CASE 2 GI
A 54-year-old man was admitted to hospital because of diarrhea, vomiting, and weight loss.
The patient was well until approximately 2.5 years before admission, when abdominal cramping
and non-bloody diarrhea developed 1 day after he came back from a trip to Colorado, USA; the
symptoms persisted for the duration of his 4-day vacation. Four days after returning home, he
went to the emergency department of another hospital because of persistent symptoms, where
he was told he had a stomach virus. The next day, he has an opd consult, and ciprofloxacin was
administered, without benefit. One month later, he saw a gastroenterologist. Routine laboratory
studies were normal. A stool specimen showed many leukocytes and no ova or parasites; a
stool assay for Clostridium difficile and a stool culture were negative. A course of metronidazole
was administered for 10 days, and the symptoms nearly resolved.
Two years before this admission, esophagogastroduodenoscopy reportedly revealed an inlet
patch ( an area of ectopic gastric mucosa) involving the circumference of the cervical
esophagus and extending at least 4 cm in length, multiple erosions of the gastric antrum, antral
gastritis, superficial ulcerations in the duodenum, and a prominent mucosal fold in the gastric
side of the gastroesophageal junction. A colonoscopy showed several small polyps.
Pathological examination of the biopsy specimens of the proximal portion of the esophagus
reportedly showed squamous mucosa and gastric-type mucosa, with intestinal metaplasia that
was thought to be consistent with Barrett's esophagus. Pathological examination of a biopsy
specimen of a polyp in the transverse colon revealed adenomatous changes and low-grade
dysplasia; a hyperplastic rectal polyp and normal fragments of duodenal mucosa were also
seen. Testing for Helicobacter pylori and giardia was negative. Proton-pump inhibitors were
prescribed.
Nine months later, the patient again awoke with abdominal cramps and watery diarrhea (up to
one episode per hour); 3 days later, nausea and vomiting developed. Examination of a stool
specimen at that time revealed Blastocystis hominis, and the symptoms again resolved after
treatment with metronidazole.
Four months before admission, the patient traveled to the Middle East. While traveling, he
stayed in hotels and drank only bottled water. The day after arrival, abdominal cramping
developed, with watery, non-bloody diarrhea occurring every 1 to 2 hours during the day and
occasionally awakening him at night. His discomfort increased with eating. On the sixth day,
nausea and non-bloody, nonbilious vomiting (two to three episodes daily) occurred, in
association with increased diarrhea and without fevers or diaphoresis. None of his 15 travel
companions had symptoms. Twelve days later, the patient returned home. His symptoms
persisted, and 3 weeks after their onset, he went to a second hospital for evaluation;
intravenous fluids and metronidazole were administered, but the symptoms worsened.
Examination of the stool for pathogens and screening for H. pylori were negative. During the
next 3 months, anorexia developed, and the patient lost 15.9 kg. Approximately 2 weeks before
admission, his physician prescribed trimethoprim–sulfamethoxazole, with partial improvement of
diarrhea.
Eight days before admission, the patient was seen in the infectious-disease clinic. On
examination, the blood pressure was 114/86 mm Hg and the pulse was 88 beats per minute; the
remainder of the physical examination was normal. The platelet count, erythrocyte
sedimentation rate, red-cell indexes, and serum levels of glucose, urea nitrogen, calcium,
vitamin B12, C-reactive protein, cortisol, thyrotropin, amylase, and lipase were normal, as were
the results of liver-function tests. Testing for IgA antibodies to gliadin, endomysial antigen,
and tissue transglutaminase was negative; other test results showed 19 mg/dl of hemoglobin
and normal wbc count. Stool specimens showed no enteric pathogens, ova, or parasites, and
testing for C. difficile toxin was negative. During the ensuing week, the patient's symptoms
worsened and included diarrhea (occurring hourly throughout the day), constant nausea,
vomiting within 3 minutes after oral intake, and weakness, with orthostatic lightheadedness. He
came to the emergency department of this hospital.
The patient reported no fever, chills, sweats, flushing, or headache. His only medication was
omeprazole, 20 mg daily, which he took for symptoms of gastroesophageal reflux. He had no
known allergies. He worked in a service industry, and was monogamous with his girlfriend. He
drank alcohol in moderation, had smoked as a young adult, and did not use illicit drugs.
He had had no exposures to sick persons or animals and had no history of ingestion of
unpasteurized milk products or raw meats. His father was 82 years of age and had dementia,
his mother was deceased and had a history of Parkinson's disease and heart disease, and an
uncle reportedly had stomach cancer.
On examination, the blood pressure was 133/94 mm Hg and the pulse 120 beats per minute;
the temperature, respirations, and oxygen saturation while the patient was breathing ambient air
were normal, as was the remainder of the examination. The platelet count, activated partial-
thromboplastin time, and serum levels of calcium, phosphorus, magnesium, and prealbumin
were normal, as were the results of liver-function tests; An electrocardiogram was normal.
Normal saline was infused.
Computed tomography (CT) of the abdomen and pelvis after the oral and intravenous
administration of contrast material showed thickening and enhancement of the proximal small-
bowel walls, mild dilatation in the small bowel, a large amount of fluid in the small bowel and
colon with air–fluid levels, an enlarged retroperitoneal node (1.3 cm in the short axis), calcific
atherosclerosis of the aorta, and a ground-glass nodule (0.7 cm in diameter) in the lower
lobe of the right lung (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4630533/).
Omeprazole, prochlorperazine, and ondansetron hydrochloride were administered, and
additional crystalloid solution was infused intravenously. Urinalysis revealed 1+ ketones and
albumin and was otherwise normal. During the next 2 days, levels of erythropoietin and folate
were found to be normal, and testing for human immunodeficiency virus (HIV) antibodies was
negative; other test results showed. Stool studies were again unrevealing.
On the fourth day, the level of potassium in the stool was 21.7 mmol per liter (serum level, 3.4
mmol per liter) and stool fat was 37% (reference range, 0 to 19). Esophagogastroduodenoscopy
revealed erosive or exudative circumferential lesions (grade III esophagitis, according to
the modified Savary–Miller classification, which consists of grades I through V, with grade V
indicating the metaplasia seen in Barrett's esophagus); excessive fluid (1600 ml) in the gastric
body; a partially obstructing duodenal ulcer (30 mm in the largest dimension) in the duodenal
bulb, with an ulcer crater that was suspicious for perforation; and multiple ulcers, up to 6 mm in
the largest dimension, in the second part of the duodenum. Pathological examination of biopsy
specimens of the edges of the partially obstructing duodenal ulcer showed duodenal mucosa
with ulceration, foveolar metaplasia, and hyperplasia of the Brunner's glands, with no evidence
of malignant cells. Gram's staining of an aspirate of the duodenum revealed few
polymorphonuclear cells and few yeast forms; no ova or parasites were seen. Cultures of the
duodenal aspirate grew Candida albicans and three colony types of alpha-hemolytic
streptococcus.
A diagnostic procedure was performed.
I. General Data
II. HPI
III. ROS
IV. PE
V. SALIENT FEATURES
VI. WORKING IMPRESSION
VII. Differentials
Reference:
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