POTD: Aorticenteric Fistula (AEF)

Aorticenteric Fistula (AEF):

There are two different types of AEF:

• Primary: Occurs when a chronic, untreated aortic aneurysm damages or destroys the aortic and bowel tissue.

• Secondary: Occurs due to inflammation of previous aortic graft surgery that is near a section of bowel. This type is much more common than primary AEF.

AEF must be considered in any patient with GI bleeding and history of abdominal aortic surgery. Although AEF is not the most common cause of GI bleeding in these patients, it is life threatening.

The most common location is along the third or fourth portion of the duodenum. A large abdominal aortic aneurysm can erode primarily into the duodenum at these locations, resulting in fistula formation.

Fun fact: Postoperative AEF is most often associated with a graft infection. 

Aortoenteric fistula can present with a sentinel or herald bleed that is minor, or with a sudden catastrophic bleed with hematemesis, melena, or hematochezia (so don’t rely on just upper or lower GI bleed).

If the patient is hemodynamically unstable, emergent laparotomy and blood transfusion are needed. If the patient’s condition is stable, upper GI endoscopy or CT angio of abdomen/pelvis (but you may just want to get the whole aorta). This is a good example of why it’s good to have both surgery and GI consults for your GI bleeds.

In a patient I had with this diagnosis, they had severe AKI he and we attempted to get a CTA but MRA was recommended/insisted by the radiologist (the patient was very stable). The radiologists were refusing to take this patient to CT due to the Cr. In the end, we learned that in order to get an accurate MRA, the patient needs to stay extremely still and pretty much not breath (…not practical). So after all the effort to get this patient to MRI, they ended up getting the CTA anyway, just hours later. Luckily this patient still did well but it was stressful sending them so far away to MRI land. Learn from my mistakes.

In the image below, this classic triad (GI bleed, abdominal pain and palpable mass) occurs in 6-12% of AEFs. Good for MCQs, bad for real life.

 Sources:

Text: peer review, https://www.uptodate.com/contents/aortoenteric-fistula-recognition-and-management

Photo: Rosh review

POTD: Esophageal Disorders

Question:

An elderly male comes to the ED with worsening epigastric and retrosternal chest pain, nausea, and forceful vomiting after eating some spicy food and consuming a small amount of alcohol with dinner. The most recent episode included a small amount of bright red blood.  The pain has progressively worsened, and he now has pain while swallowing and mild shortness of breath.  The patient has had dyspeptic symptoms in the past, which he self-treated with over-the-counter antacids.  He does not use tobacco or illicit drugs.  He appears pale, diaphoretic, and in moderate distress.  Temperature is 38 C (100.4 F), blood pressure is 140/90 mm Hg, pulse is 120/min, and respirations are 24/min.  Neck veins are flat.  Dullness to percussion and decreased breath sounds are present over the left basal area.  Abdominal examination reveals epigastric tenderness and decreased bowel sounds.  Stool occult blood is positive.  Upright chest x-ray reveals a small pleural effusion of the left lung, and ECG shows sinus tachycardia; the imaging results are otherwise unremarkable.

Which of the following is the most likely cause of this patient's current condition?

A) aspiration pneumonitis

B) erosive esophagitis

C) esophageal perforation

D) mallory-weiss syndrome

E) perforated gastric ulcer

The answer is (c). Vomiting + bleeding = mallory-weiss, but vomiting + PAIN + L pleural effusion = Boerhaave’s. Boerhaave’s can lead to mediastinitis (from gastric contents entering sterile sites) and lead to a left pleural effusion with accompanied pneumomediastinum. Fever can take >4 hours to develop. Mortality from mediastinis can double if not properly treated within 24 hours of diagnosis. Make sure to start broad spectrum antibiotics and obtain an emergent thoracic surgery consult!

Why L sided pleural effusion?

The mid esophagus lies next to the right pleura while the lower esophagus abuts the left pleura. Rupture occurs most commonly in the left posterolateral wall of the distal third of the esophagus with extension into the left pleural cavity.

References:

UWorld.com

Inservicetrainingprep.com

Gastrointestinal Bleeding: The Next Frontier (for TXA)

TXA has been shown to improve outcomes in cases of bleeding including postpartum hemorrhage (WOMAN trial), trauma (CRASH-2 trial), epistaxis, oral bleeding and even inhaled TXA for hemoptysis (shout out to Dr Bogach for a recent case of this).  It’s low rate of complications (remember its antifibrinolytic, NOT prothrombotic) makes it a great choice for controlling bleeding.  

Given its success in controlling hemorrhage from these sources, there has been investigation into the use of TXA in other kinds of bleeding including ICH (TICH-2 trial showed promising but inconclusive results, needs to be streamlined) and TBI (CRASH-3 trial, ongoing). Gastrointestinal bleeding (GIB) is a 

A Cochrane review on the use of TXA I'm GiB was conducted in 2012, which showed no change in transfusion needs, surgery or bleeding.  Another systematic review was conducted in 2014 that showed a reduction in mortality but noted that several of the studies used had some design flaws.  Additionally, the number of subjects in the combined studies was below the number needed to reliably find a significant result. 

Currently, the Hemorrhage ALleviation with Transexamic acid - InTestinal system Trial or HALT-IT Trial in Great Britain (I would have gone with Patient Oriented Outcomes in GiB or Stop Hemorrhage In Intestinal Tract but it is what it is) is currently enrolling patients with a goal of 8000+ subjects by summer 2019.  Treatment arm will consist of 1g IV bolus dose and then 3g IV over 24hrs (compared with CRASH-2 which gave 1g IV bolus with another 1g IV over the next 8hrs) with the control receiving NS.  Currently, TXA is not included in current recommendations in the management of nonvariceal GIB. However, given its utility in other types of bleeding and it's low risk of complications, it could be considered in severe cases. 

Summary: No evidence to support TXA in GIB but hopefully there will be some data coming out within the next year. Consider it in cases that are refractory to standard of care. 

Would live to hear from anyone with experience with using TXA for GiBs. 

The TRs