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COVID-19 and Coronavirus – Is There a Cure for the Common Cold?

Every year, the influenza virus wreaks havoc on the world, and its arrival is anticipated by hoards of people, students, and healthcare workers getting their annual “flu shot.” Influenza is its own type of virus, and is composed of two specific genetically variable markers, labeled H and N. This virus becomes genetically prevalent based on what are known as antigenic shifts, which create different combinations of H and N, making the virus unique on an annual basis. 

antigenic shifts in a virus

HN Variants

Sometimes, the HN variants are mild in nature. Other times, the HN variants are extremely contagious and potentially deadly, such as with the H1N1 outbreak a few years ago and also in 1918. The manufacturers of the influenza vaccine try to anticipate the correct H and N frequencies by combining a mixture of expected variants into their annual flu vaccine. This means that when we get our annual flu vaccinations, we are being given relative immunity for the most commonly expected types of flu for that season. Sometimes the prediction is right on. Sometimes it’s way off, and ineffective. In addition to the antigenic variance, there are two strains of influenza virus- A and B, which can also mutate through the course of a flu season or outbreak, and change their symptoms and effects on a community. 

composition breakdown of influenza virus

The coronavirus is conceptually not much different from the influenza virus, but it is important to remember that it is its own type of virus altogether. 

For perspective, it is important to remember that the common cold is most commonly caused by respiratory viruses like the coronavirus, which due to its structure is very easily spread person to person through droplets.

So what makes the novel coronavirus (COVID-19) so different? 

To start, let’s discuss how viruses work, and what makes them unique to the cellular world. Unlike bacteria, which are their own living cellular organisms, viruses are specially designed microbiotic structures that are designed to enter cells and change the way they make things. Different cells in the human body are responsible for creating different products that the body uses for its combined functions. For example, brain cells create neuroproteins designed to aid neuronal conduction. Skin cells produce sebum for lubrication and protection, and lung cells produce secretions for mucous, which delivers impurities away from the alveoli, and prevents contamination into the bloodstream. These are just a few examples, and cells can produce hundreds of unique products. 

Depending on the virus, and the type of cell it attacks, different body structures can be effected in different ways, and at times, simultaneously. When a virus has an “affinity” for a specific body tissue, its effects can be profound. 

Virus Mutations

As we mentioned with the flu, viruses are known to mutate within a community as they encounter different cellular DNA among different species. Another good historical example of this concept can be seen with the bird flu, which caused a severe mutation of the influenza virus that was derived from chickens as the host, and caused a transmission to humans that was extremely severe. The novel coronavirus is thought to be derived from bats in the Wuhan territory in China. Novel is language for new or never-before-seen. This novel virus is believed be created by a natural mutation that altered the spike protein of coronavirus, making the virus extremely virulent against humans, and specially human lung tissue. This mutation converted the common cold bug into a super virus with lethal consequences greater than the basic coronavirus. 

Genetic Predisposition

In addition to viral tissue targeting, there is a suggestion that certain genetic communities may be predisposed to varying degrees of disease severity. Research performed by Dr. Emma Hodcroft in Switzerland has documented this variance in presentation in European communities, suggesting that certain ancestral lineages (high tech talk for related people) are predisposed to getting very ill from COVID-19. As a result, this novel virus has a rapid spread between members of a population and a vastly variable effect on disease presentation, likely due to genetic factors in the host (us). The ease of transmission of novel coronavirus (COVID-19) is responsible for the high degree of concern for containing this virus, and in the great efforts we have taken to mitigate its spread. 

Preventing the Spread of COVID-19

It is likely that you have heard the phrase “flatten the curve” being used frequently in the news and in scientific circles. The field of epidemiology focuses on the prevalence of a disease and its likelihood to infect a population. In addition, it considers the resources that are needed to prevent the spread of a disease in a certain population. In the case of COVID-19, the rapid spread is highly concerning, because as transmission occurs through droplets (water vapor and exhaled particles from an infected host), and the time to develop the disease averages 5 days, the potential for a population to become quickly consumed by the contagion is very high. The disease itself does not have a high mortality rate, but the rapid drain and overburdening of healthcare resources that can manage it is profound. So profound that it quickly overwhelms the capacity of healthcare delivery, crippling hospitals, filling hallways, exhausting ventilator and provider supply, eventually wiping out any meaningful ability to manage sick patients. Clearly, a bad scenario and one that would spell disaster for a population, or even the human population. 

This rapid initial infection outbreak creates a sharp “spike” of infected people in a community. By mitigating the spread of the virus (through practices such as social distancing, public closures, mandatory PPE use, and other isolation strategies), the goal of mitigation is to slow the inevitable spread of the virus so that the public health resources can manage it, and continue to provide care to sick patients. This so called “flattening the curve” was adopted by China initially, and eventually by many other modernized nations. In the United States it led to the large swathe of closures, “lockdowns,” and other isolation techniques. 

virus spreading timeline showing the amount of people sick at once and the hospitals capacity.

Origin of COVID-19

There are several theories regarding the actual origin of COVID-19. Some believe this virus may have originated in a laboratory in China. If an evil scientist were to design the perfect biological agent to destroy a population, that agent would need to meet three requirements: 

  1. It would spread quickly by basic human transmission routes without a means of surveillance.
  2. Its disease would be rapidly progressive, highly lethal, and impossible to cure.
  3. It would be difficult to contain and track. 

This is not suggesting that the coronavirus was part of a sinister plot to infect the world, but instead to put into context the traits that make COVID-19 such a scary global concern with potential epidemiological and national security concerns. In a more likely scenario, this is a bad virus that is the result of genetic adaption and mutation through many generations of species to species transmission. 

COVID-19 Mortality

Much surrounding this outbreak and pandemic is that little is understood about the virus. This specific virus can be carried completely asymptomatically and transmitted without them knowing it, making the true number of “infected” people even higher, and unknown. The walking well who have the virus may never be sick enough to know they need testing, and if they were, they would likely dilute the true mortality of this infection to an even lower percentage. Based on data from mid May, 2020, the actual overall mortality of coronavirus is approximately 80,000 people in the United States. With an estimated US population of 328 million people, the overall mortality attributed to COVID-19 is .02%. As of mid-March 2020, the CDC has estimated that the total of number of deaths attributed to influenza is between 29,000 and 59,000 for the year 2020. By comparison, the overall mortality of common causes of death in the United States is as follows: 

Cardiovascular Disease647,457
Cancer599,108
Accidents169,936
Chronic Lower Respiratory Diseases160,201
Cerebrovascular Diseases146,383
Alzheimer’s disease121,404
Diabetes83,564

Source: National Vital Statistics Reports, Vol. 68, No. 9, June 24, 2019, CDC 

It is likely that, as the final tally of mortality for 2020 is recorded, COVID-19 will surpass Diabetes as a common cause of death. Very sobering, with the exception of a few discrepancies in reporting that may be falsely elevating data. For example, in the city of New York, arguably the largest COVID-19 epicenter in the world, nearly all deaths are being diagnosed as COVID-19. This includes myocardial infarctions, strokes, cancer, and other common causes of mortality that are attributed to the virus instead of their actual and (more likely) cause. Conversely there is also variability in the diagnosis of common diseases that may actually be due to COVID-19 due to limited testing. While we may never know the true number of COVID-19 deaths, mitigation strategies put in place will likely cause an overall decline in mortality from the virus as time moves forward. 

Then there’s the children mystery. For whatever reason, COVID-19 initially seemed to leave children largely unaffected, and pregnant mothers who tested positive for the virus were having babies who were testing negative, initially suggesting the virus did not cross the placenta, and does not impact fetal cells. Additional studies are beginning to demonstrate that there may be intrauterine transmission after all. To confound things even more, children are also now appearing with vascular inflammation and a Kawasaki-like syndrome as a result of this infection, causing even more confusion. 

It is highly likely that the evolving disease presentation and changing clinical findings are the result of viral mutation. The latest estimates from mid-May 2020 suggest that the actual number of COVID-19 viral strains is around 14, with even more being likely. In fact, it is estimated that the majority of worldwide infections since mid-march are caused by the newest of these 14 strains. This has far- reaching implications for the pandemic because as the virus changes, its effects on different organ systems is impacted. Furthermore, this data was published while vaccination research based on prior known strains had previously begun, thwarting progress made to this point. These mutations make disease more variable, transmission more rapid, and also open the door to reinfections of those who had previously been infected. 

The Viral Reaction of COVID-19

So there you have the current situation- a novel strain of a likely genetically targeted virus that is not well understood, transmitted globally, and causing death. While the mortality data may be unreliable, there is no doubt that public sentiment is led by fear of the unknown. People don’t handle panic well, and the media feeds on scenarios such as this to garner attention and viewers. Fact checking is a challenge because multiple sources are changing their information daily and, well, relying on the Chinese to provide us with accurate data is a challenge even with good news. In short, the hysteria surrounding COVID-19 may be well-founded, or may be a byproduct of emotional reactions generated by unfounded fear. Only time will tell. What we do know is that after a short 3 month time period, COVID-19 infections declined in China- if you trust their data. However, as China reopened their doors and businesses, a second wave of outbreaks has occurred. 

This virus has led to an unprecedented reaction from the international community, resulting in closed borders, cruise ships being denied portage, and literally entire cities being placed on lockdown to avoid spreading of the virus. Similar to movies involving zombie apocalypse themes and other fictional disease themes. The truth is that the scientific community must assume the worst, and governments must, despite political and economic pressures, do what is right for the global community. 

Perhaps more concerning about this “viral reaction” is the discovery of how woefully unprepared we are as a nation and a world. The US CDC has suggested that a 6 foot radius is ideal to avoid transmission of droplets from one person to another. Alternatively, wearing face masks can reduce the need for this spacing. However, the type of mask (surgical, N95, etc) has not been universally agreed upon by epidemiologists and public health authorities. The reality is that even if there was a consensus about the right type of mask, there aren’t enough in the world to safely protect everyone. While production efforts are increasing, it will be a long time before supply reaches demand. Also, the misuse and overuse of PPE will contribute to this shortage. Anyone who has seen a person driving their own car alone, wearing a mask and face shield can appreciate how good intentions can lead to cumulative misunderstanding. 

Human Hygiene

Hand hygiene has also been recommended and while a shortage of soap may not be likely, hand sanitizer is also in short supply. These known limitations have rendered all guidance from the CDC effectively meaningless, and without a miracle production of face masks and hand sanitizer, the only “easy” solution to limit the spread of the virus is to quarantine people and keep them out of the public domain. Factories have closed. Food production facilities have been shuttered due to internal infections, and the food supply of our nation may be under threat. As we enter a phase of reopening, there is little consistency between state to state regarding what a cohesive plan will be, but it appears to be data-driven and appropriate for disease prevalence. The general public can only be locked away for so long before they yearn to be free, and as public sentiment against isolation and lockdown turns toward re-opening and a return to normalcy, it is likely that public health initiatives will fail in favor of commerce and economic recovery. After all, this is also an election year! 

Self Isolation

Despite these clear limitations, we are still isolating high risk people who are symptomatic and require COVID-19 testing, which is also in short supply and with limited availability. The initial testing guidelines suggested that patients with a fever, AND a cough, AND a history of travel should be tested for COVID-19. Over time this has morphed to include patients with risk factors such as obesity, hypertension, immunocompromised states, and age over 65. Current guidelines also include screening for loss of taste, smell, chills, sweating, or general weakness. It will only be a matter of time before every possible symptom of any infection will meet a screening criteria, leading to the eventual need to either test everyone for COVID-19 or treat everyone as if they are infected. 

COVID-19 Testing

Even if we decide testing is warranted, there is still differing consensus at the state and even local level about who should administer the test and where patients should wait for the results, which can take as long as 48 to 72 hours after the test is received. Rapid tests (45 minutes or less) are being developed, but their accuracy is in question, with reported sensitivities ranging from 45% to 85%. Even those being used in the White House at this time have a reported low sensitivity. These low-sensitivity tests are discouraging because the number of false negative patients in our community will continue to contribute to the disease transmission. 

Then there’s the multi-billion dollar question: What is the utility of a positive test result? If a patient has a cough, fever, and they are 18 years old without any risk factors, they are very unlikely to experience major complications. So why do we test? 

We know that the disease progression can be severe and that a certain percentage of patients, for whatever reason, will develop severe pulmonary disease. Recent data has suggested there is a tipping point between the mild symptoms and the severe pulmonary disease that causes high mortality rates. Overall, it should be noted that over 80% of all COVID-19 positive patients experience only a mild upper respiratory illness. 

We also like to have answers, which make us feel better about our likely illness outcome and allow us to identify those who should be isolated. The bigger question we should ask is how do we test those who have already been infected, and will be become immune. Most human viruses we are are familiar with confer a life-long immunity. Measles, Mumps, Rubella, Chickenpox – to name a few – are usually a “one and done” infection, and vaccination leads to permanent immunity. It would be ideal if we could test for COVID-19 antibodies that confirm immunity exists. There has been much in the media and in national planning surrounding antibody testing as a possible means to navigate the pandemic. In a brief nutshell, acute exposure to a disease cause an initial spike of Immunoglbulin M (IgM) which can be seen by itself in the bloodstream for up to 10 days. The solo appearance of IgM implies an acute infection period exists. As the 

IgG and IgM Antibody levels and symptoms timeline

immune system recognizes the virus and begins to create antibodies to treat it, there is a testable overlap between IgM and IgG in the blood. Is IgG begins to appear, IgM disappears, and IgG remains as the final proof of prior exposure. 

With common human viruses, the presence of IgG defines immunity, meaning that a person who has IgG for a specific virus has previously been infected and can’t get infected again. We are learning that this is not the case with COVID-19, as people are testing positive for the virus again – with acute infections – weeks and months after initially getting the disease. This is very concerning because it suggests that there may not be any form of immunity to the virus, making attempts at production of a vaccine meaningless. The old saying that “there is no cure for the common cold” may apply. 

It is possible that this virus could mutate or reappear in a similar fashion for years to come. It may never be eradicated. 

Byproduct of COVID-19

Perhaps the most sobering thought is that our nation’s hospitals and emergency departments, known as safe havens for identification and treatment of disease, have become areas feared by our population, and avoided. While the data is not known, it is reasonable to postulate that more patients will die without seeking emergency or hospital care, and other disease mortality will increase. Cardiovascular deaths will rise, untreated and undiagnosed cancers will become more prevalent, and preventable severe illness from diabetes and other diseases will soar. Medical science may go backwards because people are afraid to see their own doctors, and the fear of COVID-19 may blunt the reality of other more common diseases. 

Progressing Through COVID-19

As we progress into the mitigation phase of the disease, we must all realize that containment is no longer a possibility, and the virus will run its course in our communities and across the nation. As the phase implies, the best we can hope for at this time is to reduce the number of people who get this disease, and limit their transmission to others as a whole. Reopening will proceed with diligence and data as their driving forces, and it is likely that, as disease outbreaks continue to appear in pockets of the country, and a re-emergence of the disease becomes a possibility, we may resume the containment-mitigation process all over again, leading to more closures, and a reconfinement of our society. 

We must each do our part to watch for signs and symptoms in ourselves, and avoid exposing each other when they present. Pandemics and epidemics are a natural part of disease transmission, and since the 20th century have mostly been viral in nature. 

As we move into the next few months, we owe it to ourselves and each other to be vigilant, careful, and responsible with our bodies and exposures. COVID-19 may not be the global killer that we fear, but if transmission remains high, that could equate to more severe illnesses and deaths. The reality is that by controlling the disease exposure rate, and keeping total infection rates low, the total lives lost will equate to a very small and imperceptible fraction of that total number. 

A healthcare providers, we are determined to diagnose and treat our patients, and we are used to a world and a healthcare system that supports us in this endeavor. As this pandemic continues, and this specific novel virus continues to evolve, our world, our economy, and our entire healthcare system, will evolve with it. These are truly amazing times to be alive, despite the devastation and tragedy we must experience. We at Provider Practice Essentials are proud to be with you as we all experience these extraordinary times and hope to one day have a cure for the common cold.

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Heart Failure

Cardiology Essentials

Definition

Syndrome characterized by impaired myocardial performance and progressive maladaptive neurohormonal activation of the cardiovascular system leading to circulatory insufficiency to meet the body’s demands.

Systolic heart failure or heart failure with reduced ejection fraction (HFrEF): Clinical diagnosis of heart failure and an EF of less than 50%.

Diastolic heart failure or heart failure with preserved ejection fraction (HFpEF): Clinical signs and symptoms of heart failure with evidence of normal or preserved EF and evidence of abnormal LV diastolic function by Doppler echocardiography or cardiac catheterization

Right heart failure: Majority of cases are a result of left heart failure, although isolated pulmonary diseases can also cause this syndrome.

Etiology

  • Non-ischemic dilated cardiomyopathy (familial or idiopathic)
  • Hypertrophic cardiomyopathy
  • Restrictive cardiomyopathy
  • Cardiomyopathy as a result of fibroelastosis
  • Mitochondrial disease
  • Left ventricular non-compaction
  • Ischemic cardiomyopathy
  • Stress induced cardiomyopathy
  • Valvular obstruction or insufficiency
  • Hypertensive cardiomyopathy
  • Inflammatory (lymphocytic, eosinophilic, giant cell myocarditis)
  • Infectious (Chagas, Lyme disease, HIV, viral, bacterial, or fungal infections)
  • Endocrine disorders (thyroid disease, adrenal insufficiency, pheochromocytoma, acromegaly)
  • Familial storage disease (hemochromatosis, glycogen storage disease, Hurler syndrome, Anderson-Fabry disease)
  • Amyloidosis
  • Connective tissue disease (SLE, polyarteritis nodosa, scleroderma, myositis, sarcoidosis)
  • Muscular dystrophies
  • Neuromuscular disease (Friedreich ataxia, Noonan disease)
  • Toxins (alcohol, anthracyclines, radiation)
  • Tachyarrhythmia

Pathophysiology

Progressive disorder initiated by a form of myocardial injury either sudden (MI or myocarditis) or chronic insults (familial, metabolic, HTN, valve disease, shunting) that result in maladaptive compensatory mechanisms.

These mechanisms include activation of the sympathetic nervous system and activation of the RAS system which overtime lead to pump dysfunction and circulatory collapse.

Differential Diagnosis

Other entities that may look like acute decompensated heart failure:

  • Acute coronary syndrome
  • Interstitial lung disease
  • Pneumonia
  • ARDS
  • Other sources of volume overload such as CKD/ESRD vs cirrhosis, pulmonary hypertension, PE, cardiac tamponade, constrictive or restrictive pericarditis

Patient History

Ask about the signs and symptoms:

  • Worsening dyspnea at rest or exertion?
  • Fatigue?
  • Orthopnea?
  • PND?
  • Weight gain?
  • Increased edema?
  • Lightheadedness?
  • indigestion?
  • Chest heaviness?
  • Fever?
  • Chest pain?
  • Timing of symptom onset?

Ask about triggers of acute decompensation:

  • dietary indiscretion? foods high in Na like lunch meats, chips, canned foods, fast foods?
  • missed medication doses (diuretic)?
  • are they weighing themself daily? adjusting diuretics?
  • any signs or symptoms that an ischemic event has occurred?
  • do they consume alcohol excessively?

Physical Exam

  • Weight gain (if possible look at previous discharge weights)
  • Elevated jugular venous pulsations (Key!), hepatojugular reflux
  • Orthopnea
  • Pulmonary rales
  • Third and/or fourth heart sound
  • Pedal edema
  • Sacral edema in patients who are mostly in bed

Work Up

Laboratory

  • Renal function panel, liver function panel (CMP): Patients who are volume overloaded due to acute decompensated heart failure often have an acute kidney injury and hepatic congestion.
  • Potassium, calcium (CMP), magnesium. May need to check more frequently (e.g. bid) especially if pt will be diuresed.
  • CBC: Anemia is present in up to 40% of patient with heart failure.
  • Consider pro-BNP if volume exam not helpful; compare to prior.
  • If patient is presenting newly with HF and/or etiology is unclear:
    • troponin and lipid profile, especially if HFrEF the pt may need further work up for ischemic disease
    • TSH
    • in the right patient, consider iron studies (hemochromatosis), serum ceruloplasmin (Wilson’s), trypanosoma cruzi IgG (chagas), blood alcohol level or CDT etc.

Imaging

  • ECG, chest x-ray, echocardiography

Other imaging and diagnostic modalities that can be considered based on the patient’s history:

  • Cardiac MR
  • Nuclear imaging
  • Right heart catheterization
  • Left heart catheterization
  • CT angiogram.
  • Endomyocardial biopsy

 

Triage

Strongly consider step-down or ICU if evidence of decompensation with hypoperfusion (cold and wet):

Altered mental status, Cold extremities, evidence of organ hypoperfusion: increasing lactate or rising creatine, narrow pulse pressures

Risk Stratification

The American College of Cardiology/American Heart Association (ACC/AHA) Heart Failure Classification is a system used to classify heart failure into four stages based on the severity of symptoms and degree of functional impairment.

The four stages of heart failure in the ACC/AHA classification are:

  1. Stage A: At high risk of developing heart failure due to underlying conditions or risk factors such as hypertension, diabetes, or coronary artery disease.

  2. Stage B: Structural heart disease is present, but there are no symptoms of heart failure. This stage includes patients with a history of myocardial infarction (heart attack) or left ventricular remodeling after a cardiac injury.

  3. Stage C: Structural heart disease is present, and there are symptoms of heart failure such as fatigue, shortness of breath, and decreased exercise tolerance. This stage includes patients with past or current symptoms of heart failure who are responding to treatment.

  4. Stage D: Advanced heart failure that is refractory to standard treatments. This stage includes patients with severe symptoms of heart failure at rest, despite maximal medical therapy. Patients in this stage may require advanced interventions such as heart transplant or mechanical circulatory support.

The ACC/AHA Heart Failure Classification is based on a combination of factors, including clinical symptoms, physical examination findings, imaging studies, and laboratory tests. This classification system is useful for guiding treatment decisions and predicting outcomes in patients with heart failure. It can also help clinicians identify patients at high risk for developing heart failure and initiate preventive interventions to improve outcomes.

The New York Heart Association (NYHA) Functional Classification is a system used to classify heart failure into four stages based on the severity of symptoms and degree of functional impairment. The classification system was developed in 1928 and is still widely used today.

New York Heart Association functional classification

The NYHA Functional Classification is based on the patient’s subjective symptoms and limitations related to physical activity. It is often used in clinical practice to assess the severity of heart failure, guide treatment decisions, and predict outcomes. Patients with more severe symptoms are more likely to have poorer outcomes, and may require more aggressive treatment or consideration of advanced interventions, such as heart transplantation or mechanical circulatory support.

It’s important to note that the NYHA Functional Classification is just one aspect of the overall assessment of heart failure and should be used in conjunction with other clinical and diagnostic findings.

The Seattle Heart Failure Model (SHFM) is a clinical prediction model that provides an estimate of the probability of death and other adverse outcomes in patients with heart failure. It was developed to help clinicians make more informed decisions about treatment and to assist in risk stratification of patients with heart failure. The SHFM incorporates a wide range of patient characteristics, including demographics, clinical symptoms, laboratory values, and medication use, to predict the likelihood of various outcomes, such as mortality, hospitalization, and quality of life. The model is based on data from over 11,000 patients with heart failure and has been validated in several independent cohorts. To use the SHFM, a clinician inputs data on the patient’s age, sex, symptoms, medical history, laboratory values, and medication use into a web-based calculator. The model then generates a personalized estimate of the patient’s probability of death and other outcomes at 1 year and 5 years. The SHFM also provides a range of other information, such as the estimated survival time, probability of hospitalization, and predicted quality of life. The SHFM has been shown to have good accuracy in predicting outcomes in patients with heart failure, and it can be useful in guiding treatment decisions and in risk stratification of patients. However, it is important to note that the SHFM is just one tool among many that can be used in the management of heart failure, and it should be used in conjunction with clinical judgment and other diagnostic and prognostic tools.  

The MAGGIC (Meta-Analysis Global Group in Chronic Heart Failure) risk score is a prognostic model that is used to predict mortality in patients with chronic heart failure. It was developed using a large international database of over 39,000 patients with heart failure from 30 different studies.

The MAGGIC risk score takes into account a range of patient characteristics and clinical features that have been shown to be predictive of mortality in heart failure, including age, sex, systolic blood pressure, NYHA functional class, heart rate, serum sodium, serum creatinine, ejection fraction, etiology of heart failure, and use of certain medications such as ACE inhibitors, beta blockers, and diuretics.

The MAGGIC risk score assigns points to each of these variables based on their estimated contribution to mortality risk. The total number of points is then used to estimate the patient’s probability of mortality at 1 year and up to 5 years. The MAGGIC risk score has been shown to have good discrimination and calibration in predicting mortality in patients with heart failure.

The MAGGIC risk score is useful for identifying high-risk patients who may benefit from closer monitoring and more aggressive treatment, as well as for guiding clinical decision-making and communication with patients and families about prognosis. However, it is important to note that the MAGGIC risk score is just one tool among many that can be used in the management of heart failure, and it should be used in conjunction with clinical judgment and other diagnostic and prognostic tools.

CHA2DS2-VASc score: The CHA2DS2-VASc score is a tool used to estimate the risk of stroke in patients with atrial fibrillation. Since atrial fibrillation is a common comorbidity in heart failure, this score can be useful in managing heart failure patients with concurrent atrial fibrillation.

The CHA2DS2-VASc score is a clinical prediction rule that is primarily used to estimate the risk of stroke in patients with non-valvular atrial fibrillation. It is not specifically used in the management of heart failure, but rather in the management of comorbidities that may be present in patients with heart failure.

Patients with heart failure are at an increased risk of developing atrial fibrillation and other cardiovascular diseases, such as stroke, myocardial infarction, and peripheral vascular disease. As such, the CHA2DS2-VASc score can be used in the management of heart failure as a tool to identify patients who are at an increased risk of developing these conditions, and to guide clinical decision-making regarding the use of prophylactic therapies such as anticoagulation.

The CHA2DS2-VASc score takes into account a range of patient characteristics and clinical features that have been shown to be predictive of stroke and other cardiovascular events, including age, sex, history of stroke or transient ischemic attack, hypertension, diabetes, heart failure, and vascular disease. The score assigns points to each variable based on its estimated contribution to the risk of stroke or other cardiovascular events.

While the CHA2DS2-VASc score is not specifically designed for use in heart failure, it is an important tool that can be used to guide clinical decision-making in the management of patients with heart failure and comorbidities. It can help identify patients who may benefit from prophylactic therapies and other interventions aimed at reducing the risk of stroke and other cardiovascular events.

 

Heart failure with reduced ejection fraction (HFrEF) is a condition where the heart muscle weakens and can’t pump blood effectively. Treatment for HFrEF usually involves a combination of lifestyle changes, medication, and other interventions.

The HFrEF therapy calculator is a tool that can help healthcare professionals determine the most appropriate treatment plan for patients with HFrEF. The calculator takes into account the patient’s age, sex, blood pressure, kidney function, and other factors, and recommends medications and doses that have been shown to be effective in treating HFrEF.

The calculator is based on guidelines developed by the American College of Cardiology, American Heart Association, and Heart Failure Society of America. These guidelines recommend a combination of medications that target different aspects of heart failure, including angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), beta blockers, and aldosterone antagonists.

The HFrEF therapy calculator takes into account the patient’s current medications and adjusts the recommendations accordingly. It also provides guidance on when to start or stop certain medications, and how to titrate the doses to achieve the maximum benefit while minimizing side effects.

The Renal Risk Score is a tool that helps predict the risk of developing acute kidney injury in patients with heart failure who are undergoing intravenous diuretic therapy.

The renal risk score is a tool that is primarily used to estimate a patient’s risk of developing acute kidney injury (AKI) after undergoing cardiac surgery. However, the risk of AKI is also a concern in patients with heart failure, particularly those who are hospitalized or receiving treatment with certain medications.

In patients with heart failure, the risk of AKI is often related to factors such as low cardiac output, fluid overload, and the use of medications that can affect kidney function. Some of these medications include diuretics, angiotensin-converting enzyme inhibitors (ACE inhibitors), angiotensin receptor blockers (ARBs), and nonsteroidal anti-inflammatory drugs (NSAIDs).

Several studies have looked at the use of the renal risk score in patients with heart failure. One study, published in the journal Circulation Heart Failure in 2014, found that the renal risk score was able to predict the risk of AKI in patients hospitalized with heart failure. The study also found that patients with higher renal risk scores were more likely to require dialysis or have a longer hospital stay.

Another study, published in the Journal of Cardiac Failure in 2018, evaluated the use of the renal risk score in patients with heart failure who were receiving treatment with sacubitril/valsartan, a medication used to treat heart failure with reduced ejection fraction. The study found that the renal risk score was able to predict the risk of AKI in these patients and could be used to guide dosing of the medication to minimize the risk of kidney injury.

Overall, while the renal risk score was developed for use in patients undergoing cardiac surgery, it may also be a useful tool for predicting the risk of AKI in patients with heart failure. By identifying patients at higher risk of AKI, healthcare providers can take steps to minimize the risk of kidney injury and improve outcomes for these patients.

Treatment

Acute Decompensated Heart Failure

IV diuresis:

Determine home regimen and try to give an increased dose. Patients with anasarca DO NOT ABSORB ORAL MEDS. Remember patients who are naïve to diuretics may not require high doses for good urine output. As a rule of thumb, the furosemide dose can be initially calculated at 40 (mg) X serum creatinine. Titration will be performed according to initial response. Common diuretics include furosemide, torsemide, metolazone, and Chlorothiazide. For ESRD patients who no longer make urine, volume removal will be via ultrafiltration and may need to be done more aggressively as tolerated by BP. Be sure to check electrolytes twice a day and aggressively supplement (keep K around 4 and magnesium around 2.4. Check daily weights (standing if possible) and monitor Ins and Outs.

Afterload reduction in systolic heart failure:

If no kidney injury is detected you can consider an ACE-Inhibitor, otherwise hydralazine with/or without nitrates. In more severe cases, one may consider sodium nitroprusside

Inotropy: Usually in severe cases or if effective diuresis is not achieved despite other efforts.

Dobutamine or milrinone

Remember to hold beta blockers in acute decompensated heart failure

Chronic Heart Failure Therapies

Mortality reducing agents:

  • ACE inhibitors/ARBs
    • start in all pt’s with current or prior sx’s of HFrEF unless contraindicated; try ACEi first and then try ARB if not tolerated
    • caution in pts with ↓SBP, renal insufficiency, or ↑serum potassium (>5.0 mEq/L). Angioedema occurs in < 1% of pts with ACE inhibitors.
  • ANRIs (angiotensin receptor–neprilysin inhibitor: valsartan/sacubitril)
    • start in pt’s with NYHA class II-III HFrEF who tolerate an ACE inhibitor or ARB, replacement by an ARNI is recommended to further reduce morbidity and mortality. Harmful if started concomitantly with ACEi/ARB – wait 36 hrs after stopping ACEi/ARB to inititate
  • Beta blockers (metoprolol succinate, bisoprolol, and carvedilol)
    • start in all pt’s with current or prior sx’s of HFrEF unless contraindicated
  • ISDN + Hydralazine
    • clear benifit in African American pt’s with NYHA class III-IV HFrEF
    • likely beneficial for all pt’s with HFrEF, though utility somewhat limited by TID dosing
  • Aldosterone receptor blockers (eplerenone, spironolactone)
    • recommended in patients with NYHA class II–IV HF and who have LVEF of 35% or less

HF Hospitalization Reducing Agents

  • Digoxin
  • Ivabradine (inhibits the If current in the SA node, ↓HR)
    • can use in NYHA class II-III stable chronic HFrEF (LVEF ≤35%) who tolerate maximum BB in NSR with HR of 70 bpm or more at rest[2]

Advanced Therapies

  • Left ventricular assist device (right heart must be able to tolerate this)
  • Heart transplantation

References

  1. Khot UN, Jia G, Moliterno DJ, et al. Prognostic importance of physical examination for heart failure in non-ST-elevation acute coronary syndromes: the enduring value of Killip classification. JAMA. 2003;290(16):2174-81. [PMID:14570953]
  2. Yancy CW, et al: 2016 ACC/AHA/HFSA Focused Update on NewPharmacological Therapy for Heart Failure: An Update of the 2013 ACCF/AHA Guideline for theManagement of Heart Failure, Journal of the American College of Cardiology (2016), doi: 10.1016/j.jacc.2016.05.011.
  3. Griffin BP, Callahan TD, Menon V, et al. Manual of Cardiovascular Medicine. Lippincott Williams & Wilkins. 2013 4th edition; Heart Failure and Transplant 125-159
  4. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;62(16):e147-239. [PMID:23747642]

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Dermatology Overview

Dermatology Essentials

Definition

Cellulitis: infection of dermis and subcutaneous fat

Impetigo: superficial purulent lesions, esp. on face and extremities. Commonly with bullae and/or golden crust

Erysipelas: raised erythematous lesion with clear borders

Folliculitis: hair follicle inflammation. Superficial and limited to the epidermis.

Furunculosis: hair follicle infection that extend to dermis. Multiple = carbuncle

Necrotizing Infection: Deeper SSTI that involve fascial and/or muscle compartments

Etiology

Microbiology

  • Cellulitis: primarily Staph and Strep, incl. MRSA. In immunocomp./diabetics, GNRs also
    • Other etiologies: cat/dog bite P. moltocida; gardening Sporothrix; salt water Vibrio vulnificus; puncture wound → Pseudomonas
  • Impetigo: Strep or Staph
  • Erysipelas: group A Strep usu.
  • Folliculitis/furunculosis: S. aureus, Pseudomonas
  • Necrotizing Infections: Polymicrobial (eg strep and GNRs in Type I, Fournier’s), Group A Strep, S. aureus, Aeromonas hydrophila, Vibrio vulnificus

At risk: athletic teams, military, prison, MSM, communities with MRSA infxn, Diabetic

High risk for more aggressive infection: splenectomy, immunocompromised

Differential Diagnosis

  • Cellulitis
  • Impetigo
  • Erysipelas
  • Folliculitis
  • Furunculosis
  • Necrotizing fasciitis
  • Myonecrosis
  • Calciphylaxis
  • Cutaneous metastasis from neoplasms (especially adenocarcinoma)
  • Graft-versus-host disease (in appropriate population)
  • Sweet syndrome

Patient History

  • Recent trauma to the affected area?
  • Any recent surgeries (hip replacement is risk factor)?
  • Ask about the presence of HIV, diabetes, liver disease, or kidney disease.
  • History of IV drug abuse or subcutaneous injection.
  • Recurrent Cellulitis: Assess for predisposing conditions such as edema, obesity, eczema, venous stasis, and toe web abnormalities.
  • Recurrent Abscesses: Search for local causes such as pilonidal cyst, HS, or foreign body. Consider 5-day decolonization (intranasal mupirosin, daily chlorhexidine). Consider neutrophil disorder if abscesses began in childhood.

Physical Exam

  • Evaluate affected area for erythema, edema, warmth, and pain on palpation.
  • Look for lymphangiitis (erythematous tracks under the skin marking an inflamed lymphatic system), palpate for lymphadenopathy.
  • Assess for evidence of necrotizing infection: systemic toxicity with high temperature, hypotension, disorientation, lethargy, skin discoloration or bullous lesions, anesthesia, firm skin with wooden-hard induration, pain extending beyond cutaneous erythema, pain out of proportion to exam

Work Up

Note: Diagnosis is largely clinical

Laboratory:

  • CBC with diff, ESR/CRP if concern for osteo, CK if concern for necrotizing infection or pyomyositis.
  • Furuncle/pustule can be aspirated for gram stain and culture.
  • For cellulitis, blood cultures are generally low yield, but should be obtained in patients undergoing chemo, neutropenic patients, and those who suffered animal bites.

Imaging:

  • If concern for osteo, xray; consider MRI
  • If concern for necrotizing infection can look for gas in fascial planes on x-ray or CT, but this is highly insensitive

Triage

More serious presentations of skin and soft tissue infections:

  • Toxic shock syndrome: fever, HA, vomiting, myalgias, pharyngitis, diarrhea, diffuse rash with desquamation. Hypotension and shock.
  • Osteomyelitis: infection of bone due to hematogenous seeding or direct spread from overlying focus.
  • Necrotizing fasciitis: infection and necrosis of superficial fascia, subq fat, and deep fascia. Clues: rapidly spreading cellulitis, systemic toxicity (inc TSS), pain out of proportion to exam, bullae formation, gangrene, crepitus. Surgical and medical emergency.
  • Gas gangrene: Clostridial myonecrosis, a fulminant skeletal muscle infection. C. perfringins usually in the setting of trauma; C. septicum in setting of cancer. Surgical and medical emergency.

Treatment

Purulent (furuncle/carbuncle/abscess):

  • Mild: I & D
  • Moderate: I & D, send for culture and sensitives
    • Empiric treatment: Bactrim 1-2 DS tab BID or Doxycycline 100mg BID
    • Defined treatment: MRSA: Bactrim 1-2 DS tab BID, MSSA: Dicloxacillin 250 Q6H or Cephalexin 500 Q6H or Cefadroxil 500mg po q12.
  • Severe: I & D, send for culture and sensitiivies
    • Empiric treatment: Vancomycin or Daptomycin or Linezolid or Ceftaroline
    • Defined treatment: MRSA: similar to empiric, MSSA: Nafcillin or Cefazolin or Clindamycin (if Susceptible)

Nonpurulent (necrotizing infection/cellulitis/erysipelas):

  • Mild: impetigo: topical mupirocin; oral treatment: Penicillin VK or Cephalosporin (eg Cephalexin 500mg PO Q6H) or Dicloxacillin 500mg PO Q6H or Clindamycin 300mg PO Q8H
  • Moderate: IV therapy: penicillin or Cefriaxone or Cefazolin or Clindamycin 300mg PO Q8H or 600mg IV Q8H
  • Severe: emergency surgical evaluation/debridement to rule out necrotizing process
    • Empiric treatment: Vancomycin PLUS Piperacillin/Tazobactam
    • Defined treatment for necrotizing infections:
      • Strep. pyogenes:Penicillin PLUS Clindamycin
      • Vibrio vulnificus:Doxycycline PLUS Ceftazidime
      • Aeromonas hydrophila:Doxycycline PLUS Ciprofloxacin
      • Polymicrobial: Vancomycin PLUS Piperacillin/Tazobactam

Duration of Therapy: 5-7 Days

Treatment Notes:

Erythema may initially worsen with antibiotics 2/2 local bacterial killing.

– For cellulitis, elevation of the affected extremity is essential to treatment.

– For Staph aureus infections (eg suppurative cellulitis) in 2014 at Hopkins susceptibilities were: TMP-SMX 87-88%, Tetracycline 89-91%, and Clindamycin 46-60%.

– For Beta-hemolytic Strep infections (eg non-suppurative cellulitis) all strains are susceptible to penicillin. At Hopkins there are high rates of resistance to TMP-SMX and tetracyclines and variable rates of resistance to Clindamycin.

– If you are concerned for a necrotizing infection, CONSULT SURGERY. Empiric antibiotic treatment with vancomycin (or linezolid) PLUS zosyn (or carbapenem) should be initiated. Clindamycin can be added to inhibit toxin production.

References

  1. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):e10-52. [PMID:24973422]
  2. Swartz MN. Clinical practice. Cellulitis. N Engl J Med. 2004;350(9):904-12. [PMID:14985488]

Resources

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Airway Anatomy and Assessment

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Indications for Airway Management

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Airway Options

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Intubation Drugs

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Introduction to Ultrasound

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Biliary Ultrasound

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DVT Ultrasound

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eFAST Ultrasound

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Ocular Ultrasound

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Pelvic Ultrasound

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Pulmonary Ultrasound

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Renal Ultrasound

  • Anatomy and probe placement
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Soft Tissue Ultrasound

  • Probe selection and settings
  • Foreign body, cellulitis, abscess, and cyst identification
  • Next clinical steps

Ultrasound for Vascular Access

  • Anatomy of peripheral and central veins
  • Application of Ultrasound to assist with line placement
  • Visualization of landmarks and expected clinical findings

Abdominal Aorta Ultrasound

  • Anatomy and ultrasound placement
  • Expected normal and abnormal findings
  • Next clinical steps and application

3-Day Clinical Skills & Procedure Workshop + The Airway Course

Day 1 Morning

Airway Anatomy and Assessment

  • How to assess an airway
  • Identification of landmarks
  • Predicting a difficult airway
  • Special scenarios
  • Airway classification and grading

Indications for Airway Management

  • Clinical conditions
  • Respiratory status
  • Anatomy
  • Predictors of airway need
  • Common approaches

Non-Invasive and Invasive Airway Management

  • Escalation of intervention
  • Sequential oxygenation
  • BIPAP
  • CPAP
  • Endotracheal Intubation
  • Airway Adjuncts (LMA, OPA)

Airway Options and Medications

  • Types of airway devices
  • Airway equipment
  • Laryngoscopes
  • Fiberoptic and Video Scopes
  • Induction agents and dosing

Induction and Intubation

  • Procedure organization and setup
  • Stepwise airway protocols
  • Anatomy
  • Endotracheal Intubation
  • Hands-On Procedure Practice

Tube Confirmation and Difficult Airway Management

  • Confirmatory tests
  • Defining an intact airway
  • How to manage a failed airway
  • Difficult airway algorithm and management
  • Fiberoptic laryngoscopy
  • Laryngeal mask airway
  • Video laryngoscope

Day 1 Afternoon

procedure

Difficult Airway Algorithm and Simulation

  • Application of the difficult airway algorithm
  • Simulated patient scenarios
  • Intubation with video laryngoscopy
  • Hands-On airway procedure lab
  • Individual review with instructor
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Day 2 Morning

Cardiac

Cardiac Disorders

  • Course Introduction
  • Cardiac Overview
  • EKG Interpretation
  • Acute MI (recognition, management)
  • Common Dysrhythmias
  • Electrolyte Abnormalities and rhythm impacts
  • Condition blocks
  • Bundle Branch Blocks
  • Application to practice
Pulmonary

Pulmonary Disorders

  • Pulmonary Overview
  • Basic Airway Assessment
  • Pneumothorax
  • Asthma Management
  • COPD Management
  • Supplemental Oxygenation
  • Wells Criteria
  • PERC Rule
  • Using D-Dimer
  • Pulmonary Embolism
  • Treatment of Pulmonary Embolism

Introduction to Radiology – Chest and Abdomen

 
  • Overview of Radiograph Interpretation
  • Chest, Shoulder, Clavicle Radiographs
  • Systemic Reading Process
  • Abnormal Radiographs
  • Radiographic Signs of Major Diseases
  • Suggested treatment guidelines based on findings
  • Radiographic Signs of High Impact Injuries
  • Foreign body ingestion, aspiration, and insertion
  • Pediatric foreign body aspiration and management

Day 2 Afternoon

procedure

Procedure Overview

  • Procedural Overview
  • Needle Decompression
  • Chest Tube Insertion
  • Tracheostomy Replacement
  • Shoulder Reduction and Immobilization
  • Upper Extremity Joint Aspiration
  • Trigger Point Injection
  • Nail Trephination
  • Nail Removal
  • Foreign Body and Fish Hook Removal
    Introduction to Suture Techniques
     
suturing

The Suturing Course

  • Suture Clinic and Equipment Introduction
  • Knot Tying
  • Simple Interrupted
  • Simple Running
  • Mattress
  • Subcutaneous/Multiple Layer Closure
  • Staples
  • Skin Adhesive
  • Surgeon’s Knot
  • Buried Knot
  • Billing and Documentation for Sutures
  • Local Injections and Digital Blocks
 
procedure

Procedure Workshop

  • Knee Injection and Aspiration
  • Shoulder Injection
  • Needle Decompression
  • Chest Tube Insertion

Day 3 Morning

Cervical Spine Injuries

  • Long Board and Collar Removal
  • NEXUS Criteria
  • Unstable Fractures
  • Mechanisms of Common Fractures
  • Immobilization
  • Ordering the Correct Studies
  • Correct Consult and Referral
 

Thoracic and Lumbar Spine Injuries

  • Spine form and function
  • Mechanisms of Injury
  • Unstable Fractures
  • Mechanisms of Common Fractures
  • Cauda Equina Syndrome
  • Epidural Abscess
  • Ordering the Correct Studies
  • Correct Consult and Referral
 
Extremity

Upper and Lower Extremity Injuries

  • Speaking Orthopedics
  • Common Patterns of Fractures
  • Common Dislocation and Reduction Techniques
  • Splinting Techniques and Compartment Syndrome
  • Clavicle, Shoulder, Humerus, Elbow, Radius. Ulna. Paired fractures, Wrist and Carpal Bones, Hand
  • Amputations
  • When to Consult Orthopedics
  • When to Consider Transfer/EMS
  • What to send home

Day 3 Afternoon

skin

Skin Conditions Not to Miss

  • Skin and Soft Tissue Conditions
  • Emergent Rash Identification
  • Cellulitis
  • Abscess Incision and Drainage
  • DVT Identification and Decisions Rules
  • Burn Care and Referral Criteria
  • What Not to Send Home
procedure

Procedure Workshop

  • Procedure Clinic
  • Lumbar Puncture
  • Splinting Workshop
  • Intraosseous Access
  • Central Venous Catheter Insertion

3-Day Clinical Skills & Procedure Workshop + The Ultrasound Course

Day 1 Morning

Introduction to Ultrasound

  • Ultrasound Physics
  • Probe functions and types
  • Methods of scanning (sliding, rocking, other movements and techniques)
  • Probe Settings (depth, “knobology”)
  • Hand movements and dexterity
ultrasound

Abdominal Ultrasound

  • Aorta (all views, normal anatomy, pathology)
  • Biliary Quadrant (gallbladder, stones, techniques)
  • Kidney (hydronephrosis, pyelonephritis)
  • Trans-abdominal Pelvis
procedure

Trauma Ultrasound

  • eFAST exam
  • Right upper quadrant imaging
  • Left upper quadrant imaging
  • Bladder Imaging
  • Cardiac Imaging
  • Lung Imaging
procedure

Free Scan with Live Models

  • Small groups, team led with hands-on guidance and findings

Day 1 Afternoon

Specialty Ultrasound

  • Ocular Ultrasound (retinal detachment, foreign bodies)
  • Foreign body imaging
  • Ultrasound-Guided IV and Central access technique
  • Lower Extremity Vascular Ultrasound
procedure

Afternoon Free Scan

  • Small groups, team led with hands-on guidance and findings
  • Review and individual practice sessions with instructors
  • Additional ultrasound applications
  • Wrap-Up and Closing

Day 2 Morning

Cardiac

Cardiac Disorders

  • Course Introduction
  • Cardiac Overview
  • EKG Interpretation
  • Acute MI (recognition, management)
  • Common Dysrhythmias
  • Electrolyte Abnormalities and rhythm impacts
  • Condition blocks
  • Bundle Branch Blocks
  • Application to practice
Pulmonary

Pulmonary Disorders

  • Pulmonary Overview
  • Basic Airway Assessment
  • Pneumothorax
  • Asthma Management
  • COPD Management
  • Supplemental Oxygenation
  • Wells Criteria
  • PERC Rule
  • Using D-Dimer
  • Pulmonary Embolism
  • Treatment of Pulmonary Embolism

Introduction to Radiology – Chest and Abdomen

 
  • Overview of Radiograph Interpretation
  • Chest, Shoulder, Clavicle Radiographs
  • Systemic Reading Process
  • Abnormal Radiographs
  • Radiographic Signs of Major Diseases
  • Suggested treatment guidelines based on findings
  • Radiographic Signs of High Impact Injuries
  • Foreign body ingestion, aspiration, and insertion
  • Pediatric foreign body aspiration and management

Day 2 Afternoon

procedure

Procedure Overview

  • Procedural Overview
  • Needle Decompression
  • Chest Tube Insertion
  • Tracheostomy Replacement
  • Shoulder Reduction and Immobilization
  • Upper Extremity Joint Aspiration
  • Trigger Point Injection
  • Nail Trephination
  • Nail Removal
  • Foreign Body and Fish Hook Removal
    Introduction to Suture Techniques
     
suturing

The Suturing Course

  • Suture Clinic and Equipment Introduction
  • Knot Tying
  • Simple Interrupted
  • Simple Running
  • Mattress
  • Subcutaneous/Multiple Layer Closure
  • Staples
  • Skin Adhesive
  • Surgeon’s Knot
  • Buried Knot
  • Billing and Documentation for Sutures
  • Local Injections and Digital Blocks
 
procedure

Procedure Workshop

  • Knee Injection and Aspiration
  • Shoulder Injection
  • Needle Decompression
  • Chest Tube Insertion

Day 3 Morning

Cervical Spine Injuries

  • Long Board and Collar Removal
  • NEXUS Criteria
  • Unstable Fractures
  • Mechanisms of Common Fractures
  • Immobilization
  • Ordering the Correct Studies
  • Correct Consult and Referral
 

Thoracic and Lumbar Spine Injuries

  • Spine form and function
  • Mechanisms of Injury
  • Unstable Fractures
  • Mechanisms of Common Fractures
  • Cauda Equina Syndrome
  • Epidural Abscess
  • Ordering the Correct Studies
  • Correct Consult and Referral
 
Extremity

Upper and Lower Extremity Injuries

  • Speaking Orthopedics
  • Common Patterns of Fractures
  • Common Dislocation and Reduction Techniques
  • Splinting Techniques and Compartment Syndrome
  • Clavicle, Shoulder, Humerus, Elbow, Radius. Ulna. Paired fractures, Wrist and Carpal Bones, Hand
  • Amputations
  • When to Consult Orthopedics
  • When to Consider Transfer/EMS
  • What to send home

Day 3 Afternoon

skin

Skin Conditions Not to Miss

  • Skin and Soft Tissue Conditions
  • Emergent Rash Identification
  • Cellulitis
  • Abscess Incision and Drainage
  • DVT Identification and Decisions Rules
  • Burn Care and Referral Criteria
  • What Not to Send Home
procedure

Procedure Workshop

  • Procedure Clinic
  • Lumbar Puncture
  • Splinting Workshop
  • Intraosseous Access
  • Central Venous Catheter Insertion

1-Day Advanced and Difficult Airway Course Schedule

Day 1 Morning

Airway Anatomy and Assessment

  • How to assess an airway
  • Identification of landmarks
  • Predicting a difficult airway
  • Special scenarios
  • Airway classification and grading

Indications for Airway Management

  • Clinical conditions
  • Respiratory status
  • Anatomy
  • Predictors of airway need
  • Common approaches