Preparticipation Evaluation & Athlete Health
Screen by history, clear by condition, return by protocol
The preparticipation evaluation
History first. The sports physical looks chiefly for conditions that cause sudden cardiac death, and the history is its most powerful tool. Cardiac red flags:
- Chest pain, syncope or near-syncope, excessive dyspnea, or palpitations during exercise.
- A previously noted murmur or elevated blood pressure.
- A relative with sudden unexplained death or disabling heart disease before age 50, or known HCM, long QT syndrome, other channelopathy, or Marfan syndrome.
Syncope during exertion is ominous, whereas collapse just after finishing a race is usually benign post-exertional hypotension. Any red flag means withholding clearance until an ECG, echocardiogram, and cardiology evaluation are complete. A routine screening ECG for every athlete is not required in the United States.
Targeted exam. Listen supine and standing. The HCM outflow murmur is a harsh systolic crescendo–decrescendo murmur at the left sternal border that grows louder with Valsalva or standing and softer with squatting, handgrip, or passive leg raise; anything that shrinks the left ventricular cavity worsens the obstruction. An aortic stenosis murmur instead softens with Valsalva, and an innocent flow murmur softens on standing. Look for Marfan habitus (tall stature, arm span exceeding height, arachnodactyly, pectus deformity, lens subluxation), palpate femoral pulses for coarctation, and measure blood pressure.
Sudden cardiac death in athletes
| Cause | Clue | Key test |
|---|---|---|
| Hypertrophic cardiomyopathy | Leading cause in young US athletes; dynamic outflow murmur, family history | Echocardiogram, ECG |
| Anomalous coronary artery | Second most common; left coronary from the right sinus; exertional angina or syncope with a normal ECG | CT coronary angiography |
| Arrhythmogenic RV cardiomyopathy | Fibrofatty right ventricle; epsilon wave, T inversion V1–V3 | ECG, cardiac MRI |
| Channelopathies and WPW | Long QT, Brugada, CPVT; exertional or emotional syncope; pre-excitation | ECG, family screening |
| Myocarditis | Recent viral illness, chest pain, arrhythmia | Troponin, cardiac MRI |
| Marfan syndrome | Aortic root dilation, dissection or rupture | Echocardiogram |
| Commotio cordis | Chest blow in a structurally normal heart | None: immediate CPR and AED |
Commotio cordis. A blunt, nonpenetrating blow to the precordium from a baseball, hockey puck, lacrosse ball, or fist, landing during the vulnerable upstroke of the T wave, triggers ventricular fibrillation. Survival depends on immediate CPR and early defibrillation, which is why every venue needs an AED and a rehearsed emergency action plan.
Clearance decisions
| Condition | Concern | Decision |
|---|---|---|
| Infectious mononucleosis | Splenic rupture, highest risk in the first 3 weeks | No contact or collision sports or heavy exertion for at least 3–4 weeks from onset, and until afebrile and well |
| Solitary kidney | Loss of the only kidney | Individualized; counsel and use protective padding for contact sports |
| Functionally one-eyed | Best-corrected acuity worse than 20/40 in the weaker eye | Polycarbonate sports eye protection for all sports; avoid boxing and full-contact martial arts |
| Down syndrome | Atlantoaxial instability | Neurologic history and exam; image if symptoms or signs |
Mononucleosis details. Most patients with EBV have splenomegaly, and rupture can occur with minimal or no trauma. Palpation is insensitive, routine ultrasound is not required, and the monospot can stay positive for months, so it cannot time return. Left upper quadrant pain radiating to the left shoulder (Kehr sign) means splenic rupture until proven otherwise.
Atlantoaxial instability. Ligamentous laxity produces radiographic instability in about 10–20% of people with Down syndrome, but only about 1–2% are symptomatic. Ask about neck pain, torticollis, gait change, weakness, and bowel or bladder change, and examine for hyperreflexia and clonus. Symptoms or signs call for prompt neutral-position cervical spine radiographs, MRI, urgent neurosurgical referral, and restriction from collision and neck-flexion sports. Routine screening films in asymptomatic children are no longer advised, although some organized programs still require them. The same instability matters during intubation, when neck hyperextension should be avoided.
Sport-related concussion
Definition and recognition. Concussion is a trauma-induced functional disturbance of the brain with normal structural imaging. Symptoms include headache, confusion, amnesia, dizziness or imbalance, nausea, light sensitivity, fogginess, and mood change; loss of consciousness occurs in fewer than 10%. Any suspected concussion means immediate removal from play, evaluation with a standardized sideline tool, and no return the same day, even if symptoms clear within minutes. Head CT is reserved for red flags such as worsening headache, repeated vomiting, seizure, focal deficit, declining consciousness, or skull fracture.
- Relative rest24–48 hours, then symptom-limited daily activity and a gradual return to learning.
- Light aerobic exerciseWalking or stationary cycling that does not worsen symptoms.
- Sport-specific and noncontact drillsRunning and skill work without head impact, then harder noncontact training.
- Full-contact practiceOnly when symptom-free at rest and with exertion and cleared by a clinician.
- Return to competitionEach stage lasts at least 24 hours; recurrent symptoms send the athlete back a stage.
Second impact syndrome. A second head blow before recovery from the first can abolish cerebral autoregulation, causing vascular engorgement and rapid diffuse brain swelling with herniation. It is rare, often fatal, and mostly affects adolescents. Repeated concussions also contribute to persistent post-concussive symptoms, managed with graded symptom-limited aerobic exercise and targeted vestibular, cervical, or cognitive therapy rather than prolonged rest, and to chronic traumatic encephalopathy, a tauopathy diagnosed at autopsy.
Female athlete triad and RED-S
Pathophysiology. Low energy availability, with or without disordered eating, suppresses hypothalamic GnRH pulsatility, lowering LH, FSH, and estradiol and producing functional hypothalamic amenorrhea. Estrogen deficiency and undernutrition reduce bone density, leading to stress fractures of the tibia, metatarsals, and pelvis. Leanness sports such as distance running, gymnastics, and ballet carry the highest risk. Relative energy deficiency in sport (RED-S) broadens the concept to male athletes and to other systems: bradycardia, hypotension, anemia, impaired immunity, and mood disturbance.
Evaluation. Amenorrhea is evaluated with a pregnancy test first, then TSH, prolactin, and FSH. DXA, interpreted with Z-scores, is obtained after prolonged amenorrhea, a stress fracture, or an eating disorder.
Treatment. Restore energy availability by eating more and/or training less, with a sports dietitian, mental health care for disordered eating, and adequate calcium and vitamin D. Return of spontaneous menses is the key sign of recovery. Combined oral contraceptives do not restore bone density and mask ongoing suppression with withdrawal bleeds; if estrogen is needed, transdermal estradiol with cyclic progestin is preferred. Bisphosphonates are avoided in young women.
Anabolic-androgenic steroid misuse
Endocrine effects. Exogenous androgens suppress LH and FSH, causing testicular atrophy, low sperm counts, and infertility, while aromatization to estradiol causes gynecomastia. Women develop virilization (deep voice, clitoromegaly, hirsutism) and amenorrhea, and adolescents suffer premature physeal closure with short stature. Stopping causes hypogonadal symptoms and depression that drive continued use.
Systemic effects and labs. Look for acne, aggression and mood swings, hypertension, left ventricular hypertrophy or cardiomyopathy, and tendon rupture. Labs show low HDL with high LDL, erythrocytosis with thrombosis risk, and liver injury ranging from cholestatic jaundice to peliosis hepatis and hepatic adenomas with oral 17α-alkylated agents. LH and FSH are suppressed; serum testosterone is high with testosterone esters but low with synthetic androgens. Suppressed gonadotropins separate steroid use from Klinefelter syndrome, in which LH and FSH are high.