Think before you drink
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Transcript Think before you drink
Joint Hospital Surgical Grand Round
Dr. WH She
Queen Mary Hospital
52/M
Bipolar and delusional disorder
Drank unknown amount of self made cocktail
Strong acidic solution, pH < 2
Coca Cola
Complained of dysponea and epigastric pain
Physical examination
Tachycardia
Tenderness and guarding over epigastrium
Resuscitated and intubated
Blood results
Metabolic acidosis (pH 7.2, HCO3 -13 mmol/L, base
excess -14 mmol/L)
Acute renal failure (201 umol/L)
Raised AST level (252 U/L)
Chest X-ray – no abnormality detected
Upper endoscopy
Gangrenous appearance of the esophageal and gastric
mucosa, distally to duodenum
Laparotomy
Findings
Full thickness gangrene of stomach with fundal
perforation
Esophagus
Mucosal gangrene, spare muscle and adventitia
Duodenum
1st part gangrenous changes
Some involvement of 2nd part
Patches fat necrosis at pancreatic tail
Proximal jejunum normal
Procedures
Total gastrectomy, distal exclusion of esophagus, feeding
jejunostomy and tracheostomy
Post operative period
Remained critical and septic
Further laparotomies
Findings
Pancreatic necrosis
Perforated esophageal and duodenal stumps
Procedures
Pancreatic necrosectomy
Esophageal drain and controlled duodenostomy
Caustic ingestion
Accidental
Usually in children
Intentional
Usually adults
Higher concentration
Larger amount
More severe
Gumaste VV et al. Am J Gastroenterol 1992
Schaffer SB et al. J La State Med Soc 2000
Satar S et al. Am J Ther 2004
Mckenzie LB et al. Pediatrics 2010
pH < 3 or > 11
Extent of injury
Type of agent
Concentration
Quantity
Physical form
Duration of contact
Acid
Lick the esophagus and bite the pyloric antrum
Coagulation necrosis
Eschar formation, prevent deeper tissue penetration
Estrera A et al. Ann Thorac Surg 1986
Gumaste VV et al. Am J Gastroenterol 1992
Ertekin C et al. Hepatogastroenterology 2004
Acid
Pool in stomach
Pyloric spasm
Gastric perforation and stricture
Schaffer SB et al. J La state Med Soc 2000
Kochhar R. et al. J Gastroenterol Hepatol 2004
Tohda G et al. Surg Endosc 2008
Example
Hydrochloric acid, sulphuric acid
Toilet bowl cleaners or swimming pool cleaners
Alkaline
Highly viscous, longer duration of contact
More uniformly severe mucosal injury to esophagus
Liquid form
More distal injuries
Solid form
Adhere to mucosa of mouth, upper airway and
esophagus
Spare stomach
Schaffer SB et al. J La State Med Soc 2000
Alkaline
Liquefactive necrosis
Denaturation of proteins and collagen
Sponification of fats
Dehydration of tissues
Thrombosis of blood vessels
Example
Drain cleaners
Hair relaxers
Detergents
Disk batteries
Schaffer Sb et al. J La State Med Soc 2000
Ertekin C et al. Hepatogastroenterology 2004
Acute problems
Laryngeal spasm, edema
Perforation
Upper gastrointestinal bleeding
Acute pancreatitis
Death
Tracheoesophageal fistula
Aorto-enteric fistula
Chronic problems
Esophageal stricture
Gastric outlet obstruction
Esophageal carcinoma
Management
Resuscitation
Endoscopy
Conservative management
Operative management
Zwischenberger JB et al. Am J Respir Crit Care Med 2001
Endoscopy
Classification by Zargar
0
Normal findings
1
Edema, hyperaemia of mucosa
2a
Friability, blisters, haemorrhaging, erosions, whitish
membranes, exudates, and superficial ulcerations
2b
Deep discrete or circumferential ulcerations in addition to
grade 2a
3a
Small scattered areas of multiple ulcerations and area of
necrosis (brown-black or grayish discoloration)
3b
Extensive necrosis
Zargar SA et al. Gastroenterology 1989
Zargar SA et al.Gastrointest Endosc 1991
Zargar SA et al. Am J Gastroenterol 1992
Grade 1
Grade 2a
Grade 2b
Grade 3
Endoscopy
Timing of upper endoscopy
No consensus yet
Early endoscopy
First 24 hours
Assess the severity and extent of injury
Risk of perforation
Ramasamy K et al. J Clin Gastroenterol 2003
Tohda G Et al. Surg Endosc 2008
Cheng HT et al. BMC Gastroenterol 2008
Celik B et al. Dis Esophagus 2009
Endoscopy
Unable to assess the depth of lesion
Despite concomitant use of endoscopic ultrasound
Kirsh MM et al. Ann Thorac Surg 1976
Chiu HM et al. Gastrointest Endosc 2004
Three phases of tissue injury from
alkaline ingestion
Phase Tissue injury
Onset
Duration
Inflammatory response
1
Acute necrosis 1-4days
1-4days
Coagulation of intracellular
proteins inflammation
2
Ulceration
and
granulation
3-5days
3-12days
Tissue sloughing
Granulation of ulcerated tissue
bed
3
Cicatrization
and scarring
3 weeks
1-6months Adhesion formation scarring
Conservative management
Clinically stable without peritonitis
Usually for Zargar’s grade I and II
Grade III injury in the absence of clinical and
biological signs of severity
Low mortality rate
Zerbib P et al. Ann Surg 2011
Operative management
Clinically unstable or signs of perforation
Aim
Resect the necrotic tissues
Prevent extension of the injury to the adjacent organs
Delayed presentation or operation
Massive ingestion of strong corrosive agents
Cattan P et al. Ann Surg 2000
Esophago-gastrectomy, cervical esophagostomy and
feeding jejunostomy
High mortality rate
Pancreatoduodenectomy
Extensive duodenal necrosis
Reconstruction
Stable, and survive from complications
Sarfati E et al. Br J Surg 1987
Cattan P et al. Ann Surg 2000
Use of nasogastric tube
Controversial
For
Decrease incidence of stricture formation and allowed
nutritional support
Ramasamy K et al. J Clin Gastroenterol 2003
Atabek C et al. J Pediatr Surg 2007
Use of nasogastric tube
Against
Long term indwelling N/G insertion would cause long
strictures of the esophagus
Gumaste VV et al. Am J Gastroenterol 1992
Ramasamy K et al. J Clin Gastroenterol 2003
Use of steroid
Debatable
For
Decrease strictures
Dosage matters
Howell JM et al. Am J Emerg Med 1992
Mamede RC et al. Dis Esophagus 2002
Pelclova D et al. Toxicol Rev 2005
Use of steroid
Against
Risk of the use of steroids
Randomized trial
No difference
Small sample size
Anderson KD et al. N Engl J Med 1990
Meta-analyses
No difference
Pelclova D et al. Toxicol Rev 2005
19% (steroid treated group) vs 40% rate of stricture
Ramasamy K et al. J Clin Gastroenterol 2003
Outcome
Depends on
Amount of caustic substances ingested
Severity of injury
Clinical status
Our patient
Unknown amount of caustic substances ingestion
Clinically unstable
Metabolic acidosis
Acute renal failure
Endoscopic Zargar’s grade IIIb
Upper airway injury
Esophageal necrosis
Gastric perforation
Duodenal involvement
Poor biochemical predicting factors
pH < 7.2
Base deficit > 16 mmol/L
Two fold increase of serum AST
Chou SH et al. World J Surg 2010
Conclusions
Difficult to manage
High morbidities and mortality
Early recognition of the type, amount and duration of
caustic ingestion
Decision on appropriate investigations and treatments
Acknowledgement
Prof. S Law
Dr. D Tong