Autotransfusion Methods and Replacement of Blood Loss in Neurosurgical Operations

V.V. Gromova, A.Yu. Lubnin, O.B. Sazonova, A.A. Imaev, A.A. Ogurtsova

Burdenko Research Institute of Neurosurgery, Russian Academy of Medical Science, Moscow, Russia

 

Hemotransfusion in oncologic cases has such a serious side effect as immunosuppression. Thus, one can understand a natural desire of researchers and clinicians to use all possible methods of blood loss replacement without applying components of donor blood.

The goal of the present research was clinical study of possibility and safety of using different autotrasnfusion methods and their combinations for replacement of blood loss in neurosurgical interventions.

Materials and Methods. There were 125 patients with different intracranial tumors. We used the following methods and their combinations for ensuring adequate replacement of blood loss:

Parameters of a patient's state, studied by us, were as follows: systemic hemodynamics, hemoconcentration and hemocoagulation indices of blood, results of cerebral oximetry (CO) and EEG.

Results. A volume and speed of blood loss, peculiarities of autotransfusion tactics served the basis for dividing all patients into 3 groups:
A - Cases with moderate blood loss (2-2.5% from a body mass)
B - Cases with considerable blood loss (2.6-5% from a body mass)
C - Cases with massive blood loss (more than 5 % from a body mass)

The patients of group A (blood loss of not more than 1.5 l) had cysts and cystic lesions of different localization, intracerebral glial tumors, metastases, small neurinomas, fibrosarcomas. The cases of this group were selected for using PAD with the purpose of complete avoidance of probable transfusion of whole blood components. It was caused either by blood group rarity or necessity of an individual approach to whole blood selection. In case of small blood loss (up to 1-1.2 l), we managed to optimize hemoconcentration and hemocoagulation parameters only with the help of stored components of autoblood.

Group B included the cases with supposed intraoperative blood loss of 1.5-3 l. They had moderately vascularized meningiomas of the posterior or middle cranial fossa, craniofacial and cranioorbital tumors of different histology (meningiomas, angiofibromas, cancer), spread cholesteatomas, and chondroid-chondromas. There were two types of transfusion tactics in these cases:
a) a combination of PAD with moderate IVHD (800-1200 ml) and IARPRC;
b) in case of technical impossibility of carrying out IARPRC in some interventions (use of Cell-Saver in parallel operations), we combined PAD with more profound IVHD (1600-2000 ml).

Group C was represented by cases with such giant and highly vascularized tumors, as meningiomas, hemangiopericytomas, angiofibromas and hemangiosarcomas. A volume of blood loss in this group varied from 2 up to 12 l. Such extremely massive blood loss demanded transfusiologic support, which would differ from the above methods. We did not use packed red cells of a patient and limited ourselves to preparing a big volume of autoplasma and planning to restore an erythrocytic link with the help of IARPRC. Profound IVHD with separation was chosen as an additional method of blood replacement. When amounts of autoblood products were insufficieint, we had to use components of donor blood. However, it was done less frequently and in smaller volumes, than in operations without applying autotransfusion methods.

Autodonoship did not lead to increase of convulsive activity in cases with epileptic syndrome.

Conclusions

  1. Adequate choice of autotransfusion methods in neurosurgical interventions allows to achieve complete replacement of operative blood loss, exceeding 100% of a circulating blood volume.
  2. Taking autoblood in neurosurgical patients with epileptic syndrome does not result in aggravation of the brain electric activity; on the contrary, it leads to normalization of EEG results in many cases.
  3. PAD with subsequent administration of antifibrinolyitics promotes correction of hemocoagulation in patients with hyperfibrinolysis, caused by meningovascular tumors.