Outcomes of croup in children: COVID-19 versus non-COVID-19 cases.

Objectives: The emergence of COVID-19 has revealed its association with croup. The objective of this study was to compare outcomes of COVID-19 related croup to non-COVID-19 related croup during the COVID-19 pandemic. Methods: This retrospective propensity matched study used data from 2020-2023 in the United States Cohort of the TriNetX database that includes 56 major health care organizations. The analysis compared the outcomes of 2 cohorts of patients between 2 months and 7 years of age: Cohort A had croup and a positive test for COVID-19 and Cohort B had croup without a positive COVID-19 test, both within 1 week before or after presentation with croup. Outcomes were death, admission to the hospital, intensive care unit (ICU) admission, respiratory rate >60, and oxygen saturation <90 within 7 days after the diagnosis of croup. Results: There were 2590 patients with COVID-19 related croup and 103,439 patients with non-COVID-19 croup. The final propensity matched cohort included 5180 patients evenly divided between groups. When both groups were compared based on outcomes after matching, there was twice the risk of the patient being admitted to the hospital with COVID-19 croup (risk ratio [RR] = 2.12; 95% confidence interval [CI] 1.59-2.84; P < 0.001). Those with COVID-19 related croup had significantly increased risk of being admitted to the ICU (RR = 4.90; 95% CI 3.11-7.73; P < 0.001). The patients with COVID-19 related croup were more likely to have a respiratory rate ≥60 (RR = 2.00; 95% CI 1.18-3.37; P = 0.008) and oxygen saturation ≤90% (RR = 2.12; 95% CI 1.21-3.70; P = 0.007). There were no deaths in the final cohorts. There were no worse outcomes in the Omicron COVID-19 related croup group. Conclusions: The patients with COVID-19 related croup exhibited more severe disease manifestations. These children were more likely to be admitted to the hospital/ICU and had more significant respiratory distress.

At the intersection of toxicology, psychiatry, and genetics: a diagnosis of ornithine transcarbamylase deficiency.

Ornithine transcarbamylase (OTC) deficiency is a genetic disorder involving a mutation of the ornithine transcarbamylase gene, located on the short arm of the X chromosome (Xp21.1). This makes the expression of the gene most common in homozygous males, but heterozygous females can also be affected and may be more likely to suffer from serious morbidity. Most males present early in the neonatal period with more devastating outcomes than their female counterparts. Up to 34% will present in the first 30 days of life (J Pediatr 2001;138:S30). Females often have partially functioning mitochondria due to uneven distribution of the mutant gene secondary to lyonization ("X-chromosome Inactivation". Genetics Home Reference, 2012). Occasionally, symptomatic females may not even present until they are placed under metabolic stress such as a severe illness, fasting, pregnancy, or new medication (Roth KS, Steiner RD. "Ornithine Transcarbamylase Deficiency". EMedicine, 2012). The urea cycle is the body's primary tool for the disposal of excess nitrogen, which is generated by the routine metabolism of proteins and amino acids. Mitochondrial dysfunction impairs urea production and result in hyperammonemia (Semin Neonatol 2002;7:27). The sine qua non among all degrees of OTC deficiency at presentation is hyperammonemia. As in adults, children will have similar symptoms of encephalopathy, but this may be expressed differently depending on the child's developmental level. We present an unusual case of OTC deficiency in an older child with undifferentiated symptoms of an anticholinergic toxidrome, liver failure, iron overdose, and mushroom poisoning.

Prospective pilot derivation of a decision tool for children at low risk for testicular torsion.

OBJECTIVE: The purpose of this study was to derive a pilot clinical decision tool with 100% negative predictive value for testicular torsion based on prospectively collected data in children with acute scrotal pain. METHODS: This was a prospective cohort study of a convenience sample of newborn to 21-year-old males evaluated for acute (72 hours or less) scrotal pain at an urban children's hospital emergency department (ED). A pediatric emergency medicine fellow or attending physician documented history and examination findings on a standardized data collection form. The study investigators used ultrasound (US), operative reports, or clinical follow-up to identify patients who had testicular torsion. Pearson's chi-square test and odds ratios (OR) were used to identify factors associated with the diagnosis of testicular torsion. The authors also used a recursive partitioning model to create a low-risk decision tool for testicular torsion. RESULTS: Of the 450 eligible patients, 228 (51%) were enrolled, with a mean (± SD) age of 9.9 (± 4.1) years, including 21 (9.2%, 95% confidence interval [CI] = 5.8% to 13.7%) with testicular torsion. The derived clinical decision tool consisted of three variables: horizontal or inguinal testicular lie (OR = 18.17, 95% CI = 6.2 to 53.2), nausea or vomiting (OR = 5.63, 95% CI = 2.08 to 15.22), and age 11 to 21 years (OR = 3.9, 95% CI = 1.27 to 11.97). These variables had a sensitivity of 100% (95% CI = 98% to 100%) and negative predictive value of 100% (95% CI = 98% to 100%) for the diagnosis of testicular torsion. CONCLUSIONS: Based on a decision tool derived with recursive partitioning, study patients with all of the following characteristics had no risk of testicular torsion: normal testicular lie, lack of nausea or vomiting, and age 0 to 10 years. Future research should focus on externally validating this tool to optimize emergent evaluation when testicular torsion is likely, while minimizing routine sonographic evaluation when patients are unlikely to have a serious condition requiring immediate management.

Laser Doppler flow and brain tissue PO2 after cortical impact injury complicated by secondary ischemia in rats treated with arginine.

BACKGROUND: Traumatic brain injury (TBI) makes the brain susceptible to secondary insults such as ischemia. This study tested the hypothesis that L-arginine would increase regional CBF (rCBF) and brain tissue PO2 (PbtO2) at the injury site. METHODS: A secondary insult model was employed in rodents. rCBF was measured with laser doppler flowmetry (LDF) and PbtO2 with a PO2 catheter at the impact site. Animals were randomized to receive L-arginine, D-arginine or saline intravenously, 5 minutes after impact. RESULTS: In animals who received L-arginine, the percentage rCBF from baseline (%CBF) was higher at the impact site after impact (p < 0.001), during bilateral carotid occulation (BCO) (p = 0.001) and during reperfusion (p = 0.032). In contrast, PbtO2 was not significantly increased throughout the experiment for the L-arginine group. CONCLUSIONS: Administration of L-arginine increased rCBF in the injured brain tissue, and resulted in better preservation of CBF during BCO than D-arginine and saline.

Oxidative DNA lesions in a rodent model of traumatic brain injury.

BACKGROUND: Oxidative DNA lesions have not been well studied in traumatic brain injury (TBI). METHODS: TBI was induced with a controlled cortical impact injury in rats. Brain tissue was examined for 8-hydroxy-2'-deoxyguanosine (oh8dG) using mono-clonal antibodies at different time frames; 15 minutes (n = 4), 30 minutes (n = 7), 60 minutes (n = 6), and 240 minutes (n = 5). The control group consisted of sham-operated animals undergoing the same surgery without the controlled cortical impact injury (n = 5). RESULTS: An elevation of oh8dG was detected in the nuclear and perinuclear (mitochondrial) regions of the ipsilateral cortex, but seldom in those of the contralateral cortex. The amount of oh8dG in those animals with TBI was significant in all time frames when compared with sham-operated controls (p < 0.001). The oh8dG levels were more prominent at 15 minutes (p < 0.0001) when compared with controls. CONCLUSION: Oxidative DNA lesions occurred in this model of TBI maximally early after TBI. This suggests that oh8dGs may affect genetic material of the brain and that oh8dGs may adversely affect gene expression that occurs early after head injury.