Discuss the management of upper gastrointestinal haemorrhage

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DISCUSS THE MANAGEMENT OF UPPER GASTROINTESTINAL HAEMORRHAGE

DR BASHIR YUNUSSURGERY DEPARTMENT

AKTH14th October 2014

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OUTLINE

•INTRODUCTION

•PRINCIPLE OF MANAGEMENT

•COMPLICATIONS

•PROGNOSIS

•CONCLUSION

•REFERENCES

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INTRODUCTION

• The gastrointestinal tract extend from the mouth to the anus and divided into two parts;

• Upper GIT

• Lower GIT

• By the ligament of treitzat the duodenojejunaljunction.

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INTRODUCTION

• The part above the ligament is the upper GI

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Definition:Any bleeding from GI tract proximal to ligament of treitz.

It is a common cause of emergency hospital admission and accounts for 5-10% mortality which increase in the elderly.

INTRODUCTION

• modes of presentation

– Hematemesis- 40-50%

– Melena-70-80%

– Hematochezia- 15-20%

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INTRODUCTION

• Hematemesis Vomiting of fresh or old blood

(40-50%) Proximal to Treitz ligament

Bright red blood = significant bleeding

Coffee ground emesis = no active bleeding

• Melena Passage of black & foul-smelling stools

(70-80%) Usually upper source – may be right colon

• Hematochezia Passage of bright red blood from rectum

(15-20%) If brisk & significant → UGI source

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PRINCINPLES OF MANAGEMENT

• INITIAL ASSESSMENT

• RESUSCITATION

• DETERMINATION OF BLEEDING SITE

• TREATMENT/INTERVENTION

• PREVENTION OF RECURRENCE

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PRINCIPLES

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Immediate Assessment

Stabilization of hemodynamic status

Identify the source of bleeding

Stopping the active bleeding

Treat the underlying

Prevent recurrent bleeding

ASSESSMENT

Patient presenting with cardiovascular instability requires prompt resuscitation before detailed history and examination to find the cause of bleeding and other co-morbidity

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ASSESSMENT

Severity of bleeding can be determined:

• Level of consciousness - obtundation

• Pulse rate >100bpm

• Postural hypotension.

• Severe blood loss—Vagal slowing of the heart

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ASSESSING SEVERITY

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eeding

Bleeding severity Vital Signs Blood loss (%)

Minor Normal < 10 %

Moderate Postural

(Orthostatic hypotension)

10 – 20 %

Massive Shock

(Resting hypotension)

20 – 25 %

RESUSCITATION

• Aggressiveness of resuscitation depends on the bleeding severity

• Resuscitation is proportional to bleeding severity

• Inadequate resuscitation leads to Multi-organ failure.

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RESUSCITATION• Ensure a patent airway and breathing.

• Elevate foot of bed to about 15⁰

• Secure IV access, take samples; PCV, U/Ecr, GXM, Platelet count, LFT.

• IV crystalloid, N/S R/L 1L over 30-45min

• Pass urethral catheter, empty the bladder then monitor urine output. (0.5-1ml/kg/min)

• Reassess PR,BP,CVP, urine output, to determine the rate of infusion

• Supplemental Oxygen---enhances oxygen carrying capacity of blood

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RESUSCITATION

• Pass N-G tube-– Decompression, prevent aspiration– Cold saline lavage

• Transfuse;– significant blood loss or pcv <30– on going bleeding,– inadequate response to fluid resuscitation,– elderly and – presence of cardiopulmonary disease

• Sedation– Phenobarb to quieten patient.

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HISTORY

• History to find the cause, co-morbidity and character(onset, volume and frequency) of bleeding. Careful history and physical examination may yield no definitive cause in 50%.– HX of PUD

– Alcohol ingestion

– NSAID

– Dysphagia

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HISTORY

• COMMON CAUSES

• Duodenal ulcer

• Gastric ulcer

• Stress ulcer

• Oesophageal varices

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HISTORY

• LESS COMMON CAUSES

• Oesophagitis

• Mallory- Weiss syndrome

• Malignant gastric tumours

• Benign gastric tumours

• Oesophageal ulcers or tumour

• Para-oesophageal hiatal hernia

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HISTORY

• RARE CAUSES

– Duodenal tumours

– Aorto-enteric fistula

– Blood dyscrasia

– Hereditary talengiectasia

– Angiodysplasia

– Dieulafoy’s lesion

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EXAMINATION

– Pallor

– Sweating

– Cold extremities

– Nostrils/ pharynx

– Epigastric tenderness

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EXAMINATION

• Collapse subcutaneous veins

• Tachycardia

• Hypotension

• Restlessness

• Features of CLD, gastric ca, abdominal masses,

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RISK SCORING

• ROCKALL’S RISK SCORE

• Score that predicts poor prognosis, i.e. rebleeding and mortality from upper GI haemorrhage

• It uses clinical criteria (increasing age, co-morbidity, shock) as well as endoscopic finding (diagnosis, stigmata of spontaneous haemorrhage -SSH)

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ROCKALL’S SCORE

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Risk category: High (> 5)Intermediate (3–5)Low (0–2)

MANAGEMENT AS PER RISK

• Low risk (0-2);usually 80% of patients recovers spontaneously with medical treatment(PPI) + hospitalization for 24hrs and may be discharge if uneventful.

• Intermediate risks(3-5); same treatment + hospitalization for at least 72 hrs.

• High risk(>5); same treatment + hospitalization in ICU

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DETERMINATION OF BLEEDING SITE

• NG-tube aspiration

• Endoscopy

• Barium studies

• Angiography

• Tagged rbc scan

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LOCALIZATION

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N-G TUBE ASPIRATION

Nasogastric aspiration with saline lavage is beneficial

• to detect the presence of intragastric blood,

• to determine the type of gross bleeding,

• to clear the gastric field for endoscopic visualization

• to prevent aspiration of gastric contents.

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ENDOSCOPY

• Diagnostic; direct visualization of source of bleeding

• Therapeutic; control of active bleeding

• To assess the prognostic indicator using the Forrest classification

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Modified Forrest Classification for Upper GI bleeding

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BARIUM MEAL

• In the absence of endoscopy, barium is attempted. It may show ulcer craters, varices, filling defect or tumors in the stomach.

• Double contrast is preferred; it shows small ulcers

• Disadvantages;

– Source remains undetected in ≥ 50% of patients

– Blood clot obscures gross lesion

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ANGIOGRAPHY

• It identifies the bleeding vessel

• Targeted therapy for ongoing hemorrhage; may prevent need for surgery (with embolization).

• Angio ≥ 1 ml/min

• Disadvantages; Invasive,expensive,requiresspecial expertise, exposure to radiation, risk of contrast media–induced nephropathy, bleeding from arterial puncture site

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TAGGED RBC SCAN

• Utilizes technetium labelled rbc extravasation into bowel is detected by scintillation camera.

• RBC scan may not accurately locate bleed.

• 0.5 – 1 ml/min bleeding requirement,set up req. 1-2 hours, test time 1-2 hours

• Contraindicated in;– initial Hct < 24,

– hemodyn unstable patient,

– ongoing > 100-200 cc/h bleed

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TREATMENT

• Non-operative

• Operative

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NON OPERATIVE

Peptic ulcer disease• Endoscopic• PPI• Elimination of H. pylori

• Endoscopic therapy: – Injection of adrenaline at the base of the vessel/

Sclerotherapy– Bipolar electro- / thermal probe coagulation– Argon plasma / laser photocoagulation– Hemostatic materials, including biologic glue

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ENDOSCOPIC MODALITIES AVAILABLE FOR THE MANAGEMENT OF U.G.I. BLEED

INJECTION

Adrenalin

Fibrin glue

Human Thrombin

Sclerosants

Alcohol

THERMAL Heater Probe

Bicap Probe

Gold Probe

Argon plasma coagulation

Laser therapy

MECHANICAL

Haemoclips

Banding

Endoloops

Staples

Sutures

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NON-OPERATIVE

• If bleeding controlled:• PPI- proton pump inhibitor

– omeprazole/pantoprazole, 80 mg bolus then 8 mg/hr infusion x 24 hrs. then 40 mg IV OD/BDthen transition to oral PPIs for 6-8 wks.

• Helicobacter pylori treatment, if presenttriple drug regimen x 2-3 wks.recurrent colonization 70-90% within few month to years.

• Repeat endoscopy < 6-8 wks.

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NON-OPERATIVE

• VARICES• Balloon tamponade• Pharmacological • Endoscopic• Transjugular intrahepatic portosystemic stent-shunt (TIPSS)

– Balloon tamponade:– Initially temporizing measure in all pts, now < 10%

temporary hemostasis in 85%, near 100% re-bleed on removal– 20% complication rate

Esophageal rupture, Tracheal rupture, Duodenal rupture, Respiratory tract obstruction, Aspiration, Tracheoesophagealfistula, Esophageal necrosis / ulcer

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Sengstaken blakemore tube

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Sengstaken blakemore tube

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• Pharmacologic treatment :• Vasopressin splanchnic vasoconstriction; 20IU in 250ml

of 5% DW over 30min, 4hrly. It improves hemostasis. Telipressin (pro-drug) better hemostasis and survival benefits. And longer duration of action.– Side effects

• Pallor• Hypertension• Abdominal colic• Cerebral and coronary ischemia• purgation

– Nitroglycerine 40 mcg/min may be given simultaneously to prevent coronary ischemia.

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• Nitroglycerine systemic hypotension and venous pooling, counteract cardiac effects of vasopressin; titrate to SBP 90-100.

• Glypressin; contains both nitroglycerin and vasopressin

• Beta-Blockers: Propranolol 40 mg bd; lowers portal pressure. Daily oral dose after bleeding has stopped is found to stop re-bleeding in about 80%.

• Octreotide: 250 mcg bolus, 250 mcg/hr infusion; Decreases gastric acid, pepsin, gastric blood flow

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Endoscopy

• Sclerotherapy;– Ethanolamine oleate (3-5ml) or sodium morrhuate

is injected into each varies.

– If the bleeding is controlled, injection is repeated weekly, then at 3weeks and at 3monthly until varies obliterate.

– Use of cyanoacrylate tissue adhesive.

• Initial success rate -> 90%, re-bleed 30-50%

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• Band Ligation; is efficacious and is now preferred to Sclerotherapy

• Endoscopic surveillance;

– 3 monthly for 1year then

– 6monthly for 1year then

– Annually

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• TIPSS;

– In refractory bleeding after sclerotherapy or band ligation.

– A shunt is established between the portal vein and the right or middle hepatic vein

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OPERATIVE

• Indications;– Massive bleeding

– Severe haemorrhage continues or recurs/not responsive to resuscitative efforts

– Associated perforation

– Blood not readily available

– Failure of medical therapy and endoscopic hemostasis with persistent / recurrent bleeding

– A second hospitalization for peptic ulcer hemorrhage

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OPERATIVE

• Factors predicting further bleeding from a peptic ulcer and possible need for surgery– Age > 60years

– Hb <8g/dl

– Shock on admission

– Visible spurting vessel on endoscopy

– Giant ulcer >2cm

– Ulcer on the posterior lesser curvature or posterior inferior wall of the duodenal bulb

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OPERATIVES

• AIMS;

– To stop the bleeding

– To prevent a recurrence

– To cure underlying cause

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DEFINITIVE PROCEDURES

• Peptic ulcer disease

– Laparotomy

– Upper mid-line incision

– Duodenal ulcer: most common, posterior bleed;

• longitudinal anterior duodenotomy

• Under-run the vessel (i.e. gastroduodenal artery) using non-absorbable suture preferable prolene 4-O.

• Quickest and safest operation

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Anterior longitudinal duodenotomy

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• Common complications

– Re-bleeding

– Injury to the common bile duct.

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Gastric ulcer: 1• wedge excision gastric ulcer – (always send for frozen to r/o

cancer)• Under-running the vessel• Followed by post-OP PPI, H.P. therapy, follow-up endoscopy• Effective and quicker

2Billroth 1 partial gastrectomy

3truncal vagotomy and pyloroplasty with excision of the ulcer

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vagotomy

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vagotomy

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• Complications

– gastric atony,

– alkaline reflux gastritis,

– Dumping

– diarrhea.

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VARICES

• Surgical Shunts:• Goal: decompression of the high-

pressure portal venous system into a low-pressure systemic venous system and devascularization of the distal esophagus and proximal stomach

• Portacaval shunt (end-to-side, side to side, interposition graft)

• Mesocaval shunt (Large- or small diameter interposition graft)

• Distal splenorenal (Warren) shunt

• Esophagogastricdevascularization,

• Esophageal transsection, & reanastomosis

• Orthotopic liver transplantation• Splenectomy (for splenic vein

thrombosis)

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VARICES

• Surgical Shunts:

• bleeding control rate >90%

• No differences in survival rates: ~5%.

• Complications;

– Re-bleeding

– Encephalopathy

– Ascites

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• Stress ulcers– Numerous ulcers- vagotomy + hemi-gastrectomy

– Few - oversewn

• Mallory-Weiss syndrome– Mucosal laceration is sutured

• Aorto-enteric fistula– Fistula disconnected and closed

– Aorta grafted with antibiotic primed graft and covered with omentum

– Antibiotic cover

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NEGATIVE LAPAROTOMY

• No lesion may be found in the eosophagus, stomach or duodenum

• The small and larged intestined are carefully examined for possible source of bleeding

• If negative, the abdomen is closed

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COMPLICATION OF UPPER GI BLEEDING

• Anaemia

• Sepsis

• DIC

• MODS

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PROGNOSIS

• Overall mortality is 10-15%• 33% in patient over 70years• 70-80% of bleeding peptic ulcer stop bleeding

sponteneously• Predictors of mortality:

– Age– Shock– Co-morbidities– Delay in diagnosis – Re-bleeding

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PROGNOSIS

• 20% re-bleed in 5-10years when treated conservatively

• When treated surgically, 4.5% re-bleed in 5-10years

• With H.pylori eradication, the re-bleeding rate is likely to go down.

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CHALLANGES

• ICU space limited

– Hemodynamic instability

– Massive

• Delayed definitive diagnosis

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CONCLUSION

• Even though 70-80% stops spontaneously,

• Bleeding frighten the patient it requires expeditious work-up ,prompt diagnosis and treatment.

• Accurate patient evaluation and early resuscitation before esophagogastroduodenoscopy (EGD) is critical to decrease the morbidity and mortality.

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REFERENCES

• E.A. Badoe, E.Q. Arcampompong, J.T Rocha; “Principles and Practice of surgery including pathology in the tropics”. 4th edition, Assembly of God Literature Center ltd, 2009. P 637-641

• Souba, Wiley et al; “ACS Surgery principles and practice” 6th edition, WebMD Inc. (Professional Publishing), 2007.

• Sriram Bhat M; “SRB’s Manual of surgery” . 4th edition, Jaypee brothers medical publishers ltd, 2013.

• Mitchell S. Cappell, David Friedel,; Initial Management of Acute Upper Gastrointestinal Bleeding: From Initial Evaluation up to Gastrointestinal Endoscopy.Med Clin N Am 92 (2008) 491–509

• Ingrid Lisanne Holster, Ernst Johan Kuipers; Management of acute nonvaricealupper gastrointestinal bleeding: Current policies and future perspectives. World J Gastroenterol 2012 March 21; 18(11): 1202-1207

• Jiwon Kim; management and prevention of upper GI bleeding: Gastroenterology and Nutrition. PSAP -VII

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»THANK YOU

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