Gastric paralysis

Amonronx, J., Gnillevin, L. Bladder neuropathy and gastric paralysis... 

Abiltrmiruri distension, resulting from gastric paralysis or gas Cj Ihetapy and rttanagcmenlof actrlegastric toxicosis... 

Usually intravenous pre-oxygenation followed by a small dose of an opioid, e.g., fentanyl or alfentanil to provide analgesia and sedation, followed by propofol or, less commonly, thiopental or etomidate to induce anaesthesia. Airway patency is maintained with an oral airway and face-mask, a laryngeal mask airway (LMA), or a tracheal tube. Insertion of a tracheal tube usually requires paralysis with a neuromuscular blocker and is undertaken if there is a risk of pulmonary aspiration from regurgitated gastric contents or from blood. 

Exposure should be terminated as soon as possible either by removal of the patient or by fitting the patient with a gas mask if the atmosphere remains contaminated. Contaminated clothing should be removed immediately the skin and mouth should be washed with copious amounts of water. Gastric lavage should be conducted if necessary. Artificial respiration should be administered if required, and administration of oxygen may be necessary. If the convulsion persists, diazepam (5-10 mg intravenously) or sodium thiopental (2.5% intravenously) should be administered, and the patient should be treated for shock. Atropine should be administered in sufficiently large doses, but atropine is without any effect against peripheral neuromuscular activation and subsequent paralysis. Pralidoxime (1 or 2 g infused intravenously) should be administered for all the peripheral effects. 

Indications Spleen and stomach qi vacuity. Chronic gastritis, gastric and duodenal ulcer, gastrointestinal weakness and dysfunction, gastroptosis, irritable bowel syndrome, diabetes mellitus, periodic paralysis, uterine fibroids, anemia, vomiting, and diarrhea... 

Atropine is able to oppose these muscarinic effects. In addition, neostigmine, which has both a direct action as well as an indirect action that is mediated by acetylcholine on end-plate nicotinic receptors, may produce muscular fascicula-tion, muscular cramps, weakness, and even paralysis. These effects are not countered by atropine. Furthermore, neostigmine enhances gastric contraction and secretion. Neostigmine itself is metabolized by plasma acetylcholinesterase. 

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