Breastfeeding is associated with a lower risk of SIDS. It is not clear if co-sleeping among mothers who breastfeed without any other risk factors increased SIDS risk.

SIDS rates decrease with increasing maternal age, with teenage mothers at greatest risk. Delayed or inadequate prenatal care also increases risk. Low birth weight is a significant risk factor. In the United States from 1995 to 1998, the SIDS death rate for infants weighing 1000–1499 g was 2.89/1000, while for a birth weight of 3500–3999 g, it was only 0.51/1000. Premature birth increases the risk of SIDS death roughly fourfold. From 1995 to 1998, the U.S. SIDS rate for births at 37–39 weeks of gestation was 0.73/1000, while the SIDS rate for births at 28–31 weeks of gestation was 2.39/1000.

Anemia has also been linked to SIDS (note, however, that per item 6 in the list of epidemiologic characteristics below, extent of anemia cannot be evaluated at autopsy because an infant's total hemoglobin can only be measured during life.). SIDS incidence rises from zero at birth, is highest from two to four months of age, and declines toward zero after the infant's first year. Baby boys have a ~50% higher risk of SIDS than girls.

Fetal mortality refers to stillbirths or fetal death. It encompasses any death of a fetus after 20 weeks of gestation or 500 gm. In some definitions of the PNM early fetal mortality (week 20-27 gestation) is not included, and the PNM may only include late fetal death and neonatal death. Fetal death can also be divided into death prior to labor, antenatal (antepartum) death, and death during labor, intranatal (intrapartum) death.

Preterm birth is the most common cause of perinatal mortality, causing almost 30 percent of neonatal deaths. Infant respiratory distress syndrome, in turn, is the leading cause of death in preterm infants, affecting about 1% of newborn infants. Birth defects cause about 21 percent of neonatal death.

Populations groups at risk:

- In the US:

- Children and young adults: Drowning rates are highest for children under 5 years of age and persons 15–24 years of age.

- Males: Nearly 80% of people who die from drowning are male.

- Minorities: The fatal unintentional drowning rate for African Americans between 2005 and 2009 was significantly higher than that of whites across all ages. The fatal drowning rate of African American children of ages from 5 to 14 is almost three times that of white children in the same age range, and 5.5 times higher in swimming pools. These disparities might be associated with lack of basic swimming skills in some minority populations.

Behavioral and physical factors:

- In the US:

- Use of alcohol increases the risk of drowning. Among adolescents and adults, alcohol use is involved in almost a quarter of emergency department visits for drowning.

- Inability to swim: Participation in formal swimming lessons can reduce the risk of drowning among children aged 1 to 4 years.

- Free access to water: Effective barriers prevent young children from gaining access to the water

- Ineffective supervision: Drowning can occur anywhere there is water, and even in the presence of lifeguards.

- Risk can vary with location depending on age. Children between 1 and 4 usually drown in home swimming pools. Drownings in natural water settings increase with age. More than half of drownings among those 15 years and older occurred in natural water environments.

- Failure to wear life jackets or personal flotation devices was implicated in 88% of the boating related drownings in the US during 2010.

- For persons with seizure disorders, drowning is the most common cause of death by unintentional injury, largely in the bathtub.

Drowning is a major worldwide cause of death and injury in children. Long term neurological outcomes of drowning cannot be predicted accurately during the early stages of treatment and although survival after long submersion times, mostly by young children, has been reported, many survivors will remain severely and permanently neurologically compromised after much shorter submersion times. Factors affecting probability of long term recovery with mild deficits or full function in young children include the duration of submersion, whether advanced life support was needed at the accident site, the duration of cardiopulmonary resuscitation, and whether spontaneous breathing and circulation are present on arrival at the emergency room.

Data on long-term outcome are scarce and unreliable. Neurological examination at the time of discharge from hospital does not accurately predict long term outcomes. Some victims who suffered from severe brain injury and were transferred to other institutions died months or years after the drowning and are recorded as survivors. Non-fatal drownings have been estimated as two to four times more frequent than fatal drownings.

Promoters of this suicide method recommend it to terminally ill patients. However, across the world, most people who use suicide bags are physically healthy. Instead of having incurable cancer or other life-threatening physical diseases, most of the users have psychiatric disorders or substance abuse problems that might possibly be addressed through medical and psychological treatment. The demographics of its users varies; in one survey, the method had been used mostly by middle-aged adults in failing health, who were attracted to the relative nonviolence of the method.

This suicide method is also typically used by younger or middle-aged adults, rather than by older adults. In the US, it is more commonly chosen by non-Hispanic white males than by women or people of other races.

Disorders like congenital central hypoventilation syndrome (CCHS) and ROHHAD (rapid-onset obesity, hypothalamic dysfunction, hypoventilation, with autonomic dysregulation) are recognized as conditions that are associated with hypoventilation. CCHS may be a significant factor in some cases of sudden infant death syndrome (SIDS), often termed "cot death" or "crib death".

The opposite condition is hyperventilation (too much ventilation), resulting in low carbon dioxide levels (hypocapnia), rather than hypercapnia.

Respiratory stimulants such as nikethamide were traditionally used to counteract respiratory depression from CNS depressant overdose, but offered limited effectiveness. A new respiratory stimulant drug called BIMU8 is being investigated which seems to be significantly more effective and may be useful for counteracting the respiratory depression produced by opiates and similar drugs without offsetting their therapeutic effects.

If the respiratory depression occurs from opioid overdose, usually an opioid antagonist, most likely naloxone, will be administered. This will rapidly reverse the respiratory depression unless complicated by other depressants. However an opioid antagonist may also precipitate an opioid withdrawal syndrome in chronic users.

Suicides using bags or masks and gases are well documented in the literature.

Suicide bags have been used with gases other than inert gases, with varying outcomes. Examples of other gases are propane-butane and natural gas.

Suicides using a suicide bag and an inert gas produce no characteristic post-mortem macroscopic or microscopic findings. Forensic death investigations of cause and manner of death may be very difficult when people commit suicide in this manner, especially if the apparatus (such as the bag, tank, or tube) is removed by someone after the death. Petechiae, which are often considered a marker of asphyxia, are present in only a small minority of cases (3%). Frost reported that of the two cases he studied that featured death from inert gas asphyxiation using a suicide bag, one had "bilateral eyelid petechiae and large amounts of gastric content in the airways and that these findings challenge the assumption that death by this method is painless and without air hunger, as asserted in "Final Exit"." A review study by Ely and Hirsch (2000) concludes that conjunctival and facial petechiae are the product of purely mechanical vascular phenomena, unrelated to asphyxia or hypoxia, and do not occur unless ligatures were also found around the neck. The authors wrote,

There are also documented cases of suicide attempts using the suicide bag that failed. A case report study in 2015 discussed the risks associated with failed attempts using this method. The authors wrote, "If the process is interrupted by someone, there is no gas or the tube slips out of the bag, there is a high risk of severe hypoxia of the central nervous system."

The Lazarus phenomenon raises ethical issues for physicians, who must determine when medical death has occurred, resuscitation efforts should end, and postmortem procedures such as autopsies and organ harvesting may take place.

Medical literature has recommended observation of a patient's vital signs for five to ten minutes after cessation of resuscitation before certifying death.

Lazarus syndrome, (the Lazarus heart) also known as autoresuscitation after failed cardiopulmonary resuscitation, is the spontaneous return of circulation after failed attempts at resuscitation. Its occurrence has been noted in medical literature at least 38 times since 1982. It takes its name from Lazarus who, as described in the New Testament of The Bible, was raised from the dead by Jesus.

Occurrences of the syndrome are extremely rare and the causes are not well understood. One hypothesis for the phenomenon is that a chief factor (though not the only one) is the buildup of pressure in the chest as a result of cardiopulmonary resuscitation (CPR). The relaxation of pressure after resuscitation efforts have ended is thought to allow the heart to expand, triggering the heart's electrical impulses and restarting the heartbeat. Other possible factors are hyperkalemia or high doses of epinephrine.

Consistent risk factors include:

- Severity of seizures, increased refractoriness of epilepsy and presence of generalized tonic-clonic seizures: the most consistent risk factor is an increased frequency of tonic–clonic seizures.

- Poor compliance. Lack of therapeutic levels of anti-epileptic drugs, non-adherence to treatment regimens, and frequent changes in regimens are risk factors for sudden death.

- Young age, and early age of seizures onset.

- Male gender

- Poly-therapy of epilepsy. It remains unclear whether this is an independent risk factor or a surrogate marker for severity of epilepsy.

- Being asleep during a seizure is likely to favour SUDEP occurrence.

Pallor mortis results from the cessation of capillary circulation throughout the body. Gravity then causes the blood to sink down into the lower parts of the body, creating livor mortis.

A living person can look deathly pale. This can happen when circumstances make the blood escape from the surface of the skin, as in deep shock. Also heart failure ("insufficientia cordis") can make the face look grey; the person then also has blue lips. Skin can also look deathly pale as a result of vasoconstriction as part of the body's homeostatic systems in cold conditions, or if the skin is deficient in vitamin D, as seen in people who spend most of the time indoors, away from sunlight.

Brainstem death is a clinical syndrome defined by the absence of reflexes with pathways through the brainstem—the “stalk” of the brain, which connects the spinal cord to the mid-brain, cerebellum and cerebral hemispheres—in a deeply comatose, ventilator-dependent patient.

Identification of this state carries a very grave prognosis for survival; cessation of heartbeat often occurs within a few days although it may continue for weeks or even months if intensive support is maintained.

In the United Kingdom, the formal diagnosis of brainstem death by the procedure laid down in the official Code of Practice permits the diagnosis and certification of death on the premise that a person is dead when consciousness and the ability to breathe are permanently lost, regardless of continuing life in the body and parts of the brain, and that death of the brainstem alone is sufficient to produce this state.

This concept of brainstem death is also accepted as grounds for pronouncing death for legal purposes in India and Trinidad & Tobago. Elsewhere in the world the concept upon which the certification of death on neurological grounds is based is that of permanent cessation of all function in all parts of the brain—whole brain death—with which the reductionist United Kingdom concept should not be confused. The United States' President's Council on Bioethics made it clear, in its White Paper of December 2008, that the United Kingdom concept and clinical criteria are not considered sufficient for the diagnosis of death in the United States of America.

The sudden cardiac deaths of 387 young American athletes (under age 35) were analyzed in a 2003 medical review:

While most causes of sudden cardiac death relate to congenital or acquired cardiovascular disease, an exception is commotio cordis, in which the heart is structurally normal but a potentially fatal loss of rhythm occurs because of the accident of timing of a blow to the chest. Its fatality rate is about 65% even with prompt CPR and defibrillation, and more than 80% without.

Age 35 serves as an approximate borderline for the likely cause of sudden cardiac death. Before age 35, congenital abnormalities of the heart and blood vessels predominate. These are usually asymptomatic prior to the fatal event, although not invariably so. Congenital cardiovascular deaths are reported to occur disproportionately in African-American athletes.

After age 35, acquired coronary artery disease predominates (80%), and this is true regardless of the athlete's former level of fitness.

Until recently, medical literature did not indicate a connection among many genetic disorders, both genetic syndromes and genetic diseases, that are now being found to be related. As a result of new genetic research, some of these are, in fact, highly related in their root cause despite the widely varying set of medical symptoms that are clinically visible in the disorders. Anencephaly is one such disease, part of an emerging class of diseases called ciliopathies. The underlying cause may be a dysfunctional molecular mechanism in the primary cilia structures of the cell, organelles present in many cellular types throughout the human body. The cilia defects adversely affect "numerous critical developmental signaling pathways" essential to cellular development and, thus, offer a plausible hypothesis for the often multi-symptom nature of a large set of syndromes and diseases. Known ciliopathies include primary ciliary dyskinesia, Bardet-Biedl syndrome, polycystic kidney and liver disease, nephronophthisis, Alström syndrome, Meckel-Gruber syndrome, and some forms of retinal degeneration.

Exsanguination is a relatively uncommon cause of death in human beings. Traumatic injury can cause exsanguination if bleeding is not promptly controlled, and is the most common cause of death in military combat. Non-combat causes can include gunshot or stab wounds; motor vehicle crash injuries; suicide by severing arteries, typically those in the wrists; and partial or total limb amputation, such as via accidental contact with a circular or chain saw, or becoming entangled in operating machinery.

Patients can also develop catastrophic internal hemorrhages, such as from a bleeding peptic ulcer, postpartum bleeding or splenic hemorrhage, which can cause exsanguination without any external signs of distress. Another cause of exsanguination in the medical field is that of aneurysms. If a dissecting aortic aneurysm ruptures through the adventitia, massive hemorrhage and exsanguination can result in a matter of minutes.

Blunt force trauma to the liver, kidneys, and spleen can cause severe internal bleeding as well, though the abdominal cavity usually becomes visibly darkened as if bruised. Similarly, trauma to the lungs can cause bleeding out, though without medical attention, blood can fill the lungs causing the effect of drowning, or in the pleura causing suffocation, well before exsanguination would occur. In addition, serious trauma can cause tearing of major blood vessels without external trauma indicative of the damage.

Alcoholics and others with liver disease can also suffer from exsanguination. Thin-walled, normally low pressure dilated veins just below the lower esophageal mucosa called esophageal varices can become enlarged in conditions with portal hypertension. These may begin to bleed, which with the high pressure in the portal system can be fatal. The often causative impaired liver function also reduces the availability of clotting factors (many of which are made in the liver), making any rupture in vessels more likely to cause a fatal loss of blood.

The cause of anencephaly is disputed by medical professionals and researchers.

Folic acid has been shown to be important in neural tube formation since at least 1995, and as a subtype of neural tube defect, folic acid may play a role in anencephaly. Studies have shown that the addition of folic acid to the diet of women of child-bearing age may significantly reduce, although not eliminate, the incidence of neural tube defects. Therefore, it is recommended that all women of child-bearing age consume 0.4 mg of folic acid daily, especially those attempting to conceive or who may possibly conceive, as this can reduce the risk to 0.03%. It is not advisable to wait until pregnancy has begun, since, by the time a woman knows she is pregnant, the critical time for the formation of a neural tube defect has usually already passed. A physician may prescribe even higher dosages of folic acid (5 mg/day) for women having had a previous pregnancy with a neural tube defect.

In general, neural tube defects do not follow direct patterns of heredity, though there is some indirect evidence of inheritance, and recent animal models indicate a possible association with deficiencies of the transcription factor TEAD2. Studies show that a woman who has had one child with a neural tube defect such as anencephaly has about a 3% risk of having another child with a neural tube defect, as opposed to the background rate of 0.1% occurrence in the population at large. Genetic counseling is usually offered to women at a higher risk of having a child with a neural tube defect to discuss available testing.

It is known that people taking certain anticonvulsants and people with insulin-dependent diabetes have a higher risk of having a child with a neural tube defect.

The United Kingdom (UK) criteria were first published by the Conference of Medical Royal Colleges (with advice from the Transplant Advisory Panel) in 1976, as prognostic guidelines. They were drafted in response to a perceived need for guidance in the management of deeply comatose patients with severe brain damage who were being kept alive by mechanical ventilators but showing no signs of recovery. The Conference sought “to establish diagnostic criteria of such rigour that on their fulfilment the mechanical ventilator can be switched off, in the secure knowledge that there is no possible chance of recovery”. The published criteria—negative responses to bedside tests of some reflexes with pathways through the brainstem and a specified challenge to the brainstem respiratory centre, with caveats about exclusion of endocrine influences, metabolic factors and drug effects—were held to be “sufficient to distinguish between those patients who retain the functional capacity to have a chance of even partial recovery and those where no such possibility exists”. Recognition of that state required the withdrawal of fruitless further artificial support so that death might be allowed to occur, thus “sparing relatives from the further emotional trauma of sterile hope”.

In 1979, the Conference of Medical Royal Colleges promulgated its conclusion that identification of the state defined by those same criteria—then thought sufficient for a diagnosis of brain death—“means that the patient is dead” Death certification on those criteria has continued in the United Kingdom (where there is no statutory legal definition of death) since that time, particularly for organ transplantation purposes, although the conceptual basis for that use has changed.

In 1995, after a review by a Working Group of the Royal College of Physicians of London, the Conference of Medical Royal Colleges formally adopted the “more correct” term for the syndrome, "brainstem death"—championed by Pallis in a set of 1982 articles in the British Medical Journal —and advanced a new definition of human death as the basis for equating this syndrome with the death of the person. The suggested new definition of death was the “irreversible loss of the capacity for consciousness, combined with irreversible loss of the capacity to breathe”. It was stated that the irreversible cessation of brainstem function will produce this state and “therefore brainstem death is equivalent to the death of the individual”.

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.

Sudden unexpected death in epilepsy (SUDEP) is a fatal complication of epilepsy. It is defined as the sudden and unexpected, non-traumatic and non-drowning death of a person with epilepsy, without a toxicological or anatomical cause of death detected during the post-mortem examination.

While the mechanisms underlying SUDEP are still poorly understood, it is possibly the most common cause of death as a result of complications from epilepsy, accounting for between 7.5 and 17% of all epilepsy-related deaths and 50% of all deaths in refractory epilepsy. The causes of SUDEP seem to be multifactorial and include respiratory, cardiac and cerebral factors, as well as the severity of epilepsy and seizures. Proposed pathophysiological mechanisms include seizure-induced cardiac and respiratory arrests.

SUDEP occurs in about 1 in 1,000 adults and 1 in 4,500 children with epilepsy a year. Rates of death as a result of prolonged seizures (status epilepticus) are not classified as SUDEP.

While the diagnosis of brain death has become accepted as a basis for the certification of death for legal purposes, it should be clearly understood that it is a very different state from biological death - the state universally recognized and understood as death. The continuing function of vital organs in the bodies of those diagnosed brain dead, if mechanical ventilation and other life-support measures are continued, provides optimal opportunities for their transplantation.

When mechanical ventilation is used to support the body of a brain dead organ donor pending a transplant into an organ recipient, the donor's date of death is listed as the date that brain death was diagnosed.

In some countries (for instance, Spain, Finland, Poland, Wales, Portugal, and France), everyone is automatically an organ donor after diagnosis of death on legally accepted criteria, although some jurisdictions (such as Singapore, Spain, Wales, France, Czech Republic and Portugal) allow opting out of the system. Elsewhere, consent from family members or next-of-kin may be required for organ donation. In New Zealand, Australia, the United Kingdom (excluding Wales) and most states in the United States, drivers are asked upon application if they wish to be registered as an organ donor.

In the United States, if the patient is at or near death, the hospital must notify a transplant organization of the person's details and maintain the patient while the patient is being evaluated for suitability as a donor. The patient is kept on ventilator support until the organs have been surgically removed. If the patient has indicated in an advance health care directive that they do not wish to receive mechanical ventilation or has specified a do not resuscitate order and the patient has also indicated that they wish to donate their organs, some vital organs such as the heart and lungs may not be able to be recovered.

Yunnan sudden death syndrome is a label used to define unexplained cases of cardiac arrest, which afflicted significant numbers of rural villagers in Yunnan province, in southwest China. Cases occurred almost always during the midsummer rainy season (from June to August), at an altitude of . The cause turned out to be a mushroom now blamed for an estimated 400 deaths in the past three decades.

The mysterious fatalities were recorded for decades before researchers from the Chinese Center for Disease Control and Prevention isolated a significant factor common in every case: a tiny unknown mushroom which was unintentionally gathered and consumed during wild mushroom harvests in the region. Previously the syndrome was thought to be caused by Keshan disease, caused by the Coxsackie virus.

The mushroom, "Trogia venenata", is also known as 'Little White'. It has been determined that families collecting fungi to sell have been eating these Little White mushrooms as they have no commercial value. Three amino acids present in the mushrooms have been shown to be toxic. The mushrooms have also been shown to contain very high quantities of barium, and it may be that some of the deaths are simply from barium poisoning.

In the hours before death, about two-thirds of the victims had such symptoms as nausea, dizziness, heart palpitations, seizures and fatigue.

However, in December 2012 it was announced that Dr Xu Jianping (徐建平) has been collecting samples of "Trogia venenata" in Yunnan for the past three years, and his research now shows that barium levels in the wild mushroom are no higher than those of common foods such as poultry and fish. Nonetheless, it appears the mushroom will still likely play a role. Since publication of the widely circulated 2010 "Science" article, no instances of Yunnan sudden death syndrome have been reported.