Captain Morgan hip reduction

4 Aug

quick review of this technique, which works great, and takes much less effort than standing on the bed breaking a sweat (my personal recent N of 3 in recent months has been a 3 for 3 success rate)

CONCEPT:tumblr_lriey37dpa1qafl51o1_1280

Provider’s leg up on the stretcher, a-la Captain Morgan’s pose.

Patients leg bent over provider’s thigh

Provider pushes up with their foot, pulls down (lever-action) on patient’s lower leg

Pop’s back into place.

VIDEO ASSIST: (start at the 0:45 mark if you’re short on time)

 

ORIGINAL ARTICLE (Hendey & Avila):

12/13 successful reduction; only failure had an intra-articular fragment that needed the OR

 

There you go. Add it to the toolbox.

 

References: video, picture, article

 

Calcaneal Fracture

15 Jul

submitted by Christina Brown, M.D.

 

Definition – Fracture of the calcaneus secondary to fall from significant height. calcaneal_fracture Attributed to shear stress adjoined with compressive forces combined with a rotary direction.  The calcaneus, also known as the heel bone, is the largest of the tarsal bones and articulates with the cuboid bone anteriorly and the talus bone superiorly.

 

Signs and Symptoms

Most common symptoms = pain upon plantar flexion and palpation of heel.  

Other symptoms include: Inability to bear weight, limited mobility. 

“Mondor sign” = Hematoma extending to sole of foot; pathognomonic for calcaneal fracture [3].   

Associations – Vertebral compression fractures occur in approximately 10% of these patients [1].  A trauma-focused clinical approach should be implemented to evaluate for tibial, knee, femur, hip tenderness.

 

Diagnostic Imaging:

Xray’s – Recommended views = Axial, AP, Oblique [1].

CT – Best for visualization of subtalar joint

 

Intraarticular vs Extra articular:

Intraarticular fractures = more common and tends to involve the posterior talar articular facet of the calcaneus. 

  1. Type I – Non-displaced fractures (displacement < 2 mm).
  2. Type II – Single intraarticular fracture that divides the calcaneus into 2 pieces.
  3. Type III – Two intraarticular fractures that divide the calcaneus into 3 articular pieces.
  4. Type IV – More than three intraarticular fractures.

 

Treatment:

Non-surgical treatment is indicated for intraarticular fractures and Sanders Type I intraarticular fractures. Recommendations include no weight-bearing for a few weeks followed by range-of-motion exercises and progressive weight bearing for a period of 2–3 months.

Displaced intra-articular fractures require surgical intervention within 3 weeks of fracture, before bone consolidation has occurred. 

 

Complications:   Skin blisters may become infected if medical attention is delayed, which can lead to necrotizing fasciitis or osteomyelitis, causing irreparable muscle/bone damage [4].

 

References:

  1. Stoller, D. W.; Tirman, P. F. J.; Bredella, M. (2004). “Ankle and foot, osseous fractures, calcaneal fractures”. Diagnostic imaging: orthopaedics. Salt Lake City: Amirsys. pp. 70–4.
  2. Calcaneus Fractures at eMedicine
  3. Richman, JD; Barre, PS (1986). “The plantar ecchymosis sign in fractures of the calcaneus”. Clinical Orthopaedics and Related Research (207): 122–5.
  4. Heier, Keith A.; Infante, Anthony F.; Walling, Arthur K.; Sanders, Roy W. (2003). “Open Fractures of the Calcaneus: Soft-Tissue Injury Determines Outcome”. The Journal of Bone and Joint Surgery. American Volume 85–A (12): 2276–82.
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THORACIC AORTIC DISSECTION

27 Jun

submitted by Christina Brown, M.D.

Definition – Blood entering intimal tear in aortic wall.  Blood subsequently dissects through the media under aortic systolic pressure.

Risk Factors – HTN, Tobacco abuse, pregnancy, congenital heart disease (bicuspid AV, Coarctation), Marfan’s, Ehler’s Danlos, Inflammation (Lupus, syphilis, endocarditis, GCA)

Location:

a_dissection

Proximal – Occur at the aortic root, coronary ostia and/or pericardium.  

Distal – Dissect distally to involve any or all branches of the aorta ie -carotid and subclavian arteries.

Stanford classification:

  • Type A: Ascending aorta
  • Type B: Distal to ascending aorta

Peak Age for Occurrence

  • Proximal dissection: 50–55 yr
  • Distal dissection: 60–70 yr

Complications:

  • Occlusion of the coronary ostia, aortic valve incompetence, or cardiac tamponade.

 

Signs & Symptoms

Chest Pain:

  • May be absent in as many as 15% of patients
  • Acute onset, sharp
  • Substernal -> type A dissection
  • Intrascapular -> descending thoracic dissection
  • Lumbar -> abdominal aorta involvement

Back pain:

  • Commonly interscapular or lumbar. May present as combination of chest, back, and abdominal pain.

Neurologic complaints: Stroke symptoms, Vision changes

 

Physical Exam

Hypertension: 35–40% may be normotensive.

Pulse deficits: Discrepancies in BP in upper extremities

Neurologic/spinal cord deficits

New murmur of aortic regurgitation: Occurs in up to 31% of patients

 

Management

EKG – Dissection may involve coronary ostia and cause MI:

  • Inferior MI (RCA territory) is more common than LCA territory.
  • A normal EKG + severe, acute-onset chest/back pain/shortness of breath – high suspicion for aortic dissection.

Labs

  • CBC, BMP, UA – Evaluate renal function, hematuria
  • Amylase – May be elevated d/t bowel ischemia
  • Troponin – May be elevated d/t myocardial ischemia

 

Imaging

Unstable Patient:

CXR – Widened mediastinum or abnormal aortic contour.

Echocardiogram – Transthoracic vs Transoesophageal (if intubated) – Tamponade, valvular incompetence for evaluation. 

Stable Patient:  CT, Aortography

 

ED Treatment

BP Control = Reduce shear force on aortic wall and slow down the dissection process.

  • Esmolol (IV) or labetalol (IV): Start before Nitroprusside therapy to prevent reflex tachycardia. 
    • Contraindications:Bradycardia,  COPD, hypotension
  • Nitroprusside

 

Emergent surgery:

  • Treatment of choice for type A dissection
  • Treatment for type B dissections in those who have failed medical therapy

Medical management:

  • Treatment of choice for stable type B dissections

 

Disposition

ADMIT – All patients with an evolving aortic dissection should be admitted to the ICU.  C/S  cardiothoracic surgery for type A dissection.

 

References

1] Jeffrey I. Schneider and Jonathan S. Olshaker.  Aortic Dissection, Thoracic. Rosen & Barkin’s 5-minute Emergency Medicine Consult.
2] Erbel R, Alfonso F, and Boileau C et al.: Diagnosis and management of aortic dissection. Eur Heart J. 2001; 22(18):1642–1681. [PMID: 11511117]
[3] Hagan P G, Nienaber C A, and Isselbacher E M et al.: The international registry of acute aortic dissection: New insights into an old disease. JAMA. 2000; 283(7):897–903. [PMID:10685714]
[4] Khan I A and Nair C K.: Clinical, diagnostic, and management perspectives of aortic dissection. Chest. 2002; 122(1):311–328. [PMID: 12114376]
[5] Klompas M.: Does this patient have an acute thoracic aortic dissection? JAMA. 2002; 287:2262–2272. [PMID: 11980527]
[6] Mészáros I, Mόrocz J, and Szlávi J et al.: Epidemiology and clinicopathology of aortic dissection. Chest. 2000; 117(5):1271–1278. [PMID: 10807810]
[7] Moore A G, Eagel K A, and Bruckman D et al.: Choice of computed tomography, transesophageal echocardiography, magnetic resonance imaging, and aortography in acute aortic dissection: International registry of acute aortic dissection. Am J Cardiol. 2002; 89:1235–1238. [PMID:12008187]
picture

 

tox bradycardias: fingerstick for clues

7 Jun

often taught, often forgotten clue to help differentiate beta-blocker vs. calcium channel blocker overdoses:

REMINDER:

Calcium Channel Blockers can present with hyperglycemia (CCBs prevent insulin release)

Beta Blockers can present with hypoglycemia (BBs  inhibits both glycogenolysis and gluconeogenesis)

 

VISUAL AIDS:

The above difference has been difficult to remember for me, and I frequently look it up as a reminder, so here’s an attempt to associate/remember which is which:

CALCIUM CHANNEL BLOCKERS:

HYPERglycemia

visual association:

046435__53574_stdbabydeal-keo-gummy-2

 

BETA BLOCKERS:

hypOglycemia

stop-the-sugar

 

 

Appreciate any other tips/mnemonics y’all have on remembering the difference.  

 

References: emdocs post, beta blocker, ODs, picture 1, 2, 3

 

 

tendon repair – Kessler stitch

2 Jun

via a nice quick review of tendon lac repair concepts in last December’s ACEP Now:

modified Kessler stitch for tendon repair:

basic idea: stronger stitch, tension distributed across multiple points (e.g. with mattress sutures)

the stitch:

acep_1215_pg13c

concept walkthrough (tune in from 2:00-4:00 if tight on time):

live action video (start at 0:30 if tight on time)

There you go. Add one more technique to the toolbox.

 

References: ACEP Now article (& picture); concept video; live video

insulin memory aid: Can I tell from the name if its short or longer acting?

30 May

nice memory tool pulled from an April emdocs post:

 

INSULINs:

rapid acting: LOGs (e.g. NovoLog, HumaLog)

short to intermediate acting: LINs

  • Lin R – Short acting (NovoLin R, HumuLin R)
  • Lin N – Intermediate acting (NovoLin N, HumuLin N)

long acting: other stuff (e.g. Lantus, Levemir)

 

There you go. Check out the original post, which has a nice chart on the pharmacokinetics, as well as this handy visual aid, too.

screen-shot-2015-08-16-at-10-53-37-am

 

References: http://www.emdocs.net/core-em-pharmacology-of-insulins/

Cranial Nerve VI Palsy

23 May

Submitted by Christina Brown, M.D.

Definition 

  • Abducens nerve, CN VI
  • a somatic, efferent (motor) nerve that controls a single muscle; lateral rectus. 
  • sixth cranial nerve has the longest subarachnoid course of all the cranial nerves. 
  • sixth nerve nucleus is located in the pons, just ventral to the floor of the fourth ventricle and just lateral to the medial longitudinal fasciculus (MLF) [5].

RBO revisada JAN-FEV-13-en.pmd

Epidemiology 

study of 213 patients with unilateral isolated sixth nerve palsies, non-traumatic

  • 78% experienced spontaneous recovery of their palsy,
  • 37% recovering by 8 weeks
  • 74% by 24 weeks [3].
  • Only 16% failed to recover; of this group, however, almost 40 percent had serious underlying pathology accounting for their palsy.

 

Presentation 

  • primarily c/o horizontal diplopia (double vision producing a side-by-side image with both eyes open). 
  • Patients with idiopathic sixth nerve palsy often present with the sudden onset of horizontal diplopia that is better at near and worse at a distance.
  • Patients also may present with a head-turn to maintain binocularity and to minimize diplopia. [5].  
  • A sudden onset distinguishes idiopathic sixth cranial nerve palsies from tumor or myasthenia gravis [6]. 
  • Other things to pay particular attention to when dealing with sixth nerve palsies
    • fifth nerve (reduced facial sensation, often around the upper face and cornea) pointing to a lesion in the cavernous sinus
    • papilledema, suggesting a mass lesion causing raised intracranial pressure and displacement of the brainstem and thus stretching of one or both sixth nerves.

 

DDx – Giant cell arteritis, Mass Lesion, Myasthenia Gravis, Lyme disease, syphilis, cavernous sinus lesion, Medial Orbital Wall Fracture, Horner’s Syndrome, diabetes, meningitis [1,6]

Evaluation – For idiopathic CNVI palsy, spontaneous improvement over several weeks to months is expected, and failure to improve suggests more serious intracranial pathology.

  • 1st – Onset of presentation? A sudden onset distinguishes idiopathic sixth cranial nerve palsies from tumor or myasthenia gravis.
  • 2nd – Is a single nerve involved? Involvement of other nerves, even the opposite cranial nerve (eg, bilateral sixth nerve palsy), suggests a more serious underlying pathology.
  • 3rd – Is there a medical excuse for the problem? Diabetes, myasthenia gravis, etc.  As an example, one is more likely to work up a young person with a sixth nerve palsy than an older person in his seventies.
  • 4th – Headache? The presence of severe headache of sudden onset demands an urgent evaluation for cerebral aneurysm
  • 5th – Signs of improvement over time? Almost always point to a benign process. Isolated fourth or sixth never palsies can be observed for a few weeks. More extensive work-up should be done if the palsy does not resolve or if other symptoms appear. Persistent esotropia may require a surgical procedure.

 

Management 

  • Ophthalmology C/S if bilateral nerve involvement, CNV involvement, persistent esotropia.
  • Neuroimaging if high clinical suspicion for mass lesion, cerebral aneurysm.
  • If elevated ESR, CRP pointing toward temporal arteritis, start high dose steroids.

 

References: 

  1. http://www.uptodate.com/contents/overview-of-diplopia?source=search_result&search=sixth+nerve+palsy&selectedTitle=1~50#H23
  2. Patel SV, Holmes JM, Hodge DO, Burke JP. Diabetes and hypertension in isolated sixth nerve palsy: a population-based study. Ophthalmology 2005; 112:760.
  3. King AJ, Stacey E, Stephenson G, Trimble RB. Spontaneous recovery rates for unilateral sixth nerve palsies. Eye (Lond) 1995; 9 ( Pt 4):476.
  4. Gutman I, Levartovski S, Goldhammer Y, et al. Sixth nerve palsy and unilateral Horner’s syndrome. Ophthalmology 1986; 93:913.
  5. http://emedicine.medscape.com/article/1198383-overview
  6. Kline LB, Glaser JS. Bilateral abducens nerve palsies from clivus chordoma. Ann Ophthalmol 1981; 13:705.
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