This systematic review explores the association between herpes zoster (HZ) infection and Ogilvie's syndrome (acute colonic pseudo-obstruction), evaluating how varicella-zoster virus (VZV) reactivation may contribute to autonomic dysfunction leading to intestinal obstruction. A comprehensive search was conducted in PubMed, Scopus, and Cochrane Library databases up to October 2024, in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Eligible studies included case reports, clinical images, and letters reporting Ogilvie's syndrome secondary to HZ or VZV infection. After screening 219 publications and additional grey literature, 27 studies describing 28 cases met the inclusion criteria. Data were extracted on patient demographics, clinical manifestations, diagnostic methods, and outcomes. The quality of studies was assessed using the Joanna Briggs Institute critical appraisal checklist. The results from 27 studies encompassing 28 patients with intestinal pseudo-obstruction secondary to VZV or HZ infection indicated a mean age of 60 years, predominantly affecting males (71.5%). Notably, 47.6% had underlying immunosuppressive conditions. The primary clinical manifestations included abdominal distention and severe constipation. Most patients (93%) exhibited a herpetiform rash, primarily in thoracic dermatomes. Symptoms of pseudo-obstruction often preceded the rash (58%), and imaging in the vast majority revealed colonic distension with no intra-abdominal pathology. Treatment focused on conservative management of both pseudo-obstruction and HZ symptoms, with 93% of patients achieving full recovery, while the mortality rate was identified at 7%. The findings suggest that HZ-induced Ogilvie's syndrome may be an underdiagnosed condition, requiring a high index of suspicion, particularly in immunocompromised patients. Early recognition and conservative treatment can prevent unnecessary surgical interventions. Further studies are needed to clarify the pathophysiological mechanisms linking VZV reactivation to colonic pseudo-obstruction.

Herpes zoster (HZ) infection occurs in approximately 10% to 30% of individuals. Visceral neuropathies secondary to HZ can cause cystitis and urinary retention. But colonic pseudo-obstruction can also occur. Peripheral neuropathy may reveal segmental motor paresis of either upper or lower limbs, the abdominal muscles or the diaphragm. We report the case of a 62-year-old male patient who presented with abdominal distention and cutaneous vesicular eruption on the left side of the abdominal wall. Plain X-rays and computed tomography scan showed distended small bowel. A diagnosis of intestinal pseudo-obstruction was made secondary to segmental paresis of the small intestine and visceral neuropathy. Conservative management was successful and the patient was discharged uneventfully. Intestinal pseudo-obstruction ought to be considered when dealing with non-obstructive (adynamic) conditions of the digestive tract associated with HZ infection; since early recognition may help to avoid unnecessary surgery.

To critically review the literature addressing the definition, epidemiology, aetiology and pathophysiology of acute colonic pseudo-obstruction (ACPO).

A systematic search was performed to identify articles investigating the aetiology and pathophysiology of ACPO. A narrative synthesis of the evidence was undertaken.

No consistent approach to the definition or reporting of ACPO has been developed, which has led to overlapping investigation with other conditions. A vast array of risk factors has been identified, supporting a multifactorial aetiology. The pathophysiological mechanisms remain unclear, but are likely related to altered autonomic regulation of colonic motility, in the setting of other predisposing factors.

Future research should aim to establish a clear and consistent definition of ACPO, and elucidate the pathophysiological mechanisms leading to altered colonic function. An improved understanding of the aetiology of ACPO may facilitate the development of targeted strategies for its prevention and treatment.

The very unusual association between herpes zoster and Ogilvie syndrome has received scant attention in the published literature.

This review discusses the published experience since 1950 and attempts to increase clinical awareness about the co-existence of both conditions.

An 84-year-old male patient affected by herpes zoster presented with advanced acute colonic pseudo-obstruction and was successfully treated with colonic diversion.

Twenty published studies (1950-2008) of 28 patients in whom the two conditions co-existed are reviewed. The review included 22 male and 7 female patients (24%) aged 32-87 years (mean, 61 years). Significant co-morbidities were present in 45% of the patients. The majority of patients were observed and treated conservatively (83%). Two patients died (7%), both suffering from respiratory complications and malignancy.

Recognition of the combined syndrome may help to avoid unnecessary surgery. Laparotomy should be reserved as a last resort for when the obstruction cannot be successfully managed by endoscopy. A diverting colostomy can be used to monitor the blood supply and thus provide early warning for an impending abdominal catastrophe.

Gastrointestinal symptomatology as a complication of herpes zoster (HZ) is extremely rare, with the majority of reported cases showing only temporal or radiological evidence of GI tract involvement by varicella zoster virus (VZV) infection. We present the first case of documented direct VZV infection in the muscularis propria of the gut presenting as intestinal pseudo-obstruction (Ogilvie's syndrome). The patient was a 34-yr-old HIV+ man who developed small bowel pseudo-obstruction in association with disseminated cutaneous HZ. A partial ileocolectomy specimen demonstrated a focal ulcer in the terminal ileum. Immunohistochemistry against VZV gpI demonstrated diffuse staining of the muscularis propria and myenteric plexi throughout the length of the specimen. Viral particles consistent with Herpesviridae were shown to be present ultrastructurally. We postulate that the viral infection in the neuronal plexi and muscularis propria caused muscle injury leading to pseudo-obstruction.

Gastrointestinal motility is the function of gastrointestinal smooth muscle. It is controlled by both the intrinsic and extrinsic nerves of the gastrointestinal tract and, to a lesser degree, the gastrointestinal hormones. Therefore, any abnormality of the above factors, theoretically, can cause gastrointestinal dysmotility. In a clinical situation, commonly seen is gastrointestinal dysmotility caused by either smooth muscle or intrinsic and extrinsic nerves dysfunction. Diseases that cause smooth muscle dysfunction include familial visceral myopathies, nonfamilial visceral myopathies, collagen disease, muscular dystrophies, amyloidosis, thyroid disease, and so on. Diseases that cause enteric nerve dysfunction include familial visceral neuropathies, nonfamilial visceral neuropathies, diabetes mellitus, Chagas' disease, ganglioneuromatosis of the intestine, visceral neuropathy of carcinomatosis, Parkinson's disease, and so on. The patients with neuromuscular disease of the gastrointestinal tract have a wide range of clinical manifestations regardless of the underlying cause. At one end of the spectrum, the patients may be asymptomatic, and at the other end of the spectrum, the patients may have functional obstruction of the gastrointestinal tract. Plain abdominal x-rays, upper gastrointestinal (UGI) and small bowel x-rays, enteroclysis, barium enema, and manometric studies are useful for the work-up of these patients. Enteroclysis is especially helpful in ruling out mechanical obstruction of the small intestine in patients with chronic intestinal pseudo-obstruction. Treatment is mainly symptomatic and supportive. There is no effective drug to improve gastrointestinal motility. Surgery may be helpful in selected cases of severe gastrointestinal dysmotility.

Herpes zoster is a cutaneous vesicular eruption resulting from recrudescence of the chickenpox virus. It is mainly a disease of adults, with a predisposition for the elderly or immunocompromised. Although usually localized, the disease can disseminate to visceral organs. Diagnosis is often made based on the characteristic pattern of the lesion and clinical features. Tzanck smear, viral isolation, seroconversion, antibody titers, and monoclonal antibodies may further aid or confirm the diagnosis. Clinical features of herpes zoster may follow a progression through 3 stages, prodromal, acute, and chronic. The prodromal and acute phases seldom require more than symptomatic management. The chronic pain syndrome, postherpetic neuralgia (PHN), demands a more aggressive approach. Pharmacologic intervention, neuroaugmentation, and/or surgery may prevent or alleviate PHN, but universal response to any of these therapeutic approaches is unlikely. Tricyclic antidepressants remain the first choice in treating this pain syndrome. A trial of antiviral therapy may be warranted in patients with disseminated disease or in immunocompromised patients with localized disease. Of the antiviral agents, acyclovir is considered the drug of choice by most clinicians.

We report a patient who developed delayed gastric emptying with vomiting and weight loss simultaneously with herpes zoster in the sixth right thoracic dermatome. Sequential radionuclide solid egg meal gastric emptying studies were used to document gastroparesis, the response to metoclopramide and its transient nature. We present a possible explanation for this phenomenon within the context of the known pathophysiology of varicella-zoster infection.

The vast majority of the more than 300,000 annual cases of herpes zoster in the United States occur among healthy, immunocompetent persons. Most patients recover from reactivated varicella-zoster infection, but some experience complications. The most common of these is postherpetic neuralgia, but other neurologic as well as ocular and dermatologic complications can occur as well. Zoster during pregnancy is not of serious concern. Ongoing trials of antiviral agents are aimed at resolving the infection quickly and decreasing the incidence and severity of postherpetic neuralgia.

This study analyzes 400 cases of acute pseudo-obstruction of the colon (Ogilvie's syndrome). Seven cases were reported at St. Elizabeth Hospital Medical Center between October 1982 and February 1985; 393 cases were reported in the literature from 1970-1985. Ogilvie's syndrome is most commonly reported in patients in the sixth decade, and is more predominant in men. It is caused by an unknown disturbance to the autonomic innervation of the distal colon, and is associated with different conditions. Plain abdominal roentgenogram is the most useful diagnostic test. If the cecal diameter is 12 cm or greater, or conservative management is unsuccessful, colonoscopic or operative decompression is needed. The mode of treatment, age, cecal diameter, delay in decompression, and status of the bowel significantly influence the mortality rate, which is approximately 15 percent with early appropriate management, compared with 36 to 44 percent in perforated or ischemic bowel.