General information

Hexachlorophene has been extensively used as an ingredient of innumerable kinds of consumer goods and medical formulations. Since 1961, when it was reported that daily bathing of newborn infants with a 3% hexachlorophene suspension prevented colonization of the skin by coagulase-positive staphylococci, hexachlorophene has been widely used in hospital nurseries.

However, hexachlorophene readily penetrates excoriated or otherwise damaged skin and absorption through intact skin has also been described. The most dramatic complication reported was due to accidental use in talcum powder in neonates, with neurological and other features and many deaths [ ]. Since then there has been reticence to use hexachlorophene in young infants at all, and certainly the customary 3% emulsion is too strong [ ].

As a result of investigations of the toxicity of hexachlorophene in animals and reports of accidental intoxication in France, the FDA in 1972 banned all non-prescription uses of this drug, restricting hexachlorophene to prescription use only, as a surgical scrub and hand-wash product for health-care personnel. Hexachlorophene was excluded from cosmetics, except as a preservative in concentrations not exceeding 0.1%. Other countries followed suit. An extensive critical review of hexachlorophene is given by Delcour-Firquet [ ].

Organs and systems

Respiratory

  • Occupational asthma occurred in a pediatric nurse who had worked with hexachlorophene for 15 years [ ]. The initial symptom was rhinitis but at the time of diagnosis she also had attacks of asthma.

Nervous system

Neurotoxicity has been observed after dermal application of hexachlorophene to large areas of burned or otherwise excoriated skin, after accidental application of extremely high concentrations on intact skin, and after ingestion. If hexachlorophene is applied in high concentrations or at frequent intervals to the intact skin, excoriation will result, increasing the risk of systemic effects.

In animals, there is a clear relation between dosage, blood concentrations, duration of treatment, and morphological and functional disturbances of the nervous system. In the lower dose range, there is unequivocal histological evidence of neurotoxicity, but without symptoms of neurotoxicity [ ].

Five Chinese patients aged 14–39 years were treated for Conorchiasis sinensis infection with oral hexachlorophene 20 mg/kg for 5–6 days [ ]. They developed nausea, vomiting, diarrhea, abdominal pain, general muscle weakness, and soreness in the eyeballs and legs. Of eight children treated similarly, one became comatose on the fourth day, with temporary loss of light reflex, alternating dilatation and contraction of the pupils, and positive cerebrospinal tract signs; the fundus showed papillary edema; recovery followed symptomatic treatment. [ ]

In experimental animals, hexachlorophene can cause cerebral edema [ ], and occasional cases have also been reported in humans [ ]. It affects exclusively the white matter of the brain and spinal cord and produces a spongiform encephalopathy, transforming the white matter into an extensive network of cystic spaces lined by fragments of myelin. Electron microscopy shows intramyelinic edema, with splitting and separation of the myelin lamellae. Nerve damage due to hexachlorophene appears to be reversible, although it takes many weeks for all the holes in the white matter to disappear. However, extensive edema occurring within a rigid structure such as the spinal canal can result in infarction of nervous tissue. In one study of all premature infants who weighed under 1400 g at birth and who survived at least 4 days, there was a significant association between repeated whole-body bathing in 3% hexachlorophene soap (undiluted pHisoHex) and a vacuolar encephalopathy of the brainstem reticular formation [ ].

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