CVCT
Uploaded by
Dr. Sajid AbbasCVCT
Uploaded by
Dr. Sajid AbbasDr.
Sajid Abbas
DVM UVAS Lahore (Pakistan)
Bronze Medalist
Senior Vet. Officer
EverFresh Farms (Pvt). Ltd.
EverFresh Farms (Pvt). Ltd.
+923072044623
+923072044623
CAUDAL VENA CAVAL THROMBOSIS
AND METASTATIC PNEUMONIA
ETIOLOGY
Origin is most commonly septic thromboemboli originating from abscess at
hilus of liver showering caudal vena cava, right heart, and pulmonary arterial
circulation. Potentially, other septic foci that are nonhepatic in origin, such as
abdominal abscesses caused by hardware and deep digital sepsis, can also
be source of thromboembolic showering.
SIGNS
Although most cattle do not show signs of illness
when shower occurs, some cattle experience
acute death from massive pulmonary infarction
or have acute onset of profound respiratory
distress at time of thromboembolic episode.
SIGNS
Cattle having inapparent seeding of pulmonary
arteries or survive acute respiratory distress
Episode may eventually develop dyspnea,
hemoptysis and anemia. Epistaxis is most common
clinical sign observed in cows with hemoptysis.
PATHOGENESIS
Pathogenesis starts in forestomach or abomasum and involves inflammatory or
ulcerative mucosal lesions that allow bacterial seeding of portal circulation
with subsequent formation of liver abscesses. Therefore rumenitis, ruminal
acidosis, abomasal ulcers, and similar disorders predispose to condition.
Location is much more important than number of abscesses, however,
because only those at hilus of liver or adjacent to post cava represent
significant risk.
F. necrophorum and T. pyogenes are most common organisms isolated from
liver abscesses in dairy cattle. Most cattle with liver abscesses show no clinical
signs of illness unless abscess erodes into vena cava or multiple large
abscesses develop. This disease occurs sporadically in heifers and adult cattle
but rare in calves. This may be result of calves being fed less intensive diets
than heifers or lactating animals.
SUDDEN DEATH SYNDROME
Acute rupture of liver abscess into caudal vena cava may result in massive
release of thromboemboli to right heart and subsequent pulmonary artery
thrombosis, pulmonary infarction, exotoxemia or endotoxemia, and anoxia.
Close attention to perihilar area of liver and caudal vena cava should always
be part of thorough gross pathological examination in such cases.
ACUTE RESPIRATORY DISTRESS
SYNDROME
This appears in one animal within group or herd. Affected cow has per acute
onset of respiratory distress, fever(103.0° to 106.0°F [39.44° to 41.11°C]), labored
breathing, and increased respiratory and heart rates. Pulmonary edema, SC
emphysema, and open-mouth breathing may also be observed. Auscultation
of thorax reveals reduced airway sounds resulting from pulmonary edema,
pulmonary infarction, and bullous emphysema brought on by exertional
respiratory efforts. Key to diagnosis is fact that only one animal is affected with
severe lower airway disease, and to owner’s knowledge, the
cow has had no unique stress or previous problems.
HEMOPTYSIS, EPISTAXIS, CHRONIC
PNEUMONIA, ANEMIA SYNDROME
Septic thromboemboli create pulmonary abscesses at their endpoint in pulmonary
arteries, and aneurysms develop proximal to each abscess within affected pulmonary
artery. Because pulmonary arterial branches in cattle course close to bronchi,
eventual enlargement of abscesses predisposes to their rupture into airways. Sudden
discharge of purulent material into airway creates septic bronchopneumonia followed
immediately by minor or major hemorrhage from arterial aneurysm now
communicating directly into airway. Hemorrhage may be sufficient to result in
hemoptysis and subsequent epistaxis. Affected cattle are unthrifty and frequently
have been treated for recurrent bronchopneumonia characterized by fever (103.0°
to 106.0°F [39.44° to 41.11°C]), increased respiratory rate, as well as auscultable rales,
crackles, or wheezes within localized areas of lung. Some affected cattle develop
endocarditis caused by septic thrombus in caudal vena cava persisting as source of
chronic bacteremia through right heart and pulmonary arteries.
Epistaxis or hemoptysis may be slight and intermittent or may be profound and acute
and result in sudden death. Epistaxis with coughing and chronic bronchopneumonia
indicates extremely guarded prognosis because of irreversible nature of pathology in
CVCT. Other signs ascites, generalized visceral edema, and diarrhea are possible if
thrombosis occludes caudal vena cava and results in portal hypertension. Right heart
failure and chronic passive congestion of liver may also develop in chronic cases.
DIAGNOSIS OF SUDDEN DEATH SYNDROME
➢Affected animals have appeared completely healthy before death
➢Only one animal is affected in the herd
➢Careful necropsy when sudden death results
➢Necropsy will typically reveal hilar liver abscess with rupture into caudal vena
cava
➢Lungs may show bullous emphysema, pulmonary edema, pulmonary
infarction, and pulmonary arterial thrombosis
DIAGNOSIS OF ACUTE
RESPIRATORY DISTRESS SYNDROME
➢Thoracic radiography, demonstrates focal or multifocal pulmonary infarction
and densities resulting from septic emboli, diffuse pulmonary edema, and
bullous emphysema. Enlargement of thoracic vena cava between cardiac
silhouette and diaphragm may also be detected
➢History and physical examination
➢Sudden onset of respiratory distress in a single cow within a herd
DIAGNOSIS OF CLASSICAL CAUDAL VENA CAVAL
THROMBOSIS WITH EPISTAXIS, HEMOPTYSIS, ANEMIA,
AND CHRONIC BRONCHOPNEUMONIA
➢Thoracic radiography or ultrasonography is helpful in identifying distinct
pulmonary abscesses. Transabdominal ultrasonography of right 8th through
12th ICSs can be useful to identify liver abscesses and allows visualization of
hilus and abdominal caudal vena cava close to hilus
➢Thoracic radiography assists in identifying severity of pulmonary pathology
and may also identify an enlargement of thoracic vena cava close to
diaphragm in cases of CVCT
➢Causative thrombus may be lodged in caudal vena cava and may also
sometimes be visualized ultrasonographically or else its presence inferred by
significant intrahepatic vessel enlargement on ultrasonography alongside an
increase in diameter of perihilar vena cava (normal diameter, 2–5 cm)
➢Endoscopy will help confirm origin of hemorrhage in lower airway and will
allow collection of tracheal wash material for cytology and culture if desired
PROGNOSIS
Prognosis is poor because a large thrombus tends to persist in caudal vena
cava, and constant or intermittent embolic showering is likely to continue.
Treatment of CVCT with classic signs of pneumonia, epistaxis, hemoptysis, and
anemia seldom is worthwhile because of extensive pathology that exists. Few
cattle have survived long term.
When epistaxis has been observed and confirmed to originate from lower
airway, prognosis is extremely guarded.
TREATMENT
Therapy for CVCT causing acute respiratory distress is symptomatic and
includes:
➢Broad-spectrum antibiotics such as oxytetracycline, ceftiofur, or penicillin to
control septic thromboemboli. F. necrophorum and T. pyogenes are the
primary organisms found in these abscesses
➢Furosemide (250–500 mg IM twice daily per adult animal) if pulmonary
edema is present
➢Atropine (2.2 mg/45 kg body weight SC twice daily) as a supportive
bronchodilator and to dry bronchial secretions
➢Aspirin or another NSAID in standard dosages as an anti-inflammatory drug.
Initially, flunixin meglumine may be used (250–500 mg/450 kg body weight)
to counteract possible endotoxemia
CONTROL
Prevention or control of CVCT in cattle involves nutritional changes. Highly
acidic diets that predispose to clinical or subclinical rumenitis and abomasal
ulceration have to be tempered by buffers, prefeeding hay before high
energy grains such as high moisture corn, or most commonly by feeding total
mixed rations. Dairy rations should not be fed to yearling or bred heifers. High
production herds are most at risk for rumenitis and abomasal ulceration
secondary to intensive feeding of high-energy, acidic diets. When more than
an occasional case of CVCT appears in a herd, immediate evaluation of the
herd’s nutritional program is in order. One cow in a herd with CVCT is
unfortunate but a common clinical problem. More than one cow in same herd
with CVCT, however, signals a potential serious economic loss and requires
changes in the feeding program.
THANKS FOR YOUR ATTENTION
