CLINICAL CASES

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CLINICAL CASES

• CHOLESTASIS

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CASE I
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• 24 yrs old male patient presented with jaundice,
  pruritus ,dark colored urine, epigastric pain
  ,vomiting and weight loss of one month duration.
• There was a history of occasional alcohol intake
  few months earlier.
• On examination the patient was jaundiced with
  scratch marks.
• No hepatomegaly ,splenomegaly or ascites.

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• Urine analysis bile pigments
• CBC normal
• Liver functions
• Total Bilirubin 9.5mg/dL
• Conjugated 4.9mg/dL
• ALT90 U/L
• AST109 U/L
• ALP301 U/L
• GGT 72 U/L
• PC 100
• FBS98mg/dL

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ABDOMINAL U.S.

• Liver is average in size, homogenous echo pattern
  with considerable dilatation of IHBRs and
  dilatation of the proximal part of the CBD8mm
  yet no definite stones seen inside. No HFL. PV
  is not dilated.
• No other abnormal findings were noticed.

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ABDOMINAL C.T.

• Moderate dilatation of the IHBRs as well as CBD
  down to the porta hepatis with normal caliber
  down to the duodenum ,no definite masses or
  stones.
• Pancreas and para-aortic area are free with no
  focal lesions or lymphadenopathy.

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Differential Diagnosis

• Luminal lesions e.g. stones ,worms.
• Wall lesions
• Cholangicarcinoma
• Benign bile duct stricture (e.g. PSC, benign
  tumors of the biliary tree).
• Extra-luminal lesions
• carcinoma of the pancreas
• chronic pancreatitis
• cystic lesions of the pancreas
• enlarged lymph node.

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ERCP

• Revealed a stricture in the CHD ,marked IHBR
  dilatation and a 19Fr 12cm stent was inserted
  with good drainage.
• On the following day, the pt. developed fever,
  rigors, Rt. hypochondrial pain , rising bilirubin
  (up to 21.6) and leucocytosis (most probably
  cholangitis).
• He received antibiotics and the condition started
  to improve gradually within few days.

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• Serum bilirubin was falling gradually but very
  slowly.
• A follow up abdominal U.S. showed
• No evidence of IHBRs dilatation.
• CBD is not dilated( 4mm at the level of hepatic
  hilum).
• A biliary stent is seen inside it reaching
  proximally into its intra-hepatic portion.

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Hepatitis Viral Markers

• HBsAg Negative
• HB core total and IgM were Negative.
• HAV IgM Negative.
• HCV Ab. Negative.

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• CA 19-9 354.2ng/ml (37.0ng/ml)
• CEA 6.5ng/ml. (5.0ng/ml)
• Anti fascoila antibodies 1/80.
• MRCP revealed
• Pancreatic cystic lesion related to the
  pancreatic tail at the region of lesser sac.
• No biliary tree obstruction Normal caliber of
  the CBD and IHBRs.

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• Surgical intervention was performed revealing
• -A cystic lesion(3x2x2cm) at the area of the
  pancreatic body.
• -The lesion was excised with part of the body
  and neck of the pancreas with resection of the
  lesser sac of the stomach related to the cyst.
• -Roux en Y pancreatic jujonostomy was done
  for drainage.

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Histo-pathological examination

• Aspirated fluid from the cyst showed inflammatory
  cells.
• Sections examined from the cyst wall revealed a
  pyloric wall showing a pseudo-cystic lesion lined
  by septic granulation with evidence of marked
  fibrosis and hemorrhage. The cyst is adherent to
  the pancreatic tissue with evidence of
  pancreatitis.
• No evidence of specific inflammation or
  malignancy.
• Conclusion pancreatic pseudocyst adherent to the
  pyloric wall and pancreas.

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PANCREATIC PSEUDO-CYST

• Definition a localized fluid collection that is
  rich in amylase and other pancreatic enzymes,
  that has a nonepithelialized wall consisting of
  fibrous and granulation tissue, and that usually
  appears several weeks after the onset of
  pancreatitis.
• Number Pancreatic pseudocysts can be single or
  multiple.
• Size varies from 2-30 cm.
• Site About 1/3rd of pseudocysts manifest in the
  head of the gland, and 2/3rd appear in the tail.

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• Etiology 75-85 of cases are caused by alcohol
  or gallstone diseaserelated pancreatitis.
• Sex The male predominance mirrors the male
  predominance in the incidence of pancreatitis.
• Age Pseudocysts may occur after pancreatitis in
  any age group.

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Clinical picture

• History
• consider the possibility of a pseudocyst in a
  patient who has persistent abdominal pain,
  anorexia, or abdominal mass after a case of
  pancreatitis.
• Rarely, patients present with jaundice or sepsis
  from an infected pseudocyst.
• Physical
• Patients very frequently have a tender abdomen.
• Patients occasionally have a palpable mass in the
  abdomen.
• Peritoneal signs suggest rupture of the cyst or
  infection.
• Other possible findings include Fever ,jaundice
  pleural effusion.

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Lab studies

• Serum tests have limited utility.
• Amylase and lipase levels are often elevated but
  may be within reference ranges.
• Bilirubin and LFT findings may be elevated if the
  biliary tree is involved.
• Analysis of the cyst fluid may help differentiate
  pseudocysts from tumors.
• CEA and CA-125 tumour marker levels are low in
  pseudocysts.
• Amylase levels are usually high in pseudocysts
  and low in tumors.
• Cytology is occasionally helpful in diagnosing
  tumors, but a negative result does not exclude
  tumors.

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Imaging studies

• Abdominal ultrasound ultrasound is not the study
  of choice for diagnosis.
• Abdominal CT scan
• CT scan is the imaging criterion standard for
  pancreatic pseudocysts. It has a sensitivity of
  90-100 and is not operator dependent.
• ERCP
• It is not necessary in diagnosing pseudocysts
  however, it is useful in planning drainage
  strategy.

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Imaging studies

• MRI
• MRI is not necessary for the diagnosis of
  pseudocysts however, it is useful in detecting a
  solid component to the cyst and in
  differentiating between organized necrosis and a
  pseudocyst.
• Endoscopic ultrasound
• Endoscopic ultrasound (EUS) is not necessary for
  diagnosis but is very important in planning
  therapy, particularly if endoscopic drainage is
  contemplated.

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Medical Care

• The goal of therapy is avoidance of
  complications.
• About 10 of pseudocysts become infected.
• Pseudocysts can also rupture.
• A controlled rupture into an enteric organ can
  sometimes cause GI bleeding.
• A free rupture into the peritoneal cavity
  produces abdominal pain and, rarely, peritonitis
  or even death.
• Most pseudocysts resolve without interference and
  only require supportive care.
• Indications for drainage include the following
• Complications
• Symptoms
• Concern about possible malignancy

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CASE II
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• A 46years old male patient presented to us with
  jaundice ,pruritus and pale stools of one month
  duration following an attack of abdominal pain ,
  vomiting .He lost 12kg within the period of
  illness .
• Examination revealed deep jaundice ,scratch marks
  but no hepato-splenomegaly ,ascites or other
  significant clinical finding.

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• Urine analysis bile pigments
• CBC was normal
• ESR was 50 in the 1st hour.
• Bilirubin Total 4.6 mg/dL
• Direct 3.4 mg/dL
• ALT118 U/L
• AST30 U/L
• ALP342 U/L (up to 104)
• GGT 22U/L
• PC 100
• FBS94mg/dL
• Serum bil. has raised up to 63 during hospital
  stay.

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• Abdominal U.S.
• Liver Average sized with bright echo pattern. No
  IHBR dilatation or HFL. Main portal vein is not
  dilated. CBD is not dilated.
• No other abnormal findings in the U.S.

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DIFFERENTIAL DIAGNOSIS

• Causes of intra-hepatic cholestasis
• Cholestatic viral hepatitis
• Drug induced cholestasis
• PBC
• PSC
• Septicemia
• Rare causes Benign recurrent cholestasis,
  Hodgkins disease and amyloidosis.

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Hepatitis Viral Markers

• HBsAg Negative
• HB core total and IgM were Negative.
• HAV IgM Negative.
• HCV Ab. Negative.
• EBV IgG Positive.
• EBV IgM Negative.
• CMV IgG 75.8 (up to 15)

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AUTOANTIBODIES

• ANA
• SMA
• AMA
• LKM
• ANCA

NEGATIVE
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• Protein electrophoresis showed mild
  hypo-proteinemia and hypo-albuminemia.
• Serum amylase was 54 (90)
• Abdominal C.T was normal.

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• Ultra-sound guided Liver biopsy was done and
  histopathological examination of the specimen
  revealed
• canalicular / hepatocellular cholestasis
  ,predominant acinar zone 3 involvement with
  minimal reactive inflammation unremarkable
  portal pathology.

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• On reviewing drug history there was occasional
  intake of NSAIDS for headache.

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DRUG INDUCED HEPATO-TOXICITY

• Common causes of drug induced hepatic reactions
  are antibiotics, NSAIDs, cardiovascular drugs and
  CNS modifiers.

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DRUG INDUCED HEPATO-TOXICITY

• Drug toxicity mechanisms
• Intrinsic or predictable drug reactions The
  injury can be due to the drug itself or to a
  metabolite. Acetaminophen and carbon
  tetrachloride are classic examples.
• Idiosyncratic drug reactions
• Hypersensitivity Phenytoin is a classic. The
  response is characterized by fever, rash, and
  eosinophilia and is an immune-related response
• Metabolic-idiosyncratic This type of reaction
  occurs through an indirect metabolite of the
  offending drug. The response rate is variable and
  can occur within a week or up to one year later.
  It occurs in a minority of patients taking the
  drug, and no clinical manifestations of
  hypersensitivity are noted. INH toxicity is
  considered to fall into this class.

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CASE III
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• 57 years old male presented to us with jaundice
  of 4 months duration, dark colored
  urine,pruritus, pale colored stools, bleeding
  tendency in the form of bleeding gums, but no
  fever or abdominal pain.
• The patient reported bilateral lower limb
  swelling 1 month prior to the onset of jaundice
  and recurrent attacks of DCL for 2 years which
  resolve with enemas, lactulose, hepamerz.

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• Examination revealed-
• General examination
• Pulse88/min regular BP110/70
• Disturbed conscious level
• Jaundice
• Flapping tremors.
• Bilateral soft pitting lower limb edema till
  knees.
• Generalized scratch marks.

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Abdominal examination

• Shrunken liver
• Splenomegaly 5cm from the costal margin, firm,
  smooth surface, rounded border, not tender.
• NO ascites

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• Urine analysis bile pigments
• HB 11 TLC 5,700 PLAT94000
• Liver biochemical profile
• Bil T25.9 Bil D14.12
• AST85 ALT29
• ALP125 GGT67(11-49)
• T.proteins6.3 Albumin2.1
• PC 55
• Normal kidney functions.

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• Abdominal Ultrasounddetailsssss
• Liver cirrhosis with IHBR dilatation centrally
  more in right lobe.
• Chronic calcular cholecystitis.
• Splenomegaly
• Mild pelvic ascites.
• Upper endoscopy
• -portal hypertensive gastropathy.
• -superficial duodenal ulcer on the posterior
  wall.

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ERCP

• Selective cannulation was done with some
  difficulty due to resistance in the lower most
  part of the CBD.Contrast injection revealed
• markedly dilated CBD with a short tight stricture
  segment at its lower most part.
• Dilatation of the stricture was done using a 10
  Fr dilator.
• A 10 cm 10 Fr stent was placed with good bile
  flow seen coming from the stent.
• Internal biliary drainage is established.

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• Tumor markers
• CEA5.6( )
• CA19-9 172( )
• (40xCEA CA19-9) 396
• Alfa feto protein3.1( )

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Follow up

• Bilirubin(T) 8.00
• Bilirubin(D)5.00
• Abdominal ultrasound
• -No dilated IHBR
• -Good function of the stent.

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Gall Stones in Liver Cirrhosis
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• An increased prevalence of gallstones was
  demonstrated in patients with liver cirhosis,
  higher in the advanced stages of the disease.
  Some studies have found impaired emptying of the
  gallbladder in cirrhotic patient
• Cirrhotic patients showed a higher prevalence of
  gallstones than healthy subjects (41 vs 15, P
  0.003), and the prevalence increased with the
  progression of liver cirrhosis (Child-Pugh class
  A 26, B 44, and C 65, P 0.02).
• Gallbladder contractility is impaired in patients
  with liver cirrhosis and gallstones. Hypomotility
  is proportional to the severity of liver disease.
  Gallbladder hypomotility might contribute to the
  increased gallstone formation in patients with
  advanced cirrhosis.