Transcript Case Conference

June 22, 2009
Rivera, Rivere, Robosa, Rodas, Rodriguez, Rogelio, Roque, Ruanto,
Sabalvaro
Section D Group 1




• J.D., 49 y/o, Male
• Married
• Filipino, Roman Catholic
• Jeepney driver
• Gnawing, non-radiating, RLQ pain, 2-3/10
• Relieved: antacid; Aggravated: heavy meal intake
13 yrs PTA • Sought consult at a local clinic; prescribed: Buscopan- dosage unrecalled
2 days PTA
• One episode of Melena
• No consult done
• Severe, non-radiating epigastric pain, 9/10
• Sought consult at a local clinic and was adviced to take Clarithromycin and
7 hrs PTA
Omeprazole (both afforded temporary relief)
• Persistent Severe, non-radiating epigastric pain, 9/10
• Pain became generalized all over the abdomen
6 hrs PTA • Rushed to USTH ER
ADMISSION


• No hypertension, diabetes, or asthma
• No previous surgeries or transfusions

(‐) asthma, DM, hypertension




• Smoker, 40 pack years
• Occasional alcoholic beverage drinker
• Diet: mixed
• Denies illicit drug use













• No fever, no weight loss, no weakness, no anorexia
• No rashes, no increased pigmentation
• No visual dysfunction, no redness, no itchiness, no eye pain,
excessive lacrimation
• No deafness, no tinnitus, no aural discharge
• No epistaxis, no nasal discharge
• No gum bleeding, no throat soreness
• No dyspnea, no shortness of breath, no chest pain, no
palpitations
• No diarrhea, no constipation, no nausea, no vomiting, no
heartburn,
(+) melena
• No dysuria, hematuria, incontinence
• No limitation of movements, joint pains and swelling of joints
• No heat or cold intolerance, no polyphagia, polydipsia, polyuria
• No convulsions, no headache, no sleep disturbances
• General
– conscious, coherent, not in cardiorespiratory
distress
 • Vital Signs:
 – BP: 140/90 mmHg
 – PR = 90 bpm, regular
 – RR = 22 cpm
 – T = 37.6 C
 • Skin
 – Warm, moist
 – no active dermatoses












• HEENT
– pink palpebral conjunctivae, anicteric scelrae, no
nasoaural
discharge, moist buccal mucosa, tonsils not enlarged,
nonhyperemic posterior pharyngeal walls
– Supple neck, no palpable cervical lymph nodes, thyroid
not enlarged
• Thorax
– symmetric chest expansion, (‐) retractions, resonant on
both lung fields, equal and clear breath sounds
• Cardiovascular
Adynamic precordium, AB 5th LICS MCL, apex S1>S2,
base
S2>S1, (‐) murmurs








• Abdomen
– Flat, no scars or striae, NABS, tympanitic upon
percussion,
Traube’s space not obliterated, (+) direct and rebound
tenderness in upper abdominal region with guarding
(‐)Rovsing’s sign, (‐) psoas sign
• DRE:
– no skin tags seen, tight sphincteric tone, smooth
rectal
mucosa, (‐) palpated masses, (‐) pararectal
tenderness,
brown stool on tactating finger











• Extremities
– Pulses were full and equal, no cyanosis, no edema, no
limitation of movement in all extremities were noted.
• Neurological Examination
– Conscious, coherent, oriented to 3 spheres
– Cranial nerves: pupils 2‐3 mm ERTL, EOMs full and
equal,
V1V2V3 intact, can clench teeth, can raise eyebrows, can
close eyes tightly, can smile, can frown, can puff cheeks,
no
facial asymmetry, no hearing loss, can turn head from side
to side with resistance, can shrug shoulders, tongue
midline on protrusion.







• Neurologic Exam
– Motor: MMT of 5/5 on all extremities
– Cerebellar: can do FTNT & APST
– DTR’s: ++ on all extremities
– No sensory deficit
– (‐) Babinski
– (‐) nuchal rigidity







49 y/o, Male, jeepney driver
(+) melena
Generalized, persistent, severe, non-radiating
epigastric pain, 9/10
(+) direct and rebound tenderness in upper
abdominal region with guarding
– BP: 140/90 mmHg
– RR = 22 cpm
Smoker, 40 pack years





Gastric ulcer
Duodenal ulcer
Erosive gastritis
Zollinger- Ellison Syndrome
Gastrointestinal tumors


Majority of GUs can be attributed to either H.
pylori infection or NSAID induced mucosal
damage
Type I - located near the angularis incisura on
the lesser curvature, close to the border
between the antrum and the body of the
stomach. These patients usually have normal
or decreased acid secretion.




Type II - associated with active or quiescent
duodenal ulcer disease
Type III - prepyloric
Type IV- near the gastroesophageal junction,
and acid secretion is normal or below normal
Type V- any location, associated with NSAID
use



Acid secretory abnormalities that is also
caused by H. pylori infection
Bicarbonate secretion is significantly reduced
in patients with DU
Role of NSAIDS in inducing mucosal damage




caused by many factors, including infection,
injury, certain drugs, and disorders of the
immune system.
involves both inflammation and wearing
away of the stomach lining.
results from irritants such as drugs, especially
aspirin and other nonsteroidal antiinflammatory drugs
Painless upper GI bleeding in ICU setting


increased levels of the hormone gastrin are
produced, causing the stomach to produce
excess hydrochloric acid
a tumor (gastrinoma) of the duodenum or
pancreas producing the hormone gastrin.
Gastrin then causes an excessive production
of acid which can lead to peptic ulcers in
almost 95% of patients.


one of the most common mesenchymal
tumors of the gastrointestinal tract
Patients present with trouble swallowing,
gastrointestinal hemorrhage or metastases


H. pylori and NSAID induced injury account for the majority
of DUs and GUs.
Caused by mild gastric acid hypersecretion resulting from
(1) increased release of gastrin due to the stimulation of
a. antral G cells by cytokines released by inflammatory
cells
b. diminished production of somatostatin by D cells, both
resulting from H. pylori infection
(2) an exaggerated acid response to gastrin due to an
increased parietal cell mass resulting from gastrin
stimulation
H. pylori infection is virtually always associated with
a chronic active gastritis
 The particular end result of H. Pylori infection is
determined by a complex interplay between
bacterial and host factors






HP is able to facilitate gastric residence, induce mucosal
injury, and avoid host defense
Urease allows the bacteria to reside in the acidic stomach
and generates NH3 which can damage epithelial cells
produce surface factors that are chemotactic for
neutrophils and monocytes which further contribute to
injury
Proteases and phospholipases break down the
glycoprotein lipid complex of the mucus gel and reduces
the efficacy of the first line of mucosal defense
Adhesins are expressed to facilitate attachment



Inflammatory response to H. pylori includes
recruitment of neutrophils, lymphocytes (T
and B), macrophages, and plasma cells
Pathogens lead to injury by binding to class II
MHC molecules expressed in gastric epithelial
cells, leading to apoptosis
Elevated concentrations of multiple cytokines
contribute to the mucosal and systemic
humoral response that further compounds
cell injury
Summary of potential mechanisms by which H. pylori
may lead to gastric secretory abnormalities.


PGs play a critical role in maintaining
gastroduodenal mucosal integrity and repair
Interruption of PG synthesis can impair
mucosal defense and repair, thus facilitating
mucosal injury

Smoking
 Decreases both gastroduodenal prostaglandin
production and pancreaticoduodenal bicarbonate
production
 Impairs blood flow and healing

Alcoholism
 Not been proved to directly cause peptic
ulceration, but alcoholic cirrhosis is associated
with an increased incidence of peptic ulcers

Gnawing
 characteristically peptic ulcer disease

Epigastric pain
 Location of duodenum
Acid-induced activation of chemical receptors in the
duodenum
 Enhanced duodenal sensitivity to bile acids and
pepsin
 Altered gastroduodenal motility

Final common pathway to ulcer formation is
peptic acid injury of the gastroduodenal
mucosal barrier

Classically associated with gastric ulcers

Possibly due to increased acid secretion
during digestion
As an ulcer continually erodes the duodenal
wall, blood vessels are also damaged, causing
bleeding.



Tarry stools – Upper GI
Bleeding can be confirmed by nasogastric
aspiration
Principal indication for surgery
http://nyp.org/health/stomach-duodenal-ulcers.html
To compensate for the blood loss so as to not
compromise circulation
Chemical infection due to release of enzymes
Date 05/14/09
HGB: 136
HCT: 0.41
Platelet: 332
WBC: 12.7
Neut: 0.83
Lymph: 0.17
Ref. Range
120-170
0.37-0.54
150 – 450
4.5 – 10.00
0.50 – 0.70
0.20 – 0.40
INT
N
N
N
HIGH
HIGH
LOW
Date 05/14/09
Color : Dark yellow
Transparency: Sl. Turbid
pH: 6.0
Sp. Gravity: 1.020
Albumin: Negative
Sugar : ++
RBC: 0-3/hpf
WBC : 0-3/hpf
Date 05/14/09
Sodium 136
Potassium 3.5
Ref. Range
137-147
3.5-5.1
INT
N
N
Date 05/14/09
Amylase 65.0
Lipase 31.8
Ref. Range
10-130 IU/L
13-60 IU/L
INT
N
N
• There is a linear lucency noted in
the subdiaphragmatic area
suggestive of
Pneumoperitoneum
• Suspicious infiltrates are seen in
the right apex and right
infraclavicular area.
• The heart is not enlarged
• The right hemidiaphragm is
slightly elevated
• Sulci are intact



Reduce acid output
Increase mucosal protection
Eliminate infectious agents

Antacids –





Aluminum hydroxide
Calcium carbonate
Magnesium hydroxide
Sodium bicarbonate
H2-receptor antagonists
 Competitively blocking binding of histamine to H2 receptors
 Cimetidine,famotidine,nizatidine,ranitidine

Proton pump inhibitors
 Omeprazole,lansoprazole
 Binds to H/K ATPase suppressing secretion of hydrogen ions into the
gastric lumen

Sucralfate
 Impairs HCl and prevents degradation of mucus
by pepsin

Colloidal Bismuth
 inhibit activity of pepsin, increase mucus secretion
and interact with proteins in necrotic mucosal
tissue





Amoxicillin
Bismuth compounds
Clarithromycin
Metronidazole
Tetracycline

Cefoperazone –3rd gen. cephalosporins
 Inhibits the bacterial cell wall synthesis, and

Sulbactam – acts as a beta-lactamase
inhibitor, to increase the antibacterial activity
of cefoperazone against beta-lactamase
producing organisms

Indications for Surgery:
 Hemorrhage
 Perforation
 Obstruction
 Intractibility


Emergency exploratory laparotomy
Primary repair with omental buttress

Perforation
 Typically seen in anterior wall of the duodenal
bulb.
 Classic presentation is sudden severe epigastric
pain that rapidly spreads
 Generalized boardlike rigidity of the abdomen

Optimize condition of patient
 Nasogastric tube placed
 Fluid resuscitation and hydration
 Pre-op monitoring
 Antibiotics
 Screening of other condition that will interfere
with treatment
Under general anesthesia
Incision:
 an incision is made into the
patient's abdomen. Fascia is
divided. The lining of the
abdominal cavity, the
peritoneum, is cut
Abdominal Exploration: Surgeon
explores the abdominal cavity
for disease or trauma
Closure: organs and related
structures are returned to their
normal anatomical position.
The incision may then be
sutured (stitched closed).

Sutures are placed
across the perforation
 And a piece of
omentum is placed on
top of the perforation
 Sutures are securely
tied to entrap the
omentum as a plug




NGT maintained
Hydration continued – D5 NR
IV Antibiotics
 Pantoprazole 40mg/IV OD
 Sulperazone 1.5g/IV q8 hrs





Continue medications at home
Continue. daily wound care
Resume moderate daily activities
Follow up after a week or earlier if any
problem arises
Advise patient to avoid skipping meals and
take small but frequent meals
Diagnostic, Treatment, Harm, Prognosis
1130-0108/2004/96/9/599-605
REVISTA ESPAÑOLA DE ENFERMEDADES DIGESTIVAS
Copyright © 2004 ARÁN EDICIONES, S. L.
REV ESP ENFERM DIG (Madrid)
Vol. 96. N.° 9, pp. 599-605, 2004
Recibido: 16-10-03.
Aceptado: 27-01-04.
Correspondencia: Manuel Castro Fernández. Servicio de Aparato Digestivo
(9ª planta izda.). Hospital Universitario de Valme. Ctra. de Cádiz, s/n.
41014 Sevilla. e-mail: [email protected]
M. Castro Fernández, D. Sánchez Muñoz, E. García Díaz, M. V. Galán Jurado and C.
Rodríguez Alonso
Service of Digestive Diseases. Hospital Universitario de Valme. Sevilla. Spain

Introduction: the sensitivity of invasive
diagnostic methods
for Helicobacter pylori (H. pylori) infection,
particularly of urease
rapid test, is decreased in cases of
gastroduodenal ulcer and
upper gastrointestinal bleeding.

Objectives: to assess the influence of blood
in the stomach or recent bleeding endoscopic
signs in the diagnostic sensitivity of urease
rapid test among patients with bleeding
duodenal ulcer, as well as the influence of
simultaneously collected corporal and antral
biopsy samples.

120 patients, 85 male and 35 female,with an average
age of 62 (18-88) years, who were admitted to our
Hospital due to bleeding duodenal ulcer and who
received an endoscopic diagnosis within 24 hours of
admission were included.

None of the patients had been under treatment with
non-steroideal antiinflammatory drugs, protonpump inhibitors or antimicrobial drugs in the two
weeks prior to the bleeding event, and none had
received eradicating therapy for H. pylori. In this
group of selected patients an H. pylori infection rate
nearing 100% was assumed.

H. pylori infection was ruled out using antral biopsy (69
cases) or both antral and fundic biopsies (51cases) for urease
rapid testing (Jatrox®-H.p.-Test). Patients were classified in
three groups according to their endoscopic bleeding signs: a)
presence of blood in the stomach or recent bleeding ulcer(21
cases); b) ulcer showing non-recent bleeding signs (38
cases);and c) ulcer without bleeding signs (61 cases).

The sensitivity of the urease rapid test was compared
between patient groups.

Similarly,urease test results with an antral biopsy sample
were compared in 100 patients with non-bleeding duodenal
ulcer.

urease test was positive in 93% of patients with nonbleeding
duodenal ulcer, and in 83% of patients with upper
gastrointestinal bleeding, which reached statistical
significance (p = 0.019).

This test was positive in 82.6% of patients with an antral
biopsy, and in 82.3% of patients with combined antral and
fundic biopsies.

In group A, urease test was positive in 90.5% of patients; in
group B, it was positive in 89.5% of patients, and in group C,
the test turned positive in 75.4% of patients. Statistical
differences were only reached when patients in group C were
compared to patients in groups A and B together (p = 0.037).

1. The presence of either blood in the stomach or
recent bleeding endoscopic signs appeared not to
be the conditioning factor for the decreased
sensitivity of urease test among patients with
bleeding duodenal ulcer.

2. The decreased sensitivity of this test in patients
with upper gastrointestinal bleeding is more evident
during the resolution stage, and it does not seem to
occur because of H. pylori migration from the
antrum to the corporal gastric region.
Wing T. Siu, MBChB (HK), FRCSEd (Gen),* Heng T. Leong, MBBS (HK), FRCSEd,* Bonita K. B. Law, MBChB (HK),
FRCSEd (Gen),* Chun H. Chau, MBBS (Jinan), LMCHK (HK), FRCSEd (Gen),* Anthony C. N. Li, MBBS (HK), FRCSEd,*
Kai H. Fung, MBBS (HK), FRCR (UK),† Yuk P. Tai, MBBS (Lond), FRCSEd, and * Michael K. W. Li, MBBS (Lond), MRCS
(Eng.), LRCP
(Eng.), FRCS (Eng.), FRCSEd*
From the Departments of *Surgery and †Diagnostic Radiology, Pamela Youde Nethersole Eastern Hospital, Chai Wan,
Hong Kong, SAR, China
OBJECTIVE
To compare the results of open versus
laparoscopic repair for perforated peptic ulcers.
SUMMARY BACKGROUND DATA
 Omental patch repair with peritoneal lavage is the mainstay of
treatment for perforated peptic ulcers in many institutions.
Laparoscopic repair has been used to treat perforated peptic
ulcers since 1990, but few randomized studies have been carried
out to compare open versus laparoscopic procedures.
• 130 patients with a clinical diagnosis of perforated ulcer were randomly assigned to undergo
either laparoscopic omental patch repair.
JAN 1994 –
JUNE 1997
• Patients were excluded for a history of upper abdominal surgery, concomitant evidence of
bleeding from the ulcer, or gastric outlet obstruction.
• Patients with clinically sealed-off perforations without signs of peritonitis or sepsis were
treated without surgery. Laparoscopic repair would be converted to an open procedure for
technical difficulties, nonjuxtapyloric gastric ulcers, or perforations larger than 10 mm
• A Gastrografin meal was performed 48 to 72 hours after surgery to document sealing of the
perforation.
Primary
endpoint
perioperative
parenteral
analgesic
requirement.
Secondary
endpoint
operative time
postoperative pain
score
length of postoperative
hospital stay
complications and
deaths
date of return to normal
daily activities
CONCLUSION
 Laparoscopic repair of perforated peptic ulcer
is a safe and reliable procedure.
 It was associated with a shorter operating
time, less postoperative pain, reduced chest
complications, a shorter postoperative hospital
stay, and earlier return to normal daily activities
than the conventional open repair.
H. Lau
Department of Surgery, University of Hong Kong Medical Center, Tung Wah
Hospital, 12 Po Yan Street, Sheung Wan, Hong Kong, China
Received: 14 October 2003/Accepted: 7 January 2003/Online publication: 12
May 2004

To compare the safety and efficacy of open and
laparoscopic repair of perforated peptic ulcer in an
evidence-based approach using meta-analytical
techniques
SUMMARY BACKGROUND DATA
• Although laparoscopic repair combines the
principles of open repair with the advantages of
minimal access surgery, it has not been widely
accepted by general surgeons

Literature search: Search of electronic databases, including MEDLINE and
EMBASE between January 1990 and December 2002

Inclusion criteria: All prospective randomized trials or case–control studies that
compared the outcomes of laparoscopic and open repair of perforated peptic
ulcer were included. For the laparoscopic treatment group, only patients who
underwent laparoscopic suture repair were recruited

Data extraction: Standardized data abstract form

Data pooling and statistics: An effect size for the outcome parameter of
individual studies was calculated by the odds ratio (OR). The effect sizes of all
trials were tested for heterogeneity by Q Statistics. A qualitative review of the
outcome data was performed when a formal meta-analysis was not feasible.
Statistical analysis was performed with the Statistical Package for the Social
Sciences (SPSS, Chicago, IL,USA) software program and Comprehensive Metaanalysis

All reports (13) were critically appraised with respect to their methodology and
outcome

Meta-analyses demonstrated a significant reduction in the wound infection rate
after laparoscopic repair, as compared with open repair, but a significantly higher
reoperation rate was observed after laparoscopic repair.

Factors considered in the comparison of laparoscopic and open surgery were
as follows:
Length of operation
Conversion
Postoperative pain
Postoperative complications
Reoperation
Mortality
Length of hospital stay
Recovery variables
Length of operation: Five studies demonstrated a significantly longer operative
time for laparoscopic repair
Conversion: Reported rates of conversion to open repair ranged from 0% to 29.1%
Postoperative pain: A postoperative assessment of pain score consistently showed
a lower pain score after laparoscopic repair than after open repair
Postoperative complications:
Chest infection was the most common postoperative morbidity. Naesgaard et al.
in their retrospective study, demonstrated a significantly higher incidence of
chest infection in the laparoscopic group. But subsequent meta-analyses showed
a lower overall chest infection rate after laparoscopic repair
Wound infection was the next most common morbidity after open repair of
perforated peptic ulcer. Subsequent meta-analyses proved that laparoscopic
repair conferred a significant reduction in wound infection rate, as compared
with open repair.
Reoperation: The overall reoperation rate was 3.7% (n = 11) for laparoscopic repair (n
= 294) and 1.9% (n = 7) for open repair (n = 364). Leakage was the chief reason for
reoperation. Subsequent meta-analyses found a significantly lower reoperation
rate after open repair.
Mortality None of the mortality was attributed directly to the adoption of
laparoscopic repair. The subsequent pooled estimate of the overall mortality
favored laparoscopic repair.
Length of hospital stay All the studies showed that the length of hospital stay after
laparoscopic repair was either shorter than or equal to that associated with open
repair.
Recovery variables: Only Katkhouda et al. showed significantly earlier resumption
of the normal diet after laparoscopic repair. Siu et al. found that patients
returned to normal activities after laparoscopic repair within an average of 10 ±
6.9 days, which was significantly earlier than the return of those who underwent
open repair (26 ± 15.1 days).

The rationale for the sutureless technique is both to simplify the procedure and
to shorten the operative time. However, sutureless repair using a plug of gelatin
sponge with fibrin glue has not gained wide acceptance because of its associated
higher leakage rate, particularly if the ulcer is larger than 5 mm in diameter.

One main drawback of laparoscopic repair was the increase in operating time.

Another disadvantage of laparoscopic repair was a significantly increased
reoperation rate, which was a consequence of postoperative leakage. The higher
incidence of leakage after laparoscopic repair may be attributable in part to a
faulty technique of laparoscopic closure. Furthermore, the higher incidence of
intraabdominal collection was secondary to inadequate lavage and suctioning
of the peritoneal cavity. Perfection and standardization of the laparoscopic
technique for the repair of perforated ulcer is therefore necessary.

Laparoscopic repair is effective and superior to open repair in terms of early
postoperative outcomes including pain, wound infection, and functional
recovery.

However, the relative benefits of the laparoscopic approach must be weighted
against the increased risk of mortality, which can be reliably predicted by
preoperative assessment of Boey’s risk factors and the APACHE II score. It is
therefore of paramount importance that patients be selected carefully for the
laparoscopic approach. Patients who have one or more of Boey’s risk factors
are therefore less suitable for laparoscopic surgery.

Other relative contraindications for laparoscopic repair include the concomitant
presence of other ulcer complications such as bleeding and obstruction, large
perforation, technical difficulty, previous upper abdominal operations, and
serious associated cardiopulmonary diseases.

Meta-analyses of the 13 recruited trials demonstrated that laparoscopic repair
was associated with a significantly lower wound infection rate. Laparoscopic
repair of perforated peptic ulcer also was associated with reduced postoperative
pain and diminished analgesic consumption.

Currently, the main drawbacks of laparoscopic repair are a longer operation and a
higher reoperation rate. Both laparoscopic and open repairs of perforated peptic
ulcer, being complementary to each other, have their roles in the management of
perforated peptic ulcer.
**Boey’s risk factors: concurrent major medical illness, preoperative shock, and
delayed presentation of more than 24 hours
Mariëtta J. O. E. Bertleff, 1 Jens A. Halm,2 Willem A. Bemelman,3 Arie C. van
der Ham,4 Erwin van der Harst,5 Hok I. Oei,6 J. F. Smulders,7 E. W.
Steyerberg,8 and Johan F. Lange2
OBJECTIVE
To evaluate whether laparoscopic closure of a
PPU is as safe as conventional open correction.
SUMMARY BACKGROUND DATA
Laparoscopic surgery has become popular during the last
decade mainly because it is associated with fewer postoperative
complications than the conventional open approach.
It remains unclear, however, if this benefit is observed after
laparoscopic correction of perforated peptic ulcer (PPU).
• The study was based on a randomized controlled trial in which nine
medical centers from the Netherlands participated.
• A total of 109 patients with symptoms of PPU and evidence of air under
the diaphragm were scheduled to receive a PPU repair.
• After exclusion of 8 patients during the operation, outcomes were
analyzed for laparotomy (n = 49) and for the laparoscopic procedure (n =
52).


Operating time was significantly longer in the
laparoscopy group (75 min versus 50 min),
which is comparable to reports in the
literature [3, 10]
Laparoscopic correction of PPU causes less
postoperative pain [6, 12, 17, 18]
Open repair > Laparascopic
Open repair > laparascopic

Results of the LAMA trial confirm the results of other
trials that laparoscopic correction of PPU is safe,
feasible for the experienced laparoscopic surgeon,
and causes less postoperative pain.

Operating time was longer in the laparoscopic group
and there was no difference in length of hospital stay
or incidence of postoperative complications.