Case Report Singapore Med J 2009; 50(8) : e298

Acute naphthalene poisoning following

the non-accidental ingestion of mothballs
Lim H C, Poulose V, Tan H H

ABSTRACT due to school stress. She did not have any past medical
Ingestional naphthalene mothball poisoning history. She complained of giddiness and dark-coloured
l e a d i ng to p r o l o ng e d haemolysis and urine a few hours after the ingestion, but only sought
methaemoglobinaemia can present with medical help because of persistent symptoms. On the
diagnostic and therapeutic challenges. A 19- day of presentation, she vomited once and had mild
year-old woman ingested 12 mothballs, and suprapubic pain. Clinically, she was efebrile, her pulse
presented two days later with haemolysis rate was 109/minute, respiratory rate 16/minute, blood
and methaemoglobinaemia. She was treated pressure 102/71 mmHg, oxygen saturation (SpO2) 82% on
with red blood cell transfusions, intravenous 100% oxygen via facemask. She was pale, jaundiced and
methylene blue, N-acetylcysteine and ascorbic appeared to have cyanosis. Heart sounds were dual with
acid. Continuous venovenous haemofiltration a grade 2/6 ejection systolic murmur heard at the heart
was conducted for 45 hours. Haemolysis with apex. The lungs were clear with good air entry bilaterally.
anaemia and methaemoglobinaemia persisted The abdomen was mildly tender in the suprapubic region,
even after five days post-ingestion. Clinical and but soft and not guarded. No organomegaly was noted.
biochemical parameters improved. We describe Neurological examination was normal.
a case of ingestional naphthalene poisoning with Urinary catheterisation collected dark-brown urine,
a good outcome after treatment. which tested positive for blood on dipstick. The urine
microscopy did not reveal significant red blood cells
Keywords: haemolysis, methaemoglobinaemia, (RBC) content or casts, suggesting haemoglobinuria.
mothball ingestion, naphthalene, poisoning Electrocardiogram showed normal sinus rhythm, with
Singapore Med J 2009; 50(8): e298-e301 no ischaemic changes. At that time, the provisional
diagnosis was haemolysis, haemoglobinuria and possibly
Introduction methaemoglobinaemia secondary to naphthalene
Naphthalene mothballs, as a choice agent for deliberate toxicity. She did not bring any remaining mothball for
ingestion in suicide, is uncommon in Singapore. examination. Supportive management with oxygen and
Other more common agents that have led to patients intravenous (IV) fluid was provided. Gastric washout
requiring intensive care include organophosphates and and activated charcoal administration were not performed Department of
Emergency Medicine,
carbamates, benzodiazepines, tricyclic antidepressants, in view of delayed presentation. Alkalinisation of urine Changi General
and phenothiazine.(1) The fatal dose for naphthalene in was initiated in the emergency department in an effort Hospital,
2 Simei Street 3,
humans is unknown, but as little as one mothball can to prevent renal tubular damage, and she was admitted Singapore 529889

result in toxicity in children. Deaths have been reported to the intensive care unit (ICU) for further management. Lim HC, MBBS,
MRCSE, FAMS
following ingestion of naphthalene balls.(2,3) Haemolytic Alkalinisation of urine was continued there. Consultant
anaemia and methaemoglobinaemia from poisoning can Her initial full blood count revealed haemoglobin
Tan HH, MBBS,
pose a diagnostic and therapeutic challenge to clinicians (Hb) 9.7 g/dL with haematocrit 27.4%, reticulocyte count FRCSE, FAMS
Consultant
because it is not commonly encountered. We present a 0.8%, total white cell count 26.6 ×103/μL, and neutrophil
case of prolonged naphthalene-induced haemolysis and 84.1%. Intravascular haemolysis was confirmed by serum Division of
Respiratory Medicine
methaemoglobinaemia from a non-accidental ingestion of jaundice with total bilirubin measuring 84.0 μmol/L and
Poulose V, MBBS,
12 naphthalene mothballs, and reviewed the mechanism a highly-raised indirect bilirubin level, associated with FCCP
Consultant and
of its toxicity, diagnostic dilemma and management low serum haptoglobulin 0.09 g/L. Her platelet count Director, Medical
recommendations. and coagulation profile were normal. Renal function Intensive Care Unit

and the serum creatinine kinase were also normal. Liver Correspondence to:
Dr Tan Hock Heng
Case Report enzyme aspartate transaminase was raised at 98 U/L, Tel: (65) 6850 1687
A 19-year-old female foreign student presented 40 hours but alkaline phosphatase and alanine transaminase were Fax: (65) 6260 3756
Email:hock_heng_tan
after intentional oral ingestion of 12 mothballs. This was normal. Arterial blood gas (ABG) analysis did not reveal @cgh.com.sg
 Singapore Med J 2009; 50(8) : e299

any acidosis; pH 7.423, pCO2 34.4 mmHg, pO2 380.0 Hb (g/dL) MetHb (%)
IV methylene blue
mmHg, base excess −1.7 mmol/L, HCO3 21.9, O2 Sat
Start CVVH
100.0%. Serum lactic acid was normal. 14
Her first methaemoglobin (MetHb) level was 9.6% 12

Hb and MetHb levels

(Hb 8.6 g/dL). This increased to 13% on the second day 10
of admission, with Hb dropping to 7.5 g/dL. IV methylene 8
blue 60 mg (1.5 mg/kg) was prescribed on Day two of 6
admission and she was transfused two units of RBC 4 Blood transfusion Blood transfusion
(2 units) (2 units)
concentrate (total 730 ml). Oral ascorbic acid 300 mg 2

and N-acetylcysteine (NAC) 1.2 g daily was started. On 0

Day 1
Day 3 Day 2
Day 4 Day 5 Day 10
Day 3 of admission, the Hb remained at 7.5 g/dL, and Day of admission
there was only some improvement of MetHb to 7.8%. Fig. 1 Graph shows the haemoglobin (Hb) and methaemoglobin
(MetHb) levels vs. day of admission. The use of methylene
Ongoing haemolysis was suspected based on the failure blue and blood transfusions resulted in the improvement in
of Hb to improve as well as the continued collection of clinical and biochemical parameters. Continuous venovenous
haemofiltration (CVVH) was introduced on Day 3 of admission.
dark-brown urine. Another two units of blood (total 780
ml) were transfused and continuous renal replacement
therapy (CRRT) in the form of continuous venovenous
haemofiltration (CVVH) was started. This continued for mothballs are not freely available in Singapore. Bedside
almost 45 hours till Day 5. Blood samples on Days 1 and 3 differentiation is important to the clinician because
of admission were qualitatively positive for naphthalene; identifying a mothball containing paradichlorobenzene
however, the urine sample on Day 1 was negative for can often lead to outpatient management, saving both
naphthalene. On Day 4, her laboratory parameters money and undue worry.(5) One method is to test the
improved. Hb stabilised at 9.4 g/dL without further blood ability of the mothball to float in water and concentrated
transfusion; total bilirubin had dropped from 77.6 to 38.5 salt solution. A naphthalene mothball floats in saturated
μmol/L, with AST in the downward trend as well. Her salt solution but sinks in water. If it sinks in both liquids,
renal function remained normal and alkaline diuresis was it is a paradichlorobenzene mothball. Camphor, in
stopped. The urine was noted to be clear, and there was contrast, floats on water.(6) Radiography may also be
decreased cyanosis. The pulse oximeter begin to register helpful as paradichlorobenzene is radiopaque whereas
consistently > 95% by late afternoon that day. naphthalene is not.(7)
At this time, blood glucose-6-phosphate Naphthalene is a bicyclic aromatic hydrocarbon
dehydrogenase (G6PD) activity was confirmed present, with a molecular weight of 128 (C10H8). It is poorly
and her Hb electrophoresis was suggestive of Hb-E alpha soluble in water, and one mothball (depending on size)
thalassaemia. By Day 5 of admission, her Hb level had can contain between 0.5–5 g of naphthalene. The clinical
stabilised at 9.8 g/dL with normalisation of leucocyte consequences of naphthalene ingestion may include
count and serum total bilirubin level. Renal function was headache, vomiting, diarrhoea, abdominal pain, fever
preserved and MetHb was reduced to 1.8%. CVVH was and altered mental status.(5) Oxidative stress from the
discontinued and she was sent to general ward after five hepatic metabolites of naphthalene causes haemolysis
days in the ICU. Radioimaging tests for her abdominal and methaemoglobinaemia. The presence of one should
pain were normal and her urine pregnancy test was prompt the exclusion of the other. Laboratory studies
negative. The pain resolved spontaneously. She stayed a have also demonstrated that naphthalene induces
total of ten days in the hospital. On discharge, her Hb was toxic manifestations by enhanced production of free
10.3 g/dL and MetHb 1.1%, with no renal or neurological oxygen radicals, resulting in lipid peroxidation and
sequelae. Subsequently, she was lost to outpatient follow- deoxyribonucleic acid damage.(8) Ascorbic acid was
up. Table I and Fig. 1 illustrate the progression of her given to our patient to counteract this effect; it has also
biochemical parameters and the important interventions been used in one previously-described case(9) though its
performed while she was admitted. efficacy is questioned as it is a weak reducing agent.
Haemolysis occurs through either Hb (Heinz
Discussion bodies formation) or cell membrane effects, particularly
Mothballs retailed for household use in Singapore in patients with a low tolerance to oxidative stress
may contain naphthalene or paradichlorobenzene, (4)
of (G6PD deficiency). Renal failure as a complication of
which the latter poses less harm if ingested. Camphor naphthalene-induced haemolysis and haemoglobinuria
 Singapore Med J 2009; 50(8) : e300

Table I. Progression of biochemical parameters while the patient was admitted.

Day of admission: Day 1 Day 2 Day 3 Day 4 Day 5 Day 10

Haemoglobin (g/dL) 8.6 7.5 7.5 9.4 9.8 10.3

Methaemoglobin (%) 9.6 13 7.8 NA 1.8 1.1
Qualitative serum naphthalene Positive ND Positive ND ND ND
Urine colour Brown Brown Brown Clearing Clear NA

NA: not available; ND: not done

has been reported.(10) Haemolysis and haemoglobinuria show enhanced reduction in human volunteers.(14,15) Other
are treated with IV hydration ensuring brisk urine output, than the specific therapies described above, management
urinary alkalinisation and packed RBC transfusion. of naphthalene toxicity is mainly supportive. If the
Urinary alkalinisation and IV hydration with diuresis patient presents early, decontamination procedures like
are aimed at minimising the deposition of Hb in kidney the use of activated charcoal, gastric lavage and whole
tubules. However, regular monitoring and correction of bowel irrigation should be considered.
blood and urine pH as well as blood electrolytes need to Our patient demonstrated persistent haemolytic
be maintained. anaemia and methaemoglobinaemia up to five days
Methaemoglobinaemia is caused by the oxidation post-ingestion. This is also shown in other cases of
of ferrous (Fe ) to ferric (Fe ) Hb. It renders the
2+ 3+
naphthalene ingestion where the haemolysis and metHb
Hb incapable of carrying oxygen and shifts the persisted more than a week.(10) No studies have quantified
oxyhaemoglobin curve to the left. Cyanosis is clinically the rate and extent of naphthalene absorption in humans
detectable at >10% metHb in a patient with a Hb 15 following ingestion. Extended urinary excretion has
g/dL (> 1.5 g/dL of metHb). However, the presence of been observed following the ingestion, with metabolites
anaemia could mask this clinical sign at the same metHb still detectable in the urine 13 days post-ingestion.(16) The
fraction. Pulse oximetry may become unreliable in the postmortem finding of one patient who swallowed 40
setting of methaemoglobinaemia, registering a false mothballs and died five days later revealed 25 remaining
high in patients with severe methaemoglobinaemia and a mothballs in the stomach.(3)
false low in patients with mild methaemoglobinaemia.(11) There is little in the literature on the use of
Routine ABG of these patients measures serum PO2 extracorporeal elimination modalities to treat acute
(which is normal) and calculates a falsely normal oxygen poisoning with naphthalene. One man with naphthalene
saturation. A co-oximeter type of blood gas analyser is poisoning had survived following haemodialysis.(17)
needed to directly measure the oxygen saturation and Free naphthalene and its metabolites should cross the
metHb levels. Clinical suspicion of metHb should be haemofilter readily, but naphthalene is poorly water-
raised when there is cyanosis that does not respond to soluble, and its volume of distribution is not defined. The
high-flow oxygen with no obvious cardiorespiratory role of CRRT in the removal of excessive fluid overload,
causes, like right-to-left shunting. especially in haemodynamically-unstable patients, is
Standard treatment includes the use of methylene well established. However, its role in poison elimination
blue and exchange transfusion. Methylene blue increases remains ill-defined.(18) Its use in lithium poisoning to
the rate of conversion of metHb to Hb by accepting reduce the rebound of lithium level post-haemodialysis
an electron (in the presence of nicotinamide adenine has been reported.(19) This is mainly because CRRT
dinucleotide phosphate [NADPH] and metHb reductase), can be used over 24 hours. The CRRT technique to
to form leucomethylene blue, which can then donate this enhance elimination was utilised in this case because of
electron to reduce metHb. (12)
It is important to note that continued haemolysis despite full supportive care and
methylene blue itself may induce haemolysis (through blood transfusion. In the presence of delayed extended
the development of Heinz bodies) and cause paradoxical absorption of naphthalene from the gastrointestinal
methaemoglobinaemia, especially in G6PD deficient tract or sequestration of the poison in the body fats, it
patients.(13) The use of NAC as a direct reducing agent in could provide ongoing removal of toxins, reducing the
treating methaemoglobinaemia is still being investigated. likelihood of rebound toxicity. The institution of CVVH
It presents the potential benefit in G6PD deficiency coincided with clinical improvement in our patient.
because glutathione synthesis is not dependent on However, we could not confirm whether it made a real
NADPH.(13) However, recent studies with NAC failed to difference in the patient’s recovery, and more studies
 Singapore Med J 2009; 50(8) : e301

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