May 2016 | Volume 16 Issue 5

Why was needle aspiration preferred over incision and drain-age for the breast abscess? For cosmetic reasons, they recom-mend needle aspiration under direct visualization, usually by in-terventional radiology under ultrasound guidance. Breast tissue is extremely vascular, especially in lactating women. Abscesses are amenable to needle aspiration, although it may take 2-3 at-tempts to remove all the pus before it heals.

Current recommendations advise needle aspiration of the ab-scess under direct visualization, usually with ultrasound. They also recommend irrigating the abscess through the same needle. Needle aspiration is recommended up to three times. Incision and drainage is recommended if the infection is not resolved by this time. This technique is successful up to 60% of the time.

This is better from the patient’s perspective. There is no disfig-uring scar and they heal faster.

There are some caveats.

If the abscess is very superficial and the skin has thinned around it, a stab incision is recommended for drainage.

If a woman is breastfeeding, she may continue to breast feed with the affected breast. Draining the breast helps. Pumping may help if the child is unable to breastfeed from the breast.

Antibiotics are recommended for these patients as the abscess is aspirated rather than incision and drainage. If the mother is breastfeeding, you need to give medications compatible with breastfeeding such as cephalosporins or trimethoprim-sulfame-thoxazole.

Observations on the management of abscesses in general.

The Yankauer suction may be used to evacuate pus in large ab-scesses such as pilonidal cysts. This decreases the smell. If you are a fan of irrigation, you can irrigate into the abscess and aspi-rate the irrigant.

If the abscess is too small for an incision that accommodates the Yankauer suction catheter, you can still suction the pus from the skin.

You can tape a blue drape to the skin under the abscess to pre-vent pus from dripping down the patient’s skin.

EM:RAP Written Summary May 2016: Volume 16, Issue 5 1

Introduction:Hematuria and AAARob Orman MD and Anand Swaminathan MD

Hematuria in abdominal aortic aneurysm. An aortocaval fistu-la is a cause of gross hematuria. This is rare. Abdominal aortic aneurysms can sometimes cause microscopic hematuria due to the proximity of the aneurysm causing local irritation of the ureter. This can lead to a false diagnosis of renal colic.

There is very limited literature on this topic.

Keep abdominal aortic aneurysm on your differential diagnosis in an elderly patient with microscopic hematuria and flank pain.

Community Medicine Rants:Breast AbscessAl Sacchetti MD

Take Home Points Current recommendations advise needle aspiration of

breast abscesses under direct visualization, usually with ultrasound.

Superficial abscesses may be treated with stab incision.

Patients should be given an antibiotic consistent with breast feeding such as a cephalosporin.

Patients may continue to breast feed with the affected breast.

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

www.emrap.org

CASEA young woman presented with a breast abscess. She was postpartum and breastfeeding. She developed a cellulitis and had been treated for several days with cephalexin and tri-methoprim-sulfamethoxazole. She returned for a repeat visit. She had a significant amount of surrounding cellulitis. Ultra-sound showed an abscess extending deep into the breast tis-sue. A consult was placed with the surgical service to request incision and drainage in the OR. The surgical service declined to drain the abscess and recommended interventional radiol-ogy for needle aspiration. Surgery agreed to admit the patient for IV antibiotics.

EM:RAP Written Summary | www.emrap.org2

Medical Myths:Toxicology MythbustingAnand Swaminathan MD and Bryan Hayes PharmD

Take Home Points A retrospective chart review found no fatal dysrhythmias

and no difference in mortality in patients with hyperkale-mia and digoxin toxicity that were given calcium.

However, there is little literature on patients who have acute digoxin toxicity.

Patients with acute cocaine toxicity need benzodiaze-pines, sedatives and cooling, not beta-blockers.

Flumazenil may precipitate benzodiazepine withdrawal, which may be life-threatening.

We have been taught that if you give calcium to a patient with digoxin toxicity, you will kill them. Patients with digoxin toxicity will often be hyperkalemic. The EKG will look scary and you will want to give calcium.

What if hyperkalemia is due to cardiac glycoside poisoning like digoxin? This has traditionally been considered a contraindica-tion to giving IV calcium. Why? Cardiac glycoside overdose can lead to an increase in intracellular calcium concentrations. If you give more calcium, it is thought that you will cause an irrevers-ible non-contractile state due to impaired diastolic relaxation. This is the “stone heart” theory.

The early literature seemed to show some validity to this mechanism. There are five human case reports showing a temporal relationship between calcium administration and death in digoxin toxicity. There were several animal models that also seemed to show an increase in mortality and mor-bidity after administration of calcium in digoxin toxicity.

However, review of the five case reports shows a question-able association. The case reports were primarily from the 1930s and 1950s. The symptoms of digoxin toxicity were not described. No levels of digoxin were measured. Only two cas-es showed a strong temporal association but this does not imply causation.

The animal models were also flawed. The animals were made severely hypercalcemic before they received digoxin. This is not what we see in digoxin toxic patients. Subsequent animal models failed to demonstrate adverse effects.

Levine, M et al. The effects of intravenous calcium in patients with digoxin toxicity. J Emerg Med. 2011 Jan;40(1):41-6. PMID: 19201134.

This was a retrospective chart review including 161 patients. They looked for potentially fatal dysrhythmias within an hour

of IV calcium administration. They found five deaths in pa-tients who received calcium (about 22%). There were 27 deaths among patients who did not receive calcium (about 20%). There was no difference in the percentage of death be-tween patients who received calcium and those who didn’t. There were no fatal dysrhythmias in either group within 4 hours of calcium administration.

However, almost all of these patients had chronic digoxin tox-icity. There is little evidence on acute digoxin toxic patients.

Stone heart probably isn’t going to happen but giving calcium probably won’t help much either. The real treatment is to give the patient Digibind. However, if you have a patient with un-differentiated hyperkalemia, give the calcium and later find out they had digoxin toxicity; you shouldn’t feel bad about it.

You have a patient who has been freebasing cocaine and then develops chest pain and atrial fibrillation. Don’t beta-blockers cause unopposed alpha agonism and death?

There are some studies from the 1980s in which patients going to the cath lab were given cocaine. Patients were then given propranolol with resulting vasoconstriction of the coronary vas-culature. When patients were given phentolamine (an alpha-an-tagonist), the vasoconstriction reversed.

The patients with acute cocaine toxicity presenting with agi-tation, diaphoresis, hyperthermia and sympathomimetic over-drive should not be given beta-blockers. You need benzodiaz-epines, sedatives and cooling, not beta-blockers.

What about cocaine toxic patients with chest pain?

In 2008, guidelines recommended against giving beta-block-ers to patients with cocaine use and chest pain. However, there were no studies that actually looked at this patient pop-ulation. Since these guidelines were published, there are now several studies looking at beta-blockers in cocaine chest pain patients.

However, these studies were retrospective, observational cohorts that utilized urine toxicology screens to identify co-caine use. These may be positive for several days. It is unclear when the patients actually used cocaine. Patients with co-caine use who are most likely to have an MI and bad outcome usually have it within the first few hours of use, not several days later.

The use of beta-blockers in acute chest pain patients is not as simple as initially thought. Although it may be ok to use be-ta-blockers in patients with acute cocaine toxicity, it is unneces-sary. You can control the chest pain with nitrates and benzodi-azepines.

Thus, even though the existing data appears to support be-ta-blocker use in cocaine chest pain, the studies did not cap-ture the correct patient population.

3

Should we give flumazenil? Flumazenil has been around since the 1990s. It is very similar to naloxone. The dosing is similar to naloxone. The duration of effect is about 45 minutes to an hour. It can reverse CNS depression in patients with benzodiazepine overdose.

Benzodiazepines in isolation are not that toxic. Most patients do well with benzodiazepine overdoses unless other CNS depres-sants are involved. Do you need to reverse the benzodiazepine?

Flumazenil can lead to re-sedation after the medication wears off. If you put a patient into withdrawal from benzodiazepines, it is worse than opiate withdrawal. Benzodiazepine withdrawal is similar to alcohol withdrawal and can lead to seizures.

Three articles published in 2012 attempted to prove the safety of flumazenil in overdose.

Kreshak, AA et al. A poison center’s ten-year experience with fluma-zenil administration to acutely poisoned adults. J Emerg Med. 2012 Oct;43(4):677-82. PMID: 22766408.

904 cases were included. 13 seizures and 1 death occurred after administration of flumazenil. This doesn’t seem too bad.

Kreshak, AA et al. Flumazenil administration in poisoned pedi-atric patients. Pediatr Emerg Care. 2012 May;28(5):448-50. PMID: 22531190.

83 patients were included. There were no seizures or deaths noted.

Veiraiah, A et al. Flumazenil use in benzodiazepine overdose in the UK: a retrospective survey of NPIS data. Emerg Med J. 2012 Jul;29(7):565-9. PMID: 21785147.

This was also a retrospective survey of poison center data. Flumazenil was given to 80 patients; there was one seizure and no patients died.

These studies are somewhat misleading. The patients who are likely to experience a bad outcome from flumazenil are those with chronic benzodiazepine use. This is most likely in adult pa-tients. Most adult patients with overdose do not use only one drug. Some of these agents may lower the seizure threshold and the benzodiazepine may actually be helping.

Retrospective poison center data should not be used to prove the safety of the drug. It is a voluntary reporting center. You do not know the denominator in terms of safety. You don’t know how many others were given flumazenil with a bad outcome that went unreported. All three of these studies suffer from this same flaw.

Penninga, E et al. Adverse events associated with flumazenil treat-ment for the management of suspected benzodiazepine intoxi-cation – a systematic review with meta-analyses of randomised trials. Basic Clin Pharmacol Toxicol. 2016 Jan;118(1):37-44. PMID: 26096314.

May 2016: Volume 16, Issue 5 | www.emrap.org

This meta-analysis and systematic review concluded that flumazenil should not be used routinely and the harms and benefits should be carefully considered in each patient.

“The use of flumazenil in a population admitted at the emer-gency department with known or suspected benzodiazepine intoxication is associated with a significantly increased risk of serious adverse events compared with placebo.”

Perinatal DisastersChristopher Doty MD

Take Home Points The Turtle sign, when the head comes out and then goes

back in, is a sign of shoulder dystocia.

If shoulder dystocia occurs, you need to get the baby out quickly.

If a nuchal cord is tight, place two clamps and cut the cord between them.

Management of a prolapsed cord is a surgical delivery.

What does it mean when the patient in labor has an urge to defecate? The colon is being compressed by the baby.

If the delivery is imminent, it will happen in the ED. You don’t want to have the delivery in the elevator – which will happen if you try to get to Labor and Delivery.

If you have some time, get some more information.

When was the onset of labor? Frequency of contractions?

What is the age of the fetus? At twelve weeks, the uterus is at the pelvic brim. At twenty weeks, the fundus is at the um-bilicus. Full term is all the way up the abdomen.

Are they bleeding? Did membranes rupture? Is there meco-nium staining? If there is meconium staining, can you transfer out?

Is delivery eminent? Do they have the urge to push? Is there bulging of the perineum?

After the patient is dilated to 2 inches (5 cm), they may prog-ress quickly.

Use the ultrasound.

Is the head up? You will need to prepare for a breech delivery.

You can check the fetal heart rate. You are looking for a heart rate between 120 and 160.

What happens during the delivery?

The child will usually come out occiput-anterior (face down).

EM:RAP Written Summary | www.emrap.org4

The baby will spontaneously turn to a transverse lie and look at either thigh.

Suction the mouth.

See and feel for a nuchal cord. If it is loose, you may be able to gently pull it over the baby’s head. Check to make sure there is no double cord.

If a nuchal cord is tight, don’t yank on it. Place two clamps and cut between them. Once you cut that cord, the baby is not getting any placental blood or oxygen.

Push down to get the anterior shoulder out. Reverse the movement and deliver the posterior shoulder.

What if the head comes out but then goes back in? This is called turtle sign. This is a sign of shoulder dystocia. The anterior shoul-der becomes impacted below the pubic bone. This is a problem. It is associated with large babies, gestational diabetes and late term pregnancies. This occurs in 1% of births. You might see this.

Once you identify shoulder dystocia, you need to get the baby out quickly.

Get help. If you have an obstetrician or midwife on call, call them.

Drain the bladder. Straight cath and get as much room in the pelvis as possible.

Episiotomy. You can consider it but usually the bone keeps the kid in the pelvis and not the perineum.

McRoberts technique. Flex the knees all the way to the chest with the patient on their back. Have slight abduction of the hip.

Suprapubic pressure. This changes the angle of the pelvic in-clination and straightens the sacrum. Some small studies have shown benefit. Push over the pubic rim, not at the fundus.

There are some rotational procedures that rotate the baby’s body, not their head. Delivering the arm equals delivering the shoulder. If you see the arm pop out, the shoulder is delivered.

The mother can roll onto her hands and knees with knees to the chest.

If nothing works, you may have to break the baby’s clavicle. Pinch the midpoint of the clavicle and snap it.

You see a bluish gray cord of tissue in the vagina. Cord prolapse results in compression of the cord when the head engages. This prevents the baby from receiving oxygen. If you see a prolapsed cord, you can’t safely deliver the baby vaginally. This means a surgical delivery.

To temporize, have the mom stop pushing. Elevate the hips. Push the head back up. Give the mother oxygen.

Don’t reduce the cord. You can’t get the cord back inside effi-ciently. Cover it with a moist towel and send for C-section.

There are some case reports recommending inflating the bladder with saline to push the vertex back up.

You can consider tocolysis.

The baby is coming out and you see a foot. If there is one foot coming out, make it two. Drain the bladder. Deliver the first leg, then the second leg. Grasp both legs and deliver to the umbili-cus. Most of the time this happens spontaneously.

Place the baby’s butt up and deliver the chest. Spin the baby 90 degrees. Sweep out one arm. Spin the baby back 180 de-grees and deliver the other arm. Deliver the shoulders.

Put your finger in the baby’s mouth and pull down to deliver the head. This provides flexion and lets you pull on the baby without stretching the neck. Suprapubic pressure may help here.

There is a lot of bleeding after the delivery. What do you do?

External massage of the uterine fundus.

Inspect for tears. Inspect the placenta.

Medications such oxytocin, methylergonovine, misoprostol and carboprost.

You may need to do bimanual compression. Put a fist in the vagina and tamponade the bleeding between your two hands.

Why does postpartum hemorrhage occur? Uterine atony for whatever reason. Laceration. Bleeding disorders are less likely. Retained placenta. Placenta accreta may be an issue.

Pediatric Pearls: Pediatric Thoracic TraumaIlene Claudius MD, Sol Behar MD and Elizabeth Benjamin MD

Take Home Points

The incidence of blunt aortic injury in children is extremely low and would require significant force.

Do not routinely order CT scans of the chest in children with seatbelt sign.

Children aren’t good candidates for discharging home with a Heimlich valve in place as they are likely to dislodge it.

A child in a motor vehicle accident has some abdominal ten-derness and a seatbelt sign. You are ordering a CT abdomen and pelvis. Should you also order a CT of the chest or is plain film sufficient? Chest x-ray is a great screening tool. In the adult population, we worry about missing aortic injuries. The incidence of blunt aortic injury in children is extremely low and would require significant force. Children rarely even experience

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Are smaller chest tubes sufficient for hemothoraces?

Inaba, K et al. Does size matter? A prospective analysis of 28-32 versus 36-40 French chest tube size in trauma. J Trauma Acute Care Surg. 2012 Feb;72(2):422-7. PMID: 22327984.

Chest tube size was less relevant than the technique and placement of the tube.

Small tubes are sufficient for pneumothorax and also are ef-fective for hemothorax.

There is little evidence on how to proceed with thoracotomy in the pediatric population. We have to extrapolate from adult data. However, there is not much consensus in the adult data. The most recent guidelines cite a survival rate of 2%. Nothing is worse than a child dying. It is hard to not perform thoracotomies if there is a chance.

Is REBOA an option? Unfortunately, there is no balloon avail-able for children. Most of the catheters are large profile and require a large artery for insertion. The REBOA is meant as a bridge to additional therapy. It is a good option to allow trans-port to the operating room or angiography in patients with bad pelvic fracture or intra-abdominal bleeding.

Is there a role for permissive hypotension in the pediatric pop-ulation? There is no data available. The physiology and reason-ing behind it can likely be applied to the pediatric population however. We don’t know the magic number. We should avoid resuscitation to maintain blood pressure with high volumes of crystalloid. This will result in hemodilution, coagulopathy and DIC. Start your resuscitation with blood products.

There is not much data on tranexamic acid in children. The lim-ited data available suggests it is safe. There is no reason to think it should not be used in the same way as in adults.

Ovarian TorsionMatt DeLaney MD

Take Home Points

Patients with ovarian torsion have abrupt onset of symp-toms only 60% of the time.

15% of ovarian torsions happen in pediatric patients.

1/3 of confirmed ovarian torsion cases had normal blood flow on Doppler.

CT is as good as ultrasound at identifying torsion and ovarian or adnexal pathology.

There are a lot of misconceptions regarding ovarian torsion.

Patient history. The classic history is a patient of reproductive

rib fractures. Routine CT scan screening of the chest in children to identify blunt aortic injuries in children is difficult to justify.

The decision to scan the chest should be made in concert with the trauma team and consider mechanism of injury, other injuries and abnormalities noted on plain films or ultrasounds.

What findings would prompt CT scan of the chest? Seatbelt sign of the chest is not an indication for CT scan. There aren’t any clear-cut physical exam findings that indicate an aortic in-jury. The literature in adults cites the mechanism of an abrupt stop. It is more difficult to generate this force in children due to the elasticity of their tissue.

You should be more concerned in children with a significant thoracic injury burden such as pulmonary contusions and rib fractures.

The pediatric population is a wide group; 3-4 year old children are different from 16-17 year old children. Many of the studies include children under the age of 17. Older children have physi-ology more similar to adults.

Small pneumothoraces may be identified on CT scan that weren’t appreciated on plain films. How should these be man-aged? Are these important to diagnose? Management depends on the clinical picture.

You need to treat a large pneumothorax (greater than 20%).

Many of the patients with small pneumothoraces may be monitored. Place on oxygen and observe. Repeat the chest x-ray to determine if they are able to resorb the pneumotho-rax on their own.

What if the patient has a head injury and is intubated? You should have a lower threshold to place a chest tube in this situation. However, an occult pneumothorax in an intubated patient doesn’t mandate chest tube placement. You can still watch the patient but you need to need to determine the capability of your environment. If the patient is going to be transferred via helicopter to another facility, they may need chest tube placement. If the patient will be transported emer-gently to the operating room, they don’t need a chest tube placed in the ED.

What about a small hemothorax? If the lung is compressed for too long and the hemothorax persists you can develop an in-fection or trapped lung. It will be more difficult for the lung to re-expand in the future. A significant hemothorax may prevent re-expansion of the lung resulting in decreased function. Man-agement and consideration of the risks versus benefit should be done in conjunction with the trauma team.

Can children be discharged home with a Heimlich valve in place? Children are more likely to dislodge the tube which could result in complications.

EM:RAP Written Summary | www.emrap.org6

age presenting with sharp, sudden, unilateral pain with a waxing and waning component. However, reviews of ovarian torsion show abrupt symptoms in only 60% of cases. Patients often re-port a sharp or stabbing pain, about 70% of the time. More than 70% of patients report associated nausea and vomiting.

Who gets ovarian torsion? The majority of patients are women of reproductive range. However, 15% of cases happen in pedi-atric patients and another 15% occur after menopause. About 20% of cases of ovarian torsion occur in pregnancy.

Historical features that increase the likelihood of ovarian torsion include previous episodes of pelvic inflammatory dis-ease, pelvic surgery, masses or cysts on the ovary. About 25% of patients with confirmed ovarian torsion have no previous pelvic pathology.

The literature supporting pelvic exam in the diagnosis of ovari-an torsion is terrible. One study found that 30% of patients with torsion will have no abdominal or pelvic tenderness on exam. The sensitivity of pelvic exam for detecting ovarian or adnexal masses is awful. The sensitivity to detect a mass in an operative setting with a patient under general anesthesia with an attend-ing gynecologist performing the exam was only 15-36%. You can’t rule out torsion based on exam.

The data on imaging cases of potential torsion is surprising.

Ultrasound performs fairly poorly with a sensitivity of 35-85%. There is a lot of variability. About one third of cases of ovarian torsion confirmed in the operating room had normal blood flow documented on Doppler studies.

Swenson, DW et al. Ovarian torsion: case-control study compar-ing the sensitivity and specificity of ultrasonography and comput-ed tomography for diagnosis in the emergency department. Eur J Radiol/ 2014 Apr;83(4):733-8. PMID: 24480106. The data seems to show that CT scan is just good as ultrasound at iden-tifying torsion and ovarian or adnexal pathology.

What about patients with intermittent torsion? The literature provides few answers. It is unclear which features help us iden-tify these patients. The data seems to show that the chance of ovarian torsion is very low in the absence of ovarian or adnexal pathology. If you have a normal CT or ultrasound in a patient with medium pre-test probability, you probably don’t need to work it up further. However, we need to be careful. If you have a negative work-up but the presentation is highly concerning for torsion, involve your consultant gynecologist. These patients may be admitted for laparoscopy or serial examinations.

There is no support in the literature for obtaining an ultrasound after a negative CT. CT and ultrasound are tolerable studies in identifying ovarian torsion. There are significant limitations to both. If the patient has a vague story of abdominal pain and the CT scan is negative, you don’t need to proceed with a pelvic ultrasound.

What are the risks of missing a diagnosis of ovarian torsion?

There isn’t much literature demonstrating significant infertil-ity. Animal studies show that having only one ovary doesn’t lead to significant infertility. The human studies suggest that this is probably true.

Patients may have morbidity from the operation.

There is a risk of lawsuits for the ED providers. These cases often involve a younger patient with atypical symptoms with a complaint that torsion was missed initially. These lawsuits often settle for a significant amount.

How can we protect ourselves? Discuss this possibility with the patient and document carefully. There will be missed cas-es of ovarian torsion including after a negative work-up. It is reasonable to say, “I don’t think this is intermittent torsion and do not believe the patient needs further work-up.”

Trauma Surgeons Gone WIld:Traumatic Seat Belt SignsMizuho Spangler DO and Kenji Inaba MD

Take Home Points

The incidence of clinically significant intra-abdominal in-jury is much higher (about 8 fold) in patients with an ab-dominal seatbelt sign than those without.

If the imaging does not show an obvious injury but has some concerning features like trace free fluid, stranding or bowel wall thickening, the patient should be observed for 12 to 24 hours.

What should you do about an abdominal seatbelt sign in an adult patient?

The East guidelines say that detection of intraperitoneal fluid by FAST or CT in a patient with an abdominal seatbelt sign mandates a DPL or an exploratory laparotomy. Patients with a negative CT scan and an abdominal seatbelt sign should be admitted for observation and serial physical exams.

This may not be feasible for many sites.

If a stable patient has an abdominal seatbelt sign with no peri-tonitis and an adequate CT scan that is completely negative, it may be reasonable to send them home?

What does the literature say? There is no good large prospec-tively collected data set. The available studies are either small or retrospective. There is no accurate compilation of the physical exam and this is difficult to ascertain retrospectively.

The incidence of clinically significant intra-abdominal injury

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is much higher (about 8 fold) in patients with seatbelt sign than those without. It is worthwhile to obtain imaging in pa-tients with an abdominal seatbelt sign.

If the imaging shows a clinically significant injury, the patient can go the operating room.

If the imaging does not show an obvious injury but has some concerning features like trace free fluid, stranding or bowel wall thickening, the patient should be observed for 12 to 24 hours.

Do they need repeat imaging? Not usually. The likelihood of detecting a change prompting intervention is very low.

If the patient is improved with resolution of pain after 12 to 24 hours and able to tolerate oral intake, they are discharged home.

If the patient develops peritonitis, they are taken to the op-erating room.

Does the location of the seatbelt sign correlate with the area of bowel that is injured? Bucket-handle injuries result from shear-ing of the mesentery from the bowel after compression against the spine. The bowel remains intact and the patient may not have peritonitis initially. Over the next several hours, the seg-ment of bowel becomes progressively ischemic and perforates. This can increase pain, fevers and the white blood cell count, prompting operative exploration. Injuries to the colon and duo-denum may also occur. A full bladder may lead to rupture.

Is It or Isn't It a STEMIMike Weinstock MD, Anand Swaminathan MD, Amal Mattu MD and Mark Calvert

Take Home Points

Findings that increase the likelihood ratio of ruling in for ACS include chest pain with diaphoresis, chest pain with vomiting, chest pain that worsens with exertion and chest pain associated with radiation, especially to the right arm or bilaterally.

Patients should receive aspirin prior to transport to the cath lab.

The history of present illness per the emergency physician. “Patient presents for the evaluation of ongoing chest pain which began at 11pm at night. The symptoms began gradually and the patient currently has continued symptoms. However, they are improved relative to the onset. The pain is most severe in the left chest and radiates to the arm. The pain moved from the an-terior chest to the back. It is associated with nausea but no vom-iting. It is associated with diaphoresis and shortness of breath. The maximum severity was moderate and the current severity is mild. There is nothing that exacerbates the pain.”

The physical exam and vital signs were unremarkable. The pulse was in the 60s. The blood pressure was 107/65.

The EKG was obtained 7 minutes after arrival. This showed normal sinus rhythm with relatively high voltage indicating bor-derline left ventricular hypertrophy. There was some ST seg-ment depression in the inferior leads. There was ST elevation or J point elevation in the right anterior precordial leads.

The emergency physician documented concave ST elevation in the anterior leads. Was this a STEMI? It wasn’t clear. The EKG was faxed to the on-call cardiologist.

The actual diagnosis of STEMI is not made on the 12 lead ECG. The diagnosis is made in the cath lab or based on serial rising troponins or the development of Q waves. The 12 lead ECG is only to risk stratify to presumed STEMI.

What do you do when the ECG is not diagnostic? Correlate the presentation with the ECG. Initiate treatment. Consult the car-diologist.

The emergency physician saw the patient promptly, started the patient on a nitroglycerin drip within 20 minutes and contacted the cardiologist right away. The case was discussed with the car-diologist 9 minutes later.

What conditions warrant activating the cath lab? STEMI in two contiguous leads. This is more concerning with convex upwards (e.g. non- smiley face) ST elevation or reciprocal changes.

Who activates the cath lab? This varies depending on institu-tion. In some facilities, the emergency physician activates the cath lab. In other places, the cardiologist activates the cath lab after consultation by the ED physician.

The cardiologist contacted stated he was not on call and ad-vised contacting a different cardiologist. The physician con-tacted a second cardiologist who did not believe the patient had a STEMI and started the patient on a heparin drip and gave him morphine. He advised admission to the ICU.

The troponin was 0.08. This was within the normal range.

The physician documented that beta-blockers would not be given secondary to a heart rate of 55. Critical care time was 30 minutes.

CASEA 57 year old man developed chest discomfort and diaphoresis at 11pm. He called 911. Medics administered sublingual nitro-glycerin and his pain decreased from 6/10 to 4/10. He was given aspirin and transported to the emergency department at 11:56pm.

EM:RAP Written Summary | www.emrap.org8

The patient was diagnosed with unstable angina and admitted to the intensive care unit.

Should you get a second troponin earlier? It isn’t necessarily helpful. There may be an increase in troponin whether it is a STEMI or NSTEMI.

The physician repeated the EKG in 30 minutes. There was no change. The ST changes remained concave upwards.

Repeat ECGs may show changes in acute cardiac ischemia such as increased ST depression, increased ST elevation, change in the morphology of the T waves, etc.

There are only four findings that increase the likelihood ratio of ruling in for ACS; chest pain with diaphoresis, chest pain with vomiting, chest pain that worsens with exertion and chest pain associated with radiation, especially to the right arm or bilaterally.

What medications should patients receive prior to transport to the cath lab? Aspirin between 162mg and 325mg. Addition-al medications are institution and cardiologist specific. Heparin is necessary for all of these patients but it doesn’t need to be started in the ED.

The patient was admitted to the ICU at 2:48am. A repeat EKG at the time of admission looked like a well-defined anterior STEMI. There was a new right bundle branch block.

At 5:07am, a repeat EKG showed new lateral changes. At 5:32am, a fifth EKG was performed. At 6:07am, the CPK and MB fraction was elevated.

At 6:55am, the initial cardiologist who was contacted arrived and took the patient to the cath lab. While the patient was in the cath lab, the repeat troponin had increased to 4.5.

While in the cath lab, the patient became hypotensive and received pressors. He was combative and intubated. He de-veloped third degree AV block and had an intra-aortic balloon placed. He was found to have a thrombus in the LAD and PCI was performed. He was then transferred to another facility for a higher level of care.

There was a bad outcome and it resulted in a lawsuit. The emergency physician was steadfast that the emergency care was appropriate. However, the documentation and medical de-cision making was lacking.

Calvert was the defense attorney. What is his ideal documen-tation? “Possible STEMI. Call to IC on call (list name) and re-ferred to another IC (list name). Spoke at (time) and expressed concerned about possible STEMI and ACS. Faxed ECGs to Dr. (name). He feels no STEMI at this time. Instructed for ICU ad-mission and he will come in to see him.”

The emergency physician in her deposition:

“The first EKG in the ER was completed at 12:03 am. The

EKG showed some ST elevation but it was in the non-inferior leads. Also, the EKG was not significantly different from those performed by EMS so it did not show evolving changes. In my opinion, the 12:03 EKG did not show a clear cut STEMI but I thought it was a possible STEMI and catheterization was a possibility for this patient so I promptly contacted the cardiol-ogist listed as on call for the cath lab.”

“He informed me that another doctor was the interventional cardiologist covering call that evening so I immediately had the interventional cardiologist paged. I spoke with the inter-ventional cardiologist and told him about the patient’s pre-sentation, condition and my concerns about the 12:03 EKG. The interventional cardiologist asked me to fax him the 12:03 EKG and to do a repeat EKG.”

“I instructed the nurse to fax the EKG to the interventional cardiologist’s fax number which I had written on the 12:03 EKG and I ordered a repeat EKG which was completed at 12:36am. This EKG was also sent to the interventional cardi-ologist at approximately 12:40am.”

“I discussed the case with the interventional cardiologist shortly thereafter and we discussed the two EKGs, the car-diac enzyme results which were all within normal limits and the patient’s condition. I reiterated my concern about the pa-tient’s status and I inquired whether the patient needed to go to the cath lab. The cardiologist felt the patient was suffering from unstable angina and needed to be admitted to the ICU for careful monitoring. He indicated he would come and see the patient later. I followed his instructions, contacted a spe-cialist in internal medicine and arranged to admit the patient to her care.”

Mattu served as the expert witness. This was the turning point of the case. Next month we will continue with its conclusion.

National Lecture Series: Things Intensivists Wish We Did Peter DeBlieux MD

Take Home Points

Ketamine is ideal for rapid sequence intubation in shock states.

Resuscitate before you intubate if possible.

Document difficult intubations so the intensivist is aware and can wean the patient from the ventilator accordingly.

Document discussions of end-of-life goals so future pro-viders are privy to the conversation.

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Consider ketamine. Our intensivists often think that our choices for RSI make our patients sicker. There is data to support this.

Ketamine is ideal for shock states. It is one of the safest drugs we can give in the ED. It drives blood pressure up. There is a small elevation in the intracranial pressure. However, it also raises the mean arterial pressure to an even greater degree and overall cerebral perfusion pressure is enhanced by ketamine.

In a sick patient, you need to consider whether the patient will be more or less likely to tolerate intubation after 15 minutes of your best efforts. RSI is not safe. We are giving drugs that alter blood pressure and performing positive pressure ventila-tion that alters physiology. This decreases venous return. If the patient is already in a shock state, then RSI can tip them over the edge.

If the patient won’t be more stable in 15 minutes, despite your best care, intubate. For example, hemorrhagic shock.

If the patient may be better in 15 minutes after receiving a fluid bolus and initiating vasopressors, then we should wait. Resuscitate before you intubate. Non-invasive positive pressure ventilation. In acidotic patients, you can bag them through the procedure. Flu-id resuscitation. Pre-emptive fluid boluses in COPD and asthma patients if you have time. Bicarbonate in patients with profound acidosis.

Don’t be afraid to document difficult intubations. Your col-leagues need to know. Future intubations should be prepared with a cric kit at the bedside. This can affect the decision to wean the patient from the ventilator. Discuss the airway with your intensivists so they know what they are getting into if they decide to extubate.

Keep the patient comfortable. We use long term paralytics but don’t use long term sedatives. We are better than this. Order your sedative medications along with your RSI medications. Avoid benzodiazepines. Use fentanyl for pain. Consider dexme-detomidine (if available) or propofol. Short-acting agents are a better choice. Patients in the ICU are assessed every 8 hours with a spontaneous breathing trial to see who can be extubated.

Elevate the head of the bed. Place OG or NG tubes.

Remember low tidal ventilation. 6cc/kg of ideal body weight. Maintain plateau pressures less than 30.

Use the ultrasound. Look for inferior vena cava variation from 15% to 50%. This indicates a patient that will likely tolerate a fluid bolus. If the IVC is static, you don’t know how they will re-spond. When you give a fluid bolus, make it small and reassess.

If the blood pressure is not responsive after the first liter of flu-ids, you should be asking the nurse to mix up norepinephrine. Don’t wait until the second, third and fourth liter to make this decision.

After initiating vasopressors, you need to assess response. As-sess the heart with ultrasound. Use the ultrasound to identify a vigorous, active heart with the left ventricle collapsing on its chamber compared to a heart that is barely contracting. If the ventricle is barely contracting, add dobutamine.

What fluid should be used for resuscitating septic shock? There is nothing normal about normal saline. It has a lot of chloride and a lower pH than our blood. Consider giving a balanced solution to patients with sepsis to avoid the hyperchloremic, metabolic acidosis seen with large volumes of normal saline. Retrospective studies hint at danger from resuscitation with large volumes of normal saline.

The SPLIT study found no difference in acute kidney inju-ry between small volumes of normal saline versus buffered crystalloid solution like Plasmalyte. However, patients only received about two liters of fluid on average.

Young, P et al. Effect of a buffered crystalloid solution vs sa-line on acute kidney injury among patients in the intensive care unit: the SPLIT randomized clinical trial. JAMA. 2015 Oct 27;314(16):1701-10. PMID: 26444692.

Early institution of the right antibiotic saves lives. We need to ask the patient questions. Have you recently been on an antibi-otic? Have you received wound care at home? Have you been admitted to the hospital within the last three months? These increase the likelihood that the patient has multi-drug resistant infections.

Culture blood and urine prior to antibiotics and identify a source. Don’t withhold antibiotics if you are unable to obtain blood cultures.

CASE 1A 74 year old woman with insulin dependent diabetes presents with three days of fever and progressive altered mental status. She is tachycardic with a heart rate in the 120s, hypotensive with a respiratory rate in the 30s with a temperature of 102 (38.9%). Her oxygen saturation is only 86% on a non-rebreath-er mask. She is 5 feet tall and 200kg.

CASE 2The patient is febrile, hypotensive and hypoxic. They also have a history of congestive heart failure.

CASE 3A 49 year old woman with insulin dependent diabetes, hyper-tension and end stage renal disease presents to the ED with complaints of fever and a red painful arm at the site of her dialysis vascular access. She is hypotensive, tachycardic and tachypneic.

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Give broad spectrum antibiotics first. A typical antibiotic regi-men for a patient with sepsis or septic shock is usually vanco-mycin and something like piperacillin-tazobactam or cefepime. Give the piperacillin-tazobactam before the vancomycin be-cause the vancomycin is administered slower. The dose of vancomycin should be 15-20 mg/kg of total body weight. The maximum dose is 2 grams. If the patient is obese and requires a higher dose, go with linezolid.

Don’t renally dose the initial antibiotic doses.

Acetaminophen for fever. Intensivists often follow the fever curve to determine response to antibiotics so you may consider not treating the fever.

Document the neurologic exam prior to and after intubation. Documentation of serial neurologic exams is essential when determining the need for repeat imaging. Consider short term paralytics and sedatives with a short half-life.

For non-convulsive status and seizure patients with altered mental status, assess for fine hand and foot tremor as well as tics to the lips, face and eyes to determine likelihood of non-convulsive status. Order an EEG.

Elevate the head of the bed. Make sure that the oxygen satura-tion is greater than 90% but the patient is not supersaturated. Aim for oxygen saturation between 94-97%.

Maintain cerebral perfusion pressure between 50 and 70. If the patient has elevated ICP, you need to target a MAP greater than 65. Aim for 75-85.

Avoid hypoglycemia, hyperglycemia and hypothermia.

Identify life planning goals for critically ill patients. Is there a living will? Do we know? Establish realistic expectations for the patient and family members. If you think you may need to de-liver bad news, lay down a pre-emptive strike. “There is a good likelihood that we will have this conversation later today and it may involve bad news. If there is bad news, do you want to hear this solo or with friends or family here?” About 80% of US citizens want to hear the news solo; they do not want to have their family members present.

Document what you discussed so future providers are privy to the conversation.

Cardiology Corner:Door To Balloon TimeRob Orman MD and Amal Mattu MD

Take Home Points

Aggressive measures to reduce door to balloon time were associated with an increased incidence of false positive STEMI and in-hospital mortality.

False positive cath lab activations have consequences such as cost, increased morbidity and mortality.

Aortic dissections are not reliably diagnosed on cardiac catheterization

When the patient with the STEMI arrives at the emergency department, the clock starts ticking. Door to balloon time has become a sacred number.

Fanari, Z et al. Aggressive measures to decrease “door to balloon” time and incidence of unnecessary cardiac catheterization: poten-tial risks and role of quality improvement. Mayo Clin Proc. 2015 Dec;90(12):1614-22. PMID: 26549506.

Aggressive measures to reduce door to balloon time were asso-ciated with an increased incidence of false positive STEMI and false positive STEMI in-hospital mortality.

There is a lot of pressure on emergency medicine from CMS, hospital administrators and cardiologists to get the patient to the cath lab as quickly as possible. There are unintended con-sequences. There is an increase in false positive cath lab activa-tions. Not all ST elevation is due to STEMI.

False positive cath lab activations have consequences. There is an associated cost. The cost of a false positive cath lab activa-tion has been cited as around $14,000. Resulting fatigue of the cath lab team can affect cases the following day. There is a po-tential increase in morbidity and mortality.

Researchers in this study looked at false positive STEMIs before and after a systems intervention designed to cut door to bal-loon time to less than 60 minutes. The door to balloon times did decrease from an average 76 minutes to 61 minutes. The false positive STEMI activation rate increased from 7.7% to 16.5%. There was a significant increase in in-hospital mortality in pa-tients with negative caths; 5.6% to 21.6%.

There was no significant decrease in mortality with the de-creased door to balloon time in true STEMIs. All of the studies have shown a significant drop in mortality if you can get the

CASE 4A 34 year old man with a history of closed head injury and seizures presents post-ictal after a witnessed seizure that lasted 5 minutes and required two doses of lorazepam per EMS providers.

CASE 5A 74 year old man with Parkinson’s disease and dementia is transported by EMS from a nursing home for dyspnea and de-creased responsiveness. The patient looks sick.

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door to balloon time under 90 minutes. However, any further reductions probably don’t make a big difference.

EKGs were frequently misread in the patients with false posi-tive catheterizations. Left ventricular hypertrophy consistently is one of the main reasons that STEMI is over- or undercalled. There is not a good reliable set of criteria that clearly differen-tiates between LVH and STEMI. Other misreads included early repolarization, left bundle branch block and pericarditis.

There are a handful of deadly conditions that often produce ST elevations. Misdiagnosis or delays in proper diagnosis was often associated with a fatal outcome. This includes conditions such as sepsis, intracranial hemorrhage, massive or submassive pul-monary embolism and aortic dissections.

Aortic dissections are not reliably diagnosed on cardiac cath-eterization.

We are more aggressive in transporting out-of-hospital cardiac arrests to the cath lab. This likely affected the mortality.

Once the angiogram is negative, the interventional cardiologist is not always the best provider to continue the remainder of the work-up.

Spend the extra five to ten minutes to take a good history and physical exam. Consider the differential diagnosis and decide whether the patient should go to the cath lab.

What is the take-home message? You have to know EKGs. Prac-tice, practice, practice. Spend the extra 5-10 minutes to do a good history or physical exam. Reducing the door to balloon time below 90 minutes does not improve outcomes.

After they recognized the increased mortality, they performed a second set of educational interventions to teach about the false positive rate and STEMI mimics. They looked at the false positive rate, mortality rate and door to balloon time. They were able to maintain a door to balloon time of 60 minutes. They were able to drop the mortality in false positive activations from 21.6% to 4.5%.

The Happy MD’s Guide to Physician Wellness Dike Drummond MD and Rob Orman MD

Take Home Points

Physician wellness and burnout prevention need to be pri-oritized by hospitals and group practices.

The mission statements of most hospitals talk about caring for the patient. The focus is not on caring for the health care providers.

The culture of medicine has changed over the years; many of the changes have led to an increase in physi-cian burnout.

The Happy MD encourages creating a burnout preven-tion working group that does 3 things: educate about burnout, establish a feedback mechanism whereby providers can identify causes of stress, and ‘get on it’.

Physician wellness is not prioritized by hospitals, either through financial funding or other means of support. In medical training, we are conditioned to diagnose and treat. We are always focused on problems. Wellness is something that we rarely deal with in our day-to-day practice. Many hospitals have physician wellness committees which, while well-intentioned, have little to no impact. Burnout preven-tion committees, on the other hand, often receive support, money, and the necessary protected time to make changes. Hospitals put their organizational backbone behind prevent-ing burnout.

Mission statements in medicine.

A mission-led endeavor, where the mission is consciously created and you live it, is an extremely important success factor in any business, including health care.

The challenge is that in health care, the mission state-ment almost always focuses only on the patient. It might talk about quality of care, but it doesn’t mention any of the people who work inside the organization. This blind spot gives the leadership the ability to ignore the needs, or even abuse the providers inside the system. We are con-ditioned that the patient comes first and that conditioning sets us up for burnout. If the patient always comes first, you can’t recharge your own energy levels and eventually, you won’t have anything more to give.

A mission statement is not supposed to be a static thing. It is not meant to be a half-day retreat, never to be looked at again. Organizations often have a mission statement posted on their websites, but employees are unfamiliar with it and had no part in crafting it.

The Happy MD mission is to give physicians the tools that they need to lower their stress levels and prevent burnout. Most of the time, doctors are simply running through the patients on their ‘gerbil wheel’, heads down, in survival mode without any thought of their mission. Phy-sicians need to be aware of their mission and live it, if they want it to have any impact on what they’re doing.

Which job would you take?

One where you are working in an organization where all you are is an RVU generator and nobody really cares about you as a person. This job compensates very well.

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One where you are part of a team and everybody has each other’s back. In this job, people care about their lives outside of medicine and everybody gets along.

The culture of medicine has changed over time, which has led to an increase in burnout. Previously, many were in small group practices which encouraged socialization outside of med-icine and a culture of teamwork and camaraderie. Now, these small groups have been absorbed by hospitals and large medical groups. Nobody knows anybody else. There is a lack culture and cohesiveness, which contributes to burnout.

It’s a tragedy and a missed opportunity that the vast majority of healthcare organizations have no signs of caring about the health of the front line providers in their mission statements. The statement does not include wordage indicating that the or-ganization supports the well being or happiness of the people who deliver the medical care. Nurses, medical assistants, and physicians are all taught, conditioned, and driven to take good care of their patients. It happens automatically, as long as the providers are healthy and have adequate energy stores. Most organizations do not support the wellness of the people provid-ing the medical care.

Burnout is inevitable if you can’t shut out, “The patient comes first’, when you leave the office. If you are only focused on the patient, you can’t recharge yourself and perform at your best the next day.

How do we change the culture of medicine, so we aren’t car-ing just about patients; that we are also caring about ourselves and each other?

Socialize more often; don’t underestimate the power of piz-za and beer. This encourages cohesiveness.Form a burnout prevention working group which has 3 spe-cific steps.

Fill the educational holes around burnout. Talking about burnout normalizes the conversation. 40% of physicians are suffering from burnout on any given day, but doctors fear showing weakness and rarely feel comfortable talking about stress or burnout.Establish a feedback mechanism for front-line providers with the focus on their level of satisfaction. Ask the fol-lowing questions in a survey. (The answers to these ques-tions create the project list for the burnout prevention working group.)

On a scale from 1-10, what is your satisfaction with your current practice?What are the 1st, 2nd, and 3rd most stressful things in your workday.How would you describe the culture around here in one sentence?What would you like the culture to be like?

Get on it. Address the issues that come up in the survey publicly, loudly, and get administrative support. Commu-nicate every little bit of progress that is made. Repeat the surveys every year to ensure that you are always working on improving the things that people point out as causing stress.

Critical Care Mailbag: Peripheral Pressors and IV FluidT emperatureRob Orman MD and Scott Weingart MD

Take Home Points

Warm all fluids and blood products administered to trau-ma patients.

Peripheral administration of pressors seems to be safe if done correctly.

Have a protocol in place for frequent checks of the IV site and management of extravasation.

Don’t use ultrasound guided deep brachial or IVs in the hand for pressors.

Does the administration of room temperature crystalloid fluids have a detrimental effect on a critically ill patient? Theoreti-cally, it may be beneficial to cool these patients. However, the HEAT trial found no benefit to controlling fevers although they were using acetaminophen rather than cool fluids.

Young, P et al. Acetaminophen for fever in critically ill patients with suspected infection. N Engl J Med. 2015 Dec3;373(23):2215-24. PMID: 26436473.

However, trauma patients may become profoundly hypo-thermic from room temperature fluids. This worsens coag-ulopathy. Blood products are often ice cold. Giving patients unwarmed blood products or other fluids is bad. You should put all fluids and blood products administered to trauma pa-tients through a fluid warmer first.

The HEAT trial is based on the thought that the ability to mount a fever is a product of evolution and allows the body to help clear infections. However, it is not unreasonable to give acetaminophen to treat discomfort in patients with a fever. This is especially true in children who may not eat or drink when fe-brile. Your focus should be on comfort rather than the actual number.

From Kenji Inaba. Why the hate for IV fluids in trauma pa-tients? We have accumulated a lot of data that shows increased risk of complications although not increased mortality. Proac-tive resuscitation with blood and blood products has been asso-ciated with better outcomes.

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What should you do if there is an infiltration?

In the Ricard trial, the patients were just observed for compli-cations.

In the Mayo trial, they used phentolamine and nitroglycerin. None of the patients with extravasations had complications.

What does Weingart do? Leave the angiocath in place tem-porarily. Suck out everything you can, even if it is only 3-4 cc. Phentolamine is administered through the angiocath andsubcutaneously in the areas that appear vasoconstriction.

Is there any evidence to support the use of phentolamine? There is some old literature available from the 1960s. Zucker, G et al. Treatment of shock and prevention of ischemic necro-sis with levarterenol-phentolamine mixtures. Circulation. 1960 Nov;22:935-7. PMID: 13788877.

You need to have a protocol in place for extremity checks and management of extravasation.

Management of extravasation

Step IIf the patient is relying on the agent for their hemodynamic stabil-ity, switch the pressor to another IV or place an immediate IO or central line.

Step IIDo not pull the cannula yet.

Step IIISuck out as much as you can.

Step IVAdminister subcutaneous phentolamine mesylate using a 25 or smaller needle.

This comes in 5 mg per 1ml vials. Place in 9ml of NS.

A dose of 0.1-0.2 mg/kg (up to a maximum of 10mg) should then be injected subcutaneously around the site.

Administer as soon as the extravasation is detected, even if the area initially looks just a little white or OK.

You should see near immediate effects; otherwise consider ad-ditional dose. Now pull the catheter.

May cause systemic hypotension (but they should be on pres-sors at another site).

Step VConsult plastics.

Is there a role for some crystalloid? Yes. No matter where you work, they will likely arrive with fluids hanging. This serves as a challenge and can help determine disposition (i.e. rapid transport to the OR). It also provides a bridge until you can get blood products on board. If the patient is stable, you can stop the fluids.

Some physicians are reluctant to start pressors as it requires central line access. There may be complications and it is time-consuming when you are busy in the ED. There has been increasing literature on peripheral administration of pressors. The consensus seems to be that peripheral pressors are safe. This is a controversial topic. Patients should not be left on pe-ripheral pressors for a prolonged period of time. However, it is probably safe up to 12 to 24 hours. Some patients may be able to get off the pressor in that period of time.

If you are going to do it, you need to be safe. Have a policy of regular inspection of the arm. Use a reasonable size IV in a reasonable vein. Ultrasound guided IVs are high risk for extrava-sation and the deeper location means extravasation may remain undetected for longer. Don’t use IVs in the hand.

Ricard, JD et al. Central or peripheral catheters for initial venous access of ICU patients: a randomized controlled trial. Crit Care Med. 2013 Sep;4(9):2108-15. PMID: 23782969. This found it was safe.

Cardenas-Garcia, J et al. Safety of peripheral intravenous ad-ministration of vasoactive medication. J Hosp Med. 2015 Sep;10(9):581-5. PMID: 26014852. They found it was safe. They used peripheral IV’s for prolonged period of times.

Which pressor can be used? Phenylephrine is considered safe when injected subcutaneously. The two trials above used nor-epinephrine which traditionally was the most feared. Dopamine is often considered safe peripherally. However, there are multi-ple case reports and lawsuits regarding dopamine induced injury.

Ultrasound guided IV placement with a reasonably sized nee-dle gauge and relatively superficial placement are probably ok to use. However, the deep vessels with a long angiocath are higher risk for extravasation. When the vessels are deep, not much of the angiocath actually enters the vessel. If the patient moves their arm, the angiocath could fall out of the vessel and you may not detect it right away.

Midline catheters go up to the shoulder but do not enter the central circulation. If you place the line and are still able to draw blood, there is probably 4-5 inches of the line in the ves-sel and the chances of extravasation are miniscule. Howev-er, there are no available studies on peripheral vasopressors through a midline.

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Strayerisms: Anaphylaxis RebuttalRuben Strayer MD

Take Home Points

An allergic reaction is dangerous when it involves the air-way, breathing or circulation.

Change in voice, stridor, mishandling of secretions and air-way posturing demonstrate airway compromise.

Order epinephrine in a dose of 300 to 500mcg IM. Don’t worry about calculating 1:1000 or 1:10000.

Consider glucagon in patients not responding to treatment.

A recent segment on anaphylaxis by Howie Mel, Anand Swa-minathan and Bryan Hayes advised a low threshold to give epinephrine. This is true. When in doubt, give epinephrine. They also discussed that evolving changes to the definition of anaphylaxis are confusing and lead to suboptimal care. This is also true. However, they cited the World Allergy Organization Guidelines definition which is three parts, confusing and impos-sible to remember.

Emergency medicine physicians care whether this allergic re-action is dangerous. It doesn’t matter how many systems are involved. It matters which system is involved.

An allergic reaction is dangerous when it involves the airway, breathing or circulation and that is all. If you have rash and ab-dominal pain, you do not need to give epinephrine. If you have rash and hand tingling, you do not need to give epinephrine. If you have involvement of the airway, breathing or circulation without another system involved, you must use epinephrine.

What are the signs of airway compromise? There are four: Change in voice. Stridor. Mishandling of secretions. Airway posturing.

Airway posturing is not tripoding which is using the arms to splint the lungs. Airway posturing is assuming a sniffing posi-tion. It is usually seen in children with epiglottitis. If you see it, you should be alarmed.

Many patients develop tingling or scratching in the back of their throat. Some are anxious and screaming that they can’t breathe. If you aren’t sure, give a dose of epinephrine and prepare for airway management. However, if the patient is screaming they can’t breathe but using full sentences with a normal voice and no signs of airway compromise, you can be more measured in your approach.

What are signs of breathing compromise? Wheezing and evi-dence of lung dysfunction such as tachypnea, increased respira-tory effort and hypoxia.

What are signs of circulatory compromise? Hypotension, hy-poperfusion and syncope.

Don’t try to understand 1:1000 and 1:10,000. Even if you un-derstand it, the person you are shouting verbal orders to will not and will give you the wrong dose. Know the dose so you can give the right dose. The correct dose is 300-500mcg IM. If you call for this, you will get the right dose whether your nurse has the 1:1000 or 1:10,000 available.

Should you use push dose epinephrine? This is difficult to do and is going to get screwed up. If you are managing the crashing anaphylaxis patient, do not try to draw up and push 5mcg of epinephrine.

How do you manage the crashing anaphylaxis patient? Give 500mcg (1/2 of 1 mg) of epinephrine intramuscularly and get ready to manage the airway while someone else establishes IV access. If your patient is not improving in a few minutes, give a second dose of 500mcg IM epinephrine and start an intrave-nous epinephrine drip.

How do you start an intravenous epinephrine drip? Take 1 mg of epinephrine in any concentration you like. The crash cart epinephrine is preferred because it comes drawn up in a syringe. Add 1mg of epinephrine to a liter of saline and drip it in. This takes 30 seconds to set up. You get epinephrine in a concentration of 1mcg/cc. 20 drops per cc. 2 drops/second is about 6mcg/min which is your target. Use the knob on the IV tubing to titrate up and down to effect. When things settle down, you can switch to formal drip on a pump.

Using vasopressors as bolus doesn’t make sense because their effect lasts for seconds to minutes.

When a patient can’t breathe from dynamic airway obstruc-tion such as trauma, burns or anaphylaxis, there is a reason-able chance that you will not be able to pass an endotracheal tube through the cords for the same reason the patient can’t breathe through the cords. Announce to your team and to your-self that this patient is likely going to require a surgical airway but you will look via laryngoscopy to be sure. Be prepared for cricothyrotomy. Have your colleague standing next to you with a scalpel in their hand.

If the patient is still not responding to epinephrine despite all your best efforts, reach for glucagon. The patient may be on a beta-blocker. There is weak evidence to support vasopressin and methylene blue as therapies for anaphylaxis in patients who are deteriorating despite everything. However, almost all ana-phylaxis patients will respond to epinephrine.

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Snake BitesStuart Swadron MD and Sean Nordt MD

Take Home Points Antivenin should be given in snake bites for progression

of swelling or lab abnormalities.

Antivenin is indicated for platelets less than 100 or fibrin-ogen less than 100.

Patients may develop delayed thrombocytopenia unre-sponsive to antivenin so follow-up is important.

How much antivenin should you give? The decision to give an-tivenin is based on two criteria; progression of swelling and lab abnormalities.

To evaluate progression of swelling, measure the leading edge in a straight line over an hour. If it is rapidly progressing, this is an indication alone for antivenin. If the line is progressing, keep giving antivenin every hour. Continue to give antivenin until you achieve initial control. This is cessation or minimal progression of swelling.

Elevate the extremity.

Platelets and fibrinogen. If the platelet count is 100 or trend-ing toward 100, give antivenin. If the fibrinogen is trending toward 100 or less, give antivenin.

Platelets may decrease in the beginning phase and a week lat-er. The initial decrease in platelets is likely secondary to a se-questration phenomenon. For most patients, the platelet count will recover after antivenin. However, patients may have a dip in platelets at 4 to 14 days after the bite. This does not respond to antivenin. It is unclear why it happens but may be an immuno-logical response. Patients should have follow-up for repeat CBC between 7-10 days.

What do fasciculations mean? Fasciculations are common on the West Coast because rattlesnakes have Mojave toxin which is a neurotoxin. Respiratory paralysis is rare. These can result in rhabdomyolysis. Fasciculations are not an indication for anti-venin but you should monitor the patient for rhabdomyolysis.

How do you treat rattlesnake bites differently depending on location? You should be aggressive in treating bites on the hand. It is unusual for patients to die from rattlesnake bites but they can have morbidity and loss of function. Nordt recommends six vials of Crofab for bites on the hand. There is no available sup-porting data however.

What do you do when the patient presents? Measure the lead-ing edge of swelling. Watch over an hour. If you elect to give antivenin, give 4 to 6 vials over an hour. Wait an hour and look

for progression of swelling. If there is progression, give another 4 to 6 vials. When the labs return, give antivenin if the platelets or fibrinogen is less than 100.

How do you redose after gaining control? The package insert describes maintenance dosing of 2 vials every 8 hours for three doses. Most toxicologists don’t do this. Call your local poison center or toxicologist for guidance.

Annals of Emergency Medicine: Penetrating Neck TraumaPaul Jhun MD, Mizuho Spangler DO and Kenji Inaba MD

Take Home Points Zones of the neck are no longer used to determine man-

agement of penetrating injury.

CT angiogram allows us to image the entire neck and screen for any injuries.

Hard signs include hemodynamically instability or hemop-tysis, hematemesis, arterial bleeding, rapidly expanding hematoma, vascular or neurologic deficit or bruit or thrill.

Are zones of the neck still used to determine management? Not currently, although the zones can help us communicate lo-cation to other physicians. We rely on evaluation of hard signs, soft signs and no signs.

Previously zone I and III injuries were evaluated by imaging before surgery because they were difficult technically to ex-plore. Zone II injuries were taken to the OR because they were surgically accessible and easy to explore.

There were a lot of negative explorations of zone II. Also, patients with Zone I and III injuries were subjected to a va-riety of invasive tests including angiography, bronchoscopy, esophagoscopy and swallow evaluations.

CASEA 7 year old girl presented to the emergency department with right shoulder and chest pain after falling with a pencil in her hand. Clinical examination demonstrated only a small pene-trating injury in her anterior chest wall and she was discharged home. A week later, she returned with persistent pain and lim-ited movement of her neck. CT angiography was performed. The patient was taken to the OR where a 10cm pencil and 1cm lead tip were removed without complication.

EM:RAP Written Summary | www.emrap.org16

Injuries entering in one zone may involve neighboring zones. CT angiogram allows us to image the entire neck and screen for any injuries.

What are hard signs? Hemodynamically unstable or hemopty-sis, hematemesis, arterial bleeding, rapidly expanding hemato-ma, vascular or neurologic deficit or bruit or thrill (HARD Bruit).

Although subcutaneous emphysema, hoarse voice and stridor are not considered hard signs, this may be due to their rarity. These patients may be candidates for emergent transfer to the operating room.

You need to determine whether the patient is safe to go to the CT scanner for preoperative imaging or not.

Would a screening x-ray have been useful? The entry wound was periclavicular, which is concerning for chest pathology with downward tracking. The radiation burden of a chest x-ray is low and it could be very helpful. The patient could have a large pneumothorax which could complicate surgery. The chest x-ray can help identify a need to continue the CT angiogram down into the chest.

Could a duplex evaluate a vascular injury? It may be useful. However, the sensitivity of ultrasound is highly variable. There may be some operator variability and there is a lot of variability among patients. Access to duplex ultrasound may also be a lim-iting factor depending on where you work.

CT angiogram gives you the big picture and allows you to rule out injury to the vascular and aerodigestive structures. It can give a good idea of the wound trajectory. This can influence management. CT angiogram is preferred as it will allow you to detect nonvascular injuries. The sensitivity to rule out vascular and aerodigestive injuries is very good. The specificity for inju-ries to the vascular structures is good. However, the specificity for airway and esophagus is less.

How do you evaluate Zone 1 injuries? These are difficult. For any external wounds in the thoracic inlet, there is concern that that they may track downwards and into the mediastinum where the vessels and heart lie. Are there hard signs, soft signs

or no signs? Remember that the vascular outflow is not just to the neck and head but also the arms. Aerodigestive injuries may be seen in the pleural space on a chest x-ray.

Get a chest x-ray and do a clinical exam including the vascu-lar supply to the arm. If the patient doesn’t have a completely normal physical examination and chest x-ray, the next step is to image the area with a CT angiogram.

Should patients with stable penetrating neck injuries, a nega-tive CT angiogram, no hard signs or evidence of aerodigestive injury but a laceration that may involve the external jugular vein be seen by surgery or can the ED physician repair it? It depends on your practice setting and your comfort level. If it is extensive, the patient may be more comfortable with repair in the operating room.

From The Mailbag:ACEP Stroke GuidelinesRob Orman MD and Anand Swaminathan MD

From the mailbag regarding the new ACEP stroke guidelines. “With a goal to improve functional outcomes, IV tPA should be offered and may be given to selected patients with acute ischemic stroke within three hours after symptom onset at in-stitutions where systems are in place to safely administer the medication”. What does this mean?

Do you need to have a neurosurgeon in house? No. “Systems in place” means each hospital should have a preplanned protocol on how to manage acute stroke whether it is in house, telemed-icine or transfer.

Quit calling emergency departments “shops”. What we do and say matters. This word aligns our profession with commerce. We were outraged when a neurologist in the New York Times com-pared us to garage mechanics. We aren’t doing ourselves any favors. An auto mechanic doesn’t have to tell a patient that their spouse is dead.