Laboratory Signs of Enteric Failure - Predictors of Pressure Ulcers in Traumatic Spinal Cord Disease

Relevance. Among the complications of traumatic spinal cord disease (SCD) pressure ulcers occupy a special place, with incidence reaching 68% and showing no tendency for decreasing. Literature reviews one of the main reasons for the formation of decubital ulcers is enteral insufficiency, the timely detection of which is still a common problem for many medical specialties, and laboratory indicators pointing to its manifestation remain in the zone of a controversial issue. New knowledge regarding laboratory predictors of pressure ulcer formation in the acute period of trauma will reduce the risk of decubital ulcerative defects.Purpose of the study. Based on the analysis of laboratory blood levels in the acute and early periods of hip joint injury, to identify predictors of the formation of pressure ulcers in patients with spinal trauma.Materials and methods. 68 case histories of adult patients with hip injury were retrospectively analyzed. The victims were treated in the City Clinical Hospital No. 39 of the Kanavinsky District of Nizhny Novgorod for the period from 2013 to 2020.Results and discussion. A comparative analysis of blood levels on the first day after injury showed that patients with subsequently developed bedsores at the early stages of treatment got hypoproteinemia and a decrease in serum creatinine levels more often than patients without bedsores. In addition, white blood cell count in patients with pressure ulcers was elevated, compared to normal values and patients without pressure ulcers white blood cell count. For a year creatinine and total protein values in patients of the main group tended to be or completely became normal, which is most likely associated with adequately administered enteral nutrition. The white blood cell count of the study group decreased to the normal range.Conclusion. Increased white blood cell, a decrease creatinine levels and total protein values in patients with HSC in the first hours after injury confirms the catabolic orientation of metabolism in the acute period of spinal cord injury, so it leads to conclusion that the early intensive therapy aimed at arresting protein losses and inflammation is needed, which in turn will prevent the formation of pressure ulcers in the early period of traumatic spinal cord disease.

A case of combined spinal cord disease due to lead poisoning from dishes

At the beginning of 1898, at the very time when the question of noon was discussed in St. Petersburg not only by the medical press, but also by the general press, I came across a case that, in addition to the everyday interest associated with this issue, undoubtedly deserves attention and clinical attention. While a whole literature has already been formed about peripheral lead paralysis, diseases of the central nervous system and, in particular, of the spinal cord due to lead poisoning have been described by relatively few and only recently. All this prompts me to report my observation, despite the fact that he was destined to remain without posthumous research.

Genetics of Degenerative Cervical Myelopathy: A Systematic Review and Meta-Analysis of Candidate Gene Studies

Degenerative cervical myelopathy (DCM) is estimated to be the most common cause of adult spinal cord impairment. Evidence that is suggestive of a genetic basis to DCM has been increasing over the last decade. A systematic search was conducted in MEDLINE, EMBASE, Cochrane, and HuGENet databases from their origin up to 14th December 2019 to evaluate the role of single genes in DCM in its onset, clinical phenotype, and response to surgical intervention. The initial search yielded 914 articles, with 39 articles being identified as eligible after screening. We distinguish between those contributing to spinal column deterioration and those contributing to spinal cord deterioration in assessing the evidence of genetic contributions to DCM. Evidence regarding a total of 28 candidate genes was identified. Of these, 22 were found to have an effect on the radiological onset of spinal column disease, while 12 genes had an effect on clinical onset of spinal cord disease. Polymorphisms of eight genes were found to have an effect on the radiological severity of DCM, while three genes had an effect on clinical severity. Polymorphisms of six genes were found to have an effect on clinical response to surgery in spinal cord disease. There are clear genetic effects on the development of spinal pathology, the central nervous system (CNS) response to bony pathology, the severity of both bony and cord pathology, and the subsequent response to surgical intervention. Work to disentangle the mechanisms by which the genes that are reviewed here exert their effects, as well as improved quality of evidence across diverse populations is required for further investigating the genetic contribution to DCM.

The Natural History of Adrenal Insufficiency in X-Linked Adrenoleukodystrophy: An International Collaboration

Context Primary adrenal insufficiency is an important clinical manifestation of X-linked adrenoleukodystrophy (ALD). Other manifestations include spinal cord disease and/or inflammatory demyelinating cerebral disease. Implementation of newborn screening requires natural history data to develop follow-up recommendations. Objective To delineate the natural history of adrenal insufficiency in male patients with ALD and to assess associations between the risk for developing adrenal insufficiency, spinal cord disease, or cerebral disease and plasma C26:0/C22:0 and C24:0/C22:0 ratios, which are diagnostic biomarkers for ALD. Design Retrospective review of medical records. Setting Two international tertiary referral centers of expertise for ALD. Patients Male patients with ALD followed at the centers between 2002 and 2016. Main Outcome Measures The primary endpoint was adrenal insufficiency; secondary endpoints were spinal cord and cerebral disease. Results Data on 159 male patients was available. The probability of developing adrenal insufficiency was described with survival analysis. Median time until adrenal insufficiency was 14 years (95% CI, 9.70 to 18.30 years). The cumulative proportion of patients who developed adrenal insufficiency was age-dependent and highest in early childhood [0 to 10 years, 46.8% (SEM 0.041%); 11 to 40 years, 28.6% (SEM, 0.037%); >40 years, 5.6% (SEM, 0.038%)]. No association between clinical manifestations and plasma ratios was detected with Cox model or Spearman correlation. Conclusions Lifetime prevalence of adrenal insufficiency in male patients with ALD is ~80%. Adrenal insufficiency risk is time-dependent and warrants age-dependent follow-up. Besides on-demand testing if symptoms manifest, we suggest a minimum of adrenal testing every 4 to 6 months for patients age ≤10 years, annual testing for those age 11 to 40 years, and solely on-demand testing for those age >40 years.