Acute conditions in gastroenterology

MUDr. Komorníková, PhD, MUDr. Vlčková

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

Part 1

Gastrointestinal bleeding

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

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

• 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

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 %

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

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

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

Prognostic factors – Rockall score

• Mortality risk stratificationLow risk ˂ 5High risk ˃ 5Score ˃ 8 – high mortalityAge over 90 – 40 % mortality

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

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

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

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

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

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

Forrest classification

Forrest classification

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

Sengstaken-Blakemore tube

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

Endoscopic treatment

• Endoscopic treatment

– Sclerotherapy

– Variceal ligation with a small band

– Injection of tissue adhesives

– Use of polymers

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

Part 2

Acute pancreatitis

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

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

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

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

• APACHE II

• non-specificsystem for AP

• ˃ 8 points –severe AP

• sensitivity 83%, specificity 91%

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

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

Part 3

Foreign bodies in GI tract

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

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

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

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

• 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

Case report

• 56 years old female

– History of arterialhypertension, hypothyroidism, duodenal ulcer

• Came to hospital due to stabbing abdominalpain

Case report

Case report

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.

Part 4

Caustic injuries of GI tract

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)

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

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

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

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

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

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

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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