Chemical Mediator in a Spilled Hot Water Burn
Prostaglandins (D) are the primary chemical mediator in a spilled hot water burn, playing a crucial role in the inflammatory response that follows thermal injury.
Pathophysiology of Burn Injury
When hot water contacts the skin, it causes tissue damage that initiates an inflammatory cascade:
- Burn injuries trigger inflammation, hypermetabolism, and capillary leakage, leading to the release of various inflammatory mediators 1
- At the site of injury, several inflammatory mediators are released, including monoamines, cytokines, prostanoids (prostaglandins), and peptides 1
- These mediators are sensed by nociceptors and activate C and Aδ fibers, which transmit pain signals to the dorsal horn of the spinal cord 1
Role of Prostaglandins in Burn Injury
Prostaglandins are the predominant chemical mediator in thermal burns for several reasons:
- Prostaglandins are synthesized by the enzyme cyclooxygenase (COX) and play a major role in the inflammatory response following tissue damage 2
- They function as vasodilators that potentiate plasma exudation produced by other permeability-increasing mediators like histamine or bradykinin 3
- Prostaglandins are responsible for many of the cardinal signs of inflammation seen in burns, including pain, swelling, and edema 2
- The inducible enzyme COX-2 is particularly important in producing pro-inflammatory prostaglandins after tissue injury 2
Other Chemical Mediators in Burns
While prostaglandins are the primary mediator, other substances also contribute to the burn response:
- Bradykinins (option B) do play a role in burn inflammation, but they primarily act by sensitizing nociceptors to heat stimuli through a mechanism that depends on prostaglandin synthesis via both COX-1 and COX-2 4
- Serotonin (5-HT) (option A) functions more as a transmitter in the inhibitory pain system rather than as a primary inflammatory mediator in burns 1
- Thromboxane (option C) is another prostanoid but is not the predominant mediator in thermal burns 1
Clinical Implications
Understanding prostaglandins as the key mediator in burns has important treatment implications:
- Non-steroidal anti-inflammatory drugs (NSAIDs) can help manage burn pain by inhibiting COX enzymes, thus reducing prostaglandin production 2
- Multimodal analgesia is recommended for burn pain management, with titration based on validated pain assessment scales 1
- Cooling the burn site can help reduce pain and limit burn depth progression by affecting the inflammatory cascade 1
- Covering burns with appropriate dressings can reduce pain by protecting nerve endings from external stimulation 1
Management Considerations
When treating thermal burns, consider these evidence-based approaches:
- For small to moderate burns (< 20% TBSA in adults, < 10% in children), cooling the burn can limit deepening and reduce pain 1
- Short-acting opioids and ketamine are effective for managing burn-induced pain 1
- Non-pharmacological treatments such as cooling limited burned surfaces and covering burns with appropriate dressings can improve pain control 1
- In severe cases, general anesthesia may be required for wound care procedures 1
Understanding that prostaglandins are the primary chemical mediator in thermal burns helps guide appropriate anti-inflammatory and analgesic therapy to improve patient outcomes.