Annals of Burns and Fire Disasters - vol. XI - n. 3 - September 1998


Faggiano G., De Donno G., Verrienti P., Savoia A.

Centro Ustioni, Ospedale Di Summa, Brindisi, Italy

SUMMARY. Electrical burns have traditionally been considered as distinct from thermal burns. The management of high-voltage electrical burns, in particular, poses certain therapeutic challenges for the surgeon. We present our experiences with a series of such patients admitted to the Burn Unit of Brindisi Hospital (Italy).


Electrical burns occur less frequently than flame or liquid burns, but they give rise to a series of very complex problems. They account for 3-9% of all patients treated in burns centres. Such cases are distinguished as highvoltage burns (over 1000 V) and low-voltage burns (less than 1000 V).
An electric current can cause two types of tissue damage, due to:

  • local generation of heat owing to passing of current (main mechanism)
  • direct action (mechanism not fully understood), probable damage to endothelial membrane

The factors determining the degree of tissue damage are shown in Table I.

Contact time
Pathway of current
Type of current

Table 1 - Factors causing tissue damage

Voltage (V) is the electromotor force generated by a power, while amperage (A) is the intensity of the electric current per unit of time; they are related by the formulae A = V/J and J = IRT. The joule (J) is the heat produced by the current (1) when it meets a resistance (R) during its passage per time unit (T); the resistance depends on the quantity of water in the tissues, water being a good conductor.
The most resistant tissues are bone, followed by fat, tendon, skin, muscle, vessels and nerves (Tables II, III).


Wet skin                   =        1,000 ohm/cm2

Dry skin                    =      10,000 ohm/cm2

Calloused palm skin = 1,000,000 ohm/cm2

Table II - Resistance to passage of current

Table III - Skin resistance

In high-voltage burns the entry point of the current is the area of contact with the electric source; the exit point is often an area of damp skin such as the sweaty areas of the axilla, the sole of the foot, the elbow and the hands.
The severity of the burn is directly proportional to the duration of the contact, although even extremely short exposure to high-voltage current can cause massive tissue damage.
The pathway of the current is unpredictable but usually follows the vessels, as these offer least resistance.
The passage of current from one hand to the other is extremely dangerous because in this case it passes through the thorax, with an elevated rise of cardiac fibrillation.

Material and methods

A retrospective analysis was carried out with regard to four patients suffering from high-voltage electrical burns admitted to our burns centre in Brindisi, Italy, over a oneyear period (Table IV).



Number of



stay (days)













M. M.












Table IV - Patients admitted

All the patients were male; the mean voltage was 15,000 V; the patients were admitted to the burns centre within 3 h of the accident; the current entry point was the lower limbs (two cases), the right thigh (one case), and the right buttock (one case).
The mean burned body surface area was 12%; no patient required cardiovascular resuscitation; all four patients received infusion therapy (Baxter formula); one patient was subjected to fasciotomy of the upper limb, with topical treatment involving use of silver sulphadiazine and salicylic vaseline; and several surgical debridement procedures were performed, with skin graft coverage. One patient, suffering from advanced AIDS, died on day 4; the other three patients were discharged after about 50 days.


In high-voltage burns the body surface involved is often relatively limited, but all the burns are deep, unlike those caused by electric tlash (Figs. 1a, 1b, 2a, 2b).

Fig. la - Electrical burn. Fig. 2a - Electrical bum.

Fig. la - Electrical burn.

Fig. 2a - Electrical burn.

Fig. lb - Electrical burn. Fig. 2b - Electrical bum.

Fig. lb - Electrical burn.

Fig. 2b - Electrical burn.

The skin at the entry point often appears mummified and depressed, with a clear outline due to the rapid evaporation of water. The skin adjacent to the exit point is often ulcerated, with the formation of outwardly oriented craters that conceal deep and severe muscular lesions.
The deep tissues are damaged by the direct action of the heat produced, by progressive devascularization secondary to thrombosis, or by the inevitable infections. In typical cases the muscle is dark in colour, noncontractile, not bleeding: the hand looks as if it has been boiled.
Sometimes a compartment syndrome develops because of massive perilesional oedema, with an increase in cutaneous tension that may exceed 30 mm Hg and a consequent loss of tissue perfusion. In such situations fasciotomy becomes imperative. This is performed along the major axis of the limb, as in escharotomy. The underlying muscle is then inspected, and debridement is thus facilitated. Early debridement of the muscle and necrotic tissue, and if necessary the amputation of nonviable extremities, reduce the risk of infection and the possibility of renal damage due to massive myoglobinuria.
Tissue cleaning may have to be repeated several times; definitive coverage is performed when there is no more devitalized tissue. In our patients coverage was effected on about day 20 using full-thickness autologous skin grafts.
Cardiac complications in this type of patient range from reversible asystoles to systemic hypertension, hypovolaemic shock, and the rupture of aneurysms of large vessels.
Death is often due to acute kidney failure with massive myoglobinuria, to DIC (disseminated intravasal coagulation), or to direct damage caused by the electric current. The central nervous system may be involved either directly or subsequently; the literature contains cases of coma of varying gravity, hemiplagia, aphasia and epilepsy.
Peripheral neuropathies are very frequent as a result of direct damage by the current to the nerve myelin or because of vascular thromboses; these consequences cause irreversible and very incapacitating damage.
The bone structure is also frequently involved in highvoltage electric burns as a result of violent muscular spasms that cause fractures as a result of direct destruction of the bone by heat or devascularization. Hydroclectrolytic hydrating treatment is based on the same principles as those followed in classic flame burns, with the use of Ringer's lactate or hypertonic solutions, except that the quantity of fluid necessary to obtain satisfactory renal and tissue perfusion is approximately double the normal amount, and particular attention has to be paid to the presence of myoglobinuria, which requires a considerable wash-out in order to prevent the precipitation of pigments in the renal tubules.
If this risk is present, an infusion of mannitol maintains a more effective diuresis. There is a high risk of Staphylococcus aureus and Pseudomonas aeruginosa infection in these patients. flowever, wide-range antibiotic prophylaxis is not recommended. Topical therapy with silver sulphadiazine will reduce the bacterial charge.


Our experience in the field of electric burns confirms the absolute priority of appropriate infusion therapy in the first hours post-burn, special care with regard to the current entry point, and early surgical treatment with subsequent skin coverage by means of free grafts or local and distant flaps.


RESUME. Il est tradition de considérer les brûlures électriques comme un problème distinct de celui posé par les brûlures thermiques. La gestion des brûlures électriques causées par la haute tension pose des problèmes thérapeutiques particuliers pour le chirurgien. Les Auteurs presentent leurs expériences avec des patients de ce type traités dans l'Unité de Brindisi (Italie).


  1. Baxter C.R.: Present concepts in the management of major electrical injury. Surg. Clin. North Am., 50: 1401, 1970.
  2. Skoog T.: Electrical injuries. J. Trauma, 10: 816, 1970.
  3. Daniel R.K., Ballard P.A., Heroux P. et al.: High-voltage electrical injury: acute pathophysiology. J. Hand Surg., 13A: 44, 1988
  4. Cabanes J.: Prevention des brGlures 6lectriques. Ann. Medit. Burns Club, 4: 38-41, 1991.
  5. Luce A.E., Gottlieb J.: "True" high-tension electrical injuries. Am. Plast. Surg., 84: 321, 1984.
  6. Zelt R.G., Daniel R., Ballard P. et al.: High-voltage electrical injury: chronic wound evolution. Plast. Reconstr. Surg., 82: 1027, 1988.
  7. Lee R.C., Gottlieb J., Krizak T.: Pathophysiology and clinical manifestations of tissue injury in electrical trauma. Adv. Plast. Reconstr. Surg., 8: 1, 1992.
  8. Luce E.A.: Electrical injury. In: McCartey, "Plastic Surgery", Saunders, Philadelphia, vol. 1, chap. 24.
  9. Logan M.A.: Electrical burned caused by fishing rod contact with overhead electric cables. Burns, 19: 535, 1993.
This paper was received on 25 March 1998.

Address correspondence to:
Dr G. Faggiano
Centro Ustioni, Ospedale Di Summa
Brindisi, Italy.


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