monochloroacetic acid

Also found in: Dictionary, Encyclopedia.

monochloroacetic acid

; CH3ClCOOH; monochlor strongly caustic and keratolytic topical agent used to destroy skin lesions, e.g. verrucae (see Table 1 and Table 2); application typically causes pain (pain develops typically ~48 hours after application, and subsides 4–5 days after application); it may be applied as a saturated solution directly to an unmasked lesion, or as a tiny crystal (approximate size of salt grain) strapped directly to a masked lesion (see mask (2)), or as a tiny crystal embedded in 40–70% salicylic acid contained in a cavitied felt pad applied over a masked lesion; has a deeply penetrating action and must be used with caution (i.e. not suitable for lesions overlying bony prominences, involving the nail apparatus, or in patients with reduced fibrofatty padding, peripheral vascular disease or diabetes); patients must be advised of likely effects (e.g. pain, deep action) and appreciate that the dressing must be kept dry and in situ, and reattend in 3–7 days; see Table 3
Table 1: Factors that should be considered in the use of chemical cauterizing agents to destroy verrucae
Lesion siteSuperficial lesion, non-weight-bearing skin – use liquid caustics
20% salicylic acid in collodion
Trichloroacetic acid, saturated solution (+75% sliver nitrate)
Deeper lesion, weight-bearing skin, good fibrofatty padding – either liquid or solid caustics
Monochloroacetic acid, saturated solution
40–70% salicylic acid ointment
Number and size of lesionsLarge lesions: ointment-based caustics
40–70% salicylic acid ointment Smaller and satellite lesions: caustic solutions
Alternating layers of trichloroacetic acid, saturated solution and 75% silver nitrate
Skin textureSweaty or hyperhidrotic skin
Padding cannot be retained in situ
Fair skin or atopic individuals; atrophic or dry skin
Tend to overreact/undergo tissue breakdown, to applied caustics
CirculationReduced arterial supply (diabetes, atherosclerosis)
Caustics may cause ulceration or predispose to infection as healing response is depressed (use astringents or mild keratolytics)
Impaired venous or lymphatic drainage (oedematous tissues)
Avoid strong caustics (use astringent agents or mild keratolytics)
NeuropathyImpaired pain awareness (as in diabetic neuropathy)
Do not use caustics (use astringents or mild keratolytics)
AvailabilityStrong acids should not be used unless both practitioner and patient are available for emergency appointments
Caustics may not be treatment of choice if patient cannot return weekly for ongoing treatments (consider a ‘one-off’ treatment, e.g. cryotherapy)
Opt for self-applied milder, topical ongoing treatments, if in patient's best interests
AgeStrong caustics should be avoided in young patients with a low pain threshold
Caustics that require padding to be retained in situ between treatments may be contraindicated in patients who cannot keep foot dry (e.g. swimmers)
Previous treatmentsIt is pointless continuing with a treatment that has already proved to be ineffective, or has caused an adverse reaction
Single treatmentsVerrucae pedis do not often respond to a single treatment, but methods include:
• Cryotherapy (application of liquid nitrogen, optimally every 3 weeks; ice ball must extend beyond lesion edge; contraindicated in patients with peripheral vascular disease)
• Electrosurgery (peripheral tissues must also be removed in order to clear all virally infected cells; requires local anaesthesia; contraindicated in patients with peripheral vascular disease or those with an indwelling pacemaker)
Alternative treatmentsAlternative treatments may be indicated for cases that have not responded to other forms of treatment: many of these therapies have not been tested by formal research
Thuja tincture: painted on lesion once or twice a day
Kalanchoe leaves: fleshy leaves split open and fleshy pulp left in situ on lesion; changed every 24–48 hours
Tea tree oil: painted on lesion daily, and covered
Banana skin: small piece of banana skin cut to size of lesion and strapped in place, pith side against lesion; changed every 24–48 hours
Table 2: Keratolytic and caustic agents
Keratolytic/caustic agentIndicated use
Whitfield's ointment (3% salicylic acid and 6% benzoic acid in white soft paraffin)Treatment of mild tinea pedis
5% salicylic acid ointmentApplied daily for 7 days to soften hyperkeratosis and facilitate its removal
12% salicylic acid in collodionMacerating agent; painted over callosity and left in situ for 7 days, to assist removal of heavy callosity
20–40% salicylic acid plasterApplied topically and left in situ for 1–2 days to aid removal of corns
40–70% salicylic acid ointmentApplied topically in a cavitied pad and left in situ for 7 days for verruca treatment; the lesion should be masked
Calmurid cream (10% urea)To hydrate anhidrotic skin; applied daily to treat dyskeratosis
40% urea creamA strongly keratolytic agent, applied under an occlusive dressing and left in situ for 7 days, to soften, macerate and aid the reduction and removal of hypertrophied nails in patients who are unsuitable for nail avulsion
Monochloroacetic acidA deeply penetrating caustic that is painful in use Applied, retained in situ and reviewed within 3–7 days, for the treatment of verrucae:
1. as a saturated solution to the lesion
2. as a tiny crystal strapped over a masked lesion
3. as a tiny crystal embedded in 40–70% salicylic acid retained by a cavitied pad
Trichloroacetic acidA self-limiting caustic with a superficial action
Applied directly to the verruca, after initial scalpel debridement of the lesion
May be used in conjunction with 75–95% silver nitrate (see below) as a diagnostic or a final treatment of verrucae
75–95% Silver nitrateA self-limiting caustic with a superficial action, causing a dark brown discoloration of the skin to which it is applied; it is used for the treatment of shallow or mosaic verrucae.
Note: Some patients show an idiosyncratic local sensitivity or inflammatory reaction to applied silver nitrate
1. Applied directly to the lesion, after overlying callosity has been debrided off
2. Applied directly to the lesion in alternating layers with trichloroacetic acid
3. As a diagnostic aid to identify verrucous tissue; viral-infected skin cells show up as bright white dots within a few moments of the application of the layers of silver nitrate and trichloroacetic acid
Potassium hydroxide (KOH)A powerful keratolytic caustic with a great affinity for water that penetrates deeply dissolving precipitated protein; used to destroy soft tissues
1. Overlying hyperkeratosis is debrided off the verruca and the foot is immersed in water for 5 minutes to hydrate the skin, then dried; a KOH pellet is rubbed into the lesion; the foot is reimmersed in water and the jelly-like material formed by the KOH on the lesion surface is debrided off. The process is repeated once or twice until the lesion appears to have gone, then glacial acetic acid is applied to neutralize the KOH
2. A similar protocol may be used to ablate nail matrix after removal of the overlying section of nail plate
3. KOH 5% liquid applied to heavy callosity and left in situ for 5 minutes softens heavy callosity to ease its removal
Pyrogallol (pyrogallic acid)A powerful analgesic, non-self-limiting, caustic reducing agent. It may be used in the treatment of recalcitrant verrucae or neurovascular corns in areas of skin overlying a healthy layer of fibrofatty padding. It should only be used with great caution as its action continues after application has ceased and can lead to severe tissue breakdown that is slow to heal. It is incompatible with alkalis, iron salts, oxidizing agents and ammonium salts
1. 20% pyrogallol ointment for the treatment of neurovascular corns
2. 40% pyrogallol ointment for the treatment of VP
3. WP ointment (20% pyrogallol, 20% wheat germ oil) for the treatment of tough, fibrous, hyperkeratotic plantar lesions
PhenolAn analgesic, corrosive caustic. It is used as an 80% solution (liquefied phenol) to destroy soft-tissue lesions such as VP, or nail matrices (three applications, each of 1 minute duration). Its action is quenched by dilution with IMS or isopropyl alcohol. Healing is delayed for several weeks after its application
Glacial acetic acidA weakly acidic mild caustic that is crystalline at 14°C
1. As a paint to hard or vascular corns, or VP (return period 14–21 days)
2. As a paint to VP, alternating with silver nitrate 75% (in a similar manner to trichloroacetic acid)
3. To neutralize KOH (see above: KOH, point 1)
Nitric acidA powerful analgesic oxidizing caustic agent with a superficial action that offers a ‘one-off’ VP treatment
1. Applied to VP with a glass rod and left in situ for 5 minutes, followed by phenol solution 10%; the skin stains bright yellow
2. The lesion is saturated with phenol solution 5% for 5 minutes, then with nitric acid for 20–30 seconds, then once again with phenol solution 5%
Strong iodine solution (iodine solution 10%; iodine fortis)A strong astringent and vesicant agent. It is incompatible with many topical medicaments, and can cause sensitivity reactions in some patients
1. to shrink nail tufts
2. to shrink hypergranulation tissue
FormaldehydeA strongly astringent and antiseptic agent used in the treatment of VPs (the skin surrounding the lesion should be protected with petroleum jelly; sensitivity is likely)
1. 10% formaldehyde in collodion, painted on daily
2. 36% formaldehyde solution, painted on daily
Thermal caustics
CryosurgeryThe topical application of liquid nitrogen (at -196°C) or nitrous oxide (at -88.5°C) to destroy small soft-tissue lesions; the cell cytoplasm must be reduced to and maintained at -24°C or lower for at least 1 minute, and repeated for two further freezing episodes between which the area has been allowed to thaw. Cryosurgery is more effective when any overlying hyperkeratosis is removed before freezing
HyfrecationTissue destruction by initial fulguration (outlining and superficial charring) of the lesion by the application of high-frequency electrical energy), then electrodesiccation (electrocautery) of the lesion by the release of electrical energy whilst the probe is inserted into the lesion
ElectrosurgeryTissue removal using high-frequency energy waves to incise through tissue

Note: Please also refer to the text entries for each listed agent.

IMS, industrial methylated spirit; VP, verrucae pedis.

Table 3: Caustic agents used in podiatric practice to achieve local tissue destruction
AgentActionSpecial precautionsContraindications
Monochloroacetic acid (crystals or saturated solution) e.g. single VPKeratolytic; hydrolysing agent
Deep penetration
Do not use mask if applying solution
Use a mask if applying crystals
Review in 5–7 days
Neutralize with foot bath ± NaHCO3 or NaCl
Soft-tissue atrophy
Peripheral vascular disease
Sensory neuropathy
Salicylic acid paste (40–70%) e.g. single VP; plantar hard cornKeratolytic; hydrolysing agentMacerates tissues
Review in 7–14 days
May be used in conjunction with monochloroacetic acid crystals
Neutralize with foot bath ± NaHCO3 or NaCl
Soft-tissue atrophy
Peripheral vascular disease
Sensory neuropathy
Pyrogallic acid e.g. single VPKeratolytic; oxidizing agentDeep penetration
Review in 3–5 days
Prolonged caustic action
Do not apply more than 3 times sequentially
Stains skin black/brown
Use with great care: may cause deep tissue breakdown
Soft-tissue atrophy
Peripheral vascular disease
Sensory neuropathy
Trichloroacetic acid (saturated solution; 10% solution) e.g. mosaic VPMild keratolytic
Protein precipitant
Shallow penetration
Neutralize with foot bath ± NaHCO3 or NaCl
Review in 3 weeks
Peripheral vascular disease
Sensory neuropathy
Silver nitrate (70% solution; 75–95% stick) e.g. mosaic VP; as a protective skin application below a maskProtein precipitant
Stains skin black/brown
Maximum effect occurs within 24 hours
Some patients show hypersensitivity to silver nitrate (or experience acute pain)
Neutralize with NaCl foot bath
May be applied in alternate layers with trichloroacetic acid
Peripheral vascular disease
Known sensitivity
Potassium hydroxide (KOH; 85% pellets)Strong keratolyticPotentially deep penetration
Action of KOH stopped by application of 5% acetic acid after macerated coagulum has been removed
Single treatment
Soft-tissue atrophy
Peripheral vascular disease
Sensory neuropathy
Phenol (80% solution or 100% crystal)Protein precipitateAction retarded by flooding with industrial methylated spirit
Skin overspill flooded with glycerine
Review as per postoperative protocol
Peripheral vascular disease (phenol suppresses inflammatory response)

VP, verruca pedis.

References in periodicals archive ?
This dehalogenase cleaves the carbon-halogen bond of a specific enantiomer of each of D-2-chloropropionate and monochloroacetic acid (MCA) and has been further characterized (Huyop et al.
Biodegradation of monochloroacetic acid by a presumptive Pseudomonas sp.
European Union Risk Assessment Report Monochloroacetic acid (MCAA).
AkzoNobel (Euronext: AKZA) has expanded the capacity of its plant for the manufacture of monochloroacetic acid (MCA) in China.
This report presents a detailed overview of the global and regional Monochloroacetic Acid (MCAA) markets (CIS countries in particular) by contemplating and analyzing its various parameters.
Firstly, a brief introduction to the industry is provided where Monochloroacetic Acid (MCAA) properties, application areas and manufacturing technologies are covered.
II-14 Cellulose Acetate & Acetic Anhydride II-14 End-use Applications of Cellulose Acetate II-15 Acetylates (Esters and Acetates) II-15 Ethyl Acetates II-15 Production Process II-15 Recent Developments II-15 Consumption Pattern II-16 Butyl Acetate II-16 Acetic Anhydride II-16 Other II-16 Monochloroacetic Acid II-16
This report analyzes the worldwide markets for Monochloroacetic Acid in Millions of Pounds.
CABB holds a strong market and technology position for its main product, monochloroacetic acid (MCAA), an important intermediate for applications in industries such as agro chemistry, detergents, plastics and pharmaceuticals.
based in the Netherlands, today agreed to plead guilty and pay a USD 12 million fine for participating in a price-fixing and market-allocation conspiracy in the United States monochloroacetic acid (MCAA) industry from September 1995 through August 1999.