364

replacement. The premature discharge of the child resulted fromthe widespread but grave misconception that the rat poisonconsisted of a short-acting warfarin compound. When the child wastraced a month later he had, despite no evidence of bleeding, aprothrombin time of 23-4 s (control 15) and a PTT of 60 s (control38). Specific factor assays showed decreased vitamin-K-dependentfactors VII (37%), IX (42 %), and X (42%) and a protein in vitaminK absence (PIVKA) level of 28% (normal 0-2%).The reason for the initial discrepancies between prothrombin

time, PTT, and specific factor levels is not known. Clotting profileswere repeated three times on the admission day to monitor theresponse of specific therapy. It is possible that the factor assaysfollowed part of this therapy. There could have been a delay in thefactor assays with a sponaneous rise in factor levels.On clinical grounds there can be little doubt that the prothrombin

time and PTT were correct. Repeatedly high PIVKA levels and thewhole presentation, as recounted in the letter, indicates that this wasa bromodialone-induced coagulation disorder involving the

vitamin-K-dependent factors.

Department of Paediatrics,University of Witwatersrand,Bersham 2013, South Africa M. C. GREEFF

ALARMING ELECTROCARDIOGRAPHIC CHANGESCAUSED BY INADEQUATELY INSULATEDTEMPORARY EPICARDIAL ELECTRODES

SiR,—Temporary epicardial electrodes are commonly used forthe diagnosis and treatment of cardiac arrhythmias after open heartsurgery,l especially valvular and anti-arrhythmic operations. Suchelectrodes (one attached to each atrium and two to the rightventricle) were implanted in a 41-year-old man after successfulendocardial resection of a left free-wall accessory pathway for thecontrol of drug refractory arrhythmias associated with the Wolff-Parkinson-White syndrome. The external ends of the temporaryelectrodes were situated near the lower end of the sternum and were

inadequately insulated in the early postoperative period. Analarming electrocardiogram in V4 was recorded (figure). It was

subsequently shown that both direct and indirect contact (throughconducting gel) between the recording lead of an

electrocardiographic machine and the epicardial electrode couldseverely distort the electrocardiographic appearance by combinedrecording of epicardial electrogram and the surface

electrocardiogram. Changes in the repolarisation phase couldsimulate acute myocardial ischaemia and infarction. Although thechanges were best seen in lead V4, more extensive changes (fromV3-6) could be produced depending on the positions of theepicardial wires and the recording leads and the amount of

conducting gel in the field.

Electrocardiographic appearances recorded in lead V4 with

epicardial electrodes in indirect contact through conducting gel.

Normal electrocardiogram is shown top left. RA and LA = right and leftatrial electrodes and RV = right ventricular electrode.

It is known that epicardial electrodes should be properlyinsulated to prevent electric discharges to the heart from externalelectric fields. We found that inadvertent recording fromuninsulated epicardial electrodes could cause changes in the

electrocardiogram that simulate myocardial damage. Such changesare usually localised to anterior chest leads and are not seen in thelimb leads.

Department of Cardiological Sciences,St George’s Hospital Medical School,London SW17 0RE

C. P. LAUN. STRATIGIS

A. J. CAMM

1. Waldo AL, MacLean WAH Diagnosis and treatment of cardiac arrhythmiasfollowing open heart surgery: Emphasis on the use of atrial and ventricular wireelectrodes. Mount Kisco, NY. Futura Publishing, 1980.

INCIDENTAL NEUROBLASTOMA

SIR,-Dr Kosloske and her colleagues (Sept 5, p 565) report 7cases of neuroblastoma detected "incidentally" duringexaminations for another complaint. 3 patients were more than 12months old at diagnosis. 6 had thoracic neuroblastomas and 1 had anabdominal neuroblastoma. 5 tumours were stage 1,1 stage II, and 1stage III. All 7 children had done well.Mass screening for neuroblastoma at 6 months of age was

initiated at some districts in Japan in 1985 and by the end of 1986,89cases had been detected.1 86 were symptom-free; the other 3 hadfever with sweating, anaemia, and poor weight gain. In 25 (31 %) ofthe 80 cases with abdominal neuroblastoma an abdominal mass wasnot palpable on routine physical examination by a paediatriconcologist, but all 80 abdominal masses were detected byechography, and the patients demonstrated increasing urinaryvanillylmandelic acid (VMA) excretion. The 9 thoracic neuro-blastomas had no abnormal findings on physical examination butwere detected by chest X-ray. 66 neuroblastomas were diagnosedbefore the age of 8 months (the screening being done at 6 months).19 tumours were stage I, 39 stage II, 11 stage VIII, 12 stage IV, and 8were stage IVs. The removed primary masses weighed 4-260 g(median 50).

-

2 children with abdominal neuroblastomas have died-1 with

progressive neuroblastoma at 5 years of age and the other from acomplication of surgery. Both thoracic and abdominal neuro-blastomas detected by screening had a good prognosis.An "incidental neuroblastoma" simply means a small primary

mass which is detected earlier than it would be otherwise. AlthoughKosloske et al suggest that careful physical examination and reviewof routine X-rays may lead to early detection of neuroblastomas, wewould recommend the addition of measurement of urinarycatecholamine metabolites and abdominal echography forabdominal neuroblastomas or chest X-ray for thoracic

neuroblastomas, because we find these examinations to be mostuseful.

Supported by grants from the Japanese Ministry of Health and Welfare.

Department of Paediatricsand Children’s Research Hospital,

Kyoto Prefectural University of Medicine,Kamikyoku, Kyoto, 602 Japan

TADASHI SAWADAHIDEKAZU KAWAKATUYOSHIHIRO HORIITOHRU SUGIMOTO

1. Sawada T, Sugimoto T, Matsumura T, et al. Mass screening for neuroblastoma ininfancy. Presented at the Children’s Hospital of Philadelphia fourth symposium onadvances m neuroblastoma research. (Philadelphia, May 16, 1987).

SOMATOSENSORY EVOKED POTENTIALS ANDSPINAL DECOMPRESSION SICKNESS

SiR,—Or Palmer and colleagues (Dec 12, p 1365) report on spinalcord degeneration in three of eleven divers who died accidentally.We have done an electrophysiological study of ten amateur diversadmitted to hospital with type II decompression sickness. Thesenine men and one woman aged 16-40 had 1-7 years of divingexperience and the alleged greatest depth was 18-41 m. All hadneurological symptoms (paraesthesiae in the legs 8, lower lunbparesis 2, headache or limb pain 7, sphincter disturbance 3). Theneurological examination revealed lower limb paresis (2,

365

Central conduction time (CCTT) from T12 to cortex as function ofconduction distance in ten divers.

There are two points from each patient representing results from left andright tibial nerve stimulation. Solid line and broken lines indicate mean and95% confidence interval of controls.

hyperreflexia (6), extensor plantar responses (4), and hypoaesthesia/dysaesthesia (8).

All patients were put into a pressure chamber and decompressed.Symptoms and signs disappeared within a few days except in thetwo patients with paraparesis. One of the two recovered completelywithin 3 weeks, but the other still had a paresis of the left leg withhyperreflexia and an extensor plantar response 8 months after theaccident. Neurophysiological tests were done 1-2 days after theaccident. Somatosensory evoked potentials (SEP)l were recordedover cortical hand and foot areas (ie, C3 or C4 after median nervestimulation and Cz after tibial nerve stimulation; International10-20 system). Recordings were also made over the supraclavicularfossa and at the C7 spinous process after median nerve stimulation,and over the gluteal crease and T12 spinous process following tibialnerve stimulation. Central conduction time (CCT) between C7 andcortex and between T12 and cortex was calculated. Findings inpatients were compared with values from age-and-sex matchedcontrols.

Latencies of peripheral, spinal, and cortical potentials and centralconduction times (figure) were normal in all patients except the onewho turned out to have a persistent leftsided lower limb paresis.SEPs were recorded in this patient three times during the next 8months and remained unchanged.

This suggests that SEPs can be used to predict the outcome inspinal decompression sickness. Normal neurophysiologicalfindings indicate a good prognosis with later complete functionalrecovery, whereas abnormal findings indicate persistent damage tothe spinal cord, in accord with neuropathological findings in

divers.2,3 SEP measurement seems to be a sensitive test since

subclinical abnormalities have been found in HIV-seropositive menwithout AIDS,’ and major chariges have been revealed in patientswith acute transverse myelopathy.s

Laboratory of Clinical Neurophysiology,Rigshospitalet,Copenhagen, DK-2100 Denmark

TORBEN SMITHWERNER TROJABORG

1 Trojaborg W, Petersen E Visual and somatosensory evoked potentials in multiplesclerosis. J Neurol Neurosurg Psychiatry 1975; 42: 323-30

2. Palmer AC, Calder IM, McCallum RI, Mastaglia FL Spinal cord degeneration in acase of "recovered" spinal decompression sickness Br Med J 1981; 283: 888.

3 Palmer AC, Calder IM, Hughes JT. Spinal cord degeneration in divers. Lancet 1987;ii: 1365-66.

4 Smith T, Jakobsen J, Gaub J, Helweg-Larsen S, Trojaborg W. Clinical andelectrophysiological studies of HIV-seropositive men without AIDS. Ann Neurol(in press).

5 Wulff CH. Evoked potentials in acute transverse myelopathy. Dan Med Bull 1985; 32:282-87

SPINAL-CORD DEGENERATION IN COMMERCIALDIVERS

SiR,—The demonstration by Dr Palmer and colleagues (Dec 12,p 1365) of occult myelin degeneration in three professional divers isalarming. -

There is a tendency to relate risk of serious decompressionsickness to the increasing depth of a dive or to the use of advancedtechniques, like helium and oxygen saturation diving.Paradoxically, diving to over 300 m with helium and oxygen is saferthan shallow diving with compressed air. The safety conferred byhelium and oxygen mixtures compared with compressed air wasfirst noted in the US Navy and attributed to the much lowersolubility of helium in the lipids of the nervous system. Theobservation was confirmed in the North Sea, with many cases ofneurological decompression after diving with compressed air,which is used in the gas-fields off East Anglia. Despite much longerdives, almost no cases were seen after diving in the Northernoilfields where helium and oxygen mixtures are used.2The Department of Energy has funded a study of decompression

sickness in North Sea diving,3 which has shown that about fifteendivers suffer neurological decompression sickness every year. Mostof the cases arise from the use of a military diving technique called"surface decompression", in which full stoppages appropriate to thedepth and duration of the dive are omitted. The diver is brought tothe surface and rapidly recompressed in a chamber on deck tocontrol the release of dissolved nitrogen. Surface decompression isprohibited by law in France.

All divers must start their careers diving with compressed air andseveral young men are made permanently unfit every year becauseof residual neurological damage. Cases have even arisen whensurface decompression has been used during training. Regrettably,despite the recognition of this problem, no concerted effort has beenmade to remedy matters. If demyelination is fourid where there hasbeen no recorded decompression sickness, it is likely that manycommercial divers have more extensive damage, such as that

previously described by Palmer et al .4 This demands urgent action.For diving below 30 m helium and oxygen mixtures should be

used, together with submersible decompression chambers, whichwould improve other aspects of diving safety. These procedures arerequired by law in dives below 50 m. Thus the change to 30 mwould only require a minor revision of the diving regulations.Department of Community Medicine,Wolfson Institute of Occupational Health,Medical School,Ninewells, Dundee DD1 9SY P. B. JAMES1 Behnke AR, Yarbrough OD. Physiologic studies of helium. Navy Med Bull 1938, 36:

542-502. Shields TG, Lee WB. The incidence of decompression sickness arising from

commercial offshore air-diving operations in the UK sector during 1982, 83Aberdeen: Robert Gordon’s Institute of Technology and Grampian Health BoardHyperbaric Medicine Unit, 1985.

3. James PB. A review of neurological decompression sickness. In: James PB, McCallumRI, Rawlins JSP, eds Proc VII Ann Cong Eur Undersea Biomed Soc. CambridgeNorwich Union, 1981: 9-15.

4. Palmer AC, Calder IM, McCallum RI, Mastaglia FL Spinal cord degeneration in acase of recovered spinal decompression sickness. Br Med J 1981, 283: 888

PLASTIC DEVICES: NEW FIELDS FOR OLDMICROBES

SIR,-Your Jan 2/9 editorial suggests that early treatment ofdeveloping infection associated with plastic devices may besuccessful but, when infection is established, antimicrobial therapyis usually futile. Using a novel model we have studied the effect ofseveral antibiotics on cannulae colonised with a slime producing,fully antibiotic sensitive strain of Staphylococcus epidermidzs. 1

Cannulae can become colonised with bacteria within 20 min ofinitial contact. Once attached these bacteria may remain viable inthe presence of apparently lethal concentrations of various

antibiotics. Of the anti-staphylococcal antibiotics tested,vancomycin and ciprofloxacin were most effective at reducing thenumber of colonising organisms. However, in many experimentssome bacteria remained attached and viable despite exposure evento these antibiotics (table). Similarly exposure of staphylococci tothe antibiotics for an hour before addition of cannulae did not

prevent subsequent colonisation.Thus prophylaxis for an hour before insertion of plastic devices

may be inadequate in the prevention of colonisation and longerperiods should be considered. Agents such as vancomycin andciprofloxacin are potentially most useful in the treatment ofline-associated infections but success may be limited, as commonly