POTD: Complications of Blood Transfusion

>> Hemolytic:

  • Acute Intravascular Hemolytic Reaction

    • Overview:

      • Occurs when recipient's antibodies recognize and induce hemolysis of donor's RBCs

        • Most of the transfused cells are destroyed, which may result in activation of the coagulation system, DIC, and release of anaphylatoxins and other vasoactive amines

      • Caused by ABO incompatibility; usually the result of technical errors

      • Risk is 1 to 4 per million units transfused

      • Serum haptoglobin will be decreased, serum lactate dehydrogenase will be elevated, and direct antigen (Coombs) test usually will be positive

    • Signs/Symptoms: Fever, chills, low back pain, flushing, dyspnea, tachycardia, shock, hemoglobinuria

    • Management:

      • Immediately stop transfusion

      • IV hydration to maintain diuresis; diuretics may be necessary

      • Cardiorespiratory support as indicated

    • Evaluation:

      • Retype and repeat cross-match

      • Direct and indirect Coombs test

      • CBC, creatinine, prothrombin time, activated partial thromboplastin time

      • Haptoglobin, indirect bilirubin, lactate dehydrogenase, plasma free hemoglobin

      • Urine for hemoglobin

  • Delayed Extravascular Hemolytic Reaction

    • Often have low-grade fever but may be entirely asymptomatic

    • Usually presents days to weeks after transfusion

    • More common than intravascular hemolytic reaction; rarely causes clinical instability

    • Hemolysis most commonly occurs in the spleen and occasionally in liver and bone marrow

    • Requires hemolytic workup as above to investigate the possibility of intravascular hemolysis

      • May be identified by a positive Coombs test, elevated unconjugated (indirect) bilirubin level, and less than expected increase in hemoglobin from the transfusion

>> Febrile:

  • Overview:

    • Characterized by fever during or within a few hours of a blood transfusion

    • Quite common => occurs in approximately 1 per 300 units of PRBCs infused 

    • Most common in multiparous women or multiply transfused patients (pts who have been exposed to foreign blood antigens)

    • For patients with recurrent febrile reactions, use of leukocyte-reduced blood products may be helpful

  • Signs/Symptoms: Fever, chills

  • Management:

    • Stop transfusion

    • Initially manage as intravascular hemolytic reaction because one cannot reliably distinguish between the two

    • Can treat fever and chills with Acetaminophen

    • Consider infectious workup

  • Evaluation:

    • Hemolytic workup as above

>> Allergic:

  • Overview:

    • Caused by an immune response to transfused plasma proteins

    • Pts with immunoglobulin A deficiency may experience severe anaphylactic reactions due to presence of immunoglobulin A in donor products

      • Washing the plasma from the RBCs minimizes this type of reaction

  • Signs/Symptoms: 

    • Mild: urticaria, pruritus

    • Severe: anaphylaxis => dyspnea, bronchospasm, hypotension, tachycardia, shock

  • Management:

    • Stop transfusion

    • If mild, reaction can be treated with Diphenhydramine; if symptoms resolve, can resume transfusion

    • If severe, may require cardiopulmonary support; do not restart transfusion

  • Evaluation:

    • For mild symptoms that resolve with Diphenhydramine, no further workup is necessary

    • For severe reaction, do hemolytic workup because initially may be indistinguishable from a hemolytic reaction

>> Infectious:

  • HIV-1: 1 per 6 million units transfused

  • HIV-2: Unknown, but extremely low

  • Human T-cell Lymphotropic Virus Types 1 and 2: 1 per 640,000 units transfused

  • Hepatitis B: 1 per 1 million units transfused

  • Hepatitis C: 1 per 100 million units transfused

  • Parvovirus B19: 1 per 10,000 units transfused

  • Note: Blood is not tested routinely for CMV unless recipient is seronegative AND either pregnant, a potential or present transplant candidate, immunocompromised, or a premature infant

    • Leukocyte-reduced blood components further decrease the risk of CMV transmission to susceptible populations because most of the virus resides in leukocytes

>> Transfusion Related Acute Lung Injury:

  • Thought to be due to granulocyte recruitment and degranulation within the lung

  • Usually a complication of fresh frozen plasma or platelet transfusion; rare after PRBC transfusion alone

  • Presents with respiratory distress and bilateral pulmonary infiltrates due to noncardiogenic pulmonary edema, during or within 6 hours of transfusion

  • Often self-limiting and resolves spontaneously with supportive care

>> Other:

  • Hypervolemia

    • Rapid volume expansion may occur leading to transfusion-associated cardiovascular overload

    • Pts with limited cardiovascular reserve (infants, severe chronic anemia, elderly) => highest risk

  • Electrolyte Imbalance

    • Hypocalcemia, hypokalemia or hyperkalemia rarely occur

    • The anticoagulant citrate is a component of many blood preservatives and chelates calcium

      • Pts with normal hepatic function metabolize the citrate to bicarbonate

    • Rarely, hepatic metabolism is overwhelmed; hypocalcemia can develop and/or the excess bicarbonate generated causes alkalemia, driving potassium into cells and causing hypokalemia

    • Potassium content in stored blood products increases during storage; uncommonly, pts with renal insufficiency or neonates can develop hyperkalemia


POTD: Painless Visual Loss


  • CRAO: Occlusion of the main artery that supplies the retina or its branches (BRAO); typically due to an embolus from proximal atherosclerotic disease

  • CRVO: Occlusion of the main veins draining the retina; results in secondary hemorrhage and ischemia

Risk Factors: Older age, Vasculopathy


  • Sudden painless monocular vision loss or partial loss

  • Can be transient, stuttering, or permanent


  • Classic fundoscopy findings of CRAO: pale retina with a cherry red spot over the macula as a result of ischemia and edema

  • Classic fundoscopic finding of CRVO: blood and thunder

  • Fundoscopic findings may be subtle in:

    • Pts who present early

    • Pts with intermittent symptoms

    • Pts with branched retinal artery occlusions (BRAO)


  • Most therapies that have been studied are not very effective

  • Eyeball massage and globe paracentesis are sometimes used for CRAO

  • Intra-arterial tPA has also been used for CRAO

>> Retinal Detachment


  • May occur as a result of trauma, but the majority of cases are spontaneous

  • Typically preceded by posterior vitreous detachment (PVD)

    • As the vitreous humor dehydrates and shrinks with age, it can detach from retina

    • The resulting traction on the retina then puts the pt at risk for retinal detachment 

  • The symptoms of PVD are primarily floaters and flashers

  • Most cases of PVD are self-limited

    • However, the risk of progression to retinal detachment is high in the days and weeks following the initial symptoms

  • Can be difficult to distinguish PVD from early retinal detachment!

    • Unless symptoms are chronic and unchanging, consider retinal detachment when pts present acutely with flashers and floaters

Risk factors: Older age, Severe myopia (nearsightedness), Glaucoma, Cataract surgery, Diabetic retinopathy


  • Early warning sign is acute onset of flashers and floaters

  • Curtains moving across visual field

  • Visual field cuts

  • Painless monocular vision loss


  • Visual acuity may be completely normal if early; it is important to test visual fields

  • An advanced detachment can be seen with direct fundoscopy


  • Macula on: vision is preserved; emergent surgery may halt progression and preserve vision

  • Macula off (the macula has detached): severe vision loss in central visual field

  • Presumed retinal detachment requires emergent Ophthalmologic evaluation to preserve the pt's vision!

>> Vitreous Hemorrhage

Risk factors: Diabetes, Hypertension, Vasculopathy


  • Sudden or staggered loss of monocular vision

  • May present similarly to PVD or RD

  • May also present as blurry vision


  • Decreased red reflex; may be difficult to see fundus

  • Ultrasound is very effective at identifying blood in the vitreous!


  • Pts may follow up urgently in Ophthalmology clinic for treatment

  • Return precautions for worsening symptoms/pain

  • Anticoagulation is generally not discontinued


POTD: Painful Visual Loss

>> Acute Angle Closure Glaucoma


  • Extremely painful (deep, boring pain); frequently associated with vomiting


  • A red, angry appearing eye, firm to touch

  • Cloudy “steamy” cornea

  • Decreased visual acuity (may be profound)

  • Markedly elevated IOP (generally > 40 mm Hg)


  • Treat pain and give antiemetic

  • Consult Ophthalmologist emergently

  • Carbonic anhydrase inhibitors - Acetazolamide

  • Topical beta blockers - Timolol

  • Mannitol or Glycerol IV

  • Alpha agonist drops - Apraclonidine

  • Definitive therapy is surgical; involves laser iridectomy

>> Optic Neuritis

Causes: Multiple sclerosis (1/3 of patients with optic neuritis will develop MS), Other causes - idiopathic, infections (syphilis, measles, TB, crypto, etc), and autoimmune diseases


  • Painful monocular vision loss

  • Pain behind eye and with eye movements 


  • Loss of central vision; peripheral vision is preserved

  • Afferent pupillary defect (APD)

    • Anything that affects the optic nerve will cause an APD

    • Not specific to optic neuritis; may occur in any condition where light cannot reach the retina

  • Red desaturation test

    • Take a dark red item and have the patient look at it covering one eye and then the other

    • Affected eye will see it as lighter red or pink


  • Consultation with Ophthalmology and Neurology are both appropriate

  • MR brain looking for plaques of MS

  • Admit for IV steroids (Methylprednisolone); very high doses are used

>> Giant Cell Arteritis


  • Painful monocular vision loss

  • May have headache, especially over the temporal areas

  • Strong association with Polymyalgia Rheumatica (painful chronic condition in older patients causing fatigue and muscle pain)

  • Jaw claudication (aching pain with chewing) is an important clue


  • Palpate and inspect area near temporal arteries for tenderness and nodularity


  • Patients with any visual loss should be admitted for IV steroids

    • Methylprednisone 0.5-1 gm daily x 3 days (similar to optic neuritis or MS)

  • If no vision loss, you can start Prednisone 1 mg/kg PO

  • ESR should be draw; temporal artery biopsy should then be performed in the next week to confirm diagnosis


POTD: Ultrasound Guided Transversus Abdominis Plane (TAP) Block

>> What is it?

  • A well-established regional anesthetic block used for perioperative pain control of the anterior abdominal wall

  • Will block innervation to anterior cutaneous branches of T10 to L1 (grayed area Figure 1)

>> Block Volume: 20 - 30 mL

>> Uses in ED: Appendicitis

>> Probe Placement:

  • Transverse orientation above the iliac crest at the mid- to anterior-axillary line (Figures 2) so that the external oblique, internal oblique, and transversus abdominis muscle layers are easily visualized (Figure 3) 

>> Approach and Needle Trajectory:

  • Place your patient supine and exposed from the inferior costal margin to the iliac crest

  • Place the needle in-plane (enter medial to lateral/posterior) and advance until the needle reaches the interfascial plane between the internal oblique and transverse abdominis muscles

  • Inject anesthetic. Deposition can be confirmed by visualization of anechoic fluid tracking between the internal oblique and transverse abdominis muscles (Figure 3)

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Figure 1: Surface landmarks that should be palpated include the inferior costal margin and the iliac crest.

Figure 1: Surface landmarks that should be palpated include the inferior costal margin and the iliac crest.

Figure 2: Place the ultrasound transducer between the inferior costal margin and iliac crest. The probe marker should point lateral/posterior.

Figure 2: Place the ultrasound transducer between the inferior costal margin and iliac crest. The probe marker should point lateral/posterior.

Figure 3: Note the external oblique, internal oblique, and transverse abdominis muscles on the ultrasound screen. The goal is to deposit anesthetic in the potential space just above the transverse abdominis muscle and just below the internal oblique muscle.

Figure 3: Note the external oblique, internal oblique, and transverse abdominis muscles on the ultrasound screen. The goal is to deposit anesthetic in the potential space just above the transverse abdominis muscle and just below the internal oblique muscle.

Figure 4: An ultrasound representation demonstrating where anesthetic should be placed when performing a TAP block.

Figure 4: An ultrasound representation demonstrating where anesthetic should be placed when performing a TAP block.


POTD: Peri Partum Cardiomyopathy

>> Definition:

  • Development of HF toward the end of pregnancy (last month) or within 5 months following delivery

  • LV systolic dysfunction with an LVEF < 45%

>> High incidence of PPCM in Haitian (1:300) and Nigerian (1:100) women

>> High incidence in Nigeria may be related to a local custom of eating Kanwa, a dry lake salt for 40 days after delivery.

>> It has been suggested that the development of PPCM in these patients may be related in part to hypervolemia and hypertension.

>> Risk Factors:

  • Age greater than 30 years

  • African descent

  • Multiple gestation pregnancy

  • Hx of preeclampsia, eclampsia, or postpartum hypertension

  • Maternal cocaine abuse

  • Long-term (>4 weeks) oral tocolytic therapy with β-adrenergic agonists such as Terbutaline

>> Management Considerations:

  • Women with HF during pregnancy should be treated similarly to other patients with HF. 

  • Diuretics: Both HCTZ and Furosemide are safe during pregnancy and lactation.

  • β blockers: Although safe during pregnancy, β1-selective blockers are preferred over nonselective β-blockers to avoid anti-tocolytic action induced by β2-receptor blockade.

  • ACE-I/ARB: Improve survival but are contraindicated in pregnancy.

    • Also, since they are secreted in breast milk, breastfeeding must be stopped before starting therapy.

  • In the setting of atrial fibrillation (most common arrhythmia in patients with PPCM):

    • Rhythm control (all safe during pregnancy): Digoxin, Procainamide, Quinidine.

    • Refractory atrial fibrillation requires placement of permanent pacemakers and implantable cardioverter-defibrillators.

    • REMEMBER: Warfarin is teratogenic

>> Prognosis:

  • Death due to PPCM is usually caused by progressive pump failure, sudden death, or thromboembolic events.

  • A subset of patients with PPCM will achieve full recovery of LV function (LVEF > 50%).

    • However, LV dysfunction can re-occur despite initial full recovery.

  • Women with PPCM and persistent LV dysfunction or LVEF ≤ 25% at diagnosis are at high risk for recurrent PPCM.

    • The recommendation in this case is to avoid future pregnancies.

  • Since up to 20 to 60% of women with PPCM have complete recovery of LVEF by 6 months to 5 years, ICD placement should be deferred at least 3 months following presentation.

  • Patients with PPCM are at high risk for thrombus formation and thromboembolism due to both the hypercoagulable state of pregnancy and stasis of blood due to severe LV dysfunction.

    • Still, there is no consensus on prophylactic AC.

      • General recommendation to start AC for EF < 30% or in setting of atrial fibrillation.

  • Notes regarding contraception:

    • Estrogen-Progestin contraceptives (e.g., pills, patch, vaginal ring) may increase fluid retention, which may worsen HF.

    • In general, Estrogen-Progestin contraceptives should be avoided, particularly early after diagnosis and in women with persistent LV dysfunction due to increased risk of thromboembolism.


POTD: critical appraisal: decision rules for the use of radiography in acute ankle injuries

 ·   · 

stiell i, et al


march 3, 1993

2 university emergency rooms

ottawa and toronto, canada

ankle xrays.

it matters! ankle pain is one of the most common ED complaints!

...and only 15% of those getting xrays are POSITIVE

the study validated and refined previously derived clinical decision rules


stage I

validate and refine the original rules

stage II

validate the refined rules


n (stage I) = 1032 of 1130 available patients

n (stage II) = 453 of 530 available patients

stage I: original rules: 

sensitivity: 1.0 (95% CI, 0.97 to 1.0) for detecting 121 malleolar zone fx & 0.98 (95% CI, 0.88 to 1.0) for detecting 49 midfoot zone fx

stage II: refined rules:

sensitivity: 1.0 (95% CI, 0.93 to 1.0) for detecting 50 malleolar zone fx & 1.0 (95% CI, 0.83 to 1.0) for detecting 19 midfoot zone fx

refined ottawa rules -->

100% sensitive for fractures & 30% decrease in unnecessary xrays


POTD: stemi equivalents -- when to call the cath lab

1. ppm/LBBB + unstable/sgarbossa

ppm = percuatenous pacemaker (LBBB morphology + pacer spikes)


LBBB = left bundle branch block (widened QRS >120ms)


sgarbossa criteria (inappropriate concordance)


modified smith criteria (excessive discordance)


2. VR st elevation

left main artery occlusion

VR st elevation >1mm


3. deWinters

proximal left anterior descending artery occlusion

precordial lead st depression + hyperacute t waves

4. posterior MI

right coronary artery occlusion (90%)

left coronary artery occlusion (10%)

V1-3 st depression

5. out-of-hospital cardiac arrest WITHOUT unfavorable features

unfavorable features = 

traumatic arrest

unwitnessed arrest

unwitnessed cpr


>30min ROSC

pH <7.2 | lactate >7 | age >85yr

credits: UptoDate | RebelEM | WikEM | Google images


POTD: Pulmonary Embolism Decision Rules - Beyond the Basics

Screen Shot 2019-04-26 at 6.26.05 PM.png

Special thanks to Dr. Errel Khordipour for giving this amazing review and Dr. Anna Bona for taking meticulous notes during this talk!


  • PE carries an 8% 30-day mortality after diagnosis (some studies higher)

  • CTA has a very high false positive rate

  • Step 1: based on the patient's history and presentation, do you think the patient has a PE? If yes, proceed. If no, STOP

    • Read more below for nuances re: features that makes a patient risky for PE

  • Step 2: Using your clinical decision rules (Well's, Geneva, or clinical gestalt), is the patient low, medium, or high risk?

    • Low risk: PERC

    • Medium: D-dimer --> then CTA if positive

      • Age adjust your d-dimer if possible

    • High Risk: CTA

  • Step 3: Treat! (or don't treat!)

    • Unstable --> tPA and MICU

    • Stable --> get labs, echo

      • Labs abnormal or echo w/ RV strain --> heparin +/- half-tPA

      • Labs/echo normal --> determine the pt's PESI score

        • High --> heparin

        • Low --> lovenox and discharge

  • Subsegmental PEs in patients < 50 with stable vitals have a very low risk of adverse outcome

    • May consider discharging without anticoagulation if no DVT is present and there are no risk factors for recurrence

  • If the study is inadequate, refer to the d-dimer

    • If d-dimer positive, get bilateral lower extremity dopplers

      • Discharge if negative

      • If positive, consider anticoagulation based on risk factors and labs and f/u with PMD for repeat doppler in 3-7 days. 

Interested? Let's get more specific!

Let’s consider a patient that rolls into your emergency department. They’re complaining of chest pain and shortness of breath. You’re working with a medical student and they list pulmonary embolism as a differential diagnosis. How do we risk stratify our patients using our decision making tools.

First off, why do we care? First off, PE is a very much-feared missed diagnosis, which carries an 8% 30-day mortality** after diagnosis (this was much lower than I expected, to put this into context, hemorrhagic strokes carry a 25-40% mortality depending on your source and hip fractures carry a 4-10% mortality rate depending on your source).

**some studies show a 30% mortality, however those were autopsy studies, so it is unknown whether the patients died with a PE or as a result of a PE.

That being said, our testing methods are very much imperfect! The false positive rate on CTA for segmental PE is 25% and even scarier, the false positive rate for subsegmental PEs is 60%!! Not a great test! Plus, a CTA is not a benign test. Contrast can cause anaphylactoid reactions and lifetime risk of malignancy increases with each CT. Plus, once a patient is labeled as having a PE (even subsegmental), they’re much more likely to get scanned in the future.

So let’s talk about how we can determine who is high risk and who is low risk.

Screen Shot 2019-04-26 at 6.47.06 PM.png

Step 1: Consider the patient’s presentation and history

Vital signs:

Screen Shot 2019-04-27 at 6.00.56 PM.png

Risk Factors

Prior VTE (PE/DVT): Was the last PE/DVT unprovoked or provoked? More concerning if the last PE/DVT was unprovoked (e.g. the patient was not immobilized for a long period of time). This does not change if testing for hypercoagulability was negative. If provoked, this is less concerning.

Malignancy History: Higher risk with active cancer. This either means active treatment within the last 6 months or metastatic disease. Chemotherapy patients are also more at risk. Not all malignancies are created equal, though! Your risk is even higher with pancreatic cancer, multiple myeloma, colon cancer, glioblastoma, and melanoma.

Immobility: certain types of immobility are higher risk than others! Examples: patients in casts, hospitalized trauma patients (others not at higher risk). Surgical patients are higher risk if they were intubated, received general anesthesia, or received an epidural (e.g. knee surgery, abdominal surgery, neurological surgery). Being in a continuous seated position for > 6 hours might be a risk factor.

OCPs: estrogen of any form increases risk (e.g. OCPs, estrogen replacement, intra-vaginal estrogen). For transgendered patients, more study is needed to determine increased risk.

Pregnancy: Highest risk 2 weeks postpartum. If a patient is pregnant and symptomatic, they have a 70% risk of PE.

Increased risk at age 50: Risk of PE perpetually increases with age. 


Chest painpleuritic chest pain suggest peripheral PE (65%)

Hemoptysis: more indicative of pulmonary hemorrhage, not infarct

Exertional Dyspnea: concerning! You do not need to have chest pain to have a PE!! There is a syndrome that consists of subacute dyspnea that gets worse over days that is predictive of central PE.

Calf pain/Calf swelling: unilateral calf pain (the symptom) and calf swelling (the physical exam finding) are both concerning.

Syncope: corresponds to a large clot burden, but syncope  (likely does not confer an increased likelihood of PE)

Anticoagulation: if they are compliant with anticoagulation, they are less likely to have PE. While this is definitely true with NOACs, with Coumadin, it’s less certain because levels will vary regardless of compliance with medication. Symptoms that are not significant: orthopnea, palpitations, anxiety, dizziness 

Physical Exam Findings:

Abnormal pulmonary exam - decreases likelihood of PE

Clinical signs of DVT - such as calf swelling, redness, etc. increases likelihood 

STEP 1 (cont): Do you, based on the information above, feel that a PE is possible? Meaning, it is ABOVE the 2% threshold for PE. 

Professional recommendation: if the patient has risk factors in 2 or more of the above categories (e.g. vital sign and risk factors, or risk factors and exam findings), and there is no alternative explanation for the patient's presentation, you can say adequately that you have suspicion for PE. 

If you have less than a 2% clinical suspicion for PE, STOP. You do NOT think there is a PE and you do not evaluate further. I repeat - STOP! Evaluate for other suspected pathologies). ACEP Guidelines: 2% is an acceptable cutoff recognizing limitations of testing and risk of false positives (in latest NSTEMI guidelines) Now that you truly think your differential should include PE...  


It doesn't matter if you use Well's Score vs. Geneva vs. Gestalt; all have been shown to be equal. Keep in mind these decision tools SHOULD NOT used to rule out. They are only to RISK STRATIFY. Meaning that you clinically have a suspicion of said disease before you use them. This means you should NEVER document "Well's score low, not likely PE". 

 High risk: get a CTA! May consider empiric heparin before or after CTA.  

Moderate: D-dimer. 

  • In general, you should use age adjusted cutoffs for patients > 50. The conversion depends on which unit you use. 

    • FEU (fibrinogen unit, cutoff usually ~ 500): add the age x 10

    • DDU (d-dimer unit, cutoff usually ~ 250): add the age x 5


STEP 3: Further Management

Ever get a reading that said "evaluation for sub-segmental suboptimal due to motion artifact? What do you do? (Only if vital signs are stable)

  • Get a d-dimer (if not already obtained)

  • Positive --> LE dopplers

    • Yes DVT: anticoagulate!

    • No DVT: discharge with or without anticoagulation based on risk factors and lab values; follow-up with PMD for repeat surveillance ultrasound in 3-7 days. 

  • Negative -->  Discharge 

Now let's go over what you do if a PE is found...


Disposition: depends on if the patient is stable or unstable

Unstable: hypotensive, signs of shock, etc

  • Give tPa and admit to MICU

Stable: labs (BNP, troponin), echo

  • If the patient as abnormal labs or right heart strain, give heparin +/- half-dose tPA and admit to ICU/tele

  • If normal, determine the patient's PESI Score

    • High PESI score --> give heparin and admit to floor

    • Low PESI score --> give lovenox** and discharge

** There inadequate evidence and no FDA approval for NOACs at this time
  Subsegmental PEs in patients < 50 with stable vitals have a very low risk of adverse outcome, so you may consider discharging without anticoagulation if no DVT is present and there are no risk factors for recurrence and have the patient f/u with PMD for surveillance of PE symptoms


POTD: UTI? How to interpret your UAs and micros.

We diagnose UTIs nearly everyday, but are all of these true UTIs? Below, I will go into a quick review of what makes a UTI positive and various other tidbits. As usual, TL;DR is on the bottom of the post.

First off, patient should be instructed to provide a mid-stream sample, preferably clean-catch, however studies have shown that cleaning does not decrease contamination. 

Once collected, samples should be send immediately or refrigerated within 2 hours. This is to prevent proliferation of bacteria within the container itself. That being said, samples should still be analyzed expeditiously because refrigeration can also alter urinary leukocytes. 

Before you consider ordering any tests at all, consider this - does your patient really need testing?

UTI is a clinical diagnosis! In patients with classic symptoms for UTI (dysuria, urinary frequency, urinary urgency in the absence of symptoms that could suggest cervicitis or vaginitis), a negative dip or UA may actually falsely reassure you due to false negative results. In short, a negative result should not change your management 

Likewise, in a non-pregnant, asymptomatic patient, a false positive may lead to unnecessary treatment (besides, asymptomatic bacturia in a non-pregnant patient should not be treated anyway!!)

Now if you think a patient should be tested...

Nitrites are found in urine as a result of conversion of urinary nitrates to nitrites by gram negative bacteria that have been sitting in the bladder for > 4 hours. Studies have shown that they are highly specific (92-100%), but not very sensitive (19-48%). False negatives occur because nitrites require > 4 hours incubation, are not formed by some bacteria (Enterococcus faecalis) or are formed in small amounts, low urinary pH, or ingestion of foods/drugs that color the urine red. However, false positives can occur due to treatment with pyridium (phenazopyridine) and testing with strips that have been exposed to air. 

Leukocyte Esterase
Leukocyte esterase (if you remember back to your microbiology days) is produced by neutrophils and is associated with pyuria (positive requires > 10 WBC/hpf). Abnormal LE has been found to be highly sensitive (72-97%), butnot very specific (41-86%). To put that in perspective, the PPV is only 43-56%, meaning that of the patients that test positive, on the high end of the spectrum, only 56% of patients will have a culture-confirmed UTI. False positives can occur from contamination, false negatives occur from glycosuria, ketonuria, proteinuria, high urine specific gravity (increases cell lysis), vitamin C, or some oxidizing drugs (e.g. keflex, macrobid, tetracycline, gentamicin).  

What about microscopy?
So we tend to look a lot at the WBC/hpf to aid in our decision making. This is actually the less accurate method for determining pyuria - things like vaginal secretions can affect the leukocyte count. The more accurate method is hemocytometry. However, using what we have available, up to date recommends using a cut off of 8cells/microL, which corresponds to 2-5 cells/hpf. The question is how to use this information knowing that contamination can falsely increase your WBC count.

Some biostats:

  • Bacteria: sensitivity 46-58%, specificity 89-94%

  • > 5 WBC/hpf: sensitivity 90-96%, specificity 47-50%

Looks pretty similar to your stats for nitrites and leuk esterase, right?

There are several situations which can arise: 

  • Bacteria without pyuria: absence of pyuria with a UTI are rare, so this is usually indicative of contamination and a repeat test should be done. However if the patient has symptoms, they may have an entity called "acute urethral syndrome". Likewise, if your sample is from a patient that is chronically catheterized, lack of pyuria is likely due to colonization and not infection. Keep in mind though, patients that are immunosuppressed may not have pyuria due to blunted immune response. 

  • Sterile pyuria: can occur in patients that have already taken antimicrobials (your "partially treated" UTIs), contamination by sterilizing cleaning solution used to clean the urethra, vaginal leukocytes, dehydration, chronic interstitial nephritis, interstitial cystitis, uroepithelial tumors, appendicitis, diverticulitis, or atypical organisms such as ChlamydiaUreaplasma, and TB. 

Take home points:
Don't test all urine! In a young, non-pregnant female with symptoms typical of UTI, go ahead and treat! A negative result may cloud your judgement. In other situations (pregnant female, symptomatic males, the elderly with AMS that may be due to UTI), learn to use your UA and microscopy to aid in your decision making. Figure out what can cause false negatives and false positives. Positive nitrites and positive leuks? Treat! Only have bacteria? Test again! Only have leuks? Look for other causes! In short, only use testing as an adjunct to your clinical decision making. 


  • Think about who you're testing! Not everyone needs a UA. 

  • Nitrites are highly specific, but not sensitive

  • Leukocyte esterase is highly sensitive, but not specific

  • Absence of pyuria is rare in UTI, so if you see bacteria, but no pyuria, it's likely not a UTI

  • Pyuria can occur in many different conditions, so if you have pyuria without bacteria, think about alternative diagnoses



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

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

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


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

Special cases:

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

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

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

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

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

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

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

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

  • Affected vein segment < 5cm

  • Remote from the saphenofemoral/saphenopopliteal junction

  • Low risk for VTE

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

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

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

  • NSAIDs

  • Warm/cool compresses

  • Elevation of the extremity

  • Compression stockings

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

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


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

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

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

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

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

  • Antibiotics for suppurative thrombophlebitis

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



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



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

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

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

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

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

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

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


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

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



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

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

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

  4. Aspirate and inject 2mL anesthesia in each position

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

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

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

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

What about sickle cell disease?

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


  • Ischemic priapism is painful and is a urological emergency

  • Call urology consult!

  • Provide analgesia/perform a dorsal nerve block

  • Aspirate with two needles laterally

  • Phenylephrine if this fails

  • Further management with urology if this fails

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




Wellness Wednesday POTD: Imposter Syndrome

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

Imposter Syndrome

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

Dr. Clance described six potential characteristics:

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

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

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

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

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

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

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

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

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

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

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

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

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

How to deal with imposter syndrome

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

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

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

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

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

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


POTD: Measles (Part 2)

Part two in our two part series about measles! 

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

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

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

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

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

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


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

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

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

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

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

  • Otitis media

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

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

  • Neurologic

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

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

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

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

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

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

      • Stage IV: death

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

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

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


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

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

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

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

  • Diagnose via IgM, IgG, nasopharyngal swab

  • Treatment primarily supportive

  • Consider vitamin A and ribavirin



POTD: Measles (Vaccination and Post-Exposure Prophylaxis)

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

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

Scroll to the bottom for the TL;DR version. 



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

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


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

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

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

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

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

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

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

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


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

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

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

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

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

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

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


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

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

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

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

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

  • Post exposure:

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

    • Infants < 12 months should receive IMIG within 6 days

    • Pregnant women and immunocompromised should received IVIG within 6 days

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



POTD: Lithium Toxicity (Toxicology Thursday)

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

There are three categories of toxicity:

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

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

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


Toxicity from chronic ingestions occur from impaired excretion due to:

  • Reduced GFR (NSAIDs, ACE inhibitors)

  • Increased renal tubular reabsorption (thiazides, spironolactone)

  • Calcium channel blockers (unknown mechanism)

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

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




  • Coarse tremor

  • Hyperreflexia

  • Nystagmus

  • Ataxia

  • Altered mental status

  • Seizures/non-convulsive status epilepticus


  • Nephrogenic diabetes insipidus

  • Sodium losing nephritis

  • Nephrotic syndrome

Cardiovascular (usually mild)

  • Wandering atrial pacemaker

  • Sinus bradycardia

  • ST-segment elevation

  • Prolonged QT syndrome

  • T-wave flattening


  • Nausea/vomiting

  • Diarrhea

  • Ileus

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


  • Hypothyroidism (inhibition of hormone synthesis)

    • Also worsens lithium toxicity


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

However, generally:

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

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

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


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

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

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

Hemodialysis for severe toxicity or renal failure

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


POTD: High-Pressure Injection Injury

High-Pressure Injection Injury

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

·      Their condition often rapidly deteriorate

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

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

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

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

·      Initial emergency department management:

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

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

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

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

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

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

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

potd high pressure.jpg

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

potd finger.png

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


POTD: Varicella-zoster virus (VZV)

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

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

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

    • Buzz words: asynchronous vesicular lesions

potd varicella.jpg

·      Requires airborne precautions

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

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

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

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

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

·      Who is most at risk for complications from varicella?

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

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

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

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

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

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

o   Special attention to airway monitoring

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

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

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

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




Peer IX

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


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

Let’s start with a case:

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

potd diaph.png

What does this patient have?

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

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

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

  • No longer true! more or less the same frequency

  • Right sided injury with greater mortality

    • d/t force required for injury is higher

    • more delay in diagnosis

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

  • Keep in mind that ptx is more common

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

  • o    size of the diaphragmatic tear

  • o   amount of abdominal viscera that is herniated

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

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

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

·      Small injuries are notoriously very difficulty to detect

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

·      Complications

o   tension gastrothorax, visceral ischemia, perforated viscus



ACEP Clinical Policy on acute blunt abdominal trauma


Peer IX

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


POTD: Idiopathic Intracranial Hypertension

POTD: Idiopathic intracranial hypertension


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

·      rare condition

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

·      + papilledema/ swelling of the optic disc on fundoscopy

potd eye papill.jpg

·      optic sonography

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

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

·      Classic presentation: young, obese female

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

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

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

·      Definitive dx: Lumbar puncture

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

  • normal CSF analysis.

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

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

·      Treatment

  • Repeat LPs  

  • Acetazolamide

  • Surgical shunt if severe and refractory

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

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




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

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

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

  • Peer IX


POTD: TB in the ED

Approach to TB in the ED.

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

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

Who is at high risk?

Those with no “usual source of care”

  • ethnic minorities

  • foreign born

  • HIV patient

  • drug users

  • nursing home patients

  • homeless patients

  • prisoners

Why is it often missed?

Non-specific presentation of TB

  • Cough present: 64%

  • Cough was chief complaint: 20%

  • Only 36% had respiratory complaint at triage

What to do if for high suspicion of TB:

  • Negative pressure isolation room

  • N95 fitted masks

  • CXR and rapid HIV

    • Why HIV test?

      • HIV increases risk of having reactivation TB

      • Immunosuppression will give you atypical cxr findings

  • Looking primarily for active tuberculosis 

Confirmatory testing:

  • PPD: Sensitivity 60-100%

  • QuantiFERON Gold: Sensitivity 81-96%

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

    • Variable Sensitivity: 20-60%

    • High specificity: 90-100%

  • Culture

    • Slower results: 7days- 8 weeks

    • Gold standard: 99% sensitivity

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

    • Respiratory for assistance in collection

    • 5 ml specimen

    • Rifampin resistance detection

    • Supposed to be a 2 hr turnaround

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

    • Sensitivity about 75-93%

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

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