Fellowship revision > Major vascular > Flashcards
Major vascular Flashcards
What are the indications for open aortic surgery
-Requiring AAA repair with anatomy unfavourable for endovascular approach (generally EVAR done on infrarenal AAA)
-Aortic thrombosis or repair of aortic rupture from any cause, even when control of the haemorrhage initially achieved by an endovascular method
-Pt has a relative lack of comorbidities & has the functional/cardiovascular reserve to tolerate open
What has higher technical success rate & lower rate of severe perioperative complications? Abdominal aortic endografting or open surgical repair?
EVAR
How does the periop M&M and long-term survival compare between EVAR & open AAA repair?
EVAR has lower periop M&M but EVAR & open repair have similar LT survival; likely because while open higher intra-op stressors, population for EVAR likely higher risk; 1/12 postop mortality 1.8% EVAR & 4.3% open AAA repair but survival trajectories converged with time
With EVAR, are early or late complications more likely than with open? Why?
Late, since the endograft is dynamic
What type of repair has higher reintervention rate? Endovascular or open? Stats?
endovascular- 9% vs 1.7%
What’s the initial success rate of endovascular aortic repair?
High- 99%
What are some causes of immediate or early complications with endovascular abdominal aortic repair?
Issues with the endograft placement, eg. vascular access probs, vascular damage (arterial rupture or dissection), accidental coverage of visceral vessels, atheroembolism, probs with deployment of the graft, structural integrity/stability of the endograft (eg. endoleak, endograft migration, endograft collapse), LL ischaemia due to graft limb kinks or graft limb occlusion
What’s one of the MOST common complications after endovascular aortic repair?
vascular access problems eg. haematoma, acute thrombosis, distal embolisation, dissection, pseudoaneurysm, AV fistula
what’s the rate of re-intervention with EVAR due to late endograft complications?
30%
rate of conversion to open?
2%- unclear from literature if higher M&M w open
what are some late endograft complications?
angulation/kinking, migration or thrombosis, infection
what are some causes of ischaemic complications with EVAR?
embolism, positioning of endograft
What organs may be impacted by ischaemic complications of EVAR?
Kidneys, spinal cord, intestines, pelvic organs, extremities
As per the Monroe-Kellie doctrine, what 3 things are contained within the fixed enclosed space of the spinal column?
Spinal cord (extending to L1 in adults), CSF (60mL in the spinal column, 60mL in the cranium, 500mL/day produced, turned over 4x/day, normal CSF pressure 5-15mmHg)
SS_NS 1.2 “Describe the blood supply to the spinal cord”
2/3 from single ASA which arises from vertebral arteries & extends down length of spine in anterior median fissure.
Supplies motor regions (ant horns of gray matter, corticospinal & spinothalamic tracts).
Reinforced by 6-8 radicular vessels which originate from vertebral arteries, intercostal arteries or aorta & enter the spinal canal through intervertebral foramen, most important= artery of Adamkiewicz which arises from lower thoracic/upper lumbar aorta (from inf intercostal or lumbar arteries, generally at the T9-12 level), supplies most of the flow to the lower 2/3 of the ASA (lower thoracic & upper lumbar cord)
1/3 from posterior spinal arteries (2), arise from posterior inferior cerebellar arteries or vertebral arteries & reinforced by a greater number of radicular arteries, supply posterior horns/dorsal columns (sensory components of SC)
Venous drainage is via 2 major spinal veins, one ant & one posterior, draining into a series of radicular veins, emptying into interna & external vertebral plexuses to the azygous & pelvic venous systems; since valveless, increased intra-abdominal pressure can increase venous pressure & decrease spinal cord perfusion pressure
Watershed areas btwn Cx, Tx & Lx sections of the cord, poor vertical anastamoses
Spinal cord perfusion pressure = MAP - intraspinal pressure (or vertebral venous plexus pressure, whichever is higher)
also, spinal cord blood flow = spinal cord PP/spinal vascular resistance
Describe anterior spinal artery syndrome. What are risk factors? Rates?
Flaccid paralysis of lower extremities with bladder & bowel dysfunction but sparing of sensation/proprioception, due to selective watershed ischemia of the anterior spinal cord, risks= aortic cross-clamp/occlusion during AAA repair, hypotension.
0.2% risk with elective infrarenal AAA EVAR, 8% in elective thoracic aneurysm repair (?<3% thoracic aorta EVAR) & 40% in dissection or rupture involving thoracic aorta. Risk increased with duration of X-clamp.
What’s spinal cord perfusion pressure?
MAP-intraspinal (CSF) pressure (or vertebral plexus venous pressure, whichever highest)
What’s the hagan poiseulle equation?
flow= 8nl/pi(r4)
What are some causes of renal insufficiency during EVAR?
embolism, positioning of endograft, IV contrast (allergic reaction, contrast-induced nephropathy)
What are the branches of the abdominal aorta (from sup to inf)
Inferior phrenic (2)
Suprarenal (2)
Coeliac
Superior mesenteric
Renal (2)
Gonadal (2)
Inferior mesenteric
Common iliac (2)
is salty canned soup really good in cup
at what level do the common iliac arteries usually arise?
L4
At what level does the common iliac bifurcate into the external & internal iliacs?
Pelvic inlet
What does the internal iliac artery supply?
Pelvic viscera & muscles
What does the external iliac artery become? At what point?
Common femoral artery as it emerges beneath inguinal ligament
What’s the most common approach for endovascular aortic graft placement?
Femoral
what is a mycotic aneurysm?
a dilation of an artery due to damage of the vessel wall by an infection
Are evar or open patients TYPICALLY higher risk?
EVAR as they’re often older
what are specific pt-related risk factors for EVAR?
Age >=60, ASA>=3, at least one comorbidity (cardiac, pulm, renal)
which group have more pulmonary complications? Open or EVAR?
Open
which group have more bleeding complications? Open or EVAR?
EVAR
Are there typically more cardiac, cerebrovascular or renal complications with open or evar?
No difference at 3.4yr follow-up but the overall incidence of systemic complications following endovascular repair is lower than with open
Why are pts with AAA by default at risk for CV events eg. MI? what’s the preop implication of this?
they are considered to have coronary heart disease equivalent. They should have their risk factors (BP, lipids) controlled b4 AAA repair
what’s the incidence of periop cardiac complications following AAA repair?
2-5%
why is IV contrast needed during EVAR?
during the placement of the grafts, contrast essential to ensure proper positioning of the graft & to ensure a lack of endoleaks
what are some contrast-related complications?
contrast-induced nephropathy & contrast allergy
what’s the rate of severe renal dysfunction following elective Tx or abdo EVAR?
0.7-2%
what are some causes of renal dysfunction following elective EVAR?
Renal ischaemia due to impingement by the graft or due to embolic debris (eg. from manipulation of IV cathethers & wires near the renal arteries), or the administration of IV contrast, hypotension
what are some of the causes of renal ischemia with EVAR?
renal artery embolism, thrombosis, dissection or impingement of the origin of the renal artery by the endograft, hypotension
What factors increase pt risk of contrast nephropathy?
pre-existing renal impairment
Age >70
Multiple prev use of IV contrast (eg. graft surveillance/reintervention)
What strategies may reduce risk of contrast nephropathy?
Judicious use of dilute contrast
CO2 angiography
Intravascular US
surveillance protocols that reduce or eliminate the need for exposure to IV contrast
what’s the overall risk of ischaemic complications after EVAR?
9%
is the incidence ischaemia higher with EVAR or open aortic repair?
EVAR
why might the risk of ischaemia be higher with EVAR vs open repair?
risk of endograft limb occlusion
where’s the most common site of ischaemia following EVAR?
Lower extremity
aside from endograft limb occlusion, what are some other potential causes of lower extremity ischaemia following EVAR?
endograft limb occlusion (70%). Less common causes of lower extremity ischemia= embolisation, common femoral artery thromboses
what’s the most common form of intestinal ischaemia following EVAR? site of this?
colonic ischaemia, thought to be due to endograft coverage of the inferior mesenteric artery (esp if there’d been previous hypogastric embolisation) or thromboembolism
is the risk of bowel ischaemia higher for EVAR or open repair?
same, however risk for COLONIC ischaemia is higher with EVAR vs open repair
what’s another name for the hypogastric artery?
internal iliac
what are some symptoms which may indicate complication in pts who’ve had hypogastric artery embolisation prior to endovascular repair of AAA?
erectile dysfunction or buttock claudication (either can occur in up to 40% of these pts)
what’s the overall risk of acute kidney injury following EVAR?
6-7%
are endovascular or open AAA repair more associated with AKI
open
what’s the risk of spinal cord ischemia with EVAR for infrarenal AAA vs thoracic aorta repair?
0.2% vs 12%
what are other compliations of EVAR (aside from graft, cardiopulmonary, IV contrast & ischemic complications)?
abdominal compartment syndrome (IAP >20mmHg), intra-abdominal HTN (IAP>12mmHg), postimplantation syndrome
what is abdominal compartment syndrome?
organ dysfunction caused by intra-abdominal hypertension (IAP >12mmHg, compartment syndrome when IAP >20mmHg)
risk increased in pts with ruptured AAA due to the fluid resus & volume effect of retroperitoneal haematoma
what’s postimplantation syndrome wrt EVAR, it’s incidence & associated factors?
transient flu-like inflammatory syndrome associated with new-onset thrombus & possibly the material composition of the stent graft. 13-60%
what’s the treatment of postimplantation syndrome?
aspirin & surveillance, there’s NO role for antibiotics
at what location are the AAAs typically treated with EVAR?
infrarenal
is endograft infection common after abdo aortic repair? Its mortality?
no, it’s rare (up to 3%) but it has high mortality rate (25%
what are 2 main reasons why EVAR may be associated with less periop morb/mort cf open aneurysm repair?
no intrathoracic or intraabdo exposure of the aorta needed, no aortic cross-clamping needed
what are options for anaesthetising pts for EVAR? What’s most commonly used? Evidence?
- LIA at the femoral or iliac arterial access, supplemented by ilioinguinal & iliohypogastric nerve blocks or bilat tap blocks + MAC for sedation/analgesia/anxiolysis
- Neuraxial (single-shot spinal, CSE or epidural with dermatomes T6-L3 covered, lasting 3-4hrs) +/- MAC or GA
Most done under LA or neuraxial (OR paravertebral!)- observational studies suggest that LIA or neuraxial reduce LOS & morbidity & they may also be useful wrt early detection of anaphylaxis or detection of rupture (c/o retroperitoneal pain) however no randomised trials, small number of total events & heterogeneity among studies
Is there likely to be much pain after EVAR?
no, as only groin incisions or even less painful percutaneous access
in which situations is GA needed?
if femoral or iliac access not possible & retroperitoneal vascular access necessary, if pts extremely anxious or unable to cooperate with maintaining supine motionless (eg. HF or back pain), or if need to use TOE
what are some potential benefits of LIA or neuraxial vs GA?
avoid myocardial depression of GA drugs, avoid catecholamine release with intubation & other risks of airway instrumention, potential to identify anaphylaxis or rupture (retroperitoneal pain) sooner, less alteration in pulm mechanics, shorter ICU & hospital LOS
what are some potential benefits of GA?
pt still, elimination of issues of pt anxiety/discomfort being supine, able to satisfactorily suspend respiration during stent deployment, less bowel peristalsis (may improve quality of intraop imaging)
how is vascular access for EVAR achieved?
femoral vessels (or retroperitoneal vascular access) via percutaneous access or access via small incisions
what’s the risk of a periop cardiovascular event following Tx or abdo EVAR?
at least 1%
what is a major risk factor for major postop cardiac complications (incl mortality, nonfatal cardiac arrest, MI, CHF, stroke) after major vascular surgery?
Known pre-existing RV dysfunction
what are the recommendations re: evaluation & Mx of cardiac risk in pts undergoing intermediate-risk noncardiac surgery?
pre-op ECG (useful as baseline if postop ecg abnormal), looking for Q-waves or sig ST-elevation or depression, LVH, QTc prolongation, BBB or arrhythmia. Additional cardiac testing only indicated if it would change management & only for pts w high risk for periop CV events (recent MI, unstable angina, decomp HF, high-grade arrhythmias, haemodynamically important valvular heart disease)
what are the specific goals of anaesthetising a pt for EVAR?
-Choosing a technique which facilitates pts ability to lie still for 1-3hrs
-If GA, limit SNS response to intubation (pts @ cardiac risk)
-preparation for massive transfusion (rare)- IV access, group & hold measurement of serial haematocrits
-art line, fastidious BP control & have drugs ready to decrease MAP upon request (eg. @ the time of device deployment)
-manage anticoagulation (initiation, monitoring & reversal)
-temp control (incl active warming)
-ensure adequate hydration to limit risk contrast nephropathy
what may be a useful indicator of intra-op myocardial ischemia w EVAR?
ST depression >1mm (computerised trending is superior to visual interpretation & multi-lead monitoring more sensitive than single)
is direct arterial monitoring usually employed for EVAR?
yes usually but there’s no evidence for benefit cf NIBP
during thoracic evar where should the radial artery catheter be placed?
R) radial if there’s any concern that the stent may cover the L) subclavian- after the surgeon has deplyed the stent they may whan to monitor the distal limb pressure to check for adequate flow- pressure tubing connected to the distal limb artery can be passed to be attached to our monitors
is a CVC or PAC needed?
CVP & PAP + CO measurements generally AREN’T required, but if vasoactive infusions are likely, reliable venous access + the info obtained with CVC can be useful esp w Tx EVAR
is neuro monitoring for spinal cord ischemia required? If so, how?
generally not- risk for abdo aortic procedures is extremely rare (0.3% if pt has not had prior thoracic aortic aneurysm repair, however in pts undergoing thoracic EVAR if they’ve had prev abdo EVAR, risk spinal cord ischemia 14.3%! Primary determinant of spinal cord ischemia is extent of the aorta covered by endografts (incr risk if >20cm aortic coverage). If surgeon decides to use CSF drainage as a protective strategy to minimise SC ischemia, SC monitoring with SSEPs +/- MEPs is required.
What is the setup for SSEPs?
electrical stimulation of distal nerves of lower extremity (eg. post tibial & peroneal) & recording of resultant cortical electrical potentials via scalp electrodes. This monitors the continuity of lateral & posterior column function.
how are MEPs set up?
electrical stimulation of the scalp over the motor cortex, waves travel down corticospinal tract to nerve root & peripheral nerve which cause muscle action potentials in a peripheral muscle group (eg. tib ant), the evoked motor response is recorded
What’s the definition of intraop haemodynamic instability wrt BP management during EVAR?
SBP <90mmHg or 40% below preop levels for 10 mins intraop
what might intraop haemodynamic instability increase the risk of?
postop renal insufficiency
What 2 things may the surgeon request @ the time of device deployment?
lowering MAP & breath hold (lungs off in anaesthetised, awake pts hold their breath)
how could I lower the MAP for device deployment?
propofol 10-30mg increments, esmolol 10-30mg
what are some example concentrations & doses of meds to rapidly treat HTN or hypoT or arrhythmias that should be immediately available?
phenylephrine(eg, 100 mcg/mL, administered in 100 to 200 mcg boluses),ephedrine(eg, 5 to 10 mg/mL, administered in 5 to 20 mg boluses),vasopressin(eg, 1 unit/mL, administered in 1 unit boluses),nicardipine(eg, 100 mcg/mL, administered in 100 to 500 mcg boluses),labetalol(eg, 5 to 10 mg/mL, administered in 5 to 20 mg boluses),esmolol(10 mg, administered in 10 to 50 mg boluses), andatropine(0.4 mg/mL, administered as 0.2 to 0.4 mg boluses).
what’s a risk of spinal cord ischaemia in elective abdominal EVAR patients without prior thoracic aortic aneurysm repair?
0.3%
what’s a risk with lumbar CSF drainage?
rapid drainage/low CSF pressures if drain open & bag falls on floor
kinking/blockage, catheter fracture/dislodgement
PDPH
CSF leak
bleeding complications (asymptommatic blood in CSF, SAH, ICH)
in which abdominal EVAR cases should lumbar CSF drainage be considered? how about in pts w desc Tx aortic surgery?
in pts with a PHx of a repair of a large descending Tx aneurysm
for pts @ high risk paraparesis/paraplegia eg. those who had prev aortic surgery, extended aortic segment coverage, those with crawford II extent, some pts with extensive coverage of crawford I to III, if having L) subclavian coverage without revasc to L) UL, anticipated prol XC time, emergency surgery if time permits.
what’s the risk of spinal cord ischemia with thoracic EVAR?
<3%
what’s the risk of CSF drain placement?
similar to the risk of spinal cord ischemia with thoracic EVAR (<3%)
in which thoracic aortic aneurysm repairs is CSF drainage considered?
if >20cm of aorta is covered or if a prior abdo aortic aneurysm has been repaired
Generally don’t use CSF drainage for abdo evar since the risk of SC ischaemia is 0.3%, outweighed by risks of using CSF drain (approx 3%), but consider if pt has had prev larg Tx aortic repair.
However, TEVAR risk SC ischaemia is <3%, similar to risks CSF drain placement, consider whether to place a graft if >20cm covered, prior abdo aortic aneurysm repair esp if artery of adamkiewicz previously excluded.
in what type of anatomy is the risk of spinal cord ischemia greatest?
if the artery of Adamkiewicz was previously excluded, since that artery supplies most of the flow to the lower 1/3 of the anterior spinal artery
when CSF drainage is used, what is the goal for CSF & MAP to maintain spinal cord perfusion pressure >=80mmHg?
Keep CSF pressure at 8-10mmHg (<10cmH2O) while increasing MAP in 5mmHg increments (via vasopressors +/- intravascular volume expansion) to 80-100mmHg), to keep spinal cord perfusion pressure >=80mmHg
what are the goals for drainage of CSF via the intrathecal drain if management for spinal cord ischemia is required?
drain to decrease CSF pressure to <10cmH2O, limit the CSF drainage to <20mL in the first hour of surgery & limit it to <40mL during any 4-hour period (as per Venu, rate shouldn’t exceed 15mL/hr)
what are the goals with anticoagulation during EVAR?
systemic anticoagulation (usually hepairn 5000-8000 units) initiated, aiming for ACT >=200 seconds. The anticoagulation is reversed & ACT rechecked after device deployment.
aside from limiting CSF pressure & augmenting MAP to ensure adequate spinal cord perfusion pressure >=70mmHg, what other targets will help limit risk of spinal cord ischemia?
adequate oxygenation, eg. with Hct >25%
symptoms of AAA? what diameter of abdominal aorta is considered aneurysmal? Indication for repair?
AAAs generally symptomless until rupture
if a localised dilatation is identified and the diameter of that dilatation is increased >50% relative to normal aortic diameter; generally >3cm is considered aneurysmal
risk of rupture is low if <5cm
elective surgery may prevent rupture of abdo aortic aneurysms but mortality is 5-6% (1 in 17)
risks of rupture exceed risks of elective repair if >5.5cm or if it’s expanded >0.5cm within 6/12 or symptomatic AAA; current guidelines= offer operative intervention when aneurysm exceeds 5.5cm provided pt is fit enough for surgery.
Pts w AAA diameter <5.5cm should have surveillance, risk evaluation & risk modification
aneurysms >6cm annual rate rupture 9%, 25% annual rate rupture for aneurysms >8cm diameter. 5yr surfival for pts w aneurysms >5cm & no OT is about 20%.
most aortic aneurysms are infrarenal; suprarenal AAA ass’d w greater bleeding risk, renal impairment. XC above coeliac & SMAs–> risk visceral ischaemia & profound acidosis.
what proportion of pts with infrarenal AAA tend to get EVAR?
almost 2/3
how does the short-term mortality of endovascular vs open aortic repair compare among the pts at highest risk (ASAIV)
5 vs 20% at 30 days
what’s the overall complication rate for endovascular aneurysm repair?
10%
what haematological perturbations may occur after EVAR?
decrease in platelet count or increase in FDPs due to the thrombus in the aortic aneurysm consuming coagulation factors & platelets
why may the surgeon request the MAP be dropped @ the time of graft deployment?
to decrease the risk of distal stent migration
which pts should go to ICU postop?
those @ high risk for CV, pulm, renal, bleeding or SC complications
what proportion of pts are anatomically suited to EVAR?
65%
do women or men benefit more from EVAR?
women
What to do if traumatic epidural needle/catheter placement?
Delay surgery 24hrs (as intraop anticoagulation)
From where does the L) subclavian artery arise? and the R)?
L) from aortic arch (to the L) of L) common carotid), R) from brachiocephalic artery (which arises from aortic arch to the R) of the L) common carotid & gives off the R) common carotid & the R) subclavian)
What’s intermediate risk for a perioperative cardiovascular event?
at least 1%
What proportion of males & women >65 have an AAA?
10% & 3%
What’s the most important risk factor for development & progression of AAA?
cigarette smoking.
prevalence in chronic smokers >4x than lifelong non-smokers, progresses in size more rapidly in smokers.
What’s the most common cause of AAA? and some rare causes?
atherosclerosis
rare= marfan, salmonella, tuberculosis, brucellosis & takayasu’s arteritis
What’s the mortality after a ruptured AAA?
80% among those who reach hospital. 50% in those who undergo emergency surgery for ruptured AAA.
What’s the 30-day operative mortality for elective AAA repair?
7%
By how much is O2 consumption increased during abdominal vascular surgery?
40%
What are the benefits of having a pre-anaes consult by vascular anaesthetist ASAP after listed for elective open AAA repair?
identify high risk pts
optimise medical Mx of comorbidities
adequately consent
What pre-op Ix do pts require b4 elective AAA repair?
baseline ECG
additional cardiac testing in pts w changes in cardiac symptoms & functional status
What’s the risk of postop MI, cardiac arrest, mortality in elective AAA repair?
3%, 3.2% & 8.7%
What subjective test= predictor of poor outcome prior to elective AAA surgery?
inability to walk up a flight of stairs or 6mph on level ground
What are some major cardiac risk factors prior to elective AAA surgery?
decomp HF, sig arrhythmias, unstable/severe angina, MI <1/12 ago, severe valvular disease, recent PCI
Useful to use the RCRI
What’s the yield of pharmacological stress test b4 elective AAA surgery?
Low PPV (20-30%) but high NPV (95-100%) for periop cardiovascular complications.
What should be the next step if a pt has a +ve pharmacological stress test before elective AAA surgery? Then the use of this?
coronary angiogram.
No sig difference in periop death or MI or LT mortality with coronary revascularisation b4 non-cardiac surgery (aspirin & statins have negated benefit of revasc). PCI rarely indicated (traumatises endoluminal surface, makes it thrombogenic until healed & stent re-endothelialised- antiplt therefore indicated after PCI & high risk in-stent thrombosis if interfere w antiplatelets.
If significant (>50%) L) main stenosis, severe (>70%) 2 or 3 vessel disease +/- LV dysfunction, CABG should be performed on prognostic grounds b4 AAA repair (which should then be deferred 3/12 after CABG).
What should be the step if pt has murmur before elective AAA surgery?
echo
What’s a CPET & threshold level for high periop mortality?
cycle ergometer w simultaneous resp gas analysis & ecg.
Anaerobic threshold <11mL/kg/min (1MET=3.5mL/kg/min), esp if ass’d w ecg evidence of ischemia, is ass’d w high periop mortality.
CPET can contribute to estimates of survival & mortality risk.
What education should be given @ pre-anaes consult b4 elective AAA repair?
Lifestyle advice:
-smoking cessation
-structured exercise programs to improve cardioresp fitness
Medication advice:
-continue regular on day of OT except ACE-I & ARBs (discontinue 24-48hrs pre-op)
-antiplatelets protect vs thromboembolic complications of CV disease
Postop discussion/advice:
incl DB&C 10x & 3 coughs hourly from when regain consciousness until fully mobile (reduce PPCs by almost 50%)
What are the intra-op considerations for elective AAA repair?
A: intubating w conditions to minimise SNS surge (CV risk), HTN risks aneurysm rupture
B:
C:
MAINTAIN NORMOVOLAEMIA
High risk blood loss-
EBL highly variable & often high (5% >5L)
2x wide-bore IV
Valid G&S
Art line
CVC
intra-op cell salvage
if require transfusion, rotem-guided
familiarisation/preparedness for MTP
Target Hb >90, Hct >27% (high risk CAD)
MAINTAIN HAEMODYNAMIC STABILITY- ESP W X-CLAMPING (see haem effects)
D:
have heparin ready, protamine if bleed & surgeons advise (give slowly, ass’d w pulm HTN, anaphylaxis, myocardial depression)
E:
NORMOTHERMIA
Exposure: open abdo risks heat & fluid loss
utilise heat conservation, warm fluids, increase OT temp & actively warm pt BUT make sure under-body bair hugger off during X-C as reduced cutaneous perfusion predisposes to thermal injury
Temp probe IDC
F:
Fluid losses w open abdo can be significant but don’t want to overload pt before X-C on- monitor UO to help guide re: volume status
G:
gastroprotection as high surg stress (PPI)
glycaemic control
H:
I:
J:
K:
RENAL injury a risk.
-mainstay= maintain O2 delivery & avoid nephrotoxics & limit X-C time.
-Normovolaemia important: adequate circulating vol reduces need for Na+ & H2O reabsorption in the renal medulla which reduces renal medullary O2 requirement & reduces risk renal hypoxic injury
-During infra-renal X-clamp RBF can reduce 40% due to RAAS system alterations (incr renal vascular resistance, reduce GFR)
-NO level 1 evidence supporting use of loop diuretics, dopamine, mannitol.
Monitoring:
Standard SpO2, 5-lead ecg
art line
central line
BIS
NMT
temp probe IDC (temp & UO)
PAFC generally not used; consider in high-risk pts w impaired ventricular function to obtain optimal SV value
P:
STIMULATING PROCEDURE & HIGH LEVELS POSTOP PAIN
balanced GA w high-dose opioid, low-dose volatile (may impr tolerance to myocardial ischaemia via effects on mitochondrial & sarcolemmal ATP-regulated K+ channels)
Tx epidural ameliorates stress response to surg & improves postop pain control, limiting demands on CV system, reduces pulm complications (promotes early extubation, deep breathing, mobility) BUT no evidence it improves mortality. issue= intraop hypoT.
Since heparin given prior to X-clamp (reduces thrombotic & embolic events, reduces periop mortality from MI), if have bloody epidural tap the surgery needs to be delayed
Alternative= spinal morphine, tap blocks or rectus sheath catheters + systemic opioids via PCA for postop
multimodal
Adequate anti-emetics to promote early enteral nutrition postop
Disposition= typically extubate elective AAA @ end of procedure. ICU w effective analgesia (Tx epidural infusion of low-dose LA + opioid, multimodal, if no epidural, TAP blocks or RSCs with PCA), anti-emesis, glycaemic control, antacid, instructions re: deep br exercises (10x 3 coughs hourly until fully mobile, make part of preop eduction redues PPCs by almost 50%)
thromboembolic & antibiotic proph
followup re: risk DCV events (monitor MAP, serial ECGs/troponin)
monitor postop blood loss 7 coags
-monitor postop renal performance; 5% renal dysfunction after infrarenal AAA surgery, mortality >25% if renal failure occurs. risk factors= pre-existing renal insufficiency, DM, HTN, incr age, NSAIDs, prol XC, intra-op hypoT, suprarenal XC
monitor for ischaemic colitis (bloody diarrhoea, abdo pain, metabolic acidosis w rising lactate)
monitor for SC ischaemia
distal circulation (risk atheroembolism)
Normal haematocrit for men? women?
40-50, 35-45
What’s the target Hct & Hb for elective AAA repair?
> 27% & >90 (pt population w high incidence CAD)
What are the 4 main intra-op goals for anaesthesia for elective open AAA repair?
- Normovolaemic
- Haemodynamically stable
- Normothermic
- Pain well-controlled on completion of surgery
What factors influence the pt’s physiological response to X-clamping?
myocardial function
amount of collateral circulation
SNS function
volume status
What’s the most common initial physiological response to placement of X-clamp? why? how to anticipate/manage this? What other cardiac physiological demands arises?
a) Arterial HTN (rise in BP 7-10%), due to 30% incr SVR; sudden large incr in LV systolic afterload may–> myocardial ischaemia or LV failure
(for Tx aorta: TOE may be useful electively or rapidly deployed to detect RMWAs & guide relief of LV preload eg. w partial L) heart bypass (if utilise L) heart bypass, dose heparin w goal ACT approx 250sec, after bypass reverse w protamine))
the pronounced incr MAP prox to aortic XC is ass’d w incr production of CSF, incr CSF pressure & ICP)
Strategies:
Run the pt dry prior to X-clamp
May manage w analgesia, deep anaesthesia, frusemide (only if not hypovolemic), could add in GTN as further vasodilator which is useful for heart failure signs and reduces LV preload & dilates coronaries (BUT risks organ ischaemia by reducing perfusion pressure in collateral circulation)
b) increased cardiac filling pressures (LV systolic & EDP, LVEDV) due to incr volume in the central veins proximal to X-clamp, reduced venous capacitance in organs distal to the clamp (volume redistribution from vasculature distal to clamp to that prox to clamp), combo of passive recoil of vessels distal to clamp & incr catecholamines & active venoconstriction (if the XC is infrarenal & the splanchnic vasculature isn’t vasoconstricted, preload won’t increase). Diseased coronary system may be unable to deal w the increased cardiac workload (CorPP=ADP-LVEDP). Incr LV pressure may –> heart failure (esp if too much volume before X-clamp)
c) CO reduces 9-33% after infra-renal X-clamp for most (but in some pts w good cardiac performance (contractility, coronary blood flow, level of clamp & whether the blood is sequestered in splanchnic circulation). CO may increase, anrep effect (myocardial contractility incr w afterload)
d) risk multiorgan ischaemia/impairment depending on level & duration of XC
-renal blood flow can reduce 40% w infrarenal XC (RAAS effects, circulating catecholamines, reduced CO)
-risk GIT ischaemia if XC above coeliac & sup mesenteric (desc colon IMA)
-ScPP (MAP-SC CSF pressure, risk impaired perfusion if interrupt artery of adamkiewicz or other collaterals & inadequate MAP to support collateral flow), also X=XC incr CSF pressure
haemodynamic effects more dramatic with more prox XC
other changes during XC: incr SmvO2
What are the anticipated physiological changes on release of aortic X-clamp?
a) dramatic BP drop due to reduction in afterload & release of vasoactive metabolites with reperfusion of ischemic LL tissues.
May get central hypovolaemia due to sequestration of blood in reperfused organs (proportional to X-C time), there may be incr microvasc permeability; anticipate this by loading w crystalloids/blood products pre XC removal; basically aim for normotension when XC on, CVP 5mmHg greaterthan baseline by the time of unclamping).
“declamping hypoT” minimised by ensuring adequate filling prior to removal of X-C, clear communication w surgeons, may attenuate w GRADUAL release of the clamp, discontinuation/reduction of vasodilators, may require vasopressors (eg. NAdr) BUT may get preferential VC of the vessels above the clamp, may use +ve inotropes. If severe refractory hypoT may require re-clamping
Consider CCl (cardiac protection from hyper K), NAdr
b) May have myocardial depression w ensuing metabolic (lactic) acidosis
may attenuate w incr MV, consider sodibic
risk arrhythmias
reduce thromboembolism, incr RVSP & RHF
If epidural, limit boluses until aorta closed (easier to manage unclamping hypoT w intact SNS)
What are the complications ass’d w hypothermia during elective open AAA surgery?
-myocardial ischemia (55% reduction in MACE when AAA actively warmed!)
-dysrhythmias (prol PR, QRS, brady, decr CO, vasoconstriction)
-coagulopathy (decr plt count, slowing of enzymes of coagulation cascade, enhanced fibrinolysis due to vascular injury)
-wound infections (hyperglycaemia, decr MRO2, L)-shift HbO2 dissn curve)
-shivering (incr O2 consumption)
-slowed metabolism of drugs
-emergence delirium
-respiratory funciton worsens
INDEPENDENTLY ass’d w higher rates organ dysfunction, in-hospital mortality, prol hospital LoS
bl temp should be monitored, heat conservation & actively warm (theatre, fluids, FAWD but DON’T use lower body active warming during XC)
pre-emptive warming important
-don’t warm legs on XC
-only extubate when temp >36degC
What’s the risk of postop renal dysfunction following infrarenal AAA repair? mortality if renal failure occurs?
5%, mortality > 25% if renal failure occurs
What are some of the complications following AAA repair?
bleed
pulm
renal failure
ischemic colitis
spinal cord ischaemia (more common after Tx aneurysm);
-increase tolerance of spinal cord to ischaemia (consider mild or deep hypothermia; typically permissive hypothermia to about 34 degC prior to XC, may use heat exchanger incorporated in pefusion circuit during partial L) heart bypass. decreases neuronal injury in the brain or SC by decr neuronal O2 consumption & metabolic rate, promotes tolerance to ischaemia. Cerebral MRO2 decr by a factor of 2.3 for every 10degC decr body temp, may also attenuate excitatory NTs & inflamm mediators & prevent neuronal apoptosis after ischaemic injury. (during asc aorta or aortic arch surgery, achieve deep hypothermia <28degC w DHCA. Adverse effects w hypothermia: coag, cardiac arrhyth, hyperglyc, decr metn anaes agents & drugs, eliminates or masks MEP/SSEP response. care w rewarming (avoid systemic hyperthermia; typically warm IVT, irrigate Tx w warm saline, FAWB, some may use heat exchanger in partial L) heart bypass perfusion circuit.)
-minimise duration of cord ischaemia (eg. limit XC time, shunts to aorta beyond XC eg. gott shunt of blood from prox aorta to distal aorta beyond XC, partial L) heart bypass (redirect flow to distal aorta; dual benefit of unloading LV during XC to prevent excessive proximal HTN, perfuses kidneys, mesentry, LLs; also can control systemic temp by adding a heat exchanger to the partial L) heart bypass perfusion circuit. typically UL MAP maintained >=80mmHg & lower body >=50mmHg during partial L) heart bypass), may employ selective perfusion (eg. with cold crystalloid or blood) or reimplantation of segmental spinal arteries eg. intercostal arteries) that supply the artery of adamkiewicz.
atheroembolism distal circulation
CVA, MI (ischaemic from hypoperfusion or emboli)
What are the current guidelines/advice re: when to intervene with a AAA?
if it exceeds 5.5cm provided pt fit enough for OT; the annual rupture rate if >8cm is 25%, >6cm 9%. 5-yr survival for pts w aneurysms >5cm & no OT is 20%.
How does 1/12 postop mortality compare w EVAR vs open? and later?
1.8% vs 4.3% but the survival trajectories converge, likely because while open higher surg stress, the pop for ever more comorbid.
SS_VS 1.7: How may the anaesthetic approach differ w ruptured AAA?
how to minimise blood loss (SS_VS 1.8)?
once receive notification that pt enroute to ED, notify theatre coordinator & my anaesthetic nurse
advise that we need: O neg/cross-matched blood, cell saver, warm line, art line, central line & rapid infusor eg. belmont; 2nd pair of anaesthetic hands/senior Reg to prepare drugs (need ketamine, fentanyl, roc, prop, metaraminol, ephedrine, NAdr, GTN)
Go to ED & escort the pt to OT sans delay (clear multi-D communication vital for effective Mx of rAAA; there is USUALLY time (if haem stable contained rupture) for CT angiography to confirm Dx, Ax aneurysm morphology, possible suitability for EVAR (minimal pt movement/rolling during CT)
If EVAR, pros= avoids risks of laparotomy but issues related to remote anaesthesia (eg. limited access to OT staff familiar w resus of a critically ill emerg pt). Emergency EVAR has rate of conversion to GA up to 25%, due to pain/restlessness w expanding retroperitoneal haematoma, risk of acute LL ischaemia with intra-aortic occlusive devices, buttock pain if int iliac occluded, resp insufficiency w expanding retroperitoneal haematoma, fem fem crossover if LL ischaemia after EVAR.
The timing of intervention depends on pt’s haemodynamic stability; may be stable with expanding contained rupture; pre-op preparation occurs quickly but may get time for pre-induction art & CV lines
haemodynamically unstable rupture–> resuscitative measures vital (limits mortality); restore IV volume w blood & crystalloid (but try to limit crystalloid), judicious vasoconstrictors, rapid surgical control (immediate surgical priority= XC aorta). Under the best situations there’s 40-50% mortality (risk arrest, hypoperfusion). Risk MI, ARF, resp failure, coagulopathy, prol LoS in ICU.
minimal/focussed Hx (rapid Ax functional status, most significant medical Hx (eg. IHD, HF, renal impairment) & allergies, risk stratification (Hardman index 1 point if age >76, LoC after present, Hb <90g/L, serum Cr >190micromol/L, ECG signs of ischaemia; if Hardman score >=2, high mortality (>80%). rAAA specific & validated for both open & EVAR. If pt has cardiac arrest or terminal malignancy, OT futile.
MINIMISE pt movement during preparation
Pt needs a large-bore IVC 14g, 5-lead ecg, IDC
Art line & CVC likely asleep due to time constraints
Have cell saver, pressurised warmed fluids, vasopressors & inotropes ready. TOE may be useful for detecting aortic dissection.
Activate MTP (rotem-guided)
-wait until surgeons scrubbed/prepped/draped & ready b4 induce, blood products in OT, as soon as tube in: “you may commence”- the abdo relaxation reduces tamponade effect & may–> bleeding ++, inhibition of SNS tone also incr risk vasodilation, IPPV decr preload.
-for open, GA w modified RSI carefully titrated, aim haem stability & avoid hypoT; midaz, ketamine, roc, vasopressors titrated, remi infusion (care w hypotension) but avoid SNS response to intubation.
-EVAR it may be possible to use LA/regional (no RCTs compare influence of anaes technique for EVAR on outcomes in rAAA)
-CRITICAL to keep SBP >70mmHg (an important prognostic indicator in rAAA, IMPROVE trial reports sig association btwn lowest SBP preop & 30-day mortality, which was 51% if SBP went <70mmHg but 34% if lowest SBP >70mmHg) BUT avoid aggressive fluid resus before XC (similar to elective, care w fluid before X-C; dilutes clotting factors, risks blood loss, dilutes clotting factors, excess fluid ass’d w incr 30-day mortality), only use 250mL boluses to maintain SBP >70mmHg
-heparin 5000U mins before XC on.
-when XC on, short-acting VD or opiates to control BP increases
-anticipate post-XC vasodilation; load w crystalloid or blood products, vasopressors ready
-basically aim for normotension when XC on
-with release of XC, sudden decr afterload, ischaemia-reperfusion w hypT, acid-base disturbances, lactic acidosis; attenuate w gradual XC release (communicate w surgeons), stop vasodilators, vasopressors (care re pref VC above where XC was), inotropes, if refractory hypoT may re-clamp
-volume management: IV volume depleted by haemorrhage, insensible losses with open abdo, evaporative
-target Hb >90, replace crystalloids approx 5mL/kg/hr & use colloids if unresponsive to crystalloids; utilise ROTEM-guided transfusion
utilise cell-salvage (auto-transfused blood is deficient in plasma, CFs, plts); aim for UO 1mL/kg/hr to prevent renal failure
-AKI also an independent predictor of postop mortality; limit this w normotension goal, limit XC time, avoid nephrotoxic drugs
-normothermia & warm (limit coagulopathy & myocardial dysfunction), BUT lower body warmers OFF when XC on (heat injury)
-ICU postop (high risk postop cardiac, resp, renal complications, intra-abdo HTN, ileus). Likely to t/f intubated due to risks hypothermia, acid-base electrolyte/coag abnormalities, large fluid shifts, likely massive transfusion.
for emergency case wouldn’t consider Tx epidural (risk delay, bloody tap) so anticipate postop pain, HTN, tachy along w shivering; in ICU ongoing rewarming, fluid resus, CVS & resp support, monitoring of renal function, coagulation, Hb & acid base balance.
Minimising blood loss: PBM pillars of optimising blood volume & red cell mass, limiting bleeding & tolerance of anaemia; for emergency ruptured AAA, avoid excess crystalloid (just use small boluses to keep SBP >70mmHg), don’t want HTN which may disrupt clot, worsen bleeding & excess fluid dilutional coagulopathy.
Blood loss highly variable & may be massive. When native aorta opened, may have back bleeding from Lx arteries (need to be controlled). massive bleeding can occur from leaking anastamoses. ICS to limit allogenic transfusion.
aim Hb >90 & hct >27% (since high risk coronary artery disease).
use POCT if any bleeding.
targets normal pH, normothermia, TxA to prevent fibrinolysis, avoid hypocalcaemia.
Senior surgeon.
does TTE rule out dissection?
no
SS_VS 1.7: Discuss the perioperative management, including postoperative analgesia and perioperative fluid management of patients having an emergency vascular procedure for the following: Aortic dissection.
What’s an aortic dissection?
Blood entering medial layer of aortic wall, creates a false lumen
Distension of the false lumen causes intimal flap to compress the true lumen–> malperfusion
Asc aorta dissection is the most common catastrophe of aorta, 2-3x more common than AAA rupture
mortality= 1-2% per hr for the first 48hrs
Survival improved w prompt Dx, BP & HR control & early surgical repair
Risk factors:
pt:
HTN (75%)
Genetic disorders (marfans, bicuspid AV, turner, ehlers-danlos, loeys-dietz, CoA)
Atherosclerosis (most common cause)
cocaine use
intense weight lifting
pregnancy
iatrogenic
trauma (2nd most common cause, usually due to deceleration injuries @ level of ductus arteriosus)
inflammatory (giant cell arteritis, takayasu arteritis, Bechet)
infection (syphilis)
Hx: Presents w acute severe chest/back pain w sudden onset, sharp/ripping/stabbing nature. May present w acute HF from severe AR or syncope from aortic rupture & tamponade or acute neuro complications (CVA, limb or mesenteric ischaemia, AMI)
Examination: may have pulse deficit (unequal or absent), AR murmur (soft, high-pitched, early diastolic decrescendo @ L) 3rd ICS, end-exp w pt sitting up & leaning forward)
CXR: widened mediastinum, L)-sided pleural effusion, acute haemothorax, ecg often inf infarct if the dissection involves RCA. CT will demonstrate widened aorta & abnormal contour. Contrast CTA, MRI & TOE all have high S&S.
Mx: type A urgent surgery (risk life-threatening tamponade, aortic rupture, CVA, CHF); 14 day mortality for type A w surgical Rx=25%
Type B prompt BP reduction: B-block (esmolol, labetalol) before vasodilator (GTN or hydralazine); vasodilators can cause reflex catecholamine release. if refractory HTN, may have renal artery HTN due to dissection flap causing renal malperfusion. Mortality of type B w medical Rx is 10%, if complicated by malperfusion, shock or surgery higher mortality (25-50%) so initial medical Mx or endovascular therapy first (lower mortality than surg). endovascular involves deployment of expandable prosthetic graft (generally via femoral artery sheaths).
Analgesia: pain worsens HTN.
Surgery will involve excising the intimal tear, obliteration of the false channel (oversew aortic edges), reconstitute aorta (usually dacron interposition arch. May need aortic valve repair or root replacement or AV replacement along w the root.
Mx:
Pre-op:
When hear about pt, inform OT coord, anaes nurse; art line, CVC, fluid warmers w rapid infusion device, blood O neg or XM 6units, plt, FFP, cryo in OT, have cell saver & call massive transfusion. NAdr, GTN, metaraminol in OT
TxA
Ax haemodynamics, severity of dissection & discuss surgical Mx plan w surgeons
(if using MEPs need TIVA, aortic root or arch replacement need cerebral oximetry (deep hypothermia, cessation of brain electrical activity or cerebral perfusion by retrograde or antegrade)
Arrange post-op ICU bed
pt will have temp probe IDC.
Intra-op: asc aorta needs median sternotomy & CPB
transverse aortic arch median sternotomy, bypass, DHCA (may require femoral artery cannulation, subclavian or inominate if arch is involved, antegrade (eg. through IA & L) CA) or retrograde (through SVC) may occur
desc (type B) often L) lateral thoracotomy w XC distal to L) subclavian. R) radial art line. & likely also L) femoral to Ax lower body perfusion.
Principles of my Mx:
limit fluids (may worsen dissection)
anti-hypertensives
gentle midaz/fent-based induction, meticulous Mx of any haemodynamic instability, acidosis, coagulopathy & low UO. pt needs continuous TOE.
Airway & ventilation may be difficult (risk deviation/compression, esp w L) mainstem bronchus, tracheal displacement or disruption
If doing thoracotomy, DLT with OLV.
Thoracic may consider Lx CSF drain.
type A art line on L) side, big drip, CVL
rewarm after wean from CPB.
consider that DIC can occur (prol CPB, hypothermia or massive transfusion)
Postop ICU for haem monitoring/control, I&V Mx, fluid balance, analgesia, anticoagulation, monitoring of CSF drain.
ventilate until warm & haem stable w anti hypertensives onboard.
neuro exam awap
ecg, csr & coag monitoring, monitor renal function
Long-term needs strict BP control, genetic evaluation, follow-up imaging & education
What’s the Stanford classification of aortic dissection?
DeBakey?
Type A- involves ascending aorta, can extend distally, surgery usually indicated
Type B- involves aorta beyond L) subclavian only (doesn’t involve asc aorta), often managed with BP control promptly w B-blocker to reduce shear stresses (IV esmolol or labetalol, consider SNP, GTN, hydralazine; B blockers first as vasodilators may cause reflex catecholamine release (or surgical or endovascular therapy if complicated by visceral ischaemia or limb ischaemia, impending rupture, refractory pain).
DeBakey I= dissection begins in asc aorta & extends to or beyond arch.
II= involves asc aorta only
III= begins in desc aorta, most often distal to L) subclavianOR
While TTE can NOT rule out aortic dissection, it’s diagnostic for what proportion of aortic dissections?
75% for type A
40% for type B
How does TOE, CT & MRI compare for diagnostic accuracy of an aortic dissection?
similar
What’s the reduction in renal blood flow with infrarenal aortic XC? Why?
up to 40%, due to incr renal vascular resistance of up to 75%
Why may renal & hepatic flow be relatively preserved with infrarenal aortic XC in modern anaesthesia cf splanchnic?
kidney has intrinsic autoregulation, liver has dual supply of blood flow (hepatic arterial buffer response), GI region may lack these mechanisms
Why may renal & hepatic flow be relatively preserved with infrarenal aortic XC in modern anaesthesia cf splanchnic?
kidney has intrinsic autoregulation, liver has dual supply of blood flow (hepatic arterial buffer response), GI region may lack these mechanisms
What happens to descending aortic flood flow & cardiac index during infrarenal aortic XC?
significant decrease, likely due to increased afterload & myocardial dysfunction
What happens to descending aortic flood flow & cardiac index during infrarenal aortic XC?
significant decrease, likely due to increased afterload & myocardial dysfunction
what’s the clinical importance of splanchnic hypoperfusion (which occurs with descending aortic blood flow reductions during XC)?
associated with delayed postop recovery of GI function, prolonged GI intramucosal acidosis is ass’d with periop M&M
What are some procedural complications of TAVI?
Vascular access issues (iliofemoral or aortic), ventricular wall perforation, valvular complications, arrhythmias, coronary artery occlusion, MI, CVA, death.
Complications that may occur or be detected after TAVI?
AKI, high-degree AV block, myocardial injury, vascular complications, tamponade after removal of temporary wire, valve migration or embolisation, mitral valve dysfunction.
Are the rates of stroke or TIA higher after TAVI or surgical AVR?
TAVI, at 30 days, 1 year & borderline @ 2 yrs but no diff stroke or all-cause mortality at 5yrs
Are the rates of stroke or TIA higher after TAVI or surgical AVR?
TAVI, at 30 days, 1 year & borderline @ 2 yrs but no diff stroke or all-cause mortality at 5yrs
What has higher risk of major bleeding & AF? How about the rates of short-term AV reintervention, pacemaker implantation, mod/severe HF symptoms & AR?
SAVR higher rates of major bleeding & AF but TAVI higher rates of stort-term AV reintervention, pacemaker implantation, mod or severe HF symptoms & AR
What is associated with higher risk AKI or mortality? TAVI or surgical AVR?
SAVR higher rates AKI. Surgical AVR higher mortality in the short-term, same long-term mortality
Which is associated with higher gradient across valve & smaller prosthetic valve areas- TAVI or SAVR?
SAVR
What has higher 30-day transfusion requirement? TAVI or SAVR?
SAVR
How do the rates of all-cause mortality & disabling stroke compare btwn TAVI & SAVR @ 2yrs (PARTNER 2A trial)?
similar
What’s associated with higher major vascular complications & paravalvular regurg? TAVI or SAVR?
TAVI
What’s associated with higher rates of AKI, severe bleeding & new-onset AF? TAVI or SAVR?
What’s associated with higher rates of AKI, severe bleeding & new-onset AF? TAVI or SAVR?
What’s associated with higher rates of AKI, severe bleeding & new-onset AF? TAVI or SAVR?
AV conduction disturbances & need for a PPM
What’s associated with higher rates of AKI, severe bleeding & new-onset AF? TAVI or SAVR?
AV conduction disturbances & need for a PPM
:) what antimicrobial prophylaxis is required for patients undergoing vascular surgery? how long redose lincomycin? when is the ideal timing of pre-incision ABx?
arterial surgery involving prosthesis, abdominal aorta or a groin incision requires s. aureus, s. epidermis, enteric GN bacilli
cefazolin, lincomycin or vancomycin
for LL amputation, same coverage along with clostridia- same drugs, same doses
8hrs
15-60mins pre-incision
:) Discuss the periop cardiovascular evaluation & management of patients undergoing non-cardiac surgery
60% of pts w peripheral vascular disease have underlying coronary artery disease
25% of vascular pts have CAD correctable by surgery
Peripheral arterial disease= 6.6x incr RR death from coronary heart disease
Pts who have postop MI have incr 30-day mortality (11%!)
Incr risk for CV death & non-fatal MI persists for 6/12 after surgery
- EMERGENCY surgery: life or limb threatened if not in OT in <6hrs
-determine clinical risk factors influencing peri-op management, proceed to OT with appropriate monitoring & Mx strategies (eg. Cath lab capabilities on-site, relevant disciplines aware/have given input)
*Urgent life or limb threatened if not in OT 6-24hrs
*Time-sensitive: delay of >1-6 wks will negatively affect outcome (most oncologic procedures)
*Elective: could delay for up to 1yr - Has the patient had an ACS? If yes, refer for cardiology evaluation & Mx according to guideline-directed medical therapy
Clinic:
Identify those @ elevated risk of periop ischaemia (ACC/AHA guidelines)
- Quantify the extent of that risk wrt SURGICAL & PATIENT variables:
SURGICAL:
-low risk procedure= combined surgical & pt characteristics ass’d w <1% risk MACE (MI or death), eg. Cataract, some plastic surgery (even if the pt has multiple risk factors, these procedures confer low periop risk). Those w MACE risk >=1% are elevated risk.
-procedures with highest periop risk incl OT for peripheral vascular disease.
PATIENT:
PRIOR CAD:
-60 days should have elapsed within MI (without coronary intervention) & noncardiac surgery. MI within 6/12 of noncardiac surgery incr risk of CVA, which is ass’d w 8-fold incr periop mortality rate
-unstable angina very high M&M (ischaemic symptoms suggestive of an ACS (rest angina >20mins, new onset angina markedly limiting function, incr angina freq/duration/with less exertion) but no elevation in troponins, with or without ecg changes). Cf NSTEMI where manifestations same as UA but elevated troponins present. Initial management for UA & NSTEMI is the same since trop elevations may not be detectable for hours after presentation. The initial therapy (should be instigated within 20 mins of presentation) is the same as for acute STEMI w the exception that there’s no benefit (possibly harm) from fibrinolysis).
Anti-ischaemic & analgesic therapy:
-O2 to maintain SpO2 >=94% (unnecessary if saturating well & no signs resp distress)- DETO2X-AMI study found routine use O2 doesn’t decr risk all-cause death, recurrent ischaemia, MI, HF, arrhythmia, risks hyperoxia= coronary vasoconstriction.
-nitroglycerin s/l, followed by IV if persistent pain after 3x s/l GTN tabs, HTN or HF. aim to relieve symptoms or MAP 10% below baseline normotensive, 30% hypertensive. keep SBP >90mmHg. 5-10microg/min (0.6-1.2mL/hr). Avoid if hypoT likely or may have sig adverse implications eg. RV infarction or severe AS, CI if had PDE-I for ED within the prev 24hrs.
-Afterload-reducing agent for L) heart failure (GTN), frusemide IV, consider NIPPV for some pts.
-Metoprolol 25mg if no heart failure or not @ high risk heart failure, haemodynamic compromise, bradycardia, severe reactive airways disease. If hypertensive, IV B blocker.
BMS higher risk re-stenosis but lower risk thrombosis. DES inhibit smooth muscle proliferation so lower risk re-stenosis but slows stent endothelialisation so greater risk thrombosis without DAPT.
-morphine ONLY if unacceptable pain refractory to nitrates & other anti-ischaemic therapies (ass’d w higher adj risk of death among those in the CRUSADE initiative). Morphine may interfere w antiplatelet effect of P2Y12 receptor blockers.
-B-blockers in all pts sans CIs (they must be haemodynamically stable), cardioselective (eg. Metoprolol) preferred.
-statins: high-intensity, irrespective of LDL cholesterol.
Atorvastatin 80mg asap ideally before PCI.
Antithrombotic:
-aspirin & P2Y12 receptor blocker for ALL NSTEACS pts
-aspirin @ time of Dx, 163-325mg, then discharge 75-100mg daily.
-prasugrel lower rates of CV death, MI, stroke but higher rates of major bleeding. Ticagrelor lower composite primary end point (death from vascular causes, MI, stroke) vs clopidogrel, no sig diff in rates of major bleeding.
All pts aspirin 325mg non-enteric.
Clopidogrel 300mg <75, 75mg >75.
No reperfuson: ticagrelor 180mg.
Primary PCI ticagrelor or prasugrel. Clopidogrel 600mg if high risk bleeding.
UFH for pts w primary PCI if had ticagrelor or prasugrel. Bivalirudin if clopidogrel.
-insufficient evidence to suggest which superior prasugrel or ticagrelor.
-anticoagulation asap -UFH if managed with an early invasive strategy (higher bleeding rates with enoxaparin)
-transfusion thresholds: severe symptomatic anaemia eg. Hb 80-100 w haem instability or ongoing ischaemia, otherwise <80g/L
-normalise electrolytes (K+ 3.5-4.5, correct hypoMg++)
-stop NSAIDs (incr risk CV events)
Cocaine-related ACS: give BZD. Standard therapies but NO beta blockers.
High risk for APO, arrhythmias, cariogenic shock; monitor w continuous ECG & manage in CCU while awaiting definitive Rx.
Pts undergo a risk score, if indicates intermediate-high risk, in-hospital angiography. If low risk, ischaemia testing first (unless high-risk features eg. Significant egg changes, recurrent ischaemia).
Reperfusion strategy; primary PCI strongly preferred esp if cariogenic shock, heart failure, late presentation, contraindications to fibrinolysis. Activate Cath lab. >12hrs can’t have fibrinolysis but PCI considered. Fibrinolysis if can’t get PCI within 2hrs & symptom onset <12 hrs & no contraindications.
Pts with STEMI presenting within 12hrs of onset of pain (or if evidence of ongoing ischaemia) should be offered PCI; if it can’t be achieved within 2hrs, fibrinolysis. Offer PCI to pts w cariogenic shock. Fibrinolysis NOT recommended if ischaemic symptoms present for >=12hrs. Most pts should have angiography within 24hrs.
Pts have anti platelet, anticoagulant.
AGE:
>=55yo incr prevalence of cardiovascular, cerebrovascular disease & DM (all incr MACE risk for noncardiac surgery)
>65yo incr ischaemic stroke for noncardiac surgery
>62yo independent risk factor for periop stroke
If aged >70 & frail (ie. Cognitive impairment & dependence on others for iADLs), more postop complications, incr hospital LoS, higher risk inability to return home after hospitalisation
Hx CEREBROVASCULAR DISEASE:
-incr risk periop MACE
Hx HEART FAILURE:
-pts w a HISTORY of HF undergoing major surgical procedures have higher ++ risks operative death, if active HF (symptoms or exam findings of peripheral oedema, jugular venous distension, rales, S3, CXR w pulm vascular redistribution & pulm oedema), higher risk 30-day postop death than if AF or CAD. *MUST emphasise active HF in periop risk-prediction models.
Signs & symptoms of decompensated HF= highest risk, but LVEF <30% (severely decreased)= independent contributor to periop outcome, long-term risk factor for death in HF patients undergoing elevated-risk noncardiac surgery.
Pts with HFrEF have higher all-cause mortality than HFpEF (risk of death doesn’t incr notably until LVEF falls <40%).
Mortality in HFpEF still higher cf pts sans HF. Diastolic dysfunction with & without systolic dysfunction ass’d w sig incr rate of MACE, prol hospital LoS, higher rates postop HF.
An echo should not be performed to Ax ventricular function in pts without signs or symptoms of cardiovascular disease in the preop setting. However, do perform an echo to Ax LV function in pts w dyspnoea of unknown origin, for pts w HF & worsening dyspnoea or other changes in clinical status, for pts with previously documented LV dysfunction but no echo within 1yr (even if clinically stable, to re-Ax LV function). Pre-op Low EF has low sensitivity but relatively high specificity for prediction of peri-op cardiac events. Complication risk is greatest if EF<35%.
Pre-op natriuretic peptide levels independently predict CV events in the first 30 days after vascular surgery & they significantly improve the predictive performance of the RCRI. It may be helpful in assessing pts w HF & diagnosing postop HF but further research needed to Ax utility of this.
CARDIOMYOPATHY:
-restrictive: eg. Amyloidosis, hemochromatosis, sarcoidosis: preload & HR dependent. Multi-D optimisation of pathology, volume status & HF status incl medication adjustment
-hypertrophic: defend preload, afterload & avoid incr contractility, likely on B blockers
-arrhythmogenic RV CM: in an autopsy study of SCD in pts w arrhythmogenic RV CM, death occurred in 9.5% of cases during the periop period so close periop evaluation & monitoring for ventricular arrhythmia is vital. Most require consideration of ICD.
-PPCM: a form of DCM, 1:1000 deliveries, manifests during last few months of preg or first 6/12 postpartum. Prognosis depends on recovery of LV contractility & resolution of symptoms within the first 6/12 after disease onset. Optimise fluid, avoid myocardial depression, maintain stable intra-op haemodynamics.
VALVULAR HEART DISEASE:
-if clinically suspected moderate or greater valvular stenosis or regurg, should have pre-op echo if none within the last year or if a significant change in clinical status or physical exam since last evaluation.
-if the pt meets indications for valvular replacement/repair based on symptoms & severity, intervention before elective non-cardiac surgery is effective in reducing peri-op risk, eg:
-pts eligible for valvular intervention (open mitral commissurotomy or perc mitral balloon commissurotomy (no data before non-cardiac surg but excellent outcomes for high-risk pregnancies) for MS, surgical AVR for AS (options incl TAVR (no data for safety/efficacy of TAVR for pts undergoing noncardiac surgery), perc aortic balloon dilatation as temporisation, or proceed with appropriate monitoring & optimising of loading conditions) should have intervention before elective noncardiac surgery.
Along with echo to quantify severity of stenosis or regurg, calculate systolic function & est R) heart pressures, evaluation for concurrent CAD is also warranted; electrocardiography exercise testing, stress echo or nuclear imaging studies or coronary angiography.
Elevated-risk elective non-cardiac surgery using appropriate intraop & postop haemodynamic monitoring may be reasonable in asymptomatic pts with severe valvular lesions.
If emergency noncardiac surgery must be undertaken in the presence of an uncorrected significant valvular heart disease, risk can be minimised by:
-having an accurate diagnosis of the type & severity of valvular heart disease
-choosing an anaesthetic approach appropriate to the valvular heart disease
-considering a higher level of peri-op monitoring (eg. TOE)
-appropriate level of postop care
1-year mortality in untreated symptomatic severe AS approaches 50%.
Pts w mod-severe AS have 30-day mortality 2.1% after nonemergency noncardiac surgery (cf 1% in propensity score-matched pts sans AS); postop MI more frequent in pts w AS (3% vs 1%). Higher risk of 30-day mortality & postop MI if higher risk surgery (OR 7.3), symptomatic severe AS (OR 2.7), coexisting mod-severe MR (OR 9.8) or pre-existing CAD (OR 2.7). If a pt meets criteria for AVR before noncardiac surgery but they are too high risk or ineligible for surgical AVR, can either:
-proceed with noncardiac surgery with invasive haemodynamic monitoring & optimisation of loading conditions
-percutaneous aortic balloon dilation as bridging (mortality 2-3%, stroke risk 1-2 % but recurrence & mortality rates are 50% by 6/12 after the procedure)
-transcatheter aortic valve replacement: PARTNER RCT: TAVI has superior outcomes for pts who aren’t eligible for surgical AVR & had similar all-cause mortality @ 1yr (noninferiority trial) in pts who are @ high risk for surgical AVR, but those who had TAVI had higher rates of stroke. No data specific to the efficacy & safety of TAVR for pts w AS undergoing noncardiac surgery.
PARTNER 2 trial: TAVI is non-inferior to surgical AVR in intermediate risk candidates for surgery. More recent Cochrane review support expansion of TAVI to low & intermediate risk groups: no diff in all-cause mortality, stroke, MI & cardiac mortality with TAVI & it was ass’d w reduced risk of postop AF, AKI & bleeding.
Indications for TAVI continue to broaden as new evidence emerges.
A multi-D “heart team” should be involved (incl interventional cardiologists, CTS, cardiac anaesthetist, referring cardiologist, cath lab staff) to weight risks/benefits/alternatives of TAVI vs other approaches, considering pt comorbidity, arterial access, valve & other cardiac characteristics.
Indications currently: Severe AS if surgical AV replacement isn’t suitable & pt is likely to gain improved QoL.
Factors favouring TAVI= severe comorbidity, age >=75, previous cardiac surgery, favourable vascular access, porcelain aorta, intact CABGs, chest wall deformity
Factors favouring surgical AVR: Euroscore <10% (mort after cardiac surgery), valvular endocarditis, short distance btwn coronary ostial & AV annulus, size of AV out of TAVI range, unfavourable valve morphology (bicuspid), LV thrombus, severe coronary, mitral, tricuspid or aortic disease requiring surgery).
Only absolute contraindication to TAVI is active endocarditis. Relative Cis: frailty precluding improved QoL or life expectancy <2yrs, annulus has to be adequate size.
Usually done via femoral arteries, alternative= subclavian
MITRAL STENOSIS: crucial to maintain intravascular volume (but NOT hypervolaemic), aggressively avoid AF, avoid tachycardia & hypotension- want to avoid excessive rises in LA pressure & PCWP that could precipitate APO. R) heart considerations.
AR & MR generally better tolerated than stenotic lesions but still incr cardiac risk during noncardiac surgery; maintain preload, avoid excessive afterload (augment forward flow, reduce regurgitant volume).
Worse prognosis in AR is LVEF <55% and renal dysfunction, high surgical risk & lack of preop cardiac med Mx.
Mod-severe MR predictors of postop adverse outcomes after noncardiac surgery= EF <35%, ischaemic cause of MR, Hx DM, Hx CEA.
ARRHYTHMIAS:
Presence of any arrhythmia in the preop setting should prompt Ix into underlying cardiopulmonary disease, MI or myocardial ischaemia, drug toxicity, metabolic derangements, depending on nature, acuity of arrhythmia & pts Hx.
AF: generally no modification of medical Mx (aside from anticoagulation) if clinically stable.
Ventricular arrhythmias (single PVCs or nonsustained VT) usually don’t require therapy unless haemodynamic compromise or significant structural heart disease or inherited electrical disorders; while these are risk factors for development of intraop & postop arrhythmias, they aren’t ass’d w periop MI or cardiac death. If a pt does develop sustained or nonsustained VT during the periop period, they may require referral to cardiologist for futher evaluation, incl Ax of ventricular function & screening for CAD.
High-grade cardiac conduction abnormalities, such as complete AV block, if unanticipated, may incr operative risk & necessitate temporary or permanent transvenous pacing.
Pts with intraventricular conduction delays, even if L) or R) BBB, if no history of advanced heart block (aka 3rd degree AV block) or symptoms, will rarely progress to complete AV block perioperatively.
Presence of sinus node dysfunction & AV block requires caution if periop B-blockers are being considered. Isolated BBB & bifascicular block generallly don’t contraindicated B blockers.
CIEDs:
PULM HTN:
Ideally these pts undergo their preop risk Ax & Mx at a centre with medical & anaesthetic expertise in pulm HTN incl echo evaluation of R) heart function. R) heart cath helps confirm severity of illness & distinguish primary pulm HTN from secondary causes of elevated pulm artery pressures. Optimise pulm HTN & RV status preoperatively.
ADULT CONGENITAL HEART DISEASE:
Optimal to perform preop evaluation & surgery of these pts at a centres specialising in congenital cardiology, esp pt populations @ particularly high risk (prior fontan, cyanotic ACHD, pulm art HTN, clinical HTN, sig dysrhythmia).
QUANTIFY METs w DASI:
-1 MET is resting or basal O2 consumption of a 40yo, 70kg male
-excellent functional capacity is >10METs, good is 7-10METs, moderate 4-6METs, poor <4METs, unknown
-periop cardiac & long-term risks are increased in pts unable to perform 4 METs during ADLs.
APPLY VALIDATED RISK-PREDICTION TOOL FOR PERIOP MACE IN PTS UNDERGOING NON-CARDIAC SURGERY
3, estimate periop risk of MACE:
Generally use -Lee’s RCRI. ACS NSQIP surgical risk calculator outperforms RCRI in discriminative power (best estimation of surgery-specific risk of MACE & death), esp for vascular surgery, specifies if emergency case or not, includes 21 pt-specific fariables.
4, if the pt is low risk MACE, further testing not recommended (ie Lee’s RCRI 0-1= LOW risk of MACE (30-day risk death, MI, cardiac arrest). >=2 predictors= elevated risk). 0 points= 3.9%, 1=6, 2=10.1, 3+=15
5, if thpt is @ elevated risk MACE, determine functional capacity. If >=4METs, proceed to OT sans further evaluation.
6, if poor (<4METs) or unknown functional capacity, consult w pt & periop team to determine if further testing will impact decision making. If yes, pharmacological stress testing:
-Dobutamine stress echo or pharmacological (dipyridamole/ adenosine/ radionucleide MPI) is appropriate (little data on exercise stress echo or radionuclide myocardial perfusion imaging but expected to perform similarly to pharmacological stress testing if pt able to exercise adequately; exercise stress test does provide functional info as well as info re: inducible ischaemia & haem response.
<5METs or HR<100/min high risk.
7METs or HR >130 low risk. mod-large reversibleperfusion defect= high risk postop MI or death) for elevated risk noncardiac surgery
If stress test abnormal (on radionucleide MPI, presence of mod-large areas of REVERSIBLE perfusion defect, reflecting myocardial ischaemia, ass’d w incr risk periop MI or death; old MI on rest imaging is of little predictive value for periop MI or cardiac death. (reversible myocardial perfusion defect predicts periop events, fixed perfusion defects predict LT cardiac events)
Normal study has high NPV (TN/TN+FN)
consider coronary angio & revascularisation depending on extent of the abnormal test
Dobutamine stress echo: safe & feasible, ability of a +ve test result to predict nonfatal MI or death is 0-37%. NPV high (90-100%). Avoid dobutamine in pts w serious arrhythmias or severe HTN.
*CTCA has BEST 88-100% sens & 85-97% spec
stress echo has sens 80-85% & spec 88-95%
Nuclear imaging 87-92% sens & 88-95% spec
exercise test the least sens & spec (approx 70%)
For pts with L) BBB, exercise MPI has unacceptably low specificity (septal perfusion defects not related to CAD)- do pharmacological stress MPI over exercise stress imaging. Also, pharmacological DSE or MPI good solution for pts w indication for stress testing who can’t perform adequate exercise. Avoid adenosine or dipyridamole for pts w sig HB, bronchospasm, critical carotid occlusion or condition preventing them from being withdrawn from theophylline or other adenosine antagonists.
Avoid any stress test in unstable pts.
CPET may be considered for pts w elevated risk OT but functional capacity unknown- low anaerobic threshold (approx. 10mLO2/kg/min= optimal discrimination point). Can estimate w DASI or incremental shuttle walk but some pts who perform poorly in these have satisfactory peak O2 & anaerobic threshold on CPET (that study didn’t look @ postop outcomes)
Routine preop coronary angio doesn’t improve outcomes in pts w stable coronary disease who would not otherwise be considered. Routine revascularisation before noncardiac surgery exclusively to reduce peri-op cardiac events is not recommended; should weigh cumulative mort & morb risks of coronary revascularisation procedure & the noncardiac surgery in light of pts health/functional status. PCI should only be performed for: L) main disease with comorbidities precluding bypass without undue risk. Pts w unstable CAD who are candidates for appropriate emerg or urgent revascularisation. Pts w STEMI or non-STEMI ACS. If the surgery is time-sensitive, a strategy of balloon angioplasty or BMS implantation should be considered.
Recommendations for preop echo& angiography may be different for pts having kidney or liver transplant.
7, if testing won’t impact decision making or care, proceed to surgery according to GDMT or consider alternative strategies eg. Non-invasive Rx
Optimise management prior to surgery:
As per 2021 ACC/AHA coronary revascularisation guidelines: for PCI for stable IHD, DES should have at least 6/12 DAPT; if high bleeding risk can have monotherapy w P2Y12(-) after 3/12. If no bleeding risk after 6/12, can continue DAPT for up to 12/12. BMS should have at least 1/12 DAPT; if high bleeding risk. If no bleeding risk, can continue DAPT up to 12/12.
Aggressive medical Mx & myocardial protection with B blockers (rationale in preventing PMI= improve myocardial O2 balance (slow HR, reduce contractility, improve diastolic coronary filling, reduce haemodynamic stress that may promote plaque rupture, but risk brady, hypoT & stroke. Decision to commence considers risk for stroke other relative contraindications (eg. Decomp HF). Pts at more risk of morbidity may incl prev CVA, bleeding, sepsis, anaemia; it may be reasonable to begin B blockers pre-op if intermediate or high-risk myocardial ischaemia on preop stress testing or 3 or more RCRI risk factors, there’s insufficient evidence if the pt has a compelling long-term risk factor (eg. Known CCF, known CAD) but no >2 RCRI indicators (for those may be better to commence after OT). If commencing, should allow at least 1 day before OT to Ax tolerability & effectiveness (2-7 days preferred), tight HR control doesn’t need to be achieved (tolerability more important). POISE suggested that B blockers reduce risks of cardiac events (MI, cardiac death & to a lesser degree, new-onset AF) but overall higher risk (stroke & death from noncardiac complications) but POISE criticised for high dose long-acting B blocker immediately before. Should be continued in pts who’ve been on them chronically but postop Mx & careful titration to BP & HR paramount to minimise risk)
Should continue statins, peri-op initiation for vascular surgery reasonable.
Alpha-2 agonists not recommended for prevention of cardiac events in NCS
CCBs may reduce myocardial ischaemia & SVT; most benefits to reduced death & MI are attributed to diltiazem; those with sig -ve inotropic effects (verapamil, diltiazem) may precipitate or worsen HF in pts w depressed EF & clinical HF.
ACE-Is & ARBs could reasonably be continued perioperatively. Data re: risk/benefit is limited to observational studies. Continuation ass’d w higher risk hypotension but no change in important CV outcomes (death, MI, stroke, renal failure). Maintaining continuity of these drugs in the setting of Rx for HF or HTN is supported by CPGs.
Management of periop antiplatelets therapy should be determined by consensus of pt, cardiologist, surgeon, anaesthetist, weighing risk bleeding & stent thrombosis. Risk of in-stent thrombosis during noncardiac surgery is low but higher than if there was no surgery; risk decreases w time, may be stable by 6/12 after DES. Magnitude of incr risk bleeding w DAPT vs aspirin alone is uncertain.
Pts w mechanical MVs taking VKAs or pts with aortic valve & >=1 additional risk factor (eg. AF, prev thromboembolism, LV dysfunction, hypercoaguable state) may require bridging periop.
For pts taking aspirin to prevent ischaemic complications who are unstented, POISE-2 trial showed aspirin (continuation or initiation) didn’t protect against MACE or death but was ass’d w risk major bleeding. However, only a small proportion had known CAD so continuation may be reasonable in pts w known CAD; ie it may be reasonable to continue aspirin if perceived risk of cardiac events outweighs risk of bleeding. Patients taking it for vascular surgery should remain on it.
Periop AF: incidence as high as 30% after major noncardiac Tx surgery peaks 1-3 days postop. Rate control usually w B block or nondhp CCBs; digoxin if systolic HF or Cis/inadequate response to other agents. Care that BBs & CCBs w sig -ve inotropic effects may worsen HF if depressed EF or clinical HF. Cardioversion of minimally symptomatic AF/flutter generally not required (correction of underlying issues may restore sinus). IV amiodarone may assist restoring or maintaining sinus if benefits outweigh risks of hypoT or other side effects. Cardiovert if haem unstable.
Frequent ventricular ectopy or runs of NsVT may require antiarrhythmics if symptomatic or result in haemodynamic compromise. New-onset complex ventricular ectopy, esp polymorphic VT, should be evaluated for myocardial ischemia, electrolyte abnormalities or drug effects. They may respond to IV B-blockers, lignocaine, procainamide or amiodarone. Cardiovery if haemodynamic compromise. Consider ICD if inherited arrhythmia or chronic cardiomyopathy with ventricular arrhythmias despite GDMT.
Bradyarrhythias periop are usually sinus brady due to meds, electrolytes, acid-base disturbance, hypoxaemia, ischaemia, pain (heightening vagal tone). Symptomatic brady due to sinus node dysfunciton & AV block will respond to temporary pacing.
Inform patients of risks/benefits/alternative of ay GDMT, coronary or valvular interventions & the surgery itself, seeking their opinions & involving them in shared decision making as part of informed consent.
:) crawford classification of thoracoabdominal aortic aneurysms
I: below subclavian artery origin (above 6th ICS), ends above infrarenal aortic segment
II: entire desc Tx aorta up to bifurcation (from above 6th ICS, extends distal to include infrarenal aortic segment)
III: starts in distal Tx aorta (below 6th ICS), extends down to bifurcation
IV: confined to abdo aorta (from diaphragm to aortic bifurcation)
V: from below 6th CIS, extends into abdo aorta but limited to visceral segment
:) what are risk factors for aortic dissection?
chronic HTN
atherosclerotic vascular disease
Marfan
:) what are some non-aortic surgeries that may be associated with spinal cord ischaemia?
spine surgery, bowel resection, hepatectomy, caesarean; surgical injury to radicular feeding artery likely the etiology..
:) What’s Marfan syndrome?
One of the most common inherited disorders of connective tissue. Predominantly autosomal dominant. Can be sporadic.
Broad range of clinical severity, there can be poor correlation btwn severity of CV & ocular or skeletal manifestations.
Diagnosis based on characteristic manifestations, Dx based on 2010 revised Ghent Criteria.
Places greatest weight on AR dilatation/dissection & ectopia lentis (cardinal features of MFS) & on testing of FBN1 mutations.
For ectopia lentis & features of systemic score, can only add to Dx for MFS after exclusion of Shprintzen-Goldberg, Loeys-Dietz or vascular EDS.
If no FHx:
-aortic criterion (diameter Z score >=2 or aortic dissection) AND ectopia lentis
-aortic criterion AND a causal FBN1 mutation
-aortic criterion AND *systemic score >=7
-ectopia lentis AND a causal FBN1 mutation
If FHx:
ectopia lentis, *SS >=7 points or aortic criterion
*SS= those scoring points in Ghent nosology
OCULAR:
-ectopia lentis (dislocation of lens) in 50-80%, from failure of supporting ciliary zonules
-myopia (incr AL) (*1)
-flat cornea
-hypoplastic iris
-hypoplastic ciliary m (reduced miosis)
-glaucoma, cataracts, retinal detachment
CNS: DURAL ECTASIA (*2) (very common in NF1, also can occur w EDS, LDS, ank spond):
-ballooning/widening of dural sac, lack of epidural fat
-may be ass’d with posterior vertebral body scalloping, herniation of nerve root sleeves out of foramina (& foraminal widening), meningocoeles, arachnoid cysts
can be a source of back pain, headaches, radicular pain, LL weakness, UI
May be accompanied by spondylolisthesis, scoliosis, vertebral erosions/#s
Neuraxial not contraindicated but may be complicated; incr risk dural puncture w epidural attempts, risk inadequate block w intrathecal.
CARDIOVASCULAR:
-mitral valve prolapse (*1) (more common w older age & in females w marfans), ass’d w degrees of MR
-aortic root aneurysmal dilatation/dissection (main cause of M&M in MFS), often accompanied by AR- while dilated, aorta tends to be stiffer & less distensible than controls
-May have dilatation of other segments of Tx aorta, abdo aorta, PA root or carotid & intracranial arteries (less frequent than with LDS)
-6-monthly echo for initial diagnosis & Ax stability of aortic dimensions. Use nomograms/Z-scores (normal range varies w body size & age).
if dissection, generally a type 1 De Bakey
-there’s often a FHx dissection
SKELETAL: excess linear growth of long bones, joint laxity OR reduced joint mobility (esp elbow (1) & digits)
-PAIN common
-incr arm span:height ratio
-reduced upper segment:lower segment ratio (1)
-scoliosis (cobb angle >=20degrees) or kyphosis (1)
-arachnodactyly: +ve wrist sign, +ve thumb sign (both is 3, 1 is 1)
-pectus deformity: CARINATUM (2) more specific vs excavatum or chest asymmetry (1)
-hindfoot valgus (2), pes planus (1)
-acetabular medial protrusion (>=3mm beyond ilioischial line) (2)
-FACIAL FEATURES: retrognathia (diff laryngoscopy), malar hypoplasia (diff BMV), enophthalmos, downsloping palpebral fissures, dolichocephaly (reduced width/length of face) (1 point for >=3/5)
LUNG
-emphysematous changes, lung bullae esp in upper lobes, predisposes to spont pneumothorax (*2)
-sleep-disordered breathing
SKIN
-striae, often in uncommon locations (eg. mid back) (*1)
Other features not in symptom score eg. high arched palate, risk C-spine instability/joint laxity, recurrent herniae
:) what are some DDx of Marfan?
loeys-dietz (bifid uvula, cleft palate, arterial tortuosity, hypertelorism, diffuse aortic & arterial aneurysms, craniosyntosis, clubfoot, C-spine instability, easy bruising)
shprintzen-goldberg: pectus, scolisoss, arachnodacytlyl, craniosyntosis, mental retardation
ehlers-danlos: vascular type ass’d w aortic anuerysm/dissection (also translucent skin, dystrophc scars, intestinal or uterine rupture)
cardiac valvular type (MVP, joint hypermobility, severe AR/MR, atrophic scars, skin hyperelasticity), kyphoscoliotic type (aortic ilatation/dissection, kyphoscoliosis, joint laxity
:) Pregnancy & Marfan’s:
need multi-D care (pregnancy heart team), high risk (if Marfan’s w AD >4.5cm, modified WHO 4 (should have elective repair prior to preg). if 4-4.5cm, 3 (incr risk aortic dissection), if <4cm sans dissection, class 2-3).
Pregnant pts w MFS require regular f/up, freq & imaging indificualised. MR without gadolinium contrast= preferred imaging for entire aorta during pregnancy.
Main goal= minimise shear forces on aorta.
Should be on B blocker (labetalol or metoprolol) to minimise progressive aortic dilation & risk dissection.
Strict BP control.
Method of delivery individualised. Early epidural recommended if VD, neuraxial pref for CS. dural ectasia is not an absolute CI to epidural but higher risk failed block, dural puncture, PDPH. consider pre-neuraxial symptoms (LBP, headache, LL pain/weakness/numbness). Invasive monitoring. avoid ergometrine.
Type A dissection during T1 or T2, urgent repair w fetal monitoring. During T3, urgent CS & aortic repair.
Type B: nonsurgical may be safest.
:) Outline the pathophysiology of peripheral vascular disease incl common co-morbidities:
Peripheral vascular disease:
a common manifestation of generalised atherosclerosis; 60% of pts w PVD have underlying CAD. PAD= 6.6x incr RR death from CAD.
pathogenic processes underlying the disease= same as for coronary & cerebral circulations: dyslipidaemia, endothelial dysfunction, inflammation, oxidative stress, hypercoaguability, chronic infection.
LL more commonly effected vs UL, atherosclerotic plaques in med/large arteries.
progressive luminal reduction, exercise-induced symptoms of tissue ischaemia (intermittent claudication) or acute ischaemia if acute occlusion eg. plaque rupture & thrombosis.
Ankle brachial (BP @ ankle vs arm) index <0.9 strongly suggestive of PAD.
Prevalence incr w age. risk factors:
-male:female 2:1
-smokers 4x more likely, those who continue more likely to need amputation/other intervention vs those who quit
-DM 2x more likely to develop PVD, amputations 5-10x more common in DM vs non-DM. good glycemic control paramount (1% incr HbA1C ass’d w 26% incr chance PVD)
-dyslipidaemia: high chol, LDL, TGs & low HDL higher risk PVD.
-HTN (BP >160/95 2.5x risk claudication men, 4x risk women)
-CKD: accelerated atherosclerosis; promotes dyslipidaemia & HTN, inflammatory mediators are often elevated, RAAS frequently activated.
:) What are the risks of HTN among pts undergoing non-cardiac surgery? whether to defer? recommendations for antihypertensives?
incr risk periop cardiovascular adverse events & mortality, related to:
-cardiovascular responses due to pre-existing HTN incl diastolic dysfunction from LVH, systolic dysfunction leading to CCF, renal impairment, cerebrovascular & coronary occlusive disease
-incr risk of adverse periop outcomes if the HTN has caused endo-organ diseases (eg. heart failure, renal impairment)
-haemodynamic lability eg. responses to SNS activation may be more pronounced (BP & HR increases, risking CVA, myocardial ischaemia), may have exaggerated intraoperative hypotension risking reduced myocardial O2 supply
-incr risk perioperative MI, CVA, dysrhythmias, renal failure.
BP reading alone is not grounds for canceling surgery; decision depends on accuracy of reading, presence of severe end-organ effects (eg. signs of renal dysfunction, CVA, myocardial ischaemia, aortic dissection) requiring urgent BP lowering & Mx, cause of HTN (eg. phaeochromocytoma high periop mortality), type of surgery (eg. ophthal procedures requiring phenylephrine must have SBP <180 & DBP <100, CEA must have BP optimised risk cerebral hyperperfusion), urgency of surgery (eg. emergency such as UGI bleed, likely temporise with acute BP management & proceed with careful haemodynamic management)
Continue all antihypertensives up to & including day of OT; if significant OT w haemodynamic swings consider witholding ACEI & ARBs morning of surgery UNLESS they are for heart failure or poorly controlled HTN. also consider witholding diuretics on day of OT unless pt has HF with fluid balance difficult to manage.
:) considerations for DM, COPD, renal failure
DM: optimise glycaemic control (HbA1c guide for LT glucose control) in liaison w endocrine. Assess for & risk mitigate end-organ effects (CAD, renal, ANS neuropathy (eg. suggested by orthostatic hypoT, resting tachy, peripheral neuropathy).
smoking & co-existent resp disease risks postop pulm compns. Assess severity & type & reversibility (eg chance for optimisation, if reversibility preop BD may be useful). ABG may be useful wrt Ax underlying pulm failure.
CKD: postop renal dysfunction incr mortality, Cr >177mmol/L baseline indep risk factor for predicting MACE.
SS_VS 1.3: impact of vascular disease on
-wound dehiscence & infection
-positioning injury
-periop stroke
-periop renal failure
-PVD–> incr rates microvascular disease & impaired wound healing (compounded by DM, smoking whcih decr fibroblast function & impair normal wound healing)
intra-op optimise temp management, prophylactic ABx, maintain MAP, tissue DO2 (Hb, PaO2), limit stress response (adequate analgesia), limit fasting
postop: aim to maintain map, tissue oxygenation (ie. Hb), nutritional needs
-stretch, ischaemia & compression due to poor joint positioning/prolonged pressure areas may predispose to intra-operative nerve & soft tissue injury. disruption of intraneural blood vessels (vaso nervorum) may contribute to patchy ischaemia, particularly in setting of microcirculatory impairment with peripheral vascular disease. significant stretching may tear intra-neural connective tissue–> haemorrhage & necrosis. Compression may damage schwann cells & myelin. Prolonged surgery, thin pts, obese pts, contractures/deformities, malnutrition, DM, hypothermia, hypotension, PVD all contrite.
-periop stroke risk in up to 3% of pts having peripheral vasc OT, up to 6% in CEA & up to 9% undergoing surgery for aorta. most CVAs due to embolic phenomena vs hypoperfusion ass’d w anaesthesia.
risk factors:
advanced age, female, Hx HTN, DM, CKD, smoking, PVD, CAD, CHF, prev TIA/stroke, carotid stenosis, asc aorta atherosclerosis, abrupt discontinuation of antithrombotic therapy prior to surgery, postop HF/ dehydration/ arrhythmia/ hyperglycaemia.
-CKD common in PVD
aortic surgery high rates postop renal dysfunction related to location & duration of AXC
suprarenal clamps risk renal hypoperfusion & postop AKI, blood loss, preop dehydration are other risks
care with contrast
SS_VS 1.4: Surgical requirements & implications for anaes Mx of pts having elective surgery for peripheral arterial occlusive disease
Procedure:
-may be emergency for ischaemic limb (unfasted (RSI), limited time for Ax/optimisation)
-whether endovascular or open depends on location, surigcal preference, vascular access; if in IR, considerations for remote location & radiation safety
-pt may be anticoagulated on heparin infusions; neuraxial may be contraindicated
-often prolonged, consider this w choice of neuraxial/LA/GA
Pathology:
-may be painful & on strong analgesics
-consider source (atherosclerotic plaques or from cardiac emboli)
-anticipate metabolic disturbance after re-perfusion: high CO2, lactate, potassium, release of vasoactive agents which can contribute to vasodilated state; 100% O2, consider calcium gluconate prepared, hyperventilation, checking ABG
Patient:
-likely multi co-morbid (eg. CAD in 60%, often DM, smokers, Hx TIA/CVA, HTN, renal impairment, consider pts ability to lie flat, cognitive status if electing for LA/sedation or neuraxial
-risks of GA may be high, likely requirement for invasive arterial pressure monitoring, 5 lead ecg, consider defib if significant cardiac comorbidity
-check & optimise electrolytes & fluid status
-consider multi-D input re: comorbidities
Potential complications:
-distal emboli with pain in recovery (procedure is otherwise not usually painful, surgeons can infiltrate wound w LA, PO analgesia usually adequate)
-renal impairment or anaphylaxis from contrast
-pressure injury from prolonged procedure
-bleeding particularly at vascular access site (consider postop instructions wrt time lying flat), limit pain & emesis, BP control to limit bleeding risk
-radiation safety concerns
risk/benefit of surgical Rx for carotid atherosclerotic disease in setting of recent CVA/TIA?
prevents subsequent stroke & improves mortality but periop stroke rate is 5-6%
benfit of stabilising intimal plaque balanced against risk distal emboli & subsequent stroke if incomplete CoW
SS_VS 1.10: Discuss the prevention, diagnosis and management of intra- operative complications associated with vascular surgery including (also refer to the Resuscitation, trauma and crisis management clinical fundamental):
MAJOR HAEMORRHAGE (for desc Tx aortic surgery):
art line(s)- either just R) rad or R) rad & femoral
large bore IVC x2 or 1+ RIC & CVC IJV
6 units red cells, 6 FFP, 6 plt xmatched, checked & ready prior to incision
rapid infusers, warm fluids, cell salvage
Prophylactic TxA
transfuse for Hb >=80 or >=90g/L if evidence bleeding or organ ischaemia, use POCT to guide transfusion. fib conc for hypofibrinogenemia.
May be occult or torrential
SPINAL CORD ISCHAEMIA
-Risk identification (ASA syndrome, flaccid paralysis of LLs w bladder & bowel dysfunction but sparing of sensation/proprioception due to selective watershed ischaemia of anterior spinal cord):
Procedure risks: 8% risk in elective Tx aneurysm repair, 40% in dissection or rupture involving Tx aorta, <3% TEVAR, 0.2% risk elective infrarenal AAA EVAR.
For open incr risk w incr duration of XC (perfusion to the SC during this time dependent on collateral perfusion; if critical vessels have prolonged interruption or are covered or ligated & the pt has inadequate collateral flow, ischaemia may result), larger grafts, emergency vs elective procedure; for both EVAR & open, incr blood loss, crawford I& II aneurysms incr risk. Complications of any drain (eg. blockage, catheter fracture/dislodgement, CSF leak, PDPH, meningitis, bleeding complications (IVH, SAH, epidural haematoma, asymptomatic blood in CSF). mortality related to CSF drainage 0.9%.
For EVAR, endograft length >20cm, placement over origin of artery of adamkiewicz (T9-12), placement over subclavian artery without revascularisation, placement over internal iliac & compromise of hypogastric artery flow (internal iliacs collaterals to spinal cord!), placement of 3+ stents, prol procedure
-Pt factors; atheromatous aorta/more extensive disease, advanced age, previous aortic intervention (risk SC ischaemia for pts having Tx evar w prev abdominal EVAR risk 14.3%, previous aortic surgery particularly risk if hypogastric artery compromised), acute aortic dissection, female, CKD, DM, anaemia, COPD, HTN
-Anaes factors: hypoT (MAP <70mmHg), haemorrhage
Management:
-Limit risk by managing pt modifiable risk factors (eg. smoking cessation, BP control, pt blood management strategies (Hb target >=100 intraop, have 6 U red cells, six units FFP, 1 unit plt ready & available), aim normoglycaemia (incl intra-op, hyperglycaemia detrimental for ischaemia, also avoid hypo, avoid hyperthermia))
-Intra:
SC PP= MAP-intra-spinal CSF pressure (or spinal venous pressure) so ensure adequate MAP (80-100mmHg with vasopressors or fluid; some pts w pre-existing HTN may need higher MAP to prevent SC ischaemia (such pts are @ higher risk), MAP goal may be higher if pt has higher baseline MAP). Rationale for high ScPP is to ensure flow through collateral network of small vessels within the spinal canal communicating with ASA & PSA. Periop hypotension below 70mmHg is indep predictor of postop neurol deficit.
Meticulous surgical attention to avoid ligation/blockage/damage of artery of adamkiewicz (CT demonstrating location of artery) or other important collaterals, avoid raised spinal venous pressure eg. excessive intra-abdominal pressure) to optimise spinal cord perfusion.
-for open, limit XC time, optimise tolerance to ischaemia (eg. cooling to mild or deep hypothermia (impacts on our placement of warming devices), pharmacological neuroprotection steroids barbiturates no evidence benefit), augment SC perfusion (eg. lumbar CSF drain or deliberate HTN), bypassing/shunts to distal aorta eg. atrifemoral bypass or selective perfusion of renal or other arteries (eg. they may use cold saline or blood, selectively perfusing segmental intercostal or Lx arteries or reimplanting Tx intercostals that supply artery of adamkiewicz, rencanalisation of occluded collaterals like int iliac artery). Plans for bypass will affect intra-arterial monitoring sites.
-consider prophylactic CSF drain (timed appropriately with thromboprophylaxis meds) for thoracic or thoracoabdominal endovascular aortic repair reduces risk of SC ischaemia (reduces risk of paraplegia @ discharge & improves 1-year survival). Insert into subarachnoid space @ level of L3-4 disc. Inserting in lateral position may decr amount of CSF loss during insertion. 16g epidural kit, occlude the 16g touchy needle while advancing. thread 6-8cm in SA space unless paraesthesia; withdraw until Sx subside. GOAL OF CSF DRAINAGE= MAINTAIN ScPP >80mmHg. Generally achieve w CSF pressure <10cmH2O (7.3mmHg) & MAP 80-100mmHg. monitor CSF pressure continuously. Drain CSF when the pressure approaches 10cmH2O (>12mmHg), drain in 5-10mL increments until pressure returns below 10mmHg; drainage shouldn’t exceed 15mL/hr. opening pressure should be recorded, CSF transducer is zeroed at RA level, keep drainage chamber 10-15cmH2O above RA. CSF drain reduces CSF pressure, optimising SC perfusion pressure (which we want to maximise to preserve flow through collaterals supplying SC). If CSF drainage becomes bloody, discontinue immediately & obtain SC MRI asap. drainage indicated if high CSF pressure, refractory signs ischaemia on neuromonitoring, hypotension, signs of backbleeding, iliac artery injury. Aim to remove drain <72hrs postop (vascular surgeons & ICU decide).
Maintain MAP within 20% of baseline, ensure adequate oxygenation, keep Hct >25%, limit XC time, regularly monitor Hb & PaO2 to optimise DO2, use POCT if active bleeding, limit coagulopathy (normothermia, avoid acidosis). If insert CSF drainage to minimise SC ischaemia, SC monitoring with MEPs required (stimulate scalp over motor cortex, waves travel down CS tract to nerve root & peripheral nerve, muscle APs in peripheral group *eg tib ant) & evoked response recorded (can measure I & D waves in epidural space or compound muscle action potential). This requires TIVA (prop/remi useful) or volatile <=0.5MAC (incl avoid N2O), m relaxant if used for intubation reversed. ketamine may augment MEP amplitude. caveats: reversible intraop changes don’t nec correlate w paraplegia, intraop MEP has low sens but high specificity for motor deficits @ time of hospital discharge. hypothermia incr latencies & stimulation threshold.
SSEPs also require TIVA or technique w volatile <=0.5MAC as volatiles or N2O delay conduction & decr amplitude SSEPs ketamine may augment. post columns monitored w SSEPs miss the ant columns (of greater interest during XC for ASA sysndrome risk). High NPV >99%, PPV may be as low as 60%. Hypothermia also may delay conduction time decr amplitude (flaxe +ve).
SSEPs stimulate post tib or peroneal nerve, record cortical electrical potentials via scalp electrodes. monitors lat & post column function.
-postop: early & regular neuro exam (neurologic deficit from ischaemic SC injury usually presents immediately after surgery but may be delayed several days), ongoing haemodynamic monitoring & avoid hypoT
If signs SC ischaemia (eg. on MEPs), communication btwn anaesthetist, surgeon, neuromonitoring team to urgently confirm changes, determine etiology, initiate Rx interventions. Ensure anaes not interfering w neuromonitoring, communicate w surgeon to ensure they’re not directly impacting SC perfusion if able to modify, Rx a MAP of <80mmHg in 5mmHg increments up to 100mmHg. Manage CSF pressure >10mmHg, decrease it to 8-10mmHg by draining 5-10mL at a time (don’t drain >20mL in the first hour of surgery & no more than 40mL in any 4-hour period thereafter). Goal = maintain ScPP >=70-80mmHg. Check CVP, if CVP > CSF pressure, incr MAP further to incr likelihood of ScPP >=80mmHg.
Ensure optimal CO, O2 content (high PaO2, Hb>=80). if ongoing evidence ischaemia, continue to incr MAP up to 100mmHg, CSF pressure 8-10mmHg, ScPP >=70mmHg, consider additional surgical Rx (reimplantation of intercostal vessels, distal aortic perfusion). Plan for meticulous postop monitoring for SC ischaemia.
Management of delayed paralysis:
-ongoing monitoring of neuro function, MAP, CSF pressure & temp necessary to recognise & treat postop neuro complications. may be evidence of SC ischaemia hours or days postop. hourly neuro Ax until pt can report.
If postop weakness or paralysis with normal pulses, urgently:
-drain CSF to keep pressure <10cmH2O (8-12mmHg)
-MAP augmented; 80-100mmHg unless pts baseline is higher
-optimise DO2 to SC (maintain CO, optimal CaO2 w normal high SpO2, PaO2, Hb >=80g/L).
-avoid fever which may exac ischaemic neurol injury.
**for pts with complex aneurysms consider MAP >=90mmHg & Hb >=100g/L, CSF drain.
RENAL IMPAIRMENT:
Pts @ risk due to prolonged XC, embolism of atherosclerotic debris into renal arteries, haem instability, blood loss, dehydration; renal dysfunction ass’d w worse outcomes, elevated preop Cr a risk of postop renal impairment.
prevention= identification of pts @ risk:
PT:
pre-existing HTN, DM, elderly, HF
pre-renal:
volume depletion
renal:
pre-existing renal disease/impairment (particularly severely impaired, eGFR <30) or AKI are @ particular risk CIN (consider other tests for these pts incl non-con CT, MRI, US). pts w eGFR stable >=30 & those anuric on chronic haemodialysis are lower risk (UTD: pts w near-normal kidney function are @ low risk for contrast-associated AKI, few precautions needed aside from avoidance/correction of volume depletion. CA-AKI risks= eGFR <60, those w proteinuria. Those w eGFR <30 or <45 & proteinuria/diabetes are highest risk). Intra-arterial contrast higher risk than IV contrast.
nephrotoxics (eg. ACE-I, nSAIDs, diuretics)
post-renal obstruction
PROCEDURE:
IV contrast risks CIN (judicious dilute, aim for at least 24hrs btwn, avoid volume depletion & NSAIDs)
longer procedure/less experienced, complex procedure
repeated contrast within 7 days of prev
PRE-OP:
optimise modifiable risk factors (eg. glycaemic control, renal function) with relevant specialists
limit fasting, ensure adequate HYDRATION w isotonic saline, maintain optimal IV volume status & haem stability throughout periop period, fluid load prior to contrast & continue during & for several hours after (for those pts @ highest risk), monitor UO, ensure >0.5mL/kg/min
judicious use of dilute contrast for endovascular (senior surgeon to help limit OT time/contrast use)
avoid nephrotoxics, withold metformin 48hrs prior to IV contrast
minimise XC time (lower risk infra-renal XC), partial L) heart bypass +/- systemic hypothermia during Tx aortic surgery minimises renal, mesenteric & SC injury. surgeons may selectively perfuse renal & visceral arteries with cold crystalloid or blood (not based on prospective evidence).
defend MAP within 20% of baseline intra-op, dynamic or CO monitoring (may be useful info re: circulatory status
POSTOP:
monitor urine output postop & defend MAP
HDU for early identification & intervention
early nephrology advice
no benefit for acetylcysteine, mannitol or other diuretics or hemodialysis for prophylaxis.
MYOCARDIAL ISCHAEMIA:
-identify @ risk pts, optimise modifiable factors in liaison w appropriate specialists, continue medical management (aspirin, B blockers, statins) & have appropriate monitoring (eg. art line, 5-lead) intra-op.
-Dx with ST changes (continuous leads II & V5 monitoring, computerised ST-segment trending for identification ischaemic changes. confirm with expanded 12 lead ecg, liaise with cardiology immediately with ST elevation & have defib ready), hypotension/reduced CO (for desc Tx aortic surgery, insert 2 intra-arterial catheters if proximal & distal arterial BP required, ie. R) radial & L) femoral) eg. reduced EtCO2, elevated troponin, if TTE/TOE, RWMAs
-correct modifiable supply/demand imbalances: increase FiO2 & optimal ventilation, notify room & stop surgical stimulation as able, deepen anaesthesia/analgesia (reduce O2 demand), if hypotensive, augment MAP to defend diastolic perfusion (DBP >60mmHg, aim MAP >75, SBP 100-120mmHg) by titrating vasoconstrictor (avoid excess afterload, want to avoid elevated LVEDP, cotrol filling pressures)., check Hb & correct any volume loss (w blood if anaemic), CONTROL RATE & manage any arrhythmias (electrolytes, consider B blocker, lignocaine or amiodarone or DC shock), if hypertension control w B blockers or GTN if not inferior infarction or tight AS, control HR aiming 50-60bpm (B block, narcotic), to limit afterload/myocardial O2 demand, when volume & BP are corrected carefully titrate GTN infusion (which dilates coronaries & reduces LVEDP), manage fever & shivering, support contractility (consider inodilator or inotrope). If persistent ischaemia suspect NSTEMI, cardiology will advise re: medical management, angiogram/PCI, otherRx eg. IAABP. Timing wrt completion of procedure depends on urgency of the surgery, if emergency eg. ruptured AAA may need to complete as able & urgent cath lab t/f afterwards
communicate w NOK to update
STROKE:
Prevention & Mx:
Vigilance for at-risk pts & Dx asap; risk identification:
*older age, generally progressive from age 62 onwards, esp 85
cardiovascular disease (HTN, *recent MI, *AF (CHA2DS2-vasc CHF(1),HTN(1),age>=65(1)>=75(2)DM(1) Stroke/TIA Hx(2)-PVD(1), female gender; predict 1-yr risk of TE event in non-anticoagulated pt w non-valvular AF; 1=0.6%,2=2.2%,3=3.2%,4=4.8%,5=7.2%6=9.7%,7=11.2%,8=10.8%,9=12.2%), *HF, *cardiac valvular disease)
*prior CVA or TIA, particularly in the last 9/12
*renal disease
*DM
*COPD
*female
*carotid stenosis (esp symptomatic)
*tobacco use
PFO, migraine, atherosclerosis of asc aorta, OSA, long bone #, DVT, thrombophilias, infection, ?dyslipidaemia, obesity, cessation of anticoagulants
Surgical: cardiac, neuro, CEA, major vascular, major intra-abdo, pulm resection, transplant, arthroplasty, shoulder surg in beach chair position, head&neck surgery, trauma
mechanisms incl cerebral atherosclerosis, low flow states, cardioembolism from AF, air/fat/paradoxical emboli, arterial dissection of neck arteries
Anaes: position excessive neck E/F, blood loss, intra-op hypoT, arrhythmia
Pre:
DELAY ELECTIVE SURGERY after ischaemic stroke- *at least 6/12, IDEALLY 9 MONTHS, to reduce the risk of recurrent stroke (balance risks w risks ass’d w delaying surgery)
use cardio-selective vs nonselective B-block where possible & continue them if chronically on (don’t start acutely)
Appropriate anticoagulation Mx for pts w AF & other conditions predisposing to TE (consider bridging if high risk CHA2DS2-Vasc 7-9, mech heart valve, VTE within 3/12, severe thrombophilia (prot C, S or AT defic, antiphosphoalipid antibodies, multiple abNs) OR av filters considered in multi-D discussion.
Continue statins, those who are @ high risk of CVD should start statin asap before surgery (weak evidence for benefit of starting preop but low risks)
Continue other antihypertensives & anti plt agents where procedure permits (consider any antiplts after PCI in discussion w surgeon cardiologist, neurologist & pt), smoking cessation, manage any arrhythmias (correct electrolytes, rate control, euvolaemia)
normoglycaemia (8-10mmol/L)
BP management
limit fasting time & optimise hydration/volume status
Intra:
-weak evidence for anaes technique; base it on standard pt/surg/anaes factors but observational studies report that for THR, ass’n btwn neuraxial & lower risk periop stroke (no causal ass’n est)
-short-acting opioids & agent for quick wake-up to Ax neurology
-Maintain BP within 20% of baseline (despite lack of evidence for intra-op hypoT in periop stroke etiology)
-if require acute admin B blockers intra-op, use esmolol or labetalol rather than metoprolol
-decision re: transfusion & Hb targets complex & multifactorial; balance pt factors (*pts taking B blockers may be more sensitive to anaemia, attenuation of cerebral compensatory VD by B blockers), ongoing blood loss, risks of transfusion
-Neuroprotective avoid hyoxaemia, maintain normocapnia, normoglycaemia, BIS 40-60 (not too low)
Cerebral oximetry can be used to detect unilat or bilat cerebral hypoperfusion (use for beach chair, CEA under GA, aortic arch surgery). Unilat cerebral desat may indicate disruption cerebral blood flow (eg. arterial dissection). If bilat decr cerebral O2 saturation >10% cf baseline, incr DO2 eg:
-incr MAP w vasopressor
-ensure CO adequate
-ensure adequate SaO2 (incr FiO2 if necessary)
-ensure PaCO2 not <35mmHg (avoid cerebral VC; normal-high PaCO2)
-decr CMRO2 (deepen anaesthesia)
-transfuse if Hb <80g/L
-normoglycaemia (avoid hypo, Rx hyper if >14)
-if beach chair, ensure MAP at CoW baseline
-cognisant of changes suggestive of VAE (watch EtCO2, MAP)
-euvolaemia
Postop:
high index of suspicion for @ risk pts; DDx of failure to wake, neuro deficit (Face arms, speech, time).
pharm (once haemostasis assured) & non-pharmacological VTE prophylaxis, maintain MAP within 20% of baseline & euvolaemia, manage any infection, glycaemic state
Identification of stroke is important, time is brain & delayed recognition is common. Most noncardiac periop strokes occur in the first few postop days; assessment can be confounded by postop delirium, cognitive dysfunction & pain. FAAST scale ((face uneven, UL/LL numbness or weakness, anaesthesia (residual effect), speech (slurring), time (get help immediately)) useful for screening.
ischaemic stroke syndromes:
ACA: motor +/- sens deficit (leg >face, arm), gait apraxia, abulia, paratonic rigidity
MCA: dominant aphasia, CL hemiparesis/hemisensory disturbance face, arm > leg > foot, homonymous hemianopia. non-dominant: neglect, anosognosia, motor, sens deficit, homonymous hemianopia.
PCA: homonymous hemianopia, alexia sans agraphia, visual hallucinations/perseverations, sens loss, choreoathetosis, pain, III nerve palsy, paresis of vertical eye movements, motor deficit
vertebrobasilar: CN palsy, crossed sensory deficit, diplopia, dizziness, N&V, dysarthria, dysphagia, limb & gait ataxia, motor deficit, coma.
ICA: stuttering onset of MCA +/- ACA territory syndrome if inadequate collateral supply.
Urgent neurology consult & neuroimaging & consideration of mechanical thrombectomy should be obtained if suspicion of new neurological deficit & stroke protocol activated. eligibility for acute endovascular intervention for pts emerging from GA w new neuro deficit may extend to 16-24hrs after stroke onset. Other Mx thrombolysis (may be CI soon after OT; depends on the site, higher risk of surgical site haemorrhage if major surgery, CI if intracranial or intraspinal OR or severehead trauma within 3/12, GI haemorrhange within 21/7, active internal bleeding, therapeutic (not prophylactic) LMWH, CAUTION to be exercised if major surgery in the previous 14 days), endovasular thrombectomy (for pts w ischemic stroke caused by proximal lg artery occlusion in ant circulation if can be treated within 24hrs of symptom onset (can consider if posterior circulation LAO)), aspirin, TE prophyl, anti-thrombotic discharge, statin, BP reduction after acute phase passed, lifestyle (smoking cessation, exercise, WL, mediterranean)
ABC, ensure medical stability; consider I&V if decr LoC, bulbar dysfunction, incr ICP
SpO2 should be >94%, avoid hypercapnia
BP control, Rx of abnormal BGL, correct IV volume depletion (isotonic fluids to limit cerebral oedema), Rx fever & infection
aim glucose >=10 (7.8-10mmol/L); very tight glucose control doesn’t improve functional outcome & risks hypos.
swallowing Ax (risk aspiration)
avoid fever (Ix source, Rx w paracetamol)
stroke care unit
BP targets <=185/<=105mmmHg before thrombolysis, maintain <180/<105 for @ least 24hrs. If not having thrombyliss, DON’T acutely Rx HTN unless it’s extreme (SBP >220mmHg, DBP >120mmHg) or if active ischaemic coronary disease, HF, aortic dissection, hypertensive encephalopathy, PET/eclampsia; if Rx, cautiously lower by 15% per 24hrs.
correct systemic hypotension & hypovolaemia
consider 30 deg head of bed elevation if elev ICP, aspn, cardiopulm decomp; otherwise however pt comfortable (horizontal for cerebral perfusion unproven)
Hx time of onset (<4.5hrs eligible for thrombolysis, <24hrs mechanical thrombectomy)
DDx sugar, seizure, syncope, shocking migraine, drug toxicity.
Acute onset headache & vomiting favours SAH.
Examination: neurologic, can use NIHSS w 3 most predictive exam findings for acute stroke= facial paresis, arm drift/weakness, abnormal speech
Urgent noncon brain CT or MRI, fingerstick BGL, SpO2
other tests cbc trops, coags, ecg, echo if suspect endocarditis, shouldn’t delay Rx (eg. unless suspect bleeding abnormality)
ACUTE ARRHYTHMIA:
-anticipate around times of: reperfusion, high SNS stimulation (eg. intubation, XC placement/release), esp in pts @ high risk (underlying AF)
-have anti-arrhythmics available, along w Adr & vasopressors
-confirm real ecg trace & Ax stability (art line)
-temporise w 100% O2, ensure adequate anaes depth, Rx any known likely precipitants (eg. electrolytes, volume correction, temp management, hypoxia, PTx, tamponade, thrombosis or toxin)
-communicate & delegate team (drugs, defib, timekeeper/scribe, CPR)
-SVT adenosine 6-12mg, verapamil
-AF metoprolol or if signs HF, digoxin or amiodarone, flutter rate w B blocker
-broad complex DCCV 200J if unstable, amiodarone 300mg IV over 20-30mins
-torsades Mg++ 2g over 10 mins
THROMBOEMBOLISM:
-prevention: non pharm (risk identify/stratify, smoking cessation, limit fasting, TEDS/SCDS, early mobn (analgesia/anti-emesis), prohylactic LMWH. regional reduces VTE rates
-Dx w CTPA or V/Q, LL US for DVT
-Mx w therapeutic anticoagulation; if haem compromise may require ICU, invasive monitor & CV/vent support, consideration clot retrieval or thrombolysis
LIMB ISCHAEMIA Dx & Mx:
Pre-op symptoms claudication (reproducible discomfort of m group induced by exercise, relieved by rest. due to imbalance in supply & demand of blood flow (fails to satisfy ongoing metabolic requirements).
Buttock= aortoiliac
Thigh: aortoiliac or CFA
upper 2/3 calf: SFA
lower 1/3 calf pop artery
foot: tib, peroneal.
ischaemic rest pain w severe decreases in perfusion- digits & forefoot, typically @ night, may be relieved w dependent positioning of foot
nonhealing wounds/ulcers (may become infected, risk osteomyelitis)
diminished pulses, pallor, Buerger test (normally takes <20secs to reperfuse dependent extremity)=, abnromal delayed, pallor w elevation, dusky flush in dependent positin).
ABI <0.9 high sens & spec for PAD.
sensory loss (distal to prox) may have superimposed diabetic sensory neuropathy (glove & stocking, vibn, 2-point)
Clinical features acute lmb ischaemia:
initially pain, then pallor/pulselessness, paraesthesia, cold & paralysis later.
likely arterial line if prolonged, may need US guidance to insert
likely IV UFH before XC, if epidural UFH can be 1 hr after. ACT 200-250s or approx 2x baseline- may use protamine (1mg per 100U heparin, considering time since dose, half-life heparin (45mins). also use if endovascular, 180-240secs typically target ACT. often withold protamine after endovascular procedures.
risk reperfusion syndrome (this is also relevant to prol gut or limb ischaemia; basically reperfusion gives load of cytokines, acid, K, lactate–> vasodilation, reduced myocardial contractility, pulm oedema arrhythmias, risk CVS collapse; anticipate this (& expected impact cognisant of pts CV reserve)).
art line in assists w keeping MAP within 20% of baseline throughout.
RHABDOMYOLYSIS prev, Dx, Mx:
-characterised by muscle necrosis & release of intracellular m constituents into the circulation
-Causes:
Traumatic/compression:
crush, compartment syndrome or ischaemia
multi trauma, vascular/ortho surg, immobilisation
non-traumatic:
extreme exertion, sickle cell, seizures, myopathies, MH, NMS, ETOH, drugs/toxins
*important to rapidly recognise & treat compartment syndrome, may be a CAUSE of rhabdo or MAY DEVELOP AFTER FLUID RESUS/worsening oedema of the muscle (non-pitting) & peripheral (pitting)
-compartment syndrome exists when incr pressure in closed anatomic space threatens viability of the m & nn within the compartment due to compromised perfusion & local ischaemia.
-Dx:
triad= myalgias, m weakness, redbrown urine (myoglobinuria- detect on urinalysis DDx haematria). elev serum CK.
-ARF on b/g predisposing factors (eg. long lie)
-may be asymptomatic CK elevation or life-threatening electrolyte imbalance (esp hyper K+ which is more prominent if oliguric AKI, may get profound hypocalcemia, may have hyperuricemia, hyperphosphatemia, metabolic acidosis w incr AG, 25% get hepatic impairment), hypobol & ARF (CK >5000 ass’d w ARF in 50% of cases), rarely DIC w severe rhabdo
-muscle pain, weakness, malaise, fever, tacycardia, N&V, abdo pain.
-may get cardiac dysrhythmias/risk arrest if severe hyperK.
serum CK (usually >5x ULN, half life 1.5 days), urinalysis (myoglobin), renal function, CBC (evidence infection or hemolysis), electrolytes (K+, hyperphosphate, hypoCa), abg (met acidosis), serum alb (hypo may be seen w systemic capillary leak syndrome)
ecg
consider coags or cultures if suspect DIC or infection
-Mx:
-IVT (isogonic saline, 1-2L/hr, irrespective of renal function continue until it’s clear the plasma CK gets <=5000U/L & isn’t increasing, neeed urine output 200-300mL/hr & avoid vol overload), correct electrolytes (esp K+ & Ca++), monitor, haemodynamic support
-correct causes (esp prompt Mx compartment syndrome)
-If progressive ARF, consider haemodialysis w correction of hyperK, volume status (overload or hypovol from myoglobinuria), acidosis
-sodium bicarb IV to alkalinise urine & treat metabolic acidosis & hyper K
diuretics no proven benefit but consider if volume overload
Main complications with open desc Tx aortic surgery?
ischaemia (brain, SC, kidney, viscera, extremities), embolic complications, large blood los, prolonged duration
SC ischaemia risk with open is similar to endovascular
Plans for induction & airway managmeent for desc Tx aortic surgery (open)
DLT or BB if aortic dissection or XC above the diaphragm
induction agents to limit risks myocardial ischaemia, hypoT, HTN, tachy
temp monitoring (oropharyngeal & bl), want to reestablish normothermia after any systemic hypothermia
pt likely ICU ntubated as unlikely to meet extubation criteria (eg. residual hypothermia, coaguloapthy, acidosis).
SS_VS 1.5: Discuss options for postoperative analgesia and perioperative fluid therapy for these procedures
Thoracic aortic open repair: PCA, regional w bilat PVB (epidural risk haematoma)
fluids: balanced crystalloid, large volumes of N/S risk hyperchloraemic metaolic acidosis, renal VC, decr GFR & renal injury. starches renal injury.
normovolaemic, run pt dry prior to XC, consider fluid load before XC removal
for endovascular procedures utilising contrast, vavoid hypovolaemia, fluid load prior to & continue IVT during & for several hrs post contrast (eg. 3mL/kg in first hr, 1.5mL/kg/hr thereafter provided comorbidities allow
SS_VS 1.4: Aortic & aorto-iliac disease:
High risk MACE (suprainguinal vacular)
for aorto-bifemoral bypass & axillary-femoral bypass, significant comorbidities & functional decline due to claudication, reginal ideal if pt not anticoagulated. Epidural may be best (often open), best to avoid GA & IPPV, bloody tap not a CI to surgery, need PCA if no epidural. pt needs to be still so pt selection important & care re: disinhibition w sedation.
Pre-op Ix 5-lead ecg, echo, PFTs, CT abdo w contrast (care re: CIN), FBC, E/LFT, coags
major blood loss risk: G&H w XM 6U
cell salvage available
2x large IVC, IAL, generally CVL not nec, HDU likely required due to pt/surg factors
SS_VS 1.6: Evaluate the risks and benefits of regional anaesthesia and analgesia in vascular surgery
TEA for open abdo aortic surgery: reduces pain intensity, time to tracheal extubation, ICU time, time to oral intake, rate of resp failure/MI/GI bleed cf IV opioids but no mortality benefit. MASTERS trial: small reduction in resp failure in epidural group but no diff in mortaity or major morbidity in high-risk pts undergoing major abdo surgery w epidural + GA cf GA alone.
TEA adverse effects: epidural haematoma, epidural abscess & temp/perm neuro deficit, resp depression & adverse effects of drugs added, hypotension (depends on dose), treatment failure, prolonged motor blockade & sensory disturbance confounding assessment of neuromuscular function (eg. for pts @ risk of SCI)
rectus sheath catheters and TAP blocks also beneficial for post-open AAA analgesia
ITM 200microg + GA for abdo aortic srugery= better postop analgesia vs GA only.
ITM adverse effects: OIVI (generally minimal risk with lower dose <300microg; use lowest effective dose & surveillance for OIVO at least 18-24hrs following single dose; hourly first 12 hrs then 2hrloy, LOC, rasp rate, pulse ox longer monitoring for high risk pts), pruritis dose-related, PONV, urinary retention (tends to be more of an issue for minor surgery), reactivation of HSV, theoreticsal caution if pt is @ risk of SC ischaemia.
Regional (brachial plexus block) advantageous over LA only or GA, sympatholysis provides arterial & venous dilation & improves fistula patency, reducing re-intervention rate, lower rates vasospasm (supraclav & infraclav)
supraclav relatively quick onset, sympatholysis/vasodilation, risks ulnar sparing, PTx (may be delayed), phrenic n injury 30%, horner’s, bleeding (non-compressible site, vascular so use colour doppler.
infraclav: technically challenging (3-5cm deep), poorly compressible site, risk PTx if too medial, larger dose as higher volume (20-30mL) needed
axillary: minimal risk damage critical structures, multiple reangulations so useful for teaching but risk sparing radial & musculocutaneous
all spare intercostobrachial (tourniquet)
CEA: Cochrane 2021: incidence of stroke & death not diff in GA vs LA for CEA, either fine.
GALA trial for CEA: no diff in outcomes for stroke but reduced incidence periop MI in LA group
LL surgery & bypass grafting, regional avoids complications of GA, may be ass’d w reduced rates of graft failure & embolectomy, 2x cohort study of >17000 & >20,000 procedures showed RA ass’d w lower surgical & general complicaitons & lower 30-day mortality, lower renal & cardiopulm complications, one showed lower LoS. May be ass’d lower stress response.
sciatic & perineural catheters help w postop phantom limb pain & telecsoping following LL amputations
SS_VS 1.7: Discuss the perioperative management, including postoperative analgesia and perioperative fluid management of patients having an emergency vascular procedure for the following:Major vessel occlusion or limb ischaemia
Acute thrombus= urgent exploration under GA to restore perfusion; likely unfasted, RSI, likely significant pain, may be after hours, may be in remote location
chronic ischaemia less urgent, likely fem-pop bypass graft w autologous saphenous vein graft or w Gore-tex
Both procedures can be long (1-6hrs, pressure areas, fluid balance, temp etc, GA more likely appropriate despite comorbidities given duration) & significant blood loss (0.5-1L) but usually no major haemodynamic stress. occasionally if small level bypass limited duration may be appropriate for LMA w fem nerve block. While regional avoids complications of GA, may be ass’d w reduced rates of graft failure & embolectomy, 2x cohort studies of >17,000 & >20,000 procedures showed RA ass’d w lower surgical & general complicaitons & lower 30-day mortality, lower renal & cardiopulm complications, one showed lower LoS. May be ass’d lower stress response, Long operations (typically >3hrs) make regional largely impractical.
Ax exercise tolerance (often difficult to Ax if claudication)- useful to know pts CV reserve w risks of reperfusion syndrome., Hx angina/UA, COPD, smoking, DM, CVA
either GA ETT, LMA w FNB, spinal w ITM for short procedures, consider CSE longer, prop tci sedation
neuraxial may be contraindicated depending on anticoagulation status
Ax severity of occlusion, duration of ischaemia, other comorbidities (CVS, resp, renal, DM incl glycaemic control) & stability, current fluid status & analgesia
open or endovascular? (remote anaesthesia considerations for IR suite)
IV 14 or 16g, likely art line if >2hrs or expect haem instability, along w 5-lead ecg, nibp, for fluid status monitoring
want to serially monitor abgs esp if prolonged ischaemia, risk reperfusion syndrome (this is also relevant to prol gut or limb ischaemia; basically reperfusion gives load of cytokines, acid, K, lactate–> vasodilation, reduced myocardial contractility, pulm oedema arrhythmias, risk CVS collapse; anticipate this (& expected impact cognisant of pts CV reserve)).
heparin 3000-5000IU prior to clamping, reverse w protamine (1mg/100U heparin)
*communication vital w surgeons re: duration if ischaemia, extent, timing of embolus removal (risk sudden reperfusion injury w profound hypoT, hyperkalaemia, acidosis, risk arrest); pre-empt w vasopressors, electrolyte Mx (Ca++, insulin/dextrose), hyperV, fluids, consider bicarb
Postop: consider HDU/ICU for haem monitoring, analgesia, neurovascular monitoring (risk graft occlusion requiring urgent re-exploration), also nonitoring of pH & K+ (reperfusion may be a slow process esp if prolonged limb//GIT ischaemia). aim= to extubate if pt fits criteria.
SS_VS 1.7: Discuss the perioperative management, including postoperative analgesia and perioperative fluid management of patients having an emergency vascular procedure for the following: limb amputation
below knee, through knee, above knee or indivicual digits (r/o necrotic or infected tissue due to vasc ischaemia)
generally short procedure (30-120mins), significant pain & chronic posotp pain possible, generally not major blood loss (200-500mL), often spinal +/- sciatic & femoral block +/- sedation
Pre-op:
commonly multi comorbid pts w significant poorly controlled DM, significant CVS disease, repeated revascularisation attempts
Often DM, smokers, COPD, IHD, PVD, prev CVA
often in significant pain (less if DM neuropathy) & may be on large doses enteral or parenteral opioids (poor pain control incr risk phantom limb pain & regional pain syndromes)
High risk periop mortality postop
Pt may be septic from necrotic tissue but postponing for Ix/optimisation may not be possible if source control required; do manage decomp HF, tachyarrhythmias, HTN, optimise COPD w bronchodilators +/- steroids, commence tight BSL control w insulin
Hx of comorbidities & control/end organ effects, anaes & medication Hx, cardioresp exam, bloods w eLFT, FBC, G&H, coags (particular consideration for regional/neuraxial), ecg, echo (Ax of valve & ventricular function helps guide GA vs RA). PFTs may help quantify degree of resp disease.
plans re: DM management, anticoagulation esp wrt neuraxial, postop analgesia.
Intra-op:
generally spinal & sedation excellent anaesthesia, epidural good post-op analgesia & can do pre-op or as a CSE; ALSO PERIOP EPIDURAL REDUCES INCIDENCE OF SEVERE PLP. Regional pref if significant airways disease.
can do gentle GA w sciatic, femoral block.
periop ketamine may prevent severe PLP
morphine, gabapentin, ketamine & dextromethorphan reduce PLP cf placebo, calcitonin reduces acute but not chronic PLP
5 lead ecg, art line, usually short procedure w minimal blood loss but keep pt warm & consider BGL control
postop:
regional analgesia best (multi-comorbid, risk postop chronic pain)- otherwise PCA
phantom limb pain a problem for 60-70% of amputees!
pre-emptive analgesia w epidural is believed to reduce incidence & severity of CPSP in amputation, can use combined fem/sciatic nerve blocks as an alternative to epidural esp if pt on anticoagulation
multi-modal; paracetamol, TCA, or gabapentinoids useful for neuropathic pain, consider ketamine & lignocaine infusions intra-op if high risk persistent postsurgical pain, best to avoid NSAIDs w risk renal impairment.
PCA opioids.
Phantom limb pain APMSE:
-PERIOP (pre- intra-post) EPIDURAL DOES REDUCE INCIDENCE OF SEVERE PLP 12/12 postop (NNT 5.8)
-periop ketamine may prevent severe PLP
-continuous regional block via nerve sheath catheters provides postop analgesia post amputation but doesn’t prevent PLP
-oral & IV morphine (in the short term), ketamine, dextromethorphan gabapentin, reduce PLP cf placebo (level 1 coch review)
-amitryptiline & tramadol may assist PLP (level II)
-IV salmon calcitonin reduces acute (<7 days post amputation) but not chronic PLP, while epidural calcitonin reduces incidence chronic PLP, allodynia & hyperalgesia @ 6&12/12
-non-pharmacological:
Rx aiming at cortical reorganisation (eg. mirror therapy, sensory discrimination training & motor imagery may reduce chronic PLP)
anxiety may be a predictor of PLP
SS_VS 1.12: Discuss the diagnosis and management of postoperative complications associated with vascular surgery including: Post-amputation pain
phenomena that may emerge following amputation incl:
-residual limb pain (stump pain) @ the site of amputation. may be acute (usually nociceptive) or chronic (usually neuropathic), most common in immediate postop period. risk incr by presence of severe preamputation pain, pre-op anxiety.
-phantom sensation: sensory perception of the missing body part, not painful. common; range from vague awareness & paraesthesia to complete sensation of the missing part (incl temp, movement)
-phantom limb pain: noxious sensory phenomenon in the missing body part. incidence 30-85% after amputation, usually in the distal portion of the missing limb. 75% report PLP in the first few days post amputation but it may be delayed onset. typically intermittent & diminishes w time. Predictors= severity of preamputation pain, degree of postop stump pain, chemo or radiotherapy, catastrophising, longstanding preop chronic pain, depression/anxiety. afferent input plays a role (given that peripheral nerve blocks help).
These phenomena are common; only 15% are pain-free after amputation. 75% have PLP, 42% residual limb pain, 35% both.
SS_VS 1.7: Discuss the perioperative management, including postoperative analgesia and perioperative fluid management of patients having an emergency vascular procedure for the following: arterial laceration
may be other ass’d trauma
potential for massive haemorrhage depending on vessel; typically I/M tourniquet until repaired
big drip, art line, GA/ETT, possible massive transfusion
SS_VS 1.19 Outline the advantages and disadvantages of interventional radiological procedures as compared with open procedures for management of:
Aortic aneurysm
& 1.16: Outline the implications for patient safety of the location of the interventional radiology service
EVAR more options for anaesthetising the pt (depending on pt factors) eg. LIA @ femoral or iliac art access, neuraxial, benefits of early detection of anaphylaxis or detection of rupture (retroperitoneal pain), this may reduce LoS but pt selection important (eg. anxious, HF or back pain unable to lie still) & GA allows motionless pt (optimal surgical conditions), ability to lower MAP & suspend respn during stent deployment may be easier, less bowel peristalsis (intro imaging quality), pt comfort.
Minimal pain w EVAR.
EVAR has higher technical success rate & lower rate severe peri-op complications but similar LT survival. Late complications (related to endograft) & re-intervention more likely w EVAR.
Immediate & early complications relate to endograft placement (eg. vascular access problems; thrombosis, rupture or dissection, accidental occlusion of visceral vessels with endograft or embolism—> ischaemic complications to kidneys (hypotension, embolisation, graft impinging on renal artery flow), SC (blood loss/hypotension reducing MAP hence ScPP, placement of graft over artery of adamkiewicz T9-12), intestines (colonic ischaemia if endograft covers inf mesenteric artery or thromboembolism), pelvic organs, extremities; endoleak or graft migration, graft occlusion & LL ischaemia).
Conversion to open 2% (25% emergency)
IV contrast= risk physiologic or hypersensitivity reaction or contrast-induced nephropathy.
Less pulmonary complications vs open but EVAR more bleeding (eg. residual heparinisation) & ischaemic complications with EVAR (eg. renal, LL) due to risk endograft limb occlusion; LL= most common site of ischaemia following EVAR). Cardiac, cerebrovascular & renal complications no diff at 3.4yr f/up open vs EVAR but AKI more common following open vs EVAR, risk MACE still at least 1% after EVAR. may require hypogastric artery embolisation to limit endo-leaks; risk buttock claudication & erectile dysfunction (& SCI if future aortic procedures).
Post-op may get retroperitoneal haemorrhage/haematoma & abdominal compartment syndrome (intra-abdo HTN IAP>20mmHg); risk organ dysfunction (may get SC ischaemia from this; flank pain, may get hypotension/tachy, bilat absent reflexes/motor weakness but intact light touch)
All IR procedures have considerations related to remote anaesthesia:
-distance from main OT; if complication or require extra hands/equipment it may be delayed; notify/request additional support appropriate to the case (eg cardiac anaesthetist, pads) if difficulty anticipated
-unfamiliar or inadequately stocked equipment; arrive early & check machine, oxygen, suction sources, monitors, medication drawers & have all plan A/B/C airway/drugs, standard & emergency equipment available & in working order (eg. pt warmer)
-skilled anaesthetic assistant best suited to remote anaesthesia, brief them on plans
-We may need to bring our own anaesthetic machine
-patient access may be limited: meticulous set-up with secure airway or pt’s airway visible if unsecured, lines carefully secured with backup & long extensions, free of II/O-arms, dummy run any screening equipment to ensure won’t catch/kink on lines or tubing
-space may be limited- arrange room to optimise airway access & allow ability to see pt/machine/monitor, have emergency drugs & equipment immediately accessible along with cognitive aids for specific emergency situations
-recovery & monitoring facilities must be appropriate
-emergency procedures pose particular issues for remote anaesthesia eg. emergency buzzer & equipment/drugs, personnel for insertion of lines, ongoing resuscitation, checking & administration of blood products; anticipate this & establish who’ll provide assistance in event of any crises & plan for transport to other locations
-other staff may not be known to me & may be unfamiliar with anaesthetic procedures/requirements particularly emergency, similarly their environment & procedures may be unfamiliar to me; discuss issues during multi-D team brief (particularly important in unfamiliar locations & with unfamiliar teams)
-process for multi-D review (eg. debriefs) & audit of adverse events
-pts may be particularly frail/comorbid in IR- higher clinical needs
-risks of radiation; this is an important consideration for younger pts having EVAR, who require endograft surveillance eg. CT angiography, repeated radiation exposure ass’d w incr lifetime Ca risk. Repeated contrast may also contribute to progressive decline in renal function.
-staff regularly exposed to radiation risks should wear dosimeter badges to monitor cumulative radiation exposure
-radiation dose is determined by: -distance (amount of radiation decreases in proportion to the square of the distance from the source); always wear lead aprons, thyroid collars & use portable shields, stand as far away as possible, ideally in an observation room -ionizing radiation for diagnostic & interventional procedures may cause DNA damage (through free radicals interfering with chemical bonds between molecules, causing structural damage @ cellular or molecular level) increasing the risk of further Ca. -Effective dose can provide an estimate of potential harms caused by low doses of radiation for diagnostic imaging, measured in sieverts (Sv); 100rem=1Sv=1000mSv. The effective dose is considered in the context of annual effective dose to individuals from natural background radiation sources; background is approx 3mSv. An individual dose of 50mSv or lifetime dose of 100mSV hasn’t been associated with health risks so they’re the upper thresholds for diagnostic imaging. If a pt receives a whole-body radiation dose of 1Sv, 4-5% incr RR of fatal Ca. Whole-body CT is 12mSv, CT angiogram aorta is 24mSv, PA or lateral CXR: 0.1mSv, CT chest 8mSv, CTPA 15mSv, coronary angioplasty or stent: 15mSv. V/Q 2.2mSv.
Dissection: endovascular vs open OT for type B reduced mortality, deploying stent/graft, risk occlusive issues, likely spinal drain for Tx. radiation risks.
CAS: can be LA only, no diff stroke/survival, if neuro changes IR can do angiogram to immed Dx vasospasm/embolisation/dissection, <90mins, less risk conversion to GA vs CEA. risks not suitable for some pts (supine), brady/lability w balloon inflation, risk groin haematoma (& heparin not reversed), contrast.
SS_VS 1.17: Discuss the procedural requirements and implications for anaesthetic management of patients having interventional radiological procedures including:
Vascular embolisation
Vascular stenting
Insertion of intravascular devices including aortic
grafts
Radiological-guided biopsy under anaesthesia
vascular embolisation:
For Rx vascular malformations, tumours & haemorrhage.
Superficial procedures, those involving AV malformations or using ETOH for the embolisation are painful ++ & require sedation or GA.
PPH: single procedure completely arrests bleeding in 89% of ages. pt MUST be stable. Fentanyl for placement of balloon under IR. have cell saver, XM blood in OT fridge x4, CSE spinal morphine or epidural titrated w 0.75% ropivacaine to avoid opiate before delivery, lateral position or GA w IAL, RICC, BIS. close common w abs during case. epidural for postop pain.
may be used for uterine fibroids: typically percutaneous transcatheter embolisation under fluoroscopic guidance. Typically under LA or epidural anaesthesia for post pain. LA at groin puncture site. sedation. lidocaine into uterine aa during & after UAE reduces post procedural pain & narcotic use. IV dexamethasone + postop PCA / epidural. APMSE: epidural improves pain scores but incr complications & costs.
Brain AVM: onyx polymer= a common embolising agent, may cause transient desaturation. Small but present risk of the agent migrating through AVM to distal venous circulation or R) heart & pulm circulation—> pulm HTN, proceduralist may request hypoT or adenosine-induced asystole during polymer injection to minimise passage into draining vv & the systemic circulation.
onyx embolisation= distinctive garlic smell up to 24-48hrs post procedure (metabolism of the solvent)
shunting: balloon-tipped catheter insert into narrow or blocked vessel. balloon inflated. stent may be placed to keep it open. GA may not be required.
TIPS: pt supine, GA or sedation/LA. MAY TAKE SEVERAL HRS to access the portal vein. TIPS may worsen encephalopathy, generally pts w significant encephalopathy are excluded from TIPS but GA if cognitive impairment or can’t tolerate supine (or if massive ascites & aspiration risk, there may be limited access to the airway, Ax & correct coagulopathy before procedure (put >50K, fibrinogen >2. G&S. volume resuscitations may be needed if variceal haemorrhage. if large paracentesis prior to procedure, give Alb vs crystalloid. If significant hyponatremia, 25% albumin preferred (contains less sodium than 5% alb). immediate procedure risks incl vascular injury, haemorrhage, PTx, dysrhythmia. TIPs creates rapid incr VR to the heart, may unmask cardiac dysfunction or pulm HTN. haemodynamic deterioration intra- or post procedure may occur.
EVAR: simple infra-renal AAA is minimally invasive, femoral/iliac artery catheterisation; expandable grafts into abdo aorta under fluoroscopic guidance. juxta- and supra-renal aneurysms w fenestrated grafts specifically for the pt. in some cases the stent inserted from above; surgeon cannulating a brachial or subclavian artery. establish this before site art lines. more complex grafts incr skill required from the operator & procedural time, fluoroscopy time & dose of iodinated contrast, incr risk renal impairment. there may be blood loss from vessel damage. highest risk for acute rupture of aneurysm= stent deployment. complex ears may result in significant blood loss (consider cell salvage, rapid infusion device for complex EVARs.
pts need to do breath hold for image quality of DSA. consideration of femoral/iliac artery occlusion & ischaemic pain in legs/buttocks w awake pts (other limitations to awake= respiratory insufficiency, if emergency abdo pain w expanding haematoma, agitation if metabolic disturbance/ypotension)
hybrid OT appropriate (ability to convert to open).
Emergency EVAR: IMPROVE trial showed that @ 3yrs, cf open repair, endovascular for suspected ruptured AAA survival advantage, QALY gain, similar levels of reintervention, reduced costs.
risks of conversion to open (eg. w pain of retroperitoneal haematoma) so hybrid OT preparing for emergency repair.
aortic dissection HR <120bpm, SBP 100-120mmHg (minimise aortic wall stress). aortic rupture SBP aim >70mmHg, <100mmHg.
emergency LA sedation OR GA (neuraxial inappropriate).
IF GA, don’t induce until surgical team prepared to deploy aortic balloon or open abdo rapidly & apply aortic XC (loss of tamponade effect & SNS stimulation w GA agents, risk catastrophic bleeding). can cannulate access vessels & insert expandable balloon under LA.
most pts have perc biopsy sans sedation. can premed w BZD +/- opioid if anxious. pt needs to cooperate w breathing maneuvers.
Risks incl bleeding, PTx.
SS_VS 1.18: Discuss the diagnosis and management of complications associated with interventional radiological procedures including:
REACTION TO IV CONTRAST:
Indication for contrast should be carefully considered & used appropriately (avoid inaccurate/unnecessary tests/radiation exposure).
Identify/define features of previous reaction- ensure to iodinated contrast, clinical details of the reaction, severity, physiologic or allergic-like, duration, therapy. Determines the likelihood & probable severity of recurrent reaction & need for premed prophylaxis (hydrocort 200mg IV 5 & 1hr before, antihistamine 1hr before)
Chemotoxic & vasovagal reactions (aka physiological)- depend on infusion rate & dose. Varying severity, some self-limited, some need Rx & severe.
Chemotoxic: warmth, flushing, nausea, emesis, arm pain, mild HTN, chills, metallic taste, headache, seizures, chest pain, arrhythmia, vasovagal signs (vagal tone depresses SA & AVN activity, inhibit AV conduction–> faintness, hypoT, brady. Mx by slowing infusion rate).
Hypersensitivity:
Idiosyncratic, independent of dose & infusion rate. can occur in response to minute amounts of contrast
Occur mins to within 1hr: flushing, pruritis, urticaria, angioedema, erythema, tachy, bronchospasm, wheeze, laryngeal oedema, stridor, hypoT, LOC, shock. Sx within 5 mins of contrast. Some, particularly severe, may be IgE-mediated anaphylaxis & equally severe. In most cases non-IgE mediated (mast cell activation, complement, serotonin). Skin testing is helpful.
delayed hypersensitivity: type IV, T-cell mediated, from later to 1hr to 10 days after contrast, mild-mod cutaneous eruptions, urticaria, angioedema. Maculopapular exanthem= most common presentation. severe= DRESS (drug reaction w eosinophilia & systemic symptoms, SJS, TE). allergy evaluation can help determine if the exanthem related to contrast vs viral.
Decision re: what to use- if severe or mod could presumptively Rx the path, alternative test or proceed w counselling/consent/resus team/premed w steroid or antihistamine.
always discuss reaction w radiologist & team. if mild reaction, urgent Ix shouldn’t be delayed for premed.
allergist for skin testing may identify safer agents for that individual.
Mx= immediately cease infusion
Mx as per the anaphylaxis guidelines
Simultaneously communicate issue (ask them to stop contrast & procedure) & request assistance & anaphylaxis cards, assess pt & monitors (perfusion/colour/etCO2), temporise w 100% O2, minimal GA agent.
cardiac arrest: immediate CPR, 1mg IV Adr, elevate legs, 2L crystalloid.
assign leader, reader of cards, scribe.
airway: capnography trace (confirm present, FiO2 100%)
intubate early (risk airway oedema)
500mL bolus (mod), 1L (life-threatening) IVT
ensure large-bore IV access, warm IV fluids if possible
Adr: severe (hypoT/bronchospasm) 50-100microg (0.5-1mL of 100microg/mL). If no response, 200microg.
mod 10-20microg (0.1-0.2mL), if no response, 50microg (0.5mL)
dose every 1-2mins, if >3boluses, infusion: 3mg/50mL
start @ 3mL/hr (3mcg/min, max 40mL/hr)
refractory: consider calling arrest code (more help); maximise fluid resus (extra 50mL/kg bolus), remove occult triggers (eg. chlorhex, synthetic colloid), consider art line/TOE/TTE/CVC
Add 2nd line vasopressor to Adr infusion
-NAdr infusion (3-40microg/kg/min)
-vasopressin 1-2U bolus then 2U/hr
glucagon 1-2mg IV every 5 min until response if B-blockers
Bronchospasm: ensure not oes intubation, circuit or device issue, tension PTx. continue Adr infusion, alt bronchodilators: salbutamol 12 puffs MDI, IV 100-200microg bolus ++/- 5-25microg/min infusion
Mg++ 2g (8 mmol) over 20mins
consider volatiles, ketamine
consider ecmo
Preg: L) manual UD, CS if peri-arrest (within 5 mins)
tryptases, refer.
AORTIC OCCLUSION:
catastrophic occurrence that results in high risk limb loss & death. extensive collateralisation usually prevents acute ischaemic phenomena
can be due to acute embolism obstructing aortic bifurcation, thrombosis of existing aorto-iliac occlusive disease, thrombosis of endograft, small vessel size, distal aortic coarctation.
severe pain, LL paralysis/paresis, other ischaemic manifestations of intestine, kidney.
If noted absent pulses, immediate heparinisation & angiogram.
Rx depends on the etiology (eg. embolectomy, aorta femoral bypass, axillary femoral bypass, thrombectomy, haematologic workup), aim- restore flow asap. mortality 20-50%, amputation 30%, paraplegia, renal insufficiency, visceral ischemia other complications.
M&M affected by duration of ischaemia, local & systemic complications of re-perfusion injury.
What’s an emergency (as per ESC)?
Life or limb threatening, time for VERY limited clinical evaluation, typically <6hr
Urgent is also life or limb threatening, time for limited clinical evaluation, typically 6-24hrs
What are active or unstable cardiac conditions?
UA
acute HF
significant arrhythmias
symptomatic valvular heart disease
Recent MI or residual myocardial ischaemia
What are active or unstable cardiac conditions?
UA
acute HF
significant arrhythmias
symptomatic valvular heart disease
Recent MI (WITHIN 60 days) or residual myocardial ischaemia
What are some of the medical management guidelines recommended by ESC?
known IHD or myocardial ischaemia: consider low-dose B blocker titrated
if HF, ACE-I considered
vascular: statin
1MET
3.5mL/kg/min O2, 1.2Kcal/kg/hr
Difference w ESC guidelines:
Steps 1-4 the same:
emerg?
unstable cardiac condition?
low combined pt/surgical risk (<1%), proceed
if >1% consider METs; if METs >=4, proceed
If <4METs:
-Intermediate surgery, consider noninvasive testing (IIb), ECG if pt has one or more clinical risk factors (level 1 recommendation); main pt risk factor for cardiac events= HF, then stroke & renal insufficiency equal. then DM & angina.
-If high (>5%) risk surgery, consider pt risk factors (IHD, HF, stroke or TIA, renal dysfunction (Cr >176.8micromol/L), DM insulin)
-If <=2 risk factors, rest echo (also TTE should be considered if high NT-proBNP/BNP, new murmurs, unexplained dyspnoea (decline functional capacity, suspect mod-severe valve, known CCF no echo within 12/12)) & biomarkers (level 1 recommendation for trops (pre, 24, 48hrs), IIb for BNP), then surgery
if >=3 risk factors, cardiac stress test. If no or mod stress-induced ischaemia, surgery. If extensive ischaemia, consider risks/benefit of surgery cf medical therapy or revascularisation.
If balloon, surgery can be performed >2wks later w aspirin continuation
BMS can do surgery >4wks later, continuation of DAPT @ least 4 wks
new-gen DES: can do surgery within 6/12
CABG
continuation of aspirin for the procedure depends on bleeding vs thrombotic complications
Pre-op, they suggest:
No Ix for low-risk NCS for anyone
Intermediate-risk NCS:
pts >=65yo OR with CV risk factors (HTN, smoking, dyslipidaemia, DM, FHx CVD) OR those w established CVD should have ecg & biomarkers (hs-CTn +/- BNPs) & functional capacity Ax (DASI or 2 flights stairs)
High-risk NCS:
consider an ECG & biomarkers in pts >45yo
ecg, biomarkers (I), functional capacity (IIa) if >=65yo or CV risk factors
If known CVD, ecg & biomarkers is class 1 recommend, functional capacity IIa, cardiology consult & multi D
How long should elective NCS be delayed after PCI & ACS as per ESC 2022?
6/12
12/12
Significant findings of manage study wrt MINS
MINS had a HR of 3 to incr risk of MI at 6/12, while a true MR HR of 5
HOWEVER, heart failure at 6/12, HR of 5 if had MINS (“trip leak” vs 3 if had MI
CARP RCT TBL & relevant ACC/AHA guideline
pts undergoing elective major vascular surgery with known CAD, no mortality benefit in performing coronary artery vascularisation
Level 1 recommendation to revascularise before non-cardiac surgery in circumstances where it’s OTHERWISE recommended, but calss III recommendation that routine coronary revasc not be performed prior to NCS exclusively to reduce periop CV events
