Resiliency is the human character trait to suffer an insult and return to a state of dis-despair, to return to one’s homeostatic equilibrium. In life we all will encounter problems, errors, disasters. How we deal with it, is how we come to be resilient.

As physicians, we must take our own advice and practice what may seem the least glamorous part of medicine: preventative care. One way in which we can do this is by taking advice from improvisational comedy. The concept of “Yes, and…” is practiced by an comedian agreeing with another’s statement and then furthering the point along a similar train of thought. In a way, employing it is to accept what’s been presented, foster an armistice with it, and from it create something more. Forge a new solution together. See more in this article, or listen to drunkroomates. Conflict resolution is easy when both parties cooperate as opposed to compete.

One tactic you can employ when another person is competing, and aggressively, is to react with non-complementary behavior. When you walk into the room and someone is already yelling at you, the usual response is to react in kind; you yell back. They expect this, but if you were to act in a different behavior, discordant with their disruptive flow, and more akin to how you would want the conversation to go, namely pleasantly, they may also respond in kind. Listen here on NPR.

And when we finally suffer the pangs of life, we must cope. As students, we memorize the mature and immature and we ought to apply them to ourselves. Mature coping mechanisms consist of sublimation, altruism, humor, suppression. In all of these, you focus your negative emotions around a stressor into something more productive: athletics or a hobby, a park cleanup or good deed for your neighbor, a joke, or into the nothingness that they are worth to you. Read on with the positive psychology program.

Coping immaturely will likely cause more problems then cures. Withdrawal, avoidance, isolation, acting out, passive aggression. We all commit these sins. As bad habits, out of necessity, as rationalizations for our selfish well-being – they are the easiest way out. Knowing what these are and recognizing when commit them is the goal of introspection and self-awareness. Through this, we can fulfill the Kantian moral duty of self-improvement.

Finally, tell your story. Verbalize it, make it tangible, impart it to a listener. Experience another’s empathy and allow yourself to be nurtured. Be grateful for them. Then be grateful for yourself for having the courage to be vulnerable.

Pediatric Pearl – Anaphylaxis


By: Hima Khamar, PGY3

4-year-old female presents to ED with parents due to 1 week of cough, fever, congestion, irritability, and decreased PO intake. CXR shows RLL pneumonia, patient is started on Ceftriaxone. 5 mins after the initiation of Ceftriaxone infusion, patient begins to complain of itchy scalp, starts coughing uncontrollably (much worse than throughout her entire ED stay), and some urticaria is noted on her abdomen. Per mom, patient has never been on antibiotics, but has allergies to many fruits and foods. THIS WAS A REAL PATIENT OF MINE*


-Correctly identify and diagnose anaphylaxis
-Don’t be afraid to give epinephrine and give it in a timely manner
-Monitor frequently and if not improving, don’t be afraid to take the airway
-Provide epinephrine auto-injector to go home with, if stable for discharge
-Give parents and patient (if old enough) education of anaphylaxis and how to use autoinjector


-What are the manifestations
-What time did attack(s) start
-How long did episode(s) last
-Treatments administered
-Potential causes
-Previous attacks, including severity
-Atopic status, particularly presence of asthma

-Vital Signs
-Skin: Hives, pruritis, or flushing
-Edema: Mucosal tissue, lips, tongue, uvula
-Airway: Stridor, hoarseness, cough, trouble swallowing
-Breathing: Cough, dyspnea, wheezing, retractions, hypoxemia
-Circulation: Hypotension, tachycardia, delayed capillary refill, poor perfusion
-Neurologic: Change in mental status, syncope, sense of impending doom
-Gastrointestinal: Persistent vomiting, abdominal pain, diarrhea

Anaphylaxis Criteria

Criteria 1:

  • Acute onset of an illness with involvement of the skin, mucosal tissue, or both (e.g., generalized hives, pruritis or flushing, swollen lip-tongue-uvula)
    • Respiratory compromise, Reduced BP or associated symptoms of end-organ dysfunction, Persistent GI Symptoms, Significant abdominal pain and/or significant vomiting

Criteria 2:

  • Two or more of the following that occur rapidly after exposure to a LIKELY ALLERGEN
    • Involvement of the skin-mucosal tissue, Respiratory compromise, Reduced BP or associated symptoms, Persistent gastrointestinal symptoms

Criteria 3:

  • Reduced BP after exposure to KNOWN ALLERGEN

Anaphylaxis Caveats

  • While the majority of anaphylaxis cases involve skin symptoms, 10% of patients do not have hives or other skin manifestations; these patients often have the most severe symptoms.
  • Isolated skin findings alone (generalized hives) should not automatically be defined as anaphylaxis.
  • In a patient with exposure to a known allergen that has previously caused anaphylaxis that presented with hives alone, threshold should be low for the diagnosis of anaphylaxis.
  • The above signs/symptoms obviously can be due to non-allergic causes.
  • The absence of exposure to a known allergen should never preclude the diagnosis of anaphylaxis.
  • Patients on beta blockers should get glucagon if the first dose of epinephrine is ineffective.


(Very important in helping diagnose, so here is a quick review)

New born 30-50 120-160 50-70 30-60 2-3
Infant (<1 yr) 20-30 80-140 70-100 53-66 4-10
Toddler (1-3) 20-30 80-130 80-110 53-66 10-14
Preschooler (3-5) 20-30 80-120 80-110 55-69 14-18
School Age (6-12) 20-30 70-110 80-120 57-71 20-42
Adolescent (>13) 12-20 55-105 110-120 66-80 >50

*Every degree Celsius rise in temperature should show a 10% rise in HR



  • <5 kg – 5mg/hr cont
  • 5-10 kg – 5mg/hr cont
  • 10-20 kg – 25mg/hr cont
  • >20 kg – 15mg/hr cont


  • Methyprednisolone IV 2mg/kg (max 60mg)
  • Prednisone PO 2mg/kg (max 60mg)
  • Dexamethasone PO 0.3-0.6mg/kg (max 12mg)

Racemic Epi (stridor)

  • <5 kg: 25 mL
  • 5-10 kg: 5 mL


  • Diphenhydramine IV/PO 1mg/kg (max 50mg)
  • Ranitidine IV 1mg/kg (max 50mg) or PO 4mg/kg (max 150mg)
  • Cetirizine PO <24mths 2.5mg/day, 2-5yrs 2.5-5mg/day, >6yrs 5-10mg/day


  • Epinephrine 01-0.1 mcg/kg/min

Glucagon (if on beta blockers) à 20-30 mcg/kg (max 1mg) over 5 mins

Anaphylaxis Red Flags

-History of biphasic or severe reactions
-Progression of / or persistent symptoms
-History of severe asthma
-1 ICU admission and/or 3 in-pt admissions/year
-Current asthma flare
-Hypotension during ED stay
-Requires >1 Epinephrine dose
-Requires fluid bolus
-Upper airway obstruction i.e. stridor

Discharge Criteria

  • Complete clinical resolution of all serious symptoms (rash may persist)
  • If epinephrine was administered, observe 4 hours from time of epinephrine administration
  • Parental comfort with discharge with good access to ED if symptoms recur
  • Epinephrine auto-injector physically available to family
  • Counseling regarding allergen avoidance
  • Allergist referral

Case of the Week COW #21

Resident: Yenisleidy Paez Perez 

CC:“I”m bringing in my son. He has been having tooth pain since last night, and I gave him Tylenol but then he seemed to pass out and had white stuff at the mouth and his face and hands look blue”

HPI: 5-year-old male presents to ED brought by his mother today after she noticed his mouth, legs, arms, and legs started turning blue. Patient was brought immediately after mother noticed the symptoms. Prior to arrival, patient was given Tylenol which mom bought a local store for a toothache he’s been having for the past few days. Patient has appointment with the dentist tomorrow. Patient’s mother denies any change in behavior, HA, dizziness, or syncope episode. Denies fever, chills, recent illnesses, nausea, vomiting, diarrhea, generalized weakness, or lethargy, abdominal pain, limitations in his activities, difficulty breathing, cough or URI symptoms. Upon arrival, patient is hypoxic, saturating 77% on room air. Despite this, pt denies SOB or Chest pain.

Physical Exam:
T: 35.6 °C (Tympanic) HR: 126 (Monitored) RR: 14 BP: 102/73 SpO2: 82% (on Non-rebreathing Mask) WT: 18.60 kg

Constitutional: Awake, alert, comfortable but irritable, crying but consolable by the mother. Head: Normocephalic, atraumatic


ENT: External ears are unremarkable. B/L external auditory canals are normal and clear, no cerumen impaction, non-erythematous. B/L TMs are normal, nonerythematous, no bulging or dullness or effusion. Posterior pharynx is grossly normal, non-erythematous, no tonsilar enlargement, or exudates. Multiple dental cavities with mild tenderness on palpation of right lower jaw.

Neck: Supple, full range of motion, no mass Chest: Normal appearance and motion, no deformity or crepitus.

Cardiovascular: Tachycardia. Rhythm is regular. Normal S1 and S2, No gallops, murmurs, or rubs., symmetric pulses bilaterally

Respiratory: Normal chest rise and fall, no respiratory distress or stridor despite hypoxia and cyanosis, equal breath sounds bilaterally, clear to auscultation bilaterally, no wheezing, rales or rhonchi. No stridor.

Abdomen/GI: Soft, non-tender, no rebound tenderness or guarding, nondistended, no organomegaly

Neuro: Alert and oriented, Mentation is appropriate for age, moves all fours, good tone. GCS 15. 5/5 strength in all extremities. Sensory intact

MS/extremity: ROM intact in all extremities. Pulses equal. Neurovascularly intact.

Skin: Acrocyanosis and periorbital cyanosis noted, no rashes, no erythema,

Laboratory Data:
Blood work was drawn and the blood was noticed to be chocolate brown

CMP: Na: 137    K+: 3.9    Cl: 104    CO: 21    BUN: 12    Cr: 48    Glucose: 116 Alk Phos: 279    AST: 25    ALT: 9

CBC: WBC: 8.4    Hg: 12.7    Hct: 38.1    Platelet: 312    PT: 13. 7    INR: 1    PTT: 32.6

D-dimer: 0.43      Troponin: < 0.010      VBG & MetHb: Pending!


Pertinent Images/EKG:
EKG: Sinus Tachycardia at 126 bpms. Normal PR- Interval and QRS- interval. No T waves changes.
Chest X ray: Normal chest X-ray, NO cardiomegaly, NO increased interstitial lung markings , no consolidation, no PTX.

Working Diagnosis at time of Disposition: Methemoglobinemia , CO Poisoning  and Anemia


VGB (Mixed Venous Gas) pH: 7.39   pCO2: 36   pO2: 265   HCO3: 21.8   Lactate 2.6   COHb: 0.2   MetHb: 30

5-year-old male presented to the ED with hypoxia, saturating 77% on room air. His saturations went up only to 85% – 87% while on a non-rebreather mask.. No evidence of anaphylaxis, no wheezing, rales or decreased breath sounds on exam. No rashes, no vomiting or abdominal pain. Chest x-ray did not reveal cardiomegaly or pulmonary infiltrate or pneumothorax. Blood work was drawn as well as Met hemoglobin levels, VBG and carboxyhemoglobin levels were obtained. Met hemoglobin level return at greater than 30%.

This is a case of methemoglobinemia, which was treated with Methylene blue (2mK/kg over 15 minutes). After it was administered, patient’s saturation increased to 97% while on non-rebreather mask.

On further questioning, patient’s mother asked the grandfather who had been taking care of him if he had given him any new medications. He admitted to administering Oragel to the patient’s teeth multiple times per day for the past couple of days.

In ED patient was given: methylene blue: 37 mg (2mg/kg over 15min) (02/24/19 12:02:00 EST) Sodium Chloride 0.9%: 372 mL (02/24/19 11:27:00 EST)

Hospital Course: ABG was repeated and MethB had normalized. Patient did not have return of cyanosis and never experience respiratory distress during his hospital stay. OMFS was also consulted for his toothache and patient started on IV Unasyn for right buccal swelling, which was fluctuant, erythematous and tender with palpation. He underwent drainage of dental abscess and tooth removal. He was transitioned Amoxicillin PO for 1 week, and discharged the next day

WHAT IS IN ORAGEL? 20% Benzocaine!

Pearls & Take Away: Methemoglobinemia!


  • Definition: An abnormal elevation of Methemoglobin, which refers to, the ferric form of hemoglobin (Fe+3) that is unableto bind to O2.
  • An abnormal MetHb level is any level > 1%
  • Suspect in any patient with cyanosis not responsive to supplemental oxygen!!!
  • Pulse Oximetry readings are inaccurate in the presence of MetHb


  • Oxidized Fe+3 sites on MtHb are unable to bind to oxygen
  • This results in a leftward shift in the oxyhemoglobin dissociate curve which leads to decreased oxygen delivery
  • Methemoglobinemia occurs when there is a deficiency of the reducing enzyme (NADH MetHb reducatase) OR when there is increased oxidative stress to the body


  1. NADH reductase deficiency – unable to reduce ferric to ferrous iron (Fe3+→ Fe2+)
  2. Exposure to oxidizing agent
  3. Benzocaine and other local anesthetics
  4. Contaminated well water
  5. Nitrofurantoin, Nitroprusside
  6. Sodium Nitrite, Amyl nitrite
  7. Antimalarials: Quinolones
  8. Dapsone (used to treat leprosy, PCP pneumonia, toxoplasmosis, dermatitis herpetiformis, brown recluse bite)
  9. Aniline dyes
  10. Phenazopyridine[3]


  • Patients with anemia or preexisting cardiopulmonary disease will show symptoms sooner (i.e. CHF, Pneumonia, COPD, anemia, etc)
  • Important diagnosis feature (Saturation < 85% without response to 100% FiO2)
  • Wavelength averaging by the pulse oximeter causes a falsely low O2 reading
  • Symptoms depend on level of metHb:
  • < 20%:Asymptomatic or very mild symptoms; gray-blue cyanosis, chocolate brown colored blood
  • 20-50%:Anxiety, HA, weakness, lightheadedness, tachycardia, dyspnea, dizziness, syncope
  • 50-60%:Myocardial ischemia, dysrhythmias, ischemia, tachypnea, depressed mental status due to CNS hypoxia, seizure
  • >70%:Severe hypoxia, Death


  • Emergent: Anaphylaxis, Angioedema, Airway Obstruction, Aspiration, Asthma, Cor pulmonale, Non-cardiogenic or Cardiogenic pulmonary edema, Pneumonia, Pulmonary Embolism, Tension Pneumothorax, Tamponade, MI, Pericarditis, Myocarditis
  • With normal/increased Respiratory effort—-Anemia, CO Poisoning, Salicylate toxicity, DKA, Sepsis, renal failure, metabolic acidosis


  • ABCs
  • Provide 100% Fio2, —-lack of response should raise concern for methemoglobinemia. If patient does response to supplemental oxygen then most likely it is from a cardiovascular or pulmonary etiology
  • Venous blood gas (VBG)
  • Arterial blood gas (ABG) would reveal a normal
  • Co-Oximeter panel for MetHb level (Can use VBG or ABG) : Measures levels of oxyhemoglobin, Carboxyhemoglobin,methemoglobin, reduced hemoglobin
  • “Chocolate brown” color of blood
  • If no response to Oxygen —– Draw MetHb concentration

MetHB > 30% ——àSpO2 will fall to 80-85% and will not increased despite additional oxygen.  This occurs due to light absorption of both oxyHb and deoxyHb.

  • Who gets treatment?
  1. MetHb < 25% with symptoms, abnormal vital signs, metabolic acidosis or end organ dysfunction (AMS, seizure, etc)
  2. MetHb > 25% regardless of symptoms


  • Initiate treatment if symptomatic OR asymptomatic with MetHB > 25%
  • 1-2mg/kg Methylene Blue IV over 5-15 minutes, repeat if no effect with initial dose. Flush line after infusion completed
  • Clinical improvement seen within 20 minutes
  • Contraindicated in G6PD deficiency as it can induce acute hemolytic anemia
  • Exchange transfusion for symptomatic patients with G6PD deficiency as well.
  • Hyperbaric oxygen when methylene blue ineffective or contraindicated



Pediatric Pearl: UTI (February)

FEBRUARY UTI – Hima Khamar

Pediatric Urinary Tract Infection
By: Hima Khamar, PGY3

In a previous pediatric pearl, we discussed how to treat febrile infants below 60 days. This pearl discussed management of pediatric urinary tract infection (UTI), but also discusses patients above the age of 60 days with a fever with no obvious source in whom UTI as a source.

History and Physical

Duration of fever
Symptoms that suggest an alternative source
Hydration status History of recurring fever without source
History of UTI
History of constipation
Dysfunctional voiding by history
FH of vesicoureteral reflux (VUR) or renal diseases

Vital signs
Suprapubic, flank tenderness
Abdominal mass, palpable bladder
Evidence of spinal lesion
Other GU abnormalities

Signs and Symptoms of UTI: Most common to least common*
Infants < 3 months Fever
Poor feeding
Failure to thrive
Abdominal pain
Offensive urine
Infants > 3 months – preverbal Fever Abdominal pain
Loin tenderness
Poor feeding
Offensive urine
Failure to thrive
Verbal – 18 years Frequency
Dysfunctional voiding
Changes to continence
Abdominal pain
Loin tenderness
Offensive urine
Cloudy urine

Risk factors for UTI
Infants >56 days who are not toilet trained

Female risk factors
–       Non-black
–       T ≥ 39°C
–       Fever ≥ 2 days
–       No source
–       < 12 months
>3 risk factors consider screening>4 risk factors recommend screening
Male risk factors
–       Non-black
–       T ≥ 39°C
–       Fever ≥ 2 days
–       No source
–       < 6 monthsCircumcised:
≥ 3 consider screening
≥ 4 recommend screening
≥ 2 consider screening
≥ 3 recommend screening
Fully toilet trained – 18 yrs
–       Symptoms referable to urinary tract
–       Prior history of UTI, fever ≥ 2 days
–       Prolonged fever (≥ 5 days)Recommend screening for any of the above factors


The AAP recommends obtaining a catheterized specimen for diagnosis of UTI, but this is a level C recommendation. Upon further reading, they basically state a bagged specimen is acceptable as well. SO BASICALLY, GET THE URINE IN WHATEVER WAY YOU CAN.

UTI Definition

Catheterization with >50,000 cfu/ml
Clean catch with >100,000 cfu/ml
Leukocyte esterase and nitrite positive
Nitrite positive, leukocyte esterase negative
Pyuria and bacteriuria positive
Bacteriuria positive and pyuria negative
Catheterization with >10,000 cfu/ml
Clean catch with >50,000 cfu/ml
Leukocyte esterase positive, nitrite negative = only treat if good evidence for UTI
Leukocyte esterase and nitrite negative = no UTI
Pyuria positive and bacteriuria negative = only treat for UTI if have good evidence
Bacteriuria and pyuria negative = no UTI

Whom to culture?

– Infants and children who are suspected to have acute pyelonephritis/upper urinary tract infection
– Infants under 3 months
– Infants and children with a positive result for leukocyte esterase or nitrite – EVERY POSITIVE URINALYSIS SHOULD BE CULTURED
– Infants and children with recurrent UTI
– Infants and children with an infection that does not respond to treatment within 24–48 hours, if no sample has already been sent

Urine Pathogens
E. coli, Proteus sp.
Enterococcus sp.
Pseudomonas sp.
Serratia sp.
Corynebacterium Urealyticum
Klebsiella sp.
Enterobacter sp.
Group B streptococci
Staphylococcus aureus

Common Contaminants
Lactobacillus sp.
Corynebacterium sp.
Coagulase-negative staphylococci
Alpha-hemolytic streptococci


Oral vs. Parenteral Antibiotics
– Most patients will tolerate oral antibiotics. Patients should receive parenteral antibiotics if patient is ill appearing, not able to tolerate PO, or has any other contraindication to oral antibiotics.

-Antibiotics are recommended for 7-14 days. Shorter courses result in spread of infection and renal scarring.

Ceftriaxone 75 mg/kg Q24h

Cefotaxime 150 mg/kg divided into Q6-8h

Ceftazidime 100-150 mg/kg divided into Q8h

Gentamicin 7.5 mg/kg divided into Q8h

Tobramycin 5 mg/kg divided into Q8h

Piperacillin 300 mg/kg divided into Q6-8h

Amox-clav 20-40 mg/kg divided into Q8h

TMP 6-12 mg/kg SMX 30-60 mg/kg divided into Q12h

Cefixime 8 mg/kg Q daily

Cefpodoxime 10 mg/kg divided into Q12h

Cefuroxime 20-30 mg/kg divided into Q12h

Cephalexin 50-100 mg/kg divided into Q6h


– Toxic appearance
– Dehydration requiring IVF
– Failed outpatient therapy
– Febrile infants < 60 days
– Non-febrile infants 31-60 days can be considered for outpatient therapy if they have good follow up within 24 hours


ALL patients should have a renal bladder US (RBUS) after their first febrile UTI. RBUS should be obtained after the patient has recovered from the acute infection (4-6 weeks). Studies have shown that in the acute phase can have false positives due to structural changes that are transient caused by the infection, such as hydronephrosis. (THIS IS FOR THE OUTPATIENT PHYSICIAN)
-Obtain the RBUS during acute illness if: Hospitalized; Ill, concern for sepsis; Abdominal, pelvic mass; Inadequate response to 48 hours of therapy.
-Voiding cystourethrogram (VCUG) should not be obtained routinely after first febrile UTI.
-Obtain VCUG if RBUS is abnormal.


1. CHOP Clinical Pathways
2. Seattle Children’s Hospital Clinical Pathways
3. AAP Guidelines on UTI
4. NICE Guidelines on UTI



Presenting Resident: Katrina D’Amore, PGY4
Chief  Complaint: Palpitations

Brief HPI: 36 y/o F G4P2012 at 18 weeks gestation presents complaining of palpitations that began this morning. Patient reports a history of “SVT” multiple times in the past and she even underwent ablation in 2012.  Patient states that “Adenosine never ever works for me.” Patient  denies any other symptoms and was in her usual state of health until the symptoms began this morning. Patient does report she was recently
started on Synthroid by her OB for subclinical hypothyroidism.

Pertinent PE and Vitals
VS: Afebrile, HR 203 bpm, BP 125/86, 98% on RA
Patient appears uncomfortable but not in distress. PE unremarkable except for tachycardia.

Pertinent Imaging/EKG

Working Diagnosis at time of Disposition:
Wide Complex Tachycardia: Ventricular Tachycardia vs SVT with aberrant conduction

ED & Hospital Course
Patient noted to be on 240 mg PO verapamil daily at home. Decision made to give Verapamil 5 mg IVP x 1.  Patient immediately converted to Sinus rhythm at a rate of 100 bpm. Patient seen by both OB and EP at bedside. Electrolytes and troponin WNL. Normal Echo from 01/2019. Patient ultimately d/c with close f/u. Advised by EP to take extra ½ dose of Verapamil PO if palpitations recurred at home. Synthroid

Pearls & Takeaways
Diagnosis: Idiopathic Ventricular Tachycardia AKA Fascicular VT AKA Verapamil-sensitive VT AKA Belhassen-type VT
• Behaves like a reentrant tachycardia – usually seen in young adults (aged 15-40) w/o any  structural heart disease (thus the term idiopathic)
• Mainly affects males (60-80% of cases)
• Fascicular VT is the most common idiopathic VT arising from the LEFT ventricle (thus the term fascicular)
• Most have QRS only modestly prolonged (~120-140ms) and fast initial forces (RS interval 60-80 ms)
• QRS relatively “narrow” due to the origin of the tachycardia being very early in the His-Purkinje system.
• Classified based on the site of origin/EKG morphology
o Posterior fascicular VT (95% of cases) – RBBB + LAD
o Anterior FT (5%) – RBBB + RAD
o Upper septal FT (very rare) – narrow QRS with RBBB
• OFTEN misdiagnosed as SVT with a RBBB – presence of capture or fusion beats indicates it is a ventricular tachycardia
• Usually stable despite high ventricular rates (>200/min)
• Will not respond to vagal maneuvers, adenosine, etc
• Belhassen et al first described its sensitivity to Verapamil
• Treatment: VERAPAMIL 2.5-10mg IVP (thus the term verapamil-sensitive VT)
• If you are uncertain of the diagnosis, first line treatment is synchronized cardioversion.

Reviriego S. Idiopathic fascicular left ventricular tachycardia. European Society of Cardiology 2010; 9 (13)
Belhassen B, Rotmensch HH, Laniado S. Response of recurrent sustained ventricular tachycardia
to verapamil. Br Heart J 1981; 46: 679-82.



By: Hima Khamar M.D., PGY3

Tranexamic acid (TXA) has become a huge asset in the world of emergency medicine when it comes to controlling hemorrhage. The main use in the ED is in traumatic hemorrhage, but there are many other uses for TXA. In this article, I will discuss some of the other uses of TXA in the hopes that the next time you come across a patient whose hemorrhage you are unable to control with conventional methods, TXA maybe an addition to your toolbox.

TXA is an antifibrinolytic agent. It reversibly binds plasminogen which prevents plasmin activation. Decreased plasmin activation results in inhibition of fibrin clot degradation, thereby stabilizing the clot. This increase in clot formation and stabilization is how TXA works to control hemorrhage.

TXA comes in both oral and intravenous formulations. The oral form comes in 500mg or 650mg tablets and is cheaper. The intravenous form comes in a vial that is usually 1000mg/10ml. Both of these formulations are used in different disease processes, which will be further discussed below.

Despite the many uses of TXA, there are only two indications for which it is approved: tooth extractions for hemophiliac patients (to be given prior to the procedure) and control of heavy menstrual bleeding (this is given orally on an outpatient basis). All the other uses are off label, despite many of them having great evidence.


  1. Traumatic hemorrhage

1g IV bolus over 10 minutes loading dose, followed by 1g IV infusion over 8 hours – MUST BE GIVEN WITHIN THE FIRST 3 HOURS.

Evidence for this came out of the CRASH 2 trial in 2010. The study concluded that TXA reduced all-cause mortality and reduced risk of death due to bleeding when compared to the placebo group. Also, the subgroup analysis showed only effective when given within 3 hours.

  1. Epistaxis

Topical. Soak cotton pledget or any other epistaxis control device, such as RhinoRocket in TXA prior to placing in the nostril.

Evidence for this came out of an RCT by Zahed et al. in 2017. The study showed topical TXA resulted in quicker resolution of epistaxis, decreased ED length of stay, decreased re-bleeding rate, and increased patient satisfaction when compared to placebo.

  1. Dental bleeding in relation to dental procedures (FDA use approved only for hemophilia patients)

Mouthwash. Create by either using 5mg of intravenous solution (1000mg/10ml) in 5ml to make 5% solution OR 650mg tablet crushed and placed in 20ml. A paste can also be created with the tablets and saline to placed directly onto the bleeding region.

Evidence for this came from multiple studies in the dental literature starting around the mid-2000s which showed TXA reduced bleeding when used in a mouth wash formulation both during the procedure and for 2-3 days after the dental procedure when compared to placebo. This was also proven in hemophilia patients and in patients on anticoagulants, such as Warfarin.

  1. Cyclic heavy menstrual bleeding (FDA approved use)

1300 mg PO 3x daily for up to 5 days.

Evidence for this came from multiple RCTs and is also in the ACOG guidelines for management of heavy menstrual bleeding.

  1. Traumatic hyphema

25 mg/kg PO 3x daily for 5-7 days.

There is not a lot of evidence for this use, but it has been looked at in small studies and it is a use recommended by the American Academy of Ophthalmology on a case by case basis. There was a study looking at topical (via drops), but the study was very small so not generalizable.

  1. Orthopedic and cardiac surgery

This is not in our realm, but orthopedic studies are by far the most numerous looking at various doses and various formulations to decrease intra-operative bleeding.

  1. Postpartum hemorrhage

1g IV bolus over 10 mins, if continues to have bleeding after 30 mins or has another re-bleed within 24 hours then give another 1g IV bolus over 10 mins. (Dosing based on study)

Evidence for this comes from the WOMAN trial published in 2017. The study concluded that “Tranexamic acid reduces death due to bleeding in women with post-partum haemorrhage with no adverse effects. When used as a treatment for postpartum haemorrhage, tranexamic acid should be given as soon as possible after bleeding onset.”

  1. Hemoptysis

1g of TXA in 20ml of saline nebulized over 30 mins. (Dosing is controversial)

Evidence for this is based on various case reports. No large RCT exists at this time. This is very experimental, but definitely worth a try in those post-tonsillectomy patients (including pediatrics), cancer patients (oral or lung), or any other causes of hemoptysis.

These are just some of the uses documented in the literature. I think over time we will see more uses of TXA. I have personally used it in penile bleeding secondary to a false track created by a misplaced Foley catheter. I have also used it to stop bleeding topically for varicose veins. There are also current ongoing studies looking at its use in GI bleeding as well. SO, CONSIDER TXA THE NEXT TIME YOU ARE IN A BIND.



  1. Bryant-Smith et al. Antifibrinolytics for heavy menstrual bleeding. Cochrane Database Syst Rev. 2018 Apr 15.
  2. Carter et al. Current concepts of the management of dental extractions for patients taking warfarin. Aust Dent J. 2003 Jun;48(2):89-96.
  3. Carter et al. Tranexamic acid mouthwash: a prospective randomized study of a 2-day regimen vs 5-day regimen to prevent postoperative bleeding in anticoagulated patients requiring dental extractions. Int J Oral Maxillofac Surg. 2003 Oct;32(5):504-7.
  4. Coetzee, M J. 2007. The use of topical crushed tranexamic acid tablets to control bleeding after dental surgery and from skin ulcers in haemophilia. Haemophilia. 2007 Jul;13(4):443-4.
  5. Hankerson et al. Nebulized Tranexamic Acid as a Noninvasive Therapy for Cancer-Related Hemoptysis. Journal of Palliative Medicine. 2015. Volume 18, Number 12, 1060-62.
  6. Jahadi et al. Comparison between Topical and Oral Tranexamic Acid in Management of Traumatic Hyphema. Iran J Med Sci. 2014 Mar;39(2 Suppl):178-83.
  7. Komura et al. Hemoptysis? Tryi inhaled tranexamic acid. The Journal of Emergency Medicine. 2018. Vol. 54, No. 5, pp. e97–e99.
  8. Management of acute abnormal uterine bleeding in nonpregnant reproductive-aged women. Committee Opinion No. 557. American College of Obstetricians and Gynecologists. Obstetric Gynecology 2013;121:891–6.
  9. Nuvvula et al. Efficacy of tranexamic acid mouthwash as an alternative for factor replacement in gingival bleeding during dental scaling in cases of hemophilia: A randomized clinical trial. Contemp Clin Dent. 2014 Jan;5(1):49-53.
  10. Shakur et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet 2010; 376: 23–32.
  11. Shakur et al. Effect of early tranexamic acid administration on mortality, hysterectomy, and other morbidities in women with post-partum haemorrhage (WOMAN): an international, randomised, double-blind, placebo-controlled trial. Lancet 2017; 389: 2105–16.
  12. Zahed et al. Topical Tranexamic Acid Compared With Anterior Nasal Packing for Treatment of Epistaxis in Patients Taking Antiplatelet Drugs: Randomized Controlled Trial. Academic Emergency Medicine. 2018 Mar;25(3):261-266.

Pediatric Pearl – January


By: Hima Khamar, PGY3  &  Dr. Patel, PGY16

Sickle cell disease (SCD) is a common disease process we encounter in the ED. There are multiple complaints related to SCD that patients present with such as: pain, fever, stroke like symptoms, anemia. In this pediatric pearl article, we will discuss pain management during vaso-occlusive crisis (VOC) in the pediatric sickle cell patient.
We as emergency medicine physicians often tend to undertreat pain in SCD patients, we tend to be even more cautious with pediatric patients. The goal of this pediatric pearl article is to emphasize trusting patient reported pain, treating pain adequately, realizing opioids are the main stay for VOC, discussing dosing of various pain medications along with routes, and hopefully making you more comfortable treating VOC in pediatric patients.

Primary Goal on Arrival (provided patient’s ABCs are stable and the patient is neurologically intact): PAIN ASSESSMENT

  • Assess, document pain – TRUST the PATIENT’S self-reported score
  • Recent pain medication, dose, time of last dose
  • Allergies to any medication (if they need Benadryl, ONLY PO, avoid use of IV or IM. DO NOT re-dose with every administration of pain medication. Dose every 4-6 hours as you normally do when using Benadryl.)
  • Order pain medication immediately (ideally should be administered within 30 mins of arrival)
History and Physical

Pain Assessment
–          Pain typical of previous VOE?
–          Location, quality, duration, intensity
Prior Hx of Complications of SCD
–          Acute chest syndrome
–          Aplastic crisis (Parvovirus Infection)
–          Documented bacteremia
–          Stroke, TIA
–          Splenic sequestration
–          Gall bladder disease
–          Osteomyelitis, septic arthritis

Past Medical History
–          Baseline pulse oximetry reading
–          Previous admissions, ICU admissions
–          Transfusion history
–          Vaccination history

–          Penicillin prophylaxis
–          Hydroxyurea
–          Folic acid
–          Chronic pain medications
 AllergiesPhysical Exam
–          VS, pulse oximetry reading
–          General appearance, jaundice
–          Pain assessment
–          Respiratory, Circulatory, Neurologic                     status
–          Evidence of focal infection
–          Spleen size
–          Presence of rash or petechiae


  • CBC w/ differential – determine if there is any hemolytic or inflammatory process
  • Reticulocyte count – determine if there is any hemolytic or inflammatory process
  • Type and Screen
    • Pale, persistent tachycardia, ill appearing
    • Suspected splenic sequestration
    • Acute chest syndrome
    • Focal neurologic findings
    • Hgb < 5 g/dL or Hgb drop > 2 g/dL from baseline Hgb
    • Reticulocyte count < 1% (unless hemoglobin > 10 g/dL)
  • Chest Radiograph – new hypoxia, chest pain, clinical suspicion for pneumonia/acute chest syndrome
  • HCG – any females ≥ 12 years or < 12 with menarche
  • Blood cultures – if infection is suspected



  • Recommended onlyif O2 saturation is less than 92%


    • Recommended: D5 ½ NS.
    • As clinically indicated for: clinical dehydration/intravascular volume depletion
    • If need to place patient on maintenance fluids because they are not tolerating adequate PO, then place on hypotonic solution, not hypertonic or isotonic solution. Note: IVF offers no therapeutic benefit for patients with VOE who have no signs of volume depletion.
Ketorolac IVP or IM 0.5 mg/kg
(Max 30mg/dose)
Ensure patient has no history of renal insufficiency
Fentanyl IN 0.2 mcg/kg
(Max 100mcg/dose;
Max volume
Great for those patients who are in a lot of pain, while you are trying to get IV access.
Morphine IV 0.1-0.15 mg/kg/dose
(Max 8 mg/dose)
Hydromorphone IV 0.015-0.02 mg/kg/dose
(Max 2 mg/dose)
Diphenhydramine PO 1mg/kg/dose
(Max 50mg/dose)
No indication to give IM or IV, unless patient truly can’t tolerate PO, but may try giving PO after giving anti-emetic.
Oxycodone PO < 6 yrs: 0.15 mg/kg/dose up to 2.5 mg
6-12 yrs: 0.2 mg/kg/dose up to 5 mg
> 12 yrs: 0.2 mg/kg/dose up to 10 mg
For outpatient management. Give up to 3 days, until they can see their heme-onc doctor.
Tylenol PO 10-15mg/kg/dose
(Max 975mg/dose)
Use as an adjunct to decrease opioid use provided there is no contraindication.
Motrin PO 10 mg/kg/dose
(Max 600mg/dose)
Use as an adjunct to decrease opioid use provided there is no contraindication.


      • Provide to all patients who are admitted for VOC.
      • This will help decrease development of acute chest syndrome. Acute chest syndrome normally develops during inpatient stay. (We will discuss this in depth in another pearl.)


      • Based on studies, high dose methylprednisolone may help in the acute event, but has been associated with high rate of rebound pain after stopping steroids.
      • Currently, it is not routinely recommended for VOC.

Ketamine – need more studies

      • In ED recommend 0.25-1 mg/kg; inpatient can place on continuous infusion of 3-5 mcg/kg/min
      • Has been shown to be effective in some case series, but need more data and large, randomized control trials

Nitrous oxide – needs more studies

      • May try as another modality to control pain
      • Has been shown to be effective in some case series, but need more data and large, randomized control trials

Patient controlled analgesia (PCAs) – RECOMMENDED FOR ADMITTED PATIENTS

      • Pain management, which is under anesthesia can help with setting this up. You can get pager number from the operator. Recommended for patients who are admitted, and pain is not controlled with opioid pushes. Discuss with heme-onc team and may consider starting in ED, especially if patient is not going to get a bed for some time.

Other adjuncts

      • Laxatives should be provided around the clock to prevent side effects of opioids.
      • Antiemetics as needed.
      • Antipyretics as needed.


The website listed below can help you convert a patient’s home medication into the parenteral dose you should be starting at in the ED. You can also do it manually using the conversion table provided below. On the right side is an example case on how to use the table. Whenever you are converting opioids, always convert to morphine and then convert to another opioid agent.



  • < 3 months of age
  • Focal neurologic findings
  • Acute chest syndrome
  • Splenic sequestration
  • Reticulocyte count < 1 % (unless Hgb > 10 g/dL)
  • Severe anemia (Hgb < 5 g/dL)


  • Patients with pain relief: After 1 – 3 doses of IV analgesia
  • Patient continues to be pain free at least 60 minutes after PO analgesia
  • Discharge with 3 days of PO analgesia until they can follow up with heme-onc doctor
  • Absence of other complications of sickle cell disease


  • TRUST the patient’s self-reported pain score
  • Vital signs can be normal even if patient is in pain, so do not rely on vital signs as an indicator of pain.
  • There is no lab test to definitively say a patient is having VOC or not.
  • Acute VOC is considered acute, not chronic pain, and opioids are indicated and should be used to treat pain.
  • Rapidly initiate analgesic therapy within 30 minutes of triage or within 60 minutes of registration.
  • In adults and children with SCD and a VOC associated with mild to moderate pain who report relief with NSAIDS in the absence of contraindications to the use of NSAIDS, continue treatment with NSAIDS.
  • In adults and children with SCD and a VOC associated with severe pain, rapidly initiate treatment with parenteral opioids.
  • Calculate the parenteral (IV or subcutaneous) opioid dose based on total daily short-acting opioid dose currently being taken at home to manage the VOC.
  • Administer parenteral opioids using the subcutaneous route when intravenous access is difficult.
  • Reassess pain and re-administer opioids if necessary for continued severe pain every 15–30 minutes until pain is under control per patient report.
  • Maintain or consider escalation of the dose by 25 percent until pain is controlled.
  • Reassess after each dose for pain relief and side effects.
  • In adults and children with SCD and a VOC, do not use meperidine unless it is the only effective opioid for an individual patient.
  • In adults and children with a VOC, administer oral NSAIDS as an adjuvant analgesic in the absence of contraindications.
  • In adults and children with a VOC who require antihistamines for itching secondary to opioid administration, prescribe agents orally, and do not re-administer with each dose of opioid in the acute VOC management phase. Re-administer every 4 to 6 hours if needed.
  • To reduce the risk of acute chest syndrome in adults and children hospitalized for a VOC. Encourage use of incentive spirometry while awake. Encourage ambulation and activity as soon as possible.
  • In adults and children with VOC, use adjunctive nonpharmacologic approaches to treat pain such as local heat application and distraction.
  • In euvolemic adults and children with SCD and a VOC who are unable to drink fluids, provide intravenous hydration at no more than maintenance rate to avoid over-hydration.
  • Assess all patients with sickle cell disease who present with acute pain to determine whether their pain is being caused by an acute painful sickle cell episode or whether an alternative diagnosis is possible, particularly if pain is reported as atypical by the patient.
  • Patients who experience three or more acute painful episodes per year that require treatment with parenteral opioids in a medical facility are considered to have severe disease.

Physician burnout

As physicians, we all decided to help others. Those of us in Emergency Medicine decided to help others at their most ill, at the most traumatic moment in their lives, or at their wits end as far as where to seek answers. Sometimes we can help, and sometimes we cannot. Regardless of what their reason or our ability to meet their expectations, patients come to offload some of their burdens of life. Maybe they can no longer care for themselves because their sepsis has drained them of all their energy. Or their addiction to substances (despite the number of times you’ve counseled them on breaking their habit) has brought them back to us either for either intoxicant effects or the pangs of being without for too long.

Regardless, we can feel the burden and it manifests as burnout. Burnout is a syndrome exemplified by emotional exhaustion, depersonalization and a sense of lack of accomplishment. It manifests in those whose careers aim at working with others. While stress is a normal part of life and work, when we cannot defuse the stress between shifts thereby allow it to build up will we be in danger of experiencing burnout. The syndrome can lead to us making clouded medical decisions which can have disastrous consequences.

Some studies suggest 1 of 3 physicians are experiencing burnout at any given time. The Medscape Physician Lifestyle Survey shows an increase of self-reported burnout from 39.8% in 2013 to 46% in 2015. Whether we don’t have enough time off between shifts, work too many shifts to pay off loans, or simply keep our feelings inside, it exists and knowledge of it is essential. Many of these habits perhaps are inculcated from medical pedagogy since day one of our education.

But there is a cure. Recognize it. In ourselves. In others. Talk about it. Talk to each other. Be there for one another. Recommend healthy coping strategies. Provide an ear. The National Academy of Medicine has validated tools for you to determine if you are burnt out.

As physicians, we have an obligation to patients. But as humans, we have an obligation to ourselves.

Case of the Week COW #20

Resident: D’Amore/Clayton

CC: “My heart is racing.”

HPI: 26 year old male with no past medical history presents to the Emergency Room with complaints of palpitations. Patient states that while exercising at the gym just prior to arrival, he suddenly developed palpitations along with associated lightheadedness. He reported one similar episode in the past that self-remitted. He denies chest pain, shortness of breath, nausea or vomiting but was experiencing intermittent lightheadedness. He denies taking any medication prior to arrival. Patient states he drinks ETOH infrequently with his last drink several days ago. He denies tobacco or illicit drug use. Patient also denies any family history of heart disease or arrhythmias.

Physical Exam:
Vitals: HR: 221 BP: 117/74 RR: 20 T: 98.8 Pulse Ox 100% on Room Air
General: Patient is awake, appears uncomfortable
Respiratory: No respiratory distress. Lungs are clear to auscultation.
Cardiovascular: +S1/+S2, tachycardic, irregular. No murmurs, rubs or gallops.
Abdomen: Soft, non-tender, non-distended
Extremities: Palpable, rapid pulses. No cyanosis, clubbing, or edema.
Neurological: Alert and oriented to person, place, time, and situation, following all commands, strength and sensation intact and equal bilaterally.

Laboratory Data:
Lab work and radiography including troponins, complete blood count, complete metabolic panel, thyroid stimulating hormone, chest x-ray, and urine drug screen were all within normal limits. Image 1 is the EKG on presentation. The patient quickly became hypotensive 90/52 and complained of lightheadedness. The patient was quickly sedated and cardioverted with 150 joules. He returned to sinus rhythm at which time the underlying conduction was more apparent.


  1. What EKG abnormalities do you notice?
  2. EMS requests permission to administer 6mg of Adenosine to treat the arrhythmia.

What is your recommended treatment plan?


  1. This EKG demonstrates Wolff-Parkinson-White Syndrome with Atrial Fibrillation.
  2. Advise EMS not to treat with Adenosine or other A-V nodal blocking agents as this may precipitate ventricular tachycardia or ventricular fibrillation.


Wolff-Parkinson-White Syndrome is a pre-excitation syndrome where myogenic bundles known as the Bundles of Kent directly link the atria to the ventricles, bypassing the atrioventricular (AV) node and the organized infranodal system [source: Tintinalli]. Atrial Fibrillation (AFib) in Wolff-Parkinson-White Syndrome (WPW) is a presentation of this syndrome in up to 20% of cases.

Features include an irregularly irregular rhythm, very rapid ventricular rates often in the range of 250 to 300, and widened QRS complexes that differ in duration and morphology from one to the next.The accessory pathway present in patients with WPW allow for the multitude of additional ectopic atrial impulses present in AFib to bypass the AV node and conduct to the ventricles, accounting for the unusually rapid ventricular rates. The variation in QRS duration and morphology can also be attributed to simultaneous conduction through the traditional AV node-His-Purkinje pathway as well as the Bundle of Kent-Ventricle route.

WPW with AFib is often misdiagnosed as a supraventricular tachycardia (SVT), ventricular tachycardia (VT) or atrial fibrillation with a bundle branch block, all of which can be safely treated with AV nodal blockers such as Adenosine, Diltiazem, and Amiodarone. WPW in the presence of atrial fibrillation makes degeneration into ventricular fibrillation more likely and thus synchronized cardioversion, delivering 0.5 – 2 Joules/kilogram, is the first-line treatment. Second-line treatments include Procainamide or Ibutilide whose mechanism prolongs the refractory period of the accessory pathway and whose dosing is weight-based. Stable WPW in the presence of narrow-complex SVT can be treated with the traditional vagal maneuvers, adenosine, and calcium channel- or betablockers [source: Tintinalli]. Patients with WPW should undergo ablation as this syndrome can lead to sudden cardiac death by means of ventricular fibrillation.

Take Home Pearls:

  • Wolff-Parkinson-White with Atrial Fibrillation presents as an irregularly irregular tachycardia with widened QRS complexes that vary in morphology and result in ventricular rates often greater than 250.
  • If the QRS complex is widened, avoid use of any AV nodal blockers as they can precipitated ventricular arrhythmias.
  • Procainamide and synchronized Cardioversion are the treatment of choice for WPW with AFib.