Severe metabolic acidosis following assault chemical burn.

Assault chemical burns are uncommon in northern Europe. Besides local toxicity, systemic manifestations are possible after strong acid exposure. A 40-year-old woman was admitted 1 h after a criminal assault with sulfuric acid. The total burned surface area was 35%, third degree. Injury was due to sulfuric acid (measured pH 0.9) obtained from a car battery. Immediate complications were obstructive dyspnea and metabolic acidosis. The admission arterial pH was 6.92, with total bicarbonate 8.6 mEq/l and base deficit 23.4 mEq/l. The correction of metabolic acidosis was achieved after several hours by the administration of bicarbonate and lactate buffers. The patient developed several burns-related complications (sepsis and acute renal failure). Cutaneous projections of strong acids may cause severe metabolic acidosis, particularly when copious irrigation and clothes removal cannot be immediately performed at the scene.

INTRODUCTION

Assault chemical burns are uncommon in northern Europe as compared with Africa or Asia.[1-4] Besides extensive skin lesions leading to functional and aesthetic sequelae, projection of strong acids such as sulfuric acid may also cause severe metabolic disturbances requiring aggressive resuscitation.

CASE REPORT

A 40-year-old (45-kg weight) previously healthy woman was admitted to the intensive burn care unit approximately 90 min after an assault chemical burn following conjugal violence. The total burned surface area was estimated at 35% (neck, face, head, arms, thorax, abdomen, and left leg), third degree [Figure 1]. There were severe bilateral eyes and ears lesions. Injury was due to sulfuric acid (battery acid, pH measured at 0.9). As the patient and relatives were in panic, irrigation with water was not performed at the scene of the accident but was started immediately after the arrival in the burn center. The emergency medical team began fluid resuscitation (Parkland's formula), and orotracheal intubation was performed on-site after evidence of the severity of facial burns. The patient was sedated for hospital transfer and presented the following vital signs: arterial blood pressure 70/30 mmHg, pulse 110 bpm, SpO2 >90% with normal lung auscultation.

Figure 1

Admission examination with third-degree caustic lesions extending to the neck (incisions), trunk, and arms

The admission electrocardiogram and chest X-ray examination did not reveal significant abnormalities. Laboratory investigations mainly revealed a profound metabolic acidosis with a pH at 6.92, PaCO2 42 mmHg, total bicarbonate 8.6 mEq/l, base deficit 23.4 mEq/l, sodium 148 mEq/l, potassium 4.1 mEq/l, chloride 117 mEq/l, calcium 6.1 mg/dl, and phosphorus 15.1 mg/dl. The lactate level was within the normal range: 1.7 mmol/L. Renal function was initially preserved (serum creatinine 0.83 mg/dl), with no evidence for rhabdomyolysis. Blood coagulation tests on admission were disturbed, with fibrinogen 117 mg/dl, activated partial thromboplastin time (APTT) 69 s, and International Normalized Ratio (INR) 2.23. Platelets count was 169 000/mm3. Metabolic acidosis was progressively corrected by the administration of a total of 300 mmol of sodium bicarbonate over 14 h and of 140 mmol of lactate from Hartmann's solution over the first 24 h Table 1. The adjustment of the ventilator settings was complicated by the progressive development of a thoracic rigidity secondary to the chemical burns.

Table 1

Evolution of blood gas analysis from admission and correction with bicarbonate buffer

During the ICU stay, the patient developed several complications. Mechanical ventilation was required for 40 days, and a percutaneous tracheostomy had been performed after 1 month. The hemodynamic condition required mild inotropic support (maximal dose of dobutamine, 5 μg/kg/min) for a period of 15 days. Echocardiography demonstrated a moderate alteration of the left ventricular function. While urine output was maintained during the first week, continuous venovenous hemofiltration had to be started after this interval and was continued for 7 weeks. The patients also developed multiple episodes of wound-related sepsis treated by adapted antimicrobial therapy. In addition, iterative surgery was required with a total of 15 procedures for excision and grafting. After 5 months, the patient left the intensive care unit for rehabilitation.

DISCUSSION

According to a recent systematic review, the annual incidence of severe burns in Europe (1985-2009) was 0.2 to 2.9/10 000 inhabitants, with a predominance of male patients younger than 16 years.[1] Flames, scalds, and contact burns were the most prevalent causes in the total population. Chemical burns were less frequent than electrical burns, and when they occurred, they were mainly encountered after accidental professional exposure. While the major risk factors for death are older age and total percentage of burned surface area after severe burns from all origins, no specific prognostic factors exist for chemical burns.[1]

Assault chemical burns are uncommon in northern Europe in comparison with Africa or Asia.[2-4] There is a predominance of female victims in the case of aggression, mainly after domestic disputes.[4] After an assault chemical burn, the face, head, and neck are predominantly injured but extension to the trunk and upper limbs is not rare. The physical and psychological outcomes are usually poor, with disfigurement, loss of vision, and requirement for a long series of surgical interventions.

As it appears inexpensive and readily available from exhausted automobile batteries, sulfuric acid is one of the agents most often involved in acid burns.[5] In the present observation, the chemical agent was analyzed in a specialized military laboratory, which confirmed the nature of the agent and the extremely low pH measured at 0.9. It appeared that the aggressor had collected the total content of a car battery. Sulfuric acid and its precursor sulfur trioxide cause injury by inducing dehydration damage and by creating excessive heat in the tissues. The result is the development of necrotic coagulation eschars with thrombus formation in the lesion's microvasculature.[6]

The immediate management of a chemical burn relies on the removal of agent from contact with the patient. However, minimal literature on the science of decontamination of sulfuric acid exposure exists.[7] Early treatment suggested in the literature is controversial and is not always supported by experimental data. In a paper published in 1974, Jelenko stressed that water lavage should be avoided in sulfuric acid burns due to the propensity of the agent to produce an exothermic reaction on contact with water.[89] He suggested neutralization with magnesium oxide, lime water, or soap. Lime water is an aqueous solution of calcium hydroxide. Theoretically, irrigation with lime water could offer the possibility to neutralize sulfuric acid while minimizing exothermic reactions. The reaction between sulfuric acid and lime water should be written as follows:

H2SO4 + Ca(OH)2 -> CaSO4 + 2 H2O

The only experimental study that focused on sulfuric acid appeared in 1927.[10] Water lavage was superior to neutralization with sodium bicarbonate in the treatment of 96% sulfuric acid burns in rats. With 50% and 25% sulfuric acid, there was no difference between the rats treated by neutralization or with pure water.

No recent experimental data, however, suggest that neutralizing agents should be effective and safe. Therefore, immediate copious irrigation with tap water seems essential as the only early treatment. Penner evaluated the in vitro dilution of concentrated sulfuric acid with water and found an instantaneous increase in temperature. If the amount of water was increased 20-fold, the temperature increase was less, encouraging larger volumes of a neutralizing solution to minimize the temperature changes.[11]

CONCLUSION

This observation emphasizes the possibility of severe systemic toxicity after dermal exposure to some agents. This has been well demonstrated with hydrofluoric acid causing hypocalcemia and ventricular fibrillation or for formic acid and intravascular hemolysis. As assault sulfuric acid burns mainly occur in countries with a limited access to primary emergency care, the exact occurrence of severe metabolic acidosis with such an agent is not precisely known but should be suspected according to the nature of the product, the duration of exposition, and the extent of the lesions. In the present observation, the severity of the metabolic acidosis was also related to the absence of the initial irrigation.