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 cirrhosis 4. 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 rupture Oesophageal / gastric ischaemia ulceration or necrosis Extent of subcutaneous bleeding remains unseen Patient non compliance / discomfort Risk to airway – Intubation usually required To 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 / Terlipressin Antidiurectic 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 cirrhosis Blood transfusion Fresh frozen plasma Platelets Cryoprecipitate Vitamin 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 forms COX I - the constituitive enzyme COX 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 H 2 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