Ankle fractures

Ankle fractures:

Start with good H&P:


Mechanism, height of the fall, direction of the foot inversion

Consider age, steroid use, hx of neoplasm, prior surgeries, hardware



Start from the knee down, neurovascular intact, ROM, strength, severe tenderness, instability, rash/ulcers

Ottawa Ankle rules 


Classification of the injury: stable/unstable?

Many classifications are available but for ED we can use Closed Ring System: 


Think of an ankle as a ring of bone and ligaments surrounding the talus consisting of the tibia, the medial malleolus and medial deltoid ligaments, the fibula and lateral ligaments and calcaneus.


A single disruption in the ring - stability most likely preserved

Two disruptions - think instability and will likely cause the joint to shift.

Exceptions: Lateral malleolus fracture even with no medial injury may become unstable.

Isolated syndesmosis injury



Approach to ankle injuries x-ray interpretation

Here is an EM focused summary

Look at the cortical disruption of each bone

Look at the soft tissue swelling

Look at the spaces between the bones

Look within the bones

Ask for a mortise view (no, it’s not a GOT character) in addition to the standard AP and lateral views

Look at the tib/fib, knee and base of the 5th metatarsal

Key areas:

Talar shift: look to make sure there is congruence between the clear space on either side of the talus; go further - measure the medial clear space and the lateral clear space. If they are incongruent or the medial clear space is >4mm the ankle is likely unstable.

Talar tilt: The lines in red below should be parallel. Talar tilt indicates an unstable ankle 


Just a few commonly missed fractures at the ED:


High ankle sprain: The isolated syndesmosis injury - isolated distal tibiofibular syndesmosis injury, with ligamentous disruption can result in unstable ankle injury.

Look at the tibio-fibular clear-space: Measure the gap between the tibia and fibula 1cm proximal to the tibial plafond on both the AP view and mortise view. They should be <6mm. If  >6mm, suspect a syndesmosis injury.

Tillaux fracture - fracture is an intra-articular Salter-Harris class III fracture of the distal tibia with avulsion of the anterolateral tibial epiphysis.

Remember that in children, the ligaments tend to be stronger than the growth plate. Tillaux fractures can be considered “the syndesmosis injury of children

Snowboarder’s fracture - A snowboarder’s fracture is a lateral process of the talus fracture that is commonly misdiagnosed as a simple ankle sprain. 

Lateral process of the talus fracture also known as a snowboarder’s fracture



Bottom line: 

Reassess including the if the pt is still neurovascular intact

If pt can’t ambulate get further workup

If in doubt call radiology

Persistent pain but pt wants to go hoe, splint with ortho follow up



References: CoreEM, EMDoc, Uptodate, Radiopedia


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Acute respiratory distress syndrome (ARDS) 

acute inflammatory lung injury that causes non-cardiogenic pulmonary edema by increasing alveolar capillary permeability. 

The thickened diffusion barrier leads to hypoxemia via:

decreased lung compliance

inefficient gas exchange

Pulmonary hypertension

increased physiological dead space

Predisposing factors:

Direct lung injury: pneumonia, gastric aspiration, pulmonary contusion, near drowning, inhalation injury, transfusion-related acute lung injury

Indirect lung injury: sepsis, shock, acute pancreatitis, burns, crush injury, fat embolism, and massive transfusion

Diagnosis criteria for ARDS – Berlin definition (all 4 components must be present):

  1. Acute onset (1 week or less)

  2. Hypoxemia (PF ratio* < 200 mmHg with a minimum of 5 cmH2O PEEP (or CPAP))

  3. Pulmonary edema (bilateral opacities on CXR)

  4. Non-cardiogenic (not caused by cardiac failure)

*PF (PaO2/FiO2) ratio is the ratio of arterial oxygen partial pressure to fractional inspired oxygen. PaO2 value can be obtained from ABG, and FiO2 is 0.21 at sea level (room air) or depends on supplemental O2.


ARDS is a diagnosis of exclusion so consider first: 

Cardiogenic pulmonary edema, severe multilobar pneumonia, acute exacerbation of pulmonary fibrosis, diffuse alveolar hemorrhage, idiopathic acute eosinophilic pneumonia, dissemination of lymphoma/leukemia, and several others. 



Labs: CBC, BMP, LFTs, Coags, VBG followed by ABG, troponin, BNP, lipase, consider DD

Imaging: CXR, POCUS US ECHO and CHEST and consider CT



ED Management:

Supplemental O2

Treat the underlying condition (pneumonia, sepsis, etc.)

Tempered diuresis – non-cardiogenic pulmonary edema takes much longer to respond to treatment than cardiogenic CHF, so avoid being overly aggressive with diuresis, as this may worsen underlying shock and increase likelihood of multi-organ failure

Glucocorticoids — consider steroids when ARDS precipitated by a steroid-responsive process (eg, acute eosinophilic pneumonia)

Be cautious when using non-invasive positive pressure ventilation – the benefit of NIPPV in the initial management of ARDS remains controversial. 

Mostlikely patient will end up being intubated, for vent management suggested strategies are:

Use low tidal volume (6-8 mL/kg) to avoid barotrauma (ideal body weight should be calculated)

And careful FiO2:PEEP ratio titration:


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ARDS severity (mortality) predictor 

Mild ARDS – The PaO2/FiO2 is >200 mmHg, but ≤300 mmHg, on ventilator settings that include positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) ≥5 cm H2O


Moderate ARDS – The PaO2/FiO2 is >100 mmHg, but ≤200 mmHg, on ventilator settings that include PEEP ≥5 cm H2O

Severe ARDS – The PaO2/FiO2 is ≤100 mmHg on ventilator settings that include PEEP ≥5 cm H2O.

ST Elevation - Scary or Not?


EKG #1

36 year old, swole, healthy male, sharp diffuse anterior chest pain after pumping mad weights at the gym yesterday. He has a snake tattoo on his shoulder.
Like, what? Why?

  1. How would you describe this EKG over the phone to a consultant?

  2. What's the most likely EKG diagnosis? Anything else on your ddx?

  3. Name two EKG findings that support your diagnosis.

  4. Are you getting a troponin on this patient? If so, how many?

EKG #2

28 year old female, recent fever/cough, now with pleuritic/central/sharp chest pain. Kind of whiney. She’s on her phone.


1.     What’s the most likely diagnosis?

2.     Name two findings that support your diagnosis.

3.     Is this EKG different from the previous? If so, how?

EKG #3

46 year old male with chest pain


1.     What is the diagnosis? What about the EKG supports your diagnosis?

2.     Is this EKG different from the previous two? If so, how?


EKG #1

Benign Early Repolarization

·      BER is a super common EKG pattern, so be familiar!

·      Two main findings:

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o   Diffuse concave ST elevation, more-so in the precordial leads (usually < 2mm)

o   Elevation & notching at the J-point.

§  Notching best seen in V4 – may look slurred in other leads

·      Importantly, there are NO RECIPROCAL CHANGES

·      Be suspicious of this diagnosis in patients over 50yo, consider ischemia

·      With regards to the troponin, this is probably a style point, and I’m not sure there’s a right answer. Some attendings probably won’t get one. Most will just order one at the onset and call it a day. Some will argue that you can’t rule out ACS without serial troponins.

EKG #2


·      Like BER, pericarditis also has diffuse concave ST elevation!

So how do we distinguish between BER and pericarditis??

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EKG #3

Anterior STEMI

THIS IS AN IMPORTANT EKG. Our job isn’t to diagnose BER – it’s to see if our patient is having a heart attack.


Why is this an AMI and not benign early repolarization?

1.     ST segments are nearly linear and lack the obvious concavity of the other EKGs

2.     There is reciprocal change in lead III (look to inferior leads in anterior STEMI)

3.     Leads V2-V4 have scary (pathologic) Q waves

4.     There is poor R wave progression (there should be at least 3mm in V3 – here it’s 0mm)


Finally, for those of you who want to take it to the next level…


·      This is actually an anterior MI, which is super frightening.

·      It’s concave, there aren’t Q waves, there’s not reciprocal depressions (?III is inverted), though there is poor R wave progression and the T waves look big.

·      There is a crazy formula you can use to distinguish BER from an AMI.

 (1.062 x STE at 60 ms after the J-point in V3 in mm) + (0.052 x computerized QTc) - (0.151 x QRSV2) - (0.268 x R-wave Amplitude in V4 in mm)

·      >18.2 is likely an LAD occlusion.

·      More important than knowing this formula is knowing…

o   Just because you don’t see a STEMI doesn’t mean they’re not infarcting

o   If you’re suspicion is high enough, get a repeat EKG


Benign Early Repol -

Pericarditis -

Anterior STEMI vs BER -

Anterior STEMIs -


For a super crazy next level anterior STEMI lesson…




Approach to a pt with thrombocytopenia

Definition: definition of thrombocytopenia is a platelet count < 150 × 10E9/L



Often asymptomatic when first detected (significant or spontaneous bleeding rarely occurs with a platelet count > 50 × 10E9/L; 5-fold increase in risk <50 x 10E9/L)

Purpura, petechiae and bleeding from the gums and into the knee

Bleeding from venipuncture sites

Spontaneous intracerebral haemorrhage (<0.5% in ICU, higher risk if platelets <10 x 10E9/L)










Increased destruction

Immunologic: collagen vascular disease, infection, ITP, lymphoma/CLL, drugs (heparin, sulfonamides, aspirin, phenytoin, digoxin, vancomycin, B-lactam antibiotics)

Mechanical: TTP, HUS, DIC, chronic dialysis patient



Decreased production

Decreased megakaryocytes: drugs (EtOH, thiazide, chemo, linezolid), toxins, infection, leukemia

Splenic sequestration



Massive transfusion, ECMO, exchange transfusion


Suggested work-up:

Repeat platelet count – Ensure value is accurate

CBC – TTP-HUS presents with anemia AND thrombocytopenia. Abnormal platelets and abnormal WBC count is concerning for primary hematologic etiology.

Peripheral smear (call the lab and ask them to add a peripheral smear) – Look for schistocytes, and also for platelet clumping to rule out pseudothrombocytopenia. 

PT/PTT/INR/fibrinogen – These will be abnormal in DIC and unaffected in other etiologies.

Consult Heme/onc



Whom to consider admitting:

Severe thrombocytopenia (i.e. < 20)

Platelet count drop > 50% of baseline

Suspected leukemia, TTP-HUS, or DIC

Active bleeding


Diagnosis to consider:


Heparin-induced thrombocytopenia AND thrombosis

Use the 4T score: Timing (5-10 days after heparin exposure), degree of Thrombocytopenia (> 50% drop from baseline), no other clear etiology, and Thrombosis

If intermediate probability, send anti-platelet (PF4) antibody test

If high probability, start alternative anti-coagulation with argatroban (hepatically-cleared) or bivalirudin (renally-cleared)


Dx of exclusion

Acute => child, viral prodrome days-weeks prior, platelets <20, self-limited, supportive care unless active bleeding (steroids, IVIG, anti-Rh Ig)

Chronic => adult, no prodrome, gradual, platelets 30-100

Life-threatening bleeding: plt transfusions, steroids, IVIG



Usually idiopathic but can be 2/2 meds (clopidogrel, ticlopidine, quinine) or infection (E. coli)

Thrombocytopenia + microangiopathic hemolytic anemia (pentad of fever, anemia, thrombocytopenia, renal involvement, and neuro involvement)

Acute management is with plasmapheresis

If not available FFP and arrange for transfer. NO PLATELETS.



Look for high white counts, but sometimes can present with leukopenia

Patients should be started on all-trans retinoid acid (ATRA) as soon as the diagnosis is suspected

When to transfuse platelets: <10 or <50 + active bleeding or <50 + invasive procedure. Of note: transfused platelets last 3-5 days.



Pulmonary hypertension

Pulmonary Hypertension (PH): 

pulmonary hypertension news.jpg

Pulmonary hypertension (PH) is present when mean pulmonary artery pressure exceeds 25 mm Hg at rest or 30 mm Hg with exercise (Normal PA systolic pressures range from 10-30)

Definitive diagnosis via right heart catheterization, rare cause of SOB

In general, there is no cure besides supportive care and treating the precipitant, high rate of mortality


Pulmonary vasculature is meant to be a high-flow, low-resistance circuit.

Cardiac causes

LA or LV disease => ↑ LA pressure => ↑ pulmonary venous pressure => ↑ pulmonary artery pressure => ↑pulmonary vascular resistance

L to right shunt will also cause high pulmonary vascular pressure

Respiratory causes

hypoxic vasoconstriction -> PH

Which leads to => vasoconstriction => altered vascular endothelium and smooth muscle function

 => cellular remodelling => increased vascular contractility => lack of relaxation in response to various endogenous vasodilators => fibrosis of vascular tissue


Dyspnea (with rest or with exertion), Fatigue, Chest Pain, Syncope, Exertional lightheadedness

Patients with severe pulmonary HTN can develop signs of R heart failure (JVD, hepatomegaly, ascites, edema)


Five types of PH: 

Group 1: Pulmonary arterial HTN


Genetic/Heritable abnormalities

Drug/Toxin induced

Associated with known risk factors (HIV, liver disease, collagen vascular disorders)

Group 2: Pulmonary venous HTN (left heart disease)

Systolic or diastolic dysfunction

Mitral or aortic valve disease

Group 3: Chronic hypoxemic lung disease

Obstructive lung disorders (COPD)

Interstitial Lung Disease

Idiopathic Pulmonary Fibrosis

Sleep-Disordered breathing (OSA)

Group 4: Embolic disease (PE)

Group 5: Miscellaneous


The Workup


Most common abnormality is right axis deviation

Signs of R heart strain: S1Q3T3, right atrial enlargement in the inferior leads, incomplete/complete RBBB


CBC, CMP often nonspecific

BNP often elevated and correlates with outcomes

Elevations in troponin are associated with higher morbidity and mortality


Can demonstrate signs of RV failure – enlarged RA, RV, pulmonary arteries

Can demonstrate underlying etiology – hyperinflation, ILD, edema


Best initial diagnostic test

Apical four chamber helpful to evaluate size of RV relative to LV and assess for septal deviation

US not helpful in assessing volume status in these patients!



Start with ABC’s 

Give home medications

If known PH consult pulmonology early

Consider 3 Ps: Preload, Pump and Pipes

RV function determined by 3Ps: Preload, Pump, Pipes


Consider gentle hydration (250cc IVF) vs. gentle diuresis 


Cardiovert dysrhythmias as indicated

Consider inotropic support

Dobutamine 2-10 mcg/kg/min

Milrinone 50mcg/kg bolus -> 0.2-0.8mcg/kg/min (can cause hypotension)

Consider low dose norepinephrine (0.05–0.75mcg/kg/min) to maintain coronary artery perfusion

Pipes: (afterload)

Consider Pulmonary vasodilators

Prostanoids, endothelin receptor antagonists, and phosphodiesterase-5 (PDE-5) inhibitors

Prostanoids are treatment of choice

Epoprostenol is the only therapy proven to improve survival

inhaled nitric oxide 20-40ppm (good in bypass, doesn’t cause systemic hypotension as inactivated when bound to Hb)

Treat underlying etiologies

If need to provide respiratory support consider doing it in consultation with pt’s pulmonologist:

Always start with NRB before positive pressure ventilation (PPV)

PPV can cause rapid cardiovascular collapse due to increased Pulmonary Vascular Resistance and decreased preload

If you must intubate, have vasopressors at bedside: phenylepherine + NE + vasopressin are all OK

Low TV, low PEEP ventilation strategy

aggressively treat hypercarbia, acidosis, hypothermia (all increase PVR), which can increase pulmonary vascular resistance, pulmonary artery pressure, and RV strain


References: LITFL, EMDocs, UpToDate


systematic approach to reading CXR and hidden pneumonias

For this pearl of the day we will talk about systematic approach to reading CXR and hidden pneumonias:

The key is to be very systematic when approaching CXRs and that is what radiologists do each time.

Here is the suggested approach by the Brown EM program (

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When ready to review the x-ray, consider the commonly used “A, B, C, D, E, F” system.

A - Airway- trachea, carina, right and left main bronchi

B - Bones and soft tissue- clavicles, ribs- posterior and anterior, vertebral bodies, and sternum on lateral films. Look for any fractures, dislocations, or lytic lesions.

C - Cardiac- cardiac silhouette and mediastinum. The cardiac silhouette should be less than half of the thoracic cavity. AP films exaggerate heart size, so this rule does not apply. Assess the borders of the heart and the hilar structures

D - Diaphragm- right should be higher than left and you should see a gastric air bubble on the left. Is there any free air under the diaphragm? Evaluate the costophrenic angle and pleura (normally invisible due to thinness).

E - Everything else (lines and tubes, pacemakers, artificial valves)

F - Fields- FINALLY, evaluate the lung fields. Lungs are the area of greatest interest, so it is helpful to keep this at the end to prevent distraction. Divide each lung into three “zones” when reading a chest x-ray. These do not correlate with the lobes. Remember, there are 2 lobes on the left (upper and lower) and 3 on the right (upper, middle and lower). 

Hidden pneumonias:

Go through your ABCDEFs and look at the signs of hidden pneumonias:

Silhouette sign

The loss of the normal silhouette of a structure is called the silhouette sign.  - It enables us to find subtle pathology and to locate it within the chest.

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R middle lobe pneumonia


LLL pneumonia

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LLL pneumonia

Hidden areas

There are some areas that need special attention, because pathology in these areas can easily be overlooked:

apical zones

hilar zones

retrocardial zone

zone below the dome of diaphragm

These areas are also known as the hidden areas.

But in doubt get another view or a chest CT.


Looking at wellness: "Happiness and Resilience in the Life of an Emergency Physician"

Today’s POTD will be focused on wellness.

I will attempt to briefly summarize an amazing piece on “Happiness and Resilience in the Life of an Emergency Physician” from ACEP Wellness Guidebook. But more importantly the piece is written by our amazing and hardworking wellness advocate Dr. Arlene Chung in collaboration with Dr. Rosanna Sikora and Dr. Laura McPeake.

The first paragraph is talking about defining happiness and resilience. My favorite quote is “Engagement and meaning appear to be the strongest contributors to living a happy life” and that “You can strengthen happiness and resilience by practicing”. But at the end of the day it is very individualized and we, ourselves “ must choose what is most meaningful in our lives along the way to be happy”. 

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The part that I would like to draw your attention to are the suggested specific strategies by the authors that can help to build resilience in the practice of emergency medicine:

Writing a journal or recording oral narratives. 

Transforming your traumatic experiences into a written or recorded piece will not only help you to cope with difficult emotions but also put the situation in perspective and even learn from it. 

Meditation or mindfulness exercises. 

Mindfulness can be as simple as taking in a deep breath and exhaling very slowly, resulting in a parasympathetic charge of feeling peaceful and settled.

Peer mentoring.

Discussing stressful events with a supportive and empathic colleague is some of the best medicine that we have, and if our emergency medicine atypical humor is involved, all the better. Humor is a great coping strategy. 

Niche development. 

“Research has demonstrated that physicians who have developed a niche within emergency medicine have lower rates of burnout, better career longevity, and more career satisfaction.” This one is specifically very important for the senior class. Thinking about what can improve your clinical practice after graduation (and I am not only talking about fellowship) but rather looking into different areas of interest that can potentially become your niche.


I’ve heard teaching is rewarding and improves doctors satisfaction :)

Personal coaching. 

Develop a mission statement and a career plan and the examples that authors suggest: personal organization, time management courses, and learning to say “no” to obligations outside your mission statement.

Focus on empathy. 

Consider books, workshops, and podcasts. Connect with your family, friends, and co-workers outside of the fluorescent lights of the emergency department. 

Take care of your own needs. 

We need to take care of ourselves before we can care for others. Remember to MOVE your body: “A jog a day keeps depression away.” Make time for what you enjoy. Place it on your calendar and treat it like a shift.

Limit stressful downtime.

Balance your high-stress activities with low-stress activities. 

Please read the full article at ACEP emergency physician-focused wellness guide

Variceal Bleeding

Active Gastroesophageal Varices bleeding



Gastroesophageal varices bleeding is associated with a mortality rate approaching 20-30%.  

Bleeding from varices stops spontaneously only in 50% of patients



Prior complications, medications, fever, abdominal/chest pain, vomiting, melena, syncope/pre-syncope, hematemesis, cause of cirrhosis, prior interventions on varices, weights.


Evaluate hemodynamic status immediately (consider use of beta blockers). 

Look for signs of chronic liver disease – spider angiomata, palmar erythema, jaundice, ascites (shifting dullness, fluid wave, etc.), coagulopathy (petechiae, purpura), ENT exam (pharynx), CV, pulmonary, extremities, mental status.


ECG, CBC, coags, renal function, VBG/lactate, Ammonia level, electrolytes, LFTs, type and cross, fibrinogen, CXR and EKG 


First obtain bilateral IV access (large bore advised), monitors, supplemental oxygen. Wear personal protective equipment. 



This is one of the most difficult airways to management due to shock state, difficulty with visualization, rapid desaturation with sedative/paralytic, and extensive blood loss.

Use NG tube to decompress stomach (remove the ticking time bomb). 

May use metoclopramide 10 mg or erythromycin 250 mg IV to assist in moving blood through GI tract

Place in Trendelenberg if vomiting (keep blood out of lungs).

Bleeding and Circulation:

Hemostatic Resuscitation: Do not rely on PT/PTT/INR to assess coagulation status. Consider use of TEG instead. May need to start MTP

Consider pRBCs if Hb <7 g/dL (goal of Hb between ≥7 g/dL (70 g/L) and <9 g/dL). If pt received >6 units of pRBCs in <3 hours check serum ionized calcium concentration (due to citrate binding of ionized calcium) 

Platelets – if initial platelet count is < 50,000/microL 

Prohemostatic products – consider fresh frozen plasma, PCC on case by case basis, cryoprecipitate targeting fibrinogen 150-200 mg/dL. Consider to use TXA 1g IV. 

Target resuscitation end points of mentation, capillary refill, MAP, urine output. 

Source Control: Emergency GI and IR consults. 

May use erythromycin or metoclopramide to improve view for EGD. 

Use octreotide 50 mcg IV bolus, 50 mcg/hr IV infusion (or vasopressin with nitroglycerin), which is associated with decreased products transfused. 

Be ready with other devices: Sengstaken-Blakemore, Minnesota, Linton-Nachlas tubes.

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Prevent and Treat Complications

Infection associated with 25-65% of upper GI bleeds from varices (UTI, SBP, pneumonia):

Ceftriaxone 1 g IV or cefotaxime 2 g IV associated with NNT of 22 to prevent death and NNT of 4 to prevent infection. 

Albumin also useful in patients meeting certain criteria (Cr 1.5, BUN > 30, bilirubin > 4)

Consider NG tube placement for stomach decompression (Whether placement of a nasogastric tube can help prevent aspiration has not been well studied)

Beware of renal failure and encephalopathy, which are further complications.


References: EMCrit, EMDoc, UpToDate

ECG: What about U waves?

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What is the U wave? 

Small 0.5mm deflection following T wave: and best seen in V2 and V3 

Usually in the same direction as T wave 

Usually better visible at slow heart rates < 65 bpm

Grows bigger as HR decreases

Usually < ¼ of the T wave voltage, if much bigger (or >2mm)- its abnormal


Where is it coming from?

May be Purkinje fibers repolarization

May be some kind of after-potential

No one really knows


Abnormal U waves:

Prominent U wave - >1-2mm or 25% of the height of the T wave

Common causes: 


Severe hypokalemia.




Raised intracranial pressure

Left ventricular hypertrophy

Hypertrophic cardiomyopathy


Drugs associated with prominent U waves:


Phenothiazines (thioridazine)

Class Ia antiarrhythmics (quinidine, procainamide)

Class III antiarrhythmics (sotalol, amiodarone)





U waves associated with left ventricular hypertrophy


U waves associated with digoxin use

 Inverted U waves:

A negative U wave is highly specific for the presence of heart disease

Common causes of inverted U waves

Early MI

Coronary artery disease


Valvular heart disease

Congenital heart disease




Inverted U waves in a patient with NSTEMI 


References: UpToDate. LITFL,, ecg weekly





Thyroid storm

Thyroid Storm


mask thyroid.gif




Thyroid storm is a rare yet mortality rates reported between 10-30%

It is often presents in patients (pts) with established hyperthyroid disease (Graves' disease, toxic multinodular goiter, solitary toxic adenoma)


Precipitating Factors: Trauma, infection, DKA, CVA, PE, MI, etc.


Presentation and Diagnosis


Thyroid storm is a clinical diagnosis of a severe and exaggerated form of thyrotoxicosis.  

Look for a triad:

Extreme Fever (often >104F)

Tachycardia (can be accompanied with AFib, widened pulse pressure)

Altered Mental Status

Other findings:


Lid Lag

Proptosis/Periorbital Edema

Pretibial plaques/nodules/non-pitting edema

Goiter/Thyroid Nodules




low TSH and high free T4 and/or T3 concentrations

mild hyperglycemia, mild hypercalcemia, abnormal liver function tests, leukocytosis, or leukopenia





Supportive Care

Fever: Cooling measures and antipyretics. 

Agitation: Benzodiazepines 

Vascular instability: IV fluids


Beta Blockers:

β blockade is critical in the management of the peripheral actions of increased thyroid hormone.

Propranolol 0.5-1mg IV over 10 mins followed by redosing 1-3mg every few hours OR 60-80mg PO q4h

Alternative metoprolol, esmolol or atenolol 

Thionamides - Inhibit New Synthesis by blocking T4-to-T3 conversion

PTU for the acute treatment of life-threatening thyroid storm -

Propylthiouracil (PTU) 600-1000mg PO loading dose with 200-400mg PO q6-8h, Hepatotoxic

Methimazole for severe, but not life-threatening for a longer duration of action 

Methimazole 20-25mg PO q4-6h - longer half-life compared to PTU.

Iodines - blocks the release of pre-stored hormone, and decreases follicular transport and oxidation.

SSKI 5 drops PO q6h or Lugol’s Solution 4-8 drops PO q6-8h

Works through “Wolff-Chaikoff effect,” in which high levels of iodide will inhibit T3/T4 synthesis and release

Give AFTER antithyroid drugs, no sooner than 30-60 mins following PTU/Methimazole.

Lithium 300mg PO q6-8h - for iodine allergy or contraindication to iodine usage 


Other therapies to consider: 

Steroids (Inhibit Peripheral Conversion) Hydrocortisone 300mg IVx1 and then 100mg IV q8h or Dexamethasone 2-4mg IV q6h

Cholestyramine (4 g orally four times daily) - bile acid sequestrants to reduce enterohepatic circulation of thyroid hormone

Plasmapheresis: Offers temporary stabilization for a patient that has been unresponsive to antithyroid medications

References: EMDocs, UpToDate

Case of eclampsia in your resus bay


  • new-onset tonic-clonic, focal, or multifocal seizures in the absence of other causative conditions (eg, epilepsy, cerebral arterial ischemia and infarction, intracranial hemorrhage, drug use), 

  • typically but does not have to be present in the presence of preexisting hypertensive disorder of pregnancy (preeclampsia, gestational hypertension, HELLP syndrome)


  • Hypertension 

  • Headache (persistent frontal or occipital headaches or thunderclap headaches)

  • Visual disturbances (scotomata, loss of vision [cortical blindness], blurred vision, diplopia, visual field defects [eg, homonymous hemianopsia], photophobia)

  • Right upper quadrant or epigastric pain 

  • Asymptomatic 


  • Start with ABCs

  • Consider alternative causes of seizures based on additional information other than eclampsia: hyponatremia, ICH, hypoglycemia, etc.

  • Usually eclamptic seizures subside on its own

  • If pt is seizing => administer Mg Loading dose 4-6 g IV over 15 to 20 minutes. An alternative dose/route is magnesium sulfate 5 g intramuscularly into each buttock for a total of 10 g

  • Followed by Maintenance dose – magnesium sulfate 2 g/hour as a continuous IV infusion to women with good renal function.

  • If pt is in status => in cases refractory to magnesium sulfate (patient is still seizing at 20 minutes after the bolus or more than two recurrences), administer sodium amobarbital (250 mg IV over three minutes), thiopental, or phenytoin (1250 mg IV at a rate of 50 mg/minute). In this case pt will need to be intubated.

If need to consider intubation:

  • Medications:

    • Induction - consider propofol (category B)

      • You want to avoid: Etomidate - lowers seizure threshold and Ketamine - worsens HTN


    • Paralytics - rocuronium or succinylcholine, yet both of the medications are category C so use minimal dose to reach the desired effect, avoid additional doses

pregnancy medications.jpg

Next consider hypertensive control if BP diastolic pressures greater than 105 to 110 mmHg or systolic blood pressures ≥160 mmHg:

  • Labetalol - 20 mg IV gradually over 2 minutes.

  • Hydralazine - 5 mg IV gradually over 1 to 2 minutes.

  • Nifedipine immediate release - 10 mg orally.

  • Nicardipine (parenteral) - The initial dose is 5 mg/hour intravenously by infusion pump and can be increased to a maximum of 15 mg/hour.

Proceed with labs, consider HELLP syndrome labs, type and screen, fluids. 

Call OB/GYN early

The definitive treatment for eclampsia is prompt delivery.  

5th metatarsal fracture


Normal Apophysis in children runs parallel to the bone.  

Dancer’s or Avulsion (pseudo-Jones) Fracture @ cuboid articulation - hard sole shoe for 4-6 weeks and weight bearing as tolerated (WBAT) with orthopedics follow up in a week

Jones Fracture @ intermetatarsal articulation - high risk of non union, pt will need a splint and non weigth bearing activity (NWB) for 6-8 weeks with orthopedics follow up

Metatarsal shaft fracture - high risk of non union, will need a splint, NWB for 10-20 weeks, with orthopedics follow up

Below is a 5 minute video by amazing Dr. Anna Pickens (former Maimo attending) for visual review of the fractures:

What kind of mood elevator are you on?


Lithium toxicity



Uses: Lithium often prescribed for Bipolar disorder

Has a narrow therapeutic index: therapeutic dose close to a toxic dose

Mechanism of action is still incompletely understood. Lithium increases serotonin release and receptor sensitivity as well as inhibiting release of dopamine and norepinephrine. 

Elimination: Lithium is excreted exclusively by the kidneys. Any insult to kidneys can lead to impaired elimination 



For acute overdose mainly intentional overdose

For chronic Li+ toxicity with present body stores any changes changes in absorption or elimination lead to lithium levels above the narrow therapeutic window like:

  • volume depletion

  • salt restriction

  • advanced age with resultant decrease in GFR, 

  • thiazide diuretics, NSAIDs, ACE inhibitors

  • heart failure



Workup at the ED:

  • Basic labs: CBC, BMP

  • Lithium level

  • Urinalysis

  • thyroid function panel 

  • Co-ingestants: acetaminophen, salicylates if intentional overdose is suspected 


Acute Lithium Toxicity presentation:

  • GI symptoms such as nausea, vomiting, and diarrhea, at times with significant volume loss. 

  • Dry mouth 

  • Lack of coordination

  • systemic and neurologic findings manifest late in acute lithium toxicity because  it takes time for lithium to distribute into tissues and the CNS


Chronic Lithium Toxicity presentation:

  • Potent neurotoxin,altered mental status, seizures, tremor, hyper-reflexia, clonus, fasciculations, and extra-pyramidal symptoms which can persist for month regardless of serum concentration 

  • serotonin syndrome, as well as neuroleptic malignant syndrome. 

  • nephrogenic diabetes insipidus (creates resistance to vasopressin)

  • abnormal ECG findings, including QT prolongation, T-wave inversions across the precordial leads, sinoatrial dysfunction, bradycardia, complete heart block, or unmasking of a Brugada pattern. 

  • Hypothyroidism 

  • hyperthyroidism and thyrotoxicosis

  • hyperparathyroidism and hypercalcemia


Treatment and Disposicion:

  • Supportive care and fluids at the ED

  • Consult Poison control center 

  • Renal service, for hemodialysis in severe intoxications

  • Psychiatric service, for patients with intentional overdose

  • Pt will most likely require admission for monitoring of electrolytes and renal function, hydration, medication adjustment





Epistaxis is one of the most commonly encountered ENT emergencies in the US

Main causes: 

Local: Epistaxis digitorum (nose picking), Foreign bodies, Intranasal neoplasm/polyp, Irritants (e.g., cigarette smoke), Medications (e.g., topical steroids), Rhinitis, Septal deviation/perforation, Trauma, Vascular malformations/telangiectasias

Systemic: Hemophilia, Leukemia, Medications , Conditions causing platelet dysfunction , Thrombocytopenia


The vascular supply - from branches of the internal carotid arteries and  branches of the external carotid arteries

The anterior portion of the nasal septum - Kiesselbach’s plexus - majority of epistaxis 

Posterior epistaxis - mainly sphenopalatine artery and terminal branches of the maxillary artery



Where do you start with nosebleeders?


  • The usual: ABCs? Is your pt tolerating his/her secretions? Vitals? => Have the pt lean forward applying direct pressure on bilateral nares for at least 10 min, now we can ask some questions.


  • Onset, duration, and laterality of the current bleed?

  • Frequency, associated factors?

  • Review of systems: skin rashes (petechiae/pupura), easy bruising

  • Previous medical history: hepatic disease (cirrhosis), renal disease (uremia), nasopharyngeal carcinoma 

  • Social history: smoking (irritant), recreational drug use (specifically cocaine and other inhalants)

  • Medication review: NSAIDs, aspirin, ADP receptor blockers, anticoagulants

  • Family history: coagulation disorders


Management: the bleeding does not stop after direct pressure. What’s next?

  • => have the pt blow her nose to get rid of the clotts, examine the nares, look at the posterior oropharynx, if seems like an anterior nosebleed use topical vasoconstrictors (oxymetazoline and LET), cocaine and topical hemostatics like TXA soaked pledget 

  • => if patient continues to bleed, look for the source and attempt to cauterize chemically with silver nitrate or electrically.  Although that may not work on active bleeding

  • => if that did not work next step is nasal packing with nasal tampons, Rhino Rocket or balloon devices


Nasal tampon:


 Rhino Rocket:

What if the bleeding doesn’t stop?

It's most likely a posterior bleed and now you should be sweating…

  • Call ENT/OMFS/IR/in some places Surgery

  • Get labs

  • Consider Posterior nose packing: foley that should be available at every institution or specialized devises like Storz.

  • Consider antibiotics Antibiotics:

First Line: PO cephalexin 250–500 mg QID or PO amoxicillin/clavulanate 250–500 mg TID

Second line: PO clindamycin 150–300 mg QID or PO trimethoprim/sulfamethoxazole DS

Therapy should be continued for 7-10 days.

 Foley Catheter in Posterior Epistaxis




The Emergency Department Management of Posterior Epistaxis

EMCrit C3 Epistaxis


POTD: "Push-pull" boluses - keep them sterile!

 ·   · 

How do I appropriately use the push-pull technique to deliver a bolus to a pediatric patient?

Push-pull Technique

push pull technique.png
  1. Hook up 3 way stopcock to IV tubing and attach syringe to 3rd port.

  2. Turn off to patient, draw fluid from bag.

  3. Turn off to bag, push bolus into patient with steady pressure.

  4. Repeat 2-3 until full amount of bolus given.


  • To deliver adequate fluid resuscitation in a timely fashion to pediatric patients (superior to gravity)

  • Similar flow rates as pressure bag, but with higher accuracy of volume

  • For difficult IVs, you are able to feel resistance when giving the bolus and recognize a blown vein earlier

Contamination Concern!?

  • A study showed that with repeated use, the contents inside the syringe may become contaminated (see fluorescein study below)

  • Gross!!! This implies we may unwittingly introduce bacteria into systemic circulation....

Tips for Improvement

  • Use syringe that is larger than the amount of the individual pushes (e.g. use a 60ml syringe to give 30ml at a time or a 20ml syringe to give 10ml at a time)

  • Consider wearing sterile gloves and maintain aseptic technique

  • Avoid touching the "ribs" (see below)


Trauma Tuesday POTD: Shock

 ·   · 

How do I recognize shock in a trauma patient? 

We learn that shock in a trauma patient is usually hemorrhagic shock

Vitals are vital! 

Here's a chart from LITFL that goes through the different stages of hemorrhagic shock: 


The take away is that the patient can be in stage 1 hemorrhagic shock with normal vitals. Early signs are: 

  1. Widened pulse pressure (difference between systolic and diastolic)

  2. Cool extremities/pale skin

  3. Mild anxiety (but which patient isn't anxious coming into the trauma bay?)

Patients don't read textbooks

The stages are useful to conceptualize, but there are several reasons a patient's  response may vary from the chart above: 

  • Elderly patients have a blunted response

  • Pediatric patients are able to compensate well

  • Medications (e.g. beta blockers and other antihypertensives) or intoxication

  • Extreme pain or anxiety

  • Comorbidities

  • Blunt vs penetrating trauma can have different physiologic responses

Bradycardia is possible with hemorrhagic shock

  • Several theories exist as to why this happens (vagal stimulation, sympathetic response, post catecholamine surge...)

  • Seen more with acute, severe blood loss

  • Up to 1/3 of patients with hemorrhagic shock may be bradycardic

Give blood early!


POTD: Heatstroke Cooling in High Humidity

 ·   · 

How do I cool my patient with heatstroke?


  • AMS

  • Core body temp > 40.5 C (105 F)

  • Exposure to high temperatures or exercise

Cooling down their core temperature ASAP provides mortality and morbidity benefit

  • Delayed treatment can have a mortality as high as 70%!

We learn that evaporative cooling is the best method 
(spraying tepid water and cooling with fans). 

HOWEVER, when humidity is high this may not work! 

  • Because sweat on the skin cannot evaporate into the surrounding air and body temperature cooling fails.

  • This occurs in some studies at humidity levels >50-55%

So what else can you do?

Ice Bath

  • Practically speaking, place the patient in a body bag up to their neck and add ice and water.

If an ice bath isn't possible, apply ice packs to neck, armpits, and groin. 

Stay cool!


Wellness POTD: Sleep

 ·   · 

Importance of sleep:

  • Helps with memory consolidation and improving retention of new knowledge

  • Increases metabolism

  • Improves mood

  • Improves cardiovascular health

  • Boosts immune system

Effects of sleep restriction:

  • First thing to go is compassion and empathy, NOT medical judgment

  • Increased cortisol levels

  • Increased insulin resistance

  • Increased hunger

  • Irritability

  • Testosterone levels drop

  • Reaction times diminished

  • Driving while sleep deprived can be similar to driving while intoxicated

Sleep hygiene tips

  1. Make a bed time routine

  2. Avoid screen time (TV, phone, computer) before sleep

  3. If you must have screen time before bed, use a computer app that decreased blue light when its dark out (I like Flux)

  4. Use your bed only for sleeping

  5. Avoid caffeinated drinks a few hours before bed

  6. Exercise regularly


POTD: Neonatal Procalcitonin

 ·   · 
  • Neonates will have physiologically elevated procalcitonin.

  • Normalizes around 3 days.

procalcitonin neonates.jpg
  • Studies show that procalcitonin is useful in detecting/managing sepsis in neonates.

    • Neonates who have procalcitonin trended seem have shorter duration of antibiotic therapy.


  • Chiesa C, Panero A, Rossi N, Stegagno M, DeGiusti M, Osborn JF, Pacifico L: Reliability of Procalcitonin concentrations for the diagnosis of sepsis in critically ill neonates. Clin Infect Dis. 1998, 26: 664-672. 10.1086/514576.

  • Stocker, M., Hop, W. C., & van Rossum, A. M. (2010). Neonatal Procalcitonin Intervention Study (NeoPInS): Effect of Procalcitonin-guided decision making on Duration of antibiotic Therapy in suspected neonatal early-onset Sepsis: A multi-centre randomized superiority and non-inferiority Intervention Study. BMC Pediatrics, 10(1).doi:10.1186/1471-2431-10-89



POTD: Treat methotrexate neurotoxicity with cough syrup!

 ·   · 

How do I treat methotrexate neurotoxicity?

(Yes it's a thing) 

Case from today 

12yo M w/ ALL on methotrexate therapy presents with 1 day of worsening R facial droop and R sided weakness. MRI showed non-enhancing, hyperintense signal on T2 and flair consistent with MTX leukoencephalopathy.


  • Folic acid antagonist

  • Used as chemotherapeutic agent or DMARD

  • May be given orally, IV, or intrathecally


  • Can occur anytime after methotrexate use (hours to days to weeks)

  • Symptoms include seizure or stroke-like signs: hemiparesis, hemisensory deficits, aphasia, dysarthria, diplopia, dysphagia

Proposed Mechanism

  1. Methotrexate interferes with metabolism of homocysteine

  2. Homocysteine levels rise in blood and CSF

  3. Downstream effect is NMDA receptor agonism as well as neurotoxicity


Treatment: Dextromethorphan

  • Theoretically, NMDA inhibitor could counteract these effects...

  • Dextromethorphan is a noncompetitive NMDA receptor antagonist.

  • Case series show improvement and even resolution of symptoms after administration of dextromethorphan.

  • Symptoms may resolve in minutes, but on average took half a day. Some patients still had neuro symptoms months later.


  • Afshar, M., Birnbaum, D., & Golden, C. (2014). Review of Dextromethorphan Administration in 18 Patients With Subacute Methotrexate Central Nervous System Toxicity. Pediatric Neurology, 50(6), 625–629. doi:10.1016/j.pediatrneurol.2014.01.048

  • Drachtman, R. A., Cole, P. D., Golden, C. B., James, S. J., Melnyk, S., Aisner, J., & Kamen, B. A. (2002). DEXTROMETHORPHAN IS EFFECTIVE IN THE TREATMENT OF SUBACUTE METHOTREXATE NEUROTOXICITY. Pediatric Hematology and Oncology, 19(5), 319–327. doi:10.1080/08880010290057336

  • Radiopedia: Methotrexate-related leukoencephalopathy <>