57 year old female s/p appendectomy (>20 years ago), s/p laparoscopic hysterectomy and b/l oophorectomy (3 mos ago) presents with foul-smelling vaginal discharge x 1 day.Read More
Welcome to the Pulse!
By Nicholas Otts, MD
Edited by Gal Altberg, MD and Abbas Husain, MD
A Common Problem:
11 year old male complaints of two episodes of testicular pain associated with nausea and vomiting, but in the emergency department the pain resolved. His testicular exam is non contributory. Ultrasound of his scrotum shows increased flow to left testicle. Torsion ruled out?
A Small Dose of EBM:
Testicular torsion has a bimodal distribution - initial peak during first year of life followed by the pubertal surge in adolescence; thus, torsion is primarily a PEM problem. Classically, ED residents are taught to evaluate torsion with an ultrasound, using power doppler to assess flow to involved testicle. If no or decreased flow compared to other side, there is a much higher concern for torsion.
What about normal or even increased flow? Does that rule out torsion? What if pain has resolved. What about intermittent torsion?
Intermittent testicular torsion, in which the spermatic cord twists and spontaneously resolves, is often a harbinger of final torsion. It is a problem that needs surgical correction, and, thus a diagnosis that cannot be missed.
On ultrasound, however, it can look like other causes of testicular pain. With flow returned to the testicle, the subsequent inflammation can appear as increased flow on doppler, which can be mistaken for orchitis. Further, the epididymis, near the spermatic cord, is often inflamed with or without return of flow, appearing enlarged and hyperemic on ultrasound, leading one to possibly suspect epididymitis.
Enter the Whirlpool
Whirlpool sign on ultrasound is another marker of torsion, and is created by a twisting of the spermatic cord (1,2,3). A good retrospective study at Texas Children’s showed that in patients with a surgical diagnosis of intermittent torsion, the whirlpool sign on ultrasound is a significant marker and can help distinguish this from other causes of testicular pain when doppler is non-diagnostic (4).
So, the next time you suspect torsion, think about intermittent torsion and make sure the ultrasound evaluation includes a good examination of the spermatic cord.
A good article with video of whirlpool sign:
1. Vijayaraghavan SB. Sonographic differential diagnosis of acute scrotum: real-time whirlpool sign, a key sign of torsion. J Ultrasound Med 2006; 25:563-574
2. Baud C, Veyrac C, Couture C, Ferran JL. Spiral twist of the spermatic cord: a reliable sign of testicular torsion. Pediatr Radiol. 1998;28:950–954
3. Esposito F, Di Serafino M, Mercogliano C, Vitale V, Sgambati P, Vallone G. The “whirlpool sign”, a US finding in partial torsion of the spermatic cord: 4 cases. Journal of Ultrasound. 2014;17(4):313-315.
4. Munden MM, Williams J, et. al. Intermittent Testicular Torsion in the Pediatric Patient: Sonographic Indicators of a Difficult Diagnosis. American Journal of Roentgenology. 2013;201: 912-91
by Nicholas Otts, MD
Edited by Gal Altberg, MD
A Common Problem:
3 year old male presents w/ decreased oral intake associated w/ ulcerative and vesicular lesions in his mouth and irritability. Normal amount of wet diapers, no signs of dehydration on exam. Vesicular lesions on palms and soles as well.
To give or not to give viscous lidocaine in an attempt to increase oral intake in a patient you do not wish to admit?
A Small Dose of EBM:
Treating pediatric viral stomatitis is a challenge. The primary goal is to avoid dehydration, and thus, admission for a primarily viral problem that will resolve with time. Oral medications commonly attempted in the ED include diphenyhydramine, coating agents (maalox), and viscous lidocaine (including combinations). For years, much of the EBM supporting either was case based and anecdotal. The desire to do something for these patients and their suffering parents is strong.
The most potentially toxic (1,2) but also potentially helpful medication is lidocaine. Thankfully, a recent blinded, randomized, placebo-controlled trial examined this exact question (3).
In 2014, a trial out of Australia tested 2% viscous lidocaine against a placebo with improved oral intake after one hour as the primary outcome measure. The study had a good design and was powered appropriately.
In the end, however, the oral intake in both groups was not significantly different. Viscous lidocaine appeared to make no difference for all of the measured outcomes. Further, because viscous lidocaine has the most potential to cause harm out of the agents frequently used, it is a less than desirable choice.
Because both the placebo and lidocaine groups in general showed significant improvement in oral intake as compared to the reported oral intake at home, it is suggested that simply the attention and instruction by the ED staff to the parents contributed significantly to the better outcomes.
This is a good trial, but there are some problems. First, as pointed out by the famous NYC toxicologist Dr. Hoffman in a letter to the editor in response to the article (4), the trial did not account for pain at all as an outcome measure. One can only use this trial to say that lidocaine did not improve oral intake, not that it does not relieve pain.
Further, the study only accounted for the first hour of oral intake post administration, and a longer term benefit of lidocaine was not assessed (but the timing was applicable to standard emergency department goals of disposition in these types of patients).
Bottom line: right now, due to potential for toxicity and no proven benefit in increasing oral intake, lidocaine may not be the best option for ulcerative lesions in the mouth. Good instruction to the parents and bringing attention to the issue of dehydration, however, may make all the difference.
1. Hess GP, Walson PD. Seizures secondary to oral viscous lidocaine. Ann Emerg Med. 1988; 17(7) 725.
2. Questions and Answers: Reports of rare, but potentially serious and potentially fatal adverse effect with the use of OTC benzocaine gels and liquids applied to gums or mouth. www.fda.gov/Drugs/DrugSafety/ucm250029.htm
3. Hopper SM, McCarthy M, Tancharoen C, et al. Topical Lidocaine to improve oral intake in children and painful infectious mouth ulcers: a blinded, randomized, placebo-controlled trial. Ann Emerg Med. 2014; 63: 292-299.
4. Hoffman R. Viscous Lidocaine Treatment for Painful Oral Infections in Children: Disappointingly Dismissive of Pediatric Pain. http://dx.doi.org/10.1016/j.annemergmed.2014.02.026
This EKG comes courtesy of Dr. Dan Peterson.
We thank EP Cardiologist Dr. Seth Keller for his contribution to this edition of EKG of the Week.
A 71 year old male presented to the ED complaining of palpitations. His vital signs are: Pulse 150, BP 110/70. His EKG is below.
1. What is the rhythm?
2. What are the treatment options?
The EKG shows a regular narrow complex tachycardia without P waves at a rate of approximately 150. This can be caused by SVT or atrial flutter.
Adenosine can be used initially. This may be therapeutic in the setting of SVT or diagnostic in the setting of atrial flutter. Other options include calcium channel blockers and beta blockers.
The EKG shows a regular narrow complex tachycardia without P waves at a rate of approximately 150. This can be caused by SVT or atrial flutter. Remember that whenever you see an SVT at a rate of 150, you should consider atrial flutter in the diagnosis. If you look closely at this EKG in leads III and aVF, you can see flutter waves present (arrows).
This patient was initially treated with diltiazem which resulted in EKG b.
Here you see a heart rate of 75 with flutter waves present (arrows below). This EKG is somewhat interesting in that the atrial rate is relatively slow for atrial flutter (150) and there is 2:1 AV conduction resulting in a ventricular rate of 75.
This patient was already on anticoagulation and had an INR of 2.9. At this point, the patient was cardioverted which resulted in EKG c.
Now the patient is in sinus rhythm at a rate of 50.
The following algorithm is useful in diagnosing tachyarrhythmias:
This EKG comes courtesy of Dr. Kong.
A 64 year old female presents to the ED complaining of fluttering in her chest. She has no past medical history and is on no medications.
Her vital signs are: Pulse 40, Respirations 16, BP 130/80.
Her EKG is below.
1. What is the rhythm?
2. How would you manage this patient?
The rhythm is 2nd degree AV block type I (AKA Wenckebach block).
2nd degree AV block type I usually requires no specific emergency treatment.
The EKG shows some dropped P Waves (P waves with no QRS complexes following them). This can be caused by 2nd degree or 3rd degree AV block. 2nd degree AV block has 2 types: type I and type II. In type I 2nd degree AV block, there is progressive lengthening of the PR interval followed by a dropped P wave. Then the cycle begins again. In type II 2nd degree AV block, the PR interval is constant and there are dropped P waves.
A quick way to differentiate type I from type II 2nd degree AV block is to compare the PR intervals before and after the dropped P waves. In type I, the PR interval before the drop will be longer than the PR interval after the drop. In type II, the PR interval before the drop and after the drop should be the same. (Note: This method is inaccurate in 2:1 AV block.)
On the EKG below, the red arrows are pointing at the dropped P waves. The PR intervals before and after the drop are circled in blue. Note that the PR interval before the drop (0.40 seconds) is longer than the PR interval after the drop (0.20 seconds). This is consistent with 2nd degree type I AV block.
An approach to interpreting a bradycardic EKG is below.
2nd degree AV block type I usually requires no specific emergency treatment. It can occur in the setting of an inferior wall MI. In that case the treatment is to treat the ischemia. If it occurs as an adverse effect of a medication, the medication should be withdrawn.
This EKG comes courtesy of Dr. Khodorkovsky.
An 87 year old male with a history of HTN presents to the ED for chest pain and shortness of breath which began the night before. He vomited this morning.
V/S: Pulse 102, Respirations 16, BP 86/52.
He is ill appearing on exam.
His EKG is below.
1. What does the EKG demonstrate?
2. What is the diagnosis?
3. How would you manage this patient?
The EKG shows sinus tachycardia with an anterolateral ST elevation MI.
The diagnosis is Cardiogenic shock
Cardiogenic shock is managed with aspirin, anticoagulation, vasopressors, and urgent cath.
The EKG demonstrates ST elevations in leads V1-V6, I and aVL with reciprocal depressions in leads II, III and aVF. This is consistent with an anterolateral STEMI. It usually suggests a proximal LAD occlusion.
The patient’s clinical condition (acute MI with tachycardia and hypotension) is consistent with cardiogenic shock. Cardiogenic shock is a state of heart failure that results in inadequate cardiac output, hypoperfusion, and end-organ dysfunction. The most common cause is LV dysfunction from an acute MI. It carries a very high mortality rate (50-80%).
The acute MI should be managed as all other MI’s with aspirin and anticoagulation. To manage the shock, Dobutamine can increase cardiac output but it causes hypotension. Norepinephrine is the preferred first-line adrenergic agent.
Cardiac cath with PCI is the treatment of choice.
Our patient went to the cath lab and was found to have a 100% occlusion of the proximal left main, as well as 70% occlusion of the proximal RCA. His ejection fraction was 10%. An intra-aortic balloon pump was placed. He was treated with vasopressors. Unfortunately he expired the following day.
Reference: Moskovitz et al. Cardiogenic Shock. Emerg Med Clin N Am 33 (2015) 645–652.