Unexpected Death: Causes and Contributing Factors
[you are now on Dr. Shaw's personal
In the world of medical examiners, coroners, and
pathologist involved in forensic autopsies, "sudden death" does not necessarily mean instantaneous death.
This outline is an outgrowth of the category referred to as SIDS (sudden infant death
syndrome). I suppose that one could say we are talking about deaths "in less than 24 hours". But the implication is of a rapid
and unexpected death...mostly unwitnessed...and without obvious cause when the body was
found. I offer the following, not as an expert on all of them, but as a semi-comprehensive list just so that there might be a file
available to the public to indicate how many possible causes there are for sudden unexpected death.
In evaluating death, we must keep in mind that the dead body is a static (as with a single still photograph or pic "snapshot") and not a dynamic (as with a video portraying changing conditions) representation of the state of health at the moment of death. And, that whole postmortem situation is tainted with any number of (1) agonal (things changing during the dying process) and (2) postmortem (after death) artifacts. Therefore, I would tell you that courtroom and television or movie representation of forensic death investigation has been made to seem to have more exactitude than is truly possible. In a large number of situations, there must be "common sense" consideration of all circumstantial factors and evidences. Then, an intelligent execution of a mix of the art and science of death evaluation is made.
I. PRIMARILY CARDIAC-ABNORMALITY
DEATHS: Keep in mind that trauma or
metabolic vacillations of acute and chronic illness superimposed on significant cardiac
lesions can trigger acute or chronic electrical or mechanical decompensation and
1. Epicardial Coronary Artery Abnormalities:
A. Coronary Atherosclerosis:
- Chronic...segmental or
- Acute myocardial
atherosclerosis with chronic changes in myocardial parenchyma.
- Constriction of
Congenital abnormalities of coronary arteries:
- Anomalous origin from
- Other type of
coronary AV fistula.
- Origin of left
coronary artery from right sinus of Valsalva.
- Origin of right
coronary artery from left sinus of Valsalva.
- Hypoplastic or
aplastic coronary arteries.
Other coronary problems:
- obstucting/stenosing ostial mural folds
("flutter valve-like"), calcific spurs or constrictions, or partial orcircumferential intimal webs (FA-06-90).
- aneurysm with rupture
D. Coronary artery
embolism or thrombosis from:
- Thrombosis over an artery lesion.
- Aortic or mitral
- Prosthetic aortic or mitral
- Abnormal native valves or left-sided mural
- Polyarteritis nodosa, progressive systemic
sclerosis, giant cell arteritis.
- Mucocutaneous lymph node syndrome
(Kawasaki's disease) with arteritis, then aneurysms.
- Syphilitic coronary ostial
- Focal/segmented arteritis, NOS (A80-547,
mechanical obstruction of coronary arteries:
- Ulceration of an atherosclerotic
- Coronary artery dissection in Marfan's
- Coronary artery dissection in
- Prolapse of aortic valve myxomatous polyps
into coronary ostia.
- Dissection or rupture of sinus of
- Coronary vasospasm: especially if on
cocaine; even transmural infarcts without apparent coronary lesions (American Heart J. 88:219,
- Occult trauma to a normal-appearing
- Mural thickening due to metabolic deposits
or intimal proliferation (JAMA 231:952, 1975):
Juvenile intimal sclerosis (idiopathic arterial calcification of
Intimal hyperplasia associated with contraceptive steroids or with postpartum
Coronary fibrosis associated with radiation therapy.
2. Endomyocardial coronary artery perforating
B. mural thickening arteriolopathies.
3. Hypertrophy of Ventricular
A. Left ventricular hypertrophy associated with chronic
stenosing coronary atherosclerosis.
B. Hypertensive heart disease without significant coronary
atherosclerosis (be especially careful to view
heart weight in view of the body
C. cardiomyopathy of morbid obesity: (relative cardiomegally
[heart to total body wt. ratio normal], LV
dilation, and myocyte hypertrophy in absence of
interstitial fibrosis); 50% = sudden cardiac death.
D. Hypertrophic myocardium secondary to valvular heart
E. Hypertrophic cardiomyopathy (HCM): by late 2001, some 10
genes have been noted in association with
HCM...afflicting 1/500 adults.
F. Primary or secondary
pulmonary hypertension (remember, they can be found dead before there is that much increase in RV thickness; so need lots of lung
sections to rule this out):
- Advanced chronic right ventricular
- Pulmonary hypertension in
4. Myocardial Diseases and Heart
A. Chronic congestive heart failure:
- Idiopathic cardiomyopathy (A90-893,
- Post-myocarditis cardiomyopathy
- Chronic CHF, NOS: and don't overlook
additional causes of high-output failure such as occult shunts (Paget’s disease of bone can do
B. Dilated cardiomyopathy: Do to
practically any of the above or below influences on the heart muscle, the
heart enlarges, then the chambers dilate (etiologies:
idiopathic, inflammatory, metabolic, genetic, toxic,
peripartum, infiltrative, hypersensitivity,
arrhythmogenic, and rheumatologic).
C. Acute cardiac failure:
- Massive acute myocardial
- Acute or chronic myocarditis (A-02-1,
- Acute alcoholic cardiac
- Ball-valve malfunction in aortic stenosis
- Mechanical disruptions of cardiac
- Rupture of ventricular free wall.
- Disruption of valvular apparatus:
- Acute pulmonary edema in noncompliant
- Myocardial bridging - is supposedly fairly
common at autopsy, being mostly in the left coronary, the first 10 to 20 mm. Deaths ascribed
mostly when also involves the posterior circulation (average death is a 31 year old, with or
without associated physical activity or excitement) or associated with some other lesion in the
(anterior versus posterior) opposite coronary system. The thicker the bridge, the more likely
- Infarction associated primarily with
oxygen “supply-demand” disproportion (JAMA 231:952, 1975):
Aortic stenosis, all forms [FA13-129].
Incomplete differentiation of the aortic valve.
Carbon monoxide poisoning.
- Miscellaneous odd infarctions (JAMA
AMI with normal coronaries.
5. Inflammatory, Infiltrative Neoplastic, and Degenerative
A. Acute viral myocarditis with or without ventricular
B. Myocarditis associated with the
D. Progressive systemic sclerosis.
E. Amyloidosis (A78-350).
F. Hemochromatosis (FA91-607).
G. Idiopathic giant cell myocarditis.
H. Senile myocardium: usually a small heart & myocardium
soft (elderly person found dead of "old age")
J. Arrhythmogenic right ventricular (fatty) dysplasia (ARVD) cardiomyopathy [as opposed to
more ordinary fatty infiltration]: ARVD tends to be fatty change out of all proportion to
the body weight or usual epicardial fat and involving into the myocardial interior...focally transmural...myocardium] (A79-451,
FA-94-57, FA-95-9, FA-95-36, A-01-2, FA-01-72, A10-10, FA10-196, FA13-195). Some 85% of diagnoses of ARVD are made only at
the time of sudden unexpected adult death.
K. Neuromuscular diseases (e.g., muscular dystrophy, Friedreich's ataxia,
myotonic dystrophy) (FA-94
L. Intramural tumors:
Primary benign or
M. Obstructive intracavitary tumors:
- Neoplastic - benign or malignant.
- Thrombotic - enlarging chronic
- Chronic lymphocytic myocarditis: this can
be very subtle and may require numerous cardiac sections in order to locate at least several
microscopic foci of lymphocytic infiltrates (FA86-261, FA91-605, FA91-631,
- Myxoid heart syndrome: mucosubstances in
conduction system, valves, etc. (See I,5,c.); a forme frustMarfan's [Nat'l Marfan's Foundation]
- Intramural arteritis, NOS (A82-655) or
other arterial occlusions.
- Hurler's (and other similar storage
disease) syndrome (gargoylism): accumulation of mucopolysaccharide in RES
- Fabray's disease: foamy accumulation in
smooth muscle, endothelial and perithelial cells.
- Pompe's disease: excessive glycogen
storage in heart muscle.
- Look for signs of other storage
6. Diseases of the Cardiac
A. Valvular aortic stenosis/insufficiency.
B. Mitral valve disruption, see above.
C. Prolapse of myxoid, floppy mitral valve having
accumulation of acid mucosubstances.
E. Prosthetic valve dysfunction.
7. Congenital Heart Disease:
- Congenital aortic or pulmonic valve
- Right-to-left shunts with Eisenmenger’s
> Advanced disease.
> During labor and delivery.
- After surgical repair of congenital
lesions; e.g., tetralogy of Fallot.
- CHARGE Syndrome (the Foundation) [note the
coloboma...abnormal eye pupil shape...plus various cardiac defects]
A. Abnormalities of the electrical conducting
- Fibrosis of the His-Purkinje
Primary degeneration (Lenegre's disease).
Secondary to extension of fibrosis and calcification from the mitral valve ring/"cardiac
skeleton" (Lev's disease).
Post-viral conducting system fibrosis.
Hereditary conducting system disease.
B. Prolonged Q-T interval
syndromes [2/3's have history of fainting/syncope] (SADS Foundation):
- With deafness.
- Without deafness.
3. Romano-Ward syndrome: sudden childhood deaths or death at
any age on induction of anesthesia.
- Drug effect.
- Electrolyte abnormality [FA10-160, which was actually accidental!].
- Toxic substances.
- CNS injury.
5. Idiopathic ventricular
fibrillation (does not cause heavy lungs if happens abruptly and not super
imposed on another CHF event):
- Absence of identifiable structural or
functional causes, even with extensive sampling of conduction system
- Sleep-death in refugees of Southeast Asia,
9. Electrical Instability Related to Neurohumoral and Central
Nervous System Influences:
A. Catecholamine-dependent lethal
B. Central nervous system related:
- Psychic stress, emotional extremes:
- psychiatric deaths:
psychosis..."acute exhaustive mania".
- Neuroleptic malignant syndrome.
- Phenothiazine-related arrhythmias.
- Auditory/sight related...scared to death by noise/startling
- "Voodoo" death in primitive cultures.
- Diseases of the cardiac nerves.
- Congenital Q-T interval prolongation.
II. SUDDEN INFANT DEATH SYNDROME (SIDS)
AND SUDDEN DEATH IN CHILDREN:
1. Sudden infant death syndrome:
- Immature respiratory
- Susceptibility to
lethal arrhythmias for uncertain reasons.
- Congenital heart
- Fatty liver,
2. Sudden death in
- Eisenmenger syndrome:
aortic stenosis, hypertrophic cardiomyopathy, pulmonary atresia.
- Uhl's anomaly : focal or complete severe
thinning of right ventricular non-septal myocardium.
- After corrective surgery for congenital
- histiocytoid cardiomyopathy: genetic
aberration causes presence of enlarged foamy cells & granular (excess mitochondria)
cardiocytes (cardiac myocytes) & tends to be female infants.
- Acute laryngotracheobronchitis without
croup history [FA09-9].
- "Overlying"/bed-clothing suffocation: (1)
prone sleeping...blanched postmortem skin around mouth & nose while lividity is elsewhere
in the prone position hints at a type of auto-suffocation as the baby's head bobs and lands
face down in thick soft covers or pillow; BUT, it does not rule out a cleverly set up homicide.
By the same token, prone lividity with blanched contact spot on cheek or side of face does not
rule out bobbing auto-suffocation with a terminal, agonal seizure that turns the head to the
side. (2) a parent or other large person who is impaired or maybe a fitful but very deep
sleeper can miss and "overly" an infant and suffocate it.
- Reye's syndrome: liver may not be grossly
- Occult carbon monoxide poisoning: consider
circumstances and note the bright red postmortem blood, being also relatively bright red even
after formalin fixation.
- Homicidal/accidental: suffocation; chest
wall compression; shaken infant; neglect...dehydration;hypothermia/hyperthermia.
- pulmonary aspiration of gastric contents
with laryngospasm while ill with something else (FA10-147).
III. SUDDEN DEATH in PREGNANCY/POSTPARTUM:
any of those already noted; and...
- ruptured ectopic
pregnancy with sudden massive hemorrhage (FA10-44)
- toxemia (usually before/beginning of
cardiomyopathy (usually postpartum)
- ruptured Berry
- amniotic fluid
- acute fatty liver of
- pulmonary embolism
especially SS & SC.
- thrombophilia with
PE or arterial thrombosis (cardiac or CNS).
- Sudden death during
extreme physical activity (such as in military recruits [JAMA 256:2696, 1986]; sometimes the
exertion is not extreme [JAMA 225:1319, 1973]; intense football practice in those with sickle-cell
trait (Mike Bianchi, The Orlando Sentinel, & in The State newspaper 7/20/08 page C12);
otherwise healthy persons being acutely restrained and struggling...acute metabolic
acidosis; personally intentional over-exertion in the heat to "sweat off" weight [FA10-160].
- Agitated delirium
(violently combative, out-of-control reaction): often in a setting of drug use such as cocaine,
amphetamines, etc. (invariably febrile...40.2 degrees C. average...and 2/3rds die @ scene or
during transport; if to hospital, complicated by rhabdomyolysis, DIC, renal
interferences with venous return:
Acute cardiac tamponade.
Massive pulmonary embolism: obese lady with necrotic, infected submucosal
- Dissecting aneurysm
of the aorta.
Electrolyte disturbances: [FA10-160...a 60+ year old man has become determined to lose weight and decides to do it by working out in the heat of the day and/or in the gym and at home and sweating the weight off. The autopsy was without evidence of disease. An arrhythmogenic electrolyte abnormality...accidentally induced by extreme exercise to sweat weight off was left as the presumed cause of death...making it an accidental death. ].
Proarrhythmic effects of anti-arrhythmic drugs.
Proarrhythmic effects of noncardiac drugs.
Be on the lookout for acetaminophen-induced central lobular hepatic
Diabetic: the first "diabetic attack" can be the last (postmortem
urinalysis; look for the Armanni-
Epstein renal lesion).
Insulin overdose (FA07-38).
Polypharmacy and/or single-medication overdose.
Endocrine "storms" or deficits.
> hypo- or hyperthyroidism
> hypo- or hyperparathyroidism: hyper (FA08-47)
acute septic hemorrhage:
relative adrenal insufficiency in
assoc. with other highly stressful disorders
- Mimics of sudden
"Cafe coronary"...choking on food.
Acute alcoholic states ("holiday heart").
Acute asthmatic attacks, primarily bronchospasm with relatively little mucus
plugging & may require lots of lung sections to diagnose if is a "first asthmatic attack".
"Seasoned" asthmatics will usually create quite a stir and be nearly hysterical if they begin
to have restricted breathing that is non-responsive...if it is possible to alert anyone, depend
on them to do it. People with an asthmatic background can die of other causes and non-natural
manners of death...suspect this when no evidence of agitation in the scene
Air (look for air in atria and/or pulmonary arteries) or amniotic fluid
embolism (note squames in pulmonary circulation). But, remember that a little air or amniotic
fluid is not an obligatory killer!
- Acute Septicemia
(some found dead & no real complaints):
I autopsied a 12 year old boy who went to bed with a sore throat; found dead
the next morning; autopsy essentially negative; postmortem blood culture was positive for group
A strep (FA-85-157).
(A-81-617) An 86 year old man dies in 12 hours, jaundiced with fever:
undiagnosed bile duct cancer obstruction (emergency surgery could not find it). Undiagnosed
colon cancer perforated (FA07-28).
(FA-02-14) A 63 year old male dies at home in 24 hours with flu-like onset;
we found an acute bacterial abscess of unknown etiology.
People who have lost their spleens (FA-95-12), even if vaccinated because of
it, are liable to odd infections from such as dog bites (the CDC DF-2
(FA11-7) A 36 y/o male may have had slight fever before bedtime & found
dead in bed next morning. Autopsy found infected cholesteatoma & associated brain abscess
(multiple anaerobe bacteria). In retrospect inquiry with his dad, he'd had a bad headache
Some other of our septic-type case examples are HERE.
- Acute anaphylaxis:
try to retain frozen serum at 20 degrees C to test for elevated blood tryptase and
allergen-specific IgE...larynx need not be edematous.
causes: edema, hemorrhage, tumor (FA91-662), meningitis/encephalitis, trauma (e.g. ice-pick
stab)...these findings can sometimes be fairly subtle.
- Acute massive
polymyositis: the case I had (A98-15) took 30 days from onset (as if a flu-like illness) to
death...so is not really a sudden unexpected death (but you may find one that is even more
- Severe acute or
chronic fatty liver:
Alcoholic: possibly as terminal seizure or an effect on the prolonged QT
interval common in chronic alcoholics; DT's if negative blood alcohol; fatal dysrhythmia
(A-79-423, FA94-57): markedly enlarged (absolute hepatomegally), highly fatty,
- Homicidal asphyxia:
with or without significant drug or alcohol levels, associated with suspicious circumstances
(look carefully for tiny abrasions over the tip of the nose and for seizure-like bites of
tongue and cheek mucosa).
- One should always be
very skeptical on hearing of a multi-injury death (multiple gunshot wounds; multiple stab
wounds) being ruled as a suicidal manner of death [FA09-40]!
deaths: remember homicidal manner of death masked as accidental drownings of "high" young drug
users; carbon monoxide (particularly in the elderly) poisoning [a case
- Idiopathic seizure
disorder with CNS negative and all else negative: remember the lesions that produce syncope and
that syncope may produce seizures; everything being negative, then presume a fatal
obesity...especially where there is a history of sleep apnea and tonsil
- Senility when >90
- Electrocution: 40%
of low voltage (e.g., a lamp) cases have no burn; and, victim may even be able to walk into
another room before flipping into the terminal dysrhythmia
- Trauma with negative
Blows to the head: Forensic pathologist, Dr. Charles "Buddy" Garrett, during his time as a
Deputy Medical Examiner in Virginia, told me that he was standing next to an otherwise healthy,
relatively young male who was being booked in the police station...he became rowdy. A policy
officer popped the defendant on the back of the head with a blackjack; the defendant fell to
the floor unresponsive and could not be resuscitated. Dr. Garrett, himself, very painstakingly
performed the autopsy and could not find any evidence at all of a CNS lesion.
Blows to the chest: these can induce a terminal lethal dysrhythmic
When primarily laryngospasm, there can be negative findings of nothing more
While many experts consider that there are no specific markers of drowning,
there can be homicidal and suicidal drownings are set up to seem accidental [check out
Soft foods stuck in the posterior pharynx in the elderly, infirm, or
Food/material obstructing, but removed during transport or by resuscitating
personnel (medical examiner subsequently not informed of this)...autopsy seems
Prolonged chest compression: such as when apprehended by many people in a
crowd; a person compressed in a wreck.
Positional asphyxia (such as someone who is passed out drunk with a
tracheostomy and the chin occludes the stoma); or an obese person fainting or passing out
Gastric contents aspiration: not infrequently being a lethal secondary event
(laryngospasm?) triggered by trauma in a "high"/intoxicated individual
Post obstruction pulmonary edema (POPE): this can happen postoperatively
following extubation and onset of an episode of acute laryngospasm and attempts by the patient
at respiratory inspiration against a closed glottis (high negative intrathoracic pressure)...or
any other mechanism that acutely closes the glottis. The subject has quick onset of foaming
reddish frothy pulmonary edema. [FA-04-87].
- Pulmonary artery
Common pulmonary emboli, see above.
Carcinomatous (A91-911) diffuse micro-occlusions and other types of
occlusions not readily visible to the naked eye exam.
- Occult severe
chronic liver disease:
Other metabolic derangements.
- Sudden Adult Death
Syndrome: A complete autopsy with toxicology of a death without suspicious circumstances fails
to find a cause (FA08-133). Many pathologists in both coroners' & medical examiners'
systems write many of these type cases off as a cardiac death due to fatal arrhythmia. But, the
real truth is simply that a cause of death that a select group of seasoned pathologists would
agree upon is NOT found. Society cannot deal with this "truth"; therefore, a "cause" is given.
I estimate about 100 per year in S. C. and at least about 1500 cases per year in the
- Sheppard, MN, "The fittest person in the morgue?", Histopathology 60:381–396, 2012.
check out Autopsy/forensics page
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(this file begun 7 April 1995; posted 7 Sept.
1998; latest addition July 2013)