Pyelonephritis (PN) represents an important cause of morbidity in the pediatric population, especially in uropathic patients. The aim of the study is to demonstrate differences between PNs of uropathic patients and PNs acquired in community in terms of uropathogens involved and antibiotic sensitivity; moreover, to identify a proper empiric therapeutic strategy. A retrospective study was conducted on antibiograms on urine cultures from PNs in vesicoureteral reflux (VUR) patients admitted to pediatric surgery department and from PNs in not VUR patients admitted to Pediatric Emergency Unit between 2010 and 2020. We recorded 58 PNs in 33 patients affected by VUR and 112 PNs in the not VUR group. The mean age of not VUR patients at the PN episode was 1.3 ± 2.6 years (range: 20 days of life–3 years), and almost all the urine cultures, 111 (99.1%), isolated Gram-negative bacteria and rarely, 1 (0.9%), Gram-positive bacteria. The Gram-negative uropathogens isolated were Escherichia coli (97%), Proteus mirabilis (2%), and Klebsiella spp. (1%). The only Gram-positive bacteria isolated was an Enterococcus faecalis. As regards the antibiograms, 96% of not VUR PNs responded to beta-lactams, 99% to aminoglycosides, and 80% to sulfonamides. For the VUR group, mean age was 3.0 years ± 3.0 years (range: 9 days of life–11 years) and mean number of episodes per patient was 2.0 ± 1.0 (range: 1–5); 83% of PNs were by Gram-negatives bacteria vs. 17% by Gram-positive: the most important Gram-negative bacteria were Pseudomonas aeruginosa (44%), Escherichia coli (27%), and Klebsiella spp. (12%), while Enterococcus spp. determined 90% of Gram-positive UTIs. Regimen ampicillin/ceftazidime (success rate: 72.0%) was compared to ampicillin/amikacin (success rate of 83.0%): no statistically significant difference was found (p = 0.09). The pathogens of PNs in uropathic patients are different from those of community-acquired PNs, and clinicians should be aware of their peculiar antibiotic susceptibility. An empiric therapy based on the association ampicillin + ceftazidime is therefore suggested.
Dinoflagellates associated with coral reefs produce ciguatoxin which is concentrated in the marine food chain and subsequently ingested by humans resulting in ciguatera poisoning.' It is an endemic and underreported* problem in Queensland. We present two cases of cardiac dysfunction temporally related to ciguatera poisoning.A 65-year-old Vietnamese male (Case 1) presented to the Princess Alexandra Hospital with findings consistent with ciguatera poisoning. He described paraesthesia of the tongue, abdominal skin, distal extremities and perioral region. Temperature sensation reversal, nausea, vomiting and mild diarrhoea were noted. These symptoms began within 24 hours of eating portions of a large reef fish, including the head and liver. Others who shared the meal had the same typical but milder symptoms of ciguatera poisoning.On examination the patient was shocked, without fever or signs of dehydration. Blood pressure (BP) was 75 mmHg systolic with a relative bradycardia of 60 beatshinute. The ECG showed only non-specific minor ST shift. Serial serum creatine phosphokinase levels were normal.The patient responded to fluid loading. The cardiac findings resolved over three days and the non-cardiac symptoms cleared over the subsequent 14 days.A 54-year-old Caucasian male (Case 2) was admitted to Townsville General Hospital with progressive dyspnoea, dizziness and peripheral oedema dating from his ingestion of several large portions from a large coral trout two weeks previously. He also complained of perioral paraesthesia, myalgia, arthralgia, and limb hyperaesthesia. Diarrhoea, abdominal pain and temperature sensation reversal were not described. Others from the group who had eaten the same fish had typical symptoms of ciguatera poisoning. Pulse rate was 110 beatdminute, BP 165/95 mmHg, third and fourth heart sounds were evident, the JVP was raised and the apex beat displaced. Diminution of light touch, pin prick and vibration sense was noted below the level of the knees with ankle and knee jerks being absent. Proprioception was impaired and the gait ataxic.
An anterior congenital diaphragmatic hernia (CDH) is a diaphragmatic defect that allows the passage of abdominal organs into the thorax. It is typically asymptomatic (the diagnosis is incidental) and it requires surgical correction. In this paper we present a 6 year-old girl affected by spinal muscular atrophy (SMA) who was diagnosed with anterior CDH. Four years after laparoscopic closure of the defect by interrupted suture the girl returned for hernia recurrence. Another laparoscopic procedure was performed and the defect was closed using a GORE-TEX patch. We postulate a mechanism of altered respiratory dynamic and increased abdominal pressure related to scoliosis favouring CDH recurrence in patients with neuromuscular pathologies such as SMA. In these patients patch interposition should be considered in the first place in order to reduce tension over margins. Laparoscopy is a safe and feasible procedure for CDH correction also in case of recurrence and when the interposition of a patch is required.
Our early results suggest that the "double N" laparoscopic technique to close the internal inguinal ring in children is safe and efficient. We therefore suggest using this approach in children with a patent internal inguinal ring of >1 cm. The recurrence rate is low, but it should be better assessed by studies with longer follow-up.
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