Accidental dural puncture and post-dural puncture headache: a retrospective review in an Irish maternity hospital.

BACKGROUND: Accidental dural puncture (ADP) during epidural catheter insertion and the possible consequent post-dural puncture headache (PDPH) remain challenging complications in obstetric anaesthesia. ADP/PDPH can represent a considerable degree of morbidity for the parturient and require immediate diagnosis and appropriate management to ensure recovery and avoid complications. AIM: This retrospective audit was carried out to identify the accidental dural puncture and post-dural puncture headache rates at the Coombe Women and Infant University Hospital in Dublin. METHODS: Cases of ADP and PDPH were identified retrospectively from a register used to record these cases. Demographic and obstetric data was retrieved using the patients' medical records. Analysis was carried using MS Excel. RESULTS: In 1 year (June 1, 2018 to June 1, 2019), there were 25 cases of ADP during epidural catheter insertion and this is 0.78% of epidurals done in this period. Seventeen of these (68%) subsequently developed PDPH. In total, there are 32 cases of PDPH: 27 after epidural analgesia using an 18G Touhy needle and 5 after a spinal anaesthetic using a 25G Whitacre needle. All PDPH cases received first-line conservative treatment and 9 (28.1%) required an epidural blood patch (EBP). No-one required a second EBP. DISCUSSION: The incidence of ADP at our hospital (0.78%) is within the range quoted in the literature (0.1-1.5%) and below the UK standard of 1%. The incidence of PDPH after recognized ADP (68%) is also consistent with other published reports.

Managing opioid consumption after caesarean delivery: a quality improvement initiative.

INTRODUCTION: Caesarean delivery is the most common major surgical procedure performed worldwide and pain management after caesarean delivery remains challenging. Finding a balance between sufficient postoperative pain relief and excess sedation secondary to opioids is often difficult in this patient population. This quality improvement project aimed to manage the amount of opioid consumption after caesarean delivery using a new postoperative analgesic regimen. METHODS: The current practice was analysed in 52 patients before introducing the new regimen. Oxycodone consumption, pain scores and quality of recovery were recorded. Following this pre-implementation audit, a new postoperative analgesic protocol was introduced. All patients received standard doses of intrathecal morphine, paracetamol and diclofenac. Regular oxycodone sustained-release (SR) was replaced with oxycodone immediate-release (IR) as needed. These changes also coincided with education to improve midwifery assessment of pain and the delivery of analgesia. RESULTS: The outcome measures were re-audited in 178 patients which showed that oxycodone consumption had reduced median (IQR) 30 mg (20-40) vs 10 mg (5-15) (p < 0.001). There was no significant difference in the pain scores between the before and after groups at rest median (IQR) 2.0 (0-4.8) vs 2.0 (0.8-4.0) or at movement 5.0 (3.0-6.0) vs 5.0 (3.0-6.3) (p = 0.292, p = 0.482 respectively). The quality of recovery scores were also equivalent mean (SD) 78.6 (20.6) vs 77.8 (19.0) (p = 0.792). CONCLUSION: The results of this study suggest that postoperative opioid consumption can be reduced with specific analgesic protocols and allow us to improve patient's quality of recovery.

Impact of experimental obesity on diaphragm structure, function, and bioenergetics.

Obesity is associated with bioenergetic dysfunction of peripheral muscles; however, little is known regarding the impact of obesity on the diaphragm. We hypothesized that obesity would be associated with diaphragm dysfunction attributable to mitochondrial oxygen consumption and structural and ultrastructural changes. Wistar rat litters were culled to 3 pups to induce early postnatal overfeeding and consequent obesity. Control animals were obtained from unculled litters. From postnatal day 150, diaphragm ultrasound, computed tomography, high-resolution respirometry, immunohistochemical, biomolecular, and ultrastructural histological analyses were performed. The diaphragms of obese animals, compared with those of controls, presented changes in morphology as increased thickening fraction, diaphragm excursion, and diaphragm dome height, as well as increased mitochondrial respiratory capacity coupled to ATP synthesis and maximal respiratory capacity. Fatty acid synthase gene expression was also higher in obese animals, suggesting a source of energy for the respiratory chain. Myosin heavy chain-IIA was increased, indicating shift from glycolytic toward oxidative muscle fiber profile. Diaphragm tissue also exhibited ultrastructural changes, such as compact, round, and swollen mitochondria with fainter cristae and more lysosomal bodies. Dynamin-1 expression in the diaphragm was reduced in obese rats, suggesting decreased mitochondrial fission. Furthermore, gene expressions of peroxisome γ proliferator-activated receptor coactivator-1α and superoxide dismutase-2 were lower in obese animals than in controls, which may indicate a predisposition to oxidative injury. In conclusion, in the obesity model used herein, muscle fiber phenotype was altered in a manner likely associated with increased mitochondrial respiratory capability, suggesting respiratory adaptation to increased metabolic demand.NEW & NOTEWORTHY Obesity has been associated with peripheral muscle dysfunction; however, little is known about its impact on the diaphragm. In the current study, we found high oxygen consumption in diaphragm tissue and changes in muscle fiber phenotypes toward a more oxidative profile in experimental obesity.