Senior Report 8.19


 Case Presentation by Laura Smylie, MD

A 14 year old girl who presents with nausea and vomiting for one day and an abrupt onset of chest pain.
Vitals: BP 100/67, HR 121, RR 25, Temp 36.7, 100% on room air.




1. What is the diagnosis based upon the above x-rays?
a) Foreign body
b) Pneumothorax
d)Apical pneumonia

2. What is the likely etiology of the radiographic finding?
a) alveolar rupture secondary to forceful retching
b) esophageal rupture secondary to forceful retching
c) acute PE
d) no abnormality on chest x ray.

3. What is the most appropriate initial management of this patient?
a) place on continuous pulse oximetry, place a left sided chest tube
b) place on continuous pulse oximetry, 4mg ondansetron, NPO.
c) place on a continuous cardiac monitor, start heparin drip, consult cardiology.
d) send blood cultures, start antibiotics, encourage PO intake.


Answers and discussion:

1) C
2) A
3) B

1) C – Pneumomediastinum. You can see air tracking in the soft tissues of the neck and the upper aspects of the mediastinum. Although there could potentially be a pneumothorax (B) associated with this this, no pneumothorax can be seen in this study. No foreign body (A) is present and there is no infiltrate to suggest pneumonia (D).



2) A – Alveolar rupture secondary to forceful retching is the most likely etiology of the pneumomediastinum, although you should also be concerned for possible esophageal rupture secondary to forceful wretching (B) also known as Boerhaave’s esophagus. Review of the literature shows that in similar presentations, esophograms are typically negative for tears in the esophagus. Acute PE (C) has not been shown to present with free air. On a chest xray, the most concerning (and classically pimped) findings for acute PE are Hampton’s Hump and Westermark’s sign. Hampton’s Hump, represented in the first image below, shows a wedge shaped area of hyperdensity along the lung parenchyma periphery, indicative of an infact/PE. Westermark’s sign, as shown in the second image below, shows a focal peripheral hyperlucency secondary to oligemia, with or without dilation of the central pulmonary vessels.



3) B – Although there is no obvious pneumothorax on the initial chest x ray, you must keep a high level of suspicion for a small pneumothorax. This would not necessitate chest tube placement (A), but a nonrebreather and continuous pulse oximetry are appropriate if a small pneumothorax is present. Given that the retching led to the pneumomediastinum, treat her nausea with ondansetron. She should be kept NPO until an esophagram can be obtained (as an inpatient or in the observation unit) to definitively rule out Boerhaave’s esophagus. As an inpatient, the chest x ray should repeated in 6-8 hours. C is the treatment for a non-massive PE or NSTEMI; D is the treatment for pneumonia, neither of which applies in this case.


The percentage of pneumothorax will guide therapy. This picture illustrates that 2 cm pneumo is typically the cut off point for inserting a chest tube with a spontaneous pneumo but not necessarily with a traumatic pneumo.




Spontaneous pneumomediastinum: diagnostic and therapeutic interventions. Al-Mufarrej F, Badar J, Gharagozloo F, Tempesta B, Strother E and Margolis M. Journal of Cardiothoracic Surgery 2008, 3:59 doi:10.1186/1749-8090-3-59

BMJ Case Rep. 2012 Oct 10;2012. pii: bcr0320091647. doi: 10.1136/bcr.03.2009.1647.

Gantner J, Keffeler JE, Derr C. Pulmonary embolism: An abdominal pain masquerader. J Emerg Trauma Shock [serial online] 2013 [cited 2015 Mar 26];6:280-2. Available from:

Intern Report 7.14

Case Presentation by Luda Khait, MD

CC: “My chest hurts”

HPI: The patient is a 56yo female who presents to the emergency department as a medical code for tachycardia. She is well known to the emergency department for multiple admissions for DKA. The patient is complaining of chest pain that started earlier today, however, is unable to provide us with any more history due to confusion. She is thrashing on the stretcher, moaning, and not fully responding to questions.

ROS: Unable to obtain secondary to medical condition

Past medical history: Diabetes mellitus with multiple admissions for DKA, glaucoma, hypertension, renal insufficiency, chronic anemia
Past surgical history: Unknown
Social history: Per EMR positive history of remote drug abuse.
Family history: Diabetes
Medications: Reports she is compliant with her Insulin 70/30 10U BID, other medications unknown
Allergies: NKDA
PMD: She states she has no regular doctor

Physical Exam:
– T: 36.0 – orally
– P: 119
– BP 124/70
– R 20
– O2 sat 98% RA

GENERAL: The patient appears agitated and is hyperpnic. She is wearing clothes that appear dirty and have holes in them. She does open her eyes spontaneously, she is unable to coherently answer questions, however, is moaning in response to questions and pain.

HEENT: Head normocephalic, atraumatic Conjunctivae are pink without pallor. Pupils are 3mm bilaterally, equal, round and reactive to light.

NECK: Supple. Trachea midline.

HEART: Tachycardic rate, regular rhythm, no murmurs, rubs or gallops

LUNGS: Lungs are clear to auscultation bilaterally, no wheezes, rales, or ronchi, increased ventilation, no retractions or use of accessory muscles.

ABDOMEN: The abdomen is soft, nondistended. It is diffusely tender to palpation no rebound or peritoneal signs, no increased tenderness at McBurney’s point, negative Murphy’s sign.

EXTREMITIES: Dorsalis pedis and radial pulses are 2+ bilaterally. No pedal edema.

NEUROLOGIC: The patient is alert. Her face appears symmetric. She smiles and closes her eyes symmetrically. She responds to some commands and moving all 4 extremities with good strength and purpose. We are unable to evaluate her speech at this time, since she is moaning in response to questions.

ED Course: 
In the resuscitation bay, the patient was immediately placed on an O2/cardiac monitor, which revealed an O2 sat of 98% on room air and sinus tachycardia. Nursing staff placed two large bore peripheral IV lines and basic labs were drawn. Two boluses of NS were started wide open. Accucheck revealed a CBG >600.

A 12-lead ECG was obtained:









Chest XR revealed no pneumothorax or pulmonary infiltrates.

BMP: Na 142, K 4.7, Cl 91, HCO3 5, BUN 42, Cr 2.25 BG 1,037
AG: 46
CBC: WBC 11.4, Hgb 9.6, Hct 31.5, Pl 438
ABG: 7.15/15/126/8.1
Beta Hydroxybuterate: >100


Question 1: What is the most likely cause of this patient’s change in mental status?
A)   Hyperglycemia
B)   Dehydration
C)   Hyperosmolarity
D)   Acidosis
E)   Hyponatremia

Question 2: In the treatment of DKA, what is the ABG pH for which bicarbonate therapy is recommended?
A) pH < 6.8
B) pH < 7.0
C) pH < 7.1
D) pH < 7.3

Question 3: In a diabetic patient with refractory hypoglycemia, what medication are you most suspecting responsible for this finding?
A)   Pioglitazone
B)   Glyburide
C)   Metformin
D)   Rosiglitazone

Part B: Name a treatment for hypoglycemia associated with Type II DM (not glucose in any form).


Answers & Discussion
1) C
3) B
Bonus) Octreotide

Question 1: C. The pathophysiology of DKA involves concurrent insulin deficiency and glucagon excess that combine to produce a hyperglycemic, dehydrated, acidotic patient that has profound electrolyte abnormalities. Although all of the above can contribute to altered mental status, the most important factor is hyperosmolarity, a result of hyperglycemia and dehydration. The renal tubules begins to excrete glucose in the urine (glycosuria) when the blood glucose reaches a level above 160-180 mg/dl; the proximal renal tubules become overwhelmed at that level and are unable to resorb the excess glucose. The excess glucose in the renal tubules draws water and other electrolytes, via an osmotic effect, into the urine. This osmotic diuresis along with dehydration from poor oral intake and vomiting promotes hyperosmolarity and altered mentation. Ketoacidosis is also an important factor that can determine mentation, however, it has a contributory effect with hyperosmolarity, rather than absolute effect on its own in DKA.

The formula for serum osmolality is = 2(Na+) + Glucose/18

One must be very careful when interpreting the laboratory values in a patient with suspected DKA. The serum sodium levels are often misleadingly low in hyperglycemic states. In profound dehydration, sodium levels are usually on the lower end secondary to hyperglycemia, hypertriglyceridemia, low salt intake, increased GI/renal losses, along with perspiration/insensible losses. The pathophysiology of falsely low sodium is due to water flowing from cells into the intracellular space due to the marked hyperosmolarity, creating a dilutional hyponatremia. The true value of sodium can be calculated by adding 1.3-1.6 to the sodium lab value for every 100mg/dL of glucose above the normal value. This calculation cannot be accurately used, however, if profound hyperlipidemia is noted. Hypertriglyceridemia is a common finding in DKA, owing to the fact of impaired lipoprotein lipase activity and overproduction of hepatic VLDLs. These lipids further promote dilution of the blood and falsely decrease sodium concentrations.












Question 2: B. The use of bicarbonate therapy in treating DKA is controversial. Successful treatment of DKA involves correction of dehydration, hyperglycemia, and electrolyte imbalances. Initially, ABCs should be established. The initial fluid therapy is directed toward total intravascular volume expansion as well as restoration of renal perfusion. Typically, normal saline is used at a rate of 15-20ml/kg /hr. If the patient is in hypovolemic shock, more fluids may be necessary. If the patient has other co-morbidities, such as heart failure or CKD, it is important to monitor the patient hemodynamically so to not fluid overload the patient.

In general, insulin administration shuts of ketogenesis and in turn will correct the acidosis. Bicarbonate therapy is generally not recommended by the ADA, unless the pH is below 7. Bicarbonate therapy has not been shown to improve outcomes and has actually been shown to worsen prognosis in patients with pH ranges of 6.9-7.1, and in fact, lower pH has been shown to directly inhibit further ketogenesis via a feedback mechanism. Bicarbonate shifts the oxygen-hemoglobin dissociation curve to the right via 2,3-DPG deficiency, worsening oxygen release in tissues. Also, quickly correcting the intravascular acidosis will terminate Kussmaul respirations, allowing the CO2 to cross readily into the brain circulation across the blood-brain barrier, making CSF acidic. In addition, administration of bicarbonate will drive potassium further into the cells, making hypokalemia even more pronounced. Finally, overaggressive use of bicarbonate administration may produce alkelemia later on in the treatment course, secondary to ketones being metabolized into CO2, water, and bicarbonate.

This is a guideline and the complete clinical picture should be considered, not just a number.











Question 3: B. Hypoglycemia is a major and most dangerous complication associated with both type 1 and type 2 diabetes. Severe hypoglycemia is typically defined as blood glucose levels below 40-50mg/dL associated with altered mentation. It occurs when patients use too much insulin/oral hypoglycemic medication and either have decreased oral intake, increased energy expenditure, or increase their insulin dosage. Patients that have had multiple bouts of hypoglycemia may become immune to the warning symptoms, causing what is known as hypoglycemia unawareness. This in turn can result in significant morbidity and mortality. Since their blood sugar can plummet without their awareness, these patients may become unresponsive and unarousable very quickly and without warning. Signs and symptoms of hypoglycemia are a result of adrenergic drive of epinephrine. These signs and symptoms include sweating, nervousness, tremor, tachycardia, and altered mentation.

Pioglitazone and Rosiglitazone are within the thiazolidinedione class of oral hypoglycemics. This class of medications reverses insulin resistance of the muscle and fat cells, and also acts on hepatocytes to a lesser degree decreasing gluconeogenesis. Hypoglycemia is not a known side effect of thiazolidinediones. Glyburide, on the other hand, is a longer acting oral hypoglycemic belonging to the sulfonylurea class. This class of hypoglycemics is known to cause hypoglycemia, especially after exercise or missed meal, after being discharged from the hospital, with use of longer acting medications, and malnourished patients, amongst others. This class of medications increases insulin release from the beta cells of the pancreas at any blood glucose concentration. Metformin does not typically cause hypoglycemia because it only works when there is a baseline insulin level within the body. It acts to increase insulin’s action rather than to stimulate its release.

Patients with suspected overdose on oral hypoglycemic agents should be observed for 24 hours if hypoglycemia recurs after initial treatment in the ED. Patients that are most at risk for refractory hypoglycemia are those with impaired renal function, pediatric patients, and those patients who have just been started on an oral hypoglycemic.

In addition to frequent glucose monitoring and replacement, treatment with an agent to inhibit insulin release, like octreotide (a somatostatin analogue) canbe used. The recommended dose for adults ranges from 50-100 mcg IV or SC every 12 hours. In fact, giving patients multiple doses of D50 to raise their blood sugar in turn will stimulate more insulin to be produced, given the sulfonylureas still in the system. Although the exact mechanism of action is not known, Octreotide will block the insulin release that is caused both by the sulfonylureas and dextrose.

Prior to discharge, a meal should be given to the patient to make sure that the patient can tolerate oral feedings and this meal can begin to replenish the glycogen stores. Close outpatient follow-up is necessary to re-evaluate the oral hypoglycemic agent dose.


Conn’s Current Therapy 2014 Edward T. Bope, Rick D. Kellerman; Elsevier Inc, 2014

Rosen’s Emergency Medicine

Kitabchi A, et al. Hyperglycemia Crisis in Adult Patients with Diabetes. Diabetes Care, Volume 29, #12. December 2006.











Senior Report 7.13

Case Presentation by Dr. Tim Scott, DO

CHIEF COMPLAINT: “MY chest hurts”

HISTORY OF PRESENT ILLNESS:  62yo white male presents from home with chest pain.  He states it is substernal and non-radiating and started 30 mins prior to arrival while he was helping his wife in the garden.  He was kneeling down cutting thorns off of a rose bush.  It states it felt like indigestion and he tried to burp a couple of times but it did not help.  It was 8/10 initially and is now 6/10.  He went in the house and sat down and drank a glass of water but this did not help.  He takes an aspirin daily and did not try any other medications.  He states he feels a little sweaty and light headed but denies any other symptoms.  Otherwise usual state of health.  States he has hypertension, no previous history of heart attack or coronary artery disease he is aware of.

Constitutional: Denies weight losst
Cardiovascular: Denies palpitations or syncope
Respiratory: Denies hemoptysis
Gastrointestinal: Denies rectal bleeding
Genitourinary: Denies hematuria

PAST MEDICAL/SURGICAL HISTORY: HTN – only surgery was tonsillectomy many years ago



SOCIAL HISTORY: Pt denies smoking, socially drinks alcohol and denies ever using any illicit drugs

VITAL SIGNS: Blood pressure 106/54, pulse 92, respirations 20, temperature 36.3, SpO2 95% on RA
GENERAL:  Well-developed, well-nourished, alert and oriented x3 and mildly uncomfortable secondary to acute condition.
HEENT: Head is normocephalic and atraumatic with no gross signs of trauma.  The pupils are equally round bilaterally with extraoccular movements grossly intact and no conjunctival pallor.  Sclera are icteric and non-injected.  Mucous membranes of the mouth are moist without erythema.
Neck:   No adenopathy. Trachea is midline.
LUNGS: Clear to auscultation bilaterally without wheezes, rales or other adventitious breath sounds.  Good airflow, no accessory muscle use.
HEART: Regular rate and rhythm.  S1-S2 noted.  No clicks rubs or gallups auscultated. No murmurs auscultated.
ABDOMEN: Soft, non-tender, non-distended.  No pulsatile masses appreciated.
MSK/EXTREMITIES: Normal strength bilaterally in upper and lower extremities.  Peripheral pulses are present and symmetric bilaterally at 2+ in all extremities.  Homan sign negative bilaterally. Good pulses at radial and posterior tibial arteries bilaterally
Skin: No edema. Warm and moist. No calf erythema.
NEURO: Patient is awake alert and oriented x3 with normal speech and normal hearing.  Patient is responding and cooperating appropriately to exam.  Face is symmetrical.

ED Course
Pt placed on a cardiac monitor and 2L O2 via NC and an IV is established with an accucheck performed before you ever see the patient (yes, you are at an outside institution … a very rural ED to be exact).  The nurse grabs you because the monitor looks funny.  You agree and order a 12 lead EKG.  You are handed the following gem:








Lucky for you, the cardiologist happens to be in the ED seeing another patient.  You grab an old EKG which shows an obvious LBBB and you show this new one and the old one to the cardiologist.  The cardiologist tells you to go ahead and admit to him for “repeats and serials” …

It is a perfect world.  You have mentally ruled out PE and Aortic Dissection and you are right.

1)  Your next step is to …
A: Give the patient 325mg ASA PO.  Order CXR and labs including CBC, lytes with BUN/Cr, troponin now and 3 hours from now, PT/INR.
B: Give the patient 325mg ASA PO.  Order CXR and labs including CBC, lytes with BUN/Cr, troponin now and 3 hours from now, PT/INR. Perform a rectal exam with FOBT and start the patient on Heparin.
C: Give the patient 325mg ASA PO.  Order CXR and labs including CBC, lytes with BUN/Cr, troponin now and 3 hours from now, PT/INR. Perform a rectal exam with FOBT and start the patient on tPA via STEMI protocol
D: Give 325mg ASA PO.  Repeat an EKG in 15 minutes and evaluate for evolution of suspected acute ischemia.

2) If you agree with the cardiologist, you know you will be monitoring the patient until the first troponin comes back.  At that time, if it is elevated you know this cardiologist will want you to transfer the patient to a place that can do an interventional left heart cath and has a CCU.  If you didn’t agree with the cardiologist and pushed tPA you know you have to do the same.  Either way, you know you have to consider your transfer options. You ask the secretary to find out if flight is available today (yes they do these things) and what your ground crew options are.  She tells you that you have BLS and ALS ground, no ICU transfer via ground team.  You have fixed-wing and helo both flying and available at both can be to your hospital and ready to ship in equal amounts of time.  Should you need to transfer this patient, what will you choose and why?
A: ALS ground because the first troponin came back at 0.125 and you and your cardiology friend decided this was a classic NSTEMI but he is scared to admit so you have to transfer the patient to a tertiary care center
B: ALS ground because you immediately pushed tPA and the crew can be there 30 minutes quicker than the helo team.  Time for ground transport is 1hr 45 minutes.
C: Fixed-wing because you immediately pushed tPA and you feel that it is safer than helo (though it may take slightly longer overall).
D: Helo because you immediately pushed tPA and you feel it is the fastest.

3)  Which of the following is NOT an indication for Air Medical Transport (AMT)?
A: Use of local ground transport would leave the local area without adequate EMS coverage.
B: Based on information available at the time and your best clinical judgement, you determine need for AMT.
C: The roads are icy and it is late at night. Ambulance driver says “I can do it, but I don’t like it”.
D: The interventional cardiologist at the tertiary care center was screaming in your ear on the phone “YOU HAVE TO SEND THIS PATIENT HERE ASAP in a HELICOPTER!!!!!!”
E: Local ground crew says “sorry doc, we cant go more than 100 miles” (tertiary hospitals is 150 miles away)

Bonus Question:
4)  PCI and thrombolytics are the standard of care for treatment of acute STEMI.  One of the known complications of either one of these is a reperfusion injury which is though to be induced by the restoration of blood flow to previously ischemic tissue as the reintroduction of oxygen and energy into a now anaerobic and acidotic environment can lead to further myocyte damage.  Which of the following are true regarding coronary reperfusion? (More than one acceptable answer)
A: ST-segment normalization and terminal T-wave inversion in the first hour after thombolysis are poor and clinically insignificant indicators for reperfusion
B: Factors contributing to reperfusion injury include: mitochondrial damage, myocyte hypercontracture, free radical formation, inflammatory mediators, platelet activation and complement activation
C: The arrhythmia that is most commonly associated with reperfusion is atrial fibrillation.
D: Ventricular tachycardia and ventricular fibrillation can also occur after thrombolytic therapy; however, these arrhythmias are more likely to reflect persistent occlusion and infarction than a reperfusion injury … but more importantly, they are the most common cause of spontaneous death in the reperfused patient and sphincter tone should elevate to catastrophic levels when this is encountered.

Answers & Discission:

1) C
2) D
3) D
4) B & D

1. C – This is a STEMI. Clinically and electrographically this is a STEMI. Using Sgarbosa and/or modified Sgarbosa criteria, this is a STEMI. Your sister in third grade thinks this is a STEMI. You are 150 miles from a tertiary care center so you must do something to attempt to treat this STEMI until you can get them to the definitive spot. You should tell your nurses to initiate the in-house STEMI protocol. Give the patient 325mg of ASA. Ask the clerk to get whatever interventional cardiologist on the line that your hospital has a transfer agreement with. Tell them you will be giving ASA and thrombolytics (unless you encounter an absolute contraindication) and transporting the patient to them. Ask them if there is anything else they want. Hang up. Go through the tPA checklist, making sure there are no absolute contraindications. Explain the risks and the benefits to the patient. This can be as easy as saying: “Risks include bleeding in your gut, your chest and your head. You could die or become permanently disabled from this medication. Benefits: Those things I said rarely happen and you have also have a chance (somewhat higher) of dying if you don’t get this medication.” DOCUMENT that you did all this. (At the end of all of this, don’t forget to document your critical care time minus all billable procedures as well… I digress)

2. D – How to transfer a patient can be one of the toughest decisions to even the most seasoned physician. There are multiple modalities, most of which are listed above and pretty self-explanatory. The correct answer here is D. Helo is fast and though it is dangerous, ambulances and airplanes crash too. If the skies are clear and the team is available to fly helo, it is no doubt the fastest form of travel (with rare exception) and in stroke and STEMI which are the most common time sensitive conditions requiring medical transport, time is tissue and it is your job to get them where they need to be. A is wrong because this is NOT an NSTEMI. B is wrong because the helo or fixed-wing transport will still be quicker than ambulance in this scenario despite the initial delay. C is wrong because helo is faster. Fixed-wing is ARGUABLY safer but it is slower and anything can crash. If you still want to argue with me and say “Fixed-wing isn’t that much slower and I think the benefit of less fixed-wing crashes outweighs the risk of the small time delay vs helo” … then I say fine. When you are out there, you can make whatever decision you want but think of this. You have a very important morning meeting today and you woke up late. If you arrive late to this meeting, you might die. You don’t have to get on the national transportation safety website to know that more car crashes and vehicular deaths occur on the expressways than the surface streets every year. You know your risk of crash and death is higher if you take the expressway. Are you really going to take the back roads? …. I have included some more information for your leisurely reading on the types of transport teams.

BLS bus usually staffs EMT-B and refers to the use of emergency care without the use of advanced therapeutic interventions and includes airway management (oral and nasal, BMV), CPR, hemorrhage control, fracture and spine immobilization, and child birth assistance. They often have an AED as well.

ALS bus usually staffs EMT-I, EMT-P or equivalent and offers more comprehensive service such as an advanced airway, IV line placement and medication distribution en route, cardiac monitoring and manual defibrillation and certain invasive procedures.

ICU transport varies considerably but in generally you want this team when the patient is intubated, or you have a high index of suspicion they could need it en route (though if this is the case more often than not you should intubate before you send them out). ICU transport teams can run a vent and manage drips such as pressors, paralytics and sedatives and vasoactive agents. Almost all flight crews are staffed by an ICU team.


3. D is an incorrect answer. A, B, C and E are all true statements. I will refer you to Box 191-3 from Rozen’s










A refers to #8 and is self-explanatory. B refers to #9. Remember you are the one with the training and the knowledge. There might be a million protocols and suggestions out there but it is your job to integrate all things available to you from patient history, presentation and condition to hospital and city policies to what may happen on the way, to where the patient is going. You have the full clinical picture, you make the call. C refers to # 1 and 2. Your ambulance driver knows these roads and he/she has probably made the trip you are sending them on many times. If they are suggesting to you that they don’t think the drive is safe for some reason or another, don’t let them be a hero. Explore your next option. D refers to #9 again and look at my previous explanation. The cardiologist doesn’t make the call, you do.

4. B and D are correct.

There is a very good discussion of reperfusion injury on UpToDate, which is where I pulled this info from. I’m not going to copy and paste it but I highly suggest you read it. I don’t usually like UpToDate and you will rarely hear me say something good about it, but this article is a solid 30 minute read.

A is wrong. ST segment normalization and terminal T-wave inversion within the first hour are good markers for reperfusion. You can argue which is better, but that isn’t the question. Please pay attention to your patient first and foremost, they are a pretty good marker too for what is going on post thrombolytics. If they say “I don’t feel good, something isn’t right”, be scared. Don’t walk away yet. Watch the monitor and watch them and charge some paddles.

B is correct. These are all pathologic causes of reperfusion injury. Cell ischemia gets the ball rolling and nature does the rest.

C is wrong. An accelerated idioventricular rhythm (AIVR) is the most common arrhythmia seen with reperfusion after thrombolytics. AIVR usually pretty easy to distinguish on the monitor but you have to be thinking about it or you will be tricked into thinking it is a standard BBB. Basically an AIVR means a rhythm being paced by the ventricles. Now anytime you have a ventricularly paced rhythm you can count on a wide QRS so you know this will be present. And normally, ventricles would pace at less than 50bpm, so in AIVR you have a rate >50 and a wide QRS with a BBB morphology. More often than not, it is originating from the left ventricle. One more caveat, if the rhythm is driven by the ventricles and the rate goes greater than 120, you are out of the realm of AIVR and you are now talking Vtach (and be ready for Vfib, either way, get ready for some electricity and draw up some amiodarone, you might need both soon).

Recap of this. AIVR is the MC reperfusion arrhythmia and is characterized by a wide QRS and a rate greater than 50 but less than 120.

D is correct. It is pretty clear. Again, check out this article UpToDate

Intern Report 7.13

Case Presentation by Justin Stimac, MD

CC: “Chest pain”

HPI: 67 year old male from Bolivia presents to the Emergency Department with chest pain that is central, non-radiating, sharp, and lasts for only a few seconds.  Chest pain has been present for years, however it has been acting up more lately. He has never gone to the doctor before today.  Today his son felt that he should have his chest pain evaluated.   He also endorses the occasional brief episode of palpitations.  He denies pre-syncope, syncope, and diaphoresis.  At his baseline he does become short of breath when he goes upstairs or walks more than a half kilometer. This shortness of breath has been present for years.  He feels that he occasionally has fevers but he does not own a thermometer.  He also has a long history of constipation for which he tries to drink plenty of fluids and eat foods that are high in fiber.  He denies headache, abdominal pain, weakness, dysuria, melena, hematochezia, hematuria, bleeding disorders, hearing loss, emesis, and dysphagia.  He immigrated to the United States to live with his son who works at the embassy.  The patient speaks no English, but is able to communicate with you via the interpreter. He grew up in a small village in the cloud forest of Bolivia.  He is a farmer.

ROS: Negative except as listed above in the HPI.

Medications: None
PMH: Has never gone to the doctor and is not sure.
Past Surgical History: None
Family History:  Both his mother and father had diabetes and HTN
Social History:  Denies smoking. Endorses drinking “canaso” a sugar cane based home made liquor occasionally during holidays. He later states that he does love to dance cumbia  and when he dances he drinks.  Denies ever snorting cocaine or other recreational drug use.  However, he did chew coca leaves daily for the majority of his life until he moved to the US.

Physical Exam:

Vital signs: BP 120/86, HR 102, RR 17, Temp 38.0, Pulse Ox 96% on room air
General: Appears his stated age.
Eyes: PERRL, mild conjunctival pallor, EOMI
Neck: Supple, no cervical LAD, no stiffness
Cardiac: Regular rhythm and tachycardic.   No MRG.
Respiratory: CTAB except for some faint bibasilar crackles.
GI: Abdomen is soft, non tender. No distention, rebound, guarding, or masses.
Musculoskeletal: Moves all extremities equally.  Strength bilaterally 5/5 with regards to bicep flexion, tricep extension, hip flexion and extension, knee flexion and extension, dorsiflexion and plantar flexion.
Skin: Multiple large scars on his lower leg.  He states that they are from machete accidents.
Neurological: Awake and moving all extremities spontaneously. No facial droop. Pupils are equal, round and reactive to light. Strength is 5/5 in upper and lower extremities bilaterally. No ataxia.
Extremities: +2 pitting edema.

Labs: Pending








Cardiac ultrasound:





#1. Which is associated with the most likely cause of the patient’s presentation.
A. Anopheles mosquito
B. Reduviid bug
C. Sandfly- L. donovani
D. Taenia Solium

#2. What other symptom/exam finding is most associated with this disease?
A. Anemia
B. Dysphagia
C. Painless skin ulcers
D. Seizure

#3. What is the disposition for this patient based on the information presented above?
A. Admit to medicine with Infectious Disease Consult
B. Cardiac Catheterization
C. Discharge to home
D. Observation unit with telemetry



  1. B
  2. B
  3. B










Question 1

1 . B:  This case is most consistent with a patient suffering from Chagas disease ( T. Cruzi). The triad of dysphagia, cardiomyopathy, and constipation are most commonly seen.   The vector lives in the walls and roofs of houses in Central and South America. It can be eradicated completely with simple public health home remodeling. Chagas disease can be obtained from bug bites or via blood transfusion. Trypomastigotes migrate to the smooth muscle, cardiac muscle and autonomic ganglia of the heart, esophagus, and colon (1).

The problem transcends the borders of Bolivia. In Latin America 18 million people are infected and approximately 30% these individuals develop major heart disease decades after the acute infection.   The WHO warns that 100 million people are at risk, and it is estimated that Chagas disease causes four times the burden of malaria, schistosomiasis, leprosy and leishmaniasis combined (2). Great strides have been made in eliminating the vector through public health strategies; however, many patients will continue to progress from the Intermediate Stage (seropositive but asymptomatic) to the chronic symptomatic phase (irreversible dilated cardiomyopathy, megacolon, and mega-esophagus).   Thus a treatment for the larger number of patients with Intermediate Chagas disease is crucial.

Chagas disease includes patients with both asymptomatic and symptomatic disease.   It is unclear on how we should go about treating these different subgroups of patients, especially those in the chronic phase.

The majority of experts agree that acute Chagas should be treated with Benznidazole (BZD). Acute infection is asymptomatic in most cases, but can present with malaise, fever, lymphadenopathy, mild splenomegaly, myocarditis and meningoencephalitis. If acute Chagas is detected, the patient should receive treatment. Up to 70% of these acute patients remain xenodiagnostically and serologically cured. No RCTs have been conducted on long term benefits of treating acute Chagas; however, it is generally accepted that all acute disease and reactivated disease should be treated with trypanocidal therapies (3).

Chagas can be diagnosed with the Chagas StatPak. The manufacturer reports a sensitivity of 98% and specificity of 95%. In order to officially have the diagnosis of Chagas a patient also needs to test positive with either the PCR or ELISA technique.

The two main trypanocidal medicines in use since the 1960s are Nifurtimox (NFTMX) and Benznidazole (BZD). Both of these medications are reported to have high noncompliance rates due to side effects, especially NFTMX. Side effects of NFTMX include nausea, vomiting, abdominal pain, weight loss, severe anorexia, paresthesias, insomnia and seizure. Side effects are seen in up to 40% of patients treated with NFTMX.   The most serious side effects seen are leucopenia, peripheral neuropathy, and allergic dermopathy (4).

The Romana sign, painless unilateral swelling of the eye, which is often quoted in the literature is extremely rare. Many seasoned Bolivian physicians have never seen it.

Question 2

  1. B: Anemia is most consistent with Malaria. The Sandfly is associated with both cutaneous and visceral leishmaniasis which are associated with a painless skin ulcer.   Seizure is most associated with cysticercosis and cerebral malaria.

Mega-esophagus is a known complication of Chagas disease.   Dysphagia is one of the classic findings of Chagas disease. This is due to damage to the myenteric plexus of the colon.


Question 3

  1. B: The patient has a LBBB. A new LBBB is no longer considered an automatic trip to the cath lab. We need to apply Sgarbossa’s criteria to help us look for signs of ischemia. This patient has concordant ST depression of greater than 1 mm in leads V2 and V3 which is consistent with a myocardial infarction.

Sgarbossa’s criteria states that ST segment elevation of 1 mm or more that is concordant to the QRS in any lead receives a score of 5 points. ST segment depression of at least 1 mm that is concordant in leads V1-V3 is worth 3 points. ST segment elevation of greater than 5 mm that is discordant values a score of 2.   If a patient has a score of at least 3 there is a 90% specificity for myocardial infarction.   However, the criteria are not very sensitive (5).















  1. Marx, Hockberger, & Walls. (2010). Rosen’s Emergency Medicine Concepts and Clinical Practice. 7th Edition. Philadelphia:Mosby. Page 1765.
  2. Schmunis G. American Tripanosomiasis as a public health problem. Chagas’ disease and the nervous system. Washington, DC: PAHO, 1994:3–29.4
  3. Bern C, Montgomery SP, Herwaldt BL, Rassi A Jr, Marin-Neto JA, Dantas RO, Maguire JH, Acquatella H, Morillo C, Kirchhoff LV, Gilman RH, Reyes PA, Salvatella R, Moore AC 2007. Evaluation and treatment of Chagas disease in the United States. A system­atic review. JAMA 298: 2171-2181.
  4. Marin-Neto J Antonio, Rassi Anis. The BENEFIT trial: testing the hypothesis that trypanocidal therapy is beneficial for patients with chronic Chagas heart disease Mem Inst Oswaldo Cruz, Rio de Janeiro, Vol. 104(Suppl. I): 319-324, 2009
  5. Goldberger. Up to Date. Electrocardiographic diagnosis of myocardial infarction in the presence of bundle branch block or a paced rhythm. Viewed 4/20/14.

radER Case 13.1





Case 1 Questions

54 YOM presents to emergency department complaining of midsternal chest pain that he states has been coming and going for the past few years.  He states it has worsened over the past week becoming more constant.  He denies exertional component to his chest pain.  He denies any shortness of breath or difficulty breathing.  He does state that he intermittently feels nauseated but does not have any episodes of emesis.  He denies any fevers, chills, and productive cough.  He states that he has a history of hypertension, diabetes, and coronary artery disease with CABG x3.

The patient’s physical examination is unremarkable.

1. What significant abnormality is noted on the PA view of his patient’s chest film?
A. Acute Infiltrate
B. Increased Pulmonary Vascular Congestion
C. Esophageal dilatation
D. Westermark Sign

2. What is the most preferred initial screening/diagnostic test if the above condition is suspected?
A. Barium Swallow
B. CTA Thorax
C. D-Dimer
D. Echocardiogram

3. What is the preferred initial pharmacotherapy?
A. Heparin bolus with subsequent heparin ggt
B. Calcium Channel Blockers or Nitrates
C. Cetriaxone and doxycycline
D. Fondaparinux with warfarin overlap

Case 1 Answers

1. Correct Answer C. Esophageal dilatation with air-fluid level is the most notable abnormality on the PA view of his chest x-ray. This is often seen in an advanced achalasia as the lower esophageal sphincter as constricted and not allowed any liquid or solids to pass causing significant dilatation of the esophagus. No acute infiltrate is noted in the chest x-ray to suggest pneumonia.  No increased pulmonary vascular congestion is appreciated. Pulmonary embolism should be considered however no shortness of breath or history of DVT/PE exists.  No Westermark Sign is noted on his chest x-ray.

2.  Correct Answer A. Barium Swallow is the preferred initial screening test if achalasia is suspected.  Extensive esophageal dilatation is typically only noted 1 chest x-ray in advanced cases. A CTA thorax is the preferred modality for diagnosis of acute pulmonary embolus.  A d-dimer should only be used in the low risk patient’s suspected of having a pulmonary embolus with a Well’s score of less than 2. An echocardiogram is also a good screening test for both acute pulmonary embolism with right heart strain as well as for acute heart failure however it serves no role in the diagnosis of achalasia.

 3.  Correct Answer B. Calcium Channel Blockers or Nitrates are the preferred initial pharmacotherapy for smooth muscle relaxation in patients with achalasia.  Ceftriaxone and doxycycline are preferred for patient’s being admitted with acute community acquired pneumonia. Heparin bolus with subsequent drip is preferred in patients with acute pulmonary embolus that may undergo PCI. Fondaparinux with Coumadin overlap is preferred for stable patient’s with acute pulmonary embolus.

Senior Report 6.25

Case Presentation by Dr. John Wilburn

CC: Chest pain


24 year-old male presents to the emergency with complaints of chest pain, he points to the left upper sternal border and left upper chest. He reports it began about a month ago.  He describes it as a constant, dull pressure. He reports the intensity of the pain has significantly increased over the past 5 days and is now radiating to the right side of his chest.  Patient has not tried anything to alleviate this pain.  He reports taking a deep breath exacerbates his pain. He denies any fevers. He reports a dry cough that is non productive, which he attributes to smoking. He denies any trauma or dyspnea.


Constitutional: Denies night sweats, fatigue or weight loss.

Cardiovascular: Denies syncope

Respiratory: Denies hemoptysis

Gastrointestinal: Denies Abdominal pain

Genitourinary: Denies scrotal masses

Musculoskeletal: Denies extremity pain or swelling

PMH: Denies hypertension, pneumothorax, or diabetes

PSH: None

Allergies: None

Medications: None

FHx: Reports Hypertension denies CAD

Social Hx: Patient smokes cigarettes daily, and marijuana occasionally. Denies IVDU or Cocaine. Reports to socially drinking less than 3 times per month.

Physical Examination:

General/Psychiatric: WNWD non-toxic appearing male sitting upright in the stretcher in no acute respiratory distress, speaking in full sentences. A&Ox3.

Vital signs: 122/65 HR: 58 RR 14 Temperature 37 C Pulse oximetry 96% RA

HEENT: NC/AT PERRL EOMI. No nasal discharge, or nasal flaring.. Mucous membranes of the mouth are moist. No tonsil enlargement no erythema.

Neck: Supple, No JVD Trachea Midline. Full Range of Motion, No lymphadenopathy.

Back: No Tenderness to palpation

Chest: Left sided chest wall tenderness to palpation – front back level?.

Respiratory: CTAB no wheezes rhonchi or rales.

Cardiovascular: S1S2 present no M/R/G.

Abdomen: Thin Soft ND/NT no rigidity or rebound tenderness.

Musculoskeletal: Strength 5/5 in the upper and lower ext. Palpable and symmetric radial and dorsalis pedis pulses. No edema or asymmetry. No tenderness to palpation.

Neuro: Normal speech and gait..

Medical Decision Making/Course in the ED:

Patient Received Motrin and Maalox, ECG and CXR obtained







1) Where is the abnormality located in this patients chest radiograph?

a) Anterior Mediastinum

b) Ascending Aorta

c) Carina

d) Right Atrium

e) Posterior Mediastinum

2) Which of the following statements is correct?

a) The anterior mediastinum extends from the sternum anteriorly to the esophagus posteriorly.

b) The anterior mediastinum contains the thymus gland.

c) The anterior mediastinum contains the transverse arches of the aorta.

d) The middle mediastinum contains the esophagus.

e) All of the above are correct.

3) Which is the most appropriate next step in this patient’s management?

a) Obtain blood cultures, start antibiotics and consult cardiothoracic surgery.

b) Obtain a CT-Thorax with contrast.

c) Obtain a Transthoracic Echocardiogram.

d) Perform a Color Doppler Ultrasound Guided Thoracentesis.

e) Start the patient on Heparin and admit to the hospital.

4) Which of the following is the most common tumor of the anterior mediastinum?

a) Bronchogenic Cysts

b) Germ Cell Tumors

c) Lymphoma Hodgkin’s disease

d) Non-Hodgkin Lymphoma

e) Thymoma

5) What is the initial diagnostic study of choice?

6) Bonus Question: What was this patient’s final diagnosis?

a) Empyema

b) Germ Cell Tumor

c) Lymphoma Hodgkin’s Disease

d) Thymoma


Answers & Discussion:

1) Answer: a. Anterior Mediastinum

Brief review of radiographic anatomy eliminates b, c, d.


Patient’s Radiograph:  The radiograph does demonstrate two findings helpful in identifying the location of the mass. See below.


3 3b


The Hilum overlay sign is a useful tool to help identify probable location of a mediastinal mass

Another way to evaluate for mass in either the middle or posterior mediastinum is look for the azygoesophageal recess reflection. (below)


2)Answer: b. the thymus is located in the anterior mediastinum

The mediastinum is divided into 4 compartments

  1. The Anterior Mediastinum– extends from the sternum anteriorly to the pericardium and brachiocephalic vessels posteriorly


  • Thymus and residue of thymus
  • Fat
  • Lymph glands

The Middle Mediastinum– lies between the anterior and posterior mediastina.


  • Heart
  • Pericardium
  • Ascending aorta
  • Trachea
  • Main bronchi
  • Lymph nodes
  • Pulmonary artery
  • Pulmonary veins
  • Phrenic nerve

Posterior Mediastinum– bounded by the pericardium/trachea anteriorly and the vertebral column posteriorly.


  • Descending aorta
  • Esophagus
  • Azygous vein
  • Hemiazygous veins
  • Lymph glands
  • Thoracic duct
  • Autonomic nerves
  • Vagus nerve

Superior Mediastinum– bounded superiorly by the thoracic inlet and inferiorly by and arbitrary plane passing horizontally and posteriorly from the manubriosternal joint to the junction of T4/T5 vertebra.  Anteriorly bounded by the sternum and posteriorly by the upper thoracic vertebra.


  • Trachea
  • Esophagus
  • Great vessels
  1. Arch of aorta
  2. Thoracic portions of left common carotid and left subclavian arteries
  • Veins
  1. Innominate veins
  2.  Upper ½ superior vena cava
  • Thymus
  • Phrenic and vagus nerves
  • Thoracic duct
  • Lymph glands


3) Answer: b. CT Thorax w/ contrast should be ordered next. (Explanation below).




 4) Answer: e. Thymoma

The most common causes of anterior mediastinal masses: Thymoma (20%) Germ Cell Tumors (seminoma, teratoma, etc(15%)); thyroid disease (15%); and lymphoma HD and non-HD (10%). Masses of the middle mediastinum are typically congenital cysts. Neurogenic tumors are the most common cause of posterior mediastinal masses.  Overall, two thirds of mediastinal tumors are benign, however masses in the anterior compartment are more likely to be malignant.



The clinical sequelae can range from asymptomatic to symptoms of cough, chest pain, dyspnea, and fevers/chills. The likelihood of malignancy is influenced by mass location, patient age, and the degree of symptoms. Age is a strong predictor of malignancy, lymphomas and germ cell tumors (GCTs) occur mostly during the second and fourth decades. Symptomatic patients are more likely to have a malignancy. Symptoms may be delineated between localizing symptoms (mass effect) and systemic symptoms (hormonal/antibody effect). In Davis et al,7 85% of patients with a malignancy were symptomatic at presentation, compared to 46% of patients with benign neoplasms.

The initial workup of a suspected mediastinal mass involves obtaining posteroanterior and lateral chest radiographs. CT scanning is used to further characterize mediastinal masses (cystic, vascular, and soft-tissue structures) and their relationship to surrounding structures.

Other more rare imaging modalities include, fluoroscopy, and barium swallow. MRI may be used in evaluating a neurogenic tumor, and identifies vascular invasion and cardiac involvement.

Tissue diagnosis is almost always required. Biopsy may be obtained via, transthoracic or transbronchial needle aspiration, mediastinoscopy, anterior mediastinotomy, or video-assisted thoracic surgery. Modality of choice is sometimes case dependent.  Fluoroscopic or CT guided transthoracic needle biopsy, has been shown to be faster, cheaper, and better tolerated by patients. It has been shown to have good diagnostic accuracy, although sometimes specimens are inconclusive requiring further investigation.

5) Answer: CT Guided Transthoracic Needle Biopsy, however some evidence suggests Thoracoscopic biopsy is just as safe and slightly more accurate.

 6) Answer: b. Germ Cell Tumor (Seminoma)



A Diagnostic Approach to Mediastinal Abnormalities

Camilla R. Whitten, MRCS, FRCR, Sameer Khan, MRCP, FRCR, Graham J. Munneke, MRCP, FRCR and Sisa Grubnic, MRCP, FRCR

2)Tumors of the Mediastinum

Beau V. Duwe, MD; Daniel H. Sterman, MD. FCCP; Ali I. Musani, MD, FCCP

Chest. 2005; 128(4):2893-2909.


4)Harrison’s Principles of Internal Medicine 16th edition

5) Anterior mediastinal masses: utility of transthoracic needle biopsy.

S J HermanR V HolubG L Weisbrod and D W Chamberlain

Department of Radiology, Toronto General Hospital, Ont, Canada.


Thoracoscopic diagnosis and treatment of mediastinal masses

Ann Thorac Surg 1993;56;92-96

7)Davis, RD, Jr, Newland Oldham, H, Jr, Sabiston, DC, Jr Primary cysts and neoplasms of the mediastinum: recent changes in clinical presentation, methods of diagnosis, management and results. Ann Thorac Surg 1987; 44, 229-237 [CrossRef] [PubMed]


Percutaneous Transthoracic Needle Biopsy

Jack L. Westcott, MD

Department of Radiology, Hospital of Saint Raphael, New Haven, CT.

Intern Report 6.4

Case Presentation by Dr. Daniel Hutchens

History of Present Illness:

A 52 year old man with a past medical history of hypertension presents to the ED with complaints of acute onset chest pain for 8 hours.  The patient was sitting at home when it started and denies any exertional component.  The pain is sharp, located retrosternally, and radiates to the left neck and shoulder.  The pain is worse during inspiration and when lying flat, and is relieved by sitting upright and leaning forward.  Patient took his blood pressure medication at home and did not feel relief so he came to the ED.  He does not take aspirin.  He feels SOB and states that he had a URI 1 week ago.  There has been no recent travel.  He states toward the end of the exam that he is worried about the cost of his care as he just lost his job.

Review of Systems:

Admits to a mild cough and occasional dizziness, otherwise negative except as per HPI.

Past Medical History: Hypertension

Past Surgical History: No surgical history

Medications: HCTZ

Allergies: NKDA

Social History: Denies tobacco, occasional alcohol, occasional marijuana

Family History: HTN, father with an acute MI (AMI) at 65

Physical Examination:

VS: BP 142/92 mmHg, HR 110, RR 20, O2 Sat 97% on room air, Temp 38.0°C
Head: Atraumatic
ENT: PERRLA, EOMI, throat is non-erythematous
Neck: Supple, no carotid bruits
Heart: RRR, there is a high pitched scratching sound heard that remains with suspension of respiration
Lungs: CTAB, no wheezing, no rales, ronchi are heard that remain with suspension of respiration
Abdomen: Soft, nontender, nondistended, positive bowel sounds
Skin: No rash
Neurologic: Gait is normal.

IV access was established; patient was put on oxygen, cardiac monitoring, and given an aspirin.  12 lead EKG was obtained.

ECG 6.4

A line was placed and labs were sent including a BMP, CBC, coagulation panel, and troponin.  CXR was obtained.

cxr 6.4

Cardiac ultrasound (US) was performed at the bedside.

us 6.4

Labs came back and Troponin I was <0.017.  Serum electrolytes as well as BUN and Cr were wnl.  CBC and coagulation studies were wnl.


1.) What is the best treatment in this patient’s case?
a. Indomethacin
b. Ibuprofen
c. Colchicine
d. Prednisone

2.) What is a distinguishing factor for acute pericarditis vs. AMI on EKG?
a. PR interval elevation
b. Inverted T waves in the anterior and inferior leads
c. ST-segment depressions in the precordial leads with reciprocal changes
d. Diffuse ST-segment elevations with no reciprocal changes

3.) How can you use serum biomarkers with EKG to help diagnose acute pericarditis over AMI?
a. Biomarker elevation will be moderate compared to what would be expected in AMI given the EKG findings
b. Biomarker elevation will be higher compared to what would be expected in AMI given the EKG findings
c. Biomarker elevation is never seen in acute pericarditis
d. There is no relation between biomarker elevation and EKG findings in acute pericarditis


Answers to the questions:

1.) b. Ibuprofen

2.) d. Diffuse ST elevations with no reciprocal changes

3.) a. Biomarker elevation will be moderate compared to what would be expected given the EKG findings


The characteristics of this patient’s pain, the physical exam finding of a friction rub, and the EKG findings make the most likely diagnosis acute pericarditis.  Acute pericarditis is classified as chest pain for <6 weeks and can resemble cardiac ischemia.  It is often severe, retrosternal and left precordial, and referred to the neck, arms, or left shoulder.  Pain is often pleuritic but sometimes it is a steady, constricting pain that radiates into either arm.  Characteristically, pericardial pain is relieved by sitting up and leaning forward, something you would not see classically with AMI.  EKG changes in acute pericarditis will show diffuse, concave ST elevation across multiple leads, usually with PR depression early, then isometric T-waves progressing to ST depression.  This is in contrast to EKG changes in AMI, where you would expect more convex ST elevations present in anatomically contiguous leads with reciprocal changes.  Acute pericarditis is often accompanied by some degree of myocarditis causing serum biomarkers (troponin) to rise, termed myopericarditis.  These elevations, if they occur, are often quite modest compared to the elevations in AMI given the extensive EKG findings of ST-segment elevation.

A pericardial friction rub will be audible in anywhere from 50-85% of patients with acute pericarditis and is pathognomonic.  It will have a rasping, scratching, or grating quality.  The best way to hear it is to have the patient sit up and lean forward while placing your stethoscope over the lower sternal edge or apex.  It is heard best at end-expiration and won’t disappear with cessation of respirations as would a pleural rub.  More than 50% of rubs are triphasic and will include an atrial systolic rub preceding S1, a ventricular systolic rub occurring between S1 and S2, and an early diastolic rub occurring after S2.  It is not uncommon for patients with acute pericarditis to have a pericardial effusion and a pericardial friction rub can be heard at the start.  After enough effusion has accumulated the rub will disappear.  US is the best initial test which will show free fluid in the pericardial space.  The US from the case shows a small pericardial effusion near the right atrium.

Within the diagnosis of acute pericarditis it is necessary to determine an underlying cause.  Different etiologies of are grouped into infectious, noninfectious, or autoimmune.  Infectious etiologies include: viral (1-10% of cases, peaks in spring and fall); pyogenic (bacterial from direct pulmonary extension, hematogenous spread, myocardial abscess/endocarditis, post-surgery); tuberculous (suspect in high risk groups and developing countries).  Noninfectious etiologies include: post-MI (Dressler’s syndrome); uremia (usually secondary to ESRD or dialysis, will often have normal EKG because little epicardial inflammation occurs); neoplastic (both primary and metastatic); myxedematraumaticaortic dissectionsarcoidosis.  Autoimmune etiologies include: rheumatic feverSLERAsclerodermaWegener’s granulomatosisdrug-induced (procainamide, hydralazine, phenytoin, isoniazide, minoxidil, anticoagulants).  An idiopathic cause is responsible for 26-28% of acute pericarditis diagnoses and is the most common etiology given.  Many idiopathic cases are likely due to undiagnosed viral infections.

Pericardiocentesis is indicated in patients with effusions larger than 250 mL, effusions where the size increases despite intensive dialysis for 10-14 days, or effusions with evidence of tamponade.  The procedure can be performed with or without US guidance, although if it is available US should be used.  Before you perform the procedure you should ensure the patient has IV access, is receiving supplemental oxygen, is connected to a cardiac monitor, and continuous pulse oximetry.  If time permits you can place an NG tube to decompress the stomach and reduce the risk of a gastric perforation.  Either subxyphoid or left sternocostal margin approaches are most often used.  The procedure should be performed in a sterile fashion using a spinal needle connected to a syringe with the patient supine if there’s no US guidance, and at 30-45 degrees head elevation if there is.  When you’re not using US the needle should be inserted at a 45 degree angle to the abdominal wall and directed toward the left shoulder.  With US guidance, insert the needle at a 15-20 degree angle and direct it just under the rib cage toward the left should.  The needle is inserted ~5cm while applying negative pressure to the syringe until a return of fluid is noted or a change on the EKG strip is seen.  If the EKG pattern shows cardiac injury (ST segment elevation) then you have gone too far, are in direct contact with the myocardium, and should withdraw the needle until the pattern has returned to normal.  Withdraw as much fluid as possible.  Complications of this procedure are production of pericardial tamponade, laceration of a coronary artery, and induction of cardiac dysrhythmias.  Pericardial fluid should be analyzed for red and white blood cells, cytologic studies for cancer, microscopic studies, and cultures.  Fluid that returns as an exudate is likely from an inflammatory cause (most commonly viral).  Transudative fluid is seen in pressure-related conditions such as congestive heart failure.  If red blood cells are seen in the fluid this could represent a complication from acute rheumatic fever, post-cardiac injury, or renal failure (such as in uremic pericarditis).  If adenosine-deaminase activity is high, tuberculous pericarditis should be suspected.

Treatment includes empiric anti-inflammatory therapy for acute and recurrent pericarditis secondary to viral or idiopathic cases that are most commonly seen.  Currently, aspirin and NSAIDs are the mainstay of therapy.  An “attack dose” should be given for 1-2 weeks.  For aspirin this is 2-4 g/day, ibuprofen is 600mg TID, indomethacin is 50mg TID.  After the attack dose drug tapering may be considered.  Colchicine is added in autoimmune conditions and cases of recurrent pericarditis.  It interferes with WBC activity and is good for these cases.  Attack dose is not necessary with colchicines and 0.5mg BID can be given for 3 months if it’s the first attack or 6-12 months with recurrent attacks.  Corticosteroids should be reserved for difficult cases requiring multi-drug therapies and specific medical conditions.  This is because while they offer a fast remission, there is a higher risk of recurrences, prolonged course, and side effects with corticosteroids.  The corticosteroid of choice is prednisone and is dosed at 0.2-0.5 mg/kg/day.  Treatment length for aspirin, NSAIDs, and corticosteroids are usually until symptoms resolve and CRP normalizes.  If it is a uremic pericarditis aggressive dialysis is indicated and NSAID therapy will have little effect.  Corticosteroids can be used in these cases but typically don’t produce a response for 1-2 weeks.

Disposition depends on etiology.  For idiopathic acute pericarditis, high-dose NSAID therapy is the mainstay of treatment and should be continued for 1-4 weeks.  At a week’s time, however, if the current NSAID therapy is not working then the NSAID should be switched to another.  60% of patients will recover in 1 week and 80% by 3 weeks.  18% of patients can have recurrent pericarditis which warrants additional therapy with corticosteroids or colchicines.  Patients without clinically poor prognostic predictors (fever >38°C, subacute onset, immunosuppression, trauma, oral anticoagulant therapy, myopericarditis, severe pericardial effusion, cardiac tamponade) can be considered “low-risk cases” and assigned to outpatient treatment with high-dose oral NSAID therapy.  Otherwise, hospital admission is warranted with a consult to cardiology and any other subspecialties required (ex. In the case of uremic pericarditis you should also consult nephrology).

Clinical Pearls:

  • Suspect acute pericarditis if chest pain is sudden onset, relieved by sitting up and leaning forward, and is associated with a friction rub.
  • EKG in acute pericarditis will show diffuse ST-segment elevations with no reciprocal changes and PR depression early on.
  • Cardiac US should be performed in patients with acute pericarditis to rule out a pericardial effusion.
  • If a pericardial effusion is present, CXR may show a typical “water bottle” heart, where the heart is enlarged in the shape of a flask or water bottle.
  • Aspirin or NSAID therapies remain the mainstay of treatment for the majority of cases of acute pericarditis.  However, other etiologies should be investigated with each case and treated appropriately.


Imazio M, Adler Y.  “Treatment with aspirin, NSAID, corticosteroids, and colchicines in acute and

recurrent pericarditis.”  Heart Fail Rev 4 Jun. 2012.  Pubmed.  Web.  16 Nov. 2012.

Imazio M, et al.  “Day-hospital treatment of acute pericarditis: a management program for outpatient

therapy.”  J Am Coll Cardiol.  2004; 43(6): 1042-46.

Longo D, et al.  “Acute Pericarditis.”  Harrison’s Online 18e: Part 10 Disorders of the Cardiovascular

System: Section 4 Disorders of the Heart: Chapter 239 Pericardial disease.  Web.  16 Nov. 2012.

Pericardial Disease (Pericarditis).  Rosen’s Emergency Medicine.  7th edition.  2010.  Print.

Spangler MD, Sean.  “Acute Pericarditis.”  Medscape Reference 10 Oct. 2011.  Medscape.  Web.  16 Nov.