Anorexia nervosa and pancreatitis

Acute pancreatitis is a condition whereby erroneous activation of trypsin and zymogen results in pancreatic autodigestion. There are many aetiologies, with alcohol intake and gallstones being the most common. Anorexia nervosa is an eating disorder in which patients' reduced food intake and psychological aversion of weight gain can result in low body weight and malnourishment. The link between pancreatitis and anorexia nervosa is not well understood; this article explores the theorised pathophysiology connecting the two conditions, as well as the optimal management of patients when the conditions co-exist based on current literature. A literature search was performed using MEDLINE, EMBASE and CINAHL databases for all journal articles on the topic of presentations of acute or chronic pancreatitis in adults with anorexia nervosa. The literature proposes various links between anorexia nervosa and pancreatitis. It is theorised that pancreatitis may arise as a result of malnourishment itself or secondary to the refeeding process. Some explanations focus on the histopathological changes to the pancreas that malnourishment induces, while others focus on the enzymatic changes and oxidative damage that arise in the malnourished state. More mechanical mechanisms such as gastric dilatation, gastrointestinal ileus and compartmental fluid shift during refeeding have also been proposed as explanations for the link between the conditions. Some medications used in the management of anorexia nervosa have also been linked to pancreatitis.

LLower body negative pressure reduces jugular and portal vein volumes, and counteracts the cerebral vein velocity elevation during long-duration spaceflight

Purpose: Cephalad fluid shifts in space have been hypothesized to cause the spaceflight-associated neuro-ocular syndrome (SANS) by increasing the intracranial-ocular translaminal pressure gradient. Lower body negative pressure (LBNP) can be used to shift upper-body blood and other fluids towards the legs during spaceflight. We hypothesized that microgravity would increase jugular vein volume (JVvol), portal vein cross-sectional area (PV), and intracranial venous blood velocity (MCV) and that 25mmHg LBNP application would return these variables towards preflight levels. Methods: Data were collected from 14 subjects (11 male) before and during long-duration ISS spaceflights. Ultrasound measures of JVvol, PV, and MCV were acquired while seated and supine before flight and early during spaceflight at days 45 (FD45) and late (FD150) with and without LBNP. Results: JVvol increased from preflight supine and seated postures (46 ± 48 % and 646 ± 595 % on FD45 and 43 ± 43 % and 702 ± 631 % on FD150, p<0.05), MCV increased from preflight supine 44 ± 31 % on FD45 and 115 ± 116 % on FD150 (p<0.05), PV increased from preflight supine and seated (51 ± 56 % and 100 ± 74 %) on FD150 (p<0.05). Inflight 25mmHg LBNP restored JVvol, and MCV to preflight supine and PV to preflight seated level. Conclusions: Elevated JVvol confirms the sustained neck-head blood engorgement inflight, while increased PV area supports the fluid shift at the splanchnic level. Also, MCV increased potentially due to reduced lumen diameter. LBNP, returning variables to preflight levels, may be an effective countermeasure.

Overnight Rostral Fluid Shifts Exacerbate Obstructive Sleep Apnea After Stroke

Background and Purpose: Overnight shifts of fluid from lower to upper compartments exacerbate obstructive sleep apnea (OSA) in some OSA populations. Given the high prevalence of OSA after stroke, decreased mobility and use of IV fluids among hospitalized patients with stroke, and improvement in OSA in the months after stroke, we hypothesized that overnight fluid shifts occur and are associated with OSA among patients with subacute ischemic stroke. Methods: Within a population-based project, we performed overnight sleep apnea tests (ApneaLink Plus) during ischemic stroke hospitalizations. Before sleep that evening, and the following morning before rising from bed, we assessed neck and calf circumference, and leg fluid volume (bioimpedance spectroscopy). The average per subject overnight change in the 3 fluid shift measurements was calculated and compared with zero. Linear regression was used to test the crude association between each of the 3 fluid shift measurements and the respiratory event index (REI). Results: Among the 292 participants, mean REI was 24 (SD=18). Within individuals, calf circumference decreased on average by 0.66 cm (SD=0.75 cm, P <0.001), leg fluid volume decreased by a mean of 135.6 mL (SD=132.8 mL, P <0.001), and neck circumference increased by 0.20 cm (SD=1.71 cm, P =0.07). In men, when the overnight change of calf circumference was negative, an interquartile range (0.8 cm) decrease in calf circumference overnight was significantly associated with a 25.1% increase in REI ( P =0.02); the association was not significant in women. The relationship between overnight change in leg fluid volume and REI was U shaped. Conclusions: This population-based, multicenter, cross-sectional study showed that in hospitalized patients with ischemic stroke, nocturnal rostral fluid shifts occurred, and 2 of the 3 measures were associated with greater OSA severity. Interventions that limit overnight fluid shifts should be tested as potential treatments for OSA among patients with subacute ischemic stroke.

Effects of Venoconstrictive Thigh Cuffs on Dry Immersion-Induced Ophthalmological Changes

Neuro-ophthalmological changes named spaceflight associated neuro-ocular syndrome (SANS) reported after spaceflights are important medical issues. Dry immersion (DI), an analog to microgravity, rapidly induces a centralization of body fluids, immobilization, and hypokinesia similar to that observed during spaceflight. The main objectives of the present study were 2-fold: (1) to assess the neuro-ophthalmological impact during 5 days of DI and (2) to determine the effects of venoconstrictive thigh cuffs (VTC), used as a countermeasure to limit headward fluid shift, on DI-induced ophthalmological adaptations. Eighteen healthy male subjects underwent 5 days of DI with or without VTC countermeasures. The subjects were randomly assigned into two groups of 9: a control and cuffs group. Retinal and optic nerve thickness were assessed with spectral-domain optical coherence tomography (OCT). Optic nerve sheath diameter (ONSD) was measured by ocular ultrasonography and used to assess indirect changes in intracranial pressure (ICP). Intraocular pressure (IOP) was assessed by applanation tonometry. A higher thickness of the retinal nerve fiber layer (RNFL) in the temporal quadrant was observed after DI. ONSD increased significantly during DI and remained higher during the recovery phase. IOP did not significantly change during and after DI. VTC tended to limit the ONSD enlargement but not the higher thickness of an RNFL induced by DI. These findings suggest that 5 days of DI induced significant ophthalmological changes. VTC were found to dampen the ONSD enlargement induced by DI.

Ambulance deceleration causes increased intra cranial pressure in supine position: a prospective observational prove of principle study

Background Ambulance drivers in the Netherlands are trained to drive as fluent as possible when transporting a head injured patient to the hospital. Acceleration and deceleration have the potential to create pressure changes in the head that may worsen outcome. Although the idea of fluid shift during braking causing intra cranial pressure (ICP) to rise is widely accepted, it lacks any scientific evidence. In this study we evaluated the effects of driving and deceleration during ambulance transportation on the intra cranial pressure in supine position and 30° upright position. Methods Participants were placed on the ambulance gurney in supine position. During driving and braking the optical nerve sheath diameter (ONSD) was measured with ultrasound. Because cerebro spinal fluid percolates in the optical nerve sheath when ICP rises, the diameter of this sheath will distend if ICP rises during braking of the ambulance. The same measurements were taken with the headrest in 30° upright position. Results Mean ONSD in 20 subjects in supine position increased from 4.80 (IQR 4.80–5.00) mm during normal transportation to 6.00 (IQR 5.75–6.40) mm (p < 0.001) during braking. ONSD’s increased in all subjects in supine position. After raising the headrest of the gurney 30° mean ONSD increased from 4.80 (IQR 4.67–5.02) mm during normal transportation to 4.90 (IQR 4.80–5.02) mm (p = 0.022) during braking. In 15 subjects (75%) there was no change in ONSD at all. Conclusions ONSD and thereby ICP increases during deceleration of a transporting vehicle in participants in supine position. Raising the headrest of the gurney to 30 degrees reduces the effect of breaking on ICP.

Intraocular pressure and choroidal thickness respond differently to lower body negative pressure during spaceflight

Spaceflight associated neuro-ocular syndrome (SANS) develops during long-duration (>1 month) spaceflight presumably because of chronic exposure to a headward fluid shift that occurs in weightlessness. We aimed to determine whether reversing this headward fluid shift with acute application of lower body negative pressure (LBNP) can influence outcome measures at the eye. Intraocular pressure (IOP) and subfoveal choroidal thickness were therefore evaluated by tonometry and optical coherence tomography (OCT), respectively, in 14 International Space Station crewmembers before flight in the seated, supine, and 15° head-down tilt (HDT) postures and during spaceflight, without and with application of 25 mmHg LBNP. IOP in the preflight seated posture was 14.4 mmHg (95% CI, 13.5-15.2 mmHg) and spaceflight elevated this value by 1.3 mmHg (95% CI, 0.7-1.8 mmHg, P<0.001). Acute exposure to LBNP during spaceflight reduced IOP to 14.2 mmHg (95% CI, 13.4-15.0 mmHg), which was equivalent to that of the seated posture (P>0.99), indicating that venous fluid redistribution by LBNP can influence ocular outcome variables during spaceflight. Choroidal thickness during spaceflight (374 µm, 95% CI, 325-423 µm) increased by 35 µm (95% CI, 25-45 µm, P<0.001), compared to the preflight seated posture (339 µm, 95% CI, 289-388 µm). Acute use of LBNP during spaceflight did not affect choroidal thickness (381 µm, 95% CI, 331-430 µm, P=0.99). The finding that transmission of reduced venous pressure by LBNP did not decrease choroidal thickness suggests that engorgement of this tissue during spaceflight may reflect changes that are secondary to the chronic cerebral venous congestion associated with spaceflight.

Mechanical Countermeasures to Headward Fluid Shifts

Head-to-foot gravitationally-induced hydrostatic pressure gradients in the upright posture on Earth are absent in weightlessness. This results in a relative headward fluid shift in the vascular and cerebrospinal fluid compartments and may underlie multiple physiological consequences of spaceflight, including the Spaceflight Associated Neuro-ocular Syndrome. Here, we tested 3 mechanical countermeasures (lower body negative pressure [LBNP], veno-constrictive thigh cuffs [VTC] and impedance threshold device [ITD] resistive inspiratory breathing) individually and in combination to reduce a posture-induced headward fluid shift as a ground-based spaceflight analog. Ten healthy subjects (5 male) underwent baseline measures (seated and supine postures) followed by countermeasure exposure in the supine posture. Noninvasive measurements included ultrasound (internal jugular veins [IJV] cross-sectional area, cardiac stroke volume, optic nerve sheath diameter, noninvasive IJV pressure), transient evoked otoacoustic emissions (OAE; intracranial pressure index), intraocular pressure, choroidal thickness from optical coherence tomography imaging, and brachial blood pressure. Compared to the supine posture, IJV area decreased 48% with application of LBNP (mean ratio: 0.52, 95% CI: 0.44-0.60, P<0.001), 31% with VTC (mean ratio: 0.69, 95% CI: 0.55-0.87, P<0.001), and 56% with ITD (mean ratio: 0.44, 95% CI: 0.12-1.70, P=0.46), measured at end-inspiration. LBNP was the only individual countermeasure to decrease the OAE phase angle (Δ -12.9 degrees, 95% CI: -25 to -0.9, P=0.027), and use of combined countermeasures did not result in greater effects. Thus, LBNP, and to a lesser extent VTC and ITD, represent promising headward fluid shift countermeasures, but will require future testing in analog and spaceflight environments.

Detection of hysteroscopic fluid in the pouch of Douglas: a prospective cohort study about the predictability of bilateral tubal occlusion

Purpose To determine whether an increase in cul de sac (CDS) fluid after hysteroscopy is predictive of tubal patency. Methods In a prospective clinical cohort study, 115 subfertile women undergoing laparoscopic and hysteroscopic surgery at the Medical University of Vienna were invited to participate. The primary outcome was determining whether an increase in fluid in the pouch of Douglas was reflective of unilateral or bilateral tubal patency. Vaginal sonography before and after hysteroscopy was performed to detect fluid in the pouch of Douglas, directly followed by laparoscopy with chromopertubation. Results Laparoscopic chromopertubation revealed bilateral Fallopian tube occlusion in 28 women (24.3%). Twenty-seven/40 patients (67.5%) with no fluid shift had bilateral occlusion during the consecutive laparoscopy (p < 0.001). One/75 patients (1.3%) showing a fluid shift had bilateral occlusion (sensitivity of a present fluid shift for uni- or bilateral patency 85.1%, 95% CI: 81.7–99.9, specificity: 96.4%, 95% CI: 75.8–91.8). Intracavitary abnormalities (odds ratio, OR, 0.038; p = 0.030) and adhesions covering one or both tubes (OR 0.076; p = 0.041) increased the risk for a false abnormal result, i.e., uni- or bilateral tubal patency despite the lack of a fluid shift. Conclusion When CDS fluid does not change after hysteroscopy, this is a sensitive test for tubal occlusion and further testing may be warranted. However, if there is an increase in CDS fluid after hysteroscopy, particularly for a patient without fluid present prior, this is both sensitive and specific for unilateral or bilateral tubal patency.

EXPRESS: Hypoxemia during Sleep and Overnight Rostral Fluid Shift in Pulmonary Arterial Hypertension: a pilot study

Introduction. Sleep-related breathing disorders, including sleep apnea and hypoxemia during sleep, are common in pulmonary arterial hypertension (PAH), but the underlying mechanisms remain unknown. Overnight fluid shift from the legs to the upper airway and to the lungs promotes obstructive and central sleep apnea, respectively, in fluid retaining states. The main objective was to evaluate if overnight rostral fluid shift from the legs to the upper part of the body is associated with sleep-related breathing disorders in PAH. Methods. In a prospective study, a group of stable patients with idiopathic, heritable, related to drugs, toxins, or treated congenital heart disease PAH underwent a polysomnography and overnight fluid shift measurement by bioelectrical impedance in the month preceding or following a one-day hospitalization according to regular PAH follow-up schedule with a right heart catheterization. Results. Among 15 patients with PAH (women: 87%; median [25th;75th percentiles] age: 40 [32;61] years; mean pulmonary arterial pressure 56 [46;68] mmHg; pulmonary vascular resistance 8.8 [6.4;10.1] Wood units), 2 patients had sleep apnea and 8 (53%) had hypoxemia during sleep without apnea. The overnight rostral fluid shift was 168 [118;263] mL per leg. Patients with hypoxemia during sleep had a greater fluid shift (221 [141; 361] mL) than those without hypoxemia (118 [44; 178] mL, p = 0.045). Conclusion. This pilot study suggests that hypoxemia during sleep is associated with overnight rostral fluid shift in PAH.