Pyloric Stenosis as Cause of a Venous Hypertensive Syndrome Mimicing True Shaken Baby Syndrome
|Institute of Reproductive and Developmental Biology, Imperial College School of Medicine, Queen Charlotte’s Hospital, UK|
|Corresponding Author :||D.G.Talbert
Institute of Reproductive and Developmental Biology
Imperial College School of Medicine
Queen Charlotte’s Hospital
Du Cane Road, London W12 0NN, UK
E-mail: [email protected]
|Received November 25, 2011; Accepted December 23, 2011; Published December 05, 2011|
|Citation: Talbert DG (2011) Pyloric Stenosis as Cause of a Venous Hypertensive Syndrome Mimicing True Shaken Baby Syndrome. J Trauma Treatment 1:102. doi:10.4172/2167-1222.1000102|
|Copyright: © 2011 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.|
A syndrome of bleeding in the brain with retinopathy, but no external evidence of trauma, is known in infants. There is an association with excessive crying and feeding difficulties in this condition. This has led to the hypothesis that the injuries arise during violent shaking by an angry carer, causing the brain to rotate relative to the skull, (Shaken Baby Syndrome, SBS).
An alternative hypothesis, described here, (Dysphagic Infant Death Syndrome DIDS), is that injuries similar to those in SBS can result from venous hypertension during excessive coughing or vomiting. Such injuries occur “naturally” during paroxysms of coughing in Whooping Cough. High intra-abdominal pressure drives abdominal venous blood up into the head, rupturing intracranial veins and capillaries. This results in subdural haemorrhages, petechiae in skin and Valsalva Retinopathy in the eyes. This article considers when the excessive intra-abdominal pressures are caused by violent vomiting and retching in pyloric stenosis.
Some DIDS additional features, not occurring in SBS, may give warning of impending intracranial catastrophe. Infant skull suture growth rate depends on local stretch induced in the underlying Dura Mater. This will be increased during venous hypertension, accelerating head growth rate analogous to the hydrocephalous mechanism. The prolonged inconsolable crying would be explained by Mallory-Weiss tears at the oesophageal-stomach junction during repeated vomiting. Edema resulting from local leakage from over-distended cerebral veins and capillaries may temporarily disable axon transmission, causing temporary loss of consciousness. Transient “spiking” fevers may seen in this condition if the temperature limiter center in the hypothalamus is temporarily disabled by such flooding. (Brainstem tissue is drained by the vertebral vein system whose tortuous nature smoothes out pressure spikes. This provides some protection of breathing and cardiac mechanisms which may remain normal.)
It is concluded that, unlike SBS, preventative measures should be possible for DIDS.