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 Table of Contents  
CASE REPORT
Year : 2012  |  Volume : 9  |  Issue : 1  |  Page : 40-43

The dilemma of managing childhood poisoning without adequate history in a resource-poor environment: Report of 4 cases


Department of Pediatrics, Aminu Kano Teaching Hospital, Kano, Nigeria

Date of Web Publication10-Oct-2012

Correspondence Address:
Helen Oluwadamilola Akhiwu
Department of Pediatrics, Aminu Kano Teaching Hospital, Kano
Nigeria
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0331-8540.102116

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  Abstract 

The dilemma of managing childhood poisoning without adequate history poses a serious challenge, especially in resource-limited settings where facilities for toxicology studies are not readily available. We reported 4 cases of childhood accidental poisoning who were admitted to our center with inadequate history. Two were cases of haloperidol poisoning, another was that of potassium bromate poisoning and the fourth was that of organophosphate poisoning. While meticulous history was helpful in the making of the diagnosis of the first 3 cases, the use of electronic literature solved the riddle in the fourth.

Keywords: Childhood, inadequate history, poisoning


How to cite this article:
Akhiwu HO, Ibrahim JS, Abdullahi SU, Akibu OO. The dilemma of managing childhood poisoning without adequate history in a resource-poor environment: Report of 4 cases. Niger J Basic Clin Sci 2012;9:40-3

How to cite this URL:
Akhiwu HO, Ibrahim JS, Abdullahi SU, Akibu OO. The dilemma of managing childhood poisoning without adequate history in a resource-poor environment: Report of 4 cases. Niger J Basic Clin Sci [serial online] 2012 [cited 2022 Dec 3];9:40-3. Available from: https://www.njbcs.net/text.asp?2012/9/1/40/102116


  Introduction Top


Accidental poisoning is common in pediatrics. Children younger than 5 years account for majority of pediatric poisoning, [1] virtually all of which are considered accidental. The natural inquisitiveness and impulsivity of toddlers make them vulnerable hosts for toxic ingestions. Most poisonings happen at home and are often by substances in sight but unattended by an adult. Most poisoning in children is usually from medications, cosmetics, insecticides, plants etc. [2]

Children frequently present to the emergency department after poisoning without a specific history of toxic exposure and this poses a challenge in diagnosis and management of these children, especially in resource-limited settings where toxicology studies are not readily available.


  Case Series Top


Case 1

A 13-months-old girl who was rushed to the emergency unit in May 2011. She was found collapsed on the floor in her mother's room a few minutes after she entered the room to play. Neither history of toxic substance ingestion nor other relevant history surrounding the circumstance was obtained from the caregiver.

Prior to presentation, she was said to have been a healthy child and growing normally. She had not been on any medication, and no member of the family was on any medication. No first aid treatment was given to the child before presentation.

On presentation to the emergency room, the child was comatose with a Glasgow coma score of 3/15. Her pupils were 4 mm in size bilaterally and reactive to light. She was in respiratory distress with brownish secretions from her mouth. There was no abnormal characteristic odor. She was hypoxic with oxygen saturation of 50%. Her pulse rate was 120 bpm regular moderate volume. Blood pressure was 80/60 mmHg, heart sounds were normal. There was no other significant abnormality.

She was hyperglycemic with a random blood sugar of 28 mmol/L. Bedside urinalysis revealed a pH of 6, blood ++, proteins ++, glucose ++++, ketones negative, and nitrite negative. Packed cell volume of 32% and no malaria parasite was demonstrable on blood film.

Poisoning was suspected. The internet was accessed and search of electronic literature showed she was presenting with symptoms of organophosphate poisoning.

The patient was then managed with intravenous fluid, atropine, and intranasal oxygen. The specific antidote (pralidoxin) was not available. The respiratory distress subsided and oxygen saturation improved to 96%. The blood sugar was closely monitored, and by the following morning, the patient was normoglycemic with a random blood sugar of 5.4 mmol/L. Patient regained full consciousness by the next day. Her serum urea, electrolytes, and blood counts were essentially normal.

Case 2

A 3-year-old girl, admitted in May 2011 who had cough for two days, after which she was noticed to have developed difficulty in breathing and was wheezing. She had several similar episodes in the past, and there was a positive family history of asthma. She was examined and found to be in respiratory distress and had widespread polyphonic rhonci in the chest. A diagnosis of acute asthmatic attack was made, and patient was nebulized with salbutamol with remarkable improvement. She was subsequently placed on oral salbutamol and a suspension of ampicillin with cloxacillin as outpatient. The following day, the parents noticed the child to be sitting still and staring forward for long periods at a time, not responding to call, drooling saliva, rolling her tongue, and hyper extending her neck. She was also having occasional tonic contractions of the upper limbs. The patient was rushed to the emergency pediatric unit. Dystonic drug reaction was suspected, and the drugs the patient had been on were examined, and it was observed that she had been given haloperidol in place of salbutamol, and the patient had received 10 mg of haloperidol. She was managed conservatively with intravenous fluid, and later patient was encouraged to take liberal oral fluids. Trihexyphenidyl was avoided due to its associated side effects. About 24 hrs later, all symptoms had subsided and she was discharged home.

Case 3

A 3-year-old girl who was brought in by her grandmother to the emergency pediatric unit in April 2011 with complaints of abnormal body movements of 8 hrs duration in a child that had been previously healthy. Significant clinical findings were those of a restless child with dystonic features. Further enquiry of the whereabouts of the mother revealed that the mother was a psychiatric patient who has been on haloperidol, and the child had been found in the room where the drugs were kept with the tablets on the floor.

The child was managed as a case of haloperidol overdose. The patient was managed conservatively like the second case. Her recovery was uneventful, and she was discharged after 36 hrs.

Case 4

A 1-year-old boy who was brought to the emergency room in April 2011 with complaints of inability to pass urine, vomiting, and facial puffiness all of 3 days duration. There were no other urinary symptoms. Facial puffiness was said to have been noticed some hours after he had stopped passing urine, usually worse in the mornings and regresses as the day progresses.

Further questioning revealed that the patient was observed to have come from the neighbor's house a day prior to the onset of the symptoms licking a whitish substance from his hands. The neighbor bakes bread commercially. Patient was seen at a peripheral center where the serum urea and electrolytes were assessed. Urea was 10.6 mmol/l, Cr 234 μmols/L, bicarbonate of 18 mmol/l; other electrolytes were normal.

A diagnosis of acute renal failure was made, and the kidneys were challenged with frusemide and intravenous fluids, but to no avail, hence the referral.

On presentation, patient was fully conscious with periorbital edema. His pulse rate was 102 bpm regular with a blood pressure of 90/70 mmhg. There was no other abnormality. A urethral catheter was passed, but no urine was obtained. A diagnosis of acute renal failure following ingestion of suspected potassium bromate was made. Parents were later asked to bring the whitish substance the patient was said to have ingested and it was observed to be potassium bromate. The U/E on admission was urea of 16.6 mmol/L, Na 140 mmol/L, K 6.5 mmol/L, bicarbonate 18 mmol/l, Cl 103 mmol/l, and Cr 231 μmmol/L

Patient was placed on IVF 400 mls/m 2 with strict input output monitoring. After the first 24 hrs, patient had not made any urine, but he was otherwise stable. At 48 hrs after admission, patient made 20 mls of urine and by the 3 rd day, he was making 4 mls/kg / hr. The repeat urea and electrolytes on the 3 rd day showed urea 11.1 mmol/L, Na 127 mmol/L, K 4.7 mmol/L, Cl 107 mmol/L, Cr 107 μmol/L. The packed cell volume was 26%.

Subsequent urea and electrolyte results gradually normalized, and patient was discharged home 11 days after admission.


  Discussion Top


Each year, in the United States, over 1 million children are reported poisoned [3] with more than half of the poisonings involve children under the age of 6 years. Most of the poisonings occur at home [3] as evidenced by this report.

Organophosphate compounds are a group of chemicals used in both domestic and industrial settings. The mechanism of action of organophosphate pesticides is inhibition of carboxyl ester hydrolases, particularly acetyl cholinesterase. [4] Once inactivated, acetylcholine accumulates throughout the nervous system, resulting in overstimulation of muscarinic and nicotinic receptors. Clinical effects are manifested via activation of the autonomic and central nervous systems and at nicotinic receptors on skeletal muscle. [5] Although most patients become symptomatic within a short period, the onset and severity of symptoms usually depends on the specific compound, amount, route of exposure, and rate of metabolic degradation. The common features of organophosphate poisoning are salivation, diaphoresis, diarrhea, lacrimation, urination, miosis, bronchospasm and bronchorrhea, emesis, muscle twitching, cramping, fatigue, paralysis, respiratory muscle weakness, and decreased respiratory effort. Others are anxiety, emotional liability, restlessness, confusion, headaches, slurred speech, hypotonia, ataxia, tremors, seizures, and coma. It also presents with non-ketotic hyperglycemia. [6] The child in case 1 had presented with most of the life-threatening features of organophosphate poisoning.

Haloperidol is used for the symptomatic management of psychotic disorders. It is also used for treatment of severe behavioral problems in children and for the short-term treatment of hyperactive children with excessive motor activity and accompanying conduct disorders. It can also be used in the control of tics and vocal utterances of Gilles de la Tourettes syndrome. [7] Features of haloperidol overdose include depressed consciousness, which can progress to coma. It is worthy of note that paradoxically, some patients manifest with confusion, excitement, and restlessness. Tremor or muscle twitching, muscle spasm, rigidity, and convulsions can also be seen. Extra pyramidal signs can include dystonia, sometimes severe enough to impair swallowing or breathing; torticollis and opisthotonos posturing. The pupils may be constricted or dilated, hypotension and tachycardia are common. Sometimes, there can be cardiac arrhythmias and cardiac arrest. [8] The children in case 2 and 3 presented with the extrapyramidal effects of haloperidol overdose. They were managed conservatively due to the associated side effects of the antidote itself. They did well on this conservative treatment and were discharged home in less than 48 hrs.

Potassium bromate is an oxidizing agent typically used as a flour improver. It causes strengthening of the dough and allowing higher rising. In the acute phase of poisoning, vomiting and diarrhea with abdominal pain are the main symptoms. Subsequently, the patient develops features of renal impairment: Oliguria, anuria. [9] Other reported features include deafness, vertigo, hypotension, depression of the central nervous system, and thrombocytopenia. [10] The use of potassium bromate has been banned in Nigeria, but it is sad to note that it is still in use.

These 4 cases were seen within a time period of 2 months. Most of these poisoning are preventable. It goes to show that dangerous drugs and chemicals are still kept within the reach of children.

There is a need for a high index of suspicion when a child presents in the emergency room with impaired consciousness, especially when the child had otherwise been healthy and had a period of not having been attended to by an adult. This is especially important in our environment where we do not have facilities for toxicology tests. The first case illustrates how the use of internet facility can be put to good use in the making of diagnosis. One would advise such facility in the children's emergency room since it might be cost-effective in developing countries when compared with facilities for toxicology tests.

There is also the need to teach parents practices to minimize the risk of poisoning by ensuring safety efforts at home.

 
  References Top

1.Memon Y, Majeed R, Kolachi HB, Querashi K, Sheikh S. Clinical spectrum and outcome of accidental poisoning in children. Biomedica 2010;26 : 92-5.   Back to cited text no. 1
    
2.McGuigan MA. Common culprit in childhood poisoning: Epidemiology, treatment and parental advice for prevention. Paediatric Drugs 1999;1:313-24.  Back to cited text no. 2
[PUBMED]    
3.Watson W, Litovitz TL. Annual report of the american association of poison control centers' toxic exposure surveillance system. Am J Emerg Med 2002;21:353.  Back to cited text no. 3
    
4.Bajgar J. Organophosphates/nerve agents poisoning. Mechanism of action, diagnosis, prophylaxis and treatment. Adv Clin Chem 2004;38:151-216.  Back to cited text no. 4
[PUBMED]    
5.Okeniyi JA, Lawal OA. Accidental poisoning with otapiapia: A local organophosphate containing rodenticide. A case report. Nig Med Pract 2007;52:100-1.  Back to cited text no. 5
    
6.Meller D, Fraser I, Kryger M. Hyperglycemia in anticholinesterase poisoning. CMAJ 1981;124:745-8.   Back to cited text no. 6
[PUBMED]    
7.Serrano AC. Haloperidol-its use in children. J Clin Psychiatry 1981;42:154-6.  Back to cited text no. 7
[PUBMED]    
8.Joy CB, Adams CE, Lawrie SM. "Haloperidol versus placebo for schizophrenia". Cochrane Database Syst Rev 2006;(4):CD003082.  Back to cited text no. 8
[PUBMED]    
9.Okeniyi JA, Aladekomo TA, Oyelami OA. Acute renal failure following accidental potassium bromate poisoning. A case report. Nig J Paed 2003;30:150-3.  Back to cited text no. 9
    
10.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;12:204-9.  Back to cited text no. 10
[PUBMED]    




 

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