Search

Background Sepsis is associated with a deflection of inflammatory and coagulative parameters, since some clotting factors are known to be involved in the host’s defense against infection and inflammation. These parameters could play a crucial role in the course of sepsis and be used as prognostic markers in critically ill children. Methods A total of 250 critically ill pediatric patients diagnosed with sepsis were retrospectively analyzed to identify routinely measured predictors for in-hospital mortality at the peak level of C-reactive protein. Those parameters entered multivariate logistic regression analysis as well as a decision tree for survival. Results Multivariate logistic regression analysis revealed fibrinogen, platelets and activated partial thromboplastin time (aPTT) at the peak level of C-reactive protein to be predictors for survival (p = 0.03, p = 0.01 and p = 0.02, respectively). An increase in fibrinogen and platelets is linked to survival, whereas an aPTT prolongation is associated with higher mortality; adjusted odds ratios (95% CI) for an increase of 100 mg/dl in fibrinogen are 1.35 (1.04–1.82) per 50 G/l platelets 1.94 (1.3–3.29) and 0.83 (0.69–0.96) for an aPTT prolongation of 10 s. Decision tree analysis shows that a fibrinogen level below 192 mg/dl (90.9% vs. 13% mortality) is most distinctive in non-survivors. Conclusions High levels of fibrinogen and platelets as well as a non-overshooting aPTT are associated with a higher survival rate in pediatric patients with diagnosed sepsis. In particular, hypofibrinogenemia is distinctive for a high mortality rate in septic critically ill children. Electronic supplementary material The online version of this article (10.1186/s13613-018-0457-8) contains supplementary material, which is available to authorized users.

The authors report two cases of delayed post-operative anterior spinal artery syndrome (ASAS) following posterior correction with Cotrel Dubousset (CD) instrumentation for adolescent idiopathic scoliosis. Sensory pathways were continuously monitored from skin incision to awakening. In both cases intraoperative SEPs were normal and the wake-up test revealed no neurological deficit. Both patients were presented with incomplete paraplegia (no sensory impairment) three and ten hours after surgery. Without delay, both patients underwent revision surgery, and the CD instrumentation was removed. Immediately after surgery, both patients' motor power in their lower extremities improved rapidly. In cases with delayed ASAS after posterior scoliosis correction, the removal of the instrumentation system was shown to be sufficient to regain full motor recovery caudal to the level of impairment.

More efficacious anticoagulant and antiplatelet agents have been introduced in vascular medicine and in the prevention of perioperative venous thromboembolisms. Patient management should be guided by familiarity with thepharmacology of coagulation-altering drugs and by consensus statements. The present paper reviews recommendations from the Austrian Task Force for Perioperative Coagulation which are based on thorough evaluation of the available pharmacological information and case reports. The consensus statement focuses on neuraxial and peripheral techniques and is designed to encourage safe and quality patient care.

Resuscitation of patients in hemorrhagic shock remains one of the most challenging aspects of trauma care. We showed in experimental studies that vasopressin, but not fluid resuscitation, enabled short-term and long-term survival in a porcine model of uncontrolled hemorrhagic shock after penetrating liver trauma. In this case report, we present two cases with temporarily successful cardiopulmonary resuscitation (CPR) using vasopressin and catecholamines in uncontrolled hemorrhagic shock with subsequent cardiac arrest that was refractory to catecholamines and fluid replacement. In a third patient, an infusion of vasopressin was started before cardiac arrest occurred; in this case, we were able to stabilize blood pressure thus allowing further therapy. The patient underwent multiple surgical procedures, developed multi-organ failure, but was finally discharged from the critical care unit without neurological damage.

Hemorrhage after traumatic injury results in coagulopathy which only worsens the situation. This coagulopathy is caused by depletion and dilution of clotting factors and platelets, increased fibrinolytic activity, hypothermia, metabolic changes and anemia. The effect of synthetic colloids used for compensating the blood loss, further aggravates the situation through their specific action on the hemostatic system. Bedside coagulation monitoring permits relevant impairment of the coagulation system to be detected very early and the efficacy of the hemostatic therapy to be controlled directly. Administration of fresh frozen plasma (FFP), platelet concentrates and antifibrinolytic agents is essential for restoring the impaired coagulation system in trauma patients. Clotting factor concentrates should be administered if coagulopathy is based on diagnosed depletion of clotting factors, if FFP is not available and if transfusion of FFP is insufficient to treat the coagulopathy. Recombined FVIIa is frequently employed during severe bleeding which could not be treated by conventional methods but the results of on-going clinical trials are not yet available.

Author details 1Haemostasis Research Unit, Centre for Haemostasis and Thrombosis, Department of Haematology and Oncology, Guy’s and St Thomas’ Hospital & NHS Trust Foundation, King’s College London School of Medicine, 1st Floor, North Wing, St Thomas’ Hospital, Westminster Bridge Road, London SE1 7EH, UK. 2Institute of Anesthesiology, University Hospital Zurich, CH-8091 Zurich, Switzerland. 3Department of Anaesthesiology and Critical Care Medicine, Innsbruck Medical University, Anichstrasse 35, A-6020 Innsbruck, Austria. 4Working Group on Perioperative Hemostasis, Department of Anaesthesiology, University Hospital of Munich, Nussbaumstrasse 20, 80336 Munich, Germany. 5Department of Anaesthesiology, University Hospital Aachen, RWTH Aachen University, Pauwelsstrasse 30, 52074 Aachen, Germany. Published: 18 March 2011