Abdominal imaging
Case TypeClinical Cases
AuthorsM. V. Pavlov, N. V. Orlova, Yu. V. Kulezneva, A. B. Abduraimov, K. A. Lesko
Patient20 years, female
A 20-year-old woman with complaints of eructation and vomiting. She was diagnosed with autism when she was 3 years old. The patient is given probiotics, intestinal antiseptics, antibiotics, laxatives and enemas. She has followed a gluten-free diet since she was 5 years old. The patient already had episodes of such symptoms in the previous 12 years.
Abdominal X-ray showed severe dilation of the stomach, small bowel and colon without any signs of pneumoperitoneum or gas-fluid levels. The diameter of the colon was 70 mm approximately. The stomach was dilated and hypotonic. Periodically the stomach bended and became angulate. Gastric tone and peristalsis could be observed only in the antrum. Cardia gaped periodically. Barium study revealed continuous rugal pattern and fine mucosal relief without pooling of contrast material, filling defects and convergence of mucosal folds. Also it revealed stomach bending without signs of gastric volvulus. Real obstruction was excluded by barium passage through stomach and small intestine. There was adequate flow of contrast material out of the stomach.
Large studies confirmed that some syndromes are more prevalent in people with autism, compared with non-autistic persons. The US Centers for Disease Control and Prevention analysis found that children with autism have a much higher sensibility to a wide group of diseases including gastro-intestinal disorders [1].
The mortality rate from gastrointestinal diseases was 40.8 times higher in patients with moderate to severe autism compared with non-autistic persons [2].
Food and respiratory allergies, including atopic manifestations and food intolerance are common in patients with autism [1, 3]. Large double-blind studies confirmed that patients with a history of allergic and atopic manifestations suffer from food sensitivities, but not due to coeliac disease [4, 5].
In the passt decade, gastrointestinal comorbidities in people with autism were recognised, such as increased permeability of the intestine wall, diarrhea, constipation, gastroesophageal reflux disease, deficiency of digestive enzymes and goitre [6-10]. Moreover, studies confirmed that the presence of gastrointestinal dysfunction in children with autism is not related to their eating habits or different side effects of drugs.
Analysis of the gut flora in patients with autism showed the presence of abnormal bacteria and atypical localisation of normal bowel bacteria [11, 12]. Serum levels of endotoxin were significantly higher in patients with autism and inversely and independently correlated with the severity of autism symptoms [13].
E. Emanuele et al [13] suspect that this phenomenon is a result of increased development of pathogenic bacteria in the gut and increased intestinal permeability in patients with autism. These studies revealed a spectrum of digestion disturbances in patients with autism including absorption pathology in the upper digestive tract, putrid and fermentative dyspepsia, abnormal metabolism of proteins and lipids, colitis as well as disturbances of motor-evacuation function of the large intestine. The latter is a part of neuronal and neuromuscular abnormalities, which are caused by increased intestinal permeability and immune imbalance, as well as disorders of neurological and neuroimmunological development [14]. Neuromuscular abnormalities can also lead to pseudo-obstruction.
Diagnostic radiology plays an important role in diagnosis and follow up of gastrointestinal disorders in patients with autism. Abdominal radiography and fluoroscopy are useful in these patients due to serious problems in communication and complaints revealing. These techniques are simple enough and relatively cheap for usage as a routine follow up method in this group of patients. Oral contrast study, including barium study, in patients with autism may help to differentiate stomach and pseudo-obstruction with small bowel obstruction and stomach volvulus.
[1] Kohane, I.S., McMurry, A., Weber, G., et al. (2012) The Co-Morbidity Burden of Children and Young Adults with Autism Spectrum Disorders. PloS one 7(4): e33224 (PMID: 22511918)
[2] Shavelle, R.M., Strauss, D.J. and Pickett, J. (2001) Causes of death in autism. Journal of Autism and Developmental Disorders 31(6): 569-576 (PMID: 11814268)
[3] Schieve, L.A., Gonzalez, V., Boulet, S.L., et al. (2012) Concurrent medical conditions and health care use and needs among children with learning and behavioral developmental disabilities, National Health Interview Survey, 2006-2010. Research in developmental disabilities 33(2): 467-476 (PMID: 22119694)
[4] Carroccio, A., Mansueto, P., Iacono, G., et al. (2012) Non-Celiac Wheat Sensitivity Diagnosed by Double-Blind Placebo-Controlled Challenge: Exploring a New Clinical Entity. The American Journal of Gastroenterology 107(12): 1898-906 (PMID: 22825366)
[5] Massari, S., Liso, M., De Santis, L., et al. (2011) Occurrence of nonceliac gluten sensitivity in patients with allergic disease. International archives of allergy and immunology. International archives of allergy and immunology 155(4): 389-394 (PMID: 21346369)
[6] Horvath, K., Papadimitriou, J.C., Rabsztyn, A., et al. (1999) Gastrointestinal abnormalities in children with autistic disorder. J. Pediatr 135(5): 559-563. (PMID: 10547242)
[7] Kushak, R.I., Lauwers, G.Y., Winter, H.S., et al. (2011) Intestinal disaccharidase activity in patients with autism Effect of age, gender, and intestinal inflammation. Autism 15(3): 285-294 (PMID: 21415091)
[8] Williams, B.L., Hornig, M., Buie, T., et al. (2011) Impaired carbohydrate digestion and transport and mucosal dysbiosis in the intestines of children with autism and gastrointestinal disturbances. PloS one 6(9): e24585 (PMID: 21949732)
[9] Wasilewska, J., Jarocka-Cyrta, E. and Kaczmarski, M. (2009) Gastrointestinal abnormalities in children with autism. Polski merkuriusz lekarski: organ Polskiego Towarzystwa Lekarskiego 27(157):40-3 (PMID: 19650428)
[10] Persico, A., Napolioni, V. (2013) Urinary p-cresol in autism spectrum disorder. Neurotoxicology and Teratology 36:82-90 (PMID: 22975621)
[11] Finegold, S.M., Dowd, S.E., Gontcharova, V., et al. (2010) Pyrosequencing study of fecal microflora of autistic and control children. Anaerobe 16: (4): 444-453 (PMID: 20603222)
[12] Parracho HM, Bingham MO, Gibson GR, McCartney AL. (2005) Differences between the gut microflora of children with autistic spectrum disorders and that of healthy children. J Med Microbiol 54(Pt 10):987-91 (PMID: 16157555)
[13] Emanuele, E., Orsi, P., Boso, M., et al. (2010) Low-grade endotoxemia in patients with severe autism. Neuroscience letters 471: (3): 162-165 (PMID: 20097267)
[14] Goyal D.K., Miyan J.A. (2014) Neuro-immune abnormalities in autism and their relationship with the environment: a variable insult model for autism. Front Endocrinol (Lausanne) 5: 29. 1-10 (PMID: 25110424)
URL: | https://eurorad.org/case/15759 |
DOI: | 10.1594/EURORAD/CASE.15759 |
ISSN: | 1563-4086 |
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.