UGI Bleed - Duodenal Ulcer

8/10/2019 UGI Bleed - Duodenal Ulcer

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UGI Bleed

Obie M. Powell, M.D.Joseph A. Iocono, M.D.

Department of Surgery

University of Kentucky


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Mr. Mellenna

57 year-old white male with recent history of

dark stools presents to the emergency room

complaining of a two hour history of vomiting

blood and feeling faint.

On presentation the patient is pale and lethargic

complaining of abdominal pain.


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History

What other points of the history do

you want to know?


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History, Mr. Mellenna

Characterization of

symptomsTemporal sequence

Alleviating /

Exacerbating factors:

Pertinent PMH, ROS,

MEDS.Relevant family hx.

Associated signs and

symptoms

Consider the Following


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Characterization of Symptoms

Un-relenting nausea with associated burning

epigastric discomfort

Pain is steady and rates it as a 5 on a scale of 1-

10.


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Temporal Sequence

Dark stools off and on for approximately 6 months.

Often has some mild epigastric pain to which he payslittle attention. This pain has been occurring for thesame duration.

Today he has been feeling light headed for about 3-

4 hours, and has been throwing up blood for 2 hours.


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Alleviating / Exacerbating Factors

Standing erect worsens his light headedness and laying

down improves it.

Nothing improves the pain or nausea

In the past eating food sometimes relieved hisabdominal pain.


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PMH

The patients past history is significant for

HTN

MI 3 years prior treated with angioplastyand stenting.

COPD

OsteoarthritisNo prior abdominal surgery


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PMH

Medications

ASA - supposed to be on it but it bothers his

stomach

Metoprolol 50mg po BID

Simvastatin 10mg po daily

Ibuprofen 400mg po QID prn, none in past 2

weeks

NKDA


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Family/Social History

Family History

Non-contributory

Social History

Married

Computer programmer ETOH- 6 pack per week


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ROS

As in HPI.

The patient denies chest pain, shortness of breath,

fever, chills, anorexia, and dysuria

ROS should emphasize further characterization of

the active disease process AND risk factors that maycomplicate surgery such as active infection, active

CAD, poor exercise tolerance

Wh i Diff i l


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What is your Differential

Diagnosis?


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Differential Diagnosis

Esophageal varices

Gastric varices

Erosive gastritis

Mallory Weiss tear

Reflux esophagitis

Gastric malignancy

Vascular malformations

Nose bleed

Aorto-enteric fistula

Gastric ulcer

Duodenal ulcer

Consider the following


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Physical Exam

What are you looking for?


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Physical Exam

What to look for

Vital signs: instability, respiratory distress, beware

of beta blockade

Overall appearance: signs of anemia, dehydration

Abdominal exam: probe for peritonitis

Rectal exam: mandatory. Look for perianal causes

of bleeding.


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Physical Exam, Mr. Mellenna

Vital signs: Temp. 97.8, Pulse 90, BP 95/63Resp. 30

Patient is alert and oriented. Pale skin and dry

mucous membranes.

During your examination the patient has a large

maroon bowel movement


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Physical Exam

Head is atraumatic /normocephalic, eyes sunken,pale conjunctiva

Neck-No lymphadenopathy,flat neck veins.

Oropharynx - dried blood, noactive bleeding, dry mucusmembranes.

CV- Regular rate and rhythm, nomurmur, rubs, or gallops

Chest-Mild tachypnea,respirations are clear bilaterally norales, rhonchi, or wheezes

Abdomen is scaphoid, soft,mildly tender in mid-epigastrum. Bowel sounds are

present and hyperactive.

Extremities show no clubbing,

cyanosis, or edema. Rectal exam shows gross blood,

enlarged smooth prostate, nopalpable masses, nohemmorhoids or other peri-anal

disease


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Would you like to revise your initial

differential diagnosis?


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What Labs do you need ?


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Laboratory studies:What is necessary?

Type and Cross

CBC: Do you expect anemia?

CMP: evaluate for hepatic dysfunction and

renal compromise

Coags: active hemorrhage can cause

coagulopathy and requires aggressive

replacement

ABG: probe for acidosis


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Laboratory Values

140 110

4.3 20

10.2

31.1

144108

55

1.1

11

ABG: 7.23 | 28 | 80 | 18 | -5

PT: 18 (1.5) PTT: 36

LFTs: Normal


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What do you think about the labs?


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Laboratory Values Discussion

An elevated BUN to Creatinine ratio can be a sign ofupper GI bleed due to the digestion of blood or

prerenal azotemia.

A patient actively hemorrhaging will show a normal

Hgb/Hct prior to being resuscitated. Chronic bleeding

presents with typical iron deficiency anemia.


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What would you do now?


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Interventions to consider

ABCs Ensure adequate airway protection and adequate

respirations

Start 2 large bore IVs.

Fluid bolus either NS or LR

Foley Catheter

NG with gastric lavage

STAT Upper endoscopy


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Endoscopy

Upon upper endoscopy theesophagus appears normal.

There is a large amount of clot inthe stomach, irrigation reveals

normal appearing mucosawithout signs of ulcer orgastritis.

On passing through the pyloruscopious gross blood is

encountered with a activelybleeding ulcer on the posteriorwall of the duodenum.


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What would you do now?


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Endoscopy

Attempt at injecting with epinepherine, andeven direct pressure prove unsuccessful withcontinued brisk pulsatile bleeding.

Are there any particular endoscopic findingsthat suggest a higher risk of failed therapy or re-

bleeding?


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What would you do next?

Repeat Hct is 18

He is actively bleeding in Endoscopy


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Surgery for Bleeding Ulcers

Indications

Pre-operative preparation

Operative approach

Relevant Anatomy

Potential complications


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Operative Indications

Duodenal ulcers located on the anterior wallare prone to perforation and present asperitonitis and free air. Those on the posterior

wall, which is the more common location, leadto bleeding.

The gastroduodenal artery passes just distal tothe pylorus and posterior to the duodenum. If

it or one of its branches are in the ulcer craterthey may erode and result in massive bleeding.


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Operative Technique

Patients are explored through an upper midlineincision.

An incision is made in the anterior duodenum

through the pylorus and distal stomach.

The site of bleeding is identified. The bleeding canthen usually be controlled by placing sutures in 3-4

quadrants around the ulcer base.

The gastroduodenal artery may be ligated ifnecessary


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Operative Technique

Once bleeding has been controlled, thehorizontal opening through the pyloric channel

is closed vertically resulting in a Heineke-

Mikulicz pyloroplasty.A truncal vagotomy is then added for long-term

ulcer control. Specimens of both vagal trunks

are sent to Pathology to document the vagotomy


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Gastrointestinal Bleeding

Bleeding can arise anywhere along the GI tract.Bleeding represents the initial symptom of

gastrointestinal disease in 1/3 of all patients.

The majority of bleeding will stopspontaneously.


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Hematemesis- Vomiting of blood. Can be either grossblood and blood clots representing rapid bleeding or

coffee-ground emesis signifying chronic bleeding.

Hematemesis is the result of bleeding from the

oropharynx to the ligament of Treitz.

Melena- Passage of black and tarry stool caused by

digested blood.


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Melena is usually the result of severe upper GIbleeding. Melena without hematemesis is

caused by severe bleeding distal to the ligament

of Treitz. Hematochezia- Passage of maroon to red blood

and blood clots.


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As little as 50-60 mL of blood in the GI tractproduces melena. Melena can persist from 5-7days after a 2 unit bleed and stools can remain

occult positive up to 3 weeks. With upper GI blood loss blood urea nitrogen

levels may be elevated to 30-50 mg/dL. ABUN: Creatinine ratio greater than 36:1 likely

represents blood loss from an upper GI source.


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Upper Gastrointestinal Bleeding

Some dependency on socioeconomic factors.Peptic ulcers are more common in suburbanhospitals, while gastritis and varices are morecommon in urban centers. Patients 60 years oldand older represent ~ 60% of patients presentingwith upper GI bleeding with a mortality rate of20-25%. For younger patients the mortality rate

drops to 4%.


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Nose bleeds-Rarely the cause of majorbleeding. It must be ruled out by a careful

examination of the posterior pharynx to insure

blood is not running down the esophagus,causing hematemesis .


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Esophagitis- Hiatus hernia and refluxesophagitis are not common causes of upper GIbleeding. Reflux esophagitis is more likely toresult in chronic occult bleeding usuallyassociated with grade II-III esophagitis withfriable mucosa. Significant bleeding in this areais more commonly associated with para-

esophageal hernias.


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Varices- In pediatric patients 95% of all upper GIbleeds are caused by variceal hemorrhage, usually as aconsequence of extra hepatic portal venous obstruction.In patients with cirrhosis and portal hypertension

variceal hemorrhage accounts for 50-75% of all upperGI bleeds. Variceal hemorrhage is usually precipitated

by ulceration of the varix secondary to refluxesophagitis or increased pressure within the varix.


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Varices- In patients with liver disease bleedingis precipitated by the inability of the liver to

synthesize clotting factors. Initial therapy

includes sclerotherapy, ligation and vasopressin.Ligation is as effective as sclerotherapy with

fewer complications. If unsuccessful shunting

or transplant may be necessary.

U G t i t ti l Bl di


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Mucosal tear (Mallory-Weiss)

Esophagogastric mucosal tear or Mallory-Weiss tear

account for 5-10% of all upper GI bleeds. Mallory-Weiss

tears present in a classic pattern. Initially the patient has

vomiting without blood. Continued emesis leads to pain

from the tear and eventually the patient developshematemesis. 90% of Mallory-Weiss bleeding resolves

spontaneously and require no further therapy.

If bleeding persists, endoscopic therapy with injection of

vasoconstrictive agents, IV vasopressin or balloontamponade with Sengstaken-Blakemoore tube may be

necessary.


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Gastritis Up to 1/3 of upper GI bleeds are caused by diffuse

gastritis. Erosions are usually multiple and foundprimarily in the fundus and body of the stomach. Chronicslow bleeds are most commonly associated with H. pylori,

while more brisk bleeding is usually a result of ingestedsubstances harmful to the gastric mucosa such as NSAIDs,alcohol, steroids, or other drugs.

Treatment is with vasopressin, iced saline lavage,sucralfate, H2 blockers, and proton pump inhibitors.

Bleeds refractory to these treatments may requireelectrocautery, vagotomy and antrectomy or even totalgastrectomy.


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Peptic ulcer Most common cause of upper GI bleed, encompassing 1/2-

2/3 of patients. Bleeding is presenting symptom in up to

10% of these patients. Duodenal bleed is four times more

common than gastric ulcer bleed. Duodenal ulcers areusually posterior and involve branches of the

gastroduodenal artery.

Benign gastric ulcers bleed more than malignant ulcers.

There will be significant bleeding in 10-15% of pepticulcers and surgical intervention is needed in 20% of these

patients


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Stress ulcers Stress ulcers refer to acute gastroduodenal lesions that

arise after episodes of shock, sepsis, surgery, trauma, burns(Curlings ulcer), or intracrainial pathology or surgery(Cushings ulcer). Specific risk factors associated with

these ulcers are, multi system trauma, hypotension,respiratory failure, sepsis, jaundice, recent surgery andburns.

It is believed that stress ulceration is the result of bilereflux damage to the gastric protective barrier combined

with decreased gastric blood flow secondary to splanchnicvasoconstriction. Sepsis, coagulopathy, and activation ofcytokines may also play a role in the formation of stressulcers.



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Other causes Miscellaneous causes may contribute up to 18% of upper

GI bleeds. Gastric neoplasmsboth malignant and benigncan cause bleeding which is usually mild and chronic.

Dieulafoysvascular malformationsare dilated arteriallesions usually amendable to endoscopic injection.

Aorto-enteric fistulascan present as a herald bleedfollowed by a massive bleed in patients with prior aorticreconstructions. Hematobiliacan be found in patientsfollowing hepatic injuries or manipulations.



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Management- Complete history with inquiries ofpeptic ulcer disease, alcohol use, cirrhosis, heart burn,reflux, and medications. Exam looking for signs ofcirrhosis including spider angiomata, palmererythema, prominent abdominal veins, caput medusa,and ascites. Examine mucous membranes formelanin spots associated with Puetz-Jegherssyndrome. Perform rectal exam and check for occult

blood in the stool.


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Management- Fluid resuscitation, foley, naso-gastric tube, gastric lavage and arterial line.

Labs- Complete blood count with platelets,

comprehensive metabolic panel with liverfunctions, and coagulation studies. Cross

match for blood transfusion.



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Studies/Treatment :

EGD with sclerotherapy or electrocautery,

tagged red blood cell scan, arteriography with

embolization.

If esophageal bleeding does not respond to

sclerotherapy, ligation, or intravenous

vasopressin, Sengstaken-Blakemoore tube

should be used.



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TIPS- for portal hypertension

Trans jugular intrahepatic porto-systemic shunt.

Used for bleeding secondary to portal hypertension.Associated with in hospital mortality rate of 35-56%.

Encephalopathy rate is the same as for patients who

undergo porto-caval shunts. Stenosis or occlusion of

TIPS is up to 50% at one year.

L G i i l Bl di


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Lower Gastrointestinal Bleeding

Small Bowel- Small bowel accounts for 10-15% ofall lower GI bleeds. Usually a diagnosis of exclusion.Seeing blood exiting the ileo-cecal valve accounts for10% of diagnoses. Causes include, Meckels

diverticulum, Crohnsdisease, intussusception,neoplasm, vascular malformations, intestinal varices,

blood dyscrasias, non-Meckelsdiverticulum,mesenteric thrombosis, drug reactions, enteric

infections, and polyps.

L G t i t ti l Bl di


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Colon- Most often related to polyps orneoplastic disease (occult). Right sided lesions

usually present through anemia and guaiacpositive stools. Larger bleeds can arise from

diverticuli or angiodysplastic lesions on either

the right or left side.


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Angiodysplastic lesionshave the followingcharacteristics. They are not congenital or neoplastic

but degenerative. They are not associated with othervascular lesions. They increase with age. They are

usually small < 5mm. They can be diagnosed bycolonoscopy. 80% of angiodysplastic bleeds will stopspontaneously and 50% will re- bleed within 3 years.

Ulcerative colitis- Usually cause chronic bloodydiarrhea, but massive bleeds can occur


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Management- Complete H&P. Fluid

resuscitation, foley, naso-gastric tube, gastric

lavage and arterial line.

Labs- Complete blood count with platelets,

comprehensive metabolic panel with liver

functions, and coagulation studies. Cross

match for blood transfusion.

L G t i t ti l Bl di


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Studies/Treatment: Normalize coagulation. Colonoscopy, tagged

red blood cell scan 91% sensitive and 100%

specific. Angiography with or without coilembolization.

Local resection of defined bleeds, otherwise ifbleeding continues and no source can be

identified within the colon, total colectomy isindicated.

R t l d A l Bl di


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Rectal and Anal Bleeding

Fresh red blood on the exterior of stool usuallyrepresents hemorrhoids, fissures, or proctitis.

Bleeding that drops into the toilet water is most

likely the result of fissures or hemorrhoids. Allrectal bleeding should be fully investigated with

full H&P, anoscopy / proctoscopy and if

necessary exam under anesthesia.

QUESTIONS ??????


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QUESTIONS ??????


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UGI Bleed - Duodenal Ulcer