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Small Bowel Obstruction, Acute Pancreatitis,Upper GI Bleeding:
An Update
Jonathan Terdiman, MDProfessor of Clinical Medicine and Surgery
University of California, San Francisco
Disclosures: Nothing to disclose
Acknowledgements: Jon Carter, MD and John Cello, MD
Abdominal plain films
CT abdomen and pelvis
bowel wall edema, collapsed colonsmall bowel feces sign present
• What is the cause of the patient’s intestinal obstruction?
• Is the obstruction strangulating or non-strangulating?
• Can any tests differentiate patients whose non-strangulating obstructionwill resolve with time?
• How long should non-operative management be tried?
• Can adhesiolysis reduce the risk of recurrent SBO?
What is the cause of the patient’s intestinal obstruction?
Etiology Incidence, %
Adhesions20% within 1 month of surgery30% within 1 year of surgery25% years 1-525% after 5 years
60
Cancer 20
Hernia 10Inflammatory Bowel Disease 5
Volvulus 3
Miscellaneous 2
Pathogenesis: adhesive disease
Procedure Incidence, %
Appendectomy 23
Colorectal surgery 21Gynecologic surgery 12Foregut surgery 9
Small bowel surgery 8
Multiple laparotomies 24
Is the obstruction strangulating or non-strangulating?
Is the obstruction strangulating or non-strangulating?
Silen et al., Strangulation obstruction of the small intestine. Arch Surg 1962;85:121-129. “The results of this study indicate that the clinical differentiation between simple and strangulating obstruction is often impossible.”
The “classic signs” of strangulating obstruction are:* continuous (rather than colicky) pain* fever* tachycardia* peritoneal signs* leukocytosis
….but alone, or in combination, sensitivity / specificity low
Clinical Study
• Retrospectively reviewed 192 cases operated on for a small bowel obstruction (1996-2006) at UCSF Medical Center.
• A predictor model was created based upon operative findings: strangulated (n=44) or non-strangulated (n=148).
• Independent Predictors of strangulation: WBC > 12K, Rebound/Guarding at PE, Reduced Enhancement of SB at CT.
Is the obstruction strangulating or non-strangulating?
The best initial study is a CT abdomen/pelviswith IV contrast and without (positive) oral contrast
“I don’t buy it. You just have to use your judgment.”
Madhulika G. Varma, MD, Chief Section of Colon and Rectal Surgery, UCSF
Can any tests differentiate patients whose non-strangulating obstruction will resolve non-operatively?
Complete obstruction = absence of significant flatus or stool for 12 hours and no colonic gas seen on KUB.
Complete obstruction = 20% success rate with non-operative treatment, 20-40% risk of strangulation
Partial obstruction = 80% success rate with non-operative treatment, low risk of strangulation (3-6%)
OLD: CLINICAL PRESENTATION
Can any tests differentiate patients whose non-strangulating obstruction will resolve non-operatively?
NEW: ORAL WATER SOLUBLE CONTRAST ADMINISTRATION
Instill 50-150cc of gastrograffin (water-soluble contrast) orally or via NGT. Obtain abdominal plain films at 4, 8, and/or 24 hours
Presence of gastrograffin in the colon at 8 hours predicts non-operative resolution with 95% sensitivity and 99% specificity. PPV = 99%, NPV =85%.
At 24 hours, 99% sensitivity, 97% specificity, 99% PPV, 97% NPV
Can any tests differentiate patients whose non-strangulating obstruction will resolve non-operatively?
Possible therapeutic role for gastrograffin:
PROPORTION NEEDING SURGERY
“I don’t buy it. You just have to use your judgment.”
Madhulika G. Varma, MD, Chief Section of Colon and Rectal Surgery, UCSF
How long should non-operative management be tried?
85-95% of patients with adhesive SBO who are destined to recover without surgery will show marked improvement within 72 hours
EAST guidelines 2009:3-5 days
Bologna guidelines 2010: 3 days
Can adhesiolysis reduce the risk of recurrent SBO, readmission, or reoperation?
Review of 500 patients Norway operated upon for adhesive SBO from 1961-1995.All patients interviewed at median follow-up of 11 years, 85% follow-up rate
For patients with > 2 prior bouts of adhesive SBO,
Surgery:
reduced risk of readmission (RR 0.55)
…but did not change risk of future operations (RR 0.79)
Can adhesiolysis reduce the risk of recurrent SBO, readmission, or reoperation?
Surgery…had no effect on total readmissions (32% vs 34%)but spaced out readmissions over time (median 0.7 vs 2 years)and had no difference in reoperation rate (14% vs 11%)
Special cases
virgin abdomen • confirm diagnosis (no ileus)• exam to rule out hernia• CT abdomen/pelvis to look for intussusception, tumor, Crohn’s, malrotation, etc.
• diagnostic laparoscopy and LOA
intra-abdominal malignancy •1/3 caused from adhesions that can be lysed.•1/3 caused from tumor than can be resected or bypassed.
•1/3 nothing can be done surgically• high failure rate / mortality with nonoperative management.
intussussception • if <3cm in length, spontaneous resolution expected.
• operate for obstruction, pain, intransigence.
hernia • operate on all hernias causing SBO.• relative contraindication for laparoscopy• zebras are: obturator, paraduodenal, transmesenteric, transomental, congenital hernias
Crohn’s • treat medically initially. Surgery for intransigence.
tumors • GIST, adenoma, lipoma, hamartoma, hemangioma, adenocarcinoma, lymphoma, carcinoid, metastasis• Rx is resection
early postoperative(within 30 days of surgery)
• risk of strangulation low• success rate of nonoperative management is 85% at 7 days, 90% at 14 days
Acute Pancreatitis
DefinitionsMorphological Definition: Tissue is rarely available.
Mild: Interstitial edema andlimited fat necrosis
Severe: Hemorrhage, extensive necrosis ofpancreas & peripancreatic tissue
Severe systemic disease - oftenmulti-organ failure
Importance: Nearly 2-3% of all patients admitted to acute care hospitals
Incidence– Acute pancreatitis 5 to 75 cases per 100,000/year
Scotland: 24 cases per 100,000Finland: 73 cases per 100,000
– Gallstone pancreatitis: 35-75% of all casesMortality– Overall for acute pancreatitis: 10%
Etiology - Acute Pancreatitis
1. Mechanical Factors – most common
Gall stones – about 75% of cases worldwideTrauma/post-operativeERCP - about 1- 4 % of proceduresParasites - Ascaris, Clonorchis, Opisthorchis,
Fasciola hepaticaDuct obstruction – tumorPancreas divisum
Etiology - Acute Pancreatitis
2. Metabolic
AlcoholHypertriglyceridemia ( usually TG > 2500 )Drugs ( thiazides, 6-MP, MTX, DDI, DDC, sulfa )Scorpion stingOrganophosphate insecticidesHeredofamilial disease – familial pancreatitis
cystic fibrosis“Tropical" pancreatitis
Etiology - acute Pancreatitis
3. Other Factors
Infections - mumpshepatitis A/B/CCMV, cryptosporidiosis, microsporidiosisHIV (AIDS papillary stenosis)
Vasculitis - lupus
Idiopathic - much may be microcalculi
Sphincter of Oddi disfunction
Gallstone Pancreatitis
Most common etiology world-wideCholelithiasis – pancreatitis risk about 2% over 30 yrs.Structural risk factors: small stones, large cystic duct diameter, common distal channel.
Acute Alcoholic Pancreatitis –Epidemiologic and Experimental DataUsually demographics – steady state alcohol usage with normal, nutritious diet Mean age of onset of “acute” pancreatitis is 10 years later than “chronic” pancreatitis.Most patients with acute pancreatitis already have “chronic pancreatitis” histologically – on autopsy.Effect of alcohol/ nutritious diet in primates and canines – increased pancreatic juice viscosity, increased protein concentration and decreased pancreatic “stone protein” and trypsin inhibitory protein.
Diagnosis of Acute Pancreatitis – use of serum enzymes
(Steinberg et al. Ann Int Med 1985; 102:576)
Sensitivity % Specificity %
Amylase 95 86
P-amylase 92 83
Trypsinogen 97 83
Lipase 87 95
Severity Assessment• Ranson criteria of historical interest• Multiple other scoring systems• BISAP (Bedside Index for Severity of Acute Pancreatitis)
is likely best• BISAP assessed in first 24 hours
– BUN > 25 mg/dl– Glasgow coma score < 15– Age > 60– Pleural effusion– SIRS present*
*2 of the following 5 present•T < 36, > 38•RR > 20 or PaCO2 < 32•HR > 90•WBC < 4 or > 12 or >10% bands
BISAPWu BU, Gut 2008;57:1698-703
CT can see fluid collections around pancreas, but also presence &
amount of
pancreatic necrosis
<30%
30-50%
> 50%More necrosis = worse prognosis
Degree of necrosis
Management: “Golden Hours”• Management in the first 24 hours:• Aggressive fluid resuscitation is the key
– 2000 ml bolus in ED– 250-300 ml/hr– Use lactated Ringer’s– UO of at least 0.5 ml/kg/hr
• Under resuscitation– Pancreatic hypoperfusion occurs– SIRS, Pancreatic Necrosis, Mortality all
increase
Early Fluid ResuscitationWarndorf MG, Clin Gastroenterol Hepatol 2011;9:705-9
• Early resuscitation– SIRS at 72 hours 10% vs 23%– Organ Failure 5% vs 10%– ICU care 6% vs 17%– Hospital Stay 8 d vs 11 d
Mortality Benefit in other studies as much as 0 versus 20%Banks PA, Am J Gastroenterol 2006;101:2379-400Gardner TB, Pancreatology 2009;9:770-6
What Doesn’t Help• NG Suction• H2 blockers or PPIs• Atropine or Glucagon• Somatostatin or Octreotide• Protease Inhibitors• TPN• Peritoneal lavage• Antibiotics and ERCP?
Nutritional SupportTotal Enteral Nutrition (TEN)Enteral feeds should be post ligament of
Treitz (not gastric or duodenal feeds!!)– Advantages:
reduced cost compared to TPN or PPNno associated risk of catheter line sepsisprevents gut atrophy and bacterial translocation and infection
– Disadvantages:risk of proximal migration of the tube tip into the duodenum or stomachpatient refusal due to discomfort
Prophylactic Antibiotics• Wittau M, Scand J
Gastroenterol 2011;46:261-70• 14 trials with 841 patients• Infected pancreatic necrosis:
– RR 0.78 (95% CI, 0.6-1.1)
• Non pancreatic infections:– RR 0-.70 (95% CI, 0.46-1.1)
• Mortality: – RR 0.74 (95% CI, 0.5-1.1)
Bai Y, Am J Gastroenterol 2008;103:104-10
Early Treatment of Acute Biliary Pancreatitis
Acute ERCP (97 pts.) vs. Conservative (98 pts) Acute ERCP Converv. P value
mortality (overall) 5% 9% NS
overall morbitity 18% 29% NS
morbidity (patients 16% 33% 0.03 with stones)
systemic complications 10% 14% NS
local complications 10% 12% NS
biliary sepsis 0 12% 0.003
Fan ST et al. NEJM 1993;328:228-32.
20-50% biliary pancreatitis recurrence within 8 weeks, so prior to discharge or soon after ERCP with sphincterotomy or cholecystectomy is needed
Early ERCP/Papillotomy compared with Conservative Treatment for Acute Biliary
Pancreatitis
Parameter ERCP Conservative Treatment P Value
Patients randomized 126 112
ERCP performed 121 22
ES/ Stone removal 58 13
Overall deaths 14 7 NS
Pancreatitis deaths 10 4 NS
Respiratory failure 15 5 0.03
Renal failure 9 4 NS
Cholecystitis 13 20 NSJaundice 1 12 0.02Cholangitits 17 13 NS
Folsch, Nitsche, Ludtke et al NEJM 1997;336:237-42.
ERCP for all versus only for ongoing obstruction and sepsis
UK 1995(N=4137)
US-CORI 2004
(N=7822)
Canada2002
(N=1869
Hong Kong2007
PUD 35% 21% 50% 60%Erosive disease 21% 43% 10% 13%
MW Tear 5% 4% 3%Varices 4% 11% 4%Malignancy 4% 1% 4%AVM 5% 0.3%Esophagitis 15% 17% (w/erosive)Other 6% 4%No Dx Made 25% 4% 11%
Upper GI Bleeding
Definition of Low Risk: < 5 % Rebleeding, < 1 % Mortality
BlatchfordSystolic BP > 110 Pulse < 100 Hgb > 12 (women), 13 (men)BUN < 6.5 mmol/LComorbities: none
Clinical RockallSystolic BP > 100Pulse < 100Age < 60 yearsComorbidities: none
Early Endoscopy: Risk Assessment and Therapy
Stigmata Prevalence (%) Rebleed (%)
Arterial bleed 10 90
Visible vessel 25 50
Adherent clot 10 25Clean ulcer base 35 < 5
Endoscopic Treatments for PUD with High-risk Stigmata (active bleeding / visible
vessels)Injection:• Epinephrine (1:10000)Thermal:• Contact
thermocoagulation: MPEC, heater probes
Mechanical:• Endoclips: loops, bandsCombination: • Epi injection + thermal
or mechanicalOutomes: Reduction in rebleed, LOS, Tx, Surgery, Mortality by >/= 50%
Combination Monotherapy # Trials / N OR Rebleeding (95 % CI)
Epi + Thermal Epi alone 3 / 376 0.363 (0.177-0/727)
Epi + Clips Epi alone 4 / 362 0.334 (0.177-0.629)
Epi + Thermal Thermal alone 3 / 425 0.699 (0.405-1.206)
Epi + Clips Clips alone 3/ 234 1.045 (0.447-2.449)
Pooled Rebleeding
0.597 (0.444-0.802)
Marmo R, Am J Gastro 2007;102:279
Combination Therapy vs Monotherapy: Is It Better?
This image cannot currently be displayed.
Early EGD Reduces LOSCooper GS et al. Medical Care 1998;4:462
Cooper GS et al. Gastroinest Endos 1999;49:145
PPIs• > 25 randomized controlled trials• Considerable heterogeneity with respect
to intervention and outcomes measured• Study outcomes: PPI > placebo, EGD >
PPI, PPI + EGD > PPI, EGD + PPI > EGD + placebo– rebleeding, transfusion need– surgery
Sung, J. J.Y. et. al. Ann Intern Med 2009;150:455-464
Kaplan-Meier estimate of the cumulative percentage of patients with recurrent bleeding within 30 days
Meta-Analysis: RCTs of PPI vs Placebo After Endoscopic Therapy of Ulcers with
High-risk StigmataEndoscopic Therapy Followed by High-dose IV PPI
PPI Placebo OR (95% CI)
Rebleeding 5.2%* 12.8% 0.39 (0.18-0.87)
Surgery 5.2%* 9.4% 0.53 (0.31-0.89)
Mortality 5.7% 5.6% 0.98 (0.25-3.77)
Endoscopic Therapy Followed By Oral or Low-dose IV PPI vs Placebo
Rebleeding 10.2%* 17.2% 0.52 (0.35-0.78)
Surgery 6.6% 9.9% 0.59 (0.33-1.05)
Mortality 2.4% 2.4% 1.00 (0.42-2.35)
Leontiadis G, BMJ 2005• 21 RCTs: 2915 pts
IV PPI Infusion vs Placebo Before EGD
• Endoscopic Tx:– Peptic Ulcers: 22.5%
(PPI) vs 36.8% (placebo) (p< 0.05)
– Other bleeding sources: no difference
• Hospitalized < 3 d– 61 % PPI vs 49%
placebo (P< 0.05)• No effect of PPI on:
– Urgent endoscopy– Transfusions– Rebleeding– DeathLau J, 2007;356:1631.
• N = 638 UGIB: 377 PUD (60%)• Omeprazole 80 mg bolus, 8 mg/hr X 72 hr
Date of download: 9/3/2012
Copyright © The American College of Physicians. All rights reserved.
From: International Consensus Recommendations on the Management of Patients With Nonvariceal Upper Gastrointestinal Bleeding
Ann Intern Med. 2010;152(2):101-113. doi:10.7326/0003-4819-152-2-201001190-00009
Summary of Consensus Recommendations for the Management of Patients With Nonvariceal Upper Gastrointestinal Bleeding
Figure Legend:
Endoscopic Therapy Initial Control
Permanent Control
80-90%
Rebleeding
Endoscopic TherapyPermanent
Control75%
Rebleeding
Angiography
25%
ER Endoscopy
IV PPIOctreotide
Erythromycin
Treatment Algorithm
At discharge: 1) test and treat and test again for HP, 2) if ASA or plavix needed, resume with PPI, 3) if NSAID needed, change to cox-2 inhibitor with PPI
Recommended