1. GI Problem in Critical
Patients
Naichaya Chamroonkul MD.
Division of Gastroenterology and Hepatology
Department of Internal Medicine
Prince of Sonkla University

2. Agenda
• GI problem that common in critical care
patients.
– Stress related mucosal disease
– Motility disorder in ICU patients
• GI disease that need intensive care team
– Severe acute pancreatitis
– Acute liver failure
– Massive GI bleeding

3. Stress-related mucosal disease (SRMD)
Synonym
• Stress ulcer
• Stress erosion
• Diffuse mucosal injury
• Acute erosive gastritis
Lucus CE, et al.Arch Surg. 1971;102:266-273.

4. Stress : ulcers or erosions occur in
stomach and duodenum during
stressful conditions

5. Diagnostic criteria Prevalence (%)
1. ICU patient with decreasing
hematocrit and positive
stool occult blood
100
2. Positive endoscopes
finding in ICU patients
75-100
3. Clinically significant UGI
bleeding
30

6. Clinical important of SRMD
• 70-90% of ICU pts got SRMD
• Important bleeding contribute to death in
30-80% (more than bleeding in other
condition)
• Prolong length of hospitalization , the
excess length of ICU stay attributed to stress
ulcer bleeding is estimated at 4 days-8 days
• Cost-effectiveness in prophylaxis strategy.
Ben-Menacham, et al. Crit Care Med. 1996;24:338-45.

8. Risk factors of UGI bleeding in SRMD
Retrospective studies
• Respiratory failure required ventilator
• Hypotension or shock
• Sepsis
• Multiple or severe trauma
• Extensive burn
• Severe CNS injury
• Hepatic failure
• Renal failure
• Post major surgery

9. Risk factors for clinically important bleeding among
2252 patients admitted to an intensive care unit
Cook DJ, et al. N Eng J Med. 1194;330(6):377-81.

10. Prophylaxis of bleeding in SRMD
1. Increase gastric pH > 4
2. Improved homodynamic state
3. Increase mucosal defense

11. Regimens in SRES prophylaxis
1. Antacid 30-60 ml
2. Cimetidine 37.5-100 mg
3. Ranitidine 0.25-12.5 mg
4. Proton pump inhibitor
McAlhary JC, et al. J Trauma. 1976;16:645-8.
Lichtenstein DR, et al. Gastrointestinal pharmacotherapy, Philadephia WB Sounders, 1993;47-84.
Cantu TG, et al. Ann Intern Med. 1991;114:1027-34.

12. Stress induced gastritis and ulcer
0
5
10
15
20
25
30
All studies Occult
bleeding
Overt
bleeding
Placebo
Cimetidine
Antacids
Efficacy of stress prophylaxis Shuman et al, Ann Intern Med 1987
%
907 580 646 187 178 188720 402 458

14. PPI/H2RA

18. Motility disorders in critically ills.
• Delay Gastric Emptying time
• Ileus (small bowel and or large bowel
disorder)
• Acute intestinal Pseudo-obstruction

19. Delay of Gastric Emptying Time
• Prevalence
– 50 % of patients on mechanical ventilator.
– 80% in pts with increase ICP from head injury
• Clinical
– feeding intolerance  residual of gastric content
– vomitting
Tarling MM et al. A model of gastric emptying using paracetamol absorption in
intensive care patients. Intensive Care Med 1997
Kao CH et al. Gastric emptying in head-injured patients. Am J Gastroenterol 1998

20. Clinical Impact of Delay Gastric
Emptying Time
• Impaired enteral nutrition
– nutritional outcome  can reduced mortality and
increase ventilator free days.
– risk of infection (maintenance gastric immunology
and barrier)
• Risk of pulmonary aspiration of pooled
gastric content

21. Factors May Alter Gastric Emptying in
Critically Patients
• Premorbid diagnoses
– Diabetes mellitus
– Previous vagotomy
– Systemic sclerosis
– Chronic intestinal pseudo-
obstruction
– Myopathies/dermatomyositis
• Admission diagnoses
– Head injury
– Burns
– Extensive abdominal surgery or
trauma
– Spinal cord injury
– Pancreatitis
 Biochemical abnormalities
 Hyperglycemia
 hypokalemia
 Drugs
 Opiate
 Anticholinergics
 Erythromycin
 Stress
 Pain
 Sepsis
1.Reduce
vagal efferent
2.inhibit NO
inhibiting
neurotransmitter
relaese, alter
excitibility
Preexisting GI
motility disorder

22. Management of Delayed Gastric
Emptying
• Pharmacologic treatment
• Direct Delivery of Nutrients to the
Upper Small Intestine via feeding tube
–When treatment of gastric stasis fails or is
contraindicated

23. Problems with NJ Feeding
 Placement may need endoscopy or
fluroscopy-guidance
 Frequent tube displacement

24. Prokinetics for ICU patients
• Metoclopramide : 10-20 mg IV q 6-8 hr
• Erythromycin : 250– 500 mg IV/NG q 6
hr
• Combination treatment

25. Erythromycin
• Increase phase III contraction of MMC
• Action on motilin receptor on smooth
muscle
• Induction of anthral contractility by
intrinsic cholinergic pathway

26. Limitation of Erythromycin
• Development of drug resistance bacteria
– May be cross action with other ATB, can be
transfer through Bacterial Spp.
– Recommend not longer than 3-4 days
• Desensitization of therapy
• Long QT syndrome : caution in cardiovacular
risk positive patients and co with class III
antiarrhythmic drugs.

27. Ileus
• Impairment of coordinated propulsive
intestinal motility
• Absence of a mechanical bowel obstruction
Prevalence
• Small bowel motility disorder
– > 20% of pts have feeding intolerance and
diarrhea
– In head injury > 90% of underfeeding related to
ileus

28. Clinical Impacts of ileus
• Gastroduodenal reflux/aspiration
• Fluid sequestration
• Bacterial overgrowth
• Bacterial translocation
• Increase abdominal pressure

30. Cause of Ileus in Critical illness.
• Postoperative Ileus
• Sepsis-induced Ileus
• Drugs.
• Metabolic (hypo K, hypo Mg, hyposmolality )
• Head injury and neurosurgical procedure
• Intra-abdominal inflammation and
peritonitis

31. Drugs with possible adverse side
effects on motility
Opioids
Antiepileptic drug
Benzodiazepine group
Anticholinergic effect drug
(tricyclic antidepressant, antihistamine,
antipsychotic)
Warfarin
Antacid

32. Catecholamines
• Direct dose- dependent inhibitory effect on
small bowel motility
• Fail to convert fasting motility to feeding
motility after enteral feeding
• Decrease response of prokinetics agent such
as Erythomycin or metoclopramide

33. Ileus Pseudo-
obstruction
Mechanical
Obstruction
(Simple)
Symptoms Mild
abdominal
pain,
bloating,
nausea,
vomiting,
obstipation,
constipation,
Crampy
abdominal pain,
constipation,
obstipation,
nausea,
vomiting,
anorexia
Crampy
abdominal pain,
constipation,
obstipation,
nausea,
vomiting,
anorexia

34. Physical
Examinat
ion
Findings
Silent
abdomen,
distension,
tympanic
Borborygmi,
tympanic,
peristaltic waves,
hypoactive or
hyperactive
bowel sounds,
distension,
localized
tenderness
Borborygmi,
peristaltic
waves, high-
pitched bowel
sounds,
rushes,
distension,
localized
tenderness
Ileus Pseudo-
obstruction
Mechanical
Obstruction
(Simple)

35. Plain
Radiogra
phs
Large and
small bowel
dilatation,
diaphragm
elevated
Isolated large
bowel dilatation,
diaphragm
elevated
Bow-shaped
loops in ladder
pattern,
paucity of
colonic gas
distal to
lesion,
diaphragm
mildly
elevated, air-
fluid levels
Ileus Pseudo-
obstruction
Mechanical
Obstruction
(Simple)

36. Evalu
ation
No Obstruction
(n=5)
Partial Obstruction
(n=15)
Complete
Obstruction (n=16)
True
Nega
tive
Fals
e
Posi
tive
Specif
icity
(%)
True
Posit
ive
False
Nega
tive
Sensit
ivity
(%)
Tru
e
Pos
itive
Fals
e
Nega
tive
Sensiti
vity
(%)
Clinic
al/
plain
film
5 0 100 2 13(10
)
13 3 13(1
1)
19
CT 5 0 100 15 0 100 16 0 100
David H. Frager, AJR, 1995

37. Therapeutic Consideration
• Fluid management and circulatory
support
• Stimulation of gastric and intestinal
motility
• Nutritional consideration
• Abdominal decompression

38. Prokinetics Drugs in Critical Care
Setting
Study Population (n) Intervention Outcome P Value
Jooste et al. Mixed ICU (10) MET 20 g IV Placebo
(crossover)
Increase in Cmax; increase in
AUC120
9/10;8/10
1/10;2/10
.04
MacLaren et
al.
Mixed ICU (14) MET 10 mg NG
CIS 10 mg NG
Tmax Cmax,AUC120 ;gastric
residual
< .05 vs
placebo
NS
Calcroft et
al.
Mixed ICU (16) MET 10 mg IV Placebo AUC60 Data not report .04
MacLaren et
al.
Mixed ICU (10) MET 10 mg NG
ERY 200 mg NG
CIS 10 mg NG
Placebo
MRTabs gastric residuals
8.6 min; 125 mL
28.1 min; 69 mL
6.5 min; 142 mL
20.5 min; 127 mL
NS vs
placebo
Yavagal et
al.
Mixed ICU (305) MET 10 mg NG
Placebo
Pneumonia; Mortality
24/174(17%); 56%
22/131(14%); 53%
NS

39. Cisapride
• 5 HT4 receptor
• Enhances esophageal peristalsis
• Increases lower esophageal tone
• Accelerates gastric emptying
• Shortens small bowel and colonic transit time
• Long QT syndrome  withdrawal from may
country FDA.

40. Study Population (n) Intervention Outcome P Value
Williums Mixed ICU (27) CIS 10 mg NG
Placebo
Tolerance to feeds
6/13(46%)
11/14(79%)
NS
Goldhil et
al.
Mixed ICU (27) CIS 60 30 30 mg PR
Placebo
AUC 60
Data no reported
.07
Spapen et
al.
Mixed ICU (21) CIS 10 mg NG
Placebo
Gastric residuals; t1/2 of
Te99
18mL;18min
95mL;78min
<.01;<.01
Heyland et
al.
Mixed ICU (72) CIS 20 mg NG
Placebo
-40 min; +49μmol/L
-4 min; +12μmol/L
.02;<.01
Booth, et al. Crit care med. 2002

41. Neostigmine
• Inhibitor of acetylcholine esterase
• Reduce the time to first passage of gas and
stool
• Narrow concentration window, higher dose
inhibit small bowel motility
• Most study pts  post op ileus

42. Ogilvie syndrome
• Acute colonic pseudo-obstruction
• Definition
–Colonic dilation without mechanical
obstruction
–s/s: abdominal distension without pain
–Plain film: massive colonic dilation, esp.
of the cecum and right colon
• If not decompressed the colon, patient risks
perforation, peritonitis, and death.

44. Pathophysiology
• not clearly understood
• It is thought to result
from an imbalance in the
regulation of colonic
motor activity by the
autonomic nervous
system.
– parasympathetic
nervous dysfunction
• Usually associated with a
recent, significant medical
illness or surgical
procedure.
– Recent surgery
– Severe pulmonary disease
– Severe cardiovascular disease
– Severe electrolyte disturbance
– Severe constipation
– Malignancy
– Systemic infection
– Medications

45. Treatment
• Medical Care
– Supportive care (NPO, NG decompression, fluid
resuscitation, enema)
– neostigmine
– Colonoscopic decompression of the colon
• Surgical Care
– Tube cecostomy
– Subtotal colectomy

46. Neostigmine
• The use of neostigmine should be careful in patient
underlying:
– bradyarrhythmias
– bronchospasm
– renal impairment
• The effect of neostigmine treatment, compare with
– conservative therapy
– Colonoscopy
– Surgery

47. Abdominal Decompression
• In colonic distension : led marked reduction of
intestinal dilatation in more than 80% of case
• Relapse rate up to 44% (1)
• Colonic tube placement for 2-3 days after
decompressive colonoscopy ore effective than
decompressive colonoscopy alone (2)
(1) Vanek VW.Disease of the Colon and Rectum, 1986
(2) Harig JM, et al. Gastrointest Endosc, 1988

48. Abdominal Decompression
• Indicated when supportive measures have
failed
• Colonic diameter progress  11- 13 cm or
there is evidence of clinical deterioration.
• Bowel preparation should not be
administered.
• Water enemas can be administered gently via
a rectal tube.

49. Abdominal Compartment Syndrome
• The IAP is usually 0 mmHg during spontaneous
respiration, and is slightly positive in the patient on
mechanical ventilation
• Direct relation to body mass index
• One report, supine hospitalized patients had a mean
baseline value of 6.5 mmHg
Definition : increase intraabdominal pressure above 20 to
25 mmHg
• Emergency condition

50. ETIOLOGY
• Massive volume resuscitation is the leading
cause of ACS.
• Incidence of ACS in trauma patients is
between 2-9 %
• > 30 % of patients following OLT.
• Mechanical limitations on the abdominal wall,
due to tight surgical closures or burn scars.

51. Systemic effects of abdominal
compartment syndrome
• Central nervous
system
– Intracranial pressure
– Cerebral perfusion pressure
• Cardiac
– Hypovolemia
– ↓ Cardiac output
– ↓ Venous return
– ↑ PCWP and CVP
– ↑ SVR
 Pulmonary
 ↑ Intrathoracic pressure
 ↑ Peak inspiratory pressure
 ↑ Airway pressures
 ↓ Compliance
 ↓ PaO2
 ↑ PaCO2
 ↑ Shunt fraction
 ↑ Vd/Vt

52. Systemic effects of abdominal
compartment syndrome
• Hepatic
– ↓ Portal blood flow
– ↓ Mitochondrial
function
– ↓ Lactate clearance
• Abdominal wall
– ↓ Compliance
– ↓ Rectus sheath
blood flow
 Gastrointestinal
 ↓ Celiac blood flow
 ↓ SMA blood flow
 ↓ Mucosal blood flow
 ↓ pHi
 Renal
 ↓ Urinary output
 ↓ Renal blood flow
 ↓ GFR

53. Bladder pressure transduction system

54. Treatment
Surgical decompression
• Only treatment that reverses all of the
physiologic derangements resulting from ACS,
the timing of this procedure remains
controversial.

55. Burch, et al.. Surg Clin North Am 1996

56. Acute Pancreatitis

57. Gallstone
Idiopathic /
Tropical
HereditaryAlcohol
Obstructive
PC, IPMN, PD, SOD
Hyper TG
Post ERCP
Trauma
Drugs
CP
APAP

58. Pathogenesis of AP
Intracellular enzyme activation
Acinar cell damage
Circulating
Activated enzymes
Inflammatory mediators
Cytokines
SIRS
Trigger factors
Activation of
Coagulation cascade

59. Lungs
Pleural effusion
ARDS
Heart
Pericardial
effusion
Arrhythmia
Circulation
Hypovolemia
Shock
Brain
Purtscher’s
retinopathy
Encephalopathy
Metabolic
Hypocalcemia
Hyperglycemia
Coagulation
DIC
Kidneys
Oliguria
ARF
Rare
Panniculitis

60. Natural Course of AP
Acute Pancreatitis
Sterile
Pancreatic
Necrosis
Infected
Necrosis
Pancreatic
Abscess
3%
Acute Pseudocyst
6%
Phase 1
0-1 week
Phase 2
2-4 weeks
Phase 3
4-6 weeks
?
SIRS
Sepsis
MOF Death
~50%
~30%
~20%
~20%
Initiating Events

61. Natural Course of AP
Acute Pancreatitis
Infected
Necrosis
Pancreatic
Abscess
3%
Acute Pseudocyst
6%
Phase 1
0-1 week
Phase 2
2-4 weeks
Phase 3
4-6 weeks
?
SIRS
Sepsis
MOF Death
~50%
~30%
~20%
~20%
Initiating Events
Sterile
Pancreatic
Necrosis

62. 1. Abdominal pain
• >95% of patients
• Anywhere in the abdomen
• 50% radiate to back
• Painless AP
• ICU / post-operative
• Organophosphate poisoning
• Peritoneal dialysis
• Legionnaire’s disease
1. ICU/ post-op patients with unexplained shock or
deterioration
Presenting Symptoms & Signs
of Acute Pancreatitis

63. Mild AP
• Aggressive fluid and
electrolyte replacement
• Monitoring
 Vital signs
 Urine output
 O2 saturation
 Pain
• Analgesics
• Anti-emetics
• NG tube (if ileus)
Treatment of Acute Pancreatitis
Severe AP
 Admit to ICU
 Urgent ERCP
(in GS pancreatitis)
 CT scan
 Antibiotics
 FNA
 Surgery
 Nutrition support

64. Mild AP
 Aggressive fluid and
electrolyte replacement
 Monitoring
 Vital signs
 Urine output
 O2 saturation
 Pain
 Analgesics
 Anti-emetics
 NG tube
Severe AP
• Admit to ICU
• Urgent ERCP
(in GS pancreatitis)
• CT scan
• Antibiotics
• FNA
• Surgery
• Nutrition support
Treatment of Acute Pancreatitis

65. Severe Acute Pancreatitis
Atlanta Definition 1992
1. Presence of organ failure
• Shock : systolic BP < 90 mm Hg
• PaO2 < 60 mm Hg
• Cr > 2 mg/dl
• GI bleeding > 500 ml/24 hr
• DIC (plt < 100,000/mm3
, fibrinogen <1 g/dl, FDP > 80 µg/ml)
• Calcium ≤ 7.5 mg/dl
2. Pancreatic necrosis, abscess or pseudocyst
3. Unfavorable prognostic signs (‘predicted
severe AP’)
• Ranson score > 3
• Modified Glasgow score > 3
• APACHE II score > 8
• CRP ≥ 150 mg/dl
Bradley EL III. Arch Surg 1993; 128: 586-90
(Persistent)

66. Severity Assessment of AP
 Bedside clinical assessment
 Clinical, OF, SIRS, obesity, CXR, Hct
 Scoring systems
 Ranson, Glasgow, APACHE-II, APACHE-O
 Serum markers
 C-reactive protein
 TAP
 Cytokines
 CT scan
Dervenis C. Int J Pancreatol 1999; 25: 195-210

67. Cutaneous Signs
 Cullen’s sign: periumbilical ecchymosis
 Grey-Turner’s sign: flank ecchymosis
 Fox’s sign: ecchymosis below inguinal
ligament
 Walzel’s sign: livedo reticularis
Grey-Turner’s Sign Cullen’s Sign

68. CXR Hematocrit
 Hct > 44%
 Hct < 44% but fails to decrease in
24 hr
 Infiltrates
 Bilateral effusion
 Left effusion
 Right effusion

69. Ranson Criteria
Alcohol Biliary
On admission
Age > 55 yr > 70 yr
WC > 16,000/mm3
> 18,000 /mm3
Blood glucose > 200 mg/dl > 220 mg/dl
LDH > 350 U/L > 400 U/L
SGOT > 120 U/L > 210 U/L
(>250 S.F.) (>440 S.F.)
During 48 hr
Hct decrease > 10% > 10%
BUN > 5 mg/dl > 5 mg/dl
Serum calcium < 8 mg/dl < 8 mg/dl
PaO2 < 60 mm Hg -
Base deficit > 4 mEq/L > 2 mEq/L
Fluid sequestration > 4 L > 6 L
Cutoff ≥ 3

70. Modified Glasgow (Imrie) Criteria
During initial 48 hr
WC > 15,000/mm3
PaO2 < 60 mm Hg
Blood glucose > 180 mg/dl
BUN > 45 mg/dl
Serum calcium < 8 mg/dl
Serum albumin < 3.2 g/dl
LDH > 600 U/L
SGOT > 200 U/L
Corfield et al. Lancet 1985
Cutoff ≥ 3

71. APACHE II Score

72. APACHE II Score
 Score ≥ 8
 Advantages
 Accuracy at 24 hr ~ other scoring system
at 48 hr
 Can be used for follow-up
 Disadvantages
 Complicated

73. Dx of AP
Mild Severe
CT scan
(>48 hr)
Supportive Rx ERCP
within 72 hr
Biliary
Pongprasobchai S. Thai J Gastroenterol 2004;5:111-22
Enteral
Nutrition
Dx of GS-AP
Assessment of severity

74. Effects of Impacted / Retained CBD
Stone in ABP
 Causes concomitant
ascending cholangitis
(incidence 3-14%)
 May increase severity
of ABP?
>80%
<20%

75. Indications
 Concomitant cholangitis
 Impacted stone at ampulla
Timing
 Within 72 hr after symptoms
Always perform ES?
 Probably yes
Urgent ERCP ± ES in ABP
Conclusions

76. Dx of AP
Mild Severe
CT scan
(>48 hr)
Supportive Rx ERCP
within 72 hr
Biliary
Pongprasobchai S. Thai J Gastroenterol 2004;5:111-22
Enteral
Nutrition
Dx of GS-AP
Assessment of severity

77. Importance of
Nutritional Management in AP
 AP is catabolic (esp. severe AP)
• Total energy expenditure = 1.5x of REE*
 Inability to maintain adequate oral
intake
• Abdominal pain
• N-V
• Reluctance of physician, fear of disease
exacerbation
*Bouffard YH. JPEN 1989;13:26-9.

78. Enteral
Pros
 Improve gut barrier & intestinal
permeability
 Reduce bacterial translocation
Cons
 Stimulation of pancreatic
secretion
EN and PN in Severe AP
Parenteral
Pros
 No stimulation of
pancreatic
secretion
Cons
 Infections
 Metabolic
(hyperglycemia
and hyper TG)

79. EN versus TPN in Severe AP
 NJ feeding
 Meta-analysis of 6 studies, 263 patients
RR [95%CI]
 ↓ Infectious complications 0.45 [0.26-0.78]
 ↓ Surgical interventions 0.48 [0.22-1.00]
 ↓ LOS 2.9 d [1.6-4.3 d]
 Noninfectious complications 0.61 [0.31-1.22]
 Mortality 0.66 [0.31-1.22]
Marik PE. BMJ 2004

80. Problems with NJ Feeding
 Placement may need endoscopy or
fluroscopy-guidance
 Frequent tube displacement

81. How to Initiate Enteral Feeding in AP
 Can start within 48 hr (after
classifying pt. as SAP)
 Regardless of abdominal
pain, bowel sound or
amylase/lipase level
 NJ or NG route based on
convenience and local
expertise
 Low fat, semi-elemental
formula
 Start with 10-30 ml/hr
 Observe pt’s symptoms
 Titrate rate until target
calorie is met
 If adequate calorie not
achieved within 5 days,
consider PPN

82. Dx of AP
Mild Severe
CT scan
(>48 hr)
Supportive Rx ERCP
within 72 hr
Biliary
Pongprasobchai S. Thai J Gastroenterol 2004;5:111-22
Enteral
Nutrition
Dx of GS-AP
Assessment of severity

83. Current Indications & Timing
of CT Scan in AP
Indications
 Clinically severe AP
 Persistent organ failure
 Clinical deterioration or not improved after
48-72 hr
Timing
 Usually not necessary within the first 48 hr
 6-10 days after admission*
 No need of ‘emergency’ CT
*UK Guidelines 2005. Gut 2005; 54(Suppl III): 1-9

84. Contrast-Enhanced CT

85. Infected Pancreatic Necrosis
 Incidence ~30 of
pancreatic necrosis
 Increase mortality 3x
from sterile necrosis
(10% → 30%)
 Indication for surgery
 Difficult to diagnose

86. Diagnosis of
Infected Pancreatic Necrosis
1. Clinical suspicion
– Sepsis syndrome: not accurate
1. Gas in pancreatic necrosis***
- Uncommon but definite
1. Fine needle aspiration (FNA)*****
– CT- or US-guidance
– Not widely available

87. Pancreatic Gas
Uncommon but definite

88. Diagnosis of Infected Pancreatic
Necrosis by FNA
Gerzof SG. Gastroenterology 1987; 93: 1315-20
Gold standard
but usually unavailable

89. Dx of AP
Mild Severe
CT scan
(>48 hr)
Supportive Rx
No necrosis Necrosis
ATB
Surgery
ERCP
within 72 hr
Biliary
Pongprasobchai S. Thai J Gastroenterol 2004;5:111-22
Enteral
Nutrition
Gas
Dx of GS-AP
Assessment of severity

90. Antibiotic Prophylaxis in PN
Guidelines for Clinicians
 Patient
• Area of necrosis >30%
• Presence of OF
• Newly developed SIRS or OF
• EN cannot be initiated
• (High incidence of IPN)
 Choice of antibiotics
• Imipenem, meropenem
• Quinolones + metronidazole
 Duration
• <14 days
AGA Institute Medical Position Statement on AP. GE 2007; 132: 2019-21

91. Indications of Surgery in AP
 Infected pancreatic necrosis**
• Positive FNA
• Gas in pancreatic necrosis
(Recommendation Grade B)
 Selected case of sterile necrosis*
• Unimproved organ failure after 3-4 weeks
(Recommendation Grade B)
IAP Guidelines 2002. Uhl W, et al. Pancreatology 2002; 2: 565-573

92. Acute Liver Failure

93. 06/20/14 Free template from www.brainybetty.com 93
Defenition
• Rapid development of hepatocellular
dysfunction  coagulopathy and enceph
alopathy in a patient without known pre
existing liver disease
• Interval between the onset of illness and
appearance of encephalopathy of < 8-12
weeks

94. 06/20/14 Free template from www.brainybetty.com 94
Classification
O'Grady Classification
• Hyperacute liver failure: < 7 days, more likely
to develop cerebral edema and to recover wit
hout liver transplantation
• Acute liver failure: 8-28 days
• Subacute liver failure: 4-24 weeks, more likely
to present with evidence of portal
hypertension such as ascites and to have a lo
w rate of survival without transplantation

95. 06/20/14 Free template from www.brainybetty.com 95
• Dx: physical examination (altered mental
status) and supportive laboratory findings (hy
perbilirubinemia, prolonged prothrombin time
)
• DDx: sepsis, systemic disorders with liver and
brain involvement (e.g. SLE, TTP), and an acut
e decompensation of chronic liver disease

96. Etiology of ALF
• Viral hepatitis
• Drug – induced hepatitis
• Toxin induced hepatitis
• Wilson’s disease
• Mushroom (Amanita phalloides) poisoning
• Budd-Chiari syndrome
• New-onset autoimmune hepatitis
• Malignant infiltration of the liver
• Combine 5-30%

97. Clinical features
• Initial presentation : nausea, vomiting, and
malaise, and jaundice
• Impaired elimination of bilirubin; depressed
synthesis of coagulation factors and diminished gluc
ose synthesis.
• Decreased uptake and increased generation of
intracellular lactate  lactic acidosis
• Increases risk of gastrointestinal and intracranial
hemorrhage; hypoglycemia can contribute to brai
n injury; and acidosis can contribute to hypotensi
on

98. Initial evaluation and Manangement
• Rapid identification of the underlying cause,
with an emphasis on treatable conditions
– Acetaminophen: NAC
– Amanita mushroom poisoning: immediate gastric
lavage and instillation of charcoal, hemodialysis
can remove toxins from the serum; intravenous p
encillin
– Herpes simplex: intravenous acyclovir
– Rapid delivery for pregnant women with acute
fatty liver of pregnancy, HELLP syndrome, and pr
eeclampsia

99. Initial Management of ALF
• ICU care
• Serial lab: base-acid, arterial NH3, INR
• Urgent transfer to a liver transplantation
center before the development of advanced e
ncephalopathy or other complications of acut
e liver failure

104. 06/20/14
Predictor of outcome
Acetaminophen Cases
• Arterial pH < 7.3 or
Arterial lactate level >3.5mmol/L at 4
hours or
Arterial lactate level >3.0mmol/L at 12
hours or
• INR > 6.5 (PT > 100 seconds)
• Serum creatinine >3.4 mg/dL
• Stage 3 or 4 encephalopathy
• Single factor
mortality 55%
• Acidosis
mortality 95%

105. 06/20/14
Non-Acetaminophen
Cases
• INR > 6.5 (PT > 100 seconds) or
• any 3 of the following:
-Age <10 or >40 years
-Duration of jaundice >7 days
-Etiology: idiosyncratic
drug reaction; non-A, non-B he
patitis; halothane hepatitis; ind
eterminate
-Serum bilirubin >17.5 mg/dL
-INR > 3.5 (PT > 50 seconds)
• Single predictor
mortality 80%
• 3 predictors
mortality 95%

106. 06/20/14 Free template from www.brainybetty.com 106

107. Liver transplantation
• Short-term survival rate of 80% and a 1-year
survival rate of 70%
• Contraindications to transplantation
– Irreversible brain damage
– Active extrahepatic infection
– Multiple organ failure syndrome

108. • EXTRACORPOREAL LIVER SUPPORT
• Albumin dialysis (e.g., the molecular
adsorbent recirculating system, or MARS)
• Information about the safety and efficacy of
these systems in patients with acute liver failu
re is limited

109. • Bioartificial liver devices contain liver cells
grown within specialized hollow-fiber cartridg
es through which the patient's plasma is perfu
sed
• trial failed to demonstrate a significant benefit
in outcome but can lead to a trend toward
improvement in metabolic, hemodynamic, an
d clinical parameters

110. 06/20/14 Free template from www.brainybetty.com 110

111. Management Goals For
Upper GI Bleeding
• Resuscitation
• Identification of bleeding site
• Cessation of active bleeding
• Prevention of recurrence of
bleeding

112. Initial Management
• Early intensive-care monitoring*
–Reduce time to hemodynamic
stabilization
–Reduce mortality rate
• UGI bleeding team**
–Improve overall MR 8% compared
with 14%
*Baradarian R. Am J Gastroenterol. 2004
**Sander DS. Eur J Gastroenterol Hepatol 2004

113. Initial Assessment &Initial Assessment &
ResuscitationResuscitation
Supportive Treatment
 Maintain airway
 Hx and PE for assessment of severity
and causes
 NG irrigation
 Fluid resuscitation
 Blood for CBC, cross-match

114. Airway Management
• Indication for Intubation in Upper Gi
Bleeding (high risk for aspiration)
–Altered Mental Status
–Massive Upper Gi Bleeding

115. Classification of
Hypovolumic Shock in
AdultClass I Class II Class III Class IV
Blood loss
volume (ml)
<750 750-1500 1500-2000 >2000
Blood loss (%of
circulating blood)
0-15 15-30 30-40 >40
SBP No change Normal Reduced Very reduced
DBP No change Raised Reduced Very reduced
/unrecordable
Pulse rate Slightly
tachycardia
100-120 120 >120
RR Normal Normal > 20 >20
Mental state Alert, thristy Anxious or
aggressive
Anxious
aggressive or
drowsy
Drowsy confused
or unconcious
Management of Hypovolumic Shock,BMJ ;1990

116. Resuscitation
Colloid and crystalloid in use of
resuscitation prior to administering
blood component.
Perel P. The Cochrane review, 2007

117. Goals of Transfusion
• To keep Hb more than 10 gm/dl in non
variceal bleeding
• To keep Hb more than 7-8 gm/dl in variceal
bleeding

118. Factor that Consider Before
transfusion
• Age
• Hemodynamic status
• Sign and symptom of blood loss
• Cardiovascular reserve
• Baseline Hematocrit
• Rate of blood loss and recent Hematocrit
• Co morbid : Heart, lung, renal, liver etc.

119. 1. Confirm diagnosis of UGIB
negative in 10% of DU bleeding
2. Clear stomach, prepare for EGD
3. Assess severity of bleeding
Do not stop bleeding !!!
Gastric Lavage

120. Hematemesis / Melena
Initial Assessment and Resuscitation
Risk Stratification
Low Risk High Risk

121. Risk StratificationRisk Stratification
High risk
• Host factors
- Age > 60 years
- Co-morbid conditions (e.g.
renal failure, cirrhosis,
CVS disease, COPD)
- Hemodynamic instability
(e.g. orthostatic
hypotension, P>100/min,
SBP < 100 mmHg
- Coagulopathy, including
drug-related
• Bleeding character
- Continuous red
blood from NG
after irrigation
- Red blood per
rectum
• Patient course
- Rebleeding
- Inpatient

122. Rockall scoring system for risk of rebleeding and death
after admission to hospital for acute UGIB
score
Variable 0 1 2 3
Age(Y) <60 60-79 ≥80
Shock No shock
(SBP>100,P<
100)
Tachycardia
(SBP>100,
P>100)
Hypotension (SBP<100,
P>100)
Comorbidity Nil major Cardiac failure, ischemic
heart disease, any major
comorbidity
Renal failure, liver
failure,
disseminated
malignancy
Diagnosis MWT, no
lesion, and
no SRH
All other
diagnosis
Malignancy of upper GI tract
Major SRH None or dark
spot
Blood in UGI tract, adherent
clot, visible spurting vessel
Each variable is scored and the total score calculated by simple addition SRH,stigmata of
recent hemorrhage. MWT,Mallory Weiss tear
Gut 2002;51

123. Correlation Between Rockall Score and
Rebleeding and Mortality
Rockall et al. Gut 1996; 38: 316-21.
Sanders DS. Am J Gastroenterol 2002
A total score of <3 is associated with excellent outcome,
where as a score >8 carries a high mortality

124. Clinical Rockall Score
• Retrospective observational study
• 102 non-variceal UGIB patients
• Results
– Score 0: no adverse outcome, no blood
transfusion
– Score 1-3 : no adverse outcome, 29% need blood
transfusion
– Score > 3 : 21% rebleeding, 5% need surgery, 10%
death.
• Low-risk patients  elective endoscopy
Tham TC. Postgrad M J 2007

125. Hematemesis / Melena
Initial Assessment and Resuscitation
Risk Stratification
Low Risk
Supportive Treatment
and Monitoring
Elective Endoscopy
High Risk
6. PPI for Suspected
Non-variceal
Bleeding
7. Somatostatin for
Suspected Variceal
Bleeding

126. Variceal Non-variceal
Painless bleeding Pain or painless
Hematemesis Hematemesis,
coffee
ground,
melena
Usually hemodynamic Vary
change or Hct<30%
Signs of portal HT Absent
(superficial dilated vein,
splenomegaly, low plt)
Underlying Cirrhosis
chronic liver disease
Variceal & Non-variceal bleeding

127. Non Variceal Bleeding

128. Treatments of Non-variceal
UGIH
 Medical treatment
 Endoscopic treatment
 Surgical treatment

129. Empirical Therapy
Nonvariceal upper GI haemorrhage
- Acid related disease: > 75%
- Bleeding peptic ulcer
~ 75% stop spontaneously
~ 25% recurrent bleeding
Laine L, N Engl J Med, 1994

130. Pharmacologic Therapy
• Acid suppressing agents
– H2-receptor antagonists (H2RAs),
– proton pump inhibitors (PPIs)
• Splanchnic blood pressure modifiers
– vasopressin, somatostatin, octreotide
• Anti-fibrinolytic agents
– tranexamic acid

131. Suspected High-RiskSuspected High-Risk
Nonvariceal BleedingNonvariceal Bleeding
 Continuous IV PPI infusion or bolus PPI or oral
PPI double dose
 If endoscopy is available within 8 hr, PPI may not
be needed
Continuous IV infusion PPI
- Pantoprazole /Omeprazole 80 mg iv bolus then iv drip
8 mg/hr
Bolus PPI
- Pantoprazole /Omeprazole 40 mg iv q 12 hr
Oral PPI
- Double normal dose

132. Day 0 Day 1 Day 2 Day 3
UGIB
Risk stratification
PPI Before
Endoscopy + Therapeutics
PPI After endoscopy
Role of PPI in Non-variceal UGIB
TIME

133. Timing for Endoscopy in High
Risk non-variceal UGIB
• Study compare 0-6 hr and 6-24 hr for
endoscopy
• Retrospective review in 169 patients
(77 /0-6 hr and 92 /6-24 hr)
• No difference in
– Rebleeding
– Surgery
– Mortality
– Readmission within 30 days
Targownik LE, et al. Can J Gastroenterol 2007;21:425

134. Endoscopic Treatment

135. SRH of Ulcer
Clean
base
Spot Adherent
clot
NBVV Active
bleeding
Endoscopic treatment
Rebleeding Surgery Death
Clean base 5% 0.5% 2%
Spot 10% 6% 3%
Adherent clot 22% 10% 7%
NBVV 43% 34% 11%
Active bleeding 55% 35% 11%
Continuous IV infusion PPI
- Omeprazole / pantoprazole 80 mg iv bolus then
iv drip 8 mg/hr
IV PPI drip 3-5 d +

136. • Injection • Thermal
Coagulation
• Mechanical
(hemoclip)
Combination of adrenaline injection and Thermal or mechanical
Method are recommend

137. Adjuvant iv PPI improves
Outcome
.0
.2
.4
.6
.8
1.0
ProbabilityofNoRecurrentBleeding
0 5 10 15 20 25 30
No. at Risk
Omeprazole
Placebo
120 115 113 113 113 113 112
120 94 93 93 93 93 93
Omeprazole
Placebo
Lau JY. N Engl J Med. 2000;343:310–316
•Epinephrine injection + 3.2mm
heater probe treatment
•Omeprazole 80mg+ 8mg/h for
72h Versus Placebo
Hazard Ratio, 95%CI
4.8 (1.9-12)

138. 1. Continued active bleeding and
unable to perform endoscopy
2. Require blood transfusion > 6 units
3. Failure of endoscopic treatment
3. Rebleeding after successful
endoscopic treatment
Indication for Surgery

139. Acute UGI bleed
Bleeding continues
or recursBleeding stops
Survival Death
20%
~8%
80%
Longestrech GF. Am J Gastroenterol 1995; 90: 206-10.
Silverstein FE, et al. Gastrointest Endosc 1981; 27: 80-93.
Outcome of Acute UGI Bleeding

140. • Clinical signs
– Previous documented of EV or GV
– Signs of portal HT e.g. splenomegaly,
ascites, HE, dilated superficial vein
– Clinical cirrhosis with thrombocytopenia
and/or splenomegaly
• Medications
– Somatostatin 250 µg iv bolus, followed by iv
drip 250 µg /hr
– Octreotide 50 µg iv bolus, followed by iv drip
50 µg /hr
– Prophylaxis ATB : 3 rd generation
cephalosporin
• If endoscopy can be performed urgently,
somatostatin or its analogue may not be needed
Suspected Variceal BleedingSuspected Variceal Bleeding
(Always High-Risk)(Always High-Risk)

141. Pre-Endoscopy Treatments
of Variceal Bleeding
Current Recommendation
1. Pharmacological Rx:
• “First-line treatment”
• Choice depends on local availability
• Terlipressin is preferred if available
2. Balloon tamponade:
• “Rescue Rx”
Bosch J, et al. J Hepatol 2003; 38: S54-S68

142. Endoscopic
treatment
Somatostatin S-B tube
Stop bleed
Rebleeding
Complicatn
Onset
Cost
70-90%
20%
2-22%
immediate
+++
60-75%
40%
Low
1-2 hrs
++++
80-100%
50%
15-68%
immediate
+
Treatment of Variceal
Bleeding

143. Pharmacologic TreatmentPharmacologic Treatment
• Somatostatin / Octreotide
- Stop bleeding in 75-80 %
− ↓ Blood transfusion ~ 1 unit
− ↓ Need for S-B tube ~ 30 %
- Do not affect rebleeding rate and mortality
• Terlipressin
− ↓ Mortality rate 18 % (NNT = 6)
Gotzsche PC, et al. Cochrane Systematic Reviews 2003
Ioannou G, et al. Cochrane Systematic Reviews 2001

144. Endoscopic treatment in
Variceal Bleeding
• Esophageal
Varices band
ligation for EV
Cyanoacrylate injection for gastric
varices

145. EV Banding

146. Glue Injection

147. Variceal Bleeding
Pharmacotherapy (Somatostatinor analogue)
Endoscopy Avialable
yes no
EVL/EIS SB 24-48 hrs
Bleeding stop Ongoing bleed
TIPS or Surgery
fail
SB 24-48 hrs
Success
Rebleed
Re endoscopy with EVL Fail or rebleed

148. Sengstaken-Blakemore
Tube

149. • Gastric balloon is inflated with
250 ml air & doubly clamp.
• Esophageal tube is then
inflated to a pressure of 20-40
mmHg.
• 500 ml bag of saline,taped to
the tube & hang over the side
of bed
• The head of bed is raised
• The position of the tube is
checked by x-ray
Sengstaken-Blakemore Tube

150. Balloon Tamponade
• Efficacy in 118 cases
- 92 % could stop bleeding at least 24 hr
- 50 % could stop bleeding until D/C
- 50 % rebleed after deflated balloon
- 50 % within 24 hr
- 50 % after 24 hr (~ 4.5 days)
- 20 % had minor complications
- 10 % had major complication i.e. aspiration pneumonia
Panes J, et al. Dig Dis Sci 1988; 33: 454-9

151. Cautions on the Use of S-B TubeCautions on the Use of S-B Tube
 Use only when variceal bleeding is very
likely
 Always test the balloon before use
 ET tube may be needed if patient has HE
grade III-IV
 Blow gastric balloon with air 200-250 cc
 Tract the tube with 0.5 kg weight only
 Put NG tube in the esophagus
 Blow esophageal balloon with air 30-40
mm Hg using 3-way and manometer
 Do not leave SB tube > 24-48 hr

152. ขอบคุณค่ะ