SIDS is a diagnosis of exclusion and should be applied to only those cases in which an infant's death is sudden and unexpected, and remains unexplained after the performance of an adequate postmortem investigation, including:

1. an autopsy (by an experienced pediatric pathologist, if possible);

2. investigation of the death scene and circumstances of the death;

3. exploration of the medical history of the infant and family.

After investigation, some of these infant deaths are found to be caused by accidental suffocation, hyperthermia or hypothermia, neglect or some other defined cause.

Australia and New Zealand are shifting to the term "sudden unexpected death in infancy" (SUDI) for professional, scientific, and coronial clarity.

The term SUDI is now often used instead of sudden infant death syndrome (SIDS) because some coroners prefer to use the term 'undetermined' for a death previously considered to be SIDS. This change is causing diagnostic shift in the mortality data. In addition, the U.S. Centers for Disease Control and Prevention (CDC) has recently proposed that such deaths be called "sudden unexpected infant deaths" (SUID) and that SIDS is a subset of SUID.

Sudden infant death syndrome (SIDS), also known as cot death or crib death, is the sudden unexplained death of a child less than one year of age. Diagnosis requires that the death remains unexplained even after a thorough autopsy and detailed death scene investigation. SIDS usually occurs during sleep. Typically death occurs between the hours of 00:00 and 09:00. There is usually no evidence of struggle and no noise produced.

The exact cause of SIDS is unknown. The requirement of a combination of factors including a specific underlying susceptibility, a specific time in development, and an environmental stressor has been proposed. These environmental stressors may include sleeping on the stomach or side, overheating, and exposure to tobacco smoke. Accidental suffocation from bed sharing (also known as co-sleeping) or soft objects may also play a role. Another risk factor is being born before 39 weeks of gestation. SIDS makes up about 80% of sudden and unexpected infant deaths (SUIDs). Other causes include infections, genetic disorders, and heart problems. While child abuse in the form of intentional suffocation may be misdiagnosed as SIDS, this is believed to make up less than 5% of cases.

The most effective method of reducing the risk of SIDS is putting a child less than one year old on their back to sleep. Other measures include a firm mattress separate from but close to caregivers, no loose bedding, a relatively cool sleeping environment, using a pacifier, and avoiding exposure to tobacco smoke. Breastfeeding and immunization may also be preventive. Measures not shown to be useful include positioning devices and baby monitors. Evidence is not sufficient for the use of fans. Grief support for families affected by SIDS is important, as the death of the infant is sudden, without witnesses, and often associated with an investigation.

Rates of SIDS vary nearly tenfold in developed countries from one in a thousand to one in ten thousand. Globally it resulted in about 19,200 deaths in 2015 down from 22,000 deaths in 1990. SIDS was the third leading cause of death in children less than one year old in the United States in 2011. It is the most common cause of death between one month and one year of age. About 90% of cases happen before six months of age, with it being most frequent between two months and four months of age. It is more common in boys than girls.

Perinatal mortality (PNM), also perinatal death, refers to the death of a fetus or neonate and is the basis to calculate the perinatal mortality rate. Variations in the precise definition of the perinatal mortality exist specifically concerning the issue of inclusion or exclusion of early fetal and late neonatal fatalities. The World Health Organization defines perinatal mortality as the "number of stillbirths and deaths in the first week of life per 1,000 total births, the perinatal period commences at 22 completed weeks (154 days) of gestation and ends seven completed days after birth", but other definitions have been used.

The UK figure is about 8 per 1,000 and varies markedly by social class with the highest rates seen in Asian women. Globally about 2.6 million neonates died in 2013 before the first month of age down from 4.5 million in 1990.

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.

There are several terms which were in general use, but are no longer recommended.

Drowning is most often quick and unspectacular. Its media depictions as a loud, violent struggle have much more in common with distressed non-swimmers, who may well drown but have not yet begun to do so. In particular, an asphyxiating person is seldom able to call for help. The instinctive drowning response covers many signs or behaviors associated with drowning or near-drowning:

- Head low in the water, mouth at water level

- Head tilted back with mouth open

- Eyes glassy and empty, unable to focus

- Eyes open, with fear evident on the face

- Hyperventilating or gasping

- Trying to swim in a particular direction but not making headway

- Trying to roll over on the back to float

- Uncontrollable movement of arms and legs, rarely out of the water.

Frank Pia, a lifeguard and researcher of rescue techniques and drowning, notes that drowning begins at the point a person is unable to keep their mouth above water; inhalation of water takes place at a later stage. Most people demonstrating the instinctive drowning response do not show obvious prior evidence of distress.

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.

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.

Pallor mortis occurs almost immediately (within 15–25 minutes) post-mortem; paleness develops so rapidly after death that it has little to no use in determining the time of death, aside from saying that it either happened less than 30 minutes ago or more, which could help if the body were found very soon after 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.

In the UK, the formal rules for the diagnosis of brainstem death have undergone only minor modifications since they were first published in 1976. The most recent revision of the UK's Department of Health Code of Practice governing use of that procedure for the diagnosis of death reaffirms the preconditions for its consideration. These are:

1. There should be no doubt that the patient’s condition – deeply comatose, unresponsive and requiring artificial ventilation—is due to irreversible brain damage of known cause.

2. There should be no evidence that this state is due to depressant drugs.

3. Primary hypothermia as the cause of unconsciousness must have been excluded, and

4. Potentially reversible circulatory, metabolic and endocrine disturbances likewise.

5. Potentially reversible causes of apnoea (dependence on the ventilator), such as muscle relaxants and cervical cord injury, must be excluded.

With these pre-conditions satisfied, the definitive criteria are:

1. Fixed pupils which do not respond to sharp changes in the intensity of incident light.

2. No corneal reflex.

3. Absent oculovestibular reflexes – no eye movements following the slow injection of at least 50ml of ice-cold water into each ear in turn (the caloric reflex test).

4. No response to supraorbital pressure.

5. No cough reflex to bronchial stimulation or gagging response to pharyngeal stimulation.

6. No observed respiratory effort in response to disconnection of the ventilator for long enough (typically 5 minutes) to ensure elevation of the arterial partial pressure of carbon dioxide to at least 6.0 kPa (6.5 kPa in patients with chronic carbon dioxide retention). Adequate oxygenation is ensured by pre-oxygenation and diffusion oxygenation during the disconnection (so the brainstem respiratory centre is not challenged by the ultimate, anoxic, drive stimulus). This test—the apnoea test—is dangerous – and may prove lethal.

Two doctors, of specified status and experience, are required to act together to diagnose death on these criteria and the tests must be repeated after “a short period of time ... to allow return of the patient’s arterial blood gases and baseline parameters to the pre-test state”. These criteria for the diagnosis of death are not applicable to infants below the age of two months.

Hypoventilation may be caused by:

- A medical condition such as stroke affecting the brainstem

- Voluntary breath-holding or underbreathing, for example, hypoventilation training or Buteyko

- Medication or drugs, typically when taken in accidental or intentional overdose. Opioids in particular are known to cause respiratory depression. Examples of opioids include pharmaceuticals such as oxycodone and hydromorphone.

- Hypocapnia, which stimulates hypoventilation

- Chronic mountain sickness, a mechanism to conserve energy.

It is very important for family members and health care professionals to be aware of natural movements also known as Lazarus sign or Lazarus reflex that can occur on a brain-dead person whose organs have been kept functioning by life support. The living cells that can cause these movements are not living cells from the brain or brain stem, these cells come from the spinal cord. Sometimes these body movements can cause false hope for the family members.

A brain-dead individual has no clinical evidence of brain function upon physical examination. This includes no response to pain and no cranial nerve reflexes. Reflexes include pupillary response (fixed pupils), oculocephalic reflex, corneal reflex, no response to the caloric reflex test, and no spontaneous respirations.

It is important to distinguish between brain death and states that may be difficult to differentiate from brain death, (such as barbiturate overdose, alcohol intoxication, sedative overdose, hypothermia, hypoglycemia, coma, and chronic vegetative states). Some comatose patients can recover to pre-coma or near pre-coma level of functioning, and some patients with severe irreversible neurological dysfunction will nonetheless retain some lower brain functions, such as spontaneous respiration, despite the losses of both cortex and brain stem functionality. Such is the case with anencephaly.

Note that brain electrical activity can stop completely, or drop to such a low level as to be undetectable with most equipment. An EEG will therefore be flat, though this is sometimes also observed during deep anesthesia or cardiac arrest. Although in the United States a flat EEG test is not required to certify death, it is considered to have confirmatory value. In the UK it is not considered to be of value because any continuing activity it might reveal in parts of the brain above the brain stem is held to be irrelevant to the diagnosis of death on the Code of Practice criteria.

The diagnosis of brain death needs to be rigorous, in order to be certain that the condition is irreversible. Legal criteria vary, but in general they require neurological examinations by two independent physicians. The exams must show complete and irreversible absence of brain function (brain stem function in UK), and may include two isoelectric (flat-line) EEGs 24 hours apart (less in other countries where it is accepted that if the cause of the dysfunction is a clear physical trauma there is no need to wait that long to establish irreversibility). The patient should have a normal temperature and be free of drugs that can suppress brain activity if the diagnosis is to be made on EEG criteria.

Also, a radionuclide cerebral blood flow scan that shows complete absence of intracranial blood flow must be considered with other exams – temporary swelling of the brain, particularly within the first 72 hours, can lead to a false positive test on a patient that may recover with more time.

CT angiography is neither required nor sufficient test to make the diagnosis.

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.

Meronanencephaly is a rare form of anencephaly characterized by malformed cranial bones, a median cranial defect, and a cranial protrusion called area cerebrovasculosa. Area cerebrovasculosa is a section of abnormal, spongy, vascular tissue admixed with glial tissue ranging from simply a membrane to a large mass of connective tissue, hemorrhagic vascular channels, glial nodules, and disorganized choroid plexuses.

The most common type of anencephaly, where the brain has entirely failed to form, except for the brain stem. Infants rarely survive more than one day after birth with holoanencephaly.

Brain death is the complete loss of brain function (including involuntary activity necessary to sustain life). It differs from persistent vegetative state, in which the person is alive and some autonomic functions remain.

Brain death is used as an indicator of legal death in many jurisdictions, but it is defined inconsistently. Various parts of the brain may keep functioning when others do not anymore, and the term "brain death" has been used to refer to various combinations. For example, although a major medical dictionary says that "brain death" is synonymous with "cerebral death" (death of the cerebrum), the US National Library of Medicine Medical Subject Headings (MeSH) system defines brain death as including the brainstem. The distinctions can be important because, for example, in someone with a dead cerebrum but a living brainstem, the heartbeat and ventilation can continue unaided, whereas in whole-brain death (which includes brain stem death), only life support equipment would keep those functions going. Patients classified as brain-dead can have their organs surgically removed for organ donation.

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.

Cardiac arrest is preceded by no warning symptoms in approximately 50% of people. For those who do, they have non specific symptoms such as, new or worsening chest pain, fatigue, blackouts, dizziness, shortness of breath, weakness, and vomiting.

When the arrest occurs, the most obvious sign of its occurrence will be the lack of a palpable pulse in the person experiencing it (since the heart has ceased to contract, the usual indications of its contraction such as a pulse will no longer be detectable). Certain types of prompt intervention can often reverse a cardiac arrest, but without such intervention the event will almost always lead to death. In certain cases, it is an expected outcome of a serious illness where death is expected.

Also, as a result of inadequate blood flow to the brain (cerebral perfusion), the patient will quickly become unconscious and will have stopped breathing. The main diagnostic criterion to diagnose a cardiac arrest (as opposed to respiratory arrest which shares many of the same features) is lack of circulation; however, there are a number of ways of determining this. Near-death experiences are reported by 10–20% of people who survived cardiac arrest.

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.

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.

Coffin birth, also known as postmortem fetal extrusion, is the expulsion of a nonviable fetus through the vaginal opening of the decomposing body of a deceased pregnant woman as a result of the increasing pressure of intra-abdominal gases. This kind of postmortem delivery occurs very rarely during the decomposition of a body. The practice of chemical preservation, whereby chemical preservatives and disinfectant solutions are pumped into a body to replace natural body fluids (and the bacteria that reside therein), have made the occurrence of "coffin birth" so rare that the topic is rarely mentioned in international medical discourse.

Typically during the decomposition of a human body, naturally occurring bacteria in the organs of the abdominal cavity (such as the stomach and intestines) generate gases as by-products of metabolism, which causes the body to swell. In some cases, the confined pressure of the gases can squeeze the uterus (the womb), even forcing it downward, and it may and be forced out of the body through the vaginal opening (a process called "prolapse"). If a fetus is contained within the uterus, it could therefore be expelled from the mother's body through the vaginal opening when the uterus turns inside-out, in a process that, to outward appearances, mimics childbirth. The main differences lie in the state of the mother and fetus and the mechanism of delivery: in the event of natural, live childbirth, the mother's contractions encourage the infant to emerge from the womb; in a case of coffin birth, built-up gas pressure within the putrefied body of a pregnant woman pushes the dead fetus from the body of the mother.

Cases have been recorded by medical authorities since the 16th century, though some archaeological cases provide evidence for its occurrence in many periods of human history. While cases of postmortem fetal expulsion have always been rare, the phenomenon has been recorded under disparate circumstances and is occasionally seen in a modern forensic context when the body of a pregnant woman lies undisturbed and undiscovered for some time following death. There are also cases whereby a fetus may become separated from the body of the pregnant woman about the time of death or during decomposition, though because those cases are not consistent with the processes described here, they are not considered true cases of postmortem fetal extrusion.

Cardiac arrest is a sudden loss of blood flow resulting from the failure of the heart to effectively pump. Symptoms include loss of consciousness and abnormal or absent breathing. Some individuals may experience chest pain, shortness of breath, or nausea before cardiac arrest. If not treated within minutes, it usually leads to death.

The most common cause of cardiac arrest is coronary artery disease. Less common causes include major blood loss, lack of oxygen, very low potassium, heart failure, and intense physical exercise. A number of inherited disorders may also increase the risk including long QT syndrome. The initial heart rhythm is most often ventricular fibrillation. The diagnosis is confirmed by finding no pulse. While a cardiac arrest may be caused by heart attack or heart failure, these are not the same.

Prevention includes not smoking, physical activity, and maintaining a healthy weight. Treatment for cardiac arrest is immediate cardiopulmonary resuscitation (CPR) and, if a shockable rhythm is present, defibrillation. Among those who survive, targeted temperature management may improve outcomes. An implantable cardiac defibrillator may be placed to reduce the chance of death from recurrence.

In the United States, cardiac arrest outside hospital occurs in about 13 per 10,000 people per year (326,000 cases). In hospital cardiac arrest occurs in an additional 209,000. Cardiac arrest becomes more common with age. It affects males more often than females. The percentage of people who survive with treatment is about 8%. Many who survive have significant disability. Many U.S. television shows, however, have portrayed unrealistically high survival rates of 67%.

After ingestion, toxic features usually develop within a few minutes. The major lethal consequence of aluminium phosphide ingestion is profound circulatory collapse, and is reportedly secondary to these toxins generated, which lead due to direct effects on cardiomyocytes, fluid loss, and adrenal gland damage. The signs and symptoms are non-specific, dose dependent and evolve with time passing. The dominant clinical feature is severe hypotension refractory to dopamine therapy. Other features may include dizziness, fatigue, tightness in the chest, headache, nausea, vomiting, diarrhoea, ataxia, numbness, paraesthesia, tremor, muscle weakness, diplopia and jaundice. If severe inhalation occurs, the patient may develop acute respiratory distress syndrome (ARDS), heart failure, arrhythmias, convulsion and coma. Late manifestation include liver and kidney toxicities.

The diagnosis of AAlP usually depends on the clinical suspicion or history (self-report or by attendants). In some nations, tablets of AlP are also referred to as "rice tablets" and, if there is a history of rice tablet ingestion, then it should be treated differently from other types of rice tablets that are made up of herbal products. For a silver nitrate test on gastric aspirate, diluted gastric content can be positive.

Holiday heart syndrome is an irregular heartbeat pattern presented in individuals who are otherwise healthy. Coined in 1978 the term is defined as "abnormal heart rhythms sometimes following excessive alcohol consumption; usually temporary".

Holiday heart syndrome can be the result of stress, dehydration, and drinking alcohol. It is sometimes associated with "binge drinking" common during the holiday season. The condition can also occur when individuals consume only moderate amounts of alcohol.

Irregular heartbeats can be serious. If palpitations continue for longer than a few hours patients should seek medical attention. Some arrhythmias associated with HHS after binge drinking can lead to sudden death, which may explain some of the sudden death cases commonly reported in alcoholics. Atrial fibrillation is the most common arrhythmia in holiday heart syndrome. Symptoms usually resolve themselves within 24 hours.

Holiday heart can also cause abnormal burning sensation whilst urinating and/or the feeling of passing blood similar to a kidney stone. This generally subsides in days or weeks.