Impact of Focused Abdominal Ultrasound Utilization on Outcomes for Children With Midgut Volvulus.

BACKGROUND: Ultrasound (US) is gaining acceptance for the evaluation of midgut volvulus in children. However, its impact on clinical outcomes is unknown. We aim to determine whether using US as a first-line modality changes imaging mobilization, time to surgery and re-feeding, length of stay, and frequency of bowel necrosis, short bowel syndrome, and death. METHODS: An IRB-approved retrospective cohort study was performed at a tertiary pediatric institution. Eighty children with surgically confirmed midgut volvulus from 2014 to 2021 were compared before and after implementation of US as first-line imaging and based on the modality used to diagnose midgut volvulus. RESULTS: Outcomes were not statistically different pre- versus post-implementation. Compared with patients who had UGI only, those who had US only or both had significantly quicker imaging mobilization (median: -33 min; 95% CI: -61.2, -4.8; p = 0.023 and median: -31 min; 95% CI: -58.5, -3.6; p = 0.028 respectively). Patients with US only were less likely to have bowel necrosis compared with those who had UGI only (9.1% versus 43.8%, p = 0.042). Patients who had US only or both were less likely to develop short bowel syndrome compared to UGI only (4.8% US only, 0% both, 40% UGI only; p = 0.027 for US only, p = 0.005 for both). CONCLUSIONS: No statistically significant change in outcomes was found after implementation of US as first-line imaging for midgut volvulus. However, patients diagnosed with US only or US in combination with UGI had quicker imaging mobilization and decreased frequency of bowel necrosis and short bowel syndrome. Findings suggest that US has potential to improve patient outcomes. LEVEL OF EVIDENCE: III.

Imaging of pediatric pancreas tumors: A COG Diagnostic Imaging Committee/SPR Oncology Committee White Paper.

Primary pancreatic tumors in children are rare with an overall age-adjusted incidence of 0.018 new cases per 100,000 pediatric patients. The most prevalent histologic type is the solid pseudopapillary neoplasm, followed by pancreatoblastoma. This paper describes relevant imaging modalities and presents consensus-based recommendations for imaging at diagnosis and follow-up.

Solitary long-bone epiphyseal lesions in children: radiologic-pathological correlation and epidemiology.

BACKGROUND: Solitary epiphyseal lesions are rare and present with nonspecific imaging features. Knowledge regarding etiologies of pediatric epiphyseal lesions is limited to small studies. OBJECTIVE: The purpose of this study was to determine the relative incidence of pathologies affecting the pediatric epiphysis based on biopsy-proven cases with imaging. MATERIALS AND METHODS: We conducted a retrospective review of imaging studies including the terms "biopsy" or "resection" and entities known to affect the epiphysis and cross-referenced these with pathology reports, recording the relevant clinical data. Two radiologists performed comprehensive imaging review and recorded relevant features. RESULTS: Forty-nine children and adolescents met inclusion criteria. The long-bone epiphyseal lesion etiologies included chondroblastoma (n=22, 45%), nonspecific nonmalignant pathology (n=11, 22%), osteomyelitis (n=9, 18%), lymphoma (n=2, 4%) and 1 case of each of aneurysmal bone cyst, chondrosarcoma, enchondroma, hemangioendothelioma, and non-Langerhans cell histiocytosis. Median age was 13.1 years old (range 1.5-18.6 years). We performed comparative analysis of the two most common lesions in our series, chondroblastoma and osteomyelitis. Chondroblastoma was significantly more likely to be peripherally located (94% vs. 33%, P=0.002) and to demonstrate a discrete T1-weighted hypointense rim (94% vs. 33%, P=0.002); there were no significant differences in enhancement or intrinsic signal properties. Children with chondroblastoma were older (15.1 years vs. 7.3 years, P=0.001), and chondroblastoma lesions were significantly larger, with mean maximum lesion diameter of 25 mm (interquartile range [IQR] 20-30) vs. 12 mm (IQR 11-18) (P=0.001) and lesion volumes of 4.4 mL (IQR 2.4-7.9) vs. 0.4 mL (IQR 0.2-1.4) (P=0.01). CONCLUSION: This study reports the relative frequency of pathology of pediatric solitary epiphyseal lesions and describes several features that might assist in differentiating between chondroblastoma and osteomyelitis.

Contrast-enhanced ultrasound of liver lesions in children.

Initial pediatric imaging of the liver heavily relies on ultrasonography (US) because it is free of ionizing radiation, easily portable and readily available. Although conventional US (gray-scale and color Doppler) is often an excellent screening tool, its relative low specificity compared to CT/MRI limits liver lesion characterization. The United States Food and Drug Administration's recent approval of an intravenous US contrast agent for pediatric liver lesion characterization (sulfur hexafluoride lipid-type A microspheres) and its excellent safety profile have spurred increased interest in contrast-enhanced US for definitive diagnosis of pediatric liver lesions. This review focuses on the safety of contrast-enhanced US, role of contrast-enhanced US in the evaluation of focal liver lesions, basic contrast-enhanced US technique for liver imaging, and interpretation principles. The authors review common focal liver lesions, with special attention to the role of contrast-enhanced US in the pediatric oncology population.

Clinical metric for differentiating intracranial hemangiopericytomas from meningiomas using diffusion weighted MRI.

PURPOSE: Intracranial Hemangiopericytomas (IHP) are dural based tumors that frequently recur/metastasize. Unfortunately, their imaging appearance overlaps significantly with more benign meningiomas. We evaluated the use of diffusion weighted imaging (DWI) to differentiate IHP from meningioma. METHODS: We compared MRI of IHP tumors (WHO Grades II/III) (n = 20) to meningioma (n = 48, WHO Grade I/II). FINDINGS: ADC values differed between IHP (1.05 × 10-3 mm2/s) and meningiomas (0.89 × 10-3 mm2/s) (p = 0.05). Normalized ADC ratios (nADC), differed between IHP and meningiomas (1.30 vs 1.07, p = 0.03). CONCLUSION: Importantly, a nADC cutoff of >1.3 was specific (96%) but not sensitive (35%) for identifying IHP.

Polymerase delta interacting protein 2 sustains vascular structure and function.

OBJECTIVE: On the basis of previous evidence that polymerase delta interacting protein 2 (Poldip2) increases reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 4 (Nox4) activity in vascular smooth muscle cells, we hypothesized that in vivo knockdown of Poldip2 would inhibit reactive oxygen species production and alter vascular function. APPROACH AND RESULTS: Because homozygous Poldip2 deletion is lethal, Poldip2(+/-) mice were used. Poldip2 mRNA and protein levels were reduced by ≈50% in Poldip2(+/-) aorta, with no change in p22phox, Nox1, Nox2, and Nox4 mRNAs. NADPH oxidase activity was also inhibited in Poldip2(+/-) tissue. Isolated aortas from Poldip2(+/-) mice demonstrated impaired phenylephrine and potassium chloride-induced contractions, increased stiffness, and reduced compliance associated with disruption of elastic lamellae and excessive extracellular matrix deposition. Collagen I secretion was elevated in cultured vascular smooth muscle cells from Poldip2(+/-) mice and restored by H2O2 supplementation, suggesting that this novel function of Poldip2 is mediated by reactive oxygen species. Furthermore, Poldip2(+/-) mice were protected against aortic dilatation in a model of experimental aneurysm, an effect consistent with increased collagen secretion. CONCLUSIONS: Poldip2 knockdown reduces H2O2 production in vivo, leading to increases in extracellular matrix, greater vascular stiffness, and impaired agonist-mediated contraction. Thus, unaltered expression of Poldip2 is necessary for vascular integrity and function.

Red blood cells stored for increasing periods produce progressive impairments in nitric oxide-mediated vasodilation.

BACKGROUND: Clinical outcomes in transfused patients may be affected by the duration of blood storage, possibly due to red blood cell (RBC)-mediated disruption of nitric oxide (NO) signaling, a key regulator of vascular tone and blood flow. STUDY DESIGN AND METHODS: AS-1 RBC units stored up to 42 days were sampled at selected storage times. Samples were added to aortic rings ex vivo, a system where NO-mediated vasodilation could be experimentally controlled. RESULTS: RBC units showed storage-dependent changes in plasma hemoglobin (Hb), RBC 2,3-diphosphoglycerate acid, and RBC adenosine triphosphate conforming to expected profiles. When freshly collected (Day 0) blood was added to rat aortic rings, methacholine (MCh) stimulated substantial NO-mediated vasodilation. In contrast, MCh produced no vasodilation in the presence of blood stored for 42 days. Surprisingly, the vasoinhibitory effects of stored RBCs were almost totally mediated by RBCs themselves: removal of the supernatant did not attenuate the inhibitory effects, while addition of supernatant alone to the aortic rings only minimally inhibited MCh-stimulated relaxation. Stored RBCs did not inhibit vasodilation by a direct NO donor, demonstrating that the RBC-mediated vasoinhibitory mechanism did not work by NO scavenging. CONCLUSIONS: These studies have revealed a previously unrecognized vasoinhibitory activity of stored RBCs, which is more potent than the described effects of free Hb and works through a different mechanism that does not involve NO scavenging but may function by reducing endothelial NO production. Through this novel mechanism, transfusion of small volumes of stored blood may be able to disrupt physiologic vasodilatory responses and thereby possibly cause adverse clinical outcomes.

Effect of medial calcification on vascular function in uremia.

The contribution of medial calcification to vascular dysfunction in renal failure is unknown. Vascular function was measured ex vivo in control, noncalcified uremic, and calcified uremic aortas from rats with adenine-induced renal failure. Plasma urea was 16 ± 4, 93 ± 14, and 110 ± 25 mg/dl, and aortic calcium content was 27 ± 4, 29 ± 2, and 4,946 ± 1,616 nmol/mg dry wt, respectively, in the three groups. Maximal contraction by phenylephrine (PE) or KCl was reduced 53 and 63% in uremic aortas, and sensitivity to KCl but not PE was increased. Maximal relaxation to acetylcholine was impaired in uremic aortas (30 vs. 65%), and sensitivity to nitroprusside was also reduced, indicating some impairment of endothelium-independent relaxation as well. None of these parameters differed between calcified and noncalcified uremic aortas. However, aortic compliance was reduced in calcified aortas, ranging from 17 to 61% depending on the severity of calcification. We conclude that uremic vascular calcification, even when not severe, significantly reduces arterial compliance. Vascular smooth muscle and endothelial function are altered in renal failure but are not affected by medial calcification, even when severe.