Case of the Month – July 2017 – Answer

We had three wonderful answers to last month’s COTM, but Dr. Segarra’s comprehensive response takes the cake.


For a complete review of the case, please click here.


Just to recap:


50-year-old woman with DM2, HTN, GERD, recently completed 6 months of TB therapy, presented with abdominal pain, N/V, weight loss, and anorexia. Her exam was notable for a diffusely tender abdomen, most pronounced in the right lower quadrant, and bilateral costovertebral angle tenderness. Labs were notable for a leukocytosis and bandemia of 11%, thrombocytopenia, hyponatremia of 116 (uncorrected), anion gap of 17 (20 when corrected for Albumin of 2.8), hyperglycemia of 526, creatinine of 3.23, large leukocyte esterase in the urine. CT imaging was notable for massively enlarged kidneys, ascites, hepatomegaly, and a large bulky uterus. The patient was initially tachycardic and hypotensive but after a 2L bolus, the hemodynamics improved, creatinine decreased to 2.89, glucose decreased to 435, and sodium decreased to 107 (uncorrected).


What is your differential diagnosis for the patient’s presentation?

Dr. Segarra gave a wide differential diagnosis and went through the process of paring down the possibilities. For this patient, labs ruled out DKA (no ketonemia), and CT excluded appendicitis, pancreatitis, hepatitis, cholecystitis, and bowel obstruction. The remaining diagnoses included sepsis (patient had a leukocytosis/bandemia and tachycardia), hematologic disorders, endocrine disorders such as SIADH and adrenal insufficiency, and infiltrative diseases. All of our respondents included extra-pulmonary tuberculosis as part of their differential diagnosis. The treatment regimen for drug-susceptible renal and disseminated tuberculosis is the same as for pulmonary tuberculosis, and as such, our patient had recently completed treatment (Nahid, 2016).


What antibiotics would you choose?

It all depends on what is being treated and which organisms may be responsible. Piperacillin/tazobactam was the initial choice in the ED based on the suspicion for an intra-abdominal infection as it offers coverage for both Gram negatives and anaerobic organisms (in addition to pseudomonas which was not likely to be a culprit in this case). The only risk factor that she had for TB is her previous infection; otherwise, she had no previous history of incarceration (recall that she works in the police department), and she had been adherent to her therapy (this was confirmed by the medicine team with the DOH). So, her risk for multidrug resistant TB was deemed to be low. Nevertheless, in such patients, the use of a fluoroquinolone, despite its broad-spectrum activity, would be controversial as it also is effective against Mycobacteria species and is generally given as part of a multi-drug regimen to avoid development of resistance. Piperacillin/tazobactam is an acceptable choice, but ceftriaxone with metronidazole would be most appropriate for the treatment of community-acquired intra-abdominal sepsis.

Does this patient need to be on isolation?

Based on CDC guidelines, respiratory isolation is not required. The patient had very recently completed a treatment regimen and did not have any respiratory symptoms.

How would you characterize the sodium disturbances, both on initial presentation and after the initial interventions?  How would you address them?

The sodium derangements are somewhat masked by the hyperglycemia. Her initial value indicates some degree of pseudohyponatremia, with the corrected value being either 123 or 126 depending on whether you use 1.6 or 2.4 as your correction factor. That the serum sodium decreased to 107 (112 or 115 depending again on choice of correction factor) despite infusion of crystalloid containing 154 mmol/L indicates that she is suffering from either too much free water retention or from too much loss of salt. Her corrected values still represent hyponatremia, but it is important to recognize that the concomitant hyperglycemia has an impact.

As Dr. Segarra noted, it’s helpful to break down hyponatremia based on serum osmolality and then on volume status (Spasovski, 2014). Calculation of this patient’s serum osmolarity would be affected by her hyperglycemia, but her downtrending creatinine (3.23 to 2.89 after 2L of fluids), and initial vital sign abnormalities all point towards an initial hypovolemic state. The resolution of her tachycardia/hypotension and downtrending creatinine also indicate that her initial hypovolemia had improved, and she was now closer to a euvolemic state. Euvolemic hyponatremia is usually caused by endocrine derangements such as hypothyroidism, adrenal insufficiency, and syndrome of inappropriate antidiuretic hormone (SIADH).

Further diagnostic work-up for the exact etiology of her hyponatremia would likely include serum cortisol, serum TSH, serum osmolarity, urine electrolytes, urine osmolarity, and urine creatinine. However, much of this work-up typically continues after the patient has left the ED.

Treatment of hyponatremia requires assessing whether the patient is symptomatic, characterizing the time-course during which it had developed, and clarifying the underlying etiology. Acute (e.g. developing within 48 hours) severe (Na < 125 mmol/L) hyponatremia has severe complications including altered mental status, hallucinations, seizures, coma, decerebrate posturing, respiratory arrest, and ultimately, death (Berl, 2007). While the available information does not definitively tell us how long the patient’s hyponatremia had been present, the lack of any of these signs/symptoms points towards a more chronic picture. Chronic hyponatremia may cause milder or even no neurologic symptoms (like our patient).

Assessment of time-course and presence (or absence) of symptoms will determine the treatment plan (Berl, 2007). A patient with documented acute (e.g. <48 hours) severe hyponatremia or chronic severe hyponatremia with symptoms, should received 3% hypertonic saline at 2 mL/kg/hr and IV furosemide, with a goal of 2 mmol/L/hr increase in serum sodium (Berl, 2007). Spasovski et. al describes alternative dosing regimens for treatment of symptomatic severe hyponatremia.  Patients may require ICU level of care for monitoring and administration of hypertonic saline (Berl, 2007).


A patient with an unclear time-course and moderate symptoms (symptoms not including coma or seizures) should get 0.9% saline with IV furosemide, with a goal of 0.5-2 mmol/L/hr increase and a goal of 8-10 mmol/L increase in serum sodium in the first 24 hours (Berl, 2007). Alternatively, the patient may receive a single bolus of 2 mL/kg 3% hypertonic saline over 20 minutes, cause-specific therapy, and discontinuation of any inciting factors (Spasovski, 2014).

An asymptomatic patient should have fluid restriction with dietary salt or urea (at 0.25-0.5 g/kg). Use of ADH antagonists is controversial, and based on 2014 European guidelines, it is not recommended due to the fear that it may increase the rate of sodium correction (via free water excretion) beyond a safe level (Spasovski, 2014).

In the event of overcorrection of serum sodium (e.g. a rise in >10 mmol/L during the first 24 hours, or >8 mmol/L in any 24 hour period afterwards), the saline treatment should be discontinued, and the prospect of starting D5W at 10 mL/kg over 1 hour should be discussed (Spasovski, 2014).


Fluid restriction would be appropriate for treatment of our asymptomatic patient’s hyponatremia. However, this creates a dilemma because she also has an AKI (suggested by the fact that her creatinine is downtrending after the initial 2L bolus). As such, it may also be reasonable to give 0.9% saline as detailed above, withholding the furosemide (which would counteract the goal of increasing her intravascular volume). The key is to avoid over-correction as it can cause Osmotic Demyelination Syndrome.

What is the ultimate disposition for this patient?

Ultimately the disposition depends on the treatment plan. Continuous administration of 3% hypertonic saline would likely require placement of a central line and close observation that would only be possible in an ICU. If treatment is fluid restriction, then a stepdown unit (as we have at UHB) would be appropriate as it would allow for closer observation than a floor bed, in case the patient then develops the significant symptoms of hyponatremia.


Clinical Course

This patient was admitted to the stepdown unit and initially treated with maintenance normal saline.  After approximately 12 hours, her sodium decreased to 114 (corrected). Her treatment was switched to fluid restriction and oral salt, and her home insulin regimen was restarted. The Department of Health reported that she had drug-susceptible TB and corroborated that she had completed antimycobacterial therapy. Urine AFBs were negative. Urine studies were indicative of a pre-renal etiology behind her AKI, and ruled out renal sodium loss as the etiology behind her hyponatremia. Renal, Hematology/Oncology, and Infectious Diseases were consulted. Her hyponatremia was attributed to SIADH; her leukocytosis/bandemia and initial hemodynamic instability was attributed to sepsis. Urine and blood cultures ended up growing ESBL E. coli, and her antibiotics were switched to IV meropenem. After approximately 48 hours of fluid restriction and oral salt, the serum sodium increased to 120 mmol/L (corrected). Maintenance fluid was restarted and oral salt continued, and after one week, the sodium was 130 mmol/L and remained stable until discharge.

The patient experienced dramatic improvement in her urine output during her hospitalization, and an abdominal ultrasound done prior to discharge demonstrated marked reduction (but not resolution) of her ascites. There were 24-hour intervals during which maintenance fluids were discontinued, but it was quickly restarted after the patient experienced a rise in her creatinine. Eventually, her serum creatinine decreased and remained stable at 1.5. The patient was discharged home after completion of her antibiotic course.

Unfortunately, the ultimate etiology behind the patient’s enlarged kidneys, organomegaly, and ascites was never fully elucidated during her hospitalization. Therefore, the patient was discharged with follow up appointments with gynecology (for further characterization of her large bulky uterus), nephrology (for possible biopsy of her massively enlarged kidneys), and hepatology (for her hepatomegaly and ascites).

Thanks to our respondents!  Stay tuned for the next installment of Case of the Month!



Berl, D. E. (2007). The Syndrome of Inappropriate Antidiuresis. New England Journal of Medicine, 1064-1072.

Nahid, D. A. (2016). Official American Thoracic Society/CDC/IDSA Clinical Practice Guidelines: Treatment of Drug-Susceptible Tuberculosis. Clinical Infectious Diseases, e147-e195.

Spasovski, V. (2014). Clinical Practice Guidelines on Diagnosis and Treatment of Hyponatraemia. Nephrology Dialysis Transplantation, 1-39.

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Bored Review – “Lai Tai” after a Mai Tai

It’s Friday night, and you get a second in between patients. You are dreaming of sipping a Mai Tai by the beach, when your dream is quickly brought to an end. A 35-year-old young man walks into the ED, complaining of an episode of “passing out” after a few drinks. “Mai Tai’s?” you ask. “Oh no, just vodka,” he says. Oh, come on, you tell yourself, as you sign up for him and order an ECG and fingerstick. You think he just must have had a bit too much, and you casually hop over the stretcher-lined hallway to get a history.

He surprisingly does not seem intoxicated and has no significant past medical history. He says he had three shots of vodka, and after about an hour, “passed out”. This occurred about 4 hours prior. He felt light-headed and had palpitations just prior to the event. He does not recall how long he was down, although his friends mentioned about one to two minutes. He was not confused afterward, did not report any pain or weakness, but he did feel a bit light-headed. This has happened to him twice over the past 4 years, and both times were during alcohol intake.

His physical exam including neurologic/cerebellar function is within normal limits. His fingerstick is 110. You get his ECG back as you are talking and “aha”…

1. What do you see, and why does it concern you?
  • ST segment elevation in V1-V3 with corresponding inverted T waves
  • This is concerning for possible Brugada Syndrome


2. What is Brugada Syndrome?
  • Brugada syndrome is a disorder caused by a mutation in a cardiac sodium channel gene, SCN5A,(1) causing conduction abnormalities and dysrhythmias.
  • In Southeast Asia, it has been connected with a known phenomenon called SUNDS – Sudden and Unexpected Death during Sleep. In Thailand, studies have shown a Brugada-like ECG in 16 of 27 men, referred for a phenomenon called “Lai Tai” – or death during sleep.(1)
  • It is associated with ventricular fibrillation and sudden cardiac death, often in otherwise healthy young adults without known structural heart disease.


3. How does it present?
  • Clinically, it can present with ventricular fibrillation, aborted sudden cardiac death (more common at night or during sleep), syncope, palpitations, chest pain or discomfort, or nocturnal agonal respiration.(2)
  • ECG changes and clinical manifestations can be transient and unmasked or altered by various factors, some of which include alcohol intake, fever, ischemia, hypothermia, hypokalemia, DC cardioversion, cocaine, and various drugs listed below:(1)
    • Sodium channel blockers
    • Alpha-adrenergic agonists
    • Beta blockers
    • Tricyclic antidepressants
    • First generation antihistamines – i.e diphenhydramine, chlorpheniramine
    • Vagotonic drugs – i.e nitrates
    • Lithium


4. How common is Brugada Syndrome, and who gets it?
  • The prevalence of Brugada Syndrome is estimated at 1-5 per 10,000 people worldwide, more common in men, and is even higher (greater than 5 per 10,000 people) in South-East Asia, particularly in Thailand and the Philippines where it is considered one of the major causes of death in young people.(1)
  • Given that it is often concealed, masked, or missed, the actual prevalence may vary from the numbers above.
  • The mean age at sudden death due to the syndrome is 41 years, and the age range for diagnosis ranges from 2 days to 84 years,(1,3)


5. How do you diagnose Brugada Syndrome?
  • Although there are three ECG phenotypes classically associated with Brugada Syndrome, only Type I is truly diagnostic.
  • Type I: Coved ST segment elevation greater than or equal to 2 mm followed by negative T wave.
  • Type II: Saddle-back appearance with initial ST segment elevation greater than or equal to 2 mm. This is followed by an elevated trough in the ST segment greater than or equal to 1 mm and then, in turn, a positive or bi-phasic T wave.
  • Type III: Saddle-back or coved appearance with ST segment elevation of less than 1 mm.
  • A diagnosis of Brugada syndrome is definitively made when a Type I ECG is present in more than one precordial lead, in the presence or absence of a sodium channel blocker, in conjunction with one of the following: ventricular fibrillation, polymorphic ventricular tachycardia, family history of sudden cardiac death at less than 45 years of age, similar coved ECG types in family members, syncope, nocturnal agonal respiration, or inducible VT with programmed electrical stimulation.(1)
  • Doing the 12-lead ECG with leads V1-V2 (right precordial leads) in a superior position, using a sodium channel blocker challenge to help unmask ECG characteristics, and imaging to rule out structural heart disease may aid in diagnosis.


6. What is your differential?
  • In a young patient without known structural heart disease, several conditions can predispose to tachydysrythmias.
    • Long QT Syndrome: QTc greater than 440-450 ms in men, and greater than 460 ms in women
    • Ventricular Pre-excitation Syndromes/Accessory Conduction Pathways:
      • Wolf-Parkinson White – Shortening of PR interval less than 120 ms, widened QRS, “delta wave” – slurred upstroke of initial part of R wave
      • Lown-Ganong-Levine Syndrome – Shortening of PR interval less than 120 ms, but no delta wave.
    • Hypertrophic Cardiomyopathy: Left ventricular hypertrophy and/or prominent Q waves in leads II, III, aVF, V5, and V6


7. How will you manage this patient?
  • Given the presence of syncope and a diagnostic Type I Brugada pattern on ECG, this patient should be presumed to have Brugada Syndrome
  • Initial emergency management, ABCs, and cardiac monitoring should be applied to all patients while in the ED. ACLS protocol should be applied to patient’s in ventricular tachycardia, ventricular fibrillation, and cardiac arrest.
  • Cardiology should be involved, on an inpatient or outpatient basis, depending on your patient’s disposition. Given that our patient is symptomatic (presenting with syncopal episodes) and has a diagnostic Type I ECG, he should be admitted to telemetry with cardiology consult for implantable cardioverter defibrillator (ICD) placement.
  • Currently, an ICD is the only definitive management.
  • In patients with a diagnostic ECG presenting with aborted sudden cardiac death, ICD placement is generally recommended given high risk for recurrence.
  • In an asymptomatic patient with a type I ECG or any stable patient with a type II or Type III ECG, it may be reasonable to follow closely in an outpatient setting, with risk stratification and electrophysiological studies.(3)


  1. Antzelevitch C. Brugada Syndrome . Pacing Clinical Electrophysiology 2006; 29(10): 1130–59.
  2. MDedge [Internet]. MDedge. [cited 2017 Aug 7];Available from:
  3. Brugada Syndrome [Internet]. LITFL • Life in the Fast Lane Medical Blog. 2016 [cited 2017 Aug 7];Available from:
  4. Brugada Syndrome [Internet]. Practice Essentials, Background, Pathophysiology. 2017 [cited 2017 Aug 7];Available from:
  5. Toscano J. Review of Important ECG Findings in Patients with Syncope . American Journal of Clinical Medicine 9(2):92–6.




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Bored Review – Clavicle Fracture

A fit, young female dressed in cycling gear presents to your emergency department with a chief complaint of shoulder pain. Just prior to arrival, she was participating in a bike race in Prospect Park. As she was sprinting to the finish, a menacing squirrel leaps out aggressively and tries to take a bite out of her legs!

She slammed on the brakes trying to avoid the rabid squirrel, but ended up flipping right over her handlebars, landing on her outstretched arm.

She immediately felt pain in her shoulder with a noticeable bulge. As an astute emergency physician, you’ve heard and seen this story before. This young female has a clavicle fracture and is yet another victim of the rabid squirrel of Prospect Park.


What is the anatomy of the clavicle?

The clavicle is the only bony connection between the arm and the trunk, articulating distally with the acromion (acromioclavicular joint) and proximally with the sternum (sternoclavicular joint). The clavicle protects the adjacent lung, brachial plexus, and subclavian and brachial blood vessels.

Picture Credit: UpToDate

What is the typical history and presentation?

The clavicle accounts for 5% of all fractures and is the most commonly fractured bone in children. The mechanism of injury is usually from high-energy trauma to the shoulder or from a fall on an outstretched hand.

Patients will present with pain over the fracture site and tend to hold the affected extremity close to his or her body.

Of note, clavicle fractures also occur in newborns during delivery, though this article will focus on injuries of children, adolescents, and adults.

What are the key physical exam features of clavicle fracture?

It is important to perform a neurovascular exam in patients with clavicle fractures because the clavicle overlies the subclavian artery, the subclavian vein, and the brachial plexus. Although rare, high-impact anterior forces on the proximal clavicle can lead to pneumothorax and/or pulmonary injuries.

The skin over the area of injury may show tenting, ecchymosis, or bleeding. Since the clavicle is very superficial, any skin tenting (see arrow below) can progress to an open fracture due to pressure necrosis of the skin from the clavicle itself.

Picture credit: Medscape

How are clavicle fractures diagnosed?

Standard shoulder and clavicle X-rays are very sensitive. For more subtle fractures, positioning the patient in the upright position or a 45-degree cephalad tilt view may be used. CT should be considered if clinical suspicion for fracture is high, it is not clear on X-ray, or if there is concern for neurovascular or pulmonary injury.

Mid-Clavicular Fracture

Picture credit: Rosen’s Emergency Medicine

Clavicle fractures can also be seen on ultrasound, which can be especially helpful in saving younger children from exposure to radiation.

Normal Clavicle Ultrasound

Fractured Clavicle Ultrasound


How are clavicle fractures classified?

Clavicle fractures are classified anatomically into three groups. It is important to recognize these groups, because it has a large influence on additional workup and disposition. The groups are listed below in order of incidence.

  1. Middle (~ 80% of fractures) – The usual mechanism is a direct force applied to lateral aspect of the shoulder as a result of fall, sporting injury, or MVC.
  2. Lateral (~15% of fractures) – The usual mechanism is a direct blow to the top of the shoulder. There are 3 types of lateral fractures.
    • Type I – The coracoclavicular ligament is intact.
    • Type II – The coracoclavicular ligament is torn. These tend to displace because the proximal fragment lacks any stabilizing forces. There is a high risk of nonunion so operative management may be indicated.
    • Type III – These are intra-articular fractures through the acromioclavicular (AC) joint.
  1. Medial/Proximal (~5% of fractures) – The usual mechanism is a direct blow to the anterior chest. Medial/Proximal injuries result from high impact and are often associated with intrathoracic injuries. As a result, there should be a low threshold to explore for associated neurovascular or pulmonary injuries.

How do we manage clavicle fractures?

In the emergency department, immediate orthopedic consultation should be sought for open fractures or fractures associated with neurovascular injuries, skin tenting, or interposition of soft tissues.

Otherwise, clavicle fractures can usually be managed non-operatively with immobilization. Patients should wear a sling until repeat X-rays of the clavicle show callus formation. This can take up to 2 to 4 weeks in younger children and 4 to 8 weeks in adolescents and adults. This can either be done with primary care follow up (for mild, nondisplaced fractures) or orthopedic follow up (for more displaced fractures with significant shortening).

Sling Over Swathe (Left) | Velpeau Sling Immobilization (Right) 

Picture Credit: Rosen’s Emergency Medicine

The orthopedic literature also suggests clavicular or figure-of-eight splints which can be applied after closed reduction of the clavicle fracture, though the evidence for its efficacy in the emergency setting is slim.

Figure-of-Eight Splint

Picture Credit: Rosen’s Emergency Medicine

There is growing evidence that operative management improves outcomes. This is especially true for any patients with risk factors for non-union such as shortening greater than 2cm, comminuted fractures, or 100% displaced fractures. Orthopedics evaluation should be offered to all patients with these risk factors.



Hatch, Robert L, James r. Clugston, and Jonathan Taffe. Clavicle fractures. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on July 30, 2017.)

Marx, John A, Robert S. Hockberger, Ron M. Walls, Michelle H. Biros, and Peter Rosen. Rosen’s Emergency Medicine: Concepts and Clinical Practice. Philadelphia, PA: Elsevier/Saunders, 2014. Print.

Tintinalli, Judith E, J S. Stapczynski, O J. Ma, David Cline, Garth D. Meckler, and Donald M. Yealy. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. , 2016. Print.



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