South African Experience with Ingestion Injury to Children

Robin Brown & Sebastian van AsTrauma 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 IngestionForeign 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

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 causefor admission to Trauma Unit!

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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

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Object -material

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Metal Plastic CoatedPaper

Textile(Cloth)

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Nail in stomach

Screw in right main bronchus

Object – nature

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Coin Ball Bone Pin Paper Food Other

Anatomical site

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Removal

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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 cricopharynxUncomfortable

Remove: Endoscopically Under G.A.

Balloon catheter

Sharp pointed objects Remove by endoscope under G.A.

Rest of objects Observe x12 hoursStill persist , remove

B: STOMACH80% will 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 severe consequences

Common household corrosives

conc caustic agent

Acids sulphuric acidshydrochloric acids 15 – 99%oxalic acid

Alkaline Na hydroxide 0.5 – 54%K hydroxideNa carbonate

Ammonia Am hydroxide

Detergents Na hypochlorite <15 – 49%

Condy’s crystals K permanganate

Across the counter availability of caustic material

Can you spot the danger

Caustic - Mechanism of Injuries

Time period - 1 sec contact = necrosis

Causative factor Hydroxyl ion

acid

exothermia

pH 2 7 12Acid

9-99%Alkali

0.5-54%

AETIOLOGYAlkali NaOH Drain/ oven cleanerspH >12 KOH Soap manufacture

Na2CO3 Fruit Drying

Tasteless increased ingestion

Immediate pain

Causes liquefactive necrosis and thrombosis deep burn

Max. Upper Oes

AETIOLOGYAcids sulphuric batteriespH<2 metal cleaners

oxalic paint thinnershyrdrochloric solvent

metal cleanertoilet/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 eventsCaustic 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 necrosis4-7 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

4 weeks

Transmural fibrosis, regenerating epithelium covering granulation tissue

13 weeks

Epithelium covering a thick layer of fibrosis

18 weeks

Evolution of esophageal caustic injury

L H Bosher J Thoras surg 1951

Regenerated epithelium and extensive fibrosis

SYMPTOMSSYMPTOMS

• History History

• Evidence of corrosive ingestion – 25%Evidence of corrosive ingestion – 25%

• Pain on swallowingPain on swallowing

• Salivation, droolingSalivation, drooling

• Oro-pharyngial signs – may be absentOro-pharyngial signs – may be absent

• Upper airway obstructionUpper airway obstruction

Grade 0 normalGrade I edema and hyperemia of mucosaGrade IIa friability haemorrhage erosion

blisters, exudates, or whitish membranes, superficial

ulcers Grade IIb Grade IIa plus deep discrete or

circumferential ulcerationGrade IIIa Small scattered areas of necrosis,

areas of brownish black or grey discoloration

Grade IIIb extensive necrosis

Acute caustic injury – findings at esophagoscopy

ConsequencesAspiration

Esophageal Bronchial perforation

Esophageal strictures

Gastric outlet obstruction

ACUTE MANAGEMENTACUTE MANAGEMENT

• NPMNPM -- assess esophagus firstassess esophagus first

• EndoscopyEndoscopy -- confirm injuryconfirm injury-- quantitate injuryquantitate injury

• NG TubeNG Tube -- early feedingearly feeding

• Oral FeedingOral Feeding -- when patient can swallowwhen patient can swallow

• DysphagiaDysphagia -- esophagogramesophagogram

• StrictureStricture -- dilatationdilatation

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 grade I - III

Can the Diagnosis be ImprovedEsophageal 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 abnormalitiesExtensive unyielding strictures

Pseudo diverticular formation

Excessive eccentricity and tortuosity

Multiple strictures

Cause caustic injury

Prograde dilatation E. Panieri, H. Rode, R.A.Brown et al. JPS 1996

Perforation

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 71% - Sx size at first dilatation 20 vs 31 F maximum size in first 3 months 28 vs 43 F average size of dilatation 24 vs 33 F

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