Vous êtes sur la page 1sur 10

Phlegmasia Cerulea Dolens: '

A 10-Year Review
J. MANLY STALLWORTH, M.D., GILBERT B. BRADHAM, M.D., RICHARD R. KLETKE, M.D.,
RICHARD G. PmcE, JR.,"* M.D.
From the Department of Surgery, Medical College of South Carolina and
Roper Hospital, Charleston, South Carolina

PHLEGMASIA CERULEA DOLENS, although injected with a sclerosing agent during


recognized 400 years ago,'5 continues to a saphenous vein operation in 1949. Gre-
have a mortality rate of 25 per cent and an goire,23 in 1938, described this condition as
amputation incidence of 50 per cent.45 The phlegmasia cerulea dolens.
purpose of this study is to review 55 cases In the early 1900's there were several
previously recorded in the literature be- case reports, some of which appeared to
tween 1954 and 1964 and to report 14 ad- include arterial thrombosis in addition to
ditional cases. Each patient in this series venous occlusion. In 1939 DeBakey, Burch
was observed by at least one of the authors. and Oschner" found that either chemical
Cases reported prior to 1954 have been phlebitis or ligation of the iliofemoral vein
reviewed by Moser.45 produced severe arterial spasm which could
be relieved by sympathectomy. They fur-
History ther demonstrated that similar arterial
Following the first recognition of gan- spasm was initiated when an exudate was
grene from venous thrombosis by Fabricius produced by irritating chemicals injected
Hildanus in 1593,15 it was nearly 300 years adjacent to the veins. McMasters and Par-
before Cruveilhier 9 described that this con- sons 40 pointed out that in the absence of
dition was produced only by extensive arterial pulsations the lymph flow was slow,
thrombosis of large and small veins. In while in the presence of pulsations the
1859 and 1894 Heuter 28 and Gaillard 20 re- flow was rapid. Thus a generalized hy-
ported isolated cases. In 1924 Buerger5 pothesis implied a relationship of veins,
reiterated the massive venous occlusion arteries and lymph vessels in the extremity
theory and clarified the clinical picture. during an acute thrombotic process. It was
In 1937 Fontaine and deSouza-Pereira 18 shown that venous irritation by mechanical
showed that complete ligation of the ve- occlusion, inflammatory occlusion or peri-
nous circulation in the leg of the dog pro- venous inflammatory changes resulted not
duced gangrene, as it was already known only in venostasis but also in severe arterial
to do in the intestine. This phenomenon spasm which, in turn, could markedly im-
was reproduced unintentionally in man pede the lymphatic return and cause fluid
when the femoral vein was ligated and retention in the limbs of experimental ani-
mals.
*
Presented before the Southern Surgical As- Leriche,34 however, thought that the
sociation, Dec. 8-10, 1964, Boca Raton, Fla. edema was due to peripheral vasospasm
**
Present address: Beaufort, South Carolina.
Supported in part by the John A. Hartford and that sympathetic block relieved the
Foundation. edema. Laufman et al.,33 utilizing the mi-
802
'olume 161 PHLEGNIASIA CERULEA DOLENNS
Number 5 803
croscopic observation technics of Knise-
l1ey,Ul. 3' studied the intravasctlar cellular
flow following experimental vascular oc-
clusion in the mesenteric vessels and dem-
onstrated that there x-vas moderate dilation
of tributary veins and miarked spasm (lup
to original caliber) of associated arteries.
The capillaries, wvhile usually mcarkedly-
dilated, wvere occasionally narrow-ed as if
thiey wvere in spasm. After venous occlusion
was released the arteries remained in
spasm. During prolonged venous occlusion
there were increased aggregcates of red
blood cells, followved 1y clumping and in-
travascular thrombosis of both arteries and
v-eins.
In 1951 Veal and associates restudied
the effects of major vein occltusion in the
mesenterv of dogs cand observed that after
one hour of occluision, venouis pres-
venoius
sture reached865 mm. wvater and(I the bowel
became "deep purple, edematotus and pete-
clhial. Hemorrhcages wvere present thfroui gl-
ouit the mesenterv." Arterial pressture wV1as FIG. 1. F. M., 57-year-old wN-oman wvith early
miaintained buit puilsations wvere "hardlxv phlegmasia ceruleacldolens, shjowNNinig v,iolet discolor-
altion swelling, early bullate formation an(I impend-
demonstrable . the arterial svstem re-
. .
ing gaangrene of the toes.
mained open and spasm did niot develop.
The blood flow\N came to a stan(Istill when The disease occcurs Imlost frequently be-
the venouis pressuire realched its peak." tw-een the ages of 40 to 49, (Fig. 2) and is
equally pre'valent anmong mein and women.
Methods and Materials There w-ere no Negro patients among the
Clinical Picture 69 cases with plhlegmasia cerulea dolens.
The classical picture of phlegmllasia certi- More than 91% of p-atients (Table 2)
lea dolens asdeilmonstrated in the 69 pa- described somile form of thrombophlebitis,
tients reported is suddenipain ( 7.5% ) in diseaLse or operation immediately preceding
the involved extremity followN-ed by swelling, the onset of acute symnptoms. About one
and a blue-violet color in the skin (Fig. 1). fourth gave a hiistory of chronic thrombo-
In one fouirth of the cases, the onset of the phlebitis hile another one fourth de-
triad of symptoms gradual (Table 1).
was scribe(d acuite plhlegmasia alba dcolens as

FIG. 2. Incidence ac-


cording to age and sex.
There wvere 34 males and
34 females (sex not men-
tioned in one report).
804 STALLWORTH, BRADHAM, KLETKE AND PRICE Annals of Surgery
May 1965
TABLE 1. Occurrence of Symptoms: Pain, Edema As the process continues, bullae may de-
and Cyanosis velop and para-esthesias or motor paralysis
Prev. Pres. Av. may ensue (Fig. 3A). Renal damage or
Occurrence Cases Series Total %/c failure may follow rapidly as the anoxic
process extends. If death does not prevail,
Gradual onset 12 5 17 24.7
Sudden onset 43 9 52 75.3 gangrene (Fig. 3B) of varying degree de-
velops in about 31.9% of patients (Table
4), resulting in major amputation (Fig.
the forerunner of phlegmasia cerulea 3C). Of the entire group, 29%o show evi-
dolens. In approximately 50% of the pa- dence of pulmonary emboli, but only 7.2%o
tients there was a history of cancer, ulcera- died as a result of the emboli. Approxi-
tive colitis, pneumonia, heart failure, dia- mately 46.8% of the survivors develop the
betes or tuberculosis as antecedent dis- typical post-phlebitic syndrome (Table 4).
eases. A history of recent operations was Included in this group are those who had
present in 20% of the patients. (Many pa- non-fatal pulmonary emboli or tissue loss
tients describe carcinoma and operation or or both.
phlebitis and operation as concomitant dis- At any stage the acute process may sub-
orders.) No history of any preceding dis- side spontaneously or be aborted by sup-
order was reported by 8.7% of the patients. portive measures. Death occurred in 31.9%o
On examination, the extremity is blue, of the patients (Table 5); the major single
edematous and painful in practically all cause was advanced cancer (36.3%o), yet
(over 95%) patients (Table 3). Some show this severe type of phlebitis and its compli-
signs of varying degrees of shock since cations accounted for 49.9% of the deaths.
enormous quantities of fluid may be trapped
in the involved part. Often the massive Treatment
edema prevents adequate detection of distal The management of patients with phleg-
pulses which may account, in part, for the masia cerulea dolens has been rather loosely
absence of pulsations in about 52% of pa- categorized, and combinations of methods
tients. On the other hand, these pulse find- have made accurate appraisal of treatment
ings may be a distinguishing feature of the impossible. However the impressions have
disease. About 88%o of the patients are been summarized in Tables 6 and 7.
described as having coolness of the in- Elevation of the part to prevent im-
volved extremity. pedance to the already partially ob-
TABLE 2. Antecedent Conditions TABLE 3. Physical Findings

Prev. Pres. Av. Prev. Pres. Av.


Conditions Cases Series Total 7 Findings Cases Series Total 5

Chronic Blue discol-


phlebitis 17 3 20 28.9 oration 55 14 69 100
Acute Edema 53 14 67 97.1
phlebitis 12 4 16 23.2
Pain 53 13 66 95.6
Disease* 29 6 35 50.7
Pulses
Operation 13 1 14 20.3 present 23 11 34 49.3
(Total) (91.3) Pulses
None 2 4 6 8.7 absent 32 3 35 51.7
Decreased
*
Cancer, ulcerative colitis, pneumonia, heart failure, skin temp. 47 14 61 88.4
diabetes or tuberculosis.
Volume 161
Number 5
PHLEGMASIA CERULEA DOLENS 805

FIG. 3. A. A. C., 39-year-old woman. Advancing stage of phlegmasia cerulea dolens, showing early
gangrene of toes and advanced bullae formation. B. Progression of disease showing frank gangrene of
toes and forefoot C. Symes amputation. End result of disease process seen in A and B.

structed venous flow was generally prac- propagation of the clot and in postoperative
ticed (73.9%). management to prevent reformation of clot.
Heparin was used in 81.3%o of the cases Exercise, both active and passive, was
studied. Ordinarily its use was avoided advocated by Veal 56 in 1957. In the present
when bleeding from a concomitant disease, study seven patients were treated in this
such as ulcerative colitis, existed. It was manner, three of whom sustained fatal pul-
used in nonoperative treatment to prevent monary emboli. Of the survivors two had
post-phlebitic symptoms.
Sympathetic blockade-as first recom-
TABLE 4. Results
mended by Leriche 35 and later by De-
Prev. Pres. Av.
Results Cases Series Total 6X TABLE 5. Associated Diseases as Cause of Deatl/

No residual 15 2 17 36.2** Prev. Pres. Av.


Causes Cases Series Total ;
Post-phlebitic
syndromet 18 4 22 46.8**
Pulmonary emboli 4 1 5 22.7
Loss of tissue* 11 4 15 31.9**
Metastatic disease 7 1 8 36.3
Pulmonary
emboli 13 7 20 29.0*** Phlegmasia cerulea
dolens 4 2 6 27.2
Death 16 6 22 31.9
Myocardial infarction 1 1 4.5
* Gangrene in varying degree. Bleeding diathesis 1 1 4.5
** % of those living. None given 1 1 4.5
* % of total; 7.2%o died.
t Including those with loss of tissue and nonfatal Total 16 6 22 31.9
pulmonary emboli.
806 STALLWORTH, BRADHAM, KLETKE AND PRICE Annals of Surgery
May 1965
TABLE 6. Types of Treatment in Total Series of Patients
No Post Tissue Av.
Treatment Residual Phlebitis Loss Death Emboli Total %
Heparin, elevation 3 2 3 7 3 14 20.2
Heparin, elevation, exercise 2 2 0 3 3 7 10.1
Heparin, elevation, block 4 5 3 2 2 13 18.8
Heparin, elevation, block, vasodilator 3 1 4 2 2 9 13.0
Heparin, block, thrombectomy 1 2 1 0 1 3 4.3
Heparin, thrombectomy, ligation 2 1 0 0 1 3 4.3
Heparin, thrombectomy, ligation, block 0 1 0 0 0 1 1.4
Heparin, block, fasciotomy, vasodilator 0 0 0 1 1 1 1.4
Heparin, thrombectomy 0 0 2 3 2 4 5.7
Heparin, fasciotomy 0 1 0 0 0 1 1.4
Elevation, ligation 0 1 0 0 1 1 1.4
Elevation, ligation, block 0 1 0 0 0 1 1.4
Elevation, thrombectomy, ligation, block 1 0 0 0 0 1 1.4
Elevation, thrombectomy, ligation, and vaso-
dilators 1 2 1 1 2 5 7.2
Thrombectomy 0 0 0 1 1 1 1.4
Block, ice pack 0 0 0 1 1 1 1.4
Vasodilators 0 2 0 1 0 2 2.8
Not specified 0 1 1 0 0 1 1.4
Total 17 22 15 22 20 69 100.0

Bakey,12 Edwards 14 and others-was ef- loss. Where the process had extended far-
fected as a lumbar sympathetic block, ther, nerve block was useless. In 30 pa-
spinal anesthesia or caudal anesthesia. tients who received sympathetic block,
Those patients treated by nerve block either alone or in combination with other
within 6 hours of onset showed very good measures, the mortality was 20%. In 33%
results, not only temporarily but, at times, of cases there resulted a postphlebitic syn-
permanently when the process was rather drome and in 30%o there was no residue.
dramatically reverted from phlegmasia ce- Vasodilation as a form of treatment has
rulea dolens to phlegmasia alba dolens. varied from reflex heating methods to
Even in the later stages, after demarkation chemicals such as alcohol, Priscoline®,
of gangrenous parts was partially deline- Ilidar®, nicotinic acid, papaverine, etc. In
ated, sympathetic interruption often re- several instances, Priscoline® given intra-
lieved pain and produced clinical evidence arterially and Ilidarg given intravenously
of increased blood flow to the level of tissue seemingly improved the color and tempera-
ture of the extremity. Otherwise the results
TABLE 7. Sutmmary of Types of Treatment appeared equivocal.
Thrombectomy with central ligation of
Treatment (alone or with No. drainage veins, as advocated by DeBakey 12
other methods) Patients %c
in 1949, has in the past 10 years been used
Elevation 51 73.9 along with various other nonoperative
Heparin 56 81.3 methods of treatment in 27 instances. There
Exercise 7 10.1
43.5 were three deaths (11%). Four patients
Sympathectic block 30
Vasodilators 17 24.6 (15%) survived without residual disease.
Thrombectomy & ligation 27 39.1 In these 27 patients the surgical measures
Thrombectomy 8 11.6
Fasciotomv 2 2.9 included ligation of the vein, not only
adjacent to the clot but also at higher levels,
Volume 161
Number 5
PHLEGMASIA CERULEA DOLENS 807
such as vena cava ligation followed by There were four deaths and only one pa-
common femoral thrombectomy. tient lived without residual damage.
In addition to this group, there were two Fasciotomy as a means of relieving tissue
patients who had venous ligation without tension was tried several times along with
thrombectomy. Both survived but had the many other forms of treatment. Results are
typical postphlebitic syndrome. difficult to evaluate, but each author be-
Thrombectomy-as recommended previ- lieved that the diminished tissue tension
ously by Mahorner, 6 Haller,25 Fogerty 16 afforded evidence of improvement, although
and others-without venous ligation, but sometimes only temporary.
in combination with various other methods Medicinal therapy such as cortisone, fi-
of treatment, was used in eight instances. brinolysin, Butazolidin®, antibiotics, etc.,

TABLE 8. SummarAy of Patients on Present Series

Age
Name Sex Symptoms Past History Examination Treatment Result (cause of death)

E. A. 76 Gradual pain, edema, Chronic phlebitis, Pain, edema, blue, Block, heparin, Tissue loss, B-K amp.
F blue, cold, (3 ex- Ca gall bladder cold, pulses + fibrinolysin, (bilat.)
tremities) (found at cortisone
autopsy)
S. C. 45 Sudden pain, edema, Operation Pain, edema, bltue, Thrombectomy Death (bleeding diathesis
M blue, cool cool, pulses + attempted, following pulm. em-
pulm. emboli bolectomy, pulm.
in OR emboli)
A. C. 39 Gradual pain, edema, Acute phlebitis, Pain, edema, blue, Block, heparin, Tisstue loss, Sy-mes amp.
F blue, cool broken ankle cool, ptulses + elevation,
vasodil.
J. E. 56 Sudden pain, blue, None related Pain, edema, blue, Block, heparin, Post-phlebitic syndrome
M edema, numbness cold, pulses + elevation (mild)

F. F. 57 Sudden edema, blue, Diabetes, lupus Edema, blue, cool, Thrombectomv, Death (myocard. infarct)
F cool erythematosis pulses +, no heparin, p1ulm. emboli (in-
pain cortisone cidental)
A. G. 59 Sudden pain, edema, None related Pain, edema, blue, Block, heparin, Death (phlebitis an-I
M blue, cool cool, pulses + vasodilators p)ulm. emboli)
L. H. 20 Gradual pain, edema, Acute phlebitis Pain, edema, blue, Block, heparin, Death (renal fail-tissue
F bltue, cool cool, pulses - elev., vasodil., necrosis, limb)
fasciotomv
F. M. 57 Sudden pain, edema, Acute phlebitis, Pain, edema, blue, Block Death (metastatic Ca)
F blue, cold diabetes (cont'd) cold, pulses -
p)ulm. emboli (inci-
dental)
T. McA. 55 Sudden pain, edema, Chronic phlebitis, Pain, edema, blue, Block, heparin, Post-phlebitic syndrome
M blue, cold operation cool, pulses + thrombectomy (moderate)
W. R. 19 Sudden pain, edema, Chronic phlebitis, Pain, edema, blue, Block, heparin, Post-phlebitic syndrome,
M blue, cool old pulm. emboli cool, pulses + vasodil., tissue loss, skin graft,
thrombect, pulm. emboli
elevation
W. S. 19 Gradual pain, edema, None related Pain, edema, blue- Block, heparin, Complete recovery
M blue, cool red, cool, pulses+ cortisone,
vasodil.
K. V. 49 Suidden pain, edema, None related Pain, edema, blue, Treated else- Tissue loss, toe amp.
M blue, cool cool, pulses - where
P. WV. 76 Gradual pain, edema, Congestive heart Pain, edema, blue, Block, heparin, Death (pulm. emboli)
F blue, cool failure cool, pulses + elevation
J. WV. 29 Sudden pain, edema, Acute phlebitis Pain, edema, blue, Block, heparin, Complete recovery
F blue, numb after pneumonia cool, pulses - elevation,
vasodilators
808 STALLWORTH, BRADHAM, KLETKE AND PRICE Annals of Surgery
Mlay 1965
could not be appraised accurately. In in- addition, the recent operative approach-
dividual instances cortisone or antibiotics removal of the major thrombus-actually
were used to treat associated diseases. reverses the process originally instigating
Transfusion and other forms of suppor- the massive venous occlusion. Obviously, if
tive treatment were often used, especially progressive venous occlusion and vasospasm
when there was acute loss of fluid in the are not relieved before tissue necrosis oc-
edematous limb. curs, neither thrombectomy, sympathetic
Discussion block nor any other method of treatment
will help.
The cause of phlegmasia cerulea dolens In some instances of massive carcinoma-
is unknown, but accumulated data afford tosis, no combination of methods of treat-
certain theoretical impressions. Massive ve- ment was affective; however, in uncom-
nous occlusion, no matter what the etiology, plicated cases, evacuation of the forward
produces marked venous pressure eleva- clot and release of vasospasm appeared
tion locally,14 56 concomitant venous dilata- paramount in preventing harmful sequelae.
tion,33 sludge formation and minute propa- The importance of heparin and, to a
gating thrombi.33 There is arterial spasm'2' lesser degree, vasodilators, is well estab-
33 without changes in arterial blood pres- lished. Elevation of the diseased parts to
sure,56 but with marked diminution of ar- promote gravity drainage is sound.
terial flow * resulting in ischemia of the Exercise in the presence of unfixed blood
capillary system and producing an abnor- clot has resulted in a high rate of pulmonary
mal escape of fluid and red blood cells. embolus and death. In the case of opera-
With diminished blood flow there is slowed tive thrombectomy, this embolic phenome-
lymphatic return,40 thus aiding in the re- non is apparent when passive motion is
tention of fluid. If tissue tension from swell- used to effectively expel distal clot. The
ing exceeds arterial pressure, additional physical action of muscle tension propels
ischemia results. centrally, not only blood but also any float-
When the major venous occlusion is re- ing object in it.
leased experimentally, associated venous There had been some underlying disease
pressure returns to normal, but diminished process or recent operation in 91.3% of all
arterial flow tends to remain lowered. Since patients. Strict precautionary measures de-
inflow arterial blood pressure remains un- signed to prevent venostasis and to promote
changed and outflow venous pressure re- venous return to the heart are indicated.
flects only mechanical obstruction, there This is especially true in postoperative pa-
appears to be some partial obstructive force tients and in those with either acute throm-
in smaller vessels. Whether this is arterial bophlebitis or sequelae of chronic phlebitis.
or venous in origin is conjectural. There is In two patients the application of heat to
obvious venostasis in capillaries and ven- the early acute phlebitic limb was be-
ules as shown by blue skin or bowel. The lieved to have increased swelling and prob-
entire process can be established in a ably aided in conversion from phlegmasia
shorter time than is needed for normal in alba dolens to phlegmasia cerulea dolens.
vivo clotting. Impedence to blood flow Severe pain accompanying the usual phle-
could be due to sludging and ultimate clot- bitis may be the first sign of impending
ting of red blood cells in smaller vessels or massive thrombosis. Early decision re-
to small vessel spasm or both. If the latter garding anticoagulants, sympahtetic block,
prevails, the theory of sympathetic block is thrombectomy, etc. is strongly indicated if
supported from a physiologic aspect. In the thrombotic process is to be relieved be-
* This
experimental work to be published later. fore tissue necrosis occurs.
Volume 161 PHLEGMASIA CERULEA DOLENS 809
Number 5
The possibility of venous and arterial ing refrigeration anesthesia and tourniquet
spasm in addition to the obvious venous when indicated in preparation for amputa-
thrombosis has been debated for centuries. tion.30
In the present review many dramatic con- Summary
versions from the blue phlebitis to ordinary
white phlebitis have been noted to follow During the past 10 years, 55 patients with
sympathetic interruption. Pain, in almost all phlegmasia cerulea dolens have been re-
instances, was relieved or improved whether ported. In the same interval 14 additional
or not tissue necrosis was present. Return patients were observed by the authors.
of warmth to the skin was sometimes only These 69 patients comprise the basis for
transient. Best results from sympathetic the present study.
block were derived during the first 6 hours Despite the recent advances in treatment
after onset of the acute phase. of vascular diseases, the basic physiopatho-
Thrombectomy, as recommended by logic differences between phlegmasia alba
many authors12, 14,16, 36 has also yielded dolens and phlegmasia cerulea dolens are
many excellent results. Failures, which oc- not entirely understood. There is, unequivo-
curred about as often as successes, appear cally, massive venous occlusion, but there
to have been due to reformation of clot, must be other factors, since at times spon-
pulmonary emboli and inability to remove taneous recovery and dramatic improve-
clots from tributary veins. Thrombectomy ment follow thrombectomy, simple ligation
after venous ligation, while popular as a of the vena cava or sympathetic blockade.
form of treatment in the early part of the The exact causes of ischemia and gangrene
past decade, has recently been replaced are conjectural, but obstruction to blood
almost entirely by thrombectomy alone. flow at the arteriole-capillary-venule level
There was no reported instance where par- is probably a factor. This obstruction may
tial occlusion of the vena cava was prac- be due to spasm of the vessels or stasis
ticed in this series of patients, although thrombosis or both.
total occlusion was performed several times Since the occlusive process may involve
with satisfactory results. more than one venous system in distant
The principles of treatment appear to be parts of the body and is often associated
as follows: with malignant disease there may be an
associated but unrecognized chemical re-
1. Recognize the disorder which precedes action.
the phlebitis and meticulously prevent Regardless of the type of treatment, the
venostasis. overall mortality is 31.9%. Of surviving pa-
2. Relieve venous and arterial spasm by tients, 31.9% lose tissue and 46.8% have
some form of sympathetic blockade. post-phlebitic syndrome. Once the disorder
3. Promote venous return by elevation of is recognized, the described principles of
the involved parts in relationship to the management should be observed.
level of the heart.
4. Remove major offending thrombus References
when possible. 1. Anlyn, W. C., G. D. DeLaughter, Jr., J. I.
5. Be prepared to partially or completely Fabrikant, J. W. Sullenberger and W. T.
Weaver: Management of Acute Venous
occlude the vena cava when there is evi- Thromboembolism. J.A.M.A., 168:725, 1958.
dence of pulmonary emboli. 2. Anlyn, W. G., J. K. Isley, J. F. Schauble, G.
J. Baylin and R. W. Postlethwait: Labora-
6. Prevent additional thrombosis by main- tory Studies in the Evaluation of Postphle-
taining adequate heparin levels. bitic Disease. Arch. Surg., 76:228, 1958.
3. Boyd, D. P. and F. M. Clarke: Phlegmasia
7. Amputate gangrenous tissue early us- Cerulea Dolens. Surgery, 51:19, 1962.
810 STALLWORTH, BRADHAM, KLETKE AND PRICE Annals of Surgery
4. Boyd, J. F. and G. Smith: Gangrene due to 28. Heuter: Fall von Gangran in Folge von
Acute Massive Venous Occlusion of a Limb. Venenoblit. Virchows Arch. Path. Anat., 17:
Brit. J. Surg., 44:179, 1957. 483, 1859.
5. Buerger, L.: The Circulatory Disturbances of 29. Humphrey, D. C. aiid R. M. Davie: Phleg-
the Extremities. Phila., W. B. Saunders, Co., masia Cerulea Dolens. Guy's Hosp. Rep.,
1924. p. 628. 108:76, 1959.
6. Carroll, B. J.: Clinical Observations in the 30. Jeffords, J. V. and J. M. Stallworth: The Use
Treatment of Phlebothrombosis with Fi- of Refrigeration Anesthesia (Regional Hypo-
brinolysin. Angiology, 10:308, 1959. thermia) for Amputation in Poor-Risk Pa-
7. Carroll, B. J. and C. Lomack: Phlegmasia tients with Peripheral Vascular Diseases.
Cerulea Dolens Treated with Fibrinolysin Amer. Surg., 22:998, 1956.
(Human). Angiology, 13:315, 1962. 31. Kniseley, M. H.: Method of Illuminating Liv-
8. Catchpole, B. N.: Massive Thrombophlebitis. ing Structures for Microscopic Study. Anat.
Lancet, 1:343, 1957. Rec., 64:499, 1936.
9. Cruveilhier, J.: Traite d'Anatomie Pathologique 32. Kniseley, M. H.: Improved Fuses Quartz Liv-
Generale, Tome IV Paris, J. B. Bailliere et ing Tissue Illuminator. Anat. Rec., 71:503,
Fils, 1862. p. 288. 1938.
10. Cywes, S. and J. H. Louw: Phlegmasia Ce- 33. Laufman, H., W. B. Martin and S. W. Tuell:
rulea Dolens: Successful Treatment by Re- The Pattern of Vasospasm Following Acute
lieving Fasciotomy. Surgery, 51:169, 1962. Arterial and Venous Occlusions. Surg. Gynec.
11. DeBakey, M., G. E. Burch and A. Oschner: & Obstet., 87:641, 1948.
Effect of Chemical Irritation of a Venous 34. Leriche, R. and Jund, A.: Recherches Experi-
Segment on Peripheral Pulse Volume. Proc. mentales sur les Oedemes Chirurgicaux des
Soc. Exp. Biol. Med., 41:585, 1939. Membres d'origine Phlebitique. J. Chir.
12. DeBakey, M. and A. Oschner: Phlegmasia Orthop., 37:481, 1931.
Cerulea Dolens and Gangrene Associated 35. Leriche, R. and J. Kunlin: Traitment Immediat
with Thrombophlebitis. Surgery, 26:16, 1949. des Phlebites post-operatoires par Infiltration
13. DeTakats, G.: Vascular Surgery. Phila., W. Novocainique due Sympatheque Lombaire.
B. Saunders, Co., 1959. p. 271. Presse Med., 43:1481, 1934.
14. Edwards, W. S.: Observations on the Patho- 36. Mahorner, H., J. W. Castleberry and W. 0.
genesis and Management of Massive Venous Coleman: Attempts to Restore Function in
Occlusion. Surgery, 43:153, 1958. Major Veins which are the Site of Massive
15. Fabricius Hildanus, G.: De Gangraena et Thrombosis. Ann. Surg., 146:510, 1957.
Sphacelo. Cologne, 1593. 37. Mahorner, H.: A New Method of Management
16. Fogerty, T. J., J. J. Cranley, R. J. Krause, E. for Thrombosis of Deep Veins of the Ex-
S. Strasser and C. D. Hafner: Surgical Man- tremities. Amer. Surg., 20:487, 1954.
agement of Phlegmasia Cerulea Dolens. 38. Manheimer, L. H. and L. M. Levin: Phleg-
Arch. Surg., 86:256, 1963. masia Cerulea Dolens. Angiology, 5:472,
17. Fontaine, R.: Remarks Concerning Venous 1954.
Thrombosis and Its Sequelae. Surgery, 41: 39. McDonald, S. T., W. N. Person and L. M.
6, 1957. Taylor: Thrombophlebitis Cerulea Dolens.
18. Fontaine, R. and A. deSouza-Pereira: Ob- Arch. Surg., 80:350, 1960.
literations et Resections Veineuses Experi- 40. McMasters, R. J. and P. D. Parsons: The Ef-
mentales; Contributions a l'etude de la Cir- fects of the Pulse upon the Formation and
culation Collaterale Veineuse. Rev. Chir. Flow of Lymph. J. Exp. Med., 68:353, 1938.
Orthop., 75:161, 1937. 41. Meek, J. R. and J. J. Maurer: Phlegmasia
19. Fontaine, J. R. and D. Taverner: Gangrene of Cerulea Dolens. Amer. J. Surg., 97:104,
the Three Limbs Resulting from Venous Oc- 1959.
clusion. Ann. Intern. Med., 44:549, 1956. 42. Miles, R. M.: Phlegmasia Cerulea Dolens-
20. Gaillard, L.: Gangrene Humide du pied Successful Treatment by Vena Cava Liga-
gauche par Thrombose de la Veine Femorale tion. A Case Report. Surgery, 30:718, 1951.
chez une Cancereuse de 27 ans. Bull. Mem. 43. Mills, E. S. and R. C. Bennetts: Phlegmasia
Soc. Med. Hosp. Paris, 11:315, 1894. Cerulea Dolens as a Cause of Gangrene of
21. Giles, E. J.: Phlegmasia Cerulea Dolens. Amer. the Fingers. Canad. Med. Ass. J., 72:917,
J. Surg., 95:429, 1958. 1955.
22. Gillenwater, J. Y., I. H. Breslow and S. Lisker: 44. Moore, R. F. and G. B. D. Scott: Gangrene of
Phlegmasia Cerulea Dolens. Circulation, 25: Venous Origin. Brit. J. Surg., 43:591, 1955-
39, 1962. 56.
23. Gregoire, R.: Blue Phlebitis (Phlegmatia 45. Moser, M., S. M. Babin, G. W. Cotts and A.
Caerulea Dolens). Presse Med., 46:1313, G. Prandoni: Acute Massive Venous Occlu-
1938. sion: Report of a Case Successfully Treated
24. Hains, R. D., C. D. McMillan and J. C. with Exercise. Ann. Intern. Med., 40:361,
Stinson: Phlegmasia Cerulea Dolens. Tex. 1954.
Med. J., 51:707, 1955. 46. Myhre, J. and R. S. Ylvisakee: Venous Gan-
25. Haller, A. J.: Thrombectomy for Acute Ilio- grene with Thrombosis of the Inferior Vena
femoral Venous Thrombosis. Arch. Surg., Cava. Arch. Surg., 69:732, 1954.
83:136, 1961. 47. Nelson, T. R., P. H. Mullally and D. A.
26. Haimovici, H.: Gangrene of the Extremities Sherrin: Phlegmasia Cerulea Dolens; Report
of Venous Origin. Circulation, 1:225, 1950. of Two Cases. Ohio Med. J., 59:58, 1963.
27. Harden, R. N. and W. R. Deaton, Jr.: Phleg- 48. Oschner, J. L. and J. K. Ronald: Phlegmasia
masia Cerulea Dolens. N. C. Med. J., 17: Cerulea Dolens after Aorto-Iliac Operations.
372, 1957. J.A.M.A., 182:144, 1962.
Volume 161
Number S
PHLEGMASIA CERULEA DOLENS 811
49. Osuis, E. A.: Acute Massive Venous Occlusion. naires: Effet Therapeutique de l'acetyl-
Arch. Surg., 65:19, 1952. choline. Bull. Med. Paris, 43:1101, 1929.
50. Rasmussen, J. A., S. E. Potter and R. R. Best: 53. Wailer, J. V.: Venous Thrombosis Simulating
The Management of Acute Massive Venous Arterial Embolization with Major Gangrene.
Occlusion. Surgery, 40:387, 1956. J.A.M.A., 165:344, 1957.
51. Ross, J. V., A. H. Baggenstoss and J. I. 54. Watt, J. H. and H. Leider: Phlegmasia Cerulea
Juergens: Gangrene of Lower Extremity Sec- Dolens, Complicated by Pulmonary Em-
condary to Extensive Venous Occlusion. Cir- bolism. New York J. Med., 54:1373, 1954.
culation, 24:549, 1961.
55. Wright, R. B.: Phlegmasia Cerulea Dolens.
Scot. Med. J., 1:267, 1956.
52. Tremoliere, F. and P. Veran: Syndrome d'ob- 56. Veal, J. R., T. J. Dugan, W. L. Jamison and
literation Arterielle due Membre Inferieur R. E. Bauersfeld: Acute Massive Venous Oc-
droit Apparue an cours d'une phlebite Super- clusion of the Lower Extremities. Surgery,
ficielle et Profonde avec Embolies Pulmo- 29:355, 1951.

DIscusSION amazing series of events takes place. The bowel


DR. MARK M. RAV1TCH (Baltimore): This is an becomes violently blue within a few minutes, the
extraordinary clinical phenomenon which Dr. Stall- veins become quite dilated, the capillaries are
worth has described so elegantly. I would like to markedly distended, whereas the arterioles become
report on a recent experience of Dr. Richard W. somewhat more narrowed as though in spasm.
Steenburg with a patient at the Baltimore City The flow virtually stops as time goes on.
Hospital, a young woman who had severe and The next slide shows the tracing from a dog
extensive bums, who developed a perfectly classi- experiment in which in the upper level, one sees
cal picture of sudden pain with a great blue-violet the measured mesentery artery flow, in the second
swollen leg. A thrombectomy was done immedi- line the mesentery artery pressure, and in the
ately, but the observation was made that the third line the mesentery venous pressure. As the
femoral artery appeared not to be pulsating. It was vein is occluded, one can see that the mesenteric
incised and a well-organized thrombus was re- artery flow is markedly diminished and goes almost
moved from it. to the zero point where it is maintained until the
She did well, and we have been wondering ever vein is released; then it becomes elevated but not
since, if this is an isolated observation or if-for quite to the point of flow that was existent before.
instance in a series like Dr. Stallworth's-there is If this period of occlusion is allowed to remain
evidence (arteriographic or postmortem dissection for half an hour, the return of arterial flow is quite
evidence) to show that this occurs occasionally, slow. If the clamp stays on longer, this flow is zero,
never or often. even though the mesentery artery pressure at this
time remains constant. The artery pulse seems to
DR. ROBERT P. MCBURNEY (Memphis): I would be normal, but there is no forward flow of blood.
like to ask Dr. Stallworth a question. He had eight At the same time the venous pressure, interestingly
cases in which he used the thrombectomy technic enough, within 2 minutes will approach that of the
described by Mahomer, Heller and others, with mean artery pressure, and is maintained until the
four deaths, and I wondered if he would give us vein is released.
some more details on those deaths. I believe that If this clamp remains on the mesenteric veins
this is the preferred treatment of this condition, for a sufficient length of time, all vessels are oc-
having used it in three cases. All of my three cases cluded by thrombus, and I imagine this is what
have been early cases, to be sure, but each has happened in Dr. Ravitch's patient.
been a gratifying success. As to Dr. McBurney's comment, it was not my
If he creates the impression that there is a 50% intent to condemn any procedure. I am simply re-
mortality with this treatment, I think it might porting what has been described in the literature
discredit what I think probably is the best treat- up to the present time. There were four deaths
ment. among those 8 patients who had thrombectomies,
and who did not have an associated venous liga-
DR. J. MANLY STALLWORTH (closing): I think tion. Three of these deaths were due to emboli,
perhaps this slide will answer Dr. Ravitch's ques- and the fourth was one of our own group of pa-
tion, at least in the experimental lab. This experi- tients who developed pulmonary embolus, while
ment has been used for a number of years, be- his leg was being prepared in the operating room
ginning in the 1800's, repeated again in 1951 by for thrombectomy. His chest was opened, he was
Dr. Veal and here we have added nothing more connected to a hear-lung pump, the clot was re-
to it than the flow meter. The pressure transducer moved, but the patient, unfortunately, had some
is attached to the proximal artery going into an type of bleeding diathesis, and continued to hemor-
isolated segment of the bowel, a venous catheter rhage from all sources over the next 3 or 4 hours.
is inserted for pressure, and a flow meter probe He subsequently died. His death was due to some
is placed on an artery in the isolated mesentery. type of clotting phenomenon, which was not con-
The vein is intermittently occluded and a rather trollable.