Upper gastrointestinal bleed

Prepared by; Siti Nazhatul

Raudhah Azurien Nurul ‘Atiqah

Poncius Siti Rashidah

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

• 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

• 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

• 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

• 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.

• 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

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

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

Nervous System

• No LOC• No vertigo• No giddiness• No feeling of numbness• No blurring of vision

MSSK

• No muscle pain• No joint pain

• 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.

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

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

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

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

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.

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.

SYSTEMIC EXAMINATIONCENTRAL NERVOUS SYSTEMAll are intact.

PROVISIONAL DIAGNOSIS

• Upper gastrointestinal bleed

DIFFERENTIAL DIAGNOSIS

• Oesophageal varices• Oesophagitis • Peptic ulcer• Carcinoma of stomach

INVESTIGATIONS

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

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

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

Oesophagogastroduodenoscopy (OGDS)

Results:• 3 columns of grade 2-3 oesophageal varices • Banding was done• No fundal varices• No blood seen

Other investigation

• BUSE• Renal profile• Ultrasound of abdomen• Hepatitis B and C screening

FINAL DIAGNOSIS

UGIB secondary to oesophageal varices grade 2-3

MANAGEMENT

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.

DEFINITIVE TREATMENT

• Endoscopic banding• Vasopressin (IV Telepressin 2mg stat)

UPPER GASTROINTESTINAL BLEEDING

• Bleeding of GIT proximal to ligament of treitz• Ligament of treitz:- a fibromuscular band

which extends from right crus of diaphragm to duodenojejunal flexure

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

PAIN NO PAIN1. Peptic ulcer diseases2. Acute gastric erosion3. Oesophagitis

1. Carcinoma of stomach2. Esophageal varices

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

Bailey & Love’s Short Practice of Surgery, 25th ed

INDICATION FOR BLOOD TRANSFUSION

1. Systolic BP <110mmHg2. Postural hypotension3. Pulse >110/min4. Haemoglobin <8g/dL5. Angina or cardiovascular disease with

haemoglobin <10g/dL

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

Peptic Ulcer Disease

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.

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.

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

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.

Cont.

Duodenal ulcer

• Pain before meal.

• Relieved by taking food, milk.

Gastric ulcer

• Pain while eating.

• Relieved by vomiting

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.

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

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.

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

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)

Gastric Carcinoma

Worldwide, the fourth most common cancer and the second most common

cause of death.

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

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)

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

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

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

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.

Oesophagitis

• 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

Symptoms

• Heartburn (often at night, worsened by lying flat, initiated by bending, stooping or heavy lifting)

• Bitter taste in the mouth • Dysphagia (long term)

Investigation

• Barium swallow and barium meal– Oesophageal ulcer and peptic strictures

• Endoscopy – For patients who do not improve on medical trial,

long – standing symptoms

Treatment

• Proton Pump Inhibitor: Pantoprazole, Omeprazole

Esophageal Varices

• Caused by portal hypertension ( > 10mmHg )• Portal hypertension are caused by:– Liver cirrhosis– Hepatitis– Alcohol

Signs and symptoms

• Hematemesis• Melena• Ascites, splenomegaly, spider naevi, flapping

tremor• Anemia symptoms– Fatigue– Dizziness– Pallor– Shortness of breath

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

Japanese Classification

Management

• General– Secure airway, breathing and circulation– Resuscitation– Administer vitamin K– Short term antibiotic prophylaxis for 7 days

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