Let Apneic Oxygenation Reign!

We have talked about this topic briefly in the past but it is extremely important and deserves more dedicated attention.  Past mantra has dictated using a bag-valve mask (BVM) whenever a patient was thought to not be breathing adequately, or even not breathing at all.  Current evidence emphasizes the danger of the BVM and its inappropriate use.  The BVM can be summarized nicely: 1) It increases intrathoracic pressure thus decreasing preload and coronary artery perfusion, 2) opens the lower esophageal sphincter(even if you are good at ventilating) causing a high risk for vomiting from gastric insufflation, 3) causes over-distention of the alveoli resulting in oxygen shunting and decreased capillary PaO2. and 4) decreases cerebral blood flow. So what can we do to ensure oxygenation in those patients who just don’t require a BVM?  Apneic oxygenation!

The most common time the apneic oxygenation strategy will be employed is during the preoxygenation period and peri-intubation period of airway management.  The principles of apneic oxygenation may also be applied to patients who require supplemental oxygen but may not be able to be intubated at the time (i.e., predicted difficult airway or RSI meds are not available).  The goal is to maintain a SpO₂ > 93% without using a BVM.  If the patient is unconscious during preoxygenation, this can be accomplished with a nasopharyngeal airway (NPA), nonrebreather (NRB) and high-flow nasal cannula (HFNC) set to at least 15 Lpm.  To review, the purpose of preoxygenation is to provide nitrogen washout.  As we know, nitrogen is the most common atmospheric gas and also predominates in your lungs.  If you remove the nitrogen by flooding the airway, including the dead space, with 100% O2 you can increase the functional reserve capacity and buy yourself time and reassurance during the apneic period of intubation. 

The best way to provide oxygenation during the apneic period of intubation is obviously to continue oxygenation.  Place an NPA (or two, yes two, NPAs) and passively oxygenate past the tongue through the glottis.  HFNC may actually provide bubbles or assist in visualization of the trachea; voila you have your view!  Through the use of HFNC during the apneic period of intubation the alveoli will continue to take up oxygen despite a lack of diaphragmatic movement or lung expansion.  Ideally the patient should remain in the upright 20 degree position ensuring that the airway remains patent with an NPA, OPA, jaw-thrust, head-tilt-chin-lift or, preferably, a combination to allow oxygen gas to pass down the nasopharynx into the deeper airway structures and then to the alveoli for passive diffusion.

Recent evidence has reviewed the effectiveness of the HFNC when used in the apneic period of intubation using RSI.  The study was conducted by an Australian helicopter emergency medical service (HEMS).  The HEMS service consisted of a physician and paramedic.  Intubation attempts were split evenly between the physician and paramedic in the pre-intervention arm of the study but favored the paramedics during the institution of apneic oxygenation.   They reviewed RSI intubations pre and post implementation of an apneic oxygenation protocol.  They had a significant decrease in desaturation during intubation in the group that received apneic oxygenation (22.6% to 16.5%).  They also noted a decrease in cardiac arrests (5.6% to 1.4%) and episodes of bradycardia (7% to 1.4%) related to desaturation during intubation after apneic oxygenation was implemented.  In conclusion, avoid the BVM whenever possible and always use a HFNC during intubation. 

So here is what I do EVERY TIME I am getting ready to intubate.  (Not in this order)

1. Have a BVM ready with PEEP valve on at all times. 
2. Have suction ready. 
3. Quantitative ETCO₂ ready to place on ETT.  (Remember, it needs to “zero” to the atmosphere first anyway.)
4. Nasal cannula at least 15 LPM or as high as you can go. 
5. Apply NRB at 100% over nasal cannula
6. Bag only if RR<4 and SpO₂ <93%.  If RR>4 and SpO₂ <93% use oxygen for 3 MINUTES to see if saturation will come up.  If it does not come up… you can ventilate with BVM slowly (no more than 6 times per minute)

Bonus:  If systolic BP is less than 90 mmHg, add…

1. IV fluid bolus as fast as possible
2. Push-dose Epi 10 µg/min until SBP >90 mmHg

References

Weingart, SD. “Preoxygenation, Reoxygenation, and Delayed Sequence Intubation in the Emergency Department.” J Emerg Med 2010.

Weingart, SD, Levitan, RM. “Preoxygenation and Prevention of Desaturation During Emergency Airway Management.” Ann Emerg Med 2011.

Wimalesena Y, Burns B, Reid C, Ware S, Habiq K. “Apneic Oxygenation Was Associated With Decreased Desaturation Rates During Rapid Sequence Intubation by an Australian Helicopter Emergency Medicine Service.” Ann Emerg Med 2014. 

More Than Just Shock Value?

*Note - this discussion is only pertinent to modern biphasic defibrillators with self adhesive electrodes applied only anterior/posterior or anterior/lateral, with the compression provider wearing two pairs of gloves (double-gloving), with a maximum defibrillation energy of 360J.*

We have all heard the chant, “I’m clear, you’re clear, we’re all clear,” prior to a provider double, triple, sometimes quadruple checking him or herself before pushing that magic red button with the white lightning bolt - “shock”!  Recent literature has spurred quite the discussion on hands-on defibrillation (HOD) - CPR where compressions continue throughout the defibrillation - as it is widely known that interruptions in chest compressions lead to poor patient outcomes and are all too common, for example, during intubation, providing ventilations, AED analyzing, charging, and during defibrillation shocks.  This pearl is meant to provide a very brief explanation of what your risks might be, what protection devices you might use, anecdotal and published accounts on HOD, and suggestions for your clinical practice.

There are numerous factors in regards to energy and the effect it may have on the provider during HOD.  Energy is the product of voltage, current and time.  Neither factors, independently, are sufficient in inducing damaging effects.  For example, several thousand volts are experienced during static electricity, although the current is very low.  Current is determined by the resistance between the electrodes of the defibrillator, the electrode gel, the gel-skin contact, and the tissue resistance.  Glove integrity, skin moisture and the actual current pathway will determine the amount of escape current.  Biphasic defibrillators provide voltages up to approximately 2200 V over approximately 15-20 msec.  The maximum permissible leakage current, per the International Commission on Non-Ionizing Radiation Protection is 1mA; the threshold for perception is 2.5-4.0 mA; and pain is experienced at 6-10 mA.²  Sullivan and Chapman studied the voltage-current curves for gloves.  They note the international safety standard on 1mA and explain that at this level, it would take 1-3 seconds of current flow to induce VF in <5% of the population.  While defibrillation shocks are usually less than 20 msec, even if the pulse is timed appropriately in the rescuer’s cardiac cycle, as much as 500 mA would be required to induce VF.¹ For reference, the current exposure from a home body fat monitoring scale is 500 uA.

In one of the most exciting studies, Lloyd et al measured current between “rescuers” and patients undergoing cardioversion at up to 360 J and found the highest current leak measured was 907 uA,⁴ with no “rescuers” experiencing a “shock.”  Neumann et al found HOD was safely performed on pigs by rescuers, HOD shortened pauses during CPR, and it more quickly restored coronary perfusion pressure.⁴  Kurz and Sawyer, in their letter to the editor of Resuscitation, advocate eliminating effects of no-flow time, perhaps by using HOD.⁷ Dr. Scott Weingart writes that in the 4 years that he and his colleagues have been performing HOD, there have been no rescuer complications, although occasional perceptions of tingling have been reported.  He himself reported arm soreness after 3 shocks, all at 360 J with the electrode pads notably in the anterior/anterior position.

In opposition, Lemkin et al derive an equation called the rescuer-received dose, to try to better qualify defibrillation risk.  Noting that energy values greater than 1 J reportedly can cause VF, they deem HOD unsafe as values above 1 J were calculated in their cadaver study, though effects of gloves were not accounted for.  Two studies from the UK found that medical examination gloves do not provide rescuer safety and even demonstrate further glove breakdown of the gloves worn by rescuers who perform compressions.  According to Sullivan and Chapman, HOD with medical examination gloves will produce no sensation at all unless the gloves completely break down.¹  

Although there are no reported fatalities or serious consequences to rescuers performing HOD under ideal conditions - using a biphasic defibrillator with electrodes placed appropriately, with rescuers double gloved - we should take note that any change to a safety protocol should not be undertaken without ensuring rescuers' safety.  I have personally performed HOD, as have my colleagues in the emergency department.  While none of us have experienced any detrimental consequences or even the reported tingling, considering the literature, perhaps we should currently hold off on changing our protocols to mandate hands-on defibrillation.  Protocols that need to be changed or followed are as follows:

• High quality CPR remains of utmost importance.  Set a metronome at 100 beats per minute and compress the chest to 1.8” (or as close to it as possible) every time.
• Have no interruptions in chest compressions - not for intubation, not for starting an IV, not for inserting a central line, not for transporting, and not for charging the defibrillator!
                

The use of HOD needs to reflect your clinical decision made in the best interest of you, your co-rescuers, and your patient.  If you chose to do so, please double-glove, please place the electrodes anterior/posterior, and communicate your practice to your colleagues.    

References

1.  Sullivan JL, Chapman FW. Will medical examination gloves protect rescuers from defibrillation voltages during hands-on defibrillation? Resuscitation. 2012 Dec;83(12):1467-72. doi: 10.1016/j.resuscitation 2012.07.031. Epub 2012 Aug 25. PubMed PMID: 22925991

2.  Petley GW, Cotton AM, Deakin CD. Hands-on defibrillation: theoretical and practical aspects of patient and rescuer safety. Resuscitation. 2012 May;83(5):551-6. doi: 10.1016/j.resuscitation.2011.11.005. Epub 2011 Nov 15. Review. PubMed PMID: 22094984.

3.  Sullivan JL. Letter by Sullivan regarding article, "Hands-on defibrillation: an analysis of electrical current flow through rescuers in direct contact with patients during biphasic external defibrillation". Circulation. 2008 Dec 2;118(23):e712; author reply e713. doi: 10.1161/CIRCULATION AHA.108.803718. PubMed

PMID: 19047587.

4.  Lloyd MS, Heeke B, Walter PF, Langberg JJ. Hands-on defibrillation: an analysis of electrical current flow through rescuers in direct contact with patients during biphasic external defibrillation. Circulation. 2008 May 13;117(19):2510-4. doi: 10.1161/CIRCULATION AHA.107.763011. Epub 2008 May 5. PubMed PMID: 18458166.

5.  A note of caution on the performance of hands-on biphasic defibrillation. Weingart SD. Resuscitation. 2013 Mar;84(3):e53. doi: 10.1016/j.resuscitation.2012.12.014. Epub 2012 Dec 22. PMID: 23266533

6. Lemkin DL, Witting MD, Allison MG, Farzad A, Bond MC, Lemkin MA. Electrical exposure risk associated with hands-on defibrillation. Resuscitation. 2014 Oct;85(10):1330-6. doi: 10.1016/j.resuscitation.2014.06.023. Epub 2014 Jun 30. PubMed PMID: 24992873.

7.  Petley GW, Deakin CD. Do clinical examination gloves provide adequate electrical insulation for safe hands-on defibrillation? II: Material integrity following exposure to defibrillation waveforms. Resuscitation. 2013 Jul;84(7):900-3. doi: 10.1016/j.resuscitation.2013.03.012. Epub 2013 Mar 16. PubMed PMID: 23507465.

8.  Deakin CD, Lee-Shrewsbury V, Hogg K, Petley GW. Do clinical examination gloves provide adequate electrical insulation for safe hands-on defibrillation? I: Resistive properties of nitrile gloves. Resuscitation. 2013 Jul;84(7):895-9. doi: 10.1016/j.resuscitation.2013.03.011. Epub 2013 Mar 16. PubMed PMID: 23507464.

Did you get the orthostatics yet?

A 70 y/o male presents from a nursing facility with symptoms of weakness after 2 days of diarrhea.  He states it has been watery and occurring 4-5 times per day.  His heart rate is 80 bpm and regular, BP 130/70, respirations of 16, skin warm and dry. He appears well but shows a little general weakness overall.  He knows he takes medications for his blood pressure; however, he is not sure of the name.

Q: Would you get orthostatic vital signs on this patient to assess for volume loss?

Orthostatic vital signs have been used to assess for volume loss by measuring the body’s response to positional change.  Upon standing from a supine position, vasoconstriction and changes in heart rate help to maintain perfusion.  It is thought that when a person is hypovolemic this system fails and blood pools in the lower extremities causing a drop in blood pressure and/or an increase in heart rate.   Symptoms of orthostatic hypotension are lightheadedness, dizziness, blurred vision, weakness, fatigue, cognitive impairment, nausea, palpitations, tremulousness, headache, and syncope.  Orthostatic vital signs are considered positive when there is a drop in systolic blood pressure of ≥ 20 mmHg, drop in diastolic blood pressure of ≥ 10 mmHg, or heart rate increase of ≥ 30 beats per minute within 3 minutes of standing from a supine position.¹

The utility of orthostatic vital signs came into question over 20 years ago.  A study in 1990 looked at orthostatic vitals in 132 self-proclaimed euvolemic patients aged 18-80 years old (mean 34.1 +/- 13.6 years).  Of these patients 43% tested positive.  The study concluded that normal patients may present with orthostatic vitals given the current criteria.²

In 1997, a study examined orthostatics in 911 non-acutely ill patients aged greater than 60 from 45 different nursing homes.  To be included in the study, patients had to be able to stand for at least one minute.  The study found that over 50% of patients had orthostatic changes at baseline and it was most prevalent in the morning when patients first rise.³

Besides the elderly, orthostatic vitals were examined in adolescents as well.  307 healthy high school students aged 15-17 were checked for orthostatic vitals.  The study found pulse changes within the population to be 61% sensitive and 56% specific.  They also found orthostatic blood pressure changes to be within the adult range for 98% of adolescents, and a third of participants experienced orthostatic symptoms.  The study concluded the orthostatic heart rate criterion to be likely inappropriate for adolescents.⁴  Another study examining blood pressure changes in 23 healthy adolescents concluded transient orthostatic hypotension is common in their population.⁵

In addition to examining orthostatics in the non-acutely ill and adolescents, they were also studied in patients with known blood volume loss.  A study in 1992 examined 100 blood donors aged 19-83 years old and 100 senior center volunteers aged 55-94. The blood donors all gave 450 mL of blood.  Orthostatics had no clinical difference between ages.  Furthermore, a pulse rise >20 bpm or a diastolic BP drop > 10 mmHg had a specificity of 17%, sensitivity of 98%.  Systolic changes yielded no better.⁶ A similar study from 1994 looked at orthostatics in blood donation of 450 mL between two age groups, patients <65 and patients 65 or older.  These were healthy volunteers at baseline prior to blood donation.   A pulse change >20 bpm was found to have a sensitivity of 43% and a specificity of 94% in patients less than 65 years old.  In the age 65 and older group, pulse change was found to have a sensitivity of 25% and a sensitivity of 100%.  When they looked at blood pressure, they found it was worse than the flip of a coin.⁷

Besides blood volume loss, fluid volume loss and orthostatics were also studied. A study of 23 pregnant women with hyperemesis gravidarum studied the sensitivity of orthostatics in pre and post rehydration of 6 liters of lactated Ringer’s solution.  The study found that orthostatic changes lack sufficient sensitivity to be effectively used as quantitative screening tests for dehydration.⁸

In summary, the review above shows that using orthostatic vital signs alone to determine volume loss is highly unreliable.  Many patients can test positive for orthostatic signs even when asymptomatic.  We would never want to utilize a test that is so sensitive yet essentially with minimal specificity.  This would then cause the healthcare provider to act on all of the “positive” results by assuming the patient is hypovolemic. To make matters worse, the proportion of patients on beta blockers causing a blunting of the testing would make this even more unreliable than it already is.  When patients were known to have volume loss, orthostatic vitals still lacked a sufficient sensitivity to be deemed an effective test.  Looking for orthostatic clinical signs, not the numbers, is a far more reliable means to assess volume loss.  If the patient stands up and feels either lightheaded or passes out, this is sufficient enough to determine significant hypovolemia.  

References

1.         Naccarato M, Leviner S, Proehl J, et al. Emergency Nursing Resource: orthostatic vital signs. Journal of emergency nursing: JEN : official publication of the Emergency Department Nurses Association. Sep 2012;38(5):447-453.

2.         Koziol-McLain J, Lowenstein SR, Fuller B. Orthostatic vital signs in emergency department patients. Annals of emergency medicine. Jun 1991;20(6):606-610.

3.         Ooi WL, Barrett S, Hossain M, Kelley-Gagnon M, Lipsitz LA. Patterns of orthostatic blood pressure change and their clinical correlates in a frail, elderly population. Jama. Apr 23-30 1997;277(16):1299-1304.

4.         Skinner JE, Driscoll SW, Porter CB, et al. Orthostatic heart rate and blood pressure in adolescents: reference ranges. Journal of child neurology. Oct 2010;25(10):1210-1215.

5.         Stewart JM. Transient orthostatic hypotension is common in adolescents. The Journal of pediatrics. Apr 2002;140(4):418-424.

6.         Baraff LJ, Schriger DL. Orthostatic vital signs: variation with age, specificity, and sensitivity in detecting a 450-mL blood loss. The American journal of emergency medicine. Mar 1992;10(2):99-103.

7.         Witting MD, Wears RL, Li S. Defining the positive tilt test: a study of healthy adults with moderate acute blood loss. Annals of emergency medicine. Jun 1994;23(6):1320-1323.

8.         Johnson DR, Douglas D, Hauswald M, Tandberg D. Dehydration and orthostatic vital signs in women with hyperemesis gravidarum. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. Aug 1995;2(8):692-697.

Things We Can Do Better in 2015!

Here's my list of the top 20 things we can do better in 2015 based on what we learned in 2014 (or even before).

1. High-flow nasal cannula (HFNC), at least 15 Lpm, on all patients undergoing intubation or who might need intubation.
2. PEEP valve on every BVM.
3. No longboards for ANY patient.  Continue to use spinal precautions as appropriate, but that doesn't mean you need a long spinal board.
4. Ketamine, followed by ketamine, rounded out by MORE KETAMINE for RSI induction.
5. No Versed (midazolam) for intubation or post-intubation.
6. No interruptions in compressions for any reason.  Your survival decreases by 7% for every five seconds without compressions. We should be working on improved CPR and "see-through CPR" monitor technology, and don't you dare hold compressions while the monitor is charging!
7. Tranexamic acid (TXA) for all hemodynamically unstable trauma patients.
8. Let the fentanyl flow for intubations, especially after intubation. Pre-intubation benefits in head trauma.
9. More intranasal medications.
10. Use D25 instead of D50 when available.
11. Treat septic nursing home patients like the real emergencies they are.  IV fluids with 30-40 cc/kg bolus.  IV access at a minimum to speed up the time to first antibiotics.
12. Agitated/emotionally-disturbed patients should be recognized as real emergencies as well.  These may be excited delirium.  Treat with ketamine IM; doses as high as 4 mg/kg IM shown to be safe.
13. No etomidate for sepsis or hypotensive patients.
14. Push dose epinephrine for peri-intubation hypotension.
15. Rotate people doing compressions at least every 3 minutes.
16. Stop using BVMs on patients if RR is at least 4 or SPO2 is at least 94%. Instead, use high-flow nasal cannula with a nonrebreather on top.
17. Every BLS should have a pulse oximeter.  They are very affordable these days.
18. Use a metronome for every cardiac arrest!  If your monitor doesn't have one, download an app.
19. No more nitroglycerin paste.
20. Starting dosage of Zofran (ondansetron) for adults should be 8 mg.

2015: The Death of Longboards (Hopefully)

Myths in medicine take too long to go away.  Longboards are yet another modality that serve no purpose except to harm our patients.  Luckily this unnecessary tool used by EMS is going away around the world.  Many states and cities have completely stopped using longboards for ALL patients.  These places include areas within Connecticut, Los Angeles, Kansas, Oregon, Missouri, Houston, New Mexico,.etc.  No matter what your injuries are, in many regions throughout the world, you will not be placed on a longboard, because they are not being used at all.

These devices have hurt our patients since they offer no benefit, yet we continue to use them in our region.  The misconceptions about these devices are enormous, yet the science tells us the following...

Longboards:

1.      Worsen the pain of patients resulting in more unnecessary imaging tests and more radiation exposure.

2.      Cause respiratory compromise/decreased pulmonary function by lying patients flat.

3.      Delay on-scene time for trauma patients.

4.      Result in pressure sores for patients by rapid tissue breakdown from the board.

5.      Increase the risk of aspiration.

Unfortunately, we continue to have folks who spread misconceptions about these devices, which prevent us from moving forward with evidence based medicine.  Luckily, a lot of places are ignoring these folks and moving forward.  Some of the incorrect EMS statement that we have heard are:

1.      The DOT makes me put everyone on a longboard.

2.      I will get my license/certification taken away if I don’t use a longboard.

3.      The DHSS does not allow patients to be brought to hospitals without a longboard.

4.      If someone else puts a patient on a longboard, I cannot take the patient off.

5.      It splints the back.  (No, in fact it was only designed to help extricate patients.)

6.      I will get sued if I don’t put someone on a longboard

These are all ridiculous, and it is great that many places around the country are moving forward with the science.  Lets make 2015 the year we get rid of these terrible devices in New Jersey and around the country.

Following the science, in January 2015, we will be telling EMS providers that they do not need to place anyone on a longboard that is brought into our hospital.  Please join us in getting rid of this outdated modality and provide the same information to EMS.

References:

1. Chan D, Goldberg R, Tascne A, et al. The effect of spinal immobilization on healthy volunteers. Ann Emerg Med. 1994;23:48-51.

2. March JA, Augband SC, Brown LH. Changes In Physical Examination Caused By Use Of Spinal Immobilation. Prehospital Emerg Care. 2002; 6: 421-424.

3. Schriger DL, Larmon B, LeGarrick T, et al. Spinal immobilization on a flat backboard: Does it result in neutral position of the cervical spine? Am J Emerg Med. 1991;20:878-81.

4. Schafermeyer RW, Ribbeck BM, Gaskins J, et al. Respiratory effects of spinal immobilization in children. Ann Emerg Med. 1991;20:1017-1019.

5. Bauer D, Kowalski R. Effect of spinal immobilization devices on pulmonary function in the healthy nonsmoking man. Ann Emerg Med.-1988; 17:915-8.

6. Barney RN, Cordell WH, Miller E. Pain associated with immobilization on rigid spine boards (Abstract). Ann Emerg Med.1989; 18:918.

 7. Chan D, Goldberg, RM,  Jennifer Mason, J et al., Backboard Versus Mattress Splint:  A Comparison Of Symptoms. The Journal of Emergency Medicine. 1996. 14:193-298.

8. Totten VY, Sugarman DB, Respiratory Effects Of Spinal Immobilization. Prehosp Emerg Care 1999;3:347-352

9.  Hauswald M,  McNally T. Confusing Extrication with Immobilization: The Inappropriate Use of Hard Spine Boards for Interhospital Transfers. Air Med J. 2000; 19: 126-127

10. Hauswald M,Braude D.Spinal immobilization in trauma patients: is it really necessary?_Current Opinion in Critical Care 2002;8:566–70.

11. Hauswald M,Ong G,Tandberg D,Omar Z. Out-of-hospital spinal immobilization:  its effect on neurologic injury.  Academic Emergency Medicine 1998;5:214-219.

12. S. Abram S, Bulstrode C. Routine spinal immobilization in trauma patients: What are the advantages and disadvantages? The Surgeon. 2010;8:218–222.

13. Connell RA, Graham CA, Munro PT. Is spinal immobilization necessary for all patients sustaining isolated penetrating trauma? Injury. 2003;34: 912–914.

14. Kaups KL, Davis JW. Patients With Gunshot Wounds To The Head Do Not Require Cervical Spine Immobilization And Evaluation. J Trauma. 1998; 44:865– 867.

15. Haut ER,  Efron DT,  Adil H, Haider AH et al. Spine Immobilization in Penetrating Trauma: More Harm Than Good? The Journal of Trauma. 2010;  68.

16. Cornwell EE, Chang DC, Bonar JP, et al. Thoracolumbar immobilization for trauma patients with torso gunshot wounds: is it necessary? Arch Surg. 2001;136:324 –327.

17. Hauswald M, Ong G, Tandberg D, Omar Z. Out-of-hospital spinal immobilization: its effect on neurologic injury. Acad Emerg Med. 1998;5:214 –219.

18. Kaups KL, Davis JW. Patients with gunshot wounds to the head do not require cervical spine immobilization and evaluation. J Trauma. 1998;44:865–867.

19. Mark Hauswald, MD, Darren Braude, MD, MPH .Diffusion of Medical Progress: Early Spinal Immobilization in the Emergency Department. Academic Emergency Medicine 2007; 14:1087–1089.

Ebola - Just the Facts!

Editor note:  Thankfully, a lot of the hype has already passed on this disease.  This is the clinical pearl written a month ago, prior to the blog.  Unfortunately, I don't think we've heard the last about Ebola, as it still comes up.

Before I start this Clinical Pearl, let me say that Ebola is a scary disease, but, with any disease, we must put science and fact above panic and rumor.  People ask… am I worried about Ebola for the general population?  The answer is no… I am worried about diseases that are likely to kill the general population, such as heart disease, stroke, cancer, trauma, distracted driving, COPD, etc..  If we were to put Ebola into perspective and spend the amount of time discussing it based on the likelihood it will kill any of us compared to the previous diseases…  Well, we would never bring it up.  Unfortunately, too much confusion and too many myths surround this filovirus.  People often say, “Ebola is a lot more likely to kill someone than the diseases I just mentioned.”  That is completely untrue.  In fact, if you took patients with STEMIs or cancer and put them in areas of Ebola outbreaks, which are remote areas of Liberia, Sierra Leone, Nigeria, Senegal and Guinea, the mortality would probably be higher than Ebola is now.  Any disease process in remote areas yields a high mortality rate because of unavailable medical resources.  The actual mortality rate of Ebola in West Africa based on the first 4507 recent cases is 70 percent.  The mortality rate in hospitalized patients is 64.7 percent and 56 percent in health care workers.  So, even without substantial medical care (intravenous fluids), 30 percent of all patients survive and 44 percent of healthcare workers survive.  What is the mortality rate of Ebola patients who contracted it in the United States?  ZERO percent.  Although we have given plasma transfusions and monoclonal antibodies to these patients, we have no evidence that we help any patient beyond supportive care of IV fluids.  Even the one patient who was transferred to Germany, in septic shock with significant hypotension, received 30 liters of fluids and survived.  In the first 9 months of the recent outbreak, we know a couple of things.  The most common presenting symptoms are like anything else:  Fever (87%), fatigue (76%), decreased appetite (65%), vomiting (67%), and diarrhea (65%).  Less than five percent of patients had unexplained bleeding.  So, fever is not present in 13 percent of patients, which makes it the most common yet an unreliable finding to screen patients.  These symptoms could explain many diseases which are much more likely than Ebola.

            The transmissibility of diseases is explained by the R₀  factor.  From the first 4507 patients during the recent outbreak with Ebola or probable Ebola, this factor is 1.7-2.  The Sierra Leone type is the highest.  To put this into perspective, measles is 17-19. This represents the number of patients who will contract the disease from one individual without isolation.  The incubation period is 11.4 days and the rate of conversion to a positive Ebola test is within 4 days.  Of the twenty-seven outbreaks since 1967, none have resulted in a pandemic.

            So if mortality is not as bad as we initially thought, many people are afraid of Ebola because they never thought the disease would come to the United States.  This is not the first time we have seen Ebola in the United States.  In fact it was predicted that this was going to happen.  The book “The Hot Zone” by Richard Preston in 1992 predicted the reemergence of Ebola based on a monkey outbreak in Reston, Virginia (about 10 miles from Washington, D.C.).  On Oct 2, 1989, 100 monkeys were shipped via Amsterdam through Tokyo, Tipai to New York City.  They traveled down I-95 to Reston, Virgina.  On November 1, 1989, the monkeys began dying and were incorrectly diagnosed with Simian Hemorrhagic Fever, which turned out to be Ebola Virus.  The Level 4 Biosafety Lab at Fort Dietrick correctly analyzed the tissues of the monkey.  Interestingly, although no protection was initially used in Reston, not one person contracted Ebola from the sick monkeys.  The monkeys were euthanized and significant disinfection was performed over the next 11 days.

            Another fear is the amount of personal protective equipment (PPE) one must wear around these patients.  In fact, this is really no different than any other potentially infectious disease when patients are acutely ill with diarrhea or vomiting.  In many ways, it is less since Ebola is not naturally aerosolized.  I would not come into contact with bodily fluid of any acutely ill person without universal precautions. Ebola is no different in terms of many diseases except it is less transmissible than many.  We should be observing the same universal precautions in all patients.

            Quarantining patients has been a source of great debate.  We have marked 21 days in patients as a “magical number.”  Yet this is not true.  Five percent of patients may show symptoms past the 21 day mark.  However we must follow science and folks who have dealt with this process for a long time.  Doctors without Borders is one of the amazing agencies that have dealt with this disease for years and based recommendations on science on fact.  Quarantining is not necessary unless patients are symptomatic.  Of note they also agree that, “Ebola is a hard disease to catch.”  Unless you are in contact with diarrhea or feces or vomiting, no real risk exists.  I would add that you should not come into contact with these bodily fluids as a healthcare worker and simple gloves are not enough.  I have heard of folks going into rooms with a mask and gloves, but, like all patients, this is not universal precaution, and the mask does nothing for Ebola, which is not aerosolized.

            The host of Ebola seems to be the fruit bat, and coming into contact with patients who have the highest viral load or people who have recently died poses the greatest risk of disease transmission.  Additionally, other species which are taking secretions of tissues from fruit bats seem to be at risk as well, such as apes.

            Finally, my advice is to keep this virus in perspective.  Worry about diseases which result in bad outcomes every day.  Continue to use the same precautions that hopefully you have been using for years and do not believe rumors.  Use science and the community of infectious disease folks and evidence based articles to guide you.

Ebola Virus Disease in West Africa — The First 9 Months

of the Epidemic and Forward Projections NEJM Oct 16, 2014

Transmission dynamics and control of Ebola virus disease (EVD): A Review

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