SAEM Clinical Images Series: Below the Chin, Badness Lies Within

neck swelling

A 50-year-old male with insulin-dependent Type 2 Diabetes presented to the emergency department with three days of pain and swelling on the right side of his neck. He endorsed progression of his symptoms, reporting that he was now having fevers, myalgias, and intermittent difficulty swallowing solid foods.

Vitals: BP 153/96; HR 110; T 100.0°F; RR 16; O2 sat 97%

General: Appears uncomfortable

HEENT: Mild right-sided facial swelling. No trismus. No gingival inflammation or swelling or induration to suggest abscess. There is focal swelling and tenderness to palpation, without overlying erythema, throughout the right submandibular triangle, and along the sternocleidomastoid.

MSK: Limited active right shoulder range of motion secondary to pain

WBC: 10.4

Hgb: 14.4

Plts: 213

Na: 131

K: 3.7

A1C: 13

Lemierre syndrome (LS) is a rare complication of bacterial pharyngitis/tonsillitis and involves an extension of the infection into the lateral pharyngeal spaces of the neck with subsequent septic thrombophlebitis of the internal jugular vein (as seen on CT). Patients may present with trismus, dysphagia, and fever. Due to the possibility of widespread septic emboli, patients may experience sequelae of systemic infection with dyspnea, focal neurologic deficits, and abdominal pain. Treatment consists of prompt antibiosis and rapid source control.

Most cases of bacteremia in Lemierre syndrome are caused by Fusobacterium necrophorum, an anaerobic gram-negative rod that colonizes the oropharynx. This bacterium causes platelet aggregation and thrombus formation through hemagglutinin production and direct activation of the coagulation cascade. However, up to one-third of patients are found to have a polymicrobial infection with streptococcus and staphylococcus species frequently present.

Take-Home Points

  • Lemierre syndrome (LS) is a rare infection. However, the incidence of LS has been increasing in recent decades due to more judicious use of antibiotics for pharyngitis.
  • A high index of suspicion must be maintained to diagnose Lemierre syndrome, with special attention to alternative diagnoses such as Ludwig angina, retropharyngeal abscess, or meningitis.
  • A thorough investigation of associated symptoms is imperative as these may represent sequelae of septic emboli.

  • Foo EC, Tanti M, Cliffe H, Randall M. Lemierre’s syndrome. Pract Neurol. 2021 Oct;21(5):442-444. doi: 10.1136/practneurol-2021-002928. Epub 2021 May 7. PMID: 33963085.
  • Forrester LJ, Campbell BJ, Berg JN, Barrett JT. Aggregation of platelets by Fusobacterium necrophorum. J Clin Microbiol. 1985 Aug;22(2):245-9. doi: 10.1128/jcm.22.2.245-249.1985. PMID: 4031037; PMCID: PMC268368.

Cocaine for Epistaxis: What was old is new again

cocaine for epistaxis

Droperidol is back! Routine use of calcium for cardiac arrest is out? TPA is… well, we won’t go there. The landscape of medicine is continuously being reshaped. New research may question the effectiveness of an existing medication or promote the arrival of a novel treatment. Once beloved medications sit dust-laden in the back of a hospital pharmacy. But sometimes, just sometimes, an old medicine arises from that dust. Phenobarbital for alcohol withdrawal comes to mind.

Could cocaine hydrochloride be one of those medications to be resurrected?

Cocaine is effective in the treatment of epistaxis. Epistaxis is an exceedingly common complaint, accounting for approximately one in 200 emergency department (ED) visits in the United States [1, 2]. If you ask any seasoned emergency physician their ideal approach to epistaxis management, chances are high that it used to include cocaine. They will exclaim how superior it was to anything used today and claim, “Not only did it vasoconstrict, but it anesthetized, as well!” If this is the case, why is cocaine hydrochloride no longer used?

This post will chronicle cocaine’s fascinating yet troubled history in medicine and expose you to another tool for your arsenal in the ED management of epistaxis.

History

The coca plant, native to South America, Mexico, Indonesia, and the West Indies, derives its name from the Aymaran word Khoka meaning “the tree” [3]. Coca leaves contain approximately 0.25 to 0.9% cocaine. Their use medicinally dates as far back as 1000 BC by the indigenous people of South America. The leaves were chewed for energy supplementation and altitude sickness relief. During the Incan Empire of the 13th to 16th century, the leaves were revered as sacred and served as a panacea or cure-all. Coca was used to aid in digestion, pain relief, mitigation of hunger, wound healing, and even as a local anesthetic for invasive procedures, such as cranial trephination [3, 4].

It was not until the mid-1800s that cocaine’s journey began in Europe with the German chemist, Albert Nieman. Neiman isolated the alkaloid cocaine from the coca leaf and noted its numbing properties when placed on the tongue [5]. Its anesthetic and vasoconstricting properties were soon recognized by Austrian Professor C.D. Schroff and Peruvian physician, Dr. Thomas Mareno y Maiz [4]. Its popularity in medicine, however, had yet to catch on [4–6].

1884 marked a pivotal year for cocaine use in medicine. Austrian ophthalmologist, Dr. Carl Koller, introduced cocaine as a local anesthetic for cataract and other eye surgeries, which was a groundbreaking advancement. He additionally suggested its use for additional procedures of the nose, pharynx, and larynx [4, 5, 7]. Simultaneously, Sigmund Freud, the famed Austrian neurologist, became fascinated with cocaine’s various applications and wrote Uber Coca, the first of his 5 papers on the subject. He touted it as a “magical substance” without addictive properties. Ironically – and unfortunately – Freud later realized his misjudgment and spent years grappling with cocaine addiction [4, 5, 7].

Cocaine’s use as a local and regional anesthetic spread widely across Europe and to America from there. Influential American surgeons like Dr. William Halstead, a founder of Johns Hopkins School of Medicine, and his student, Dr. James Corning, further advanced its clinical applications by using cocaine as the first agent for regional nerve blocks and spinal anesthesia [8]. Like Freud, Dr. Halsted became addicted to cocaine and later morphine, which he used to wean his cocaine addiction.

In the early 1900s the medical use of cocaine declined due to increased reports of side effects, the development of safer alternatives such as procaine, and strict regulatory measures such as the 1914 Harrison Narcotics Tax Act [9].

Today’s Use in Medicine

Most of today’s medical use of cocaine is by the Ear, Nose and Throat (ENT) community. In fact, the American Academy of Otolaryngology-Head and Neck Surgery has had a position statement on cocaine since 1886 that reads [10]:

The American Academy of Otolaryngology-Head and Neck Surgery considers cocaine to be a valuable anesthetic and vasoconstricting agent when used as part of the treatment of a patient by a physician. No other single drug combines the anesthetic and vasoconstricting properties of cocaine.

FDA Approval

Cocaine hydrochloride is FDA-approved for local anesthesia for adult nasal procedures. Though not FDA-approved, it is also commonly used by ENT physicians as a hemostatic agent to prevent post-procedure bleeding and as a decongestant to promote a clearer view of the nasal passageways during surgery [11–14]. In the ED, it has been used off-label to treat epistaxis [11, 13, 15, 16] and as an anesthetic and analgesic before fiberoptic nasotracheal intubation [8].

Mechanism of Action

Cocaine is an alkaloid ester with weak basic properties. The addition of hydrochloride salt forms cocaine hydrochloride. In this form, cocaine is soluble in aqueous solution and can be used for ENT procedures. Its anesthetic properties occur via blockage of voltage-gated sodium channels. Vasoconstriction and hemostasis occur due to inhibition of catecholamine reuptake, including norepinephrine [9, 11].

Pharmacokinetics

  • Intranasal absorption: 4-33% [17–19]
  • Onset: 2-5 minutes [8]
  • Duration: 30-45 minutes [8]

Preparations

Cocaine hydrochloride is a clear, green solution. It comes in a single-unit bottle with concentrations ranging from 4-10%. Only the 4% solution is currently recommended as it has similar efficacy to higher concentrations with fewer side effects [11, 22]. The 10% solution should be avoided as it has been associated with toxicity and adverse events [8, 17, 20, 23]. Typically the 4% solution is dispensed in 1 mL or 4 mL single-use bottles.

Efficacy

There is limited research available on the use of intranasal cocaine in the ED for epistaxis management, or any other condition. Studies from the ENT literature have shown that cocaine has similar efficacy to most vasoconstrictors including epinephrine and phenylephrine for preventing bleeding after intranasal procedures [26–30]. The literature is mixed on oxymetazoline (Afrin) in epistaxis with some studies showing it may have superior efficacy in preventing post-procedure epistaxis [31, 32]. However, oxymetazoline lacks any anesthetic properties.

Safety

Concerns about cocaine hydrochloride’s intranasal use primarily revolve around its potential for systemic cardiovascular toxicity. Historical case reports of varying quality have documented significant adverse events including myocardial infarction (MI) and cardiac arrhythmias following intranasal use during ENT procedures and epistaxis management [21, 33, 34]. A dive into these reports, however, shows that a concentration and dose over the accepted 4% concentration and 200 mg maximum dose was frequently used in these cases. Many confounders also existed, such as a history of cardiac disease and concomitant medication administration (including general anesthesia) [34, 35]. There have been many contemporary studies comparing cocaine to other vasoconstricting/anesthetic agents in the ENT literature. In these studies, cocaine has not been shown to cause serious adverse CNS or cardiac events including MI, dangerous arrhythmias, or death [28, 32, 36–41].

It is important to note that most of the randomized control studies excluded patients with cardiac disease. It is therefore recommended to avoid the use of cocaine in patients with a history of MI, CAD, congenital heart disease, or uncontrolled hypertension [18, 34]. Cocaine should also be avoided in patients on beta-blocker therapy, from limited studies demonstrating increased coronary vasoconstriction with concomitant administration [20, 42].

Side Effects

The most common side effects are mild blood pressure elevation, mild tachycardia, non-emergent headache, and anxiety [18, 43]. Although rare, signs to watch for that could indicate severe CNS or cardiovascular toxicity include: agitation, seizure activity, hyperthermia, significant hypertension, significant tachycardia or arrhythmias, chest pain, and MI [25, 34].

It is recommended that patients receiving intranasal cocaine should have continuous cardiac monitoring and frequent vital sign checks, assessing for hypertension and tachycardia [21].

Contraindications [11, 24, 25]

Absolute

  • History of allergy to cocaine or substitutes of topical solution

Relative

  • History of cardiovascular disease (uncontrolled hypertension, unstable angina, MI, coronary artery disease, congestive heart disease, congenital heart disease): Increased risk of cardiac adverse event
  • Seizure/epilepsy history: May decrease seizure threshold
  • Active asthma exacerbation: May cause bronchoconstriction
  • Drug interactions:
    • Beta-blockers: May lead to hypertensive crisis through unopposed alpha-adrenergic vasoconstriction
    • Lidocaine/category 1A & 1C antiarrhythmics: Concurrent sodium channel blockade
    • Epinephrine or phenylephrine: Historical reports of MI and ventricular arrhythmia
    • Succinylcholine: Co-metabolism by plasma cholinesterase may lead to increased toxicity
    • Selective Serotonin Reuptake Inhibitors (SSRIs): Increased risk of seizures
    • Monoamine Oxidase Inhibitors (MAOIs): Prevent breakdown of catecholamines and can lead to toxicity
    • Disulfiram: Increases plasma cocaine and could lead to toxicity

Special Populations

  1. Pregnancy: Category C (may cause fetal harm). Avoid use during pregnancy [24, 25].
  2. Lactation: Avoid use during lactation [25].
  3. Pediatric: Not well studied

Barriers to Use

  1. Regulations
    • Schedule II drug (high potential for abuse with potentially severe psychological or physical dependence)
    • Requires storage in a locked cabinet and maintenance of separate written records of use
  2. Time to treatment: May take longer to obtain from the pharmacy compared to alternatives, given storage considerations and whether dispensed from the hospital (rather than ED) pharmacy
  3. Drug testing: Discuss with patients before use that cocaine may be detected up to 1 week in blood and even longer in urine [25].

Applying Cocaine in Epistaxis (24, 25)

  1. You will need at least 80 mg of 4% cocaine hydrochloride.
    • If your hospital stocks the 1 mL bottle of 40 mg/mL cocaine hydrochloride, you should obtain 2 vials (80 mg total). Use 2 separate pledgets, immersing each one in its own bottle.
    • Alternatively, if your hospital stocks the 160 mg/4 mL solution, soak 4 pledgets in the entire 4 mL solution.
    • Each pledget will absorb approximately 1 mL of the 4% solution.
  2. Once fully adsorbed, place 1-2 pledgets in the nasal cavity with epistaxis, positioned against the septum.
  3. Leave the pledgets in place for up to 20 minutes.
  4. Assess for hemostasis.
  5. If needed, you can use a maximum of 2 additional pledgets, if epistaxis does not resolve. The maximum dose should be the lower dose of 200 mg or 2 mg/kg.

Proposed ED Epistaxis Algorithm [16, 44]

Takeaways

  1. In the right patient, cocaine may have a place in the management of epistaxis. Avoid in patients with cardiovascular disease.
  2. Cocaine is the only single agent that both vasoconstricts and anesthetizes.
  3. Insert 1-2 pledgets soaked each with 40 mg of cocaine hydrochloride into the affected nare for 20 minutes.
  4. The maximum dose is 2 mg/kg or 200 mg, whichever is lower.

  1. Newton E, Lasso A, Petrcich W, Kilty SJ. An outcomes analysis of anterior epistaxis management in the emergency department. J Otolaryngol – Head Neck Surg J Oto-Rhino-Laryngol Chir Cervico-Faciale. 2016;45:24. doi:10.1186/s40463-016-0138-2. PMID: 27066834
  2. Pallin DJ, Chng YM, McKay MP, Emond JA, Pelletier AJ, Camargo CA. Epidemiology of epistaxis in US emergency departments, 1992 to 2001. Ann Emerg Med. 2005;46(1):77-81. doi:10.1016/j.annemergmed.2004.12.014. PMID: 15988431
  3. Biondich AS, Joslin JD. Coca: The History and Medical Significance of an Ancient Andean Tradition. Emerg Med Int. 2016;2016:4048764. doi:10.1155/2016/4048764. PMID: 27144028
  4. Brain PF, Coward GA. A review of the history, actions, and legitimate uses of cocaine. J Subst Abuse. 1989;1(4):431-451. PMID: 2485453
  5. Redman M. Cocaine: What is the Crack? A Brief History of the Use of Cocaine as an Anesthetic. Anesthesiol Pain Med. 2011;1(2):95-97. doi:10.5812/kowsar.22287523.189. PMID: 25729664
  6. Grzybowski A. [The history of cocaine in medicine and its importance to the discovery of the different forms of anaesthesia]. Klin Oczna. 2007;109(1-3):101-105. PMID: 17687926
  7. Cocaine – Definition, Crack & Plant. HISTORY. Published August 21, 2018. Accessed January 3, 2024.
  8. Roberts JR, Custalow CB, Thomsen TW, eds. Roberts and Hedges’ Clinical Procedures in Emergency Medicine. Seventh edition. Elsevier; 2019.
  9. Goldstein RA, DesLauriers C, Burda A, Johnson-Arbor K. Cocaine: history, social implications, and toxicity: a review. Semin Diagn Pathol. 2009;26(1):10-17. doi:10.1053/j.semdp.2008.12.001. PMID: 19292024
  10. American Academy of Otolaryngology—Head and Neck Surgery Committee. Position Statement: Medical Use of Cocaine. Published online July 31, 2014. Accessed January 3, 2024.
  11. Lutfallah SC, Brown E, Spillers NJ, et al. Topical Cocaine Hydrochloride Nasal Solution: Anesthetic and Surgical Considerations. Cureus. 2023;15(8):e42804. doi:10.7759/cureus.42804. PMID: 37664274
  12. De R, Uppal HS, Shehab ZP, Hilger AW, Wilson PS, Courteney-Harris R. Current practices of cocaine administration by UK otorhinolaryngologists. J Laryngol Otol. 2003;117(2):109-112. doi:10.1258/002221503762624530. PMID: 12625882
  13. Reid JW, Rotenberg BW, Sowerby LJ. Contemporary decongestant practices of Canadian otolaryngologists for endoscopic sinus surgery. J Otolaryngol – Head Neck Surg J Oto-Rhino-Laryngol Chir Cervico-Faciale. 2019;48(1):15. doi:10.1186/s40463-019-0337-8. PMID: 30885260
  14. Long H, Greller H, Mercurio-Zappala M, Nelson LS, Hoffman RS. Medicinal use of cocaine: a shifting paradigm over 25 years. The Laryngoscope. 2004;114(9):1625-1629. doi:10.1097/00005537-200409000-00022. PMID: 15475793
  15. Seikaly H. Epistaxis. N Engl J Med. 2021;384(10):944-951. doi:10.1056/NEJMcp2019344. PMID: 33704939
  16. Tunkel DE, Anne S, Payne SC, et al. Clinical Practice Guideline: Nosebleed (Epistaxis). Otolaryngol–Head Neck Surg Off J Am Acad Otolaryngol-Head Neck Surg. 2020;162(1_suppl):S1-S38. doi:10.1177/0194599819890327. PMID: 31910111
  17. Liao BS, Hilsinger RL, Rasgon BM, Matsuoka K, Adour KK. A preliminary study of cocaine absorption from the nasal mucosa. The Laryngoscope. 1999;109(1):98-102. doi:10.1097/00005537-199901000-00019. PMID: 9917048
  18. Dwyer C, Sowerby L, Rotenberg BW. Is cocaine a safe topical agent for use during endoscopic sinus surgery? The Laryngoscope. 2016;126(8):1721-1723. doi:10.1002/lary.25836. PMID: 27075241
  19. McGrath J, McGrath A, Burdett J, Shokri T, Cohn JE. Systemic Pharmacokinetics of Topical Intranasal Cocaine in Healthy Subjects. Am J Rhinol Allergy. 2020;34(3):336-341. doi:10.1177/1945892419896241. PMID: 31856588
  20. Lange RA, Cigarroa RG, Yancy CW, et al. Cocaine-induced coronary-artery vasoconstriction. N Engl J Med. 1989;321(23):1557-1562. doi:10.1056/NEJM198912073212301. PMID: 2573838
  21. Richards JR, Laurin EG, Tabish N, Lange RA. Acute Toxicity from Topical Cocaine for Epistaxis: Treatment with Labetalol. J Emerg Med. 2017;52(3):311-313. doi:10.1016/j.jemermed.2016.08.006. PMID: 27693072
  22. Lu IC, Hsieh YH, Hsu HT, et al. Comparison of 4% and 6% topical cocaine solutions for reduction of epistaxis induced by nasotracheal intubation. Acta Anaesthesiol Taiwanica Off J Taiwan Soc Anesthesiol. 2014;52(1):17-21. doi:10.1016/j.aat.2014.05.001. PMID: 24999214
  23. Gurudevan SV, Nelson MD, Rader F, et al. Cocaine-induced vasoconstriction in the human coronary microcirculation: new evidence from myocardial contrast echocardiography. Circulation. 2013;128(6):598-604. doi:10.1161/CIRCULATIONAHA.113.002937. PMID: 23812179
  24. Genus Lifesciences Inc. GOPRELTO- cocaine hydrochloride solution Reference ID: 4195367. Published online December 2017.
  25. Micromedex Solutions. Cocaine Hydrochloride. Published online November 30, 2023.
  26. Rector FT, DeNuccio DJ, Alden MA. A comparison of cocaine, oxymetazoline, and saline for nasotracheal intubation. AANA J. 1987;55(1):49-54. PMID: 3551442
  27. Gross JB, Hartigan ML, Schaffer DW. A suitable substitute for 4% cocaine before blind nasotracheal intubation: 3% lidocaine-0.25% phenylephrine nasal spray. Anesth Analg. 1984;63(10):915-918. PMID: 3551442
  28. Valdes CJ, Bogado M, Rammal A, Samaha M, Tewfik MA. Topical cocaine vs adrenaline in endoscopic sinus surgery: a blinded randomized controlled study. Int Forum Allergy Rhinol. 2014;4(8):646-650. doi:10.1002/alr.21325. PMID: 24678064
  29. Sessler CN, Vitaliti JC, Cooper KR, Jones JR, Powell KD, Pesko LJ. Comparison of 4% lidocaine/0.5% phenylephrine with 5% cocaine: which dilates the nasal passage better? Anesthesiology. 1986;64(2):274-277. doi:10.1097/00000542-198602000-00028. PMID: 3946816
  30. Campbell JP, Campbell CD, Warren DW, Prazma TU, Pillsbury HC. Comparison of the vasoconstrictive and anesthetic effects of intranasally applied cocaine vs. xylometazoline/lidocaine solution. Otolaryngol–Head Neck Surg Off J Am Acad Otolaryngol-Head Neck Surg. 1992;107(5):697-700. doi:10.1177/019459989210700511. PMID: 1279502
  31. Katz RI, Hovagim AR, Finkelstein HS, Grinberg Y, Boccio RV, Poppers PJ. A comparison of cocaine, lidocaine with epinephrine, and oxymetazoline for prevention of epistaxis on nasotracheal intubation. J Clin Anesth. 1990;2(1):16-20. doi:10.1016/0952-8180(90)90043-3. PMID: 2310576
  32. Riegle EV, Gunter JB, Lusk RP, Muntz HR, Weiss KL. Comparison of vasoconstrictors for functional endoscopic sinus surgery in children. The Laryngoscope. 1992;102(7):820-823. doi:10.1288/00005537-199207000-00012. PMID: 1614253
  33. Ross GS, Bell J. Myocardial infarction associated with inappropriate use of topical cocaine as treatment for epistaxis. Am J Emerg Med. 1992;10(3):219-222. doi:10.1016/0735-6757(92)90213-H. PMID: 1586432
  34. Higgins TS, Hwang PH, Kingdom TT, Orlandi RR, Stammberger H, Han JK. Systematic review of topical vasoconstrictors in endoscopic sinus surgery. The Laryngoscope. 2011;121(2):422-432. doi:10.1002/lary.21286. PMID: 21271600
  35. Meyers EF. Cocaine toxicity during dacryocystorhinostomy. Arch Ophthalmol Chic Ill 1960. 1980;98(5):842-843. doi:10.1001/archopht.1980.01020030836006. PMID: 7378007
  36. MacNeil SD, Rotenberg B, Sowerby L, Allen B, Richard L, Shariff SZ. Medical use of cocaine and perioperative morbidity following sinonasal surgery-A population study. PloS One. 2020;15(7):e0236356. doi:10.1371/journal.pone.0236356. PMID: 32730351
  37. McGrath J, McGrath A, Burdett J, Shokri T, Cohn JE. Investigation of topical intranasal cocaine for sinonasal procedures: a randomized, phase III clinical trial. Int Forum Allergy Rhinol. 2020;10(8):981-990. doi:10.1002/alr.22561. PMID: 32384578
  38. Pfleiderer AG, Brockbank M. Cocaine and adrenaline: a safe or necessary combination in the nose? A study to determine the effect of adrenaline on the absorption and adverse side effects of cocaine. Clin Otolaryngol Allied Sci. 1988;13(6):421-426. doi:10.1111/j.1365-2273.1988.tb00315.x. PMID: 2465851
  39. Delilkan AE, Gnanapragasam A. Topical cocaine/adrenaline combination in intransal surgery–is it necessary? Anaesth Intensive Care. 1978;6(4):328-332. doi:10.1177/0310057X7800600406. PMID: 736254
  40. Alhaddad ST, Khanna AK, Mascha EJ, Abdelmalak BB. Phenylephrine as an alternative to cocaine for nasal vasoconstriction before nasal surgery: A randomised trial. Indian J Anaesth. 2013;57(2):163-169. doi:10.4103/0019-5049.111844. PMID: 23825816
  41. Kara CO, Kaftan A, Atalay H, Pinar HS, Oğmen G. Cardiovascular safety of cocaine anaesthesia in the presence of adrenaline during septal surgery. J Otolaryngol. 2001;30(3):145-148. doi:10.2310/7070.2001.20197. PMID: 11771042
  42. Lange RA, Cigarroa RG, Flores ED, et al. Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med. 1990;112(12):897-903. doi:10.7326/0003-4819-112-12-897. PMID: 1971166
  43. Drivas EI, Hajiioannou JK, Lachanas VA, Bizaki AJ, Kyrmizakis DE, Bizakis JG. Cocaine versus tetracaine in septoplasty: a prospective, randomized, controlled trial. J Laryngol Otol. 2007;121(2):130-133. doi:10.1017/S0022215106002386. PMID: 17274862.
  44. Gottlieb M, Long B. Managing Epistaxis. Ann Emerg Med. 2023;81(2):234-240. doi:10.1016/j.annemergmed.2022.07.002. PMID: 36117013

11 Tips to Improve Epistaxis Management in the Emergency Department

epistaxis 11 tips

Managing epistaxis is often challenging, time-consuming, and takes practice. Even under the best circumstances, epistaxis often results in return visits for rebleeding and poor outcomes. Rarely should you do “nothing” for adults who present to the ED with or following epistaxis. If it produced enough blood to seek care (even without hemodynamic compromise), epistaxis frequently recurs even if currently resolved. This is a less true in pediatric patients. A careful and comprehensive evaluation is essential in both populations, whether epistaxis is ongoing.

The following 11 pearls with a bonus tip should help you avoid common pitfalls, improve outcomes, and increase both patient and physician satisfaction:

  1. Wear proper protection during the procedure, including a face shield and gown. Nasal manipulation often causes patients to cough or sneeze, resulting in blood spray.
  2. Prepare your equipment in advance. Work with your nurses or techs to develop a policy where it is placed at the bedside when the patient is roomed. A bright, focused light is essential, ideally as a headlamp so both hands are free. This way, no assistant is needed. Cordless headlamps are easier to use but should be charged after each use.
  3. Although an elevated blood pressure or hypertension can worsen epistaxis, acute treatment is generally not required. Help your patient relax by establishing a calm presence, demonstrating confidence, and explaining your approach in advance. Done well, these actions are often sufficient to reduce their blood pressure.
  4. Have your patient slowly but firmly blow their nose to remove any clots that have formed, which not only will reduce or prevent medications from absorbing but will also interfere with visualization. After this, have your patient hold firm pressure with a clip or clamp for at least 15 minutes while you gather your supplies. If available, spray a vasoconstrictor such as oxymetazoline into the affected nostril(s) prior to holding firm pressure.
  5. Tight packing of your selected medications and your preferred method of their administration (e.g., cotton balls, pledgets, swabs) is crucial, as the vasoconstrictor/anesthetic won’t be well absorbed without direct contact and pressure. Tight packing also helps tamponade any bleeding. It may be necessary to pack both nasal cavities to achieve adequate tamponade because the septum is mobile.
  6. Avoid touching the nasal septum when using the nasal speculum. This is likely the area of bleeding and can be sensitive. Carefully insert the tip along the inner edge of the ala, open the speculum, then pull out with gentle traction to provide optimal visualization with your high-intensity light.
  7. If using silver nitrate to cauterize a friable area or visible vessel, ensure the field is dry and the site is anesthetized. Chemical burns are painful, and this area is sensitive. Using light pressure with a gentle rolling motion, cauterize an area slightly wider than the area of bleeding, limiting the number of repeat cautery attempts.
  8. If using commercial nasal packing that is too large (they come in several sizes, although some EDs stock only the largest sizes), shorten and trim the tip at an angle. Apply a topical antibiotic ointment to the nasal tampon to aid with insertion; this serves both as an antibiotic and lubricant. In some situations, using a hemostatic agent with the nasal tampon or in the nasal cavity may prove helpful. Follow the contour and direction of the nasal passage to ease insertion and minimize pain. Some patients poorly tolerate the placement of nasal packing and/or the packing itself.
  9. Add 1-3 ccs of water or saline using a syringe (no needle) to wet the packing following insertion. This allows the packing to expand and soften. Be prepared for a small amount of leaking, coughing, or spitting. If using an inflatable device for packing, be prepared to inflate the balloon to the optimal size with air or appropriate fluid (depending on the device).
  10. Do not immediately discharge a patient after successful epistaxis management. Observe your patient for a post-procedure recheck to ensure the bleeding remains well-controlled, your patient is tolerating the packing or balloon, and the vital signs are stable. This can be 15–30 minutes (or longer) depending on the amount of blood loss, the findings, the procedure, and your patient’s comorbidities.
  11. Know how and when to call for help. Call for help early in situations such as hemodynamic compromise due to blood loss, hypoxia or acute cardiopulmonary distress, post-surgical epistaxis, bleeding tumors (especially those that have been irradiated), patients with underlying bleeding disorders, an inability to control the bleeding, or other circumstances that make poor outcomes more likely.

Charting Bonus Tips: You can complete your patient’s discharge paperwork while waiting for the pre-procedure topical anesthetic/vasoconstrictor to take effect. During the post-procedure observation period, complete your chart and document your findings, the procedure, whether the patient tolerated the procedure, and any complications while observing your patient and awaiting the final set of vital signs before discharge.

Additional recommended reading

  • Gottlieb M, Long B. Managing Epistaxis. Ann Emerg Med. 2023;81(2):234-240. doi:10.1016/j.annemergmed.2022.07.002. PMID 36117013

Updated March 23, 2023

By |2023-03-23T23:41:34-07:00Mar 3, 2023|ENT|

Trick of the Trade: Managing Epistaxis with Merocel Nasal Packing and an Angiocatheter


There are many ways to manage epistaxis. Once nasal clamping and cauterization fail, the next step is to consider using tranexamic acid (TXA) and performing nasal packing. Inflatable packing devices such as a Rhinorocket are painful to insert and do not conform well to the shape of the naris. The expandable Merocel nasal packing, a compressed, dehydrated sponge, provides a softer, alternative option, although the insertion process can be painful given its initial rigid, edged structure. We propose 2 strategic tricks to optimize your nasal packing technique using the Merocel sponge.

Trick of the Trade: Strategic expansion of the Merocel sponge

The common approach for Merocel packing involves inserting the unexpanded sponge into the nose, tilting the patient’s head back, and dripping in TXA solution to expand the sponge to tamponade the bleeding.

Trick #1: Wet the tip of the Merocel’s sharp edge to allow for a softer cushion to slide the packing more comfortably and deeper into the naris.

Trick #2: Use an angiocatheter to deliver the TXA solution directly onto the mid-portion of the packing. Commonly, the TXA solution is dripped onto the outer end, which may cause an uneven and inadequate expansion at the site where the bleeding may be occurring. Because blood also can react with the packing, it is likely the blood will expand the packing before TXA reaches the center by osmosis. Another benefit of Merocel expansion starting at the center is that it will help anchor the sponge in place. In contrast, TXA administration at the outer tip first may pull the sponge out of the naris a few millimeters.

Equipment

  • 20g or 22g angiocatheter (closed IV catheter system)
  • Tranexamic acid solution
  • A syringe
  • Merocel nasal dressing

Technique

merocel sponge nasal packing trick setup

1. Insert the angiocatheter needle into the Merocel packing about ⅓ the distance from the external end of the packing. Remove the needle, leaving the plastic angiocatheter in place.

merocel tip moisten txa trick

2. Soak the insertion tip of the nasal packing with a drop of TXA to soften it. Or apply a light coat of an antibiotic ointment or petroleum jelly to the insertion tip for lubrication. This will make it easier to advance the packing and also less painful for patients. Advance the Merocel into the affected naris just as you would a nasogastric tube. Some additional tips are in the ALiEM article about nasogastric and nasopharyngeal tube insertion.

3. Once the nasal packing is fully inserted, expand the sponge by administering TXA via the attached angiocatheter. The mid-portion of the sponge should expand first, thus preventing outward slippage of packing. Also TXA more quickly reaches the area of bleeding rather than from a more gradual osmotic effect when dripped in from the external tip.

SAEM Clinical Image Series: A Rapidly Spreading Rash

spreading rash

A 40-year-old male with a past medical history of HIV presented for evaluation of a non-pruritic rash. Six days ago, he suddenly felt a stinging sensation at the back of his head and neck similar to a bug bite. He then noticed bumps were starting to form and developed a shock-like pain in the area. Three days ago, the rash spread from the back of his head towards his chest. Yesterday, the rash spread further and now extends medially and upwards covering most of his left neck and ear. The pain continued to worsen, at which point the patient shaved the left side of his head in an attempt to help the rash. Today, the pain became unbearable, which prompted his visit to the emergency department for further evaluation and management.

Head: Normocephalic, atraumatic; left side of patient’s head is shaved.

Eye: Pupils equal, round, reactive to light; extraocular movements intact; no corneal ulcers or dendritic lesions with fluorescein staining.

Visual acuities: Right 20/25, left 20/25, baseline 20/25

Ear, nose, throat: Mucous membranes are dry; oral thrush and tonsillar erythema appreciated; localized erythema, crusting and blistering rash of varying sizes and ages along with the outer ear including the tragus, antihelix, and antitragus; helix mildly swollen. On otoscopy, the tympanic membranes appear pearly grey, shiny, translucent with no bulging, and without cerumen impaction.

Neck: Full range of motion appreciated but both horizontal and vertical movement is slow secondary to pain; no lymphadenopathy.

Neurological: Awake, alert, and oriented to date, place, and person; moves all extremities; cranial nerves II through XII grossly intact; strength 5/5 in all extremities; gait steady; no ataxia, dysmetria, or dysarthria.

Skin: Erythematous, localized, crusted, blistering vesicular rash of various sizes and ages appreciated along the left V3 distribution, C3 to T3 dermatomes anteriorly, and C2 to C6 dermatomes posteriorly.

HIV-1 antibody: positive

CD4 helper t-cells: 48 (L)

HIV-1 RNA PCR: 36,490

The lesions can be characterized as vesicles in various stages of healing. Some lesions are crusted, others are bullous, and a few are pustular. The C2-C6 dermatomes are affected posteriorly, and the C2-T3 dermatomes are involved anteriorly.

The diagnosis is Disseminated Herpes Zoster. The rash in reactivation varicella zoster virus (VZV) is preceded by tingling, itching, or pain, and begins as maculopapular then progresses to vesicles, pustules, and bullae. The rash typically involves a single dermatome and does not cross the midline. Rash present in multiple dermatomes (>3) or a rash that crosses the midline signifies disseminated disease. Hutchinson’s sign is a lesion on the lateral dorsum and tip of the nose indicating the involvement of the nasociliary branch of the ophthalmic division of the trigeminal nerve. The nasociliary branch innervates the eye, thus these lesions are highly suspicious for herpes zoster ophthalmicus. Herpes zoster ophthalmicus on fluorescein examination appears as pseuododendritic lesions with no terminal bulbs (not to be confused with herpes simplex virus (HSV) keratitis, which has dendritic lesions with terminal bulbs). Vesicles in the auditory canal (herpes zoster oticus) may be a part of Ramsay Hunt syndrome with ear pain and paralysis of the facial nerve.

The patient is immunocompromised and requires hospitalization for intravenous (IV) antiviral therapy and pain management. VZV primary infection results in viremia, diffuse rash, and seeding of sensory ganglia where the virus establishes latency. Herpes zoster is the result of viral reactivation with spread along the sensory nerve in that dermatome. Antiviral therapy aids in the resolution of lesions, reduces the formation of new lesions, reduces viral shedding, and decreases the severity of acute pain, but does not affect the development of post-herpetic neuralgia.

Immunocompetent patients may receive Valacyclovir 1 g PO q8hrs (preferred) or Acyclovir 800 mg PO 5x/day x 7d if the onset of rash is <3 days or >3 days with the appearance of new lesions.

Immunocompromised, transplant, and cancer patients are all at high risk for dissemination, chronic skin lesions, acyclovir-resistant VZV, and multi-organ involvement. Immunocompromised patients and patients with disseminated zoster require aggressive multimodal treatment, admission to the hospital, and IV antiviral therapy regardless of the time of onset of rash. Recommended therapy is Acyclovir 10 mg/kg IV q8h or Foscarnet 40 mg/kg IV q8h for acyclovir-resistant VZV. All patients require adequate analgesia, typically with non-steroidal anti-inflammatory drugs, opioids, Gabapentin, Nortriptyline, and Lidocaine patches on intact skin.

Take-Home Points

  • Disseminated herpes zoster is defined as reactivation of VZV in three or more dermatomes. It requires admission, IV antiviral therapy, and pain control.
  • If VZV reactivation involves the face, one must evaluate for herpes zoster ophthalmicus and oticus.
  • Perform a thorough neuro exam including evaluation of cranial nerves V, VII, and VIII.
  • VZV requires airborne precautions.
  1. Cohen JI. Clinical practice: Herpes zoster. N Engl J Med. 2013 Jul 18;369(3):255-63. doi: 10.1056/NEJMcp1302674. PMID: 23863052; PMCID: PMC4789101.

 

 

 

SAEM Clinical Image Series: Edema Got Your Tongue?

angioedema

A 57-year-old male presented to the emergency department with a swollen mouth for three hours. He reported never having experienced this before and denied starting any new medications. The patient endorsed a feeling that his mouth was swollen and had difficulty swallowing. The edema had been increasing in size since its onset. He had been drooling for the past hour and endorsed mild pain around the area. He denied any shortness of breath, rash, nausea, vomiting, or other areas of edema. His past medical history included hypertension, diabetes, and allergies, with no known drug allergies. His family history was unknown. His medications included Metformin and Lisinopril.

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SAEM Clinical Image Series: Left Ear Mass

ear mass

A 25-year-old male who was previously healthy presents to the emergency department with a painful left posterior ear mass. The mass began as a “pimple” and has been increasing in size for the last 6 months. He has an associated headache, dizziness, and malaise. He denies fever, trauma, drainage, known insect bite, dysphagia, dyspnea, trismus, and hearing loss. He emigrated to the United States from Honduras 8 months ago. He was seen in the emergency department 4 months prior for a similar complaint, which was diagnosed as lymphadenopathy by point-of-care ultrasound.

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