Senior Report 8.8

seniorreport

Case Presentation by Sarah Michael, DO

 

Chief Complaint: “My chest has been bothering me.”

History of Present Illness:

A 67-year-old female patient presents to the ED complaining of chest discomfort slowly worsening over the past 10-12 hours. It has been relatively mild but constant since the time of onset. The patient reports a left substernal nonradiating pressure sensation. She has never experienced anything similar in the past and has not taken anything for pain. She is not short of breath, diaphoretic, dizzy, or lightheaded. When questioned further, the patient reports she thinks her symptoms are “due to stress” as she has been hosting several extended family members at her home over the past few days. She drove herself to the ED.

 

Past Medical History: hypothyroidism, hyperlipidemia

Past Surgical History: none

Medications: simvastatin, levothyroxine

Allergies: NKDA

Social: Lives alone. Drinks alcohol infrequently (none recently). No tobacco or drug use.

Family History: Denies significant family history. No family history of early myocardial infarction.

Physical Exam:

BP 138/86

HR 82

RR18

T 37.5

Oxygen saturation 100% RA

General: Alert, oriented, well-appearing Caucasian female, sitting in a chair without distress. She speaks in complete sentences.
Cardiovascular: Regular rate & rhythm. No murmurs. No chest wall tenderness or exacerbation of pain with palpation.
Respiratory: Clear to auscultation bilaterally
GI: Abdomen soft, non-tender, non-distended
Neuro: Alert, oriented, appropriate. Strength 5/5 in all extremities.
Psychiatric: No acute psychiatric decompensation is noted. She is appropriate, lucid and able to formulate and articulate complex thought processes without delusions. No evident anxiety.

A cardiac workup was initiated and the following EKG was obtained.

 

Web Case EKG

1. Where does the pathology demonstrated in the EKG localize?

A. right coronary artery
B. left circumflex artery
C. left anterior descending artery
D. pericardium

The following bedside echocardiogram was obtained in the ED.

 

echo

2. On the basis of the echocardiogram, where does the patient’s pathology localize?

A. right ventricle
B. left ventricle
C. mitral valve
D. pericardium

3. What is the underlying pathologic mechanism resulting in this clinical picture?

A. catecholamine surge
B. plaque rupture
C. inflammation with PMN infiltration
D. infection of a pletelet-fibrin nidus with circulating bacteria

 

Answers:

1. C

2. B

3. A
Explanations:

1. C. Let’s start by agreeing that this is not pericarditis (D). The concavity can be misleading, but recognize that the ST segments are not globally elevated. There is also a giant pathologic Q wave with deeply inverted T wave in III and a fragmented (potential goes up, then down, then up) small voltage QRS in V2. These features are far more consistent with infarct than with pericarditis.

There is ST elevation in V2-V6 consistent with anterolateral infarct. The remaining leads have been mapped on the hexaxial reference figure below.

LAD2

The infarct predominantly affects the anterolateral aspect with involvement of aVR and III. What vessel supplies all of these regions? A “wraparound” type III LAD, which, when obstructed, can produce ST elevations in any inferior, anterior or lateral leads. Caution is required because an obstruction of this vessel can create a compelling pericarditis mimic. (A) A dominant RCA is unlikely to cause this degree of anterior ST elevation. (B) Similarly, the circumflex (obtuse marginal) artery does not perfuse a large enough percentage of myocardium to cause diffuse ST elevation.

2. B. Takotsubo cardiomyopathy takes it’s name from “Tako-tsubo,” the Japanese word for “octopus pot.” With its wide base and narrow neck, this eartherware structure is an ideal home for unsuspecting cephalopods. It also nicely describes the shape of the LV apex in people afflicted with this condition, which is also called “left ventricular apical ballooning syndrome.” On echocardiogram, you will typically see dilation and hypokinesis of the apex with relative sparing of the base. There is typically not primary involvement of the other chambers or valves. Underlying left ventricular outflow tract obstruction exacerbates the disease.

octopus pot

Takotsubo cardiomyopathy typically presents in times of emotional distress and most commonly occurs in post-menopausal women. The initial presentation is often indistinguishable from STEMI and evidence of inferior, lateral, or anterior localization may be seen. Cardiac catheterization will reveal non-occlusive coronary arteries and apical dilation on left ventriculogram, shown below. Ejection fraction is often moderately to severely reduced and troponin is typically positive.

vgram
3. A. There are many names for the condition and in the lay media it is often referred to as “broken heart syndrome” because it presents during times of emotional stress, though the trigger may be relatively minor, as seen in this case. The definitive mechanism has not been elucidated, but there is clearly a catecholamine surge, which when combined with a relative decrease in endothelial NO after menopause, is thought to cause distal coronary artery vasospasm and myocardial ischemia.

(B) Plaque rupture would be expected in the case of obstructive atherosclerotic coronary artery disease. (C) Inflammation and PMN infiltration is typically seen in the setting of acute pericarditis. (D) Infection of a platelet-fibrin nidus is the mechanism by which endocardial vegetations form.

 

References:

1. Smith, S. Pericarditis, or Anterior STEMI? The QRS proves it. Dr. Smith’s ECG Blog. http://hqmeded-ecg.blogspot.com/2012/08/pericarditis-or-anterior-stemi-qrs.html

2. Merchant, et al. Takotsubo Cardiomyopathy: A Case Series and Review of the Literature. West J EM. 2008 vol. 9 no. 2. http://westjem.com/case-report/takotsubo-cardiomyopathy-a-case-series-and-review-of-the-literature.html

3. Takotsubo Cardiomyopathy. Circulation. December 16/23, 2008 vol. 118 no. 25 2754-2762. http://circ.ahajournals.org/content/118/25/2754/F4.expansion.html

Intern Report Case Discussion 1.2

intern-report

Presented by Jeff McMenomy, MD

History of Present Illness:
A 75-year-old woman is brought to the Emergency Department by EMS. Her family states the patient complained of gradually worsening generalized weakness and decreased responsiveness over the course of the previous week.  They also state that she is “not being herself”.  EMS noted the patient to be minimally responsive, bradycardic, and hypotensive en route to the hospital.

PMHx: hypertension
PSHx: unknown
FHx: unknown
SocHx: unknown
Allergies: codeine, penicillin
Medications: unknown

Physical Exam

Vitals: T 36.2 C, HR 40, BP 86/43, RR 18, O2 97% on 15 L nonrebreather
Gen: obtunded, oriented x 1, responds to name but not oriented to place or time
HEENT: NC/AT, PERRL, EOMI, no conjunctival pallor, TMs clear b/l, mucous membranes dry, no tonsillar exudates or erythema, + gag reflex
Neck: supple, FROM, no JVD, trachea midline, no cervical LAN
Heart: bradycardic, regular rhythm, no murmurs, rubs, or gallops.
Lungs: clear to auscultation b/l in all fields, no wheezes/rales/rhonchi, normal respiratory effort
Abdomen: soft, nontender, nondistended, bowel sounds normoactive, no rebound/masses/guarding
Vascular: capillary refill 3 seconds, pulses thready but palpable in all four extremities.
Neuro: responds to her name, follows commands. Eyes open spontaneously.  Tongue and uvula are midline.  Moving all four extremities.
Skin: + mild diaphoresis, no rashes

Electrocardiogram:

ecg1

QUESTIONS:

1. Given this patient’s overall clinical picture, what would be the most appropriate initial course of action?

A.   Place patient on a monitor, establish IV access, and administer 0.5 mg doses of atropine while preparing for transcutaneous pacing.

B.   Place patient on a monitor, establish IV access, and administer 325 mg of aspirin, 0.4 mg nitroglycerin sublingual, and morphine at 0.1 mg/kg.

C.   Place patient on a monitor, establish IV access, and administer CPR while preparing a cardiac defibrillator.

D.   Place patient on a monitor, establish IV access, and administer adenosine 6 mg rapid IV push.

E.   Place patient on a monitor, establish IV access, and administer a one liter fluid bolus of normal saline

___
2. Electrical capture by transcutaneous pacing is confirmed by which of the following?

A.   A p-wave, QRS complex, and t-wave showing a first-degree heart block pattern

B.   A pacing spike followed by a p-wave, QRS complex, and t wave all of normal morphology

C.   A return to normal rate with no change in rhythm

D.   A return to normal sinus rhythm with normal rate

E.   A widened QRS after each pacing spike

___

3. Which of the following statements regarding cardiac pacing is true?

A.   Although alternative approaches are acceptable, the femoral vein is the preferred site of percutaneous access for placement of the transvenous pacer.

B.  Hypothermia is a relative contraindication to transvenous pacing.

C.  Second degree heart block type I (Wenckebach)  is among the indications for transvenous pacing.

D.  Transvenous pacing is underutilized in traumatic cardiac arrest and evidence suggests that it may be beneficial in some cases

E.  When compared with the blind insertion technique, ECG-guided transvenous pacer insertion has been shown to be faster.

Discussion

A 75-year-old female presented to the emergency department with hypotention and bradycardia.  ACLS guidelines for symptomatic bradycardia were initiated including IV fluid resuscitation, administration of repeat doses of atropine 0.5mg IVP and placement of transcutaneous pacer.  Her HR remained below 60 bpm with these interventions and therefore transcutaneous pacing was initiated.  Her condition was refractory to transcutaneous pacing as well and so a transvenous pacer was placed.

The right internal jugular was chosen as the site to place the transvenous pacer.  The patient was draped in a sterile fashion and ultrasound guidance was used to obtain percutaneous access of the right internal jugular vein.  After inserting of the transvenous pacing catheter the catheter balloon was inflated and the catheter was floated down the internal jugular vein with ECG-guidance to the superior vena cava, into the right atrium.  Pacing was confirmed by an ECG pattern of an electrical spike followed by a wide QRS complex (see illustration below). After placement of this pacer, the heart was paced at a rate of 60 bpm.  Check out this review article on transcutaneous pacing.

pic

When a patient presents with bradycardia one must first determine if emergent intervention is warranted.  A small percentage of the population has a physiological heart rate of less than 60 bpm.  This patient, in contrast, was having generalized weakness and decreased responsiveness and therefore symptomatic bradycardia.  According to ACLS guidelines, hypotension is one of the “signs or symptoms of poor perfusion caused by the bradycardia.”  Atropine administration, transcutaneous pacing, and later transvenous pacing were all employed to stabilize this patient.  She eventually achieved stability with transcutaneous pacing.

These interventions were administered emergently before any laboratory results had returned.  Laboratory results indicated that electrolyte imbalances and dehydration were contributing factors.  The patient was admitted to the MICU and was eventually discharged after correction of her electrolyte abnormalities and dehydration.

When one is presented with a medical code situation in the emergency department whose conditions fit the criteria for one of the ACLS algorithms, the steps for the appropriate algorithm must be followed emergently.  The underlying cause will often not be apparent at initial presentation to the emergency department.  And once it is discovered it must be addressed.

ANSWERS

1.  The correct answer is A, “Place patient on a monitor, establish IV access, and administer 0.5 mg doses of atropine while preparing for transcutaneous pacing.”  The patient’s ECG shows a junctional bradycardia.  Proper treatment of this patient requires following ACLS guidelines for symptomatic bradycardia.  Current ACLS guidelines for intervention in bradycardia are for patients who have “signs or symptoms of poor perfusion caused by the bradycardia.”  Treatment includes administration of atropine 0.5 mg IV while preparing for transcutaneous pacing.  Atropine may be repeated to a total of 3 mg, otherwise the patient is at risk for anticholinergic toxicity.  Epinephrine and dopamine may also be considered.  If the patient’s condition is refractory to medical management, transcutaneous pacing, followed by  transvenous pacing may be indicated.

(B) is incorrect because it specifies the proper treatment indicated in the ACLS algorithm for acute coronary syndrome, not for symptomatic bradycardia.  Although ACS may be on this patient’s initial list of differential diagnoses, her condition should be treated immediately as symptomatic bradycardia.  If during the course of treatment the patient’s clinical picture begins to exhibit signs or symptoms more specific to ACS, then this patient may need to be treated with aspirin, nitroglycerine, and morphine.

(C) is incorrect because this patient has palpable pulses and CPR is only indicated in patients who are pulseless.  Asynchronous cardioversion is indicated only in pulseless patients and synchronized cardioversion is indicated in certain cases of tachycardia with pulses.  Neither form of cardioversion is indicated in bradycardia.

Administration of adenosine is indicated in the stable patient who is suspected to have a supraventricular tachycardia (AVnRT and AVRT). Answer choice (D), therefore, is incorrect.

Although a fluid bolus is often indicated in hypotension, it is not part of the symptomatic bradycardia treatment algorithm and therefore (E) is incorrect.  This patient’s hypotension may be thought of as a clinical sign of “poor perfusion caused by the bradycardia”  And improving the bradycardia will likely result in an improved blood pressure.  Nonetheless, fluids should be started to augment the patient’s blood pressure.

2.  The correct answer is E, “A widened QRS after each pacing spike.”  Under physiologic conditions, the ventricles of the heart are depolarized rapidly by the rapid progression of an electrical current through the His-Purkinje system, causing the QRS complex to take on a narrow appearance.  When the heart is paced from an external pacing source, such as and artificial pacer, ventricular depolarization takes more time, causing the QRS complex to take on a wide appearance.  The initiation of the electrical impulse by the pacemaker itself can be seen on the ECG as a very narrow spike.

An electrical impulse that begins at the SA node and progresses down all of the heart’s physiological pathways would be required to produce a P-wave, QRS complex, and T-wave of normal morphology, or to produce a pattern consistent with first-degree heart block.  Transcutaneous cardiac pacing does not begin at the SA node and does not progress in this manner.  Answer choices A and B, therefore, are incorrect.

Transcutaneous pacing therapeutically changes the cardiac rate and it also changes the rhythm so that the ECG shows pacing spikes followed by wide QRS complexes when capture is achieved.  Therefore C and D are both incorrect answers.

3.  The correct answer is: B, “Hypothermia is a relative contraindication to transvenous pacing.”  Introducing a transvenous pacer into a patient who is hypothermic has a theoretical potential of causing the patient to have a terminal dysrhythmia.  Hypothermia, therefore, is considered a relative contraindication to transvenous pacing.  Hypothermic patients should be warmed according to standard hypothermic care.

When placing a transcutaneous pacer, either the right internal jugular vein or the left subclavian vein should be considered first as they have been shown to have “the highest rates of proper placement in code situations” (Harrigan et al).  Answer choice A, therefore, is incorrect.  The femoral approach may be indicated in the coagulopathic patient.

Although electronic cardiac pacing may be considered in advanced forms of AV nodal block, second degree heart block type I (Wenckebach) is relatively benign and an invasive procedural is generally not warranted.  Answer choice C, therefore, is incorrect.

Answer choice D is incorrect because cardiac pacing is not indicated in traumatic cardiac arrest.

Although there are advantages to the ECG-guided technique for transvenous pacer insertion, speed is not one of them.  The blind technique is, in fact, faster, making answer choice E incorrect.

References
Harrigan RA, Chan TC, Moonblatt S, Vilke GM, Ufberg JW. Temporary Transvenous pacemaker placement in the emergency department. J Emerg Med 2007;32: 105-11.

This case discussion presented by Jeff McMenomy, MD.

Morrison’s Pouch: Answer 1.1

morrisons-pouch-redo1

Although we had many submissions – there were NO WINNERS this week

A 75-year-old woman presents with left lower extremity swelling and pain behind the knee for the past few days.  She has been taking ibuprofen and was referred from her PMD, who was concerned that she may have a DVT.  The patient has a history of hypertension and diabetes.  She smokes cigarettes daily.   Her vital signs are within normal limits.  On physical exam, her legs are symmetric in size, her dorsalis pedis pulses are 2+ and symmetric, there is no erythema, but she is tender to palpation in the popliteal fossa.

Questions:

1.  What is the diagnosis?
2. Which veins of the lower extremity are visualized in the DVT examination?
3. Name a finding seen on ultrasound exam that is consistent with the diagnosis of DVT?

Answers:
1.  Baker’s cyst
2. from the exam includes the veins from the iliofemoral junction to the popliteal fossa.
3. Veins that are not completely compressable are indicative for a DVT.

This patient’s leg veins were fully compressible, so a DVT was ruled out.  The ultrasound exam demonstrated a Baker’s cyst, which explains the pain she is having behing her knee.  The patient was discharged with pain medications and instructions to follow-up with her PMD for a repeat ultrasound in 1-week.

baker2-labelled

pop2-labelled4 saph2-labeled4 split2-labeled3

Discussion:
As ED physicians, we are using ultrasound with increasing frequency to evaluate the lower extremity for DVT, Baker’s cyst, and abscesses.  A Baker cyst is a synovial cyst that is located posterior to the medial femoral condyle, between the tendons of the medial head of the gastrocnemius and semimembranous muscles. It usually communicates with the joint by way of a slitlike opening at the posteromedial aspect of the knee capsule just superior to the joint line. An extension of the knee joint, a Baker cyst is lined with a true synovium.  The common symptoms of baker cysts include localized swelling and pain, and decreased range of motion of the extremity. Baker cysts commonly resolve following rest; analgesics and extremity elevation help to reduce swelling and pain. If symptoms persist, an orthopedic surgeon can excise the cyst.

Over the past decade, emergency ultrasound is well established in its use to detect lower extremity DVT.  The exam is traditionally performed by ultrasounding from the iliofemoral vein junction to the popliteal vein. After identifying these vessels, the vein is followed and compressed at 1-centimeter intervals. Full collapse indicates that no DVT is present, while partial or incomplete collapse is diagnostic of DVT.
Several studies have shown that ED ultrasound interpertation is equivalent to formal ultrasound studies. A 2000 study showed ED ultrasound exams and formal ultrasound studies agreeing in 110 of 112 cases of possible DVT. Of the two discrepancies, one was a false positive ED reading. The other was an ED-positive exam that was initially read as negative by formal ultrasound but later shown to be DVT-positive by venography. Another study done in 2004 showed that 154 of 156 DVTs were diagnosed by ED ultrasound, the remaining two being false positive results.

In addition, the ED evaluation of DVT saves time in correctly diagnosing the presence or absence of DVT, prevents a potentially unstable patient from having to leave the ED department for a study, and ensures the timely diagnosis even when an ultrasound technician is unavailable.

This case prepared by Dr Sam Lee, PGY-1 Emergency Medicine Resident, Detroit Receiving Hospital

Bibliography

  1. Blaivas, Lambert, Harwood, Wod, Konicki. Lower-extremity Doppler for Deep Vein Thrombosis – can emergency physicians be accurate and fast? Academic Emergency Medicine. Feb 2000. Vol. 7, number2. pgs. 120-1262.
  2. Stephen A. Shiver MD and Michael Blaivas. Acute Lower extremity pain in an adult patient secondary to bilateral popliteal cysts. Journal of EM: Volume 34, issue 3, April 2008. pgs 315-3183.
  3. Theodoro, Blaivas, Duggal, Snyder, Lucas. Real-time B-mode Ultrasound in the emergency department saves time in the diagnosis of Deep Vein Thrombosis American Journal of EM Vol 22, no. 3, may 2004. pgs. 197-200

“Morrison’s Pouch” is an educational module that utilizes ultrasound video clips from case presentations in the Emergency Department.  The section is hosted by Dr. Daniel Morrison, Director of Emergency Medicine Ultrasound for Detroit Medical Center, and case presentations are submitted by the EM residents of Detroit Receving Hospital.

Answer Tracings Vol 1.2

Winners

Allison Loynd          Marjan Siadat       Richard Gordon

David Mishkin         Brian Kern

Case

ecg2

ECG Interpertation

  • anterolateral wall STEMI
  • ST-elevation in leads I, AVL and precordial leads V2-V6.
  • Evolving Q waves are seen in several leads.

There is, in addition, complete heart block (CHB). The atrial rate is 125 bpm, while the ventricles are beating at 52 bpm. The arrows in ECG#2 show P waves (except the 8th P wave, which is buried in a QRS complex) marching through the QRS complexes.

Remember: you have AV dissociation but NOT CHB if the atria and ventricles are dissociated BUT the ventricular rate is FASTER than the atrial rate.

Discussion

CHB occurs in about 5% of STEMIs. When it occurs in association with anterior wall MI, the prognosis is grave with mortality as high as 70-80%. This apparently is not causally related to the CHB itself but reflects that large MIs, which have worse outcomes, are more likely to have associated CHB.

In this case the patient was taken rapidly from the ED to the cath lab, where the LAD was found to have a proximal ruptured plaque with thrombus resulting in a 99% stenosis. This was successfully stented. A large troponin leak peaked at >22.78.

Although complete heart block with STEMI is generally considered to be an indication for at last temporary pacemaker placement, in this case after stenting the heart block resolved and it was felt that the patient did not need a pacemaker.

Echocardiogram on the 2nd hospital day showed a small LV cavity with concentric hypertrophy, severe hypokinesis of the mid
to distal and anterior septal wall, and akinesis of the apex. Ejection Fraction was 35%.

The patient was discharged home on the 4th hospital day.

Tracings is a learning module involving actual cases of patients and their ECGs that present to the Emergency Department.  Topics chosesn are dervied from the EM Model for Resident Education. Cases are prepared by Dr. William Berk.

Tracings Vol 1.2

A 79-year-old Bangladeshi man arrived in the ED via private car.  He describes having chest pain for 4 hours that is worse on the left side than the right. He speaks no English and it is impossible to immediately obtain a more detailed recent history.  His past medical history includes Type 2 diabetes and a  “thyroid problem.” His medications include glipizide 5 mg once daily and levothyroxine 50 mcg once daily. On exam, his BP is 154/71 mm Hg, P 62 beats per minute, R 18 breaths per minute, and T 96.7. He is alert and as far as can be ascertained, oriented. There are no other significant exam findings.
A 12-lead ECG was obtained as seen below.

ecg1

Questions:

1.  What is your ECG interpretation?
2.  What is your disease differential diagnosis?
3.  What would you do?

Please post your answer in the “reply box” or click on the “comments” link  You will not see your answer post until next week when all of the submitted answers will be posted.  Good luck!

Tracings is a learning module involving actual cases of patients and their ECGs that present to the Emergency Department.  Topics are derived from the EM Model for Resident Education. Cases are prepard by Dr. William Berk.