Perioperative haemotherapy: I. Indications for blood component transfusion

The practice of transfusion medicine has undergone substantial change over the last decade. Much of the impetus for the change has come from the isolation of human immunodeficiency virus (HIV) and the linkage of HIV transmission to blood transfusion. The purpose of this paper is to collate and review the literature relating to the indications for blood transfusion and provide recommendations for the appropriate utilization of blood products. Peer-reviewed and published studies and reviews relating to aspects of clinical blood transfusion were identified through computer searches and searching of the bibliographies of identified articles. Emphasis was placed on the literature published within the last decade and particularly in the years 1985-91. Material was chosen which was of proved clinical importance and in which findings were consistent among different investigators or different centres. Less emphasis was placed on material reporting new findings of uncertain clinical relevance or findings that were not consistent with majority reports. It is concluded that the only indication for red cell transfusion is to increase the oxygen carrying capacity of the blood and that an adjustment downwards in the haemoglobin concentration at which blood is transfused (transfusion trigger) from the traditional level of 100 g.L-1 is supported by the physiological and clinical data. Perioperative haemoglobin concentrations of 80 g.L-1 are acceptable in otherwise healthy young patients. The transfusion trigger should be adjusted upwards from this in medically compromised patients and in the elderly (greater than 60 yr). Fresh frozen plasma (FFP) is only indicated when there are documented deficiencies of coagulation factors. Platelet concentrates (PC) are indicated for the treatment of clinical coagulopathy resulting from thrombocytopaenia or platelet dysfunction. Routine or prophylactic administration of either FFP or PC after cardiopulmonary bypass or during resuscitation from haemorrhage is not indicated.     

Persistent Hypotension Associated with Hypermedullipinemia: A New Syndrome

A new syndrome is described in a patient with advanced renal insufficiency. This consists of severe and persistent hypotension causing weakness but associated with a clear mental status. Also present is evidence for decreased vascular reactivity. The hypotension was not orthostatic. The hypotension was associated with a circulating vasodepressor substance having the characteristics of medullipin I. The medullipin appears to have been derived from the remaining right kidney. Hypotension existed despite the presence of major prohypertensive mechanisms, including an endstage kidney, hyperreninemia and hyperaldosteronemia. It is likely that hypotension due to hypermedullipinemia is an entity occurring in the human being.     

Stabilization of acetylcholine receptors at the neuromuscular synapse: the role of the nerve.

The majority of acetylcholine receptors (AChRs) at innervated neuromuscular junctions (NMJs) are stable, with half-lives averaging about 11 days in rodent muscles. In addition to the stable AChRs, approximately 18% of AChRs at these innervated junctions are rapidly turned over (RTOs), with half lives of less than 24 h. We have postulated that RTOs may be precursors of stable AChRs, and that the motor nerve may influence their stabilization. This hypothesis was tested by: (i) labeling AChRs in mouse sternomastoid (SM) muscles with 125I-alpha-BuTx; (ii) denervating one SM muscle in each mouse, and (iii) following the fate of the labeled AChRs through a 5-day period when RTOs were either stabilized or degraded. The hypothesis predicts that denervation should preclude stabilization of RTOs, resulting in a deficit of stable AChRs in denervated muscles. The results showed a highly significant (P less than 0.002) deficit of stable AChRs in denervated as compared with innervated muscles. Control experiments excluded the possibility that this deficit could be attributed to independent accelerated degradation of either RTOs or pre-existing stable AChRs. The observed deficit was quantitatively consistent with the deficit predicted by a mathematical model based on interruption of stabilization following denervation. We conclude that: (i) the observed deficit after denervation of NMJs is due to failure of stabilization of pre-existing RTOs; (ii) RTOs at normally innervated NMJs are precursors of stable AChRs; (iii) stabilization occurs after the insertion of AChRs at NMJs, and (iv) motor nerves play a key role in stabilization of RTOs. The concept of receptor stabilization has important implications for understanding the biology of the neuromuscular junction and post-synaptic plasticity.     

Panfacial fractures: analysis of 33 cases treated late.

PURPOSE: The aim of this retrospective study was to analyze the characteristics of delayed panfacial fractures and evaluate treatment results. PATIENTS AND METHODS: Thirty-three patients with delayed panfacial fractures were treated in the Maxillofacial Trauma Center of Peking University, School and Hospital of Stomatology between 1998 and 2004. Each patient was examined by computed tomography (CT) scans before operation. For those who had no severe opening restriction, dental impressions were taken to fabricate dental casts. For those with severely comminuted fractures, 3-dimensional (3D) models of the facial skeleton were used. Re-establishing the continuity of the mandible was the first step and then used as a platform to reconstruct the maxillary fractures via maxillomandibular fixation after Le Fort I osteotomy. The third step was to restore the mid- and upper-facial width and projection by coronal approach to expose the zygomatic complex and frontal bone/sinus and/or naso-orbito-ethmoid (NOE) fractures. RESULTS: There were 3 types of mandibular fractures that affected the treatment plan: 1) type I, mandibular body/symphysis fracture(s) (17/33, 51.52%); 2) type II, mandibular angle and/or condylar fracture(s) (6/33, 18.18%); and 3) type III, both mandibular body/symphysis and angle/condylar fractures (10/33, 30.30%). Fourteen cases were associated with NOE fractures (42.42%) and 3 cases had frontal sinus fractures (9.1%). Twelve cases had enophthalmos (36.36%) and 3 lost 1 eyeball. The order of treatment was dependent on the mandibular fracture type. For type I fractures, reconstructing the mandibular arch was the first step. For type II fractures, repairing the angle, ascending rami, and condylar areas was the first step. For type III fractures, when both mandibular height and arch were disrupted, freeing the malunited angle or condyle was the first step before restoring the mandibular arch form. Reconstruction of the mandibular height and projection was then carried out. For all 3 types, the second step was to restore the mid- and upper facial width and projection by reducing the zygomatic complex and frontal bone/sinus or NOE fractures. Maxillary fixation across the Le Fort I level was the last step. Le Fort I osteotomy was used for all 33 cases. Bone grafts and soft tissue suspension also were used. Twenty-one cases (63.64%) had good results, 7 (21.21%) cases were acceptable, and 5 (15.15%) were not good. There were 7 cases (21.21%) that still had soft tissue problems that needed secondary operations. CONCLUSIONS: Reconstruction of the mandible first with Le Fort I osteotomy is a good way to treat delayed panfacial fractures. Computed tomography and 3D CT, model surgery, and occasionally 3D models are necessary aids for diagnosis and treatment. Soft tissue problems, including lacerations and asymmetries, were often the factors that caused an unfavorable outcome.     

Crystal deposits in the human intervertebral disc: implications for disc degeneration.

BACKGROUND CONTEXT: Although crystal deposition in cartilage and synovial fluid has received much attention, crystal formation and the role that crystal deposits play are virtually unexplored in the intervertebral disc. In articular cartilage matrix, crystal deposits are associated with altered extracellular matrix (ECM) and cell phenotypic features, but crystal deposition in the human intervertebral disc has received much less attention. PURPOSE: To determine the incidence of crystal deposits in the annulus and to evaluate associated disc cell and ECM features. STUDY DESIGN/SETTING: Human intervertebral disc annulus tissue was obtained in a prospective study of the presence of crystals in the disc ECM. Human Subjects Institutional Review Board approved experimental studies. PATIENT SAMPLE: Two hundred eight sequential disc specimens were submitted from surgical disc procedures performed on individuals with herniated discs, degenerative disc disease, or recurrent disc herniation. During this same time period, three disc specimens were received from nonsurgical donors and added to the study population. OUTCOME MEASURES: Histologic features with special attention to crystal deposition. METHODS: Specimens were processed undecalcified and examined for the histologic presence of crystal deposits and ECM features around the crystals. RESULTS: The proportion of specimens containing crystals was determined to be 14.7%; crystals displayed varying sizes, morphology, and polarized light birefringence features. Pyrophosphate crystals were most common, but oxalate-like crystals were also present. ECM in crystal regions showed previously recognized alterations. CONCLUSIONS: This study shows that the incidence of crystal deposits in discs is approximately 15% and is thus a relatively common occurrence. These data are important because masses of crystals not only disrupt disc ECM but may also accelerate preexisting degenerative changes via an elevation in matrix metalloproteinases (as previously recognized in cartilage). Because failure of the structural integrity of the disc can result in annular tears and subsequent disc herniation, the mechanisms of crystal formation and the relationship between crystals and disc degeneration merit further investigations.