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Wernicke Encephalopathy (WE) is an acute and serious secondary neurological syndrome caused by a deficit of thiamine or vitamin B1. Although it rarely presents with the classic triad, the most frequent presenting symptoms are: mental confusion, ocular-motor dysfunction and ataxia. Laboratory and image studies can be useful, but diagnosis is fundamentally clinical, and if this syndrome is suspected treatment must be started as soon as possible. The most frequent cause in our setting is chronic alcoholism; however, there are increasing numbers of reported cases secondary to parenteral nutrition not correctly supplemented with vitamins. Here we present a case of WE secondary to parenteral nutrition not correctly supplemented with vitamins. This patient presented the classic clinical triad and was therefore diagnosed and treated rapidly, responding to treatment in an effective manner. Thus, the clinical presentation corresponded to a deficit of other vitamins associated with the same vitamin complex iv that was not administered, including a regenerative anemia and eczema craquele. This case emphasizes the need to supplement parenteral nutrition with thiamine and other vitamins. At the same time, it stresses the importance of suspecting this syndrome in all clinically compatible patients with non-vitamin supplemented parenteral nutrition.
Keywords: Wernicke Encephalopathy (WE); Home parenteral nutrition; Thiamine deficiency; Wernicke Encephalopathy (WE); Home parenteral nutrition; Thiamine deficiency
both external rectus muscles and one horizontal rotatory nystagmus, constantly in all positions of gaze. From the motor HPN is indicated in patients with an inability use the aspect, muscular balance was normal (motor strength 5/5), as digestive tract, as occurred in our patient, who presents chronic were the osteotendinous reflexes, with the exception of the intestinal insufficiency due to actinic enteritis, indicating stanachilles which were bilaterally absent. The cutaneous plantar dard parenteral nutrition of 1,700 kcal, to which is added daily a reflexes were flexors. The sensitivity study revealed a mild discomplex of minerals and multivitamins adjusted to their needs. tal hypopalesthesia in the inferior extremities, without other Poor praxis or adherence to the treatment can give rise to a noteworthy changes. The patient also presented ataxia of the state of calorific-protein or micronutrient malnutrition, causing trunk which made seating difficult and bipedal ambulation im- 1,2 the typical symptoms of each deficiency.
possible without aid.
Wernicke syndrome is a neurological complication, Regarding additional tests that were carried out, the relatively common, stemming from a deficit of thiamine or vianalytic study detected the presence of thrombocytopenia tamin B1 and which can lead to an extremely negative outcome (102,000 platelets/ml) and normocytic normochromic anemia with high mortality if not correctly identified and treated. Thi- (hemoglobin 10,3 g/dl, mean corpuscular volume 87,5 fl), in amine is a water soluble vitamin which is involved in energyaddition to hypoalbuminemia of 2,53 g/dl, indicating moderproducing enzymatic cascades during glucose metabolism. ate protein deficiency. The remainder of the additional tests, With reduced activity of these enzymes, it produces inhibition including radiography of the thorax, abdomen and a CT scan of normal glucose metabolism, causing damage to certain areas of the cranium obtained results within normal parameters. of the brain. Wernicke syndrome is characterized clinically by the triad of mental confusion, ocular-motor dysfunction and Considering the clinical history and the described ataxia. Nevertheless, the presence of this triad is more of an findings on physical examination, Wernicke syndrome was susexception than a rule and the conjunction of the three symppected, and for this reason treatment was started with 300 mg toms is in a third of patients. Confusion is the most frequent of thiamine iv every 8 hours, subsequently continuing with 300 presenting symptom, followed by ataxia and ocular problems.5 mg iv/day of the vitamin for one week, while simultaneously Our patient presented the classic triad, which greatly facilitated reintroducing parenteral nutrition with vitamins and minerals diagnosis.
incorporated. It should be taken into account that since the patient attended on the weekend, it was not possible to carry out Although the most frequent cause in our setting is a Magnetic Resonance Imaging (MRI) scan or any non-urgent
2,16,17 caused by any other medical condition which produces malnuwhich are linked the use of parenteral nutrition to WE. Givtrition.6 This includes prolonged administration of parenteral en that the majority of patients for whom TPN is indicated have nutrition without the correct vitamin supplements, as occurred no other way of acquiring said vitamin, its deficiency is due to in our case.2 While laboratory and image studies can be useful, the lack of supplementation of the same in the parenteral nutri- EW diagnosis is fundamentally clinical and often it is the clinition bag. The recommended dose of thiamine for a healthy adult cal response to treatment that confirms the suspected diagnosis.7 is 1,4 mg per day or 0,5 mg per 1000 kcal consumed. It is calcu- The sensitivity and specificity of laboratory tests in symptomlated that the reserve of thiamine in the body is approximately atic patients is uncertain. There usefulness is questionable due 30 g, from which we can calculate that the symptoms will appear to the fact that a finding of normal thiamine does not exclude after 18-20 days of exogenous non-availability of the vitamin.18 a diagnosis of WE and that in the majority of healthcare centers it is not possible to obtain results immediately, requiring
treatment to be administered empirically on suspicion of the syndrome.8 In this case, confronted with the suspicion of WE In conclusion, we consider the supplementation of and the impossibility of requesting thiamine levels in advance, thiamine and other vitamins in patients with TPN to be an abestablishment of opportune treatment proceeded, obtaining solute necessity. It is important to come to the suspicion of this said levels, which were normal, at a later stage.
syndrome in those patients when they present compatible symptoms, with the objective of establishing treatment with thiamine Imaging studies are also unnecessary in all suspected as soon as possible. Likewise, with thiamine included in a vita- WE patients and the initiation of treatment should not be demin complex, it is common to find other deficiencies which must layed.9 However, imaging diagnosis can be useful in providalso be ruled out.
ing evidence of WE and help eliminate possible alternative diagnoses. CT scan can show small, symmetrical signs of low