Trauma Tuesday: Electrocution Injuries

 Epidemiology

-       3 primary age groups

o   Toddlers – household sockets, appliances, etc.

o   Adolescents – risk-taking behavior

o   Adults – occupational hazard

-       Lightning strikes – account for 50-300 deaths per year in US (mostly Florida)

-       ~6,500 injuries and 1,000 deaths annually from all electrocution injuries

 

Classification

-       Low voltage: ≤1000 volts (V)

o   Household outlets in US typically 120 V

-       High Voltage: >1000 V

o   Power lines > 7000 V

-       Alternating current (AC) = electrical source with changing direction of flow  household outlets

o   Induces rhythmic muscle contraction  tetany  prolonged electrocution as individual is locked in place

o   Although generally lower voltages, can be more dangerous than DC as the time of electrocution is much higher

-       Direct Current (DC) = electrical source with unchanging direction of current of flow  lightning strikes, cars, railroad tracks, batteries

o   Usually induces a single, forceful muscle contraction  can throw an individual with significant force  higher risk of severe blunt trauma 

 

Mechanisms of Injury

-       Induced muscle contraction  rhabdomyolysis

-       Blunt trauma

-       Burns

o   Internal thermal heating – most of damage caused by direct electrocution

o   Flash/Arc burns – electricity passes over skin causing external burns

o   Flame – electricity can ignite clothing

o   Lightning strikes can briefly raise the ambient temperature to temperatures greater than 54,000F

 

Severity of Injury – is determined by…

-       Type of current – AC vs. DC

-       Duration of contact

-       Voltage

-       Environmental circumstances (rain, etc.)

 

Clinical Manifestations

-       Cardiac – 15%, mostly benign and occur within few hours of hospital stay

o   Arrhythmias - Most occur shortly after the event, though non-life-threatening arrhythmias can occur a few hours after the event and are usually self-resolving. Generally, …

§  DC = asystole

§  AC = ventricular fibrillation

o   Other EKG findings – QT prolongation, ST elevations, bundle branch blocks, AV blocks, atrial fibrillation

-       Pulmonary

o   Respiratory paralysis – diaphragmatic muscle

o   Blunt trauma – pneumothorax, hemothorax, pulmonary contusions, etc.

-       Neurologic – generally, patient can APPEAR DEAD but is the cause of neurologic electrocution and may be temporary. IE.

o   Coma

o   Fixed, dilated pupils

o   Dysautonomia

o   Paralysis or anesthesia

-       Renal – Rhabdomyolysis

-       Skin – All kinds of burns

-       MSK – from severe muscle contractions

o   Always assume C-spine injury

o   Compartment syndrome

o   Fractures/Dislocations

 

Management – we’ll divide them into categories of severity. Basically, always do an EKG!!

 

1)    Mild (<1000V) – examples include brief house outlet shock, stun gun

a.     EKG – other work-up such as troponin and CPK usually unnecessary

b.     If history/physical unremarkable (patient endorses brief contact with house outlet) patient can be discharged without further work-up

c.     If PMH puts patient at higher risk of arrhythmia (cardiac disease, sympathomimetics) can do a brief period of telemetry observation

d.    Can always observe 4-8 hours to be on the safe side

e.     High Risk Features

                                               i.     Chest pain

                                             ii.     Syncope

                                            iii.     Prolonged exposure

                                            iv.     Wet skin

2)    Severe Electrocution (>1000V) – industrial accidents, lightning strikes

a.     Coding – pursue usual ACLS

                                               i.     Keep in mind traumatic causes of arrest (tension pneumothorax, etc.)

                                             ii.     KEY FACT: remember that patients with fixed, dilated pupils, no respiratory effort, and no spontaneous movement may only have TEMPORARY neurologic stunning

                                            iii.     Pursue resuscitation longer than usual as patient with ROSC can still have good outcomes  does not appear to be any definitive guidelines on when to terminate, at physician discretion

b.     Otherwise, broad medical and traumatic work-up and likely admission for telemetry monitoring (basically just send all the labs and images)

                                               i.     Start with primary/secondary trauma survey and further imaging as required

                                             ii.     Don’t forget CPK to assess for rhabdomyolysis

c.     Consider transfer to burn center

 

TL;DR

-       Treat as you would a trauma/burn patient

-       Most household outlet shocks – history/physical, EKG, and likely quick discharge unless high risk features

-       Industrial shocks – at best admit for telemetry. At worst prolonged ACLS as good outcomes are possible. Don’t forget traumatic causes such as tension pneumothorax

 

http://brownemblog.com/blog-1/2020/4/14/acute-care-of-the-electrocuted-patient

http://www.emdocs.net/electrical-injury/

http://www.emdocs.net/em3am-electrical-injuries/

http://www.emdocs.net/em-cases-electrical-injuries-the-tip-of-the-iceberg-view-larger-image/

https://www.tamingthesru.com/blog/air-care-series/electrocution

 

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POTD: Peripartum Cardiomyopathy

POTD: Peripartum Cardiomyopathy

Causes:

  • Infectious (EBV, CMV, HSV)

  • Genetics

  • Pre-eclampsia

  • Fetal cells present in the maternal system that elicit an inflammatory response

Clinical Findings (same as CHF findings):

  • Tachycardia

  • Decreased pulse oximetry (should be ≥ 97% at sea level).

  • Blood pressure may be normal. (systolic >140 mm Hg and/or diastolic >90 mm Hghyperreflexia with clonus suggest preeclampsia).

  • Elevated jugular venous pressure

  • Third heart sound (turbulent ventricular filling secondary to poor wall relaxation from dilated ventricle)

  • Loud pulmonic component of the second heart sound (increased right sided flow)

  • Mitral or tricuspid regurgitation

  • Pulmonary rales

  • Peripheral edema

  • Ascites

  • Hepatomegaly

Management:

  • CBC- to see if there is significant thrombocytopenia

  • CMP- to see if there is any dysfunction in creatinine, LFTs, albumin

  • Urine dipstick- to check if there is any proteinuria

  • EKG

  • Echocardiogram

  • CXR

  • Stress testing

  • OBGYN, Cardiology consult in addition to reaching out to potential transplant hospitals

Treatment:

  • Digoxin: first line in pregnancy

  • Loop diuretics; Start with 10 mg of furosemide, as pregnant women have an increased glomerular filtration rate (GFR) that facilitates secretion of the drug into the loop of Henle.

  • Hydralazine and nitrates: afterload and preload reduction

  • B- Blockers (carvedilol or metoprolol): decrease all-cause mortality and hospitalization in those with systolic dysfunction.

  • Heparin for EF<30% (high risk of venous and arterial thrombosis)

  • LVAD

  • May ultimately need heart transplant

  • Delivery- Unless the mother is decompensating, you can manage her medically until delivery is possible. If the mother is not responding to medical therapy or if the fetus must be delivered for obstetric reasons, the best plan is to induce labor with the goal of a vaginal delivery. C-section can lead to a lot of dynamic fluid changes which can lead to maternal decompensation

Disposition: 

  • ICU vs potential transfer to a center that offers tertiary care services for both the mother and the fetus.

Stay well,

TR Adam

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Pressors in cardiogenic shock

“Pressors” in Cardiogenic Shock in adults

 

  • Vasopressors- Pure vasoconstriction without any inotropy eg Phenylephrine and Vasopressin

  • Inotrope- Increase cardiac contractility à improving SV and cardiac output without any vasoconstriction eg Milrinone

  • Inopressors - a combination of vasopressors and inotropes, because they lead to both increased cardiac contractility and increased peripheral vasoconstriction eg Norepinephrine, Epinephrine and Dopamine

 

Norepinephrine- Inopressor

  • Considered the safest Inopressor

  • Less arrhythmogenic than Epinephrine and Dopamine


Mechanism of action

  • Stimulates alpha-1 and alpha-2 receptors

  • Small amount of beta-1 agonist- modest inotropic effect

  • Increased coronary blood flow and afterload

  • Increases venous tone and return with resultant increased preload

Adverse effects

  • Norepinephrine is considered safer than both epinephrine and dopamine.

  • Still carries risk of toxicity to cardiac myocytes, cardiac arrhythmias, and peripheral vasoconstriction leading to tissue ischemia

Indications

  • Norepinephrine is considered first-line in cardiogenic shock with profound hypotension (SBP < 70 mm Hg)

  • Should be used in conjunction with dobutamine in patients with cardiogenic shock and blood pressure higher than 70 mm Hg who fail to respond to dobutamine.

Dosing

  • Use weight-based dosing to avoid the adverse effects associated with norepinephrine use

  • Weight-based dosing is based on GFR

  • Norepinephrine has a rapid onset of action (minutes) and can be titrated every 2-5 minutes

 

Dobutamine- Inopressor

Mechanism of action

  • Stimulates beta-1 and beta-2 receptors at approximately a 3:1 ratio

  • At high doses (greater than 15 ug/kg/min), dobutamine also becomes a mild alpha-1 agonist.

  • Because it mainly stimulates beta-1 receptors, dobutamine is mostly an inotrope

  • Dobutamine’s stimulation of beta-2 receptors can result in peripheral vasodilation, though the magnitude of this effect is variable à blood pressure in some (but not all) patients.

  • Due to its vasodilatory effects, dobutamine has been shown to improve capillary perfusion independent of changes in blood pressure and cardiac index.

Adverse Effects

  • Studies have demonstrated increased myocardial oxygen demand and malignant arrhythmias typically occuring at doses higher than 15 ug/kg/min

  • Many patients experience hypotension associated with dobutamine use and should be used with caution in patients with systolic blood pressure less than 90 mmHg

  • Dobutamine should only be used in patients with adequate fluid resuscitation


Indications

  • Current ACC/AHA guidelines à first-line agent in management of hypotension associated with acute myocardial infarction

  • But because dobutamine can lower BP, it should only be used if SBP is between 70-100 mmHg, with norepinephrine ready (or already infusing) as well.

  • Dobutamine is typically recommended as the first line agent in cardiogenic shock , but this is not a strong recommendation because several studies have demonstrated benefits to norepinephrine in this setting.

  • If dobutamine is used as a first-line agent, then norepinephrine should be second-line or already infusing, followed by milrinone.


Dosing

  • Dobutamine can be started at 2 mcg/kg/min and titrated to effect, with a maximum dose of 20 mcg/kg/min.

  • Onset of action is 1-2 minutes and the half-life is also approximately 2 minutes à rapidly reversible.


Milrinone- Inodilator

Mechanism of action

  • Milrinone is a phosphodiesterase-3 (PDE3) inhibitor à leads to cardiac smooth muscle relaxation and peripheral vasoconstriction

  • Potent inotropy + diastolic relaxation and vasodilation à to reduced preload, afterload, and systemic vascular resistance (SVR)

  • Milrinone has no beta-adrenergic activity à minimal chronotropic effects.


Adverse Effects

  • Because milrinone decreases preload (and therefore often leads to hypotension), it should only be used in patients who have undergone appropriate fluid resuscitation

  • Use of milrinone often necessitates concurrent vasopressor administration.

  • Because milrinone is metabolized in the kidneys, it should be avoided in patients with renal disease


Indications

  • Recommended for use in patients with daily beta-blocker use and in patients with long-standing heart failure who have developed resistance to catecholamine derivatives

  • Due to PDE’s vasodilatory effect on pulmonary vasculature à theoretical benefit in patients with pulmonary hypertension

Dosing

  • The starting dose of milrinone should ideally be chosen based on that patient’s renal function. The general range is 0.25-0.75 mcg/kg/min.

  • Avoid its use in patients with creatinine clearance less than 50 mL/min.

  • Because of its long onset of action and half-life, milrinone should be titrated every 2 hours (or slower, in the presence of renal disease).


Vasopressin- Pressor

Mechanism of action

  • Vasopressin is an endogenously released hormone (also known as anti-diuretic hormone) à vasopressin receptors in the kidneys à improve GFR

  • Vasopressin receptors on the peripheral vasculature à vasoconstriction.

  • Also causes coronary and cerebral vasodilation


Adverse Effects

  • Vasopressin increases the risk of digital ischemia more significantly than the catecholamine derivatives.

  • No evidence to support the use of vasopressin through a peripheral intravenous line

  • Vasopressin does not have an antidote if extravasation does occur.

Indications

  • Due to its increased risk for digital ischemia à avoid vasopressin in patients with known PVD

  • It has been proposed that because vasopressin leads to coronary vasodilation, it may be a preferable agent in cardiogenic shock but few RCTs investigating vasopressin use in cardiogenic shock.

  • Vasopressin may not lead to pulmonary vasoconstriction à ideal pressor choice in hypotension secondary to pulmonary hypertension à but not enough literature to support routine use in this setting


Dosing


Vasopressin is an endogenous à no utility to titrating vasopressin à used at a set dose of 0.04 U/min, regardless of weight.

 

Epinephrine- Inopressor

 

Mechanism of action

  • Beta-1 and beta-2 receptors agonism à more inotropic effects than norepinephrine

  • Epinephrine greatly increases chronotropy (heart rate) and thus stroke volume

  • Some stimulatory effect on alpha-1 receptors

  • Lower doses (1-10 mcg/min) à a beta-1 agonist

  • Higher doses (greater than 10 mcg/min) à an alpha-1 agonist

 

Adverse effects

  • Associated with an increased risk of tachycardia and lactic acidosis

  • Hyperglycemia

  • Increased incidence of arrhythmogenic events associated with epinephrine

  • More difficult use lactate as a marker of the patient’s response to treatment

 

Indications

Should be used with extreme caution in cases of cardiogenic shock:

  • RCT of 219 patients with cardiogenic shock found epinephrine to be independently associated with increased 90-day mortality and worsened renal function compared to dobutamine and norepinephrine (not validated).

  • Known increased incidence of arrhythmogenic events associated with epinephrine

 

Dosing


  • doses of 1-10 mcg/min predominantly activate beta-1 receptors, while doses greater than 10 mcg/min begin to primarily affect alpha-1-mediated vasoconstriction.

 

 

Phenylephrine: Not recommended in Cardiogenic shock

 

 

Resource: Awesome chart summarizing plessors

 http://www.emdocs.net/wp-content/uploads/2018/02/Inopressor-Summary_chart.pdf

 

References:

http://www.emdocs.net/evidence-based-approach-pressors-shock-part/

emDOCs.net – Emergency Medicine EducationAn Evidence-Based Approach to Pressors in Shock: Part I - emDOCs.net - Emergency Medicine Education

www.emdocs.net


 

http://www.emdocs.net/evidence-based-approach-pressors-shock-part-ii/

emDOCs.net – Emergency Medicine EducationAn Evidence-Based Approach to Pressors in Shock: Part II - emDOCs.net - Emergency Medicine Education

www.emdocs.net


 

Tarvasmäki T, Lassus J, Varpula M, Sionis A, Sund R, Køber L, et al. Current real-life use of vasopressors and inotropes in cardiogenic shock-adrenaline use is associated with excess organ injury and mortality. Critical Care. 2016;20(1):208.

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