A fatal case of complicated congenital peritoneopericardial diaphragmatic hernia in a Holstein calf

Abstract

Congenital peritoneopericardial diaphragmatic hernia is a rare condition most commonly reported in cats and dogs. A 6-week-old Holstein heifer calf with a congenital peritoneopericardial diaphragmatic hernia complicated by a perforated abomasal ulcer is described. The clinical signs and pathological findings are compared with those reported in other species.

Peritoneopericardial diaphragmatic hernia is a rare condition characterized by direct communication between the abdomen and the pericardial sac via a defect in the diaphragm which allows migration of organs from the abdominal cavity into the pericardial cavity. In humans, this hernia occurs either as a result of abnormal development of the retrosternal septum transversum or, more commonly, diaphragmatic trauma (1). The pericardium is firmly attached to the central tendinous aponeurosis of the diaphragm in humans, thus rendering this area susceptible to traumatic rupture and herniation (2). Pigs, seals, and beavers similarly have a fixed pericardial attachment (2). In contrast, other animals have a ligamentous attachment, the ventral phrenicopericardial ligament in dogs and cats and the caudal sternopericardial ligament in horses and ruminants, rendering them less susceptible to a traumatic etiology (2). Of the two types of attachment, the phrenicopericardial ligament is the more tenuous and, with no fixed contact between pericardium and diaphragm, all peritoneopericardial diaphragmatic hernias in dogs and cats are reported to be congenital (3). Faulty development of, or prenatal injury to, the lateral pleuroperitoneal folds and/or septum transversum may result in peritoneopericardial communication in animals (4,5).

Congenital peritoneopericardial diaphragmatic hernia (CPDH) is the most common congenital anomaly of the pericardium in dogs and cats (3). A prevalence of 0.29% is reported in cats (6). Over representation of this anomaly is reported in Weimaraner dogs and Himalayan and Maine coon cats, suggesting a possible heritable basis in these breeds (3,6,7). Concurrent congenital skeletal and/or cardiac anomalies and umbilical hernias have been reported in association with CPDH in both dogs and cats (6–8). Thus, CPDH can present as either a single congenital anomaly or as part of a syndrome of multiple congenital anomalies.

In contrast to dogs and cats, reports of CPDH in other species are sparse and comprise an alpaca (9), a Standardbred horse (10), and a Holstein calf (11). Multiple congenital anomalies including CPDH were reported in 3 Japanese Black calves (12). Accordingly, there is limited knowledge regarding the clinical presentation, pathological findings, and outcome of CPDH in species other than dogs and cats. In the current report, a CPDH in a 6-week-old Holstein heifer calf complicated by a perforated abomasal ulcer is described.

Case description

On February 2, 2010, a 6-week-old Holstein heifer was presented for necropsy to the Animal Health Centre in Abbotsford, British Columbia, with a history of acute onset of fever and respiratory signs followed by rapid death. Upon opening the carcass, foul, turbid, tan-colored fluid containing bits of ingesta filled the abdominal cavity. Marked enlargement of the pericardial sac within the thorax was observed. Incision of the right wall of the pericardial sac revealed the presence of similar exudate to that observed in the abdomen and the left lobe of the liver resting against the caudal border of the heart. Reflecting the liver, the abomasum with proximal duodenum was found to be wedged between the liver, the heart, and the underlying greater omentum which was adherent to the wall of the pericardial sac. Fibrinous exudate coated the heart, abomasum, omentum, and liver. A 2- to 3-cm diameter ruptured abomasal ulcer was present along the greater curvature of the abomasum immediately adjacent to the apex of the heart. An 18-cm diameter defect in the right ventrolateral diaphragm continuous with the pericardial sac was identified. The edges of the diaphragmatic defect were smooth and fibrous. No other gross abnormalities were noted. Routine bacteriological culture produced a heavy growth of alpha-hemolytic Streptococcus species and non-hemolytic Escherichia coli in the pericardial exudate and a light to moderate growth of both bacteria in the lung, liver, and spleen.

Discussion

The diaphragmatic defect in the calf exhibited smooth fibrous edges continuous with the pericardial sac suggestive of a congenital etiology. This finding is similar to gross observations of the diaphragmatic defect reported in the horse (10), alpaca (9), and Holstein calf (11). A congenital etiology for all peritoneopericardial diaphragmatic hernias has been established in cats and dogs, based on the absence of any fixed point of anatomic contact between the diaphragm and pericardial sac (3). Although the pericardial sac of ruminants is more firmly attached to the sternum than is the case with dogs and cats (2), there is no fixed point of contact with the diaphragm and thus a congenital pathogenesis for the peritoneopericaridal hernia is most likely.

Cats and dogs with CPDH can remain asymptomatic for many years before developing clinical signs which would prompt an owner to present their pet for veterinary advice. Age at time of diagnosis ranges from 6 wk to 10 and 17 y in dogs and cats, respectively (3,4,6). Clinical signs are not specific; however, gastrointestinal and respiratory signs are most common (4). Gastrointestinal signs include vomition and diarrhea (4). Dyspnea, tachypnea, coughing, and/or wheezing are the most common respiratory signs and these predominate in cats (3,7). Dogs more commonly present with gastrointestinal signs, usually vomition (3). The liver, gall bladder, small intestine, and omentum are most frequently herniated with occasional involvement of the stomach, spleen, and colon (3,6,7). Adhesions of abdominal viscera to the pericardial sac are also occasionally observed (3,6). While the liver is the most commonly herniated organ in both cats and dogs, the small intestine is more commonly involved in dogs (3). This may explain why gastrointestinal signs are more often a presenting complaint in dogs (3).

Animals with CPDH may not be symptomatic at the time of diagnosis. In a retrospective study of 66 cats, 60% were detected as a result of presentation for clinical complications arising directly from the hernia and 40% were found incidental to the presenting complaint or on routine physical examination (6). Muffled heart sounds are the most common finding on physical examination in CPDH, reported in about 50% of cats and dogs (3,6). Animals with the most severe clinical signs tend to undergo surgery and prognosis is good for both surgical and conservative treatment in uncomplicated cases (3,6). However, recurrence of clinical signs is common where conservative treatment is elected (6,7).

Less is known about the clinical presentation and outcome of CPDH in large animals. The alpaca was clinically normal until he developed colic at 18 months of age (9). By the time he was transported to a veterinary teaching hospital for examination, the colic had resolved. Clinical examination revealed small body size, normal heart rate and heart sounds, and increased peritoneal fluid with leukocytosis. Conservative treatment for enteritis/peritonitis was instituted and recovery was uneventful. Three months later he was presented for colic and again his heart rate and heart sounds were normal but analysis of blood and imaging studies revealed changes compatible with inflammation and small intestinal obstruction. Surgery was performed for jejunal adhesions and obstruction. Gaseous compartment distension, peritonitis, dyspnea, and muffled heart sounds developed 12 h following surgery and the alpaca died. At necropsy, CPDH involving the liver was found, although this was not considered to be the primary cause of the clinical signs or death.

The Standardbred horse was also reported to be clinically normal until intermittent colic associated with fecal impaction commenced at 18 months of age (10). Increasingly frequent episodes of impaction prompted the owner to present the horse at 3 years of age to a veterinary teaching hospital. Heart sounds were dull and referred over a wider than normal area with a grade 2/5 systolic murmur and fluid sounds in the hemithorax. Radiography revealed diaphragmatic hernia involving the intestine. The horse was taken to surgery where the diaphragmatic flexure of the dorsal colon was found to be impacted and herniated within the pericardial sac via a 30 × 20 cm defect in the right ventral diaphragm continuous with the pericardial cavity. The hernia was reduced and the impaction treated, but the gap was too large to be closed. Nevertheless, the horse recovered without incident and was successfully racing 1 y post surgery.

In contrast to the alpaca and the horse, the 3 Japanese Black calves had CPDH complicated by other, more severe, congenital anomalies (12). Two of the 3 calves died at 1 day of age with ventricular and atrial septal defects, Tetralogy of Fallot, pulmonary stenosis, hypoplastic lungs, vertebral anomalies, and hydranencephaly. The third calf died at 28 days of age with patent ductus arteriosus, hypoplastic lungs, and supernumerary ribs.

The previously reported Holstein calf had been mauled by its dam at birth and reportedly failed to thrive despite normal appetite (11). At 6 weeks of age, the calf developed fever and anorexia. Physical examination by a veterinarian revealed tachypnea, tachycardia, cyanosis, muffled heart sounds on the left side, and increased lung sounds. Diaphragmatic hernia was suspected; however, at surgery the pericardial cavity was found to be continuous with the peritoneal space and contained the liver, abomasum, and small intestine. The defect was repaired but the calf died following surgery.

The Holstein heifer calf described herein was reported by the owners to be clinically normal until the acute onset of clinical signs and rapid death at 6 weeks of age. The horse (10) and many cats and dogs previously reported (3,4,7) were similarly considered to be normal by their owners prior to the onset of clinical signs which lead to detection of CPDH. In contrast, the alpaca was reported to be small for its age (9) and the previously reported Holstein calf was reported to be poor doing (11), both nonspecific longstanding signs which might be associated with CPDH. Stunted growth, poor weight gain, and/or weight loss were presenting complaints by owners reported in 9 cats and 3 dogs, whereas intermittent anorexia was reported in 27 cats and 2 dogs (3,6,7), indicating that, in a subset of animals with CPDH, nonspecific and longstanding clinical signs may be present. Whether an affected animal develops specific and/or nonspecific signs or remains asymptomatic prior to detection is dependent on the extent of the herniation and the organs involved (4).

The Holstein heifer calf described herein exhibited a CPDH complicated by a ruptured abomasal ulcer with secondary peritonitis, pericarditis and sepsis, the presumed cause of the acute onset of her clinical signs and death. Abomasal ulceration is a common, often clinically inapparent, condition in calves (13). Perforation of an ulcer usually presents as sudden death (13). Abomasal ulceration is correlated with stressful circumstances including abomasal displacement (14). Displacement of the abomasum within the pericardial sac was likely a significant contributing factor in the development of the ulcer.

In summary, a 6-week-old Holstein heifer died secondary to complications arising from a CPDH. Herniation of the liver, omentum, abomasum, and proximal duodenum into the pericardial sac was complicated by a perforated abomasal ulcer, marked septic pericarditis/peritonitis and death. CVJ