The message below was sent to me by Peter Shane. Some of you may be interested in this course...
As promised, I am writing in the hope that you might be able to publicize to your students my winter quarter (for them) course in The Internet, Democracy, and the Law. The course description appears below. Many thanks, Peter
THE INTERNET, LAW AND DEMOCRACY
Professor Peter Shane
Since the advent of the Internet, hopes have loomed large for its potential role in invigorating the quality of democratic life in both developing and post-industrial countries. This course will analyze the ways in which the production, consumption, and legal regulation of Internet speech and digital technologies shape the Internet's political impact on democracy, with special, but not exclusive reference to the experience of the United States.
The course will begin with an introduction to the Internet as a technological and political phenomenon, plus a brief survey of democratic theory. We will then consider the Internet as an information medium, as we might consider newspapers or broadcast journalism. A third section of the course will look at the Internet as a vehicle for governance and political action.
Our readings will introduce the idea of "e-democracy," and the challenges posed for e-democracy by issues of access, inclusion, and the digital divide. We will then consider the uses of the Internet for mobilizing interest groups, conducting electoral campaigns, as well as the phenomenon of "e-government." Following this survey, we will consider how law treats the Internet in its capacity as a "public square"or general forum for free speech. Specific topics will include fighting words, national security limits on speech, the regulation of obscenity, and defamation. We will then discuss the legal regulation of digital technologies as its affects their democratic prospects. Of particular concern will be debates over treating internet service providers as common carriers, mandating "net neutrality," promoting broadband deployment, and regulating technologies for sharing information. We will take a brief look at copyright issues and their potential impact on democracy, and then survey political and legal perspectives on data mining, data protection and freedom of information.
In order to accommodate potential enrollment by graduate students from other departments, the course is offered during the College of Law spring semester, but compressed into thirty 70-minute sessions taught over the ten-week winter quarter. Grading will be based 70 per cent on an all-essay take-home final examination, 20 per cent on student contributions to an online discussion forum, and 10 per cent on class participation. Because the College of Law spring semester begins one week later than Winter Quarter, 2009, graduate students from other departments will start this course during the second week of the quarter, and will be responsible only for the material in Classes 1-27. They will be welcome to attend the last three classes, which focus on the law of privacy, but attendance will be optional and the exam for non-law students will not cover this material. Law students and non-law students will be graded on separate curves.
Our primary texts will be Andrew Chadwick, Internet Politics: States, Citizens and New Communication Technologies (Oxford University Press, 2006), and Madeleine Schachter and Joel Kurtzberg, Law of Internet Speech (Carolina Academic Press, 3d ed., 2008).
COPS alumnus in the thick of TN election polling
COPS Ph.D. alumnus Jason Reineke, only a few months after graduation, is already getting attention with his work running the MTSU Poll. Here we seem him interviewed by local news discussing findings from a recent poll regarding the race between Obama and McCain in Tennessee. While completing the Ph.D., Jason also completed the graduate interdisciplinary specialization in survey research, which no doubt increased his value on the job market and helped him secure this position.
Miller: Makover Nation
Makeover Nation
The United States of Reinvention
Toby Miller
Life is very much a project in the United States—but not a straightforwardly individual one. A duality of individual free choice and disciplinary institutional governance is the grand national paradox. Simply being—leading life without a bumper sticker avowing one’s elective institutional affinities—seems implausible in a country consumed by the makeover—the idea that what you were born as need not define you forever.
As Toby Miller writes in his introduction: “I come neither to bury the makeover nor to praise the makeover, but to criticize it, even as I stand alternately bewildered, amused, appalled, and attracted by it.” In Makeover Nation he does just that in a witty, no-holds-barred style. Miller looks at the power of various forms of knowledge about people and their emotions as they have been applied to the US population, from talk therapy to drug treatment. He is particularly interested in young people—in examining how childhood is constructed—and pays close attention to the much-favored (and overused) diagnosis and treatment of ADHD/ADD. He also focuses his attention on metrosexuals and right-wing Christians to disclose how these opposing groups manifest their drive toward self-creation. Miller believes that we must question the pleasures of reinvention even as we embrace them.
COPS Globetrotters
In the past couple of weeks COPS members have been traveling the globe sharing their research with colleagues and students in the U.S. and abroad. For instance, Andrew Hayes just returned from a trip to England and Amsterdam. In England, he presented the paper "Self-Censorship as a Psychological Syndrome" to the Morrell Centre for Toleration Workshop on Self-Censorship at the University of York. He then hopped a plane to the Amsterdam School of Communication Research (ASCOR) to deliver a workshop on applied statistics. Meanwhile, Lance Holbert -- feeling the first chill of autumn in Columbus -- flew south to the University of Texas at Austin to participate in a gathering of 20 political communication scholars to celebrate the 40th anniversary of the landmark agenda setting study of McCombs and Shaw.
Fortunately, as we start the first day of the autumn quarter, our friends are back in Columbus safe and sound.
Fortunately, as we start the first day of the autumn quarter, our friends are back in Columbus safe and sound.
Meta Analysis of Election Polls 2008
Princeton is at it again this year, with its meta-analysis of election polls. COPS members with an interest in politics, public opinion, and methodology (i.e., every single one of you) will find their web page very interesting, and even addicting.
Bruno: Justified by Work
Justified by Work
Identity and the Meaning of Faith in Chicago’s Working-Class Churches
Robert Anthony Bruno
In Justified by Work, Robert Anthony Bruno sheds light on the simple but rarely asked question: “What role do faith and religious observance play in the everyday lives of working people?” While some historical work has been done on middle-, upper-, and professional-class notions of faith, money, time, and business ethics, the theological beliefs and experiences of working-class Americans have been practically ignored. Bruno’s book is embedded in the contemporary religious practices and beliefs of working-class Chicago-area congregations to show both how faith is inextricably interwoven in the everyday lives of the people who regularly attend places of worship and how class impacts the daily manifestation of these people’s religion (from theology to practice).
Most past religious scholarship has drawn a dichotomy between urban and suburban churches and has compared religious observance and denominational membership by race, gender, ethnicity, and recently, around the emergence of a “knowledge” and “entrepreneurial” class forms of church practice. Diverging from previous models, Justified by Work, based on author interviews with a wide spectrum of working-class Chicagoans, offers a comparative study of working-class religious practice and faith, across race and ethnic identity. Christian churches are represented by a Catholic Mexican congregation, an African American Baptist church, and a mixed eastern European church. Bruno examines as well how religious observance affects the life and attitudes of working-class Jews and Muslims in Chicago.
Acute Bronchitis
Acute Bronchitis
Susan Davids, MD, MPH and Ralph M. Schapira, MD in Rakel & Bope:
Acute bronchitis is one of the most common diagnoses made by primary care physicians in the
Acute bronchitis manifests as an acute respiratory illness of less than 3 weeks' duration, with or without sputum production. Acute bronchitis is a clinical diagnosis and must be distinguished from other respiratory diseases, such as pneumonia, acute exacerbation of chronic bronchitis (episode of worsening of symptoms and expiratory airflow obstruction in patients with chronic obstructive pulmonary disease), and the onset of asthma. Most cases of acute bronchitis occur in the fall and winter. The etiology of acute bronchitis is infectious, and viruses appear to be the cause of most cases. Influenzas A and B are the most common viruses isolated, although a wide variety of infectious agents have been identified, such as adenovirus, coronavirus, parainfluenza virus, respiratory syncytial virus, coxsackievirus, Mycoplasma pneumoniae, Bordetella pertussis, and Chlamydia pneumoniae.
Diagnosis of acute bronchitis is based on findings of a prominent cough that may be accompanied by wheezing and sputum production. Most patients are otherwise healthy and without preexisting respiratory disease. Nonspecific constitutional symptoms may also be part of acute bronchitis. Appropriate management of acute bronchitis is essential because it is one of the most common illnesses that present to physicians in the outpatient setting. Antibiotics are often prescribed unnecessarily for acute bronchitis and other respiratory tract illnesses; these prescriptions may potentially lead to adverse events (i.e., allergic reactions and gastrointestinal side effects) and bacterial resistance. Other medications, such as inhaled bronchodilators and antitussives, are often prescribed for acute bronchitis despite questionable evidence to support their routine use.
Pathophysiology of acute bronchitis involves an acute inflammatory response involving the mucosa of the trachea and bronchi, resulting in injury to the respiratory tract epithelium. Sputum production is increased and bronchoconstriction (potentially resulting in airflow obstruction and wheezing) can occur. Positron emission tomography (PET) of a patient with acute bronchitis confirms that the primary inflammatory changes occur in the trachea and bronchi and not the remainder of the lower respiratory track.
| CURRENT DIAGNOSIS |
| 1. Normal healthy adult with cough 2. Predominance of cough 3. Lasts 1 to 3 weeks 4. With or without sputum 5. Can be accompanied by other respiratory and constitutional symptoms 6. Absence of abnormal vital signs and physical exam suggesting pneumonia,particularly Heart rate >100 beats per minute Respiratory rate >24 breaths per minute Temperature >100.4°F (38°C) Lung findings suggest a consolidation process |
Diagnosis
Cough, phlegm (which may be purulent as both bacteria and viruses can cause purulent sputum), and wheezing help differentiate acute bronchitis from upper respiratory infections such as pharyngitis and sinusitis. Acute bronchitis must be differentiated from acute bacterial pneumonia. The absence of abnormalities in vital signs (heart rate >100 bpm, respiratory rate >24 breath/min, oral temperature >100.4°F [38°C] and physical examination of the chest) supports the diagnosis of acute bronchitis and makes the need for chest radiography unnecessary in most cases. The treatment and outcome of acute bronchitis and pneumonia are very different; a chest radiograph should always be obtained if there is uncertainty about the diagnosis. Chest radiography will demonstrate no lung infiltrates in a patient with acute bronchitis. In contrast, lung infiltrates are present in pneumonia. Pertussis or whooping cough should be considered in adults with cough in the setting of what appears to be an upper respiratory infection, even in those previously immunized. Typically, the cough of pertussis, unlike acute bronchitis, lasts for longer than 3 weeks. Other respiratory diseases, such as previously undiagnosed asthma, can also mimic acute bronchitis, although several features differentiate asthma from acute bronchitis (see Section 12). Rapid testing to diagnose influenza viruses A and B (the most common causes of acute bronchitis) as a cause of acute bronchitis should be considered given the availability of effective treatment if initiated in the first 48 hours.
Treatment
ANTIBIOTICS, INHALED BRONCHODILATORS, AND ANTITUSSIVES
Existing evidence does not support the routine use of antibiotics for uncomplicated cases of acute bronchitis. Although most cases of acute bronchitis are caused by viral infections, upwards of 60% of patients are prescribed antibiotic therapy, which is contributing to the rise of bacterial resistance to commonly used antibiotics. Meta-analyses examining the effectiveness of antibiotic therapy in patients without underlying lung disease suggest no consistent effect of antibiotics on the severity or duration of acute bronchitis. A recent study evaluated children and patients with colored sputum and found that they also did not benefit from antibiotics. This study also found that compared to other populations, the elderly were less likely to benefit from antibiotics. Smokers with acute bronchitis are even more likely to be prescribed antibiotics.
Their response to antibiotics was either equal to or worse than that of nonsmokers.
| CURRENT THERAPY |
| Antibiotics not routinely recommended If influenza is highly probable and patient is presenting within the first 48 hours, consider treatment with : a. Oseltamivir (Tamiflu) 75 mg b. Zanamivir (Relenza) 10 mg bid by inhalation for 5 days (influenza A/B) [*] c. Amantadine (Symmetrel) 100 mg bid or 200 mg once daily for 5 days (influenza A) [*] d. Rimantadine (Flumadine) 100 mg bid for 5 days (influenza A) In patients with evidence of bronchial hyperresponsiveness, consider treatment with a. β2-agonists for 1 to 2 weeks b. Antitussives in those with cough for 2 to 3 weeks c. Antipyretics and analgesics as needed d. Smoking cessation Education: cough likely to last 3 weeks or more. ' Due to emergence of antiviral resistance, use of these agents has been discouraged by the CDC. |
One possible reason for overuse of antibiotics is the concern by physicians about patient satisfaction. Studies show that patients presenting to the doctor expecting antibiotics were more likely to be prescribed antibiotics; studies also suggest that satisfaction is more related to appropriate patient education than to receiving antibiotics. Patient education should include information regarding the duration of symptoms associated with acute bronchitis. It was found that patients presented on average after 9 days of cough and that the cough persisted for an additional 12 days after the physician visit. This information can impart a realistic expectation of illness duration to the patient.
If influenza is highly suspected and the patient presents within 48 hours of the onset of symptoms, rapid diagnostic testing and treatment should be considered. Both amantadine (Symmetrel) and rimantadine (Flumadine) are effective for influenza A, and neuraminidase inhibitors, inhaled zanamivir (Relenza), and oral oseltamivir (Tamiflu) are effective for influenzas A and B. If these medications are initiated within the first 48 hours of symptoms (and ideally within 30 hours), the duration of illness can be shortened.
The evidence supporting the use of inhaled bronchodilators for the treatment of the symptoms has been variable. Two small trials reported a shorter duration of cough with the use of inhaled ß-agonists; another study reported benefit in those with evidence of bronchial hyperresponsiveness. Current recommendations support the use of ß-agonists only in patients with evidence of bronchial hyperresponsiveness (wheezing or spirometry demonstrating a forced expiration volume in 1 second [FEV1] <80%>
Antitussive agents have not been shown to improve the acute or early cough but did show some improvements in cough lasting longer than 3 weeks. The current recommendations are to use antitussives, namely dextromethorphan (Benylin) or codeine, in patients with cough of 2 to 3 weeks' duration.
Acute uncomplicated bronchitis is most often a viral illness in which antibiotics are not routinely indicated. Patients presenting with an acute respiratory illness, who are younger than 65 years old without existing pulmonary disease or other significant comorbid illness, should have a thorough physical examination, including vital signs. If the vital signs are normal and physical examination of the chest is clear, pneumonia can most likely be ruled out. In patients who present within 48 hours of onset of symptoms, influenza should be considered as effective therapy is available for acute bronchitis caused by influenzas A or B. Otherwise, the evidence for treatment with antibiotics does not support their routine use. Bronchodilators should be considered in those with evidence of bronchial hyperresponsiveness; cough suppressants should be considered in those with 2 to 3 weeks of cough. Patient education is an integral part of the treatment, and patients should receive information that provides realistic expectations regarding the duration of cough.
Football, of sorts
In spite of the OSU vs. USC hoopla of late, it isn't all about football at OSU. Ok, maybe football matters, but sometimes of a different kind. The Columbus Crew is currently #1 in the MLS, and we have a number of soccer fans, students and faculty, who enjoy attending the Crew games. For instance, here we see Jorg Matthes, Erik Nisbet, Andrew Hayes, and Ray Pingree watching the Crew win again. Maybe it doesn't look that exciting from this photo, but it is. Granted, if you really want to have fun, you have to hang with the grad students in the fan section.
Young Mie's article in Journal of Communication
You may be interested in reading the press release related to the paper published by Young Mie Kim and former graduate student John Vishak in the Journal of Communication. This study, about the relative informational effects of network news and late night comedy programs, taps into a topic that has received a lot of attention in recent years. I expect that this study is going to generate some news coverage both locally and nationally. Congrats to Young Mie and John on their interesting study being published!
Acne Vulgaris
Acne ulgaris
Major points
2. Affects 85% of adolescents aged 15–17 years
a. Microcomedone: microscopic plugging of the hair follicle that is the precursor lesion to
acne vulgaris
b. Open comedone (blackhead): plugging at the follicular opening; cellular plug of stratum
corneum with oxidized melanin within the follicle (Figure 1)
Figure 1 Comedonal acne - on forehead with open and closed comedones
c. Closed comedone (whitehead): plugging of the pilosebaceous unit just below the
follicular opening with cystic swelling of the duct; filled with cellular debris
2. Inflamatory lesions: papules, pustules, cysts, sinus tracts (Figures 2–4)
3. Scars: depressed, pitted, macular, papular, hypertrophic, keloidal
Figure 2 Papulopustular acne - numerous erythematous papules and pustules on the face
Figure 3 Cystic acne on the chest with erythematous nodules, crusts and scarring
Figure 4 Inflammatory acne with comedones, erythematous papules and nodules on the back of a teenager
Pathogenesis
References
Cunliffe WJ, Holand DB, Clark SM, Stable GI. Comedogenesis: some new aetiological, clinical and therapeutic strategies. Br J Dermatol 2000; 142: 1084–91
Harper JC, Thiboutot DM. Pathogenesis of acne: recent research advances. Adv Dermatol 2003; 19: 1–10
Lee DJ, VanDyke GS, Kim J. Update on pathogenesis and treatment of acne. Curr Opin Pediatr 2003; 15: 405–10
Leyden JJ. A review of the use of combination therapies for the treatment of acne vulgaris. J Am Acad Dermatol 2003; 49: S200–10
Lucky AW, Biro FM, Simbartl LA, et al. Predictors of severity of acne vulgaris in young adolescent girls: results of a five-year longitudinal study. J Pediatr 1997; 130: 30–9
Weiss JS. Current options for topical treatment of acne vulgaris. Pediatr Dermatol 1997; 14: 480–8
Major points
- Most prevalent skin disorder in pediatrics
2. Affects 85% of adolescents aged 15–17 years
- Lesion types:
a. Microcomedone: microscopic plugging of the hair follicle that is the precursor lesion to
acne vulgaris
b. Open comedone (blackhead): plugging at the follicular opening; cellular plug of stratum
corneum with oxidized melanin within the follicle (Figure 1)
Figure 1 Comedonal acne - on forehead with open and closed comedonesc. Closed comedone (whitehead): plugging of the pilosebaceous unit just below the
follicular opening with cystic swelling of the duct; filled with cellular debris
2. Inflamatory lesions: papules, pustules, cysts, sinus tracts (Figures 2–4)
3. Scars: depressed, pitted, macular, papular, hypertrophic, keloidal
- Acne is one of the earliest stages of adrenarche
- Lesion type often correlates with pubertal stage
1. Comedonal acne is predominant type in prepubertal children
2. Inflammatory acne is more prevalent in adolescents
- Develops in areas with high numbers of pilosebaceous units: face, chest, back
- Increased severity often predicted by earlier onset and positive family history of scarring acne
Figure 2 Papulopustular acne - numerous erythematous papules and pustules on the face
Figure 3 Cystic acne on the chest with erythematous nodules, crusts and scarring
Figure 4 Inflammatory acne with comedones, erythematous papules and nodules on the back of a teenagerPathogenesis
- Acne development is a complex process that involves four main contributing factors :
1. Abnormal keratinization and obstruction of the pilosebaceous unit
a. Initial lesion is a microcomedone; caused by obstruction of the follicular opening with
the accumulation of cellular debris
b. Obstruction is due to abnormal keratinization of the cells lining the follicle with delayed
shedding and increased cohesiveness
2. Hormonal stimulation and increased sebum production
a. Increased secretion and accumulation of sebum within the follicle which is stimulated
by increased adrenal and gonadal androgens that occur with adrenache
b. Poly cystic ovary syndrome, a heterogeneous disorder with altered gonadotropin
secretion, hyperandrogenism (acne, hirsutism and virilization), chronic anovulation,
obesity and insulin resistance
3. Bacterial overgrowth
a. Propionibacterium acnes overgrows within the dilated follicle
b. Bacterial lipases convert accumulated sebum triglycerides into free fatty acids that
cause inflammation
c. P. acnes also releases other proteolytic enzymes and chemotactic factors that further
stimulate inflammation and recruitment of polymorphonuclear cells (PMNs)
4. Inflammatory reaction
a. Inflammatory cells including PMNs are recruited to the area
b. Ingestion of bacteria by PMNs causes release of hydrolytic enzymes that causes
rupture of the follicular wall
c. This leads to intense inflammation and a surrounding foreign body reaction
- Clinical findings
- Drug-induced acne
- Chemical-induced acne
- Rosacea
- Gram-negative folliculitis
- Pityrosporum folliculitis
- Topical retinoids: important for normalizing keratinization (e.g. tretinoin, adapalene)
- Topical keratolytics: salicylic acid, azelaic acid
- Topical benzoyl peroxide preparations
- Topical antibiotics: clindamycin, erythromycin
- Systemic antibiotics for inflammatory lesions
1. Doxycycline, tetracycline and minocycline most commonly used in those >9 years of age - Systemic retinoids for severe cystic acne or early scarring
- Oral contraceptives
- Can have significant impact on social interactions and self-esteem and can lead to depression in severe cases
- May produce significant scarring in inflammatory and cystic lesions
- Can rarely be associated with an underlying endocrine disorder
Cunliffe WJ, Holand DB, Clark SM, Stable GI. Comedogenesis: some new aetiological, clinical and therapeutic strategies. Br J Dermatol 2000; 142: 1084–91
Harper JC, Thiboutot DM. Pathogenesis of acne: recent research advances. Adv Dermatol 2003; 19: 1–10
Lee DJ, VanDyke GS, Kim J. Update on pathogenesis and treatment of acne. Curr Opin Pediatr 2003; 15: 405–10
Leyden JJ. A review of the use of combination therapies for the treatment of acne vulgaris. J Am Acad Dermatol 2003; 49: S200–10
Lucky AW, Biro FM, Simbartl LA, et al. Predictors of severity of acne vulgaris in young adolescent girls: results of a five-year longitudinal study. J Pediatr 1997; 130: 30–9
Weiss JS. Current options for topical treatment of acne vulgaris. Pediatr Dermatol 1997; 14: 480–8
Bullous Pemphigoid
Bullous Pemphigoid
Major points
Figure 1. Bullous pemphigoid - large bullae on erythematous patches
Figure 2. Pemphigoid gestationis - in a young pregnant woman. Her child was unaffected
Bullous pemphigoid (BP) antigens are proteins in the hemidesmosomes (HDs). Autoantibody binds both inside the cell to plaques of HDs and outside cells to the extracellular section of HDs
BP antibodies are directed against both BPAg-1 (230 kDa) component and also BPAg-2 (180kDa) (also called type XVII collagen)
BP IgG can activate complement by the classical pathway causing leukocyte adherence to the basement membrane, degranulation of polymorphonuclear leukocytes and subsequent dermal–epidermal separation
Diagnosis
Histology: Subepidermal blister without necrosis, and superficial dermal infiltrate with lymphocytes, histiocytes and eosinophils
DIF: linear pattern of C3 and IgG at BMZ
Differential diagnosis
BP may be self-limited and can last several months to many years
Prognosis is good. In adults, half of treated patients go into remission in 2.5–6 years
- Large, tense blisters arising on normal or erythematous skin
- Mucous membrane involvement in 10–35%
- Sites of predilection: lower abdomen, inner thighs, flexor forearms or generalized
- Bullae may have clear or hemorrhagic fluid
Figure 1. Bullous pemphigoid - large bullae on erythematous patches
Figure 2. Pemphigoid gestationis - in a young pregnant woman. Her child was unaffected- Erosions tend to re-epithelialize quickly
- Nikolsky sign is negative
- New vesicles may form at the edge of old blisters
- Blisters do not tend to scar but may be hyperpigmented
- Mild to moderate pruritus
- Early lesions tend to look urticarial
- Rare in childhood
Bullous pemphigoid (BP) antigens are proteins in the hemidesmosomes (HDs). Autoantibody binds both inside the cell to plaques of HDs and outside cells to the extracellular section of HDs
BP antibodies are directed against both BPAg-1 (230 kDa) component and also BPAg-2 (180kDa) (also called type XVII collagen)
BP IgG can activate complement by the classical pathway causing leukocyte adherence to the basement membrane, degranulation of polymorphonuclear leukocytes and subsequent dermal–epidermal separation
Diagnosis
Histology: Subepidermal blister without necrosis, and superficial dermal infiltrate with lymphocytes, histiocytes and eosinophils
DIF: linear pattern of C3 and IgG at BMZ
Indirect immunoflourescence: 70–80% of patients will have circulating IgG which binds to stratified squamous epithelium; titers do not correlate with disease extent or activity ~50% have elevated IgE, and sometimes eosinophilia, which correlates with pruritus
Differential diagnosis
- Bullous insect bite reactions
- Bullous impetigo
- Bullous erythema multiforme
- Chronic bullous disease of childhood
- Prednisone 1–2mg/kg per day until activity is suppressed. Once under control, steroids should be tapered to avoid side-effects
- Steroid-sparing agents can be used as an adjunct: cyclophosphamide, azathioprine, cyclosporine, methotrexate, or gold
- Localized BP can be treated with high-potency topical steroids
- Some patients respond to sulfones, tetracycline, or nicotinamide
BP may be self-limited and can last several months to many years
Prognosis is good. In adults, half of treated patients go into remission in 2.5–6 years
More Forthcoming Faculty and Student Publications
Here are just a few of the forthcoming faculty publications from COPS group members that I have learned about. I'm sure there are more to follow!
William Eveland and Myiah Hively, "Political discussion frequency, network size, and 'heterogeneity' of discussion as predictors of political knowledge and participation" in Journal of Communication.
Myiah Hively and William Eveland, "Contextual antecedents and political consequences of adolescent political discussion, discussion elaboration, and network diversity" in Political Communication.
Lance Holbert, Heather LaMarre, and Kristen Landreville, "Fanning the flames of a partisan divide: The role of debate viewing in the formation of partisan-driven post-election evaluations of personal vote count accuracy" in Communication Research.
Young Mie Kim, “Issue publics in the new information environment: Selectivity, domain-specificity, and extremity” in Communication Research.
Andrew Hayes and Teresa Myers, “Testing the 'proximate casualties hypothesis': Local troop loss, attention to news, and support for military intervention” in Mass Communication and Society.
William Eveland and Myiah Hively, "Political discussion frequency, network size, and 'heterogeneity' of discussion as predictors of political knowledge and participation" in Journal of Communication.
Myiah Hively and William Eveland, "Contextual antecedents and political consequences of adolescent political discussion, discussion elaboration, and network diversity" in Political Communication.
Lance Holbert, Heather LaMarre, and Kristen Landreville, "Fanning the flames of a partisan divide: The role of debate viewing in the formation of partisan-driven post-election evaluations of personal vote count accuracy" in Communication Research.
Young Mie Kim, “Issue publics in the new information environment: Selectivity, domain-specificity, and extremity” in Communication Research.
Andrew Hayes and Teresa Myers, “Testing the 'proximate casualties hypothesis': Local troop loss, attention to news, and support for military intervention” in Mass Communication and Society.
LaMarre, Beam and Landreville Paper and Shen Paper Accepted at Press/Politics
The LaMarre, Beam and Landreville paper that won the top student paper award in AEJMC's Mass Communication & Society division last month -- "The irony of satire: Political ideology and the motivation to see what you want to see in The Colbert Report" -- was recently accepted for publication in the journal Press/Politics. Congrats Heather, Michael, and Kristen! This follows up the acceptance of Chris Shen's #2 student paper award winner in the same division -- "Staying alive: The impact of media momentum on candidacy attrition in the 1980-2004 primaries" -- also accepted for publication in Press/Politics. Congrats Chris!
Venomous Snakebite
Venomous Snakebite
Epidemiology
Venomous snakes (Fig. 1) of the world belong to the families Viperidae (subfamily Viperinae: Old World vipers; subfamily Crotalinae: New World and Asian pit vipers), Elapidae (including cobras, kraits, coral snakes, and all Australian venomous snakes), Hydrophiidae (sea snakes), Atractaspididae (burrowing asps), and Colubridae (a large family, of which most species are nonvenomous and only a few are dangerously toxic to humans). Bite rates are highest in temperate and tropical regions where the population subsists by manual agriculture. Estimates indicate >5 million bites annually by venomous snakes worldwide, with >125,000 deaths.
Figure 1. Types of highly venomous snakes. (A).The Viperidae, (B). The Elapidae, (C). Hydrophiidae (D). Atractaspididae
Snake Anatomy/Identification
The typical snake-venom apparatus consists of bilateral venom glands located below and behind the eye and connected by ducts to hollow, anterior maxillary teeth. In viperids (vipers and pit vipers), these teeth are long mobile fangs that retract against the roof of the mouth when the animal is at rest. In elapids and sea snakes, the fangs are smaller and are relatively fixed in an erect position. In ~20% of pit viper bites and higher percentages of other snakebites (e.g., up to 75% for sea snakes), no venom is released ("dry" bites). Significant envenomation probably occurs in ~50% of all venomous snakebites.
Differentiation of venomous from nonvenomous snake species can be difficult. Viperids are characterized by somewhat triangular heads (a feature shared with many harmless snakes); elliptical pupils (also seen in some nonvenomous snakes, such as boas and pythons); enlarged maxillary fangs; and, in pit vipers, paired heat-sensing pits (foveal organs) on each side of the head. The New World rattlesnakes generally have a series of interlocking keratin plates (the rattle) on the tip of the tail; the rattle is used to warn potentially threatening intruders. Color pattern is notoriously misleading in identifying most venomous snakes. Many harmless snakes have color patterns that closely mimic venomous snakes found in the same region.
Venoms and Clinical Manifestations
Snake venoms are complex mixtures of enzymes, low-molecular-weight polypeptides, glycoproteins, and metal ions. Among the deleterious components are hemorrhagins that promote vascular leakage and cause both local and systemic bleeding. Proteolytic enzymes cause local tissue necrosis, affect the coagulation pathway at various steps, and impair organ function. Myocardial depressant factors reduce cardiac output, and neurotoxins act either pre- or postsynaptically to inhibit peripheral nerve impulses. Most snake venoms have multisystem effects in their victims.
Envenomations by most viperids and some elapids with necrotizing venoms typically cause progressive local swelling, pain, ecchymosis (Fig. 2), and (over a period of hours or days) hemorrhagic bullae and serum-filled vesicles. In serious bites, tissue loss can be significant (Fig. 3). Systemic findings can include changes in taste, mouth numbness, muscle fasciculations, tachycardia or bradycardia, hypotension, pulmonary edema, hemorrhage (from essentially any anatomic site), and renal dysfunction. Envenomations by neurotoxic elapids such as kraits (Bungarus spp.), many Australian elapids [e.g., death adders (Atractaspis spp.) and tiger snakes (Notechis spp.)], some cobras (Naja spp.), and some viperids [e.g., the South American rattlesnake (Crotalus durissus) and some Indian Russell's vipers (Daboia russelii)] cause neurologic dysfunction. Early findings may consist of cranial nerve weakness (e.g., manifested by ptosis) and altered mental status. Severe poisoning may result in paralysis, including the muscles of respiration, and lead to death due to respiratory failure and aspiration. After elapid bites, the time of onset of venom intoxication varies from minutes to hours depending on the species involved, the anatomic location of the bite, and the amount of venom injected. Sea snake envenomation usually causes local pain (variable), myalgias, rhabdomyolysis, and neurotoxicity; these manifestations are occasionally delayed for hours.
Figure 2. Northern Pacific rattlesnake (Crotalus oreganus oreganus) envenomations. Top: Moderately severe envenomation. Note edema and early ecchymosis 2 h after a bite to the finger. Bottom: Severe envenomation. Note extensive ecchymosis 5 days after a bite to the ankle.
Figure3. Early stages of severe, full-thickness necrosis 5 days after a Russell's viper (Daboia russelii) bite in southwestern India
Treatment
Field Management
The most important aspect of prehospital care of a victim bitten by a venomous snake is rapid delivery to a medical facility equipped to provide supportive care (airway, breathing, and circulation) and antivenom administration. Most first aid recommendations made in the past are of little benefit, and some can actually worsen outcome. It is reasonable to apply a splint to the bitten extremity in order to lessen bleeding and discomfort and, if possible, to keep the extremity at approximately heart level. In developing regions, indigenous people should be encouraged to seek care quickly at health care facilities equipped with antivenoms as opposed to consulting traditional healers.
Although mechanical suction has been recommended in the field management of venomous snakebite for many years, there is now evidence that this intervention is of no benefit and can actually be deleterious in terms of local tissue damage.
Techniques or devices used for centuries in an effort to limit venom spread remain controversial. Lympho-occlusive bandages or tourniquets may limit spread only at the cost of greater local tissue damage, particularly with necrotic venoms. Because tourniquets lead to higher rates of amputation and loss of function, they absolutely should not be used. Elapid venoms that are primarily neurotoxic and have no significant local tissue effects may be localized by pressure-immobilization, in which the entire limb is immediately wrapped with a bandage (e.g., crepe or elastic) and then splinted. The wrap pressure must reach ~40–70 mmHg to be effective. Furthermore, if more than a few minutes from medical care, the victim must be carried out from the scene of the bite. Otherwise, muscular pumping will promote venom dispersal, even in bites to the upper extremities. In short, pressure-immobilization should be used only in cases where the offending snake is reliably identified and has a primarily neurotoxic venom, the rescuer is skilled in pressure-wrap application, and the victim can be carried to medical care—an uncommon combination of conditions. Besides tourniquets, other forbidden measures include incising or cooling the bite site, giving the victim alcoholic beverages, and applying electric shocks. The best first aid advice, as coined by Dr. Ian Simpson of the World Health Organization's Snakebite Treatment Group, is to "do it 'RIGHT'": reassure the victim, immobilize the extremity, get to the hospital, and inform the physician of telltale symptoms and signs.
Hospital Management
In the hospital, the victim should be closely monitored (vital signs, cardiac rhythm, oxygen saturation, urine output) while a history is quickly obtained and a rapid, thorough physical examination is performed. Victims of neurotoxic envenomation should be watched carefully for evidence of difficulty swallowing or respiratory insufficiency, which should prompt definitive securing of the airway by endotracheal intubation. To provide objective evidence of the progression of envenomation, the level of swelling in a bitten extremity should be marked and limb circumferences measured in several locations every 15 min until swelling has stabilized. Large-bore IV access in unaffected extremities should be established. Early hypotension is due to pooling of blood in the pulmonary and splanchnic vascular beds. Later, hemolysis and loss of intravascular volume into soft tissues may play important roles. Fluid resuscitation with isotonic saline should be initiated for clinical shock. If the blood pressure response to administration of crystalloid (20–40 mL/kg) is inadequate, a trial of 5% albumin (10–20 mL/kg) is prudent. If tissue perfusion fails to respond to volume resuscitation and antivenom infusion (see below), vasopressors (e.g., dopamine) can be added. Invasive hemodynamic monitoring (central venous and/or pulmonary arterial pressures) can be helpful in such cases, although obtaining access is risky if coagulopathy has developed.
Blood should be drawn for typing and cross-matching and for laboratory evaluation as soon as possible. Important studies include a complete blood count (to evaluate degree of hemorrhage or hemolysis and effects on platelet count), studies of renal and hepatic function, coagulation studies (to identify consumptive coagulopathy), and testing of urine for blood or myoglobin. In developing regions, the 20-min whole-blood clotting test (WBCT) can be used to diagnose coagulopathy reliably. A few milliliters of fresh blood are placed in a new, plain glass receptacle (e.g., test tube) and left undisturbed for 20 min. The tube is then tipped once to 45° to determine whether a clot has formed. If not, coagulopathy is diagnosed. In severe envenomations or with significant comorbidity, arterial blood gas studies, electrocardiography, and chest radiography may be helpful. Any arterial puncture in the setting of coagulopathy, however, requires great caution and must be performed at an anatomic site amenable to direct-pressure tamponade. After antivenom therapy (see below), laboratory values should be rechecked every 6 h until clinical stability is achieved.
The key to management of venomous snakebite is the administration of specific antivenom. Circulating venom components bind quickly with heterologous antibodies produced in animals immunized with the venom in question (or a very closely related venom). Antivenoms may be monospecific (for a particular snake species) or polyspecific (covering several medically important species in the region) but rarely offer cross-protection against snake species other than those used in their production unless the species are known to have homologous venoms. In the United States, assistance in finding antivenom can be obtained 24 h a day from regional poison control centers.
Indications for antivenom administration in victims of viperid bites include any evidence of systemic envenomation (systemic symptoms or signs; laboratory abnormalities) and (possibly) significant, progressive local findings (e.g., soft tissue swelling crossing a joint or involving more than half the bitten limb in the absence of a tourniquet). Care must be used in determining the significance of isolated soft-tissue swelling as, in many countries, the saliva of some relatively harmless snakes causes mild edema at the bite site. In such bites, antivenoms are unhelpful and unnecessary.
In the developing world (e.g., much of Asia and Africa), elapid bites are generally treated similarly to viperid bites. Systemic symptoms such as ptosis, other manifestations of cranial nerve impairment, or respiratory compromise constitute grounds for antivenom administration. Decisions about antivenom administration to victims with isolated local signs or symptoms are based on the criteria listed above for viperid bites.
Production of the only antivenom currently available in the United States for coral snake bites has been discontinued, and remaining stocks will be exhausted or will expire shortly. Until a suitable substitute is produced or imported, physicians caring for victims of Micrurus bites may have to rely on sound supportive care, especially airway management and respiratory support.
The package insert for the selected antivenom can be consulted regarding species covered, method of administration, starting dose, and need (if any) for re-dosing. The information in antivenom package inserts, however, is not always accurate and reliable. Whenever possible, it is advisable for treating physicians to seek advice from experts in snakebite management regarding indications for and dosing of antivenom. For viperid bites, antivenom administration should generally be continued as needed until the victim shows definite improvement (e.g., stabilized vital signs, reduced pain, restored coagulation). Neurotoxicity from elapid bites may be harder to reverse with antivenom. Once neurotoxicity is established and endotracheal intubation is required, further doses of antivenom are unlikely to be beneficial. In such cases, the victim must be maintained on mechanical ventilation until recovery occurs, which may take days to weeks.
The newest available antivenom in the United States (CroFab; Fougera, Melville, NY) is an ovine, Fab fragment antivenom that covers systemic venom effects of all North American pit viper species and carries a low risk of allergic sequelae. Table 1 compares the two antivenoms recently available for the treatment of pit viper bites in the United States. The manufacturer of Antivenin (Crotalidae) Polyvalent has recently discontinued its production, leaving CroFab as the current drug of choice for the management of indigenous pit viper envenomations in the United States. Use of any heterologous serum product carries a risk of anaphylactoid reactions and delayed-hypersensitivity reactions (serum sickness). Skin testing for potential allergy is insensitive and nonspecific and should be omitted. Worldwide, the quality and availability of antivenoms are highly variable. In many developing countries, antivenom resources are scarce, contributing to high morbidity and mortality rates in these regions. The rates of acute anaphylactoid reactions to some of these products exceed 50%. If the risk of allergic reaction is significant, pretreatment with appropriate loading doses of IV antihistamines (e.g., diphenhydramine, 1 mg/kg to a maximum of 100 mg; and cimetidine, 5–10 mg/kg to a maximum of 300 mg) may be considered. In some regions, a prophylactic SC or IM dose of epinephrine is given in an effort to reduce the risk of reaction. Further research is necessary to determine whether any pretreatment measures are truly beneficial. Modest expansion of the patient's intravascular volume with crystalloids could blunt an acute adverse reaction.
Pretreatment is not recommended by the manufacturer of CroFab. Epinephrine should, however, always be immediately available, and the antivenom dose to be administered should be diluted in an appropriate volume of crystalloid according to the package insert. Antivenom should be given only by the IV route, and the infusion should be started slowly, with the physician at the bedside during the initial period to intervene immediately at the first signs of any acute reaction. The rate of infusion can be increased gradually in the absence of a reaction until the full starting dose has been administered (over a total period of ~1 h). Further antivenom may be necessary if the patient's clinical condition fails to stabilize or worsens. After stabilization, additional doses of CroFab are often recommended as the small-molecular-weight Fab fragments are rapidly cleared from the circulation. Larger, whole IgG or F(ab)2 antivenoms have longer half-lives that eliminate the need for re-dosing after initial stabilization unless definitive symptoms of envenomation reappear.
If the patient develops an acute reaction to antivenom, the infusion should be temporarily stopped and the reaction immediately treated with IM epinephrine and IV antihistamine and steroids (Chap. 311). If the severity of envenomation warrants additional antivenom, the dose should be further diluted in isotonic saline and restarted as soon as possible. Rarely, in recalcitrant cases, a concomitant IV infusion of epinephrine may be required to hold allergic sequelae at bay while further antivenom is administered. The patient must be very closely monitored, preferably in an intensive care setting, during such therapy.
Blood products are rarely necessary in the management of the envenomated patient. The venoms of many snake species can cause a drop in platelet count or hematocrit and depletion of coagulation factors. Nevertheless, these components usually rebound within hours after administration of adequate antivenom. If the need for blood products is thought to be great (e.g., for a dangerously low platelet count in a hemorrhaging patient), these products still should be given only after adequate antivenom administration to avoid adding fuel to ongoing consumptive coagulopathy.
Rhabdomyolysis and hemolysis should be managed in standard fashion. Victims who develop acute renal failure should be evaluated by a nephrologist and referred for dialysis (peritoneal or hemodialysis) as needed. Such renal failure, usually due to acute tubular necrosis, is frequently reversible. If bilateral cortical necrosis occurs, however, the prognosis for renal recovery is more grim, and long-term dialysis with possible renal transplantation may be necessary.
Acetylcholinesterase inhibitors (e.g., edrophonium and neostigmine) may promote neurologic improvement in patients bitten by snakes with postsynaptic neurotoxins. Victims with objective evidence of neurologic dysfunction after snakebite should receive a trial of acetylcholinesterase inhibitors as outlined in Table 2. If they respond, additional doses of long-acting neostigmine can be continued as needed. Special vigilance is required to prevent aspiration if repetitive dosing of neostigmine is used in an attempt to obviate endotracheal intubation.
Care of the bite wound includes application of a dry sterile dressing and splinting of the extremity with padding between the digits. Once the administration of an indicated antivenom has been initiated, the extremity should be elevated above heart level to relieve edema. Tetanus immunization should be updated as appropriate. Prophylactic antibiotics are generally unnecessary after bites by North American snakes, as the incidence of secondary infection is low. Antibiotics can be considered, however, if misguided first-aid efforts have included incisions or mouth suction. In some regions of the world, secondary bacterial infection is more common and the consequences are dire. In these regions, prophylactic antibiotics (e.g., cephalosporins) are commonly used.
Most snake envenomations involve subcutaneous deposition of venom. On occasion, however, venom can be injected more deeply into muscle compartments. If swelling in the bitten extremity raises concern that subfascial muscle edema may be impeding tissue perfusion (muscle-compartment syndrome), intracompartmental pressures (ICPs) should be checked by any minimally invasive technique—e.g., wick catheter or ICP monitor (Stryker Instruments, Kalamazoo, MI). If any ICP is high (>30–40 mmHg), the extremity should be kept elevated while further antivenom is given. A dose of IV mannitol (1 g/kg) can be given in an effort to reduce muscle edema if the patient's hemodynamic status is stable. If, after 1 h of such therapy, the ICP remains elevated, a surgical consultation for possible fasciotomy should be obtained. While evidence from studies of animals suggests that fasciotomy may actually worsen myonecrosis, compartmental decompression is still required to preserve nerve function. Fortunately, the incidence of muscle-compartment syndrome is very low following snakebite.
Wound care in the days after the bite may require careful aseptic debridement of clearly necrotic tissue once coagulation has been restored. Intact serum-filled vesicles or hemorrhagic blebs should be left undisturbed. If ruptured, they should be debrided with sterile technique.
Physical therapy should be started when pain allows in order to return the victim to a functional state. The incidence of long-term loss of function (e.g., reduced range of motion, impaired sensory function) is unclear but is probably quite high (>30%), particularly after viperid bites.
Any patient with signs of venom poisoning should be observed in the hospital for at least 24 h. In North America, a patient with an apparently "dry" viperid bite should be watched for at least 8 h before discharge, as significant toxicity occasionally develops after a delay of several hours. The onset of systemic symptoms is commonly delayed for a number of hours after bites by several of the elapids (including coral snakes), some non–North American viperids [e.g., the hump-nosed pit viper (Hypnale hypnale)], and sea snakes. Patients bitten by these reptiles should be observed in the hospital for at least 24 h. Unstable patients should be admitted to a monitored setting.
At discharge, victims of venomous snakebite should be warned about signs and symptoms of wound infection and serum sickness as well as other potential long-term sequelae, such as pituitary insufficiency in Russell's viper (D. russelii) bites. If the victim had evidence of coagulopathy early on, this abnormality can recur during the first 2–3 weeks after the bite. Such victims should be warned to avoid elective surgery or activities posing a high risk of trauma during this period. Outpatient analgesic treatment and physical therapy should be continued.
In the event of serum sickness (fever, chills, urticaria, myalgias, arthralgias, and possibly renal or neurologic dysfunction developing 1–2 weeks after antivenom administration), the victim should be treated with systemic glucocorticoids (e.g., oral prednisone, 1–2 mg/kg daily) until all findings resolve, at which point the dose is tapered over 1–2 weeks. Oral antihistamines (e.g., diphenhydramine in standard doses) provide additional relief of symptoms.
Morbidity and Mortality
The overall mortality rates for venomous snakebite are low in areas with rapid access to medical care and appropriate antivenoms. In the United States, for example, the mortality rate is <1% for victims who receive antivenom. Eastern and western diamondback rattlesnakes (Crotalus adamanteus and C. atrox, respectively) are responsible for the few snakebite deaths occurring in the United States. Snakes responsible for large numbers of deaths in other regions include cobras (Naja spp.), carpet and saw-scaled vipers (Echis spp.), Russell's vipers (D. russelii), large African vipers (Bitis spp.), lancehead pit vipers (Bothrops spp.), and tropical rattlesnakes (C. durissus).
The incidence of morbidity—defined as permanent functional loss in a bitten extremity—is difficult to estimate but is substantial. Morbidity may be due to muscle, nerve, or vascular injury or to scar contracture. In the United States, such loss tends to be more common and severe after rattlesnake bites than after bites by copperheads (Agkistrodon contortrix) or water moccasins (A. piscivorus).
Epidemiology
Venomous snakes (Fig. 1) of the world belong to the families Viperidae (subfamily Viperinae: Old World vipers; subfamily Crotalinae: New World and Asian pit vipers), Elapidae (including cobras, kraits, coral snakes, and all Australian venomous snakes), Hydrophiidae (sea snakes), Atractaspididae (burrowing asps), and Colubridae (a large family, of which most species are nonvenomous and only a few are dangerously toxic to humans). Bite rates are highest in temperate and tropical regions where the population subsists by manual agriculture. Estimates indicate >5 million bites annually by venomous snakes worldwide, with >125,000 deaths.
Figure 1. Types of highly venomous snakes. (A).The Viperidae, (B). The Elapidae, (C). Hydrophiidae (D). AtractaspididaeSnake Anatomy/Identification
The typical snake-venom apparatus consists of bilateral venom glands located below and behind the eye and connected by ducts to hollow, anterior maxillary teeth. In viperids (vipers and pit vipers), these teeth are long mobile fangs that retract against the roof of the mouth when the animal is at rest. In elapids and sea snakes, the fangs are smaller and are relatively fixed in an erect position. In ~20% of pit viper bites and higher percentages of other snakebites (e.g., up to 75% for sea snakes), no venom is released ("dry" bites). Significant envenomation probably occurs in ~50% of all venomous snakebites.
Differentiation of venomous from nonvenomous snake species can be difficult. Viperids are characterized by somewhat triangular heads (a feature shared with many harmless snakes); elliptical pupils (also seen in some nonvenomous snakes, such as boas and pythons); enlarged maxillary fangs; and, in pit vipers, paired heat-sensing pits (foveal organs) on each side of the head. The New World rattlesnakes generally have a series of interlocking keratin plates (the rattle) on the tip of the tail; the rattle is used to warn potentially threatening intruders. Color pattern is notoriously misleading in identifying most venomous snakes. Many harmless snakes have color patterns that closely mimic venomous snakes found in the same region.
Venoms and Clinical Manifestations
Snake venoms are complex mixtures of enzymes, low-molecular-weight polypeptides, glycoproteins, and metal ions. Among the deleterious components are hemorrhagins that promote vascular leakage and cause both local and systemic bleeding. Proteolytic enzymes cause local tissue necrosis, affect the coagulation pathway at various steps, and impair organ function. Myocardial depressant factors reduce cardiac output, and neurotoxins act either pre- or postsynaptically to inhibit peripheral nerve impulses. Most snake venoms have multisystem effects in their victims.
Envenomations by most viperids and some elapids with necrotizing venoms typically cause progressive local swelling, pain, ecchymosis (Fig. 2), and (over a period of hours or days) hemorrhagic bullae and serum-filled vesicles. In serious bites, tissue loss can be significant (Fig. 3). Systemic findings can include changes in taste, mouth numbness, muscle fasciculations, tachycardia or bradycardia, hypotension, pulmonary edema, hemorrhage (from essentially any anatomic site), and renal dysfunction. Envenomations by neurotoxic elapids such as kraits (Bungarus spp.), many Australian elapids [e.g., death adders (Atractaspis spp.) and tiger snakes (Notechis spp.)], some cobras (Naja spp.), and some viperids [e.g., the South American rattlesnake (Crotalus durissus) and some Indian Russell's vipers (Daboia russelii)] cause neurologic dysfunction. Early findings may consist of cranial nerve weakness (e.g., manifested by ptosis) and altered mental status. Severe poisoning may result in paralysis, including the muscles of respiration, and lead to death due to respiratory failure and aspiration. After elapid bites, the time of onset of venom intoxication varies from minutes to hours depending on the species involved, the anatomic location of the bite, and the amount of venom injected. Sea snake envenomation usually causes local pain (variable), myalgias, rhabdomyolysis, and neurotoxicity; these manifestations are occasionally delayed for hours.
Figure 2. Northern Pacific rattlesnake (Crotalus oreganus oreganus) envenomations. Top: Moderately severe envenomation. Note edema and early ecchymosis 2 h after a bite to the finger. Bottom: Severe envenomation. Note extensive ecchymosis 5 days after a bite to the ankle.
Figure3. Early stages of severe, full-thickness necrosis 5 days after a Russell's viper (Daboia russelii) bite in southwestern IndiaTreatment
Field Management
The most important aspect of prehospital care of a victim bitten by a venomous snake is rapid delivery to a medical facility equipped to provide supportive care (airway, breathing, and circulation) and antivenom administration. Most first aid recommendations made in the past are of little benefit, and some can actually worsen outcome. It is reasonable to apply a splint to the bitten extremity in order to lessen bleeding and discomfort and, if possible, to keep the extremity at approximately heart level. In developing regions, indigenous people should be encouraged to seek care quickly at health care facilities equipped with antivenoms as opposed to consulting traditional healers.
Although mechanical suction has been recommended in the field management of venomous snakebite for many years, there is now evidence that this intervention is of no benefit and can actually be deleterious in terms of local tissue damage.
Techniques or devices used for centuries in an effort to limit venom spread remain controversial. Lympho-occlusive bandages or tourniquets may limit spread only at the cost of greater local tissue damage, particularly with necrotic venoms. Because tourniquets lead to higher rates of amputation and loss of function, they absolutely should not be used. Elapid venoms that are primarily neurotoxic and have no significant local tissue effects may be localized by pressure-immobilization, in which the entire limb is immediately wrapped with a bandage (e.g., crepe or elastic) and then splinted. The wrap pressure must reach ~40–70 mmHg to be effective. Furthermore, if more than a few minutes from medical care, the victim must be carried out from the scene of the bite. Otherwise, muscular pumping will promote venom dispersal, even in bites to the upper extremities. In short, pressure-immobilization should be used only in cases where the offending snake is reliably identified and has a primarily neurotoxic venom, the rescuer is skilled in pressure-wrap application, and the victim can be carried to medical care—an uncommon combination of conditions. Besides tourniquets, other forbidden measures include incising or cooling the bite site, giving the victim alcoholic beverages, and applying electric shocks. The best first aid advice, as coined by Dr. Ian Simpson of the World Health Organization's Snakebite Treatment Group, is to "do it 'RIGHT'": reassure the victim, immobilize the extremity, get to the hospital, and inform the physician of telltale symptoms and signs.
Hospital Management
In the hospital, the victim should be closely monitored (vital signs, cardiac rhythm, oxygen saturation, urine output) while a history is quickly obtained and a rapid, thorough physical examination is performed. Victims of neurotoxic envenomation should be watched carefully for evidence of difficulty swallowing or respiratory insufficiency, which should prompt definitive securing of the airway by endotracheal intubation. To provide objective evidence of the progression of envenomation, the level of swelling in a bitten extremity should be marked and limb circumferences measured in several locations every 15 min until swelling has stabilized. Large-bore IV access in unaffected extremities should be established. Early hypotension is due to pooling of blood in the pulmonary and splanchnic vascular beds. Later, hemolysis and loss of intravascular volume into soft tissues may play important roles. Fluid resuscitation with isotonic saline should be initiated for clinical shock. If the blood pressure response to administration of crystalloid (20–40 mL/kg) is inadequate, a trial of 5% albumin (10–20 mL/kg) is prudent. If tissue perfusion fails to respond to volume resuscitation and antivenom infusion (see below), vasopressors (e.g., dopamine) can be added. Invasive hemodynamic monitoring (central venous and/or pulmonary arterial pressures) can be helpful in such cases, although obtaining access is risky if coagulopathy has developed.
Blood should be drawn for typing and cross-matching and for laboratory evaluation as soon as possible. Important studies include a complete blood count (to evaluate degree of hemorrhage or hemolysis and effects on platelet count), studies of renal and hepatic function, coagulation studies (to identify consumptive coagulopathy), and testing of urine for blood or myoglobin. In developing regions, the 20-min whole-blood clotting test (WBCT) can be used to diagnose coagulopathy reliably. A few milliliters of fresh blood are placed in a new, plain glass receptacle (e.g., test tube) and left undisturbed for 20 min. The tube is then tipped once to 45° to determine whether a clot has formed. If not, coagulopathy is diagnosed. In severe envenomations or with significant comorbidity, arterial blood gas studies, electrocardiography, and chest radiography may be helpful. Any arterial puncture in the setting of coagulopathy, however, requires great caution and must be performed at an anatomic site amenable to direct-pressure tamponade. After antivenom therapy (see below), laboratory values should be rechecked every 6 h until clinical stability is achieved.
The key to management of venomous snakebite is the administration of specific antivenom. Circulating venom components bind quickly with heterologous antibodies produced in animals immunized with the venom in question (or a very closely related venom). Antivenoms may be monospecific (for a particular snake species) or polyspecific (covering several medically important species in the region) but rarely offer cross-protection against snake species other than those used in their production unless the species are known to have homologous venoms. In the United States, assistance in finding antivenom can be obtained 24 h a day from regional poison control centers.
Indications for antivenom administration in victims of viperid bites include any evidence of systemic envenomation (systemic symptoms or signs; laboratory abnormalities) and (possibly) significant, progressive local findings (e.g., soft tissue swelling crossing a joint or involving more than half the bitten limb in the absence of a tourniquet). Care must be used in determining the significance of isolated soft-tissue swelling as, in many countries, the saliva of some relatively harmless snakes causes mild edema at the bite site. In such bites, antivenoms are unhelpful and unnecessary.
In the developing world (e.g., much of Asia and Africa), elapid bites are generally treated similarly to viperid bites. Systemic symptoms such as ptosis, other manifestations of cranial nerve impairment, or respiratory compromise constitute grounds for antivenom administration. Decisions about antivenom administration to victims with isolated local signs or symptoms are based on the criteria listed above for viperid bites.
Production of the only antivenom currently available in the United States for coral snake bites has been discontinued, and remaining stocks will be exhausted or will expire shortly. Until a suitable substitute is produced or imported, physicians caring for victims of Micrurus bites may have to rely on sound supportive care, especially airway management and respiratory support.
The package insert for the selected antivenom can be consulted regarding species covered, method of administration, starting dose, and need (if any) for re-dosing. The information in antivenom package inserts, however, is not always accurate and reliable. Whenever possible, it is advisable for treating physicians to seek advice from experts in snakebite management regarding indications for and dosing of antivenom. For viperid bites, antivenom administration should generally be continued as needed until the victim shows definite improvement (e.g., stabilized vital signs, reduced pain, restored coagulation). Neurotoxicity from elapid bites may be harder to reverse with antivenom. Once neurotoxicity is established and endotracheal intubation is required, further doses of antivenom are unlikely to be beneficial. In such cases, the victim must be maintained on mechanical ventilation until recovery occurs, which may take days to weeks.
The newest available antivenom in the United States (CroFab; Fougera, Melville, NY) is an ovine, Fab fragment antivenom that covers systemic venom effects of all North American pit viper species and carries a low risk of allergic sequelae. Table 1 compares the two antivenoms recently available for the treatment of pit viper bites in the United States. The manufacturer of Antivenin (Crotalidae) Polyvalent has recently discontinued its production, leaving CroFab as the current drug of choice for the management of indigenous pit viper envenomations in the United States. Use of any heterologous serum product carries a risk of anaphylactoid reactions and delayed-hypersensitivity reactions (serum sickness). Skin testing for potential allergy is insensitive and nonspecific and should be omitted. Worldwide, the quality and availability of antivenoms are highly variable. In many developing countries, antivenom resources are scarce, contributing to high morbidity and mortality rates in these regions. The rates of acute anaphylactoid reactions to some of these products exceed 50%. If the risk of allergic reaction is significant, pretreatment with appropriate loading doses of IV antihistamines (e.g., diphenhydramine, 1 mg/kg to a maximum of 100 mg; and cimetidine, 5–10 mg/kg to a maximum of 300 mg) may be considered. In some regions, a prophylactic SC or IM dose of epinephrine is given in an effort to reduce the risk of reaction. Further research is necessary to determine whether any pretreatment measures are truly beneficial. Modest expansion of the patient's intravascular volume with crystalloids could blunt an acute adverse reaction.
Pretreatment is not recommended by the manufacturer of CroFab. Epinephrine should, however, always be immediately available, and the antivenom dose to be administered should be diluted in an appropriate volume of crystalloid according to the package insert. Antivenom should be given only by the IV route, and the infusion should be started slowly, with the physician at the bedside during the initial period to intervene immediately at the first signs of any acute reaction. The rate of infusion can be increased gradually in the absence of a reaction until the full starting dose has been administered (over a total period of ~1 h). Further antivenom may be necessary if the patient's clinical condition fails to stabilize or worsens. After stabilization, additional doses of CroFab are often recommended as the small-molecular-weight Fab fragments are rapidly cleared from the circulation. Larger, whole IgG or F(ab)2 antivenoms have longer half-lives that eliminate the need for re-dosing after initial stabilization unless definitive symptoms of envenomation reappear.
If the patient develops an acute reaction to antivenom, the infusion should be temporarily stopped and the reaction immediately treated with IM epinephrine and IV antihistamine and steroids (Chap. 311). If the severity of envenomation warrants additional antivenom, the dose should be further diluted in isotonic saline and restarted as soon as possible. Rarely, in recalcitrant cases, a concomitant IV infusion of epinephrine may be required to hold allergic sequelae at bay while further antivenom is administered. The patient must be very closely monitored, preferably in an intensive care setting, during such therapy.
Blood products are rarely necessary in the management of the envenomated patient. The venoms of many snake species can cause a drop in platelet count or hematocrit and depletion of coagulation factors. Nevertheless, these components usually rebound within hours after administration of adequate antivenom. If the need for blood products is thought to be great (e.g., for a dangerously low platelet count in a hemorrhaging patient), these products still should be given only after adequate antivenom administration to avoid adding fuel to ongoing consumptive coagulopathy.
Rhabdomyolysis and hemolysis should be managed in standard fashion. Victims who develop acute renal failure should be evaluated by a nephrologist and referred for dialysis (peritoneal or hemodialysis) as needed. Such renal failure, usually due to acute tubular necrosis, is frequently reversible. If bilateral cortical necrosis occurs, however, the prognosis for renal recovery is more grim, and long-term dialysis with possible renal transplantation may be necessary.
Acetylcholinesterase inhibitors (e.g., edrophonium and neostigmine) may promote neurologic improvement in patients bitten by snakes with postsynaptic neurotoxins. Victims with objective evidence of neurologic dysfunction after snakebite should receive a trial of acetylcholinesterase inhibitors as outlined in Table 2. If they respond, additional doses of long-acting neostigmine can be continued as needed. Special vigilance is required to prevent aspiration if repetitive dosing of neostigmine is used in an attempt to obviate endotracheal intubation.
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Most snake envenomations involve subcutaneous deposition of venom. On occasion, however, venom can be injected more deeply into muscle compartments. If swelling in the bitten extremity raises concern that subfascial muscle edema may be impeding tissue perfusion (muscle-compartment syndrome), intracompartmental pressures (ICPs) should be checked by any minimally invasive technique—e.g., wick catheter or ICP monitor (Stryker Instruments, Kalamazoo, MI). If any ICP is high (>30–40 mmHg), the extremity should be kept elevated while further antivenom is given. A dose of IV mannitol (1 g/kg) can be given in an effort to reduce muscle edema if the patient's hemodynamic status is stable. If, after 1 h of such therapy, the ICP remains elevated, a surgical consultation for possible fasciotomy should be obtained. While evidence from studies of animals suggests that fasciotomy may actually worsen myonecrosis, compartmental decompression is still required to preserve nerve function. Fortunately, the incidence of muscle-compartment syndrome is very low following snakebite.
Wound care in the days after the bite may require careful aseptic debridement of clearly necrotic tissue once coagulation has been restored. Intact serum-filled vesicles or hemorrhagic blebs should be left undisturbed. If ruptured, they should be debrided with sterile technique.
Physical therapy should be started when pain allows in order to return the victim to a functional state. The incidence of long-term loss of function (e.g., reduced range of motion, impaired sensory function) is unclear but is probably quite high (>30%), particularly after viperid bites.
Any patient with signs of venom poisoning should be observed in the hospital for at least 24 h. In North America, a patient with an apparently "dry" viperid bite should be watched for at least 8 h before discharge, as significant toxicity occasionally develops after a delay of several hours. The onset of systemic symptoms is commonly delayed for a number of hours after bites by several of the elapids (including coral snakes), some non–North American viperids [e.g., the hump-nosed pit viper (Hypnale hypnale)], and sea snakes. Patients bitten by these reptiles should be observed in the hospital for at least 24 h. Unstable patients should be admitted to a monitored setting.
At discharge, victims of venomous snakebite should be warned about signs and symptoms of wound infection and serum sickness as well as other potential long-term sequelae, such as pituitary insufficiency in Russell's viper (D. russelii) bites. If the victim had evidence of coagulopathy early on, this abnormality can recur during the first 2–3 weeks after the bite. Such victims should be warned to avoid elective surgery or activities posing a high risk of trauma during this period. Outpatient analgesic treatment and physical therapy should be continued.
In the event of serum sickness (fever, chills, urticaria, myalgias, arthralgias, and possibly renal or neurologic dysfunction developing 1–2 weeks after antivenom administration), the victim should be treated with systemic glucocorticoids (e.g., oral prednisone, 1–2 mg/kg daily) until all findings resolve, at which point the dose is tapered over 1–2 weeks. Oral antihistamines (e.g., diphenhydramine in standard doses) provide additional relief of symptoms.
Morbidity and Mortality
The overall mortality rates for venomous snakebite are low in areas with rapid access to medical care and appropriate antivenoms. In the United States, for example, the mortality rate is <1% for victims who receive antivenom. Eastern and western diamondback rattlesnakes (Crotalus adamanteus and C. atrox, respectively) are responsible for the few snakebite deaths occurring in the United States. Snakes responsible for large numbers of deaths in other regions include cobras (Naja spp.), carpet and saw-scaled vipers (Echis spp.), Russell's vipers (D. russelii), large African vipers (Bitis spp.), lancehead pit vipers (Bothrops spp.), and tropical rattlesnakes (C. durissus).
The incidence of morbidity—defined as permanent functional loss in a bitten extremity—is difficult to estimate but is substantial. Morbidity may be due to muscle, nerve, or vascular injury or to scar contracture. In the United States, such loss tends to be more common and severe after rattlesnake bites than after bites by copperheads (Agkistrodon contortrix) or water moccasins (A. piscivorus).
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