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Vascular Surgery > ALI > Flashcards

ALI Flashcards

1
Q

What is Compartment Syndrome?

A

Increased intracompartmental pressure impairs tissue perfusion (ICP)

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2
Q

What are the major two causes of CS and what are examples of each?

A

Vascular

Ischemia-reperfusion
CS 21% of acute ischemia
IR causes muscle tissues injury, interstitial edema. Oxygen free radicals increase permeability
Trauma
Arterial occlusion initiates IR
Fasciotomy for blunt 11%, penetratig 30%
Venous outflow obstruction
Phelgmesia cerulea dolens, harvesting of deep veins from thigh
Hemorrhage
Rapid increase in compartment pressure

Non-Vascular

Fracture
Tibia or forearm most common cause of ortho
Muscle swelling, bleeding
Anterior compartemenr and flexor compartement most prone
Comminuted fracture more likely to result in CS
Crush injry
Iatrogenic
Extra of large volumes, or caustic medications. Punctures in coagulopathic patients

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3
Q

What is secondary compartment syndrome?

A

CS with no overt evidence of trauma
diffuse microvascular permeability from trauma induced systemic inflammatory response syndrome combined with massive fluid resuscitation

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4
Q

What are clinical findings of CS?

A

disproportionate pain
tense, swollen
pain on passive movement elicits pain
loss of 2 point discrimination
absence of clinical findings
Numbness interweb space (ant)

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5
Q

What pharmacological interventions can decrease CS?

A

mannitol
allopurinol

they reduce oxygen free radicals and reduce impact of schema-reperfusion

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6
Q

What are two different techniques in fasciotomy?

A

Single vs double incision

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7
Q

Describes each surgical approach for fasciotmy.

A

Single-incision

Lateral incision over fibula from neck to 3-4cm above lateral malleolus
Sc flap anterior direction to access anterior and lateral compartments
Posterior flap to access superficial posterior compartment
Flexor hallucis longus identified and dissected off fibula in subperiosteal plane
Fascial attachement of PT to the fibula is incised to open deep post compartment. Most do not perform a fibulectomySingle-incision

Double-incision

Lateral incicions over intermuscular spetum b/w ant and lat compartements, apporx 4cm lateral to crest of the tibia. anterior and lateral compartments.
Medial aspect of leg incision 1-2cm posterior to the tibia, for posterior decompression incision over gastroc, for deep compartment divide soleal attachments off tibia and incise fascia

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8
Q

What are advantages/disadvantages for each surgical technique of fasciotomy?

A

single
one incision
tedious
potential injury to perineal nerve

double
simple
but two large incision have high morbidity

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9
Q

Describe technique for thigh fasciotomy.

A

Incision on lateral thigh. Start just distal to intertrochanteric line and extending distal to lateral epicondyle
Iliotibial band exposed and incised longitufinally to decomp anteriror
Vastus lat reflected medially to exposed lateral IM septum which is then incised

Medial usually does not need decomp
Incision over adductor muscle group

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10
Q

What are different was of closing fasciotomies?

A

delayed primary
secondary intention
dradual dermal apposition
split-thickness grafting
myocutaneous flap

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11
Q

What are complications of CS?

A

myonecrosis
amputation 5-20%
neuro deficits 5-35%

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12
Q

what complications are related to myonecrosis?

A

hyperK
hypocalcemia
elevated LFT
DIC
myoglobinuria
RF

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13
Q

What are complications for missed CS?

A

50% require amp
90% neuropathy
after 3-4 days decompression not indicated b/c myonecrosis too high
Volkmanns contracture

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14
Q

What is chronic compartment syndrome?

A

exercise induced pain and tightness of the lower legs esp ant compartment
within 20-30 mins abates 15-30mins
bilat 82%

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15
Q

What are pressure criteria for diagnosis of chronic compartment syndrome?

A

1 resting ICP >15mmHg
2 ICP >30mmhg 1-2 mins after completion of exercise
3 ICP >20mmhg 5 mins after completion of exercise

one or more for diagnosis

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16
Q

What is tx for chronic CS?

A

avoidance of inciting factors
surgical decompression

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17
Q

What muscles are in the anterior compartment?
What vessels?
what nerves?

A

enclosed by the crural fascia

tibialis anterior 
extensor digitorum longus 
extensor hallucis longus (mid-distal) 
peroneus tertius (very distal)

anterior tibial

peroneal nerve

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18
Q

What muscles are in the superficial posterior compartment?
what vessels?
what nerves?

A

gastrocnemius
soleus
plantaris

medial sural cutaneous nerve

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19
Q

What muscles are in the deep posterior compartment?
What vessels?
what nerves?

A

flexor digitorum longus
flexor hallucis longus
Tibialis posterior
Popliteus

posterior tibial
peroneal

tibial nerve

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20
Q

What muscles are in the lateral compartments?
What vessels?
what nerves?

A

peroneus longus
peroneus brevis

no vessel

superficial peroneal nerve

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21
Q

What is the techniques for closed fasciotomies for compartment syndrome?

A

Transverse incision
Close the skin

22
Q

What are causes of acute limb ischemia.

A

Afib
thrombi post MI
endocarditis
cardiac tumor
atheroembolism
aortic mural thrombi
hypercagulable state
vasospasm
dissection
occlusion of graft

23
Q

What is the most common cause? The most common site?

A

Afib
femoral bifurcation

24
Q

What is the earliest sign of ALI?

A

paresthesia
then muscle weakness
muscle tenderness sign advanced ischemia

25
Q

When does irreversible muscle loss occur?

A

6-8 hours

26
Q

What are the five Ps?

A

pain
pallor
paresis
pulselessness
paresthesia

27
Q

What is the classification of ALI?

A

I. viable
no sensory loss, no muscle weakness. positive A, V doppler signals
IIa marginally threatened
salvageable is treated promptly
minimal sensory loss, no muscle weakness. inaudible A. audible V
IIb immediately threatened.
Salvageable with immediate revasc. sensory loss more then toes with rest pain, mild-mod muscle weakness. inaudible A, audible V.
III irreversible
major tissue loss or permanent nerve damage inevitable.
sensory profoundly anesthetic, profound paralysis, inaudible A and V.

28
Q

What is the presentation of aortic occlusion.

A

mottled to above inguinale ligament
often paralysis

29
Q

What is the mortality associated with acute aortic occlusion?

A

close to 100% if embolic
in-situ thrombosis usually has collateral

30
Q

What are the causes of acute aortic occlusion?

A

saddle embolus
thrombosis of atherosclerotic aorta
thrombosis of small abdo aneurysm
aortic dissection

31
Q

What is the treatment for acute aortic occlusion?

A

if embolic, bilat transfer embolectomies
otherwise extra-anatomical bypass

32
Q

What are contra-indications to lysis?

A

active bleeding disorder
GI bleed within 10d
CVA within 6 months
intracranial/spinal surgery within 3 months
head injury within 3 months

33
Q

What class schema can lysis be considered

A

IIa

34
Q

What is the cause of UE ischemia?
What is the natural hx?

A

embolic
usually cardiac

50% have late complications if left untreated (contracture, amputation)

35
Q

What is presenting symptoms of UE ALI?

A

usually cold and numb rather then pain.

36
Q

What are amputation, mortality and limb salvage rates for LE ALI?

A

15%, 20%, 70% at 2 years.

37
Q

What structures can be injured during a fasciotomy?

A

lateral incision
common superficial and deep perineal nerve

medial incision
SV and nerve

38
Q

What are relative indications for fasciotomy?

A

Ischemia >6
Combined arterial and venous trauma
Phlegmatic cerulea dolens
Tense compartment after crush or fracture

39
Q

What are absolute indications for fasciotomy?

A

tense compartment with neuro defects
tense compartment in obtunded or serial exam is not indicated
ICP-MAP

40
Q

What is the main cause of injury during ischemia?

A

From hypoxia/anoxia and stasis in microcirculation

41
Q

Describe how ischemic injury occurs.

A

Mitochondria without O2 cannot produce ATP by oxidative phosphorylation
ATP falls, with ADP and AMP rise.
Glycolysis stimulated but insufficient for the cell
Lactic acid builds up making intracellular pH decrease, this then inhibits glycolysis
To compensate ion pumps are supposed to pump H ions out however there is pump dysfunction as no O2. Intracellular Ca rises are a consequence
This leads to eventually cell memebrane damage and cell death
During process reactive O2 species produced and accum in mitochondria
Increase ROS and Ca causes cell necrosis

42
Q

What are the main causes of injury during reperfusion?

A

Metabolic, thrombotic, inflammatory

43
Q

Describe reperfusion injury.

A

Burst of ROS production, increased Ca uptake into mito, shift of pH towards enutral
Mitochondrial oxidative damage leads to cell death through apoptosis and necrosis
Increased ROS during ischemia and reperfusion initiated apptosis and necrosis

Elicits inflamm response dependent of complement
Imflamm mediators delivered to reperfused tissue (mac, lumphocytes, neutrophils, mast cells and plt)
Edema

44
Q

List clinical manifestations of reperfusion injury.

A

myocardial stunning
arrhthmia
tissue edema
multi-organ dysfunction
compartmenet syndrom
bacterial translocation
RF
ARDS
no reflow phenomena

45
Q

Describe myocardial stunning.

A

Reversible, decreased ATP resunthesis, coronary spasm, cytotoxic injury

46
Q

Describe arrhythmia.

A

Rapid and sudden changes in ions concentration

47
Q

Describe tissue edema.

A

Disruption to blood brain barrier can cause increased ICP

48
Q

Which organ most injured in multi-organ dysfunction.

A

Lungs most frequently injured

49
Q

How long before nerve ischemia is permanent in CS.

A

12-24 hours

50
Q

What causes bacterial translocation.

A

increased intestinal permeability.

51
Q

What is no reflow phenomena?

A

Downstream microembolization of plt, neutrophils, thrombus, and atheroma particles cause occlusion. absence of obstruction in named arteries

Vascular Surgery (37 decks)

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