Acute situations in gastroenterology - FMED UK...Acute pancreatitis • inflammatory disease of the...
Transcript of Acute situations in gastroenterology - FMED UK...Acute pancreatitis • inflammatory disease of the...
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Acute conditions in gastroenterology
MUDr. Komorníková, PhD, MUDr. Vlčková
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Acute conditions in gastroenterology
• Gastrointestinal bleeding
• Acute pancreatitis
• Foreign bodies in the GI tract
• Caustic injuries
• Acute abdomen
– ileus, obstruction
– splanchnic ischemia
– perforation of the GI tract
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Part 1
Gastrointestinal bleeding
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Gastrointestinal bleeding
• The most common situation in gastroenterology
• Upper/lower GI tract – borderline lig. Treitzi
• Acute/Chronic bleeding (compensatory mechanisms in case of longer duration)
• Variceal/non-variceal bleeding
• Incidence 25 – 50/100 000/year
• Higher incidence with increasing age, prescription of anticoagulant and
antiplatelet therapy, overuse of NSAIDs
• Mortality 5 – 15 %
• 3 – 15 % require surgery
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Basics of GI bleedings
• Haematemesis - vomited blood with coffee-like appearance (after contact
of blood with HCl - conversion of heme to dark chlorhaemin)
• In more active bleeding/achlorhydria – clear red blood
• Melena - excretion of black tarry stool with typical smell (requires at least
50 - 100 ml of blood in the large intestine, after 8 hours sulfides are
formed by the action of intestinal bacteria, causing black stool
discoloration)
• Enterorrhagia/haematochezia - bleeding below
Ligament of Treitz
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• In 1 – 10 % cases is source of bleeding undetected → search for the cause of bleeding in the small intestine - angiodysplasia 40%, lymphoma, IBD, leiomyoma
The most common Often Rare
Upper GIT Esophageal varicesMallory-Weiss syndromeGastric erosionsGastric/duodenal ulcers
EsophagitisCarcinoma of esophagus/stomach/duodenumBulbitisUlcer in anastomosisVascular enteral fistula
HemoptysisNasopharyngeal bleedingHaemobiliaAngiodysplasia
Lower GIT HaemorrhoidsProctitisIBDDiverticulosisIschemic colitisAngiodysplasiaPolyps of colon
Anal fissureInfectious enterocolitisCarcinoma of colonPost-radiation colitisMeckel diverticulumMassive bleeding from upper GIT
AmyloidosisPseudomembranous colitis
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Epidemiology
• Peptic ulcer 36 – 50 %
• Erosion 8 – 15 %
• Esophagitis 5 – 15 %
• Varices 13 – 18 %
• Mallory-Weiss syndrome 15 %
• Cancer 1 %
• Vascular malformation 5 %
• Others 5 %
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Diagnostics• History – type of bleeding, duration, abdominal pain,
comorbidities, weight loss, family history –
oncological disease?
• Physical examination – vital signs, color of the skin,
signs of hepatic disease – palmar erythema,
gynecomastia, spider nevi, ascites, hepato- and
splenomegaly
• Per rectum
• Labs – blood count – first hours without decrease in
Hgb, Hct, later normocytic normochromic anemia
(complete hemodilution after 24 hours), platelet
count, coagulation (warfarin, DOAC) + renal, hepatic
parameters, ionogram
• Esophagogastroduodenoscopy
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Pathogenesis of GI bleeding
• Sudden loss of 1/3 circulating volume – hemorrhagic shock
• If the blood loss lasts more than 24 hours – larger loss is well tolerated, activation
of compensatory mechanisms, fluid transfer from tissues to the intravascular
space – contribute to maintaining of the intravascular volume and BP
• release of catecholamines → peripheral vasoconstriction, tachycardia → normal
BP at the beginning, followed by ↓ blood pressure, ↓ hour diuresis →
vasodilation, release of toxic metabolites from the ischemic tissue →
progression of metabolic acidosis → irreversible
hemorrhagic shock
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Clinical features
• Depend on the extent of GIT bleeding + co-morbidities
• Pale, sweaty, cold acral parts, weakness, malaise, syncope, thirst
• Normal BP at the beginning → hypotension, tachycardia
• In case of CVS diseases – chest pain, dyspnea
• systolic BP below 100 mmHg, PF above 100 /min, centralization of circulation →
symptoms of hypovolemic shock – require intensive approach
• Complications - worsening of the underlying disease (DM, liver cirrhosis, CHF,
CKD/dialysis, stroke, malignancy, EtOH abuse) → cardiorespiratory failure, ARDS
disseminated intravascular coagulation, irreversible hypovolemic shock
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Prognostic factors – Rockall score
• Mortality risk stratificationLow risk ˂ 5High risk ˃ 5Score ˃ 8 – high mortalityAge over 90 – 40 % mortality
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Glasgow-Blatchford score
• Focused on the need of intervention– Blood transfusion, or– Endoscopy
• Score 0-1 = low risk– No intervention /
hospitalization required
• Who gets score 0– Hemoglobin >129 g/L
(men) or >119 g/L (women)
– SBP >109 mmHg– Pulse <100/minute– Blood urea <6.5 mmol/L– No melena or syncope– No past or present liver
disease or heart failure
Values Score
Blood urea 6,5 – 7,9 2
8,0 – 9,9 3
10,0 – 24,9 4
˃ 25,0 6
Hemoglobin in males (g/l)
120 – 129 1
100 – 119 3
˂ 100 6
Hemoglobin in women (g/l)
100 – 119 1
˂ 100 6
Systolic blood pressure (mmHg)
100 - 109 1
90 - 99 2
˂ 90 3
Other markers Pulse over 100/min 1
Melena 1
Syncope 2
Hepatic disease 2
Heart failure 2
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What to do in case of confirmed high risk GI bleeding?
• Nothing per os• Withdrawal of antiplatelet / anticoagulation drugs, consider
antidote – warfarin – vitamin K or prothrombin complex concentrate– dabigatran – idarucizumab (Praxbind), – Xabans and LMWH – no specific antidote now (andexanet
alpha in development), prothrombin complex can be used
• Intensive monitoring of BP, pulse, diuresis, ECG, satO2 • Peripheral access (at least 2x i.v. access) / central access• IV fluids• Hemostyptics – Pamba (paraaminobenzoic acid), Dicynone
(etamsylate)• Intubation as a prevention of aspiration
– in case of continued hematemesis, agitation, encephalopathy, impaired consciousness
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What to do next...• PPI - decrease acidity, prevents dissolution of blood coagula and facilitates
healing of ulcer - Pantoprazole 80 mg i.v. bolus, followed by 8 mg/h
continuously i.v. during 72 hours (for lesions with hemostasis + Forrest IIb)
• Vasopressor support
• Bloods units if anemia (in case of thrombocytopenia below 50 x 10/9 → correction of PLT,
hypocoagulation state → fresh frozen plasma, prothrombin complex concentrate)
• GFS - finding of the source of bleeding + treatment
• In case of recurrent bleeding after GFS successful hemostasis - repeat GFS, if this second attempt fails
/ unsuccessful primary GFS → catheter angiographic embolization or surgery
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What to do next...
Transfer higher risk patients to ICU
• age over 60 years
• serious associated diseases
• persistence of active bleeding
• hypotension or shock
• the need of higher amount of transfusions - ˃ 6
• severe coagulopathy
• recurrence of the bleeding during hospitalization
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Preparation before acute endoscopy
• Hemodynamic stabilization - significantly reduces the
incidence of myocardial infarction and reduces mortality
• Antibiotic prophylaxis – in valve diseases and prosthesis,
history of endocarditis (Not recommended anymore by ESC
Guidelines 2015)
• Correction of coagulation parameters
• Sedation if needed
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Endoscopic examination + therapeutic modality → GFS
• Endoscopic hemostasis significantly reduces the incidence of recurrent bleeding, the need for surgical
treatment, mortality, shortens the length of hospitalization
• Urgent GFS - ˂ 12 hours - high risk patient, hemodynamic instability, Glasgow-Blatchford ≥ 12
• Early GFS - within 24 hours
• Delayed GFS - no need for hospitalization if Glasgow-Blatchford ≤ 1
• Second look GFS - within 24 hours only in patients at high risk of bleeding
• Hemostasis – the use of endoscopic methods depends on the type of bleeding
– Injection of vasoconstrictors – adrenaline
– Injection of sclerosing agents (Etoxisclerol)
– Tissue adhesives, hemostatic sprays
– Ligation
– Metal clips
– Thermal methods - laser, argon plasma coagulation, bipolar coagulation
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Forrest classification
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Forrest classification
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Bleeding from esophageal varices
• Complication of portal hypertension, mortality 10 - 20% 6 weeks after bleeding
• Therapy - similar to nonvariceal bleeding• + Use of a balloon tube
• Linton - Nachlas - stomach balloon, for subcardial varices + traction • Sengstaken-Blakemore - stomach + esophageal balloon, air filling,
application for max. 12-24 hours (decubitus), unsuitable for subcardialvarices
• Minnesota - stomach + esophagus balloon
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Sengstaken-Blakemore tube
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Management of variceal bleeding
• Reducing pressure in the portal region → Terlipressin 2 mg i.v.,
if necessary 1 mg every 4 hr i.v. for 5 days (CAVE - coronary
ischemia)
• OR somatostatin or sandostatin (CAVE – hypoglycemia)
• + in advanced cirrhosis - ATB prophylaxis - quinolones / III.
generation cephalosporins
• + treatment of hepatic encephalopathy - lactulose, rifaximin
• Paquet classification
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Endoscopic treatment
• Endoscopic treatment
– Sclerotherapy
– Variceal ligation with a small band
– Injection of tissue adhesives
– Use of polymers
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What’s next?
• In case of recurrent bleedings from esophageal varices, Child/Pugh C/B with active bleeding (ideally up to
24-72 hours) – insertion of TIPS – transjugular intrahepatic portosystemic shunt via the jugular vein →
hepatic veins → v. portae –
– less invasive
– risk of hepatic encephalopathy
– risk of obliteration
• Esophageal stent Danis – covered self-expandable metal
stent
• Surgical treatment of portosystemic shunts - if conservative treatment of esophageal varices, despite
medical and endoscopic treatment , is not successful, the approximate
prognostic criterion is the number of blood transfusions – if amount of
red-cells concentrates is ›4/24hod – surgical management is indicated
• Liver transplant
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Part 2
Acute pancreatitis
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Acute pancreatitis
• inflammatory disease of the pancreas with
variable course
• The most frequent acute abdomen of non-surgical character
• 10 - 80/100 000 cases/year
• Etiology – alcohol-induced, biliary, diseases of major duodenal papilla – tumors,
dysfunction, diverticulum, dyslipidemias, hypercalcemia, congenital abnormalities of
the pancreas, drug-induced, blunt force trauma of the abdomen, penetrating gastric
ulcers, viruses, bacteria, parasites, cystic fibrosis, iatrogenic post-ERCP....
• Forms – mild, severe necrotizing → fluid collections, necrosis, pseudocyst, abscess
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Clinical presentation
• Various picture – acute pain, localized in epigastrium, propagation along left costal
margin up to the left scapula, to sternum, hypogastrium, nausea, vomiting (paralytic
ileus!), fever, icterus, cholangitis?
• + tachycardia, hypotension, dyspnea/respiratory failure, changes in consciousness,
delirium, oliguria, renal insufficiency, ascites, fluidothorax → ARDS, ARI, DIC, SIRS, MODS,
MOF
• + delirium – in case of active alcohol abuse
• Grey-Turner sign – ecchymosis
on lateral side of abdomen, costovertebral angle
• Fox sign – ecchymosis in the groins
• Cullen sign – periumbilical ecchymosis
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Diagnosis
• History + clinical presentation + laboratory evaluation
• Serum amylase (non-specific – parotitis, trauma, ileus, peritonitis,
macroamylasemia, diabetic ketoacidosis), amylase in urine, lipase,
total bilirubin + conjugated bilirubin, liver function test, urea,
creatinine, CRP, PCT, IL-6, WBC, hematocrit, coagulation test
• chest and plain abdominal X-ray, abdominal ultrasound
• MRCP, ERCP
• CT staging
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Criteria for severity of AP
• Mild form 80 – 85%, severe form 15 – 20%
• Modified Glasgow criteria – during 48 hours
• Severe pancreatitis – 3 and more criteria
P Arterial PaO2 < 9 kPa
A Albumin < 32 g / L
N Urea Nitrogen > 10 mmol / L
C Calcium < 2 mmol / L
R Raised White blood count > 15 000 per uL
E Enzyme Lactate dehydrogenase > 16 ukat / L
A Age > 55 years
S Sugar (Glucose) > 10 mmol / L
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• APACHE II
• non-specificsystem for AP
• ˃ 8 points –severe AP
• sensitivity 83%, specificity 91%
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CT staging
• Balthazar classification – level of damage + extent ofnecrosis → severity index
• Mild 0-2 (mortality 2%)
• Moderate 4 – 6
• Severe 8 – 10 (17 % mortality)
• Initial CT – severe AP up to 72 hours
• Repeat CT - A-C in case of deterioration of the condition
- D-E after 7-10 days, or according to the
condition of the patient
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Treatment• Monitoring of the patient – BP (CVP), Pulse, SpO2, diuresis, level of consciousness
• Nothing per os
• i.v. access
• nasogastric tube in case of vomiting/ileus
• PPI
• appropriate hydration – massive in the first 12-24 hours, 250-500 ml crystalloid/hour – monitoring of urea,
creatinine, lactate, hematocrit – parameters of hydration, adequate tissue perfusion → maintaining
diuresis of 0,5 ml/kg body weight/hour
• analgesia
• ATB treatment only for severe forms – G – bacteria - E coli, Enterobacter, Pseudomonas, Serratia + Staph.
Aureus, Streptococcus faecalis
• Parenteral nutrition/nasojejunal tube– if NPO for more than 5 days
• ERCP – in case of biliary etiology/acute cholangitis
• In case of infected necrosis of pancreas – fine-needle aspiration
• surgical removal of necrosis – after 2 weeks
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Part 3
Foreign bodies in GI tract
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Foreign bodies in GIT
Occurs in:– children (80%)– older patients – patients with personality disorders/psychiatric patients– prisoners– alcohol intoxication
Character of the foreign body:– food bolus (meat, fish, bones, …) – the most common (associated with
anatomical and motor abnormalities – peptic strictures, rings, tumor, ...)– real foreign bodies – rare (coins, dentures, ...)– iatrogenic foreign bodies – pills, dental instruments, ...
Localization:– 10 - 20% FB stay in esophagus (4 physiological narrowings, pathological
narrowing)– 80 - 90% FB reach the stomach
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Clinical presentation• the location of difficulties doesn’t have to correlate with the real
location of the FB• the FB sensation can persist even for a few hours after it passes
through
• dysphagia• odynophagia, retrosternal pain, sore throat• foreign body sensation, nausea, vomiting• Complete esophageal obstruction - hypersalivation, inability to
swallow fluids• Trachea compression, aspiration - asphyxia, stridor, dyspnea
Complications:• Bowel obstruction• Perforation – fever, tachycardia, subcutaneous emphysema• Laceration of esophagus
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Evaluation
• History– character of the foreign body
• Physical examination
• X-ray of the neck, chest (PA+lateral view), abdomen– suspicion of radio-opaque object
– unknown object
• X-ray with water –soluble contrast agent– if the object is not visible on plain X-ray
• CT scan– suspicion of perforation with possible surgical treatment
• Endoscopy- diagnostic and therapeutic possibilities
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Management
• Outpatient monitoring - 80-90% spontaneous passage through GIT (4-6 days)
- asymptomatic patients
- blunt objects ‹2-2,5cm in diameter (pylorus, ileocecal valve), ‹5-6cm long (duodenal flexure), which have already passed through esophagus
- checking X-ray 1x/week
• Surgical treatment - ‹1%
- stop in the passage of the object through GIT
- bowel obstruction
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• Endoscopic intervention - 10-20%
– Emergent (‹2 hours, max. 6 hours)
- complete esophageal obstruction
- sharp-pointed objects
- batteries in the esophagus
– Urgent (‹24 hours)
- sharp pointed objects and batteries in the stomach/duodenum
- larger objects, magnets
- smaller objects in the esophagus
– Nonurgent (‹72 hours)
- smaller and middle size objects after esophagus
- blunt small objects that fail to pass stomach in 3 to 4 weeks
Observational hospitalization• after a technically difficult intervention
• mucosal injury caused by the foreign body/ endoscopic intervention
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Case report
• 56 years old female
– History of arterialhypertension, hypothyroidism, duodenal ulcer
• Came to hospital due to stabbing abdominalpain
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Case report
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Case report
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Case report
• The sewing needle was removed from leftlobe of liver by laparoscopic surgery
• Further course was uncomplicated
• Patient later recounted, that she was sewingher grandson trousers some 10 days ago.
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Part 4
Caustic injuries of GI tract
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Caustic injuries of the gastrointestinaltract
• Injury of GIT by acid or alkaline substances (esp. pH ‹2/›12)– affects mostly esophagus, stomach, but also oral mucosa, pharyngeal area,
upper airways, duodenum– mostly household cleaning products
• Occurs in: – children (1 to 5-years old) – accidental ingestion, small amounts (spitting out
of the substance), lower rate of complicated cases– adults (30-40-years old) – intentional suicide attempts, greater injury
• The severity and extent of injury depends on:– length of time of tissue contact– amount and state of the substance– characteristics of the substance (pH, concentration, ability to penetrate
deeper to the tissue)
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ALKALIES• usually colorless, tasteless, with less marked odour, more viscous –
ingestion of greater amount
• reaction with proteins and fats – proteinases, soaps - liquefactive necrosis– deeper penetration with a greater likelihood of transmural injury
• affects mostly esophagus (+oro/hypopharynx), injury of stomach less frequent (neutralization by acidic content)
ACIDS• pungent odor, taste – ingestion of smaller amount
• reaction with proteins – coagulation necrosis – formation of eschar/coagulum (prevents transmural spreading)
• mostly affects stomach, in 20% small intestine
• the risk of absorption – metabolic alkalosis, hemolysis, ARI, death
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Clinical presentation
• Upper GIT, esophagus: – hypersalivation
– dysphagia, odynophagia
– sensation of pyrosis, retrosternal pain/
back pain
• Stomach: – nausea, vomiting, hematemesis
– epigastric pain
Perforation: - worsening of pain, fever, tachycardia, shock
- can occur at any time during the first 2 to 3 weeks of ingestion
• Airways: – cough, dyspnea
– hoarseness, stridor, aphonia
(involvement of epiglottis and larynx)
• symptoms do not always correlate with the degree of injury• mainly depend on the location of damage
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Diagnosis
• History, identification of corrosive agent• Physical examination
– CAVE – the absence of clinical signs of burns in the oropharyngeal area does not rule out the presence of gastric or esophageal injury
• Laboratory evaluation– CBC, pH, electrolyte panel, renal parameters, liver function test, lactate
• X-ray of the chest, abdomen, X-ray with a water soluble contrast agent, CT scan– free air in mediastinum, abdominal cavity– if perforation is suspected – water soluble
contrast agent (less irritating)
• Endoscopy
• ! distinguishing of patients who require emergency surgery from patients who are eligible for non-operative management
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Endoscopy in caustic GI injuries
• Contraindications– shock, hemodynamic instability
– necrosis in the oral cavity, hypopharynx
– esophageal/gastric perforation
– edema of the airways
• evaluation of the extent of the damage, determination of prognosis and management
• during the first 12-48 hours• not advised 5 to 15 days after caustic ingestion – tissue
friability during the healing stage, the risk of iatrogenic perforation
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Endoscopic classification of caustic injuries(Zargar et.al.)
Endoscopic finding
0 normal mucosa
I edema and erythema of the mucosa
II A hemorrhage, erosions, blisters, superficial ulcers
II B circumferential lesions
III A focal scattered areas od necrosis
III B extensive necrosis
IV perforation
0 1 2A 2B 3A 3B
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Management
• hospitalization• airway stabilization• supportive treatment
– NPO– fluid resuscitation, parenteral
nutrition– PPI– analgesia– ATB – in case of perforation,
infection– corticosteroids – airway
involvement
• surgical treatment– urgent – necrosis, perforation– later – reconstruction of strictures
• NO:– supine position– inducing emesis
• re-exposure of mucosa to corrosive agent
– gastric lavage• risk of perforation, aspiration
– neutralization by a weak acid/ base• exothermic reaction
– dilution by milk, water• risk of vomiting• exothermic reaction of water with
acid
– activated charcoal• poor adsorption• endoscopic interference
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Prognosis
• I, IIA complete healing, good prognosis, no complications
• II B 70% risk of strictures
• IIIA 90% risk of strictures
• IIIB 70% early complications, 65% mortality
• stricture formation – the most common late complication (3weeks to 1 year)
• esophageal malignancy - ›1000 times higher risk than in the general population (latency up to 40 years) - FOLLOW UP
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Thank you for your attention