CASE REPORT

CASE REPORT
ANEMIA EC HEMATEMESIS MELENA SUSPEK GASTRITIS EROSIVA
PRECEPTOR:
dr. Hj. Ihsanil Husnah, Sp.PD
ARRANGED BY:
Rizki Febrian
(2012730088)
KEPANITERAAN KLINIK STASE ILMU PENYAKIT DALAM

RUMAH SAKIT ISLAM JAKARTA CEMPAKA PUTIH
FAKULTAS KEDOKTERAN DAN KESEHATAN
UNIVERSITAS MUHAMMADIYAH JAKARTA
Case Report Anemia ec Hematemesis Melena Suspek Gastritis Erosiva

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CHAPTER I
PATIENT STATUS
A. PATIENTS IDENTITY
Name : Mrs. T
Age : 65h years old
Address : St. Kayu Mas, North Jakarta
Religion : Christian
Occupation : Housewife
Marital status : Married
Education : Senior High School
Date of admission : 11 August 2017
MR. Number : 00973941
B. ANAMNESIS
a. Chief Complaint
Vomited like coffee grounds since 6 day before entering the hospital.
Another Complaint
Nausea, limp, dizzy, abdominal pain, tarty stool, sweaty

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b. History of Present Illness
Patient came to Emergency Departement Islamic Hospital of Jakarta Cempaka
Putih with vomited like coffee grounds since 6 day before entering the hospital.
Vomite contain fluid colored black like coffe grounds mixed mucus and cloggy with
the frequency more than 4 times, she estimates that he has vomited about a half cup
(approximate 100 cc). She has been nauseous for several days. Vomited be
accompanied with epigastric pain, pain like burning especially before she had a meal.
Patient complaining that she fell languid and dizzy especially when she woke
up. Since one day ago patient complaining tarty stool with the consistency soft and no
slime. She denies having any fever, Diarrhea and lose wheigh and urinated normally.
c. History of Past Illness
She denied any previous episodes of hematemesis and melena
Hypertension since 10 years ago
Stroke since 6 years ago
She had gastritis
d. History of Family
Her father having history of hypertension and stroke
No history of diabetes mellitus
No history of cardiovascular disease
e. History of Allergy
Patient has no allergy to food, drugs and weather.

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f. History of Treatment
She take any medication for Hypertensi,valsaltran 80 mg
She said 3 month ago she came to neurologist for pain on her knee then neurologist
give her 3 kind of drugs but she forgot abot the drugs name.
g. Habits
Patient said that she likes to eat spicy and sour foods. Pasient eat 3 times a day. Patient
no smoked and not drink alcohol.
C. PHYSICAL EXAMINATION
- Generalis status : Mild ill
- Conciusness : Composmentis
Vital sign
- Blood pressure : 130/70 mmHg
- Heart rate : 88x/minute
- Respiratory rate : 20x/minute
- Temperature : 36.2 C
Anthropometric status
- Body weight : 54 kg
- Body high : 160 cm
- BMI : 21 kg/m2
D. GENERAL PHYSICAL EXAMINATION
Head : normocephal, deformity (-)
Eyes : anemic conjungtiva (+/+), icteric sclera (-/-)

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Nose : epistaksis (-/-), deviasi septum (-/-)
Mouth : the oral mucosa moist
Neck : mass (-), lymphadenopathy (-)
Thorax
Inspection : the movement of the chest symmetrical
Palpation : same vocal fremitus in dextra and sinistra
Percussion : Sonor
Auscultacion : vesicular breath sounds + / +, ronkhi - / -, wheezing - / -
Heart
Inspection : ictus cordis not seen
Palpation : ictus cordis not palpable
Percussion : Right heart margin :sternalis line sinistra ICS-V
left heart margin :midclavicula line sinistra ICS-V.
Auscultation : Regular 1st & 2nd heart sounds, murmur (-), gallop (-)
Abdomen
Inspection : looked flat
Auscultation : bowel (+) sounds, 6x/minutes
Palpation : pressure pain at regio epigastrium (+), ascites (-)
Percussion : timpani, shifting dullness (-)

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Extremities
Superior : Edema (- / -), warm akral(+ / +), RCT <2 seconds (+ / +)
Inferior : Edema (-/ -), warm akral (+ / +), RCT <2 seconds (+ / +)
E. LABORATORY EXAMINATION
Date : 11 August 2017
Examination Result Normal Value
8,1 g/dL 11,7- 15,5

Hemoglobin
9,38 103/ L 3,60-11,00

Leukosit
24 % 38-47
Hematokrit
304 103/L 150-440

Trombosit
2,85 106/L 3,80-520

Eritrosit
83 fl 80-100
MCV
28 pg 26-34
MCH
34 g/dL 32-36
MCHC

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Examination Result Normal Value
Chemical clinic
144 mEq/L 135-147

Natrium
4,2 mEql/L 3,5- 5,0

Kalium
96 mEql/L 94-111
Klorida
diabetes
191 mg/dL 70-200

Plasma glucose
F. RESUME
Mr. S, 65th years old, came with complaints of hematemesis since 4 days. Hematemesis
complaining with epigastric pain like burn, especially before she had a meal , nausea and
languid. She complaint melena since one day ago and feel dizzy especially when she woke up.
Patient has history of hypertension and stroke, she consumtion valsaltran 80mg, she liked to
eating spicy and sour foods.
Physical examination : BP: 130/70 mmHg, HR: 88x/minute, RR: 20x/minute, Temp :
36.2 C. anemic conjungtiva (+/+) and pressure pain at region epigastrium (+)
Laboratory examination: Hb: 8,1 g/dL, Hematokrit: 24%, Eritrosit: 2,85 106/L

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G. PROBLEM LIST
Anemia
Hematemesis
Melena
H. ASSESSMENT
1. Anemia
S : Patient complaining that she fell languid and dizzy especially when
she woke up.
O : BP: 130/70 mmHg, HR: 88x/minute, RR: 20x/minute, Temp : 36.2 C.
conjungtiva anemic (+/+), HB: 8,1 g/dL
A : Anemia
P : Transfusion PRC
HB x BBx 4 (12-8,1)x54x4= 842 cc
2. Hematemesis
S : vomited like coffee grounds since 6 day before entering the hospital. Vomite
contain fluid colored black like coffe grounds mixed mucus and cloggy with the
frequency more than 4 times.
O : BP: 130/70 mmHg, HR: 88x/minute, RR: 20x/minute, Temp : 36.2 C.
A : Hematemesis
P : Ranitidine 2x1
Asam Traneksamat 1x 2 amp
Vitamin K 1x 10 mg IM
Omeprazole 2x 20 mg
Ondancentron 1x 8 mg

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Ringer laktat 20 tpm
3. Melena
S : Since one day ago patient complaining tarty stool with the consistency soft
and no slime.
O :BP:130/70mmHg, HR:88x/minute, RR:20x/minute, Temp : 36.2 C.
A : Melena
P : Asam Traneksamat 1x 2 amp
Vitamin K 1x 10 mg IM
I. PROGNOSIS
Quo ad vitam : dubia ad bonam
Quo ad functionam : dubia ad bonam
Quo ad sanationam : dubia ad bonam

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CHAPTER II
LITERATURE REVIEW
GASTROINTESTINAL BLEEDING
GASTROINTESTINAL BLEEDING
1. Acute Upper Gastrointestinal Bleeding
ESSENTIALS OF DIAGNOSIS
Hematemesis (bright red blood or coffee grounds).
Melena in most cases; hematochezia in massive upper gastrointestinal bleeds.
Volume status to determine severity of blood loss; hematocrit is a poor early indicator of
blood loss.
Endoscopy diagnostic and may be therapeutic.
General Considerations
There are over 250,000 hospitalizations a year in the United States for acute upper
gastrointestinal bleeding, with a mortality rate of 410%. Approximately half of patients are
over 60 years of age, and in this age group the mortality rate is even higher. Patients seldom
die of exsanguination but rather from complications of an underlying disease. The most
common presentation of upper gastrointestinal bleeding is hematemesis or melena.
Hematemesis may be either bright red blood or brown coffee grounds material. Melena
develops after as little as 50100 mL of blood loss in the upper gastrointestinal tract, whereas
hematochezia requires a loss of more than 1000 mL. Although hematochezia generally suggests

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a lower bleeding source (eg, colonic), severe upper gastrointestinal bleeding may present with
hematochezia in 10% of cases. Upper gastrointestinal bleeding is self-limited in 80% of
patients; urgent medical therapy and endoscopic evaluation are obligatory in the rest. Patients
with bleeding more than 48 hours prior to presentation have a low risk of recurrent bleeding.
Etiology
Acute upper gastrointestinal bleeding may originate from a number of sources. These
are listed in order of their frequency and discussed in detail below.
A. Peptic Ulcer Disease
Peptic ulcers account for half of major upper gastrointestinal bleeding with an overall
mortality rate of 6%. However, in North America the incidence of bleeding from ulcers is
declining, perhaps due to eradication of H pylori and prophylaxis with proton pump inhibitors
in high-risk patients.
B. Portal Hypertension
Portal hypertension accounts for 1020% of upper gastrointestinal bleeding. Bleeding
usually arises from esophageal varices and less commonly gastric or duodenal varices or portal
hypertensive gastropathy. Approximately 25% of patients with cirrhosis have medium to large
esophageal varices, of whom 30% experience acute variceal bleeding within a 2-year period.
Due to improved care, the hospital mortality rate has declined over the past 20 years from 40%
to 15%. Nevertheless, a mortality rate of 6080% is expected at 14 years due to recurrent
bleeding or other complications of chronic liver disease.

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C. Mallory-Weiss Tears
Lacerations of the gastroesophageal junction cause 510% of cases of upper
gastrointestinal bleeding. Many patients report a history of heavy alcohol use or retching. Less
than 10% have continued or recurrent bleeding.
D. Vascular Anomalies
Vascular anomalies are found throughout the gastrointestinal tract and may be the
source of chronic or acute gastrointestinal bleeding. They account for 7% of cases of acute
upper tract bleeding. The most common are angioectasias (angiodysplasias) which are 110
mm distorted, aberrant submucosal vessels caused by chronic, intermittent obstruction of
submucosal veins. They have a bright red stellate appearance and occur throughout the
gastrointestinal tract but most commonly in the right colon. Telangiectasias are small, cherry
red lesions caused by dilation of venules that may be part of systemic conditions (hereditary
hemorrhagic telangiectasia, CREST syndrome) or occur sporadically. The Dieulafoy lesion is
an aberrant, large-caliber submucosal artery, most commonly in the proximal stomach that
causes recurrent, intermittent bleeding.
E. Gastric Neoplasms
Gastric neoplasms result in 1% of upper gastrointestinal hemorrhages.
F. Erosive Gastritis
Because this process is superficial, it is a relatively unusual cause of severe
gastrointestinal bleeding (< 5% of cases)

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and more commonly results in chronic blood loss. Gastric mucosal erosions are due to NSAIDs,
alcohol, or severe medical or surgical illness (stress-related mucosal disease).
G. Erosive Esophagitis
Severe erosive esophagitis due to chronic gastroesophageal reflux may rarely cause
significant upper gastrointestinal bleeding, especially in patients who are bed bound long-term.
H. Others
An aortoenteric fistula complicates 2% of abdominal aortic grafts or, rarely, can occur
as the initial presentation of a previously untreated aneurysm. Usually located between the graft
or aneurysm and the third portion of the duodenum, these fistulas characteristically present
with a herald nonexsanguinating initial hemorrhage, with melena and hematemesis, or with
chronic intermittent bleeding. The diagnosis may be suspected by upper endoscopy or
abdominal CT. Surgery is mandatory to prevent exsanguinating hemorrhage. Unusual causes
of upper gastrointestinal bleeding include hemobilia (from hepatic tumor, angioma, penetrating
trauma), pancreatic malignancy, and pseudoaneurysm (hemosuccus pancreaticus).
Initial Evaluation & Treatment
A. Stabilization
The initial step is assessment of the hemodynamic status. A systolic blood pressure <
100 mm Hg identifies a high-risk patient with severe acute bleeding. A heart rate over 100
beats/min with a systolic blood pressure over 100 mm Hg signifies moderate acute blood loss.
A normal systolic blood pressure and heart rate suggest relatively minor hemorrhage. Postural
hypotension and tachycardia are useful when present but may be due to causes other than blood
loss. Because the hematocrit may take 2472 hours to equilibrate with the extravascular fluid,

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it is not a reliable indicator of the severity of acute bleeding. In patients with significant
bleeding, two 18-gauge or larger intravenous lines should be started prior to further diagnostic
tests. Blood is sent for complete blood count, prothrombin time with international normalized
ratio (INR), serum creatinine, liver enzymes, and blood typing and screening (in anticipation
of need for possible transfusion). In patients without hemodynamic compromise or overt active
bleeding, aggressive fluid repletion can be delayed until the extent of the bleeding is further
clarified. Patients with evidence of hemodynamic compromise are given 0.9% saline or lactated
Ringer injection and crossmatched for 24 units of packed red blood cells. It is rarely necessary
to administer type-specific or O-negative blood. Central venous pressure monitoring is
desirable in some cases, but line placement should not interfere with rapid volume
resuscitation. Placement of a nasogastric tube is not routinely needed but may be helpful in the
initial assessment and triage of selected patients with suspected active upper tract bleeding.
The aspiration of red blood or coffee grounds confirms an upper gastrointestinal
source of bleeding, though up to 18% of patients with confirmed upper tract sources of bleeding
have nonbloody aspiratesespecially when bleeding originates in the duodenum. An aspirate
of bright red blood indicates active bleeding and is associated with the highest risk of further
bleeding and complications, while a clear aspirate identifies patients at lower initial risk.
Erythromycin (250 mg) administered intravenously30 minutes prior to upper endoscopy
promotes gastric emptying and may improve the quality of endoscopic evaluation when
substantial amounts of blood or clot in the stomach is suspected. Efforts to stop or slow
bleeding by gastric lavage with large volumes of fluid are of no benefit and expose the patient
to an increased risk of aspiration.
B. Blood Replacement

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The amount of fluid and blood products required is based on assessment of vital signs,
evidence of active bleeding from nasogastric aspirate, and laboratory tests. Sufficient packed
red blood cells should be given to maintain a hemoglobin of 79 g/dL, based on the patients
hemodynamic status, comorbidities (especially cardiovascular disease), and presence of
continued bleeding. In the absence of continued bleeding, the hemoglobin should rise
approximately 1 g/dL for each unit of transfused packed red cells. Transfusion of blood should
not be withheld from patients with massive active bleeding regardless of the hemoglobin value.
It is desirable to transfuse blood in anticipation of the nadir hematocrit. In actively bleeding
patients, platelets are transfused if the platelet count is under 50,000/mcL and considered if
there is impaired platelet function due to aspirin or clopidogrel use (regardless of the platelet
count). Uremic patients (who also have dysfunctional platelets) with active bleeding are given
three doses of desmopressin (DDAVP), 0.3 mcg/kg intravenously, at 12-hour intervals. Fresh
frozen plasma is administered for actively bleeding patients with a coagulopathy and an INR >
1.8; however, endoscopy may be performed safely if the INR is < 2.5. In the face of massive
bleeding, 1 unit of fresh frozen plasma should be given for each 5 units of packed red blood
cells transfused.
C. Initial Triage
A preliminary assessment of risk based on several clinical factors aids in the
resuscitation as well as the rational triage of the patient. Clinical predictors of increased risk of
rebleeding and death include age > 60 years, comorbid illnesses, systolic blood pressure < 100
mm Hg, pulse > 100 beats/min, and bright red blood in the nasogastric aspirate or on rectal
examination.

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1. High riskPatients with active bleeding manifested by hematemesis or bright red blood on
nasogastric aspirate, shock, persistent hemodynamic derangement despite fluid resuscitation,
serious comorbid medical illness, or evidence of advanced liver disease require admission to
an intensive care unit (ICU). After adequate resuscitation, endoscopy should be performed
within 224 hours in most patients but may be delayed in selected patients with serious
comorbidities (eg, acute coronary syndrome) who do not have signs of continued bleeding.
2. Low to moderate riskAll other patients are admitted to a step-down unit or medical ward
after appropriate stabilization for further evaluation and treatment. Patients without evidence
of active bleeding undergo nonemergent endoscopy usually within 24 hours.
Subsequent Evaluation & Treatment
Specific treatment of the various causes of upper gastrointestinal bleeding is discussed
elsewhere in this chapter. The following general comments apply to most patients with
bleeding. The clinicians impression of the bleeding source is correct in only 40% of cases.
Signs of chronic liver disease implicate bleeding due to portal hypertension, but a different
lesion is identified in 25% of patients with cirrhosis. A history of dyspepsia, NSAID use, or
peptic ulcer disease suggests peptic ulcer. Acute bleeding preceded by heavy alcohol ingestion
or retching suggests a Mallory-Weiss tear, though most of these patients have neither.
A. Upper Endoscopy
Virtually all patients with upper tract bleeding should undergo upper endoscopy within
24 hours of arriving in the emergency department. The benefits of endoscopy in this setting are
threefold.

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1. To identify the source of bleedingThe appropriate acute and long-term medical
therapy is determined by the cause of bleeding. Patients with portal hypertension will
be treated differently from those with ulcer disease. If surgery or radiologic
interventional therapy is required for uncontrolled bleeding, the source of bleeding as
determined at endoscopy will determine the approach.
2. To determine the risk of rebleeding and guide triage Patients with a nonbleeding
Mallory-Weiss tear, esophagitis, gastritis, and ulcers that have a clean, white base have
a very low risk (< 5%) of rebleeding. Patients with one of these findings who are < age
60 years, without hemodynamic instability or transfusion requirement, without serious
coexisting illness, and who have stable social support may be discharged from the
emergency department or medical ward after endoscopy with outpatient follow-up.All
others with one of these low-risk lesions should be observed on a medical ward for 24
48 hours. Patients with ulcers that are actively bleeding or have a visible vessel or
adherent clot, or who have variceal bleeding usually require at least a 3-day
hospitalization with closer initial observation in an ICU or step down unit.
3. To render endoscopic therapyHemostasis can be achieved in actively bleeding
lesions with endoscopic modalities such as cautery, injection, or endoclips. About 90%
of bleeding or nonbleeding varices can be effectively treated immediately with injection
of a sclerosant or application of rubber bands to the varices. Similarly, 90% of bleeding
ulcers, angiomas, or Mallory-Weiss tears can be controlled with either injection of
epinephrine, direct cauterization of the vessel by a heater probe or multipolar
electrocautery probe, or application of an endoclip. Certain nonbleeding lesions such
as ulcers with visible blood vessels, and angioectasias are also treated with these
therapies. Specific endoscopic therapy of varices, peptic ulcers, and Mallory- Weiss
tears is dealt with elsewhere in this chapter.

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B. Acute Pharmacologic Therapies
1. Acid inhibitory therapyIntravenous proton pump inhibitors (esomeprazole or
pantoprazole, 80 mg bolus, followed by 8 mg/h continuous infusion for 72 hours) reduce the
risk of rebleeding in patients with peptic ulcers with high-risk features (active bleeding, visible
vessel, or adherent clot) after endoscopic treatment. Oral proton pump inhibitors
(omeprazole, esomeprazole, or pantoprazole 40 mg; lansoprazole or dexlansoprazole 3060
mg) once or twice daily are sufficient for lesions at low-risk for
rebleeding (eg, esophagitis, gastritis, clean-based ulcers, and Mallory-Weiss tears).
Administration of continuous intravenous proton pump inhibitor before endoscopy results in a
decreased number of ulcers with lesions that require endoscopic therapy. It therefore is standard
clinical practice at many institutions to administer either an intravenous or a highdose oral
proton pump inhibitor prior to endoscopy in patients with significant upper gastrointestinal
bleeding. Based on the findings during endoscopy, the intravenous proton pump inhibitor may
be continued or discontinued.
2. OctreotideContinuous intravenous infusion of octreotide (100 mcg bolus, followed by
50100 mcg/h) reduces splanchnic blood flow and portal blood pressures and is effective in
the initial control of bleeding related to portal hypertension. It is administered promptly to all
patients with active upper gastrointestinal bleeding and evidence of liver disease or portal
hypertension until the source of bleeding can be determined by endoscopy. In countries where
it is available, terlipressin may be preferred to octreotide for the treatment of bleeding related
to portal hypertension because of its sustained reduction of portal and variceal pressures and
its proven reduction in mortality.

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C. Other Treatment
1. Intra-arterial embolizationAngiographic treatment is used in patients with persistent
bleeding from ulcers, angiomas, or Mallory-Weiss tears who have failed endoscopic therapy
and are poor operative risks.
2. Transvenous intrahepatic portosystemic shunts (TIPS)Placement of a wire stent from
the hepatic vein
through the liver to the portal vein provides effective decompression of the portal venous
system and control of acute variceal bleeding. It is indicated in patients in whom endoscopic
modalities have failed to control acute variceal bleeding.
2. Acute Lower Gastrointestinal Bleeding
ESSENTIALS OF DIAGNOSIS
Hematochezia usually present.
Ten percent of cases of hematochezia due to upper gastrointestinal source.
Evaluation with colonoscopy in stable patients.
Massive active bleeding calls for evaluation with sigmoidoscopy, upper endoscopy,
angiography, or nuclear bleeding scan.
General Considerations
Lower gastrointestinal bleeding is defined as that arising below the ligament of Treitz,
ie, the small intestine or colon; however, up to 95% of cases arise from the colon. The severity
of lower gastrointestinal bleeding ranges from mild anorectal bleeding to massive, large-
volume hematochezia. Bright red blood that drips into the bowl after a bowel movement or is
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mixed with solid brown stool signifies mild bleeding, usually from an anorectosigmoid source,
and can be evaluated in the outpatient setting. In patients hospitalized with gastrointestinal
bleeding, lower tract bleeding is one-third as common as upper gastrointestinal hemorrhage
and tends to have a more benign course. Patients hospitalized with lower gastrointestinal tract
bleeding are less likely to present with shock or orthostasis (< 20%) or to require transfusions
(< 40%). Spontaneous cessation of bleeding occurs in over 75% of cases, and hospital mortality
is < 4%.
Etiology
The cause of these lesions depends on both the age of the patient and the severity of the
bleeding. In patients under 50 years of age, the most common causes are infectious colitis,
anorectal disease, and inflammatory bowel disease. In older patients, significant hematochezia
is most often seen with diverticulosis, angiectasias, malignancy, or ischemia. In 20% of acute
bleeding episodes, no source of bleeding can be identified.
A. Diverticulosis
Hemorrhage occurs in 35% of all patients with diverticulosis and is the most common
cause of major lower tract bleeding, accounting for 50% of cases. There is 1.35- to 3.49-fold
increased risk of diverticular hemorrhage among patients who use aspirin or nonsteroidal anti-
inflammatory agents. Diverticular bleeding usually presents as acute, painless, large-volume
maroon or bright red hematochezia in patients over age 50 years. More than 95% of cases
require < 4 units of blood transfusion. Bleeding subsides spontaneously in 80% but may recur
in up to 25% of patients.
B. Angioectasias
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Angiectasias (angiodysplasias) occur throughout the upper and lower intestinal tracts
and cause painless bleeding ranging from melena or hematochezia to occult blood loss. They
are responsible for 4% of cases of lower gastrointestinal bleeding, where they are most often
seen in the cecum and ascending colon. They are flat, red lesions (210 mm) with ectatic
peripheral vessels radiating from a central vessel, and are most common in patients over 70
years and in those with chronic renal failure. Bleeding in younger patients more commonly
arises from the small intestine. Ectasias can be identified in up to 6% of persons over age 60
years, so the mere presence of ectasias does not prove that the lesion is the source of bleeding,
since active bleeding is seldom seen.
C. Neoplasms
Benign polyps and carcinoma are associated with chronic occult blood loss or
intermittent anorectal hematochezia. Furthermore, they may cause up to 7% of acute lower
gastrointestinal hemorrhage. After endoscopic removal of colonic polyps, important bleeding
may occur up to 2 weeks later in 0.3% of patients. In general, prompt colonoscopy is
recommended to treat postpolypectomy hemorrhage and minimize the need for transfusions.
D. Inflammatory Bowel Disease
Patients with inflammatory bowel disease (especially ulcerative colitis) often have
diarrhea with variable amounts of hematochezia. Bleeding varies from occult blood loss to
recurrent hematochezia usually mixed with stool. Symptoms of abdominal pain, tenesmus, and
urgency are often present.
E. Anorectal Disease

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Anorectal disease (hemorrhoids, fissures) usually results in small amounts of bright red
blood noted on the toilet paper, streaking of the stool, or dripping into the toilet bowl; clinically
significant blood loss can sometimes occur. Hemorrhoids are the source in 10% of patients
admitted with lower bleeding. Rectal ulcers may account for up to 8% of lower bleeding,
usually in elderly or debilitated patients with constipation.
F. Ischemic Colitis
This condition is seen commonly in older patients, most of whom have atherosclerotic
disease. Most cases occur spontaneously due to transient episodes of nonocclusive ischemia.
Ischemic colitis may also occur in 5% of patients after surgery for ileoaortic or abdominal
aortic aneurysm. In young patients, colonic ischemia may develop due to vasculitis,
coagulation disorders, estrogen therapy, and long distance running. Ischemic colitis results in
hematochezia or bloody diarrhea associated with mild cramps. In most patients, the bleeding
is mild and self-limited.
G. Others
Radiation-induced proctitis causes anorectal bleeding that may develop months to years
after pelvic radiation. Endoscopy reveals multiple rectal telangiectasias. Acute infectious
colitis (see Acute Diarrhea, above) commonly causes bloody diarrhea. Rare causes of lower
tract bleeding include vasculitic ischemia, solitary rectal ulcer, NSAIDinduced ulcers in the
small bowel or right colon, small bowel diverticula, and colonic varices.
Clinical Findings
A. Symptoms and Signs

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The color of the stool helps distinguish upper from lower gastrointestinal bleeding,
especially when observed by the clinician. Brown stools mixed or streaked with blood predict
a source in the rectosigmoid or anus. Large volumes of bright red blood suggest a colonic
source; maroon stools imply a lesion in the right colon or small intestine; and black stools
(melena) predict a source proximal to the ligament of Treitz. Although 10% of patients
admitted with self-reported hematochezia have an upper gastrointestinal source of bleeding
(eg, peptic ulcer), this almost always occurs in the setting of massive hemorrhage with
hemodynamic instability. Painless large-volume bleeding usually suggests diverticular
bleeding. Bloody diarrhea associated with cramping abdominal pain, urgency, or tenesmus is
characteristic of inflammatory bowel disease, infectious colitis, or ischemic colitis.
B. Diagnostic Tests
Important considerations in management include exclusion of an upper tract source,
anoscopy and sigmoidoscopy, colonoscopy, nuclear bleeding scans and angiography, and small
intestine push enteroscopy or capsule imaging.
1. Exclusion of an upper tract sourceA nasogastric tube with aspiration should be
considered, especially in patients with hemodynamic compromise. Aspiration of red blood or
dark brown (coffee grounds) guaiac-positive material strongly implicates an upper
gastrointestinal source of bleeding. Upper endoscopy should be performed in most patients
presenting with hematochezia and hemodynamic instability to exclude an upper
gastrointestinal source before proceeding with evaluation of the lower gastrointestinal tract.
2. Anoscopy and sigmoidoscopyIn otherwise healthy patients without anemia under age 45
years with smallvolume bleeding, anoscopy and sigmoidoscopy are performed to look for

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evidence of anorectal disease, inflammatory bowel disease, or infectious colitis. If a lesion is
found, no further evaluation is needed immediately unless the bleeding persists or is recurrent.
In patients over
age 45 years with small-volume hematochezia, the entire colon must be evaluated with
colonoscopy to exclude tumor.
3. ColonoscopyIn patients with acute, large-volume bleeding requiring hospitalization,
colonoscopy is the preferred initial study in most cases. The bowel first is purged rapidly by
administration of a high-volume colonic lavage solution, given until the effluent is clear of
blood and clots (48 L of GoLYTELY, CoLYTE, NuLYTE given orally or 1 L every 30
minutes over 25 hours by nasogastric tube). For patients with stable vital signs and whose
lower gastrointestinal bleeding appears to have stopped (> 75% of patients), colonoscopy can
be performed electively within 24 hours of admission. For patients with signs of
hemodynamically significant bleeding (unstable vital signs) or who have signs of continued
active bleeding during bowel preparation (< 25% of patients), urgent colonoscopy should be
performed within 12 hours of completing the bowel purgative, when the bowel discharge is
without clots. The probable site of bleeding can be identified in 7085% of patients, and a high-
risk lesion can be identified and treated in up to 20%.
4. Nuclear bleeding scans and angiographyTechnetium- labeled red blood cell scanning
can detect significant active bleeding and, in some cases, can localize the source to the small
intestine, right colon, or left colon. Because most bleeding is slow or intermittent, less than half
of nuclear studies are diagnostic and the accuracy of localization is poor. Thus, the main utility
of scintigraphy is to determine whether bleeding is ongoing in order to determine whether
angiography should be pursued. Less than half of patients with a positive nuclear study have

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positive angiography. Accordingly, angiograms are performed only in patients with positive
technetium scans believed to have significant, ongoing bleeding. In patients with massive lower
gastrointestinal bleeding manifested by continued hemodynamic instability and hematochezia,
urgent angiography should be performed without attempt at colonoscopy or scintigraphy.
5. Small intestine push enteroscopy or capsule imaging
Up to 5% of acute episodes of lower gastrointestinal bleeding arise from the small
intestine, eluding diagnostic evaluation with upper endoscopy and colonoscopy. Because of the
difficulty of examining the small intestine and its relative rarity as a source of acute bleeding,
evaluation of the small bowel is not usually pursued in patients during the initial episode of
acute lower gastrointestinal bleeding. However, the small intestine is investigated in patients
with unexplained recurrent hemorrhage of obscure origin. (See Obscure Gastrointestinal
Bleeding below.)
Treatment
Initial stabilization, blood replacement, and triage are managed in the same manner as
described above for Acute Upper Gastrointestinal Bleeding.
A. Therapeutic Colonoscopy
High-risk lesions (eg, angioectasias or diverticulum, rectal ulcer with active bleeding,
or a visible vessel) may be treated endoscopically with epinephrine injection, cautery (bipolar
or heater probe), or application of metallic endoclips or bands. In diverticular hemorrhage with
highrisk lesions identified at colonoscopy, rebleeding occurs in half of untreated patients
compared with virtually no rebleeding in patients treated endoscopically. Radiation proctitis is

| 25
effectively treated with applications of cautery therapy to the rectal telangiectasias, preferably
with an argon plasma coagulator.
B. Intra-arterial Embolization
When a bleeding lesion is identified, angiography with selective embolization achieves
immediate hemostasis in more than 95% of patients. Major complications occur in 5% (mainly
ischemic colitis) and rebleeding occurs in up to 25%.
C. Surgical Treatment
Emergency surgery is required in < 5% of patients with acute lower gastrointestinal
bleeding due to the efficacy of colonoscopic and angiographic therapies. It is indicated in
patients with ongoing bleeding that requires more than 6 units of blood within 24 hours or more
than 10 total units in whom attempts at endoscopic or angiographic therapy failed. Most such
hemorrhages are caused by a bleeding diverticulum or angioectasia. Surgery may also be
indicated in patients with two or more hospitalizations for diverticular hemorrhage depending
on the severity of bleeding and the patients other comorbid conditions.
3. Obscure Gastrointestinal Bleeding
Obscure gastrointestinal bleeding refers to bleeding of unknown origin that persists or
recurs after initial endoscopic evaluation with upper endoscopy and colonoscopy. Obscure-
overt bleeding is manifested by persistent or recurrent visible evidence of gastrointestinal
bleeding (hematemesis, hematochezia, or melena). Up to 5% of patients admitted to hospitals
with clinically overt gastrointestinal bleeding do not have a cause identified on upper
endoscopy or colonoscopy (and therefore have obscureovert bleeding).

| 26
Obscure-occult bleeding (discussed below) refers to bleeding that is not apparent to the
patient. It is manifested by recurrent positive FOBTs or FITs or recurrent iron deficiency
anemia, or both in the absence of visible blood loss (as described below). Obscure bleeding
(either occult or overt) most commonly arises from lesions in the small intestine. In up to one-
third of cases, however, a source of bleeding has been overlooked in the upper or lower tract
on prior endoscopic studies. Hematemesis or melena suggest an overlooked source proximal
to the ligament of Treitz (ie, within the esophagus, stomach, or duodenum): erosions in a hiatal
hernia (Cameron erosions), peptic ulcer, angioectasia, Dieulafoy vascular malformation,
portal hypertensive gastropathy, gastroduodenal varices, duodenal neoplasms, aortoenteric
fistula, or hepatic and pancreatic lesions. In the colon, the most commonly overlooked lesions
are angioectasias and neoplasms. The etiology of obscure bleeding that arises from the small
intestine depends on the age of the patient. The most common causes of small intestinal
bleeding in patients younger than 40 years are neoplasms (stromal tumors, lymphomas,
adenocarcinomas, carcinoids), Crohn disease, celiac disease, and Meckel diverticulum. These
disorders also occur in patients over age 40; however, angioectasias and NSAID-induced ulcers
are far more
common.
Evaluation of Obscure Bleeding
The evaluation of obscure bleeding depends on the age and overall health status of the
patient, associated symptoms, and severity of the bleeding. In an older patient with significant
comorbid illnesses, no gastrointestinal symptoms, and occult or obscure bleeding in whom the
suspected source of bleeding is angioectasias, it may be reasonable to limit diagnostic
evaluations, provided the anemia can be managed with long-term iron therapy or occasional
transfusions. On the other hand, aggressive diagnostic evaluation is warranted in younger

| 27
patients with obscure bleeding (in whom small bowel tumors are the most common cause) and
symptomatic older patients with overt or obscure bleeding. Upper endoscopy and colonoscopy
should be repeated to ascertain that a lesion in these regions has not been overlooked. If these
studies are unrevealing, capsule endoscopy should be performed to evaluate the small intestine.
Capsule endoscopy is superior to radiographic studies (standard small bowel follow through,
enteroclysis, or CT enterography) and standard push enteroscopy for the detection of small
bowel abnormalities, demonstrating possible sources of occult bleeding in 50% of patients,
most commonly vascular abnormalities (25%), ulcers (1025%), and neoplasms (< 110%).
Further management depends on the capsule endoscopic findings. Laparotomy is warranted if
a small bowel tumor is identified by capsule endoscopy or radiographic studies. Most other
lesions identified by capsule imaging can be further evaluated with enteroscopes that use
overtubes with balloons to advance the scope through most of the small intestine in a forward
and retrograde direction. Neoplasms can be biopsied or resected, and angioectasias may be
cauterized. For massive or hemodynamically significant acute bleeding, angiography may be
superior to enteroscopy for localization and embolization of a bleeding vascular abnormality.
Abdominal CT may be considered to exclude a hepatic or pancreatic source of bleeding. A
nuclear scan for Meckel diverticulum should be obtained in patients under age 30. With the
advent of capsule imaging and advanced endoscopic technologies for evaluating and treating
bleeding lesions in the small intestine, intraoperative enteroscopy of the small bowel is seldom
required.
4. Occult Gastrointestinal Bleeding
Occult gastrointestinal bleeding refers to bleeding that is not apparent to the patient.
Chronic gastrointestinal blood loss of < 100 mL/d may cause no appreciable change in stool
appearance. Thus, occult bleeding in an adult is identified by a positive FOBT, FIT, or iron
| 28
deficiency anemia in the absence of visible blood loss. FOBT or FIT may be performed in
patients with gastrointestinal symptoms or as a screening test for colorectal neoplasia (see
Chapter 39). From 2% to 6% of patients in screening programs have a positive FOBT or FIT.
In the United States, 2% of men and 5% of women have iron deficiency anemia (serum
ferritin < 3045 mcg/L). In premenopausal women, iron deficiency anemia is most commonly
attributable to menstrual and pregnancy-associated iron loss; however, a gastrointestinal source
of chronic blood loss is present in 10%. Occult blood loss may arise from anywhere in the
gastrointestinal tract. Among men and postmenopausal women, a potential gastrointestinal
cause of blood loss can be identified in the colon in 1530% and in the upper gastrointestinal
tract in 3555%; a malignancy is present in 10%. Iron deficiency on rare occasions is caused
by malabsorption (especially celiac disease) or malnutrition. The most common causes of
occult bleeding with iron deficiency are (1) neoplasms; (2) vascular abnormalities
(angioectasias); (3) acid-peptic lesions (esophagitis, peptic ulcer disease, erosions in hiatal
hernia); (4) infections (nematodes, especially hookworm; tuberculosis); (5) medications
(especially NSAIDs or aspirin); and (6) other causes such as inflammatory bowel disease.
Evaluation of Occult Bleeding
Asymptomatic adults with positive FOBTs or FITs that are performed for routine
colorectal cancer screening should undergo colonoscopy (see Chapter 39). All symptomatic
adults with positive FOBTs or FITs or iron deficiency anemia should undergo evaluation of
the lower and upper gastrointestinal tract with colonoscopy and upper endoscopy, unless the
anemia can be definitively ascribed to a nongastrointestinal source (eg, menstruation, blood
donation, or recent surgery). Patients with iron deficiency anemia should be evaluated for
possible celiac disease with either IgA anti-tissue transglutaminase or duodenal biopsy. After

| 29
evaluation of the upper and lower gastrointestinal tract with upper endoscopy and colonoscopy,
the origin of occult bleeding remains unexplained in 3050% of patients.
In younger patients (age < 60) with unexplained occult bleeding or iron deficiency, it
is recommended to pursue further evaluation of the small intestine for a source of obscure-
occult bleeding (as described above) in order to exclude a small intestinal neoplasm or
inflammatory bowel disease. Patients over age 60 with occult bleeding who have a normal
initial endoscopic evaluation and no other worrisome symptoms or signs (eg, abdominal pain,
weight loss) most commonly have blood loss from angioectasias, which may be clinically
unimportant. Therefore, it is reasonable to give an empiric trial of iron supplementation and
observe the patient for evidence of clinically significant bleeding. For anemia that responds
poorly to iron supplementation or recurrent or persistent chronic occult gastrointestinal blood
loss, further evaluation is pursued for a source of obscure-occult bleeding (as described above).
When possible, antiplatelet agents (aspirin, NSAIDs, clopidogrel) should be discontinued.

| 30
REFERENCES
Djojoningrat, Dharmika.2009. Dispepsia Fungsional dalam Buku Ajar Ilmu Penyakit
Dalam. Jilid I. Edisi ke-5,p 529-33. Jakarta: Internal Publishing
Sudoyo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiati S. 2009. Buku Ajar Ilmu
Penyakit Dalam. Edisi ke-5. Jakarta : Pusat Penerbitan Departemen Ilmu Penyakit
Dalam Fakultas Kedokteran Universitas Indonesia
Tarigan, Pengarapen. 2009. Tukak Gaster dalam Buku Ajar Ilmu Penyakit Dalam.Jilid
I. Edisi ke-5. Jakarta : Pusat Penerbitan Departemen Ilmu Penyakit Dalam Fakultas
Kedokteran Universitas Indonesia
Papadakis A, Maxine, 2015, Gastorintestinal Disorders in CURRENT MEDICAL
DIAGNOSIS & TREATMENT, Mc Gam Hill Education. New York
Rani A, Soegondo S, Nasir A, Wijaya I. 2009. Panduan Pelayanan Medik Perhimpunan
Dokter Spesialis Penyakit Dalam Indonesia. Jakarta : Interna Publishing
Jawetz, Melnick, Adelbergs. Medical Microbiology. Edisi ke-24. United States of
America : McGraw-Hill ; 2007.
Hirlan.2009. Gastritis dalam Buku Ajar Ilmu Penyakit Dalam.Jilid I. Edisi ke-5. Jakarta
: Pusat Penerbitan Departemen Ilmu Penyakit Dalam Fakultas Kedokteran Universitas
Indonesia

| 31

CASE REPORT - DR Ihsanil

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ANEMIA EC HEMATEMESIS MELENA SUSPEK GASTRITIS EROSIVA

KEPANITERAAN KLINIK STASE ILMU PENYAKIT DALAM

Case Report Anemia ec Hematemesis Melena Suspek Gastritis Erosiva

Age : 65h years old

Address : St. Kayu Mas, North Jakarta

Marital status : Married

Education : Senior High School

Date of admission : 11 August 2017

MR. Number : 00973941

Nausea, limp, dizzy, abdominal pain, tarty stool, sweaty

Case Report Anemia ec Hematemesis Melena Suspek Gastritis Erosiva

Patient came to Emergency Departement Islamic Hospital of Jakarta Cempaka

c. History of Past Illness

She denied any previous episodes of hematemesis and melena

Hypertension since 10 years ago

Stroke since 6 years ago

She had gastritis

Her father having history of hypertension and stroke

No history of diabetes mellitus

No history of cardiovascular disease

Patient has no allergy to food, drugs and weather.

Case Report Anemia ec Hematemesis Melena Suspek Gastritis Erosiva

She take any medication for Hypertensi,valsaltran 80 mg

no smoked and not drink alcohol.

- Generalis status : Mild ill

- Blood pressure : 130/70 mmHg

- Heart rate : 88x/minute

- Respiratory rate : 20x/minute

- Body high : 160 cm

D. GENERAL PHYSICAL EXAMINATION

Head : normocephal, deformity (-)

Eyes : anemic conjungtiva (+/+), icteric sclera (-/-)

Mouth : the oral mucosa moist

Neck : mass (-), lymphadenopathy (-)

Inspection : the movement of the chest symmetrical

Palpation : same vocal fremitus in dextra and sinistra

Auscultacion : vesicular breath sounds + / +, ronkhi - / -, wheezing - / -

Inspection : ictus cordis not seen

Palpation : ictus cordis not palpable

Percussion : Right heart margin :sternalis line sinistra ICS-V

left heart margin :midclavicula line sinistra ICS-V.

Inspection : looked flat

Auscultation : bowel (+) sounds, 6x/minutes

Palpation : pressure pain at regio epigastrium (+), ascites (-)

Percussion : timpani, shifting dullness (-)

Case Report Anemia ec Hematemesis Melena Suspek Gastritis Erosiva

Superior : Edema (- / -), warm akral(+ / +), RCT <2 seconds (+ / +)

Date : 11 August 2017

Examination Result Normal Value

8,1 g/dL 11,7- 15,5

9,38 103/ L 3,60-11,00

304 103/L 150-440

2,85 106/L 3,80-520

Case Report Anemia ec Hematemesis Melena Suspek Gastritis Erosiva

144 mEq/L 135-147

4,2 mEql/L 3,5- 5,0

191 mg/dL 70-200

eating spicy and sour foods.

Case Report Anemia ec Hematemesis Melena Suspek Gastritis Erosiva

she woke up.

O : BP: 130/70 mmHg, HR: 88x/minute, RR: 20x/minute, Temp : 36.2 C.

conjungtiva anemic (+/+), HB: 8,1 g/dL