Heat Rash

Heat Rash

PATHOPHYSIOLOGY

Heat associated rash is known by several names including; miliaria rubra, sweat rash, and lichen tropicus. Most commonly it is referred to as prickly heat. In prolonged exposure to high heat and humidity, aspect of the stratum corneum may become macerated and obstruct the sweat gland pore. Heat rash is an inflammatory reaction occurring as a result of the blockage of these eccrine sweat glands. Pore obstruction often results in a super imposed staphylococcal infection. Heat rash affects all ages, ethnicities, and genders, although younger children tend to be at a slightly higher risk (Lyons R, 1982).

Heat rash may develop in anyone experiencing excessive sweating. Common risk factors for heat rash include:

– High ambient temperature environments

– High humidity conditions

– Sustained physical exertion

– Occlusive clothing

– Lack of acclimatization to new environment

CLINICAL PRESENTATION & DIAGNOSIS
Diagnosis of heat rash remains clinical in nature with characteristic rash in induvial with a history of excessive sweating. Heat rash will typically present as erythematous 2-4 mm papules or vesicles superimposed on an erythematous background. Simple heat rash will typically be vesicular in nature [Figure 1A] while a secondary staphylococcal infection will typically manifest as pustular lesions [Figure 2B]. It is important to note that close examination of the rash is required to ensure the vesicles or pustules are not follicularly based which would indicate folliculitis rather than heat rash.
Figure 1 – A and B

AB
Reference: Habif TP: Clinical Dermatology, ed 3, St. Louis, 1996, Mosby.

The rash is often intensely pruritic with complete anhidrosis of the affected areas due to the sweat gland pore blockage. A keratin plug may develop in the obstructed pore which will produce a deeper vesicle within the dermis days to weeks after the initial rash occurrence. This is known as the profunda stage and may result in a secondary vesicular eruption after the initial rash has subsided. Profunda stage vesicles are typically not pruritic (Lyons R, 1982).

DIFFERENTIAL

– Viral infection – herpes vs varicella

– Bacterial infection – folliculitis

– Acne

– Drug reaction

– Viral exanthem

– Allergic reaction

– Cholinergic urticaria

TREATMENT

Heat rash is typically self-limiting and will resolve spontaneously. In mild cases, simply moving to a cooler environment and removing constrictive clothing is often the only intervention required. Gentle exfoliation will also help open obstructed pores. Heat rash tends to recur but as acclimatization to higher ambient temperature occurs the risk of recurrence decreases dramatically. Generally, any measure aimed at reducing sweating will be beneficial in patients with heat rash. More severe cases are distinguished by the formation of pustules rather than simple vesicles. In these patients a topical corticosteroid such as hydrocortisone 2.5% BID for seven days may help to resolve symptoms sooner. Caution should be advised to avoid the face and areas of thin skin when applying corticosteroid creams. Topical antibiotics may rarely be required and coverage for staphylococcal and streptococcal organisms is advised if considering treatment. Mupirocin is a reasonable choice in this regard (Platt, 2014).

Dr. Erik Leci and Dr. Graham Briscoe (February 2, 2020 PR – ND)

References:

Lyons R, L. R. (1982). Miliaria rubra, a manifestation of staphylococcal disease. Archives of Dermatology, 282-6.

Osilla, a. S. (2019). Physiology, Temperature Regulation. Tampa, Florida, USA : StatPearls Publishing .

Platt, a. P. (2014). Heat Illness . In H. W. Marx, Rosen’s emergency medicine: Concepts and clinical practice (8th ed.) (pp. 1896 – 1905). Philadelphia, PA: Elsevier/Saunders.