epa D. S., Gnanathasan A., and Rajapakse S., “Hypothyroidism Causing Paralytic Ileus and Acute Kidney Injury‐Case Report,” Thyroid Research 4, no. 1 (2011): 7, 10.1186/1756-6614-4-7.

13. Beach E. C. and De Jesus O., “Ileus,” in StatPearls (StatPearls Publishing, 2025), https://www.ncbi.nlm.nih.gov/books/NBK558937 .

Associated Data

Data Availability Statement

Data and materials available upon request from corresponding author.

ИП Урсолов Владлен Сергеевич

ИНН 500118482352 · ОГРНИП 314500117700049

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