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.

Case: An 18 year old female with a past medical history of anxiety, 2 weeks post-op from tonsillectomy presents for chest pain. She woke up today with severe, non-radiating central chest pain. Her daily medications include sertraline and oral contraceptives. Vitals are BP 118/86, HR 119, Temp 97.7F, RR 24, SpO2 96% on room air. On exam, she is uncomfortable appearing and tearful. Her oropharynx is clear without signs of erythema or drainage. She is tachycardic without murmurs and has clear lung sounds bilaterally. There are no signs of lower extremity swelling. EKG and point-of-care cardiac ultrasound are shown below:

EKG interpretation: Sinus tachycardia with rightward axis and T wave inversions in anterior leads

POCUS interpretation: Normal LV ejection fraction. No pericardial effusion. Elevated RV to LV ratio. Dilated IVC with < 50% collapse with inspiration. RV free wall hypokinesis with apical hyperkinesis. Tricuspid annular plane systolic excursion 1.0 cm.

Case continued:  Due to high concern for pulmonary embolism, the patient is empirically started on heparin. CTA chest results with acute pulmonary embolism with right heart strain. High sensitivity troponin results markedly elevated at 306 mg/dL. Patient is admitted to the ICU with interventional cardiology consultation. Patient underwent pulmonary arteriogram which demonstrated elevated PA pressures without need for thrombectomy and was discharged in good condition on hospital day #4.

Pearls:

• Infants and toddlers can have normal T wave inversions in the anterior leads known as “juvenile T waves” which should turn upright by age 7.
  • Any T wave inversion in these leads after they have flipped upright is abnormal.
• While the S1Q3T3 EKG finding is classically associated with pulmonary embolism, more common EKG findings suggestive of PE include sinus tachycardia, rightward axis, incomplete right bundle branch block, and T wave inversions in the anterior leads.
• Empirically start anticoagulation in patients with high concern for pulmonary embolism prior to definitive imaging.
• Right ventricular free wall hypokinesis with apical hyperkinesis is known as McConnell’s sign and is pathognomonic for acute pulmonary embolism.
  • Other POCUS findings include an RV:LV ratio > 1 which is sensitive but not specific. A tricuspid annular plane systolic excursion (TAPSE) < 17 mm is a quantitative measure to diagnose right heart dysfunction on echocardiogram.

References:

Kline JA. Venous Thromboembolism Including Pulmonary Embolism. 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.

Goodacre, S., & McLeod, K. (2002). ABC of clinical electrocardiography: Paediatric electrocardiography. BMJ (Clinical research ed.), 324(7350), 1382–1385. https://doi.org/10.1136/bmj.324.7350.1382

Alerhand S, Hickey SM. Tricuspid Annular Plane Systolic Excursion (TAPSE) for Risk Stratification and Prognostication of Patients with Pulmonary Embolism. J Emerg Med. 2020;58(3):449-456. doi:10.1016/j.jemermed.2019.09.017

Case: A 69 year old male with a past medical history of hypertension and type 2 diabetes arrives via EMS for chest pain and weakness. EMS found patient with a heart rate of 30, systolic BP 100, awake and and alert. Vitals upon arrival to the ED are BP 92/41, HR 42, Temp 97.7F, RR 20, SpO2 98% on room air. On exam, he is conversant with bradycardia and clear lung sounds. EKG is shown below:

EKG interpretation: sinus bradycardia with left bundle branch block pattern, Sgarbossa criteria negative

Differential diagnosis: acute cardiac ischemia, hyperkalemia, medication overdose (beta blockers, calcium channel blockers, digoxin, clonidine)

Management:

• Transcutaneous pacer pads
• 1 mg atropine given with no response
• 500 mL IV fluid bolus improved SBP to 100
• Cardiology consult with concerns for acute ischemia given chest pain and new left bundle branch block with bradycardia

Case continued: 40 minutes after arrival, patient suffered a brady-asystolic cardiac arrest. ACLS was started immediately and 1 mg epinephrine and 1 g calcium gluconate were administered. ROSC was achieved with 3 minutes, and patient became awake and alert. Critical lab values resulted with a potassium of 7.7 and creatinine of 3.7 (unknown baseline). The patient was admitted to the ICU on vasopressors, maintained adequate urine output, and did not require emergent hemodialysis. He was discharged in good condition two days later.

Diagnosis: BRASH Syndrome – Bradycardia, Renal failure, AV nodal blocking agents (beta blockers in this case), Shock, and Hyperkalemia

• Check out this excellent summary of BRASH syndrome from the Journal of Emergency Medicine here.

Pearls:

• Hyperkalemia is a common cause of bradycardia.
• Unstable patients should be treated empirically with IV calcium while waiting for lab confirmation.
• A VBG with lytes may provide a faster laboratory confirmation, though the specimen may have unrecognized hemolysis.
• The combination of acute renal failure (sometimes from vomiting/diarrhea) in conjunction with AV nodal blocking agents may result in BRASH syndrome.
• Acute treatment is aimed as for management of hyperkalemia and emergency hemodialysis may be required if patient is anuric or unresponsive to treatment.

References:

Farkas, Joshua et al. BRASH Syndrome: Bradycardia, Renal Failure, AV Blockade, Shock, and Hyperkalemia. Journal of Emergency Medicine 59 (2); 216-223.

Case: A 12-year-old male was hit in the right eye with a baseball just prior to arrival, now with headache, nausea, and vomiting, with swelling and pain around his right eye.  Patient was unable to look upward, and had pain with looking downward. When he presented to the Emergency Department, his initial heart rate was 44 BPM. Patient received emergent CT head which showed small volume retrobulbar hematoma, concern for entrapment of the right lateral rectus muscle, and acute mildly displaced right orbital floor fracture. Ophthalmology and OMFS were emergently consulted and recommended transfer for pediatric oculoplastic evaluation for retrobulbar hematoma, right orbital floor fracture, and high concern for entrapment.

Pearls:

• A drop in heart rate by more than 20%, with associated nausea, syncope, or hypotension, after force is exerted on the extraocular muscles or globe of the eye, is known as the oculocardiac reflex. The bradycardia that develops is typically sinus bradycardia. In some cases, this reflex has been known to cause arrhythmias, asystole, and cardiac arrest.  This reflex can occur with facial trauma and nerve blocks, however, it is most commonly found during ophthalmologic surgery.
• This reflex occurs with activation of the vagus nerve from nerve pathways originating from the stimulation of the opthalmic division of the trigeminal nerve.  The vagus nerve activation results in a diminished chronotropy, creating the response.

Treatment:

• Removal of the cause, which in the setting of trauma, means consulting ophthalmology for an intervening procedure.
• In the interim, patients can be stabilized using management for bradycardia, such as atropine, placing the patient on the pacing pads, and careful cardiac monitoring. 
• If signs and symptoms are concerning for oculocardiac reflex in the setting of trauma, emergent CT and ophthalmology consult is recommended.  Evidence of ocular muscle entrapment, such as limited extra-ocular movements, diplopia, or proptosis, is an indication for emergent ophthalmology consult.

References:

1. Cavuoto, K, Barmettler, A, Prakalapakorn, G, Yen, M, Puente, M. Oculacardiac Reflex. EyeWiki from American Academiy of Opthalmology. March 30, 2023. https://eyewiki.aao.org/Oculocardiac_Reflex.

2. Dunville LM, Sood G, Kramer J. Oculocardiac Reflex. [Updated 2022 Sep 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499832/

3. Sires BS, Stanley RB Jr, Levine LM. Oculocardiac reflex caused by orbital floor trapdoor fracture: an indication for urgent repair. Arch Ophthalmol. 1998;116(7):955-956.

4. Walker RA, Adhikari S. Eye Emergencies. 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. Accessed September 16, 2023. https://accessemergencymedicine-mhmedical-com.ezproxy.rowan.edu/content.aspx?bookid=2353&sectionid=222404436