Influence of external cardiac pacing on cerebral oxygenation measured by near‐infrared spectroscopy in children after cardiac surgery

Background: The brain of children in the early period after repair of congenital heart defects with cardiopulmonary bypass (CPB) may be more vulnerable to hemodynamic changes because of impaired cerebral autoregulation. During postoperative testing of the external temporary safety pacer, we performed desynchronizing ventricular pacing (VVI) while monitoring cerebral oxygenation using near‐infrared spectroscopy (NIRS). Methods: We prospectively investigated 11 children (6 girls, 5 boys). Mean age was 6.1 months (±3.8 months) and mean weight: 5.3 kg (±1.5 kg). We performed measurements at four study steps: baseline I, VVI pacing, baseline II and atrial pacing (AOO) to exclude effects of higher heart rate. We continuously measured the effects on hemodynamic and respiratory parameters as well as on cerebral tissue oxygenation index (TOI). Hemoglobin difference (HbD) was calculated as a parameter for cerebral blood flow (CBF). Results: Ventricular pacing leads to a significant decrease in arterial blood pressure and central venous saturation accompanied by an immediate and significant decrease in TOI (63.3% ± 7.6% to 61.5% ± 8.4% [P < 0.05]) and HbD (0.51 ± 1.8 μmol·l⁻¹ to −2.9 ± 4.7 μmol·l⁻¹ [P < 0.05]). Conclusion: Cardiac desynchronization after CPB seems to reduce CBF and cerebral oxygenation in children.     

The association of hypotension during non‐cardiac surgery,before and after skin incision,with postoperative acute kidney injury: a retrospective cohort analysis

Intra‐operative hypotension is associated with acute postoperative kidney injury. It is unclear how much hypotension occurs before skin incision compared with after, or whether hypotension in these two periods is similarly associated with postoperative kidney injury. We analysed the association of mean arterial pressure < 65 mmHg with postoperative kidney injury in 42,825 patients who were anaesthetised for elective non‐cardiac surgery. Intra‐operative hypotension occurred in 30,423 (71%) patients: 22,569 (53%) patients before skin incision; and 24,102 (56%) patients after incision. Anaesthetised patients who were hypotensive had mean arterial pressures < 65 mmHg for a median (IQR [range]) of 5.5 (0.0–14.7 [0.0–60.0]) min.h^?1 before skin incision, compared with 1.7 [0.3–5.1 [0.0–57.5]) min.h^?1 after incision: a median (IQR [range]) of 36% (0%–84% [0%–100%]) of hypotensive readings were before incision. We diagnosed postoperative kidney injury in 2328 (5%) patients. The odds ratio (95%CI) for acute kidney injury was 1.05 (1.02–1.07) for each doubling of the duration of hypotension, p < 0.001. Postoperative kidney injury was associated with the product of hypotension duration and severity, that is, area under the curve, before skin incision and after, odds ratio (95%CI): 1.02 (1.01–1.04), p = 0.004; and 1.02 (1.00–1.04), p = 0.016, respectively. A substantial fraction of all hypotension happened before surgical incision and was thus completely due to anaesthetic management. We recommend that anaesthetists should avoid mean arterial pressure < 65 mmHg during surgery, especially after induction, assuming that its association with postoperative kidney injury is, at least in part, causal.     

Pre‐operative anaemia,intra‐operative hepcidin concentration and acute kidney injury after cardiac surgery: a retrospective observational study

Acute kidney after cardiac surgery is more common in anaemic patients, whereas haemolysis during cardiopulmonary bypass may lead to iron‐induced renal injury. Hepcidin promotes iron sequestration by macrophages: hepcidin concentration is reduced by anaemia and increased by inflammation. We analysed the associations in 525 patients between pre‐operative anaemia (haemoglobin < 130 g.l^?1 in men and < 120 g.l^?1 in women), intra‐operative hepcidin concentration and acute kidney injury (dialysis or > 26.4 μmol.l^?1 or > 50% creatinine increase during the first two days after cardiac surgery. Rates of pre‐operative anaemia and postoperative kidney injury were 109/525 (21%) and 36/525 (7%), respectively. The median (IQR [range]) intra‐operative hepcidin concentration was 20 (10–33 [0–125]) μg.l^?1 and was lower in anaemic patients than those who were not: 15 (4–28 [0–125]) μg.l^?1 vs. 21 (12–33 [0–125]) μg.l^?1, respectively, p = 0.002. Four variables were independently associated with postoperative kidney injury, for which the beta‐coefficients (SE) were: minutes on cardiopulmonary bypass, 0.016 (0.004), p < 0.001; intra‐operative hepcidin concentration, 0.032 (0.008), p < 0.001; pre‐operative anaemia, 1.97 (0.56), p < 0.001; and Cleveland clinic risk score, 0.88 (0.35), p = 0.005. Contrary to generally increased rates of kidney injury in patients with higher hepcidin concentrations, rates of kidney injury in anaemic patients were lower in patients with higher hepcidin concentrations, beta‐coefficient (SE) ?0.037 (0.01), p = 0.007. In cardiac surgical patients the rate of postoperative acute kidney injury predicted by the Cleveland risk score might be adjusted for pre‐operative anaemia and intra‐operative cardiopulmonary bypass time and hepcidin concentration. Pre‐operative correction of anaemia, reduction in intra‐operative bypass time and modification of iron homeostasis and hepcidin concentration might reduce acute kidney injury.