UMEM Educational Pearls - Vascular

Bleeding Dialysis Fistula?

Ever see a patient in the ED c/o "my fistula won't stop bleeding"? If you haven't, you probably will in the future.

Here are some helpful tips on getting these bad boys to stop oozing:

• Local pressure for 10 minutes will stop many of these bleeders
• Can also try locally applied gel foam/thrombin
• Pharmacologic adjuncts may be required, especially if the patient has missed dialysis-DDAVP can be given (makes platelets stickier by causing endothelial cells to release von Willibrand Factor). You can also give platelets, since platelets don't work well in a uremic state. Many dialysis patients are on coumadin because of chronic line clots, so don't forget to reverse this if present
• Probably as a last resort you can tie a superficial circular suture at the puncture site. This works quite well.

Pulmonary Embolism-Myths and Misconceptions

Just wanted to mention a few myths/misconceptions about acute PE that I have recently heard discussed in the ED.

1. Emergency physicians have to "get help" to give thrombolytic therapy. Sure it makes sense that we consult critical care and perhaps interventional radiology in some cases. But we do not need permission to use this drug by ourselves if indicated. Consider using lytics ESPECIALLY if the patient is unstable or if there is evidence of RV dysfunction (elevated troponin, echo criteria for dysfunction, or CT with large RV and bowing of the septum). What about the patient with RV dysfunction and a normal BP? Evidence is mounting that lytics are indicated to reduce the severity of pulmonary hypertension. 

2. "Just get a d-dimer." Be very careful. Lots of false positives. D-dimer often clouds the picture more often than not. 

3. "The mortality rate of missed PE is high." Often quoted as a 30%+ mortality rate if missed. Recent data suggests that it is < 5%. 

Can you use a serum d-dimer to rule out aortic dissection?

The answer to the question, in 2010, is no.  

There has been a flurry of recent literature about the use of serum d-dimer to rule out aortic dissection. Some studies have shown a sensitivity of nearly 100%, but other studies have shown sensitivities of only 60-70%....pretty abysmal sensitivities. And despite some of the authorities on the subject touting how good the test is, there is not firm literature to support it. Better yet, there are some active medical malpractice cases I am aware of in which the diagnosis of aortic dissection was missed based on a "negative d-dimer."

My suggestion, and the vascular pearl for the day, is to avoid using d-dimer as a aortic dissection rule out strategy until good evidence (if it ever becomes available) exists. I know that people are using this test to rule out the disease, just realize that EVERY time I have ever given a talk on acute aortic disasters, 2-3 people from the audience always share that they had a case of a "d-dimer negative dissection." 

Be careful....

Evaluation of the acutely ischemic limb

Some considerations when evaluating/treating patients with acute limb ischemia:

• Strongly consider anticoagulation (usually with Heparin) early
• Consider the source of the ischemia (LV/LA thrombus, AAA mural thrombus, in situ limb thrombosis)
• Always consider aortic dissection as an etiology of acute limb ischemia (chest pain and leg ischemia)
• Early vascular consult and/or transfer
• Obtain bedside ABIs on suspected cases and remember that diabetics may have normal to falsely elevated ABIs secondary to calcified vessels.
• Common theme in laws suits for missed or delayed cases of limb ischemia: failure to perform and document ABIs

How to stop dialysis fistula/graft bleeding

The number of patients being placed on hemodialysis seems to be increasing. And the ED is where they will go when there is a any complication from their fistula or graft.

Hemodialysis shunts require cannulation with large bore instruments. This combined with heparinization may lead to prolonged bleeding from puncture sites. 

What to do when a patient shows up in the ED with persistent bleeding from a fistula puncture site:

• Simple pressure may be all that is required in many cases. 
• If this doesn't work, place a single circular suture around the puncture site/incision. In some small studies this has been shown to be very useful in stopping persistent oozing

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Effort Thrombosis

Effort thrombosis, also called Paget von Schrotter disease, occurs when either the axillary and or subclavian veins thrombose. The condition is more common in young, healthy (>males) patients and presents with the usual DVT symptoms of arm pain, swelling, and pain.

The disease was originally described in patients performing vigorous activities, like weight lifting or repetitive over-the-head lifting. This type of activity has been reported to kink the subclavian vein and lead to clot formation.

Diagnosis and therapy is the same for any other type of DVT.

A varicocele is a collection of venous varicosities in the spermatic veins in the scrotum. This is caused by imcomplete drainage for the pampiniform plexus. This may be seen is up 20% of males and is asymptomatic most of the time. Most are found on the left side.

Why should you care, you might ask? Well, the right spermatic vein drains into the IVC and then into the renal vein, whereas the left spermatic vein drain drains directly into the renal vein.

In the patient with new onset, unilateral varicocele, consider an IVC thrombus/tumor if right sided and a left renal clot if left sided.

A case we had recently was a 30 yo male with nephrotic syndrome (a HUGE risk factor for renal vein thrombosis) who presented with left-sided scrotal swelling. He was found to have a left-sided varicocele. Based on this finding, a renal sono was performed and the diagnosis of left renal vein thrombosis was made.

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Got some interesting info today on the costs of some commonly used antihypertensive medications. Keep in mind that in patients with severe hypertension, your options of IV drips are limited.

Here is some info from our hospital:

Fenoldopam - $113.28
Nicardipine - $94.67
Esmolol - $82.15
Nitroprusside - $20.86
Labetalol - $14.40
Nitroglycerin - $2.90

Although Fenoldopam (Corlopam), which has been around for years, is more expensive than Nitroprusside, it is just as effective and without the side effects.

A new drug on the market that we don't have yet, Clevidipine, is just as effective as the big guns Nipride and Fenoldopam. Costs at this point are unknown.

More on antihypertensive medications next week....

Painless thoracic aortic dissection (TAD) and syncope

Patients with TAD do not always present with chest pain. In the International Registry of Aortic Dissection (IRAD) study, 2.2% of TAD cases were painless and approximately 13% of TAD cases presented with isolated syncope (i.e. NO PAIN). Other studies have shown that as many as 15% of TAD cases are painless.

Patients with TAD may present after a syncopal episode. The underlying pathophysiology of syncope is related to proximal rupture into the pericardium with resultant tamponade.

Add TAD to your differential diagnosis of unexplained syncope, especially in older folks and especially if a patient "looks bad" and you don't have a reason.

Unusual Presentations of AAA

Many unusual presentations of AAA have been reported in the literature and include:

• Musculoskeletal complaints (thigh or groin pain)
• Bilateral testicular pain
• Unexplained inguinal pain-VERY well described
• Femoral neuropathy
• Abdominal pain and urge to deficate (and, NO, I am not making that one up)

One more note on the whole urge to deficate thing: any thing that leads to hemoperitoneum may cause this strange complaint (ruptured AAA, ruptured ectopic pregnancy).

Beware of older patients with groin pain!

Lower abdominal pain (mimicking diverticulitis) and isolated groin/hip pain are relatively common presentations of AAA and iliac artery aneurysm and rupture. As many as 15-20% of symptomatic AAAs wil present with hip and/or groin pain.

Bottom line: AAA and iliac artery aneurysm should at the very least be considered in older patients (and in patients with vascular disease) who present with unexplained groin/hip pain.

New Antihypertensive agent coming our way...

Well, we have nitroprusside, labetalol, nicardipine, fenoldopam, etc. Say hello to a new drug that is "reported" to be a great drug for ED patients with severe hypertension (emergencies)....Clevipidine (Cleviprex).

Clevidipine is an ultrashort acting calcium channel blocker that has been found to be a powerful antihypertensive medication.

Unique properties of the drug:

• Very short half life-quick on, quick off
• Not affected by renal/liver disease-drug is broken down into inactive metabolites by plasma esterases
• Reportedly as effective as nitroprusside and the other big guns we have for severe hypertension
• Starting dose is 1-2 mg/hour and can titrate up every 1-2 minutes.
• Contraindicated in patients with allergies to soy products and egg products

Remains to be seen if this drug will play in a role in the treatment of our severely hypertensive patients....stay tuned...

Hypertensive Encephalopathy

Hypertensive encephalopathy (HE) is one of the true hypertensive emergencies. Although usually seen with diastolic BPs greater than 120 mm Hg, it can occur in patients with lower numbers. And the diagnosis can be really tricky to make. Sometimes the diagnosis isn't clear until symptoms resolve from BP reduction .

The presentation is variable and includes:

• Seizures
• Altered mental status
• Coma
• Vomiting

The goal of treatment is to reduce the BP NO MORE THAN 25% (of the MAP) within the first few hours. In addition, drugs like Hydralazine (which may lead to a precipitous decline in BP) and Clonidine (which can alter mental status) should be avoided.

Medications to consider for treating HE include intravenous drips-Fenoldopam, Nicardipine, Labetalol. Drugs like Nipride are probably best avoided since cyanide toxicity may alter a patient's mental status further.

Transvenous pacing

We had a very interesting case the other day in the ED. A 60 yo male presented after a syncopal episode. After arriving in the ED he was awake (with a pulse of 50) but then became asystolic, without warning. He then woke up and 10 minutes later became asystolic again. He then woke up again. So, we decided to put in a transvenous pacer.

Some considerations when putting in a transvenous pacer:

• You need to use a small cordis (e.g. 6 French)
• Right IJ is the preferred approach so that when the balloon is inflated you will have easy entry into the right heart
• You will need transvenous pacing wires, obviously.
• Once you open the wire kit, you will find 2 adaptors that fit over the two ports of the pacemaker wire. Snap them on, then these connect to the ventricular leads of the pacer box-ignore the atrial side. Here is the key: the POSITIVE lead connects to the PROXIMAL port on the pacemaker (PROXIMAL=POSITIVE) and the distal lead connects to the distal port.
• Turn the pacer on then set rate to 80 or so. And start the mAmp at 20.
• Advance the wire through the Cordis and after the wire has cleared the Cordis, blow up the balloon with a syringe and lock it.
• The key is in determining capture: While the patient is on the monitor, and as the wire is being slowly advanced, look for pacer spikes and the development of wide complexes. This indicates electrical capture. Be sure to check for mechanical capture by checking the patient's pulse.
• After capture, the mAmps can be turned down to the capture point.
• DON'T forget that transcutaneous pacing is clearly the first option as this is easy to initiate.

Risk of PE/DVT in patients with microalbuminuria....another risk factor to consider??

Microalbuminuria (protein in the urine) is a known risk factor for arterial thromboembolic disease, and recent studies suggest that arterial thromboembolism and venous thromboembolism (VTE) have common risk factors. In a prospective community-based cohort study in the Netherlands, researchers enrolled 8574 adults (age range, 28-75) who were followed for 9 years. People with insulin-dependent diabetes or pregnancy were excluded.

Of 129 identified episodes of VTE, roughly half were deep venous
thromboses, and half were pulmonary embolisms. The annual VTE incidence
rate was 0.12% in patients with normoalbuminuria (<30 mg/24 hours)
versus 0.40% in those with microalbuminuria. After adjustment for known VTE
risk factors and other factors (including hypertension, known coronary arterydisease, and elevated C-reactive protein level), the hazard ratio for
VTE in people who had microalbuminuria, compared with those who had
normoalbuminuria, was 2.0.

Comment: The importance of this study is not in the clinical value of
usingmicroalbuminuria as a marker for VTE risk, because the absolute risk
conferred by microalbuminuria is very low, and the therapeutic
implicationsare unclear. Rather, this study suggests that microalbuminuria is a
marker for endothelial dysfunction in both arterial and venous systems, and it
suggests a mechanism for how statins interact with the endothelium to
prevent VTE (JW Cardiol Mar 29 2009).

So, does this affect us as emergency physician? Unclear. But it may very well mean that we might be dealing with a new risk factor that needs to be taken into consideration when evaluating patients with chest pain or SOB. Obviously, we might need medical records to find this risk factor...can you imagine asking a patient if they have microalbuminuria?

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Nitroprusside-Friend or Foe?

Nitroprusside is a direct venous and arteriolar vasodilator and is very effective at lowering blood pressure. It has been used for the treatment of hypertensive emergencies for many years and most of are comfortable with using it.

The problems with the drug:

• May cause precipitous drops in BP and lead to overshoot of BP target goals
• The drug is inactivated by light so the infusion bag and tubing must be protected  from light
• Frequently causes nausea, vomiting, and muscle twitching
• Most importantly, cyanide (CN) is released from nitroprusside in a dose-dependent fashion and may cause clinical toxicity
• Good alternatives exist: Fenoldopam as an example. Just as effective and without any of these side effects.

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Follow-up for the Hypertensive Patient

We see hypertensive patients every day, every shift. And, we discharge many of them. So, when do you get them follow-up?

The JNC-7 recommends that patients with BPs > 180/110 mm Hg have follow-up within 7 days. Like most of the HTN recommendations in the primary care setting, this recommendation is based on a "smart person" concensus....and no data.

This is a tremendous issue for us in the ED, because we don't want to see a bad outcome in our discharged hypertensive patients.

Some pearls regarding discharging the very hypertensive (but asymtomatic) patient:

• Since there isn't any realy data on follow-up, it would be wise to use caution and have very high BPs checked the next day and to NOT wait a week.
• Discharge instructions should note when/where (if you have to...use the ED as a recheck) the patient is to follow-up
• ALWAYS warn patients about what can/will happen if they don't seek follow-up: MI, stroke, renal failure/need for dialysis, death, and disability and write this in the chart. The last thing you want to hear is that the patient went on to develop renal failure/stroke, etc. and that they claim they were not warned about what could happen.
• When it is possible, contact the patient's doctor to discuss management

Evaluation of End Organ Damage in Hypertensive Patients

No evidence to date supports the ED workup for end-organ damage in asymptomatic hypertensive patients.

End-Organ Damage Pearls:

• Rarely, if ever, will an aimless search for lab abnormalities lead to any clinically meaningful change in patient management
• An elevated creatinine does NOT define acute, end-organ damage. Most of the time it is due to the effects of chronic hypertension.
• There is some evidence that a UA that has BOTH no protein and no red cells predicts a normal creatinine. The studies that have looked at this, however, are very small. Also, HTN in and of itself may cause some protein leak, even in the setting of normal renal function
• A CXR and/or ECG is not needed in an asymptomatic patient.
• Prompt followup is always necessary especially if no ED workup is started. All of this can be dome in the primary care doctor's office.

Bleeding AV Fistulas

It is not an uncommon complaint for dialysis patients to present with bleeding from their fistula.  They can lose a large amount of blood in a short period of time if not treated promptly, and if treated too agressive their fistula can clot off. Some tips on how to control the bleeding.

Most of the bleeding occurs at the site that the needle puntured the fistula. If it is due to an ulcer eroding into the fistula these tips may not be effective.

• The easiest and safest way to control the bleeding is with simple diret pressure directly over the site of bleeding with a single finger. No guaze.  [Gown up and wear goggles or eye protection]. The use of a big wad of guaze or a pressure dressing tends to just hide the continued bleeding or result in the clotting off of the fistula.
• Injecting lidocaine with epinephrine at the site can also help and helps set you up for the next step,
• A figure eight stitch at the puncture site can help close the puncture wound.
• Of course you should call your vascular surgeon if you are having trouble controlling the bleeding, want close follow up or finger is going numb from holding pressure.

I typically check a CBC and coags.  Once the bleeding is controlled observe the patient for awhile [typically the hour to hour and half to get the labs back] and then road test them with a walk around the Emergency Department to ensure it does not start bleeding again.

BEWARE sudden onset thoracic back pain

Just reviewed a case last week of a person who presented with back pain (thoracic) as the sole manifestation of an aortic dissection. No chest pain, belly pain, etc. JUST severe, acute, thoracic back pain.

Keys to staying out of trouble:

• Any sudden onset pain should be explained. Musculoskeletal pain doesn't normally present like this. Look for risk factors like HTN. If a person with HTN (even if not that high in the ED) presents with acute, severe, thoracic back pain the diagnosis of dissection should at the very least be considered.
• The key to making the diagnosis begins with thinking about the diagnosis.
• At the very least, include aortic dissection in EVERY patient you see with back pain, especially if sudden onset. I am not talking about the 95%+ people who don't really have anything wrong with them and who stumble into urgent care asking (begging) for Percocet.
• Sudden onset back pain should also prompt consideration for a AAA
• Just like all else in Emergency Medicine, always ask yourself if a "worst case scenario" could be present?, and the list for acute back pain is pretty short: dissection, AAA, fracture (by history), cancer, infection. Most of these, however, do not present acutely.

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