Case: A 63 y.o. female with PMH of migraines and chiari malformation presents with headache. Patient reports that for the past 10 days, she has had a right-sided migraine that she describes as similar in quality to her prior migraines but longer-lasting. However, at 2 PM yesterday, she experienced an acute worsening of the severity of her headache – additionally, the pain became bilateral and occipital at this time. The patient reports dizziness, nausea, and photophobia, and her husband states that the patient has been slower to respond to questions for the past day. Denies vomiting, visual changes, or fever.

Vitals: BP: 133/90 | Pulse: 71 | Temp: 98.1F | Respiratory Rate: 18 | SpO2: 99%

Exam: Neuro exam is non-focal. Patient appears tired, but responds to questions appropriately. 

Clinical Course: Patient is given Tylenol, 10 mg IV Compazine, and 1 L lactated ringers with significant improvement in symptoms. Given change in headache quality from prior migraines and acute worsening of headache, CT Head without contrast ordered. 

CT revealed a large hemorrhagic neoplasm in the right frontal region with associated mass effect and 1.2 cm leftward midline shift resulting in obstructive hydrocephalus. Patient subsequently noted to be increasingly somnolent compared to initial presentation. Neurosurgery was consulted who recommended decadron, Keppra for seizure prophylaxis, and admission to the ICU.

Headache Pearls: The majority of headaches are due to primary headaches such as tension headache, migraine, or cluster headache. However, as 18% of patients with chief complaint of headache may be experiencing a secondary headache disorder. Many of these secondary headaches represent life-threatening emergencies such as intracranial bleeding or CNS infection. The SNOOP mnemonic is a helpful tool for remembering “red flag” headache symptoms to identify headache patients who warrant further imaging/laboratory work-up in the ED. Additionally, improvement in symptoms with medication does not decrease the likelihood of a secondary headache disorder.

Systemic: Systemic signs or conditions such as fever, weight loss, immunocompromised, HIV, cancer

Neuro: Neurologic findings including mental status changes, vision changes, seizure, confusion, or focal neuro findings on exam

Onset: Onset that is acute with progression to worst severity within minutes

Older: Older patient (50 y.o. or older) with new headache or a progressive headache

Previous: No history of previous headaches, or in a patient with history of headaches, a change in severity/symptoms/location from prior headaches

Pregnancy: Headache in pregnant or post-partum patient

References:

Ashenburg Nick, Marcolini Evadne, Hine Jason. Approach to Headache. In: Mattu A and Swadron S, ed. CorePendium. Burbank, CA: CorePendium, LLC. https://www.emrap.org/corependium/chapter/rec8eRzSrPsVUiMuV/Approach-to-Headache#h.pq7xksb5a2qy. Updated October 8, 2022. Accessed December 22, 2023.

Dodick DW. Clinical clues and clinical rules: primary vs secondary headache. Adv Stud Med 2003;3:87–92.

Do TP, Remmers A, Schytz HW, et al. Red and orange flags for secondary headaches in clinical practice: SNNOOP10 list. Neurology. 2019;92(3):134-144. doi:10.1212/WNL.0000000000006697

HPI: 

• A 58 year old male with a past medical history of CAD s/p PCI, cardiomyopathy with EF 30-35% c/b VF arrest s/p ICD presents via EMS as a STEMI alert. 
• While en route, patient had episode of VT on the cardiac monitor and was defibrillated by the ICD almost immediately, returning to narrow complex rhythm. 
• He remains neurologically intact and states that 1 hour ago he started having crushing substernal chest pain and feels like he is going to die.  

Physical Exam:

Vitals: BP 84/40, HR 39, RR 20, SpO2 94%

• GCS 15, moves all extremities equally
• Appears pale, diaphoretic, in obvious extremis
• Bradycardic with cool extremities
• Trace pitting edema in bilateral lower extremities

EKG interpretation: Junctional rhythm with PVCs in pattern of bigeminy. Inferior STEMI with reciprocal ST segment depressions in lateral leads. 

Case continued:

• Patient was given 324mg aspirin en route by EMS. Additionally given 300 mg amiodarone bolus, 4000 U heparin bolus, and 500 cc LR bolus upon arrival to ED.
• During initial resuscitation, cardiac rhythm converts to VT and patient is immediately defibrillated by ICD with ROSC and remains neurologically intact. 
• Patient persistently hypotensive and norepinephrine infusion is initiated to MAP > 65.
• Patient experiences another episode of VT and is again immediately defibrillated by ICD with ROSC and remains neurologically intact. 
• Decision is made in junction with cardiology and interventional cardiology to transport patient immediately to catheterization lab. During the procedure, the patient continues to have multiple episodes of VT and VFib and undergoes general anesthesia and is intubated. The angiogram demonstrates a 100% occlusion of the proximal RCA. The patient recovers in the CCU and was discharged on hospital day 5.

Pearls:

• Electrical storm is defined by 3 or more sustained episodes of VT, VFib, or appropriate shocks from an ICD within 24 hours. 
• Initial management adheres to ACLS protocol with strict attention to airway, breathing, and circulation.
  • Medications include epinephrine, amiodarone, and lidocaine
• Consider the following for refractory VT/VF (electrical storm):
  • Esmolol or other beta blockade agents
  • Dual sequential defibrillation
    • https://www.youtube.com/watch?v=Ov-BBUhKdJU
  • Ultrasound guided stellate ganglion block
    • https://www.youtube.com/watch?v=B6ROeVFUJSY
  • VA-ECMO

References:

Eifling M, Razavi M, Massumi A. The evaluation and management of electrical storm. Tex Heart Inst J. 2011;38(2):111-121.

Driver BE, Debaty G, Plummer DW, Smith SW. Use of esmolol after failure of standard cardiopulmonary resuscitation to treat patients with refractory ventricular fibrillation. Resuscitation. 2014;85(10):1337-1341. doi:10.1016/j.resuscitation.2014.06.032

Submitted by Rahul Gupta M.D.

HPI

• 43-year-old female p/w sudden onset vertigo, nausea, vomiting, and severe R sided headache 1 hour PTA
• HA is R sided, radiates into neck
• No weakness, numbness, tingling, speech changes
• Pt notes balance issues
• States that the vertigo is positional in nature.

Physical Exam

Vitals: BP 210/89, P 75, RR 18, SPO2 98%

• Neuro exam: Cn II-XII intact, motor strength normal, normal finger to nose, no nystagmus noted
• Gait was unable to be assessed secondary to vertigo

DDx

• subarachnoid hemorrhage, posterior circulation stroke, primary headache, vertebral artery dissection, peripheral vertigo

Case course

• A stroke alert was called
• CTA Head and neck demonstrated R vertebral artery occlusion. MRI demonstrated an acute infarct of the cerebellar vermis.

Pearls:

• Initial work-up of vertigo is stratifying between central and peripheral vertigo. The below table provides general patterns for both, but this is variable in nature.

• HINTS exam should be performed only when patient has persistent vertigo, nystagmus, and a normal neurological exam. When used correctly and performed appropriately, the HINTS exam has impressive sensitivity (100%) and specificity (96%) for posterior circulation stroke as compared to MRI
• See the HINTS exam in action here:

• The Dix-Hallpike maneuver can be performed if BPPV is in the differential. Dix-Hallpike is only 50-85% sensitive for BPPV. If positive, consider the Epley Maneuver for treatment.
  • Consider teaching the patient the maneuver if they find relief after the Epley maneuver.
  • Other treatments for peripheral vertigo include:
    • 1^st line: Diphenhydramine 25-50mg IM/IV/po q4hr, Meclizine 25mg po QID
    • 2nd line: Diazepam 2-10 mg po/IV q4h-q8h, Lorazepam 0.5-2mg po/IM/IV q4h-q8h

References

1. Barraclough K, Bronstein A. Vertigo. BMJ. 2009;339:b3493
2. Kuo CH, Pang L, Chang R. Vertigo – part 1 – assessment in general practice. Aust Fam Physician. 2008;37(5):341-7
3. Newman-Toker, D. E., Kattah, J. C., Alvernia, J. E., & Wang, D. Z. (2008). Normal head impulse test differentiates acute cerebellar strokes from vestibular neuritis. Neurology, 70(24 Pt 2), 2378–2385. https://doi.org/10.1212/01.wnl.0000314685.01433.0d
4. Sacco RR et al. Management of Benign Paroxysmal Posi- tional Vertigo: A Randomized Controlled Trial. J Emerg Med. 2014 Apr;46(4):575-81

Case: A 35 year old Hispanic male presents to the Emergency Department for acute onset weakness, particularly in the bilateral upper and lower extremities. Symptoms started abruptly last night after a stressful work day. He denies any recent illnesses, insect bites, or rashes. Vitals are within normal limits. On exam, there is pronounced weakness in his proximal muscles with his lower extremities slightly weaker than his upper extremities. His grip strength is preserved. Reflexes are normal.

Differential diagnosis includes: thyrotoxic periodic paralysis, hypokalemic periodic paralysis, myasthenic crisis, Guillain-Barre syndrome, transverse myelitis, tick paralysis

Case continued: Labs are notable for a potassium 1.7, magnesium 1.5, TSH < 0.01, Free T4 5.9, Free T3 23.5. EKG showing sinus rhythm with prolonged QTc. Management included IV and PO repletion of potassium which improved the patient’s symptoms rapidly. He was also started on methimazole for hyperthyroidism. Finally, he was admitted to a telemetry monitored bed to check serial BMPs and monitor for rebound hyperkalemia.

Teaching Pearls:

• Thyrotoxic periodic paralysis is a form of acquired hypokalemic periodic paralysis, often precipitated by rest after strenuous exercise or high carbohydrate load.
• Treat with potassium repletion, continuous cardiac monitoring, and monitor potassium levels for rebound hyperkalemia.
• For acute weakness episodes not responsive to potassium replacement, use Propranolol.
• Treat hyperthyroidism – attacks should cease with euthyroid state.

References:
Chaudhry MA, Wayangankar S. Thryotoxic Periodic Paralysis: A concise review of the literature. Curr Rheumatol Rev. 2016;12(3):190-194.

Kung AW. Clinical review: Thyrotoxic periodic paralysis: a diagnostic challenge. J Clin Endocrinol Metab. 2006 Jul;91(7):2490-5. Epub 2006 Apr 11.

Vijayaumar A, Ashwath G, Thimmappa D. Thyrotoxic periodic paralysis: clinical challenges. J Thyroid Res 2014;2014:649502

Case: 64 M with no PMH presenting with continuous oozing from mass in posterior pharynx. Vital signs significant for: T 98.5, HR 72, BP 130/84, RR 16, SPO2 98%. Patient also found to have petechia on lower extremities. IV access established, and it is noted that there is bleeding from the IV sites.

Pathophysiology of DIC:

Causes of DIC:
– Most common: Sepsis
– Carcinomas, leukemias, TBI, pancreatitis, snake bites, ARDS, transfusion reactions, transplant rejection, crush injuries, burns, fat embolism, liver disease
– Pregnancy associated: Placental Abruption, Amniotic Fluid Embolism, Septic Abortion, HELLP syndrome, Acute fatty liver of pregnancy

Laboratory Testing:

PT used for monitoring over course

Bleeding Differential Diagnosis:

Management:
– Treat to treat underlying trigger
– If purpura fulminans present, treat with protein C concentrate
– Consider heparin if thrombosis is primary symptom
– Repletion to be considered if significant bleeding or impending procedure

• Fibrinogen < 100 = Cryoprecipitate
• Platelets <50K with bleeding, <10K without bleeding = Platelets
• PT/PTT over 1.5x normal limit = FFP
• Vitamin K and Folate
  

References:

Tintinalli’s Emergency Medicine Manual, 8e Eds. Rita K. Cydulka, et al. McGraw Hill, 2018

Uptodate.com

Step 1: Modified Valsalva

• Have the patient lie in a semi-recumbent position and blow into a standard 10 mL syringe as long as they can.
• Lay the patient supine and elevate the lower extremities for 1 minute.

Step 2: Escalating adenosine doses

• If standard dose of 6 mg of IV adenosine fails to terminate SVT, escalate subsequent doses by 6 mg.
• Doses up to 36 mg has been successful in case reports.

Step 3: Attempt an infusion of a Calcium Channel Blocker

• Diltiazem or verapamil can be given as a slow bolus.
  • Has been shown to be at least as successful, if not more successful, than adenosine in terminating SVT
  • May cause hypotension – treat with fluids and/or IV calcium gluconate

Step 4: If cardioverting, use propofol as sedative

• Propofol has terminated a variety of tachyarrhythmias in multiple case series.
• Remember to administer pain medication as propofol has no analgesic effects.
• Synchronized cardioversion of SVT only requires 50 Joules as initial dose.

References:
Lim SH, Anantharaman V, Teo WS, Chan YH. Slow infusion of calcium channel blockers compared with intravenous adenosine in the emergency treatment of supraventricular tachycardia. Resuscitation 2009; 80:523-528.

Bailey AM, Baum RA, Rose J, Humphries RL. High-Dose Adenosine for Treatment of Refractory Supraventricular Tachycardia in an Emergency Department of an Academic Medical Center: A Case Report and Literature Review. J Emerg Med. 2016 Mar;50(3):477-81.

Appelboam A, Mann C, et al. Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet 2015; 386:1747-53

Case: A 12 year old male with a history of autism spectrum disorder and chronic sinusitis presents for forehead swelling. Mother reports that she noticed progressive forehead swelling for about 1 month. She has followed up with the patient’s pediatrician and ENT and given oral cephalexin and fluticasone nasal spray which has not made any changes in symptoms. Patient denies any fevers or headache. Vitals include BP 100/58, HR 90, Temp 97.4F, RR 18, SpO2 98%. Exam is notable for a 3x3cm area of fluctuance centrally located over the forehead with no drainage or surrounding erythema that is minimally tender to palpation.

Differential diagnosis includes: abscess, cyst, lipoma

CT of the facial bones with contrast:

CT interpretation: “Bifrontal and ethmoid sinusitis associated with osseous destruction resulting in a 5 cm bifrontal complex loculated anterior epidural abscess as well as a 3 cm midline frontal subgaleal extracranial scalp abscess. Findings are most consistent with osteomyelitis of the frontal bone and sinuses.”

Case continued: ENT and Neurosurgery are emergently consulted and both recommend transfer to a Pediatric Center for advanced surgical and medical management given extensive nature of infection and reconstruction required post-operatively. The patient is started on broad spectrum antibiotics with vancomycin, ceftriaxone, and metronidazole and transferred to a Pediatric Center ICU with neurosurgical consultation. He was taken to the OR for a bifrontal craniotomy for epidural abscess evacuation and did well post-operatively, discharged on hospital day #4.

Pearls:

• Pott’s puffy tumor is a rare, life-threatening complication of frontal sinusitis characterized by osteomyelitis of the frontal bone with associated subperiosteal abscess causing swelling and edema over the forehead and scalp.
• It can be found in all age groups but most common in adolescents.
• MRI brain with and without contrast is the preferred imaging modality due to increased sensitivity to detect early intracranial and osseous abnormalities.
• Treatment is typically surgical intervention with at least 6 weeks of intravenous antibiotics.
  • The infection is typically polymicrobial warranting gram-positive, gram-negative, and anaerobic antibiotic coverage.

References:

Sharma, P., Sharma, S., Gupta, N., Kochar, P., & Kumar, Y. (2017). Pott puffy tumor. Proceedings (Baylor University. Medical Center), 30(2), 179–181. https://doi.org/10.1080/08998280.2017.11929575

Masterson L, Leong P. Pott’s puffy tumour: a forgotten complication of frontal sinus disease. Oral Maxillofac Surg. 2009;13(2):115-117. doi:10.1007/s10006-009-0155-7

Case: A 34 year old male with a past medical history of polysubstance use is brought in via EMS for an “allergic reaction.” He woke up this morning with tightness in his jaw and legs which has progressed to the inability to open his mouth or walk. Per chart review, the patient was in the ED yesterday acutely agitated and received intramuscular sedation with haloperidol and midazolam. On exam, his vitals are within normal limits. He speaks in full sentences through clenched teeth. Visualization of the oropharynx is limited due to inability to open his jaw. His bilateral lower extremities demonstrate rigid hyperflexion and inversion at the ankle joints. He is otherwise neurologically intact without abnormal findings on skin or lung exam.

Differential diagnosis includes: allergic reaction, extrapyramidal reaction, tetanus

Pearls:

• This patient is likely presenting with an extrapyramidal reaction secondary to receiving haloperidol, a high-potency antipsychotic.
  • Extrapyramidal symptoms include acute dystonia, akathisia, Parkinsonism, tardive dyskinesia, and neuroleptic malignant syndrome.
  • The pathophysiology involves an imbalance of dopaminergic and cholinergic activity, not a true allergic reaction.
• Acute dystonia is typically self-limited and not life-threatening with the exception of rare cases of laryngospasm.
  • Treatment includes benztropine (dopamine agonist) or diphendydramine (anticholinergic).
  • Patients that are discharged from the ED with resolution of symptoms should be given PO benztropine or diphenhydramine for 2 to 3 days due to prolonged effects of antipsychotics that can result in rebound dystonia.
• Drug induced Parkinsonism and tardive dyskinesia usually develop after prolonged use of antipsychotics and are less likely to be reversible.

Case continued: The patient received 50 mg IV diphenhydramine with near immediate resolution of his symptoms. He was observed for a brief period in the emergency department, ambulated, and tolerated PO without difficulty and was shortly thereafter discharged.

References:

Levine M, LoVecchio F. Antipsychotics. 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; 2020.