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Hydrogen fluoride (HF) is a relatively weak and poorly dissociated acid. It is used widely in industry in concentrated solutions (>20%) for glass and computer chip etching, petroleum processing, and fluoridated hydrocarbon production. Other forms of fluoride are available such as ammonium bifluoride used in solder fluxes and rust removers. These have the potential to be as toxic as the acid form of HF.
Products containing less concentrated HF (6–10%) are freely available to the public for use as rust removal agents and aluminium and chrome cleaning solutions.
The most common sites for exposure are the hands and digits of individuals working with HF. Immediate tissue damage is mild unless the solution is concentrated or there has been a prolonged tissue contact time.
Tissue damage results primarily from the fluoride ion which complexes with intracellular divalent cations, resulting in cell death.
Several pathologic mechanisms may be involved in both local and systemic fluoride poisoning.
Oral absorption is very rapid.
Dermal absorption is also rapid but the rate of onset of symptoms correlates with the concentration of HF. Exposure to > 3% body surface area has the potential to produce systemic hypocalcaemia.
With oral ingestions or dermal exposures that are either large in area or high in concentration, significant hypocalcaemia, hypomagnesaemia, and hyperkalaemia may occur as well as metabolic acidosis.
Secondary to local hypocalcaemia, hypomagnesaemia or hyperkalaemia in cardiac myocytes as well as systemic electrolyte abnormalities.
Upper airway damage and pulmonary oedema can occur after inhalational exposure.
Oral ingestions may result in corrosive damage to the oesophagus and stomach.
In cases of isolated digital exposure to HF it is unlikely that systemic toxicity will result.
In cases where there is more than 3% body surface area exposure to HF the following investigations are indicated.
Systemic exposure resulting in hypocalcaemia or hyperkalaemia: think of other causes of these electrolyte abnormalities.
In dermal exposure the presence of delayed onset of pain at the exposure site out of proportion to the local clinical findings does not occur with any other acid or caustic substance. It is virtually pathognomonic of HF exposure.
Differences in toxicity are virtually always due to differences in HF concentration.
All oral ingestions should be considered potentially fatal regardless of concentration.
Patients with dermal exposures to low concentrations < 10% may present late with pain (i.e. more than 8 hours following the exposure). These patients are at low risk of death. Diagnosis may be problematic in these cases as there are few clinical signs and severe local pain. Patients may not ascribe the presenting clinical features with recent use of HF.
Always suspect HF exposure when severe local pain out of proportion to any physical signs is present. Little or no evidence of dermal damage may be present in the early post-exposure phase.
Patients who develop local pain at the dermal exposure site within 30 minutes of exposure should be assumed to have had an exposure to a high concentration of HF (>20%) and are therefore at greater risk of early tissue damage.
Patients exposed to HF with a concentration greater than 20% should be considered at high risk of tissue damage regardless of the extent of exposure.
Treatment is based around preventing ongoing absorption and aggressive correction of electrolyte abnormality.
Correction of hypocalcaemia, hypomagnesaemia and hyperkalaemia.
Correct any significant acidosis.
Aspirate gastric contents if recent (< 1 hour) oral exposure.
For dermal exposures remove clothes and wash area with water or normal saline.
Ophthalmic exposures should be irrigated copiously with water or normal saline or Hartmann's solution. Early referral to ophthalmologist is available. Consider the addition of small amount of Ca gluconate to the irrigating fluid (e.g.. 10 mL of 10% Ca gluconate in 1 litre of N/saline). Calcium solutions should not be applied directly to the eye as these may be directly toxic to the cornea.
Recently, hexafluorine (Prevor, France) has been marketed for HF eye and skin decontamination. There is limited information available on efficacy and some studies show less effect than calcium gluconate gel (Höjer et al, 2002).
Treatment of HF acid cutaneous burns remains a therapeutic challenge.
Local chelation of fluoride ions with exogenously supplied divalent cations such as calcium gluconate or magnesium sulphate is accepted current therapy. Calcium and magnesium salts have been delivered by a number of methods including: topical gel, intradermal or subcutaneous infiltration, and intra-arterial infusion. Each method has limitations and possible adverse effects.
Calcium currently appears to be the most commonly used cation for chelation. Intra-arterial magnesium may result in increased tissue damage.
Topical application (calcium gel)
Topical application of calcium or magnesium salts may result in chelation of only the most superficial cutaneous fluoride ions and is often ineffective when more concentrated solutions are implicated in the exposure.
Intradermal and subcutaneous injections of calcium gluconate
Intradermal and subcutaneous injections are painful and the amount of calcium delivered is limited.
The technique may be impractical at digital sites where the subcutaneous tissue space is small and may already exhibit oedema from chemical exposure. While nail removal and local infiltration of calcium intradermally may be required for subungual exposures it is no longer be seen as first line therapy for digital exposures. Palmar fasciotomy has been advocated for fingertip exposures to prevent high tissue pressures.
Intradermal infiltration for exposures to the trunk or more proximal sites on the limbs may be the only option for these sites.
Regional-ischaemic intravenous infusion of calcium gluconate
Regional-ischaemic intravenous infusion of calcium gluconate using a Bier block technique has been reported to successfully abolish the pain from HF exposures to the hands in two case reports and one case series. This technique is simple, does not require arterial line placement, and is less invasive than local dermal infiltration or intra-arterial (IA) therapy.
The case series only showed a 60% success rate with this technique with less success seen following high concentration HF (> 20% concentration) exposures to the digits.
Regional IV calcium infusion may be better suited to lower HF concentration exposures or as a temporising measure for higher concentration exposures if there will be a delay to IA line placement.
Regional infusion dose
Intra-arterial infusion of calcium gluconate
Intra-arterial infusion of calcium gluconate is currently the gold-standard therapy for HF exposures to the digits. It requires the placement of either a radial, ulnar, or brachial arterial line.
Previously reported complications of arterial puncture include arterial vasospasm, median and ulnar nerve palsies from haematoma accumulation at the puncture site, arterial dissection, and carpal tunnel syndrome.
Up to ten consecutive four-hour intra-arterial infusions have been safely administered to patients for ongoing pain from HF exposure.
Intra-arterial infusion dose
An arterial transducer should be connected to a 3-way valve in the circuit so that the arterial wave form may be checked every 30-60 minutes to ensure that the arterial line is fully patent.
All digital exposures should be reassessed at 24 hours following successful therapy for evidence of tissue loss as this may take 24-48 hours to become evident.
Referral to a hand surgeon should be considered in any cases where there is evidence of necrosis or tissue loss.
In most cases, where adequate early therapy with calcium has been instituted, a favourable outcome can be expected with minimal or no tissue loss.
Be wary of patients who present late or are exposed to high concentrations of HF as these are more likely to result in tissue loss and require surgical referral.
Dr Rama Rao New York Poisons Centre Hydrofluoric Acid07.ppt
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