Townsville University Hospital (TUH), formerly The Townsville Hospital (TTH), is a public tertiary care hospital on Angus Smirth Drive, Douglas, Townsville, Queensland, Australia. It is the largest facility within the Townsville Hospital and Health Service (HHS) geographic area. It provides healthcare across the entire North Queensland region, with patients from as far as Mount Isa and Cape York being airlifted or transported to the hospital on a daily basis. This is the third general hospital to be built in Townsville and is relatively new (completed 2001). The next main referral hospital is the Royal Brisbane and Women's Hospital, in Herston, Brisbane some 1,375 kilometres (854 mi) distant.
Introduction:Treatment uncertainties influenced by organ intrafraction motion complicate the widespread adoption of hypofractionated radiotherapy. This study aims to identify imaging features on pre-treatment magnetic resonance imaging (MRI) scans that describe prostate and seminal vesicle (SV) intrafraction motion, with the goal of informing and improving treatment planning. Materials/methods:Thirty prostate cancer participants treated on an Elekta Unity 1.5T MR-Linac were recruited, with a series of volumetric MR images acquired pre-, during and post- treatment over multiple fractions. nnU-Net was used to automatically contour the prostate, rectum, SV and bladder. These contours quantified prostate and SV intrafraction motion and enabled extraction of imaging features. A linear regression model assessed relationships between the organs intrafraction motion, treatment margins, and the extracted features. Results:Bladder filling during treatment influenced both SV and prostate intrafraction motion, especially, when baseline bladder volume was <190 mL for both prostate (R2 = 0.142) and SV (R2 = 0.258). Rectum volume showed no strong correlation with motion. Baseline bladder volume below 332 mL increased the required SV treatment margins to 5.8 mm, compared to 3.5 mm for larger volumes. Conclusion:This study demonstrated that the baseline bladder volume at start of a treatment fraction predicts for both SV and prostate intrafraction motion, by mediating the effect of bladder filling, and that SV treatment margins could be reduced for a favourably sized bladder. These findings may support refining treatment protocols such as aiming for an initial bladder volume of at least 190 mL.
Background/Objectives: Dysnatraemia is common in severe traumatic brain injury (TBI) and independently associated with increased case-fatality. However, existing analyses treat serum sodium as a static variable, discarding prognostic information embedded in its temporal pattern. This study investigated whether various sodium trajectory phenotypes carry differential 90-day case-fatality risk in severe TBI. Methods: This retrospective cohort study included adults (≥ 18 years) with severe TBI (Glasgow Coma Scale (GCS) ≤ 8 at intensive care unit (ICU) admission) treated at the four tertiary neurosurgery referral hospitals in Queensland, Australia. Serum sodium values from the first 96 hours were aggregated into four 24-hour windows, and latent growth mixture modelling (LGMM) classified patients into trajectory groups. The association with 90-day all-cause case-fatality was evaluated using Bayesian parametric Weibull survival models, adjusting for age, sex, admission GCS, illness severity, and osmotherapy exposure. Results: Of 1,465 patients, LGMM identified two trajectory classes: eunatraemia-stable (Class 1; n = 1,222, 83.4%), with admission sodium 139.5 ± 4.4 mmol/L remaining stable; and persistent hypernatraemia (Class 2; n = 243, 16.6%), with admission sodium 142.2 ± 5.6 mmol/L rising to 145.9 ± 5.8 mmol/L by 72–96 hours. Overall, 90-day case-fatality was 20.8% (304 deaths), with 19.0% in Class 1 and 29.6% in Class 2 (p < 0.001). Under the primary non-informative prior, persistent hypernatraemia was independently associated with increased case-fatality (posterior median hazard ratio 1.79, 95% credible interval 1.36–2.34; P[HR > 1 | data] = 0.9998). The association was consistent across weakly informative and literature-informed priors and robust to sensitivity analyses, including removal of osmotherapy covariates and restriction to patients with complete sodium windows. Conclusions: Among adults with severe TBI, LGMM identified two biologically plausible sodium trajectory phenotypes with substantially different 90-day case-fatality. The persistent hypernatraemia trajectory was independently associated with increased case-fatality across Bayesian prior specifications, supporting trajectory-based sodium assessment as a complement to static thresholds in neurocritical care.
Introduction: Diabetic ketoacidosis (DKA) is a common complication of diabetes mellitus characterized by metabolic acidosis, ketogenesis, hypovolemia, hyperglycemia, and electrolyte depletion. During treatment of DKA with intravenous fluids and insulin, some electrolyte disturbances can worsen. Hypophosphatemia is one such electrolyte disturbance that has not been well characterized in patients with severe DKA requiring Intensive Care Unit (ICU) admissions. This study sought to evaluate the incidence, severity, associations, and outcomes of hypophosphatemia in DKA. Methods: This retrospective multicenter study was conducted across DKA admissions to Queensland ICUs from 2016 to 2021. Adult patients (>18 years) requiring ICU admission for management of DKA were included in this study. Patients with DKA were stratified by lowest recorded phosphate level as: normal ≥ 0.80 mmol/L, mild 0.50–0.79 mmol/L, moderate 0.30–0.49 mmol/L and severe < 0.3 mmol/L. Patient demographics, comorbidities, ICU-related supports, and medications (including fluid, insulin administration, phosphate, and other electrolyte replacement) were collected. Univariate analysis was performed between hypophosphatemia severity and normophosphatemia subgroups to determine risk factors, outcomes, replacement, and progression of hypophosphatemia in the ICU. Phosphate replacement and administered insulin was compared to nadir serum phosphate level. Multivariate analysis and linear regression were performed to identify risk factors for the development of hypophosphatemia. Results: A total of 842 admissions of 669 unique patients due to DKA were included; 436 of 842 (51.8%) admissions maintained normophosphatemia in the ICU, while 220 (26.1%, n = 220/842) had mild hypophosphatemia, 124 (14.7%, n = 124/842) had moderate hypophosphatemia and 62 (7.4%, n = 62/842) had severe hypophosphatemia. Patients with higher BMI, higher APACHE II/III score, cerebrovascular disease and all blood gas parameters (excluding PaO2) were found to have more severe hypophosphatemia. Lower serum phosphate was associated with greater replacement and greater insulin administration per kilogram body weight. ICU length of stay, hospital length of stay and mortality were not affected by degree of hypophosphatemia (p > 0.05). Linear regression revealed that standard base excess was strongly associated with the development of hypophosphatemia (β = 0.02, 95% CI 0.01–0.02, p < 0.001). Conclusions: Increasing severity of hypophosphatemia was associated with increasing severity of DKA. Increased ICU length of stay was related to increased severity of hypophosphatemia.
