BACKGROUND & AIMS: Clinically active inflammatory bowel disease (IBD) is associated with an increased risk of adverse pregnancy outcomes. However, the validity of clinical scores to assess antenatal disease activity is questionable. We aimed to assess whether active disease defined by intestinal ultrasound (IUS) may predict adverse pregnancy outcomes. METHODS: This international prospective cohort study recruited pregnant individuals with IBD from 2017 to 2023 from 3 specialist IBD pregnancy services. Participants underwent clinical assessments and fecal calprotectin (FCP) testing in the first (T1), second (T2), and third (T3) trimesters, and 6 weeks postpartum. IUS was performed in T1 or T2 when referral timing allowed. Univariable and multivariable log-binomial regression analyses were used to estimate the impact of IUS activity on pregnancy outcomes. Cohen's k coefficients were used to determine agreement between FCP, IUS, and clinical disease activity. RESULTS: The study recruited 377 participants, 198 with Crohn's disease (CD), and 234 women underwent an IUS during pregnancy. A maximal bowel wall thickness (BWT) >6 mm in T2 was associated with a 4-fold increased risk of prematurity (relative risk [RR], 4.01; 95% confidence interval [CI], 1.26-12.72; P =.018) and 2-fold increased risk of lowbirth-weight delivery (RR, 2.19; 95% CI. 1.01-4.72; P =.046). Hyperemia on IUS in T2 was associated with a 3-fold increase in preeclampsia risk (RR, 3.46; 95% CI, 1.03-11.12; P =.046). Each 1-mm increase in BWT in T2 was estimated to increase the risk of gestational diabetes (RR, 1.08; 95% CI, 1.088-1.089; P <.001) Agreement between clinical (Harvey Bradshaw index or Simple Clinical Colitis Activity Index) and IUS/FCP activity during pregnancy was weak, particularly for CD. CONCLUSIONS: Active IBD on IUS in pregnancy is associated with an increased risk of adverse pregnancy outcomes, independent of clinical activity and FCP. Use of IUS monitoring antenatally should be considered to guide therapeutic decision-making.

BackgroundPeripheral parenteral nutrition (PPN) provides an alternative nutrition support strategy to centrally administered PN for specific patients requiring short-term PN. Previous studies have demonstrated limited use of PPN and variable complication rates. This study aimed to evaluate PPN complications and usage at this center.MethodsThis was a single-center retrospective observational study of all adult patients who received at least 1 day of PPN from June 2018 to December 2023. Demographic and clinical data were collected, including complications, indications for PN and reason for PPN, duration of therapy, reason for cessation of PPN, nutrition status, energy and protein provision, and central line insertion rates.Results381 patients were included, the median age was 62 (interquartile range = 28-74) years, and 235 were men (61.7%). The most common indication for PN was ileus (n = 153, 40%) followed by gastrointestinal obstruction (n = 93, 24%). The median time receiving PPN was 3 (2-4) days. Patients received a median of 65% (55%-75%) of energy and 58% (50%-69%) of protein requirements with PPN. Malnutrition was diagnosed in 47.5% (n = 181) of this cohort. Total complication rates were 8.7% (n = 33), with cannula infiltration being the most common complication (6.6%, n = 25). 213 (56%) patients proceeded to central line insertion.ConclusionPPN proved to be a safe and effective therapy for short-term PN when managed by a nutrition support team. PPN has the potential to attenuate short-term nutrition deficits and prevent central venous access device insertion in selected patients, making it a valuable nutrition support therapy.

This study explored the use of transperineal intestinal ultrasound (TPIUS) for assessment of ulcerative colitis (UC) in pregnancy. 8 pregnant women with UC underwent TP-US, clinical assessment and fecal calprotectin. TP-IUS was well tolerated and feasible with adequate rectal views obtained in all trimesters of pregnancy. No correlation between TP-IUS, clinical, or biochemical rectal disease activity assessment was found in this small cohort. Further studies are required to define the optimal technique and references ranges in the pregnant population.

Objective Sexual dysfunction is common in patients with inflammatory bowel disease (IBD). Data on IBD disease activity and IBD patients’ desire to seek specialist advice regarding sexual dysfunction are lacking. We aimed to identify sexual healthcare needs in patients with IBD. Design/method We conducted a cross-sectional survey of adult patients with IBD at a tertiary teaching hospital. Clinical disease activity was assessed using the Harvey-Bradshaw Index for patients with Crohn’s disease and the Patient-Simple Clinical Colitis Activity Index for patients with ulcerative colitis. Sexual health questions were derived from the validated IBD-Specific Female Sexual Dysfunction and IBD-Male Sexual Dysfunction Scales. Comparisons between those with inactive and active disease were made using Fisher’s exact test. Results 101 respondents completed the survey, of which 53 (52%) were female and 57 (56%) had Crohn’s disease. The median age was 38 (IQR 28–52). 34 respondents (34%) had active disease. Respondents with active Crohn’s disease trended towards having more significant sexual dysfunction than those in remission for all domains on the sexual dysfunction scale. 74% reported interest in accessing specialist advice regarding their sexual function while 20% have attempted to seek this advice. 36% would wish to be contacted by the IBD team if a sexual health service became available. Conclusions Negative impacts on sexual function were common in our cohort, particularly in the presence of active disease. Most patients with IBD are interested in obtaining advice regarding their sexual function. This is an unmet need among IBD services.

BACKGROUND & AIMS:Vedolizumab and ustekinumab pharmacokinetics in pregnancy and the infant after in utero exposure remain incompletely defined. We aim to define the antenatal stability of ustekinumab and vedolizumab levels and the time at which infant drug levels become undetectable. METHODS:This multicenter prospective observational cohort study recruited pregnant or preconception women with inflammatory bowel disease receiving vedolizumab or ustekinumab. Trough drug levels, clinical data, and biochemical data were documented preconception, during each trimester of pregnancy, and postpartum. Maternal and cord blood drug levels were measured at delivery and in infants until undetectable. Infant outcomes were assessed until 2 years of age. RESULTS:A total of 102 participants (vedolizumab, n = 58) were included. The majority of mothers were, and remained, in clinical and biochemical remission. Maternal vedolizumab levels decreased over the course of pregnancy in association with increasing weight, rather than increasing gestation. Maternal ustekinumab levels remained stable. The median time to drug becoming undetectable in the infant was shorter for vedolizumab (11 wk; range, 5-19 wk; n = 32) than ustekinumab (14 wk; range, 9-36 wk; n = 17) and correlated positively with infant delivery level. Thirty-two of 41 (88%) and 17 of 30 (67%) vedolizumab- and ustekinumab-exposed infants had undetectable drug levels by 15 weeks of age, respectively. Pregnancy and infant outcomes were favorable. Twenty infants with undetectable drug levels received the rotavirus vaccine, with no adverse reactions reported. CONCLUSIONS:Maternal vedolizumab levels decreased, whereas ustekinumab levels remained stable over the course of pregnancy. Most vedolizumab- and approximately half of ustekinumab-exposed infants had undetectable drug levels by 15 weeks of age. No concerning maternal or infant safety signals were identified.

Background:Exposure to maternal inflammation is associated with an increased risk of neurocognitive and developmental disorders in offspring. Early diagnosis and intervention improves childhood motor and cognitive functioning. Neonatal cerebral MRI and remote app-based generalised movement assessments (GMAs) are both predictive of adverse neurocognitive outcomes but have only been used in infants at significantly increased risk for these outcomes, rather than following in utero exposure to maternal inflammatory disorders. Methods:Pregnant women with inflammatory bowel disease were assessed clinically and biochemically in each trimester of pregnancy in this single centre prospective study. Neonatal cerebral MRIs were performed at 6-12 weeks post-corrected term. Two GMA videos were filmed using the 'BabyMoves' app from 12 to 16 weeks of age. MRIs and GMAs were assessed by a blinded highly qualified practitioner using validated scoring systems. Results:40/53 of invited maternal-infant dyads were recruited. C-reactive protein was elevated antenatally in less than 13%. 5/37 neonatal MRIs had incidental or obstetric trauma related gross anatomical abnormalities, with none abnormal on validated gross abnormality scoring. 3/35 GMAs were abnormal, with one GMA abnormality being clinically significant. Of those with abnormal GMAs, 2/3 were in exposed to severely active IBD in-utero. Conclusion:Neonatal cerebral MRI and GMA for neurocognitive screening is feasible in the setting of maternal inflammatory bowel disease, where the risk of cerebral palsy is poorly defined and thus burdensome screening interventions are less appealing to parents. Larger studies are required to stratify adverse neurocognitive outcome risk in infants born to women with maternal inflammatory disorders, but these data are reassuring for women with IBD in remission antenatally.

Rationale: Peripheral parenteral nutrition (PPN) may negate the need for central venous access device insertion in a subset of patients requiring short-term parenteral nutrition. Previous studies have reported adverse complications of up to 50% with PPN.1 This study aimed to evaluate the use of PPN at a tertiary referral centre where the therapy is initiated and overseen by a dedicated nutrition support team.

BACKGROUND:Despite reassuring clinical safety data, thrombocytosis, anemia, lymphopenia, and liver function derangements have been observed in infants born to women with inflammatory bowel disease (IBD) treated with thiopurines and biologics. We aimed to define the prevalence, course, associations, and clinical impact of hematological and biochemical abnormalities in such infants. METHODS:This multicenter prospective cohort study assessed clinical, hematologic, and biochemical outcomes of infants exposed to thiopurines or biologics in utero for management of maternal IBD. Liver transaminases, full blood examination, and infant thiopurine metabolites (where exposed) were taken at delivery and 6 weeks of age. Abnormal results were repeated until normalization. Infants were followed clinically by a pediatric gastroenterologist up to 2 years of age. RESULTS:A total of 130 infants were included. Thrombocytosis and elevated alanine transaminase (ALT) were seen in over half of infants up to 6 months of age with no significant clinical impact. Elevated ALT was associated with increasing maternal C-reactive protein in second trimester, while thrombocytosis was associated with increasing maternal C-reactive protein and fecal calprotectin in third trimester. Preceding infection and vaccination were associated with an increased risk of elevated alkaline phosphatase at 3 months. In those exposed to thiopurines, increasing maternal 6-methylmercaptopurine at delivery was associated with increased ALT to 6 months. CONCLUSIONS:Infants born to women with IBD commonly developed thrombocytosis, elevated alkaline phosphatase, and elevated ALT. These findings were associated with exposure to maternal inflammation, elevated 6-methylmercaptopurine at delivery, and infant vaccinations and infections, and had minimal clinical consequence.

Background and Aims: The risk of intrahepatic cholestasis of pregnancy [ICP] is increased in thiopurine-exposed pregnancies. Thiopurine 'shunting', with a 6-methylmercaptopurine [MMP] to 6-thioguanine [TGN] ratio of >11, progresses over pregnancy, and may promote ICP development. We aimed to explore the association between thiopurine exposure and ICP, including the hypothesised impact of thiopurine shunting, and identify risk minimisation strategies. Methods: This prospective multicentre cohort study compared thiopurine and biologic monotherapy-exposed pregnant participants. Disease activity and obstetric outcome data, thiopurine metabolites, bile acids, and transaminases were obtained before conception, in each trimester, at delivery, and postpartum. Thiopurine dose management was at the discretion of the treating physician. Results: Included were 131 thiopurine and 147 biologic monotherapy-exposed pregnancies. MMP/TGN ratio increased from preconception to third trimester [p <0.01], with approximately 25% of participants shunting in pregnancy. Second trimester split dosing led to a decrease in the median MMP/TGN ratio from 18 (interquartile range [IQR] 6-57) to 3 [IQR 2-3.5] at delivery [p = 0.04]. The risk of ICP was increased in thiopurine-exposed pregnancies (6.7% [7/105] vs 0% [0/112], p <0.001), with all ICP cases occurring in the setting of antenatal thiopurine shunting. Thiopurine dose increases (risk ratio [RR] 8.10, 95% confidence interval [CI] 1.88-34.85, p = 0.005) and shunting in third trimester [6.20, 1.21-30.73, p = 0.028] and at delivery [14.18, 1.62-123.9, p = 0.016] were associated with an increased risk of ICP. Conclusions: Thiopurine exposure is associated with an increased risk of ICP, particularly following dose increases antenatally and with shunting in late pregnancy. The latter may be effectively managed with split dosing, although further studies are warranted.

Autoimmune and inflammatory disorders, including inflammatory bowel disease (IBD), commonly affect women of childbearing age, warranting the use of immunomodulatory agents at a time where pregnancy may be desired. In utero exposure to pro-inflammatory mediators from maternal IBD, IBD-associated intestinal dysbiosis, and immunomodulatory drug use may impact neonatal immune system development during what is considered to be a critical period, with potential long-lasting impacts on susceptibility to disease. Both the innate and adaptative immune systems of the neonatal differ to that of the adult in terms of both cellular composition and sensitivity to antigenic and innate stimulation. The infant immune system gradually develops to more closely resemble that of the adult. Exposure to maternal inflammation in utero may aberrantly impact this period of infant immune system development, with maternal autoimmune and inflammatory disorders shown to affect the physiologic changes in serum cytokine abundance observed during pregnancy. The maternal and neonatal intestinal microbiome greatly influence infant mucosal and peripheral immune system development, and thereby impact the susceptibility to short-term inflammatory diseases, the adequacy of vaccine response, and later life risk of atopic and inflammatory disorders. Maternal disease, mode of delivery, method of feeding, time of weaning to include solid foods in the diet, and neonatal antibiotic exposure all influence the composition of the infant microbiome, and thereby infant immune system maturation. How exposure to specific immunosuppressive medications in utero alters infant immune cell phenotype and response to stimulation has been explored, but with existing studies limited by the time at which samples are performed, heterogenicity in methods, and small sample size. Furthermore, the impact of more recently introduced biologic agents have not been explored. Evolving knowledge in this field may influence therapeutic preferences for individuals with IBD planning to conceive, particularly if substantive differences in the risk of infant infection and childhood immune disease are identified.

Restorative proctocolectomy with ileal pouch-anal anastomosis (IPAA) remains the preferred surgical option for medically refractory ulcerative colitis. Management of individuals with an IPAA prior to and during pregnancy presents challenges that can have serious consequences. Infertility, mechanical obstructive and inflammatory pouch complications are frequently encountered in pregnant women with an IPAA. Mechanical obstructions occur due to a variety of underlying aetiologies, including stricturing disease, adhesions and pouch twists. Conservative management of such obstructions often results in resolution of symptoms without a need for endoscopic or surgical intervention, although endoscopic decompression may be attempted in isolation or as a bridge to definitive surgical intervention. Parenteral nutrition, and early delivery, may also be necessary. Faecal calprotectin and intestinal ultrasound, both of which are accurate in pregnancy, are useful in the setting of suspected inflammatory pouch complications, in some circumstances allowing for avoidance of pouchoscopy. Penicillin-based antimicrobials can be considered first line in pregnancy for the management of pouchitis and pre-pouch ileitis, and biologics can be safely instituted in the setting of refractory disease or suspected Crohn’s disease-like inflammation of the pouch or pre-pouch ileum. Pragmatism, clear patient communication and multidisciplinary discussion are essential in approaching pregnant women with complications of an IPAA, particularly given the lack of definitive evidence to guide therapeutic decisions.

Ascites is the pathological accumulation of fluid in the peritoneal cavity.1 Cirrhosis is the commonest cause of ascites in developed countries, followed by malignancy and cardiac failure.1 Ascites is a common presenting sign of hepatic decompensation in cirrhosis, with important prognostic implications.1 Spontaneous bacterial peritonitis is bacterial infection of ascites without any obvious source of infection.1, 2 It occurs in 1–4% of outpatients and 10% of inpatients with ascites secondary to cirrhosis, and can be asymptomatic initially but life-threatening when diagnosis is delayed.1, 3 Ascitic fluid analysis is recommended to evaluate the cause of clinically apparent (grade 2 and 3) ascites (Box 1) at first presentation and to exclude spontaneous bacterial peritonitis in patients with known cirrhosis, clinical deterioration (new neurological, liver or renal dysfunction) or acute gastrointestinal bleeding.1 Paracentesis (from the Greek parakentein, meaning "to pierce at the side") is therefore a useful clinical skill to master. Large volume paracentesis can provide symptomatic relief in patients with tense ascites or pleural effusions secondary to ascites (hepatic hydrothorax).1-3 Up to 30 mL of peritoneal fluid is physiologically normal (especially in menstruating females). Transabdominal ultrasound can detect ≥10 mL of fluid. Shifting abdominal dullness on examination requires about 1500 mL of fluid.1 Ascites volume is graded clinically from mild to large (Box 1).1, 2 No treatment is recommended for grade 1 ascites.2 Large volume paracentesis is arbitrarily defined as drainage of > 5000 mL of ascitic fluid in a single procedure, as removal of > 5000 mL in patients with cirrhosis requires plasma expansion (usually with albumin) to avoid post paracentesis circulatory dysfunction.2 Secondary bacterial peritonitis is the rare occurrence of peritonitis in a patient with cirrhosis secondary to organ perforation or poor aseptic technique, suggested by focal abdominal pain, very high neutrophil count, and multiple organisms on ascites culture (Box 2).1 Paracentesis is a low bleeding risk procedure which can be carried out safely even in patients with advanced cirrhosis.1, 3-6 Guidelines recommend that coagulopathy or thrombocytopenia should not be routinely corrected, but patients with platelet count < 20 × 109/L or chronic kidney disease may be at higher risk of bleeding.4-6 Antibiotic prophylaxis is not required before paracentesis; neither is withholding anti-platelet or anti-coagulant medications.5 Published major bleeding rates following paracentesis range from 0 to 2.7% and are lower with use of ultrasound guidance.1 A drug history should be taken to guide anti-coagulant reversal if significant bleeding occurs. Baseline full blood count, and liver and renal function blood tests are useful to assess baseline organ function and calculate the serum albumin ascites gradient. Serum (blood) brain natriuretic peptide should be requested in an ethylenediaminetetraacetic acid (EDTA) tube if cardiac failure is suspected as the cause of ascites. Elevated levels of brain natriuretic peptide (> 300 pg/mL) may serve as a marker of disease severity and subclinical cardiac dysfunction in patients with cirrhosis.7 Ultrasound of the liver can document organomegaly, liver or peritoneal lesions, established cirrhosis, and signs of portal hypertension. Paracentesis requires informed patient consent, including for intravenous albumin replacement if large volume paracentesis is being performed.1, 2 The most common clinically significant complications of paracentesis are fluid leak (3–13%), bleeding (0–2.7%) and organ puncture (< 1%), although routine use of ultrasound for paracentesis likely reduces these risks.1, 8, 9 Caution is advised in patients with clinical signs of bowel or bladder obstruction, significant central adiposity, grade 1 ascites (Box 1), loculated ascites and during pregnancy. Such patients often require paracentesis by experienced proceduralists with imaging guidance. Paracentesis is regularly performed at the bedside under local anaesthetic, with minimal discomfort, by a variety of health care professionals.1 Paracentesis is an aseptic procedure requiring strict skin antisepsis and sterile gloves. Diagnostic paracentesis can be performed with a long 22-gauge needle, 20 mL syringes and an antibacterial skin cleaning solution. A disposable drape is useful. A single EDTA blood tube, three plain sterile pots and two blood culture bottles are required for ascites biochemistry, cytology and microscopy. Sending ≥ 80 mL of ascites for testing significantly increases the diagnostic yield of cytology, as does use of sterile blood culture bottles if infection is suspected.1, 10 Box 2 lists the tests to request, depending on the patient's presentation and suspected cause.1, 3 For large volume paracentesis, commercially available paracentesis drains are available consisting of a 15 cm plastic drainage catheter with multiple drainage holes near the tip, on a long 18-gauge puncture needle (coaxial technique) (Box 3). Once the central needle is removed, rapid fluid drainage occurs through the catheter, which can be secured to the patient. Using an intravenous cannula for large volume paracentesis is discouraged; these are often too short and prone to kinking or dislodging. Note multiple side holes on the drainage catheter and auto-retracting needle tip. Reproduced with the kind permission of Rocket Medical. The patient should be positioned supine or slightly head up. Bedside ultrasound is recommended to assess the most suitable site for drainage.1 Ultrasound allows confirmation of ascites and the estimated volume, location of viscera, and the depth from the anterior abdominal wall to the fluid. Ultrasound marking of the proposed skin entry site should be performed with a permanent marker immediately before paracentesis, with the patient in the same position. Avoid access through infected skin, haematomas, peritoneal masses and scars.11 Experienced clinicians can use ultrasound guidance to advance the needle tip under continuous vision into the ascites, which allows grade 1 ascites to be targeted safely. If ultrasound is not available, then a skin entry site one-third of the way along a line drawn from the anterior iliac spine to the umbilicus in the left iliac fossa is an easily identifiable surface landmark (contralateral McBurney's point) (Box 4). The anterior abdominal wall is thinnest here; it is lateral to the inferior epigastric artery and away from the mobile caecum.11 Alternatively, the right iliac fossa or 2 cm inferior to the umbilicus can be used.11 If the infra-umbilical puncture site is chosen, the patient should be encouraged to empty their bladder beforehand to avoid bladder injury. The anterior abdomen needs to be widely exposed and the skin cleaned with a suitable antiseptic. The chosen entry site is anaesthetised down to the peritoneum with 5–10 mL of 1% lidocaine using a 25-gauge needle. An oblique trajectory between the skin and the peritoneal puncture sites may reduce the chance of post paracentesis fluid leak. A small skin nick with a number 11 blade can facilitate drain passage. Using the same trajectory as the anaesthetic needle, the paracentesis needle is advanced slowly into the peritoneal cavity while aspirating on the attached syringe, until ascites is aspirated. The free hand can steady the needle shaft to prevent sudden forward movement as the peritoneum is pierced. Often a drainage catheter is inserted; similar to intravenous cannulation, the plastic catheter is slid forward off the needle once the peritoneum is punctured and the drainage catheter is secured to the skin (coaxial technique) (Box 3). A small randomised controlled trial suggested that the z-tract technique, where the abdominal wall skin is retracted during skin puncture and released before peritoneal puncture, is more painful for the patient, more difficult for the proceduralist, and has no difference in post paracentesis fluid leakage.9 Dispose of all sharps and write a brief procedure note in the patient's medical record, including when the drain should be removed (within 4 hours for large volume paracentesis to avoid secondary infection) and whether albumin replacement is required (routinely for large volume paracentesis of > 5000 mL in patients with cirrhosis).1, 2 Radiologists often use locked pigtail drains, which have an internal suture holding the pigtail tightly in a loop after placement. The locking mechanism is visible at the catheter hub (Box 5). Locked pigtail drains require unlocking before removal to allow the pigtail to uncurl — this will be documented in the procedure note. A video of the paracentesis procedure can be reviewed along with this article to refresh knowledge before performing the procedure.12 Note locking mechanism at the catheter hub, which must be undone before drain removal. Media provided courtesy of Boston Scientific. © 2022 Boston Scientific Corporation or its affiliates. All rights reserved. Routine clinical observations and puncture site checks for leakage or haematoma are required, as well as regular monitoring of drainage output. Small fluid leaks or haematomas are usually successfully treated with direct manual pressure. Haemorrhagic ascites (> 10 000 red blood cells per microlitre) is uncommon and is usually spontaneous due to advanced liver disease or secondary to hepatocellular carcinoma, rather than a complication from paracentesis.13 In patients with haemorrhagic ascites or clinical suspicion of active bleeding (expanding haematoma, acute cardiovascular instability) or suspected organ perforation (spontaneous rupture of hepatocellular carcinoma, iatrogenic injury, secondary bacterial peritonitis), a low threshold for urgent computed tomography of the abdomen with intravenous contrast is advised, followed by discussion with the local surgical team or interventional radiology.1, 13 Ascitic fluid leak is the most common complication of paracentesis.1, 9 Leaks can be minimised by only making a small skin nick or avoiding this entirely, using a small diameter catheter (≤ 8 Fr) and an oblique catheter insertion technique. Persistent leakage usually indicates significant residual ascites which can be treated by repeat paracentesis. Otherwise, a skin suture can be considered.1 Pressure dressings should be avoided as they rapidly soak and can damage the skin.1 Patients with cirrhosis require intravenous albumin infusion (8 g albumin/L drained) after drainage of 5000 mL of ascites, to avoid post paracentesis circulatory dysfunction. For example, 40 g albumin should be infused if 5000 mL ascites is drained.1-3 This is equivalent to two 100 mL bottles of 20% salt poor albumin. Limiting paracentesis to ≤ 8000 mL in a single session over 4 hours before drain removal may reduce post paracentesis circulatory dysfunction and infection.1 Patients with malignant ascites do not require routine albumin replacement and can be drained to dryness over 8 hours, often as a day case procedure.14 We do not recommend longer drainage times, as these increase protein losses and the risk of secondary infection. Depending on the cause of the ascites, the patient will need referral to the appropriate specialist for further care.1-3 Patients with cirrhosis and refractory ascites can be considered for transjugular intrahepatic portosystemic shunt insertion or liver transplantation in specialised units.1-3 Patients with refractory malignant ascites can be considered for tunnelled drain insertion, with quality-of-life benefits and cost savings over repeated paracentesis.15 However, the role of tunnelled drains for refractory ascites in patients with advanced cirrhosis is unclear and should be decided on a case by case basis after multidisciplinary team discussion.15 Open access publishing facilitated by The University of Melbourne, as part of the Wiley - The University of Melbourne agreement via the Council of Australian University Librarians. No relevant disclosures. Not commissioned; externally peer reviewed.

Sexual dysfunction is prevalent in inflammatory bowel disease (IBD) and occurs in up to half of women and one-quarter of men.1 Addressing issues of sexual dysfunction is necessary to improve quality of life and functioning.2,3 Chronic pain4 and persistent fatigue,5 both quite common in patients with IBD, adversely affect sexual desire and arousal. Arthralgias and arthritis may also result in limited mobility and reduced sexual pleasure. Body image concerns may arise from diarrhea, incontinence, perianal complications, draining fistulae, skin tags, scars, and the presence of an ostomy all may increase embarrassment and decrease confidence and therefore impair sexual function.1 Importantly, psychiatric disorders are associated with sexual dysfunction and must be addressed, given the prevalence of depression and anxiety in IBD.1 Patients with IBD value sexual health highly but describe a lack of conversation with their treating physicians.6 Despite this discrepancy in...

Abstract Background Active Inflammatory Bowel Disease (IBD) in pregnancy is associated with adverse obstetric and neonatal outcomes. PICCOLO-X is an ongoing prospective cohort study of pregnant women with IBD, aiming to describe rates of biochemically active IBD in the current therapeutic landscape, and associations with adverse outcomes. Methods Participants were evaluated preconception, in each trimester and postpartum with clinical and biochemical data collected. Univariate and multivariate logistic regression was performed to identify the relative risk (RR) of adverse outcomes by relevant exposures. Fischer’s exact test was used to compare group medians. Results 164 completed pregnancies were included, with 62% exposed to biologic therapy and 56% having Crohn’s Disease (Table 1). Clinically active disease (PGA ≥1) was reported in 23.9% in trimester 1 (T1), 18.8% in trimester 2 (T2) and 17.5% in trimester 3 (T3), and was less common in biologic exposed patients (Table 2 & 3). The median faecal calprotectin (FC) was <50μg/g in all trimesters, and was lower in those receiving biologics (24.9 vs 86μg/g T1 p=0.02, 26.25 vs 46μg/g T2 p=0.02, 30 vs 58μg/g T3 p=0.04) (Table 3). Adverse pregnancy outcome rates were equivalent to the normal population (Table 2). Corticosteroid (CCS) exposure in T2 was associated with an increased risk of preterm delivery (PTD) on multivariate analysis (RR 8.12, 95%CI 1.23–53.72, p=0.03). T1 FC ≥250μg/g (RR 2.41 95% CI 0.5–4.31, p=0.01), clinically active disease in T3 (RR 4.7, 95% CI 1.02–26.61, p<0.01) & T3 FC 100–250 (RR 6.8 95% CI 1.71–26.0, p<0.01), but not T3 FC ≥250μg/g (RR 1.6, 95% CI 0.41–8.25, p=0.6) were associated with an increased risk of PTD on univariate analysis (Table 4). Biologic exposure was associated with a reduced need for CCS; no participants on a biologic had CCS in T1, with RR 0.14 (95% CI 0.03–0.66, p=0.01) in T2 and 0.11 (95% CI 0.02–0.46, p=0.003) in T3. On multivariate analysis, FC >100μg/g in T2 was associated with an increased risk of emergency caesarean section (RR 1.65, 95% CI 0.47–2.82, p<0.01), whilst FC >100μg/g in T2 (RR 1.65 95% CI 0.4–2.91 p=0.01) and T3 (RR 2.47,95% CI 1.36–8.82, p<0.01) were associated with an increased risk of neonatal intensive care unit admission. Conclusion PICCOLO X describes low rates of biochemical and clinical active disease in pregnant women with IBD as compared to historical cohorts, possibly due to the cohort’s high rate of biologic use. Pregnancy outcomes were favourable overall. Clinical and biochemical inflammation and CCS exposure were associated with an elevated risk of adverse pregnancy outcomes. Biologic therapy reduces FC and the need for steroids.

Although available clinical outcome data are reassuring, the consequences of in utero exposure to inflammatory bowel disease (IBD) pharmacotherapies on the development of the neonatal immune system remain ill-defined. So too does the converse effect on immunological maturation of fetal exposure to maternal inflammatory activity. Both warrant elucidation to appropriately stratify antenatal IBD care.