Efforts to Reduce Infections in Delayed Sternal Closure Patients: A Survey of Pediatric Practice.

BACKGROUND: Pediatric patients with sternum left open after cardiac surgery experience a higher risk for sternal wound infection (SWI). These infections are costly for programs, payers, and patients and their families. Despite efforts by individual programs to reduce infections in patients undergoing delayed sternal closure (DSC), there are no established guidelines that address preventive procedures. The purpose of this study was to determine the practice of pediatric cardiac surgery programs to prevent infection in their DSC patients and if preventive measures were associated with less infections. METHODS: A 33 question survey on institutional practices was sent to chief surgeons at pediatric cardiac surgery programs in the United States. RESULTS: Twenty-eight (35%) surgical programs responded. The mean number of pediatric cardiac bypass operations performed by programs in 2016 was 227 (range: 69-872). Data represented 6,484 patients <18 years of age who underwent cardiac surgery with 807 (12%) of those undergoing DSC. One hundred fifty-eight (2.4%) of all patients and 51 (6.3%) of the DSC patients developed a SWI. Patients with DSC who received preoperative baths were less likely to become infected (5.9% vs 15.8%; P = .015). Patients in programs with feeding protocols had fewer infections (5.7% vs 14.8%; P = .008). CONCLUSIONS: The results of this survey of children's cardiac surgery programs describe their practices to reduce infection rates in DSC patients. A multicenter project on wound care and closure techniques that might impact this costly complication is needed.

Multicenter Quality Improvement Project to Prevent Sternal Wound Infections in Pediatric Cardiac Surgery Patients.

BACKGROUND: Children undergoing cardiac surgery are at risk for sternal wound infections (SWIs) leading to increased morbidity and mortality. Single-center quality improvement (QI) initiatives have demonstrated decreased infection rates utilizing a bundled approach. This multicenter project was designed to assess the efficacy of a protocolized approach to decrease SWI. METHODS: Pediatric cardiac programs joined a collaborative effort to prevent SWI. Programs implemented the protocol, collected compliance data, and provided data points from local clinical registries using Society of Thoracic Surgery Congenital Heart Surgery Database harvest-compliant software or from other registries. RESULTS: Nine programs prospectively collected compliance data on 4,198 children. Days between infections were extended from 68.2 days (range: 25-82) to 130 days (range: 43-412). Protocol compliance increased from 76.7% (first quarter) to 91.3% (final quarter). Ninety (1.9%) children developed an SWI preprotocol and 64 (1.5%) postprotocol, P = .18. The 657 (15%) delayed sternal closure patients had a 5% infection rate with 18 (5.7%) in year 1 and 14 (4.3%) in year 2 P = .43. Delayed sternal closure patients demonstrated a trend toward increased risk for SWI of 1.046 for each day the sternum remained open, P = .067. Children who received appropriately timed preop antibiotics developed less infections than those who did not, 1.9% versus 4.1%, P = .007. CONCLUSION: A multicenter QI project to reduce pediatric SWIs demonstrated an extension of days between infections and a decrease in SWIs. Patients who received preop antibiotics on time had lower SWI rates than those who did not.

Prevention of sternal wound infection in pediatric cardiac surgery: a protocolized approach.

BACKGROUND: Sternal wound infections (SWIs) are a costly complication for children after cardiac surgery, increasing morbidity, mortality, and financial cost. There are no pediatric guidelines to reduce the incidence of SWI in this vulnerable population. METHODS: A quality improvement, multidisciplinary team was formed, and a protocol to prevent SWI was developed. A prospective review of patients who underwent pediatric cardiac surgery was conducted over a two-year period to follow adherence to the protocol and incidence of SWI. The Centers for Disease Control definitions for surgical site infections were used to determine the depth and presence of infection. RESULTS: Three hundred and eight children <18 years of age had sternotomies during the study period. There was a reduction in all SWI between the first and second years of the study (odds ratio [OR] = 0.35; confidence interval [CI] 95% 0.12-1.01; P = .059). Delayed sternal closure (DSC) was associated with increased risk of SWI (OR = 5.4; CI 95% 2.13-14.9; P ≤ .001). Institution of a protocol in patients with DSC was associated with decreased infections during the second year (first year: n = 7 (14%), second year: n = 2 (4%), P = .14). CONCLUSIONS: Institution of a protocol was associated with a decreased number of infections in children. A multicenter study of a bundled protocol approach to SWI prevention is needed. Children with DSC had a significantly higher risk of developing a wound infection. Initiating strategies to reduce SWI with a focus on children with DSC may result in improved overall infection rates.

Sternal wound infections in pediatric congenital cardiac surgery: a survey of incidence and preventative practice.

BACKGROUND: Guidelines exist for prevention of sternal wound infections (SWI) in adults. There are no guidelines for pediatric patients and limited reports on SWI incidence. The purpose of this study was to determine the incidence of, and preventative practice regarding pediatric SWIs with a long-term aim to develop best practice guidelines. METHODS: Eighty-nine congenital heart programs were sent a 31 question on-line survey regarding pediatric SWI. RESULTS: Thirty eight (43%) of the 89 programs responded. They reported 8,774 pediatric congenital procedures with a mean SWI rate of 1.53% (range, 0 to 9.09). Mean yearly volume was 237 operations (range, 50 to 720). Neither program size nor delayed sternal closure was associated with increased incidence of SWI. Variations in preoperative measures, antibiotic regimens, and wound care did not statistically impact incidence of SWI. Programs with protocols to monitor and control blood glucose levels postoperatively had statistically lower infection rates (1.04 vs 2.35, p = 0.03), and those that sent mediastinal cultures at time of delayed sternal closure reported lower infection rates (1.34 vs 1.74, p = 0.051). CONCLUSIONS: This report provides a multiinstitutional SWI incidence from pediatric programs of 1.53%. Despite variations in clinical practice between programs, this survey revealed two strategies resulting in reduced SWIs; protocol-based management of glucose levels and mediastinal wound cultures sent at time of closure. Pediatric programs do not consistently follow adult preventative guidelines. Multicenter randomized research is needed to formulate preventative guidelines to reduce the incidence of pediatric SWI.

Resuscitation from hemorrhagic shock with HBOC-201 in the setting of traumatic brain injury.

Outcomes after mild or moderate head trauma are worsened with associated hypotension, and secondary brain injury can be reduced with timely resuscitation. This study was performed to investigate HBOC-201 as a resuscitation therapy in a combined hemorrhagic shock and brain injury model. Anesthetized rats sustained moderate brain injury using a controlled cortical impact device, followed by rapid hemorrhage to a mean arterial pressure of 30 mmHg. After 30 min of hypotension, animals were resuscitated with HBOC-201, autologous shed blood (SB), or lactated Ringer solution (LR). Brain injury was assessed by measurements of cerebral blood flow (CBF) and cerebral vasoreactivity to hypercapnia (CVH) using a laser Doppler flowmeter. Contusion volume was evaluated histologically, and cerebral edema was determined by total water content. The HBOC rats required significantly less resuscitation volume versus LR and SB. The CBF was significantly diminished at 60 min after resuscitation with HBOC (70.1% +/- 3.8% baseline) compared with LR (105.8% +/- 10.1% baseline; P < 0.01) and SB (96.8% +/- 5% baseline; P < 0.05). The CVH was preserved in the HBOC and SB groups. The CVH was significantly diminished compared with baseline in the LR group at 30 min after resuscitation and showed a significant loss compared with HBOC at 60 min after resuscitation. The contusion volume for HBOC (45.1 mm3) and SB (35.1 mm3) was less than LR (63.5 mm3, P < 0.01). Although CBF was diminished after resuscitation in the HBOC group, HBOC-treated animals maintained CVH and experienced significantly smaller contusion volume than those treated with LR. These results suggest that resuscitation with HBOC-201 protects autoregulatory mechanisms and may reduce secondary brain injury in traumatic brain injury.

Reversal of attenuation of cerebrovascular reactivity to hypercapnia by a nitric oxide donor after controlled cortical impact in a rat model of traumatic brain injury.

OBJECT: Traumatic brain injury (TBI) attenuates the cerebral vasodilation to hypercapnia. Cortical spreading depression (CSD) also transiently reduces hypercapnic vasodilation. The authors sought to determine whether the CSD elicited by a controlled cortical impact (CCI) injury masks the true effect of TBI on hypercapnic vasodilation, and whether a nitric oxide (NO) donor can reverse the attenuation of hypercapnic vasodilation following CCI. METHODS: Anesthetized rats underwent moderate CCI. Cerebral blood flow was monitored with laser Doppler flowmetry and the response to hypercapnia was determined for injured and sham-injured animals. The effect of the NO donor, S-nitroso-N-acetylpenicillamine (SNAP), on this response was also assessed. At an uninjured cortical site ipsilateral to the CCI, a single wave of CSD was recorded and the CO2 response at this location was significantly attenuated for up to 30 minutes (seven rats, p < 0.05). At the injured cortex, hypercapnic vasodilation continued to be attenuated for 7 hours. The cerebral vasodilation to CO2 was 37 +/- 5% in injured rats (six) compared with 84 +/- 10% in the sham-injured group (five rats, p < 0.05). After 30 minutes of topical superfusion with SNAP, hypercapnic vasodilation was restored to 74 +/- 7% (nine rats, p > 0.1 compared with that in the sham-injured group). In contrast, papaverine, an NO-independent vasodilator, failed to reverse the attenuation of the CO2 response to CCI. CONCLUSIONS: The authors conclude that CSD elicited by CCI can mask the true effect of TBI on hypercapnic vasodilation for at least 30 minutes. Exogenous NO, but not papaverine, can reverse the attenuation of cerebrovascular reactivity to CO2 caused by TBI. This result supports the hypothesis that NO production is reduced after TBI and that the NO donor has a potential beneficial role in the clinical management of head injury.

Chronic administration of indomethacin increases role of nitric oxide in hypercapnic cerebrovasodilation in piglets.

Hypercapnia-induced cerebral vasodilation is associated with prostanoids in the piglet, but is a primarily nitric oxide (NO) associated response in many adult models. Hypercapnia-induced cerebral vasodilation is both NO and prostanoid associated in the juvenile pig. We hypothesized that with chronic administration of indomethacin the piglet would advance the role of the NO system in cerebrovascular responses. The closed cranial window technique was used in piglets to determine pial arteriolar response. Chronically indomethacin treated newborn animals dilated in response to CO2 similarly to control newborns (40.9+/-4.4% vs 48.4+/-4.1%). Topical n-nitro L-arginine (L-NA, 10(-3) M), attenuated CO2 induced dilation in the chronically indomethacin treated animals (11.7+/-3.3% vs 40.9+/-4.4%; p < 0.001), but had no effect on the response to hypercapnia of piglets not treated with indomethacin. Neither indomethacin nor L-NA altered response to topical isoproterenol (10(-6) M). We conclude that with chronic indomethacin administration there develops a significant hypercapnia-induced cerebral vasodilation in which NO has an important role. The chronic inhibition of the newborn's principal dilator system appears to increase the role of NO in newborn cerebral hemodynamics.