MINI-INCISIONAL LIGATION OF INCOMPETENT PERFORATING VEINS OF THE LEGS
Queral LA, Criado FJ
J Vasc Surg 1997; 25:437-41
ABSTRACT AND COMMENTARY BY:
John J. Bergan, MD
Professor of Surgery
Loma Linda University Medical Center
Clinical Professor of Surgery
University of California, San Diego
Uniformed Services University of the Health Sciences
In this work from the Maryland Vascular Institute, 18 patients with venous ulcerations
in 26 limbs were operated upon with the single objective of closing incompetent perforating
veins diagnosed by duplex scanning. All of the ulcerations were medially located and all patients had one to four perforating veins per leg, identified by the
duplex scan. Only one patient had greater saphenous incompetence, but 17 of the
18 patients had incompetence at the popliteal and tibial veins. Treatment was by
gel-paste boot until the day of surgery, and the perforating veins and corresponding fascial
defects were marked with indelible ink after localization was performed with the
duplex scanner. All patients had open ulcers at the time of surgery. After surgery,
a gel-paste boot was placed as a final step in the procedure. Duplex confirmation of closure
was obtained within two weeks of the procedure, and weekly applications of the gel-paste
boots were done until full healing of the venous ulcers took place.
The technical steps of the operation were unique to this procedure. Four, 6 to 8
mm, vertical incisions were placed circumferentially around the fascial defects located
by duplex. These incisions were placed directly in the skin affected by lipodermatosclerosis. The purpose of the incision was to identify the fascia clearly and to allow
placement of a 2-0 nylon suture on the fascia. A large needle was used for this
purpose. The suture passed circumferentially around the fascial defect and then
was snugly tied. This obliterated the fascial defect and interrupted flow through the incompetent
perforating vein.
A continuous-wave, hand-held Doppler transducer was used to verify the success of
the procedure and obliteration of flow in the perforating vein. Skin incisions were
left open, and after two hours of observation, the patients were discharged home.
No postoperative anticoagulation was used. The operation ranged from 6 to 25 minutes in
duration and between one and four fascial defects (mean 2.3) were obliterated. There
were no wound complications. All incisions healed and initial success in interrupting
the perforating veins was achieved in 24 of 26 legs.
In the 24 legs with perforator closure, full healing of ulceration occurred within
six weeks of the procedure. During a mean followup of 22 months, three recurrent
perforating veins had been uncovered. Permanent healing of the ulcers has been achieved
in 21 of the 26 legs.
Purse-string suture is placed through mini-incisions around fascial defect, which harbors incompetent perforator. Suture is then snugly tied, obliterating defect and interrupting flow in perforator.
COMMENTARY
This focus on perforating veins in limbs with proven deep venous incompetence isolates
the complex problem of severe chronic venous insufficiency. Clearly, superficial
venous incompetence was not addressed in this patient cohort, yet early healing of
ulcerations and lack of recurrence during the first two years of observation strongly
suggests that perforating veins are an important part of the chronic venous insufficiency
syndrome.
This operation adds another instrument to the surgical armamentarium which now includes
subfascial endoscopic perforator vein interruption, duplex ultrasound-guided sclerotherapy,
and ablation of superficial venous insufficiency in those limbs with gravitation reflux. One could envision combining this procedure with subfascial endoscopic
perforator vein surgery in order to close retromalleolar and inframalleolar perforating
veins which are outside of the visual field of the endoscope. As duplex scanning
may miss as many as 25% of perforating veins, surgeons must be aware of the fact that
failure to identify a perforating vein in a limb with clear venous etiology of cutaneous
ulceration should not exclude the patient from surgical therapy. 6338b
UPPER EXTREMITY DEEP VEIN THROMBOSIS: RISK FACTORS, DIAGNOSIS AND COMPLICATIONS
Prandoni P, Polistena P, Bernardo E, et al.
Arch Intern Med 1977; 157:57-62
ABSTRACT AND COMMENTARY BY:
Anil Hingorani, MD & Enrico Ascher, MD
Division of Vascular Surgery
Maimonides Medical Center
Brooklyn, New York
This article attempts to identify factors associated with upper extremity deep venous
thrombosis (DVT), to compare the diagnostic accuracy of ultrasonographic methods
of detection of upper extremity DVT, including venography, and to investigate the
frequency of early and long-term complications.
A total of 58 consecutive patients with signs and symptoms suggestive of upper extremity
DVT between September 1990 and July 1994 underwent blood sampling for antithrombin
III, protein C and S levels, resistance to activated protein C, and lupus-like anticoagulants. All underwent compression ultrasonography, Doppler ultrasonography, and
color-flow Doppler imaging followed by venography. If found to have an upper extremity
DVT (n = 27), a chest radiograph and perfusion scan of the lungs were also done.
Ventilation scans or pulmonary angiograms were also performed in patients with clinical
suspicion of pulmonary embolism (PE). Patients with objective findings of PE underwent
real-time compression ultrasonography and/or color-flow Doppler imaging of the lower extremities. Patients were treated with a standard anticoagulation protocol for
at least three months and were followed up at three and six months and then every
six months.
By univariate analysis, factors found to be significantly associated with upper extremity
DVT included indwelling catheters, thrombophilic states, and a previous lower extremity
DVT. Thrombophilic states were identified in 26%. Sensitivity and specificity of real-time compression ultrasonography, Doppler ultrasonography, and color-flow
Doppler imaging were 96% and 93%, 81% and 77%, and 100% and 93%, respectively. A
total of 11% were found to have symptomatic PE, and 26% of 19 asymptomatic patients
were found to have PE based on the perfusion lung scan. During followup, five patients
died of their neoplasms, two had recurrent thromboembolism, and four had moderate
to severe postthrombotic sequelae.
COMMENTARY
The authors have attempted to further characterize a disease process which has been
poorly studied with few large prospective studies. However, this present study leaves
many concerns about the methodology. For example, timing of blood sampling for the
hypercoagulable state is unclear. It has been documented that antithrombin III, protein
C, and protein S levels can be expected to decrease in the presence of acute lower
extremity deep venous thrombosis.1 If the samples were taken with a short time interval from the initiation of upper
extremity DVT, one might expect that these factors would be falsely decreased and
might return to normal if repeat testing were done at a later date. In addition,
no values are given for what the authors considered normal for antithrombin III, protein C,
and protein S. Thus, the reader is left to assume that the results for these values
were not included in the study if the patient was receiving any heparin or warfarin,
respectively.
Further assays may have demonstrated a higher incidence of a thrombophilic state.
No attempt was made to assess the activities of antithrombin III, protein C and
protein S and the level of anticardiolipin antibodies. Further characterization
of the protein C resistance by performing a factor V mutation (arginine 506 to glycine) might
be of interest.
In our series of 50 patients with upper extremity DVT undergoing a hypercoagulable
workup, we found that 45% had some underlying hypercoagulable disorder (alterations
in protein C, protein S, antithrombin III activity or antigen, activated protein
C resistance, factor V Leiden mutation, lupus anticoagulant, or anticardiolipin antibody).
The methodology of real-time compression ultrasonography is not completely clear
as the authors state if the subclavian vein was fully compressible, the test was
regarded as normal. Therefore, we must surmise that the intrathoracic subclavian
vein was not evaluated. This leads one to question the conclusion that compression ultrasonography
should be a preferred method of diagnosis over color-flow Doppler imaging. The authors
state that color-flow Doppler imaging is an expensive, time-consuming technique requiring considerable expertise. However, in many laboratories, it has become
the standard and is complementary to compression ultrasonography.
Risk factors for upper extremity DVT were analyzed by univariate analysis but a multivariate
analysis was not done.
The authors chose to evaluate the incidence of PE by perfusion scanning and chest
radiographs and to use ventilation lung scans and pulmonary angiograms in an unspecified
manner. Inconsistent use of the ventilation scan and pulmonary angiograms suggests
that the protocol followed was not standardized. In our series of 180 patients with
upper extremity DVT, we found only an 8% incidence of symptomatic PE.2 In addition, the authors compared their results to a paper citing an incidence of
asymptomatic PE of 15 to 26% and symptomatic PE of 3 to 6%.
The authors grade the severity of postthrombotic signs and symptoms into mild, moderate,
and severe but there is a failure to specify what was included in each category.
With only 6 of 27 patients being followed four years, it appears that very little
can be stated about long-term sequelae of upper extremity DVT.
The final conclusion that upper extremity and lower extremity DVT are manifestations
of the same disease process grossly oversimplifies upper extremity DVT. We reviewed
the profiles of 52 patients from our database of 180 patients with upper extremity
DVT and compared these to 430 patients with lower extremity DVT diagnosed during the
same 18-month period.3 We found that those with upper extremity DVT had a six-month mortality rate of 48%
compared to 12% for patients with lower extremity DVT. This significant difference
remained despite eliminating those with PE, metastatic neoplasm, or age greater than
75 years from the analysis. Despite having the same average age, those with lower extremity
DVT seemed to have more severe underlying medical problems as documented by higher
APACHE III scores. We suggest that patients with upper extremity DVT and lower extremity DVT are not similar.
The present study makes an attempt to further characterize upper extremity DVT. However,
flaws in methodology cloud the results. We agree with the need for larger prospective
studies but improvements in methodology are needed to obtain better characterization of upper extremity DVT. 6588b
REFERENCES
1. Bennet JS. Thrombotic Disorders. In: Textbook of Internal Medicine, 3rd ed.
W Kelley (ed). Lippincott, Raven Press, 1995.
2. Monreal M, Raventos A, Lerma A, et al. Pulmonary embolism in patients with upper
extremity DVT associated with venous central lines: A prospective study. Thrombo
Haemost 1994; 72(4): 548-50.
3. Hingorani A, Ascher E, Hanson J, et al. Upper extremity versus lower extremity
deep venous thrombosis: An analysis of morbidity and mortality. Submitted to Am
J Surg.
770 CONSECUTIVE SUPRACLAVICULAR FIRST RIB RESECTIONS FOR THORACIC OUTLET SYNDROME
Hempel GK, Shutze WP, Anderson JF, Bukhari HI
Ann Vasc Surg 1996; 10:456-63
ABSTRACT AND COMMENTARY BY:
Richard J. Sanders, MD
Denver, Colorado
Over a 28-year period, 770 supraclavicular first rib resections and scalenectomies
were performed, 92% for neurogenic thoracic outlet syndrome (TOS), 2% for arterial
TOS, and 6% for venous TOS. Good to excellent improvement was noted in 86%, fair
improvement in 13%, and failure in 1%. There were no brachial plexus injuries, permanent phrenic
nerve injuries, or vascular injuries. There was one lymphatic leak and two instances
of causalgia requiring sympathectomy.
A total of 47 patients (6%) had venous TOS, including several with primary subclavian
vein thrombosis, who were initially treated with lytic therapy and anticoagulation.
Supraclavicular first rib resection and scalenectomy were performed two to three
weeks later. The authors note excellent clinical improvement in all patients although
followup venograms were not performed.
COMMENTARY
Neurogenic TOS comprised over 90% of the cases in this study which is similar to our
own experience. Like the authors, we also prefer the supraclavicular route for scalenectomy
and first rib resection when dealing with neurogenic or arterial TOS. However, for venous TOS or subclavian vein obstruction, we employ a transaxillary approach.
The etiology of primary subclavian vein thromboses is congenital narrowing of the
passage of the subclavian vein at the costoclavicular ligament. This space must
be enlarged to prevent recurrent thrombosis, and this cannot be done through the
supraclavicular approach. In freeing the vein, not only must the costoclavicular ligament and
subclavius muscle be divided but often portions of the costal cartilage and manubrium
must also be resected. Because the authors did not perform followup venograms, the
patency and caliber of the veins postoperatively is unknown. Long-term followup of these
patients would be of interest to see if thrombosis recurred.
Our protocol in managing primary (effort) subclavian vein thrombosis is similar to
that of the authors. Initial therapy is thrombolysis with the catheter embedded
in the thrombus. The patient is also started on heparin and warfarin concomitantly
with lytic therapy. Transaxillary or infraclavicular first rib resection and venolysis is
performed within a few days of thrombolysis, and anticoagulation is continued for
the next few months. Residual stenosis in the subclavian vein is usually not treated
at the time of rib resection unless it is severe. In most patients, no further treatment
is needed. If postoperative pain and swelling develop, balloon angioplasty is tried
first. If unsuccessful, endovenectomy with a vein patch or juguloaxillary vein transposition is performed along with a temporary arteriovenous fistula. The fistula
is removed two to three months later. 6589b
IS THROMBOLYSIS OF VENOUS THROMBOSIS AN OPTION IN TREATMENT?
Cairols MA
Vasc Surg 1996; 30:451-2
ABSTRACT AND COMMENTARY BY:
Patricia E. Thorpe, M.D.
Associate Professor of Radiology & Surgery
Creighton University
Omaha, Nebraska
The treatment of acute venous thrombosis has remained administration of heparin followed
by Coumadin. There is no doubt that fibrinolytic agents can dissolve thrombi but
these have been infrequently applied. Spontaneous lysis of venous thrombi occurs
in varying degrees and is important in recanalization of the occluded vein. It has been
discovered that valvular competence remains in approximately one-third of affected
limbs, and valvular competence is directly related to rapidity of spontaneous lysis.
Some years ago, we treated 57 consecutive patients with acute deep venous thrombosis
with streptokinase. Thirty-one of these were followed up to five years by repeat
ultrasound examinations. In the femoropopliteal segment, complete lysis was achieved
in 74% and venous valve function was preserved in 77%. We also discovered that the
earlier the lytic agent was given, the more likely it was to achieve complete lysis.
In the iliofemoral segment, the problems were more formidable. Only 20% of patients
with this problem were found to have lysis and preservation of valve function. Unfortunately,
many patients have a contraindication to fibrinolytic therapy but many absolute contraindications
are being revised to relative contraindicatives.
Catheter-directed thrombolysis may improve results, and most studies in print at this
time describe systemic administration which does not give the drug directly into
the thrombus.
COMMENTARY
Dr. Cairols asks if thrombolysis is a therapeutic option for patients with deep vein
thrombosis (DVT). This is a legitimate question now that almost 40 years have transpired
since the first reported success of this lytic therapy in venous occlusion.1 Standard therapy continues to be bedrest, elevation, and heparin followed by warfarin.
Therapeutic options for DVT have increased but there has been little evolution in
the nomenclature which describes venous disorders. This has limited meaningfulness
in discussion about different therapies. Quite simply, all DVT is not the same. Thus,
consideration of an appropriate therapy must begin with an accurate definition of
the clinical problem. Yet in the mid-1990s, most physicians regard DVT as a single
entity, paying no attention to the pathophysiology behind the signs and symptoms.
In practice, there is a significant difference between patients presenting with their
first truly acute episode of DVT versus a subsequent pseudo-acute episode where the
"acute" clot is superimposed upon chronic venous changes. Patients in each category
may clinically present with "acute" DVT but response to therapy and long-term prognosis
differs.
Furthermore, DVT can be a little or a lot. Stratification of DVT distinguishes single-segment
from multi-segment thrombosis but this is rarely considered. The difference is pertinent
when discussing recanalization, an acclaimed natural process, which rarely succeeds in reopening totally occluded iliofemoral thrombosis. Further, iliofemoral
occlusion rarely occurs in isolation and is usually associated with thrombus in the
leg.2 Many reports of recanalization do not address the issue of restoration of venous
flow relative to postthrombotic clinical status. Although recanalization is widely
observed, approximately 70% of patients with DVT have some degree of pain and swelling
later. Thus recanalization alone does not adequately restore flow in extensively occluded,
multi-segment thrombosis. Thus, it is limited to being sufficient, endogenous therapy
only in single-segment, short thrombosis where injury is focal and residual obstruction or narrowing does not cause hemodynamic imbalance.
Recent investigations support the notion that rapid elimination of clot, whther endogenously
or with lytic therapy, offers the best chance of restoring valve function as Cairols
notes. But he refers to the Kakkar study which concluded that the advantage of valvular protection from early lysis was lost over time. We presume that some patients
in that study had occult chronic changes from prior episodes of DVT and were not
treated with lytic therapy. Were there already impending late sequelae from prior
DVT? Also, perhaps the lysis was incomplete and residual obstructing thrombus beyond
a valve resulted in increased venous pressures which affected distal valves over
time.3
Cairols believes in thrombolysis but he limits this option to acute DVT with symptoms
less than one week in duration. He cautions that a majority of acute DVT patients
may be excluded due to contraindications. We note that the exclusionary criteria
for lytic therapy continue to diminish, even in postoperative patients who were the focus
of Markel's analysis.4 In fact, some prior absolute contradications (e.g. older thrombus and perioperative
situations) have become relative because of safer, more efficient catheter-delivery
techniques. These optimize therapeutic results and minimize risks. Also, criteria
developed for inpatient postoperative patients does not apply to the many ambulatory,
low-risk outpatients who present in clinics or the emergency room with acute DVT
or pulmonary embolus. In recent experience, patients with symptoms for more than
seven days have repeatedly benefitted from lytic therapy. This is often augmented with stent
placement across mechanically recanalized iliofemoral occlusions.5
Therefore, we agree with Cairols that lytic therapy should be an option if acute DVT
is diagnosed and if no contraindication to therapy, including anticoagulation, exists.
However, we disagree that thrombosis older than seven days is a contraindication.
As with arterial thrombolysis, growing experience with venous thrombolysis using
catheter-delivery systems allows far greater success with variable-aged thrombus
than was ever achieved with systemic infusions in the past. Moreover, these improved
results can be achieved with fewer complications due to these technical advances.
A question remains regarding the role of lytic therapy for chronic venous disorders.
There are many patients in whom the initial diagnosis of DVT was missed during the
"acute" presentation. Later on, a subsequent event occurs which aggravates the underlying venous pathology. The future challenge is to see if thrombolysis in this setting
can mitigate the signs and symptoms of the postthrombotic syndrome. Even more importantly,
will this decrease the incidence of recurrent DVT? If we aggressively identify and treat the truly acute thrombosis as Cairols advocates, perhaps the magnitude
of chronic venous disorders will begin to diminish. 6175b
REFERENCES
1. Tsapogas MJ, Flute PT, et al. Lysis of experimental thrombi by streptokinase.
Br J Surg 1962; 50:334.
2. Bauer G. A venographic study on thromboembolis problems. Acta Chir Scand 1940:
61.
3. Lindner DJ, Edwards JM, et al. Long-term hemodynamic and clinical sequelae of
lower extremity deep venous thrombosis. J Vasc Surg 1986; 4:436-42.
4. Markel A, Manzo RA, Strandness DE Jr. The potential role of thrombolytic therapy
in venous thrombosis. Arch Intern Med 1992; 152:1265.
5. Nazarian GK, Bjarnason H, et al. Iliofemoral venous stenoses: Effectiveness of
treatment with endovascular stents. Radiology 1996; 200:193-99.
PHLEGMASIA CAERULEA DOLENS AND VENOUS GANGRENE
Perkins MJT, Magee TR, Galland RB
Br J Surg 1996; 83:19-23
ABSTRACT AND COMMENTARY BY:
Bernhard H Nachbur, MD
Berne, Switzerland
The authors have compiled a review article on a clinical phenomenon which is characterized
by its forceful and dramatic presentation. A chapter on the pathophysiology of phlegmasia
caerula dolens (PCD) and venous gangrene is followed by an enumeration of the putative etiologic factors, an overview of the clinical features, and finally
a chapter on the treatment of this highly dangerous venous disorder.
The pathophysiology of PCD and venous gangrene is especially well presented. It is
most important because it is generally not well known and is barely understood.
In contradistinction to the much more common "ordinary" deep venous thrombosis where
adequate collaterals can develop, both PCD and venous gangrene are characterized by thrombotic
occlusion of practically the entire venous cross-section of one or both lower limbs
with near total obstruction of venous return. Bilateral PCD can, of course, only
occur if the causative occlusive mechanism is situated in the inferior vena cava.
Accordingly, it is much less frequent than unilateral PCD which, not surprisingly,
favors the left lower extremity (venous spur, crossover of the right common iliac
artery).
The authors describe the buildup of venous pressure (up to 15 fold) and thereafter
of the interstitial pressure (to 25 to 48 mmHg) which will eventually overcome the
arterial hydrostatic pressure. Arterial inflow is automatically throttled and the
hydrostatic arterial pressure progressively decreases to values of 50 mmHg and less. Peripheral
pulses can disappear and be absent while femoral pulses in the groin become noticeably
weaker.
When interstitial pressure exceeds the hydrostatic arterial pressure, the so-called
'critical closure pressure' is overcome and the arterioles will occlude. Thus, ischemia
of the foot and calf muscles will ensue and venous gangrene will develop. Venous
gangrene is brought on by arterial insufficiency and is, in the last analysis, arterial
in nature.
The etiology is manifold. The authors present a long list of possible thrombogenic
factors, hypercoagulable states, and intrinsic deficiencies. They notably point
out the association between PCD, venous gangrene, and malignancies in 20 to 40% of
the cases. When malignancy is present, it is advanced and a sign of terminal illness attending
emaciated persons. This factor accounts a great deal for the poor prognosis of therapy
in these cases.
The clinical features are governed by massive swelling, cyanosis, bursting pain, motor
deficiency, and gradual loss of sensitivity. In this section, it is pointed out
that ascending contrast venography might be technically unfeasible and useless when
veins cannot be visualized because of complete obstruction. Therefore, the authors recommend
strongly duplex sonography to which they attribute a sensitivity of 93% and a specificity
of 98%.
The section on treatment of these two conditions becomes rather wobbly. This is not
surprising since the authors analyze all forms of treatment ever suggested and tried
over the past decades. In fact, no treatment modality such as anticoagulation, thrombolysis, and thrombectomy, alone or in any combination, appears to satisfy the authors
who point out that results are fairly good for PCD but invariably poor for venous
gangrene. They conclude that the best first-line management for PCD is steep limb
elevation, fluid resuscitation (to make up for trapped loss of plasma into the interstitium),
and anticoagulation with heparin. In the back of their minds, they suspect that
fibrinolysis might or should become the logical treatment of choice if only its effect could be proven.
COMMENTARY
In this painstaking review of the literature, the authors present an excellent understanding
of the pathophysiology and a good review of the etiology and clinical features of
PCD and venous gangrene. However, in the section on treatment they betray a lack of personal experience or at least refrain from presenting their opinion. Thus,
they arrive at contradictory conclusions.
For instance, after having correctly explained that PCD and venous gangrene are characterized
by massive swelling of the extremity, cyanosis, and a tendency towards shock due
to extravasation of fluid and plasma into the interstitium with a subsequent dramatic rise in interstitial and venous pressure due to an almost complete occlusion
of the entire venous cross section with resulting ischemia and a critical drop in
arterial arterial pressure (loss of peripheral pulses), they surprisingly come to
the conclusion that steep elevation of the affected limb and intravenous fluid replacement (and
heparin) constitute first-line treatment. In reality, a patient writhing with bursting
pain symptoms of acute ischemia will simply not tolerate steep elevation of the leg for the number of hours necessary to lower substantially the interstitial pressure.
Rather, rapid lowering of the intolerably high interstitial pressure is necessary.
The dispatch with which this goal can be achieved depends upon the etiology of PCD
and venous gangrene. If PCD occurs as a first-time manifestation of a venous disorder
(i.e., following surgery or postpartum), rapid decompression can be achieved by immediate iliofemoropopliteal venous thrombectomy in virtually all cases using local or
spinal anesthesia. On the other hand, if PCD follows one or many previous bouts
of deep venous thrombosis, recanalization of the key veins in the groin will prevent
venous thrombectomy and the surgeon must proceed immediately to fasciotomy. This lowers compartment
pressure dramatically and permits leg elevation.
The authors claim that fasciotomy holds the danger of wound infection and therefore,
they dismiss this form of treatment. Such skepticism suggests to this reviewer that
the authors have limited personal experience. This also explains the high amputation
rate in the review of their chosen literature.
This paper demonstrates the urgent need for a competent, strategic outline regarding
the treatment of PCD and venous gangrene. 6590b