Gastric Emergencies

Principles of Critical Care Module

Session length 1hour

Contents Introduction - What is a gastric emergency?

Learning objectives for session

Oesophageal Varices Pathophysiology Management options

Gastric / duodenal Ulcers Pathophysiology Management options

Summary

Introduction

This session will focus on the more commonly seen

gastric emergencies presenting within critical care settings – A. Bleeding varices B. Gastric / Duodenal ulcers

The pointecaste will explore the pathophysiology of these types of GI

bleed, looking at immediate management options, and the longer term

care issues patients with these conditions present to critical care

settings.

GI bleeds present numerous challenges for critical care with many

factors affecting prognosis. Overall mortality from variceal haemorrhage

ranges from 30%, reaching 50% in Child’s grade C (Kumar & Clark, 2001).

Objectives

Understand the pathophysiological processes underpinning common gastric emergencies

Identify different treatment options for each gastric emergency and implications for use

Recognise treatment priorities within the critically ill patient using a systematic approach

Understand the longer term implications of common gastric emergencies and management strategies within critical care

A. Oesophageal Varices

Pathophysiology

Portal vein is formed by the union of the superior mesenteric and splenic vein

Internal pressure 5 – 8mmHg with only a small gradient across the liver to the hepatic vein in which the blood is returned to the heart via the inferior vena cava. Oesophageal varices develop when blood through this area is obstructed Prehepatic - egThrombosis Intrahepatic – eg Cirrhosis, Hepatitis Posthepatic – eg Budd-Chiari syndrome

Net result of obstruction is a rise in internal pressure within portal vein

Portal Hypertension

As portal pressure rises above

10 – 12mmHg venous system dilates and collaterals occur at the gastro-oesphageal junction, the rectum, left renal vein, the diaphragm etc

The collaterals at the gastro-oesophageal junction are superficial in position and tend to rupture

Critical Care Management

In emergency situations, the care is directed at,

1. Stopping haemorrhage 2. Maintaining plasma volume 3. Correcting disorders in coagulation

induced by cirrhosis4. Antibiotic prophylaxis (sepsis / spontaneous

bacterial peritonitis)

Management options

Sengstaken-Blakemore tube

Drugs – Vasopressin, Beta Blockers, Octreotide

Endoscopy Variceal ligation, or

banding Sclerotherapy

Transjugular intrahepatic portosystemic shunt (TIPS)

Distal splenorenal shunt procedure

Liver transplantation

1. Stopping the Haemorrhage

Sengstaken-Blakemore Tube

Aim - to tamponade the bleeding varices

Oesophageal/ gastric balloon inflated with up to 60mls, and gastric and oesophageal lumens for drainage

Recommended balloon pressures vary from 25-40mmHg (McCaffrey,

1991) 50-60mmHg (Sung 1997)

May require tension for optimal functioning but this is controversial (Woodrow, 2000)

Can you think of any potential complications?

What are the potential complications associated with using a Sengstaken-Blakemore tube?

Can you think of 5?

(Press the pause button while you do this activity)

Other types of tube available

Linton-Nachlas tube, with large gastric balloon, and gastric and oesophageal aspirates

Minnesota four-lumen balloon with oesophageal and gastric balloons, and oesophageal and gastric aspirates.

Sengstaken-Blakemore Tube

Potential complications

Oesophageal / gastric ruptureOesophageal / gastric ischaemia

ulceration or necrosisExtent of subcutaneous bleeding

remains unseenPatient non compliance / discomfortRisk to airway – Intubation usually

requiredTo aid insertion tubes should be chilled –

Do you know where they are kept on your unit?

Limitations

Balloon tamponade controls 85 – 92% of bleeds, but rebleeds are common (Boyer &

Henderson, 1996)

Balloon tamponade is often used as only a temporary emergency measure – due to complications limit balloon use to 24hrs (Hudak etal, 1998)

Drug treatments

Vasopressin / Desmopressin / TerlipressinAntidiurectic hormone causes splanchnic arterial vasoconstriction, thus reducing portal hypertension. Temporarily controls haemorrhage in 28 – 70% of patients (Boyer & henderson, 1996).

Cautions – up to one third may rebleed during treatment (Boyer &

henderson, 1996). Used as a holding measure until definitive treatment obtained

Octreotide (a somatostatin analogue) Causes splanchnic vasoconstriction without significant systemic vascular effects. Reduces splanchnic blood flow and acid secretion

Beta-Blockers Also cause splanchnic vasoconstriction, thus reducing portal hypertension in approx 60% of patients with cirrhosis

Endoscopy - Sclerotherapy & Banding

Sclerotherapy – Endoscopic injection of 5% Ethanolamine Oleate (or similar) into varices

Banding – Endoscopic ligatation with bands

Arrest bleeding in approx 80% of cases (Kumar & Clark, 2001)

Transjugular Intrahepatic Portosystemic Shunt (TIPS)

Fistula created between the portal and hepatic veins and expandable shunt inserted to maintain patency

2. Maintaining circulation

Maintaining plasma volume

Close haemodynamic monitoring CVP monitoring BP monitoring Capillary refill times / evidence of compensation? Patient history Fluid balance - vomited blood (fresh or altered) /

evidence of malaena Fluid replacement

Blood / clotting products Plasma expanders eg Voluven or Gelofusion Crystalloids eg 0.9% Saline

3. Coagulation

Platelets

Fresh frozen plasma

Packed red cells

Cryoprecipitate

Coagulation

Correcting disorders in coagulation induced by cirrhosisBlood transfusionFresh frozen plasmaPlateletsCryoprecipitateVitamin K

B. Gastric / Duodenal ulcers

A bacterial infection - Helicobacter pylori infection

Medication, nonsteroidal anti-inflammatory drugs (NSAIDs) - aspirin, ibuprofen and naproxen

Stress Diet Hypersecretory states

eg Zollinger-Ellison syndrome

Signs and symptoms

Loss of weight / appetite

Pain, heartburn, or indigestion

Feeling of abdominal fullness or distention

Pain triggered or aggravated by eating 90 mins – 3hrs after eating

Mucosal erosion

Gastric Ulcer

Ulcer crater may extend beyond duodenal wall into nearby structures eg pancreas and liver

Ulcer crater may erode through blood vessels

NSAIDs

Aspirin and other NSAIDs deplete mucosal prostaglandins by inhibiting the cyclooxygenase (COX) pathway – leading to mucosal damage

Cyclooxygenase occurs in two formsCOX I - the constituitive enzymeCOX II - the inducible form which is

produced by cytokine stimulation in areas of inflammation (Kumar & Clark, 2001)

Investigations

Endoscopy – direct visualisation Carbon-13 urea breath test reflects activity of

H.pylori Barium swallow X Ray Occult blood in stools WBC count elevated Gastric secretory studies – excess

hydrochloric acid

Management options

Immediate ABCDE assessment and intervention

Proton pump inhibitor eg Omeprazole, Pantoprazole

H2 receptor antagonists eg Ranitidine

Endoscopy – injection with adrenaline + sclerosant vessel coagulated with heat probe or laser therapy

Surgical oversewing or resection of area

ABCDE approach

Airway Is patient maintaining airway – aspiration risk? Oxygen / suction / airway adjuncts / elective intubation

Breathing Respiratory rate / oxygen sats / ABGs

Circulation Signs of shock – capillary refill time / compensation (peripherally shut down) Observations – Pulse / BP / CVP / JVP Early large bore venous access Bloods – FBC / Clotting / LFTs / U&Es / cross match Fluid replacement – Blood products / colloid / crystalloids Fluid balance / input - output

Disability GCS / AVPU score / Blood sugar

Exposure Source of bleeding / volume Patient history Pain control Temperature

Exercise

Go and read / ask around on this topic and enter you findings on the discussion board

Some areas to consider….. What are the problems associated with using

nasogastric tubes in these patients? When should you allow eating and drinking? Whether you should use traction on a

Sengstaken tube? What nursing interventions do these patients

require?

Summary

GI bleeds can occur from multiple pathologies from cancer to infection. Or can result from the knock on effect of a disease process elsewhere in the body such as oesophageal bleeds as a result of portal hypertension

Management should reflect the severity of the bleed with initial priority aimed at haemorrhage control and fluid management

Longer term management aimed at finding / controlling the cause such as drugs or infection