Ascitic Fluid

Brief HPI:

A 56 year-old male with a history of alcoholic cirrhosis complicated by esophageal varices presents to the emergency department with abdominal distension. He notes gradually worsening symptoms over the past 2 weeks – roughly correlating with the timing of his last paracentesis. He has limited access to medical care and typically presents to emergency departments for palliative paracenteses. He is otherwise in his usual state of health and denies fevers, chills, abdominal pain, vomiting blood, or dark/bloody stools.

Vital signs are notable for a heart rate of 97bpm and blood pressure of 110/65mmHg – otherwise normal. Examination demonstrates a distended abdomen which is non-tender, dull to percussion and with a palpable fluid wave. Bedside ultrasonography shows large, homogenous-appearing ascites with readily-accessible pockets for drainage in the bilateral lower quadrants. A palliative paracentesis is performed with uncomplicated extraction of 4 liters of translucent, straw-colored fluid. Ascitic fluid analysis shows 90 white blood cells of which 10% are polymorphonuclear. The patient is observed briefly in the emergency department, noted symptomatic improvement and was discharged with a plan for telephone follow-up of fluid culture results.

An Algorithm for the Analysis of Ascitic Fluid

Algorithm for the Analysis of Ascitic Fluid

References

  1. Runyon BA. Care of patients with ascites. N Engl J Med. 1994;330(5):337-342. doi:10.1056/NEJM199402033300508.
  2. Wong CL, Holroyd-Leduc J, Thorpe KE, Straus SE. Does this patient have bacterial peritonitis or portal hypertension? How do I perform a paracentesis and analyze the results? JAMA. 2008;299(10):1166-1178. doi:10.1001/jama.299.10.1166.
  3. Tarn AC, Lapworth R. Biochemical analysis of ascitic (peritoneal) fluid: what should we measure? Ann Clin Biochem. 2010;47(Pt 5):397-407. doi:10.1258/acb.2010.010048.
  4. Li PK-T, Szeto CC, Piraino B, et al. ISPD Peritonitis Recommendations: 2016 Update on Prevention and Treatment. Perit Dial Int. 2016;36(5):481-508. doi:10.3747/pdi.2016.00078.
  5. MacIntosh T. Emergency Management of Spontaneous Bacterial Peritonitis – A Clinical Review. Cureus. 2018;10(3):e2253. doi:10.7759/cureus.2253.

Resuscitative Thoracotomy

Brief HPI:

A call is received from pre-hospital providers regarding an inbound trauma patient. An estimated 30 year-old male with unknown history sustained a penetrating wound to the right flank. On EMS arrival the patient was unresponsive but had a weakly-palpable radial pulse which was lost en-route. Their estimated time of arrival is 5 minutes.

Algorithm for the Selection of Patients for Resuscitative Thoracotomy

Algorithm for the Selection of Patients for Resuscitative Thoracotomy

References:

  1. Seamon MJ, Haut ER, Van Arendonk K, Barbosa RR, Chiu WC, Dente CJ, et al. An evidence-based approach to patient selection for emergency department thoracotomy: A practice management guideline from the Eastern Association for the Surgery of Trauma. J Trauma Acute Care Surg. 2015 Jul;79(1):159–73.
  2. Burlew CC, Moore EE, Moore FA, Coimbra R, McIntyre RC, Davis JW, et al. Western Trauma Association critical decisions in trauma: resuscitative thoracotomy. J Trauma Acute Care Surg. 2012 Dec;73(6):1359–63.
  3. Sherren PB, Reid C, Habig K, Burns BJ. Algorithm for the resuscitation of traumatic cardiac arrest patients in a physician-staffed helicopter emergency medical service. Crit Care. 2013 Mar 12;17(2):308.
  4. Cothren CC, Moore EE. Emergency department thoracotomy for the critically injured patient: Objectives, indications, and outcomes. World J Emerg Surg. 2006 Mar 24;1:4.

Red and Painful Eye

Brief HPI

A 60-year-old female with rheumatoid arthritis presents with unilateral eye pain and redness without reported vision changes. Physical examination demonstrates radially-oriented engorged episcleral vessels and normal visual acuity – she was diagnosed with episcleritis and discharged with follow-up.

Algorithm for the Evaluation of the Red and Painful Eye

Algorithm for the Evaluation of the Red and Painful Eye

Overview

The red or painful eye is a common presentation in the emergency department and the rapid identification and management of potentially sight-threatening causes is critical.

The diagnostic approach to the red or painful eye begins with identifying a history of caustic exposure where immediate and copious irrigation (even before detailed examination) may limit further injury. Alkaline agents induce more severe liquefactive necrosis leading to keratoconjunctivitis, while acidic agents are generally less destructive. Management is identical for both: irrigation with lactated Ringer solution through a Morgan lens applied to a topically anesthetized eye for 5-10 minutes repeated until the pH of the eye is neutral1.

Ocular or facial trauma presents a spectrum of differential diagnoses. Suspicion for globe rupture is increased by a suggestive mechanism such as a high-velocity projectile or high-impact blunt facial trauma. Characteristic examination findings include obvious globe deformity, an irregularly-shaped pupil, extrusion of vitreous, markedly decreased visual acuity, or parting of fluorescein (Seidel sign). If globe rupture is suspected, further manipulation is unadvisable and the affected eye should be shielded. Measures should be taken to avoid increases in intra-ocular pressure including elevation of the patient’s head-of-bed, anti-emetics (to prevent intra-ocular hypertension with vomiting), and the avoidance of medications potentially implicated in intra-ocular hypertension (ketamine, succinylcholine). Tetanus and antimicrobial prophylaxis should be provided while awaiting emergent ophthalmology consultation2,3.

Another traumatic diagnosis warranting rapid identification and possible intervention is retrobulbar hematoma – identified by proptosis, eye pain, decreased visual acuity, and elevated intra-ocular pressure. Pressures exceeding 40mmHg warrant lateral cantholysis in conjunction with medical management to prevent optic nerve ischemia and preserve vision4,5.

Diagnostic Approach

The evaluation of the non-traumatic red or painful eye follows a systematic and anatomically-based approach, starting with external components and moving inward:

1. External

The examination begins externally with an assessment of function (visual acuity) and inspection and palpation of the periorbital region. Periorbital edema, erythema, and tenderness to palpation in the setting of systemic illness (fever) is concerning for orbital cellulitis. When associated with elevated intra-ocular pressure or proptosis, a retrobulbar abscess may be present. Both warrant admission and parenteral antibiotics and the latter may require operative management such as aspiration or cantholysis. Less severe features without impact on visual acuity is suggestive of a periorbital cellulitis which may be treated as an outpatient with close follow-up2,6.

2. Lids and Lashes

Several non-emergent processes may affect the lids and lashes including blepharitis (inflammation of the eyelid margin), chalazion (inflammation of the Meibomian glands), hordeolum (eyelash follicle abscess), or dacrocystitis (infection of the lacrimal sac)2,7,8.

3. Conjunctiva and Sclera

Again, proceeding from superficial to deeper structures we encounter the epithelial layer (including palpebral and bulbar components) covering the sclera which is subject to allergic or infectious inflammation. Conjunctivitis is characterized by engorgement of superficial conjunctival blood vessels, potentially associated with conjunctival edema (chemosis), or discharge. Most conjunctivitis is self-limited and not sight-threatening, treatment is aimed at symptomatic relief though topical antibiotics have few adverse effects and may be prescribed if the diagnosis of bacterial conjunctivitis is unclear9.

When associated with pain, a deeper inflammatory process is implicated. Scleritis is a frequently immune-mediated inflammatory process (though infection, malignancy and medications have been implicated) associated with pain, photophobia, and examination findings of globe tenderness and engorged scleral blood vessels. Management in the emergency department is trivial (systemic NSAID’s), however ophthalmology consultation should be secured due to the risk of vision-compromising complications, as well as the intimation of an underlying systemic disorder9,10. Episcleritis is similarly immune-mediated, though generally self-limiting. The diagnosis is made by identification of characteristic, radially-oriented engorged episcleral vessels. When the diagnosis of scleritis versus episcleritis or conjunctivitis is in question the application of a topical vasoconstrictor (phenylephrine 2.5%) will blanch vessels in the conjunctival or superficial episcleral plexuses – sparing scleral vessels10,11.

4. Cornea

Keratitis can be caused by infection, ultraviolet light exposure, or contact lens use. Patients may have photophobia and a foreign-body sensation. Gross inspection or slit-lamp examination will show epithelial erosions that stain with fluorescein or the characteristic dendritic pattern accompanying herpes simplex virus infection. Management includes ophthalmology consultation, topical antibiotics if a bacterial process is suggested, and close follow-up7-9,12.

5. Anterior Chamber

A critical process occurring in the anterior chamber is angle-closure glaucoma. The patient commonly presents with severe pain, circumcorneal injection, and a pupil fixed at mid-dilation. Diagnosis is confirmed by the measurement of elevated intra-ocular pressure (greater than 20mmHg). Reduction of intra-ocular pressure with topical and systemic agents should begin immediately while awaiting emergent ophthalmology consultation13.

The slit-lamp microscope facilitates examination of the anterior chamber. The presence of cells (floating white and red blood cells, or layering hypopyon or hyphema) and flare (protein) suggest inflammation in the anterior segment caused by a systemic inflammatory process, infection, or trauma and warrants close ophthalmologic follow-up2,7,9.

6. Vitreous

An ocular examination mimicking orbital cellulitis with evidence of anterior chamber involvement, particularly in a patient with a history of recent ocular surgery or trauma suggests endophthalmitis. Management requires admission for parenteral antibiotics with ophthalmology consultation2.

Additional Diagnostic Modalities

Advanced imaging may be useful in the diagnosis of traumatic and non-traumatic orbital pathology. Multi-detector computed tomography (MD-CT) is readily available and rapidly performed in the emergency department and can aid in the diagnosis of critical infectious processes, including extension beyond the orbital septum in orbital cellulitis, scleral thickening in endophthalmitis, and characterization of hematoma or abscess in the retrobulbar space. The addition of intravenous contrast media can identify critical vascular processes such as cavernous sinus thrombosis14,15. For traumatic pathology, CT can assist with the evaluation of globe integrity, lens position, vitreous/retinal detachment, and foreign bodies16. Imaging cannot be relied upon exclusively to exclude pathology, and the patient’s presentation and clinician’s examination should determine the need for consultation and evaluation. For globe rupture, for example, in one study of 59 patients with severe ocular trauma and diagnostic uncertainty regarding the presence of globe rupture, CT failed to diagnosed open globe injury in 1/3 of patients (with surgical scleral inspection as a reference standard)17. Another retrospective analysis of 48 eyes sustaining trauma revealed sensitivity ranging from 56-68% for CT identification of open globe injury18.

In addition to potential diagnostic inaccuracy, computed tomography exposes patients to risks including ionizing radiation, and the possibility of contrast-induced nephropathy19. Ultrasound is becoming increasingly accessible and comfortable for the emergency physician, and has the benefit of being relatively non-invasive – including facilitating ocular examination in patients with significant periorbital swelling limiting eye-opening. Ocular ultrasound may aid with the diagnosis of a wide variety of ocular pathology including vitreous hemorrhage, retinal detachment, central retinal arterial/venous occlusions, foreign body identification, lens dislocation and retrobulbar hematoma. In one study of 61 patients presenting with trauma or acute vision changes, ultrasound interpretation agreed with criterion standard (orbital computed tomography or ophthalmology evaluation) for 98% of cases20.

View Ocular Ultrasound Algorithm

References

  1. Messman AM. Ocular Injuries: New Strategies In Emergency Department Management. Emergency Medicine Practice. 2015;17(11):1–21–quiz21–2.
  2. Wright JL, Wightman JM. Red and painful eye. … Concepts and Clinical Practice 8th ed …. 2014.
  3. Romaniuk VM. Ocular trauma and other catastrophes. Emerg Med Clin North Am. 2013;31(2):399-411. doi:10.1016/j.emc.2013.02.003.
  4. Babineau MR, Sanchez LD. Ophthalmologic Procedures in the Emergency Department. Emerg Med Clin North Am. 2008;26(1):17-34. doi:10.1016/j.emc.2007.11.003.
  5. Rowh AD, Ufberg JW, Chan TC, Vilke GM, Harrigan RA. Lateral canthotomy and cantholysis: emergency management of orbital compartment syndrome. J Emerg Med. 2015;48(3):325-330. doi:10.1016/j.jemermed.2014.11.002.
  6. Henderson M, Tierney L, Smetana G. The Patient History: Evidence-Based Approach. McGraw Hill Professional; 2012.
  7. Alteveer JG, Mccans KM, Hemphill RR. The Red Eye, The Swollen Eye, And Acute Vision Loss. … Practice+ Em Practice …. 2002.
  8. Leibowitz HM. The red eye. N Engl J Med. 2000;343(5):345-351. doi:10.1056/NEJM200008033430507.
  9. Mahmood AR, Narang AT. Diagnosis and management of the acute red eye. Emerg Med Clin North Am. 2008. doi:10.1016/j.emc.2007.10.002.
  10. Albini TA, Rao NA, Smith RE. The Diagnosis and Management of Anterior Scleritis. International Ophthalmology Clinics. 2005;45(2):191.
  11. Roscoe M, Landis T. How to diagnose the acute red eye with confidence. JAAPA. 2006;19(3):24–30–quiz45–6.
  12. Deborah S Jacobs MD. Evaluation of the red eye. UpToDate. https://www.uptodate.com/contents/evaluation-of-the-red-eye. Published February 24, 2016. Accessed April 18, 2017.
  13. Prum BE, Herndon LW, Moroi SE, et al. Primary Angle Closure Preferred Practice Pattern(®) Guidelines. Ophthalmology. 2016;123(1):P1-P40. doi:10.1016/j.ophtha.2015.10.049.
  14. LeBedis CA, Sakai O. Nontraumatic orbital conditions: diagnosis with CT and MR imaging in the emergent setting. Radiographics. 2008;28(6):1741-1753. doi:10.1148/rg.286085515.
  15. Platnick J, Crum AV, Soohoo S, Cedeño PA, Johnson MH. The globe: infection, inflammation, and systemic disease. YSULT. 2011;32(1):38-50. doi:10.1053/j.sult.2010.12.003.
  16. Dunkin JM, Crum AV, Swanger RS, Bokhari SAJ. Globe trauma. YSULT. 2011;32(1):51-56. doi:10.1053/j.sult.2010.09.003.
  17. Hoffstetter P, Schreyer AG, Schreyer CI, et al. Multidetector CT (MD-CT) in the diagnosis of uncertain open globe injuries. Rofo. 2010;182(2):151-154. doi:10.1055/s-0028-1109659.
  18. Arey ML, Mootha VV, Whittemore AR, Chason DP, Blomquist PH. Computed tomography in the diagnosis of occult open-globe injuries. Ophthalmology. 2007;114(8):1448-1452. doi:10.1016/j.ophtha.2006.10.051.
  19. Custer PL, Kent TL. Pitfalls of ophthalmic radiographic imaging. Curr Opin Ophthalmol. 2014;25(5):432-435. doi:10.1097/ICU.0000000000000064.
  20. Blaivas M, Theodoro D, Sierzenski PR. A study of bedside ocular ultrasonography in the emergency department. Academic Emergency Medicine. 2002;9(8):791-799.

Pericardial Effusion

HPI:

43F with a history of HTN and diastolic heart failure presenting with two days of shortness of breath. Reports that symptoms are worse at night when lying down to sleep and associated with a cough productive of white sputum. She also reports intermittent left-sided chest pain, described as sharp and exacerbated by cough or deep inspiration. She denies fevers/chills, nausea/vomiting, sick contacts or recent travel.
m

PMH:

  • Hypertension
  • Diabetes Mellitus (Type II)
  • Hyperlipidemia
  • Diastolic heart failure

PSH:

  • Cesarean section

FH:

  • Father with MI at 76 years-old

SHx:

  • Lives at home.
  • Denies tobacco, alcohol or drug abuse.

Meds:

  • Lasix 40mg p.o. daily
  • Lisinopril 20mg p.o. daily
  • Atenolol 50mg p.o. daily
  • Omeprazole 20mg p.o. daily
  • Lantus 14 units daily
  • Novolin 6 units t.i.d

Allergies:

NKDA

Physical Exam:

VS: T 98.2 HR 81 RR 19 BP 219/91 O2 95% RA
Gen: Adult female in no acute distress, alert and responding appropriately to questions.
HEENT: PERRL, EOMI, mucous membranes moist.
CV: RRR, no murmurs appreciated, no JVD.
Lungs: Crackles at right lung base.
Abd: Soft, non-tender, non-distended, without rebound/guarding.
Ext: 1+ pitting edema in bilateral lower extremities to knee.
Neuro: AAOx4, grossly normal peripheral sensation and motor strength.

Labs/Studies:

  • Troponin: 0.15
  • Procalcitonin: 0.15
  • CBC: 10.9/9.1/26.4/296
  • BMP: 134/4.6/104/22/56/2.87/214

Imaging:

Pericardial Effusion

Pericardial Effusion

Measured in the largest dimension, suggestive of a moderate to large pericardial effusion.

E-Point Septal Separation

E-Point Septal Separation

E-Point Septal Separation (EPSS), estimated here is the smallest distance between the anterior leaflet of the mitral valve and intraventricular septum. Values > 12mm are suggestive of depressed ejection fraction.

Left Ventricular Hypertrophy

Left Ventricular Hypertrophy

Thickened left ventricular wall.

Pericardial Effusion - Subxiphoid

Pericardial Effusion - Subxiphoid

Pericardial Effusion - Parasternal Long

Pericardial Effusion - Parasternal Long

Pericardial Effusion - Parasternal Short

Pericardial Effusion - Parasternal Short

  • CXR: Consolidation involving the majority of the right lung, cardiomegaly.
  • Bedside Echo: LVEF 55%, concentric LVH, no wall motion abnormality, moderate pericardial effusion noted, RV not collapsed.

Assessment/Plan:

43F with a history of HTN, diastolic heart failure presenting with SOB.

#SOB: CXR finding of right-sided consolidation with history of productive cough, evidence of leukocytosis with neutrophil predominance, and relative hypoxemia suggestive of community-acquired pneumonia. No evidence of systemic inflammatory response. PE unlikely, patient is not bed-bound and alternative diagnosis more likely.
– Start empiric antimicrobial therapy ceftriaxone 1g IV q24h, azithromycin 500mg IV q24h.

#Pericardial Effusion: Noted on bedside echo, no evidence of RV collapse to suggest cardiac tamponade. Also, no JVD and pulsus paradoxus measured at 8mmHg.
– Obtain formal transthoracic echocardiogram to evaluate effusion.
– Consult cardiology if worsening hemodynamics

#Elevated Troponin: No ECG changes suggestive of acute ST-elevation MI. May represent NSTEMI though historical features not consistent with ACS.
– Trend troponin/EKG q.8.h. x3
– Give aspirin 325mg, consider anti-coagulation.
– Consider stress echo prior to discharge

#Elevated Creatinine: Baseline unknown, likely acute component with or without chronic kidney disease.
– Volume resuscitation as tolerated, follow repeat chemistry.

#Hypertension: Asymptomatic, resume home medications.

Physiology of Cardiac Tamponade 1

  • Intrapericardial pressure (IPP) normally reflects intrathoracic pressure (ITP).
  • Inspiration: low ITP → low RAP → increased RA filling.
  • Expiration: high ITP → low LAP → increased LA filling.
  • Increased pericardial fluid → increased IPP → increased LA/RA filling pressures (diastolic dysfunction) → increased variation with respiration.
  • Earliest hemodynamic change in cardiac tamponade is JVD or IVC dilation.

IVC variation as marker for RAP 1

IVC Diameter (cm) Change with Respiration (%) RAP (mmHg)
<2.1 >50% 0-5
<2.1 <50% 5-10
>2.1 >50% 5-10
>2.1 <50% >15

Grading Pericardial Effusions 1

Grade Echo-free space (mm) Size (mL)
Small <10 100
Moderate 10-20 100-500
Large >20 >500

History and Physical Exam in Patients with Acute Pericarditis 2,3

Symptom/Sign ACS Pericarditis PE
Quality Pressure Sharp Sharp
Pleuritic No Yes Yes
Positional No Yes (worse when supine) No
Duration Minutes to hours Hours to days Hours to days
Improves with NG Yes No No
Friction Rub No Yes No
S3 Maybe No No

Differential Diagnosis of Pericardial Effusion 2-8

Differential Diagnosis of Pericardial Effusion

References:

  1. Schairer, J. R., Biswas, S., Keteyian, S. J., & Ananthasubramaniam, K. (2011). A Systematic Approach to Evaluation of Pericardial Effusion and Cardiac Tamponade. Cardiology in Review, 19(5), 233–238. doi:10.1097/CRD.0b013e31821e202c
  2. Khandaker MH, Espinosa RE, Nishimura RA, et al. Pericardial Disease: Diagnosis and Management. Mayo Clinic Proceedings. 2010;85(6):572-593. doi:10.4065/mcp.2010.0046.
  3. Lange, RA, Hillis, LD. Clinical practice. Acute pericarditis. The New England journal of medicine. 2004;351(21), 2195–2202. doi:10.1056/NEJMcp041997
  4. Imazio M, Adler Y. Management of pericardial effusion. Eur Heart J. 2013;34(16):1186-1197. doi:10.1093/eurheartj/ehs372.
  5. LeWinter MM. Clinical practice. Acute pericarditis. N Engl J Med. 2014;371(25):2410-2416. doi:10.1056/NEJMcp1404070.
  6. Vakamudi S, Ho N, Cremer PC. Pericardial Effusions: Causes, Diagnosis, and Management. Prog Cardiovasc Dis. 2017;59(4):380-388. doi:10.1016/j.pcad.2016.12.009.
  7. Imazio M, Mayosi BM, Brucato A, et al. Triage and management of pericardial effusion. J Cardiovasc Med (Hagerstown). 2010;11(12):928-935. doi:10.2459/JCM.0b013e32833e5788.
  8. Maisch B, Seferović PM, Ristić AD, et al. Guidelines on the diagnosis and management of pericardial diseases executive summary; The Task force on the diagnosis and management of pericardial diseases of the European society of cardiology. Eur Heart J. 2004;25(7):587-610. doi:10.1016/j.ehj.2004.02.002.

Low Voltage ECG

Definition

  • QRS in limb leads <5mm
  • QRS in precordial leads <10mm

General Causes

  • Fluid, fat or air attenuating signal
  • Myocardial infiltration
  • Loss of viable myocardium

Example

Low Voltage ECG
Low Voltage ECG

Low Voltage ECG

ECG of patient with pericardial effusion

Baseline ECG
Baseline ECG

Baseline ECG

Old ECG from same patient

Differential Diagnosis of Low Voltage ECG

Differential Diagnosis of Low-Voltage ECG

References

  1. Madias JE. Low QRS voltage and its causes. J Electrocardiol. 2008;41(6):498–500. doi:10.1016/j.jelectrocard.2008.06.021.
  2. WikEM: Low ECG voltage

Palpitations

Brief H&P

48F with a history of Grave disease (off medications for 4 months), presenting with palpitations. Noted gradual onset of palpitations while at rest, describing a pounding sensation lasting 3-4 hours and persistent (though improved) on presentation. Symptoms not associated with chest pain, shortness of breath, loss of consciousness, nor triggered by exertion. She reported a history of 8-10 episodes in the past for which she did not seek medical attention. Review of systems notable only for heat intolerance.

On physical examination, vital signs were notable for tachycardia (HR 138bpm). No alteration in mental status, murmur, tremor or hyperreflexia appreciated.

Labs

  • Hb: 14.7
  • Urine hCG: negative
  • TSH: <0.01
  • Total T3: 311ng/dL
  • Free T4: 2.64ng/dL

ECG

Palpitations - Sinus Tachycardia

Sinus Tachycardia

Impression/Plan

Palpitations due to sinus tachycardia from symptomatic hyperthyroidism secondary to medication non-adherence. Improved with propranolol, discharged with methimazole and PMD follow-up.

Algorithm for the Evaluation and Management of Palpitations1, 2

Algorithm for the Evaluation and Management of Palpitations

Evaluation of Palpitations

History and Physical

Subjective description of symptom quality
Rapid and regular beating suggests paroxysmal SVT or VT. Rapid and irregular beating suggests atrial fibrillation, atrial flutter, or variable conduction block.
Stop/start sensation: PAC or PVC
Rapid fluttering: Sustained supraventricular or ventricular tachycardia
Pounding in neck: Produced by canon A waves from AV dissociation (VT, complete heart block, SVT)
Onset and offset
Random, episodic, lasting instants: Suggests PAC or PVC
Gradual onset and offset: Sinus tachycardia
Abrupt onset and offset: SVT or VT
Syncope
Suggests hemodynamically significant arrhythmia, often VT
Examination
Identify evidence of structural, valvular heart disease

ECG1

ECG Finding Presumed etiology
Short PR, Delta waves WPW, AVRT
LAA, LVH Atrial fibrillation
PVC, BBB Idiopathic VT
Q-waves Prior MI, VT
QT-prolongation VT (polymorphic)
LVH, septal Q-waves HCM
Blocks  

References

  1. Zimetbaum P, Josephson ME. Evaluation of patients with palpitations. N Engl J Med. 1998;338(19):1369-1373. doi:10.1056/NEJM199805073381907.
  2. Probst MA, Mower WR, Kanzaria HK, Hoffman JR, Buch EF, Sun BC. Analysis of emergency department visits for palpitations (from the National Hospital Ambulatory Medical Care Survey). The American Journal of Cardiology. 2014;113(10):1685-1690. doi:10.1016/j.amjcard.2014.02.020.
  3. Abbott AV. Diagnostic approach to palpitations. Am Fam Physician. 2005;71(4):743-750.

Seizure

Brief HPI

A 72 year-old male with a history of hypertension and hiatal hernia presents to the emergency department with one week of generalized weakness. His family report decreased oral intake with frequent emesis over the past four days. He denies chest pain, shortness of breath, abdominal pain, or other complaints. During the interview he has a generalized tonic-clonic seizure which persists for five minutes despite the administration of 4mg of lorazepam.

An Algorithm for the Management of Seizures

The management of active seizures is algorithmic, starting with a rapid assessment of airway patency, supporting ventilation (with appropriate positioning, nasopharyngeal airway adjuncts and bag-valve mask if needed) and ensuring adequate perfusion. Patients should have continuous vital sign monitoring, supplemental oxygen to maintain oxygen saturation >92% and intravenous access1.

Pharmacologic treatment follows a stepwise approach, detailed in the algorithm below. The focus is on immediate stabilization and progressively escalating anti-epileptic drugs eventually requiring endotracheal intubation and continuous infusions of sedatives2-4.

An Algorithm for the Management of Seizures

Pathophysiology

Seizures are caused by excessive and disorganized neuronal activation, typically induced by global alterations in the production and transmission of impulses (electrolyte derangements, drugs/toxins, infection), or foci of increased irritability (hemorrhage, stroke, mass) – a pathophysiologic motif that mimics cardiac tachyarrhythmias (sympathomimetic toxicity or scarred myocardium for example)1. Status epilepticus, defined as a seizure lasting greater than five minutes or recurrent seizures without a return to normal baseline, shares an equally high short-term mortality – greater than 20%5.

Syncope vs. Seizure

The algorithm below details historical and examination features that may assist with distinguishing epileptic seizure from non-epileptic activity6,7.

Clinical Features Distinguishing Seizure from Syncope

Case Conclusion

The patient continued to seize and a point-of-care chemistry panel revealed a serum sodium of 108mEq/L. Seizures abate after the infusion of hypertonic saline (100mL of 3% saline over 10 minutes, repeated until cessation of seizures). While hyponatremia is generally corrected slowly – owing to the risk of osmotic demyelination – immediate correction in this setting is critical8.


The remainder of the patient’s evaluation demonstrated urine osmolarity is 389mOsm/kg and urine sodium is 53mmol/L, in the setting of relative euvolemia on examination these findings were consistent with SIADH. Head computed tomography is obtained and reveals a sellar mass.

View Hyponatremia Algorithm

References

  1. McMullan JT, Davitt AM, Pollack CV Jr. Seizures. In: Rosen’s Emergency Medicine. Mosby Incorporated; 2002:2808. doi:10.1016/S1474-4422(06)70350-7.
  2. Billington M, Kandalaft OR, Aisiku IP. Adult Status Epilepticus: A Review of the Prehospital and Emergency Department Management. J Clin Med. 2016;5(9):74. doi:10.3390/jcm5090074.
  3. Huff JS, Morris DL, Kothari RU, Gibbs MA, Emergency Medicine Seizure Study Group. Emergency department management of patients with seizures: a multicenter study. Academic Emergency Medicine. 2001;8(6):622-628.
  4. Prasad M, Krishnan PR, Sequeira R, Al-Roomi K. Anticonvulsant therapy for status epilepticus. Prasad M, ed. Cochrane Database Syst Rev. 2014;16(9):CD003723. doi:10.1002/14651858.CD003723.pub3.
  5. Logroscino G, Hesdorffer DC, Cascino G, Annegers JF, Hauser WA. Short-term mortality after a first episode of status epilepticus. Epilepsia. 1997;38(12):1344-1349.
  6. Sheldon R, Rose S, Ritchie D, et al. Historical criteria that distinguish syncope from seizures. J Am Coll Cardiol. 2002;40(1):142-148.
  7. McKeon A, Vaughan C, Delanty N. Seizure versus syncope. Lancet Neurol. 2006;5(2):171-180. doi:10.1016/S1474-4422(06)70350-7.
  8. Goh KP. Management of hyponatremia. Am Fam Physician. 2004;69(10):2387-2394.

Cardiac Arrest

Brief HPI:

An overhead page alerts you to an arriving patient with cardiac arrest. An approximately 35-year-old male was running away from police officers and collapsed after being shot with a stun gun. The patient was found to be pulseless, CPR was started by police officers and the patient is en route.

An Algorithm for the Evaluation and Management of Cardiac Arrest with Ultrasonography

An Algorithm for the Evaluation and Management of Cardiac Arrest with Ultrasonography

Causes of Cardiac (and non-cardiac) Arrest

Sudden cardiac arrest (SCA) leading to sudden cardiac death (SCD) if not successfully resuscitated, refers to the unexpected collapse of circulatory function. Available epidemiologic data for in-hospital and out-of-hospital cardiac arrest (OHCA) point appropriately to cardiac processes as the most common cause, though extra-cardiac processes (most frequently respiratory), comprise up to 40% of cases1-3.

Identifying the underlying cause is critical as several reversible precipitants require rapid identification. However, the usual diagnostic techniques may be challenging, limited or absent – including patient history, detailed examination, and diagnostic studies.

The initial rhythm detected upon evaluation is most suggestive of the etiologic precipitant. Pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VF) is suggestive of a cardiac process – most commonly an acute coronary syndrome although heart failure or other structural and non-structural heart defects associated with dysrhythmias may be at fault4.

Pulseless electrical activity (PEA) presents a broader differential diagnosis as it essentially represents severe shock. The most common extra-cardiac cause is hypoxia – commonly secondary to pulmonary processes including small and large airway obstruction (bronchospasm, aspiration, foreign body, edema). Other causes include substance intoxication, medication adverse effect5,6, or electrolyte disturbances7. Finally, any precipitant of shock may ultimately lead to PEA, including hypovolemia/hemorrhage, obstruction (massive pulmonary embolus8, tamponade, tension pneumothorax), and distribution (sepsis).

Asystole is the absence of even disorganized electrical discharge and is the terminal degeneration of any of the previously-mentioned rhythms if left untreated.

Management of Cardiac Arrest

Optimizing survival outcomes in patients with cardiac arrest is dependent on early resuscitation with the prioritization of interventions demonstrated to have survival benefit. When advanced notice is available, prepare the resuscitation area including airway equipment (with adjuncts to assist ventilation and waveform capnography devices). Adopt the leadership position and assign roles for chest compressions, airway support, application of monitor/defibrillator, and establishment of peripheral access.

High-quality chest compressions with minimal interruptions are the foundation of successful resuscitation – and guideline changes prioritizing compressions have demonstrated detectable improvements in rates of successful resuscitation9,10. Measurement of quantitative end-tidal capnography can guide adequacy of chest compressions11,12 and an abrupt increase may signal restoration of circulation without necessitating interruptions of chest compressions13,14. Sustained, low measures of end-tidal CO2 despite appropriate resuscitation may signal futility and (alongside other factors) guides termination of resuscitation11,12.

The next critical step in restoring circulation is prompt defibrillation of eligible rhythms (pVT/VF) when detected. The immediate delivery of 200J (uptitrated to the device maximum for subsequent shocks) of biphasic energy and restoration of a perfusing rhythm is one of few interventions with clear benefits. For pVT/VF that persists despite multiple countershocks (more than three), the addition of an intravenous antiarrhythmic appears to improve survival to hospital admission. The ARREST trial was a randomized controlled study comparing amiodarone to its diluent as placebo for OHCA with refractory pVT/VF showing significant improvement in survival to hospital admission for the amiodarone group15. This was followed by the ALIVE trial comparing amiodarone and lidocaine which showed significantly higher rates of survival to hospital admission in the amiodarone group16. However, a more recent randomized trial comparing amiodarone (in a novel diluent less likely to cause hypotension), lidocaine, and placebo in a similar patient population showed less convincing results, with no detected difference in survival or the secondary outcome of favorable neurological outcome for either amiodarone or lidocaine compared with placebo17. The heterogeneity of available data contributed to current guidelines which recommend that either amiodarone or lidocaine may be used for shock-refractory pVT/VF18.

Current guidelines also recommend the administration of vasopressors (epinephrine 1mg every 3-5 minutes). In one randomized controlled trial exploring the long-standing guideline recommendations, epinephrine was associated with increased rates of restoration of spontaneous circulation, though no significant impact on the primary outcome of survival to hospital discharge was identified19. Physiologically, increased systemic vascular resistance combined with positive beta-adrenergic impact on cardiac output would be expected to complement resuscitative efforts. However, more recent studies have suggested that arrest physiology and unanticipated pharmacologic effects may complicate this simplistic interpretation – particularly when patient-centered outcomes are emphasized. Research exploring the timing and amount of epinephrine suggest that earlier administration and higher cumulative doses are associated with negative impacts on survival to hospital discharge and favorable neurological outcomes20-22.

Ultimately, treatment should focus on optimal execution of measures with clear benefits (namely chest compressions and early defibrillation of eligible rhythms). Other management considerations with which the emergency physician is familiar with including establishing peripheral access and definitive airway management can be delayed.

Rapid Diagnostic Measures for the Identification of Reversible Processes

Traditional diagnostic measures are generally unavailable during an ongoing cardiac arrest resuscitation. The emergency medicine physician must rely on the physical examination and point-of-care tests with the objective of identifying potentially reversible processes. Measurement of capillary blood glucose can exclude hypoglycemia as a contributor. Point-of-care chemistry and blood gas analyzers can identify important electrolyte derangements, as well as clarifying the primary impulse in acid-base disturbances.

End-tidal capnography was discussed previously for the guidance of ongoing resuscitation, but it may have diagnostic utility in patients with SCD. In one study the initial EtCO2 was noted to be significantly higher for primary pulmonary processes (with PEA/asystole as presenting rhythm) compared to primary cardiac processes (with pVT/VF as presenting rhythm)23.

The use of point-of-care ultrasonography, particularly in PEA arrest where non-cardiac etiologies dominate, may help identify the etiology of arrest and direct therapy. Bedside ultrasonography should be directed first at assessment of cardiac function – examining the pericardial sac and gross abnormalities in chamber size. A pericardial effusion may suggest cardiac tamponade, ventricular collapse can be seen with hypovolemia, and asymmetric right-ventricular dilation points to pulmonary embolus where thrombolysis should be considered8. If cardiac ultrasound is unrevealing, thoracic ultrasound can identify pneumothorax24-27.

In the absence of ultrasonographic abnormalities, attention turns to other rapidly reversible precipitants first. If opioid toxicity is a consideration, an attempt at reversal with naloxone has few adverse effects. If any detected rhythm is a polymorphic ventricular tachycardia characteristic of torsades de pointes – rapid infusion of magnesium sulfate should follow defibrillation. Other potentially reversible medications or toxins should be managed as appropriate.

Post-Resuscitation Steps

After successful restoration of circulation, the next management steps are critical to the patient’s long-term outcomes. A definitive airway should be established if not already secured (and if restoration of circulation was not associated with neurological recovery sufficient for independent airway protection). Circulatory support should continue with fluid resuscitation and vasopressors to maintain end-organ perfusion.

An immediate ECG should be performed to identify infarction, ischemia or precipitants of dysrhythmia. ST-segment elevation after return of spontaneous circulation (ROSC) warrants emergent angiography and possible intervention. However, given the prevalence of cardiac causes (of which coronary disease is most common) for patients with pVT/VF arrest, the presence of ST elevations is likely of insufficient sensitivity to identify all patients who would benefit from angiography. Several studies and meta-analyses have explored a more inclusive selection strategy for angiography (patients without obvious non-cardiac causes for arrest), all of which identified survival benefits with angiography and successful angioplasty when possible28-30.

Finally, the induction of hypothermia (or targeted temperature management) has significant benefits in survivors of cardiac arrest and can be instituted in the emergency department. Studies first targeted a core temperature of 32-24°C, with a randomized controlled trial demonstrating higher rates of favorable neurological outcome and reduced mortality31. More recent studies suggest that a more liberal temperature target does not diffuse the positive effects of induced hypothermia. A randomized trial of 939 patients with OHCA comparing a targeted temperature of 33°C vs 36°C suggested that a lower temperature target did not confer higher benefit to mortality or recovery of neurological function32. The more liberal temperature target may alleviate adverse effects associated with hypothermia which include cardiovascular effects (bradycardia), electrolyte derangements (during induction and rewarming), and possible increased risk of infections33. Targeted temperature management is achieved with external cooling measures or infusion of cooled fluids, rarely requiring more invasive measures34. Aggregate review of available data in a recent meta-analysis further supports the use of targeted temperature management after cardiac arrest as standard-of-care35.

References

  1. Bergum D, Nordseth T, Mjølstad OC, Skogvoll E, Haugen BO. Causes of in-hospital cardiac arrest – Incidences and rate of recognition. Resuscitation. 2015;87:63-68. doi:10.1016/j.resuscitation.2014.11.007.
  2. Wallmuller C, Meron G, Kurkciyan I, Schober A, Stratil P, Sterz F. Causes of in-hospital cardiac arrest and influence on outcome. Resuscitation. 2012;83(10):1206-1211. doi:10.1016/j.resuscitation.2012.05.001.
  3. Vaartjes I, Hendrix A, Hertogh EM, et al. Sudden death in persons younger than 40 years of age: incidence and causes. European Journal of Cardiovascular Prevention & Rehabilitation. 2009;16(5):592-596. doi:10.1097/HJR.0b013e32832d555b.
  4. Zheng ZJ, Croft JB, Giles WH, Mensah GA. Sudden cardiac death in the United States, 1989 to 1998. Circulation. 2001;104(18):2158-2163.
  5. Hoes AW, Grobbee DE, Lubsen J, Man in ‘t Veld AJ, van der Does E, Hofman A. Diuretics, beta-blockers, and the risk for sudden cardiac death in hypertensive patients. Ann Intern Med. 1995;123(7):481-487.
  6. Siscovick DS, Raghunathan TE, Psaty BM, et al. Diuretic therapy for hypertension and the risk of primary cardiac arrest. N Engl J Med. 1994;330(26):1852-1857. doi:10.1056/NEJM199406303302603.
  7. Gettes LS. Electrolyte abnormalities underlying lethal and ventricular arrhythmias. Circulation. 1992;85(1 Suppl):I70-I76.
  8. Kürkciyan I, Meron G, Sterz F, et al. Pulmonary embolism as a cause of cardiac arrest: presentation and outcome. Arch Intern Med. 2000;160(10):1529-1535.
  9. Callaway CW, Soar J, Aibiki M, et al. Part 4: Advanced Life Support: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. In: Vol 132. American Heart Association, Inc.; 2015:S84-S145. doi:10.1161/CIR.0000000000000273.
  10. Kudenchuk PJ, Redshaw JD, Stubbs BA, et al. Impact of changes in resuscitation practice on survival and neurological outcome after out-of-hospital cardiac arrest resulting from nonshockable arrhythmias. Circulation. 2012;125(14):1787-1794. doi:10.1161/CIRCULATIONAHA.111.064873.
  11. Touma O, Davies M. The prognostic value of end tidal carbon dioxide during cardiac arrest: a systematic review. Resuscitation. 2013;84(11):1470-1479. doi:10.1016/j.resuscitation.2013.07.011.
  12. Levine RL, Wayne MA, Miller CC. End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest. N Engl J Med. 1997;337(5):301-306. doi:10.1056/NEJM199707313370503.
  13. Garnett AR, Ornato JP, Gonzalez ER, Johnson EB. End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. JAMA. 1987;257(4):512-515.
  14. Falk JL, Rackow EC, Weil MH. End-tidal carbon dioxide concentration during cardiopulmonary resuscitation. N Engl J Med. 1988;318(10):607-611. doi:10.1056/NEJM198803103181005.
  15. Kudenchuk PJ, Cobb LA, Copass MK, et al. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation. N Engl J Med. 1999;341(12):871-878. doi:10.1056/NEJM199909163411203.
  16. Dorian P, Cass D, Schwartz B, Cooper R, Gelaznikas R, Barr A. Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation. N Engl J Med. 2002;346(12):884-890. doi:10.1056/NEJMoa013029.
  17. Kudenchuk PJ, Brown SP, Daya M, et al. Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest. N Engl J Med. 2016;374(18):1711-1722. doi:10.1056/NEJMoa1514204.
  18. Neumar RW, Shuster M, Callaway CW, et al. Part 1: Executive Summary: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. In: Vol 132. American Heart Association, Inc.; 2015:S315-S367. doi:10.1161/CIR.0000000000000252.
  19. Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL. Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial. Resuscitation. 2011;82(9):1138-1143. doi:10.1016/j.resuscitation.2011.06.029.
  20. Hagihara A, Hasegawa M, Abe T, Nagata T, Wakata Y, Miyazaki S. Prehospital epinephrine use and survival among patients with out-of-hospital cardiac arrest. JAMA. 2012;307(11):1161-1168. doi:10.1001/jama.2012.294.
  21. Dumas F, Bougouin W, Geri G, et al. Is epinephrine during cardiac arrest associated with worse outcomes in resuscitated patients? J Am Coll Cardiol. 2014;64(22):2360-2367. doi:10.1016/j.jacc.2014.09.036.
  22. Andersen LW, Kurth T, Chase M, et al. Early administration of epinephrine (adrenaline) in patients with cardiac arrest with initial shockable rhythm in hospital: propensity score matched analysis. BMJ. 2016;353:i1577. doi:10.1136/bmj.i1577.
  23. Grmec S, Lah K, Tusek-Bunc K. Difference in end-tidal CO2 between asphyxia cardiac arrest and ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest in the prehospital setting. Crit Care. 2003;7(6):R139-R144. doi:10.1186/cc2369.
  24. Rose JS, Bair AE, Mandavia D, Kinser DJ. The UHP ultrasound protocol: a novel ultrasound approach to the empiric evaluation of the undifferentiated hypotensive patient. American Journal of Emergency Medicine. 2001;19(4):299-302. doi:10.1053/ajem.2001.24481.
  25. Hernandez C, Shuler K, Hannan H, Sonyika C, Likourezos A, Marshall J. C.A.U.S.E.: Cardiac arrest ultra-sound exam—A better approach to managing patients in primary non-arrhythmogenic cardiac arrest. Resuscitation. 2008;76(2):198-206. doi:10.1016/j.resuscitation.2007.06.033.
  26. Chardoli M, Heidari F, Shuang-ming S, et al. Echocardiography integrated ACLS protocol versus con- ventional cardiopulmonary resuscitation in patients with pulseless electrical activity cardiac arrest. Chinese Journal of Traumatology. 2012;15(5):284-287. doi:10.3760/cma.j.issn.1008-1275.2012.05.005.
  27. Zengin S, Yavuz E, Al B, et al. Benefits of cardiac sonography performed by a non-expert sonographer in patients with non-traumatic cardiopulmonary arrest. Resuscitation. 2016;102:105-109. doi:10.1016/j.resuscitation.2016.02.025.
  28. Spaulding CM, Joly LM, Rosenberg A, et al. Immediate coronary angiography in survivors of out-of-hospital cardiac arrest. N Engl J Med. 1997;336(23):1629-1633. doi:10.1056/NEJM199706053362302.
  29. Dumas F, Cariou A, Manzo-Silberman S, et al. Immediate Percutaneous Coronary Intervention Is Associated With Better Survival After Out-of-Hospital Cardiac Arrest: Insights From the PROCAT (Parisian Region Out of Hospital Cardiac Arrest) Registry. Circulation: Cardiovascular Interventions. 2010;3(3):200-207. doi:10.1161/CIRCINTERVENTIONS.109.913665.
  30. Millin MG, Comer AC, Nable JV, et al. Patients without ST elevation after return of spontaneous circulation may benefit from emergent percutaneous intervention: A systematic review and meta-analysis. Resuscitation. 2016;108:54-60. doi:10.1016/j.resuscitation.2016.09.004.
  31. Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002;346(8):549-556. doi:10.1056/NEJMoa012689.
  32. Nielsen N, Wetterslev J, Cronberg T, et al. Targeted Temperature Management at 33°C versus 36°C after Cardiac Arrest. N Engl J Med. 2013;369(23):2197-2206. doi:10.1056/NEJMoa1310519.
  33. Polderman KH, Peerdeman SM, Girbes AR. Hypophosphatemia and hypomagnesemia induced by cooling in patients with severe head injury. J Neurosurg. 2001;94(5):697-705. doi:10.3171/jns.2001.94.5.0697.
  34. Polderman KH, Herold I. Therapeutic hypothermia and controlled normothermia in the intensive care unit: Practical considerations, side effects, and cooling methods*. Critical Care Medicine. 2009;37(3):1101-1120. doi:10.1097/CCM.0b013e3181962ad5.
  35. Schenone AL, Cohen A, Patarroyo G, et al. Therapeutic hypothermia after cardiac arrest: A systematic review/meta-analysis exploring the impact of expanded criteria and targeted temperature. Resuscitation. 2016;108:102-110. doi:10.1016/j.resuscitation.2016.07.238.

Atrial Fibrillation

A 64-year-old male with a history of hypertension and hyperlipidemia presents with palpitations. He reports intermittent symptoms over the past 3 days, associated with dyspnea on exertion, but no chest pain, dizziness or syncope. His vital signs are notable for tachycardia (HR 129bpm) without hypotension or hypoxia. An ECG shows atrial fibrillation with rapid ventricular response.

Evaluation and Management

While the patient’s tachyarrhythmia is not yet associated with hypotension or evidence of malperfusion, preparation is key and includes continuous telemetry and vital sign monitoring, establishment of intravenous access, and application of cardioversion pads 1.

The presence of atrial fibrillation is new and the rapid ventricular response (RVR) may be symptomatic of more serious and potentially reversible pathology. A thorough history and physical examination may elucidate a precipitant and should precede attempts at rate- or rhythm-control. RVR may be provoked by any of the processes that would otherwise induce a sinus tachycardia, including bleeding, infection, toxic/metabolic etiologies and endocrinopathies 2, 3

Candidacy for Cardioversion

In hemodynamically stable patients with new-onset atrial fibrillation, candidacy for cardioversion includes:4-6

  • Stable without ischemia, hypotension or acute CHF
  • Clear onset of <48 hours
  • Non-severe symptoms
  • Few prior episodes/treatments
  • Existing anti-coagulation with warfarin and therapeutic INR (at least 3 weeks)
  • Absence of high-risk features: rheumatic/valvular disease, severe left-ventricular dysfunction, prosthetic valves, or history of thromboembolism

Cardioversion may be pharmacologic (with procainamide, or amiodarone), or electrical (synchronized at 100-200J). Electrical cardioversion for acute atrial fibrillation is both more effective and results in shorter lengths-of-stay in the emergency department – though stable patients should participate in shared decision-making7. Another important consideration when cardioversion is pursued is the prevention of systemic embolization. While atrial fibrillation of duration less than 48-hours is rarely associated with systemic embolization, certain populations are at higher risk8. One retrospective study of 3143 patients with atrial fibrillation for less than 48-hours demonstrated an overall risk of 0.7% for thromboembolic events – though the rate was significantly higher in patients older than 60 years or with other comorbidities (heart failure, diabetes)9. The risk of embolic events should be weighed against the risk of bleeding.

CHA2DS2VASc10-12

C Congestive Heart Failure 1
H Hypertension 1
A2 Age >75 2
D Diabetes Mellitus 1
S2 Stroke, TIA, Thromboembolism 2
V Vascular disease 1
A Age >65 1
Sc Sex Category Female 1

 

  • 0: low risk (may not require anti-coagulation)
  • 1: low-moderate risk (consider anti-platelet or anti-coagulation)
  • ≥ 2: moderate-high risk (anti-coagulation recommended)

HAS-BLED13,14

H Uncontrolled hypertension 1
A Abnormal renal/liver function
Renal (renal replacement therapy, creatinine >2.3mg/dL) 1
Liver (cirrhosis, bilirubin >2x, AST/ALT >3x) 1
S Stroke 1
B Bleeding history/anemia 1
L Labile INR 1
E Elderly (>65) 1
D Drugs
Anti-platelet agent, NSAID 1
Alcohol (>8 drinks/week) 1

 

  • 0: low risk (0.6-1.13% annual risk of major bleeding)
  • 1-2: intermediate risk (1.02-3.2% annual risk of major bleeding)
  • ≥ 3: high risk (4.9-19.6% annual risk of major bleeding)

Pharmacologic Management

For patients who are not candidates for cardioversion, rate-control should be pursued. Options include AV nodal blocking agents such as calcium channel blockers and beta-blockers15. The most frequently studied agents of each category are metoprolol and diltiazem. Both classes show comparable efficacy and safety profiles with trends favoring diltiazem16, 17.

Algorithm for the management of atrial fibrillation with rapid ventricular response:

Algorithm for the management of atrial fibrillation with rapid ventricular response

References

  1. Atzema, C.L. and T.W. Barrett, Managing atrial fibrillation. Ann Emerg Med, 2015. 65(5): p. 532-9.
  2. January, C.T., et al., 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: Executive Summary. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society, 2014. 64(21): p. 2246-2280.
  3. Scheuermeyer, F.X., et al., Emergency Department Patients With Atrial Fibrillation or Flutter and an Acute Underlying Medical Illness May Not Benefit From Attempts to Control Rate or Rhythm. Ann Emerg Med, 2015. 65(5): p. 511-522 e2.
  4. Stiell, I.G., et al., Association of the Ottawa Aggressive Protocol with rapid discharge of emergency department patients with recent-onset atrial fibrillation or flutter. CJEM, 2010. 12(3): p. 181-91.
  5. von Besser, K. and A.M. Mills, Is discharge to home after emergency department cardioversion safe for the treatment of recent-onset atrial fibrillation? Ann Emerg Med, 2011. 58(6): p. 517-20.
  6. Cohn, B.G., S.M. Keim, and D.M. Yealy, Is emergency department cardioversion of recent-onset atrial fibrillation safe and effective? J Emerg Med, 2013. 45(1): p. 117-27.
  7. Bellone, A., et al., Cardioversion of acute atrial fibrillation in the emergency department: a prospective randomised trial. Emerg Med J, 2012. 29(3): p. 188-91.
  8. Weigner, M.J., et al., Risk for clinical thromboembolism associated with conversion to sinus rhythm in patients with atrial fibrillation lasting less than 48 hours. Ann Intern Med, 1997. 126(8): p. 615-20.
  9. Airaksinen, K.E., et al., Thromboembolic complications after cardioversion of acute atrial fibrillation: the FinCV (Finnish CardioVersion) study. J Am Coll Cardiol, 2013. 62(13): p. 1187-92.
  10. Friberg, L., M. Rosenqvist, and G.Y. Lip, Evaluation of risk stratification schemes for ischaemic stroke and bleeding in 182 678 patients with atrial fibrillation: the Swedish Atrial Fibrillation cohort study. Eur Heart J, 2012. 33(12): p. 1500-10.
  11. Lip, G.Y., et al., Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro heart survey on atrial fibrillation. Chest, 2010. 137(2): p. 263-72.
  12. Ntaios, G., et al., CHADS(2), CHA(2)S(2)DS(2)-VASc, and long-term stroke outcome in patients without atrial fibrillation. Neurology, 2013. 80(11): p. 1009-17.
  13. Lip, G.Y., et al., Comparative validation of a novel risk score for predicting bleeding risk in anticoagulated patients with atrial fibrillation: the HAS-BLED (Hypertension, Abnormal Renal/Liver Function, Stroke, Bleeding History or Predisposition, Labile INR, Elderly, Drugs/Alcohol Concomitantly) score. J Am Coll Cardiol, 2011. 57(2): p. 173-80.
  14. Pisters, R., et al., A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation: the Euro Heart Survey. Chest, 2010. 138(5): p. 1093-100.
  15. Goralnick, E. and L.J. Bontempo, Atrial Fibrillation. Emerg Med Clin North Am, 2015. 33(3): p. 597-612.
  16. Demircan, C., et al., Comparison of the effectiveness of intravenous diltiazem and metoprolol in the management of rapid ventricular rate in atrial fibrillation. Emerg Med J, 2005. 22(6): p. 411-4.
  17. Fromm, C., et al., Diltiazem vs. Metoprolol in the Management of Atrial Fibrillation or Flutter with Rapid Ventricular Rate in the Emergency Department. J Emerg Med, 2015. 49(2): p. 175-82.
  18. DiMarco, J.P., Atrial fibrillation and acute decompensated heart failure. Circ Heart Fail, 2009. 2(1): p. 72-3.

Blunt Cardiac Injury

Case Presentation

A 35-year-old female with no past medical history is brought in by ambulance to the emergency department. She was struck by a firework (“Roman Candle”) which lodged in her mid-chest until the propellant was consumed. She transiently lost consciousness but was awake upon EMS arrival. She complains of pleuritic chest pain. Examination reveals a circular 4x4cm full-thickness burn to the mid-chest with surrounding deep and superficial partial-thickness burns. Her ECG shows normal sinus rhythm, the initial serum troponin I is 32.9 (normal <0.012). CT angiography of the thorax is obtained.

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Mechanisms

Blunt cardiac injury (BCI) may be induced by multiple forces including direct thoracic trauma, crush injury of mediastinal contents between the sternum and thoracic spine, rapid deceleration causing tears at venous-atrial confluences, abrupt pressure changes from rapid compression of abdominal contents, blast injury, or laceration from bone fracture fragments1. The most common mechanisms of injury are motor vehicle collisions (50%), auto versus pedestrian (35%), motorcycle accidents (9%) and falls from significant height (>6m)2.

BCI represents a spectrum of conditions. Diagnosis is both challenging and critical as clinical manifestations can be absent or rapidly fatal.

At one end of the spectrum is myocardial contusion. The lack of a gold-standard for the diagnosis of this clinical entity has led to a preference for describing associated abnormalities if present3,4, including cardiac dysfunction (identified on echocardiography) or the next entity along the spectrum – arrhythmia.

The most common arrhythmia identified in blunt cardiac injury is sinus tachycardia, followed by premature atrial or ventricular contractions, T-wave changes, and atrial fibrillation or flutter5. Commotio cordis is a unique arrhythmia induced by untimely precordial impact (often in sports) during a vulnerable phase of ventricular excitability, resulting in ventricular fibrillation2.

ST-segment elevations after blunt cardiac injury should raise concern for myocardial infarction due to coronary artery dissection, laceration or thrombosis (often in already-diseased vessels) 5,6.

The remaining disease entities are increasingly rare, require careful examination or imaging for diagnosis, and are more likely to be non-survivable. Septal injury can range from small tears to rupture. Valvular injury most commonly affects the aortic valve (followed by mitral and tricuspid valves) and involves damage to leaflets, or rupture of papillary muscles or chordae tendineae. The clinical presentation is of acute valvular insufficiency, including acute heart failure and murmur2,7,8. A widened pulse pressure may be noted with aortic valve injury, and the manifestations of valvular injury may be delayed9. Finally, myocardial wall rupture is unlikely to be survivable, though patients may present with cardiac tamponade if rupture is small or contained2.

Evaluation

The primary diagnostic modalities for the assessment of BCI in the emergency department include assessment for pericardial fluid during the Focused Assessment with Sonography for Trauma (FAST), electrocardiography and cardiac enzymes.

While specific for identifying patients at risk of complications of BCI, electrocardiography alone is not sufficient to exclude BCI. In one study, only 59% of patient with echocardiographic evidence of BCI (wall-motion abnormalities, other chamber abnormalities) had initially abnormal ECG’s10. In another study, 41% of patients with initially normal ECG’s developed clinically significant abnormalities11. The use of specialized electrocardiography including right-sided ECG (proposed to better detect right-ventricular abnormalities which are more commonly associated with BCI) and signal-averaged ECG is not supported11,12.

Several studies have supported the use of serum troponin for the detection of clinically significant BCI – particularly in combination with electrocardiography. A prospective study in 2001 evaluating patients with blunt thoracic trauma using ECG at admission and 8-hours, as well as troponin I at admission, 4- and 8-hours had a negative predictive value of 100% for significant BCI (arrhythmia requiring treatment, shock, or structural cardiac abnormalities) in patients with initially normal ECG and troponin13.

Another prospective study adding to the population evaluated by Salim et al. included 41 patients with normal ECG’s and troponin levels at admission and 8-hours who were admitted for significant mechanisms, none developed significant BCI (again described as arrhythmia requiring treatment, shock, or structural cardiac abnormalities) after 1 to 3 days of observation14. The precise timing of serum troponin analysis remains unclear.

While FAST may detect hemopericardium warranting immediate intervention, formal echocardiography is indicated for patients with unexplained hypotension (to evaluate for valvular injury or regional wall-motion abnormalities) or persistent arrhythmias (to evaluate for arrhythmogenic intramural hematomas)15. The presence of sternal fractures was previously thought to increase risk of BCI and mandate echocardiography, however this notion is no longer supported16-18. The role of advanced imaging including helical CT (cardiac-gated), and MRI remains unclear19.

Algorithm for the Evaluation of Blunt Thoracic Trauma

Notes:
† Arrest in ED, immediate chest tube output >20ml/kg (>1.5L) or >200mL/hr for 2-4hr.

Management

Management of BCI depends on the pathologic process localized along the spectrum defined above. Persistent hypotension after appropriate evaluation for alternative etiologies may represent myocardial contusion with cardiac dysfunction and should be evaluated with echocardiography. Similarly, echocardiography and observation with continuous telemetry monitoring is indicated for any new arrhythmia or persistent and unexplained tachycardia. Patients with only elevation of the serum troponin without electrocardiographic abnormalities or obvious cardiac dysfunction should also be admitted for observation and serial cardiac enzymes. Traumatic myocardial infarction, valvular injury, or post-traumatic structural myocardial defects should be managed in consultation with cardiothoracic surgery5,19-21.

Case Conclusion

The CT interpretation noted the soft-tissue defect identified on examination as well as associated pulmonary contusions and a non-displaced sternal fracture. The patient went to the operating room for washout and debridement. A transthoracic echocardiogram demonstrated trace mitral regurgitation and a small pericardial effusion. She remained hemodynamically stable and serial troponin measures downtrended – no dysrhythmias were noted on telemetry monitoring. She was discharged on hospital day four with a negative-pressure wound dressing.

References

  1. Schultz JM, Trunkey DD. Blunt cardiac injury. Crit Care Clin. 2004;20(1):57-70.
  2. Yousef R, Carr JA. Blunt cardiac trauma: a review of the current knowledge and management. Ann Thorac Surg. 2014;98(3):1134-1140. doi:10.1016/j.athoracsur.2014.04.043.
  3. Mattox KL, Flint LM, Carrico CJ, et al. Blunt cardiac injury. The Journal of Trauma: Injury, Infection, and Critical Care. 1992;33(5):649-650.
  4. Sybrandy KC, Cramer MJM, Burgersdijk C. Diagnosing cardiac contusion: old wisdom and new insights. Heart. 2003;89(5):485-489.
  5. Elie M-C. Blunt cardiac injury. Mt Sinai J Med. 2006;73(2):542-552.
  6. Edouard AR, Felten M-L, Hebert J-L, Cosson C, Martin L, Benhamou D. Incidence and significance of cardiac troponin I release in severe trauma patients. Anesthesiology. 2004;101(6):1262-1268.
  7. Cordovil A, Fischer CH, Rodrigues ACT, et al. Papillary Muscle Rupture After Blunt Chest Trauma. Journal of the American Society of Echocardiography. 2006;19(4):469.e1-469.e3. doi:10.1016/j.echo.2005.12.005.
  8. Pasquier M, Sierro C, Yersin B, Delay D, Carron P-N. Traumatic Mitral Valve Injury After Blunt Chest Trauma: A Case Report and Review of the Literature. The Journal of Trauma: Injury, Infection, and Critical Care. 2010;68(1):243-246. doi:10.1097/TA.0b013e3181bb881e.
  9. Ismailov RM, Weiss HB, Ness RB, Lawrence BA, Miller TR. Blunt cardiac injury associated with cardiac valve insufficiency: trauma links to chronic disease? Injury. 2005;36(9):1022-1028. doi:10.1016/j.injury.2005.05.028.
  10. García-Fernández MA, López-Pérez JM, Pérez-Castellano N, et al. Role of transesophageal echocardiography in the assessment of patients with blunt chest trauma: correlation of echocardiographic findings with the electrocardiogram and creatine kinase monoclonal antibody measurements. Am Heart J. 1998;135(3):476-481.
  11. Fulda GJ, Giberson F, Hailstone D, Law A, Stillabower M. An evaluation of serum troponin T and signal-averaged electrocardiography in predicting electrocardiographic abnormalities after blunt chest trauma. The Journal of Trauma: Injury, Infection, and Critical Care. 1997;43(2):304–10–discussion310–2.
  12. Walsh P, Marks G, Aranguri C, et al. Use of V4R in patients who sustain blunt chest trauma. The Journal of Trauma: Injury, Infection, and Critical Care. 2001;51(1):60-63.
  13. Salim A, Velmahos GC, Jindal A, et al. Clinically significant blunt cardiac trauma: role of serum troponin levels combined with electrocardiographic findings. The Journal of Trauma: Injury, Infection, and Critical Care. 2001;50(2):237-243.
  14. Velmahos GC, Karaiskakis M, Salim A, et al. Normal electrocardiography and serum troponin I levels preclude the presence of clinically significant blunt cardiac injury. The Journal of Trauma: Injury, Infection, and Critical Care. 2003;54(1):45–50–discussion50–1. doi:10.1097/01.TA.0000046315.73441.D8.
  15. Nagy KK, Krosner SM, Roberts RR, Joseph KT, Smith RF, Barrett J. Determining which patients require evaluation for blunt cardiac injury following blunt chest trauma. World J Surg. 2001;25(1):108-111.
  16. Roy-Shapira A, Levi I, Khoda J. Sternal fractures: a red flag or a red herring? The Journal of Trauma: Injury, Infection, and Critical Care. 1994;37(1):59-61.
  17. Hills MW, Delprado AM, Deane SA. Sternal fractures: associated injuries and management. The Journal of Trauma: Injury, Infection, and Critical Care. 1993;35(1):55-60.
  18. Rashid MA, Ortenwall P, Wikström T. Cardiovascular injuries associated with sternal fractures. Eur J Surg. 2001;167(4):243-248. doi:10.1080/110241501300091345.
  19. Clancy K, Velopulos C, Bilaniuk JW, et al. Screening for blunt cardiac injury: an Eastern Association for the Surgery of Trauma practice management guideline. J Trauma Acute Care Surg. 2012;73(5 Suppl 4):S301-S306. doi:10.1097/TA.0b013e318270193a.
  20. El-Menyar A, Thani Al H, Zarour A, Latifi R. Understanding traumatic blunt cardiac injury. Ann Card Anaesth. 2012;15(4):287-295. doi:10.4103/0971-9784.101875.
  21. Hockberger RS, Walls RM. Rosen’s Emergency Medicine. Mosby Incorporated; 2002.

Arterial Pressure Indices

Indications

  • Assess for peripheral arterial disease (PAD)
  • Assess for risk of arterial injury in trauma

Test characteristics

  • PAD: ABI <0.90 sensitivity 95%, specificity 100% for >50% stenosis on arteriography1
  • Trauma: API <0.90 sensitivity 95%, specificity 97% for major arterial injury2

Technique for obtaining arterial pressure indices3

  1. Patient lies supine with extremities at level of the heart for 10 minutes
  2. Ankle: cuff positioned just above malleolus
  3. Brachial: cuff positioned just above antecubital fossa
  4. Doppler SBP
  5. Sequence: first arm, first PT, first DP, other PT, other DP, other arm. If SBP of first arm >10mmHg compared to second arm, repeat first arm and disregard first measure
  6. Calculation: ABI = higher of DP or PT / higher arm

Interpretation of ABI for PAD3

Value Interpretation
0-0.40 Severe PAD, rest pain, gangrene
0.41-0.90 PAD, claudication
0.91-1.30 Normal
>1.30 Non-compressible, severely calcified

Algorithm for the Evaluation of Arterial Injury4, 5

Algorithm for the Evaluation of Arterial Injury

Notes:

  • † If unable to palpate pulses due to patient habitus or shock/hypothermia, reattempt with oversized cuff and after appropriate rewarming/resuscitation. If remains challenging, proceed with imaging.
  • ‡ Proximal LE arterial injuries refers to the major named arteries of the thigh (excluding the profunda femoris) and proximal to the anterior tibial artery and tibioperoneal bifurcation.

Arteries of the Lower Leg

References:

  1. Mohler ER. Peripheral arterial disease: identification and implications. Arch Intern Med. 2003;163(19):2306-2314. doi:10.1001/archinte.163.19.2306.
  2. Johansen K, Lynch K, Paun M, Copass M. Non-invasive vascular tests reliably exclude occult arterial trauma in injured extremities. The Journal of Trauma: Injury, Infection, and Critical Care. 1991;31(4):515–9–discussion519–22.
  3. Aboyans V, Criqui MH, Abraham P, et al. Measurement and interpretation of the ankle-brachial index: a scientific statement from the American Heart Association. Circulation. 2012;126(24):2890-2909. doi:10.1161/CIR.0b013e318276fbcb.
  4. Feliciano DV, Moore FA, Moore EE, et al. Evaluation and management of peripheral vascular injury. Part 1. Western Trauma Association/critical decisions in trauma. J Trauma. 2011;70(6):1551-1556. doi:10.1097/TA.0b013e31821b5bdd.
  5. Fox N, Rajani RR, Bokhari F, et al. Evaluation and management of penetrating lower extremity arterial trauma: an Eastern Association for the Surgery of Trauma practice management guideline. J Trauma Acute Care Surg. 2012;73(5 Suppl 4):S315-S320. doi:10.1097/TA.0b013e31827018e4.
  6. Inaba K, Branco BC, Reddy S, et al. Prospective evaluation of multidetector computed tomography for extremity vascular trauma. J Trauma. 2011;70(4):808-815. doi:10.1097/TA.0b013e3182118384.

Weakness

A systematic approach to motor weakness progresses along an anatomic tract from the cerebral cortex to individual sarcomeres. Impulses are generated in the primary motor cortex mapped to the homunculus, then aggregate as they descend through the internal capsule. Fibers decussate in the medulla and descend in the contralateral lateral corticospinal tract. These upper motor neurons (UMN) synapse with the lower motor neuron (LMN) in the anterior horn of the spinal cord. The lower motor neuron is bundled with neighboring fibers into a peripheral nerve and activates the target muscle fibers at the neuromuscular junction.

Algorithm for the Evaluation of Weakness

Algorithm for the Evaluation of Weakness

Upper Versus Lower Motor Neuron Findings

Finding Upper Lower
Reflexes
Atrophy
Weakness
Fasciculation
Tone
Summary
Recalling these findings can be simplified by understanding the underlying process. Denervation near the target muscle fibers (lower motor neuron disease) results in dampening of the efferent limb of spinal reflexes, resulting in hyporeflexia. The absence of nourishing stimulation leads to muscle atrophy and disorganized interpretation of proximal activity produces fasciculation.

Comparison Between Myopathy, Neuropathy and Neuromuscular Junction Processes

Finding Myopathy Neuropathy Neuromuscular Junction
Example Polymyositis Guillain-Barre Syndrome Myasthenia Gravis
Distribution Proximal > Distal Distal > Proximal Diffuse, Bulbar
Reflexes Normal
Sensory
Fatigue
CK Normal Normal

Motor Strength Grading

Grade Description
5 Normal
4 Reduced, moves against resistance
3 Moves against gravity
2 Moves only with elimination of gravity
1 Fasciculation only
0 None

Reflex Grading

Grade Description
4 Increased amplitude, spread to adjacent, clonus
3 Increased
2 Normal
1 Decreased
0 None

References

  1. Ganti L, Rastogi V. Acute Generalized Weakness. Emerg Med Clin North Am. 2016;34(4):795-809. doi:10.1016/j.emc.2016.06.006.
  2. Asimos AW. Weakness: A Systematic Approach To Acute, Non-traumatic, Neurologic And Neuromuscular Causes. Emergency Medicine Practice. 2002;4(12):1-28.
  3. Morchi R. Weakness. In: Rosen’s Emergency Medicine. Elsevier Inc.; 2014:2521.

Epistaxis

Brief HPI:

A 63 year-old female with a history of hypertension, diabetes, and deep venous thrombosis on warfarin presents with epistaxis. She noted the spontaneous onset of nose bleeding 15 minutes prior to presentation. She had attempted compression but symptoms persisted so she was brought to the emergency department. On initial evaluation, she was in no acute distress and vital signs were normal. She was compressing her distal nares and was spitting up blood.

Oxymetolazone was administered and the patient was instructed regarding the appropriate position for compression, however bleeding continued when reassessed at 10- and then 30-minutes of compression. A bleeding focus could not be visualized on rhinoscopy so a nasal tampon was inserted with resolution of bleeding. Bleeding did not recur after two hours of observation in the emergency department. The patient’s INR was therapeutic two days prior to presentation and she was instructed to continue her usual regimen. At primary care follow-up two days later, the compression device was successfully removed.

Algorithm for the Management of Epistaxis1,2

Algorithm for the Management of Epistaxis

Epistaxis site of compression

Site of compression

External Compression

Begin with simple measures while preparing the necessary equipment and medications. Request that the patient gently blow their nose to clear clots, administer oxymetolazone 0.05% two sprays into the affected side. Apply firm pressure below the nasal bridge continuously for at least 10 minutes before reassessment. Commercial compression devices are available, or can be fashioned with tongue depressors3. Alternatively, the patient can apply pressure themselves.

Cautery

Again ask the patient to blow their nose to remove clots. Apply topical anesthetic for patient comfort prior to inspection with a nasal speculum. Additional suction (small tip, Frazier) may be required to improve visualization. If the bleeding site is identified, apply silver nitrate circumferentially around the source, then directly over the site. Avoid prolonged exposure or exposure to opposing sides of the nasal septum. If hemorrhage control is successful, patients may be discharged with a topical antimicrobial ointment such as polymixin-bacitracin-neomycin.

Packing 4,5

Multiple commercial anterior packing devices are available. Placement technique is similar for most, generally involving lubrication of the device with antimicrobial ointment or sterile water, sliding the device along the floor of the nasal cavity, followed by injection or inflation of the device to support tamponade. The incorporation of tranexamic acid (500mg in 5mL) into any phase of anterior packing may be beneficial 6,7. Packing the contralateral side to further support tamponade may be required.

Commonly used commercial devices are:

  • Merocel: lubricate with antimicrobial ointment, once deployed can rehydrate with saline or topical vasoconstrictor
  • Rapid Rhino
  • Rhino Rocket

Packing material should remain for 48-72 hours, during which patients should be re-evaluated. Prophylactic systemic antibiotics for the prevention of sinusitis or toxic shock are likely not required8.

Thrombogenic materials such as Floseal or Surgicel can also be used and may be better tolerated than packing materials9.

Posterior Control

If bleeding persists despite the above measures, a posterior site should be considered. Dual-balloon commercial devices are available for the control of posterior epistaxis and are deployed in a similar fashion to anterior devices. Once inserted, the posterior balloon should be inflated with air – with the volume guided by tension of the pilot cuff. The anterior balloon can then be inflated in a similar fashion. The posterior balloon cuff should be reinspected after 5 minutes as additional inflation may be required.

Commonly used commercial devices are:

If a commercial device is unavailable, a Foley catheter may be used. The catheter is introduced into the affected side. Once the tip is visualized in the posterior oropharynx, the balloon is inflated with approximately 10mL of sterile water. The catheter is then withdrawn gently to seat the balloon posteriorly. The catheter is secured in position against the nares with a clamp (taking care to pad the nares with gauze to prevent trauma) 10,11.

Patients with posterior epistaxis should be admitted with otolaryngology consultation. If bleeding continues despite these measures, emergent otolaryngology consultation for operative management is warranted.

Causes of Epistaxis12

Causes of Epistaxis

References

  1. Leong SCL, Roe RJ, Karkanevatos A. No frills management of epistaxis. Emerg Med J. 2005;22(7):470-472. doi:10.1136/emj.2004.020602.
  2. Barnes ML, Spielmann PM, White PS. Epistaxis: a contemporary evidence based approach. Otolaryngol Clin North Am. 2012;45(5):1005-1017. doi:10.1016/j.otc.2012.06.018.
  3. Moxham V, Reid C. Controlling epistaxis with an improvised device. Emergency Medicine Journal. 2001;18(6):518. doi:10.1136/emj.18.6.518.
  4. Singer AJ, Blanda M, Cronin K, et al. Comparison of nasal tampons for the treatment of epistaxis in the emergency department: A randomized controlled trial. Ann Emerg Med. 2005;45(2):134-139. doi:10.1016/j.annemergmed.2004.10.002.
  5. Iqbal IZ, Jones GH, Dawe N, et al. Intranasal packs and haemostatic agents for the management of adult epistaxis: systematic review. J Laryngol Otol. 2017;131(12):1065-1092. doi:10.1017/S0022215117002055.
  6. MD RZ, MD PM, MD SA, PhD AG, MD MS. A new and rapid method for epistaxis treatment using injectable form of tranexamic acid topically: a randomized controlled trial. American Journal of Emergency Medicine. 2013;31(9):1389-1392. doi:10.1016/j.ajem.2013.06.043.
  7. Kamhieh Y, Fox H. Tranexamic acid in epistaxis: a systematic review. Clin Otolaryngol. 2016;41(6):771-776. doi:10.1111/coa.12645.
  8. MD BC. Are Prophylactic Antibiotics Necessary for Anterior Nasal Packing in Epistaxis? YMEM. 2015;65(1):109-111. doi:10.1016/j.annemergmed.2014.08.011.
  9. Mathiasen RA, Cruz RM. Prospective, Randomized, Controlled Clinical Trial of a Novel Matrix Hemostatic Sealant in Patients with Acute Anterior Epistaxis. The Laryngoscope. 2005;115(5):899-902. doi:10.1097/01.MLG.0000160528.50017.3C.
  10. Holland NJ, Sandhu GS, Ghufoor K, Frosh A. The Foley catheter in the management of epistaxis. Int J Clin Pract. 2001;55(1):14-15.
  11. Hartley C, Axon PR. The Foley catheter in epistaxis management–a scientific appraisal. J Laryngol Otol. 1994;108(5):399-402.
  12. Kucik CJ, Clenney T. Management of epistaxis. Am Fam Physician. 2005;71(2):305-311.

Ocular Ultrasound

Brief HPI:

Intraocular foreign body

Intraocular foreign body

A middle-aged male with no past medical history presents with blurred vision. He reported that he was hammering while at work approximately 3 days prior to presentation and felt something enter his left eye. He denies eye pain, has noted some eye redness and increased tearing. Denies prior eye surgery or procedures. Physical examination demonstrates normal visual acuity, minimal left nasal conjunctival injection sparing the limbus, and an irregular left pupil that is minimally reactive. A no-pressure ocular ultrasound was performed and demonstrated a hyperechoic structure in the globe suggestive of foreign body which was confirmed on computed tomography of the orbit. The patient was taken to the operating room for removal.

Imaging

iofb_14
iofb_14
iofb_13
iofb_13
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iofb_12
iofb_11
iofb_11
iofb_10
iofb_10
iofb_09
iofb_09
iofb_08
iofb_08
iofb_07
iofb_07
iofb_06
iofb_06
iofb_05
iofb_05
iofb_04
iofb_04
iofb_03
iofb_03
iofb_02
iofb_02
iofb_01
iofb_01

CT Orbit without contrast

Punctate density within the left globe compatible with foreign body.

Algorithm for the Evaluation of Visual Complaints with Ocular Ultrasonography

Algorithm for the Evaluation of Visual Complaints with Ocular Ultrasonography

Gallery

The POCUS Atlas
The ultrasound images and videos used in this post come from The POCUS Atlas, a collaborative collection focusing on rare, exotic and perfectly captured ultrasound images.
The POCUS Atlas

Orbital Abscess

Lens dislocation

Retinal detachment

Vitreous hemorrhage

Posterior vitreous detachment

ONSD (increased)

Central retinal artery flow (normal)

Central retinal artery occlusion


Applications1,2

Useful for the evaluation of intraocular processes:

  • Retinal detachment
  • Vitreous hemorrhage/detachment
  • Intraocular foreign body
  • Lens dislocation
  • Retroorbital hemorrhage/abscess
  • Retinal vascular processes (CRAO)

Augmentation of physical examination when limited due to facial swelling or trauma:

  • Pupil size and reactivity
  • Extraocular movements

ONSD

  • Normal <5mm adults (>15yo)
  • Normal <4.5mm children (1-15yo)
  • Normal <4mm infants (<1yo)
  • By convention, measurements of the optic nerve sheath diameter are made 3-mm posterior to the globe

Technique

  • Apply Tegaderm, ensuring no air bubbles trapped
  • Apply copious ultrasound gel
  • Use no-pressure technique, anchoring hand against the patient’s forehead, nasal bridge or maxilla
  • Probe indicator to the patient’s right for transverse views
  • Probe indicator to the patient’s head for longitudinal views
  • Start with medium gain then increase to identify subtle findings

Test Characteristics

Prospective observational study evaluating patients presenting with ocular trauma or acute vision complaints underwent ocular ultrasound. Ultrasound findings agreed with the confirmatory test: ophthalmology consultation or advanced imaging (usually computed tomography) in 60 of 61 cases3.

Specific Findings 4,5

Retinal Detachment6-9

Appears as a highly reflective membrane floating in the substance of the vitreous body, moves within vitreous body with eye movement. Remains anchored at the optic nerve and ora serrata.

Posterior Vitreous Detachment10

Both retinal detachments and posterior vitreous detachments show a linear hyperechoic line in the posterior chamber. However, posterior vitreous detachments are not tethered to the optic nerve and will appear to cross midline.

Vitreous Hemorrhage

Seen more easily with high-gain, enhanced by eye movements which demonstrate hyperechoic particles swirling around in the vitreous body.

Retrobulbar Hematoma

Identified by the presence of a hypoechoic structure posterior to the globe. Should prompt a measurement of intra-ocular pressure if simultaneous globe rupture is not suspected.

Lens Dislocation

Usually secondary to blunt trauma, lens displaced from normal position and appears as an echogenic ovoid structure floating freely in the vitreous or over the retina.

Globe Rupture

If the diagnosis of globe rupture is obvious, ultrasound should be avoided. However, the “no-pressure” technique described above likely does not significantly impact intra-ocular pressure and should be safe11,12. Globe rupture can be identified by scleral buckling, anterior chamber collapse, or globe collapse/irregularities.

Optic Nerve Evaluation13-18

Though not a direct assessment of ocular pathology, evaluation of the optic nerve sheath diameter (ONSD) serves as a reliable surrogate for elevated intracranial pressure – emulating fundoscopy for papilledema. See normal measurements and image acquisition above.

Intraocular Foreign Body

The preferred imaging modality for evaluation of intraocular foreign body is orbital computed tomography. Ultrasonographically, foreign bodies are typically hyperechoic.

Central Retinal Artery Occlusion19,20

A more advanced technique, the addition of color Doppler over the central retinal artery may reveal decreased systolic amplitude and diastolic flow in embolic or thrombotic occlusion.

All illustrations are available for free, licensed (along with all content on this site) under Creative Commons Attribution-ShareAlike 4.0 International Public License.

Downloads Page License

References

  1. Kimberly HH, Stone MB. Chapter E5 – Emergency Ultrasound. Ninth Edition. Elsevier Inc.; 2018:e49-e66. doi:10.1016/B978-0-323-35479-0.00204-X.
  2. Knoop KJ, Dennis WR. Ophthalmologic, Otolaryngologic, and Dental Procedures. Seventh Edition. Elsevier Inc.; 2019:1295–1337.e2. doi:10.1016/B978-0-323-35478-3.00062-2.
  3. Blaivas M, Theodoro D, Sierzenski PR. A study of bedside ocular ultrasonography in the emergency department. Academic Emergency Medicine. 2002;9(8):791-799.
  4. Roque PJ, Hatch N, Barr L, Wu TS. Bedside ocular ultrasound. Crit Care Clin. 2014;30(2):227–41–v. doi:10.1016/j.ccc.2013.10.007.
  5. Kilker BA, Holst JM, Hoffmann B. Bedside ocular ultrasound in the emergency department. European Journal of Emergency Medicine. 2014;21(4):246-253. doi:10.1097/MEJ.0000000000000070.
  6. Yoonessi R, Hussain A, Jang TB. Bedside ocular ultrasound for the detection of retinal detachment in the emergency department. Acad Emerg Med. 2010;17(9):913-917. doi:10.1111/j.1553-2712.2010.00809.x.
  7. Shinar Z, Chan L, Orlinsky M. Use of ocular ultrasound for the evaluation of retinal detachment. J Emerg Med. 2011;40(1):53-57. doi:10.1016/j.jemermed.2009.06.001.
  8. Chu HC, Chan MY, Chau CWJ, Wong CP, Chan HH, Wong TW. The use of ocular ultrasound for the diagnosis of retinal detachment in a local accident and emergency department. Hong Kong Journal of Emergency Medicine. 2017;24(6):263-267. doi:10.1177/1024907917735085.
  9. Vrablik ME, Snead GR, Minnigan HJ, Kirschner JM, Emmett TW, Seupaul RA. The diagnostic accuracy of bedside ocular ultrasonography for the diagnosis of retinal detachment: a systematic review and meta-analysis. Ann Emerg Med. 2015;65(2):199–203.e1. doi:10.1016/j.annemergmed.2014.02.020.
  10. Schott ML, Pierog JE, Williams SR. Pitfalls in the Use of Ocular Ultrasound for Evaluation of Acute Vision Loss. J Emerg Med. 2013;44(6):1136-1139. doi:10.1016/j.jemermed.2012.11.079.
  11. Chandra A, Mastrovitch T, Ladner H, Ting V, Radeos MS, Samudre S. The utility of bedside ultrasound in the detection of a ruptured globe in a porcine model. West J Emerg Med. 2009;10(4):263-266.
  12. Berg C, Doniger SJ, Zaia B, Williams SR. Change in intraocular pressure during point-of-care ultrasound. West J Emerg Med. 2015;16(2):263-268. doi:10.5811/westjem.2015.1.24150.
  13. Tsung JW, Blaivas M, Cooper A, Levick NR. A rapid noninvasive method of detecting elevated intracranial pressure using bedside ocular ultrasound: application to 3 cases of head trauma in the pediatric emergency department. Pediatr Emerg Care. 2005;21(2):94-98.
  14. Kimberly HH, Shah S, Marill K, Noble V. Correlation of optic nerve sheath diameter with direct measurement of intracranial pressure. Acad Emerg Med. 2008;15(2):201-204. doi:10.1111/j.1553-2712.2007.00031.x.
  15. Blaivas M, Theodoro D, Sierzenski PR. Elevated intracranial pressure detected by bedside emergency ultrasonography of the optic nerve sheath. Academic Emergency Medicine. 2003;10(4):376-381.
  16. Moretti R, Pizzi B. Optic Nerve Ultrasound for Detection of Intracranial Hypertension in Intracranial Hemorrhage Patients. Journal of Neurosurgical Anesthesiology. 2009;21(1):16-20. doi:10.1097/ANA.0b013e318185996a.
  17. Rajajee V, Vanaman M, Fletcher JJ, Jacobs TL. Optic Nerve Ultrasound for the Detection of Raised Intracranial Pressure. Neurocrit Care. 2011;15(3):506-515. doi:10.1007/s12028-011-9606-8.
  18. Major R, al-Salim W. Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. BET 3. Ultrasound of optic nerve sheath to evaluate intracranial pressure. Emerg Med J. 2008;25(11):766-767. doi:10.1136/emj.2008.066845.
  19. Riccardi A, Siniscalchi C, Lerza R. Embolic Central Retinal Artery Occlusion Detected with Point-of-care Ultrasonography in the Emergency Department. J Emerg Med. 2016;50(4):e183-e185. doi:10.1016/j.jemermed.2015.12.022.
  20. Catalin J Dragos, Jianu S Nina, Munteanu M, Vlad D, Rosca C, Petrica L. Color Doppler imaging features in patients presenting central retinal artery occlusion with and without giant cell arteritis. VSP. 2016;73(4):397-401. doi:10.2298/VSP140814087C.

Thromboelastography

Thromboelastography (TEG) is an assessment of hemostatic function intended to evaluate in vivo coagulation parameters, guiding the targeted correction of coagulopathy1. TEG has predominantly been studied in cardiac surgery, though research has extended to other peri-operative and peri-procedural transfusion management2-5.

Recently, a randomized trial explored the use of TEG to guide transfusion in trauma patients requiring massive transfusion6. 111 patients meeting requirements for massive transfusion protocol activation were randomized to a conventional coagulation assay (CCA) or TEG-guided transfusion algorithm. Patients in the TEG group demonstrated significantly decreased mortality at 28 days and reductions in plasma and platelet transfusion requirements.

More research is needed before TEG can be recommended for use in trauma resuscitation or other common emergency department applications7,8, however it may be useful to prepare by becoming familiar with the most basic aspects of thromboelastography.

Thromboelastography Summary

Thromboelastography Summary

Examples

Normal

Normal

Anti-coagulants

Anti-coagulants

R,K: Increased
Angle: Decreased

Anti-Platelet

Anti-Platelet

R: Normal
K: Increased
MA: Decreased

Hypercoagulable

Hypercoagulable

R,K: Decreased
MA: Increased

FIbrinolysis

FIbrinolysis

MA: Decreasing
LY30: Increased

DIC (Phase 1)

DIC (Phase 1)

R,K: Decreased
MA: Increased
LY30: Increased

DIC (Phase 2)

DIC (Phase 2)

R,K: Increased
MA: Decreased

References

  1. Bolliger D, Seeberger MD, Tanaka KA. Principles and Practice of Thromboelastography in Clinical Coagulation Management and Transfusion Practice. Transfusion Medicine Reviews. 2012;26(1):1-13. doi:10.1016/j.tmrv.2011.07.005.
  2. Porte RJ, Bontempo FA, Knot EA, Lewis JH, Kang YG, Starzl TE. Systemic effects of tissue plasminogen activator-associated fibrinolysis and its relation to thrombin generation in orthotopic liver transplantation. Transplantation. 1989;47(6):978-984.
  3. Rahe-Meyer N, Solomon C, Hanke A, et al. Effects of fibrinogen concentrate as first-line therapy during major aortic replacement surgery: a randomized, placebo-controlled trial. Anesthesiology. 2013;118(1):40-50. doi:10.1097/ALN.0b013e3182715d4d.
  4. Weber CF, Klages M, Zacharowski K. Perioperative coagulation management during cardiac surgery. Current Opinion in Anaesthesiology. 2013;26(1):60-64. doi:10.1097/ACO.0b013e32835afd28.
  5. De Pietri L, Bianchini M, Montalti R, et al. Thrombelastography-guided blood product use before invasive procedures in cirrhosis with severe coagulopathy: A randomized, controlled trial. Hepatology. 2016;63(2):566-573. doi:10.1002/hep.28148.
  6. Gonzalez E, Moore EE, Moore HB, et al. Goal-directed Hemostatic Resuscitation of Trauma-induced Coagulopathy. Ann Surg. 2016;263(6):1051-1059. doi:10.1097/SLA.0000000000001608.
  7. Afshari A, Wikkelsø A, Brok J, Møller AM, Wetterslev J. Thrombelastography (TEG) or Thromboelastometry (ROTEM) to Monitor Haemotherapy Versus Usual Care in Patients with Massive Transfusion. Vol 24. (Afshari A, ed.). Chichester, UK: John Wiley & Sons, Ltd; 1996:404–3. doi:10.1002/14651858.CD007871.pub2.
  8. da Luz LT, Nascimento B, Rizoli S. Thrombelastography (TEG®): practical considerations on its clinical use in trauma resuscitation. Scand J Trauma Resusc Emerg Med. 2013;21(1):29. doi:10.1186/1757-7241-21-29.

Simplified Airway Management Algorithm

An airway management algorithm, developed with Dr. Diane Birnbaumer, has been previously developed on ddxof: airway management algorithm. The algorithm provides detailed, step-by-step recommendations for specific airway classifications – divided into normal, anticipated difficult, crash, and failed airways.

While helpful as an educational tool, the algorithm is likely too complex for rapid review or bedside application. Admittedly sacrificing some detail, this simplified airway management algorithm highlights the critical steps, incorporates only the most commonly-used airway adjuncts, assumes imminent respiratory decompensation and failure of progressive intubation attempts.

Simplified Airway Management Algorithm

Simplified Airway Management Algorithm

Febrile Seizure

Brief HPI:

An 8-month old female, fully-immunized, otherwise healthy is brought in by paramedics after 1 minute of witnessed generalized tonic-clonic shaking. The patient had otherwise been well, eating and behaving normally earlier that day. On EMS arrival, the patient was post-ictal but grew increasingly responsive en-route and upon presentation to the pediatric emergency department she was crying and appeared normal to her parents. Capillary glucose was 118g/dL. On examination the patient was noted to be febrile with a rectal temperature of 39.4°C. The remainder of the physical examination was normal.

ED Course:

The patient received anti-pyretics and a urinalysis was obtained which was not suggestive of urinary tract infection. During the 3-hour period of observation in the emergency department the patient remained at her normal baseline, had no further seizure activity, and tolerated oral intake with difficulty. The patient was suspected to have a simple febrile seizure and was discharged home.

Algorithm for the Diagnosis of Febrile Seizure

Algorithm for the Evaluation of Febrile Seizure

References

  1. Syndi Seinfeld DO, Pellock JM. Recent Research on Febrile Seizures: A Review. J Neurol Neurophysiol. 2013;4(165). doi:10.4172/2155-9562.1000165.
  2. Whelan H, Harmelink M, Chou E, et al. Complex febrile seizures-A systematic review. Dis Mon. 2017;63(1):5-23. doi:10.1016/j.disamonth.2016.12.001.
  3. Millichap JJ, Gordon Millichap J. Methods of investigation and management of infections causing febrile seizures. Pediatr Neurol. 2008;39(6):381-386. doi:10.1016/j.pediatrneurol.2008.07.017.
  4. Subcommittee on Febrile Seizures, American Academy of Pediatrics. Neurodiagnostic evaluation of the child with a simple febrile seizure. Pediatrics. 2011;127(2):389-394. doi:10.1542/peds.2010-3318.

Leukemoid Reaction

Brief HPI:

An approximately 80-year-old male with unknown medical history is brought to the emergency department from a skilled nursing facility after unwitnessed arrest – EMS providers established return of spontaneous circulation after chest compressions and epinephrine. On arrival, the patient was hypotensive (MAP 40mmHg) and hypoxic (SpO2 85%) with mask ventilation. The patient was intubated, resuscitated with intravenous fluids and started on vasopressors. Imaging demonstrated lung consolidation consistent with multifocal pneumonia versus aspiration. Laboratory studies were obtained:

  • CBC: WBC: 49.2 (N: 64%, Bands: 20%)
  • ABG: pH: 7.07, pCO2: 73mmHg
  • Lactate: 9.1mmol/L
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CT Pulmonary Angiography

Peribronchial opacities and patchy consolidation in the lungs which may represent multifocal pneumonia and/or aspiration in the appropriate clinical setting.
Mildly dilated main pulmonary artery suggestive of pulmonary arterial hypertension.

ED Course:

The patient was admitted to the medical intensive care unit for cardiopulmonary arrest presumed secondary to hypoxia and septic shock from healthcare-associated pneumonia or aspiration. The markedly elevated white blood cell count was attributed to a combination of infection and tissue ischemia from transient global hypoperfusion.


Definition: 1

  • Markedly elevated leukocyte (particularly neutrophil) count without hematologic malignancy
  • Cutoff is variable, 25-50k

Review of Available Literature

Retrospective review of 135 patients with WBC >25k 2
48% infection
15% malignancy
9% hemorrhage
12% glucocorticoid or granulocyte colony stimulating therapy
Retrospective review of 173 patients with WBC >30k 3
48% infection (7% C. difficile)
28% tissue ischemia
7% obstetric process (vaginal or cesarean delivery)
5% malignancy
Observational study of 54 patients with WBC >25k 4
Consecutive patients presenting to the emergency department
Compared to age-matched controls with moderate leukocytosis (12-24k)
Patients with leukemoid reaction were more likely to have an infection, be hospitalized and die.

Differential Diagnosis of Leukemoid Reaction 1,5-8

Differential Diagnosis of Leukemoid Reaction

References

  1. Sakka V, Tsiodras S, Giamarellos-Bourboulis EJ, Giamarellou H. An update on the etiology and diagnostic evaluation of a leukemoid reaction. Eur J Intern Med. 2006;17(6):394-398. doi:10.1016/j.ejim.2006.04.004.
  2. Reding MT, Hibbs JR, Morrison VA, Swaim WR, Filice GA. Diagnosis and outcome of 100 consecutive patients with extreme granulocytic leukocytosis. Am J Med. 1998;104(1):12-16.
  3. Potasman I, Grupper M. Leukemoid reaction: spectrum and prognosis of 173 adult patients. Clin Infect Dis. 2013;57(11):e177-e181. doi:10.1093/cid/cit562.
  4. Lawrence YR, Raveh D, Rudensky B, Munter G. Extreme leukocytosis in the emergency department. QJM. 2007;100(4):217-223. doi:10.1093/qjmed/hcm006.
  5. Marinella MA, Burdette SD, Bedimo R, Markert RJ. Leukemoid reactions complicating colitis due to Clostridium difficile. South Med J. 2004;97(10):959-963. doi:10.1097/01.SMJ.0000054537.20978.D4.
  6. Okun DB, Tanaka KR. Profound leukemoid reaction in cytomegalovirus mononucleosis. JAMA. 1978;240(17):1888-1889.
  7. Halkes CJM, Dijstelbloem HM, Eelkman Rooda SJ, Kramer MHH. Extreme leucocytosis: not always leukaemia. Neth J Med. 2007;65(7):248-251.
  8. Granger JM, Kontoyiannis DP. Etiology and outcome of extreme leukocytosis in 758 nonhematologic cancer patients: a retrospective, single-institution study. Cancer. 2009;115(17):3919-3923. doi:10.1002/cncr.24480.