Incarcerated or strangulated prolapsed rectal polyps are an incredibly rare phenomenon, seldom reported in the literature. Given the overall low incidence of rectal prolapse, these instances in which polyposis - a relatively common condition - progress and become emergent are clinically significant. We present a case of a 49-year-old with an acutely incarcerated rectal prolapse of dysplastic villous adenomatous polypoid tissue. The patient presented to our facility with a large, painful rectal mass, passing mucus and bright red blood per rectum after two hours of straining to have a bowel movement. She denied past colonoscopies, anal receptive intercourse, and any personal or family history of bowel disease or cancer. On computed tomography (CT) scans, the incarcerated mass appeared as a full-thickness rectal prolapse with signs of edema and ischemia, prompting emergent surgical intervention. A diagnostic laparoscopy showed no pathology to the large bowel or rectum. The prolapsed mucosal mass was circumferentially resected, and the rectum was reduced. A temporary diverting loop sigmoid colostomy was then created. Surgical pathology reported villous adenoma, extensive high-grade dysplasia, and foci of pseudo-invasion with no evidence of invasive carcinoma. A follow-up rectal exam under anesthesia and flexible sigmoidoscopy identified multiple large rectal polyps but no evidence of rectal ischemia. The patient had an uneventful postoperative course and was discharged home on hospital day 11 for outpatient follow-up with Colorectal Surgery. Abdominal perineal resection versus transanal transabdominal rectal resection, preserving gastrointestinal continuity, have been offered as options for definitive treatment. Rectal prolapse can be predisposed to occur in the setting of a variety of clinical conditions. Management of prolapses can be complex. In the setting of these rare incarcerated or strangulated prolapsed dysplastic polyps, emergent surgical intervention is still indicated.

Tuberculous meningitis (TBM) is the most severe form of central nervous system (CNS) tuberculosis and carries significant morbidity, particularly when diagnosis is delayed. Cranial nerve involvement is a recognized complication, most frequently affecting the abducens nerve (CN VI); bilateral oculomotor nerve (CN III) palsy, however, is exceedingly rare and typically signifies pathology at the level of the midbrain. The oculomotor nerve originates from paired nuclei in the midbrain tegmentum at the level of the superior colliculus; any compressive or inflammatory lesion at this site can produce bilateral CN III deficits. We report a 70-year-old man with type 2 diabetes mellitus presenting with subacute fever, headache, and altered sensorium, who subsequently developed bilateral ptosis with ophthalmoplegia. The brain MRI demonstrated multiple disseminated tuberculomas with a focal midbrain lesion at the oculomotor nuclear-fascicular complex and communicating hydrocephalus. This case highlights an uncommon neuro-ophthalmological manifestation of TBM and emphasizes the critical role of early clinico-radiological correlation in diagnosis and management.

Pleomorphic adenoma of the lacrimal gland is a benign epithelial neoplasm and can rarely undergo cystic degeneration, mimicking other conditions with similar radiological findings. It commonly presents as a slow growing, painless mass in the outer upper eyelid, characterised by exophthalmos, ptosis, diplopia and reduced ocular movements. Here, we present one such case of a male in his mid-30s presenting with a painless, progressive fullness in the left upper eyelid with mild proptosis and restricted ocular movements which was initially suspected to be due to an underlying dermoid cyst owing to the cystic nature of the lesion on imaging. Surgical intervention involving complete excision was preferred, rendering no recurrence on follow-up. Histopathological examination however revealed microscopic features suggestive of a pleomorphic adenoma with cystic changes contrary to the initial diagnosis of a dermoid cyst. This case highlights the challenges faced in arriving at the right diagnosis with successful treatment outcomes.

Recurrent urinary tract infection (UTI) is defined as two or more UTIs within 6 months or three or more within 1 year. The annual recurrence rate of UTI in women is approximately 14% to 25%. Risk factors for recurrent UTI include antimicrobial exposures, more frequent sexual activity, use of spermicidal agents or diaphragms, peri- or postmenopausal status, personal hygiene practices, urinary stasis from incomplete bladder emptying, pelvic organ prolapse, and voiding dysfunction. When women present with recurrent UTI symptoms, urinalysis and urine culture should be obtained. Management guidelines recommend empiric treatment with a first-line antibiotic based on prior culture results, then changing the antibiotic if the new culture shows resistance, or waiting for culture results before selecting an antibiotic. Longer duration of therapy does not reduce the risk of recurrent UTI. Asymptomatic bacteriuria should not be treated, except in patients who are pregnant or undergoing invasive urologic procedures. Prevention of recurrent UTI begins with behavioral modification and hygienic practices. The next step is prescription of antibiotic prophylaxis with shared decision-making. Nonantibiotic methods are also used to prevent recurrent UTI, and evidence of their effectiveness varies. These methods include use of cranberry products, Lactobacillus probiotics, vaginal estrogen, methenamine supplements.