Aug 192011

Hi people!

The idea behind this podcast and blog is to provide a quick 5-minute review of each of the LLSA* articles. In the past three years, we’ve taken the exam in the 11th hour, quite literally. Obviously, there is a better way.

Here’s our solution. We’re going to create 5 minute audio summaries of each article.  Our goal is to catch up to the 2012 test in a year’s time. We’ve decided to share it with everyone.

You can also find this on iTunes, look for “Procrastinators Guide.” We’ve already completed the podcasts for 2009 and will soon be starting 2010.

If you find this useful, have some questions, comments or criticisms or if you’d like to contribute your own 5-minute summary of one of the LLSA articles (we’d love this to be a community effort), please e-mail us at emergencyprocrastinator at gmail [dot] com. Or you can call us and leave a message at 773-377-LLSA.

Feel free to leave comments below! Thanks.

– Scott & Rahul

* The LLSA (Lifelong Learning and Self-Assessment) is a program by the American Board of Emergency Medicine (ABEM) to keep all board-certified ER physicians up to date with the literature.  Each year there is a reading list of articles intended to keep us learning for a lifetime.

 Posted by at 7:03 am
Mar 152013

Singer AJ, Dagum AB.  Current Management of Acute Cutaneous Wounds.  N Engl J Med.  Sept 2008;359(10):1037-1046.  (Test questions will only be written from the article, but ABEM also encourages diplomates to watch the video.)

Wounds are something with which we frequently deal.  More than 11.8 million wounds were treated in the US EDs in 2005.  This article summarizes evidence-based management where available, and includes small studies and expert opinion where data is lacking.  This summary will be full of the article’s recommendations.

General principles

Thoroughly cleanse with tap water or saline.  High pressure for heavy contamination. Update tetanus.  A moist environments accelerates healing.  Use topical antibiotic or an occlusive dressing.  Wet dressings that macerate the tissue should be avoided.


First irrigate and remove foreign bodies.  This may be difficult with large and deep abrasions.  If particles are not removed, post-traumatic tattooing will develop. Removing the particles within 24 hours produces the best results, so do your best and don’t pawn it off on the plastic surgeon next week.  Use scrub brushes, topical and infiltrative anesthetics, opioids, and sedation liberally to facilitate proper care.


Traumatic lacerations are reviewed in another articles.  The authors do note that for simple low-tension lacerations skin adhesives and surgical tapes can be used effectively rather than sutures.

Skin Tears


If no tissue loss, wound edges can be approximated with surgical tapes and covered with a nonadherent dressing.  If there is tissue loss, there are a number of petroleum-based gauzes, hydrogels, foams, hydrocolloids, nylon-impregnated gauzes, and silicone-coated dressings available (though I’ve never seen these in my ED).  A Dermabond-like adhesive can be used for all types of skin tears.


Plantar puncture wounds


2-10% will develop cellulitis (Staph or strep).  Puncture wounds in patients wearing tennis shoes saturated with sweat have been associated with pseudomonas osteomyelitis.   Cleanse well and evaluate for foreign bodies.  Prophylactic antibiotics for sweaty shoes, and for immunocompromised–in others abx are debatable.  Close follow-up required.


Mammalian Bites


Dog bites get infected 3-18% and cat bites are 28-80%.  Studies have suggested it is safe to close after high-pressure irrigation up to 12 hours (even on extremities).  Punctures and scratches should heal by secondary intention.  Bad ones may benefit from delayed primary closure.  Do not close “clenched-fist bites”.  Irrigate, give antibiotics, and consider surgeon.  Prophylactic antibiotics have only been shown to help human bites and bites to hands (though most of us give them for everything).

Subungual hematomas

Historically the nail was removed for hematomas involving more than 50% of the nail bed.  However, simple trephination has been shown to be effective without deformities or complications.  Save nail removal for ones that have disruption of the nail or surrounding nail folds.  The authors do not replace the nail plate or put aluminum foil or gauze to separate the nail fold from nail bed unless surgical repair is necessary.


May progress over 2-3 days so frequent assessment is necessary.  Therapy is based on the deepest part of the burn.

First degree are limited to the epidermis and are red and painful.  Second degree burns involve all the epidermis and part of the underlying dermis.  Superficial second-degree (partial thickness) burns have clear blisters and weeping.  They are painful and blanch with pressure.  They heal in 2 weeks with minimal scarring.  Deep second-degree burns are difficult to distinguish from full thickness, or third-degree burns.  They involve deep layers of dermis and are characterized by white or red dermis that doesn’t blanch.  There are several ways to estimate burn area: “rule of nines”, Lund-Browder chart, 1% x palm surface area.

Use of cold tap water within 30 minutes reduces pain, depth and extent of injury.  Ice or ice water may worsen tissue injury.  Hypothermia from cooling large burns has been claimed, but the authors seem to question this fact.

Blisters < 3 cm should be left alone, but if > 3 cm or over mobile areas then should be aspirated sterilly.  If ruptured, cleanse with soap and water and remove dead epidermis.


First-degree burns may benefit from topical NSAIDS or aloe vera.

Deep second-degree burns and third degree burns should be covered with topical abx, and referred.

Superficial second-degree burns can be treated with topical antimicrobial or an absorptive occlusive dressing (which may be less painful and promote more rapid healing).  There seem to be many new products summarized in the article that are better than silver sulfadiazine.


Chemical burns

Remove elemental metals if present, then copious water lavage.  Hydrofluoric acid can cause hypocalcemia, may require admission and excision of wound.



Rapid rewarming over 20 minutes in water at 40-42’C.  Do not massage area.  Watch skin over 1-2 days to determine extent of injury.  Use ibuprofen 400 bid to reduce levels of prostaglandin and thromboxane.  TPA given within 24 hours has been shown to be helpful.

In summary, irrigate and debride, protect from trauma and bacteria, create a moist environment, and judiciously use antibiotics, and you’ll be a wound master.

Mar 152013

Ropper AH, Gorson KC.  Concussion.  N Engl J Med.  Jan 2007;356(2):166-172.

Special guest author for summary:  Dr. Nedra Vincent.  Thanks!!!


Defined as an immediate and transient LOC with a brief period of amnesia after a blow to the head. Highest rates noted among young children, Bicycles and sports are most common cause among 5-14 year olds and falls and vehicular accidents most common among adults.

Concussion does not cause loss of autobiographical info such as name or DOB. This would suggest hysteria or malingering.

The brief LOC appears to be caused by rotational forces exerted at the junction of the upper midbrain and thalamus causing disruption of the reticular neurons. It is unknown what accounts for the amnesia.

It is prudent to insist that any concussion pt be taken to an ED for evaluation although some will object

The concern is that of a subdural, epidural or intraparenchymal hemorrhage. But less than 10% will have bleeding after concussion and less than 2% require neurosurgical intervention
Noncontrast CT is adequate to detect these, MRI in not necessary.
Clear neuro signs such as hemiparesis or poor arousal certainly necessitate CT, but predicting which patients are likely to have CT findings and yet avoiding unnecessary scans has proved difficult. Evidence that the injury was minor, including a normal neuro exam does not ensure absence of intracranial lesion. 2 rules for clinical decision making have been prospectively validated- The New Orleans Criteria and the Canadian CT Head Rule. The only criteria they have in common is older age and vomiting. In two prospective studies it was shown that the presence of any of the clinical features in these rules identified essentially all patients requiring immediate neurosurgical intervention. Both rules had low specificity, but it was slightly higher for the Canadian rule. Patients 15 years and younger were excluded from one of the original studies and both of the validation studies, so the applicability to this age group is uncertain.

For patients 16-65 years old with no postconcussive symptoms except mild headache, no external signs of injury or basilar skull fracture, and a normal neuro exam, the frequency of clot requiring neurosurgical intervention is so low (<1%) that it is reasonable to forego CT. Imaging is routinely suggested for age <16, for intoxicated patients, those on anticoagulants or having other bleeding tendencies, and those who cannot be reliably observed after discharge.

2 hour observation is appropriate for patients with normal neuro exams and no systemic injuries. Having a responsible person to observe is imperative as well as complete written discharge instructions. It is generally suggested that patients not return to normal activity until they are free of headache and dizziness.

New hemiplegia, drowsiness or aphasia after concussion is cause for concern about delayed subdural/ epidural and warrants exam and imaging. If focal signs are not due to IC bleeding, the possibility of CVA or carotid dissection should be considered.
CT findings of small surface contusion or limited amounts of SAH can occur in up to 5% but seldom cause neuro findings apart from headache. These findings would warrant overnight observation. Fracture through the middle meninigeal groove also warrants repeat imaging.

Post concussion symptoms consist of sometimes disabling syndrome of headache, difficulty concentrating, dizziness and others in the days/weeks post injury. Symptoms may persist for months. Controlled trial data is lacking, but reassurance and education about symptoms may decrease incidence and duration of symptoms at 6 months. Clinical experience suggests benefit from use of mild analgesics for headache, avoidance of narcotics and the use of meclizine, promethazine and vestibular exercises for dizziness.

Concussion in athletes: Testing of several hundred athletes after single concussion has demonstrated return to baseline cognitive and motor performance within weeks. Studies of collegiate rugby and soccer players have shown decreased scores on some neuropsychological tests in proportion to number of reported head injuries, but a recent study of Australian football players suggests no such association. There has been more clear cognitive decline noted in boxers.

Second impact injury within a short period causing catastrophic neuro damage is largely unfounded. It is based on rare and disputed cases.

There are scant data to guide when to allow players to return to sports after concussion.
American Academy of Neurology recommendations are included in the article and are currently under revision.

Mar 152013

Heard KJ.  Acetylcysteine for acetaminophen poisoning.  N Engl J Med.  July 2008;359(3):285-292.

Acetaminophen (or paracetamol, for you non-americans) poisoning killed 300 and accounted for 70,000 visits in 2005, either as a single ingestion, or dosing too frequently or too much.

There are 4 phases:

  • preclinical toxic effects (normal ALT)
  • hepatic injury (elevated ALT)
  • hepatic failure (elevated ALT plus encephalopathy)
  • recovery

If treated in the first phase, recovery is full.  In the second phase, it is variable.  In the third phase mortality rises to 20-40%.


There are two pathways of the metabolism of acetaminophen to know.  About 95% undergoes glucouronidation and sulfation to nontoxic metabolites, while 5%is metabolized by cytochrome p450 to NAPQI (N-acetyl-p-benzoquinone imine), which is toxic to the liver.  NAPQI is detoxified by glutathione which is typically plentiful.  Glutathione is synthesized from glutamate, glycine, and cysteine.  Cysteine is not as plentiful.  Acetylcysteine is readily absorbed and converted to cysteine in cells, thus forming glutathione and saving the liver cells from NAPQI.

Clinical evidence and use

Acetylcysteine has proven useful even in patients with hepatic failure (from acetaminophen) with a 21-28% reduction in mortality, but there have not been systematic studies comparing its use in hepatic injury but not failure.  Even a Cochrane review concluded that acetylcysteine should be given but acknowledged the limited evidence.

The Rumack-Matthew nomogram is useful in a single acute ingestion.  Most poison centers recommend treatment if the level falls in the “possible toxicity” zone, but apparently some centers and other countries recommend treatment only when in the “probable toxicity” zone.  Be careful where you decide to overdose!

The nomogram is not useful if one does not know the time of ingestion, it was not done at a single time, or when the patient has been taking too much acetaminophen chronically.  The authors recommend treatment for patients who chronically take > 4g a day and have an elevated ALT.

Oral versus IV.  The authors recommend IV for altered or vomiting patients, hepatic failure, and pregnancy (though oral probably would work).

Oral is given 140 mg/kg load, with 70 mg/kg q4h x 17 doses.  IV is 150 mg/kg load over an hour, followed by 12.5 mg/kg over 4 hr, and then 6.25 mg/kg over 16 h.  Oral costs $50.  IV is $470.

Acetylcysteine is not pleasant, and vomiting is common.  Up to 15% treated with IV might have an anaphylactoid reaction (though in the study the medication was only discontinued in 2%).

When patients do not meet criteria to use the nomogram, the treatment recommendations are more variable.  The author seems to have a very low threshold for starting a treatment course.  Given the dramatic improvement in outcomes, and safety profile of the medication, this approach seems to make sense.

Mar 152013

Cucchiara B, Ross M.  Transient ischemic attack: risk stratification and treatment.  Ann Emerg Med.  Aug 2008;52(2):S27-S39.

After a TIA, the two main concerns are what’s the chance of a stroke happening and how should the patient be treated. This article reviews both the risk stratification of TIA for stroke and treatment options. So let’s start with risk stratification.

There are three main ways of risk stratifying patients:

  1. clinical risk scores: analagous to risk scores in ACS
  2. diffusion weighted imaging: similar to cardiac enzyme levels as it is a direct measure of neuronal death
  3. vascular imaging: is similar to cath

And if we were to draw an analogy to ACS, then they would correspond as…

  1. MRI would be like transient ischemic changes on EKG (this hasn’t been studied well yet).

Clinical Risk Scores
There are three main scores: California, ABCD and the hybrid of the two ABCD2:
The Cali score is:

  • age > 60 y/o
  • DM
  • > 10 min Sx
  • S/Sx weakness
  • Speech impairment

Each gets a point. For patients with all five risk factors, 34% experienced a stroke, about half of which within 2 days

The ABCD score

  • Age > 60
  • BP > 140 / 90
  • Clinical features of unilateral weakness
  • Duration of Sx <10, 10-60, >60 min

These are weighted differently, see Table 1 in the article to see how to calculate and the Odds ratios or Hazard ratios for these. No patients with ABCD < 3 had a stroke within 1 week. Greater than 3 had increasing chances of stroke. This one doesn’t have DM in it.

Combining these two data sets and using some statistical magic, they came up with the ABCD2 score. This one is basically like the ABCD score but it includes DM and speech impairment (carried over from the Cali score).

These risk scores should supplement, but not replace clinical judgement.

Diffuse-Weighted Imaging
Patients with TIA’s have lesions in DW MRI in 16-67% of patients. Nice range. When present, it says a stroke has occurred. So they are a high risk group. It’s like the high troponin. A lesion doubled the risk of a stroke. In patients with symptoms > 1 hour and a lesion, four times risk of stroke. One study saw 4.2% risk of stroke in DWI negative patients and 14.7% in DWI positive patients (P=0.10, not good – is this a typo?). One study showed the hazard ratio is larger for DWI-positive than ABCD=5.

Vascular Imaging
Symptomatic large vessel disease is associated with a high-risk of short term stroke. Hemispheric TIA + carotid disease of any severity was noted to have a 20.1% risk of 90-day stroke (NASCET trial), though the greater the stenosis – they didn’t find greater risk of stroke.

Who should be hospitalized? Should something go wrong, it’s nice to be in the hospital – and they can get tPA pretty quickly. On the other hand, most patients don’t get a stroke. One Texan study found the 30d-risk of stroke in hospitalized patients was 2% and 7% in discharged patients. Some benefit of hospitalization? Current guidelines vary, but a consensus panel declared hospitalization should be considered for patients with a first TIA (within 24-48h), recommended for patients with crescendo attacks or >1h Sx or carotid stenosis > 50% or known source of embolus or hypercoagulable state or an elevated Cali score or ABCD score. Maybe the intensive study you get in house?

The EXPRESS study found that a stroke clinic visit decreased the 90-day-likelihood of stroke. Just going to your PCP, though, isn’t as good because you likely won’t get the full workup (Goldstein showed in a study with 95 patients). An obs stay with an accelerated diagnostic protocol was shown to have similar clinical outcomes, but at less cost and less time in the hospital.

We can divide the treatment into two groups: the hyperacute period (to prevent stroke, before testing has been finished) and longer term prevention. So first we look at the hyperacute period.

Hyperacute period
Anticoagulation – no evidence of net benefit. Bleeds may offset any prevented strokes. This is an area of uncertainty.

Long-Term Stroke Prevention
CEA – patients with 70% stenosis are referred for CEA. There was a 10-15% absolute reduction.
Anticoagulation for Dissection (Carotid or Vert) – the mural hematoma can occlude the vessel or embolize – causing a stroke. Many experts advocate anticoagulation. Non-randomized data says no difference between anti-platelet and anti-coagulant meds.
Atrial fibrillation – warfarin reduces risk, 39% relative risk reduction compared to anti-platelet therapy alone. ASA + plavix – doesn’t substitute for warfarin
Infectious endocarditis – anticoagulation should be avoided due to high risk of intracranial bleeding
Anti-platelet therapy

  • aspirin – low dose just as good as high dose, but has less side effects
  • clopidogrel / ticlopidine – plavix had a similar side effect profile but 8.7% relative risk reduction for stroke compared to aspirin; ticlid has caused severe neutropenia so no good
  • combination therapy – ASA + dipyridamole was better than either alone (and all 3 better than placebo); clopidogrel + ASA was just as effective as clopidogrel alone in high risk patients, but more risk of bleeding.

The one figure in the paper tells it all (talk the way through it).

Mar 152013

Sprung CL, Annane D, et al.  Hydrocortisone therapy for patients with septic shock.  N Engl J Med.  Jan 2008;358(2):111-124.

The gist of this article is that hydrocortisone doesn’t improve survival or reversal of shock in patients with septic shock. We have been using steroids in patients who remained hypotensive after fluid boluses and vasopressors in patients whose plasma cortisol didn’t rise after a corticotropin stim test. This multicenter, randomized, double-blind, placebo-controlled trial,

  • 251 patients got steroids hydrocortisone 50 mg q6h x 5d [125 did not have a response] {118 did} ?8-unknown
  • 248 got placebo [108 did not have a response] {136 did} ?4
  • With an outcome of death at 28 days in those who didn’t have a response to the corticotropin stim test. Secondary response was death at 28 days in patients who DID have a response to the stim test. They also looked at all patients. And the rates of death at 1 year.

No difference in mortality between the two groups @ 28 days. Also no difference in those who did have a response. Though in those whose shock was reversed, it happened quicker in those receiving steroids.

Mar 152013

Venkat A, Piontkowsky DM, et al.  Care of the HIV-positive patient in the emergency department in the era of highly active antiretroviral therapy.  Ann Emerg Med.  Sept 2008;52(3):274-285.  

This article discusses the change in the spectrum of illness since the introduction of HAART (highly active anti-retroviral therapy) in 1995. Previously opportunistic infections predominated, these are the ones WE learned in medical school: pneumocystis jiroveci (carinii), candida albicans, mycobacterium species (Tb, avium, intracellulare), cytomegalus, cryptococcus neoformans. The prevalence of these has decreased while other illnesses are on the rise, like kidney problems, lymphomas and psychiatric illnesses.

I don’t really know anything about HAART, so let’s go over this briefly. HAART therapy is indicated when the CD4 drops below 350. Also pregnant patients, those with renal failure, an AIDS defining illness, hepatitis B should, too. HAART consists of:

  • 2 nucleoside-analog reverse transcriptase inhibitors AND
  • either a non-neucleoside reverse transcriptase inhibitor or a protease inhibitor.

Examples of these are:

  • nucleoside-analog reverse transcriptase inhibitor: tenofovir/emtricitabine or zidovudine/lamivudine
  • non-nucleoside reverse transcriptase inhibitors: efavirenz
  • protease inhibitor: atazanavir+ritonavir, fosamprenavir+ritonavir, or lopinavir+ritonavir

If you want to see more possibilities, look at table 1 which also shows their side effects. All these drugs can call hepatotoxicity. The nucleoside reverse transcriptase inhibitors can cause lactic acidosis. The levels can get as high as 10 (wow) and present fairly subtly – fatigue, vomiting and mylagias. I’m going to check a lactate level on all my HIV patients on these meds.

If they’re not responding to meds, then they need salvage therapy as second line therapy.

  • Enfuvirtide, a fusion inhibitor (that is it prevents HIV from fusing to the CD4 cell)
  • maraviroc – prevents entry into the cell
  • raltegravir – which prevents the HIV DNA from integrating into the host DNA

They all have side effects.
Immune Reconstitution Inflammatory Syndrome
When the immune system of the patient gets better, patients on HAART can develop a syndrome where previously dormant opportunistic infections act up, like MAC.  It usually happens within the first 8 weeks and therapy is supportive, maybe needing anti-inflammatories and steroids. You don’t have to stop HAART.

Cardiovascular Disease
Patients on protease inhibiros get hyperlipidema, truncal obesity and hyperglycemia. There is a 26% increased relative risk of MI with patients on HAART. Basically, HAART meds increase a patient’s risk for MI – even in young patients. They can also get dilated cardiomyopathy.

Pulmonary Illness
P jiroveci’s incidence has fallen, and strep pneumonia remains the number one cause of pneumonia. And it will look like non-HIV patient’s on XR. That sounds like it’d be a test question. HIV patients also are at risk for COPD, which responds to standard inhaler and steroid therapy. 0.5% get pulmonary hypertension.

Renal/urological disease
HIV nephropathy is an indication for starting HAART. Patient’s can get Fanconi’s syndrome, in which all sorts of stuff gets spit out into the urine in the prox tubules and not reabsorbed. Renal failure is a leading cause of death of HIV patients in the HAART era.

Indinavir and other drugs can cause kidney stones.

The pre-HAART illnesses inclue toxo and C neoformans. Obviously, CT should be obtained before LP. Progressive multifocal leukoencephalopathy is still a lethal cause of encephalitis despite HAART, though the incidece has decreased. HAART is the mainstay of therapy, with stabilization as opposed to cure. CNS lymphoma has also decreased.

Strokes – patients are getting older so they’re at greater risk, HAART produces lipid profiles assocaited with atherogenesis, and HIV itself is a risk factor for stroke. So get that head CT.

HIV and the meds can also cause sensory neuropathies.

Opportunitistic infections have decreased, like C albicans. C difficile is the most likely cause of diarrhea. Advanced AIDS are at risk for crypto and microsporidia, so you’ll need special stool studies. Hep B and C are the most serious hepatic compliations, and they are at 2-3 times the risk. Patients with Hep C don’t respond as well to HAART. A few of the anti-retroviral meds have activitis against hep B. Othe rmeds can cause Gilbert’s disease, pancreatitis and lactic acidosis.

Anemia is caused by HAART, macrocytic, normocytic or hemolytic. HAART can improve neutropenia and thrombocytopenia. They are at increased risk for DVT (2-10 x), but you have to be careful with monitoring warfarin use. HIV can cause TTP despite HAART. In fact TTP plus hemolytic anemia should trigger the consideration of Dx of HIV.

Certain cancers are increased: Hodgkin’s, anal and lung cancers.

Endocrine disease
Protease inhibitors cause hyperlipidemia and truncal obesity, and at risk for insulin resistance. HIV can cause low testosterone levels. Grave’s disease or thyrotoxicosis can happen during IRIS.

Psychiatric Illness
Demoralization (which doesn’t respond to anti-depressants). This differs from depression by lacking complete anhedonia. This jeopardizes compliance with thearpy. AIDS mania and AIDS dementia.

Before HAART, patients got arthritis, polymyositis and diffuse infiltrative lymphocytosis. Patient’s on HAART get septic arthritis, staphylococcal pyomyositis (usually in the thigh). IRIS can cause sarcoid or autoimmune thyroiditis. Osteoporosis and osteonecrosis, normally of the hip. Remember to watch out for lactic acidosis and rhabomyolysis.

Many sorts of dermatologic lesions can present, derm conditions are the most common clinical ailment in HIV-infected patients. Folliculitis with Staph aureus is common. Molluscum with HAART use and pre-malignant warts (which require urgent referral).

Mar 152013

Gallagher TH, Studdert D, Levinson W.  Disclosing harmful medical errors to patients.  N Engl J Med.  June 2007;356(26):2713-2719.   

The IOM report from 1999 “To Err Is Human: But Doctors are Just Crazy Dangerous Killing Machines” reports that we cause anywhere from 44,000 to 98,000 deaths per year. Now some of those are equipment failure, systems errors, all of these errors led to patient harm. There’s a disconnect between physicians who would like to sympathize with those injured but fear litigation if they do so. So we get very vague about the errors or just cover it up entirely. This is not congruent with a patient’s wish to know and right to know if they are a victim of a medical error.

Since 2001 the Joint Commission requires that patients are informed of all of their outcomes, even the “unanticipated outcomes.” They don’t specify what you’re supposed to tell them, but at least they require you to say something. In 2005, a little over two thirds of hospitals had a disclosure policy in place to meet this requirement. Other countries, namely Australia and England, have disclosure policies though compliance with them are not mandatory.

In 2006, the National Quality Forum (a patient safety organization) endorsed elements of a disclosure. The patient should be told facts of the event, the presence of any error or system failure and the results of any analysis in addition to being given a formal apology. The hospitals should create a disclosure support system and integrate patient-safety, risk-management into the disclosure process. Physicians, risk managers and other health care workers should receive coaching and emotional support. And performance should be measured and tracked.

The Leapfrog Group, formed by several large US corporations affected by the rising costs of health care for their workers leveraged their purchasing power to increase patient safety and health care quality, use these NQF practices and publishes an institution’s compliance on the Internet so it can be compared to other hospitals.

Legislatively there are a spattering of relevant laws. Then Senators Hillary Clinton and Barack Obama proposed the National Medical Error Disclosure and Compensation Act (MEDiC – cute) but it failed to pass. Seven states have disclosure laws (NV, FL, NJ, PN, OR, VT, CA) and 34 states have “apology laws” which prevent an apology from being used in court as an admission of guilt. This, however, only applies to the apology. If you explain why you are sorry, that information can be used. So how helpful can that be?

There are only a few case reports of institutions which established disclosure policies:

COPIC Ins. Co.  (Colorado) 3 R Program — Recognize, Respond, Resolve

  • Saved 33% costs from traditional adversarial process – limited payouts to $30,000
  • 98% of claims resolved without litigation
  • Lawyers not permitted to participate
  • Patients are not forbidden from suing
  • Not reportable to the practitioner database

Veterans’ Administration Medical Center, Lexington, KY apology program

  • Average payout for medical claims $16,000 vs. $98,000 national average – 84% savings
  • 2 lawsuits have gone to trial during 10 year period

University of Michigan Health System apology program

  • Reduced malpractice claims by 50%
  • Reduced average time to process a claim from about 20 months to about 8 months
  • Reduced the cost per claim by 50%

Personally, I feel we should involve patients in all aspects of their care, including medical errors. Though, I’ll admit worry about any litigation it would trigger may prevent me from doing so. So there is still a lot of work to be done on this, but the winds of change are blowing.

Mar 152013

Karounis H, Gouin S, et al.  A randomized, controlled trial comparing long-term cosmetic outcomes of traumatic pediatric lacerations repaired with absorbable plain gut versus nonabsorbable nylon sutures.  Acad Emerg Med.  July 2004;11(7):730-735.

This is a randomized clinical trial that aimed to answer whether there is any difference between non-absobable (nylon) and absorbable (plain gut) in traumatic pediatric lacerations.  Short answer?  There is none.  They found no difference in cosmesis, dehiscence or wound infections.

Apparently there is a dearth of good literature on this topic, and thus the authors sought to provide solid evidence.  The authors note that most of us were taught to use nylon on the skin layer of lacerations because of a lower infection and dehiscence rate.  However, there had been some recommendations especially by surgeons to use plain gut, so the authors wanted to show that this recommendation could apply to the ED setting as well.  50 kids got plain gut, and 45 had nylon.  At 4 months they were evaluated by a plastic surgeon.  Scar revision was only recommended in 3, and 2 of those were nylon closures.  There was no difference in the complication rate.

I was one of those that was taught to always use nylon.  It made life simple.  Now I’ll have to think.

Mar 152013

Edwards ED, Jacob BP, et al.  Presentation and management of common post-weight loss surgery problems in the emergency department.  Ann Emerg Med.  Feb 2006;47(2):160-166.

With the rampant increase in obesity, there has been a huge increase in the number of weight-loss surgeries performed, and thus many more complications that may be seen in the emergency department.  We will briefly discuss the surgeries, complications, and treatments.

Vertical Banded Gastroplasty

Mostly of historical significance as lap-band has taken its place.  A pouch is made by stapling the lesser curvature of the stomach, then a nonadjustable band is placed.  A significant portion of patients regain weight after two years and go onto other surgeries.

Laparascopic Adjustable Gastric Banding

An adjustable band is placed around the upper stomach to limit the size, with a port implanted under the skin.  It should be 30-45’ from horizontal on the plain films.
Early Complications: gastroesophageal obstruction and proximal movement of the band.  If the obstruction is from the edema, conservative treatment with iv hydration is ok.  Proximal movement requires surgery.
Late complications:  “slippage” leads to gastric dilation and food intolerance.  It may lead to gastric necrosis and perforation.  The band should be deflated as quickly as possible.  The skin above the port should be anesthetized, and the port should be accessed with large-bore needle withdrawing up to the 5ml the port will hold.  Another problem is gastric erosion which can occur in 6.8% and requires surgery.

Roux-en-Y gastric bypass

This is the most common surgery for morbid obesity.  It reduces the amount of food one can eat, and bypasses a section of bowel leading to incomplete digestion.  A small gastric pouch is created that will hold only 15-30 ml of indigested food and liquid.  This is connected to the small intestine, with a variable amount bypassed (thus gastric BYPASS).

Early complications usually relate to major abdominal surgery like anastamotic leak, PE, bleeding, etc.  Occasionally there is obstruction of the “roux” limb that causes gastric dilation.  IR can decompress this.

Late complications include malnutrition, stricture, ulcer, reflux, and most concerning, internal hernia.  As with any abdominal surgery there can be adhesions leading to chronic pain and obstruction.

For all potentially surgical complications, CT is the test of choice, ideally with oral and iv contrast.  Since these patients can’t tolerate 1 liter of oral contrast, the author’s practice is to allow them to sip it over 3 HOURS!!! and then proceed to ct regardless of how much they drank.

A stricture will present with food intolerance and ct will be normal.  Upper endoscopy with sequential balloon dilation is usually successful.

Internal hernias occur when a loop of bowel herniates through the mesenteric defect created by surgery.  They present as intermittent, crampy pain that often radiates to the back.  Exam is usually unrevealing unless there is ischemic bowel.  20% can have normal CT’s, and most will have normal wbc counts.  Therefore the author makes this statement: “Any patient with unexplained abdominal pain, regardless of laboratory or radiologic findings, should be considered for surgical exploration.”  Good luck getting your community surgeon to buy that one.

Since absorption is affected, deficiencies in iron, b12, vit d, and calcium occur.  Most patients have secondary hyperparathyroidism, which causes decreased bone density.  Long-term effects of the decreased density are not clear.

Biliopancreatic diversion:

It involves decreasing the size of the stomach and creating an extensive bypass of the doudenum and jejunum.  These patients have similar complications to the Roux-en-Y patients but have a higher incidence of nutritional complications.

Bottom line, as obesity increases, the number of surgeries and thus complications will increase, causing all of us in the ED to cringe when we have to decide how hard to push our surgeons and how many CT’s to get.

Mar 152013

Appelbaum PS.  Assessment of patients’ competence to consent to treatment.   N Engl J Med.  Nov 2007;357(18):1834-1840.

 Valid informed consent depends on three factors: giving information to a competent individual and allowing them to make a voluntary choice. Really “competency” is a definition made in a court room, as physicians we judge capacity to make a decision – though we use these terms interchangeably. The trouble we can run into is in obtaining consent from a patient who lacks capcity is invalid. We need to be looking for a substitute decision maker. The article references a study in which physicians missed three quarters of patient’s lacking capacity to make a decision. This incapacity comes mostly from neurologic and infectious causes, but psychiatric conditions also affect capacity.

So it’s important to know what comprises the competence to consent for treatment, and while it varies it generally concerns:

  1. the ability to communicate a choice
  2. ability to understand relevant information
  3. ability to appreciate the medical consequences of a situation
  4. and the ability to reason about treatment choices.

Table 1 in the article presents this in greater detail with suggested questions to ask, for example:

  1. to assess the ability to communicate a choice, you could ask: “have you decided to follow the recommended treatment? if not, why not? why are you having a hard time deciding?”
  2. to assess the ability to understand relevant information, you can ask: “can you tell me in your own words what you understand about this choice? the risk? the benefits? the alternatives?”
  3. to assess the ability to appreciate their medical condition, you can ask: “what do you think is wrong with your health right now? do you believe you need treatment? do you know what that treatment will do? Do you know what will happen if you choose not to have the treatment? why do you think we recommend this treatment?”
  4. and finally to assess their ability to reason about treatment choices, you can ask: “how did you choose to pick the option you did? what makes this better than the alternative?”

Application of these rules depends on how serious the consequences of the patient’s decisions are? The more severe the consequences, the more stringent you should be.

In the absence of any reason to doubt their competence, assume that they are capable of making decisions. If there is reason to doubt, then there are standardized question sets which can be asked. The mini-mental status exam correlates very well, with a score ranging from 0 to 30, those less than 19 are more likely to lack capacity to make decisions and those above 23 to 26 are more likely to possess it. These questions are probably better asked by a social worker or someone else trained to do so, as it is time consuming for the EP to do. Plus, it’s also good to get another opinion on the chart. Similarly, there’s a structured interview called the MacArthur’s Competence Assessment Tool for Treatment which takes 20 minutes to administer which has better interrater reliability than just clinical assessment alone.

First be sure that patients have all the information needed to make a decision, this includes:

  • the nature of their condition
  • the nature and purpose of the proposed treatment
  • the risks and benefits of the treatment
  • the alternatives to treatment including the option of no treatment at all

It’s also better to perform two evaluations at two different times.

Once you’ve determined your patient lacks the capacity to make treatment decisions, if urgent treatment isn’t needed, first try to reverse any causes which can be: fever, hypoxia, medications, hypoglycemia, psychosis, etc. If fear or anxiety is the cause, find someone who can calm the patient down.

If the patient is still unable to display capacity, then find a surrogate decision maker. There may be someone named in an advanced directive, otherwise contact family members, usually in this order: spouse, adult children, parents, siblings then other relatives. If there is disagreement among family at the same priority level, it may need to be resolved in a court room.