Resuscitation 1, 35-44

A case of poisoning with mercuric chloride

MARGARET J. MURPHY, ELIZABETH J. CULLIFORD and V. PARSONS

Kings College Hospital Renal Unit, Dulwich Hospital, East Dulwich Grove,
London, SE22

Summary

A male patient was admitted to hospital 12 h after self-poisoning with mercuric

chloride. He suffered multiple complications including acute renal failure, ulcerative
colitis, anaemia, disseminated intravascular coagulation, chronic sepsis and severe
weight loss. Initially he responded well to resuscitative measures and intensive
supportive therapy, which included ventilation of the lungs, haemodialysis, dimercap-
rol, antibiotics, parenteral feeding and gastrointestinal surgery. Unfortunately the
sepsis was never satisfactorily eradicated despite satisfactory serum concentrations of
the appropriate antibiotics. On day 43 after poisoning he had a grand ma1 fit; after this
there were focal neurological signs and on lumbar puncture he was found to have a
raised protein concentration and raised pressure in his cerebrospinal fluid. The
condition of the patient rapidly deteriorated and on day 47 he died. Post-mortem
examination revealed a large cerebellar abscess. The literature on mercury poisoning is
reviewed.

Introduction

Self-poisoning with inorganic mercury is now extremely rare, whereas overdosages

with barbiturates, tranquillizers, antidepressants, aspirin and paracetamol are com-
monly seen in hospital practice. Accidental poisoning with elemental mercury,
inorganic and organic mercury compounds still results occasionally from occupational
and environmental exposure. Acute and chronic cases have been reported and
reviewed. We report here a case of self-poisoning with mercuric chloride and the
management of the patient and the complications which occurred.

Case history

A 35year-old man was admitted approximately 12 h after swallowing an unknown

quantity of mercuric chloride. Vomiting occurred shortly after taking the poison
followed by incontinence of faeces, with colicky abdominal and oropharyngeal pain.
On examination he was found to have oropharyngeal oedema with ulceration,
35
 36 M. J. MURPHY AND OTHERS

Table 1. Sumniary of tindings and procedures to the time of death

DAY No. I 2 3 4 5 6 7 8 9 10 11 I2 13 14 15 16 17 18 19 ;

Hacmodialysis x x x x x x x x x x x x x x X X

Transfusion (units of blood) 2 4 3 I 2 2 2 2 2 2 5

Haemoglobin (g/dl) 13.5 13.7 12.9 10.5 7.5 - 8.9 9.7 10.9 10.3 13.0 14.6 12.8 10.5 11.7 12.1 14.0 13.2 11.5 1

Blood urea (mmolll) 6.7 17 23 31.2 41.6 48.5 49.7 41.5 30.5 31.8 34 40 37.5 30.0 24.5 43.2 37.1 56.9

Bilirubitt (3-20 pmol/l) 80 134 189 180 144 113

Alkaline phosphatax
(3&85 i.u./l) 48 77 126 200 240 275

Aspartate transaminase
(IO-50 i.u:/l) > 250 244 197 95 75 77

Hydroxybutyrate
dehydrogenasc
(lOCL250 ix/l) >600 >6QCI >600 S600 410 333

Prothrombin time
[patient control (2)] 19/13 19113 21/13 14113 15113

Urine volume (ml/day) 265

Infection

DAY No. 1 2 3 4 5 6 7 8 9 10 II 12 13 14 I5 16 17 18 19
 MERCURY POISONING 37

24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47

X x x X X x x X X

2 14 2 16 4 I1 2 2 2 2 5 4 2 2 I

11.7 10.3 9.3 - 90 10.8 II.3 11.6 II0 14.2 12.4 13.6 12.6 12.1 12.1 - 12.0 10.7 8.9 9.5 9.9

32 42.1 35.8 31.7 27.5 34.8 48.3 36.2 50 34 17.5 34 25.1 42 36 42 27.5 32 38 38.5 41.5

41 22 27 43 37 70 80 I15

360 177 X0 181 I57 I22 85 I17

77 54 31 67 53 44

217 133 61 321 242 244 2.50 310

16/13 15113 IQ13 2O,'l3

800 550 600 - 950 160: 120'

3
.Ej
a 2 2
P E
B
B .s
e
P
E
& 2
za
2 -u
a i 4u g ti$
v4 4rr)
-
- - -
2
sI 3B 8$ iiz z :
, . s B
24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47
38 M. J. MURPHY AND OTHERS

laryngeal stridor and cyanosis.
mmHg. An X-ray of his chest
Investigations included the
g/dl; serum Na+, 141 mmol/l;
creatinine, 0.17 mmol/l.
His pulse was 64/min and his blood pressure was 130/70
showed extensive pulmonary oedema.
following, whose values are given: haemoglobin, 13.5
serum K+, 3.0 mmol/l; blood urea, 6.7 mmol/l; blood

Management
Tracheostomy was performed to facilitate ventilation of the lungs. Stomach washout
was not undertaken because of the friable state of the mucosa of his upper
gastrointestinal tract. Intravenous fluid replacements were determined according to
the central venous pressure.
Treatment was begun with dimercaprol (BAL), 250 mg intramuscularly, 4 hourly,
methyl prednisolone, 500 mg, 8 hourly for 24 h and prophylactic antibiotics (ampicillin,
500 mg intravenously, 6 hourly and flucloxacillin, 500 mg intravenously, 6 hourly). He
remained anuric from the time of his admission and after 6 h was given an infusion of
500 ml of 20% mannitol and frusemide, 375 mg, intravenously, without effect. After
three 250 mg doses of dimercaprol this was discontinued because of the risk of toxicity
in the presence of acute renal failure.
During the weeks that followed he had many problems which will be reviewed
systematically.

Kidney
During the first 24 h after admission the blood urea, creatinine and potassium
concentrations rose sharply (blood urea 6.7--17 mmol/l; blood creatinine 0.17--0.4
mmol/l; serum K+ 3.@-6.5 mmol/l). Haemodialysis was therefore commenced and
continued daily for 13 days, during which time he remained anuric and severely
catabolic. It was hoped that by dialysis some of the mercury would be eliminated. On
day 15 he passed 265 ml of urine and after this was put on a regimen of dialysis on
alternate days. Variation in his urine output (Table 1) and his slowly recovering renal
function were largely dependent on his general condition, gastrointestinal com-
plications and surgical procedures. On day 40 he was incontinent of urine and
subsequently passed increasing daily volumes, requiring no further dialysis. He was
haemodialysed on a total of 26 occasions.

Gastrointestinal tract and nutrition

On day 2 parenteral feeding was given during dialysis to avoid fluid overload in the
presence of anuria. This was continued. An oesophageal X-ray during a Gastrograffin
swallow on day 8 showed no evidence of perforation or stricture, so oral feeding
proceeded. This caused intense retrosternal pain, possibly due to severe oesophagitis (a
second radiological examination showed no lesion). He would only accept high-calorie
frozen feeds. Profuse diarrhoea persisted and the perianal skin excoriated despite
intravenous morphine, 5 mg, 4 hourly, during the first 2 days and later kaolin and
morphine mixture, 10 ml orally, 2 hourly, Lomotil, 10 mg, 8 hourly, and methylcel-
lulose added to feeds.
 MERCURY POISONING 39

T&e 2. Intravenous feeding and transfusion

Vamin 10% 20% 20% 50%

Aminosol glucose A.F.E. Intralipid Intralipid glucose glucose Plasma Blood

Total (I) 5: 4+ 42 3 lti 16 1st 44 units 86 units

Calories
given 1925 2925 18900 3300 21000 12000 29062

On day 14 he was weighed for the first time, and his weight was found to be 70 kg, a
loss of 12 kg from his estimated admission weight. On day 17 severe abdominal pain
and diarrhoea led to a radiological examination, which showed fluid levels and gas in
the large bowel, but no gross dilatation. He became shocked on day 19 after passing 1
litre of fresh blood per rectum. Repeated examinations revealed dilatation of the small
bowel with multiple fluid levels. Despite a good response to blood transfusion and
insertion of a gastrostomy tube on day 27 for feeding and administration of drugs, he
had another massive gastrointestinal tract haemorrhage. Toxic dilatation of the colon
led to a decision to perform a total colectomy with the construction of a terminal
ileostomy. On examination of the specimen removed, it was seen that the colon had
suffered extensive mucosal loss with a few surviving islands of mucosa; in places there
was full-thickness ulceration of the muscularis.
Feeding through the gastrostomy was recommenced but by day 32 he weighed only
47 kg. Faecal fistulae developed and these were confirmed at laparotomy on day 39:
further ileostomies were fashioned and feeding via the gastrostomy was then continued.
The extent of intravenous feeding is shown by the administration of large volumes of
synthetic mixtures and blood (Table 2).
Respiratory tract and ventilation
Pulmonary ventilation was needed until day 5. Radiological examinations showed a
steady clearing of diffuse fluffy shadows in all zones, leaving some consolidation in both
lower zones. The tracheostomy tube was used for bronchial toilet until day 13. On day
21 bronchopneumona developed, with increasing cyanosis; the tracheostomy was
again used for ventilation and sputum aspiration to prevent segmental collapse.
Diffuse infection of the lungs and bronchi persisted with much sputum. After each
surgical procedure he was kept sedated and intermittent positive-pressure ventilation
was continued for various periods of time.

Infection
Pseudomonas aeruginosa was cultured from his sputum daily from day 2. At first this
was only a light growth but when it became heavier he was started on gentamicin. After
initial loading doses this was regulated according to serum concentrations. Ampicillin
and flucloxicillin were discontinued on day 8 but as on days 11 and 12 Streptococcus
faecalis was also cultured, the flucloxicillin was recommenced. When on day 20 he was
found to have a Pseudomonas septicaemia, carbenicillin, 2 g intravenously, 6 hourly,
was added to his antibiotic regimen. After abdominal surgery mixed organisms were
40 M. J. MURPHY AND OTHERS

cultured from the wounds and drains. These were mainly Gram-negative organisms.
Blood cultures on day 35 grew Proteus species and Bacteroides, and his sputum
continued to grow Pseudomonas aeruyinosa as well as Proteus species. Lincomycin, 600
mg intravenously, 2 hourly, and rifampicin, 600 mg orally, daily, were prescribed.
Throughout his illness he had a leucocytosis with neutrophilia (leucocyte count
13 OOG-50000//J with 70-95X neutrophils). His immunoglobulins on day 35 were
within normal limits (IgC = 13.0 g/l, IgA = 2.53 g/l and IgM =0.6 g/l).

Haematoloyy
After admission anaemia was a constant feature, associated with bloody diarrhoea
and gastrointestinal haemorrhages (Table 1). During the initial 2 weeks he became
jaundiced, his reticulocyte count rose to 8% and his grossly elevated serum
hydroxybutyrate dehydrogenase (HBD) suggested haemolysis in addition to a degree
of liver failure.
On day 3 his prothrombin time was prolonged to 19 s, compared with a control value
of 13 s; he was thrombocytopaenic, with a platelet count of 40 x 103/p1 and the partial
thromboplastin time (PTT) and the thrombin clotting time (TCT), although normal at
this time, became prolonged 4 days later when the PTT was 48 s with a control of 33 s,
and the TCT was 15 s with a control of 12 s. On day 4 the plasma was labelled with I-
labelled fibrinogen, the half-life of which was 35 h (normally 337 days), a finding
consistent with a consumptive coagulopathy. He was not heparinized and by day 11 the
clotting variables were all normal. His bone marrow was aspirated from the iliac crest
on day 4 and it showed active erythropoiesis consistent with an acute anaemia. Initially
his haemoglobin was maintained by transfusing him during dialysis. His transfusion
requirements increased as a result of his major haemorrhages and surgical operations
and he was given a total of 86 units of blood.

During days 2--13 he was jaundiced. HBD, aspartate transaminase (AST), .alkaline
phosphatase and bilirubin were elevated throughout his admission, indicating
hepatocellular damage (Table 1). Initially the HBD, AST and bilirubin were extremely
high, and on days 8--10 he was given vitamin K, 10 mg intramuscularly, daily. The
raised bilirubin and HBD may also have been associated with intravascular
haemolysis. His liver-function tests showed gradual improvement until the end of week
4, when, after colectomy, he developed a septicaemia and rifampicin, 600 mg daily, was
introduced into his drug regimen. There was a gradual rise in serum bilirubin and
alkaline phosphatase from that time.

Central nervous system

He was conscious and alert after cessation of ventilation on day 5 and was able to
communicate by writing until the tracheostomy tube was removed. During the first 2
weeks he complained of blurred vision and diplopia. There was no obvious cornea1
damage or extraocular muscle palsies, and his fundi appeared normal. On day 45 he
had a grand ma1 tit, after which he had focal neurological signs. A lumbar puncture was
 MERCURY POISONING 41

TabIe 3. Mercury concentrations reported in human organs and in the present case of mercury poisoning.

Chronic Fatal
Normal subjects Normal poisoning poisoning
(Joselow et al., subjects (Davis et al., (Bidstrup, Present
1967) (Eyl, 1971) 1974) 1964) case

Range Average
(p.p.m.) (p.p.m.) (pg/ml) (p.p.m.) @g/ml)

Cortex
2.1 p.p.m.
Kidney (t26.3 2.75 421.5
Medulla
8.2 p.p.m.
Liver SO.9 0.3
Brain O-O.6 0.1 0.26 p.p.m.
Small intestine O-O.9 0.1 3.0 p.p.m.
Stomach 4.7 p.p.m.
Day 4
4.8 pg/ml
Day 14
Blood 0.05-0.65 0.1-1.2
2.4 pg/ml
Day 18
1.5 pg/ml

performed; the pressure was 300 mm of cerebrospinal fluid and its protein content was
2880 mg/l. No organisms were seen or cultured from the fluid. A cerebral abscess was
the most likely diagnosis. As his condition deteriorated he required large doses of
anticonvulsants to suppress the fits. He was given diazepam, 10 mg intravenously, to
arrest each fit, and started on phenytoin sodium, 150 mg, 8 hourly, and an infusion of
chlormethiazole, 0.8%. at the rate of 500 ml. Three days later the fits stopped - no
sedation was required and as an electroencephalogram showed no activity ventilation
was discontinued.

Post-mortem examination
At post-mortem examination a large cerebral abscess was found occupying the left
lobe of the cerebellum and the right occipital lobe. The lungs were congested and
oedematous with areas of confluent bronchopneumonic consolidation. The stomach
was surrounded by dense fibrous adhesions and the peritoneal cavity contained locules
of pus and necrotic matter. There were three areas of infarction in the small bowel, the
liver was enlarged and soft, and the kidneys were swollen and pale.

Mercury analysis
Three blood samples were taken on days 4,14 and 18 for analysis of serum mercury
concentrations. These showed falling concentrations. Tissue mercury concentrations
were estimated from post-mortem specimens (Table 3).
42 M. J. MURPHY AND OTHERS

Discussion
Blood and tissue mercury concentrations in cases of poisoning and in the normal
population have been analysed (Bidstrup, 1964; Joselow, Goldwater &Weinberg, 1967;
Eyl, 1971). Although the quantity of mercury ingested by our patient was never known
the concentrations of mercury in the blood and tissues indicated that a large amount
was absorbed (Table 3). The blood concentrations fell, probably as the combined result
of excretion from the gut, haemodialysis and to some extent the BAL therapy.
Unfortunately, by the time this patient presented there was such extensive corrosive
damage to the upper gastrointestinal tract that gastric lavage was thought to be
hazardous, and as he had vomited it would probably have been of little benefit. BAL
was administered, but since this was 12 h after poisoning, this also probably did not
help very much.
Although there was no initial circulatory collapse, the patient developed acute renal
failure, severe gastrointestinal complications, corrosive ulceration, ulcerative colitis,
toxic dilatation and haemorrhage. Secondarily to these changes, he was severely
catabolic and approximately halved his body weight. The administration of adequate
feeding, parenterally, orally or in combination, proved impossible. His average daily
calorie intake of 2000 kcal/day (Table 2) was grossly inadequate. His severe anaemia
was due mainly to blood loss, since the bone marrow aspiration showed no evidence of
toxic suppression. The terminal events were the result of chronic sepsis. Pseudomonas
aeruyinosu, which was cultured from day 2, was never successfully eradicated despite
adequate blood concentrations of antibiotics, normal immunoglobulins and a
leucocytosis. Finally the patient developed a septicaemia and cerebellar abscess. There
was hepatocellular damage with gross elevation of liver enzymes preceding the
septicaemia. Apart from one case with fatty vacuolation of the liver (Sanchez-Sicilia,
Seto, Nakamoto & Kolff, 1963) we can find no previous reports of hepatic dysfunction
in cases of acute poisoning. It is not, however, surprising that it occurs in view of the fact
that a high proportion of injected mercury is seen in experimental situations to be taken
up by the liver (Rothstein & Hayes, 1960).
Mercuric chloride is a highly corrosive substance, which has both local and distal
effects after ingestion or application. The mercuric ion forms bonds with thiol groups
present in protein molecules, resulting in cellular destruction. It is excreted mainly by
the kidneys and colon, but also in small amounts by sweat and salivary glands, and in
milk. The kidneys are the main route of excretion, and thus proportionally high
concentrations of mercury occur in these organs after exposure (Joselow, Louria &
Browder, 1972). Experimentally it has been shown that 2 weeks after intravenous
administration, 90% of the total quantity of mercury in the body is deposited in the
kidneys (Rothstein & Hayes, 1960). Although there are many similarities, the
syndromes which occur after mercury poisoning depend upon whether the exposure is
acute or chronic and to which form of mercury, elemental, salt or organic compound,
the individual has been exposed (Eyl, 1971; Department of Employment, 1972; Hilmy,
Rahim & Abbas, 1976).
Acute exposure to 100 mg or more of inorganic mercuric salts has been reported to
give rise to the following symptoms: a bitter metallic taste in the mouth; a sense of
constriction of the throat; gastritis; abdominal pain; nausea; vomiting; corrosive ulcers
in the mouth; bloody diarrhoea; shock and oliguria or anuria (Schreiner & Maher,
1965). Inorganic mercurous salts, which in the past have been used widely as laxatives
(calomel or mercurous chloride), teething powders, ointments, antisyphilitics and
 MERCURY POISONING 43

antihelminthics, have given rise to similar but less severe symptoms. Cases of poisoning
from mercurous chloride laxatives are still being reported (Davis, Wards, Weiss, Price
& Girling, 1974).
The variation in the syndromes which occur after poisoning with other forms of
mercury results from different duration of exposure, methods of distribution and the
biotransformation of some mercury compounds (Kurland, Fard & Siedler, 1960;
Rothstein & Hayes, 1960; Hayes & Rothstein, 1962; Clarkson, 1965, 1968).
Only very small amounts of mercuric ion can cross the blood-brain barrier, whereas
unionized mercury and organic mercury salts are selectively taken up by the brain; in
the central nervous system they are degraded with the release of the toxic mercuric ion.
This is a slow metabolic process and therefore symptoms of organic poisoning develop
long after exposure.
Poisoning with mercuric chloride was relatively common before the beginning of
this decade (Hull & Mone. 1934; Longcope, Leutscher, Calkins. Grab, Bush &
Eisenberg, 1946; Doolan, Hess & Kyle, 1953; Sanches-Sicilia et al., 1963; Schreiner &
Maher, 1965; Frang, Csata, Hamvasi & Toth, 1966). The development during world
war 2 of the chelating agent British Anti-Lewisite (BAL, dimercaprol), which is now
used extensively in the treatment of mercury poisoning, has greatly improved the
prognosis. Longcope and his colleagues reported treating 23 cases of mercuric chloride
poisoning with BAL with only one death (4.49, mortality). compared with 34 deaths
from 263 cases (12.9% mortality) admitted to the Johns Hopkins Hospital between
1925 and 1945 (Longcope et al., 1946). Great emphasis is placed on the promptness with
which BAL is administered, and on the administration of an adequate dose. Renal
lesions begin to develop within the first 3 h and therefore, ideally, the first dose of BAL
should be given within this period. When acute renal insufficiency occurs the dose of
BAL should be reduced or discontinued if severe toxicity is to be avoided (Doolan et al.,
1953). Tissue damage, after it has occurred, is not corrected by BAL.
Various reports have recommended different dose regimens for BAL. Martindale
(1977) recommends that in mercury poisoning an initial dose of 5 mg/kg body weight
should be given intramuscularly, followed by two or three injections of 2.5 mg/kg body
weight in the next 12 h. This can be continued with 200400 mg on days 2 and 3 and
100-200 mg/day subsequently in divided doses.
Of patients receiving doses of 4-5 mg/kg body weight 50% can be expected to suffer
minor toxic reactions, including nausea, vomiting, headache, stomatitis, lachrimation,
salivation, paraesthesiae, a constricting sensation in the throat, chest pain, muscle
spasm, hypertension and tachycardia. These symptoms are most severe 15-20 min after
injection and may be alleviated by either an antihistamine or 25-50 mg of ephedrine
sulphate given half an hour before each BAL injection (Martindale, 1977).
There are three stages in the syndrome which develops from acute inorganic mercury
poisoning, but whereas not all patients develop all the features, any one of them or their
complications can result in death. Within the first 24 h the patient may become shocked
and develop circulatory failure, probably from hypovolaemia. Secondly the patient
may develop renal insufficiency with its complications, including fluid overload,
uraemia, hyperkalaemia and susceptibility to infections. Thirdly the patient may
develop a severe membranous or ulcerative colitis. Besides specific therapy with BAL
and haemodraiyz &p%tienGf beg ?o survrve, must be supported during each of
these phases. More people have survived since the introduction of BAL and
haemodialysis.
44 M. J. MURPHY AND OTHERS

Sanchez-Sicilia et al. (1963) list the therapeutic aims in acute inorganic mercury
poisoning as follows:
1. Immediate removal of poison by gastric lavage.
2. Prevention of its toxicity with early administration of BAL
3. Continuous use of BAL for 7 days or longer.
4. Early and frequent haemodialysis to support the patient through the period of
oliguria and possibly to remove the toxic mercury ion.
5. Colectomy and removal of the rectum when haemorrhage from ulcerative colitis
becomes a threat to life.

Acknowledgments
We thank Mr M. Bewick and Mr C. Rudge for their surgical assistance; the staff of the
Ventilation Unit, Dulwich Hospital for their devoted nursing care; Dr R. Goulding for
his help with the case report, and Dr D. Gibbons of Harwell Industrial Research for the
tissue analysis of mercury content.

References
Bidstrup, P. L. (1964) Toxicity of Mercury and its Compounds, p. 81. Elsevier, London.
Clark, T. W. (1965) Toxicological aspects. Ann. Occup. Hyg. 8, 73-80.
Clarkson, T. W. (1968) Biochemical aspects of mercury poisoning. J. Occup. Med. 10, 351-355.
Davis, L. E., Wards, J. R., Weiss, S. A., Price, D. L. & Girling, E. F. (1974)Central nervous system intoxication
from mercurous chloride laxatives. Arch. Neural. 30, 428-431.
Department of Employment, London (1972) Chief Employment Medical Adoisers Notes of Guidance:
Mercur).
Doolan, P. D., Hess, W. C. & Kyle, L. H. (1953) Acute renal insufficiency due to bichloride of mercury. SJ.
Engl. J. Med. 249, 273-276.
Eyl, T. B. (1971) Organic mercury food poispning. N. Eng. J. Med. 284, 7CltG709.
Frang, D., Csata, S., Hamvasi, G. & Toth, M. (1966) Acute renal insufficiency caused by mercury poisoning,
Oru. Hetil. 107, 1118-1120.
Hilmy, M. I., Rahim, S. A. & Abbas, A. H. (1976) Normal and lethal mercury levels in human beings.
Toxicology 6, !55-159.
Hayes, A. D. & Rothstein, A. (1962) The metabolism of inhaled mercury vapour in the rat studied by isotope
techniques. J. Pharmucol. 138, l-10.
Hull, E. & Mone, L. A. (1934)Bichloride of mercury: a statistical study of 302 cases. Southern Med. J. 27,918-
924.
Joselow, M. M., Goldwater, L. J. & Weinberg, S. B. (1967) Absorption and excretion of mercury in man:
mercury content of normal human tissue. Arch. Environmental Health 15,64-66.
Joselow, M. M., Louria, D. B. & Browder, A. A. (1972) Mercurialism, environmental and occupational
aspects. Ann. Intern. Med. 76, 119-130.
Kurland, L. T., Fard, S. N. & Siedler, H. (1960) Minamata disease. World Neural. 1, 370-380.
Longcope, W. T., Luetscher, J. A., Jr, Calkins, E., Grob, D., Bush, S. W. & Eisenberg, H. (1946)Clinical uses of
2,3 dimercaptopropanol (B.A.L.). J. Clin. Incest. 25, 557- 567.
Martindale (1977) Dimercaprol, in: The Extra Pharmacopoeia, 27th edn,.p. 331. Ed. Blacow, N. W. The
Pharmaceutical Press, London.
Rothstein, A. & Hayes, A. D. (1960) The metabolism of mercury in the rat studied by isotope techniques. J.
Phurmacol. 130, 166176.
Sanchez&cilia, L., Seto, D. S., Nakamoto, S. & Kolff, W. J. (1963) Acute mercurial intoxication treated by
haemodialysis. Ann. Int. Med. 59, 692-706.
Schreiner, G. E. & Maher, J. F. (1965) Toxic nephropathy. Am. J. Med. 38, 40949.