Stress Ulcer Prophylaxis - Wild Apricot wills.pdf · Stress Ulcer Prophylaxis: Guideline Update April 2014 Rob Wills, Pharm.D., BCPS ... PPI’s vs. H2RA’s vs. sucralfate What are

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Stress Ulcer Prophylaxis: Guideline Update April 2014

Rob Wills, Pharm.D., BCPS

Clinical Manager of Pharmacy

PGY1 Residency Program Director

St. Luke’s Boise-Meridian Medical Centers

Disclosure Statement

�No conflict of interest

Idaho Society of Health System Pharmacists2014 Spring Conference

Objectives� Who should be receiving stress ulcer prophylaxis in your institution?

� Pathophysiology

� Risk Factors

� What medications are best to use to prevent stress ulcers?

� The great debate: PPI’s vs. H2RA’s vs. sucralfate

� What are the complications of providing stress ulcer prophylaxis?

� Strategies for gaining back the control


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Why is this important?� Unnecessary Costs

� Meds without an indication

� Inappropriate use

� Patients sent home on SUP agents

� Opportunistic Infections

� C. difficile

� Pneumonia

� Readmissions


Question 1

�Who’s been anxiously awaiting the release of the new Stress Ulcer Prophylaxis guidelines?

A. Check ASHP website at least weekly

B. What Guidelines

C. I thought this was a Law Talk?

D. None of the above


ASHP GuidelinesDocument Publishe

d

Next

Review Date

Estimated

Publication Date

Antimicrobial Prophylaxis in Surgery

2013 2016 --

Clinical Practice Guidelines for Sustained Use of Neuromuscular Blockade in the Adult Critically Ill Patient

2002 In process

--

Clinical Practice Guidelines for the Management of Pain Agitation and Delirium in Adult Patients in the ICU

2013 2016 --

Gastrointestinal Stress Ulcer Prophylaxis

New In process

Q1 2014

www.ASHP.org accessed 3/3/14


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The Guidelines

� Last updated 1999

�What’s missing?

�Are they still relevant?

ASHP Therapeutic Guidelines on SUP. AJHP.1999;56(4):347-379.



History

1800’s

Erosions & Gastric Ulcers have been known to develop

1970’s

Gastric Acid linked as possible cause of stress ulcer development

1980’s

Incidence of stress-ulcer related bleeding was found to be decreased by

increasing gastric pH

ASHP Therapeutic Guidelines on SUP. AJHP.1999;56(4):347-379.Schuster DP. Crit Care Med. 1993;21:4-6.Schuster DP, et al. Am J Med. 1984;76:623-630.Sesler JM. ACCN. 2007;18(2):119-128.


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Background� 1970

� Skillman and Silen reported a clinical syndrome of lethal “stress ulceration” in patients with� respiratory failure� hypotension� sepsis in the ICU

� 1971� Lucas et al labeled this as “stress-related erosive syndrome”

� Today� Stress Related Mucosal Disease

Skillman JJ, Silen W. Acute gastroduondenal “stress” ulceration: Barrier disruption of varied pathogenesis? Gastroenterology. 1970;59:478-482Lucas CE, SugawaC, Riddle J, et al. Natural history and surgical dilemma of “stress” gastric bleeding. Arch Surg. 1871;102:266-273.


Terminology� Stress Ulcers

� Ulceration

� Stress erosions

� Stress gastritis

� Hemorrhagic gastritis

� Erosive gastritis

� Peptic Ulcers

� Gastric Ulcers

� Stress-Related Mucosal Disease

� SRMD

Sesler JM. ACCN. 2007;18(2):119-128.


CHEST. 2001;119(4):1222-1241. doi:10.1378/chest.119.4.1222

Proposed mechanisms for development of stressulceration. SRMD results from the complex interaction of multiplesystems. The specific relationships depicted remain somewhatspeculative. Reprinted with permission from Bresalier.44

Figure Legend:


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GI Complications in Patients Receiving Mechanical Ventilation*

CHEST. 2001;119(4):1222-1241. doi:10.1378/chest.119.4.1222

Proposed mechanisms for the development of GI complications during MV. MV can contribute to the pathogenesis of GI problems in much the same way as critical illness by affectingsplanchnicblood flow and leading to increased release ofproinflammatorymediators. SIRS = systemic inflammatory response syndrome; TNF-α = tumor necrosis factor-α.

Figure Legend:


Pathogenesis of stress ulcerationOccurs in 50 to 70% of ICU patients within 12 to 24 hours

GI Mucosal Ischemia

Impaired defense mechanisms:� H+ back-diffusion� Mucous/bicarbonate barrier� Prostaglandin production� Epithelial renewal

Stress Ulceration

Gastrointestinal bleed

Mortality rate is 50 to 70%

Acid Secretion

H. Pylori infection?

Cohen H. Stop Stressing Out: The new stress ulcer prophylaxis guidelines are finally here. 2013 ASHP

Clinical Midyear Meeting. Orlando, FL


Classification of GI Bleeding

Outcome Measure of GI Bleeding

DefinitionIncidence in ICU

patients

Endoscopic EvidenceEndoscopic evidence of gastroduodenal SRMD lesions

74 to 100%

Occult Guaiac-positive stools or nasogastric aspirate 15 to 50%

Overt ORClinicallyevident

Hematemesis, gross blood or coffee grounds material in nasogastric tube aspirate, hematochezia or melena

5 to 25%

Clinically Significant

Overt bleeding accompanied by- Hemodynamic compromise

- Decrease in BP by 20 mmHg- Need for blood transfusion

- Decrease in Hgb by 2 g/dL AND transfusion of 2 units of blood

- Need for surgeryShould be used as outcome measure for all trials

< 5%

Table 1

Naylor DF. Clinical Applications of Stress Ulcer Prophylaxis. Soc of Crit Care Med. 2012 conference.Cook et al. NEJM.1994;330:377-381.


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Appearance� Appearance

� Diffuse sub-epithelial hemorrhage with or without erosions

CHEST. 2001;119(4):1222-1241. doi:10.1378/chest.119.4.1222


Where is this occurring?�Acid-producing areas of stomach

� Upper body

� Fundus

Accessed from www.webmd.com

8-2012


Outcomes

�Morbidity

� Increases length of ICU stay from 4 to 8 days, or even 11 days longer stay

�Mortality

� 50% - 75% of patients with clinically significant bleed

� ~ 12% directly attributable to the bleed

�Cost of bleed

� $7000 in 1999

Cook et al. NEJM.1994;330:377-381.Sesler JM. ACCN. 2007;18(2):119-128.

AJHP. 1999:56;347-379.


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Question 2

�Which of the following is a risk factor for stress-related ulcer bleeding in a 73 year old critically ill patient?

A. An INR of 5

B. Acute renal failure

C. ARDS with ventilator support for 72 hours

D. All of the above

Cohen H. Stop Stressing Out: The new stress ulcer prophylaxis guidelines are finally here. 2013 ASHP

Clinical Midyear Meeting. Orlando, FL


Critical Illness

Splanchnic Hypoperfusion

Reduced HCO3 Secretion

Reduced Mucosal Blood Flow

Decreased GI Motility

Acid Back Diffusion

Decreased Cardiac Output

Increased Catecholamines

HypovolemiaProinflammatory Cytokine Release

Acute Stress Ulcer

Increased Vasoconstriction

Mutlu GM, Mutlu EA, Factor P. GI complications in patients receiving mechanical ventilation. Chest. 2001;119:1222-1241.


Risk factors for Stress Ulcer Bleeding in Critically Ill Patients

Study Design

� N=2252

� Primary Diagnosis� CV surgery (48.5%)

� Respiratory (12%)

� Head Injury (1.2%

� Sepsis (1.6%)

� Multiple trauma (0.8%)

� APACHE II score: 21± 9 (moderate-severe illness)

Risk Factor Multiple Regression: Odds Ratio for Developing GI Bleed

Respiratory failure 15.6*

Coagulopathy 4.3*

Hypotension 3.7

Sepsis 2.0

Hepatic Failure 1.6

Renal Failure 1.6

Cook et al. NEJM.1994;330:377-381.

.

*Identified as independent risk factors; P< 0.001

Cohen H. Stop Stressing Out: The new stress ulcer prophylaxis guidelines are finally here. 2013 ASHP Clinical Midyear Meeting. Orlando, FL


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Risk factors for SRMD� Respiratory failure requiring mechanical ventilation ≥ 48 hrs

� Coagulopathy (INR > 1.5, PTT > 2x control or Thrombocytopenia)

� Acute renal insufficiency

� Acute hepatic failure

� Sepsis, Shock requiring vasopressors

� Multi-organ Failure

� Extensive burn or thermal injury involving more than 35% of the BSA

� Severe head or spinal cord injury

� History of gastrointestinal bleeding

� Organ transplantation

� Ulcerogenic Drugs (NSAIDS, Aspirin, Corticosteroids)

� Fibrinolytics, Anticoagulants

Cook et al. NEJM.1994;330:377-381.Sesler JM. ACCN. 2007;18(2):119-128.

AJHP. 1999:56;347-379.Cohen H. Stop Stressing Out: The new stress ulcer prophylaxis guidelines are finally here. 2013 ASHP Clinical Midyear Meeting. Orlando, FL


Degree of Acid Suppression Required Varies Depending on Indication

Gastric pH Physiologic Activity

≥ 3.5 Decreased incidence of stress-induced bleeding

≥ 4.5 Pepsin inactivation

5 99.9% acid neutralization

< 5 to 7 Alterations in coagulation and platelet aggregation

≥ 7 Potential decrease in incidence of rebleeding

≥ 8 Pepsin destruction

Prevention of Stress-Related Mucosal Disease

Prevention of Stress-Related Mucosal Disease



Question 3� 57 year old male admitted to the ICU with sepsis 2 days ago� Placed on Mechanical Vent at that time due to respiratory

failure

� Also experiencing some acute

renal failure, thrombocytopenia, and hypotension

� Which of the following can be used as first-line stress

ulcer bleeding prevention?

A. Famotidine IV

B. Esomeprazole IV

C. Omeprazole NGT

D. Sucralfate NGT

Accessed from heart-valve-surgery.com August 2012



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Therapeutic Options

�Antacids

� Sucralfate

� Histamine 2 Receptor Antagonists (H2RA)

� Proton Pump Inhibitors (PPI)


AntacidsDose: 30 – 60 mL q 1 – 2 Hrs with pH monitoring

� Rarely used today

�Disadvantages� Labor intensive – frequent dosing and frequent monitoring

� Dosed to pH of 3.5 to 4

� Required frequent monitoring

� High volume may pre-dispose patients to aspiration pneumonia

� GI disturbances

� Electrolyte imbalances (magnesium and aluminum)

� Metabolic acidosis

� Numerous drug interactions (digoxin, quinolones, iron)

� Not cost effective

Blogs.cbn.comCohen H. Stop Stressing Out: The new stress ulcer prophylaxis guidelines are finally

here. 2013 ASHP Clinical Midyear Meeting. Orlando, FL


SucralfateDose: 1 to 2 grams Q 4 – 8 Hours

� Doesn’t change the pH of the stomach� Thought to have less risk of pneumonia� No pH monitoring required

� MOA:� In acidic environment forms a polymer that eventually binds with the protein cations in the exposed ulcer

� Disadvantages� Not available intravenously� Requires timing spaced from enteralfeeds

� Feeding tube occlusion� Aluminum toxicity� Hypophosphatemia� Constipation� Drug Interactions via chelation

� Quinolones, digoxin, warfarin, quinidine, levothyroxine, azoles

Drsfosterandsmith.comCohen H. Stop Stressing Out: The new stress ulcer prophylaxis guidelines are finally



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Histamine-2 Receptor Antagonists (H2RA’s)Cimetidine, Ranitidine, Famotidine, Nizatidine

Started in the mid 90’s with cimetidine infusion = well studied

� IV and PO formulation

� Cimetidine IV = only H2RA FDA approved for SUP

� Intermittent vs Continuous infusions

� No advantage to pH monitoring vs no pH monitoring

� Tachyphylaxis with CI

� Renal dosing required

� Cost effective – generics available

www.medicineworld.orgCohen H. Stop Stressing Out: The new stress ulcer prophylaxis guidelines are finally



IV PPI For Management of UGI Bleed: ToleranceOmeprazole 80 mg + 8 mg/hr vs Ranitidine 50 mg + 0.25 mg/hr x 72 hrs

DB crossover with gastric pH

Results (n=34 healthy

volunteers)Day One Day Three

Median pH Omeprazole*

6.1 6.3

Median pH Ranitidine 5.1 2.7

% pH > 4 Omeprazole* 95% >99%

% pH > 4 Ranitidine 70% 26%

% ph > 6 Omeprazole 59% 71%

% pH > 6 Ranitidine 30%# 7%*

* p ranitidine > nizatidine > famotidine

� Pneumonia – CAP

� Rapid IVP: hypotension and arrhythmias

� Pseudo-renal failure with cimetidine

� CYP-450 drug interactions: 3A4, 2D6, 2C19, 1A2

� Phenytoin, warfarin, amiodarone, colchicine, BZDs, CCBs

� Cimetidine >> ranitidine (low) > nizatidine: famotidine (none)



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H2RA-Induced Thrombocytopenia

� Structure Related

�Onset is 4 – 7 days

�Can occur earlier with prior exposure

�Cross reactivity is 100%

http://oregonstate.edu/instruct/bb350/textmaterials/ch03.html


Sucralfate vs. Ranitidine for Prevention of Upper GI Bleeding in Mechanically Ventilated Patients

0

20

40

60

80

100

120

GI Bleeding Ventilator Associated

Pneumonia

Occurrence Rate (%)

Events

Sucralfate (n=596)

Ranitidine (n=604)

N=1200

P=0.19

Cook D et al. N Engl J Med 1998;338:791-797.

Ranitidine 50 mg IV Q8H vs. Sucralfate 1 gm Q6H

RR = 0.44

P=0.02



Question 4

�Which of the following is an adverse effect of PPIs?

A. Interstitial nephritis

B. Hypomagnesemia

C. C. difficile diarrhea

D. All of the Above



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Proton Pump Inhibitors (PPIs)Pantoprazole, Omeprazole, Lansoprazole, etc.� Activated by protination in parietal cells and then binds to H/K counter exchange ATPase to block acid production

� Most potent of gastric acid secretion agents

� Superior to H2RA’s in other settings

� Consistent pH control

� IV and PO forms

� Most trials studied enteral PPIs for SUP

� Lack of data for IV PPIs

� Becoming less expensive

� ADR’s

� Pneumonia

� C.diff

� Possible drug interactions

� P450’s and Clopidogrel

� Latest Sepsis Guidelines seem to favor PPIs

Cloudfront.net Cohen H. Stop Stressing Out: The new stress ulcer prophylaxis guidelines are finally here. 2013 ASHP Clinical Midyear Meeting. Orlando, FL


Medication Route DoseMetabolism by Hepatic CYP450enzymes

Excretion

EsomeprazolePONG & IV

40 mg daily 2C19 > 3A480% renal inactivemetabolites, < 1% parent drug in urine

LansoprazolePONG & IV

15 or 30 mg daily

15 mg = 81%30 mg = 91%

14 – 25% renalInactive metabolites, < 1%Parent drug in urine 67% bile

OmeprazolePONG

20 to 40 mg daily

2C19 > 3A477% renal inactive metabolites, “minimal” parent drug in urine 19% bile

PantoprazolePONG & IV

40 mg daily 2C19 > 3A4

71 – 82% renal inactive metabolites, no active drug in urine 18 – 20% fecal

RabeprazolePONG

20 mg daily 2C19 = 3A490% renal inactivemetabolites, no active drug in urine10% fecal

PPI Dosing

ASHP Therapeutic Guidelines on SUP. AJHP.1999;56(4):347-379.Lexi-comp Online. Accessed 8-2012Sesler JM. ACCN. 2007;18(2):119-128.



PPI Adverse Effects� Gastrointestinal

� Diarrhea, nausea, vomiting, abdominal pain

� Headaches (3 to 5%)� Acute Interstitial Nephritis

� Rash, fever, arthralgias� Oliguric ARF, eosinophillia, eosinophilluria, pyuria, hematuria

� Pneumonia – CAP, HAP, VAP� C. difficileDiarrhea� Hip Fractures

� PPIs >> HrRAs

� Hypomagnesemia with chronic use (3 months)� Seizures reported� PPIs may change interstitial absorption of Mg� Pantoprazole plus Magnesium supplements have been used



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Clostridium difficile

� FDA Warning links PPIs to C. difficile-Associated Diarrhea

� Feb 8th, 2012� FDA Safety Alert warned that PPI’s may be associated with an increased risk for Clostridium difficile associated diarrhea

Pharmacy Practice News – March 2012


PPIs and Risk of Community-Acquired CDAD- 317 cases of community-acquired C. difficile-associated disease treated with oral vancomycin and 3167 controls

Exposure within 90 days Odds ratio for C. difficile-

associated disease

95% CI

Antibiotic 8.2 6.1 – 11.0

PPI 3.5 2.3 – 5.2

Questions• Epidemiologic studies have limitations• C. difficile-associated disease involves a complex interaction between host, pathogen, and environment

Cunningham R. CMAJ. 2006;175:757-758.Cohen H. Stop Stressing Out: The new stress ulcer prophylaxis guidelines are finally here. 2013 ASHP Clinical Midyear Meeting. Orlando, FL


Copyright © 2012 American Medical

Association. All rights reserved.

Use of Gastric Acid–Suppressive Agents and the Risk of Community-Acquired Clostridium difficile–Associated

Disease

JAMA. 2005;294(23):2989-2995. doi:10.1001/jama.294.23.2989


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Howell et al. Arch Intern Med. 2010;170(9):784-790.


Howell et al. Arch Intern Med. 2010;170(9):784-790.


Odds Ratios for Health Care–Associated Clostridium difficile Infection and Colonization According to Various Patient and Pathogen Characteristics.

Loo VG et al. N Engl J Med 2011;365:1693-1703


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Times to Health Care–Associated Clostridium difficile Infection and Colonization during Hospitalization.

Loo VG et al. N Engl J Med 2011;365:1693-1703


Risk of Recurrent C. difficile

� 1166 patients� Metronidazole or Vancomycin treated CDI

� 527 (45.2%) received PPI’s

� Similar antibiotic exposure in both groups

� Results� 42% increased risk of recurrence

Linsky et al. Arch Intern Med. 2010;170(9):772-778.


Proton Pump Inhibitors and Risk for Recurrent Clostridium difficile Infection

Arch Intern Med. 2010;170(9):772-778. doi:10.1001/archinternmed.2010.73

Recurrence-free survival in those exposed vs unexposed to proton pump inhibitors (PPIs) during treatment for incident Clostridium difficile infection. Time to recurrence started from the incident toxin finding or the start of antibiotic treatment (≤3 days after thediagnosis).

Figure Legend:


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Use of Proton Pump Inhibitors and the Risk of Community-Acquired Pneumonia: A Population-

Based Case-Control Study

Arch Intern Med. 2007;167(9):950-955. doi:10.1001/archinte.167.9.950

Association between current use of proton pump inhibitors (PPIs) and community-acquired pneumonia, according to the timing of first PPI prescription. ORs indicates odds ratios.

Figure Legend:


Community-Acquired PneumoniaComparing the Literature

Current PPI Use

OR (CI)

Current H2RA Use

OR (CI)

Arch Intern Med 2007

1.5 (1.3 – 1.7) 1.10 (0.8 – 1.3)

Ann Intern Med 2008 1.02 (0.97 – 1.08) 0.99 (0.95 – 1.04)

JAMA 2004 1.89 (1.36 – 2.62) 1.63 (1.07 – 2.48)

JAMA. 2004;292(16):1955-1960. doi:10.1001/jama.292.16.1955


Ann Intern Med. 2008;149(6):391-398.

Naylor DF. Clinical Applications of Stress Ulcer Prophylaxis. Soc of Crit Care Med. 2012 conference.


Community-Acquired PneumoniaRecent PPI Initiation & Increased Risk

PPI Initiation & CAP Risk

OR (95% CI)

Ann Intern Med 2008 2.45 (2.04 – 2.95)

Arch Intern Med 2007 2.30 (1.22 – 4.35)

JAMA 2004 2.24 (1.42 – 3.54)

Epidemiol 2009 1.21 (0.9 – 1.63)

Am J Med 2010 1.83 (1.24 – 2.70)

Overall CAP Risk*: 1.92 (1.40 – 2.63)

JAMA. 2004;292(16):1955-1960. doi:10.1001/jama.292.16.1955

Eurich D, et al. Am J Med 2010:123


Ann Intern Med. 2008;149(6):391-398.

Naylor DF. Clinical Applications of Stress Ulcer Prophylaxis. Soc of Crit Care Med. 2012 conference.

* Dose response relationship also noted with high dose PPI use


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Long-Term PI Use and Hip Fractures- Nested case-control study of patients aged > 50 years- 13,556 patients with hip fracture and 135,386 controls

� Association stronger in men than women� Possible mechanisms

� Calcium malabsorption secondary to acid suppression� Reduction in bone resorption through inhibition of osteoclasticvacuolar proton pumps

� Did not include information on OTC calcium and vitamin D use

Yang y-X, et al. JAMA. 2006;296:2947-53Cohen H. Stop Stressing Out: The new stress ulcer prophylaxis guidelines are finally here. 2013 ASHP Clinical Midyear Meeting. Orlando, FL

Exposure Group Adjusted Odds Ratio

for Hip Fracture

95% CI

> 1 year of PPI therapy

1.44 1.30 – 1.59

Long-term high-dose PPI therapy

2.65 1.80 – 3.90


Stress

Impaired Proton Removal

Reperfusion Injury

Free Radical Formation &

Inflammation

Acid Injury

Impaired Proton Buffering

Pepsinogen Activation

Mucosal Ischemia

Impaired Blood Flow

Impaired Defense Mechanism

Acute Stress Ulcer


GI BleedMacLaren R. A Review of StressUlcer Prophylaxis. J Pharm Prac. 2002;15:147 -157


Stress


Reperfusion Injury


Inflammation

Acid Injury



Mucosal Ischemia

Impaired Blood Flow


Acute Stress Ulcer



PPI’s& H2RA’s


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Stress


Reperfusion Injury


Inflammation

Acid Injury



Mucosal Ischemia

Impaired Blood Flow


Acute Stress Ulcer



PPI’s

H2RA’s H2RA’s


Does Enteral Nutrition Help?� Benefits in critically ill

� Improves splanchnic blood flow

� Reduces macroscopic ulceration

�Does it reduce the risk of developing SRMD?

� Lack of significant evidence

� Bottom line

� Don’t use Enteral nutrition as sole SRMD prophylaxis measure


H2RA vs PPI - Clinically Important GI Bleeding- Meta-Analysis

AlhazzaniW. et al. Proton Pump Inhibitors Versus Histamine 2 Receptor Antagonists for Stress Ulcer Prophylaxis in Critically Ill Patients: A Systematic review and Meta-Analysis. Crit Care Med.2013;41(3):693-705.



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H2RA vs PPI - Clinically Important GI Bleeding- Bias Risk




H2RA vs PPI - Comparison of H2RA’s: Up-close



Trial N PPI H2RAUpper GI Bleeding

Cases

PPI H2RA

Conrad (2005) 350Omeprazole/Bicarb

NGTCimetidine IV 7 10

Kantorova (2004) 143 Omeprazole IV Famotidine IV 1 2

Solouki (2009) 129 Omeprazole NGTRanitidine IV 50

mg BID3 14

Levy (1997) 32OmeprazolePO/NGT

Ranitidine IV 2 11

Somberg (2008) 200 Pantoprazole IV Cimetidine IV 0 0


Is Stress Ulcer Prophylaxis Needed?(Prophylaxis is recommended for ICU patients with one or more risk factors)

No Risk Factors Present

Continue daily assessment for stress ulcer risk factors

Discontinue when risk factors are no longer present. If patient was on pre-existing H2RA or PPI, evaluate indications for continued treatement.

AntisecretoryIV H2RA (first line)

PPI (if H2RA not tolerated)

GastroprotectiveSucralfate

(only via gastric access)Can be used when H2RAs

or PPIs are contraindicated or not

tolerated

Functional GI tract?

Consider oral therapy

IV therapy

YES NO

NO

NO

YES



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When Do We Stop?

� Patients should be reassessed daily

�Once the indication is removed the med should be discontinued


652 ICU Admissions

248 patients initiated on Stress Ulcer Prophylaxis in

ICU

215/248 (84%) transferred from ICU on SUP

24% Discharged from hospital on SUP without appropriate indication

523 ICU Admissions

357 patients received SUP in

ICU

316/357 (89%) were transferred out of ICU on SUP

24% Discharged from hospital on SUP with no indication

Transitions of Care

Wohlt et al. Ann of Pharmacotherapy. 2007;41:1611-1616.

Murphy et al. Pharmacotherapy. 2008;28:968-766.


What can we do?

� Start with education

� Hatch et al. 2010

� Looked at educational intervention to reduce non-indicated prescribing of gastric acid suppressants for SUP

Hatch JB, et al. Ann of Pharmacotherapy. 2010;44:1565-71.


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Pharmacist Intervention

1. Dosing card with indications

2. Pharmacist interaction during multidisciplinary rounds

3. Medication reconciliation by RPh at discharge



Results356 patients included in study

158 (44%) were using acid-

suppressing meds prior to admission

Compared to 25.6% in Wohlt’s

study

308 received SUP while in

ICU

11% had no identifiable indication

259 continued upon transfer out of the ICU

84 (24%) had no clear indication

Improvement of 50.7% from previous study

After discharge

197 continued acid-suppression

therapy

31 (8.7%) not having a clear indication

64.3% reduction


Wohlt et al. Ann of Pharmacotherapy. 2007;41:1611-1616.


Pharmacy Protocol

� Worked with the intensivists to create a Stress Ulcer Prophylaxis per Pharmacy Protocol

� When ‘SUP Per Pharmacy’ ordered the pharmacist would

� Identify risk factors


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Applying this to your practiceH2RA’s are the preferred agent for initial prevention of GI hemorrhage resulting from Stress Related Mucosal Disease in patients that are at risk

PPI’s should be reserved for patients unable to tolerate H2RA’s

Antacids are not recommended for prevention of SRMD

Sucralfatemay be used for SUP when H2RA’s and PPI’s cannot be used

The need for SUP should be evaluated daily, and pharmacotherapy should be discontinued when the patient no longer has risk factors for SRMD

Naylor DF, Rebuck JA, Maclaren R, et al. Clinical Applications of Stress Ulcer Prophylaxis. 2012. SCCM Annual Conference.



Documents

Stress Ulcer Prophylaxis - Wild Apricot wills.pdf · Stress Ulcer Prophylaxis: Guideline Update April 2014 Rob Wills, Pharm.D., BCPS ... PPI’s vs. H2RA’s vs. sucralfate What are