Related Experiment Video

Updated: May 15, 2026

Open Tracheostomy Gastric Acid Aspiration Murine Model of Acute Lung Injury Results in Maximal Acute Nonlethal Lung Injury
09:16

Open Tracheostomy Gastric Acid Aspiration Murine Model of Acute Lung Injury Results in Maximal Acute Nonlethal Lung Injury

Published on: February 26, 2017

A lethal cocktail: gastric perforation following liquid nitrogen ingestion

James Scott Pollard1, Joanne Elizabeth Simpson, Moatasiem Idris Bukhari

  • 1Department of Surgery, Royal Lancaster Infirmary, Lancaster, UK. james.pollard@doctors.net.uk

BMJ Case Reports
|January 10, 2013
PubMed

More Related Videos

Inducing Acute Liver Injury in Rats via Carbon Tetrachloride (CCl4) Exposure Through an Orogastric Tube06:12

Inducing Acute Liver Injury in Rats via Carbon Tetrachloride (CCl4) Exposure Through an Orogastric Tube

Published on: April 28, 2020

Related Concept Videos

Esophageal Perforation-I: Introduction01:22

Esophageal Perforation-I: Introduction

Esophageal perforation is a severe medical condition characterized by a breach in the integrity of the esophageal wall. This breach can occur due to various factors such as trauma, medical procedures, or underlying diseases. When the esophageal wall is compromised, it allows food, fluids, and digestive juices into the chest cavity or adjacent structures, leading to potential complications and health risks.
The location of esophageal perforation can vary, occurring anywhere along the esophagus.
Esophageal Perforation-II: Clinical Manifestations and Management01:28

Esophageal Perforation-II: Clinical Manifestations and Management

Esophageal perforations manifest in various clinical forms, influenced by factors such as the perforation's cause and location (cervical, intrathoracic, or intra-abdominal), the extent of contamination, and potential injury to adjacent mediastinal structures. The timing between the perforation occurrence and treatment initiation also affects the clinical presentation.
Clinical Manifestations:
Prevention of Further Absorption of Poison01:14

Prevention of Further Absorption of Poison

In cases of acute poisoning, the primary objective is to prevent further absorption of the toxic substance into the body. Immediate interventions using various decontamination techniques targeting the gastrointestinal (GI) tract can achieve this. Decontamination is crucial to prevent poison from entering the systemic circulation, which involves washing affected areas with water and mild soap and removing contaminated clothing. Once external decontamination is done, attention must be turned to...
Intestinal Obstruction II: Pathophysiology01:07

Intestinal Obstruction II: Pathophysiology

Intestinal obstruction triggers a series of physiological responses, starting with gas and fluid accumulation in the bowel segment proximal to the obstruction, leading to distension. This distended intestine compresses the diaphragm, hindering lung expansion and potentially leading to reduced respiratory effort, atelectasis, and pneumonia.To overcome the blockage, the gut intensifies contractions, causing colicky abdominal pain, nausea, and vomiting, which reduces fluid and food intake and...
Pyloric Obstruction01:11

Pyloric Obstruction

Pyloric obstruction, also referred to as gastric outlet obstruction, is a condition characterized by narrowing or blockage at the pylorus—the muscular valve regulating the flow of stomach contents into the duodenum. When this passage becomes impaired, the stomach cannot effectively empty its contents into the small intestine. This disruption leads to a range of gastrointestinal symptoms, including early satiety, bloating, epigastric pain, postprandial nausea, persistent vomiting, and...
Peptic Ulcer01:27

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...