847

fall. In 1976-78 17/33 (52%) of infants weighing 501-1000 gand 16/95 (17%) of those weighing 1001-1500 g died, givinga total mortality-rate for infants weighing 1500 g or less of33/128 (25-8%). Trend-analysis of mortality-rates for VLBWinfants born in U.C.H. from 1961 to 1978 shows a highly sig-nificant (p << 0.001) and continuing reduction in mortality.The prevalence of major handicap in surviving VLBW in-

fants born at Hammersmith Hospital in 1961-75 was 5.3%(19/357) of the total population of infants’ or 13-3% (19/143)of the long-term survivors. Our follow-up study at U.C.H. didnot start until 1966. The prevalence of major handicap overthe ten years 1966-75 was 4.4% (11/248) of the total popula-tion or 8.0% (11/138) of the long-term survivors.2 The preva-lence of major handicap in surviving infants from the two hos-pitals is not, therefore, very different.We think that two main conclusions can be drawn from the

U.C.H. study. Firstly, the introduction of modern methods ofobstetric and neonatal care was associated with, and we believecaused,2 a large and progressive increase in the chances of sur-vival for VLBW infants. Secondly, the vast majority of the in-fants who survive are proving at follow-up to be normal

healthy children.

We thank Mr Derek Lowe of the M.R.C. Statistical Unit for his

help.

Departments of Paediatrics and Obstetrics,University College Hospital and Medical School,London WC1

ANN L. STEWARTE. O. R. REYNOLDS

BLINDNESS AND PARAPLEGIA IN SEVERECHILDHOOD HYPERTENSION

SIR,&mdash;Dr Hulse and colleagues (Sept. 15, p. 553) describethree children in whom optic atrophy and blindness developedduring episodes of severe arterial hypertension. They state that"there is much evidence refuting a clear association betweenraised intracranial pressure and hypertension." However, inone of the four references cited, Taylor et al.’ demonstratedthat there is such an association in the presence of papill-edema. Hulse et al. do not report on CSF pressures. Were theymeasured? Might these patients have had severely increasedCSF pressure (pseudotumor cerebri)? If their CSF pressureswere above 600 mm, would shunting have been considered?High CSF pressure can increase arterial pressure, decrease cere-bral perfusion, and contribute to optic atrophy.

Department of Medicine,Albert Einstein College of Medicine,Bronx, N.Y. 10461, USA QUENTIN B. DEMING

**This letter has been shown to Dr Hulse and colleagues,whose reply follows.-ED. L.

SIR,&mdash;Dr Deming suggests that our three patients had pseudo-tumor cerebri and the effects of raised intracranial pressure.However, the renal aetiology of their systemic hypertension wasclearly demonstrated, and there was’no evidence of ventricularcompression on the computerised tomographic scans. CSFpressure was not measured because it is very labile in hyper-tensive encephalopathy and the results are uninterpretable,quite apart from the unacceptable risks of such procedures.Taylor et al. measured CSF pressure in 200 patients with andwithout papilledema and stated that "in hypertensive patients

2 Stewart A, Turcan D, Rawlings G, Hart S, Gregory S. Outcome for infantsat high risk of major handicap. In: Major mental handicap: methods andcosts of prevention (Ciba Found Symp 59). Amsterdam: Elsevier, 1978:151-64.

3 Reynolds EOR. Neonatal intensive care, and the prevention of major handi-cap. In: Major mental handicap: methods and costs of prevention (CibaFound Symp 59). Amsterdam: Elsevier, 1978: 77-106.

1 Taylor RD, Corcoran AC, Page IH. Increased cerebrospinal fluid pressureand papill&oelig;dema in malignant hypertension. Arch Intern Med 1954; 93:818-24.

1. Ledingham JGG, Rajagopalan B. Cerebral complications in the treatment ofaccelerated hypertension. Quart J Med 1979; 48: 25-41.

2. Thien TA, Huysmans FTM, Gerlag PGG, Koene RAP, Wijdeveld PAGAB.Treatment of severe hypertension and of hypertensive crisis by infusion ofdiazoxide. Clin Pharmacol Ther 1979; 25: 795-99.

3. Mroczek WJ, Leibel BA, Davidov M, Finnerty FA Jr. The importance of therapid administration of diazoxide in accelerated hypertension. N Engl JMed 1971; 285: 603-06.

with papilledema the statistical significant -correlation(between diastolic pressure and CSF pressure) was not suffi-cient to indicate causation" and that "papilledema and in-creased CSF pressure are specific manifestations or hyperten-sive disease unrelated as cause and effect." Only 1 of their 400measurements of CSF pressure was over 600 mm. Surely thetreatment of hypertensive encephalopathy is to lower the sys-temic blood-pressure.

Hospital for Sick Children,London WC1N 3JH

J. A. HULSEM. J. DILLOND. S. I. TAYLOR

ACUTE BLOOD-PRESSURE REDUCTION INMALIGNANT HYPERTENSION

SIR,&mdash;Although we agree with your Sept. 8 editorial on thedangers of acute blood-pressure reduction in malignant hyper-tension, we would like to add the following comments.The high incidence of neurological complications reported

by Ledingham and Rajagopalan cannot be ascribed solely tothe use of diazoxide. Their treatment protocol was unusuallyaggressive. The mean maximum reduction of the averagearterial pressure (MAP) in their patients was 50% (range34-71%). Most patients received a combination of differentdrugs that were often given several times, so there is no con-vincing evidence that diazoxide alone was responsible for theserious complications. We have treated 35 patients with bolusinjections of diazoxide and have not encountered neurologicalcomplications. This might be related to the fact that the meanmaximal MAP decrease achieved was 29% (range 10-48%)which is much smaller than that attained by Ledingham andRajagopalan. However, it cannot be denied that the rapid in-jection of diazoxide is potentially harmful; and since 1975 wehave been administering diazoxide by slow infusion and wehave reported earlier on the results in 15 patients.2 We havenow treated 29 patients in a hypertensive crisis. Diazoxide (15mg/ml) was administered at a constant rate of 15 mg/min toa total amount of 5 mg/kg body-weight, which resulted in aninfusion-time ranging from 20 to 30 min. In contrast to whathas been reported by others3 this way of administering diazox-ide was effective. The mean maximal reduction in MAP was25% (range 13-33), and this value was reached after a meantime of 26 min. Neurological complications did not occur. Theinfusion results in a gradual decline of the blood-pressure andcan easily be interrupted if the initial response is too great.Since monitoring of the patient with this approach is muchsimpler than with the fast (and short) acting drug nitroprus-side, we consider slow infusion of diazoxide to be the treatmentof choice in hypertensive crisis.

Department of Internal Medicine,Division of Nephrology,St. Radboudziekenhuis,University of Nijmegen,Nijmegen, Netherlands

TH. THIENF. T. M. HUYSMANSR. A. P. KOENE

DEEP-VENOUS THROMBOSIS IN CHILD DURINGHALOFEMORAL TRACTION

SIR,&mdash;Postoperative deep-venous thrombosis (DVT) of thelower limb is rare in children, and it has not been describedas a complication of skeletal traction in this age-group. Halo-femoral traction is used for preoperative correction of scoliosisin otherwise fit children. A halo is attached to the skull byscrews and Denham pins are inserted through the supracondylar