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Clinicopathological and ultrasonographic findings in 40 water buffaloes ( Bubalus bubalis ) with traumatic pericarditis T. Mohamed Veterinary Record 2010 167: 819-824
doi: 10.1136/vr.c3113
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Papers
Papers Clinicopathological and ultrasonographic findings in 40 water buffaloes (Bubalus bubalis) with traumatic pericarditis T. Mohamed Forty buffaloes with traumatic pericarditis were examined to characterise the ultrasonographic findings in buffaloes with traumatic pericarditis, determine the extent of the lesions and assess the prognosis. The most noticeable clinical presentations were presternal oedema (73 per cent) and jugular and mammary vein distension (88 per cent). Laboratory findings included neutrophilic leucocytosis, elevated total protein concentration, hypoalbuminaemia, hypergammaglobulinaemia and increased concentration of free fatty acids. Ultrasonographically, fluid in the pericardium appeared as either mild or massive anechoic accumulations containing fibrin threads or were imaged as homogenous, echogenic pericardial effusions. Moderate to severe corrugation of the reticular wall was observed. Deposits of fibrinous tissue interspersed with fluid pockets were seen between the reticulum, dorsal ruminal sac and diaphragm. Perireticular and mediastinal abscesses were imaged and appeared as echogenic lines with anechoic, echogenic, homogenous or heterogeneous contents. Additional ultrasonographic findings included hepatomegaly, dilation of the caudal vena cava, hepatic and portal veins, ascites, echogenic pleural effusions and vegetations of the tricuspid, mitral and pulmonary valves. The ultrasonographic findings were confirmed at postmortem examination. Traumatic reticuloperitonitis and its sequelae are well-recognised conditions in bovids (Ward and Ducharme 1994, Braun 2009a, b). The condition is usually caused by long, thin, sharp foreign bodies (wire, needles, nails) that penetrate the reticulum, peritoneum, diaphragm and pericardial sac, eventually leading to traumatic peri carditis. This leads to inflammation of the pericardium, with accumulation of serous or fibrinous inflammatory products (Gründer 2002). Pericarditis attributable to haematogenous spread of infectious diseases (such as colibacillosis, pasteurellosis, salmonellosis and anaerobic infections) is much less common and is usually masked by signs of septicaemia (Gründer 2002). Idiopathic pericarditis, which is seen in human beings, dogs and horses, is rare in cattle (Jesty and others 2005). The pathology associated with these conditions includes proliferative inflammatory adhesions, tissue hyperplasia and sepsis (Herzog and others 2004). Traumatic pericarditis is extremely common in developing countries, possibly due to unregulated small-scale farming and unsatisfactory standards of animal management and feeding (Misk and others 1984). Pregnancy and parturition may aggravate the condition in cattle (Peek and McGuirk 2007). The water buffalo (Bubalus bubalis) can compete very successfully with and even surpasses the cattle genus Bos in its ability to adapt to hot climates and swampy land (Wilson 1998); therefore, water buffaloes have special importance in milk and meat production in the
Veterinary Record (2010) 167, 819-824 T. Mohamed, DVM, MS, PhD, Department of Animal Medicine, Faculty of Veterinary Medicine, Zagazig University, PO Box 44579, Zagazig, Egypt
doi: 10.1136/vr.c3113
E-mail for correspondence:
[email protected] Provenance: not commissioned; externally peer reviewed
Nile River valley in Egypt (GOVS 2005). The risk of traumatic reticuloperitonitis and its sequelae is considerably higher in buffaloes than in cattle (Misk and Semieka 2001). Ultrasonography is the method of choice for imaging and characterising pericardial effusion (Buczinski 2009). The ultrasonographic appearance of traumatic pericarditis in cattle has been described in a few case reports (Moeller 1997, Schweizer and others 2003) and in a study of 22 cows (Braun and others 2008). There are no reports describing the ultrasonographic findings in water buffaloes with traumatic pericarditis. The present study was, therefore, designed to characterise the ultrasonographic findings in water buffaloes affected with traumatic pericarditis, determine the extent of the lesions and assess the prognosis. The results were compared with the findings determined following physical and postmortem examinations.
Materials and methods
Animals, history, clinical, laboratory and postmortem examinations
Forty buffaloes were examined. Ultrasonographic examinations were carried out at the veterinary teaching hospital of Zagazig University, Egypt, between 2004 and 2007. The animals were aged seven months to 10 years and weighed 260 to 670 kg (mean [sd] 450 [140] kg). These buffaloes were referred for examination because of anorexia (n=34) and presternal oedema (n=29). The animals had been ill for three to 30 days before admission; the duration of the clinical signs was unknown in six animals. All animals underwent a thorough clinical examination as described previously (Rosenberger 1990, Radostits 2000), which included observations of the general behaviour and condition; auscultation of the heart, lungs, rumen and intestine; measurement of heart rate, respiratory rate and rectal temperature; swinging auscultation; percussion auscultation of both sides of the abdomen; and rectal examination. MT examined all the animals. A confirmatory diagnosis was made on postmortem November 20, 2010 | Veterinary Record
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Papers
FIG 1: Clinical presentation in a buffalo affected with traumatic pericarditis. Presternal oedema and distension of the jugular vein (arrow) are evident
examination of 23 cases. For unknown reasons, the owners of the remaining buffaloes did not notify the author at the time of their slaughter. Therefore, in these latter cases, inclusion in this study was made strictly on the basis of the following criteria: physical findings (presternal oedema, pain tests and distension of the jugular and mammary vein) and cardiac abnormalities (muffled heart sounds, non-detectable murmurs), and ultrasonography (corrugated reticular wall, echogenic deposits between the reticulum and diaphragm, and fibrinous or suppurative pericarditis). Other causes that may lead to signs of congestive heart failure, such as pleuritis and hypoprotein aemia, were excluded by thoracic ultrasonography and serum chemistry profiling, respectively. Two blood samples were collected by puncture of the jugular vein, one into EDTA, and the other without an anticoagulant. A complete blood count (haematocrit, haemoglobin, total and differential leucocytes) was carried out on 18 blood samples. After centrifugation of the second blood sample, 18 serum samples were collected and then frozen for later clinical chemistry analysis. Commercial kits were used to determine the serum concentrations of total protein, albumin, calcium, glucose, free fatty acids (FFA), urea nitrogen, creatinine, sodium, potassium and chloride. The serum activities of aspartate aminotransferase and γ-glutamyl transferase were also measured. Serum protein fractions were determined by electrophoresis. Control values were obtained by measuring the haematological and biochemical parameters in 15 apparently healthy buffaloes with a mean (sd) age of 5.7 (2.7) years.
Ultrasonographic examination and aspiration technique
Ultrasonographic examination was carried out while the animals were standing, using 3.5 and 5.0 MHz sector transducers (240 Parus; Pie Medical). In preparation for ultrasonography, the third to 11th intercostal spaces and the entire abdomen were clipped, shaved and swabbed with alcohol to remove excess oil, and coupling gel was applied. Animals were examined on both sides of the thorax, according to standardised examination techniques (Braun and others 1996, Babkine and Blond 2009). Examination of each lung area was performed with the transducer held parallel to the ribs, from the third to the 11th intercostal space. Each thoracic sonogram was evaluated according to appearance of the parietal and visceral pleura, as well as lung parenchyma; fluid in the pleural space; differentiation of the parietal and visceral pleura; normal, well-ventilated lungs (pleural reflective band and reverberation artefacts); comet tail artefacts; and consolidation and echo patterns – degree of echo density. Echocardiographic examinations were made while the animals were standing, by the methods described previously (Braun and others 2001, Mohamed and others 2004b, Mohamed and Oikawa 2007, Buczinski 2009). The third, fourth and fifth intercostal spaces in the cardiac region were examined ultrasonographically on the right and then on the left side of the thorax. The thoracic limbs were moved Veterinary Record | November 20, 2010
cranially to facilitate better contact between the probe and the intercostal space. In the cardiac area, the heart and major blood vessels and the mediastinal region were imaged. The tricuspid, mitral, pulmonary and aortic valves were also scanned. Ultrasonographic examination of the jugular and milk veins was carried out using an 8.0 MHz linear transducer (240 Parus; Pie Medical). Abdominal ultrasonography was carried out as described previously (Mohamed and Oikawa 2007, Braun 2009b). The peritoneum, rumen, reticulum, omasum, abomasum, spleen, small and large intestines, liver, pancreas and right kidney were examined. Pericardiocentesis was planned to be carried out; however, before the procedure, the author informed the owners about the few possible complications. As a result, all refused pericardiocentesis of their animals, but 11 accepted aspiration of perireticular and thoracic abscesses under ultrasound guidance. After sterilisation by a standard surgical disinfection technique, the area was infiltrated with 10 ml 2 per cent procaine hydrochloride. Ten minutes later, a small incision was made with the point of a scalpel blade, immediately adjacent to the transducer, through the skin, in either the abdominal or thoracic wall. A 14 G x 170 mm spinal needle (Kurita) was advanced through the skin and guided ultrasonographically towards the abscess and, with a slight thrust, was pushed through the lesion. The end of the needle within the abscess was usually visible in the ultrasonograms. The lesion was punctured percutaneously where it was best visualised ultrasonographically. The stylet was then removed and 5 to 10 ml of the contents was aspirated for macroscopic and microscopic examination.
Statistical analysis
Data of the haematological and biochemical parameters were analysed in the diseased and control buffaloes using one-way analysis of variance.
Results
Clinical, haematological and biochemical findings
Thirty-nine (97.5 per cent) of the buffaloes examined in this study were females; 34 (85 per cent) were pregnant, of which 12 (30 per cent) were in the first trimester of pregnancy, five (12.5 per cent) were in the second trimester; and 17 (42.5 per cent) were in the third trimester. Five animals (12.5 per cent) were not pregnant, and one (2.5 per cent) was male. Clinical findings and history in the 40 buffaloes affected with traumatic pericarditis are summarised in Table 1; the most noticeable clinical presentations were non-inflammatory presternal oedema (73 per cent) and jugular and mammary vein distension and pulsation (88 per cent) (Fig 1). The buffaloes had not responded to previous conventional therapy that included antibiotic injection and oral administration of magnets, laxatives, antacids and ruminotonics. Abnormal heart sounds were evident in 63 per cent of the buffaloes. Various pain tests, such as the back grip test, pole test and pain percussion on the xiphoid region, were positive only in 10 per cent of the buffaloes. Complete blood count findings included neutrophilic leucocytosis in 16 animals (88.8 per cent) (P>0.001). Abnormalities identified from the chemistry profile included elevated total protein concentration in 15 buffaloes (83.3 per cent) (P>0.05), hypoalbuminaemia in 11 buffaloes (61 per cent) (P>0.05), hypergammaglobulinaemia in 14 buffaloes (77.7 per cent) (P>0.001) and elevated concentration of FFA in 16 buffaloes (88.8 per cent) (P>0.001). Compared with the controls, other measured serum values did not differ significantly (Table 2).
Ultrasonographic findings
Ultrasonographic findings in the 40 buffaloes with traumatic pericarditis are summarised in Table 3. Ultrasonographic imaging of the presternal oedema revealed excessive accumulation of anechoic fluid separated with echogenic septa. The distended and pulsating jugular vein was round in shape when scanned; however, the distended and pulsating milk vein was oval. Pericardial effusions were imaged in 93 per cent of the examined buffaloes, where fluids in the pericardium appeared as either mild or massive anechoic accumulations (Fig 2a), contained fibrin threads (fibrinous pericarditis) (Fig 2b) or were imaged as homogenous echogenic pericardial effusions (Fig 2c).
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Papers TABLE 1: History and clinical findings in 40 buffaloes with traumatic pericarditis Parameter Cardiovascular-related findings Jugular and mammary vein distension and pulsation Presternal oedema Muffled heart sounds Splashing heart sounds Other findings Anorexia Recurrent or chronic tympany Decreased milk production Constipation Systemic reactions* Ruminal atony Dyspnoea Depression and recumbency Pain tests Diarrhoea
Number (%) of buffaloes manifesting clinical signs 35 (87.5) 29 (72.5) 18 (45) 7 (17.5) 34 (85) 33 (82.5) 30 (75) 12 (30) 9 (22.5) 8 (20) 5 (12.5) 5 (12.5) 4 (10) 4 (10)
* Include moderate to severe rise in rectal temperature (39.0 to 41.5ºC), respiratory rate (40 to 80 breaths/minute) and pulse rate (80 to 120 bpm)
TABLE 2: Mean (sd) haematological and biochemical findings in 18 buffaloes with traumatic pericarditis and 15 control buffaloes Parameter Haematocrit (%) Haemoglobin (g/l) Leukocyte count (x 109 cells/l) Neutrophils (x 109 cells/l) Lymphocytes (x 109 cells/l) Total protein (g/l) Albumin (g/l) α-globulin (g/l) β-globulin (g/l) γ−globulin (g/l) Albumin:globulin ratio Glucose (mmol/l) Calcium (mmol/l) Aspartate aminotransferase (U/l) γ-glutamyl transferase (U/l) Free fatty acids (mmol/l) Sodium (mmol/l) Potassium (mmol/l) Chloride (mmol/l) Urea nitrogen (mmol/l) Creatinine (µmol/l)
Affected
Controls
32 (8) 120 (30) 18.72 (6.40)** 11.98 (3.37)*** 5.24 (2.25) 86 (8)* 19 (5)* 11 (2) 11 (7) 45 (14)*** 0.3 (0.1)** 3.6 (1.1) 2.0 (0.6) 65 (10) 33 (18) 1.3 (0.5)*** 136 (7) 4.3 (1.5) 100 (5) 11 (13) 97 (62)
35 (3) 122 (15) 7.46 (1.22) 3.37 (0.65) 4.82 (1.84) 69 (12) 32 (5) 9.5 (2.8) 8 (3) 20 (5) 0.85 (0.2) 2.9 (0.4) 2.7 (0.5) 57 (22) 25 (6) 0.13 (0.04) 141 (8) 4.8 (0.7) 102 (5) 9 (3) 84 (0.21)
* P
