Erythema Ab Igne

CORRESPONDENCE:

Lindsay Tjiattas-Saleski, DO | LRTJ55@yahoo.com

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A 39-year-old female with a past medical history of chronic back pain, due to scoliosis and associated leg length discrepancy, pres-ents to the emergency room with a rash on her diffuse lower back. Her pain had worsened over the past week due to a change in weather and was unrelieved by her normal prescription and over the counter pain control regimen. She had applied a heat pack to her lower back while she was sitting in a chair studying and accidentally fell asleep for an hour. When she woke up, she took a shower and noticed a stinging/burning sensation to her lower back, which she attributed to a burn from the heat pack. When she woke up the next morning, her husband noted the following rash on her back, which persisted for 1 week prior to presentation to physician (Figures 1 and 2).

She initially noted a few blisters which had resolved. She denies associated fevers, chills, myalgias, arthralgias, pruritis, insect bites or rash elsewhere on her body and denies previous episodes of the rash. The patient does admit to frequent heating pad usage for back pain.

QUESTIONS:

1. The most likely etiology of this patient's dermatologic presentation is:

   1. Contact dermatitis

   2. Exposure to thermal heat

   3. Livedo Reticularis

   4. Vasospasm after heat pad removal
      

2. What is the recommended treatment?

   1. Removal of the offending heat source

   2. Treat the underlying cause of pain

   3. Monitor skin changes for hyperkeratotic changes

   4. All of the above

ANSWERS

1. The most likely etiology of this patient's dermatologic presentation is:

   
   

   The correct Answer is:

   The correct Answer is:

   D) All of the above

   The rash will generally fade over weeks to months without treat- ment.6 In this case, the underlying cause of back pain should be addressed so as to assist the patient in avoiding further thermal heat use. If a patch of EAI fails to fade, or if there are hyperkeratot- ic plaques present, it may be reasonable to consult a dermatologist.

   
   

   DISCUSSION

   Erythema ab igne (Latin, meaning “redness from fire”), also known as “toasted skin syndrome”, presents as an erythematous, macu- lar dermatosis that develops due to chronic exposure to low level thermal heat.1,2,3,4 While known as being a historical disease, this skin condition has since seen a reemergence that reflects modern- ized technology. Formerly, the condition occurred on the shins of elderly people due to lengthy and close proximity to coal fires or stoves.3 With the arrival of central heating, most cases now are due to the use of heating pads, heated car seats, laptop computers, and electric heaters.4,7 Acutely, the skin changes associated with EAI manifest as coalescing red bands with erythema present diffusely. Only after repeated exposure will microscopic changes in the skin result in a more defined pigmentary variation.3,8

   It is reported that the rash can appear with as little as two weeks of heat exposure, however the time course depends on the tempera- ture of the heat source.9 The acute presentation of this mottled rash may be viewed as benign, however, over time there is concern about the development of thermal keratosis and, rarely, squamous cell carcinoma (SCC), cutaneous marginal zone lymphoma, and Merkel cell carcinoma.1,3,10

   German dermatologist Abraham Buschke first described erythe- ma ab igne in the early 1900’s.11 As with many diseases, there are certain distinguishing cultural and geographical features that are associated with EAI. Most cases have been reported in countries with a cooler climate where people resorted to alternative ways of maintaining their body heat during the cold months.12 One of these very characteristic cases were the Chinese kang cancers. A Chinese kang is a long, traditional platform made of clay or bricks that was heated by a cooking fire and used for general living and warmth during sleep, thus the greater trochanter was a common area for EAI and SCC to develop.13

   The early appearance of EAI is that of a transient macular ery- thema that is distributed in a reticular, or net-like, pattern and is blanchable.4 The lesions are characteristically painless, but the patient may complain of a diffuse minor burning sensation or pru- ritus that resolves as the rash fades.4,6 The rash may exhibit mul- tiple colors simultaneously, with areas differing from light pink, to a duskier rose and brown.4 Over time, and with chronic exposure to the source of thermal heat, the dermatosis progresses into a dusky hyperpigmentation and no longer blanches.4 If the source of heat persists, skin hyperpigmentation may be permanent. Scarring is probable if bullae have formed.7 Livedo reticularis, a vasospastic vasculopathy, produces a rash similar to that seen in early EAI and thus should be included in the differential diagnosis.3,10 Cutis mar- morata and Poikiloderma should also be considered.4

   Thermal heat damages the epithelium by several mechanisms. First, is direct injury to the cellular structure of the tissue, and second by the release of local mediators such as cytokines.14 Heat provokes an inflammatory response within the tissue resulting in the release of toxic cytokines as well as free oxygen and nitrogen radicals which potentiate the injury by damaging essential pro- teins, lipids, and DNA. One of these cytokines is TNF, an acute phase reactant that plays a role in systemic inflammation and cell apoptosis.15 Cell membranes are specifically prone to these oxida- tive stresses.15 Mast cells recruited to burned tissue release hista- mine, resulting in local vasodilation and edema.14 Histologically, there may be an abundance of inflammatory cells, connective tis- sue disintegration, and hemosiderin deposition.14 The rash pattern parallels the dermal venous plexus, where hemosiderin deposition results in the net-like reticular appearance.4,9

   Many patients do not associate their rash with the source of heat exposure. It may be up to the clinician to perceive the markings of EAI and then question the patient about a possible persistent ex- posure to a heat source. Specific questioning should focus on occu- pation and hobbies, as certain exposure patterns have been noted (EAI on the forearms of bakers, or the face and arms of glass blow- ers and foundry workers).4,6 In other instances, patients may be us- ing heat as a means of pain relief. EAI is often seen in patients with longstanding back and abdominal pain who find comfort with the application of heat.3 EAI in the lumbosacral region suggests a mus- culoskeletal dysfunction.4 It has also been seen in the setting of malignancy or visceral disease, specifically pancreatitis, peptic ul- cer disease, primary cancers, as well as metastatic neoplasms.4,7,16 In these cases, EAI ensued after the chronic use of a heating source to mitigate pain associated with these underlying processes.7

   Within a longstanding patch of EAI, a keratotic skin lesion called a thermal keratosis (TK) may emerge.11 TKs will appear as hyperker- atotic papules and plaques. There has been reported evolvement of these lesions to invasive squamous cell carcinoma from TKs, however there is little information in the literature with reference to the percentage of progression of TK to invasive SCC or of the prognosis of thermal SCC.1,7,10,13

   The diagnosis of EAI is a clinical diagnosis with labs and imaging offering little benefit. If there is uncertainty of the diagnosis, how- ever, or if there are hyperkeratotic plaques or papules within the patch, a punch or shave biopsy is indicated.1,3,13,17 If multiple lesions exist, the clinician should pick the largest, most representative le- sion in the least cosmetically important area for biopsy.18 When concerned regarding SCC, sample from the most central and thick- ened area of the lesion.18 The most important step in treatment is to remove the offending heat source. In most cases, the rash will fade over weeks to months without treatment.6 If there are cos- metic concerns due to hyperpigmentation, topical tretinoin may be used to improve the appearance of the rash.6,17,19 Laser therapy and cryosurgery are also acceptable options if tretinoin is contra- indicated. If a patch of EAI fails to fade, or if there are hyperkera- totic plaques present, it may be reasonable to consult a derma- tologist. 5-fluorouracil cream has been used if the lesions exhibit pre-cancerous morphology on punch biopsy.3,8

   Osteopathic manipulative therapy (OMT) may have proven helpful in this particular patient. The OSTEOPATHIC trial was a random- ized double blind trial that demonstrated that OMT treatment did result in moderate to substantial improvement in low back pain symptoms when used to complement other co-treatments. OMT also decreased the need for prescription medications. Some of the techniques utilized in the study were high-velocity, low-amplitude thrusts, soft tissue stretching, kneading, and pressure, myofascial stretching and release, and positional treatment of myofascial ten- der points.8

   In summary, EAI presents as a localized, erythematous, and reticu- lated rash that develops due to a low level of heat below the point for a thermal burn. Over time, if continued thermal damage occurs, squamous atypia may appear histologically, which can progress to a cutaneous malignancy, namely SCC. First and foremost, the physician should determine the underlying reason for the use of heat. Many patients who present with EAI are attempting to allevi- ate chronic pain, in rare cases hinting at an underlying malignancy.8 EAI itself can be very easily identified and allow prevention of pro- gression to more serious cutaneous disease. The ICD 10 code for EAI is L59.0.

   
   

   REFERENCES:

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   2. Ladizinski B, Sankey C. Erythema ab igne. The Journal of Emergency Medicine 2014;49(1):29–29.

   3. Riahi RR, Cohen PR, Robinson FW, Gray JM. Erythema ab igne mimicking livedo reticularis. International Journal of Dermatology 2010;49:1314– 1317.

   4. Other Vascular Disorders: Livedo Reticularis. Bolognia Dermatology,

      Third Edition. 106, 1747-1757.

   5. Ustane, Richard and Riojas, Marcela, MD. Diagnosis and Management of

      Contact Dermatitis. Am Fam Physician. 2010 Aug 1;82(3):249-255.

   6. El-Ghandour A, Selim A, Khachemoune A. Bilateral lesions on the legs.

      Journal of Family Practice 2007;56(1):37–39

   7. Lopiccolo M, Crestanello J, Yoo SS, et al. Facial erythema ab igne of rapid onset. Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology 2008:38–39.

   8. Steadmon MJ, Riley KN. Erythema Ab Igne: A Comeback Story. The Journal of Pediatrics 2013:1789–1789.

   9. 9. Botten D, Langley RGB, Webb A. Academic branding: erythema ab igne and use of laptop computers. Canadian Medical Association Journal 2010:57–57. doi:10.1503/cmaj.091868.

   10. Sigmon JR, Cantrell J, Teague D. Poorly differentiated carcinoma arising in the setting of erythema ab igne. American Journal of Dermatopathology 2013. doi:10.1097/DAD.0b013e3182871648

   11. Asilian A, Abtahi-Naeini B, Pourazizi M. Rapid onset of bullous erythema ab igne: A case report of atypical presentation. Indian Journal of Dermatology Indian J Dermatol 2015:325–325. doi:10.4103/0019- 5154.156488.

   12. Chan C-C, Chiu H-C. Erythema Ab Igne. The New England Journal of Medicine 2007:8–8.

   13. Fitzpatrick TB. Thermal Burns and Other Heat-Induced Skin Disorders. In: Fitzpatrick's Dermatology in General Medicine. 8th ed. New York [etc.: McGraw-Hill Medical; 2012.

   14. Adams J. Thermal Burns and Other Heat-Induced Skin Disorders. In: Emergency Medicine Clinical Essentials. 2nd ed. Philadelphia, Pa: Elsevier/ Saunders; 2013.

   15. Marx JA. Pathophysiology of Burns. In: Rosen's Emergency Medicine Eight Edition. Elsevier; 2014.

   16. Ashby M. Erythema ab igne in cancer patients. Journal of the Royal

       Society of Medicine 1985;78:925–925.

   17. Sesay M, Dhanji S. Case Report: Erythema Ab Igne in a Patient with

       Diabetic Neuropathy. American Family Physician 2009.

   18. Coffman, Donna. Punch Biopsy (General Surgery) Procedures Consult. https://www-clinicalkey-com.vcom.idm.oclc.org/#!/content/medical_ procedure/19-s2.0-mp_GS-071Accessed on Clinical Key. 6/6/2016.

   19. Bassi A, Berti S, Galeone M. Erythema ab igne . Quarterly Journal of Medicine 2014. doi:10.1093/qjmed/hcu049.

   
   

   FIGURE LEGEND:

   Figure 1 and 2: EAI