gastric emergencies principles of critical care module session length 1hour
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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
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