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Home , Acute pericarditis, Pericardial effusion, Pericardial friction rub, Pericarditis, Sinus tachycardia, Tachycardia

Postgrad Med J: first published as 10.1136/pgmj.43.502.534 on 1 August 1967. Downloaded from Postgrad. med. J. (August 1967) 43, 534-538.

CURRENT SURVEY

Acute non-specific R. G. GOLD * M.B., B.S., M.RA.C.P., M.R.C.P. Senior Registrar, Cardiac Department, Brompton Hospital, London, S.W.3

Incidence neck, to either flank and frequently through to the Acute non-specific pericarditis (acute benign back. Occasionally is experienced on swallow- pericarditis; acute idiopathic pericarditis) has been ing (McGuire et al., 1954) and this was the pre- recognized for over 100 years (Christian, 1951). In senting symptom in one of our own patients. Mild 1942 Barnes & Burchell described fourteen cases attacks of premonitory may occur up to of the condition and since then several series of 4 weeks before the main onset of symptoms cases have been published (Krook, 1954; Scherl, (Martin, 1966). is very common, and is 1956; Swan, 1960; Martin, 1966; Logue & often severe and accompanied by listlessness and Wendkos, 1948). depression. The latter symptom is especially com- Until recently Swan's (1960) series of fourteen mon in patients suffering multiple relapses or patients was the largest collection of cases in this prolonged attacks, but is only partly related to the country. In 1966 Martin was able to collect most length of the illness and fluctuates markedly from of his nineteen cases within 1 year in a 550-bed day to day with the patient's general condition. hospital. The is thus by no means rare and occurs in almost every patient at warrants greater attention than has previously some stage of the illness. It is usually sinus incopyright. been aceorded it, despite its usually benign course. origin and may outlast all other symptoms and signs by several months (Dressler, 1966). James Clinical features (1962) has shown that because of the close prox- Acute non-specific pericarditis can occur at any imity of the sinus node to the epicardium it is age but is most common in the third and fourth usually involved in pericarditis. decades (Bradley, 1964). The sex incidence has in pericarditis thus indicates irritation of the sinus been variously reported as equal (Bradley, 1964), node. Other dysrhythmias, e.g. atrial M/F 3 :1 (McGuire, Kotte & Helm, 1954) and (Soffer, 1960), supraventricular and ventricular M/F 8-5 :1 (Martin, 1966). A history of an upper ectopics and tachycardia, and may http://pmj.bmj.com/ respiratory tract about 2 weeks before is occur. Pyrexia of more than 100°F is present in common (McGuire et al., 1954). The onset is most patients at the onset of the illness but a few almost always acute and pain the almost universal patients remain afebrile throughout. presenting symptom. The pain is usually severe A is probably present in and may be accompanied by and hypo- most patients at some stage of the illness. How- tension (Martin, 1966). It may be sharp and stab- ever, it may be extremely transitory and may

bing and aggravated by respiration, or dull and disappear completely within a matter of hours or on October 2, 2021 by guest. Protected aching. It is unrelated to exertion though may be be replaced by a pericardial click. of prolonged and aggravated by the patient's failure the several times a day during the acute to rest. The pain is very often aggravated by rotat- stages is, therefore, advisable to detect it. The ing the trunk (McGuire et al., 1954), by bending behaviour of the pericardial rub is independent of forward at the waist (Bradley, 1964), or in extreme the intensity of pain. The effect of respiration on recumbency and lying on the left side (Friedberg, the intensity of the pericardial rub is very variable 1966). The site of the pain is frequently retro- and occasionally the patient's position is crucial, sternal and if also dull and pressing may result in the rub only being heard, for example, when the a wrong diagnosis of . It may patient bends forward (Bradley, 1964). The heart radiate to one or both shoulders and arms, to the sounds are otherwise normal apart from being dulled at times by . *Present address: Shotley Bridge General Hospital, The occurrence of pericardial effusion in acute Shotley Bridge, Co. Durham. non-specific pericarditis is extremely variable, the Postgrad Med J: first published as 10.1136/pgmj.43.502.534 on 1 August 1967. Downloaded from Current survey 535 reported incidence ranging from 20% (Martin, may demonstrate pericardial thickening and loss 1966) to 73% (Bradley, 1964). Pericardial tam- of mobility of the right heart border. At the same ponade should be suspected if there is marked time the right atrial pressure wave form may show elevation of the with a the systolic descent characteristic of pericardial systolic descent in the wave form (Gibson, 1960) tamponade or constriction (Gibson, 1960). accompanied by . The presence should be performed as a of a third heart sound does not indicate pericardial therapeutic measure where is tamponade or constriction but is a sign of under- suspected and as a means of obtaining fluid for lying myocardial failure (Gibson, 1960). A positive bacteriological, virological and cytological study Kussmaul's sign (elevation of the mean jugular where the diagnosis is in doubt. The pericardial venous pressure on inspiration) is likewise mis- fluid may be serous or, especially when anti- leading and can occur in any situation producing coagulants have been given for a mistaken diag- marked elevation of the jugular venous pressure, nosis of myocardial infarction, blood stained (Liu notably cardiac failure. Pleural effusion and/or & Garcia, 1965). pneumonitis occur not infrequently and produce The electrocardiogram is frequently unreward- the corresponding physical signs in the lungs. ing in acute non-specific pericarditis. It may range from normal to the type of tracing suspicious of Special investigations acute or chronic coronary disease (Bradley, Since the diagnosis of acute non-specific peri- 1964). In one of our patients whose illness lasted is largely one of exclusion, special tests 4 months the only electrocardiographic abnor- are as much directed at ruling out other causes of mality was intermittent mild ST segment depres- pericarditis, e.g. bacterial infection, including sion in several leads coinciding with clinical ; collagen disease, notably systemic exacerbations of her illness. The classical pattern erythematosus and peri-arteritis nodosa; in pericarditis of raised ST segment, retaining its and , as in confirming the natural concavity, returning within a few days to diagnosis. the isopotential level or becoming depressed with Chest X-ray may be completely normal. Its subsequent flattening or inversion of the , copyright. principal value is to rule out tuberculous or malig- was first described by Porte & Pardee (1929). The nant foci, or other causes of pericarditis which variations of this pattern in acute non-specific could result from direct spread and to establish pericarditis have been comprehensively reviewed the presence and follow the course of significant by Soffer (1960). pericardial effusions. Bradley (1964) points out Blood. Anaemia, if present at all, is never more that 250 ml of fluid may be present in the peri- than mild. The erythrocyte sedimentation rate is cardium in the adult before the heart appears usually moderately elevated in the early stages, enlarged radiologically, and suggests a lateral film generally between 20 and 30 mm/hr, Westergren with the patient leaning forward to show fluid in (Martin, 1966). However, as in our patient who http://pmj.bmj.com/ the below and in front of the heart had been ill for 8 months, the ESR may be normal shadow. The most significant radiological finding throughout. A return to normal from a previously is a sudden change in heart size in the absence of high reading must not be used as an indication clinical evidence of . Rapid increase in for ambulation of the patient, especially if heart size associated with clinical evidence of a are being used (Bradley, 1964). Leucocytosis with raised jugular venous pressure with a systolic absolute neutrophilia is present in about half the

descent in its wave form and pulsus paradoxus patients on admission to hospital (Johnson et al., on October 2, 2021 by guest. Protected should suggest the development of cardiac tam- 1961). Most of the remainder have a normal total ponade. Conversely, progressive reduction in heart white cell count with or without some relative size without resolution of these clinical signs neutrophilia (Bradley, 1964). In two of our own should suggest that the patient may be developing patients and in one of Martin's (1966), neutro- pericardial constriction. Pleural effusions are pre- paenia was observed. Serum transaminases are sent in two-thirds of the patients with pericardial universally normal in uncomplicated acute non- effusions (Bradley, 1964). specific pericarditis (Bradley, 1964) and are a Fluoroscopy is of limited value but may show useful means of distinguishing between post- some diminution in the pulsation of the heart in myocardial infarction syndrome and an extension pericardial effusion or constriction. of the original myocardial infarction. and angiography are studies. A search for evidence of recent seldom justified except where pericardial constric- virus infection particularly with the Coxsackie B tion is suspected, when injection of contrast group should be made in every suspected case of medium into right with cine-angiography acute non-specific pericarditis. The virus may be Postgrad Med J: first published as 10.1136/pgmj.43.502.534 on 1 August 1967. Downloaded from 536 Current survey cultured from faeces or from throat washings, and Myocardial infarction. The distinction between its association with the current illness confirmed this and uncomplicated acute non-specific peri- by the demonstration of a rising titre in the appro- carditis is usually not difficult provided adequate priate neutralization tests on the patient's blood. In attention is paid to the history. A history of pain the event of failure to grow the virus, examination related to breathing, sudden changes of posture of paired sera is seldom practicable due to the and swallowing should militate strongly against a multiplicity of strains of the Coxsackie virus. diagnosis of myocardial infarction. The pericardial friction rub of either condition may be evanescent. That of myocardial infarction is usually so while Other forms of pericarditis. In acute bacterial the rub of pericarditis usually persists several days. pericarditis the patient is usually much more The second sound occasionally shows reversed severely ill than with acute non-specific peri- splitting (i.e. splitting on expiration instead of carditis. The patient's history or physical examina- inspiration) in acute coronary insufficiency or tion may reveal the source of such an infection myocardial infarction but is always normal in and cultures of blood and purulent pericardial pericarditis. The electrocardiogram will usually fluid will usually disclose the specific cause. differentiate between the two conditions. The QRS is much more insidious complex is never affected in pericarditis whereas in onset. Pericardial effusion is almost always conduction defects are not uncommon with in- present and pain is uncommon. Pericardiocentesis farction. The distinction between myocardial should be performed for culture and guinea-pig infarction and post-myocardial infarction peri- inoculation of the . carditis is more difficult as the , raised ESR Spirochaetal, fungal and parasitic pericarditis and leucocytosis of the infarction may still be are all rare in this country. present at the time when the pericarditis develops. Malignant pericarditis is seldom of such acute The changing T waves and ST segments of a heal- onset as acute non-specific pericarditis. It results ing infarct may mask those of pericarditis. Pain of different character from the original infarct and

from copyright. direct spread of the process from the sur- in rounding structures. The site of origin may be pericardial quality occurring 1 or more weeks revealed by chest X-ray. Blood-stained pericardial after the infarction favours a diagnosis of post- effusion is usual and cytological examination of myocardial infarction syndrome (Dressler, 1959a). this will often reveal the true aetiology. Post-traumatic and post-operative pericarditis Aetiology can usually be eliminated by their association with The cause of acute non-specific pericarditis recent operation or trauma. However, the post- remains unknown. Its assocpation with Bornholm pericardiotomy syndrome may occur 3 months or disease was described by Bing in 1933. Since 1957, when the first cases of pericarditis associated with more after the operation, when the distinction http://pmj.bmj.com/ becomes more difficult. As most authorities now Group B Coxsackie virus were described regard acute non-specific pericarditis, post- (Fletcher & Brennan, 1957; Weinstein, 1957), pericardiotomy syndrome and post-myocardial there have been numerous reports strengthening infarction syndrome as representing the same the association between infections with this virus disease process, whose treatment is the same in and pericarditis (Smith, 1966). However, associa- each case, the distinction is largely academic. tion does not necessarily mean direct causation and it is difficult to explain the 2 weeks' delay Rheumatic pericarditis is frequently associated frequently noted between the development of the on October 2, 2021 by guest. Protected with other serious rheumatic manifestations, in infection and the onset of pericarditis on the basis particular carditis and cardiac failure. The patient of direct infection of the heart and pericardium is usually much more seriously ill. The ESR is with the virus. Furthermore, an identical clinical usually higher and the anti-streptolysin titre raised. picture of acute non-specific pericarditis can be Prolongation of the PR interval in the electro- seen following other infections such as Reiter's cardiogram is common in rheumatic pericarditis disease (Csonka & Oates, 1957), infectious mono- but is not seen in acute non-specific pericarditis. nucleosis (Gardner, 1959) and lymphogranuloma Collagen , in particular systemic lupus venereum (Sheldon et al., 1948). Likewise in peri- erythematosus, may exhibit pericarditis as part of carditis following heart operations (Engle & Ito, a much more generalized disease process. Abnor- 1961); following myocardial infarction (Dressler, mal findings in other systems, e.g. hepatic or renal 1959a); gunshot wounds to the heart (Wood, involvement, the finding of LE cells in the blood, 1956); following traumatic haemopericardium and muscle biopsy will help to reveal the true (Tabatznik & Isaacs, 1961); as a result of drug cause of the pericarditis. therapy (Costa, Holland & Pickren, 1961; Shafar, Postgrad Med J: first published as 10.1136/pgmj.43.502.534 on 1 August 1967. Downloaded from Current survey 537 1965) and with hypersensitivity (Schoen- feel that, until further research establishes which wetter & Silber, 1965), the clinical features are the cases are likely to benefit from therapy, the same. This suggests that an autoimmunity reaction view of the British Medical Journal (1965) that rather than direct causation by all the various 'there need be no hesitation in giving these agents' agents may be responsible. Anti-heart antibodies is not justified. If steroids are used the initial dose have been found in the post-pericardiotomy and should be high (40-60 mg of per day) post-myocardial infarction syndromes (van der and reduction of the dose must be made gradually Geld, 1964) and in one of our patients with an to avoid precipitating a relapse. 8-month history of smouldering non-specific peri- Patients with pericardial effusion may require carditis the titre of anti-nuclear factor rose to and where predominates 1 320 after being negative on two occasions 8 digitalization may be necessary. The treatment of months previously. This patient also gave a pre- cardiac tamponade is immediate pericardiocentesis vious history of recurrent attacks of the same and aspiration of as much of the fluid as is pos- symptoms over the previous 7 years. A similar sible, followed if necessary by surgical drainage of course has been described in many patients (Swan, the pericardium if aspiration affords inadequate or 1960 ; Dressler, 1962) and this time interval renders too short-lived relief. We prefer the apical purely viral causation unlikely. approach rather than the xiphisternal route as the former is less likely to result in damage to the Treatment heart or in confusion due to aspiration of blood The epicardium is always involved to a greater from the right atrium rather than from the peri- or lesser degree in pericarditis and it is this involve- cardial space. ment which is responsible for the ECG changes. is the only effective treatment Occasionally the myocarditis may be greater than once pericardial constriction has occurred. In the pericarditis (Smith, 1966). Because of this, and patients with recurrent attacks of acute non- because complete bed rest is the most important specific pericarditis sufficiently severe and pro- measure in minimizing the degree and duration of tracted to result in chronic invalidism, pericardiec- the acute attack (Bradley, 1964), the patient should tomy has brought complete relief to the majority copyright. be kept in bed for at least a few days after pain, (Zinsser et al., 1959). More recently, Goldfarb fever and the pericardial rub have subsided, and et al. (1966) have described the persistence of convalescence should then be gradual. Simple anal- pericardial pain after pericardiectomy. Such gesics such as or paracetamol may be radical treatment should therefore be reserved for sufficient to treat the pain of the moderate attack patients with pericardial constriction or recurrent but more severe attacks may require , large pericardial effusions and only undertaken as dextromoramide, pethidine or even for a last resort for the relief of symptoms. relief. Especially in more prolonged attacks the

patient's morale needs boosting at every oppor- Prognosis http://pmj.bmj.com/ tunity, and suitable mood-elevating drugs may be The usual course of acute non-specific peri- necessary. carditis is complete recovery from the initial attack The administration of is still a in between 2 weeks and 3 months, the average matter of considerable controversy. In many duration being 6-8 weeks. However, 20% or more patients, their administration results in a dramatic of patients suffer one or more relapses (Wood, relief of symptoms and marked general improve- 1956) and Swan (1960) described a patient with ment in the patient's condition. However, there is seventeen attacks in 16 years. Usually the patient on October 2, 2021 by guest. Protected as yet no good evidence that hormonal therapy in finally recovers completely, but rarely the disease addition to suppressing the toxic and inflammatory progresses to constrictive pericarditis (Krook, reactions does anything to eliminate the cause or 1954; Rabiner et al., 1954). Pericardial constric- in any way influence the natural history of the tion may develop as quickly as 4 weeks after the disease (Dressler, 1962). In one patient (Dressler, onset of the acute attack (Caddell, Friedman & 1959b) flare-ups of pericarditis, and Johnson, 1960; Gibbons, Goldbloom & Dobell, pneumonitis were observed after 1 and 2 years, 1965). respectively, of continuous steroid therapy, on The retention of the term 'benign' for a condi- each occasion on attempting to withdraw the drug. tion which has been responsible for twelve North & Jamplis (1962) describe a 23-year-old reported deaths (Liu & Garcia, 1965) and which housewife who developed a severe relapse while has been followed by constrictive pericarditis in on 40 mg of prednisolone per day. One of our approximately twenty-five patients (Krook, 1954; own patients, a woman of 31, also suffered a Gibbons et al., 1965), is perhaps inappropriate. Of relapse while on the same dose. For this reason we the twelve reported deaths, five were patients with Postgrad Med J: first published as 10.1136/pgmj.43.502.534 on 1 August 1967. Downloaded from 538 Current survey

,no associated heart disease who died of cardiac GIBSON, R.V. (1960) Proceedings of the Third European tamponade. Three of these patients had been given Congress of , Part A, p. 279. GOLDFARB, B., GOLD, D., LATTS, E., WEXLER, H. & WANG, anticoagulant therapy. These three, and two other Y. (1966) Recurrent 'pericardial pain' after pericardiectomy patients in the series who were also on anti- for recurrent acute benign pericarditis. Circulation, 33, coagulant therapy, all had sanguineous pericardial 283. effusions. Six of the twelve had associated JAMES, T.N. (1962) Pericarditis and the sinus node. Arch. patients intern. Med. 110, 305. cardiac disease. The inference to be drawn from JOHNSON, R.T., PORTNOY, B., ROGERS, N. & BUESCHER, E.L. Liu & Garcia's (1965) review of fatal cases is that (1961) Acute benign pericarditis. Arch. intern. Med. 108, accurate diagnosis of the condition, prompt recog- 823. nition and treatment of cardiac KROOK, H. (1954) Acute non-specific pericarditis: Study in tamponade and 24 cases including descriptions of two with later develop- the withholding of anticoagulant therapy from any ment into constrictive pericarditis. Acta med. scand. 148, patient in whom there is a suspicion of peri- 201. carditis would render a fatal outcome extremely Liu, H.Y. & GARCIA, R. (1965) Acute idiopathic pericarditis. Report of a fatal case, with brief review of the literature. unlikely in acute non-specific pericarditis, except Amer. Heart J. 69, 677. where this condition is superimposed on pre- LOGUE, R.B. & WENDKOS, M.H. (1948) existing heart disease. of benign type. Amer. Heart J. 36, 587. MARTIN, A. (1966) Acute non-specific pericarditis. A description of 19 cases. Brit. med. J. ii, 279. References MCGUIRE, J., KOTTE, J.H. & HELM, R.A. (1954) Clinical BARNES, A.R. & BURCHELL, H.B. (1942) Acute pericarditis progress. Acute pericarditis. Circulation, 9, 425. simulating coronary occlusion: A report of 14 cases. 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(1957) Cardiac compli- postpericardiotomy and postmyocardial-infarction syn- cations of Coxsackie virus infection. Lancet, 1, 913. dromes. Lancet, H, 617. FRIEDBERG, C.K. (1966) Diseases of the Heart. Saunders, WEINSTEIN, S.B. (1957) Acute benign pericarditis associated Philadelphia. with Coxsackie virus group B, type 5. New Engl. J. Med. GARDNER, C.C. (1959) Acute pericarditis as the initial 229, 423. manifestation of infectious mononucleosis. Amer. J. WOOD, P. (1956) Diseases of the Heart and Circulation. med. Sci. 237, 352. Eyre & Spottiswoode, London. GIBBONS, J.E., GOLDBLOOM, R.B. & DOBELL, A.R.C. (1965) ZINSSER, H.F., BLAKEMORE, W.S., KIRBY, C.K. & JOHNSON, Rapidly developing pericardial constriction in childhood J. (1959) Invalidism due to recurrent idiopathic pericarditis following acute non-specific pericarditis. Amer. J. Cardiol. with a recovery after pericardiectomy. J. Amer. med. Ass. 15, 863. 171, 274.