Category Archives: #GI

MR with Jossy and Dr. Shlager: Acute Liver Failure in a patient on Azathioprine

A middle aged female with history of renal transplant (in 2013 2/2 ANCA vasculitis) on immunosuppression presents with one month of jaundice, light stools, and vague abdominal pain. Her initial labs showed a bilirubin of 16 with transaminases in the 80s-90s, INR of 1.3, and AKI on CKD without evidence of structural obstruction on imaging. Her initial workup included a liver biopsy, after which she became more encephalopathic with a rising INR, meeting criteria for ALF. UCSF was then contacted for potential transplant. The etiology of her ALF is still not clear, but thought most likely a result of azathioprine hepatotoxicity
*One confusing thing in this presentation were the relatively low AST/ALT. We discussed that the patient could have had an insult several weeks ago and her liver enzymes are now just ‘burnt out’; because of this, she should still be worked up for all of the usual causes of ALF (i.e. hepatitis, autoimmune disease, etc) that are usually associated with higher transaminases.
*Definition of Acute Liver Failure: INR > 1.5 + Encephalopathy in a patient without pre-existing liver disease (often defined as developing in <26w)
-While only INR + encephalopathy define ALF, we discussed the following signs of poor prognosis as ALF progresses: hypoglycemia, signs of HRS (creatinine rising or oliguria), hypotension
*My patient with had negative hepatitis serologies in the last 5 years and is low risk. Do we need to resend these? What should we send?
In the case ALF (or concern for progression towards ALF), repeat hepatitis serologies AND viral loads should almost always be sent. We often forget about hepatitis A, but this is common and the biggest risk factor for this progressing to liver failure is age.
-Would send: hep A IgM, hep A IgG, hepB surface Ab, hepB core Ab, hepB surface Ag, hepB DNA, hepC ab, hepC RNA
*What causes ALF?
Acute Liver Failure actually has a nice differential because it’s actually quite limited with a few big categories: Toxins, Viral, Vascular, Metabolic, Other
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And, random antibiotic pearls:
*For every antibiotic you choose, ask yourself what you are covering and what you are missing. It is the only way to learn the nuances of these drugs over time!
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Monday – MR with Jenny Zhang: Autoimmune hepatitis and pyelephlebitis

 

A middle aged patient with a hx of cirrhosis secondary to autoimmune hepatitis on azathioprine and prednisone who presented with acute on chronic abdominal pain called to the ED for Gram Negative bacteremia.  CT abdomen demonstrated thrombi within the peripheral branches of the portal venous system consistent with pylephlebitis.  The patient was treated with antibiotics and the decision was made to not anticoagulate.

 

Learning Points

-Anticoagulation for pylephlebitis is NOT recommended unless there is evidence of progression of thrombosis or fever or bacteremia despite antibiotic therapy

-The most common predisposing infections leading to pylephlebitis are diverticulitis and appendicitis.

-Typical antibiotic choice for these patients is at least 4-6 weeks

MR with Jessica Duhe + Lyle Shlager: HCV management in the new treatment era

A middle aged woman presents for management of HCV. She has cirrhosis w/ portal hypertension; she was treated unsuccessfully 20 years ago with IFN + ribavirin, then again with addition of a third agent in 2012. With the advent of new therapies, she was re-treated and achieved SVR; however, she continued to require active management of decompensated cirrhosis and HCC screening.
*See this excellent NEJM take on updates in treatment of patients with cirrhosis: https://resident360.nejm.org/content_items/treatment-of-patients-with-cirrhosis
1. Who qualifies for HCV treatment?
-With the new therapies, EVERYONE! Asymptomatic patients, cirrhotics, AND decompensated cirrhotics can all be treated; if someone has decompensated cirrhosis, they should be listed for transplant in addition to being treated.
2. Who is at risk of treatment failure?
-Cirrhotics and patients on BID PPI. 
-Patients with HBV are at risk of HBV flare during HCV treatment; hence all patients must be tested for HBV prior to treatment initiation.
3. Once someone achieves SVR, are they cured for life?
-In short, yes (99% sustained cure for life) but they can always be re-infected (with same or different genotype)
4. When should beta blockers be used for varices in cirrhotics?
-Though BB used to be given to any cirrhotic with varices, new data shows a decline in survival when these are used in end stage cirrhotics, thought due to negative effects on already poor cardiac reserve. This has led to the “window hypothesis”, which essentially states that BB should be used during a specific period when someone has known medium to large varices but does not yet have refractory ascites or hypotension.
 
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MR with Sonia + Dr. Robbins: Cholecystitis + Crohn’s

A young female w/ history of Crohn’s in remission presents with fever + RUQ pain found to have transaminitis + neutropenia with an odd-looking “collapsed gallbladder” on imaging. She is being treated broadly for cholecystitis, but the underlying cause of her imaging findings is still unclear; GI and Surgery are involved.
1. Although PSC more commonly occurs in UC patients, it is also (though less) associated with Crohn’s Disease.
2. Acute Liver FAILURE requires the presence of INR > 1.5 and encephalopathy. This patient did NOT have acute liver failure.
3. Neutropenic fever pearls
-As Morgan noted, the diagnosis and management of “neutropenic fever” we often discuss strictly applies to chemotherapy-induced neutropenia. The infectious risk in patients with non-chemotherapy neutropenia of unclear etiology ranges from benign to life-threatening; the infectious risk is highest when neutropenia is related to bone marrow suppression or vasculitis. However, when the risk is unknown it is reasonable to manage ALL people with neutropenic fever with broad-spectrum antibiotics including pseudomonal coverage.
-Infectious risks are highest when ANC < 500 AND duration of neutropenia is >7 days

MR with JLo and Dr. Robbins: Hidden Diverticulitis

A middle aged woman w/ obesity who presents with sudden onset profuse diarrhea and SIRS. She was initially sent home after a CT was negative at her first ED visit, but represented two days later with worsening symptoms and temperature to 104. A CT was ultimately repeated with IV and PO contrast, and showed diverticulitis c/b contained perforation.

*The sensitivity and specificity of abdominal CT [with oral AND IV contrast] for the diagnosis of acute diverticulitis are 94 and 99 percent, respectively

*25% of patients with acute diverticulitis have associated complications – complications include bowel obstruction, abscess development, fistula, or a colonic perforation (as seen in this case)

*Indications for urgent surgery:  failure of medical treatment, obstruction, abscess failing nonoperative intervention

9/1 Morning Report w/ Teresa: MI Mimic

An elderly male w/ CAD and prior MI, afib, CHB now paced, HTN presents with chest pain “that feels like my last MI”. He had a fairly negative workup and was treated briefly with heparin for MI vs PE, but this was ultimately stopped when LFTs showed transaminitis with a late-peaking bilirubin, most consistent with a passed stone.
How do I interpret signs of ischemia in someone who is ventricular-paced? (Hint – there’s no foolproof way…)
-Compare to prior EKGs and look for changes
-Most pacemakers pace from the RV yielding a LBBB pattern; hence, you can consider using Sgarbosa criteria but these are less specific for ischemia in RV pacing. Other criteria have been proposed (http://en.ecgpedia.org/index.php?title=MI_Diagnosis_in_LBBB_or_paced_rhythm ) but if you’re clinically worried about ACS, call cards!
-Look for ANY non-paced beats that conduct via the AV node (ie narrow QRS). All of these native beats are still interpretable for ischemia
The definition of hepatojugular reflux:
We discussed this often confusing physical exam maneuver. The most important thing is that you hold pressure for at least 10-20 seconds to see if the rise in JVP sustains – if it sustains that long, then the test is abnormal. Normal subjects will have a JVP that rises initially but returns to normal within seconds.

8/22 MR with Justin + Dr. Schlager: Dysphagia + Food impaction

An elderly woman w/ a history of esophageal cancer (s/p endoscopic mucosal resection) presents with acute on chronic dysphagia. Her initial workup was unrevealing for stricture and CT showed a nonspecific filling defect, which was ultimately found to be an undigested hot dog!
Management of foreign body impaction: 
Emergent endoscopy
-Complete esophageal obstruction with inability to handle oral secretions
-Disk batteries int he esophagus
-Sharp pointed objects in the esophagus
Urgent endoscopy (within 24h)
-Esophageal objects that are blunt
-Esophageal objects without complete obstruction
-Magnets
-Anything > 6cm in length
Non-Urgent endoscopy
-Blunt objects that fail to pass the stomach or advance in the duodenum in 3-4 weeks
-Disk batteries in the stomach
Conservative management (observe with weekly radiographs and determine need for endoscopy later)
-Blunt objects that have already made it to the stomach or beyond