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[...]the article discusses the new and surprisingly effective use of ketamine. Of that group, the prevalence of depression was more than three times as great as in those not using such medications.14 Risk factors for developing MDD include low social support, divorce, substance use disorder, and chronic medical conditions.9,10 The process may be bidirectional in that patients with MDD appear to have a higher risk of developing diabetes and coronary artery disease and a lowered pain tolerance.15 Adverse events in childhood, including physical and sexual abuse, increase the risk of an individual developing MDD, possibly by permanently altering corticotropin-releasing cells in the hypothalamus, causing exaggerated responses to future stress.5,11 Epidemiology Estimates of depression’s societal impact are staggering. Antidepressant Medications23,24,37,41,43,44 Class Examples Toxicity Monoamine oxidase inhibitors (MAOIs) * Phenelzine (Nardil)* Selegiline (Eldepryl)* Tranylcypromine (Parnate) * Hypertensive crisis with tyramine-containing substances (beer, wine, cheese)* Serotonin toxicity when mixed with other serotonergic agents Tricyclic antidepressants (TCAs) * Amitriptyline (Elavil)* Imipramine (Tofranil)* Clomipramine (Anafranil)* Nortriptyline (Pamelor, Aventyl)* Doxepin (Sinequan) * Significant anticholinergic effects* Cardiotoxicity — lethal arrhythmias* Coma, seizures Tetracyclics (TeCAs) * Maprotiline (Ludiomil)* Amoxapine (Asendin) * Similar toxicity to TCAs but generally milder Selective serotonin reuptake inhibitors (SSRIs) * Fluoxetine (Prozac)* Paroxetine (Paxil)* Sertraline (Zoloft)* Citalopram (Celexa)* Escitalopram (Lexapro) * Mild toxicity* Potential for serotonin toxicity when mixed with other serotonergic agents Serotonin norepinephrine reuptake inhibitors (SNRIs) * Duloxetine (Cymbalta)* Desvenlafaxine (Pristiq)* Nefazodone (Serzone)* Venlafaxine (Effexor) * Toxic profiles similar to SSRIs Atypical agents * Bupropion (Wellbutrin, Zyban)* Mirtazapine (Remeron)* Trazodone (Desyrel) * Generally mild toxicity* Bupropion associated with seizures Hundreds of clinical trials since the 1950s have demonstrated that ADMs relieve symptoms to an extent 20-30% greater than placebo.23 The beneficial effect appears stronger in moderate to severe depression than in milder forms of the disease.23 The choice of an optimal agent for a given patient involves a knowledge of side effects, interactions, and comorbidities, and often involves a period of trial and error.24 Some ADMs have indications for other conditions, including chronic pain and anxiety disorder. Serotonin Toxicity48-51 Presenting Symptoms Differential Diagnosis Treatment * Autonomic excess (fever, diaphoresis, tachycardia, hypertension, mydriasis)* Neuromuscular hyperactivity (spontaneous clonus is pathognomonic, induced clonus, ocular clonus, hyperreflexia, rigidity)* Altered mental status (confusion, restlessness, excitement, headache, coma)* Gastrointestinal irritation (nausea, vomiting, diarrhea) * Neuroleptic malignant syndrome (exposure to dopaminergic agent, slower onset, no clonus, more rigidity, bradyreflexia)* Malignant hyperthermia (exposure to inhalational anesthetic or depolarizing paralytic, mottled skin, rigidity, hyporeflexia)* Anticholinergic toxicity (dry skin, urinary retention, normal tone and reflexes)* Meningitis/encephalitis* Sedative-hypnotic withdrawal, including delirium tremens* Sympathomimetic toxicity * Stop potential triggering agents* Supportive care* Benzodiazepines* Intravenous hydration* Check for rhabdomyolysis* Active cooling* Consider cyproheptadine (a serotonin antagonist)* Paralysis and airway control in severe cases The Hunter Criteria for Serotonin Toxicity (HCST) currently is the diagnostic gold standard, with a sensitivity of 84% and a specificity of 97%.48 HCST is positive if a patient has been exposed to a serotonergic agent and has at least one of the following features: spontaneous clonus, inducible clonus plus agitation or diaphoresis, ocular clonus plus agitation or diaphoresis, tremor and hyperreflexia, or hypertonia and fever > 38° C plus ocular or inducible clonus.51 For the purposes of helping clinicians keep serotonin toxicity on the radar screen, remember the mnemonic SNAGGLE: sympathetic (autonomic) excess (fever, diaphoresis, tachycardia, mydriasis); neuromuscular hyperactivity (tremors, myoclonus, clonus, hyperreflexia, rigidity); altered mental status (excitement, restlessness, agitation, confusion); gastrointestinal upset (nausea, diarrhea); gait disturbance (and go look up the Hunter criteria); and LE, for the symptoms being more prominent in the lower extremities.

EXECUTIVE SUMMARY* Syncope can be divided into reflex (neurally mediated) syncope, hypotensive syncope, and cardiovascular syncope. Presyncope is less serious, but in general should be evaluated like syncope.* Reflex syncope has three major causes: vasovagal, carotid sinus, and situational.* Cardiac syncope can be from abnormal rhythms or structural heart disease. The electrocardiogram (ECG) may show some abnormalities, although the critical rhythm may have normalized.* All patients with syncope should have an ECG to assess for abnormal rhythm and Brugada.

• Patients are presumed to be capable of making choices for themselves, unless proven otherwise; the physician is required to determine incapacity. • Capacity is essential for valid consent for medical care and treatment. • Capacity is NOT a test result, diagnosis, or score on an assessment tool. • Capacity involves the process of decision making and does not depend on the specific choice that is made. • Capacity assessment focuses on the specific abilities that a patient requires to make a decision about a specific situation. • People who are capable can make rational decisions that are based on their values and goals, as well as on their knowledge and understanding of the issues they face. Capable people can identify and accept risks. • Capacity is not one ability that people have or do not have. People employ different abilities to make different types of choices. Capacity is specific to the task. • Assessment of capacity is domain-specific; six recognized domains are healthcare, nutrition, clothing, shelter, hygiene, and safety. Patients may have capacity in one domain but they may lack capacity in another. • Assessing capacity requires considering the whole person — it is not related to an illness, a diagnosis, or a living situation. Being homeless, being a resident of a long-term care facility, or abusing drugs or alcohol does not automatically render a patient incapable of medical decision making. • Assessment of capacity relates to two ethical principles: the need to balance autonomy (self-determination) and beneficence (protection). • Incapacity often is reversible. Illnesses and intoxications can temporarily impair capacity. Patients can regain capacity on recovery.

Although the most common cause of facial nerve weakness is Bell’s palsy, pursue a careful history along with a detailed otolaryngologic and neurologic exam to avoid missing other causes.* The facial nerve is primarily a motor nerve; associated sensory and parasympathetic components of this nerve may produce symptoms when this nerve is diseased.* The long course of the facial nerve and its many branches may produce symptoms and physical findings in addition to facial weakness.* An important distinction when evaluating acute unilateral facial weakness is whether the weakness is confined to the lower face vs. weakness involving both the upper and lower face.* The inability to fully close the eyelid may lead to corneal dryness; initiate artificial tear ointment and nocturnal patching to prevent permanent damage.* Send serologic testing and initiate empiric antibiotic therapy for Lyme disease when facial nerve palsy presents from an endemic area.Emergency medicine clinicians routinely encounter patients with facial paralysis and need a straightforward way to filter through the wide range of differential diagnoses. Although the majority of these patients can be diagnosed and appropriately treated based on the results of the history and exam, clinicians must be confident they can identify those individuals with more serious and potentially life-threatening conditions presenting with facial palsy and understand the next steps in evaluation.This article reviews the fundamentals of facial paralysis, including its epidemiology, anatomy, and differential diagnosis. The article’s primary goal is to provide clinicians with a practical, straightforward approach to reaching the correct diagnosis and avoiding pitfalls along the way. The article also gives a state-of-the-science review of treatment modalities, with special attention to the treatment of Lyme disease — an increasingly major concern in endemic areas for patients who present with facial paralysis.

* Depression is a clinical diagnosis that must be present for at least two weeks. It may be associated with suicidal thoughts. * Antidepressants generally are started by outpatient physicians, but they can be started in the ED if there is communication with an outpatient physician. * SNAGGLE is a mnemonic for serotonin syndrome, which can be seen after overdose (monoamine oxidase inhibitors) or with a combination of medications. * Ketamine appears to have antidepressant activity that starts shortly after infusion. In the future, this may become an ED medication.

• Cool, running tap water is an effective method for reducing injury from superficial and superficial partial-thickness burns. • Inhalation injuries are more common in enclosed-space fires and in conditions causing impaired consciousness. • Consider carbon monoxide poisoning or cyanide toxicity as potential causes of impaired consciousness in thermal burn victims. • Full body exposure is necessary to accurately estimate the extent of burn involvement. • Areas that are superficially burned are not included when calculating the percentage of body area injured by a thermal burn. • Initiate fluid resuscitation using lactated Ringer’s solution based on the extent of the burn injury. • Do not apply opaque ointments to burns prior to transfer to a burn center.

• Hand injuries are common, and there are a number of pitfalls for emergency physicians and providers who treat them. When in doubt, consult a hand surgeon for advice, and provide follow-up for patients. • A common injury is a \"bite\" to the metacarpals with tendon involvement. The injury is sustained when an individual punches another in the mouth, and the skin is lacerated by the teeth. Patients often are intoxicated or deny the mechanism of the injury. • High-pressure spray devices for paint or grease, or even pressure washers, can penetrate the skin with little to no external injury. Pain nearly always is present. Many of these will require surgical treatment. • A herpetic whitlow is an infection with the herpes virus. It can look like a paronychia on the finger. Be suspicious of this if there are vesicles present, particularly in healthcare workers, although the use of gloves has decreased this injury.

I am, I believe, about to be sued. A lawyer has pulled the medical records of a case I dealt with in the emergency room of my hospital last year. I remember the patient well—a middle-aged man from another state, passing through town, who had a bad drinking habit and who finally decided to get help.

The fungal pathogen Candida albicans is frequently associated with catheter-based infections because of its ability to form resilient biofilms. Prior studies have shown that the transcription factor Bcr1 governs biofilm formation in an in vitro catheter model. However, the mechanistic role of the Bcr1 pathway and its relationship to biofilm formation in vivo are unknown. Our studies of biofilm formation in vitro indicate that the surface protein Als3, a known adhesin, is a key target under Bcr1 control. We show that an als3/als3 mutant is biofilm-defective in vitro, and that ALS3 overexpression rescues the biofilm defect of the bcr1/bcr1 mutant. We extend these findings with an in vivo venous catheter model. The bcr1/bcr1 mutant is unable to populate the catheter surface, though its virulence suggests that it has no growth defect in vivo. ALS3 overexpression rescues the bcr1/bcr1 biofilm defect in vivo, thus arguing that Als3 is a pivotal Bcr1 target in this setting. Surprisingly, the als3/als3 mutant forms a biofilm in vivo, and we suggest that additional Bcr1 targets compensate for the Als3 defect in vivo. Indeed, overexpression of Bcr1 targets ALS1, ECE1, and HWP1 partially restores biofilm formation in a bcr1/bcr1 mutant background in vitro, though these genes are not required for biofilm formation in vitro. Our findings demonstrate that the Bcr1 pathway functions in vivo to promote biofilm formation, and that Als3-mediated adherence is a fundamental property under Bcr1 control. Known adhesins Als1 and Hwp1 also contribute to biofilm formation, as does the novel protein Ece1.

Farnesoid X receptor (FXR) plays an important role in maintaining bile acid and cholesterol homeostasis. Here we demonstrate that FXR also regulates glucose metabolism. Activation of FXR by the synthetic agonist GW4064 or hepatic overexpression of constitutively active FXR by adenovirus-mediated gene transfer significantly lowered blood glucose levels in both diabetic db/db and wild-type mice. Consistent with these data, FXR null mice exhibited glucose intolerance and insulin insensitivity. We further demonstrate that activation of FXR in db/db mice repressed hepatic gluconeogenic genes and increased hepatic glycogen synthesis and glycogen content by a mechanism that involves enhanced insulin sensitivity. In view of its central roles in coordinating regulation of both glucose and lipid metabolism, we propose that FXR agonists are promising therapeutic agents for treatment of diabetes mellitus.