Social Media and Medicine: Do FaceBook and Twitter Put Your License at Risk?

The interest in this was generated from a conversation on the CORDem List-serve.

My take-home from the paper is that medical boards are more concerned about your Social Media behavior than you likely are.


"Thought everyone might be interested, on the heels of ****'s social media policy inquiry, to read this article (Greysen SR, Ann Intern Med. 2013;158:124-130.) on how surveyed State Medical Boards might view certain posts by practitioners on social media sites. Thought provoking. The highlights of the article are as follows:

The state medical boards who responded to the survey had a variety of opinions about what kinds of social media activity would prompt an investigation. There was wide consensus about some things, and very little consensus about others.

HIGH CONSENSUS: Things nearly all medical boards agree would trigger an investigation

Misinformation on a physician's website.
Posting photos of patients receiving medical treatment without their consent.
Contacting a patient through a dating website for a date.

MODERATE CONSENSUS: Less than three-quarters but more than half of medical boards said this would trigger an investigation.

Posting a photo onto a social media site of doctor clearly intoxicated.
Posting patient narratives containing potential identifiers.
Using discriminatory language on a blog or social media site.

LOW CONSENSUS: Things fewer than half of state medical boards said would trigger an investigation.

Posting something to a blog or social media site that is disrespectful of patients but doesn't contain potential identifiers.
Posting a photo to a social media site that shows doctors drinking but not clearly intoxicated."


WashU Journal Club:  

The Washington University in St. Louis Emergency Medicine Residency discussed whether Endotracheal Intubation by paramedics in the field impacts Pt outcome.  Here is a brief summary.

The Problem

You are on your favorite rotation of residency, EMS!  You are having a dinner discussion with some of your favorite attendings...EMS ones of course.  You ask the group "what do you think is the best way for EMS to manage the airway of cardiac arrest patients?" 
Dr. Levine responds: "I still have my medics intubate.  Endotracheal tubes are cheap and I also don't want my medics to lose their intubation skills by using alternate methods such as alternate airways or bag-valve-mask (BVM) ventilation."
The very intelligent and well-respected Dr. Svancarek gracefully responds: "But Dr. Levine, we now know that chest compressions are emphasized more than ever and intubation attempts in the field are difficult and timely and cause a significant number of chest compression interruptions.  I say the best way is an alternate airway or 2-rescuer BVM."
Dr. Tan then states:"I agree with Dr. Svancarek.  My medics go to the King first, although they have the option to intubate first if they feel it is a potentially easy airway."
Dr. Keeperman sighs and rolls his eyes.
Dr. Rathert: "What did I get myself into?"
Dr. Gilmore then pulls his ipad out: "You guys have clearly not been keeping up on the research.  Let’s pull some of the latest articles up and that should clear things up."

Or will it?

Bottom Line

Each year in the United States, Emergency Medical Services (EMS) treat approximately 300,000 cases of OOHCA (Lloyd-Jones 2009), with less than 10% of these patients surviving to hospital discharge (McNally 2011).  Several studies have suggested that EMS protocols which focus on minimizing interruptions in chest compressions, such as minimally interrupted cardiac resuscitation and cardiocerebral resuscitation protocols, improve rates of neurologically intact survival in OOHCA, as discussed at a previous Journal Club.   This has led to the American Heart Association placing more emphasis on chest compressions in CPR, deemphasizing the importance of definitive airway management (Field 2010).


ETI is often considered the standard method of definitive airway management.  Safety concerns with prehospital ETI, including unrecognized esophageal intubation (Bair 2005) and interruptions in chest compressions during CPR (Wang 2009), have led many to propose alternative techniques such as BVM ventilation, SGA insertion, and passive ventilation (Guyette 2007Hayes 2007Jensen 2010Deakin 2010).  Even with alternate airways, the risk for hyperventilation remains, which has been shown to increase thoracic pressure and decrease coronary perfusion pressure in a pig model (Aufderheide 2004), and decreases cerebral blood flow (Raichle 1972).


Much debate still exists as to the proper management of oxygenation and ventilation in OOHCA.  The majority of the literature on the subject is composed of observational studies, many based on pre-existing datasets (Bobrow 2009,Studnek 2010Wang 2012).  Dr. Henry Wang, one of the leading researchers in the area, has himself questioned the utility of such observational data (Wang 2010).  However, many barriers exist to performing prospective or randomized trials in the prehospital arena, including lack of funding and issues of obtaining consent in this setting, as previously documented by the Resuscitation Outcomes Consortium.  The FDA has made several recommendations regarding approval for Exception from Informed Consent (EFIC) (Table 1) which help illustrate this difficult process. While a large prospective, randomized trial to assess optimal airway management in OOHCA would be most helpful, we must utilize the current body of literature to develop EMS protocols.


Unfortunately, the current literature does not provide a clear answer to our clinical question.  While ETI leads to interruptions in chest compression during CPR (Wang 2009), the impact of such interruptions is not immediately apparent.  When passive ventilation was compared to BVM ventilation, improved neurologically intact survival was seen in patients with shockable rhythms; however, no significant difference was seen in the primary outcome, overall neurologically intact survival (Bobrow 2009).  One study showed a negative association between prehospital ETI and survival (Studnek 2010), while another study showed an association between successful ETI and survival (Wang 2012).  Such conflicting results leave a consensus far out of reach.  Additionally, EMS training has often focused on the development of technical skills, ETI among them.  Emphasis on continued use of ETI has persisted in part due to the association between clinical exposure and the likelihood of success on subsequent ETI attempts(Warner 2010Wang 2005).  The pride that many paramedics feel towards mastery of ETI complicates the implementation of strategies that place less emphasis on definitive airway management when definitive evidence to support  such strategies is lacking.




Prolonged CPR May Improve Outcomes

An article released yesterday in The Lancet shows that Pts who suffer in-hospital cardiac arrest appear to benefit from prolonged CPR.  Analysis of data from the Get With The Guidelines—Resuscitation registry in the US shows that Pts in hospitals where median CPR time was 25 minutes in non-survivors had a greater survivability to hospital discharge in those who survived when compared to those with median CPR time of 16 minutes.

While the study cannot tell you what is the appropriate time for CPR it does seem that for in-hospital cardiac arrest prolonged CPR may provide some benefit.


Innovative New Therapy for Severe Asthma Patients

The NY Times today discussed an innovative new therapy for severe asthma Pts. It involves the use of bronchial thermoplasty.  A bronchoscope is inserted down to the depths of of the bronchials where it is heated to 149 deg. F.  This atrophies the smooth muscles which in turn decreases their inflammation during asthma exaccerbations allowing airways to remain more patent.  For Pts with severe asthma it may prevent freqent ED visits and save lives.  Unfortunately it also costs $20,000 and isn't covered by many insurance companies.  Hopefully this therapy will help decrease the mortatlity of asthma which results in approcimately 3,400 deaths per year.  For the full article you can go the New York Times at .


New Phlebovirus Causing Severe Febrile Illness in My Own Back Yard

A New Phlebovirus is causing severe febrile illnesses in my own state of Missouri.  Read the attached New England Journal of Medicine article.

A New Phlebovirus Associated with Severe Febrile Illness in Missouri

Laura K. McMullan, Ph.D., Scott M. Folk, M.D., Aubree J. Kelly, M.S., Adam MacNeil, Ph.D., Cynthia S. Goldsmith, M.G.S., Maureen G. Metcalfe, B.S., Brigid C. Batten, M.P.H., César G. Albariño, Ph.D., Sherif R. Zaki, M.D., Ph.D., Pierre E. Rollin, M.D., William L. Nicholson, Ph.D., and Stuart T. Nichol, Ph.D.

N Engl J Med 2012; 367:834-841August 30, 2012

The phlebovirus genus contains more than 70 antigenically distinct viruses, which are divided into virus complexes according to whether they are borne by sand flies, mosquitoes, or ticks.1 Sand-fly–borne viruses are found in the Americas, Asia, Africa, and the Mediterranean region, and infection with these viruses commonly results in a self-limiting 3-day fever, with the exception of Toscana virus, which can cause aseptic meningitis.2 The prototype mosquito-borne phlebovirus is Rift Valley fever virus, which causes large-scale epizootics; human infection is often a self-limiting febrile illness that can progress to hepatitis, encephalitis, or hemorrhagic fever.3 The only tickborne phlebovirus known to cause human disease is severe fever with thrombocytopenia syndrome virus (SFTSV), which was recently identified in central and northeastern China.4


Patient 1

Patient 1 was a healthy 57-year-old man who lived on a 70-acre farm in northwestern Missouri. In early June 2009, he noticed a small nymphal tick embedded on his abdomen. The tick was subsequently removed with tweezers. There was no rash or localized itching. The following day, fever developed, which was followed by severe fatigue, headache, anorexia, nausea, and nonbloody diarrhea. Four days later, he was admitted to the hospital with a temperature of 37.9°C, which increased to 39.1°C the next day. Laboratory tests revealed a low white-cell count of 1900 cells per cubic millimeter, a low platelet count of 115,000 cells per cubic millimeter, and a low sodium level of 132 mmol per liter. Serum levels of liver aminotransferases were slightly elevated, with an alanine aminotransferase level of 57 U per liter and an aspartate aminotransferase level of 44 U per liter. The serum level of C-reactive protein was elevated at 2.9 mg per deciliter. (Laboratory details are provided in Table S1 in the Supplementary Appendix, available with the full text of this article at

The patient was hospitalized for 10 days. There was progression from moderate to severe thrombocytopenia, with a nadir of 37,000 cells per cubic millimeter on day 5 and 40,000 cells per cubic millimeter on days 6 and 7. Leukopenia continued throughout the hospitalization, with notable lymphopenia and mild neutropenia that progressed to moderate neutropenia on day 7 (Figure 1AFIGURE 1Laboratory Values for Patients 1 and 2.). Band forms were detected on days 2 and 8. An erythrocyte sedimentation rate was within the normal range at 9 mm per hour, and the erythrocyte count and hemoglobin were unremarkable and stable. The hematocrit was slightly low during hospitalization (Figure 1C). The prothrombin time and partial-thromboplastin time were normal.

Serum hepatic aminotransferase levels increased and peaked, with an alanine aminotransferase level of 315 U per liter and an aspartate aminotransferase level of 431 U per liter on day 8 (Figure 1B). Serum alkaline phosphatase levels rose within normal limits and peaked at 101 U per liter on day 9. Levels of creatinine and blood urea nitrogen remained normal. Urinalysis showed trace protein and 1+ ketones and was otherwise normal. Serum albumin levels were low, and serum sodium and calcium levels were mildly low.

On the second day of hospitalization, blood was sent to the Rickettsial Zoonoses Branch of the Centers for Disease Control and Prevention (CDC) and was subsequently shown to be negative forE. chaffeensis, E. ewingii, and rickettsiae of the spotted fever group on PCR assay. Serologic analysis later confirmed negative results of IgM and IgG assays for the spotted fever group and typhus. A rapid test for influenza A and B antigens was negative (Meridian Bioscience). Two blood cultures were sterile.

The patient was empirically placed on doxycycline (100 mg) intravenously twice daily for 14 days for suspected ehrlichiosis. Nonbloody diarrhea persisted through the fourth day of hospitalization. Stool specimens were negative for leukocytes, Clostridium difficile toxins, and salmonella, shigella, and campylobacter species. The results of two-dimensional echocardiography and chest radiography were normal.

The patient has reported fatigue and recurrent headaches in the 2 years since his hospitalization, but these symptoms cannot be clearly attributed to the viral infection. In addition, he initially had short-term memory difficulty, which has slowly improved, and anorexia, which resolved 4 to 6 weeks after discharge.

Patient 2

Patient 2 was a 67-year-old man with a 5-year history of type 2 diabetes who was otherwise healthy. He lived on an approximately 100-acre farm in northwestern Missouri. While on his property in early 2009, he received an average of 20 tick bites daily for approximately 2 weeks. He removed the embedded ticks with his fingers and tweezers. The last tick bite was noticed 1 week before hospitalization. Approximately 4 days before hospitalization, subjective fever, fatigue, and anorexia developed. Additional symptoms included myalgia, dry cough, and nonbloody diarrhea. No rash was noted before or during hospitalization.

On hospital admission in June 2009, his temperature was 38.1°C and reached 39.1°C the following day. Laboratory studies that were conducted on admission showed a low white-cell count of 2100 cells per cubic millimeter, a low platelet count of 78,000 cells per cubic millimeter, and a slightly elevated aspartate aminotransferase level of 54 U per liter (Figure 1A, 1B, and 1C). The serum sodium level was slightly low at 130 mmol per liter, as was the calcium level at 7.8 mg per deciliter (1.95 mmol per liter). The results of urinalysis were normal.

The patient was hospitalized for 12 days. After day 2, thrombocytopenia progressed from moderate to severe, with a nadir of 34,000 cells per cubic millimeter on days 5 and 6. Platelet numbers increased starting on day 8 and reached a normal level by day 11 (Figure 1C). Testing for antiplatelet antibodies was negative. Leukopenia continued until day 10, with mild neutropenia progressing to moderate neutropenia on days 6 to 8 (Figure 1A). Band forms were present on days 2 to 7, and lymphocytes gradually increased to a normal range by day 8 (Figure 1A). Erythrocyte counts and hemoglobin were within normal limits, and the hematocrit was slightly low throughout hospitalization. The prothrombin time, partial thromboplastin time, and fibrinogen levels were normal, but the serum D-dimer level was elevated, at 4.08 mg per liter.

Blood was collected on day 2 of hospitalization and sent to the CDC. PCR results were found to be negative for E. chaffeensis and a range of ehrlichia and anaplasma species. Testing that was specific for borrelia antibody (Quest Diagnostics) was negative.

Alanine and aspartate aminotransferase levels were elevated and increased to 355 U per liter on day 8 and 302 U per liter on day 10, respectively (Figure 1B). The alkaline phosphatase level was temporally high on day 10 but then resumed normal levels. Levels of creatinine and blood urea nitrogen remained normal. Levels of serum albumin and sodium remained low throughout hospitalization. Low serum calcium levels increased to normal by day 10. Results on chest radiography and abdominal ultrasonography were normal.

A bone marrow aspiration and biopsy were performed on day 2 of hospitalization. Trilineage hematopoiesis was detected, with less than 1% blasts and no ringed sideroblasts. There was notable defective development of erythrocytes (dyserythropoiesis) and megakaryocytes (dysmegakaryocytopoiesis). Flow cytometry confirmed 3 to 4% plasma cells with monoclonal lambda restriction, indicating response to infection. Cultures for fungi and mycobacteria were sterile.

The patient was initially treated empirically with intravenous piperacillin–tazobactam and was switched to ceftriaxone on hospital day 2 and to oral doxycycline (100 mg) twice daily on day 3 for suspected ehrlichiosis. He completed a 14-day course of doxycycline.

After hospital discharge, the patient noted fatigue, short-term memory difficulty, and anorexia. All the symptoms abated after 4 to 6 weeks and have not recurred in 2 years. Six months after discharge, the CDC confirmed the patient was negative for E. chaffeensis and Anaplasma phagocytophilum on IgG assay.


Clinical Specimens and Virus Culture

EDTA-treated blood was collected and leukocytes separated with the use of Ficoll histopaque gradients and inoculated onto the canine monocyte cell line DH82.5 Adherent and nonadherent cells were examined with the use of a modified rapid Wright–Giemsa stain (Diff-Quik). Culture supernatant was collected and transferred to Vero E6 cells and LLC-MK2 cells for virus propagation.

Virus Genome Sequencing

Total RNA was extracted from infected cell culture media with the use of TriPure (Roche) and RNeasy (Qiagen) columns and nonspecifically amplified by means of random primers in a one-step reverse-transcriptase PCR reaction (SSIII RT–Platinum Taq HiFi Enzyme Mix, Invitrogen). Complementary DNA products were sequenced by means of next-generation sequencing (Roche 454) and analyzed with the use of bioinformatics tools.6 (Details are provided in the Supplementary Appendix.)


Isolation of a Virus from Patient Leukocytes

Leukocytes were collected from both patients on day 2 of hospitalization and inoculated onto cultures of DH82 cells. These cultures showed cytopathic effects similar to early cultures of E. chaffeensis. However, cellular vacuoles did not contain bacterial morulae. Transfer of culture supernatants onto fresh DH82 cells resulted in similar cytopathic effects within 9 to 11 days. Cytopathic effects were less evident but also noted in Vero E6 cells 9 days after inoculation.

Studies were initiated to identify the suspected virus. Thin-section electron microscopy revealed enveloped particles averaging 86 nm in diameter, typical of a virus in the Bunyaviridae family (Figure 2FIGURE 2Thin-Section Electron Microscopy of Vero E6 Cells Revealing Virus Particles.).

Genetic Analysis of a Novel Phlebovirus

Total RNA was isolated from infected culture media and subjected to next-generation sequencing. The resulting full-length genome sequences were found to be similar to those of phleboviruses in the Bunyaviridae family, which are single-stranded, negative-sense RNA viruses comprised of three genome segments. We called this newly discovered virus the Heartland virus.

The phleboviruses share a similar genome organization.7 The L segment is 6.4 kb in length and encodes a large RNA-dependent RNA polymerase. The M segment is 3.4 kb in length and encodes a polyprotein processed into the virus glycoproteins Gn and Gc, which are used for virion entry and assembly. The S segment is 1.7 kb in length and encodes the nucleoprotein that encapsidates the genomic RNA and a nonstructural (NSs) protein in an ambisense coding strategy. The genomes of virus isolates from both patients were sequenced in their entirety and found to be closely related, with 98%, 95%, and 99% identity for the S, M, and L virus segments, respectively. The high genetic identity indicates that both patients were infected with the same phlebovirus strain, but the differences between the isolates suggest that the two patients were infected independently.

Phylogenetic Analysis

Phylogenetic analysis of the aligned amino acid sequence of the polymerase, glycoprotein, nucleoprotein, and NSs protein suggested that the novel virus is a distinct member of the phlebovirus genus, clustering with the tickborne viruses and most closely related to SFTSV4,8(Figure 3FIGURE 3Phylogenetic Analyses of Amino Acid Sequencing of Representative Members of the Phlebovirus Genus.). This relationship is distant; however, pairwise comparisons of the viral polymerase and nucleoprotein (the two most conserved virus proteins) showed differences of 27% and 38%, respectively. Greater differences are found among the phlebovirus complexes that are borne by ticks, sand flies, and mosquitoes, which differ by at least 35%.

The novel virus was also distinct from an uncharacterized bunyavirus called lone star virus, which was isolated in 1967 from a nymphal Amblyomma americanum tick found on a woodchuck in western Kentucky.9 Comparison of the polymerase amino acid sequence showed that lone star virus shared only 34% identity with the novel virus.

Viral RNA and Antigen in Bone Marrow Specimen

RNA of the novel virus was detected in bone marrow aspirate obtained from Patient 2. Immunohistochemical staining revealed the virus nucleocapsid protein in large mononuclear cells that did not resemble mature granulocytes, erythroid cells, or megakaryocytes. Staining was primarily cytoplasmic and seen in association with fragmented nuclear debris, which was a prominent finding in the biopsy specimen. No immunostaining was seen in control bone marrow–biopsy specimens or in normal rabbit serum used as a negative control (Figure 4FIGURE 4Histopathological and Immunohistochemical Staining of a Bone Marrow–Biopsy Sample from Patient 2., and the Methods section in the Supplementary Appendix).

Long-Term Presence of Reactive IgG Antibody

Patient serum samples were tested for the presence of antibodies reactive to the novel virus. In October 2011, more than 2 years after the onset of infection, blood was collected from both patients and serum samples were tested on enzyme-linked immunosorbent assay (ELISA) to detect IgG reactive with virus antigen (inactivated virus-infected cell lysate). Both serum samples were strongly positive, with titers of more than 6400.


Although Koch's postulates have not been completely fulfilled, our findings are consistent with the identification of a new pathogenic virus in the United States. This novel virus (which we called the Heartland virus) is a distinct member of the phlebovirus genus and is most closely related to tickborne phleboviruses, notably the recently isolated SFTSV. Clinical evaluations of the illness in the two patients who are described here probably do not reflect the entire spectrum of symptoms associated with this virus, yet both patients had a similar clinical course. Symptoms in the two patients included fever, fatigue, anorexia, and diarrhea.

Common laboratory findings were leukopenia with moderate neutropenia, thrombocytopenia, and elevated hepatic aminotransferase levels. Both patients had viremia on day 2 of hospitalization, approximately 7 days after the onset of symptoms. The temporal trends in white-cell and platelet counts and in aminotransferase levels were also strikingly similar between the two patients. Both patients presented with neutropenia that continued to decline to levels below 700 cells per cubic millimeter on days 6 and 7 of hospitalization. Thrombocytopenia continued until day 7 for both patients. Initially, the aminotransferase levels were only slightly elevated but spiked on days 7 and 8. After this time, there were increased levels of circulating neutrophils, lymphocytes, monocytes, and platelets, and aminotransferase levels began to normalize. Clinical evidence did not suggest respiratory or kidney involvement in either patient.

Many of the clinical and laboratory facets of this illness are similar to those reported for the tickborne phlebovirus SFTSV.2 However, we did not observe coagulation abnormalities despite a markedly low platelet count, whereas a minority of patients with SFTSV infection had an elongated partial thromboplastin time and thrombin time, an elevated fibrinogen level, and symptoms of gingival bleeding and hemorrhage, with fatalities from disseminated intravascular coagulation and cerebral hemorrhage.10,11 There have been numerous reports of person-to-person transmission on exposure to SFTSV-infected blood, and SFTSV has been detected in blood, throat swabs, urine, and feces obtained from patients with the infection.10-13 It remains to be determined whether the novel virus can be transmitted from person to person, since no family members or caregivers of either patient reported symptoms resembling those of the patients. It will be important to determine how patients acquire this viral infection in order to promote risk-reduction practices.

The clinical laboratory results, symptoms, and occurrence of tick bite are similar to those of ehrlichiosis infections.5 The novel virus should be considered as a possible etiologic agent in these instances, particularly when suspected ehrlichiosis does not improve within a few days of doxycycline treatment.

Although we did not isolate the novel virus from ticks, and tick specimens from the patients were not available, one potential vector is the lone star tick, A. americanum. Recent ecologic studies in central and southern Missouri found that 99.9% of captured ticks were A. americanum.14 A. americanum is abundant in northwestern Missouri and found throughout the southeastern and south–central United States, extending up the Atlantic coast to Maine.15 Both patients resided in areas with fragmented deciduous forest and old fields, suitable habitats for A. americanum. Studies will be required to determine the vector and potential hosts of this virus.

Although these two patients had severe disease, the incidence of infection with the novel virus and range of disease severity are currently unknown. Given the largely nonspecific symptoms observed, this virus could be a more common cause of human illness than is currently recognized. Epidemiologic and ecologic studies are needed to identify disease burden, risk factors for infection, and natural hosts of this new virus.

The findings and conclusions of this report are those of the authors and do not necessarily represent the views of the CDC.

Disclosure forms provided by the authors are available with the full text of this article at

Drs. McMullan and Folk contributed equally to this article.

We thank Christopher Paddock and Jana Ritter for their consultation on histopathological and immunohistochemical analyses, Amy Denison for extraction and quality assessment of nucleic acids from bone marrow–biopsy samples, Mike Flint and Anita McElroy for discussions and editorial assistance in the preparation of the manuscript, and Ute Ströher and the Viral Special Pathogens Branch diagnostics group for providing ELISA data on viral IgG.


From the Viral Special Pathogens Branch (L.K.M., A.M., C.G.A., P.E.R., S.T.N.) and the Infectious Disease Pathology Branch (C.S.G., M.G.M., B.C.B., S.R.Z.), Division of High-Consequence Pathogens and Pathology, and the Rickettsial Zoonoses Branch, Division of Vector-Borne Diseases (A.J.K., W.L.N.), Centers for Disease Control and Prevention, Atlanta; and Heartland Regional Medical Center, St. Joseph, MO (S.M.F).

Address reprint requests to Dr. Nichol at the Viral Special Pathogens Branch MS G14 or to Dr. Nicholson at the Rickettsial Zoonoses Branch MS G13, Centers for Disease Control and Prevention, 1600 Clifton Rd. NE, MS G-14, Atlanta, GA 30333, or at  or.