|
|
|
|
OJHAS Vol. 8, Issue 3: (2009
Jul-Sep) |
|
|
|
Response: Accidental Potassium Bromate Poisoning Causing Acute Renal Failure |
|
| Kazeem A. Oshikoya, Department of Pharmacology, Lagos State University College of
Medicine, and Department of Paediatrics, Lagos State University Teaching
Hospital, Ikeja, Lagos, Nigeria. |
|
|
| |
|
|
|
|
|
|
Address For Correspondence |
Academic Division of Child Health,
University of Nottingham,
Derby Royal Children’s Hospital,
Derbyshire DE 22 3 DT,
United Kingdom.
E-mail:
med_modhospital@yahoo.com |
|
|
|
|
|
Oshikoya KA. Response: Accidental Potassium Bromate Poisoning Causing Acute Renal Failure. Online J Health Allied Scs.
2009;8(3):19 |
|
|
|
|
Submitted: Jul 3, 2009; Accepted:
Jul 10, 2009 Published: Nov 15, 2009 |
|
|
|
|
|
|
|
| |
| |
| Abstract: |
|
No abstract
Key Words:
Potassium bromate,
Poisoning
|
|
I have read with keen interest the
case of accidental ingestion of potassium bromate by a two year old boy reported
by Adeleke and Asani.1 I
sincerely congratulate them for their high index of suspicion of potassium
bromate poisoning and for successfully managing the patient amidst inadequate
facilities in Nigeria to manage such a case. However, I would like to raise a
few points about the history and management of the patient.
Even though the body temperature was
not reported, vomiting, diarrhoea, abdominal pains, lethargy and
hepato-splenomegaly, as initially presented by the patient, are symptoms and
signs of malaria2 or
inflammatory gastroenteritis.3Perhaps
this was the reason for the initial diagnosis of acute diarrhoea with some
dehydration made by the authors. The degree of dehydration of the patient at
presentation was not reported, however, the passage of frequent and loose watery
stools with weakness may indicate moderate to severe dehydration. Moderate to
severe dehydration may result in acute renal failure.4
There is a high possibility of the
child ingesting potassium bromate especially when the mother rinsed his mouth
with water. However, the quantity swallowed may be small and this may perhaps
explain the mild symptoms and signs initially presented by the child. The
quantity of potassium bromate ingested by children from previous reports was
very small5,6 compared
to adults7, 8 and
this have accounted for the relatively mild symptoms observed in the children.
Hepato-splenomegaly has not been reported in previous cases of acute potassium
bromate poisoning but this may be caused by a massive intravascular haemolysis.
Massive haemolysis and thrombocytopenia may be seen in children with bromate
poisoning9 but
were not present in the patient reported by Adeleke and Asani.1 However,
mild haemolysis was reported as evident by anaemia (PCV- 28%). Thus, malaria or
inflammatory gastroenteritis may explain the hepo-splenomegaly reported in the
patient. It might have been useful to do complete blood count, blood film
morphology and malaria parasites study of the patient. Electrolyte and urea are
very important in patients with moderate to severe dehydration which should have
served as early pointers to acute renal failure but unfortunately they were
delayed until the 4th day
of admission.
The mechanism of bromate toxicity is
not clearly understood9 but
it has been proposed that renal failure could result from direct tubular
toxicity due to induction of active oxygen radicals10,
reduced renal perfusion from dehydration and possibly decreased vasomotor tone.7,11 Haemolytic anaemia with
haemoglobinaemia may also play a role.12 Asymptomatic
phase of a few hours may follow bromate poisoning before overt renal failure
develops and anuria is usually apparent within 1-2 days of bromate ingestion11 similar
to the onset of anuria in the patient reported by Adeleke and Asani.1 Perhaps,
a urethral catheterisation would have been more appropriate to monitor urinary
output rather than suprapubic needle aspiration performed by the authors.
The authors have centred their
discussion on the management of acute bromate poisoning with reference to animal
studies which could not be extrapolated to human and may not be very relevant in
the clinical management of the patient. The principles of management of acute
bromate poisoning are largely empirical and supportive. They include reducing
bromate to less toxic bromide ion with specific antidotes. 10% sodium
thiosulphate solution, 10- 50 ml (0.2- 1 ml/kg) i.v has been successfully used
as a specific antidote in the treatment of acute bromate poisoning in children.5-7,11 Methaemoglobinaemia may
require the use of methylene blue.8 In
the early stage, patient can be decontaminated with sodium bicarbonate (baking
powder) to prevent formation of hydrobromic acid in the stomach9;
it might have been worth a trial in this patient. Large recent bromate ingestion
may require gastric lavage with a 2% sodium bicarbonate or activated charcoal.9,12 Peritoneal dialysis was
performed in the patient not only to reverse the renal failure but to enhance
bromate ion elimination since bromates are primarily excreted renally.9
Tinnitus and irreversible sensorineural
deafness may complicate bromate poisoning and may be delayed for several days in
children or may go unnoticed.9,11,12 Thus, audiometry at
presentation and follow-up was very important in the management of this patient.
Polyneuropathy, characterised by severe burning pain to the leg, is an unusual
symptom seen in bromate poisoning in adult and may present very late; although
it may resolve spontaneously after a month.13 Thus,
a neurological examination should have formed part of the follow-up evaluation
of this patient.
- Adeleke SI, Asani MO. Accidental
potassium bromate poisoning causing acute renal failure.
Online J Health
Allied Scs. 2009;8(1):11.
- Bhutta ZA. Acute gastroenteritis in
children. In: Kliegman RM, Behrman RE, Jenson HB, Stanton BF, eds. Nelson
Textbook of Paediatrics. 18th ed. Philadelphia: Saunders Elsevier, 2007:
1065-1618.
- Molyneux ME. Malaria- clinical
features in children. J Royal Soc Med 1989;17(Suppl):35-38.
- Ford DM. Fluid, electrolyte, and
acid-base disorders and therapy. In Hay WW, Levin MJ, Sondheimer JM,
Deterding RR, eds. Current diagnosis and treatment in pediatrics. 18th ed.
USA: McGraw-Hill, 2007: 1274-1282.
- Warshaw BL, Carter MC, Hymes LC,
Bruner BS Rauber AP. Bromate poisoning from hair permanent preparations.
Pediatrics 1985;76:975-978.
- Kearnery TE, Redetki HM, McElwee NE.
Sodium bromate poisoning in an infant who ingested a home cold wave
neutralizing solution. Vet Hum Toxicol 1986;28:482.
- Matsumoto I, Morizono T, Paparella
NM. Hearing loss following potassium bromate: two case reports. Otolaryngol
Head Neck Surg 1980;88:625-629.
- Kutom A, Bazilinski NG, Magana L,
Dunea G. Bromate intoxication: hairdresser’s anuria. Am J Kidney Dis 1990;15:84-85.
- Olson KR, Anderson IB, Benowitz NL,
Blanc PD, Clark RF, Kearney TE, Osterloh JD. Poisoning and overdose. 5th ed.
USA. Mc Graw Hill. 2006. pp 128-130
- Kurokawa Y, Maekawa A, Takahashi M,
Hayashi Y. Toxicity and carcinogenecity of potassium bromate- a new renal
carcinogen. Environ Health Perspect 1990;87:309-335.
- Gradus D, Rhoads M, Bergstrom LB,
Jordan SC. Acute bromate poisoning associated with renal failure and deafness
presenting as haemolytic uremic syndrome. Am J Nephrol 1984;4:188-191.
- De Vriese A, Vanholder R, Lameire N.
Severe acute renal failure due to bromate intoxication: report of a case and
discussion of management guidelines based on a review of the literature.
Nephrol Dial Transplant 1997;12:204-209.
- Wang V, Lin K Tsai C, Kao K. Bromate
intoxication with polyneuropathy. J Neurol Neurosurg Psychiatry 1995;58:516-517.
|
