HPI: Pt is a 41 y/o male who presents to the ED w/ significant wrist pain s/p MVC. He was the unrestrained driver of a car, T boned at a moderate speed, + broken windshield, + airbag deployment, – entrapment. R wrist is swollen tender over the mid dorsal aspect w/o any open lacerations. 

Vitals: HR 101, BP 121/91, Temp 98F, RR 15

Physical Exam: GCS 15 Cardiac, Pulm & Abd unremarkable.

Extremities: LUE, LLE, RLE – unremarkable. RUE: Strength 5/5 throughout, sensation intact at C5-T1 and distally, able to make an “okay”, “thumbs up” sign. Point tenderness over R dorsal mid wrist and snuff box w/o deformity or skin changes, + swelling, compartments soft. Limitation w/ flexion/extension of the R wrist, normal finger cascade when closing hand,

Differential: Scaphoid fracture, scapholunate dissociation, proximal MCP fracture, distal radius or ulnar fracture, other carpal injury.

Xray

Scapholunate Dissociation is a common result of hand trauma and it may be acute (traumatic) or chronic (in the setting of degenerative injuries). Often associated w/ intraarticular distal radius and other carpal fractures. Mechanism typically involves forced wrist extension and ulnar deviation. Think FOOSH injury.

Associated injury often is a “DISI” – Dorsal Intercalated Segmental Instability. A scapholunate dissociation causes the scaphoid bone to rotate anterior while lunate rotates posteriorly – if untreated can progress to chronic degenerative arthritis.

Diagnosis: XR AP radiograph: > 3mm of widening between the scaphoid and lunate on a “clenched fist view”.

Signet Ring Sign: indicative of a scapholunate dissociation. As the scaphoid rotates the scaphoid tubercle appears more rounded. Can also be seen in perilunate and lunate dislocations.

Treatment: Pain control, splinting (sugar tong or thumb spica) and repeat imaging in 1-2 weeks w/ ortho followup. Often requires operative fixation in outpt setting. If associated w/ perilunate, lunate, scaphoid dislocation – requires urgent reduction prior discharge.

Complications: Chronic pain and degenerative disease of associated structures, neurovascular compromise, joint instability

References:

1. Stevenson M, Levis JT. Image diagnosis: Scapholunate dissociation. The Permanente journal. 2019. Accessed January 14, 2025. https://pmc.ncbi.nlm.nih.gov/articles/PMC6443367/#f1-18-237. 

2. Scapholunate ligament tear – cortical ring sign | radiology case | radiopaedia.org. Accessed January 15, 2025. https://radiopaedia.org/cases/scapholunate-ligament-tear-cortical-ring-sign. 

3. Scapholunate Ligament Injury & Disi. Orthobullets. Accessed January 14, 2025. https://www.orthobullets.com/hand/6041/scapholunate-ligament-injury-and-disi. 

4. Rap corependium. EM. Accessed January 14, 2025. https://www.emrap.org/corependium/chapter/recrf1uDQslSAzIEL/Wrist-Dislocations#h.t4rehgq0mdhi. 

On a busy mid shift, you are handed this EKG for a 76 y/o pt presenting with known CAD complaining of chest pain. VS stable. What’s your interpretation and what’s your next step?

Aslanger – An Occlusive Myocardial Infarction Equivalent

13% of acute anterior myocardial infarctions

Found in 6.3% of NSTEMI

ECG Criteria: (must meet all criteria)

Isolated ST Elevations in lead III (not any other inferior leads)

ST Depressions in V4, V5 or V6

ST segment in V1 > V2

Next Step -> Call the STEMI phone!

References:

1. Liu M, Li H, Li A, et al. A patient with acute myocardial infarction with Electrocardiogram Aslanger’s pattern – BMC cardiovascular disorders. BioMed Central. January 2, 2024. Accessed January 8, 2025. https://bmccardiovascdisord.biomedcentral.com/articles/10.1186/s12872-023-03678-x. 

2. Buttner R, Cadogan M, Cadogan RB and M. Aslanger pattern: Another omi? Life in the Fast Lane • LITFL. January 28, 2021. Accessed January 8, 2025. https://litfl.com/aslanger-pattern/. 

By Dr. Edward Guo

Case: A 70 year old male with a past medical history of hypertension, type 2 diabetes, and atrial fibrillation on warfarin presents for visual changes. He is accompanied by his daughter who states that about one hour ago, his vision on the right side became blurry. There is associated right facial numbness and headache. His daughter believes that he has become more confused over this time period. Fingerstick glucose is 220. An EKG is obtained which shows atrial fibrillation at a rate of 92.

Exam: BP 151/75, HR 92, T 97.8F, RR 18, SpO2 98%

Comfortable appearing in no acute distress. GCS E4 V4 M6. No facial droop. Decreased sensation to right side of face. 5/5 strength and sensation in all extremities. No difficulty with rapid alternating movements. Extraocular motion intact. Left gaze preference with right sided homonymous hemianopia. 

Differential diagnosis: acute ischemic stroke, spontaneous intracranial hemorrhage, complex migraine, toxic-metabolic encephalopathy

Case continued: Neurology is emergently consulted and a stroke alert is activated. CT/CTA of the head and neck shows no acute intracranial hemorrhage and no large vessel occlusion. Labs are notable for an INR of 1.6. The decision is made in conjunction with neurology to administer thrombolytics, and the patient is admitted to neurology critical care. Repeat head CT 24 hours later demonstrates a left parieto-occiptal infarct. 

Pearls:

• This patient’s neurologic deficits including right sided facial numbness, right homonymous hemianopsia, left sided gaze preference, and aphasia localize to a cortical distribution as noted above.
• Warfarin use alone is not a contraindication to thrombolytics for acute ischemic stroke. The INR must be > 1.7 in addition to be an exclusion criterion.
  • This patient had multiple previous subtherapeutic outpatient INR levels which likely precipitated an embolic stroke.
• In patients without contraindications, the decision to administer thrombolytics for acute ischemic stroke should be clinical without waiting for results of laboratory testing with the exception of a point of care glucose and patients with suspected coagulopathy. 
• Other common exclusion criteria to the use of thrombolytics in acute ischemic stroke include previous head trauma or stroke within 3 months, any previous intracranial hemorrhage, SBP > 185 or DBP > 110, or known intracranial mass such as neoplasm or aneurysm. 

References:

Go S, Kornegay J. Stroke Syndromes. 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.
Powers WJ, Rabinstein AA, Ackerson T, et al. 2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association [published correction appears in Stroke. 2018 Mar;49(3):e138] [published correction appears in Stroke. 2018 Apr 18;:]. Stroke. 2018;49(3):e46-e110. doi:10.1161/STR.0000000000000158

By Dr. Edward Guo

Case: A 70 year old male with a past medical history of hypertension, type 2 diabetes, and atrial fibrillation on warfarin presents for visual changes. He is accompanied by his daughter who states that about one hour ago, his vision on the right side became blurry. There is associated right facial numbness and headache. His daughter believes that he has become more confused over this time period. Fingerstick glucose is 220. An EKG is obtained which shows atrial fibrillation at a rate of 92.

Exam: VS: BP 151/75, HR 92, T 97.8F, RR 18, SpO2 98%.  Pt is comfortable appearing in no acute distress. GCS E4 V4 M6. No facial droop. Decreased sensation to right side of face. 5/5 strength and sensation in all extremities. No difficulty with rapid alternating movements. Extraocular motion intact. Left gaze preference with right sided homonymous hemianopia. 

Differential diagnosis: acute ischemic stroke, spontaneous intracranial hemorrhage, complex migraine, toxic-metabolic encephalopathy

Case continued: Neurology is emergently consulted and a stroke alert is activated. CT/CTA of the head and neck shows no acute intracranial hemorrhage and no large vessel occlusion. Labs are notable for an INR of 1.6. The decision is made in conjunction with neurology to administer thrombolytics, and the patient is admitted to neurology critical care. Repeat head CT 24 hours later demonstrates a left parieto-occiptal infarct. 

Pearls:

• This patient’s neurologic deficits including right sided facial numbness, right homonymous hemianopsia, left sided gaze preference, and aphasia localize to a cortical distribution as noted above.

• Warfarin use alone is not a contraindication to thrombolytics for acute ischemic stroke. The INR must be > 1.7 in addition to be an exclusion criterion.

• This patient had multiple previous subtherapeutic outpatient INR levels which likely precipitated an embolic stroke.

• In patients without contraindications, the decision to administer thrombolytics for acute ischemic stroke should be clinical without waiting for results of laboratory testing with the exception of a point of care glucose and patients with suspected coagulopathy. 

• Other common exclusion criteria to use of thrombolytics in acute ischemic stroke include previous head trauma or stroke within 3 months, any previous intracranial hemorrhage, SBP > 185 or DBP > 110, or known intracranial mass such as neoplasm or aneurysm. 

References:

Go S, Kornegay J. Stroke Syndromes. 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.

Powers WJ, Rabinstein AA, Ackerson T, et al. 2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association [published correction appears in Stroke. 2018 Mar;49(3):e138] [published correction appears in Stroke. 2018 Apr 18;:]. Stroke. 2018;49(3):e46-e110. doi:10.1161/STR.0000000000000158

By: Dr. Sean Coulson

HPI: Pt is a 38 y/o male with hx of sickle cell (SS) who presents for generalized headache, facial droop and difficulty speaking. Last known normal was 19 hours PTA. No anticoagulation.

Objective: HR 91, BP 155/91, RR 20, Temp 98F, Accu Check 129 NIH 2 – mild left lower facial droop and mild dysarthria. No other neurologic deficits. Stroke alert is called and CT CTA do not show any acute hemorrhagic infarct or large vessel occlusion. Labs and EKG are sent and the only pertinent result includes a Hb of 6.1 (prior baseline 9).

DDX: acute hemorrhagic / ischemic stroke, seizure, dural venous sinus thrombosis, myasthenia gravis, botulism, complex migraine etc.

Management: Given that this patient was outside of the 4.5 hour window and there was a low suspicion for thromboembolic etiology, TNK was held. In discussion with neurology and hemonc, a shiley dialysis catheter was placed and exchange transfusion was initiated.

Exchange transfusion: Goal is to reduce HbS to < 30% preventing further sickling. In hemorrhagic stroke (primary or secondary to an ischemic stroke), exchange transfusion is still indicated however the goal is to prevent secondary vasospasm and recurrent strokes – data is less clear in terms of overall benefit. If exchange transfusion is not possible, simple regular transfusions are indicated immediately and can act as a bridge until exchange transfusion is established. Hb goal determined in discussion w/ Hematology.

Pearls:

~ Sickle cell is a common cause of acute stroke in children and young adults.

~ SS causes increased risk for cerebral aneurysms and other arterial abnormalities (high risk for carotid dissection, subarachnoid, dural venous thrombosis etc)

~ It is still important in acute strokes to apply general sickle cell crisis management (O2, fluids, pain control, transfusion)

~ Exchange transfusions lower risk of recurrent stroke

~ SS is not an absolute contraindication to TPA

*** Thrombolytics can be given in sickle cell patients if there is a high pretest probability for thromboembolic etiologies of the acute stroke (CAD, PVD, Afib etc) and the patient meets typical inclusion/exclusion criteria. However the benefit of thrombolytics in stroke secondary to sickled RBCs is questionable – data is limited.

~ If exchange transfusion is not possible, discussion w/ hematology and neurology about Hb parameters is paramount.

References

Hulbert ML, Scothorn DJ, Panepinto JA, et al. Exchange blood transfusion compared with simple transfusion for first overt stroke is associated with a lower risk of subsequent stroke: a retrospective cohort study of 137 children with sickle cell anemia. J Pediatr. 2006;149(5):710-712. doi:10.1016/j.jpeds.2006.06.037

Alakbarzade V, Maduakor C, Khan U, Khandanpour N, Rhodes E, Pereira AC. Cerebrovascular disease in sickle cell disease. Pract Neurol. 2023;23(2):131-138. doi:10.1136/pn-2022-003440

Tintinalli J. TINTINALLI’S EMERGENCY MEDICINE : A Comprehensive Study Guide. Mcgraw-Hill Education; 2019:1136.

EM:RAP CorePendium. EM:RAP CorePendium. Published 2024. Accessed August 10, 2024. https://www.emrap.org/corependium/chapter/recZWicqx0K20uwsz/Sickle-Cell-Disease#h.1h9pp1rguxde

Sean Coulson D.O.

HPI: Pt is a 24 y/o male who presents for fall, complaining of right lateral anterior palm pain. No medical hx, TDap up to date, no anticoagulation.

Physical Exam: Tender to palpation over the medial right palm on the anterior aspect. Radial pulse 2+, Cap refill intact, Strength and sensation intact, no abrasions / lacerations / skin changes. When the patient closes the right hand and makes a fist, the right 2nd finger angulates and bends overtop the 3rd phalanx (as seen below).

Pertinent Information About 2nd-5th Metacarpal Fractures:

Is it an open vs closed? Does it involve the intra articular space? Cascade of finger placement, malrotation / scissoring (see photo below)?

What are acceptable degrees of angulation based on the digit?

1st metacarpal: < 10 degrees

2nd: <20 degrees

3rd: < 30 degrees

4th: < 40 degrees

If less than the stated degree, may consider reduction, splint and discharge with orthopedic follow up if no other concerning features are present.

Other Indications for operative management and in ED orthopedic consult

Angulation greater than what’s stated above

Shortening > 5mm

Intraarticular or open fracture

Abnormal finger cascade regardless of degree of angulation

Multiple metacarpal fx

Management

+/- Ortho evaluations w/ operative fixation as described above

4th / 5th MCP fx: ulnar gutter splint

2nd / 3rd MCP fx: radial gutter splint

References:

https://jkfs.or.kr/ViewImage.php?Type=F&aid=593409&id=F1&afn=104_JKFS_31_2_61&fn=jkfs-31-61-g001_0104JKFS

https://www.ncbi.nlm.nih.gov/books/NBK551532

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7355092

https://www.journal-cot.com/article/S0976-5662(20)30230-7/fulltext

https://www.orthobullets.com/hand/6037/metacarpal-fractures

Pt is a 55 y/o F w/ hx of SLE who presents to the ED for hypotension. Pt is altered and not providing any information. Pt arrives with family who notes she has had progressively worsening mental status and abdominal pain w/ vomiting non bilious material x 3 days. Not compliant with medications during this time 2/2 vomiting. Unclear what medications she takes.

HR 119, BP 71/48, Temp 94F, RR 20, Acc Check 51

Physical Exam:
GCS 11, arousable to gentle stimuli 

Extremities warm w/o pitting edema

Abdomen soft and nontender

Lungs CTA b/l

Heart rate tachycardia and regular

POCUS unremarkable

Pertinent Labs:

CBC: WBC 15k w/ increased lymphocytosis

BMP: Na 128, K 5.8, AG 18, Cr 2.1

Differential diagnosis: Distributive shock 2/2 sepsis w/ unclear source vs adrenal insufficiency, hypovolemia, myxedema coma etc.

Physiology

• Primary adrenal insufficiency (Addisons) – direct loss of glucocorticoids (cortisol) and mineralocorticoid (aldosterone)
• Secondary adrenal insufficiency – loss of ACTH / CRH
  • More common secondary to chronic steroid therapy – leads to loss of glucocorticoids
  • Aldosterone is largely unaffected because its regulated by RAAS so typical electrolyte abnormalities are not as common / pronounced and hypotension is less severe

When to consider

• Shock refractory to fluid resuscitation / vasopressors
• Typical lab findings: HypoNa, HyperK, HypoGlycemia, HypoThermia, HypoTension, AMS
• Azotemia
• If leukocytosis -> likely eosinophilia w/ lymphocytosis > neutrocytosis
• Fever of unexplained origin

High Risk Groups

• Included in the ddx for shock refractory to pressors / volume resuscitation

• Pts on long term steroids
• Autoimmune disorders
• HIV and TB
• Head trauma, tumors and pituitary apoplexy (sheehan syndrome)
• Bacterial meningitis
• Neonates w/ congenital adrenal hyperplasia
• Infiltrative disorders
• Chronic opioid use and withdraw can suppress the HPA axis as well

Diagnosis

• In the ED, its a clinical diagnosis. Suspect? = Treat!
• Cortisol < 20 ug/dl is highly suggestive however not definitive
• Confirm w/ cosyntropin test (to be done on floor/ICU)

Management

• Hydrocortisone 100mg IV then 50mg q6: 1st line as it has glucocorticoid and mineralocorticoid effects – however it will affect the cosyntropin test. Can consider adding fludrocortisone for added mineralocorticoid benefits but not typically recommended.
  • If affecting the cosyntropin test is a large concern – consider starting dexamethasone 6mg IV (glucocorticoid). Must rx fludrocortisone as well (mineralocorticoid)
• Low threshold for empiric levothyroxine as well
• If pt truly has adrenal crisis – pt should have some clinical improvement within a few hours after receiving the above steroids

Prevention

• Patients on chronic steroids who present w/ acute illness – take at home steroid dose and triple – this is their new maintenance dose for the next 1-3 days or until their acute presentation improves.

References:

By Dr. Jacob Martin, MD

HPI:

• 30 yo healthy male p/w generalized fatigue, b/l UE and LE weakness and pain for several hours
• Denies strenuous activity, change in diet, falls, trauma, midline back pain, bowel and or bladder incontinence
• Hospitalized 3 months prior for unexplained hypokalemia (K <2.0) that resolved with IV repletion

PE:

Vitals: BP 182/78 | Pulse 61 | Temp 97.7 °F (Oral) | Resp 22 | SpO2 100% 

• Awake and alert, appears fatigued
• Dry MM, cap refill greater than 3 seconds
• 4/5 strength b/l UE
• 3/5 strength b/l LE
• Sensation to light touch intact in bilateral upper and lower extremities
• 2+ patellar reflexes bilaterally
• Unable to ambulate due to weakness

Ddx for Generalized Weakness:

• Hypokalemia/hyperkalemia vs rhabdomyolysis vs periodic paralysis vs spinal cord compression vs Guillain-Barre syndrome

Initial Diagnostics:

• Initial labs notable for K 1.9, Mg 1.5, and Phos 1.1
• Initial ECG (see below)

Management:

• Electrolytes repleted as follows…
  • 40 mEq oral K, 20 mEq IV K
  • 2 gm Mg over 2 hours
  • 2 tablets of Neutra-Phos

Case Progression:

• Ultimately diagnosed with hyperthyroidism, likely secondary to Graves’ disease
  • TSH <0.01
  • Ultrasound thyroid
    • Enlarged heterogeneous thyroid with diffusely increased vascularity
    • Thyroid nodule of the isthmus
• Started on Methimazole and Propranolol
• Presenting symptoms and electrolyte abnormalities attributed to thyrotoxic periodic paralysis

Thyrotoxic Periodic Paralysis (TPP)

• Potentially life-threatening
• Defined as the triad of
  • Muscle paralysis
  • Acute hypokalemia
  • Hyperthyroidism
• Less than half of TPP patients exhibit clinical signs of hyperthyroidism
• Rapid recognition and termination are mandatory to avoid potentially fatal complications of severe hypokalemia
  • Cardiac arrhythmias
  • Respiratory failure
• Management complicated by the thin line between refractory hypokalemia and rebound hyperkalemia
• KCl supplementation is essential but often not enough to control TPP
• IV propranolol has been reported to reverse weakness and hypokalemia in patients unresponsive to KCl administration

References:

Bilha S, Mitu O, Teodoriu L, Haba C, Preda C. Thyrotoxic Periodic Paralysis-A Misleading Challenge in the Emergency Department. Diagnostics (Basel). 2020;10(5):316. Published 2020 May 18. doi:10.3390/diagnostics10050316

Lin SH, Huang CL. Mechanism of thyrotoxic periodic paralysis. J Am Soc Nephrol. 2012;23(6):985-988. doi:10.1681/ASN.2012010046