|Year : 2016 | Volume
| Issue : 2 | Page : 76-78
Acute intravascular hemolysis following accidental ingestion of naphthalene: A rare case report
Rachita Sarangi1, Sarita Pradhan2, Bikrant Kumar Prusty1, Sitaram Mahapatra3
1 Department of Paediatrics, IMS and SUM Hospital, Siksha O Anusandhan University, Bhubaneswar, Odisha, India
2 Department of Pathology, Division of Hematology Laboratory, IMS and SUM Hospital, Siksha O Anusandhan University, Bhubaneswar, Odisha, India
3 Department of Pathology, SCB Medical College, Bhubaneswar, Odisha, India
|Date of Web Publication||14-Jul-2016|
Department of Pathology, Division of Hematology Laboratory, IMS and SUM Hospital, Siksha O Anusandhan University, K8, Kalinga Nagar, Bhubaneswar - 751 003, Odisha
Source of Support: None, Conflict of Interest: None
Naphthalene toxicity, an unusual form of poisoning, is often missed as a probable diagnosis for acute onset of intravascular hemolysis in children. It has an unpredictable clinical course and proper management in children relies heavily on high index of clinical suspicion. We report a rare case of naphthalene toxicity in a 1½-year-old child who presented with acute onset of intravascular hemolysis following accidental ingestion of a single mothball. She was put on supportive therapy. We have reported the present case to highlight the spectrum of acute symptoms that a single accidental ingestion of a moth ball can cause. The idiosyncrasy of the chemical toxicity and the myriad of symptoms that it can cause has to be kept in mind to impart timely and right treatment to save precious human lives.
Keywords: Hemolysis, mothball ingestion, naphthalene
|How to cite this article:|
Sarangi R, Pradhan S, Prusty BK, Mahapatra S. Acute intravascular hemolysis following accidental ingestion of naphthalene: A rare case report. J Appl Hematol 2016;7:76-8
|How to cite this URL:|
Sarangi R, Pradhan S, Prusty BK, Mahapatra S. Acute intravascular hemolysis following accidental ingestion of naphthalene: A rare case report. J Appl Hematol [serial online] 2016 [cited 2020 Jul 11];7:76-8. Available from: http://www.jahjournal.org/text.asp?2016/7/2/76/186328
| Introduction|| |
Naphthalene toxicity is a rare form of poisoning, and it poses a diagnostic and therapeutic challenge due to its complicated clinical course. Lack of adequate history regarding the intake of toxic substance, especially in pediatric age group, poses a big hurdle in the management of these cases.  It has an unpredictable clinical course and therefore adequate knowledge regarding its manifestation becomes mandatory for appropriate line of management. We have reported this case to highlight the intensity of clinical signs and symptoms that single naphthalene-containing mothball can cause. Therefore, appropriate and timely management depends on the high index of clinical suspicion.
| Case report|| |
A 1½-year-old female child presented to pediatrics emergency unit with a complaint of dark urination. Mother gave the history of accidental ingestion of single moth ball during her play 12 h back. She did not experience any vomiting, abdomen pain, or headache after the ingestion.
On examination, she was conscious (Glasgow Coma Scale = 15/15), afebrile, with heart rate of 144/min, respiratory rate of 36/min without any distress. Blood pressure was 82/40 mm Hg and oxygen saturation 96% with room air. She was found to be severely pale and icteric. Abdomen was soft, nontender without organomegaly. Neurological and cardiovascular examination revealed no abnormality.
Investigation showed her hemoglobin (Hb) was 4.9 g/dl, hematocrit 13.4%, total leukocyte count 12,950/mm 3 , neutrophil 62%, and platelet count 3.27 lakh/mm 3 . Peripheral smear had evidence of hemolysis in the form of nucleated red blood cell (RBC), fragmented RBC [Figure 1]a and b and schistocytes. Heinz body was positive. Urine was dark brown, and it was positive for Hb, whereas urine microscopy did not show any RBCs. Her serum bilirubin was 7.5 mg/dl, indirect fraction being 7.2 mg/dl with normal liver enzymes. Serum lactate dehydrogenase was high (1575 U/L). Arterial blood gas analysis did not reveal evidence of acidosis. Her renal function, coagulation profile, electrolytes, and glucose-6-phosphate dehydrogenase (G6PD) activity were unremarkable. The malaria parasite test was also negative. Thus, provisional diagnosis of intravascular hemolysis and hemoglobinuria secondary to naphthalene toxicity was made.
|Figure 1:Microphotograph shows fragmented red cells (a) at ×100 and (b) at ×40|
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She was treated with rapid infusion of normal saline, three units of packed RBC, and 100 ml each. Methylene blue treatment was not given as there was no cyanosis which excluded any possibility of methemoglobinemia. The urine color becomes lighter and clear after 4 days. Her Hb improved to 10.2 mg/dl after transfusion and bilirubin declined to 1 mg/dl, indirect fraction being 0.6 mg/dl on day 5 of admission. Her general condition improved and she was discharged after 5 days of hospitalization. She is doing well and her G6PD status was also normal on follow-up.
| Discussion|| |
Mothballs containing naphthalene are a widely used as an insect repellent in Indian household and exposure can occur through inhalation, dermal absorption, and ingestion. It's easy accessibility in clothes and cupboards to children often becomes hazardous. Naphthalene is a bicyclic aromatic hydrocarbon which is poorly soluble in water and depending on size, one mothball can contain between 0.5 and 5 g of naphthalene.  After exposure, naphthalene is readily absorbed and metabolized into reactive epoxides and quinone metabolites by cytochrome P450 oxidation. It is excreted in the urine as mercapturic acids, methylthio-derivatives, and glucuronide conjugates. After metabolism in liver, the most potent derivative of naphthalene, naphthol-alpha causes hemolysis and Heinz bodies formation. G6PD deficient patients are more prone for hemolysis due to increased susceptibility to oxidative stress. , However, evaluation for G6PD deficiency is often misleading during the acute hemolytic episode as it may be falsely normal. Hence, the patients should be evaluated for underlying G6PD deficiency after the hemolysis regressed. 
Clinically, naphthalene has a wide spectrum of toxicity. There have been deaths associated with naphthalene toxicity.  After ingestion, naphthalene causes abdominal cramps with nausea, vomiting, and diarrhea. Patients may have lethargy, listlessness, myalgia, headache, sweating, and irritability. Patients may present with convulsions and coma in severe poisoning. Urinary bladder irritation may cause urgency, dysuria, and the passage of dark urine with or without cast and albumin. Severe toxicity may happen through dermal and inhalational exposure, particularly in newborns exposed to diapers and blanket stored in moth ball.
Acute intravascular hemolysis is the most common sign, particularly in G6PD deficient persons. It is accompanied by anemia, leukocytosis, fever, methemoglobinemia, hemoglobinuria, acidosis, jaundice, and renal insufficiency. Death can result from acute renal failure in adults or kernicterus in young infants. 
Methemoglobinemia is caused by the oxidation of ferrous (Fe 2+ ) to ferric (Fe 3+ ) Hb, which renders the Hb incapable of carrying oxygen and shift the oxyhemoglobin curve to left. Cyanosis is clinically detectable at >10% metHb. Pulse oximetry may become unreliable in the setting of methemoglobinemia because of false high in patients with severe methemoglobinemia and false low in patients with mild methemoglobinemia. Clinical suspicion of meth Hb should be raised when there is cyanosis that does not respond to high flow oxygen with any obvious cardiorespiratory causes such as the right to left shunting. Our patient did not have cyanosis with an oxygen saturation of 96% thereby excluding any possibility of methemoglobinemia.
Treatment is usually supportive but close monitoring is mandatory. Hemolysis requires blood transfusions and hemoglobinuria should be managed with urinary alkalinization if necessary. Severe kidney injury due to hemolysis often requires hemodialysis.  Methylene blue is reduced to leucomethylene blue by accepting electrons from NADPH and leucomethylene blue donates an electron to reduce methemoglobin to Hb. , G6PD deficient has low levels of NADPH, which is required for methylene blue to be effective. Hence, methylene blue is not recommended in G6PD deficient individuals. ,
| Conclusion|| |
The index case had a history of single mothball ingestion with rapid onset of massive intravascular hemolysis and dramatic recovery following supportive therapy prompted us to report this case. More so over, it is to draw the attention of regulatory bodies and clinician about it's over jealous, nonregulated use in household which is potentially toxic and can be a cause of chronic anemia in children. Extensive public health awareness campaigns of both medical and general sections of society are extremely important in decreasing the morbidity and mortality associated with this unusual medical emergency.
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Conflicts of Interest
There are no conflicts of interest.
| References|| |
Sekar A, Paudel S, Sivakumar SP, Verma A. Methemoglobinemia and uremia from an unusual poison. J Clin Toxicol 2014;4:217.
Kuffner EK. Camphor and moth repellants. In: Nelson LS, Lewin NA, Howland MA, Hoffman RS, Goldfrank LR, Flomenbaum NE, editors. Gold Frank′s Toxicologic Emergencies. 9 th
ed. New York: McGraw-Hill; 2011. p. 1150-92.
Sillery JJ, Lichenstein R, Barrueto F Jr., Teshome G. Hemolytic anemia induced by ingestion of paradichlorobenzene mothballs. Pediatr Emerg Care 2009;25:252-4.
Lim HC. Mothballs: Bringing safety issues out from the closet. Singapore Med J 2006;47:1003.
Kurz JM. Naphthalene poisoning: Critical care nursing techniques. Dimens Crit Care Nurs 1987;6:264-70.
Siegel E, Wason S. Mothball toxicity. Pediatr Clin North Am 1986;33:369-74.
Agarwal SK, Tiwari SC, Dash SC. Spectrum of poisoning requiring haemodialysis in a tertiary care hospital in India. Int J Artif Organs 1993;16:20-2.
Nascimento TS, Pereira ROL, Mello HLD, Costa J. Methaemoglobinaemia: From diagnosis to treatment. Rev Bras Anestesiol 2008;58:651-64.
Wright RO, Lewander WJ, Woolf AD. Methaemoglobinaemia: Etiology, pharmacology and clinical management. Ann Emerg Med 1999;34:646-56.