World Veterinarian Prize Quiz - 2

Introduction

• Jaundice is French word means yellow
• Icterus is Greek word means jaundice/yellow jaundice.
• Jaundice is sign, it is not a disease.
• Definition: It is the yellowish discoloration of the tissues, particularly those with high elastic tissue content, including the sclera and aorta, due to an increase in bilirubin termed hyperbilirubinemia.

Or

• A yellow discoloration of tissue that is especially evident in tissue rich in elastin, such as the aorta and sclera, due to increased concentration of conjugated or unconjugated bilirubin in blood.
• Normal Value: 0.5 -1.0 mg/ dL
• Discoloration occurs only when bilirubin levels rise above 2.0 mg/dL. So the animal can be hyperbilirubinemic but not icteric.

Here, what is jaundice and icterus / when we called that is jaundice or icterus?

• When an excessive accumulation of a yellow pigment into blood and tissues. This is known as an icterus.
• But when icterus has present for any length of time and discolor many tissues of body and that is become visible as jaundice on most body surfaces areas and the skin.
• In case of horses bilirubin have a wider reference range and may not be hyperbilirubinemic at this concentration. So maximum accumulation of bilirubin in tissues of horse takes approximately 2 days, and that’s why horse with acute hepatic failure or obstruction may have seen icterus.
• Unconjugated Bilirubin:in this Bilirubin is bound to a certain protein (albumin) in the blood is called unconjugated or indirect
• Conjugated Bilirubin:  In the liver, bilirubin is conjugated with glucuronic acid by the enzyme glucuronyltransferase ans it is  water soluble.

Mechanism how to develop Jaundice/icterus

• Overproduction of bilirubin due to increase hemolysis
• Reduced liver uptake due to lake of enzyme
• Impaired conjugation
• Impaired intrahepatic secretion of bilirubin due to

                                           Hepatic damage,

                                           Intrahepatic cholestasis and

                                           Biliary obstruction

• Impaired extrahepatic secretion of bilirubin due to bile duct obstruction.

Classification of Jaundice

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        ⇓                                 ⇓                           ⇓

     Haemolytic or                                                     Toxic or                                           Obstructive or 

     prehepatic jaundice                                  intrahepatic jaundice                     posthepatic jaundice

Haemolytic or prehepatic jaundice

• 80% or more of the serum bilirubin is unconjugated (unconjugated hyperbilirubinaemia)
• Overproduction of bilirubin   

                           •      RBC destruction

• Reduced liver uptake:

        •      Certain drugs such as rifampin, an antitubercular drug

• Impaired conjugation:

      •   Activity of glucoronosyl transferase is low at birth – neonatal Jaundice

      •   Hereditary, or acquired deficiency

Etiology

• Bacteria : Leptospirosis, Clostridium haemolyticum,
• Virus : Equine infectious anaemia (EIA)
• Protozoa : Babesiosis, Trypanosomosis Anaplasmosis, Haemobartonellosis,
• Nutritional : Phosphorus deficiency - Post parturient haemoglobinuria(PPH)
• Phytotoxins : Saponin, Resin.
• Animal toxin : Snake venom
• Chemicals : Copper and  selenium toxicity in sheep
• Icterus neonatarum, incompatible blood supply
• Haemolytic anaemia
• Zn toxicity or onion toxicity   

Pathogenesis 

In to Blood Extravascular or intravascular haemolysis

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Unconjugated bilirubin in Blood

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Then blood reach to liver and in hepatocyte unconjugated bilirubin convert into conjugated bilirubin by glucuronosyl transferase

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Then conjugated bilirubin by biliary system goes to small intestine  

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In Small intestine conjugated bilirubin à urobilinogen

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Here urobilinogen 90% excreted by faeces so sometimes yellow faeces seen.

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While 10% urobilinogen by portal vein to blood and excreted by kidney so abnormal intense yellow urine seen. 

Toxic or intrahepatic jaundice

•  Both unconjugated and conjugated bilirubin accumulate in the blood
• Damage to liver cells may impair both conjugating and secretory mechanisms

Etiology

• Bacteria : Salmonellosis and Leptospirosis
• Virus : Infectious canine hepatitis(ICH)
• Phytotoxins : crotalaria and Senecio
• Chemicals : Phosphorus, chronic copper poisoning, chloroform, carbon tetrachloride.
• Acute or chronic hepatitis, hepatotoxicity, cirrhosis, Necrosis

 Pathogenesis

Cell necrosis reduces the liver's ability to metabolize and excrete bilirubin and unconjugated bilirubin in the blood

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The blood contains an abnormally raised amount of conjugated bilirubin and bile salts which are excreted in the urine

NOTE : Both unconjugated and conjugated bilirubin accumulate in the blood

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Acute or chronic hepatitis or biliary cirrhosis leading to an increase in plasma conjugated bilirubin because there is excretion of conjugated bilirubin into the bile

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Here unconjugated bilirubin still enters the liver cells and becomes conjugated

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So this conjugated bilirubin is returned into the blood by rupture of the congested bile canaliculi and direct emptying of the bile into the lymph leaving the liver

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So most of the bilirubin in the plasma becomes the conjugated than the unconjugated type

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And this conjugated bilirubin which not goes into intestine to become urobilinogen gives the urine the dark color.

Obstructive or post hepatic jaundice

 

• secretion (excretion) of conjugated bilirubin is impaired
• Grey or putty like faeces
• Urine contain bilirubin 

 Etiology

• Blocking of bileduct from within

                                       Ascaris lumbricoides in swine

                                      Thysanosoma astiniodes (fringed tape worm)

                                      Fasciola gigantica in cattle

                                       Gall stones

• Pressure on bile duts from outside by Fibrosis, Abscesses, Enlarged pancreas or lymph nodes

 Granulomas, Tumours,

• Inflammatory processes in biliary system like

                                         Dicrocoelium dendriticum                                        

                                          cholecystitis

                                          fascioliasis,

• Closure of bile duct due to Duodenitis and thickening of mucosa
• Biliary atresia, 
• Cholangiocarcinoma, 
• Pancreatitis are also responsible.

 

Pathogenesis

In complete obstruction of the bile duct

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Not found urobilinogen in the urine, so bilirubin has not access to the intestine

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and in the intestine the bilirubin converted to urobilinogen to be later released into the general circulation of animal body

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Presence of bilirubin (conjugated) in the urine without urine-urobilinogen suggests obstructive jaundice

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Also if presence of pale stools and dark urine suggests an obstructive or post hepatic.

Clinical sign

 

       Prehepatic Jaundice                                      Hepatic Jaundice

Intravascular or extravascular anaemia                                 Weight loss

Weakness                                                                                     Anorexia

Pale mucous membranes                                                          Ascites

Tachycardia and tachypnea                                                      Vomiting and Diarrhoea

Haemoglobinemia                                                                      Polydipsia/polyuria

Haemoglobinuria ('port wine' urine)                                      Coagulopathy and

                                                                                                      Hepatoencephalopathy

Post hepatic Jaundice

• If complete obstruction so pale gray faeces
• Bleeding disorders 
• If acute pancreatitis so seen anorexia, vomiting, diarrhoea and abdominal pain in animals
• If jaundice is associated with biliary rupture so resorption of bile pigments and accumulating in the peritoneal cavity and ascites.   

Diagnosis

 Base on the…

• Hematology Parameter
• Serum biochemistry
• Urinalysis
• Faeces

If presence of Jaundice in tissue

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Perform Complete Blood Count(CBC) and Serum Biochemistry

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If hyperbilirubinemia is conformed so seen the PCV/HCT

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If PCV/HCT < 15% so it is pre hepatic Jaundice

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But If PCV/HCT >=  15% so next step is ultrasonography (USG)

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In USG If bile duct and Gall bladder not dilated so hepatic Jaundice

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If bile duct and Gall bladder dilated so it is Post hepatic Jaundice.

Van den Bergh Reaction

 It is used for determine type of bilirubin

• mixing Ehrlich's reagent (diazotized sulphanilic acid) with plasma or serum
• form a colored compound known as azobilirubin

Direct : Immediate reaction with conjugated bilirubin : pink or purple  obstructive jaundice

Indirect: Unconjugated bilirubin gives a delayed reaction: Within 10 minutes, a golden colour appears - haemolytic jaundice

Biphasic reaction:  a brownish-red colour appears during the first two minutes, - toxic jaundice

Differential Diagnosis of jaundice

 

Parameter               Haemolytic                        Toxic                         Obstructive

 

Bilirubin                     Increase unconjugated             Increase conjugated &               Increase conjugated

                                                                                         Increase unconjugated             

 

Van de bergh                    Indirect                                        Biphasic                                              direct

 

Urine bilirubin                         -                                                      +                                                       +

 

Urnine                              Slight                                           present                                                  not

Urobilinogen                   present                                                                                                     present

 

Liver Function                Negative                                       Positive                                               Negative

     Test

 

Serum                              Normal                                         Decrease                                            Increase

Colostrum

 

Haemoglobinuria          Present                                             Absent                                               Absent

 

Faeces                         Intense yellow                                 Normal                                            Pale or Greyish

                                     No smell                                                                                                      foul smelling 

 Macroscopic Pathology

Microscopic Pathology

Treatment 

• First identify the primary cause of jaundice.
• Haemolytic jaundice : prevent the haemolysis and Given Haemoprotozoan drugs.
• Obstructive jaundice : Find the cause of obstruction If there are endoparasite so given anthelmintic drug. If  there is any neoplasm growth or stone so surgically removal.
• Toxic jaundice : Treatment as a hepatitis.
• Fluid therapy :  Dextrose (DNS) Orally or Panretally.
• Suggest for Fat free and salt free diet.

References

https://www.vin.com/doc/?id=7259263

https://en.wikipedia.org/wiki/Jaundice

ecoursesonline.iasri.res.in/mod/page/view.php?id=130402

labpeda.net

(A Courtesy Dr. M.D. McGavin, College of Veterinary Medicine, University of Tennessee.)

(ACourtesy School of Veterinary Medicine, Purdue University.)

(ACourtes Dr. A. Confer, Center for Veterinary Health sciences, Oklahoma State University.