Trauma

The female athlete triad is a combination of menstrual dysfunction, low energy availability with or without an eating disorder, and decreased bone mineral density often seen in young women in competitive sports.

The new term for this entity is Relative energy deficiency in sport [RED-S].

Classically female athlete triad was defined as consisting of disordered eating, amenorrhea, and osteoporosis.

In 2007, the inclusion criteria were broadened

• Disordered eating- replaced by low energy availability or without an eating disorder, the spectrum ranging from optimal energy to low energy
• Amenorrhea- Menstrual condition spectrum ranging from eumenorrhea to functional hypothalamic amenorrhea
• Osteoporosis – a spectrum ranging from “optimal bone health” to “osteoporosis”

Energy availability is the cornerstone on which the other two 2 components of the triad build upon. This component is thus key to correction.

Female athlete triad can have a significant impact on the health of the athlete. The full impact of this syndrome may not be realized until these women reach menopause when bone loss is accelerated.

Relative energy deficiency in sport” or “RED-S” is considered more accurate as it also describes the of health issues affected by decreased energy availability which include[metabolic rate, menstrual function, bone health, immunity, protein synthesis, cardiovascular and psychological health. This term is also to include men, who could also be affected by an imbalance in energy availability. But the term is not adopted yet.

Sports that have an aesthetic component ( ballet, or gymnastics) or have group classification based on weight (judo, or wrestling) have a higher prevalence of affected female athletes.

Majority of cases are diagnosed only after advanced symptoms become apparent. To diagnose milder cases, one needs a high index of suspicion.

In women who participate in sports that emphasize aesthetics or leanness, secondary amenorrhea can be as high as 69%, compared with 2% to 5% in the general population.

The prevalence of clinical eating disorders among female elite athletes ranges from 16% to 47%.

Pathophysiology

Reduced energy availability

It is defined as dietary energy intake minus exercise-energy expenditure. This could be due to
• Undereating
• Weight concerns

Disordered eating is the spectrum of behaviors ranging from not taking enough food to offset energy expenditure to preoccupation with eating and a profound fear of becoming fat.

These tend to each unrealistic weight and body fat goals dictated by their sport which is detrimental to their health.

Menstrual dysfunction

The spectrum ranges from normal menstrual function [eumenorrhe] to amenorrhea. Earlier amenorrhea was the criteria but present definition also will include a large portion of athletes who may have low estrogen levels but who still experience menstruation.

Menstrual dysfunction which may be present are

• Luteal suppression – short luteal phase, prolonged follicular phase, ovulation present, menstruation present
• Anovulation – low estrogen and progesterone, absent ovulation, irregular menses
• Oligomenorrhea
• Primary/secondary amenorrhea

Impaired bone health

It determined by BMD (or bone mineral content) and bone quality.

Bone quality cannot be measured as yet.

It refers to factors related to bone turnover rates

• Resorption versus formation
• Microarchitecture
• Time taken for maturation of the new bone matrix
• bone geometry and size).

This inability to measure may explain why some athletes with the same poor bone mineral density as their colleagues may suffer more fractures.

Dual-energy x-ray absorptiometry is used as a quantitative measure of bone health.
[more on BMD and scores]

T-score is used to gauge fracture risks for postmenopausal woman.

In athletes, therefore, Z-score is used for chronologic age.

Athletes with a Z-score 2 SDs below the mean are to be termed low bone density below the expected range for age.

But as athletes already have a higher BMD than nonathletes, an athlete with a BMD Z-score below -1.0 is recommended to get further work up.

The bones of the lower extremities, pelvis, and vertebrae are the ones most commonly affected by poor bone health in women with the female athlete triad, typically manifested by stress fractures or and frank fractures of these areas are the typical manifestations.

It is interesting to note that menstruating athletes gain approximately 2-4% of bone mass per year, whereas amenorrheic athletes tend to lose 2% per year.

Other physiologic dysfunction

Following conditions can occur concurrently with the female athlete triad

•  Anemia
• Chronic fatigue
• Increased risk of infection
• Esophagitis
• Electrolyte imbalance
• Slowing of the metabolic rate
• Decreased production of growth hormone
• Unfavorable lipid panels
• Endothelial dysfunction
• Reduced muscle protein synthesis
• Depression.

In addition, there is a possibility of long-term reproductive adverse effects.

Theories Behind Female Athlete Triad

There is a negative calorie balance. this energy drain disrupts the hypothalamic-pituitary-ovarian axis, resulting in decreased gonadotropin-releasing hormone (GnRH) pulsatility and low levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels.

This causes decreased estrogen production which causes menstrual dysfunction. The decreased estrogen levels, in turn, affect calcium resorption and bone accretion, causing decreased bone health.

Another theory considers the hormone leptin, which is secreted by adipocytes. It influences the metabolic rate, and levels are proportional to body mass index. It may be a significant mediator of reproductive function as studies have shown low levels of leptin correlating positively with amenorrhea and infertility.

Leptin receptors have been found on hypothalamic neurons involved in the control of GnRH pulsatility and in bone, which may also affect osteoblastic function.

Emotional stressors often lead to disordered eating and excessive training and may contribute.

Clinical Presentation

The athlete might be identified as at risk at health examination or might present with a stress fracture or menstrual disturbances.

A  multidisciplinary approach should be used. A detailed history is obtained to look for the contributing factors and conditions. Specific histories to be obtained are

• History of fractures
• Endocrine disorders history
  • Thyroid abnormalities
  • Panhypopituitarism
  • Diabetes
• Menstrual history
  • Age of menarche
  • Length of menses, and menstrual cycle
  • Any missed periods
  • Pregnancy
• Psychosocial history
  • Addiction history
  • Sexual or physical abuse
  • Depression/Suicidal tendencies
  • Anxiety
  • Previous eating disorders
  • Recent trauma or illness
  • Change in coaches
  • Significant personal/academic events.
  • Lack of a familial or social support system
• Exercise history
• Nutritional intake assessment
• Current medications
  • Prescription medications
  • contraceptive medications,
  • Use of hormones

A complete screening physical examination should be performed which should include

• General physical examination
• Gynecological examination
• Psychological examination
• BMI Measurement

Causes of menstrual dysfunction and/or poor bone health and secondary physiologic issues should be looked for the triad.

The diagnosis of the female athlete triad is largely clinical.

Diagnostic Considerations

• Hypogonadotropic hypoestrogenism
• Hypothalamic disorders
• Hyperthyroidism
• Luteal-phase inadequacy
• Nutritional deficiencies
• Gonadal dysgenesis or ovarian defects
• Pituitary disorders

Laboratory Studies

Obtain the following in a female suspected of having the female athlete triad

• Urine or plasma pregnancy test to rule out pregnancy
• Urinalysis to establish volume status
• Complete blood cell for anemia
• ESR and CRP to check inflammation or infection
• Complete metabolic panel
  • Liver function
  • Electrolyte levels
  • Kidney function
• Hormone levels
  • Thyroid panel
  • Follicle-stimulating hormone and luteinizing hormone [for pituitary and possible premature ovarian failure]
  • Prolactin test [pituitary function]
  • Testosterone and dehydroepiandrosterone
  • Estradiol levels

Imaging

X-rays

If the athlete presents with bone pain, as with a stress fracture, appropriate plain radiographs should be obtained.

Dual Xray Absorptiometry

Indication for DEXA are

•  ‘High risk’ triad risk factors:
  • History of a DSM-V diagnosed ED
  • BMI ?17.5 kg/m², < 85% estimated weight, OR recent weight loss of ?10% in 1 month
  • Menarche >16 years of age
  • Current or history of < 6 menses over 12 months
  • Two prior stress reactions/fractures, one high-risk stress reaction/fracture, or a low-energy nontraumatic fracture
  • Prior Z-score of <–2.0 (after at least 1 year from baseline DXA)
• Moderate risk” triad risk factors:
  • Current or history of DE for 6 months or greater
  • BMI between 17.5 and 18.5, < 90% estimated weight, OR recent weight loss of 5–10% in 1 month
  • Menarche between ages 15 and 16 years
  • Current or history of 6–8 menses over 12 months
  • One prior stress reaction/fracture
  • Prior Z-score between –1.0 and –2.0 (after at least 1 year
  • interval from baseline DXA)

In addition, the following may be considered for DEXA

• A history of >1 nonperipheral or >2 peripheral long bone traumatic fractures (nonstress) should be considered for DXA testing if there are one or more moderate or high-risk triad risk factors.
• Athletes on medications for 6 months or greater that may impact bone (such as depot medroxyprogesterone acetate, oral prednisone, and others).

Follow up DEXA scans depend on the severity of disease, the success of treatment and the ongoing status of the athlete.

In case of concern, scans every 1-2 years may be necessary to evaluate the ongoing bone health of the athlete.

Other Imaging Studies

• MRI head for pituitary dysfunction
• Pelvic ultrasonography for ovaries
• Hand images for bone age.
• Bone for a suspected stress fracture,
• ECG when resting heart rate <50 beats/min.

Other Tests

Progesterone Challenge

It is used to determine if the uterine endometrium has been primed with estrogen and thus is ready to be shed, as in normal menstruation. 5 or 10 mg of oral progesterone is given for 10 days to induce menstrual bleeding.

Lack of bleeding indicates that the uterine endometrium has not been adequately exposed to estrogen since the last menses.

Endometrial Biopsy

It is done to determine the stage of growth of the endometrial tissue and, thus, the effects or presence of estrogen and progesterone.

Treatment of Female Athlete Triad

Lack of Available Energy

The treatment has to be approached by multiple team members, given the complexity of the issue.

The cornerstone of the female athlete triad is decreased energy availability. It is the key element to be corrected.

It is done by increasing caloric intake and/or decreasing energy expenditure.

However, the participation of the athlete is very important.

In case non-pharmacological approach fails, antidepressant medication may be useful in aiding treatment.

Correction by dietary and habit changes would also correct menstrual dysfunction and BMD.

Nonpharmacological therapy is considered for one year.

Lack of response to therapy has been defined as

• A clinically significant reduction in z-scores after at least 1 year of nonpharmacological therapy or
• The occurrence of new clinically significant fractures during nonpharmacological treatment over the course of 1 year

BMD

For BMD, indications for drug treatment are

• after lack of response to at least one year of nonpharmacological therapy
  • Z-scores less than or equal to -2.0 with a clinically significant fracture history
  • Z-scores between -1.0 and -2.0 with a clinically significant fracture history plus greater than or equal to 2 additional triad risk factors [or even1 according to some authors]

The drug treatment considered is

• Transdermal estradiol replacement with cyclic progesterone
• Calcium supplementation [1300-1500 mg/day]
• Vitamin D supplementation [1500 and 2000 mg/day]

Symptomatic treatment for other musculoskeletal conditions may be done.

Surgery is usually not indicated except in some fractures

Hormone replacement therapy and oral contraceptive pills are not commonly used in athletes with the female athlete triad.

Restoration of menstrual function

If lack of energy availability is corrected by meeting the calorie requirement, the menstrual function gets corrected.

The availability of energy will restore gonadotropin-releasing hormone (GnRH) and luteinizing hormone (LH) pulsatility, as well as menstruation.

If the nonpharmacologic treatment does not work, transdermal estradiol with cyclic progesterone has been found to be helpful.

Bisphosphonates are indicated in postmenopausal athletes with severe osteoporosis.

Prevention of Female Athlete Triad

Female athlete triad is difficult to diagnose, hence its prevention becomes quite significant.

Regular screening and identification of at-risk athlete is one strategy.

The preparticipation physical examination presents an ideal opportunity to screen all female athletes for signs or symptoms of the female athlete triad.

Athletes should be encouraged to report missed periods or scanty periods because they might indicate underlying issues. Therefore athletes need to be educated on the issue.

Misconceptions like amenorrhea is a sign of hard work should be addressed.

Physicians need to keep a stronger vigil and high index of suspicion too.

Prognosis

For many, the long-term prognosis is good.

Few athletes with the female athlete triad require inpatient treatment. Some may die from their disease or serious complications, such as cardiac arrhythmias.

Others may have significant long-term morbidity affecting them later in life.

References

• Sabatini S. The female athlete triad. Am J Med Sci. 2001 Oct. 322(4):193-5.
• Sanborn CF, Horea M, Siemers BJ, Dieringer KI. Disordered eating and the female athlete triad. Clin Sports Med. 2000 Apr. 19(2):199-213.
• Nichols JF, Rauh MJ, Lawson MJ, Ji M, Barkai HS. Prevalence of the female athlete triad syndrome among high school athletes. Arch Pediatr Adolesc Med. 2006 Feb. 160(2):137-42.
• Thein-Nissenbaum J. Long-term consequences of the female athlete triad. Maturitas. 2013 Jun. 75(2):107-12
• Committee on Adolescent Health Care. Committee Opinion No.702: Female Athlete Triad. Obstet Gynecol. 2017 Jun. 129 (6):e160-e167.

Swimmer’s shoulder is an umbrella term covering a range of painful shoulder in the competitive swimmer lead to a spectrum of overuse injuries seen in the swimmer’s shoulder, the most common of which is rotator cuff tendinitis.

Shoulder pain is the most common musculoskeletal complaint in swimming with swimmer’s shoulder.

Reports of incidence of disabling shoulder pain in competitive swimmers ranging from 27% to 87%.

Relevant Anatomy of Shoulder

[Read anatomy of shoulder]

The shoulder girdle is anatomically designed to achieve the greatest range of motion. Glenohumeral and scapulothoracic joints part of this system designed for the mobility whereas the acromioclavicular and sternoclavicular joints provide stability along with tendon ligaments and muscles.

This mechanism allows the shoulder to withstand large external forces while providing enough mobility. It is especially true for overhead movements.

It is composed of

3 bones

• Scapula
• Clavicle
• Proximal humerus)

2 Joints

• Glenohumeral
• Acromioclavicular

Various ligaments, muscles, and tendons stabilize and enhance the function of the shoulder.

The subacromial bursa is present between rotator cuff and acromion provides the cuff with some mechanical protection.

There are three glenohumeral ligaments (inferior, middle, superior), which are thickened regions of the joint capsule. The inferior glenohumeral ligament is most important. Their role is to help stabilize the glenohumeral joint.

Rotator cuff is formed by the subscapularis, supraspinatus, infraspinatus, and teres minor.

It functions as the dynamic and functional stabilizer of the glenohumeral joint with contributions from the long head of the biceps tendon

These ligaments, tendons, and muscles can be overused and injured in activities like swimming where the shoulder has a dominant role to play.

Out of these, the supraspinatus is most commonly injured.

The other muscles involved in activity are those which power the shoulder movements [ the latissimus dorsi, pectoralis, and deltoid] are less common to sustain an injury.

External stabilizers of shoulder girdle are the trapezius, levator scapulae, rhomboids, and serratus anterior muscles. These also help n positioning the scapula and shoulder girdle and play important role in swimming.

These are also less commonly injured.

Biomechanics of Swimming

Swimming requires several different shoulder motions

• Circumduction in clockwise and counter-clockwise directions
• Varying degrees of internal and external rotation
• Scapular protraction and retraction

There are four different types of stroke in swimming – freestyle, butterfly, backstroke, and breaststroke. Most strokes are divided into two primary phases referred to as the pull-through and recovery. The pull-through is where propulsion is achieved.

Increased shoulder flexibility and range of motion are desirable and beneficial to all strokes. But this can lead to increased laxity of the glenohumeral joint capsule and ligaments and hence affecting stability.

The acquired anterior laxity permits excessive external rotation but places greater demand on the rotator cuff and the long head of the biceps to reduce humeral head elevation and anterior translation.

The rotator cuff tries to balance this laxity, to keep the humeral head centered in the glenoid socket during the stroke. It acts as a fulcrum of upper limb as it works through the water. It stabilizes the glenohumeral joint to allow efficient use of power by power muscles.

Failure of the rotator cuff and the scapular stabilizers to can lead to excessive humeral head migration and either increased tensile stress on the tendons or compression of the tendons due to the humeral head abutment.

It has been found that after about 3 months of training, subacromial space distance decreases in swimmers and there is an increase in forward shoulder posture compared to other athletes who do not have so much overhead shoulder use.

The proposed mechanism of failure initiates muscle fatigue. During high demands, rotator cuff muscles generally fatigue before the power muscles, allowing micromotion and subluxation of the humeral head.

This can lead to decreased stroke efficiency and may injure the rotator cuff, biceps tendon, and glenoid labrum.

Superior subluxation of the humeral head impinges the rotator cuff tendons against the acromion above, leading to tendinitis and/or tears.

Bursitis can result in the overlying subacromial bursa.

Primary subacromial impingement and secondary impingement may be contributive.

Another proposed impingement mechanism involves the microvasculature of the rotator cuff.

With shoulder abduction, vessels of the supraspinatus and long head of the biceps are filled and emptied during adduction causing vascular compromise leading to fatigue.

In addition, overuse of the shoulder would cause microtrauma.

Clinical Presentation of Swimmer’s Shoulder

There is pain which at first occurs during or after swimming. Often it is ignored and it starts paining with non-swimming activities of the shoulder as well.

Eventually, the worsening may cause pain at rest too.

A history of a recent growth spurt, an increase in the level of training and competition, or both may be there.

A break from swimming may improve the condition but often recurs with swimming if no rotator cuff strengthening is done.

The pain is often poorly localized and felt deep in the shoulder, often in the posterior aspect of the shoulder or less commonly, at the deltoid insertion area of the upper arm.

On examination, a common postural deviation is often observed in swimmers called forward head, rounded shoulder posture.

This posture includes

• Increased thoracic kyphosis
• Decreased cervical lordosis
• Protracted scapulae
• internally rotated/anterior humeral head.

[This posture is seen in players without Swimmer’s shoulder also]

Soft tissue findings associated with this posture are

• Restricted anterior shoulder musculature
• Lengthened and weak medial scapular stabilizers,
• Tight glenohumeral posterior capsule
• Weak anterior cervical flexors

Physical examination of swimmer’s shoulder may reveal asymmetry, particularly in scapular position, or rotator cuff muscle mass (atrophy).

Mostly,  both internal rotation and external rotation are increased as compared to the general population.

Swimmers with impingement may have a painful arc from 60-120 degrees.

Weakness in the involved muscle, most commonly the supraspinatus, may be noted in advanced cases.

Altered scapulohumeral rhythm may be observed with excessive elevation or upward rotation of the scapula.

The range of motion will usually show excessive external rotation and horizontal abduction due to hypermobility of the anterior glenohumeral joint capsule.

In most swimmers’ shoulders, a mild-to-moderate increase in laxity is noted, indicating multidirectional laxity. Occasionally, this can lead to symptomatic instability in which the swimmer complains of the shoulder subluxing or shifting with use.

Following signs may be noted

• Sulcus sign [hypermobility]
• Positive load and shift test
• Positive relocation test
• Positive apprehension sign.

The weakness of the rotator cuff and scapular stabilizers will be noted when instability is present.

Positive impingement tests and painful resisted tests indicate underlying inflammation.

Shoulder Apprehension Test

Place the shoulder in maximum abduction and external rotation (90-90 position) and apply an anteriorly-directed force to the shoulder from behind. To be positive, it must elicit a feeling of apprehension or instability. Generally, the only discomfort is seen in swimmers rather apprehension or sense of instability.

Load and Shift Test

With the patient seated, stabilize the scapula to the thorax with one hand, while the other hand is placed across the posterior glenohumeral joint line and humeral head, and the web space across the patient’s acromion. The index finger should the over the anterior GH joint line.

Load and shift of the humeral head across the stabilized scapula in an anteromedial direction to assess anterior stability, and in a posterolateral direction to assess posterior instability is done.

Normal motion anteriorly is half of the distance of the humeral head, more movement is considered to be a sign of glenohumeral joint laxity.

Strength Assessment of Rotator Cuff

Subscapularis

• Internal rotation movement against resistance
• Lift-off test
  • Shoulder in internal rotation with the back of the patient’s hand against the small of the back.
  • The patient attempts to lift hand away from back against the examiner’s resistance.

Infraspinatus, teres minor

External Rotation against resistance [shoulder in the neutral position at the side and the elbow flexed to 90°.

Supraspinatus

• Resisted shoulder elevation with the arms extended, internally rotated, and positioned in the scapular plane (approximately 30-45° anterior to the coronal plane).
• If weak, retest the supraspinatus in the same arm position except with the arms externally rotated (ie, thumbs pointing upwards).

Sulcus Sign [Assessment of Joint Laxity]

The arm is pulled inferiorly and gap or sulcus is looked between the humeral head and lateral edge of the acromion. This indicates inferior subluxation of the humeral head.

• Grade 1 – Less than 1 finger breadth (< 1 cm)
• Grade 2 – One finger breadth (1-2 cm)
• Grade 3 – Greater than 1 finger breadth (> 2 cm)

Compare to the opposite shoulder (should be similar). If not then consider unilateral traumatic injury.

In addition, check for generalized ligamentous laxity.

Tests for Labral Tear

A labral tear is suggested by a painful click is noted during the recovery phase of an overhand stroke. Often, this click can be reproduced during the exam.

O’Brien test for Labral Tear [SLAP Lesion]

A downward force is applied with the extended in the forward flexed position, adducted 15° toward the midline, with the shoulder in the maximal internal rotation (thumb pointing down).

A pain that occurs in this position and relieved when external rotation is done suggests a SLAP lesion.

Differential Diagnoses

• Acromioclavicular Joint Injury
• Labral Tears
• Biceps Tendinopathy
• Bony Avulsion of Anterior Inferior Glenohumeral Ligament
• Cervical Radiculopathy
• Rotator Cuff Tear
• Multidirectional Instability
• Rheumatoid Arthritis
• Shoulder Impingement Syndrome
• Subacromial Bursitis
• Supraspinatus Tendonitis
• Thoracic Outlet Syndrome

Lab Studies

Generally normal.

Imaging Studies

X-rays

X-rays are performed to rule out bony causes of shoulder pain like a stress fracture or lesion or loose body. X-rays should be obtained if the pain persists after 6 weeks of rest and rehabilitation.

The desirable x-rays are anteroposterior (AP) y-scapular or outlet view and axillary view of the shoulder.

Magnetic Resonance Imaging

MRI is able to tell about rotator cuff pathology and status of the bones, ligaments, and other tendons in the shoulder.

But in most of the cases, the MRI is normal or in some cases may demonstrate some increased signal in the substance of the supraspinatus tendon.

Fluid in the subacromial bursa may signify bursitis.

MRI arthrogram with intraarticular gadolinium is able to depict labral tear.

Diagnostic Subacromial Injection

Subacromial injection of an anesthetics agent like lignocaine can be used for diagnosis. Immediate relief of pain following the injection suggests an injury of the rotator cuff and/or the overlying bursa.

Intra-articular injection providing relief, on the other hand, suggests intraarticular pathology.

Treatment of Swimmer’s Shoulder

In the acute phase, pain relief is the main aim. This involves

• resting the shoulder.
• Modify/restrict activities
• Regular icing
• Nonsteroidal anti-inflammatory medications or NSAIDs

For the restoration of strength, physical therapy and exercise follow. Measures taken could involve

• Supervised exercise program for the rotator cuff
• Ultrasound
• Phonophoresis
• Iontophoresis
• Electrical stimulation

Surgery for Swimmer’s Shoulder

If the patient does not improve even after  6 months of guided rest and rehabilitation.

The procedures include a diagnostic arthroscopy and a  surgical tightening of the lax capsule (capsulorrhaphy).

If there is an evidence of impingement on arthroscopy, a subacromial decompression is performed.

After decompression surgery patient may not return to the same level of swimming. The athlete should know this before undergoing the procedure

After capsulorrhaphy,  immobilization in an arm sling or immobilizer for 4-6 weeks is done.

After this rotator cuff strengthening program in physical therapy.

Before swimming,  80% of normal motion and strength in the shoulder should be there.

The patient with Swimmer’s shoulder can return to swimming between 6 and 12 months following surgery.