Anticoagulation with Heparin-How to Reverse?

So you just started Heparin on that ACS patient? Just bolused the patient in room 12 with the large PE with a slug of Heparin? The nurse tells you that one of them just vomited blood and the other just had a large bloody bowel movement. What to do, oh, what to do?

How to reverse Heparin...use Protamine:

• Protamine is obtained from the sperm of salmon and other species of fish....glad you know that now?
• Given IV, it binds to Heparin (Unfractionated Heparin) and inactivates it
• Administer Protamine (IV) at a dose of 1 mg for every 100 Units of Heparin given within the last four hours. Max dose 50 mg of Protamine. May give more than 50 mg, but use caution as may lead to bleeding
• If the dose of Protamine is exceeded, patients may bleed. Protamine is actually an anticoagulant. 
• Give slowly over 10 minutes as may cause anaphylactoid reaction
• Can use to reverse LMWH as well: 1mg Protamine per 1 mg of LMWH (Lovenox)

Cerebral Venous Sinus Thrombosis (CVST)

An uncommon but very serious entity that leads to three distinct types of presentations:

• Headache
• Seizures
• Stroke

Caused by thrombosis of one of the intracerebral venous sinuses (most commonly the transverse sinus) The major risk factor is hypercoagulable disease. May be the underlying cause of a majority of cases of idiopathic intracranial hypertension.

When to suspect:

• Headache with negative CT, negative LP, but high opening pressure
• In any patient with new onset idiopathic intracranial hypertension (i.e. pseudotumor cerebri). Can't be formally diagnosed without a negative MRI.
• Stroke syndrome that doesn't quite fit. May see bilateral infarcts in the posterior regions. These are actually venous infarcts secondary to the sinus thrombosis.

Diagnosis:

• Just like a lot of other things in medicine, "If you don't think about it, you can't diagnose it."
• 1 in 3 head CT scans will be normal
• MRI with MRV (venous phase) is the diagnostic standard

Treat:

• Anticoagulation with heparin then warfarin

 Does Hypertension (elevated BP) Cause Headache?

This is an age old question that many of us have struggled with in the ED for many years...

Other questions include: Does elevated BP cause headaches? Do we need to scan hypertensive patients with headache just because they have a headache? At what level of BP does the BP actually cause headache? 

A few quick pearls:

• Although incredibly high BPs (diastolics above 130 mm Hg) have been correlated with headache, the general concensus is that hypertension doesn't really cause headaches. 
• At really high blood pressures (again, diastolic BP > 130-140), cerebral autoregulation breaks down and may lead to cerebral edema and headache...hypertensive encephalopathy.
• Elevated systolic BP may actually be protective for developing headaches
• CT scanning the hypertensive patient with a headache is not warranted a lot of the time, unless the patient has a neuro deficit, or if the headache was acute onset or associated with other findings of hypertensive encephalopathy.
• Patients with HTN are as likely to have a headache in the ED as non-hypertensive patients

Avoidable Pitfalls in Managing the Hypertensive Patient

We all see very hypertensive patients on almost every shift. Dr. Winters has an earlier pearl related to pitfalls in treating patients with hypertensive encephalopathy, but I thought it was time to reiterate just a few points.

• No evidence to date has ever shown a benefit to acutely lowering someone's BP in the ED prior to discharge
• Probably the best thing you can do for the patient with out of control BP is to arrange (and make sure they have) followup for the next day or two after discharge
• In patients with severe HTN (eg. admitted patients with pressure to high to go to their inpatient bed), avoid agents like IV Hydralazine. This agent is pretty reliable in being completely unpredictable when it comes to BP response. Some will really bottom out their BPs.
• Avoid Clonidine unless the patient is on it and stopped taking it recently (rebound HTN). May worsen someone's already crappy mental status.
• If a patient is being admitted, say to a unit or step down unit, don't bother titrating oral agents for people with pressures > 240/130 mm Hg or so. Consider a drip-oral agents may "stack" and take effect, thus lowering someones BP way lower than you wanted.
• Don't treat the number, treat the patient.

So, how good is a screening CXR for aortic dissection?

• Classic CXR finding is a wide mediastinum
• Pooled literature shows that the overall sensitivity of a CXR is about 67-70% for aortic dissection (even if upright, or PA and Lateral)
• Most authorities agree that a screening CXR alone is not sufficient to r/o aortic dissection

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Key Cardiovascular complications of cocaine:

• Myocardial ischemia and infarction
• Myocarditis and cardiomyopathy
• Aortic dissection
• Vessel thrombosis
• Stroke (usually hemorrhagic) 
• Visceral ischemia

Pearls:

• Cocaine and abdominal pain=mesenteric ischemia, hemoperitoneum (described)
• Cocaine and chest pain=MI, aortic dissection
• Cocaine and extremity pain=arterial thrombosis, aortic dissection
• ~ 6% of cocaine chest pain patients rule in for MI

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 Management of acute limb ischemia

Just a few pearls regarding acute limb ischemia

• Presents with an acutely painful extremity (may be pale and cool as well)
• Common etiologies include atrial fibrillation, embolism from aortic plaques, and thrombosis of extremity vessels
• Most patients need to be anticoagulated (heparin) 
• Vascular surgery should be consulted immediately or the patient needs transfer to a facility that can handle acute vascular emergencies
• Use caution when performing the physical examination, because there may be a pulse present
• Perform bedside ABI to the best of your ability and document
• Diabetics with stiff vasculature may have ABIs of 1 or greater so may be less reliable

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 Quick Pearls for Intubating:

1. When intubating, make sure to use two hands!

• Have the person holding cricoid pressure let up...cricoid pressure many times makes your job more difficult
• You as the intubator then swing your right hand around and manipulate the larynx (left, right, up, down, etc)
• When you get the view you want, have someone take over pressure and then pass the tube
• Using two hands makes your job so much easier

2. Resist the urge to look for cords

• Your job is to get the tube in the airway
• If you can identify the two arytenoid cartilages, you are home free. Aim north of these structures.
• You don't have to see cords to intubate. All you need are the landmarks that identify the entry into the glottis....just pass the tube north!
• I had a case just a few days ago where the only thing we saw were the two arytenoids (covered in blood). No cords were seen, but we passed the tube above (i.e. north) the arytenoids and we were in.

3. Stylet shape is crucial

• Shape your tube with the "straight to cuff" technique
• The tube is straight and then bent 15-20 degrees at the beginning of the cuff
• This shape will prevent the tube from actually obscuring your view and will increase your success.

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Complications of Subarachnoid Hemorrhage

The three dreaded complications of SAH include the following:

• Rebleeding
• Hydrocephalus-occurs in as many as 33-50% of patients with SAH. Intraventricular blood (in 20% of cases) acutely occludes the foramen of Monroe and Luschka and obstructs CSF outflow. This is treated by inserting a ventriculostomy catheter. 
• Vasospasm-Usually develops several days after the initial SAH. May be an asymptomatic angiographic phenomenon or cause cerebral ischemia-an important cause of morbidity after SAH. Prophylactic administration of Nimodipine improved outcomes. 

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Currently Approved LMWHs for the Treatment of Acute PE:

• Enoxaparin-1 mg/kg every 12 hours subcut
• Tinzaparin 175 Units/kg once daily subcut
• The pentasaccharide: Fondaparinux- at a dose of 5 mg for body weight <50 kg, 7.5 mg for 50-100 kg, and 10 mg for >100 kg, once daily

Make sure to monitor platelet counts regardless of agent chosen.

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 Necrotizing Fasciitis Pearl

A few things to remember about treating necrotizing soft tissue infections:

• Often polymicrobial and most of the time we in the ED won't have a microbial diagnosis
• If due to strep, patient may benefit from the addition of Clindamycin. Streptococcal species may stop multiplying in a wound/cellulitis and continue to produce large amounts of tissue toxin. In this case, many antibiotics (like the ubiquitous Zosyn-which works on dividing bacteria) may not work well. Clindamycin will actually affect toxin binding. The phenomenon of Strep species  dividing but continuing to produce toxin is referred to as the Eagle affect. 

So, when shot-gunning the antibiotics in a patient with a really bad soft tissue infection (not the run of the mill cellulitis) consider adding Clindamycin to the regimen. 

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Causes of an Elevated D-Dimer 

Don't forget the multiple causes of an elevated d-dimer:

• PE/DVT
• Sepsis/infection
• Malignancy 
• Renal disease
• Pregnancy
• MI
• Stroke

**See attached PDF-Differential Diagnosis of Elevated D-Dimer

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Attachments

• 0807301959_Causes_of_Elevated_D-Dimer.pdf (43 Kb)

How good was that CT Pulmonary Angiogram You Ordered?

CT is currently the gold standard imaging modality for pulmonary embolism. Since we order these quite a bit in the ED, we should know some of the important nuances regarding interpretation of the scan. All of us at some point have looked at a pulmonary CTA and thought that it looked a bit "fuzzy" or perhaps it didn't "look right"  This happens more often in obese patients. There is good literature to show that a suboptimal CTA misses clinically significant PE. So, it is important for emergency physicians to know a little about the CT scan ordered for our patients. 

How can you know if the CT scan YOU ordered to rule out PE is really "good enough" to rule out PE?

• Well, you can rely on the radiologist. But remember they may not comment of the quality of the scan. Or, they may simply recommend another test.
• Look at the Hounsfield Units (HU). For those who have PACS or some other computer radiology display,all you need to do is move the cursor to the main pulmonary artery and see what value (usually on the bottom of the screen) is displayed. 
• A HU >280 indicates that the CT is "good" (i.e. good enough contrast bolus to detect clot). By the way, >350 looks white.

So, a 34 yo obese patient who gets a CT scan to rule out PE, who has 170 HU in the main pulmonary artery, has not had an optimal CT. Thus, you really haven't ruled out PE even if the read is "negative." Often this is due to poor bolus timing. 

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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.

Abstract

PURPOSE: To prospectively evaluate (a) the diagnostic performance of D-dimer assay for pulmonary embolism (PE) in an oncologic population by using computed tomographic (CT) pulmonary angiography as the reference standard, (b) the association between PE location and assay sensitivity, and (c) the association between assay results and clinical factors that raise suspicion of PE. MATERIALS AND METHODS: This HIPAA-compliant study had institutional review board approval; informed consent was obtained. Five hundred thirty-one consecutive patients were clinically suspected of having PE; 201 were enrolled (72 men, 129 women; median age, 61 years) and underwent CT pulmonary angiography and D-dimer assay. Relevant clinical history, symptoms, and signs were recorded. CT images were interpreted, and the location of emboli was recorded. The negative predictive value (NPV), positive predictive value (PPV), sensitivity, specificity, and diagnostic likelihood ratios of the D-dimer assay results were calculated. RESULTS: Forty-three patients (21%) had pulmonary emboli at CT. D-Dimer results were positive in 171 patents (85%). The NPV and sensitivity were 97% and 98%, respectively. The specificity and PPV were 18% and 25%, respectively. No association was shown between clinical history, symptoms, or signs and NPV, PPV, sensitivity, or specificity or between location of PE and sensitivity. CONCLUSION: D-Dimer results have high NPV and sensitivity for PE in oncologic patients and, if negative, can be used to exclude PE in this population. Combining the assay with clinical symptoms and signs did not substantially change NPV, PPV, sensitivity, or specificity.

Whether this is ready from prime time or not remains to be determined, but it is interesting that we might be able to do this in the future to r/o PE in 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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 Pregnancy and Acute Pulmonary Embolism

Women who are pregnant or in the postpartum period and women who take hormonal therapy are at an increased risk of pulmonary embolism.

Some facts:

• Risk of first episode of venous thromboembolism is 15 times as high in the postpartum period as during pregnancy
• Diagnostic workup and initial ED therapy is the same as it is for non-pregnant patients
• Although there are still some concerns about pulmonary CTA, both the American College of Obstetrics & Gynecology and the American College of Radiology agree that it is safe. It is unknown what happens to fetal nephrons after exposure to circulating contrast in the mother. Despite this, CTA can be used without fear if indicated. 
• Warfarin is a teratogen and should not be used for anticoagulation.

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 Thrombolytic Therapy for PE

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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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