POTD: Superficial Thrombophlebitis (feat. Dr. Doge Pologe)

Today's POTD is inspired by resident extraordinaire Dr. Doge Pologe. As usual, TL;DR is below the main text. 

Thrombophlebitis is essentially a composite of two diagnoses: phlebitis, which is a clinical diagnosis in the setting of an erythema and pain overlying a vein and an identified thrombus. In the lower extremities, this is most likely to occur in varicose veins. 


In general, risk factors for thrombophlebitis are the same as for DVT (think Virchow's Triad of hypercoagulability, hemodynamic changes (stasis/turbulence), and endothelial injury/dysfunction). These include pregnancy, history of vein excision/ablation, history of prior thrombosis, malignancy, and prior IV catheter placement. 

Special cases:

  • "Mondor": thrombophlebitis of a breast vein, anterior chest vein, or of the dorsal penile vein. The two former should prompt a search for breast cancer and the later is usually due to repetitive trauma

  • "Trousseau's sign of malignancy": migratory thromboembolism, has a strong association with adenocarcinoma of the pancreas and lung

Diagnosis of phlebitis is clinical. Ultrasound should be used to identify a thrombus to distinguish between phlebitis and thrombophlebitis. Patients should also have duplex ultrasound to identify a DVT especially if the area of concern is above the knee. This is important because the rate of concurrent DVT in all cases is 25% and the rate of concurrent PE is 5%. 

Thrombophlebitis on ultrasound will demonstrate heterogeneous internal echoes within a superficial vein. Unlike an abscess or a lymph node, this will not be discrete and you should be able to trace it out. in the words of the Doge:

"it looks like a weird continuous twisty spaghetti
abscess thing; 
but it's not to be feared, 
mostly superfluous, so get frisky and ultrasound that biddy, 
color doppler, diagnosis, ka-ching". 

There may be flow present (which can help distinguish an abscess from thrombophlebitis; abscess = no flow). Some examples (by the Doge Pologe and myself):

Screen Shot 2019-04-15 at 6.57.02 PM.png

As with treatment of below the knee VTE, the treatment of superficial thrombophlebitis is controversial. Patients can be considered low risk (for VTE) if they meet these criteria:

  • Affected vein segment < 5cm

  • Remote from the saphenofemoral/saphenopopliteal junction

  • Low risk for VTE

**Repeat duplex should be obtained in 7-10 days or for worsening symptoms to check for propagation!

NB: thrombophlebitis post-ablation are always low risk and do not require treatment

For these uncomplicated cases, treatment is aimed at alleviating symptoms and prevention of propagation. This includes the following:

  • NSAIDs

  • Warm/cool compresses

  • Elevation of the extremity

  • Compression stockings

Patients that do not qualify as low risk or if they have recurrent thromboembolism should be considered for anticoagulation. Although studies looking at anticoagulation for SVT are small and flawed, NSAIDsLMWH, and fondaparinux have all been shown to decrease incidence of DVT. Patients can also be discharged on Xarelto (this is the only NOAC to be studied for this indication). 

In addition, thromboembolism can become suppurative. Signs and symptoms include high fever (as opposed to the low-grade fever that accompany simple thrombophlebitis) and purulent drainage (duh). In these cases, consider antibiotics


  • Thrombophlebitis = phlebitis (redness/pain along vein) + thrombus

  • Find the thrombus on ultrasound! Look for internal echoes.

  • Low risk patients = below the knee, affected vein < 5cm, distance remove from saphenofemoral/saphenopopliteal junction can be managed with NSAIDs, compression stockings, warm/cool compresses, elevation

  • Low risk patients should get repeat study in 7-10 days to check for propagation

  • High risk patients: consider anticoagulation with LWMH, fondaparinux, or Xarelto

  • Antibiotics for suppurative thrombophlebitis

Special thanks to Dr. Jonas Pologe, Dr. Lawrence Haines, and Dr. Leily Naraghi Bagher Pour. 



Sunday Funday POTD: Priapism - a hard problem to solve?



Named after the Greek god of fertility, Priapus, priapism is defined as an erection that lasts for longer than 4 hours that is not associated with sexual stimulation. Why do we care? Because 90% of men with persistent erections > 24 hours will have permanent erectile dysfunction. There are three types: non-ischemic, ischemic, and recurrent. 

Non-Ischemic ("high flow"):
The less common type, this is due to an excess of blood via a fistula between the cavernosal artery and the corpus cavernosum, usually in the setting of trauma. 

Ischemic ("low flow"):
The more common type, this is due to obstruction of venous outflow as a result of impaired relaxation of cavernosal smooth muscle. This is a urological emergency

Recurrent ("stuttering"):
A form of ischemic priapism that occurs in men with sickle cell disease. It's characterized by initially short erections that progressively worsen. 

History should include: duration of current erection, prior episodes, any medications used (legal or otherwise), history of hematological disorders (specifically sickle cell), history of trauma, how severe the pain is. 

Your entire workup is used to distinguish between ischemic and non-ischemic priapism. The table below summarizes the characteristics. 

Screen Shot 2019-04-15 at 11.22.03 AM.png


Call urology!! (if available)
If unavailable, believe it or not, high flow or non-ischemic priapism, can resolve spontaneously, actually does not require treatment, and can be managed as an outpatient by urology. 

First of all, analgesia should be provided. An easy way to do this is to perform a dorsal penile nerve block.



  1. Obtain consent, grab your materials (lidocaine), syringe, needle, alcohol/iodine, cleanse the area

  2. Insert a small needle at the 2 o'clock and 10 o'clock position at the base of the penis

  3. Feel for the pop of scarpa's (superficial) fascia

  4. Aspirate and inject 2mL anesthesia in each position

This can also be done under ultrasound guidance!
Second, the American Urological Association recommends primary aspiration of cavernosal blood. To do this, insert an 18 gauge needle to the lateral aspect of the penis one in each corporal body. 30-60ccs of blood should be removed. 

If this is sufficient, stop here. If tumescence persists, phenylephrine injection may be attempted. This should be given in 1mL aliquots of a 100-500mcg/mL concentration. To mix this, take a vial of phenylephrine (10mg/mL) and take out 1mL, mix this in a 100mL bag of NS. To make it easier, don't take the needle out of the penis and simply attach a syringe with the medication to the needle. This may be repeated every 3-5 minutes for an hour until resolution. 

Fun fact: epinephrine can be used as well based on several case series. The dosing: 2mL of a 1:100,000 (10mcg/mL) concentration. This is essentially your push-dose dose (ie. 1mL of code cart epi in 9mL NS)

If this fails, the patient will need urological surgery... won't bore you with the details here!

What about sickle cell disease?

Priapism in sickle cell disease should be managed in the same way as ischemic priapism. It is rare that standard therapies do not work, but if they do not, exchange transfusion or simple transfusion can be considered. Don't forget to get a retic level in these patients!


  • Ischemic priapism is painful and is a urological emergency

  • Call urology consult!

  • Provide analgesia/perform a dorsal nerve block

  • Aspirate with two needles laterally

  • Phenylephrine if this fails

  • Further management with urology if this fails

  • Consider exchange transfusion in patients with sickle cell disease with priapism that doesn't resolve with these measures




Wellness Wednesday POTD: Imposter Syndrome

As the academic year is coming to and we all adjust to our new roles within our residency programs or as new attendings or fellows, I thought this would be a good time to talk about this.

Imposter Syndrome

Originally described by psychologists Suzanne Imes, PhD and Pauline Rose Clance, PhD in the 1970s, it is defined as an "internal experience of intellectual phoniness". Essentially, this means that people with imposter syndrome feel that their achievements are undeserved and worry about being "found out"that they are less than adequate despite evidence indicating success and/or competence. 

Dr. Clance described six potential characteristics:

Screen Shot 2019-04-03 at 10.22.16 PM.png
  1. The imposter cycle
    The cycle starts with a task, which is then met with anxiety, lead to either over-preparation for the task or procrastination (which is over-compensated with frenzied preparation). When the task is completed, there is relief, but this is short-lived despite positive feedback. Instead, the person believes that their success is either due to their hard work or luck, but not due to their ability

    The result is a feeling of self-doubt, depression, and anxiety and a tendency to overwork

  2. The need to be special or the very best
    Those with imposter syndrome are secretly comparing themselves to others, which leads to a feeling of inadequacy.  

  3. Super(wo)man aspects
    Related to the need to be the best, people with imposter syndrome set unrealistic goals for themselves. 

  4. Fear of failure
    This can also be identified as the main motivational factor for most people with imposter syndrome. 

  5. Denial of competence and discounting praise
    Adding onto feelings of inadequacy, those with imposter syndrome have difficulty internalizing success and will even make excuses about why praise is not deserved. 

  6. Fear and guilt about success
    Although people with imposter syndrome crave success, they also fear it because it makes them feel isolated in their success. They also fear taking on more responsibilities as they're more likely to be "found out" with higher expectations. 

This was further elucidated by Dr. Valerie Young who broke down the syndrome into five different personality types in her book The Secret Thoughts of Successful Women:

  1. Perfectionists: people who set unrealistic goals and feel like failures despite the level of completion of these goals

  2. Experts: people who need to know every piece of information and will overeducate themselves. They are also afraid of looking stupid and will hesitate to assert themselves

  3. Natural geniuses: people that are used to achieve success effortlessly, which leads to feelings of inadequacy when any effort is needed

  4. Soloists: people who feel that asking for help is a sign of failure

  5. Super(wo)men: people who need to work harder than everyone else around them in order to succeed in all aspects of life

How to deal with imposter syndrome

As with any problem, the first step is identifying and recognizing the problem. From there, overcoming imposter syndrome requires a lot of self-reflection and much of this comes from reframing your mindset on what qualifies as success. Some potential methods:

  • Seek help: this can be found in a mentor, a friend, or a therapist. Vocalizing feelings and concerns can help in several ways. First, it can help identify characteristics that are typical of imposter syndrome, which can lead to increased self-awareness. Talking can also help with the realization that imposter syndrome is not an uncommon occurrence, which helps to normalize the condition. 

  • Lean to internalize validation: people with imposter syndrome tend to dismiss positive feedback. Learning to reframe your mindset by resisting this response to positive feedback can help put things into perspective.  

  • Be realistic about expectations: the expectations that those with imposter syndrome set for themselves are unrealistic. It is important to realize that nobody is perfect and to properly reflect on one's own successes. Likewise, it's important to recognize that everyone has strengths and weakness and to reflect on one's strengths and not to see weaknesses as failures. 

  • Figure out your true goals: it's possible the goals that you've set for yourself would not actually ones that would make you happy. Take stock in what really matters and that may also help to redirect your ambitions. 

Abrams A. Yes, Imposter Syndrome is Real. Here’s How to Deal With It. Time Website. http://time.com/5312483/how-to-deal-with-impostor-syndrome/
Roche J. 10 Ways to Overcome Imposter Syndrome. The Shriver Report Website. http://shriverreport.org/10-ways-to-overcome-impostor-syndrome-joyce-roche/
Sakulku J, Alexander J. The imposter phenomenon. International Journal of Behavioral Science. 2011;6(1):75-97.
Weir K. Feel Like a Fraud?. American Psychological Association Website. https://www.apa.org/gradpsych/2013/11/fraud
Wilding M. 5 Different Types of Imposter Syndrome (and 5 Ways to Battle Each One). The Muse Website. https://www.themuse.com/advice/5-different-types-of-imposter-syndrome-and-5-ways-to-battle-each-one


POTD: Measles (Part 2)

Part two in our two part series about measles! 

Again, TL;DR at the bottom and here's another plug for Dr. Anna Pickens' EM in 5: http://www.emdocs.net/em-in-5-measles/

This section goes over the diagnosis, management, and complications of measles. 

Measles virus is a single-stranded, enveloped, RNA virus of the genus Morbillivirus within the family Paramyxoviridae. It is spread via respiratory droplets that may remain in the air for up to two hours

Clinical Presentation
 period: 6-21 days (median 13 days)

Prodrome (days 2-4): fever, malaise, and anorexia followed by “the 3C’s” (conjunctivitis, coryza, and cough). This phase of infection can last up to 8 days. 

Koplik spots typically present 48 hours prior to the onset of the exanthem. They are white/gray/bluish elevations, described as “grains of salt” on an erythematous base. These are typically seen on the buccal mucosa, but may spread to the soft and hard palates. These generally last for 12-72 hours. 


Exanthem: starts 2-4 days after onset of fever. Classically is a blanching, maculopapular rash that starts on the hairline and progresses downward and outwards to the extremities. It tends to coalesce and become non-blanching with time. 

Patients will become clinically better within 48 hours of the appearance of rash, the rash will darken in color, and eventually desquamate. 

Measles may vary in severity and there are several clinical variants including: modified measles (milder symptoms) in those with pre-existing measles immunity, those who have received IVIG, and in babies with passive immunity from placental migration of immunoglobulins; atypical measles in those who have received the killed virus vaccine (not seen frequently now), which is characterized by higher and more prolonged fevers, pneumonitis, and transaminitis. Patients that are immunocompromised will also not present classically. 

Immunocompromised patients and pregnant patients are more likely to develop complications. 

Superimposed infection is common because T-cells and dendritic cells are directly infected, which leads to immune suppression that can persist for up to three years. Infections include:

  • Otitis media

  • Gastrointestinal (most common) - diarrhea, gingivostomatitis, appendicitis

  • Pulmonary (most common cause of death) - bronchopneumonia, croup, bronchiolitis

  • Neurologic

    • Encephalitis: occurs several days after rash. Patients have neurodevelopmental sequelae in 25% of cases, fatal in 15% of cases

    • Acute Disseminated Encephalomyelitis (ADEM): occurs several weeks after rash. Demyelinating disease likely due to immune response to the virus. Fatal in 10-20% of cases and survivors commonly have residual neurologic abnormalities. 

    • Subacute Sclerosing Panencephalitis (SSPE): occurs 7-10 years after infection. More likely the younger the time of infection

      • Stage I (weeks-years): insidious neurological symptoms (trouble concentrating, lethargy, personality changes, strange behavior)

      • Stage II (3-12 months): dementia, myoclonus

      • Stage III (variable): myoclonus resolves, neurologic function deteriorates leading to flaccidity/decorticate rigidity, autonomic dysfunction

      • Stage IV: death

First off, isolate your patient if you suspect measles!! Place the patient in a negative pressure room. Despite the high efficacy of MMR, there is still a 1% chance that you are not immune. As such, everybody entering the room should wear an N95 mask and the patient should wear a mask during transport. 

Test used depends on the prevalence of disease and the local governing body for infection control. In general, IgM and IgG are tested in the serum and a nasopharyngeal swab should be obtained for serological testing. False positive PCR does not rule out infection

Mainly supportive and treating any superimposed bacterial infections. In children, they tend to have low vitamin A levels, which can contribute to delayed recovery and more complications. Low vitamin A levels also causes blindness in children in the developing world. As such, children benefit from vitamin A supplementation. Ribavirin can also be considered especially for higher risk individuals (< 12 months, requiring ventilatory support, and severe immunosuppression). 


  • Measles is transmitted airborne, stays in the air for 2 hours

  • Characterized by a prodrome of fever, malaise, coryza, conjunctivitis, and cough for 2-4 days followed by a maculopapular rash that progresses downward

  • Measles can be complicated by bacterial infections. Most common cause of death is from pneumonia

  • Long-term effects include severe neurological sequelae: encephalitis, acute disseminated encephalomeningitis, and subacute sclerosing panencephalitis

  • Diagnose via IgM, IgG, nasopharyngal swab

  • Treatment primarily supportive

  • Consider vitamin A and ribavirin



POTD: Measles (Vaccination and Post-Exposure Prophylaxis)

Ok guys, time for a big topic very relevant in current events - Measles! This is going to cover mostly immunization and post-exposure prophylaxis recommendations and not the clinical symptoms.

Our former clerkship director Dr. Anna Pickens has a great video summarizing all things measles available on emdocs.net:

Scroll to the bottom for the TL;DR version. 



A little bit of background first. One of the most infectious pathogens, measles was targeted for eradication in the 1960s because of its highly infectious nature and it's human-only infectivity, which led to a dramatic decrease in the number of cases in developed countries. Before this, about 90% of children acquired the virus before age 15. In the United States, the immunization program has resulted in a staggering 99% percent decrease in the number of cases. Since then, largely due to under-vaccination or unvaccinated populations, cases have been on the rise since 2008. Most of these cases are imported from abroad. Of the cases in the US, 85% of cases were unvaccinated despite being eligible for vaccination. 

Measles is highly contagious and carries a 90% infectious rate when a susceptible person is exposed. Population immunity of > 95% is needed to stop ongoing transmission. 


In the US, two doses of vaccination MMR is recommended, the first at 12-15 months (conferring 95% immunity) and a second dose at 4-6 years of age (conferring 99% immunity) or at least 28 days after the first dose. 

Fun fact: vaccination is recommended no earlier than 12 months because maternal antibodies seem to interfere with seroconversion (87% seroconversion if administered at 9 months, 95% at 12 months, and 98% at 15 months). 

A third dose is not routinely recommended as it is not associated with any more protection than two doses. 

For those who received two doses of MMR based on the CDC recommended schedule, the CDC, NYCOH, and NYCOHMH all discourage serologic testing if the vaccine history is available. 

What this means: if your patient has had two doses of MMR, they do not need titers and if they have titers, it doesn't matter!!

For those born before 1957, they are presumed to have immunity to measles and mumps. This is not the case for rubella (not covered here). 

Pregnant women are at higher risk than the general public of measles related morbidity and mortality and should therefore be counseled by their ob/gyn regarding vaccination status. As with all adults, pregnant women that have evidence of two doses of MMR are considered immune and should not have titers performed. If documentation is not available, pregnant women should not receive MMR due to a theoretical risk of vertical transmission of rubella to the fetus. MMR vaccine should then be administered after delivery. That being said, studies on neonates that are born to women that have inadvertently received MMR shows no risk of of MMR vaccine to the fetus. 

Healthcare workers are also considered a special population due to our frequent exposure to communicable disease. The recommendations for vaccination and testing are the same as the general public regardless of date of birth (ie. two doses or serological evidence is always required). Additionally, during outbreaks, healthcare workers without evidence of immunity should receive 2 doses MMR. 


First things first: who qualifies as "being exposed to measles"? You qualify if you have shared the same air as someone while they were infectious. The infectious period lasts from 4 days before until 4 days after the onset of rash. 

Un-vaccinated individuals should receive MMR vaccination within 72 hours of exposure if there are no contraindication (ie. pregnancy, immunocompromise, anaphylactic reaction to any of the vaccine components, infants < 12 months of age). Between 72 hours and 6 days of vaccination, they should receive IMIG (0.5mL/kg IM, max 15 mL). 

Infants < 12 months of age exposed to measles should receive IMIG 0.5mL/kg IM, max 15 mL within 6 days of exposure. 

Because of the increased risk of complications and death in pregnancy, pregnant women exposed to measles should receive IVIG 400mg/kg within 6 days of exposure. Additionally, peri-partum, pediatrics should be made aware of the potential risk of congenital measles if born to a mother with measles. 

Immunocompromised individuals should also receive IVIG 400mg/kg within 6 days after exposure regardless of vaccination status.

Infants exposed to measles (< 12 months of age) should receive IMIG 0.5mL/kg (max 15 mL)

Healthcare workers who do not show evidence of immunity either by records or serological testing should receive MMR and be removed from work for 21 days following exposure. Those who do not receive MMR should be removed from work for 21 days following exposure even if they have received IMIG. If there is only one dose documented, they may remain at work and should receive a second dose. 


  • Measles very contagious, MMR has been successful in greatly decreasing cases

  • Most outbreaks have been due to under-vaccination or unvaccinated populations

  • Recommended schedule: 1st dose at 12-15 months, 2nd dose at 4-6 years or 28 days after the first dose

  • Titers are not necessary if there is evidence of two appropriately administered vaccinations for everyone

  • If record/evidence of vaccination is not available, serological testing should be performed

  • Post exposure:

    • Unvaccinated individuals should receive MMR within 72 hours of exposure or IMIG 72 hours-6 days after exposure

    • Infants < 12 months should receive IMIG within 6 days

    • Pregnant women and immunocompromised should received IVIG within 6 days

  • Exposed healthcare workers who do not have evidence of immunity should not return to work for 21 days following exposure regardless of whether they received MMR or IMIG. 



POTD: Lithium Toxicity (Toxicology Thursday)

Lithium has been used to treat patients with bipolar disorder since the 1870s and is still widely used today, but has a very narrow therapeutic index! Toxicity can due to acute deliberate ingestions (18%) or, more commonly, chronic ingestions.

There are three categories of toxicity:

Acute: due to ingestion in a lithium naive patient, generally, an ingestion of > 7.5mg/kg of elemental lithium or 40 mg/kg of lithium carbonate. Prognosis tends to be better in acute poisoning because there is not sufficient time for distribution, which decreases the risk of neurotoxicity.

Acute-on-Chronic: an acute ingestion in a patient chronically on lithium

Chronic poisoning: occurs when chronic ingestion exceeds elimination. Highest risk of neurotoxicity because there is sufficient time to accumulate. Also the half life of lithium in chronic toxicity is prolonged due to underlying renal impairment.


Toxicity from chronic ingestions occur from impaired excretion due to:

  • Reduced GFR (NSAIDs, ACE inhibitors)

  • Increased renal tubular reabsorption (thiazides, spironolactone)

  • Calcium channel blockers (unknown mechanism)

 Renal processing is similar to that of sodium – meaning if the kidneys find any reason to retain sodium, it will also retain lithium! A major example is dehydration.

Serum lithium levels may be high, but the patient may be asymptomatic because effects only occur when moved intracellularly.




  • Coarse tremor

  • Hyperreflexia

  • Nystagmus

  • Ataxia

  • Altered mental status

  • Seizures/non-convulsive status epilepticus


  • Nephrogenic diabetes insipidus

  • Sodium losing nephritis

  • Nephrotic syndrome

Cardiovascular (usually mild)

  • Wandering atrial pacemaker

  • Sinus bradycardia

  • ST-segment elevation

  • Prolonged QT syndrome

  • T-wave flattening


  • Nausea/vomiting

  • Diarrhea

  • Ileus

**this can worsen toxicity due to increased renal reabsorption of sodium and lithium


  • Hypothyroidism (inhibition of hormone synthesis)

    • Also worsens lithium toxicity


Labs including TFTs, renal function, calcium, serum lithium level, EKG, cardiac monitoring. Make sure the tube was not treated with lithiated heparin. Remember, the serum level does not reflect the intracellular level, so a patient may be asymptomatic with high levels and normal levels do not exclude toxicity!!

However, generally:

  • Mild intoxication (1.5-2.5 mEq/L): nausea/vomiting, lethargy, tremor

  • Moderate intoxication (2.5-3.5 mEq/L): confusion, agitation, delirium, tachycardia, hypertonia

  • Severe intoxication (> 3.5 mEq/L): coma, seizures, hyperthermia, hypotension 


Symptomatic treatment (e.g. benzos for seizures, magnesium for torsades).

IVF – the goal is to preserve GFR so that lithium does not get reabsorbed!

Activated charcoal does not work, but you may consider gastric lavage or whole-bowel irrigation for acute ingestions.

Hemodialysis for severe toxicity or renal failure

Patient should be admitted to a monitored setting. Admit to ICU for severe symptoms!! If patients are asymptomatic with a lithium level < 1.5 mEq/L, they may be discharged.


POTD: High-Pressure Injection Injury

High-Pressure Injection Injury

·      Patients present with seemingly innocuous findings after high-pressure injection injury

·      Their condition often rapidly deteriorate

·      Substances can be paint, paint stripper, grease, oil, water or air.

·      This is a surgical emergency and early consultation is critical for surgical decompression and debridement

·      Less viscous substances can penetrate deeper with less pressure, leading to worsened outcomes, even if initially the wound may appear benign on the exterior, and even if the patient’s pain is initially minimal

·      Paint and paint thinners produce a large and early inflammatory response leading to ischemia and tissue death and the rate of associated amputation is high.

·      Initial emergency department management:

o   pain control, radiographs (look for free air), elevation, splinting, IV antibiotics, tdap, emergent hand specialist consultation

o   These injuries are not high-risk injuries for tetanus, and prophylaxis, even if indicated, therefore tdap should not delay other steps in management.

o   In fact, none of the emergency department interventions, (besides pain control), is as important as recognition of the potential severity of the injury and early consultation with a hand specialist

o   There is no amount of cleansing this wound in the ED that is recommended because the penetration is deep and this patient needs to go to the OR.

·      It is interesting to note that although digital blocks are excellent tools to relieve pain and provide anesthesia, they are not recommended in high-pressure injection injury as one of our major concerns is compartment syndrome.

o   Digital blocks can lead to an increase in compartment pressure and worsen injury/tissue ischemia. Systemic pain control is recommended.

The below picture is of a hand in the OR, you can see the initial presentation appears someone benign and once the hand is opened up, you see a lot of tissue necrosis.

potd high pressure.jpg

Below pictures show benign physical exam findings and some free air on xray

potd finger.png

Sources: Tintinalli, Rosen's Emergency Medicine, uptodate, Peer IX, ortho blog for photos: http://www.cmcedmasters.com/ortho-blog/high-pressure-injection-injuries


POTD: Varicella-zoster virus (VZV)

Noticing the trend in decreased vaccination, let’s review varicella.

  • Varicella-zoster virus (VZV): one of eight herpesviruses known to cause human infection

  • full-body rash that starts on the trunk and is characterized by lesions in various stages of development.

    • Buzz words: asynchronous vesicular lesions

potd varicella.jpg

·      Requires airborne precautions

·      Chickenpox used to be very common in the United States.

o    Each year, chickenpox caused about 4 million cases, about 10,600 hospitalizations and 100 to 150 deaths.

·      Two doses of the vaccine are about 90% effective at preventing chickenpox.

·      Although varicella is usually a self-limited disease and usually management is supportive

o   Exception to this is if you are at risk for complication or develop complications. 

·      Who is most at risk for complications from varicella?

o   Older patients, pregnant patients, and anyone who is immunocompromised (think on chronic steroids or immunosuppressants who are not vaccinated).

·      Complications: hepatitis, pneumonia, superimposed cellulitis, meningitis and encephalitis

·      Pneumonia is more frequent complication in these at risk populations (especially pregnant patients) who develop varicella.

·      Severe complications of varicella pneumonia in pregnant patients: development of congenital varicella syndrome in the baby and, if the mother develops varicella rash right before or after delivery, risk for neonatal varicella.

·      When associated with pregnancy, varicella pneumonia is the leading cause of varicella-related illness and death in adults, with a reported maternal mortality rate of up to 44%.

·      Patients with severe varicella disease should be admitted and treated with intravenous acyclovir.

o   Special attention to airway monitoring

·      When do we give Varicella-zoster immune globulin (VZIG)?

o   VZIG is indicated for prophylaxis in susceptible pregnant women who have been exposed to the varicella-zoster virus.

o   The primary purpose of VZIG prophylaxis is to prevent or attenuate maternal disease.

·      PO acyclovir for those cases that are not severe and can be managed with close outpatient follow up




Peer IX

Uptodate: varicella: https://www.uptodate.com/contents/treatment-of-varicella-chickenpox-infection


POTD: Trauma Tuesday. Blunt Abdominal Trauma: What's the injury?

Let’s start with a case:

19 year-old Male presents after MVC as unrestrained driver in head on collision. He appears tachypneic and is noted to have decreased breath sounds on his left side. Just as the Trauma Team is prepping for a chest tube, POCUS shows +lung sliding at the apex and something that looks strange at the bases…

potd diaph.png

What does this patient have?

·      Diaphragmatic rupture with herniation of the abdominal contents into the thoracic cavity

·      Pathophysiology? Blunt trauma causes compression of the abdominal cavity and the pressure gradient between the thoracic and abdominal cavities

o   Previously thought to be more common on left side due to absence of liver

  • No longer true! more or less the same frequency

  • Right sided injury with greater mortality

    • d/t force required for injury is higher

    • more delay in diagnosis

o   Proceed cautiously if considering chest tube placement in these patients to avoid visceral injury from the chest tube

  • Keep in mind that ptx is more common

·      Can lead to respiratory distress and the degree of his respiratory distress is related:

  • o    size of the diaphragmatic tear

  • o   amount of abdominal viscera that is herniated

·      The mortality rate higher with blunt trauma than penetrating trauma because blunt diaphragmatic injury tends to lead to larger defects.

·      If the injury is large enough, it can be detected on cxr

·      CT scan can help identify these injuries when they are not visible on chest xray

·      Small injuries are notoriously very difficulty to detect

  • Patients can even present from weeks to months to years later with symptoms from a previously undiagnosed injury

·      Complications

o   tension gastrothorax, visceral ischemia, perforated viscus



ACEP Clinical Policy on acute blunt abdominal trauma


Peer IX

Cxr from: https://www.semanticscholar.org/paper/Blunt-diaphragmatic-rupture%3A-four-year%E2%80%99s-experience-Matsevych/35f84bfd12f4633dcb29539464a67e9cca51bd29/figure/3


POTD: Idiopathic Intracranial Hypertension

POTD: Idiopathic intracranial hypertension


Idiopathic intracranial hypertension (IIH) aka pseudotumor cerebri and benign intracranial hypertension

·      rare condition

·      presents with gradual onset and chronic headache, vision changes, nausea, vomiting, and tinnitus

·      + papilledema/ swelling of the optic disc on fundoscopy

potd eye papill.jpg

·      optic sonography

potd us eye.jpg
  • ONSDs should be measured 3 mm behind the papilla, an average of less than 5 mm is considered normal.

  • ONSD > 5 mm has been shown to be 90% sensitive and 85% specific for ICP > 20.

·      Classic presentation: young, obese female

·      + association has been found with this diagnosis and the use of oral contraceptive medications, tetracycline, anabolic steroids, and vitamin A

·      Pathophysiology is not well understood but thought to be caused by an imbalance in CSF production and reabsorption

·      Diagnostic criteria include an alert patient with either a normal neurologic examination or findings consistent with papilledema, visual field defect, or an enlarged blind spot

·      Definitive dx: Lumbar puncture

  • done in a recumbent position reveals an elevated CSF opening pressure of more than 20 mm Hg in an obese patient (normal being up less than 20 mm Hg).

  • normal CSF analysis.

·      CT head may show “slit like” or normal ventricles without mass effect

·      DDx: glaucoma, venous sinus thrombosis, ICH, IC mass.

·      Treatment

  • Repeat LPs  

  • Acetazolamide

  • Surgical shunt if severe and refractory

  • offending agents such as oral contraceptive medications should be discontinued.

·      Permanent loss of vision can occur in up to 10% of patients, and higher if left untreated




  • Dubourg J, Javouhey E, Geeraerts T, Messerer M, Kassai B. Ultrasonography of optic nerve sheath diameter for detection of raised intracranial pressure: a systematic review and meta-analysis. Intensive Care Med. 2011;37(7):1059-68. [pubmed]

  • Blaivas M, Theodoro D, Sierzenski PR. Elevated intracranial pressure detected by bedside emergency ultrasonography of the optic nerve sheath. Acad Emerg Med. 2003;10(4):376-81. [PDF]

  • https://www.ultrasoundoftheweek.com/uotw-5-answer/

  • Peer IX


POTD: TB in the ED

Approach to TB in the ED.

TB might be more common than you think: In NY alone, in 2016, 3.9 cases per 100,000 people, 761 cases in NY in 2016.

Reactivation TB is about 90% of active TB in the United States. 

Who is at high risk?

Those with no “usual source of care”

  • ethnic minorities

  • foreign born

  • HIV patient

  • drug users

  • nursing home patients

  • homeless patients

  • prisoners

Why is it often missed?

Non-specific presentation of TB

  • Cough present: 64%

  • Cough was chief complaint: 20%

  • Only 36% had respiratory complaint at triage

What to do if for high suspicion of TB:

  • Negative pressure isolation room

  • N95 fitted masks

  • CXR and rapid HIV

    • Why HIV test?

      • HIV increases risk of having reactivation TB

      • Immunosuppression will give you atypical cxr findings

  • Looking primarily for active tuberculosis 

Confirmatory testing:

  • PPD: Sensitivity 60-100%

  • QuantiFERON Gold: Sensitivity 81-96%

  • Sputum Looking for AFB on smear (Ziehl-Neelson stain)

    • Variable Sensitivity: 20-60%

    • High specificity: 90-100%

  • Culture

    • Slower results: 7days- 8 weeks

    • Gold standard: 99% sensitivity

  • Rapid TB testing/ Cepheid Xpert MTB/RIF PCR assay

    • Respiratory for assistance in collection

    • 5 ml specimen

    • Rifampin resistance detection

    • Supposed to be a 2 hr turnaround

    • 2 negative sputum specimens at least 8 hrs apart: can remove from isolation

    • Sensitivity about 75-93%

Screen Shot 2019-03-22 at 11.11.35 AM.png

*This is a sample rule out TB protocol that I adapted from Annals of Emergency Medicine October 2016 : http://www.annemergmed.com/article/S0196-0644(16)30920-9/fulltext

potd tb.png

POTD: Tongue Blade Test in Minor Mandibular Blunt Trauma

Minor trauma with mild swelling and want to avoid imaging the patient?

Tongue blade test:

How is it done? Have the patient attempt to "clamp down on” a tongue blade between the teeth with enough force that the examiner is unable to pull it out from the teeth.

When the examiner twists the blade, a patient should be able to generate enough force to break or crack the blade.

A positive test: if the patient cannot clench the tongue blade between the teeth or if the examiner cannot break the blade while it is held in the patient’s bite. If the test is positive, imaging is indicated.  

A negative test: If the blade can be gripped by the patient and be broken by the examiner, fracture of the mandible is much less likely, and additional imaging is likely not needed. In a prospective series of 110 patients with suspected mandible fracture, the test was found to be approximately 96% sensitive and 65% specific.

Who is not likely to benefit from this test? Major trauma that would indicate further imaging, signs of mandibular fracture such as: intraoral bleeding, tooth malocclusion, trismus, ecchymosis, and intraoral swelling.

Sources: https://www.aliem.com/2010/07/trick-of-trade-tongue-blade-is-as/

^ Check out this awesome aliem post and especially for the video demonstration

Alonso L, Purcell T. Accuracy of the tongue blade test in patients with suspected mandibular fracture. J Emerg Med. 1995;13(3):297-304. [PubMed]

Peer IX


POTD: Trauma Tuesday: Lateral Canthotomy

When to perform it?

·      To release orbital compression syndrome, most commonly due to retrobulbar hematoma.

·      IOP > 40, the pressure that indicated that you need to cut and release the compartment syndrome.

·      Without decompression, irreversible vision loss due to increasing orbital pressure may occur in as little as 90-120 minutes.

Clinical situation: trauma to the head/face.

Physical exam:



CT head and face


familiarize yourself with the anatomy

potd anatomy eye.png

Before starting, highly consider sedation.


1)    Generously inject 1% Lidocaine with epi to numb that lateral canthus to the orbital rim.

  • Do this by directing the needle away from the globe itself

  • Helps with bleeding and with pain.

2)    Using the needle driver as your hemostat, advance from the lateral canthus to outer orbit rim. Clamp down and hold for 1- 2 minutes.

3)    Using your small scissors, cut the lateral canthus to the orbital rim.

4)    Then cut inferiorly to cut the inferior crus of the lateral canthus (you may need to probe around to feel the structures)

5)    Repeat IOP. If the IOP is not immediately lower, then cut the superior crus of the lateral canthus and recheck pressure.


·      There is a lot of swelling. It can be hard to fit your hemostat in place and to feel your landmarks. Use you instruments to feel/probe around.

·      Also, do not worry about cutting too much. You are doing this to save this patient’s vision. After discussing this with optho, these are repaired quite easily days/weeks later. For example, Dr. Tome Levy performed this once on a patient that I later followed up with in split flow about 2 weeks later. There was no physical evidence on physical exam that this had ever happened. At first I thought I had the wrong patient in front of me… but the patient confirmed that a week and half ago he had in fact had the optho plastic surgery to repair it.  




This is an excellent emrap video that reviews the procedure: https://www.youtube.com/watch?v=tgQaKVGynFA


POTD: Ludwig’s Angina

History: Named after German physician, Wilhelm Frederick von Ludwig, who first described this condition in 1836.


•        Submandibular Space Cellulitis

•        Bilateral

•        Aggressive, fast spreading

•        70% of Ludwig’s angina is dental in origin

•        Real risk of airway compromise: This can result in rapid airway decompensation.

Physical Exam (useful things to document the presence of absence of in the chart):

•        Floor of the mouth: is described as: “woody,” which means firm, indurated, taut

•        Tongue: displaced superiorly and posteriorly

•        This result in: Slow suffocation, drooling, sniffing position, muffled voice, stridor

•        Labs

•        Vbg, cbc 7, blood cultures

•        Imaging

•        CT face and neck with IV contrast

•        Be very cautious if you are sending them to CT without airway secured

•        Consults

•        ENT, anesthesia



•        ABCs…A! Airway obstruction in 33%

•        sit upright

•        Secure/verify integrity of airway

•        Awake fiberoptic nasal intubation

•        Mentally prepare yourself for a surgical airway. This is the time to have the materials set up at the bedside.

•        Abx: polymicrobial

  • Oral anaerobes and aerobes

  • PCN G + flagyl

  • Unasyn

  • Clinda

  • Immunocompromised? Cefepime +flagyl

•        Steroids

  • Dexamethasone  8-12 mg IV

•        Dispo

  • ICU

  • 3-4 day process, gets worse before better


•        Mortality usually associated with airway compromise

•        with appropriate treatment, 8% mortality

•        Spread of infection: IJ thrombophlebitis, intracranial infection, mediastinitis


Brush up!

Brush up!

Sources: LIFL https://lifeinthefastlane.com/ccc/ludwigs-angina/

Uptodate Lugwig’s angina

Tintinelli’s Lugwig’s angina


POTD: Foreign Body of the Nose

potd nose pic.png

Foreign body of the Nose

•        Most common age range: 2-5 yo

•        Most common FB: beads, beans, peanuts, toy parts

•        Beware of: button batteries and two magnets, as always.

•        Can lead to septal perforation/necrosis of tissue.

•        Be suspicious of nasal FB when you see unilateral discharge, often malodorous

•        Complications: infection, aspiration, epistaxis


To remove:

•        Topical lidocaine or afrin?

  • Pro: improve tolerance of/cooperation with the procedure

  • Con: risks displacement of the FB


How to remove

1) Mechanical extraction: You need a cooperative child and good visualization.

2) Suction: must exercise extreme caution not to push further back and aspirated into the trachea

3) Positive Pressure: Parent’s kiss, bag mask, continuous pressure

  • Start by asking the child to blow their nose, occluding the unaffected nostril as they do this. Sometimes, this alone may expel the foreign body.

  • Parent’s Kiss: One of my preferred methods. Has a 50 % success rate.

Kissing parent: The technique is performed by a parent by placing their mouth over the child’s (giving a ‘big kiss’), while they occlude the unaffected nostril. The parent then exhales into the child’s mouth, generating positive pressure, similar to that of nose blowing. See picture below for demonstration.

Nothing working? You may need an ENT consult because the FB is so posterior that above methods are futile.

Now that it’s removed:

·       Don’t forget to inspect for trauma or retained FB


•        PEM playbook foreign bodies: excellent peds podcast by Dr. T Horeczko - ‎2015

•        Wiki EM: Nose foreign body

Look at this retro parent’s kiss!

Look at this retro parent’s kiss!


POTD: Foreign bodies, Ears!

potd kid ear.png

This is a two part series for POTD. Foreign bodies: Ears and Nose! Today, Ears!

potd anatomy ear.png

Quick Anatomy review to help locate that FB:

•        Anatomy

–       medial 2/3 is fixed in temporal bone –where many FBs are lodged and/or where trauma

•        Ask yourself: is it graspable or non-graspable?

–       Graspable: 64% success rate, 14% complication rate

–       Non-graspable: 45% success rate, 70% complication rate

•        What instrument/method should I use for what?

–       Alligator forceps: think something graspable like paper, foam

–       Suction tip: think something non graspable like a round object such as a bead

–       Irrigation: think something non graspable like a bead (note: do not irrigate organic material as will swell or break apart)

–       Glue: something non graspable like a bead or organic material that might swell or break if irrigated


Pearls on insect FB:

·       Kill it first. They will fight.

-        What to use? Lidocaine jelly, viscous lidocaine (2%), lidocaine solution, isopropyl alcohol, or mineral oil.

-        After they are dead, you can remove or can send to ENT for removal (most patients will want it out, can you blame them?)

o    An ENT friend of mine says to keep the insect in the ear and let them remove because we tend to cause trauma. Something to keep in mind.


What if I caused or the FB (like that insect fighting for their life) caused local trauma?

•        TM rupture?

–       Keep dry

•        When to use otic abx drops

–       Any trauma or dirty FB injury (think: that insect crawling around) or canal lacerations/abrasions.

–       What to give? Ofloxacin drops or the very expensive ciprodex.

•        ENT f/u



•        Inspect after removal

–       Something else in there? Abrasions/trauma and need prophylactic antibiotic ear drops

•        If at first you don’t succeed, try again. But consider changing the technique of removal. Remember the law of diminishing returns.



Pem playbook: excellent peds podcast by Dr.  T Horeczko - ‎2015

Wiki EM: Ear foreign body


POTD Trauma Tuesday: Name that fracture!

A 36-year-old man presents by ambulance following a motorcycle crash. He told the EMTs that he lost control and fell sideways, bracing his fall with his outstretched right hand. His R arm looks deformed but is neurovascularly intact. An xray is obtained.

xray potd.png

What’s the name of this one again?!

Galeazzi fracture! Named after an Italian surgeon from Milan.

What is it? a fracture-dislocation of the distal third of the radius associated with dislocation-subluxation of the distal radial ulnar joint, or DRUJ.

Why do we care? With Galeazzi fractures, there is a high risk of malunion, loss of function, infection, and chronic pain in adult patients. For this reason, surgical management with internal fixation and possible open reduction is required. The repair should occur promptly, so the emergency physician or another clinician should contact the orthopedic consultant emergently to coordinate care.

What about in peds? Emergent orthopedic consultation is still required but interestingly, in children, some Galeazzi fractures are treated conservatively with closed reduction by an orthopedic surgeon. Disruption of the DRUJ can be subtle, so a high suspicion should be maintained when a patient presents with a fracture of the distal third of the radius.

Pearls of the Peal:

* Look for fracture-dislocation of the distal radius and ulna after a fall onto an outstretched arm. This injury can’t be missed: it requires immediate orthopedic involvement.

* Skin tenting associated with the Galeazzi fracture-dislocation puts the patient at risk for skin necrosis and conversion to an open fracture.

Wasn’t there some way to remember this compared to other one?? Why, yes! See below:



Comic: Medcomic.com

Xray and clinical information: PEER IX


POTD: Straight leg test. A leg up on clinical testing!

A little background:

Lumbar disc herniation is the most common cause of lumbar radiculopathy, or sciatica, a shooting or burning pain from the low back radiating down the posterior leg distal to the knee.

Two tests used to evaluate these symptoms are

The straight leg raise.

·       The straight leg raise test is highly sensitive but not very specific for disc herniation.

·       This is performed by lifting the leg affected by the radiating pain.

·       The patient lies supine with one leg either straight or flexed at the knee with the sole of the foot flat on the stretcher.

·       The examiner then raises the affected leg up, extended, to 30 to 70 degrees.

·       Reproduction of low back pain that radiates down the posterior affected leg at least past the knee is considered a positive result. Not just pain to the lower back, which is a common misconception.

·       The SLR test can also be performed with the patient in a sitting position, by stretching the sciatic nerve by extending the knee; the test is positive if pain radiates to below the knee.


The crossed straight leg raise.

·       It is highly specific (90%) for disc herniation

·       You perform the same test as the straight leg but on the unaffected leg.

·       A positive test: reproducing both the back pain + the radiation down the affected leg.

Sources: Peer IX, Tintinelli’s, Dr. Sergey Motov, Uptodate


POTD: Young woman with upper abdominal pain clinical vignette

25-year-old woman presents with RUQ abdominal pain she has had for 1 week. She denies fever and vomiting. She also describes some vague pelvic pain for the past month. She is unsure if her vaginal discharge is abnormal. She thinks she was treated for an STI a few years ago, also unsure. No urinary symptoms.

Examination reveals tenderness to palpation in the right upper quadrant, negative murphy’s sign. You do a bedside u/s that does not show GS/cholecystitis. LFTs/lipase are nl. GI cocktail doesn’t help. Being a thorough emergency physician you decide to do a pelvic exam and find +purulent discharge with an erythematous cervix and mild cervical tenderness to palpation. No adnexal ttp b/l.

Dx? Management?

Fitz-Hugh-Curtis syndrome (FHCS).

FHCS is a relatively rare secondary infection of the perihepatic region following pelvic inflammatory disease (PID). Patients generally have mild to moderate PID findings on pelvic examination. Most infections are chlamydial; gonococci are another infectious etiology. Because the infection does not affect the liver or biliary system itself, liver function test results and ultrasound examination results are normal. Abdominal CT can be diagnostic for FHCS; perihepatic inflammation will be noted.

Outpatient treatment for Fitz-Hugh-Curtis syndrome is similar to that for PID: ceftriaxone, 250 mg IM once, and doxycycline, 100 mg PO twice daily for 14 days, with or without metronidazole, 500 mg PO twice daily for 14 days. Patients who are hemodynamically stable may be discharged home with OBGYN f/u.

Although this is a rare diagnosis just keep it in the back of your mind. Chlamydia and gonorrhea are often asymptomatic in women, undiagnosed and lead to infertility (vs men where they tend to have symptoms).  So if the clinical scenario fits, do the pelvic exam.

Sources: Peer IX, uptodate


POTD: Aorticenteric Fistula (AEF)

Aorticenteric Fistula (AEF):

There are two different types of AEF:

  • Primary: Occurs when a chronic, untreated aortic aneurysm damages or destroys the aortic and bowel tissue.

  • Secondary: Occurs due to inflammation of previous aortic graft surgery that is near a section of bowel. This type is much more common than primary AEF.

AEF must be considered in any patient with GI bleeding and history of abdominal aortic surgery. Although AEF is not the most common cause of GI bleeding in these patients, it is life threatening.

The most common location is along the third or fourth portion of the duodenum. A large abdominal aortic aneurysm can erode primarily into the duodenum at these locations, resulting in fistula formation.

Fun fact: Postoperative AEF is most often associated with a graft infection. 

Aortoenteric fistula can present with a sentinel or herald bleed that is minor, or with a sudden catastrophic bleed with hematemesis, melena, or hematochezia (so don’t rely on just upper or lower GI bleed).

If the patient is hemodynamically unstable, emergent laparotomy and blood transfusion are needed. If the patient’s condition is stable, upper GI endoscopy or CT angio of abdomen/pelvis (but you may just want to get the whole aorta). This is a good example of why it’s good to have both surgery and GI consults for your GI bleeds.

In a patient I had with this diagnosis, they had severe AKI he and we attempted to get a CTA but MRA was recommended/insisted by the radiologist (the patient was very stable). The radiologists were refusing to take this patient to CT due to the Cr. In the end, we learned that in order to get an accurate MRA, the patient needs to stay extremely still and pretty much not breath (…not practical). So after all the effort to get this patient to MRI, they ended up getting the CTA anyway, just hours later. Luckily this patient still did well but it was stressful sending them so far away to MRI land. Learn from my mistakes.

In the image below, this classic triad (GI bleed, abdominal pain and palpable mass) occurs in 6-12% of AEFs. Good for MCQs, bad for real life.


Text: peer review, https://www.uptodate.com/contents/aortoenteric-fistula-recognition-and-management

Photo: Rosh review

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