Senior Report 8.8


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


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.



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



1. C

2. B

3. A

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.


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.

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.



1. Smith, S. Pericarditis, or Anterior STEMI? The QRS proves it. Dr. Smith’s ECG Blog.

2. Merchant, et al. Takotsubo Cardiomyopathy: A Case Series and Review of the Literature. West J EM. 2008 vol. 9 no. 2.

3. Takotsubo Cardiomyopathy. Circulation. December 16/23, 2008 vol. 118 no. 25 2754-2762.

Senior Report 8.7


 Case Presentation by Heather Bowman, MD


Chief Complaint: “I took all of my pills”


History of Present Illness:

A 40 year old male with PMH DM, HTN, depression and recent cocaine use comes in reporting he wanted to kill himself. He admits to taking 10 tablets of remeron (mirtazapine) (15 mg tablets), and “whatever was left in the bottle”, possibly up to 30 tablets of simvastatin (20mg) as well as 8 tablets of a “cold medication”. He reports some chest pain and ringing in his ears. Otherwise denies nausea, vomiting, difficulty breathing, abdominal pain, or headaches. He denies taking any other substances including other pills, alcohol or drugs.


Past Medical History: DM, HTN, depression, closed head injury

Past Surgical History: “head surgery” following closed head injury

Medications: aspirin, lantus, lisinopril, simvastatin, remeron

Allergies: Tylenol

Social: no smoking or drinking, last use cocaine 4-5 days ago, no IVDA

Family History: HTN



Vitals: BP 193/106, HR 77, resp 18, temp 36.3, oxygen saturation 100% RA

Cardiovascular: regular rate & rhythm, no murmurs. Radial and DP pulses strong and symmetric, chest pain is not reproducible

Respiratory: clear to auscultation bilaterally

GI: Abdomen soft, non-tender, non-distended

Neuro: pupils 3mm, round reactive to light, facial smile symmetric, alert & oriented x 3, interacting appropriately

Psychiatric: admits to suicidal ideation, no homicidal ideation, no visual or auditory hallucinations



1. What is the most important study to get on the patient?

A. CBC and chem-7
C. Aspirin level
D. Urine drug screen


2. Chem 7 shows Na=140, K+=3.9, Cl=107, HCO3=25, BUN=13, creatinine=0.9, glu=346, Ca=0.9, Mg=1.8. EKG is as pictured. Aspirin level is negative. UDS shows cocaine otherwise negative. ECG as below; HR 81, PR interval 138, QRS 106, QTc 529

What is your next step?

A. Make sure magnesium >2mg/dL, potassium >4 mMol/L, and calcium and phosphorous are normal and call MICU
B. Tell pharmacy to mix 3 amps of bicarb in 250cc of normal saline and begin bicarb infusion on the patient and admit the patient.
C. Give the patient a few liters of normal saline, maybe some insulin, and clear the patient for psych when glucose is <300
D. Order a troponin and get ready to call CCU


3. Which substance that the patient took is likely causing the above EKG findings?

A. Remeron (mirtazapine)
B. Simvastatin
C. Cocaine
D. Antihistamine cold medication


4. (Bonus Question) Which dysrhythmia do you worry about above EKG progressing to?

A. Ventricular tachycardia
B. Bradycardia
C. Torsades
D. Atrial fibrillation



1. B. EKG: While the policy at many institutions is to get basic labs as part of the screening protocol for a psych patient these labs are often of low utility. Labs are often used for screening on a psychiatric patients with an exacerbation of their psychiatric illness to rule out other medical conditions. Laboratory results are used to clear your patient who has no other complaints but in a potential overdose situation an EKG is a better answer. While you may not expect any EKG changes with remeron or simvastatin, it is a cheap and easy test that should be obtained for any unknown medication overdose. In many cases of overdose, patients may not report all co-ingestions. One should not expect symptoms with salicylate overdoses in quantities less than 150mg/kg (6.5g). This patient reported taking 8 tabs of a cold medication which could have contained 325mg aspirin each, however this dose would not be close to the dose needed to induce tinnitus. It is prudent to consider aspirin and acetaminophen ingestion with any overdose as these are medications readily available in patient’s medicine cabinets. While we often order a UDS, toxicologists will tell you that it does not screen for all drugs and has many false positives. The patient admitted which tabs he took and disclosed his cocaine use, so a UDS is probably of lower utility than an EKG.
2. A. Make sure magnesium >2mg/dL, potassium >4 mMol/L, and calcium and phosphorous are normal and call MICU
This patient has a QT and a QTc of 456/529. A normal QTc is 350-440 in a female and up to 460 in a male. The poison center uses a cutoff of 500 as their cutoff for a worrisome EKG. Treatment for QTc prolongation is to make sure electrolytes are normalized and optimized (magnesium >2, potassium >4, and calcium and phosphorous are normal). When the potassium concentration in the blood rises the action potential shortens making arrhythmias less likely, so you should aim for a potassium a little higher than normal (4 instead of 3.5).

PLEASE DON’T GIVE BICARB AS THIS IS A GOOD WAY TO KILL THE PATIENT. Bicarb is treatment for QRS prolongation (as is seen in TCA overdose), not for QTc prolongation. While the patient is also hyperglycemic and option C would be a good answer if they had a normal EKG, in this case they need more than their glucose corrected before being cleared for psych. Not every EKG abnormality needs a heart catheterization. In this case his EKG abnormalities are from his ingestion, not cardiac disease.
3. D. Antihistamine cold medication
D. Antihistamine poisoning can include delirium, psychosis, seizure, coma, hypotension, QRS widening, QT interval changes and ventricular dysrhythmias including torsades. Although this patient was never able to confirm which medication he took based on EKG changes we suspect his “cold medication” contained a diphenhydramine type substance. Diphenhydramine is a reversible competitive histamine-1 receptor antagonist with significant effects including anticholinergic, sedative, anti-vertigo, antiemetic, antidyskinetic and local anesthetic properties. Presentation of diphenhydramine toxicity can include nervous system manifestations such as impaired consciousness, seizures, hallucinations, extrapyramidal movement disorders, toxic psychoses, ataxia, tachycardia, hypertension, hypothermia, convulsions, delirium, syncope and respiratory failure from crossing blood brain barrier. Anticholinergic effects can include fever, tachyarrhythmias, hallucinations, urinary retention, blurred vision and mydriasis. In addition to tachycardia, cardiac effects can include hypertension or hypotension, which may relate to other factors such as age, hydration status, co-morbid conditions and vascular tone. Through inhibition of fast sodium channels, patients can develop wide complex tachycardias. At higher diphenhydramine concentrations patients will also develop potassium channel inhibition which results in QT interval prolongation.
Remeron (mirtazapine) has sedative effects due to histamine receptor antagonism and orthostatic hypotension due to alpha 1 adrenergic antagonism. It has low incidence of anticholinergic side effects.
Simvastatin’s overdose effects are an extension of adverse effects including nausea/vomiting/diarrhea/abdominal pain, rhabdomyolysis, elevated LFTs, tendon rupture etc. Cocaine increases sympathetic activity and vasospasm and in overdose antagonizes cardiac sodium channels, thus the common complaint of cocaine induced chest pain. Severe toxicity can present with seizures or severe agitation.

4. C. Torsades

Dr. Nefcy

Senior Report 8.6


Case Presentation by Katherine Shulman, MD

Chief Complaint: Difficulty swallowing

History of Present Illness: This is a 66-year-old male with no significant medical history who comes in to emergency department complaining of difficulty in swallowing beginning 3 months ago. He further describes it as a foreign body sensation in his throat and has started eating a soft diet, which he tolerates well. He reports only mild discomfort with swallowing. Also, three months ago he noticed a change in his voice. He reports a “very mild” baseline shortness of breath over the same timeframe. He denies any neck pain, chest pain, fevers, night sweats, or headaches. No recent dental procedures. Denies any URI symptoms in the past several months.

Past Medical History: none

Medications: None

Social History: Denies tobacco, alcohol, or illicit drug use.

Family History: His brother just died of laryngeal cancer two months ago.


Physical Exam:

Vital Signs: BP 145/82; HR 98; RR 16; Temp 36.8; 98% RA

General: Patient sitting semi-fowler in stretcher in no acute apparent distress, with no acute respiratory distress. Handling oral secretions well. Speaking in full sentences with a muffled voice. Resting comfortably.

Head: normocepahlic; atraumatic

Eyes: EOMI; PERRL; pink conjunctiva

Mouth: moist mucous membranes, no tongue or submandiblar swelling, good overall dental hygiene, uvula midline; significant area of swelling in the right oropharynx just posterior to the tonsil with normal appearing overlying mucosa; no erythema, exudates, ulcerations in the anterior or posterior pharynx.

Neck: Supple; trachea midline; no palpable lymphadenopathy

Cardiovascular: s1, s2; regular rate and rhythm; no murmur

Respiratory: no stridor, lungs clear to auscultation bilaterally; symmetrical chest rise and fall; no accessory muscle use


Workup: We obtained laboratory tests and a CT – Neck w/ contrast.







1. What is the most likely diagnosis?

A. Peritonsillar Abscess

B. Nasopharyngeal Carcinoma

C. Diphtheria

D. Ludwig’s Angina


2. What is the most likely causative organism?

A. Streptococcus Species

B. Staphylococcus Aureus

C. Haemophilus Influenzae

D. Fusobacterium


3. What are the next steps in management?

A. Initial dose IV Clindamycin, discharge home w/ PO Clindamycin, and ENT f/u

B. IV Unasyn, consult ENT, medicine admit

C. IV Zosyn, consult ENT, ICU admit for compromised airway

D. Consult ENT, obtain blood cultures, medicine admit



1) A

2) A

3) B

1. A. The diagnosis is right peritonsillar abscess. The CT scan shows a large peripherally enhancing complex cystic mass arising from the right peritonsillar region (best seen in the first image) causing significant mass effect. The structure measures 5.4 centimeters in the greatest dimension, and the airway measures 1 centimeter at the narrowest dimension. This is a relatively uncommon presentation of peritonsillar abscess. Usually, the progression of disease occurs within a week, signs and symptoms include: odynophagia, dysphagia, drooling, trismus, muffled voice. Additionally, fever, malaise, and dehydration are common systemic symptoms.

B. Nasopharyngeal carcinoma is uncommon in the US, difficult to detect early, and usually presents with the following: cervical lymphadenopathy, sore throat, nasal discharge or bleeding, bloody saliva, ear infection or pain, changes in hearing, tinnitus, headaches.

C. Diphtheria usually presents with an upper respiratory tract illness with sore throat, low-grade fever, and an adherent grey pseudomembrane covering the posterior aspect of the pharynx. Due to vaccinations, there has been only one case in the US in the past ten years.

D. Ludwig’s Angina is a fulminant disease process that may lead to death within hours or days. It generally occurs secondary to a dental infection, causing progressive cellulitis of the submandibular space extending to the deep tissues of the floor and mouth.


2. A. Common organisms associated with peritonsillar abscess include the following: Streptococcus pyogenes (most common aerobic), Staphylococcus aureus, Haemophilus influenzae, Neisseria species, Fusobacterium (the most common anaerobic), Peptostreptococcus, Prevotella, and Bacteroides. For most abscesses, a mixed profile of both aerobic and anaerobic organisms proliferates. The final culture in the case above was positive for Streptococcus viridans, negative for anaerobic organisms.


3. B. IV antibiotics should be started. Unasyn, Zosyn, clindamycin, a combination of penicillin G and metronidazole, are all good options for treatment of inpatient peritonsillar abscess. Mainstay of therapy is needle aspiration or incision and drainage, which in this case should be performed by ENT. The patient has a large peritonsillar abscess and an airway measuring 1 cm in diameter at the narrowest point, thus, the patient should be admitted. A medicine floor admission is an appropriate disposition. ICU is not indicated at this time, as the patient is stable and not showing signs of respiratory distress. He is neither hypoxic nor tachypneic. Physical exam demonstrates a comfortable, well appearing male. In general, peritonsillar abscesses do not take such an indolent course as described in the case above.


Steyer, Terrence E. Peritonsillar Abscess: Diagnosis and Treatment. Am Fam Physician. 2002; Jan 65(1):93-97.
Marx, John A, et al. Rosen’s Emergency Medicine, 7th Ed. Philadelphia: Mosby Elsevier, 2010. Print.