Mortality in paediatric cardiac surgery has fallen dramatically over the past 20 years. The focus in the current era is on reducing morbidity through prediction, prevention and anticipatory management of cardiac critical illness and perioperative care. Care of children with congenital heart disease often requires prolonged periods of complex intensive care with prolonged central venous access increasing risk of venous thrombosis. Thrombi in the central veins impair placement of central venous catheters making vascular access a challenge, and limit or prevent the establishment of cavopulmonary connections to secure pulmonary blood flow. Thrombotic occlusion of femoral veins can impede the performance of cardiac catheterisation for diagnostic or therapeutic interventions. Todd Tzanetos [
48] used ultrasound surveillance and serial measurements of biomarkers of coagulation and fibrinolytic pathways to determine the prevalence of thrombus and to describe the time course of biomarkers of coagulation and fibrinolysis in a group of 16 children undergoing early stage palliation for complex congenital heart disease. Thrombus was detected in 31 % of 16 babies studied despite the administration of heparin and aspirin, with impaired ventricular function, low antithrombin III and increased tissue plasminogen activator levels being associated with the occurrence of thrombus. There is no consensus on how thrombotic risk should be managed in these vulnerable patients, and larger structured studies are needed to further explore risk factors and treatment strategies for central venous thrombosis. Algra et al. [
49] studied a cohort of 412 children following cardiac surgery and detected infection defined by Center for Disease Control definitions in 25 % of them. Of the patients developing infections, 26 % developed surgical site infections and 25 % bloodstream infections. A panel of clinical variables available to bedside clinicians at 48 h after cardiac surgery were subjected to regression analysis, and a simple bedside ‘infection prediction’ rule including age (<6 months), delayed sternal closure (>48 h) and PICU stay (>48 h) was tested and shown to have a positive predictive value of 54.5 %, and negative predictive value of 79.5 %. Whilst the rule is helpful it is probably no surprise for experienced intensivists to learn that smaller children, sick enough to stay in for more than 48 h with an open sternum are at risk of infection. Those interested in this topic should also read the paper by Barker et al. [
50] which reports data derived from the large US Society of Thoracic Surgeons database. Clinically important ‘low cardiac output’ is a common complication seen in infants and young children following cardiac surgery. Wernovsky et al. [
51] developed a descriptive inotrope score (IS) as a means of comparing levels of inotropic support in a paediatric critical care setting. Gaies et al. [
52] updated the original IS adding noradrenaline and ‘new’ drugs, milrinone and vasopressin, naming this the vasoactive inotrope score (VIS). Davidson et al. [
53] recently undertook an evaluation of the VIS and IS in children following cardiac surgery and determined that a higher VIS at 48 h following cardiac surgery is strongly associated with poorer short-term outcomes including length of ventilation and PICU stay. VIS was superior to IS in predicting short-term outcome. The VIS may soon have to be modified again, if the use of levosimendan gains traction in paediatric cardiac critical care [
53]. Ricci et al. [
54] recently reported on its use in a small randomised controlled trial of levosimendan versus ‘usual inotropes’ in this population. Children were allocated to receive either levosimendan, a novel inodilator agent belonging to the family of calcium sensitiser agents, or ‘usual inotropic therapy’. The incidence of clinically assessed ‘low cardiac output’ was lower in the levosimendan group than in the control patients (37 vs. 61 %) [
54]. Whilst the positive inotropic and vasodilating properties and unique pharmacodynamics suggest a strong rationale for the use of levosimendan in paediatric perioperative care, it is a great shame that despite pressure from the clinical community, the drug’s manufacturer has so far not conducted or supported any sizable clinical trials in children. In a prospective observational study, Hassinger et al. [
55] hypothesised that elevated preoperative levels of asymmetrical dimethylarginine (ADMA), an endogenous competitive inhibitor of nitric oxide synthase which is known to be associated with disruption of endothelial function, might be associated with worse outcomes following paediatric cardiac surgery. ADMA levels were measure before cardiac surgery in 100 patients aged 0–18 years. Raised ADMA levels were found in 29 (29 %). Using logistic regression including a range of common short-term clinical outcomes, the authors determined that preoperative ADMA level (odds ratio 452.9; 95 % CI 7.9, 999;
p = 0.003), cardiopulmonary bypass (CPB) time (odds ratio 1.03; 95 % CI 1.01, 1.05;
p = 0.002) and peak inotrope score (odds ratio 1.27; 95 % CI 1.01, 1.59;
p = 0.042) carried independent risk for poor short-term outcomes. Mastropietro et al. [
56] sought to investigate the paradox that some children appear to have increased arginine vasopressin (AVP) levels following cardiac surgery whilst others who are hypotensive respond favourably to exogenously administered AVP. A great difficulty in studying AVP is its short half-life and demanding assay techniques. Copeptin is a more stable and easily measured product of pro-AVP metabolism and may therefore act as a useful surrogate for endogenous AVP production. The investigators found that relative AVP deficiency occurred in a portion of infants and children following cardiac surgery. Plasma AVP and copeptin concentrations were positively associated in these patients, supporting a basis for additional studies of larger cohorts of children to determine if copeptin will prove useful in identifying these patients and therefore children who could benefit from exogenous AVP administration.
The maintenance of stable haemodynamic conditions whilst inducing sedation of anaesthesia during critical illness is challenging. Some of the most commonly used sedatives in critical care such as midazolam and propofol are poorly tolerated in cardiovascularly compromised children. Etomidate, an alternative sedative-anaesthetic has a more favourable cardiovascular profile but is associated with competitive inhibition of cortisol production which itself may be harmful unless supplemental corticosteroid is given. The inert gas xenon has long been recognised as an effective inhaled anaesthetic agent. Its rarity in the atmosphere and therefore its expense have to date severely limited its clinical application. Chakkarapani et al. [
57] recently reported the effect of 18 h 50 % xenon (Xe) inhalation at normothermia (NT 38.5 °C) or hypothermia (HT 33.5 °C) on mean arterial blood pressure, inotropic support and heart rate (HR) following an induced perinatal global hypoxic-ischaemic insult (HI) in newborn pigs. Xe maintained stable blood pressure, thereby reducing the inotropic support requirements during and after administration independently of induced HT-current neonatal encephalopathy treatment. If supply, delivery and recapture issues can be resolved, Xe may in future offer haemodynamic benefits during neuroprotection and also in other haemodynamically critical situations in paediatrics such as the induction of anaesthesia in children with sever septic shock or end-stage heart failure (cardiomyopathy, acute fulminant myocarditis). Whilst ‘myocardial depression’ or ‘low cardiac output’ are often imputed from clinical findings in neonates and young children in the perioperative period, routine measurement of cardiac output is both difficult and as yet of unproven benefit in patient management [
57]. Grollmuss et al. [
58] investigated the use of a noninvasive and continuous method of measuring stroke volume, electrical velocimetry (EV) with intermittent transthoracic Doppler measurements, and found the two methods to be interchangeable. EV has the potential to become a useful tool for continuous cardiac output measurement and guiding goal-directed therapy in critically ill infants with heart failure. Even blood pressure can be challenging to measure in the critically ill preterm neonate [
58]. Konig et al. [
59] studied 60 infants of less than 32 weeks gestation and compared noninvasive cuff measurements with intra-arterial measurements obtained from umbilical arterial catheters. Although the authors found that overall the average differences between invasive and noninvasive measurements were acceptable, the range of under- and overestimation was large, making reliance on noninvasive measurements in guiding circulatory management ‘problematic’. Clearly better cardiovascular noninvasive monitoring methods are needed for our smallest patients. The majority of papers published in the paediatric pages of the journal relate to critical care undertaken in the developed world. Nguah et al. [
60] remind us of the huge burden of critical illness in underdeveloped and developing countries, and what can be achieved in those settings. These investigators reported on observations of cardiac function and haemodynamic status of 183 children with severe malaria at presentation and after recovery, including details of echocardiographic evaluation of 121 children in the cohort. There is huge potential for studies in sepsis in such settings which have the potential both to improve local clinical care and provide key populations for clinical trials with potentially worldwide application, as we have recently seen from the FEAST trial [
61].
Cyclosporine has been shown to reduce myocardial cell death following ischaemia–reperfusion. Therefore Gill et al. [
62] hypothesised that cyclosporine treatment may attenuate asphyxia-related intestinal injury in neonates. In an asphyxiated newborn piglet model, anaesthetised asphyxiated piglets were block-randomised to receive cyclosporine (10 mg/kg) or placebo (normal saline) boluses at 5 min of reoxygenation (
n = 8/group). Within 2 h of hypoxia, piglets had cardiogenic shock with hypotension and acidosis and decreased superior mesenteric perfusion. Cyclosporine treatment increased superior mesenteric arterial (SMA) flow (114 ± 6 vs. 78 ± 19 % of baseline of controls, respectively) with improved intestinal tissue lactate (all
p < 0.05) [
62].
This is the first study to demonstrate that post-resuscitation administration of cyclosporine improves mesenteric perfusion and attenuates necrotising enterocolitis (NEC)-like intestinal injury in newborn piglets following asphyxia-reoxygenation.