[Intramedullary placement of intraosseous cannulas inserted in the preclinical treatment of polytrauma patients : A retrospective, computed tomography-assisted evaluation]. / Intramedulläre Lage von präklinisch angelegten intraossären Zugängen bei polytraumatisierten Patienten : Retrospektive, computertomographisch gestützte Evaluation.

BACKGROUND: Use of intraosseous access to the vascular system is rare in the pre-hospital setting (<1%). However, as patients for which the use of an intraosseous device is indicated are usually in a critical condition, awareness of possible application errors is vital. A survey was performed to evaluate intramedullary needle placement by means of computed axial tomography. METHODS: In the period of 01/01/2011 to 31/12/2015 all multislice-CT trauma scans performed in a trauma center were monitored for intraosseous devices in situ. The placement site, type of intraosseous device and needle deployed, thickness of bone and soft tissues, site for optimum needle placement, and both deviation from gold standard placement and visible complications were also recorded. RESULTS: In 11 out of 982 patients with suspected polytrauma that were studied during the observation period, 13 intraosseous cannulas were found (1.12%). In all cases, the EZ-IO® (Teleflex, P.O. Box 12600, Research Triangle Park, NC 27709, USA) intraosseous vascular access system was used. All applications were placed correctly in the medullary cavity, but none concurred with the current guidelines: The site of the puncture deviated laterally in seven cases, medially in two cases, cranially in four cases, and caudally in two cases. The most common error in all 13 cases was overshooting during needle introduction. CONCLUSION: Even though clinical criteria may suggest correct placement of an intraosseous device, the results of this survey provide evidence that deviations in positioning are common. Placement of the needle too deep can cause complications within the soft tissues or potentially impede intraosseous infusion.

[Acquired von Willebrand's disease type 2A following arteriovenous fistula for haemodialysis?]. / Erworbenes von-Willebrand-Syndrom Typ 2A als Begleiterscheinung eines Dialyseshunts?

Acquired von Willebrand's disease (aVWD) is considered to be an underestimated cause of unexplained bleeding. Adsorption of von Willebrand factor (VWF) to tumour cells or hydroxyethyl starch and elimination of VWF by autoantibodies as well as shear stress-induced mechanical alteration of VWF with concomitant cleavage by enzymes may lead to an acquired deficiency of VWF and a bleeding disorder. We report a 39-year-old woman who developed spontaneous bleeding five years after surgical creation of an arteriovenous fistula (AVF) for haemodialysis treatment. AVWD type 2A was diagnosed after successful renal transplantation. One year after surgical closure of the AVF, the aVWD could not be verified again. Thus, the aVWD may have developed because of altered blood flow and shear stress inside the arteriovenous fistula.

[Acquired hemophilia A as a cause of postoperative bleeding]. / Erworbene Hämophilie A als postoperative Blutungskomplikation.

Acquired spontaneous hemophilia is a rare but potentially life-threatening disease, which poses a major challenge to intensive care medicine. We report a case in which the disease occurred postoperatively in a patient following uncomplicated lumbal discectomy. The clinical sequelae involved hemorrhagic shock (cHb 4.1 g/dl; hct 17 %; systolic BP 60 mmHg; HR 130/min; saO2 73 %) due to retroperitoneal hematoma eight days after neurosurgical intervention. While lesions of the retroperitoneal vessels were not found during emergent angiography and laparotomy, the laboratory results showed a slightly prolonged activated prothrombin time (aPTT; 47 s). However, application of fresh frozen plasma (FFP) even prolonged the aPTT (53 s). Analysis of clotting factors proved a deficiency of factor VIII with a reduced activity of about 20 %, which was resistant against therapy with desmopressin (DDAVP) and substitution of factor VIII. Thus, the plasma-mix-test was performed, showing complete inactivation of the factor VIII-activity of the pooled plasma. This evidenced the presence of acquired inhibitors against factor VIII. Hemostasis was successfully and immediately restored with the application of recombinant factor VIIa (rFVIIa), including boluses of 60 - 80 microg/kg every 6th - 8th hour (supplemented with tranexamic acid, 3 x 1 g/d), leading to a continuous infusion of 12 microg/kg per hour. With prednisolone (1 mg/kgBW/d) over the ensuing 8 weeks, the antibodies were sufficiently suppressed and no additional substitution of factor VIII was necessary to maintain normal hemostasis.