THE EYE IN GENERAL VASCULAR DISEASE HYPERTENSION AND ARTERIOSCLEROSIS

61 Pages·2007·19.13 MB·English

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Brit.J. Ophthal. (1957) 41, 641. O
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THE EYE IN GENERAL VASCULAR DISEASE* l: firs
HYPERTENSION AND ARTERIOSCLEROSIS t p
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BY lish
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ROBERT LEISHMAN d a
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DepartmentofOphthalmology, UniversityofGlasgow 1
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THE HUMAN eye is a natural transparent chamber and its retinal vascular 1
3
system is easily accessible to direct and repeated observations in vivo. The 6
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behaviour of its arterioles, capillaries, and venules in health and disease jo
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should provide data applicable to the study of systemic vascular disorders. 1
With the introduction ofthe ophthalmoscope, a little over a hundred years .11
ago, abnormal fundus pictures were soon observed to occur in conditions .64
1
ofgeneralized disease, and, since then, many clinical observations and histo- o
n
logical studies have been contributed to the ophthalmic literature. It is, 1
however, a serious limitation of ophthalmoscopy that, even with the most N
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modern instruments, a direct study ofthe retinal blood vessels at a cellular ve
m
level is not possible, and it has proved most difficult to translate the descrip- b
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tive terminology derived from ophthalmoscopic studies into terms of basic cr 1
pathology. o9
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It has been said, with perhaps somejustification, that "specialism, though yrig7. D
favourable to the accumulation offacts, is bad for the philosophy ofknow- ht.ow
ledge". Most ophthalmologists would claim to recognize "copper-wire" n
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and "silver-wire" arteries in the retina, butfewwould profess to have a clear a
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conception ofthe meaning ofthese appearances in detailed terms ofmorbid e
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histology. There is a danger that the faithful recording of clinical signs, fro
such as "copper-wire" arteries, calibre variations, arterio-venous ratios, and m
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the vagaries of the vascular light reflex, may become the self-imposed limit ttp
of legitimate clinical thought concerning the retinal vessels; and, having ://b
built up a series ofuncommon attributes, it is easy to convey the implication jo
that the retinal vessels are fundamentally different from other blood vessels. .bm
Inthefield ofgeneral medicine, theinvention ofthe sphygmomanometerin j.c
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1896 came at a time when physicians were preoccupied with arteriosclerosis, m
and, almost immediately, attention was diverted to a new factor in vascular o/
n
disease, highblood pressure. This disorder has come to be known as hyper- M
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tension; its study from many different aspects has led to great advances in rc
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the understanding of cardiovascular derangements. Abundant data are 8
now available with regard to both hypertension and arteriosclerosis, but the , 2
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data lack integration; it is still not generally appreciated that these disorders 2
3
are to some extent complementary to one another, so that neither condition b
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* ReceivedforpublicationMay6,1957. ue
41 641 s
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B
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642 ROBERT LEISHMAN O
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can be adequately assessed without considering the effect ofthe other. For th
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this reason, physicians at the present time find it difficult to classify their lm
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cthaissesisofacamradjioorvahsicunldarrandcieseatsoetihnetoagprpoliucpastiwohnicohfatrheeclnieniwcalklnyohwolmeodggeenetooutsh;e l: firs
assessment and management of cases, and to the rational use of the many t p
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new hypotensive drugs which are now becoming available. b
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Since conventional ophthalmoscopic interpretations and descriptive ocular h
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data do not appear to fit well with modern conceptions of related systemic d
a
diseases, it might be more profitable to reverse the method of approach. s
1
After consideration of the knowledge derived from research along general 0
.1
clinical, experimental, and pathological lines, a working hypothesis integrat- 1
3
ing hypertension with arteriosclerosis has been formulated, and this hypo- 6/b
thesis has been tested in the ocular field. jo
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1
GENERAL CONSIDERATIONS .1
1
The existence of arterial disease has been known for several centuries. .64
1
The atheromatous lesion was observed first. Atheroma occurs in arteries of o
n
all sizes; it is a patchy, subendothelial, fatty, degenerative lesion with associ- 1
ated fibrosis. It occurs with, or without, high blood pressure, and its origin N
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is not known. ve
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Later, the name arteriosclerosis was coined to describe a diffuse hardening b
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or stiffening of the arteries, contrasting with patchy atheroma. The com- cr 1
mon type is that which is due to high blood pressure. The initial response op95
inthe arterywallisphysiological hypertonus; thisisfollowed byhypertrophy yrig7. D
and hyperplasia in the media, and iftime is allowed, by replacement fibrosis, ht.ow
changes which are considered to be ofa reactive nature. n
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It is to Allbutt (1896), that we attribute the recognition of high blood a
d
pressure as a disease entity with a course of its own. He segregated the e
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condition during a clinical study of arteriosclerosis. His essential thesis, fro
however, was not so much the recognition of hyperpiesia, but rather the m
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differentiation of the decrescent from other types of arteriosclerosis. De- ttp
crescent or involutionary sclerosis is defined as an ageing process affecting ://b
arteries and arterioles, appearing histologically as a relative or replacement jo
fibrosis ofpatchy distribution. The condition is not caused by, but may be .bm
associated with, high blood pressure. j.c
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It was natural, in the first instance, that arteriosclerosis and high blood m
pressure should be regarded as cause and effect, and, when this assumption o/
n
was discredited, interest in arteriosclerosis waned. But, although arterio- M
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sclerosis does not produce high blood pressure, we have seen that continued rc
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hypertension may ultimately cause reactive sclerosis. 8
Hypertension is now considered to result from increased peripheral resist- , 2
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ance, whichinturnis due to generalized andwidespreadhypertonus. Tonus 2
3
is a sustained physiological contraction and is not to be confused with spasm b
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which implies a sudden violent contraction oflimited duration. The main- g
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B
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THE EYE IN GENERAL VASCULAR DISEASE 643 O
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tenance of sustained tonus is not associated with increased expenditure of tha
energy, for the tissue, while in this condition, uses no more oxygen than lm
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wtehnesnioinn(tLhoevartetlaExveadnsst,ate1,94e1v).en though it may be exerting quite considerable l: firs
High diastolic pressures have been shown to cause necrotic lesions in the t pu
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walls of arterioles, but arteriosclerosis is thought to provide some defence lis
against the necrotizing effects of severe hypertension (Wilson and Byrom, he
d
1939). This concept ofdefence by sclerosis is conceived in the limited sense a
s
that the reactive changes induced in a vessel wall as a result ofhypertension 1
0
appear to protect the wall from the more severe acute degenerative lesions .1
1
of high blood pressure. The idea of "defence by sclerosis" may have a 3
6
muchwiderapplicationthanthiswithregardto highbloodpressure. Sclero- /b
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sis may not only protect the wall from necrosis, but also, may in some cases .4
predetermine, and in others modify, the whole course of the hypertensive 1.1
disorder, a theme which we shall now proceed to develop more fully. 1.6
4
1
HYPOTHESIS AND ARGUMENT on
Ifwe accept Allbutt's differentiation ofinvolutionary sclerosis as an ageing 1 N
process in the arteries, independent of, but sometimes associated with, high o
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blood pressure, we may divide the general population of non-hypertensive m
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subjectsintotwo groupsinordertoconsidertheeffects ofhighbloodpressure e
upon them: cr 1
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(1) Those significantly affected by involutionary sclerosis. yrig7. D
(2) Those not affected. ht.ow
Involutionary sclerosis is of almost universal occurrence after the sixth nlo
decade (Duke-Elder, 1940), and must therefore be regarded as a normal ad
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concomitant of old age. It may occur prematurely in younger persons, d
whereas in some elderly people it may have progressed little at an advanced fro
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age. It commonly affects the aorta and larger arteries, but may also be h
found in the arterioles. Fibrosis ofthe larger vessels will result in elevation ttp
of the systolic pressure without corresponding elevation of the diastolic ://b
level, provided the heart muscle is sound and attempts to maintain the jo.b
peripheral circulation. m
The ophthalmoscopic features ofthe retinal arterioles in senile involution- j.co
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arysclerosisarewellknown(Fig. 1,overleaf). Thearteriolesappearrelatively o/
straight anddiffuselynarrow,withacute-angledbranchings, andthe colourof n
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the blood column is ofdiminishedintensity. Ithas been suggested thatthis
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appearance is due to contraction of maturing fibrous tissue in the walls of rc
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the vessels, but histologists have found no evidence of diffuse fibrosis or of 8
fibrous thickening ofthe vessel walls. It is probable that the pale, straight, , 2
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narrow retinal arterioles of normal old age, are merely a manifestation of 23
lowered peripheral pressure resulting from relative rigidity of the larger by
arteries. Patchyrelativefibrosismaywellbepresentinsuchretinalarterioles, gu
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644 ROBERT LEISHMAN O
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7~~~~j%h~ .~~..~.g~~y.~..FIG..~1..-D.i~adgraLm ~sof tseni~l~e dretina~l blis ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
sclerosis without hypertension (blood he
pressure 225/85). The arterioles are d
* diffuselystraightandnarrow,withacute- as
angledbranchings, and thecolourofthe- 1
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tadnclbldood column is diminished. .1
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but since there is no increase of wall thickness and no deposition of 4
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abnormal elements, there should be no demonstrable alteration in the trans- o
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lucency ofthe arteriolar wall. 1
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Hypertension, by definition, means a persistent elevation of both the sys- o
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tolic and diastolic levels of blood pressure. It is considered to result from e
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the increased peripheral resistance offered by widespread diffuse arteriolar b
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hypertonus. This conception assumes that the arterioles are capable of cr 1
diffuse active constriction and takes no account of the state of the vessel op95
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walls with regard to fibrosis. Rigidity ofthe large arteries will tend to oper- rig. D
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ate against elevation of the diastolic pressure, and patchy fibrosis of the t.ow
arterioles will tend to reduce the area capable' of effective hypertonus, so nlo
lessening the degree of increased peripheral resistance. Thus, if hyper- a
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tension ensues in a person whose vessels are significantly affected by involu- d
tionary sclerosis, he will be protected from serious elevations of diastolic fro
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pressure in proportion to the degree and extent of his sclerosis. h
Should hypertension occur in senile arterioles (Fig. 2), only those portions ttp
which are unaffected by fibrosis and still contractile, will become hypertonic; ://b
the blood column will become more narrow, and, since it is less bulky, will jo.b
appear less red in colour when seen with the ophthalmoscope. In other m
portions of the wall, contractile elements will have been degraded into col- j.co
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lagen fibres without actual increase in wall thickness. Such portions, with o/
reduced contractility, will tend to dilate passively as a result of raised pres- n
sure; the blood column will become wider and more intense in hue, and M
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elongation of the vessel wall will be revealed by slight localized curving of rc
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the wide portion of the column. In the course of time, as involutionary 8
sclerosis advances, replacement fibrosis will extend into the hypertonic por- , 2
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2
tions; the fibrotic segments will become confluent, and the whole vessel will 3
then appear diffusely wide, red, and tortuous as a result ofpassive dilatation by
and elongation (Fig. 3, opposite). gu
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THE EYE IN GENERAL VASCULAR DISEASE 645 O
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FinIG.a2c.a-seDioafgrianvmolouftsieonnialreyrestcilnearlosairsterwiiotlhe FinIGa.c3as.e-oDfiaadgvraanmceodfisnevnoilleutrieotnianarlyasrctleerriooslies 1 on
hypertension (blood pressure 200/120). withhypertension(bloodpressure250/140). 1
Hypertonicportionsofthevessel,wherethe The main arteriole is diffusely wide, deep N
wall is normal, are straight, narrow, and incolour, andtortuous. ov
palein colour. Other portions, where the e
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wall is fibrous, are wide, deeper in colour, b
andmorecurvilinear. e
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If this reasoning is correct, aged retinal arteries which are usually pale, op95
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straight, and narrow in health, should become hypertonic in those parts of rig. D
the arteriole which are still contractile; the blood column will remain pale, ht.ow
straight, andnarrowinsuchportions, andthevesselwallshouldbeofnormal nlo
thickness and cell content in histological sections. Other segments which ad
are fibrous, situated proximally, will become more red, wide and curvilinear; ed
inthese portions, with persistent rise ofpressure, the walls mayeven become fro
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thinner than normal, and there should be a relative excess ofcollagen, while h
cell nuclei should be disproportionately few. ttp
Since hypertonus is a physiological state, and involutionary sclerosis is a ://b
change which is on the border line between physiology and pathology, it is jo.b
probable that neither condition willcause appreciable alteration in the trans- m
lucency ofthe arteriolar wall. A vessel whose wall has undergone replace- j.co
mwielnltofffiebrrogsirseastherourledsibsetacnocmeetolessstreeltacshtiicngafnodrcmeso.reBruitgi,d,whinentheitsiesnssuebtjheactteidt onm/
to persistent abnormal pressure, it will tend to yield. In proportion to the Ma
degree offibrosis, a vessel will lose the property ofelastic recoil or resilience, rc
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and the more it is deficient in cellular elements, the more it will lose the 8
power ofactive contraction. , 20
We shall now consider the case of arteries not significantly affected by 23
involutionary sclerosis. In the child or young person, age-fibrosis should by
be minimal. The normal child has well-coloured, wide, sinuous retinal gu
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B
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646 ROBERT LEISHMAN O
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arterioles (Fig. 4). Such vessels would be expected to respond actively and th
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diffuselyinhypertonus. Shorteningofcircularly andlongitudinallydisposed lm
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cbolnotordactcioleluemlenmewnhtiscwhouwlodulldeadbetocochmaengsetsraiinghtth,enaaprpreoawr,ancaendofmtohreeartpearlieolairn l: firs
colour in the hypertensive state (Fig. 5). The arteriole will react diffusely t p
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throughout its length, and the response will extend further in a proximal blis
direction than in elderly subjects. The youthful resilience of the large h
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arteries, together with the intensity and extensity ofthe peripheral reaction, d a
will result in high levels of diastolic pressure. The state of hypertonus in s 1
youthful vessels in response to early hypertension is physiological in nature, 0.1
and the vessel walls should appear normal in histological section. 13
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FIG.hamoscoiagamly,nral youeedwFlGc5nDananrgmofanynownfrmedtsup- jo.b
pretinal arterioents shon-hyprtfensivoe areioleind sohypertensive chilourblod h m
bwodrcehiildd.-e,Tnndsnotwurmss,igntgi.ahesweawlirdcaelt-soasrendlredistpooraclilrgcaturer1oc6twh0eoav1nedsm0el0eabrpatelrleilTthiilsain i j.com
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THE EYE IN GENERAL VASCULAR DISEASE 647 O
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also appear finely variable in calibre. Thus, a hyperplastic portion of an th
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artery might appear clinically as a region which is excessively pale, with a lm
bpolrotoidoncowleurmentowhcirocshsias vneairnrothweraendwofuilnedlybevacroianbcleealimnecnatliobfret,heanvdeinif.such a ol: firs
From this stage onwards, the further course ofthe arteriolar reaction will t p
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depend on the severity ofthe hypertensive stimulus. b
In cases offulminating hypertension, there will be no timefor replacement lish
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fibrosis; hyperplasia will proceed to acute arteriolar necrosis. d
a
In other cases, when the hypertensive stimulus. is less severe, diffuse s
1
replacement fibrosis has time to supersede hyperplasia in the arteriole, 0
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diminishing its cellular content and hence its reactivity, and offering some 1
3
protection against the necrotizing effects of high diastolic pressure. Since 6/b
hypertonus merges into hyperplasia and in turn into fibrosis, all three jo
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processes may occur at the same time but in different portions of the same 1
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arteriole. Hypertonic branches will remain straight, narrow, and pale in 1
colour; thick-walled hyperplastic portions will appear excessively pale and .64
1
finely variable in calibre and will cause concealment at arterio-venous o
n
crossings; portions undergoing replacement fibrosis will be red, wide, and 1
curvilinear (Fig. 6). N
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FIG.6.-Diagramofretinal o9
arterioleinacaseofhyper- py57
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If the patient survives until the stage of advanced reactive sclerosis is j.c
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attained, a diffuse replacement fibrosis will have extended throughout the m
larger arterioles. The main arterioles will appear red, wide, and even tor- o/
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tuous throughout theirentire length; minor branches, less capable offibrosis, M
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may still appear straight, narrow, and pale in colour, indicating hypertonus rc
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(Fig. 3). Thus the patient might reach a state ofacquired benign hyperten- 8
sion resulting from reactive sclerosis, but differing in pathogenesis from , 2
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benign hypertension which is predetermined by involutionary sclerosis. 2
3
Fromthese data a hypothetical clinical classification has been constructed. b
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This is summarized in Table I (overleaf). g
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648 ROBERT LEISHMAN O
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OLD ARTERIES YOUNG ARTERIES tha
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GROUP I NORGMRAOLUPYO4UTH l: firs
NORMAL OLD AGE t p
(Involutionary Sclerosis) u
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C=ONSET OF HYPERTENSIONl- he
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GROUP 5 s 1
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B EARLY .1
E HYPERTENSION 13
NI GROUP 2 6/b
NG INVWOILTUHTIHOYNPAERRYTESNCSLEIROONSIS GROUP 6 jo.41
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H GROUP 7 FULMINATING 1
py SEVERE HYPERTENSION HYPERTENSION .641
E - WITH o
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R REACTIVE SCLEROSIS 1
T GROUP 3 N
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NS ADVANCED TABLE I vem
INVOLUTIONARY SCLEROSIS
CLASSIFICATION OF FUNDUS PICTURES IN b
N0 WITH HYPERTENSION HYPERTENSION AND ARTERIOSCLEROSIS coer 19
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METHOD rig. D
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The phenomena provided by disease processes cannot be simplified arti- t.ow
ficially in order to fulfil the criteria ofa good experiment, and the resulting nlo
observations must be pondered and interpreted to a point rarely necessary ad
e
in designed laboratory experiment. d
Tahe investigations to be described are mainly clinical; and it has proved fro
m
extraordinarily difficult to make consecutive studies ante and post mortem h
in the same patient. Thus, in such studies, thought must travel ahead of ttp
pathological confirmation. On the other hand, a hypothesis which is based ://b
on physiological as well as pathological phenomena cannot be proved in all jo.b
respects by pathological methods. m
Thestepsto betakeninanidealinvestigation ofthis type are as follows: j.co
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(1) Consecutive ophthalmoscopicstudieswithserialphotographicrecordsinlife. o/
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These records of the fundus appearances were obtained by multiple M
wexeproesufirtetseduisnitnogeaachZeoitshesr-Ntoordfeonrsmena ccoammpeorsai.teTpihceturpehootfogthreapahrieca oprfitnhtes arch
(2) Phfoutnodgursapuhnydeorfotbhseefrvuantdiuosn.just before death. 8, 20
2
(3) Early fixation ofthe eyes and removal ofthe posterior halves ofthe globes 3
after death. by
(4) Slit-lamp examination ofthe retina in situ. g
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THE EYE IN GENERAL VASCULAR DISEASE 649 O
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(5) Photography and microscopic examination of the retina in bulk after th
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clearing in glycerine. lm
(6) Microscopic examination of serial sections of the retina, cut, quadrant by o
quadrant, in a direction at right angles to the course of the main vessels. l: firs
Adjacent sections taken for study by different staining methods. t p
(7) Special localization and study ofselected features. u
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Needless to say, the practical realization fell short of the ideal in most lis
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cases, but the above principles were adhered to in so far as was practicable. ed
a
OPHTHALMOSCOPIC GRADING s
1
The hypothesis was tested in the first instance by the method of clinical 0.1
ophthalmoscopy. 1
3
The initial problem was two-fold. First, it was necessary to determine 6/b
whether the existence ofthe hypertensive state could be recognized solely by jo
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ophthalmoscopic examination. This was found to be possible except in a 1
.1
very few cases, and the magnitude oferror was well within the limits usually 1
.6
permitted in a clinical experiment. Secondly, it had to be discovered 4
1
whether or not the various hypothetical fundus pictures could be segregated o
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by means of the ophthalmoscope alone, without reference to other general 1
N
medical data. The observed fundus pictures fell into seven groups as in o
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Table I: e
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Group 1. Involutionary Scle- ; cr 1
rosis.- Since involutionary op95
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sclerosis is almost universal rig. D
after 60 years of age, this ht.ow
represents the normal fundus in n
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old age. In the elderly, the a
d
optic disc is usually pale and ed
often slightly hollow like a fro
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shallow saucer. The ocular h
media become hazy; in the ttp
fundusbackground, reflexes are ://b
diminished, the hue is dull, jo
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retinal pigmentation is dis- m
turbed, and colloid bodies are j.c
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usually present and often FIG. 7.-Section of normalretinalarteriolefrom a m
numerous. The retinal ar.teries non-hypertensive elderly subject, showing a wall of on/
rurn ua arnerlealtaitivveellyy ssttrraaiigghhtt ccoouurrssee,, adinmdinsicsahnetydntuhcilcekin.essxwi4t00h.relativeexcess ofcollagen Ma
arediffusely narrow andslightly rc
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pale, andtendto branch atanacuteangle; thewalls, inhealth, arenotvisible. 8
The veins are not congested distal to arterio-venous crossings. , 2
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The retinal arterioles of non-hypertensive, elderly subjects have walls of 23
normal ordiminished thickness, inwhich there is a relative excess ofcollagen b
y
and cell nuclei are disproportionately few (Fig. 7). g
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650 ROBERT LEISHMAN O
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This fundus picture is usually associated with raised systolic pressure th
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without a corresponding rise in diastolic pressure, a condition which has lm
ebnejeonycgaloloedd shyesatlotlhicfhoyrpetrhteiernsyieoanr.s, tAhlethsotautgehotfhetshee egledneerrlaylpheeraslotnhsaunsduatlhley ol: firs
blood pressure readings are consistentwithextensive involutionary sclerosis, t p
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and the various features ofthe fundus picture are explicable as the manifes- b
tations ofdiminished peripheral pressure (Fig. 8). lish
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