AAA aortic surgery Endoleak EVAR

Does AAA rupture after EVAR, and how ‘dramatic’ the presentation is?

01/04/2017

ref. JVS Jan 2017

Comparison of the outcomes between those occurring after endovascular repair (group 1) and those occurring without previous endovascular treatment (group 2) was made using the data collected and combining the results obtained by a previous study that analyzed the same findings between 1992 and 2003 from the same center to provide a total 22-year experience (1992-2014) at a single quaternary referral center.

Results

From May 1992 to September 2014, there were 1921 elective repairs of intact infrarenal AAAs, with 1288 endovascular and 633 open repairs. During 22 years, 40 of the 1288 patients (3.1%) who underwent endovascular repair for AAA had rupture. The proportion of patients with hypotension at presentation in group 1 (13/40) was significantly less than in group 2 (108/138; P < .01). The difference in perioperative 30-day mortality rate in group 1 (8/40 [20%]) compared with group 2 (68/138 [49%]) was significant (P < .01).

Conclusions

This study confirmed that endovascular AAA repair does not prevent rupture in all patients. The data suggest that rupture, when it does occur, may not be accompanied by such major hemodynamic changes and higher mortality rate as with rupture of an untreated AAA. Strict surveillance and follow-up are required, especially in patients with relatively large initial AAA diameter or presence of endoleak and graft migration, to reduce the rate of ruptures after endovascular repair. Complete prevention will remain challenging because rupture may occur without any predisposing abnormalities. With the advent of new-generation devices, continuous larger long-term studies are required to document reduction in rupture rates after endovascular aneurysm repair.

Aortic dissection

predicting the behaviour of dissection from level of CT enhancement!

01/04/2017

ref: JVS Jan 2017:

This relatively easy method of comparing the degree of enhancement of thrombus in the false lumen is easily obtainable and useful to a) understand the dynamics and b) predict outcome.

A total of 65 patients (42 men; mean age, 75 years) with type B IMH were evaluated retrospectively. On initial CT scans, attenuation of the false lumen (AFL) was determined before enhancement and in the early and delayed phases of contrast enhancement. Then enhancement of the false lumen (EFL) was calculated (AFL in the delayed image − AFL in the precontrast image). The Cox proportional hazards model was employed to estimate the risk of IMH-related events, including death or surgical repair.

Results

The mean AFL for precontrast CT, arterial phase enhanced CT, and delayed phase enhanced CT was 56.3 ± 10.5, 59.9 ± 10.8, and 63.7 ± 11.1 Hounsfield units, respectively, whereas the mean EFL was 7.4 ± 9.0 Hounsfield units. EFL was the only independent predictor of IMH-related events (n = 23; hazard ratio, 1.008; 95% confidence interval, 1.03-1.15; P = .0044) and IMH-related death/surgical repair (n = 10; hazard ratio, 1.111; 95% confidence interval, 1.017-1.213; P = .0197).

Conclusions

In patients with IMH, EFL is the most powerful predictor of IMH-related events, as well as IMH-related death or surgical repair.

carotid artery disease carotid disease Carotid stenting

Restenosis following Carotid endarterctomy: open redo or stenting??

01/04/2017

Source: JVS Jan 2017:

This is a challenging question for real life cases … here is the results from this very large cohort of patients:

We studied all patients in the Vascular Quality Initiative (VQI) database who underwent CEA or CAS after prior ipsilateral CEA between January 2003 and April 2015. Univariate methods (χ2 and t-test) were used to compare patients’ characteristics and outcomes ≤30 days and up to 1 year. Multivariate logistic and Cox regression analyses, adjusting for patients’ demographic and clinical characteristics, were used to compare the procedures with respect to ipsilateral stroke, death, myocardial infarction (MI), stroke/death, and stroke/death/MI.

Results

This cohort of patients with prior ipsilateral CEA underwent 2863 carotid interventions, 1047 (37%) CEA, and 1816 (63%) CAS. Characteristics were similar in both groups. The 30-day ipsilateral stroke rate comparing CEA vs CAS was 2.2% vs 1.3% (P = .09) for asymptomatic patients and 1.2% vs 1.6% (P = .604) for symptomatic patients. The 30-day mortality was 1.3% vs 0.6% (P = .04), and MI occurred in 1.4% of CEA vs 1.1% of CAS patients (P = .443). Cranial nerve injury occurred in 4.1% of the redo-CEA cases, and access site complications occurred in 5.3% of the CAS cases. CEA was associated with higher mortality at 30 days (adjusted odds ratio [aOR], 2.83; 95% confidence interval [CI], 1.13-7.14; P = .027) and at 1 year (adjusted hazard ratio, 2.17; 95% CI, 1.03-4.58; P = .042). However, there were no differences in postoperative stroke (aOR, 0.54; 95% CI, 0.20-1.45, P = .22), MI (aOR, 0.98; 95% CI, 0.31-3.10; P = .97), stroke/death (aOR, 1.38; 95% CI, 0.72-2.67; P = .22), and stroke/death/MI (aOR, 1.38; 95% CI, 0.80-2.37; P = .25) between CEA and CAS after adjusting for patient characteristics, and freedom from stroke at 1 year was also similar (CEA: 96.7% vs CAS: 96.4%; P = .78).

Conclusions

In this population-based study, we have shown higher mortality but similar stroke and MI associated with redo CEA compared with CAS after prior ipsilateral CEA. We recommend avoidance of redo CEA in very sick patients. Smoking cessation remains a potent target for improvement of outcomes of carotid revascularization in these patients.

AAA aortic surgery bypass carotid artery disease chewing gum complex AAA; FEVAR; BEVAR EVAR Ileus

Can chewing Gum be useful after surgery? well, there is a fairly good evidence now!

10/14/2016

Ref: BJS Oct 2016

Randomized clinical trial of chewing gum after laparoscopic colorectal resection

Chewing gum may enhance intestinal motility after surgery. This trial studied whether chewing gum could lead to a further reduction in ileus in patients who had a laparoscopic colorectal resection and followed an enhanced recovery programme.

Forty-one patients were randomized into each group. Thirty-seven patients underwent rectal resection and 45 had a colonic resection. Time to passage of flatus was shorter (18 versus 34 h; P = 0·007), first bowel motion occurred earlier (19 versus 44 h; P = 0·001) and time to feeling hungry was earlier (16 versus 25 h; P = 0·001) in the intervention group. There was no difference in the duration of hospital stay (5 days in the intervention group versus 5·5 days in the control group). No adverse events were attributed to chewing gum.

 

Chewing gum is probably a simple intervention that speeds intestinal transit in patients managed with a recovery programme after laparoscopic colorectal resection, but also can be used in other non-colorectal surgery such as vascular surgery. VERY NICE!!

Registration number: NCT02419586

carotid artery disease carotid disease

Would you operate on a mild (<50%) symptomatic carotid stenosis?

10/01/2016

Source: EJVES Sep 2016

According to the trials, NO …. but what would you do when the plaque is ‘vulnerable’? Well … this study from Sweden for three years showed that the recurrent rate for stroke is about 7% in 3 yrs in Symptomatic mild stenosis. This is too high.

The commentary on the article put very nice rules:

A combinations of mild (20–49%) and moderate (50–69%) percent stenosis with stable or unstable plaque morphology is given in the following 2 × 2 matrix.

The four combinations for recurrent stroke risk are:

  • (a) low % stenosis and stable plaque,
  • (b) low % stenosis and unstable plaque,
  • (c) moderate % stenosis and stable plaque, and
  • (d) moderate stenosis and unstable plaque.

One might predict that

  • (a) be strongly considered for current best medical therapy and that
  • (d) be recommended for CEA.
  • The optimal management outcomes for (b) and (c) are unknown and clearly deserve a trial.
  • If I had a TIA or minor stroke and (b), mild stenosis and an unstable plaque, I would strongly consider CEA.
  • In contrast, if I had (c), moderate stenosis, and stable plaque, I might choose current best medical management, unless I was already on it.

This is really interesting argument …

 

AAA aortic surgery complex AAA; FEVAR; BEVAR complex EVARs EVAR Spinal cord ischaemia

Protecting patients with complex aneurysm repair from paraplegia. Possible?

10/01/2016

Source: EJVES Sep 2016

The first large TEVAR series reported comparable neurological adverse events to open surgery, at ~ 30% of cases!

Bidirectional and reversible flow patterns in the longitudinal arteries suggest the existence of watershed zones. These are vulnerable whenever the arterial inflow becomes diminished, or if the collateral circulation becomes inadequate. Grey and white matter blood supply depends primarily on systemic and local blood pressure. Local spinal cord haemodynamics are also significantly influenced by venous drainage.

Delayed paraplegia is a complex phenomenon and probably follows aggravation of intraoperative subclinical spinal cord damage because of postoperative reductions in blood pressure, insufficient local haemodynamics, and reactive, inflammatory processes.

SCI is a multifactorial phenomenon where contributory factors vary within individuals, as well as interacting differently between individuals. Accordingly, the pragmatic approach (while accepting that many pathophysiological mechanisms remain unknown) is to revascularise as many inflow arteries as possible while also optimising haemodynamic management, cerebrospinal fluid (CSF) drainage, and strategies that aid the development of collateral arteries.

Approaches –

  • Monitoring motor evoked potential (MEP) – highly sensitive for assessing spinal cord function. If critical spinal cord perfusion is identified, then protective measures can be taken:

    • increasing mean arterial pressures

    • draining more CSF

    • restoring flow early to the internal iliac arteries

    • staging the procedure

    • MEP monitoring is a relatively complex technique, requiring dedicated and experienced neurophysiological support, and requires the procedure to be performed using no muscle relaxants. Spinal near-infrared spectroscopy might, however, become an alternative and easier technique for the future.14

  • Temporary aneurysm sac perfusion – during both open and endovascular repair of extensive TAAAs, staged repair has resulted in significant reductions in SCI.8

  • CSF drainage remains controversial.

    • A Cochrane review concluded that only limited data supported the role of CSF drainage.9

    • A recent meta-analysis demonstrated that CSF drainage decreased SCI by nearly half. However, this significant difference did not extend to patients who developed delayed paraplegia.10

    • Another systematic review reported an overall SCI rate less than 4%, with no difference between prophylactic CSF drainage and no drainage following TEVAR.11

    • Another recent study on endovascular TAAA repair reported a 16% rate of SCI, with no reduction using prophylactic CSF drainage, and CSF drainage was associated with a 6% rate of cranial hypotension syndrome.12

    • Despite these conflicting data, however, CSF drainage continues to be used by almost all aortic teams during TAAA repair.

  • Other methods –

    • Assessment of CSF biomarkers for neuronal injury. Recently, two biomarkers for axonal injury (T-tau and NFL) were shown to rise significantly in patients with postoperative SCI. Unfortunately, however, these biomarkers did not increase until after clinical signs of paraplegia had appeared.15

    • Regenerative medicine for spinal cord injury, mainly after trauma.16 Scientists expect to be able to regenerate injured spinal cord within a decade.

    • High-resolution computed tomography and magnetic resonance imaging allow anatomic assessment of crucial collateral pathways and can guide surgical and endovascular strategies. However, functional and dynamic information is lacking.

 

 

AAA AAA SCORE Frailty

Can we objectively measure ‘frailty’ in elderly population in preparation for a major vascular surgery? 

05/14/2016

REF. BJS Jan 16 special issue. Wiki on sarcopenia. 

We appearantly can, and this is how: 

Similarly to the 1996 World Health Organization (WHO) methodology for definitive diagnosis of osteoporosis, which uses DEXA, which uses a cut point of 2 standard deviations below the mean of DEXA results for gender specific healthy young adults to define osteoporosis. In here, we use a measure of lean mass rather than bone mineral density (BMD).  

The European society on clinical nutrition and metabolism special interest group on geriatric nutrition had a concerns us definition for sarcopenia: 

1) A low muscle mass, >2 standard deviations below that mean measured in young adults (aged 18–39 years in the 3rd NHANES population) of the same sex and ethnic background, and

2) Low gait speed (e.g. a walking speed below 0.8 m/s in the 4-m walking test).

Linda Fried / Johns Hopkins Frailty Criteria Edit

A popular approach to the assessment of geriatric frailty encompasses the assessment of five dimensions that are hypothesized to reflect systems whose impaired regulation underlies the syndrome. These five dimensions are:
unintentional weight loss,

exhaustion,

muscle weakness,

slowness while walking, and

low levels of activity.[1]

Corresponding to these dimensions are five specific criteria indicating adverse functioning, which are implemented using a combination of self-reported and performance-based measures. Those who meet at least three of the criteria are defined as “frail”, while those not matching any of the five criteria are defined as “robust”. 

The Bmj (based on research commissioned by  National Institute for Health Research (NIHR) under the Collaborations for Leadership in Applied Health Research and Care (CLAHRC) programme for North West London) provided another way of measuring fragility, as in the following figure: 


Authors in the BJS JAN 2016 measured the psoas as volume as a proxy for sarcopenia, and showed a significant predictive power to estimate the risk of frailty on patients undergoing major HBP surgery.

Nhs England has produced a document on how to measure frailty and how to provide a better care to elderly population. 

Thrombolysis Uncategorized

Is it necessary to admit patients to level 2 care to administer intraarterial catheter-directed thrombolysis?

05/13/2016

Ref. EJVES MAY 2016- Type: cohort study

This cohort study says NO. The outcome of 252 patients treated with thrombolysis was not different on the site of admission: 

There were no differences in the frequency of non-bleeding related complications between Centre 1 and Centre 2. Patients on the vascular ward had a higher frequency of minor bleeding (p = .002) but there was no difference in major bleeding (p = .12). Eleven patients on the ward required an increased level of care for medical reasons and six were moved for a lack of resources. The presence of cardiac disease was an independent risk factor for patient transfer (OR 3.2; 95% CI 1.04–9.8, p = .04).

claudication; bypass; angioplasty; Uncategorized

Adjuvant AV fistula in high risk lower limb bypass surgery: is it useful?

05/13/2016

Ref. EJVES MAY 2016

It is well described and well know; yet again, there is no evidence that it helps in improving latency rate. Things are slightly different on using a synthetic graft. It appears that the patency rate improves primarily (as compared to secondary intervention)

Two randomised controlled trials and seven retrospective cohort studies comprising 966 participants were included. Pooled standardized data showed no difference in primary graft patency (pooled RR = 1.25, 95% CI 0.73–2.16), secondary patency (pooled RR = 1.16, 95% CI 0.82–1.66), or limb salvage at 12-months (pooled RR = 1.13, 95% CI 0.80–1.60) for the peripheral bypass with AVF group compared with peripheral bypass alone. Subgroup analysis indicated a reduction in reintervention rates associated with AVF when performed in conjunction with a synthetic graft (pooled RR = 0.55, 95% CI 0.30–0.98).

AAA ruptured aneurysm Uncategorized

Ruptured AAA are NOT necessarily associated with coagulopathy

05/13/2016

Ref. EJVES MAY 2016

This is the first systematic review of this kind. Very interesting findings. 

Seven studies, comprising 461 patients were included in this systematic review. Overall weighted prevalence of coagulopathy was 12.3% (95% CI 10.7–13.9), 11.7% for INR (95% CI 1–31.6), 10.1% for platelet count (95% CI 1–26.8), and 11.1% for aPTT (95% CI 0.78–31). Fibrinogen serum concentration level was normal in 97%, and 46.2% (n = 55) of patients had elevated D-dimer. Only 6% of the entire population demonstrated significant coagulopathy. DIC was noted in 2.4% of the population.

So the question is: do you consider heparin for those patients? 

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