1035 have occurred in 46 women with SLE who have attended Hammersmith Hospital".

RECURRENT SUBARACHNOID HÆMORRHAGES IN

Princess Alexandra Hospital, Harlow, Essex CM20 1QX

SIR,-Common causes of subarachnoid hemorrhage include hypertensive arteriosclerotic disease, and arteriovenous malformations but there are many other possible causes, including coagulation disorders and anticoagulant therapy. 1,2 We describe here a patient with recurrent subarachnoid haemorrhages and Hageman factor (factor xn) deficiency. A 32-year-old male was admitted to hospital on May 24,1977, because of persistent headaches that woke him at night and lasted for five days. He also vomited and had mild fever. Clinical neurological examination was normal but his blood-pressure was 160/95 mm Hg. The diagnosis of subarachnoid haemorrhage was supported by the cerebrospinal-fluid findings (see table). Laboratory findings were normal except for ’Thrombotest’ (Medica, Finland) values of 46-48% (normal lower limit 70%). Occult blood was detected in faeces. A week later electroencephalography (E.E.G.) showed diffuse episodic theta activity in the left posterior temporal lead, and isotope scanning revealed some diffuse uptake in the same area, suggesting intracerebral haemorrhage. On carotid angiography, done 2 weeks from the beginning of symptoms, no aneurysms were detected; minor dislocation of the middle line frontal arteries was observed, possibly due to secondary local cerebral oedema. While in hospital the patient had signs of recurrent subarachnoid haemorrhage and lumbar punctures confirmed the diagnosis (table). After 4 weeks the patient left hospital with no symptoms, his brain scan being unchanged. 4 days later the patient had another intense headache which lasted for several days, and he returned to hospital. c.s.F. was contaminated with artefactual blood. However, the sample was xanthochromic. After 2 weeks’ bed rest the patient was dis-

pregnancies

DENIS HARDY

C.S.F. LACTIC ACID FOR DIFFERENTIAL DIAGNOSIS OF MENINGITIS

SIR D’Souza

et

al. have commented

on

the value of esti-

mating cerebrospinal-fluid (c.s.F.) lactic-acid concentrations in the differential diagnosis of meningitis, but their letter left several aspects of the merit of c.s.F. lactic-acid assays unresolved. For two years we have been using the Boehringer lactate test kit to measure lactic acid in C.S.F..2 We have done more than 800 such measurements in children. A level of 25 mg/dl seems to be a cut-off point in the differentiation between viral and bacterial meningitis: c.s.F. lactates above 30 mg/dl were compatible with a diagnosis of bacterial meningitis, while lactic-acid levels below 25 mg/dl were compatible with viral meningitis or no meningitis. With 5 exceptions, the test has been remarkably free of false positives or false negatives. We find the method very sensitive in the detection of bacterial meningitis, providing cellular responses to the bacteria had occurred, as indicated by finding more than 10 white blood-cells/µl in the c.s.F. The only exceptions were 3 cases of Staphylococcus epidermidis meningitis after installation of shunts; c.s.F. lactate values stayed below 25 mg/dl despite positive c.s.F. cultures and raised white-blood-cell counts in the c.s.F. In 2 other newborn babies with bacterial meningitis and no cellular response c.s.F. lactic-acid concentrations were not raised at first; however, 8-10 h later, on a repeat lumbar tap, when the cell-count had risen above 10 cells/µl, lactic-acid levels also rose. Normal levels of c.s.F. lactate in the newborn may be slightly greater than those noted as normal in older children. D’Souza et al. indicated that some cases of part-treated bacterial meningitis had lactic-acid levels similar to those of normal c.s.F. or of c.s.F. in viral meningitis; however, they did not indicate the duration and type of previous treatment. We have found’ that lactic-acid levels in the c.s.F. fall to normal after 2 or 3 days of therapy, and in D’Souza’s patients the low lactic-acid concentrations may represent just such a response to therapy. In tuberculous meningitis, we find that c.s.F. lacticacid levels are high in the initial stages of the infection,3 but with therapy they slowly regress to normal over 7-14 days. Here again, low lactate levels cannot be evaluated without knowledge of the duration of acute tuberculosis therapy. It is difficult to comment on the higher-than-normal values found by D’Souza et al. in some cases of viral meningitis because the technique of reading lactic-acid varies from one laboratory to another. However, their data suggest no overlap between the viral and the purulent meningitis cases, where a line of demarcation can be drawn at 43 mmol/l (39 mg/dl). extensive experience lactic-acid measurements are we believe that this rapid test should be used as an adjunct to the early differentiation between bacterial and viral meningitis. Data in cases of treated bacterial meningitis have to be evaluated according to type, duration, and amount of therapy given to the patient before c.s.F. lactate was measured. ITZHAK BROOK WILLIAM J. RODRIGUEZ Children’s Hospital National Medical Center, GUIDO CONTRONI Washington, D C. 20010, U.S.A. SYDNEY Ross In

our

reliable, and

PATIENT WITH HAGEMAN FACTOR DEFICIENCY

charged. For over a year the patient was healthy, except for occasional nosebleeds. In October, 1977, a brain isotope scan was normal. The patient took drugs to control mild hypertension. In August, 1978, the recurrent subarachnoid hxmorrhages necessitated transfer to a central hospital. Episodic theta activity was seen, principally in the left lateral and temporobasal leads of the E.E.G. The middle-line dislocation was not observed on echo encephalography. A brain scan was normal. On Sept. 6, he had another attack. Carotid and vertebral angiography revealed neither aneurysms nor arteriovenous

malformations. The main laboratory findings were: slightly increased alanine aminotransferase (56-68 I.u./l); abnormal clottingtime (20 min); normal bleeding-time; occult blood in faeces; thrombotest 70-66%; partial thromboplastin time, which measures the factors vill, ix, xi, and xn, clearly prolonged at more than 180 s (normal upper limit 43); factor-xn deficiency (5% of normal plasma value); and normal bone-marrow. Earlier the patient had been healthy and he had no history of liver disease. Clonidine, hydrochlorthiazide, and potassium had been used to control hypertension since the first hxmorrhagic episode. The family history revealed no bleeding disorders. Besides recurrent subarachnoid haemorrhages this patient had two other signs of an abnormal clotting system-nosebleeds and traces of blood in faeces. There was no clear blood disorder, no evidence of collagen disease, no coagulant-factor abnormalities except for Hageman factor deficiency, no aneurysms, and no arteriovenous malformations. The patient had mild hypertension; this was being treated but a slight contributory effect of blood-pressure cannot be excluded. His Hageman factor value was only 5% of normal. Complete absence of factor xu requires two abnormal alleles;’* the sibH. I., Reveich, M. in Scientific Approach edited by E. S. Goldensohn and S H. Appel), vol.

1. Hurtig, 1

D’Souza, E., and others. Lancet, 1978, ii, 579. 2. Controni, G., Rodriguez, W. J., Hicks, J. M., Ricke, M., Ross, S., Friedman, 3

G., Khan, W. J. Pediat 1978, 91, 379. Brook, I., Bricknell, K. S., Overturf, G. D., Finegold, 1978, 137, 384.

S.

M. J infect. Dis.

to

Clinical

i, p. 769.

Neurology Philadelphia,

1977

2. Pakarinen, S Acta neurol. scand 1967, suppl. 29, p. 43. 3. Silverstein, A. Archs Neurol 1960, 3, 141. 4 Colman, R. W., Wong, P. Y Thrombos Hœmostas. 1977, 38, 751.

C.S.F. lactic acid for differential diagnosis of meningitis.

1035 have occurred in 46 women with SLE who have attended Hammersmith Hospital". RECURRENT SUBARACHNOID HÆMORRHAGES IN Princess Alexandra Hosp...
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