UMEM Educational Pearls

Evaluating for Pulmonary Embolism During Pregnancy

Highest risk of PE is within the first week postpartum

Acceptable, safe, and medico-legally sound strategies to rule out PE in pregnancy:

• Pulmonary CTA-this strategy is safe and accepted. Plenty of data to support you if you choose this strategy. Some evidence recently that shielding the baby may actually increase scatter radiation to the fetus. Check with your Radiologist. 
• V/Q scan-also an acceptable strategy. Probably more radiation to the fetus. If you choose this test, remember that many experts recommend you insert a foley to drain the bladder (reduces radiation exposure to the fetus). 
• Negative PERC (Pulmonary Embolism Rule Out Criteria) + Negative, trimester adjusted d-dimer level. Adjusted trimester cutoffs for d-dimer in pregnancy are: 1st 750 ng/dL, 2nd 1000 ng/dL, and 3rd 1250 ng/dL. So, figure out what trimester your patient is and if they are PERC - and the d-dimer falls below the cutoff,  you are done. Remember to adjust the pulse to 105 bpm if using the PERC rule for rule out as heart rate goes up in pregnancy.
• Start with lower extremity US, if DVT +, you are done

**For explanation of PERC rule, see earlier pearl.

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D-Dimer levels are known to be elevated in pregnancy. But how high is too high and can this test be used in the workup of VTE in pregnant patients?

Recent literature indicates that D-dimer levels in each of the three trimesters are approximately 39% higher: 700, 1000, and 1400 ng/dL for each trimester (normal cutoff 500 ng/dL). So, figure out what trimester your patient is in and use the corresponding D-Dimer level for that trimester.

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Ruling Out PE in Cancer Patients: Use D-Dimer??

Most of us are aware of the data that suports using a highly-sensitive d-dimer combined with low-moderate risk score to r/o PE. Sounds simple enough. What about using d-dimer in a cancer patient to rule it out? Well, this is being studied more and more.

Most of us would be a little uneasy about using a d-dimer as a stand-alone test to r/o PE in a cancer patient. After all, they have cancer, aren't they high risk?

The following study showed that the there was a VERY high negative predictive value and a VERY high sensitivity of a negative d-dimer in this group of cancer patients.

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Does a normal d-dimer rule out aortic dissection?

A lot of research seems to be focused on using d-dimer as a rule-out strategy for acute aortic dissection. The idea is that a d-dimer <500 (which is what we use for ruling out PE in low-mod risk patients) rules out dissection as well.

A few pearls and pitfalls regarding this:

• Studies look very promising, but NO accepted cutoff point (d-dimer) has been defined
• This practice has NOT been widely accepted yet
• A d-dimer <100 ng/dL rules out aortic dissection with a sensitivity of 100%
• A d-dimer of <500 ng/dL rules out aortic dissection with a sensitivity of 98%
• Experts in this area seem to be advocating this as a potential rule out strategy
• Critics of this approach point out the fact that a subset of patients with dissection (those with intramural hematomas-i.e. no intimal tear) may not release d-dimer into the circulation. But almost all studies include patients with this variant and their d-dimers are almost always elevated.

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Clinical Presentation of AAA

Everyone is familiar with the "classic," textbook, presentation of AAA:

• Abdominal pain
• Pulsatile mass
• Hypotension

This presentation, however, is not all that common. Many patients simply present with unexplained abdominal and/or flank pain.

Consider the diagnosis in anyone with risk factors (i.e. older folks, family history, etc) who presents with abdominal and/or flank pain. In most cases, CT scanning of this group of patients is the way to go.

And, one last pearl: put the US probe on early. May make a huge difference in time to diagnosis.

Be afraid, be very afraid.

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What study should we be getting to evaluate for DVT in patients with suspected VTE (venous thromboembolic disease)?

Ultrasound of the legs seems to be equivalent to CT Venography (CTV). 

Drawbacks of CT Venography (CT scanning into the abdomen/pelvis/legs after pulmonary CTPA):

• Radiation (TONS of radiation!)
• Cost
• Never been proven superior to non-invasive ultrasound

Despite the fact that leg ultrasound obviously doesn't evaluate for deep pelvis clots and intraabdominal clots (IVC, etc), outcome studies and other studies in recent years show ultrasound is just as good as  CTV. 

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Management of Ruptured AV Fistula

This pearl pertains to a case I had 2 weeks ago. A 65 yo male presented with a massively swollen left forearm in the region of his AV fistula. On ultrasound he had a 6 X 6 cm aneurysm. He was seen by vascular and transplant surgery and taken to the OR for repair.

So, the question came up, what would an emergency physician do if this bad boy actually ruptured? Well, obviously we would hold pressure. But what if that didn't work? Well, shouldn't the patient go to the OR? The answer is a resounding yes, but what if there is no surgeon around. There is not much literature on how to handle this devastating vascular catastrophe.

As a rule of thumb, if an AV Fistula ruptures (not leaks) and the patient is exsanguinating in front of you:

• Strongly consider a tourniquet (don't worry about the arm, they are about to die). Yes, that is right, a tourniquet. Sounds like common sense, but according to the vascular surgeons I have spoken with, too often this isn't done, and the patient ends up dying. If the patient is dying, tie the arm off.
• Consult a vascular surgeon ASAP

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Side Effects of Hydrochlorothiazide

 Consider the following when prescribing HCTZ from the emergency department:

The side effects of hydrochlorothiazide include hypokalemia,hypercalcemia, hypomagnesemia, metabolic alkalosis, hyponatremia, hyperuricemia (may worsen gout), hyperglycemia, hypercholesterolemia, hypertriglyceridemia.

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Hemorrhage Volume on Head CT 

Ever wanted to speak the same language as our neurosurgical colleagues? Ever wonder what they are doing, calculating, or thinking about as they look at the head CT of the large intracranial hemorrhage? 

Most of the neurosurgeons want to know basic information about patients with head bleeds. One thing they always calculate is the hemorrhage volume...i.e. how many mLs of blood are in the bleed? This can be easily done in the ED by using the following formula: called the ABC formula. 

A X B X C/2 X 0.6= mL of blood

A= largest width of the bleed (in cm)

B=largest width perpindicular to A

C=number of cuts you see blood on

So, if A=2cm, B=2cm and the bleed is seen on 3 cuts.....

2 X 2 X 3/2 X 0.6=3.6 mL of blood (not very much in the opinion of a neurosurgeon)

Most of the big bleeds that neurosurgeons drain or take to the OR are 50 cc or so. So, when you call a neurosurgeon and tell them that the patient has 60 mLs of blood, you will definitely get their attention. 

 PEA Arrest...Look for AAA rupture and Cardiac Tamponade

If a patient presents in cardiac arrest (particularly PEA), consider the following diagnoses in addition to the causes commonly taught in ACLS:

• AAA with rupture
• Aortic Dissection complicated by tamponade

A 2004 study in Resuscitation by Meron et al. showed the following:

• Approximately 50% of the patients who presented in PEA arrest from a AAA rupture did NOT have abdominal or flank pain prior to arrest
• Approximately 50% of the patients who presented in PEA arrest from cardiac tamponade (from aortic dissection) did NOT have chest pain prior to arrest
• Bedside US was diagnostic in all cases in this subset of patients with PEA arrest of unknown cause

Take home point for the emergency physician:

• Pull the US machine out very early on in the resuscitation of the PEA arrest patient....get the probe on as soon as you can. 

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DVT and Asymptomatic Pulmonary Embolism

A few important pearls about PE:

• Remeber that up to 50% of patients with proven DVT will have asymptomatic PE at the time of presentation
• Large, even central PE may be asymptomtic
• Normal vital signs DO NOT rule out PE

Journal of Thrombosis and Hemostasis and Chest-2006, 2007

Treatment of Pulmonary Embolism

Treatment of acute PE:

• Unfractionated Heparin (80 units/kg intravenous bolus followed by 18 units/kg/hour) or,
• Fractionated (i.e. low molecular weight heparin) Heparin. For example, Enoxaparin, in a dose of 1 mg/kg subcutaneously every 12 hours. Some also give this dose IV every 12 hours.

If administering thrombolytic therapy (currently tPA is the only FDA approved drug) for massive PE, most authorities recommend UFH (Unfractionated Heparin) because the infusion needs to be turned off while the tPA hangs for 2 hours.

Although other agents are being promoted for the treatment of acute PE, like direct thrombin inhibitors, many institutions do not have these drugs available yet. Plus, they are expensive and have not been shown to be superior to standard therapy (at least yet)

References: Kline, Journal of Thrombosis and Hemostasis, 2005, 2006, 2007

Direct Renin Inhibitor-Aliskiren (Tekturna)

This drug is the 1st in a new class of antihypertensives called direct renin inhibitors-1st approved in 2007. This drug, along with three others being developed, inhibits the entire Renin-Angiotensin-Aldosterone System (RAAS) which has been shown to lead to definitive 24 hour blood pressure control.

Why should emergency physicians care, you ask?

• It is only matter of time before we start seeing patients on this drug. I saw my first just a few weeks ago, and according to some of our nephrologists we can expect to see a whole lot more.  Emergency Physicians should at the very least know about this new class of drug.
• Side effects of the drug are similar to ACE inhibitors (ACE-I), like hyperkalemia.
• The drug can cause angioedema, so development of angioedema on this drug pretty much takes all three angiotensin drugs (ACE inhibitors, angiotensin receptor blockers, and direct renin inhibitors) off the list of potential BP meds for the patient. All three can cause angioedema.

J Hypertension March 2007

AAA...be afraid, be very afraid

Abdominal Aortic Aneurysm (AAA)  is known as the great masquerader in the elderly for good reason....

• May look EXACTLY like a kidney stone
• May cause vague abdominal and/or back pain....probably one of the reasons we scan older folks with abdominal pain. Presentations of AAA in the older patient may not be impressive!
• May be associated with the "blue toe syndrome" (where mural thrombus flips distally and occludes small vessels in the feet and toes)
• A pulsatile mass is frequently absent
• 10% of urology referrals for older (>65) patients with suspected kidney stones result in a diagnosis of AAA

Physical Examination finding in inferior vena cava thrombosis

Consider IVC thrombosis if you ever see vertically oriented, dilated abdominal wall veins, or dilated veins on the back. As opposed to abdominal wall veins that radiate out from the umbilicus in patients with cirrhosis-known as caput medusae.

Etiologies include hepatic tumors abutting the IVC, renal cell tumors, open abdominal surgery, catheter related, IVC filter-related.

Fenoldopam Pearls

Intravenous Fenoldopam has been shown in recent years to be a very effective antihypertensive medication. Studies have compared it to Nitroprusside (Nipride), the older generation "gold standard" antihypertensive, and have found to be just as effective.

• Think of Fenoldopam as Nipride without the toxicity....taste great, less filling
• Works by peripheral dopamine agonism
• Increases renal blood flow and induces a natriuresis (patient pees sodium)-so works well in our chronic kidney disease and ESRD patients
• Easy to titrate and very well tolerated
• Contraindication in patients with glaucoma-The drug elevates IOP.

Journal of Hypertension 2007

Pulmonary CTA Sensitivity and PIOPED II

The publication of PIOPED II has led some to doubt the sensitivity of pulmonary CTA for pulmonary embolism. This study reported an overall sensitivity of 83% which could be increased to nearly 90% with the addition of CTV (CT Venography). 83% is a horrible sensitivity. So, why should you care?

• This study used 16 detector CTs...not the 64+ head scanners we are now using. This study, like many others, suffers from the explosion of CT technology. As soon as a study is published, the technology the study used becomes outdated. Most studies now look at OUTCOME...i.e., what % of patients with a negative CT who do not receive anticoagulation develop a PE at 30, 60, 90 days? Current literature shows that the chances of VTE at 90 days for patients with negative CTAs is less than 2%.
• Bottom line, don't be too discouraged by the PIOPED II study.  In addition, many of the authors of the study actually advocate for CTA/CTV to rule out PE. This is a tremendous amount of radiation and has NOT been validated as a "standard" approach to ruling out PE.
• Lastly, it is generally a good idea to try to limit the use of CT scans (yes, that is what I said) by using a d-dimer/pretest probability or PERC/clinical gestalt approach. This is a defensible strategy.

Optimal pulmonary artery opacification  for detecting pulmonary embolism-how good was the CT you ordered?

The PE literature is pretty clear about one thing: a CT with well-timed opacification of the pulmonary arteries is very sensitive for detecting pulmonary embolism. This means that there needs to be enough contrast in the central pulmonary arteries to be able to detect clot. So how can you be really sure the PE Protocol CT you ordered is adequate? Have you really ruled out PE?

What does this mean for the emergency physician?

• The pulmonary arteries on CT should be approximately 200 or so Hounsefield units (HU).
• What this means is that you slide the cursor over the pulmonary arteries and see what their HUs are. On the computer screens at UMMS, Hounsefield units are on the bottom of the screen and change as you roll the cursor over different densities (bone, soft tissue, calcium, etc).
• If the central pulmonary arteries are a lot less than 200 Hounesfield units (e.g. 100 HU) the scan would be considered suboptimal.

Some predict that in the future WE (the emergency physician) may in fact be held accountable for knowing whether or not a CTPA (CT Pulmonary Angiography) is optimal or not.

References:

(1) Kline-Carolinas Medical Center (2) Journal of Thrombosis and Hemostasis 2007 (3) AJR 2006,2007

Risk Factors for Pulmonary Embolism

• Remember that as many as 20-25% of patients with proven VTE (DVT and PE) will not have identifiable risk factors at the the time you evaluate them.
• 6 hours of flight (or car ride) with the knees flexed at about 90 degrees is considered by many to be a risk factor.
• Inflammatory bowel disease (Crohns and Ulcerative Colitis) are hypercoagulable disorders and have been linked to VTE.

Can you imagine one of  our patients saying"Dr. Abaraham, I have what is known in the hematology community as a Factor 5 Leiden mutation"?

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