An audit of patient-controlled analgesia after appendicectomy in children

Summary

Background

Patient-controlled analgesia (PCA) is commonly used after appendicectomy in children.

Aim

The aim of this study was to characterize the analgesic use of children prescribed PCA after appendicetomy, in order to rationalize future use of this modality.

Methods

We retrospectively audited all cases of acute appendicitis over a 4-year period in a single pediatric hospital, recording demographics, surgical approach, pathology, analgesia use, pain scores, and duration of PCA. We preplanned subgroup analyses for surgical approach, pathology, and intraoperative nonsteroidal anti-inflammatory drug (NSAID) administration. We subsequently identified a patient subgroup who were unlikely to require PCA and conducted a (2 months) prospective audit of such patients (uncomplicated appendicitis with intraoperative NSAID) having non-PCA (oral) analgesia.

Results

Of the 649 patients undergoing appendicectomy for acute appendicitis, 85% were prescribed an opioid PCA, 8% received an opioid infusion (younger patients), and 7% received neither PCA nor infusion. Of the 541 bolus only PCA patients, 49% had laparoscopic surgery, 36% had complicated appendicitis, and 49% received intraoperative NSAID (diclofenac). Mean (SD) duration of PCA was shorter with uncomplicated vs complicated appendicitis (21.9 ± 10.7 vs 32.8 ± 21.1 h, P < 0.001, difference in means [95% CI]: 10.9 [7.7–14.1]), and with intraoperative NSAID (23.2 ± 14.4 vs 28.4 ± 17.4 h, P < 0.001, difference in means [95% CI]: 5.2 [2.5–7.9]). There was no difference in the time to PCA cessation between laparoscopic and open approach. Morphine consumption and pain scores were lower in the early postoperative period for those patients receiving intraoperative NSAID. In the prospective audit, 44 of 69 patients had uncomplicated appendicitis. Thirty-eight of these were prescribed oral analgesia and none required any parenteral opioid or acute pain service intervention postoperatively. Parental satisfaction level was high (>90%) with oral analgesia.

Conclusions

It is feasible that children with uncomplicated appendicitis given intraoperative NSAID can be successfully managed without PCA.

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A novel 5q11.2 microdeletion in a child with mild developmental delay and dysmorphic features

5q11.2 Deletion is a very rare genomic disorder, and its clinical phenotype has not yet been characterized. This report describes a patient with an 8.6 Mb deletion, showing hypotonia, mild developmental delay, short stature, and distinctive dysmorphic features (frontal bossing, square face, deep-set eyes, prominent columella, long philtrum, thin lips). © 2016 Wiley Periodicals, Inc.

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Homozygosity for moyamoya disease risk allele leads to moyamoya disease with extracranial systemic and pulmonary vasculopathy

Moyamoya disease is characterized by diffuse distal intracranial stenosis. Recently, RNF213 has been identified as a susceptibility gene in the development of this condition. Pulmonary hypertension is a rare progressive vasculopathy with an unknown etiology. The co-occurrence of pulmonary hypertension and Moyamoya disease has been described in four patients; however, whether this co-occurrence represents a chance association or a common vascular pathology has remained unknown. Here, we report two unrelated male patients who presented during their childhood with dyspnea on exertion. Systemic vascular imaging studies revealed the presence of pulmonary hypertension and Moyamoya disease in both patients. Medical exome sequencing revealed that both patients had a homozygous mutation for p.Arg4810Lys in RNF213. We suggest that homozygosity in RNF213 may lead to a novel entity involving the brain and lung. Interestingly, when present in a heterozygous state, this mutation causes a classic cerebral vascular disease, Moyamoya disease. In the homozygous state, the exact same mutation led to Moyamoya disease with extracranial systemic vasculopathy in at least two patients. From a clinical standpoint, cerebrovascular or pulmonary vascular investigations may be warranted in patients with pulmonary hypertension or Moyamoya disease, respectively. © 2016 Wiley Periodicals, Inc.

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Diagnosis of Van den Ende–Gupta syndrome: Approach to the Marden–Walker-like spectrum of disorders

Marden–Walker syndrome is challenging to diagnose, as there is significant overlap with other multi-system congenital contracture syndromes including Beals congenital contractural arachnodactyly, D4ST1-Deficient Ehlers–Danlos syndrome (adducted thumb-clubfoot syndrome), Schwartz–Jampel syndrome, Freeman–Sheldon syndrome, Cerebro-oculo-facio-skeletal syndrome, and Van den Ende–Gupta syndrome. We discuss this differential diagnosis in the context of a boy from a consanguineous union with Van den Ende–Gupta syndrome, a diagnosis initially confused by the atypical presence of intellectual disability. SNP microarray and whole exome sequencing identified a homozygous frameshift mutation (p.L870V) in SCARF2 and predicted damaging mutations in several genes, most notably DGCR2 (p.P75L) and NCAM2 (p.S147G), both possible candidates for this child's intellectual disability. We review distinguishing features for each Marden–Walker-like syndrome and propose a clinical algorithm for diagnosis among this spectrum of disorders. © 2016 Wiley Periodicals, Inc.

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SETD5 loss-of-function mutation as a likely cause of a familial syndromic intellectual disability with variable phenotypic expression

Loss-of-function de novo mutations in the SETD5 gene, encoding a putative methyltransferase, are an important cause of moderate/severe intellectual disability as evidenced by the results of sequencing large patient cohorts. We present the first familial case of a SETD5 mutation contributing to a phenotype of congenital heart defects and dysmorphic features, with variable expression, in two siblings and their father. Interestingly, the father demonstrated only mild intellectual impairment. Family based exome sequencing combined to careful parental phenotyping may reveal a more complex clinical picture in newly recognized syndromes. © 2016 Wiley Periodicals, Inc.

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Early atherosclerosis development in female apolipoprotein E-deficient mice is associated with an increased vascular oxidative stress

2016-07-03T15-29-41Z
Source: Oxidants and Antioxidants in Medical Science
Livan Delgado-Roche, Yanet Hernandez, Ivonilce Venturi, Irina Wilkins, Dalia Alvarez.
Objective: The mechanisms of atherosclerosis development in the apolipoprotein E-deficient (apoE−/−) mice have been clearly described. In this genetically modified strain, oxidative stress contributes with atherosclerotic lesion progression. However, there are controversial criteria on the vulnerability of female apoE−/− mouse to oxidative stress and atherosclerosis during the fertile period. Thus, the aim of the present work was to examine the implication of vascular oxidative stress during early atherosclerosis development in young apoE−/− female mice. Methods: AQ1 Please provide a brief methodology Results: Hematoxylin/eosin staining demonstrated the presence of early atherosclerotic lesions in the apoE−/− mice, which progressed with age. Dihydroethidium staining of aortic sections revealed a significant increase of superoxide anion generation in apoE−/− compared with the wild type mice. The increment of this reactive oxygen species was associated, at least, with the overexpression of Nox2 mRNA levels. In addition, the 8-week-old apoE−/− mice had a significant increment of lipid and protein damage, as well as a disruption of superoxide dismutase and catalase activity, together with a deprivation of reduced glutathione and an impairment of nitric oxide availability. Conclusion: The present study shows that early atherosclerotic lesion formation in young apoE−/− female mice is associated with an increment of Nox2-mediated reactive oxygen species generation with the subsequent redox disruption, suggesting a key role of oxidative stress during atherogenesis in fertile apoE−/− female mice.


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Patients with mild enteropathy have apoptotic injury of enterocytes similar to that in advanced enteropathy in celiac disease

Severity of villous atrophy in celiac disease (CeD) is the cumulative effect of enterocyte loss and cell regeneration. Gluten-free diet has been shown to benefit even in patients having a positive anti-tissue transglutaminase (tTG) antibody titre and mild enteropathy.

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Prescription drugs associated with false-positive results when using faecal immunochemical tests for colorectal cancer screening

The most common side effect in population screening programmes is a false-positive result which leads to unnecessary risks and costs.

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Low testosterone in non-responsive coeliac disease: A case series, case–control study with comparisons to the National Health and Nutrition Examination Survey

Adults with coeliac disease (CD) often report persistent fatigue, even when CD appears well controlled for unknown reasons.

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Predictive factors of poor response to therapy in Autoimmune Hepatitis

To evaluate "ex ante" the predictive factors of incomplete/absent response to the standard therapy in a well characterized series of Autoimmune Hepatitis (AIH) patients from Italy.

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Patients with mild enteropathy have apoptotic injury of enterocytes similar to that in advanced enteropathy in celiac disease

Severity of villous atrophy in celiac disease (CeD) is the cumulative effect of enterocyte loss and cell regeneration. Gluten-free diet has been shown to benefit even in patients having a positive anti-tissue transglutaminase (tTG) antibody titre and mild enteropathy.

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Prescription drugs associated with false-positive results when using faecal immunochemical tests for colorectal cancer screening

The most common side effect in population screening programmes is a false-positive result which leads to unnecessary risks and costs.

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Low testosterone in non-responsive coeliac disease: A case series, case–control study with comparisons to the National Health and Nutrition Examination Survey

Adults with coeliac disease (CD) often report persistent fatigue, even when CD appears well controlled for unknown reasons.

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Predictive factors of poor response to therapy in Autoimmune Hepatitis

To evaluate "ex ante" the predictive factors of incomplete/absent response to the standard therapy in a well characterized series of Autoimmune Hepatitis (AIH) patients from Italy.

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