Erythema Multiforme

●Erythema multiforme (EM) is an acute, immune-mediated disorder that involves the skin and/ormucosal surfaces. The treatment of acute EM varies according to the severity of the acute eruption and the presence or absence of recurrent disease.

●Many cases of EM occur secondary to herpes simplex virus (HSV) infection. In patients with HSV-induced EM, treatment with oral antivirals in the acute setting does not alter the course of EM, and is not indicated.

●Most patients with EM can be managed with symptomatic therapy alone. For patients with cutaneous disease and/or mild oral mucosal involvement, treatment with topical corticosteroids, oral antihistamines, and/or an anesthetic mouthwash is sufficient.

●Severe oral mucosal involvement may be accompanied by intense pain and an inability to eat or drink. For patients with severe oral mucosal involvement, we suggest treatment with oral prednisone (40 to 60 mg/day) tapered over the course of two to four weeks (Grade 2C). Patients with disabling symptoms may require hospitalization for nutrition and pain control.

●Ocular involvement rarely may lead to keratitis, conjunctival scarring, or visual impairment. Patients with ocular symptoms should be referred to an ophthalmologist.

●Some patients with EM develop recurrent disease. When feasible, the inciting agent should be identified and eliminated. For patients with HSV-induced or idiopathic EM that recurs ≥6 times per year, or who have fewer, but disabling episodes, we recommend treatment with continuous antiviral therapy (Grade 1B).

●For patients with severe, recurrent EM who fail to respond to continuous systemic antiviral therapy, we suggest treatment with azathioprine, mycophenolate mofetil, or dapsone (Grade 2C). Other options for therapy include other immunomodulatory drugs.

NonSustained Ventricular Tachycardia

Non Sustained V Tachycardia:::

●A variety of definitions of nonsustained ventricular tachycardia (NSVT) have been published, but the most commonly used definition is three or more consecutive ventricular beats, a heart rate of >120 beats per minute, and a duration of arrhythmia of less than 30 seconds.

●Patients with NSVT are usually asymptomatic, although some patients may notice symptoms associated with episodes of NSVT. The type and intensity of symptoms, which may include palpitations, chest pain, shortness of breath, syncope, or presyncope, will vary depending upon the rate and duration of the NSVT along with the presence or absence of significant comorbid conditions.

●Few physical examination findings in patients with NSVT are unique and specific. By definition, patients will have a pulse exceeding 100 beats per minute during the episode. In addition, if the physical examination coincides with an episode of NSVT, this can reveal evidence of atrioventricular (AV) dissociation, including marked fluctuations in blood pressure, variability in the occurrence and intensity of heart sounds (especially S1), and cannon A waves.

●All patients with suspected NSVT should have a 12-lead electrocardiogram (ECG), although NSVT is frequently identified on continuous telemetric monitoring, in which case only one or two leads may be available for review.

●Once nonsustained ventricular tachycardia (NSVT) has been identified, reversible causes of arrhythmia should be sought, including electrolyte imbalances, myocardial ischemia, hypoxia, adverse drug effects, anemia, hypotension, and heart failure. For patients who have only a single asymptomatic episode of NSVT, often no further investigation is required. However, for patients with multiple episodes or for those with symptoms felt to be related to NSVT, a thorough diagnostic evaluation to exclude structural heart disease is warranted, including cardiac imaging and ambulatory ECG monitoring for most patients and invasive electrophysiology studies (EPS) only on rare occasions.

●Treatment of patients with NSVT is as follows:

•Patients with NSVT and no identified symptoms do not require any specific therapy directed toward the NSVT. However, some patients with NSVT who are found to have a cardiomyopathy with significantly reduced left ventricular systolic function may be evaluated for implantable cardioverter defibrillator (ICD) placement for primary prevention of sudden cardiac death related to sustained ventricular tachyarrhythmias.

•For the initial treatment of patients with symptomatic NSVT, we suggest beta blockers rather than calcium channel blockers or antiarrhythmic medications (Grade 2C).

•For patients with NSVT who remain symptomatic in spite of beta blockers, or who are unable to tolerate beta blockers due to side effects, we suggest adding a nondihydropyridine calcium channel blocker (ie, verapamil or diltiazem) rather than an antiarrhythmic medication

•For some patients who have frequent, highly symptomatic NSVT not adequately suppressed by beta blockers or calcium channel blockers, the addition of antiarrhythmic medications (table 1) may be helpful. We suggest amiodarone as the initial choice, rather than other antiarrhythmic drugs, based on its efficacy (Grade 2C).

•In patients who have very frequent, symptomatic monomorphic NSVT not controlled by medications or who are unable or unwilling to take medications, catheter ablation can be effective for reducing or eliminating NSVT and associated symptoms

Some FLASHCARDS in ED: FOAMed worth-sharing

credits: @foampodcast

qSOFA: UPDATED 2017

This is the latest Published article so far:

Sepsis: qSOFA More Accurate Than Previous Criteria in ED
Nicola M. Parry, DVM
January 19, 2017

In the emergency department (ED) setting, the quick Sequential Organ Failure Assessment (qSOFA) score is better than previous criteria for predicting in-hospital mortality among patients with suspected infection, a new study suggests.

Yonathan Freund, MD, PhD, from Pitié-Salpêtrière University Hospital, Paris, France, and colleagues published the results of their multicenter prospective cohort study online January 17 in JAMA.

"Among patients presenting to the [ED] with suspected infection, the use of qSOFA resulted in greater prognostic accuracy for in-hospital mortality than did either SIRS [systemic inflammatory response syndrome] or severe sepsis [criteria]," the authors write.

In 2016, a task force of experts was convened to redefine sepsis in the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). In the previous guideline, the definition of sepsis was based on SIRS criteria, which are nonspecific. In Sepsis-3, the experts redefined sepsis as life-threatening organ dysfunction resulting from a dysregulated host response to infection.

In patients with infection, organ dysfunction is now be identified by an increase in the SOFA score of at least 2 points. The experts recommend that clinicians use qSOFA in settings such as the ED to more rapidly identify patients with sepsis.

Dr Freund and colleagues therefore set out to prospectively validate qSOFA as a mortality predictor in the ED and to compare the accuracy of the new criteria with both the previously used SIRS criteria and the previous definition of severe sepsis (namely, at least two elements of SIRS and a blood lactate level of more than 2 mmol/L (18 mg/dL).

They conducted the study during a 4-week period in 30 EDs in France, Switzerland, Spain, and Belgium, including adult patients with a suspicion of infection who visited the recruiting EDs. Patients were screened and followed until death or hospital discharge.

For each patient, the ED physician recorded the three components of the qSOFA at their worst level during the ED stay (highest respiratory rate, lowest systolic blood pressure, and lowest Glasgow Coma Scale score). The presence of an altered mental status was also recorded independent of Glasgow Coma Scale.

The analysis included 879 patients with a median age of 67 years; 414 (47%) were women. Respiratory tract was the most common site of infection (n = 379; 43%).

"Overall, in-hospital mortality was 8%," the authors note. Patients with a qSOFA score lower than 2 had a 3% mortality rate (95% confidence interval [CI], 2% - 5%), whereas those with a score of 2 or higher had a 24% mortality rate (95% CI, 18% - 30%; absolute difference, 21% [95% CI, 15% - 26%]).

The researchers found qSOFA to be better at predicting in-hospital mortality (area under the receiver operating curve [AUROC], 0.80; 95% CI, 0.74 - 0.85) than the SIRS criteria (AUROC, 0.65; 95% CI, 0.59 - 0.70) and severe sepsis criteria (AUROC, 0.65; 95% CI, 0.59 - 0.70; P < .001 compared with qSOFA).

qSOFA had a sensitivity of 70% (95% CI, 59% - 80%) and specificity of 79% (95% CI, 76% - 82%) for prediction of in-hospital mortality. The test had a positive likelihood ratio of 3.40 (95% CI, 2.80 - 4.17) and a negative predictive value of 97% (95% CI, 95% - 98%).

After adjusting for patient age and site of infection, a qSOFA of 2 or higher was associated with in-hospital mortality with a hazard ratio (HR) of 6.2 (95% CI, 3.8 - 10.3; Harrell C, 0.83). In comparison, using the previous definition of severe sepsis, the HR was 3.5 (95% CI, 2.2 - 5.5).

"One of the strengths of this study is that it prospectively validates the [task force's] findings and highlights how these findings particularly apply to ED patients with even stronger results," the authors conclude.

An accompanying editorial emphasizes the importance of timely identification of patients with possible sepsis.

"[C]linicians must rely on clinical judgment, potentially augmented by clinical criteria validated to identify sepsis among patients with infection," write François Lamontagne, MD, from the University of Sherbrooke, Canada, and David A. Harrison, PhD, and Kathryn M. Rowan, PhD, both from the Intensive Care National Audit & Research Centre, London, United Kingdom.

According to the editorialists, studies have mainly used predictive validity to assess qSOFA. They highlight one particular study of patients with suspected infection that compared use of qSOFA with use of the more complex SOFA or Logistic Organ Dysfunction System tests for patient encounters in hospital settings. In the intensive care unit setting, qSOFA had a worse predictive validity for in-hospital mortality than SOFA or the Logistic Organ Dysfunction System had. However, outside the intensive care unit, qSOFA had a similar or better predictive validity than the other two tests had, despite its relative simplicity.

Although the editorialists acknowledge that qSOFA could therefore be most useful outside the intensive care unit, they stress that the test still needs further evaluation in other settings. For example, in some settings, factors such as how quickly patients with a suspected infection present to the hospital might vary substantially and could affect the test's predictive validity.

Dr Lamontagne and colleagues also suggest that use of qSOFA could be replaced by any highly accurate, rapid diagnostic tests for sepsis that might emerge. However, at least for now, "qSOFA appears a simple, rapid, inexpensive, and valid way to identify — among patients with suspected infection — those at a higher risk of having or developing sepsis," they conclude.

Dr Freund received lecturer fees from Daichi-Sankyo. One coauthor received personal fees from ThermoFisher Brahms, CrossJect, Sanofi, and LFB. Dr Lamontagne served as investigator for a study funded by GlaxoSmithKline and E-Motion, both of which funded remuneration of research staff. The other coauthors and editorialists have disclosed no relevant financial relationships.

JAMA. 2017;317:267-268, 301-308. Article abstract, Editorial extract

Evaluation of Patients with Suspected PE: Updated guidelines 2017

Evaluation of Patients With Suspected Acute Pulmonary Embolism:

Best Practice Advice From the Clinical Guidelines Committee of the American College of Physicians

Raja AS, Greenberg JO, Qaseem A, Denberg TD, Fitterman N, Schuur JD; Clinical Guidelines Committee of the American College of Physicians
Ann Intern Med. 2015;163:701-711

The diagnosis of pulmonary embolism (PE) is definitely one of the great challenges in acute care medicine. I can't think of any condition that is so frequently worked up with negative results and yet is also so often underdiagnosed, with catastrophic results and resulting litigation. In addition, we in EM are often chastised for overordering D-dimer levels and CT pulmonary angiograms (CTPAs), yet we continue to practice in this way for lack of an acceptable standard method of working up patients. However, there may finally be some good news that will decrease workups, misdiagnoses, and litigation.

In November 2015, the American College of Physicians' Clinical Guidelines Committee published a set of recommendations for best practice with regard to working up PE. The document was evidence-based, straightforward, and clinically relevant. The document essentially serves as a guideline recommendation from a major national organization, which provides strong medicolegal protection when following the recommendations.

There were six pieces of "Best Practice Advice" from the Committee, which I have listed below.

Best Practice Advice 1: Clinicians should initiate their evaluation of patients with possible PE by using validated clinical prediction rules (eg, Wells or revised Geneva scores) to estimate the pretest probability of PE as low, intermediate, or high risk.

Best Practice Advice 2: Clinicians should not obtain D-dimer measurements or imaging studies in patients with a low pretest probability of PE and who meet all of the pulmonary embolism rule-out criteria (PERC). If the patient with low pretest probability is PERC-negative, PE is considered ruled out and the workup is completed. If the patient is PERC-positive, a D-dimer value may then be obtained.

Best Practice Advice 3: A high-sensitivity D-dimer test (enzyme-linked immunosorbent assay) should be obtained as the initial diagnostic test in patients who (1) have a low pretest probability for PE but are PERC-positive, or (2) have an intermediate pretest probability of PE. If the D-dimer value is within normal limits, imaging is deferred and the workup for PE is completed. D-dimer testing should not be performed for patients with high pretest probability for PE (see Best Practice Advice 6, below).

Best Practice Advice 4: Clinicians should use an age-adjusted D-dimer threshold (top normal level = age × 10 ng/mL rather than a generic 500 ng/mL cutoff) for patients older than 50 years to determine whether imaging is necessary.

Best Practice Advice 5: Clinicians should not obtain imaging studies in patients with D-dimer levels below the cutoffs noted above.

Best Practice Advice 6: Clinicians should obtain imaging with CTPA in (1) patients with high pretest probabilities for PE, or (2) patients with elevated D-dimer levels based on the evaluations noted above. Clinicians should reserve ventilation/perfusion scans for patients with contraindications to CTPA or when CTPA is not available.

The authors add a recommendation to obtain lower-extremity ultrasound before CTPA in patients who have lower-extremity symptoms or in pregnant patients during the first trimester.

This set of recommendations, when taken as a whole, is certain to reduce testing, especially imaging and radiation exposure for many patients. The guidelines are a quick read and are chock-full of useful clinical information; they are a must-read for anyone who has an interest in the topic or who desires some of the background information behind these Best Practice Advice statements.

Anion Gap and the role of Carbonic Anhydrase: Simplified

Anion Gap and the role of Carbonic Anhydrase

Carbonic anhydrase catalyses the first part of the reversible reaction in which carbon dioxide and water are converted to carbonic acid (and vice versa):
CO2 + H2O ←→ H+ + HCO3-

In the kidney, carbonic anhydrase is found in the proximal convoluted tubule.

The equation is normally shifted to the left allowing the formed carbon dioxide to diffuse back into the systemic circulation. In the presence of a carbonic anhydrase inhibitor, such as acetazolamide, the equation is shifted to the right and more H+ and HCO3- is produced. The H+ is reabsorbed alongside chloride ions. However, the bicarbonate is passed in the urine as it is not easily absorbed in the nephron. This results in a hyperchloraemic, normal anion gap metabolic acidosis.

This effect can be used therapeutically to prevent acute mountain sickness. Whereas normally the hypoxic high altitude would stimulate ventilation resulting in a respiratory alkalosis, acetazolamide use causes net renal excretion of bicarbonate, correcting this abnormality.
With respiratory alkalosis the kidneys would physiologically excrete bicarbonate, but this takes two to three days. Acetazolamide speeds this process.
The anion gap is a simple method for discerning causes of metabolic acidosis. It relies on the fact that the concentration of cations in a solution (that is, plasma) must equal the concentration of anions. Cations have positive charge, anions have negative charge.
[Cations] = [Anions]
Most ions are unmeasured and individually have a low concentration. The measured ions in sufficient concentration are sodium, potassium, chloride and bicarbonate.

Therefore:
[Na] + [K] + [unmeasured cations] = [Cl] + [HCO3] [unmeasured anions]

And rearranging:
([Na] + [K]) - ([Cl] + [HCO3]) = [unmeasured anions] - [unmeasured cations].

In health the difference between unmeasured anions and unmeasured cations, known as the anion gap, is between 10-18 mmol/l. This value is helpful in discerning causes of metabolic acidosis, as if it is raised the acidosis is due to an unmeasured ion - such as lactate, ketones, salicylate in lactic acidosis, diabetic ketoacidosis and aspirin overdose respectively.

A normal anion gap suggests an acidosis due to bicarbonate or chloride handling - such as renal tubular acidosis, diarrhoea, ammonium chloride ingestion or, in this case, acetazolamide.

Acetazolamide is a carbonic anhydrase inhibitor which may result in a metabolic acidosis. This is not the result of an increase of unmeasured anion so therefore results in a normal anion gap. Therefore it is the best answer in this case. Other causes of a metabolic acidosis with normal anion gap are renal tubular acidosis, diarrhoea, pancreatic fistula and chloric acid (such as ammonium chloride) ingestion.

A metabolic acidosis with raised anion gap occurs in the setting of an additional unmeasured anion.
This occurs in lactic acidosis, diabetic ketoacidosis, aspirin overdose and methanol or ethylene glycol poisoning.

A metabolic alkalosis may be seen in vomiting, from other diuretics or excessive bicarbonate or antacid therapy.

Respiratory acidosis is defined by a raised pCO2 and is typically related to type 2 respiratory failure. It is seen in severe COPD, asthma, pneumonia or pulmonary oedema and hypoventilation due to sedatives, muscular disease (for example, myasthenia gravis) or chest wall trauma.

Respiratory alkalosis is seen in any cause of hyperventilation, either due to anxiety, or in hypoxic states such as asthma where adequate ventilation is preserved.

Orbital Cellulitis: Ophthalmology Emergencies

What are recommendations for patients with Orbital Cellulitis? 

Orbital cellulitis is an infection involving the contents of the orbit (fat and ocular muscles). Preseptal cellulitis and orbital cellulitis involve different anatomic sites, with preseptal cellulitis referring to infections of the soft tissues anterior to the orbital septum and orbital cellulitis referring to infections posterior to it . Although the two entities may initially be confused with one another, it is important to distinguish between them because they have very different clinical implications. Preseptal cellulitis is generally a mild condition that rarely leads to serious complications, whereas orbital cellulitis may cause loss of vision and even loss of life. Orbital cellulitis can usually be distinguished from preseptal cellulitis by its clinical features (ophthalmoplegia, pain with eye movements, and proptosis) and by imaging studies; in cases in which the distinction is not clear, clinicians should treat patients as though they have orbital cellulitis. Both conditions are more common in children than in adults.

●The most common underlying factor that leads to orbital cellulitis is acute sinusitis, particularly ethmoid sinusitis; less common causes are ophthalmic surgery and orbital trauma.

●Orbital cellulitis is often a polymicrobial infection. The most commonly identified pathogens in orbital cellulitis are Staphylococcus aureus and streptococci .

●The diagnosis of orbital cellulitis is suspected clinically and can be confirmed by contrast-enhanced computed tomography (CT) scanning of the orbits and sinuses. During the initial evaluation, it is critical to distinguish preseptal cellulitis from the more serious orbital cellulitis . It is also important to evaluate for complications of orbital cellulitis, such as subperiosteal abscess, orbital abscess, visual loss, and intracranial extension. Although both preseptal cellulitis and orbital cellulitis typically cause eyelid swelling with or without erythema, features such as ophthalmoplegia, pain with eye movements, and/orproptosis occur only with orbital cellulitis.

●The diagnosis of orbital cellulitis is made by a combination of physical examination findings (including formal assessments of extraocular movements, visual acuity, and proptosis), and radiologic assessment with CT scanning.

●We recommend that patients with suspected orbital cellulitis with any of the following features undergo a contrast-enhanced CT scan of the orbits and sinuses to confirm the diagnosis of orbital cellulitis and detect potential complications:

•Proptosis

•Limitation of eye movements

•Pain with eye movements

•Double vision

•Vision loss

•Edema extending beyond the eyelid margin

•Absolute neutrophil count (ANC) >10,000cell/microL

•Signs or symptoms of central nervous system (CNS) involvement

•Inability to examine the patient fully (usually patients less than one year of age)

•Patients who do not begin to show improvement within 24 to 48 hours of initiating appropriate therapy

●Complications of orbital cellulitis may develop rapidly and include subperiosteal and orbital abscesses, extension to the orbital apex causing vision loss, or intracranial extension causing epidural abscess or subdural empyema, intracranial abscess, meningitis, or cavernous sinus thrombosis.

●For patients with orbital cellulitis, we suggest initial empiric antibiotic treatment with parenteral broad-spectrum therapy with activity against S. aureus(including methicillin-resistant S. aureus [MRSA]), streptococci, and gram-negative bacilli; this should include vancomycin plus one of the following:ampicillin-sulbactam, piperacillin-tazobactam,ceftriaxone, or cefotaxime . If ceftriaxone or cefotaxime is employed and there is concern for intracranial extension, we suggest thatmetronidazole be added to the regimen to cover anaerobes .

●Signs and symptoms should begin to show improvement within 24 to 48 hours following the initiation of appropriate therapy; if this does not occur, repeat imaging should be performed and surgery should be considered.

●For patients with uncomplicated orbital cellulitis, we suggest that antibiotics be continued until all signs of orbital cellulitis have resolved, and for a total of at least two to three weeks (including both intravenous and oral therapy). A longer period (at least four weeks) is recommended for patients with severe ethmoid sinusitis and bony destruction of the sinus. The management of the complications of orbital cellulitis is discussed separately.

●Although initial treatment may consist of intravenous antibiotics alone, management should be in consultation with an ophthalmologist and an otolaryngologist because the physical examination requires ophthalmic and/or otolaryngologic expertise and surgery is sometimes required. The main indications for surgery are a poor response of the infection to antibiotic treatment, worsening visual acuity or pupillary changes, or evidence of an abscess, especially a large abscess (>10 mm in diameter) or one that fails to respond promptly to antibiotic treatment.