TRAUMA VASKULAR

subagjo

PKB IKABI malang

Background
Result from - penetrating - blunt If not recognized and treated rapidly, resulting ; - loss of life - loss of limb

Pathophisiology
Upper extremity, high-risk areas: axilla, medial/anterior upperv arm, and antecubital fossa - Injuries to a single distal artery can often be managed by ligation ( 95% the palmar arches are complete) Lower extremity, high-risk locations: inguinal, medial thigh, and poplitea fossa. - Injury to a single distal trifucation are unlikely to produce serious limb ischaemia.

Patofisiologi
Bentuk lesi tergantung penyebab atau mekanisme trauma, Dapat berupa:
kontusio lobang kecil (puncture) robekan dengan atau tanpa ada bagian yang hilang (laceration) terpotong melintang (transection) robekan intima yang dapat menutup aliran darah, atau hematoma intra mural dengan trombosis (pada trauma tumpul)

Patofisiologi
Arteri yg transeksi spasme + penurunan tekanan darah sistemik clotting Bentuk trauma vaskuler biasanya tangensial atau transeksi komplit Perdarahan >> pada lesi arteri yang inkomplit, karena ketidakmampuan pembuluh darah untuk beretraksi Pembuluh yang putus seluruhnya akan retraksi dan konstriksi sehingga dapat mengurangi atau menahan perdarahan

Patofisiologi

The three basic patterns of arterial injury

 Hypoxia : is a pathological condition in which the body as a whole (generalized hypoxia) or region of the body (tissue hypoxia) is deprived of adequat oxygen supply. Hypoxemia : The reduction of oxygen specifically in the blood. Hypoxic hypoxia : hypoxia resulting from a defective mechanism of oxygenation in the lungs. Anoxia : the extreme form of hypoxia where there is no oxygen present Anaemic hypoxia : a state where the oxygen content of blood is low and the cause is anaemia. Ischemia : a medical term for hypoxia where there is a restriction in blood supply, generally due factors in blood vessels.

 Ischemia tissue hypoxia or anoxia Metabolism of glucose (glycolysis) 2 molecules of piruvic acid If suffucient oxygen available, piruvic acid converted in to acetyl coenzym A main input for Krebs cycle 36 ATP.

2ADP Glucose

2ATP Glucose Piruvic acid

Acetyl CoA

Acetyl CoA O2 CO2

O2

O2 CO2 + H2O

36ADP ATP

36 ATP

H2O
Cell membrane

H2O

Mitochondrion

 If insufficient oxygen is available, piruvic acid is broken down anaerobically to Lactic acid using enzym Lactate dehydrogenase and Coenzym NADH. Ischemia Lack of Oxygen

Cell normal process for making ATP for energy fail

Anaerobic metabolism

Producing Lactic acid

Anaerob metabolism

ATP reliant ion transport pump fail

Active transport Na+ and K+ throught cell membrane diminished

Na+ and K+ intracelluler increased

Cell begin to swell

ATP reliant ion transport pump fail

Ion Ca2+ flow in to cell

Increased Ca2+ intracelluler

Released of harmful chemical like free radicals, phospolipase, and Calcium dependent enzym such as Calpain, endonuclease, ATPase

Necrosis Initiating Insult

Increased Ca2+

Calpains

Released Cathepsins protease

 Cell membrane is broken down by phospolipase more permeable more ions flow in to cell Mitochondrial breakdown, releasing toxins and apoptotic factors in to cell The caspase dependent apoptosis cascade is initiated, causing cell to commit suicide necrosis cell.

What is ischemia reperfusion ( I/R) injury ?

Reperfusion injury refers to damage to tissue cause when blood supply returns to the tissue after a period of ischemia. The absence of oxygen and nutrients from blood create a condition in which the restoration of circulation result in inflamation and oxidative damage from the oxygen rather than restoration of normal function.

What is the clinical relevance of reperfusion injury ?

Relevant to many fields of medicine For cardiologist I / R injury can occurs following every successfully balloon angioplasty or tPA induced thrombolysis. For the plastic surgeon I/R injury threatens the integrity of every free flap. For the orthopaedist it may take the form of a decompression fasciotomy for a severe compartment syndrome.

What is the mechanism for reperfusion injury ?

During an ischemia episode, hypoxanthine is formed as breakdown product of ATP metabolism. With the restoration of normoxia, hypoxhantine substrate is combine with oxygen to produce xanthine and oxygen radical.
Xanthine oxidase

Hypoxanthine + O2

Xanthine + Oxygen radical

 Leukocyte polimorphonuclear ( neutrophil ) carried to the area by blood flow release a host inflamatory factors such as interleukin as well as free radical Neutrophyl contain an NADPH oxidase that reduces molecular oxygen to the superoxide anion. Damage to cells membrane may turn cause the release of more free radicals. Leukocyte may also build up in small capillaries, obstructing them and leading to more ischemia.

The Oxygen paradox

Because oxygen free radicals exert such a damaging effect, it would seem that the provision of hyperbaric oxygen (HBO) therapy would further fan the flames of oxygen mediated reperfusion injury. Although in numerous experimental designs HBO has been shown to improve the outcome of flaps and extremities subjected to reperfusion injury, it is only recently that mechanism have been uncovered to explain the paradoxical effects of high dose oxygen.

What is the effect of HBO on reperfusion injury?

Experiments conducted to evaluate leukocyte endothelial adherence in the presence of HBO showed a striking inhibition of leukocyte adherence. Thom ( 1993 ) eloquently showed that HBO selectively inhibits the B2 integrin function of neutrophils that is responsible for persistent adherence of neutrophils to the endothelium.

What are the clinical implications for HBO ?

The clinical implications of current research findings would argue for early aggressive intervention with HBO whenever significant reperfusion injury is suspected. It opens up the possibility of using HBO in a prophylactic capacity whenever reperfusion injury is anticipated.

Frequency
US : pheripheral injuries, 80% all cases of vasclar trauma. The lower extremities in two thirds of all vascular injuries. Penetrating trauma, 70 90% of vascular injury.

Mortality/Morbidity
Death due to extremity vascular trauma is uncommon ( except by exsanguination or development of a necrotizing myofascial infection. Limb survival is threatened by delays in diagnosis and treatment ( more than 6 hours) Extensive assosiated musculoskeletal, nerve and skin injuries indicate a poor prognosis.

Sex
90% of patients with vascular trauma are male
Age

Vascular trauma most often occurs in patients aged 20-40 years.

History
- The mehanism of injury is an important prognostic factor. Shotgun and military rifle injuries as well as knee dislocations are particularly high risk. - The time interval between injury and evaluation must be considered. > 6 hours, irreversible nerve and muscle damage in 10 % of patients. -Previous history of vascular injury or disease -Extensive or pusatile external hemorrhage -Anticoagulation therapy or impaired hemostatic function

Phisical
The presence of hard signs has a 92-95% sensitivity for injuries requiring intervention: - bruit or thrill - active or pulsatile hemorrhage - pulsatile or expanding hematoma - signs of limb ischaemia and elevated compartem,ent pressure including the 5P: pallor, paresthesias, pulse deficit, paralysis, and pain.

Physical
Soft sign, predicting abnormal findings 35% - hypotension or shock - neurologic deficit due to primary nerve injury occurs immediately after injury. - stable, nonpulsatile or small hematoma - proximity of the wound to major vascular structures

Other Problems to be Considered:

- Embolic vaso-occlusive disease - Vasospasm ( due to cocaine or extravasated dopamine)

Lab Studies :
- The arteriel pressure index is useful in detecting patients with major vascular injury: systolic affected is divided normal extremity, < 90% is abnormal -ABI, is calculated by dividing the higher of the systolic dorsalis pedis or posterior tibial pressure by the ipsilateral brachial artery pressure -The Allen test is useful for injuries distal to the brachial artery bifurcation

Lab Studies
Angiography, for evaluation of vascular injuries: - the disadvanges include cost, significant time delay. - dye load and renal function are important presudy considerations Duplex ultrasonography currently plays a role in the evaluation of patient presenting with soft signs. Helical CT Angiography sensitivity 90 - 100%

Prehospital Care
- Stabilize the extremity in the anatomic position - Control hemorrhage with direct pressure -Applay a tourniquet proximal to the injury if direct pressure is not effective in controlling hemorrhage.

Emergency Departement Care

Immediately reduce displaced or angulated fractures if any evidence or suspicion of vascular compromise exists. External hemorrhage can be controlled with direct pressure. Once the patient has been stabilized, identify peripheral vascular injuries and restore normal circulation as rapidly as possible. Do not apply clamps or hestats to Vascular structures, since this may make definitive repair more difficult and damage surrounding tissues

Further Inpatient Care

Surgical exploration and repair is performed as soon as possible for patients with hard sign of vascular injury Patients with soft signs of injury can be further evaluated by either duplex ultrasonography or helical CT arteriography -Certain igh-risk injuries, such as shotgun wounds and major vessel proximity injuries. -Low-risk injuries without hard and soft sign should be observed for possible progression of injury either in the hospital or on an outpatient basis.

Further Outpatient Care

Low-risk injuries without hard and soft signs may be managed on an outpatient basis with careful follow-up and a strict schedule of repeat evaluations. All other patients should be admitted for either definitive repair or futher evaluation or observation.

Penatalaksanaan
rekonstruksi pembuluh darah
anastomosis ujung ke ujung anastomosis dengan graft vena safena magna. Dianjurkan pemakaian graft bila kehilangan arteri lebih dari 1,5 cm Ligasi a.femoralis dan a.poplitea tidak dibenarkan, karena komplikasi amputasi Perbaikan a.tibialis anterior dan a.tibialis posterior tergantung dari keadaan vaskularisasi distal Pada semua kelainan sendi harus dicari apakah ada kelainan/cedera vaskuler

end-to-end anastomosis

The arterial repair

Complications
Delayed diagnosis and treatment may result in thrombosis, embolization, or rupture with exsanguinating hemorrhage. Risk factors for amputation include elevated compartment pressure, arterial transection, associated open fractures and the combination of injuries above and below the elbow and knee. Nonocclusive injuries do not disrupt flow and include the following: - AV fistule. - Pseudoaneurysms

Medical/Legal Pitfals
Failure to appreciate the severity of injury is a major risk. Failure to recognize that injuries may require repair even when pulses are intact. Inappropiate delay in radiographic evaluation and surgical in tervention. Failure to perform an appropiate examination, including objective test, in all patients including those who lack hard signs of vascular injury Clamping vascular structures.