Fecalomas are masses of hardened stool that are typically impacted in the sigmoid colon and rectum. Fecalomas are commonly associated with chronic constipation, Hirschsprung's disease, Chagas disease, and multiple psychiatric conditions. We present a case of a giant fecaloma resulting in complete large bowel obstruction and suggest a five-year abdominal ultrasound monitoring of adults presenting with chronic constipation and/or chronic nonspecific gastrointestinal (GI) complaints.

INTRODUCTION: “Flood syndrome,” also known as spontaneous umbilical hernia rupture, is a rare complication of end-stage liver disease and persistent ascites. We present a case of a patient who developed Flood syndrome prompting emergent surgical management. CASE DESCRIPTION/METHODS: A 63-year-old man with cryptogenic cirrhosis and ascites presented with worsening diffuse abdominal pain. Physical exam revealed a massively distended abdomen with generalized tenderness and a large umbilical hernia (UH) with ulceration of the overlying skin. Abdominal CT scan revealed large, loculated, abdominopelvic ascites with a large ventral hernia containing ascites (Figure 1). Despite undergoing two large-volume therapeutic paracentesis, he experienced spontaneous rupture of an ulcerated UH while attempting to defecate during this hospitalization. Likely greater than 10 L of ascitic fluid poured out leading to hypotension and prompt emergent exploratory laparotomy with repair of the defect in the abdominal wall. DISCUSSION: UH is seen in up to 20% of patients with cirrhosis and persistent ascites [1]. It is the result of the chronically weakened state of the abdominal wall surrounding the umbilicus in the setting of increased intra-abdominal pressure. Flood syndrome can occur when the tense pressure of ascites leads to spontaneous rupture of an umbilical hernia site with drainage of a large volume of ascitic fluid. It is a serious condition, with a mortality of over 60%. Rupture of an umbilical hernia site in Flood syndrome can be provoked by vomiting, coughing, or straining with defecation. In Flood syndrome, treatment begins with fluid resuscitation and antibiotics to prevent infection. Once stable, emergent surgical repair of the abdominal wall defect is essential. Non-surgical management is not advised and is associated with higher mortality. To prevent complications and improve mortality, these patients should be treated immediately with surgical intervention [2].

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INTRODUCTION: GI investigation of pts with A-IDA typically begins with both upper (U) and lower (L) GI endoscopy. Guidelines tend to recommend bidirectional endoscopy (BDE) sequencing based on age stratification, or starting with LGI endoscopy. The aim of this study was to determine the most efficient BDE sequence among patients with A-IDA by investigating the relative frequencies of identified associated sources of bleeding by UGI or LGI endoscopy. METHODS: We performed a retrospective chart review of clinical characteristics of pts ≥18 yrs who had BDE performed within 6 months of A-IDA diagnosis between the yrs 2014-2019. Pts were excluded if they had GI tract surgery within 10 yrs, active pregnancy, active GI bleeding, an obvious site of non-GI blood loss or ferritin >100. McNemar's test was used to compare frequency of lesions identified across the general population and stratified for age < 50 and >50 yrs. Bivariate analyses of characteristics associated with UGI and LGI lesions were performed using t-test, Chi-squared test, or Fisher's exact test. Multivariate logistic regression estimated odds ratios. RESULTS: 497 pts were available for analysis (65% female, mean age 63 yrs; Table 1). BDE found IDA-associated lesions in 307 (61.8%) pts comprising 196 (39.4%) exclusively UGI lesions, 66 (13.3%) exclusively LGI lesions, and 45 (9.1%) both UGI and LGI lesions. In our cohort, UGI lesions were more common than LGI lesions [241 (48.5%) vs 111 (22.3%); P < 0.001], regardless of age (P < 0.001) (Table 1). Protective variables against an LGI lesion included female sex [OR 0.51 (0.32-0.86); P = 0.01], BMI [OR 0.96 (0.93-0.99) per unit inc.; P = 0.01] and Hgb [OR 0.88 (0.78-0.98) per unit inc.; P = 0.03]. CKD was associated with LGI lesions [OR 1.99 (1.12-3.48); P = 0.02]. Hgb was higher in pts with only UGI than only LGI lesions (9.4±1.6 vs 8.5±1.5; P = 0.001). PPI use predicted absence of identifiable lesions [OR 0.66 (0.45-0.96); P = 0.03]. The most common UGI lesions were H. pylori-associated (HP-A) gastritis (24.2%) and peptic ulcer disease (17.6%) (Figure 1a). The most common LGI lesions were large polyps (37.7%) and colon CA (16.2%) (Figure 1b). CONCLUSION: Our results indicate 1) pts with A-IDA are more likely to have an UGI than LGI source; thus starting with UGI endoscopy may be prudent; 2) women are less likely to have a LGI source of A-IDA than men; 3) low BMI, low Hgb and CKD predict a LGI source of A-IDA. 4) HP-A UGI lesions account for a significant portion of A-IDA; 5) PPI use predicts the absence of lesions.

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