Acrocallosal syndrome (also known as ACLS) is a rare autosomal recessive syndrome characterized by corpus callosum agenesis, polydactyly, multiple dysmorphic features, motor and mental retardation, and other symptoms. The syndrome was first described by Albert Schinzel in 1979.

It is associated with "GLI3".

Acrocallosal syndrome (ACLS, ACS, Schinzel-Type) is a rare, heterogeneous, autosomal recessive disorder [3]. The heterogeneity of this condition refers to the multiple genes that may function to contribute to varying degrees of this syndrome [3] and is often linked to consanguinity [2,5]. Characteristics of this syndrome include agenesis of the corpus, macrocephaly, hypertelorism, polydactyly, mental and motor retardation [2], craniofacial dysmorphism, hallux dudplication [3], and sometimes palatal clefting [5]. It has also been reported that there are many similar signs and symptoms between ACLS, Greig cephalopolysyndactyly, and Hydrolethalus Syndrome (HLS), although there is little evidence to support common genetic causation at this point [3].

Women in sports such as association football, basketball, and tennis are significantly more prone to ACL injuries than men. The discrepancy has been attributed to gender differences in anatomy, general muscular strength, reaction time of muscle contraction and coordination, and training techniques.

Gender differences in ACL injury rates become evident when specific sports are compared. A review of NCAA data has found relative rates of injury per 1000 athlete exposures as follows:

- Men's basketball 0.07, women's basketball 0.23

- Men's lacrosse 0.12, women's lacrosse 0.17

- Men's football 0.09, women's football 0.28

The highest rate of ACL injury in women occurred in gymnastics, with a rate of injury per 1000 athlete exposures of 0.33

Of the four sports with the highest ACL injury rates, three were women's – gymnastics, basketball and soccer.

According to recent studies, female athletes are two to eight times more likely to strain their anterior cruciate ligament (ACL) in sports that involve cutting and jumping as compared to men who play the same particular sports (soccer, basketball, and volleyball). Differences between males and females identified as potential causes are the active muscular protection of the knee joint, the greater Q angle putting more medial torque on the knee joint, relative ligament laxity caused by differences in hormonal activity from estrogen and relaxin, intercondylar notch dimensions, and muscular strength.

High school athletes are at increased risk for ACL tears when compared to non-athletes. This risk increases with certain types of sports. Among high school girls, the sport with the highest risk of ACL tear is soccer, followed by basketball and lacrosse. The highest risk sport for boys was basketball, followed by lacrosse and soccer. Children and young athletes may benefit from early surgical reconstruction after ACL injury. Young athletes who have early surgical reconstruction of their torn ACL are more likely to return to their previous level of athletic ability when compared to those who underwent delayed surgery or nonoperative treatment. They are also less likely to experience instability in their knee if they undergo early surgery.

In the UK, 28,354 cases of hypothermia were treated in 2012-13 – an increase of 25% from the previous year. Some cases of hypothermia death, as well as other preventable deaths, happen because poor people cannot easily afford to keep warm. Rising fuel bills have increased the numbers who have difficulty paying for adequate heating in the UK. Some pensioners and disabled people are at risk because they do not work and cannot easily get out of their homes. Better heat insulation can help.

Alcohol consumption increases the risk of hypothermia by its action as a vasodilator. It increases blood flow to the skin and extremities, making a person "feel" warm, while increasing heat loss. Between 33% and 73% of hypothermia cases are complicated by alcohol.

The risk factors for SCD are similar to those of coronary artery disease and include age, cigarette smoking, high blood pressure, high cholesterol, lack of physical exercise, obesity, diabetes, and family history. A prior episode of sudden cardiac arrest also increases the risk of future episodes.

Current cigarette smokers with coronary artery disease were found to have a two to threefold increase in the risk of sudden death between ages 30 and 59. Furthermore, it was found that former smokers risk was closer to that of those who had never smoked.

These possible causes are remembered as the 6 Hs and the 6 Ts. See Hs and Ts

- Hypovolemia

- Hypoxia

- Hydrogen ions (Acidosis)

- Hyperkalemia or Hypokalemia

- Hypoglycemia

- Hypothermia

- Tablets or Toxins (Drug overdose)

- Cardiac Tamponade

- Tension pneumothorax

- Thrombosis (e.g., myocardial infarction, pulmonary embolism)

- Tachycardia

- Trauma (e.g., hypovolemia from blood loss)

This list is not fully comprehensive. Most notably, it does not include anaphylaxis. Pressure effects associated with artificial ventilation may also contribute to significant reduction in cardiac output, resulting in a clinical diagnosis of PEA.

The possible mechanisms by which the above conditions can cause pulseless in PEA or the same as those recognized as producing circulatory shock states. These are (1) impairment of cardiac filling, (2) impaired pumping effectiveness of the heart, (3) circulatory obstruction and (4) pathological vasodilation causing loss of vascular resistance and excess capacitance. More than one mechanism may be involved in any given case.

Arrhythmias not due to structural heart disease account for 5 to 10% of SCDs.

Examples of arrhythmic syndromes associated with SCD include: Long QT syndrome, Wolff-Parkinson-White Syndrome, Brugada Syndrome, Catecholaminergic polymorphic ventricular tachycardia.

Long QT syndrome, a condition often mentioned in young people's deaths, occurs in one of every 5000 to 7000 newborns and is estimated to be responsible for 3000 deaths each year compared to the approximately 300,000 cardiac arrests seen by emergency services. These conditions are a fraction of the overall deaths related to cardiac arrest, but represent conditions which may be detected prior to arrest and may be treatable.

Sudden cardiac arrest is the leading cause of death in the industrialised world. It exacts a significant mortality with approximately 70,000 to 90,000 sudden cardiac deaths each year in the United Kingdom, and survival rates are only 2%. The majority of these deaths are due to ventricular fibrillation secondary to myocardial infarction, or "heart attack". During ventricular fibrillation, cardiac output drops to zero, and, unless remedied promptly, death usually ensues within minutes.

Pulseless electrical activity leads to a loss of cardiac output, and the blood supply to the brain is interrupted. As a result, PEA is usually noticed when a person loses consciousness and stops breathing spontaneously. This is confirmed by examining the airway for obstruction, observing the chest for respiratory movement, and feeling the pulse (usually at the carotid artery) for a period of 10 seconds.

Myofibre break-up, abbreviated MFB, is associated with ventricular fibrillation leading to death. Histomorphologically, MFB is characterized by fractures of the cardiac myofibres perpendicular to their long axis, with squaring of the myofibre nuclei.