Intra-Arterial Calcium Gluconate Treatment After Hydrofluoric Acid Burn of the Hand
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Hydrofluoric acid (HF) is a colorless corrosive acid used in different industrial branches. Exposure to HF typically results from spills, and most often the hand or fingers are involved. Tissue damage through cutaneous HF exposure occurs through corrosive burns due to the free hydrogen ions and through skin penetration of the fluoride ions, causing a depletion of calcium in the deep tissue layers, ultimately leading to cell death and tissue necrosis. Treatment of HF burns consists of thoroughly flushing the exposed area with water and applying calcium gluconate gel to the skin. If topical treatment does not suffice, subcutaneous injections, as well as intravascular—both intravenous and intra-arterial—calcium gluconate therapy, have been advocated. We report for the first time a case of HF burn of the hand and digits associated with vasospasm. Pain and vasospasm were successfully treated by repeated intra-arterial calcium gluconate injection. We conclude that intra-arterial calcium gluconate injection is a successful and well-tolerated therapy for HF burn associated with Raynaud’s syndrome. Intra-arterial injection allows for well-controlled delivery of therapy as well as assessment of the vascular status.
KeywordsIntra-arterial therapy Acid burns
Hydrofluoric acid (HF) is a colorless, highly corrosive acid widely used in different industrial fields. Highly concentrated HF is typically used for glass and computer chip etching and in the petroleum industry. Additionally, it can be found at lower concentrations in various household products such as rust removers and aluminum brighteners.
Exposure to HF typically results from spills or splashes, and most often the hand or fingers are involved. Tissue damage through cutaneous HF exposure occurs through two distinct mechanisms . Typical corrosive burns due to the free hydrogen ions produce a stinging, burning pain briefly after exposure, which may be accompanied by erythema, focal edema, or more overt burn signs if the acid was highly concentrated. However, especially in the case of exposure to low-concentration HF (e.g., 20%), patients will seek medical attention after a symptom-free interval (18–24 h) following a delayed onset of symptoms. In these cases no significant skin injury is apparent. However, the fluoride ions easily penetrate the horny layer of the skin and move into deeper tissues. Here they complex with bivalent cations (primarily calcium and, to a lesser extent, magnesium), causing a depletion of calcium. This in turn alters electrical membrane function and impairs cellular metabolism, ultimately leading to cell death, resulting in liquefaction necrosis.
Immediate treatment of HF burns consists of thoroughly flushing the exposed area with water and applying calcium gluconate gel to the skin in an attempt to neutralize the fluoride ions before they penetrate to deeper tissue layers. Often topical treatment alone does not suffice to prevent deeper tissue damage. In this case subcutaneous injections as well as intravascular—both, intravenous (Bier’s block) and intra-arterial (i.a.)—calcium gluconate therapy have been administered in cases where topical therapy did not prevent the progression of poisoning [2, 3, 4, 5, 6].
We report a case of low-concentrated HF burn of the hand and digits associated with vasospasm, which was successfully treated by i.a. calcium gluconate injection. To our knowledge, Raynaud’s syndrome in all affected fingers as in this case has not been described previously to occur with an HF burn.
The catheter was removed, but the sheath left in place and intravenous heparin continued. Within the next 6 h the pain in the right hand returned, although there was no recurrence of vasospasm. Therefore local i.a. calcium gluconate infusion was continued for another 4 h, at an identical dosage and catheter position. The arterial sheath was eventually removed after another 8-h pain-free interval, and the patient was discharged from hospital after normalization of the PTT value. Repetitive blood test showed normal electrolyte values during the entire hospital stay. Calcium overload due to calcium gluconate infusion was not observed. An X-ray of the patient’s hand showed no signs of atopic calcification. Motor and sensor neurography were performed before patient discharge and were normal. Two months after discharge the patient was contacted again and asked about her hand. She reported occasional dysesthesia and numbness of her hand following prolonged manual labor, but no pain or discomfort during normal use.
HF burns present with a variety of symptoms that are mostly related to the two mechanisms through which the substance exerts its deleterious effects on tissue: first, the actual burn through the hydrogen ions and, second, the tissue damage and necrosis due to the calcium deprivation related to tissue penetration of fluoride ions. The predominant effect and presentation of symptoms depend on a number of factors such as the concentration of HF, duration of contact, time to local treatment, and kind of initial treatment (i.e., thorough rinsing, local calcium gluconate gel) as well as the location of the injury.
In this respect the presented case is exemplary. Because of the brief exposure and immediate optimal treatment as well as the rather low concentration of HF, no relevant signs of chemical burn were apparent on the patient’s skin at the time of presentation at the ED. Only a slight paleness of the exposed skin was found, and no hemorrhage or vesicles were present. This finding was in sharp contrast to the increasing stinging pain experienced by the patient as a result of the tissue penetration of fluoride ions and the subsequent calcium depletion. As has been described previously, perfusion of the affected tissue with 10% or 20% calcium gluconate is the most effective therapy for HF related burns [3, 4, 5, 6, 7, 8]. Following the drug’s package insert, slow infusion of calcium gluconate is warranted (i.e., >3 min/10 ml 10% calcium gluconate for i.v. use; Calcium-Sandoz; Sandoz Pharmaceuticals, Germany) to avoid calcium deposition in soft tissue. However, in the case of HA burns, only slow perfusion rates are needed, and calcium deposition or other side effects, even after repeated i.a. injection, have not been reported [4, 5]. The recommended dosage for i.a. delivery varies between 10 and 20 ml of 10%calcium gluconate or 10 ml of 20% calcium gluconate in 40–50 ml of 5% dextrose or 40–50 ml of 0.9% NaCl over 4 h, according to the literature and poison control centers [4, 5, 6, 7]. As an alternative to i.a. infusion, tissue perfusion may be accomplished indirectly by intravenous administration of calcium gluconate using a Bier Block technique or local subcutaneous infiltration [2, 3, 4, 5, 6, 7, 8]. Of these, the Bier Block technique is the less invasive. Using this technique an intravenous cannula is placed on the dorsum of the affected hand. The veins are exsanguinated by elevation and torniquet technique. During infusion a double-cuffed pneumatic torniquet is inflated and placed above the elbow, resulting in ischemia of the effected extremity. Ischemia is maintained for about 25 min. This therapeutic approach, however, is associated with relevant discomfort. Also, 25 min may not be long enough for all free fluoride ions to be bound, and final treatment failure, where only i.a. injection could successfully relieve the patient’s pain, has been reported . Both therapies were compared in a porcine model and both were found to be effective, with a trend to lesser burn depth for the i.a. therapy . Repeated local calcium infiltrations have been advocated by some authors . However, intradermal and subcutaneous injections are painful, the amount of calcium delivered is limited, and the technique is impracticable in the digits, where subcutaneous tissue space is small and may be edematous from early HF exposure. The apparent ischemia of the patient’s fingers was a compelling reason to choose an i.a. approach in our case. Because it was unclear what exactly had caused the ischemia, and i.a. therapy seemed to be the best method to treat the burn, no other option was considered in our case. Raynaud’s syndrome in all affected fingers as in this case has not previously been described to occur with an HF burn. To our knowledge, only one report of angiographic findings in digital HF burns has been published to date . The authors describe increased local perfusion in burned fingers, comparable to the mild hyperemia we observed in two of the five exposed fingers 4 h after calcium gluconate therapy. They argue that the increased perfusion may be related to a nonspecific local inflammatory response or the deprivation of calcium directly inducing vasodilation of the respective blood vessels. They found a vascular defect in just one patient’s finger tip, ultimately requiring surgical debridement. It remains unclear, though, whether the vascular defect was due to preexisting necrosis or was the cause thereof. Physiologically the reason for Raynaud’s syndrome in our patient remains unclear. It may have been caused by pain-related stress, as direct effects of the fluoride ions and subsequent calcium deficit are not very likely to be the reason. On the other hand, no Raynaud’s syndrome was apparent at the time of the second infusion, when the pain had returned to the patient’s hand and fingers. Exposed tissue, if not showing a full-thickness burn, will appear rather pale after the first symptoms of a chemical burn have ceased and by the time deep tissue pain caused by fluoride ions develops. This, in fact, may be a symptom of local vasoconstriction as well but, again, cannot be fully explained by the effect of the fluoride ions. However, both he syndrome and the paleness completely resolved with the i.a. calcium injection, as has been described previously in the case of paleness .
In conclusion, i.a. calcium gluconate injection was a successful and well-tolerated therapy for HF burn associated with Raynaud’s syndrome. Repeated i.a. injection allowed for well-controlled delivery of therapy as well as assessment of vascular status and therapy response in our patient.
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