It is well-known that the active form of thiamine pyrophosphate plays an important role in the pentose phosphate pathway and the tricarboxylic acid cycle, which are essential in the metabolism of carbohydrates and lipids. The active form of thiamine pyrophosphate also plays an important role in energy metabolism as a cofactor for enzymes such as transketolase, pyruvate dehydrogenase, and alpha ketoglutarate dehydrogenase. Lacking thiamine, the excessive metabolism of brain cells will suffer from cell energy deficit, acidosis and even cellular death[6]. Vitamin B1 deficiency can lead to WE because it disturbs glucose metabolism of the brain, which results in lactic acid accumulation and acidosis and hinders the production, release and reuptake of neurotransmitters. The consumption of vitamin B1 also increases with the supplementation of glucose[7]. Since the body’s reserve of thiamine is exhausted after nearly 20 days of scant supplementation, thiamine deficiency may occur within as few as 18-20 days in patients receiving severe thiamine-free diets. In our case, the patient was given total parenteral nutrition and a large quantity of glucose to promote post-operative rehabilitation. Hypermetabolism, nutrition without vitamin B1 and the acceleration of vitamin B1 consumption by glucose eventually leads to WE.
Wernicke encephalopathy is a universally known neurological complication of thiamine deficiency that mostly occurs in alcoholic persons and is regarded as a rare complication of severe acute pancreatitis. The diagnostic criteria of WE proposed by the 2010 European Union of Neuroscience Association includes (1) dietary deficiencies; (2) ophthalmopathy; (3) cerebellar dysfunction; and (4) either an altered mental state or mild memory impairment. We can diagnose WE clinically when patients exhibit at least two of the four elements[7]. As it is presented, doctors will take WE into account when the patient presents with the classic triad of Wernicke’s encephalopathy, including ophthalmopathy, ataxia and confusion. However, Wernicke’s encephalopathy might be underdiagnosed and even misdiagnosed because there is often non-specific clinical presentation and because approximately 19% of patients have none of the symptoms of the specific triad[8]. There are few case reports in patients with Wernicke’s encephalopathy who suffered from severe acute pancreatitis and received cholecystectomy and exploratory biliary tract surgery.
In our case report, the patient did not manifest the complete triad, and the most obvious symptoms and signs were mental status changes. The systematic clues to this disease are anorexia, confusion, blindness, amyasthexia, nystagmus, irritability and recurring vomiting episodes[9]. From the typical clinical manifestation, Wernicke’s encephalopathy could be diagnosed[10]. The patient has a long history of dietary deficiency and showed mental status changes. Serum thiamine B1 was lower than normal, his brain MRI supported WE, and his condition recovered after vitamin supplementation. WE was eventually definitively diagnosed. The differential diagnosis between Wernicke’s encephalopathy in a patient with severe acute pancreatitis after cholecystectomy and exploratory biliary tract surgery and other psychiatric and/or neurological disorders includes pancreatic encephalopathy, hepatic encephalopathy, septic encephalopathy, and cerebral vascular accidents. Pancreatic encephalopathy is a complication of severe acute pancreatitis that manifests as confusion, restlessness, and altered mentality, and there is evidence of diffuse demyelination and white matter changes in cerebral imaging[12]. Sometimes, it is difficult to distinguish the difference between Wernicke’s encephalopathy and other encephalopathies due to the overlap of neuropsychiatric manifestations and to the multiple concomitant clinical and metabolic alterations capable of explaining the neurologic alterations. Regarding these difficulties, some physicians who joined the discussion still insisted on their initial diagnosis of the other encephalopathies, and they did not give up their opinions until the condition of the patient was recovered by intravenous vitamin B1. Therefore, when difficulties in distinguishing between Wernicke’s encephalopathy and other psychiatric and/or neurological disorders appear, intravenous vitamin B1 could be regarded as a discriminative method or a pre-emptive treatment.
According to some sensitive clinical signs related to a patient, combined with serum thiamine levels and brain images, WE would be more likely to be diagnosed[13]. The most valuable method used to diagnose Wernicke’s encephalopathy is brain magnetic resonance imaging, with a high (93%) specificity. However, due to poor sensitivity (53%), it is not reliable enough for normal magnetic resonance imaging to exclude the disease[14]. The typical magnetic resonance imaging findings of WE include symmetrically increased T2 signals in the thalami, mammillary bodies, tectal plate, and periaqueductal grey matter. Other changes could also be seen in MRI, such as abnormal signal-intensity in the cerebellum, the cerebellar vermis, the cranial nerve nuclei, the dentate nuclei, the red nuclei, the caudate nuclei, the corpus callosum, and the cerebral cortex[15, 16].
Wernicke’s encephalopathy can emerge in post-operative patients who have prolonged total parenteral nutrition without sufficient thiamine supplementation, which makes the addition of thiamine indispensable. It is reported that a delay in treatment with thiamine before the magnetic resonance imaging findings can lead to progressive and irreversible damage and even death. Thus, early parenteral supplementation with thiamine after cholecystectomy and exploratory biliary tract surgery can quickly reverse symptoms and prevent further injury[17].
In conclusion, human beings may develop Wernicke’s encephalopathy at any age, and persons who suffers from severe acute pancreatitis after cholecystectomy and exploratory biliary tract surgery may be at higher risk. Wernicke’s encephalopathy should be taken into consideration when patients with prolonged total parenteral nutrition present one or more symptoms of ophthalmopathy, ataxia and altered mentality. The most valuable examination for WE is brain magnetic resonance imaging. After cholecystectomy and exploratory biliary tract surgery, a multivitamin and thiamine regimen should be provided for patients to prevent and treat Wernicke’s encephalopathy[7].