“Pressors” in Distributive Shock in Adults

“Pressors” in Distributive Shock in Adults

Thank you, Dr Dastmalchi, for requesting this POTD. I will review “pressors” for cardiogenic shock separately

  • Vasopressors- Pure vasoconstriction without any inotropy eg Phenylephrine and Vasopressin

  • Inotrope- Increase cardiac contractility à improving SV and cardiac output without any vasoconstriction eg Milrinone

  • Inopressors - a combination of vasopressors and inotropes, because they lead to both increased cardiac contractility and increased peripheral vasoconstriction eg Norepinephrine, Epinephrine and Dopamine

Norepinephrine- Inopressor

  • First line vasopressor in septic shock per Surviving Sepsis Guidelines

  • Less arrhythmogenic than Epinephrine and Dopamine


Mechanism of action

  • Stimulates alpha-1 and alpha-2 receptors

  • Small amount of beta-1 agonist- modest inotropic effect

  • Increased coronary blood flow and afterload

  • Increases venous tone and return with resultant increased preload

Adverse effects

  • Norepinephrine is considered safer than both Epinephrine and Dopamine.

  • ARR of 11% compared to dopamine with NNT 9

  • NE superior in improving CVP, urinary output, and arterial lactate levels compared to Epinephrine, Phenylephrine, and Vasopressin.

Indications

  • First-line pressor choice in distributive shock, including both neurogenic and septic shock

  • Norepinephrine as the only first-line pressor per SSC guidelines

Dosing

  • Use weight-based dosing to avoid the adverse effects associated with norepinephrine use

  • Weight-based dosing is based on GFR

  • Norepinephrine has a rapid onset of action (minutes) and can be titrated every 2-5 minutes

Epinephrine- Inopressor

Mechanism of action

  • Beta-1 and beta-2 receptors agonism à more inotropic effects than norepinephrine

  • Epinephrine greatly increases chronotropy (heart rate) and thus stroke volume

  • Some stimulatory effect on alpha-1 receptors

  • Lower doses (1-10 mcg/min) à a beta-1 agonist

  • Higher doses (greater than 10 mcg/min) à an alpha-1 agonist

Adverse effects

  • Associated with an increased risk of tachycardia and lactic acidosis

  • Hyperglycemia

  • Increased incidence of arrhythmogenic events associated with epinephrine

  • More difficult use lactate as a marker of the patient’s response to treatment

Indications

  • SSC guidelines recommend epinephrine as a second-line agent, after norepinephrine

  • “push-dose pressor”

  • Due to beta-2 receptors agonism causing bronchodilation, epinephrine is first-line agent for anaphylactic shock

Dosing

  • Guidelines for anaphylactic shock recommend an initial bolus of 0.1 mg (1:10,000) over 5 minutes, followed by an infusion of 2-15 mcg/min however associated with adverse cardiovascular events

  • For septic shock start epinephrine at 0.05 mcg/kg/min (generally 3-5 mcg/min) and titrate by 0.05 to 0.2 mcg/kg/min every 10 minutes. maximum drip rate is 2 mcg/kg/min

Dopamine- Inopressor

  • Fallen out of favor

  • Associated with higher arrhythmogenic events

Mechanism of action

  • Effects are dose-dependent

  • Low doses à dopaminergic receptors à leads to renal vasodilation à increased renal blood flow and GFR although studies failed to demonstrate improved renal function with dopamine use clinically

  • Moderate doses à beta-1 agonism à increased cardiac contractility and heart rate

  • High doses à alpha-1 adrenergic effects à arterial vasoconstriction and increased blood pressure

Adverse Effects

  • Several large, multi-center studies that demonstrate increased morbidity associated with its use

  • Significantly higher rates of dysrhythmias à NNH 9

Indications

  • Rescue medication when shock is refractory to other medications

Dosing

  • Start at 2 mcg/kg/min and titrate to a maximum dose of 20 mcg/kg/min.

  • Less than < 5 mcg/kg/min à vasodilation in the renal vasculature

  • 5-10mcg/kg/min à beta-1 agonism

  • 10 mcg/kg/min à alpha-1 adrenergic

Vasopressin- Vasopressor

  • Add vasopressin (doses up to 0.04 units/min) to norepinephrine to help achieve MAP target or decrease norepinephrine dosage

  • Restore catecholamine receptor responsiveness, particularly in cases of severe metabolic acidosis.

  • pH independent

  • Pure pressor à increase vasoconstriction with minimal effects on chronotropy or ionotropy

Mechanism of action

  • At low doses (< 0.04 units/min) à increases vascular resistance (V1)

  • No effect on heart rate and cardiac contractility

Adverse Effects

  • Vasopressin has been shown to be as safe as norepinephrine at lower doses

  • Increases SVR and afterload and decreases cardiac output although unclear if effect significant at lower doses

Indications

  • Second line vasopressors per SSC guidelines for septic shock

  • pH independent- Vasopressin in combination with epinephrine demonstrated improved ROSC in cardiac arrest patients with initial arterial pH <7.2 compared with epinephrine alone

Dosing

  • Steady dose at 0.03-0.04 units/min

  • Vasopressin is not titrated to clinical effect as are other vasopressors

  • Think about it more as a replacement therapy and treatment of relative vasopressin deficiency

Phenylephrine- Vasopressor

  • Pure pressor à increase vasoconstriction with minimal effects on chronotropy or ionotropy

  • SSC guidelines does not make rated recommendations on Phenylephrine

  • Limited clinical trial data

Mechanism of action

α1 agonism with peripheral vasoconstriction

Adverse Effects

  • Bradycardia - decrease in heart rate mediated by the carotid baroreceptor reflex 2/2 increase in SVR

  • Increases SVR and afterload and decreases cardiac output

Indications

  • Patients that are susceptible to beta-adrenergic generated arrhythmia

  • Push dose formulation

  • Refractory shock

Dosing

0.1-2mcg/kg/min (onset: minutes, duration: up to ~20 minutes)

References:

Emdocs

LITFL

Pollard, Sacha, Stephanie B. Edwin, and Cesar Alaniz. "Vasopressor and inotropic management of patients with septic shock." Pharmacy and Therapeutics 40.7 (2015): 438.

Amlal, Hassane, Sulaiman Sheriff, and Manoocher Soleimani. "Upregulation of collecting duct aquaporin-2 by metabolic acidosis: role of vasopressin." American Journal of Physiology-Cell Physiology 286.5 (2004): C1019-C1030.

Khanna, Ashish, and Nicholas A. Peters. "The Vasopressor Toolbox for Defending Blood Pressure."

Turner, DeAnna W., Rebecca L. Attridge, and Darrel W. Hughes. "Vasopressin associated with an increase in return of spontaneous circulation in acidotic cardiopulmonary arrest patients." Annals of Pharmacotherapy 48.8 (2014): 986-991.

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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
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. 

TL;DR:

  • 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

Sources:
https://www.aafp.org/afp/2005/0315/p1153.html
http://epmonthly.com/article/lowly-urinalysis-avoid-common-pitfalls/
https://www.uptodate.com/contents/sampling-and-evaluation-of-voided-urine-in-the-diagnosis-of-urinary-tract-infection-in-adults
https://www.acepnow.com/article/avoiding-overdiagnosis-overtreatment-urinary-tract-infection-emergency-department/
https://emergencymedicinecases.com/uti-myths-misconceptions/

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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. 

Transmission
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
Incubation
 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. 

koplik+spots.jpg

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. 

Complications
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

Diagnosis:
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

Treatment:
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). 


TL;DR:

  • 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

Sources:
https://www.uptodate.com/contents/measles-clinical-manifestations-diagnosis-treatment-and-prevention
http://www.emdocs.net/em-in-5-measles/
http://epmonthly.com/article/ready-for-the-measles-comeback/


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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:
http://www.emdocs.net/em-in-5-measles/

Scroll to the bottom for the TL;DR version. 

Vaccine_Measles_Vials-1296x728-Header.jpg

Measles

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. 


Vaccination

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. 


Post-Exposure

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. 


TL;DR

  • 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. 

Sources:
https://www.uptodate.com/contents/measles-mumps-and-rubella-immunization-in-adults
https://www.uptodate.com/contents/measles-mumps-and-rubella-immunization-in-infants-children-and-adolescents
https://www.health.ny.gov/prevention/immunization/toolkits/docs/health_advisory.pdf
https://www.cdc.gov/mmwr/preview/mmwrhtml/rr6007a1.htm
http://www.emdocs.net/em-in-5-measles/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4552307/

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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

Sources:

https://www.cdc.gov/vaccines/vpd/varicella/index.html

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3155623/

Peer IX

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

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POTD: TB in the ED

Approach to TB in the ED.

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

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

Who is at high risk?

Those with no “usual source of care”

  • ethnic minorities

  • foreign born

  • HIV patient

  • drug users

  • nursing home patients

  • homeless patients

  • prisoners

Why is it often missed?

Non-specific presentation of TB

  • Cough present: 64%

  • Cough was chief complaint: 20%

  • Only 36% had respiratory complaint at triage

What to do if for high suspicion of TB:

  • Negative pressure isolation room

  • N95 fitted masks

  • CXR and rapid HIV

    • Why HIV test?

      • HIV increases risk of having reactivation TB

      • Immunosuppression will give you atypical cxr findings

  • Looking primarily for active tuberculosis 

Confirmatory testing:

  • PPD: Sensitivity 60-100%

  • QuantiFERON Gold: Sensitivity 81-96%

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

    • Variable Sensitivity: 20-60%

    • High specificity: 90-100%

  • Culture

    • Slower results: 7days- 8 weeks

    • Gold standard: 99% sensitivity

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

    • Respiratory for assistance in collection

    • 5 ml specimen

    • Rifampin resistance detection

    • Supposed to be a 2 hr turnaround

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

    • Sensitivity about 75-93%

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

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

potd tb.png
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POTD: Ludwig’s Angina

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

Overview:

•        Submandibular Space Cellulitis

•        Bilateral

•        Aggressive, fast spreading

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

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


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

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

•        Tongue: displaced superiorly and posteriorly

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

•        Labs

•        Vbg, cbc 7, blood cultures

•        Imaging

•        CT face and neck with IV contrast

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

•        Consults

•        ENT, anesthesia

 

Treatment

•        ABCs…A! Airway obstruction in 33%

•        sit upright

•        Secure/verify integrity of airway

•        Awake fiberoptic nasal intubation

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

•        Abx: polymicrobial

  • Oral anaerobes and aerobes

  • PCN G + flagyl

  • Unasyn

  • Clinda

  • Immunocompromised? Cefepime +flagyl

•        Steroids

  • Dexamethasone  8-12 mg IV

•        Dispo

  • ICU

  • 3-4 day process, gets worse before better


Complications

•        Mortality usually associated with airway compromise

•        with appropriate treatment, 8% mortality

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

 

Brush up!

Brush up!

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

Uptodate Lugwig’s angina

Tintinelli’s Lugwig’s angina

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POTD: Young woman with upper abdominal pain clinical vignette

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

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

Dx? Management?

Fitz-Hugh-Curtis syndrome (FHCS).

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

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

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

Sources: Peer IX, uptodate

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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%.

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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.

Presentation

  • 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.

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Evaluation

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

Treatment

  • 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

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Ebola virus disease

One reason I know that I went into the right speciality is that

we HAVE to know about Ebola

. Virology is uber fascinating, and we aim to hammer out everything the EP provider needs to know regarding this Ebola virus disease (EVD). 

Aside from being an interesting topic,

there is currently a budding outbreak of EVD in the Congo.

Due to armed conflict, healthcare and quarantine measures are impeded. See news article below: 

https://www.beckershospitalreview.com/quality/101-dead-in-congo-s-ebola-outbreak-as-safety-risks-mount-for-health-workers.html

If you recall from the last outbreak, there were several notable US cases, one of which  received treatment in NYC. 

It is thought that there is animal reservoir (likely fruit bats) and the animal to human transmission of the virus may come from individuals handling bushmeat. 

Ebola is a filovirus (meaning it looks like a string). It is a negative sense single stranded RNA virus. 

Below is an colorized scanning electron microscope image of the virus, (included because it is just gorgeous!)

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image curtesy of CDC

Transmission is via contact

of viral particles to mucus membranes or broken down skin.  

Incubation time is 9-11 days.

The ebola virus is one of the most infectious agents known to man.

A single ebola virion is enough to be infectious

. This is in stark contrast to most other infectious agents which typically require a large inoculum to cause clinically significant disease. 

Symptoms typically develop by infection day 5

-fever, fatigue

-GI upset: vomiting, watery diarrhea, abdominal pain

-this can progress to seizures and cerebral edema

-renal failure

-hepatic failure

-eccymoses and petechial rash are also possible

-hemorrhage is uncommon, but reported in 18% of patients (typically GI)

Patients with severe disease typically die within 6-16 days. Mortality rate in west Africa was ~40-70%. Of 27 patients treated in the United States, the fatality rate was 18.5%.

The mechanism for the hemorrhagic fever is thought to be massive activation of macrophages and other immune cells causing a cytokine storm, which then leads to break down of the vascular endothelium and results in leaking. Other research suggests the virus itself has proteins which lead to endothelial dysfunction and leakage.

You can utilize ELISA, PCR, or virus isolation to test for the disease. These

tests for ebola are only available in consultation with a governmental health agency. 

Mainstay of treatment is supportive.

However, you can transfuse convalescent serum from recovered and now immune individuals. A more elegant and certainly more expensive treatment is

ZMapp

, which is a mix of “3 humanized monoclonal antibodies” against Ebola.  There also several vaccines including rVSV-ZEBOV which have been experimentally deployed in west Africa. 

As per the CDC, travelers from endemic outbreak regions should self monitor their health for 21 days. Febrile patients who may had contact with ebola, should be placed on contact precautions and NYDOH should be immediately contacted. 

Hopefully this is something we never see. But preparedness is critical for our specialty. Thank you for taking the time to read and have a great weekend.

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POD- Lyme Disease Prophylaxis

LYME DISEASE: When to give prophylaxis for a tick bite? Patient must meet ALL of the following criteria:

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  1. I. scapularis tick

  2. Tick attached >36 hours

  3. Prophylaxis begins within 72 hours of tick removal

  4. Bite occurred in area with high rate of infection

  5. Doxycycline not contraindicated

    1. Patient > 8 years of age

    2. Not pregnant or lactating

Prophylaxis=Doxycycline 4mg/kg max 200mg one-time dose

*** If patient does not meet the criteria for antibiotic prophylaxis recommendation is that they be observed and only treated if signs of symptoms of Lyme Disease develop

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Anti-NMDA Encephalitis

Today we are going to attempt to broaden your differential of altered mental status in the “young” patient.  While we attribute AMS or psychotic/bizarre behavior in many young patients to toxicologic causes or schizophrenia, there are other organic causes which are probably far more common than diagnosed. We are going to focus on one of these causes: Anti-NMDA Encephalitis

 

Symptoms

  • Many different presentations. Typically progresses in four stages.

  • Phase 1

o   May be prodrome of URI, flu-like syndrome, or headache.

  • Phase 2

o   Typically begins with a behavioral change

o   Cognition, memory, speech problems.

o   Odd behavior, however no prodrome: agitation, paranoia, psychosis.

o   Seizures

  • Phase 3

o   Automatisms: Twitching, lip smacking.

o   Catotonia, LOC

  • Phase 4

o   Autonomic dysfunction, hypoventiliation

 

Demographics

  • Mean age is 21 years old!

  • Mainly affects women (~80%).

  • 38% have a paraneoplastic syndrome, almost all of these are women (97%), typically associated with a teratoma (which contain tissue with NMDA receptors).

  • It appears to be the most common individual cause of encephalitis in those youngers than age 30, even more common than HSV encephalitis.

Cause

  • Thought to be an autoimmune issue caused by an antagonist again the NR1 subunit of the NMDA receptor.

  • Some of this autoimmune activity is thought to be invoked by tumors (teratoma, ovarian).

 

Workup

Rule out other causes ruled out (meningitis, toxicologic causes, herpes, etc).

Should get CSF.  Send for oligoclonnal bands.  You should also send CSF to test for the anti-NMDA antibody (in addition to HSV, etc).

Otherwise patient should get EEG, MRI, CSF (probably already performed) which show non-specific abnormalities.

Treatment

IVIG and Steroids (1G/day methylprednisone).  Consider plasmapheresis. Secondarily immunotherapy (rituximab) or cyclophosphamide.

 

Prognosis

Many patients take months to get better.  Phases of symptoms are generally reversed as patient improves. Those with masses do better as masses are removed. Additionally those with early treatment  do better.

Hopefully this helps to expand your differential in new onset AMS.  Remember to rule out other causes: meningitis, toxicologic, etc!

EM:RAP, David Carr

Aliem

California Encephalitis Project

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