Neurological complications associated with parenteral treatment: central pontine myelinolysis and Wernicke's encephalopathy.

Thompson, P. D.; Gledhill, R. F.; Quinn, NP; Rossor, Martin N.; Stanley, Philip M.; Coomes, E. N.

doi:10.1136/bmj.292.6521.684

Cited by 27 publications

(16 citation statements)

References 10 publications

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“…Features were, however, sufficiently similar to the spectrum of changes recognised in CPM to make the diagnosis with reasonable confidence. Other findings in case OL103 included a single, small, recent but well 16 who sustained at least one increase of > 12 mmol/l/day (in 15 this coincided with transplantation), 19 with preoperative hyponatraemia, and 12 who became hypernatraemic for at least one postoperative day (table 2). There were no significant differences between this group and the patients with CPM with respect to the incidence of any of these factors taken individually.…”

Section: Methodsmentioning

confidence: 96%

Central pontine myelinolysis in liver transplantation.

et al. 1991

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Gross external findings were determined at necropsy and the brains then fixed whole by suspension in 10% formalin for three to six weeks before slicing. In the 47 cases collected prospectively the brain stem and cerebellum were detached and the cerebrum sliced coronally at one cm intervals. Any grossly obvious lesions were sampled for histological examination. Routinely, blocks were also taken from frontal, temporal, parietal and occipital lobes, hippocampus, basal ganglia, thalamus, cerebellum and medulla. The pons was carefully examined for evidence of CPM and blocks taken at mid-pontine level. In cases where the clincal history suggested pontine disease or where there was evidence of CPM in the first block, additional blocks were taken to include rostral and caudal pons. In three cases only single random blocks of pons were available for study.The tissue was processed to paraffin wax using a standard technique and sections were cut and stained with haematoxylin and eosin and luxol fast blue. In cases where initial sections were suspect for CPM, immunohistochemical stains for glial fibrillary acidic protein (GFAP) and neurofilament protein were prepared using an indirect immunoperoxidase technique,30 and further blocks of tissue were stained with oil red 0 to detect neutral fat.All clinical records were carefully scrutinised and particular note was made of neurological features and serum sodium changes in both the periods before and after transplantation.

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Section: Methodsmentioning

confidence: 96%

Central pontine myelinolysis in liver transplantation.

et al. 1991

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“…But, in our case hyponatremia was corrected gradually, but the clinical features of CPM and encephalopathy improved fast with thiamine supplementation. There are reports of CPM associated with WE in literature [9] and few reports show that CPM is completely reversible, though radiologic normalization takes many months [10]. Thus, it was higly suggestive of WE associated polyneuropathy as the cause of CPM in our case.…”

Section: Discussionmentioning

confidence: 59%

“…Reports were suggestive of hyperthyroidism with serum thyroid stimulating hormone (TSH) = 0.06 mIU/mL (0.4-5.5), total triiodothyronine (T3) = 321 pg/mL (90-200) and total thyroxine (T4) = 18 ng/mL (8)(9)(10)(11)(12)(13)(14)(15). But, T3/T4 ratio was \20:1 and hyperthyroid features were subtle leading to differential diagnosis of transient hyperthyroidism of hyperemesis gravidarum (THHG).…”

Section: Case Reportmentioning

confidence: 99%

Hyperemesis Gravidarum is a Syndrome of Metabolic and Endocrine Disturbances: A Case Description

Gayathri

Bhargav

2013

Ind J Clin Biochem

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Hyperemesis gravidarum is a clinical syndrome characterized by excess vomiting, dehydration and weight loss associated high human chorionic gonadotropin levels, usually occurring in the first trimester of gestation. It often presents with severe electrolyte imbalance, mental confusion and may be associated with thyroid dysfunction. We are describing the management of one such case riddled with multiple metabolic events.

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“…The rates proposed as acceptable by Ayus et al [13] (25 mEq/1 in 48 h) and Berl [15,16] (20 mEq/l/day) strike us as being too rapid. Many cases of hyponatremia have ended in CPM despite being corrected at rates slower than allowed by these guidelines [49][50][51][52][53][54][55][56][57][58][59][60][61], The recommenda tion of Sterns et al [2][3][4][5][6] that the rate of correction is not to exceed 12mEq/l/24h is safe for most patients with symptomatic hyponatremia. However, cases have been described in which CPM developed after correction of hyponatremia at a rate slower than 12 mEq/l/day.…”

Section: Our Recommendationsmentioning

confidence: 99%