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Abaxis University 


Evaluating for Liver Damage and Dysfunction 




Andrew J Rosenfeld, DVM ABVP 



      Section I:  Pre‐Case and Case Worksheet 


Abaxis University Case Work Sheet

Evaluating for Liver Damage and Dysfunction 


A. Rosenfeld, DVM ABVP    

© 2009 

Instructions:    Prior  to  taking  the  on‐line  course,  please  review  the  course  notes  and evaluate the hospital case.  Please take some time and fill out the pre‐course  section  of  the  case  to  the  best  of  your  ability.    Once  in  lecture,  the  case  will  be  discussed  and  new  diagnostic  testing  and  treatment  options  will  become  available.    As  the  class  progresses,  each  team  member  will  outline  diagnostic  testing  and  treatment  concerns  to  help  identify  the  primary  and  secondary  concerns  of  the  patient,  understand  treatment  options  and  be  able  to  discuss  these concerns with the client.  Good luck.  Pre‐course Section – Please fill out prior to attending the on‐line classroom ‐‐‐‐‐‐‐‐  Signalment:  “Pewter”, 20 kg Male Neutered    5 year old English bulldog  CC:  Lethargic, depressed, anorexic and having soft  stool for 7 days.      Initial Triage Examination  • • • • • • • • Temp:  101.2 degrees Fahrenheit  Pulse:  160   Resp: 50‐60 breaths / min  CRT:  2 secs  MM: Light Pink   Hydration: 8% dehydrated  Mentation: Depressed  Abdomen:  Sore and painful to touch  

1 | E v a l u a t i n g   f o r   L i v e r   D a m a g e   a n d   D y s f u n c t i o n    

History – Please list questions that you would like to ask during your medical  history.    1.    2.    3.    4.    5.    6.    7.    8.    9.    10.     What Clinical Diagnostics should be completed at this time?    1.    2.    3.    4.    5.    6.    7.    8.    9.    10.        
2 | E v a l u a t i n g   f o r   L i v e r   D a m a g e   a n d   D y s f u n c t i o n    

0‐7.5 mg/dl)    Complete Blood Count:    Test   WBC   Lymphocytes   Monocytes   Neutrophils   Eosinophils   Basophils   RBC   HCT   Hemoglobin   Platelet   Findings  7500  1250 (l) 1000  4500  750  0   6000  32% (l)  11 (l)  328000  Normal  5.Initial Database Available:  • Tubes:  • Purple Top  • Red Top  • Packed Cell Volume  • PCV:   24 % (l)     (25‐45%)  • Total Protein  6.5‐15  200000‐500000   3 | E v a l u a t i n g   f o r   L i v e r   D a m a g e   a n d   D y s f u n c t i o n     .500   1500‐7000   0‐850  2500‐12500   0‐1500  0‐100  5500‐8500   35‐55%  9.500‐19.2    (5.

2  5.5  4 (l)  9.2 g/dl   4 | E v a l u a t i n g   f o r   L i v e r   D a m a g e   a n d   D y s f u n c t i o n     .4 mg/dl  60‐110 mg/dl  138‐160 mEq/l  3.8 mg/dl  2.3‐1.3‐5.3  (l)  143  112  752  0.9‐6.8  (l)  6.6 mg/dl  0.2  3.8 mEq/l  5.4‐8.4  115  (h)  149  2.5‐4.9  Normal   2.Chemistry:    Test   Albumin   Alk Phos   ALT   Amylase   T Bilirubin   BUN   Calcium   Phosphorus   Creatinine   Glucose   Na   K   TP   Globulin       Findings  2.7‐5.2 g/dl   2.4 g /dl   20‐150 IU/L   10‐118 IU/L   200‐1200 IU/L  0.6  1.6‐11.6 mg/dl  7‐25 mg/dl   8.1‐0.

   8.    8.   14.   11.    5.    6.    6.    4.    7.    2.    9.   5 | E v a l u a t i n g   f o r   L i v e r   D a m a g e   a n d   D y s f u n c t i o n     .    10.    5. please identify a  problem list for the patient:    1.   12.    4.    3.   13.    2.    7.    10.    3.    9.Based on Physical Exam and Clinical Diagnostics thus far.     Please list other diagnostics that need to be completed:      1.

   7.    3.    2. what are secondary concerns that medical  team must monitor for?      1.    6 | E v a l u a t i n g   f o r   L i v e r   D a m a g e   a n d   D y s f u n c t i o n     .    8.    9.    4.    6.Given the concerns of the patient.     STOP ‐‐‐‐‐‐‐‐ The rest of the case will progress during the on‐line class.    5.     10.

On‐Line Class Portion:  Please review each diagnostic test ordered. copy down  the abnormal and list concerns based on these findings:  Clinical Diagnostic #1:                    Problem List:                7 | E v a l u a t i n g   f o r   L i v e r   D a m a g e   a n d   D y s f u n c t i o n     .

Clinical Diagnostic #2:                      Problem List:                  8 | E v a l u a t i n g   f o r   L i v e r   D a m a g e   a n d   D y s f u n c t i o n     .

Clinical Diagnostic #3:                      Problem List:                9 | E v a l u a t i n g   f o r   L i v e r   D a m a g e   a n d   D y s f u n c t i o n     .

Clinical Diagnostic #4:                      Problem List:                10 | E v a l u a t i n g   f o r   L i v e r   D a m a g e   a n d   D y s f u n c t i o n     .

Clinical Diagnostic #5:                    Problem List:                11 | E v a l u a t i n g   f o r   L i v e r   D a m a g e   a n d   D y s f u n c t i o n     .

                        12 | E v a l u a t i n g   f o r   L i v e r   D a m a g e   a n d   D y s f u n c t i o n     . 5. 6. 4. and clinical diagnostics:    1. physical  exam.    4. 2.     As  we  treat  this  patient.    6.    3.    8.   13. 3.  what  are  some  monitoring  diagnostics  that  will  be  necessary to evaluate the effectiveness of our treatment options and concerns  of secondary disease conditions?  1.    5.    7. 8.    10.    9.   11.Please list a completed problem list based on the case including history.   15.    12.   14.    2. 7.

                Section II:  Lecture Notes                        .

1/12/2010 Evaluating for Liver Damage and Dysfunction Andrew J Rosenfeld. 2010 Case I : Pewter • Signalment: 20 kg Male Neutered 5 year old English Bull Dog • CC: Lethargic. 1 . Ames Io. Rosenfeld. S. depressed. A and Dial. DVM ABVP © 2009 Material Courtesy of Clinical Pathology for the Veterinary Team. Wiley Blackwell. anorexic and having soft stool for 7 days.

10. 6. 5. 9. 3. 7. 2.2 degrees Fahrenheit Pulse: 160 Resp: 50-60 breaths / min CRT: CRT 2 secs MM: Light Pink Hydration: 8% dehydrated Mentation: Depressed • Abdomen: Sore and painful to touch History – What should we ask? 1. 8. 8. 6.1/12/2010 Initial Triage Exam • • • • • • • Temp: 101. 4. 4. 7. 5. 3. Now What? What should be in our clinical database? 1. 2 . 2.

1-0.2 3.7-5.3-1.4 mg/dl 60-110 mg/dl 138-160 mEq/l 3.0-7.5 4 (l) 9.8 mg/dl 2.8 mEq/l 5.500-19.6 mg/dl 0.3 (l) 143 112 752 0.6 1.9-6.6 mg/dl 7-25 mg/dl 8.6-11.5-4.2 g/dl 3 .500 1500-7000 0-850 2500-12500 500 500 0-1500 0-100 5500-8500 35-55% 9.4 115 (h) 149 2.0 (35-55%) (5.9 Normal 2.3-5.1/12/2010 Initial Database • Tubes: – Purple Top – Red Top p • Packed Cell Volume – PCV : 34 % (L) – Total Protein: 6.2 g/dl 2.4 g /dl 20-150 IU/L 10-118 IU/L 200-1200 IU/L 0.5-15 200000-500000 Chemistry Test Albumin Alk Phos ALT Amylase T Bilirubin BUN Calcium Phosphorus Creatinine Glucose Na K TP Globulin Findings 2.2 5.8 (l) 6.4-8.5 mg/dl) Complete Blood Count Test WBC Lymphocytes Monocytes Neutrophils eut op s Eosinophils Basophils RBC HCT Hemoglobin Platelet Findings 7500 1250 (l) 1000 4500 500 750 0 6000 32% (l) 11 (l) 328000 Normal 5.

4. 7. 4. 6. 8. 10. 2. 3. 7. 5. 6. 9. 6. What are secondary concerns that medical team must monitor for? 1. 3. 10. 3. What other diagnostics are needed to be completed? 1. 8. 9. 9. 5. 2.1/12/2010 Problem List 1. 7. 8. 2. 4. 10. 4 . 5.

Liver Physiology • The liver has many functions in the body. and nutrients that are in the portal blood supply. • To do this the liver architecture is divided into i di id d i t sinusoids where oneid h cell thick layers of hepatocytes filter blood flowing from the portal vein to the hepatic central vein • The function of these cells is to absorb all toxins. microbes and toxins into a large venous system called the Portal Venous System System. can have blood work parameters within normal limits. bacteria. • The other concern is that a patient with have severe debilitating liver disease with poor function. • • Liver Detoxification • For the liver to be able to detoxify blood. the ability to evaluate liver damage vs. The large portal vein carries all of these substances into the liver where intracellular chemicals (enzymes) detoxify toxins into inert waste products. 5 . The small intestine absorbs all food stuffs. harvesting necessary nutrients and removing toxins.1/12/2010 Introduction • As opposed to clinical diagnostic evaluation of renal disease and kidney function. However. the most important is detoxification of toxins. hepatic function is much more complex. the internal architecture of the liver must be adapted to filter blood. • Team members must be able to understand the importance and the limitation of hepatic clinical diagnostics when approaching a patient with potential liver disease. this does not y always mean the liver is non-functional. • The goal of this chapter is to understand that patients with liver trauma have changes in liver enzymes.

the active toxins can build up into the blood stream and tissues. energy and fats needed by the body and then released back into the blood venous flow for general circulation. running between layers of hepatocytes.1/12/2010 Liver Detoxification • The nutrients are absorbed. altered into other proteins. weight loss. neurologic signs can be closely associated with feeding. • These canniculi lead to the bile ductules. vomiting and diarrhea. This can produce anorexia. Of these factors. called Canniculi. weakness. • Liver Production • The liver produces many of the body’s building blocks necessary for normal maintenance. the liver produces – – – – Glycogen Red Blood Cells Precursors Clotting Factors Body Proteins (Albumin) 6 . growth and production. Further specific toxins can penetrate the central nervous system producing neurologic symptoms such as – – – – – • Seizures Acute blindness Circling Head pressing Abnormal behavior • • Neurologic symptoms produced secondary to decrease hepatic function is called Hepatic encephalopathy. • The toxins and bacteria are deactivated and then released into channels. Liver Detoxification • If the body is unable to detoxify these compounds. Since this process is stimulated by the absorption of nutrients and improper detoxification of toxins. which then move all deactivated sludge and debris into the gall bladder.

– If severe. Risks of patients with reduced hepatic function • Alteration in Protein Production – The liver also produces a protein molecule called albumin. large amounts of fluid accumulation can occur within the abdomen (ascites). anorexia. weakness and weight loss. – In order to move albumin through the blood stream. Risks of patients with reduced hepatic function • Decreased Production: – Anemia: • Due to lack of Red Blood Cell precursors. Further medical team members must be extremely cautious with hospitalize patients on intravenous fluids with low albumin levels since these patients have increased risk of pushing larger amounts of fluids into the tissue. large amounts of fluid must be ll d from th ti b pulled f the tissue. • Animals with chronic hepatic disease may develop chronic anemia and may have decreased ability to clot blood.1/12/2010 Risks of patients with reduced hepatic function • Issues with Detoxification: – Hepatic Encephalopathy: Development of neurologic symptoms secondary to improper detoxification of microbes and toxins which remain in the body affecting the central nervous system. – Increased Clotting Time: • The liver produces clotting factors that finalize clot formation. – Physical Symptoms due to build of toxins and bilirubin: Increased toxins can produce nausea. increasing the amount of fluid returning to the tissue. – This increases risks of moving fluid into lung tissue producing pulmonary edema and developing fluid overload. no jugular blood collection should ever be attempted with patients suffering from potential hepatic disease or dysfunction. 7 . – Albumin’s function is to carry other molecules and hormones around the blood stream in a deactivated form until the body requires the chemical. – Loss of albumin production secondary to liver dysfunction can decrease oncotic pressure. • With this concern. – This physiological draw of fluid that albumin exerts on the tissue is called Oncotic Pressure. diarrhea. depression. vomiting.

Lymphoma. increasing fluid accumulation in the body producing ascites. Common metabolic diseases of the liver include: – Hepatic Lipidosis: This disease syndrome occurs commonly in the cat and horse (pony) when these animals have a diseases entity that produces a profound anorexia. Hypoalbunemia: Due to lack of blood albumin. vomiting. Hepatic Cholangioadenocarcinoma. Porto-caval Shunts: In some patients. • Cancer (Neoplasia): The liver is both the site of primary cancer and a common site of secondary metastatic disease. weakness and weight loss. toxins can damage normal liver tissue affecting function. The animals shunt large amounts of fat into the liver to transform it into sugar. depression. amyloidosis can be associated with kidney and liver disease and inflammatory changes in joint capsule.1/12/2010 Liver Function Concern of Dysfunction • Hepatic Encephalopathy: Development of neurologic symptoms secondary to improper detoxification of microbes and toxins which remain in the body affecting the central Detoxification • nervous system. bacterial. a small blood vessel. called a shunt. Some common cancers that primarily affect the liver are Hepatic Adenocarcinoma. Physical Symptoms due to build of toxins and bilirubin: Increased toxins can produce nausea. • • Formation of Building Blocks • Anemia: Lack of Red Blood Cell precursors Increased Clotting Time: The liver produces clotting factors that finalize clot formation. This antigenic stimulation produces an influx of white blood cells through healthy liver causing damage and irritation. and Mast Cell tumor. This build up of this abnormal protein is most commonly seen in the Shar-pei breed. the body can shift fluid from the vascular supply to the tissue. chronic or end stage (Cirrhosis). • 8 . fungal and parasites pathogens can infect and invade normal liver tissue producing acute or chronic disease and debilitation • Inflammatory Disease: Hepatitis is the activation of the immune system by some foreign antigen within the liver. Inflammatory disease can be acute. Protein: Amyloidosis is an accumulation of an inert protein in the liver which can chronically destroy normal liver tissue. diarrhea. can occur from the portal vein to the caudal vena cava producing a by-pass of blood flow around the liver. Glucose Storage • Hypoglycemia (rare) Causes of Liver Disease • Infectious Liver Disease: Viral. anorexia. The movement of fat into the liver is so severe that normal liver architecture and liver function can be affected. In this breed. edema and pulmonary edema (with patients on IV fluids). Causes of Liver Disease Metabolic Disease: This form of liver disease occurs as inert compound build-ups within the liver. destroying the normal architecture and liver function. – • Toxin Disease: Since the liver is the major detoxifying organ in the body.

injury. these clinical diagnostics do not represent a build up toxin. which affect the muscular skeletal system (e. However. a specific level of each enzyme leaks from the hepatocyte into the blood stream.g. • • • Liver Damage Enzymes • ALT (Alanine aminotransferase): – Alanine aminotransferase (ALT) is responsible for the conversion of 2oxoglutarate to pyruvate and glutamate in the liver cells (hepatocytes). – The increase blood levels do not indicate the severity of the damage to the hepatocytes or degree of reversibility of the disease process. secondary to injury. trauma or seizure) – Disease. Hepatic Dysfunction • Within the liver cells are enzymes that function to change or produce specific body building blocks or detoxify toxic chemicals in the body. but the liver may not be functional. Low ALT activity is not generally associated with – Increased AST activity: As with ALT. • Further AST activity can also be increased secondary to: – Disease. there may enough hepatic enzymes within the blood stream to produce normal blood levels in clinical testing. • Increased activity of the enzyme in the blood occur when there are alterations in the lipid membrane of the hepatocytes. inflammations or infection within the liver. • The increase blood levels do not indicate the severity of the damage to the hepatocytes or degree of reversibility of the disease process.1/12/2010 Identifying Liver Damage vs. – Further ALT activity can also be increased secondary to: » Chronic use of anticonvulsants. since there is significant levels of AST in red blood cells. steroids and other drugs » Physical trauma » Cardiac Disease Liver Damage Enzymes • Aspartate aminotransferase (AST or SGOT): Aspartate aminotransferase (AST) is an intracellular enzyme in all cells. AST blood levels in the blood occur when there are alterations in the lipid membrane of the hepatocytes secondary to injury hepatocytes. Normally. 9 . which produce red blood cell destruction (e. The following patterns in the AST level can be observed: – Decreased AST activity: disease conditions.g. but do not always suggest liver dysfunction. Acute trauma to hepatocytes can produce sharp elevations of liver enzymes. Clinically we evaluate the following intracellular enzymes: – – – – Alanine aminotransferase (ALT) Aspartate aminotransferase (AST) Gamma-Glutamyltransferase (GGT) Alkaline Phosphatase (Alk Phos) ( ) • Unlike evaluating kidney disease by monitoring azotemia. but has higher levels of activity in muscle and liver cell damage. – The following patterns in the ALT level can be observed: • Low ALT activity is not generally associated with disease conditions. inflammations or infection within the liver. Immune Mediated Hemolytic Anemia). Increases in these liver enzymes support liver trauma. but rather normal enzymes produced within the hepatocytes. with chronic to end stage disease.

– A red bl d cells age. GGT is present in all cells except it has higher concentration in renal epithelial. th As d blood ll they are removed from circulation in the spleen. GGT does not “leak” from hepatocytes. Similar to GGT. ALP’s activity increases because of increased production of the enzyme (induction) in response to disease. – The remaining chemical is bilirubin. GGT is an intracellular enzyme responsible for cleaving C-terminal glutamyl groups from one substrate or molecule to another. Some conditions that increase Alkaline Phosphatase activity are: • • • • Hyperadrenocorticism Liver and Gall Bladder Disease Long Term Medication Bone growth – Liver Dysfunction Enzymes • Bilirubin: – Bilirubin is a toxic metabolite produced from the red blood cell destruction in the spleen and the breakdown of hemoglobin. kidneys and placenta. bile duct and hepatic cells. • Liver Damage Enzymes • Alkaline Phosphatase (SALP or ALP): Alkaline Phosphatase is present within the liver. Increased Alkaline Phosphatase activity: High ALP can originate from diseases and non-diseased conditions. – Elevations in GGT: • Increased GGT activity can be associated with decreased bile flow (cholestasis) • Unlike AST and ALT. lysed. and is thought to be involved in pathways used to protect cells from oxidative injury. which is moved to the liver to be detoxified and excreted through the gall bladder.1/12/2010 Liver Damage Enzymes • Gamma-glutamyltransferase (GGT): Gamma-glutamyltransferase is more an indicator of gall bladder obstruction or lack of bile flow. and the iron molecule removed from the hemoglobin molecule to be used again. On most chemistry panels. Alkaline Phosphatase activity represents the combined activity all combined tissue alkaline phosphatase levels. bone. its activity is increased due to increased production (induction) of the enzyme in response to disease. The following patterns of GGT levels can be observed: – Decreased GGT activity: Low GGT activity is not generally associated with disease conditions. 10 . intestine. The following patterns of ALP can be observed: – Decreased ALP activity: Low ALP activity is not generally associated with disease conditions.

at least 75% of normal liver function must be lost before albumin concentration is decreased. and two hours later another bile acid level is collected. Immune-mediated Hemolytic Anemias) or gall bladder obstruction. – Further. low body albumin can also be associated with Kidney disease. Low protein diets can also result in a low BUN. – To evaluate bile acids. – In liver disease. 11 . Then the animal is fed a high energy food. – – – – Liver Dysfunction Enzymes • Bile Acids – Hepatocytes also produce chemicals called bile acids that help to emulsify fat within the small intestine. increase levels of Bilirubin also can be associated with increase intravascular red blood cell destruction (e. When observed on clinical diagnostics. – After fat is emulsified. bile acids are then rapidly reabsorbed by the small intestine. – • Albumin: – Albumin is a small carrier protein that binds to hormones and other components in the blood stream to maintain and move necessary elements throughout the body. When attributable to liver disease. As a general rule. the patient is fasted for 12 hours and a baseline level of bile acids are drawn.g. – Bile acids then empty through the g bladder and into the common bile py g gall duct. – In an animal with liver dysfunction. it may suggest a liver dysfunction. bile acids are not properly reabsorbed and represent a true liver dysfunction. – However. A low BUN by itself does not always indicate liver dysfunction.1/12/2010 Liver Dysfunction Enzymes • Bilirubin: – The buildup of bilirubin in the serum and body in association with liver disease indicates liver dysfunction. Liver Dysfunction Enzymes • Blood urea nitrogen (BUN): – A low BUN level can be associated with the liver’s inability to produce take ammonia molecules and produce BUN. however not all patients with liver dysfunction are icteric. However. bleeding and intestinal disease. Decreases in blood albumin concentration can occur generally with a number of disease syndromes that effect production or loss of the protein molecule. it should be noted that although patients that are icteric secondary to liver disease have liver dysfunction. – Bile acids are stimulated when the patient eats. hypoalbuminemia can be an indicator of altered liver function. pre-feeding (pre-parandial) bile acids are high and post feedings post-parandial bile acids are even higher. A decrease in functioning hepatocytes will compromise the liver’s ability to produce albumin.

the medical team must also evaluate the history. chronic anemia may be present secondary to the lack of precursors for cellular components. clotting times and a blood film should be evaluated to determine if the patient has a non-regenerative anemia vs.e. platelet number. Also chronic liver disease can affect the patient’s ability to clot blood. – Platelets: • • With concerns of decreased clotting factors and an inability to finalize the clotting process (coagulopathy). however general trends should be monitored for: – Red Blood Cells: • • • With chronic waning disease. tissue biopsy.1/12/2010 Hepatic Clinical Diagnostics • Since liver disease. a liver biopsy (fine needle. white blood cell elevations can be severe with extremely abnormal cytology and high white blood cell. changes in white blood cells should be evaluated. or core biopsy) may be recommended to obtain a final diagnosis and help outline treatment protocols. and jugular sticks should not be attempted if there is concern of a coagulopathy. chronic bleeding concerns. platelets counts should also be closely monitored. Further. physical examination and other diagnostic aids. With significant anemia. blood work can appear normal and there can still be significant liver dysfunction. With certain forms of cancer (i. If the medical team determines that hepatic dysfunction is occurring. Hepatic Clinical Diagnostics • Blood Film: – Changes in Red Blood Cell Morphology • Acanthocytes / Echinocytes • Burr Cells – Hepatic Lipidosis • Schistocytes – White Blood Cell : Lymphoma – Abnormal Lymphocytes / White cells – Low Platelet Number 12 . hepatic lymphoma). Animal should be carefully assessed for bruising. non regenerative – White Blood Cells: • • With concerns of infectious disease. • • • Hepatic Clinical Diagnostics • Complete Blood Count: Components of the complete blood count can vary dependent on the form of liver disease. There are many potential forms of liver disease. trauma and dysfunction can be difficult to evaluate based on blood work alone. clinical diagnostics and imaging alone are often not sufficient to diagnose the cause of the liver disease present.

However this can be a normal finding in Dalmatians. Bilirubinuria will be seen before hyperbilirubinemia in dogs with early hepatic disease.35 A normal to low pCO2 A low base excess (BE) A low Sodium Bicarbonate Level (NaHCO3) A normal to high Anion Gap (AG) • In most cases. Activated Partial Thromboplastin Time (APTT)) can help detect early trends of the patient’s ability to clot blood. hemolysis. The diseases that cause of bilirubinuria are the same as those that result in hyperbilirubinemia.1/12/2010 Hepatic Clinical Diagnostics • Chemistry: – Liver Damage Enzymes: • • • • ALT AST GGT Alk Phos – Liver Dysfunction Enzymes: • • • • • Elevated Total Bilirubin Paired Bile Acids Hypoalbunemia (Suggestive) Low Blood Urea Nitrogen (Suggestive) Hypoglycemia (Rare) Urinalysis • A urinalysis should always accompany all blood work evaluations to help determine and indicate multiple organ issues. Since liver disease can produce all these components. treating the underlying liver disease will resolve the metabolic acidosis. 13 . monitoring blood gas helps the medical team understand the response to treatment and allows for a more accurate prognosis to be made. the presence of bilirubin in feline urine is always significant. • – Urine Sediment: • Ammonium Biurate Crystals can be seen in neutral to high urinary pH and are associated with liver disease and portocaval shunts. Key concepts to monitor are: – – Urine Specific Gravity: Determine Renal Azotemia vs. it should not be completely discounted. increase toxins and toxic metabolites and increase the loss of bicarbonate rich fluids. bile duct obstruction and sepsis. Bilirubin crystals are seen in any urinary pH and are associated with liver disease and immune-mediated hemolytic anemia • Hepatic Clinical Diagnostics • Coagulation Screen: Evaluating clotting times (Activated Clotting Time (ACT). In cats. However. a metabolic acidosis can be noted. a metabolic acidosis can be produced by disease which decrease glomerular filtration. Partial Thromboplastin Time (PT). liver disease. noted The following parameters are observed with metabolic acidosis: – – – – – Blood pH < 7. Although bilirubinuria can be found in normal dog urine. Blood Gas: As discussed in Renal Course of Abaxis University. Pre-renal Azotemia Bilirubinuria: • Dog urine can have trace to 1+ bilirubin with no underlying disease.

1/12/2010 Hepatic Clinical Diagnostics • Abdominal Radiography: Abdominal radiographs can help assess for changes in hepatic size and shape. • – – • Exploratory Surgery: In some cases. Cellular or tissue biopsy is possible through ultrasound guided biopsy techniques. evidence of gall bladder for stones (Cholelithe). Abdominal Ultrasound: – Abdominal ultrasound can assess the internal architecture of the abdominal organs g for changes suggestive of focal or diffuse hepatic disease. changes in the gall bladder wall suggestive of infection or obstruction. It is important to note that changes in hepatic architecture can only suggest focal or diffuse disease and rarely helps the medical team confirm diagnosis. 14 . exploratory or laparoscopic surgery and wedge or core biopsy of the liver may need to be completed. when ultrasonic biopsy or fine needle aspirate is non-diagnostic. and any other changes in the abdomen that can suggest serious disease. and identification of abnormal blood vessels that could suggest a Porto-caval shunt.

                Section III:  Appendix                        .

  • • Anemia:  Lack of Red Blood Cell precursors  Increased  Clotting  Time:  The  liver  produces  clotting  factors  that  finalize  clot  formation.  • Hypoalbunemia:    Due  to  lack  of  blood  albumin.  weakness  and  weight  loss.  depression.  the  body  can  shift  fluid  from  the  vascular  supply  to  the  tissue.    Abaxis University Appendix    Evaluating for Liver Damage and Dysfunction A.  vomiting.  increasing  fluid  accumulation  in  the  body  producing  Formation of Building Blocks  . DVM ABVP     Table I:  Secondary Concerns of Liver Dysfunction  Liver Function  •   © 2009  Concern of Dysfunction Hepatic  Encephalopathy:    Development  of  neurologic  symptoms  secondary  to  improper detoxification of microbes and toxins which remain in the body affecting  Detoxification  • the central nervous system.  anorexia. Rosenfeld.  Physical  Symptoms  due  to  build  of  toxins  and  bilirubin:    Increased  toxins  can  produce  nausea.  diarrhea.

  Normal Level:    • Canine:  10‐43 IU/L  . but has higher levels of activity  in muscle and liver cell damage. edema and pulmonary edema (with patients on IV fluids).   Normal Level:    • Alanine  aminotransferase  (ALT or SGPT)     • • Canine:  6‐70 IU/L  Feline:  28‐76 IU/L  The following patterns in the ALT level can be observed:  • • Low ALT activity   Not associated with disease conditions  Increased activity of the enzyme occurs with:  • • • • ACUTE LIVER DAMAGE  Chronic Drug Therapy (Anticonvulsants.ascites.  Glucose Storage  • Hypoglycemia (rare)    Table II:  Enzymes which evaluate Liver Damage   • • Alanine  aminotransferase  (ALT)  is  responsible  for  the  conversion  of  2‐oxoglutarate  to  pyruvate  and  glutamate in the liver cells (hepatocytes). Steroids)  Physical Trauma  Cardiac Disease  Aspartate  aminotransferase   (AST or SGOT)  • • Aspartate aminotransferase (AST) is an intracellular enzyme in all cells.

  and  is  thought  to  be  involved  in  pathways  used to protect cells from oxidative injury.• • Feline:  12‐40 IU/L  The following patterns in the ALT level can be observed:  • • Low AST activity   Not associated with disease conditions  Increased activity of the enzyme occurs with:  • • • ACUTE LIVER DAMAGE  Disease.      . Immune Mediated Hemolytic  Anemia). which affect the muscular skeletal system (e. bile duct and hepatic cells. GGT does not “leak” from hepatocytes.    GGT  is  an  intracellular  enzyme  responsible  for  cleaving  C‐terminal  glutamyl  groups  from  one  substrate  or  molecule  to  another.g.g. its activity is increased due to  increased production (induction) of the enzyme in response to disease. trauma or seizure)  Disease.   • Gamma‐glutamyltransferase  (GGT):    Gamma‐glutamyltransferase  is  more  an  indicator  of  gall  bladder  obstruction  or  lack  of  bile  flow. GGT is present in all cells except it has higher concentration in  renal epithelial. which produce red blood cell destruction (e.   Normal Level:    • Canine:  0‐8 IU/L  Feline:  0‐1  IU/L  • Gamma‐ glutamyltransferase  (GGT):    • • The following patterns in the ALT level can be observed:  • • Low GGT activity   Not associated with disease conditions  Increased activity of the enzyme occurs with:  • • • ACUTE LIVER DAMAGE  Increased GGT activity can be associated with decreased bile flow (cholestasis)  Unlike AST and ALT. since there is significant levels of AST in red blood cells.

 Some conditions that increase Alkaline Phosphatase  activity are:    • • • • Hyperadrenocorticism  Liver and Gall Bladder Disease  Long Term Medication  Bone growth    .  On most chemistry panels. Similar to GGT. Alkaline Phosphatase activity represents the  combined activity all combined tissue alkaline phosphatase levels. bone.  kidneys and placenta. intestine. ALP’s activity increases because of increased production of the  enzyme (induction) in response to disease.• Alkaline Phosphatase (SALP or ALP): Alkaline Phosphatase is present within the liver.  Normal Level:    • • Canine:  8‐76 IU/L  Feline:  8‐62  IU/L  • • Alkaline Phosphatase  (SALP or ALP):  The following patterns in the ALT level can be observed:  • • Low Alk Phos activity   Not associated with disease conditions  I Increased Alkaline Phosphatase activity:  High ALP can originate from diseases and non‐diseased  conditions.

  Bili)  Canine:  0‐0.5 g/dl  Feline:  2.1 g/dl  • Low Albumin levels may indicate:  • Decreases  in  blood  albumin  concentration  can  occur  generally  with  a  number  of  disease  .  Normal Level:  • • • Bilirubin  (Total Bilirubin or T.  However.1‐4.6 mg/dl  Feline:  0‐0. Immune‐mediated Hemolytic Anemias) or gall bladder  obstruction.g.  it  should  be  noted  that  although  patients  that  are  icteric  secondary  to  liver disease have liver dysfunction. however not all patients with liver dysfunction  are icteric.4‐4.  Further. increase levels of Bilirubin also can be associated with increase intravascular  red blood cell destruction (e.  Normal Level:  • • Canine:  3.  • • • Albumin  Albumin  is  a  small  carrier  protein  that  binds  to  hormones  and  other  components  in  the  blood  stream to maintain and move necessary elements throughout the body.4 mg/dl  The following patterns in the ALT level can be observed:  • • Low Bilirubin activity   Not associated with disease conditions  Increased activity of the enzyme occurs with:  • • The  buildup  of  bilirubin  in  the  serum  and  body  in  association  with  liver  disease  indicates liver dysfunction.Table III:  Enzymes which evaluate Liver Dysfunction  • • Bilirubin is a toxic metabolite produced from the red blood cell destruction in the spleen and the  breakdown of hemoglobin.

  Bile Acids    • Normal Level:  • • Canine:  Pre‐parandial: 0‐5.   Bile acids are stimulated when the patient eats.  When observed on clinical diagnostics.  low  body  albumin  can  also  be  associated  with  Kidney  disease.0 µmol/l     Post‐Parandial:  5.  As a general rule.syndromes that effect production or loss of the protein molecule.  bleeding  and  intestinal disease.  Low protein diets can also result in a  low BUN.9‐12. hypoalbuminemia can be a suggestion of altered liver  function. • A  decrease  in  functioning  hepatocytes  will  compromise  the  liver’s  ability  to  produce  albumin.7 µmol/l       Feline:  Pre‐parandial: 0‐5.0‐10.0 µmol/l       • Alterations in Bile Acids can indicate a true liver dysfunction.  After fat is emulsified. it may suggest a liver dysfunction.0 µmol/l     Post‐Parandial:  3.    –   .  However.  When attributable to liver disease.   A low BUN by itself does not always indicate liver dysfunction.  • •   Blood urea nitrogen  (BUN)    A low BUN level can be associated with the liver’s inability to produce take ammonia molecules and  produce BUN.   Hepatocytes also produce chemicals called bile acids that help to emulsify fat within the small intestine.  Bile acids then empty through the gall bladder and into  the common bile duct. bile acids are then rapidly reabsorbed by the small intestine. at least 75% of normal liver function must be lost before albumin  concentration is decreased.

  Blood Smear:  Non‐regenerative Anemia due to secondary to lack of erythropoietin. Schistocytes)  AST  ALT  ALK PHOS  GGT  Total Bilirubin (Hepatic Disease)  Blood chemistry –  Liver Dysfunction  (See Table II)  Low Albumin (Hepatic Disease)  Low BUN  +/‐ Blood Glucose  Elevations in Post‐Parandial Bile Acids    Urine Specific Gravity (USG):  to help differentiate renal from pre‐renal azotemia  Urinalysis  Urine Stick: Bilirubinuria:  >+1 (Canine)  / > Trace (Feline)  Urine Sediment:  Ammonium Biurate Crystals & Bilirubin crystals  Blood chemistry –  Liver Damage  (See Table II)  . fungal.  leukocytosis  Complete blood count  Platelets:  Low Platelet count can support chronic bleeding secondary to decreased clotting factors. and red blood cell abnormalities (Acanthocytes / Echinocytes. Concerns of Chronic Anemia  White Blood Cell Count: Bacterial. Burr Cells – Hepatic  Lipidosis. possible decreased  platelet number.Table IV: Suggested Overview of Clinical Diagnostics of Liver Dz  Red blood cell count:  Elevations of HCT / PCV – Dehydration. parasitic or protozoal causes of infectious hepatic disease.  thrombocytopenia.

35  A normal to low pCO2   A low base excess (BE)  A low Sodium Bicarbonate Level (NaHCO3)  In most cases.  monitoring blood gas helps the medical team understand the response to treatment and allows for a  more accurate prognosis to be made.Elevations in: • Coagulation Profile  • • Activated Clotting Time (ACT)  Partial Thromboplastin Time (PT)  Activated Partial Thromboplastin Time (APTT))  Metabolic Acidosis ‐The following parameters are observed with metabolic acidosis: – – – – Blood Gas  – A normal to high Anion Gap (AG)   Blood pH < 7. treating the underlying liver disease will resolve the metabolic acidosis.     .  However.

 changes in the gall bladder wall  suggestive of infection or obstruction. and any other changes in the abdomen  that can suggest serious disease. and identification of abnormal blood vessels that  could suggest a Porto‐caval shunt.    Cellular or tissue biopsy is possible through ultrasound guided biopsy techniques. when ultrasonic biopsy or fine needle aspirate is non‐ diagnostic.    It is important to note that changes in hepatic architecture can only suggest focal or  diffuse disease and rarely helps the medical team confirm diagnosis.    . evidence of gall bladder for stones (Cholelithe). exploratory or laparoscopic surgery and wedge or core biopsy of the liver may need  to be completed.     Other Possible  Diagnostic Exams  – – • Exploratory Surgery:  In some cases.• Abdominal Radiography:  Abdominal radiographs can help assess for changes in hepatic size and  shape.      • Abdominal Ultrasound:    – Abdominal ultrasound can assess the internal architecture of the abdominal organs for  changes suggestive of focal or diffuse hepatic disease.