Clinical evaluation and surgical intervention for diaphragmatic eventration mimicking peritoneopericardial hernia in a cat

Abstract

A 2-year-old spayed female British Shorthair cat presented with an increased frequency and duration of cough since infant period. Based on radiographic, ultrasonographic, and computed tomography findings, peritoneopericardial diaphragmatic hernia was considered so that repair surgery was planned. During celiotomy, lax diaphragm was identified instead of defect. Transabdominal diaphragmatic plication was performed to resolve lax diaphragm and to prevent recurrence by overlapping relatively normal part of diaphragm. Diagnosed with diaphragmatic eventration postoperatively, the cat showed improvement in clinical signs and imaging results. Transabdominal diaphragmatic plication is a suitable treatment; the patient maintained normally during a 14-month follow-up period.

INTRODUCTION

Peritoneopericardial diaphragmatic hernias (PPDH) are hernias in which communication occurs between the pericardial and pleuroperitoneal membranes. PPDH can occur congenitally or traumatically [1]. In contrast to PPDH, diaphragmatic eventration (DE) is uncommon in human medicine and has been also rarely reported in veterinary medicine [2,3,4]. Despite its unclear etiology, DE can result from a nerve injury or congenital developmental deformity of the central tendon or diaphragmatic muscle [2,5,6,7]. In humans, DE can be treated surgically with diaphragmatic plication [2]. There are a few reports on surgically treated DE in veterinary medicine, but there are no reports on surgical intervention with long-term clinical evaluation in feline patients [4]. This is a rare report of DE mimicking PPDH and the first report of close clinical evaluation including echocardiographic and Computed tomography (CT) evaluation and long-term follow-up including blood examination and radiographic and ultrasonographic evaluation of surgically treated DE in a cat.

CASE PRESENTATION

A 2-year-old spayed female British Shorthair cat, weighing 3.7 kg, was referred with a history of coughing. Coughing has been present since infant period and has become more severe recently.

Physical examination revealed muffled heart sounds on the right side, along with an increased respiratory rate of 51 rpm. Blood test results were within normal range, except high aspartate aminotransferase and lactate levels. In addition to an enlarged cardiac silhouette and a connection between the silhouette and diaphragm on radiographs, a small liver volume was observed (Fig. 1A and B). Ultrasonography revealed that displaced liver and gallbladder is adjacent to heart (Fig. 1C). The displaced liver is more hypoechoic than the abdominal liver. Echocardiography revealed pericardial effusion, a dilated right atrium, and tricuspid valve regurgitation (Fig. 1D and E). CT revealed a displaced gallbladder and displacement of the hepatic lobes. Based on these results, PPDH was considered.

Fig. 1. Lateral and ventrodorsal radiographic view of the thoracic cavity (A, B) and ultrasonographic evaluation of displaced abdominal contents and heart (C-E). Enlarged cardiac silhouette that is not separated from the diaphragm and cranial deviation of gastric axis is present due to reduced liver size (dotted line). On the ultrasonographic evaluation, large amount of pericardial effusion (asterisk) is observed around the heart (thin arrow). Displaced liver (arrowhead) and gallbladder (thick arrow) are also identified. Dilated right atrium and tricuspid valve regurgitation are detected (dotted arrow).

Surgical intervention to reduce the displaced organs and repair the defect of diaphragm was initiated to prevent further damage to the gallbladder and liver, and interference with pulmonary function, and to resolve respiratory symptoms and pericardial effusion. A ventral midline incision was made for laparotomy and displaced abdominal contents were observed (Fig. 2A). The displaced contents were then retracted into the abdominal cavity. During dissection of the adhesion between the liver and diaphragm, the diaphragm adjacent to the pericardium became perforated, causing leakage of pericardial effusion. Discoloration of the displaced liver section and a tortuous common bile duct were identified. No diaphragmatic defects were observed after dissection; instead, the central tendon was abnormally loosened (Fig. 2B). Displacement of the abdominal contents was suspected owing to the lax tendon. As the central tendon appeared normal to the left and right sides of the abnormal lax section, diaphragmatic plication was performed to resolve lax part and prevent recurrence of displaced abdominal contents (Fig. 2C). A thoracic tube was placed through the diaphragmatic perforation, and the fluid and air in the pericardium were removed using a syringe. The tube was gradually retracted, and the perforation was closed simultaneously using a purse-string suture. The abdominal wall, subcutaneous tissues, and skin were closed.

Fig. 2. After celiotomy, the herniated organs (arrow) are identified (A). The herniated liver and gallbladder are retracted to the abdominal cavity using stay sutures. A thin and lax central diaphragm (asterisk) was confirmed instead of a diaphragmatic defect and an iatrogenic perforation (thin arrow) was made during dissection of adhesion of the liver (thick arrow) and gallbladder (arrowhead) to the diaphragm (B). To prevent further eventration, mattress sutures are used on each side of the central tendon (C). The mattress suture pattern was used by passing the suture needle from right to left through the abnormal section, then again from left to right through the abnormal section, and tying off the ends. Two additional sutures with the same pattern were made ventral to the first suture site and cranioventral to the liver. Radiographic evaluation of the thoracic cavity was performed immediately after surgery (D). The cardiac silhouette is distinctly separated from the diaphragm. On day 26, radiography revealed cranial deviation of the diaphragm (E). Although the diaphragm is deviated more cranially from day 138 onward, similar deviation is maintained during the 14-month follow-up (F).

The patient recovered uneventfully after anesthesia. Radiography revealed that the diaphragmatic protrusion disappeared immediately after surgery (Fig. 2D). Two days after surgery, the patient was discharged. Improved heart sounds and respiratory signs were also observed 12 days after surgery; however, thoracic radiographs revealed a mild protrusion of the diaphragm (Fig. 2E). On day 138, coughing became less frequent. Thirteen months postoperatively, the pericardial effusion and pulmonary hypertension disappeared, and the severity of tricuspid valve regurgitation decreased, without evidence of right-sided heart failure on echocardiography. No changes were observed in the echotexture of the liver, and the gallbladder was in a normal position. Blood test results were normal. At the last follow-up, 14 months after surgery, the protrusion of diaphragm was still observed (Fig. 2F). However, the protrusion is much milder than preoperative evaluation and the patient survived with normal blood test results and showed no clinical signs.

DISCUSSION

The present case represents a case of DE that mimicked PPDH. Similar cases have rarely been reported in humans [7,8,9]. A congenital eventration is called a “true DE” [2,6]. True DE has a relatively low incidence of histological changes, including fibroelastic changes and lack of muscle fibers in the eventrated portion, while acquired DE has a relatively high incidence of normal muscle fibers [2]. Histological examination was not requested in this case; however, a true DE was tentatively diagnosed based on clinical signs, history, and clinical presentation. First, this patient was young, with no signs of traumatic events. Second, coughing was observed during infancy. Lastly, no evident defects were detected, and the lax and thin parts of the central tendon were found grossly during surgery.

Elevation of the diaphragm on radiographic images is remarkable for DE but cannot differentiate it from a diaphragmatic hernia [3,10]. Histopathological evaluation provides a definitive diagnosis, and ultrasonography and CT may assist in diagnosis in humans [2,3,10]. Although accurate differentiation is challenging due to the limited reports and difficulty detecting the lax diaphragm on CT images in veterinary patients, we found that some findings on CT in this case differed from the typical findings of PPDH, despite the similarity in radiographic findings. In this case, the protruding abdominal contents had smooth margin, and the shape of the margin was similar to that of the diaphragm. In addition, the suspected diaphragmatic defect portion is wider than the cranial part of the displaced organs, which are surrounded by a thin diaphragm and gradually protrude into the pericardial sac (Fig. 3A). In the case of PPDH, there is no membrane to prevent the herniation of abdominal contents, the margin appears irregular, and a large volume of abdominal contents, such as the liver, passes through a narrow defect into the pericardial sac; the volume returns to normal, resulting in a narrow defect with a large volume of abdominal contents (Fig. 3B). This feature might help differentiate between the two diaphragmatic disorders; however, more cases and further studies are required.

Fig. 3. CT images of this DE case (A) and a typical case of PPDH (B) to compare to this case. The radiographic findings including connection between cardiac silhouette and diaphragm and inapparent liver are similar to that of DE and CT findings revealed the herniated gallbladder and liver to the pericardial cavity (red asterisk). Shape of herniated organs in DE case (blue arrow) is smoother compared to PPDH (yellow arrow) and a base which is presumed to be diaphragmatic defect is wider compared to displaced organs in DE case (blue dotted line). A base in PPDH case is narrower compared to herniated orgeans (yellow dotted line).

CT, computed tomography; DE, diaphragmatic eventration; PPDH, peritoneopericardial diaphragmatic hernia.

Herniation of the gallbladder can cause torsion or rupture of the gallbladder and biliary obstruction [11,12], which is a medical emergency. In the present case, a tortuous common bile duct was confirmed. Dilation of the right atrium with regurgitation and pericardial effusion were also observed on preoperative echocardiography. After surgery, most findings improved. As the suspected pulmonary hypertension was no longer detectable, we attributed this improvement to the removal of the compressive lung lesion. This suggests that not only the severity of the clinical signs, but also the preoperative evaluation of the displaced contents and echocardiography can help decide the surgical intervention, and further complications can be prevented through surgical repair.

In humans, diaphragmatic plication for symptomatic DE can be performed through either the thoracic or abdominal cavity using open transthoracic, thoracoscopic, open transabdominal, or laparoscopic plication [2]. Open transabdominal plication is an alternative to the transthoracic technique, but its outcome data are insufficient in human and veterinary medicine [2,13]. The transabdominal technique has advantages, including access to both sides of the diaphragm, no requirement for selective ventilation, and a less morbid incision; however, accessing the posterior portion of the diaphragm is challenging [2]. In this case, a celiotomy was performed because the lesion was initially considered a result of PPDH, which is typically approached by celiotomy. Diaphragmatic plication using a celiotomy may be advantageous because an additional incision is not required although DE is misdiagnosed as PPDH. Eventration was confirmed on the ventral side; therefore, challenges associated with the transabdominal technique were not addressed when treating case of DE mimicking PPDH.

Although the clinical signs and blood, radiographic, and ultrasonographic results improved, recurrent protrusion was detected on radiographs. However, the severity of the protrusion was mild compared to that on preoperative radiographs; this mild protrusion was maintained from day 138, and only a small part of the liver continued to protrude. Thus, according to the owner’s opinion, conservative management with periodic monitoring was selected to evaluate the severity of the protrusion and clinical signs. In humans, a study reviewing 109 cases revealed that the recurrence rate after surgical intervention for true DE was 8.3% [14]. Repair of DE by mesh is known in human medicine, and the mesh can be implanted to maintain the tone of the diaphragm when the overall diaphragm is too lax to maintain tone. It could be also used for revision surgery for recurrent DE, as in our case [2,15]. Secondary surgery with mesh would be performed if clinical signs became severe, gallbladder displacement recurred, protrusion became severe, or other remarkable findings were detected.

This report presents a detailed clinical evaluation of feline DE using various diagnostic imaging modalities, informed procedures, and good long-term outcomes after diaphragmatic plication. DE should be considered when diagnostic imaging findings are suggestive of PPDH in cats. CT may be helpful in differentiating DE from PPDH, and transabdominal diaphragmatic plication is a successful surgical option.