2. 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

3. Introduction Trauma leading cause childhood deaths Child Accident Prevention Foundation of Southern Africa since 1978 Childsafe Database at Red Cross Children’s Hospital

4. Aim Reduce intentional and unintentional injuries of all severity through: Research Education Environmental change Recommendations for legislation

5. EXAMINATION: Up to 50% asymptomatic (including 9/25 button batteries) Dysphagia/ odynophagia Increased salivation Vomiting/ choking/ refusal to eat Fever

6. 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

7. Database of all trauma patients 1991-2013 >150 000 entries Approximately 50 variables Largest Single-Centre Database on childhood injuries worldwide

8. Foreign body 5 th most common cause for admission to Trauma Unit!

9. Anatomy

10. Aim To study our experiences with ingested foreign bodies in children

11. Materials and Methods Retrospective study; 2 years 241 hospital folders analysed

12. Gender

13. Age

14. Object -material

15. Nail in stomach

16. Screw in right main bronchus

17. Object – nature

18. Anatomical site

19. Removal

27. Ingestion toys

29. Recently; Magnets!

31. 4 Months old baby

32. After removal…

33. MANAGEMENT: Depends on: -type of foreign body -site of impaction

34. A: OESOPHAGUS: 90% lodgement of FB’s Site 50% cricopharynx 30% mid oesophagus 20% lower oes Uncomfortable

35. Button battery EMERGENCY because of local damage. Remove endoscopically under G.A. Follow up scope

36. CoinMax cricopharynx Uncomfortable Remove: Endoscopically Under G.A. Balloon catheter Sharp pointed objectsRemove by endoscope under G.A. Rest of objectsObserve x12 hours Still persist, remove

37. B: STOMACH 80% will pass spontaneously Button battery:Remove endoscopically after 72 hours Long, sharp/big round objects:Remove after 72 hours All rest remove 3/ 52

38. 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

39. COMPLICATIONS: Max if : Delayed presentation / Prolonged impaction >48 hours Other anatomical abnormalities Perforation / Stricture / Atony / Fistula / Bleeding

40. Abbreviated Injury Score (AIS)

41. Conclusion Foreign bodies common in South Africa Metal coins most common Majority removed surgically Complications rare

43. 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

44. Common household corrosives conc caustic agent Acids sulphuric acids hydrochloric acids15 – 99% oxalic acid Alkaline Na hydroxide0.5 – 54% K hydroxide Na carbonate Ammonia Am hydroxide Detergents Na hypochlorite<15 – 49% Condy’s crystals K permanganate

45. Across the counter availability of caustic material

46. Can you spot the danger

47. Caustic - Mechanism of Injuries Time period - 1 sec contact = necrosis Causative factor Hydroxyl ion acid exothermia pH 2 712 Acid 9-99% Alkali 0.5-54%

48. AETIOLOGY AlkaliNaOHDrain/ oven cleaners pH >12KOHSoap manufacture Na2CO3Fruit Drying Tasteless  increased ingestion Immediate pain Causes liquefactive necrosis and thrombosis  deep burn Max. Upper Oes

49. AETIOLOGY Acidssulphuricbatteries pH<2metal cleaners oxalicpaint thinners hyrdrochloricsolvent 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

50. Sequence of events Caustic ingestion intense spasm Liquifactive necrosis anatomical narrowings cricopharyngeal muscle aortic arch, left main bronchus diaphragmatic hiatus 2-3 days antrum, pyloricregions 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 3 rd, 4 th and 5 th decades

52. Exudate and necrotic tissue Granulation tissue

54. 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

55. SYMPTOMS History History Evidence of corrosive ingestion – 25% Evidence of corrosive ingestion – 25% Pain on swallowing Pain on swallowing Salivation, drooling Salivation, drooling Oro-pharyngial signs – may be absent Oro-pharyngial signs – may be absent Upper airway obstruction Upper airway obstruction

56. Grade 0normal Grade Iedema and hyperemia of mucosa Grade IIafriability haemorrhage erosion blisters, exudates, or whitish membranes, superficial ulcers Grade IIbGrade IIa plus deep discrete or circumferential ulceration Grade IIIaSmall scattered areas of necrosis, areas of brownish black or grey discoloration Grade IIIbextensive necrosis Acute caustic injury – findings at esophagoscopy

57. Consequences Aspiration Esophageal Bronchial perforation Esophageal strictures Gastric outlet obstruction

58. ACUTE MANAGEMENT NPM -assess esophagus first NPM -assess esophagus first Endoscopy -confirm injury Endoscopy -confirm injury -quantitate injury NG Tube -early feeding NG Tube -early feeding Oral Feeding -when patient can swallow Oral Feeding -when patient can swallow Dysphagia -esophagogram Dysphagia -esophagogram Stricture -dilatation Stricture -dilatation

59. 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

60. 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

61. Can Risk Factor for Esophageal Perforation be Identified 11/2970 dilatations (<1%) Anatomical abnormalities Extensive 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

62. Can Risk Factors for Failure of Esophageal Dilatations be Identified Delay presentation > 1 month80% - Sx Tracheostomy100%- Sx Length stricture > 5cm94% - Sx Dilatation pattern unable to dilate at first attempt 71% - Sx size at first dilatation 20 vs 31 F maximum size in first 3 months28 vs 43 F average size of dilatation 24 vs 33 F E. Panieri, H. Rode R.A. Brown et al. PSI 1998

63. 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