ALiEM AIR Series | HEENT Module (2025)

 

Welcome to the AIR HEENT Module! After carefully reviewing all relevant posts in the past 12 months from the top 50 sites of the Digital Impact Factor [1], the ALiEM AIR Team is proud to present the highest quality online content related to related to HEENT emergencies in the Emergency Department. 4 blog posts met our standard of online excellence and were approved for residency training by the AIR Series Board. More specifically, we identified 2 AIR and 2 Honorable Mentions. We recommend programs give 2 hours of III credit for this module.

 

AIR Stamp of Approval and Honorable Mentions

 

In an effort to truly emphasize the highest quality posts, we have 2 subsets of recommended resources. The AIR stamp of approval is awarded only to posts scoring above a strict scoring cut-off of ≥30 points (out of 35 total), based on our scoring instrument. The other subset is for “Honorable Mention” posts. These posts have been flagged by and agreed upon by AIR Board members as worthwhile, accurate, unbiased, and appropriately referenced despite an average score.

 

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Highlighted Quality Posts: HEENT 2025

 

SiteArticleAuthorDateLabel
EMCritEpiglottitisDr. Josh FarkasJuly 22, 2024AIR
EMDocsAuricular HematomaDr. Jacob Tauferner, Dr. Mihir PatelApril 13, 2024AIR
EMDocsMalignant/Necrotizing Otitis ExternaDr. Russ Burgin, Dr. Rachel BridwellApril 27, 2024HM
Taming the SRUDiagnostics and Therapeutics: Ear Emergencies in the DepartmentDr. Nicole LewisNovember 14, 2023HM

 

(AIR = Approved Instructional Resource; HM = Honorable Mention)

 

If you have any questions or comments on the AIR series, or this AIR module, please contact us!

Reference

    1. Lin M, Phipps M, Chan TM, et al. Digital Impact Factor: A Quality Index for Educational Blogs and Podcasts in Emergency Medicine and Critical Care. Ann Emerg Med. 2023;82(1):55-65. doi:10.1016/j.annemergmed.2023.02.011, PMID 36967275

 

 

SAEM Clinical Images Series: Alternative Block

A 10-year-old female with a history of constipation presented with intermittent lower abdominal pain with difficulty urinating. Pain was in the suprapubic area. The patient stated she last urinated the morning of presentation and typically urinates 1-2 times a day. She reported that it is sometimes hard to initiate urination and that she has pain at the conclusion of urination. She typically takes MiraLAX daily for constipation but ran out one week ago. She denied fever, chills, nausea or vomiting.

Constitutional: Awake, alert and in no acute distress.

HEENT: PERRLA. Moist mucus membranes.

Cardiovascular: Regular rate and rhythm. No murmur.

Pulmonary: Breath sounds normal. No increased work of breathing.

Abdominal: Abdomen soft. There is tenderness in the suprapubic area. There is no guarding or rebound.

Neurologic: Awake and alert. At neurologic baseline. No focal deficits.

UA: Trace ketones, 100 protein.

Post void residual: 430 cc.

X-ray of the abdomen is normal without obstruction or a significant stool burden. Ultrasound demonstrates a distended fluid-filled vagina.

Imperforate hymen. The opening of the vagina is typically surrounded by a thin membrane with an opening in the center, called the hymen. In the case of an imperforate hymen, the membrane does not have an opening and therefore blocks the vaginal canal. Symptoms of imperforate hymen vary. It can present early in life if normal mucous builds up and causes a bulge of the membrane. Imperforate hymen may not be diagnosed until adolescence when menstruation begins. Symptoms at that time include amenorrhea, back pain, lower abdominal pain, or difficulty with urinating or stooling. In an adolescent with imperforate hymen, physical exam may demonstrate a vaginal bulge with a bluish discoloration, caused by the accumulation of blood in the vagina (hematocolpos). This patient had urinary retention secondary to imperforate hymen and accumulation of blood in the vaginal canal that compressed the urethra. A genitourinary exam was later performed and confirmed the diagnosis. Imperforate hymen is treated with a minor surgical procedure to remove the extra tissue.

Take-Home Points

  • Imperforate hymen occurs when the hymen covers the vaginal entire vaginal opening, therefore blocking it. It may present early in life or later during adolescence.

  • Consider imperforate hymen as a differential diagnosis for female patients who present with lower abdominal or back pain, amenorrhea, or difficulty with urinating or stooling.

  • Diagnosis and management of hymenal variants. ACOG. (2019, May 23). https://www.acog.org/clinical/clinical-guidance/committee-opinion/articles/2019/06/diagnosis-and-management-of-hymenal-variants

  • Hamouie A, Dietrich JE. Imperforate Hymen: Clinical Pearls and Implications of Management. Clin Obstet Gynecol. 2022 Dec 1;65(4):699-707. doi: 10.1097/GRF.0000000000000703. Epub 2022 Mar 11. PMID: 36260009.

By |2025-02-26T14:55:11-08:00Feb 28, 2025|Ob/Gyn, Pediatrics, SAEM Clinical Images|

SAEM Clinical Images Series: Short of Breath and Short on Time

A 62-year-old female presented with shortness of breath that started two days ago which she described as mild to moderate, worse with activity. She denied chest pain, abdominal pain, fever, diaphoresis, syncope, cough, wheezing, sputum production, or emesis. Past medical history was significant for rectal adenocarcinoma metastatic to liver. She was status post radioembolization of liver metastasis from the left lobe and her last chemotherapy was approximately one month prior to presentation.

Vitals: T 36.5°C; BP 87/57; HR 91-115; RR 12; O2 sat 94% on 2L NC

General: Ill-appearing.

Cardiovascular: Normal rate and regular rhythm, diminished heart sounds.

Chest: Pulmonary effort normal, normal breath sounds.

Gastrointestinal: Abdomen flat, soft, nontender.

MSK: Cyanotic toes bilaterally with decreased capillary refill.

Neurologic: Diffuse motor weakness, no focal deficit present.

CBC: WBC 18.0, Hgb 9.6, Plt 348

PT: 19.4

INR: 1.6

BMP: Na 126, K 4.4, Cl 100, CO2 13 (20-29), Anion Gap 13, Glucose 107, BUN 54 (7-25), Cr 1.96, Ca 7.7

BNP: 410 (0-100)

Lactic acid: Initial 2.5, repeat 4.0 (0.5-2.0)

EKG: Normal sinus rhythm, normal rate, low voltage QRS.

Pneumopericardium, the presence of air within the pericardial sac, is discovered on imaging. The accumulation of air can result in compression of the heart and interfere with normal functioning. Pneumopericardium on imaging can appear as a characteristic radiolucency around the heart on chest X-ray and CT scan, or as direct visualization of air within the pericardial sac on ECHO. Causes include trauma introducing air into the pericardial sac, infection with gas-producing organisms, procedural complications, barotrauma, or spontaneous occurrence.

Gastropericardial fistula is a rare, life-threatening condition whereby an abnormal communication is created between the stomach and pericardial sac, with less than 100 cases reported in modern literature. This condition usually occurs in the setting of prior gastroesophageal surgery, ulcer perforation, or as in this case, malignant perforation due to breakdown of malignant implants between the liver and the gastric wall adherent to the diaphragm and pericardium. This can lead to frank pneumopericardium and tension physiology, ultimately resulting in death if not promptly diagnosed and treated with urgent pericardial drain placement to ameliorate tension physiology. Definitive therapy is surgical repair.

Take-Home Points

  • Gastropericardial fistula is a rare cause of pneumopericardium, usually in the setting of patients with prior gastroesophageal surgery, gastric ulceration, or malignancy of the stomach.

  • Diagnosis is usually made with a combination of imaging modalities including esophagram/upper GI, CT with water soluble oral contrast, and echocardiogram.

  • Prompt diagnosis and treatment are necessary to prevent the onset of tension physiology.

  • Azzu V. (2016). Gastropericardial fistula: getting to the heart of the matter. BMC gastroenterology, 16(1), 96. https://doi.org/10.1186/s12876-016-0510-8

  • Rathur, A., Al-Mohamad, H., Steinhoff, J., & Walsh, R. (2021). Chest Pain from Pneumopericardium withGastropericardial Fistula. Case reports in cardiology, 2021, 5143608. https://doi.org/10.1155/2021/5143608

Is Ondansetron for Nausea and Vomiting Prophylaxis Necessary with Opioids?

prophylactic ondansetron with opioids example 4+4
Ondansetron is the most documented medication given in emergency departments (ED) throughout the United States [1]. We have all heard someone ask, “Can I get an order for 4 and 4 for this patient?” in reference to 4 mg of IV morphine and 4 mg of IV ondansetron. It has become common practice in many institutions to provide a prophylactic antiemetic prior to administering an IV opioid.

Logic for giving ondansetron with opioid

This dual therapy seems to make initial sense because all opioids carry a FDA warning that nausea may occur [2]. So why not administer an antiemetic to prevent it? Opioids cause nausea and vomiting due to its interaction on the chemoreceptor trigger zone (CTZ), increased vestibular sensitivity, and hindered gastric emptying [3]. The logic is to provide these patients with a 5-HT3 antagonist (i.e., ondansetron) to inhibit the opioid from exerting emetogenic properties on 5-HT3 receptors in the CTZ and prevent nausea and/or vomiting.

How common is nausea and vomiting associated with IV opioids?

Multiple studies illustrate that morphine-induced nausea and vomiting is low, ranging from 2.0–20.2% in ED patients [4-9]. When discussing with ED nurses, nausea and vomiting are anecdotally associated with how quickly the IV opioid is administered and generally occurs within 5 minutes of administration.

So we should give IV ondansetron to prevent this, right? A common misconception with IV ondansetron is its onset of action. In fact, it can take anywhere between 27-34 minutes before there is a 50% decrease in nausea severity following the administration of ondansetron [10, 11]. This begs the question, does it really make sense to provide prophylactic antiemetics with IV opioids?

Literature Review

StudyInterventionOutcomeConclusion
Bradshaw et al. [5]

RCT- double blinded

Performed in United Kingdom

IV morphine + placebo (n=136)

IV morphine + metoclopramide 10 mg (n=123)

N/V between the 2 groups was not statistically significant (p=0.3).

Overall incidence of N/V was low in both treatment groups (3.7% in placebo and 1.6% metoclopramide)

Pre-treating patients with metoclopramide was not necessary.

Overall N/V associated with IV morphine was very low and recommended using antiemetics for patients who develop N/V.

Bhowmik et al. [8]

RCT, double blinded

Performed in India

IV morphine + placebo (n=53)

IV morphine + promethazine (n=54)

IV morphine + ramosetron (n=54)

IV morphine + metoclopramide (n=54)

Overall incidence of N/V was low in all treatment groups (9.4% ramosetron, 18.5% metoclopramide, 10.2% in promethazine and 6.2% in placebo)

Rate of N/V was not statistically significant between any of the groups.

 Patients should receive antiemetic therapy only if experience N/V and not as a prophylactic agent with IV opioids.

Patients that received (morphine + placebo) had less N/V compared to other treatment groups; however, NOT statistically significant.

Sussan et al. [9]

Randomized, double- masked multicenter trial

Performed in 9 countries

Investigated 2,574 patients that received IV opioids and randomized 520 patients that developed N/V associated with IV opioids.

Group 1: placebo (n=94)

Group 2: ondansetron 8 mg (n=214)

Group 3: ondansetron 16 mg (n=211)

Resolution of N/V was statistically more significant (p < 0.001) when comparing ondansetron therapy with placebo.

Group 1: 45.7% N/V resolved

Group 2: 62.3% N/V resolved

Group 3: 68.7% N/V resolved

The best practice seems to treat patients’ N/V after development in patients that receive IV opioids.

Trial determined the prevalence of N/V is minimal and exposing patients to medication they do not need puts them at risk for additional adverse drug reactions.

Each of the 3 trials concluded that there was no statistical significance in outcomes when adding prophylactic antiemetics with IV opioids. After these institutions analyzed their findings, the investigators at their respective institutions made it common practice for patients to only receive antiemetics AFTER a patient developed nausea or vomiting.

Prophylactic ondansetron practice

So why is ondansetron still commonly used to pre-treat patients that receive IV opioids in the ED?

The limited literature primarily focused on these anti-emetic agents: metoclopramide, promethazine, and ramosetron (5-HT3 antagonist). Literature related to specifically ondansetron is minimal.

Two randomized, placebo-controlled studies comparing ondansetron, metoclopramide, and saline in ED patients complaining of nausea showed no clinically important difference in the reduction of nausea between treatments and placebo [12, 13]. Yet in the ED, we still order ondansetron more than any other medication.

Some nerd (me!) put together a prospective multiple-site study (n=133) at 2 academic medical institutions where patients were administered IV opioids, with or without IV ondansetron [14]. Patients were observed for nausea and vomiting at baseline, 5 minutes, and 30 minutes after opioid administration, and then for a total of 2 hours. The results showed that 17.3% of patients developed nausea, with no significant difference in the rate of nausea, emesis, or the need for rescue antiemetics between the group receiving ondansetron and the group receiving opioids alone.

Of note, ondansetron is not FDA approved for the treatment or prophylaxis of acute nausea and/or vomiting (N/V) outside of chemotherapy, radiation, and postoperative use. It also, not surprisingly, has side effects!

Take Home Point

  1. Concurrent treatment with anti-emetics (including ondansetron) is unnecessary, increases costs, and adds potential for adverse drug reactions.
  2. The next time the request for “4 + 4” comes through, consider holding off on the unnecessary ondansetron with your IV opioid order.
  3. You can use this isopropyl alchohol vapor inhalation trick of the trade for those 2-20% of patients that do develop nausea.

References

  1. National Hospital Ambulatory Medical Care Survey: 2011 Emergency Department Summary. Accessed 19 Dec 2024.
  2. Red Book: pharmacy’s fundamental reference. Montvale, NJ: Thompson Healthcare Inc.; 2010
  3. Smith H, Smith J, Seidner P. Opioid-induced nausea and vomiting. Annals of Palliative Medicine 2012;1(2):121-129
  4. Paoloni R, Talbot-Stern J. Low incidence of nausea and vomiting with intravenous opioid analgesia in the ED. Am J Emerg Med 2002;20:604-608.
  5. Bradshaw M, A Sen. Use of prophylactic antiemetic with morphine in acute pain: randomized controlled trial. Emerg Med J 2006; 23:210-212.
  6. Talbot-Stern J, Paoloni R. Prophylactic metoclopramide is unnecessary with intravenous analgesia in the ED. Am J Emerg Med 2000;18(6):653-7.
  7. Lambie B, Chambers J, Herbison P. The role of prophylactic anti-emetic therapy in emergency department patients receiving intravenous morphine for musculoskeletal trauma. Emer Med 1990; 11(4): 240-243.
  8. Bhowmik A, Dasgupta I, Barua S, et al. Evaluation of the need of prophylactic antiemetic with injection morphine in treating acute musculoskeletal pain in the Indian population. IJAR 2014;2:53-58.
  9. Sussan G, Shurman J, Creed M, et al. Intravenous ondansetron for the control of opioid-induced nausea and vomiting. Clinical Therapeutic. 1999; 21:1216-1227.
  10. Cotton J, Rowell L, Hood R, et al. A comparative analysis of isopropyl alcohol and ondansetron in the treatment of postoperative nausea and vomiting from the hospital setting to the home. AANA J. 2007; 75(1):21-6.
  11. Winston A, Rinehart R, Riley G, et al. Comparison of inhaled isopropyl alcohol and intravenous ondansetron for treatment of postoperative nausea. AANA J. 2003; 71(2):127-32.
  12. Barrett TW, DiPersio DM, Jenkins CA, et al. A randomized, placebo-controlled trial of ondansetron, metoclopramide, and promethazine in adults. Am J Emerg Med. 2011 Mar;29(3):247-55.
  13. Egerton-Warburton D, Meek R, Mee MJ, et al. Antiemetic use for nausea and vomiting in adult emergency department patients: randomized controlled trial comparing ondansetron, metoclopramide, and placebo. Ann Emerg Med. 2014 Nov;64(5):526-532.
  14. Culver MA, Richards EC, Jarrell DH, et al. Use of Prophylactic Ondansetron With Intravenous Opioids in Emergency Department Patients: A Prospective Observational Pilot Study. J Emerg Med. 2017;53(5):629-634. PMID 28987314. DOI

SAEM Clinical Images Series: When it is Not Just a Knot

knot

A 12-year-old male with a history of hydrocephalus status post ventriculoperitoneal (VP) shunt placement presented with an abdominal “knot.” The patient’s mother noticed the knot two days ago, on the right anterolateral thorax, which has steadily been increasing in size. The patient had no known trauma to the area or had been bitten or stung by any insect. He has otherwise been complaining of a headache, generalized, without positional changes, improved with home acetaminophen, ice pack, and rest. There were otherwise no associated vision changes, nausea, vomiting, mental status changes, or fever.

Vitals: T-36.2°C; HR 74 bpm; BP 144/75 mm Hg; RR 20; O2 Sat 96% RA

General: Well-appearing teenager in NAD.

HEENT: NC/AT. PERRL approximately 2-3 mm bilaterally. EOMI.

Neck: Supple, no meningismus.

Chest Wall: Induration to the right anterolateral thorax 5 cm x 4 cm without erythema, fluctuance, or drainage, non-tender to palpation.

Neurological: Alert. No focal neurological deficit observed.

The cause of the knot is subcutaneous cerebrospinal fluid from a shunt malfunction. The ultrasound images show characteristic “cobblestoning,” indicating fluid in the subcutaneous tissue, around a linear hyperechoic object, the catheter of the VP shunt. On the plain film imaging, a disconnect was found between the thoracic and abdominal portions of the VP shunt. Up to 80% of patients with VP shunts will have experienced a shunt malfunction after 12 years, according to one study, with fractured tubing causing shunt failure in around 15% of all cases (1).

Nausea, vomiting, headache, irritability, or decreased mental status are common but nonspecific findings in shunt malfunction. Pediatric patients may present with other signs such as bulging fontanelles, increasing head circumference, or feeding and behavioral changes. An increase in the interval ventricular size can be seen in neuroimaging but can be absent in as many as 20% of patients (2). If there is a high degree of clinical suspicion for shunt malfunction, normal or unchanged neuroimaging should not preclude neurosurgical consultation.

Take-Home Points

  • In the United States, mechanical causes of VP shunt malfunction are the most common presentation, such as catheter obstruction, fracture along the clavicle or ribs, degradation of tubing, and migration of the distal catheter due to changes in height or weight.
  • Rarely, patients can develop an accumulation of CSF at the distal catheter of the VP shunt due to migration into the abdominal wall forming an abdominal pseudocyst.
  • In patients with VP shunts, abdominal complications should be considered as a sign of shunt malfunction.
  • Consider pertinent physical exam findings and POCUS to confirm the diagnosis of shunt malfunction at the distal catheter.

  • Sainte-Rose C, Piatt JH, Renier D, Pierre-Kahn A, Hirsch JF, Hoffman HJ, Humphreys RP, Hendrick EB. Mechanical complications in shunts. Pediatr Neurosurg. 1991-1992;17(1):2-9. doi: 10.1159/000120557. PMID: 1811706.

  • Reynolds RA, Ahluwalia R, Krishnan V, Kelly KA, Lee J, Waldrop RP, Guidry B, Hengartner AC, McCroskey J, Arynchyna A, Staulcup S, Chen H, Hankinson TC, Rocque BG, Shannon CN, Naftel R. Risk factors for unchanged ventricles during pediatric shunt malfunction. J Neurosurg Pediatr. 2021 Sep 24;28(6):703-709. doi: 10.3171/2021.6.PEDS2125. PMID: 34560626.

SAEM Clinical Images Series: A Rare Gastrointestinal Complication of an Endocrine Emergency

A 54-year-old woman with a history of hypothyroidism, diabetes mellitus type II, COPD, asthma, anxiety, and depression presented to the emergency department via EMS with three days of fatigue, weakness, chills, and shortness of breath without chest pain or cough. Symptoms had been progressively worsening, and she stated she felt as if she could not move her body on presentation. She also noted diarrhea without abdominal pain, melena, or hematochezia. Just prior to arrival the patient’s daughter thought she looked paler and shorter of breath and called EMS after a near syncopal episode. EMS reported that the family was concerned that the patient’s blood glucose level was low. Blood glucose upon EMS arrival was 90 and rose to 150 following their administration of oral glucose. The patient denied fever, recent sick contacts, urinary changes, hematuria, or leg swelling. She reported two missed doses of levothyroxine which was prescribed at a dose of 25 mcg daily. No recent antibiotic use reported.

Vitals: Temp 36.4°C; BP 106/64 mmHg; HR 62 bpm; Resp 16/min; SpO2 96% on RA

General: Patient drowsy, slow to answer questions, sitting with eyes closed. No obvious distress.

Skin: Warm and dry.

Cardiovascular: Regular rate and rhythm without murmur.

Respiratory: Lungs clear to auscultation bilaterally. No respiratory distress.

Abdomen: Soft, non-distended, normal bowel sounds, diffuse abdominal discomfort to palpation, which she states is chronic.

Neurological: Oriented to person, place, time. CN II-XII intact. No focal neurological deficit observed, strength 4+/5 throughout able to hold all extremities up when placed above the body.

Extremities: No obvious swelling.

CBC: Hb 11.5, WBC 9.5, Plt 186

BMP: Na 141, K 3.8, Cl 105, CO2 24, BUN 17, Cr 1.3

LFTs: AST 20, ALT 11, Bili 0.4

VBG: pH 7.28, PCO2 60, HCO2 28

Mg: 1.7

CK: 333

TSH: 196.80

The abdominal CT scan demonstrates multiple fluid-filled mildly dilated loops of large bowel with air-fluid levels, some minimally dilated loops of small bowel, and no clear transition point identified which is concerning for developing colonic pseudo-obstruction (Ogilvie Syndrome). There are many predisposing factors that may cause Ogilvie Syndrome including recent surgery, infection, trauma, respiratory failure, cancer, and other metabolic conditions.

Given our patient’s history of hypothyroidism with missed doses of levothyroxine and an elevated TSH her cause of Ogilvie syndrome is most likely hypothyroidism. This is also known as myxedema ileus, a rare entity. Management of myxedema ileus consists of bowel decompression with a nasogastric tube and treatment of the hypothyroid condition. In our case, the patient received 200 mcg of levothyroxine, and 12.5 mcg of liothyronine while undergoing further endocrinologic workup

Take-Home Points

  • In patients with a history of hypothyroidism presenting with gastrointestinal concerns, myxedema ileus, while not common, should be considered.
  • Colonic pseudo-obstruction (Ogilvie syndrome) has many causes and the radiographic appearance of a bowel obstruction without an obvious transition point.
  • Myxedema ileus should be managed with bowel decompression and treatment of the underlying hypothyroidism. ICU level care is often needed for this severe endocrine emergency

  • Saunders MD. Acute colonic pseudo-obstruction. Best Pract Res Clin Gastroenterol. 2007;21(4):671-87. doi: 10.1016/j.bpg.2007.03.001. PMID: 17643908.

  • Vanek VW, Al-Salti M. Acute pseudo-obstruction of the colon (Ogilvie’s syndrome). An analysis of 400 cases. Dis Colon Rectum. 1986 Mar;29(3):203-10. doi: 10.1007/BF02555027. PMID: 3753674.

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