J . small Anim. Pruct. (1982) 23,483-500.

Idiopathic pericardial haemorrhage in dogs : a review of fourteen cases

C H R I S T I N E G I B B S * , C . J , G A S K E L L T , P . G . G . D A R K E t q : A N D P . R . W o T T o N t Q

Departments of Veterinary Surgery* and Veterinary Medicine?, University of Bristol School of Veterinary Science. Langford House. Langford, Bristol BS 18 7DU.

A B S T R A C T

The clinical and radiological findings in 14 cases of idiopathic pericardial haemorrhage are reported. Seven dogs recovered following treatment by pericardial drainage (six cases) or pericardectomy (one case). Four cases later relapsed of which two were again treated successfully. One dog apparently responded to conservative treatment but died of a relapse one month later. In the remaining six animals, which all died or were destroyed during either investigation or treatment, pericardial haemorrhage was confirmed at post-mortem examination.

I N T R O D U C T I O N

Pericardial effusion in the dog has most often been recognized in association with neoplasia, particularly heart base turnours (Luginbuhl & Detweiler, 1965; Knaur, 1977). Thrall & Goldschmidt (1978) recorded pericardial effusion in two out of six cases of mesothelioma, while Kleine. Zook & Munson (1970) reported that atrial rupture with pericardjal haemorrhage had caused sudden death in seven out of 30 dogs with right atrial haemangiosarcoma. Pericardial haemorrhage may also occur as a result of right atrial splitting in aged dogs with mitral insufficiency (Buchanan & Kelly, 1964). The developnient of pericardial transudates as a consequence of congestive heart failure, hypoproteinaemia and congenital

$ Present address: Small Animal Practice Teaching Unit. Royal (Dick) School of Veterinary

$ Present address: Department of Veterinary Medicine. Royal Veterinary College Field Station. Studies. Summerhall. Edinburgh.

Hawkshead House, Hawkshead Land, North Mymms. Hatfield. Hem.

0022-4510/S2/0900-0~83$02.00 @ 1982 BSAVA

483

484 C H R I S T I N E G I B B S E T A L .

pericardiodiaphragmatic defects is well recognized (Ettinger & Suter, 1970; Bolton, 1975; Knaur, 1977; Detweiler et a!., 1979). Pericarditis of traumatic or infective origin has also been reported (Schwartz et al., 1971 & Thompson, 1971; Straw et al., 1979) and Millman et al. (1979) mention pericardial effusion among the radiological features of canine coccidiomycosis. Marion eC al. (1970) described a case in which a pericardial effusion was apparently related to a fibrotic cyst.

While authors of standard texts on pericardial disease mention that benign sanguineous pericardial effusions may occur occasionally (Ettinger & Suter, 1970; Bolton, 1975; Knaur, 1977; Detweiler et al., 1979), idiopathic pericardial haemorrhage does not appear to be widely recognized as a distinct clinical entity. However, in a discussion of the clinical aspects of canine cardiology, Detweiler (1955) referred to a condition of unknown aetiology characterized by ‘massive sanguineous pericardial effusion’, commenting that aspiration of the accumulated fluid resulted in dramatic alleviation of clinical signs and that the condition might recur. Subsequently, similar cases have been described by Price & Mullen (1966) and Downey & Sumner-Smith (1971) and illustrated in a review of pericardial disease (Harris, 197 1).

The purpose of this paper is to report 14 further cases of idiopathic pericardial haemorrhage referred to the University of Bristol Veterinary School between 1974 and 1980. These represent more than three-quarters of the confirmed cases of pericardial effusion recorded during that time, the remainder being due either to infection or neoplasia.

C L I N I C A L F I N D I N G S

Breed, age and sex distribution together with histories and presenting signs are summarized in Table 1. St Bernards were most commonly affected (five cases) followed by Great Danes (four cases), Golden Retrievers (three cases), an Old English Sheepdog and a Labrador Retriever. Two of the St Bernards were closely related, Case 13 being the sire of Case 6. Ages ranged from 1 to 10 years and the sex incidence was predominantly male (1 1 out of 14 cases).

The duration of signs ranged from four days to three months. Onset was usually insidious and, in four dogs, coincided with an apparently unrelated transient illness (Table 1). A further dog had suffered a severe attack of gastro-enteritis three months before the onset of signs.

Abdominal distension due to ascites was the most consistent presenting sign and occurred in all cases except one. In five dogs, this sign was the first abnormality observed by the owners. Lethargy and decreased exercise tolerance were also common features, usually noted early in the course of the disease. Weight loss became apparent later in six dogs and was one of the earlier presenting signs in one. Twelve dogs showed respiratory distress at the time of presentation and in one, dyspnoea had been observed throughout the entire illness. One or more episodes of collapse were reported in three dogs. In one case (5). referred for investigation of

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486 C H R I S T I N E G I B B S E T A L .

a chronic cough, evidence of pericardial effusion was found incidentally on radiographic examination.

Clinical examination revealed similar features in all cases. Heart rates were uniformly elevated ( 120/min- 170/min at rest) with weakening of the pulse. With the exception of two cases which were normal on auscultation, heart sounds were either mufiled (eight cases) or inaudible (four cases), Electrocardiographic recordings were obtained from 10 dogs and showed reduced voltage with diminished QRS complexes in eight and no abnormality in the other two. Routine haematological and biochemical tests at the time of admission showed no significant variations from normal in any case.

R A D I O G R A P H I C E X A M I N A T I O N

Radiological findings are recorded in Table 2. In all cases plain radiographs showed evidence of cardiomegaly (Figs 1, 2a, 3b & c and 5a & b) and with one exception (Case 9, pleural effusion. In general, the clarity of the cardiac silhouette depended upon the amount of pleural fluid present. In one case (9), the heart itself could not be identified but enlargement was inferred from dorsal elevation of the carina and distal trachea on the lateral recumbent projection and in three further cases (2, 3 and 13), the degree of cardiomegaly could not be assessed until fluid had been removed from the pleural cavity (Fig. 3a, b & c).

In 11 cases, fluoroscopy was carried out in order to determine whether or not

TABLE 2. Radiological signs in 14 dogs with idiopathic haemopericardium

Diagnosis of pericardial Cardiomegaly Pleural effusion Fluoroscopy ‘still heart’ effusion from X-ray signs

1. ++++ + Yes Yes 2. +++ ++ Yes* Yes 3. ++ ++++ Yes* Yes 4. ++++ +++++ Yes* Yes 5. +++ - Yes Yes 6. +++ + Yes Yes 7. + + ++ Yes Yes 8. ++ +++ Suggestive Suspected 9. +++t +++++ Not done Yes

10. +++ + Yes Yes 1 1 . +++ ++ Not available No (C.M.O.) 12. ++++ + Yes Yes 13. ++ ++++ Inconclusive* No (C.M.O.) 14. +++++ + Not done Yes

* Examination performed after removal of fluid from the pleural cavity. t Cardiac silhouette obscured by fluid-enlargement inferred from tracheal elevation. C.M.O. Cardiomyopathy.

I D I O P A T H I C P E R I C A R D I A L H A E M O R R H A G E IN D O G S

FIG. 1. Case 14. Lateral radiograph, taken on admission, showing very gross enlargement of the heart shadow which almost completely fills the chest. The trachea is displaced dorsally to such an extent that it is compressed. The dog died shortly after this radiograph

was taken.

( b) FIG. 2. Case 1. Dorso-ventral radiographs taken-(a) at first admission showing gross enlargement of the heart shadow which is almost globular in shape. A fissure line between the right cardiac and apical lobes indicates a small pleural effusion. (b) three days after aspiration of one litre of blood from the pericardium and diuresis. The cardiac silhouette is now normal and the pleural effusion has subsided.

48 7

488 C H R I S T I N E G I B B S E T A L .

FIG. 3(b)

I D I O P A T H I C P E R I C A R D I A L H A E M O R R H A G E I N D O G S 48 9

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490 C H R I S T I N E G I B B S E T A L

FIG. 3 ( r )

I D I O P A T H I C P E R I C A R D I A L H A E M O R R H A G E I N D O G S 49 1

FIG. 4. Case 12. Lateral radiograph taken 24 hours after aspiration of 850 ml blood from the pericardium. The overall size of the heart shadow is almost normal but the left atrium remains moderately enlarged. This dog developed atrial fibrillation the following

day and died.

normal ventricular contractions could be observed. In nine of these dogs. the cranial and caudal cardiac borders were either immobile or showed only slight ‘shimmering’ movements, thus confirming the presence of pericardial fluid. In one of the remaining cases ( 13), small ventricular contractions synchronous with the peripheral pulse could be seen and this finding contributed to an erroneous diagnosis ‘by exclusion’ of cardiomyopathy, while in the other (Case 8), lack of image contrast due to the presence of pleural fluid prevented accurate observation. All cases were monitored radiographically throughout the period of hospitalization.

FIG. 3. Case 3. (a) Lateral radiograph taken on admission. The heart shadow is obscured by free pleural fluid but the distal trachea is slightly elevated. (b) & (c) Lateral and dorso- ventral radiographs taken after aspiration of 800 ml of fluid from the pleural cavity: cardiomegaly can now be appreciated. (d) Lateral radiograph taken after aspiration of 200 ml blood from the pericardium. The cardiac silhouette is reduced in size but some pleural fluid remains. (e) Lateral radiograph taken at the time of discharge 14 days later. after diuretic treatment, showing a normal cardiac silhouette and complete resolution of

the pleural effusion.

492 C H R I S T I N E G l B B S E T A L

I D I O P A T H I C P E R I C A R D I A L H A E M O R R H A G E I N D O G S 493

T R E A T M E N T

Details of treatment and outcome are summarized in Table 3 . A variety of therapeutic measures had been employed prior to admission and in five dogs, transient remission of signs had been achieved by diuresis.

In all cases, diuretic therapy was instituted immediately following radiographic confirmation of pericardial and/or pleural fluid.

Pericardial aspiration was performed in 10 cases. In four of these, the procedure was preceded by thoracocentesis which yielded blood-stained modified transudates. When possible, the animal remained standing during pericardiocentesis; otherwise it was restrained in sternal recumbency. A left-sided approach was invariably used. After surgical preparation and injection of local anaesthetic into the skin and intercostal muscles between the 6th and 7th ribs at the junction of the middle and lower thirds of the chest wall, a 16 BWG needle catheter (e.g. Vistacan: Portex) was introduced through a small skin incision and directed medially across the pleural space. Some resistance to its passage could usually be appreciated as it penetrated the pericardium. Once a free flow of fluid was established, the needle was withdrawn and drainage continued through the catheter which could be manipulated freely within the pericardial sac. In all cases, the resulting fluid resembled blood but did not clot. On haematological examination of samples from nine dogs, cellular parameters, packed cell volume and haemoglobin concentrations were within, or close to, the normal range for whole blood.

Pericardiocentesis was not attempted in four cases for the following reasons. In two (Cases 11 and 13), pericardial effusion was not convincingly demonstrated radiographically (Fig. 5a), due either to lack of fluoroscopic facilities (Case 11) or inconclusive fluoroscopic findings (Case 13). In both, cardiomyopathy was erroneously diagnosed. One of the remaining two dogs, (Case 14) died before fluoroscopy could be performed and the other (Case 8). which showed only moderate cardiomegaly and equivocal fluoroscopic signs, responded favourably to conservative treatment.

Antibiotic cover was given in all cases in which thoracic puncture had been performed. Two dogs received steroid therapy (Case 8, corticosteroid and Case 10, anabolic steroid). Five cases, in which diuretic therapy was intended to be sustained, were also given potassium chloride (Slow-K, Ciba Ltd.). Three cases (2, 10 and 11) were digitalized and four (2, 10, 11 and 12) which developed atrial fibrillation, received quinidine sulphate.

Pericardectomy using the technique described by Sumner-Smith & Archibald (197 1 ) was performed on one case (5) in which repeated pericardial aspiration had failed to produce a significant reduction in the size of the cardiac silhouette on radiography.

FIG. 5. Case 11. (a) and (b) Lateral and dorso-ventral radiographs taken three days after admission and diuretic treatment showing moderate cardiomegaly and a small pleural effusion. This case was misdiagnosed as cardiomyopathy but pericardial haemorrhage

was found at post-mortem examination four days later.

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O U T C O M E

Eight dogs (Cases 1-8) made a satisfactory clinical recovery from the initial episode of pericardial haemorrhage. In four cases (1, 3, 4 and 6) pericardial aspiration and diuresis resulted in dramatic alleviation of clinical signs. Case 2 developed atrial fibrillation two days after pericardiocentesis but the heart returned rapidly to normal rhythm following administration of quinidine sulphate. In all these animals chest radiographs were normal at the time of discharge between one and two weeks after admission (Figs. 2b and 3e). Case 2 remained in good health for five years when it died of an unrelated disease. Cases 3 and 6 were alive and well three years and one year respectively after treatment. Cases 1 and 4 both suffered a recurrence, five years and nine months respectively, after the initial episode. Both recovered after further similar treatment and were in good health one year and 15 months later.

Surgical recovery of the dog subjected to pericardectomy was complicated by wound infection. On chest radiographs at the time of discharge and at several follow-up examinations, heart size was considerably reduced but never returned to normal. However, the dog remained clinically well until it died of an acute recurrence 15 months later. Case 7 showed marked clinical improvement after aspiration of 70 ml of blood from the pericardium and diuresis but at discharge, two weeks later, there was still radiographic evidence of cardiac enlargement. The clinical signs recurred after five months when the dog died as a result of ventricular laceration during pericardiocentesis. Case 8 made an apparent clinical recovery following conservative treatment with diuretic, antibiotic and corticosteroid. There was marked radiographic improvement, but not complete resolution. The dog was discharged after two weeks but died suddenly one month later. Post mortem examination revealed gross pericardial haemorrhage.

The remaining six dogs either died during treatment or were destroyed because of failure to respond. In all cases, pericardial haemorrhage was confirmed post mortem. Pericardial aspiration had been performed successfully in two cases (10 and 12) but both subsequently developed atrial fibrillation which could not be reversed with quinidine sulphate. In the latter dog, although radiographs taken 24 hours after pericardiocentesis showed marked reduction in heart size, the left atrium remained distinctly enlarged (Fig. 4). In Case 9, repeated attempts to aspirate the pericardial fluid failed to produce more than a small sample of blood and no significant Improvement was achieved with medical treatment. This dog eventually died during induction of general anaesthesia for surgical drainage of the pericardium. Cases 1 1 and 13, misdiagnosed as cardiomyopathy, were destroyed because of failure to respond to medical treatment and Case 14, presented in extremis, died within one hour of admission.

D I S C U S S I O N The disorder exhibited by these 14 dogs is compatible with that described by

Detweiler (1955), Price & Mullen (1966) and Downey & Sumner-Smith (1971).

I D I O P A T H I C P E R I C A R D I A L H A E M O R R H A G E IN D O G S 497

Post-mortem examination of seven of the nine dogs which died or were destroyed revealed no gross lesions to account for the haemorrhage. I n the remaining dogs, the diagnosis of idiopathic haemorrhage was based on the results of pericardial aspiration, together with radiographic evidence of a reduction in size of the cardiac silhouette immediately following this procedure.

The breed distribution of the cases in this series indicates that the condition affects larger dogs and that St Bernards and Great Danes may be particularly susceptible. These observations are supported by other case reports which concern a Labrador Retriever (Price & Mullen, 1966) and a St Bernard (Downey & Sunmer-Smith, 1971). The sex incidence is predominantly male, but the age range in this series (1-10 years) showed wide variation. By contrast, both subjects of previous case reports were less than one year of age (Price & Mullen, 1966 and Downey & Sumner-Smith, 197 1).

The presenting signs, characterized by general debility, ascites and latterly, respiratory difficulty with tachycardia and a weak pulse, were essentially those of gradually developing heart failure. The predominance of right-sided signs can be attributed to the compression effect of accumulated pericardial fluid on the thin- walled right ventricle.

Conditions to be considered in differential diagnosis include other forms of pericardial effusion, haemorrhage from intrapericardial tumours and particularly myocardial failure, due to the so-called idiopathic myopathy of large and giant breeds (Ettinger, 1975).

Radiographic examination made an important contribution to arriving at a provisional diagnosis of pericardial effusion. On plain films, gross generalized cardiomegaly, as shown by marked increase in both cranio-caudal and ventro- dorsal dimensions of the heart with elevation of the carina on the lateral view and a globular cardiac silhouette on the dorso-ventral view, is strongly suggestive of pericardial effusion. These signs, however, are not definitive, since a heart in the late stages of myocardial failure may assume similar dimensions, although the tendency of idiopathic cardiomyopathy to produce mainly left atrial enlargement is a useful differential feature. For diagnostic confirmation, fluoroscopy is essential and is particularly valuable in those cases in which cardiomegaly is not gross.

The presence of fluid within the pericardium obliterates, or attenuates markedly the normal movements which take place during atrial and ventricular contraction. The cardiac silhouette remains immobile or shows only slight shimmering movements, except at the base, where pulsations of the aortic arch cause inter- mittent indentation of the atria, synchronous with ventricular contractions. In animals with marked respiratory distress, some difficulty may be encountered in distinguishing between cardiac and respiratory movements. However, it was found that the absence of normal ventricular contractions could be observed most reliably in the region of the caudal border of the heart, the movement of which could be related to the respiratory excursions of the diaphragm. Since large pleural effusions seriously hinder fluoroscopic observation of the heart, it may be necessary to aspirate fluid from the thorax prior to examination.

49 8 C H R I S T I N E G I B B S ET A L .

In the absence of fluoroscopic facilities, electrocardiographic examination must play an important part in differentiating pericardial effusion from primary myocardial disease. While reduction in voltage with decreased amplitude of the QRS complexes was a frequent finding in this series, no case, at the time of presentation, showed evidence of atrial fibrillation or ectopic ventricular con- tractions which characterize cardiomyopathy .

The sanguineous nature of the pericardial aspirate excludes transudation and empyema, but further investigations may be required in order to rule out neoplasia as the underlying cause of haemorrhage. Cytological examination of the aspirate or radiography following the introduction of air into the pericardium would be helpful in this respect, but in this series, the absence of neoplasia was either con- firmed at surgery or post mortem or inferred by the failure of haemorrhage rapidly to recur.

The outcome of the cases in this series suggests that recovery is dependent upon successful aspiration of the pericardial contents. That the condition may recur (Detweiler, 1955) after a prolonged period of clinical normality is confirmed by Cases 1 and 4, both of which were re-admitted with identical signs at respective intervals of five years and nine months after the initial episode and were re-treated successfully, and Case 5 which died of an acute recurrence one year after peri- cardectomy. It may be significant that in the two dogs which suffered an earlier recurrence (Cases 7 and 81, pericardial aspiration either had not been attempted or had yielded only a small volume. In both these animals, chest radiographs made at the time of discharge showed residual cardiomegaly and persisting pleural effusion.

The risk of ventricular damage during pericardiocentesis is illustrated by Case 7, in which post mortem examination revealed a 5 cm tear in the left ventricle. However, with further experience it has been found that this complication should be avoidable if the needle is withdrawn immediately it contacts the moving ventricle. The risk is also reduced by the use of a catheter.

Atrial fibrillation appears to be a serious complication. It occurred two days after pericardiocentesis in three dogs (Cases 2, 10 and 12) and was presumed to be the cause of death of the latter two. Case 2, however, made a complete recovery. All these dogs were treated with quinidine sulphate. Cases 2 and 10 had also received digoxin. One of the two cases misdiagnosed as cardiomyopathy also developed atrial fibrillation following digitalization and it may be significant that this complication has not been encountered since the use of digoxin in the treatment regimen has been discontinued. The reason for its occurrence in Case 12, however, would then remain unexplained.

Surgical drainage of the pericardium was not required in the majority of cases in this series, but is indicated if immediate recurrence or continuation of haemorrhage is demonstrated by radiographic evidence of persisting cardiac enlargement following pericardiocentesis (Case 5 ) or failure to obtain adequate drainage (Case 7). Sumner-Smith & Archibald (197 1) described two techniques: pericardial

I D I O P A T H I C P E R I C A R D I A L H A E M O R R H A G E I N D O G S 499

fenestration, which consists of creating a ‘window’ in the pericardium to allow drainage of its contents into the pleural cavity from which they can then be more readily absorbed or aspirated, and pericardectomy, when total excision is performed. They suggest that the latter technique should be reserved for cases in which there is gross thickening of the pericardium and epicardial roughening.

The pathogenesis of this disorder remains unexplained. In the seven dogs examined post mortem, the only relevant reported pathological changes were the presence of free and clotted blood within the pericardial sac and fibrous thickening of the epicardium and pericardium, interpreted as a secondary response to the presence of effusion. From the insidious onset of clinical signs and the degree of pericardial distension which can be attained without inducing fatal cardiac tamponade, it can be inferred that bleeding must occur slowly or intermittently over a considerable period of time. It is possible, however, that the disease may also result in severe haemorrhage and sudden death; such a rapid course was exhibited during recurrence by Cases 5 and 7. In normal circumstances, these acute cases would be unlikely to reach a referral clinic. The fact that a number of dogs made a complete recovery indicates that haemorrhage may also cease spontaneously. The incidence of recurrence, however, suggests that individual animals may have a particular susceptibility to the condition.

A C K N O W L E D G E M E N T S

We are indebted to Miss R. J. Robins for permission to include Case 3, and to colleagues in the Department of Pathology, University of Bristol for pathological reports. The photographs were prepared by Mr J. Conibear and the script was typed by Mrs V. Beswetherick and Mrs C. Francis.

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