Gastrointestinal prophylaxis in - Manssmh.mans.edu.eg/files/pdf/conf/2013/Gastro-Prophylaxis.pdf ·...
Transcript of Gastrointestinal prophylaxis in - Manssmh.mans.edu.eg/files/pdf/conf/2013/Gastro-Prophylaxis.pdf ·...
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Gastrointestinal prophylaxis in
critically ill patients
Ehab Abdel-Khalek, M.D.
Professor of Hepatology and Gastroenterology, Faculty of Medicine, Mansoura University
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Conflict of Interest
I did not receive any financial
support from the pharmaceutical
companies whose medications were
mentioned in this presentation.
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Critical illness - Definition
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A critical illness or injury acutely
impairs one of more vital organ
systems with a high probability of
imminent life threatening
deterioration in the patient’s
condition.
Messmann H. Crit Care Med 2013; 15(2):139-43.
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Early, specific signs of GI
complications are rarely present.
Because of late or missed diagnosis,
morbidity and mortality related to
these complications can be high.
Martin B. Adv Crit Care 2007; 18(2):158-66.
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Preventive measures
Cost.
Stay.
Morbidity.
Mortality.
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Strategies related to GIT
Stress Ulcer.
Gastric Overdistension.
Nutritional Support.
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Stress ulcerStress-related mucosal disease
(SRMD)
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Outline
Definition
History
Epidemiology
Pathophysiology
Guidelines
Agent Selection & Administration
Complications
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Definition
Gastrointestinal mucosal injury related to
critical illness.
Stomach
Duodenum
Ileum
Jejunum
Macroscopic bleeding
ASHP Therapeutic Guidelines on Stress Ulcer Prophylaxis. 2009; 15(2):139-43.
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History
1842: Curling described series in burn
patients
1932: Cushing reported ulcers with
surgery and trauma
1970s: Development of H2 receptor
antagonists
Maton PN. Aliment Pharmacol Ther. 2005 Dec;22 Suppl 3:45-52.
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History
1990’s: Dr. Cook and the Canadian
Critical Care Trials Group perform
landmark trials on ICU usage of H2
receptor antagonists.
1990s to 2000: Proton Pump inhibitors
make more efficient gastric
alkalinization possible.
Maton PN. Aliment Pharmacol Ther. 2005 Dec;22 Suppl 3:45-52.
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Epidemiology
Up through the 1970, stress ulcers were
much more common (>30% of ICU
patients)
Today, less than 5% of ICU patients
have stress ulcers with macroscopic
bleeding
Del Valle J. Peptic Ulcer Disease and Related Disorders , 2010.
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Pathophysiology
Etiology is complex
Decreased Gastric pH
Ischemia
Decreased mucus production
Usually occur within 24-48 hours of
trauma/stress
Del Valle J. Peptic Ulcer Disease and Related Disorders , 2010.
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Pathophysiology
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Pathophysiology
Absent
mucosal
barrier +
gastric acid =
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Guidelines
American Society of Health-system
pharmacists (ASHP) Therapeutic
Guidelines on Stress Ulcer Prophylaxis
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Key Guideline Points – The Big 3
1. Coagulopathy
Platelet count of <50,000mm3
INR>1.5
PTT of >2 times the control
2. Mechanical Ventilation
Longer than 24 hours
3. Recent GI ulcers/bleeding
Within 12 months of admission
ASHP Therapeutic Guidelines on Stress Ulcer Prophylaxis, AJHP 1999;56(4): 347-379.
Pathophysiology and prophylaxis of stress ulcer in ICU patients. J Crit Care. 2005 Mar;20(1):35-45.
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Key Guideline Points – The Little
2 or more of the following:
1. Sepsis
2. ICU>1 week
3. Occult Bleeding within 6 days
4. High dose corticosteroids
250mg Hydrocortisone
50mg Methylprednisone
ASHP Therapeutic Guidelines on Stress Ulcer Prophylaxis, AJHP 1999; 56(4): 347-379.
Pathophysiology and prophylaxis of stress ulcer in ICU patients. J Crit Care. 2005 Mar;20(1):35-45.
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Prophylaxis
Antacids
Sucralfate
Histamine2 receptor antagonists
Prostaglandin analogues
Proton pump inhibitors
Enteral feeding
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Prophylactic Options
Antacids:
- Neutralize acid.
- Must be given frequently and in larger
volumes to be effective.
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Prophylactic Options
Sucralfate:
- Adheres to epithelial cells and “restores” a cytoprotective barrier.
- Binds bile salts
- Stimulates prostaglandin synthesis
- Stimulates local epidermal growth factor
Goodman & Gilman’s Pharmacological Basis of Therapeutics. 2011.
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Prophylactic Options H2 Blockers:
- Inhibit acid secretion in a dose-dependent competitive manner.
- Reduce volume of gastric acid and [H+]
- Well absorbed with half life of 2 to 3 hours.
- Most trials show lower risk of significant GI
hemorrhage.
Shuman, RB. Ann Int Med 2006; 106: 562-8.
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Prophylactic Options
Prostaglandin analogues:
- PGE 2 and PGI 2 inhibit acid secretion
and increase mucus and bicarbonate.
- May have a more useful role in patients
who are dependent on NSAIDS.
Goodman & Gilman’s Pharmacological Basis of Therapeutics. 2011.
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Prophylactic Options
Proton pump inhibitors:
- The final mediator of acid secretion is the H+,
K+ -- ATPase pump unique to the parietal cell.
- PPIs are prodrugs that are activated by
protonation and covalently bind to a cysteine
residue and inactivate the ATPase enzyme.
Goodman & Gilman’s Pharmacological Basis of Therapeutics. 2011.
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Prophylactic Options
NUTRITION
In multiple burn studies, enteral
nutrition alone had a significantly lower
GI hemorrhage when compared to H2
Blockers.
Raff, T. Burns 1997; 23:313
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Agents and Dosing
IV Agents
Pantoprazole 40 mg (Q12-24h)
Ranitidine 50mg (Q8h)
Oral Agents
PPI 40mg (Q24h)
Ranitidine 150mg (Q12h)
Sucralfate 1-2 grams 4 times per day
Management Strategic Healthcare Group and the Medical Advisory Panel 2010; 39: 48-55.
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Proton pump inhibitors are at least
as effective as histamine 2 receptor
antagonists, as a large number of
clinical trials have demonstrated.
Maton PN. Aliment Pharmacol Ther. 2010; 3:45-52.
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New data suggest that PPI
inhibitors suppress acid production
more completely in critically ill
patients.
Stollman N, Metz DC. J Crit Care. 2012; 20(1):35-45.
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Negative Health Outcome
Risks Associated With Acid Suppression
Hospital Acquired Pneumonia(HAP).
C. Difficile.
Osteoporosis & Hip Fractures.
1. Herzig HJ et al, JAMA 2009;301(20):2120-2128
2. Dial, S, Delaney, AC, Barkun AN, et al. JAMA 2005;294(3):2989-2995
3. Yang et al. JAMA 2006:296(24):2947-2953
4. Targownik, LE et al. CMAJ 2008:179(4):319-326
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This patient with no Helicobacter infection got this ulcer during a
period of severe somatic stress due to a heart disease.
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Gastric overdistension
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Mechanical ventilation in critically ill patients
is theoretically associated with a number of
gastrointestinal complications, including stress
ulcers, hypomotility and diarrhoea.
Other aspects of critical illness or the therapies
used to treat it may further affect
gastrointestinal function.
Crit Care Resusc 2010; 12: 182–185
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Although gastrointestinal dysfunction is
not a priority in the critically ill,
intestinal hypomotility may lead to:
Malabsorption.
Vomiting.
Aspiration pneumonia.
Bacterial overgrowth.
Endotoxaemia.
Crit Care Resusc 2010; 12: 182–185
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Acute gastrointestinal (GI)
dysfunction and failure have been
increasingly recognized in critically
ill patients.
A. R. Blaser et al., Intensive Care Med 2012; 38:384–394
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The international Working Group on
Abdominal Problems (WGAP) of the
European Society of Intensive Care
Medicine (ESICM) developed the
definitions for GI dysfunction in
intensive care patients.
A. R. Blaser et al., Intensive Care Med 2012; 38:384–394
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Acute gastrointestinal injury (AGI)
is a malfunctioning of the GI tract
in intensive care patients due to
their acute illness.
A. R. Blaser et al., Intensive Care Med 2012; 38:384–394
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AGI grade I =
Risk of developing GI dysfunction or failure
(a self-limiting condition).
AGI grade II =
GI dysfunction
(a condition that requires interventions).
AGI grade III =
GI failure
(GI function cannot be restored with interventions).
AGI grade IV =
Dramatic GI failure with severe impact on distant organ
function
(a condition that is immediately life-threatening).
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AGI grade I
AGI grade I (risk of developing GI
dysfunction or failure).
Transient and partial impairement GI
function.
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AGI grade I
Examples :
- Nausea and vomiting after abdominal
surgery.
- Postoperative absence of bowel sounds.
- Diminished bowel motility in the early phase
of shock.
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AGI grade I
Management :
- Fluid replacement by IV infusions.
- Early enteral feeding, 24–48 h after the
injury.
- Limitation of drugs impairing GI motility
(e.g. catecholamines, opioids).
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AGI grade II
AGI grade II (gastrointestinal dysfunction)
The GI tract is not able to perform digestion
and absorption adequately.
There are no changes in general condition of
the patient related to GI problems.
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AGI grade II
Examples:
- Gastroparesis with high gastric residuals or reflux.
- Paralysis of the lower GI tract.
- Intra-abdominal hypertension grade I. (IAP = 12–15
mmHg).
- Visible blood in gastric content or stool.
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AGI grade II
Management:
- Prokinetic therapy.
- Enteral feeding should be started or continued.
- Initiation of postpyloric feeding in patients with
gastroparesis.
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AGI grade III
AGI grade III:
Loss of GI function, where restoration of
GI function is not achieved despite
interventions and the general condition
is not improving.
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AGI grade III
Examples:
- Feeding intolerance is persisting despite
treatment.
- High gastric residuals, persisting GI
paralysis.
- Progression of IAH to grade II (IAP 15–20
mmHg).
- Low abdominal perfusion pressure (APP)
(below 60 mmHg).
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AGI grade IIIManagement:
-Undiagnosed abdominal problems
(cholecystitis, peritonitis, bowel ischaemia)
should be excluded.
- The medications promoting GI paralysis
have to be discontinued as far as possible.
- Challenges with small amounts of EN should
be regularly considered.
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AGI grade IV
AGI grade IV:
GI failure with severe impact on distant
organ function.
AGI has progressed to become directly
and immediately life threatening, with
worsening of MODS and shock.
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AGI grade IV
Examples:
- Bowel ischaemia with necrosis.
- GI bleeding leading to haemorrhagic
shock.
- Ogilvie’s syndrome.
-Abdominal compartment syndrome
(ACS) requiring decompression.
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Ogilvie syndrome
acute pseudoobstruction and
dilatation of the colon in the absence
of any mechanical obstruction in
severely ill patients.
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Abdominal compartment
syndrome
- The abdomen becomes subject to increased
pressure.
- Cause: sepsis and severe abdominal trauma.
- Increasing pressure reduces blood flow to
abdominal organs and impairs pulmonary,
cardiovascular, renal, and GI function,
causing MODS and death.
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AGI grade IV
Management:
Condition requires laparotomy or other
emergency interventions.
There is no proven conservative
approach to resolve this situation.
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Nutritional support
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Critical illness increases nutrient requirements
as well as alters metabolism.
Patients in the ICU are unable to nourish
themselves orally.
Jeejeebhoy KN. Nutr Rev. 2012 Nov;70(11):623-30.
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ICU patients rapidly become malnourished
unless they are provided with involuntary
feeding either:
- Enteral nutrition (EN): through a tube
inserted into the GI tract, or
- Parenteral nutrition (PN): directly into the
bloodstream.
Jeejeebhoy KN. Nutr Rev. 2012 Nov;70(11):623-30.
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Between the 1960s and the 1980s, PN was the
modality of choice which led to overfeeding
regimens called hyperalimentation.
Later, the dangers of overfeeding,
hyperglycemia, fatty liver, and increased
sepsis associated with PN became recognized.
Acosta E scribano J Med Intensiva, 2011 Nov;35 Suppl 1:77-80.
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In contrast, EN was not associated with these
risks and it gradually became the modality of
choice in the ICU.
Hence, the balanced perspective has been
reached of using EN when possible but
avoiding underfeeding by supplementing with
PN when required.
Acosta E scribano J Med Intensiva, 2011 Nov;35 Suppl 1:77-80.
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Early EN is superior to delayed EN in the
critically ill
The expert committee, however favours that
critically ill patients, who are haemodynamically
stable and have a functioning gastrointestinal
tract, should be fed early (< 24 h), if possible.
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EN in critically ill patients
During the acute and initial phase of critical
illness, an exogenous energy supply of 20–25
kcal/kg BW/day is needed.
During recovery (anabolic flow phase), the aim is
to provide 25–30 total kcal/kg BW/day.
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Protein requirement 1.5 g/kg/day.
2 g/kg/day in patients with trauma, severe burns, and
head injury.
2.5 g/kg/day in adult patients treated with continuous
renal replacement therapy (CRRT).
nutritional support can only limit the loss
of the body’s protein and calorie stores.
The goal is to administer sufficient nitrogen to provide a
positive or neutral nitrogen balance.
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Lipid requirements
0.5 – 1 g/kg/d [ 20-40% of energy ]
Lipid clearance is reduced in stressed patients due to decreased activity of lipoprotein lipase.
infusion rate should not exceed 0.12 g/kg/hr to avoid the development of elevated TG levels.
Source of essential FA , fat soluble vitamins.
Avoid Omega 6 [ linoleic is a precursor of arachinodic acid].
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Parenteral nutrition
Indications:
- In patients who cannot be fed sufficient
enterally.
- Intolerant to EN
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Complications of PN
PN associated with a more pronouncedproinflammatory response than EN.
Complications of excess dextrose infusion
hyperglycemia
hypertriglyceridemia
hepatic steatosis,
respiratory decompensation
depression of immune function
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SUMMARY
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Acute gastrointestinal injury (AGI)
is a malfunctioning of the GI tract
in intensive care patients due to
their acute illness.
A. R. Blaser et al., Intensive Care Med 2012; 38:384–394
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AGI grade I =
Risk of developing GI dysfunction or failure
(a self-limiting condition).
AGI grade II =
GI dysfunction
(a condition that requires interventions).
AGI grade III =
GI failure
(GI function cannot be restored with interventions).
AGI grade IV =
Dramatic GI failure with severe impact on distant organ
function
(a condition that is immediately life-threatening).
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Guideline Summary
Big 3
1. Coagulopathy
2. Mechanical Ventilation
3. GI Bleeding within 12 months
Little 4 (2 or more)
1. Sepsis
2. ICU>1 week
3. Occult Bleeding within 6 days
4. High dose corticosteroids
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