Predicting Volume Responsiveness in the Emergency Department

Authors: Paolo N. Grenga, MD (EM Resident Physician, University of Rochester Emergency Medicine Residency), Ryan P. Bodkin, MD (Program Director, University of Rochester Emergency Medicine Residency), and Jason M. Rotoli, MD (Assistant Program Director, University of Rochester Emergency Medicine Residency // Edited by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)

The ED physician commonly encounters undifferentiated shock.  As is the case with many shock states, rapid intravenous (IV) fluid administration is often the initial therapy of choice during initial resuscitation.  Yet, it has been established in the literature that only about ~50% of hemodynamically unstable patients will respond favorably to fluid administration [1-4].  What options exist to predict which patients will respond favorably to a fluid challenge?  Recent debate over various indices and ultrasonographic techniques for indirectly assessing volume responsiveness in critically ill patients suggests that there may be fewer options than previously proposed.


You are working in the critical care bay of a tertiary medical center when you receive a transfer from an outside hospital.  The patient is a 67-year-old female with advanced atherosclerosis who presented to her local hospital with multiple days of abdominal pain, nausea, vomiting, and diarrhea.  Computed tomography of the abdomen and pelvis showed non-specific but extensive small and large bowel inflammatory changes including bowel wall edema concerning for colitis versus obstruction.  She arrives to your facility toxic appearing – she is febrile, hypotensive, tachycardic, and tachypneic.  On review of the accompanying medical records you find that she has been under-resuscitated, having received minimal intravenous fluids prior to transport.


Undifferentiated Shock – Workup and Resuscitation Occur in Tandem

One of the challenges in caring for a patient in shock is that the workup must occur simultaneously with the resuscitation.

The approach suggested by Winters et al. can help to narrow the differential diagnosis, which begins with a rapid and deliberate physical examination [5].  Distended neck veins in the hypotensive patient may represent elevated central venous pressure in patients with obstructive shock, as is seen in pulmonary embolism, tension pneumothorax, and pericardial tamponade.  This same clinical presentation can also be seen in patients with pump failure secondary to cardiogenic shock from a variety of etiologies.  Urticaria, angioedema, facial swelling, and respiratory distress may accompany hypotension in anaphylaxis leading to a vasodilatory shock.  In the setting of hypotension, warm extremities may suggest pathologic vasodilation, as is seen in sepsis and anaphylaxis.  Cold extremities, however, are a result of sympathetic compensation for hypotension and may point toward hemorrhagic, hypovolemic, or cardiogenic shock.  Hematemesis or a rectal examination positive for blood (melena/gastrointestinal blood) may suggest a hemorrhagic cause of hypovolemic shock.

Early diagnostic testing is also helpful and should include the following:

  • Blood glucose
  • ECG – dysrhythmia and ischemia
  • Chest radiograph – pneumothorax, hemothorax, pulmonary edema, pneumonia
  • Pregnancy test – ectopic pregnancy


Case (Continued)

The patient’s blood pressure improves modestly with the administration of two liters of IV normal saline.  Shortly after fluid administration you are called to the bedside by her nurse, who is concerned about the patient’s work of breathing.  You arrive at the bedside and find the patient in tripod posture, tachypneic with increased accessory muscle use.  She is hypoxic.  A non-rebreather is applied, but before her oxygen saturations improve she suddenly has an episode of emesis and becomes unresponsive.  She loses pulses and CPR begins.  She receives two rounds of CPR and epinephrine for pulseless electrical activity in the setting of hypoxic respiratory arrest, the patient is intubated, and ROSC is achieved.  Post-intubation chest x-ray shows the endotracheal tube in appropriate position and near-complete opacification of the right lung.  She remains hypotensive.


Fundamentals of Fluid Responsiveness

Only ~50% of hemodynamically unstable patients will respond favorably to a fluid challenge, defined as an increase in stroke volume after fluid loading [1-4].  Further, overly aggressive fluid administration is associated with worse outcomes [1, 6-9].  Responsiveness of the heart to a fluid challenge can be anticipated by where its output lies on the Frank Starling curve.

As right atrial pressure (RAP, a function of ventricular preload) increases, stroke volume and therefore, cardiac output (recall that CO = HR x SV) increases.  Other parameters affect the shape of the curve.  For example, the curve will move upward with decreased afterload, decreased contractility, and decreased heart rate.

Ventricular preload is determined by venous return, which is comprised of three parts, 1) mean systemic filling pressure (MSFP), or the volume of blood not in capacitance vessels that is able to create a transmural pressure above zero, 2) RAP, and 3) the resistance to venous flow (Rv).  The relationships of these components is shown in the following equation:

Venous return = (MSFP – RAP)/Rv

Venous return can be increased by 1) increased MSFP, 2) decreasing RAP, and 3) decreasing resistance to venous flow (Rv).  The MSFP drives venous return and may be increased by fluid loading or by venoconstriction, whereas options to modulate the latter two parameters are limited in the ED [1].

Cardiac output cannot increase without a corresponding increase in venous return, which can be directly augmented by fluid loading.  This is only the case, however, when the heart is operating on the steep portion of the curve.  For example, consider the decreased cardiac function curve seen below.  Point II indicates that, despite an increase in venous return, there is no corresponding increase in cardiac output.  This is the case in cardiogenic shock, as the heart does not have the ability increase its contractility regardless of IV fluid administration.

Case (Continued)

The patient continues to be hypotensive despite receiving multiple liters of intravenous fluids.  She requires initiation of a norepinephrine drip to keep her MAP > 65 mmHg.  Hours later, however, her MAP begins to fall again despite increasing the dose of the norepinephrine, administration of calcium, and stress dose steroids. 

Should this patient receive further intravenous fluid administration?  How can we determine whether her hemodynamics will improve with a volume challenge?


Predictors of Fluid Responsiveness

Despite their continued use in many ICU settings, static markers of central venous pressure (i.e. ventricular end diastolic volume, pulmonary artery occlusion pressures, etc.) have consistently been shown not to correspond to volume responsiveness [1, 10, 11].  Central filling pressures (classically considered to be cardiac filling pressures) are poor predictors of volume responsiveness for three reasons.  First, CVP is an intramural pressure only, which does not take extramural pressures into account. This can be problematic in patients with elevated intrathoracic pressures, such as in mechanically ventilated patients.  Second, preload is made up by CVP and ventricular end-diastolic radius. The latter is determined by ventricular compliance, which varies widely between patients and disease states.  Lastly, even low CVP does not imply that a patient can be fluid responsive (consider point I on the previous figure) [1].  For these reasons, dynamic markers of CVP have been deemed preferable to static markers and have been described in the literature for the past 20 years.  So, which of these, then, would be of use to the ED physician?

Pulse Pressure Variation/Stroke Volume Variation

Pulse pressure (difference between the systolic and diastolic blood pressures) during mechanical ventilation has been used in the past to estimate stroke volume.  Cyclic variation of the pulse pressure during mechanical ventilation (or pulse pressure variation) can predict response of cardiac output to volume expansion.  For example, insufflation during positive pressure ventilation decreases preload of the right ventricle.  If this decrease in preload is transmitted to the left ventricle, then both ventricles may be thought of as preload dependent.  Pulse pressure variation has the largest body of evidence supporting its use, with a recent meta-analysis showing a pooled sensitivity of 88% and specificity of 89% for predicting volume responsiveness [10, 12].  The usefulness of this technique in patients with ARDS is questionable, however, as these patients are ventilated with smaller tidal volumes that may not be able to generate enough insufflation to appreciably modify the pulse pressure.  This technique is also less accurate in the spontaneously breathing patient and in the setting of dysrhythmia.

Variations of Vena Caval Dimensions

Variation in the diameter of the inferior vena cava (IVC) measured by transthoracic echocardiography has been used to predict fluid responsiveness.  Compared to patients using PPV, evaluation of vena caval dimension in spontaneously breathing patients is less studied and less accurate.  In a 2014 meta-analysis of 8 studies, the pooled sensitivity was 76%, and the pooled specificity was 86% [10, 13].  Unlike pulse pressure variation, it can be used in patients with cardiac dysrhythmias.

End Expiratory Occlusion Test

As mentioned earlier, positive pressure ventilation decreases ventricular preload by way of decreased venous return.  Temporarily stopping mechanical ventilation, end-expiratory and/or end-inspiratory holds, depending on the strategy being employed, can stop this impediment to venous return.  If cardiac output increases during this brief pause in positive pressure ventilation, then it can be expected to be volume responsive.  This test is easy to perform (simply a < 15 second pause in mechanical ventilation) and is valid in patients with ARDS.  However, the change in cardiac output is measured by pulse contour analysis in studies validating its use.  Pulse contour analysis is based on the observation that the area under the arterial pressure waveform is proportional to stroke volume.  Systems that perform this calculation (i.e. FloTrac, PiCCO) are not always immediately available in the ED, and depending on the system, requires central venous and/or arterial cannulation [14].  Furthermore, only recently has echocardiography been studied as a means for measuring the change, and implementing the appropriate technique may require advanced training in echocardiography [10, 15].

Fluid Challenge

Perhaps the most direct way to predict fluid responsiveness is to administer a bolus of IV fluids and then assess for improved cardiac output. This has the benefit of being easy to perform; however, it is a therapeutic endeavor just as much as it is diagnostic and may lead to deleterious effects if given when contraindicated.  There is evidence that using a small fluid bolus (~100 mL) can produce changes in left ventricular outflow velocities (detected by transthoracic cardiac ultrasound), but this requires exceedingly sensitive cardiac output monitoring [10]. 

Passive Leg Raise

The passive leg raise (PLR) is essentially a fluid bolus of about ~300 mL that can be repeated interminably without infusing any additional fluid.  This test has the benefit of being easy to perform and highly accurate in predicting volume responsiveness.  Two meta-analyses of these studies have been recently published showing a pooled sensitivity of 85% and specificity of 91% for predicting volume responsiveness [10, 16-17].  However, invasive, direct measures of cardiac output must be used in order to accurately make this determination.  When substituting direct measurement of cardiac output for pulse pressure, specificity is unchanged but sensitivity is decreased.

Case Resolution

The patient’s MAP improved with PLR and fluid challenge, showing volume responsiveness.  She received additional crystalloid with improvement in her hemodynamics.  An emergent surgical consult was made, and after further stabilization, the patient was brought to the OR for exploratory laparotomy, where she underwent partial small bowel resection for obstruction.


The Verdict? No Substitute for Clinical Judgment

So how does one predict which patients will be responsive to administration of IV fluids?  Like the start of many investigations in medicine, the answer begins with a thorough history and physical exam and is dependent on clinical judgment as well as other additional pieces of information.  Indeed, there are instances where the expected response to fluid administration is obvious, such as the initial phase of septic shock (prior to IV fluid administration) or hemorrhagic shock (as may be seen in trauma) [10, 18].  Yet, emergency physicians must be cognizant of the adverse effects of fluid overload, as has been observed in septic patients [19].

No single method for predicting volume responsiveness is without limitation.  Further, none of the techniques have 100% sensitivity or specificity for detecting which patients will respond favorably to fluid administration.  Emergency physicians increasingly use bedside ultrasound in clinical decision making. However, recent literature review of the ability of IVC diameter to predict fluid responsiveness demonstrates unreliability and unpredictability in certain patients.  Ultrasonographic protocols like the RUSH exam may be more useful in sorting out undifferentiated shock and which patients could benefit from fluid administration [5].  In the meantime, the PLR, a low risk and simple maneuver, appears to have stronger evidence supporting its use and may help emergency physicians at the bedside decide whether to continue to administer intravenous fluids. Ultimately, the evaluation of the patient in undifferentiated shock should not be based on a single technique.  Instead, it should be a multi-faceted approach that includes as much information as necessary to positively influence the patient’s care.


References / Further Reading:

  1. Cherpanath, T. G. V., B. F. Geerts, W. K. Lagrand, M. J. Schultz, and A. B. J. Groeneveld. “Basic concepts of fluid responsiveness.” Netherlands Heart Journal21.12 (2013): 530-36. Web.
  2. Marik PE, Cavalazzi R, Vasu T, et al. Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature. Crit Care Med. 2009;37:2642–7.
  3. Michard F, Teboul JL. Predicting fluid responsiveness in ICU patients: a critical analysis of the evidence. Chest. 2002;121:2000–8.
  4. Marik, Paul. “ISepsis – Vena Caval Ultrasonography – Just Don’t Do It!” EMCrit. N.p., 08 July 2017. Web. 28 July 2017.
  5. Winters, Michael E., Deblieux, Peter, Marcolini, Evie G., Bond, Michael C., Woolridge, Dale P. Emergency Department Resuscitation of the Critically Ill. Dallas: American College of Emergency Physicians, 2011.
  6. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345:1368–77.
  7. Holte K, Kehlet H. Fluid therapy and surgical outcomes in elective surgery: a need for reassessment in fast-track surgery. J Am Coll Surg. 2006;202:971–89.
  8. Wiedemann HP, Wheeler AP, Bernard GR, et al. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med. 2006;354:2564–75.
  9. Boyd JH, Forbes J, Nakada TA, et al. Fluid resuscitation in septic shock: a positive fluid balance and elevated central venous pressure are associated with increased mortality. Crit CareMed. 2011;39:259
  10. Monnet, Xavier, Paul E. Marik, and Jean-Louis Teboul. “Prediction of fluid responsiveness: an update.” Annals of Intensive Care 6.1 (2016): n. pag. Web.
  11. Kory, Pierre. “COUNTERPOINT: Should Acute Fluid Resuscitation Be Guided Primarily by Inferior Vena Cava Ultrasound for Patients in Shock? No.” Chest151.3 (2017): 533-36. Web.
  12. Yang X, Du B. Does pulse pressure variation predict fluid responsiveness in critically ill patients? A systematic review and meta-analysis. Crit Care. 2014;18:650.
  13. Zhang Z, Xu X, Ye S, Xu L. Ultrasonographic measurement of the respiratory variation in the inferior vena cava diameter is predictive of fluid responsiveness in critically ill patients: systematic review and meta-analysis. Ultrasound Med Biol. 2014;40:845–53.
  14. Mehta, Yatin. “Newer methods of cardiac output monitoring.” World Journal of Cardiology 6.9 (2014): 1022. Web.
  15. Jozwiak M, Teboul JL, Richard C, Monnet X. Predicting fluid responsiveness with echocardiography by combining end-expiratory and inspiratory occlusions (abstract). Ann Intensive Care. 2016 (in press).
  16. Cherpanath TG, Hirsch A, Geerts BF, Lagrand WK, Leeflang MM, Schultz MJ, et al. Predicting fluid responsiveness by passive leg raising: a systematic review and meta-analysis of 23 clinical trials. Crit Care Med. 2016;44:981–91.
  17. Monnet X, Marik P, Teboul JL. Passive leg raising for predicting fluid responsiveness: a systematic review and meta-analysis. Intensive Care Med. 2016.
  18. Grenga, Paolo. “ED Management of the MVC Patient: Pearls and Pitfalls.” – Emergency Medicine Education. N.p., 14 June 2017. Web. 28 July 2017.
  19. Genga, Kelly, and James A. Russell. “Early Liberal Fluids for Sepsis Patients Are Harmful.” Critical Care Medicine 44.12 (2016): 2258-262. Web.

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EM@3AM – Epididymitis

Author: Erica Simon, DO, MHA (@E_M_Simon, EMS Fellow, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 29-year-old male, with no previous medical history, presents to the emergency department for three days of progressively worsening dysuria and left testicular pain. The man denies fever, abdominal pain, hematuria, urethral discharge, and testicular trauma. He reports unprotected intercourse with two new sexual partners within the previous 30 days.

Initial VS: BP 119/76, HR 77, T 99.7F Oral, RR 14, SpO2 99% on room air.

Physical examination:
General: Thin, well-developed male; appearing as stated age.
Abdomen: Soft, non-tender, non-distended; no guarding, or rebound.
GU: Tanner stage V, no evidence of inguinal hernia, no scrotal edema, urethral discharge, or visible lesions. TTP of the left epididymis.

What do you suspect as a diagnosis? What’s the next step in your evaluation and treatment?

Answer: Epididymitis1-5

  • Epidemiology: Epididymitis accounts for > 600,000 visits to physicians in the U.S. annually.1
  • Pathogens:
    • Males < age 35: C. trachomatis (most common) and N. Gonorrhoeae are the major pathogens.1
    • Males > age 35: Gram negative coliforms, enterococci, and Pseudomonas species frequently isolated from cultures.2
  • Clinical Presentation: Patients frequently report dysuria. Testicular pain, urethral discharge (rare in the setting of C. trachomatis infection), suprapubic discomfort, and fever may also occur.1
    • Sexually transmitted infections (STIs): median interval from exposure to clinical manifestation: 10 days.3
      • Males may carry chlamydiae for long periods before developing overt epididymitis.3
    • Gram negative coliforms, enterococci, and Pseudomonas species: onset commonly subacute (1-2 days).
      • Infection may occur weeks to months (rare) following urethral catheterization or surgical manipulation.
      • Epididymitis may rarely occur following genital trauma.1
  •  Evaluation and Treatment:
    • Assess the ABCs and obtain vital signs.
    • Perform a thorough H&P: Obtain sexual history and question regarding recent urethral instrumentation.
    • GU examination may be significant for:
      • Epididymal TTP (posterior aspect of the scrotum).
      • TTP and swelling of the involved testis (suspect epididymo-orchitis).
      • Presence of a hydrocele => inflammatory fluid collection between the layers of the tunica vaginalis.
      • Urethral discharge.
    • Laboratory evaluation: Urinalysis, urine culture, STI testing as appropriate (e.g. urine nucleic acid amplification test (NAAT), urine culture, urethral swab).
    •  Treatment:
      • Epididymitis thought secondary to sexual exposure: ceftriaxone + azithromycin or doxycycline.
        • Requires patient counseling regarding treatment of sexual partner.
        • Requires communicable disease reporting if NAAT or culture positive .4
      • Epididymitis thought secondary to coliforms: empiric antibiotic therapy directed against gram negative rods and gram positive cocci (utilize culture to target therapy).
    •  Complications: Untreated bacterial epididymitis may result in: bacteremia, testicular infarction, scrotal abscess, pyocele, a chronic draining scrotal sinus, chronic epididymitis, and infertility.
  • Pearls:
    • In children presenting with epididymitis (absent indications/findings consistent with sexual abuse) => suspect anatomic urinary tract abnormality.1
    • Patients taking amiodarone may present with signs/symptoms of epididymitis:5
      • Amiodarone is known to induce epididymalgia in 3-11% of individuals compliant with prescribed therapy => mechanism is currently unknown; hypothesized that accumulation of a metabolite in epididymal tissue results in focal fibrosis and lymphocytic infiltration (UA and culture are negative).  Analgesia is the treatment of choice.5
    • Failure of resolution of epididymitis signs/symptoms within 72 hours of therapy: re-evaluation required => consider testicular abscess, carcinoma, testicular infarction, or fungal epididymitis.


  1. McGowan C, Krieger J. Prostatitis, Epididymitis, and Orchitis. In Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. 8th ed. Philadelphia, PA. Elsevier Saunders. 2015; 112: 1381-1387.e2.
  2. Doble A, Taylor-Robinson D, Thomas B, et al. Acute epididymitis: a microbiological and ultrasonographic study. Br J Urol. 1989; 63:90-94.
  3. Berger R, Alexander E, Harnisch J, et al. Etiology, manifestations, and therapy of acute epididymitis: a prospective study of 50 cases. J Urol. 1979; 121: 750-754.
  4. Chorba, Berkleman, Safford, and Hull. Mandatory Reporting of Infectious Diseases by Clinicians. Centers for Disease Control and Prevention. 1990. Accessed 12 Aug 2017. Available from:
  5. Shen Y, Liu H, Cheng J, Bu P. Amiodarone-induced epididymitis: a pathologically confirmed case report and a review of the literature. Cardiology. 2014; 128(4):349-351.


For Additional Reading:

Foley Catheter Patients: Common ED Presentations/Management/Pearls & Pitfalls


Foley Catheter Patients: Common ED Presentations / Management / Pearls & Pitfalls

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EM@3AM – Central Retinal Vein Occlusion

Author: Olivier Levac-Martinho, MD, BSc (@OlMartinho, Resident Physician, University of Ottawa) and Erica Simon, DO, MHA (@E_M_Simon, EMS Fellow, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 52-year-old male, with a previous medical history of CAD (CABG x3), HTN, DM, and smoking (30 pack years), presents to the emergency department following the painless loss of vision in his left eye. The patient denies headache, slurred speech, and motor and sensory deficits. He denies contact lens wear and denies a requirement for glasses. The man reports an eye examination within the previous year, stating “my eyes have been perfect.”

Initial VS: BP 123/76, HR 66, T 99.9F Oral, RR 12, SpO2 97% on room air.

Visual Acuity:
OD: 20/20
OS: 20/400
OU: 20/200

Pertinent physical exam findings:
HEENT: PERRLA, 2mm bilaterally, EOMI. OS: Tonometry: IOP 18 mmHg. Fundoscopy: retinal hemorrhages, cotton-wool spots, optic disc edema.
Cardiovascular: S1, S2, regular rate and rhythm. No carotid bruits.

What’s the next step in your evaluation and treatment?

 Answer: Central Retinal Vein Occlusion (CRVO)1-4

  • Epidemiology: CRVO typically occurs in persons > 65 years of age with a history of atherosclerotic disease. Risk factors include DM, HTN, vasculitis (systemic lupus erythematosus, HIV, syphilis, sarcoidosis, etc.), glaucoma (increased IOP = bowing of the lamina with subsequent impingement of the central retinal vein), and hypercoagulable states (hyperviscosity syndromes, protein C deficiency, protein S deficiency, etc.).1,2 Population studies report the prevalence of CRVO as 0.1-0.4% (incidence highest among African American individuals).1,2
  • Etiology: Occurs secondary to a thrombus occluding the lumen of the central retinal vein, compression of the central retinal vein by an atherosclerotic central retinal artery, or occlusion of the central retinal vein secondary to inflammation.1,3
  • Clinical Manifestations: Sudden onset, or progressively worsening, painless, monocular vision loss.1,4
  • Evaluation and Treatment:
    • Obtain visual acuity (vision often significantly reduced in the affected eye (> 20/200)).2,3
    • Perform a thorough H&P:
      • Question specifically regarding the aforementioned risk factors. Obtain a complete family history to include systemic thrombotic diseases and rheumatologic diseases.
    •  Ocular examination: pupillary exam may demonstrate an ipsilateral afferent pupillary deficit.2
      • Fundoscopic retinal exam: retinal hemorrhages in all quadrants of the fundus (“blood and thunder” appearance), optic nerve head swelling, splinter hemorrhages, cotton-wool spots, and macular edema +/- breakthrough vitreous hemorrhage.1,2
    • Consider a more extensive evaluation in persons < 65 years of age presenting without known risk factors for CRVO (e.g. blood dyscrasias: CBC, coags, etc.).
    •  Treatment => Emergent ophthalmology consult.
      • Available therapies include aspirin, anticoagulation, photocoagulation, and intravitreal injections (anti-vascular endothelial growth factors, steroids, etc.)1
      • Treatment of, or referral for, the management of CRVO systemic vascular risk factors (e.g. HTN, DM, etc.) is advised.
  • Pearls:
    • Nearly 7% of persons presenting with unilateral CRVO develop the condition in the contralateral eye within 5 years of onset of the first eye.1
    • The differential diagnosis of CRVO includes: stroke, TIA, amarosis fugax, temporal arteritis, retinal detachment, and posterior vitreous detachment.1



  1. Oellers P, Hahn P, Fekrat S. Central Retinal Vein Occlusion. In Ryan’s Retina. 6th ed. 2018. Philadelphia, Elsevier. 57; 1166-1179.
  2. Cugati S, Ten-year incidence of retinal vein occlusion in an older population: the Blue Mountains Eye Study, Arch Ophthalmol. 2006 May; 124(5):726-32.
  3. Klein R, The epidemiology of retinal vein occlusion: the Beaver Dam Eye Study; Trans Am Ophthalmol Soc. 2000;98:133-41
  4. Green WR, Central retinal vein occlusion: a prospective histopathologic study of 29 eyes in 28 cases, Trans Am Ophthalmol Soc. 1981; 79:371-422.


For Additional Reading:

Acute Visual Loss in the Emergency Department: Pearls and Pitfalls

Acute Visual Loss in the Emergency Department: Pearls and Pitfalls

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