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Matary Vascular Surgery 2013
Matary Vascular Surgery 2013
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Arteritis
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VASCULAR,
SURGERY
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Lack of blood flow due to sudden DGomp.: Gena, Gat, Volk, Rat occlusion of a previously patent t.: art. (duplex, angio), Systems (ECHO) artery with no time for collaterals to open. ,,ogeratiove, Post. (cause, comp.) Patholooical definition: fusion of tissues affecting the cellular functions and metabolism
1) Embolism. 2) Thrombosis. 3) Trauma e.g. catheter, arteriography. lntra-arterial drug injection 4) Others (pressure from outside e.g. tourniquet, plaster cast, aortic dissection, phlegmasia
The most common causes are embolism and vascular injury
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- Sudden in embolism. - Less dramatic in thrombus. - Following trauma in arterial injury. Presentation:
2.
1. fain:
sudden severe pain, usually felt in the most peripheral part of the limb. Paralysis ) The toes cannot be moved in contrast with venous occlusion muscle function is not affected and gradually movement becomes more difficult. Onset of motor paralysis indicates impending gangrene.
2
3.
4.
lallor:
5.
6.
deoxygenated blood ) mottled appearance o Later on capillaries rupture ) fixed blue staining of skin (irreversi ble changes). fulselessness ) absent pulsations distal to the site of embolism ,but the femoral pulse may be palpable, even thrusting, as distal occlusion results in forceful expansion of the artery with each pressure wave despite the leak of flow. Progressive coldness of the limb (Poikilothermia). There is poor capillary refilling
o At first leg is marble white and veins are empty. o 6-12 hrs later VD occurs and capillaries fill with stagnant
B.
Picture of chronic ischemia eg: Trophic change, rigid blood vessel Tapering stenosis Diffuse atherosclerosis Extensive collaterals
Fixed color changes (blue staining). Signs caused by muscle necrosis (tense calf, fixed planter flexion, bulging anterior leg compartment). Acute paraplegia may occur in saddle aortic aneurysm.
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r.
Occurs if:
2.
1-
Embolus does not cause complete occlusion. Pre-existing good collaterals in cases of thrombosis. oflsetris more gradual and the symptoms are less severe.
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After circulatory arrest widespread distal intravascular thrombosis occurs. Thrombosis may also affect the artery proximal to the site of obstruction. Gompartmental slrndrotnet lschemic muscles get swollen which exaggerates the effect of ischemia. After revascularization further edema of the muscles occurs Ieading to more interruption of the circulation. Eady fasciotomy of the muscles compartments can avoid this problem. As a result of stasis of blood in the arterial tree, blood stagnates in the veins
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Complete recovery Complications: o Gangrene ( wet type) o Chronic ischemia o Volkmann's ischemic contracture o Reperfusion injury: - Definition: body response following restoration of arterial continuity due to release of high concentration of metabolic prodpctsinto generat circulatidn (e.g. K*, Myoglobin, lactate). - This leads to: o Svstemic effect: Crush syndrome, pulmonary edema, ARDS, myocardial dysfunction. . Local effect: compartmental syndrome
7. Metabolic: Gout. 8. Others: cramp. B-Inooflooo stde.s. C- .,1 ade o cchrc ian ofp IL.,flortic disection.
- Fracture. - Dislocation. 2. lnflammation: - Rheumatoidarthritis. 3. lnfective: - Cellulitis. - Osteomyelitis. 4. Deqenerative: - Osteoarthritis. 5. Vasculan: - Deep venous thrombosis. - lntermittent claudication. 6. Neuroloqical: - Sciatica.
Crush injury.
- Backer's cyst.
- Acute arterial occlusion.
- Peripheral neuropathy.
ap lite al an
dfemaral
ant eutys nu
+
thrombus.
VASCULAR SUR.GERY
A. Site of impaction: 1- Doppler& Duplex scan: localizes and identifies the presence of embolism 2- Arterioqraphv: (Mainly preoperative,it is not done in threatened limb).
and
Its value is in cases of diagnosed acute thrombosis because it provides information that is essential before doing an afterial reconstruction. This information includes: a- Site of occlusion. b- Proximal inflow, i.e., if there is another proximal arterial narrowing. c- Distal run-off, i.e., flow distal to the obstruction.
to detect
AF.
C. For complications:
12-
High hemoglobin, BUN and creatinine indicate intravascular hypovolemia due to fluid sequestration in the limb. Acidosis and raised creatinine phosphokinase and WBCs ) if muscle necrosis.
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Treatment
Pre-operative preparation 2. Operative: a. Embolism. b. Thrombosis. c. lnjury. 3. Post-operative: a. Cause. b. Complications.
1.
:
.
a
a o
Hospitalization Morphine: for pain. l.V fluids to correct dehydration if present Prophylacti c anti biotics. - Heparin : Start with a loading of 80 lU/kg followed by a maintenance dose of 18 lU/kg/hour. The dose is monitored by checking APTT every 12 hours, which should be maintained at 2.53 times the baseline level. Care of the cardiac condition (Oz, digitalis)
dose
O Operation:
if ischemia is not so severe that immediate operation is essential, it may be possible to treat either embolus or thrombosis by intra-arterial thrombolysis. . Embolism: o Urgent embolectomy (within 6 hours) by Fogerty catheter + FaSciotomy (done in late coses as a prophylaxis to prevent comportmental syndrome). o Followed by anticoagulant. o Acute Thrombosis on top of chronic: thrombolytics followed by revascularization surgery.
- Pulse did not return ) explore the artery. Definitive treatment (within 6 hours). accordrnq to type of ,nrury
3;:,1[:
. .
ible dilatation using Fogerty catheter, if failed ) excision & graft. Partial tear ) repair with graft. Complete tear ) repair if large artery & ligate if small artery.
VASCUIAR
SUR.GERY
Post-operative:
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Treatment of the cause: - Embolism) antiarrhythmic drugs if AF. - Exclusion graft if aneurysm. - Thrombosis) conservative treatment of chronic ischemia.
Volkmann's ischemic contracture )muscle or tendon transfer. Crush syndrome )lV fluids + alkalinization of urine. Prognosis: the most important prognostic sign is muscle turgor.
'
Ischemia is not severe in case of atherosclerosis as pre-existing collaterals thrombosis with gradual onset and less severe symptoms
In acute limb ischemia based on history and clinical examination ) Do not wait for investigation as ischemia timc is very precious, hand Doppler cxamination is cnough (absent Doppler signals)
Arterial Embolism
"Embolus is a Greek word that means a plug or stopper"
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(A, V, rare) A body that is foreign to the blood )Etiology: Hrt 80%, out of heart 20% (in order) Fefe & Popos Be Calm )lncidenece: stream becomes lodged into a 6ps blood vesse! causing obstruction. >C/P: >lnvest.: art. Cause, comp. )TTT: pre, operative (Fogerty embolectomy), post A- Cardioqenic (80%): From the heart (most common): - Mitral stenosis with AF Ithe commonest I Q7%) - Left atrial myxoma- mural thrombus Ml - Subacutebacterialendocarditis. B- Non-cardioqenic (1 0%): 1. From large aileries (i.e. arterioarterial embolization). - Atherosclerosis. - Aneurysms. 2. From veins: venous thrombi through patent VSD or ASD + Eisenmenger ) paradoxical emboli. 3. Other types: - Air embolism, fat embolism (in bone fracture) therapeutic embolization (in treatment of tumors & bleeding), parasitic embolism (e.9. pulmonary bilharzial and bilharzial Corpulmonale) and amniotic fluid embolism. - Malignant cell emboli (hypernephroma and cardiac myxoma). C- ldiopathetic (10%).
As acute ischemia
* >Def.: Plug.
An embolus in the arterial tree is usually arrested at the sites of bifurcation of arteries where sudden reduction in the size of the arterial lumen occurs. The lower limb is more commonly affected. 2. lmmediate cut off of the blood supply )severe ischemia + vasoconstriction of collaterals (reflex due to severe pain).
1.
VASCULAR. SUR.GERY
3. Muscle necrosis within 4 -6 hours. 4. 2ry thrombosis after circulatory arrest widespread
distal intravascular thrombosis occurs. Thrombosis may also affect the artery proximal to site of obstruction. 5. DVT (as a result of stasis of blood in arterial tree = blood stagnates in veins). 6. Gompartmental syndrome (if prolonged ischemia): ischemic muscle gets swollen and this in turn exaggerates the effect of ischemia. After revascularization further edema of muscle occurs leading to more interruption of circulation.
Artery narrowed by atherosderosis & embolism from heart obstructing the lumen (Acute on top of chronic)
descendinq order of frequencv are: 1- The bifurcation of common femoral artery into
2345-
superficial and deep femoral arteries (40%). The aortic bifurcation (saddle embolus). The bifurcation of popliteal artery. The bifurcation of the brachia! artery. The bifurcation of common carotid artery.
off
from clot
to
the
Leg:
blocking blood
o o
is most commonly
See before (acute ischemia). Complications are more severe because of little or no collaterals. Gauses of acute limb pain: see before. Of the cause e.g. thrombus.
Site of impaction:
. Doppler
U/S, Duplex
(unress coexistins atheroscrerosis) B. Detection of the cause ECG, Echo, U/S if due to aortic aneurysm. c. Detection of complications: muscle necrosis )4TLC, 4 CPK
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Ansiographv3
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possible.
Preoperative Preparation
1. Hospitalization. 2. Heparin: (details as in acute ischemia) To deal with the cardiac problem. To prevent the propagation of the thrombus.
VASCULAR
SUR.GERY
3. Antibiotics (prophyla cti c a gai nst infective endocarditis). 4. Analgesic. 5. Care of the cardiac condition: e.g. digitalis, diuretics, antiarrhythmics ,but the acute ischemia has the priority.
B.
I
1.
By Fogerty catheter (can be done under local , general & epidural anesthesia) ' For embolism of femoral artery )common femoral transverse arteriotomy ' For embolism of aortic bifurcation ) bilateral femoral arteriotomies till above embolus.
be passed distally to extract any
2. 3.
table to ensure clearance of arterial tree. lnject heparin into blood vessel. Closure by venous patch. Heparin is continued postoperatively according to the cardiac condition of the patient. The source of arterial emboli should be corrected if possible +/- Fasciotomy (if prolonged acute ischemia to prevent compartmental $.). Signs of adequate embolectomy: - Pulses are felt during operation. - Color & temperature. - Reverse bleeding. - lntra-operative angiography, Doppler.
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C Postoperative Care
Treatment of the cause e,g: Anticoagulant (Heparin lV, then continue on oral anticoagulants), antiarrythmic if A.F, exclusion graft if aneurysm. Treatment of complications o lf gangrene )amputation. o lf Volkmann's contracture ) muscle or tendon transfer, if crush syndrome )lV fluids + alkalinization of urine. o lf MVO )treat, (see GIT).
Gompl ications of treatment bv Foqeftv's catheter:
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VASCULAR. SUR.GERY
)Etiology: old (pt., wall, blood, )G/P:6ps )lnvest.: art. Cause, comp.
>
aneurysm).
Tfi
amputation), post
3.
) diseased wall: - Afterial narrowing due to atherosclerosis(commonest cause). - Endothelial inflammation as in typhoid fever and pneumonia Preci p itati n g factors) stasis & hyperviscos ityr: - Dehydration(diarrhea). - Blood disease (polycythemia).
lt is acute on top of chronic ischemia due to atherosclerosis (fibrofatty streaks, elevated plaques) ) collaterals are opened ) ischemia is less severe.
acute but less dramatic than embolism.
e IrmD may
. .
A. Site of impaction
B. Detection of the cause ) CBC, lipid profile in blood, FBS, ECG C. Detection of complications: muscle necrosis )4TLC, ACPK. | . Preoperative Preparation
e.g.dehydration.
Treatment of the cause: conservative TTT of chronic ischemia. Treatment of complications: (as embolism).
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VASCULAR. SUR.GERY
tear. signs.
Peripheral arterial injury accounts for 80% of all the cases of vascular trauma
= -
Wth Tear
Tear: may be
a) Complete
b)
ends retract, constrict, thrombose ) present with ischemia rather than hemorrhage. lncomplete ) ends retract leading to widening of the gap ) usually present with hemorrhage - lf such bleeding remains within tissue )pulsating hematoma will develop ) false aneurysm - Less commonly if concomitant injury to adjacent artery and vein may lead to A-V fistula.
. . -
Wthout Tear
Spasm: - Present by ischemia. Arterial spasm should not be diagnosed except exploration of the artery to exclude contusion and thrombosis. Arterial contusion and thrombosis is the commonest type in cases of closed injuries. - Patients present by ischemia.
History of the cause: trauma, bleeding (if external). General examination ) shock, associated injuries. Loca! examinations are the bases for diagnosis . Hard siqns: these are sure signs of arterial injury. 1. Externa! bleeding (pulsatile hemorrhage). 2. Loss of distal pulsations. 3.6Ps. 4. Pulsating or expanding hematoma. 5. Palpable thrill or audible bruit heard at or distal to area of injury. . &!!Siqns,: these are less specific signs 1. Small or moderate sized. hematoma that is not pulsating and not expanding. 2. Proximity of penetrating wound to a major vascular structure. 3.Adjacent nerve injury producing neurological deficit.
VASCULAR SUR.GERY
II
4. History of pre hospital hemorrhage that has stopped or presentation with shock that cannot be explained by other injuries. 5. Delayed capillary refilling time.
Threatening ischemia is caused only by injury to brachial artery proximalto the origin of profunda brachii or occlusion of both ulnar and radial arteries , this is due to extensive collateral circulation and small muscle mass
1. Acute ischemia. 2. Hematoma. pulsatinq hematoma lnjury to artery false traumatic aneurysm (the wall is fibrous tissue & not normal vesse! wal!). lnjury to artery & vein A-V fistula varicose veins & ischemia). (according 3. Muscle affection to collaterals)
- volKmann's tscnemtc
supply is partial. lschemic fibrosis of the muscles. trial to extend fingers passively is associated with flexion of the wrist. NB: Flexion of the wrist ) J clawing . ) wet gangrene. to urgent exploration.
) )
. ln patient with hard siqns: no need for investigations, proceed . ln patient with soft siqns: urgent investigations
- Angiography (most accurate
). A traumatic A-V fistula shows early venous filling Doppler. X-ray for associated fractures. lf soft sign is shock )no investigations should be done, resuscitation &monitoring is the first priority. Arteriography can be done in operating room
It could be isolated
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Breathinq hemothorax
@ Circulation
Disability
e e
Head to toe examination of undressed & stable patient. History of any (AMPLE H/O). Urgent investigation after basic life support.
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VASCUTAR SUR.GERY
te wound with saline. Wound debridement. .W.excise 1 lo 2 cm from edges. . Fascia : open tense fascia. .Muscle: excise dead muscle (bluish in color, doesn't contract on pinching, doesn't bleed on cut). .Nerue: mark with black silk for delayed repair. .Blood vesse/: see later. Closed: @ lf due to fracture ) reduce fracture 1"t & wait for 20 min - Pulse return ) follow up. - Pulse did not return ) explore the artery. @ On Exploration ) Deal according to type of injury. 1. Spasm ) paint the artery with papaverine, if failed) forcible dilatation using catheter, if failed ) excision & graft. ln spasm, paint the artery 2. Partial tear ) repair with
lf less than 112 circumference sutures )Saphenous v patch. lf more lhan 112 circumference
Proline
with Papaverine
3. Complete tear
Repaired by direct end to anastomosis. 4. Gontusion: excision of the whole s reconstruction with interposition graft
synthetic).
Then
Local heparin, fasciotomy, adequate sKn covenng (graft) anct prophylactic antibiotics.
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Repair in oblique line
2-
3-
o Thrombosis of repaired vessels . Reperfusion injury Earlv postoperative: . Venous thrombosis r lnfection in the area of vascular reconstruction o Disruption of suture line and hemorrhage Late complications: . Aneurysmal changes in the vein graft use o Chronic venous insufficiency after venous thrombosis or ligation.
lmmediate postoperative:
VASCULAR SUR.GERY
The most commonly punctured arteries are the brachial and radial arteries. Glinical features: 1- Burning discomfort extending from the point of injection to the tips of fingers immediately after injection. This followed by severe pain and blanching. 2- Edema develops rapidly and may be severe. 3- Coldness and cyanosis. 4- The distal pulses are often normal. 5- Digital gangrene and less commonly total extremitiy gangrene. 6- Arteriography should not be done. '#,- !..-. -.=t, rl U'r YsJIIIIEIUI
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2- Dexamethazone 4mg l.V every 6 hours. 3- Low molecular weight dextran minimizes platelet aggregation. 4- Strong analgesics. 5- Limb elevation to decrease edema. 6- Fasciotomy is frequently needed due to chemical myopathy.
Asymptomatic peripheral arterial diseases (PDA) > 10% of elderly population) lntermittent claudication ) 5% of elderly population CLI ) 0.05 % of elderly population iJtro[Yar;r.,vr rrrJr-.:))J
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Atherosclerosis
the most common cause
Diabetic
Presen ile atherosclerosis
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1-
Male Female D.M. (the most important risk factor) Buerger's-Aderitis Raynaud's-Arteritis Old age Smoking 3 times {r the incidence of PDA Hypertension >BP> 160 / 95 mmHg > i 4 times incidence of PDA Dyslipidemia Hyperhomocystenemia
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Atheroscterosis
It is a systemic disease characterized by deposition of fibro-fatty streaks under the intima of the arteries forming atheroma.
(Thrombansifis obliterans)
It is an occlusive disease of the small and medium sized arteries, thrombophlebitis of
wall.
the superficialand deep veins and Raynaud's phenomenon. . lnflammatory disease of the neurovascular bundle in all 3 layers of the arterial wall + perivascular space (veins & nerves). . The lumen of the artery is obstructed by a thrombus, which becomes organized. . Affection of the neryes by the inflammatory process and the early block of arteries explain the severe pain that is present
. . . .
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2- Glaudicant Patient
a-Type of patient:
s-
Z-
Asymptomatic
Caludicant
cl-t
patient
]
i i
Atherosclerosis
Male >50 year with risk factors e.g.: - DM. - Obesity. - HTN. - Hvoercholesterolemia.
Buerger's
(Thrmobansitis obliterans)
Male 20 -4O year, heavy smoker.
b-
forms)
a) lntermittent claudication: - Site ) depends on the leve! of obstruction (see later). - Cause: is due to stimulation of nerve endings in the muscle by accumulated metabolites during exercise, which will be washed out during rest. Character ) cramp-like Comes on ) walking & exercise. Relieved bv ) standing still.
ii.
Associated other systemst . CVS ) heart failure, angina pectoris & Ml. . CNS ) TIA and stroke (loss of memory, fainting, blindness or
Claudication distance ) o ln early stgges of the disease, patient gets the pain after walking for a certain distance (claudication distance) but he can continue his walk. Later on, pain gets worse and forc'es the patient to stop for few minutes, as the disease progress: ) Claudication distance ) gradually shortens. ) Period of the rest ) gradually increase.
VASCULAR. SUR.GERY
r5
' Kidney (atherosclerotic kidney) ) pain, hematuria, hypertension and renalfailure. . Genital ) impotence in males. (Leri che synd rome = aortobi-i liac o bstruction). . GIT ) cramping pain in the abdomen in relation to meal.
(Post-ci bal abdominal angina).
hemiparesis).
Sisns:
i. General examination:
'
.
Chest E
) )
Vitat signs
ii. Local
aneurysm AVF. state of vessel wall: rigid in atherosclerosis. examlnmlon (fmb in layers): 1. Skin: Cold sensation: ischemic limb is colder than the other limb but an ischemic limb tends to equilibrate with the temperature of its surrounding and may feel quite warm under the bed clothes. Trophic chanqes: Loss of hair (1"t trophic change). fhin, atrophic, stretched, dry skin
)continuous
systolic
Color chanqes - Pale + bluish or red + blackish (cLr). - lt is affected by change of pos as affected legs blanch on elevation and develop a purple discoloration on dependency.
Pallor is due to decrease blood flow to the skin. Cyanosis and redness are due to stagnation of blood in markedly dilated capillaries under the effect of accumulated vasodilator metabolites. The color at flrst red then later on becomes bluish due to extraction of Oz by tissues. 2. Nails ) brittle. 3. Subcutaneous tissues: - J Limb circumference. 4. Muscles: - Atrophy ) weakness.
- Fibrosis.
t5
VASCULAR SUR.GERY
5. Nerves: - Sensory ) paraesthesia, hypo or hyperaesthesia (proprioception is the first to be lost). - Motor ) weakness (fine_movements are the first to be lost). - Reflexes ) weak ankle (Sr,z) & knee reflexes (L3,a). 6. Veins: - Slow venous refilling. - DVT (2ry to stasis). - Migrating superficial thrombophlebitis ) in Buerger's only. 7. Arteries: Palpation: - Weak (in presence of good collateral) or absent peripheral pulsations according to level. . Peroneal a. o Dorsalis Pedis a. . Anterior tibial a. o Posterior tibial a. - Expansile pulsation ) may indicate an aneurysm. - Stenosis or occlusion with a well developed collateral circulation may allow distal pulses to be normal in palpation. ln this case, the sign of disappearing pulse may be useful. 8. Bone ) osteoporosis. 9. Specialtests Capillary refllling test, Buerger angle, Harvey's venous refilling time test (see oral questions)
o) Type
of patient:
As claudicant
b) Presented with.' one of 4 diagnostic criteria I. Rest Pain: o Site: never comes above the ankle s Cause: ischemic neuritis s Character: severe pain awakes the patient from sleep o Comes on: rest and characteristically it worse at night q Relieved by: hanging the foot out of bed and by sleeping on a chair q Exacerbated by: lying down and elevation of the foot
q Site: between the toes ,in the dorsum of the foot or around the malleoli u Edge: Punched out o Margin: blackened and mummified o Floor: granulation or pus u The ulcer is extremely tender & its base is difficult to be palpated III. Ganqrene: (usually dry unless with HF or infection). IV. Absence of palpable pulse:
Stage Stage Stage Stage l: asymptomatic. ll: intermittent claudication. llt: rest pain. !V: ulceration or gangrene.
VASCULAR SURGER,Y
t7
=
=
released the color returns. ln an ischemic limb, the return of color is slow and is called sluggish capillary circulation.
seconds'
to right angle until all veins empty. lt is then brought down to the horizontal position. Normally the veins fill in '10-15
) normal distal pulse ) exercise up to claudication ) decrease pulse ) 1-2 minutes they reappear. - The explanation is that exercise produces vasodilatation below the obstructing lesion and the increase in afterial inflow is less than the increase in the vascular space so the pressure falls and the pulse disappear.
- Arterial occlusion + good collaterals
- ln patient with chronic ischemia, dorsalis pedis pulse disappears after exercise.
= A. Diagnosis: =
1- Doppler flow study
a. Doppler, Duplex.
b. Angiography.
de-
f-
Stenosed or occluded segments can be detected. Collateral refilling of the postoccluded or post-stenosed arteri Measurement of the ankle/brach ial (A/B ) index: o Normally A/B index is 1-1.2 . Less than 0.9 denotes ischemia . Less than 0.7 indicates severe ischemia . Less than 0.3 indicates impending gangrene
2- Duplex scanning
Visualizes the arteries and detects the areas of stenosis and block
r8
3- Arteriography
VASCULAR. SUR.GERY
This invasive method is done only if revascularization surgery is intended. Techniques: a- Direct femoral arteriography: this technique is losing popularity nowadays in favour of more informative aortography. b- Translumbar aortography: this is performed only if both femoral pulses are not palpable. c- Transaxillary aortography: performed only if the whole distal aorta is occluded.
' .
,-
b-
Exact site of arterial block State of the proxima! arteries. c- Distal run-off.
2- Hemorrhage 3- Diminished pulse 4- Pulsatile mass (hematoma 5- lnfection (at puncture site)
false aneurysm)
a.
1. Non-invasive. b. Disadvantaqes:
1- Expensive. 2- New technique
c not Therapeutic
Advantaqes:
Digital subtraction artriography of the right leg of the same patient showing a stump in the take off of the superficial femoral artery
Magnetic
r e s onantce
arfuiogr aphy
showing
bilateral total superficial femoral occlusions in a patient with a non-healing ulcer of the right lower extremity. (CFA = Common femoral artery, PFA = Profunda femoral artery, SFA = Distal superficialfemoral aftery filling from collateral flow from the profunda femoral aftery with no visible
VASCUIAR
SUR.GERY
I9
ln claudicant patient starfs the investigation with non-invasive vascular laboratory test and then proceed to one of the imaging fesfs only if non-invasive tesf results are insignificants e ln CLI do the non-invasive vascular lab test together with one of the imaging fesfs according to the clinical situation
q-
uidy:t_qjjIUnIl
Conseruative Treatment
Treatment is mainly consewative
Spontaneous improvement occurs in many patients over the l"t 6 months after an occlusive episode as collateral vessels develop. Symptoms oJ'PAD ) Clinical and Duplex assessment ) Claudication
I
Critical
I
I
lschemia
lmproved
Surgicalreconstruction +
(BMT)
3- Vaso-active druos (may have a role in intermittent caludication) a- Naftidrituryl (Praxilane) b- Cilostazol (PIetal) 4- Care of foot Gspeciallv in diabetics) a- Avoid cutting angles of the nails, avoid tight shoes. b- Good hygiene & dryness of foot. 5- Exercise traininq: Walking to near maximum pain producing distance 3 times per week improves
ln dications (as en darterectomy) Short segment affection in a big vessel (2cm or less). Non-calcified Not done in occlusion below knee Ievel. - Good outflow
Complications:
. .
Recurrenoe. Hematoma.
A-V fistula.
B.
the elastic recoil of the arterial wall and keep the lumen patent)
(Surgery in this case aims in saving the limb and thas called limb salvage sargery)
ischcnicl
1.
2. 3.
4. 5.
Starting gangrene (to avoid spread of gangrene). Pregangrene. Severe claudication pain interfering with patient's work (differs according to each patient). Ulcers resistant for hpaling. Long segrnent occlugion > 12 cm
VASCULAR. SUR.GERY
$argical tcchnioues laccoriling to angiogranhyl:
2t
Endarterectomy
(Short segment affection in big vessel).
Bypass
(Long segment affection in small vesse[).
femoro-femord or
l'emoral
arlllo
Amputation Indications:
. .
Spreading or massive gangrene Spreading infbction. Severe uncontr-ollable pain (patient himself asks for amputation)
2- Bvoass surger:y:
a. For aorto-iliac disease: done using synthetic graft made of Dacron or PTFE. b. For superficial femoral arterv block: The standard operation is femoro-popliteal bypass using the saphenous vein. To overcome the valves of long saphenous vein one of two techniques is used: Reversed saphenous venous graft. o ln situ saphenous vein graft. The valves are destroyed and the tributaries are ligated.
Graft
Blockage
22
VASCULAR SUR.GERY
1.
2.
Atherosclerosis except with tissue loss (ulcer resistant for healing) ) improves collaterals) improves healing (as it shifts blood to skin) (done in combination with direct arterial surgery)' Diabetics, as the patient is already sympathectomized.
1. lschemia of UL ) Ceruico-dorsal sympathectomy. T2,3,4 are transected. . T1 (or stellate ganglion) is left to avoid Homer's syndrome.
2.
lschemia of LL
- L2,3,4
Lumbar sympathectomy.
ejaculation.
Stellate Ganglion
are transected.
blood supply to skin & J blood worsen supply to muscles of claudication pain (steal
Save T1
T2,3, 4 (dorsal)
phenomenon).
Save
Ll
L2,3,
(lumbar)
hypersensitivity.
a-
lndications:
'
VASCULAR. SUR.GERY
2T
. Lumbar svmpathectomv: a- Open lumbar sympathectomy. b- Chemical sympathectomy: require the injection of small quantities of
dilute aqueous phenol into the lumbar sympathetic chain under radiographic control.
3- levet o[ amoutation:
a. b. c.
lf the popliteal pulse is felt, below knee amputation is done. lf the popliteal pulse is not felt, above knee amputation is done.
/,
Forefootamputation.
DD of claudicating pain
1. Osteoarthritis: pain on the first step
2. Lumbar prolapse: pain not relieved by standing still. 3. Venous claudication: 1 on prolonged standing & J on lying flat. 4. Flat foot: pain on standing or walking (due to pressure on plantar nerves).
affecting claudication distance: = Factors 1- Speed of walk (high speed decreases it).
2- The presence of hills or soft floor (reduces it). 3- Upstairs movement. 4- Degree of ischemia. 5- General health such as anemia or heaft failure. Arm claudication:
lt may occur in upper limb in subclavian, axillary, brachialartery obstruction. The pain being brought on by such activities e.g. writing or manua! labour.
- Warmth stimulates tissue metabolism) lischemia. - Patient tends to uncover his limb (J metabolism).& put it in dependant position blood supply). - Rubbing of dorsum of foot
(f
24
. . . .
VASCUIAR SUR.GERY
Subclavian steal phenomenon
Thrombosis on top of atherosclerosis affecting the 1"t part of subclavian artery before origin of vertebral artery. So the vertebral artery provide a collateralcirculation by reversing its direction of flow. This may cause periods of cerebral ischemia due to shift of blood from the basilar artery. However, the classic syndrome of syncopal attacks and visual disturbance associated with arm exercise and diminished BP in affected limb is rare, asymptomatic reversalof flow is much more common. . ln symptomatic patient, PTA or operation is indicated The acutely ischemic limb is frequently paralyzed and without sensation but chronic ischemia does not cause paralysis, but hyperesthesia is common especially in those areas of skin on borderline of gangrene.
Factors affecting the severity: 1. Size of the vessel occluded. 2. The collaterals available for blood flow. Signs of impending limb gangrene: 1. Rest pain.
Degree of ischemia can be determined by: 1. Degree of pain (claudication distance). Claudication distance <50m and rest pain ) severe ischemia. 2. Color changes: fixed color changes ) severe ischemia. 3. Trophic changes. 4. Capillary circulation (sluggish > 2sec). 5. Venous fillino: orolonoed > 2min ) severe ischemia. The levet of ischemia c-an be d'etermined by:
Site of claudication. Color changes. 3. Trophic changes. 4. Temperature changes. 5. Level of pulse.
1.
2. Edema. 3. Color changes. 4. Hyperthesia. 5. Ankle pressure < 30 mmHg. 6. With or without ulceration.
2.
VASCULAR SURGERY
$ite ot ilisease Aorto-iliac obstruction
25
Type of operation
Clinical finding
Claudication in both buttocks, thighs and calves (1't muscle to be affected is vastus medialis). Femoral and distal pulses are absent in both limbs. Bruit over aorto-iliac region. lmpotence (common in Leriche). Unilateral claudication in the thigh and the calf and sometimes the buttock. Bruit over the iliac region. Unilateral absence of femoral and distal pulse.
lliac obstruction
Aortofemoral bypass (Dacron bifurcation bypass grafting is the best for Leriche syndrome Only 1 iliac artery is involved
+
Axillo-femoral bypass
PTA
Femoropopliteal obstruction
Unilateral claudication in the calf. Femoral pulse is palpable with absent unilateral distal pulse.
Superficial femoral
I Mird
+
occlusion
Available
Moderate or severe
Technical
support
Conservative treatment
++ PTA
)
Not available
Femero-poplitial bypass
smal! vein prosthetic
VAiCU[nn'iiiilciir
>Ulcer >lnfection >Vasculopathy )Gangrene
Term used to describe complex pathology in a diabetic patient's foot. lt is related to duration and control of disease.
Diabetic patients are susceptible to serious foot infections due to: 1- Peripheral neuropathy: diminished sensations makes the patients unaware of foot
2- Vascular affection: due to premature atherosclerosis and microangiopathy. 3- Compromise of the immune system: both the humoral and cellular immunity
disturbed.
injuries.
are
a
a
o
a a
Neuropathic ulcer. Diabetic foot infection. Di abetic vasculopathy. Mixed types. Gangrene.
o Neuropathic
B.
G/P:
Ulcer
Patient is unaware of his foot injury ) neglected ) ulcer
A. Gauses:
)foot
Painless, deep ulcer, may reach the bone, at pressure sites e.g heal, ball of the big toe.
G. Treatment:
45o/o of
diabetic foot ulceration are purely neuropathic in origin , 10o/o are purely ischemic, 45o/o of mixed neuroischemic origin. "ra Infection,,(usually start by minor trauma or infection) o Diabetic Foot A. Causes: - Decrease resistance (both humoral and cellular immunity are disturbed). - Glycosylation of tissue. ' +l- ischemia. - Neuropathy. B. C/P: - Persistent ulcer - Severely swollen Iimb, red, hot & tender. - Pus loculus , tissues becomes dark and slough . - May spread )osteomyelitis, septic shock.
VASCUIAR SUR.GERY
C. Treatment:
Prophvlactic: - Care of patient: control diabetes. - Carefultrimming of toes to avoid their injury.
27
to look for
- Avoidance of walking barefooted. - Daily feet care by washing, drying and powdering them. Curative: - Hospitalization. - Rest in bed and elevation of the foot. - Blood sugar is estimated and controlled better by crystalline insulin. - Broad-spectrum antibiotics are started immediately before C&S. '
Anaerobes are commonlY involved.
Drainaqe of infection and debridement: 1- Under general anaesthesia all pockets of pus should be drained. All sloughs should be excised. A gangrenous toe needs to be
234-
amputated leaving the wound open. lf the patient is in septicemia, a major amputation is necessary to save the patient Iife. Repeated dressing and repeated debridement. When the wound becomes completely free of infection, plastic skin covering is considered to shorten recovery time.
c. Treatment:
Microangiopathy: (all pulses are felt, no bleeding from cut wound) )surgicaldebridment, antibiotics, skin flap to promote healing . Macroangiopathy (pulse is not felt).
u
Doppler & Angiography
Run in & run off +short segment I Endarterectomy Percutaneous translumena! angioplasty
Bypass
Mixed Type
o Gangrene
-
- Dry gangrene on top of chronic ischemia. - (C/P & TTT see gangrene).
28
VASCULAR. SUR.GERY
Vasospastic Disorders
W{fittltrint
}UL > LL 1. Recurrent lschemic attacks. >3 colors (white, blue, red) 2. Precipitated by exposure to cold or >Raynaud's: 1ry,2ry emotional stress. >TTT: Conservative, Surgery, Cause 3. Common in UL & rare in LL. 4. It consists of: 1 Pallor (white) ) due to VC. 2 Cyanosis (blue) ) due to sluggish blood flow. 3 Rubor (red) ) due to reflex VD (accumulation of metabolites).
Raynaudt Disease
Aqe & sex
DD
Il ry)
Raynaud's phenomenon(2ry)
Vary according to underlying cause - Collagen ) SLE, scleroderma. - Arterial obst ) Atherosclerosis, Buerger's disease. - Nerve injury ) Thoracic outlet $, carpal tunnel $. - Environmental ) Vibrating tools - Druqs ) beta-blockers. - May affect LL. - May be unilateral. - lf bilateral, it is asvmmetrical. More prominent.
May be absent.
Cause
young females (20 - 40 yrs) Not exactly know, certain factors are suggested e.g.: 1- lncrease sympathetic tone. 2- Psychological instability. 3- Abnormal sensitivity of small arteries and arterioles of hand to cold.
It affects UL (may affect LL).
Distribution Trophic changes& oanorene Radial & ulnar oulse Follow up Investiqation
Absent or minimal.
Present.
Treatment
No progression & no evidence of Progressive. underlvinq disease. manifestations of undedvinq dis. Should be directed to the suspected underlying cause Conservative (in earlv stases) - Treatment of the cause. Care of patient - Vasodilators and beta-blockers may - Stop smoking. be used. - Avoid cold weather. - TTT of anemia if present. - No benefit from sympathectomy as Control diabetes there may be: Care of Hand Vasculitis. - Good hygiene, dryness of the hand and * * Cryo-antibodies ) cause VC in wear woolen gloves in winter case of lowered blood temp. to - Hand exercise. Druos: as chonic. lschemia + 36-36.50 c - Vasodilators ) phenoxybenzamine, nifedipine. - Baby aspirin (prophylactic for fear of vaso-obliteration). - CCB.
Cervicodorsa I Sympathectomy. lmmediate results are good, but may recur after one or two years (due to denervation hvperse nsitivity).
VASCULAR. SUR.GERY
29
a. Painless. b. Not paroxysmal. c. Cyanosis is marked and reticular. d. Affects upper and lower limbs. e. Associated with lower limb paraesthesia.
TTT: in severe
ses
sympathectomy.
. C/O: occurs due to cold exposure , Patholoqv: there is damage in vessel wall followed by transudation and edema . C/P: severe burning pain in affected part, blistering and gangrene may follows . Ig!44!i The proper emergency treatment is immersion of the affected part in warm water at 4O ) 44 C
1ry Raynaud's in 24-year-old female
trostBlte;
Apparently normal angiogram of 24 year old femal with primary Raynaud's syndrome
b) Intensive vasospasm prevents filling of digital vessels after cold exposure in the same patient c) cigarette smoking has the same vasospastic effect
VASCULAR SURGERY
The etiology is unkown. . Affects males only. . Starts between 2040 years old. . Occurs exclusively in smokers; it may represent allergic reaction for nicotine. o Interdigitalfungal infection is a common association.
The disease should be suspected in a young male who is a heavy smoker complaining of chronic ischemia in one or more limbs. The disease is preceded by migrating thrombophlebitis. may be superimposed.
Distal vessels with patchy distribution lnflamed neurovascular bundle and thrombi that block the lumen Usually present
. o .
ls rarely needed to confirm the diagnosis. This is because the disease affects the distal vessels and the distal run-off is known to be absent. So there is no possibility for reconstruction, and consequenfly no need for
1- Smoking must be stopped. 2- Sympathectomy gives good results. 3- Amputation of one or more toes or digits is indicated for persisting pain or
VASCULAR SURGERY
a
a
lt
a a
(Pulseless disease of young females) autoimmune arteritis affecting the thoracic and abdominal aorta and their major branches and is usually fatal.
on
Acute
Saddle embolism
Chronic
Old
age
Leriche syndrome
Etrd|ergy
1. Gervical rib: lt is an extra-rib articulates with C7. Present in 0.5 % of population. May be bilateral. - Usually asymptomatic. The rib may be: articulates anterior with manubrium or. Complete with a free bulbous or Fibrous band anteriorly. lncomplete
72
VASCULAR SURGERY
2. Scalene syndrome: Very strong scalene muscles. Weak shoulder girdle muscles. 3. Malunion of fracture clavicle. 4. Pancost tumor. 5. Tumors or infection of the 1"t rib. 6. Post fixation of the brachial plexus: ln this case the lower root of brachial plexus arises fromT2 instead of T1, so becomes severly bended over the 1't rib. .t'
The condition occurs more frequenlly in females. lt is usuallv unilateral affectinq the rioht arm (dominant arm), but is sometimes bilateral.
Neural
Compression of the lowertrunk of the brachial plexus (C8 & Tl ). lt is the main structure to be comoressed.
1- Subclavian or axillary vein limb: thrombosis a- Claudication pain with exercise. (Effort thrombosis). b- 2ry Raynaud's phenomenon (on exposure to cold) (due to irritation of C/O: acute pain and swelling (DVT). sympathetic fibers supplying U.L.) 2- Chronic venous 2- Post+tenotic dilatation: may insufficiency. develop a thrombus inside. This 2- Motor ) C/O: chronic heaviness Weakness & thrombus may send a shower of and swelling. embolito the index and middle atrophy of direct continuation small finger as they are the muscles of of the brachial artery. This emboli the hand. can oroduce dioital oanqrene. - I Sensation. - Unequalpulse on both sides. - ms weakness . Positive Addison's lesl ) ask the patient to: - Extend the head. & atrophy. - Look at opposite side. - Take a deep breath. - Then palpate radial pulse while arm is pulled down. lf oositive ) radial pulse becomes weak - A oaloable cervical rib mav be felt at root of neck especially if bulbous. 1- Chronic ischemia of upper
7- Sensory)
tingling & numbness along the ulnar side of hand & forearm.
. .
Other causes of localized pressure on nerve: cervical spondylosis, carpal tunnel syndrome. Other causes of Raynaud's phenomena: Raynaud's disease, systemic lupus.
VASCULAR. SUR.GERY
Plain x-ray ) cervical rib. 2. Arteriography ) show post - stenotic dilatation. 3. Nerve conduction studres ) Reveal prolonged nerye conduction time. ) Very useful to differentiate carpal tunnel syndrome from thoracic outlet syndrome.
1.
Cervical rib compresses subclavian artery & there is poststenotic dilatation Electrical Studies ) reveal prolonged nerve conduction time
Phltsiotherapv & shoulder exercises ) to develop shoulder girdle muscles. Severe cases with vascular symptoms or failure of conseruation
T*.*#[[i",,f #-ff-,i.,wffi f*ffi Osteotomy and internalflxation of clavicle. Radio and chemotherapy for pancost tumor.
ilary
l4
t!;ufl,it,fr,lfgiit
VASCULAR. SUR.GERY
. . .
C
)i4 r,
iTq-,i ) FrE
I gt
ft
with size)
Middle age female or male with slowly growing swelling adjacent to hyoid bone, anterior to sternomastoid muscle, smooth, compressible, pulsatile, moves from side to side not vertical
CT scan Angiography: widening the carotid artery bifurcation Excision with preservation of ICA
ilnv+4fr*:,itrunr;
. .
Tr=;'.[ri-f4iii
Gangrene
iD'eft;t,fi,tl g)t,t . Macroscopic death of tissues
due to loss of blood supply and is usually associated with bacterial invasion and
Others
t1
lt often affects the distal part of a limb because of arterial obstruction (thrombosis, embolism or arteritis)
aE'il.rdfei.Il
1. lschemic ) thrombosis, embolism, vasospastic disease. 2. Neuropathic ) syringomyelia, leprosy. 3. Venous Gangrene (see below). 4. Traumatic ) direct:e. g bed sores, 5.
lnfective
6.
) indirect: e. g arterialinjuries. Specific infection: e.g. clostridialgas gangrene. Non-specific infection e.g. carbuncle, anaerobic cellulites. Physiochemical ) bums, caustics, frostbite,... ) )
:rfggr+t
VASCULAR
SUR.GERY
35
(There are 3 types ofgangrene depending on rate oflocal death in the presence ofinfection)
l- Dry Gangrene
(cause)
Putrefaction Odor
Gross Line of demarcation Separation
Chronic ischemia ) allows dryness of tissues.
Minimal.
Dry. Hard.
Verv offensive
well defined
Fate
Due to presence of line of demarcation appears between the dead & viable tissues. Leaving a conical stump (deeper tissue has better blood suoolv).
1.
The five cardinal signs of local death are: Lost (pulsation, Sensation, Heat, Function of affected part) fixed color changes.
CIP
Treatment
NB. Patient suffering from threatened gangrene have all the above signs but the tissues are still viable and local pressure causes some modification of color, which returns when the pressure is released. 2. The affected part is ) see gross. 3. Minimal toxemia ) better general 3. Severe toxemia ) poor general condition. condition. - Amputation till the level of See chronic ischemia pulsation (acute condition) - Limb salvage (conservative (non-conservative amputation). amputation). - Non-conservative amputation. - Later on ttt of the cause if possible.
o o
Etioloqv:
. .
lnfection of sterile gangrene (2ry infective gangrene). lnfection of tissues with virulent organisms leading to gangrene (1'v infective gangrene)
Glinical Picture:
. . .
The affected limb becomes swollen, edematous and markedly inflamed. The skin appears moist with bullae filled with serum. The limb emits a very offensive odour and may crepitate due to gas formation.
t5
VASCULAR. SUR.GERY
. Line of demarcation : between dead and healthy tissue o Line of separation: level at which thc necrotic tissuc separatcs from healthy
tissue.
Treatment
1. Prevention.
- Air mattress.
2 hours. 2. Curative - Debridement. - Leave the wound open until healing + repeated dressing with glycerin magnesia to help separation of the slough. - Then, antibiotics (can not be given alone as it is dead tissue so it will not benefit from it) - Skin flap.
- Skin should be kept dry & clean. - Frequent change of position every
(Fourneir's Gangrene):
- Sudden onset of scrotal inflammation + sudden onset of gangrene Due to mixed infection (synergism) by Strept, Staph., E. coli, Cl. Welchii,....etc. May be associated with necrotizing fasciitis & wide surgica! excision.
TreatmeXlrrbiotics
VASCULAR. SURGERY
Pathological definition:
A sac filled with blood communicating with an artery.
1. Congenital. e.g. aneurysms in circle of Willis "Berry's aneurysm" I t rupture causing spontaneous subarachnoid hemorrhage. { 2. Pathological due to: - Atherosclerosis (commonest cause). - Trauma. - Syphilis. - Mycotic (i.e. arterialwall is weakened by infection e.g.following embolization from SBE. - Collagen disease e.g Ehlar Danlos, Behchet. 3. Traumatic: o A blunt trauma may weaken part of its wall Later this weak area progressively yields Ieading to aneurysmal dilatation. o A penetrating injury to the artery leading to hematoma surrounding the artery .Later on, this clot is surrounded by organized fibrous capsule leading to false aneurysm.
7.
Saccular.
2. Fusiform.
3. Drssectrnr.
False AneurYsm
True Aneurysm
Fusiform
Type of patient
.
Age:
- old age: atherosclerosis and syphiftic aneurysm. - Yong age: traumatic aneurysms are common. Sex-' more common in males.
saccular
SymptOmS
. May be asymptomatic.
. Swelling (external) or pressure manifestation (internal). . lschemic manifestations due to: - The cause (atherosclerosis) ) chronic ischemia. - The patient may be presented by complications: Dissecting o Embolism ) acute ischemia. o Rupture ) acute ischemia, shock.
38
Sims
VASCULAR. SUR.GERY
. Local:
lnspection
-Swelling. -Along the course of an artery. - Expansile pulsation (systolic) (most important sign) Palpation Consistenqr ) cystic. Movement ) across but not along an artery. Compression - Totally compressible. - Partially compressible ) thrombosis. - Proximal compression ) on feeding artery ) | size & pulsation becomes weak. - Distal compression ) on affected artery ) f size & become tenser. Auscultation ) soft systolic bruit may be heard over it.
1. 2.
3.
g e
) fatal hemorrhage (suspect if diameter >6 cm, 0 elastase in blood) - lnfection: may lead to rupture and 2ry hemorrhage. - Pressure manifestations: o Nerve ) sensory, motor loss. o Bone )erosion. oVein ) obstruction, thrombosis. - lschemia due to: o Thrombosis. o Embolism. o Associated atherosclerosis.
- Rupture (most serious complication)
1. 2.
Plain x ray: may accidentally discovered calcification in wall of artery. U/S) best if aortic aneurysm is suspected ) non-invasive, cheap & can determine the diameter and extension of the aneurysm. 3. CT scan: is the accurate investigation to determine the diameter of the aneurysm
. . .
CT accurately determines the true extension of the aneurysm ln aortic aneurysm lt is important to determine if the upper limit of the aneurysm is below, at, or above the renal arteries because the operative treatment is different in each situation lt is important to determine if the iliac afteries are also involved.
4. Angiography: Angiography does NOT show the true diameter of the aneurysm. lt only shows the diameter of the patent lumen
. Recently, CT angiography with 3D reconstruction of the arterial tree is graduiiry:r"ii{
:''/:''?ii]:i:
.lt
is more accurate than older CT & less invasive than angiography as the dye in injected
VASCULAR. SUR.GERY
Conservative. 2. Surger;t lndications
l9
l.
1. Symptomatic aneurysm. 2. Asymptomatic if the diameter is >55mm. 3. Asymptomatic in high-risk patient e.g. hypertension.
Technique . Excision ) for small or unimportant artery. . Excision & grafting ) for aneurysm of large artery. . Exclusion graft (open the sac ,place the graft then close the sac End ovascul ar su rgery: ntra! u mi nal self-i nfl atable g raft .
i
See before + affecting abdominal aorta. Mainly due to atherosclerosis. (95%) Rarely due to other Gauses (mycotic, syphilitic, collagen disease).
)lnvest.:
CT scan, U/S
Silent in 75 7o of cases. lf symptomatic ) pain (commonest symptom) ) vague abdominal pain with flank and backache (due to vertebral compression). May present with complications) Rupture : Types of rupture aneurysms: 1- lntra-peritoneal rupture (free rupture) isfatal. Patients usually don't reach hospital
2-Retro-peritoneal rupture is an extreme emergency. lt has a high operative mortality (this the reason way we prefer to repair large (>4cm) asymptomatic aortic have much lower mortality.
Symptoms
. . .
Sudden severe onset of epigastric pain. Collapse with severe hypotension. May have history of aneurysm under surveillance.
Signs
. .
Cardinal sign: unexplained rapid onset hypertension, pain and sweating. A pulsatile abdominal mass is not always present.
+o
VASCULAR SUR.GERY
CT scan is the investigation of choice to investigate painful, leaking or ruptured aneurysm Arterio-aortic embolism: mural thrombus within the aneurysm can detach and cause distal emboli Embolization may be spontaneously (blue toe syndrome) or iatrogenic during surgery (trash foot).
. i-QJ-PJ
Pseudopancreaticcyst:transmitted pulsations.
-r
See before
U/S, CT, MRA, Angiography. For other system affection ECG, CBC, lipid profile.
Foraneurysm
'
- US is the screening test of choice to documents or to role out the presence of aneurysm -Arteiography may appear normal despite presence of large AAA if the aneurysm is occupied by thrombous so it is not used to diagnose AAA or to assess its dimension, is is only of value if the patient is suspected to have associated occlusive disease.
Tltaf,illt.rEnIi
Plain of
management: Treatment
I
I
Look for indications tbr surserv (accordins to the caliber)
l
l
of acute expansion.
*ns
Indicated
Symptomatic regardl ess size
Asyrnptomatic
ertr
I
Exclusion graft ( standard mcthod) Endoluminal self inflatable graft
/U.8.
Endovascular repair of AAA via insertion of endoluminal stented graft through bilateral femoral arteriotomies is expensive and recurrence of aneurysm can occur so, only indicated for: 1- High risk patient who can not tolerate anaesthesia or open surgery 2- High risk local abdominal factors (intra-abdominal infection)
VASCULAR. SUR.GERY
+t
Aneurysm opened
Note the clots and cholesterol debris. These may cause distal emblization
The bifurcated graft is first sutured to the aorta from inside of the aneurysm
They are usually single, affecting large or small vessels (causes ischemia); it is common in the thigh (butcher's thigh), axilla or neck.
2. Patholoqical tvpes: a- Arteriovenous aneurysm: the communication between the artery and vein is not direct and there is an intervening hematoma, which later organizes. vein is direct and b- Aneurysmal varix: the communication between the. there is no swelling in between.
3.
Glinical Picture:
General ) tachycardia, {t cardiac output with high systolic blood pressure and low diastolic blood pressure ) water hammer pulse.
Local lnspection
A!
Aneurysmal varix
+2
Palpation On the swelling
VASCUIAR SUR.GERY
thrill. Compression - Totally compressible. - Partially compressible ) thrombosis. - On feeding artery (at site of fistula) ) Upulse "Branham's bradycardia" (AV fistula -+ tCOp, on compression -+ JCOp-+ Vpulse). machinery murmur may be heard over it. Auscultation Distal: secondary varicose veins, ischemia.
4. lnvestiqations
1- Arteriography
shunting of the blood from the artery to the vein or show both arteries and veins at the same time due to rapid venous filling.
5. Treatment
2- Doppler)
1. Reconstruction of the artery & vein. 2. Quadriple ligation: - lf Reconstruction is difficult (as in HF). - Unimportant artery.
B
i:
Endovascular Su
.
@F,st:f ftfei,i'fi -ellt
Management of vascular diseases percutaneously through a puncture to deal with a lesion in a remote site.
System: 1- Arterial.
2- Venous. Purpose: 1- Diagnostic. 2- Theraputic.
1- Angioplasty.
2- lntravascular stents. 3- Thrombolytic therapy. 4- Atherectomy. 5- Peripheral laser angioplasty. 6- Endoluminal grafts. 7- IVC filters. 8- Catheter vascular access implantation of a catheter
vesselfor either: a- hemodialysis in chronic renal failure.
to access a central
b-
Chemotherapy.
lndications:
1- Critical ischemia.
2- Severe claudication that interferes ldeal Iesion: 23Stenosis <5cm length. Best in lliac
I I
Aim:
rMay inserted in the same session after PTA to prevent its drawbacks (dissection and elastic recoil) in order to maintain its patency of the artery.
2- Recurrent pulmonary embolism. 3- Chronic pulmonary embolism in patients 4pulmonale. Complications of anti
Principle:
I
I
.A combination of a stent with prosthetic graft positioned with a delivery system. Uses:
of an
i i
Acute DVT. Acute thrombotic ischemia. 3- Acute coronary occlusion. 4- Occlusion of vascular grafts. 5- Pulmonary embolism. 6- Acute embolic ischemia. 7- Restoring patency of recently occluded central venous catheters. .lt is betterdone in an l.C.U underclose observation.
12-
Contraindications:
1-
Active bleeding.
E The commonest
E
E E E
o
E
E E
ln diabetic patients with critical limb ischemia, the ankle/brachial index may be falsely high, so they may develop calcification of leg arteries. Approximately 50% of popliteal artery aneurysms are associated with aneurysms at other sites. The 1"t thing to do after diagnosis of acute L.L. ischemia is to give the patient heparin to prevent clot propagation. Thrombolysis is contraindicated in patients with history of stroke within the previous 2 months or major surgery within the previous 10 days because of risk of bleeding. Aorto-iliac reoonstruction su1gery has good long-term outcome. lntra-arterial thrombolysis is best achieved with pulse-spary TPA. ln fat embolsim the fat is most likely to arise from chylomicrons. Therapeutic embolization is used for arrest of hemorrhage, TTT of A-V malformations & shrinkage of tumor growth. Venous gangrene occurs in presence of venous & arterial occlusion, embolism or diabetes. Bowel strangulation is an example of moist gengrene. Cessation of cigarette smoking is the 1ry therapy for Buerger's disease. Buerge/s disease is characterized by recurrent exacerbations & remissions. Intermittent claudication is usually the 1"t symptom in Buerger's disease & it may end in gangrene. Endovascular Aortic Aneurysm Repair (EVAR) leads to absolute reduciton in early mortality (within 30 days) compared to open repair
Superficial veins. Deep veins: occur mainly in the calf or iliofemoral veins. Less common sites
2-
are lVC, subclavian, axillary or portal veins. Predisposinq factors (Virchow's triad): 1. Velocity: slow circulation: Prolonoed rest in bed.
Pregnancy.
y [:is:;,i",ll''g:JtrX'nt
- f*lflTation
Previous DW
b-
Phlebothrombosis: with this type, the venous thrombosis is not associated with infection. Therefore, the thrombus will not be adherent to the vein wall and it may detach resulting in pulmonary embolism. Thrombophlebitis: the venous thrombosis is associated with inflammation of the affected vein, so the thrombus with be adherent to the vein wall.
. General ) FAHM. , Local ) pain & tenderness at the site of the affected vein.
. The vein is felt as tender, firm, cord Iike structure. . The overlying skin is red & edematous.
1. 2-
3. Pulmonary
Extension to deep veins via communicating veins. embolism (very rare because the thrombus is very adherent to the vesselwall except big veins as saphenous vein).
VENOUS SUR,GERY
1. Rest & compression by elastic stockings 2. Anti-inflammatory drugs e.g. aspirin.
special conditions:
17
or compression bandage.
3. Antibiotics (only if there is evldence of infection). 4. Anticoagulant therapy (heparin and warfarin) is given in severe cases (ascending
thrombophelbitis or if associated DW).
Thrombonhlebitis M
It is a type of superficial thrombophlebitis that resolves spontaneously in a few weeks to reappear in another area. !t occur with: 1. Buerger's disease. 2. lt is the earliest sign of visceral cancer (stomach, pancreas) "Trousseau's sign" due to break down of the tumor which causes hypercoagulation of the blood. Migratory Thrombophelbitis 3. Polycythemia & polyarteritis nodosa. 4. Ulcerative colitis & ,
SLE.
1- The process usually starts in the calf venous sinuses or in the iliac and femoral veins by adherence of platelets to the endothelial surface forming qrey cluster. 2- Fibrin and RBCs are deposited as layers in-between the platelets giving a laminated appearance known as !@!!4es of Zahn.
18
VENOUS SUR.GERY
When the vein is totally occluded, non adherent, jelly-like propagated thrombus spreads up the vessel as far as the next major tributary. This thrombus is dark red and consists onlv of fibrin and red cells. At this stage the thrombus is looselv attached and it can be easily detached leading to pulmonary embolism. 4- Later, the thrombus becomes tightly adherent to the vein wall by fibrin deposition. lt then organizes and contracts thus producing destruction of the vein valves which is responsible for the development of oost-phlebitic !imb. 5- Later on the process of fibrinolysis and phagocytosis starts and helps in recanalization of the vein but the valves are permanently destroyed. 90% of occluded veins will be recanalized within 9 months while 10% of affected veins remain occluded for life.
Deeo Vein Th?ombosis
(DYf)
Embolus
. . . .
Classical triad of pain, swelling, tenderness. Depends upon the site of the thrombosis. 1- Pain: there is usually aching discomfort and tightness in the involved calf or thigh, which are aggravated by muscular exercise. 2- Swelling (it is the most reliable physical sign) ln calf thrombosis swelling is limited to foot and ankle. ln femoralthrombosis swelling involves calf and lower part of thigh. ln iliofemoral thrombosis swelling affects the whole lower limb. 3- Tendemess: present on grasping the affected calf or thiohND, e+hrimbosis: blood clots occurring in sitting on computers for
Homan siqn
putmonary embolism.
Vascular SUR.GERY
87 Non-Hodghn's
Hodgkin's
Macroscopically A) L.N. - Sites:
- CG's: - Usually lower deep cervical axillary ) mediastinal
matted later.
- Cut section:
Microscopically
Characteristic giant cell (ReedSternberg cell) with lymphocytes, histiocytes & PNL (pleomorphism). 1 - Lymphocytic predominance 2- Nodular sclerosis 3- Mixed cellularity 4- Lvmphocvtic depletion
- Adolescent & middle age
(bimoda!)- d
- Extreme of age - d
3-Swelling:
matted later.
4-Pain:
5-Pressure manifest.
VENOUS SUR.GERY
b- Local a) Early: 1. Phlegmasia alba dolens: massive
+9
iliofemoral DVT may be associated with severe arterial spasm and lymphangitis, so the limb becomes pale, white and massively swollen with absent peripheral pulsation.
2. Phlegmasia
and cyanosis and the whole lower limb looks massively swollen and blue and if not probably treated, it may lead to venous gangrene.
b) Late:
1.
2.
Post phlebitic limb (secondary V.V due to destroyed valves 2ry to recanalization) Venous gangrene (phlegmasia alba & cerulea dolens).
>
A- Uniloterol: l)Acute:
laotn previous conditions (No2 & 3) occur during exercise and can produce swollen painful calf which is usually difficult to distinguish from DVT. Duplex scan is needed to establish the diagnosisl.
1. Varicose veins
Cardiac Renal
3. 4.
. .
. .
DVT is a potentially fatal disease and its clinical picture overlaps with many other conditions. So once clinically suspected, the diagnosis of DW must be confirmed / excluded by accurate investigations, as clinical examination is not reliable in 50% of cases.
2. Duplex. (accurate in 90 -100) most errors are in below knee veins 3. Recently radioactive fibrinogen)detect active uptake by thrombus). 4. Recently )spiral CT (most accurate). 5. Venography (not done now) (it is the gold standard but invasive)
(accurate in 80-85%)
50
VENOUS SUR.GERY
Venous blood flow in the SFV
Colored Duplex US: Acute DW of the superficial femora! vein with a floating tail
1. Spiral CT or ViQ Iung scan or pulmonary 2. Ventilation /perfusion scan. 3. Pulmonary angiography. 4. Chest xray. If Recurrent FW in Young Patient
arteriography
Treatment
Treatment of DW
1)
2)
Treatment of complications
Prophylaxis: - For all patients. - For high risk patients Curative: - General. - Drug therapy. - Operative.
:
A. Treatment of DVT:
Prophylactic
For high risk patients e.g. major surgery, elderly patients, history of DVT or PE
-1-
Early ambulation after operation. 2- Active leg exercises while in bed. ?- Adeq uate postoperative hydration.
Prophylactic heparinization should be avoided if a large raw area is left after surgery
VENOUS SUR.GERY
Curative
5r
A. General:
.
. .
Complete bed rest for 7-10 days till the thrombus is adherent to the vessel wall. '1't day elastic stockings. Vitamin E (helps absorption and recanalization of thrombus). Foot elevation in bed 15-20" to decrease edema and pain and increase venous return. Thrombi usually takes 7-10 days to become adherent to the vein wall. During this period the patient should be kept in bed then gradual ambulation with elastic stocking support is allowed but standing and sitting with legs dependent are forbidden. These measures are continued for 3-6 months until recanalization and collaterization develops.
B.I)rug treatnent:
>
ai'+r--qf
r.M
Tvpes of heparin: 1- Low molecular weight heparin (fractionated heparin): . Tinzaparin lT5lUlkglla hours S.C. , Enoxaparin 1 mg/kg/12 hours S.C. 2- Untractionated heparin is administrated either by: . Continuous l.V infusion. A Ioading dose of 80 lU/kg then maintenance dose of 18lU/kg/hour. . This is the ideal method, but it requires hospitalization and a pump that controls the dose per hour. . Bolus therapy. A loading dose of 80 lU/kg then maintenance dose of 70 lUlkgl4
. Heparin is given
2.
hours.
until all sings of active thrombosis disappear which is clinically known by disappearance of pain and tenderness on grasping. This usually take 7-1 0 days.
. .
Administration:
2- Discontinue heparin after 3 days of overlap treatment. 3- 5 days after the start of therapy and PT should be measured
by 5 mg daily dose.
and adjusted to
45-
keep it at30-40%PC and PT are repeated every 2 weeks and the INR should be between 2-3 times the control value. Oral anticoagulants are given for 3-6 months which is the time needed for recanalization. ln some patients who are liable for rethrombosis warfarin is given for life.
P$,e.r@
rrBtE
52
VENOUS SUR.GERY
if given in the first 3 days of thrombosis, as after that they have no advantages over heparin)
. .
- lsolated ilio-femora! DW - lmpending venous gangrene as phlegmasia cerulea dolens - Urokinase. - Streptokinase. - Recombinant tissue plasminogen activator (advantages: less allergic and more effective).
Tvpes:
lndications:
t Action: - Conversion of plasminogen into plasmin, which has a proteolytic effect on fibrin & fibrinogen. . Advantages: - I cvtto 4G.50 - I valve damage . Complications:
c.@!
streptokinase'
AIL"J:fiJiffHHJ:
lndications:
1-
'8.
Tre
a
I
done): Bv Fosertv catheter if: - Massive illiofemoral thrombosis. - Phlegmasia cerulea dolens. - Pulmonary embolism.
:of,,
Pulmonary embolism: mo;phia, 02, thropbolytics, anticoagulants, embolectomy. Post phlebitic limb: compression bandage.
VENOUS SUR.GERY
5T
Heparin
23HaH
Enhances the activity of naturally occuning antithrombin lll. The antithrombin lll-heparin complex neutralizes the effect of thrombin. Neutralizes factors lX, X and Xl. Mav have mild thrombolytic effect as it can cause mild activation o
Mode of action
AntiXa
12 hours S.C Not required- if needed ---level of Xa <2% May be taken at home
l.v
APTT
1-5%
. Control:
The dose of heparin is monitored by measureing APTT which should be kept between 2-2.5 times the controlvalue.
23-
bruises, epistaxis, bleeding gums or G.l.T bleeding. The antidote of heparin is protamine sulphate 1 mg lV for every 100 lU of heparin. The use of S.C low molecular weight heparin is less likely to cause bleeding. Failure to respond to heparin (heparin resistance). lt may be mild and requires only increasing the dose of heparin. Heparin induced thrombo'cytopenia occurs usually in the 2nd week of therapy. lf the platelet count drops below 100000/mm3, heparin should be stopped.
. Mode of action:
Oral anti-coagulants
These drugs blocks the synthesis of at least 4 vitamin k dependant clotting factors (prothrombin and factors Vll, lX and X). For this effect its anticoagulant effect is delayed. Ora! anticoagulants inhibit the synthesis of protein S and C which has an anticoagulant effect and so there is a period of relative hypercoagulability during the 1"' few days of warfirurin therapy. This period should be covered by continuing heparin therapy together with the warfarin for the last 3 days.
2-
'@ A. Absolute:
B- Relative:
the dose and by vitamin K injection in a dose of 10-20 mg. lnteraction may occur between oral anticoagulants and other drugs as aspirin, barbiturates and H2 blockers.
3- History of cerebral hemorrhage. 4- Blood pressure above 1801120 mm Hg. 5- Peptic ulcer.
2-3
o/o
of all cases of DW
activity)
1- 1ry spontaneous (usually preceded by unusual muscle 2- Secondary to: a- Central venous catheter b- Metastatic tumor (axilla)
12?- Prominent venous collaterals over the shoulder and anterior chest wall 4- The limb may be cyanosed
As in DVT of the Iower limb + lf the vein is compressed at the thoracic outlet, resection of the first rib or scalenus anterior muscle mav be reouired.
I I
BIock the synthesis of vit. K dependarlt factors Il, IIV, IX, X Prevents synthesis of protgin C and profein S which have anticoagulant effeqt Basal levels of PT and Prothrombin concentration (PC) are estimated before the start of warflarin therapy then measured again 5 days after treatment then every 2-3 weeks
. .
lnitial dose: 10 mg followed by 5 mg daily dose. Given together with heparin for 2 days then stop heparin (3 times /day twice then once lday. Till INR 2% -3l,Control PT of the patient INR = Normal PT
then
. .
VENOUS SUR.GERY
A. Absolute 1- Trauma or recent
55
operation
2- Hemorrhagic diathesis 3- Septic phlebitis 4- Bacterial endocarditis B. Relative 2- Major acute fracture 3- History of cerebral hemorrhage 4- Peptic ulcer 5- HTN. Bo > 180 I 120
I 1. Bleeding is the main problem treated by vit. K. 2. lnteraction with aspirin and non-steroidal inflammatory drug 3. Skin necrosis.
1-
1- Bleedinq
- Management:
4-
Osteoporosis
VENOUS SUR,GERY
2-3o/o
r
1.
o r
Usually secondary to DVT. lnfective endocarditis. Other emboli: fat, air, infected, tumor embolism.
r Recurrent smallemboliwill lead to pulmonary hypertension. 2. Medium-sized emboli (impacted in branches of pulmonarv artery):
. Usually silent.
pain.
b. Dyspnea.
c. Hemoptysis.
3.
'9!!rlica!-P!glure:
f'' .
/'
" ellii evidence of DW in the lower limbs. rt failure in a hospitalized patient is very suggestive of
'"'
' '
l i
I l
1. Spiral CT (recent): most accurate. The clot appears as a filling defect 2. Ventilation Perfusion test: - By ventilation & then injection of isotope material. - Shows filling defect in perfusion scan with norma! ventilation scan (in fibrosis ) defect in both ventilation & perfusion scan). 3. Blood tests - 1 LDH & serum alkaline phosphatase & normal bilirubin (f in case of heart failure). - BIood qases: hypoxia (PaO2<80%mmHg, PaCOz remains normal) 4.
ECG
while in fibrosis there is JPCOz). P-pulmonale. Axis deviation to the right, right ventricular strain pattern ( in 40% of cases).
VENOUS SUR.GERY
57
5.
6. -
of cases). Wedge shaped peripheral opacity is rare. 'l or J vascularity. Pleural effusion.
Pulmonarvangiography
ls the most accurate, yet not commonly done (invasive). Can show hypoperfusion.
Start with D-dimer
if +ve
Ttir'siliiirEitrt
Prophylaxis & TTT of DVT is very important in prevention of PE (mention)
For Pulmonary Embolism: a. Curative: . Small and medium-sized pulmonary embolism are treated by anticoagulants. . Patients with massive pulmonary embolism (surgical emergency):
Ventilation
Cardiac catheterization (in pulmonary artery) Thrombolytics e.g. streptokinase 600.000 unit followed by 100.000 unit / hour for 72 hours. The cardiac functions should improve within 6 hours in favorable cases, if failed ) urgent pulmonary embolectomy is performed. Prophylaxis against recurrence of pulmonary embolism by IVC filter.
- perfusion scan (V/Q scan): is a radioisotope scan that can measure and compare the amount of blood flow to each lung (perfusion) and the amount of air that goes to each lung
(ventilation) pulmonary embolism, the perfusion of a segment of the lung is impaired (because the embolus occludes one of the branches of the pulmonary anery) while the ventilation of the same segment is normal. That is called, ventilation - perfusion mismatch
Tn
r(&i
:.',.'.,.
Septicthrombophlebitis
small -+ multiple foci of infection in the lung.
e
I
Itpilrg9 $,?ly
.gloq9d
91!9. .9J.i
ntection.
It is a rare condition. 95% of fat emboli are associated with fractures which disrupt venous channels in the bone marrow, allowing fat particles to enter the venous pirculation.
Dyspnea. Cyanosis. Tachypnea. Pleural rub (12-96 hours after injury). (as Cerebral symptoms confusion, delirium or coma). Peticheal on chest wall, axilla & flanks
e e
Clinical Definition:
Patholoqical Definition:
Veins that allow reversal of blood flow through damaged valves).
1.
Recanalization of the thrombus ) damage of the valve ) reflux of blood ) this postulates an unusual strain on the superficial veins which have Iittle external support ) they progressively dilate.
VENOUS SUR.GERY
59
3.
Due to compression of the pelvic veins. Also hormones of pregnancy e.g. progesterone and relaxin action on veins.
i
valvular ncompetence) a- Congenital: local gigantism (Klipple-Trenaunay syndrome), Parkes Weaber Syndrome (collection of varicose veins secondary to microscopi c A-V fistula) b- Acquired: butcher's thigh. 4. Aneurysm. 5. Buerqeds disease.
j.N \:' \,
,'f
r))
Pregnancy
Comprgssion by tumor
A-V listula
DVT
Site
Macroscopic Picture 1. Tubulartype: ) dilated main veins (common in 1ry V.V.). Tff 2. $pider type: ) veins are thin & blue (dilated skin venules). 3. Serpentine type: ) veins are coiled.
ffi
4. $accular type:
BIow out dilated superficial system in front of incompetent perforators. Palpable defect in the deep fascia opposite it. Saphena Varix is a saccule opposite an incompetent saphenofemoral unction.
50
Microscopic Picture
VENOUS SUR.GERY The wall is thickened. The muscle & elastic layers are replaced by fibrous tissue.
. . . . . , .
Above & below knee perforators can be called communicators as they join the long saphenous directly, while the ankle & lateral perforators join branches of the long & short saphenous respectively. Communicators = direct pedorators. Perforators = indirect perforators. The muscle pump (soleus acts as peripheral heart). Theunidirectionalvalves. Negative intrathoracic pressure. Transmitted arterial pulsations to venae commitans.
Qultryttrg,i'tbllr;(uvei{u't-fli{tlr;t}i!{4*i!i{4)
Venous Complications 1. Superficial thrombophlebitis: due to sluggish circulatio 2. Hemorrhage after trauma (profuse) due to f pressure. 3. Edema of the LL: due to f venous pressure. Skin Complications 1- Piqmentation. Dermatitis & Eczema: >Due to f venous pressure ) capillary dilatation ) RBCs get out in the S.C fat )phagocyted ) hemosedrin in SC tissue ) pigmentation & irritation ) eczema. 2- Yaricose Ulcer: see later. 3duration of the leg associated .pa+ina nain pain t,,r uursting
From
shortening of
1)
6 together with chronic leg pain constitute postfhlebitic syndrome as they usually follow previous DVT with incompetent perforators.
Cfriffir,[)WrvitfirE
Type of patient . Primary V.V usually occurs around 30 years, rare < 20 years. Symptoms [May be aqymptomatic) 1. Gosmetic disfiq urement. 2. Achinq and discomfort: of the limb usually described as dull-aching, heavy, bursting sensation with sense of hotness usually at the end of the day or on prolonged standing and is relieved by elevation of the limb. 3. Niqht cramps: due to congestion of the muscles (in severe cases). 4. Mild swellinq: ocours at the end of the day (mainly with secondary) 5. Svmptoms of complications: e.g. pigmentation, itching (common), ulceration, etc....
VENOUS SUR.GERY
Signs A. General: 1- Pulse and BP changes in cases of A-V fistula. 2- Heart examination for signs of peripheral of A-V fistula. 3- Flat foot and kyphosis (signs of mesenchymal weakness) B. Abdominal: Scars of previous operation, dilated veins crossing inguinal region, abdominal or pelvic swelling.
6t
1-
2-
lnspection: LL is inspected for: a- Varicosity and its anatomical site. b- Any swelling (saphena varix), scar, edema. c- Skin complications: e.g ulcer, pigmentation. d- Corona phlebectatica: ankle / maleolar flare (one of the earliest manifestations of CVI in form of dilated subdermal veins at or just below the medial maleolus with thin fragile overlying skin ) blue bleb appearance. Palpation: a- Thrill on cough at saphena varix or incompetent saphenopopliteal junction but may be spontaneous in case of A-v fistula. b- Fascial defect: felt at the site of incompetent perforator (Fegan sign) c- Superficial thrombophlebitis: firm tender nodule. d- Skin temperature and peripheral arterial pulsation to exclude associated arterial disease.
[f!
',
3- Percussion: Schwartz's test (tapping test) to detect: Dilated veins belong to sfort or long saphenous. Denotes incompetent valves in superficial system 4- Auscultation: for machinery murmer (A-V fistula) 5- DRE or PV: for pelvic tumors. 6- Soecial test: For Iocalization of incompetent perforator (Trendlenburg's test, multiple tourniquet test) Differentiate between occluded and patent deep systems (Perthe's , J test)
. .
jerthe's
VENOUS SUR.GERY
PrimaryW
Etiology
Pain
ldiopathic Slight or absent Along the long or short saohenous veins Minimal or absent
Distribution Complications
Secondary Secondary to DVT, A-V fistula, pelvic tumors or oreqnancv Marked Haphazard veins crossing the qroin mav be seen More common
The aim of investigations is detection of sites of incompetent perforators and to verify the patency of deep system. In most cases of lry V.V clinical asse
'@itshows:
- Reversal
of blood flow.
- Venous thrombosis.
- Descendinq: shows
For Complications . Ag[qlqgf3plE in case of arteriovenous fistula. . Plain X-ray: in case of varicose ulcer)if periostitis
is suspected.
l. PrimaryW.
A. Gonservative treatment:
Early uncomplicated 1ry .V. Patient unfit for operation or refusing operation. Method: 1. Reassurance. 2. Removal of any predisposing factor. 3. Compression therapy: this is done by graduated elastic compression stockings which exerts 40 mmHg at the ankle and 20 mmHg just below knee (this retards the progression of CVI) 4. Elevation of the LL to prevent congestion. 5. Vitamins, antioxidants, veno-tonics.
Treatment
Of V.V:
lndications:
b.
Secondary.
'TTm1i:]l':s..
VENOUS SUR.GERY
lndications:
57
1.
2. 3. 4.
Moderate cases of 1ry V.V. with main complai nt of cosmetic disfi gurement. ResidualV.V after operation. Lower leg perforators. Recurrent V.V.
lf the main complaint is pain, injection will not cause ,,"T":llt0"""r"" pressure is still high, so we should refer to surgery.
lil-
Complications:
2. 3.
1.
Syncope due to drug sensitivity. Extravasation leading to sloughing & necrosis of the overlying skin. DVT (may occur if large amount of sclerosant material reaches the deep system undiluted.
Contraindications:
C. Suroical treatment:
1. rndications:
- Large 1ry V.V. - Presence of complication.
2' Pt":"+-.
s.%nbandageisappIiedtothelimbattheendofthe
4. Complications of surgery:
operation to prevent excessive bruising.
a- Bruises and discomfort. b- Pain (requires only mild analgesic) c- Sensory nerve injury may occur (1% o'f operation). d- Motor nerve injury (uncommon). e- Venous thrombosis is often seen in residual varices
following surgery.
2.ZryYY
A, Post phlebitic (i.e. following DW). The majority of these cases are treated conservatively by elastic stpckings. Rarely the varicosities are large enough to require active treatment. In these cases verifi7 that the deep system is patent by Duplex, and then treat as 1ry V.V. B. - V.V complicating A-V fistula. Surgical treatment of the fistula is usually followed by marked regression of the varicosities. - lf residual veins remain, treat as 1ry V.V. c. V.V occurring during pregnancy. A complete elastic stocking from the toes up to the groin is applied all through the period of pregnancy. After labour any residual V.V are treated as 1ry V.V.
Ptgnentatio-r-&-eqemal Localcleanliness & avoid itching. ii) Rest & elevation. iii) Hydrocortisone & zinc oxide ointment. see below Yefr-cgSe-Uggl elevation & pressure bandage. tlgnerlhgge excision by safety margin &cross leg flap. $_aflo_1tfl9_qlget physi othera py. IaljpeS _eguj[eg saucerization. PetigSflig_
i)
) )
VENOUS SUR.GERY
Superlicial infrerior epigastric vein Femora
55
rein
SuperfEialextffil
pudardal vein
More Details
1. lniection sclerotherpav:
- The patient lies supine. - The leg is hanged down beside the bed, so the veins will be distended &
the needle for injection is inserted inside the vein.
- Then the leg is elevated on the bed & the vein is compressed by the index
& middle fingers which are applied around the needle.
- The sclerosing solution is injected into the empty vein. - A firm bandage is applied to allow fibrosis of the intima. - The patient is asked to walk to allow the blood to dilute the irritant substance
to avoid blocking of the deep system.
- The interval of injection: every 4 weeks. - The commonest sclerosing material used is ethanolamine oleate 5% (bad
cosmetics) which damages the vein intima, so that a septic thrombosis and later on fibrosis will occur. The dose injected should not exceed 2ml per site, since larger doses will easily reach the deep veins and cause thrombosis.
3- Injection should be done during the patient is reclining not standing 4- Compress above and below the injection site for 1 min. 5- A compressive elastic bandage is applied and the patient is actively ambulated
immediately
- Lower third of the leg - At ankle - On foot - lnfant legs - ln post-phlebitic stasis dermatitis 2- No more than 0.5 ml of the sclerosant sodium tetradecyl sulfate 3% - Hypertonic saline - Morrhuate Saline
55
VENOUS SUR.GERY
G stands for Clinica! classification . Co No visible or palpable signs of venous disease. . C1 Telangiectasis or reticular vein. Veins less than 3 mm . C2Varicose veins. Veins over 3 mm . C3 Edema . C4 Skin and subcutaneous changes Now divided to better define severity:
'.
Further descriptors "a" for asymptomatic, "s" symptomatic for Etiology Ec: Congenital Ep: Primary Es: Secondary (post-thrombotic) En: No venous cause identified
'Ad:
. Pr: Reflux . Po: Obstruction , Pr,o: Reflux and obstruction . Pn: No pa identifiable
)Method: - The patient Iies supine. - The leg is hanged down beside the bed, so the veins will be distended & the
)Material used: - The commonest sclerosing material used is ethanolamine oleate 5% (bad
needle for injection is inserted inside the vein. Then the leg is elevated on the bed & the vein is compressed by the index & middle fingers which are applied around the needle. The sclerosing solution is injected into the empty vein. A firm bandage is applied to allow fibrosis of the intima. The patient is asked to walk to allow the blood to dilute the irritant substance to avoid blocking of the deep system. The interval of injection: every 4 weeks.
cosmetics) which damages the vein intima, so that a septic thrombosis and later on fibrosis will occur. The dose injected should not exceed 2ml per site, since larger doses will easily reach the deep veins and cause thrombosis.
)Effect: - The injected material causes irritation of the endothelium & obliteration
veins by fibrosis.
of the
lF,FEf rffit
ri.
88
o o
U/S & C.T. puncture. BM g. Staging laparotomy is rarely used (replaced by C.T). 1. blood (mainly chemotherapy as transfusion, iron therapy. it is multicenteric) 2. Definitive treatment Hodgkin's lymphoma Staoe l. l! & llla radiotherapy but: a- lf above diaphragm )ManUe. In nodular tvpe b- If below diaphragm )lnverted Y. chlorambucil c- lf llla)Both mantle & inverted Y ln diffuse tvpe cyclophosphamide, Staqe lll b & lV Ghemotheraov. Vincristine & MOPP (Mustine, Oncovine, Prednisone. Prednisone & Procarbazine)
t.
d. cxR. e. Abdominal
General )Vitamins, )
As ) )
VENOUS SURGERY
Chronic Le Ulcers
lt is flrst produced by trauma then it becomes chronic from negligence and repeated infection. - Finally it becomes fixed to the bone and this prevents contraction of the base of the ulcer and interferes with the groMh of the epithelium. e.LllSp..q.; Wounds, burns, radiation, bedsores.
- Srfe: Skin over medial side of tibia or bony prominence. - Edqes: Punched out. - EIW Healthy or unhealthy granulations. - Ease: lndurated. - Marqin: Pigmentation or inflammation. - Discharqe: Serous or purulent. - lnquinal L.N.:Firm, tender, mobile.
Conseruative: Like varicose ulcer. : Cover with skin graft or flap.
Tr.ea.tmen.t;
a. Chronic osteomyelitis ulcer See orthopedics. b. Chronic specific ulcers: Rare, T.B., Syphilis, Madura
sulphur granules.
foot discharge
Syp
iu-tis. .IJlq p..r ; - lt is rare nowadays. S[e: lt occurs on the medial surface or urb Numben lt may be solitary or multiple. Edqe is punched out and may be serpiginous. Flootis covered with yellowish (wash leather)slough. Base may be fixed to bone. - W.R is positive.
T.uh p.rs.u I p..u.r..U.Is.er; - lt results from the breaking out of a tuberculous arthritis or osteitis. - Edqe: thin undermined - Margin: bluish. El oor. pale g ranulation tissue Base: Slight induration
Primary skin tumors as sq. cell carcinoma, melanoma Marjolin's ulcer on top of chronic benign ulcer. Ulcerating deep malignancy as osteosarcoma, fibrosarcoma
-1.,.Sgue.mera$:9..9[..qfl r.-c.i.+.qm?..e..r..epitlr..elisF-t+.; - lt may occur de novo in the skin or on the top of a chronic scar when it is known as Marjolin's ulcer. - Premaliqnant conditions include chronic venous ulcer and prolonged irritation of the skin by chemicals e.g. dyes, tar or soot. Shape is irregular in outline. Edoes are raised and everted.
1.
2. 3. 4. 5. o. 7.
Acute septic lymphadenitis Chronic lymphadenitis TB lymphadenitis (caseous) $ (first stage). Metastasis. Early lymphomas Lymphogranuloma inguinale Filarial
Leukemia
4.
3.
. Rubbery.
No calcification.
58
VENOUS SUR.GERY
Base is indurated and soon becomes attached to the deeper structures. Discharqe: A blood-stained occurs and increases if there is superadded secondary infection. lnguinal lvmph nodes are first not palpable but Iater they become involved and become hard.
2:.Malignfl.Itt.rrele.p..q.mp.;..(pp..e.sp..r.erpl) - lt usually affects adults. - lt may start de novo as a pigmented (dark brown or black) lesion,
which grows progressively with a tendency to ulcerate and bleeding. Sometimes it takes the form of a rapidly growing, fleshy, ulcerated skin tumor (amelanotic melanoma). Satellite nodules may be present around the tumor (due to spread by lymphati c permeation). lnguinal lymph nodes are first not involved but later become palpable & hard. Blood borne metastases may be seen in liver & lungs in advanced cases.
Punched out
Hyperemic
Granulation or pus
Base
Difficult to be oaloated
bulta.
skin anesthesia in some neurologica! diseases e.g. peripheral neuritis, nerve injuries or DM. sole of the foot at ball of the big toe or heel (pressure areas). Skin anesthesia ) trauma not felt by the patient ) callosity & adventitious bursae ) infection of bursae ) separation ) deep penetrating ulcer to bone & joints... lT'S PAINLESS.
Pafh-ol.o.gy.
Treatment:
a. Conservative treatment + control neurologic disease. b. Amputation if destroyed bone or joints.
As sickle cell anemia & congenital spherocytosis. SLE, rheumatoid arthritis.
VENOUS SUR.GERY
59
Discontinuity of epithelium of the skin resulting in a 3D conical defect with well formed edge, margin, floor and base in relation to high venous pressure of the lower limbs. Constitutes 90% of ghronic leg ulcers. Usually post phlebitic limb due to DW. Less common due to A-V fistula. e to primary varicose veins. Recanalization of DW is commonly followed by dysfunction of the valves of both deep veins and the perforating veins. As the skin of the lower part of the leg is drained directly by the perforators which drain into the deep system, it follows that incompetence of these perforators leads to high venous pressure in the skin particularly that lying on the medial aspect of the lower third of the Ieg (ulcer bearing area). Ambulatory venous hypertension ) skin capillaries become glomerulous-like ) trapping of more leucocytes which become activated and release proteolytic enzymes that damage the capillaries ) fibrotic process in skin and subcutaneous tissue (lipodermatosclerosis). The combination of venous hypertension, eczema and Iiposclerosis will eventually lead to ulceration after minor trauma. Local hypoxia due to venous stasis and impaired nutrition lead to the liberation of free oxygen radicals which are toxic to the tissuses.
.
-
Site ) in the ulcer bearing area (Gaiter area) just above the medial malleolus. Number ) usually solitary. Size
lnfected ulcer ) dirty granulation tissue. Non-infected ulcer j healthy granulation tissue. Base ) lndurated (hard). Edge ) - At first ) irregular, slopping & serrated then ) punched out. Margin ) the skin around the ulcer is pigmented and may show contact dermatitis. LNs ) +ve if 2ry infection or malignant changes.
Floor -
Variable. In severe cases, it may encircle lower part of leg above ankle.
70
VENOUS SUR.GERY
lnfection, hemorrhage, osteomyelitis, periostitis, marjolin ulcer, talipes equinovarus.
Mention:
lschemic ulcer: at pressure sites, deep, painful + ischemic changes of L.L. Neurotrophic ulcer: painless, deep, penetrating to bone, at pressure sites. Malignant ulcers: everted edge, necrotic floor, indurated base. TB ulcer: undermind edge, cyanotic margin, caseous material. Syphilitic ulcer: punched out edge, wash Ieather floor, WR +ve. Chronic traumatic ulcer: punched out, over bony prominence, LNs firm, tender,
mobile.
For the cause e.g.: Doppler, duplex (functional & anatomical), biopsy if suspecting malignancy.
Treatment of Ulcer Consentative treatment for early ulcer (main line of treatment):
i.
Rest. Elevation of the limb. Compression stockinq (below knee) exerts 40 mmHg pressure at the ankle and 20 mmHg below knee. lt is the most important item in treatment.
Dressinq with saline & not antiseptics because of eczema. Most ulcers heal in 3-4 weeks. Debrideme4[ removal of any dead tissue on the wound is essential for proper healing. are said to accelerate ulcer healing as:
:"?:#""-i;ffi
ii.
. Prostaglandin E1 analouge. . Diosmin. Conservative treatment is usually successful in allowing the ulcer to heal. The problem is that, once the patients return to normal activity, most ulcers will recur.
Surgical For resistant ulcer: - lf there is evidence of incompetent perforators in the Ieg, they can be either
injected or excised
Nf,f Previous
operations as Cockett's or endoscopic subfascial ligation of perforatt are not commonly performed nowadays.
iii.
Prevention of recurrence
- Continue use of elastic stocking after treatment. - Leg elevation whenever possible.
CVI is a chronic disease in which venous return is impaired usually over number of years of - Calf muscle failure Reflux - Obstruction This Ieads to venous
A- Chanqes in macrocirculation:
. o o
B- Ghanqes in microcirculation 1- Fibrin-cuff theorv: widening of pores between endothelial cells allow passage
of large molecules out of intra-vascular space into the tissue then fibrin accumulation at this sites around the capillaries forming cuff (barrier to 02 , nutrients) ) lack of supply to skin, interstitial tissue ) Iocal tissue ischemia, cell death ) ulceration Cutenous iron Over Ioad - llt hydrostatic pressure within capillaries combined with {t capillary
2-
o"'1"?,oJlY,i#:E="fl""f
tissue destruction
;iT,t3;,[:tJ#illi,,ripioperoxides)
a
I I I
Family history of DW, W Obesity Smoking Pregnancy Jobs requiring long periods of standing or sitting Venous hypertension DVT Phelbitis enital absence or weakness of valves in the leg veins
I I
;Type of.patient
. .
With
S,y,r-qp-tpm$r,!.tl t 1- Ankle, symptom) typically edema worse at end of day lmproves by leg elevation 2- Leg discomfort: heaviness.aching or burning sensation 3- V.V 4- Lipodermatosclerosis tJlcers
leg
VENOUS SUR.GERY
1) Color coded Duplex Ultrasound scan: (Salient investigation method) Identify deep v. obstruction ldentify deep vein valve incompetent (RefluxO Presence and location of incompetent perforators
Measures the pressure in dorsalfoot vein in standing & in walking Normally: pressure on walking decreases CVI walking venous hypertension
1. Vascutar:
-DVT
3.
Post-phlebiticsyndrome. Lymphedema.
2. Dermatoloqic:
- Cellulitis. i
Endocrinal and
4.
metabolic:
Dermatitis.
Mainly conservative
A- Conseruative: 1- Avoid prolonged standing or sitting
L Surgical Treatment
E E E E E E E
Pressure in superficial veins in the leg is 80 mmHg & it falls during exercise. Acute lipodermatosclerosis is treated by anti-inflammatory drugs & external compression. Acute suprficialthrombophlebitis is treated py systemic anti-inflammatory drugs & external compression. Duplex UiS is the accurate non-invasive investigation used to evaluate venous reflux & patency. Phlegmasia alba dolens is due to iliofemoral vein thrombosis + lymphatic obstruction. Treatment of phlegmasia cerulae dolens is nearly always surgical. The commonest cause of fatal pulmonary embolism is iliac vein thrombosis.
I,JL
pNAT
LYMPHATIC SUR.GERY
)1ry,Zry
. . .
>G/P: swelling, pain, disability )Comp.: infection, elephantiasis, sarcoma interstitial space due to lymphatic )TTT: mainly conservative. affection with edema of the srgn overlying skin, which becomes thick corrugated. Edema at first pitting later on non-pitting. May run in families "Milory's disease". lt affects extremities, scrotum, external genitalia and rarely the breast.
1
. Female : male = 2:
I-
Congenital Lymphedema
According to age:
1.
A. Hvpoplasia
ln which the number of lymph vessels is reduced in the affected limb. Example in the thigh there one or two vessels instead of the usual five or more. B. Aplasia: no lymph vessels are demonstrated. C. Varicose lvmphatics: destroyed valve. . The condition is often associated with incompetent valves.
. .
2- Aeguired hrmphedema
1. Repeated attacks of streptococcal lymphangitis (i.e. cellulitis). 2. Filariasis (commonest cause). a. W. bancrofti --> in UL- & scrotum. b. W. malyi --> in LL & breast. 3. lrradiation. 4. Surgical excision of LNs which drain the limb (as after radical mastectomy). 5. Obstruction of the lymphatic by malignant tumor. 6. Burns at site of LN. 7. lniuries as circumferential scars of the limbs.
1.
2. 3.
4.
5.
6.
Swelling oiirm or telgs Heavy: tightness of arm or leg Restricted range of mobility Aching or discomfort of arm or leg Recurrent infection in the affected limb Hardening and thickening of skin and axilla
LYMPHATIC SUR.GERY
Q Clinical
classification of lvmphedema (Burnerl
75
Crade
Latent
I
Clinical
Excess interstitial fluid and histological abnormalities of Ivmphatics but no clinical lvmphedema Edema pits on pressure and swelling disappears on elevation and bed rest Edema does not pit and reduce on elevation Edema is associated with irreversible skin changes, fibrosis, papillae (elephantiasis)
!I
Iil
Q Complications of Lvmphedema:
1- lnfection: 2lt makes the vulnerable arm or leg more Iiable to infection including cellulitis, lymphangitis Elephantiasis: - lt occurs when arm or leg becomes so hardened with thickened skin that you have difficulty to move it Lvmphanqiosarcoma (rare) - lt orioinates from LN and h vessels
3-
Palliative:
fndicated in early cuses
1. Exercise and manual Iymphatic massage 2. lntermittent pneumatic compression 3. lntermittent limb compression pump. 4. Antibiotics for infection (long acting penicillin) : 1,200,000 5.
weeks. Treatment of the cause (Filariasis). - Hetrazan. - Anti-mosquito measures.
B. Surgical Treatment:
The only indication is disabilin as results of surgery are not promising.
Q ldea:
-
1. Swiss-roll cake operation: (Thompson operation) - Excess skin is not removed but shaved and buried in muscle-like swiss 2. Amputation: - lndicated if the limb is hugely swollen, ulcerated & infected.
Diversion of the lymphatic flow through the deep fascia to lymphatics of the muscles.
roll.
Other options: 1- Gharle's operation: total excision of skin, SC tissue, deep fascia then covering using split skin graft.
75
LYMPHATIC SUR.GERY
Filariasis
J'-t -J ) J
4 stases: 1. Stage of soft pitting edema early. 2. Stage of lymphorrhea due to rupture of lymphatic vessels discharging lymph in subcutaneous tissue. 3. Stage of fibrosis: O protein ) excites fibrosis ) non-pitting edema. 4. Stage of elephantiasis: thick rough skin from severe flbrosis ) pigmentation and ulceration, varicosity of the lymphatics.
)t t
i
to detect microfilaria.
Ilrrlt^-tl 2JJ))))'-!)
3.
. Endemic area for filarial. . Past history of mastectomy or irradiation. . Recurrent erysipelas. 2. Proqressive edema: . ffi!, it's a slightly pitting edema. . Latter on, it becomes non-pitting due to subcutaneous flbrosis.
Skin then becomes thick. rouqh & dark (Elephantiasis). . Ulceration with bad odor & toxemia. . Chylous ascites & hydrocele. . Chylous fistulae on the scrotum & groin. ,J Elephantoid fever. 'ir
"
4.
. l.t
Sfemmer's sign
D')
+
(of swollen limb): Accordinq to the distribution: A. Localized swellinq:
1. 2.
B. Generalized swellinq:
Accordinq to lateralitv A- Bilatera!: causes of generalized edema. B- Unilateral: causes of peripheral welling.
1. Lymphangiography ) obstruction. 2. Lymphoscintigraphy. 3. Duplex: for venous insufficiency. 4. CT & MRI: better. 5. For the cause e.g. midqight thick blood film for microfilaria. . Hetrazan (diethylcarbamazine citrate).
. Anti mosquito measures.
. . .
Affected Iymphatics appear as tender, hot lines Toxemia is often severe Suppuration may occur is evidenced by general malaise, fever, swelling of
. . . .
Bed rest Rest of affected limb, elevation lf suppuration ) incision and drainage
. .
78
LYMPHATIC SUR,GERY
Non-specific
; Slphilis ; Sarcoidosis
Acute Lymphadenitis
I I
Acute inflammation of LNs carried to it by lymphatics from area drained by involved gland Lymphatics show no evidence of disease except in some strep. lnfections
I I
a
Genera!: FAHM Local: painful enlarged LNs with congested edematous, hot overlying skin Major cases resolve but suppuration may occur
Antibiotics, local heat, pus drainage if formed
Enlarged LNs with little pain or tenderness, firm discrete, non-adherent to skin with little tendency to suppuration
Of the primary focus
Vascular SUR.GERY
79
TB lvmnhadenitis
. .
Stained by Z.N. stain because it is acid fast bacilli. Cultured upon: 1. Dorset egg media. 2. Lowenstein Jensen media which is selective for TB bacilli as it contains Malachite Green.
::,"1;iitiy!,Jg,l/
Tubercles are formed in which there is: 1. Epitheloid cells. 2. Giant cells (Langhan's cells).
Lymphocytes. 4. Fibroblast. 5. Caseation Depending on the resistance of the patient caseation & fibrous fissue is formed.
)
3.
i{Frlrslfug!'efiilf
. Tuberculous lvmphadenitis is common in children & young adults. . Those who have been in contact with open human tuberculosis or who drink infected milk. . TB bacilli might reach the lymph node through the blood (blood bornoid tvpe) or throuqh the tics tic born Lymphatic bome Blood bome [fibrocaseous)
Age
More common in elderly. Generalized affection. Occurs in milliary TB. OR Blood borne from pulmonary or renal TB.
Origin
Pathology
Organisms reach L.N. through arterial supply in hilum ) affection of medulla - Not affecting capsule (periadenitis) - No matting. - Late caseation. - No cold abscess or sinus is ever seen clinically in this type.
More common in children. Localized affection (from catchment area) ) Iry complex - Upper deep cervical LNs (the commonestr'4 ) portal is tonsils (organism pass without reaction) - Mediastinal LNs ) from pulmonary TB. - Mesenteric LNs ) lntestinalTB Organisms reach L.N. through afferent lymphatics ) affection of
cortex
Early affecting capsule (periadenitis) Early matting. Early caseation forming cold abscess ) perforate deep fascia ) Collar stud ) Abscess may break down ) sinuses
80
LYMPHATIC SUR.GERY
G/O:
)
1- Manifestations of
pulmonary TB.
o/E:
2-
Glinical picture
2- Affected LNs )
enlarged,
3-
(2N21) Manifestations of Pulmonary TB. (dyspnea, cough, expectoration & hemoptysis) Affected L.N. enlarged, not tender, firm early multiple then
DD
. . . .
1.
2. 3.
matted Cold abscess ) fluctuant (But not as hot as pyogenic abscess) 5- Multiple sinuses with undermined edge & cyanotic margins. - LNs secondaries For Cold abscess (from other swelling in the neck) For Sinus (from sinuses in neck) thvroolossal - branchial-actinomvcosis
4-
From tonsils the infection spreads by lymphatics to the nearest lymph node i.e. the upper deep cervical LNs ) coalesce ) cold abscess. The caseous material perforates the deep fascia ) (Gollarstud abscess). This skin gradually, breaks down, & forms a sinus. Patient usually has tuberculous toxemia.
GtE t' n I
lfiyrq:i'twj'trqffi
4. 5. 6.
Gold abscess formation which is called so because there is no signs of inflammation (no redness, or hotness). 2 ry infection which is called hot cold abscess Sinus & ulcer formation. Pressure on nearby structure e.g. mediastinal $. Galcifications Systemic Spread.
@,r;a*ry*tiF=t;i....))
ti Frq,{'{ru F:
n
l.
Blood . Anemia.
T.B.
sinus
. Guinea pig inocutation. . Culture on Dorset egg media for tuberculous bacilli. 3. Smear fromsinus & examination for TB bacitli: 4. Lymph nOde biOgSy 8t CU[tUfet better under general anesthesia.
Vascular
SUR.GERY
8l
For pulmonary TB
5. )GRarChest
Pulmonarytuberculosis. Mediastinal node affection. Calcified lymph node. Iuberculin test it is a good negative test.
& culture on Lowenstein Jensen media.
. . .
a) Tuberculous lymohadenitis before caseation: . The general condition of the patient is improved by good diet and nutrition. . At least two antituberculous drugs are prescribed for at Ieast g months. . A combination of rifampicin and isonicotonic acid hydrazide (lNH) is very
efficient.
for a single group of lymph nodes showing no response to medical treatment after a period of 6 months. A tuberculous abscess or sinus maybe included with the nodes during excision.
c)
of streptomycin solution. The rules of aspiration of a cold abscess should be followed to avoid sinus formation : 1. The needle iq inserted in a healthy part of the skin away from the abscess. 2. The site of puncture should be in a non dependant part. 3. - The needle should also pass in a valvufar manner. - The points of entry through skin and abscess cavity should not be close and opposite each other. - To accomplish this the needle pricks the skin is advanced some distance through the subcutaneous tissue, and is finally thrust deeply to enter abscess cavity. lncision is indicated in the followinq conditions 1. Secondary infection transforming the cold abscess into acute pyogenic abscess. 2. lf the abscess is imminent to rupture , it is incised , curetted , powdered with streptomycin and closed. Excision toqether with underlvinq lvmph nodes is done if the nodes need excision
nlls: . General antituberculous treatment . Dressing with streptomycin powder every three days until it closes. . Excision with underlying nodes, if resistant to conservative measures.
Treatment of Blood borne Type:
prescribed.
LYMPHATIC SUR.GERY
t-@
.
Affected in the 3 stage Genital chancre: ) shotty nodes i.e. firm painless, mobile & discrete. Extra-genital chancre enlarged, painful, tender, soft (1 w after chancre & disappear 1 m after it)
ab-
2-25tags.
Generalized & shotty (sp. epitrochlear & on posterior border of sternomastoid) + condyloma + mucus patches + +ve W.R. 3- Tertiarv S (oumma) 1- Gumma of L.N. rare. 2- lnfected Gumma ) acute lvmphadenitis.
. These are malignant tumors of RES (liver, spleen, BM, blood) . The malignant cells are not present in the blood stream (localized in the RES)
I Leukemia.
>Cervical
axillary
mediastinal
abdominal
>
hernotherapy, Radiotherapy
Abdominal (2o/o) Axillary (9o/.). It usually starts in one group & later on it involves other groups of LNs. Liver intestine & BM (i.e. extra-nodal lesion)
l. LNs:
+
Site:
. Usually
then axillary
then mediastinal
. .
Enlarged + satellites Discrete early ) matted Iater. . They are rubbery in consistency.
Vascular SUR.GERY
. Pink in color . Homogenous
.
Cut section:
87
ll.
with loss of architecture (no differentiation between the cortex & medulla) With intact capsule in early cases. No caseation.
affected:
Iate case.
2. After irradiation.
3. After biopsy because of the 4. After
lnfection.
fibrosis.
plasma cel
J
I
4.
OSIS
Each stage is further subdivided into two groups (a) & (b) according to absence or presence of general symptoms. The general manifestations; as: weight loss > 10 % in 6 months, night sweats and fever.
Staee
. . . . .
II:
Two groups of lymph nodes are affected on the same side of diaphragm OR Single extranodal site and 1 or more LN areas on same side of diaphragm.
One group of lymph node is affected above the diaphragm & another group is affected below it. The spleen is enlarged (some considers enlarged spleen as stage llls). Other consider the spleen to be a group of LNs. Extra-nodal affection especially liver & bone marrow.
Q Staee IV:
8r+
LYMPHATIC SUR.GERY
Type of patient
Adolescent or middle-aged male complaining of painless enla deep cervical LNs May be associated with:
q q
which lasts for 2 to 3 weeks followed by remission for few weeks.) - Pruritis. - Pain with alcohol "Gordon's tesf" HepatoSplenomeqalv of unknown etiology in 30% of the cases
Other manifestations:
1.
2.
3.
4. Metastasis:
Mediastinal svndrome: dyspnea, dysphagia, hoarseness & horner's Jaundice: a. Obstructive jaundice: due to enlarged LNs in porta hepatis. b. Hepatocellular: due to infiltration of the liver by Hodgkin's tissue c. Hemolytic: due to autoimmune antibodies Cachexia - Weakness. - Asthenia. - Anemia. Skin metastasis. Paraplegia.
- Bony metastasis.
Local examination:
. .
Earlv: LN is enlarged, rubbery, not matted etc... (see macroscopic). Late: LN enlarged matted.
A) Routine investigations
l. CBC
2. 3.
EBS
O(k - Mediastinal LN enlarg. appears as wide mediastinum, - Paralyzed copula of the diaphragm (due to phrenic nerve invasion). - Rib andlor Lung metastasis, pleural effusion.
4. ECG 5. LFT
Abnormal serum alkaline phosphatase, - Abnormal bilirubin level. 5. Kidney function tests: - Enlarged abdominal LNs might obstruct the course of the ureter. - During ttt excessive tissue destruction ) urate stones (tumor lysis syndrome). : +ve in stage 4 7.
Vascular SURGERY
85
B) For diagnosis
lt is better to delay lymph node biopsy for 2 or 3 wks (Don't rush for
1. 2.
flfi.fr:lJl|i;
G) For staging
r.
- Better
Avoid hypersplenisim. Protect the kidney from irradiation as we can remove the spleen instead of its irradiation which will affect the kidney. Liver biopsy from both Iobes. Abdominal LN biopsy. Putting silver clips on the affected L.Ns. to mark the site for better ttt with irradiation. ln females in the child bearing period suture the ovaries behind the uterus to protect them from the irradiation. Appendectomy to see its lymphoid tissue.
. The high accuracy of CT and MRI . The risk of ovenruhelming post splenectomy infection.(OPSI)
Tttr--g,jl1,fg;1,it
1. Ggnefal: . Radiotherapy
.
General scheme for therapy for stage la, lb, lla. Stage llb is treated by radiotherapy and 6 cycles of combination chemotherapy. Stage !ll, lV are treated by 12 cycles of chemotherapy (Mustin,oncovine procarbazine, prednisone ; MOPP) while radiotherapy is supplement to control bulkv cervical LNs.
for
85
LYMPHATIC SUR,GERY
Depends upon histological type and grade 5 years survival is obtained in 80% with proper treatment - for stage la with lymphocytic predominance results may reach 100%
'
Hodgkin's disease
Age Site Skin overlvino Consistencv
Younq
Non
n's disease
old
Mobility
Tenderness Proqnosis
Multicenteric May be red, hot, & dilated veins Hard Amulgamated early
-ve
Good
-ve
Bad
Lukes
l-
r.
. .
(Mainly by chemotherapy as if is multicenteric) As Hodgkin's lymphoma but: ln nodular type single agent chemotherapy is given (chlorambucil), ln diffuse type combination chemotherapy is recommended which is cyclophosphamide 400 mg/m2, Vincristin e 1.4 mglm2, prednisone 40 mgiday.
. . . .
ls a highly malignant B-cell tumor that may involve sites other than LNs & RES. There is strong evidence that it may be due to EBV & may be related to malaria. lt is common between ages under 12years, more in males from eastern Africa. Commonly multifocal, affect the jaw (59%) forming painless progressive swelling, ovaries, retroperitoneal tissues & CNS
His..tqp.+.th.-o.l.qry;. Dark blue lymphocytes & starry shaped faint histiocytes (Starry sky appearance).
Treefus.nt;.