Tag Archives: vascular

blood pressure targets (strokes, bleeds, and tears)

15 Sep

 

Adapted from an old post, but a good refresher that came up again recently, with a new little table from a recent emed journal article that includes some recommendations for BP targets in stroke (ischemic or otherwise):

neuroBP

 

(and from a previous post):

IS SOMETHING BLEEDING (OR ABOUT TO)?  MINIMIZE THE DAMAGE:

ICH:

–lowering to SBP 140-160 probably safe

–theory: less/slower hematoma growth

–options: nicardipine (less cerebral vasospasm)

 

AORTIC DISSECTION:

SBP 100-120, HR <60

–theory: reduce shear forces

–options: beta blocker (labetolol push, esmolol drip), nitroprusside

 

RUPTURED AAA:

–goal SBP 80-100

–theory: permissive hypotension; bleed slower, less likely to blow out the few clots they’re making

Reference(s): emed-journal articleuptodate.com: Ruptured abdominal aortic aneurysm, management of aortic dissection, Spontaneous intracerebral hemorrhage: Prognosis and treatment, Kodama K, et al. Tight heart rate control reduces secondary adverse events in patients with type B acute aortic dissection, picture

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ACUTE LIMB ISCHEMIA

14 Jul

manifests as:

  • ischemic rest pain
  • ischemic ulcers
  • gangrene

 

ETIOLOGY 

  • Embolus from a proximal source lodging into a more distal vessel
  • dissection of an artery or direct trauma to an artery

 

RISK FACTORS

  • atrial fibrillation,
  • Recent myocardial infarction
  • Aortic atherosclerosis,
  • aneurysmal disease (eg, aortic aneurysm, popliteal aneurysm)
  • Prior lower extremity revascularization (angioplasty/stent, bypass graft),
  • Risk factors for aortic dissection (HTN, etc)
  • Arterial trauma
  • Deep vein thrombosis (paradoxical embolism)
  • left ventricular dysfunction
  • debris from prosthetic valves and infected cardiac valves (septic emboli)

 

Arterial Trauma — Acute arterial occlusion following interventional procedures has become a more frequent cause — the incidence of arterial complications following interventional cardiac catheterization is ~1.5 to 9 percent 

 

6 P’s

  • paresthesia,
  • pain,
  • pallor,
  • pulselessness,
  • poikilothermia,
  • paralysis

 

Variations Blue toe syndrome — sudden appearance of a cool, painful, cyanotic toe(s) or forefoot in the often perplexing presence of strong pedal pulses and a warm foot.  The blue toe syndrome is usually due to embolic occlusion of digital arteries with atherothrombotic material from proximal arterial sources.

IMAGING 

First LineComputed tomographic angiography with runoff, noninvasive duplex ultrasonography, or magnetic resonance angiography

 

MANAGEMENT

intravenous heparin bolus followed by a continuous heparin infusion 

Preoperative eval, including blood tests (PT/PTT, CBC) and electrocardiography (ECG)

Surgical thromboembolectomy and bypass grafting – Were the mainstays of therapy for many years. Subsequently, thrombolytic therapy and percutaneous transluminal angioplasty (PTA) have become treatment options for selected patients. 

Consult Vascular Surgery.

Submitted by Christina Brown.

 

References: uptodate.com, Norgren L, Hiatt WR, Dormandy JA, et al. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). J Vasc Surg 2007; 45 Suppl S:S5Nasser TK, Mohler ER 3rd, Wilensky RL, Hathaway DR. Peripheral vascular complications following coronary interventional procedures. Clin Cardiol 1995; 18:609.Alonso-Coello P, Bellmunt S, McGorrian C, et al. Antithrombotic therapy in peripheral artery disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012; 141:e669S.Yeager RA, Moneta GL, Taylor LM Jr, et al. Surgical management of severe acute lower extremity ischemia. J Vasc Surg 1992; 15:385.; picture 

Quick Hit: D-Dimer false positives

30 Jun

Thinking about ordering a D-Dimer for PE rule-out? What are the clinical conditions to consider thatmay make your D-Dimer falsely elevated?

  • Myocardial infarction
  • Stroke
  • Atrial fibrillation
  • Preeclampsia and eclampsia
  • Cardiovascular disease
  • Congestive heart failure
  • Severe infection
  • Surgery/trauma
  • Sickle cell disease
  • Severe liver disease (decreased clearance)
  • Malignancy
  • Renal disease
  • Pregnancy

 

Source: uptodate.com; picture

 

Submitted by K Estes.

Catheter-related upper extremity DVT

26 Mar

QUICK PEARLS:

The majority (70-80%) of thrombotic events in the upper extremity deep veins (subclavian, axillary, brachial) occur in the presence of IV catheters.

 

Any catheter has the potential to cause thrombosis. Think about PIV, PICC, tunneled and non-tunneled central catheters, ports and pacemakers.

 

In addition to the classic risk factors that you commonly consider for DVT (prior surgery, malignancy, h/o DVT, etc.), specifically catheter-associated thrombosis is more likely with:

large-diameter catheters (more likely to have stagnate blood v. free flowing)

PICC as compared to centrally placed catheters

-catheter malposition (In one study, DVT developed in 46% of patients whose catheter tip was in the innominate vein or junction of the immoninate vein with the SVC, compared with 6% of patients with a properly positioned catheter)

-chemical irritation (potassium chloride, antibiotics such as vancomycin, diazepam, hypotonic and hypertonic electrolyte solutions)

 

Clinical presentation: inability to withdraw blood, phlebitis, extremity edema

 

Diagnosis is made with Doppler ultrasound.

 

Treatment involves observation, anticoagulation to prevent embolization, and removal of the catheter. Prophylactic systemic anticoagulation is not routinely recommended in this population.

 

Submitted by K Estes.

 

References:  Luciani, et. Al. Catheter-related upper extremity deep venous thrombosis in cancer patients: a prospective study based on Doppler US. Radiology. 2001;220(3):655. PMID 11526263

Uptodate.com; picture

strength in numbers: aortic dissection

24 Feb

just to scare you, and/or keep you on your toes (from the Oct/Nov EMRA mag):

5% of acute aortic dissections will NOT have associated pain

 

38% will NOT have a widened mediastinum on CXR

 

12% will have syncope

 

2-5% have concurrent MI (proximal dissection into the RCA)

 

up to 30% have acute neuro deficits

 

References: EMRA article, picture

 

aortoenteric fistula: fear it

13 Oct

QUICK PEARLS:

Aortoenteric fistula: a communication between the aorta and the GI tract

consider in anyone with a GI bleed and a history of aortic surgery.

Can involve any part of the bowel but 75% involve the third part of the duodenum.

Mean time to presentation from surgical date is 32 months, but can run the gamut.

 

Can be primary (from AAA, but this is rare), but often related to aortic graft

 

Herald Bleeds

  • often have self-limited “herald bleeds”, can be intermittent
  • Stops from vasospasm or thrombus formation
  • Followed by massive GI bleed over the next month; 30% of these are within next 6 hours

 

DIAGNOSIS:

  • Conventional CT
  • CTA (most sensitive with “detection rate” of 61%)
  • EGD (25-62.5% or primary fistulas are identified)
  • Laparotomy

 

TREATMENT OPTIONS:

  • Endovascular stent for those than cannot tolerate surgery
  • Graft resection, repair of duodenal wall, and new bypass (mortality rate: 30-40%)
  • Gentle resuscitation: SBP goal 60-100
  • Survival rates with treatment: 30-70%

 

References:  MacDougall, L et al. Aorto-enteric fistulas: a cause of gastrointestinal bleeding not to be missed.  BJMP. 2010; 3(2): 317.   Ranasinghe, W et al. Primary aortoenteric fistulae: the challenges in diagnosis and review of treatment. Ann Vasc Surg. 2011; 25(3): 386; picture

Mesenteric Ischemia: quick review

22 Sep

What is it?

A reduction in intestinal blood flow, due to

arterial occlusion, usually SMA (85-95%)

nonocclusive ischemia/hypoperfusion, usually related to low cardiac output (20-30%)

-venous occlusion, usually SMV (5%)

 

 

What are the risk factors?

Advanced age, atherosclerosis, low cardiac output states, cardiac arrhythmias, cardiac valvular disease, recent MI, and intra-abdominal malignancy

 

In younger patients, mesenteric venous thrombosis is the major cause of ischemia

 

 

How does it present?

Rapid onset of severe periumbilical abdominal pain out of proportion to physical exam findings, +/- associated nausea and vomiting

 

Be cautious of a more insidious presentation for venous thrombosis; pain may be present for several days to weeks

 

 

How is it diagnosed?

Mostly clinical suspicion

 

A personal history of previous embolism is present in 1/3 of patients with acute embolic mesenteric ischemia; a personal or family history of DVT or PE is present in ½ of patients with acute mesenteric venous thrombosis

 

Lactate is 100% sensitive, 42% specific for intestinal ischemia/infarction

 

CT angiography (CTA) should be done without oral contrast (to avoid obscuring mesenteric vessels) shows findings of acute ischemia:

-bowel wall thickening

-intestinal pneumatosis with portal venous gas

-bowel dilation

-mesenteric stranding

-portomesenteric thrombosis

-solid organ infarction

 

What is the treatment?

Systemic anticoagulation +/- surgery (embolectomy, thrombectomy, bowel resection)

 

Anticoagulation alone may be reasonable in patients with good collateral blood flow

 

Consider hypercoaguable workup for venous thrombosis.

 

 

Submitted by K Estes.

 

Source: uptodate.com; picture