Thermal Lesions of the External Nose: Burns and Frostbite

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Thermal nasal injuries may develop when extremely high or low temperatures damage the skin and underlying tissues of the nose.

Nasal burns

Etiology of nasal burns

Burns are caused by exposure of the nasal area to hot liquids, steam, or high doses of UV radiation (sunburns). The higher the temperature and exposure time of the liquid (steam) is, the more damage a patient can incur.

Anatomic Pathology of Nasal Burns

Nasal burns may be classified by depth of injury:

  • Superficial burns (first-degree burns): Only the upper layer of the skin (the epidermis) is damaged;
  • Superficial partial-thickness (second-degree burns): Damage extends to both the epidermis and superficial dermis layers (papillary layer);
  • Superficial full-thickness (third-degree burns): The epidermis, dermis, fatty layer of the subcutaneous tissue, and skin appendages (hair follicles and sweat glands) are involved;
  • Deep full-thickness (fourth-degree burns): The lesions extend beyond the skin, causing necrosis of muscles, tendons, and cartilage, thus exposing the bone.

The first two types of burns heal when the wound surface heals through epithelialization, whereas third- and fourth-degree lesions require scar tissue formation.

Clinical Manifestations of Nasal Burns

Any type of burn triggers severe pain in the affected area.

In first-degree burns, the skin typically appears hyperemic. The burn site is painful upon palpation and turns pale when pressed.

In second-degree burns, hyperemic skin develops serous blisters filled with clear fluid; the wound bed is pink. In such cases, blisters may form within 24 hours from the moment of injury. Tenderness on palpation is also observed.

Second-Degree Nasal Burn
Second-Degree Nasal Burn — 3D-Model

Third-degree burns are characterised by serous hemorrhagic blisters on hyperemic and infiltrated skin. Coagulation necrosis may also be observed. The lesion is moderately painful or painless, hairs can easily be pulled from their roots.

Fourth-degree deep full-thickness burns are characterized by black scab. An exposed bone becomes the wound bed, which is otherwise painless.

Note that nasal burns are rarely observed alone. Other body parts are typically damaged as well.

Classification of nasal burns by depth of injury

Grade Lesion depth Local changes Soreness Healing
First Epidermis only Hyperemic (red) skin. On palpation, there is soreness. The area blanches when pressed Moderate pain when touched Epithelization, without scarring
Second Epidermis and superficial layers of dermis (papillary layer) Hyperemic skin develops serous blisters filled with clear fluid.
The bottom of the bubbles are pink.
Blisters may appear within 24 hours
Pronounced Epithelization, without scarring
Third Epididymis, dermis, fatty layer of subcutaneous tissue, skin appendages Serous or hemorrhagic blisters, coagulation necrosis.
The skin is hyperemic and infiltrated.
Hairs are easy to remove
Reduced or none Scarring
Fourth All layers of skin, muscles, tendons, cartilages, possibly bones Black crusts, an exposed bone becomes the wound bed. Extensive necrosis None Thick scarring

Diagnosisof Nasal Burns

Diagnosis is based on a detailed history of the trauma and an ENT exam. During a prehospital check-up, the patient’s airway patency must be assessed. Subsequently, the nasopharyngeal mucosa is regularly reassessed for early detection of burns, reactive mucosal edema, and prevention of respiratory failure. To devise a treatment plan, a healthcare professional should evaluate the depth of the lesion and the percentage of the total body surface area (TBSA) affected. In cases of extensive burns, blood tests, urinalysis, and an ECG are performed to anticipate any systemic complications.

Treatment of nasal burns

First and foremost, any contact with the damaging factor should be terminated. If a patient has inhaled smoke, humidified oxygen is administered at a prehospital stage.

Whenever possible, the damaged body area should be cooled down and an adequate level of analgesia should be provided. For superficial burns, local therapy is recommended. Dressings with antibacterial ointments are prescribed. Blisters are managed differently depending on their size: small lesions should remain as they are, while larger blisters require excision. Deep burns necessitate skin graft transplantation.

Patients with large and deep burns must be admitted to a specialized burn unit.

Nasal frostbite

Etiologyof Nasal Frostbites

Frostbites typically develop on exposed skin areas subjected to low temperatures for extended periods. However, frostbites may occur even at temperatures above zero if the weather conditions are unfavorable (high humidity and strong wind).

Anatomic Pathologyof Nasal Frostbites

Moreover, cold exposure triggers vasoconstriction of peripheral blood vessels to provide more blood flow to the vital organs. The tissues become ischemic, leading to cell death. In some cases, it may be challenging to assess the degree of a frostbite immediately, as typical alterations may develop only a few days later. For instance, blisters are observed within the first 4–8 hours, and necrosis borders become demarcated several days after the event.

  • First-degree frostbites affect the superficial layers of the dermis, making the skin look pale.
  • In second-degree frostbites, serous blisters erupt on the pale skin.
  • Deep skin lesions are observed in third-degree frostbites. These are represented by blisters filled with hemorrhagic fluid.
  • Fourth-degree frostbites are characterized by full-thickness necrosis of the skin and underling tissues. This stage presents with dry gangrene, black dry crusts over the distal areas, and in extreme cases, autoamputation. The skin is cyanotic, marbled. Such damage is also accompanied by second- and third-degree manifestations and leads to blisters filled with different types of fluids.

Clinical Manifestations of Nasal Frostbites

Initially, frostbites cause burning sensations and numbness in the affected area. The frostbitten skin is pale, cold to the touch, hard, and mottled. Upon warming, patients start to feel severe pain. Pain intensity correlates with the lesion degree. The skin becomes highly hyperemic and edematous. As described earlier, depending on the degree, frostbites present with specific local skin alterations.

Classification of Nasal Frostbites by Lesion Severity

Grade Lesion depth Local changes Soreness Healing
First Superficial layers of the dermis Skin pallor, numbness, burning, cold area. Hyperemia and edema develop after warming. No blisters form Moderate pain which intensifies upon warming Rapid with no scars left
Second Epidermis and superficial layers of dermis (papillary layer) Hyperemic skin develops serous blisters filled with clear fluid within 4–8 hours. The skin is pale and cold. Edema and hyperemia develop later Pronounced Complete, possible hyperpigmentation
Third Deep skin layers Blisters with hemorrhagic contents, the skin is cyanotic, marbled. The hair on the affected area falls out. Eventual necrosis Severe, then decreased Slow, with scarring
Fourth All skin layers and underlying tissues (fatty layer of subcutaneous tissue, muscles, bones) Dry gangrene, black dry scab, autoamputation It is often accompanied by second- and third-degree signs. Demarcation after a few days Absent due to nerve endings dying Slow, with tissue loss and thick scarring

Diagnosis

Diagnosis is based on medical history and patient’s complaints. A healthcare professional should conduct an assessment of both general condition and local changes.

Treatment of nasal frostbite

The damaged body area should be warmed up. Under no circumstances should the skin be massaged. Direct exposure to open flame should also be avoided, as frostbites reduce skin sensitivity to stimuli, which can lead to burns. The affected body part may be immersed in warm water or covered with a dry, warm dressing.

An adequate level of analgesia should be provided; sometimes opioids may be indicated. In cases of general hypothermia, warm fluids and thermal blankets may be used. Locally, blisters may be treated with antibacterial ointments and sterile dressings. To improve tissue perfusion, anticoagulants, antiplatelet agents, and vasodilators are indicated. If dry gangrene is present, amputation is performed after a few days.

FAQ

1. Why is frostbite degree not always immediately identifiable?

Deep tissue changes do not appear right away. Blisters develop within 4–8 hours, and the necrosis borders become demarcated several days after the injury. The final severity assessment is conducted dynamically.

2. Why should frostbitten skin not be rubbed?

Rubbing tissues that have lost sensitivity can cause mechanical damage and may result in thermal burns if direct heat sources are used. Ischemia and cell death increase the risk of secondary complications and infections. In such cases, passive warming with warm water or dry heat is the optimal approach.

3. How does the treatment of burns and frostbite differ?

For burns, it is crucial to eliminate the heat source, provide an adequate level of analgesia, and prevent infection. Frostbites require gradual rewarming, restoration of blood flow, and treatment of vascular disorders. In some cases, necrotic tissue may require surgical removal.

4. Is it possible to sustain both a burn and frostbite simultaneously?

In certain clinical situations, particularly when attempting to warm frostbitten tissue improperly with an open flame or hot objects, a thermal burn can be superimposed on frostbitten tissues. This significantly worsens the condition, increases the extent of necrosis, and raises the risk of complications.

5. What complications can arise from nasal burns and frostbites?

Major complications include wound infection, thick scar formation, and deformities of the external nose. In cases of deep burns and frostbites, damage to the cartilaginous framework may occur, potentially leading to chronic breathing difficulties and impaired olfactory function. Additionally, if the nasal mucosa is affected, edema often develops, obstructing nasal breathing and increasing the risk of secondary infection.

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