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Introduction: Acute gastric dilatation (AGD) is a massive distension of the stomach caused by the accumulation of gas, gastric secretions, or food material. AGD is a radiological diagnosis with no clear etiopathogenesis and is often misdiagnosed owing to a lack of clear diagnostic criteria and physician awareness. Case Presentation: In this case series, we describe the clinical presentations and outcomes of 4 patients with AGD. Three (75%) of the patients were female, and one (25%) was male. The patients’ ages ranged from 53 to 84 years, with an average age of 73.5 years. Abdominal pain, nausea, and vomiting were the most frequently reported complaints. Two (50%) patients had cancer, one (25%) had an acquired duodenal stenosis, and the fourth patient experienced an ileus. Conclusion: AGD is a surgical emergency with a 50–100% mortality rate; thus, prompt diagnosis and management are crucial. Herein, we describe a case series of AGDs that were diagnosed and managed at our institution. We aim to raise awareness about this fatal yet underrecognized clinical entity. [ABSTRACT FROM AUTHOR]

Introduction: Acute gastric dilatation (AGD) is a massive distension of the stomach caused by the accumulation of gas, gastric secretions, or food material. AGD is a radiological diagnosis with no clear etiopathogenesis and is often misdiagnosed owing to a lack of clear diagnostic criteria and physician awareness. Case Presentation: In this case series, we describe the clinical presentations and outcomes of 4 patients with AGD. Three (75%) of the patients were female, and one (25%) was male. The patients’ ages ranged from 53 to 84 years, with an average age of 73.5 years. Abdominal pain, nausea, and vomiting were the most frequently reported complaints. Two (50%) patients had cancer, one (25%) had an acquired duodenal stenosis, and the fourth patient experienced an ileus. Conclusion: AGD is a surgical emergency with a 50–100% mortality rate; thus, prompt diagnosis and management are crucial. Herein, we describe a case series of AGDs that were diagnosed and managed at our institution. We aim to raise awareness about this fatal yet underrecognized clinical entity.

Superior mesenteric artery (SMA) syndrome is a rare cause of proximal bowel obstruction due to duodenal compression by the SMA. The morbidity and mortality associated with delayed diagnosis and its complications make it an important differential cause for bowel obstruction. We report a case of mega-stomach secondary to SMA syndrome requiring total gastrectomy. An 18-year-old male presented with vomiting, abdominal pain and shock after a buffet. Computed tomography (CT) imaging revealed a grossly distended stomach (113 × 187 × 350mm) and a transition point at the third part of the duodenum, along with pneumatosis and portal venous gas. Emergency gastroscopy showed blood and necrotic mucosa. Laparotomy confirmed full thickness necrosis and the patient underwent a total gastrectomy with Roux-en-Y reconstruction. Postoperatively, he had a brief intensive care stay and recovered without complications. This case underscores the importance of considering SMA syndrome during presentations of acute gastric dilatation. [ABSTRACT FROM AUTHOR]

Abstract Background Herpes zoster is a common disease that can affect men and women at any age. Sensory neuropathy is the most common complication while motor neuropathy of the abdominal muscles is rare complication appearing in ~ 0.7% of patients. Furthermore, visceral nerve involvement causing gastroparesis is an extremely rare postherpetic complication. We present an extremely rare case of acute gastric dilatation with segmented abdominal paresis as a rare manifestation of herpes zoster infection. Case presentation A 91-year-old Asian man was admitted to hospital with 2-day history of vomiting and left abdominal protrusion. He was previously treated for a rash on the left abdominal wall as herpes zoster infection with oral valaciclovir 2 weeks prior. On physical examination, characteristic herpes zoster rash scars and an ipsilateral abdominal bulge were observed on the left side. Computed tomography revealed no abdominal wall defect, mass, or stenosis. Remarkable distension of the stomach, asymmetrical left flank wall bulge, and a thinner abdominal wall on the left compared with the right side were shown. He was diagnosed as acute gastric dilatation owing to gastroparesis and segmental paresis of the abdominal musculature associated with herpes zoster infection. The patient showed significant improvement in symptoms and abdominal paresis within a month of conservative treatment, including nasogastric tube decompression and mosapride administration. Conclusion Acute gastric dilatation with abdominal paresis is an extremely rare complication of herpes zoster infection, and to date there have been no reports in the literature. It alerts us that, when examining patients with abdominal bulge, we should be conscious of this rare pathology for the optical diagnosis, avoiding unnecessary invasive examination or surgical exploration.

Background: Herpes zoster is a common disease that can affect men and women at any age. Sensory neuropathy is the most common complication while motor neuropathy of the abdominal muscles is rare complication appearing in ~ 0.7% of patients. Furthermore, visceral nerve involvement causing gastroparesis is an extremely rare postherpetic complication. We present an extremely rare case of acute gastric dilatation with segmented abdominal paresis as a rare manifestation of herpes zoster infection. Case presentation: A 91-year-old Asian man was admitted to hospital with 2-day history of vomiting and left abdominal protrusion. He was previously treated for a rash on the left abdominal wall as herpes zoster infection with oral valaciclovir 2 weeks prior. On physical examination, characteristic herpes zoster rash scars and an ipsilateral abdominal bulge were observed on the left side. Computed tomography revealed no abdominal wall defect, mass, or stenosis. Remarkable distension of the stomach, asymmetrical left flank wall bulge, and a thinner abdominal wall on the left compared with the right side were shown. He was diagnosed as acute gastric dilatation owing to gastroparesis and segmental paresis of the abdominal musculature associated with herpes zoster infection. The patient showed significant improvement in symptoms and abdominal paresis within a month of conservative treatment, including nasogastric tube decompression and mosapride administration. Conclusion: Acute gastric dilatation with abdominal paresis is an extremely rare complication of herpes zoster infection, and to date there have been no reports in the literature. It alerts us that, when examining patients with abdominal bulge, we should be conscious of this rare pathology for the optical diagnosis, avoiding unnecessary invasive examination or surgical exploration. [ABSTRACT FROM AUTHOR]

Abstract Background Acute gastric dilatation can develop in patients with anorexia nervosa who are being refed to achieve weight restoration. If unrecognized, this condition is associated with significant morbidity and mortality. Patients with acute gastric dilatation usually have abdominal pain, nausea, and vomiting. Abdominal imaging confirms the diagnosis. This study aims to identify risk factors associated with the development of acute gastric dilatation in patients with severe restrictive eating disorders in order to hasten diagnosis and guide treatment. This study also aims to define the clinical outcomes of patients with acute gastric dilatation. Methods In this retrospective case series, 15 patients with a restrictive eating disorder were studied. Multiple variables were assessed for significant correlation with stomach size. Results 15 patients with a restrictive eating disorder were identified as being diagnosed with acute gastric dilatation through chart review during the study period. The average dilated stomach size was 20.5 cm. There was no significant correlation of stomach size with any of the following: % ideal body weight on day of admission, % ideal body weight on day of imaging study, rate of weight gain (kg per week), or duration of illness. Serum levels of sodium, potassium, phosphorus, magnesium, calcium, bicarbonate, blood urea nitrogen, glucose, albumin, and hematocrit on the day of imaging, did not correlate with stomach size. All patients were treated with conservative management. None of the patients required surgical intervention or progressed to gastric necrosis or perforation, and there were no recurrences of the acute gastric dilatation. Conclusions There are no specific risk factors significantly associated with the development of acute gastric dilatation in patients with severe restrictive eating disorders. Clinicians should maintain a high index of suspicion for this condition when patients are experiencing abdominal pain, nausea, or vomiting. When promptly diagnosed and treated, outcomes are good. If diagnosis is delayed, the outcome can be dire.

Background: Acute gastric dilatation can develop in patients with anorexia nervosa who are being refed to achieve weight restoration. If unrecognized, this condition is associated with significant morbidity and mortality. Patients with acute gastric dilatation usually have abdominal pain, nausea, and vomiting. Abdominal imaging confirms the diagnosis. This study aims to identify risk factors associated with the development of acute gastric dilatation in patients with severe restrictive eating disorders in order to hasten diagnosis and guide treatment. This study also aims to define the clinical outcomes of patients with acute gastric dilatation. Methods: In this retrospective case series, 15 patients with a restrictive eating disorder were studied. Multiple variables were assessed for significant correlation with stomach size. Results: 15 patients with a restrictive eating disorder were identified as being diagnosed with acute gastric dilatation through chart review during the study period. The average dilated stomach size was 20.5 cm. There was no significant correlation of stomach size with any of the following: % ideal body weight on day of admission, % ideal body weight on day of imaging study, rate of weight gain (kg per week), or duration of illness. Serum levels of sodium, potassium, phosphorus, magnesium, calcium, bicarbonate, blood urea nitrogen, glucose, albumin, and hematocrit on the day of imaging, did not correlate with stomach size. All patients were treated with conservative management. None of the patients required surgical intervention or progressed to gastric necrosis or perforation, and there were no recurrences of the acute gastric dilatation. Conclusions: There are no specific risk factors significantly associated with the development of acute gastric dilatation in patients with severe restrictive eating disorders. Clinicians should maintain a high index of suspicion for this condition when patients are experiencing abdominal pain, nausea, or vomiting. When promptly diagnosed and treated, outcomes are good. If diagnosis is delayed, the outcome can be dire. Plain English summary: The mainstay of treatment of patients with severe restrictive eating disorders is initiation of nutrition to gain weight. One potential complication when patients are started on nutrition is the development of a massively enlarged stomach, also called acute gastric dilatation. If a patient's care provider does not recognize the development of acute gastric dilatation, it can lead to serious problems, including death. Patients with this condition usually have abdominal pain, nausea, and vomiting. These are common symptoms in patients with anorexia nervosa and are often dismissed. Identifying risk factors associated with developing acute gastric dilatation could help providers recognize this condition and promptly start treatment. This study sought to identify risk factors associated with developing acute gastric dilatation in patients with severe restrictive eating disorders. Several variables, including patient age, duration of illness, body mass index, %ideal body weight, laboratory values, medications, type of nutrition, and rate of weight gain were analyzed. This study found that there are no specific risk factors significantly associated with development of acute gastric dilatation in patients with severe restrictive eating disorders being initiated on nutrition. Therefore, providers need to listen to their patients, evaluate symptoms, and have a high index of suspicion for underlying acute gastric dilatation. [ABSTRACT FROM AUTHOR]

Hepatic portal vein gas (HPVG) is caused by the influx of gastrointestinal gas into the intrahepatic portal vein as a result of gastrointestinal wall fragility due to ischemia or necrosis. Gastrointestinal tract necrosis is fatal in severe cases. We observed a case of food intake-induced acute gastric dilatation (AGD) in a healthy young male who developed HPVG and underwent conservative treatment. A 25-year-old male presented to our hospital with epigastric pain and nausea the day after excessive food intake. Computed tomography (CT) revealed gas along the intrahepatic portal vein and marked gastric dilatation with large food residue. AGD-induced HPVG was considered. Esophagogastroduodenoscopy (EGD) was not performed at this stage because of the risk of HPVG and AGD exacerbation, and the patient was followed up with intragastric decompression via a nasogastric tube. Food residue and approximately 2 L of liquid without blood were vomited 1 h after the nasogastric tube placement. His symptoms improved after the vomiting episode. An EGD was performed 2 days after undergoing CT. Endoscopic findings revealed extensive erosions and the presence of a whitish coat extending from the fornix to the lower body of the stomach, indicating AGD. HPVG disappeared on the CT scan taken during EGD. Thereafter, symptom relapse and HPVG recurrence were not observed. [ABSTRACT FROM AUTHOR]

Introduction: We present a case of acute massive gastric dilatation in a 16-year-old patient with previous gastric fundoplication, who developed unusual multiple organ sequelae which have seldom been described in this context. Case presentation: The patient presented with acute massive gastric dilatation, and subsequently developed acute pancreatitis, superior mesenteric artery syndrome, the nutcracker phenomenon, and after resolution developed acute bowel obstruction. He had adhesiolysis and gradually returned to baseline with prokinetics and dietary interventions. Conclusion: We discuss the sequence of events as they unfolded and a presumed mechanism for this unusual course. This case demonstrates several sequelae of an acute massive gastric dilatation as a late complication of fundoplication, which physicians should keep in mind when treating such patients.

Abstract We present a case of a 55‐year‐old woman complaining of abdominal distension owing to acute gastric dilatation. Her localized skin mottling had spread from the lower abdomen to both knees. The skin mottling in the area affected by gastric dilatation improved immediately after stomach emptying using a gastric tube and upper endoscopy.

Gastric volvulus leading to acute gastric dilatation is a surgical emergency that should be considered as a differential in patients who present to the emergency department with severe epigastric pain and evidence of gastric outlet obstruction. This condition requires a high index of suspicion that enables early diagnosis and treatment. [ABSTRACT FROM AUTHOR]

Acute gastric dilatation (AGD) is a rare but potentially life-threatening condition, commonly associated with mechanical obstructions or systemic conditions such as diabetes and eating disorders. This report describes a 46-year-old man who was brought to the emergency department with frequent vomiting as his chief complaint. He was a habitual heavy drinker and had consumed a large amount of alcohol the night before his admission. He had a previous hospitalization for AGD triggered by excessive alcohol intake a year earlier. Abdominal computed tomography (CT) revealed gastric distension, and his symptoms improved following nasogastric decompression. No significant abnormalities were found during an upper gastrointestinal endoscopy performed after his admission. He was discharged on the fifth day without any complications. This case represents a rare instance of acute gastric dilatation triggered by excessive alcohol consumption. AGD induced by alcohol presents unique clinical challenges compared to typical cases caused by overeating. Specifically, frequent vomiting following heavy alcohol intake can lead clinicians to consider diagnoses such as acute alcohol intoxication or alcoholic ketoacidosis, which may divert attention from the potential for concurrent AGD. This case underscores the importance of considering AGD in the differential diagnosis for patients presenting with frequent vomiting after excessive drinking, illustrating the critical need for careful evaluation to avoid misdiagnosis., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Zokumasu et al.)

Abstract Gastric volvulus leading to acute gastric dilatation is a surgical emergency that should be considered as a differential in patients who present to the emergency department with severe epigastric pain and evidence of gastric outlet obstruction. This condition requires a high index of suspicion that enables early diagnosis and treatment.

Abstract Background Acute gastric dilatation (AGD) leading to gastric necrosis and perforation has been reported to be a rare but fatal complication in young patients with eating disorders, particularly anorexia nervosa. Case presentation We report a case of a Canadian female patient presenting with mild abdominal pain, with a history of anorexia nervosa, the binge/purge subtype, who was found to have severe acute gastric dilatation on subsequent computed tomography imaging. Her clinical course was uncomplicated after gastric decompression. The cause of her AGD was thought to be secondary to dysmotility disorder caused by her anorexia nervosa. Conclusion Our case report demonstrates the importance of clinical identification of AGD and subsequent diagnosis and management. Because of the urgency to rule out obstruction or perforation through consultation or additional imaging modalities, recognition and correct diagnosis of this condition is necessary for appropriate patient management. In addition, our case report adds to an underreported but important complication of anorexia nervosa.

Acute gastric dilatation is the radiological finding of a massively enlarged stomach as seen on plain film X-ray or a computerized tomography scan of the abdomen. It is a rare entity with high mortality if not treated promptly and is often not reported due to a lack of physician awareness. It can occur due to both mechanical obstruction of the gastric outflow tract, or due to nonmechanical causes, such as eating disorders and gastroparesis. Acute hyperglycemia without diagnosed gastroparesis, such as in patients with diabetic ketoacidosis, may also predispose to acute gastric dilatation. Prompt placement of a nasogastric tube can help deter its serious complications of gastric emphysema, ischemia, and/or perforation. We present our experience of 2 patients who presented with severe hyperglycemia and were found to have acute gastric dilation on imaging. Only one of the patients was treated with nasogastric tube placement for decompression and eventually made a full recovery.

We present a case of a 55‐year‐old woman complaining of abdominal distension owing to acute gastric dilatation. Her localized skin mottling had spread from the lower abdomen to both knees. The skin mottling in the area affected by gastric dilatation improved immediately after stomach emptying using a gastric tube and upper endoscopy. [ABSTRACT FROM AUTHOR]

Acute gastric dilatation is the radiological finding of a massively enlarged stomach as seen on plain film X-ray or a computerized tomography scan of the abdomen. It is a rare entity with high mortality if not treated promptly and is often not reported due to a lack of physician awareness. It can occur due to both mechanical obstruction of the gastric outflow tract, or due to nonmechanical causes, such as eating disorders and gastroparesis. Acute hyperglycemia without diagnosed gastroparesis, such as in patients with diabetic ketoacidosis, may also predispose to acute gastric dilatation. Prompt placement of a nasogastric tube can help deter its serious complications of gastric emphysema, ischemia, and/or perforation. We present our experience of 2 patients who presented with severe hyperglycemia and were found to have acute gastric dilation on imaging. Only one of the patients was treated with nasogastric tube placement for decompression and eventually made a full recovery. [ABSTRACT FROM AUTHOR]

• Ischemic gastric necrosis could be provoked by acute gastric dilatation. • Early diagnosis is crucial to increase survival from fundic gastric necrosis. • Conservative treatments should be considered as first-line management. • Surgical treatment is advised when massive gastric necrosis is encountered. Gastric fundus ischemia is a rare event, which does not account for many significant clinical studies. This disorder could have different etiologies, but authors agree that a prompt diagnosis and a proper treatment could avoid dangerous complications and ultimately the death of the patient. We herein report an interesting idiopathic case of acute gastric dilatation and fundus ischemia of an 83-year-old Caucasic woman who was admitted to the Emergency Department complaining of abdominal discomfort, vomiting and constipation. In literature, only a few case reports about this condition are reported. Possible risk factors, etiologies, and the different therapeutic options available for this condition are examined, in order to try to favor clinicians to formulate a timely diagnosis and provide patients with rapid healthcare services. Further investigations are still needed to analyze the pathophysiological pathways responsible of gastric fundus ischemia and to provide a definitive treatment to this dangerous disorder. [ABSTRACT FROM AUTHOR]

Highlights • A man developed gastric necrosis secondary to acute gastric dilatation. • He was seen at 3 different hospitals and discharged home. • Early diagnosis and prompt treatment are required for treatment. Abstract We report a case of sudden death in a patient who developed extensive gastric necrosis secondary to acute gastric dilatation. A 36-year-old man with mental retardation (but without difficulties in activities of daily living), developed an illness after a meal out with friends, necessitating 3 hospital visits. He returned home after receiving drug therapy; however, his condition deteriorated, and he was transferred to our hospital via ambulance. Whole-body computed tomography performed upon admission revealed gastric dilatation. A stomach tube was inserted, and 2000 mL of gastric aspirate was obtained. The patient died approximately 5 h later despite receiving treatment. Autopsy revealed 1000 mL of gastric contents and extensive gastric necrosis. He was diagnosed with extensive gastric necrosis secondary to acute gastric dilatation. [ABSTRACT FROM AUTHOR]

Pneumoperitoneum caused by acute gastric dilatation (AGD) is a very rare complication. We report a case of pneumoperitoneum and acute pulmonary edema caused by AGD in a patient with Parkinson’s disease. A 78-year-old woman presented with pneumonia and AGD. We inserted a nasogastric tube and administered empirical antibiotics. We performed an endoscopy, and perforation or necrosis of the stomach and pyloric stenosis were not observed. Thirty-six hours after admission, the patient suddenly developed dyspnea and shock, and eventually died. We suspected the cause of death was pneumoperitoneum and acute pulmonary edema caused by AGD during the conservative treatment period. Immunocompromised patients with chronic illness require close observation even if they do not show any symptoms suggestive of complications. Even if the initial endoscopic or abdominal radiologic findings do not show gastric necrosis or perforation, follow-up with endoscopy is essential to recognize complications of AGD early.

We present a case of acute massive gastric dilatation in a 16-year-old patient with previous gastric fundoplication, who developed unusual multiple organ sequelae which have seldom been described in this context. The patient presented with acute massive gastric dilatation, and subsequently developed acute pancreatitis, superior mesenteric artery syndrome, the nutcracker phenomenon, and after resolution developed acute bowel obstruction. He had adhesiolysis and gradually returned to baseline with prokinetics and dietary interventions. We discuss the sequence of events as they unfolded and a presumed mechanism for this unusual course. This case demonstrates several sequelae of an acute massive gastric dilatation as a late complication of fundoplication, which physicians should keep in mind when treating such patients. [ABSTRACT FROM AUTHOR]

Acute gastric dilatation is a rare surgical condition in children, which often results from blunt abdominal trauma. This condition is characterized by the gut-brain connection disorder or gastric muscular layer damage, which results in atony. Gradual gastric stretching with fluid contents and gases in the end leads to the development of various types of intestinal obstruction. When conservative measures are not sufficient (in rare cases), it is reasonable to resort to operative intervention. Several cases of such a pathology have been published around the world. This condition has been observed not only at the blunt abdominal trauma, but also at lesions of central and peripheral nervous systems and in patients with anorexia nervosa and bulimia in the event of excessive food consumption. The article presents a clinical case study and a follow-up analysis of a child with posttraumatic acute gastric dilatation. The authors describe clinical manifestations, pathogenesis and diagnostic algorithm, which allowed establishing this rare diagnosis. Along with the conventional drugs and intensive care measures, the treatment involved a complex of mini-invasive endosurgical and endoscopic manipulations, including laparoscopic jejunostomy, which was performed in order to provide long-term enteral feeding. The clinical case study demonstrated that the use of diagnostic laparoscopy helps to establish nature of the gastric damage correctly and formulate the following optimal treatment tactics on the basis of the obtained data.

Objetivos: Mostrar mediante un caso clínico, la repercusión sistémica y las complicaciones orgánicas, que pueden darse tras una dilatación gástrica aguda, ocasionada por un atracón bulímico. Caso clínico: Mujer joven, diagnosticada de bulimia nerviosa, acude a urgencias tras un atracón. A su llegada, presenta gran distensión abdominal y refiere dificultad para provocarse el vómito. Con el paso de unas horas, comienza a presentar signos de inestabilidad hemodinámica y oliguria. Se realiza un TC urgente, en el que se aprecian infartos renales bilaterales por compresión de la aorta abdominal y algunas de sus ramas viscerales. Intervenciones: El proceso de evaluación incluyó la medida del volumen gástrico mediante TC. Se realizó una gastrostomía de descarga, que permitió la evacuación de gran contenido alimenticio y la restauración de la vascularización intraabdominal, que mejoró la perfusión renal. Conclusiones: El TC es una herramienta diagnóstica fundamental que, no sólo permite cuantificar la dilatación gástrica aguda, sino que también permite valorar la integridad de los órganos adyacentes que pudieran estar sufriendo hipoperfusión por compresión.Objectives: To demonstrate through a clinical case the systemic effetcss and complications that can arise after an acute gastric dilatation caused by an eating binge. Clinical case: A young woman diagnosed of bulimia nervosa presents to the emergency room after a massive food intake. She shows important abdominal distention and refers inability to self-induce vomit. A few hours later she commences to show signs of hemodynamic instability and oliguria. A CT scan is performed; it shows bilateral renal infarctions due to compression of the abdominal aorta and some of its visceral branches. Interventions: The evaluation procedures included quantification of the gastric volume by CT. A decompression gastrostomy was performed; it allowed the evacuation of a large amount of gastric content and restored blood supply to the abdomen, which improved renal perfusion. Conclusions: CT is a basic diagnostic tool that not only allows us to quantify the degree of acute gastric dilatation but can also evaluate the integrity of the adjacent organs which may be suffering compression hypoperfusion.

ABSTRACT Objective Medical problems that arise due to severe restricting and/or purging may be misdiagnosed or suboptimally treated, from outpatient clinics to top medical hospitals. A symptom may be presumed to be a psychological manifestation of the eating disorder and inappropriately dismissed for further medical evaluation. Alternatively, a detailed medical workup may be performed, overlooking a classic relationship between starvation and a physical finding, which delays referral to eating disorder care. This review article focuses on rare medical issues (also called 'zebras' in medical training), diagnoses that may be missed in patients with eating disorders, and best practices for management, organized by organ system. Method A PubMed search was performed, using search terms 'eating disorder,' 'anorexia nervosa,' and 'bulimia nervosa' in combination with different words for each organ system and known medical manifestations of severe eating disorders, with high quality and relevant studies from the past 20 years cited. Discussion Adults with eating disorders may present with extreme organ dysfunction and atypical signs and symptoms of typical medical problems. Timely diagnosis, risk awareness, appropriate treatment, and avoidance of harm are all vital. With judicious management and nutritional rehabilitation, most of these complications will significantly improve or resolve. © 2015 Wiley Periodicals, Inc. (Int J Eat Disord 2016; 49:331-344). [ABSTRACT FROM AUTHOR]

Acute gastric dilatation is a rare complication of anorexia nervosa binge/purge subtype that results from gastrointestinal abnormalities, including decreased gastric motility and delayed gastric emptying. Early diagnosis and intervention is critical since delay may result in gastric necrosis, perforation, shock, and death. We report a 26-year-old female with anorexia nervosa binge/purge subtype, who presented with abdominal pain and nausea after a binge episode. Abdominal radiography and computed tomography showed a grossly dilated stomach measuring 32 cm Χ 17.9 cm consistent with acute gastric dilatation. She underwent exploratory laparotomy with gastrotomy and gastric decompression, and recovered uneventfully. Initially, the patient denied the binge episode, as many patients with eating disorders do, but later revealed an extensive history of anorexia nervosa binge/purge subtype. This case stresses the importance of obtaining a thorough history of eating disorders and maintaining a high index of suspicion for acute gastric dilatation in young women who present with abdominal pain and distention.

Acute gastric dilatation is a low-incidence nosologic entity, and potencially fatal due to high risk of gastric perforation. Its mortality is reported from 80 to 90%. It has been described with higher frecuency in women suffering from nutritional diseases such as anorexia nervosa, bulimia and psychogenic polyfagia, however, by means of a meticulous search, we can find a large number of case reports about diseases associated to acute gastric dilatation. This fact causes its physiopathology to be non-clear, but allows to identify risk factors and to create a therapeutic algorithm. Throughout this text we describe a case report of acute gastric dilatation in a female postoperated of Nissen fundoplication who simultaneosly coursed with acute gastroenteritis; finally we aimed to make a concise review towards this disease based on the data reported so far in the literature. We present the case of a 54-year-old female who underwent Nissen fundoplication four months before. She coursed with acute gastroenteritis, and afterwards she began with incapacitant abdominal pain and upper gastrointestinal bleeding followed by hemodynamic instability. She was treated with gastric decompression by exploratory laparotomy and gastrostomy catheter colocation. Acute gastric dilatation is a rare disease associated to Nissen fundoplication, and it must be considered a probable cause in the approach algorithm of abdominal pain, specially in patients that have the risk factors described in this text, regarding that its prevention and opportune treatment lower its mortality due to necrosis and gastric perforation. [ABSTRACT FROM AUTHOR]

The purpose of this study is to determine the relationship between blood lactate and pyruvate concentrations in Japanese monkeys. On the basis of these results, I investigated whether measurement of blood lactate concentrations in ill animals with acute gastric dilatation was useful in identifying an earlier diagnosis and prognosis. Blood lactate and pyruvate concentrations were determined in 43 Japanese monkeys. Using a portable lactate analyzer, blood lactate concentrations in 4 ill animals were examined at the on set of acute gastric dilatation and after the recovery from this disease. The present results revealed that blood lactate concentrations linearly correlated with pyruvate concentrations in Japanese monkeys: y=0.7214+0.0142x, r=0.7813 (P<0.01). At the onset of acute gastric dilatation, the monkeys showed high lactate concentrations. Blood lactate levels in these ill animals remained elevated under uneventful circumstances. After emergency treatment, their lactate concentrations apparently decreased to the reference range (P<0.05). It was probable that persistent mechanical compression by the expanded stomach on the portal vein and/or caudal vena cava obstructed the blood flow, resulting in persistent hyperlactic acidemia from anaerobic metabolism. I concluded that blood lactate concentrations could serve as a reliable diagnostic predictor of clinical outcome in Japanese monkeys suffering from acute gastric dilatation. Monkeys with remarkable post-treatment decreases in blood lactate concentrations showed an excellent improvement in survival. [ABSTRACT FROM AUTHOR]