Acute Upper Gastrointestinal Bleeding in a Patient With Bipolar II Disorder and Catatonia: A Case Report

A 60-year-old male was diagnosed with bipolar II disorder 30 years before the current visit (Figure 1). During that 30-year period, he was hospitalized four times and received various pharmaceutical treatments. The patient's condition stabilized after the use of Depakin and quetiapine for the previous 7 years. One week before the current visit, the patient was diagnosed with cervical spondylosis, and he began to worry about his physical condition. He gradually developed symptoms such as depressed mood, lack of motivation, and social withdrawal. His condition worsened 1 day before admission, with stupor, mutism, ambitendency, posturing, and sometimes tension, fear, restlessness, systemic sweating, and increased muscle tension. The patient did not pass stool for 5 d. On the basis of the patient's past medical history of bipolar II disorder and current symptoms, he was diagnosed with a major depressive episode combined with catatonia. After admission, he received escitalopram 10 mg qd and quetiapine fumarate 0.4 g qn. Moreover, a glycerin suppository was administered to assist with bowel movements, and the color of the stool was normal. At the time of admission, the hemoglobin level was 171 g/L, and the red blood cell count was 5.05 × 1012/L. After no contraindications were identified, modified electroconvulsive therapy (MECT) was started on the 3rd day after admission. After two rounds of MECT, the patient developed a fever. The white blood cell count was 13.19 × 109/L, and the hemoglobin level was 128 g/L. Thus, the MECT was stopped. The symptoms of tension, excitement, and agitation did not significantly resolve. After a glycerin suppository was administered again, the patient passed a large amount of dark-brown loose stool. An emergency blood test revealed that the hemoglobin level was 116 g/L and that the patient's stool was positive for occult blood (OB). After the gastroenterology consultation, acute upper GIB was considered. The doctor told the patient to refrain from drinking and eating immediately and used medications to treat gastrointestinal bleeding. However, the hemoglobin level continued to decrease over the next 2 d, with levels of 109 g/L and 99 g/L, respectively. Emergency gastroscopy revealed multiple bulbous ulcers in the duodenum (2 ulcers approximately 0.8–1.5 cm in size at the anterior wall near the pyloric opening and surrounding mucosal edema). The endoscopic diagnosis was multiple bulbous ulcers in the duodenum (Stage A1, Forrest Stage III). After endoscopic titanium clip hemostasis, the patient's hemoglobin level gradually increased. A routine blood test was conducted three times within 7 days, and the hemoglobin levels were 108 g/L, 112 g/L, and 109 g/L, respectively. The relative stabilization of the hemoglobin level indicated that there was no active bleeding. After 15 days, follow-up gastroscopy revealed that the mucosa was congested and swollen, but no active bleeding was detected (Figure 2). During this period, escitalopram treatment was stopped, and treatment was switched to milnacipran 25 mg bid. The dose of milnacipran was gradually increased to 75 mg/d, and the dose of quetiapine was increased to 0.6 g. The patient's tension symptoms disappeared, and his mood improved. He was asked again about his medical history, and he still denied any previous history of gastrointestinal diseases or symptoms. However, test results were positive for HP IgG antibody and for HP congenital infection protein. Given the depression, tension, and upper gastrointestinal bleeding of the patient, anti-HP treatment has not yet been administered. The patient was discharged after 27 days of hospitalization with no gastrointestinal or physical discomfort; his hemoglobin level was 109 g/L, and the color of his stool was brown. After discharge from the hospital, the patient continued to take ilaprazole enteric-coated tablets and chewable aluminum carbonate tablets for acid suppression and gastric mucosal protection, respectively. He also took milnacipran and quetiapine for emotional stability. Eight months after discharge, the patient was emotionally stable and in a good mental state, and he had no gastrointestinal discomfort. Routine blood tests revealed that the hemoglobin level was 139 g/L, and the red blood cell count was 4.32 × 1012/L, both of which are within normal limits. When patients with BD develop catatonia, sudden shifts in the autonomic nervous system and catecholamine metabolism occur. In addition, patients with catatonia have adrenal–sympathetic nerve impulses similar to the stress response, manifested as autonomic instability, with sympathetic nerve activation as the main manifestation [1]. Catatonia can lead to stress, which can cause excessive activity of the sympathetic nervous system, increasing the levels of several catecholamine metabolites, especially epinephrine and norepinephrine. These changes cause patients to develop symptoms such as tachycardia, fever, increased blood pressure, and sweating [1]. Sympathetic nerve excitation can increase catecholamine metabolites, which can lead to reduced blood flow perfusion of splanchnic nerves and mucosal membranes and, in turn, reduced bicarbonate secretion, reduced mucosal blood flow, weakened gastrointestinal motility, and acid back-diffusion, thus leading to stress ulcers [2]. However, few reports of acute stress ulcers as complications of catatonia exist. This patient had a 30-year history of BD and had no catatonic features in previous attacks. However, this time, the patient was hospitalized due to a major depressive episode with catatonic features. He had no previous history of gastrointestinal diseases or gastrointestinal symptoms except for HP infection. His routine blood test at admission revealed a normal hemoglobin level. During hospitalization, black stools and a progressive decrease in the hemoglobin level developed. Gastroscopy revealed multiple bulbous ulcers in the duodenum (2 ulcers approximately 0.8–1.5 cm in size on the anterior wall near the pyloric opening), combined with upper GIB. After the bleeding stopped following the use of the titanium clip under the endoscope, the patient's hemoglobin level gradually increased to a normal level. The patient had no history of peptic ulcers or gastrointestinal bleeding. During severe depressive episodes combined with catatonia, acute duodenal ulcers developed in the patient, which led to acute massive GIB. One cohort study revealed that patients with BD have a greater probability of subsequently developing peptic ulcers, and the underlying mechanism may involve the hypothalamus–pituitary–adrenal (HPA) axis disorders and glucocorticoid resistance. Patients with BD have hippocampal damage and HPA axis disorders caused by disinhibition [3]. In addition, BD is also associated with chronic neuroinflammation, which can induce glucocorticoid resistance under chronic conditions, and under chronic stress, glucocorticoids cause damage to the gastric mucosa [3]. Therefore, BD itself may increase the risk of peptic ulcers, but in these studies, peptic ulcers were not classified into chronic peptic ulcers and acute stress ulcers. This patient received two rounds of MECT before the development of acute upper GIB. However, in the past 60 years, there have been no case reports of peptic ulcers combined with bleeding caused by ECT. Currently, serious adverse events associated with ECT are rare, and stress ulcers and acute GIB have not been reported as complications of ECT. In addition, the patient had been taking drugs such as Depakin, quetiapine, and escitalopram for a long period of time. Depakin may cause thrombocytopenia and eventually cause bleeding. Escitalopram has antiplatelet effects [4]. However, the patient's routine blood test results several times after admission to the hospital revealed that the PLT count was within the normal range. Therefore, the possibility of bleeding caused by drug-induced thrombocytopenia was excluded. After the patient's acute massive upper GIB resolved, the test result for HP antibody was positive. A detailed medical history was obtained. The patient did not have any history of digestive tract diseases or gastrointestinal symptoms before admission, and the hemoglobin and red blood cell levels were within the normal range at the time of admission. Therefore, the possibility of peptic ulcers and acute or chronic GIB existing before admission was excluded. HP infection is the leading cause of peptic ulcers; HP infection mainly leads to the development of peptic ulcers by promoting gastric acid secretion and destroying the mucosal barrier [2]. Depression-associated stress may activate the release of some proinflammatory cytokines, and these proinflammatory cytokines may activate HP, thereby triggering the development of ulcers [5]. In summary, a long-term history of BD increases the probability of peptic ulcer development. When BD occurs in combination with catatonia, acute stress peptic ulcers and complicated GIB can occur. These factors may trigger the body's stress response during catatonia, especially when people are infected with HP, which increases the likelihood of ulcers. The authors would like to thank the patient for his consent to the presentation of this case report. The informed consent is available from the patient for the illustrations/images. The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.