Acids injuries

Schematic diagram of a primary afferent neuron mediating pain, its synapse with a secondary afferent in the spinal cord, and the targets for local pain control. The primary afferent neuron cell body is not shown. At least three nociceptors are recognized acid, injury, and heat receptors. The nerve ending also bears opioid receptors, which can inhibit action potential generation. The axon bears sodium channels and potassium channels (not shown), which are essential for action potential propagation. Synaptic transmission involves release of substance P, a neuropeptide (NP) and glutamate and activation of their receptors on the secondary neuron. Alpha2 adrenoceptors and opioid receptors modulate the transmission process.

Many of the deep dermal papillae actually survive the acid injury when it starts to affect the Grenz zone. 

Allergic and irritant contact dermatitis and acute caustic chemical or acid injuries are the most common toxin-related skin problems. Systemic toxicity may occur (p 157) but is not a common complicating factor. 

Bonnans C., Fukunaga K., Levy M. A., Levy B. D. 2006. Lipoxin A4 regulates bronchial epithelial cell responses to acid injury. American. Journal of Patholoev. 

Chemical skin injuries 7 % (n = 80) 70 (87.5 %) acid injuries 18-month Add assault injuries 4 % of aU bum injury patients, 57.5 % of aU chemical period skin injury patients (n=46)... 

In a cross-sectional study of a bum registry from Sri Lanka for a period of 18 months, chemical splash injuries with acids represented 4 % of all patients and deliberate chemical assaults comprised 57 % of all chemical skin injuries. There were 14 formic acid injuries (41.3 %), 1 nitric acid injury (2.1 %), and 26 cases of unknown acid injuries (56.5 %). Prehospital water decontamination was done in 26 cases (56.5 %) and not done in 20 cases (43.5 %). Long-term sequelae were hypertrophic scars with constriction bands, ectropion, and microstomia. Scar revision surgery was required in 5 cases (10.8 %) and there were 2 fatalities [192]. 

CavaUini M, Casati A. A prospective, randomized, bUnd comparison between saline, calcium gluconate and diphoterine for washing skin acid injuries in rats effects on substance P and beta-endorphin release. Eur J Anaesthesiol. 2004 21 389-92. 

Yano K, Hosokawa K, KaMbuchi M, Hikasa H, Hata Y. Effects of washing acid injuries to the skin with water an experimental study using rats. Burns. 1995 21(7) 500-2. 

Trap R, Christensen 1. Hydrofluoric acid injuries pathogenesis and treatment. Ugeskr Laeger. 1990 152(22) 1570-2. 

At a pH of 2.0 and below, the limits of the HC03 response are greatly exceeded, and the intercellular spaces will acidify even more and to a deeper level. At this stage, the ability of the epithelial cells to maintain constant intracellular pH may be overcome due to the high add load, with resultant erosion. As the nxire superficial cells are eroded, pepsin may also back diffuse, adding proteolytic insult to acid injury. 

The severity of acid exposures depends on several factors the type, concentration, and amount of acid involved, and the time and type of tissue exposure to the acid. Injury caused by acid bums usually involves a coagulation necrosis of the tissue with a precipitation of protein resulting in scab formation. This injury generally does not result in a deep penetration of tissues. 

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