Intro to
Dworken (GI)
Intern Boot Camp
Jacob Sadik, PGY3
What You Will Learn
 How
to survive Dworken
 How to recognize when a GI patient is sick
 How to diagnose/manage a few commonlyencountered GI diseases
 (Biliary
disease, transaminitis, comprehensive
discussion on GIB, hepatitis and cirrhosis covered
in other boot camp lectures)
High-Yield Slides
Dworken
 Lksd
55 is your home
 2 interns, 1 senior, 2 fellows, 2
attendings (liver, GI)
 Spend time in the endoscopy
lab when you can!
 Your senior/fellow are always
there to help!!
The only stupid
question is the
one you didn’t
ask!
Dworken Patients
 Take




a GI-focused history
Prior GI diagnoses
Prior endoscopic studies (EGD, C-scope, CE, ERCP)
NSAIDs, anti-platelets, anticoagulation
Shadow of a doubt?...make NPO!
 Know
your overnight admissions well!!!
 Notify primary gastroenterologist re: admission
 Rectal exams on all bleeding patients (even if
done in the ED)
 No consults for hemoccult positive stools!!!
 OARRS…. is….everything
The OARRS Report
 Ohio
reporting system for narcotics and other
controlled substances
 Get access today!

https://www.ohiopmp.gov/Portal/Registration/Defa
ult.aspx
Case 1
A 56 y/o M with a h/o DMT2, DLD, PUD and EtOH abuse
arrives on Lksd 55 from the ED with a 1-week h/o
progressively worsening, gnawing epigastric abdominal
pain radiating to his back.
VS: T 36.1, P 118, R 20, BP 100/80, SpO2 96% RA
Orthostatics negative
FOCUSED EXAM:
HEENT: Sclera anicteric, no palatal jaundice
SKIN: No jaundice, +axillary sweat, no truncal
ecchymoses
ABD: Soft, ND, significant TTP over epigastrium without
peritoneal signs, no organomegaly
NEURO: AAOx3
PERTINENT LABS:
Hgb 15
BUN 10, Cr 0.9, lipase 4600
Acute Pancreatitis
Classification
 Type


Edematous, interstitial acute pancreatitis
Necrotizing acute pancreatitis
 Severity


Mild-mod (absence/transient organ failure <48 hrs)
Severe (persistent organ failure >48 hrs)
Acute Pancreatitis
Diagnosis
 Requires



2 or more of the following:
1) Acute, persistent, severe epigastric abdominal
pain (often radiating to the back)
2) Elevated serum lipase or amylase ≥3x upper limit
of normal
3) CT/MRI/ultrasound evidence of AP
 (NOTE:
imaging is not required for uncomplicated mild
AP if #1 and 2 are present)
Acute Pancreatitis
Initial Evaluation
 Assess
severity. ICU transfer may be indicated if 1
or more of the following are present:







P <40 or >150
SBP <80
RR >35
PaO2 <50 mmHg
pH <7.1
Anuria
Coma
Acute Pancreatitis
APACHE II SCORING SYSTEM
Acute Pancreatitis
“Surgical” Abdomen
 Be

concerned about…
Rigidity, guarding, rebound tenderness, illappearance
 Portable
KUB STAT
 Acute care surgery consult STAT
 ICU transfer


If no acute surgical intervention per ACS
Your senior/fellow will help you with this
Acute Pancreatitis
Think About Etiology…
 Gallstones***
 EtOH***
 Hypertriglyceridemia
(TG >1000s)
 Trauma (e.g. panc laceration, post-ERCP)
 Drugs

Steroids, azathioprine, Januvia, tetracycline,
furosemide, thiazides, flagyl, valproate, HAART,
etc..
 Infection
 Other
mechanical
 Autoimmune
 Toxins (e.g. scorpion sting)
 Hypercalcemia
 Idiopathic
Acute Pancreatitis
Supportive Workup
 RFP(includes
Ca) and CBC
 LFTs
 Lipid
panel (for TG level)
 Lactate
 Blood EtOH level (if indicated)
 Abdominal ultrasound
 ABG (if altered, SpO2 <90%, bicarb low, etc)
 CT abd/pelv with contrast


CAUTION in those with AKI
Diagnostic or to assess for complications in severe AP
 EUS/MRCP
vs. ERCP (in suspected or overt gallstone
pancreatitis)
Acute Pancreatitis
Management
 1)



 2)

 2)


 4)
Fluid resuscitation!!!
Generally ~>200 cc/hr
Decreases morbidity/mortality w/in the 1st 12-24 hrs
Monitor for improvement (via VS, BUN, Cr, Hct, UOP)
Pain control
IV opiates
Bowel rest
NPO  CLD  Soft, low-residue, low-fat, soft diet
NJ feeding (post-ligament of Treitz) > TPN/PPN
Metabolic/electrolyte correction
Acute Pancreatitis
AP Sequelae
 Non-discrete
peri-pancreatic fluid collections
 Walled off fluid collections (or “pseudocysts”)
 Necrotizing pancreatitis (+/- secondary infection)
 Pancreatic ascites
 Hemorrhagic pancreatitis
 Abdominal compartment syndrome
 Pseudoaneurysms
Acute Pancreatitis
Non-Discrete Fluid Collections
Acute Pancreatitis
Walled-Off Fluid Collections
Acute Pancreatitis
Pancreatic Necrosis
Acute Pancreatitis
Management of Infected
Necrosis
 Empiric
antibiotics with good pancreatic
penetration (e.g. carbapenems*, quinolones,
flagyl)
 Cover GNRs and anaerobes
 Trend towards conservative management with
ABx and observation for several weeks vs.
immediate surgical resection
 Limited role for CT-guided FNA
 Open/endoscopic partial/total necrosectomy
may eventually be required
Acute Pancreatitis
Hemorrhagic Pancreatitis
Cullen’s Sign 
 Grey Turner’s Sign
Acute Pancreatitis
Pancreatitis Take Home
Points
 Once

Dx is known, assess severity first
Does your patient need ICU level care?
 FLUIDS!
 Close
monitoring (VS, UOP, BUN, lactate, etc.)
 Etiology will help guide management
 Be mindful of complications
Case 2
A generous NF resident gives you an overnight patient. Pt
is a 56 y/o M who presents to the ED with a 1-week h/o
progressively worsening left quadrant/flank pain and
fever. Endorses associated anorexia, nausea and fatigue.
Had a colonoscopy ~1 week ago, revealing scattered,
non-bleeding diverticuli.
VS: T 38.2, P 100, R 22, BP 128/86, SpO2 100% on RA
FOCUSED EXAM:
GEN: Well-nourished CM in mod distress d/t pain
SKIN: No jaundice
ABD: Soft, ND, mild TTP over LLQ without peritoneal signs,
no organomegaly
NEURO: AAOx3
PERTINENT LABS:
WBC 13K with left shift, CRP 10
What is your DDx?
 Pyelonephritis
 Acute
uncomplicated/complicated diverticulitis
 Nephrolithiasis
 Iatrogenic microperforation
 Acute pancreatitis
 Infectious colitis
 Crohns disease
 CRC
 Acute appendicitis
What do you order next?
A CT scan! What is the Dx?
Acute Diverticulitis
Presentation
 Mean
age ~60s
 LLQ abd pain
 Fever
 Leukocytosis
 N/V/constipation
 Recurrence is ~20-40% after initial attack and
20% may have chronic abd pain
Acute Diverticulitis
Classification
 1)
Uncomplicated
 2) Complicated





Perforation
Abscess
Fistulas
Obstruction
Peritonitis
Acute Diverticulitis
Management
 Bowel
rest
 Antibiotics covering GNRs and anerobes


Amp/sulbactam, pip/tazo
May be transitioned to PO Augmentin prior to
discharge
 Pain
control with IV opiates
 +/- Surgery consult



Indicated for acute complications
Surgery decided on case-by-case basis
<40 y/o, R-sided disease, immunocompromised
Acute Diverticulitis
Management
 Colonoscopy
due at least 6-8 weeks out from
onset to exclude CRC

NOT during acute flare given risk of iatrogenic
perforation
Acute Diverticulitis
Your patient asks, “I read that seeds, nuts and popcorn are bad for
my diverticulitis. What do you think?
Case 3
You get called from the DACR at 6:50 because a 68 y/o F with
a h/o osteoarthritis and SLE (on chronic hydroxychloroquine
and prednisone) is in the ED complaining of a 2-day h/o
frequent black, tarry stools and lightheadedness. She has been
taking Ibuprofen for the past 7 days because of knee pain.
VS: T 37, P 120, R 24, BP 104/80, SpO2 99% on RA
Orthostatics negative
FOCUSED EXAM:
GEN: Lethargic, in NAD
HEENT: Conjunctival pallor, dry mucous membranes
ABD: Soft, ND, epigastric TTP without rebound/rigidity/guarding
NEURO: AAOx3
LABS:
Hgb 6.4 (baseline 12)
BUN 18, Cr 1.34, bicarb 18, K 3.2
Lactate 1.8
GIB
What else do you want to
know?
 Use
of NSAIDs, anti-platelets, anticoagulants
 Abdominal pain? Relation to food?
 Stool color, character, quantity
 Previous GIB
 Previous EGD/colonoscopy/CE?
 EtOH abuse
 H/o cirrhosis or visualized varices
 Primary thrombophilia
 Recent pepto or iron ingestion  darkens stools
GIB
Initial Management
 NPO
 CBCs
q6h and active T&S with blood consent
 RFP, LFTs, coags
 2 18-gauge (large-bore) PIVs
 Bolus NS/LR for orthostatic hypotension
 Stop all NSAIDs, anti-platelets and anticoagulants
 Hold pharmacologic DVT prophylaxis
 +/- NG lavage
 Oxygen as needed
 Abdominal pain?  KUB prior to endoscopy
 Transfer to ICU? (discuss with your senior)
GIB
Transfusion Goals
 Transfuse
pRBCs for Hgb <7 (consider <8 in
patients with cardiac disease)
 Transfuse platelets for…



Active bleeding with PLT <50K
Pre-procedural PLT <50K with/without bleeding
Any PLT <10K
 Transfuse
FFP for INR >1.5 in the setting of active
bleeding or pre-procedural in some cases
GIB
Prep Basics
 EGD


NPO
+/- erythromycin 3 mg/kg IV q8h (off-label) to clear
stomach contents for better visualization – ask GI
 Flexible

sigmoidoscopy or ileoscopy
Tap water enemas 30 minutes apart x 3 or until
clear
 Colonoscopy



Golytely “split-prep” (2L in the evening, 2L in the
early morning; i.e. 7PM, 3AM)
Movi-Prep (Gatorade)
NG tube if refusing PO
GIB
Concerning GIB
 Active
bloody bowel movements
 Hemodynamic instability
 Drop in Hgb >/= 2 gm/dL or poorly incrementing
Hgb after transfusion (1 unit pRBCs should bump
Hgb by 1-1.5 g/dL)
 Change in mental status or symptomatic
anemia
 REMEMBER!
Blood is a laxative.
Hemodynamically-significant GI blood loss will
present itself.
Case 4

Your covering the Dworken team pager on NF when
you are paged by nursing about a 36 y/o F with a h/o
ulcerative colitis who is having multiple, small-volume
bloody bowel movements. She has been taking
Keflex for the past week for a soft tissue infection.
What do you do?!?

Examine the patient
VSS? Pain? Mentation? Abd exam? DRE?





“Show me the stool!”
CBC STAT
Orthostatics
Send C.diff PCR!
IBD
IBD
 2nd-3rd

decade of life
Crohns disease has bimodal distribution (7th-8th
decade)
 Disease
predilection for developed countries
and the northern hemisphere
 Look for extraintestinal manifestations




Episcleritis, uveitis, iritis
Ankylosing spondylitis
Pyoderma gangrenosum
Eythema nodosum
IBD
Genetic
Predisposition
IBD
Immune
System
Dysregulation
Environmental
Triggers
IBD
Crohns Disease
 Risk
factors: smoking, “western” diet
 Protective factors: high-fiber diet
 Transmural bowel wall inflammation
 Entire GI tract (TI most commonly involved)
 “Skip” cobblestone lesions
 Rectal sparing
 Abdominal pain, diarrhea,
fatigue, weight loss, kidney
stones
IBD
Diagnosis of CD
 Colonoscopy
with intubation of the terminal
ileum and biopsy acquisition is the gold standard
 MRE is preferred for initial Dx of small bowel CD
 Consider CE in difficult-to-diagnose cases
 MRI or EUS to evaluate perianal CD
IBD
Tx Strategies in CD
 “Step-Up”
 Slow-release
5ASA for ileitis
 Sulfasalazine for
colitis
 Antibiotics
if not
improving
 Biologic
agent
 Immunomodulator
 “Top-Down”
 Biologic
agent
 Immunomodulator
 Slow-release
5ASA for ileitis
 Sulfasalazine for
colitis
IBD
Ulcerative Colitis
 Bloody
diarrhea, tenesmus, fecal urgency,
fatigue weight loss and sometimes fever
 DDx: infectious, ischemic, CD, radiation-induced
 High CRC risk
 Predisposition to C.diff colitis
 Erythematous, engorged
mucosa
 Rectal involvement with
continuous progression
 Crypt abscesses
IBD
Dx of UC
 Consider
flex sig if inpatient for severe active
flare due to risk of iatrogenic complications with
colonoscopy
 Colonoscopy if flare not severe
IBD
Acute IBD Flares
 Severe




flares
Fever (>/= 37.5C)
Tachycardia
Anemia (Hgb <7 g/dL)
Elevated inflammatory markers (ESR, CRP)
 Corticosteroids
 NPO
 Fluid
resuscitation
 Electrolyte correction
 Consider 5-ASA compound (for those who are
not on maintenance therapy)
IBD
Back to our Patient…
 Initiate
supportive care
 CRP, ESR, CBC, RFP, LFTs
 C.diff PCR, stool studies first
 If C.diff PCR negative, would start steroids
 High-dose 5-ASA compound (e.g. sulfasalazine)
Now you know a little bit about….
 The
Dworken team
 How to recognize a sick patient
 Prep Basics
 Acute pancreatitis
 Diverticular Disease
 GI bleeding (briefly)
 IBD (briefly)