Neonatal spongioform myelinopathy after restricted application of hexachlorophane skin disinfectant.

Anderson, J.; Cockburn, F.; Forfar, J. O.; Harkness, R. A.; Kelly, R W; Kilshaw, B. H.

doi:10.1136/jcp.34.1.25

Cited by 21 publications

(6 citation statements)

References 11 publications

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“…During the 1980s, several papers were published showing that the use of antiseptics such as chlorhexidine on neonatal umbilical stumps delayed the time to cord separation (26,142,227,272). Because of the resulting increase in community midwives' workload due to the delay in cord separation, as well as rare isolated cases of hexachlorophane toxicity causing spongiform myelinopathy after percutaneous absorption (10,237), hospitals have gradually stopped using antiseptic umbilical cord care. This move has occurred despite previous studies demonstrating that the use of antiseptics for cord care is essential for preventing staphylococcal infection and cross-infection in hospitals (47,244).…”

Section: Outbreaks Of Ssssmentioning

confidence: 99%

Clinical, Microbial, and Biochemical Aspects of the Exfoliative Toxins Causing Staphylococcal Scalded-Skin Syndrome

et al. 1999

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SUMMARY The exfoliative (epidermolytic) toxins of Staphylococcus aureus are the causative agents of the staphylococcal scalded-skin syndrome (SSSS), a blistering skin disorder that predominantly affects children. Clinical features of SSSS vary along a spectrum, ranging from a few localized blisters to generalized exfoliation covering almost the entire body. The toxins act specifically at the zona granulosa of the epidermis to produce the characteristic exfoliation, although the mechanism by which this is achieved is still poorly understood. Despite the availability of antibiotics, SSSS carries a significant mortality rate, particularly among neonates with secondary complications of epidermal loss and among adults with underlying diseases. The aim of this article is to provide a comprehensive review of the literature spanning more than a century and to cover all aspects of the disease. The epidemiology, clinical features, potential complications, risk factors, susceptibility, diagnosis, differential diagnoses, investigations currently available, treatment options, and preventive measures are all discussed in detail. Recent crystallographic data on the toxins has provided us with a clearer and more defined approach to studying the disease. Understanding their mode of action has important implications in future treatment and prevention of SSSS and other diseases, and knowledge of their specific site of action may provide a useful tool for physiologists, dermatologists, and pharmacologists.

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Section: Outbreaks Of Ssssmentioning

confidence: 99%

Clinical, Microbial, and Biochemical Aspects of the Exfoliative Toxins Causing Staphylococcal Scalded-Skin Syndrome

et al. 1999

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“…Optic nerve vacuolization was seen in all bromethalin-dosed cats (cat Nos. [1][2][3][4][5]. Axons in vacuolated areas were normal when stained with hematoxylin and eosin and by Bodian's method.…”

Section: Methodsmentioning

confidence: 99%

Neuropathologic Findings of Bromethalin Toxicosis in the Cat

1992

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Abstract. Ten random source male domestic shorthair cats, 2 to 6 years old and 3.0-4.4 kg body weight, were each given a single oral dose (1.5 mg/kg) of bromethalin (cat Nos. 1-5) or bait vehicle carrier (cat Nos. 6-10). Bromethalin-dosed cats developed a toxic syndrome characterized by ataxia, focal motor seizures, vocalization, decerebrate posture, decreased conscious proprioception, recumbency, depression, and semicoma. Bromethalin-dosed cats were euthanatized if seizure activity or hindlimb paralysis developed. Survival times were 48 hours (cat No. l), 89 hours (cat No. 2), 90 hours (cat No. 3), and 97 hours (cat No. 4). Control cats (cat Nos. 6-10) and one bromethalin-dosed cat (cat No. 5 ) were euthanatized on day 20 after dosing. Spongy change (edema-characterized by the formation of vacuoles in extracellular spaces and myelin lamellae), hypertrophied fibrous astrocytes, and hypertrophied oligodendrocytes were observed in the white matter of the cerebrum, cerebellum, brain stem, spinal cord, and optic nerve of all bromethalin-dosed cats. Spongy change occasionally extended into contiguous cerebellar Purkinje cell layer and cerebral cortical gray matter. The severity of lesions varied among cats but was most pronounced in cat No. 5 (480 hours after dosing). A leukocytic inflammatory response, gitter cell (macrophage) response, or axonal degeneration was not observed in the vacuolated areas. Ultrastructural findings included separation of myelin lamellae at the interperiod lines with the formation of intramyelinic vacuoles (intramyelinic edema), rupture and coalescence of intramyelinic vacuoles into larger extracellular spaces (spongy change), and pronounced cytosolic edema of astrocytes and oligodendroglial cells. MO), and Trounce@ (Agricultural Feeds, St. Louis, MO). Bromethalin and its primary N-demethylated metabolite (desmethylbromethalin) are effective uncouplers of oxidative p h o s p h o r y l a t i~n .~J~*~~ Uncoupling of this reaction may result in a lack of adequate adenosine 5'-triphosphate and diminished sodium and potassium adenosine 5'-triphosphatase-dependent ion channel pump activity. Bromethalin also induces lipid peroxidation in the brain of rats.7 Cerebral edema and elevated cerebrospinal fluid pressure develop in lethally poisoned dogs and rat^.^.^ Bromethalin-based rodenticides are highly neurotoxic to cats. Experimentally induced bromethalin toxicosis in the cat develops within 2 to 7 days of dosing and is characterized clinically by the development of hindlimb ataxia, paresis, paralysis, central nervous system depression, tremors, and decerebrate posture, as well as focal and generalized seizure^.^ A spontaneous case of bromethalin toxicosis in the cat was r e~0 r t e d . l~ This cat had progressive depression, ataxia, extensor rigidity, and opisthotonus associated with diffuse white matter vacuolization. Dogs and rats given bromethalin also developed diffuse spongy degeneration of the white matter that was characterized ultrastructurally as intramyelinic edema.10,29Other toxic caus...

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“…Huge, well documented, progressive improvements in neonatal outcomes have been interspersed with multiple setbacks. These disasters have included: an epidemic of retinopathy of prematurity due to unregulated administration of oxygen [1], followed by an increase in cerebral palsy rates when oxygen therapy was too severely restricted [2]; the grey baby syndrome from the use of chloramphenicol when no adequate pharmacokinetic studies had been performed [3]; a gasping syndrome from the use of untested bacteriostatic chemicals in flush solutions [4]; and a neurological syndrome due to bathing infants with hexachlorophene and its unexpected absorption through the skin [5]. All of these disasters have the common underlying cause of introducing therapies into the care of the most fragile of patients without adequate investigation of their potential harm.…”

Section: Introductionmentioning

confidence: 99%

The adverse neuro-developmental effects of postnatal steroids in the preterm infant: a systematic review of RCTs

2001

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BackgroundRecent reports have raised concerns that postnatal steroids may cause neuro-developmental impairment in preterm infants. This systematic review was performed with the objective of determining whether glucocorticoid therapy, to prevent or treat bronchopulmonary dysplasia, impairs neuro-developmental outcomes in preterm infants.MethodA systematic review of the literature was performed. Medline was searched and articles retrieved using predefined criteria. Data from randomized controlled trials with adequate neuro-developmental follow up (to at least one year) were entered into a meta-analysis to determine the effects of postnatal treatment of preterm infants with glucocorticoids. Cerebral palsy rates, and neuro-developmental impairment (developmental score more than 2SD below the mean, or cerebral palsy or blindness) were analyzed. The studies were divided into 2 groups according to the extent of contamination of the results by treatment of controls with steroids after the initial study period, those with less than 30% contamination, and those with more than 30% contamination or size of contamination not reported.ResultsPostnatal steroid therapy is associated with an increase in cerebral palsy and neuro-developmental impairment. The studies with less contamination show a greater effect of the steroids, consistent with a real direct toxic effect of steroids on the developing central nervous system. The typical relative risk for the development of cerebral palsy derived from studies with less than 30% contamination is 2.86 (95% CI 1.95, 4.19). The typical relative risk for the development of neuro-developmental disability among followed up infants from studies with less than 30% contamination is 1.66 (95% CI 1.26, 2.19). From this subgroup of studies, the number of premature infants who need to be treated to have one more infant with cerebral palsy (number needed to harm, NNH) is 7; to have one more infant with neuro-developmental impairment the NNH is 11.ConclusionsPostnatal pharmacologic steroid treatment for prevention or treatment of bronchopulmonary dysplasia is associated with dramatic increases in neuro-developmental impairment. As there is no clear evidence in the literature of long term benefit, their use for this indication should be abandoned.

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Neonatal spongioform myelinopathy after restricted application of hexachlorophane skin disinfectant.

Cited by 21 publications

References 11 publications

Clinical, Microbial, and Biochemical Aspects of the Exfoliative Toxins Causing Staphylococcal Scalded-Skin Syndrome

Clinical, Microbial, and Biochemical Aspects of the Exfoliative Toxins Causing Staphylococcal Scalded-Skin Syndrome

Neuropathologic Findings of Bromethalin Toxicosis in the Cat

The adverse neuro-developmental effects of postnatal steroids in the preterm infant: a systematic review of RCTs

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