EsoTensive Colic: The Screaming InfantD G Talbert*
Institute of Reproductive and Developmental Biology, Imperial College School of Medicine, London, UK
- *Corresponding Author:
- D G Talbert
Institute of Reproductive and Developmental Biology
Imperial College School of Medicine, Du Cane Road, London W12 ONN, UK
Tel: 020 8969 8151
E-mail: [email protected]
Received date: August 21, 2014; Accepted date: February 24, 2017; Published date: February 28, 2017
Citation: Talbert DG (2017) EsoTensive Colic: The Screaming Infant. J Gastrointest Dig Syst 7:488. doi:10.4172/2161-069X.1000488
Copyright: © 2017 Talbert DG. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: Infantile colic is considered a benign process in which an infant has paroxysms of inconsolable crying for more than three hours per day, more than three days per week, for longer than three weeks. It affects approximately 10% to 40% of infants worldwide and peaks at around six weeks of age, with symptoms resolving by three to six months of age. The incidence is equal between the sexes, and there is no correlation with the type of feeding (breast vs. bottle), gestational age, or socio-economic status. Some colicky infants have attacks of screaming with associated motor behaviours such as flushed face, furrowed brow, clenched fists and legs pulled up to the abdomen. Crying occurs in prolonged bouts. The infants do not respond to normal comforting techniques. Crying onset is unpredictable, spontaneous and unrelated to environmental events. The cause of infantile colic is unknown. It is proposed that there is a form of infant colic, resulting from Mallory-Wiess tears near the esophageousstomach junction, caused by distension of the stomach cardiac orifice during vomiting.
Physiology: Projectile vomiting is associated with severe colic. Very high intra-abdominal pressures are required to propel vomit several feet, greatly exceeding those involved in Gastro-oesophageal reflux disease. These pressures are generated by simultaneous maximal contraction of diaphragm and abdominal wall muscles, compressing abdominal contents. Pressurised chyme overwhelms the lower esophagus sphincter and enters the lower esophagus, distending and possibly tearing it.
Conclusions: A) There is a form of colic caused by Mallory-Weiss tears at the gastro-esophageal junction during violent vomiting. Subsequently, any reflux flowing over the exposed wound will cause sudden pain. B) Screaming will commence largely unrelated to external events, and last until the reflux disperses. C) Diet will have no effect, unless it induces vomiting. D) There will be no gender bias.