Management of abdominal compartment syndrome during extracorporeal life support.

OBJECTIVE: To describe the successful use of a peritoneal dialysis catheter for emergent decompression of abdominal compartment syndrome during extracorporeal life support for septic shock. DESIGN: Case report. SETTING: Pediatric intensive care unit at a freestanding tertiary children's hospital. PATIENT: Two-year-old toddler with influenza A complicated by methicillin-resistant Staphylococcus aureus pneumonia and septic shock. INTERVENTIONS: Placement of peritoneal dialysis catheter. MEASUREMENTS AND MAIN RESULTS: Changes in hemodynamic and respiratory parameters. Improvement in extracorporeal membrane oxygenation venous drainage with subsequent survival. CONCLUSIONS: Although the standard therapy for abdominal compartment syndrome is decompressive laparotomy, a minimally invasive percutaneous approach may be effective and should be considered in selected patients.     

Successful intra-arterial thrombolytic therapy for a right middle cerebral artery stroke in a 2-year-old supported by a ventricular assist device

Embolic stroke is a common complication in patients on ventricular assist devices in both adults and children. The reported incidence of strokes in children supported by VAD's varies from 7 to 38%. The rapid increase in recent years in the availability of both adult and pediatric VADs will likely add to the overall prevalence of strokes in patients being bridged to heart transplant. Strokes in this population can be lethal as they frequently necessitate withdrawal of the extracorporeal device support and withdrawal from the organ transplant waiting list. We present a case of a fully anti-coagulated 29-month-old supported on a Berlin EXCOR LVAD (Berlin, Germany) with embolic stroke which was treated successfully with direct thrombolysis with recombinant tissue plasminogen activator. This is the first report which uses intra-arterial thrombolytics while on a ventricular assist device in a pediatric patient.     

Adrenal Insufficiency in Hemodynamically Unstable Neonatesafter Open-Heart Surgery

Objective. To investigate if the low dose (1 µg) ACTH stimulation test appropriately assesses adrenal responsiveness in neonates undergoing open-heart surgery requiring cardio-pulmonary bypass. Design. In this retrospective study, adrenal axis response was assessed on the first post-operative day with the low-dose (1 µg) ACTH stimulation test. Age, gender, weight, RACHS category, inotrope score, and baseline and post-stimulation cortisol levels were collected. The association between basal serum cortisol levels and degree of response to the ACTH stimulation test was also investigated. Setting. Tertiary care referral center. Patients. Twenty-one neonates who underwent neonatal cardiac surgery on cardiopulmonary bypass and underwent an ACTH stimulation test. Interventions. Hydrocortisone 50 mg/m² bolus in four divided doses daily. Outcome Measures. Response to the low dose (1 µg) ACTH stimulation was assessed. Results. All neonates with hemodynamic instability in the immediate post-operative period had low basal serum cortisol levels. The basal mean serum cortisol level for the 21 patients who underwent the low dose ACTH stimulation test was 7.3 µg/dL (median 2.2, range 0.7–42). The mean serum cortisol level increased after the ACTH stimulation test in the 21 patients to 39.6 µg/dL (median 38, range 79–17). The mean inotrope score in the first 24 hours after surgery was 24 (median 17.5, range 7–76.5) and decreased to 17 (median 14, range 5–52.3) 24–48 hours after surgery. At 48 hours post-surgery the mean arterial pressure in the groups with a serum cortisol increase after ACTH stimulation (<30 µg/dL vs. >50 µg/dL) was significantly different (P value 0.026). Conclusions. The low dose (1 µg) ACTH stimulation test is a valid test to assess adrenal responsiveness among neonates after open heart surgery requiring CPB. Traditionally used basal serum cortisol level cutoff of <20 µg/dL used to define relative adrenal insufficiency may not be applicable in neonates undergoing open heart surgery on CPB thus indicating the need for re-defining adrenal insufficiency in this patient population.     

Outcomes after extracorporeal cardiopulmonary resuscitation (ECPR) following refractory pediatric cardiac arrest in the intensive care unit

AimTo describe our experience using extracorporeal cardiopulmonary resuscitation (ECPR) in resuscitating children with refractory cardiac arrest in the intensive care unit (ICU) and to describe hospital survival and neurologic outcomes after ECPR.MethodsA retrospective chart review of a consecutive case series of patients requiring ECPR from 2001 to 2006 at Arkansas Children's Hospital. Data from medical records was abstracted and reviewed. Primary study outcomes were survival to hospital discharge and neurological outcome at hospital discharge.ResultsDuring the 6-year study period, ECPR was deployed 34 times in 32 patients. 24 deployments (73%) resulted in survival to hospital discharge. Twenty-eight deployments (82%) were for underlying cardiac disease, 3 for neonatal non-cardiac (NICU) patients and 3 for paediatric non-cardiac (PICU) patients. On multivariate logistic regression analysis, only serum ALT (p-value = 0.043; OR, 1.6; 95% confidence interval, 1.014–2.527) was significantly associated with risk of death prior to hospital discharge. Blood lactate at 24 h post-ECPR showed a trend towards significance (p-value = 0.059; OR, 1.27; 95% confidence interval, 0.991–1.627). The Hosmer–Lemeshow tests (p-value = 0.178) suggested a good fit for the model. Neurological evaluation of the survivors revealed that there was no change in PCPC scores from a baseline of 1–2 in 18/24 (75%) survivors.ConclusionsECPR can be used successfully to resuscitate children following refractory cardiac arrest in the ICU, and grossly intact neurologic outcomes can be achieved in a majority of cases.     

Netrin-1 inhibits leukocyte migration in vitro and in vivo

Cell migration plays important roles in embryonic development and inflammation, and this process is highly regulated to ensure tissue homeostasis. A number of barriers exist to prevent the inappropriate migration of leukocytes into healthy peripheral tissues, including retention of these cells in the inactive state and maintenance of the integrity and charge of the vascular endothelium. However, active signals also are likely to exist that can repulse cells or abolish existing cell migration. One such paradigm exists in the developing nervous system, where neuronal migration is mediated by a balance between chemoattractive and chemorepulsive signals. The ability of the guidance molecule netrin-1 to repulse or abolish attraction of neuronal cells expressing the UNC5b receptor makes it an attractive candidate for the regulation of inflammatory cell migration. Here, we show that netrin-1 is expressed on vascular endothelium, where it is regulated by infection and inflammatory cytokines. The netrin-1 receptor UNC5b is strongly expressed by leukocytes, upon which netrin-1 acts as a potent inhibitor of migration to different chemotactic stimuli both in vivo and in vitro. These data suggest that endothelial expression of netrin-1 may inhibit basal cell migration into tissues and that its down-regulation with the onset of sepsis/inflammation may facilitate leukocyte recruitment.