Gastro Clinical Cases

8/21/2019 Gastro Clinical Cases

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Hepatitis C and Alcohol Abuse - What is the Treatment Plan? Author: V. Dimov, M.D.

Reviewer: S. Randhawa, M.D.

A 57-year-old African American male (AAM) with a past medical history (PMH) of hepatitis C, alcohol (EtOH) abuse, and

hypertension (HTN) is referred to the GI clinic because of elevated liver function tests (LFTs). He has no complaints.

Past medical history (PMH)

Intravenous drug abuse (IVDA) with heroin and cocaine abuse 3o years ago, hepatitis C, heavy alcohol abuse, HTN. Rectal

bleeding for 2 months - a colonoscopy showed 9 benign polyps (one tubular adenoma and 8 hyperplastic polyps).

Medications

Tenormin (atenolol), lisinopril.

Social history (SH)

Drug abuse as described above. He told his PCP that he is "in remission" from alcohol. On closer questioning, the patient

admitted to long term alcohol abuse in binging sprees, drinking 3-5 bottles of wine whenever he can afford it. The last binge

was just 2 weeks ago. He finances his EtOH abuse with the money he is receives for disability because of his liver disease.

Physical examination

WD/WN in NAD.

No signs of chronic liver disease.

HEENT: no teeth (lost in brawls as per patient).

The rest of the examination was normal.

What is your diagnosis?

Hepatitis and alcohol abuse.

What laboratory wor k-up would you order?

CBC, CMP, AFP.

Liver ultrasound (U/S).

What about hepatitis C genotype?

The treatment response in hepatitis C depends on the genotype. The response in HCV type 1 is only 40% with interferon

(INF) plus ribavirin for 12 months. HCV type 2 and 3 have a better response rate of 80% after 60 months.

Our patient's genotype was 1a.

Laboratory results

CMP, hepatitis profile (left). Hepatitis C viral load and genotype (right) (click to enlarge the images).

The patient already had laboratory work several months ago that showed elevated LFTs. His HDL level it is high because of

EtOH abuse. AFP is 6.2.

Would you recommend antiviral treatment with INF and ribavirin?

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No. EtOH abuse is a contraindication to the antiviral treatment of hepatitis C.

What happened?

The patient was referred to a drug abuse counseling center and a follow-up (F/U) appointment was made in 1 month to

monitor the progress. Liver U/S and repeat LFT were ordered.

All patients with chronic hepatitis C need AFP and liver U/S every 6 months to screen for hepatocellular CA.

What did we learn from this case?

Take a careful history of drug abuse. You cannot treat hepatitis C patients if the patient is still drinking heavily. EtOH abuse

has a detrimental effect on hepatitis C liver disease (interestingly, this is not typically the case with hepatitis B).

Even if you decide to treat this patient, his chance of response would be virtually zero because of the genotype and EtOH

abuse. The studies show that African American patients also have a lower response rate. In conclusion, we should f irst help

this patient stop drinking before treating his hepatitis C.

A "Green" Patient Treated with Valproate Develops Toxic Hepati tis Author: V. Dimov, M.D.Reviewer: S. Randhawa, M.D.

A primary care physician (PCP) called in a direct admission: "She's at the office and she's green".

The patients is a 30-year-old African American female (AAF) with a past medical history (PMH) of diabetes type 1 (DM1) with

multiple admission for diabetic ketoacidosis (DKA), and depression.

Patient has had nausea, vomiting and diarrhea (N/V/D) for 2 weeks. She went to the emergency room (ER) 2 weeks and

was told that she was having hepatitis C. Since then, the nausea and vomiting (N/V) are better but the d iarrhea worsened to

the point that she was having 15 watery bowel movements (BM) per day.

She went to see her PCP and was sent to the hospital as a direct admission with the above mentioned "green" color.


Depression, for which she is treated with aripiprazole (Abilify) and Depakote (divalproex), gastroparesis and bouts of

diarrhea. DM1 is not controlled due to noncompliance with insulin treatment and HA1c is usually in the 13-15 range.

What is the most likely diagnosis?

Infectious hepatitis is the number one cause on the differential list but there are other possible diagnoses as well.

Liver function test (LFTs) elevation can be due to drug toxicity (Depakote), autoimmune hepatitis or alcohol. However, she

denies drinking.

Diarrhea may be due to autonomic dysfunction secondary to poorly controlled diabetes but the cause may also be C. diff.

colitis since she has been in and out of ERs and hospitals over the last 2 weeks.


Visibly exhausted.

VS: Orthostatic changes.

Dry mucosal membranes, jaundice.

Abdomen: Soft with active BS, not painful .

The rest of the examination was not remarkable.


3/11

What laboratory test w ould you order?

CBCD, CMP, UA, acute hepatitis profile.

Stool WBC, C.diff. toxin x 2, O&P, C&S (O&P are rarely diagnostic but this is part of the standard diagnostic tests)

Why amylase and lipase? She had some episodic abdominal pain 3 weeks ago.

What happened?

AST and ALT were elevated in the range of 500-700 IU.

GGT was 1300, AP 500 and bilirubin 11 mg/dL, most of it was direct bilirubin (the repeated total bilirubin was 8 mg/dL, direct

7 mg/dL).

Lipase was more than 2000, amylase 214.

CMP in hepatitis; Lipase levels (click to enlarge the images).

Does she have pancreatiti s?

A CT scan of the abdomen was ordered and it did not show evidence of pancreatitis.

A GI consult was called and cholecystitis was ruled out with a negative HIDA scan.

Stool C. diff. was negative and diarrhea resolved with IVF and Immodium.

What is t he most likely diagnosis at this point ?

Pancreatitis?

Abilify can cause pancreatitis as a rare adverse event but the psychiatr ist who was consulted restarted the medication on

day 3 and the patient did not have any further complaints.

Repeated lipase was still elevated but with a negative CT scan of the abdomen and no pain pancreatitis was unlikely.

Amylase and lipase can be falsely elevated for a number of reasons and one of them is uncontrolled DM1/DKA.

TG level was just 74.

Hepatic Hydrothorax - An Uncommon Compl ication Of Cirrhosis

Author: M. Auron, M.D, Department of Hospital Medicine, Cleveland Clinic, OHReviewer: V. Dimov, M.D., University of Chicago, IL

A 63-year-old female was admitted to the hospital with a progressive dyspnea of one-week duration. She also had orthopnea

but denied chest pain, cough, palpitations, wheezing, fever or chills. Past medical history was significant for well-controlled

hypertension. Social history was positive for smoking; the patient denied using drugs or alcohol. Family history was

unremarkable.

Medications

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Amlodipine 10 mg daily and propranolol 40 mg BID.


Normal vital signs.

Anicteric.

Lung exam showed decreased air entry bilaterally, mostly on the right side with decreased vocal resonance and tactile

fremitus, with dullness to percussion over the right infra-axillary and infra-scapular areas.

Abdominal and cardiac exam was unremarkable.

The patient had bilateral pitting edema of lower limbs.

What is t he most likely diagnosis?

Pleural effusion.

What laboratory tests would you suggest?

- CXR (PA, lateral and decubitus).

- Complete blood count with differential (CBCD)

- Basic chemistry profile (BMP)

- Hepatic function panel (LFT) including coagulation profile (PT, INR and aPTT).

- Serum LDH

- Ascites fluid albumin, LDH, glucose, pH, cytology

- Thyroid function test

- BNP.

- Transthoracic echocardiogram to assess ejection fraction

Laboratory results

Chest roentgenogram revealed a large right sided pleural effusion.

LFTs showed hypoalbuminemia (2.5) and hyperbilirubinemia (Total 3.0, direct 2.5). INR was elevated (1.8) and PTT was

normal. Transaminases were normal.

The remaining of the tests was normal.

What treatment would you start for this patient?

The patient was started on diuretics and a salt/fluid restricted diet. A CT of the chest and abdomen was requested for further

evaluation of the effusion.

What happened?

The CT-scan of chest and abdomen showed liver appearance suggestive of cirrhosis without ascites.

Cirrhosis was confirmed via liver biopsy. Hepatitis serology was negative.

Work up for autoimmune hepatitis, alpha-1-antitrypsin deficiency, hemochromatosis and Wilson’s disease was negative.

Alpha fetoprotein was normal. Lipid prof ile showed elevated total cholesterol (280 with elevated LDL 200), suggesting NASH(Non-alcoholic steatohepatitis) as the etiology of cirrhosis.

(click to enlarge the images)

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What happened next?

One liter (1 L) of pleural fluid was drained via thoracentesis (pleural tap) and sent for analysis.

(click to enlarge the images)

The pleural effusion recurred despite conservative measures and frequent thoracocentesis. Hepatic hydrothorax was

considered as the most likely diagnoses in the setting of recurrent transudative pleural effusion in a patient with cirrhosis.

The patient underwent talc chemical pleurodesis and chest tube placement with clinical improvement and resolution of the

effusion.

Final diagnosis

Hepatic hydrothorax secondary to NASH-induced cirrhosis.


Hepatic hydrothorax is a recurrent transudative pleural effusion that occurs in patients with cirrhosis even in the absence of

ascites or other manifestations of portal hypertension. Most commonly is associated with persistent diaphragmatic defects

associated with relatively slow forming ascites; this results in pleural effusion as long as the rate of ascites formation does

not exceed the volume capacity of the pleural space. The only definitive treatment is liver transplantation.

Diverticulosis - a Typical Case Plus Colonoscopy Procedure Info A 79 yo AAF with a PMH of diverticulosis, diagnosed by colonoscopy 2 years ago, is admitted to the hospital with CC:

intermittent rectal bleeding for 3 days. She also c/o lower abdominal pain but no fever or chills.

PMH:

Diverticulosis, GERD, seizures, DM2, gout.

Meds:

Dilantin, Nexium, Colchicine, Seroquel.

SH:

Lives alone, no EtOH, smoking or drugs.

Physical examination:

VSS, no orthostatic changes. Please remember to check f or orthostatic changes in all patients with a suspected GI problem.

Examination: unremarkable.

What do you think i s going on?

Diverticulosis? (very likely)

Diverticulitis? The abdominal pain points to diverticulitis but the patient does not have fever or chills, CBCD is also important

to make the diagnosis.

Other causes of lower GI bleed seem less likely.

Remember the mnemonic H-DRAIN for DDx of lower GI bleed:

Hemorrhoids

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Diverticulosis / Diverticulits

Radiation colitis

AVM

Infection / IBD / Ischemic gut

Neoplasm

What tests would you or der?

CBCD, CMP, INR/PTTH&H q 8 hrs

Type and screen 2U PRBC. Please do not "type and cross" since if the units are not transfused, that blood is wasted.

GI consult

What happened?

Laboratory results

H&H was relatively stable but she continued to have bloody BM.

What is the next step?

A colonoscopy

Colonoscopy report (click to enlarge)

In terms of procedure length, a colonoscopy is reminiscent of a long journey as opposed to an EGD which resembles a short

commute. The colonoscope has to go all the way to the ileocecal valve and back. In this patient, there was some old brownblood in the rectum. The further north it went, the more blood we saw, and it became fresher and brighter. There were a lot

of diverticuli and you have to be very careful not to take a side road in one of the blind diverticuli pouches. Most of the blood

was in the upper descending and transverse colon. Going further, and the blood disappeared. By the time the colonoscope

reached the ileocecal valve, the mucosa was pale and shiny, with no sign of blood whatsoever. It looked like a low grade

continuous oozing somewhere in the transverse colon but there was no focal source of bleeding.

Final diagnosis:

Diverticulosis

What is usually the bleeding source in diverticulosi s?

Usually, the source is one ruptured vessel in one of the diverticuli and it is very difficult to see which one of the may

diverticuli pouches is to blame.

How do you anesthetize the patient during the procedure? All patients are hooked to a portable monitor which shows their HR, BP and SpO2, they have supplemental O2 by NC.

Versed and Demerol are the standard sedatives. Patients are often uncomfortable due to the gas inflation of the bowel

during the colonoscopy and they are encouraged to pass gas during the procedure.

What happened?

Hemoglobin slowly decreased to 9.1 mg/dL and stayed there, this was a drop of 3 grams since admission. Patient was

hemodynamically stable but continued to have a small amount of rectal bleeding with stools. This made us a little nervous

and we ordered a RBC Tc-tagged scan which was negative (no evidence of active bleeding). Patient was stable and was

D/C'd home with a stool softener and MoM PRN.

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Q & A

Does inflammation of d iverticulitis and bleeding of diverticulosis o ccur in the same area?

No. Diverticulitis affects the sigmoid colon almost exclusively although you can certainly find diverticuli all over the colon. The

bleeding on the other hand most commonly occurs in the descending to transverse colon.

What did we learn from this case? Common things happen commonly. This patient had a typical picture of diverticulosis as expected by history.

Usually the bleeding stops spontaneously, in this patient it just took a little more time (4 days).

Abdominal Pain and Diarrhea for 2 Months: Is it IBD? A 26-yo CF with a negative PMH comes to the GI lab f or a colonoscopy referred by her PCP with the CC: abdominal pain

and diarrhea for 2 months. She had noticed some mucus in her stools but no blood. No weight loss.

What do you think i s going on?

Infectious diarrhea vs. IBD?

Ask for any ABx use for URTI, UTI, etc.

Anybody else in the family with the same complaint?Diarrhea at night?

What happens if she is fasting?

Colonoscopy:

Loss of the normal vascular pattern, granular mucosa, a lot of mucus.

All this is suggestive of IBD - UC.

What labs would you ord er? CBCD, CMP, ESR

Stool C/S, O/P, C.diff x 2, WBC

How would you treat this patient?

Start 5-ASA and adjust any further treatment according to the labs and the colon biopsy.

What did we learn from this patient?

Always rule out infection f irst when a patient is having chronic diarrhea.

Patient may also need a biopsy to diagnose IBD.

Q&A

How to diagnos e UC?

History and stool examination permit a presumptive diagnosis of UC. Always confirm by sigmoidoscopy. Colonoscopy is not usually necessary before treatment and may be dangerous in active

stages because of the risk of perforation.

Source: Merck manual

How to diagnose Crohn's?

Diagnosis is usually made by x-ray - barium enema or small-bowel series.

CT can detect extramural complications but it is not routinely needed for initial diagnosis.

Source: Merck manual

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How to tr eat UC?

Check the guidelines from AFP

How to treat Crohn's?

Check the guidelines from AFP

References:

Management of Inflammatory Bowel Disease - AFP 1998Inflammatory Bowel Disease - NEJM 1996

Inflammatory Bowel Disease - Medical Progress - NEJM 2002

How does UC look on c olonoscopy?

It depends on the severity of the disease - mild, moderate, severe. Mild colitis produces redness and swelling of the mucosa,

resulting in a loss of the normal vascular pattern, an overall granular appearance, and friability (fragility with ease of

bleeding), mucosal granularity, exudate and superficial ulceration.

Small Bowel Obstruction (SBO) and Gas in the Portal System Author: V. Dimov, M.D., Allergist/Immunologist and Assistant Professor at University of Chicago

Reviewer: S. Randhawa, M.D., Allergist/Immunologist and Assistant Professor at LSU (Shreveport) Department of Allergy

and Immunology

86-year-old Caucasian female (CF) was admitted from a nursing home (NH) with a one week history of loose stools, and a 4-

day history of nausea and vomiting. She also complained of (c/o) distended abdomen with crampy abdominal pain. For the

last two days, attempts have been made at managing her at the nursing home with intravenous (IV) fluids and antiemetics.

She had no urinary complaints.


Coronary artery disease (CAD), congestive heart failure (CHF), hypertension (HTN), peptic ulcer disease (PUD),

osteoporosis and macular degeneration.

Past surgical history (PSH)

Hysterectomy and p lacement of a permanent pacemaker.

Medications

Potassium (KCl), atorvastatin (Lipitor), lisinopril, Protonix (pantoprazole), aspirin, Coreg (carvedilol), Digitek (digoxin oral),

and Lasix (furosemide).

Al lergies

She has reportedly multiple allergies including penicillin (PCN), Altace (ramipril), Prevacid (lansoprazole), Norvasc

(amlodipine), Ceclor (cefaclor), and Meclomen (meclofenamate).

Physical examination:

Vital signs (VS) 36-74-36-158/88. Appears acutely ill, she is in moderate distress and lethargic but arousable

Chest: bibasilar rhonchi, tachypneic

CVS: Clear S1S2

Abdomen: Distended and tympanic. She has generalized epigastric tenderness with mild guarding and rebound. Bowel

sounds are hyperactive. Rectal exam showed heme negative stool.

What is the most likely diagnosis?

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- Small bowel obstruction (SBO) vs. large bowel obstruction (LBO)

- Digoxin ("Dig") toxicity

- Ischemic colitis

- Gastroenteritis

- C. diff. colitis

What laboratory workup would you suggest?

CBCD, CMP, Dig level, UA, Stool WBC, C&S, O&P, KUB

What about a CT of the abdomen?

Laboratory results: WBC 16.4/mm3, hemoglobin 13 mg/dL, platelets were 269,000/mm3. She had 86% PMN, and no bands.

Her white count at earlier this morning was 10.8/mm3.

CBCD, note the elevated WBC with 86% PMN and the appearance of bands (36%) several hours later (click to enlarge the

images).

BMP in SBO - note the development of metabolic acidosis (click to enlarge the images).

Amylase and lipase are normal. Urinalysis is normal. Digoxin level is 1.2.

Abd ominal X-r ays - 3 views:

AXR: Lateral view, SBO, dilated small bowel loops, one air-fluid level (right). Pacemaker; Air-fluid level close-up (click to

enlarge the images).

SBO, multiple dilated small bowel loops. Close-up: note the valvulae crossing the lumen from side to side; in LBO the

haustrae cross only half-way (click to enlarge the images).

Radiology report: Very prominent gaseous distention of multiple loops of small bowel overlying the lower abdomen and

pelvis. Associated air fluid levels are noted on decubitus films. These findings are suspicious for SBO, with associated

prominent gastric distention and large air fluid level overlying stomach. No obvious free air is identified. There is severe

dextroscoliosis.

What happened?

The patient was admitted to the intensive care unit. She also had CT scan of the abdomen and pelvis in the ER. The working

diagnosis was bowel obstruction.

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Before the patient went to CT scan, a NG was put and 1200 cc of fecal like material was drained, and then about 400 cc of

contrast was passed per NG tube prior to CT.

What happened next?

The CT scan showed gas in the portal system.

CT chest and abdomen: Note the metallic reflections in the heart due to the pacemaker wires. Calciffication in the aorta,

contrast in the stomach (click to enlarge the images).

Gas in the portal system. Note also the severe scoliosis (click to enlarge the images).

Gas in the portal system. Dilated stomach half-filled with contrast (click to enlarge the images).

Dilated small bowel loops with air-fluid levels (click to enlarge the images).

Radiology report of CT abdomen and pelvis with IV and oral contrast:

Severe dextroscoliosis, resulting in distortion of upper abdominal anatomy. There is associated tortuosity and calcification of

the abdominal aorta. A NG tube terminates within the stomach, which is distended with contrast proximally. There is very

prominent distention of multiple loops of small bowel, with fluid distention more proximally and with fecal material being

suggested more distally. The findings are suspicious for severe distal SBO. No abnormal colonic distention is seen. No intra-

abdominal free air or generalized ascites is seen. There is extensive gas in the portal system. The uterus is presumed

surgically absent.

Impression:

1. Findings suspicious for high grade distal SBO. Surgical consult recommended.

2. No free air or generalized ascites.

3. Extensive gas in the portal system, of uncertain etiology.

Note: CT abdomen was initially read as pneumobilia (gas in the biliary system) which was later corrected. Pneumonilia is

central in distribution as opposed to the peripheral distribution of the gas in the portal system seen in this patient.

A surgical consult was called urgenlty. The preoperative diagnosis of small bowel obstruction was confirmed during the

laparotomy.The operation consisted of exploratory laparotomy and adhesiolysis.

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Upon entering the abdomen, multiple loops of densely adherent and distended small bowel loops were encountered. By

tracing the bowel down to the area of the ileocecal valve, the surgeon found dense adhesions which originated from the

pelvis. These were lysed, after which the loops of bowel were then seen to decompress themselves in the distal bowel and

into the cecum itself. The bowel appeared to be dusky but viable upon closer inspection. It was noted that the patient's

mesentery pulsations were quite diminished, although no ischemia was noted.

After surgery, the pat ient improved and was discharged to the nursing home.

Final diagnosis

Small bowel obsctruction (SBO) secondary to adhesions, and gas in the portal system.


Bowel obstruction is on top of the list in elderly patients with abdominla pain and N/V, especially with a history of previous

abdominal surgery.

CT abdomen is important in the diagnosis of SBO. Consult a surgeon early.

Comparison of small bowel obstructi on (SBO) and LBO features :

Small bowel------------------------Large bowel

Bowel diameter (cm)

>3 and 5

Position of loops

Central-----------------------------Peripheral

Number of loops

Many-------------------------------Few

Bowel markings

Valvaulae---------------------------Haustra

(all the way across)-----------------(partially across)

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