OF PERIPHERAL VASCULAR T)ISEASR HCGH MONTGOWTRY, M.D..” MEYER NAIDE, M.D., AND

NORMAN R. FREEMAN, M..l>.

PHILADEL~~HIA, Pn.

D URINCT the past fe\~ years nl~merous methods for estimating the degree and distribution of peripheral arterial occlusion and VRSO-

constriction have been described. These methods have added great,]) lo our clinical knowledge of vascular diseases such as arteriosclerosis oblit.erans, thromhoangiit,is ohlitcrans, various vnsospastic conditions. and numerous less common peripheral v:~scnlar disorders. They are aids in diagnosis a.nd prognosis and help indicaie appropriate therapy. In the past seven years 1,027 patients have been st.ndicd in the Peripheral Va,scnlar Clinic of the Hospital of the University of Pennsylvania. Onl! 75 per cent. of Ihis number were found to have peripheral vascular disease (Table T). The present wmmnnic~ation is presented in order to show the usefulness of diagnostic tests in c~alllai.ing t.hc circnlatnry disorder from the standpoint; of prognosis and t,reatmcnt (Table I1 1.

Frequently the t,ests served tf~ confirm pathologic and functiona. diagnoses based on history and physical cxaminntion. usually they gave some additional information, and riot uneommonl: they changed the diagnosis. In a scrjes of scvcnty-onr consecntivc CHWS of peripheral arteriosclerosis. t hromhoangiitis obl it crans, or abnormal vasoconst,ric- tion (Table IIT), the diagnosis whit+ was mndc from the hist,ory and physical examination was confirmed by diagnostic tests in 53 per cent, was amplified (’ ‘ functional diagnosis’ ’ 1 in 30 per cent,. and was reflcted in 17 per cenl. Accuracy of prognosis was gent~rally improved as il,

result, of employing t,he diagnostic tcwt s, nlihollgh thcl rrmittcnt charackr of the disrasc in many cases dctcrmined the ~llt~imatc~ outcome.

Vasodilatation tests gave the most wliwhlc information. F’requently they wcrc used to substantiate th(i clinical impression formed from the hist.ory and physical examination, and in such instances t.he>F est.ablished the diagnosis JllOrC firmly on a physiologic basis. 1 n those cases in which the tests were functionally diagnost ita the immediate prognosis was estab- lished. In no case was misleading information gained Prom properly per- formed tests. A list of the tests is given in Table TV.

ELEVATION AND DEl’E:NDFNCX OF I&‘v~BS

Several tests are a, part of the routine examination of patients who are suspected of having peripheral art,erial disease. The simplest of these is

From the Robinette Foundation. Medical Clinic of the Hospit%i, and The Harrison Department of Surgical Research, IJniversity of Pennsylvania.

Presented before the American Heart Association, June 8. 1440, New York, N. Y. Received for publication Aug. 2, 1940. *Henrietta Heckscher Memorial Fellow in Medical Research.

780

MONTGOMERY ET AL.: PERIPHERAL VASCULAR DISEASX 781

TABLE I

DIAGNOSES OF ALL PATIENTS SEEN IN THE PERIPHERAL VASCULAR CLINIC 1933.1949*

-

“ STRICTLY ’ ’ PERIPHERAL VASCULAR DISEASE DIAGNOSES ___-

:: 3. 4.

5. 6.

7. 8. 9.

10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 2ti. 27. 28. 29 30:

Arteriosclerosis-without diabetes 252 Arteriosclerosis-with diabetes 94 Thromboangiitis obliterans 121 Abnormal vasoconstriction (a) Raynaud ‘R disease 1 !I

Varicose veins (b) other

Thrombophlebitis (a) acute (b) chronic

Embolism Acrocyanosis Scleroderma Lymphedema Varicose ulcer Erythromelalgia Scalenus anticus syndrome Congenital arteriovenous fistula Cervical rib Sensitivity to tobacco Thrombosis saphenous vein Recurrent lymphangitis (idiopathic) Femoral artery thrombosis of unknown origin Recurrent phlebitis of unknown origin Traumatic aneurysm femoral artery Traumatic arterial occlusion (by cast) Traumatic arterial spasm Thrombosis $ of abdominal aorta Axillary artery thrombosis, cause unknown Traumatic vasospasm (pneumatic hammer) Oil embolus (bismuth in oil) Traumatic arteriovenous aneurysm Thrombosis common iliac veins Axillary vein thrombosis

3ti 16

7 lti 13 11

9 9 5 4 3 2 2 2 2 2 0

i 1 1

2 1 1 1 1

722

OTHER PERIPHERAL VASCULAR DISEASES

1. Cerebral vascular, symptoms in extremities 10 2. Frostbite of digits 3. Hypothyroidism-coldness in extremities i 4. Polycythemia Vera-erythromelalgic symptoms 2 5. Localized scleroderma-morphoea 2 6. Poliomyelitis 1 7. Edema of unknown origin 1 8. Postoperative carcinoma of breast 1 9. Injury to lymphatics with obstruction 1

10. Stump edema-poor lymphatic return 1 11. Thrombosis of central retinal artery 1 12. SurgicaIIy induced hypotension 1 13. Arteriosclerosis of spinal cord 1 14. Arterial spasm secondary to coronary artery disease 15. Causalgia :

33

*Final diagnoses in 1,027 cases from the Peripheral Vascular Clinic of the Hospititl of the University of Pennsylvania.

1. 2. n 4. 5.

i;: s. 9.

1 Il. 11. 1” 15: 14. 15. 16. 17 1s: 19. 20. “I.

.> D --. “3. 24. 25. 06. “7. “II. 29. ::o. 31. ::“. 33. 24. 3.i. ::ti. 37. 3. 30. 40, 41. 42. 43.

1)iseases with symptoms in extremities not diugnosetl in the Peripheral Vawular Clinic

‘l’ot,al number of patients examined -.____-

7::

1027

observation of t,he effect of position on skin color. While the pat.ient W- clines, the legs are raised and the degree and rate of blanching of the feet are noted. Normally, blanching is incomplete and slow; but, blanch- ing is complete within several seconds when many art,eCes are occluded. The patient, then sits up and places the feet on the tloo~*. 3 f the snbj~t

TABL

E II

~~TR

wTvR

AL

ASD

FVW

TION

AL

&WSI

FICA

TION

O

F PE

RIPH

ERAL

AR

TERI

AL

COND

ITIO

NS

IN

RELA

TION

TO

PR

OGNO

SIS

A;1D

PR

INCI

PLES

O

F TR

EATM

ENT

“DIA

GNOS

IS

’ ’

1. No

rmal

2. Ab

norm

al va

soco

nstric

tion

or sp

asm

3. Oc

clusio

n LSea

ere

(a)

Unco

mp.

for

by

colla

t.

(b)

Partly

ca

mp.

for

by

co

llat.

(c)

Fully

cam

p.

for

by

colla

t. Pn

rtial

(a

) Un

com

p. for

by

co

llat.

(b)

Partly

ca

mp.

for

by

co

llat.

(c)

Fully

cam

p.

for

by

colla

t.

4. M

ixed

abno

rmal

vaso

cons

trictio

n an

d pa

rtial

occlu

sion

(a)

Occl.

un

com

p. for

by

co

llat.

(b)

0~1.

partly

ca

mp.

for

by

co

llnt.

(c)

0~1.

fully

cam

p.

for

by

colln

t.

PULS

E OR

OW

ILLA-

TI

ONS

tt

tt or

t

0 0 (!

I) to

+

0 to

t 0

to +

0 to

+ 0

to t

0 to

+

BLOO

D FL

OW

Max

. ra

nge

of blo

od

flow,

va

ry-

ing

prom

ptly

and

autom

atica

lly

depe

nding

up

on

the

need

s of

the

tissu

es

Max

. ra

nge

of blo

od

flow

in re

- sp

onse

to

stron

g sti

muli

, bu

t flo

w fai

ls to

increa

se

autom

at-

ically

in res

pons

e to

som

e of

the

need

s

Pu’eg

ligibl

e ra

nge

of blo

od

flow

(usua

lly fix

ed,

sl.

vaso

dilata

- tio

n)

Decre

ased

ra

nge

of blo

od

flow

Norm

al ra

nge

of blo

od

flow

Decre

ased

ra

nge

of blo

od

5ow

Decre

ased

ra

nge

of blo

od

5ow

Norm

al ra

nge

of blo

od

50~

Decre

ased

ra

nge

of blo

od

flow

Decre

ased

ra

nge

of blo

od

flow

Vorm

al ra

nge

of blo

od

flow

PROG

NOSI

S PR

INCI

PLE

OF

TREA

TMEN

T $ E ;:

----

------

------

----

0 z m

a r:

Good

\T

asod

ilator

“: F:

a

Poor

De

creas

e tis

sue

need

s G

Oive

tim

e for

co

llat.

Lc

33

Mech

anica

l m

ethod

s of

incr.

bl.

5 flO

W

$

Fair

Yam

e,

less

inten

se

4 Fa

ir Pr

otect

from

tra

uma

;r -z

Fair

Fair

Fail

Fair

Fair

Fair

to

Decre

ase

tissu

e ne

eds;

give

time

fur

colla

teral

Sam

e, les

s int

ensiv

e Pr

otect

from

tra

uma

Vaso

~lilat

or,

tlecre

nse

need

s Sa

me,

less

inten

se

Vaso

dilato

r go

od

-1

m w

TABL

E III

CLIN

ICAL

VA

LUE

OF

TEST

S

PERI

PH.

ARTE

RIAL

DI

AG..

I’ATI

I. AK

D FU

NCTI

ONA

L

SEX

AGE

FRO

hI

HIS

T.

AND

I-‘HY

S.

EXAh

l. FR

OM

H

IST.

, P.

ES

. AN

D TE

STS

VA

LVE

OF

TES

TS

FOT.

LO\V

UP

- -

No

Perip

hera

l Va

sczL

lal-

Dise

ase

F 57

BA

rterio

ocl.

No.

P.V.

di

seas

e Di

azno

stic

6 vr.

No

P.

V.D.

.’

F 46

F

36

M 3s

M

55

F 23

No

per,

%-a

s. di

seas

e %

Per.

vas.

di.s

ease

No

pe

r. va

s. di

seas

e Di

abet

es,

ulce

r, no

P.

V.D.

No

ne

r. l-a

s.

dis.

__-_

__

M M F M M M M M M F l\r

M M M

63

Brtg

riosc

l. a

seve

rit)

65

Abno

rmal

vaso

cons

t. 66

Ar

terio

sc.

mod

erat

e 68

Ar

terio

scl.

sex-

ere

54

Arte

riosc

., 1

grad

e 75

Ar

terio

sc.

mod

. se

vere

5s

Ar

terio

sc.

sere

re

53

Arte

riosc

. ga

ngre

nrl

57

Arte

riosc

. se

vere

70

Irt

erio

sc.

sligh

t 56

Sr

terio

sc.

,? d

egre

e 70

SA

rterio

sclcr

osis

80

Arte

riosc

. se

vere

6.

7 c,

Art,e

riosc

. m

oder

ate

M F iv E’

F

Arte

riosc

. se

vere

Ar

terio

sc.

seve

re

Arte

riosc

. se

\-ere

Sr

terio

sc.

mod

erat

e Ar

terio

sc.

sere

re

Srte

riosc

. m

oder

ate

hrte

riosc

. m

oder

ate

Arte

riosc

. RC

~CW

?A

rterio

ev.

Srte

riow.

‘?

gra

de

Arte

riosc

. wv

ere

Arte

riosc

. se

vere

?2

rterio

sc.

mod

erat

e Ar

terio

sc.

seve

re

?Arte

riosc

. Ar

terio

sc.

mod

erat

e

No

P.V.

D.

No

P.V.

D.

No

P.V.

D.

No

P.V.

D.

No

P.V.

D.

ConL

nato

ry

Diag

nost

ic Co

nfirm

ator

y Co

nfirm

ator

y Co

nfirm

ator

v

2 $r

. No

P.

V.D.

2

yr.

No

P.V.

D.

2 yr,

No

P.

V.1)

. 2

yr.

No

P.V.

D.

2 yr.

No

P.

V.1)

. ---

.~

trtcr

iosc

lero

sis

Rifh

O

cclzl

sion

__-

Arte

riosc

l. go

ad

colla

t.

A-L

Func

t. di

w.

Diag

nost

ic‘

Conf

irmat

ory

Conf

irmat

ory

Func

t. di

ag.

Func

t. di

ag.

Func

t. di

ag.

Func

t. di

ag.

Func

t. di

ag.

Conf

irmxto

r>

Func

t. di

ag.

Diag

nost

ic Co

nfirm

ator

y c.‘

onfir

mat

or>

Arte

riosc

. g>

od

colla

t. Ar

terio

sc.

good

co

llat.

Arte

riosc

. se

vere

Ar

terio

sc.

good

co

llat.

Arte

riosc

. go

od

colla

t. ilr

terio

sc.

good

co

llat.

Srte

riosc

. fa

ir co

llat.

Arte

riosc

. fa

ir co

llat.

Artcr

iow.

sligh

t. -4

rterio

sc.

mod

erat

e hr

terio

sc.

seve

re

Arte

rinsr

. po

or

colla

t. ar

terio

sc.

good

co

llat.

- Di

nbet

ic 11

rterio

scler

osis

TFirh

Oc

clusio

n

Arte

riosc

. se

vere

br

terio

sc.

good

co

llat.

.Ilrte

riosc

:. fa

ir co

llat.

Arte

riosc

. po

or

colla

t. -4

rterio

sc.

fair

colla

t. Ar

terio

sc.

rath

er

seve

re

Arte

riosc

. go

od

colln

t. Ar

terio

sc.

seve

re

Arte

riosc

. sp

astic

el

emen

t Ar

terio

sc.

mod

. co

llat.

Art.e

riosc

. fa

ir co

llat.

Arte

riosc

. se

vere

Ar

terio

sc.

mod

erat

e Ar

terio

sc.

good

co

llat.

Arte

riosc

lero

sis,

mild

Ar

terio

sc.

fair

colla

t.

5 yr.

As

ympt

. 2

yr.

Aste

riosc

. 7

yr.

mod

erat

e 2

yr.

Asym

pt.

3 yr.

As

ympt

. 3

yr.

Asym

pt.

5 yr.

As

ympt

. 5

yr.

Asym

pt.

2 yr.

As

ympt

. 4

yr.

Asym

pt..

9,

i yr.

As

gmpt

. 2

1-r.

no

vlmng

e 3

yr.

Asym

pt.

3 vr.

In

ter.

Cln.

(-‘on

firmat

ory

Func

t. di

ag.

Func

t. di

ng.

F’un

ct.

diag

. E’

unct

. dia

g. Co

nfirm

ator

> Co

nfirm

ator

> Co

nfirm

ator

?~

Diag

nost

ic Fu

net.

diag

. Fu

nct.

diag

. Co

nfirm

ntor

?,

Conf

irmat

ory

Fun&

. di

ag.

Diag

nost

ic C’

onfirm

xtorv

.--

---

S yr.

As

ympt

. ?I

yr.

dsym

pt.

5 yr.

.\s

ympt

. 3

w.

Asym

pt.

5 >r

r. As

ympt

. 2

1-r.

Asym

pt.

1’ &

-. lm

prov

cd

2 yr.

Im

prov

ed

r; yr.

Aa

ympt

. 1

J-I+

. Im

prov

ed

j 7’

. As

ympt

. ?

yr.

no

chan

ge

t’ yr.

no

eh

a.ng

e 2

yr.

Imp.

, Fa

il. S

w.

Imar

oved

M M M M M M M M M M M M M M M x M M M ii M 2 M M M 3 M

25

T.A.

O.

seve

re

35

T.A.

O.

seve

re

33

T.A.

O.

seve

re

28

T.A.

O.

seve

re

37

T.A.

O.

seve

re

41

T.A.

O.

seve

re

45

T.A.

O.

a gr

ade

30

T.A.

O.

seve

re

51

T.A.

O.

seve

re

46

T.A.

O.

mod

erat

e 42

Ab

norm

al va

soco

nstri

ctio

n 32

T.

A.O

. se

vere

43

BA

rteria

l oc

clusio

n 44

T.

A.O

. m

oder

ate

28

T.A.

O.

seve

re

56

T.A.

O.

seve

re

49

T.A.

O.

seve

re

41

T.A.

O.

mild

45

T.

A.O

. fa

ir co

llat.

28

T.A.

O.

seve

re

39

T.A.

O.

seve

re

30

T.A.

O.

seve

re

31

T.A.

O.

seve

re

48

T.A.

O.

seve

re

45

T.A.

O.

seve

re

49

T.A.

O.

seve

re

59

T.A.

O.

and

arte

riosc

. 5s

T.

A.O

. an

d ar

terio

sc.

mod

. 52

T.

A.O

. an

d di

ab.

art.

seve

re

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.A.

O.

T.,4

.0.

Elig

ht

colla

t. go

od

colla

t. so

me

colla

t. ne

glig

ible

co

llat.

sligh

t co

llat.

negl

igib

le

colla

t. go

od

colla

t. se

vere

se

vere

se

vere

po

or

colla

t. fa

ir co

llat.

fair

colla

t. go

od

colla

t. fa

ir ca

llat.

poor

co

llat.

seve

re

good

co

llat.

poor

co

lIat.

seve

re

som

e co

llat.

poor

co

llat.

poor

co

llat.

seve

re

seve

re

poor

co

llat.

etc.

se

vere

et

c.

fair

col.

etc.

po

or

colla

t.

Conf

irmat

oYy

Func

t. di

ag.

Confi

rmato

r: Co

nfirm

ator

y Co

nfirm

ator

y Co

nfirm

ator

y Co

nfirm

ator

y Co

nfirm

ator

y Co

nfirm

ator

y Fu

nct.

diag

. Di

agno

stic

Fun&

. di

ag.

Diag

nost

ic Fu

nct.

diag

. Fu

nct.

diag

. Co

nfirm

ator

y Co

nfirm

ator

y Co

nfirm

atoq

Fu

nct.

diag

. Co

nfirm

ator

y Co

nfirm

ator

y Co

nfirm

ator

y Co

nfirm

ator

y Co

nfirm

ator

y Co

nfirm

ator

y Co

nfirm

ator

y Co

nfirm

ator

y Co

nfirm

ator

,v Co

nfirm

ator

y

- 2

heal

ing

3 yr.

he

aled

2

yr.

just

he

aled

ti

yr.

recu

r. ul

c.

5 yr.

re

cur.

4 yr.

As

ympt

. 5

yr.

Inte

r. Cl

a.

3 yr.

In

ter.

Cla.

2

yr.

Impr

oved

2

yr.

heal

ing

4 yr.

wo

rse

3 yr.

m

uch

impr

. 3

yr.

Asym

pt.

5 yr.

no

ch

ange

2

yr.

Asym

pt.

2 yr.

In

ter.

Cla.

2

yr.

Toes

Xm

put.

3 yr.

As

ympt

. 4

yr.

Recu

r. ul

cer

2 yr.

Re

cur.

ulc’

s 2

yr.

Recu

r. ul

c’s

3 yr.

Re

cur.

ulc’

s 5

yr.

Ampu

t. le

g 5

yr.

wors

e 2

yr.

Ampu

t. to

es

3 yr.

Am

put.

leg

2 yr.

Pr

egan

gr

‘9

6 yr.

Im

prov

ed

4 yr.

Am

put.

legs

Ab

norm

al lra

socw

nstri

cttin

-

M 57

Di

abet

ic ar

terio

sc.

Abno

rmal

vaso

cons

tr.

Diag

nost

ic 3

yr.

Asym

pt.

F 24

Di

abet

ic ar

terio

sc.

Abno

rmal

vaso

cons

tr.

Diag

nost

ic 8

yr.

Asym

pt.

F 36

$A

rterio

scle

rotic

Ab

norm

al va

soco

nstr.

Di

agno

stic

3 yr.

Ab

n.

Vaso

con.

F

34

Arte

riosc

l. se

vere

Ab

n.

vaso

con.

, m

ild

arte

riosc

l. Di

agno

stic

6 yr.

As

ympt

. M

49

Abno

rmal

vaso

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ESI’OSLRI’: TO COLD

Patients who present a history of’ ahnormal vasoconstrirtion which is not apparent at the time of cxanlination are tested by exposure to cold air or 11s immersing the aflcctcd limb in cold water (15 degrees (.!. for ten minutes). U’hen the vasoronstriction is confinctl to the upper ex- tremities, evidence of the presence of a cervical rib alld the scalenus anticus syndrome1 is sought.

MONTGOMERY ET AL. : PERIPHERAL \-ASCI-l,hR DISEASE 787

VASODILATATION TESTS

The outcome of physiologic studies on the peripheral circulation is largely influenced by variations in vasomotor tone, that is, the degree of peripheral vasodilatation or vasoconstriction which is present at the time the test is made, for most of the tests estimate the rate of blood flow, and the circulation decreases in proportion to the degree of vasomot,or tone. Wide fluctuations in vasomotor tone occur in response to variouti factors. Vasodilatation occurs in the skin in response to infection, tc local heating, to heat applied elsewhere to the body, to a rise in hod? temperature, and to meals. Blood may flow through exercising muscle as much as ten to twenty times as fast as through resting muscle,2 and through warm skin as much as a hundred times as fast as through coo1 skin.” Changes in environmental temperature alter vasomotor tone to such an extent that there may be an even fast,er blood flow in a warm extremit.y in which t.here is some occlusion of vessels t.han in a cool ex- tremity with normal vessels. Consequently, in studying t,he peripheral circulation it is essential to estimat,e the degree of vasomotor tone or to remove vasomotor tone at the time the examination is made.

The significant part played by vasomotor tone is illustrated hy eom-

paring the physical signs in a limb (a) when there is normal vasocon- striction, and (b) when there is full, normal vasodilatation. When a person feels chilly he usually has a cold, pale foot, and the veins are small and the pulses small or indistinct. When Ohe same person feels warm the feet are warm and pink, and the veins and pulses are prominent.

An example of such a change in the appearance of vascularity is afforded by comparing the two normal feet of a subject after block of the right lumbar sympathetic ganglia with novocain. The left foot is pale, cool (skin temperature 22” C.), and moist; the veins are small,

the arteries small, the pulses fine, and the oscillations one space (aneroid sphygmomanometer) . Blanching on elevation is complete in 10 seconds, and color returns to the foot and the small veins fill only after forty seconds of dependency. The right foot is bright pink: warm (skin tem- perature 34” C.), and dry. The veins are large (diameter 3 times those of left), the arteries large (diameter about 2 times those of left), and the pulses are more rradily felt than those on the left. Oscillations are two spaces and blanching on elevation is incomplete, and the color returns and the veins fill after three seconds of dependency.

The diagnostic tests which most, capably control the factor of variable vasomotor tone are the so-called vasodilatation tests. In these tests, vasomotor tone is either inhibited reflexly or depresed by an anesthetic. After vasodilatation is initiated it continues to its maximum if the condi- tions of its initiation are maintained. The resulting blood flow equals the undamaged circulation plus the collateral circulation. The collateral,

iht k;, t’he nortp~~lsatilc cirruI;ltion, (‘ill1 thc>n I)(, cStim;lt& 1)~ colnr);lping

this b100d flow wit,11 the degrc~ of c];m~ag:c estimat(l(l from a.bscnt pnlsps and decreased oscillations (src Fig. 4). ~asodilatation t&s can mi~asllrfl even a slight decrease in circulation, ilHd mtaslirc~ l.he CircllliltiOI~ in t.hP more distal tiswcs, mhcrr, in l)ati(~nts Tvith ptriphcA arterial diseases. the ischemia is usually most sevcro.

AS a ~UIC t.hc ra.tc of blood flow ill thcsc tests is cstimat.ed clinically hi mea.surements of surface icrnpcrnt~~~~c. Skin t cwrwrat~llrp is con vcnicntly measured by means of a fllcl~lt~c,c~onplc or skin thermometer.” A radiometer is less applicable 10 the small areas of skin on the tips of digi&” Experimentally. l~lcthlr-snlo$raphic and calorimetric methods of measuring peripheral blood flow i1 r(’ ~iscd.“~ i* 4, n, I”

A vasodilatat,ion test is l~~rl’o~~u~c~l in the following manner. The paGent, reclines, lightly clatl, in a co111 room, prcferahly in a constant tem- perature room at 20 cltg~~s C”. The fcrt. or hiln(lS, depending upon which a.re to 1~ studied, >I re c~sl~osc~l to roonl air throughout t,hc test. Digital skin tcmperaturr is takcln at ten-minute interva,ls, and, when it has decreased to 21-20 dcgrccs C”.. vasodilatation is reflexly induced by one of several methods. Vasoclil;~tatiot~ begins within a few minutes IO an hour, depending upon th(~ rtlc+hod card to elicit it. In the nor- mal subjert, when vasodilatatioll is cotjlp1et.e the skin temprrat.lirc’ 01 the digits will rise to a Ipv(~I Iw~xvP(~~ 31 and 33 dearers (‘. Thr mrt,h- ods for inducing vasodilatation illcallrdc reflex heat.“, “. “* “9 ‘,‘* ” arti-

ficial fever,‘:. I* ingestion of i~lcohol,~~’ posterior I ihiill 01’ lrln;iY uwv

block with procaine,*“~ ?I, ??. “‘j sl)inal anesthesia.“, X. ” gencl*ill nnes- thesia, and injection of the 1~1mhn r thoracic ganglion with procaincl.“’ Heat cannot,, of course, he applictl dircctl;- to 111~ clst,remihp which is being studied. The skin tenlpcraturc rises more rapidly in rcspor~s~ to

an&hetizatiOn of the s;vmpat 1lct.ic.s than to ot.1lt.r proccdnrcs~ and to a slightly higher level (ahont 2 degrt~~s ( !.) h(~cillls(~ 01’ thca lac?k of swrnting

and perhaps of her factors. Witll frill VilSOtlil~t;lliOt~ the trmperatllrr of the fingers iS normally- OIICJ 01’ I \YO cl~~gr’c~s highcar t ban that of the tops.

The choice of one rather t,han iIIIothcl* means of induPing v2lsOdihtation

in the ext,remitirs depends upon 1 tw sllb.iect. ;incl. to some rstrnt, upon

t.hc syndrome presented. 111 a~~~ <‘ilW, the 1llc~t110~l vhosen must r)~(~dl~(*~~ rasodilatation ; if it fails, another met hot1 is select rd ( SIT Table IL* 1. I”07 t,he first trial wp rhoose rcflcx heat, hecansc it is innocuous. simple. and is effective in about. 90 pvr cent of the cases. Eutisfaetory vasodilata- tion is produced lqr applying hea.ting pads to the estremitics which are not being tested, and coverin, (r the body with blankets.*

Landis and G ihhon”, lz inlmcrsed the extremit.irs which were not being tested in water at 45 degrees L:. Water immersion is r*nmhersome. but is

*Pickering has shown that heat applied to a part of the body induces vasodilatation elsewhere by raising the temperature of the blood (ref. Heart 16: 115, 1932). Presum- ably the “vasomotor center” responds to the rise in blood temperature, and lessens vasomotor tone.

MONTGOMERY ET AL.: PERIPHERAL VASCIII,AR. DISEASE xx-i

even more effective than heating pads in initiat,ing vasodilatation. Jf reflex heat fails to induce a rise of at least 2 degrees C. in skin tempera- ture, one cannot be sure that vasomotor tone has been abolished, and, although some abnormal vasoconstriction is indicated by this failure, either peripheral nerve block, spinal anesthesia, general anesthesia, or procaine injection of sympathetic ganglia is resorted to. Otherwise, no estimate of the degree of arterial occlusion is gained. When some means other than reflex heat is required (about 10 per cent of the eases), any one of the second choices is nearly always successful in producing maximum vasodilatation.

Vasodilatation tests are, for the most part, easily interpretable (see Table V). Strictly speaking, the interpretation applies solely to blood flow in the skin under the thermocouple, but this is usually repsesenta- tive of surrounding Gssues. With a cool room temperature, a rise in skin temperature to 31 degrees C. means that the flow of blood is equal to that of a normal person with full vasodilatation. This level is reached in a limb with no arterial occlusion, or with arterial occlusion which has been completely compensated for by collateral circulation. A rise which falls short of the 31 degrees C. level indicates arterial occlusion-more if the rise is slight,, less if the skin temperature ap- proaches 31 degrees C.

Vasodilatation tests are useful (1) in diagnosing or helping to estimate arterial vasoconstriction, (2) in diagnosing early arterial occlusion, (3) in quantitating all but the most severe grades of occlusion, (4) in help- ing to measure the collateral circulation, and (5) in measuring the capacity for vasodilatation, and hence in deciding a,bout the propriety of vasodilatation therapy, such as sympathectomy. The tests are useful because they remove that important variable, vasomotor tone. They are not indicated in the most severe grades of uncompensated occlusion, for clinical signs and the histamine test afford all of the necessary in- formation in these cases.

TESTS OF ABNORMAL VASOCONSTRXCTION

Vasoconstriction is a normal, reversible, physiologic process which con- trols the blood flow to various tissues in accordance with the total economy of the body. Contraction of blood vessels is produced by short- ening of the smooth ruuscle fibers of the media in response to sympathetic nerve impulses or circulating substances.

Before discussing tests for vasoconstriction, it will be necessary to de- fine certain terms. “Normal vasoconstriction” is the degree of contrac- tion of blood vessels which results from physiologic stimuli. It is not sufficiently intense to interfere with tissue nubrition and does not pro- duce signs or symptoms of ischemia. The cool hands of a subject who is exposed to a cold environment illustrate “normal vasoconstriction. ”

c Heat applied to the arnls (to test toea) ; 01 to legs (to test fingers)

2. Posterior tibia1 ulnar) nerve block be used only after 1

(01 ctu d).

3. High spinal anesthesia (applicable only for le:! symptoms).

4. Novocain iniection of sympathetic. Chain (lum bar or dorsal).

( 1)) Urlayc~l riw t 0 normal level.

(I’) Partial rise, to below 1101.nI:tl lrvel.

(a) Rise to normal.

(h) Partial rise to below normal (in presence of numbness indicating succex3ful injection of nerve j ,

Cc) No riw, or continue{1 fall (in presence trf numbnrss, etc.. ) .

“ Abnormal vasoconstrittion’ ’ is an excessive c+ontraction of blood vessels in response to physiologir stimuli, or contraction as a result of abnormal stimuli. The vasoconstriction is sufficiently intense to inkrferc with the normal metabolic demands of the tissues and prodnces signs and symptoms of ischeniia. The results of abnormal vasoconstr,i~tioli aim, usually, coldness, cyanosis, and I)ain, and, ult.imat.el~, superficial necrosis. “,4bnormal vasoconstriction” is frequently seen in association with or- ganic vascular occlusion, as in thromhoangiitis c~hlitrrans.

‘ ’ Vasospasm ’ ’ is a term which has been loosely ustd to indkalr ah- normal vasoconstriction. It seems to us that it should be used specifically to denote an actual spasm of blood vessels, with complete circulatory arrest. The classical manifestations of’ vasospasm occur in t,he blanched fingers of patients with Raynaud’s disease. It may also follow arterial trauma, as in acut.e embolism of peripheral arteries, and is occa- sionally seen in patients with acute iliofemoral t hrombophlebitis. Pro- longed spasm, although rare, will cause gangrene.

“ Capacity for vasodilatation ” is the measured increase in circulation which occurs when vasoconstrictor tone is removed, as it is in one of the vasodilatation tests. It does not necessarily mean that iLvasospasnl ” or “abnormal vasoconstriction” is present, but simply indicates that the blood vessels have an increased capacity when the vasoconst,rictor tone is removed. Some capacity for vasodilatation is a prercyuisite for a diagnosis of normal or abnormal vasoconstriction or vasospasm.

TESTS OF VASOCOKSTRICTIO~

With these definitions in mnid, vasoconstrici ion is revealed clinically by intermittent coldness, blanchin g, or cyanosis, and is frequently asso- ciated with excessive sweating, or pain, in a limb which has its pulses and at least some capacity for vasodilatation. No tests hare been devised to differentiate between normal and abnormal vasoconstriction and raso- spasm. If the patients are free from symptoms at the time of examina- tion, exposure to cool air or the immersion of ali cxt,reniity in cold water may help establish the diagnosis of abnormal vasoconstriction. When vasodilatation produced by reflex heat fails to relieve vasoconstriction, and relief is obtained by more vigorous procedures such as anesthetiza- tion of sympathetic nerves, the patient can be said to have abnormal vasoconstriction, but there are other pat,ients with undoubtedly abnormal vasoconstriction who obtain prompt relief from reflex heat.

Vasoconstriction produces ischcmic symptoms which are indiscernible from those of organic arterial occlusion. The vasotlilatation tests play an important part in the study of various grades of vasoconstriction, in t,hat they measure the capacity for vasodilatation, thereby excluding. or measuring the degree of, organic occlusion. It is most. difficult to differentiate vasoconstriction from occlusive vascular disease when the latt,er is accompanied b.v abnormal vasoconstriction. In such cases, care- ful attention to the history, examination, and vasodilatation tests gives a remarkably accurate picture of the abnormal vascular system.

Clinical oscillometry affords a measure of the total pulsation trans- mitted by the heart’s beat to the vessels encompassed by the oscillometel CUfl*2G, 27 In normal subjects, arteries large enough to carry a palpable pulse contribute most of the pulsation, and the smaller arteries and arterioles make up the rest. Aside from alterations in the strength or rhythm of the heartbeat, the oscillometrie readings in a limb become abnormal because of several common disturbances in the peripheral arterial circulation. The oscillations are lessened (1) by obstruction to the pulse wave, such as that caused by arterial occlusion and aneurysm, even in the presence of an adequate collateral circulation, and by arterial or arteriolar spasm, (2) by lessened flexibility of arteries and arterioles, such as occurs in arteriosclerosis, (3) by a diminution in the size of the arterial, arteriolar, and probably venous bed, (4) b>- a profound decrease

in blood pressure, and (5) by an inflexible. C&t skin such as that, of scleroderma. The oscillations are increased ( 1 i 1)~ vasodilatatioll, whether it be physiologic or pathologic, and (2) b.v escape of arterial blood directly into veins, as with single or multil~lc art~+ovenons fistulas.

Great fluctuations in blood flow. such as arc induced by cold and heat in the skin, and by rest and exercise in muscle, thange the oscillometric readings. In a normal subject with peripheral rasoc’c,l~strictioll os~illo- metric readings from a finger arc increased about sixfold, from a tar about threefold,3 and from the ankle about twofold when l’ull peripheral vasodilatation is induced b,v hcui (‘)scillomet,ric readings from the rest - ing calf are about doubled immctlintel,v after cscr(Aisc, in spite 01’ a concomitant slight decrease in the bIood Aow through the skin of thtl calf. Therefore, if minimal osrillations are rated iL< 0, anti maximal normal oscillations as 1, the range of rlornlal at unklc level is betwcsen $6 and 1 when the subjects arc under controlled c*ondit,ions with respect, to exercise and warmth. The amplitude of the oscillations is more nearly standardized when measurements arc made only afttar vasomot(Jr tow is released, or when, in a single subject, readings ar(’ ~*ompa.red at identical levels of the two legs. Slight discrepancies in atljnstment of the cuff still contribute some error. Muscle spasm, anomalous arteries, card&r weakness, severe scleroderma. and the size of the snhject rarclp confuse the interpretation.

The clinical use of oseillomet,ry is most helpful ( 1 ) in ascert.aining the exact level of arterial occlusion, (2) in helping to establish the presence or absence of pulses which arc not palpable beeausv of overlaid muscle, fat, or edematous tissue, (3) in measuring past vascular damage which may or may not have been compensat,ed for by a nonpulsat.ile collateral circula.tion, (4) in detecting t,he site of artcriovpnous fis~.ulas, and i5’1, when combined with a vasodilatation test in estimating the extent of the collateral circulation (when collateral circulation rcluals blood flow minus undamaged circulation).

Several types of oscillomet,ers are available for clinical use; in all of them the pulsations are transferred from a cuff lo a tambour with a recording needle. A recording instrument has the advantage of pro- ducing a permanent record. The ordinary aneroid s~llygmomanonleter is a nonrecording form of oscillometer which is satisfactory for most purposes. With this instrument the normal reading at the ankIe is be- tween one and two scale markings, when each marking indicates 2 mm. Hg. Similar instruments which are market,ed as oscillometcrs have larger and more easily read scales.

CUTANEOUS HISTAMINE REACTIONS

Unless there is marked cutaneous vasoconstriction, histamine, when in- troduced into the skin of a normal person, produces a localized wheal within three minutes after injection. If the blood flow to the part has been completely arrested no wheal appears.*8 If the blood flow is greatly

MONTGOMERY ET AL.: PERIPHERAL VASCULAR DISEASE 793

decreased, either the wheal will not appear or its appearance will he delayed.2”l 3o Starr has utilized this phenomenon as a measure of blood flow. Any delay in wheal formation of more than five minutes indicates severe ischemia. When no wheal appears t,he life of the tissues is endangered, and gangrene is usually imminent unless blood flow can be made to increase. Moderate grades of occlusive disease fail to alter the time of appearance of the wheal.

This test, like the vasodilatation test, is a t,est of capacity for cutaneous blood flow only, but this is hardly a limitation because failure of the cutaneous circulat,ion is t,he cause of most of the more serious conne- quences of peripheral vascular disease. The histamine test is morr sensitive than the vasodilatation test only in the lowest range of blood flow estimated by the latter.

The test is performed by placing a small drop of l/1,000 histamine acid phosphate on dried, cleaned, nonedematous skin (preferably not over bone), by needling the skin several times through the drop, and by feel- ing for a wheal.” Any palpable irregularity is considered a satisfact,ory wheal. A necessary precaution is that vasoconstriction be relieved before this test for arterial occlusion is performed; a cold, white, or blue skin should be prepared by gentle warming. There are exceptions in Ray- naud’s disease and in acrocyanosis, as described below.

The histamine test is indicated mainly when occlusive arterial disease is known to be present. We have never seen a wheal fail to appear wit.h- in five minutes, when the test was properly performed, in patients who have a fairly good or good cutaneous circulation, as indicated bp the vasodilatation test. The reaction is unaffected by moderate degrees of arterial occlusion ; the test is sensitive to slight changes in severe arterial occlusion. It is most useful in making a prognosis of the viability of ischemic tissues. Skin which fails to develop a wheal after histamine injection, when the precaution against vasoconstriction has been taken, is too isehemie to enable incisions to heal, whereas delayed wheal forma- tion indicates that healing is improbable. Wheal formation within 3 to 5 minutes indicates that there is sufficient blood flow for the healing of incisions, but infection, because of its great demands on blood flow, can upset conclusions based on the histamine test. The test should not be performed on, or adjacent to, necrotic tissue, but is sometimes most use- ful a few centimeters above a line of demarcation. The test is sometimes helpful in determining the lowest level at which an amputation wound can be expected to heal, but in this connection Starr has emphasized the need for taking all data available into account in deciding the ques- tion whether amputation should be done, and at what level.

The test is useful in differentiating between Raynaud’s disease and acrocyanosis. In Raynaud’s disease the spasm is predominantly in the small and large arteries, and, in acrocyanosis, in the arterioles. When

*Histamine for this purpose ca,n be kept for months when chloretone is added tq make a 1 per cent solution,

MONTGOMERY ET AL.: PERIPHERAI, YAWlTAR DISr?r\SR 7%

tightly by the observer, the hand lowcrc~d, opened, and, after three minutes, the wrist released. Heating the hand is less necessary than heating the foot because vasomotor tone is less readily maintained in the hand. The resulting flush is interpreted in the same way as that in the foot. A useful modification serves to demonstrate patency or occlu- sion of the ulnar artery when the ulnar pulse cannot l)e palpated. The modification follows the above directions, with the addition that the radial pulse is held compressed from the time the pressure is being rc- leased. Care should be taken that compression of’ the radial bc prevented from extending to the ulnar artery. In like itiam~r, occlusion of a single one of the paired digital arteries can br demonstrated. Thcsc modifications of the test are occasionally of diagnostic valac early in the course of thromboangiitis obliterans.

One of the earliest forms of the reactive h+vpercmia test is the most complete, and, in its special application, the most useful. MataP de- signed the test to estimate the extent of the collateral circulation in a limb with an art,eriovenous fistula prior to operation. The whole circula- tion is arrested by an Esmarch bandage, and the main artery just, above the fistula is compressed digitally or instrumentally to a degree sufficient to occlude it. The bandage is removed while arterial compression is maintained. Reactive hyperemia results through the collateral circula- t,ion only. The test, demonstrates the extent of the collateral circulation, and, therefore, shows whet,her or not it is safe to undertake surgical procedures such as ligation and excision. Halstead”” suggested a some- what similar procedure, in which a metal band is adjusted so that, it will partly occlude an artery above an arteriovcnous fistula. This procedure is both a test and a therapeutic method. The tightness of the band is repeatedly adjusted to maintain a bare1.v adequate blood flow, thus diminishing the symptoms from the fistula and encouraging growth of collateral circulation without causing undue ischemia. An opportunit) is thus afforded for final arterial closure with lessened danger to the limb.38, 30

METHODS OF ESTIMATING BLOOD FLOW THROGGH MUSCLE

(TESTS OF INTERMITTENT CIALJDI~ATION)

Intermittent claudication results from interference with normal arterial blood flow through muscle. An adequate estimat,e of muscle blood flow can usually be obtained from the patient’s statement concern- ing the walking distance necessary to precipitate pain, or more accurately by having the patient walk at some standard rate, such as 120 steps

per minute.40 A satisfactory estimate can be made by having the patient alternately press and raise the foot against a pedal.4’ The most objective method of measurin, 0 intermittent claudication in the muscles of the calf is that of Hitzrot, Naide, and Landis.42 In the operation of this test the patient, reclines, with the foot resting against a board which is support,ed by a spring. A mifom electrical stimulus

is applied intermittently to the calf muscles, and t II~~ rrsuli ant c+ontracd- t ion is recorded graphically. ‘l’hc rt’czord obt aincd is c~ompared with a normal graph. This method has the, advantages OVOI’ othtlr tests of int.cq*- mitt,ent claudication in Cat the rec~ortl is more ol,jcc+ti \:(I, and one tan, to some extent. subdivide the pat.ient ‘s muscle ischcm ia into (a) taxtent of ischemia and (b) intensity of ischemia. Widesprrnd iscahemia of large muscle groups results in a very much reduced amplitrtdr of contraction before pain develops. Intense ischcmia of a small ttIIIsc’lt> group results in pain before a significant decrease in amplitude occurs. With this device the stimulus for contraction remains lhe SNIIC when the pain he- gins. Decrease in contraction resolts from muscle I’atigue.

Claudication fest,s are ol’ valuc~ ( 1 i when pat.it>nts arta unable to give a satisfactory history OS internliti c>nt rlaudication, (2) in differentiating between intermittent claudicntion, faulty mechanistlt of an &hope&* uature, neurologic disorders, and nvuroses, and !S 1 in Cotlowing changes in the severity of intermittent clautlieation.

PHYSIOLOGIC CONSIDER.\TIONS

In arterial disease two major processes are at work : (1) obstruction of arteries and (2) development of collateral circulation. Superim- posed upon these structural changes arc two additional factors. namely, the varying needs for blood flow and reflex vasoconstriction. Only b; evaluating the circulation from the standpoint of past damage, its extent and location, previous repair: funct.iomal capacity. and superimposrd vasoconstriction can the clinical statlls of each individual patient be en- tirely appreciated.

Tests of the peripheral circulation can be divided into two general categories: (1) Those which measure previous damage, i.e., past occlu- sion (oscillometry, careful palpation of pulses, arteriography,4Q and per- haps blanching of the limb on elevation) and (2) those which measure blood flow, e.g., reactive hyperemia tests, various vasodilatation tests, and the histamine wheal test (see Table IV). It must be emphasized that past arterial damage is by no means necessarily synonymous with present functional defect. A comparison of the results of two of the tests for past damage (i.e., oscillomctry and palpation of the pulses) with the results of two tests of present function (i.e., t,hc reflex vasodilatation test and the histamine test) illustrates this fact.

In Fig. 1, digital blood flow, as measured by the air plethysmogruph, is plotted against the temperature of the adjacent digit. The normal varitl- bility of digit,al blood flow is shown in terms of both blood flow and skin temperature. The values arc taken at random from fifteen normal SUM)- jects. During marked vasoconsi.riction, normal digital blood flow is as low as 1 CC. of blood per 100 CC. of tissue per minute, and during vaso- dilatation as much as 100 times that amount. In a cool room the skin temperature of a normal finger varies from 20 to 34 degrees, depending upon the rate at which blood is flowing.

Ii4ONTGOMERP ET AL.: PERIPHERAL VASCULAR DISEASE 797

Fig. 2 shows the clinical significance of the skin temperature of digits with maximal vasodilatation and a room temperature of 21” C. (70” F.), and illustrates the capacity for vasodilatation within the digits. The normal skin temperature, with maxim-al vasodilatat,ion, of a toe is about 31° C. At 29” the skin temperature is subnormal hut, “good”; at

D~e~tal skin tanparature (Thermocouple)

30

26

22

Data obtamed from fi normal sub]ects m wk skm temperature and had been constant fol .

em :h both ,lood flow Over

Fig. I.-Relationship of digital skin temperature to blood flow through adjacent Anger.

Fig. Z.-Clinical significance of digital skin temperature.

23O it is “minimal,” and gangrene is imminent. With this low capacity for vasodilatation, and here only, the histamine wheal test offers a finer differentiation of functional capacity.

By and large, oscillations and pulses are closely similar measurements of past damage. Fig. 3 illustrates this relationship. Ankle pulses are plotted against oscillations at the ankle. Absent pulses and minimal

Ankle pulses

I

Both present

Osci.llations.

Both present

pulses No palpable

26-29 29-305 30 5 and above

Digital temperature with maximum reflex vasodilatation

a low skin temperature, and normal limbs us~lally have hoth ankle pulses and a high skin tem~)ernt~u*c~, there ww 176 limbs in which there were no pulses and yet considerable Mood flow. These observations are iherpreted as evidence of fail- to excellent function of a nonpulsatile

collateral circulation. Ot.her points which fall out of line wit,h good pulses but lessened function are interpreted as abnormal vasoconstriet,ion” or distal occlusion. The data on nonpulsatile coIlatera1 flow are again presented in Fig. 5. This figure shows the results obtained from t,he vasodilatation test on all limhs in which no ankle pulses were felt. The

Number of limbs Bitbout ankle pulses

I25 T

26-29 29-305 30-5 and above

Digital temperature t;lith max\mum reflex vasodilatation.

Fig. 5.-Vasodilatation test in patients with arterial occlusion.

Ankle pulses

I

Minutes- OQ

Time of appearance of wheal or flare. Fig. 6.-Relationship of ankle pulses to histamine test.

200 legs. Each large square represents

largest group of these limbs had poor function, but there were three other large groups in which the function was fair or even excellent, show- ing the great frequency with which a collateral circulation follows severe damage.

That the pulse wave does not necessarily indicate the functional

For simplicity in Figs. 3, 4. and 6, ‘kpasm.”

“abnormal vasoconstriction” has been termed

Number of hmbs subseouentlu amputated

15-

10 -

I

5 d.-

I i

“C- B elok 26 26-29 29-305 30.5

and above

The prognoslie significance of f.he va.sodilat:tt ion lest. and or t hc hist.amine test is shown in Figs. 7 znd S. A%m put at ion is seldom required if the vasorliletation test or l-hc histamine test shows good fun&m.

A structural and functional classjfiration 01’ caonditions of the periph- ctral arteries is presented in Tahlc IL Progwsis and therapy folloll principles already indicated, bui arc of cnursc influenced hy knowledge gained from the history, physical examination, ronvcntional diagnosis, and a knowledge of the metabolic* nr~ds of’ bhe peripheral tissues. Espe- cially if there is a lesion, the metabolic needs may determitw prognosis quite as much as does the capaci1.y for blood flow.

Number of limbs subseauently amputated

Di~it~~l temperature with maximum reflex vasodilatation.

Time of appearance of wheal or flckre.

Fig. II.-Clinical significance of vmodila- tation test.

Fig. X.-Clinical significance 0C Ibista- mine test.

In peripheral arterial discasc t,here arc two J\Iajor processes at work: (1) obstruction of arteries and (2) formation of rollateral circulation. Either damage or repair may hecome dominant. Collateral circulation means functional repair. Vasodilatation tests, the histamine test, and reactive hypcremia tests are t,ests of function, and when pmt vascular damage is estimated by oscillomctry or palpation of pulses these tests help to estimate the extent. of t,hc collateral circulation. Superimposed abnormal vasoconst,riction may confuse the picture. Only by evaluating the circulation from the standpoint of past damage, its extent and location, repair, funct,ional capacity, and supcrimposcd vasomot,or tone can the clinical status of each individual patient he entirely appreciated. Various tests of peripheral arterial conditions are important adjuncts to information gained from a complete history and physical examination.

MONTGOMERY ET AL.: PERIPHERAL VASCTJLAR D~SEASl? 801

REFERENCES

3. Ochsner, A., Gage, M., and DeBakey, M.: Scalenus Anticus (Naffziger) Syn- drome, Am. J. Surg. 28: 669, 1935.

3. Krogh, A.: The Anatomy and Physiology of Capillaries, ed. 3, New Haven, 1929, Yale University Press.

3. Burton, A. C.: The Range and Variability of the Blood FIow in the Human Fingers and the Vasomotor Regulation of Body Temperature, Am. J. Physiol. 127: 437, 1939.

4. Murlin, John R.: Skin Temperature, Its Measurement and Significance for Energy Metabolism, Ergebn. d. Physiol. 42: 153, 1939.

5. Hardy, J. D.: Radiation of Heat From the Human Body: Instrument for Measuring Radiation and Surface Temperature of Skin, J. Clin. investigation 13: 593, 1934.

6. Hewlett, A. W., and Van Zwaluwenberg, J. G.: The Rate of Blood Flow in the Arm, Heart 1: 87, 1909.

7. Kunkel, Paul, and Stead, Eugene A., Jr.: Blood Flow and Vasomotor Reactions in the Foot in Health, in Arteriosclerosis, and in Thrombo-Angiitis Obliterans, J. Clin. Investigation 17: 715, 1938.

8. Kegerreis, R.: Calorimetric Studies of the Extremities. II. Experimental Apparatus and Procedures, J. Clin. Investigation 3: 357, 192627.

9. Stewart, G. N.: Studies on the Circulation in Man, Heart 3: 33, 1911-12. 10. Brown, G. E.: Calorimetric Studies of the Extremities. III. Clinical Data

on Normal and Pathologic Subjects With Localized Vascular Disease, J. Clin. Investigation 3: 369, 1926.

17. Landis, E. M., and Gibbon, J. H., Jr. : A Simple Method of Producing Vaso- dilatation in the Lower Extremities, With Reference to Its Usefulness in Studies of Peripheral Vascular Disease, Arch. Int. Med. 52: 785, 1933.

12. Gibbon, J. H., Jr., and Landis, E. M.: Vasodilatation in the Lower Ex- tremities in Response to Immersing the Forearms in Warm Water, J. Clin. Investigation 11: 1019, 1932.

13. Coller, F. A., and Maddock, W. G.: The Differentiation of Spastic From Organic Peripheral Vascular Occlusion by the Skin Temperature Response to High Environmental Temperature, Ann. Surg. 96: 719, 1932.

14. Lewis, T.: Vascular Disturbances of the Limbs, New York, 1936, The Macmillan Co., and Lewis, T., and Pickering, G. W.: Vasodilatation in the Limbs in Response to Warming the Body, With Evidence for Sympathetic Vasodilator Nerves in Man, Heart 16: 33, 1932.

15. Pickering, G. W.: Vasomotor Regulation of Heat Loss From Human Skin in Relation to External Temperature, Heart 16: 115, 1932.

16. Uprus, V., Gaylor, J. B., and Carmichael, E. A.: Vasodilatation and Vasocon- striction in Response to Warming and Cooling the Body, Criticism of Methods, Clin. SC. 2: 301, 1936.

17. Brown, G. E.: Treatment of Peripheral Vascular Disturbances of Extremities, J. A. M. A. 87: 379, 1926.

18. Brown, G. E., Allen, E. V., and Mahorner, H. R.: Thrombo-Angiitis Obliterans, Philadelphia, 1928, WV. B. Saunders Co.

79. Cook, E. N., and Brown, G. E.: Vasodilating Effects of Ethyl Alcohol on Peripheral Arteries, Proe. Stat?? Meet., Mayo Clin. 7: 449, 1932.

30. White, J. C.: Diagnostic Blocking of Sympathetic Nerves to Extremities With Procaine; Test to Evaluate the Benefit of Sympathetic Ganglionectomy, J. A. M. A. 94: 1382, 1930.

21. White, J. C.: Diagnostic Novocaine Block of Sensory and Sympathetic Nerves; Method of Estimating Results Which Can Be Obtained by Their Permanent Interruption, Am. J. Surg. 9: 264, 1930.

22. Scott, W. J. M., and Morton, J. J.: Sympathetic Activity in Certain Diseases, Especially Those of the Peripheral Circulation, Arch. Int. Med. 48: 1065, 1931,

23. Scott, W. J. M., and Morton, J. J.: The Differentiation of Peripheral Arterial Spasm and Occlusion in Ambulatory Patients, J. A. M. A. 97: 1212, 1931.

54. Brill, S., and Lawrence, L. B.: Changes in Temperature of the Lower Ex- tremities Following the Induction of Spinal Anesthesia, Proc. Sot. Exper, Biol. & Med. 27: 728, 1930.

25. Morton, J. J., and Scott, W. J. M.: Methods for Estimating the Degree of Sympathetic Vasooonstriction in Peripheral Vascular Diseases, New England J. Med. 204: 955, 1931.

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Starr, I., ir.: Change in the Keacatil,u of the Skin to Histamine as Flvidence (II Deficient Circ~ulation in the Lowvchr Extremities, .T. A\. M. A. 90: SW, 193X.

ldem : The T’alue of the (‘utaneous Hixtamin Reaction in the Prognosis of

Pedal Lesions in Diat~ett+ M<bllit us ; After-Histllrity of S!l Patients fol I<‘ive Years. Am. J. 111. Rc. 188: 54s. 1934.

Prognostic i’alue in “ Nephritii ” With (+eneralizrd Edema, .T. A. hf. A. 82: 142.5 192-r.

Ritlr, Auguit : Die Entstrhung (lrs ~‘ollatrrxlkreirla~~f~. ‘I‘hril II. Utlr Riickflus:: 11~s Rlutes aus ischiimis~~hrn Kiirl~crtlleilc‘n, A\rc~l~. f. Imtli. Aliat. u. f. klin. Mwl. 153: 306. 1898.

Med. 11: 373, InNI. .

Barker, X. W., Brown, U. E., and Koth, Q. %I.: Kffect uf Tissue E>xtracts on Muscle Pains of lsvh~rui~~ Origin (Intermittent (‘laudi(~:lticlu I, .4rrl. .I. M. SC. 189: 36, 1935.

Simmons, 11. T.: Interlllitt~~llt (‘Iautli~~:ction autl Its Quantitativt~ &asurrlrlrnt. Lancrt 1: 72, 1936

Hitzrot, I,. H., Naide. >I., and I,andis, E. &I.: Intermittent C’laudicatir~rl Studied 11y a Graphic Method, Au. HEART J. 11: 513, 7936.

Veal, J. K.: Adequate (Circulation in the Extremities. ’ Arterlogra1)h.v as a Test for I)rttbrmining Its Linrits. l+limin:rry Rrl)orf I<:ts;r~l on %I $,mpnt:k- tions. .T. A. hf. A. 104: .5-i!?, 1935.

DR. NEI,SON W. B~P,KRK ( KwhehtcAr, Minn.).-1 think that this presentation is

an excellent statement of thch prohlrn~ of study in WS~B of prripheral vaWular dis-

ease. Two comparatively simple tests were not dis(*ussc~d: ( 1) The ~~laudic~ation test. which can be done in sever;rl different w:~ys, eitht>r with apparatus or by having the patient take a tixed number of steps per minute under standard mvironmental conditions in order to ascertain thr time necessary for czlaudicnt,ion to tlevelop. Thir is a test of the functional cap:u+itg ol’ the (*irculation of the muscles, whereas most of the other tests measure the fun&onsl capacity of tllc (lirl*ulation of the skin. (Z) The elevat,ion-dependencay test, tlrr value of whi(lh 1 would like to emphasize.

This requires no apparatus, hut sl~ould he done under cont~rolled environmental temperatures, and, when comparxt iv(l t rsts are matlt~, they shoul~l be done at the same time of the day and at the samcl time after ingeat.ion of food. The patient’s

feet should he elevated for a fixed period until maximal blanching has occurred; then the feet are rapidly plaw~l in the dependent position, and the time required for

I\IOSTGOMERY ET AT.. : PER1PHER.U. C.\SCI‘IAR DISEXSR 803

the color to return is recorded. Thir; simple test gives considerable information RR

to the functional rapacity of the circulation of the skin of the fed.

1 ~-oul(l like to emphasize another fact whi(~h has some hewing on prOgnOSis. ilrterial insufficienr,v of consid~r:~hle d~jqec which has conic on rapi+ ma)’ he a

rnuc~h greater h:~zrtrtl as far a8 the development of gangrene is concerned than the same degree of arterial insufficiency which has wme on gr:lduallg or llXs been present for a considerable period of time. The tissues ma-y develop :L capacity to exist under cwnditions of considerahlo iwhemia if it does not ~lerelol~ to0 rapidly.

DR. I). 11’. I<MMI.:K (Pt~iladelpliia).--I was please11 tcl he:tr Dr. Montgomery’s pflptV. I tllink cirwlatory function teats have now rcnrl~etl the point where they nrr c~onsitlercd as neceess;nr,v procedures in diagnosing perit~hcrd vnsrulnr diSO~dP~%

It is now generally recognizetl that a hidory and nn rs:lmination of the peripheral

puls~h HI’C not sufficient because the patient niny have :I good tlorrralis pedis pulse

:~nd still have gangrene. On the other hand, the Ilordix ldis lmlre m:ly be absent even when the patient 112s an effieienf circulation.

There are about thirty twts which rn~y he ernploye~l. Some of them are more practical than others. Home are prohibitive hewwe elf their expense and ran only he employed in hospitals anil clinics.

I wts glad to hear Dr. Montgomery tliscusa tfle oscillometer. This method of studying the circulation has been unduly I.riticaized. Althou$~ it 11:~s its tlrawbacaks, it

does give definite information. particularly pertaining to mass pulsation of the lrlrger vessels.

Thr histamine test is :I simple procrdurr thnt is inexpensive and wn he per- formecl in the offire. It gives us definite information 3s to the caapillary rwponsr rind, indirectly, the rondition of the underlying vessels.

Caloromctric: and thermometric ,&dies we helpful in tlcridiq whether We are tlealing tvith organic ocdusive conditions or vaso~pwm. However, all of these tests still require checking up ant1 further investigation.

Even our views concerning skin surfwe tempewture studies, which we accept as our most reliable method, nl:iy some tlap rquire moilific:dion. -4t the present time I have two patients who apparently have the classid clinical mnnifestntions of

thromhoanyiitis obliterans, but their skin surfacse temperature can be made to rise to maximum limits. This would indicate that we mere dealing entirely with v:~sosp:~rr~, hut I doubt whether this was true in these particular l*ases.

I hope that, others will continue to investigde the various ciwulntory function test* and help establish their value in interpreting the various pathologic~ ilisordrrs of the

peripheral circulatory system.

DR.. HI~GII i%owr(:oBrERv (Plrilxtlrlpllia).--Tliere is, of course, s long list of tests. T\-e started out to ~liswss approximately twenty-five of ttiqm. hut raw that I llis was impossildr.*

Certainly the claudication test has c~onsiderahle value, dthough I think not as much :LS some of the others, because walking alone will give very good information concern- ing the funrtion of the cd or foot musrlrs, except in unusual (aircumstances.

I do not altogether agree with Dr. Barker that the elevation ant1 dependency test is fairly acwratr. We look on it more, I think it is fair to s:~p, as x part of the pllysid examination. Very useful inftrrmation (aan he gained from it, as it certainly

can be from the physicnl ex:Unination in general, flntl we xre not trying in any way to leave the impression that these tests take the plwe of a thorough physical exarnina- tion.

I Wts wondering whether Dr. Kramer ‘8 patient LVVRS not one whtr did have thromho- angiitis ohliterans, but nevertheless hat1 perfectly m,rrn:d fundion-in other words, R patient who Ilad ohtainetl his ~ollnteral cirrulation.