Thrombolytic infusion for occluded central venous catheters

For patients with long-term indwelling central venous catheters (dialysis catheters, Hickmans, etc) who develop catheter occlusion, consider infusion of thrombolytic therapy for catheter salvage.

How do you do it, you ask?

• Infuse 2 mg of tPA through the affected port
• Can also use Urokinase if this is all you have

This treatment is very safe and is well tolerated.

Journal of Vascular Access, 2006

The PERC Rules revisted

How can I rule out PE without ANY testing, you ask? Do I have to get a d-dimer on that low risk patient?

Do these things keep you up at night like they do me?

Consider using the PERC rule (Pulmonary Embolism Rule Out Criteria)

This set of rules was mentioned in an earlier pearl, but there are now 3 large studies (and one on the way) that validate the use of these rules.

So, if you have a patient who is LOW risk for PE but you would like to document something in the chart that proves you thought about the diagnosis and clinically ruled it out:

If the patient is LOW risk for PE by your clinical gestalt and if the answer to ALL of the following questions is YES, then the patient is considered PERC negative:

• Age < 50 years
• Pulse < 100 bpm
• SpO2 > 95%
• No unilateral leg swelling
• No hemoptysis
• No recent trauma or surgery
• No prior PE or DVT
• No hormone use

PERC negative + Low Risk clinical gestalt = PE ruled out

Caution!

• Most people are comfortable with: LOW risk + negative d-dimer = PE ruled out but use of the PERC rules has not gained wide acceptance yet. Experts in this area predict this will change.
• Clinical gestalt must be used and the patient must be LOW risk for PE
• The PERC rule is not intended for use in moderate risk patients or in patients without an alternative diagnosis.
• The rule is really only intended to avoid testing in the patient you were really not thinking about PE in the first place. Some experts agree that writing "PERC negative" in the chart is defensible.

Jeff Kline, PERC rule. Journal of Thrombosis and Hemostasis. 2007/2008

Secondary Causes of Hypertension

Although not that common, consider the following (with accompanying history and/or physical examination findings) in patients with hypertension:

• Renovascular hypertension (renal artery stenosis)-abdominal bruits, older patients
• Pheochromocytoma-episodic flushing, htn, headache, new onset htn in younger patient
• Cushing's disease-abdominal striae (not very specific in Baltimore), new onset hyperglycemia, classic electrolyte abnormality: hypokalemic metabolic alkalosis
• Primary Aldosteronism-new onset htn and hypokalemia
• Hyperparathyroidism-htn and hypercalcemia
• Aortic coarctation-younger patients (even young adulthood), unequal upper and lower extremity blood pressures
• Sleep apnea-typically obese patients (but not necessarily), excessive snoring, day time sleepiness (again, not specific)
• Thyroid disease (hypo or hyper)-signs and symptoms of thyroid disease

Although most of the time the patient will end up having essential hypertension, these entities should at the very least be considered.

Journal of Hypertension 2007

Subarachnoid hemorrhage: Unilateral or bilateral headache?

Pretty good evidence exists that most patients with subarachnoid hemorrhage will have a bilateral headache.

In fact, unilateral headache is helpful in the history in ruling out SAH in most cases. Presence of an unruptured aneurysm, however can be present with a unilateral headache.

J NeuroSurg 2006

ECG gating CTs for aortic dissection/aneurysm rule out

• Increasing evidence supports the use of ECG gating when performing CTs to rule out aortic pathology-dissection and aneurysm.
• The most common artifact on CT is a "psuedo-dissection" flap caused by excessive motion at the aortic root. Administering beta blockers before CT will limit this motion and decrease the chance of this false positive.

AJR 2007

A few pearls regarding Acute Aortic Dissection...

• CXR has been shown to have an overall sensitivity of only 67%!
• Recent literature and a large, recently published, authoratative book by one of the world's leading authorities on aortic dissection support the notion that a negative highly sensitive d-dimer rules out aortic dissection.
• CT scan is the test of choice, but be aware that many authorities are starting to recommend beta blockade before CT to reduce the most common artifact, motion at the aortic root that simulates a dissection flap
• MRI and TTE are reasonable alternatives if a CT can not be ontained
• The most common theme found in malpractice claims against emergency physicians is failure to address the combination of chest/back, back/abdominal pain.

Elefteriades. Acute Aortic Disorders. 2007

 

Patients with aortic dissection (Type A or B) who develop intestinal/renal, etc. ischemia should be considered for aortic fenestration-a procedure in which holes are literally created in the aortic lumen to connect the true and false lumen-this allows perfusion of the involved vessel to occur from true lumen into the false lumen into the involved vessel.

Patients with large vessel malperfusion have a VERY HIGH mortality rate, AND most CT surgeons will not operate even on a Type A unless the involved vessels have been opened up.

This procedure is useful when major vessels (SMA as an example) branch from the aortic false lumen.

So, when to consider this procedure:

• Aortic Dissection (A or B) with severe abdominal pain, elevated lactate, OR imaging study showing malperfusion to a vessel (SMA, renal, etc)
• Most of the time in the ED we will see this on CT in a sick patient.

Who do you call?

• Vascular Surgery and IR-normally perormed percutaneously via a femoral approach

Remember that PE can clinically look exactly like pneumonia:

Both can present with:

• Cough
• Pleuritic chest pain
• Leukocytosis (WBC as high as 20-30)
• Elevated temperature (as high as 105F!)
• CXR that "looks" like pneumonia
• Both can present acutely

Be afraid, be very, very afraid....

Splenic Artery Aneurysm

• According to autopsy studies, splanchnic artery aneurysms (spleen, celiac, etc.) may be more frequent than AAA
• Most asymptomatic and detected incidentally on CT
• Splenic artery aneurysms most common splanchnic aneurysm
• With increased use of abdominal CT, emergency physicians will be seeing this diagnosis more often

Who cares, you ask?

• Splanchnic artery aneurysms are at risk for rupture
• This type of vascular abnormality will be discovered more often because of increased CT use
• Aneurysms > 2cm indication for repair
• Consider consultation and /or expeditious followup if this is encountered
• May be treated with catheter embolization or surgery

Degree of D-Dimer elevation and Mortality Rates

Evidence now exists that links the degree of D-Dimer elevation with mortality rate. The higher the D-Dimer, the higher the PE mortality rate.

Consider this when risk stratifying patients with PE. This adds to our use of biomarkers for risk stratification. Elevation of BNP, D-Dimer, and Troponins have been shown to predict mortality.

 

 

Blue Toe Syndrome

This syndrome refers to acute digital ischemia caused by athero-microembolism and is associated with cool, painful, cyanotic toes in the presence of palpable distal pulses.

Presence of this syndrome should prompt the Emergency Physician to search for the proximal source. Failure to identify the source and aggressively treat may lead to limb loss.

Common etiologies include:

• AAA
• Iliac artery aneurysm
• Popliteal artery aneurysm

 

There is no good evidence for what type of workup an asymptomatic hypertensive patient should get in the ED.  An ECG is likely to show LVH, a cxr will be normal in most cases, and many patients will have some degree of proteinuria.

So, what is a safe and reasonable strategy to workup these patients?

• Consider checking a serum creatinine. I say consider because even this recommendation isn't terribly evidence-based. Elevated creatinine may NOT indicate that a hypertensive emergency is present, but if the creatinine is elevated it might persuade you to choose a different antihypertensive agent (HCTZ won't lower BP effectively if the creatinine near 2.0, and many of us would be a little hesitant to start an ACE-I if the creatinine is elevated). Although there is one study that showed absence of proteinuria and hematuria was correlated with a normal serum creatinine, many patients with asymptomatic HTN will have proteinuria.
• Repeat the BP several times. One study has shown that as many as 1/3 of patients with high BP in the ED do not have elevated BP when followed up as an outpatient. Many patients' BPs will spontaneously decline (regression to the mean).
• In the asymptomatic patient a CXR and ECG will likely not help you manage a patient, so don't waste your time and the patient's money getting it.

American College of Emergency Physicians 2006 Guidelines on the evaluation of asymptomatic HTN.

 

 

Suspect an aortoenteric fistula in patients who present with an upper GI bleed if they have ever had a AAA repair. This occurs when a fistula forms between the abdominal aorta and the GI tract (most commonly the duodenum). Patients may present stable or may present critically-ill. Unstable patients with an upper GI bleed and a history of AAA repair should proceed to the OR for laparotomy.

Stable patient may undergo CT scanning and/or endoscopy. Bottom line: If a patient with a history of AAA repair presents with an upper GI bleed, rally your troops (GI, Surgery, etc) ASAP and don't mess around. If you are wrong, and the patient doesn't have a fistula, no big deal. If you are wrong, and the patient does have a fistula, the patient may very well die on you as you struggle to get a regular ICU bed.

 

 

Surgical repair of thoracic aortic aneurysms is generally dictated by size. Aneurysms need repair to prevent rupture. Anything over 6 cm (which is the magic number , according to authorities) will make almost all cardiothoracic surgeons anxious. -For non-marfans patients Most cardiac surgeons will use a cut off for surgery of: ascending aorta > 5.5 cm and descending aorta > 6.5 cm -Patients with Marfans: Threshold to operate is a bit lower. ascending >5 cm and descending > 6 cm So, who cares, you ask? #1-We scan a lot of chests and we will be diagnosing this in the ED. #2-As emergency physicians we should have some familiarity with the aortic size that makes Cardiothoracic surgeons nervous and the size that can get outpatient followup. Calling a CT surgeon to the ED to see a patient with an incidental 4.8 cm ascending aortic aneurysm in many cases is not necessary...depends on the patient, followup, etc. They will definitely not be excited about a 4.8 cm aneurysm. Sure, it looks HUGE on CT, but most won't operate on this size.

Indications for the placement of an IVC filter: 1. Patients with acute VTE who have a contraindication to traditional anticoagulation (surgery, GI bleed, bleeding) 2. Patients with a DVT who have severely compromised cardiopulmonary reserve or who already have pulmonary hypertension 3. Patients with VTE who have developed clot on anticoagulation Reference: Buller, HR, et al. Antithrombotic therapy for venous thromboembolic disease: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy, Chest 2004

Hypertensive encephalopathy is a condition in which cerebral blood flow and autoregulation are altered in the setting of very high blood pressure. Although there is no evidence-based cutoff for what BP value defines this condition, most people will have a diastolic above 120 mm Hg or so. In many cases, you may not be able to make the diagnosis until BP is reduced and other conditions have been ruled out (meningitis, etc.) Patients with this condition may have: 1. altered mental status of any sort 2. seizures 3. stroke-ischemic or hemorrhagic Pearls: 1. Avoid hydralazine-will bottom some peoples' BP out 2. Forget oral meds-unreliable and may lead to "stacking" and eventual abrupt decline in BP 3. Aim for a 25% reduction in MAP over 2-3 hours....then stop reducing the BP! 4. Early signs of this condition may be subtle (mild confusion, somnolence, seizure)

Pearls regarding truly asymptomatic, but severely elevated, BP: 1. Repeat blood pressure a few times in the ED before acting on it. Many patient's blood pressure will regress to the mean. 2. Anyone being discharged with elevated BP should have some type of plan for followup. Avoid "followup with your doctor as needed." 3. No evidence exists that acute lowering of BP in an asymptomatic patient does any good (despite scary BP numbers). Avoid "treating the numbers." and.... 4. Avoid NSAIDS in patients with out of control BPs. NSAIDS induce sodium retention and essentially obliterate the effects of antihypertensive medications.

There has been an explosion in recent years in the PE literature on CT scanning. Older literature, and even some current studies, emphasized the sensitivity of CT scanning for pulmonary embolism. In other words, how well does CT detect PE? The current trend in PE research is to report outcomes. So, a patient is evaluated for PE and the CT is negative. What is that patient's outcome (PE, DVT, death) at 30, 60, 90 days, etc? Dozens of studies in recent years have shown that patients generally have a superb outcome after negative CTs. Several recent studies have shown this, and in these studies the only imaging modality was CT (no ultrasound, etc). Pearl: Despite the difference in sensitivity for PE between single slice, multislice, and multidetector CT studies have shown that the outcome rates are relatively equal. Multidetector CT clearly picks up small, subsegmental clots better than single slice or 16, 32 slice CT. This might very well mean (according to some) that subsegmental (small, tiny) clots may not be that significant. We may very well be approaching an era where we don't treat small, peripheral clots. Pulmonary Embolism, second edition, Paul Stein 2007

Well, I know you have been having trouble sleeping lately since you have been asking yourself, "What are some really weird causes of thoracic aortic aneurysms?" So, here is a short list: 1. Syphilis 2. Takayasu's arteritis 3. Behcet's disease 4. Psoriatic arthritis 5. Relapsing polychondritis Great pearl for an upcoming Visual Diagnosis Jeopardy....oh yeah, baby, it's coming to a wednesday conference near you!

A retrospective study by Gaul et al. of 102 patients with aortic dissection showed that 29% of patients presented with neurologic symptoms. Interestingly, almost 1/3 of these patients reported NO chest or back pain...i.e. painless aortic dissection with neurologic manifestations. Neurologic presentations discussed in the study include: stroke-like symptoms, syncope, ischemic neuropathy, somnolence, seizures, coma, and spinal ischemia. Pearl: Consider the possibility of aortic dissection in patients with neurologic symptoms especially if symptoms are unusual or combined with other findings. Gaul C, et al. Stroke 2007 From Emergency Medical Abstracts (July 2007)