This 47-year-old male presented with abdominal pain and fever and was found to have a contained perforated duodenal ulcer. He had a history of diabetes, hypertension, cholecystectomy, and pancreatitis. Imaging revealed distention of the left colon, air fluid levels, and stranding around the pancreas. He underwent laparotomy which showed a contained anterior duodenal ulcer perforation resulting in a large left subphrenic abscess. The abscess was drained and the perforated ulcer was sutured. Diabetics are at higher risk for complications of peptic ulcer disease such as perforation due to reduced pain sensitivity.

1. Case Presentation
Kristina DeMarco ANP-BC
7/16/17
NURS 664

2. Chief Complaint & HPI
CC-Abdominal pain and fever.
HPI-This is a 47 year old male with a hx of CCY, HPTN, and DM who is
currently intubated in the ICU. HX is per chart and wife: Pt had 2
recent evaluations for upper abdominal pain, nausea, vomiting and
non bloody diarrhea in the last 7 days. Out patient labs and
Abdominal Xray were unremarkable and stool studies for enteric
pathogens were normal. He was started on PPI, and advised to stay
on liquid diet. He was given a referral to a local gastroenterologist if
symptoms persisted. He was presumed to have infectious
gastroenteritis. He returned to the ED yesterday with fever, SOB,
and severe stabbing, radiating to the right shoulder, upper
abdominal pain more intense on the left side since last night.

3. Medical/Family/ Social History
PM/SHX
Diabetes for 5 years
Neuropathy
Hypertension
CCY 2 years ago
Hemorrhoidectomy
Pancreatitis X 3 10 years ago
Family HX-Mom alive HX DM, Dad with HX of CAD, 2 Br hx DM
SOC HX-Drinks heavily more than 10 years ago. Sober. No hx of tobacco
or drug use. Married and works in sales.

4. MEDICATION
Medications Prior to admission-
Metformin
Quinapril
ASA 81 mg
OTC
Pepto Bismol (last 3 days)
Mylanta
Omeprazole
Acidophilus

5. Upon admissionUpon admission --Plain x-ray of chest and abdomenPlain x-ray of chest and abdomen
revealed distended left colon, air fluid levels in the SB andrevealed distended left colon, air fluid levels in the SB and
left colon, and an elevated left diaphragm. This wasleft colon, and an elevated left diaphragm. This was
followed by a CT scan of the abdomen and pelvis withfollowed by a CT scan of the abdomen and pelvis with
contrasts. No free air. Duodenal thickening and pericontrasts. No free air. Duodenal thickening and peri
pancreatic stranding are noted at the HOP. Amylase levelpancreatic stranding are noted at the HOP. Amylase level
was slightly elevated.was slightly elevated.

6. At this point:
1. What do you suspect most strongly in
your differential and why?
2. What pertinent facts will you promptly
try to elicit from pt’s family while he is
unable to speak for himself?

9. A little more info
His wife mentions to you that his mild to moderate upper
abdominal pain became more severe approximately 20-
30 minutes after any meal or in the middle of the night.
He has had frequent belching, and that he began to take
Pepto Bismol for his symptoms 3-4 days go.
She also reports that he used to drink heavily 10 years
ago. No prior GI bleed. He did have 3 admission for
pancreatitis while he was an active drinker. He had his
GB removed for continued pain and the presence of GB
sludge.

10. Questions
The pt has black heme positive stool. Is this a reliable
finding?
Does a hx of pancreatitis, DM with neuropathy and
alcohol abuse lead you down other paths in your
differential?

11. Physical Exam Highlights
 BP 100/58, Pulse 110 min, Temp 101.8 F, RR 22, Oxygen Saturation 96%
on RA
GENERAL-Toxic appearing in obvious pain.
HEENT-Anicteric, orally intubated. No JVD.
LUNGS-CTA&P, Decreased @ Left base.
HEART-S1S2 REG, –MRG, 119/min. PMI non displaced.
ABD-Asymmetry with moderate distention of the LUQ. Upper abdominal
tenderness L>R. Guarding but no rebound present. No shifting dullness or
fluid wave.
RECTAL exam with dilated rectum without stool or blood.

12. Diagnostic Testing
 Chest Xray
 Abdominal Xray
 Abdominal US
CMP, CBC diff
Amylase, Lipase
Lactate, procalcitonin
Pt, PTT, D-dimer
Suggested by current
literatureDiagnostics
 Plain film upright ABD xray and CXR if free
air/stop.
 If no free air-spiral CT abd/pelvis with
water soluble contrast. This is superior to
US.
 FOBT-considered variable and unreliable.
False positive with Pepto Bismol
AZER, 2016.
Anand 2017.

13. Blood results
CBC 18.2> 9.9<109,000
27 MCV lo
Iron
TIBC
38
482
BMP BUN 47 146 113 >180
CR 1.9 2.9 20
Ferri-
tin
14
LFT SGOT-nl
SGPT-nl
ALK PHOS 210
TBILI nl
ALB 2.8
ABG PH 7.38
PcO2 36
PO2 90
HCO3 24
40 percent Fio2
Amylase
Lipase
250
nl
PT
PTT
Normal
D Dimer Elevated Type
/cros
s
Lactate Elevated
Procalci-
tonin
Elevated

14. Free air under diaphragm
taken from Dheer

15. free
perforation

16. Free air
perforation

17. 3 days later3 days later -an abdominal US was done and revealed-an abdominal US was done and revealed
leftleft sub-diaphragmatic abscesssub-diaphragmatic abscess and pt was taken to theand pt was taken to the
OR for a laparotomy, and drainage of a large leftOR for a laparotomy, and drainage of a large left
subphrenic abscess. Exploration revealed that this ptsubphrenic abscess. Exploration revealed that this pt
had a contained anterior duodenal ulcer perforationhad a contained anterior duodenal ulcer perforation
resulting in abscess formation and sepsis. The DU wasresulting in abscess formation and sepsis. The DU was
sutured and an omental patch was performed. Thesutured and an omental patch was performed. The
abscess was causing extrinsic compression of theabscess was causing extrinsic compression of the
bowel and elevation of the left hemi-diaphragm. Oncebowel and elevation of the left hemi-diaphragm. Once
the abscess was drained, the dilation of the left colonthe abscess was drained, the dilation of the left colon
that was extrinsically compress, resolved.that was extrinsically compress, resolved.

18. My Treatment Recommendations
Admit to ICU
NPO
Normal Saline 150 cc/h
Protonix 80 mg bolus followed by 8mg per hour
continuous infusion
Stat blood culture times 2
Invanz 1 gm IV daily after culture
1
https://www.uptodate.com/contents/overview-of-the-complications-of-peptic-ulcer-
disease?source=search_result&search=perforated%20duodenal
%20ulcer&selectedTitle=1~106ferences for treatment

19. My Treatment Recommendations
Suggested Consultations
Surgical Consultation-to determine if urgent
surgery is necessary.
IR evaluation for possible percutaneous
drainage of contained abscess
Gastroenterology-is endoscopy indicated

20. TREATMENT
 Coordination of care — Medicine, Intensivist, Gastroenterologist,
Surgery, and interventionalists. Early collaboration with team and
family.
 NPO
 Urgent surgery is necessary in patients with uncontrolled
hemorrhage or with a perforated ulcer with continued leakage.
Depending on the site of perforation and the condition of the
surrounding are, a patch vs partial gastrectomy may be performed.
 H pylori testing is indicated-best done with stool antigen or direct
collection. In this case, the patient was negative.

21. Evidence-Based Literature
Diagnostic options in suspected DU.
Endoscopy has become procedure of choice in suspected
DU. Direct visualization. Treatment and sampling
capacity. Invasive and costly. Risks.
Double contrast UGI series-single contrast may miss up to
40% of DU whereas double contrast images can pick up
as many as 95% DU > 10mm. Not good if recurrent. No
specimen or treatment.
CT and Ultrasound are best at visualizing subphrenic
collections. They are a common sequella of perforated
DU.
Dheer*

22. Evidence-Based Literature
DU occurs in 10 percent of the adult population.
Perforation should be suspected with sudden, severe
diffuse pain.
 Perforation will complicate up to 10 % PUD. Of those
60% will be DU, 20% antral, and 20% gastric body
1/3 of PUD=DU
Typically benign whereas GU may be malignant in 5% of
cases.

23. Evidence-Based Literature

24. PATHOPHYSIOLOGY
Leakage of Gastric and duodenal contents -severe chemical
peritonitis.
If food particles leak- bacterial peritonitis develops.
Distal Small Bowel contain aerobes and anaerobes such as
E.coli and bacteroides fragilis.
Bacteria in the peritoneal cavity-influx of inflammatory cells
leading to localization, phlegmon, local hypoxia, more
bacteria….abscess, sepsis, bacteremia
Contained perforation occurs when adjacent organs slow
the process and wall it off.

25. Pathophysiology
Gastric and duodenal mucosa are protected with mucous
impermeable to acid and pepsin. Other cells produce
bicarb. Prostaglandin E aids in mucous and bicarb
production. When there is imbalance between acid
production and mucosal defenses-injuries occur.
NSAIDS
HPYLORI-alkalinizes and survives was causing
inflammation
BILE SALTS
ACID
PEPSIN

26. ACID SUPPRESSION THERAPY-intravenous
pantoprazole, omeprazole, 80 mg bolus followed by 8 mg/hr
infusion. Lower-dose continuous infusions and bolus
intravenous dosing may produce comparable results. Both are
reasonable.
Intravenous form takes effect within minutes and can decrease
the rate of active bleeding by rapid and profound acid
inhibition on fibrin formation and ulcer healing.
If surgery is indicated for perforation, it should not be
delayed. Perforation – Persisting or advancing signs of
peritonitis and a preoperative delay of greater than 12 hours
increase risk of death. Perforated gastric ulcers appear to have
a poorer prognosis than duodenal ulcers.
.
Evidence-Based Literature

27. Evidence-Based Literature
Comorbid disease, bleeding, perforation, ulcer size,
advanced age, malnutrition, hypotension, ARF, metabolic
acidosis all impact mortality in complicated peptic
disease. In a large population study, diabetic patients
had significantly increased 30-day mortality from ulcer
bleeding and perforation.

28. Follow Up
Treatment of H. pylori — 61 percent of DU pts
(non NSAID users) are positive for Pylori
H. pylori- critical to confirm successful
eradication of the organism
If H pylori testing is negative-it should be repeated
in this population of patients as bleeding and PPI
can create a false negative result
 Anand*

30. Prevention & Anticipatory Guidance
3 PHASES OF Free ULCER PERFORATION
1.Within 2 hours-sudden and severe abdominal pain. 1st
epigastric and then diffuse, may radiate to the top of the
shoulders.
2.Within 2-12 hours-Board-like rigidity. Pain improves.
Now worsens with movement. AS acidic fluid spreads
through cavity lower abdomen will become more
uncomfortable.
3.>12 hours-Worse distention but less pain. Fever and 3rd
spacing into abdomen.
WALLED OF/CONTAINED PERFS HAVE MORE
LOCALIZED SYMPTOMS
1.Uptodate*

31. Lessons Learned
SYMPTOMS —“silent” ulcers in whom complications
develop with no heralding dyspeptic symptoms to bring
them to timely medical attention. Pt with bleeding ulcers
may have lower visceral sensitivity.
Additionally, this pt. is a diabetic with neuropathy which
impacts his pain response.
 A picture is just a picture-patients with sudden change in
pain intensity, character or quality with minimal CT
findings warrants a surgical evaluation.

32. Lessons Learned
The atypical presentation of this patient led to a delay in
diagnosis and surgery. He had a favorable outcome with
minimal post operative complication. He was Hpylori
negative and will be retested in the future.
An outcome measure meaningful to this pt and staff is
that of effectiveness of 72 hour PPI GTT over bolus PPI.
Initial bleed and rebleed in those on 72 hour minimum,
drip compared to BID oral and IV therapies. Impact on
Readmits for UGI bleed?

33. Atypical DU presentations
Pneumothorax, pneumo-mediastinum,
Tension pneumo-peritoneum,
Retroperitoneal du perforation presenting as scrotal
sepsis
Duodenal Kissing Ulcer (contained anterior perforation
and posterior hemorrhage) Govaresh/vol.15, no.3,
Autumn 2010: 243-246

34. References
Peptic Ulcer Disease; predictors of poor outcomes. Retrieved from
https://www.uptodate.com/contents/overview-of-the-complications-of-
peptic-ulcer-disease
Anand, B.S.(2107). Peptic Ulcer disease. Retrieved from
http://emedicine.Medscape.com/article/181753-overview
Azer, S. (2016). Intestinal perforation. Retrieved from
http://emedicine.Medscape.com/article/195537overview#a9
Dheer, A.K. (2015). Imaging of duodenal ulcers. Retrieved from
http://emedicine.Medscape.com/article/367878-overview
Vahedian, J., (Sealed anterior perforated DU combined with hemorrhagic
posterior ulcer): Report of a case. Govaresh, 15, 243-246.