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A novel and fatal method of copper sulphate poisoning

Authors:

Abstract

Introduction Le sulfate de cuivre est largement utilisé dans le monde entier comme pesticide et fongicide pour les semences. Nombre de cas d’intoxications accidentelles par cette substance ont été signalés chez des ouvriers agricoles ayant absorbé d’importantes quantités de cette substance par voie cutanée. Ce composé a également été utilisé à des fins d’automutilation, généralement par ingestion orale. Les niveaux toxiques de la substance peuvent entraîner une méthémoglobinémie et la mort. Etude de cas Le cas d’une femme âgée de 29 ans ayant dilué et inséré du sulfate de cuivre par voie vaginale afin de mettre un terme à une grossesse non désirée est présenté. Conclusion Une étude des symptômes, du diagnostic et du traitement de la méthémoglobinémie induite par le sulfate de cuivre, ainsi que les difficultés liées au traitement de cette affection dans des structures médicales qui ne sont pas préparées à de telles complications.
CASE REPORT
A novel and fatal method of copper sulphate poisoning
Un nouveau mode d’empoisonnement, mortel, par le sulfate de cuivre
Keneilwe Motlhatlhedi
a,
*, Jacqueline A. Firth
b,c,d
, Vincent Setlhare
a
, Jackson K. Kaguamba
e
,
Mmapula Mmolaatshepe
f
a
Department of Family Medicine, University of Botswana School of Medicine, Botswana
b
Botswana University of Pennsylvania partnership, Botswana
c
Perelman School of Medicine at the University of Pennsylvania, United States
d
Department of Internal Medicine, University of Botswana School of Medicine, Botswana
e
Mahalapye District Hospital, Botswana
f
Jwaneng Mine Hospital, Botswana
Received 7 May 2013; revised 1 February 2014; accepted 2 February 2014
Introduction: Copper sulphate is widely used around the world as a pesticide and seed fungicide. Many cases of accidental intoxication with this substance have been
reported among farm workers who have absorbed large amounts of the substance through the skin. It has also been used for self-harm, generally by oral ingestion.
Toxic levels of the substance can lead to methaemoglobinaemia and death.
Case report: The case of a 29 year old woman who diluted and inserted copper sulphate vaginally in order to terminate an unwanted pregnancy is reported.
Conclusion: This article is a review of the presentation, diagnosis and treatment of copper-sulphate-induced methaemoglobinaemia, including the challenges of treating
this condition in clinical settings that are unprepared for this complication.
Introduction: Le sulfate de cuivre est largement utilise
´dans le monde entier comme pesticide et fongicide pour les semences. Nombre de cas d’intoxications acciden-
telles par cette substance ont e
´te
´signale
´s chez des ouvriers agricoles ayant absorbe
´d’importantes quantite
´s de cette substance par voie cutane
´e. Ce compose
´ae
´galement
e
´te
´utilise
´a
`des fins d’automutilation, ge
´ne
´ralement par ingestion orale. Les niveaux toxiques de la substance peuvent entraıˆ ner une me
´the
´moglobine
´mie et la mort.
Etude de cas: Le cas d’une femme aˆ ge
´e de 29 ans ayant dilue
´et inse
´re
´du sulfate de cuivre par voie vaginale afin de mettre un terme a
`une grossesse non de
´sire
´e est
pre
´sente
´.
Conclusion: Une e
´tude des symptoˆ mes, du diagnostic et du traitement de la me
´the
´moglobine
´mie induite par le sulfate de cuivre, ainsi que les difficulte
´s lie
´es au trait-
ement de cette affection dans des structures me
´dicales qui ne sont pas pre
´pare
´es a
`de telles complications.
African relevance
Many people in rural Africa may be exposed to copper sul-
phate and its toxicities, often through exposure while farm-
ing. Thus, it is important for health care providers to be
able to identify and treat copper sulphate poisoning.
The ease with which copper sulphate can be obtained in
Botswana, and perhaps in other African countries, coupled
with the high prevalence of HIV/AIDS and unwanted preg-
nancies may lead to attempted terminations of pregnancy
with use of copper sulphate. Should this be the case, this
article may serve as a guide for emergency care physicians
in our setting.
The article also highlights the diagnosis and treatment of
methaemoglobinaemia regardless of its cause and it is
important for physicians in the African setting to be able
to manage this condition.
The unavailability of the required antidote in this case, which
contributed ultimately to the patients death, may help to spark
discussion about the possible creation of toxicology plans and
centres in African health care systems. Through planning
ahead for these incidents, rarely used antidotes and clinical
guidance may be accessed when needed. This is especially
important in the African setting where access to toxicology
information, antidotes, or chelators may be limited.
Introduction
Copper sulphate (CuSO
4
) is widely used around the world as a
pesticide and seed fungicide.
1–3
Many cases of accidental
intoxication with this substance have been reported among
*Correspondence to Keneilwe Motlhatlhedi. P.O. Box 20728, Bontleng,
Gaborone, Botswana. Tel.: +267 72110741. kennymotlhatlhedi@yahoo.com
Peer review under responsibility of African Federation for Emergency Medicine.
Production and hosting by Elsevier
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http://dx.doi.org/10.1016/j.afjem.2014.02.002
Please cite this article in press as: Motlhatlhedi K et al. A novel and fatal method of copper sulphate poisoning, Afr J Emerg Med (2014), http://
dx.doi.org/10.1016/j.afjem.2014.02.002
farm workers who absorbed large amounts of the substance
through the skin.
1
It has also been used for self-harm, gener-
ally by oral ingestion.
2
Toxic levels of copper sulphate can lead
to methaemoglobinaemia and death.
3,4
A case of poisoning
due to copper sulphate inserted vaginally in order to terminate
an unwanted pregnancy is described. No other reports on cop-
per sulphate poisoning in Southern Africa or Botswana were
found; most reports in the literature are from Asia.
3,4
Case report
A 29-year-old female, 15 weeks pregnant and recently diag-
nosed with HIV infection (CD4 count unknown) presented
to the Mahalapye District Hospital emergency centre, a village
hospital with no specialist physicians and no intensive care
unit, with a history of excessive vomiting, extreme weakness,
and lower abdominal pains without vaginal bleeding. Eventu-
ally, she admitted inserting an unstated amount of copper sul-
phate powder diluted in water vaginally approximately 2 h
before presentation; her intent had been to abort an unplanned
pregnancy as her partner was unsupportive. On examination
she was conscious and alert, not pale, jaundiced, or cyanosed,
and not in respiratory distress, with a respiratory rate of 18
breaths per minute and an oxygen saturation of 96% on room
air. Her blood pressure was 128/75 mmHg with a regular pulse
of 99 beats per minute. She had mild tenderness in the supra-
pubic area.
Her underwear had bluish staining and a mucoid blue sub-
stance was observed at the cervical os. The cervix was closed
and there was no bleeding. Initial laboratory results were a
white cell count of 6.81 ·10
3
/mL, haemoglobin of 14.2 g/dL
with a haematocrit of 40.5%, serum creatinine 83 lmol/L,
AST 22.5 U/L and an ALT of 3.7 U/L. An obstetric ultra-
sound scan done at admission showed a viable 15 week old
foetus. The patient was started on 1 L ringers lactate and oxy-
gen by face mask, then admitted to the ward on 1 g IV Cefo-
taxime and 500 mg IV metronidazole 8 h, for suspected
septic abortion.
Approximately 12 h after admission the patient was cya-
notic with a decreased level of consciousness, responding only
to pain, and with amniotic liquor draining per vagina. Her
blood pressure had dropped to 90/60 mmHg, pulse was 120
beats per minute, and temperature was 37 C. She had signs
of peripheral vasoconstriction and an initial random blood
glucose of 1.5 mmol/L. Oxygen saturations were unknown
due to the lack of a monitor, but she was kept on high flow
oxygen per face mask and given a 50% dextrose 50 mL bolus
followed by 1 L 5% dextrose with simultaneous 1 L ringers
lactate bolus. Her blood sugar was 4.4 mmol/L when re-
checked. Oxygen saturations were finally obtained and found
to be 74% on oxygen by facemask. The patient developed a
bluish discolouration of her palms and feet, and her blood
was a chocolate brown colour, consistent with methaemoglobi-
naemia. Her serum creatinine had risen to 289 lmol/L, AST to
564 U/L and ALT to 57 U/L. Her white cell count was
55.89 ·10
3
/mL and her haemoglobin was 15.7 g/dL whilst
the haematocrit was 49.3%. There was no blood for transfu-
sion available at the time.
The recommended antidote for methaemoglobinaemia,
methylene blue, was not available in the hospital or in any
other hospitals contacted. Approximately 22 h after admission,
having received 2 doses of antibiotics and a total of 4 L intra-
venous fluid, the patient died. The cause of death was thought
to be tissue hypoxia and multi-organ failure.
Discussion
Ingestion of 15–20 mg of copper sulphate is reported to cause
mainly gastrointestinal symptoms, with higher doses resulting
in multi-organ damage. Lethal doses of copper sulphate inges-
tion are 10–20 g.
1,2
Gastrointestinal symptoms predominate in copper sulphate
toxicity include: vomiting, haematemesis, melaena, and diar-
rhoea. These symptoms seem to be unrelated to the mode of
poisoning, whether oral or parenteral.
1,3,5
Acute liver failure may occur due to direct toxicity of cop-
per sulphate and usually occurs in severe poisoning. Liver fail-
ure may present as hepatomegaly, icterus, or an increase in
transaminases and prothrombin time.
2,3
Renal injury may be
a result of (1) pre-renal failure resulting from the volume
depletion secondary to excessive vomiting and or diarrhoea,
(2) sepsis, (3) rhabdomyolysis, (4) intravascular haemolysis
(haemoglobinuria leading to acute tubular necrosis), or (5)
direct copper toxicity on the proximal tubules.
1–4
Sepsis and
infection may further aggravate copper sulphate poisoning
and antibiotics may be indicated.
3
The two main haematological complications of copper sul-
phate poisoning are intravascular haemolysis (due to inhibi-
tion of glucose-6-phosphate dehydrogenase or a direct effect
on the red blood cell membrane) and methaemoglobina-
emia.
1–4
In the red blood cell, copper oxidizes the iron in the haeme
complex from the ferrous Fe
2+
to the ferric Fe
3+
.
2,3
This ferric
form has a diminished oxygen binding capacity and also
increases the oxygen affinity of the remaining ferrous haeme
in the haemoglobin tetramer. This results in a shift of the oxy-
gen curve to the left; thus, oxygen is not readily released to the
cells.
6
At high levels of methaemoglobinaemia, the patient may
have tissue hypoxia despite adequate oxygenation and haemo-
globin levels, essentially a functional anaemia.
6,7
The presence
of normal arterial partial pressure of oxygen but a low SpO
2
is
called a saturation gap and is an indication of methaemoglobi-
naemia.
6,7
Symptoms of methaemoglobinaemia are not usually
seen when blood methaemoglobin levels are below 3%; cyano-
sis is usually noted at levels above 15% and the chocolate
brown colour of blood (as seen in our patient) is usually indic-
ative of levels between 15% and 30%.
8
Methaemoglobin levels
above 50% may result in central nervous system depression,
cardiac arrhythmias, and death.
8
Copper sulphate poisoning can be managed in four steps:
(1) resuscitative/supportive measures, (2) decreasing absorp-
tion, (3) chelation, and (4) management of complications. This
article focuses on the management of methaemoglobinaemia, a
complication of copper sulphate poisoning, as it was the most
immediate cause of the patient’s death.
In case of ingestion of the toxin, after initiating resuscitative
measures (ABCs) as necessary, milk, water, or activated char-
coal may be given to decrease absorption if the patient presents
within 4 h of ingestion, although there is no specific evidence to
support these measures.
2
Induction of vomiting is not recom-
mended since copper sulphate is highly emetic; for this reason
gastric lavage is also not mandatory.
1,2
2 K. Motlhatlhedi et al.
Please cite this article in press as: Motlhatlhedi K et al. A novel and fatal method of copper sulphate poisoning, Afr J Emerg Med (2014), http://
dx.doi.org/10.1016/j.afjem.2014.02.002
When the methaemoglobin levels are greater than 30% of
the total haemoglobin levels, treatment with methylene blue
is imperative.
2,6,8
Methylene blue acts by transferring an elec-
tron from NADPH to the ferric haemoglobin, thus reducing
it to the ferrous form. This dependence of methylene blue on
the availability of NADPH renders methylene blue ineffective
in people with glucose-6-phosphate dehydrogenase deficiency,
as this enzyme is required for NADPH production in the red
cell.
2,8,9
For these patients, as well as those with markedly ele-
vated methaemoglobinaemia and/or haemolysis, blood trans-
fusion or exchange transfusion is more beneficial.
1,8,9
The recommended dose of methylene blue is 1–2 mg/kg
given intravenously over 5 min. This dose can be repeated
every hour to a maximum of 7 mg/kg if cyanosis persists.
6,8
Methylene blue given at doses greater than 4 mg/kg can result
in haemolysis and caution is therefore necessary, as copper can
also cause haemolysis.
6,9
Rebound methaemoglobinaemia may
also occur if high doses are administered; therefore, where pos-
sible, serial measurements of methaemoglobin levels are rec-
ommended as additional doses of methylene blue may be
necessary.
2,9
Conclusion
Clinicians in resource-limited settings must be aware of the
possibility of methaemoglobinaemia in patients who present
with hypoxia not responsive to oxygen therapy and with a sat-
uration gap. They must also be aware of the ease with which
patients can come into contact with copper sulphate and its
potential toxicity. The powder can be bought at approximately
USD$1 over the counter at local chemists.
Some clinical and logistical questions raised by this case
include the following: (1) Is per vaginal application of copper
sulphate more toxic than oral or parenteral administration? (2)
Did the pregnancy and/or the HIV status of the patient con-
tribute to her rapid deterioration? (3) Even though copper
sulphate poisoning is rarely reported in our region, should
methylene blue be made available in our hospitals? Further
discussion of this case with the relevant authorities is ongoing.
Conflict of interest
All authors declare that there are no conflicts of interest to dis-
close. None of the authors have any financial or personal rela-
tionships with other people or organizations that could
influence their work.
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Copper sulphate poisoning 3
Please cite this article in press as: Motlhatlhedi K et al. A novel and fatal method of copper sulphate poisoning, Afr J Emerg Med (2014), http://
dx.doi.org/10.1016/j.afjem.2014.02.002
... More specifi cally, the highest prevalence (37.5%) is found in the age subgroup of 26-35 years, followed by 25.0% in the age subgroup of 16-25 years and 18.8% in the age sub-group of 46-55 years. Copper sulfate intake is often a suicidal gesture among adults; 93.75% of the cases are intentional (see Table 1) [12,26,27,30,34,35,37,39,40,43,46,49,55,68]. ...
... Furthermore, Akintonwa et al. reported deaths after the ingestion of "spiritual green water", containing more than 100 mg/L of copper sulfate [5]. In 87.5% of reported incidents, copper sulfate involved ingestion and absorption through the gastrointestinal tract [12,26,27,30,34,35,37,39,40,43,46,49,55,68]. Few studies, however, have reported parenteral copper sulfate poisoning (6.25%) [7,9]. ...
... In addition, an unusual fatal case of copper sulfate poisoning has been reported involving a 29-yearold woman, who inserted an unknown quantity of copper sulfate vaginally in order to terminate an unwanted pregnancy. She died of a septic abortion and hepatorenal failure [43]. ...
Article
A literature review of cases of acute poisoning by copper sulfate was conducted, emphasizing therapeutic interventions, and a new fatality case is reported. Specifically, the relevant literature was reviewed for incidence rates, sociodemographic variables, pathophysiology, diagnosis, prognosis, and therapeutic outcome of copper sulfate poisoning. Results conclude that copper sulfate poisoning incidence varies in different regions. It is rare in western countries, while it is very common in South Asian countries. The majority of patients belong to rural populations and are males in the third decade of their lives. The lethal dose of ingested copper is considered to be 10-20 g; 14-36% of the patients pass away within a few hours of ingestion, while the average hospitalization time is more than 20 days. The clinical features of copper sulfate poisoning include erosive gastropathy, intravascular hemolysis, methemoglobinemia, hepatitis, and acute kidney injury. The therapeutic management focuses on absorption reduction, close observation for complications, supportive therapy, and chelation therapy.
... 1 Except for South Asian countries like India, Pakistan, and Sri Lanka etc, Copper Sulfate poisoning is uncommon in the world. 1,2,3 In these countries its ingestion is accidental or deliberate self-harm related. 1,2,4 For efficient treatment of Copper Sulfate poisoning, it is mandatory that treating physicians should be well versed with this rare kind of poisoning. ...
... It has direct toxic effects which results in hepatic, gastrointestinal, hematological, and renal manifestations. 3 Indirectly, its effects are produced due to intravascular hemolysis, methaemoglobinaemia, rhabdomyolysis, hypovolemia, and sepsis etc. 3 Methaemoglobinaemia causes functional anemia i.e., hemoglobin and oxygen saturation on ABGs are normal but the patient is cyanosed. 5 Fatal dose of copper sulfate is 10-20 grams. ...
... It has direct toxic effects which results in hepatic, gastrointestinal, hematological, and renal manifestations. 3 Indirectly, its effects are produced due to intravascular hemolysis, methaemoglobinaemia, rhabdomyolysis, hypovolemia, and sepsis etc. 3 Methaemoglobinaemia causes functional anemia i.e., hemoglobin and oxygen saturation on ABGs are normal but the patient is cyanosed. 5 Fatal dose of copper sulfate is 10-20 grams. ...
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Case Report focusing Copper sulfate poisoning and its management
... Copper sulfate (CuSO 4 ) is an inorganic compound frequently used in agriculture, analytical, and tissue culture laboratories as it possesses pesticidal, redox potential, and antimicrobial actions, respectively. However, accidental or deliberate intoxication with Cu may cause multiorgan toxicity, which can be life-threatening [9,10]. The acute toxicity of CuSO 4 can cause hepatitis, jaundice, intravascular hemolysis, methemoglobinemia, erosive gastritis, acute tubular necrosis, and rhabdomyolysis [11,12]. ...
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Ingestion of strong oxidant substances may result in acquired methemoglobinemia, a clinical condition in which the oxidized blood hemoglobin is incapable of delivering oxygen to the tissues, and the patient becomes cyanotic. Traditional first-line therapy consists of infusion of methylene blue, whose action depends on the availability of reduced nicotinamide adenine nucleotide phosphate (NADPH) within the red blood cell (RBC). Some patients, particularly those who are deficient in glucose-6-phosphate dehydrogenase (G6PD), will not benefit from methylene blue. In these patients, and in some patients who have ingested very strong oxidants, methylene blue may also precipitate Heinz body hemolytic anemia. We present a case of severe, acquired methemoglobinemia in a 26-month-old, 9.8-kg boy with G6PD deficiency. He was cyanotic, in respiratory failure, intubated in a pediatric intensive care unit. In typical fashion, he did not respond to methylene blue. Manual exchange of two whole blood volumes, performed over 4 1/2 hr, also failed to resolve his severe methemoglobinemia. An automated RBC exchange (1.3 RBC volume), lowered his methemoglobin content from 31.8% to 7% in a single 40-min procedure. Thereafter his methemoglobin level continued to decrease rapidly and spontaneously. He was discharged home 2 days later, with 0.4% methemoglobin. To our knowledge, this is the first report to demonstrate the (potentially superior) effectiveness of automated RBC exchange for treatment of patients with high-risk acquired methemoglobinemia, that is, those with G6PD deficiency or who have ingested strong oxidants.
Article
Methemoglobin (MHb) may arise from a variety of etiologies including genetic, dietary, idiopathic, and toxicologic sources. Symptoms vary from mild headache to coma/death and may not correlate with measured MHb concentrations. Toxin-induced MHb may be complicated by the drug's effect on other organ systems such as the liver or lungs. The existence of underlying heart, lung, or blood disease may exacerbate the toxicity of MHb. The diagnosis may be complicated by the effect of MHb on arterial blood gas and pulse oximeter oxygen saturation results. In addition, other dyshemoglobins may be confused with MHb. Treatment with methylene blue can be complicated by the presence of underlying enzyme deficiencies, including glucose-6-phosphate dehydrogenase deficiency. Experimental antidotes for MHb may provide alternative treatments in the future, but require further study.