Traumatic Pericarditis
Traumatic Pericarditis is the inflammation of the pericardium or pericardial sac by a sharp foreign body, and the majority of the time it originates from the reticulum, subsequently leads to the development of toxaemia and signs of congestive heart failure (CHF).
Mostly, It is a sequallae of Traumatic Reticulo Peritonitis (TRP).
Clinically, it is manifested by fever, initial tachycardia followed by muffled heart sounds, jugular pulsation, and chording of the jugular vein. A tendency to develop oedema at various places is observed. The majority of the time, it is brisket, but even anasarca, ascitis, and hydrothorax can also be seen.
Etiology
A sharp foreign body originating through the reticulum (as a sequallae of TRP) is the main cause. The incidence is more common in the last trimester of pregnancy or immediately after parturition due to the constant pressure on the reticulum that causes piercing of the FB.
Pathogenesis
Penetrating foreign body causes inflammation of the pericardial sac. The introduction of microorganisms sets up the infection. Initially, there is a net increase in pericardial fluid, but later it becomes thick. Adhesions formed between the pericardial fluid surfaces cause constructive pericarditis, which leads to decreased vital space for the systole and diastole of the heart. Profound toxaemia due to infection and pressure on the heart are responsible for the majority of the clinical signs.
Limited vital space in the heart leads to incomplete filling and retention of blood in the venous circuit, which is manifested by signs of CHF. Examples are Jugular pulsation, complete anorexia, etc.
Clinical findings
Profound depression, complete anorexia, persistent fever, and rapid weight loss are commonly observed. Initially, there is tachycardia and an increased respiratory rate (40–50/min), but as the case advances increased pericardial adhesions make heart sounds less audible, which are called muffled sounds. Sometimes a fluid splashing sound is audible during auscultation.
Pericardial frictional sound is very evident on auscultation. Initially, there is jugular pulsation, which, over time, becomes engorged, leading to the chording of the jugular vein.
There is a tendency to develop oedema due to passive venous congestion. Oedema is severe at the brisket, extending to the ventral abdomen.
In a few cases, there could be the development of ascitis, clinically ascertained by fluid thrill. Other organ inefficiencies are clinically indicated by alternate diarrhoea and constipation, complete anorexia, palpable enlargement of the liver beyond the 8th coastal arch, and evidence of proteinuria indicating renal insufficiency.
Diagnosis
- Based on the History: The animal may be pregnant or recently parturated.
- Earlier signs like: Recumbancy, tympani, kyphosis, and a winged elbow are suggestive.
- Based on the clinical signs: evidence of pain near xiphoid, jugular pulsation, persistant fever, initially tachycardia followed by muffling, prolonged toxaemia, and brisket oedema.
- Lab investigation: It is done at 4–5th intercoastal space with a special needle of 18 gauge and 10 cm length. Fluid is watery in the initial stage of pericarditis and changes to thick, pasty, and smelling in the later stage.
- Radiography: Radiography can show a piercing foreign body if it is a radiopaque.
Differential diagnosis
Bovine Leukaemia like EBL, Bovine Lymphosarcoma: HF, and their crosses are more succeptible. The incidence is more common in Deoni cattle. The cardiac form of EBL almost resembles TP. Here also low HR and brisket oedema were noticed. But laboratory investigation indicates a very high leukocyte count (>30,000/µl) along with lymphocytosis. Instead of neutrophilia, immature lymphoblasts are prominent in peripheral smears and lymph node biopsy.
Treatment
There is no treatment for traumatic pericarditis that can successfully recover the animal from the condition. but prevention and control can be done.