Tuesday, December 21, 2010

Two more Cases of Takotsubo Stress Cardiomyopathy

Two more Cases of Takotsubo Stress Cardiomyopathy

Case 1.

This is the ECG of a 50 yo old woman who collapsed, was found to have a pulse, but then found to be in ventricular tachycardia. She was shocked into sinus rhythm. She presented to the ED comatose.
There is marked ST elevation especially in leads V3 to V6, as will as limb leads I and II, with no reciprocal ST depression. The cath lab was activated for STEMI, but the patient had clean coronaries. Before initiating therapeutic hypothermia, a head CT was done and showed fatal subarachnoid hemorrhage.
Case 2.
This 81 yo was found comatose.
.



There is ST elevation in V1-V3 with hyperacute T-waves and Q-waves in V2 and V3. This is highly suspicious for acute anterior STEMI. However, she was found to have a fatal pontine hemorrhage and had a maximum troponin I, at 12 hours after presentation, of 2.0 ng/ml. Echocardiogram showed an anteroapical wall motion abnormality. In this case, since no angiogram was done, it is not proven that she did not have a simultaneous anterior STEMI, but with a low maximum troponin and alternative explanation, it is highly unlikely.
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These cases demonstrate that SCM can present with STEMI pseudoinfarction patterns.

Takostubo Stress Cardiomyopathy, with Echocardiogram

Takostubo Stress Cardiomyopathy, with Echocardiogram

This case was posted on the www.hqmeded.com ultrasound site, of which this ECG blog is a part. However, only the first ECG was shown, and it was recorded before the patient became ill.

I refer you to the video case presentation by one of my colleagues, Dr. Rob Reardon (who has, by the way, a fantastic collection of ED ultrasound cases).
http://www.hqmeded.com/node/107

Briefly, this woman without significant cardiac history went into pulmonary edema with respiratory failure. Her ED echo is diagnostic of apical ballooning, also known as "stress cardiomyopathy" (SCM) or "takostubo cardiomyopathy" (because the heart, with its apical ballooning, resembles the Japanese octopus trap called a "takostubo"). The contraction at the base of the heart remains intact, while contraction of the distal or apex is very poor.

Here is the first ECG after the patient became ill.

There is sinus tach with some anterior ST elevation, however not an alarming amount.

Several hours later, she had this ECG recorded:
Theere is anterior T-wave inversion and very long QTc (680 ms). These are classic SCM findings after the hyperacute phase.


This ECG was recorded the following day:
The QTc is even longer now, at > 700 ms. T-waves are bizarre.
.
The coronaries were clean, the troponin had a small bump, and the patient recovered. The apparent trigger was stress from losing custody of children.
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SCM may happen from a wide variety of psychological or physiological stresses, including respiratory failure (although in this case a psychological stress led to poor myocardial function and then pulmonary edema, then respiratory failure) and intracranial bleeding.
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In this case, the ECG never mimicked a STEMI. I will proceed to post a couple cases in which SCM does mimic STEMI.

Sunday, October 17, 2010

Cardiac Arrest, widespread ST depression, but NOT due to ACS


Cardiac Arrest, widespread ST depression, but NOT due to ACS

This young male had ventricular fibrillation during a triathlon. He was resuscitated with chest compressions and defibrillation and 1 mg of epinephrine. On his bib it stated that he had a congenital heart disorder. He arrived in the emergency department hemodynamically stable. His initial ECG is shown here.
There is widespread ST depression. However, note that wherever there is ST depression, it is associated with a very high voltage R-wave. There is profound LVH. Such widespread ST depression maybe secondary to LVH, or due to ischemia, or to both. When there is widespread ST depression do to acute coronary syndrome, it is usually due to three-vessel disease or left main disease. This would be highly unusual in a young athlete. Therefore, one must conclude that the ST depression is either do to LVH or to demand ischemia, or both.

A bedside echo performed by the emergency physician showed no wall motion abnormality and confirmed LVH. A repeat ECG shown.

Now, there is less ST depression. The troponin returned positive, and the maximum troponin was 3.8 ng/ml. Thus, the ST depression was at least in part due to ischemia. This confirms a "Type II" myocardial infarction; that is to say, it is not due to ACS but rather to demand ischemia.

The next day, and angiogram showed normal coronary arteries. An echocardiogram confirmed aortic stenosis with a large pressure gradient. The stress of the triathlon cause demand ischemia and ventricular fibrillation

BRUGADA SYNDROME


Pseudoinfarction patterns: there are many and this is one: what is it?

This is courtesy of Mohammed S. Alo, who kindly let me reproduce a case from his blog (Mohammed Alo's blog).

This is a 40 year old male with chest pain. The cardiologist was called for management of a STEMI:



It is sinus rhythm, and there is slightly wide and abnormal appearing QRS, with an rSR' (though I don't think the duration is long enough to be RBBB, but that is a bit hard to read). There is significant ST elevation in V2 and some in V3. However, it just does not have the appearance of anterior STEMI. First, when assessing any ST-T abnormalities, one must determine if they are "primary" (due to pathology such as ischemia or hypokalemia, etc.) or "secondary" to an abnormal QRS. And here the QRS is abnormal. Then, think if it conforms to any known pathologic morphology. If you do, and you are aware of the 3 forms of Brugada syndrome, you will see that this is very similar to Type II Brugada.
Here are the 3 types:
Type I) ("Coved type") V1 has an incomplete RBBB, a wide R' wave, a downsloping ST segment, and in inverted T-wave, like this (I am sorry that due to a defect with the blogger software, this cannot be enlarged):
Types II and III) These have a saddle back ST-T wave, as in the case presented. The ST segment is at least 1 mm in Type II and less than 1 mm in Type III
There are also variants of early repolarization that can mimic Brugada. Here is one that mimics type III Brugada (again, sorry it cannot be enlarged):

Case conclusion: the man did indeed have Type II Brugada, not Anterior MI.

Monday, October 4, 2010

Risk Assessment: Minor Head Injury in Infants and Children in the Emergency Department

This is a best estimate, folks. We've presented what we think is the closest thing to the truth about this intervention, but our data is only as good as the studies that underlie it — and often, the studies aren't as complete or as good as we'd like, and in some cases the data have not been validated. We present one number here for the NNB, but please realize this is an estimate and there is a range for actual risk in a given person. That range will depend upon the person's demographic, their subtype of possible disease, the setting of the risk assessment, their general health, and literally thousands of other variables. Using these numbers in practice means taking a number of large leaps about all of these variables, and also about the veracity of the underlying research. Therefore, as with any 'high quality' data, the application of data requires a doctor's expertise and deliberate consideration.
In Summary, if you meet the below criteria for this assessment:
  • At initial examination:
    • 99.1% will not require (or undergo) neurosurgery
    • 0.9% will undergo neurosurgery*
  • After 4-6 hours have elapsed from the injury:
    • 99.8% will not require (or undergo) neurosurgery
    • 0.2% will undergo neurosurgery or deteriorate
    *There were no fatalities in the cohorts reported for this group
In Other Words:
  • At initial examination, the risk of an injury requiring neurosurgery is 1 in 110
  • After 4-6 hours have elapsed from the injury, the risk of an injury requiring neurosurgery is 1 in 500
Criteria:
  • Head injury being seen in an emergency department, and GCS=14 or 15
  • Excluded: Ground level falls, and running or walking into a stationary object, where the only visible trauma includes abrasions or lacerations (but no hematoma) were considered 'trivial' and were therefore excluded

Where We Get The Numbers:

Source: 1) Kupperman N, et al. Identification of children at very low risk of clinically-important brain injuries after head trauma: a prospective cohort study. Lancet 2009; 374: 1160–70

2) Reilly PL, et al. Patients with head injury who talk and die. Lancet, 1975; 306 (7931): 375 - 377

3) Galbraith S. Misdiagnosis and delayed diagnosis in traumatic intracranial haematoma. BMJ. 1976; 1: 1438.

4) Jennett et al. Severe head injuries in thre countries. J Neurol Neurosurg Psychiatry 1977 40: 291-298

5) Rose J, et al. Avoidable factors contributing to death after head injury. BMJ. 1977; 2 : 615

6) DaceyRG, et al Neurosurgical complications after apparently minor head injury. J Neurosurg. 1986; 65: 203-210.

7) RockswoldGL, et al. Analysis of management in thirty-three closed head iniury patients who "talked and deteriorated." Neurosurgery 1987; 21: 51-55

8) Rosckwold GL, et al. Patients who talk and deteriorate. Ann Emerg Med. 1993; 22(6): 1004-7

Harm Endpoints: Badness endpoints: Neurosurgery, death, intubation
Narrative: Minor head injury is an extremely common problem experienced by children everywhere and seen by physicians everywhere.


A small proportion of patients who appear to be neurologically normal will go on to have intracranial bleeding that will typically be treated with neurosurgery, but reliably predicting which children will have these outcomes without over-treating and over-testing has been difficult. This review examines the highest quality data available from a huge, multi-center emergency department study examining the evaluation of children with minor head injuries.(1)



The decision aids that the study presents are excellent, and present precise risk estimates in the setting of children with specific findings. Children who are under age 2 who are acting normally, do not have signs of skull fracture or a scalp hematoma (frontal hematomas are allowed), did not lose consciousness for >5 seconds, and did not have a 'severe mechanism'* have a risk of <1 in 5000 of having a major neurosurgical injury. For those over age 2 if they are neurologically normal, and have no severe mechanism*, severe headache, signs of skull fracture, or vomiting, their risk is <1 in 2000.



This is important information but should not be taken to mean that anyone with these factors is 'high risk'. Even among those children who appear to have a decreased level of consciousness (GCS of 14) or a skull fracture, 23 out of 24 children will not have a clinically important brain injury. Parents and physicians should know this information before moving to expensive radiographic imaging that carries risks and may require sedation to complete.



As with adults, when minor head injury children do have major problems such as neurologic deterioration it typically occurs in the first few hours. Rarely, it occurs beyond this time period, and a substantial body of case series literature suggests that when delayed major problems occur they occur in approximately 20% of bad outcome cases, and they occur after 4-6 hours.(2,3,4,5,6,7,8) In many cases these occur more than 12-24 hours later, making them quite delayed and in some cases detectable neither through a full day of observation nor with an immediate CT scan. Delayed hemorrhages do occur and are not always detectable with immediate imaging or observation.

Caveats: These data are from studies of head injured children being evaluated in ED's. This will not apply to many minor head injuries for whom risk is lower. In addition, enrolled children are in a subset of minor head injuries that is at higher risk than average because of the typical selection bias that comes with study enrollment (study subjects are usually higher risk than those who do not get enrolled in such studies). Therefore these risk estimates are likely to be high when applied to a general minor head injury population of children.



Alternately, the reported cohorts here were evaluated thoroughly by physicians for signs of skull fractures, neurologic abnormalities, and other signs and symptoms of brain injury. Therefore in the absence of this thorough physician evaluation it is not possible to know whether or not a specific patient is appropriately classified as a minor head injury meeting the above criteria.



Unlike data used in our review of adult minor head injury the data from the PECARN study of children that we cite (1) have not been validated. While they have been 'statistically' validated, the decision aid has not been applied to children in the clinical environment to determine how well it performs as a tool in this setting. Therefore while it is a large and excellent dataset, and it may even work better than unstructured physician judgment, this remains untested.



Finally, the above estimates of risk of delayed deterioration are based on extrapolation from case series' of patients, some of whom are pediatric and many of whom are adult, and these data are combined with the data from this large pediatric head injury study. They are not an observed set of outcomes, but rather a statistical speculation about the likelihood of delayed events after an initial 4-6 hours of normal neurologic findings in children.



*severe mechanism: car accident with ejection or fatality or rollover, pedestrian or non-helmeted bicyclist hit by a car, falls of more than 3 feet for <2 y/o and 5 feet for >2 y/o, or head struck by a high-impact object (e.g. baseball bat)

Author: David Newman, MD
Published/Updated: September 19, 2010

Risk Assessment: Minor Head Injury in Adults in the Emergency Department

This is a best estimate, folks. We've presented what we think is the closest thing to the truth about this intervention, but our data is only as good as the studies that underlie it — and often, the studies aren't as complete or as good as we'd like, and in some cases the data have not been validated. We present one number here for the NNB, but please realize this is an estimate and there is a range for actual risk in a given person. That range will depend upon the person's demographic, their subtype of possible disease, the setting of the risk assessment, their general health, and literally thousands of other variables. Using these numbers in practice means taking a number of large leaps about all of these variables, and also about the veracity of the underlying research. Therefore, as with any 'high quality' data, the application of data requires a doctor's expertise and deliberate consideration.
In Summary, if you meet the below criteria for this assessment:
  • At initial examination:
    • 99.6% will not require (or undergo) neurosurgery
    • 0.4% will undergo neurosurgery*
  • After 4-6 hours have elapsed from the injury:
    • 99.92% will not require (or undergo) neurosurgery
    • 0.08% will undergo neurosurgery or deteriorate
    *There were no fatalities or intubations in the cohorts reported for this group
In Other Words:
  • At initial examination, the risk of an injury requiring neurosurgery is 1 in 250
  • After 4-6 hours have elapsed from the injury, the risk of an injury requiring neurosurgery is 1 in 1250
Criteria:
  • Probable or definite loss of consciousness at initial injury, or memory lapse during examination
  • Neurologically normal on physician examination (other than memory loss)
  • Glasgow Coma Scale of 15 (out of 15 potential points)

Where We Get The Numbers:

Source: Stiell IG, et al. The Canadian CT Head Rule for patients with minor head injury. Lancet. 2001; 357: 1391-1396.

Stiell IG, et al. Comparison of the Canadian CT Head Rule and the New Orleans Criteria in patients with minor head injury. JAMA.2005;294:1511-1518

Smits M, et al. External validation of the Canadian CT Head Rule and the New Orleans Criteria for CT scanning in patients with minor head injury. JAMA. 2005; 294: 1519-1525.

Reilly PL, et al. Patients with head injury who talk and die. Lancet, 1975; 306 (7931): 375 - 377.

Galbraith S. Misdiagnosis and delayed diagnosis in traumatic intracranial haematoma. BMJ. 1976; 1: 1438.

Jennett et al. Severe head injuries in three countries. J Neurol Neurosurg Psychiatry 1977 40: 291-298

Rose J, et al. Avoidable factors contributing to death after head injury. BMJ. 1977; 2 : 615.

Dacey RG, et al Neurosurgical complications after apparently minor head injury. J Neurosurg. 1986; 65: 203-210.

Rockswold GL, et al. Analysis of management in thirty-three closed head iniury patients who "talked and deteriorated." Neurosurgery 1987; 21: 51-55.

Rosckwold GL, et al. Patients who talk and deteriorate. Ann Emerg Med. 1993; 22(6): 1004-7.
Harm Endpoints: Neurosurgery, death, intubation
Narrative: Minor head injury is an extremely common problem experienced by people everywhere and seen by physicians everywhere.
A small proportion of patients who appear to be neurologically normal will go on to have intracranial bleeding that will typically be treated with neurosurgery, but reliably forecasting these outcomes without over-treating (or over-testing) an unacceptable proportion has been difficult. This review examines the highest quality data available from emergency department evaluation of patients with minor head injuries, and concludes that untoward outcomes appear to occur at a consistent percentage (0.4%) across multiple minor head injury study populations.
1 2 3 4

Decision aids such as the Canadian CT Head decision aid are also useful.3 4 The aid suggests that neurologically normal patients who do not have signs of fracture on examination, who are under age 65, and who have not vomited 2 times or more will not require neurosurgery at any point. This is important information but should not be taken to mean that anyone with vomiting or over age 65, for instance, is likely to require neurosurgery. The data suggest, in fact, that neurologically normal patients over age 65 still have a 99% chance of requiring no further intervention, and physicians and their patients should be aware of these risks.

When minor head injury patients do have major problems such as neurologic deterioration it typically occurs in the first few hours. Rarely, it occurs beyond this time period. A substantial body of case series literature suggests that when delayed major problems occur they occur approximately in 20% of bad outcome cases and they occur after 4-6 hours.
5 6 7 8 9 10 11 In many cases they occur more than 12-24 hours later, making them quite delayed and in some cases detectable neither through a full day of observation nor with an immediate CT scan.
Caveats: These data are from studies of head injured patients being evaluated in ED's. This will not apply to many minor head injuries for whom risk is lower as their condition did not prompt them to seek care. In addition, many enrolled patients are in a subset of minor head injuries that is at higher risk than average because of their loss of consciousness, and the typical selection bias that comes with study enrollment (study subjects are usually higher risk than those who do not get enrolled in such studies). Therefore these risk estimates are likely to be high when applied to a general minor head injury population.

Alternately, the reported cohorts here were evaluated thoroughly by physicians for signs of skull fractures, neurologic abnormalities, and other signs and symptoms of brain injury. Therefore in the absence of this thorough physician evaluation it is not possible to know whether or not a specific patient is appropriately classified as a minor head injury meeting the above criteria.

Finally, the above estimates of risk of delayed deterioration (the 'talk and deteriorate' or 'talk and die' syndrome) are based on extrapolation from case series' of these patients, combined with the data from major minor head injury studies. They are not an observed set of outcomes, but rather a statistical speculation about the likelihood of delayed events after an initial 4-6 hours of normal neurologic findings.

Author: David Newman, MD
Published/Updated: September 21, 2010

Wednesday, September 29, 2010

Telling A Patient "I Don't Know" Takes Years of Practice.


Telling A Patient "I Don't Know" Takes Years of Practice.

Physicians don't know everything. You may or may not have been raised to believe that physicians will always have the answers to all your questions.  They don't.  Not even the subspecialists whom patients believe are supposed to know everything. They don't. 

For many physicians, one of the hardest things to learn is how to tell the patient "I don't know". Medical school and residency offers no curriculum  that teaches your doctor how to tell you "I don't know".  For many doctors, admitting failure to the patient is a form of torture.

Telling patients "I don't know" takes practice.   Actually, it takes a lot of practice. You wouldn't think so, but for many new physicians, admitting their lack of knowledge about the science of your disease process is not easy.

I remember how hard it was to get through complete history and physical examinations during my early years as a third year medical student and then having to tell the patient I didn't know what was going on.  Telling a patient you don't know is hard.  Some doctors will never get comfortable with saying it.

As a resident, physicians are expected to engage in a greater sense involvement with their patient's care plan.  They are also expected to know more and more as the years progress. But rarely does one show up in morning report with the right answer being "I don't know".  Not knowing is never an acceptable answer during the grueling physician training process.  And many physicians train to accept that as the truth once they leave their academic training centers and enter the real world. 

I remember fielding hundreds of "That's the first time anyone has ever asked me that" type questions in my resident clinic.  I always seemed to have an answer  even if it wasn't the right answer.  I remember how hard it was to sit there, face to face, with a patient asking what may or may not have seemed at the time to be simple, easy and straight forward questions.   I remember thinking to myself that I should know this, but I don't. 

After seven years as a hospitalist and thousands of patients later, I find telling patients "I don't know" to be one of the easiest parts of my job as a physician.  If I don't know an answer, I don't hesitate.  I just tell the patient up front that I don't know.  And when I don't have an answer, often times the reason is because there is no answer, at least not the answer the patient is looking for.  In my clinical practice one of the most common indications I have found for telling patients "I don't know" comes in patients with chronic pain of unexplainable etiology that only responds to that drug that starts with a D.
Happy:  Ma'am, I understand you're having 12/10 abdominal pain,  I have concerns about pursuing further evaluation given the dangers of CT scan radiation exposure we are learning more and more about every day.  I think I am comforted by the fact you have had twelve CT scans, four ultrasounds, an exploratory surgery and hundreds of esoteric labs drawn in the last year,  all of which have been normal.  I am also comforted by your ability to keep down the Big Mac your boyfriend brought you an hour ago.  I see you have previously been referred to the outpatient pain clinic but refused to take the Elavil they recommended.  I have  previously discussed my concerns with you regarding your body's evidence of tolerance and dependence to narcotics, but you declined further evalutaion of this care modality.  I don't know why you're having abdominal pain for the last three years that only responds to dilaudid, but I have nothing further to offer you in your hospital care. I'm going to discharge you to home today.
Patient:  I can't go.  I'm having too much pain.
Happy:  I'm sorry ma'am.  I don't know what's going on, but I have nothing further to offer you in the hospital.  I'll fill out your paperwork for dismissal. 
Patient:  You're going to fill my dee-luu-ded aren't you?
Happy:  No ma'am.  I have a personal policy of not prescribing narcotics for unexplained chronic pain that only responds to dilaudid.   You'll have to talk to your primary care physician about long term management. 
Patient:  F**k you.
Happy:  I don't know what to say to that.
See how easy it is?  It gets easier every year.  Do you find it hard to tell a patient, "I don't know?"