Hawke's Bay Hospital

Climate change, fueled by greenhouse gas (GHG) emissions, is a major threat to human health and demands immediate and decisive action. The effects of climate change directly harm the health of patients cared for by pulmonary, sleep, and critical care health professionals while putting healthcare delivery at risk. Ironically, the healthcare sector itself contributes to GHG emissions. In 2024, an American Thoracic Society workshop convened an international work group of adult and pediatric pulmonologists, intensivists, nurses, researchers, educators, healthcare administrators, and healthcare advocates to identify strategies to decrease pulmonary, sleep, critical care, and research laboratory-related emissions; improve quality; and support sustainability. The workshop prioritized strategies with the highest probability of reducing healthcare sector emissions significantly and urgently while considering the short- and long-term impacts of mitigation strategies on safe healthcare delivery and unintended adverse effects on vulnerable populations. Interventions were identified on micro (individual provider), meso (healthcare organization), and macro (regulatory/government/policy) levels. As trusted voices, health professionals and their professional societies are uniquely positioned to advocate for systemic change, ensuring that healthcare not only adapts to the challenges of climate change but also actively contributes to solutions that promote a healthier, more sustainable future for all.

In New Zealand, lower immunisation coverage is seen among those of Māori and Pacific ethnicity, as well as in communities with higher levels of socioeconomic deprivation. However, the impact of rurality on routine childhood immunisations has been incompletely investigated. This study aims to measure the effect of rurality on second-dose measles-mumps-rubella vaccination (MMR2) within the Taranaki region. This was a retrospective observational study using routinely collected health data. Participants were born in 2019, 2020, or 2021 and lived in the Taranaki region at age 24months. Rurality was determined using the Geographic Classification for Health (GCH). The percentage of MMR2 coverage was calculated for each rurality grouping, and logistic regression was used to adjust for confounders. A total of 4596 participants were enrolled across three GCH levels. MMR2 coverage rates were 56.2% in the most rural group (R2+3), compared to 63.0% in R1 (Rural 1) and 62.3% in U2 (Urban 2). Adjusting for ethnicity and socioeconomic deprivation produced odds ratios (ORs) of 1.33 for R1 participants and 1.18 for U2 participants, compared to R2+3. It was also shown that Māori had lower immunisation coverage than non-Māori at every GCH classification. Children living in more rural areas had lower rates of MMR2 coverage at age 24months. This may reflect inequitable impacts of the COVID-19 pandemic or uneven rollout of the 2020 changes to the National Immunisation Schedule.

Appendiceal neoplasms are rare but clinically significant findings in appendicectomy specimens. An international meta-analysis reports a malignancy rate of 1.98%. This study aimed to determine the local incidence of appendiceal neoplasms at Hawke's Bay Hospital, New Zealand, over a 10-year period and compare it with international data. A retrospective review was conducted of all appendicectomies performed at Hawke's Bay Hospital between January 2014 and December 2023. Demographic and histopathological data were extracted from electronic medical records. Neoplasms were classified as carcinoid tumours, mucinous neoplasms, or adenocarcinomas. Patients were categorised by ethnicity and rurality. Of 2333 appendicectomy specimens with complete histology, 67 (2.87%) were neoplastic. These included 27 neuroendocrine tumours (40.3%), 25 mucinous neoplasms (37.3%), and 15 adenocarcinomas (22.4%). Patients of New Zealand European ethnicity accounted for 71.6% of cases, while Māori represented 22.4%. The majority of neoplastic cases (91%) were from urban areas. Nearly half of patients with appendiceal neoplasm have their surgery at < 50 years of age (n = 33) and would therefore fall outside of the scope of routine post-appendicitis colonoscopic evaluation at our institution. The local incidence of appendiceal neoplasms (2.87%) was higher than the internationally reported rate of 1.98%. Neuroendocrine tumours were the most common subtype. The predominance of Urban and New Zealand European cases may reflect access to surgical services or demographic distribution. These findings highlight the importance of routine histopathological evaluation of appendicectomy specimens to ensure timely diagnosis and management of neoplasms.

Rapid apple decline is a syndrome primarily affecting young (<6 yr old) apple trees planted in high-density orchards throughout the eastern United States and Canada. Despite the sudden death of thousands of apple trees in North America, no definitive biotic or abiotic cause of rapid apple decline has been identified. Surveys of apple orchards in North Carolina experiencing rapid apple decline symptoms in 2017 found that ambrosia beetle infestations were associated with dead or declining trees. The exotic ambrosia beetles (Coleoptera: Scolytinae), Xylosandrus crassiusculus (Motschulsky) and X. germanus (Blandford), have been implicated in damage and decline of ornamental, fruit, and nut trees throughout the United States and are of increasing concern in other regions throughout the world. Trapping surveys across western North Carolina apple orchards over 3 yr revealed that X. crassiusculus, X. germanus, and Xyleborinus saxesenii (Ratzeburg) were the dominant species captured, with annual variation in species composition. The same 3 species of beetles were found inside the scion, rootstock, and graft union of declining apple trees collected from commercial orchards. A large diversity of fungi was associated with beetle gallery and non-gallery tissue on declining trees, including opportunistic phytopathogenic genera such as Botryosphaeria, Fusarium, and Diaporthe. No phytopathogenic fungi appeared to be exclusively associated with gallery tissue. The establishment of several genera of opportunistic fungal pathogens and ambrosia beetles in rapidly declining apple trees suggests that rapid apple decline in North Carolina has no single cause and is likely due to a combination of abiotic and biotic stress events.

Background: Neoadjuvant chemotherapy (NACT) is widely used in patients with high risk HER2-amplified (HER2+) or triple negative early breast cancer (TNBC). Advantages of NACT include allowing less extensive surgery, assessing response to treatment and guiding adjuvant therapy. NACT-related toxicities are common and can result in treatment alterations and hospitalisation, which may adversely impact outcomes. Aim: To assess NACT treatment in Hawke’s Bay (HB), New Zealand, by evaluating pathologic complete response (pCR) rates and toxicities of different regimens. Method: Data were retrospectively obtained from medical records of NACT patients. pCR rates were compared to results from previous literature. Toxicity was assessed by recording severe (grade 3 or above) toxicities, treatment-limiting toxicities (those leading to dose reductions, dose delays, early cessation), and hospitalisations for different NACT regimens. Results: A total of 71 NACT patients were included. pCR rates for HER2+ disease and TNBC were 19/45 (42%) and 8/24 (33%) respectively. The most common severe toxicities were diarrhoea, anaemia and febrile neutropaenia (all 16%) in FEC-D (5-fluorouracil/epirubicin/cyclophosphamide + docetaxel +/- carboplatin +/- immunotherapy) patients, neutropaenia (50%) in FEC-DH (FEC-D + trastuzumab +/- pertuzumab) patients and diarrhoea (38%) in TCH (docetaxel/carboplatin/trastuzumab +/- pertuzumab) patients. Comparing treatment-limiting toxicity in FEC-DH vs TCH, 9/16 (56%) vs 13/21 (62%) had dose reduction, 2/16 (13%) vs 8/21 (38%) had dose delay, 1/16 (6%) vs 5/21(24%) had early cessation and 6/16 (38%) vs 13/21 (62%) were hospitalized respectively. Conclusion: NACT was associated with high rates of severe and treatment-limiting toxicity. Despite this, pCR rates were consistent with previous literature. With the caveat of small patient numbers, FEC-DH-based therapy was associated with fewer dosing delays, early cessations and hospitalisations compared with TCH-based therapy.

Acute prolonged sitting increases blood pressure (BP) and arterial stiffness (AS). Both of these may be mitigated via light physical activity (LPA). Whether long COVID (LC), which partly manifests as vascular sequelae, predisposes a heightened sensitivity to sitting or diminished benefits from its interruption is unknown. The aims of this study were to identify whether individuals with LC: (i) exhibit a worse BP/AS response to uninterrupted sitting and (ii) a diminished mitigation of BP/AS response to sitting interrupted with LPA, compared to healthy controls. Thirty participants with LC and 15 controls completed 2 h of uninterrupted sitting and sitting interrupted with LPA. Central and peripheral systolic and diastolic BP and carotid‐femoral pulse wave velocity (cfPWV) were determined pre and post sitting. Linear mixed‐effects models demonstrated no three‐way or two‐way interactions for any variable. There was a significant main effect of time, with increases in central systolic (MD = 3.37 mmHg, SE = 0.93 mmHg, p < 0.001) and central diastolic (MD = 3.00 mmHg, SE = 0.58 mmHg, p < 0.001) BP. cfPWV was not altered in sitting in either group (MD = 0.13 m/s, SE = 0.09 m/s, p = 0.170). Uninterrupted sitting increases BP similarly, but AS is unchanged. Interrupting sitting with LPA did not mitigate sitting‐induced increase in BP regardless of LC diagnosis.

The reach of dialysis in toxicology is limited by two factors, high toxicant volume of distribution and low dialytic extraction of protein bound toxicants in blood. Therapeutic actions for lipid emulsion as antidote are thought involve a "lipid shuttle", whereby lipid droplets in the circulation "shuttle" lipophilic toxicants with "boarding" in well perfused heart and brain tissue with high toxicant concentrations and "exit" to biologically inert slower equilibrating sites such as muscle or adipose where toxicant concentrations are lower. Such a mechanism raises the conceptual possibility of an extracorporeal "exit" potentially mitigating toxicity through increased drug clearance. In experimental models drug binding nanoparticles in dialysate have been shown to mitigate the problem of blood proteins binding toxicant. We investigated whether the addition of intravenous lipid emulsion would increase extraction of amitriptyline into nanoparticle augmented peritoneal dialysate in rats orally dosed with amitriptyline for 1week. Rats were dosed with amitriptyline in drinking water for a week. On the day of the experiment, anaesthetised rats received either an initial bolus then infusion of lipid emulsion for one hour, or a bolus of saline at the initiation of the experiment equal to the total volume of lipid emulsion given. After a 50min equilibration period, a 10min pH gradient nanoparticle augmented peritoneal dialysis dwell was undertaken. Animals were humanely euthanised at the end of the experiment. Blood was sampled 0, 10, 45 and 60min and peritoneal dialysate was analysed for amitriptyline concentration. There were no significant differences in baseline physiology, initial amitriptyline blood concentration, nor pulse and blood pressure at any time between groups. Time weighted individual subject mean blood amitriptyline concentrations (median (IQR)); control 104 (87-125) nmol/l, lipid 219 (148-357) nmol/L, p = 0.03 and dialysate amitriptyline concentration; control 31(14-52) nmol/L, lipid 105 (62-185) nmol/L, p = 0.03 were greater in animals given intravenous lipid emulsion. These are the first data to our knowledge showing experimental support for the approach of simultaneously decreasing volume of distribution with an intravascular nanoparticle in conjunction with a drug binding particle in dialysate. Further work in this area is warranted.

Psychosis constitutes a cardinal component of schizophrenia and affects nearly fifty percent of those with bipolar disorder. We sought to molecularly characterize psychosis segregating in consanguineous families. Participants from eight multiplex families were evaluated using standardized testing tools. DNA was subjected to exome sequencing followed by Sanger sequencing. Effects of variants were modeled using in-silico tools, while cDNA from a patient's blood sample was analyzed to evaluate the effect of a splice-site variant. Twelve patients in six families were diagnosed with schizophrenia, whereas four patients from two families had psychotic bipolar disorder. Two homozygous rare deleterious variants in INSR (c.2232-7T>G) and NFXL1 (c.1322G>A; p.Cys441Tyr) were identified, which segregated with severe treatment-resistant psychosis/schizophrenia in two families. There were none, or ambiguous findings in the other six families. The predicted deleterious missense variant affected a conserved amino acid, while the intronic variant was predicted to affect splicing. However, cDNA analysis from a patient's blood sample did not reveal an aberrant transcript. Our results indicate that INSR and NFXL1 variants may have a role in psychosis that requires to be investigated further. Lack of molecular diagnosis in some patients suggests the need for genome sequencing to pinpoint the genetic causes.