Isolated, spontaneous superior mesenteric and celiac artery dissection: case report and review of literature

Spontaneous, isolated dissection of the superior mesenteric artery (SMA) and celiac artery (CA) is rare. Although there are known risk factors, there is no particular mechanism that is common to vascular dissections. The objectives of this study were to review the current literature on diagnosis and treatment of isolated SMA and CA dissection, and to review aortic complications in giant cell arteritis, Takayasu arteritis, and polyarteritis nodosa. Giant cell arteritis, Takayasu arteritis, and polyarterteritis nodosa are vasculitides that are associated with SMA and CA dissection. An interesting aspect of this case is that the patient was a healthy person before presentation, and ultimately, did not have an underlying etiology to explain the dissection. In addition, the patient was successfully managed without operative intervention. Although there are known risk factors in patients who present with isolated, spontaneous SMA and CA dissection, the pathogenesis is still unclear. The prognosis has improved significantly with the early use of computed tomography angiography to diagnosis this entity. Although most cases require surgical intervention, there are some, as in this case, that are managed non-operatively.     

Characterization of Renal Toxicity in Mice Administered the Marine Biotoxin Domoic Acid

Domoic acid (DA), an excitatory amino acid produced by diatoms belonging to the genus Pseudo-nitzschia, is a glutamate analog responsible for the neurologic condition referred to as amnesic shellfish poisoning. To date, the renal effects of DA have been underappreciated, although renal filtration is the primary route of systemic elimination and the kidney expresses ionotropic glutamate receptors. To characterize the renal effects of DA, we administered either a neurotoxic dose of DA or doses below the recognized limit of toxicity to adult Sv128/Black Swiss mice. DA preferentially accumulated in the kidney and elicited marked renal vascular and tubular damage consistent with acute tubular necrosis, apoptosis, and renal tubular cell desquamation, with toxic vacuolization and mitochondrial swelling as hallmarks of the cellular damage. Doses≥0.1 mg/kg DA elevated the renal injury biomarkers kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin, and doses≥0.005 mg/kg induced the early response genes c-fos and junb. Coadministration of DA with the broad spectrum excitatory amino acid antagonist kynurenic acid inhibited induction of c-fos, junb, and neutrophil gelatinase-associated lipocalin. These findings suggest that the kidney may be susceptible to excitotoxic agonists, and renal effects should be considered when examining glutamate receptor activation. Additionally, these results indicate that DA is a potent nephrotoxicant, and potential renal toxicity may require consideration when determining safe levels for human exposure.Domoic acid (DA), a water-soluble, heat-stable tricarboxylic acid produced by diatoms belonging to the genus Pseudo-nitzschia, is responsible for a condition known as amnesic shellfish poisoning in humans.^1–4 Shellfish, such as clams and mussels, and fish that accumulate DA serve as vectors of exposure to various species of birds and aquatic mammals in addition to humans.^5,6 Initially recognized as a human toxicant when more than 100 people became ill after eating contaminated mussels in eastern Canada in 1987, DA poisoning was defined by the occurrence of gastrointestinal or neurologic symptoms ranging from abdominal cramps and headache to more severe cases of memory loss, seizures, coma, and even death.^2,4 Increased awareness and governmental regulation, which set a limit of 20 μg DA/g in shellfish tissue, has reduced the incidence of DA toxicity in humans since the 1987 outbreak. However, there is concern that exposure will increase because of the growing presence of toxic diatom-producing algal blooms, which are often attributed to human factors, such as pollution, shipping, and global warming, leading to greater nutrient availability, greater distribution of algal species, and longer growth periods.^7–14 Although the overt gastrointestinal and neurologic manifestations have defined the disease, emerging evidence from animal and human studies support previously unrecognized threats and novel toxicologic syndromes caused by subclinical toxicity from acute and chronic DA exposures, which may ultimately challenge the adequacy of the current acceptable limit.^15–18DA is a potent activator of kainate receptors (KRs) as well as a subpopulation of α-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid receptors (AMPARs).¹⁹ The toxic response produced by DA is a coordinated effort, which involves initial activation of KR and AMPAR by DA and secondary activation of N-methyl-D-aspartate receptors (NMDARs) by glutamate, and it is associated with an influx of Ca²⁺ across the plasma membrane, inflammation, neuronal cell injury and death, and neurobehavioral alterations.^19–22 Although they are extensively characterized in the central nervous system, glutamate receptors are also expressed at peripheral sites and have been shown to exhibit toxicity in multiple tissues, including the kidney, where NMDARs contribute to organ damage in models of ischemia-reperfusion injury and gentamicin nephrotoxicity.^23–26 There is limited information about the effects of DA on the kidney; however, oral dosing in coho salmon has shown that the kidney is a primary site of DA accumulation in this species, and studies in rodents have shown that renal excretion is the exclusive route of systemic DA elimination.^27,28 Examination of sea lions after DA poisoning has also revealed some evidence of interstitial nephritis, renal edema, and elevated BUN, although the exact cause of these findings cannot be definitively attributed to DA toxicity.^29,30 Furthermore, sea lions with acute DA toxicosis seem to have an elevated hematocrit,³¹ suggesting that water reabsorption or red blood cell production could be affected, both of which are functions of the kidney. Despite this circumstantial evidence, a detailed examination of the renal response to DA administration has not been fully explored. The purpose of the current study was to characterize the acute renal effects of DA at doses that produce neurotoxicity and neurobehavioral changes (1.0–2.5 mg/kg) as well as several lower doses (0.0005–0.5 mg/kg), which are considered below the limit of toxicity.     

Digital imaging analysis to assess scar phenotype

In order to understand the link between the genetic background of patients and wound clinical outcomes, it is critical to have a reliable method to assess the phenotypic characteristics of healed wounds. In this study, we present a novel imaging method that provides reproducible, sensitive, and unbiased assessments of postsurgical scarring. We used this approach to investigate the possibility that genetic variants in orofacial clefting genes are associated with suboptimal healing. Red‐green‐blue digital images of postsurgical scars of 68 patients, following unilateral cleft lip repair, were captured using the 3dMD imaging system. Morphometric and colorimetric data of repaired regions of the philtrum and upper lip were acquired using ImageJ software, and the unaffected contralateral regions were used as patient‐specific controls. Repeatability of the method was high with intraclass correlation coefficient score > 0.8. This method detected a very significant difference in all three colors, and for all patients, between the scarred and the contralateral unaffected philtrum (p ranging from 1.20^?05 to 1.95^?14). Physicians’ clinical outcome ratings from the same images showed high interobserver variability (overall Pearson coefficient = 0.49) as well as low correlation with digital image analysis results. Finally, we identified genetic variants in TGFB3 and ARHGAP29 associated with suboptimal healing outcome.     

The Surgical Options and Clinical Evidence for Treatment of Wear or Corrosion Occurring With THA or TKA

Background

Wear and corrosion occurring in patients with hip and knee arthroplasty are common causes of failure leading to revision surgery. A variety of surgical approaches to these problems have been described, with varying efficacy. Polyethylene wear, metal-on-metal (MoM) hip bearing wear, and problems associated with modular taper corrosion are the areas of greatest clinical impact; results of revisions for these problems are likely to dictate a large portion of revision resources for the foreseeable future, and so they call for specific study.

Questions/purposes

We identified the most frequently reported procedures to treat hip polyethylene wear, knee polyethylene wear, MoM wear after THA, and modular taper corrosion and determined the timing and reasons these failed.

Methods

We performed systematic reviews of the published literature on the four topics using MEDLINE^® and Embase in October 2013; searches were supplemented by hand searches of bibliographies. Prespecified criteria resulted in the identification of 38 relevant articles, of which 33 were either case reports or Level IV evidence. Followup was generally at short term and ranged from 0.2 to 8 years.

Results

The most frequently reported procedures for treating clinically important wear were a partial or complete revision. When treating polyethylene wear, the more frequently reported reasons for hip and knee rerevisions were loosening, continued wear, and instability. Soft tissue reactions were more common and occasionally extensive in patients with MoM or modular taper corrosion. Patients with soft tissue reactions had more complications and higher rerevision rates.

Conclusions

Studies with longer followup and higher levels of evidence are needed to direct the treatment of wear and corrosion. When soft tissue damage secondary to MoM wear or taper corrosion is present, the results of treatment can be poor. There is an urgent need to better understand these two mechanisms of failure.