Tag Archives: Gastroenterology

AST/ALT in thousands… Acute Hepatitis A! 3/12/2019

Thanks to Kevin and Brayden for presenting a 36yo F with no medical history presenting with acute abdominal pain, nausea, and anorexia. Her AST/ALTs were in the thousands and she was ultimately diagnosed with acute hepatitis A! Incidentally her HB Core Ab came back “borderline…”

AST ALT Elevation

  • If AST/ALTs are in the thousands, there are only a few entities that can cause this:
    • Ischemia (shock liver)
    • Toxins (Tylenol is most common), Amanita aka magic mushrooms, herbal supplements (we don’t know what they put in these!)
    • Acute viral hepatitis (HAV, HBV, HCV, HEV, HSV, CMV, VZV, parvovirus)
  • Less common:
    • Autoimmune hepatitis
    • Acute Budd Chiari
    • Reactivation HBV, HDV
    • HLH (we seem to see this a lot in this hospital for some reason?)
    • Malignant infiltration
    • HELLP
    • Wilsonian Crisis (severe hemolysis and impending acute liver failure in setting of Wilson’s)
  • For acute viral hepatitis, ALT is typically higher than AST.

Hepatitis A


  • Global, 1.4 mil cases per year, can be sporadic or epidemic form
  • Fecal oral route, either person-to-person contact or ingestion of contaminated food or water.
  • Other risk factors: Sexual transmission (anal/oral sex), day care, consumption of raw or undercooked shellfish, veggies, or eating food prepared by an infected food handler.


  • Incubation period: 15-50 days, average of 28 days.
  • Acute onset N/V, fever, anorexia, abd pain are typical.
  • Bilirubinuria, pale stools can also be seen within a few days.
  • Jaundice + pruritus. Jaundice peaks within 2 weeks.
  • Exam: Jaundice, hepatomegaly, RUQ pain.
  • Serum aminotransferases often > 1000 IU/dL, bili typically < 10, alk phos can be nrl to mildly elevated. ALT is commonly higher than AST.
  • Kids: Can be asymptomatic.


  • Serum Anti-HAV IgM is diagnostic, detectable at time of symptom onset, remain detectable for 3-6 months after infection.
  • Anti-HAV IgG: remain detectable for decades, protective vs future infections. Detection of anti-HAV IgM and IgG reflects past infection or vaccination.


  • Primarily supportive, but transfer to a transplant center might be indicated if pt goes into fulminant liver failure (severe acute liver injury with encephalopathy and impaired synthetic function i.e. INR >5 in patients without pre-existing liver disease)
  • Report to public health! Fax a confidential morbidity report over to Santa Clara County Department of Public Health


  • Single Antigen inactivated virus: 2 IM doses 6-18 months apart
  • Combo HAV and HBV inactivated virus vaccine: Adults only, 0, 1, 6 mo (3 doses total)


  • Generally pretty good, less than 1% go into fulminant hepatic failure.
  • Risk factors for severe complications: > 50, underlying liver dz
  • Other Complications
    • Relapsing hepatitis: Up to to 10% of pts experience a relapse of sx 6 months after the acute episode for ~ < 3 weeks. Multiple relapses can occur. These patients usually make a complete recovery
    • Autoimmune hepatitis: HAV can trigger development of autoimmune hepatitis.
    • Cholestatic hepatitis: Prolonged period of jaundice > 3 months, typically self-resolving

Hepatitis B serologies made ridiculously simple


Disseminated cocci

Today, we talked about a middle aged man presenting with acute onset of abdominal pain and weight loss, found to have a consolidation on chest imaging, low SAAG ascites, and a nodular omentum, work up revealing disseminated cocci! For more cases like this, check out http://www.humandx.org.  If you’d like to hear some expert diagnosticians take a crack at this case and learn from their reasoning, check out thecurbsiders.com.

Clinical Pearls: 

  • Patients with immunosuppression, pregnancy, and DM2 are at risk of developing disseminated cocci.
  • The most common manifestation of cocci is pneumonia which can be consolidative, nodular, or cavitary.  Other manifestations include the skin (erythema nodosum and erythema multiforme), joints (arthralgias, vertebra, osteo), meningitis, SSTI, and visceral organs (rare).
  • Cocci should be on your differential of infections that can cause eosinophilia and a low SAAG ascites.

Approach to eosinophilia

  • Neoplasm ⇒ hypereosinophilic syndrome, T cell lymphoma, hodgkins lymphoma, solid organs (cervical, ovarian, gastric, colon, and urothelial cell carcinoma)
  • Allergies ⇒ atopy, medication induced 
  • Adrenal insufficiency ⇒ rare cause
  • Connective tissue disease ⇒ EGPA (formerly known as Churg Strauss), RA
  • Parasites/infections
    • Parasites: strogyloides, toxocara, lymphatic filariasis, isospora, dientamaeoba, sarcocystis (note Giardia does NOT cause eosinophilia) 
    • Viruses: HTLV, HIV
    • Fungi: aspergillus (ABPA), cocci, paracocci, histo, crypto
  • Primary eosinophilic syndromes (typically single organ involvement of eos, may not have blood eosinophilia) ⇒ eosinophilic fasciitis, eosinophilic cellulitis 

Differential for ascites based on SAAG

  • <1.1
    • Peritoneal carcinomatosis
    • Infections (tuberculosis, bacteria, fungi including cocci, schistosomiasis)
    • Pancreatitis
    • Biliary ascites
    • Serositis
  • >1.1
    • Portal HTN
      • Liver (cirrhosis, acute failure, alcoholic hepatitis, budd chiari, mets)
      • CHF

Coccidioidomycosis: Refer to this prior post on our blog for more details.

  • Micro
    • Airborne fungal infection transmitted by cocci immitis and cocci posadasii
  • Epi
    • Geographic distribution is southwest US and central valley
    • Most common time for transmission is summer and fall seasons
  • Risk factors for developing severe disease
    • Immunosuppression (HIV with CD4 <250, steroids, chemo)
    • Pregnancy
    • DM2 (more likely to develop cavitary disease)
  • Clinical manifestations
    • Incubation period is 7-21 days
    • Primary manifestation is CAP
    • Other manifestations
      • Skin: erythema nodosum and erythema multiforme
      • Joints: arthralgias (desert rheumatism), osteo of joints and vertebrae
      • Meningitis
      • SSTI
      • Visceral organs and omentum (rare)
  • Testing:
    • Imaging (CXR can be normal in 50% of patients)
    • Serologies:
      • Cocci EIA to screen
      • Cocci immunodiffusion and complement fixation to confirm
  • Treatment
    • Immunocompetent and minimal symptoms? No treatment, most resolve spontaneously
    • Severe disease/disseminated
      • First line is fluconazole or itraconazole
      • If no response, can try posaconazole
      • Last resort is amphotericin B
    • Duration of treatment can be up to a year
    • Repeat anti-coccidioidal Abs in 2-4 weeks after starting treatment to ensure treatment response

Dieulafoy lesion causing obscure overt GI bleed!

Today we talked about an elderly man with recent ACS on DAPT, HFrEF 25%, and h/o colonic angiodysplasia induced LGIB who presented with acute onset of obscure overt upper GI bleed, found to have a dieulafoy lesion on repeat EGD!

Clinical Pearls

  • Overt GI bleed refers to bleeding that is clinically evident (i.e. hematemesis, hematochezia, melena, etc.)
  • Occult GI bleed refers to slow bleed that primarily manifests as iron deficiency anemia and/or positive guaiac stool.
  • Obscure GI bleed refers to evident GI bleed without a clear source on EGD/colo.
    • Most common cause is angiodysplasia
    • First step in the work up of obscure GI bleed is to repeat EGD/colo.  Up to 50% of cases are successfully diagnosed this way.
  • Tachycardia is the first sign of blood loss and suggests up to 30% total blood volume loss.  Hypotension develops once blood loss >30%.
  • For people at high risk of thromboembolic events requiring anticoagulation, restart anticoagulation/antiplatelet therapy as soon as possible after acute bleeding is resolved (prior to discharge!). Be sure to discuss risk of rebleeding with endoscopist prior to restarting these agents.

Obscure GI bleed


The following is a simplified breakdown of diagnoses to consider in obscure GI bleed.  Keep in mind that many diagnoses can present as overt or occult GI bleed.  We have listed them here under the more common way in which they present:

Obscure GI bleed breakdown

  • Remember that NSAID induced ulcers can occur anywhere in the GI tract as far distally as the splenic flexure!
  • Angiodyplasia is the most common cause of obscure GI bleed.

Work up:

  • Repeat EGD/colo is the first step.  Up to 50% of the cases are diagnosed in this way.
  • If EGD/colo inconclusive, then
    • Obscure active bleed
      • Tagged RBC scan: technetium 99m-labeled RBC or sulfur colloid nuclear scans. Can detect slow bleeds with accuracy varying from 24-91%.  They can only identify a general area where bleeding is occurring (not accurate) and a follow up separate intervention is indicated if a source is identified.
      • Angiography: Can identify faster bleeds, more effective at localizing bleed, but less sensitive than tagged RBC (27-77%). Allows intervention at the same time.
      • Enteroscopy: push, single/double balloon enteroscopy are sensitive (up to 80%) and allow for intervention but are operator dependent and may not always be available
      • Intraoperative endoscopy: laparotomy or laparoscopy (sensitivity 58-80%). Last resort.
    • Obscure occult bleed
      • Capsule endoscopy: allows for imaging of the small bowel and can has a high sensitivity (83%). May be difficult to localize lesion based on imaged. Not a good tool in active bleed.
      • Enteroscopy as noted above


  • Treat the underlying etiology!
  • In the case of dieulafoy lesions, treatment with electrocautery, hemoclips, argon plasma coagulation, injection therapy, or a combination is effective.
  • For people with DAPT or on anticoagulation with warfarin, the current recommendation is to start these agents as soon as hemostasis is achieved.  The decision on when to start depends on the type of lesion, risk of bleed (based on edoscopist’s opinion), and risk of thromboembolic event (based on this cohort study and this meta-analysis).

Hemodynamics in GI bleed:

  • Tachycardia is the first vital sign abnormality in GI bleed and is noted with 15-30% blood volume loss.  With lower amounts of blood loss, tachycardia may be present upon standing.  If a patient is tachycardic while laying supine, blood loss is closer to 30%.
  • Blood loss >30% total body volume results in hypotension.  This typically begins as a widening of pulse pressure (drop in diastolic BP) followed by a drop in systolic BP.


Infected Pancreatic Pseudocyst 12/10/2018

Leah presented a case of a young/early middle age man (45 years old) with a history of NIDDM2 and two prior episodes of pancreatitis (unclear etiology) presenting with worsening abdominal pain for 2 weeks, with associated nausea and vomiting. His appetite has also been poor for the past 3 months, subjectively losing 120lbs over this time period. For the 2-3 days prior to presentation, he started endorsing fever and chills in addition to worsening abdominal symptoms…

CT AP revealed  a necrotizing pancreatitis with large multilocular thick-walled infected pseudocyst with associated phlegmon and serpiginous fluid. Ultimately the patient likely has chronic pancreatitis complicated by development of pseudocyst and walled-off pancreatic necrosis.

Fortunately he is clinically stable, pending endoscopic necrosectomy for definitive management.

Since acute pancreatitis gets all the rage attention, we will actually spend some time on chronic pancreatitis and discuss potential complications from this condition.

Just a quick recap on acute pancreatitis though…

Acute Pancreatitis

Etiology (I GET SMASHED)

  • Idiopathic, IGG4
  • Gallstones (40%)
  • Ethanol (35%)
  • Trauma
  • Steroids
  • Mumps/Malignancy
  • Autoimmune
  • Scorpion stings
  • Hypercalcemia/Hypertriglyceridemia
  • ERCP (4% of pts who undergo ERCP)
  • Drugs (1%, thiazide, Lasix, HIV meds)

Diagnosis: 2/3 required

  • Acute epigastric pain
  • Elevated lipase or amylase 3x ULN, lipase has much better sensitivity and specificity
  • Imaging findings
    • US: 1st line, rule out GS, obstruction
    • CT with con pancreatic protocol: Indicated when suspecting necrotizing pancreatitis or clinical deterioration

General Management Strategies

  • Volume: aggressive fluid resuscitation, 250-500cc/hr
    • LR has improved outcomes vs NS! Check out this and this article.
  • Pain control
  • Nutrition
    • Mild cases: PO within 48 hours, low fat/low residue diet ok
    • Severe cases with organ damage: Start enteral nutrition via NJ or NG if not eating by 3-4 days, early nutrition improves outcome.
      • Consider TPN if unable to tolerate enteral feeding

Chronic Pancreatitis

Definition: Persistent inflammation of the pancreas, resulting in permanent functional and structural damage.


  • 50% from alcoholism, M > F, other risk factors include smoking.
  • A type of pancreatitis is more common in kids and young adults patients from tropical regions, known as tropical pancreatitis.
  • Certain genetic disposition

Pathophysiology: Not well understood but there are theories

  • Chronic pancreatic ductal obstruction due to protein plugs from protein-bicarb imbalance, overtime calcifies, overtime leading to fibrosis
  • Necrosis-fibrosis: Repeated attacks of acute pancreatitis with tissue necrosis. Fibrotic tissues gradually replace the necrotic tissue, leading to development of chronic inflammation.


  • Might see the classic triad of abdominal pain, diabetes, and malabsorption.
  • Abdominal pain, chronic and often post-prandial, becomes more continuous as disease progresses.
  • Pancreatic insufficiency: steatorrhea, flatulence, distension, weight loss, fatigue, malnutrition


  • Pseudocyst (can occur 4 weeks after an acute episode or any time with chronic pancreatitis)
  • Bile duct or duodenal obstruction
  • Pancreatic ascites or pleural effusion due to disruption of the pancreatic duct
  • Splenic vein thrombosis, which can lead to gastric varices (which this patient actually has!)
  • Pseudoaneurysms of arteries
  • Inc risk of pancreatic adenocarcinoma. Those with hereditary or tropical forms are at high risk.


  • XR: May see calcifications but only in 30% of cases
  • CT: also not sensitive, may be normal early on
  • MRCP is better than CT with IV Secretin
  • EUS: High sensitivity, low spec (low rate of false negative, high rates of false positive)
  • Pancreatic function test, usually indirect i.e. serum trypsinogen, 72H fecal fat after a high fat diet (demonstrates steatorrhea but cannot establish cause of the malabsorption), fecal chymotrypsin and elastase concentration)


  • Pain control, often difficult, opiates, TCA, SSRI, gabapentin have been used with mixed results
  • Pancreatic enzyme supplements
  • Diabetes management
  • Smoking cessation, alcohol abstinence
  • Low fat diet (<25g/day) to reduce pancreatic enzyme secretion
  • ERCP

Prognosis: Generally prognosis is pretty poor once you have chronic pancreatitis



  • Usually > 4 weeks after onset of acute episode, 5-16% of cases. Starts out as peripancreatic fluid collection, progresses to pseudocyst beyond 4 weeks.
  • Can occur in both acute and chronic pancreatitis
  • Alcohol use related chronic pancreatitis is associated with highest incidence of pseudocyst formation.


  • Encapsulated fluid collection, pseudo because the cyst wall lacks epithelial or endothelial cells.


  • Uncomplicated: Asymptomatic to mild pain, can also lead to early satiety, nausea/vomiting
  • Complicated:
    • Gastric outlet or duodenal obstruction
    • Large vessel compression
    • CBD compression
    • Infected pseudocyst (10%)
    • Hemorrhage, UGIB
    • Pancreatico-pleural fistula


  • CT: Well circumscribed, usually round or oval, homogeneous, all fluid
  • Transcutaneous or endoscopic US
  • ERCP (diagnostic and therapeutic in some cases)

Routine Management

  • Observe, with serial imaging.
    • Likelihood for resolution dec if persistent for  > 6 weeks, e/o chronic pancreatitis, pancreatic duct anomaly is present, or thicker-walled pseudocyst.
  • Supportive Care
    • Pain control
    • Nutritional support
    • PPI

Complication management

  • Drainage is indicated when:
    • Evidence of infection
    • Mass effect causing ductal or duodenal blockage or pancreatic ductal stricture
    • Perforation
  • Endoscopic drainage: Preferred over percutaneous
    • Criteria (higher chance of success if the following are met):
      • Fluid collection has to be mature with well defined wall and mostly liquid,
      • The wall of the cyst must be adherent to stomach or duodenum
      • Fluid collection must be at least 6 cm in size.
  • Drainage approaches:
    • Transmural: Drain out via the stomach or duodenum
    • Transpapillary: Drain via pancreatic duct
  • Contraindication of endoscopic intervention:
    • Pseudoaneurysm, associated with fatal hemorrhage, due to erosions of the gastroduodenal or splenic artery, suspect if drop in H&H or e/o GIB or sudden expansion.

Mirizzi Syndrome

Thanks to Richard for presenting the case of a middle-aged man who presented with acute onset of lower back pain, intermittent abdominal pain, and emesis, found to be septic, work up revealing Mirizzi syndrome causing acute cholangitis which led to klebsiella bacteremia and L spine osteomyelitis! Whoosh!

Clinical Pearls

  • Klebsiella is found along the GI tract and can cause UTIs, pneumonias, osteomyelitis, GI infections, and surgical site wound infections.
  • Charcot triad of pain, fever, and RUQ pain is found in only ~50% of patients who present with acute cholangitis.  So do not rule out the diagnosis if someone doesn’t have all three.
  • Mirizzi syndrome is rare and can be accompanied by acute chonagitis, acute cholecystitis, or acute pancreatitis.  Management involves antibiotics to treat a concurrent infection in the biliary tree as well as surgical resection of the gallbladder and impacted stone.

Differential for hyperbilirubinemia:

Hyperbilirubinemia breakdown

Remember that the most common reasons for conjugated hyperbilirubinemia are extrahepatic causes and include the following:

  • Stones (30-70%)
  • Malignancy (10-50%)
  • Benign biliary strictures (5-30%)
  • Biliary stent obstruction (~20%)


Most common bacteria:

  • E coli (25-50%)
  • Klebsiella (15-20%)
  • Enterococcus (10-20%)
  • Enterobacter (5-10%)

Clinical manifestations

  • Charcot’s triad (~50% have all 3)
    • Fever
    • Abdominal pain
    • Jaundice
  • Reynold’s pentad: (rare, ~5%)
    • Above PLUS
    • Hypotension
    • AMS
  • Cholestatic LFT pattern ⇒ can progress to hepatocellular LFT pattern

Assessment of disease severity

  • Severe (suppurative) cholangitis — Acute cholangitis is considered severe if it is associated with the onset of dysfunction in at least any one of the following organs/systems:
    • Cardiovascular dysfunction – Hypotension requiring pressors
    • AMS
    • Respiratory dysfunction – PaO2/FiO2 ratio <300
    • Renal dysfunction – Oliguria, serum creatinine >2.0 mg/dl
    • Hepatic dysfunction – Prothrombin time-international normalized ratio >1.5
    • Hematological dysfunction – Platelet count <100,000/mm
  • Moderate acute cholangitis — Acute cholangitis is defined as moderate if it is associated with any two of the following:
    • Abnormal WBC count (>12,000/mm3, <4,000/mm3)
    • Fever 39°C (102.2°F)
    • Age (≥75 years)
    • Hyperbilirubinemia (total bilirubin ≥5 mg/dl)
    • Hypoalbuminemia
  • Mild acute cholangitis — Mild acute cholangitis does not meet the criteria for moderate or severe cholangitis at initial diagnosis.


  • For moderate to severe cases, consider admission to the ICU and urgent ERCP/GB decompression.
  • For mild cases, admit to the floor and monitor closely
  • Antibiotics
    • To cover gram negatives, narrow based on sensitivities
    • Duration is typically 7-10 days.
  • Address predisposing cause
    • Elective cholecystectomy after infection has resolved in those with gallstones

Mirizzi syndrome

Obstruction of the common bile duct from extrinsic compression, often from swelling or infection in the cystic duct, which can share a sheath with the CBD.

  • Commonly diagnosed intraoperatively in patients undergoing GB surgery
  • Presentations
    • Pain (54-100%)
    • Jaundice (24-100%)
    • Cholangitis (6-35%)
    • Acute cholecystitis (1/3 of patients)
    • Acute pancreatitis (rare)
  • Labs
    • Elevated bili and ALP
    • Leukocytosis if concurrent cholecystitis, cholangitis, or pancreatitis
  • Diagnosis
    • Imaging
      • Dilatation of the biliary system above the gallbladder neck
      • Presence of impacted stone in GB neck
      • Normal diameter below level of stone
    • US (23-46% sensitive)
    • CT abdomen (can r/o malignancy but sensitivity is 42%, specificity 99%)
    • MRCP (highest sensitivity)
  • Management
    • Surgery
    • Sometimes ERCP can be diagnostic and therapeutic as a temporizing measure to surgery or if patient is too high risk and unsuitable for surgery
    • Antibiotics for treatment of concurrent cholangitis or cholecystitis


Source: https://www.slideshare.net/mohamedfazly31/mirizzi-syndrome-70749345

Hemorrhagic shock secondary to GI bleed with recent PCI for NSTEMI on DAPT… Did I mention severe aortic stenosis as well? How about all of these in one patient at the same time? 11/29/2018

Narges presented a very complicated patient, who presents with 2 days of abdominal pain and melena. He had a PCI 4 days prior with a drug-eluting stent deployed at the LAD, and he was discharged on aspirin and ticagrelor (PLATO trial, superior to clopidogrel). On presentation he was in hemorrhagic shock, with notable hematochezia on exam, encephalopathy, and a 4/6 systolic murmur with carotid radiation which turned out to be an undiagnosed severe aortic stenosis.

To briefly summarize his main problem list:

  1. Hemorrhagic shock secondary to UGIB
  2. CAD with recent NSTEMI s/p DES to LAD x1 on DAPT
  3. Severe aortic stenosis, newly diagnosed

Question is, what to do if you see a patient like this? Let’s break it down.


Antiplatelet and PCI

  • Drug eluting stents (DES) are designed to have lower rates of late re-stenosis than bare metal stents (BMS), but they are at higher risk for in-stent thrombosis due to delayed endothelialization.
  • Some terminology:
    • Stent re-stenosis:
      • Gradual narrowing of the stent segment, usually occurs 3-12 months after stent placement.
      • Can present as recurrent angina vs full blown MI
    • Stent thrombosis
      • Abrupt thrombotic occlusion of a previously patent stent, usually catastrophic MI
  • Duration of DAPT? It depends! Per the 2016 ACC/AHA guidelineDAPT.png

In a nut shell:

Elective PCI in stable CAD:

  • BMS: At least 1 month of DAPT
  • DES: At least 6 months of DAPT

Exact duration is yet to be determined; there is some evidence of decreased stent restenosis (DAPT trial) with longer duration of DAPT but at the expense of all cause mortality and bleeding complications. There are also newer studies (i.e. ARCTIC Interruption) that found no benefits with longer duration of DAPT.

For PCI in setting of ACS, however, the guideline is different:

Anti-platelet duration in setting of ACS

  • Medical Therapy: At least 12 months of DAPT
  • PCI (BMS or DES, doens’t matter): At least 12 months of DAPT
  • CABG: Also at least 12 months of DAPT

In patients with high bleeding risk or personal history of bleeding and/or long term NSAID use, preemptive prophylaxis with a PPI can be considered. If bleeding risk is significant, you can potentially decrease DAPT duration to at least 6 months, on a case-to-case basis.

Now keep in mind our patient has a DES deployed 4 days ago and he’s now bleeding…

GI Bleed

Risk Factors

  • Alcohol
  • Anticoagulation
  • Cirrhosis
  • Cancer


  • UGIB: BUN/Cr ratio > 30 usually (not sensitive but specific), melena (gut transit of blood)
  • LGIB: bright red hematochezia, lower BUN/Cr ratio, but do not be fooled, can be seen in brisk UGIB (especially in this patient).


  • Airway protection
  • Large bore IVs (18 G), Cordis, IO (they work wonders in a pinch!)
  • Fluid resuscitation
  • Anti-acid (i.e. Protonix)
  • Octreotide if suspecting variceal bleed, if catastrophic variceal bleed, consider deployment of a Blakemore/Minnesota tube
  • Antibiotics for primary SBP prophylaxis if cirrhotic
  • Blood product administration
  • GI consultation, urgency depending on clinical status, EGD

High risk features on Endoscopy

The patient underwent EGD and a duodenal ulcer that was actively bleeding was found. There are certain features of an ulcer that we can use to risk stratify and determine how likely intervention will be successful, and how likely the ulcer will rebleed. This is the Forrest Classification, first published in the Lancet in 1974. Our patient in this case is class 1B, and he ended by rebleeding twice requiring additional endoscopic intervention.


Source: Alzoubaidi DLovat LBHaidry R. Management of non-variceal upper gastrointestinal bleeding: where are we in 2018? 

Failure of endoscopic therapy

  • Predictors: active bleeding at time of endoscopy, visible vessel, > 2cm, posterior duodenal ulcers, and gastric ulcers on the lesser curvature are associated with higher risk of treatment failure/rebleeding.
  • First line: 2nd endoscopic intervention
  • If recurrent bleeding persists, surgical options or IR embolization should be considered

The key question here is, when to resume DAPT? The decision will have to be individualized and most would recommend restarting ASAP as soon as patient is clinically stable… At the same time, pt has one other newly diagnosed problem that makes his management tricky…


Source: grepmed

Severe Aortic Stenosis


  1. Area < 1cm2
  2. Mean trans valvular gradient > 40 mmHg
  3. Peak velocity > 4m/s

Referral to Cardiology because it is actually more complicated than this, there is also pseudo severe where AVR is not recommended, Low flow AS, low gradient AS, or both LF LG AS.

  • Pseudo-severe: mild to moderate AS, low gradient, underlying myocardial dysfunction leading to poor valve opening. No benefit in AVR
  • LF LG AS:
    • AVA < 1cm2, but gradient < 35mmHg
    • Must distinguish from pseudo severe AS. Do dobutamine stress echo
      • If AVA remains the same, gradient inc, confirms true severe AS
      • If AVA improves while mean gradient remains the same, this is pseudo-severe AS, manage medically.


  • < 70: Suspect bicuspid aortic valve
  • > 70: Progressive valvular fibrosis/calcification
  • Developing country: Rheumatic fever


  • Over time leads to LV hypertrophy (concentric), muscle hypertrophy. Leads to heart failure over time.


  • Asx
  • Sx: SAD syncope, angina, dyspnea


  • TAVR (transcatheter) vs SAVR (surgical), TAVR is non-inferior (PARTNER A, PARTNER B, SURTAVI trials) but has other complications to consider,
  • Can think about the transcatheter approach in high surgical risk patients.

In setting of hypotension

  • Patients with critical AS are highly preload dependent:
  • Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV). In patients with severe AS, CO is fixed due to physiologic limitations of a small outlet.
    • Increasing HR can help with CO but you run the risk of increasing myocardial O2 demands…
    • Also in terms of volume, pts with severe AS usually has a degree of diastolic dysfunction (decreased compliance due to a hypertrophied ventricle). As you can imagine, if you push too much fluids into a non-compliant system, back up can occur leading to pulmonary edema thus respiratory failure…
  • Choice Pressors: no absolute contraindication to any but phenylephrine has been suggested in some anesthesia text books as first line
    • Rationale: Pure alpha, increases DBP (diastolic blood pressure), which in turns inc coronary perfusion pressure (CPP = DP – PCWP (LVEDP))
    • Won’t induce tachycardia (if anything induces a mild reflexive bradycardia which decreases myocardial O2 demands).
    • Epi has been associated with higher incidences of arrhythmias

Neutropenia and Acute Diarrhea… It’s not C.diff, it’s Norovirus (11/28/18)

Elise presented a case of a middle age man with recently diagnosed pancreatic adenocarcinoma on chemo presenting with acute loose watery stools (“too many to count”) and abdominal discomfort. He appeared septic on presentation and was found to be neutropenic. Unfortunately (or fortunately) it is not the typical C.diff colitis, but actually norovirus!

Acute Diarrhea

Definition: defined as watery stool 3x in 24 hours, < 14 days duration

Most are infectious in etiology in an acute setting

Other causes: Ingested osmoles, malabsorption


  • Secretory: High volume, watery, no systemic symptoms, usually due to small intestinal involvement
    • Most common causes are viral (rota and noro), enterotoxin, ETEC, or vibrio chlolarae.
    • Negative fecal WBC
  • Invasive: Smaller volume, bloody/mucoid, tenesmus + LLQ pain, systemic symptoms.
    • Site of involvement is the colon. Common causes are Shigella, Campylobacter, EHEC, Entamoeba histolytica
    • Positive fecal WBC
  • Importance of vomiting: Usually indicates the ingestion of a pre-formed toxin or a viral infection. Examples:
    • Staph aureus
    • B. cereus
    • Norovirus
    • Certain parasites


  • Norovirus (very common)
  • Rotavirus, enteric adenovirus, astrovirus (usually in immunocompromised adults)
  • diff (can be bloody/inflammatory)
    • Nosocomial vs community acquired
  • Clostridium perfringens (2nd most common cause of foodborne bacterial infection)
    • Associated with outbreaks in restaurants and catering facilities
    • Usually mild symptoms.
    • Associated with improperly cooked or stored meat.
    • Self-limited, supportive care often suffices
  • Enterotoxigenic E.coli (ETEC): AKA traveler’s diarrhea
    • Cruise ships, foreign countries, fecal contimation or food or water from an infected person.
  • Giardia lamblia:
    • Water & food borne outbreaks
    • Sx: 7-14 days incubation post exposure.
    • Presentation: Foul smelly stools, cramps, bloating.
    • Tx: Supportive + Metronidazole, Tinidazole, albendazole
  • Cryptosporadium
    • One of the most common parasitic foodborne diarrhea
    • Endemic in cattle, usually transmitted via infected animal or person. Food/water borne outbreaks also common.
    • Presentation: Severe, dehydrating watery diarrhea but self-limited in immunocompetent hosts.
    • Immunocompromised: More severe
  • Other bacterial
    • Staph aureus, Bacillus cereus: enterotoxins, acute diarrhea + vomiting
    • Listeria monocytogenes: Can cause systemic symptoms/spread
    • Cyclospora: Associated with sporadic outbreaks due to imported raspberries and basil.
    • Aeromonas: Distributed in watery environments, suspect if contact with fresh or brackish water.
  • Other viral: Hepatitis A

Inflammatory: bloody or mucoid diarrhea, with associated fever, abd pain. Presence of inflammatory cells in the stool. More likely bacterial.

  • Salmonella: Nontyphoidal, leading cause of acute inflammatory diarrhea
    • Association: Poultry, eggs, milk products, animal contacts
    • Incubation: 8 – 72 hours
    • Presentation: diarrhea is usually non-bloody, N/V, fever.
  • Campylobacter
    • Undercooked poultry
    • Watery or hemorrhagic diarrhea, 2-5 days after exposure
    • Association: Guillain-Barre, reactive arthritis
  • Shigella: Dysenteric diarrhea
    • Colonic infection, person to person or fecal oral transmission.
    • Mucoid or bloody diarrhea, 3-7 days after exposure.
  • EHEC: Enterhemorrhagic E.coli
    • Association: HUS
    • Presentation: Watery/progressively bloody diarrhea, 3-4 days post exposure, abd pain + fever.
  • Yersinia
    • Uncommon, can be transmitted via undercooked pork, unpasteurized milk, fecally contaminated water. 1-14 days after exposure
    • Associated with concurrent pharyngitis.
  • Others: Entamoeba histolytica, noncholera vibrios, CMV, HSV
    • CMV & HSV: Dx has to be confirmed by biopsy. Suspect these in immunocompromised patients.

Neutropenia and GI symptoms

Neutropenic enterocolitis (typhilitis), cytotoxic agent-related diarrhea, any viral/bacterial infection, but for typhilitis specifically:


  • Associated with hematologic malignancies or ingestion of food contaminated with C. perfringens
  • Pre-existing bowel wall abnormalities increases risk (i.e. diverticulitis, tumor, previous surgery).


  • Infection of the bowel wall, usually the cecum but can involve ascending colon & ileum, leading to tissue necrosis


  • Neutropenic
  • Fever, mean of 3 weeks after cytotoxic chemo
  • Abd pain, distension, N/V, watery/bloody diarrhea
  • Usually RLQ pain, can mimic appendicitis.


  • CT


  • 4th gen cephalosporins i.e. cefepime + Flagyl, surgery is generally avoid but indicated if e/o perforation


  • 50% mortality



  • Most common viral cause of gastroenteritis worldwide, all age range affected
  • 19-21 million cases every year in the US
  • Unclear reason, peak incidence during winter months.
  • Food born outbreaks is common: leafy greens, fruits, shell fish.


  • Fecal oral transmission, RNA virus
  • Different genotypes exist with further sub-groups, tend to have a preference for certain blood type.
  • Incubation: 24-48 hours, affects the small intestines
  • Very infectious, can cause full blown infection even if exposed to a small amount (< 100 viral particles)
  • Extremely stable in the environment, resists freezing or heating up to 60 degrees C, disinfection requires chlorine or EtOH
  • Viral shedding is max over the first 24-48 hours, and pts can continue to shed for up to weeks


  • Duration: 48-72 hours
  • Watery diarrhea, N/V, abd pain.
  • Vomiting usually prominent
  • Usually self-limiting but can be severe in immunocompromised patients


  • Stool PCR


  • Supportive
  • Contact plus isolation
  • Notify infection control (contact plus isolation)
  • If you have been exposed to someone with norovirus and you are symptomatic, PLEASE CALL IN SICK since this illness is highly contagious. Notify us and employee health. You have to be asymptomatic for at least 48 hours, and you have to be cleared by employee health, prior to returning to work.

Spontaneous Bacterial Peritonitis secondary to… Acinetobacter? 11/14/2018

Our doctor-in-training Jacqueline presented a middle man with infrequent medical care, with a history of heavy alcohol use, who presents with generalized swelling and anorexia. He was septic on presentation with a distended abdomen. Ascitic fluid anlysis was concerning for bacterial peritonitis, and blood cultures (4/4 bottles) were positive for acinetobacter with OXA resistance marker!

Spontaneous bacterial peritonitis

Important to distinguish between Spontaneous bacterial peritonitis (SBP) vs Secondary bacterial peritonitis (also SBP but for the sake of clarity, SBP from this point on will refer to spontaneous bacterial peritonitis)

  • Secondary: Bacterial peritonitis secondary to something else besides spontaneous, i.e. bowel perforation, surgery.
    • 100% mortality without surgical intervention. Surgical risk is high but patient mortality is almost guaranteed without surgery!
    • If Spontaneous BP, mortality can approach 80% with abdominal surgery.
  • Diagnosis: history, fluid analysis
  • Cultures from peritoneal fluid usually polymicrobial (gut flora)
  • Tertiary bacterial peritonitis: Persistence of peritonitis or abscess following adequate treatment of primary or secondary peritonitis


  • Pts with cirrhotic ascites, suspect SBP in all these patients, and also pts with ascites suffering from a GIB.
  • Organisms: E.coli, Klebsiella, strep pneumo are most common, usually single organism
  • Less common: Acinetobacter, pseudomonas, proteus
  • If polymicrobial of anaerobes, suspect secondary bacterial peritonitis
  • Rarely fungal but they have been described, poor prognosis.


  • S/S of ascites
  • May have fever, malaise, encephalopathy, decompensated liver cirrhosis, peritoneal signs sometimes.
  • Frequently an instigator for hepatorenal syndrome in cirrhotic patients.


  • PMN > 250 cells/mL
  • Positive cultures/Gram-stain
  • Absence of secondary causes


  • Antibiotics:
    • Cefotaxime 2g Q8H
    • Ceftriaxone once daily is an alterative with some evidence trending toward improved survival and less ICU stay with 2g daily dosing vs 1g.
    • Cefepime 1-2g Q8H is an alternative as well esp for resistant pathogens.
    • Fluoroquinolones: Consider alternative if pt already on a quinolone for prophylaxis prior to developing SBP. Can use Cipro, Levo, or Moxi.
    • Carbapenems
    • Beta lactam/Beta lactamase inhibitors i.e. Zosyn
    • Duration: At least 5 days
  • Albumin: Recommended, RCT published in NEJM in 1999 established the administration of albumin decreases the incidence of renal failure with albumin + antibiotics as well as decrease in mortality.
    • Patients in the study who were most likely to benefit from albumin had:
      • Bili > 4
      • Cr > 1
      • BUN > 30
    • 1.5g albumin /kg on day 1, the 1.0g/kg on day 3. Dose limited to max of 100g
  • HRS (Hepatorenal syndrome): 1.0g/kg albumin days 1 & 2 and see if renal function improves (albumin challenge)


  • Renal failure can be seen in 30-40% of patients with SBP
  • Prognosis tends to be poor once HRS sets in
  • HRS
    • Type 1: Rapid progressive decline, 50% 1 month mortality
    • Type 2: More subacute/chronic, not associated with an inciting event, median survival 6 months


  • Primary
    • Cirrhotics presenting with GIB should get primary prophylaxis, total duration of therapy x 7 days
    • Ascitic protein < 1.0 g/dL can also be considered (RCT published in Journal of Hepatology in 2008)
    • Ascitic protein <1 and Childs Pugh > 9 or T.bili > 3 or renal dysfunction: can also consider long-term primary prophylaxis, based on an RCT from Gastroenterology in 2007, drug of study was norfloxacin.
  • Secondary
    • Indicated after first episode of SBP, one year recurrence rate of 40-70%, mortality rate of 50-70%
    • Meds: Norfloxacin or cipro daily, Bactrim also an equivocal alternative
    • Life-long or until transplant

Please refer to this article for an overview of SBP.



  • Nosocomial, ICU
  • Tropical/humid environments
  • Water and soil
  • Certain strains can survive in a desiccated environment for weeks.


  • Most commonly in ventilator associated pneumonia and blood stream infection (1.5% – 2.4%)
  • Others: Central line, catheters, surgical site infection
  • Can be contamination, pts and health care workers can be colonized
  • Can also present as endocarditis or meningitis or ocular infection (contact lens)
  • Peritonitis secondary to acinetobacter usually more common in peritoneal dialysis patients.

Risk Factors

  • Prior antibiotics, especially beta lactams, carbapenems, fluoroquinolones
  • Presence of catheters, ICU
  • PD (especially in setting of peritonitis secondary to actinobacteria)
  • Trauma, burn, immunosuppression


  • Increasingly resistant, both acquired and inherent
  • ESBL phenotype also emerging


  • 1st line: cephalosporin (ceftaz, cefepime), beta-lactam/beta lactamase inhibitor, carbapenems are highly effective, ampicillin0sulbactam is also very effective.
  • Sometimes combination therapy is used i.e. with a fluoroquinolone or aminoglycoside due to concerns of emerging and acquired resistance but limited data on combo therapy vs emergences of resistance or whether clinical outcome is improved.
  • Other possible options: minocycline, tigecycline, polymyxins


  • 2x more likely to die from a carbapenem resistant strain

Abdominal Pain Secondary to… Lots of Foreign Bodies 11/6/2018

Our doctor-in-training, Jacqueline, presented a case of a 46yo man with a complicated abdominal surgical history, as well as schizophrenia, who presents with acute onset vague abdominal pain. He could not provide any remarkable history (other than abd pain and losing a bag of coins), and his exam was otherwise benign except for mild diffused abdominal pain…

The mystery was resolved on a radiography.


Foreign Body Ingestion


  • Mostly in kids, peaks 1-2 years of age
  • Adults: Typically, accidental (95% of cases) usually related to fish, chicken bones, or toothpicks. More common in older adults, pts with mental illnesses, intoxicated, or inmates (drug trafficking, packers vs stuffers).
  • Most frequent cause of esophageal obstruction = food bolus on existing stricture


  • Asymptomatic
  • Stridor/airway compromise/aspiration
  • Chest pain/abdominal pain
  • Fever, shock (perforation)
  • Hemoptysis, hematemesis


  • Imaging, clinical history


  • Will depend on stability, the location, nature of the objects ingested, and progression.
  • Expectant management for most blunt objects, ~ 70-80% of objects will pass by day 4. Consider surgical/endoscopic intervention if failure to progress


  • Presentation
    • Local necrosis secondary to pressure, electrical current, or caustic chemicals.
    • Ulceration can occur within 2-4 hours
    • Perforation can be seen as early as 4-8 hours
    • VERY IMPORTANT to distinguish between coin batteries (thicker, concentric circles) vs coins (thinner, confluent)!
    • Picture2.jpg
  • Complications
    • Vocal cord paralysis, esophageal perf, stricture, tracheal/esophageal fistula, aspiration pneumonia, mediastinitis, erosions into arteries, gastric hemorrhage, intestinal perf
  • Management
    • Esophagus: Emergent removal
    • Beyond esophagus: Depends, most (89%) will pass within 7 days
      • Surgical/Endoscopic option: consider if co-ingestion of magnets, or if remained in stomach for more than 48 hours.
      • GI symptoms
    • Cylindrical batteries: Relatively harmless and usually pass through GI tract without issues, but if stuck in stomach or esophagus, endoscopic removal is recommended


  • Presentation
    • Fistula, perforation, volvulus, obstruction, localized necrosis (pressure)
    • Higher chance of complications if multiple magnets and/or metallic objects were ingested.
    • Can react with metal external of the body and cause injury
  • Complications
    • Localized bowel necrosis, obstruction
  • Management
    • Prompt removal endoscopically if in esophagus or stomach.
    • Beyond stomach: Surgery if symptomatic or failure to progress
    • Single magnet: Expectant management, serial XR, monitor progress, don’t be around anything ferromagnetic


  • Presentation
    • High risk of perforation/injury if in esophagus, medical emergency
  • Complications
    • Esophageal perforation
    • Intestinal perforation
  • Management
    • Immediately endoscopic removal if in esophagus
    • Beyond:
      • Stomach/proximal duodenum: still consider urgent endoscopic removal, complication risk varies from as low as 10% to 40%
      • Beyond and failure to progress: Surgical intervention recommended.

Packers vs Stuffers

  • Packers: Carefully PACKING illicit substances into packages, lower chance of leakage (image adapted from Vectortoons.com)
    • Picture3.png
  • Stuffers: Hastily STUFFING illicit substances to hide evidence from law enforcement (image adapted from Family Guy), higher chance of content leakage.
    • Picture4
  • Management:
    • Decontamination:
      • Packers: Whole-bowel irrigation safe and feasible
      • Stuffers: Controversial
    • Symptomatic:
      • Opioid (CNS depression, hypoventilation, pinpoint pupils): IV Naloxone 0.05 in nonapneic patients, 0.2 – 1mg in apneic patients. Larger doses may be required if pt ingested a large amount of heroin.
      • Sympathomimetic (agitation, hypertension, hyperthermia): Symptomatic management, airway monitoring, temperature control. AVOID pure beta blockers. Can consider GI decontamination but consult Poison Control.

If suspecting ingestion of potentially toxic substance, don’t hesitate to call Poison Control!




Liver Cirrhosis Secondary to Hemochromatosis and Alcohol (10/30/2018)

Narges presented a case of a late-middle age woman with history of recurrent pancreatitis, chronic alcohol use, who presents with worsening leg swelling, nausea/vomiting, and chest pain in setting of increased alcohol intake from bereavement. She increased her alcohol intake from “several drinks” a day to a fifth of hard liquor per day for the past few weeks. She was incidentally found to have a severely elevated Transferrin Sat, and genetics study revealed HFE mutation consistent with hemochromatosis.

For those of us illiterate in EtOH… A standard drink is defined as:




  • Hereditary: Up to 10% of Caucasians in US and Western Europe are thought to be heterozygous. Homozygous roughly 0.5%.
  • Symptomatic median age around age 40 for males, later for females due to higher iron loss.


  • Disorder of iron storage, that results in increased intestinal iron absorption and iron deposition.
  • Iron deposition leads to organ damage.
  • Hereditary form
    • Most commonly secondary to mutant HFE (human hemochromatosis protein).
    • HFE codes a protein involved in cellular iron sensing and intestinal iron absorption regulation.
    • Autosomal recessive with variable penetrance.
    • Heterozygotes are asymptomatic and are not at risk of iron-overload.
    • Homozygous patients have variable disease penetrance, thought to be relatively low.
    • ***Key point: Just because someone has the mutation (can be incidentally found on genetic sequencing) does not mean they will have the disease (iron build up in the body leading to end organ damage).
    • Alcohol intake is a major risk factor for development of liver disease for patients with HFE mutation. Iron overload thought to potentiate effect of alcohol induced liver toxicity
    • Liver damage occurs without inflammation, but hence HH can occur in setting without elevated AST/ALT.
    • At least 43% of HH pts have other underlying causes i.e. fatty liver, alcohol, HBV/HCV, that leads to elevated transaminases and liver cirrhosis.
    • Most common mutant is C282Y, if heterozygous, not at risk for developing progressive or symptomatic iron overload.
    • Homozygous C282Y are at risk but again penetrance is variable.
    • Homozygous H63D are generally not at risk but might have minor abnormalities in iron studies. If symptomatic, usually has other underlying process i.e. alcohol (such as this patient).
  • Secondary iron overload (seen in frequent transfusions due to ineffective erythropoiesis)


  • Takes time to develop end-organ damage. Patients are usually asymptomatic until they have 20+ g of iron built up in the body (average iron content of an adult is 4-5g).
  • Early: Non-specific, weakness, weight loss, skin hyperpigmentation (bronze skin), abd pain, loss of libido.
  • Later: Hepatomegaly (95%), cirrhosis, HCC
  • Other organs:
    • DM (50%, pancreas) chronic pancreatitis (advanced hemochromatosis)
    • Hypogonadism (ovaries, testes), impotence/infertility
    • Hypothyroidism (thyroid)
    • Adrenal insufficiency (adrenals)
    • Arthralgia (joints, CPPD pseudogout), osteoporosis (pan hypopit leading to secondary hypogonadism)
    • Heart (heart failure, enlargement)
    • Pan-hypopit (pituitary)

Infection Risk

  • Listeria, Yersinia, and Vibrio sp have increased in an iron rich environment. Mucor sp also favors an iron-rich environment


  • Labs: Inc Fe, % transferrin sat, and serum ferritin levels.
  • Healthy pt: Fasting serum transferrin sat > 50% is abnormal and possibly suggestive of underlying hemochromatosis.
  • Serum transferrin sat: PPV of 26-39%, 80% if two separate, positive tests. NPV of 100%
  • Ferritin levels: not that useful, acute phase reactant, can fluctuate.


  • Remove excess iron!
  • Intermittent phlebotomy, goal serum iron 50-100mcg/dL
  • 1 unit of blood = 250mg Fe, hence to get 20g of iron town to a relatively normal level via phlebotomy, this might take 2-3 years.
  • Chelating agents: Deferoxamine, less effective compared to weekly phlebotomy strategy but indicated in instances when you cannot do phlebotomy, i.e. anemia.


  • IF caught early, organ damage is reversible with iron removal
  • If cirrhosis has set in, this increases risk of hepatocellular carcinoma by 20-200 fold.


  • All 1st degree family members of a patient with confirmed hemochromatosis should be screened with a genetics study +/- an iron panel.
  • Per AASLD 2011 Guideline: