Carpal Tunnel Injections: A Novel Approach Based on Wrist Width.

INTRODUCTION: Carpal tunnel steroid injections (CTIs) have the potential risk of damaging underlying critical structures, including the median nerve (MN), radial artery (RA), and ulnar neurovascular bundle (UB). The purpose of this study was to analyze the safety of a volar radial (VR) and volar ulnar (VU) CTI, using standardized anatomical "safe zones." MATERIALS AND METHODS: This study was performed on 87 cadaveric arms using a percentage of the total wrist width as a guide for placement of a VR (30 and 33% of total wrist width) and VU (60 and 66% of total wrist width) injection. RESULTS: Our results demonstrate a wide range of anatomic variations in the location of these critical neurovascular structures near the carpal canal, indicating that using superficial landmarks alone for CTIs may result in an increased risk of iatrogenic injury to these critical structures. DISCUSSION: We propose a technique using a percentage of total wrist width as a guide for CTIs. Both VR (30% of wrist width) and VU (60% of wrist width) CTIs offer relatively safe and reliable CTI locations to the carpal canal. LEVEL OF EVIDENCE: Not applicable/cadaveric study.

The diagnosis of adult-onset haemophagocytic lymphohistiocytosis: lessons learned from a review of 29 cases of bone marrow haemophagocytosis in two large academic institutions.

AIMS: Haemophagocytic lymphohistiocytosis (HLH) is divided into paediatric (primary) and adult (secondary) types. While paediatric-HLH has been extensively characterised, similar studies in adults are limited. This study aims to evaluate the significance of the HLH diagnostic criteria as well as other clinical parameters in adults with bone marrow evidence of haemophagocytosis. METHODS: We conducted a 10-year retrospective search of the pathology archives of two institutions for cases with bone marrow haemophagocytosis. We included those cases that fulfilled the currently established HLH diagnostic criteria. For the 29 cases that met inclusion criteria, we assessed clinical features, co-morbidities, therapy and clinical outcome. The effect of 19 clinical variables on mortality outcomes was assessed using logistic and hazard regression analyses. RESULTS: Of cases for which an aetiology could be identified, infectious diseases were the most common association (14 of 19, 74%). Fever and elevated ferritin were the most frequently available criteria used to establish HLH. The overall mortality rate was 61% despite HLH-specific therapy, which had been initiated in 48% of the cases. The remaining cases were treated with supportive therapy and antibiotics. The most statistically significant marker of mortality was an elevated absolute neutrophil count (ANC), a feature not typical of HLH. CONCLUSIONS: Since elevated ANC correlates with poor outcomes in sepsis, and not HLH, we postulate that many of the patients fulfilling HLH diagnostic criteria in this study likely had sepsis/systemic inflammatory response syndrome rather than HLH. Our results highlight the need to define HLH diagnostic criteria specific to the adult population.

Differential expression of ribosomal proteins in myelodysplastic syndromes.

Aberrations of ribosomal biogenesis have been implicated in several congenital bone marrow failure syndromes, such as Diamond-Blackfan anaemia, Shwachman-Diamond syndrome and Dyskeratosis Congenita. Recent studies have identified haploinsufficiency of RPS14 in the acquired bone marrow disease isolated 5q minus syndrome, a subtype of myelodysplastic syndromes (MDS). However, the expression of various proteins comprising the ribosomal subunits and other proteins enzymatically involved in the synthesis of the ribosome has not been explored in non-5q minus MDS. Furthermore, differences in the effects of these expression alterations among myeloid, erythroid and megakaryocyte lineages have not been well elucidated. We examined the expression of several proteins related to ribosomal biogenesis in bone marrow biopsy specimens from patients with MDS (5q minus patients excluded) and controls with no known myeloid disease. Specifically, we found that there is overexpression of RPS24, DKC1 and SBDS in MDS. This overexpression is in contrast to the haploinsufficiency identified in the congenital bone marrow failure syndromes and in acquired 5q minus MDS. Potential mechanisms for these differences and aetiology for these findings in MDS are discussed.