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. 

Show References

Superior Vana Cava Synrome....when to suspect

Two common causes of SVC syndrome include thrombus (secondary to CV catheters) and lung tumors/lymphoma

Consider this diagnosis in patients with a history of cancer and/or who have a central line in place and the complaint of facial swelling. Patients may not look swollen to you.

In addition, make sure to look at their necks and chest wall-presence of asymmetric, prominent veins should prompt consideration for this diagnosis. 

A useful clinical tool is to look at the patient's driver's license (assuming they have one) and compare to their appearance on presentation.

Workup in most cases will involve a CT of the chest.

Show References

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

Show References

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.

Show References

Suspected Acute Leukemia in the ED

 Key ED Interventions for patients with astronomically high WBC counts:

• Usually talking about WBC counts over 200,000 or so (can be lower in lymphocytic leukemia)
• Hydrate aggressively
• Avoid PRBC transfusions as blood products will increase the patient's cytocrit (combination of WBC, platelets, and RBC) and predispose to organ malperfusion. This may lead to WBC (or blast) sludging in the microcirculation and may result in CNS bleeds. 
• Obviously, call for help immediately! Get a hematologist on the line quickly
• Assume the patient already has Tumor Lysis Syndrome and administer Allopurinol in a dose of 300 mg orally.
• Obtain a uric acid level, and if high, give an intravenous infusion of Rasburicase-eliminates preformed uric acid released from leukemia cell lysis. Renal failure results from high uric acid levels. We have this medication at University.
• The treatment of choice is initiation of definitive chemotherapy....clearly not an option for us in the ED. You can also do leukapheresis (where you take out WBC)....also not an option unless you have a special catheter and a perfusionist/nurse. BUT, you can take off a unit or two of blood (phlebotomy). This will potentially lower the patient's cytocrit. 

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. 

Show References

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

Neutropenic Fever

A few pearls about neutropenic fever:

• Usually occurs a few weeks after chemotherapy (14-21 days)
• Defined as a fever in the setting of rapidly declining neutrophil count
• Patients who report fever at home but who are not febrile in the ED should be treated as if they are neutropenic
• ANC=absolute neutrophil count. Calculated by adding neutrophils and bands together
• Classification of neutropenia, use the ANC to calculate:  Mild: 1000-1500 cells/mm³, Moderate 500-1000 cells/mm³, and Severe Less than 500 cells/mm³.
• Mortality rate increases as the ANC drops to below 500 and the duration of neutropenia. These people die of overhwhelming bacterial infections/sepsis.
• Treatment: #1 Consider the diagnosis, #2 Broad spectrum antibiotic coverage: Imipenem, or Pip/Tazo, or Cefipime. Consider adding Vanc if the patient has a line, looks ill or is hypotensive, or if the patient has been on a fluoroquinolone.

#1 Pitfall:

• Not initiating broad spectrum antibiotic coverage fast enough. These patients can crash very rapidly.
• Patients do not have to be febrile in the ED to be diagnosed with this. Their report of fever is enough.
• Mortality rates drop the faster big gun antibiotics are given. Don't be skimpy and give Unasyn. Use the big bad boys like single agent Pip/Tazo (4.5 grams, not 3.375), Cefipime, etc. Have a low threshold for adding Vancomycin.

IDSA Guidelines on Neutropenic Fever, 2002. New Guidelines coming Summer 2008!

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

 Medical Regimen for Suspected Variceal Bleed

To review what Dr. Bond and Dr. Winters have already posted:

Three medical therapies have been shown to be effective in patients with severe upper GI bleed thought to be due to esophageal varices:

• Octreatide: 50-100 ug bolus followed by 50 ug/hour. Has been shown to lower the rebleeding rate substantially. Even if varices have not been confirmed by endoscopy, Octreatide has also been shown to be effective in ulcer bleeding as well.
• Antibiotics (3rd generation Cephalosporin): Have been to lower the rebleeding rate in variceal bleeding. 
• Intravenous Proton Pump Inhibitor: Remember that a liver patient is as likely to have a non-variceal source of bleeding (ulcer), so add a PPI drip. Raising the pH stabilizes clot. Without endoscopy, you don't know if they have an ulcer or another etiology.

Most of our gastroenterologists recommend this regimen (all three therapies)

Other things to consider:

• Platelets, FFP
• Intubate EARLY-most endoscopists will want the airway protected prior to the scope.
• Don't be too aggressive with blood replacement/IVF: The gastroenterologist don't want these patients too resuscitated with blood products. Certainly don't aim for a Hct >30.

Clinical Presentation of SVC Syndrome

SVC syndrome (caused either by tumor or thrombosis of the SVC) classically presents with facial swelling, arm swelling, and dilated chest wall veins. The problem in the real world is that often times the manifestaions are a bit more subtle.

Some SVC syndrome pearls:

• Consider the diagnosis in patients with a generalized complaint of facial swelling or "fullness," particularly if they have an indwelling catheter in place.
• Consider in patients who complain there face is swollen or red (plethoric) in the morning, or who notice this when their arms are raised (Pemberton's sign)
• The diagnosis is usually established by CT.
• Patients with SVC syndrome and the complaint of hoarseness or headache should make you nervous, as these symptoms may indicate laryngeal and cerebral edema.
• The importance of examining the neck and chest in ED patients cannot be overemphasized. Often the one clue that leads to the diagnosis is prominent and asymetric neck, upper chest, or shoulder veins.
• Treatment: For tumor related SVC syndrome-head elevation, possibly steroids, radiation therapy (along with biopsy if no cancer diagnosis established); For thrombotic-related SVC syndrome-anticoagulation, Interventional Radiology consult for lytics/stent

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

Care of the Crashing Asthma Patient

Several things should be considered in the crashing asthmatic:

• First and foremost, there is very little date on how to manage the crashing asthmatic!
• Any sick asthma patient should have IV fluid replacement-these patients have tons of insensible losses. IV fluids may also help with post-intubation hypotension cause by compression of the vena cava.
• Many EM folks have left Ketamine in the dust for intubating an asthmatic....anecdotally, it works, but creates very sticky and tenacious lung boogers that are hard to suction. Why make your job even harder?
• Sounds like common sense, but RSI the patient in the position of comfort (usually tripod) and then quickly lay them back supine.
• Consider instituting the "kitchen sink approach" to asthma care. This includes beta agonists, anticholinergics, Mg, steroids, IVF, epi, nebulized Lidocaine, perhaps non-invasive ventilation, inhaled (yes, inhaled) steriods. Our job really begins once they have been tubed.
• Sounds corny, but consider a "bedside coach." Believe it or not, some really sick asthmatics can be talked through a severe, life-threatening exacerbation. This can be a nurse, tech, physician. Someone to talk to them during this crisis. It works sometimes.
• Any intubated asthmatic who goes into PEA arrest should not be declared dead unless bilateral needle decompressions and bilateral chest tubes have been performed.
• If an intubated asthmatic codes once intubated, consider the following: (1) disconnect from the ventilator and bag VERY slowly...4-6 breaths/minute or even slower! (2) Although controversial, some consider manual chest wall compression helpful in "getting rid" of trapped air. (3) Vigorous IVF-positive pressure ventilation worsens the patients hyperinflation which compresses the vena cava, and (4) consider needle decompression and then chest tube insertion

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"?