Chemical burn secondary to propofol extravasation

Burn injuries occur when the skin and underlying tissues are damaged due to exposure to heat, electricity, chemicals, radiation, or friction. They can vary in severity, from minor superficial burns to severe deep burns that can be life-threatening.
The damage results in the death of skin cells, which can lead to a massive loss of fluid. Dehydration, electrolyte imbalance, and renal and circulatory failure follow, which can be fatal. Burn patients are treated with intravenous fluids to offset...

Intravenous anesthetics are drugs administered parenterally to induce anesthesia or sedation. Propofol is a widely used agent formulated as a 1% emulsion in soybean oil, glycerol, and egg phosphatide. It induces rapid anesthesia primarily due to its rapid distribution from the bloodstream to target tissues and is metabolized in the liver. However, it can cause significant pain on injection and hypertriglyceridemia. Fospropofol, a water-based prodrug of propofol, lacks these adverse effects.

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...

Inhalation anesthetics are drugs that induce general anesthesia upon inhalation. They work by increasing the sensitivity of GABAA receptors or inhibiting NMDA receptors, leading to a decrease in central nervous system activity. The depth of anesthesia can be rapidly adjusted by changing the concentration of the inhaled gas. Some common examples of inhalational anesthetics include volatile liquids like isoflurane, desflurane, sevoflurane and gases like xenon and nitrous oxide. Isoflurane, a...

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:

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...