Solution for case 25

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Tentative diagnosis: Hepatitis. An increase in AP, ALT and total bilirubin is indicative of liver problems. The mild elevation in total bilirubin explains the slightly yellow mucus membranes. The generalized lymphadenopathy and increased globulins could be indicative of a systemic infection that in this case is affecting primarily the liver, causing hepatitis.

Further diagnostic tests:

• Paired serum samples
• Serology
• Immunofluorescence
• Ultrasound
• Liver biopsy

Differentials:

• Infectious hepatitis: bacterial, fungal or other
• Leptospirosis
• Granulomatous hepatitis
• Toxic hepatopathy
• Fulminant infectious disease: parvovirus, canine distemper
• Portosystemic shunting

Hepatitis can have many different causes. The main disease suspected to be causing the hepatitis is leptospirosis. Leptospira interrogans serovar Bratislava is very prevalent in the area and is not covered by the leptospirosis vaccine. The vaccine only includes serovars Canicola, Icterohemorrhagiae, Grippotyphosa, and Pomona. No cross protection exists between serovars. The typical clinical signs of leptospirosis are fever, depression, lethargy, anorexia, myalgia, vomiting, lumbar pain from renomegaly and nephritis, icterus, bilirubinuria, cholestasis and/or hepatic necrosis, renal failure. It has been reported that many young dogs suffer more from liver problems and not the kidney when infected with leptospirosis.

Extrahepatic bacterial or fungal infections could also cause hepatitis, but this case was not showing clinical signs of having an infection in other body systems that could have traveled to the liver. However, since the owner was not with the dog during the entire summer the patient could have developed a primary infection, that later traveled to the liver, but at the present time is not evident.

Many hepatotoxins such as high amounts of acetaminophen, aflatoxins, blue-green algae, heavy metals; certain herbicides, fungicides, insecticides and rodenticides could cause liver problems. No ingestion or access to any of these was reported by the owner.

Other causes of hepatitis are Canine Adenovirus-1, but this patient vaccinated. Toxoplasmosis is a rare disease because the body is usually able to eliminate the infection. However some young dogs are not able to control the infection and Toxoplasma tachyzoites invade tissues throughout the body and replicate intracellularly until cells burst, causing necrosis. If the Toxoplasma tachyzoites invade the liver clinical signs associated with hepatitis could be seen.

Canine cholangiohepatitis is rare and associated with ascending biliary tract infections (Salmonella sp., Campylobacter jejuni), choleliths, coccidiosis, and surgery of the biliary tract. Clinical signs include anorexia, vomiting, diarrhea, lethargy, PU/PD, fever, abdominal pain, hyperbilirubinemia and elevated AP and GGT. To make a definitive diagnosis samples should be submitted for aerobic and anaerobic cultures and sensitivity.

Idiopathic hepatic fibrosis is a rare disease in young dogs, usually less than 2 years of age, is not associated with any underlying inflammatory conditions. Clinical signs include ascites, hepatic encephalopathy, weight loss, vomiting, diarrhea, portal hypertension, portosystemic shunt, microcytic anemia, elevated AP and ALT and hypoalbuminemia. Microhepatica can be noted on radiographs.

Hepatic amyloidosis is a rare familial disease. Clinical signs include anorexia, PU/PD, vomiting, icterus and hepatomegaly. Diagnosis is made by identifying amyloid deposits in a liver biopsy. Glycogen storage disease is caused by a rare deficiency in glucose-6-phosphatase or in amylo-1,6-glucosidase, this results in a failure of glycogen to be released from the cell. Therefore, glycogen accumulates within the liver and other organs. Enzyme analysis of fresh frozen samples of liver, muscle or skin is needed for diagnosis. Prognosis is poor and most dogs succumb to these diseases at a young age.

Treatment of possible leptospirosis: Administration of 0.9% NaCl fluids IV to prevent dehydration was started along with antibiotic treatment with Ampicillin 500mg orally TID (three times a day). The patient is to be fed three times a day l/d diet in order to prevent any further liver damage and to try to increase body weight. A CBC test is to be repeated in three days to determine if the treatment plan is being effective and assess the health status of the patient.

Need to assess the health and degree of clinical signs in patient's kins. There may be need to look into familial disease.

Case 25

Presentation: 

A six month old, intact, male, mix breed dog (pothound) was presented to AcaseAweek Clinic with a history of anorexia, weight loss and lethargy. The dog has an indoor/outdoor lifestyle, is fed puppy Science Diet, is up to date on its vaccinations and is treated for ectoparasites with Adam’s spray. The owner was away during the summer and upon return found ticks on the dog. There are four other dogs in the household, one of them is showing similar clinical signs and happens to be this patient’s brother. 

Physical examination revealed that the patient was mildly depressed, alert and responsive, had a temperature of 100.4ºF, heart rate was 100bpm, respiratory rate was 12bpm and weighted 18.2 kg.

Ears, eyes, nose, throat: mild black, thick, tarry exudate on both ears. No ocular or nasal discharge observed.

Mucus membranes: grey, pale and slightly yellow (icterus). CRT<2>

Lymph nodes: generalized lymphadenopathy.

Laboratory tests:

Snap test: Ehrlichia, Heartworm, Anaplasma and Lyme disease negative.

CBC: unremarkable, except for mild eosinophilia.

Chemistry profile:

• AP 1259 U/L (46-337)
• ALT 673 U/L (8-75)
• Glob: 4.1 g/dL (2.3-3.8)
• TBIL: 1.3 g/dL (0.0-0.8)

Urinalysis- unremarkable.

What is your tentative diagnosis? Give list of differentials.

What diagnostic test(s) will you perform to confirm your diagnosis?

How will you treat and manage this case?

Solution to this case

Solution for case 24

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Tentative diagnosis: Azotemia due to chronic renal failure (CRF).

Further diagnostic tests:
* Abdominal radiography/ultrasound to demonstrate decreased size of kidneys.

* Urine creatinine:protein ratio.

* Renal biopsy (not commonly performed).

* Blood pressure to demonstrate hypertension.

Isosthenuria is a common finding in chronic renal failure when two thirds of the functioning nephrons are lost.

Azotemia is seen when at least three fourths of the functioning nephrons are lost. Azotemia presents with increased BUN, creatinine, GI, and neurological clinical signs. This patient’s presentation would suggest that she has lost at least three fourths of her functioning nephrons.

Predisposing factors for CRF are age, chronic obstruction, infection, heart failure, and tubular disease. A urine sample taken from this patient, via a cystocentesis, ruled out bacterial infection. Patient’s heart sounded normal on auscultation. The renal failure was attributed to her age.

Management of chronic renal failure is a multifactor process. Most importantly hydration and electrolytes must be maintained with in normal limits. An appropriate renal diet will be low in protein, phosphorous, and sodium. Some other factors which must be addressed in the management of chronic renal failure include anemia, proteinuria, and gastrointestinal processes.

Anemia is due to decreased production of erythropoietin by renal peritubular cells. The anemia could also be from blood loss via GI ulcers, or iatrogenic from blood draws. The anemia is non-regenerative normochromic normocytic.

Treatment of anemia with erythropoietin (EPO) is indicated when the PCV falls below 18% and the patient is showing clinical signs of anemia/hypoxia. Caution must be used with EPO since it is of human origin. Dogs can produce antibodies against it. In severe anemia requiring immediate relief of clinical signs a blood transfusion can be done.

Proteinurea is seen because glomeruli have been damaged enough to allow loss of protein and anti-thrombin III. This decreases oncotic pressure, leading to edema. The loss of anti-thrombin III causes coagulation issues. Many of these patients have pulmonary thromboembolism as a complication.

These patients can be treated with angiotensin converting enzyme inhibitors which decreases the pressure in the glomeruli by dilating the efferent renal artery. This decrease in pressure helps prevent loss of proteins into the urine. Canine patients with CRF and proteinuria tend to have a decreased survival.

GI ulcers and nausea and vomiting are the common clinical signs seen. Uremic toxins activate the chemoreceptor trigger zone which leads to the nausea and vomiting. These uremic toxins also increase gastrin production which increases hydrochloric acid production in the stomach, leading to GI ulcers.

These complications are treated by decreasing the uremic toxins via hydration; protecting the stomach by decreasing acid production, and controlling the nausea and vomiting by blocking the chemoreceptor trigger zone. Acid production can be decreased using histamine blockers or proton pump inhibitors. Sucralfate can be used to protect/coat ulcers. The nausea can be controlled with medication targeted at dopamine antagonism, serotonin, or neurokinin.

Treatment:

Hospitalize patient
– NPO
– Fluid diuresis to decrease azotemia
* * Maintenance: 60ml/kg/24 hours = 2100ml
* * Deficit (5%) = 1715ml
* * Total fluid/day = 3850ml (160ml/hr)
– Decrease gastric acid and control N/V
* * Famotidine 20mg Q12 hours
* * Anti-emetic - Cerenia (maropitant citrate)
– Re-evaluate
* * BUN, Creatinine, Phosphorus every 48 hours
* * PCV and TP daily

The patient remained azotemic.
– After 3 days, fluids increased to 250ml/hr during the day and 160ml/hr during the evening.
– NPO
– Continue H2 blocker and Cerenia
– Continue to monitor BUN, SCr, TP, PCV, Phosphorus
The patient did not improve and was euthanized on consultation with owner.

See following Links for more info on CRF:

http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/130603.htm

http://courses.vetmed.wsu.edu/vm552/urogenital/crf.htm

http://www.marvistavet.com/html/body_chronic_renal_failure.html

http://www.felinecrf.com/what0.htm

Case 24

A 12 year old spayed female Labrador was presented to AcaseAweek Clinic with one week history of vomiting, decreased appetite and lethargy. Bad breath of the pet was also a complaint. The patient was brought to clinic 4 month back for ehrlichia and mild azotemia. She is currently on Hill’s k/d diet.

Physical exam:

• Weight: 34.8 kg
• Temperature: 100.7
• Pulse: 136
• Respiration rate: 28
• Mucus membranes: pale
• Capillary refill time: > 2 seconds.
• Dehydration: ~5%
• Abdomen was tender upon palpation.

Lab tests: (Reference Values)

• BUN: 112 mg/dl
• Creatinine: >13.6 mg/dl
• Phosphorous: 16.1
• PCV: 25%
• USG: 1.011
• TP: 6.4 mg/dl
• Albumin: 2.7 mg/dl
• Non-regenerative anemia was also noted.

What is your tentative diagnosis?

Give differentials for your diagnosis.

What further diagnostic test(s) will be performed to confirm the tentative diagnosis?

How will you treat and manage this case?

Solution for this case

Solution for case 23

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Problem List:Hemoperitoneum
Cardiac arrhythmia and murmur
Poor peripheral perfusion
Mild anemia with marked regeneration
Moderate leukocytosis due to moderate neutrophilia
Mild lymphopenia
Mild thrombocytopenia
Mild↑ALKP, ALT
Mild↑amylase
Mild↑total bilirubin
Marked↑BUN and creatinine
Marked↑phosphate
Isosthenuria (single reading)
Moderate hematuria and bilirubinuria
Mild proteinuria
Anorexia, depression, lethargy
Vomiting
Marked weight loss and muscle atrophy

Primary problems on this patient are hemoperitoneum and acute renal failure.

Differentials for hemoperitoneumHemangiosarcoma (spleen/liver)
Coagulopathy (rodenticide)
Abdominal trauma

Differentials for acute renal failure
Ischemia due to hypovolemia, hypotension, shock or DIC
Nephrotoxicity (exogenous or endogenous toxins)
Immune mediated glomerulonephritis
Infectious (e.g. Leptospirosis, pyelonephritis)

Regarding the differentials for hemoperitoneum, hemangiosarcoma is the most likely. Hemangiosarcoma is most common in middle-aged to older dogs. Marked weight loss and muscle atrophy noted on physical exam may be suggestive of neoplasia.

The patient’s history and clinical signs are consistent with sudden rupture of splenic hemangiosarcoma causing hemorrhagic effusion into the abdominal cavity. Dogs with ruptured splenic hemangiosarcoma will commonly have abdominal enlargement due to hemoabdomen, pallor and hypotension. Poor peripheral perfusion and hypovolemia are evidenced by increased CRT and pulse deficit on physical exam. CBC with ruptured splenic hemangiosarcoma typically shows evidence of a recent bleed (marked regeneration with a mild decrease in PCV). Leukocytosis due to mature neutrophilia and thrombocytopenia are common CBC abnormalities noted in dogs with hemangiosarcoma of the spleen or liver. Mild lymphopenia may be a ‘stress’ response. High liver enzyme activity may be seen with hemangiosarcoma involving the liver. Mildly elevated liver enzymes are more likely pre-hepatic in origin; secondary to hypovolemia, hypotension and poor perfusion of hepatocytes. The icterus is most likely hepatic in origin, due to impaired uptake and conjugation by the underperfused liver. Mild pancreatic amylase increase is likely also secondary to decreased perfusion.

Regarding other differentials for hemoperitoneium, coagulopathy associated with rodenticide toxicity is less likely than hemangiosarcoma since there was not evidence of intrathoracic bleeding. With hemothorax, clinical signs of coughing, thoracic pain and/or dyspnea would be expected. There was also no history of possible ingestion. Abdominal trauma was ruled out on lack of history or any other evidence of a traumatic event.

This patient’s remaining problems are consistent with acute renal failure (ARF). The patient demonstrated a marked azotemia and hyperphosphatemia due to build up of nonprotein nitrogenous waste products and phosphate which are normally removed by the kidneys. Hypovolemia indicates that there is at least a partial pre-renal component to the azotemia. However if her azotemia was strictly pre-renal with tubular function intact, urine should be concentrated (SG >1.030) in the face of reduced renal perfusion. Patient’s urine SG of 1.013 is in the isosthenuric range, implying that kidneys are unable to adequately concentrate urine despite azotemia. Unlike pre-renal azotemia, renal azotemia is usually irreversible and is caused by extensive morphological or functional glomerular lesions with a loss of more than 75% of functional nephrons. On urinalysis, proteinuria and hematuria are supportive of glomerular damage.

Clinical signs of ARF are mostly caused by severe uremia and include lethargy, vomiting, anorexia and dehydration. The rapid build up of uremic toxins often causes the animal to become profoundly systemically unwell. Severe metabolic derangements are common, particularly hyperkalemia and metabolic acidosis. Electrolytes were not run on this patient, however hyperkalemia likely contributed to the arrhythmia noted on physical exam and being non-tachycardic despite being hypovolemic/hypotensive. Diagnosis of ARF relies on evidence of a sudden elevation in urea and creatinine, but definitive diagnosis would require renal biopsy or post mortem.

The cause of ARF is debatable. The most likely scenario is that this patient had a splenic hemangiosarcoma which ruptured 2-3 days before she was presented. Subsequent uncorrected hypovolemia and hypotension caused secondary insult to abdominal organs and renal failure due to prolonged ischemia. Multiple factors may have contributed to acute renal failure, and it is possible that patient had some degree of renal insufficiency prior to the ischemic insult which merely pushed her over the edge.

Emergency treatment:
IV catheter (20 G) – L cephalic vein
LRS @ 40 mL/hour (maintenance)
Urinary catheter – closed system

Owner did not want any other diagnostic tests performed and requested euthanasia and necropsy.

Further diagnostics (if patient was not euthanized):
Coagulation panel (OSPT to rule out rodenticide toxicity)
Abdominal ultrasound (hemangiosarcoma search)
Cardiac ultrasound (splenic HSA – often concurrent R atrium involvement)
Electrolyte panel (potassium level) → correct imbalances
Repeat urinalysis (confirm isosthenuria, monitor ARF)

Treatment of hemagiosarcoma is supportive and anti-neoplastic drugs. However, prognosis is Grave.

Necropsy findings:
About 500 ml of fluid was reported in abdominal cavity. Ruptured splenic mass of about 12 cm in size was also found and submitted for histopathology. Histopathology confirmed hemangiosarcoma.

Follow these two links for more information about the hemangiosarcomas:

http://www.vet.uga.edu/VPP/clerk/frankhauser/index.php

http://vetpath.wordpress.com/2008/08/12/splenic-hemangisarcoma-in-a-cat/

http://journals.tubitak.gov.tr/veterinary/issues/vet-98-22-5/vet-22-5-13-97199.pdf

https://www.vetconnect.com.au/5min/data/06460647.htm

Case 23

A 13 year old, female spayed, mixed breed dog was presented to AcaseAweek Clinic with history of collapse, depression, lethargy and vomiting 3 times the night before presentation. The patient had been anorexic for the past 2 days and appeared healthy previously. The patient lives mostly inside and her owner reported no possibility of accidental ingestion of foreign body or chemicals. Her vaccination status is current and she is on heartworm preventative. She was treated for Ehrlichiosis with doxycycline two months back.

Physical Exam:
Remarkable weight loss and muscle atrophy.
T: 98
P: 88
R: 44
MM: pale pink
CRT> 2 sec

Cardiovascular: murmur, cardiac arrhythmia, pulse deficit.
Respiratory: lungs sound clear
Abdomen: distended, positive succession, moderately painful

CBC/Cytology:
PCV: 23% [37-55]
WBC: 28.9 x103/μL [6-16.9]
Mature Neutrophils: 26.3 x103/μL [3.3-12]
Band Neutrophils: 0.6 x103/μL
Lymphocytes: 0.3 x103/μL
NRBC: 0.9 x103/μL
Smear: Platelets: 1-4/hpf
RBC morph: marked polychromasia, moderate anisocytosis

Biochemistry:
ALKP: 267 U/L [23-212]
ALT: 164 U/L [10-100]
AMYL: 2490 U/L [500-1500]
BUN: 130 mg/dL [7-27]
CREA: 6.1 mg/dL [0.5-1.8]
PHOS: >16.1 mg/dL [2.5-6.8]
TBIL: 1.4 mg/dL [0-0.9]

Urinalysis:
Bilirubin: ++
SG: 1.013
Blood: +++
pH: 5.0
Protein: +

Abdominocentesis:10 mL fluid was withdrawn.
Abdominal Fluid Analysis/Cytology:
Color: red
Turbidity: 3+
Protein: 7.2 g/dL
PCV: 23%
Smear: many RBCs, neutrophils and macrophages, moderate lymphocytes, almost no platelets seen, few reactive mesothelial cells.

What will be your tentative and differential diagnosis?
What further diagnostic test(s) you will perform to confirm your diagnosis?
What will be your treatment plan(s)?

Solution to this case

Solution for case 22

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Tentative diagnosis: Protein-loosing nephropathy. 

Differential diagnosis: Glomerulonephritis, amylodosis, idiopathic glomerulopathy, liver disease, right sided heart failure, protein loosing enteropathy.  

Further diagnostic tests:
1. Abdominocentesis: Analysis of fluid revealed transudate nature.

2. Urine Protein:Creatinine ratio: more than 4 (less than 1 is normal)

3. 4DX snap test: Negative in this case. 

4. Renal Biopsy: To formulate prognosis by differentiating between glomerulonephritis and amylodosis. Renal biopsy was not done in this case. 

5. Fecal float for GI parasites: no parasite eggs were found. 

Although there are many causes for abdominal effusion or ascites, hypoalbuminemia, due to protein losing enteropathy or liver failure, can be ruled out at this time based on normal liver enzyme, negative fecal float and balanced diet for this patient. The abdominal fluid sample tested yielded a transudate, a potential cause could include a protein losing nephropathy/enteropathy or liver disease. In this case the hypoalbuminemia, hypercholestrolemia, proteinuria and urinary hyaline casts are hallmark of protein loosing nephropathy (nephrotic syndrome). Thromboembolism is a potential complication in such cases because of the reduced antithrombin III.

Most probable suspected cause here is the idiopathic.

This patient also had severe peridontal disease. 

Therapeutic Plan:  
Treatment is usually difficult and unrewarding. Prognosis is guarded in this case.
Abdominocentesis to make animal comfortable.
Sodium restricted diet. High quality low quantity protein diet (Hill’s k/d)
Enalapril: Vasodilator, Reduced sodium retention and reduce proteinuria and hypertesion.
Restricted activity and anticoagulants (aspirin) to reduce chances of thromboembolism.

Case 22

A 12 year old, intact female Pompek canine presented to AcaseAweek clinic for abdominal distention.  The owner reported abdominal distention worsening for last one and half week.  As the patient was eating, drinking, eliminating and otherwise showing no remarkable behavioral changes at home, the owner was unsure of the exact duration of her condition.  The dog is upto date on vaccines and deworming but not on any ectoparasite or heartworm control. Animal is fed Hill’s Science diet for senior dogs. 

Physical Exam:
Weight= 5.5 kg
T=100.9 °F
HR/PR=160 bpm  
RR=panting/open mouth breathing
EENT:  Normal, except right prolapsed third eyelid
Oral:  MM pink/moist, CRT<2s, Halitosis, Excessive tartar, gum recession, missing teeth: 101/102, 201/202, 301-303, 401/402
LLN:  Normal
Thorax:  Heart/Lung auscultate normally, with normal peripheral pulse, no jugular vein            distention
Abdomen: Distended, Firm, Unable to palpate internal organs, No pain on manipulation, +ve reaction on Ballotment
U/G: Normal, intact
Skin: Normal
MSk: BCS 2/5
Neuro: Normal

CBC/Chemistry:
PCV= 31.7% (37-55%)
Albumin= 1.2g/dl (2.6-4.0 g/dl)
Total Protein=3.8g/dl  (5.5-7.5 g/dl)
Cholesterol= 347 mg/dl (116-254 mg/dl)
All other values WNL

Urinalysis:
Protein= Dipstick protein ++++
Hyaline casts and few RBCs observed in urine sediment.

What is your tentative and differential diagnosis?
What further diagnostic tests you will perform?
What will be your treatment plan?

Solution for this case

Solution to case 21

Click here to see this case

Radiographic findings:
Globe like cardiac silhouette with distended pulmonary veins.

Ultrasound findings:
Fluid around the heart (pericardial effusion). US also showed the fluid in the abdomen around the spleen, between the diaphragm, the liver and around the bladder.

Tentative diagnosis: Right sided heart failure/pericardial effusion.

Differential diagnoses for pericardial effusion include, tumors (most common especially in dogs greater than 7 years) such as hemangiosarcomas, chemodectomas (most often in brachycephalic breeds), ectopic thyroid carcinoma, mesothelioma,  lymphosarcoma.  Idiopathic pericardial effusion is the second most common cause and is usually found in dogs 6-7 years old.  Others include anticoagulant poisoning such as rat poison and other coagulopathies, pericardial cysts, constrictive pericarditis, infectious disease, atrial tear in small breed dogs, bacteria, FB, fungus, sepsis, trauma, viruses. Top differentials in this case include hemangiosarcoma, Idiopathic, coagulopathy, infectious or constrictive pericarditis.

Anemia and hypoproteinemia due to hypoalbuminemia shown by a low PCV and low TP suggest recent hemorrhage.  The nonregenerative anemia is likely due to acute disease within the last 4 days. High BUN and Creatinine are due to dehydration (prerenal azotemia).

Large cardiac Silhouette on radiographs suggests cardiac effusion. Muffled heart sounds are characteristic for pericardial effusion. In cardiac enlargement is heart sounds are louder, pinging heart sounds if the heart was enlarged.

Characteristic findings for pericardial effusion include a large globular cardiac silhouette rounded in all views, enlarged vena cava, and occasionally distended pulmonary veins. With small effusions, these findings may not be evident. Chest x-rays should always be carefully evaluated for evidence of a heart base mass and for metastatic disease. In this case an ultrasound also showed a pericardial effusion and ascities.

Ascites is a common sequel of pericardial effusion.  Pericardial effusion can lead to pericardial tamponade and right cardiac heart failure signs such as tachycardia, ascities, swollen limbs and increased respiratory rate.

Ultrasound helps to determine and locate any tumors in the heart.  If a mass is found it is important to biopsy the mass or pieces of the pericardium.  If mass is determined to be hemangiosarcoma there is a very poor prognosis and only a 3 mo survival period for most dogs without surgery.  Chemodectomas carry a better prognosis for 3 years survival with subtotal pericardectomy.

Further diagnostic tests:

1. Coagulation panel
To rule out any coagulopathies and make sure it is safe to perform pericardiocentesis.  Also, hemangiosarcoma may lead to minor DIC and coagulopathies.

2. Pericardiocentesis and abdominocentesis
They are more therapeutic than diagnostic.  

Pericardial effusion can be differentiated from peripheral blood in that it rarely clots unless it is from very recent hemorrhage and the PCV is significantly lower than that of peripheral blood.

The most common causes of pericardial effusion cannot be diagnosed due to the fact that hemangiosarcomas and chemodectomas do not exfoliate leading to a false negative result.  Reactive mesothelial cells may be mistaken for neoplastic resulting in a false positive result.  

In this case the fluid in pericardium was blood tinged with PCV <27%.

Abdominocentesis needs to be done to determine the type of the fluid (exudate, transudate or hemorrhagic). In this case abdominocentesis was performed and the fluid was found to be transudate.

3. Blood culture and sensitivity test:
This is required to rule out any infectious etiology for the pericardial effusion. In this case no organism was isolated.

4. 4 DX snap test was negative in this case.

Therapeutic plan:
This case was treated as indiopathic pericardial effuision as no mass was seen on the ultrasound.
The patient was stabilized (iv fluids) and pericardiocentesis was performed and animal was put on predisolone. Recheck was advised in 2 weeks time.
One pericardiocentesis may be enough in idiopathic pericardial effusion in 50% of dogs.  However, if more than 2 pericardiocentesis are required a subtotal pericardiectomy is recommended. +/- prednisone for inflammation after pericardiocentesis is performed.
In this case prognosis was fair as there was no recurrence of the pericardial effusion.

Case 21

A 4 year old intact male pit-bull mix canine  was presented to ACaseAweek Clinic for generalised weakness and a swollen left hindlimb since one week. He is both indoor and outdoor and he is fed home made food which is mainly rice and chicken. He is upto date on vaccination, heartworm and ectoparasites control.

Physical Exam:
Weight 25.1Kg
T: 100.9*F
PR/HR: 90bpm
RR: 36bpm
MM: Pale
CRT: >2sec
EENT: Normal
M/S – Swollen hind limb with pitting edema that is not painful.
Thorax: Muffled heart sounds on auscultation, but regular with no arrhythmias or murmurs noted.  Possible diminished lung sounds.
Abdominal palpation – Enlarged abdomen, with fluid wave on palpation.
LN: wnl
Neuro,  rectal – not examined.
BCS:  2/5

CBC and Chemistry:PCV 27% ( 37-55)
RBC morphology: mild anisocytosis and normochromic – non regenerative
No microfilaria seen,
All other values: wnl
ALB 1.9 g/dl (2.3 -4.0)
BUN 33 mg/dl (7-27)  
Creatinine: 1.7 mg/dl (0.5-1.6)
TP 4.8 g/dL (5.2 -8.2)
Urinalysis (free catch):Mild odor,
Color: yellow
SG: 1.020
Radiographs (Click to enlarge):

 

What are radiographic and ultrasound findings?What is your tentative and differential diagnosis?
What further diagnostic tests you will perform?
What will be your treatment plan?

Solution to this case

Solution to case 20

Click here to see this case


Tentative diagnosis: FIV/FeLV

Differentials: FIV, FeLV, hemobartonella, cytoxazoon, Eosinophilic granuloma complex, superficial pyoderma, IMHA, hyperthyroidism, renal disease. 

Further diagnostic tests:IDEXX Combo FIV/FeLV snap test, blood smear for blood protozoa, impression smear of the oral lesions, skin scraping and bacterial culture and sensitivity for the skin lesions. T4 test. PCR test for hemobartonella is also available. 

In this case the IDEXX combo test was positive for FeLV. No blood protozoa was seen on the blood smear. No eosinophils were seen on the impression smear of the oral cavity. Skin scraping was negative. Culture for skin lesions was positive for Staph infection and sensitive to Potentiated Amoxicillin. T4 levels were normal.

Based on the clinical signs and results from CBC and IDEXX snap test, FeLV is at the top of the differential list.  Her general appearance, lethargy, skin condition and lymphadenopathy all are signs that the immune system is not functioning optimally. Increase in the BUN/Creatinine and total proteins is due to dehydration. 

FeLV is a retrovirus in the same family as HIV/AIDS in humans.  It is more common in outdoor cats and kittens.  It is transmitted primarily through saliva from sharing utensils or from bite wounds and licking.  It can also be transmitted via urine, tears, feces, milk and through placenta.   Its main effect is suppression of the immune system thus affected individuals have many other organ system issues. 30% of animals develop cancer (lymphosarcoma).  This virus also leads to bone marrow suppression thus this animal had non-regenerative anemia, leucopenia and thrombocytopenia. Animals can live for years with the disease but usually by the time the diagnosis is made, the cat is already viremic.  Expected lifespan is 1-2 years after diagnosis.
IDEXX combo snap test for FeLV needs to be repeated in six weeks or Immunoflourecent Antibody (IFA) test needs to be done to confirm the diagnosis.  

Treatment Plan:
Blood transfusion was done and supportive therapy was provided as follows:  
IV fluids - LRS
Antibiotics - Potentiated Amoxicillin
B-complex
a/d Hills diet (high nutrition diet for recovering sick animals)

Advised to keep the cat indoors and prevent being around others both so they are not possibly exposed to FeLV. Any secondary infections should be treated as soon as possible. FeLV in this case was repeated in six weeks and was still positive thus confirming the diagnosis.