J. M.. M W K A Y 1. ,R..%\THEWS. I. D , ROHW.. 16. BH.hTHA1, P S.. DUYER. G . , SIRIC.KL.AYD, R. G. and WHITTIWHAM. S. (19731 The spectrum of liver direaae in an Australian teaching hospital: A prospective study OS 205 patients. .Wed J Au.\I.. 2. 1085. 17 LPEW.C M. (19673: Clinical diagnosis, evaluation and treatmenr of 1hc1 disease in alcoholics, Fed Proc., 26, 1474 18 Misriiis. S P. (1968) Liver disease in pregnancy wirh particular emphasic on rhr cholestalx syndromes. A u ~ r Ann Mrd., 17, 248 19 CAROZI. J and PFarrlmor. (i. (19581: EnquPre sur les cmon$tances dittetique dc la cirrhose alcoolique en France. Yrocrvdinjir n/ World Congress on Garrroenrerologj. 1. 661 20. SCHMIDT. W arid BROYETTO, I. (1962) Death from 11wr ciirhorli and
Aust N Z J Med (1975),5,pp 57-62
specific alcoholic beierage con,umption- a n ecolog~cal study. Atnrr J . puhl H l r h , 52. 1473. ? I . Hl\rrwonrIT, H P. (1950) In Let.rure.~o n the LII’PT rrnd rls Direarea, Rlacks e l l Sc!enlitic Publications. Oxford and Edinburgh. 87 22. PFARL.A , RL!I.(.HI~Y. R and I.iPscr,m. W R (1962): Cirrhosis rnoitality in Three largc cities Imp~l~dLloilS for alcoholism and inlcrciiy comparisons. In So. Edited by Pittman, D. J and Snyder. C. R John Wile? and Sons. New York. 345 23. LtFvY. C M 119703: In Alcoholic Cirrhorii and Other 7 o . r ~Hiparopaihios. Skandia International Sympwium, Nordiska Rokhandelns Forlag. Stockhulm, 283. 24. GRtth. I R. (1965) Subclimra! acute Iwer disease d rhe alcoholic, A w l . A n n .Mud., 14, 1 I 1
_ _ -
~~
-~
CASE REPORT
Constrictive Pericarditis following Mild Non-penetrating Trauma Rudra Rasaretnam’ and A. T. S. Pault
From Thoracic Unit 1 , Colombo General Hospital, Colombo, Sri Lanka
Summary: A case of constrictive pericarditis developed within twenty-four days of mild, blunt thoracic trauma. Rapid progression from traumatic pericarditis to constriction is documented with clinical evidence, electrocardiographic changes and cardiac catheterisation data. Other manifestations of pericardial reaction after blunt chest trauma are reviewed briefly. c
The occurrence of cardiac contusion and traumatic pericarditis after blunt chest trauma is well d ~ c u m e n t e d l - ~However, . most reports deal predominantly with post mortem data, probably due to the fact that the diagnosis is missed in less severely injured patients4. Watson and Bartholomae’ found a 38% incidence of cardiac injury when routine ECGs were taken after chest trauma. A rare complication is the development of constrictive pericarditis, only twelve cases being recorded in the English ‘Assistant Thoracic Surgeon tThoracic Surgeon Accepted for publication 18 September, 1974
language literature6. In previously published reports the relationship between trauma and the subsequent development of constrictive pericarditis is inferential, particularly when there is a long time interval between the two. The present communication documents the rapidly changing clinical features with serial electrocardiograms in a boy who progressed to constriction 24 days after mild chest trauma. Case Report
JA. a twelve-year-old male, was admitted to the Colombo General Hospital on the 2nd April, 1973 with a history of falling about six feet from a tree 12 days previously, and striking his chest on some stones lying on the ground. He noticed nothing untoward at the time and participated in a school athletics meet the following day. where his performance was no less than had been achieved at practice. The following day he complained of dyspnoea, and by evening noticed that he had respiratory difficulty even at rest, and had developed an unproductive cough. He was admitted to a private hospital, but was discharged after two days. As his symptoms persisted, he was admitted the same evening to the Chilaw Hospital. where he was found to be very dyspnoeic and mildly febrile. Pulse rate was 126jmin and BP 100/70. The heart sounds were normal. Occasional adventitious sounds in the lungs were also present. and he was treated with penicillin and aspirin. After eight days, although a little improved, chest X-ray showed an un-
58
FIGURE 1. megaly.
KASAKkTN.4M A N > PAUL
VOL.
5 , NO. I
Pre-operative Chest X-ray showing cardio-
explained cardioinegaly (Fig. I). and he was then transferred to the Colombo General Hospital. There he complained of' dyspnoea, and pain in the left chest. He had a mild pyrexia. pulse rate of 13Olmin. and BP of 90/60. The jugular venous pressure was elevated. The apex beat was palpable in the 5th left intercostal space, 2 . 5 cm outside the mid-clavicular line. and the area of cardiac dullness was increased. The air entry was diminished over the left lower zone.
F I G U R E 2. Serial pre-operative electrocardiograms showing ST segment-T wave changes. (a) ECG taken 13 days after the fall; (b) 14 days; (c) 19 days: (d) 23 days.
Laboratory finding were: H b 8.7 g 100 ml. WBC 18.000, mm', ESR 98 mm in the first hour, blood urea 32 mg. IOU mi. serum cholesterol 206 mg.'100 ml. serum proteins 6 . 9 gt 100 ml. Serum electrophoresis showed a slight rise in the globulin traction. Examination of the sputum was negative for tubercle bacilli. X-ray of the chest confirmcd cardiomegaly. ECG on the 3rd .4pril (Fig. 2a) showed a slight ST segment elevation and inverted T waves in leads I and 11, with only inverted T waves in leads aVF and V2 -V6. The ST segment elevation was diminished on the 4th April (Fig. 2b). and had disappeared completely by the 9th (Fig. 2c). Increasing T wave inversion was seen until the 13th April (Fig. 2d). the day prior to operation. He ran an irregular pyrexia up to 103 degrees Fahrenheit in the days following admission. On the 4th April a pericardial rub was heard for the first time. but lasted only one
FIGURE 3. R;ght Heart pressure tracings; (a) preoperative showing 'M' form in the atrial trace, and early diastolic dip and raised end diastolic plateau in the ventricular trace; (b) post-operative trace which is essentially normal.
day. The liver edge became palpable two finger's breadth below the right costal margin. and together with the elevated JVP persisted despite treatment with digoxin and diuretics. Cardiac catheterisation on the 11th April showed a right atrial prcssure of 18 mm Hg. and a right ventricular pressure of 30'10. An early diastolic dip and end diastolic plateau were present in the right ventricular trace. and an 'M' form in the atrial trace (Fig. 3a). The catheter when wedged against the wall of the right atrium showed a gap betmen it and the outer margin of the enlarged cardiac silhouette. which was presumed to be due to a pericardial effusion. Three days later, pulsus paradoxus was noticed for the first time, and the JVP was now elevated to the level of the angle of the mandible. The precordial cardiac impulse which had previously been easily palpable was now barely perceptible. but the heart sounds were still clearly heard. The systemic HP had fallen to X@;60. Pericardiectomy was carried out on the 14th April through a left antero-lateral thoracotoniy. The pericardium was grossly thickened, measuring 5 t o 6 mm. The two layers &ere adherent to each other, hut dissection off the ventricles was not difficult. Pericardiec-
60
____._~___
RASARETNAM A N D PAUL
tomy was carried as far as the atrio-ventricular groove on the right, and as far as the entry of the pulmonary veins o n the left. a thin strip of parietal pericardium with the phrenic nerve being preserved. There was a localised collection of
-
I
'
!
VOL.
5. NO. 1
about 5-10 ml of serosanguinous fluid between the two layers of pericardium over the inferior surface of the right ventricle. The central venous pressure which had been 290 mm of salinc at the commencement of the operation had dropped to 220 mm soon after pericardiectomy. His post operative course was uneventful. and when discharged from hospital on the 4th May, the JVP was only minimally raised. and the liver edge no longer palpable. Cardiac catherisation just prior to discharge gave results summarised in Fig. 3b. Histological examination showed evidence of acute inflammation supervening on a chronic inflammatory process. There were numerous fibroblasts, together with several plasma e l l s and lymphocytes. There were in addition several polymorphonuclear leucocytes. some of which were undergoing necrotic changes; clumps of fibrin and dilated blood vessels were also seen in some areas (Fig. 4a. b.c). At review in June 1973, he was back to normal activity. The JVP was now normal, and no abnormal signs were found on clinical examination. Chest X-ray showed minimal cardiomegaly, and the ECG showed persistent T wave inversion in some leads (Fig. 5).
26.4.73
0.6.73
FIGURE 4. Histology of the excised pericardium. (a) Section showing numerous polymorphonuclear cells, some of which show degenerative changes, together with scattered macrophages and plasma cells. Dilated blood vessels are also present. (4b) Section showing fibroblasts and some fibrous tissue. Lymphocytes are also seen. (4c) Section showing clumps of fibrin, and lymphocytes and plasma cells.
FIGURE 5. Post-operative electrocardiograms on 26.4.73 and 8.6.73 showing progressive resolution towards the normal pattern by the latter date.
Discussion
The true incidence of cardiac lesions with blunt thoracic trauma is difficult to assess, as minor degrees are not recognised owing to a low index of suspicion. In more seriously injured patients, multiple injuries frequently mask the presence of the cardiac lesion. In a review of 50 consecutive fatal automobile accidents. LeinoK7 found a 16‘x incidence of macroscopic cardiac injury. Watson and Bartholomae’ reported a 38% incidence, in 44 consecutive major injuries when routine ECGs were done. The commonest pericardial reaction after trauma has been an effusion, usually of a serosanguinous character, but occasionally frankly haemorrhagic. In the majority of cases no serious sequelae occur, the effusion being s l o ~ l yreabsorbed. The occurrence of the post-pericardiectomy syndrome after penetrating chest trauma, and the usually benign course of such cases. has also been described’. Recurrent pericardial effusions occurring several weeks or months after blunt chest trauma has also been reported. but the mechanism of its development is as yet uncertain’. In the two cases presented by Goodkind et a!.’ there were recurrent episodes of cardiac tamponade, and they drew attention to the similarity between their cases and the postpericardiotomy syndrome. the post-myocardial infarction syndrome and idiopathic benign pericarditis. Initially, treatment with corticosteroids resulted in an amelioration of the signs and symptoms, but with subsequent relapses, pericardiotomy became necessary. at which time loculated effusions and adhesions between the two layers of the pericardium were present. Raker et al.“ suggested that the syndrome of recurrent effusions was analogous to the behaviour of blood clot in the subdural space, where “with liquefaction, protein molecules were split into smaller moieties, with a resultant rise in colloid osmotic pressure” and consequent attraction of fluid into the pericardial sac. However, the conservative management of penetrating cardiac wounds by aspiration has not resulted in the development of recurrent effusions or tamponade in the great majority of cases’ 1 3 . Ehrenhaft and Taber14 found experimentally that the injection of autogenous blood into the pericardial sacs of dogs failed to cause
’
the development of constrictive pericarditis, and none of the injectcd blood was found at autopsy. However, the injection of the lipid extract caused pericardial and epicardial thickening, with patchy areas of granulation tissue and adhesions in all the dogs, while one of the seven developed constrictive pericarditis at seven weeks. The first report of constrictive pericarditis occurring after trauma, and being unassociated with any other aetiological factor, was by Glenn” in 1940, the symptoms of constrictive pericarditis developing two years after blunt chest trauma sustained in an automobile accident. Twenty-five years later, Goldstein and Yu6 found only eight cases in the literature, and added four of their own. In most of the cases symptoms of cardiac involvement developed a short period after the injury, but symptoms of constrictive pericarditis did not become manifest for one to five years6. l6-’’. The presumption of trauma being the cause of the constrictive pericarditis is based on the evidence of some sort of disability developing soon after the injury, and the aspiration of haemorrhagic fluid from the pericardial sac at various times between the injury and the confirmation of the diagnosis. In only three previous cases has the constrictive pericarditis developed in under a year, the shortest period being six weeks6, 14, ’I. In the present case symptoms developed two days after trivial trauma in a previously healthy boy, and had progressed to constrictive pericarditis in 24 days. Such rapid development of constrictive pericarditis is unusual, but has been reported previously by Caddell et aZ.22 and Gibbons et aI.23, who documented the details in two children aged 7 years and 4 years, who progressed to constriction 30 days and five weeks respectively after acute non-specific pericardi tis. The reason for the development of this unusual sequence of events is unknown. The similarity of the syndrome of recurrent pencardial effusion to the post myocardial infarction syndrome of Dressler, and the response in both instances to corticosteroids has raised the possibility of an auto-immune reaction being responsible. There is however, no conclusive evidence as yet of an immune reaction,
62
RASARETNAM AND PAUL
Acknowledgements
we have pleasure
in thanking M,.. K~~~~~~~~~ cJomes for the photographs, and Miss N. Moosajee for secretarial help. References I. BAKHLR, H (1938) Trauma of [hr heart. Brrr. nted. I , 1. 4.13. 2 Hnrr. H W and M . Y R T I \ .J W (1957) Myocardial contusion. Anwr J Surg., 9 3 , 558
4
5 6 7
8 9. 10.
FR. 11 E (1Y65): Myocaidlal contusion. Arc-h inrem M u d , 115, 434. BECK.C S. (1935): Contusions of the heart, J . Amer. med. A K , 104. 109. WATSOS, J H. and BARTHOLOMAE, W. M .(1960): Cardiac q u r y due to non-penetrd?inz chest trauma. Ann. i n m n .Vrd.. 52. 871 GOL&STIIN. S a n d YL,P. N. (19651: Constrictive pericardms after hlunt chest trauma. Amer. Hear!. J . . 69, 544 LFIKOFF. H D (1940) Direct non-penetrating injuries o f t h e heart. Arch miern. Med.. 14. 653. SEGAL.F and T48~TzNih. B (1960): Post-pericardiotomy syndrome followinp penetrating stab wounds o f t h e chest. Comparison with the portcommlsrurotomy Fyndrome. Amer. H e o n I , 59, 175 GwI)KihU. M I.. B i . 1 m ~ mW. E. and GwDYER. A V N. (1960) Recurrent pencardial effiision after non-penctrating chest trauma. Report of 2 c a e c treated with adreno-cortical Fteroids, New €np/. J M e d . . 263, 874 RAKFR,I W , I . A N G I ~ H SI ~ H. ~ ~ .and GOWES.G F. (1958): Traumatic harmopericardium producing later conrtrictive pericarditis---report of a case. .4nn. S ~ r g 148. . ~ 134.
VOL.
5 , NO. 1
1 1 . R a v i r t . ~ ,M M (1952) Discussion 01 paper b) Ehrenhaft R Tabcr. J . Ihoruc. Surg., 24, 366. I ? CW1I.Y. D A . I)[ US. J R . B R W K W Y H L and DIH4KI.I. >IE. 119561.
Trearment of penetrating wounds of the heart. experimental and clinical ohservations. Surgery. 31, 8R2. J P (1956): Heart wounds: (a long I ? . DRYE.I. C.. Cot. W. S and STAMFR, term follow up of20 cases). Amer. J . Surg.. 91, 597. J. L. and T A R I RR. . E (1952): Haemopcricardium and con14. EHRENHAFT. 16. BARKEK,P S and J o l i N ~ T o ~F, D (1950). Chronic pericarditic with effusion, Circularion, 2. 134. I 7 MCKUSICK, W. A (1952) Chronic constrictiic pericarditi? Some clinical
and laboratorj data. Bufi. Johns Hopk. Horp W.3 18 OYERAOLT. R H.. BcRwrxi, C S., WOOI>RL:RY. 1 W and W & I K I : U J. H 11952): Constrictive oericarditis and constrictive Dicuritis treated bv, .nericardiectomy and pulmonary deconication. J . rhorbc. Surp., 23. 1 19. WARBFRG. E. (19551: Traumatic a m o u r heart. Arner. Hrorf 1.49, 633 20. ROWF.W S. (1959). Constrictive pencarditis following haemopericardium from mild non-penetrating trauma to the chest, M e d J . Ausl.. 2, 316 21. ADA. A . E. W , JONES. 0 R and SHEEREN, J (1950). Parrial pericardiectomy in a caSe of haemopericardium due to non-penetrating trauma. J rhoruc Surg.. 20, 105.
Y AJOHNSON, ~ J. (19601: Conbtriclivc peri22. Cwi)~t.i.. J. L.. F K ~ E ~ S~ and carditis occurrence in a child one month old following acute pericarditis w,ith effusion. Arne,. J . D6 Child. 100, 851) 27. GinuoNr. J F , Goi.i)nioon. R B. and DoBEI.~., A. R. C. (1965): Rapidly developing pericardial constriction following acuic non-specific pericarditis, Amer. . I Cnrdrol., . 15, 863.
Aust. N.Z. J. Med. (1975). 5, pp. 62 65 CASE REPORT
Dia Iys is-associated Dementia L.
J. Barratt" and J. R. Lawrencef
From the Renal Unit, The Queen Elizabeth Hospital, Woodville, South Australia
Summary: Two patients from an Australian Dialysis Centre developed a progressive neurological disorder with features similar to those recently described as the syndrome of Dementia Dialytica. These two patients are reported here and this newly recognised syndrome reviewed.
A progressive and fatal neurological syndrome associated with long term maintenance haemodialysis has recently been described in several "Assistant Director, Renal Unit tDirector, Renal Unit Correspondence Dr J R Lawrence, Renal Unit The Queen Elizabeth Hospital, Woodville, Sth Aust 501 1 Accepted f o r publication 18 September, 1974
patients from Dialysis Centres in the USA', '. In addition, a similar disorder appears to have been seen in at least one Dialysis Unit in Great Britain '. The syndrome, which is characterised by progressive dementia, dyspraxia, myoclonus and electroencephalographic changes has recently been labellcd Dementia Dialytica4. Such a syndrome has not previously been reported in Australia. We have, however, encountered two patients with features suggestive of this syndrome and describe these two patients in this report. Case Reports Case N o . 1 A 50 year old female developed Henoch Schoenlein Purpura with associated nephritis In 1965. Renal biopsy performed
Aust N Z J Med (1975),5,pp 57-62
specific alcoholic beierage con,umption- a n ecolog~cal study. Atnrr J . puhl H l r h , 52. 1473. ? I . Hl\rrwonrIT, H P. (1950) In Let.rure.~o n the LII’PT rrnd rls Direarea, Rlacks e l l Sc!enlitic Publications. Oxford and Edinburgh. 87 22. PFARL.A , RL!I.(.HI~Y. R and I.iPscr,m. W R (1962): Cirrhosis rnoitality in Three largc cities Imp~l~dLloilS for alcoholism and inlcrciiy comparisons. In So. Edited by Pittman, D. J and Snyder. C. R John Wile? and Sons. New York. 345 23. LtFvY. C M 119703: In Alcoholic Cirrhorii and Other 7 o . r ~Hiparopaihios. Skandia International Sympwium, Nordiska Rokhandelns Forlag. Stockhulm, 283. 24. GRtth. I R. (1965) Subclimra! acute Iwer disease d rhe alcoholic, A w l . A n n .Mud., 14, 1 I 1
_ _ -
~~
-~
CASE REPORT
Constrictive Pericarditis following Mild Non-penetrating Trauma Rudra Rasaretnam’ and A. T. S. Pault
From Thoracic Unit 1 , Colombo General Hospital, Colombo, Sri Lanka
Summary: A case of constrictive pericarditis developed within twenty-four days of mild, blunt thoracic trauma. Rapid progression from traumatic pericarditis to constriction is documented with clinical evidence, electrocardiographic changes and cardiac catheterisation data. Other manifestations of pericardial reaction after blunt chest trauma are reviewed briefly. c
The occurrence of cardiac contusion and traumatic pericarditis after blunt chest trauma is well d ~ c u m e n t e d l - ~However, . most reports deal predominantly with post mortem data, probably due to the fact that the diagnosis is missed in less severely injured patients4. Watson and Bartholomae’ found a 38% incidence of cardiac injury when routine ECGs were taken after chest trauma. A rare complication is the development of constrictive pericarditis, only twelve cases being recorded in the English ‘Assistant Thoracic Surgeon tThoracic Surgeon Accepted for publication 18 September, 1974
language literature6. In previously published reports the relationship between trauma and the subsequent development of constrictive pericarditis is inferential, particularly when there is a long time interval between the two. The present communication documents the rapidly changing clinical features with serial electrocardiograms in a boy who progressed to constriction 24 days after mild chest trauma. Case Report
JA. a twelve-year-old male, was admitted to the Colombo General Hospital on the 2nd April, 1973 with a history of falling about six feet from a tree 12 days previously, and striking his chest on some stones lying on the ground. He noticed nothing untoward at the time and participated in a school athletics meet the following day. where his performance was no less than had been achieved at practice. The following day he complained of dyspnoea, and by evening noticed that he had respiratory difficulty even at rest, and had developed an unproductive cough. He was admitted to a private hospital, but was discharged after two days. As his symptoms persisted, he was admitted the same evening to the Chilaw Hospital. where he was found to be very dyspnoeic and mildly febrile. Pulse rate was 126jmin and BP 100/70. The heart sounds were normal. Occasional adventitious sounds in the lungs were also present. and he was treated with penicillin and aspirin. After eight days, although a little improved, chest X-ray showed an un-
58
FIGURE 1. megaly.
KASAKkTN.4M A N > PAUL
VOL.
5 , NO. I
Pre-operative Chest X-ray showing cardio-
explained cardioinegaly (Fig. I). and he was then transferred to the Colombo General Hospital. There he complained of' dyspnoea, and pain in the left chest. He had a mild pyrexia. pulse rate of 13Olmin. and BP of 90/60. The jugular venous pressure was elevated. The apex beat was palpable in the 5th left intercostal space, 2 . 5 cm outside the mid-clavicular line. and the area of cardiac dullness was increased. The air entry was diminished over the left lower zone.
F I G U R E 2. Serial pre-operative electrocardiograms showing ST segment-T wave changes. (a) ECG taken 13 days after the fall; (b) 14 days; (c) 19 days: (d) 23 days.
Laboratory finding were: H b 8.7 g 100 ml. WBC 18.000, mm', ESR 98 mm in the first hour, blood urea 32 mg. IOU mi. serum cholesterol 206 mg.'100 ml. serum proteins 6 . 9 gt 100 ml. Serum electrophoresis showed a slight rise in the globulin traction. Examination of the sputum was negative for tubercle bacilli. X-ray of the chest confirmcd cardiomegaly. ECG on the 3rd .4pril (Fig. 2a) showed a slight ST segment elevation and inverted T waves in leads I and 11, with only inverted T waves in leads aVF and V2 -V6. The ST segment elevation was diminished on the 4th April (Fig. 2b). and had disappeared completely by the 9th (Fig. 2c). Increasing T wave inversion was seen until the 13th April (Fig. 2d). the day prior to operation. He ran an irregular pyrexia up to 103 degrees Fahrenheit in the days following admission. On the 4th April a pericardial rub was heard for the first time. but lasted only one
FIGURE 3. R;ght Heart pressure tracings; (a) preoperative showing 'M' form in the atrial trace, and early diastolic dip and raised end diastolic plateau in the ventricular trace; (b) post-operative trace which is essentially normal.
day. The liver edge became palpable two finger's breadth below the right costal margin. and together with the elevated JVP persisted despite treatment with digoxin and diuretics. Cardiac catheterisation on the 11th April showed a right atrial prcssure of 18 mm Hg. and a right ventricular pressure of 30'10. An early diastolic dip and end diastolic plateau were present in the right ventricular trace. and an 'M' form in the atrial trace (Fig. 3a). The catheter when wedged against the wall of the right atrium showed a gap betmen it and the outer margin of the enlarged cardiac silhouette. which was presumed to be due to a pericardial effusion. Three days later, pulsus paradoxus was noticed for the first time, and the JVP was now elevated to the level of the angle of the mandible. The precordial cardiac impulse which had previously been easily palpable was now barely perceptible. but the heart sounds were still clearly heard. The systemic HP had fallen to X@;60. Pericardiectomy was carried out on the 14th April through a left antero-lateral thoracotoniy. The pericardium was grossly thickened, measuring 5 t o 6 mm. The two layers &ere adherent to each other, hut dissection off the ventricles was not difficult. Pericardiec-
60
____._~___
RASARETNAM A N D PAUL
tomy was carried as far as the atrio-ventricular groove on the right, and as far as the entry of the pulmonary veins o n the left. a thin strip of parietal pericardium with the phrenic nerve being preserved. There was a localised collection of
-
I
'
!
VOL.
5. NO. 1
about 5-10 ml of serosanguinous fluid between the two layers of pericardium over the inferior surface of the right ventricle. The central venous pressure which had been 290 mm of salinc at the commencement of the operation had dropped to 220 mm soon after pericardiectomy. His post operative course was uneventful. and when discharged from hospital on the 4th May, the JVP was only minimally raised. and the liver edge no longer palpable. Cardiac catherisation just prior to discharge gave results summarised in Fig. 3b. Histological examination showed evidence of acute inflammation supervening on a chronic inflammatory process. There were numerous fibroblasts, together with several plasma e l l s and lymphocytes. There were in addition several polymorphonuclear leucocytes. some of which were undergoing necrotic changes; clumps of fibrin and dilated blood vessels were also seen in some areas (Fig. 4a. b.c). At review in June 1973, he was back to normal activity. The JVP was now normal, and no abnormal signs were found on clinical examination. Chest X-ray showed minimal cardiomegaly, and the ECG showed persistent T wave inversion in some leads (Fig. 5).
26.4.73
0.6.73
FIGURE 4. Histology of the excised pericardium. (a) Section showing numerous polymorphonuclear cells, some of which show degenerative changes, together with scattered macrophages and plasma cells. Dilated blood vessels are also present. (4b) Section showing fibroblasts and some fibrous tissue. Lymphocytes are also seen. (4c) Section showing clumps of fibrin, and lymphocytes and plasma cells.
FIGURE 5. Post-operative electrocardiograms on 26.4.73 and 8.6.73 showing progressive resolution towards the normal pattern by the latter date.
Discussion
The true incidence of cardiac lesions with blunt thoracic trauma is difficult to assess, as minor degrees are not recognised owing to a low index of suspicion. In more seriously injured patients, multiple injuries frequently mask the presence of the cardiac lesion. In a review of 50 consecutive fatal automobile accidents. LeinoK7 found a 16‘x incidence of macroscopic cardiac injury. Watson and Bartholomae’ reported a 38% incidence, in 44 consecutive major injuries when routine ECGs were done. The commonest pericardial reaction after trauma has been an effusion, usually of a serosanguinous character, but occasionally frankly haemorrhagic. In the majority of cases no serious sequelae occur, the effusion being s l o ~ l yreabsorbed. The occurrence of the post-pericardiectomy syndrome after penetrating chest trauma, and the usually benign course of such cases. has also been described’. Recurrent pericardial effusions occurring several weeks or months after blunt chest trauma has also been reported. but the mechanism of its development is as yet uncertain’. In the two cases presented by Goodkind et a!.’ there were recurrent episodes of cardiac tamponade, and they drew attention to the similarity between their cases and the postpericardiotomy syndrome. the post-myocardial infarction syndrome and idiopathic benign pericarditis. Initially, treatment with corticosteroids resulted in an amelioration of the signs and symptoms, but with subsequent relapses, pericardiotomy became necessary. at which time loculated effusions and adhesions between the two layers of the pericardium were present. Raker et al.“ suggested that the syndrome of recurrent effusions was analogous to the behaviour of blood clot in the subdural space, where “with liquefaction, protein molecules were split into smaller moieties, with a resultant rise in colloid osmotic pressure” and consequent attraction of fluid into the pericardial sac. However, the conservative management of penetrating cardiac wounds by aspiration has not resulted in the development of recurrent effusions or tamponade in the great majority of cases’ 1 3 . Ehrenhaft and Taber14 found experimentally that the injection of autogenous blood into the pericardial sacs of dogs failed to cause
’
the development of constrictive pericarditis, and none of the injectcd blood was found at autopsy. However, the injection of the lipid extract caused pericardial and epicardial thickening, with patchy areas of granulation tissue and adhesions in all the dogs, while one of the seven developed constrictive pericarditis at seven weeks. The first report of constrictive pericarditis occurring after trauma, and being unassociated with any other aetiological factor, was by Glenn” in 1940, the symptoms of constrictive pericarditis developing two years after blunt chest trauma sustained in an automobile accident. Twenty-five years later, Goldstein and Yu6 found only eight cases in the literature, and added four of their own. In most of the cases symptoms of cardiac involvement developed a short period after the injury, but symptoms of constrictive pericarditis did not become manifest for one to five years6. l6-’’. The presumption of trauma being the cause of the constrictive pericarditis is based on the evidence of some sort of disability developing soon after the injury, and the aspiration of haemorrhagic fluid from the pericardial sac at various times between the injury and the confirmation of the diagnosis. In only three previous cases has the constrictive pericarditis developed in under a year, the shortest period being six weeks6, 14, ’I. In the present case symptoms developed two days after trivial trauma in a previously healthy boy, and had progressed to constrictive pericarditis in 24 days. Such rapid development of constrictive pericarditis is unusual, but has been reported previously by Caddell et aZ.22 and Gibbons et aI.23, who documented the details in two children aged 7 years and 4 years, who progressed to constriction 30 days and five weeks respectively after acute non-specific pericardi tis. The reason for the development of this unusual sequence of events is unknown. The similarity of the syndrome of recurrent pencardial effusion to the post myocardial infarction syndrome of Dressler, and the response in both instances to corticosteroids has raised the possibility of an auto-immune reaction being responsible. There is however, no conclusive evidence as yet of an immune reaction,
62
RASARETNAM AND PAUL
Acknowledgements
we have pleasure
in thanking M,.. K~~~~~~~~~ cJomes for the photographs, and Miss N. Moosajee for secretarial help. References I. BAKHLR, H (1938) Trauma of [hr heart. Brrr. nted. I , 1. 4.13. 2 Hnrr. H W and M . Y R T I \ .J W (1957) Myocardial contusion. Anwr J Surg., 9 3 , 558
4
5 6 7
8 9. 10.
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Aust. N.Z. J. Med. (1975). 5, pp. 62 65 CASE REPORT
Dia Iys is-associated Dementia L.
J. Barratt" and J. R. Lawrencef
From the Renal Unit, The Queen Elizabeth Hospital, Woodville, South Australia
Summary: Two patients from an Australian Dialysis Centre developed a progressive neurological disorder with features similar to those recently described as the syndrome of Dementia Dialytica. These two patients are reported here and this newly recognised syndrome reviewed.
A progressive and fatal neurological syndrome associated with long term maintenance haemodialysis has recently been described in several "Assistant Director, Renal Unit tDirector, Renal Unit Correspondence Dr J R Lawrence, Renal Unit The Queen Elizabeth Hospital, Woodville, Sth Aust 501 1 Accepted f o r publication 18 September, 1974
patients from Dialysis Centres in the USA', '. In addition, a similar disorder appears to have been seen in at least one Dialysis Unit in Great Britain '. The syndrome, which is characterised by progressive dementia, dyspraxia, myoclonus and electroencephalographic changes has recently been labellcd Dementia Dialytica4. Such a syndrome has not previously been reported in Australia. We have, however, encountered two patients with features suggestive of this syndrome and describe these two patients in this report. Case Reports Case N o . 1 A 50 year old female developed Henoch Schoenlein Purpura with associated nephritis In 1965. Renal biopsy performed
