FOAMcastini – Kappa

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Reading papers is hugely important but learning how to read medical literature is an entirely different realm and many of us have statsphobia.

The Free Open Access Medical Education (FOAM)

Kappa – It’s Greek To Me

The Bread and Butter

Kappa – a coefficient indicating the degree of inter-rater reliability. How reliability are people getting the same result for a certain test or evaluation?

For example, you would want two people looking at the same chest x-ray to agree on the presence or absence of an infiltrate. Sometimes, chance comes into play and kappa tries to account for this. Similarly, clinical decision aids are often comprised of various historical and physical features. It would be nice if different clinicians evaluating the same patient would turn up the same results (thereby yielding the decision aid consistent and reliable).

To see how to calculate kappa, check this out.

The value of kappa ranges from -1 (perfect disagreement that is not due to chance) to +1 (perfect agreement that IS due to chance). A value of 0 means than any agreement is entirely due to chance [1-2].

People debate over what a “good” kappa is. Some say 0.6, some say 0.5 [1-2]. In the PECARN decision aid, for example, the authors only included variables with a kappa of 0.5 [3-4].

Limitations:

Prevalence – if prevalence is high, chance agreement is also high. Kappa takes into account the prevalence index; however, raters may also be predisposed to not diagnose a rare condition, so that the prevalence index provides only an indirect indication of true prevalence, altered by rater behavior [6].
The raters – agreement may vary based on rater skill, experience, or education. For example, when PECARN variables were looked at between nurses and physicians, the overall kappa for “low risk” by PECARN was 0.32, below the acceptable threshold as this number suggests much of the agreement may be due to chance [6].
Kappa is based on the assumption that ratings are independent (ie a rater does not know the category assigned by a prior rater).

References
1. Viera AJ, Garrett JM. Understanding interobserver agreement: the kappa statistic. Fam Med. 2005;37:(5)360-3.

2. McGinn T, Wyer PC, Newman TB, et al. Tips for teachers of evidence-based medicine: 3. Understanding and calculating kappa. CMAJ. 2004;171 (11)

3.Kuppermann N, Holmes JF, Dayan PS, et al. Identification of children at very low risk of clinically-important brain injuries after head trauma: a prospective cohort study. Lancet. 2009;374:(9696)1160-70. [pubmed]

4. Gorelick MH, Atabaki SM, Hoyle J, et al. Interobserver agreement in assessment of clinical variables in children with blunt head trauma. Acad Emerg Med. 2008;15:(9)812-8.

5. Nigrovic LE, Schonfeld D, Dayan PS, Fitz BM, Mitchell SR, Kuppermann N. Nurse and Physician Agreement in the Assessment of Minor Blunt Head Trauma. Pediatrics. 2013.

6. de Vet HC, Mokkink LB, Terwee CB, Hoekstra OS, Knol DL. Clinicians are right not to like Cohen’s κ 2013;346:f2125

Episode 25 – Skin and Skin Structure Infections

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The Free Open Access Medical Education (FOAM)

We review the post by Bryan Hayes, PharmD, FAACT on Academic Life in Emergency Medicine, Sulfamethoxazole-Trimethoprim for Skin and Soft Tissue Infections: 1 or 2 Tablets BID?

The Take Home: Most abscesses do not need antibiotics after incision and drainage. If the patient has systemic signs (fever, tachycardia), co-morbidities, or a concurrent cellulitis, they may need antibiotics. Sulfamethoxazole-trimethoprim (SMX-TMP / Bactrim) is one of the most commonly used agents in this case, as it covers MRSA.

Dosing: Two double strength (DS) tablets twice daily is a commonly prescribed regimen; yet,1 DS tablet twice daily is sufficient in most cases with exceptions for patients >100 kg, immunocompromised, or in trauma [1]. ; however, this increases the likelihood of adverse events (nausea, hyperkalemia) without notable substantial positive return.

The Bread and Butter

We cover cellulitis and abscesses, necrotizing infections, and Erythema Multiforme/Stevens-Johnson Syndrome/Toxic Epidermal necrolysis using Tintinalli (7e) Chapter; Rosen’s (8e) Chapter 137 as well as the IDSA guidelines. But, don’t just take our word for it. Go enrich your fundamental understanding yourself.

Cellulitis/Abscess

Non-purulent – cover for strep (penicillin, cephalexin/cefazolin). Even in areas with high incidences of community MRSA, the recommendations for non-purulent skin infections is strep coverage. Five days of treatment is probably enough, and IDSA and Rosenalli approved (see this post)

Purulent – Incise & Drain (I&D). Cover for MRSA in patients that failed initial I&D or those with systemic signs.

Necrotizing Infections

Presentation – pain out of proportion to exam findings, abnormal tachycardia (particularly out of proportion to degree of fever). Crepitus is not reliable (present in 13-30% of patients).

Diagnosis – clinical. X-rays, CT, and MRI have all been used but both x-rays and CT lack sensitivity and it’s probably not a good idea to send a sick patient to MRI. The gold standard diagnosis is operative findings.

The LRINEC score was derived to aid in diagnosis using lab values (sodium, creatinine, white blood cell count, hemoglobin, glucose, CRP) but has not been sufficiently predictive in validation attempts [10].

Classification

Type I – polymicrobial. Common in diabetics, immunocompromised.
Type II – monomicrobial (often Group A strep or clostridia).
Type III? – vibrio, but apparently this is controversial.

Treatment

Intravenous fluid and general resuscitation, surgical consult, and antibiotics.

Erythema Multiforme/Stevens-Johnson/Toxic Epidermal Necrolysis (for more, see this Hippo EM podcast)

Medications most associated with SJS/TEN: Antibiotics (sulfa), Anti-epileptics, Nonsteroidals

Treatment of SJS/TEN: Fluid resuscitation, Burn Center/ICU care, and IVIG

Generously Donated Rosh Review Questions

Question 1. A 22-year-old woman presents to the emergency department with a painful rash. She has had several days of malaise, arthralgias, and low-grade fever, and today developed diffuse painful erythema across her body which is beginning to blister. She takes no medications, but reports completing a course of trimethroprim-sulfamethoxazole one week ago for a urinary tract infection. Examination reveals diffuse tender erythema over her trunk and extremities with multiple ill-defined large bullae, some of which have ruptured, leaving large areas of denuded skin behind. Oral ulcerations are also noted. [polldaddy poll=8689023]

Question 2. A 54-year-old man with diabetes presents with severe leg pain. The pain has worsened over the last two days with increased swelling of the calf. He has no chest pain or shortness of breath. Vital signs are: T 101.8°F, BP 98/62, HR 118, RR 18. Physical examination is notable for erythema of the calf, mild tenderness, and crepitus. You initiate IV fluids and broad-spectrum antibiotics. [polldaddy poll=8689082]

Answers

1. This patient has toxic epidermal necrolysis (TEN). TEN is an acute inflammatory process characterized by tender erythema, painful bullae formation, and subsequent exfoliation. It often begins with prodromal symptoms such as fever, malaise, and myalgias. TEN is considered a dermatologic emergency and patients may appear toxic on presentation. Medications (within the first few months of administration) are the most common cause, with sulfa and penicillin antibiotics, anticonvulsants, and oxicam non-steroidal anti-inflammatory drugs commonly implicated. Management of TEN involves admission to a burn unit, fluid resuscitation, and prevention of secondary infection. Steroids are not an indicated treatment. Staphylococcal scalded skin syndrome (C) occurs primarily in infants and young children. Infection with exotoxin-producing Staphyloccus aureus leads to diffuse erythroderma and subsequent exfoliation. Mucous membranes are not usually involved. Treatment is fluid resuscitation and antibiotics. Infection with HSV-1 and HSV-2 results in localized skin infection, though in patients with underlying immunosuppression or malignancy it may lead to disseminated herpes simplex virus infection (A), characterized by diffuse vesicles and ulcerations and multisystem involvement. Photosensitive drug reactions (B) are characterized by confluent erythema, macules, papules, or sometimes vesicles in sun-exposed areas such as the face, neck, and arms, occurring within 1-3 weeks of the patient taking an offending agent. Medications commonly associated with photosensitivity include sulfonamides, thiazides, furosemide, and fluoroquinolones

2. Necrotizing fasciitis is an infection of the subcutaneous tissue that spreads rapidly across the fascial planes and is often fatal even with aggressive treatment. Risk factors for necrotizing infections include diabetes, vascular insufficiency, and immunosuppression. Classically patients have pain out of proportion to examination. Later findings include diffuse swelling, erythema, induration and crepitus. The gold standard for diagnosis is direct visualization in the operating room by a surgeon. Surgeons may elect to perform a bedside biopsy prior to full exploration. Management includes aggressive IV hydration, broad-spectrum antibiotics, and surgical debridement. CT scan with intravenous contrast of the lower extremity (A) may demonstrate findings suggestive of a necrotizing infection including subcutaneous gas, stranding along the fascial planes or fluid collection. However, the negative predictive value of CT scan has not been quantified and is not yet considered the gold standard. Doppler ultrasound of the lower extremity (B) may be helpful in identifying venous thrombosis as a cause of edema and fullness of the leg. Additionally, sonography may visualize an area of deep fluid collection and may demonstrate artifact from a significant amount of subcutaneous air if present. Measurement of serum lactate and CPK (C) is helpful when positive but not sensitive enough to rule out the diagnosis of necrotizing fasciitis. The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) incorporates other laboratory markers (CRP, WBC, Hemoglobin, Sodium, Creatinine, Glucose) into a decision-rule however lacks sufficient sensitivity in larger studies.

References

1.Stevens DL, Bisno a. L, Chambers HF, et al. Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infectious Diseases Society of America. Clin Infect Dis. 2014.

2. Shehab N1, Patel PR, Srinivasan A, Budnitz DS. Emergency department visits for antibiotic-associated adverse events. Clin Infect Dis. 2008 Sep 15;47(6):735-43.

3. Bourgois FT, Mandl KD, Valim C et al. Pediatric Adverse Drug Events in the Outpatient Setting: An 11-Year National Analysis. Pediatrics. Oct 2009; 124(4): e744–e750.
4. Goldman JL, Jackson MA, Herigon JC et al. Trends in Adverse Reactions to Trimethoprim-Sulfamethoxazole. Pediatrics. Jan 2013; 131(1): e103–e108.

5. Khow KS, Yong TY. Hyponatraemia associated with trimethoprim use. Curr Drug Saf. 2014;9:(1)79-82. [pubmed]

6.Antoniou T, Hollands S, Macdonald EM, et al. Trimethoprim-sulfamethoxazole and risk of sudden death among patients taking spironolactone. CMAJ. 2015.

7. Hepburn MJ, et al. Comparison of short-course (5 days) and standard (10 days) treatment for uncomplicated cellulitis. Arch Intern med 2004; 164, 1669-1674

8. Hurley HJ, Knepper BC, Price CS, et al. Avoidable antibiotic exposure for uncomplicated skin and soft tissue infections in the ambulatory care setting. Am J Med. 2013;126(12):1099–106.

9. Pallin DJ, Binder WD, Allen MB et al. Clinical Trial: Comparative Effectiveness of Cephalexin Plus Trimethoprim-Sulfamethoxazole Versus Cephalexin Alone for Treatment of Uncomplicated Cellulitis: A Randomized Controlled Trial. Clin Infect Dis. (2013) 56 (12): 1754-1762.

10.Liao CI, Lee YK, Su YC et al. Validation of the laboratory risk indicator for necrotizing fasciitis (LRINEC) score for early diagnosis of necrotizing fasciitis. Tzu Chi Medical Journal (2012) 24(2):73-76

Episode 24 – Mild Traumatic Brain Injury/Concussion

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The Free Open Access Medical Education (FOAM)

We cover the Taming the SRU podcast, “Ketamine Cagematch” (iTunes), a debate between Dr. Minh Le Cong and Dr. Chris Zammit.

Dogma persists that ketamine may increase intracranial pressure, which would be bad in traumatic brain injury (TBI) given the fixed space in the cranial vault. These are largely from Yet, these patients often need sedation, for agitation or intubation, and drops in blood pressure are also deleterious (see EMCrit on neuroprotective intubation).

PRO (Le Cong): The literature doesn’t show clinically significant deleterious outcomes from ketamine use in the head injured patient. Review in Annals on ketamine and ICP. Deleterious effects of apnea may result from other sedative agents.

CON (Zammit): Studies showing that ketamine does not increase ICP confounded by the presence of other sedatives on board. As a result, there may still be a risk to using ketamine in these patients.

The Bread and Butter

We cover key points on concussion and mild TBI from Tintinalli 254 but to be honest, Rosenalli is lacking on this topic so we’ve turned to the ACEP clinical policy, AAN guidelines, Ontario Pediatric Guidelines, and the AAP guidelines on the topic. But, don’t just take our word for it. Go enrich your fundamental understanding yourself.

Mild TBI and concussion are often referred to interchangeably and the definition varies [1-3]. Unfortunately, concussion is often thought of only in the sports population and not all-comers to the Emergency Department (ED) so patients may not receive proper .

Definition: Essentially, any alteration in mental status following head injury. Per the CDC: Head injury from blunt trauma or acceleration/deceleration with GCS 14-15 PLUS

observed or self-reported transient confusion, disorientation, or impaired consciousness
Amnesia around the time of injury
Signs of other neurologic or neuropsychological dysfunction
Any loss of consciousness (LOC) less than 30 minutes (!) [3]

For more on how reliable LOC is in these patients, see this post.

Causes: Falls and motor vehicle collisions are the most common causes in adults, whereas sports are the more common in kids.

The effects on the brain are largely a result of “secondary injury,” consistent of alterations in ion-channel, metabolic pathways, and electrochemical imbalances. These are more functional than structural.

Symptoms: There’s a good bit of overlap with migraine, more significant head trauma, and symptoms that may be confused for behavioral issues in younger populations.

Testing: Not all head injuries require imaging. Certainly, patients with focal neurologic findings warrant imaging; yet, in other cases, validated decision aids exist to help determine which patients may or may not need imaging. In adults, we like the Canadian CT Head tool , although the ACEP clinical policy uses the New Orleans Criteria. For a solid review of the two, check out this SGEM episode. In children, consider the use of the PECARN decision aid. Otherwise, a good neurologic exam and observation should suffice.

Something to consider – patients often believe that a “normal” CT scan of the head means that they don’t have a concussion. As a result, they may not take concussion precautions seriously. In this case, imaging may provide false reassurance.

There’s increased attention on biomarkers like GFAP, total tau, and S-100B but these are not ready for prime time and are not incredibly specific [3]. Further, standardized assessment tools such as SCAT3 and ACE may be useful, but are used predominantly on-site for sports related incidents.

Treatment

Education – this is one of the biggest areas in which ED providers may make a difference. Give patients or family members precautions for concussion, even if the injury or mechanism seems relatively mild. Studies show that a majority of pediatric patients do not follow up as instructed after a concussion [4]. Perhaps communication of the the potential gravity of concussion and long-term implications may improve follow up.
Rest – This the is the mainstay of initial treatment for most mild TBI [1-3, 5]. It’s unclear how strict this rest needs to be, but a recent study in the pediatric literature found no benefit to strict rest versus standard instructions (1-2 days rest + graduated return) [6].
Graduated return to activity – after a period of rest, it’s recommended to slowly resume activities, spending at least 24 hours at each level of increased activity. If an individual gets symptomatic, they should return to the level of activity at which they were asymptomatic (see the Zurich protocol).
Return to play – clearing people from the ED is NOT a good idea. For those on the sidelines, a player should be removed from activity for the day after a suspected concussion.

Why do we care in the ED?

Quality of Life – Concussive symptoms can be quite disabling. Giving patients a name for their symptoms, resources, and education may help them understand the process of recovery and available resources.
Second Impact Syndrome – A second head injury in a patient symptomatic from a concussion may experience diffuse cerebral edema, possibly from loss of cerebral autoregulation.* [2]
Post Concussion Syndrome (PCS) – a subset of the concussion population will have persistence of symptoms which, if they persist > 1 week to 3 months after the injury, is deemed PCS. * This is thought to be more prevalent in individuals with a history of depression, anxiety, or migraines and in those with more severe ED presentations [2].
Bouncebacks – Patients may present to the ED with symptoms of concussion but may not give a history of significant trauma. Remember that concussion may occur after a seemingly minor bump to the head and elderly may need extra support with activities of daily living or may bounce back with a more life threatening injury.
Lack of follow up. While some may follow up with concussion specialists, the majority of our patient population lacks the ability for meaningful or specialist follow up. We can’t assume that someone else is going to guide our patients through concussion recovery or that when we write “follow up with _____” that it will happen. Our care may be it, make it good.

*The literature on these is sparse and complicated by variable definitions, information, and standardized reporting.

Generously Donated Rosh Review Questions (scroll for answers)

Question 1. A 33-year-old man with no past medical history presents with a headache 3 days after a closed head injury. The patient states that he stood up from kneeling and hit the top of his head on a wood cabinet. There was no loss of consciousness or seizure activity. In addition to the headache, he complains of difficulty concentrating at work and dizziness. His physical examination is unremarkable.[polldaddy poll=8663736]

Question 2. A 42-year-old man is brought to the ED after he tripped and fell while he and his wife were on a walk. His wife notes that she saw him hit his head on the pavement and that he did not respond to her for 45 seconds. When he started to respond, she says that he was very confused. In the ED, his vital signs are BP 135/75, HR 88, RR 14, and oxygen saturation 98% on room air. On exam, you note some minor lacerations on the patient’s upper extremities, face, and scalp and his GCS is 15. As the wife recounts what happened, the patient does not recall any of the events and continuously asks to repeat what happened to him. A CT scan of the brain is normal. The patient is diagnosed with a concussion and is ready to be discharged from the ED. [polldaddy poll=8663741]

References

1. Tavender EJ, Bosch M, Green S, et al. Quality and consistency of guidelines for the management of mild traumatic brain injury in the emergency department. Acad Emerg Med. 2011;18:(8)880-9. [pubmed]

2. Haydel M. Management Of Mild Traumatic Brain Injury In The Emergency Department. Emergency Medicine Practice. September 2012 Volume 14, Number 9

3. Jagoda AS, Bazarian JJ, Bruns JJ, et al. Clinical policy: neuroimaging and decisionmaking in adult mild traumatic brain injury in the acute setting. Ann Emerg Med. 2008;52:(6)714-48. [pubmed]

4.Hwang V, Trickey AW, Lormel C, et al. Are pediatric concussion patients compliant with discharge instructions? J Trauma Acute Care Surg. 2014;77(1):117–22; discussion 122.

5. Brown NJ, Mannix RC, O’Brien MJ, Gostine D, Collins MW, Meehan WP. Effect of cognitive activity level on duration of post-concussion symptoms. Pediatrics. 2014;133(2):e299–304.

6.Thomas DG, Apps JN, Hoffmann RG, McCrea M, Hammeke T. Benefits of strict rest after acute concussion: a randomized controlled trial. Pediatrics. 2015;135:(2)213-23. [pubmed]

Answers

1. D. The patient presents with minor head trauma and complaints consistent with a concussion and should have neurology follow up arranged. A concussion is a minor TBI that is often seen in MVCs and collision sports (football, hockey). It is typically caused by a rotational injury or an acceleration-deceleration injury. Patients will present with a number of non-specific symptoms including headaches, dizziness, confusion, amnesia, difficulty concentrating, and blurry vision but do not have focal neurologic findings. Despite the absence of severe intracranial injury, patients can have chronic and debilitating symptoms from concussions. Neurology referral is recommended, as patients should have functional testing and tracking of their symptoms for resolution. It is vital to counsel patients to avoid contact sports or activities that increased the risk of recurrent injury as these patients are at risk for more severe injury with second impact.In the absence of focal neurologic findings, absence of antiplatelet or anticoagulant use and minor trauma, imaging is not needed (A, B, C).

2. Cerebral concussions are clinically characterized by headaches, confusion, dizziness, and amnesia for the event. Concussions are characterized by a transient loss of consciousness that occurs immediately following blunt, nonprenetrating head trauma, caused by impairment of the reticular activating system. Concussions present without focal neurologic deficits, and CT and MRI show no acute abnormalities. Although not commonly performed for concussions, functional imaging, such a PET scan, may show changes in blood flow and glucose uptake. It is critical to inform the patient and his or her family of the second impact syndrome (SIS), which occurs when a patient suffers a second concussion after being symptom-free from the first. Although SIS is more common in sports based injuries, especially among teenagers, the risk of serious sequelae following a second concussion is immense. Due to neurochemical and autoregulatory changes that may still be present, a second concussion soon after a first generally produces a rapid neurologic decline that proves fatal. Patients should be told to avoid activities that could cause falls or trauma for at least 1 week after the patient is completely asymptomatic from the first concussion. Most patients with a concussion can be discharged from the emergency department and advised to follow-up with a primary care physician within 1 week (B). Although some patients have only transient symptoms from a concussion, others may experience persistent symptoms termed postconcussive syndrome (PCS). PCS symptoms most often include headache as well as memory, sensory, sleep, and concentration disturbances. It is important to consider PCS in all patients with a concussion, but a primary care physician is generally able to care for these patients. It is unnecessary to obtain an MRI (C). Although patients should avoid trauma and falls for at least 1 week after being completely asymptomatic after the first concussion, a change insleeping position (D) is unnecessary.

Episode 23 – SBO and Mesenteric Ischemia

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The Free Open Access Medical Education (FOAM)

This week we’re covering Dr. Jacob Avila’s post on ultrasound for small bowel obstruction (SBO) located at Ultrasound of the week. He has an accompanying video on 5minSono.

Point of care ultrasound has good operating characteristics for diagnosis of SBO with a LR+ 9.5, LR- 0.04, far better than abdominal x-ray [1].

What to look for:

Dilated loops of bowel > 2.5 cm in diameter
Additional clues: “To and fro” peristalsis
The piano key sign, Tanga sign

Problems with abdominal x-ray:

Rosen’s: Abdominal x-rays are “diagnostic in approximately 50 to 60% of cases of SBO, equivocal in 20 to 30%, and normal, nonspecific, or misleading in 10 to 20%” [2].
American College of Radiology: they can “prolong the evaluation period … while often not obviating the need for additional examinations, particularly CT” [3].

Limitations:

While ultrasound can diagnose SBO, there is little evidence to suggest that we can identify transition points or strangulation/necrosis. As such, there can still be a role for CT scan, particularly in first time SBO to identify a transition point.
The EAST guidelines acknowledge the utility of ultrasound yet this practice is far from accepted in the surgical community. Surgical colleagues will likely still want concrete imaging such as an x-ray or CT; however, ultrasound performed concurrent with the history and physical may speed up patient’s disposition to definitive care/imaging.

FOAMcastini – Reflections on ACEP tPA Clinical Policy Update Draft

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As detailed in this FOAMcastini, ACEP just released a draft of an updated clinical policy on tPA for acute ischemic stroke. This came in the wake of years of controversy over the aggressive position taken in the 2012 clinical policy.

While FOAMcast is not an interview style podcast, we felt compelled to get some perspective on Emergency Physicians a little more experienced than ourselves. Here we interview:

Dr. Ryan Radecki (@emlitofnote), Assistant Professor, University of Texas – Houston

We don’t know who best benefits from tPA so elucidating which patients are “carefully selected” may get hard.
See his response to the policy on his blog here

Dr. David Newman (#draftnewman), Associate Professor of Emergency Medicine, Mount Sinai Hospital

The process for ACEP clinical policy creation seems to work. The constituency expressed concern and the college listened and went back and re-created the policy from the bottom up.
This policy reflects a move from content expert to methodologists which better reflects the evidence compared with opinions (and is the standard per USPSTF).

Dr. Anand Swaminathan (@EMSwami), Assistant Professor of Emergency Medicine, NYU

Inclusion of more rigorous methodology and review of evidence.
May be perceived as too “soft” by tPA supporters. This policy may not overtly change practice but may open up avenue of conversations.

Dr. Ken Milne (@thesgem), Chief of Staff at South Huron Hospital

When looking at “carefully selected” patients, as noted in the policy, remember to use the Evidence Based Medicine trifecta of evidence, patient values, and clinical expertise. In isolation, one component is not sufficient.
Previous discussions of NINDS, and the Cochrane tPA article

FOAMcastini – ACEP tPA Clinical Policy Update

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The Free Open Access Medical Education (FOAM)

Comment on the 2015 ACEP tPA Clinical Policy Draft here

ACEP tPA Clinical Policy 2012 – This policy has been entrenched in controversy since it was published. Why? Well, largely because the evidence was given a stronger level recommendation than the data supported, conflicts of interest abounded, and the data (mostly from NINDS (The SGEM review), ECASS, and IST-3) were problematic. This has been well covered by these reviews of the clinical policy:

Emergency Medicine Literature of Note – Dr. Ryan Radecki
SMART EM – Dr. David Newman
Practical Evidence – Dr. Scott Weingart
ACEP 2014 Debate – FOAMcast

What changed in the 2015 draft?

Episode 22 – The Knee

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This week we’re covering a post from the incredible pediatric resource, Don’t Forget the Bubbles, “Knee X-ray Interpretation” by Dr. Tessa Davis. We use a systematic approach to assessing chest x-rays, so why not knee x-rays?

Know the anatomy
Look at:
- Effusion
- Main bones
- Tibiofemoral alignment
- Tibial plateaus
- Intercondylar eminence
- Patellar tendon disruption
- Patellar fracture

The Bread and Butter

We summarize some key topics from Rosenalli, that’s Tintinalli (7e) Chapter s271, 281; Rosen’s (8e) Chapters 57, 136. But, don’t just take our word for it. Go enrich your fundamental understanding yourself.

Knee Dislocation

Anterior is most common (40%), posterior (33%)
Approximately 50% of knee dislocations may be relocated upon presentation to the hospital (this does not reduce risk of badness)
Most worrisome sequelae = popliteal artery disruption. Of patients with popliteal disruption, the amputation rate rises to 90% 8 hours after the injury without surgical intervention.
Workup may depend on your institution (ex: angiogram vs. CT angio vs. ultrasound) but all patients will need an ABI + 24 hour of pulse checks per current standards.

Screen Shot 2015-01-08 at 1.10.48 PM — Algorithm (adopted from Rosen’s)

Septic Arthritis

Most Common Organisms: S. aureus, N. gonorrhea
Hematogenous spread
Most Common Location: knee, hip

Risk factors such as immunocompromised hosts and use of steroids are risk factors for septic arthritis but the ones with the highest likelihood ratio (LR+ >10 is ideal):

Skin infection overlying prosthetic joint (LR+ 15)
Joint surgery within the preceding 3 months (LR+ 6.9)
Age > 80 (LR+ 3.5)

Diagnosis: In the red, hot, swollen, painful joint, think septic arthritis. Clinical and laboratory indicators aren’t great. Synovial fluid analysis, particularly the culture exists as the gold standard. Arthrocentesis Trick of the Trade from ALiEM. Here are the operating characteristics from Margaretten et al:

Fever: Sensitivity 57%
Lab tests: White Blood Cell count (WBC), sedimentation rate (ESR), and c-reactive protein don’t perform well
- WBC LR+ 1.4 (1.1-1.8); LR- 0.28 (0.07-1.10)
- Erythrocyte sedimentation rate 1.3 (1.1-1.8); LR- 0.17 (0.20-1.30)
- C-reactive protein 1.6 (1.1-2.5); LR- 0.44 (0.24-0.82)
Synovial fluid gram stain and culture is the “gold standard.”
- >100,000 WBCs is predictive of septic arthritis with LR+ 25
- >50,000 WBCs often used as diagnostic with 75% PMNs but 30% of patients with septic arthritis may have <50K WBCs
- Synovial Lactate in the Diagnosis of Septic Arthritis from EMJClub

Treatment: Intravenous antibiotics and washout of the joint by orthopedics in the operating room

Generously Donated Rosh Review Questions

Question 1. A 67-year-old man with a history of gout presents with atraumatic left knee pain. Physical examination reveals an effusion with overlying warmth and erythema. There is pain with passive range of motion. He reports a history of gout in this joint in the past. [polldaddy poll=8568492]

Question 2. A 27-year-old woman presents with severe left knee pain after an MVC where she was the front passenger. She states her knee hit the dashboard. An X-ray of the patient’s knee is shown below. After reduction, the physical examination reveals swelling of the knee and an Ankle-Brachial Index (ABI) of 0.8. [polldaddy poll=8569540]

Answers.

1. D. Septic arthritis is a bacterial or fungal infection of a joint typically spread hematogenously unless there is direct bacterial contamination. The synovium is highly vascular and lacks a basement membrane making it susceptible to bacterial seeding. Certain conditions predispose individuals to septic arthritis including diabetes, sickle cell disease, immunocompromise, alcoholism or pre-existing joint disease like rheumatoid arthritis or gout. Fever is present in less than half of cases of septic arthritis so with clinical suspicion an arthrocentesis is indicated. The knee is the most common joint affected and patients have pain (especially on passive range of motion) and decreased range of motion often accompanied by warmth, erythema and fever. This patient may have an acute gouty flare, but the clinician must exclude an infection. On joint fluid analysis, the white blood cell count of a septic joint is typically > 50,000. Indomethacin (B) is a non-steroidal anti-inflammatory agent commonly used in the treatment of acute gout. Gout is an arthritis caused by deposition of monosodium urate monohydrate crystals in the joint space. Acute flares involve a monoarticular arthritis with a red, hot, swollen and tender joint. Acute episodes of gout result from overproduction or decreased secretion of uric acid. However, measurement of serum uric acid (C) does not correlate with the presence of absence of an acute flare. A radiograph of the knee (D) may show chronic degenerative changes associated with gout but will not help to differentiate a gouty arthritis versus septic arthritis.

2. C. Obtain Angiography. This patient presents with a knee dislocation and signs of a popliteal artery injury requiring angiography for diagnosis. A knee dislocation refers to a dislocation of the tibia in relation to the femur and not a patellofemoral dislocation. A tibiofemoral dislocation is a limb-threatening emergency due to the high rate of popliteal artery injury. The neurovascular bundle (popliteal artery, popliteal vein and common peroneal nerve) runs posteriorly in the popliteal fossa. The popliteal artery is tethered to the femur and tibia by a fibrous tunnel and is inherently immobile making it susceptible to injury during dislocation. Knee dislocations typically occur in major trauma. An MVC where the knee strikes the dashboard is a common scenario. The dislocation is usually clinically obvious and should be emergently reduced regardless of the presence of confirmatory X-rays. The leg should rapidly be assessed for any “hard” signs of vascular injury including an absence of pulse, limb ischemia, rapidly expanding hematoma, the presence of a bruit or thrill and pulsatile bleeding. Neurologic status should also be assessed prior to and after reduction. After reduction, all patients should have ankle-brachial index (ABI) performed. A normal ABI is > 0.9. Any patient with an ABI less than this should be further investigated for a popliteal injury with angiography. Splint and elevation (D) may be appropriate once a vascular injury is ruled out. The patient should not be discharged home (A) with an abnormal ABI. Observation and repeat ABI (B) is indicated if the initial ABI is normal.

Episode 22 – The Knee

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The Free Open Access Medical Education (FOAM)

Know the anatomy
Look at:
- Effusion
- Main bones
- Tibiofemoral alignment
- Tibial plateaus
- Intercondylar eminence
- Patellar tendon disruption
- Patellar fracture

The Bread and Butter

Knee Dislocation

Anterior is most common (40%), posterior (33%)
Approximately 50% of knee dislocations may be relocated upon presentation to the hospital (this does not reduce risk of badness)
Most worrisome sequelae = popliteal artery disruption. Of patients with popliteal disruption, the amputation rate rises to 90% 8 hours after the injury without surgical intervention.
Workup may depend on your institution (ex: angiogram vs. CT angio vs. ultrasound) but all patients will need an ABI + 24 hour of pulse checks per current standards.

Septic Arthritis

Most Common Organisms: S. aureus, N. gonorrhea
Hematogenous spread
Most Common Location: knee, hip

Risk factors such as immunocompromised hosts and use of steroids are risk factors for septic arthritis but the ones with the highest likelihood ratio (LR+ >10 is ideal):

Skin infection overlying prosthetic joint (LR+ 15)
Joint surgery within the preceding 3 months (LR+ 6.9)
Age > 80 (LR+ 3.5)

Fever: Sensitivity 57%
Lab tests: White Blood Cell count (WBC), sedimentation rate (ESR), and c-reactive protein don’t perform well
- WBC LR+ 1.4 (1.1-1.8); LR- 0.28 (0.07-1.10)
- Erythrocyte sedimentation rate 1.3 (1.1-1.8); LR- 0.17 (0.20-1.30)
- C-reactive protein 1.6 (1.1-2.5); LR- 0.44 (0.24-0.82)
Synovial fluid gram stain and culture is the “gold standard.”
- >100,000 WBCs is predictive of septic arthritis with LR+ 25
- >50,000 WBCs often used as diagnostic with 75% PMNs but 30% of patients with septic arthritis may have <50K WBCs
- Synovial Lactate in the Diagnosis of Septic Arthritis from EMJClub

Treatment: Intravenous antibiotics and washout of the joint by orthopedics in the operating room

Generously Donated Rosh Review Questions

Answers.

1. D. Septic arthritis is a bacterial or fungal infection of a joint typically spread hematogenously unless there is direct bacterial http://www.mindanews.com/buy-imitrex/ contamination. The synovium is highly vascular and lacks a basement membrane making it susceptible to bacterial seeding. Certain conditions predispose individuals to septic arthritis including diabetes, sickle cell disease, immunocompromise, alcoholism or pre-existing joint disease like rheumatoid arthritis or gout. Fever is present in less than half of cases of septic arthritis so with clinical suspicion an arthrocentesis is indicated. The knee is the most common joint affected and patients have pain (especially on passive range of motion) and decreased range of motion often accompanied by warmth, erythema and fever. This patient may have an acute gouty flare, but the clinician must exclude an infection. On joint fluid analysis, the white blood cell count of a septic joint is typically > 50,000. Indomethacin (B) is a non-steroidal anti-inflammatory agent commonly used in the treatment of acute gout. Gout is an arthritis caused by deposition of monosodium urate monohydrate crystals in the joint space. Acute flares involve a monoarticular arthritis with a red, hot, swollen and tender joint. Acute episodes of gout result from overproduction or decreased secretion of uric acid. However, measurement of serum uric acid (C) does not correlate with the presence of absence of an acute flare. A radiograph of the knee (D) may show chronic degenerative changes associated with gout but will not help to differentiate a gouty arthritis versus septic arthritis.

Episode 21 – Acute Kidney Injury

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The Free Open Access Medical Education (FOAM)

Dr. Josh Farkas of the PulmCrit blog has produced a couple of blog posts on the importance of renal protection in sepsis, Renoresuscitation: Sepsis resuscitation designed to avoid long-term complications and Renal microvascular hemodynamics in sepsis: a new paradigm. Much of this is theoretical and certainly not something that is standard practice, rathery a theory extrapolated from subgroups of several trials.

Suggested renoresuscitation measures:

(1) Avoid renal failure – avoid nephrotoxins (many antibiotics, NSAIDs, ace-inhibitors), avoid hyperchloremic metabolic acidosis.

(2) Avoid volume overload – treating decreased urine output by flooding a patient with fluids is not necessarily the best move.

(3) Protect the glycocalyx of the endothelium – this suggestion proffers more questions than answers. Steroids? Albumin? Certain vasopressors? Stay tuned, as we’re not really certain what this entails.

The Bread and Butter

We summarize some key topics from Rosenalli, that’s Tintinalli (7e) Chapter 91; Rosen’s (8e) Chapter 97. But, don’t just take our word for it. Go enrich your fundamental understanding yourself.

Acute Kidney Injury – typically a creatinine 1.5-2x the patient’s baseline is classified as acute kidney injury. Urine output can be increased initially but determine whether a patient is making urine and how much, as urine output <0.5 mL/kg/h qualifies as AKI.

Importance – AKI is associated with worse outcomes, although it’s unclear as to whether this is merely a marker of

Found in 35-65% of admissions to the intensive care unit, in 5-20% of hospital admissions. Furthermore, AKI is associated with higher mortality.
Renal failure can also cause significant problems for the patient such as electrolyte abnormalities (hyperkalemia the most worriesome, but also hyperphosphatemia) and pulmonary edema.

Etiology – many causes of AKI are reversible or amenable to treatment.

Prerenal – this is one of the most common causes of acute kidney injury and basically is caused by decreased blood flow to the kidney. Associated with a high BUN/creatinine ratio, increased urine osmolality, a urine sodium concentration less than 20 mEq/L, and FENa less than 1% (this is why getting urine sodium and a concurrent chemistry panel is key).

Hypovolemia – volume depleted, hemorrhage, intravascular volume depletion from congestive heart failure or cirrhosis.
Hypotension – poor cardiac output (heart failure, valvular problems), shock
Decreased flow through the renal artery disease – Nonsteroidal anti-inflammatories: inhibit prostaglandins in the afferent arteriole. ACE inhibitors prevent the conversion of angiotensin I to angiotensin II, leading to decreased levels of angiotensin II, which when absent decreases the GFR because of dilatation of the efferent arteriole.

Post Renal (Obstructive) – Check out Episode 2 on urologic emergencies.

Benign prostatic hypertrophy (BPH) is the most common cause but medications such as anticholinergics and pseudoephedrine. Trauma, stones, strictures, and malignancy can also cause obstruction.

Intrinsic acute renal failure– divided into: tubular disease (most common), glomerular disease, vascular disease and interstitial disease.

Least common form of AKI in the ED, more common in inpatients.
Acute Tubular Necrosis (ATN) most common cause – via nephrotoxins such as aminoglycosides and contrast.
Granular “muddy brown” casts – think of necrosis from the “N” in ATN and necrosis tends to be dark.

Indications for emergent dialysis – AEIOU

A- Acidosis

E- Electrolyte emergencies (hyperkalemia!)

I- Intoxication with dialyzable toxins (ethylene glycol)

O- Overloaded with volume

U- Uremia

Generously Donated Rosh Review Questions

Question 1. A 72-year-old man is brought to the ED from a nursing home for evaluation of oliguria. He is found to have an acutely elevated BUN and plasma creatinine from baseline. A Foley catheter is placed; his urine sodium (UNa) is measured below 20 mEq/L and fractional excretion of sodium (FENa) below 1%. [polldaddy poll=8545511]

Question 2. A 54-year-old man presents to the ED in acute renal failure (ARF). [polldaddy poll=8545512]

Answer 1. D. This patient’s oliguria with acutely elevated BUN and plasma creatinine suggest that he is in acute renal failure (ARF). His UNa <20 mEq/L and FENa <1% indicate that he has intact reabsorptive function and is able to conserve sodium. This is consistent with prerenal azotemia as the cause for his ARF.

Acute tubular necrosis (ATN) (A), loop diuretics (e.g., furosemide) (B), and osmotic diuresis (e.g., mannitol) (C)all lead to UNa >20 mEq/L and FENa >1% because there is impairment in the ability to concentrate the urine. In such cases, a high-sodium load is excreted.

Answer 2. A. Acute tubular necrosis (ATN) is a severe form of impairment of tubular epithelial cells caused by ischemia or toxic injury. It is a leading cause of ARF. One of its hallmarks is the presence of brown granular casts on urinalysis. These contain cellular debris rich in cytochrome pigments. In contrast, hyaline casts (B) are usually nonspecific but present after exercise; red cell casts (C) are indicative of glomerular hematuria (e.g., glomerulonephritis); and white cell casts (D) imply renal parenchymal inflammation (e.g., acute interstitial nephritis, pyelonephritis).

Episode 20 – Anticoagulation

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The Free Open Access Medical Education (FOAM)

We review Dr. Rory Spiegel’s, A Case of Identity Part Two, post on EMNerd which is essentially a take down of dual antiplatelet therapy (DAT) in acute coronary syndrome (ACS). The bottom line? There’s no demonstrable and clinically significant benefit from DAT as demonstrated in the trials below.

CURE trial – composite endpoints of questionable clinical significance and an enormous sample size.

2.1% absolute decrease in cardiovascular death and myocardial infarction (MI), completely powered by the 1.5% absolute difference in MIs. Almost all of these MIs were Type IV and peri-procedural. Mortality between groups was identical at 30 days and end of follow up (1.0% vs 1.1% and 2.3% vs 2.4%, respectively).

ACCOAST – RCT of prasugrel or placebo prior to angiography

No difference in cardiovascular death, myocardial infarct, stroke, urgent revascularization or glycoprotein IIb/IIIa rescue therapy (10.8% vs 10.8%)
Approximately 1% increase in major bleeding

CREDO – RCT with placebo or clopidogrel 3-24 hours prior to urgent cardiac catheterization

No statistical difference in the rates of death, stroke or MI at 28 days
Statistical significance of a secondary endpoint of the 1-year outcomes with a 2% absolute reduction in the rate of death, MI, and stroke, largely the result of a 1.9% reduction of MIs.
1% increase in major bleeding events

Thienopyridine Meta-Analysis

In patients with non-ST elevation ACS, pretreatment with thienopyridines is not associated with reduced mortality but comes at a cost of a significant excess of major bleeding.

Composite endpoints are problematic (see this post, “Would You Rather“) and statistical significance claimed in these trials is largely a product of composite outcomes rather than patient oriented measures.

The Bread and Butter

We summarize some key topics from the following readings, Goldfrank (10th ed) Chapter 60, EMPractice October 2013 (there’s almost nothing in Rosenalli on this topic) but, the point isn’t to just take our word for it. Go enrich your fundamental understanding yourself!

Aspirin

Irreversibly inhibits platelets (for the duration of platelet’s life)

Ibuprofen

Reversibly inhibits platelets

Novel Oral Anticoagulants (NOACs)

NOACs have gained increased popularity and are slowly supplanting warfarin for common anticoagulation indications such as non-valvular atrial fibrillation (NVAF) as well as treatment of venous thromboembolisms such as pulmonary embolism (PE) and deep venous thrombosis (DVT).

Direct thrombin inhibitor – dabigatran (Pradaxa). This drug was the first to supplant warfarin for NVAF in the United States, billed as more patient friendly given the lack of purported need for routine monitoring. Recent investigations by Cohen et al, however, demonstrate that monitoring may, in fact, be safer. Further, in a real world, retrospective cohort of Medicare beneficiaries given either dabigatran or warfarin for atrial fibrillation, major bleeding of the dabigatran cohort was higher than in the warfarin cohort 9.0% (95% CI 7.8 – 10.2) versus 5.9% (95% CI 5.1 – 6.6) after propensity matching [Hernandez]. For more on the problems with dabigatran, check out Emergency Medicine Literature of Note.

Predominantly renal excretion
- Caution with impaired renal function (can cause dabigatran to stick around longer)
- Hemodialysis an option in acute overdose; however, most people would probably not want to put a dialysis catheter in a coagulopathic patient.
Half-life ~ 15 hours
Can elevate the PTT. If the PTT is normal, likely not coagulopathic secondary to dabigatran [Dager et al].
No reversal agent

Factor XA inhibitors – these have XA in the name….rivaroXAban, apiXAban, edoXAban.

Rivaroxaban – approved for NVAF and treatment of DVT/PE. Half life approximately 6-9 hours.

Apixaban – approved for NVAF and treatment of DVT/PE. Half life about 12 hours.

Edoxaban – approved for NVAF. Half life about 10-14 hours.

Cleared by liver and kidneys.
Can elevate the prothrombin time (PT), but not reliably. Specific assays exist but are not widely available and are expensive.
No specific reversal agent although andexanet alfa is in the pipeline. It’s a Factor Xa decoy (Andexanet Alfa) that binds up the F10A inhibitors like a sponge. Read more here.
In the setting of major bleeding, guidelines recommend 4 factor PCCs. A recent study demonstrates reduction in bleeding using 4 factor PCCs on healthy patients given edoxaban [Zahir et al, EMLitofNote]. The benefit of 4 factor PCCs is predominantly based on improvement in numbers, not patient oriented benefit and is discussed in these posts by Dr. Spiegel The Sign of Four, The Sign of Four Part 2.

More FOAM on Anticoagulation Reversal

ER Cast

Generously Donated Rosh Review Questions

Question 1. A 65-year-old man with a metal aortic valve presents with hematemesis. His vitals are BP 95/50 and HR 118. The patient is on warfarin and has an INR of 7.3. [polldaddy poll=8501352]

Question 2. A 66-year-old woman with atrial fibrillation on warfarin presents with dark stools for 2 days. Her vitals are T 37.7°C, HR 136, BP 81/43, RR 24, and oxygen saturation 94%. Her labs reveal a hematocrit of 19.4% (baseline 33.1%) and an INR of 6.1. [polldaddy poll=8505511]

Answers.

1. D. The patient presents with life-threatening bleeding and an elevated INR from warfarin use requiring immediate anticoagulant reversal regardless of the indication for anticoagulation. Warfarin acts by inhibiting vitamin K recycling thus limiting the effectiveness of vitamin K dependant clotting factors (factors II, VII, IX and X). The effect of warfarin can be measured using the prothrombin time or the INR. Warfarin is indicated for anticoagulation for a number of disorders including the presence of a metal valve. Patients with metal valves are at a higher 1-year risk of clot formation around the valve and subsequent embolic stroke. The therapeutic goal of warfarin in a patient with a metallic valve is usually between 2.5 – 3.5 or 3.0 – 4.0. Despite the increased stroke risk, patients with life-threatening bleeding should always have their warfarin reversed by administration of vitamin K and fresh frozen plasma (FFP). Alternatively, prothrombin complex concentrates can be given instead of FFP.

Warfarin is not amenable to hemodialysis (A) for removal or reversal. Although patients with a mechanical valve are at an increased stroke risk (increased 1 year risk) reversal should not be delayed (B), as the patient is more likely to die in the immediate situation from their gastrointestinal bleed. Platelet transfusion (C) will not help, as warfarin does not inhibit platelet function.

2. C. The patient has a life-threatening gastrointestinal bleed in the setting of anticoagulation with warfarin, a vitamin K antagonist. Warfarin acts by inhibiting the synthesis of vitamin K-dependant factors in the coagulation cascade (II, VII, IX, X, protein C, and protein S). The anticoagulant effect of warfarin should be reversed as part of the patient’s emergent treatment. Fresh frozen plasma (FFP) contains all factors in the coagulation cascade and should be given in patients with major bleeding and elevated INR. Vitamin K should be given IV in critically ill patients with elevated INR because it shortens the time to effect.

Vitamin K should not be given intramuscularly (B) because absorption via this route is highly variable. Vitamin K should also not be given orally (D) in critically ill patients because the onset of action will be delayed. Additionally, absorption in patients with gastrointestinal bleeding may be variable. Vitamin K should be given along with FFP (A) because the factors inhibited rely on vitamin K for function.