794 Ocr.

2, 1954 MEDICAL MEMORANDA Bou1n

MEDICAL
upper extremity, underlying and adherent to the diaphragm;
Medical Memoranda the other, 5 cm. in diameter, at the inferior margin in the
midline. The wall of the larger cavity was composed of
dense collagen with a ragged lining of necrotic material.
No amoebae or organisms were demonstrable. " Iron pig-
ment " was absent, suggesting that an origin from a recently
Liver Abscess and Polyarteritis Nodosa necrotic area of liver was unlikely. The liver appeared
fatty. There were large haemorrhagic areas, mainly in the
A case presenting with a large liver abscess, and multiple right lobe, sometimes surrounded by paler more solid areas.
infarcts due to polyarteritis nodosa, is worth recording. Other totally pale areas resembling infarcts were also pre-
CASE REPORT sent. The smaller haemorrhagic areas were circular, and
appeared to be aneurysmal sacs.
A man aged 71 presented in September, 1950, with a four- 120 and 138 g. Elastosis in the larger
months history of gnawing pain in the right hypochondrium, andKidneys.-Weights,
fibrinoid necrosis in the smaller vessels.
lassitude, loss of weight (2 st.-12.7 kg.), pallor, anorexia,
nausea, and vomiting. He had had dysentery in India in Lungs.-No vascular change.
1918, and subsequent irregularly repeated attacks of right- Spleen.-Weight, 130 g.; normal.
sided abdominal pain until 1940. Epididymis.-Aneurysmal vessels seen in the right epi-
The patient was a sallow thin man, afebrile, weight 8 st. didymis similar to those in the liver.
(50.8 kg.). A firm tender liver extended into the right iliac Suprarenals.-Vessels of the capsule showed the identical
fossa. There were signs of right basal pleurisy. B.P. 175/95. haemorrhagic change observed in the smaller hepftic vessels
Heart and C.N.S., N.A.D. Hb, 9.5 g.; R.B.C., 3,200,000. and in the epididymis.
P.C.V., 30% ; W.B.C., 12,000 (polys. 78%); E.S.R. (Wester- Hepatic A rteries.-In the portal tracts throughout the
gren), 70 mm. first hour. Trace of proteinuria. Blood urea, liver the small hepatic arteries all had thick walls and occa-
31 mg. per 100 ml.; cholesterol, 131 mg. per 100 ml.; total sionally showed hyaline or fibrinoid change. The laminae
proteins, 8.2 g. % (albumin 2.8 g., globulin 5.4 g.); bilirubin, were reduced, but there was little periarterial inflammatory
0.4 mg. per 100 ml.; thymol turbidity, 4 units; colloidal reaction. In the haemorrhagic areas the arteries were often
gold, negative; alkaline phosphatase, 20 units. Casoni test, entirely blocked by a concomitant-intrinsic hyperplasia and
negative. Hydatid C.F.T., negative. Faeces: no ova, cysts, had given rise to large areas of hepatic necrosis. In other
amoeba, or occult blood. Chest x-ray examination showed cases the necrotic arterial vessels had given way with
considerable elevation of the right hemidiaphragm.' aneurysmal dilatation.
Mesenteric Vessels.-These showed destruction of the
PROGRESS medial coat of the arteries with aneurysm formation.
Diagnostic liver puncture on December 22 revealed turbid
brown fluid. After a course of emetine hydrochloride, 10 gr. COMMENT
(0.65 g.) i.m. in 10 days, 1,500 ml. of similar fluid was aspir- It is probable that this patient had a long-standing
ated from the right lobe of the liver. The fluid was sterile on amoebic abscess and developed polyarteritis during treat-
culture (aerobic and anaerobic) and contained fat globules, ment. Atypical cases of amoebic abscesses have been
macrophages, and amorphous debris only. Subsequent diagnosed by liver aspiration (Van Raalte, 1949). The pre-
x-ray examination of the abdomen showed a large abscess sence of polyarteritis nodosa was not diagnosed during life.
cavity with a fluid level. His general condition improved There were several indications to which we should have
after a course of chloroquine sulphate (13.2 g. in divided paid more attention. The presence of proteinuria and
dosage). Recurrence of pain, weakness, anorexia, and hypertension was not readily explained, and the liver-func-
cough necessitated readmission in April, 1951. The liver tion tests were persistently abnormal, which, as Sodeman
remained enlarged and tender three fingerbreadths below the (1950) pointed out, is very unusual in amoebiasis of the
subcostal margin. Hb, 85% ; E.S.R. (Westergren), 69 mm. liver.
first hour; blood urea, 56 mg. per 100 ml.; B.P. 180/120. Pass (1935) showed that infarcts of the liver occur in poly-
Initial symptomatic improvement followed a further course arteritis nodosa, frequently becoming converted into absces-
of chloroquine (6.4 g. in 14 days), but he relapsed in May which are difficult to distinguish from amoebic or other
with severe prostrating attacks of pain, vomiting, and rigors. ses Some cases of periarteritis nodosa with hepatic
A cerebral episode developed in June with stupor, periodic abscesses.
infarcts run a course similar to this case, including pain in
respiration, papilloedema, headaches, and vomiting. B.P. liver and even collapse of the right lower lobe of the
varied between 225/150 and 190/120. E.E.G. was ab- the lung (Davson et al., 1948, Cases 10 and 11).
normal. C.S.F.: protein, 100 mg. per 100 ml.; cells, 24
lymphocytes per cubic mm. Presumptive diagnosis was andOur patient's attacks of pain, the with circulatory collapse
cerebral amoebiasis; courses of emetine (9 gr.-0.58 g.-in dyspnoea appearing during final illness, had been
nine days) and chloroquine (6.4 g. in 14 days) were followed believed to be due to the tracking of an amoebic abscess.
by improvement clinically and in the C.S.F. findings. They were due, however, to multiple infarction. The
episode of drowsiness and headache was presumably hyper-
Further enlargement of the liver, however, soon occurred. tensive
Prolonged attacks of pain, dyspnoea, pallor, and nausea encephalopathy. There was no post-mortem
evidence of amoebic encephalitis.
developed. Attacks increased in severity and duration till The polyarteritis have been caused by hypersensi-
pain became constant, with paroxysmal exacerbations. A tivity to one of themay many drugs given. These included
further course of emetine, 6 gr. (0.4 g.), was given. Further
attempts to locate pus were unsuccessful, and the patient chloroquine, emetine, penicillin, chloramphenicol, "amytal,"
died on June 30, 1951. and aminophylline.
IAN C. GILLILAND, M.D., M.R.C.P.,
Temporary Lecturer and Physician, Dept. of Medicine.
Postgraduate Medical School of London.
PATHOLOGICAL FmNDINOS
GEOFFREY C. MANNINYG, M.B., B.Ch.,
Heart.-Fibrinous pericarditis; weight, 430 g.; left ventri- Medical Registrar, Middlesex Hospital, London.
cular hypertrophy.
Lungs.-Right lung extensively adherent to right hemi- REFERENCES
diaphragm. Davson, J., Ball, J., and Platt, R. (1948). Quart. J. Med., 17, 175.
Pass, I. J. (1935). Amer. J. Path., 11, 503.
Liver.-Weight 1,400 g. Two amoebic abscesses were Sodeman, W. A. (1950). Amer. J. trot. Med.. 30, 141.
present in the right lobe: one, 20 cm. in diameter, at the Van Raalte, H. G. S. (1949). Ibid., 29, 881.