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case presentation obstructive jaundice

Case Presentation Obstructive Jaundice

Case presentation obstructive jaundice dr. ravi madhusudhana professor dr. manjunath post graduate dept of anaesthesiology. sdumc, kolar. * * * * identification of ... – powerpoint ppt presentation.

  • Dr. Ravi Madhusudhana
  • Dr. Manjunath
  • Post Graduate
  • Dept of Anaesthesiology. SDUMC, Kolar.
  • History- Relevant To Causes Of Jaundice Symptoms
  • Abdominal Examination To Differentiate Liver/ Spleen/Kidney For Ascites
  • Types Of Jaundice- LFT
  • Problems Of Hyperbilirubinemia
  • Relevance Of Child-pugh Score
  • Accumulation of Bilirubin (yellow pigment)in the skin and other tissues
  • Hemolytic Jaundice
  • Hepatic Jaundice
  • Obstructive Jaundice(Cholestasis)
  • Congenital Jaundice
  • It is due to intra- or extra hepatic obstruction of bile ducts
  • Intra Hepatic Jaundice
  • Primary Biliary Cirrhosis,
  • Drugs (contact with DDT, heavy metals, beryllium )
  • Extra Hepatic Biliary Obstruction
  • Inflammation,
  • Tumors, (Ampulla of Vater)
  • Name kalyan,
  • Age -50yrs ,
  • occupation - Farmer
  • Main complaints
  • Pain in abdomen - 15 days
  • Yellowish discoloration of urine - 12 days
  • Yellowish discoloration of eye - 10 days
  • pain at rt. Upper abdomen which is sudden in onset ,severe and colicky in nature ,increasing intensity for 2-3 min then relieved spontaneously after few minutes.
  • Frequency of pain was initially 2-3 times a day, presently 4-6 times a day.
  • Pain was non radiating in nature and increases on food intake and pt used to get mild relief on taking analgesic .
  • Pain was associated with nausea and vomiting .
  • Pain was not associated with body posture
  • Pt. also noticed clay colored stool since 12 days with yellowish discoloration of urine which gradually increased in intensity
  • No H/O of burning micturition
  • Then he also noticed yellowish discoloration of eyes followed by nail and palm.
  • Pt. is also giving h/o itching all over body since 8 days which was more in night .
  • There is also H/O decreased appetite since 4 days
  • Feeling better with less pain jaundice after an endoscopic stenting procedure done 3 days ago
  • Negative H/O-
  • no H/O fever
  • no H/O weight loss
  • no H/O similar illness previously
  • no history suggestive of
  • TB,DM ,HTN, any other chronic illness./ bleeding diathesis
  • no H/O blood transfusion / tattoo
  • pain, due to
  • gallbladder disease,
  • malignancy, or
  • stretching of the liver capsule
  • fever, due to ascending cholangitis
  • palpable and / or tender gallbladder
  • enlarged liver, usually smooth
  • palmar creases, below the breast, on the neck.
  • They indicate raised serum cholesterol of several months.
  • Xanthomas on the tendon sheaths are uncommonly associated with cholestasis.
  • xanthelasma -on the eyelids
  • scratch marks excoriation
  • finger clubbing
  • loose, pale, bulky, offensive stools
  • dark orange urine
  • Age and sex
  • Viral hepatitis is common in young adults.
  • CBD stone neoplastic jaundice seen in middle aged or elderly individuals.
  • Portal cirrhosis, primary cancer of liver pancreatic cancer predominates in males.
  • CBD Stone , PBC, carcinoma gall bladder common in females.
  • Any employment involving handling of hepatotoxic agents like
  • DDT, heavy metals, beryllium etc should be
  • Exposure to infection in medical paramedical workers ,there is a predisposition to leptospirosis among workers in rat infected premises.
  • Contact with jaundiced patients, if recent , should suggest possibility of infective hepatitis.
  • Family history
  • Association with anemia, gall stones removal of spleen suggests hemolytic jaundice.
  • Past history
  • Recent biliary tract surgery
  • History of alcohol intake in cirrhosis.
  • Use of drugs such as chlorpromazine, testosterone.
  • Sexual orientation
  • Diseases associated with male homosexuality
  • Onset of jaundice
  • Sudden Viral hepatitis, gall stones
  • Gradual more likely with cirrhosis,
  • pancreatic carcinoma, metastasis.
  • Progressive typical of malignant obstruction.
  • Fluctuating Stone in CBD, carcinoma
  • ampulla of vater or repeated
  • hemolytic episodes.
  • Strong colicky character suggests gall stones
  • Severe boring pain passing through back
  • suggests pancreatitis
  • In older patients, painless but fluctuating jaundice suggests intermittent obstruction by gall stones or necrotising papillary carcinoma.
  • Painless but progressive jaundice is usually due to
  • malignant obstruction of CBD.
  • Fever chills
  • if associated with bacterial viral infection ascending cholangitis.
  • Pruritus characteristic of cholestasis.
  • Morning anorexia , nausea retching suggests
  • alcoholism if symptoms are longstanding.
  • Urine dark coloured indicates cholestasis.
  • Stools pale stools indicate cholestatic jaundice.
  • EXAMINATION
  • Conscious cooperative and well oriented to T/P/P
  • Avg. built / Avg.nutrition
  • Hair normal
  • yellowish sclera - tongue dry and yellowish
  • Icterus present / no engorged neck vein / no enlarged lymph node / no pallor / no clubbing/no koilonychiya / no cyanosis / no edema
  • No general signs of liver cell failure gynecomastia,
  • loss axillary hair, spider naevi, clubbing, leukonychia,
  • palmar erythema, hepatic flap
  • RR- 14/min regular and abdominothoracic
  • Pulse-84/min (rt radial pulse), regular ,normal volume ,
  • no R-R delay no R-F delay , all peripheral pulses are palpable
  • BP- 130/84 (supine) rt arm ,by auscultatory method
  • Temp Afebrile
  • airway MPII, mouth opening - adequate
  • SYSTEMIC EXAMINATION
  • No added sounds
  • CVS-S1 S2 normal
  • ABDOMEN EXAMINATION-
  • INSPECTION- Contour normal flat abdomen
  • Umbilicus normal in shape and centrally placed.
  • scratch mark present on abdomen
  • no visible peristalsis seen
  • no any scar mark, no dilated vein
  • no petechiae ,no ecchymosis
  • no abdominal distension
  • local temperature normal
  • soft abdomen
  • no tenderness
  • no rebound tenderness
  • no localized swelling
  • no hepatomegaly
  • no splenomegaly
  • no palpable gall bladder
  • no fluid thrill
  • PERCUSSION-
  • tympanic note all over abdomen
  • liver dullness present and liver span is 13 cm in
  • midclavicular line
  • no shifting dullness
  • AUSCULTATION-
  • bowel sound present
  • no added sound and bruit present
  • No signs of portal hypertension
  • SHIFTING DULLNESS
  • Before ERCP
  • -Total bilirubin level of 26 mg/dL with a conjugated bilirubin of 18 mg/dL (normal level lt 0.7 mg/dl)
  • -Total bilirubin level of 8 mg/dL with a conjugated bilirubin of 6.85mg/dl
  • Aspartate aminotransferase 220 IU/L
  • Alanine aminotransferase 250 IU/L,
  • Hemoglobin level of 9 g/dL.
  • Albumin 3 g
  • CBC Normal limits
  • prothrombin time (secs) 45
  • Urinalysis positive bilirubin, normal urobilinogen
  • 50 yrs male with complaints of pain in right hypochondrium with yellowish discoloration of body associated with itching and clay colored stool without any history of weight loss, fever and chronic alcohol intake .
  • Provisional diagnosis obstructive jaundice post- ERCP status
  • D/D-choledocholithiasis
  • periampullary growth which obstruct
  • biliary tract.
  • Detection of hepatocellular injury
  • Aminotransferases
  • Lactate dehydrogenase
  • Glutathione-S-transferase
  • Assessment of hepatic protein synthesis
  • Serum albumin
  • Serum globulin
  • Prothrombin time
  • Detection of cholestatic disorders
  • (Indices of obstructed bile flow)
  • Alkaline phosphatase
  • 5 nucleotidase
  • Gamma glutamyl transpeptidase
  • Serum bilirubin(lt1mg/dl)
  • Quantitative liver tests
  • (Indices of hepatic blood flow metabolic capacity)
  • Indocyanine green(ICG)
  • Obstructive Jaundice
  • Lab Findings
  • Serum Bilirubin?
  • Feceal urobilinogen? (incomplete obstruction)
  • Feceal urobilinogen absence (complete obstruction)
  • urobilinogenuria is absent in complete obstructive jaundice
  • bilirubinuria ?
  • cholesterol ?
  • Urinary changes
  • bilirubin increased
  • urobilinogen reduced or absent
  • Faecal changes
  • stercobilinogen reduced or absent
  • ALT/SGPT-cytoplasmic(5-45 IU/L)18 hrs
  • AST/SGOT-cytoplasmic and mitochondrial(5-30 IU/L)36 hrs
  • Mild(100-249IU/l)- non-specific
  • Moderate(250-999IU/l)
  • Large(1000-1999IU/l)
  • Extreme(gt2000IU/l)
  • Mild - steatosis,
  • medications,
  • alcohol consumption,
  • cholestasis, chronic viral hepatitis,
  • haemochromatosis, neoplasms, cirrhosis
  • Moderate - acute viral hepatitis,
  • drug-induced liver injury and
  • flare-ups of chronic liver diseases
  • Large - acute on chronic active liver disease
  • Extreme - fulminant viral hepatitis,
  • severe drug induced liver injury,
  • shock liver,
  • hypoxic hepatitis,
  • autoimmune hepatitis,
  • acute biliary obstruction
  • gt4 wilsons disease
  • 2-4 alcoholic liver disease
  • lt1 non-alcoholic steatohepatitis
  • 105-333 IU/L
  • Elevated levels may reflect hepatocellular injury, extrahepatic disorders or both
  • Extreme increases signify massive liver disease
  • Prolonged concurrent elevations in LDH and AP-malignant infiltration of the liver
  • Extrahepatic- hemolysis,
  • rhabdomyolysis,
  • tumour necrosis,
  • renal infarction,
  • acute cerebrovascular accident,
  • myocardial infarction
  • Hepatocellular injury- accompanied by AST/ALT
  • Sensitive and specific test for drug induced liver injury
  • Serial measurements can reveal the time course of hepatic injury
  • In acinar zone 3
  • More sensitive than AST or ALT as a marker of centrilobular necrosis in its incipient stages.
  • To assess hepatocellular function
  • To evaluate chronic liver disease
  • Half life of nearly 3 weeks
  • Procoagulants have short half life
  • Factor VII 4 hrs, fibrinogen 4 days
  • Levels descend shortly after liver begins to fail
  • PT-measures factors II, V, VII and X
  • Prolonged PT- low level of factor VIIa
  • 20-140 IU/L(35-115 in males and 25-95 in females)
  • Circulating half life 7 days
  • To screen diseases of the liver or biliary tree- hepatitis, malignancies and cholestatic diseases
  • Extreme increases indicate
  • a) major block in biliary flow due to primary biliary
  • cirrhosis and choledocholithiasis.
  • b) hepatic malignancy compressing some
  • intrahepatic bile ducts.
  • 5nucleotidase-2-17U/L
  • Gamma glutamyl transpeptidase 0-51IU/L(lt70 in males and lt40 in females)
  • To distinguish between hepatic and extrahepatic sources of AP
  • Changes in AP secondary to hepatobiliary disease usually followed by 5NT
  • Serum AP and GGTP increase in tandem, whereas 5NT may not change for days
  • Inducible microsomal enzyme( by alcohol, anticonvulsants and warfarin)
  • Less specific than 5NT
  • Bone contains very little GGTP-therefore distinguish between osseous and hepatobiliary sources.
  • Most widely used test for hepatic excretory function
  • Normally below 1mg/dl
  • gt4mg/dl-yellowish discoloration of body tissues
  • Serological testing- viral, microbial and autoimmune
  • Genetic testing-heritable metabolic disorders
  • Tumor marker assays- hepatic malignancies
  • Total Hepatocellular mass- by measuring the clearance of a substance such as indocyanine green, bromsulphalein and rose Bengal
  • Drug metabolizing capacity
  • Caffeine clearance
  • Galactose elimination capacity
  • Aminopyrine breath test
  • Antipyrine clearance
  • Unconjugated bilirubin is toxic for neuronal cell whereas the conjugated bilirubin is responsible for renal dysfunction in patient with obstructive jaundice.
  • Bilirubin value rarely exceeds 6mg/dl in Haemolytic anaemia.
  • Intrahepatic cholestasis to cause rise in bilirubin, drainage of
  • bile in gt75 parenchyma should be blocked
  • Sepsis or renal failure should be excluded if the bilirubin exceeds 30mg/dl in patient with CBD stone.
  • Serum bilirubin will take atleast 1-2 weeks to return to normal following the relief of obstruction ( half life of bilirubin is 2weeks).
  • Negative inotropic effect by bile salt.
  • Negative chronotropic effect by bile salt.
  • Due to activation of RAS, intravascular interstitial volume expansion occurs, several types of shunts develop ,leading to hyderdynamic circulation.
  • Decreased vascular resistance( peripheral vasodilation, increased arteriovenous shunting)
  • Blood volume maintained or increased , but redistributed.(splanchnic hypervolaemia, central hypovolemia)
  • Increased blood flow in splanchnic (extrahepatic), pulmonary, muscular and cutaneous tissues.
  • Decreased total hepatic blood flow
  • maintained hepatic arterial blood flow
  • decreased portal venous blood flow
  • Beta receptor density reactivity in the myocardium of cirrhotic patients diminished, thus ionotropic responses to sympathomimetic drugs reduced in liver disease.
  • Intrapulmonary shunting caused by intrapulmonary vascular dilatations(precapillary or arteriovenous)
  • triad of chronic liver disease ,increased alveolar
  • arterial oxygen gradient and evidence of IPVD is
  • defined as hepatopulmonary syndrome.
  • Ventilation perfusion mismatch caused by impaired hypoxic pulmonary vasoconstriction, pleural effusions, ascites and diaphragm dysfunction.
  • Decrease in pulmonary diffusion capacity secondary to increased extracelluar fluid, interstitial pneumonitis,and/or pulmonary hypertension.
  • Haemodynamic instability caused by the bile salts
  • endotoxin on the cardiovascular function.
  • Three main functional abnormalities in cirrhosis are reduction in sodium excretion,
  • reduction in free water clearance,
  • decrease in renal perfusion and glomerular filtration.
  • Direct nephrotoxic effect by bile salt and conjugated
  • bilirubin .
  • Renal tubule blockade of bilirubin cast may further
  • potentiate the renal injury.
  • Decreased production of coagulation and inhibitor factors
  • Synthesis of dysfunctional clotting factors
  • Quantitative and qualitative platelet defects
  • Vitamin K deficiency
  • Decreased clearance of activated factors
  • Hyperfibrinolysis
  • elevated serum bilirubin - in proportion to duration of cholestasis returns to normal once cholestasis is relieved
  • raised serum alkaline phosphatase - to more than 3X upper limit of normal
  • LFTs - aminotransferases mildly raised raised gamma GT
  • increased urinary bilirubin
  • urinary urinobilinogen is excreted in proportion to amount of bile reaching the duodenum i.e. absence of urinobilinogen indicates complete biliary obstruction
  • The first diagnostic test to use in patients whose liver tests suggest cholestasis,
  • To look for the presence of a dilated intrahepatic or extrahepatic biliary tree or to identify gallstones.
  • In addition, it shows space-occupying lesions within the liver, enables the clinician to distinguish between cystic and solid masses.
  • Ultrasound with Doppler imaging can detect the patency of the portal vein, hepatic artery, and hepatic veins and determine the direction of blood flow.
  • Dilated ducts on ultrasound - percutaneous transhepatic cholangiograpy
  • Undilated ducts on ultrasound - endoscopic retrograde cholangio-pancreatography
  • Needle biopsy of the liver
  • Pain, jaundice (charcot s triad)
  • Hepatomegaly
  • Spleenomegaly
  • GI bleeding
  • Once Jaundice is recognized, it is important to determine whether hyperbilirubinemia is predominantly Conjugated B or UnConjugated B?
  • Differentiation of hemolytic from other type of Jaundice is usually not difficult.
  • The laboratory findings are in constant in partial biliary obstruction and differentiation from intrahepatic cholestesis is particularly difficult.
  • Jaundice- Differential diagnosis
  • Differential Diagnosis
  • Exclude UCB (e.g. hemolysis or Gilbert Synd.)
  • Distinguish hepatocellular from obstructive
  • Distinguish intrahepatic from extra hepatic cholestasis
  • DIXON FREIDMAN RISK FACTORS
  • S.Bilirubin gt 11mg/dl
  • Malignant obstruction
  • Haematocrit lt 30
  • Renal failure
  • Cholangitis
  • Hypoalbuminemia
  • If at least 3 of above mortality 60
  • If none of above mortality 5
  • Child A - Safely undergo elective surgery.
  • Child B - may undergo elective surgery after
  • optimisation with caution.
  • Child C - Contraindication for elective surgery.
  • Presence of infection
  • WBC gt 10,000
  • Treatment with gt 2 antibiotics
  • PT gt 1.5 sec over control
  • Presence of ascites
  • Malnutrition
  • Emergence surgery

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obstructive jaundice

OBSTRUCTIVE JAUNDICE

Sep 02, 2014

1.08k likes | 2.69k Views

OBSTRUCTIVE JAUNDICE. Presented by: MD. TANVIR MAJUMDER, Roll no.144 MD. MAHEDI HASAN, Roll no.150 MONIRUL HOQUE, Roll no.162 MD. SHAHADATH HOSSAIN, Roll no.163. CASE PRESENTATION ON: Obstructive jaundice. PARTICULARS OF THE PATIENT :.

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OBSTRUCTIVE JAUNDICE Presented by: MD. TANVIR MAJUMDER, Roll no.144 MD. MAHEDI HASAN, Roll no.150 MONIRUL HOQUE, Roll no.162 MD. SHAHADATH HOSSAIN, Roll no.163

CASE PRESENTATION ON: • Obstructive jaundice

PARTICULARSOFTHEPATIENT : Name : Mr. Kala Mohon Das Age : 65 years Fathers name :Late Nagar Baul Das Sex : Male Marital status: Married Religion : Sanatan Occupation: Garment worker Address: Gangabari, Pathorghata, Kotowalli, Ctg Bed no. : 18 Ward no.: 25 Date of admission :7-4-2013; 7pm Date of examination :25-4-2013;8pm

THE PRESENTING COMPLAINTS: • 1. recurrent pain in the right upper abdomen for last 1 year. • 2. yellow discoloration of eyes and skin for the same duration.

HISTORY OF PRESENT ILLNESS: According to the patient’s statement his presenting complaints started 1 year back. He developed severe pain in right upper abdomen which is colicky in nature, intermittent, radiating to the back on the tip of the scapula. The pain aggravated by taking food and relieved by medication, which was episodic occurring at an interval of 1 or 2 months. He had moderate grade, intermittent fever which was associated with chills and rigor. He also complained of vomiting after taking any food. Vomitus was non projectile, whitish in colour and contained both digested and undigested food particles. He had yellow discolouration of eyes and urine for the same duration. His bowel habit is normal. He has no history of pale colouration of stool. He has itching all over the body. He also has no history of weight loss, cough, hemoptysis, haematemesis, melaena or bone pain.

HISTORY OF PAST ILLNESS: • Patient gave no history of DM, HTN, TB, bronchial asthma.

PERSONAL AND SOCIO-ECONOMIC HISTORY: • Patient is non-smoker, non-alcoholic. • He comes from a lower-middle class family. He lives on average diet and uses sanitary latrine. FAMILY HISTORY: None of his family members is known to be suffering from the same or any other diseases.

DRUG HISTORY : He used to take analgesics and antipyretics for the last 3 months but could not mention the name of the drugs. ALLERGIC HISTORY: • He is not allergic to any drug or any particular food. TRANSFUSION HISTORY: • Patient has no history of blood transfusion.

General Examination

Appearance: Anxious • Body built: Average • Nutrition: Average • Co-operation: Cooperative • Decubitus: On choice • Anaemia: Absent • Jaundice: PRESENT (++) • Cyanosis: Absent • Clubbing: Absent • Edema: Absent • Dehydration: Absent • Pulse: 80 beats/minute • Blood pressure: 110/80 mm of Hg • Temperature: 100 degree F • Respiratory rate: 18 breaths/minute • Neck vein: Not engorged • Neck gland: Not enlarged • Peripheral lymph node: Not palpable • Hernial orifice: Intact

Abdomen examination • Abdomen is normal in shape. • Umbilicus is centrally placed, inverted, vertical slit. • No engorged vein. • No visible peristalsis. • No scar mark. • Hair distribution normal. • No visible pulsation. inspection

SUPERFICIAL PALPATION : • Hyperesthesia: absent • Tenderness: present in right hypochondriac region. • Temperature : raised • Muscle guard: absent DEEP PALPATION • Liver : not palpable • Gall Bladder: not palpable • Spleen: not palpable • Kidney: not palpable • Urinary bladder :not palpable. • Murphy’s sign: negative

Percussion • Note: Tympanic • Shifting dullness and fluid thrill absent

Auscultation • Shows no abnormality • Bowel sound present digital rectal examination

Cardiovuscular system: Peripheral pulses: All are present,symmetrical. Precordium: Apex beat: Left 5th ICS, 9 cm from midline Thrill: Absent Left parasternal heave: Absent Heart sound: Audible normally in all 4 areas Added sound: Absent

Respiratory system: Position of trachea and apex beat: Normal Chest expansion: Normal Percussion note: Resonant Breath sound: Normal Added sound: Absent

Nervous system Higher Mental function: Normal Cranial nerves: Intact Speech: Normal Signs of meningeal irritation: Absent Motor function: Intact Sensory function: Intact

SALIENT FEATURES: Mr. Kala Mohon Das, 65 years old, hailing from Kotowalli, Chittagong presented with the complaints of pain in the right upper abdomen for last 1 year, and yellow discoloration of eye and skin for the same duration. According to the patient’s statement, his presenting complaints started 1 years back when he developed pain in right upper abdomen which was severe, colicky in nature, intermittent, radiating to the back, aggravated by taking food and relieved after taking medication, which was episodic occurring at an interval of 1 or 2 months. He had moderate grade, intermittent fever which was associated with chills and rigor. He also complained of vomiting after taking any food. Vomitus was non projectile, whitish in colour and contained both digested and undigested food particles. He had yellow discolouration of eyes and urine for the same duration. His bowel habit is normal. He gives no history of pale colouration of stool. He has itching all over the body. He gave no history of weight loss, cough, chest pain, hemoptysis, haematemesis, melaena and bone pain. He has no history of blood transfusion. No member of his family is suffering from this disease. He is non-smoker, non-hypertensive, not diabetic.

On general examination, patient is anxious,co-operative,average built. He is icteric but not anaemic. Neck gland are not palpable, neck veins are not engorged, no ascites, no oedema is present. Hernial orifices are intact and all accessible peripheral lymph node are not palpable. His pulse, B.P., respiration was within normal limit and there was slight rise of body temperature. On abdominal examination, abdomen is normal in shape, umbilicus centrally placed,inverted,no scar mark, no engorged vein. Murphy’s sign is negative. There is tenderness in right hypochondriac region. Liver or other organs are not palpable. Bowel sound is present. Other systemic examination reveals no abnormality.

PROVISIONAL DIAGNOSIS: • OBSTRUCTIVE JAUNDICE due to choledocholithiasis

DIFFERENTIAL DIAGNOSIS: Obstructive jaundice due to: • carcinoma head of pancreas • Biliaryascariasis • Periampullary carcinoma • Cholangiocarcinoma

INVESTIGATIONS: 1.USG of whole abdomen with special attention to hepatobilliary system and pancreas: To visualize- -gall bladder -Liver -LN -Ascites 2.LIVER FUNCTION TEST: -serum bilirubin -SGOT -SGPT -Alkaline phosphatase -prothrombin time 3.FOR GENERAL ASSESSMENT: -CBC -urine R/E -RBS -serum creatinine -CXR -ECG

Confirmatory diagnosis: • Obstructive jaundice due to choledocholithiasis.

What is jaundice ? Jaundice may be defined as yellow discolouration of skin,sclera and mucous membrane due to an increase billirubin concentration in the body fluid above normal. Serum total bilirubin:(normal 0.3-1.2 mg/dl ) clinically detectable: >3.0 mg/dL

Anatomy of biliary system

BilLirubin Production & Metabolism:

Pathophysiologic classification of Jaundice • Hemolytic Jaundice • HepatocellularJaundice • Obstructive Jaundice

OBSTRUCTIVE JAUNDICE: • Obstructive jaundice occurs due to mechanical obstruction of the common bile duct.

CAUSES OF OBSTRUCTIVE JAUNDICE: 1.IN THE LUMEN: -gall stone -round worm 2.IN THE WALL: -congenital atresia -traumatic stricture -cholangitis -tumour of the bile duct 3.OUTSIDE THE WALL: -carcinoma head of the pancreas -carcinoma of ampulla of vater -pancreatitis -enlarged LN at portahepatis due to metastasis.

EXAMINATION FINDINGS OF OBSTRUCTIVE JAUNDICE: B.CARCINOMA HEAD OF PANCREAS: 1.Palpable liver 2.palpable mass 3.splenomegaly 4.palpable gall bladder. 5.weight loss. A.CHOLEDOCHOLITHIASIS: 1.patient-toxic,ill-looking 2.jaundice-long standing produce a deep green hue. 3.dehydrated 4.skin scratch mark all over the body. 5.increased temperature. 6.no lymphadenopathy. 7.tenderness in right hypochondriac region. 8.gall bladder is not palpable. 9.liver may be enlarged.

EXAMINATION FINDINGS OF OBSTRUCTIVE JAUNDICE: D.CHOLANGIOCARCINOMA: 1.patient is cachectic, anaemic 2.ichteric,dehydrated 3.hepatomegaly 4.palpable gall bladder-if lesion below cystic duct 5.ascitis-in advanced cases. C.PERIAMPULLARY CARCINOMA: 1.Fluctuating jaundice 2.palpable gall bladder 3.ascitis. 4.weight loss 5.palpable liver(may be)

COURVOISIER’S LAW: THE LAW STATES: 1)In case of obstructive jaundice due to stone in CBD,the gall bladder is not palpable/distended due to previous inflammatory fibrosis. 2)whereas,in obstruction of CBD due to pressure from outside(CA head of pancreas)the gall bladder become distended and palpable in an attempt to reduce the pressure in biliary system.

COMPLICATIONS OF OBSTRUCTIVE JAUNDICE: 1.Cholangitis 2.liver abscess 3.septicemia 4.hepatic failure 5.secondary biliary cirrhosis 6.acute pancreatitis 7.haemorrhage or haemobilia 8.acute renal failure. 9.gall stone ileus

Investigation

For diagnosis of obstructive jaundice: Liver function test: • Prothrombin time (markedly raised) • Serum Bilirubin (conjugated) • Fecealurobilinogen (incomplete obstruction) • Fecealurobilinogen absence (complete obstruction) • Bilirubinuria(conjugated)  • ALP markedly  • GGT & 5’ nucleosidase (most reliable)

For diagnosis of cause: • USG of whole abdomen with special attention to hepatobiliary system and pancreas (sensitivity 75-90%,specificity 80-100%) • ERCP • MRCP • CT scan • Radioisotope scanning • PTC • Endoscopic ultrasound • Routine investigation: For general anaesthesia: • CBC • Urine R/E • RBS • Serum creatinine • CXR • ECG

For staging • CXR • CT scan • MRI • PET-scan • Bone scan-if symptoms present

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Introduction, case presentation, removal of a large symptomatic retrocardiac mediastinal lipoma.

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Martina Wollheim, Lily F S Willatt, Jonas P Ehrsam, Priska Cerncic, Mario L Lachat, Othmar Schöb, Ilhan Inci, Removal of a large symptomatic retrocardiac mediastinal lipoma, Journal of Surgical Case Reports , Volume 2024, Issue 5, May 2024, rjae273, https://doi.org/10.1093/jscr/rjae273

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Large mediastinal lipomas are rare. Complete surgical resection can be difficult due to the intricate anatomy in the mediastinum. We report the case of a 75-year-old man with worsened retrosternal pressure, decline in performance and syncope episodes. Computed tomography revealed a large retrocardiac low-attenuated mediastinal lesion measuring 10 × 8 cm, compressing the left atrium and pulmonary veins bilaterally. Surgical exploration was achieved through a right anterolateral thoracotomy with a successful en bloc resection without any intraoperative complications. The total operation time was 185 min with a total blood loss of <250 ml. Stand-by extracorporeal life support was present throughout the procedure, but its use was not required. The postoperative course was uneventful. The pathological examination revealed a mature mediastinal lipoma without any evidence of malignancy. In the 12-month control the patient was completely free of symptoms and in a good general condition.

Lipomas are well-demarcated, slow-growing mesenchymal tumors originating from adipose tissue, predominantly manifesting a benign entity. Mediastinal location is rare and are mostly incidental findings. They rarely produce mediastinal compartment syndrome even at considerable sizes and can grow undetected for years. Surgical excision is usually postponed until symptomatic, leading to an increased morbidity associated with surgery, generally requiring cardiopulmonary support. Successful tumor resection is associated with a good prognosis. This case-report illustrates a safe-approach for removal of a large symptomatic retrocardiac mediastinal lipoma, not requiring extracorporeal life support (ECLS) despite cardiac manipulation. This work has been reported in line with the SCARE criteria [ 1 ].

A 75-year-old Caucasian man presented with worsened retrosternal pressure, decline in performance and syncope episodes. The patient was investigated 2-years earlier for performance intolerance, revealing a 9 × 8.5 cm mediastinal retrocardiac lesion in a computed tomography (CT)-scan, initially classified as oligosymptomatic. The progredient symptomatology prompted a new CT-scan showing a slight increase in size of the lesion to 8 × 10 cm, compression of the left atrium and pulmonary veins bilaterally ( Fig. 1A–C ). An echocardiography performed at rest demonstrated a regular cardiac output with no obstruction of flow in the pulmonary veins or arteries. A pre-operative diagnosis of a benign lipoma was suspected. Interdisciplinary concerns about a potentially abrupt and fatal insufficiency during increased exercise led to the referral to surgery.

Contrast enhanced CT scan of mediastinum demonstrating the well-defined focal fat-attenuated homogenous lesion. (A) Coronal view, (B) sagittal view, (C)axial view.

Contrast enhanced CT scan of mediastinum demonstrating the well-defined focal fat-attenuated homogenous lesion. (A) Coronal view, (B) sagittal view, (C)axial view.

The surgical exploration was achieved through a right lateral thoracotomy with a retro- and trans-pericardial approach. The thoracotomy was performed in the fifth intercostal space with division of the fifth rib in the cartilaginous portion with subsequent severing of the pulmonary ligament ( Fig. 2A ). Following circumferential dissection of the posterior pulmonary hilum the encapsulated soft tumor, reminiscent of a lipoma, became visible in the posterior mediastinum. The inferior pulmonary vein and the left atrium were intricately grown together with the tumor capsule, spanning from an extra- to intrapericardial location which required a meticulous dissection ( Fig. 2B, C ). Additionally, a 5-cm-long pericardial opening lateral to the phrenic nerve was necessary for complete resection ( Fig. 3A ). Free dissection of the superior vena cava (SVC) and azygos vein in a dorsal direction was performed to detach the tumor capsule from the retrocaval space and right atrium. An additional 8 cm long longitudinal opening of the pericardium up to the level of the anonymous vein was required. Dissection of the aperture between the SVC and aorta generated a supplementary window to further dissect the tumor capsule dorsally from these structures, the pulmonary artery and the remaining retro-pericardial area. Finally, with ventral mobilization of the heart the tumor resection could be completed ( Fig. 3B, C ). Upon re-ventilation, the lungs promptly expanded to optimal capacity.

Intraoperative images. (A) After thoracotomy giving access to mediastinum, (B) incision in posterior mediastinal pleura giving access to posterior mediastinum, (C) separating lipoma around SVC, superior pulmonary vein (SPV), ascending aorta, right atrium (RA), hidden pulmonary truncus, and right pulmonary artery.

Intraoperative images. (A) After thoracotomy giving access to mediastinum, (B) incision in posterior mediastinal pleura giving access to posterior mediastinum, (C) separating lipoma around SVC, superior pulmonary vein (SPV), ascending aorta, right atrium (RA), hidden pulmonary truncus, and right pulmonary artery.

Intraoperative images. (A) Intraoperative view of inferior pulmonary vein (IPV), SPV, phrenic nerve, right atrium, and the lipoma, (B) final removal of the Lipoma from the right incision of the dorsal mediastinum, (C) resection site after removal of lipoma before closure.

Intraoperative images. (A) Intraoperative view of inferior pulmonary vein (IPV), SPV, phrenic nerve, right atrium, and the lipoma, (B) final removal of the Lipoma from the right incision of the dorsal mediastinum, (C) resection site after removal of lipoma before closure.

The tumor was successfully resected en bloc in its capsule without any intraoperative complications. The total operation time was 185 min with a total blood loss of <250 ml. Stand-by ECLS was present throughout the procedure in case of hemodynamic insufficiency during cardiac manipulations or bleeding, but its use was not required at any point. The postoperative course was uneventful and 4-h after the operation the patient could be extubated in the intensive-care unit (ICU). 24-h post-surgery the patient could be transferred from the ICU to a regular ward and the chest-drain could be removed after 4 days. The subsequent x-ray revealed distended lungs bilaterally with an unremarkable mediastinal silhouette and the patient was discharged from the hospital in a good general condition on Day 7 post-op. The following day, the patient experienced an episode of atrial fibrillation for which he sought medical attention in his local hospital. In the 12-month control the patient was completely free of symptoms and in a good general condition.

Gross appearance showed a lobulated lesion with distinct yellow-fatty-tissue resembling a lipoma. It had a soft texture with a smooth surface covered by a thin shiny membrane. The tumor measured 10 × 8.5 cm and had a formalin-fixed weight of 172 g ( Fig. 4A ). The microscopic examination showed an encapsulated tumor composed of abundant mature adipose cells with adipocytes that exhibited uniformity in both size and shape ( Fig. 4B ). There was no detection of lipoblasts, increased mitotic rate, or zones of necrosis indicating malignancy. The definitive pathological examination was a mature retrocardiac mediastinal lipoma without any evidence of malignancy.

Macro- and microscopic findings. (A) Gross appearance of the lesion, (B) histological examination of the lesion, composed of abundant mature adipose cells with adipocytes exhibiting uniformity in both size and shape. 10× magnification, H&E stain.

Macro- and microscopic findings. (A) Gross appearance of the lesion, (B) histological examination of the lesion, composed of abundant mature adipose cells with adipocytes exhibiting uniformity in both size and shape. 10× magnification, H&E stain.

Lipomas are the most frequently encountered soft-tissue neoplasm in adults and are rarely situated in the mediastinum [ 2 ]. In this case, large mediastinal tumors occur mostly in the anterior portion and represent 1.6–2.3% of all primary mediastinal tumors [ 3 ]. A lipomatous lesion of the mediastinum tends to grow slowly and is always classified as benign except those causing mediastinal compartment syndrome. These lesions should be regarded as clinically malignant and treated with en bloc excision [ 4 ].

Liposarcomas are a diverse group of malignant soft-tissue tumors. Well-differentiated liposarcomas (WDLS) can be difficult to discern from a benign lipoma on imaging. In a study [O’Donnell et al .], experienced musculoskeletal-radiologists and orthopedic-oncologists were able to differentiate between lipomas and WDLS in imaging in 69% of cases [ 5 ]. WDLS are associated with amplification of chromosome segment 12q13-15, which carries the oncogenes MDM 2 , CDK 4 , and HMGA 2 [ 6 ]. These amplifications are not seen in lipomas and its presence helps to differentiate them from WDLS [ 7 ]. A histological exploration is therefore recommended in the pre-operative phase to differentiate these, especially in surgeries where an en bloc resection can’t be guaranteed. In our case, the suspected pre-operative diagnosis of lipoma was based on imaging in conjunction with the slow progression of the lesion over time. A fluorescence in situ hybridization to detect genetic abnormalities involving MDM 2 to rule out a malignant WDLS should have been performed.

Local recurrence of intrathoracic and mediastinal lipomas is uncommon following complete resection [ 7 ]. Generally, surgery is delayed until the lipoma is large, probably because of the morbidity associated with surgery under cardiopulmonary support. This case illustrated an original interdisciplinary, less invasive and safe approach with a good patient outcome. Such an approach allows to treat patients earlier before they develop life-threatening symptoms. Stand-by ECLS is an important pre-cautionary to have available during surgery, but may not be required.

Sohrabi C , Mathew G , Maria N , et al.    The SCARE 2023 guideline: updating consensus surgical case report (SCARE) guidelines . Int J Surg   2023 ; 109 : 1136 – 40 . https://doi.org/10.1097/js9.0000000000000373 .

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Gaerte SC , Meyer CA , Winer-Muram HT , et al.    Fat-containing lesions of the chest . Radiographics   2002 ; 22 : S61 – 78 . https://doi.org/10.1148/radiographics.22.suppl_1.g02oc08s61 .

Kandakure PR , Kambhampati S , Katta Y , et al.    Giant bilateral posterior mediastinal liposarcoma excision . Indian J Thorac Cardiovasc Surg   2018 ; 35 : 91 – 3 . https://doi.org/10.1007/s12055-018-0703-6 .

O’Donnell PW , Griffin AM , Eward WC , et al.    Can experienced observers differentiate between lipoma and well-differentiated liposarcoma using only MRI?   Sarcoma   2013 ; 2013 : 1 – 6 . https://doi.org/10.1155/2013/982784 .

Crago AM , Dickson MA . Liposarcoma . Surg Oncol Clin N Am   2016 ; 25 : 761 – 73 . https://doi.org/10.1016/j.soc.2016.05.007 .

Rizer M , Singer AD , Edgar M , et al.    The histological variants of liposarcoma: predictive MRI findings with prognostic implications, management, follow-up, and differential diagnosis . Skeletal Radiol   2016 ; 45 : 1193 – 204 . https://doi.org/10.1007/s00256-016-2409-4 .

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IMAGES

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