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Year : 2018  |  Volume : 15  |  Issue : 1  |  Page : 98-100

Autopsy findings in paediatric poisoning with otapiapia

1 Department of Pathology, Bayero University, Kano, Nigeria
2 Department of Pathology, Aminu Kano Teaching Hospital, Kano, Nigeria

Date of Web Publication23-Mar-2018

Correspondence Address:
Dr. R O Faro
Department of Pathology, Aminu Kano Teaching Hospital, Kano, PMB 3452, Kano
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/njbcs.njbcs_23_17

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Background: Otapiapia is a locally prepared insecticide composed of varying strengths of an organophosphate and kerosene. It has been occasionally associated with accidental poisoning. However, there is paucity of data on autopsy findings in pediatric deaths related to organophosphate poisoning, including otapiapia. This report of autopsy findings aims to provide valuable information in these cases and suggest ways to better manage them when they present clinically. Materials and Methods: This is a review of autopsy findings of pediatric cases of accidental poisoning with otapiapia between 2008 and 2016 in a tertiary institution in northwestern Nigeria. Results: Seven cases of otapiapia-related deaths were autopsied during the period reviewed, 4 of which were accidental while infanticide was suspected in the remaining 3. The most common autopsy findings were diffuse alveolar damage followed by cerebral edema and acute tubular necrosis in the kidneys. Conclusion: In cases of otapiapia poisoning that survive to reach medical attention, priority attention should be given to airway and fluid management.

Keywords: Autopsy, childhood poisoning, kerosene, organophosphate

How to cite this article:
Atanda A T, Yusuf I, Faro R O. Autopsy findings in paediatric poisoning with otapiapia. Niger J Basic Clin Sci 2018;15:98-100

How to cite this URL:
Atanda A T, Yusuf I, Faro R O. Autopsy findings in paediatric poisoning with otapiapia. Niger J Basic Clin Sci [serial online] 2018 [cited 2021 Jun 16];15:98-100. Available from: https://www.njbcs.net/text.asp?2018/15/1/98/228357

  Introduction Top

Pediatric poisoning occurs most commonly in children aged 3 years and below, with petroleum products and rodenticides accounting for 11.0% and 5.7% of cases in the United States of America and parts of Europe, respectively.[1],[2] In Nigeria, Oguche et al.[3] documented accidental poisoning in 0.74% of pediatric admissions over a 19-year study period, with organophosphates being responsible for 2.7% of the cases.

In Nigeria, a source of pediatric accidental poisoning is otapiapia, a locally prepared insecticide.[4] It is usually composed of two poisons; the active component, an organophosphate (OP) such as Dimethyl-OPs (Dichlorovos) or Di-ethyl-OP (parathion), generally in concentrations of 5–10% w/v, and a diluent, usually kerosene.[5] It is often dispensed in small bottles of 25 cl to 50 cl.

OP are irreversible inhibitors of acetylcholinesterase (AchE), an enzyme that phosphorylates acetylcholine (Ach), a signal transmitter found at neuromuscular junctions and cholinergic brain synapses. They form complexes (AchE-OP) with AchE, and it may take up to 31 hours for the enzyme to spontaneously reactivate.[6] Acute toxicity may have muscarinic, nicotinic, or central nervous system (CNS) effects. The CNS effects include anxiety, tremors, seizures, and coma among others.

In acute intoxication, following ingestion, OPs are promptly absorbed from the gastrointestinal system and rapidly attain a high blood concentration. Symptoms may manifest, often dramatically, and loss of consciousness may occur within 20 min.[7] Unfortunately, because of cultural disdain for autopsies, such deaths often go uninvestigated.[4] Thus, this study aims to provide information on postmortem changes in these cases as an aid to understanding their possible modes of clinical presentation and mortality.

  Materials and Methods Top

Autopsy reports of all pediatric deaths from otapiapia-related poisoning over a 9-year period (2008-2016) in a teaching hospital in northwestern Nigeria were retrieved from the archives, and information on age, sex, circumstances of death, and autopsy findings were extracted.

The centre has facilities for handling cases of poisoning if they present early enough. These include specialist pediatricians, facilities for resuscitation, and laboratory backup. This has been demonstrated by studies from the centre on the management of different types of pediatric poisoning.[8]

  Results Top

During the 9-year period, 23 nontrauma-related pediatric cases less than 13 years of age were autopsied; and 7 (30.4%) of them were associated with otapiapia poisoning. These comprised 4 accidental poisoning cases and 3 cases in which infanticide was suspected; by co-wife in 2 cases and a new husband in the third. The latter cases were excluded because the corpses were not well preserved. In the accidental poisoning cases, there were 2 males and 2 females, with a mean age of 1.7 ± 1.5 years [Table 1].
Table 1: Characteristics of the cases of accidental poisoning

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The time interval between ingestion of the poison to death could not be accurately ascertained but ranged from 1–5 h; the volume consumed could not be accurately gauged because of conflicting reports. Home remedy applied in two of the cases was forced emesis with and without administration of oral palm oil. However, they all died before any medical resuscitation could be attempted.

Factors common to these presented cases were low socioeconomic status, low level of education, and long distances to a functional hospital. Their social standing was evidenced by the fact that they were illiterate peasant farmers from localities whose distances on the map range from 20 to 50 km to the study centre. However, time spent in traffic at the time of history taking was not elicited.

On external examination, all cases showed peripheral and central cyanosis. In one of the cases, gastric contents of previously ingested food material admixed with faintly pungent smell of the poison was observed but not in any of the other three. Histological features consistent with diffuse alveolar damage (DAD) were present in all the cases [Figure 1], with two also showing additional features of cerebral edema and one acute tubular necrosis [(ATN); [Figure 2]. Other systems were essentially unremarkable.
Figure 1: Diffuse alveolar damage with hyaline membranes, Hematoxylin and Eosin ×20

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Figure 2: Extensive tubular necrosis affecting predominantly proximal tubules but intact glomeruli. Hematoxylin and Eosin ×20

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  Discussion Top

This study of acute otapiapia poisoning showed a 1:1 male-to-female ratio, mean age of 1.7 ± 1.5 years, with death occurring within few hours with major organ changes predominantly in the respiratory and neurological systems. Our study concurs with that of Osaghae and Sule,[9] that children aged 3 years and younger are more vulnerable to accidental poisoning. This can be explained by the fact that children in this age group, by their inquisitiveness, have a tendency to explore the world by sight, touch, and taste.

Risk factors identifiable in this study, are similar to other studies and include low socio-economic status,[4],[9],[10] low levels of education of victims' care givers,[3],[9],[10] and unavailability of antidote in primary care hospitals.[11] In addition, otapiapia is sold in recycled soft (soda) drink bottles and recycled pediatric syrup bottles, both of which children may mistake for something sweet to drink.

Autopsy findings in this study showed that respiratory features were most prominent and comprised cyanosis, features consistent with DAD and pulmonary edema. These may result from inhibition of lung surfactant by hydrocarbons in the poison. This would result in airway collapse, ventilation-perfusion mismatch, and hypoxia. In addition, the OP component of otapiapia can cause excessive stimulation of muscarinic receptors. This manifests as bronchoconstriction, bronchospasms, and paralysis of respiratory muscles.[6] These may also contribute to respiratory features demonstrated at autopsy.

The pungent odor of otapiapia was perceived in the gastric contents of only one of the four cases. Absence of smell of poisons in gastric contents was also reported in an autopsy-based study from India.[11] This is important because attempting to perceive gastric lavage contents, as a means of identifying poisons, may not be very helpful clinically. Absence of the smell, therefore, does not exclude the poison.

The OP component of the otapiapia also has a CNS altering effect which often manifests as drowsiness, stupor, and coma. Respiratory failure experienced by the acutely poisoned patient usually presents with hypoxia, a condition wherein the brain may result in production of lactic acid and H+ ion, release of excitotoxin (glutamate), and increase in blood–brain barrier permeability. These may cause a passive influx of Cl (and Na +) into cells causing osmotic (cytotoxic) edema as well as intercellular fluid accumulation (vasogenic edema).[12] This may explain the cerebral edema found in two of our cases.

ATN was seen in 1 of the 4 cases presented. This reflects the possibility of renal affectation by the poison. Rubio et al.[13] also documented this mode of presentation in a case report on OP poisoning. The pathogenesis of the ATN is unknown because of lack of experimental data. In laboratory animals, finding of low urinary osmolality has suggested tubular dysfunction secondary to direct tubular damage or an increase in oxidative stress.[13] When there is renal involvement, dialysis has been shown to be useful in treatment.[14]

In 2 of our cases, as well as in reports by other authors,[3],[4],[9] administration of palm oil and milk were the most common home remedies given. Unfortunately, such lipid soluble agents increase the rate of absorption of the poison and in the case of milk it may enhance absorption of water soluble OPs such as dichlorovos.[7] Raw egg may be administered as it retards gastric emptying and delays onset of toxicity.[14] If the patient is alive at presentation to the hospital, insertion of a cuffed endotracheal tube (to prevent aspiration) prior to a gastric lavage is imperative, along with frequent suctioning to remove excess secretions and oxygen administration – airway management.

In conclusion, this study has shown that otapiapia poisoning in our setting predominantly affects the respiratory system and CNS and occasionally the renal system. Therefore, prompt attention should be given to these systems as severe toxicity leading to death may occur within minutes to hours.


  1. Adoption of biological over chemical methods of pest control
  2. Banning sale of pesticides in containers without child-proof caps
  3. Induction of vomiting with palm oil or milk should be discouraged
  4. Equipment of peripheral and central hospital with requisite facilities and resources.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Litovitz TL, Klein-Schwatrz W, Rodgers GC, Cobaugh DJ, Youniss J, Onshaer JC, et al. 2001 Annual Report of the American Association of Poison Contol Centers Toxic Exposure Surveillance System. Am J Emerg Med 2002;20:391-452.  Back to cited text no. 1
Koliou M, Loannou C, Andreou K, Petridou A, Soteriades ES. The epidemiology of childhood poisonings in Cyprus. Eur J Paediatr 2010;69:833-6.  Back to cited text no. 2
Oguche S, Bukbuk DN, Watila IM. Pattern of hospital admissions of children with poisoning in the Sudano-Sahelian North eastern Nigeria. Niger J Clin Pract 2007;10:111-5.  Back to cited text no. 3
Okeniyi JAO, Lawal OA. Accidental poisoning with Otapiapia: A local organophosphate-containing rodenticide: A case report. Nig Med Pract 2007;54:100-1.  Back to cited text no. 4
Musa U, Hati SS, Mustapha A, Magaji G. Dichlorvos concentrations in locally formulated pesticide (ota-piapia) utilized in northeastern Nigeria. Sci Res Essay 2010;5:49-54.  Back to cited text no. 5
Paudyal BP. Organophosphorus poisoning. J Nepal Med Assoc 2008;47:251-8.  Back to cited text no. 6
Eddleston M, Buckley NA, Eyer P, Dawson AH. Management of acute organophosphorus pesticide poisoning. Lancet 2008;371:597-607.  Back to cited text no. 7
Akhiwu HO, Ibrahim JS, Abdullahi SU, Akibu OO. The dilemma of managing childhood poisoning without adequate history in a resource-poor environment: A report of 4 cases. Niger J Basic Clin Sci 2012;9:40-3.  Back to cited text no. 8
  [Full text]  
Osaghae DO, Sule G. Socio-demographic factors in accidental poisoning in children. J Med Med Sci 2013;4:13-6.  Back to cited text no. 9
Adejuyigbe EA, Onayade AA, Senbanjo IO, Oseni SE. Childhood poisoning at the Obafemi Awolowo University Teaching Hospital, Ile-Ife, Nigeria. Niger J Med 2002;11:183-6.  Back to cited text no. 10
Mohanty MK, Siddhartha P, Arun M, Menezes RG, Palimar V. Correlation between postmortem diagnosis and survival time in poisoning deaths. J Indian Acad Forensic Med 2005;27:23-6.  Back to cited text no. 11
Pathogenesis of cerebral edema. Available from: http://neuropathology-web.org/chapter 2/chapter 2aHIE.html. [Last accessed on 09 April 2015].  Back to cited text no. 12
Rubio CR, Fernandez CF, Bueno RM, del Pozo BAGarcia JM. Acute renal failure due to the inhalation of organophosphates: Successful treatment with haemodialysis. Clin Kidney J 2012;5:582-3.  Back to cited text no. 13
Eddleston M, Singh S, Buckley N. Organophosphorus poisoning (acute). Clin Evid 2004;12:1-15.  Back to cited text no. 14


  [Figure 1], [Figure 2]

  [Table 1]


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