Upload
bhagirath-s-n
View
3.393
Download
27
Tags:
Embed Size (px)
DESCRIPTION
A Case of Obstructive Jaundice and administration of Anesthesia in such a case
Citation preview
Obstructive JaundiceCase Discussion
Speaker: Dr S.N.Bhagirath
Panelists: Dr Hemalatha.S Dr Manjula.B.P. Dr Krithika Devi
Case Presentation
Patient details Name: Puttasomachari Age: 68 years Sex: male I.P.No.: 216363
Chief Complaints Pain abdomen – 20 days Generalised Itching – 20 days Fever – 3 days
Case Presentation……..contdHistory of presenting illness
Pain abdomen Itching Fever
Colicky type
Gradual in onset
Intermittent in nature
Over right upper part of abdomen
Non radiating
No aggravating/relieving factors
20 days duration
Gradual in onset
Progressive in nature
Generalised in extent
Relieved on medication
20 days duration
Low grade
Intermittent in nature
Not associated with chills and rigors
No diurnal variation
Relieved on medication
3 days durationHistory of yellowish discolouration of eyes and urine since 15 days
No history of Diabetes Mellitus, Hypertension, Bronchial asthma or Epilepsy
Case Presentation……..contd
Past history
No history of similar complaints in the past.
History of weight loss present since last three months (has lost about 6 kgs).
No history of previous surgery, Jaundice or contact with
jaundiced patient.
No history of drug intake except for consumption of Tab. Atarax (hydroxyzine – 25 mg) for itching and Tab. Crocin (Paracetamol – 500 mg) for fever.
No history of blood transfusions.
Case Presentation……..contd
Family history
No history of similar complaints in the family was noted. Personal history
Diet: Vegetarian
Appetite: reduced
Bowel & bladder habits: Normal. (pale stools)
Sleep: disturbed (due to itching)
Habits: Smoker since 20 years ( 8 beedis/day). Not an
alcoholic.
Case Presentation……..contd
General Physical Examination
An elderly male patient moderately built and nourished. Conscious and
oriented.
Pallor - +, Icterus - +, No cyanosis, oedema, clubbing
Scratch marks - ++ over the abdomen and peripheries.
Pulse rate – 62/min;
Blood pressure – 130/80 mm of hg;
Respiratory rate – 16/min;
Case Presentation……..contd
General Physical Examination
.
Per abdominal examination: Inspection: Normal in size and shape.No dilated veins, scars and sinuses.All quadrants move correspondingly with respiration. Palpation: Soft. Tenderness in right hypochondrium and epigastrium. Palpable hard mass of about 5 x 3 cms felt in the epigastrium with an irregular border. Hepatomegaly +, 3 cms below the costal marginNo SplenomegalyNo free fluid
Case Presentation……..contd
General Physical Examination
Cardiovascular system: S1 S2 heard, No murmurs heard.
Respiratory System: Normal Vesicular Breath Sounds heard, No added
sounds.
Central Nervous System: Normal. No neurological deficits
Impression: Obstructive Jaundice with probable carcinoma of head of pancreas
Case Presentation……..contdInvestigations
Hb: 10.4 gm%Differential count: Neutrophils – 71 Lymphocytes – 24 Monocytes – 02 Eosinophils – 03 Total count – 9, 800Platelets: 2.73 lakhs/mm3
PT INR: 1.0BT: 3’ 00”
CT: 4’ 00”
RBS: 99 mg/dlUrea: 30 mg/dl Creatinine: 1.1 mg/dlNa+: 135 mEq/l, K+: 3.9 mEq/l, Cl-: 104 mEq/l
Case Presentation……..contdInvestigations……ccontd
LFT: Total Bilirubin: 9.0 (0.1 – 1.0)
Direct Bilirubin: 5.3 (0.0 – 0.2)
Indirect Bilirubin: 3.7
Albumin: 2.8 (3.4 – 5.0)
A/G Ratio: 0.9 (1.2 – 2.5)
AST: 39 (0 – 40)
ALT: 32 (0 – 40)
Alkaline Phosphatase: 570 (37 – 147)
HIV 1 & 2: Not detected, HBsAg: Not detected
USG: Intra Hepatic Biliary radical dilatation in its entire length probably
due to stricture.
Case Presentation……..contdInvestigations……ccontd
ECG: Sinus rhythm. Within normal limits. Heart rate: 60/min.
2D ECHOCARDIOGRAPHY: Normal Left Ventricular systolic function
No Regional Wall Motion abnormalities
Ejection fraction: 59 %
Upper G.I. Endoscopy: bulging growth in Periampullary region.
C.T. Scan: Moderated dilatation of intrahepatic and common bile ducts.
Chest X – Ray: Hyperinflated lung fields (COPD changes)
Arterial Blood Gas Analysis: Mild hypoxia.
Case Presentation……..contd
Management Plan
Kausch – Whipple’s Procedure
Discussion with elaborationsHistory of presenting illness
Pain abdomen
Colicky type
Gradual in onset
Intermittent in nature
Over right upper part of abdomen
Non radiating
No aggravating/relieving factors
20 days duration
Biliary colic•Severe• intermittent•Colicky painPancreatic Pain•Dull, continous pain radiating to back• aggravated by food• relieved by sitting up or leaning forward
Hepatomegaly•Dull, continous dragging type of pain in right hypochondrium – stretching of Glisson’s capsule
Discussion with elaborationHistory of presenting illness
Fever
Low grade
Intermittent in nature
Not associated with chills and rigors
No diurnal variation
Relieved on medication
3 days duration
Viral hepatitis
• Fever at onset witharthralgias
Cholangitis
• Fever with rigors
Neoplasm
• low grade fever
Discussion with elaborationHistory of presenting illness
History of yellowish discolouration of eyes and urine since 15 days
Normal range of plasma bilirubin•Total - 0.3 – 1.0 mg/dl• Indirect – 0.2 – 0.7 mg/dl• Direct – 0.1 – 0.4 mg/dl
Clinically obvious2 – 2.5 mg/dl
•Sclera•Under surface of tongue•Palms•Nails•Skin
Bilirubin has affinity to elastin (collagenous tissue) – scleral icterus is more sensitive.
Differential diagnosis of icterus
-Carotemia(scleral icterus is absent)
Discussion with elaborationPast history
No history of similar complaints in the past. History of weight loss present since last three months (has lost about 6 kgs). -suggestive of malignancy
No history of previous surgery -retained or recurrent stone, biliary structure, recurrent obstruction from enlarging tumor
-anaesthesia exposure (post operative hepatic dysfunction, halothane hepatitis)
Jaundice-relapsing hepatitis, choledocholithiasis
Discussion with elaborationFamily and personal history
Family history of CholestasisProgressive Familial Intrahepatic Cholestasis syndrome (Dubin Johnson & Rotor syndrome)α1 antitrypsin deficiency Family history of jaundiceWilson’s diseaseProgressive Familial Intrahepatic Cholestasis syndrome (Dubin Johnson & Rotor syndrome)α1 antitrypsin deficiency
Alcohol – Alcoholic hepatitis can lead to cholestasis
Discussion with elaboration
General Physical
examination
BMI
Vital signs
Pallor: Gastrointestinal bleeding
IcterusLemon yellow – HemolyticGreenish yellow – ObstructiveOrange yellow - Hepatocellular
Pedal edema - hypoproteinemiaScratch marks - pruritis
Xanthoma - hypercholesterolemia
Bruises - Coagulopathy
Fat Soluble vitamin deficiency• Vitamin A deficiency – Bitot’s spot, hyperpigmentation• Vitamin K deficiency - Ecchymoses
Discussion with elaborationAbdominal Examination
Inspection: Abdominal distension -ascitesDilated abdominal vessels- cirrhosisOperative scar-previous surgery
PalpationRight upper quadrant tenderness (Murphy’s sign)-cholecystitis, cholangitisHepatomegaly: tender-Right heart failure, acute hepatitis, obstruction in biliary tract; Non-tender nodular–malignancy or infiltrative process e.g. amyloidosisSplenomegaly-infective hepatitis, portal HT due to cirrhosis, Right heart failure, haemolytic anaemiaDistended palpable GB (Courvoisier’s law) - in malignant obstruction of distal common bile ductFree fluid: Malignant ascites or non malignant ascites
Discussion with elaborationDifférences between extrahepatic/ intrahepatic Cholestasis
Extrahepatic IntrahepaticAbdominal Pain Present Absent
Fever Present Absent
Prodrome Absent Present
Drugs Absent Present
History of surgery Present Absent
Risk factors like transfusion Absent Present
Family History Absent Present
Stigma of cirrhosis Absent Present
Encephalopathy Absent Present
PT Normalizing with Vitamin K Present Absent
Clinical pointersNature of Jaundice
Progressively worsening jaundice - Malignant obstruction, primary biliary cirrhosis, familial cholestasis, primary sclerosing cholangitis, advanced end stage liver disease
Intermittent jaundice - choledocholithiasis, ampullary carcinoma, biliary ascariasis, relapsing viral hepatitis
Association with drug intake
Cholestatic – oral contraceptives, anabolic steroid, chlorpromazine, carbamazepine, antibiotics- erythromycin, rifampicinHepatitis- INH, halothane, phenytoin, methyldopa,
acetaminophen
Fatty liver- tetracycline, valproateToxic necrosis- acetaminophen, CCl4
Clinical pointersWhy pruritis..?
Central mechanism: ↑central opioidoergic tone in patients with cholestasis
Peripheral Mechanism: accumulation of numerous substances e.g. bile acids, histamine, serotonin & endogenous opoids in the systemic circulation subsequent to failure of elimination
Treatment:
Opioid antagonists, Cholestyramine, Rifampicin (Induce CP450 which inactivates pruritogen), Phenobarbitone, Oral guar gum, 5-HT antagonist, UDCA (Urso deoxy cholic acid), Propofol, Lidocaine, Charcoal hemofiltration, Plasmapheresis, Ileal diversion, Liver transplantation.
Bilirubin MetabolismReticuloendoth
elial system
Unconjugated bilirubin + Albumin
Bilirubin + glucuronic acid bilirubin di/ mono glucuronide
Conjugated bilirubin is hydrolyzed and converted to urobilinogen by intestinal pathogens
Stercobilin
Faeces
90% urobilinogen back to liver
10% urobilinogen
into systemic circulation Urobili
n
Clinical pointersObstructive Jaundice
Intrahepatic causes
Familial/ hereditary disorders – • Dublin Johnson syndrome, • Rotor syndrome, • Cholestatic jaundice of pregnancy, • Recurrent intrahepatic cholestasis
Acquired–•Cholestatic drugs , •viral and alcoholic hepatitis, •TPN induced, •Biliary Cirrhosis, •sclerosing cholangitis
Clinical pointersObstructive Jaundice
Extrahepatic causesBenignGallstone/ Choledocholithiasis - most common causeClinical features - Previous history of dyspepsia, Intermittent Pyrexia/ Rigors, Pain, jaundice (Charcot’s triad), O/e – positive Murphy’s sign Chronic pancreatitis, Strictures – iatrogenic, traumaParasitic infections – ascariasis, clonorchiasis, Biliary atresia , Choledochal cysts
MalignantCarcinoma of pancreas/ampulla/bile duct/gall bladderClinical features – Painless, progressive deep Jaundice, Weight loss, Courvoisier’s sign - Palpable Gallbladder (exception ampullary Ca- intermittent jaundice d/t sloughing of tumour cells)
Clinical pointersObstructive Jaundice
Lab investigations – • ↑ conj. plasma bilirubin, •bilirubinuria, •absent urobilinogen in urine, •clay coloured stools, •↑ - ALP•5-NT
Biochemical differentiators
Prehepatic Jaundice Hepatic Jaundice Post hepatic JaundiceSerum bilirubin ↑ (mostly unconjugated) ↑ (conj. & unconj.) ↑ (conjugated.) Urine Urobilinogen ++ + - Urine Bile Salts absent + / + Urine Bilirubin -- + / - ++ ↑↑ (high coloured) Fecal stercobilinogen ↑↑ N or ↓ absent (clay colour) Faecal fat N N or ↑ ↑↑Enzymes SGOT / PT N ↑↑ N or ↑(AST / ALT) (> 800 IU/L) 50-100 IU/L Alkaline PO4 N N or ↑ (x 1-2) ↑↑ (x 3-10) Plasma albumin N ↓ N or ↓
Prothrombin Time N ↑↑ ↑↑
Clinical pointersConsequences of Obstructive Jaundice
• Decreased hepatocyte function• metabolic dysfunction of cyt450• decreased synthesis of albumin and clotting factors• decreased Kupffer cell activity• bilirubinemia, pruritis, CVS depression, nephrotoxicity, hypercholesterolemia, atheromas and xanthoma. • With absence of bile, endotoxins escape into portal blood• Malabsorption of fats and vitamin A, D, E and K• Acholic stools.
Clinical pointers Investigative aids
Ultrasound - determines level & presence of intra and extrahepatic biliary dilatation - More sensitive than CT in detecting gall stone
CT - useful in obese and excessive bowel gas - stages and assesses operability of tumor
ERCP - allows biopsy, brush cytology - therapeutic – Sphincterotomy, stone removal, stricture dilatation.
PTC - 22G chiba needle, - allows biliary drainage and stenting
Clinical pointers
Surgical procedures
•Ca Gall Bladder: Radical Cholecystectomy with wedge resection
and CBD excision
•Choledocholithiasis: ERCP removal or CBD exploration/ bilio-
enteric anastamoses
•Cholangio Ca: Liver resection and or local excision of the lesion
or Whipple
•Biliary Stricture: Hepatico-jejunostomy/ liver resection
•Periampullary Ca: Whipple’s Procedure
•Chronic Pancreatitis with head Mass: Whipple/ bilio-enteric
anastamoses
Anaesthetic Perspectives
Cardiovascular system
circulating bile salts (cholemia) leads to
•Impaired myocardial contractility•Bradycardia•Vasodilatation ↓ ability to mobilise blood from splanchnic vasculature during Hemmorhage•↓ sensitivity to vasopressors•Hypotension & circulatory collapse• Small blood losses are poorly tolerated; therefore replace volume losses immediately in peri-operative period.
Anaesthetic Perspectives
Renal System
Acute renal failure
•Etiology multifactorial
•Arterial hypotension-myocardial depression
•Reduction in intravascular volume
•Nephrotoxicity - bile salt, endotoxins & inflammatory
mediators
•Incidence 5 -10%, mortality high 32 – 100%
•Level of hyperbilirubinemia correlates with postoperative
decrease in Creatinine clearance
Anaesthetic Perspectives
Sepsis
can be due to
•Associated cholangitis and bactibilia•Absence of bile salts in intestine Escape of endotoxins from intestine into portal
•blood
•Retention of bile solutes in liver ↓ Kupffer cell activity
•Prevention - Perioperative antibiotics and oral bile salts
Anaesthetic Perspectives
Coagulopathy
1.Absence of bile salts in intestine Vitamin. K malabsorption (required for gamma carboxylation of glutamyl residues of factors II, VII, IX, X) ↑ PTCorrection - pre-op. Vitamin. K 10 mg OD × 3 days 2. Long lasting biliary obstruction Sec. biliary cirrhosis ↓ syn. of coagulation factors (poor prognosis) Correction - transfusion of FFP
Anaesthetic Perspectives
Multiple Vitamin Deficiency - A, D, E, K due to absence of bile salts in intestine(A- night blindness, D – osteoporosis and muscle weakness, E- leg cramps, K-easy bruising) Haemorrhagic gastritis and stress ulcer Impaired wound healing Altered drug handling due to cholestasis Long standing extrahepatic biliary obstruction > 1yr → biliary cirrhosis → problems of liver dysfunction
Anaesthetic Perspectives
LIVER FUNCTION TESTS A. Indices of hepatocellular damage 1. Transaminases SGOT/SGPT - 0 – 35 IU/L• SGOT (AST) - extrahepatic sources- heart /skeletal muscle/ kidney/ brain, less specific• SGPT (ALP) - primarily found in liver, more specific Viral hepatitis - SGOT/SGPTAlcoholic hepatitis - SGOT/SGPT > 2 (deficiency of pyridoxine-5-PO4)In advanced liver cell injury Transaminases level may actually be normal or low due to massive loss of parenchymal tissue
How does one assess liver functions..?
Anaesthetic Perspectives
LDH – poor specificity3. Glutathione- S – transferase (GST) isoenzyme B – sensitive indicator of liver damageB. Indices of Obstructed Bile Flow 1). Alkaline Phosphatase – 35 – 100 IU/LDerived from plasma membrane of bile duct cellsExtrahepatic sources- bone, intestine, liver, placenta2.) 5- Nucleotidase - confirms hepatic origin of ALP, specific for liver disease3). Gamma glutamyl transferase (GGT) – most sensitive indicator of biliary tract disease, but limited usefulness due to poor specificity
How does one assess liver functions..? …..contd
Anaesthetic Perspectives
How does one assess liver functions..? …..contd
Aminotransferases Alkaline PO4 Diagnostic Likelihood Viral hepatitis Obstructive Jaundice > X 6 < X 2.5 90% 10%< X 6 > X 2.5 10% 80% C. Indices of hepatic synthetic function
1. Prothrombin time – factors II, V, VII & X
Coagulation. Factors have a short t ½; therefore PT is good indicator of liver function in both Acute & Chronic liver disease, good prognostic indicator of outcome of surgery in patients with liver disease Causes for prolonged PT independently of liver disease - Vit. K deficiency, Antibiotic therapy, DIC, Fibrinolysis, Coumarin administration
Anaesthetic Perspectives
How does one assess liver functions..? …..contd
Serum albuminLong t ½ - 14-20days,Liver – substantial reserve for alb. syn., daily production 10—15g/d (3.5-5.5gm %)Functions - Plasma oncotic pressure, Transport vehicle, Drug bindingNot a good indicator for acute or mild liver damage
Indicator of severity of chronic. Liver disease (< 2·5 gm% - severe damage) D. Indices of hepatic blood flow and metabolic capacity1. Indocyanine green (ICG) elimination test – for liver perfusion & function ICG has high extraction ratio2. MERG (monoethylglycinexylidide) test – for liver function. lidocaine is metabolised to MERG in liver
Anaesthetic Perspectives
How does one assess liver functions..? …..contd
OTHER PREOPERATIVE INVESTIGATIONS1. Haematological inv - Hb – decreased in concealed blood Loss, haemolysis, TLC, DLC - increased infection Platelet Count, clotting studies - BT, PT 2. Urine analysis - Urobilinogen absent, Bilirubin & Bile Salts present 3. Metabolic - Serum proteins, glucose, Urea - ↓ syn. in liver disease, Electrolyte 4. KFT – Urea, S. Creatinine, 5 Viral markers – HBV, HCV 6. Cardiorespiratory - Chest X-ray, ECG, blood gases
Anaesthetic Perspectives
RISK FACTORS for operative mortality in obstructive
jaundice patients
•Hematocrit < 30 %
•S. bilirubin > 11mg%
•Malignant cause of biliary obstruction
•Azotemia
•Hypoalbuminemia
•Cholangitis
Anaesthetic Perspectives
Maintain hepatic blood flow and oxygenation AVOID:1. Sympathetic stimulation2. Hypotension (decreased venous return / cardiac output) caused by * Haemorrhage * Cardiac depressant drugs * Regional anaesthesia e.g.; thoracic epidural analgesia3. Hypocapnia & Hypoxemia4. Pressure effects caused by * Surgical retraction * Tumors * Ascites / Laparoscopy5. Hepatic venous congestion caused by * Head down position * IPPV with PEEP, Rt. side heart failure6. Hepatotoxic drugs e.g. halothane or acetaminophen
ANAESTHETIC GOALS in Obstructive Jaundice patient
Anaesthetic Perspectives
2. Maintain Renal functionsPreoperatively• Avoid NSAIDs and nephrotoxic antibiotics e.g.; (aminoglycosides)•Oral bile salts to normalize gut flora•Prophylactic antibiotics to prevent sepsis•Drainage stent -↓ Hyperbilirubinemia•PTC, ERCP or papillotomyIntraoperatively•avoid hypotension & hypoxemia•avoid dehydration•Renal does dopamine /Mannitol / furosemide.
ANAESTHETIC GOALS in Obstructive Jaundice patient
Anaesthetic Perspectives
Choosing appropriate anaesthetic agentNo drug is contraindicated in Cholestatic liver disease. per se. Other considerations Coexisting hepatocellular disorderRenal dysfunctionHepatotoxic and Cholestatic drugs Anaesthetic agent of choiceNot dependent on hepatic metabolismMaintains hepatic O2 supply – demand relationship
PREOPERATIVE PREPARATION for Anaesthesia
Anaesthetic Perspectives
General anesthesia
Induction agent - Thiopentone/Propofol
slow titrated dose → avoid hypotension
gentle intubation → avoid sympathetic stimulation
Muscle relaxant
Suxamethonium – Rapid sequence Induction
Atracurium (drug of choice) - Hoffman’s elimination
Vecuronium 0.15mg/ kg body weight
PREOPERATIVE PREPARATION for Anaesthesia
Anaesthetic Perspectives
Opioids
•Fentanyl (DOC)- maintains hepatic oxygen supply – demand
•opioids can cause spasm of sphincter of Oddi (incidence < 3%)
leading to biliary colic , false + cholangiogram
•fentanyl> morphine> meperidine> butorphenol
•T/T naloxone, glucagon, atropine, nitroglycerine
Volatile Anesthetics
•Isoflurane - maintains hepatic blood flow & oxygen supply
•IPPV –- Maintain eucapnia, Avoid high airway pressures
Anaesthetic Perspectives
Regional anaesthesia (Epidural anaesthesia) as supplement to G.A.Supplemental for intraoperative analgesia and for postoperative analgesiaConcerns – coagulopathy & hypotension Intra Operative Monitoring RoutinePulse oximetry, ECG, NIBPEtCO2Urine outputCore temperatureNMJ monitoring Longer & extensive surgeriesIntra arterial and CVP monitoring. Biochemical – Blood Sugar, ABGs. Electrolytes.Haematology -Hb, PT
Anaesthetic Perspectives
• Conscious, adequate neuromuscular recovery, vitals stable extubate oxygen enriched air•Else - Continue IPPV• Correct Fluid & Electrolyte imbalance• Correct hypothermia• Achieve CVS stability•Adequate analgesia & chest physiotherapy•Antibiotics and H2 receptor antagonist•Maintain urine output•Replace blood and blood products
Post operative Management
References
Harrison’s Internal Medicine 16th Edition, p1888 –p1889
Clinical Anesthesia by Paul.G.Barash, 6th Edition, p1253
References
Miller’s Anaesthesia, 7th Edition, p411, p1071
A Practice of anaesthesia, seventh Edition, Wylie and Churchill
Davidson, p1253
References
Stoelting’s Anesthesia and co-existing Disease
Clinical Anesthesiology, Edward.G.Morgan, 4th Edition.