Unraveling medication errors in enteral tube administration: A cross-sectional study in geriatric patients receiving home health care

Background: Medication administration through enteral feeding tubes requires careful consideration, as several medications are unsuitable for such administration due to interactions with feeding formulas or adverse effects when crushed. These errors can lead to feeding tube obstruction, reduced drug efficacy, or drug toxicity. Objective: This study aimed to assess medication errors in geriatric patients using enteral feeding tubes who were enrolled in a home health care program. Method: This was a cross-sectional observational study conducted at the Ministry of Health Government Hospital in Makkah City, Saudi Arabia. Medication errors related to chronic oral drugs in geriatric patients using enteral feeding tubes were evaluated, including inappropriate medications for enteral tube administration, inappropriate preparation, drug-nutrient interaction, and availability of liquid formulation, following established guidelines. Results: Of the total 233 medications prescribed to 46 patients receiving enteral tube feeding at home, 49.3% exhibited at least one form of medication error, totaling 135 errors. Medication errors were highly prevalent among the patients (93.4%), with the leading cause being the administration of medications unsuitable for enteral feeding tubes (33.3%), predominantly due to the use of controlled release or enteric-coated formulations. Conclusion: This study underscores the high prevalence of medication errors in older patients receiving enteral feeding at home. To ensure patient safety and optimal outcomes, healthcare professionals should utilize available resources and seek expert advice when selecting medications and dosage forms for tube-fed patients. Pharmacists play a critical role in promoting safe drug use and can greatly contribute by educating patient caregivers on proper medication preparation and administration techniques, thus preventing harm to patients

Aminoglycoside drugs induce efficient read-through of CDKL5 nonsense mutations, slightly restoring its kinase activity

The X-linked CDKL5 gene codes for a kinase whose mutations have been associated with a suite of neurodevelopmental disorders generally characterized by early-onset epileptic encephalopathy and severe intellectual disability. The impact of these mutations on CDKL5 functions and brain development remain mainly unknown, although the importance of maintaining the catalytic activity is generally recognized. Since no cure exists for CDKL5 disorders, the demand for innovative therapies is a real emergency. The recent discovery that CDKL5 is dosage sensitive poses concerns on conventional protein and gene augmentative therapies. Thus, RNA-based therapeutic approaches might be preferred. We studied the efficacy of read-through therapy on CDKL5 premature termination codons (PTCs) that correspond roughly to 15% of all mutations. Our results provide the first demonstration that all tested CDKL5 nonsense mutations are efficiently suppressed by aminoglycoside drugs. The functional characterization of the restored full-length CDKL5 reveals that read-through proteins fully recover their subcellular localization, but only partially rescue their catalytic activity. Since read-through can cause amino acid substitution, CDKL5 patients carrying the PTC outside the catalytic domain might benefit more from a nonsense suppression therapy. Eventually, we demonstrate that non-aminoglycoside drugs, such as Ataluren (PTC124) and GJ072, are unable to induce read-through activity on CDKL5 PTCs. Although these drugs might be more effective in vivo, these results question the validity of the Ataluren phase 2 clinical trial that is currently ongoing on CDKL5 patients

Bilateral retinal hemorrhages following finger pressure against the soft palate (الترفيع) in recessive <i>CRB1</i>-related retinopathy

<p><i>Purpose</i>: To report two siblings with <i>CRB1</i>-related retinopathy who developed retinal hemorrhages following village traditional treatment of upward finger pressure against the soft palate ().</p> <p><i>Methods</i>: A retrospective case series.</p> <p><i>Results</i>: Two sisters were clinically diagnosed and genetically confirmed to have recessive <i>CRB1</i>-related retinal dystrophy. The family did not accept the condition as non-treatable and took both sisters for a traditional village therapy, consisting of several sessions of intense upward index finger pressure by the healer against the soft palate for each child. When examined following this therapy, both sisters had bilateral pre-retinal hemorrhages which were not present before the intervention and resolved without sequelae over the next several months.</p> <p><i>Conclusions</i>: The traditional village therapy may have compromised retinal venous outflow and/or provoked a Valsalva phenomenon, leading to the bilateral retinal hemorrhages. The fact that this occurred bilaterally and in both sisters supports the concept of relative vessel wall incompetence as part of <i>CRB1</i>-related retinopathy.</p

The ophthalmic phenotype of IFT140-related ciliopathy ranges from isolated to syndromic congenital retinal dystrophy

Background Conorenal syndrome is a systemic skeletal ciliopathy characterised by skeletal and renal findings and caused by biallelic mutations in the gene intraflagellar transport 140 Chlamydomonas homologue (IFT140). Most studies have focused on syndromic features and are by non-ophthalmologists. We highlight the ophthalmic phenotype. Methods Retrospective consecutive case series (2010-2014). Results Twelve subjects with confirmed homozygous mutations were identified (11 consanguineous families; 7 boys; assessed at age 10 months to 20 years, average and median age 6.5 and 4 years). All were homozygous for the same IFT140 mutation (c.1990G>A; p. Glu664Lys) except one who was homozygous for c.1541_1542delinsAA. All had poor vision and nystagmus since birth, with visual acuity after 5 years old of hand motions or light perception. In early childhood, nine were noted to stare at lights, four were noted to have a happy demeanour, high hyperopia was typical, and electroretinography was non-recordable. Fundus appearance was grossly normal before the age of 1 year but thereafter appeared dystrophic. Eight children had developmental delay, two had short stubby fingers, and one had renal disease, but four had no evident extraocular disease, including one aged 18 years who also had two older affected siblings in their twenties who remained non-syndromic and were excelling academically. Conclusions Recessive IFT140 mutations cause a severe congenital retinal dystrophy with high hyperopia and often early photophilia. Developmental delay is common but not universal and not all patients have obvious extraocular findings. The c.1990G>A mutation represents a founder effect or mutational hotspot on the Arabian Peninsula

Evaluating endothelial function of the common carotid artery: an in vivo human model

Background and aims: Flow mediated dilation (FMD) of peripheral conduit arteries is a well-established tool. to evaluate endothelial function. The aims of this study are to apply the FMD model to cerebral circulation by using acetazolamide (ACZ)-induced intracranial vasodilation as a stimulus to increase common carotid artery (CCA) diameter in response to a Local increase of blood flow velocity (BFV). Methods and results: In 15 healthy subjects, CCA end-diastolic diameter and BFV, middle cerebral artery (MCA) BFV and mean arterial blood pressure (MBP) were measured at basal conditions, after an intravenous bolus of 1 g ACZ, and after placebo (saline) sublingual administration at the 15th and 20th minute. In a separate session, the same parameters were evaluated after placebo (saline) infusion instead of ACZ and after 10 mu g/m(2) bs and 300 mu g of glyceryl trinitrate (GTN), administered sublingually, at the 15th and 20th minute, respectively. After ACZ bolus, there was a 35% maximal MCA mean BFV increment (14th minute), together with a 22% increase of mean CCA end-diastolic BFV and a CCA diameter increment of 3.9% at the 3rd minute (p = 0.024). There were no MBP significant variations up to the 15th minute (p = 0.35). After GTN administration, there was a significant increment in CCA diameter (p < 0.00001). Conclusions: ACZ causes a detectable CCA dilation in healthy individuals concomitantly with an increase in BFV. Upon demonstration that this phenomenon is endothelium dependent, this experimental model might become a valuable tool. to assess endothelial function in the carotid artery

Evaluating endothelial function of the common carotid artery: An in vivo human model.

BACKGROUND AND AIMS: Flow mediated dilation (FMD) of peripheral conduit arteries is a well-established tool to evaluate endothelial function. The aims of this study are to apply the FMD model to cerebral circulation by using acetazolamide (ACZ)-induced intracranial vasodilation as a stimulus to increase common carotid artery (CCA) diameter in response to a local increase of blood flow velocity (BFV). METHODS AND RESULTS: In 15 healthy subjects, CCA end-diastolic diameter and BFV, middle cerebral artery (MCA) BFV and mean arterial blood pressure (MBP) were measured at basal conditions, after an intravenous bolus of 1g ACZ, and after placebo (saline) sublingual administration at the 15th and 20th minute. In a separate session, the same parameters were evaluated after placebo (saline) infusion instead of ACZ and after 10mug/m(2) bs and 300mug of glyceryl trinitrate (GTN), administered sublingually, at the 15th and 20th minute, respectively. After ACZ bolus, there was a 35\% maximal MCA mean BFV increment (14th minute), together with a 22\% increase of mean CCA end-diastolic BFV and a CCA diameter increment of 3.9\% at the 3rd minute (p=0.024). There were no MBP significant variations up to the 15th minute (p=0.35). After GTN administration, there was a significant increment in CCA diameter (p<0.00001). CONCLUSIONS: ACZ causes a detectable CCA dilation in healthy individuals concomitantly with an increase in BFV. Upon demonstration that this phenomenon is endothelium dependent, this experimental model might become a valuable tool to assess endothelial function in the carotid artery

Efficacy and safety of delafloxacin, ceftaroline, ceftobiprole, and tigecycline for the empiric treatment of acute bacterial skin and skin structure infections: A network meta-analysis of randomized controlled trials

Background: This review aimed to conduct an indirect comparison using a Bayesian network meta-analysis of randomized controlled trials (RCTs) to compare the efficacy and safety of delafloxacin versus other single antibiotic regimens for the empiric treatment of Acute Bacterial Skin and Skin Structure Infections. Method: A systematic search with no start date restrictions was conducted. The Cochrane Risk of Bias tool was used to assess the quality of included RCTs. Results: Of the 577 studies initially identified, nine RCTs were included in the review. The network meta-analysis showed that ceftaroline, ceftobiprole, delafloxacin and tigecycline had similar efficacy in the indirect comparisons [Ceftaroline Odds Ratio (OR) = 1.2, 95% Crl = 0.46–3.6), ceftobiprole (OR = 1.3, 95% Crl = 0.34–3.0) and tigecycline (OR = 0.96, 95% Crl = 0.30–2.9)]. However, the ranking plot for the intention to treat (ITT) population showed that delafloxacin had a probability of 80.8% to be ranked first followed by ceftobiprole (13.1%). The analysis of the overall adverse events showed that ceftaroline (OR = 0.88, 95% Crl = 0.65–1.2), ceftobiprole (OR = 1.1, 95% Crl = 0.69–2.0), delafloxacin (OR = 0.88, 95% Crl = 0.57–1.3) and tigecycline (OR = 1.4, 95% Crl = 0.88–2.2) had similar safety profiles. Conclusion: Delafloxacin did not show any statistically significant differences when compared to ceftaroline, ceftobiprole, and tigecycline in terms of efficacy and safety. However, the surface under the cumulative ranking curve (SUCRA) probability ranked delafloxacin as the first option for the ITT population. © 2022 The AuthorsOpen access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]