POTD: Mosquito-Borne Infections, PART 1

Hi all, 

In light of it being summer, I figured I’d start out with a series of POTDs relevant to the season – mosquito borne diseases. 

It’s always been kind of a black box for me keeping all of these straight as they tend to present very similar to each other. You may not see these very frequently, HOWEVER as Dr. Strayer kindly pointed out to me, there are record-breaking numbers of Dengue Fever in countries throughout the Americas this year, exceeding the highest number ever recorded in a single year. So, you might see it sooner than you think given our patient population. 

For today, we’re going to focus on separating some very similar entities:

• Dengue Fever

• West Nile Virus

• Chikungunya Fever

DENGUE FEVER

• Dengue (break-bone fever) is a viral infection that spreads from mosquitoes (Aedes aegypti or Aedes albopictus) to people. It is more common in tropical and subtropical climates.

• Dengue fever is the fastest-spreading mosquito-borne viral disease worldwide, affecting over 100 million people annually. This disease also leads to 20 to 25,000 deaths, primarily among children, and is prevalent in more than 100 countries. Epidemics occur yearly in the Americas, Asia, Africa, and Australia.

• Traditionally, symptoms of the virus are divided into three phases:

  • Febrile Phase: During the febrile phase, individuals typically experience a sudden onset of high-grade fever, which usually lasts for 2 to 7 days. Associated symptoms during this phase include facial flushing, skin erythema, myalgias, arthralgias, headache, sore throat, conjunctival injection, anorexia, nausea, and vomiting.

  • Critical Phase: During the critical phase, defervescence marks a period when the temperature typically decreases to approximately 37.5-38 °C, occurring between days 3 and 7. This phase is associated with heightened capillary permeability, as well as a rapid decline in platelet count, accompanied by increased hematocrit levels and sometimes leukopenia. If left untreated, the critical phase can progress to shock, organ dysfunction, disseminated intravascular coagulation, or hemorrhage.

  • Recovery Phase: The recovery phase involves the gradual reabsorption of extravascular fluid over 2 to 3 days. During this period, patients often exhibit bradycardia.

• The most common laboratory findings associated with Dengue are thrombocytopenia, leukopenia, and elevated levels of aspartate aminotransferase.

• The virus antigen can be detected using enzyme-linked immunosorbent assay (ELISA) test, polymerase chain reaction (PCR), or by isolating the virus from body fluids. 

• TREATMENT: 

  • Patients with more mild symptoms (i.e. no hemodynamic instability and minimal risk factors/comorbidities) can often be managed outpatient with oral antipyretics and oral hydration. 

  • More severe symptoms require evaluation for hospitalization and should be started on IV crystalloids. Blood transfusion is indicated in cases of severe or suspected bleeding when the patient remains unstable despite adequate fluid resuscitation and hematocrit falls. Platelet transfusion may be necessary if the platelet count drops below 20,000 cells per microliter and there is a high risk of bleeding. Notably, it is essential to avoid administering aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and other anticoagulants. No antiviral medications are recommended, and no laboratory tests can reliably predict the progression to severe disease. 

WEST NILE VIRUS

• West Nile Virus is another flavivirus (same as Dengue) that also spreads from mosquitoes (most commonly the Culex genus) to people. 

• Originally seen in Uganda and other parts of Africa, West Nile virus began showing up throughout Europe, Asia, and North America in the 1990s. It is now present throughout much of the world.

• The incubation period of the West Nile virus varies from 4-14 days. Symptoms tend to last 5-7 days, however nearly 80% of those infected are asymptomatic!

• In most cases, symptoms include myalgia, malaise, and a low-grade fever. Other associated symptoms may include headache, eye pain, vomiting, anorexia, and up to 50% may have a maculopapular rash on the trunk.

• In rare cases, the virus can cause neurologic symptoms, including severe muscle weakness, changes in mental status, seizures, or flaccid paralysis. These patients initially present with features of encephalitis and/or meningitis that progresses rapidly, and they require ICU care. 

• Common laboratory findings include leukocytosis (NOTE THIS CAN HELP DIFFERENTIATE FROM DENGUE) and other nonspecific findings secondary to the viral infection. Hyponatremia may be seen when the CNS is involved, and this will typically have findings consistent with viral meningitis on lumbar puncture.

• For neuroinvasive disease, the CSF should also be tested using the ELISA test.

• TREATMENT:

  • Treatment of West Nile virus is primarily supportive care. Researchers have tried several agents including interferon, ribavirin, and intravenous immunoglobulin. No clear efficacy data exists as only one controlled study has been performed to date.

  • Individuals with milder cases can be managed symptomatically as outpatients and tend to have an excellent prognosis. However, toxic patients with neurologic symptoms usually require long-term ICU care.

CHIKUNGUNYA FEVER

• Chikungunya is a togavirus that will spread from mosquitoes (Aedes aegypti or Aedes albopictus, same as Dengue) to humans. 

• First discovered in Tanzania in 1952, it has since spread, effectively reaching the Americas in 2013, Florida in July 2014, and severely affecting various Caribbean, Central, and South American countries after that.

• Symptoms typically include (you guessed it) non-specific findings of high-grade fever and myalgia, following a 3 to 7 day incubation period, and lasting around 3 to 5 days. Bilateral symmetrical polyarthralgia ensues 2 to 5 days after the onset of fevers and preferentially involves distal over proximal joints.

• Although it is not considered to be a neurotropic virus, it has long been associated with neurologic symptoms, with encephalitis among newborns infected through mother-to-child transmission being the most common.

• Evaluation consists mainly of the clinical findings of fever and polyarthralgia in a person who recently returned from an affected region.

• Diagnosis of CHIKV can be established or confirmed by detection of viral RNA with serology and/or reverse-transcription polymerase chain reaction (RT-PCR) depending on disease time frame of presentation.

• TREATMENT:

  • Symptomatic relief is the mainstay treatment for Chikungunya fever, including adequate hydration, rest, and pain/fever relief preferably with acetaminophen. The WHO discourages the use of aspirin and most nonsteroidal anti-inflammatory drugs (NSAIDs) during the first 48 hours due to the risk of aggravating platelet dysfunction, especially in cases of possible DENV coinfection.

TL;DR

• Dengue: 

  • Spread by Aedes mosquitoes.

  • Thrombocytopenia, leukopenia, elevated LFTs.

  • High capillary permeability.

  • Supportive care, avoid ASA or NSAIDs due to low platelets.

• West Nile Virus:

  • Spread by Culex mosquitoes. 

  • Although rare, often associated with neurologic symptoms (encephalitis/meningitis). 

  • Leukocytosis; hyponatremia in CNS disease.

  • Supportive care.

• Chikungunya

  • Spread by Aedes mosquitoes.

  • Fever + polyarthralgia (bilateral symmetrical polyarthralgia, more commonly distal joints). 

  • Supportive care, avoid ASA or NSAIDs due to risk of co-infection with Dengue. 

Dengue:

https://www.ecdc.europa.eu/en/dengue-monthly 

https://www.who.int/news-room/fact-sheets/detail/dengue-and-severe-dengue#:~:text=Dengue%20(break%2Dbone%20fever),aches%2C%20nausea%2C%20and%20rash. 

https://www.ncbi.nlm.nih.gov/books/NBK430732/ 

West Nile Virus:

https://www.who.int/news-room/fact-sheets/detail/west-nile-virus 

https://www.ncbi.nlm.nih.gov/books/NBK544246/ 

https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(02)00368-7/abstract 

Chikungunya:

https://www.ecdc.europa.eu/en/chikungunya-monthly 

https://www.ncbi.nlm.nih.gov/books/NBK534224/ 

https://www.who.int/news-room/fact-sheets/detail/chikungunya 

POTD: Mind-Numbing Facts On Local Anesthetics

Hi all, 

I’ve often been confused by the differences between the myriad of choices we have for local anesthetics floating around our emergency department, so I’m dedicating this POTD to lining out some of the key differences. 

Local anesthetics vary in their potency, allowing for concentrations that range typically from 0.5 to 4%. This is largely the result of differences in lipid solubility, which enhances diffusion through nerve sheaths and neural membranes. They will interrupt neural conduction by inhibiting the influx of sodium ions through channels or ionophores within neuronal membranes. 

Local anesthetics have greater affinity for receptors within sodium channels during their activated and inactivated states than when they are in their resting states. Therefore, neural fibers having more rapid firing rates are most susceptible to local anesthetic action. Also, smaller fibers are generally more susceptible, because a given volume of local anesthetic solution can more readily block the requisite number of sodium channels for impulse transmission to be entirely interrupted.

Epinephrine is often added to a local anesthetic solution, which allows the clinician to use a lower dose of the anesthetic and improve safety. Further, epinephrine acts as a vasoconstrictor and delays absorption of the anesthetic into the peripheral arteriole, thus increasing the duration of action. The addition of epinephrine can also improve hemostasis by inducing vasoconstriction in the surgical field.

To best compare between some common choices, I figured a graph would be the best visual. I’ve highlighted the most common anesthetics we use in our emergency department. 

Interestingly, bupivacaine exists in two enantiomers (yeah I know, sorry for the PTSD from organic chemistry), which are mirror images of each other. Although structurally identical, enantiomers can exhibit clinical differences including potency and adverse effects. The discovery of a selective blockade of cardiac Na+ channels by the dextro-enantiomer of bupivacaine led to the creation and widespread use of two levo-enantiomers: levobupivacaine and ropivacaine. These exhibit lower potency at myocardial Na+ and K+ channels and have less effect on myocardial electrical conduction and contractility compared to bupivacaine. Hence our move away from bupivacaine. 

Also, don’t be fooled by all the fancy brand names – these will not tell you whether there is epinephrine present or a specific concentration. For example, Xylocaine may be on the bottle but this isn’t some specific formulation with/without epinephrine or any specific concentration – it just means lidocaine. Read your bottles carefully and calculate your maximum dose before injecting, especially on large wounds. Here for your reference:

References:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403589/ 

https://www.ncbi.nlm.nih.gov/books/NBK430894/ 

https://www.bjaed.org/article/S2058-5349(19)30152-0/fulltext

POTD - Blowing Smoke up Butts and the Formation of Modern CPR

Today I wanted to give y'all a little fun medical history lesson all about CPR. Have you ever heard the term “blowing smoke up your butt?” Have you ever wondered where that term came from?

In the 18th century there was something called the “tobacco smoke enema” that lead us to modern resuscitation. Tobacco was mainly imported from New America from the Native Americans.  At that time, Native Americans used tobacco medicinally and would physically blow tobacco smoke up the anus to ease symptoms of constipation, diarrhea, abdominal cramps, and even hernias

Prior to the Columbian Exchange, tobacco was unknown in the Old World. After explorers came to the Americans, Europeans became aware of the tobacco for its theorized medicine purposes. At that time, medical science was based heavily on humorism– Hippocrates theory that the there must be an equilibrium in the body of the vital bodily fluids (blood, phlegm, yellow bile, and black bile) and an imbalance of the humors would cause illness (later to be overturned by the understanding of germ theory). During this time, tobacco was thought to be able to soak up moisture in warm parts of the body, providing equilibrium to the body. At this time tobacco was even used to fumigate buildings to “discourage disease.” 

Slowly this information became known to Europe from travelers, mostly sailors, that came back to Europe. Richard Mead, an English physician, first published a single case report of a smoke enema that saved someone from drowning. In 1745, a woman that fell overboard in London was resuscitated after a passing sailor had told the husband of the woman to insert the stem of a pipe into her rectum and blow tobacco smoke which apparently revived the woman. 

This was revolutionary because at this time resuscitation was based solely on taking someone, warming them up, and stimulating them. At the time, artificial respiration and the blowing of smoke into the lungs or the rectum were thought to be interchangeably useful, but smoke enema was considered more potent because they believed it internally warmed and stimulated more effectively.

In the 1770s, London formed a rudimentary form of its first lifeguard crew. Drs William Haws and Thomas Cogan formed the Royal Humane Society, which was a society promoted to rescue drowning people and would pay their “guard” money for anyone successfully brought back to life. The Royal Humane Society had placed resuscitation kits that included smoke enemas along the River Thames in which young men would stand along the docks and save people from the water. First they would warm the drowned person and then would “stimulate respiration” with a smoke enema. Artificial respiration with the bellow was then used if the tobacco smoke enema failed. The lifeguards would use the below bellows:

This continued for some time and “bellowing” air into the lungs and smoke into the rectum continued to be a favored form of resuscitation. Prior to bellows in the mouth, there were documented forms of mouth-to-mouth resuscitation in the 1730s that was favored prior to the bellow. 

This became a very popular “treatment” for many ailments of the time till it fell out of favor when in 1811 English scientist Benjamin Brodie discovered that nicotine was toxic to the heart. 

Eventually artificial resuscitation evolved into many different methods prior to the ones we have today. In the 1850s, Marshall Hall, thought that the best way to artificially respirate someone was to rotate the body from the prone position to the side to increase the size of the chest cavity, followed by applying pressure to the chest to release the air. Around the same time, Henry Silvester questioned this technique and had patient’s lay on their back rather than their side, raising their arms above their head to expand the chest and allow air to flow into the lungs. He then would have the patient's arms crossed on their chest and then press on their chest to expel the air. 

These became widely accepted and used techniques until the late 1800s when open cardiac massage was discovered to restore circulation by a German scientist Moritz Schiff who was able to restore blood circulation in a dog after massaging its exposed heart in an open-chest surgery. Not but a few years later, a German surgeon Freidrich Maass was able to successfully resuscitate two patients with only external chest compressions while using respiratory ventilations for resuscitation, similar to our CPR today, however this was ignored for almost 70 years where open heart resuscitation continued to be the standard. So for 70 years people continued to have their chests cut open to have their hearts internally massaged for resuscitation. 

It wasn’t until the 1950s-1960s that CPR as we know it today actually took shape. In 1956, Peter Safar, James Elam, and Archer Gordon were able to prove that mouth-to-mouth resuscitation, which was largely abandoned for two centuries, was sufficient in resuscitating a victim. Safar, along with William Kouwenhoven and James Jude, would then in 1960 prove that combining mouth to mouth with external chest compressions was successful and would call it “cardiopulmonary resuscitation.” In the 1960s, the AHA started a program to acquaint physicians with closed-chest cardiac resuscitation and a life sized training manikin called “Resusci Anne” was born, which was used to train physicians how to perform CPR.

So every time you are coding a patient, think about how what we do currently all evolved from blowing smoke up someone’s anus!

Hannah Blakely