DON’T CALL IT A SEIZURE…

Anecdote 1:Don’t call it a seizure, start CPR

Resident: Hey, remember that patient in room 7 with the heart attack? Now he’s having a seizure!

You: That is not a seizure, let’s start CPR!

(the patient survives, and receives emergent catheterization opening a blocked vessel)

 

Cardiac arrest is often accompanied by jerking movements. The cartoons of the 1940s understood this. Bugs Bunny would typically do a few good jerking leg kicks prior to faking death with Elmer Fudd, Yosemite Sam, etc. If the setting is more appropriate for cardiac arrest, check pulses first.

 

This is probably not substantially different from convulsive syncope but I will describe that separately:

 

Anecdote 2: Don’t call it a seizure, refer to cardiology

“we never figured out why the Brugada syndrome patient had a seizure” –someone who should know better

 

Blood bank studies show that about 10% of syncope events are accompanied by a convulsion. These can look like epileptic generalized tonic clonic seizures. The differences are:

Pre-ictal: what were the setting, the symptoms, and the signs, before the event. An aura suggests a seizure. Standing in church suggests syncope. Alcohol withdrawal suggests seizure, etc.

Ictal: convulsive syncope is less rhythmic, less symmetrical, and less sustained

Post-ictal: Convulsive syncope patients regain normal arousal within a minute, seizure patients take 10-15 minutes

 

It isn’t a seizure until you have a diagnosis. It is a convulsion. Apply an appropriate differential that includes convulsive syncope.

 

Ancedote 3: Don’t call it a seizure, check the temperature

A middle aged patient is waiting to be seen for generalized weakness. The triage RN rushes them out of the waiting room because of a “seizure.” He never lost consciousness and was awake the entire time. Temp is 103 oral. You ultimately diagnose sepsis from pyelonephritis.

 

Rigors can cause tremendous shaking and can make us worry about seizure. Obviously a seizure can raise the temperature so judgment is required. But don’t automatically assume that a convulsion from sepsis is a seizure. Rigors happen when the temperature is rising, so recheck the temperature.

 

Anecdote 4: Don’t call it a seizure, educate the family

A patient is here for opioids. The doctor said no. She has a history of developing “seizures” when she does not get narcotics. Now she is screaming loudly and, wait for it…. The RN runs to you announcing a seizure and asks if you will give Ativan. Okay, I admit it, I often give Ativan if I am not sure. One time I went to the patient and said “really, you are having a seizure? Can I see the tongue biting, show me the tongue” and she proceeded to show me her teeth, biting the tongue.

 

This is tough. Don’t expect the family to understand the difference between seizures and psychogenic convulsions (also known as pseudoseizure). Educate them on the potential for psychogenic causes (but don’t prematurely rule out epilepsy either, unless it is abundantly obvious)

 

TAKE HOME POINTS:

-Our terminology can box us in. Don’t call it a seizure unless you are committing to an epileptic etiology.

-Ask about circumstances before, during, and after the event to identify possible convulsive syncope

AORTIC DISSECTION – CHECK FOR PULSE DEFICITS AND DIASTOLIC MURMUR

Morgagni in 1761 described a man who presented with a swelling on the upper part of the sternum (Seats and Causes of Diseases). The skin became thinner and blood began to leak out. The original case describes the patient pulling at his bandages and being “ordered to keep himself still, and to think seriously and piously of his departure from this mortal life, which was very near at hand, and inevitable.” The following day Morgagni describes the lesion bursting. “Nevertheless, he had the presence of mind, (as soon as) he felt the blood gushing forth, not only to commend himself to God, but to take up with his own hands a basin that lay at his bedside; and, as if he had been receiving the blood of another person, put it beneath the gaping tumour, while the attendants immediately ran to him as fast as possible, in whose arms he soon expired.” Post-mortem examination revealed the cause to be an aortic aneurysm.

 

In the 1955 movie Not as a Stranger Robert Mitchum evaluates his chief of surgery who complained of chest pain. Mitchum listens to the chest (presumably hearing a diastolic murmur), recoils in horror, then checks the bilateral pulses (presumably feeling a pulse deficit), and rushes him off to the operating room.

 

Before one gets the conclusion that we were better at physical diagnosis then, a contemporary article of that era described the antemortem diagnosis rate of aortic dissection as 11% (Levinson 1950). Hollywood has always exaggerated the abilities of its heroes to overcome the limitations of our real world. One of the leading experts on this disease has said “…difficulty in diagnosis, delayed diagnosis or failure to diagnose are so common as to approach the norm for this disease…” (Elefteriades Cardiology 2008).

 

Is there anything we can we do at the bedside to improve our history and physical examination?

 

Full history beats partial history:

Physicians who ask about onset, location, and quality have a better chance at diagnosis. Of patients who turned out to have aortic dissection, when all 3 of those were documented the condition was suspected in 91% of cases. When at least one of those is missing from the chart, the diagnosis was initially suspected in 49%.(Rosman Chest 1998)

 

Pain that is sudden, severe, or radiating to the back

Sudden and severe pain are present in up to 90% of cases (Klompas JAMA 2002). Radiation to the back occurs in 47-64% of patients (Hiratzka JACC 2010).

 

Chest pain + neurologic deficits

Other specific findings include migration of pain along the territories of the aorta and new neurological deficits, both present in up to about a quarter of patients (Sullivan Am J Em Med 2000).

 

Diastolic murmur

It turns out that Robert Mitchum’s approach is still worth doing. A diastolic murmur of aortic regurgitation is a high risk finding, occurring in 45% of patients (Hagan JAMA 2000).

 

Pulse deficit

A “pulse deficit”, which refers to an absent or asymmetrically weak pulse, occurs in 26%(Pape 2007. Klompas says 31%). Do not bother with blood pressure limb differentials in low risk populations, as it has poor specificity, being found in 19% of chest pain patients without aortic dissection (Singer 1998). Instead, palpate both limbs feeling for a difference.

 

Although it is beyond the scope of this article, many advocate using d-dimer as a screening test in those with a low (but not zero) probability of disease because it is 97% sensitive and 47% specific, at least in the first 24 hours of disease (Suzuki Circulation 2009). With time that sensitivity goes down and most experts recommend not relying on this test.

 

TAKE HOME POINTS

-Sudden and severe pain raises your concern for aortic dissection

-Check for pulse deficits and diastolic murmurs

PHYSICAL DIAGNOSIS OF CARDIAC ARREST

A patient you are caring for in the ED collapses. The nurses check pulses. One feels a pulse, one does not. Do you start CPR?

Studies do show that “feeling a pulse” does not mean a pulse is there. Many of these studies have significant limitations but overall they all seem to say the same thing. People feel pulses that are not there approximately 10% of the time.(Eberle Resuscitation 1996) One study in infants recommended using auscultation as more accurate than palpation.(Inagawa Paediatr Anaesth 2003)

We use unresponsiveness and apnea as adjuncts to recognize cardiac arrest. Apnea needs to be interpreted properly. An agonal gasping respiration raises the concern for cardiac arrest, rather than arguing against it. And respirations can continue for up to 3 minutes after ventricular fibrillation, so don’t be too rigid in using respiration to rule out the need for CPR.(Menegazzi AEM 1995)

How do we diagnose cardiac arrest? First, they have to be unconscious. Next, there needs to be some finding that indicates lack of perfusion. This can be pulselessness or apnea/gasping. Early on there is often doubt, but jump on the chest and start CPR if you don’t feel clear and obvious pulses.

Take Home Points:

-The pulse examination is not 100% sensitive or specific for cardiac arrest

-Given that we have to make decisions with imperfect information, it is better to err on the side of starting CPR

-Apnea is not 100% sensitive either, as respiration can continue for 1-3 minutes

PALPATE JUGULAR VENOUS DISTENSION

An obese patient presents with edema. You look for jugular venous distension and wonder if you see the ebbing in the neck (“Y descent”). Before you order BNP, there is one more thing you can do. Palpate the vein.

Large veins are palpable. In the days before we used ultrasound for central lines many of us had to learn to palpate central veins. They have thin walls and are full of fluid under low pressure, which is similar to the fluctuance of an abscess. An even better analogy would be a “water balloon” feel as you appose the walls of the vein and the edges are smooth against each other. This is sort of like those “magic eye” pictures that look scrambled but actually are three-dimensional. Some people simply can not perceive it. To those I say don’t give up, practice it, especially on yourself, and eventually you will get it.

Take Home Points:

If visualization is not obvious, palpate for jugular venous distension

IRREGULAR HEARTBEAT

A patient presents concerned about an irregular heart beat. You palpate the pulse and find indeed that it appears irregularly irregular.  Can you tell at the bedside whether this is atrial fibrillation?

 

Possible causes of an irregular pulse include atrial fibrillation, sinus arrhythmia, and atrial or ventricular ectopy. The physical diagnosis of these conditions has been well-described but not well studied.

 

Sinus arrhythmia can be quite irregular.  Have the patient hold the breath for 10-15 seconds. Does it become regular?

 

Ventricular ectopy does not reset the rhythm. Listen for the “beat” and nod your head along like it is a song. A few premature ventricular contractions should not change the original beats and your next head nod will come at just the right time.

 

Atrial ectopy does reset the rhythm. This one is harder to differentiate from atrial fibrillation.

 

You suspect atrial fibrillation based on the irregularly irregular rhythm. However, breath holding does make the rhythm regular. You check the EKG which confirms sinus arrhythmia.

 

Take home points:

For the patient with an irregular pulse, use breath holding to diagnose sinus arrhythmia.

PVCs do not reset the original rhythm, but PACs do

HUMAN DIVE REFLEX FOR SVT

A patient presents with racing palpitations with a heart rate of 160. Is this supraventricular tachycardia? You are waiting for the EKG. In the meantime you wonder about all those vagal maneuvers. You tried them early in your career and they didn’t work. Is it worth a second look?

 

The human dive reflex was reviewed this month in the Emergency Medicine Journal.(Smith EMJ 2012) In pediatric populations it was 90-100% effective but in adult populations for paroxysmal supraventricular tachycardia it was 5-20%. The authors note that heterogeneous studies with a low sample size limit conclusions. Until better evidence is found they recommend:

 

-Immerse the entire face, not just part of it (with cold packs)

-Employ augmentation techniques of a deep breath followed by breath holding, as well as calming measures)

-Duration of the treatment should be 30-40 seconds before abandoning it

 

Think back to your previous attempts. Did you use optimal methods? If not, maybe give it a try using the above techniques, and let me know how it goes.

 

Take Home Points

-Full face coverage

-Augmentation with deep breath, breath hold, calming techniques

-Wait 30-40 seconds before abandoning the effort

ACUTE AORTIC REGURGITATION SIGNS DIFFERENT FROM CHRONIC

Acute aortic regurgitation is distinct from chronic aortic regurgitation.  The top three causes are endocarditis, aortic dissection, and blunt trauma.  Analogous to the situation with acute mitral regurgitation (see separate posting), there has not been time for compensatory dilation of the ventricle, so back pressures rise. The left ventricular pressure rises significantly, and patients present with heart failure.

 

Because the compensatory ventricular dilation and increase in stroke volume has not yet occurred, none of the peripheral signs of aortic insufficiency are seen. No water hammer pulse, no Duroziez sign (to-and-fro murmur over the femoral artery with femoral artery compression) and no exaggerated pulsations seen distally. And in fact, the long murmur of aortic regurgitation is shortened and softened and heard mainly in early diastole (Stout, Circulation, 2009).  It is heard best with the patient sitting and leaning forward.  Augmentation maneuvers include bilateral compression of the arms, with handgrip as a less specific alternative.  Don’t be discouraged though, a search for this sign may pay off in key situations.  The International Registry of Acute Aortic Dissections has shown that the diastolic murmur of aortic regurgitation is present in as many as 44% of patients.(Hagen JAMA 2000)

 

The treatment is surgical, though afterload reduction is an important temporizing measure.

 

Take home points:

Acute aortic regurgitation presents with congestive heart failure

The murmur is shorter and more subtle than the chronic form

Peripheral signs of aortic regurgitation typically are not seen

ACUTE MITRAL REGURGITATION SIGNS DIFFERENT FROM CHRONIC

Acute mitral regurgitation is distinct from chronic mitral regurgitation.  The chronic state represents compensatory changes, including dilation of the left ventricle, which preserves cardiac output through increasing stroke volume.  In acute mitral regurgitation however, the left ventricle is typically normal in size, and the regurgitant streams shoots backward, leaving the ventricular volume pathologically low.   Forward flow is diminished, and these patients present with shock.  The retrograde flow causes pulmonary edema.

The classic teaching is that an acute murmur of mitral regurgitation suggests disruption or rupture of a leaflet, usually either from endocarditis or papillary muscle infarction.  But the murmur is different.  Sometimes it can be loud, but typically it is quieter.  The regurgitant blood quickly raises atrial pressure to equalize with the left ventricle.  Thus, regurgitation stops earlier and the murmur is earlier, shorter, and quieter (Stout, Circulation, 2009).

One other finding might help.  The pulmonary pressure is acute high, so P2 happens later.  Meanwhile the left ventricular volume is lower, so A2 happens earlier.  Thus, wide splitting of S2 is present, though this does not appear to have been well-studied recently.

The main point is that if the patient has shock and pulmonary edema without an explanation, look for signs of mitral regurgitation.  A new early systolic murmur or wide splitting of S2 is a sign that your patient may be heading to the operating room.

Take home points:

The murmur of acute mitral regurgitation may be subtle

Consider this diagnosis in unexplained shock and pulmonary edema

Listen for wide splitting of S2

RECOGNIZING THE DUCTAL-DEPENDENT LESION

A 2 week old is brought in severe distress and shock.  You suspect congenital heart disease with a ductal-dependent lesion.  Should you start prostaglandin E1?

 

The anatomy of congenital heart disease can be complex, but as one authority put it, “specific anatomical knowledge of the many complex lesions is not required for good early management.” (Brooks 2008)

 

The ductus arteriosus in the fetus bypasses the lungs, shunting blood from the pulmonary artery to the aorta.  After birth, the pulmonary resistance drops and it closes by smooth muscle contraction. This happens within the first two weeks, and that is when these patients present.

 

There are two types of ductal-dependent lesions.  Those that depend on the ductus for pulmonary flow and those that depend on the ductus for aortic flow. They present with cyanosis or shock, respectively. Prostaglandin E1 is indicated when the patient is unstable, and the examination suggests congenital heart disease.

 

Cyanosis: Apply the hyperoxia test. If the hypoxemia does not resolve with 100% oxygen, then it is assumed there is congenital heart disease.

 

Shock: Easily confused with sepsis and other systemic diseases. Specific signs of congenital heart disease should be sought, including pathological murmurs, abnormal pulses, rales, hepatomegaly, and cardiomegaly. If any of these are found, prostaglandin E1 is indicated.

 

Summary:

-Cyanosis: Failing the hyperoxia test diagnoses congenital heart disease

-Shock: Asymmetric pulses, pathological murmurs, cardiomegaly, and signs of congestive heart failure diagnose congenital heart disease

-Prostaglandin E1 is indicated in the crashing neonate with any physical signs of congenital heart disease.

PERICARDITIS

You see a patient with pleuritic chest pain.  The EKG shows ST segment elevation in the inferior leads as well as V2-V5. The closest cardiac catheterization laboratory is 120 miles away, and you normally give thrombolytics for STEMI.  But is this STEMI or pericarditis?  Can the history and physical examination help?

It has been estimated that as many as 5% of emergency department patients with noninfarction chest pain have pericarditis. (NEJM 2004)

Recognizing pericarditis is important because administration of thrombolytics may lead to hemorrhagic complications and even death.

The diagnosis of pericarditis rests on the right clinical story along with a confirmatory finding on physical examination, EKG, or echocardiogram. Describing the sensitivity and specificity of these findings is difficult because there is often no independent gold standard for diagnosis and there are no known large studies on the clinical findings in pericarditis in the emergency department.

Classic symptoms include pain localized at the area of the heart. The pain is classically pleuritic and worse with inspiration.  It is relieved with leaning forward. The pain can radiate to any cardiac referral area, but pain referred to the trapezius ridge might be more specific, caused by irritation of the phrenic nerve(NEJM 2004).

The incidence of a friction rub appears to be somewhat low, perhaps 18-34%(Cohen). It is easier to hear at the left lower sternal border with the patient leaning forward at end expiration.  In the emergency department, however, an additional maneuver for improving audibility is lowering ambient noise.  The rub is often transient and serial examination improves the sensitivity. (NEJM 2004, Spodick JAMA 2003).  Because of the poor sensitivity and specificity of clinical diagnosis, adjunctive testing is generally needed for diagnosis.

Electrocardiographic findings depend on the stage of illness.  Classically the disease starts with diffuse ST-segment elevation, which then resolves, followed by diffuse T-wave inversions, which then resolves. Diffuse PR segment depression may in fact be earlier and more sensitive than ST elevation.

Laboratory support for the diagnosis is said to include elevation in C-reactive protein and erythrocyte sedimentation rate.  However, the sensitivity and specificity for these laboratory markers for pericarditis in emergency department patients with chest pain is not known.  Troponin elevations occur in 35 to 50% , so this can not always help differentiate myocardial infarction from pericarditis.(NEJM)

Finally, an echocardiogram can be used when there is doubt about the differential diagnosis of myocardial infarction and pericarditis.  Regional wall motion abnormalities would support myocardial infarction whereas pericardial effusion, present in 58% of cases, would support pericarditis (Cohen 2008)

The patient’s pain is pleuritic but there are no additional specific signs of pericarditis.  You call the cardiologist and ask for an echocardiogram to ensure no regional wall motion abnormalities.  The cardiologist comes and though there is no effusion, there is also no regional wall movement abnormalities, so you both decide not to give thrombolytics.  Because of diagnostic uncertainty however, you transfer the patient for cardiac catheterization, and the arteries turn out to be clean. The patient’s discharge diagnosis is pericarditis.  The clinical diagnosis of pericarditis and the decision to withhold thrombolytics was felt to be courageous but well-justified, and ultimately protected the patient from exposure to hemorrhagic risks.

Summary: Confirmatory findings include

Exam – Pericardial friction rub

EKG – Classic diffuse ST elevation

Echo – Pericardial effusion