South African Experience with
Ingestion Injury to Children
Robin Brown & Sebastian van As
Trauma Unit, Red Cross Children’s Hospital
Vincent Palotti Hospital
University of Cape Town, South Africa
Introduction

Trauma leading cause childhood deaths

Child Accident Prevention Foundation of
Southern Africa since 1978

Childsafe Database at Red Cross
Children’s Hospital

Aim

Reduce intentional and unintentional
injuries of all severity through:




Research
Education
Environmental change
Recommendations for legislation
EXAMINATION:

Up to 50% asymptomatic (including 9/25
button batteries)

Dysphagia/ odynophagia

Increased salivation

Vomiting/ choking/ refusal to eat

Fever
Foreign Body Ingestion







5th commonest presentation at Trauma Unit ,
RXH
Objects: Metal (40%), Plant (25%),
Size 0.5cm (0.1-3)
Nose (40%), Oesophagus (20%), Stomach
(14%)
42% asymptomatic
57% objects removed surgically
80% GIT 20% tracheobronchial
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


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Database of all trauma patients
1991-2013
>150 000 entries
Approximately 50 variables
Largest Single-Centre Database
on childhood injuries worldwide
Foreign body 5th most common cause
for admission to Trauma Unit!
35000
30000
25000
20000
15000
10000
5000
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Anatomy
Aim

To study our experiences with ingested
foreign bodies in children
Materials and Methods

Retrospective study; 2 years

241 hospital folders analysed
Gender
120
Frequency
100
80
60
40
20
0
Male
Female
Age
60
Frequency
50
40
30
20
10
0
<1
1
2
3
4
5
6
7
Age (year)
8
9
10 11 12
Object -material
Frequency
100
90
80
70
60
50
40
30
20
10
0
Metal
Plastic
Coated
Paper
Textile
(Cloth)
Wood
Nail in stomach
Screw in right main bronchus
Object – nature
70
60
Frequency
50
40
30
20
10
0
Coin
Ball
Bone
Pin
Paper
Food
Other
No
op se
ha
g
St us
om
ac
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B
yp ow
op
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ha l
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Br ynx
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La
ry
O
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av
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Tr ty
ac
he
a
Es
Frequency
Anatomical site
100
90
80
70
60
50
40
30
20
10
0
Removal
140
Frequency
120
100
80
60
40
20
0
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on
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Fole
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Removal
Removal
Removal
Removal
Removal
Removal
Removal
Ingestion toys
Ingestion toys
Recently; Magnets!
4 Months old baby
After removal…
MANAGEMENT:
Depends on:
-type of foreign body
-site of impaction
A: OESOPHAGUS:
90% lodgement of FB’s
Site
50% cricopharynx
30% mid oesophagus
20% lower oes
Uncomfortable

Button battery
EMERGENCY because of local damage.
Remove endoscopically under G.A.
Follow up scope
Coin
Max cricopharynx
Uncomfortable
Remove: Endoscopically Under G.A.
Balloon catheter
Sharp pointed objects
Remove by
endoscope under G.A.
Rest of objects
Observe x12 hours
Still persist , remove
80%B:
will STOMACH
pass spontaneously
Button battery:Remove endoscopically
after 72 hours
Long, sharp/big round objects:Remove
after 72
hours
All rest remove 3/ 52
C: SMALL / LARGE INTESTINE


95% will pass spontaneously
Symptoms of complications for surgical
removal:
-fever, vomiting, abdominal
pain
-blood in stool
-same place on serial x-rays
-retained in rectum
COMPLICATIONS:
Max if : Delayed presentation / Prolonged
impaction >48 hours
Other anatomical abnormalities
Perforation / Stricture / Atony / Fistula /
Bleeding
Abbreviated Injury Score (AIS)
Conclusion

Foreign bodies common in South Africa

Metal coins most common

Majority removed surgically

Complications rare
Caustic Injury to the Esophagus
The problem - ingestion of corrosive
substances remains a major health
hazard
Preventative programmes –
education, labeling and packaging and
legislation
Caustic soda is in great demand for
agriculture, home industry and
cleansing agents
The victim - majority of ingestions
occur in children < 5yrs
The consequences – ± 20% will suffer
Common household corrosives
conc caustic agent
Acids
sulphuric acids
hydrochloric acids
oxalic acid
Alkaline
Na hydroxide
K hydroxide
Na carbonate
Ammonia
Detergents
Condy’s crystals
Am hydroxide
Na hypochlorite
K permanganate
15 – 99%
0.5 – 54%
<15 – 49%
Across the counter availability of
caustic material
Can you spot the danger
Caustic - Mechanism of Injuries
pH 2
7
12
Acid
9-99%
Time period
Alkali
0.5-54%
- 1 sec contact = necrosis
Causative factor
Hydroxyl ion
acid
exothermia
AETIOLOGY
Alkali
pH >12
NaOH
KOH
Na2CO3
Drain/ oven cleaners
Soap manufacture
Fruit Drying
Tasteless  increased ingestion
Immediate pain
Causes liquefactive necrosis and thrombosis 
deep burn
Max. Upper Oes
AETIOLOGY
Acids
pH<2
sulphuric
oxalic
hyrdrochloric
batteries
metal cleaners
paint thinners
solvent
metal cleaner
toilet/drain cleaner
Immediate bitter taste  expulsion
Causes coagulative necrosis  eschar  relative sparing
of oesophagus because of decreased penetration
Rapid transit through oesophagus  antral spasm and
damage
Sequence of events
Caustic ingestion
intense spasm
Liquifactive necrosis
anatomical narrowings
cricopharyngeal muscle
aortic arch, left main bronchus
diaphragmatic hiatus
2-3 days
antrum, pyloric regions
Thrombosis inflammatory reaction, mucosal ulceration
bacterial invasion cellular necrosis
4-7 days
Mucosal sloughing granulation tissue fibroblastic response
Esophageal fibrosis
7-12 days
Symptomatic stricture
> 3 weeks
Esophageal Sq Ca
3rd, 4th and 5th decades
Exudate and necrotic tissue
Granulation tissue
Evolution of esophageal caustic injury
Epithelium covering a
thick layer of fibrosis
Transmural
fibrosis,
regenerating
epithelium
covering
granulation
tissue
4 weeks
13 weeks
18 weeks
Regenerated
epithelium
and
extensive
fibrosis
L H Bosher J Thoras surg 1951
SYMPTOMS
•
History
•
Evidence of corrosive ingestion – 25%
•
Pain on swallowing
•
Salivation, drooling
•
Oro-pharyngial signs – may be absent
•
Upper airway obstruction
Acute caustic injury – findings
at esophagoscopy
Grade 0
Grade I
Grade IIa
ulcers
Grade IIb
Grade IIIa
Grade IIIb
normal
edema and hyperemia of mucosa
friability haemorrhage erosion
blisters, exudates, or whitish
membranes, superficial
Grade IIa plus deep discrete or
circumferential ulceration
Small scattered areas of necrosis,
areas of brownish black or grey
discoloration
extensive necrosis
Consequences
Aspiration
Esophageal strictures
Esophageal Bronchial
perforation
Gastric outlet obstruction
ACUTE MANAGEMENT
•
NPM
-
assess esophagus first
•
Endoscopy
-
confirm injury
quantitate injury
•
NG Tube
-
early feeding
•
Oral Feeding -
when patient can swallow
•
Dysphagia
-
esophagogram
•
Stricture
-
dilatation
Can Esophageal Injury be
Predicted
All are not symptomatic
Epiglottic edema
Prolonged salivation
Dysphagia
Abdominal pain
These symptoms are indicative
of esophageal pathology but
cannot differentiate between
Can the Diagnosis be Improved
Esophageal injury can be identified with
TC99M sucralfate scan
Sucralfate binds to injured mucosa
22 children scanned/endoscopy < 24 hours
Scan - 11 +// endoscopic findings
7 slow transit time
9 normal scans
2 false positive
Scan identified those at risk for significant
injury
Scan
+ predicted value of 84%
- predicted value of 100%
AJW Millar JPS 2001
Can Risk Factor for Esophageal
Perforation be Identified
11/2970 dilatations (<1%)
Anatomical abnormalities
Extensive unyielding strictures
Pseudo diverticular formation
Excessive eccentricity and tortuosity
Perforation
Multiple strictures
Cause
caustic injury
Prograde
dilatation
E. Panieri, H. Rode, R.A.Brown et al. JPS 1996
Can Risk Factors for Failure of
Esophageal Dilatations be Identified
Delay presentation > 1 month 80% - Sx
Tracheostomy
100%- Sx
Length stricture > 5cm
94% - Sx
Dilatation pattern unable to dilate at first attempt
Sx
size at first dilatation
31 F
maximum size in first 3 months
43 F
average size of dilatation
33 F
71% 20 vs
28 vs
24 vs
E. Panieri, H. Rode R.A. Brown et al. PSI 1998
Caustic Esophageal Injuries
Diagnosis:
clinical, flexible endoscopy
Standard therapy:
allow soft diet and liquids
Ba swallow at 3 weeks
Weekly esophageal
dilatations
Progress:
restoration of functional
esophageal lumen