The Impact of Redosing Antibiotics for Pediatric Patients Undergoing Appendectomy for Complicated Appendicitis.

Currently, there is no universally accepted, standardized protocol for pre-operative antibiotic administration in the setting of appendectomy for complicated appendicitis among pediatric patients. Strategies to mitigate surgical site infections (SSIs) must be balanced with optimal antibiotic use and exposure. We conducted a retrospective chart review to compare outcomes between patients treated pre-operatively with a single pre-operative dose of antibiotics with those who received additional antibiotics prior to laparoscopic appendectomy for complicated appendicitis between 2020 and 2022. Of 124 pediatric patients, 18% received an additional dose of pre-operative antibiotics after initial treatment dose. Surgical site infection rates between the two groups were not statistically significant (P-value = .352), thereby suggesting that redosing antibiotics closer to the time of incision may not impact SSI rates. Additional studies are necessary to make clinical recommendations.

Impact of Language Congruence on Patient Outcomes Following Gastrostomy Tube Insertion.

Inadequate health literacy poses a significant public health challenge, influencing patient treatment adherence and outcomes. This study explores outcomes in the setting of language congruence at the time of discharge for pediatric patients following laparoscopic gastrostomy tube insertion. We conducted a retrospective chart review from 2019 to 2022 at a community children's hospital, including 168 patients categorized based on language congruence. Although trends did suggest increased ER visits among Spanish-speaking patients, there were no statistically significant differences in health care utilization or patient outcomes identified. Further larger studies are needed for a comprehensive analysis of the relationship of language congruence at discharge on outcomes following surgical procedures as this may enable delivery of culturally competent medical care.

Adenine nucleotide control of coronary blood flow during exercise.

The adenine nucleotide hypothesis postulates that the ATP released from red blood cells is broken down to ADP and AMP in coronary capillaries and that ATP, ADP, and AMP act on purinergic receptors on the surface of capillary endothelial cells. Purinergic receptor activation initiates a retrograde conducted vasodilator signal to the upstream arteriole that controls coronary blood flow in a negative feedback manner. A previous study (M. Farias 3rd, M. W. Gorman, M. V. Savage, and E. O. Feigl, Am J Physiol Heart Circ Physiol 288: H1586-H1590, 2005) demonstrated that coronary venous plasma ATP concentration increased during exercise and correlated with coronary blood flow. The present experiments test the adenine nucleotide hypothesis by examining the balance between oxygen delivery (via coronary blood flow) and myocardial oxygen consumption during exercise before and after purinergic receptor blockade. Dogs (n = 7) were chronically instrumented with catheters in the aorta and coronary sinus and a flow transducer around the circumflex coronary artery. During control treadmill exercise, myocardial oxygen consumption increased and the balance between oxygen delivery and myocardial oxygen consumption fell as indicated by a declining coronary venous oxygen tension. Blockade of P1 and P2Y(1) purinergic receptors combined with inhibition of nitric oxide synthesis significantly decreased the balance between oxygen delivery and myocardial oxygen consumption compared with control. The results support the hypothesis that ATP and its breakdown products ADP and AMP are part of a negative feedback control mechanism that matches coronary blood flow to myocardial oxygen consumption at rest and during exercise.

Plasma ATP during exercise: possible role in regulation of coronary blood flow.

It was previously shown that red blood cells release ATP when blood oxygen tension decreases. ATP acts on microvascular endothelial cells to produce a retrograde conducted vasodilation (presumably via gap junctions) to the upstream arteriole. These observations form the basis for an ATP hypothesis of local metabolic control of coronary blood flow due to vasodilation in microvascular units where myocardial oxygen extraction is high. Dogs (n = 10) were instrumented with catheters in the aorta and coronary sinus, and a flow transducer was placed around the circumflex coronary artery. Arterial and coronary venous plasma ATP concentrations were measured at rest and during three levels of treadmill exercise by using a luciferin-luciferase assay. During exercise, myocardial oxygen consumption increased approximately 3.2-fold, coronary blood flow increased approximately 2.7-fold, and coronary venous oxygen tension decreased from 19 to 12.9 mmHg. Coronary venous plasma ATP concentration increased significantly from 31.1 to 51.2 nM (P < 0.01) during exercise. Coronary blood flow increased linearly with coronary venous ATP concentration (P < 0.01). Coronary venous-arterial plasma ATP concentration difference increased significantly during exercise (P < 0.05). The data support the hypothesis that ATP is one of the factors controlling coronary blood flow during exercise.

Nucleotide coronary vasodilation in guinea pig hearts.

The role of P1 receptors and P2Y1 receptors in coronary vasodilator responses to adenine nucleotides was examined in the isolated guinea pig heart. Bolus arterial injections of nucleotides were made in hearts perfused at constant pressure. Peak increase in flow was measured before and after addition of purinoceptor antagonists. Both the P1 receptor antagonist 8-(p-sulfophenyl)theophylline and adenosine deaminase inhibited adenosine vasodilation. AMP-induced vasodilation was inhibited by P1 receptor blockade but not by adenosine deaminase or by the selective P2Y1 antagonist N6-methyl-2'-deoxyadenosine 3',5'-bisphosphate (MRS 2179). ADP-induced vasodilation was moderately inhibited by P1 receptor blockade and greatly inhibited by combined P1 and P2Y1 blockade. ATP-induced vasodilation was antagonized by P1 blockade but not by adenosine deaminase. Addition of P2Y1 blockade to P1 blockade shifted the ATP dose-response curve further rightward. It is concluded that in this preparation ATP-induced vasodilation results primarily from AMP stimulation of P1 receptors, with a smaller component from ATP or ADP acting on P2Y1 receptors. ADP-induced vasodilation is largely due to P2Y1 receptors, with a smaller contribution by AMP or adenosine acting via P1 receptors. AMP responses are mediated solely by P1 receptors. Adenosine contributes very little to vasodilation resulting from bolus intracoronary injections of ATP, ADP, or AMP.