Pulmonary Embolism-Beware Two Important Atypical Presentations

Seems like we have had several atypical PE presentations recently so I thought it timely to quickly highlight some of the well-reported presentations of pulmonary embolism. Remember, although we won't and can't diagnose every case, these types of presentations should at the very least prompt us to consider the diagnosis.

Atypical PE Presentations:

• Syncope-occurs in as many as 15-20% of patients. Make sure PE is on the differential diagnosis of the syncopal patient, especially if there was any preceeding shortness of breath or chest pain.
• Abdominal pain-we just had a case of this last week. A young female 6 weeks into a course of OCPS developed RUQ pain that radiated to the left shoulder. She had NO shortness of breath. However, the RUQ pain was pleuritic. Remember the movement of the diaphragm as it is responsible for abdominal pain presentations of both PE and pneumonia. A d-dimer was obtained and returned 3000. A CT scan was then ordered which showed a large right lower PE. What's the moral of the story? Well, it isn't to rule out PE in patients with belly pain. The lesson here is that upper abdominal pain may reflect disease in the chest (lower lobe pneumona and PE) and vice versa. To make matters worse an ultrasound of the RUQ was ordered 1st which showed gallstones!

Thrombolytic Therapy for Pulmonary Embolism

Indications for administration of fibrinolytic therapy for acute PE:

• Cardiac arrest presumed to be secondary to PE-tPA 50 mg bolus, may be repeated once.
• Massive PE (hemodynamic instability)-arbitrarily defined by BP < 90 mm Hg systolic. Give 10 mg tPA bolus followed by 90 mg over 2 hours. Make sure heparin off during this time frame. tPA is the only FDA approved drug for this but some are starting to use Tenecteplase (single 0.5 mg/kg bolus).
• Submassive PE (normal hemodynamics and evidence of RV strain). This tends to be the most controversial group, although many authorities are now advocating its use. Strongly suspect strain if the Troponin/BNP are elevated and get an ECHO if they are. Most studies that advocate for lytics in this group show significant improvement in PA pressures, RV wall dilatation, etc. What is currently missing is outcome data...i.e. how short of breath and disabled are people with submassive PE at 6, 9, and 12 months? Bottom line, enough evidence exists to support giving to stable patients with RV strain as long as they are carefully screened.
• There is NO evidence that lytics are useful in stable patients without RV strain.
• The administration of thrombolytic therapy for acute PE is within the scope of practice of emergency medicine.

 

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Neurologic Manifestations of Acute Aortic Dissection

A myriad of neurologic presentations of acute aortic dissection have been reported in the literature. Although classic CVA symptoms may occur, nonspecific neurologic symptoms are much more common

These include:

• Classic stroke-like/TIA symptoms
• Encephalopathy (may look like a drug overdose)
• Seizures (ask Mike Abraham about his abdominal pain/seizure case)

Take Home Point:

• Consider the diagnosis of acute aortic dissection in patients with these findings who ALSO HAVE chest, back, or abdominal pain +/- risk factors for the disease (i.e. HTN, family history, Marfans, cocaine, etc.)

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Hypertension and Epistaxis

We commonly encounter patients with epistaxis who are found to be hypertensive. Some have taught over the years that hypertension causes nosebleeds and that some nose bleeds won't stop until the BP is lowered...

Some pearls about HTN/Epistaxis:

• Most patients we see with hypertension are not experiencing epistaxis, casting serious doubt on a causal relationship
• Studies show that the degree of blood pressure elevation does not correlate with risk of nose bleed
• No studies have ever shown that acute BP reduction in the ED for a nose bleed is beneficial or reduces bleeding
• Much of the debate is sparked by our ENT colleagues who swear that hypertension leads to nose bleeds and that bleeding will not stop until the BP is "treated." Much of this is based on experience with patients in the OR or IR suite. These blood pressures tend to be treated with IV antihypertensives by the ENT folks, and they feel pretty strongly about this relationship.

Warfarin-Induced Skin Necrosis (WISN)

Some pearls about a rare, but serious side effect of Warfarin...

• WISN Occurs in 0.01-0.1% of patients taking Warfarin
• More common in middle-age, perimenopausal women being treated for DVT/PE
• Symptoms usually begin on days 3-6 of Warfarin treatment
• Underlying pathophysiology is complex but involves thrombosis of superficial dermal capillaries
• Postulated to be associated with deficiencies of protein C, protein S, and antithrombin III
• Rash is most common on the breats, with thighs/buttocks being second most common site (see picture)
• Diagnosis usually made clinically based on appearance of rash
• Treatment is aimed at restoring Vitamin K dependent clotting factors by administering Vit K and FFP
• For patients with the need for anticoagulation (DVT/PE, etc.) Heparin therapy is usually started

 

55 yo female presented to the ED on the day of hospital discharge for evaluation of this rash.

The rash began 4 days after starting Warfarin. Was being treated for a DVT.

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• 0812012217_photo.jpg (137 Kb)

What Hypertensive Patient Needs a Workup for End-Organ Damage?

Ah, the age old question...which hypertensive patients need an ED workup for end-organ damage? The "workup" for patients includes renal function, urinalysis, CXR, ECG, etc.

Some pearls regarding working patients up: 

1. Asymptomatic patients in general do not need a workup. There is pretty good literature that shows you just won't find much (expecially anything that will change your treatment plan) if you go hunting in this group of patients.
2. If you set asymptomatic patients aside, you won't find much good data on how much of a workup other patients need. Does a 45 yo patient with a BP of 160/110 and a mild HA need a serum creatinine? What if they have had some mild, atypical CP? The answer is...no one knows. Much of what we we do depends on what we were taught and our current mood. 
3. Asymptomatic patients (truly asymptomatic) don't need chest xrays and ECGs as a rule of thumb...what you find won't help you make a decision. If you find LVH on the ECG, so what? 
4. Obtaining a serum creatinine makes sense, especially of you are going to start a BP agent. 
5. There is a pretty good study by Karas, et al. that showed that a urinalysis without protein or blood predicts a normal creatinine. Use caution, however, if you use this as a screen for renal disease, because many patients with HTN spill protein (despite a normal creatinine)

Key Pitfall to Avoid in Severely Hypertensive Patients One of the biggest pitfalls committed when treating severely hypertensive patients (asymptomatic or minimally symptomatic) is in "stacking" antihypertensive (oral) medications. Mike Winters has mentioned this previously. This occurs when several medications are given one after another...resulting in a precipitous drop in blood pressure. This could result in severe hypotension and stroke. Pearls: 1. Don't stack too many BP meds in the ED (resist the urge to do this. 2. If the patient's BP is sky high (i.e. 250/170), forget oral meds and get control of the BP with a drip. This is a safer approach than adding many different medications and taking the risk of hypotension. 3. Don't just treat the number 4. Hypertensive patients can go home (with prompt followup)

Pulmonary Embolism Rule Out Critieria (PERC) A brief reminder about the PERC rules... Use of the PERC (Pulmonary Embolism Rule-out Criteria) rule can significantly decrease work-up for pulmonary embolism. To apply this rule, the clinician must first use clinical gestalt to classify the patient as low risk. The PERC rule, which consists of eight clinical criteria including history, physical and vital signs, can then be used. If both of these criteria are met, then there is less than a 2 percent risk that this patient has a PE and no further work-up is needed. PERC Rule: Age < 50 years Pulse < 100 bpm SaO2 > 94% No unilateral leg swelling No hemoptysis No recent trauma or surgery No prior PE or DVT No hormone use This rule has now been validated in a large, multicenter trial. Bottom line: If you walk out of the room and your clinical gestalt is "no PE" and the PERC rule is negative, there is a <2% chance of pulmonary embolism (<2% probability, by the way, is what many PE experts consider the test threshold)

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Reversal of Warfarin

Reversal of Warfarin can be accomplished by administering any of the following:

• Fresh Frozen Plasma (traditional reversal agent)
• Vitamin K (po, sub q, or IV)
• Prothrombin Complex Concentrates (PCC)-not yet available for use in the US (yet)

A few pearls:

• It doesn't take many units of FFP to lower someone's INR
• Don't forget volume considerations if you use FFP
• Vit K is pretty well tolerated but some patients will have an allergic reaction (more common with IV administration)
• These medications in general will be used for life-threatening bleeding (GI, CNS bleeds, retroperitoneal bleeds, etc)
• Prothrombin Complex Concentrates-rich in factors 2,7,9, and 10...perfect drug since Warfarin depletes these factors
• PCC associated with some increased thrombosis

 

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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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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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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