Clinical Case Conference
Ranjeeta Bahirwani
August 25, 2010
Clinical Case
56 AAM with DM,HTN,CKD admitted with one day
h/o severe abdominal pain and nausea; pt reported being
in USOH until day of admission when he developed
severe crampy epigastric/RUQ pain (10/10 in intensity);
+associated nausea but no vomiting; no melena or
hematochezia, no F/C
+ cocaine use 1 day PTA
ROS: no weight loss, no early satiety, no
dysphagia/odynophagia
Clinical Case
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Past Medical History
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Surgical History
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DM
HTN
CKD (baseline Cr 2)
Hyperlipidemia
L BKA
Family History
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Mom/Dad-vasculopaths
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Social History
+ tobacco 1PPD
+ ETOH (“few beers” weekly)
+ intranasal cocaine use
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Medications
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Allergies
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None
Insulin
Lisinopril
Atenolol
ASA
Zocor
Fish oil
Physical Examination
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VS: T - 98.0, HR – 88, BP - 160/74, RR – 16, O2 Sat - 99% RA
GEN: NAD
HEENT: no scleral icterus-did not assess for deviated
septum etc etc
CV: RRR
Chest: CTA B
Abd: soft, obese, mild epigastric TTP, no rebound/guarding
Ext: L BKA
Laboratory Data
12.3
14.2
136
100
25
272
80
3.7
N-80%
1.1
27.2
TB - 0.6
AST - 45
ALT - 35
AP - 101
20
2.3
Amylase- 100
Lipase 140
Lactic acid- 4.6
Clinical Case
What’s your differential diagnosis and what
would you do next?
CT scan
Clinical Case
What next?
Endoscopy
Portal Venous Air
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Ischemia (most common)
Sepsis (pseudomonas,
Clostridium)
IBD
Colon Ca
Trauma
Iatrogenic (endoscopic
procedures)
Portal Venous Air
Pneumobilia
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Air in the biliary tree
Commonly seen in patients following biliary-enteric
anastomosis or sphincterotomy
Nonsurgical causes of pneumobilia include infection,
neoplasm, biliary-enteric fistula, emphysematous
cholecystitis and incompetence of the sphincter of Oddi
Biliary vs Portal Venous Air
Gastric Emphysema vs
Emphysematous Gastritis
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Both are causes of intramural gas in the stomach
(foregut pneumatosis intestinalis) with different (even
opposite) outcomes
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Can be differentiated radiographically and clinically
between the benign (gastric emphysema) and serious
(emphysematous gastritis) entities
Gastric Emphysema
Benign condition caused by disruption of the mucosa leading to air
dissection into the gastric wall without associated wall thickening;
can be associated with portal venous air as well
Causes include:
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GOO (PUD, pyloric stenosis, gastric volvulus)
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Increased gastric intraluminal pressure and superficial tear due to vomiting
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Partial/complete duodenal obstruction (pancreatic/ampullary Ca, duodenal
stenosis, gallstones, bezoars, SMA syndrome)
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Instrumentation (biliary stenting, NG tube placement, endoscopy, PEG)
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Cystic pneumatosis (benign idiopathic condition causing intraluminal air
bubbles)
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PTX or rupture of pulmonary bullae with dissection of mediastinal air through
paraesophageal tissues into stomach)
Clinical manifestations are non-specific including abdominal pain,
distension, N/V
Gastric pneumatosis after NG
Zenooz NA, Robbin MR, Perez V. Emerg Radiol 2007; 13: 205
Zenooz NA, Robbin MR, Perez V. Emerg Radiol 2007; 13: 205
Gastric Emphysema
D’Cruz R, Emil S. J Ped Surg 2008; 43: 2121
Emphysematous gastritis
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Phlegmonous gastritis formed by gas forming organisms arising
from local spread through the mucosa or distant hematogenous
dissemination
Stomach affected very rarely due to acidity and efficient mucosal
barrier
Common organisms include Enterobacter species, Pseudomonas,
Candida, Staph aureus, Clostridium Welchii, Streptococcus
Intramural air on imaging which is streaky and irregular/mottled
(without rounded air bubbles as in gastric emphysema), with
associated gastric wall thickening
Associated with ancillary findings of ischemia (bowel wall
thickening, arterial occlusion, PV air, mesenteric venous
engorgement, infarction of other organs
High mortality without surgical intervention
Emphysematous gastritis
Soon MS, Yen HH, Soon A et al. Worl J Gastroenterol 2005; 11:1719
Vascular supply
Gastric Ischemia
Quentin V, Dib N, Thouveny F, et al. Endoscopy 2006; 38: 529
Cocaine-induced ischemia
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Vasoconstriction via norepinephrine/dopamine release
Increased platelet aggregation leading to intravascular
thrombosis (increased thromboxane A activity and
decreased prostacycline activity)
Focal endothelial injury of the microvasculature causing
a fall in cardiac output
**Rectal and gastric involvement are NOT a common
feature of cocaine induced ischemia, reflecting the rich
arterial supply of these regions
COCAINE ASSOCIATED
ENTEROCOLITIS
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Retrospective review of 18 patients with cocaine induced
enterocolitis
Anatomical locations of disease were: proximal colon (14
pts), distal colon (3 pts), and small bowel/gastric (1 pt)
72 % patients had intranasal cocaine use (most common)
Onset of symptoms was within 72 hrs for most patients
17% total mortality
15 patients were managed conservatively and 13 had an
uneventful recovery-(one pt died of shock, one had
laparotomy for peritonitis)
Surgical intervention was performed in 4 patients (for
peritonitis); 2 died post-operatively
Ellis CN, McAlexander WW. Dis Colon Rectum 2005; 48: 2313
Take Home Points
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Portal venous air is most often seen in the setting of
ischemia
The stomach is an uncommon site for ischemia due to
its rich vascular supply
Intramural gas in the stomach (foregut pneumatosis
intestinalis) may be due to gastric emphysema
(benign) or emphysematous gastritis (serious)
Cocaine-induced ischemia is most common in the
proximal colon and resolves with conservative
management in the majority of cases