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 Past Medical History

DM HTN CKD (baseline Cr 2) Hyperlipidemia

Surgical History L BKA

Family History Mom/Dad-vasculopaths

Allergies None

Social History+ tobacco 1PPD+ ETOH (“few beers” weekly)

+ intranasal cocaine use

Medications Insulin Lisinopril Atenolol ASA Zocor Fish oil

Physical Examination

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

14.2N-80%

12.3272

136 100 25

2.3203.780

TB - 0.6AST - 45ALT - 35AP - 101

1.127.2

Amylase- 100Lipase 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 AirPortal Venous Air

Ischemia (most common) Sepsis (pseudomonas,

Clostridium) IBD Colon Ca Trauma Iatrogenic (endoscopic

procedures)

Portal Venous Air

Pneumobilia 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 Gastric Emphysema vs Emphysematous GastritisEmphysematous Gastritis

Both are causes of intramural gas in the stomach Both are causes of intramural gas in the stomach (foregut pneumatosis intestinalis) with different (even (foregut pneumatosis intestinalis) with different (even opposite) outcomesopposite) outcomes

Can be differentiated radiographically and clinically Can be differentiated radiographically and clinically between the benign (gastric emphysema) and serious between the benign (gastric emphysema) and serious (emphysematous gastritis) entities(emphysematous gastritis) entities

Gastric EmphysemaGastric EmphysemaBenign condition caused by disruption of the mucosa leading to airdissection into the gastric wall without associated wall thickening;can be associated with portal venous air as well

Causes include: GOO (PUD, pyloric stenosis, gastric volvulus) Increased gastric intraluminal pressure and superficial tear due to vomiting Partial/complete duodenal obstruction (pancreatic/ampullary Ca, duodenal

stenosis, gallstones, bezoars, SMA syndrome) Instrumentation (biliary stenting, NG tube placement, endoscopy, PEG) Cystic pneumatosis (benign idiopathic condition causing intraluminal air

bubbles) 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 EmphysemaGastric Emphysema

D’Cruz R, Emil S. J Ped Surg 2008; 43: 2121

Emphysematous gastritis 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 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

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

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 Intramural gas in the stomach (foregut pneumatosis intestinalis) may be due to gastric emphysema intestinalis) may be due to gastric emphysema (benign) or emphysematous gastritis (serious)(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