Chapter 8 :Venous Disease, Pulmonary Embolism, Fand Lymphatic System Bruce E, Jarrell R. Anthony Carabasi, Ul Mark Kahn I i E BBD venous disease oF THE LOWER EXTREMITIES A] oveniew 1 ‘Anatomy. The venous system is divided into four general areas: a The deep venous system includes the tibial, popliteal, femoral, and iliac veins. i The superficial venous eystem is made up of subcutaneous veins and the greater and lesser saphenous veins, «c. The communicating venous system is a network of veins (perforating veins) connect Ing the Superficial and deep systems with valves that allow flow only from the supe! ficial tothe deep system. 4. Venous valves are delicate web-like structures in all infta-inguinal veins that pre- Vent reverse blood flow in the veins. The valves prevent venous hypertension when the patient isin an erect position. tn addition, they assure that blood is pumped from the superficial to the degp system and back toward the heart when the patient walking, 2. Etiology. Venous disease may be caused by either congenital or acquired disorders. =. Valvular incompetence is the congenital or acquired inability of the valves to pre~ ‘vent reflux and gravitational hypertension of the venous system. b. Venous thrombosis is the formation of thrombi in the venous system. The thrombi Usually originate atthe calf vein level and progress cephalad. They occur as a result fof elements of Virchow's triad: (@) Trauma tothe vein wall (e.g. caused by surgery or physical injury) (2) Decreased velocity of venous blood flow (eg., due to postoperative immobility cor drugs, such as estrogen, which decrease venous tone), (3) Increased coagulabilty of a change inthe cellular components of blood (eg. due to surgery or polycythemia vera) El] Diordes . 1. Superficial thrombophlebitis i inflarnmation or thrombosis ofthe superficial veins. ‘A pulimonary embolus rarely is present with superficial thrombophlebitis. a. Clinical presentation (@) A tender palpable cord along tie course of a superficial vein 2) Ared, warm, indurated vein b. Treatment (1) Bed rest and elevation of the extremity 5 (2) Local application of heat for relief of pain {GY Support hose worn both during the period of inflammation and for prophylaxis (8) Nonsteroidal ant-inflammatory drugs (NSAIDs)EES 146 | Chapter 8 ¢, Complications. Chrontc recurrent superficial thrombaphfebitts Is treated with smblottes In addition to the treatment doscribed previously because the syndrome often includes a streptococcal fymphangts untreated, Iymphangt results In additional occlusion of the hmphutles, resulting In continued edema, dilatation, and inflammation, creating a vicious circle. d. Suppurative thrombophlebitis usually Is assoctated with intravenous Infusions In immunocompromised or burn patients. It is treated by excision of the infected vein, 2. Varicose veins are dilated networks in the subcutaneous venous system and result from valvular incompetence of the deep, superficial, or perforator systems. Deep venous thrombosis is not often a factor in the development of varicose veins, a. Clinical presentation (1) Local pain and edema (2) Local inflammation (3) Local hemorrhage into the surrounding tissue~ (4) Dilated superficial veins 7 (S) A positive Trendelenburg test, which is a method of Proving incompetent valves by occluding the superficial vein and demonstrating filling from the deep system b, Treatment (1) Nonoperative management principally involves the use of support hose, which keeps the superficial system collapsed and minimizes the effect of venous hyper- tension on venous dilatation. (2) Operative management (a) Indications for surgery () Previous or impending hemdrrhage from an ulcerated varicosity, Pro- * fuse painless bleeding that may occur from these'lesions can be quite alarming to pafients and physicians. This bleeding is usually controlled by a combination of elevation and direct compression, followed by | compression wraps. (ii) Recurtent pain over the varicosity or recurrent superficial phlebitis of the varicosity - (ii) Cosinetic considerations (b) Surgical procedures (Preoperative evaluation of the patency of the deep venous system. Liga- tion of the saphenous vein in the presence of a thrombosed deep system could result in riassive venous obstruction and venous gangrene. (ii) Surgical excision of the individual varicosities through small (< 1 cm) incisions (the “stab avulsion technique”), with ligation of proximal incompetent perforators ii) Ligation of incompetent perfgsting veins between the superficial and deep systems . 3. Deep venous thrombosis is thrombosis of part or all of the deep venous system of an extremity. It occurs in 250,000 individuals a year. , a. Etiology + "Gy Deep venous thrombosis usually originates in the lower extremity venous system, starting at the calf vein level and progressing proximally:to involve the popliteal, femoral, or iliac system. From 80%-90% of pulmonary emboli origi- nate here. (2) Other veins if which thrombi occasionally develop include: (a) Pelvic veins, especially during pregnancy, pelvic surgery, and from gyneco- logic cancer . - (b) Renal veins, especially when intrinsic renal disease is present » (©) Inferior. vena cava (d) Ovarian veins . + (©) Upper extremity and neck veins, especially with athletic activity or the use of intravenous cannulas (The right atrium in the presence of intrinsic cardiac disorders.‘venous Det, Plenty Embaliom and Lymphat Stem | 147 b, Clinical presentation (A) The elassic clinical syndréme includes calf or thigh pain, edema, tenderness, and a positive Homan’s sign (call pain on dorsiflexion ofthe fo00. In patients ‘with venographicaly proven deep venous thrombosis: (2) Filty percent have the classic clinical findings. (@) Fifty percent have no-associated physical findings in the extremities. (2) Pulmonary embolism isthe presenting symptom in some patients. {G) Evaluation must ascertain the presence of arterial vascular insuiciency «. Diagnosis of deep venous thrombaxis is made by means of laboratory tests. (@) ‘Duplex ultrasound has become an accurdte and commonly performed noninva- sive method to diagnose deep venous thrombosis. In experienced hands, itis as ‘accurate as venography. Duplex refers to the two modes of ultrasound evalua~ tion used in performing the test. (3) Dope ltasound flow extinaton hasan accuracy ate 0f 80%-90%. It jeermines: (i) Phasic low, the variation of flow in the examined vein with respiration. ‘Augmentation, which is increased flow in the examined vein when the more distal muscle mass is squeezed (This maneuver forces flow proxi- ally when the vein is nat occluded) ‘The presence of normal venous velocity in the feniorl, popliteal, and posterior tibial veins {iv) The presence ofa difference in ultrasound findings between the dis- easel and the normal extremily {(b) B-mode evaluation displays the ultrasound beam as an actual image of the vein being evaluated. A normal vein will be easily compressible, and the walls of the vein wll actually be seen to coapt. Because acute thrombus has 3 similar echogenicity to blood, compressibility and coaptation of the walls are felt to be more accurate in detecting acute deep venous thrombosis than the visualization of clot in the lumen. (2) Venography ofthe ascending venous system isthe traditional diagnostic method for deep venous thrombosis. Radiopaque dye is injected into the pedal veins, and a tourniquet is loosely applied atthe ankle to direct the flow of dye into the deep venous system. Inflammation or thrombosis of the veins occurs in 3% of patients who undergo venography unless the vein is flushed with a heparin solu- {ion after infusion. (3): Impedance plethysmography measures the variations in the volume of calf blood upon releasing ablood pressure cuff placed so as to cause temporary thigh venous occlusion. Ths test is accurate for about 90% of cases of deep __venous thrombosis above the knee. : 4. Treatment (1) Continuous heparin infusions given for 5-10 days followed by administration ‘of warfarin or subcutaneous administration of heparin for 3-6 months. (2) Thrombolytic therapy with streptokinase and urokinase is used if extensive deep ‘venous thrombosis results in Impaired peitusion of the extremity. Data are insut- Feeient to support the use of thrombolytic therapy to prevent or decrease the irci- dence or severity of posiphlebitic therapy, although it seems logical (3) Inferior venacaval filter or interruption is used if heparin is contraindicated or if a pulmonary embolus occurs inspite of adequate anticoagulation therapy. How- ‘ever, this treatment prevents only pulmonary embofism and does not treat the deep venous thrombosis - ‘ . Prevention (1) ‘Simple preventive measures include leg elevation, early mobilization after + “surgery the use of support hose (which comyresses superficial veins in the legs and increases flow in the deep veins), and the correction of preoperative risk factors, such as polyeylhemia vers. ae (2) Intermittent calf compression by means of'a pneumatic cuff increases leg blood flow velocity and helps to prevent stasis, as well as causing a poorly defined sys- temic lytic effect.148 | Chapter . (9) Pre. and postoperative administration of inpreventing ‘eee theomboss, An interment aaa ante : hap ia 8-12 hours. At heparin activates a 4 Inhibits platelet ay repatl (a Raver igo sais hepaingeecy Se Cee onbin aval {) Postoperative phlebitis, There wesc ey Incidence in 22% incidence in patients treated with heparin, (©) Fatal pulmonary embolism, There wer coe mi ortality rate in controls versus 2 1% mortality rate in those treated with heen £. Complications ¥ wit hearin, ay be effective se of Controls versus a ( Chronic valvular incompetence occus because of damage incurred luring the acute episode, dent aca worse 25 the day progresses ‘and asthe leg is iy @ePEndent, It usually resolves with elevation seed ao (Gi) Local superticial venous hypértension leece are and interstitial Bredtion of plasma, cells, and protein including red nag cells, white blood cells, and fibrinogen), iv) This edema and exudati 'on then lead to brawny induration from hemo- Blabin metabolism. Tissue necrosis and skin ulceration rage poor SzvBen diffusion secondary to pericapillay protein depose vey as ite blood cell release of proteolytic ensymes, supeonite radicals, and various cytokines. : (b) Treatment (© Support hose must be worn continually o prevent superficial venous . hypertension and swelling. If swelling can be prevented, man aleocs : can be prevented, Gi) Ligation of local perforating veins is used tok atthe ulcer iit will not heel ‘An Unna boot, a medicated pressure bandage, biweekly until the ulcer heals, This compress, Gv) A change of life ulceration, * 2) Phlegmasia alba dotens is caused by acute occlusion ofthe iliac and femoral veins due to deep venous thrombosis “amen (2) Clinical presentation. This phlebitis results in a pale cool leg witha dimin- ished arterial pulse due to spasm. oo (b) Treatment is thrombolytic rerapy followed by heparin administration to prevent progression to phlegmasta cerulea dolens (3) Phlegmasia ceruleadotens i secondary to acute and neatly total venous occlu sion of the extremity outflow, including the iliac and femoral veins. Its more common in the left leg. Association with another disease is commons For eaceme ple, 30% of cases occur in postoperative and postpartum patients and pelvic . malignancy is not inrequent i ta if wht saacsh te ® to Phe ilies include cyahosis of the extremiiy with massive edema, severe pain, and absent pulses, ollowed by venous gangrene, (i) Shock may occur as a result of sequestration ofa significant amount of . blood in the leg. () Treatment Cac tstaton i ic therapy followed by heparin administra G) Thambeclony ecteaenally ft eeopeie hery tensucesa (ii) Bed rest wit leg elevation lower the venous pressure is applied weekly or n heals most ulcers. style to avoid leg dependency may improve theVenous Disease Pulmonary Embolsm, and Lymphatic Sate | 149) PULMONARY EMBOLISM is a mechanical obstruction of the flow of blood in the pulmonary arterial system due to lodgment of a thromboembolus. The results of lodg- ‘ment include decreased cardiac output, pulmonary vasospasm, hypertension, impaired blood oxygenation, and bronchospasm. ‘|: Overview. Pulmonary embolism is one of the most common causes of sudden death In hospitalized patients. 1. Normal individuals can tolerate a 60%-70% occlusion of the pulmonary vasculature, but patients with preexisting cardiac or pulmonary disease tolerate much smaller occlu- sions poorly. Pulmonary embolism is frequently sudden and seemingly unheralded, although it is often preceded by the development of small and clinically unrecognized emboli. Only 10% of all autopsy-proven cases of pulmonary embolism are diagnosed pre- mortem, . Ninety percent of deaths occur within 2 hours after the onset of the initial symptoms. Therefore, ifthe patient lives longér than 2 hours, the,chance of survival is very high Pulmonary embolism develops in 10%-40% of patients with deep venous thrombosis {see |B 3). However, approximately 33% of patients with pulmonary embolism have no antecedent spose ‘of deep venous thrombosis a. Thrombosis in the venous system is cqused by (see 1A2b). _b. Pulmonary embolus formation can be prevented through the early diagnosis and pre- vention of deep venous thrombosis. 3, 4. jations described in Virchow’s triad Risk factors 1, Pregnant women and women in the postpartum period have an incidence of pule monaty embolism five times greater than the incidence in age-matched controls. Pul- monary embolus formation is a common cause of death after pregnancy. 2, Estrogen therapy is associated with an increased risk of pulmonary embolism 4~7 times that of controls. The risk is dose-dependent and is eliminated within several weeks after cessation of therapy. 3, Heart disease is. associated with a 3-4 times higher risk of pulmonary embolus forna- tion. This risk is directly related to the severity of the heart disease. 4, Obesity is associated with a 1 1/2-2 times greater risk of pulmonary embolism. 5. Carcinoma is associated with a 2-3 times greater risk of pulmonary embolism. 6, Major trauma, especially spinal cord Injury and pelvic of femoral shaft fractures, carries an increased risk of pulmonary embolus formation, history of pulmonary embolism Increases the risk of later pulmonary ‘embolus forma- tion, especially after surgery. —— 8, Varicose veins are associated with a 2 times greater risk of pulmonary embolism. 9. Older age groups are associated witha increased rk of developing pulmonary emboli, . ‘Symptoms of pulmonary embolism range {rom none to severe cardiépulmonary dysfunc tion. In general, the more complicated the symptoms, the more unreliable the elinical * diagnosis. : 1, Classic signs—hemoptyeis, pleural friction rub, cardiac galfop, cyanosis, and chest, splinting—are present in only 24% of palients.150) chapter onc a 2, Nonspecific findings, Including tachycardia (ih 60% of patlents), tachypnea (in 85% of patients), and dyspnea (In 85% of patients), are common: Bronchospasm and pleuritle chest paln also occur frequently. 3. Electrocardiographic changes, including arrhythmias and evidence of right ventricular strain, may appear, . 4. Chest x:ray may be abnormal of otally normal. m a. Occasionally, a marked diminution of the pulmonary vasculature produces increased raiolucency inthe area ofthe embolus (Westermar’ sign) b, Pleural effusion, whifch is usually hemorrhagic, or pulmonary.infiltration may be present, especially in cases 6f pulmonary infarction, which occurs in 10%-25% of cases of pulmonary embolism. ; ‘ 5, Atterial blood gases {requently show hypoxemia with a low carbéin dioxide partial pressure (Pco,) associated with hyperventilation, * a. Although serial measurements may déocumént a sudden drop in oxygen partial pres- sure (PO,), a single measurement is unlikely to confirm the diagnosis of pulmonary embolism. : 4 ¢ ol 5 b. A normal Po; does not eliminate the possibility of pulmonary embolism. Diagnosis of pulmonary embolism is based on the results of several tests. 1. Pulmonary arteriogrant js the best technique for diagnosing pulmonary embolism. This testis virtually.100% atcurate, but itis invasive, as a radiopaque dye is injected directly into the pulmonary artery. The attendant risk of cardiac arrest is small in stable patients, but It can be unacceptably high in hypotensive, unstable patients, 2. Pulmonaty radialsotope scainning is less ivasive than arteriography. a. Perfusion lung scan. A radioactive particle, small enough to black a small number of pulmonary capillaries temporarily, s injected. A camera records different views of the uptake in the vasculature, 3 (1) A major difficulty with this test is that many acute and chronic’pulmonary dis- ‘eases can result in similar perfusion defects. Iti critical to.compare,the chest x-ray with the scan to determing the presence of other abnormalities. (2) Anormial scan is very reliable in-determining the absence of a pulmonary embolus. = . , {@) The presefice of segmental or large defects predicts pulmonary embolism in 71% of patients. (b) A subsegmental or small perfusion defect is associated with pulmonary embolism in only 27% of patients. ; bb. Ventilation scan performed simultaneously with the perfusion lung scan improves | the accuracy of the latter, An inert radioactive gas, such as xenon, is Inhaled, and the patency and ventilation of the bronchial tree are assessed. (1) Ventilation-perfusion mismatch occurs when a perfusion defect is present but e the ventilation scan is normal. Matched ventilation-perfusion defect occurs when a defect in the same location Is revealed by both tests. (a) A segmental or large perfusion defect. mismatched with a'normal ventilation ‘scan Is associated witk, pulmonary embolism in 91% of patients, ; (b) A subsegmental or small perfusion defect mismatched with a normal ventila- tion scan is associated with pulmonary embolism In only 27% of patients. ()'A perfusion defect matched with a ventilation defect is associated with pul- "monary embolism In 23% of patients. : ; (2) When pulmonary embolus i clinically suspected but he lung scan i equivocal, an additional test should be performed to increase the reliability of those results. ‘A pulmonary arteriogram is most reliable. ‘leg venogram (or venous duplex) Is also useful in documenting the-presence of deep venaus thrombosis In-this situa- tion and, therefore, the likelihood of pulmonary embolism.Venous Disease, Pulmonary Embollsm, and Lymphatic System | 151 Treatment of pulmonary embolism includes both supportive measures to maintain clrcula- tory function and administration of heparin for systemic anticoagulation. 1. Cardiovascular support is frequently necessary in patients with significant pulmonary embolism and should be instituted immediately. The supportive measures include oxygen administration, assisted vertilation, correction of cardia¢ arrhythmias, and treat- ment of shock by means of adequate hydration and vasopressors. Heparin as an anticoagulant should be administered in an initial bolus of 10,000-20,000 units to halt the thrombotic process and to stabilize platelets in the embolus to prevent the:release of vasoactive and bronchoactive substances: Adminis- tration begins with a continuous intravenous drip of heparin at approximately 1000 tits an hour, he dosage Is then adjusted to malntaln the paral thromboplastin time at 1 1/2-2 times the control time. Heparin is continued for a minimum of 7 days and is followed by long-term anticoagulation therapy for 3~6 months. Thrombolytic therapy with streptokinase, urokinase; or tissue plasminogen activator may be used incases of acute ifethreatening pulmonary embolism when cardlopl- monary function is severely compromised as evidenced by shock, profound hypox- emia, or elevated pulmonary arterial pressure. Because thrombolytic therapy results in *the lysis of preexisting thrombi this therapy may be even more dangerous than heparin therapy, and it is contraindicated in patients with recent intracranial hemorrhage, recent surgery, or conditions associated with bleeding, such as peptic ulcer disease, large tumors, or urinary tract diseases associated with bleeding. Pulmonary embolectamy is reserved for very ill patients. If patients remain significantly unstable despie rapid resuscitation and, tn te opinion ofthe atending physician, are 100 unstable to endure the several-hour treatment with thrombolytic therapy, then ‘embolectomy should be considered. A closed embolectomy using a suction catheter or open embolectomy on cardiopulmonary bypass are the two most acceptable methods. “ Long-term anticoagulation may be maintained by elther oral administration of warfarin’ ‘of subcutaneous intermittent administration of heparin, The warfarin dosage should be carefully regulated to maintain the international normalized ratio (INR) at 2-3 times normal. However, warfarin interacts with many other drugs, and its effectiveness can be severely altered by these drugs and by hepatic disease. Complications of anticoagulation therapy z 1, Major hemorrhage requiring transfusions occurs In 1%-2% of patients on anticoagu- 4 lants; minor bleeding eplsodes are comricii in more than 16%; and fatal hemorthage occurs In 0.14%-1%, The risk of hemorrhage is greater if heparin is administered inter- mittently or is given to elderly or severely hypertensive patients, f+. -, Pulmonary embolism recurs despite anticoagulation therapy in 1%-8% of patients. 3. Heparin-induced thrombocytopenia occurs In up to 5% of patients on heparin and Pe may be related to the development of heparin-induced antibodies directed toward latelets. All heparin infusions must be discontinued if thrombocytopenia occurs, a Because ofthe risk of either hemorrhage or heparin-induced necrosis, aform oftissue =. necrosis that is related to localized intravascular thrombosis, in| LYMPHATIC SYSTEM . { “A] tymiphederna is a condition characterized by swelling of one’or more extremities because of lymphatic Insufficiency. 7152] Chapter 1 w Types. Lympheclema may be Idlopathlc (primary lymphedema) or may be caused by acquired insufficiency due to Infections, obstructions, or surgical destruction of the lymphatics (secondary lymphedema), a Primary lymphedema, Trea types of print Iymphedema are dsingulshed y age ofonset, (1) Congenttal lymphedema Is present at birth or occurs early In infancy. (a) I accounts for fewver than 10% of primary lymphedema cases, (6) lymphedema that is both congenital and hereditary s known as Milroy’ ease, ‘ (0) there are virtually no lymphatics present at birth, the symptoms occur at» that time, if some functioning lymphatics are present at birth, symptoms may bbe minimal of absent, As growth takes place and repeated normal damage ‘occurs from minot Infection or trauma, the remaining normal lymphatics are ‘no longer adequate and edema ocrurs. (2) Lyemphedema praecox occurs at any ime from puberty until the end ofthe third sdecade, (2) "Most cases of primary lymphedema are of this type. (b) Itis three times more common in women than in men, (3) lymphedema tarda occurs after age 30. b, Secondary lymphedema is due to obstruction from a variety of causes, including infection (see Ill C), parasites, mechanical injury (including surgery), postphlebitic syndrome, and neoplasms. : (1) In developed countries, the most conimon causes are obstruction by malignan- eles, postsurgical lymphedema (e.g,, following mastectomy), and lymphatic destruction from therapeutic radiation, (2): In less well-developed. counirles, parasitic obstruction (elephantiasis) is a com- mon cause, Wuchereria bancrott Is the most common offending parasite. 2. ‘Diagiiosis of lymphedema is usually made clinically. a The history characteristically includes edema, which begins at the ankle and pro- _Rresses proximally. Progression js slow, usually over the Course of several months. bb, Physical examination. Unlike.the edema secondary to verious disease, the swollen ‘extremity in lymphedema has no.dark brawny edema or ulceration of the ski c. Laboratory tests. The diagnosis can be proven by Iymphangiography, but this testis not done routinely because itis difficult and hazardous, 3. Treatment a. Medical treatment. Simple measures are the firsi line of treatment. a) Bevalon of the affected limb, weight reduction, and salt restriction may be helpful. (2) Compressive stockings may be of benefit if applied properly. (3) 4t is extremely important to avoid trauma and infection, because either will greatly exacerbate the condition. (4) Pulsatile compression devices may help to "squeeze" the edema from the swollen extremity in severé cases. : fb. Surgical treatment to palliate uncontrolled lymphedemna includes the following: (1) The Thompson procedure Is based on the assumption that dermal lymphatics ‘may be functional even though the.deep lymphatics are incompetent, Adermal 2 flap is buried-deep in the swollen extremity to provide competent lymphatics for drainage. (2) The a which contains an extensive lymphatic network, can also be trarisposed from theabdomen to the extremity. Although some benefit has been observed clinically by this procedure, no lymphatic communications between the omentum and the extremity have been demonstrated to develop in labora- tory experiments, . (3) The most durable operation for chronic lymphedema is a Staged resection of subcutaneous tissue and redundant skin; including muscle fascia, which was described originally by Sistruck and refined by Homans.x @ ‘Venous Disease, Pulmonary Embolism, and lymphatic System. | 153 (@) This procedure leaves a large amount of redundant skin. This skin is excised, «| and the remaining skin is closed over subcutaneous drains. z (b) The procedure is done in stages, first on the medial side and then on the outer aspect of the leg. (0 Approximately 80% of patents treated with this operation have a substantial eduction in extremity size. | (d) Periodic elevation for 30 minutes twice daily and leg. compression are neces- sary to complement the operative procedure. (4) Microsurgical anastomoses between a lymphatic and a small vein have been tried. : (@) This procedure works well when proximal lymphatics in the groin or pelvis: are obstructed. z (b) Dilated lymphatics distal to the point of obstruct’ sn can be anastomosed to nearby veins, theoretically providing a decompression mechanism for lym- . hatie fluid, Lymphatic tusiors . 1, Benign tumors are most commonly cystié hygromas. a These are derived from embryonic lymph sacs and are seen during the frst year of life. , They are most common! iediastinum. . Cystic hygromas in the neck may cause res be excised; Cranial nerves should ly found in the neck but also occur in the groin, axilla, and niratory distress and, in this case, should ‘not be sacrificed, since these tumors are benign. Lymphanglosarcoma is an‘extremely rare malignant lymphatic tumor. It can occur in any extremity affected by chronic lymphedema, but ts seen most commonly after a mastec- tomy that is Complicated by lymphedema of the arm [see Chapter 23 Il G 1 ¢ (3), 3, Lymphatic metastases are seen with many kinds of primary tumors. Lyniphangitis and lymphadenitis 1. Causes, Inflammation in the Iymohatc channels (ymphangits) and inthe lymph node (lymphadenitis) is caused by bacterial invasion, usualy byB-hemolyic srebtocree by staphylococci. 2, Clinical presentation. Usually, an extremity Is affected. a, Hyperemia occurs around the affected lymphatic, manifested by a red streak, which advances toward the draining lymph nodes. B b, Movement of the affected extremity is painful and also propels the bacteria along the lymphatic channel, exacerbating the condition, - oa hth process I not arrested by the lymph nodes, septicemia can occur. & 3. Treatment consis of Immabilizng the limb and giving antibiotics. a source of bacte- ; Hal seeding is present (6, a paronychia), itshould be drained. Uncomplicated cases 4 resolve promlly and usually without sequelae, Repeated insults can result inachronic = secondary lymphedema.ri ART ELE VASCULAR ‘A.| Atherosclerosis isa disease pro += lesions tend to occur ot cert infrarenal aorta, and the super deep femoral attery are rarely in pr 1 -e GENERAL PRINCIPLES OF PSHIPHERAL ARTERIAL DISEASE . Types of lesions. Pathological R. Anthony Carabasi, Il Bruce &, jarre!! Mark Kahn wolves both large and small arteries. Arterial such as the proximal internal carctid artery, the femoral artery, The supraceliac aorta and the distal ives. The reason for this pattem is not known, but itis ably related to different ito pattems at various locations in the arterial system. hat ieral types. a. Fatty streaks are discrete, st a lesions, which are composed of cholesterol. laden macrophages and sinooth muscle c's, These streaks may occur early in life and are not hemodynamicatly significant. 5. Fibrous plaques are more advanced lesions, which alsa contain an extracellular matrix. These plaques may progress to caus> an cbstruction to flow: ¢. Complex plaques are characierized by intisis! ulceration or intraplaque hemorthage. These plaques may cause local occlusion of tie vessel or may result in-embolization of the clot or pieces of cholesterol, causing dis. arterial occlusion, cizeulstion develops when ocelu ‘occurs over a period of time. The ability to develop collateral circulation 29 even the total occlusion of a major artery from becoming symptomatic, at feast at rest, The lick of a developed col- lateral bed is what makes an acute occlusion so much more clangerous than a slow pro- gression of chronic disease that leads to an occlusion, 2. The internal Iliac, crass pelvic, and hirabar zvievies, as well as the internal mam mary artery via the superior and inferiey epigas..‘e artestes, can form a collateral bed to help supply the leg with aortic an iliac disea: bb. Profunda collaterals supply the popliteal artery in the artery disease, és Genicutate collaterals around the knee supply the lower leg in the face of poplitéal disease, : : Rik factors (or peripheral vascula clsease are essentially the seine as those for.coro- face of the supericial femoral ” nary attery disease (CAD). These factors include cigarette smoking, diabetes mellitus, hypertension, lipid abnormatities, and a strong family history. 2. CAD is the most comnnan cause of death after major vascular surgery, whether itis carotid, aortic, of limb-salvage surgery. Ifall vascular surgery patients had preopera- Wa$22 | Caper 718 . tive coxonay \warcant cou glageaphy, approximately 25% would ina CAL sovere eacuph te ery bypass: 14% wove nt hase had elinleal evidence of CAD, fh Is Fesgneniy paxvne Ina effort to ascess rick avid decrease povierative complications This testing Is leequently adenosine or jecsaine salluny b-eause woeculr patigls are eequenily unalil o well long ‘enough to complete + sianded tess es Eh en gah torn nc ts oboe 1 Chudieationis one ofthe most characteristic symptoms of peripheral vascular la fax complain of profound auc ein ry ‘the eg the wo key leatures of cnuticaton are ts consent op aa constant distance ara is prompt rliefby fet lun rate his uss by exction never by sanding oc sting for prolonged pods: The bss. nbs adoquat at et but inadequate orth incteasad neta eran of eee 4 Symptoms appear cist ote ste of vascular occlusion (Ina lun te doco in the igh or bt fn superficial femoral artery occlusion, te symp (6) Pes or usualy absent of diminished dial wth eon, beat et may dappear ater exerse (4 attest the patient has no iscomfot,taicting that inbaheatening ischemia isnot present b, Treatment (1) Most claudication canbe managed witout surgery. In mos patients 2 rutine exerclie program and cesattn of smoking wil real na notice el npr tment in walking dsanea, Conte ofthe shersceross ik facts #5 chee leat (2) Festaifnescurey he only agent approved for the weak of ner ‘itent clacton, rradues whole blood viscosity by decresing plasm tinge ad patel: aggregation. Acenrlledsaly kay documented aig can increase in walking dstance when compared o placebo. ts agent reads tobe taken 3 times pe day for 6-8 week bloe te eect ca be raid. io AE Rc 11 3 indication that systemic vascular disease is pr cei Limb i relatively good, with only 10% of progressing to severe ischemia or limb loss in 10 years. 1 (2) Thelong-termn survival of those patients is more guarded, being 73% at 5 years and 38% at 10 yeas (3) The most common cause of death is atherosclerotic heart disease schon rest pln ess fom se ply 2 Symploms, Patients deserive intense pai, ting, or ngling, usualy acrois the tis al fat and acy which s eaceatd by lesa heat sg, wht tying sleepin bed) tmay be relieved by keeping the foot in 3 dependant postion cr by : svalhng slowiy 1 Treinen Serius consideration should be yven to exseuaization in these patients because the disability znd discomfort are sovere and she degsee of ischemia Isctitical “ { ipromisa of artaral flow, Hare the bleed! sup es 3. Gangrene tissue nero occurs when bloc fw inadequate o manta tisue via ; Sitneschemi ulcers usvlly occur a Ihe ltl tp orbetween We oes Hl ‘2, Etiology 4 (2) Caper may rel rom croc progrsive ane disease oc may esl rom i ‘embolization of cholesterol or an olganized thrombus from a proud sovtce,SA tah. Paige Att Dee 4123 2 2) Occasionally, gangree ofthe toes may occur without significant proximal erter- wae (2) ldence if toem spresents occlusion of small blood vessels owing to inn- Rertreess HX sic obliterative tisease and is seen most cornmonly in patients with diabetes and | ‘yadeno end-stage renal diseas ; a | Yceerone bs. trertment feel debridercent or apt af nave sue and unl see ‘ign oF removal of the souree of emboli to protect the remaining tissue at risk, contr the diag- {e.] Dixgnosts . onli 1, Noninvasive tests Ifthe history and physical examination suggest the presence of vas- cular disease, various noninvasive tests can confirm the diagnosis. a. Pulse volume recording (EVR) is a technique that measures the volume changes in the extremly dng the cafiec cyte. This recording i pned as a waveform for ‘view. Using waveform analysis, the presence and the location of occlusive lesions can be ascertained. a b, Szgmental arterial blood pressurés can be obtained at various locations in the arm, and leg. (G} A pressure drop distally in an eitiemity indicates aefal stenosi or occlusion. (@) The ankle brechit index (ABI) is the rato ofthe systemic blood pressure at the ankle to that ofthe brachial artery. @) Normally, the ratio should be ¥.0 or slightly greater. () Patients complaining of claudication typically have an ABI of less than 0.8. (©) Exercise testing isa Valuable to! for diagnosing clauclication secondary to arterial inguficiency, Patients with claudication may have a normal ABI at test the pani ty de to atraloceusive disse, leg pressures will lop with exercise, (8) Patients with rst pain usually have an ABI less than 0.5, (©) Calclied arteries artiicially elevate the ABI because of ircomoressible arter- ies, Diabetics frequently have calcified arteries. (3) When intepreting the PVR and ABI, the physician must remember shat a great deal of individual variation exists between a patient's symplouns and these labor ratory values. These values must be used in coiunction wi 2 thorough history and physical examination, 2, Knvasive tts for assessment of peripheral vascular disease includ digital subtraction angiography and perculancous arterial angiography. {ntravenous digital subtraction angiography (IVDSA) is performed by injecting cone trast mate into a large vein. The arterial system can be visualized by preer timing is atractive because no arterial punctur ale ry eon 1) Advan This techni ire, = thus i safe for use on oupajents Pent (2) Disadvantages, This tochnique has net lived up to expectations becausé the res: elution i onl far the conta volume i large, and fe mages i mot kee factory if the patio saws rth ming of exposure Is noteoet reithe blood sup- ay acrois the die $s, Attrial digital subtesisn a { !DSA) uses less contrast material than éon- ‘ie uyingeo verisal angiography io abta ‘terial images, DSA uses a computer to posing by Aligelly subtract baseline Im rent obtained before the contrast injec- lich, Less contrast is needed to sualize the arteries than is required in eonveriional oa bthest ; arteriography. The area imaged i: .sually smaller han the area imaged in conven. Vfonal avteriggraphy, and bony Is 1 be detected out; therefore, care must be taken stem identifying arte (i) Ssvanv 328. The patlent gree of ischemia iniral discomfort and the small amount = 1 to be ropeated if necessary, = = scm This technique regres an ariet"! puncture, and the area that - cqalltt Be sued atone time is relatively small ® Conventional z"tetography is the cuneni standarc! method for evaluating vascular ‘material is injected int the artery of interest, usualy by way of intain “issue vis:{ 424] Chapter 716 . ; femoral atery puncture, sivd sequeattal xray exposeres are wade, Atthn ; anaterial moves distally tse filling af the aneles te recede Ting the flning sequence, . . (1 Adeantags. Ades: shy ste lange lis that cle thy vos the an unen investigation, (2) Disadvantages, This prccedure s assoctated with several stove eo {a) Acute renal fallute can result cont the nephiotosielly of the dyes ea dehydration can result from the bisk diuresis induced by th perianal contrast dye. Ueoth complications ean be minimized by adequ itt pros ead © postangiographic.hyeleavion and hy limits on the total smonet af ee tnjected. An auldiiona! -ompliciéon can be an allergle reselon to (b) Acute arterial occlusi wslozally follows angiography. (i Ischerniaris most apt ty be related to technical problems, ineluling simple thrombosis ofthe ariery atthe site of needle insertion, distal embolizatton into the lower lee from a thrombus forming on the angiogram catheter or from a dislodged plaque, or subintimal dissection of an atherosclerotic plaque cluring catheter manipulation, i) Clinical Symptoms of acuie serial occlusion following angiography include absent pulses, espec ‘aly those present prior to the examination; severe and constant pais, nuiainess, or paresthesia inthe extremity ‘examined; and pallor of the skia and coolness to touch in the involved extremity, Treatment of acuté arterial occlusion during angiography depends on the underlying cause and should be initiated promptly If flow is ree estabied within 2-6 hours the reaome cocoa ror example, acute thrombosis can be tre el wit’ fytic therapy, using urokinase or streptokinase, Since this thromtoris is very fresh, rapid lysis should ‘occur, Intimal dissection that caus Ybasis requires thrombectomy | and direct arterial repair or bypass, and embolization of an athero- i sclerotic plaque may require eperalive embelsctomy. . (iv) Although arterial vasaspastn can explain this acute ischemic episode, it | occurs in fass than 3% of case © (0) Pseudoaneurysins may develop followin: catheter. This complication vsvally {quate pressure al the arterial punctur patients with high blood pressure, I (i) Pseudoaneurysms present as swelling “ullowing remo Gi) An ultrasound of the area should be obizined 19 distinguish a pseudo- | aneurysm from a simple heinatoma. If puleatile (low is ueen onside the | dye. ogeaphic i io apply ade | lumen of the artery, a pscucieanouiysm is px (ii) Pseudoaneurysm showld be Fezairei pewnptly the o d. Brachial artery catheterization (1) This study is performed frequently for cardin= when the lower extremity vessels are rnzuitol'e (2) Thrombosis of the brachial artery des’ not usu but itcan cause hand claudication, Surgical repa : ©. Axilisry artery catheterization (1) This study is performed occasi for angiography. . (2) Aperiarterial hematoma may follow this study ais: 2% 32235 the brachial ples, causing arm disability if tis not promptly dec.s.s;res:.. {his cainplication is considered a surgical emergency. athctt tzatton oF for any y result i acute hand isch iraticated, ra! vosvals are not adequate i ally when th: 3, Magnetic resonance angiography is rapidly becoming 2 more accurate sn: comiton method of assessing the arterial circulation, Although holding grow sus forthe future, most magnets and software packages do not currently prosivce infarction ats reliable ‘enough ta replace the information provided by conventional aiterioge:‘shy or DSA. ME cgi ie. : Peripheral Atrial Disease | 125 1s to improve arterial flow Nonoperative procedure 1, Percutaneous transluminal angioplasty (PTA) ; ‘irate _° & i a eae angiographic catheter is fluoroscopically gui . a infatable balloon attached to an angiographic caller Tere ce, he stenotic area. The balloon is then in! : P elinically Totism or thrombosis may follow this procedure in approx- b. Aclinically significant em imately 3% of case . c. Patency varies with anatomic location of the stenosis and with the character of the - Gisease. Focal, isolated areas of stenosis tend to show more durable results than dif: fusely diseased arteries. More proximal arteries, especially common iliac arteries, (ay cise is have the best results. Arteries with Lower flow rates, such as © the superficial femora! artery, and more distal arteries, tend not to have as high.a 2 patency rate. 2. Stents are expandable metal mesh tubes that are inserted over a balloon catheter, the Berroa fefated to expand the stent, then deflated and withdrawn. The expanded | eat eee thought to help prevent the elastic artery from restenosing, and “tacking down the intimal flaps keeps the artery from dissecting. 3 3, Lasers and atherectomy catheters . a lasers can be used to open occluded arteries so that a balloon angioplasty catheter an be inserted, They have not been shown to increase patency rates above those of SAAalone, The advent of newer guide wires has enabled short segment occlusions to be passed without the added cost of laser-equipped devices. bb, Atherectomy catheters actually remove atherosclerotic plaque from the arterial Wall, either by culting and extracting small slivers via the catheter/introducer system {eg., Simpson atherectomy device) or.by using a rapidly rotating tip that disintegrates the ploque (e.., Auth rotoblater).* 4, Piiialls in percutaneous interventional techniques . Indimal hyperplasia leading to restenosis at the sité of intervention is the pitfall with: all of these methods. Balloon angioplasty, the simplest and least expensive proce- dlure, has proven to be the most durable, with the possible exception of angioplasty in combination with stents at the common iliac artery fevel. b. Thrombosis, 23 well as early intimal hyperplasia, has proven to be a concern, espe- cially with lower flow vessels (e.g, infrainguinal). This pitfall may be managed by ; Siiiongulation with heparin and warfarine although there may be a higher eomplic cation rate from bleeding. a 4 ’ rrr RSET SETTLE Bid oiasericroor “A.} Infection and gangrene are corrtnon problems among diabetic iabetic Aas Inte bI patients, Although diabeti patients consti only 5% of tio gener population, they undergo approximately 75% of ‘al arterial revascularizaliva prox res andl i al dial arial vascularization procs on approximately 50% of all amputations. - 1, Peripheral neuropathy leading ic decreased sensation and proprioception i opathy leadi isa ; and aly complestion fay. th chage east tminor trauma being unrecog. 5 . Painless ulcers i it i nized, and therefore unteated,Patles ules? can fown ove the weight-bearing areas a with no infection and’a norma! islood.si,z:ly, these neuropathic ulcers frequently b. The affected foot is made non-weight-bearing and is properly fitted with orthotics. \paired immunity also increases the risk of infection in diabetics. Thi i : s. This reduced immu- ly has been measured as decreased leukocyte chemotaxis, adherence to vascular endothelium, phagocytosis, and intracellular killing activity.126] Cope? HA ‘ 4 Traumatized ares and painess {ions ate most common, Inely spect aniibiaties for teatmer . b, Those infections may occur ast (0 Celts ofthe drum fhe fox: (2) Adeep plantar space Infection {G) Oseomyelts of he metatarsal or phalanges bones «6. Those infections must be treated carly and aggressive a plantar abscess is suspected, urgent operative deb 18 freowuntlybescomg inset, Mint ae ance leer la wl ite atl broad-spectrum antibioties. 4, Meticulous foot care and properly filing shoes ae of critical ixporiancs ford patients 3. An adequate arterial blood supply tothe affected foot and toes must be assured for healing to occur Atterial occlusive disease occurs in a different ditibution inthe diabetic patient. 1. Diabetics tend to have more dltfuse, more distal (irapoptiteal disease than do patents Without dialetes. When contemplating tevascularization in diabetic patients, aeriopms ‘must include distal bial nd pedal arteries to completely asses intenertional options. 2 Since diabetic patents frequently have ealefied vessel, ther Al tends tobe artificially elevate, which makes evaluation of wound healing potentially more dificult. % Although pressures may be high, PVR aings may be abnormally blue in the presence of occlusive disen b Cakification frequently spares digital vessels, Toe wavelorms and pressures are re- {quently useful in evaluating wound healing potential, ©. There iso completely accurate predictor of wourd healing capabiiys clinical experience is invaluable, A isto clinical guide is tt a diabetic foot with an absent pedal pulse probably will ot heal fllowing a sound. EYL Aorromnc OCCLUSIVE DISEASE Presentation 1. Causes, Aortiliac occlusive disease fs usually caused by atherosclerosis Figure 7). (ther less comvmon eniies that can occlude the ars 7cladeTakayaat's 9 ee 4 forie coaretation. : 2. Symptoms 3” Patients may be asymptomatic or may present wih Setiock oh Leche syndrome consists of diminished femoral pes, bot ek ana cain, and impotence. b. Severe ischemia, leading to gangrene or lm los, is r8 with ec! disease, : “B.| Indications for surgery 1, Severe claudicati 2. Tissue loss 3. Peripheral arterial emboli Conse score cause by celonf dst veel inthe nes “ofthe lowe xray by pieces othe plague or patel t- ', Symptoms. The patient presents with a painful cyenotic digit "blue toe” syndeome) ormmuliple mall stn ercions. : «Treatment is exclsion of te cstised alia gment inthe proximal vessel or rest pain ~4 Pesipheral Aneral Disenie {127 Coliag axis. ‘Superior mesenterls o.. Left renal a. ‘Abdominal aorta Lumbar aa. Righ: common itiae », Right internat tae a. (hypogastric) Flght extemal tag a: Loft femoral FIGURE 7-1. Arteries ofthe abdaminal region. 4 ppotence in men when other organic or psychogenic causes have been ruled out and ‘when a hemodynamically significant vascular lesion is present __&] Operative procedures 4. Endarterectomy consists of opening the artery and Femoving the portion of the inti a and media containing the plaque. Currently, this technique fs used only for shor lesions i Of the distal aorta or common iliac arteries. % Rortebifemoral bypas: I he mos: commonly performed procedure, Graft are either woven or knitted Dacron, or exp: xed polyiesrafluoroethylene (PTFE E 2. The distal anastomosis is usual.y performed on the common femerat artety, withthe ina enlng ovr the proximal deep femoral artery. This procedure will Bypae any infrarenal aottc, iliac, and common femoral disease, : ; ». The proximal ahastomoss should be done near the renal arteries where the least aynount of disease is present in the aorta, Wis usually done inthe infrarenal Acc, & Operative morality i 1%-5%. The major cause of death fs myocardial Ianeeey, i 3, Extca-anztom!s bypass 7 &. Fermerst-fersorat byposs may be used in patients with unilateral iliac disease if the fe- maining iliac artery des not have significant obstructive disease. In well-selected exces j Pall disease inthe iliac artery providing inflow and good uno inte symp, 4 fornalc leg this procedure provides acceptable results with 70%-75% longer i patency rates. ey . AxillobHemere! bypass : (6 This procedure is used for poor risk patients who require revascularization buit annotislerate divect aortofemoral bypass, ¢ 2) (GieProcedce fs ascociated with alow motaliy rate, but the long-term patency ‘ {50% ,70%4) is tower than for aoviofemoral bypass. The gals requently require ‘ Shrombectomy to achieve long-term patency,7 at {3) Despite these dhawbacks, this eperaiion tr fl ie flowing cunts (a) In patients with severe mectic:! prodlis or those who hava had! saultiple prevlous abdominal oporations oF rads. "sn, which would male stendard aoitofemoral bypass hazardous . (0) Mfr removal of yn tected arte gf shen an azn rate Is equled ‘ for revascularization ER EXTREMITY OCCLUSIVE DISEASE In “utes ecclusive disease of the comms femoral, superficial, deep femoral, poplite: |, nd tisiatartertes (Figure 7-2), Ax} Cause. The most common cause of lower extremity disease Is atheroxzierotls, though other less commen conditions can also eause occlusive disease. 1, The superficial femoral artery isthe artery most frequently involved. Discave us.!iy : 9ccus sally where the artery passes though the sector hiatus, The mos ‘ symptom is claudication, which may not be severe if good collateral vessels ar 2. The profunda femoris artery supplies blood to the thigh and collateral flow to ; popliteal artery. The origin of this vessel frequently is stenotic, but the distal ves j usually spared by atherosclerosis. * 5. The poplitea artery may be diseased because of atherosclerosis, entrapment by the Sastiocnemius or popliteus muscle, or cysts in the adventitia ofthe artery. The falter vo Conditions should be considered if a young patient presents with claudication, i 4. The tibial arteries may be diseased by atherosclerosis or embolization, Patients with 5 diabetes frequently have disease of these vessels. Approximately 75% of femoral bypasses are in diabetic patients. Clinical presentation 1 Patients with lower extremity arterial disease may be asympiomatic or may present with Sfaudication (most common), rest pain, or tisue necrosis. Ifthe arterial inaufficiency ft Severe, tissue necrosis may produce nonhealing ulcers. 2; Ouher physical findings include loss of hat, nail changes, pallor on etevation, and dependent rubor, i C.] Surgical treatment 1+ Initcations for surgery, There are thxee commonly aécepted indications or surgery in Patients with arterial occlusive disease. i; Rise necrosis of the leg or foot isan urgent reason to proceed with surgery. i 5. Rest pain is a syndrome characterized by pain or aching across the distal feet and | toes, which occurs when the leg is elevated or when the patiers is in bed. This i in a dependent position. indicates ation for intervention. cur patients ability to wor or if they interfere severely wih the patient’ Ifesyl, su i may be offered: Ideally, surgery for claudication is performed in goo dtsk patients a period of exercise, weight reduction, and abstinence from smoking. | 2. Operative procedures 5 2. Femoropopliteal bypass, using avtogencis saphenous vein, is the basic ope 2.Ycin [Snot available or isnot suitable for bypass, an atficial prostnotic rai» : be used. : (2) Although early results with prosthetic grafs aie acceptable, these grafts are not t 4s durable as veins, and every reasonable attempt should be made to use site. enous material, q SESS ae=Dorsalis pedis a, Desp planter branch of ercuste a, ABTERIOR © postenion FIGURE 7-2. Arteries of the lower extremity. (2) The 5-year patency of vein bypasses is 65%-80%, and the limb salvage rate is 90%, (3) Mortality from the operation is primarily from myocardial infarction, and these patients should be evaluated for occult CAD, ey b, Femarotibial artery bypasé is required in patients with occlusive dise’ popliteal ans tibial vessels. (1) One technique uses a reversed saphenous vein z (2) The other technique leaves the saphenous vein in its bed but rendeis its valves incompetent (in situ technique), Both of these techniques give acceptable results; "aS years the patency rate is approximately, 70%. Limb salvage rates are approx- » imately 80%. . Be Be inthe1 130] caper? ve (3) lf he greater saphenous veln Is not usable either lesser saphenous, cephallc, ar bbrachlal veins may be used, To obtain sufficient length, pleces of veln may be anastomosed. Patency rates are ot usually as fevorabla (50% at § years) with : = thesa grafts, , (4) PTFE, Dacron, and human umbilical voln hava been used for bypasses (otal vessel The patency aes fo these ate aproxinatly 20% at year and generally used only autogenous veln Is not available, or if the patient Isa ves 00 risk and will not tolerate a long operation. «. Profindaplasty {repair ofthe origin ofthe profunda femoris artery as an isolated pro- cedure may result In relief of rest pain and healing of ulcers if applied property This procedure is used in poorrisk patients with occlusion of the superficial femoral arer- {es and severe stenosis ofthe origin of the profunda femoris artery Itcan often be cartied out under local anesthesta. 4. Lumbar sympathectomy is rarely useful in patients who have severe lower extremity aera seas: eisan uncommon operation since the inteducton ofthe femoro- bial bypass. (1) Good results may be obtained fn patiéns with mild rest pain or small areas of superticial kin uleeration in patients who have an ankle brachial index over 0.3. {@) This procedure is rarely indicated in diabetics because many of these patients have an “autosympathectomy” as a result oftheir underlying disease. (8) The Ly, Ly, and L, ganglion are removed via a retroperitoneal approach. in some Centets, sympathectomy is accomplished by injecting irritating material percuta- neously (0 destroy the ganglion. © Amputation. If reconstruction cannot be accomplished or if a patient is not a rehabil- itation candidate, amputation may be not only lifesaving but also expeditious in pro- !moting the total rehabilitation ofthe patient. Occasionally, the result is better than that of an extensive vasculat procedure, (() Indications for amputation (a) Systemic sepsis, particularly whien caused by gas-for (6) A patient who has no potential for ambulation even a larization + 40) Unreconstructable vasculir disease,” “xE_ 3g) Rehabilitation. The level of amputation should be below the knee if possible. This choice allows the greatest chance of rehabilitation. An absolute method for ing amputation healing is not available. (2). A pulsatile pulse volume recording inthe calf ora transcutaneous Po, great : than 40 mm Hg atthe site of amputation usually indicates tat the arcs will <2 heal prima (b) The rehabilitation rate depends on the level of amputation and ranges from {60%-70% for unilateral below-the-knee amputations to 10% for bilateral above-the-knee amputations, “51. (0) The healing failure rate is up to 20% for Below-the-kriee amputaticns, (3) Operative mortality rate is about 13%, with 50% of deaths occurring secondar- ~ ily to cardiac problems and 25% secondarily to respiratory problems. The long. + term mortality ate following amputation is 50% at 3 years and 70% at § years when the amputation is performed for vascular disease. ing organisms er successful revascu- BUT acute arrenat insurcictecy oF LOWER EXTREMITY imay occur : sr because of embolization or irombosis. Severe, acute ischemia may be followed by limb } + loss from nerve and muscle damage within a few hour if rapid diagnosis and prompt j \Weatment do not occur. : “A: bots, Theos cornmoin sit ofan areal embolism iat abifcation, whee th arterial lumen tends to nareow. The bifurcation of the common femoral artery into the | lolSuperficial and deep femora arteries is the most common sit popliteal, and mesenteric arteries, Peper Atel henge |131 folloived by the iliac, Mert dees hough tobe the source ofembltn OR of casey) . Al riatonspreset in then opens mores enbol, bs Mural thrombus post-myocardial, produce enbett.” infretion o from a venticular aneurysm may ‘& Apatent foramen ovale may allow a paradoxical embolism to tavel from the venous «_ Girculation into the arterial circulation. 2 Rhcurmati Valvular heatt disease isthe source of emboli in 21% of patients. 3. Arterial-aterial em Wi may occur from aorietilcerated lag penal but sintcan roup of patients may presen with agtal emboli resuhing ie es in 19%-2% of patients. Famenezanot toes (blue toe" syndrome) this syndrome may occur ass complecn tion of arterial catheterization or angi ©] fest schon econ sissies oan ik actors for aterial occlusive dca toc =<} {jhe clinical presentation from a lower extremity embolus the affected muscle groups, The 5 P's (pain, paralysis, ‘convenient inay to remember features of 1. Pain is present in 80% of paticns with jography, eased aftery may cause acute ischemia. Usually these lave a known lack of pulses, or have a number of such as cigarette smoking, diabetes, and results from acute ischemia to paresthesia, pallor, pelsles) area the ischemic limb, h an acuite arterial occlusion, and it heralds the Eegining of ichemia I pains absent maybe Because of pre anesthesia or paresthesia ey, in some patients, well developed collotecy 2, Paralysis and paresthesia (or anesthesta) devel tral nerves to anoxia, Muse! a ceatnten Cate degrees of reduced culation ands usally associated with coolness ofthe extremity." 4, Absence: of pulses helps localize the a it those wit The presence of neurol ‘the urgency of the situation, Treatment. Management of acute aiterial tious surgical correction of the occlusion, rea of occlusion Frequendy in older patents and nto of claudication, pulses may chronically be absent ornare ans the mos accurate determining factor wien deciding occlusion incides rapid diagiosis and expedi ‘+ Uspern therapy, Patents should be heparniedlnmedtly when the. clinical diagno- sis is made, 2. Hydration therapy. Patients should be urine output (preferably 100 mV), Al {rant ar wed to protect he kidney fron damage duc o myesone is with prolonged severe ischemia, given adequate hydration to maint jin kalinization ofthe urine and osmotic + frcoperative angiography should be obtained ifthe level of occision i ‘uncértain, especially ia chronic disease is suspected. Angh is frequently not necessary, and should not delay definitive therapy ins neatened fake Intraoperative angiograms are often a useful method of obtaining necded information with imal delay, 4: SaBlal therapy Revasculriaatioh shouldbe peformied within 6 hous of the onset of. symptoms for minimal mérbidity rom ‘scle and nerve damage,132] Cape? vd : a a eenfctomy is perfoved by exposing the arty ant passing a balloon peel Geter tounh the embolus and thrombus, then intatingtne betee shawrg the catheter entractng th thrombus, Limb salvage ls pest, 1°63 ~ mately 75% of the time; the mortally tn these patlents approaches 20% ker . thelr severe underlying medical problems, In a patient with an acute occlusion and chron disease, an aanglogram delines the * 1 anny aril patent distal vessel A bypass is usually the preferred therapy in these i patients, : 5. Nonsurgteal therapy, The role of lytic therapy for an acute ischemic episode is tuncleak. tn patients with no motor 5, lytic therapy may dis . In patients with motor or Ws Sensory deficits, lytic therapy is usually not he ist choice because t ean tee i & Postoperative treatment, Patients who have suflered an embolic event should neve a . 10 } Soares erae evaluation (including an echocardiogram and Holter monitod E424 for an embolic source, These patents should be andicoagulsed tosh ge chance of recurrence, . 2 q RUE iecarrmic WASCULAR DISEASE may present as an acute life-threatening emer- 1 ~ ency or ass chronic debilitating problem : : | 4] Shon mesenteric ischemia results fom slowly progresive senoss or oclusion of the | Pes rplaessels it celiac, superior mesenteric ertery arid nferor mesentric wes) | i {see Figure 7-1). There is a rich collateral bed in the visceral creelotion When symptoms : qi * occur, two of these three vessels are usually occluded, and the remaining one is highly. | wi} 3 ferloc mesenteric artery is occluded, and the celiac and superior | J i ‘mesenteric arteries are highly diseased. I b followit i i ie echoes i necrotic i 1 Clinical presentation, The signs and symptoms of chronic mesenteric ischemia includet snecrtic aa: Abdominal pain following a meal, ne to “food fear" shout be b, Weight loss secondary to avoiding focd due to pain - eine ct Anebigaunic teen | te rg . a (1) Hydra 2. Diagnosis a. Recently, dupes sahning of hcl veils as been used to screen patients (2) Theat with suspected chronic mesenteric ischemia, f j intoth ». Arteriography isthe most useful diagnostic study. Both anteriorposterio ond interal ©) Atepe Views ofthe aorta must be done to visualize the origins ofthe vicceral ves, ' wee 2s bet 3. Treatment: appropriate lesions are found, operation is recommended. (@). These 2 ypas eon hay aortas ie ona ee ‘endarterectomy of the involved during! visceral vessels is the prefered treatment, i bi. In well-selected patients, the results of operation are excellent, with 90% of palients ‘cured of their symptoms. Mesenterte yeni Typlezlly, cause ae toy wil ete. ah obs B.] Acute mesenteric cami isa suc! umergency wit an ie motaliy rat: evere tides wt { 4 abdominal pain ou of proportion to physical findings isthe most important and sched 1+ Elolog st e ign ofthe diagnosis tn the early stages of acute mesenteri chemi, nesepatens ns) : enone une im agpny wie! eden of pein, The davicprestston vases. | >. bergns has den onset of acute abdominal pain in an eldérly patient with a history of cardiac disease, hyperconcentra zg Fleguently, these patients are taking digoxin to treat arial fibrillation tnd congestive heart lumen Ils bee failure. Digoxin isa potent splanchnic vasoconstiton : reonly used,Cc. Me: Peripheral Aderial Disease | 133 is the most common cause of 1, Etiology : & Eetpolization, usually tothe superior mesenteric artery, acute mesenteric ischemia, (1) The heart is the most common source, (2): These patients usually present with a triad of symptoms, (a) Severe pain out of proportion to the physical findings (©) A history of gut emptying, Usually a massive bowel movement with or with- out vomiting (©), Atrial fibrillation or other cardi mation b, Thrombosis of visceral arteries (1) Sudden occlusion of preexisting atheroscl May cause acute mesenteric Ischemia, : (2) Patients with suspected acute mesenteric ischemia should be questioned about Dreexisting symptoms of weight loss and pain with eating, © Nonocclusive mesenteric ischemia is due to a low-flow state, such as cardiogenic ===” shock. It has been recognized in patients following car ulmonary bypass and e in patients requiring high doses of intravenous vasoconstrictors and Inottopes- (e.g, epinephrine), lac conditions that predispose to embolus for- lerotic lesions of the visceral vessels 2. Diagnosis and treatment 5 ae & Salvage of these patients depends on a high index of suspicion and prompt diagnosis * and treatment, (1) All patients suspected of acute mesenteric ischemia should have their cafdiac status optimized while being aggressively volume-resuscitated and treated with Z broad-spectrum antibiotics, (2) An angiogram can be both diagnostic and therapeutic: {a) tf an embolus is found, the treatment is prompt surgical embolectomy. (&) If mesenteric thrombosis is found, the treatment is vascular reconstruction, which usually is a bypass to the superior mesenteric artery. (c) The catheter may be leit in place for direct intra-arterial infusion of a vasodilator to relieve splanchnic vasoconstriction and spasm, Following embolectomy or reconstruction, the bowel is assessed for viability. Overly necrotic bowel is resected. If marginal viability is present in the remainin, bowel, it | should be left in place. A “second look" operation should be done in 24 hours to ! ensure viability of the residual bowel. .° If the original angiogram reveals nonocclusive mesenteric ischemia, treatment is 4 directed toward improving cardiac function’ ©" * (1) Hydration and, if necessary, inotropic therapy are begun. (2) The angiographic catheter is left in place, and ‘vasodilating drugs can be infused into the mesenteric circulation after hydration has been accomplished. * (3) A repeat angiogram is done in 24 Hours to assess the success of treatment, Vasospasm should be reversed and normal arterial perfusion restored if treatment has been effective, ; . (4). These patients may require celiotomy if perltoneal signs are present or develop during treatment, o ghee eric venolis thrombosis presents mote insidiously than acute mesenteric ischemia. "ppiealy, causes slowly progresive sbdominal pain arid distention and may be conused with intestinal obstruction, ° =~ Bit 1.. Ettology: It is frequently associated with a.hiypercoagulable state, such as a neoplasm or 2 hematologic abnormality: Poca i . eee 2 I can be diagriosed by computed tomography (C1) scan, which revea e iypeboncenasn of contrast inthe wall ofthe mesenteric vein without flow In the lumen, Itis being diagnosed more frequently as CT scans have become more com- monly used. Meg f