Fitz-Hugh-Curtis Syndrome in a Male Patient.

We report the case of a 38-year-old Middle Eastern man with intractable right upper quadrant (RUQ) abdominal pain and several emergency department visits during the last seven years, with extensive and repeated radiologic and endoscopic workups proven negative for biliary or upper gastrointestinal disease. He presented to our outpatient surgical clinic in March 2023 complaining of worsening RUQ and epigastric pain and was scheduled for a robotic cholecystectomy for presumed biliary dyskinesia following a repeat cholescintigraphy (hepatobiliary iminodiacetic acid) scan. During a cholecystectomy, extensive bilobar perihepatic adhesions were found, indicative of Fitz-Hugh-Curtis syndrome (FHCS). A thorough lysis of adhesions was performed along with a wedge liver biopsy, with subsequent histological examination showing chronic cholecystitis, perihepatic mesothelial fibrosis with mild subcapsular hepatic steatosis, and no evidence of liver fibrosis. The patient was examined in the clinic two weeks after surgery with complete resolution of symptoms. This case highlights the importance of considering FHCS in the differential diagnosis of male patients presenting with refractory RUQ abdominal pain despite a negative workup. Early recognition and prompt treatment can prevent unnecessary extensive, repeat testing and delays in intervention in these patients.

Therapeutic distant organ effects of regional hypothermia during mesenteric ischemia-reperfusion injury.

INTRODUCTION: Mesenteric ischemia-reperfusion injury (IRI) leads to systemic inflammation and multiple organ failure in clinical and laboratory settings. We investigated the lung structural, functional, and genomic response to mesenteric IRI with and without regional intraischemic hypothermia (RIH) in rodents and hypothesized that RIH would protect the lung and preferentially modulate the distant organ transcriptome under these conditions. METHODS: Sprague-Dawley rats underwent sham laparotomy or superior mesenteric artery occlusion (SMAO) for 60 minutes with or without RIH. Gut temperature was maintained at 15°-20°C during SMAO, and systemic normothermia (37°C) was maintained throughout the study period. At 6 or 24 hours, lung tissue was collected for (1) histology, (2) myeloperoxidase activity, (3) bronchoalveolar lavage (BAL) fluid protein concentrations, (4) lung wet/dry ratios, and (5) total RNA isolation and hybridization to Illumina's Sentrix BeadChips (>22,000 probes) for gene expression profiling. Significantly affected genes (false discovery rate <5% and fold change ≥1.5) were linked to gene ontology (GO) terms using MAPPFinder, and hypothermia-suppressed genes were further analyzed with Pubmatrix. RESULTS: Mesenteric IRI-induced lung injury, as evidenced by leukocyte trafficking, alveolar hemorrhage, and increased BAL protein and wet/dry ratios, and activated a proinflammatory lung transcriptome compared with sham. In contrast, rats treated with RIH exhibited lung histology, BAL protein, and wet/dry ratios similar to sham. At 6 hours, GO analysis identified 232 hypothermia-suppressed genes related to inflammation, innate immune response, and cell adhesion, and 33 hypothermia-activated genes related to lipid and amine metabolism and defense response. Quantitative real-time polymerase chain reaction validated select array changes in top hypothermia-suppressed genes lipocalin-2 (lcn-2) and chemokine ligand 1 (CXCL-1), prominent genes associated with neutrophil activation and trafficking. CONCLUSIONS: Therapeutic hypothermia during SMAO provides distant organ protection and preferentially modulates the IRI-activated transcriptome in the rat lung. This study identifies potential novel diagnostic and therapeutic targets of mesenteric IRI and provides a platform for further mechanistic study of hypothermic protection at the cellular and subcellular level.

Deposition of albuterol aerosol generated by pneumatic nebulizer in the Sophia Anatomical Infant Nose-Throat (SAINT) model.

PURPOSE: To quantify distribution of albuterol aerosol generated by a pneumatic nebulizer within the nose and lungs of a model of a 9-month-old child (SAINT) and aerosol loss to the environment, during simulated breathing at increasing tidal volumes (TVs). METHODS: (99m)technetium-labeled albuterol aerosol was generated by an IPI nebulizer with face-mask. Deposition was quantified as a percentage of emitted dose using gamma scintigraphy. RESULTS: Lung deposition was similar for all TVs, averaging 7.17 +/- 0.01%, 9.34 +/- 0.01% and 9.41 +/- 0.02% at 50, 100 and 200 mL TV, respectively. In contrast, nose deposition increased significantly with TV, averaging 4.40 +/- 0.02%, 11.39 +/- 0.02% and 22.12 +/- 0.02% at 50 mL, 100 mL and 200 mL TV, respectively (all p < 0.0167). Aerosol loss to the environment was significantly lower at 200 mL TV (53.81 +/- 0.04%), compared to 50 mL (71.99 +/- 0.02%) (p < 0.0167). CONCLUSIONS: Our results suggest that nasal deposition of albuterol aerosol generated by a pneumatic nebulizer in 9-month-old infants may be significantly affected by changes in TV, ranging between 50 to 200 mL, whereas total lung deposition may not be affected. These results also predict that environmental losses would be highest when administering to a child breathing at 50 mL TV. These data should be useful to companies who are working to improve aerosol delivery systems to treat infants.