The ambiguities make data measured using low energy x-rays unsuitable for fingerprinting active pharmaceutical ingredients and small molecule systems, and, in general, copper anode diffractometers are undesirable for this purpose; however, laboratory x-ray sources with either Mo or Ag anodes are well suited for this application.
Acute compartment syndrome (ACS) is a surgical emergency. Diagnosis depends on a high clinical suspicion and an understanding of risk factors, pathophysiology and subtle physical exam findings. The typical high risk scenario for ACS is a male patient younger than 35 years of age, involved in a high energy sport or roadway collision, resulting in a tibial shaft fracture. He will go on to develop acute compartment syndrome of the leg in less than 10 hours and require emergent fasciotomy. Diagnosis of ACS in this patient is primarily a clinical one but can be confirmed with invasive intracompartmental pressure monitoring or noninvasive near infrared spectroscopy (NIRS). Delaying the diagnosis will likely result in some degree of permanent disability and places the surgeon at high risk for litigation. This article reviews the salient features of acute compartment syndrome that should be understood by all orthopaedic residents and surgeons.
SUMMARY
The reason(s) that hepatitis A virus (HAV) infection may progress infrequently to acute liver failure are poorly understood. We examined host and viral factors in 29 consecutive adult patients with HAV-associated acute liver failure enrolled at 10 sites participating in the US ALF Study Group. Eighteen of twenty-four acute liver failure sera were PCR positive while six had no detectable virus. HAV genotype was determined using phylogenetic analysis and the full-length genome sequences of the HAV from a cute liver failure sera were compared to those from self-limited acute HAV cases selected from the CDC database. We found that rates of nucleotide substitution did not vary significantly between the liver failure and non-liver failure cases and there was no significant variation in amino acid sequences between the two groups. Four of 18 HAV isolates were subgenotype IB, acquired from the same study site over a 3.5-year period. Sub-genotype IB was found more frequently among acute liver failure cases compared to the non-liver failure cases (chi-square test, P < 0.01). At another centre, a mother and her son presented with HAV and liver failure within 1 month of each other. Predictors of spontaneous survival included detectable serum HAV RNA, while age, gender, HAV genotype and nucleotide substitutions were not associated with outcome. The more frequent appearance of rapid viral clearance and its association with poor outcomes in acute liver failure as well as the finding of familial cases imply a possible host genetic predisposition that contributes to a fulminant course. Recurrent cases of the rare subgenotype IB over several years at a single centre imply a community reservoir of infection and possible increased pathogenicity of certain infrequent viral genotypes.
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