As it is well-known, active form thiamine pyrophosphate plays an important role in the pentose phosphate and the tricarboxilic acid cycle which are essential in the metabolism of carbohydrates and lipids. Active form thiamine pyrophosphate also play an important part in energy metabolism such as transketolase, pyruvate dehydrogenase, and alpha ketoglutarate dehydrogenase. Lack of thiamine, the excessive metabolism of brain cell will suffer from cell energy deficit, acidosis and even cellula death[6]. Since the body’s reserve of thiamine is exhausted after nearly 20 days of scant supplementation, thiamine deficiency may happen within as few as 18-20 days in patients receiving severe thiamine-free diets. And the thiamine increases in demand in ill patients.
Wernicke encephalopathy is an universally known neurological complication of thiamine deficiency that mostly occurs in alcoholic persons and is regarded as a rare complication of severe acute pancreatitis. As is presented, doctors will take WE into account when there is the presence of the classical triad of Wernicke encephalopathy including opthalmopathy, ataxia and confusion. However, Wernicke encephalopathy might be underdiagnosed, even misdiagnosed because there usually be non-specific clinical presentation and about 19% of patients have none of the symptoms of the specific triad[7]. There are few case reports in patients with Wernicke encephalopathy who suffer from severe acute pancreatitis and receive a surgery of cholecystectomy and exploratory of biliary tract.
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[8]. From the typical clinical manifestation, Wernicke encephalopathy could be diagnosed primarily[9]. The differential diagnosis between Wernicke encephalopathy and other psychiatric and/or neurological disorders such as pancreatic encephalopathy is extremely significant[10]. Pancreatic encephalopathy is a complication of severe acute pancreatic which manifest as confusion, restlessness, altered mentality, and there are diffuse demyelination and white matter changes in cerebral imaging[11]. Although different pathophysiological mechanisms such as altered hemodynamic, metabolic status, electrolyte and fluid disorders, inflammatory cytokines, and a direct neurotoxic action of phospholipase were put forward, the physiopathology is not completely understood[11]. It is difficult to distinct the difference between Wernicke encephalopathy and pancreatic encephalopathy due to the overlap of neuropsychiatric manifestations, the multiple concomitant clinical and metabolic alterations capable of explaining the neurologic alterations. Regarding the difficulties, some physicians who joined the discussion still insisted on their initial diagnosis of pancreatic encephalopathy and they did not give up their opinions until the condition of the patient was recovered by intravenous by vitamin B1. Therefore, when difficulties in distinguishing between Wernicke encephalopathy and other psychiatric and/or neurological disorders appear, intravenous vitamin B1 could be regarded as a discriminative method or a preemptive treatment.
The more time waste before WE is timely and correctly diagnosed, the more dangerous the patient is. The most valuable method to diagnose Wernicke encephalopathy is brain magnetic resonance imaging, with a high(93%) specificity. However, due to poor sensitivity(53%), it is not reliable enough for a normal magnetic resonance imaging to exclude the disease[12]. The typical magnetic resonance imaging findings of WE include symmetrically increased T2 signal in the thalami, mammillary bodies, tectal plate, and periaqueductal gray matter. And 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[13, 14].
Wernicke’s encephalopathy can emerge in post-operative patients who have prolonged total parenteral nutrition without given enough thiamine supplementation, which make the addition of thiamine indispensable. It is reported that delay in treatment with thiamine before the magnetic resonance imaging findings can lead to progressive and irreversible damage and even death. So early parenteral suplement with thiamine after cholecystectomy and exploratory of biliary tract can quickly reverse symptoms and prevent further injury[15].
In conclusion, human beings may develop Wernicke’s encephalopathy at any age and not rarely in person who suffers from severe acute pancreatitis after cholecystectomy and exploratory of biliary tract. And Wernicke’s encephalopathy should be taken into consideration when patients with prolonged total parenteral nutrition present one or more symptoms of opthalmopathy, ataxia and altered mentality. The most valuable examination for WE is brain magnetic resonance imaging. After cholecystectomy and exploratory of biliary tract, a multivitamin and thiamine should be provided for patients so as to prevent and cure Wernicke’s encephalopathy[16].