UKPID MONOGRAPH
PHOSPHORIC ACID
WN Harrison PhD CChem MRSC
SM Bradberry BSc MB MRCP
JA Vale MD FRCP FRCPE FRCPG FFOM
National Poisons Information Service
(Birmingham Centre),
West Midlands Poisons Unit,
City Hospital NHS Trust,
Dudley Road,
Birmingham
B18 7QH
This monograph has been produced by staff of a National Poisons
Information Service Centre in the United Kingdom. The work was
commissioned and funded by the UK Departments of Health, and was
designed as a source of detailed information for use by poisons
information centres.
Peer review group: Directors of the UK National Poisons Information
Service.
PHOSPHORIC ACID
Toxbase summary
Type of product
A common industrial chemical used in the manufacture of fertilizers,
detergents, soft drinks and in water treatment.
Toxicity
Ten to 25 per cent phosphoric acid solutions are irritant and more
concentrated solutions corrosive.
Skin exposure, inhalation or ingestion of any quantity of a
concentrated solution can be dangerous.
5 mL of a 1.0 per cent solution was not caustic to the oral mucosa
(von Muhlendahl et al, 1978). A patient has survived ingestion of
90-120 mL of a metal cleaner containing 20 per cent "hydrogen
phosphate" (Caravati, 1987).
Features
Dermal
- Solutions greater than 10 per cent are irritating to the
skin and higher concentrations may cause burns.
Ocular
- Direct contact may irritate or burn the eye causing pain,
blepharospasm, lacrimation and/or photophobia.
Inhalation
- Cough and retrosternal discomfort may be the only early
features. Following significant exposure hoarseness,
dyspnoea and stridor (due to laryngeal oedema) may develop.
In the most severe cases the onset of non-cardiogenic
pulmonary oedema with increasing breathlessness, wheeze and
cyanosis may be delayed for up to 36 h.
Ingestion
- Ingestion of greater than 10 per cent solutions will cause
immediate burning of the mouth and throat possibly with
retrosternal and abdominal pain, nausea and vomiting.
- Severe irritant or corrosive effects are likely following
ingestion of greater than 20 per cent solutions with
hypersalivation, haematemesis and hypovolaemic shock.
- There is a risk of gastric antrum ulceration, haemorrhage
and perforation.
- The larynx may be burned, with oedema causing airway
obstruction.
- Obstructive symptoms due to oesophageal or gastric stricture
may develop weeks or months later.
- There is a single report of hyperphosphataemia,
hypocalcaemia and metabolic acidosis occurring after acute
ingestion of 90-120 mL of 20 per cent phosphoric acid
(Caravati, 1987).
Management
Dermal
1. Before attempting treatment ensure adequate measures are taken to
prevent self exposure.
2. Wear protective clothing and carry out decontamination in a well
ventilated area, preferably with its own ventilation system.
3. The patient should remove soiled clothing and wash him/herself if
possible.
4. Wash hair and all contaminated skin with copious amounts of luke-
warm water.
5. Pay special attention to skin folds, fingernails and ears.
6. Burns should be treated conventionally as thermal burns. Surgery
may be required for deep burns.
Ocular
1. Immediately irrigate the affected eye thoroughly with tepid water
or 0.9% saline.
2. Continue irrigation with saline infusion (using drip tubing) for
at least 10-15 minutes.
3. Repeated instillation of local anaesthetic may reduce discomfort
and help more thorough decontamination.
4. Corneal damage may be detected by instillation of fluorescein.
5. Patients with corneal damage, those who have been exposed to
strong acids and those whose symptoms do not resolve rapidly
should be referred for ophthalmological assessment.
Inhalation
1. Remove from exposure.
2. Give high-flow oxygen by face mask.
3. Intubation and assisted ventilation may be necessary.
4. Rarely tracheostomy may be required for life-threatening
laryngeal oedema.
5. High dose corticosteroids (prednisolone 60-80 mg/day) may be
considered for laryngeal and pulmonary oedema but there is no
confirmed evidence that they improve prognosis. Discuss with an
NPIS physician.
Ingestion
1. Secure a clear airway and support respiration as necessary.
2. DO NOT attempt gastric lavage.
3. There may be some benefit in attempting oral dilution if
performed immediately, but fluids should not be offered if there
is inadequate airway protection or severe abdominal pain.
4. Morphine may be required for pain.
5. Treat shock by replacing lost fluids and blood intravenously.
6. Monitor urine output and renal function.
7. Early fibreoptic oesophago-gastroscopy (ideally within 24 h) by
an experienced endoscopist is indicated in symptomatic patients
to grade the severity of injury and determine prognosis.
8. Corticosteroids confer no benefit and may mask abdominal signs of
perforation.
9. An aggressive surgical approach is favoured in those with
suspected perforation or severe (grade 3) burns
10. In severe cases seek specialist advice from an NPIS physician.
References
Caravati EM.
Metabolic abnormalities associated with phosphoric acid ingestion.
Ann Emerg Med 1987; 16: 904-6.
Cello JP, Fogel RP, Boland CR.
Liquid caustic ingestion. Spectrum of injury.
Arch Intern Med 1980; 140: 501-4.
Hawkins DB, Demeter MJ, Barnett TE.
Caustic ingestion: Controversies in management. A review of 214 cases.
Laryngoscope 1980; 90: 98-109.
Jeng L-BB, Chen H-Y, Chen S-C, Hwang T-L, Jan Y-Y, Wang C-S, Chen M-F.
Upper gastrointestinal tract ablation for patients with extensive
injury after ingestion of strong acid.
Arch Surg 1994; 129: 1086-90.
Mazariegos-Ramos E, Guerrero-Romero F, Rodríguez-Morán M,
Lazcano-Burciaga G, Paniagua R, Amato D.
Consumption of soft drinks with phosphoric acid as a risk factor for
the development of hypocalcaemia in children: A case-control study.
J Pediatr 1995; 126: 940-2.
Shuster J, Jenkins A, Logan C, Barnett T, Riehle R, Zackson D, Wolfe
H, Dale R, Daley M, Malik I, Schnarch S.
Soft drink consumption and urinary stone recurrence: A randomized
prevention trial.
J Clin Epidemiol 1992: 45: 911-6.
von Muhlendahl KE, Oberdisse U, Krienke EG.
Local injuries by accidental ingestion of corrosive substances by
children.
Arch Toxicol 1978; 39: 299-314.
Wason S, Gomolin I, Gross P, Mariam S, Lovejoy FH.
Phosphorus trichloride toxicity: Preliminary report.
Am J Med 1984; 77: 1039-42.
Zargar SA, Kochhar R, Nagi B, Mehta S, Mehta SK.
Ingestion of corrosive acids. Spectrum of injury to upper
gastrointestinal tract and natural history.
Gastroenterology 1989; 97: 702-7.
Substance name
Phosphoric acid
Origin of substance
Obtained commercially from phosphate rock deposits.
(CSDS, 1990)
Synonyms
Orthophosphoric acid (CSDS, 1990)
Chemical group
A compound of phosphorus, a group VA element.
Reference numbers
CAS 7664-38-2
RTECS TB 63 00000
UN 1805
HAZCHEM CODE 2 R (CSDS, 1990)
Physicochemical properties
Chemical structure
H3PO4 (CSDS, 1990)
Molecular weight
98.00 (DOSE, 1994)
Physical state at room temperature
Viscous liquid or rhombic crystals (CSDS, 1990)
Colour
Colourless (CSDS, 1990)
Odour
Odourless (HSDB, 1997)
Viscosity
NIF
pH
1.5 (0.1 N aqueous solution) (HSDB, 1997)
Solubility
Very soluble in water (CSDS, 1990)
Autoignition temperature
NA
Chemical interactions
Contact with common metals produces hydrogen which may form
flammable mixtures in air.
When used for metal cleaning may react with impurities in the
metal to release phosphine gas. (HAZARDTEXT, 1997)
Major products of combustion
Phosphorus oxides are released when heated to decomposition.
(HAZARDTEXT, 1997)
Explosive limits
NA
Flammability
Not combustible (HAZARDTEXT, 1997)
Boiling point
213°C (OHM/TADS, 1997)
Density
1.864 at 20°C (CSDS, 1990)
Vapour pressure
3.8 Pa at 20°C (DOSE, 1994)
Relative vapour density
3.4 (HSDB, 1997)
Flash point
NA
Reactivity
Reacts exothermically with water. (HAZARDTEXT, 1997)
Uses
In manufacture of superphosphates for fertilizers, phosphate
salts, polyphosphates and detergents.
Catalyst in ethylene manufacture and hydrogen peroxide
purification.
Flavour, acidulant, synergistic antioxidant and sequestrant in
food.
Pharmaceutic acid.
In dental cements.
In process engraving, metal rustproofing, latex coagulation,
analytical reagent.
As a veterinary product in the treatment of lead poisoning.
(DOSE, 1994)
Hazard/risk classification
Index no. 015-011-00-6
Risk phrases
25% Conc C; R34. Corrosive. Causes burns.
10% Conc 25% Xi; R36/38. Irritant. Irritating to eyes and skin.
Safety phrases
5(1/2-)26-45. Keep locked up and out of the reach of children. In
case of contact with eyes, rinse immediately with plenty of water
and seek medical advice. In case of accident or if you feel
unwell, seek medical advice immediately (show label where
possible).
EEC no. 231-633-2 (CHIP2, 1994)
INTRODUCTION
Phosphoric acid is a strong acid and common industrial chemical used
in the manufacture of a wide number of products, notably porcelain and
metal cleaners, detergents and fertilizers. It is also used as a food
additive and is a major constituent of many soft drinks. Low phosphate
concentrations are found in drinking water to which it is added in
some areas in order to reduce lead solubility.
There is no evidence that phosphorus poisoning occurs from phosphoric
acid exposure (Desai, 1992).
EPIDEMIOLOGY
The widespread use of phosphoric acid in industry has been the source
of both chronic (Fabbri et al, 1977) and acute exposure following
spillage, fire or explosion. Of 100, mainly occupational, cases of
chemical burns admitted to a regional burns unit over an eight year
period, two were due to phosphoric acid (Herbert and Lawrence, 1989).
Phosphoric acid in household cleaning products has been the source of
suicidal and accidental ingestion (Cello et al, 1980; Hawkins et al,
1980; Caravati, 1987).
Excessive consumption of phosphoric acid-containing soft drinks has
been associated with hypocalcaemia in children (Mazariegos-Ramos et
al, 1995) and increased recurrence of urinary stones in adults
(Shuster et al, 1992).
Historically, industrial phosphine exposure has been reported from the
use of phosphoric acid baths when elevated temperatures and the
presence of metal produced sufficient nascent hydrogen to reduce the
acid to phosphine (Anonymous, 1955).
MECHANISM OF TOXICITY
Phosphoric acid is caustic to the eyes, skin and mucous membranes of
the respiratory and gastrointestinal tracts (Hawkins et al, 1980;
Caravati, 1987; Desai, 1992).
Increased blood phosphate concentrations following phosphoric acid
ingestion have been associated with hypocalcaemia, hypotension and
acidosis (Caravati, 1987). Hypocalcaemia occurs via inhibition of
1-hydroxylase, with diminished 1,25-dihydroxyvitamin D3 formation
(Haussler and McCain, 1977). Increased serum phosphate concentrations
also inhibit bone resorption with reduced calcium release (Raisz,
1970). Hydrogen ion loads produce a metabolic acidosis which further
exacerbates hypocalcaemia (Mazariegos-Ramos et al, 1995).
TOXICOKINETICS
Absorption
Phosphoric acid can be absorbed by ingestion, inhalation and dermal
contact.
Distribution
Absorbed phosphoric acid is distributed widely in the body as
phosphate. Increased serum phosphate concentrations have been reported
rarely after phosphoric acid ingestion (Caravati, 1987).
Excretion
Absorbed phosphate is filtered at the glomerulus and partially
reabsorbed, with phosphate clearance 80 per cent of creatinine
clearance. A small amount of phosphate is excreted in faeces (Larson
et al, 1986; Reynolds, 1993).
In infants with normal renal function the serum half-life of phosphate
following single oral or rectal overdose is 5-11 hours (Larson et al,
1986).
CLINICAL FEATURES: ACUTE EXPOSURE
The Health and Safety Executive has classed phosphoric acid solutions
between 10 and 25 per cent as irritant with more concentrated
solutions corrosive (CHIP2, 1994). By contrast, the US Consumer
Product Safety Commission has suggested concentrations of 15-35 per
cent should be considered weak irritants, 35-60 per cent strong
irritants and greater than 60 per cent solutions corrosive (Meditext,
1997).
Dermal exposure
Concentrated solutions are irritating to the skin. A 75 per cent
solution will cause serious skin burns. The dust is particularly
irritating to the skin in the presence of water (CSDS, 1990).
Ocular exposure
Direct contact may irritate or burn the eye depending on the
concentration. Tested on human eyes, 0.16 M phosphoric acid buffered
to pH 2.5 caused moderate brief stinging but no injury when applied as
a single drop. The same solution adjusted to pH 3.4 caused no
discomfort. Phosphoric acid has been held responsible for burns of the
eye from superphosphate fertilizers (Grant and Schuman, 1993).
Conjunctivitis, lacrimation and blurred vision were reported after
exposure to phosphorus trichloride and its hydration products
following a spillage (Wason et al, 1984). These features plus
photophobia were reported in workers exposed occupationally to
phosphorus trichloride concentrations greater than 10 mg/m3 (Sassi,
1952; Roshchin and Molodkina, 1977).
Inhalation
Phosphoric acid has a low vapour pressure at room temperature so
significant exposure is unlikely unless it is in the form of a mist or
spray.
Pulmonary toxicity
Phosphoric acid is a respiratory tract irritant with the severity of
symptoms increasing with acid concentration. Early features include
cough and retrosternal discomfort. Hoarseness, dyspnoea and, in severe
cases, stridor due to laryngeal oedema may follow.
Following significant exposure there is a risk of delayed onset,
non-cardiogenic pulmonary oedema which may take up to 36 hours to
develop.
In the French literature a patient with no previous history of asthma
developed wheeze associated with chemical pneumonitis after accidental
phosphoric acid inhalation (Boutoux et al, 1995). Evidence of airways
hyperresponsiveness persisted one year later.
A Russian study cited by Payne et al (1993) described the response of
15 non-smoking adults aged 18-36 years exposed to phosphoric acid
aerosols. No airways irritation was reported at a concentration of 1.6
mg/m3. Eighteen per cent of subjects reported airways irritation at
7.2 mg/m3 and 82 per cent at 11.0 mg/m3.
Several studies have reported the effects of exposure to phosphorus
trichloride and its hydration products. Phosphorus trichloride is
rapidly hydrolyzed to phosphoric and hydrochloric acids on contact
with water, including moisture in the upper respiratory tract.
Exposure to a spillage of phosphorus trichloride and its hydration
products primarily caused nausea, dyspnoea and cough. Throat
irritation, headache, sputum production, chest pain, wheeze and
abdominal pain were also reported. Of 450 patients seen in hospital 15
were admitted and all discharged within two days without residual
effects. Pulmonary function tests in 17 patients showed impaired large
and small airway resistance inversely correlating with distance from
the spill (Wason et al, 1984). There was a significant improvement to
near normal lung function among seven individuals who attended a
follow-up study one month later (pre-exposure lung function was not
known).
In a review of the health of Russian workers exposed to phosphorus
trichloride Roshchin and Molodkina (1977) emphasized that features of
eye and upper respiratory tract irritation typically preceded effects
on the lower airways. Thus initial eye irritation, photophobia,
lacrimation, rhinitis, tracheitis, laryngitis, and a dry cough usually
occurred before dyspnoea, bronchitis and chest pain. Some acute
intoxications resulted in chronically increased bronchial sensitivity.
The most severe effects occurred following acute exposure to
phosphorus trichloride concentrations of 10-20 mg/m3.
Haemotoxicity
Moderate neutrophilia and an increased erythrocyte sedimentation rate
are associated frequently with pulmonary features of phosphorus
trichloride exposure (Sassi, 1952; Roshchin and Molodkina, 1977).
Hepatotoxicity
Transiently increased lactate dehydrogenase activity was reported in
six of 17 patients exposed to phosphorus trichloride and its hydration
products. It was not confirmed, however, that this was the hepatic
iso-enzyme (Wason et al, 1984).
Ingestion
The effects of acute phosphoric acid ingestion are due to its
corrosive nature, the severity of symptoms reflecting the
concentration of the solution rather than the amount taken. Where
severe gastrointestinal burns ensue there is a high risk of
multi-organ damage.
Five millilitres of a one per cent solution was "not caustic" when
held in the mouth for five seconds (von Muhlendahl et al, 1978). By
contrast, exposure of the soft tissue of the mouth to 50 per cent
phosphoric acid for more than five minutes will burn (Payne et al,
1993).
Ingestion of as little as 8 mL phosphoric acid (presumably neat) has
been reported to be the "minimum lethal dose" for a 68 kg man.
However, the original source of this information is not referenced and
its reliability is unclear (Payne et al, 1993).
A patient survived ingestion of 90-120 mL of a metal cleaner
containing 20 per cent "hydrogen phosphate" (Caravati, 1987).
Another patient survived ingestion of 240 mL of an unknown
concentration of phosphoric acid (Cello et al, 1980).
Gastrointestinal toxicity
Although there is often relative sparing of the oesophagus following
acid ingestion, with more severe stomach lesions (Hawkins et al,
1980), this is not universally true (Zarger et al, 1989). The
suggested mechanism is rapid transit to the stomach with pooling at
the pylorus due to pyloric spasm. The same mechanism, plus an alkaline
milieu, spares the duodenum where acid burns are less frequent and
less severe.
Concentrated phosphoric acid ingestion produces local caustic effects
on the mucosa of the oropharynx, oesophagus and stomach analogous to
other strong acids (Hawkins et al, 1980; Caravati, 1987). Common early
features include immediate pain in the mouth, pharynx and abdomen,
intense thirst, dysphagia, vomiting, haematemesis and diarrhoea.
Gastric and oesophageal perforation and chemical peritonitis may
ensue.
Late features include antral or pyloric stenosis, jejunal stricture
formation, achlorhydria, protein-losing gastroenteropathy and gastric
carcinoma.
Caravati (1987) reported a 64 year-old man who ingested 90-120 mL 20
per cent "hydrogen phosphate" in attempted suicide. On admission one
hour later he complained of a burning throat, hoarseness, mild
abdominal pain and nausea. He had watery stools and vomited
approximately 100 mL blood-stained liquid. The posterior pharynx was
inflamed with discrete patches of mucosal pallor, the abdomen tender
and the stool contained blood. "Prompt" endoscopy revealed partial
thickness burns of the posterior oropharynx, distal oesophagus and a
pre-existing Billroth II anastomosis. The patient recovered fully.
A patient who ingested an unstated amount of phosphoric acid sustained
extensive oesophageal burns and necrosis of the stomach, duodenum,
jejunum, and pancreas complicated by spontaneous gastric perforation
(Hawkins et al, 1980). He required four laparotomies for recurrent
abdominal haemorrhage but died 19 days after admission.
A 42 year-old man presented with oropharyngeal burns and haematemesis
one hour after ingesting 240 mL phosphoric acid (concentration
unknown) (Cello et al, 1980). Endoscopy (time post ingestion not
stated) revealed moderate distal oesophagitis and severe proximal
gastritis. The duodenum was normal. The gastric injuries healed
completely. Steroids were not employed.
Metabolic disturbances
A patient developed hyperphosphataemia, hypocalcaemia and a metabolic
acidosis after ingesting 90-120 mL 20 per cent "hydrogen phosphate"
(Caravati, 1987). Serum concentrations of calcium and phosphate were
2.05 mmol/L and 2.3 mmol/L respectively. Arterial blood gas analysis
showed pH 7.19, HCO3- 6 mmol/L and an anion gap of 23 mmol/L. These
abnormalities resolved within 36 hours following intravenous fluid and
sodium bicarbonate plus oral aluminium hydroxide (as a phosphate
binder).
Pulmonary toxicity
Features associated with corrosive acid ingestion include hoarseness,
stridor, respiratory distress and, in severe cases, laryngeal or
epiglottal oedema. Chemical pneumonitis and adult respiratory distress
syndrome (ARDS) are recognized.
Nephrotoxicity
Renal failure secondary to acute tubular necrosis may complicate
phosphoric acid ingestion although there are no reported cases.
Cardiovascular toxicity
Circulatory collapse is likely in patients with extensive
gastrointestinal burns.
Hypotension, non-specific T wave flattening in the limb leads and
inverted T waves in leads V4-6 have been reported in a patient who
developed hyperphosphataemia and hypocalcaemia after ingesting 90-120
mL of a solution containing "hydrogen phosphate" 20 per cent,
isopropanol 9 per cent, non-ionic dispersants 32 per cent and inert
ingredients 68 per cent. The abnormalities resolved within 24 hours
(Caravati, 1987).
Haemotoxicity
Disseminated intravascular coagulation and haemolysis may complicate
concentrated acid ingestion.
Injection
There are no reports of phosphoric acid injection although excess
intravenous administration of phosphoric acid salts has been reported
to cause hyperphosphataemia, hypocalcaemic tetany, hypotension, and
acute renal failure (Reynolds, 1993).
CLINICAL FEATURES: CHRONIC EXPOSURE
Inhalation
The main source of exposure to phosphoric acid mists and sprays is
occupational.
In the Italian literature chronic bronchitis was reported in 46 per
cent and an obstructive lung function defect in 37 per cent of 35
workers at a phosphoric acid production plant. However, concomitant
exposure to volatile fluorides was considered to be aetiologically
significant (Fabbri et al, 1977).
Respiratory complications have been reported also in workers exposed
to phosphorus trichloride which is hydrolyzed to phosphoric acid and
hydrochloric acid on contact with water, including moisture in the
upper respiratory tract. In the Italian literature twenty three
chemical workers developed pharyngeal irritation, dyspnoea and asthma
one to eight weeks after exposure. Emphysema was described in workers
exposed for at least one year. Poisoning was frequently accompanied by
fever and a moderate leucocytosis (Sassi, 1952).
Roshchin and Molodkina (1977) described a characteristic progression
of respiratory features among industrial workers exposed to phosphorus
trichloride with initial upper respiratory tract irritation
progressing to bronchopneumonia in those with persistent exposure.
Gastrointestinal toxicity
Inhaled phosphorus trichloride reacts with saliva to form corrosive
acids which damage the teeth (Roshchin and Molodkina, 1977).
Ingestion
The main source is phosphoric acid-containing soft drinks such as
cola.
Mazariegos-Ramos et al (1995) suggested a relationship between
ingestion of phosphoric acid-containing soft drinks and hypocalcaemia
in children. Fifty-seven children with no previously identified
chronic medical problem and serum calcium concentrations less than 2.2
mmol/L were significantly more likely (p<0.001) to consume at least
1.5 L phosphoric acid-containing drinks (Coca-Cola or Pepsi-Cola)
weekly and to be more prone to seizures (p<0.02) and cramps
(p<0.001) than 171 controls (with normal serum calcium
concentrations). The mean (± SD) serum phosphate concentrations in the
hypocalcaemic and control groups were 1.7 ± 0.4 mmol/L and 1.6 ± 0.3
mmol/L respectively.
In the above study the hypocalcaemic children (mean age 67 months)
consumed an average 2.25 L Coca-Cola or Pepsi-Cola weekly
(approximately 360-440 mg phosphate). By contrast, ingestion of up to
3000 mg phosphoric acid daily for four weeks did not have any
significant effect on the calcium balance of six adults (Payne et al,
1993).
Nephrotoxicity
Consumption of soft drinks containing phosphoric acid has been linked
to the recurrence of urinary stones in adult men (Shuster et al,
1992). The mechanism is unclear but is likely to involve increased
calcium phosphate precipitation.
MANAGEMENT
Dermal exposure
Ensure adequate self protection before attempting treatment. If
possible the patient should remove any contaminated clothing
him/herself. Affected areas of skin should be washed with copious
quantities of luke-warm water. Pay special attention to skin folds,
fingernails and ears. Burns should be treated conventionally as for
thermal burns (e.g. silver sulphadiazine dressing). Surgery may be
required for deep burns.
Ocular exposure
Irrigate immediately with lukewarm water or preferably saline for at
least 10-15 minutes. A local anaesthetic may be indicated for pain
relief and to overcome blepharospasm. Specialist ophthalmic advice
should be sought if any abnormality is detected or suspected on
examination and in those whose symptoms do not resolve rapidly.
Inhalation
Immediate management involves removal from exposure, establishment of
a clear airway and administration of supplemental oxygen if necessary.
Mechanical ventilation may be required. Rarely tracheostomy may be
necessary for life-threatening laryngeal oedema. The administration of
prednisolone 60-80 mg daily may be considered if laryngeal or
pulmonary oedema are present but there is no confirmed evidence that
their use alters prognosis. Discuss with an NPIS physician.
Ingestion
Decontamination
Gastric aspiration/lavage is contraindicated. There may be some
benefit in attempting oral dilution with milk or water, if performed
immediately, though this is controversial.
Fluids should not be offered if the patient is not fully conscious, is
unable to swallow or protect his/her own airway, has respiratory
difficulty or severe abdominal pain. Possible complications of fluid
administration include vomiting, aspiration, perforation of the
gastrointestinal tract and worsening of oesophageal or gastric
injuries.
Supportive measures
Airway support and analgesia should be provided as required. Treat
hypovolaemic shock with intravenous colloid/crystalloid and/or blood.
Monitor biochemical and haematological profiles and acid/base status.
Administer antibiotics for established infection only.
Symptoms and signs are unreliable predictors of the extent of injury
following phosphoric acid ingestion (Zargar et al, 1989) and therefore
in symptomatic patients panendoscopy should be carried out, ideally
within 12-24 hours, to gauge the severity of injury.
Grade 0: Normal examination
1: Oedema, hyperaemia of mucosa
2a: Superficial, localized ulcerations, friability, blisters
2b: Grade 2a findings and circumferential ulceration
3: Multiple, deep ulceration, areas of necrosis (Zargar et al,
1989)
Following corrosive acid ingestion endoscopic findings within the
first 36 hours have been used successfully to guide management. In a
series of 41 patients (Zargar et al, 1989) those with grade 0 and 1
burns were discharged within one or two days, those with grade 2a
burns required only supportive care for a little longer, whereas those
with grade 2b and 3 burns required nutritional support via jejunostomy
feeding (total parenteral nutrition is an alternative). All patients
with grade 0, 1 and 2a injury recovered without sequelae. Acute
complications and death were confined to those with grade 3 burns
although several patients with grade 2b burns developed oesophageal or
gastric strictures.
In view of the high morbidity associated with acid-induced upper
gastrointestinal perforation and the high incidence of later
complications requiring surgery, an aggressive surgical approach is
recommended (Jeng et al, 1994). Surgery should therefore be
considered:
1. If symptoms or signs of gastrointestinal tract perforation are
evident at initial presentation.
2. When endoscopy reveals evidence of grade 3 burns with full-
thickness necrosis (black, ulcerated mucosa) of the stomach or
oesophagus.
Corticosteroids
In a controlled trial of steroid use among 60 children with
oesophageal burns following corrosive ingestion (alkalis in the
majority) the use of steroids (intravenous prednisolone 2 mg/kg within
24 h and daily until oral intake was resumed then prednisolone
2.5 mg/kg orally daily for at least three weeks) did not influence
outcome (Anderson et al, 1990). Smaller case series have also
concluded that systemic corticosteroids confer no benefit following
acid ingestion and may exacerbate or mask symptoms of pending
perforation (Hawkins et al, 1980).
A 42 year-old man who sustained moderate distal oesophagitis and
severe proximal gastritis after ingesting 240 mL phosphoric acid
(concentration unknown) fully recovered without steroid therapy.
Steroids were also not used in the treatment of a 64 year-old man who
ingested 90-120 mL 20 per cent phosphoric acid (Caravati, 1987).
Management details were not given of a patient who suffered fatal
gastric perforation after ingesting an unstated amount of phosphoric
acid (Hawkins et al, 1980).
We do not advocate systemic steroids following phosphoric acid
ingestion.
Enhancing elimination
Hyperphosphataemia following phosphoric acid ingestion is rare and has
been managed effectively with fluid diuresis and oral phosphate
binders such as aluminium hydroxide. Haemodialysis enhances phosphate
elimination but is likely to be indicated only in the presence of
renal failure (Caravati, 1987).
MEDICAL SURVEILLANCE
Ensure adequate ventilation and air concentrations below the
occupational exposure standard. Appropriate protective equipment
should be available when working with concentrated solutions.
People with a history of asthma should be identified prior to
employment if inhalational exposure is likely.
OCCUPATIONAL DATA
Occupational exposure standard
Short-term exposure limit (15 minute reference period) 2 mg/m3
(Health and Safety Executive, 1997).
OTHER TOXICOLOGICAL DATA
Carcinogenicity
There is no reliable information on the carcinogenic potential of
phosphoric acid (Payne et al, 1993). Severe gastric burns following
acid ingestion are associated with an increased risk of gastric
carcinoma.
Reprotoxicity
There are no data regarding the reprotoxicity of phosphoric acid.
Genotoxicity
Salmonella typhimurium TA97, TA98, TA100, TA104 with and without
metabolic activation negative.
Escherichia coli without metabolic activation negative (DOSE, 1994).
Fish toxicity
LC50 96 hr) "aquatic life" 100-1000 ppm (DOSE, 1994).
EC Directive on Drinking Water Quality 80/778/EEC
Guideline level 400 µg/L; maximum admissible concentration 5000 µg/L,
as P2O5 (DOSE, 1994).
WHO Guidelines for Drinking Water Quality
NIF (WHO, 1993).
AUTHORS
WN Harrison PhD CChem MRSC
SM Bradberry BSc MB MRCP
JA Vale MD FRCP FRCPE FRCPG FFOM
National Poisons Information Service (Birmingham Centre),
West Midlands Poisons Unit,
City Hospital NHS Trust,
Dudley Road,
Birmingham
B18 7QH
UK
This monograph was produced by the staff of the Birmingham Centre of
the National Poisons Information Service in the United Kingdom. The
work was commissioned and funded by the UK Departments of Health, and
was designed as a source of detailed information for use by poisons
information centres.
Date of last revision
28/1/98
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