Thursday Conference Content

Critically Appraised Topic: Is IM vs IN Naloxone less likely to require repeat dose in opioid overdose? By Dr. Roger Rothenberg

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Study 1: A prospective, randomized, unblinded trial of patients in Victoria, Australia, with suspected opioid overdose with RR < 10 and who were unrousable. Exclusion criteria were patients who regained consciousness prior to treatment, those in whom incomplete data was recorded by EMS, and those with response associated with technical errors in recording or administration. Eligibility is not otherwise well-defined in this paper. Requirement for individual patient consent was waived. Subjects were informed of their participation by way of an information letter after regaining consciousness which allowed them to withdraw themselves from the study or seek further information. The objective of the study was to determine the efficacy of IN naloxone compared with IM naloxone for patients with acute respiratory depression secondary to suspected opiate overdose treated in the pre-hospital setting–determined by time to regain RR >  10/min. Secondary outcomes were pts with RR >  10 after 8 mins, proportion with GCS >  11 at 8 mins, proportion requiring rescue naloxone (given as 0.8mg IM dose), and rate of adverse events, defined as agitation, nausea/vomiting, headache, tremor, sweating. 155 subjects (after 27 excluded) were enrolled by paramedics to randomly receive either 2mg IN naloxone by means of a mucosal atomiser (1mg to each nostril) or 2 mg IM naloxone, in addition to BLS. Patients were followed until transport to hospital. Primary outcome of time to regain RR >  10 was 6 min in IM vs 8 min IN condition (P = 0.006). Additionally, a greater proportion of the IM group had regained RR >  10 at 8 mins (P = 0.0163). IN administration resulted in fewer incidents of agitation (P = 0.0278). Other secondary outcomes were not significantly different.

Study 2: Also a prospective, randomized, unblinded trial of patients in Melbourne, Victoria, Australia, with suspected opioid overdose (altered conscious state, pin-point pupils, respiratory rate < 10, unrousable as defined by GCS < 12 and had no major facial trauma, blocked nasal passages or epistaxis). As in the prior study, consent was waived and participation was able to be withdrawn after regaining consciousness. This study’s objective was to determine the effectiveness and safety of concentrated IN naloxone compared to IM naloxone for treatment of suspected opiate overdose in the pre-hospital setting. The primary outcome was the proportion of patients with RR >  9/min and/or GCS >  12 within 10 minutes of naloxone administration. Secondary outcomes included time to adequate response (as defined above), hospitalization, adverse event rate and requirement for ‘rescue’ naloxone (additional 0.8mg IM dose) due to inadequate primary response as judged by the treating paramedics. 172 patients were included in the study (after exclusion of 81 due to not meeting criteria, inadequate training, regaining alertness prior to intervention, and missing equipment) and enrolled by paramedics to receive 2mg IM naloxone or 2mg IN naloxone (concentrated in 1mL and administered 0.5mL per nostril), in addition to BLS. Patients were followed until transport to hospital. Primary outcomes were not significantly different between groups, nor were mean response times, however the number of patients requiring rescue dose naloxone was significantly greater in the IN group vs IM (P = 0.01), even after controlling for age, gender and suspected concomitant alcohol and/or drugs. Other secondary outcomes did not result in significant differences.

Conclusions: In these studies IM naloxone was less likely to result in need for repeat dosing with no significant difference in number of adverse events. In our practice, with patients receiving naloxone in the field and then brought to EMS triage, conditions for monitoring are not always ideal. In those patients in whom opioid overdose is suspected, IM naloxone is less likely to require repeat dosing. Based on my review of the literature, I would preferentially administer IM naloxone in patients with suspected opioid overdose.

Wednesday Image Review

What’s the Diagnosis? By Dr. Edward Guo

Edward GuoLeave a comment

A 20 year old male presents to the emergency department via EMS for left knee pain. He was playing basketball when he jumped and felt a “pop” in his left knee and has been unable to walk on his left leg since. He denies falling. On exam, the left lower extremity is distally neurovascularly intact with normal strength, sensation, and a palpable pulse. There is slight bogginess and swelling with tenderness to palpation to the inferior knee. He is unable to extend at the knee. A point of care ultrasound of the bilateral knees is performed and shown below. What’s the diagnosis?

Answer: Left patellar tendon rupture

  • Commonly occurs from forced quadriceps contraction or falling on a flexed knee.
  • Associated with a high-riding patella also known as patella alta which can be appreciated on physical exam and lateral radiographs of the knee.
  • There is emerging data demonstrating point of care ultrasound as a quick and effective method to diagnose tendon injuries in the emergency department compared to physical exam, x-ray imaging, and MRI.
  • Treatment:
    • Incomplete tears with intact extensor mechanism can be immobilized and followed up outpatient with orthopedics.
    • Complete tears or loss of extensor mechanism should prompt orthopedic consultation in the ED as expedited surgical repair is often indicated.

References:

Bengtzen R. Knee Injuries. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill Education; 2020.

Berg, K., Peck, J., Boulger, C., & Bahner, D. P. (2013). Patellar tendon rupture: an ultrasound case report. BMJ case reports, 2013, bcr2012008189. https://doi.org/10.1136/bcr-2012-008189

Wu TS, Roque PJ, Green J, et al. Bedside ultrasound evaluation of tendon injuries. Am J Emerg Med. 2012;30(8):1617-1621. doi:10.1016/j.ajem.2011.11.004

Tuesday Advanced Cases

Alcohol Withdrawal By Dr. Sandhya Ashokkumar

Edward GuoLeave a comment

HPI

  • A 53-year-old male with a history of chronic daily alcohol use presents to the ED via EMS after a witnessed seizure at home
  • The medics say he drinks every day, but his last drink was 3 days ago because he was not able to go to the store (history obtained from the sister who witnessed the seizure)

Physical Examination

T 98.3F, BP 177/106, HR 191, RR 22, Sat 93% 

  • Patient appears anxious, uncomfortable, and is actively vomiting blood tinged sputum
  • He appears confused and is not answering questions appropriately
  • He is tachycardic and his lungs are clear to auscultation bilaterally
  • Abd: soft NTND

Differential 

  • Alcohol withdrawal/ Delirium Tremens
  • Thyrotoxicosis
  • Sepsis
  • Pulmonary embolism
  • Heart failure

Workup and Management

  • The nurse informs you that the patient is seizing
  • This patient is exhibiting evidence of delirium tremens (psychomotor agitation and autonomic instability) and alcohol withdrawal seizure
  • The patient is no longer tolerating his secretions, he is confused, gurgling, and requires a definitive airway
  • After intubation, you bolus the patient with propofol and start him a propofol infusion
  • The patient is admitted to the ICU for further management

Teaching Points

  • ETOH withdrawal begins 6-8 hours after last intake and peaks in 72 hours 
  • Symptom based treatment via the CIWA score can help stratify patients, scores >15 indicate severe withdrawal
  • Start with IV diazepam at 10mg or lorazepam at 4mg and repeat them in doubling doses
  • Consider adding phenobarbital for refractory cases (i.e. after 200 mg of diazepam)
  • Consider propofol as the induction agent and sedative post-intubation as propofol potentiates GABA receptor activity and inhibits NMDA receptors Summary 
  • Delerium tremens can result in death from hyperthermia, arrhythmia and seizures

Sources:

Long D, Long B, Koyfman A. The emergency medicine management of severe alcohol withdrawal. The American Journal of Emergency Medicine. 2017;35(7):1005-1011. doi:10.1016/j.ajem.2017.02.002

Schuckit MA, Author Affiliations From the Department of Psychiatry. Recognition and Management of Withdrawal Delirium (Delirium Tremens): NEJM. New England Journal of Medicine. https://www.nejm.org/doi/10.1056/NEJMra1407298. Published February 5, 2015. Accessed December 9, 2020.

Friday Board Review

Board Review by Dr. Hilbmann (Edited by Dr. Parikh)

Vidhi ParikhLeave a comment

A 43-year-old female with a past medical history of myasthenia gravis presents to the emergency department with shortness of breath. She was just diagnosed with a urinary tract infection and being treated by her PCP with antibiotics. Prior to her developing dyspnea, the patient also mentions experiencing blurry vision and difficulty chewing. She appears in respiratory distress on exam with an SpO2 of 83% on room air. After intubation, what is the most urgent treatment for this patient?

  1. Ceftriaxone with Azithromycin
  2. Methylprednisolone
  3. Physostigmine
  4. Plasma Exchange

Answer is D.  Given this patient’s past medical history and symptoms she is most likely in myasthenic crisis, possibly exacerbated by her recent UTI. Ceftriaxone and Azithromycin (A) which could be used to treat community acquired pneumonia would not be helpful in this patient. While corticosteroids (B) are utilized in patients with myasthenic crisis, 60-80 mg of prednisone is usually the corticosteroid of choice, this treatment would not rapidly change the patient’s clinical status. Physostigmine (C.) is an acetylcholinesterase inhibitor often utilized for anticholinergic toxicity. Pyridostigmine is an acetylcholinesterase inhibitor often used as long acting treatment for myasthenia gravis. Treatment for myasthenic crisis includes treating any contributing factors (infection), beginning rapid therapy with plasma exchange or IVIG, and high dose steroids or other immunomodulators. You may want to consider discontinuing acetylcholinesterase inhibitors medications temporarily (as they can increase respiratory secretions) until beginning immunomodulating therapy. 

References:

Wendell LC, Levine JM. Myasthenic crisis. Neurohospitalist. 2011 Jan;1(1):16-22. doi: 10.1177/1941875210382918. PMID: 23983833; PMCID: PMC3726100.

Myasthenia Gravis (no date) REBEL EM – Emergency Medicine Blog. Available at: https://rebelem.com/rebel-review/rebel-review-93-myasthenia-gravis/myasthenia-gravis/ (Accessed: 11 April 2024). 

Wednesday Image Review

What’s the Diagnosis? By Dr. Edward Guo

Edward GuoLeave a comment

A 40 year old female presents to the emergency department via EMS for shortness of breath. Prior to arrival to the ED, the patient was hypoxic and in severe respiratory distress with absent left lung sounds prompting needle thoracostomy and rapid sequence intubation by EMS. Vital signs are BP 108/70, HR 102, Temp 98F, RR 16, SpO2 99% on 50% FiO2. A left sided chest tube is placed without complication. Chest x-ray confirms appropriate positioning of the endotracheal tube and chest tube with expansion of the left lung. Four hours later, the ventilator is alarming due to elevated peak and plateau pressures. SpO2 is 90%. There is no change with suctioning. A new chest x-ray is obtained and is shown below. What’s the diagnosis?

Answer: Reexpansion pulmonary edema

  • Reexpansion pulmonary edema is a rare but potentially fatal complication following drainage of a pneumothorax or pleural effusion. The pathophysiology is poorly understood but is thought to involve an inflammatory response leading to increased pulmonary capillary permeability.
  • Risk factors include large size pneumothorax, large volume pleural effusion, rapid reexpansion, and prolonged duration of symptoms (> 72 hours).
    • Prevention includes limiting drainage of pleural effusions to a maximum volume of 1.5 liters in one attempt.
  • Imaging will demonstrate unilateral airspace opacities in portions of the lung that were previously collapsed.
  • Treatment is supportive with supplemental oxygen and observation. Most patients recover without adverse outcomes.

References:

Nicks BA, Manthey DE. Pneumothorax. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill Education; 2020.

Asciak R, Bedawi EO, Bhatnagar R, et al British Thoracic Society Clinical Statement on pleural procedures Thorax 2023;78:s43-s68.

Morioka H, Takada K, Matsumoto S, Kojima E, Iwata S, Okachi S. Re-expansion pulmonary edema: evaluation of risk factors in 173 episodes of spontaneous pneumothorax. Respir Investig. 2013;51(1):35-39. doi:10.1016/j.resinv.2012.09.003

https://radiopaedia.org/articles/re-expansion-pulmonary-oedema

Tuesday Advanced Cases

Hypothermia Arrhythmia by Dr. Edward Guo

Edward GuoLeave a comment

Case: A 29 year old male with a past medical history of polysubstance use presents to the ED in December via EMS for a suspected overdose. History is limited due to patient cooperation. EMS states that he was found outside in a puddle, minimally responsive. He was given 2mg IM naloxone by EMS and became acutely agitated and combative afterward, requiring 5mg IM midazolam and 5mg IM haloperidol upon arrival. Fingerstick glucose 226. EKG is obtained and shown below.

Exam: BP 182/84, HR 111, T 86.1F, RR 18, SpO2 100%
Disheveled appearing male in wet clothes, intermittently thrashing. Cold to touch. Pupils 5mm bilaterally. No signs of trauma. GCS E3 V2 M5. Moves all extremities equally. Heart rate is tachycardic and irregular.

EKG interpretation: atrial fibrillation with rapid ventricular response with Osborn waves

Differential diagnosis: polysubstance use, environmental cold exposure, severe sepsis, hypothyroidism

Case continued: Active rewarming is initiated by removing wet clothes, administering warmed IV fluids, and placing a bair hugger. Labs are notable for a creatinine kinase of 3966. The patient’s temperature, heart rate, and mental status significantly improve within 5 hours, and his repeat EKG shows normal sinus rhythm without Osborn waves. He is ultimately admitted to medicine.

Pearls:

  • The cardiovascular response to cold is peripheral vasoconstriction and initial increase in heart rate and blood pressure. As core temperature drops below 32C, there is myocardial irritability and risk of cardiovascular collapse.
    • Atrial fibrillation and flutterare common arrhythmias associated with hypothermia.
    • Rescue collapse is a term to describe cardiac arrest that occurs during extrication or transport of a profoundly hypothermic patient due to profound myocardial irritability.
  • Osborn waves are positive deflections at the end of the QRS complex that are non-specific but may occur in temperatures below 32C.
    • Size of the wave correlates with the degree of hypothermia but has no prognostic value.
  • As temperature continues to drop, EKG changes are variable but classically include bradycardia with prolonged PR, QRS, and QTc. Heart block or ventricular dysrhythmias may be encountered as well. Asystole is the common final dysrhythmia.
  • Rewarming is the treatment of choice.
    • Atrial dysrhythmias such as atrial fibrillation will often resolve with warming.
    • Cardioversion for unstable arrhythmias should be attempted but may be refractory in severe hypothermia.

References:

Brown DA. Hypothermia. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill Education; 2020.

Hoek T. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010. 122:5829-5861

Friday Board Review

Board Review by Dr. Edward Guo (Edited by Dr. Parikh)

Vidhi ParikhLeave a comment

A postpartum 34 year old female with a past medical history of hypertension presents for shortness of breath. Symptoms have been progressive over one month. She called EMS today when she was too short of breath to walk up one flight of stairs to care for her 13 week old infant. She denies fever, cough, chest pain, or recent illness and is not taking any oral contraceptives. Vital signs include Temp 99.0F, HR 96, BP 170/90, RR 22, SpO2 95% on room air. On exam, she has conversational dyspnea with no increased work of breathing. There are rales at the bilateral lung bases and 2+ pitting edema of the bilateral lower extremities. A bedside echocardiogram is notable for a dilated left ventricle with reduced ejection fraction. Which of the following is the most likely etiology of her symptoms? 

A: Cardiac infiltrative disease

B: Coronary artery atherosclerosis

C: Venous thromboembolism

D: None of the above

Answer: None of the above

This patient is likely presenting with peripartum cardiomyopathy, a rare but potentially fatal complication of pregnancy. The cause is unknown and most commonly occurs in the last month of gestation or within 5 months of delivery. The presenting symptoms and overall management of the condition are similar to other causes of congestive heart failure. Most patients will recover normal ejection fraction within the first 6 months of delivery. Ventricular dysrhythmias caused by persistent dilated cardiomyopathy may warrant an implantable defibrillator-pacemaker.

Cardiac infiltrative diseases such as amyloidosis or sarcoidosis most commonly cause diastolic dysfunction, not systolic dysfunction. Coronary artery disease is the most common cause of congestive heart failure but is unlikely in a 34 year old with minimal risk factors. A pulmonary embolism would cause right heart failure, not left ventricular systolic dysfunction.

 

Peripartum Cardiomyopathy
Most commonly occurs in last month of pregnancy or within 5 months of delivery
Dilated cardiomyopathy without previous heart disease
Treat similarly to other causes of congestive heart failure
Majority of patients recover normal ejection fraction

References:

Young JS. Maternal Emergencies After 20 Weeks of Pregnancy and in the Peripartum Period. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill Education; 2020.

Arany Z, Elkayam U. Peripartum Cardiomyopathy. Circulation. 2016 Apr 5;133(14):1397-409. doi: 10.1161/CIRCULATIONAHA.115.020491. PMID: 27045128.

“Peripartum Cardiomyopathy – Summary 1. Definition …” GrepMed, 16 Sept. 2020, www.grepmed.com/images/10231/peripartum-treatment-diagnosis-management-cardiomyopathy. Accessed 4 Apr. 2024.

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