POTD: Cavernous sinus thrombosis (CST)

Clinical Scenario:

A 30-year-old woman presents with headache, fever, and decreased vision in her right eye over the past 24 hours. Examination reveals exophthalmos of the right eye and no pupillary reflex and a clear anterior chamber. When asked, she denies weakness and numbness.

What is the most likely diagnosis?

Last week we talked about cerebral venous sinus thrombosis (CVST), today let’s talk about cavernous sinus thrombosis (CST), or the infected subset of cerebral venous sinus thrombosis.

What is it?

  • Cavernous sinus thrombosis (CST) is a rare condition, defined as a septic thrombophlebitis of the cavernous sinus. It is caused by a bacterial infection that typically originates in the face, sinuses, ears, or orbits. Most infectious etiologies in cavernous sinus thrombosis are from Staphylococcus or Streptococcus species. 

  • The two cavernous sinuses are located on both sides of the sella turcica. Important structures are located in, or run through, the cavernous sinus, including the pituitary gland, cranial nerves III, IV, V and VI, and the internal carotid arteries (ICA)

  • It causes significant morbidity and the mortality rate is at 20-30%.


Risk Factors

  • Sphenoid and ethmoid sinusitis are the most common causes of CST. 

  • Other risk factors include dental infections, facial cutaneous infections, otitis media, maxillofacial surgery, and trauma.


  • Most patients will have fever, headache, and vision changes/ocular complaints (proptosis, periorbital edema and/or chemosis). 

  • Most will also have external ophthalmoplegia, due to venous congestion of orbital tissues, extra-ocular muscle inflammation and/or inflammation of cranial nerves III, IV and VI. 

  • Other symptoms include eyelid erythema, autonomic dysfunction, sensory changes in the ophthalmic and maxillary trigeminal nerve distributions, pupillary abnormalities, and papilledema. 

  • Vision loss is rare as the orbital nerve lies outside the cavernous sinus. 

  • CST commonly spreads from one eye to both within 24 to 48 hours.



Blood cultures, CBC, and coagulation studies (PT and PTT) should be ordered, as well as CT of the head and orbits with contrast.


  • Parenteral antibiotic treatment should be started with gram-positive coverage (nafcillin plus a third-generation cephalosporin or vancomycin if concerned for MRSA). The patient should be admitted with neurology and ophthalmology consultations

  • Anticoagulation and steroids, remain controversial.

    • Steroids may confer improved cranial nerve function.

    • Anticoagulation may confer a risk of systemic and intracranial bleeding and may result in dissemination of septic emboli. Consider anticoagulation only if there is no evidence of severe bleeding risk or current hemorrhage.

Differences between CVST and CST


POTD: Trauma Tuesdays - Concussions

Clinical scenario:

A 16-year-old boy presents after hitting his head in a collision with another player during a soccer game. He denies loss of consciousness but complains of a moderate headache, nausea, and difficulty concentrating. 

Which of the following represents appropriate next steps in management?

A. Admit the patient to the hospital for overnight observation

B. Clear the patient to play after 48 hours if his symptoms resolve

C. Discharge with instructions to get follow-up care and not return to play

D. Order a head CT to rule out the presence of an intracranial bleed or swelling

The correct answer is C. 


What is a concussion?

The term "concussion" is often used in the medical literature as a synonym for mild TBI but more specifically describes a pathophysiological state that results in the characteristic symptoms and signs that individuals may experience after a mild TBI. 


Rapid-onset short-lived neurologic function impairment that resolves on its own. These symptoms reflect functional disturbance rather than structural injury.

concussion symptoms.png


If one or more of the following:

  • Symptoms, including somatic (headache, nausea, off balance), cognitive (“ in a fog,” slow), or emotional (rapidly changing)

  • Physical signs, such as loss of consciousness, amnesia, although LOC is not required

  • Behavior changes, such as irritability

  • Cognitive impairment, such as slowed reaction times

  • Sleep disturbance, such as insomnia


  • Concussion is a clinical diagnosis, and there are a variety of sideline assessment tools (that are outside the scope of the ED) that include measurements of orientation, symptoms, gross cognition, and physical examination findings (e.g. Standardized Assessment of Concussion (SAC)Balance Error Scoring System (BESS), computerized neurocognitive testing, and the Sport Concussion Assessment Tool version 5 (SCAT5 or Child-SCAT5)).

  • Physical exam should include: 

    • assessment of the cervical spine (+/- immobilization with c-collar if cervical spine injury suspected)

    • detailed neurologic assessment (including mental status, cognitive functioning, and gait/balance)

    • structural brain imaging (i.e. CT scan or MRI) if concern for structural injury (e.g. acute brain bleed)

Discharge Precautions

This is arguably the most important part of your role in the concussed patient. Thankfully, the CDC has a ton of great literature on the subject.

Pediatric Care Packets:

  1. Pediatric Discharge Instructions

  2. Symptom-Based Recovery Tips

  3. Pediatric Care Plan

Adult Care Packets:

  1. Adult Concussion Fact Sheet

  2. Adult Concussion Brochure

  3. Adult Care Plan







POTD: Alcoholic Ketoacidosis

Today’s topic will be for the people who used this 3-day weekend for a bender:

Alcohol Ketoacidosis (AKA)

Clinical Scenario:

Someone who has been on a bender and shows up to your ED after two days of vomiting, has a low bicarb, elevated anion gap, elevated lactate, urine ketones, and an elevated BHB level...probably has AKA. 


  • Alcoholic ketoacidosis (AKA) is a starvation state in an alcoholic or binge drinker

  • Alcohol + No Food + Dehydration = AKA

  • Most often associated with acute cessation of alcohol consumption after chronic alcohol abuse

  • Can also be associated with first-time alcohol binge

  • one of the causes of anion-gap metabolic acidosis 

Clinical Features

  • episode of heavy drinking followed by vomiting and an acute decrease in alcohol consumption

  • N/V, nonspecific abdominal pain

  • can have associated gastritis or pancreatitis

  • normal mental status, but if patient is altered, look for toxic alcohol ingestion, postictal states from withdrawal seizures, or occult head injury

  • exam with acetone odor on breath

  • tachypnea (Kussmaul respiration), tachycardia, and signs of dehydration


ethanol metabolism.png

Nicotinamide adenine dinucleotide (NAD, or “Needs Additional Dextrose”) is depleted by ethanol metabolism, leading to inhibition of the Kreb’s cycle (or aerobic metabolism) in favor of ketone formation, depletion of glycogen stores, and suppression of insulin secretion  


  • low, normal, or slightly elevated glucose

  • binge-drinking that ends in N/V and decreased intake

  • wide AG metabolic acidosis, especially one without an alternative diagnosis

  • (+) serum ketones

  • can have associated hypophosphatemia, hyponatremia, and hypokalemia


  • Sugar and water!

  • Glucose stimulates insulin production, which stops lipolysis and halts further ketone formation. Glucose also increases oxidation of NADH to NAD, thereby further stopping ketone production. 

  • Start with 5% dextrose in NS. Once fluid and electrolyte losses are replaced, change fluids to 5% dextrose in 1/2 NS until oral intake is assured.

  • Give 100 mg thiamine (facilitates Krebs cycle)

  • Correct electrolytes

  • Repeat Chem7 to see if bicarb improving. If it’s not, consider ethylene glycol or methanol poisoning. This is the time for fomepizole and a call to your local toxicologist or poison center!


Discharge if tolerating PO!






POTD: Cerebral Venous Sinus Thrombosis (CVST)

Clinical Presentation:

An 18-year-old female student presented with a 7-day history of worsening frontal headache and 1 day history of vomiting. The patient described marked photophobia, but no fever or history of seizure. She was taking a combined oral contraceptive and had no other medical history. Physical examination showed no focal neurology, but fundoscopy revealed bilateral papilledema. 

Today, let’s learn about cerebral venous sinus thrombosis.

What is it?

Clot that forms within the major cerebral veins, such as the dural sinuses (super sagittal sinus, straight sinus, and transverse sinuses), cortical veins, vein of Galen, and jugular veins.


What causes it?

Thrombosis of either the cerebral veins or of the major cerebral sinuses.


  • More common in younger patients (median age = 38)

  • More common in women

  • Mortality of 10-30%

  • Risk factors: 

    • Acquired: infections (otitis, mastoiditis)surgerypregnancy, trauma, cancer, exogenous hormones

    • Genetic: inherited thrombophilia


  • Non-specific stroke-like symptoms: severe HA (90% of patients) that can be gradual in onset, weakness, paresthesias, blurred or double vision

  • If increased ICP, can see mental status changes, lethargy, decreased consciousness, papilledema 

  • If focal brain injury, can have seizures or focal neurological defecits


  • Variety of imaging modalities for diagnosis, typically can start with a non-contrast CT head and then progress to CT venogram (if MRI unavailable), or perform MR venography, MRI, or cerebral angiography


  • Manage seizures or herniations 

  • Start anticoagulation

    • Unfractionated heparin (UFH)

    • Low molecular weight heparin (LMWH): 1 mg/kg SQ Q12 hours

  • Other treatment modalities: systemic thrombolytics, cather-based interventions (thrombolytics and thrombectomy), decompressive craniectomy


POTD: AFib in Wolff-Parkinson-White Syndrome

Atrial fibrillation can occur in up to 20% of patients with Wolff-Parkinson-White Syndrome (WPW). The accessory pathway allows for rapid conduction directly to the ventricles bypassing the AV node. Rapid ventricular rates may result in degeneration to VT or VF.

ECG features of Atrial Fibrillation in WPW are:

  • Rate > 200 bpm, can be closer to nearly 300bpm!

  • Irregular rhythm

  • Wide QRS complexes due to abnormal ventricular depolarization via accessory pathway

  • QRS Complexes change in shape and morphology

  • Axis remains stable unlike Polymorphic VT


Treatment with AV nodal blocking drugs e.g. adenosine, calcium-channel blockers, beta-blockers may increase conduction via the accessory pathway with a resultant increase in ventricular rate and possible degeneration into VT or VF

  • In a hemodynamically unstable patient urgent synchronized DC cardioversion is required.

  • Medical treatment options in a stable patient include procainamide, although DC cardioversion may be preferred.

Example of EKG of WPW with afib

Example of EKG of WPW with afib

Vtach vs Afib in WPW

Vtach vs Afib in WPW


POTD: Leaving Against Medical Advice (AMA)

Over the past 2.5 years, I've heard a lot of discussion about this topic, it probably left me with more questions then answers, so I figured I'd do a review regarding AMAs, or leaving against medical advice, in a true or false format.

If a patient left AMA, insurance companies will not reimburse them for their ED visit. This is an incentive to get patients to stay.


Some patients are told that if they leave AMA, their insurance will not cover their treatment. This is false information. On this issue, the University of Chicago Medicine published an article dated February 3, 2012, which discussed their study (funded by The Agency for Healthcare Research and Quality and the National Institute on Aging) of the misconception of who picks up the tab when patients walk out. They concluded from their survey of general internal medicine doctors that two-thirds of residents and almost half of attending physicians believed that when a patient left the hospital AMA, insurance companies would not pay. They also found that some physicians go as far as using the financial obligation as a threat to persuade a patient to stay.

The researchers, all from the University of Chicago Medicine, combed through the records of more than 46,000 patients admitted to the general medicine service at the medical center's adult hospital between July 2001 and March 2010. They found that 526 patients, about 1 percent, had left against doctor's orders. Consistent with previous studies, most of these patients had government-funded insurance, either Medicare or Medicaid (78 percent), or no insurance (14 percent). The average hospital charge was nearly $28,000, of which insurance paid on average almost $6,000. (Most patients also owe a minimal co-pay.) So leaving against medical advice brought no additional financial burden to the patient. Of the 453 insured patients who left AMA, payment was initially denied in only 18 cases. All of those cases involved problems with the bill, not with the patient's behavior. None of those patients were denied coverage for leaving against doctors' orders. Furthermore, the article postulates that when a physician provides misinformation in order to influence a patient's decisions -- no matter how well intentioned -- it compounds the loss of trust.

One member of the research team, John Schuman, MD, called the insurance companies themselves and reported "I talked with VPs and media relations people from several of the nation's largest private insurance carriers. Each of them told me that the idea of a patient leaving AMA and having to foot their bill is bunk. They were glad to tell me so, as this was a rare occasion of insurance companies looking magnanimous."

Having my patient sign an AMA form will confer me legal protection if something happens to the patient.

Not necessarily.

A case where the plaintiff left AMA is most defensible if there is a thoroughly documented medical record that shows a clear, informed consent process regarding the patient’s departure. Nan Gallagher, JD, is an attorney who has defended many medical malpractice claims alleging improper AMA discharges. She urges providers to “be specific and verbose. A patient’s signature on an AMA form is not enough anymore.” Gallagher further remarks, “In our litigious society, there is a growing trend toward patients disputing the authenticity of the signatures on an AMA form and challenging the quality of informed consent communications.”

Tips on how to properly document leaving AMA in the chart. 

1. Inform the ED patient of the risks of leaving, including worsening or complications of the acute medical condition, permanent disability, or death, when these are real considerations.

“I believe that an attempt to individually list every possible complication or poor outcome from the patient’s condition is weaker than the narrative that the patient was counseled about the potential for deterioration, disability, or death,” Laura Pimentel, MD says. If the provider lists all the possible risks that come to mind, but omits something that ends up occurring, she explains, “it opens the door for the plaintiff attorney to argue that the provider didn’t properly inform the patient.”

2. Determine that the patient has the capacity to make the decision to be discharged AMA.

Remember, capacity means the patient can make an informed decision, not that they are competent, which is a legal term referring to a right to determine one's own affairs after age 18. Adults are assumed to be competent until proven otherwise. Therefore, deeming an individual “not competent” requires legal proceedings.

3. Educate the patient on the potential benefits of completing evaluation and treatment, and document the discussion.

4. Inform the patient that he or she may return at any time.

5. Give the best possible care to the patient before discharge, including recommendations for outpatient care and prescriptions.

6. Include nurses and family members in discussions with patients about the benefits of completing treatment and the risks of leaving.

Nursing documentation of the discussions can help the defense by serving as a good witness of your efforts to care for the patient

7. Make an effort to convince the patient to stay.

8. Contact patients who leave AMA by telephone, and document the call.







POTD: Blood Transfusions in Immunocompromised Patients

You have a chemo patient who’s been feeling weak and was sent by their oncologist to the ED for further evaluation. They look pale, maybe a little tachy, but otherwise stable. A preliminary VBG comes back with a Hct of 10%…what do you do?

Let’s talk about blood transfusions in the immunocompromised patient! Shout out to Dr. Allie Kornblatt for the clinical question!


What is irradiation?

Process to inactivate lymphocytes in the RBC product. 

Why is it important?

Viable donor lymphocytes can attack recipient cells in individuals who are unable to mount an immune response against them, causing transfusion-associated graft-versus-host disease (ta-GVHD). Ta-GVHD can target all hematopoietic cells as well as other tissues, leading to bone marrow aplasia and other complications that are ultimately fatal.

Who should get irradiated blood?

  • Recipients of intrauterine or neonatal exchange transfusionpremature neonates

  • Individuals with congenital cell-mediated immunodeficiency states

  • Individuals treated with specific types of potent immunosuppressive therapies (purine analogs, antithymocyte globulin [ATG], certain monoclonal antibodies); this may include those being treated for non-Hodgkin lymphoma (NHL) or other hematologic malignancies

  • Recipients of hematopoietic stem cell transplant (autologous or allogeneic)

  • Individuals with Hodgkin lymphoma (any stage of disease)

  • Individuals at risk for partial HLA matching with the donor due to directed donations, HLA-matched products, or genetically homogeneous populations

Additional Considerations

Blood ultimately has a reduced shelf life and may have a delay in arriving to the patient for transfusion.


What is leukoreduction?

Removal of leukocytes from the red cell product.

Why is it important?

These cells are present due to co-purification and do not provide any known benefit to the recipient and can potentially cause immunological mediated effects, infectious disease transmission, and repercussion injury. Some countries require universal leukoreduction of cellular blood components (RBCs and platelets), but this is not mandatory in the United States.

Who should get leukoreduced blood?

  • If cost wasn’t a factor, EVERYONE should get leukoreduced blood!

  • Patient’s that suffer from frequent febrile nonhemolytic transfusion reactions, especially if fever in these patients (e.g. immunocomprised) necessitates inpatient evaluation for occult infection

  • Patient’s awaiting organ or bone marrow transplantation and have a history of platelet refractoriness caused by Human leukocyte antigen (HLA) alloimmunization

  • Decrease the risk of postoperative infection and occult bacterial contamination

  • Patient’s with cardiac injury to prevent reperfusion injury

Additional Considerations

They have no role in preventing ta-GVHD.

CMV-Seronegative Red Cells

What are they?

RBC components that test negative for the presence of CMV using serologic methods (antibody testing).

Why is it important?

Certain immunocompromised individuals who are themselves CMV-negative may be at risk for serious infection if they receive a CMV-positive unit of blood. 

Who should get CMV-seronegative blood?

  • Solid organ transplant recipients

  • Hematopoietic stem cell transplant (HCT) recipients

  • Low birth weight neonates

  • Individuals infected with HIV

  • Pregnant women




POTD: Esophageal Disorders


An elderly male comes to the ED with worsening epigastric and retrosternal chest pain, nausea, and forceful vomiting after eating some spicy food and consuming a small amount of alcohol with dinner. The most recent episode included a small amount of bright red blood.  The pain has progressively worsened, and he now has pain while swallowing and mild shortness of breath.  The patient has had dyspeptic symptoms in the past, which he self-treated with over-the-counter antacids.  He does not use tobacco or illicit drugs.  He appears pale, diaphoretic, and in moderate distress.  Temperature is 38 C (100.4 F), blood pressure is 140/90 mm Hg, pulse is 120/min, and respirations are 24/min.  Neck veins are flat.  Dullness to percussion and decreased breath sounds are present over the left basal area.  Abdominal examination reveals epigastric tenderness and decreased bowel sounds.  Stool occult blood is positive.  Upright chest x-ray reveals a small pleural effusion of the left lung, and ECG shows sinus tachycardia; the imaging results are otherwise unremarkable.

Which of the following is the most likely cause of this patient's current condition?

A) aspiration pneumonitis

B) erosive esophagitis

C) esophageal perforation

D) mallory-weiss syndrome

E) perforated gastric ulcer

Screen Shot 2019-02-04 at 9.29.17 PM.png

The answer is (c). Vomiting + bleeding = mallory-weiss, but vomiting + PAIN + L pleural effusion = Boerhaave’s. Boerhaave’s can lead to mediastinitis (from gastric contents entering sterile sites) and lead to a left pleural effusion with accompanied pneumomediastinum. Fever can take >4 hours to develop. Mortality from mediastinis can double if not properly treated within 24 hours of diagnosis. Make sure to start broad spectrum antibiotics and obtain an emergent thoracic surgery consult!

Why L sided pleural effusion?

The mid esophagus lies next to the right pleura while the lower esophagus abuts the left pleura. Rupture occurs most commonly in the left posterolateral wall of the distal third of the esophagus with extension into the left pleural cavity.





POTD - Trauma Tuesday - Pregnant trauma

Trauma in the pregnant patient 


What's good for mommy is good for baby!! Resuscitate mom!

- Viable fetus typically at 23-24 weeks (fundus above level of umbilicus)

- Trauma incidence in up to 7% of pregnancies

- leading cause of death in reproductive females

- leading non-obstetrics cause of death in pregnant women

Assess ABCDEs first like every trauma!!!

Airway considerations -  prepare for difficult intubation (increased soft tissue edema, larger breasts, weight gain, increased aspiration risk)

Breathing - increased basal O2 requirement, fetus highly sensitive to maternal hypoxia (aim to keep Sp02 above 95%), Chest tube placement if indicated should be 1-2 intercostal spaces higher (almost in the axilla!!! a gravid uterus pushes everything superiorly)

Circulation - fluid and bloods as per ATLS, Placenta highly sensitive to vasopressors (be careful regarding placental ischemia), IVC compression from a gravid uterus can decreased CO by 30% --> decompress IVC by rolling patient to LL decubitus or just towards left side.  Defibrillation of mother has small fetal risks (mother being dead is a higher risk to the fetus).  

Uterine Rupture:  typically 2/2 direct abdominal trauma during 2nd half of pregnancy, Sx: maternal shock, abdominal distention/peritoneal signs, abnormal uterine contour on palpation, abnormal fetal lie, palpable fetal parts, fetal ascent, abnormal fHR tracing

Placental Abruption: most common cause of fetal demise in blunt trauma to pregnant mother, U/S not sensitive for this pathology, Sx: abdominal pain, uterine tenderness to palpation, vaginal bleeding (in up to 70%, may be absent if bleeding into retroperitoneum), uterine tonicity or contractions, fetal distress on monitor (decels, loss of variability).

Preterm Labor: 2x risk of preterm labor after trauma

Labs: CBC, BMP, T and S, d-dimer, fibrinogen, coags, Rh factor

Imaging: FAST, further imaging as indicated by injuries/suspicion of clinician.  Imaging should not be delayed or deferred 2/2 concern for fetal radiation exposure in the trauma setting!!!!  

If mom is stable, fetal monitoring/tocometry!  think VEAL CHOP (variable = cord compression, early = head compression, accelerations = okay, Late = placental insufficiency.

Treatment Dispo:

- Nonviable fetus (less than 23-24 weeks of age, fundus below umbilicus) - treat as standard trauma patient, consider RhoGam 50 mcg for Rh negative patient to prevent alloimmunization 

- Viable fetus (greater than 24ish weeks old) - consider RhoGam 300 mcg in Rh negative patient.  Avoid pressors which can compromise uterine and placental bloodflow and secondarily fetal SpO2.  Decreased pressure on IVF --> left lower decubitus position or roll patient 30% to left (like on a backboard if C-spine immobilized).  Tocometry monitoring 4-6 hours if no further risk factors of fetal loss.  Toco monitoring x 24 hours + if risk factors for fetal loss/placental abruption exist.

This leads me into the reason for this email:  The resuscitative hysterotomy, formerly called the perimortem C-section, but name recently changed to reflect that this procedure is good for both mother and fetus!  Potentially life saving for both as it decreases some burdens of pregnancy on maternal circulation, volume status, respiratory status, as well as it makes the newly delivered infant accessible for resuscitation, medication/fluid/blood administration, CPR, etc.  A fetus inside a mother is much harder to resuscitate.  

- Best outcome when performed within 4 minutes of Cardiac Arrest. (this patient is already dead at this point, you cannot make them worse, it is time to throw the kitchen sink)

- only attempt if gestation age is known at or above 24 weeks or if uterus appears gravid enough (fundal height above umbilicus).  

- Bare minimum supplies necessary: prep stick, Scalpel, Large scissors, hemostat, sterile gauze and then hopefully a close by OR, OB surgeon (to put patient back together again), Pediatrics to resuscitate the fetus and ICU/trauma ICU setting for patient if they make it.  A c-section or abdominal ex-lap tray is available in many ERs, and a emergency thoracotomy kit (in most EDs) will have most necessary tools.  Suction, sterile garb and copious betadine also helpful.  

I highly recommend watching some videos (Scott Weingart's: https://vimeo.com/59516684) as attached below but here are very basic steps:

  1. Widely cleanse the entire abdomen with betadine (betadine bath)

  2. midline vertical incision using scalpel from xiphoid to pubis

  3. Sharp or blunt dissection through anterior abdominal wall until abdominal cavity is entered

  4. retract abdominal walls laterally and bladder inferiorly to expose uterus

  5. Make small vertical incision at uterine fundus, insert two fingers to and lift uterus wall away from fetus

  6. use scissors to extend incision to the anterior reflection of the bladder, if encounter an anterior placenta, incise directly through it sharply.  Be careful to avoid major vessels laterally.

  7. Manually grasp and deliver fetus from uterus

  8. Clamp and cut umbilical cord and hand off infant to Peds/NICU/2nd provider

  9. Remove placenta with gentle traction.  Do not yank.  

  10. Closure depending on maternal response to resuscitation.  Closure should occur in the OR.

Remember everybody that this is all occurring during CPR!!!  Keep those compressions going throughout, but efficacy of CPR should improve if this procedure is successful.








POTD: Trauma Tuesday - Eye trauma review

Dr. Marshall's only request for POTD is that we touch on a trauma topic on the most alliterate day of the week related to trauma.  That being.... trauma Tuesday.  So here goes....

This guy comes in.  


Physical exam is key!!!

Screen Shot 2019-01-09 at 4.38.56 PM.png

Use your tool.   Use POCUS if eye is swollen shut.  Tegaderm first, lots of U/S jelly.  Is there a pupillary response to light?  Is there a consensual response?  Is the anterior chamber present?  Is the posterior chamber normal appearing (black/round/smooth throughout)?  Is there retinal detachment or vitreous hemorrhage?  What is the overall shape of the globe? (guitar pick = bad = suspicious for retrobulbar hematoma).  

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 Normal Eye U/S:


Retrobulbar Hematoma on U/S ( measure that pressure and think about clipping that lateral canthus):

Screen Shot 2019-01-09 at 4.41.21 PM.png

Traumatic ocular injuries seen in ED:

Globe rupture


Retrobulbar Hematoma

Lens dislocation

retinal detachment

corneal abrasion/ulceration

Lid Lacerations

Globe Rupture:  Prevent increased IOP (elevate HOB, avoid eye manipulation), Seidel test, cover with eye shield, pain meds, topical and systemic antibiotics and Optho consult.  

Screen Shot 2019-01-09 at 4.41.33 PM.png

Hyphema: Blood in anterior chamber, Elevate HOB, consult optho, patients at highest risk:  sicklers, trauma, bleeding diathesis, the anticoagulated

Screen Shot 2019-01-09 at 4.41.44 PM.png

Retrobulbar Hematoma:  Usually 2/2 trauma, can cause optic nerve and retinal ischemia leading to permanent blindness if untreated, A lateral canthotomy is indicated if: proptosis, decreased visual acuity or pain on EOM, afferent pupillary defect or IOP > 40 mmHG

Screen Shot 2019-01-09 at 4.41.56 PM.png
Screen Shot 2019-01-09 at 4.42.04 PM.png

Lens dislocation (aka ectopic lensis): typically 2/2 blunt trauma (less common mechanisms are electrocutions/lightning strike or in Marfan's patients.  Painful, + or - lens tremor on exam.  Emergent optho consult if elevated IOP.

Screen Shot 2019-01-09 at 4.42.15 PM.png

Retinal Detachment:  patient says they see "floaters, black dots and flashes of light." Typically acute painless vision loss.  Seen as undulated highly reflective membrane (wavy white line) on U/S.  Consult optho.

Screen Shot 2019-01-09 at 4.42.26 PM.png

Corneal Abrasion/Ulceration:  fluorescein and woods lamp.  Flip eyelid -  multiple linear abrasions often imply retained foreign body under eyelid.  Antibiotics and analgesia.  

Screen Shot 2019-01-09 at 4.42.37 PM.png

Can anyone guess what caused this corneal abrasion?!?!?

(an airbag impact on car accident)

Lid Lacerations:  What can we(as ED providers) safely repair in the ED?


POTD: When the heart fails.... congestively

Per Medscape: CHF is when "the heart, via an abnormality of cardiac function (detectable or not), fails to pump blood at a rate commensurate with the requirements of the metabolizing tissues or is able to do so only with an elevated diastolic filling pressure"

Some Generalities:

S3 = most specific exam finding (Ken-tucky, Ken-tucky)

Edema = most specific CXR finding . .

BNP : below 100 pg/ml?? -- > basically rules out CHF (90% specificity)

above 500 pg/ml? --> most likely acute decompensated CHF (87% specificity) .


Isolated left sided failure --> dyspnea, fatigue, orthopnea (WITHOUT peripheral edema or JVD).

Isolated right sided failure --> JVD, hepatojugular reflex, peripheral edema (with clear lungs sounds/CXR).

Right sided failure most common caused by left sided failure.

Systolic failure = poor contraction (low EF) and less forward blood flow

Diastolic failure = Good contractility (normal ish EF) with poor filling 2/2 stiff ventricles

NYHA Classes

  1. No symptoms

  2. Symptoms with every day activity

  3. Severely limits activity or symptoms with minimal activity

  4. Symptoms at rest

Test Pearls:

Acute CHF with STEMI on EKG --> go directly to Cath lab

Acute CHF with new systolic murmur (particular after an inferior or posterior MI) --> think Cordae Tendinae rupture --> mitral valve regurgitation 2/2 posterior leaflet of valve supplied by right coronary artery (this patient needs cardiothoracic surgery ASAP!!)

Acute CHF with syncope and/or heart murmur --> think aortic stenosis in elderly, think HOCM in the young.

Acute CHF with right sided MI --> concern for RV infarct --> fluids and/or dobutamine only if hypotensive (DO NOT TREAT LIKE TYPICAL CHF aka Nitrites and diuretics)

Acute CHF in dialysis patient with AV fistula --> think high output failure through fistula --> compress fistula site manually to decrease shunting of blood through fistula. Other types of high output failure can be seen in pregnancy, hyperthyroidism, beriberi

Obviously a tremendous topic, just scratching the surface here. Stay tuned for more POTD coming up.

Sources: In training prep video - Cardiology





Targeted Temperature Management

Targeted Temperature Management

What is it: the purposeful cooling of a patient post-cardiac arrest. Target of 32°C to 34°C (Some studies say 36, but debatable and prevent any hyperthermia) for at least 24 hours. 

Why: To improve the chance of survival and neurologic recovery, international guidelines recommend use of targeted temperature management (TTM), together with urgent coronary angiography and percutaneous coronary intervention when appropriate


  • Post cardiac arrest (any cause but most evidence supports from VF/VT shockable causes of cardiac arrest)

  • ROSC < 30 mins from team arrival

  • Time < 6 hours from ROSC

  • Patient is comatose, GCS <8 (this is try and improve neurological outcome, so someone who is neurologically intact does NOT need TTM)

  • MAP >= 65mmHg

  • depends on your hospital protocol

When: Initiate within 6 hours of ROSC and maintain for 24 hours


  • cold IVF at 2-3 mL/kg stat

  • cooling vest and cooling machine

  • sedation and paralysis



Shivering, electrolyte abnormalities, cold diuresis, infection. 


So, for post cardiac arrest patients with depressed neurological function - Keep this in mind, but consult your ICUs and plan this patient's care together for best management. TTM needs an ICU level care admission. 

Happy Learning!






And a Happy New Year of Wellness

Today's pearl will be brief and focus on Wellness. We are often super busy on our shifts and in our lives, but it doesn't take much time to stop - pause - and add a little wellness to your day. 

Here are 9 ways to have less stress in under a minute.

  1. Breathe. Take a big breath in and feel your stomach muscles relax. Hold it for a moment. Purse your lips, and blow your breath out slowly as if you are blowing out candles on a birthday cake. Feel your stomach muscles tighten as you empty your breath. Do it again 2 times or more if needed.

  2. Smile- even if you don’t feel like smiling! Smiling has been shown to decreases stress response, and even shown to lower heart rates during a stressful situation. So maybe every so often a little  "grin and bear it" can help reduce your stress!

  3. Relax your Mouth. Open your mouth, let your jaw and tongue relax, or try a jaw massage. Often times stress will lead to jaw clenching. Relaxing your jaw helps signal to your brain to reduce your stress response. 

  4. Laugh! Laughing decreased your stress levels and long-term may even boost your ability to fight sickness.

  5. Give others or yourself a hug. Hugging help reduce stress for both the giver and the receiver!

  6. Shrug your shoulders. Bring your shoulders up to your ears for a slow count of 5, then release.

  7. Exercise. Do some quick squats, jumping jacks, running in place, walk across the street to grab some tea or water, etc.

  8. Peel an orange – seriously! Then inhale the smell. Research shows that the smell of citrus relaxes people.

  9. Say Thank You. Really. Think of things you are grateful for. It is another great stress reducer! 

Wishing you a safe, happy, and healthy New Year!



Simply Smiling Can Actually Reduce Stress | Science | Smithsonianwww.smithsonianmag.comA new study indicates that the mere act of smiling can help us deal with stressful situations more easily



Do you see what eye see?

Do you see what eye see?

Eye complaints can be abundant in the ED - so what should we focus on? Today's pearl is going to focus on the diagnoses of atraumatic vision loss.

Let's break it down by symptoms: Painless or painful?

Good physical exam must include: visual acuity, visual fields, pupillary exam, fluorescein woods lamp, slit lamp and of course - a head to toe complete physical exam. 

Painless Vision Loss: 

  1. TIA/stroke: sudden vision loss usually from embolic or thrombotic event, can often be from carotid artery occlusion. If transient, often called amaurosis fugax but that can apply to any cause of transient vision loss. Risk factors: it is a stroke/TIA of the eye, so same cardiovascular risk factors. Testing: MRI, ECG, Echo, Carotid US. ED role: Don't miss it - this is a stroke and should admitted to a monitored stroke unit.

2. Central retinal artery occlusion: Sudden, permanent typically unilateral vision loss (permanent damage ~90 minutes of occlusion). Risk factors: atherosclerosisdisease (HTN, DM, Smoking, etc.) and treatment involves treating risk factors (varied success with laser treatment of pressure decreasing eye drops); or secondary to Giant cell arteritis (+/- headache, pain with hair burshing or chewing)  in which case rapid high dose corticosteroids can prevent vision loss. PE: decreased visual acuity, asymmetric red reflex, "Cherry red spot" on the macula on fundoscopy. ED role: urgent/emergent optho referral or ED consult. Recognize if cause is giant cell arteritis (CRP, ESR) and treat with high dose steroids. Consider timolol 0.5% topical drops but no strong evidence. Will need PCP to address concurrent risk factors. 

3. Central retinal vein occlusion: often times sudden but occasional gradual (days-weeks) vision loss due to swelling of the macula. Risk factors: same as above and glaucoma. Think of this as a DVT for the eye. PE: decreased visual acuity. "Blood and thunder" on fundoscopy. ED role: Evaluate for cause or presence of other pathologies secondary to a hypercoagulable state (DVT, PE, sickle cell, etc.). Refer to optho and will need PCP to address concurrent risk factors. 

retinal vein occlusion image-full.png

4. Retinal Detachment: Sudden, spontaneous "flasher and floaters" or "spots or stars" or loss of vision that is like a "curtain closing." Usually loss of peripheral vision. Risk factors: recent eye injury or surgery, severe nearsightedness (think elderly). ED Role: POCUS - look for a delicate floating line in the anechoic eyeball space. If their is no macular separation, their vision can be saved! This is an optho emergency. Unless you're Errel, err on the side of caution and call optho for all of these since we might not be able to definitively determine if the macula is involved.

5. Vitreous Hemorrhage and Posterior Vitreous Detachment: Floaters, strings, or cobwebs in their vision that change with eye movement. Flashes of light. Risk factors: retinal damage (surgery, trauma, prior retinal tear), Diabetic Retinopathy, trauma, sickle. ED role: POCUS: swirling cloud-like opacity at moves with ocular movement and is not tethered to the optic disk or retina "washing machine sign". ED role: Avoid Anticoagulation, elevate head of bed, optho referral.

6. Optic Neuritis/papillitis: painless vision loss over hours to days, typically unilateral. +/- prior episodes. +/- other neuro symptoms. May worsen with eye movement. Risk factors: typically females 18-45, multiple sclerosis. Viral: mono, zoster, encephalitis, TB. Physical exam: decreased acuity, relative afferent pupil defect, often normal fundoscopy; requires complete neuro exam. ED role: MRI brain. Diagnose underlying cause. Often required admission for continued IV high dose steroids. 

Painful Vision Loss:

1. Acute angle glaucoma: sudden, usually form bright to dark environment (movie theater). Often with headache, N/V, and light sensitivity/halos. PE: midsize, nonreactive pupil. Must include tonometry, IOP>20! Risk factors: Asian, femaile, shallow anterior chamber. ED role: timolol  0.05% 1-2 drops (beta blocker, watch for systemic absorption SE) eye drops and brimonidine (alpha agonist) eye drops to reduce IOP. Miotic agent pilocarpine (2-4% 1-2 drops q15 m). Titrate until symptoms improve, IOP decreases. Systemic carbonic anhydrase inhibitors like acetazolamide 500 mg IV. Elevate head of bed. Treat nausea and headache, too! Urgent optho referral.

2. Corneal Ulcer: foreign body sensation, red eye. PE: injected conjunctiva, gray patch on cornea. Increased fluorescein uptake on Woods lamp. Possible hypopyon purulent collection. ED role: Evaluate for foreign body. Consider HSV keratitis. Start opthalmic antibiotic drops, must have pseudomonas coverage for contact lens wearers (tobramycin), consider antifungal. **Admit for IV ceftriaxone for suspected gonococcal infection. Will need optho evaluation and ulcer culture. 


3. Uveitis/Iritis: painful, progressing red eye worse with eye movement, +photophobia suggests anterior. Floaters suggests posterior, often no pain. Can be panuveitis. Causes can be inflammatory (HLA B-27 usually bilateral, eg. reactive arthritic, psoriasis, IBD, ankylosing spondylitis; sarcoid, Kawasaki), traumatic, infectious (toxoplasmosis, CMV, HSV, adeno, measles, mumps, TB, syphilis, Lyme), or secondary to medications(sulfa). PE: injected conjunctiva with ciliary flush (erythema around the iris). Sluggish, constricted, or irregular pupils. Slit lamp shows cloudy anterior chamber and "cell and flare." ED role: evaluate for underlying cause (STD screen, CXR for TB, etc.) and refer to optho urgently and appropriate f/u. 

I am certain that this is not a comprehensive list, so please - learn on!

Buzzword pearls to part with: 


Holy smokes! Inhalation Injury

First steps (stable pt)
-treat as a trauma pt (ABCDE) and look for traumatic injuries
-place pt on NRB with O2 to 15 L/m
—add nebs 4% lidocaine early to prepare for visualization of cords with videolargynoscope
4:2:1 rule for burn pt fluid resuscitation
—give fluids even if no external burns visible, as pt will have insensible losses
-treat pain!
-evaluate cords and surrounding laryngeal structures for edema with video laryngoscope or bronch

How to risk-stratify your patient with suspected smoke inhalation injury:

Screen Shot 2018-12-27 at 12.04.46 PM.png

Rule out
carbon monoxide toxicity: obtain serial blood gases (send co-oximetry) to monitor carboxyHb. Normal levels are 5 – 12%, depending on whether or not the pt is a smoker. Also consider if family presents with similar vague symptoms.
-cyanide toxicity: cyanide levels are not reliable in excluding toxicity, as it is rapidly cleared, and don’t result for days. Use lactate>8 or rising lactate despite fluid resuscitation to raise suspicion for toxicity
—ddx for elevated lactate (=impaired tissue oxygenation) in burn pt: cyanide, metHb, hypoxia, volume depletion
-look for rhabdo and AKI

Warning signs of respiratory failure
drooling or difficulty swallowing = impending failure
-monitor for stridor, hoarseness, and respiratory distress
-PaO2/FiO2 ratio indicates degree of pulmonary shunting past injured lung. PaO2/FiO2<300 forewarns respiratory failure

-early elective intubation in a controlled setting is better than crash intubation of a pt with edematous airway structures
-Prepare multiple sizes ETTs in anticipation of vocal cord edema. Use the largest that will fit so that the pt can get a bronchoscopy upstairs. Prepare suction for soot-filled secretions. Sux is safe to use up to 24h post-burn.
-use volume controlled ARDS settings (6-8 mL/kg TV)
—airways and lung become less compliant in inhalational injury, so must prevent barotrauma and allow for permissive hypercapnea


When your Nose Knows Best

A new sick patient rolls into the busy Emergency Department, satting in the low 80s. As you prepare for a likely intubation, you appropriately assess your patient and see

download (22).jpeg



Hopes at bagging this patient's O2 sat up for pre-oxygenation start to dwindle as quickly as your fit summer body over the holiday winter season.

If only there was another way... but wait! Rudolph isn't the only nose that can be useful this holiday season!

Nasal trumpet for ambu bagging:

1. Collect Supplies: nasal trumpet, 6.0 ETT, ambu bag and access to oxygen. 

2. Separate ETT connector from ETT.


3. Connect ETT Connector to Nasal Trumpet


4. Connect joined ETT Connector-Nasal Trumpet to your ambu bag attached to the high flow oxygen (>>15 L/min, crank it all the way on)


 5. Place into patient's nasopharynx, seal patient's mouth, and bag!


Thanks to Anya for her photography skills!
As always, comments, feedback and input appreciated!

Happy airways and holidays to all! 



Dr. David Saloum's clinical teaching (even though he was not aware that this would be become today's pearl - thanks anyway!)


Fancier double trumpet anesthesia option article: http://anesthesiology.pubs.asahq.org/article.aspx?articleid=2492128

Blunt Cardiac Injury Guidelines

To trop or not to trop? Here's a brief review of the 2012 EAST trauma guidelines for BCI. 

What is BCI, anyway?

Describes a range of injuries due to blunt thoracic trauma: wall motion abnormalities, myocardial contusion, valve injuries, focal wall dilation, coronary injury, pericardial rupture, wall rupture

Right heart most commonly affected as it is most anterior.

Who to work up?

According to 2012 East guidelines: “patients with any significant blunt trauma toanterior chest should be screened.”

Also consider BCI in patients with persistent unexplained tachycardia, cardiogenic shock, or hypotension not explained by other injuries.

Now that I suspect BCI, what should I do?


Screening consists of an EKG (Level 1 evidence) and a troponin (Level 3 evidence). Early studies suggested that EKG alone is sufficient to diagnose BCI, however multiple studies since then show that such an approach does not capture the small percentage of BCI patients that present with normal initial EKG and positive troponin. 

A normal EKG and troponin rules out BCI (even in the setting of a sternal fracture, which is not predictive of BCI). Several studies show that the addition of troponin raises the NPV to 100%. Same screening approach is supported for pediatric pts.

Management & Disposition: 

Management is supportive; severe trauma may require surgical repair. 

Patients who have a new abnormality on EKG (arrhythmias, ST changes, heart block, PACs or PVCs, ischemic changes, etc) must be admitted to a telemetry floor for continuous monitoring. 

A new dysrhythmia or hemodynamic instability warrants an echo, preferably TEE over TTE.

Note that degree or persistence of elevation of troponin does not correlate with prognosis.

The chicken or the egg…did an MI precede the MVA or is it BCI?

It is important to differentiate which patients need cath with anticoagulation and which patients would be harmed from it. Can be differentiated via ekg-gated CT angiocoronaries.

Read more at:


It's getting hot in here - Pediatric Fevers

So, it's winter. Kids get sick. But really, 8-10 times a year is normal, so they're sick all the time! And they present to the ED with FEVER!!!!

What do you think about and what do you do with FEVER!?!?!?

- Fever = 38 degrees Celsius or 100.4 Fahrenheit

- Subjective fever per parents? Believe and work up/treat appropriately based on clinical presentation

- Determine exact onset and calculate fever duration (if since last night, it is only 1 day since <24 hours)

- Ask T-max
Thorough exams must include throat, ears, skin, oropharynx!

If suspect infectious etiology, treat with antipyretics:

Acetaminophen: 15 mg/kg every 4 hours, PRN

Ibuprofen (6 months and older): 10 mg/kg every 6 hours, PRN

The "alternating" approach of treating every 3 hours (Acetaminophen at 9, Ibuprofen at 12, Acet. at 3, etc) can help keep the kiddos' fever under control and keep them happy, hydrated, and hopefully home!

What to do!?

0-28 days infant: 

Orders: CBC with differential, Blood Culture, BMP, UA with culture, LP with CSF gram stain/cell count/culture/possible viral culture. +/- HSV PCR. +/- stool culture if presenting with diarrhea. CXR

Pathogens: Group B Strep, E. Coli, Listeria. Consider HSV

Treatment: Ceftazidime or cefotaxime + Ampicillin (for Listeria). or Gentamycin + Ampicillin. +/- Acyclovir (< 21 days, seizures, rash, mom w/ lesions)

**No ceftriaxone: ceftriaxone displaced bilirubin and places patient at increased risk for Kernicterus 

Dispo: Admit

29-60 days Infant: 

Similar to above, but more experienced pediatric clinicians may use clinical judgement regarding LP. In general, most general EM physicians should practice more conservative management and pursue LP. 

*Philadelphia/Rochester/Boston criteria for infants vary, hence the debate.*

Orders: CBC with differential, Blood Culture, BMP, UA with culture, LP with CSF gram stain/cell count/culture/possible viral culture. +/- HSV PCR. +/- stool culture if presenting with diarrhea. +/- CXR if respiratory symptoms. 

Treatment: Ceftazidime or cefotaxime + Ampicillin or Ceftriaxone. Skin infection: +vancomycin

Dispo: often admit, but again, clinical judgement. If you diagnose a UTI in a well appearing, eating infant and labs are normal WBCs, no bandemia, normal CSF, consider 1 dose of ceftriaxone and 24 hour follow up (be mindful of patient's family's education, access to healthcare/the hospital, reliability, health literacy, etc.). Do what is best for the patient. See reference from CHOP for an example:  https://www.chop.edu/clinical-pathway/febrile-infant-emergent-evaluation-clinical-pathway. Again - do what is best for the patient and appropriate for your level of pediatric training/experience. 

Acute Otitis Media: 

Bacteria: Strep pneumo (~80%), H. flu (especially if unvaccinated), Moraxella

Treatment: high dose Amoxicillin 90 mg/kg per day divided into 2 doses (to overcome strep pneumo's penicillin binding protein and H. flu's beta lactamase). If resistant, Augmentin (dose based off the amoxicillin) 


Most common pathogens: 

< 3 weeks: E. coli, Group B Strep, Listeria

> 3 weeks: Strep pneumonia



RSV/Bronchiolitis: Usually < 2 years old. Supportive care, often HFNC. Babies < 6 months are high risk and give good return precautions if child is well enough to go home.

Influenza: keep in mind children < 5 are all high risk, but children < 2 are at greatest risk. 

Treat with oseltamivir, even if after 48 hours for high-risk patients (young, immunosuppressed, asthmatic, renal disease, DM, neuromuscular disease, pregnant, long term care facilities). 

Oseltamivir dosing is BID for 5 days: <1 year old: 3 mg/kg. >1 year old and 15 kg or less: 30 mg. 

15-23 kg: 45 mg.  23-40 kg: 60 mg. > 40 kg: 75 mg.

Group A Strep Throat: Under 3 years old, do not develop Rheumatic heart disease so often do not require antibiotic treatments

Treatment: Low dose Amoxicillin. 45 mg/kg divided into 2 doses. 

Pyogenic Joint Infection: Most common age group is < 3 years old. 

Pathogen: Staph aureus is the most common pathogen and often with preceding trauma or URI

Treatment: Need ortho consult and include MRSA antibiotic coverage



Harriet Lane - the whole book is a reference gem, but looked up each topic


Don't be Rash about Deadly Rashes

So, let's talk about why you went into Emergency Medicine - to talk about rashes, of course! Although you might not always (or rarely?!?) know the exact etiology of the rash, there are some Can't-Miss life threatening rashes that we must be able to recognize in the ED. And rashes account for 5% of all ED visits, so you should be diligent to identify these dangerous diagnoses. 

First things first: Describe the rash 

rash pics.png

Pertinent points on managing rashes: 

- STOP IT! Stop the offending agent. Known drugs that induce SJS-TEN include sulfa drugs, penicillin, barbituric acids, aspirins, pyrazolone drugs, and anticonvulsants.

- Rashes can be like a BURN, resulting in abnormal fluid balance, thermoregulation, infection control, and electrolytes. Treat appropriately!

- Treat their PAIN (Make Motov proud!) 

- Sepsis management (Make Dickman proud!). If underlying pathology is infectious, treat early and treat appropriately

- Utilize consultants, the sooner the better! Necrotizing infections - surgery. Toxic rashes - Dermatology. ICU and Burn Centers should be on board!

- Steroids??? WAIT  -  let Dermatology/Burn Center/ICU determine the disease pathology so that steroids will not be given that may cause more harm (SJS/Tens) than good. 

There's so much information, but this is just a rough guideline. Remember to rule out life threatening rashes before sending your patient home. 

You have to determine the TYPE of rash. The algorithm divides the rashes into 6 types: Maculopapular, Petechial/Purpura, Diffuse Erythematous, Non-erythematous, Vesiculo-bullous, Pustular. 

Then branch each type of the 6 rashes into the life threatening etiologies. 


Keep in mind that this list is not comprehensive, but a guideline to help identify life threatening rash. If the patient looks ill, be concerned. 

Once you identify a life threatening rash, be aggressive and manage appropriately (too many points to address here.) Again, just a guide to look for the DANGEROUS RASHES!. Please see the original reference article attached!






Add Adenosine to the Flush

You have a patient in SVT, failed vagal maneuvers. Time to treat with adenosine. 

You all know this cute little three-way stop cock. Seems simple enough. That is until you need to use it... the stop and go seems somehow far more confusing than it really is.


And the one time you MUST know how to use it is to rapidly administer adenosine. You need access in the antecubital or proximal upper extremity.

Why the rush? Adenosine is rapidly metabolized by erythrocytes and vascular endothelial cells - so with its 10 second half-life, we have to administer and flush it quickly so it can reach the heart. 

Surely, there has to be an easier way! Well, folks. There is!

Make sure you have your ECG rhythm strip running, zoll pads on the patient, and explain the patient that this might "feel funny"  (as their heart stops for just a wee bit). 

  • Grab a 20-mL (or 30-mL) syringe.

  • Desired dose of Adenosine (6 mg or 12 mg)

  • Draw up the adenosine AND the normal saline in the same 20-mL syringe.

  • Administer via fast IV push

That's it! 

Adenosine is safe and maintains its effectiveness mixed with normal saline. One study even used OI access for conversion of SVT in an infant. 

Only have central access (hemodialysis port, central line)??? Per 2010 ACLS guidelines drop the dosing: 

  • 1st dose: 3 mg (instead of 6)

  • 2nd/3rd doses: 6 mg (instead of 12)

This lower dosing minimized risks of prolonged bradycardia. ALSO - use this lower dosing if the patient is taking dipyridamole or carbamazepine as these two medications potentiate the effects of adenosine.


J Korean Soc Emerg Med. 2003 Aug;14(3):224-227 


Weberding NT, et al. Adenosine Administration With Stopcock Technique Delivers Lower-Than-Intended Drug Doses. Ann Emerg Med 2018;71(2):220-4.