October 2016 | Volume 16 Issue 10

patients with depression, mental health issues or chemical de-pendency. The findings that will trigger a positive screen are ex-tremely common. However, suicide itself is relatively rare.

Many things kill people and we can’t screen for all of them. If we are going to do this screening in an environment where minutes are a precious commodity, we need to think about the return on time investment.

Does the screening for disease or risk factors for disease de-crease the incidence of morbidity and mortality from that dis-ease? For suicide, the answer is no. There is no evidence that screening for suicide decreases the incidence of death.

This does not discriminate for age, acuity, presenting com-plaint or mental health risk. Is it just patients being triaged? Every patient in the ED? What if the patient is in need of imme-diate intervention such as with a STEMI, respiratory distress or major trauma? Some of these patients will die from something much sooner than suicide if you don’t hurry up.

What should you do to be in compliance?

Sam Ashoo. The Joint Commission recommends many things and when they come to your institution, they will ask about each one. You do not need to have the exact same method as other institutions. They are looking to see if you have addressed the issue, have some policy or procedure in place and follow your own policies and procedures. Be careful what you put in writing as they will hold you to it.

Ashoo uses simple triage screening tools. The nurse has a task to ask a question as part of the initial triage process. The question states, “Have you had any recent thoughts of hurt-ing yourself?” The nurse has three options to check off; “Yes”, “No” or “Not applicable or available.” If the answer is yes, the information is given to the provider and it is up to them to determine the course of action.

If the patient has suicidal thoughts, you need to address it with patient. It does not mean that you need a stat psychi-atric evaluation. This needs to be referenced in the conver-sation and the patient can clarify what they meant. Some pa-tients who screen positive later clarified that their pain was so great that they wished they were dead.

Rob Orman. Patients under the age of 9 are exempt from screening at his hospital. The question asks “In the last two

EM:RAP Written Summary October 2016: Volume 16, Issue 10 1

October Introduction: Triage Suicide ScreeningRob Orman MD and Anand Swaminathan MD

Take Home Points

The Joint Commission has recommended screening all patients for suicidal ideation using a brief standardized, evidence based screening tool.

This may lead to decreased throughput and false positive results with downstream effects.

There is no evidence that screening for suicide decreases the incidence of death.

The Joint Commission publishes a sentinel event newsletter. One newsletter has gotten a lot of attention; “Detecting and treating suicide ideation in all settings.” from February 24, 2016. This looks at the concept of detecting suicide ideation in the emergency department, specifically triage screening.

“Screen all patients for suicidal ideation using a brief stan-dardized, evidence based screening tool. A waiting room questionnaire including a question specifically asking if the patient has had thoughts about killing him or herself may help identify individuals at risk for suicide who otherwise may not have been identified. Research shows a brief screening tool can identify individuals at risk for suicide more reliably than leaving the identification up to a clinician’s personal judgment or by asking about suicidal thoughts using vague or softened language.”

Joe Bellezzo: “Their solution is to screen every patient who shows up to the ED with a question like ‘Have you felt suicidal. This is going to crash throughput due to limited psychiatric cov-erage.” Patients sometimes wait for days for placement in his ED and up to 20% of beds may be occupied by psychiatric holds.

Anytime you apply a screening tool to a low risk population, you will have false positives with downstream effects. How can we meet the standard of care and effectively capture at risk patients without a negative effect on throughput?

This is an administrative standard rather than evidence-based standard of care. This screens all comers rather than higher risk

Editor-in-Chief: Mel Herbert, MDExecutive Editor: Stuart Swadron, MDAssociate Editor: Marlowe Majoewsky, MD

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EM:RAP Written Summary | www.emrap.org2

weeks, have you had thoughts about killing yourself.” If the an-swer is yes, there are mandatory follow-up questions. Are they demonstrating psychotic behavior? Have others indicated the patient is at risk to themselves or others?

Cam Berg. They have constructed a discrete field with drop-down boxes in the EMR as a component of the initial nursing assessment. This is the primary nurse assigned to the patient and does not occur in triage. The nurse does their assessment including a suicide risk assessment.

They use the PHQ-2 assessment. This is a fairly well-validat-ed primary care depression and suicide screening tool. This asks two questions. Over the past two weeks, how often have you been bothered by any of the following problems? Little interest or pleasure in doing things? Feeling down, depressed or hopeless? The screening tool uses a spectrum to assess re-sponse but Berg’s group has changed it to a binary response of yes or no. If the patient answers yes to either question, the screen is positive and the nurse informs the physician. The physician determines whether the positive screen should be addressed. The nurses may opt out due to emergent circum-stances.

If you are going to start doing this in your ED, keep it simple and consistent.

Should We Intubate Cardiac Arrest Patients?Howie Mell MD and Minh Le Cong MBBS

Take Home Points

Some are resuscitating with chest compressions only in cardiac arrest.

This may not be appropriate for pediatric patients or in specific circumstances such as drowning.

CO2 monitoring can provide some additional information regarding the efficacy of resuscitation.

Positive pressure ventilation can decrease cardiac blood flow.

Should we be intubating patients with cardiac arrest?

Le Cong.

Although Mell has been using a protocol in cardiac arrest with chest compressions only, Le Cong has concerns for certain patient populations, such as infant and pediatric patients as well as cardiac arrests due to airway obstruction, drowning or hypoxia. Out-of-hospital cardiac arrests are not one entity but rather a spectrum of ages and mechanisms.

If a patient chokes on a piece of steak and goes into cardiac arrest, it doesn’t matter how many chest compressions he re-ceives; he needs his airway cleared. He needs to be ventilated because he has had a hypoxic cardiorespiratory arrest.

Registry data from Japan has been fairly consistent that combined chest compressions and ventilation in hypoxic cardiorespiratory arrest lead to better results.

If someone is dying because they aren’t breathing, it makes sense to restore their breathing.

Mell.

The protocol is for adult patients only and excludes pediatric patients. If someone suffers an out-of-hospital cardiac arrest, either witnessed or unwitnessed, of uncertain etiology, the medics initiate compressions.

They utilize an approach called pit crew medicine. The first person who arrives begins compressions. The next person to arrive applies the pads to the patient, places an IO if appropri-ate, gives an amp of epinephrine and places a non-rebreath-er mask on the patient. They continue resuscitation for four rounds of ACLS.

Their outcome data is excellent. They have 134 cardiac ar-rests in their registry and the recovery rate is around 24%.

If the patient went into cardiac arrest due to a drug overdose or choking episode, this may not be the best approach. How-ever, about 350,000-400,000 cardiac arrests in the US are thought to be cardiogenic. This is an odds game.

Le Cong.

ACLS is made by consensus. It may not be the best evidence but it takes a public health approach providing a guideline for trained and untrained providers across all age groups. The American Heart Association still recommends ventilation.

If someone collapsed, Le Cong would perform continuous chest compressions followed by placement of an airway, de-pending on resource availability. Placing an airway provides prognostic, diagnostic and therapeutic benefit. It allows you to follow the CO2. It allows you to isolate the lung and oxy-genate the patient.

Mell.

We know that circulation around the heart depends on a low pressure state. Our heart gets circulation in diastole. If we start bagging the patient, it causes positive pressure in the chest that impedes this blood flow.

We can oxygenate patients very well with a nonrebreather; the oxygen will diffuse into the lungs via Boyle’s gas law. If we are performing good chest compressions, there will be ex-halation. CO2 will be forced out although we can’t measure it.

3

Impeding cardiac blood flow for the sake of getting a mea-surement of CO2 is not a fair trade.

Le Cong.

Ideally the patient is placed on a ventilator as bagging the pa-tient too aggressively is detrimental.

Mell.

After ten minutes, the EMS service is allowed to intubate or bag the patient.

However, we need to get over this concept that everyone who dies has to chew on a tube. It isn’t necessary.

For more information on the compressions only approach, check out azshare.gov.

Opiate WithdrawalRob Orman MD and Ken Starr MD

Take Home Points

Opiate withdrawal can benefit from agents other than clonidine.

Muscle relaxants such as tizanidine or baclofen may help.

Patients can titrate doses of gabapentin.

Patients may experience a subacute and post-acute with-drawal phase that may last for weeks after the initial acute symptoms.

We often see patients in varying degrees of opiate withdrawal. What can you do? Most patients receive clonidine and ondansetron.

Clonidine is very effective. However, there are other agents you can use.

A muscle relaxant like tizanidine 4-8mg or baclofen 10mg ev-ery 8 hours is very helpful. Baclofen has other properties that decrease cravings and it has been shown helpful in reducing al-cohol craving and withdrawal.

Gabapentin is helpful. Patients can be given a 300-400mg tab several times a day with or without a tramadol taper. A tramadol taper would be a regimen of 50mg tabs with decreasing dosing and frequency over five days. You don’t have to give tramadol but it can provide time for them to get into a clinic.

Titrating up gabapentin is recommended for neuropathic pain. We don’t necessarily need to titrate it up for sedation although higher doses may be too sedating for some pa-tients. You can start the patient on 100mg and have them take it several times daily. Patients can increase the dose up to 1600 mg daily if they are able to tolerate it.

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For insomnia, patients could receive 50-100mg of trazodone at night although studies have not shown it improves sleep. Benzodiazepines such as valium or chlordiazepoxide are very helpful. 25mg of chlordiazepoxide has a very long half-life and can help. Unfortunately, many opiate dependent patients also abuse benzodiazepines.

What is a tramadol taper? This is an option for outpatient de-toxification. The five day taper is 100mg four times daily for day, 100mg three times daily for day, 50mg three times daily for day, 50mg two times daily for a day and then 50mg once in a day. There is some evidence supporting its efficacy. It isn’t some-thing you have to do but it is an option.

Clonidine helps decrease the noradrenergic response of the central nervous system. It is very helpful for withdrawal and causes sedation. However, it won’t be helpful as monotherapy. A combination of clonidine with gabapentin, a muscle relaxant and possibly a benzodiazepine may help.

What dose of clonidine can you give? 0.1mg twice or three times a day for five days. Patients can be continued on a dose of clonidine at night for a week after they go through the acute withdrawal phase.

0.1mg of clonidine at night for a week is unlikely to result in any significant dependence. This can be combined with gab-apentin.

Patients will have symptoms for longer than you think. Patients will need a lot of medication in the first seven days and some over the next few weeks.

What can you offer patients who are no longer in acute with-drawal but still experiencing symptoms of chronic withdraw-al? Patients may continue to experience recurrent symptoms of withdrawal weeks later, especially if they were on a long-acting opiate. You can treat them symptomatically with fluids, cloni-dine and benzodiazepines.

Patients experience acute withdrawal, followed by subacute withdrawal and post-acute withdrawal. Acute withdrawal is the cramping, nausea, muscle aches and diarrhea. Subacute withdrawal has waves of these symptoms alternating with days that are improved. Post-acute withdrawal is under-recognized. These patients are very depressed, apathetic, and have low en-ergy with insomnia. This may last for months and is associated with a high relapse rate.

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ALTEs and BRUEsIlene Claudius MD and Rob Orman MD

Take Home Points Recent guidelines have replaced the term ALTE with

BRUE (brief resolved unexplained event).

Children meeting the definition of BRUE should be placed in a low or high risk category.

Lower risk children with BRUE do not need admission to the hospital for cardiopulmonary monitoring.

Home cardiorespiratory monitoring has not been shown to decrease the rate of SIDS.

ALTE previously referred to apparent life threatening event. This was described as an episode that was frightening to the caregiver and involved some combination of apnea, color change, change in muscle tone, choking or gagging.

o However, this is a relatively non-specific definition that can include a huge number of diverse pathologies. It also implies that all of them may be life-threatening, scaring families and physicians into unnecessary testing and admissions.

In the most recent guidelines, the term ALTE is replaced with BRUE (brief resolved unexplained event).

Tieder, JS et al. Brief resolved unexplained events (formerly ap-parent life-threatening events) and evaluation of lower-risk in-fants. Pediatrics. 2016 May;137(5). PMID: 27244835.

Unlike the prior definition, this specifies infants younger than a year.

The episodes must be less than one minute. They must be resolved after the event.

The patient must have a reassuring history, physical exam and vital signs at the time of evaluation.

The event must be unexplained (i.e. after an appropriate his-tory and physical exam, the clinician can’t come to a conclu-sion as to the etiology).

The event needs to meet one or more of the following cri-teria. The infant must have become cyanotic or pallid. There must have been absent, decreased or irregular breathing. There must have been a marked change in tone; either hyper-tonia or hypotonia and/or there must have been an altered level of responsiveness.

Despite literature that shows that most of these children do very well, the majority of these children previously underwent a great deal of testing and often an admission.

This guideline provides a more specific definition and guidance in what to do. It allows the provider to rely on the history and physical exam they have obtained rather than on the parents’ impression of whether the event was life threatening.

There are patients that previously would have been considered an ALTE who do not meet the new definition. For example, if the patient has not returned to baseline, they have altered men-tal status which merits a work-up. If the patient clearly has bron-chiolitis, they require appropriate treatment for that condition. There will be some patients with a brief and resolved event that lasted longer than a minute. The clinician may still struggle in determining how expansive a work-up to pursue in these cases.

Children meeting the definition of BRUE should be placed into a low or high risk category.

Features that have been defined as lower risk are age great-er than 60 days, a lack of prematurity (gestational age ≥ 32 weeks and post-conceptual age ≥ 45 weeks), a first and isolat-ed event, duration of less than one minute, no need for CPR provided by a trained medical provider and no concerning his-torical features or physical exam findings.

If the child does not meet all of the low risk criteria, they are considered higher risk and fall outside the purview of the guideline. In these patients, the clinical practice guideline does not offer further recommendations. However, a higher risk patient probably requires some observation and possibly additional work-up.

For lower risk patients, the recommendations fall into four cat-egories.

What should we do? Educate the caregivers about these events. Work with the family in shared decision making re-garding additional evaluation, disposition and follow-up. Of-fer resources in CPR training to empower the caregiver.

What should we consider? You may consider obtaining per-tussis testing, a 12-lead EKG and monitoring patients with continuous pulse oximetry and serial evaluations.

Pertussis infection has been reported to cause ALTEs in infants as it can cause gagging, gasping and color change followed by apnea. These infants may be afebrile and not demonstrate cough or lower respiratory symptoms for sev-eral days afterward.

You do not need to admit the patient to the hospital sole-ly for cardiorespiratory monitoring. “Infants presenting with lower risk BRUE do not have an increased rate of cardiovas-cular or other events during admission and hospitalization may not be required.” It is fine if the patient has to be admit-ted for another reason.

You don’t need to obtain viral respiratory testing, urinaly-sis, serum blood glucose, bicarbonate or lactic acid, check for anemia or obtain neuroimaging.

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higher. They found 22% of patients did not understand their discharge instructions. Only 30% of these patients realized that they did not understand their instructions.

There is no evidence to show that pre-printed discharge in-structions are beneficial to patients.

Lawrence, LM et al. The effect of diagnosis-specific comput-erized discharge instructions on 72-hour return visits to the pediatric emergency department. Pediatr Emerg Care. 2009 Nov;25(11):733-8. PMID: 19864969.

They looked at the transition from handwritten discharge instruction to a new system permitting computerized in-structions. They found no improvement in patient out-comes with the same amount of return visits. Adding more elaborate instructions does not help avoid bad outcomes.

As Christina Cooley MD pointed out, the written discharge instructions can increase the risk to provider in case of a bad outcome. For example, a scribe sends the patient home with discharge instructions for gastroenteritis rather than undif-ferentiated abdominal pain. This can help bolster a claim of misdiagnosis on prior visit.

Whenever you discharge a patient from the emergency de-partment, you need to give and document verbal discharge in-structions. In a lawsuit filed after a patient had a bad outcome, the discharge instructions sent home with the patient were found inadequate. However, the practitioner had given and documented additional verbal discharge instructions. The court found that even though the written discharge instructions were inadequate and fell below the standard of care, the additional verbal discharge instructions provided met the standard of care.

How can you document this? “Additional verbal discharge instructions were given and discussed with the patient.”

Talk with every patient about their discharge instructions and make a note in the chart.

There are three elements that need to be a part of all discharge instructions. Patients need information about their follow-up. Patients need to be given return instructions. There should be some discussion about prescriptions or medications you have advised them to take.

Follow-up should be both time and action specific. “This is what I want you to do and in this time frame.” There are multiple cases where the courts have maintained that patients are not respon-sible for determining the time course of their own follow-up.

In a case that resulted in a lawsuit, a patient with a lumbar wound was advised to follow-up with a plastic surgeon “when available for follow-up”. Several weeks passed and the patient was unable to get follow-up. The patient later developed an infection. The patient sued the emergency department doc-tor and won. The court maintained that saying “when avail-

We should not routinely obtain a white blood cell count, blood culture, CSF analysis or culture, serum electrolytes, cre-atinine, calcium, ammonia, blood gases, urine organic acids, plasma amino acids, acyl-carnitine, chest radiographs, echo-cardiograms, EEGs or studies for gastroesophageal reflux.

We should not initiate home cardiorespiratory monitor-ing. Infant monitors are prone to artifact and have not been shown to improve outcomes or prevent SIDS. Several studies have shown a lack of correlation between ALTEs and SIDS.

We should not prescribe acid suppression therapy or an-ti-epileptic medications. If the patient has gastroesoph-ageal reflux disease, it is not a BRUE but a patient with GERD who may require medications. You do not need to give empiric acid suppression.

Close outpatient follow-up is advised with repeat clinical history and physical exam within 24 hours to identify infants with ongoing medical concerns.

Discharge InstructionsMatt Delaney MD

Take Home Points Patients often do not understand pre-printed discharge

instructions and studies have not shown benefit.

Discharge instructions can help bolster a legal claim of misdiagnosis against the provider.

When you discharge a patient from the emergency de-partment, you need to provide and document verbal dis-charge instructions.

Three elements that should be present in all discharge in-structions are follow-up (who and what time period), re-turn instructions and a discussion about prescriptions.

The approach to discharge instructions varies widely. What is the right way to do this?

There are some common pitfalls in discharge instructions.

Focusing solely on elaborate pre-printed discharge instructions can be problematic. There is a lot of literature to support that patients don’t really understand their discharge instructions.

Engel, K et al. Patient understanding of emergency department discharge instructions: where are knowledge deficits greatest? Acad Emerg Med. 2012 Sep;19(9):E1035-44. PMID: 22978730

They looked at a study population of patients discharged from the emergency department. This was an educated group of patients with at least 65% having a college level education or

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able” or “as needed” is really not adequate in establishing a timeline for follow-up.

In another case where a patient was discharged with a diag-nosis of gastroenteritis, the doctor wrote on the chart, “I want you to see your doctor in 1-2 days.” The patient did not fol-low-up. A week later the patient presented with a perforated appendicitis. The patient sued the emergency department physician but the court found the physician was not at fault as they gave them a very clear timeline for follow-up. The pa-tient was told who they should see and they did not.

Be specific who the patient should contact for follow-up. If you have a patient who is right hand dominant and falls onto their outstretched right hand with negative radiographs, you obvious-ly want them to follow-up to rule out scaphoid fracture. “I want you to see an orthopedist or hand surgeon in 1-2 weeks.”

Multiple court cases have found that patients are not re-sponsible for recognizing when they are getting worse after discharge. In a recent case of meningitis that was missed, the patient had presented with fevers, chills and myalgias during flu season. The emergency doctor did an adequate work-up. The patient was well-appearing, was sent home with a fairly exhaus-tive list of symptoms to indicate return visit (fever/chills, inabili-ty to tolerate oral intake). The patient began developing altered mental status and neck stiffness. There was a delay between the onset of these symptoms and their return to the emergency de-partment. They brought a lawsuit saying that they weren’t told about these specific signs and symptoms.

Make the discharge instructions as welcoming and open-ended as possible. “Please return immediately if you get worse, you don’t get better or you develop any new or concerning symptoms.”

Medication warnings. This can be tricky. Almost all medications have some sort of warning. Look at your favorite prescribed medications and identify those likely to cause trouble.

Controlled substances such as opiates, antiemetics like phenergan and benzodiazepines that can alter sensorium. Have a macro that says “Don’t drive or operate heavy machin-ery while taking these medications.” When patients receive these medications at the pharmacy, the bottles have these warnings. However, there are plenty of lawsuits where the warning was given by the pharmacy rather than the physician and the physician was later held liable.

Fluoroquinolones have a risk of tendon rupture. Have a mac-ro to use any time you prescribe a fluoroquinolone and have a brief conversation with the patient.

“I discussed the medications with the patient. I gave them signs and symptoms that could indicate an adverse reaction. I have advised them to limit their activities until they can see how they respond to the medication.”

Bouncebacks: Midlevel ProvidersMike Weinstock MD, Tim Scanlon, Shonna Riedlinger PA, Jennifer Stankus MD,JD

Take Home Points

Handoffs of patient care between providers are high risk for error. Taking ownership of the patient can decrease the likelihood of error.

Critical lab values should be called to the provider while confirmatory testing is in progress, not after results are available.

If the midlevel provider feels the case is outside their scope of practice or level of expertise, the physician should take over the case without hesitation.

Scanlon reported for his shift at 11pm and assumed care of a patient assigned to the physician leaving at 1am. The patient was a 28 year old male presenting with abdominal pain. He was diaphoretic, tachycardic and slightly confused. Scanlon was con-cerned that the patient would not be wrapped up before the physician left so he approached the overnight doctor to see if they would assume care of the patient. She was unable to help and referred Scanlon to the departing physician.

What did Scanlon see? The patient was in obvious distress with a complaint of abdominal pain. He had nausea and vomit-ing. He was restless, diaphoretic and a poor historian. He had a concerned mother at the bedside. She was very impatient with questioning and evasive with some questions.

What was the differential diagnosis? Kidney stones, gallbladder disease, pancreatitis and perforated bowel. He considered toxic ingestion. The patient had previously had an appendectomy.

This was a difficult patient and the diagnosis was unclear. The CO2 was 19.

Midlevel providers need to know what they know and when to ask for help. The first physician left and Scanlon discussed the case again with the overnight physician.

The patient’s mental status continued to deteriorate. The pa-tient accidentally removed his IV several times. The patient had a low grade fever, leukocytosis and altered mental status. They considered the possibility of a CNS infection and decided to ob-tain a head CT. They ordered a drug screen and considered tox-idromes. Scanlon wished for more oversight by the physician.

“You’ve got this, right? When everything results, let’s get him admitted.” The sign-out between the physicians was minimal.

How can we make handoffs positive?

A study by Horwitz looked at the development of a hand-

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off evaluation tool for shift to shift physician handoffs. They came up with certain elements that were important to convey to the receiving physician; identifying information, problem list, medication list, anticipatory guidance and a to-do list.

Horwitz, LI et al. Development of a handoff evaluation tool for shift-to-shift physician handoffs: the Handoff CEX. J Hosp Med. 2013 Apr;8(4):191-200. PMID: 23559502.

Another study looked at potential errors of handoffs such as a high signal to noise ratio, not having a standard approach, having an ambiguous moment of transition of care and cogni-tive bias.

Incentive based models may encourage or discourage hand-offs, which could affect patient safety.

Cheung found some solutions. Reduce unnecessary handoffs. Limit interruptions and disruptions. Provide succinct over-view of the case. Communicate outstanding tasks with a clear plan. Have information available for direct review. Encourage questioning by the receiving party. Have a clear moment of transition of care.

Cheung, DS et al. Improving handoffs in the emergency department. Ann Emerg Med. 2010 Feb;55(2):171-80. PMID: 19800711.

Apker, J et al. Exploring emergency physician-hospitalist handoff interactions: development of the Handoff Communication Assess-ment. Annals of Emergency Medicine 2010 Feb;55(2):161-70. PMID: 19944486.

They looked at handoffs between emergency physicians and hospitalists. They found the power differential be-tween the physicians can decrease openness and the amount of accurate information conveyed.

Handoffs are high risk. However, it is also high risk for a provider to avoid seeing a patient because they don’t want to handoff the patient to the incoming physician. Sometimes providers may avoid ordering a test that may not provide results in a timely manner.

It is not the handoff that is the problem. The problem is that the second provider is not taking ownership of that patient. The risk of handoff significantly decreases if you take owner-ship. Go in and see the patient. Put a directed note on the chart. Make sure you discuss test results and evaluate the patient.

What was the diagnosis? The patient had salicylate toxicity. The lab was so surprised by the level of toxicity that they decided to rerun the results to confirm prior to releasing the results. The salicylate level was 119. The patient was admitted to the ICU and dialysis was arranged.

There were several aspects of communication breakdown in this case. The failure of the lab to notify the providers regarding the elevated level before confirming is a systems-based failure.

There should be an automatic call to the emergency department regarding a potentially critical lab value. There was a power dif-ferential between the midlevel provider and supervising physi-cian. Scanlon felt uncomfortable requesting the physician take over the patient.

The patient’s condition continued to decline and his respirato-ry status worsened. The intensivist decided the patient needed to be intubated. Shortly after intubation, the patient arrested and died.

Within a year, all three providers were subpoenaed for a lawsuit.

The first physician was deposed first. They were asked, “Doc-tor, don’t you think if someone has abdominal pain, tachycardia and diaphoresis, the first thing on your differential should be salicylate toxicity?” His answer was “Yes.” “Shouldn’t your PA also consider salicylate toxicity at the top of their differential diagnosis?” The answer was “Yes”.

The case was settled for $750,000. There were several contrib-uting factors to the decision to settle the case. The deposition by the first physician was not a good reflection of the realities of the case. Also, the overnight physician should have gotten involved sooner in the case. The documentation was not suf-ficient. Scanlon did not have the opportunity to document re-al-time progress notes and the documentation was not started until the patient was admitted and his shift was ending.

What could have been done differently? Scanlon wishes he was more assertive. Midlevel providers and residents look to the supervising physician and trust their input and advice but it is ok to disagree respectfully. If the midlevel provider or resident asks you for help, be receptive.

This is an interesting problem in the emergency department. Midlevel providers often have overlapping shifts with physicians resulting in sign-outs. These are more challenging as you don’t know the patient as well.

They did a good job managing the case. They made the diag-nosis and arranged for dialysis. The attorney for the plaintiff argued care was not provided in a timely manner rather than failure to diagnose. Timing is very important in these cases. The patient was likely very acidotic and had they received dialysis sooner, they may have survived.

Don’t throw another provider under the bus. However, some-one has to take ownership of the patient. The midlevel needs to have an honest conversation with the physician and let them know that they need help with the patient. The supervising phy-sician has to take ownership of the patient. This is their role.

Document times. Document what time you spoke to some-one and a brief description of what was said.

The patient presented at 11pm. They were diagnosed with sa-licylate toxicity and serum bicarbonate of 19. Nephrology and

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toxicology was consulted. They planned to place a catheter and start dialysis. Unfortunately, the patient died.

Sometimes we do everything right and there is still a bad outcome. Juries may feel sympathetic for the patient.

What is the take-home message for midlevel providers and physicians? If the midlevel provider feels the case is outside their scope of practice or level of expertise, the patient should be handed over to the physician. The physician should take over the patient without hesitation. The midlevel provider should not be placed in a position where they feel they are unable to care adequately for the patient.

Cardiology Corner: Cardiac ImagingRob Orman MD, Amal Mattu MD and Anand Swam-inathan MD

Take Home Points Stress tests look for wall abnormalities during ischemia.

They are less effective after resolution of ischemic symp-toms.

A resting SPECT (single photon emission computed to-mography) or coronary CTA may be obtained in patients with a single positive or equivocal troponin.

Hemodynamically unstable patients with possible dissec-tion should receive a bedside echo to rule out tamponade.

Emergency Department Patients With Chest Pain Writing Panel, et al. 2015 ACR/ACC/AHA/AATS/ACEP/ASNC/NASCI/SAEM/SCCT/SCMR/SCPC/SNMMI/STR/STS Appropriate utilization of cardiovas-cular imaging in emergency department patients with chest pain: a joint document of the American College of Radiology Appropriateness Criteria Committee and the American College of Cardiology Appropri-ate Use Criteria Task Force. J Am Coll Radiol. 2016 Feb;13(2):e1-e29.doi:10.1016/j.jacc.2015.09.011

Most stress tests look for wall abnormalities during ischemia. They are not as good once the ischemic symptoms have re-solved. Even more dynamic studies like resting perfusion stud-ies are only useful if they are performed within several hours of symptom resolution.

Many of our patients have symptoms that resolve prior to pre-sentation. Even if they are symptomatic, it is unlikely we will be

able to get the test done within this window.

Alternatively, you can try to provoke the symptoms and com-bine some type of stress with imaging. The stress could be the ischemic symptoms but if these have resolved, the patient could be placed on a treadmill or injected with a vasodilator like dobu-tamine.

Stress tests aren’t perfect. The sensitivity seems to range around 85-90%.

Imaging tests are not appropriate in this situation. The patient needs to go to catheterization.

This is a common scenario, especially as troponin tests have become more sensitive. This paper recommends obtaining a resting SPECT (single photon emission computed tomography) or coronary CTA.

The SPECT study is a nuclear imaging study involving the injec-tion of a radioactive tracer. The study looks for the uptake of the tracer. Viable myocardial cells will take up the tracer more than ischemic or dead cells.

These patients are lower risk or intermediate risk depending on the history.

This paper recommends obtaining a resting SPECT test or cor-onary CTA.

What if you don’t do anything? There has been a lot of recent discussion on accelerated diagnostic protocols and HEART pathway without any imaging tests. A lot of these patients do not need cardiac imaging. There was not much discussion re-garding this topic in the paper. The paper seemed to promote imaging tests and CTAs.

What patients are suitable for discharge without imaging? If the patient has a HEART score of 3 or less and two negative troponins obtained 3 hours apart, they may follow-up with their primary care doctor or cardiologist.

You are concerned about aortic dissection.

CASE The patient has ischemic symptoms that resolved hours before presentation to the emergency department.

CASE The initial EKG and/or biomarker analysis are unequivocally positive for ischemia.

CASE The initial troponin is equivocal or there is a single elevated troponin without any additional evidence of ACS.

CASE The patient has a non-ischemic EKG with a normal troponin.

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The patient is hemodynamically unstable. What is your im-aging study of choice? These patients should receive a bed-side ultrasound looking for pericardial tamponade. Why? The most likely reason for instability in dissection patient is dissection back into the pericardium with tamponade. Mattu prefers the transthoracic echo. However, the authors of the paper suggest a CT aortogram. They also said that MR aortog-raphy may be appropriate. However, we know you never send a patient who is unstable or potentially unstable to MRI.

What do you do if the patient has a dissection that has led to tamponade? Get them to the OR as quickly as possible. What if you have to wait for the cardiothoracic surgeon or transport the patient to another hospital? Maximize fluids and increase their preload. Try to control the pressure and heart rate. You don’t have a lot of options.

These are difficult patients. There isn’t much you can do. Pericardiocentesis may be a last ditch effort to salvage the patient while awaiting transport or definitive care but is un-likely to be successful.

What if the patient is hemodynamically stable? The paper rec-ommends obtaining a CT aortogram. The traditional angiogram is no longer recommended. Although the paper suggests MR aortogram as an option, you would not send a patient with sus-pected dissection to the MRI suite. TEE is usually performed by cardiologists rather than emergency physicians.

What if the patient has prior history of aortic surgery with sus-pected dissection and is hemodynamically stable?

CTA or MRA is recommended. However, MRA may be of lim-ited utility due to artifact from the prior surgery.

The paper also discusses pulmonary embolism in pregnancy.

Get a duplex ultrasound. If the duplex is negative and the pa-tient has cardiopulmonary symptoms, the paper discusses ob-taining either VQ scan or CT pulmonary angiogram.

If the patient does not have symptoms involving the leg, some will still obtain a duplex ultrasound of the leg. It is easy to obtain, non-invasive and does not involve radiation. If you get lucky and it results positive, you are done. Others will go straight to VQ scan or CT angiogram.

This paper advises that the VQ scan delivers less radiation to the mother’s breast tissue. If the patient has healthy lungs, you can often just do the perfusion portion. Either is a reasonable option.

Orman orders a CT angiogram in the first trimester and a VQ scan in the second/third trimesters.

The triple rule out scan. Chest pain patients present to the ED with complex patterns of signs, symptoms and clinical data. Al-ternate imaging pathways may be necessary if the initial ten-tative diagnosis is not confirmed. For this reason, complex pa-tients often undergo more than one imaging study to exclude all diagnoses considered life threatening.

When one test is ordered to evaluate three different diagno-ses, the sensitivity is less than if you get the CT scan to eval-uate any one diagnosis. These scans have a lower sensitivity, higher radiation dose and increased contrast dose.

Although the paper seems to support increasing the use of the triple rule out, Mattu recommends doing a good history and physical to try to narrow the differential diagnosis.

This paper did not discuss some of the well-validated acceler-ated diagnostic protocols. They also did not discuss the risk of false positive tests. False positive stress tests are very common in low risk patients. When the risk of ACS is less than 2%, you are more likely to have a false positive work-up than a true posi-tive work-up. These tests shouldn’t be done in low risk patients. False positives lead to more testing, catheterizations, surgeries, morbidity and mortality.

Pulmonary HypertensionRob Orman MD, John Greenwood MD and Anand Swaminathan MD

Take Home Points

EKG findings concerning for pulmonary hypertension in-clude dominant R wave in V1, S1Q3T3, new incomplete or complete right bundle branch block, T wave inversions in V1-V4, ST elevation in aVR and tachydysrhythmias.

Be careful rate controlling atrial fibrillation in patients with pulmonary hypertension; they may decompensate.

Critical interventions include improving hypoxia and hy-percapnia.

Patients on epoprostenol infusions may decompensate with any interruption. This may be administered via inha-lation as well.

The right ventricle gets no respect.

Greenwood, JC et al. Management of crashing patients with pulmonary hypertension. Emerg Med Clin North Am. 2015 Aug;33(3):623-43. PMID: 26226870.

CASE A pregnant patient who has symptoms involving the leg.

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What are the clinical effects of pulmonary hypertension? There are two types of pulmonary hypertension; acute and chronic. Both are very dangerous to the patient and can be difficult to manage.

The pulmonary vascular bed is a high flow, low pressure sys-tem. Normal pulmonary arterial pressure is 25/10mmHg. This is much less than the systemic blood pressure.

Acute pulmonary hypertension usually occurs due to in-creasing pressure in the main pulmonary arteries. Hypoxia, hypercapnia, acidosis, left heart failure and obstruction can increase the pulmonary artery pressure. These patients will look sick.

Chronic pulmonary hypertension patients are different. There are five classes of chronic pulmonary hypertension.

1. Pulmonary artery hypertension. This is fairly rare. There are some recent advances in management.

2. Pulmonary hypertension resulting from left ventricular failure. This is the most common.

3. Pulmonary hypertension from chronic hypoxic lung dis-ease. For example, COPD.

4. Pulmonary hypertension from pulmonary embolism.

5. Pulmonary hypertension from everything else such as connective tissue disorders or autoimmune disorders.

Why do we need to know this? All of these patients will have pulmonary vascular changes that follow similar patterns. They have pulmonary artery medial hypertrophy, intimal fibrosis, fibrinoid necrosis and develop thrombosis in situ. The pipes get thick and clogged.

The clinical presentation of these patients can be tricky unless they already carry a diagnosis of pulmonary hypertension. A majority of these patients who come in have not been previous-ly diagnosed. They may complain of chest pain, dyspnea on ex-ertion or weakness. If the disease has progressed to the point of decompensation, you may see signs of right heart failure. They may have peripheral edema or JVD.

These patients may be symptomatic for up to two years pri-or to receiving a diagnosis. They often are not diagnosed until they are in class III or IV heart failure.

The classic case is an otherwise healthy female in her 30s who has become progressively short of breath until she has a difficult time walking across her house. She has multiple pre-sentations to the emergency department.

Are there clues that indicate pulmonary hypertension is con-tributing to symptoms? This is a classic presentation of a pa-tient with shortness of breath and clear breath sounds. This differential is fairly limited; symptomatic anemia, ACS, pericar-

dial tamponade and pulmonary embolism. If they don’t have a PE, you might want to look closer. If you see signs of periph-eral edema and JVD, there are signs of pressure overload and decompensation of right ventricular dysfunction. This may be pulmonary hypertension.

The troponin and BNP may be slightly elevated. The pulmo-nary pressure is so high that the right heart strains against it and may have some mild injury.

There may be signs on the EKG suggesting right ventricular dysfunction. You may see a dominant R wave in V1, S1Q3T3, new incomplete or complete right bundle branch block, T wave inversions in V1-V4, ST elevation in aVR and tachydys-rhythmias.

New onset atrial fibrillation is especially worrisome. They lose the atrial kick which is critical for moving the blood for-ward. This may be treated with rate control like any other pre-sentation of atrial fibrillation, but as soon as you give the pa-tient a negative inotrope, they may develop hypotension and decompensate right in front of you. Be careful, especially in patients with a known diagnosis of pulmonary hypertension.

The chest x-ray may have some subtle abnormalities that are frequently overlooked. There may be mildly increased cardiac size, right atrial dilation, decreased mediastinal size in the lat-eral view due to RV hypertrophy and pulmonary vasculature pruning (the main pulmonary artery tapers down right after it branches off).

Transthoracic echocardiogram. This is much more helpful. It will show an enlarged right ventricle. If the pulmonary hyper-tension is chronic, the right ventricle wall will be thick. Thick-ness greater than 5mm is concerning and greater than 10mm is diagnostic of right ventricular hypertrophy. In the paraster-nal short axis, look for bowing of the right ventricle into the left ventricle or the “D sign”.

You could measure tricuspid annular plane systolic excur-sion test or TAPSE but this will take considerably more ul-trasound skills.

If you have access to an echo tech at your hospital, this would be a good time to use them. They can obtain accu-rate measurements for you or your cardiologist to interpret.

What are the critical interventions to prevent further deterio-ration? Address the reversible causes.

Hypoxemia is a potent pulmonary vascular constrictor. Place the patient on supplemental oxygen and get the saturation above 92%.

If the patient is hypercapneic, you need to fix it. There may be a role for non-invasive ventilation to reverse critical hy-percapnia. As the pCO2 goes up, the pH goes down and they develop a respiratory acidosis which is another potent pulmo-

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nary vascular constrictor. It is ok to use PEEP if you think it will improve the systemic oxygenation but be careful. Exces-sive positive pressure may worsen the patient’s pulmonary vascular resistance.

It isn’t wrong to give the patient a small fluid trial, especially if their blood pressure is a little low. It is difficult to predict if they will be fluid responsive. You have to be careful. Over-stretching the right ventricle can lead to collapse. Give the patient 250-500cc of fluid and see if there is a clinical im-provement of perfusion. If you don’t get anything, stop right there.

If the patient has concomitant left ventricular failure and pul-monary congestion, should you give a diuretic? If you are fairly sure the patient is perfusing the kidneys and are not in shock, go for it. Unloading the right ventricle will only help its function.

The CVP can be helpful. It fell out of favor when it was used to detect fluid responsiveness. However, trending the CVP can be helpful. It tells you the right sided filling pressure and how much pressure the RV is sensing. Follow the CVP over time and see the response to your interventions. If it remains elevated, you may need to change tactics to decrease the pressure on the right ventricle. Echocardiogram may be useful but is less accu-rate and may take more effort to obtain serial assessments to follow treatment effectiveness.

Focus on improving perfusion first rather than diuresis.

How should you manage the systemic blood pressure in a patient with pulmonary hypertension who is having severe symptoms? Maintaining a good systemic blood pressure is criti-cal in the patient with acute pulmonary hypertension. You need to ensure the coronary blood vessels are receiving blood flow in diastole. Normally the right ventricle gets blood into the right coronary artery during diastole and systole but as the right ven-tricle dilates in pulmonary hypertension, the systolic blood flow is compromised.

Ideally, the diastolic pressure should be about 20-30 points higher than the central venous pressure. A MAP greater than 65mmHg is a reasonable goal.

Patients with advanced chronic pulmonary hypertension may be on epoprostenol. This has a short half-life and is adminis-tered via continuous infusion. Even a brief interruption in the in-fusion may lead to rebound hypertension and decompensation. Resume it quickly before the patient decompensates.

Although we may not be familiar with inhaled epoprostenol, it is similar to nitrous oxide. It is much easier to use. Your respiratory therapist probably has a protocol in the ICU. The dose is 50mcg/kg/min. If the patient is intubated, the respi-ratory therapist can administer it in the circuit. There is no reason it can’t be started in the emergency department.

Start IVs. Get the patient on a monitor and start supplemental oxygen. Make sure the saturation is greater than 92%. If the pa-tient has COPD, treat him as you would treat any other COPD exacerbation with steroids, nebs, BiPAP and time. Check a VBG to make sure the respiratory acidosis is improving.

When you reassess the patient, his blood pressure is lower and he is sleepy. You are concerned he is failing BiPAP and needs to be intubated. What are your drugs of choice for RSI? Ketamine and a paralytic, either succinylcholine or rocuronium (your choice). Maximize preoxygenation. You successfully intubate the patient.

The patient is doing ok on the ventilator. You start lung pro-tective ventilation. The oxygen saturation and acidosis are im-proved.

However, the blood pressure is dropping. What do you do next? Keep it simple; tank, pump, pipes and assessment.

Start with a small fluid challenge of 250-500cc and look for response. If the blood pressure comes up and perfusion im-proves, great. If not, stop fluids. Be careful about overloading a sick right ventricle with fluids. The dilation will increase and the contractility will worsen. Cardiac output will drop.

What is the right sided filling pressure? Is there significant JVD? If there is, you might not need a central line. The patient might need an inotrope.

Use your ultrasound. Look at the left and right ventricles. Do the standard views. The right ventricle looks dilated, which is concerning. The inotrope of choice is epinephrine.

Make sure the MAP is greater than 65 and the diastolic pres-sure is high enough to perfuse the right coronary artery. Nor-epinephrine may be needed to make sure the patient does not become hypotensive.

The patient remains hypoxic. What do you do next? Start in-haled epoprostenol to improve the VQ mismatch and reverse the elevated pulmonary vascular resistance. Call the ICU.

CASE A 75 year old man with pulmonary hypertension arrives. He is severely dyspneic. What do you do?

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EKG and PERob Orman MD and Jeff Kline MD

Take Home Points

EKG findings suggestive of acute pulmonary hypertension are S1Q3T3, T wave inversions in V1-V4, ST elevation in aVR, an incomplete or complete right bundle branch block, sinus tachycardia and atrial fibrillation.

S1Q3T3 develops due to strain in the right ventricle caus-ing pressure to the left posterior fascicle.

Shopo, JD et al. Findings from 12-lead electrocardiography that pre-dict circulatory shock in pulmonary embolism; a systematic review and meta-analysis. Acad Emerg Med. 2015 Oct;22(10):1127-37. PMID: 26394330.

About 2/3 of cases Kline has reviewed regarding missed di-agnosis of pulmonary embolism had characteristic findings of acute pulmonary hypertension on ECG. You need to know this.

The only finding on EKG included in decision rules of pulmo-nary embolism is sinus tachycardia. We have been taught that the EKG is nearly worthless in diagnosing pulmonary embolism.

Marchick, MR et al. 12-lead ECG findings of pulmonary hy-pertension occur more frequently in emergency department patients with pulmonary embolism than in patients without pulmonary embolism. Ann Emerg Med. 2010 Apr;55(4):331-5. PMID: 19766353.

These findings increase the likelihood of a diagnosis of PE.

What are EKG findings suggestive of acute pulmonary hyper-tension? S1Q3T3, T wave inversions in V1-V4, ST elevation in aVR, an incomplete or complete right bundle branch block, si-nus tachycardia and atrial fibrillation. You should know these. If you see them, consider a PE. If you see them in a patient who has been diagnosed with a PE, take another look at them. They might need systemic thrombolysis or transfer to a center for catheter directed thrombolysis.

What does Kline look for when interpreting an EKG? ST seg-ment. ST deviation indicates a sick myocardium. T wave inver-sions. Conduction blocks. Then he looks for the S1Q3T3 pat-tern.

S1Q3T3 develops due to strain in the right ventricle causing pressure to the left posterior fascicle. This is an early left pos-terior fascicle block.

Next, look for a pattern indicating pulmonary hypertension such as ST elevation in aVR and anterior T wave inversion. If Kline sees these findings, he will do something to rule out PE. This indicates acute pulmonary hypertension from some-thing. Although acute exacerbations of chronic lung disease

can cause this pattern, it is uncommon. The most common cause is acute pulmonary embolism, about ⅔of the time.

The Daniels score assigns point value to the elements of pul-monary hypertension. Points are assigned to S1Q3T3, T wave inversion of V1-V4, incomplete and complete right bundle branch block and tachycardia.

New onset atrial fibrillation is bad sign if you have a pulmonary embolism, but it is not predictive of the diagnosis of PE in an undifferentiated population. The odds ratio for death is around 2.

The six EKG findings increase the risk of circulatory shock. How bad are they? Each finding independently is bad. The more findings present, the higher the probability of developing cir-culatory shock. However, they do not appear to predict overall mortality at 90 days.

What if the patient has a normal EKG? Do patients with normal EKGs die from PE? It is unknown. However, it seems unlikely.

None of the risk stratification systems (PESI, modified Geneva and HESTIA) include EKG. However, if you see these findings, send a BNP and troponin. If they are elevated, get your patient transferred or admitted for consideration of thrombolysis. Mul-tiple studies show patients with PE and right heart strain (deter-mined by elevated troponin, BNP or echocardiogram) have an increased likelihood of early decompensation.

Is Procalcitonin Useful In The ED?Rob Orman MD, Mel Herbert MD and Rory Spiegel MD

Take Home Points

Procalcitonin is an inflammatory marker that rises more precipitously with bacterial infection.

A meta-analysis evaluating procalcitonin as a marker of sepsis found a sensitivity of only 77% which may have been optimistic given the heterogeneity of the studies.

Procalcitonin does not add to clinical judgment.

Procalcitonin is gaining in popularity.

What is procalcitonin? It is a peptide precursor of the hormone calcitonin, which is used in the homeostasis of calcium. Typical-ly, the level of procalcitonin in the serum is undetectable. It only rises to detectable levels in inflammatory states. Procalcitonin is differentiated from other inflammatory markers by a rise that is more precipitous with bacterial infection.

How good is procalcitonin at differentiating infection from non-infection?

A recent meta-analysis examined the literature behind pro-

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They randomized 629 patients to traditional management or management via a procalcitonin based protocol.

The authors found a statistically significant increase in the number of days without antibiotics in the group random-ized to a procalcitonin based protocol.

However, although the difference in mortality at 28 days was not statistically significant, the procalcitonin group performed worse overall. 60 day mortality, relapse rate, superinfections and length of stay in the ICU were all high-er in patients randomized to the procalcitonin protocol.

This suggests that although the use of procalcitonin may reduce the use of antibiotics, it does not improve clinical outcomes.

Jensen, JU et al. Procalcitonin-guided interventions against infec-tions to increase early appropriate antibiotics and improve sur-vival in the intensive care unit: a randomized trial. Crit Care Med. 2011 Sep;39(9):2048-58. PMID: 21572328.

These authors performed a similar study comparing clini-cal gestalt to a procalcitonin based protocol. 1200 patients were randomized.

Unlike the PRORATA trial, the procalcitonin based group had increased antibiotic use.

There are times when we are unsure of the cause of our pa-tient’s symptoms. Procalcitonin is a mediocre test. The test characteristics are based on retrospective cutoffs designed for optimal performance. It adds nothing to clinical judgment. It of-ten leads us astray.

Congestive Heart FailureReuben Strayer MD

Take Home Points

The most important therapy for acute pulmonary edema is non-invasive ventilation.

You need to learn how to set up NIV without help from your respiratory therapist.

Give patients a bolus of nitroglycerin IV.

Phlebotomy can be a salvage therapy in renal failure pa-tients with severe volume overload and pulmonary edema.

In the February 2016 episode, Haney Mallemat and Anand Swaminathan discussed that about 50% of patients with acute pulmonary edema are euvolemic at presentation. They don’t have extra fluid but have fluid in the wrong place.

calcitonin as a diagnostic marker for sepsis. They found the pooled diagnostic characteristics of procalcitonin had a sensi-tivity of 77% and a specificity of 79%.

Even these mediocre test characteristics may have been op-timistic; the studies were very heterogeneous due to a large variation in the selected threshold.

Why was there so much variation? The authors of the stud-ies went back after the data was collected and found the val-ue that best differentiated patients with and without sepsis. They then used this cutoff to calculate their optimal diagnos-tic characteristics. Thus, the specific cutoff for this specific cohort will never work as well in an external cohort.

Wacker, C et al. Procalcitonin as a diagnostic marker for sepsis: a systematic review and meta-analysis. Lancet Infect Dis. 2013 May;13(5):426-35. PMID: 23375419.

Can you use procalcitonin to decide if your afebrile, obese pa-tient with a CHF exacerbation and cough has pneumonia?

Maisel, A et al. Use of procalcitonin for the diagnosis of pneu-monia in patients presenting with a chief complaint of dyspnea: results from the BACH (Biomarkers in Acute Heart Failure) trial. Ear J Heart Fail. 2012 Mar; 14(3):278-86. PMID: 22302662.

They looked at whether procalcitonin could determine bac-terial causes of dyspnea from other non-infectious or viral causes. They used a gold standard of the final hospital diag-nosis made by two cardiologists and one pulmonologist blind-ed to the results of the procalcitonin assay. They compared the ability of procalcitonin to identify pneumonia to the un-structured clinical judgment of the emergency physician.

Similar to the studies included in the meta-analysis, the au-thors retrospectively chose the procalcitonin threshold to optimize diagnostic capabilities.

In this trial, the threshold used was 0.25ng/mL. Despite se-lecting the optimal threshold, the test performed horribly. The area under the curve (AUC) was 0.72. It was clinically useless. The emergency physician’s gestalt performed better with an AUC of 0.84. Procalcitonin added nothing to gestalt. The AUC for chest x-ray was 0.79.

What does the area under the curve (AUC) demonstrate? The AUC demonstrates the accuracy of a test. Think of the area under the curve like grades in school. 0.9-1 is excellent and an A. 0.8-0.9 is a B. 0.7-0.8 is fair, C. 0.6-0.7 is poor, D. 0.5-0.6 is a fail.

Can procalcitonin be used to guide antibiotic use in the ICU?

Bouadma, L et al. Use of procalcitonin to reduce patients’ ex-posure to antibiotics in intensive care units (PRORATA trial): a multicenter randomised controlled trial. Lancet. 2010 Feb 6;375(9713):463-74. PMID: 20097417.

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Strayer takes it further.

The most important therapy is non-invasive ventilation. This can save your patient’s life. In order for NIV to be useful, it has to be ready. You must be able to apply it yourself without calling anyone.

If you are dependent on respiratory therapy to come down and set it up, you will be intubating a lot of these patients unneces-sarily. Setting up NIV is easy. You turn the machine on. Set the knobs to 100% oxygen and 15cm H2O of IPAP, 5cm H2O of EPAP and put the mask on the patient. You have to be ready to go.

The machine has to be plugged in and hooked up to oxygen, wall tubing and mask so when the patient arrives in extremis, you just turn it on and go. Strayer does this in the first few min-utes of any patient presenting in respiratory distress regardless of the cause. NIV will help almost all of them, either as definitive therapy or preoxygenation.

Get noninvasive ventilation started. Then you can call respira-tory therapy to optimize your settings and fit the mask. Start-ing NIV is straightforward and has to be in our skill set.

Most patients with hypertension will improve with NIV alone. The sicker patients need additional preload and afterload reduc-tion with nitroglycerin. Start high at 100-200mcg per minute. In the sickest patients, give a bolus of 500 mcg to 1mg while you are getting the drip set up.

Nitroglycerin comes in bottles of 200 mcg/mL or 400 mcg/mL. Before the nurse spikes the bottle, draw up a 1-2 mg into syringe and push a bolus. You are trying to break the hypersym-pathetic, hypertensive cycle. If you give 400mcg sublingually, it will take several minutes to reach peak levels and the bioavail-ability is around 30%.

Strayer pushes 1mg of nitroglycerin over a few seconds. He starts the drip at 200mcg/min. If they still look terrible, he gives a second 1mg bolus. [Ed.note: these doses are in signifi-cantly in excess of those recommended by most sources]

Cycle the blood pressure every 2-5 minutes while on high dose nitroglycerin. Once you break the cycle, the blood pres-sure will come down very quickly.

Temporizing with positive pressure ventilation and nitroglyc-erin may not be enough in the renal failure patient on dialysis with respiratory failure and pulmonary edema. If you are un-able to oxygenate the patient due to edema, you can consider phlebotomy. Take 200-300cc of blood and the patient will im-prove. This is a life-saving procedure supported by the literature that you should keep in mind.

Eiser, AR et al. Phlebotomy for pulmonary edema in dialysis pa-tients. Clin Nephrol. 1997 Jan;47(1):47-9. PMID: 9021241.

This was a retrospective study including 21 patients on he-

modialysis with respiratory distress due to suspected pul-monary edema. The initial treatment was nitrates (an inch of paste). If the patient did not improve, they received phlebot-omy with 500cc of venous blood removed. 17 of the patients had marked improvement. The pre-phlebotomy hematocrit was 25 and the post phlebotomy hematocrit was 22. All pa-tients who received phlebotomy survived until discharge.

This was not a randomized controlled trial and is an extreme measure.

Paper Chase 1:PCC Before LPSanjay Arora MD and Michael Menchine MD

Take Home Points PCC lowered the INR to an acceptable level within 2 hours

in 90% of patients on vitamin K antagonists prior to lum-bar puncture.

5% of patients experience a thromboembolic complica-tion.

PCC is a great drug in the correct patient population but is not benign.

Laible, M et al. Treatment with prothrombin complex concentrate to enable emergency lumbar puncture in patients receiving vitamin K antagonists. Ann Emerg Med. 2016 Apr 14 PMID: 27085368.

The bottom line: a retrospective study giving anticoagulated patients prothrombin complex concentrates prior to lumbar puncture found the INR reached an acceptable level within 2 hours in 90% of patients. However, 5% of patients experienced a thromboembolic event.

Lumbar punctures are commonly performed in the emergency department. Most regard an INR of 1.5 or greater as a contra-indication. PCC has been shown to have benefits that outweigh the risks for treatment in life-threatening intracranial or gastro-intestinal bleeding. Can we use PCC to enable an emergent LP?

This study was performed in Germany with a consecutive sam-ple of patients who received four factor PCC prior to a lumbar puncture over a 10 year period. This was at the discretion of the treating physician. It was not a randomized controlled trial.

They looked at the percent of cases that reached an INR less than 1.5 as well as complications of the procedure.

37 patients were given PCC prior to lumbar puncture. The lumbar puncture was performed approximately two hours after receiving PCC. All of the patients were on a drug similar to war-farin.

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The median INR prior to PCC was 2.2 and this dropped to a median of 1.3 after PCC.

The target INR of less than 1.5 was reached in all but 4 pa-tients.

There was no clinically relevant bleeding at the lumbar punc-ture site.

One patient had a subdural hemorrhage with multiple isch-emic strokes. Another patient had an MI. They did not at-tribute these complications to the PCC. The patient with strokes and intracranial hemorrhage developed symptoms two weeks after receiving PCC. However, the patient with an MI experienced it 10 hours after receiving PCC.

We know the clot rate for PCC is about 2%. In this paper, the clot rate was nearly 6%.

The authors concluded this practice is safe. However, we should be careful to not overuse this drug. This could change the ratio of benefit to harm. This a great drug in the right patient but it is not benign.

Paper Chase 2:Renal Colic AnalgesiaSanjay Arora MD and Michael Menchine MD

Take Home Points

IM diclofenac had a slightly better analgesic effect than IV morphine or IV paracetamol.

About one third of patients required rescue analgesia of IV morphine.

Pathan, SA et al. Delivering safe and effective analgesia for manage-ment of renal colic in the emergency department: a double-blind, multi-group, randomised controlled trial. Lancet. 2016 May 14;387(10032): 1999-2007. DOI: http://dx.doi.org/10.1016/S0140-6736(16)00652-8

The bottom line: intramuscular diclofenac had a slightly better analgesic effect than IV morphine or IV paracetamol in the ini-tial treatment of renal colic.

Renal colic is a common cause of ED visits. The patients are often extremely uncomfortable, pale and diaphoretic. The ideal medication is unclear and practice varies widely.

These authors conducted a massive randomized controlled trial in a single Qatari emergency department. This emergency department treats more than 400,000 patients per year. They compared intramuscular diclofenac with IV morphine and IV paracetamol.

The study was very well conducted with excellent allocation, concealment, etc.

The doses used were 75mg of diclofenac, 0.1mg/kg of mor-phine and 1g of paracetamol. If pain persisted, the patients were given titrated doses of 3 mg IV morphine as rescue.

The primary outcome was decrease in pain to an adequate lev-el within 30 minutes. This was defined as a 50% drop in the numeric ranking score of a scale of 1-10.

1,645 patients were enrolled over a 6 month period. 68% of the diclofenac group, 66% of the paracetamol group and 61% of the morphine group met the primary outcome. The difference be-tween morphine and the other groups was statistically significant.

Adverse events were mild but did occur more often with the morphine group (3%) versus the other groups (1%). The main side effects were nausea and sleepiness. No renal failure or GI bleeds were identified in the follow-up period. Patients who had renal dysfunction were excluded from the study.

What does this mean? This study is the largest to date compar-ing these different modalities. It found that non-narcotics are highly effective in reducing pain when given parenterally when compared to opioids. Even the best medication was effective only 68% of the time, so rescue morphine may be necessary. You can start with something that is not an opioid but a third of patients will require an opioid.

Paper Chase 3: IV Fluids For MigraineSanjay Arora MD and Michael Menchine MD

Take Home Points

The addition of IV fluids to metoclopramide for the treat-ment of migraine provides no short or long term benefits.

However, this was not a randomized controlled trial and the administration of fluids was not standardized and left to the discretion of treating physicians.

Balbin, JE et al. Intravenous fluids for migraine: a post hoc analy-sis of clinical trial data. Am J Emerg Med. 2016 Apr;34(4):713-6. PMID: 26825817.

The bottom line: there were no short or long term benefits to the addition of IV fluids to metoclopramide.

Everyone thinks they have the perfect cocktail to treat mi-graines and they are all different. Some use IV fluids as part of their regimen.

This was a post-hoc analysis of data from four emergency

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department studies that were designed to study IV metoclo-pramide for migraines. All had similar inclusion and exclusion criteria. The fluid administration was not standardized.

570 patients were enrolled in the four studies. About 20% re-ceived IV fluids.

What did they find?

The patients who received IV fluids improved by 4.5 points on a pain scale from 0-10 at 1 hour whereas the patients who did not receive fluids improved by 5.1 points.

The total duration of pain was the same in both groups. Most experienced pain for 48 hours.

66% of the patients in the IV fluid group experienced nausea compared to 52% in the group without fluids.

The authors acknowledged potential bias as the decision to administer IV fluids was by the treating physician. Patients with more severe headaches or nausea may have been given IV fluids. The study was not designed for the randomization of IV fluids. Although we need a randomized controlled trial, this study provides some data that we probably don’t need to in-clude IV fluids in our cocktail mix for treating migraine head-aches.

Paper Chase 4: Low Dose TPA For StrokeSanjay Arora MD and Michael Menchine MD

Take Home Points Low dose alteplase resulted in similar clinical outcomes

to standard dose in a study of mostly Asian patients with acute ischemic stroke.

The study was unable to prove non-inferiority.

Low dose alteplase did result in lower intracranial hemor-rhage and fatality.

Anderson, CS et al. Low-dose versus standard-dose intrave-nous alteplase in acute ischemic stroke. N Engl J Med. 2016 Jun 16;374(24):2313-23. PMID: 27161018.

The bottom line: low dose alteplase resulted in similar clinical outcomes to standard dose in a study of mostly Asian patients with acute ischemic stroke.

TPA has an indication for acute ischemic stroke within three hours (and possibly within 4.5 hours) of symptom onset. The benefit is modest improvement in clinical outcomes with a cost of a higher risk of hemorrhagic stroke and early death. Uncon-trolled studies have suggested the rate of hemorrhagic stroke

is higher among Asian populations. As a result, some organiza-tions such as the Japanese Health Authority have limited the approved dose of alteplase in acute ischemic stroke to 0.6mg/kg from 0.9mg/kg. Also, the difference in dose is significant in some countries where patients have to pay for medication out-of-pocket.

Is 0.6mg/kg non-inferior compared to 0.9mg/kg? The authors of this study conducted a randomized open-label trial in mul-tiple countries around the world comparing 0.6mg/kg versus 0.9mg/kg of alteplase for acute ischemic stroke with symptom onset within 4.5 hours.

The primary outcome was death or disability (a modified Rankin score of 2-6) within 90 days. The primary safety out-come was intracranial hemorrhage. Researchers assessing out-come were blinded to treatment allocation.

What did they find? They enrolled 3310 patients over a three year period. About 66% of the subjects were Asian and 43% were from China. 53% of patients in the low dose group had a bad clinical outcome compared to 51% in the usual dose group. This difference was slight and not statistically significant. How-ever, this difference did not clear the non-inferiority margin. It is a close call. The authors could not prove non-inferiority of the low dose alteplase.

Major symptomatic intracerebral hemorrhage occurred in 1% of participants in the low dose group and 2.1% in the standard dose group. This was statistically significant.

Fatal events within 7 days occurred in 0.5% in the low dose group and 1.5% in the standard dose group. As Rory Spiegel says, despite its statistical failure, this trial clearly demon-strates that reduced dose TPA achieves similar clinical out-comes with decreased death and ICH.

The usual FDA-approved dose of 0.9mg/kg is likely to remain the standard of care in the United States going forward. It is unclear what strategy will be adopted in Asian countries.

Paper Chase 5: Apple Juice To The RescueSanjay Arora MD and Michael Menchine MD

Take Home Points Rehydration with diluted apple juice had fewer treatment

failures than a commercial electrolyte solution in minimal-ly dehydrated children with mild gastroenteritis.

A good strategy for rehydration is 5mL of fluid every two to five minutes.

Freedman, SB et al. Effect of dilute apple juice and preferred flu-

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ids vs electrolyte maintenance solution on treatment failure among children with mild gastroenteritis: a randomized clinical trial. JAMA. 2016 May 10;315(18):1966-74. PMID: 27131100.

Bottom line: rehydration with diluted apple juice had fewer treatment failures than a commercial electrolyte solution in children with mild gastroenteritis.

The mainstay of treatment for mild gastroenteritis in children is to give oral fluids. You can use an electrolyte maintenance solution but some children don’t like the taste and it is more expensive than juice. How about diluted apple juice?

This was a single center, randomized, single-blinded, non-in-feriority trial of children between 6 and 60 months with vom-iting or diarrhea of less than 96 hours duration and minimal dehydration (cap refill less than 2 seconds). Children were ran-domized in a 1:1 ratio to half strength apple juice or an apple flavored pediatric electrolyte solution. They were still given on-dansetron if they were vomiting. Parents were instructed to give 5mL of either solution every 2-5 minutes. At discharge, parents were told to continue the intervention received in the ED.

650 children were randomized over five years. They had fol-low-up of 99.5% of the patients.

The primary outcome of treatment failure was 16.7% in the ap-ple juice group and 25% in the electrolyte solution group. This is a composite outcome failure. Children receiving the electro-lyte solution did return to the ED or primary care more often for IV fluids. However, the kids receiving apple juice had the same rates of dehydration at three days.

These children were minimally dehydrated. 70% of the kids en-rolled had no dehydration measures. This is not really the pop-ulation you are worried about rehydrating. However, this is a nice reminder that we shouldn’t be dogmatic about fluid intake. Let the kids choose their preferred fluid.

Annals of Emergency Medicine: When Cough and Fever Turn BadPaul Jhun MD, Greg Moran MD and Anand Swaminathan MD

Take Home Points Risk factors for tuberculosis include immigrant status,

homelessness, incarceration, crowding or immunosup-pression.

Chest x-ray findings concerning for tuberculosis include apical or upper lobe infiltrates, cavitation and hilar ade-nopathy.

PPD testing and interferon-gamma release assays are not useful in the work-up of acutely symptomatic patients.

What symptoms should prompt you to consider tuberculosis?

Cough and fever. Patients often have associated symptoms of weight loss, fatigue and malaise. Often the time course may indicate tuberculosis.

In this case, the patient first presented after a week of symp-toms. In most patients with a week of symptoms, TB won’t be very high on your differential unless they have high risk features such as a recent household exposure. However, as the symptoms progress, your suspicion may increase.

The most common cause of a cough with mild hemoptysis is bronchitis, which may last weeks. When should you consid-er TB? Look at risk factors. Patients born outside of the US, especially in areas where TB is endemic. TB can reactivate

CASE 1A healthy 35 year old female presented with complaints of three weeks of fever. The patient was evaluated for similar symptoms two weeks prior and was diagnosed with a non-specific viral illness. The patient reported persistent dry cough and dyspnea during this time. She denied gastrointestinal, genitourinary or gynecologic symptoms. She was a native of Haiti, living in Boston for two years. On physical exam, she was tachypneic, tachycardic, febrile but in no acute distress. Her oxygen saturation on room air was 85% and improved to 96% on 4 liters oxygen via nasal cannula. The patient’s complete blood count and chemistry panel were within normal limits. Her chest x-ray depicted faint diffuse homogenous reticulo-nodular markings throughout the lung fields bilaterally. Diagnosis? Miliary tuberculosis.

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after decades so consider it even if the patient has been in the US for a long time.

A 2009 study of patients admitted to the hospital with suspected pneumonia found immigrants were over 4 times more likely to have TB. However, TB in the US is more likely to be associated with socioeconomic factors such as homelessness, incarceration, crowding or immuno-suppression.

Moran, GJ et al. Decision instrument for the isolation of pneu-monia patients with suspected pulmonary tuberculosis ad-mitted through US emergency departments. Ann Emerg Med. 2009 May;53(5):625-32. PMID: 18760503.

What should you do if you suspect TB? Your first step should be to get a chest x-ray. This will provide a lot of information. If you see classic findings of apical or upper lobe infiltrates, cavitation or hilar adenopathy, this will increase your suspicion. You won’t always see classic findings. If the patient has an intact immune system and a negative chest x-ray, it is extremely unlikely that tuberculosis is causing their symptoms.

If there are suspicious x-ray findings, the sputum test will con-firm disease. The first sample can be sent from the ED (ideally in an isolation room!). You may even receive the results while the patient is still in the emergency department. Typically, three AFB smears and cultures are performed. If any smear results positive, you are done. Moran also performs a PCR based nu-cleic acid test. This will allow confirmation of Mycobacterium tuberculosis rather than another atypical mycobacterium. One of the tests available can determine resistance to rifampin.

If your patient is not ill-appearing, they are reliable, can comply with isolation, are not around others who are at risk (children, elderly, immunocompromised), you can contact the public health department who can arrange subsequent AFB testing.

If the patient is not immunocompetent, a negative chest x-ray does not rule out the disease. There are degrees of immuno-suppression. A patient who is HIV infected but on appropriate therapy with normal CD4 counts is not really at increased risk of tuberculosis. However, a patient with HIV and a CD4 count of 50 can have active tuberculosis without typical chest findings. They usually will have some findings on chest x-ray; a negative chest x-ray makes TB much less likely but doesn’t rule it out.

Testing such as PPD or quantiFERON-TB Gold testing is not useful in the work-up of an acutely symptomatic patient. These indicate prior exposure but don’t tell you if their current symp-toms are related to tuberculosis. If they are immunocompetent, a negative quantiFERON-TB Gold test or PPD reduces the like-lihood of TB but does not eliminate the possibility. Patients with active TB may have suppression of their immune system which reduces the sensitivity of interferon-gamma release assays.

You won’t receive these results in the emergency depart-ment. The PPD takes 48-72 hours for results and the quanti-FERON-TB Gold test takes over a day.

From The MailbagRob Orman MD and Anand Swaminathan MD

From Rob McCoy regarding Matt Delaney’s piece on ovarian torsion. “I feel that a questionable logical conclusion was made regarding imaging. Delaney pointed out the poor sensitivity of CT and ultrasound in definitively ruling out torsion. He point-ed out the surprising fact that CT has similar numbers to ultra-sound. However, a mistake was made when he concluded that if a CT has been performed and negative, pursuing an ultrasound was unnecessary.

Although the two tests have similar sensitivities, the cases in which they fail to identify the pathology won’t be the same. Asking Gyn to admit a suspected occult ovarian torsion for ob-servation without first obtaining a pelvic ultrasound won’t fly.

Delaney responds. “If these tests are looking for truly different findings then I agree. The overall sensitivity of these two tests together would be higher. It is unclear how different these tests are in practice. In reality, the vast majority of patients with tor-sion have underlying ovarian pathology such as cysts or mass-es. The incidence of torsion in patients with structurally normal ovaries is extremely low.

In a patient with an undifferentiated abdominal pain and structurally normal ovaries, adding a routine ultrasound would not necessarily help us identify the rare cases of tor-sion. Theoretically, ultrasound could detect decreased Dop-pler flow undetected on CT. If Delaney is worried enough to talk to OB/gyn, he is happy to obtain the ultrasound.

Bob Zempel discusses the well-appearing patient requesting a note for work. “I put a quick qualifier in the note indicating the time they left the ED. ‘The patient was seen and evaluated in the emergency department and discharged at this time.’” This may not be a bad idea in select patients with recurrent habits. It does not indicate regarding the patient’s intentions but states fact. It allows the patient and employer to sort out the facts.

Brooks Walsh regarding the segment on ACS in women. “Per-haps there is some statistical difference in symptom description between genders but this is highly unlikely to be clinically signif-

CASE CONTINUEDThe patient was admitted with AFB testing that confirmed the presence of Mycobacterium tuberculosis. The patient was started on five drug therapy and is doing well.

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icant or helpful at the bedside. Some studies show women do have typical symptoms of ACS. If women really have such differ-ent symptoms than men, this should be true for other diseases such as PE, pancreatitis, appendicitis and so on. Where is the evidence of women being so different in non-ACS diseases?”

Mattu responds. We are reviewing what was written in the up-to-date cardiology literature. We aren’t making the news but reporting it. The vast majority of legal cases of missed ACS that Mattu has been involved in as consultant are in young women between the mid-20s to 40s who presented atypically. The typ-ical cases don’t tend to be missed. Mattu has only seen a few cases of young men with atypical presentations that went to litigation.

Young women do present atypically more often than men. There is a lack of recognition by many physicians that these young women with atypical presentations are experiencing ACS. Although some studies question whether atypical pre-sentations are real or not, they do not represent the bulk of the literature. They did not help defend the physician for missed ACS or save the lives of young women with ACS.

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NOTES