Ogilvie syndrome caused by varicella zoster virus: A case report

Abstract

Ogilvie syndrome consists of dilatation of part or all of the colon and rectum without intrinsic obstruction or extrinsic inflammatory process. This disease has not yet been completely elucidated, but appears to be multifactorial.¹ Altered extrinsic regulation of colonic function by the sympathetic and parasympathetic nervous systems is the most commonly suggested mechanism for Ogilvie syndrome.² The relationship between varicella zoster virus (VZV) infection and the development of Ogilvie syndrome remains a rare, but clinically significant, phenomenon. VZV's impact on the autonomic nervous system is central to the development of Ogilvie syndrome, with neurogenic involvement being a primary mechanism.³ Older adults are at high risk of this disease, and the symptoms might be atypical. This paper reports a 95-year-old male patient with Ogilvie syndrome after VZV infection.

The patient, a 95-year-old man, complained of “skin rash on the back for 12 days with abdominal pain for 5 days”. Twelve days earlier, the rash appeared on the right waist and abdomen, with a flaky red rash and protruding skin surface, accompanied by itching, pain and a burning sensation. He was diagnosed with herpes zoster, and was given ganciclovir orally and fusidic acid externally. Five days earlier, abdominal pain was manifested as jumping pain in the right upper abdomen, accompanied by abdominal distension in the middle and lower abdomen, and flatulence and defecation stopped. Three days earlier, the patient went to a nearby community hospital and was diagnosed with bowel obstruction. He was given fasting, rehydration and enema therapy, and abdominal symptoms were lightly relieved. Then, the patient was admitted to our department and denied a history of chronic diseases of the digestive system. He had a red rash and blisters on the right abdomen and back, some of which were shrinking and tender (see Fig. 1a), and abdominal physical examination suggested abdominal distension. There were no obvious abnormalities in laboratory tests. Abdominal and pelvic computed tomography showed that the sigmoid colon was long and locally went to the right upper abdomen with local wall thickening, and the upper lumen expanded with accumulated gas (see Fig. 1c). Colonoscopy showed poor intestinal preparation, but all intestinal segments were unobstructed, and no obvious abnormality was found in the mucosa (see Fig. 1d).

Combined with clinical symptoms and imaging examination, both computed tomography and colonoscopy excluded the causes of mechanical intestinal obstruction, so it was considered that the patient had a high probability of pseudo-obstruction. Considering the history of herpes zoster before abdominal symptoms, and T8–12 dermatomes involved, the final diagnosis was Ogilvie syndrome caused by VZV infection, and we confirmed our diagnosis again through literature retrieval.⁴ The patient was given fasting and rehydration, oral administration of probiotics to regulate intestinal flora, trimebutine maleate to improve intestinal motility, glycerine enema to assist defecation, and acupuncture and electrical stimulation to improve intestinal peristalsis. After approximately 3 days of treatment, the patient's spontaneous defecation and flatulence significantly increased compared with before treatment. Because the patient was older and had no discomfort, he refused to undergo repeat computed tomography. At the time of discharge, the rash decreased and gradually turned into old lesions (see Fig. 1b). Within 1 year after discharge, we followed up the patient many times, and he had normal defecation and flatulence, and no intestinal obstruction occurred again.

Ogilvie syndrome was first described in 1948, and refers to massive dilation of the colon without underlying mechanical obstruction or other organic cause.⁵ Typical signs and symptoms include abdominal pain, nausea, vomiting, abdominal distension, altered bowel function, and dilation of the ascending and transverse colon without evidence of mechanical obstruction on imaging. Older patients seem to be at greatest risk. Other risk factors include recent cardiac events, electrolyte abnormalities, certain medications (opioids, anticholinergics, phenothiazines, benzodiazepines, calcium channel blockers, chemotherapeutic agents and antiparkinsonian agents), infection (cytomegalovirus, herpes zoster, tuberculosis), significant underlying medical illness, neurologic diseases and postoperative patients.⁶

Although the precise underlying mechanism is unknown, it is believed to involve viral infection at the spinal cord’ s anterior horn level as a result of the VZV spreading from the dorsal root ganglia to the brain. Pathologically, ganglion lesions, along with significant neuritis and degeneration of the motor and sensory roots, might account for the disease's electrophysiological findings.⁷ The virus in the neuronal plexus and muscularis propria also can cause muscle injury directly leading to pseudo-obstruction.

In the absence of fever, leukocytosis, abdominal tenderness, free air or cecal diameter >12 cm, first-line therapy for patients with Ogilvie syndrome includes correction of serum electrolyte abnormalities, fluid resuscitation, avoidance or minimization of narcotics, avoidance of anticholinergic medications (e.g., oxybutynin or benztropine) and bowel rest.⁸ Surgical treatment is considered a last resort. Patients with Ogilvie syndrome who undergo surgery are particularly prone to postoperative complications, so deciding when to intervene surgically in Ogilvie syndrome can be challenging.⁹

In conclusion, although Ogilvie' syndrome caused by VZV is rare, older adults are susceptible to the disease. Geriatric medical staff should improve their understanding of the disease.

This research was funded by Beijing Natural Science Foundation (7242152) and the Peking University Health Science Center International Institute of Comprehensive Health (JKCJ202102).

The authors declare no conflict of interest.

Written informed consent was obtained from the patient for publication of this case report.