upper GI bleeding
description
Transcript of upper GI bleeding
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Upper gastrointestinal bleed
Prepared by; Siti Nazhatul
Raudhah Azurien Nurul ‘Atiqah
Poncius Siti Rashidah
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History
Mr L, 58 years old, chinese, male came to the casualty with a chief complain of; I. Lower abdominal pain for 2 days II. Passing out black stool on the day of
admission III. Coffee ground vomitus on the day of
admission
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• Mr L was well until 2 days prior to admission where he started to felt pain at the lower part of the abdomen
• Site: suprapubic region • Onset: sudden • Character: dull and persistent • Radiation: no radiation to any part of the body • Associated symptom : no associated• Aggravating factor : none • Relieving factor: none • Severity: 3/10
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• On the day of admission, after waking up from sleep, he realised there is changes in the colour of his stool.
• It was black tarry dark stool. • Foul smelling• The stool was soft • No mucus or fresh blood seen
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• after passing the black stool, at around 8am, he had 1 episode of vomiting painless, large amount of coffee ground vomitus.
• He was unsure if the vomitus contains food particles because of its colour.
• The vomitus smells like blood
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• Otherwise, he had no shortness of breath, no palpitation, no dizziness, no weakness of the limbs, no chest pain, no giddiness, no fever, no early satiety and no dyspepsia.
• He also does not have any decrease in appetite or any reduce in weight.
• He has no comorbidities. • No history of blood transfusion. • He was not on any medication such as steroids,
aspirin, NSAIDS.
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• He is a chronic drinker since high school where he usually drink 4-5 bottles of alcohol per week and he drank 2 bottles of alcohol the night before he experienced melena and haematemesis
• He smoked 1 box per day (12 cigarrete) since 30 years ago.
• He is not an intravenous drug user • No history of multiple sex partner• Never had tatoo
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Systemic review
Respiratory System
• No shortness of breath• No wheezing• No hemoptysis• No cough
Cardivascular System
• No chest pain• No dyspnoea• No palpitation• No ankle swelling
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Gastrointestinal System
• No constipation• No diarrhea• bowel habit was
normal-once daily, soft in consistency
• No loss of appetite • No wight loss
Genitourinary System
• No pain during micturation
• No change in color of urine
• No urgency or incontinence
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Nervous System
• No LOC• No vertigo• No giddiness• No feeling of numbness• No blurring of vision
MSSK
• No muscle pain• No joint pain
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• No past medical and past surgical history
• Family history: Mr L is unsure of any illness that runs in the family and he was unsure if there is anyone having the same problem.
• Social history: He was divorced 2 years ago. He has 4 daughters and all of them stay with his wife. He now stays in Bercham with his friends. He works as a laundry van driver.
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General Examination• Mr L was conscious, alert
and not in pain.• Hand
• The palms were moist and warm
• IV cannula on the left dorsal part of the hand
• Capillary refilling time <2 secs• There is no palmar erythema
and no muscle wasting • No clubbing, no koilonychia
or leukonichia
• Head & mouth • The conjunctiva is pale.• No yellowish
discolouration of the sclera
• Lips were moist and hydrated
• No glossitis, angular stomatitis
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General Examination
• No palpable lymph nodes• No neck swelling• No pedal edema
• Vital signsPR : 104 bpm regular rhythm, good volumeRR : 18 breath per minTemperature : 37 oCBP : 104/69 mmHg
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Abdominal Examination
• Inspection • Abdomen is not
distended• Abdomen moves with
respiration• No visible peristalsis• The umbilicus in inverted
and lies in the midline• No scars visible on the
abdomen• No dilated veins
• Palpation• Abdomen is soft and non
tender • No guarding, no rebound
tenderness• the liver is palpable• Spleen is not palpable • Kidneys are not
ballotable
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Abdominal Examination
• Percussion• Liver span is about 14cm
right midclavicular line• Resonance traube space • No shifting dullness
• Auscultation• Bowel sounds were
present and normal• No renal bruit
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SYSTEMIC EXAMINATION
CARDIOVASCULAR SYSTEM
• No chest deformity, no visible median sternotomy scars, no visible pulsation.
• No raised in JVP• No radial-radial delay, radial-femoral delay.• Apex beat is palpable at 5th intercostal space in the left
midclavicular line, no paratsternal heave or visible thrill.• S1,S2 heard normally.• No murmur.
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SYSTEMIC EXAMINATION
RESPIRATORY SYSTEM
1)Shape of the chest is normal (elliptical), AP diameter is less than tranverse diameter, no scars, no dilated veins, trachea is in midline and not shifted, chest movement and expansion is symmetry.2)Tactile fremitus is equal on both sides.3)Percussion is resonance and equal on both sides.4)Vesicular breath sound is heard, equal air entry, no added breath sound such as crackles and wheeze. Vocal resonance are equal on both sides.
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SYSTEMIC EXAMINATIONCENTRAL NERVOUS SYSTEMAll are intact.
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PROVISIONAL DIAGNOSIS
• Upper gastrointestinal bleed
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DIFFERENTIAL DIAGNOSIS
• Oesophageal varices• Oesophagitis • Peptic ulcer• Carcinoma of stomach
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INVESTIGATIONS
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FULL BLOOD COUNTWBC 15.0 0-11.0
Hemoglobin 8.7 g/dl 13.0-18.0
Hematocrit 29.1 % 40-52
MCV 98.5 FL 76.0-96.0
MCH 29.5 PG 27.0-32.0
MCHC 29.9 G/DL 30.0-35.0
RDW 14.9 13.0-14.4
TRBC 2.95 5-6.5
Platelet 175 0-400
Neutrophil 10.54 0-7.0
Lymphocyte 3.13 0-3.0
Monocyte 1.28 2-10
Eosinophil 0.005 0.2-0.5
Basophil 0.045 0.2-0.1
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LIVER FUNCTION TESTRESULT NORMAL RANGE
Total protein 64 64-83 G/L
Total bilirubin 21.1 1-17 UMOL/L
Alkaline phosphatase 116 40-129 U/L
Albumin 33 35-52 G/L
Aspartate transaminase 85 0-40 U/L
Alanine transaminase 60 0-41U/L
Globulin 31
Haemolysis No
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COAGULATION PROFILESRESULTS NORMAL RANGE
Prothrombin time 19.5 12.3-14.3 sec
INR 1.66
Activated partial thrombin time (APTT)
31.7 28.8-45.3 sec
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Oesophagogastroduodenoscopy (OGDS)
Results:• 3 columns of grade 2-3 oesophageal varices • Banding was done• No fundal varices• No blood seen
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Other investigation
• BUSE• Renal profile• Ultrasound of abdomen• Hepatitis B and C screening
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FINAL DIAGNOSIS
UGIB secondary to oesophageal varices grade 2-3
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MANAGEMENT
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RESUSCITATION
• Secure airway, breathing and circulation• Nil per oral• Obtain IV access• Group and cross match at least 2 units of blood• Administer vitamin K, 10 mg• Antibiotics prophylaxis (IV Rocephine 1gm/day)• Administer IV saline/ packed red cells to replace
blood loss.• Bladder catheterisation performed for assessment
of end organ perfusion.
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DEFINITIVE TREATMENT
• Endoscopic banding• Vasopressin (IV Telepressin 2mg stat)
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UPPER GASTROINTESTINAL BLEEDING
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• Bleeding of GIT proximal to ligament of treitz• Ligament of treitz:- a fibromuscular band
which extends from right crus of diaphragm to duodenojejunal flexure
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ETIOLOGYNON-VARICEAL BLEEDING
(80% of cases)VARICEAL BLEEDING
(20% of cases)1. Peptic ulcer diseases (30-50%)2. Mallory-Weiss tears (15-20%)3. Gastritis or duodenitis (10-15%)4. Esophagitis (5-10%))5. Arteriovenous malformations (5%)6. Tumours (2%)7. Others (5%)
1. Gastroesophageal varices (>90%)2. Hypertensive portal gastropathy (<5%)3. Isolated gastric varices (Rare)
Sabiston Textbook of Surgery, 18th ed
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PAIN NO PAIN1. Peptic ulcer diseases2. Acute gastric erosion3. Oesophagitis
1. Carcinoma of stomach2. Esophageal varices
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UPPER GI BLEEDING
PAINFUL PAINLESS
ACUTE CHRONIC HEARTBURN ESOPHAGEAL VARICES POLYPS STOMACH
CANCER COAGULATION
1. Acute gastric erosion
1. Peptic ulcers
Gastric ulcer Duodenal ulcer
Pain at Rt HC++ by eating--- by vomitting(loss appetite)*weight ↓- thin
Pain at epigastrium++ by fasting--- by food(hunger pain)*weight ↑- Fat
1. Oesophagitis -Age (elderly)
-Family hx-Early satiety-LOW/LOA
Due to portal hypertension
PRE Hepatic HEPATIC POST Hepatic
Hepatitis B&C Alcohol
Bleeding disorders
1. Mallory-Weiss tears 2. AV malformations
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Bailey & Love’s Short Practice of Surgery, 25th ed
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INDICATION FOR BLOOD TRANSFUSION
1. Systolic BP <110mmHg2. Postural hypotension3. Pulse >110/min4. Haemoglobin <8g/dL5. Angina or cardiovascular disease with
haemoglobin <10g/dL
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1. Vomit blood on the day of admission, still continue blood in the ward with low blood pressure
2. After transfuse blood the blood pressure still low
INDICATION FOR EMERGENCY SCOPE
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Peptic Ulcer Disease
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Definition
• Disruption of the mucosal integrity of the stomach/ duodenum or both, caused by local inflammation/ decreased mucosal resistance/ hyper acidity which leads to a well-defined mucosal defect (ulcer).
• Gastric ulcers are due to decreased resistance of gastric mucosa. (older patients)
• Duodenal ulcer is predominantly occurs due to hyperacidity.
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Etiology• Helicobacter pylori infection.- Do not invade cells (only mucous membrane)- Breakdown urea to form ammonia result in breakdown of
mucosal defense.
• Non-steroidal anti-inflammatory drugs (eg. Aspirin, Ibuprofen)
• Stress
• Cigarette smoking, alcohol, spicy food.
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Pathophysiology Predisposing factors, including H.pylori infection of mucosa
Acid pepsin attack and/ or breach of mucosal protection
Acute inflammation
Destruction of mucosaMucosal ulceration
Extension through submucosal layers causing deep ulceration
Perforation
Peritonitis
Continue bleeding from mucosal surface
Erosion of major vessel
Granulation tissue formed and attempts at repair
Iron deficiency anemia
Massive hemorrhage (hematemesis and/ or malaena)
Chronic and relapsing ulceration
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Duodenal vs Gastric Ulcer
Duodenal Ulcer• More common• Occur in the 1st part of
duodenum• Fibrosis may lead to pyloric
stenosis. • Can be more than 1
duodenal ulcer at a time. • Ant. Ulcer tends to perforate
& post. Ulcer tends to bleed.
Gastric Ulcer• Less common• Occur near the lesser
curvature.• Fibrosis may lead to hour
class contraction of stomach.• Large chronic ulcers may
erode posteriorly into pancreas or into major vessels such as the splenic artery.
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Cont.
Duodenal ulcer
• Pain before meal.
• Relieved by taking food, milk.
Gastric ulcer
• Pain while eating.
• Relieved by vomiting
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Clinical Features
• Epigastric pain( described as ‘boring’, ‘gnawing’ or ‘burning’), intermittent and radiates to back (in case penetrating the pancreas).
• May described as indigestion or dyspepsia
• Bitter regurgitation : esophageal reflux & duodenal ulceration
• Hematemesis and melaena.
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Investigations
H.Pylori testing• Non invasive: – Serology tests to detect IgG antibodies– 13C-urea breath test– Stool antigen test
• Invasive:– Rapid urease test: during endoscope using CLO test kits and
results received within 3 hours– Biopsy urease test –added to a substrate containing urea and
phenol red.– Histology: on Giemsa stain
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Cont.
• Oesophageal gastro-duodeno scopy (OGDS)
- View the ulcer and take biopsy- Non malignant ulcer : sharp, punched out
defect, overhanging mucosal border with a smooth and clean ulcer base.
- Malignant ulcer will be >2cm, bleeds on touch, irregular margin with slough on the floor.
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Management
1. Control the predisposing or aggravating causes– Modify diet– Reduce alcohol intake– Quit smoking– Avoid irritant and ulcer-provoking drugs (aspirin &
other NSAIDs), – Avoid stress,– Reduce oesophageal reflux by losing weight and
attention to posture
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2. Elimination of proven H. pylori infection– Triple therapy: consists of two antibiotics
(amoxicillin, clarithromycin, and/or metronidazole) plus a PPI (omeprazole, pantoprazole) for 10 to 14 days.
3. Medical treatment– PPI: omeprazole – H2 – receptor antagonists (ranitidine, famotidine
and roxatidine)
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Gastric Carcinoma
Worldwide, the fourth most common cancer and the second most common
cause of death.
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Risk Factors
Nurritional
• Low fat and protein consumption
• High salted meat or fish
• High nitrate consumption
Environmental & social
• Poor drinking water
• Radiation exposure
• Occupational (coal mining, rubber or asbestos related
• Low socioeconomic group
• Smoking • Family history of
gastri cancer
Medical
• H. Pylori infection
• Prior gastric surgery
• Gastric atrophy and gastritis, adenomatous polyps
• Blood group A• Pernicious
anaemia
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Signs & Symptoms•Indigestion •Nausea or vomiting •Dysphagia •Postprandial fullness •Loss of appetite •Melena or pallor from anemia •Hematemesis •Weight loss •Palpable enlarged stomach with succussion splash •Enlarged lymph nodes such as Virchow nodes (ie, left supraclavicular) and Irish node (anterior axillary)
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Spread of Carcinoma Stomach
1. Direct spread– Penetrates muscularis, mucosa, adjacent
organs such as pancreas, colon, liver2. Lymphatic spread
– Spread to supraclavicular lymph node (Troisier’s sign)
3. Blood-borne metastasis– Spread to liver, lung, bone, brain
4. Transperitoneal spread– Manifest in peritoneal cavity and give
rise to ascites– Umbilicus nodules (Sister Mary Joseph’s
Nodule)– Krukenbergs’ tumor
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Investigations
1. Laboratory studies– Full blood count– Tumour markers (CEA and CA 19-9)
2. Diagnostic• Oesophagogastroduodenoscopy with biopsy• X-ray with barium meal
3. Staging– Ultrasound of the abdomen– Liver function test– CT scan of abdomen– Chest X-ray
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Management
i) Surgery• depends on the location, size, and locally invasive
characteristics of the tumor.a) Total gastrectomyb) Esophagogastrectomy for tumors of the cardia
and gastroesophageal junction c) Subtotal gastrectomy for tumors of the distal
stomach d) Lymph node dissection
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ii) Chemotherapy• Platinum-based combination chemotherapy: First-
line regimens include epirubicin/cisplatin/5-FU.
• Ramucirumab for the treatment of advanced stomach cancer or gastroesophageal (GE) junction adenocarcinoma in patients with unresectable or metastatic disease following therapy with a fluoropyrimidine- or platinum-containing regimen.
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Oesophagitis
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• Occurs when acid pepsin refluxes through the lower oesophageal sphincter onto the squamous epithelium lining of the oesophagus.
• Risk factors – Obesity– Fatty food– Caffeinated drinks– Alcohol– Drugs such as calcium channel blocker, antihistamine and
anticholinergic
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Symptoms
• Heartburn (often at night, worsened by lying flat, initiated by bending, stooping or heavy lifting)
• Bitter taste in the mouth • Dysphagia (long term)
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Investigation
• Barium swallow and barium meal– Oesophageal ulcer and peptic strictures
• Endoscopy – For patients who do not improve on medical trial,
long – standing symptoms
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Treatment
• Proton Pump Inhibitor: Pantoprazole, Omeprazole
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Esophageal Varices
• Caused by portal hypertension ( > 10mmHg )• Portal hypertension are caused by:– Liver cirrhosis– Hepatitis– Alcohol
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Signs and symptoms
• Hematemesis• Melena• Ascites, splenomegaly, spider naevi, flapping
tremor• Anemia symptoms– Fatigue– Dizziness– Pallor– Shortness of breath
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Pathophysiology
1. Caused by increased portal vascular resistance and increased portal flow / pressure
2. Due to obstruction, collaterals are formed within systemic circulation
3. The walls of the veins are easily ruptured if the pressure is high
4. Hematemesis is the most common presentation
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Japanese Classification
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Management
• General– Secure airway, breathing and circulation– Resuscitation– Administer vitamin K– Short term antibiotic prophylaxis for 7 days
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Management
• Definitive– Endoscopic scleropathy / banding– Facilities not available give pharmacologic treatment
• Vasopressin / Somatostatin to temporarily reduce portal pressure and reduce the bleeding
– To secure hemostasis, Sengstaken Blackmore tube can be inserted to achieve temporary hemostasis
– Transjugular intra hepatic porto systemic stent shunt (TIIPS) – Spleen – renal shunt – Liver transplant