352

11 Nabarro D, Chinnock P. Growth monitoring: inappropriate promotionof an appropriate technology. Soc Sci Med 1988; 26: 941.

12 Editorial. Growth monitoring: intermediate technology or expensiveluxury? Lancet 1985; ii: 1337-38.

13 Miller BD. Wife-beating in India: variations on a theme. In: CountsDA, Brown JK, Campbell JC, eds. In sanctions and sanctuary: culturalperspectives on the beating of wives. Boulder: Westview Press, 1992:173-84.

14 Liddle J, Joshi R. Daughters of independence: gender, caste and classin India. London: Kali for women and Zed Books Ltd, 1986.

15 Rohde JE. Editorial. Indian J Pediatr 1988; 55: S1.

16 Shekar M, Latham MC. Growth monitoring can and does work: anexample from the Tamil Nadu integrated nutrition project in ruralsouth India. Indian J Pediatr 1992; 59: 5.

17 Gopalan C. Growth charts in primary child-health care: time forreassessment. Nutrition Foundation of India Bulletin 1992; 13 (3): 1.

18 Chatterjee M. On the nutrition component of TINP: some lessons andissues. Workshop on Tamil Nadu Integrated Nutrition Project, July31-Aug 3, 1989, Madras.

19 Balachander J. TINP, India, in managing successful nutritionprogrammes. Geneva: ACC/SCN, 1991. State-of-the-Art series no 8:97-107.

Personal paper

Deep-vein thrombosis and pulmonary embolism

The differential diagnosis between myocardial infarction(MI) and pulmonary embolism (PE) is rarely discussed intextbooks. My experience suggests that this is a seriousomission. PE should be considered, as well as MI, in anypatient with dyspnoea or atrial fibrillation of recent originfor which there is no obvious cause.

In 1968, about 10 days after a transatlantic flight,I experienced an aching pain in the left buttock and lumbarregion. 2 days later my left leg swelled up over a matter ofminutes, and the lumbar pain disappeared. I can find noreference to lumbar pain as a premonitory symptom ofdeep-vein thrombosis (DVT) but have since come acrossanother doctor with an identical history. The lumbar painmay have been due to venous congestion from thrombosisof a pelvic! or lumbar vein, and this may have been relievedwhen the venous return diminished, due to extension of thethrombus into the femoral and great saphenous veins. Afterinitial treatment with heparin followed by warfarin theswelling gradually subsided, leaving only some dilatedveins in the calf and round the internal malleolus.

Nothing further happened until 1987 when I noticedmild exertional dyspnoea with a regular pulse. The samenight I was woken by a grossly irregular heart beat whichwas confirmed as atrial fibrillation by a general practitionerthe next morning-and by an electrocardiogram when I wasseen in the afternoon by a cardiologist. The fibrillation wasintermittent, each attack lasting 2-3 hours. The provisionaldiagnosis was paroxysmal atrial fibrillation due to an MI,though the ECG showed no evidence of infarction. Anormal rhythm was rapidly restored by digoxin, and I

returned to London where I was seen by another cardio-logist who also thought an MI to be the most likelydiagnosis. Both resting and exercise ECGs were normal, aswere a chest X-ray and an echocardiogram. There had beenno change in the veins in my left leg.Over the next two weeks I maintained normal rhythm but

the dyspnoea varied unpredictably in severity. At its worst,usually after mild exertion, I experienced a bursting pain inthe precordium. One morning, after running for a bus, I

Victoria Mill House, Framlingham, Woodbrldge, Suffolk IP13 9EG(J Black FRCP)

suddenly felt cold and clammy. Unwisely I continued withmy journey, but on the way back I felt so ill that Iabandoned the bus and took a taxi home, where I

telephoned my wife at work and our general practitioner’ssurgery. When she heard that I had taken a taxi my wifeknew at once that something was seriously wrong. Thedoctor I spoke to was not our usual one and needed to beconvinced that I was not suffering from influenza before heagreed to visit me. By the time my wife and the doctor hadarrived I was feeling better, and my pulse and bloodpressure were normal. An appointment was made to see thecardiologist and I was admitted to hospital. Chest X-rays,ECGs, and a coronary angiogram were normal, but apulmonary arteriogram revealed occlusion of the upperbranch of the right pulmonary artery. After a short course ofheparin I was given warfarin for 6 months.

2 months after stopping the warfarin, I went on holidayon an overnight flight, with very little leg room. A weeklater a small area of venous thrombosis on the dorsum of myleft foot developed. On my return to London I noticedfrequent extrasystoles, and after a few days I once more hadmild dyspnoea on exertion. A ventilation-perfusion scanrevealed three areas of hypoperfusion in the right lung. A

‘

recurrence of PE was diagnosed and I was admitted andgiven heparin for a week and warfarin indefinitely.Lumbar pain as a presenting symptom of DVT may be

more common than its absence from published worksuggests. Aeroplane journeys, especially overnight flights,are a well-known risk factor for DVT and PE. For some i

weeks before the first episode of PE I had been editing abook while seated on a wooden slatted chair. This probablyinitiated a venous thrombus which lodged in the pulmonaryartery. The initial diagnosis of MI was justified though itcould be debated whether an infarct severe enough to causedyspnoea and atrial fibrillation would have failed to

fproduce any ECG abnormality up to 3 weeks later. Atrialfibrillation, and less commonly, atrial flutter occur in

7-10% of cases of MF but in only 3% of episodes of PE3 andin many textbooks the association of PE with arrhythmias isnot mentioned. The development of extrasystoles duringthe second episode may well have been an indication ofstrain on the myocardium since it is well recognised thatextrasystoles often precede atrial fibrillation. Although

precordial pain is characteristic of MI or myocardialischaemia, there are a few descriptions of precordial pain inPE; the pain may be due to impaired transpulmonary bloodflow, with reduction in venous return to the left heart anddiminution in coronary perfusion. Alternatively the painmay be due to acute dilatation of the right ventricle, causingischaemia of the right ventricle. The variation in the

intensity of the dyspnoea and the sudden deterioration afterrunning for a bus would suggest a saddle embolus whichwas finally dislodged and occluded a main branch of thepulmonary artery.What lessons can be learned? Aeroplane journeys are a

hazard, especially for anyone with a history of DVT."Knees bend" exercises every 2-3 hours are probably thebest prophylaxis. A cushion should be used when sitting forlong periods on a hard chair. It is taught that significantemboli do not arise from peripheral vein thromboses, butsuperficial thrombophlebitis may indicate the simultaneousdevelopment of a DVT.4PE should be considered when dyspnoea or atrial

fibrillation develop for no obvious reason. The textbook

description of PE with pleuritic chest pain, haemoptysis,and changes in the chest X-ray probably occurs in only aminority of cases. The gradual onset of worsening dysp-noea, with or without arrhythmia, is probably thecommonest presentation. Finally, after one episode of PE inanyone with a previous history of DVT, it seems wise tocontinue warfarin indefinitely.

I hope that this description of my symptoms and myamateurish attempt to interpret them may lead to a betterannreciation of the clinical nicture of PE.

References

1 Ogston D. Venous thrombosis: causation and prediction. Chichester:Wiley, 1987: 52.

2 Julian DG, Camm J, Fox KM, Hall RJC, Poole-Wilson PA, eds.Diseases of the heart. London: Baillière Tindall, 1989: 515.

3 Sasahara AA, Sharma GVRK, Pietro DA. The clinical diagnosis ofacute pulmonary embolism. In: Hirst J, ed. Venous thrombosis andpulmonary embolism: diagnostic methods. Edinburgh: ChurchillLivingstone, 1987: 128-29.

4 Bergqvist D, Jaroszewski H. Deep vein thrombosis in patients withsuperficial thrombophlebitis. BMJ 1986; 292: 658-59.

BOOKSHELF

The Most Solitary of Afflictions

Madness and Society in Britain, 1700-1900. Andrew Scull. New Haven: Yale University Press. 1993. Pp 442. £29.95/$45.00. ISBN 0-300050518.

Madness, madhouses, and mad-doctors have provided medical his-

torians over recent years with much

scope for conjecture about the Englishresponses to madness in the eighteenthand nineteenth centuries. In mid-

eighteenth-century England, the madwere largely undifferentiated from

vagrants, the poor, and the mentallyhandicapped in society. Yet 100 yearslater, insanity was recognised as a

disease that was treatable by doctorswithin a society created specifically forthe mad: the asylum.

Conventionally, as Scull points out,this change in response to the mad is known as "reform" of the "treatmentof the mentally ill" and is attributed tonineteenth-century humanitarianism.However, this explanation does notsuffice for the anti-psychiatrists or

for Scull. Szasz’s claim that madness is :the product of social labelling, andFoucault’s concept of reason’s rep-ression of unreason are cursorily dis-missed. Scull argues, convincingly,that the roots of change are embeddedin much broader transformations of

English political and social structure,and especially in the growth of capi-talism.

Scull’s argument is not new. He putforward the same theory in his much-acclaimed study of the history of mad-ness published in 1979. The Most

Solitary of Afflictions is essentially arevised edition of Museums of Mad-ness, although many more referencesare cited and further details (such as ofthe treatments used and of the mean-

ings of madness) are included. Scull’s1993 version is a scholarly, well-

illustrated, and enjoyable interpreta-tion of the history of eighteenth andnineteenth century lunacy "reform",despite his grim portrayal of the role ofthe medical profession in the rise of"asylumdom".

Scull points out that for doctors toassert their authority over the care ofthe mad, a dramatic change in the

cultural meaning of madness had totake place. For most of the eighteenthcentury, madness was thought to

represent loss of reason, the differen-

tiating feature between man and

animals. Inhumane treatment of themad was the norm. Brute force, fear,and coercion were commonly appliedto the minority of the mad who were ininstitutions such as Bethlem.

: From around the 1750s, increasingnumbers of doctors began to publicisetreatments that were based, in general,on humoral principles. Violent

purging, blood-letting, and shocktreatment with cold water were just afew of the methods tried in the evolv-

ing "mad-business". George III’s

madness, says Scull, helped the medi-

cal profession to lay claim to insanityas an illness because brutish condem-nation of the King was difficult.

In 1810, a threat to the mad-doctorsemerged. Influenced by two compet-ing philosophies, Evangelicism andBenthamism, moral treatment was

developed by a Quaker layman (Wil-liam Tuke) at the York Retreat. Tukeadvocated a policy of non-restraintwhen possible, and regarded the lu-natic as a rational human being. Curewas recognised to be possible. Initialhostility from the medical professionwas followed by claims that moraltreatment should be supervised bydoctors. Medical spokesmen includ-ing Thomas Wakley, editor of TheLancet, emphasised that "insanity[was] invariably associated with bodilydisease" and physical cures for thedisease of the brain were publicised injournals for the new profession.