CASE REPORT  
Niger J Paed 2015; 42 (3):237 240  
Abdulkadir I  
Hassan L  
Abdullahi F  
Akeredolu FD  
Purdue S  
Accidental sulphuric acid poisoning  
in a newborn  
Okpe M  
Sobowale AM  
Adewumi OA  
Abdullahi U  
Onadiran MA  
Sholadoye TT  
Baba S  
Ogala WN  
DOI:http://dx.doi.org/10.4314/njp.v42i3.14  
Accepted: 18th May 2015  
Abstract: A six hour old baby  
girl presented with shortness of  
breath and haematemesis five  
hours after accidental ingestion of  
sulfuric acid. We report the clini-  
cal presentation of corrosive in-  
gestion in a neonate a rare and  
sparsely reported occurrence at  
such tender age.  
(
)
Abdulkadir I  
Hassan L, Abdullahi F, Akeredolu FD  
Purdue S, Okpe M, Sobowale AM,  
Adewumi OA, Abdullahi U  
Onadiran MA, Ogala WN  
Key words: Acid ingestion, corro-  
sives injuries, caustic substances,  
chemical ingestion, newborn.  
Department of Paediatrics  
Ahmadu Bello University Teaching  
Hospital Shika Zaria, Kaduna State  
Nigeria.  
Email: isaburamla@yahoo.com  
Sholadoye TT, Baba S  
Department of Surgery,  
Ahmadu Bello University Teaching  
Hospital Shika Zaria, Kaduna State  
Nigeria.  
Introduction and literature review  
following acid ingestion peaks between 1and 3 weeks  
5 7  
while the healing process spans 4 6 weeks  
.
Corrosives or caustics are a group of chemicals that have  
the capacity to cause tissue injury on contact by a  
chemical reaction . Ingestion of caustic substances can  
cause gastrointestinal and upper airway injuries and can  
result in lifelong complications like oesophageal stric-  
ture, laryngeal 2stenosis and later, increased risk of oeso-  
phageal cancer .  
The magnitude of the injury depends upon several fac-  
tors such as the nature of the caustic agent, volume in-  
gested, concentration, duration of mucosal exposure, age  
of the patient and the intent (suicidal or accidental) with  
1
7,8  
which the corrosive was consumed .  
Corrosive ingestion in children may cause clinical mani-  
festations varying from no injury to fatal outcome. Early  
signs and symptoms after caustic ingestion may not be  
consistent with the extent of damage and endoscopy  
performed on day 1-2 (ideally b6e,9tw,10een 12-24 hours of  
Acids and alkalis are the two primary types of agents  
most often responsible for caustic exposures but with  
3
,4  
differing injury mechanisms . While alkaline agents  
cause widespread liquefaction necrosis injury along con-  
3
tact areas, acid substances cause coagulative necrosis  
ingestion) is used to assess injury  
.
with resultant eschar formation w4hich tends to limit tis-  
sue penetration and further injury .  
Recommended management protocols include resting  
the esophagus or the entire gastrointestinal tract using  
parenteral nutrition, the use of broad-spectrum antibiot-  
ics, systemic steroids, ant1a1c,1i2ds, proton pump inhibitors  
Alkali is partly neutralized by gastric secretion thus  
minimizing gastric mucosal injury conversely acids usu-  
ally provoke the most severe gastric lesions, especially  
3
in the antropyloric region . Oesophageal wall injury  
and H  
2
receptor - blockers  
.
2
38  
Unlike in adults where ingestion is13deliberate, most in-  
gestions by children are accidental. Globally, children  
represent 80% of the corrosive ingestion injury popula1-4  
was 160 bpm, regular, and heart sounds were normal.  
There were no abnormal abdominal findings.  
8
tion with children less than 5 years most affected.  
Fig 1: Container  
with sulphuric acid  
Corrosive ingestion ac1c5o-u19nted for 0.5% of paediatric  
admissions in Nigeria.  
The probability of ingestion  
of a caustic agent is low in the newborn period and new-  
born caustic burns have been reported in16f,r1e7quently in  
Nigeria and globally and remains a rarity.  
We report  
a case of a newborn with accidental sulphuric acid in-  
gestion within the first hour of life a rare and sparsely  
reported occurrence.  
A diagnosis of accidental corrosive ingestion with com-  
plications of upper gastrointestinal (GI) bleeding and  
chemical pneumonitis was made. She was commenced  
on supportive therapy including: Nil per oral, oxygen  
therapy at 1.5L/ min via nasal catheter, intravenous flu-  
ids, parenteral antibiotics (crystalline penicillin, metroni-  
dazole and gentamicin), steroids (hydrocortisone for 48  
hours), intravenous ranitidine and a nasogastric tube  
Case report  
Baby JZ, a 6 hour old term baby girl, was rushed to the  
Special Care Baby Unit of Ahmadu Bello University  
Teaching Hospital Zaria following accidental ingestion  
of acid 5 hours prior to presentation. The acid, mistaken  
for holy water, ruwan zam zam was administered by the  
paternal grandmother who had taken the baby home for  
a bath while the mother was still in the hospital. Her 8  
year old step sister was asked to get the holy water but  
accidentally brought the acid stored in an unlabeled,  
small, white, plastic keg similar to the one containing  
the holy water (fig 1) kept in an unlocked drawer in the  
mother’s bed room. The acid was given directly from  
the container to the baby. She began to choke after tak-  
ing about two sips, and started coughing and retching  
repeatedly. She vomited blood twice, about 20-25 mls  
per bout and subsequently developed difficulty with  
breathing which persisted till presentation. There was no  
intervention at home. Baby was rushed to the Primary  
Healthcare Centre (PHC) where she was delivered and  
was then referred to our facility immediately but arrived  
about five hours later due to transportation logistics.  
There was no fever and no bleeding from any other bod-  
ily orifices.  
(
NGT) was passed. Chest x-ray (Fig 2) done at admis-  
sion showed diffuse patchy opacity while her serum urea  
and electrolyte were normal. Within 24 hours of admis-  
sion, she developed massive upper GI bleeding with  
abdominal distension, severe pallor, cold extremities,  
thready peripheral pulses and unrecordable BP, and  
NGT was draining fresh blood. She was resuscitated  
with normal saline and received multiple blood transfu-  
sions in aliquots on account of the bleeding which lasted  
rd  
for about 72 hours. On the 3 day of life, she developed  
fever, worsened abdominal distension, tenderness and  
guarding, with hypoactive bowels.  
Erect abdominal x-ray (Fig 3) showed air under the dia-  
phragm. A diagnosis of bowel perforation with peritoni-  
tis was made. Baby was managed conservatively for  
bowel perforation with improvement in clinical condi-  
tion. She was on partial parenteral nutrition of 7.5%  
dextrose in 0.18 saline and amino acid infusion at  
0
.25mg/kg/day with daily potassium maintenance in 24  
Pregnancy was supervised in a private hospital anrdd  
mother had pregnancy induced hypertension in the 3  
trimester which was controlled with antihypertensives (α  
hour fluid. Baby did not have NGT feeding asndshe devel-  
oped repeated bilious vomiting from the 2 week on  
admission. She was still opening her bowel and passing  
bile stained stools. She could not have early endoscopy  
however, gastrograffin contrast study showed normal  
oesophagus. She was planned for exploratory lapara-  
tomy and feeding jejunostomy, but her clinical condition  
deteriorated as she developed widespread petechiae rash,  
severe pallor, difficulty with breathing, severe  
methyl dopa and amiloride HCl hydrochlorothiazide  
combination). Delivery was at a PHC via spontaneous  
vertex delivery annd d baby cried immediately after birth.  
Baby was the 2 child of the mother who is a 22 year  
old house wife. Father is a 35 year old commercial mo-  
tor cycle rider who also sells perfumes. They both have  
primary education. Marriage setting is polygamous with  
two wives and six children. They reside in a 4-room  
apartment. The battery liquid was being used by the fa-  
ther to refill his motorcycle battery acid.  
electrolyte derangement and died in the course of resus-  
citation at the age of 24 days. The parents declined post-  
mortem.  
At presentation, baby was ill-looking, wheezing, pale,  
tachypnoeic and dyspnoeic SPO was 86%. There was  
2
Fig 2: Chest X - ray.  
no petechiae rash. She was conscious but irritable, ante-  
rior fontanelle was normotensive, had normal tone but  
the primitive reflexes were depressed. Mouth examina-  
tion showed dried blood on the lips, there was no hyper-  
aemia, swellings or ulcerations on lips, buccal mucosa  
or tongue. Respiratory rate was 80 cpm (tachypnoea)  
with wide spread crepitation and rhonchi. Her heart rate  
2
39  
Fig 3: Erect Abdominal X-  
ray.  
Arrow showing air under  
the (R) hemi diaghragm  
ing, retching and vomiting which could have led to aspi-  
ration and the development of difficulty with breathing  
with wide spread crepitation. Caustic agents with pH  
lower than 2 or greater than 12 are highly corrosive and  
can cause severe chemical burns in the upper gastroin-  
20  
testinal tract .  
Other complications recorded include20massive GI haem-  
orrhage and perforation. Strode et al documented that  
immediate perforation of the stomach occurs if the in-  
gested acid is concentrated. The pooling of the caustic  
acids in the prepyloric area induces pylorospasm which  
is also thought to predispose patients to gastric perfora-  
Discussion  
20  
tion and stricture .  
16  
Turan et al did document sepsis and pneumonia in  
some of their ne1o7nates who ingested caustic solution. In  
Lagos Kushimo reported severe respiratory problems  
in a neonate as complication necessitating intubation.  
Morbidity and mortality in cases of ingestion16of corro-  
Exposure to corrosive agents continues to be a major  
source of injury for children and adults however it re-  
mains a rare occurrence in newborns. Our patient in-  
gested sulphuric acid which was accidentally adminis-  
tered to her like in most cases of corrosives ingestion in  
16  
sives in newborn is very high . While Turan reported  
1
children . Sulphuric acid is one of the commonly in-  
sepsis17as the possible cause of death in their report Ku-  
shima reported necrotizing oesophago -gastritis and  
lung collapse as the cause of death in their report on a 2-  
day old neonate. Though a postmortem was not per-  
formed, the index case possibly died from a combination  
of complications including bowel perforation, metabolic  
and electrolyte derangements, consumptive coagulopa-  
thy and intracranial bleeding.  
1
gested substances associated with caustic injury . The  
types of corrosive agents commonly implicated vary  
from country to country. In a review of data on corrosive  
14  
ingestion in children from Sierra Leone , the most re-  
ported corrosive agent was caustic soda, followed by  
kerosene, sodium hypochlorite and other alkaline house-  
hold chemicals. In India, the majority of ingestions are  
due to acids and predominantly implicated are toilet  
7
cleaning fluid (hydrochloric acid) . In a ten year review  
in Turkey, corrosive injuries of oesophagus involving 8  
newborns were due to benzalkonium chloride and tri-  
Conclusion  
1
6
chloro18acetic acid 1i9ngestion . Reports from Port Har-  
court and Lagos in Nigeria have identified caustic  
soda, bleach, battery acid and shaving powder as in-  
gested corrosives. While n7 one of these reports involved  
Accidental corrosive ingestion is rare in the newborn but  
when it occurs, it is associated with high morbidity and  
mortality.  
1
newborns, Kushimo et al in Lagos however, reported a  
case of acid ingestion in a 2 day old neonate.  
Recommendations  
The ingested sulphuric acid in the index case was kept in  
an unlocked drawer in the4 house for use by the father.  
Baby JZ accidentally ingested acid mistaken for holy  
water. This could be prevented by encouraging exclu-  
sive breastfeeding (EBF) and vigorously enlightening  
parents on benefits of EBF which should negate the  
need of pre lacteal feeds, advocacy and enforcement of  
regulations of manufacturing, sales and storage of corro-  
sives and as well getting facilities to implement fully the  
essential newborn care practices part of which encour-  
ages skin to skin contact with mother from birth and  
1
Documented risk factors for corrosive ingestion in  
children include: the availability of chemicals in and  
around the home, combined with the natural curiosity of  
children, crowded living conditions and parent’s lack of  
knowledge of the hazards of corrosive substances kept  
in the house. These are factors that are however not di-  
rectly related to the newborn since it does not have the  
ability to reach out to these agents. Perhaps the most  
important risk factors in this newborn were the introduc-  
tion of prelacteal feed or drink and the use of familiar  
containers to store chemicals. This led to the care giver  
wanting to give holy water but inadvertently offering  
sulphuric acid which was easily accessible.  
nd  
encourages delaying bathing of the baby until the 2  
day of life.  
Conflict of interest: None  
Funding: None  
The PH of the ingested acid was 0.8 with resultant chok-  
2
40  
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