WRITINGS FROM A WHITEBOARD WIZARD

Pediatric Asthma

Case presentation

EMS responds to a residence for a seven-year-old male with a cough and trouble breathing. This episode began two hours ago and has been accompanied by a runny nose without any other symptoms. His mother has been treating him with albuterol by a nebulizer, but he has progressively become more short of breath.  Past medical history is notable for asthma since infancy, with multiple prior hospitalizations.  Physically, the patient appears to be in moderate respiratory distress, with suprasternal and intercostal retractions. His vital signs include a respiratory rate of 40/minute, heart rate of 120/minute, and pulse oximetry of 93 percent on room air. Lung exam is notable for diffuse inspiratory and expiratory bilateral wheezing, poor air movement and a prolonged expiratory phase. The remainder of the examination is unremarkable.

Case Discussion – Pathophysiology

Asthma is the most common chronic childhood disease, and a frequent reason for pediatric emergency medical treatment. It affects approximately 10-15 percent of all children in the United States.1 Risk factors include obesity, premature birth and a chronic environmental exposure to pollutants.  Some children are genetically predisposed, as asthma tends to be passed down through generations.  An acute asthma attack is commonly precipitated by factors such as an allergen exposure, stress, exercise, food additives, recent upper respiratory infections, exposure to cold air or tobacco smoke.

EMS professionals need to keep in mind that a child’s lower airway anatomy is proportionally smaller than an adult, and is easily compromised from a lesser degree of swelling and constriction.  In response to one of the aforementioned events, a series of reactions occur in the lower airway. First, the smooth muscle surrounding the bronchioles is stimulated by histamine and leukotriene, causing bronchoconstriction. Secondly, mucous glands and cells that line the lower airway are stimulated to secrete excessive mucous, which plugs the bronchioles. Finally, fluid shifts into the walls of the lower airway, resulting in inflammation and decrease in airway diameter. The net result is a narrowing of the small airways with increased resistance to airflow. 

These pathophysiologic changes cause distal alveoli to trap air and become hyperinflated.  As the amount of hyperinflated lung tissue expands, the child’s diaphragm is progressively flattened, causing a mechanical disruption of ventilation.  Increased workload for ventilation is transferred onto smaller and weaker intercostal and suprasternal muscles, leading to rapid fatigue and onset of respiratory failure.  The hyperinflated tissue also puts excessive pressure on pulmonary capillaries and collapses adjacent alveoli.  The acute pulmonary hypertension causes premature right ventricular failure, poor perfusion to any remaining functional alveoli and eventual hypoxemia.  Hypoxemia also develops from collapsed alveoli that are still being perfused, but are unable to participate in gas exchange. Blood flows through capillaries adjacent to the collapsed alveoli and returns to the left side of the heart, still deoxygenated.  

The increased ventilation rate in the distressed child accelerates volume loss, decreasing perfusion to multiple organ systems.  This, combined with the resultant hypoxia, leads to cellular anaerobic metabolism and systemic accumulation of lactic acid and ketones.  Once respiratory failure occurs, these by-products combine with increased levels of carbon dioxide to profoundly decrease serum pH.

Patient Presentation

During an acute attack, varying degrees of dyspnea, tachypnea, tachycardia, accessory muscle use, retractions, coughing, JVD, audible wheezing, skin color, and mental status changes manifest. Bronchiolitis may mimic asthma in children younger than two years of age, and wheezing can be a sign of foreign body ingestion in toddlers.2 Providers should observe the patient’s work of breathing as well as auscultate for abnormal lung sounds. The lack of abnormal lung sounds may be an ominous sign of poor air movement in a patient at risk for respiratory failure. Pertinent items from the patient’s history include prior diagnosis of asthma, onset, and triggers for the exacerbation, current asthma medications, and prior ED visits or hospitalizations for asthma (including intensive care unit admissions and/or intubations).

As a baseline, an acute asthma attack presents with some degree of respiratory distress. The presence of wheezing often characterizes the severity of the attack, and thus, the degree of bronchoconstriction. In a mild asthma attack, wheezing is typically audible at the end of expiration, indicating increased resistance to expiratory airflow. Oxygen saturation levels may be normal or slightly low.  During a more severe asthma attack, wheezing may be audible during inspiration and expiration, or may disappear completely. Oxygen saturation levels typically reflect hypoxemia, with readings that usually range from less than 90 to 94 percent.   Characteristically, as lower airway obstruction worsens, capnography waveforms develop a raised “shark-fin” shape. This shape progressively flattens toward the baseline if airway patency is not restored.

Status asthmaticus is a life-threatening condition of progressively-worsening bronchospasm and respiratory dysfunction due to asthma that is unresponsive to conventional therapy.  It typically progresses into respiratory failure or arrest and requires aggressive ventilatory and pharmacological interventions. The child with status asthmaticus presents with air hunger. Because of the profound bronchoconstriction and minimal airflow through the bronchioles, wheezing is either faint or completely absent. Oxygen saturation levels often reflect severe hypoxia, with readings well below 90%. As hypoxemia worsens, the workload on the ventricles of the heart increases, and the child becomes profoundly acidotic from associated hypercarbia.

Interventions and Management

Once the EMS professional concludes the most likely diagnosis is an asthma exacerbation, treatment should be centered around reversing bronchoconstriction and airway inflammation, correcting hypoxemia, rehydration and monitoring for complications – such as pneumothorax. 

First-line treatment of an asthma patient with any degree of respiratory distress should be albuterol. It relaxes bronchial smooth muscle and enhances mucous clearance. Ideally, albuterol is administered as a nebulized solution (2.5 milligrams (mg) per dose for patients less than 10 kilograms (kg), and 5 mg per dose for patients greater than 10 kg). Common side effects include tachycardia and tremors.  Rarely, children may experience arrhythmias such as supraventricular tachycardia. The addition of ipratropium bromide (0.5 mg per dose) to albuterol has been shown to positively influence a child’s outcome. The combination of ipratropium bromide and albuterol may be repeated, as needed, for persistent respiratory distress. 3,4,5,6,7 

For critically ill children, several other adjunctive therapies may be considered. Early administration of corticosteroids in addition to inhaled beta-2-agonists is recommended, typically at a dose of 2 mg/kg. Intravenous epinephrine rapidly relaxes bronchial smooth muscles and is dosed at 1.0 ml of 1:10,000 concentration, administered over one minute. Intravenous magnesium has been noted to produce good bronchodilation effects with pediatric patients in status asthmaticus.  It is dosed at 50 mg/kg.  Common side effects include skin flushing and hypotension, which is rarely clinically significant and responds well to fluid administration.

Mechanical ventilation may be necessary in rare cases. Non-invasive ventilation with bi-level positive airway pressure (BiPAP) can help stave off intubation and preserves the conscious patient’s respiratory drive. Intubation and mechanical ventilation are the last resort for patients with refractory respiratory failure and/or respiratory arrest. It is difficult to match an asthma patient’s hyperventilation, and lower tidal volumes should be used to avoid barotrauma in the setting of hyperinflation. Finally, intravenous ketamine at doses starting at 2 mg/kg, is gaining favor as an adjunctive bronchodilator, especially for agitated patients in respiratory distress.8

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References

1.            Shah MN, Cushman JT, Davis CO, Bazarian JJ, Auinger P, Friedman B. The epidemiology of emergency medical services use by children: an analysis of the National Hospital Ambulatory Medical Care Survey. Prehosp Emerg Care. 2008 Jul-Sep;12(3):269-76.

2.            Lerner EB, Dayan PS, Brown K, Fuchs S, Leonard J, Borgialli D, Babcock L, Hoyle JD, Kwok M, Lillis K, Nigrovic LE, Mahajan P, Rogers A, Schwartz H, Soprano J, Tsarouhas N, Turnipseed S, Funai T, Foltin G., Pediatric Emergency Care Applied Research Network (PECARN). Characteristics of the pediatric patients treated by the Pediatric Emergency Care Applied Research Network’s affiliated EMS agencies. Prehosp Emerg Care. 2014 Jan-Mar;18(1):52-9.

3.            Adcock IM, Maneechotesuwan K, Usmani O. Molecular interactions between glucocorticoids and long-acting beta2-agonists. J. Allergy Clin. Immunol. 2002 Dec;110(6 Suppl):S261-8.

4.            Stead L, Whiteside T. Evaluation of a new EMS asthma protocol in New York City: a preliminary report. Prehosp Emerg Care. 1999 Oct-Dec;3(4):338-42.

5.            Knapp B, Wood C. The prehospital administration of intravenous methylprednisolone lowers hospital admission rates for moderate to severe asthma. Prehosp Emerg Care. 2003 Oct-Dec;7(4):423-6.

6.            Nassif A, Ostermayer DG, Hoang KB, Claiborne MK, Camp EA, Shah MI. Implementation of a Prehospital Protocol Change For Asthmatic Children. Prehosp Emerg Care. 2018 Jul-Aug;22(4):457-465.

7.            Dylla L, Acquisto NM, Manzo F, Cushman JT. Dexamethasone-Related Perineal Burning in the Prehospital Setting: A Case Series. Prehosp Emerg Care. 2018 Sep-Oct;22(5):655-658.

8.            Gries DM, Moffitt DR, Pulos E, Carter ER. A single dose of intramuscularly administered dexamethasone acetate is as effective as oral prednisone to treat asthma exacerbations in young children. J. Pediatr. 2000 Mar;136(3):298-303.

Postpartum Emergencies

Ah, childbirth—the miracle of life. Some EMS professionals may make several calls in which they place “storks” on their preverbal career belts, while others will never get the chance. In actuality, most emergencies and maternal deaths occur after childbirth, during the postpartum period, according to the World Health Organization.   Rapid change is present within the first six to twelve hours after birth, and thus, creates a potential for an immediate crisis—postpartum hemorrhage, embolism, and pre-eclampsia being the most common emergencies. However, major changes in hemodynamics and metabolism can take place up to six weeks after birth.1

In this article, we’re going to look at our three most likely crises in different scenarios and discuss what a prepared EMS team can do.

Case 1: Postpartum Bleeding

A 32-year-old female has been home for four days after delivering an 8lb., 10 oz. baby. She has been active at home and noticed some vaginal bleeding after the first day home. The bleeding has persistently worsened the past three days. When she got up in the middle of the night to tend to the baby, her husband heard a crash, found she had fainted and called 911. She presents with pale, cool, clammy skin, BP: 86/50, Pulse: 130, RR: 24, Pulse Ox: 99% room air, and mentating normally.

Postpartum hemorrhage is the leading cause of maternal death, and accountable for 25% of all annual deaths, globally.2 It is defined as blood loss greater than 500 milliliters following a normal vaginal delivery, or greater than one liter following a cesarean section within 24 hours of birth. A useful mnemonic to help remember the major causes of postpartum hemorrhage is “Four T’s”:  Tone, Trauma, Tissue, and Thrombin (coagulopathy).

Tone refers to uterine tone, and in this instance, lack thereof. It’s the most common cause of postpartum hemorrhage, occurring once in every twenty deliveries. Causes include prolonged labor, grand multiparity, a newborn weight greater than 8.5 pounds, a maternal age greater than 35, maternal oxytocin or magnesium administration, and multiple gestations.Hemorrhage from trauma typically is induced by uterine, cervical, perineal or vaginal lacerations. Less likely causes include uterine inversion and uterine rupture. An invasive placenta can lead to retained tissue. Not only will this increase the likelihood of postpartum hemorrhage, but also the development of endometritis. An invasive placenta occurs once in every 533 pregnancies and has the potential for blood loss that exceeds three liters.4,5,6 Albeit rare, coagulation disorders, whether from an inherited form of hemophilia, or an acute case of sepsis leading to disseminated intravascular coagulation, increases the potential for massive blood loss.

Keep in mind, at full term, a pregnant female’s plasma volume increases close to 50% of her average non-pregnant volume. This equates to about 1250 milliliters that she can lose, in addition to another 1500 milliliters, before showing any visible signs of shock. Have a high index of suspicion for massive blood loss and treat aggressively before signs appear with a postpartum female. Prehospital management centers around controlling bleeding externally by placing pads over, not within, the vaginal opening; fundal massage, as needed; IV fluid replacement titrated to a sufficient mean arterial pressure, and oxygen administration.

Case 2:  Embolism

You are called to a home of a 30-year-old female with chest pain. She delivered a healthy baby one week ago, now complaining of chest pain with deep inspiration, dyspnea, and painful left leg swelling. Her lung sounds are clear, skin is pale, warm, dry; BP: 106/82; Pulse:130; RR: 28 Pulse Ox: 83% room air.

Pulmonary embolism is the second most common cause of pregnant female death in the U.S. and is fifteen times more likely to develop during the postpartum period.7 When a female is pregnant, her body naturally increases the production of products responsible for making a blood clot, while at the same time, decreasing the production of anticoagulants. The reversal of this process may take days to weeks, leaving a new mother susceptible to pulmonary vessel blockage. Another source for a maternal pulmonary embolism is from amniotic fluid. It’s a rarer condition but carries a much higher mortality, usually occurring within 48 hours after birth. Risk factors include a history of placenta previa or abruption, pre-eclampsia, recent cesarean section, and multiparity.

One prevalent theory is that the amniotic fluid enters the mother’s bloodstream via a breach in the placenta, resulting in a bubble that eventually lodges within the pulmonary trunk or the branches of the left and right pulmonary arteries. Another theory surmises that the entry of amniotic fluid into the mother’s bloodstream activates her inherent immune response, producing what appears to be an acute anaphylactic reaction. In either case, the clinical presentation is similar. The patient will have signs/symptoms of acute respiratory failure, cardiogenic shock, and disseminated intravascular coagulation.8

An amniotic fluid embolism is unpredictable, unpreventable, and has no specific management.  EMS professionals will be charged with the task of managing the presenting respiratory and cardiovascular compromise. Standard supportive BLS and ALS measures as well as oxygen administration by the most effective means, IV fluids and/or vasopressors to attain a mean arterial pressure above 60 mmHg, and intravenous or intramuscular epinephrine, if required.  Even with aggressive and proper management, these postpartum patients may not respond positively. Be prepared for cardiac arrest at all times.

Case 3:  Pre-Eclampsia

Your patient is a 38-year-old female complaining of a bad headache, blurred vision and that her stomach hurts—pointing to the upper right abdomen. She also tells you that she had her first child a week ago. Her pregnancy was normal and she has never had any medical problems. Vital signs are BP: 186/112, Pulse: 98, RR: 14, Pulse ox: 100% room air.

Pre-eclampsia is a pregnancy-related illness on a spectrum which includes eclampsia and HELLP syndrome. It typically occurs after twenty weeks’ gestation, but can also occur as late as six weeks postpartum. Pre-eclampsia is twice as prevalent with first-time mothers and occurs in 4% of all U.S. pregnancies.Risk factors include: first-time pregnancy, twins, advanced maternal age, gestational diabetes, a history of hypertension, and obesity.

It occurs secondary to an arterial malformation within the placenta. These arteries are supposed to dilate during placental development but never do. As a result, placental tissue becomes ischemic, releasing vasoconstrictive and inflammatory products into the mothers’ bloodstream.  These products cause characteristic hypertension, peripheral edema, and end-organ damage (most notably to the kidneys and liver). Liver damage manifests as HELLP syndrome, which stands for Hemolysis, Elevated Liver enzymes, and Low Platelet count. HELLP can appear anytime between 48 hours to seven days postpartum and can cause the liver to rupture, as well as increase the amount of peripheral edema, bleeding, and pain.10

Postpartum pre-eclampsia is defined by a systolic blood pressure greater or equal to 140 mmHg or diastolic blood pressure greater or equal to 90 mmHg. There are many additional criteria included to make this diagnosis, but in the prehospital setting look for the following: severe right upper abdominal quadrant or epigastric pain, bleeding, nausea/vomiting/indigestion with pain after eating, pulmonary edema, blurred vision, peripheral edema, and/or a severe, persistent headache.

The definitive treatment for women with HELLP syndrome and pre-eclampsia is the delivery of the baby. Obviously, during the postpartum period, other management strategies need to be made by EMS professionals. Unmanaged, pre-eclampsia will develop into the convulsive state known as eclampsia. Measures must be taken to prevent this, as the likelihood of maternal death increases significantly. Along with standard BLS and ALS interventions, position the patient to prevent any possible aspiration, should a seizure occur.  When an IV is established, the primary medication is magnesium sulfate. Administer a loading dose between four and six grams over fifteen minutes, per local protocol, and follow with a continuous infusion of one to two grams per hour. This is for seizure resolution/prevention as well as blood pressure reduction. Target numbers for blood pressure, generally, are less than 150 mmHg systolic and less than 100 mmHg diastolic. Additionally, various beta-blocking agents, such as labetalol, may be administered to assist in lowering blood pressure.

References
  1. Brown JS, Posner SF, Stewart AL. J Am Geriatr Soc. 1999 Aug; 47(8):980-8.
  2. Ngwenya S. Postpartum hemorrhage: incidence, risk factors, and outcomes in a low-resource setting. Int J Womens Health. 2016 Nov 2;8:647-650.
  3. Retrieved from: https://www.healthline.com/health/pregnancy/complications-delivery-uterine-atony#causes-and-risk-factors.
  4. Bowman ZS, Eller AG, Bardsley TR, et al. Risk factors for placenta accreta: a large prospective cohort. Am J Perinatol. 2014;31:799-804.
  5. Sadashivaiah J, Wilson R, Thein A, et al. Role of prophylactic uterine artery balloon catheters in the management of women with suspected placenta accreta. Int J Obstet Anesth. 2011:20:282-287.
  6. Committee on Obstetric Practice. Committee opinion no. 529: placenta accreta. Obstet Gynecol. 2012;120:207-211
  7. Retrieved from: https://www.cdc.gov/ncbddd/dvt/data.html.
  8. Benson MD. A hypothesis regarding complement activation and amniotic fluid embolism. Med Hypotheses. 2007;68:1019–25
  9. Ananth CV, Keyes KM, Wapner RJ. Pre-eclampsia rates in the United States, 1980-2010: age-period-cohort analysis. BMJ. 2013;347:f6564.
  10. Retrieved from: http://americanpregnancy.org/pregnancy complications/hellp-syndrome/

Success Tips in 3 Words

  1. Drink more water.
  2. Watch less TV.
  3. Action makes traction.
  4. Try new things.
  5. Hang in there.
  6. Celebrate small wins.
  7. Aim higher sooner.
  8. Never stop learning.
  9. Start fresh today.
  10. Write that letter.
  11. Practice deep listening.
  12. Pay yourself first.
  13. Seize the day.
  14. Life is good.
  15. Eat more vegetables.
  16. Thank your Mom.
  17. Make others shine.
  18. Ask me anything.
  19. Think WAY bigger.
  20. Focus your energies.
  21. Now beats later.
  22. Zig don’t zag.
  23. Don’t get distracted.
  24. Always ask “Why?”
  25. Amp it up!
  26. How doesn’t matter.
  27. Invite and engage.
  28. Make silly faces.
  29. Get off email.
  30. See the sunrise.
  31. Simplify, eliminate, outsource.
  32. Kiss your dog.
  33. Write it down.
  34. Ask for help.
  35. Never give up.
  36. Decide, organize, act.
  37. Sharpen your edge.
  38. Lose some weight.
  39. Hammer it out.
  40. Doodle more often.
  41. Drink hot coffee.
  42. Expand your circles.
  43. Consider crazy alternatives.
  44. Not so fast.
  45. Get a massage.
  46. Unlock, unblock, unleash
  47. Blow ’em away.
  48. More chocolate, please.
  49. Fill your bucket.
  50. Don’t shy away.
  51. Give more generously.
  52. Don’t be scared.
  53. Freshen it up.
  54. Go play outside.
  55. Thank your heroes.
  56. Respond, don’t react.
  57. Sing real loud.
  58. Schedule “me” time.
  59. Live the dream.
  60. Invest in yourself.
  61. Seek the truth.
  62. Avoid the obvious.
  63. Relationships are perishable.
  64. Avoid the news.
  65. Make that call.
  66. Hire the weirdo.
  67. Speak more honestly.
  68. Track your progress.
  69. Decisions drive momentum.
  70. Take notes everywhere.
  71. Look further ahead.
  72. Stop playing small.
  73. Sell the dream.
  74. Deliver the goods.
  75. Never shortchange yourself.

Sometimes….pizza

Depression.

Suicide.

Websites and news outlets almost on a daily basis announce another death of one of our brothers or sisters in public service.  Some are accidental or in the line of duty, but what about the others we hear about taking their own life outside of work?  What was going through their mind before he or she completed the task?  How long had they been feeling that suicide was the permanent solution to a temporary problem?  Did anyone notice, and if so, did they say anything?

It’s been estimated that 15-25% of first responders suffer from PTSD and that the rate of suicide among first responders is 2–3 times that of the general population [more than 1 in 20 EMT deaths are due to suicide (2)].  Why?  Some would say it’s inherent to the people that choose the profession of public service.  Others would say it’s the stress, the long hours with little pay, the conditions we work under, or dealing with the public, in general.

It might be any of those issues, but I’d offer up this.  According to the Center for Disease Control, it is estimated that 1 in 10 Americans suffer from some type of depression.  Additionally, 80% of the people who have symptoms of clinical depression are not receiving any specific treatment.  Realistically, the possibility you know or work with someone who suffers from depression is very high.

How many times have you noticed that a colleague, coworker, friend or family member appeared to be what you would label “depressed”?  How did you come to that conclusion?  Maybe he or she just weren’t themselves, were more withdrawn than normal, or simply just seemed to have more bad days than good?  Many times, someone we know is depressed, but we miss it, or worse, don’t bring it up in conversation. But why? There are lots of reasons, not limited to: it’s an awkward topic, the fear of upsetting that person further, simply keeping to oneself because “it’s not my business”, or you’re unsure if it really is depression and God forbid you bring up this sensitive subject and be wrong, right?

How can you tell? I’d refer you to a simple mnemonic (InSADCAGES) developed by my colleague and friend, Dwight Polk:

Interest – lack of interest in things s/he usually takes comfort
Sleep – either too much or too little
Appetite – some eat to forget, others forget to eat
Depressed mood
Concentration – can’t seem to focus, sometimes even on simple tasks
Activity – the person who abruptly seems to transform into a gym rat, or the couch potato
Guilt
Energy – lack thereof
Suicide – thoughts, words and/or attempts

People suffer from depression for a number of reasons.  Some, it’s simply a matter of screwed up physiology, and abnormal levels of serotonin and dopamine in the brain. Heredity plays a big part – researchers have identified several genes common in people with bipolar disorder and depression. Long-term use of medications for high blood pressure, birth control and even some types of sleeping pills have been linked to the development of depression, as have diets with deficiencies in folic acid and vitamin B12.  People who suffer from heart disease (depression occurs in up to half the people who have had a heart attack), stroke, diabetes, cancer, dementia, and/or an under-active thyroid gland are at a higher risk, statistically.  Even something as simple as personality can predispose someone to depression, especially those who are overly-dependent, self-critical, pessimistic or have low self-esteem.

I am one of the many who suffer with depression.  Maybe you are too.  I’ve been to therapy, took medications to no avail, read books to try and change my outlook.  I have learned to deal with it and I usually have more good days than bad.  But, the bad days still come, sometimes worse than normal and sometimes over multiple days.  I get through because I’ve learned how to cope.  It might be a sit down in the park, a drive in the car, a chat with a friend or family member, or a good rerun of a favorite movie.  Sometimes, the best thing that fixes it is just enjoying a beer and pizza. 

It is estimated that every 40 seconds, someone in the world successfully commits suicide.  Every 41 seconds, someone is left behind to try and make sense of it.  Suicide is the 10th leading cause of death in the U.S. and most recent data shows that from 2016 to 2017, the death rate increased 3.7%. (1). 

Truthfully, not everyone who is depressed is suicidal and not everyone that is suicidal is depressed.  When we hear about another suicide of a brother/sister, or anyone for that matter, we have no idea how terrible he or she must feel to get to that point.  Yet, we always say: “How could they do such a thing?”  “It was such a selfish act.”  “I would never do something like that.”  and on and on.  All the days I have felt depressed, I never had a conscious plan to take my life.  August 30, 2013 changed all that.  I was driving back from New Orleans across Lake Pontchartrain.  I hadn’t been feeling well, mentally, the entire day, but I never had thoughts of killing myself.  As I got halfway across the causeway, suddenly I felt my mind falling into the deepest, darkest, saddest, most horrible hole.  At that moment I remember thinking, to get out of that hole the solution was to drive my car off the bridge and into the water.  So, I started to do just that.  When my front tire hit the guardrail, the jolt immediately snapped me out of it and I jerked the wheel back the opposite direction.  I drove onto one of the crossovers and just sat there.  The thought was completely gone, but now my consciousness turned to “what did I just almost do?” There was no plan, no preparation.  Just a few minutes of major distress that could have had a disastrous outcome. 

I suspect there are many who have committed suicide had a similar experience.  However, there are many others that have thoughts for so much longer.  These are the people we hear or know that develop the plan, write the letters, the emails the tweets or post something on Facebook.  They say things that alert us, give away prize possessions, make funeral arrangements out of the blue, spend all their money, etc.  

I know the darkness, the pain, and the anguish that depression causes.  Maybe indirectly it lead to my near-incident.  Maybe it was something else.  Similarly, when this happens to others, maybe there just isn’t the chance to think and the result is heartbreaking.  Those are the one’s we probably can’t help, but I know there are so many more we can.  If you feel suicide is the only way out of your problem(s), consider this:  call me.  I don’t have all the answers, but I’ve been there and luckily I’m still here.  419-704-9701.  Leave me a voice mail, if need be.  I’ll call you back. 

If you don’t want to talk to me, talk to someone.  You are not worthless, a piece of shit, or anything else your mind tricks you into thinking.  Don’t have anyone or don’t want to let anyone close to you know how you’re feeling?  It’s OK.  It really is.  

I would suggest these resources:

National Suicide Prevention Lifeline 1-800-273-8255

Disaster Distress Helpline  1-800-985-5990

Fire/EMS Helpline 1-888-731-3473  or 1-206-459-3020

Veterans Crisis Line  1-800-273-8255; press 1

Police Helpline  1-800-267-5463

Traumatic Brain Injured Vets 1-866-966-1020

https://www.safecallnow.org

http://www.frsn.org

https://www.nvgc.org/programs/share-the-load-program/

http://www.copline.org

https://www.ptds.va.gov/public/treatment/therapy-med/disaster_mental_health_treatment.asp

*Help & Resources*

We always say in public service that we are the helpers and not supposed to be the help-ee’s; that we should just shrug it off, suck it up, let it go…whatever.  We’re human.  Sometimes life, the job or who we are get the best of us.  When you feel that way, don’t be afraid to say something.  Trust me, someone is always willing to listen.  Talk.  You’re too important.

WW

 

References

1. Murphy SL, Xu JQ, Kochanek KD, Arias E. Mortality in the United States, 2017. NCHS Data Brief, no 328. Hyattsville, MD: National Center for Health Statistics. 2018.

2.  Counts, C. (2018, 11/13). Making EMS Count.  Retrieved from www.ems1.com.

Musings

Over my 20 + years of teaching, I’ve come to adopt certain concepts and mantras that hold true through the test of time.  Here are some of my favorites.

  1. Retractions of any kind are just one thing – BAD
  2. Just remember, your patient didn’t read the textbook.
  3. There is Registry and then there is Reality.
  4. You bag groceries and ventilate patients.
  5. Examine thoroughly, so you can anticipate and treat properly.
  6. Just because you can, doesn’t mean you should.
  7. Always be prepared because Murphy is always watching.
  8. You can’t count respirations, but you can count ventilations.
  9. When faced with an obstacle, focus and work the problem.
  10. Physiology is how the body works, pathophysiology is how it’s busted. You must have a working knowledge of both.
  11. Every willing student can learn, s/he just won’t learn the same way as their peers.
  12. The best educators are flexible and can diversify their delivery of information.
  13. There is no substitute for a positive, encouraging, and understanding mentor.
  14. Teachers make the slides; Instructors read the slides; Educators don’t need the slides.
  15. When a student mentions the “Q” word during a clinical rotation, preceptors cringe.

 

What are some of your guiding principles that have stuck with you throughout your career?