Knowing Your Patient Population: Techniques to Capture Infants at High Risk for Physical Abuse in a Trauma Registry.

BACKGROUND: Physical abuse is a major public health concern and a leading cause of morbidity and mortality in infants. Clinical decision tools derived from trauma registries can facilitate timely risk-stratification. The Trauma Quality Improvement Program (TQIP) database does not report age for children <1 year who are at highest risk for abuse. We report a method to capture these infants despite the missing age. METHODS: Patients ≤17 years were identified from TQIP (2017-2019). The primary outcomes included injuries resulting from confirmed or suspected child abuse captured by diagnosis codes or report/investigation of physical abuse, or different caregiver at discharge available in TQIP. We used two methods to select infants within TQIP. In the first, World Health Organization (WHO) growth standards for stature or length-for-age and weight-for-age were selected to capture children younger than 1 year. In the second, a K-means machine learning algorithm was used to cluster patients by weight and height. We compared outcome and injury data with and without patients <1 year. RESULTS: Using the WHO growth standard 19,916 children <1 year were identified. A total of 20,513 patients had a report of physical abuse filed, and 9393 were infants <1 year. Increased age-adjusted odds ratios [95% CI] were seen for fractures of the upper limb (1.28 [1.22-1.34]), vertebrae (1.89 [1.68-2.13]), ribs (5.2 [4.8-5.63]), and spinal cord (3.39 [2.85-4.02]) and head injuries (1.55 [1.5-1.6]) with infants included. CONCLUSIONS: In a nationwide trauma registry, WHO growth standards can be used to capture patients under one year who are more adversely impacted by maltreatment. TYPE OF STUDY: Retrospective, Cross-sectional. LEVEL OF EVIDENCE: Level III, Diagnostic.

Clinical Outcomes in Neurologically Intact Children With Small Intracranial Bleeds and Simple Skull Fractures.

Introduction Children with minor intracranial hemorrhage (ICH) and/or simple skull fractures are often hospitalized for monitoring; however, the majority do not require any medical, surgical, or critical care interventions. Our purpose was to determine the rate of significant clinical sequela (SCS) and identify associated risk factors in neurologically intact children with close head trauma. Methods This is a retrospective observational study. Children (≤ 3 years of age) admitted with closed head trauma, documented head injuries (ICH ≤ 5mm and/or simple skull fracture), and a Glasgow Coma Scale (GCS) score of ≥14, between January 2015 and January 2020, were included. We collected demographics, resource utilization, and patient outcomes variables. SCS was defined as any radiologic progression, and/or clinically important medical or neurological deterioration. Results A total of 205 patients were enrolled in the study (65.4% male, mean age 7.7 months). Repeat neuroimaging was obtained in 41/205 patients (20%) with radiologic progression noted in 5/205 (2.4%). Thirteen out of 205 patients (6.3%) experienced SCS. Patients with SCS were more likely to be males (92.3% vs 63.5% in females, P=0.035) to have had a report filed with child protective services due to a concern for abuse/neglect (92.3% vs 61.5% in females, P=0.025), and to have had a non-linear skull fracture (P<0.001). No other factors were shown to be predictive of SCS with enough statistical significance. Conclusion Neurologically intact children with traumatic closed head injury are at low risk for developing SCS. This study suggests that most of these children may not need ICU monitoring. This study also showed that a certain subset might be at an increased risk of developing SCS.

Utility of skull radiographs in infants undergoing 3D head CT during evaluation for physical abuse.

BACKGROUND: Clinical practice guidelines recommend performing head CT and skull radiographs (SR) when evaluating infants for physical abuse. We compared the accuracy of 3-dimensional CT (3DCT) and SR for detecting skull fractures. METHODS: We reviewed children <12 months evaluated for physical abuse undergoing 3DCT and SR between January 2017 and December 2018. 3DCT and SR images were blindly read by 2 radiologists. Interrater reliability (IRR) was calculated. Diagnostic accuracy was compared using McNemar's test. RESULTS: 158 infants with a mean age of 5.0 months underwent 3DCT and SR. Consensus reading identified 46 fractures (29.1%) on 3DCT and 40 fractures (25.3%) on SR. IRR was higher for 3DCT (κ = 0.95) than for SR (=0.65). 11 fractures were identified on 3DCT but not SR. 5 fractures were identified on SR but not 3DCT. There was no difference in the diagnostic accuracy of 3DCT and SR (χ2 = 1.56, p = 0.211). CONCLUSIONS: We found no difference in the accuracy of 3DCT and SR for detecting skull fractures in infants. Because 3DCT has better IRR and evaluates for both bony and intracranial injuries it is superior to SR. Omitting SRs may be acceptable if a 3DCT is performed, and would reduce radiation exposure without compromising diagnostic accuracy.

Childhood Falls With Occipital Impacts.

OBJECTIVES: Falls are commonly reported in children who present with both accidental and inflicted brain injuries. Short falls rarely result in serious or life-threatening injuries. Our purpose is to describe a series of cases of short falls with occipital impact leading to subdural hemorrhage (SDH). METHODS: We present a series of 8 witnessed accounts of young children diagnosed as having SDHs after striking the back of their heads during a short fall. Child-abuse physicians were surveyed to determine if they had evaluated a child younger than 24 months diagnosed as having SDH, with or without retinal hemorrhages, following a witnessed fall with occipital impact. Submitted cases were analyzed. RESULTS: The median age of the children was 12.5 months. All fell backward from a standing or seated position onto a hard surface and immediately developed symptoms. There was an average of 4 witnesses per case. Physical examinations were normal; however, the majority of children had enlarged head circumferences. All were previously healthy. Six of 8 children had unilateral convexity SDH. All children had varying degrees of retinal hemorrhage but no retinoschisis. The majority of children had returned to their baseline within 24 hours of hospitalization. CONCLUSIONS: Although a larger study is needed to identify the full spectrum of injuries, we postulate that, if a history of a fall with an occipital impact is elicited during a trauma workup, accidental injury should be considered.

Esophageal foreign body: a case of a neonate with stridor.

We present a case of a 7-week-old female with a 3-week history of progressively worsening stridor who was admitted to rule out a congenital anomaly in the airway or vasculature. After 3 different imaging modalities, we discovered an esophageal foreign body causing esophagitis and proximal airway compression.Young infants with symptoms of stridor, wheezing, or retractions will often have a common diagnosis such as a viral infectious etiology, or in rarer cases an anatomic anomaly. This case illustrates that the presence of a foreign body must still remain on the differential, even in this age group.

Protein kinase C betaII peptide inhibitor exerts cardioprotective effects in rat cardiac ischemia/reperfusion injury.

Ischemia followed by reperfusion (I/R) in the presence of polymorphonuclear leukocytes (PMNs) results in a marked cardiac contractile dysfunction. A cell-permeable protein kinase C (PKC) betaII peptide inhibitor was used to test the hypothesis that PKC betaII inhibition could attenuate PMN-induced cardiac dysfunction by suppression of superoxide production from PMNs and increase NO release from vascular endothelium. The effects of the PKC betaII peptide inhibitor were examined in isolated ischemic (20 min) and reperfused (45 min) rat hearts with PMNs. The PKC betaII inhibitor (10 microM; n = 7) significantly attenuated PMN-induced cardiac dysfunction compared with I/R hearts (n = 9) receiving PMNs alone in left ventricular developed pressure (LVDP) and the maximal rate of LVDP (+dP/dt(max)) cardiac function indices (p < 0.01). The PKC betaII inhibitor at 10 microM significantly increased endothelial NO release from a basal value of 1.85 +/- 0.18 pmol NO/mg tissue to 3.49 +/- 0.62 pmol NO/mg tissue from rat aorta. It also significantly inhibited superoxide release (i.e., absorbance) from N-formyl-L-methionyl-L-leucyl-L-phenylalanine-stimulated rat PMNs from 0.13 +/- 0.01 to 0.02 +/- 0.004 (p < 0.01) at 10 microM. Histological analysis of the left ventricle of representative rat hearts from each group showed that the PKC betaII peptide inhibitor-treated hearts experienced a marked reduction in PMN vascular adherence and infiltration into the postreperfused cardiac tissue compared with I/R + PMN hearts (p < 0.01). These results suggest that the PKC betaII peptide inhibitor attenuates PMN-induced post-I/R cardiac contractile dysfunction by increasing endothelial NO release and by inhibiting superoxide release from PMNs.

Protein kinase C-zeta inhibition exerts cardioprotective effects in ischemia-reperfusion injury.

Ischemia followed by reperfusion (I/R) in the presence of polymorphonuclear leukocytes (PMNs) results in marked cardiac contractile dysfunction. A cell-permeable PKC-zeta peptide inhibitor was used to test the hypothesis that PKC-zeta inhibition could attenuate PMN-induced cardiac contractile dysfunction by suppression of superoxide production from PMNs and increase nitric oxide (NO) release from vascular endothelium. The effects of the PKC-zeta peptide inhibitor were examined in isolated ischemic (20 min) and reperfused (45 min) rat hearts reperfused with PMNs. The PKC-zeta inhibitor (2.5 or 5 microM, n = 6) significantly attenuated PMN-induced cardiac dysfunction compared with I/R hearts (n = 6) receiving PMNs alone in left ventricular developed pressure (LVDP) and the maximal rate of LVDP (+dP/dt(max)) cardiac function indexes (P < 0.01), and these cardioprotective effects were blocked by the NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (50 microM). Furthermore, the PKC-zeta inhibitor significantly increased endothelial NO release 47 +/- 2% (2.5 microM, P < 0.05) and 54 +/- 5% (5 microM, P < 0.01) over basal values from the rat aorta and significantly inhibited superoxide release from phorbol-12-myristate-13-acetate-stimulated rat PMNs by 33 +/- 12% (2.5 microM) and 40 +/- 8% (5 microM) (P < 0.01). The PKC-zeta inhibitor significantly attenuated PMN infiltration into the myocardium by 46-48 +/- 4% (P < 0.01) at 2.5 and 5 microM, respectively. In conclusion, these results suggest that the PKC-zeta peptide inhibitor attenuates PMN-induced post-I/R cardiac contractile dysfunction by increasing endothelial NO release and by inhibiting superoxide release from PMNs thereby attenuating PMN infiltration into I/R myocardium.