Transcript Document

Gastric Emergencies
Principles of Critical Care Module
Session length 1hour
Contents
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Introduction - What is a gastric emergency?
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Learning objectives for session
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Oesophageal Varices
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Gastric / duodenal Ulcers
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Pathophysiology
Management options
Pathophysiology
Management options
Summary
Introduction
This session will focus on the more commonly seen
gastric emergencies presenting within critical care settings –
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A. Bleeding varices
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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
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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
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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 gastrooesophageal 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
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SengstakenBlakemore tube
 Drugs –
Vasopressin, Beta
Blockers, Octreotide
 Endoscopy
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Variceal ligation, or
banding
Sclerotherapy
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Transjugular
intrahepatic
portosystemic shunt
(TIPS)
 Distal splenorenal
shunt procedure
 Liver transplantation
1. Stopping the Haemorrhage
Sengstaken-Blakemore Tube
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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)
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Can you think of any potential complications?
What are the potential complications
associated with using a SengstakenBlakemore tube?
Can you think of 5?
(Press the pause button while you
do this activity)
Other types of tube available
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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
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To aid insertion tubes should be chilled –
Do you know where they are kept on your unit?
Limitations
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Balloon tamponade controls 85 – 92% of
bleeds, but rebleeds are common (Boyer &
Henderson, 1996)
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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
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Arrest bleeding in approx
80% of cases (Kumar &
Clark, 2001)
Transjugular Intrahepatic
Portosystemic Shunt (TIPS)
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Fistula created
between the portal
and hepatic veins
and expandable
shunt inserted to
maintain patency
2. Maintaining circulation
Maintaining plasma volume
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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
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Blood / clotting products
Plasma expanders eg Voluven or Gelofusion
Crystalloids eg 0.9% Saline
3. Coagulation
Coagulation
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Correcting disorders in coagulation
induced by cirrhosis
Blood transfusion
 Fresh frozen plasma
 Platelets
 Cryoprecipitate
 Vitamin K
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B. Gastric / Duodenal ulcers
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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
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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
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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)
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Investigations
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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
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Immediate ABCDE assessment and
intervention
 Proton pump inhibitor eg Omeprazole,
Pantoprazole
 H2 receptor antagonists eg Ranitidine
 Endoscopy –
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injection with adrenaline + sclerosant
vessel coagulated with heat probe or laser therapy
Surgical oversewing or resection of area
ABCDE approach
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Airway
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Breathing
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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
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Respiratory rate / oxygen sats / ABGs
Circulation
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Is patient maintaining airway – aspiration risk?
Oxygen / suction / airway adjuncts / elective intubation
GCS / AVPU score / Blood sugar
Exposure
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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
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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