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\begin{document}

\title{The Stealthy Bleeder: A Case of Dieulafoy Lesion in Lower
Gastrointestinal Tract}



\author[1]{Nida Ansari}%
\author[2]{Sacide S. Ozgur}%
\author[3]{Alan Alcantara}%
\author[2]{Gabriel Melki}%
\author[2]{Ruhin Yuridullah}%
\author[2]{Oren Bernheim}%
\author[2]{Abraham El-Sedfy}%
\affil[1]{Saint Joseph's Healthcare System}%
\affil[2]{St Joseph's University Medical Center}%
\affil[3]{St Josephs Regional Medical Center}%


\vspace{-1em}



  
  \date{May 20, 2024}


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\textbf{Introduction:}

Lower gastrointestinal bleeding (LGIB) is a significant clinical
concern, accounting for about 30\% of major gastrointestinal bleeding
episodes requiring hospitalization. While upper gastrointestinal sources
are more common, lower GI bleeding presents a diverse array of potential
etiologies, ranging from diverticulosis and angioectasias to ischemic
colitis, neoplasms, and hemorrhoids {[}1{]}.

Dieulafoy lesions represent a unique vascular anomaly within the GI
tract, characterized by an abnormally large submucosal artery that
erodes the overlying mucosa without an associated ulcer or erosion,
potentially leading to significant bleeding {[}2{]}. Dieulafoy lesions
stand out as a rare but noteworthy cause of LGIB, constituting about 2\%
of acute GI bleeds {[}3{]}. These lesions are more commonly associated
with the upper GI tract, typically in the stomach near the
gastroesophageal junction, due to the vascular supply from the left
gastric artery branches. However, they can occur throughout the GI
tract, including the colon, though this presentation is rare {[}2,4{]}.

The pathogenesis of Dieulafoy lesions is not completely understood, but
arterial wall necrosis leading to rupture has been suggested.
Additionally, risk factors such as NSAIDs, tobacco, alcohol use, and
peptic ulcer disease may exacerbate the potential for bleeding from
these lesions {[}2{]}. The diagnosis is typically made endoscopically,
with criteria including the presence of a protruding vessel or active
bleeding from a small mucosal defect surrounded by normal tissue
{[}2{]}.

Endoscopic intervention remains the cornerstone of treatment, with
mechanical modalities like band ligation and hemostatic clips being
highly effective. Combination therapy has been shown to be superior to
monotherapy in achieving hemostasis, which is successful in
approximately 80-85\% of cases {[}2{]}.

The case we present emphasizes the importance of considering Dieulafoy
lesions in the differential diagnosis of LGIB, given their potential for
significant blood loss and the effectiveness of prompt endoscopic
intervention in resolving bleeding and stabilizing patients.

\textbf{Case History:}

We present a 43-year-old male with a past medical history of
hypertension, dyslipidemia, benign prostate hyperplasia, and internal
hemorrhoids who presented to the emergency department (ED) for two
episodes of bright red blood per rectum. He initially attributed his
bleeding to his hemorrhoids. While in the ED, the patient had two
further episodes of large bright red blood per rectum. He did not report
any abdominal tenderness. In the ED, his vitals revealed a temperature
of 36.8 C, heart rate of 99 beats per minute, blood pressure of 115/ 85
mmHg, and oxygen saturation of 97\% on room air. His physical exam was
benign except for bright red blood per rectum. Labs were notable for a
hemoglobin of 11.8 g/dL and lactic acid of 2.9 mmol/L. CT angiography of
the abdomen and pelvis was performed, which did not show any active
gastrointestinal hemorrhage. The patient was started on Protonix 80 mg
IV and 2 IV fluid boluses. The patient was admitted to the medical floor
for treatment. GI was consulted, and the patient was scheduled for a
colonoscopy.

\textbf{Differential diagnosis, investigations and treatment:}

Colonoscopy revealed nonbleeding internal hemorrhoids, grade 3. Hematin
was noted in the ascending colon. This distal ileum contained a single
localized nonbleeding aphtha however, no stigmata of recent bleeding was
seen. For further evaluation of bleeding, esophagogastroduodenoscopy was
performed, only notable for acute gastritis. The patient continued to
have bright red blood per rectum even after endoscopic intervention,
with an associated decrease in hemoglobin, on day 4 of his admission,
his hemoglobin was noted to be 8.5 g/dL. Due to the patient's drop in
hemoglobin and persistent rectal bleeding, a capsule endoscopy is
planned to rule out small bowel lesions. Colorectal surgery was also
consulted for internal hemorrhoid management however, no surgical
intervention at that time.

The patient's hemoglobin continued to drop, requiring a blood
transfusion. A repeat CT angiography of the abdomen and pelvis was
performed, which showed a small focus of active contrast extravasation
in the rectum with intraluminal blood in the left colon and rectum,
which was not seen on the prior imaging (Figure 1).\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

Figure 1: Computer Tomography of Chest Abdomen and Pelvis with Contrast,
Coronal View, showing a small focus of active contrast extravasation in
the rectum with intraluminal blood in the left colon and rectum.

At this time, surgery was planned for surgical intervention with
hemorrhoidectomy and recommended for a repeat colonoscopy
postoperatively as the patient had blood in ascending colon on prior
colonoscopy. However, the patient had a hypotensive episode after having
a large bloody bowel movement. At that time, the patient was undergoing
a blood transfusion. His blood pressure was noted to be 89/56, and he
had a heart rate of 107 bpm. At that time, the patient endorsed
dizziness, and he was given a 1 L IV fluid bolus with improvement of his
blood pressure to 113/72 mmHg. However patient became more disoriented.
Critical care was consulted, and an additional unit of RBC, FFP, and
platelets was recommended. Surgery was contacted, and a proctoscopy was
performed bedside, which showed a large amount of clots however, will
believed to be unlikely due to hemorrhoidal bleeding. The patient was
transferred to the ICU for further monitoring. The following day, the
patient had a colonoscopy performed to evaluate the etiology of lower GI
bleeding further, which showed an ascending colon Dieulafoy lesion with
active bleeding (Figure 2\&3). The site was treated with an epinephrine
injection and three hemostatic endoscopic clips.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

Figure 2: Colonoscopy showing ascending colon dieulafoy lesion with
active bleeding.\selectlanguage{english}
\begin{figure}[H]
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\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
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Figure 3: Colonoscopy showing lesion with endoscopic clips.

\textbf{Outcome and follow-up:}

After this intervention, the patient's bleeding slowly resolved. The
patient's clinical status improved, and the patient was subsequently
discharged.

\textbf{Discussion:}

Lower gastrointestinal bleeding (LGIB) is less common than upper
intestinal bleeding and can account for about 30\% of major GI bleeding
that requires hospitalization {[}1{]}.

Lower GI bleeding has a myriad of causes with common etiologies such as
diverticulosis, angioectasias, ischemic colitis, neoplasm, and
hemorrhoids {[}1{]}. However, there are less common causes, such as
Dieulafoy Lesions {[}1{]}. They account for about 2\% of all acute GI
bleeds {[}3{]}. Dieulafoy lesions in the lower GI tract are rare,
accounting for approximately 5\% of total cases {[}3{]}. There is a
higher predilection for males, and typically occurs after the 5th decade
{[}3{]}.

Dieulafoy lesions are vascular malformations of the gastrointestinal
tract {[}2{]}. It is an enlarged submucosal blood vessel that can bleed
without the presence of ulcers or erosions {[}2{]}. Dieulafoy lesions
are believed to occur due to pulsations or an abnormally large artery
that could disrupt the mucosal lining, exposing the artery and causing
possible bleeding {[}2{]}. Arterial thrombosis can allow for necrosis of
the arterial wall, possibly causing rupture {[}3{]}. However, the risk
of bleeding can be enhanced by other factors, including the use of
NSAIDs, tobacco, alcohol, and peptic ulcer disease {[}2{]}. It is
possible that mucosal irritation by feces can also contribute to colonic
Dieulafoy lesions {[}3{]}. Typically found in the upper GI tract, it is
often found in the stomach {[}2{]}. Specifically seen in the lesser
curvature, within 6 cm of the gastroesophageal junction, given its
arterial blood supply from the branches of the left gastric artery
{[}2{]}. Extragastric lesions can occur; however, are rarer in
presentation {[}2{]}. In a study by Baxter et al., colonic sites were
reported in less than 2\% of cases {[}4{]}.

Upon endoscopic evaluation, the following criteria are necessary for
diagnosis: Normal mucosa around the defect, with active pulsatile
bleeding that is less than 3 mm {[}2{]}. A visualized protruding vessel
from a defect or normal mucosa {[}2{]}. A fresh clot attached to the
defect of normal mucosa is observed {[}2{]}.

Treatment for Dieulafoy lesions is endoscopic intervention, with
mechanical hemostasis being the safest modality {[}2{]}. Banding
ligation and hemoclips are often utilized, and combined therapy is
superior relative to monotherapy{[}2{]}. Hemostasis is successful in
80-85\% of cases treated with endoscopy {[}2{]}. Areas can be marked
with India ink for further identification if further intervention is
warranted {[}2{]}. However, if endoscopic treatment is not therapeutic,
surgical interventions such as wide wedge resection or partial/wedge
gastrectomy can be considered {[}2{]}. In our patient, hemostasis was
achieved via hemoclips and epinephrine injection and did not report any
further rebleeding.

\textbf{Conclusion:}

Given the wide range of differential diagnoses involved when working up
hematochezia. Prompt identification of the source is needed in order to
prevent significant morbidity and mortality. Although rare, Dieulafoy
lesions should be excluded as a primary cause, as swift intervention is
associated with hemostasis in the majority of cases.

\textbf{References:}

\begin{enumerate}
\tightlist
\item
  Saltzman JR. Acute Lower Gastrointestinal Bleeding. In: Friedman S,
  Blumberg RS, Saltzman JR. eds. Greenberger's CURRENT Diagnosis \&
  Treatment Gastroenterology, Hepatology, \& Endoscopy. 4th ed. McGraw
  Hill; 2022. Available from:
  https://accessmedicine.mhmedical.com/content.aspx?bookid=3204\&sectionid=266863700.
  Accessed December 7, 2023.
\item
  Malik TF, Anjum F. Dieulafoys Lesion Causing Gastrointestinal
  Bleeding. {[}Updated April 27, 2023{]}. In: StatPearls {[}Internet{]}.
  Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available
  from: https://www.ncbi.nlm.nih.gov/books/NBK562267/.
\item
  Dokmak A, Muso E. Gastrointestinal Bleeding from Dieulafoy's Lesion in
  the Cecum. Case Rep Gastroenterol. December 29, 2022;16(3):601--606.
  doi:10.1159/000525740.
\item
  Baxter M, Aly E. Dieulafoy's lesion: Current trends in diagnosis and
  management. Ann R Coll Surg Engl. 2010;92(7):548-554.
  doi:10.1308/003588410X12699663905311.
\end{enumerate}\selectlanguage{english}
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