From: Subject: =?iso-8859-1?B?Lg==?= Date: Thu, 28 Sep 2006 11:17:28 +0530 MIME-Version: 1.0 Content-Type: text/html; charset="iso-8859-1" Content-Transfer-Encoding: quoted-printable Content-Location: file://C:\WINNT\Profiles\Administrator\Desktop\IIfolderonlearningmaterials22.9.2006\anaesthesia\Obstructive_jaundice.htm X-MimeOLE: Produced By Microsoft MimeOLE V5.00.2314.1300 =95

 

           =20

Name of the = Speciality:=20   Anaesthesia =

Case:           &n= bsp;           &nb= sp;     =20    OBSTRUCTIVE=20 JAUNDICE

Name of the = Expert:          Ravinder = Kumar Batra=20 Professor

                  &n= bsp;           &nb= sp;           &nbs= p;          =20 and

           &n= bsp;      =20            &n= bsp;             Divya=20 Sethi=20

 

All India = Institute of=20 Medical Sciences, New Delhi: 110029

 

 

 JAUNDICE- yellowish = discolouration skin=20 & mucous membranes due to excess of

           &n= bsp;        =20    plasma   bilirubin

=95        =20 Normal range = of plasma=20 bilirubin : Total :0.3-1 mg/dl

      = {(Indirect)=20 0.2-0.7mg%,   and   (Direct)=20 0.1=970.4mg%)

=95        =20 Clinically = obvious 2-2.5=20 mg/dl

=95        =20 Sites  to look for jaundice=96 = Sclera,=20 undersurface of the tongue, palms, nails, skin

=95        =20 Bilirubin=20 has high affinity to elastin ( collagenous tissue), therefore scleral = icterus is=20 a more sensitive sign of hyperbilirubinemia than generalised jaundice=20

=95        =20 D/D of = jaundice=96=20 Carotemia, treatment with Quinacrine =20 (scleral icterus =96 absent) 

 

 HISTORY =

=B7       =20 Jaundice  - onset:=20 sudden or gradual, =20 progress

=B7       =20 Prodromal = symptoms at of=20 before onset:=20 Suggestive of viral hepatits/drug induced hepatitis. Due to release of=20 endogenous interferon

=B7       =20 High coloured = urine,=20 clay coloured stool , pruritus (obstructive=20 jaundice)

=B7       =20 Anorexia, = weight loss,=20 easy fatigability (prodromal=20 symptoms-alcoholic/drug induced hepatitis, significant weight loss-=20 malignancy)

=B7       =20 Fever = (Fever=20 at onset with arthralgias-viral hepatitis; fever with = rigors-cholangitis; low=20 grade  fever-=20 neoplasm)

=B7       =20 Abdominal =  Pain

=B7       =20 Biliary=20 colic:=20 severe intermittent colicky pain

=B7       =20 Pancreatic=20 pain:=20 Dull, continuous pain  = radiating to=20 back, aggravated by food, and =20 relieved by sitting up or leaning forward

  Hepatomegaly -Dull, = continuous, dragging=20 type of pain in right hypochondrium- stretching of Glisson capsule=20

=95        =20 Gastro-Intestinal=20 bleeding (ampullary=20 malignancy or development of portal HT )

=95     Intake of=20 medications

=95        =20 Alcohol  abuse (alcoholic=20 hepatitis)

=95        =20 Injections = ,transfusion=20 of blood or blood products , promiscuous sexual behavior = (hepatitis=20 B&C)

=95        =20 Contact with = jaundiced=20 individuals

=95        =20 Travel to=20 hepatitis-endemic areas (=20 enterally transmitted hepatitis A&E)

=95        =20 Recent upper = abdominal=20 surgery

=95        =20 GI=20 Bleeding or upper abdominal pain

 

PAST HISTORY=20

=95        =20 Recent upper = abdomen=20 surgery (retained=20 or recurrent stone, biliary stricture, recurrent obstruction from = enlarging=20 tumor)

=95        =20 Anaesthesia = exposure=20 (postoperative=20 hepatic dysfunction, halothane hepatits)

=95        =20 H/o jaundice = =96=20 relapsing=20 hepatitis, choledocholithiasis

=95        =20 Recurrent = Biliary colic:=20 Cholithiasis:=20 Asymptomatic 75%, Biliary colic 20%, Cholecystitis 10%, = Cmplications  < 5%. 15% gall stones have = CBD=20 syones, 95% of CBD stones have gallstones, Normal CBD pressure 10-15cm=20 H2O. Bile flow stops at 30cm=20 H2O.

=95        =20 Past H/o = hepatotoxic=20 drugs

=95        =20 Past H/o = contact with=20 jaundiced patient

=95        =20 H/o = cholestasis during=20 jaundice

 

FAMILY HISTORY =

  1. Family=20 history of Cholestasis;

=B7       =20 Progressive=20 Familial Intrahepatic Cholestasis syndrome (Dublin Johnson & Rotor=20 syndrome)

=B7       =20 α1=20 antitrypsin deficiency

 

  1. Family=20 history of jaundice

=B7       =20 Wilson=92s=20 disease

=B7       =20 Progressive=20 Familial Intrahepatic Cholestasis syndrome (Dublin Johnson & Rotor=20 syndrome)

=B7       =20 α1=20 antitrypsin deficiency

Personal/ = Social=20 History

=B7       =20 Alcohol=20 =96 Alcoholic hepatitis can lead to cholestasis

 

GENERAL = PHYSICAL=20 EXAMINATION

=95        =20 Body mass=20 index

=95        =20 Vital=20 signs

=95        =20 Pallor:=20 GI bleeding, Hemolysis

=95        =20 Icterus=20 :Sclera, = undersurface of=20 the tongue, palms, nails, skin

      Lemon = yellow =96=20 hemolytic

      = Greenish yellow=20 =96 obstructive

      Orange = yellow =96=20 Hepatocellular

=95        =20 Pedal oedema:=20 hypoproteinemia,=20 development of cirrhosis

=95        =20 Scratch marks=20 :=20 pruritis

=95        =20 Xanthoma/ = xanthelesmas:=20 hypercholesterolemia

=95        =20 Bruises:=20 coagulopathy

=95        =20 Clinical = findings=20 associated with fat soluble vitamin deficiency: Vitamin=20 A - Bitot spot, hyperpigmentation, Ecchymosis- Vitamin K =

=95        =20 Stigmata of = chronic=20 liver disease : secondary=20 biliary cirrhosis due to long standing biliary = obstruction

=95        =20 Lymphadenopathy -=20 Troisier=92s sign(enlargement=20 of  left supraclavicular = lymph node=20 d/t secondary involvement seen in  malignancies of G.I.T., breast = and=20 testis.)

 

ABDOMINAL=20 EXAMINATION

=95    = Inspection:=20 Abdominal distension & dilated abdominal vessels-=20 cirrhosis

      = Operative=20 scar

=95        =20 Palpation

      Rt = upper=20 quadrant tenderness (Murphy=92s sign)-cholecystitis,=20 cholangitis

      = Hepatomegaly:=20 tender-Rt heart failure, acute hepatitis; nontender=20 nodular=96

      malignancy or infilterative = process e.g.=20 amyloidosis

      Splenomegaly-infective = hepatitis,=20 portal=20 HT due to cirrhosis, Rt = heart=20 failure,

      = haemolytic=20 anaemia

            Distended = palpable GB=20 (Courvoisier=92s law) - in malignant = obstruction of=20 distal

        =20    common bile duct=20

           =20 Free fluid: = Malignant=20 ascites or non malignant ascites

 

Diff=E9rences=20 between extrahepatic/intrahepatic Cholestasis

 

Extrahepatic

Intraheatic

Abdominal=20 Pain

Fever

Prodrome

Drugs

History=20 of surgery

Risk=20 factors like transfusion

Family=20 History

Stigma=20 of cirrhosis

Encephalopathy

PT=20 Normalizing with Vitamin K

 

Present=20

Present

Absent

Absent

Present

Absent

Absent

Absent

Absent

Present

Absent

Absent

Present

Present

Absent

Present

Present=20

Present

Present

Absent

 

 

 

 

Viva- voce: = Questions=20 and Answers (Obstructive Jaundice)

Q.  What are the causes of = Progressively=20 worsening jaundice and Intermittent

       = jaundice?=20

 

Progressively = worsening=20 jaundice - Malignant=20 obstruction, primary biliary cirrihosis, familial cholestasis, primary = sclersing=20 cholangitis, advanced end stage liver disease

Intermittent=20 jaundice - = choledocholithiasis,=20 ampullary carcinoma, biliary ascariasis, relapsing viral=20 hepatitis

 

Q. Name the = drugs that=20 lead to Cholestatic Jaundice?

 

Cholestatic=20 =96 oral contraceptives, anabolic steroid, chlorpromazine, = carbamazepine,=20 antibiotics- erythromycin, rifampicin

Hepatitis-=20 INH, halothane, phenytoin, methyldopa, = acetoaminophen

Fatty=20 liver-=20 tetracycline, valproate

Toxic=20 necrosis-=20 acetoaminophen, CCl4

 

Q.  Name the conditions where = family history=20 of jaundice is present?

=B7       =20 Wilson=92s=20 disease,

=B7       =20 Familial=20 Intrahepatic Cholestasis syndrome (Dublin Johnson &Rotor syndrome),=20

=B7       =20 α1=20 antitrypsin deficiency  =20

 

Q: Define = jaundice and=20 where all you will look for it?

           &n= bsp;           =20 Yellowish discolouration skin & mucous membranes due to = excess=20 of

           &n= bsp;           =20 plasma  =20 bilirubin

           &n= bsp;     =20 Sites  to look for = jaundice=96=20 Sclera, undersurface of the tongue, palms,

           &n= bsp;     =20 nails, skin

 

 

 

Q: What is the = mechanism=20 of pruritis in Jaundiced patient?

           &n= bsp; =20

Central=20 mechanism: ↑central opioidoergic tone in patients with cholestasis =

Peripheral=20 Mechanism: accumulation of numerous substances e.g. bile=20 acids,

histamine,=20 serotonin & endogenous opioids in the systemic=20 circulation

subsequent=20 to failure of elimination

Treatment:=20 Opioid antagonists, Cholestyramine, Rifampcin( Induce CP450 which = inactivates=20 pruritogen), Phenobarbitone, Oral guar gum, 5-HT antagonist, UDCA, = Propofol,=20 Lidocaine, Charcoal hemofiltration, Pasmapheresis, Ileal diversion, = Liver=20 transplantation.

 

Q.  Discuss the metabolism of=20 Bilirubin.

 

      BILIRUBIN METABOLISM =96 can = be divided=20 into 3 stages

 

Pre-hepatic=20 stage

           &n= bsp; =20

Bilirubin is = first=20 formed in macrophages of the reticuloendothelial system. 70 ~ = 80=20 % = of it is coming from breakdown of =20 hemoglobin of senescent red blood cells by RE system and the = rest 15-20% from  destruction of maturing erythroid cells in = bone marrow=20 and  turnover of Haem and Haem products in liver. =

Within=20 the macrophage, haemoglobin is broken down to:

=95        =20 Globin=20 chains; broken down into constituent amino acids for recycling=20

=95        =20 Haem=20 group

      Then, = the Haem=20 group is cleaved by the enzyme haem=20 oxygenase to liberate:

=95        =20 iron=20 cations; stored in macrophage and recycled to cytoplasmic pool=20

=95        =20 carbon=20 monoxide; expired via lungs

=95        =20 Biliverdin

Biliverdin=20 is converted to bilirubin = by the=20 enzyme biliverdin = reductase. Up to=20 250mg of  bilirubin is = produced per=20 day in the healthy adult. This is the uncong. water insoluble  bilirubin that combines = tightly with=20 albumin, in the blood stream, and is separated from albumin  just before being uptaken into = liver=20 cells. Binding with albumin also shields it from uptake by adipose = tissue with=20 subsequently reduced toxicity.

Hepatic=20 stage

In the=20 liver,  bilirubin combine = with=20 ligandin (cytosolic protein , Y-protein) and is then transferred to = smooth=20 endoplasmic reticulum were it =20 combines  with = glucuronic=20 acid under influence of the enzyme glucuronyl transferse to=20 form:

=95        =20 mainly=20 bilirubin diglucuronide=20

=95        =20 minimal=20 bilirubin monoglucuronide

The=20 glucuronide conjugated form of bilirubin is water soluble and is = excreted into=20 the bile canaliculus by active carrier-mediated transport (rate limiting = step).

 

 

Post-hepatic=20 stage

 The conjugated bilirubin is = hydrolyzed=20 and converted to urobilinogen = by the=20 intestinal pathogens.

The=20 urobilinogen is then oxidized to orange-color stercobilin and excreted in = the stool.=20 About 15 ~ 20 % of the urobilinogen is reabsorbed from the intestine = into portal=20 veins and finally 90 % of it is returned to the liver and is re-excreted = in the=20 bile, this is called entero-hepatic=20 circulation of bilirubin. The remainding 10 % gets into the systemic = circulation and finally excreted in the urine through kidney as urobilin. =

 

Q.  Classify=20 jaundice?

 

CLASSIFICATION=20 OF JAUNDICE=20

A .Based=20 on type of hyperbilirubinemia

  1. Unconjugated=20

=95        =20 Overproduction=20 =96 hemolysis,=20 ineffective erythropoiesis

=95        =20 Decreased=20 hepatic uptake =96 drugs=20 ,prolonged fasting

=95        =20 Decreased=20 glucuronyl transferase activity =96

Hereditary-=20 Gilbert=92s syndrome, Crigler Najjar ,

Neonatal=20 jaundice

Acquired=20 =96 drugs, hepatocellular disease

Sepsis

 

  1. Conjugated=20

=95        =20 Impaired=20 hepatic excretion

           =20 Familial/hereditary - Dublin=20 Johnson syndrome, Rotor syndrome, Cholestatic      = jaundice of=20 pregnancy, recurrent intrahepatic cholestasis

           =20 Acquired - drugs,=20 hepatocellular disease,sepsis

=95        =20 Extrahepatic=20 biliary obstruction

 

B. Based=20 on the mechanisms involved in the pathogenesis of the jaundice=20

 

 1. Pre-Hepatic (Haemolytic) = Jaundice =96=20 over production of bilirubin

    causes = -Absorption of=20 Haematoma,  Haemolytic=20 anaemia

   Lab inv - ↑ = unconj. plasma=20 bilirubin ,  ↑ = urobilinogen in   urine ; liver enzymes = =96=20

  =20 normal

  2. Hepatic / Hepatocellular = Jaundice=20

   Impaired hepatic uptake, = conjugation and excretion of bilirubin

   causes -=20 Viral/drugs/sepsis/hypoxia/cirrhosis

  =20 Lab inv - ↑ unconj/conj plasma bilirubin, ↑ - = ALT/AST=20

  3. Post Hepatic = (Obstructive/cholestatic)=20 Jaundice

  Obstruction to passage of = conjugated=20 bile  into=20 intestine

 

Q.  What are the causes of = Obstructive=20 Jaundice?

A.=20 Intrahepatic causes

Familial/=20 hereditary disorders  =96 = Dublin=20 Johnson syndrome, Rotor syndrome, Cholestatic jaundice of pregnancy, = Recurrent=20 intrahepatic cholestasis

Aquired=20 =96cholestatic  drugs , = viral and=20 alcoholic hepatitis, ,TPN induced, Biliary Cirrhosis, sclerosing=20 cholangitis

B.=20 Extrahepatic causes

Benign=20

Gallstone/=20 Choledocholithiasis - most common cause

 Clinical features - = Previous=20 history of dyspepsia, Intermittent Pyrexia/ Rigors, Pain, jaundice=20 (Charcot=92triad), O/e =96 positive murphy=92s sign           &n= bsp;           &nb= sp;        =20

Chronic=20 pancreatitis

Strictures=20 =96 iatrogenic, trauma

Parasitic=20 infections =96 ascariasis, clonorchiasis

Biliary=20 atresia , Choledochal cysts

 

Malignant=20

Ca.of=20 pancreas/ampulla/bile duct/gall bladder

Clinical=20 features=20 - Painless,=20 progressive deep Jaundice, Weight loss, Courvoisier=92s sign - Palpable=20 Gallbladder (exception ampullary Ca- intermittent jaundice d/t sloughing = of=20 tumour cells)

 

Lab=20 inv=20 - = ↑ conj. plasma bilirubin , bilirubinuria, = absent=20 urobilinogen in urine ,clay coloured stools, ↑ -=20 ALP,5-NT

 

Q.  How will you biochemically = differentiate=20 different types of

      = jaundice?=20

  BIOCHEMICAL = TESTS for = differentiating the=20 jaundice biochemically

 

           &n= bsp;       =20  Prehepatic=20 Jaundice          =20 Hepatic Jaundice         Post Hepatic = Jaundice   =

 

1.Serum = bilirubin           =20 ↑ (mostly unconj)  =20   ↑ (conj. & = unconj.)  =20      ↑ (conj. = )

van=20 den Bergh test       = indirect reacting           &n= bsp;       =20            &n= bsp;              d= irect=20 reacting

           &n= bsp;           &nb= sp;           &nbs= p;  =20 (total - direct)

 

2.Urine = Urobilinogen=20            ++ =20           =20            &n= bsp;      +           &n= bsp;           &nb= sp; =20 - ( if complete=20 obst.)

 

3.Urine Bile = Salts        =          absent            &n= bsp;           &nb= sp;+=20 / -            &n= bsp; =20         +

 

4.Urine = Bilirubin            &n= bsp;      -- =            &n= bsp;           &nb= sp; =20      + / -                     ++ ↑↑(high = coloured)=20

  

5.Fecal=20 stercobilinogen       =20    ↑↑=20            &n= bsp;           =20 N or ↓            &n= bsp;  =20        absent (clay=20 colour)

 

6.Faecal fat =           <= SPAN=20 style=3D"mso-spacerun: = yes">           &n= bsp;      N=20            &n= bsp;           =20 N or ↑            &n= bsp;  =20          ↑↑

 

7.  Liver Fxn. = Tests

 - Enzymes SGOT / PT           N           &n= bsp;         =20       ↑↑            &n= bsp;   =20           N= =20 or ↑

         =20 (AST / ALT)           =20            &n= bsp;           &nb= sp;     (>=20 800 IU/L)            &n= bsp;  =20   50-100 = IU/L

 

8 Alk PO4        =              &n= bsp;         N=20          =20             N or ↑ (x 1-2)         =20    ↑↑ (x = 3-10)

 

9 Plasma = albumin                   N=20            &n= bsp;           &nb= sp;  =20              &n= bsp;   =20          N=20 or ↓

 

10. PT          =20            &n= bsp;           &nb= sp;   N=20            &n= bsp;           &nb= sp;  =20 ↑↑        =20                 <= SPAN=20 style=3D"mso-spacerun: yes">  ↑↑ corrected = by vit K

 

 

Q.  How will you Evaluate a case of = Jaundice?

 

 

EVALUATION OF = A JAUNDICE=20 PATIENT

 

           &n= bsp;           &nb= sp;         =20

 

 

 

Q.=20 Describe the structural/ architectural and =20 the functional units of

     =20 Liver.

The lobule=20 is the structural unit of the liver . It is easy to observe under = microscope and=20 roughly hexagonal in shape, with portal triads at the vertices and a = central=20 vein in the middle. Portal lobule comprises of adjoining parts of 3 = hepatic=20 lobule with center around portal triad

The=20 hepatic acinus  = represents  functional unit  because it is oriented around = the=20 afferent vascular system .the hepatocytes in acinus are divided into = zones that=20 correspond to distance from the arterial blood supply .those hepatocytes = closest=20 to the arterioles in zone 1 are the best oxygenated, while those = farthest from=20 the arterioles in zone 3 have the poorest supply of=20 oxygen.

Zone I =96=20 Periportal = =96=20

=95        =20 ↑=20 mitochondria

=95        =20 Oxidative=20 and phase 2 metabolism,  =20 glycogen syn.

Zone 3 -=20 Centrilobular =

=95        =20 ↑ SER,=20 cyt-P-450,NADH

=95        =20 anaerobic  & phase 1=20 metabolism

=95        =20 Most=20 sensitive to injury from circulatory disturbances and toxic=20 byproducts

 

Q.=20 Describe the blood supply of liver and different=20 factors

     affecting=20 it?

Liver has=20 got a dual blood supply i.e., from Portal vein and hepatic artery. It = receives=20 25% of cardiac output around 1500 ml/min, out of which 30% comes form = hepatic=20 artery and 70% from Portal vein. The oxygen supply is equal from both = the=20 sources.

FACTORS=20 AFFECTING LIVER BLOOD SUPPLY

Increased=20 by:

=95       =20 Supine=20 position

=95       =20 Food

=95       =20 Hypercapnia

=95       =20 Acute=20 hepatitis

=95       =20 Drugs:=20 barbiturates, P450 enzyme inducers, b agonists

Decreased=20 by:

=95       =20 Upright=20 position

=95       =20 IPPV/PEEP,=20 Surgery

=95       =20 Hypocapnia,=20 hypoxia

=95       =20 Cirrhosis

=95       =20 Anaesthetics=20 agents   volatile,=20 inhalational, b blockers, a =20 agonists

=95       =20 Surgical=20 Manipulations

Q. What=20 are the functions of Liver ?

=95        =20 Protein=20 metabolism =96 synthesis of plasma pr( albumin & α-acid=20 glcoprotein, C-reactive protein, haptaglobin, pseudocholinestrase, = deamination=20 of A.A , formation of urea,

=95        =20 Glucose=20 Homeostasis - gluconeogenesis, glycogenolysis( glucagon),  glycogenesis (Insulin)=20

=95        =20 Fat=20 Metabolism - Synthesis of lipoproteins, cholesterol, triglycerides,  oxidation of FA to ketone=20 bodies

=95        =20 Reservoir=20 of Blood

=95        =20 Endocrine=20 Function: IGF1, Thrombopoitin, Angiotensinogen, Thyroid homeostasis, = steroid=20 hormone inactivation( Testesterone, estradiol, glucocorticoid,=20 ald.)

=95        =20 Bilirubin=20 formation & excretion

=95        =20 Drug &=20 Hormone Metabolism

       = Phase I=20 & II reactions

=95        =20 Hematological=20 function =96 haematopoiesis in fetus, heme synthesis, =

=95        =20 Immunological=20 function =96 largest RE organ, Kupffer cells - phagocytosis of  Antigen from GIT. =

=95        =20 Synthesis=20 of Coagulation factors:I,II,V,VII,IX, X,XI, XII,XIII, = prekallikrein,kininogen-=20 Anticoagulants: Antithrombin III, α1antitrypsin,=20 α2=20 antiplasmin,protein C & S, plasminogen, plasminogen activator=20 inhibitor

Q. What=20 are the pathophysiological consequences of Obstructive=20 /

      =20 Cholestatic Jaundice?

Pathophysiological=20 Consequences of Obstructive/Cholestatic = Jaundice

  • Retention of = bile=20 solutes in liver decreases =20 Hepatocyte funcunction and =20 Metabolic Dysfnunction Of Cyto-450, Synthesis of albumin = and  clotting factors is hampered = kuffer=20 cell activityis decresed.=20
  • Bile = constituents in=20 serum leads to Jaundice  = and=20 increased conjugated =20 Bilirubinemia , Pruritus ,CVS Depression , Nephrotoxicity,=20 Hypercholesterolemia  = artheromas,=20 xanthoma=20
  • Absence of = bile in=20 intestine, Escape of endotoxins into portal blood Malabsorp. fats  & vit A,D, E, K Acoholic = stools

 

 

 

 

 

 

Q. What=20 information will you get from Ultrasound, CT, = ERCP

      = &   PTC?

Ultrasound

=B7   =20 Determine=20 the presence and level of intrahepatic and extrahepatic biliary=20 dilatation

=B7   =20 For=20 obstructive jaundice ultrasound has a sensitivity 70 - 95% and = specificity 80 -=20 100%

=B7   =20 more=20 sensitive than CT scan to diagnose gallstone

=B7   =20 In future=20 endoscopic ultrasound may become more widely available , more accurate = than=20 combined CT and ERCP

CT=20 Scanning

=B7   =20 Sensitivity=20 and specificity similar to good quality ultrasound =

=B7   =20 Useful in=20 obese or excessive bowel gas

=B7   =20 Better at=20 imaging lower end of common bile duct

=B7   =20 Stages and=20 assesses operability of tumours

Endoscopic=20 retrograde cholangiogram (ERCP)

=B7   =20 Allows=20 biopsy or brush cytology

=B7   =20 Gold=20 standard to diagnose choledocholithiasis

=B7   =20  Therapeutic procedures - = Sphincterotomy ,=20 stone removal, stricture dilatation=20

 Percutaneous transhepatic = cholangiogram=20 (PTC)

=B7   =20 Rarely=20 required today

=B7   =20 Performed=20 with 22G Chiba Needle

=B7   =20 Also=20 allows biliary drainage and stenting =

 

 

 

Q. What are the surgical procedures = done for=20 obstructive jaundice?

 

Ca Gall=20 Bladder: Radical=20 Cholecystectomy with wedge ressection and CBD = excision

Choledocholithiasis: ERCP removal = or CBD=20 exploration/ bilio-enteric anastmosis

Cholangio=20 Ca:=20 Liver resection and or local excision of the lesion or=20 Whipple

Biliary=20 Stricture: = Hepatico-jejunostomy/=20 liver resection

Periampullary=20 Ca:=20 Whipple=92s Procedure

Chronic = Pancreatits with=20 head Mass: Whipple/ = bilio-enteric=20 anastmosis

 

Q. What are = the steps=20 Surgery in Whipple=92s=20 Procedure?

 

  • Exploration=20
  • Kocherization of=20 Duodenum till IVC is Visualised=20
  • Assessment = of Local=20 resectibility=20
  • Gall bladder = mobilization, CBD dissected and slinged, retracted to = right=20
  • Trace = superior=20 mesenteric vessel and tunnel it to anterior portal = vein=20
  • Transection = of common=20 hepatic duct above cystic duct insertion=20
  • Transection = of jejunum=20 10cm from DJ flesure=20
  • Transection = of neck of=20 pancrease=20
  • Jejunum = brought=20 retrocolic=20
  • Pancreaticojejunostomy-=20 end to end=20
  • Hepatico-jejunostomy =96=20 end to side=20
  • Gastrojejunostomy =96=20 end to side=20
  • Feeding = Jejunostomy=20

 

 

 

 

 

 

 

Q.  What are the Anaesthetic = problems in the=20 case of Obstructive

      =20 jaundice?

 

ANAESTHETIC=20 PROBLEMS in Obstructive Jaundice Patient

 

 A. Cardiovascular=20 dysfunction - circulating = bile salts (cholemia) lead=20 to

1.     =20  Impaired myocardial=20 contractility

2.    Bradycardia

3.   Vasodilatation = =AE  ↓ ability to mobilise = bld from=20 splanchnic vasculature during hrage

4.   ↓ sensitivity to = vasopressors=20

­=20 Hypotension & circulatory collapse

 Small blood losses are poorly = tolerated;=20 therefore replace volume losses immediately in    perioperative=20 period.

 

B.=20  Renal system - Acute = renal failure=20

Etiology=20 multifactorial           &n= bsp;           &nb= sp;           &nbs= p;         =20

1.=20 Arterial hypotension-myocardial depression

2.=20 Reduction in intravascular volume

3.=20 Nephrotoxicity - bile salt, endotoxins & inflammatory=20 mediators

 

Incidence=20 5 -10%, mortality high 32 =96 100%

Level=20 of hyperbilirubinemia correlates with postoperative decrease in = creatinine=20 clearance

 

C.=20  Sepsis=20 =96 can be due to

1.=20 Associated cholangitis and bactibilia

2.=20 Absence of bile salts in intestine =AE  Escape of endotoxins from = intestine into=20 portal  

    blood =

3.=20 Retension of bile solutes in liver =AE=20 ↓ kuffer cell activity

 

Prevention=20 - Perioperative antibiotics and oral bile salts

D.=20 COAGULOPATHY

1.=20  Absence of bile salts in = intestine=20 =AE  Vit. K malabsorption (required = for=20 gamma

     carboxylation of  glutamyl residues of  factors II, VII, IX, X) = =AE  ↑ = PT

    Correction - pre-op. Vit. K 10 = mg OD =D7 3=20 days

2.=20  Long lasting biliary obst = =AE=20 Sec. biliary cirrhosis =AE=20 ↓ syn. of coag factors (poor

     prognosis)   Correction - transfusion = of FFP=20

 

E.   Multiple Vit.=20 Deficiency=20 - A, D, E, K due to absence of bile salts in = intestine

       (A- night blindness, D =96 = osteoporosis and=20 ms weakness, E- leg cramps, K-easy

        bruising)

 

F.   Haemorrhagic gastritis = and stress=20 ulcer

 

G.  Impaired wound=20 healing

 

H.  Altered drug handling due to=20 cholestasis

 

I.   Long standing = extrahepatic biliary=20 obstruction > 1yr → biliary cirrhosis = →

      problems of liver dysfunction=20

 

 

 

 

 

 

 

 

 

 

Q.=20 How will you assess Liver functions?

 

LIVER=20 FUNCTION TESTS

 A.   Indices of hepatocellular = damage

 1. Transaminases      SGOT/SGPT   - 0 =96 35 IU/L=20

=95=20 SGOT (AST) - extrahepatic sources- heart /sk ms/ kidney/ brain, less = specific=20

=95=20 SGPT (ALP) - primarily found in liver, more = specific

 Viral hepatitis -=20 SGOT/SGPT

Alcoholic=20 hepatitis - SGOT/SGPT > 2 (deficiency of=20 pyridoxine-5-PO4)

In=20 advanced liver cell injury transaminases level may actually be normal or = low d/t=20 massive losssof parenchymal tissue

2.=20 LDH =96=20 poor specificity

3.=20 Glutathione- S =96 transferase (GST) isoenzyme B =96 = sensitive=20 indicator of liver damage

 

B.=20  Indices of Obstructed = Bile=20 Flow

 1. Alkaline phosphatase = =96 35 =96 100=20 IU/L

Derived=20 from plasma memberane of bile duct cells

Extrahepatic=20 sources- bone, intestine, liver, placenta

2.=20 5- Nucleotidase  - = confirms=20 hepatic origin of ALP , specific for liver disease

3.=20 Gamma glutamyl transferase (GGT) =96 most sensitive indicator of = biliary=20 tract disease, but limited usefulness due to poor specificity=20

 

Aminotransferases=20            A= lk=20 PO4                   &n= bsp;  Diagnostic Likelihood=20

 

                                  &n= bsp;           &nb= sp;               V= iral=20 hepatitis           =20          Obstr.Jaundice

 

>  X =20 6             &n= bsp;           &nb= sp;     =20 <  X  2.5=20            90%=20            &n= bsp;           &nb= sp;         10%

<  X =20 6            &n= bsp;           &nb= sp;      =20   >  x =20 2..5          10%=20      =            &n= bsp;               <= SPAN=20 style=3D"mso-spacerun: yes">    80%

 

       =

 

 

 

 

C.=20   Indices of hepatic = synthetic=20 function

 

1.=20 Prothrombin time =96 factors II, V, VII & X =

=95        =20 Coag.=20 Factors have a short t =BD, therefore PT is good indicator of liver = function in=20 both Acute & Chonic liver disease, good prognostic indicator of = outcome of=20 surgery in patients with liver disease

=95        =20 Causes=20 for prolonged PT independently of liver disease - Vit. K deficiency., = Antibiotic=20 therapy, DIC, Fibrinolysis, Coumarin = administration

=95        =20 Obst.=20 Jaundice prolonged PT due to vit. K malabsorption, parenteral vitK  admin.→PT normalises in = 24 =96 48=20 hrs

2.=20 Serum albumin

=95        =20 Long=20 t =BD - 14-20days,

=95        =20 Liver=20 =96 substantial reserve for alb. syn., = daily=20 production 10=9715g/d (3.5-5.5gm %)

=95        =20 Functions=20 - Plasma oncotic press. , Tansport vehicle, Drug = binding

=95        =20 Not=20 a good indicator for acute or mild liver = damage

=95        =20 Indicator=20 of severity of chr. Liver disease (<=20 2=B75 gm% - severe damage)

 

D.=20   Indices of hepatic = blood flow=20 and metabolic capacity

1.=20 Indocyanine green (ICG) elimination test =96 for liver perfusion &=20 function

    ICG has high = extraction=20 ratio

2.=20 MERG (monoethylglycinexylidide) test =96 for liver = function.

    lidocaine is = metabolised to=20 MERG in liver

 

 

 

 

 

 

 

 

Q.=20 What are the other preoperative investigations you will=20 do

      before = administering anaesthesia in these patients?

 

OTHER=20 PREOPERATIVE INVESTIGATIONS

1.=20 Haematological inv=20 - Hb =96 decreased in conceled blood Loss, = haemolysis,

          =20            &n= bsp;           &nb= sp;    TLC,=20 DLC - increased infection =20

           &n= bsp;           &nb= sp;     =20          Platele= t=20 Count, clotting studies   = - BT,=20 PT, PTTK

           &n= bsp;           &nb= sp;           &nbs= p;            = ;            =   =20

2.=20 Urine analysis=20 - Urobilinogen absent, Bilirubin & Bile Salts = present

 

3.=20 Metabolic=20 - Serum   proteins, = glucose,=20 Urea - ↓ syn. in liver dis, Electrolyte

 

4.=20 KFT =96=20 Urea, S. Creatinine,

 

5=20 Viral markers=20 =96 HBV, HCV

 

6.=20 Cardiorespiratory=20 - Chest X-ray, ECG, blood gases

 =20

RISK=20 FACTORS for operative mortality in obstructive jaundice=20 patients

=95        =20 Hematocrit=20 < 30 %

=95        =20 S.=20 bilirubin  >=20 11mg%

=95        =20 Malignant=20 cause of biliary obstruction

=95        =20 Azotemia

=95        =20 Hypoalbuminemia

=95        =20 Cholangitis

 

Q.=20 What are the risk Factors in the case of obstructed jaundice?           =20

           &n= bsp;           &nb= sp;           &nbs= p;            = ;     =20

In=20 a large retrospective study (Dixon etal =96 GUT 1983) of = 373=20 patients undergoing surgery for obstructive jaundice before 1983 the = mortality=20 rate was 9.1% and  multivariate=20 analysis identified Hematocrit  = <=20 30 %, S. bilirubin  > = 11mg%,=20 malignant cause of biliary obstruction as predictors of periop = mortalily. If all=20 these were  present, the = mortality=20 rates approached 60%,whereas none was present the mortality rate was = only=20 5%.Other Preop predictors of poor surgical outcome include =96Azotemia,=20 Hypoalbuminemia and Cholangitis. - Friedman =96Hepatology=20 June1999

 

Q.=20 What are the anaesthetic goals in this case?

 

ANAESTHETIC=20 GOALS in Obstructive Jaundice patient

           =20 Maintain hepatic blood flow and = oxygenation

 

           &n= bsp;           &nb= sp;    =20 AVOID :

=95        =20 Sympathetic=20 stimulation

=95        =20 Hypotension=20 (decreased venous return / cardiac output) caused by =

    =20 Haemorrhage

     Cardiac depressant drugs=20

     Regional = anaesthesia=20 e.g.; thoracic epidural analgesia

=95        =20 Hypocapnia=20 & Hypoxemia

=95        =20 Pressure=20 effects=20 caused by

    Surgical=20 retraction

    = Tumors

    Ascites /=20 Laparoscopy

=95        =20 Hepatic=20 venous congestion=20 caused by

    Head down=20 position

    IPPV with PEEP, = Rt. side=20 heart failure

=95        =20 Hepatotoxic=20 drugs  e.g. halothane or=20 acetoaminophen

 

 

2.=20 Maintain Renal functions

Preoperatively

=95        =20 Avoid=20 NSAIDs and  nephrotoxic = antibiotics=20 e.g.; (aminoglycosides)

=95        =20 Oral=20 bile salts to normalize gut flora

=95        =20 Prophylactic=20 antibiotics to prevent sepsis

=95        =20 Drainage=20 stent -↓ Hyperbilirubinaemia

            PTC, ERCP or = papillotomy=20

 

Intraoperatively=20

=95        =20 avoid=20 hypotension & hypoxaemia

=95        =20 avoid=20 dehydration

=95        =20 Renal=20 does dopamine /mannitol / furosemide.

 

Q.=20 How will you prepare this patient for Anaesthesia?

 

PREOPERATIVE=20 PREPARATION for Anaesthesia

=95        =20 Anxiolytic=20 =96 oral short acting Benzodiazepine

=95        =20 Oral=20 H 2 antagonist

=95        =20 Vit.=20 K (Obst. J) =96 10 mg OD X 3 day, Fresh Frozen Plasma =

=95        =20 Perioperative=20 broad spectrum antibiotics, oral bile salts

=95        =20 Rehydration=20 and adequate diuresis 1ml/kg/hr

 If Bilirubin > 8=20 mg%

 =20 I/V fluid =96 1-2 ml/kg/hr.

furosemide/ Mannitol / low dose=20 dopamine

early=20 catheterization & CVP monitoring

 

Q.=20 How will you manage anaesthetic administration in this=20 case?

 

ANAESTHETIC=20 MANAGEMENT

 

Choosing=20 appropriate anaesthetic agent

No=20 drug is contraindicated in Cholestatic liver disease. per=20 se.

 

Other=20 considerations  

Coexisting=20 hepatocellular disorder

Renal=20 dysfunction

Hepatotoxic=20 and cholestatic drugs

 

 Anaesthetic agent of=20 choice

 Not dependent on hepatic=20 metabolism

 Maintains hepatic O2 = supply =96=20 demand relationship

 

General=20 anesthesia

 

Induction=20 agent  -=20 Thiopentone/Propofol

=95        =20 slow=20 titrated dose → avoid hypotension

=95        =20 gentle=20 intubation → avoid sympathetic  stimulation

 

Muscle=20 relaxant=20

=95        =20 Suxamethonium=20 - RSI

=95        =20 Atracurium=20 (DOC) - Hoffman=92s elimination     =20

=95        =20 Vecuronium=20 0.15mg  =

 

Opioids=20  

=95        =20 fentanyl=20 (DOC)- maintains hepatic oxygen supply =96 demand

=95        =20 opioids=20 can cause spasm of sphincter of Oddi (incidence < 3%) leading to = biliary=20          colic=20 , false + cholangiogram

=95        =20 fentanyl>=20 morphine> meperidine> butorphenol

=95        =20 T/T=20 naloxone, glucagon, atropine, nitroglycerine

 

Volatile=20 Anesthetics

=95        =20 Isoflurane=20 -  maintains  HBF & oxygen=20 supply

 

IPPV=20 =96- Maintain eucapnia, Avoid high airway = pressures

 

 

 

 

 

Q.=20 What is the role of Regional anaesthesia in this = case?

 

Regional=20 anaesthesia=20 (Epidural anaesthesia)  = as=20 supplement to G.A.

=95        =20 Supplemental=20 for intraoperative analgesia and for postoperative=20 analgesis

=95        =20 Concerns=20 =96  coagulopathy &=20 hypotension

 

Q.=20 What intraoperative monitoring you will do in this=20 case?

 

Intra=20 Operative Monitoring

 Routine =

=95        =20 Pulse=20 oximetry, ECG, NIBP

=95        =20 EtCO2

=95        =20 Urine=20 output

=95        =20 Core=20 temp

=95        =20 NMJ=20 monitoring

 

Longer=20 & extensive surgeries

=95        =20 Intra=20 arterial and CVP

=95        =20 Biochemical=20 - B.Sugar, ABGS. Electrolytes

=95        =20 Hematology=20 -Hb, PT,, PTTK,TEG

 

 

 

 

 

 

 

Q.=20 How will you manage these case = postoperatively?

 

Postoperative=20 management

=95        =20 Conscious,=20 adequate NM recovery, vitals stable→ extubate → oxygen  enriched = air

=95        =20 Else   - Continue IPPV=20

           &n= bsp;   =20 - Correct Fluid & Electrolyte imbalance =

           &n= bsp;   =20 - Correct hypothermia

           &n= bsp;   =20 - Achieve CVS stability

=95        =20 Adequate=20 analgesia & chest physiotherapy

=95        =20 Antibiotics=20 and  H 2 receptor=20 antagonist

=95        =20 Maintain=20 urine output

=95        =20 Replace=20 blood and blood products