WRITINGS FROM A WHITEBOARD WIZARD

The End, and, The Beginning

Well, here it is. The last day of my forties. I’m not really sure how I feel about that. Some kind of milestone? Maybe. Beginning of another chapter? Hopefully. One thing that I know from the 49 + years so far is that time waits for no one. It’s funny to look back and realize how fast it has flown. As I get older, that flight seems to get even faster. Worst part about that is, I don’t get to collect any frequent flier miles towards a free trip! LOL

A lot of good has happened. A lot of bad has happened. Basically, life, has happened. I’m sure anyone has their own rendition of the same. Different situations and experiences, obviously, but in the end, the same outline. Given the chance, there are things I would do differently – perhaps even change. My life hasn’t been perfect by any stretch of the imagination, but it’s been mine and I have learned to own it – taking the bad with the good.

I’m grateful for the opportunities to have helped people at their worst times and to continue to educate others to do the same. I never have sought out to make a “name” for myself. Some people say I have become a “name”, and that’s OK. I’ll always be good simply being the one behind the scenes, so to speak, but still making an impact – one professional at a time. I won’t sell a lot of books or be a marquee presenter that brings in large crowds at a conference, but the people that come to listen to me always get my best every single time. I see it as a privilege, and I’ll keep doing it as long as someone allows.

I miss home and I keep hoping that I’ll be back sooner than later. I miss my family and friends. Louisiana has not been totally unkind, but it has never been a part of me – which makes me (and others) wonder why I came back a second time. Things happen and decisions always have to be made in the hope I am better off. This was one of those decisions, and I am grateful that my current situation allows me to continue doing, me.

The beginning of this new decade is the first one in a while where I find myself single. Being on my own for almost four and a half years has allowed me to do things I never had. It’s also given me a lot of down time that has been detrimental to my outlook on life, and other people. I find that my cynical side has grown, leaving a sour taste in my mouth more than a few times. I do what I can to overcome it, and for the most part, I’ve done a pretty good job. It’s still a work in progress.

I don’t mind being alone, but feeling lonely is hard and it’s been the most difficult aspect to face. People comment on how much I travel and seem to always be on the go. One reason is because I truly like to travel, plain and simple. The other, is to keep my brain occupied and minimize my down time trigger. It works, plus it makes for good conversations. How many people can say they have had a drink in two separate states at the same time, while watching a pontoon boat made from a vintage yellow VW van come into the docks? There are still many places to go and people to see. I hope I’ll have the health and the time to do a lot of both.

One of my long-term goals is to finish a half marathon in 50 states. Right now, the count includes Ohio, Kentucky, Louisiana, Mississippi, Virginia, New York and Nevada. As long as my ticker, and my knee, hold out; I’ll be attempting two more this year in the Florida Keys and South Carolina and only have 41 more to go! Might be able to sneak one more in, perhaps. It’ll be fun trying, if nothing else! I’m not getting any younger, or skinnier for that matter. Just gonna have to keep trying on the latter. I plan to get to the Caribbean, “across the pond” and the other direction toward Hawaii and points further West. They are just waiting there, so why not go see what’s it all about, right? Might even find a travel partner for some of it as well, who knows?

The inevitability of a long life is that further losses occur. I’ve already lost close friends, mentors, students and family. I don’t look forward to the day where more will be gone, but I know it will happen. My hope is that I get to know these people and be with them as much as possible before they are lost. I’ll continue to give them the love and attention I always have and that they deserve.

There is much more I could comment about, but I’m going to close out by saying this: it’s been an up and down ride, but it’s been my ride. Some days I don’t like it, but most days I do. So, here’s to good health, further adventures and making more memories. 50 years in the books. Let’s see what the next 50 has in store.

WW

Shaken, Not Stirred

Case Presentation

EMS responds to a local convenience store for a 24-year-old male having a seizure.  The patient presents lying on the floor supine and convulsing in a tonic-clonic motion. He is unresponsive to verbal commands, and there is blood oozing from his mouth. A friend who accompanied the patient states that both of them had been drinking all day while binge-watching old episodes of Game of Thrones.  When they arrived at the carryout to purchase more beer, the patient complained that the lights in the store were bothering his eyes.  Almost immediately after saying that, he suddenly collapsed.  The friend caught the patient and lowered him slowly down to the floor, where he immediately began shaking. The shaking has been ongoing now for over ten minutes.  According to the friend, similar events have occurred this past year since the patient was in a motorcycle accident and hurt his head.  Initial vital signs reveal ventilations 30/minute, shallow and gurgling; pulse 112/minute and regular; blood pressure is unobtainable; pulse oximetry 91 percent on room air; blood glucose 134 mg/dL; skin is diaphoretic and warm to the touch.

What is a Seizure?        

A seizure is a sudden attack from abnormal electrical discharges within the brain that produces various physical manifestations (convulsions, sensory disturbances, alterations of consciousness).1 There are many types of seizures, which range in severity, and vary by where and how they begin in the brain. Most seizures last from thirty seconds to two minutes but can last much longer.  A seizure that lasts longer than five minutes, or a patient having more than one seizure within five minutes without returning to a normal level of consciousness between episodes, is called status epilepticus.2 This rare condition is more common in young children and elderly adults and can lead to permanent brain damage or death.

Seizures are classified into two groups: Generalized seizures and Focal seizures (also known as partial seizures).  Generalized seizures are a result of abnormal neuronal activity that rapidly emerges on both sides of the brain, while focal seizures originate in just one part of the brain.  Focal seizures are frequently described by the area of the brain in which they originate (frontal lobe, temporal lobe, etc.) and about sixty percent of patients with epilepsy have focal seizures.Be aware that not all seizures can be easily defined as either focal or generalized. Some patients have seizures that begin as focal seizures but then spread to the entire brain.

Generalized Seizures

  • Absence seizures: Termed also as petit-mal seizures, these often occur in children.  It may cause the patient to stare blankly into space and appear to have become temporarily disconnected from reality. These seizures may occur multiple times throughout a day and induce subtle body movements, such as eye-blinking or lip-smacking.
  • Tonic seizures: These seizures cause stiffening of the back, arms and legs muscles. They usually last less than twenty seconds and often happen during sleep. However, if a patient is standing up at the time, he or she can lose their balance and fall. This seizure is more common in patients who have a specific type of epilepsy.
  • Atonic seizures: They are also called drop seizures and cause a loss of normal muscle tone, which often causes a patient to fall or drop their head involuntarily.  This presentation appears similar to a marionette having its strings cut.  Because of the risk of falling, patients who tend to have atonic seizures may be wearing a helmet when you arrive on scene.
  • Clonic seizures: Characterized by repeated jerking movements of muscles on both sides of the body, usually affecting the neck, face, and arms.
  • Tonic-Clonic seizures: Also known as grand-mal seizures, these cause a combination of symptoms; including a sudden loss of consciousness, body stiffening and shaking, and sometimes loss of bladder and/or bowel control.  Additionally, the patient may bite their tongue or cheek, and a posterior head injury may be discovered during a physical exam.
  • Myoclonic seizures: These usually manifest as sudden, brief jerks or twitches of the arms and legs, as if the patient had been shocked. As an example, he or she may suddenly throw both hands into the air. Typically, there is no loss of consciousness.

Focal Seizures

  • Simple focal seizures: A small part of the brain is affected. These seizures may cause twitching of the fingers, arms or legs and make a patient smell, hear, feel or taste something strange.  They may also see flashes of light, become acutely nauseous, dizzy or diaphoretic, but do not lose consciousness. The patient may experience sudden and unexplainable feelings of joy, anger, or sadness as well.
  • Complex focal seizures: The part of the patient’s brain that controls emotion and memory evokes these type of seizure. Unlike simple focal seizures, the patient will have a change of consciousness or awareness.  They may display strange, repetitious behaviors such as eye- blinking, lip-smacking, hand-rubbing, mouth movements (chewing or swallowing), or even continuously walk in a circle. These repetitive movements are called automatisms.

Signs and symptoms of focal seizures may be confused with other neurological disorders, such as migraine, narcolepsy or mental illness. Some patients with focal seizures may experience auras – unusual sensations that warn of an impending seizure. These auras are usually focal seizures without interruption of awareness (e.g., dejà vu).3

Seizure causes and management

The most common cause of seizures is epilepsy, but not every patient who has a seizure has epilepsy.  Other causes include:  hypoxia; hypoglycemia; renal or liver failure; high fever, which can be associated with an infection such as meningitis; sleep deprivation; specific pain relievers/antidepressants/smoking cessation therapies; head trauma; stroke; brain tumor; abuse of illegal or recreational drugs; alcohol withdrawal or extreme intoxication.4 The physical exam can be helpful to distinguish an actual seizure from other causes of loss of consciousness with convulsions. Specifically, lateral tongue biting and urinary incontinence are more suggestive of an actual seizure than a syncopal event.7 Always follow an organized approach to rule out all possible causes and don’t let past medical history lead you to a premature diagnosis.

It’s crucial to treat seizures symptomatically and protect patients from injuries that may occur during seizure activity.5 If the seizure is post-trauma or fall, the cervical spine and airway should be managed with a chin-lift and jaw-thrust until a cervical collar can be applied. This applies to all patients found at the bottom of the stairs or whenever a fall from height is suspected. Maintain the airway by suctioning, as needed, and turning the patient on his or her side to avoid airway obstruction by the tongue.  Patients should be protected from harm by keeping them from sharp objects and possibly falling off an unsafe surface.

A reversible cause should be remedied specific to its etiology, along with basic and advanced interventions to attain and maintain adequate oxygenation, ventilation, and circulation.  An infection where the patient can be treated with antibiotics or the hypoglycemic patient that can be administered glucose via an appropriate route are examples. Non-reversible causes, in addition to the initial appropriate care, need to be managed with anticonvulsant drugs such as lorazepam, diazepam, or midazolam via the intramuscular, intravenous or intranasal route.  Keep in mind, these drugs don’t cure seizures or epilepsy, but rather work to control these conditions.  Regardless, the highest priority is to stop the seizure activity. Respiratory depression is a side effect of benzodiazepines, which can be detected immediately when monitoring waveform capnography. Assist ventilation with a bag-valve mask if respiratory depression occurs, and titrate ventilation rate and tidal volume to maintain an EtCO2 between 35 and 45 mm Hg.6

Case Conclusion

The patient’s airway is suctioned, and a properly-sized nasopharyngeal airway is easily placed in the patient’s right nostril. Oxygen is administered via a non-rebreather mask at an initial rate of fifteen liters per minute to attempt to attain a pulse oximetry level higher than 94 percent.  Despite the oxygen, the patient continues to seize, and intravenous access is temporarily unattainable.  The decision is made to administer ten milligrams of midazolam by the intramuscular route, as per protocol guidelines. The seizure stops almost instantly following administration, and the patient becomes postictal with a Glasgow Coma Score of seven.  Peripheral intravenous access is attained, and blood pressure of 88/50 is auscultated.  Fluid boluses of 250 milliliters normal saline are infused to correct the hypovolemia, and the patient is positioned left lateral recumbent on the ambulance cot.  The patient is placed in the ambulance for transport, and seven minutes later his GCS score improves to 13, still very lethargic and drowsy.  Blood sugar is rechecked, reading 112 mg/dL.  He now has a pulse of 102 beats per minute, breathing at 18 times per minute – still tolerating the nasal airway, and has a SpO2 of 97 percent.  The remainder of the transport is unremarkable. He is admitted for overnight observation and is released in the morning with no neurological deficits additional to his underlying history.

References
  1. “seizure.” Merriam-Webster.com. 2019. https://www.merriam-webster.com/dictionary/seizure (5 May 2019).
  2. Status Epilepticus. (n.d.). Retrieved from https://www.hopkinsmedicine.org/health/conditions-and-diseases/status-epilepticus.
  3. What are the different kinds of seizures? (n.d.). Retrieved from https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Hope-Through-Research/Epilepsies-and-Seizures-Hope-Through#3109_10.
  4. Seizures (n.d.) Retrieved from https://www.mayoclinic.org/diseases-conditions/seizure/symptoms-causes/syc-20365711.
  5. Edgerly, D. (2011, August 2). Patient Presents with a Seizure.  Retrieved from https://www.jems.com/articles/2011/08/patient-presents-seizure.html.
  6. Sullivan, B. (2016, June 13).  3 things paramedics need to know about seizures and respiratory compromise.  Retrieved from https://www.ems1.com/capnography/articles/99193048-3-things-paramedics-need-to-know-about-seizures-and-respiratory-compromise/
  7. Dingle, H.E., Slovis, C. (2017, April 10). Guidelines for Treatment of Prolonged Seizures in Children and Adults.  Retrieved from https://www.jems.com/articles/print/volume-42/issue-4/features/guidelines-for-treatment-of-prolonged-seizures-in-children-and-adults.html.

Opioid Overdose: Fact Vs Fiction

Opioids, prescription, and illicit are currently the leading cause of drug overdose deaths.  The current data from the Centers for Disease Control reports that 70,237 drug overdose deaths occurred in the United States in 2017. Opioids were involved in 47,600 of the cases (67.8% of all drug overdose deaths), and the sharpest increase in drug overdose fatalities was related to fentanyl and associated analogs (nearly 30,000 of the 47,600).6

The states with the highest rates of death (in order) were West Virginia, then Ohio, Pennsylvania, the District of Columbia, and Kentucky.1Opioid overdoses treated in emergency departments rose 30% from July 2016 through September 2017 in 52 areas within 45 states. Overdoses in the Midwest increased by 70%, and opioid overdoses in large cities increased by 54% in 16 states in that same time period.2

Needless to say, EMS personnel will likely encounter a patient suffering from an opioid overdose sometime during their career.

Case

A 30-year-old female is dropped off at the front door of your ambulance station.  The doorbell is rung, but when you approach the door, no one but her is present.  The patient is unresponsive, limp, and cyanotic.  Her airway appears to be clear of obstruction.  She is breathing shallowly at four breaths/minute with auscultated rales in the bases of both lungs. Pulse oximetry reads 65% on room air. The patient’s other vital signs are heart rate, 106 beats/min. and irregular; blood pressure 92/64 mmHg; CO2, 70 mmHg; blood glucose 80 mg/dL; and temperature, 99.60.  Further physical exam reveals pinpoint pupils and both her upper extremities appear to be covered with what look like needle tracks, multiple abscesses, and bruises in various stages of healing.  Her skin turgor is poor with signs of malnutrition and dehydration.  Two transdermal medication patches are found on the back of her right thigh.

Discussion

Opioid toxicity should be suspected when CNS depression, respiratory depression, and pupillary constriction are present.3 The human body has three main opioid receptors, located in sensory nerves, mast cells, and in cells of the GI tract.  Stimulation of these receptors generally results in euphoria, decreased perception of pain, and drowsiness. Mast cell effects (e.g., flushing, itching) are also common. GI effects include nausea, vomiting, and constipation. With most users, peak opioid effects are reached in ten minutes with the intravenous route, ten to fifteen minutes after nasal inhalation, and thirty to forty-five minutes with the intramuscular route.5 When overstimulated, opioid receptors desensitize the brainstem to rises in carbon dioxide, which causes respiratory depression, loss of protective airway reflexes and respiratory arrest. Cardiac arrest from opioid overdoses is usually secondary to respiratory arrest. Death results primarily from hypoxia due to apnea.

Lesser common causes of morbidity and mortality from opioid toxicity are acute lung injury and pulmonary edema, status epilepticus, and cardiotoxicity. Many long-term users may also develop adverse effects due to the introduction of contaminants into their product.  Cardiac, pulmonary, and hepatic damage may also be evident due to infections such as HIV, endocarditis or hepatitis (spread by needle-sharing and non-sterile injection techniques).

Serotonin syndrome occasionally occurs when certain opioids such as fentanyl, Demerol, codeine, or oxycodone are taken along with Selective Serotonin Reuptake Inhibitors (Paxil, Celexa, Prozac, Zoloft, etc.) or Monoamine Oxidase Inhibitors (Nardil, Marplan, Parnate, etc.).4It typically presents with one or more of the following signs or symptoms: agitation, restlessness, confusion, tachycardia, hypertension, hyperreflexia, diaphoresis, seizure, muscle tremors, dilated pupils and a core temperature greater than 100°F.

Initial Opioid Overdose Management

The overriding goal of treating an opioid overdose is to restore respiratory drive and airway reflexes, prevent respiratory and cardiac arrest and avoid causing severe opioid withdrawal.7

The first step is to evaluate the extent of the patient’s respiratory depression. Even if naloxone is clinically indicated, ventilatory support should always be provided immediately. Bag-valve-mask ventilation, including inserting oropharyngeal or nasopharyngeal airways, should be used to provide adequate oxygenation and ventilation until the patient can breathe adequately. Ventilatory support by itself may result in patient recovery as the accumulated carbon dioxide is expelled, and thus naloxone administration is not necessary.8   Assess waveform capnography and pulse-oximetry to guide ventilation rate and adequacy. Upon re-establishment of a gag reflex, position the patient in a recovery position, and be ready to remove any basic airway adjuncts.  Have suction readily available to prevent aspiration of any gastric contents.

Patients that present in a prolonged respiratory arrest (especially in patients where ventilation and naloxone administration fail to improve their condition) should have advanced airway management such as a supraglottic airway device or endotracheal tube insertion as a consideration, based on the EMS provider’s level of certification.  Be ready to differentially-diagnose for other conditions that may prolong the respiratory depression.  Blood glucose determination should be routine for altered mental status and may be a useful finding in this situation.

Opioid toxicity may also cause a patient to become bradycardic and hypotensive.  Thus, determination of a central or peripheral pulse can be difficult.  If a pulse is not detected, start chest compressions and attach defibrillator pads or an AED. The 2015 American Heart Association guidelines recommend standard BLS and ACLS practices for cardiac arrest secondary to opioid overdose.7, 9 Waveform capnography and capnometry can also be useful in this instance. If a capnography waveform appears with ventilation, even if a pulse cannot be detected, the patient has a functioning heart.  AHA recommends, in this case, that naloxone be administered.7

Naloxone Administration

Naloxone reverses overdoses by binding to opioid receptors, blocking stimulation and restoring the patient’s airway reflexes.  The need for rapid access to naloxone in the pre-hospital setting has expanded its use to include both first responders and laypersons in the forms of an auto-injector for intramuscular administration and a commercial nasal spray. Consequently, this recently has struck up numerous moral and ethical debates on professional medical websites and social media. Regardless of popular opinion of administration, a retrospective study which analyzed data from northern New England revealed that basic life support practitioners are as effective as advanced life support practitioners in naloxone administration.10

Before the administration of naloxone, application of restraints in a potentially violent patient is advisable, especially in close quarters or the back of an ambulance.  Common routes of naloxone administration include intravenous, intramuscular, and intranasal. There is some debate as to which route of delivery is most effective, but overall, the medication itself is extremely safe.  One of the significant drawbacks is if it is administered too quickly and/or in high dose concentrations.  The common side effects of such includes restoration of spontaneous breathing, but with associated extreme patient agitation, vomiting, and tachycardia.  More severe, but rarer, reactions include signs of opioid withdrawal syndrome (OWS).  Findings of naloxone-precipitated OWS include hypertensive emergency, seizure, pulmonary edema, ventricular tachycardia, ventricular fibrillation, and sudden death – primarily due to the sudden release of catecholamines.11, 12, 13

Thus, the dosing of naloxone should be based on restoring adequate breathing while minimizing the risk of opioid withdrawal symptoms.  This is best accomplished with dose titration and careful monitoring.  Typically, naloxone is recommended to be administered via the intravenous route, as it reaches peak blood concentration within minutes.  However, the time it takes to establish intravenous access, combined with a long-time IV opioid abuser patient with poor vasculature, may delay naloxone administration.

A method gaining more popularity is intranasal administration. It results in a more gradual emergence from the effects of opioids and allows EMS personnel to restore ventilations and airway reflexes without causing severe opioid withdrawal.  Where this method becomes more initially ineffective than the intravenous route is when the patient has co-ingested other substances.  Alcohol, benzodiazepines, fentanyl and/or one of its analogs, such as carfentanyl, usually require a higher dose of naloxone not typically delivered via the intranasal route

Occupational Exposure

Initially, most opioid users do not intentionally seek out fentanyl or carfentanyl.  However, these synthetics, which are 50-10,000 times more potent than morphine, have created a distinct concern among public safety and EMS personnel.

Given the prevalence of synthetic opioids, law enforcement and EMS agencies have become increasingly concerned about potential exposures while responding to medical calls, crime scenes, or during drug raids.14,15,16 However, here are the facts. Fentanyl needs moisture to penetrate the skin, and toxicity can’t occur from merely being in proximity to the drug.

Inhalation is an exposure route of concern.  Aerosolized fentanyl puts it in contact with mucous membranes of the nose and/or mouth, which may supply enough moisture to allow it to penetrate the body and enter the bloodstream.  Factually, at the highest airborne concentration potentially encountered, an unprotected individual requires nearly 200 minutes of exposure to reach a dose of 100 micrograms of fentanyl.17

Incidental contact of fentanyl on dry, intact skin is also unlikely to cause opioid toxicity.  For example:  If both palm surfaces were covered with concentrated fentanyl patches, it would take approximately fourteen minutes to receive 100 micrograms of fentanyl.17 Thus, accidental exposures that are typically seen in the pre-hospital setting aren’t likely to result in opioid toxicity of first responders and EMS personnel.

Standard nitrile medical gloves and duty uniforms provide adequate dermal protection. If suspected fentanyl powder is found on skin or clothing, the dry powder should be brushed away, and then the area should be cleaned with soap and water. Alcohol-based hand sanitizers should not be used for decontamination, as they do not wash opioids off the skin and may accelerate dermal drug absorption.17,18Respiratory protection isn’t required for routine operations. In the extremely unlikely event that it’s suspected that drug droplets or particles are suspended in the air, standard disposable N95 masks provide sufficient respiratory protection. OSHA-approved protection for eyes and face should be used during tasks where there exists a possibility of splash to the face.17

Case Conclusion

Scene safety, as always, is paramount.  As this was a drop-off and she is unresponsive, there is no telling what she may or may not have on her person, or in her pockets.  Be wary of needles, syringes with blood, etc.  Take proper precaution by wearing gloves at a minimum and have eye and respiratory protection available.  Based on her presentation, insertion of a nasopharyngeal airway and ventilation via BVM is established with good compliance, but she does not regain consciousness. The pulse oximetry reading increases steadily, and the capnometry reading decreases with every ventilation.  Attaining a SpO2 higher than 94% and a CO2 between 35-45 mmHg is ideal.  Her blood pressure and pupils remain unchanged.

It is imperative to perform a good head-to-toe examination in this case, and ones similar, in which the patient is a poor historian.  Doing so reveals the two medication patches.  If these are prescribed fentanyl, the FDA mandates that they must have a name and strength in a visible color, but many patches will not have any identification. Even though research will say that these two patches may not deliver enough fentanyl to cause toxicity (especially in her case where she appears to be a long time user), they can be safely removed with gloved hands and should be.

A peripheral IV line is easily established.  The patient is administered a dose of naloxone that allows her to regain breathing at a rate of 12/minute.  She is positioned in a left lateral recumbent position on the ambulance cot and transported to the local hospital.  En route, a fluid challenge of normal saline is infused to increase her blood pressure, and she is supplied oxygen at 2 Lpm via nasal cannula, which maintains an adequate SpO2.

References
  1. Scholl L, Seth P, Kariisa M, Wilson N, Baldwin G. Drug and Opioid-Involved Overdose Deaths – United States, 2013-2017. Morb Mortal Wkly Rep. ePub: 21 December 2018.
  2. Centers for Disease Control and Prevention. Opioid Overdoses Treated in Emergency Departments. CDC Vital Signs. Available at https://www.cdc.gov/vitalsigns/pdf/2018-03-vitalsigns.pdf. March 2018.
  3. Opioid Toxicity Clinical Presentation. December 13, 2018. Medscape. Available at https://emedicine.medscape.com/article/815784-clinical#b3. Accessed: June 5, 2019.
  4. Opioid Toxicity and Withdrawal. March 2018.  Merck Manual.  Available at https://www.merckmanuals.com/professional/special-subjects/recreational-drugs-and-intoxicants/opioid-toxicity-and-withdrawal.  Accessed June 5, 2019.
  5. Opioid Toxicity Pathophysiology. December 13, 2018. Medscape. Available at https://emedicine.medscape.com/article/815784-overview#a5. Accessed: June 5, 2019.
  6. National Institute on Drug Abuse. Overdose death rates [about 7 screens]. Rockville (MD): National Institute on Drug Abuse; 2018 August [cited 2018 Sep 26]. [Internet]. https://www.drugabuse.gov/related-topics/trends-statistics/overdose-death-rates [Google Scholar]
  7. Lavonas EJ, Drennan IR, Gabrielli A, Heffner AC, Hoyte CO, Orkin AM, Sawyer KN, Donnino MW. Part 10: special circumstances of resuscitation: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Cardiovascular Care. Circulation. 2015;132(suppl 2):S501–S518.
  8. Williams K, Lang E, Panchal AR, Gasper JJ, Taillac P, Gouda J, Lyng JW, Goodloe, JM, Hedges M. Evidence-Based Guidelines for EMS Administration of Naloxone.  Prehospital Emergency Care. 17 Apr 2019. https://doi.org/10.1080/10903127.2019.1597955. [Taylor & Francis Online]
  9. Sullivan B. (2016, Jan.8). 5 things EMS providers need to know about opioid overdose and respiratory compromise. Retrieved from: https://www.ems1.com/ems-products/Capnography/articles/47753048-5-things-EMS-providers-need-to-know-about-opioid-overdose-and-respiratory-compromise/
  10. Gulec N, Lahey J, Suozzi J, Sholl M, MacLean C, Wolfson D. Basic and advanced EMS providers are equally effective in naloxone administration for opioid overdose in Northern New England. Prehosp Emerg Care. 2018;22(2):163–9. doi:10.1080/10903127.2017.1371262. [Taylor & Francis Online], [Web of Science ®], [Google Scholar]
  11. Lameijer, H, Azizi N, Ligtenberg JJ, Ter Maaten JC. Ventricular tachycardia after naloxone administration: a drug related complication? Case report and literature review. Drug Saf Case Rep. 2014;1(1):2. doi:10.1007/s40800-014-0002-0.
  12. Kienbaum P, Thürauf N, Michel MC, Scherbaum N, Gastpar M, Peters J. Profound increase in epinephrine concentration in plasma and cardiovascular stimulation after mu-opioid receptor blockade in opioid-addicted patients during barbiturate-induced anesthesia for acute detoxification. Anesthesiology. 1998;88(5):1154-1161.
  13. Kim HK, Nelson LS. Reducing the harm of opioid overdose with the safe use of naloxone: a pharmacologic review. Expert Opin Drug Saf. 2015;14(7):1137–46. doi:10.1517/14740338.2015.1037274.[Taylor & Francis Online], [Web of Science ®], , [Google Scholar]
  14. Drug Enforcement Agency. DEA Warning to Police and Public: Fentanyl Exposure Kills. 2016. https://www.dea.gov/divisions/hq/2016/hq061016.shtml.
  15. McDaniels A. Deputy, two EMS providers treated for overdose symptoms responding to call. The Baltimore Sun, Baltimore, MD. 2017. http://www.baltimoresun.com/health/bs-md-harford-opioid-exposure-20170523-story.html.
  16. Greenslade B. 3 Winnipeg police officers possibly exposed to fentanyl, self-administer naloxone. Global News. 2017.
  17. American College of Medical Toxicology. ACMT and AACT position statement: preventing occupational fentanyl and fentanyl analog exposure to emergency responders. Phoenix (AZ): American College of Medical Toxicology; 2017 Jul 12. https://www.acmt.net/cgi/page.cgi/_zine.html/The_ACMT_Connection/ACMT_Statement_on_Fentanyl_Exposure
  18. Taxel S. (2019, May 7). Fentanyl Facts and Fiction: A Safety Guide for First Responders.  Retrieved from: https://www.jems.com/articles/2019/05/fentanyl-facts-and-fiction-a-safety-guide-for-first-responders.html

Pediatric Asthma

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 obvious nasal flaring, 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.

What is significant about his presentation and assessment findings?  What are your management strategies?  How sick is this child and will he get worse?  These are questions that have to be answered in a timely manner; even more so when it involves a pediatric patient.  Let’s discuss what is happening to him and what EMS professionals can do in the prehospital setting.

Case Discussion – Pathophysiology

Asthma is a 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 lesser degrees 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 hyper-inflated.  As the amount of hyper-inflated lung tissue increases, the child’s diaphragm is progressively flattened, causing a mechanical disruption of ventilation.  The increasing workload to ventilate is transferred onto the smaller and weaker intercostal and suprasternal muscles.  Once these muscles rapidly fatigue from stress and overuse, the onset of respiratory failure is quick.  Air trapping not only increases intra-thoracic pressure but also directly puts pressure on the child’s heart – similar to the mechanics of a cardiac tamponade.  Physical compression of the superior and inferior vena cava also occurs. The result is a lesser-than-normal amount of available blood return into the right atrium – reducing right ventricular filling, and systolic output. Coupled with this lack of volume, the heart has to force blood against an increased pulmonary artery pressure.  This is due to pulmonary capillary compression from the surrounding hyper-inflated lung tissue. The acute pulmonary hypertension expedites the acute right ventricular failure, poor perfusion to any remaining functional alveoli, and hypoxemia.

Hypoxemia also develops from collapsed alveoli.  They 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.  A working hypothesis as to why the alveoli collapse suggests that a lack of alveolar surfactant develops when the asthma immune response shuts down the surfactant cells. Once the amount of surfactant is insufficient to lower the surface tension between the alveoli and capillaries, the alveoli collapse.  In addition, pulmonary surfactant is essential to maintain patency of the terminal/respiratory bronchioles.10 Lack of surfactant causes those airways to collapse and become temporarily blocked, adding to the air trapping.

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 and hasten the rapid onset of respiratory arrest, followed quickly by cardiac arrest.

Patient Presentation

During an acute attack, varying degrees of dyspnea, tachypnea, tachycardia, accessory muscle use, retractions, coughing, jugular venous distention, audible wheezing, skin color, hyper-resonant lung sounds 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 a 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 and sufficient airflow is not restored.

Status asthmaticus is a life-threatening condition of progressively-worsening bronchospasm and respiratory dysfunction due to asthma, unresponsive to conventional therapy.  It typically progresses into respiratory failure and 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 percent. During an ongoing and unbroken asthma attack, the child becomes profoundly acidotic from retained carbon dioxide, mainly due to poor inspiratory and expiratory effort and diminished air movement through the lower airways.   This may initially manifest as an increased respiratory rate.  If uncorrected, though, the respiratory rate will decrease, possibly giving the EMS professional a feeling that the patient is getting better.  The fact is, the child is tiring and is transitioning from respiratory distress into respiratory failure.

Interventions and Management

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

Hypoxia is the number one killer of asthmatic patients.  Thus, first-line treatment of a patient with any degree of respiratory distress should be oxygen administration by the most efficient delivery method.  Not only does it help reverse the patient’s hypoxemia, but oxygen also acts as a bronchodilator – helping to open the lower airways.9   Albuterol is the other mainstay medication for asthma patients by its ability to relax bronchial smooth muscle and enhance mucous clearance.  It may be administered concurrently with oxygen, but should never delay oxygen administration. Ideally, albuterol is 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 and those in status, several other adjunctive therapies should be considered. Early administration of corticosteroids in addition to inhaled beta-2-agonists is recommended, typically at a dose of 2 mg/kg. Additionally, intravenous magnesium has been noted to produce positive bronchodilation effects within pediatric patients suffering from status asthmaticus.  It is dosed at 50 mg/kg IV over 10-20 minutes.  Common side effects include skin flushing and hypotension, which is rarely clinically significant and responds well to fluid administration.

Pediatric patients in prolonged status asthmaticus may require further aggressive treatment with epinephrine.  The intramuscular route is preferred and the medication should be injected into the pediatric patient’s lateral thigh. The proper dose is 0.01 mg/kg (0.1 mL/kg), using a 1:1000 concentration.  Life-saving therapy with intravenous epinephrine may be indicated for patients who don’t improve with intramuscular epinephrine and intravenous magnesium, but only if carefully done.

Intravenous epinephrine must be given very cautiously and slowly. Never give it as a push/bolus.   Add one milligram of epinephrine (1:1000) to an IV bag of 250 mL saline or D5W, and run this infusion through a micro drip chamber drop set, starting at 15 drops per minute. Piggyback this slow drip into a high-flow IV mainline so it gets into the patient’s circulation as quickly as possible. Recheck the patient for desired effects at one-minute intervals. Slow or discontinue the drip as the patient improves or if cardiac toxicity occurs.9

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. Consider ketamine administration if sedating prior to intubation.  Intravenous ketamine with doses starting at 2 mg/kg, is gaining favor as an adjunctive bronchodilator, especially for agitated patients in respiratory distress.8

The effects of positive pressure ventilation on the cardiovascular system are well known. In normal breathing, the negative pressure phase of inspiration assists venous return, alleviates pressure on the pulmonary capillaries, and encourages flow. With positive pressure ventilation, the intrathoracic pressure increases during inspiration causing a decrease in venous return, right ventricular output, and pulmonary blood flow.  Remember, this is already occurring in the asthmatic patient from lung hyperinflation.  Ventilate with lower rates and tidal volumes to provide enough time for the patient to exhale.  This will not only delay the increase in intrathoracic pressure, but also help to avoid barotrauma and increasing workload on the patient’s heart.

______________________________________________________________________________

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.

9.            Meredith, M. (2009, September 30). Attacking Asthma: Five steps to treat pediatric status asthmaticus.  Retrieved from: https://www.jems.com/articles/print/volume-34/issue-10/patient-care/attacking-asthma-five-steps-tr.html

10.          Hohlfeld, J.M., et.al. (1999). Dysfunction of Pulmonary Surfactant in Asthmatics after Segmental Allergen Challenge. AM J RESPIR CRIT CARE MED (159), 1803–1809.

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.