Acute Colonic Pseudo-Obstruction (Ogilvie’s Syndrome) in a Patient with Decompensated Liver Cirrhosis Secondary to Chronic Hepatitis B

Introduction

Acute colonic pseudo-obstruction, also known as Ogilvie’s syndrome, is characterized by acute dilatation of the colon in the absence of a mechanical obstruction.¹ It is associated with various clinical settings, including electrolyte imbalances, major surgery, severe illness, and chronic comorbidities. In Uganda, particularly West Nile region, the region is currently battling with complications of Chronic Hepatitis B infection such as Liver cirrhosis. According to Rugaatwa et al West Nile region has 3.8% prevalence of Hepatitis B.² Prompt recognition and management are crucial to prevent complications such as bowel ischemia or perforation.

While current guidelines emphasize a stepwise approach, that is, starting with conservative management and escalating only as needed, patients with advanced liver disease present unique challenges due to their increased vulnerability to complications. This case is unique in demonstrating that, with vigilant monitoring and correction of reversible factors, conservative management can be effective even in patients with multiple comorbidities, thereby avoiding the risks associated with pharmacologic or surgical interventions.

According to unpublished internal medicine ward data at Yumbe Regional Referral Hospital, we found that there were 32 number of patients admitted with a diagnosis of decompensated Liver cirrhosis out of 178 patients admitted within a period of May 2025 to July 2025 (unpublished Hospital Data). We had only one case of Ogilvie’s syndrome in that period which is being reported.at our Hospital, Ogilvie’s not a common diagnosis and thus warranted reporting.

We present a case of Ogilvie’s Syndrome in a 65-year-old male with known Hepatitis B to highlight the role of expectant management and early intervention in improving outcomes in patients with multiple comorbidities.

Methodology

This case report was prepared following the CARE (CAse REport) guidelines to ensure comprehensive and transparent reporting. The patient was selected based on the presentation of acute colonic pseudo-obstruction (Ogilvie’s syndrome) in the context of decompensated liver cirrhosis secondary to chronic hepatitis B.

Patient Selection and Data Collection

• A 65-year-old male referred from a peripheral health center with a two-week history of progressive abdominal distention and a known history of chronic hepatitis B and liver cirrhosis.
• Clinical data were collected prospectively during the patient’s hospital admission, including history, physical examination findings, laboratory investigations, imaging studies, and details of management and clinical course.

Diagnostic Assessment

• Ogilvie syndrome is diagnosed in patients with acute abdominal distension and a tympanitic, dilated abdomen in whom mechanical obstruction is excluded by radiological investigations such as abdominal X-ray and complications (ischemia, perforation, peritonitis) are assessed. Laboratory tests (CBC, electrolytes, lactate, and TSH) may show leukocytosis or common metabolic abnormalities (especially hypokalemia, hypocalcemia, hypomagnesemia) but are not Sdiagnostic.³ Diagnosis is confirmed by abdominal CT showing proximal colonic dilatation often with a transitional zone near the splenic flexure without a structural obstructing lesion; contrast enema may be used if CT is unavailable and there is no peritonitis.³ Differential diagnoses include mechanical obstruction and toxic megacolon.
• Diagnosis was established based on clinical presentation, laboratory findings (including electrolyte disturbances), and imaging (abdominal X-ray and ultrasound) to rule out mechanical obstruction and confirm colonic dilation.
• Relevant laboratory parameters (eg, potassium, liver function tests, renal function, and complete blood count) and imaging results were documented.

Management Approach

• The patient was managed according to the current clinical guidelines for ACPO, with initial conservative measures including bowel rest, intravenous fluids, correction of electrolyte imbalances, and discontinuation of potentially offending medications.
• Pharmacological and supportive therapies were administered as indicated, and the patient’s response to treatment was closely monitored.

Outcome Documentation

• The patient’s clinical progress, resolution of symptoms, and discharge status were recorded.
• Follow-up recommendations and patient education were provided at discharge.

Case Presentation

Patient Information

A 65-year-old male with a known history of chronic Hepatitis B was referred to us from a peripheral health center. The patient presented with a two-week history of progressive abdominal distention. His surgical history included an exploratory laparotomy for intestinal obstruction four years prior, although the details were unavailable. He had no history of blood transfusions, fractures, smoking, alcohol intake, or allergies.

Clinical Findings

The patient reported progressive abdominal swelling associated with dull, generalized abdominal pain, which was relieved by lying flat and worsened while sitting. Four days prior to admission, the patient experienced loss of appetite. Two days before admission, he developed non-projectile, non-bilious vomiting, which became dark-colored on the second day. He denied dysphagia, odynophagia, per rectal bleeding, and reported normal bowel and urinary habits. There was no history of fever or convulsions. Review of other systems was unremarkable.

On examination, he appeared ill but was afebrile (37.1°C), not in respiratory distress, and had no jaundice, pallor, cyanosis, or lymphadenopathy. Notably, he had bilateral pitting edema. Abdominal examination revealed moderate distention, movement with respiration, bulging flanks, and a sub-umbilical midline incision scar. There was no tenderness, and bowel sounds were normal. Cardiovascular and respiratory examinations were unremarkable, except for mild bilateral pitting edema. Neurologically, he was drowsy but alert, with normal tone, reduced muscle bulk, normal reflexes, and a positive asterixis.

Diagnostic Assessment

Initial laboratory investigations revealed:

• Neutrophilia (9 × 10³/μL; normal: 1.5–7.0 × 10³/μL)
• Creatinine: 1.20 mg/dL (normal: 0.70–1.30)
• Urea: 27.9 mg/dL (normal: 10–50)
• Potassium: 3.50 mmol/L (normal: 3.60–5.40)
• Chloride: 100 mmol/L (normal: 90–108)
• AST: 25 U/L (normal: 0–40)
• ALT: 10 U/L (normal: 0–45)
• Albumin: 1.50 g/dL (normal: 3.50–5.30)
• Total proteins: 6.47 g/dL (normal: 6.60–8.70)
• Direct bilirubin: 0.46 mg/dL (normal: 0–0.20)
• Total bilirubin: 1.13 mg/dL (normal: 0.10–1.20)
• GGT: 50 U/L (normal: 0–55)

Abdominal ultrasound showed increased bowel gas and mild ascites. The liver was fibrosed, but gall bladder, spleen, pancreas, urinary bladder, and prostate appeared normal.

Clinical Course

The patient was initially managed with intravenous furosemide, ciprofloxacin, spironolactone, and lactulose. Three days after admission, he developed mild respiratory distress (oxygen saturation 92% on room air), gross abdominal distention, and positive fluid thrill. Four liters of peritoneal fluid were removed via paracentesis, resulting in symptomatic relief.

Subsequently, the patient developed constipation and non-bilious, non-projectile vomiting. Examination revealed moderate abdominal distention, tympanitic percussion, and increased bowel sounds. Repeat laboratory tests showed mild hypokalemia (potassium 3.39 mmol/L). Abdominal X-ray demonstrated normal bowel loops with two air-fluid levels and no evidence of perforation. Ultrasound confirmed increased bowel gas and mild ascites.

Diagnosis

A diagnosis of acute colonic pseudo-obstruction (Ogilvie’s syndrome) with mild hypokalemia was made in the context of decompensated liver cirrhosis and hepatic encephalopathy (grade II).

Management

The patient was kept nil per os, and managed with intravenous fluids (Ringer’s lactate, dextrose 10%), metronidazole, and metoclopramide. Oral erythromycin (500 mg twice daily for three days) was initiated, and dietary advice included potassium-rich foods (bananas) when he was allowed to resume oral food intake. The following day, the patient passed stool and reported no new complaints. He was monitored for three days and subsequently discharged with normal vital signs and resolution of asterixis. He was advised to avoid hepatotoxic drugs, consume plenty of greens, and attend regular outpatient follow-up.

Discussion

Ogilvie’s syndrome, or acute colonic pseudo-obstruction (ACPO), represents a rare but potentially life-threatening gastrointestinal emergency characterized by acute colonic dilatation in the absence of a mechanical obstruction. The syndrome predominantly affects elderly patients with multiple comorbidities, as exemplified by the present case of a 65-year-old male with decompensated liver cirrhosis secondary to chronic hepatitis B. The pathophysiology of Ogilvie’s syndrome is incompletely understood but is widely attributed to an imbalance in autonomic regulation of colonic motility, particularly a suppression of parasympathetic activity (S2–S4), resulting in colonic atony and progressive distension.⁴ This autonomic dysfunction may be precipitated by a variety of factors, including severe systemic illness, metabolic disturbances, recent surgery, trauma, or the use of medications such as opioids and anticholinergics (Underhill et al, 2021).

Risk factors for ACPO include advanced age, male sex, immobility, electrolyte disturbances (notably hypokalemia), and the presence of chronic comorbidities such as liver disease, cardiac disease, or infection.^5–7 A study by Rahman et al showed that individuals with chronic liver disease have a significant prevalence of electrolyte abnormalities, specifically, hypokalemia, hypernatremia and hypocalcaemia In patients with problems such as ascites and hepatic encephalopathy, these anomalies were more common and substantially correlated with the severity of liver dysfunction as assessed by the Child-Pugh classification. These findings show the relationship between liver cirrhosis and electrolyte imbalance which are important in the pathogenesis of Ogilvie’s syndrome.⁸ In patients with decompensated liver cirrhosis, acute colonic pseudo-obstruction (Ogilvie’s syndrome) appears to occur due to multiple interacting mechanisms. Portal hypertension leads to intestinal congestion and reduced bowel motility. Hypoalbuminemia contributes to bowel wall edema, further impairing peristalsis. Liver failure - related immune dysfunction promotes bacterial translocation and endotoxemia, which can depress intestinal motor activity. Additionally, common treatments in cirrhotic patients - such as diuretics and large-volume paracentesis - may cause electrolyte disturbances (especially hypokalemia), resulting in intestinal paralysis. Together, these factors disrupt autonomic regulation of the colon and predispose patients with advanced cirrhosis to reversible functional obstruction.⁹

In the current case, the patient’s decompensated liver cirrhosis and mild hypokalemia likely contributed to the development of ACPO. Hypokalemia, in particular, is both a risk factor and a potential consequence of ACPO, as colonic distension can lead to secretory diarrhea and further potassium loss, creating a vicious cycle that exacerbates colonic dysmotility.

The clinical presentation of Ogilvie’s syndrome is often insidious, with progressive abdominal distension, pain, nausea, vomiting, and constipation.⁶ Physical examination may reveal marked abdominal distension, tympanitic percussion, and variable bowel sounds, while laboratory findings frequently demonstrate electrolyte imbalances. Imaging, particularly abdominal radiography and computed tomography, is essential for diagnosis, revealing colonic dilation without evidence of mechanical obstruction.

Management of ACPO is guided by the severity of colonic distension, the presence of complications (such as ischemia or perforation), and the patient’s overall clinical status. ^5,10 Conservative management remains the cornerstone of initial therapy and includes bowel rest (nil per os), intravenous fluid resuscitation, correction of electrolyte imbalances, discontinuation of offending medications, and supportive care (Bernardi et al, 2015). In the present case, prompt correction of hypokalemia, supportive intravenous fluids, and careful monitoring led to clinical improvement and resolution of symptoms without the need for invasive intervention.

Pharmacologic therapy with acetylcholinesterase inhibitors, such as neostigmine^1,11, is indicated in patients who fail to respond to conservative measures within 48–72 hours or who exhibit progressive colonic dilation (typically cecal diameter >10–12 cm) without signs of perforation or peritonitis. Neostigmine has demonstrated high efficacy in inducing colonic decompression but requires close cardiac monitoring due to the risk of bradycardia. Recent literature also highlights emerging roles for agents such as pyridostigmine and prucalopride, though further studies are needed to establish their routine use.

Endoscopic decompression and, rarely, surgical intervention (eg, cecostomy or colectomy) are reserved for refractory cases or when complications such as ischemia or perforation develop.¹² The threshold for surgical intervention must be carefully weighed against the patient’s comorbidities and overall prognosis, as surgical morbidity and mortality are significant in this population (Alavi et al, 2021).

The prognosis of Ogilvie’s syndrome is closely linked to the timeliness of diagnosis and intervention.¹³ Mortality rates remain low in the absence of complications but increase substantially with the development of ischemia or perforation, which occur in up to 3% to 10% of patients (Alavi et al, 2021). Patients with significant comorbidities, such as advanced liver disease, are at heightened risk for adverse outcomes. In this context, early recognition and aggressive correction of reversible factors are paramount to improving outcomes (Soares et al, 2023).

In summary, this case underscores the importance of high clinical suspicion for ACPO in at-risk populations, particularly those with decompensated liver disease and electrolyte disturbances. Conservative management, with vigilant correction of underlying metabolic derangements and supportive care, is often effective and should be prioritized. Escalation to pharmacologic or invasive interventions should be reserved for refractory or complicated cases. Multidisciplinary collaboration and individualized patient assessment remain essential to optimizing outcomes in this complex and vulnerable patient population.

Limitations

This case report is subject to several important limitations. First, there is a degree of diagnostic uncertainty, as the clinical diagnosis of acute colonic pseudo-obstruction (Ogilvie’s syndrome) can be challenging in the absence of definitive imaging findings. The lack of definitive imaging, such as contrast-enhanced computed tomography or direct colonoscopic visualization, limits the ability to fully exclude mechanical obstruction or alternative diagnoses. In this patient with decompensated liver cirrhosis, abdominal distension could also be attributed to other causes, including severe ileus secondary to metabolic derangements, medication effects, or ascites-related bowel dysfunction. These factors underscore the need for a high index of suspicion and highlight the challenges in establishing a definitive diagnosis of ACPO in complex patients such as this. The investigations portray challenges typically faced at rural hospitals in Sub-Saharan Africa.

Conclusion

This case highlights the importance of early recognition and conservative management of acute colonic pseudo-obstruction in patients with decompensated liver cirrhosis and multiple comorbidities. Correction of underlying electrolyte disturbances and supportive care can lead to favorable outcomes.