Contributor: Taylor Lynch, MD

Educational Pearls:

• Delusional parasitosis is a subtype of the psychiatric condition delusional disorder
  • Defined as a fixed, false belief of infestation by parasites or other organisms
  • A somatic type of delusional disorder
• Primary delusional parasitosis
  • Occurs in the absence of other psychiatric or medical conditions
• Secondary delusional parasitosis
  • Causes include methamphetamine use disorder, schizophrenia, neurologic diseases, or medical conditions such as thyroid disease
• Pathophysiology
  • Poorly understood
  • Upregulation of striatal dopamine system is implicated
• Management
  • Form a strong therapeutic alliance and do not discredit the patient immediately
  • Perform a full physical exam
    • This helps reassure the patient and strengthen the therapeutic alliance
    • Some day there may be a patient in whom this is not a delusion
• Treatment & Management
  • Discontinuation of substances if substance-induced
  • Antipsychotic medications like risperidone or olanzapine

References

1. Lepping P, Russell I, Freudenmann RW. Antipsychotic treatment of primary delusional parasitosis: systematic review. Br J Psychiatry. 2007;191:198-205. doi:10.1192/bjp.bp.106.029660
2. Moriarty N, Alam M, Kalus A, O'Connor K. Current Understanding and Approach to Delusional Infestation. Am J Med. 2019;132(12):1401-1409. doi:10.1016/j.amjmed.2019.06.017
3. Skelton M, Khokhar WA, Thacker SP. Treatments for delusional disorder. Cochrane Database Syst Rev. 2015;2015(5):CD009785. Published 2015 May 22. doi:10.1002/14651858.CD009785.pub2

Summarized and Edited by Jorge Chalit, OMS4

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Contributor: Aaron Lessen, MD Educational Pearls:

The cause of Alzheimer’s disease is multifactorial, but the most widely suspected mechanism is the amyloid cascade hypothesis:

• Beta-amyloid proteins accumulate in the central nervous system, forming plaques that impair neuronal function.

In recent years, advances have led to the development of targeted therapies with monoclonal antibodies. These drugs:

• Work by degrading amyloid plaques
• Slow the rate of cognitive decline and disease progression
• Have major side effects, most notably the development of amyloid-related imaging abnormalities (ARIA)
  • ARIA may present as edema, effusion, or microhemorrhages, which are only detectable on MRI
  • Symptoms can include headache, vertigo, or focal neurologic deficits that mimic stroke

For patients presenting to the emergency department with stroke-like symptoms, it is important to consider whether they have a history of Alzheimer’s disease and whether they are taking these medications.

• This guides decisions about imaging and treatment:
  • The work-up may require MRI, which can delay thrombolytic or endovascular therapy in patients with true strokeConversely, treating a patient with ARIA using thrombolytics increases the risk of bleeding and other complications

References

1. Ebell MH, Barry HC, Baduni K, Grasso G. Clinically Important Benefits and Harms of Monoclonal Antibodies Targeting Amyloid for the Treatment of Alzheimer Disease: A Systematic Review and Meta-Analysis. Ann Fam Med. 2024 Jan-Feb;22(1):50-62. doi: 10.1370/afm.3050. PMID: 38253509; PMCID: PMC11233076.
2. Ma C, Hong F, Yang S. Amyloidosis in Alzheimer's Disease: Pathogeny, Etiology, and Related Therapeutic Directions. Molecules. 2022 Feb 11;27(4):1210. doi: 10.3390/molecules27041210. PMID: 35209007; PMCID: PMC8876037.
3. Perneczky R, Dom G, Chan A, Falkai P, Bassetti C. Anti-amyloid antibody treatments for Alzheimer's disease. Eur J Neurol. 2024 Feb;31(2):e16049. doi: 10.1111/ene.16049. Epub 2023 Sep 11. PMID: 37697714; PMCID: PMC11235913.

Summarized by Ashley Lyons, OMS3 | Edited by Ashley Lyons and Jorge Chalit, OMS4

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Contributor: Alec Coston, MD

Case Report Summary:

A 17-year-old female involved in a motor vehicle collision presented to a rural emergency facility via personally operated vehicle. During workup and initial CT scan, the patient began rapidly decompensating with CT revealing a 1.5cm epidural hematoma with 7mm of midline shift. The patient went from being able to walk and talk to being obtunded with a blown left pupil and unresponsive. Following intubation, the patient was being prepared for transport but potential delays required immediate emergency evacuation of the hematoma via a Burr Hole. A traditional Burr Drill was not immediately available at the facility, so an improvised Burr Drill using an Intraosseous (IO) drill was used. 35mL of blood was removed from the hematoma and the patient immediately improved from a GCS of 3 to GCS of 8. The patient was transferred to a higher level of care facility, extubated the following day, and made a full neurological recovery. 

Educational Pearls:

What is an epidural hematoma?

• An epidural hematoma is a collection of blood between the dura mater (outermost layer of the meninges) and the skull, whereas a subdural hematoma is a collection of blood between the dura mater and arachnoid mater. Both can be life threatening depending on location and size.
• Epidural hematomas tend to be arterial, and are typically secondary to trauma and can rapidly expand, but with timely recognition and evacuation of the bleed, favorable outcomes are often possible.

What are typical intracranial pressures and at what levels do they become pathologic?

• Typical intracranial pressure (ICP) varies by age, but past infancy and early childhood, adolescents and adults have a value typically between 8-15mmHg. Values exceeding 20mmHg become pathologic and rise exponentially with increased volume.
• Initial symptoms may include headache, nausea, and vomiting, but with increased pressures may progress to more life threatening symptoms such as loss of consciousness, cranial nerve palsies, pupillary constriction or dilation (sign of herniation), and respiratory irregularities.

What is the takeaway in timing of epidural hematomas?

• Older studies show that evacuation of a hematoma with lateralizing features before the two hour mark of coma symptom onset is correlated with decreased mortality (ranging from 15-17%), but beyond 2 hours the mortality increases to well over 50%.
• Though mortality statistics have grown more variable, early targeted evacuation of epidural hematomas still remains critical for improved patient outcomes. In austere conditions with limited resources, improvisation with interosseous drills and needles can improve patient outcomes and achieve the target therapy for epidural hematomas.

References

1. Haselsberger K, Pucher R, Auer LM. Prognosis after acute subdural or epidural haemorrhage. Acta Neurochir (Wien). 1988;90(3-4):111-116. doi:10.1007/BF01560563
2. Hawryluk GWJ, Nielson JL, Huie JR, et al. Analysis of Normal High-Frequency Intracranial Pressure Values and Treatment Threshold in Neurocritical Care Patients: Insights into Normal Values and a Potential Treatment Threshold. JAMA Neurol. 2020;77(9):1150-1158. doi:10.1001/jamaneurol.2020.1310
3. Pisică D, Volovici V, Yue JK, et al. Clinical and Imaging Characteristics, Care Pathways, and Outcomes of Traumatic Epidural Hematomas: A Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury Study. Neurosurgery. 2024;95(5):986-999. doi:10.1227/neu.0000000000002982

Summarized by Dan Orbidan, OMS2 | Edited by Dan Orbidan and Jorge Chalit, OMS4

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Contributor: Aaron Lessen, MD

Educational Pearls:

What is a Nursemaid's Elbow?

• A condition in which an elbow gets partially pulled out of place (a radial head subluxation)
• Usually happens in kids under 5 because the ligaments around their elbow are still loose.
• A common situation is when an adult pulls a child up by the hand or swings them by the arms. The sudden tug causes the radius to slip out of its normal spot at the elbow joint.

How are they identified?

• These don’t normally need an xray
• The child will often hold their arm close to their side and refuse to use it
• There’s usually no swelling or obvious deformity.

Treatment?

• Reduce the radial head subluxation. There are two possible techniques:
  • Flexion and supination.
    • Start with the arm extended and pronated. Then supinate the forearm. Then bend the elbow up all the way.
  • Hyper-pronation.
    • One hand stabilizes just above the child’s elbow, the other holds the wrist. Start with the arm extended. Hyperpronate the forearm. Listen/feel for a click
• The child is normally back to normal quickly, if not get the xray

Which is better?

• Hyperpronation (Aksel, 2025)
  • 10% first attempt failure rate
  • Flexion-pronation has a 25% first attempt failure rate

References

1. Aksel G, Küka B, İslam MM, Demirkapı F, Öztürk İ, İşlek OM, Ademoğlu E, Eroğlu SE, Satıcı MO, Özdemir S. Comparison of supination/flexion maneuver to hyperpronation maneuver in the reduction of radial head subluxations: A randomized clinical trial. Am J Emerg Med. 2025 Feb;88:29-33. doi: 10.1016/j.ajem.2024.11.026. Epub 2024 Nov 18. PMID: 39579408.
2. Ulici A, Herdea A, Carp M, Nahoi CA, Tevanov I. Nursemaid's Elbow - Supination-flexion Technique Versus Hyperpronation/forced Pronation: Randomized Clinical Study. Indian J Orthop. 2019 Jan-Feb;53(1):117-121. doi: 10.4103/ortho.IJOrtho_442_17. PMID: 30905991; PMCID: PMC6394198.

Summarized by Jeffrey Olson, MS4 | Edited by Jeffrey Olson and Jorge Chalit, OMS4

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Contributor: Ricky Dhaliwal, MD

Educational Pearls:

• Angioedema in anaphylaxis
  • Histamine and mast cell-mediated pathway
  • Treatment:
    • First line: epinephrine for vasoconstriction and bronchodilation
    • Second line: H1 and H2 antihistamines such as Benadryl and famotidine
• ACE inhibitor-induced angioedema
  • Different pathway from anaphylaxis
    • ACE inhibitor-induced angioedema is mediated by bradykinins
    • Therefore, anaphylaxis medications are not beneficial in patients with ACE inhibitor-induced angioedema
  • Leading cause of drug-induced angioedema in the US
  • Patients most commonly present with swelling of the lips, tongue, or face
  • Treatment:
    • Airway management: varies depending on the severity and progression of the presentation
      • If awake nasointubation is required, LMX is a 5% lidocaine water-soluble solution that provides anesthesia to the oropharynx
    • Medications:
      • Icatibant is a synthetic bradykinin B2-receptor antagonist that can be used in acute treatment
      • Tranexamic acid (TXA) inhibits the plasmin-dependent formation of bradykinin, but the data on this treatment are mixed and limited
      • Fresh frozen plasma (FFP) is thought to degrade high levels of bradykinin with subsequent resolution of angioedema
    • Discontinue ACE inhibitor

References

1. Bork K, Wulff K, Hardt J, Witzke G, Staubach P. Hereditary angioedema caused by missense mutations in the factor XII gene: clinical features, trigger factors, and therapy. J Allergy Clin Immunol. 2009 Jul;124(1):129-34. doi: 10.1016/j.jaci.2009.03.038. Epub 2009 May 27. PMID: 19477491.
2. Bova M, Guilarte M, Sala-Cunill A, Borrelli P, Rizzelli GM, Zanichelli A. Treatment of ACEI-related angioedema with icatibant: a case series. Intern Emerg Med. 2015 Apr;10(3):345-50. doi: 10.1007/s11739-015-1205-9. Epub 2015 Feb 10. PMID: 25666515.
3. Karim MY, Masood A. Fresh-frozen plasma as a treatment for life-threatening ACE-inhibitor angioedema. J Allergy Clin Immunol. 2002 Feb;109(2):370-1. doi: 10.1067/mai.2002.121313. PMID: 11842313.
4. Pathak GN, Truong TM, Chakraborty A, Rao B, Monteleone C. Tranexamic acid for angiotensin-converting enzyme inhibitor-induced angioedema. Clin Exp Emerg Med. 2024 Mar;11(1):94-99. doi: 10.15441/ceem.23.051. Epub 2023 Aug 1. PMID: 37525579; PMCID: PMC11009700.
5. Simons FE. First-aid treatment of anaphylaxis to food: focus on epinephrine. J Allergy Clin Immunol. 2004 May;113(5):837-44. doi: 10.1016/j.jaci.2004.01.769. Erratum in: J Allergy Clin Immunol. 2004 Jun;113(6):1039. Dosage error in article text. PMID: 15131564.

Summarized by Meg Joyce, MS2 | Edited by Meg Joyce & Jorge Chalit, OMS4

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Contributors: Travis Barlock MD, Jeffrey Olson MS4

Feel free to use the cases below for your own practice. All of the scenarios are completely made up and designed to hit several teaching points.

Case 1

25 M, presents to the ED with chest pain.

Stabbing, started a few hours ago, substernal. Thinks it is GERD.

After 2-3 minutes, pain worsens and radiates to the back.

VS: BP 125/50 (Right arm 190/110). HR 120. RR of 18. Sat 98% on RA.

Additional VS: Temp of 37.2, height of 6’5”, BMI of 18.

PMH: None, doesn’t see a doctor. Meds: None

FH: Weird heart thing (Mitral Valve Prolapse), weird lung thing (spontaneous pneumothorax), tall family members with long fingers and toes

Physical Exam:

Cards: Diastolic decrescendo at the RUSB, diminished S2. UE pulses are asymmetric, LE pulses are asymmetric, carotid pulses are asymmetric, BP is asymmetric

MSK: Knees, elbows, and wrists are hypermobile.

Imaging: CXR #1 normal, #2 widened mediastinum (no read yet but shows widened mediastinum), POCUS shows small effusion

CTA/MRA doesn’t come back until after the case. 

ECG: Sinus Tach

Labs:

NT-proBNP 500 pg/mL

D-Dimer: 7000 ng/L

CBC: Hemoglobin: 13.5 g/dL, WBC: 20,000/µL, Platelets: 250,000/µL

Chem 7: Na 138, K, 5.7, Cl 102, Bicarb 17, BUN 45, Creatinine: 3.5 mg/dL, Glucose: 180

LFTs: Albumin 2.4, Total protein 5.5, ALP: 140, AST: 3500, ALT: 2800, TBili: 3.2, DirectBili: 2.4,

Ca: 7.8

LDH: 2200

PT: 20.5, INR: 2.2, Fibrinogen: 170

5th gen High-Sensitivity Troponin: <3

Lactate: 7 mmol/L

VBG: pH 7.22, paCO2 28, bicarb 15

Notes: Can have patient crash somewhere in middle and show 2nd xray

Case 2: 

A 67-year-old female is brought to the ED by her daughter due to progressive weakness, confusion, and fatigue that have worsened over the past week.

Unable to get out of bed and has become increasingly lethargic. Also having some nausea, constipation. The daughter denies any preceding illness, recent trauma, or travel. Does not know her meds but will head home to get them after talking with you.

 VS: BP 88/55 mmHg, HR 110, RR 20, O2 Sat 98% on room air.

Additional VS: Temp 36.8°C.

PMH: Hypertension, osteoarthritis, and depression.

Physical exam:

General: Thin, somnolent but arousable.

HENT: Dry mucous membranes

Neuro: Confused, A&Ox1 (self), hyporeflexia

Labs (Includes many that would not return in the ED in case you want to take this case forward to the floor)

CBC: WBC 9,500, Hb 16.5, Hct: 50%, Platelets 220,000

Chem7: Na 129, K 2.1, Cl 95, HCO3 34, Creatinine 1.6, BUN 40, Glucose 115

LFTs: normal

Magnesium: 1.1

Calcium: 10.8 mg/dL (corrects to 12.8)

iCal: 3.2

Phosphate: 2.3 mg/dL

Albumin: 2

BUN:Cr ratio: 25

VBG: pH: 7.49, PaCO2 45, HCO3: 34

Lactate: 2.8

Serum Osmolality: 276 mOsm/kg (Osmolal gap of 2)

Urine Osmolality: 550 mOsm/kg

Urine Sodium (UNa): 10 mEq/L (low). Urine Potassium (UK): 25 mEq/L (elevated). Urine Chloride (UCl): 12 mEq/L (low). Urine Magnesium (UMg): 20 (Elevated). Urine Calcium (UCa): 50 in 24 hrs (Low)

100 cc of urine with foley

FeNa

Contributor: Travis Barlock MD

Educational Pearls:

• Meningitis retention syndrome is a relatively novel and rare clinical condition
  • Aseptic meningitis + acute urinary retention
  • One study reports an incidence of about 8% in patients with acute aseptic meningitis
• Clinical presentation
  • Typical meningeal symptoms including fever, stiff neck, and headache
  • Urinary retention occurs about one week after initial symptoms
• Potential pathophysiology
  • Immune-mediated dysfunction of the central nervous system
  • Detrusor muscle underactivity from inflammation of the spinal cord
• Management
  • Supportive care
  • Bladder decompression

References

1. Hiraga A, Kuwabara S. Meningitis-retention syndrome: Clinical features, frequency and prognosis. J Neurol Sci. 2018;390:261-264. doi:10.1016/j.jns.2018.05.008
2. Pellegrino F, Funiciello E, Pruccoli G, et al. Meningitis-retention syndrome: a review and update of an unrecognized clinical condition. Neurol Sci. 2023;44(6):1949-1957. doi:10.1007/s10072-023-06704-0

Summarized & Edited by Jorge Chalit, OMS4

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Contributor: Alec Coston, MD

Educational Pearls:

• Hepatic encephalopathy (HE) is defined as a disruption in brain function that results from impaired liver function or portosystemic shunting.
  • Manifests as various neurologic and psychiatric symptoms such as confusion, inattention, and cognitive dysfunction
• Although ammonia levels have historically been recognized as important criteria for HE, the diagnosis is ultimately made clinically.
  • An elevated ammonia level lacks sensitivity and specificity for HE
  • Trends in ammonia levels do not correlate with disease improvement or resolution
  • A 2020 study published in the American Journal of Gastroenterology evaluated 551 patients diagnosed with hepatic encephalopathy and treated with standard therapy
    • Only 60% of patients had an elevated ammonia level, demonstrating the limitations of ammonia levels
  • However, a normal ammonia level in a patient with concern for HE should raise suspicion for other pathology.
• In patients with cirrhosis presenting with neuropsychiatric symptoms, consider HE as the diagnosis after excluding other potential causes of altered mental status (i.e., Seizure, infection, intracranial hemorrhage)
• The primary treatment is lactulose
  • Works by acidifying the gastrointestinal tract.
  • Ammonia (NH₃) is converted into ammonium (NH₄⁺), which is poorly absorbed and subsequently eliminated from the body
  • Also exerts a laxative effect, further enhancing elimination

References:

1. Haj M, Rockey DC. Ammonia Levels Do Not Guide Clinical Management of Patients With Hepatic Encephalopathy Caused by Cirrhosis. Am J Gastroenterol. 2020 May;115(5):723-728. doi: 10.14309/ajg.0000000000000343. PMID: 31658104.\
2. Lee F, Frederick RT. Hepatic Encephalopathy-A Guide to Laboratory Testing. Clin Liver Dis. 2024 May;28(2):225-236. doi: 10.1016/j.cld.2024.01.003. Epub 2024 Jan 30. PMID: 38548435.
3. Vilstrup, Hendrik1; Amodio, Piero2; Bajaj, Jasmohan3,4; Cordoba, Juan1,5; Ferenci, Peter6; Mullen, Kevin D.7; Weissenborn, Karin8; Wong, Philip9. Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the American Association for the Study Of Liver Diseases and the European Association for the Study of the Liver. Hepatology 60(2):p 715-735, August 2014. | DOI: 10.1002/hep.27210
4. Weissenborn K. Hepatic Encephalopathy: Definition, Clinical Grading and Diagnostic Principles. Drugs. 2019 Feb;79(Suppl 1):5-9. doi: 10.1007/s40265-018-1018-z. PMID: 30706420; PMCID: PMC6416238.

Summarized by Ashley Lyons, OMS3 | Edited by Ashley Lyons & Jorge Chalit, OMS4

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Contributor: Taylor Lynch, MD

Educational Pearls:

What is atrial fibrillation with rapid ventricular response (AFib with RVR) and how does it differ from atrial fibrillation (AFib)?

• AFib is an abnormal heart rhythm in which the heart has disorganized atrial electrical activity. This causes the atria to quiver with only select signals being conducted through the Atrioventricular (AV) Node to reach the ventricles and result in ventricular contraction.
• Often described as “irregularly irregular”, a patient's EKG will present with no discernible P-waves, and irregular R-R intervals.
• AFib with RVR is distinguished from AFib when the patient’s ventricular rate is greater than 100-110 beats per minute in AFib with RVR.

What is the treatment for AFib with RVR?

• Diltiazem is considered one of the first line therapeutic agents in the treatment of AFib with RVR.
• Diltiazem inhibits L-Type calcium channels in the AV Node, reducing the amount of signals conducted to the ventricles, thus reducing the ventricular rate.

Why pretreat patients receiving Diltiazem for AFib with RVR with calcium?

• While diltiazem inhibits cardiac calcium channels, it may also cause peripheral vasodilation, resulting in diltiazem-induced hypotension.
• A recent study found that this hypotension can be blunted by pretreating with 1-2g IV Calcium Chloride (IV Calcium Gluconate can be used in the ED).
• Calcium is thought to peripherally stabilize the vascular smooth muscle, preventing vasodilation without impacting the desired calcium channel blocker action at the AV node.

Key takeaways?

• In combination with slower pushes of diltiazem for patients in AFib with RVR (AFib with ventricular rate >100-110 bpm) with borderline low blood pressures, 1-2 g of IV Calcium Gluconate can combat diltiazem induced hypotension peripherally without negating the cardiac effect of diltiazem to reduce the heart rate. 

References

1. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2024;149(1):e1-e156. doi:10.1161/CIR.0000000000001193
2. Az A, Sogut O, Dogan Y, et al. Reducing diltiazem-related hypotension in atrial fibrillation: Role of pretreatment intravenous calcium. Am J Emerg Med. 2025;88:23-28. doi:10.1016/j.ajem.2024.11.033

Summarized by Dan Orbidan, OMS2 | Edited by Dan Orbidan and Jorge Chalit, OMS4

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Contributor: Aaron Lessen, MD

Educational Pearls:

Recorded March 2025

What is the best treatment for a fever? Tylenol? Ibuprofen? Combined? Alternating the two?

• The journal Pediatrics aimed to answer this question with a meta-analysis of 31 randomized controlled trials including 5,009 febrile children.
• Results showed that both combined and alternating acetaminophen/ibuprofen regimens were significantly more effective at reducing fever at 4 and 6 hours compared with acetaminophen alone, with numbers needed to treat (NNT) of 3 and 4, respectively.
• High-dose ibuprofen alone also offered modest benefit (NNT 8).

What dose should I use?

• Oral acetaminophen
  • 10 to 15 mg/kg
  • Every 4–6 hours as needed
  • Do not exceed 75 mg/kg/day (or 4,000 mg/day maximum for older/larger kids)
• Oral ibuprofen
  • 5 to 10 mg/kg
  • Every 6–8 hours as needed
  • Do not exceed 40 mg/kg/day (or 2,400 mg/day maximum for older/larger kids)

References

1. De la Cruz-Mena JE, Veroniki AA, Acosta-Reyes J, Estupiñán-Bohorquez A, Ibarra JA, Pana MC, Sierra JM, Florez ID. Short-term Dual Therapy or Mono Therapy With Acetaminophen and Ibuprofen for Fever: A Network Meta-Analysis. Pediatrics. 2024 Oct 1;154(4):e2023065390. doi: 10.1542/peds.2023-065390. PMID: 39318339.

Summarized by Jeffrey Olson, MS4 | Edited by Jeffrey Olson and Jorge Chalit, OMS4

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