Episódios
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Contributor: Taylor Lynch, MD
Educational Pearls:
When it comes to hypoglycemia, the age dictates possible causes
Neonate:
Hormonal deficiency
Congenital Adrenal Hyperplasia (21-hydroxylase deficiency, 11β-hydroxylase deficiency)
Primary or Secondary Adrenal Insufficiency leading to cortisol deficiency
Hypopituitarism
Inborn errors of metabolism
Systemic infection (Under 30 days old should trigger a full infectious workup)
Toddler
Accidental ingestions
Sulfonylureas such as glipizide or glyburide
Older children
Addison’s Disease (Hypocortisolism)
Accidential or intentional ingestions
Exogenous insulin
How is it diagnosed?
Child or infant
Glucose
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Contributor: Kiersten Williams MD, Travis Barlock MD, Jeffrey Olson MS3
Show Pearls
Hypertensive disorders of pregnancy are one of the leading causes of maternal mortality worldwide.
Hypertension (HTN) complicates 2-8% of pregnancies
The definition of HTN in pregnancy is a systolic >140 or diastolic >90, measured 4 hours apart
There is a range of HTN disorders
Chronic HTN which could have superimposed preeclampsia (preE) on top
Gestational HTN in which there are no lab abnormalities
PreE w/o severe features
Protein in urine
Urine protein >300 mg in 24 hours
Urine Protein to Creatinine ratio of .3
+2 Protein on urine dipstick
PreE w/ severe features
Systolics above 160 mmHg
Diastolics above 110 mmHg
Headache, especially not going away with meds, or different than previous headaches
Visual changes, anything that lasts more than a few minutes
RUQ pain, which could present as heartburn
Pulmonary edema
Low platelets, if
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Estão a faltar episódios?
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Contributor: Sean Fox, MD
Educational Pearls:
Newborns may lose up to 10% of their birth weight in the first week of life
Weight loss is greatest in exclusively breastfed infants
Should regain birth weight by age 2 weeks
Newborns should gain an average of 30g (1 oz) per day in the first 3 months of life
Some will gain more and some will gain less
Infants double their birth weight by 6 months of life and triple their weight by 12 months
A 1-year-old should weigh on average 10 kg (22 lbs)
A 3-year-old should weigh on average 15 kg (33 lbs)
2-year-olds are between 10-15 kg on average
Weight assessment can help determine causes of forceful vomiting
Not all “projectile” vomiting is due to pyloric stenosis
Some infants may experience vigorous vomiting from overfeeding
Weight estimates can also provide information for quick decisions on medical management for children coming via EMS
Helps to prepare medications and dosages based on predicted average weight
References
Crossland DS, Richmond S, Hudson M, Smith K, Abu-Harb M. Weight change in the term baby in the first 2 weeks of life. Acta Paediatr. 2008;97(4):425-429. doi:10.1111/j.1651-2227.2008.00685.x
Grummer-Strawn LM, Reinold C, Krebs NF; Centers for Disease Control and Prevention (CDC). Use of World Health Organization and CDC growth charts for children aged 0-59 months in the United States [published correction appears in MMWR Recomm Rep. 2010 Sep 17;59(36):1184]. MMWR Recomm Rep. 2010;59(RR-9):1-15.
Macdonald PD, Ross SR, Grant L, Young D. Neonatal weight loss in breast and formula fed infants. Arch Dis Child Fetal Neonatal Ed. 2003;88(6):F472-F476. doi:10.1136/fn.88.6.f472
Paul IM, Schaefer EW, Miller JR, et al. Weight Change Nomograms for the First Month After Birth. Pediatrics. 2016;138(6):e20162625. doi:10.1542/peds.2016-2625
Summarized & Edited by Jorge Chalit, OMS3
Special thanks to the Carolinas Medical Center for their contribution to this episode
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Contributor: Travis Barlock, MD
Educational Pearls:
SVT: supraventricular tachycardia
Pharmacotherapy for SVT includes drugs that block the AV node, such as adenosine
EKG criteria before adenosine administration in SVT
Regular rhythm
Monomorphic: all QRS complexes are identical
If the EKG is polymorphic, with QRS complexes displaying changing morphologies, it is unsafe to administer adenosine
Adenosine can worsen polymorphic VTach and lead to VFib
References
Ganz, Leonard I., and Peter L. Friedman. “Supraventricular Tachycardia.” New England Journal of Medicine, vol. 332, no. 3, 19 Jan. 1995, pp. 162–173, https://doi.org/10.1056/nejm199501193320307.
Smith JR, Goldberger JJ, Kadish AH. Adenosine induced polymorphic ventricular tachycardia in adults without structural heart disease. Pacing Clin Electrophysiol. 1997;20(3 Pt 1):743-745. doi:10.1111/j.1540-8159.1997.tb03897.x
Viskin, Sami, et al. “Polymorphic Ventricular Tachycardia: Terminology, Mechanism, Diagnosis, and Emergency Therapy.” Circulation, vol. 144, no. 10, 7 Sept. 2021, pp. 823–839, https://doi.org/10.1161/circulationaha.121.055783.
Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3
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Contributor: Aaron Lessen, MD
Educational Pearls:
How does an automated blood pressure cuff work?
Automated blood pressure cuffs work differently than taking a manual blood pressure.
While taking a manual blood pressure, one typically listens for Korotkoff sounds (turbulent flow) while slowly deflating the cuff.
An automatic blood pressure cuff only senses the pressure in the cuff itself and specifically pays attention to oscillations in the pressure caused by when the pressure of the cuff is between the systolic (heart squeezing) and diastolic (heart relaxed) pressures.
These oscillations are at a maximum when the pressure in the cuff matches the mean arterial pressure (MAP) and therefore the machines are most accurate at reporting the MAP.
The machines then use the MAP and other information about the oscillations to estimate the systolic and diastolic pressures, which are less accurate.
What should you do if you need more accurate systolic and diastolic blood pressures?
Take a manual blood pressure.
Get an arterial-line (a-line), which provides continuous data for the blood pressure at the end of a catheter.
What happens if the cuff is too big or too small for the patient?
If the cuff is too small it will overestimate the pressure.
If the cuff is too large it will underestimate the pressure.
What should you do if the cuff cycles a bunch of times before reporting a blood pressure?
It probably isn’t very accurate so consider another method.
Bonus fact!
The MAP is not directly in the middle of the systolic and diastolic pressures but is weighted towards the diastolic pressure. The MAP can be calculated by adding two-thirds of the diastolic pressure to one third of the systolic pressure. For example if the BP is 120/90 the MAP is 100 mmHg.
References
Benmira, A., Perez-Martin, A., Schuster, I., Aichoun, I., Coudray, S., Bereksi-Reguig, F., & Dauzat, M. (2016). From Korotkoff and Marey to automatic non-invasive oscillometric blood pressure measurement: does easiness come with reliability?. Expert review of medical devices, 13(2), 179–189. https://doi.org/10.1586/17434440.2016.1128821
Liu, J., Li, Y., Li, J., Zheng, D., & Liu, C. (2022). Sources of automatic office blood pressure measurement error: a systematic review. Physiological measurement, 43(9), 10.1088/1361-6579/ac890e. https://doi.org/10.1088/1361-6579/ac890e
Vilaplana J. M. (2006). Blood pressure measurement. Journal of renal care, 32(4), 210–213. https://doi.org/10.1111/j.1755-6686.2006.tb00025.x
Summarized by Jeffrey Olson, MS3 | Edited by Meg Joyce, MS1 & Jorge Chalit, OMS3
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Contributor: Megan Hurley, MD
Educational Pearls:
Heat cramps
Occur due to electrolyte disturbances
Most common electrolyte abnormalities are hyponatremia and hypokalemia
Heat edema
Caused by vasodilation with pooling of interstitial fluid in the extremities
Heat rash (miliaria)
Common in newborns and elderly
Due to accumulation of sweat beneath eccrine ducts
Heat syncope
Lightheadedness, hypotension, and/or syncope in patients with peripheral vasodilation due to heat exposure
Treatment is removal from the heat source and rehydration (IV fluids or Gatorade)
Heat exhaustion
Patients have elevated body temperature (greater than 38º C but less than 40º C)
Symptoms include nausea, tachycardia, headache, sweating, and others
Normal mental status or mild confusion that improves with cooling
Treatment is removal from the heat source and hydration
Classic heat stroke
From prolonged exposure to heat
Defined as a core body temperature > 40.5º C, though not required for diagnosis or treatment
Presentation is similar to heat exhaustion with the addition of neurological deficits including ataxia
Patients present “dry”
Exertional heat stroke
Prolonged exposure to heat during exercise
Similar to classic heat stroke but the patients present “wet” due to antecedent treatment in ice baths or other field treatments
Management of heat-related illnesses includes:
Cooling
Rehydration
Evaluation of electrolytes
Antipyretics are not helpful because heat-induced illnesses are not due to hypothalamic dysregulation
References
Casa DJ, McDermott BP, Lee EC, et al. Cold water immersion: the gold standard for exertional heatstroke treatment. Exerc Sport Sci Rev 2007; 35:141.
Ebi KL, Capon A, Berry P, et al. Hot weather and heat extremes: health risks. Lancet 2021; 398:698.
Epstein Y, Yanovich R. Heatstroke. N Engl J Med 2019; 380:2449.
Gardner JW, JA K. Clinical diagnosis, management, and surveillance of exertional heat illness. In: Textbook of Military Medicine, Zajitchuk R (Ed), Army Medical Center Borden Institute, Washington, DC 2001.
Khosla R, Guntupalli KK. Heat-related illnesses. Crit Care Clin 1999; 15:251.
Lipman GS, Gaudio FG, Eifling KP, et al. Wilderness Medical Society Clinical Practice Guidelines for the Prevention and Treatment of Heat Illness: 2019 Update. Wilderness Environ Med 2019; 30:S33.
Summarized by Jorge Chalit, OMSIII | Edited by Meg Joyce, MS1
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Contributor: Taylor Lynch, MD
Educational Pearls:
What is Central Cord Syndrome (CCS)?
Incomplete spinal cord injury caused by trauma that compresses the center of the cord
More common in hyperextension injuries like falling and hitting the chin
Usually happens only in individuals with preexisting neck and spinal cord conditions like cervical spondylosis (age-related wear and tear of the cervical spine)
Anatomy of spinal cord
Motor tracts
The signals the brain sends for the muscles to move travel in the corticospinal tracts of the spinal cord
The tracts that control the upper limbs are more central than the ones that control the lower limbs
The tracts that control the hands are more central than the ones that control the upper arm/shoulder
Fine touch, vibration, and proprioception (body position) tracts
These sensations travel in separate tracts in the spinal cord than the sensation of pain and temperature
Their pathway is called the dorsal column-medial lemniscus (DCML) pathway
This information travels in the most posterior aspect of the spinal cord
Pain, crude touch, pressure, and temperature tracts
These sensations travel in the spinothalamic tract, which is more centrally located
These signals also cross one side of the body to the other within the spinal cord near the level that they enter
How does this anatomy affect the presentation of CCS?
Patients typically experience more pronounced weakness or paralysis in their upper extremities as compared to their lower extremities with their hands being weaker than more proximal muscle groups
Sensation of pain, crude touch, pressure, and temperature are much morelikely to be diminished while the sensation of fine touch, vibration, and proprioception are spared
What happens with reflexes?
Deep tendon reflexes become exaggerated in CCS
This is because the disruption in the corticospinal tract removes inhibitory control over reflex arcs
What happens to bladder control?
The neural signals that coordinate bladder emptying are disrupted, therefore patients can present with urinary retention and/or urge incontinence
What is a Babinski’s Sign?
When the sole of the foot is stimulated a normal response in adults is for the toes to flex downward (plantar flexion)
If there is an upper motor neuron injury like in CCS, the toes will flex upwards (dorsiflexion)
How is CCS diagnosed?
CCS is mostly a clinical diagnosis
These patient also need an MRI to see the extent of the damage which will show increased signal intensity within the central part of the spinal cord on T2-weighted images
How is CCS treated?
Strict c-spine precautions
Neurogenic shock precautions. Maintain a mean arterial pressure (MAP) of 85-90 to ensure profusion of the spinal cord
Levophed (norepinephrine bitartrate) and/or phenylephrine can be used to support their blood pressure to support spinal perfusion
Consider intubation for injuries above C5 (C3, 4, and 5 keep the diaphragm alive)
Consult neurosurgery for possible decompression surgery
Physical Therapy
References
Avila, M. J., & Hurlbert, R. J. (2021). Central Cord Syndrome Redefined. Neurosurgery clinics of North America, 32(3), 353–363. https://doi.org/10.1016/j.nec.2021.03.007
Brooks N. P. (2017). Central Cord Syndrome. Neurosurgery clinics of North America, 28(1), 41–47. https://doi.org/10.1016/j.nec.2016.08.002
Engel-Haber, E., Snider, B., & Kirshblum, S. (2023). Central cord syndrome definitions, variations and limitations. Spinal cord, 61(11), 579–586. https://doi.org/10.1038/s41393-023-00894-2
Summarized by Jeffrey Olson, MS3 | Edited by Jorge Chalit, OMSIII
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Contributor: Megan Hurley, MD
Educational Pearls:
Initial assessment of patients with severe burn injuries begins with ABCs
Airway: consider inhalation injury
Breathing: circumferential burns of the trunk region can reduce respiratory muscle movement
Circulation: circumferential burns compromise circulation
Exposure: Important to assess the affected surface area
Escharotomy: emergency procedure to release the tourniquet-ing effects of the eschar
Differs from a fasciotomy in that it does not breach the deep fascial layer
PEEP = positive end-expiratory pressure
The positive pressure remaining in the airway after exhalation
Keeps airway pressure higher than atmospheric pressure
Common formulas for initial fluid rate in burn shock resuscitation
Parkland formula: 4 mL/kg body weight/% TBSA burns (lactated Ringer's solution)
Modified Brooke formula: 2 mL/kg/% (also lactated Ringer's solution)
Less fluid = lower risk of intra-abdominal compartment syndrome
Lactated Ringer’s solution is preferred over normal saline in burn injuries
Normal saline is avoided in large quantities due to the possibility of it leading to hyperchloremic acidosis
References
Acosta P, Santisbon E, Varon J. “The Use of Positive End-Expiratory Pressure in Mechanical Ventilation.” Critical Care Clinics. 2007;23(2):251-261. doi:10.1016/j.ccc.2006.12.012
Orgill DP, Piccolo N. Escharotomy and decompressive therapies in burns. J Burn Care Res. 2009;30(5):759-768. doi:10.1097/BCR.0b013e3181b47cd3
Snell JA, Loh NH, Mahambrey T, Shokrollahi K. Clinical review: the critical care management of the burn patient. Crit Care. 2013;17(5):241. Published 2013 Oct 7. doi:10.1186/cc12706
Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit
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Contributor: Taylor Lynch, MD
Educational Pearls:
What is NMS?
Neuroleptic Malignant Syndrome
Caused by anti-dopamine medication or rapid withdrawal of pro-dopamenergic medications
Mechanism is poorly understood
Life threatening
What medications can cause it?
Typical antipsychotics
Haloperidol, chlorpromazine, prochlorperazine, fluphenazine, trifluoperazine
Atypical antipsychotics
Less risk
Risperidone, clozapine, quetiapine, olanzapine, aripiprazole, ziprasidone
Anti-emetic agents with anti dopamine activity
Metoclopramide, promethazine, haloperidol
Not ondansetron
Abrupt withdrawal of levodopa
How does it present?
Slowly over 1-3 days (unlike serotonin syndrome which has a more acute onset)
Altered mental status, 82% of patients, typically agitated delirium with confusion
Peripheral muscle rigidity and decreased reflexes. AKA lead pipe rigidity. (As opposed to clonus and hyperreflexia in serotonin syndrome)
Hyperthermia (>38C seen in 87% of patients)
Can also have tachycardia, labile blood pressures, tachypnea, and tremor
How is it diagnosed?
Clinical diagnosis, focus on the timing of symptoms
No confirmatory lab test but can see possible elevated CK levels and WBC of 10-40k with a left shift
What else might be on the differential?
Sepsis
CNS infections
Heat stroke
Agitated delirium
Status eptilepticus
Drug induced extrapyramidal symptoms
Serotonin syndrome
Malignant hyperthermia
What is the treatment?
Start with ABC’s
Stop all anti-dopaminergic meds and restart pro-dopamine meds if recently stopped
Maintain urine output with IV fluids if needed to avoid rhabdomyolysis
Active or passive cooling if needed
Benzodiazapines, such as lorazepam 1-2 mg IV q 4hrs
What are active medical therapies?
Controversial treatments
Bromocriptine, dopamine agonist
Dantrolene, classically used for malignant hyperthermia
Amantadine, increases dopamine release
Use as a last resort
Dispo?
Mortality is around 10% if not recognized and treated
Most patients recover in 2-14 days
Must wait 2 weeks before restarting any medications
References
Oruch, R., Pryme, I. F., Engelsen, B. A., & Lund, A. (2017). Neuroleptic malignant syndrome: an easily overlooked neurologic emergency. Neuropsychiatric disease and treatment, 13, 161–175. https://doi.org/10.2147/NDT.S118438
Tormoehlen, L. M., & Rusyniak, D. E. (2018). Neuroleptic malignant syndrome and serotonin syndrome. Handbook of clinical neurology, 157, 663–675. https://doi.org/10.1016/B978-0-444-64074-1.00039-2
Velamoor, V. R., Norman, R. M., Caroff, S. N., Mann, S. C., Sullivan, K. A., & Antelo, R. E. (1994). Progression of symptoms in neuroleptic malignant syndrome. The Journal of nervous and mental disease, 182(3), 168–173. https://doi.org/10.1097/00005053-199403000-00007
Ware, M. R., Feller, D. B., & Hall, K. L. (2018). Neuroleptic Malignant Syndrome: Diagnosis and Management. The primary care companion for CNS disorders, 20(1), 17r02185. https://doi.org/10.4088/PCC.17r02185
Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSIII
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Contributor: Travis Barlock MD
Educational Pearls:
Recent study assessed outcomes after ROSC with epinephrine vs. norepinephrine
Observational multicenter study from 2011-2018
285 patients received epineprhine and 481 received norepinephrine
Epinephrine was associated with an increase in all-cause mortality (primary outcome)
Odds ratio 2.6; 95%CI 1.4-4.7; P = 0.002
Higher cardiovascular mortality (secondary outcome)
Higher proportion of unfavorable neurological outcome (secondary outcome)
Norepinephrine is the vasopressor of choice in post-cardiac arrest care
References
Bougouin W, Slimani K, Renaudier M, et al. Epinephrine versus norepinephrine in cardiac arrest patients with post-resuscitation shock. Intensive Care Med. 2022;48(3):300-310. doi:10.1007/s00134-021-06608-7
Summarized by Jorge Chalit, OMSIII | Edited by Meg Joyce & Jorge Chalit
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Contributor: Taylor Lynch, MD
Educational Pearls:
Opioid Epidemic- quick facts
Drug overdoses, primarily driven by opioids, have become the leading cause of accidental death in the U.S. for individuals aged 18-45.
In 2021, opioids were involved in nearly 75% of all drug overdose deaths
The rise of synthetic opioids like fentanyl, which is much more potent than heroin or prescription opioids, has played a major role in the increase in overdose deaths
What is Narcan AKA Naloxone?
Competitive opioid antagonist. It sits on the receptor but doesn’t activate it.
When do we give Narcan?
Respiratory rate less than 8-10 breaths per minute
Should you check the pupils?
An opioid overdose classically presents with pinpoint pupils BUT…
Hypercapnia from bradypnea can normalize the pupils
Taking other drugs at the same time like cocaine or meth can counteract the pupillary effects
Basilar stroke could also cause small pupils, so don’t anchor on an opioid overdose
How does Narcan affect the body?
Relatively safe even if the patient is not experiencing an opioid overdose. So when in doubt, give the Narcan.
What if the patient is opioid naive and overdosing?
Use a large dose given that this patient is unlikely to withdraw
0.4-2 mg every 3-5 minutes
What if the patient is a chronic opioid user
Use a smaller dose such as 0.04-0.4 mg to avoid precipitated withdrawal
How fast does Narcan work?
Given intravenously (IV), onset is 1-2 min
Given intranasal (IN), onset is 3-4 min
Given intramuscularly (IM), onset is ~6 min
Duration of action is 60 mins, with a range of 20-90 minutes
How does that compare to the duration of action of common opioids?
Heroine lasts 60 min
Fentanyl lasts 30-60 min, depending on route
Carfentanyl lasts ~5 hrs
Methadone lasts 12-24 hrs
So we really need to be conscious about redosing
How do you monitor someone treated with Narcan?
Pay close attention to the end-tidal CO2 to ensure that are ventilating appropriately
Be cautious with giving O2 as it might mask hypoventilation
Watch the respiratory rate
Give Narcan as needed
Observe for at least 2-4 hours after the last Narcan dose
Larger the dose, longer the observation period
Who gets a drip?
If they have gotten ~3 doses, time to start the drip
Start at 2/3rds last effective wake-up dose
Complications
Flash pulm edema
0.2-3.6% complication rate
Might be from the catecholamine surge from abrupt wake-up
Might also be from large inspiratory effort against a partially closed glottis which creates too much negative pressure
Treat with BIPAP if awake and intubation if not awake
Should you give Narcan in cardiac arrest?
Short answer no. During ACLS you take over breathing for the patient and that is pretty much the only way that Narcan can help
Just focus on high quality CPR
References
https://nida.nih.gov/research-topics/trends-statistics/overdose-death-rates#:~:text=Drug%20overdose%20deaths%20involving%20prescription,of%20deaths%20declined%20to%2014%2C716.
Elkattawy, S., Alyacoub, R., Ejikeme, C., Noori, M. A. M., & Remolina, C. (2021). Naloxone induced pulmonary edema. Journal of community hospital internal medicine perspectives, 11(1), 139–142. https://doi.org/10.1080/20009666.2020.1854417
van Lemmen, M., Florian, J., Li, Z., van Velzen, M., van Dorp, E., Niesters, M., Sarton, E., Olofsen, E., van der Schrier, R., Strauss, D. G., & Dahan, A. (2023). Opioid Overdose: Limitations in Naloxone Reversal of Respiratory Depression and Prevention of Cardiac Arrest. Anesthesiology, 139(3), 342–353. https://doi.org/10.1097/ALN.0000000000004622
Yousefifard, M., Vazirizadeh-Mahabadi, M. H., Neishaboori, A. M., Alavi, S. N. R., Amiri, M., Baratloo, A., & Saberian, P. (2019). Intranasal versus Intramuscular/Intravenous Naloxone for Pre-hospital Opioid Overdose: A Systematic Review and Meta-analysis. Advanced journal of emergency medicine, 4(2), e27. https://doi.org/10.22114/ajem.v0i0.279
Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSII
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Contributor: Taylor Lynch MD
Educational Pearls:
Anticholinergics are found in many medications, including over-the-counter remedies
Medications include:
Diphenhydramine
Tricyclic antidepressants like amitriptyline
Atropine
Antipsychotics like olanzapine
Antispasmodics - dicyclomine
Jimsonweed
Muscaria mushrooms
Mechanism of action involves competitive antagonism of the muscarinic receptor
Symptomatic presentation is easily remembered via the mnemonic:
Dry as a bone - anhidrosis due to cholinergic antagonism at sweat glands
Red as a beet - cutaneous vasodilation leads to skin flushing
Hot as a hare - anhidrotic hyperthermia
Blind as a bat - pupillary dilation and ineffective accommodation
Mad as a hatter - anxiety, agitation, dysarthria, hallucinations, and others
Clinical management
ABCs
Benzodiazepines for supportive care, agitation, and seizures
Sodium bicarbonate for TCA toxicity due to widened QRS
Activated charcoal if patient present < 1 hour after ingestion
Temperature monitoring
Contact poison control with questions
Physostigmine controversy
Physostigmine is a reversible cholinesterase inhibitor that can cross the blood-brain barrier so in theory it would be a useful antidote BUT…
There is a black box warning for asystole and seizures when physostigmine is used this way
Therefore it is contraindicated in TCA overdoses
However, it is still indicated in certain anticholinergic overdoses with delirium
Disposition
Admission criteria include: symptoms >6 hours, CNS findings, QRS prolongation, hyperthermia, and rhabdomyolysis
ICU admission criteria include: delirium, dysrhythmias, seizures, coma, or requirement for physostigmine drip
References
1. Arens AM, Shah K, Al-Abri S, Olson KR, Kearney T. Safety and effectiveness of physostigmine: a 10-year retrospective review. Clin Toxicol (Phila). 2018;56(2):101-107. doi:10.1080/15563650.2017.1342828
2. Nguyen TT, Armengol C, Wilhoite G, Cumpston KL, Wills BK. Adverse events from physostigmine: An observational study. Am J Emerg Med. 2018;36(1):141-142. doi:10.1016/j.ajem.2017.07.006
3. Scharman E, Erdman A, Wax P, et al. Diphenhydramine and dimenhydrinate poisoning: An evidence-based consensus guideline for out-of-hospital management. Clin Toxicol. 2006;44(3):205-223. doi:10.1080/15563650600585920
4. Shervette RE 3rd, Schydlower M, Lampe RM, Fearnow RG. Jimson "loco" weed abuse in adolescents. Pediatrics. 1979;63(4):520-523.
5. Woolf AD, Erdman AR, Nelson LS, et al. Tricyclic antidepressant poisoning: An evidence-based consensus guideline for out-of-hospital management. Clin Toxicol. 2007;45(3):203-233. doi:10.1080/15563650701226192
Summarized by Jorge Chalit, OMSIII | Edited by Jorge Chalit
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Contributor: Aaron Lessen, MD
Educational Pearls:
How fast does cellulitis recover?
A recent prospective cohort study took a look at this question.
The study included 300 adults with cellulitis (excluding those with peri-orbital cellulitis or abscesses) in two emergency departments in Queensland, Australia.
They collected data from initial and follow-up surveys at 3, 7, and 14 days, and compared clinician and patient assessments at day 14.
Improvement was fastest between day 0 and day 3, with gradual progress thereafter.
At day 14, many still had skin redness and swelling, though warmth had often resolved. Clinicians reported higher cure rates than patients (85.8% vs. 52.8%).
Conclusion:
Cellulitis symptoms improve quickly at first but continue to linger for many patients.
Patients and doctors often have different views on when cellulitis is fully cured.
How should we counsel patients?
Even on antibiotics, the margins of the cellulitis may continue to spread a small amount.
Skin warmth should be the first symptom to go away.
It takes time to get better. Only about 50% of patients believed their cellulitis was cured at 2 weeks.
References
Nightingale, R. S., Etheridge, N., Sweeny, A. L., Smyth, G., Dace, W., Pellatt, R. A. F., Snelling, P. J., Yadav, K., & Keijzers, G. (2024). Cellulitis in the Emergency Department: A prospective cohort study with patient-centred follow-up. Emergency medicine Australasia : EMA, 10.1111/1742-6723.14401. Advance online publication. https://doi.org/10.1111/1742-6723.14401
Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSIII
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Contributor: Aaron Lessen MD
Educational Pearls:
A recent study assessed EMS treatment of high blood pressure in the field
2404 patients randomized to prehospital treatment (1205) vs. usual care (1199)
Included patients with prehospital BP greater than 150 mm Hg
The treatment arm’s BP goal was 130-140 mm Hg
The primary efficacy outcome was functional status 90 days out
Stroke was confirmed by imaging upon hospital arrival
On arrival, the mean SBP of the treatment arm was 159 mm Hg compared with 170 mm Hg in the usual care group
No significant difference in functional outcomes between the treatment group and the usual care group (Common Odds Ratio of 1.00, 95% CI = 0.87-1.15)
Post-imaging analysis revealed 46.5% of the undifferentiated patients had a hemorrhagic stroke
Prehospital reduction in BP did reduce the odds of poor functional outcome in hemorrhagic stroke patients alone (Common Odds Ratio 0.75, 95% CI 0.60-0.92)
Those with ischemic stroke had increased odds of poor functional outcome (Common Odds Ratio 1.30, 95% CI 1.06-1.60)
Bottom line: it is challenging to identify the stroke type in the prehospital setting and therefore not necessarily helpful to treat the blood pressure
References
1. Ren X, Zhang C, Xu P, et al. Intensive Ambulance-Delivered Blood- Pressure Reduction in Hyperacute Stroke. New England Journal of Medicine. 2024;390(20):1862-1872. doi:10.1056/NEJMoa2314741
Summarized by Jorge Chalit, OMSIII | Edited by Meg Joyce & Jorge Chalit
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Contributor: Taylor Lynch MD
Educational Pearls:
Overview: Sympathomimetic drugs mimic the fight or flight response, affecting monoamines such as dopamine, norepinephrine, and epinephrine Limited therapeutic use, often abused. Types: Amphetamines: Methamphetamine, Adderall, Ritalin, Vyvanse MDMA (Ecstasy) Cocaine (Both hydrochloride salt & free based crack cocaine) Theophylline (Asthma treatment) Ephedrine (For low blood pressure) BZP, Oxymetazoline (Afrin), Pseudoephedrine (Sudafed) MAO Inhibitors (treatment-resistant depression) Mechanisms: Act on adrenergic and dopaminergic receptors. Cocaine blocks dopamine and serotonin reuptake. Methamphetamines increase stimulatory neurotransmitter release MAO Inhibitors prevent neurotransmitter breakdown. Symptoms: Agitation, tachycardia, hypertension, hyperactive bowel sounds, diuresis, hyperthermia. Severe cases: Angina, seizures, cardiovascular collapse. Diagnosis: Clinical examination and history. Differentiate from anticholinergic toxidrome by diaphoresis and hyperactive bowel sounds. Tests: EKG, cardiac biomarkers, chest X-ray, blood gas, BMP, CK, coagulation studies, U-tox screen. Treatment: Stabilize ABCs, IV hydration, temperature monitoring, benzodiazepines. Avoid beta-blockers due to unopposed alpha agonism. Whole bowel irrigation for body packers; surgical removal if packets rupture. IV hydration for high CK levels. Observation period often necessary. Recap: Mimic sympathetic nervous system. Key symptoms: Diaphoresis, hyperactive bowel sounds. Treatment: Supportive care, benzodiazepines. Use poison control as a resource.References:
Costa VM, Grazziotin Rossato Grando L, Milandri E, Nardi J, Teixeira P, Mladěnka P, Remião F. Natural Sympathomimetic Drugs: From Pharmacology to Toxicology. Biomolecules. 2022;12(12):1793. doi:10.3390/biom12121793
Kolecki P. Sympathomimetic Toxicity From Emergency Medicine. Medscape. Updated March 11, 2024. https://emedicine.medscape.com/article/818583-overview
Williams RH, Erickson T, Broussard LA. Evaluating Sympathomimetic Intoxication in an Emergency Setting. Lab Med. 2000;31(9):497-508. https://doi.org/10.1309/WVX1-6FPV-E2LC-B6YG
Summarized by Steven Fujaros | Edited by Jorge Chalit, OMSIII
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Contributor: Travis Barlock MD
Educational Pearls:
Wide-complex tachycardia is defined as a heart rate > 100 BPM with a QRS width > 120 milliseconds
Wide-complex tachycardia of supraventricular origin is known as SVT with aberrancy
Aberrancy is due to bundle branch blocks
Mostly benign
Treated with adenosine or diltiazem
Wide-complex tachycardia of ventricular origin is also known as VTach
Originates from ventricular myocytes, which are poor inherent pacemakers
Dangerous rhythm that can lead to death
Treated with amiodarone or lidocaine
80% of wide-complex tachycardias are VTach
90% likelihood for patients with a history of coronary artery disease
In assessing a wide-complex tachycardia, it is best to treat it as a presumed ventricular tachycardia
Treating SVT with amiodarone or lidocaine does no harm
However, treating VTach with adenosine or diltiazem may worsen the condition
References
1. Littmann L, Olson EG, Gibbs MA. Initial evaluation and management of wide-complex tachycardia: A simplified and practical approach. Am J Emerg Med. 2019;37(7):1340-1345. doi:https://doi.org/10.1016/j.ajem.2019.04.027
2. Viskin S, Chorin E, Viskin D, Hochstadt A, Schwartz AL, Rosso R. Polymorphic Ventricular Tachycardia: Terminology, Mechanism, Diagnosis, and Emergency Therapy. Circulation. 2021;144(10):823-839. doi:10.1161/CIRCULATIONAHA.121.055783
3. Williams SE, O’Neill M, Kotadia ID. Supraventricular tachycardia: An overview of diagnosis and management. Clin Med J R Coll Physicians London. 2020;20(1):43-47. doi:10.7861/clinmed.cme.20.1.3
Summarized by Jorge Chalit, OMSIII | Edited by Meg Joyce & Jorge Chalit
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Contributor: Aaron Lessen MD
Educational Pearls:
The case:
A gentleman came in from a nursing home with symptoms concerning for sepsis. He was hypotensive, hypoxic, febrile, and mentally altered.
His past medical history included previous strokes which had left him with deficits for which he required a feeding tube.
Initial workup included some point of care labs which revealed a sodium of 165 mEq/L (normal range 135-145)
Hypernatremia
What causes it?
Dehydration, from insufficient fluid intake. This might happen in individuals who cannot drink water independently, such as infants, elderly, or disabled people, as was the case for this patient.
Other causes of dehydration/hypernatremia include excessive sweating; diabetes insipidus; diuretic use; kidney dysfunction; and severe burns which can lead to fluid loss through the damaged skin.
How do you correct it?
Need to correct slowly, not more than 10 to 12 meq/L in 24 hours
Can do normal saline (0.9%) or half saline (0.45%) and D5, at 150-200 mL per hour.
Check the sodium frequently (every 2-3 hours)
Will likely need ICU-level monitoring
What happens if you correct it too quickly?
Cerebral edema
Seizures
Bonus fact: Correction of hyponatremia too quickly causes osmotic demyelination syndrome (ODS).
References
Chauhan, K., Pattharanitima, P., Patel, N., Duffy, A., Saha, A., Chaudhary, K., Debnath, N., Van Vleck, T., Chan, L., Nadkarni, G. N., & Coca, S. G. (2019). Rate of Correction of Hypernatremia and Health Outcomes in Critically Ill Patients. Clinical journal of the American Society of Nephrology : CJASN, 14(5), 656–663. https://doi.org/10.2215/CJN.10640918
Lindner, G., & Funk, G. C. (2013). Hypernatremia in critically ill patients. Journal of critical care, 28(2), 216.e11–216.e2.16E20. https://doi.org/10.1016/j.jcrc.2012.05.001
Muhsin, S. A., & Mount, D. B. (2016). Diagnosis and treatment of hypernatremia. Best practice & research. Clinical endocrinology & metabolism, 30(2), 189–203. https://doi.org/10.1016/j.beem.2016.02.014
Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSIII
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Contributor: Aaron Lessem MD
Educational Pearls:
Oseltamivir (Tamiflu) is an antiviral medication used commonly to treat influenza
Trials show that the medication reduces the duration of illness by less than 1 day (~16 hours in one systematic review)
Benefit only occurs if taken within 48 hours of symptom onset
Must be taken for 5 days
A 2024 meta-analysis reviewed 15 randomized-controlled trials for the risk of hospitalization
No reduction in hospitalizations with oseltamivir in patients over the age of 12
No difference in high-risk patients over the age of 65 or those with comorbidities
The authors note that the confidence interval in these populations is wide, indicating a need for subsequent studies in high-risk populations
Oseltamivir is associated with adverse effects including nausea, vomiting, and neurologic symptoms
The risk of adverse effects may outweigh the benefits of a small reduction in the duration of illness
References
1. Hanula R, Bortolussi-Courval É, Mendel A, Ward BJ, Lee TC, McDonald EG. Evaluation of Oseltamivir Used to Prevent Hospitalization in Outpatients with Influenza: A Systematic Review and Meta-Analysis. JAMA Intern Med. 2024;184(1):18-27. doi:10.1001/jamainternmed.2023.0699
2. Jefferson T, Jones M, Doshi P, Spencer EA, Onakpoya I, Heneghan CJ. Oseltamivir for influenza in adults and children: Systematic review of clinical study reports and summary of regulatory comments. BMJ. 2014;348(April):1-18. doi:10.1136/bmj.g2545
Summarized by Jorge Chalit, OMSII | Edited by Meg Joyce & Jorge Chalit
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Contributor: Aaron Lessen MD
Educational Pearls:
Epinephrine is essential in the treatment of anaphylaxis, but is epinephrine dangerous from a cardiovascular perspective?
A 2024 study in the Journal of the American College of Emergency Physicians Open sought to answer this question.
Methods:
Retrospective observational study at a Tennessee quaternary care academic ED that analyzed ED visits from 2017 to 2021 involving anaphylaxis treated with IM epinephrine.
The primary outcome was cardiotoxicity
Results:
Out of 338 patients, 16 (4.7%) experienced cardiotoxicity. Events included ischemic EKG changes (2.4%), elevated troponin (1.8%), atrial arrhythmias (1.5%), ventricular arrhythmia (0.3%), and depressed ejection fraction (0.3%).
Affected patients were older, had more comorbidities, and often received multiple epinephrine doses.
Bottom line:
All adults presenting with anaphylaxis should be rapidly treated with epinephrine but monitored closely for cardiotoxicity, especially in patients with a history of hypertension and those who receive multiple doses.
These results are supported by a 2017 study that found that 9% (4/44) of older patients who received epinephrine for anaphylaxis had cardiovascular complications.
References
Kawano, T., Scheuermeyer, F. X., Stenstrom, R., Rowe, B. H., Grafstein, E., & Grunau, B. (2017). Epinephrine use in older patients with anaphylaxis: Clinical outcomes and cardiovascular complications. Resuscitation, 112, 53–58. https://doi.org/10.1016/j.resuscitation.2016.12.020
Pauw, E. K., Stubblefield, W. B., Wrenn, J. O., Brown, S. K., Cosse, M. S., Curry, Z. S., Darcy, T. P., James, T. E., Koetter, P. E., Nicholson, C. E., Parisi, F. N., Shepherd, L. G., Soppet, S. L., Stocker, M. D., Walston, B. M., Self, W. H., Han, J. H., & Ward, M. J. (2024). Frequency of cardiotoxicity following intramuscular administration of epinephrine in emergency department patients with anaphylaxis. Journal of the American College of Emergency Physicians open, 5(1), e13095. https://doi.org/10.1002/emp2.13095
Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit OMS II
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Contributor: Aaron Lessen MD
Educational Pearls:
Opioid overdoses that are reversed with naloxone (Narcan), a mu-opioid antagonist, can precipitate acute withdrawal in some patients
Treatment of opioid use disorder with buprenorphine can also precipitate withdrawal
Opioid withdrawal symptoms include nausea, vomiting, diarrhea, and agitation
Buprenorphine works as a partial agonist at mu-opioid receptors, which may alleviate withdrawal symptoms
The preferred dose of buprenorphine is 16 mg
Treatment of buprenorphine-induced opioid withdrawal is additional buprenorphine
Adjunctive treatments may be used for other opioid withdrawal symptoms
Nausea with ondansetron
Diarrhea with loperamide
Agitation with hydroxyzine
References
1. Quattlebaum THN, Kiyokawa M, Murata KA. A case of buprenorphine-precipitated withdrawal managed with high-dose buprenorphine. Fam Pract. 2022;39(2):292-294. doi:10.1093/fampra/cmab073
2. Spadaro A, Long B, Koyfman A, Perrone J. Buprenorphine precipitated opioid withdrawal: Prevention and management in the ED setting. Am J Emerg Med. 2022;58:22-26. doi:10.1016/j.ajem.2022.05.013
Summarized by Jorge Chalit, OMSII | Edited by Meg Joyce & Jorge Chalit
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