How Do You Know When You Can Return to Activity After Mono

Sports Health. 2014 May; half-dozen(three): 232–238.

Return to Play After Infectious Mononucleosis

Jonathan A. Becker

^†Department of Family unit and Geriatric Medicine, University of Louisville and Kentucky One Health Sports Medicine Fellowship, Louisville, Kentucky

Julie Anne Smith

^‡School of Medicine, University of Louisville, Louisville, Kentucky

Abstract

Context:

Infectious mononucleosis is a disease primarily of adolescence and early adulthood. The risk of splenic injury and chronic fatigue make return-to-play decisions a challenge for the clinician caring for athletes with infectious mononucleosis.

Prove Conquering:

Data were obtained from the PubMed and MEDLINE databases through December 2012 by searching for epidemiology, diagnosis, clinical manifestations, management, and the role of the spleen in infectious mononucleosis.

Study Design:

Clinical review.

Level of Evidence:

Level four.

Results:

Infectious mononucleosis is commonly encountered in young athletes. Its disease pattern is variable and can affect multiple organ systems. Supportive intendance is the cornerstone, with footling role for medications such as corticosteroids. Concrete examination is unreliable for the spleen, and ultrasound imaging has limitations in its ability to guide return-to-play decisions. Exercise does not announced to identify the young athlete at take chances for chronic fatigue, but determining who is at risk for persistent symptoms is a claiming.

Decision:

Render-to-play decisions for the athlete with infectious mononucleosis need to exist individualized because of the variable illness class and lack of evidence-based guidelines.

Keywords: mononucleosis, spleen imaging, splenomegaly, chronic fatigue

The question of when an athlete tin render to play following contraction of infectious mononucleosis (IM) is complex because of the serious complication of splenic rupture.^one,43 Splenic injury is rare but may occur spontaneously or with pocket-size abdominal trauma.^26,32 Protecting the athlete from splenic rupture should be at the forefront when making return-to-play decisions. The natural progression of splenic enlargement can exist unpredictable, and splenic dimensions vary with body size and blazon and so the function for ultrasonography is unclear. IM as well carries the adventure of persistent or chronic symptoms, most notably fatigue, every bit well equally neurologic, hematologic, cardiac, and respiratory complications.^one,14 The variable presentations and form of this illness pose a challenge for physicians, as bear witness-based protocols for return to competition are lacking. Therefore, decisions regarding athletic participation should be made on an private ground.

Epidemiology

Infectious mononucleosis is a cocky-limiting clinical syndrome typically caused by the Epstein-Barr virus (EBV).^i,20 Epstein-Barr virus is a member of the herpes virus family that causes benign lymphoproliferative IM merely has also been linked to Burkitt lymphoma, Hodgkin lymphoma, and nasopharyngeal carcinoma.⁴² Epstein-Barr virus exposure is common worldwide, with 90% to 95% displaying immunity by machismo.^{half-dozen,xx,30,34} Infection with EBV is often clinically silent in childhood simply results in symptomatic illness during adolescence or adulthood.⁴¹ The incidence of IM in the United states is approximately 500 cases per 100,000 persons per yr, with the highest incidence in the 15- to 24-twelvemonth-onetime age group.⁷ The incidence is almost negligible by 35 years of age.^1,20 Among college students, up to half may exist initially seronegative, with 15% of that grouping eventually developing the disease.^26,34 In that location is no sexual activity predilection for IM.⁴⁵ There is a higher incidence of IM in the white population in comparison with the African American population, believed to exist due to earlier exposure to EBV resulting in subclinical manifestations.¹⁶

While moderate do tin be beneficial to the immune system, the duration and intensity of exercise performed by the competitive athlete may impair immune function.^fourteen This has been previously described by a "J bend," where practise can initially decrease the rate of illness but has a negative outcome at more intense levels.^xiv,19 At that place is no evidence supporting IM being more prevalent in the student-athlete population in comparison to nonathletes, merely their higher incidence of trauma certainly places them at a higher adventure for complications.³⁴

Pathogenesis

Epstein-Barr virus, like other members of the herpes virus group, persists inside the host in its latent course. The virus is transmitted via saliva, giving the virus the reputation of a "kissing disease," and has an incubation period of xxx to fifty days.⁴⁵ Epstein-Barr virus targets retentivity B lymphocytes and induces their proliferation. Every bit a outcome, a jail cell-mediated amnesty response produces a clonal expansion of T lymphocytes. The cytotoxic T lymphocytes release a multitude of cytokines that cause the classical IM symptoms. Additionally, the T-lymphocyte response produces lymphoid hyperplasia, a marked lymphocytosis, and atypical lymphocytes in a peripheral blood smear.²⁶ Lytic infection of tonsillar catacomb epithelial cells and B lymphocytes results in viral reproduction and shedding into saliva, which decreases exponentially over the first twelvemonth of infection just will go on to persist for life.^xiii

Clinical Manifestations

The history and concrete examination are pertinent for making the right diagnosis. The long incubation menstruum makes it hard to determine the source or onset of IM, yet there is a archetype 3- to 5-day prodromal period consisting of angst, fatigue, and anorexia. Symptoms then progress into the archetype "triad" of IM—pharyngitis, fever, and lymphadenopathy. At times, the presentation of IM is much more than atypical and tin impact many different organ systems. Fatigue and pharyngitis are the about debilitating symptoms and often present as the main complaint. The posterior cervical lymph nodes are more than commonly involved in IM, with axillary and inguinal lymphadenopathy less probable to occur. Often, the signs of IM may be subtle, with the athlete presenting with nothing more than fatigue, lack of energy, or diminished performance. Other features of IM may include posterior palatine petechiae, jaundice, exudative pharyngitis, rash, and splenomegaly.^14,29,34

Posterior palatine petechiae occur in about one third of cases and are highly suggestive of IM.^eight This characteristic distinguishes an acute EBV infection from other causative agents, such as acute canker simplex virus infection, HIV infection, or streptococcal infection, that could be included in the differential diagnosis.⁴⁷

Jaundice is rare, occurring in less than 10% to fifteen% of patients.²⁷ However, approximately 90% of patients have mildly elevated liver enzymes facilitating in the diagnosis of IM.³⁶

Exudative pharyngitis and concomitant tonsillar enlargement can cause obstruction of the airway, leading to devastating consequences.^14,xx The exudation has been described equally white, gray, or green and even necrotic in appearance. The enlargement of the tonsil is due to lymphoid hyperplasia and pharyngeal inflammation. Oft mistaken for streptococcal pharyngitis, the clinician must exist vigilant for clues of IM such equally fatigue, the appropriate age group, or posterior cervical lymphadenopathy.²⁶ Positive testing for streptococcal pharyngitis does not completely exclude IM, since simultaneous infection may be seen in up to 30%.²⁹

A rash is seen in nigh 10% to 40% of patients. The rash is transient and generalized with maculopapular, petechial, or urticarial features (Effigy i). This is more than normally seen in a patient who has been treated with penicillin in an effort to eradicate a presumed group A Streptococcus infection. This is well-nigh pathognomonic for IM. Other antibiotic classes have been implicated, but the penicillins are the most widely reported to produce this upshot.^thirteen,14

Rash presenting with infectious mononucleosis.^v

Splenomegaly in IM occurs as a outcome of lymphocytic infiltration enlarging the spleen beyond protection from the rib cage and creating an organ that is susceptible to rupture either spontaneously or traumatically.^26,32 This infiltration may as well alter splenic architecture, resulting in a more susceptible construction.^32,43 The ability to decide the presence of splenomegaly by concrete examination is unreliable, with ane study showing every bit niggling every bit 17% of cases being identified on physical test.^one,12,43,45 Ultrasonography is the imaging modality of choice.^one,43 Linear measurements are used since measuring spleen book is technically hard. Additionally, normative information are lacking as studies accept shown that "average" spleen size tin be variable, so this tool has limitations as far equally its usefulness in predicting a safety return to play.^19,28,39,43

Since baseline spleen size measurements on competitive athletes are impractical, series ultrasound measurements may be employed to decide the course of splenomegaly in IM. A report of xix patients with IM establish normal spleen measurements in 84% at 1 calendar month after diagnosis and 100% at ii months. In this series, there were no serial or baseline measurements, leaving the possibility that the "normal" results may still take been aberrant for that individual.³² In a study where baseline spleen measurements were obtained in a large cohort of athletes, those with IM underwent serial ultrasonography. Pinnacle splenic enlargement was typically seen inside ii weeks but, in some, extended to 3.5 weeks. For the majority, splenomegaly resolved in 4 to 6 weeks.¹⁸

The long incubation flow and variable nature of the disease can make the task of identifying onset of disease a claiming. The acute phase of IM tin resolve as quickly as 7 days, only ordinarily takes between ii and three weeks from the onset of symptoms.^14,45 This is followed by a recovery catamenia that may take up to ii to 3 months.^1,14,26 IM is typically self-limiting, just an acute EBV infection is a risk factor for chronic fatigue, with symptoms lasting in excess of half dozen months.^ane,23

Diagnosis

The diagnosis of IM can be fabricated through history and physical examination as well as atypical laboratory findings (Table i).^1,20,33 The differential diagnosis includes grouping A streptococcal infection, influenza virus, herpes virus, cytomegalovirus, toxoplasmosis, acute HIV infection, and many more than bacterial and viral pathogens.^one,43 Diagnostic criteria for IM (Hoagland criteria) include greater than 50% lymphocytes and at least 10% singular lymphocytes with fever, pharyngitis, adenoapthy, and a positive serologic test.¹⁷ The presence of singular lymphocytes has a sensitivity of 75% and a specificity of 92%.⁹ Other laboratory findings that could exist suggestive of IM include transient neutropenia, thrombocytopenia, and elevated liver transaminases.^27,45 Anemia is considered a feature of complicated IM and is indicative of autoimmune hemolytic anemia, splenic rupture, aplastic anemia, and even disseminated intravascular coagulation.²⁴

Table 1.

Diagnostic tests for infectious mononucleosis, %^{13,xviii-21,44}

Test	Sensitivity	Specificity	Positive Predictive Value	Negative Predictive Value
Heterophile antibody—latex agglutination examination	87	91	52	2
Heterophile antibody—solid phase immunoassay	83	97	75	two
Singular lymphocytes ≥10%	75	92	51	3
Atypical lymphocytes ≥50%	66.3	84.five	31	iv
VCA IgM and IgG	97	94	64	0.5
PCR for EBV Dna	80	94	95	79

Heterophile antibodies are a characteristic feature of IM.^9,17,33 Epstein-Barr virus stimulates the evolution of immunoglobulin M (IgM) antibodies directed confronting viral antigens.^9,17 These antibodies and so cross-react with antigens found on sheep and horse ruddy cells. Rapid (monospot) tests for these heterophile antibodies are used to screen patients for IM. Nigh 85% to 90% of patients with confirmed IM will demonstrate a positive heterophile test by week three of illness.^17,27 Therefore, the start few weeks of illness may effect in a negative heterophile examination whereby the false-negative rate can be every bit high as 25% in the outset week and repeated testing is required at a subsequently appointment.³² A definitive diagnosis can be made for IM with more sensitive tests that find viral capsid antigens for IgM and IgG antibodies.^24,33 The negative likelihood ratio for detecting viral capsid antigens is 0.03 in comparison with the negative likelihood ratio for the heterophile antibody test, which is 0.14 to 0.18. Viral capsid antigen testing is useful for patients who initially had a negative heterophile antibody test.^2,10 Epstein-Barr virus is the causative agent in ninety% of cases of IM, but other viruses rarely produce a "mono syndrome."^eleven The most common agents are cytomegalovirus and toxoplasmosis. The illness would have the features of IM, only EBV testing would be negative.¹¹

Management and Prevention

At that place is no specific treatment for IM. Supportive therapy is the mainstay of care, which includes adequate rest, hydration, and analgesics.^{xiv,twenty,33} Over-the-counter pain medication, such as anti-inflammatories, is generally sufficient to manage the myalgias and pharyngitis. Acetaminophen is appropriate but used judiciously because of potential liver complications, equally IM ofttimes causes elevation in liver function tests.¹⁵ Aspirin should exist avoided because of bleeding risks and an association of IM with Reye syndrome in children.^14,33 There is no office for antivirals or antibiotics.^14,xv,20,34 Despite the fatigue, there is no role for strict bed rest. For patients with a quick recovery of symptoms, a return to light exercise in as fiddling as 2 weeks from the onset of illness may provide a benefit. Close follow-up is recommended to ensure resolution of all symptoms as the athlete may take chances progression to more chronic symptoms, specifically fatigue.^20,46

The function of corticosteroids in the treatment of IM is of interest only there is insufficient evidence to recommend their use in uncomplicated IM. There does non appear to be whatever comeback in elapsing of symptoms or progression to chronic symptoms.^four,44 In spite of this, a significant number of patients are given corticosteroids for symptom control in the absence of the complications of IM.⁴¹ There is general consensus that corticosteroids do accept a function when there is airway obstruction equally a outcome of laryngeal edema.^4,33,41 Other severe complications of IM warranting corticosteroid treatment include hepatitis, myocarditis, or hematologic abnormalities.^iv,33,41 Risks and benefits must exist weighed, as the adverse effects of corticosteroids in IM may include infection or even femoral head necrosis.^4,14,20,41

Manual is past shut contact via saliva, so isolation is non necessary. Mutual sense precautions such as hand washing and not sharing water bottles are typically adequate. Unfortunately, the long incubation period tin can confound efforts to prevent infecting others.^17,34 Electric current advances are being fabricated to develop an EBV vaccine. In a phase 2 trial, vaccine recipients were less probable to have symptoms of IM during master EBV infection compared with those who were non vaccinated.³⁸ Yet, the recipients were non protected against acquiring EBV.³⁸

Return-to-Play Considerations

There is general consensus that the athlete must be asymptomatic with resolution of symptoms such as fever, fatigue, and pharyngitis earlier they initiate any return to activity.^20,31,33 The majority of those with IM will not experience well plenty to pursue activity during the start weeks of affliction, which makes clinical decisions easier. They ought to exist afebrile and well hydrated.^31,33,45 Any concern for oropharyngeal bug or airway compromise would clearly prohibit any sports participation.^{14,twenty,34,45} Although their level of conditioning would exist expected to decline, the athlete should have full resolution of fatigue or risk prolonged symptoms.^1,34 Resolution of laboratory abnormalities (eg, elevated white claret prison cell counts, abnormal liver function tests) practice not play a part in assisting return-to-play decisions.³⁴ It is difficult to predict who is at hazard for prolonged symptoms, but competitive athletes may actually be at a lower level of take a chance for chronic fatigue.^1,three,34 Nonetheless, the athlete should "feel good" before considering render to play.^ane,iii,34

For those athletes who exercise have "early" resolution of symptoms, there is trivial consensus on the optimal fourth dimension for return to activity. Keeping in mind that the highest take chances for splenic injury is during the get-go 21 days of illness, it has not been shown that early return to light action causes deleterious effects.^21,26,43 The athlete should engage in very light activity at first (walking), with a gradual progression to light aerobic action.^33,36,45 Although it may have ii to 3 months for the athlete to fully recover from IM, it appears they can initiate activity well before.^ane,34,43,46

The return to activities that place the spleen at adventure for injury is a confounding matter. At this time, recommendations vary, and there is a lack of evidence-based protocols.^33,45 The concern is the athlete participating in any activeness that increases intra-intestinal pressure level and contact sports that would place the chest or belly at risk for trauma.^33,45 In ultrasound studies, peak spleen size is typically noted within the first 2 weeks of illness, but may extend to iii.five weeks.¹⁸ The majority of spleen injuries occur within the get-go 21 days of illness and are exceedingly rare at >28 days.^21,26,43 Fortunately, splenic rupture is rare, occurring in <0.v% of those with IM, but its consequences tin exist astringent.^xx,34,43

Most recommendations support that the athlete with IM should rest for 3 weeks then begin resumption of light activity.^1,20,25,34 Keeping in mind there is so much individual variability to this disease and the exact date of onset is ofttimes difficult to establish, return-to-play recommendations should be individualized. Ultrasonography may play a function in return-to-play decisions, but the variability in baseline spleen size tin can limit its utility.^19,28,39,43 Additional factors include the nature of the activeness or sport (contact vs noncontact) and the season in which the illness occurs (competitive flavor vs off-season). Any return to competition must include a detailed explanation of the risk of splenic injury, since full recovery may have months (Figure 2).

Return-to-play recommendations for infectious mononucleosis (IM). Level of show, 4.^{7,nine,24,28,32,35,twoscore,41}

There take been some novel attempts fabricated to protect the spleen from contact for collision sports with a flak jacket²² or a customized protective brace for a higher basketball season.³⁷

Conclusion

Counseling the athlete with IM remains a challenge. The disease has a long latency period, the onset of illness may exist hard to identify, and the disease course is variable. In that location is no specific physical examination finding, laboratory test, or imaging modality that provides a definitive respond. To minimize complications of IM, return-to-play decisions must exist individualized.

Footnotes

The authors report no potential conflicts of interest in the development and publication of this manuscript.

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