Death in Infancy and Young

Children

DATO DR ZAHARI BIN NOOR

MD(USM), DLM(Sheffield), DMJ(Lond),
MSc(Sheffield), DipForMed(Monash, FFFLM(Lond).

Ketua dan Pakar Perunding Forensik

Jabatan Perubatan Forensik
Hospital Pulau Pinang
 Classification of sudden death according to
the manner of death
Homicide often not different than as in adult, 2
broad categories those subjected to violent/often
impulsive attack. The other group where death
occurred due to premeditated acts such as
deliberate suffocation or poisoning. These cases
amy result into misdx of SIDS.
Accidental Falls from height, MVA, Drowning,
Firedeath and burns, accidental gunshot,
accidental poisoning, electrocution, sporting
accidents, Asphyxial death Cot/bed asphyxias,
Foreign body inhalation, Overlaying, aspirations.
Natural death
Sudden Natural death in Infancy &
young children
Death the occur in an infant who either been
completely well or have only been
sufferring from minor illness. If they did
have a major illness they have been thought
to be stable. (R W Byard. Sudden Death in Infancy, childhood and
adolescence.)
Usually within 24 hours from the time of onset of
symptoms to time of death.
 Three broad categories
Apparently completely well. Those who were
found dead, or unexpectedly collapse and died
within hours. Eg. Congenital Cardiac Defects,
Cerebral He, trauma, Sudden Infant Death.
Who were mildly unwell. Usually just with H/O
Low grade fever, URTI, non specific symptoms.
Eg Various infections, major problems missed,
ignored, or additive effect of an acquired disease
to a previously established abnormalities with
lethal consequences eg Anomalous heart condition
added with anemia thus decompensated.
Children with serious, but stable condition who
suddenly die eg Asthma and Epilepsy.
Incidence of Sudden Death in Young Children

Incidence is difficult to determine.

Death certificate diagnosis are known to be
inaccurate, particularly where autopsy are
not often performed in these cases.
 Common Causes of Death
Infancy SIDS or SID, Aspirations
Over 1 yr Infections, congenital anomalies and
malignancies .
Infections Pneumonia, bronchiolitis, tracheo-bronchitis,
sepsis, gastroenteritis and peritonitis. (Neuspel & Kuller, Sudden and
Unexpected Natural Death in childhood, JAMA, 254, 218-219, 1985)
Cardiovascular anomalies and infections myocarditis,
HCOM, DCM, Aortic Stenosis, Congenital Coronary
Anomalies, CHD such as TOF, Ebstein Anomaly,
Eisemenger syndrome, MVP, Conduction Defects (Klitzner
TS, Sudden Cardiac Death in Children, Circulation, 82, 629-32, 1990)
Others Epilepsy, IC Hge, Asthma (Neuspel & Kuller, Sudden and
Unexpected Natural Death in childhood, JAMA, 254, 218-219, 1985)
Less common haematologic, GIT, GUT, metabolic,
endocrine, genetic and immunological disorders
 Causes of sudden & unexpected death in infancy and childhood
Infective
Cardiac infections, congenital cardiac defects, cardiomyopathies,
vascular abnormalities (eg MVP), Subaortic stenosis, Conduction
defects, tumours, endocardial fibroelastosis.
Vascular Aortic abn (eg CoA), coronary artery abn, venous
(Total anomalous of pulmonary venous drainage), vascular
malformation, Pulmonary hypertension, others (fibromuscular
dysplasia).
Respiratory infections, Upper Airway obstruction, Asthma,
Bronchopulmonary dysplasia, miscellanous (eg idiopathic
pulmonary hemosiderosis).
CNS infections, Epilepsy, Hge, Tumours, Metabolic, Structural
abn,
Haematological Hemoglobinopathies, malignancies, bleeding
disorders, Anemia, misc (eg polycythemia)
GIT infection, intestinal obstruction, intestinal perforation,
Gastro-esophageal reflux/aspiration, GIT hge.
 GUT Primary renal disease (glomerulonephritis),
Urinary tract obstruction, Wilms tumour, HUS.
Metabolic Reye syndrome, Fatty acids oxidation defects
( eg MCAD), carbohydrate disorders (eg galactosaemia),
AA disorders (eg homocystinuria), Ura cycle disorders,
Organic acids disroders.
Endocrine congenital adrenal hyperplasia, Diabetes
mellitus, Thyroid disease.
Miscellaneous Connective tissue disorders (eg Marfan),
Chromosomal disroders (eg trisomy 21), skeletal disorders
(eg achondroplasia), Dermatological disorders ( eg
hypohydrotic ectodermal dysplasia), muscular conditions
(eg malignant hyperthermia), Immunological disorders (eg
anaphylaxis).
Unknown Sudden infant death syndrome or sudden death
in infancy.
 Common Causes of Infectious Conditions
Pneumonias
Airway Infections incl epiglottitis
Meningitis
Septicaemias
Viral Myocarditis
Gastro enteritis
(Royal Adelaide Hospital Autopsy Series over 30 years, 1965-1995)
Types of possible infections associated with sudden paediatric death
Cardiovascular myocarditis, rheumatic fever,
endocarditis, aortits, arteritis
Respiratory Retropharyngeal abscess,
epiglottitis, Acute LTB, bacterial tracheitis,
diphtheria, Acute bacterial pneumonia,
bronchiolitis
CNS meningitis, encephalitis, poliomyelitis
GIT AGE, primary peritonitis, botulism, hydatid
disease
GUT pyelonephritis
Generalized Septicaemia, viraemia,
endotoxaemia
Haematological dengue, malaria
(R W Byard. Sudden Death in Infancy, childhood and adolescence.1990)
 Cardiovascular Causes
Congenital cardiac defects that may cause
sudden death include TOF, Ebstein
Anomaly, Eisemenger syndrome, TGA
(Klitzner TS, Sudden Cardiac Death in Children, Circulation, 82, 629-32,
1990).
The TOF & TGA are assoc with post surgical sudden
death in apparantly stable children (Verter VF, Sudden death in
infants, children and adolescence, Cardiovasc Clinic 75, 313, 1985).
Mitral valve prolapse (24%) with or without aortic
stenosis.
Exercise related sudden death in childhood is most likely
to be cardiovascular in origin. HCOM, RV dysplasia.
Conduction Defects difficult to dx, esp. with no available
pre-collapse ECG.
Coronary anomalies congenital or acquired as in
Kawasakis.
Arrythmogenic RV Dysplasia
 Cardiovascular - Myocarditis
Infectious causes of Myocarditis
Viruses Coxsackie A & B, ECHO, polio, influenza
A&B, CMV, mumps, rubeola, rubella, EB, adenovirus,
varicella-zoster, variola, vaccinia, hepatitis B, yellow fever
Chlamydia C. psittaci, C. pneumoniaea
Rickettsia R. typhi, R. tsutsugamushi
Mycoplasma M. pneumoniae
Bacteria Corynebacterium diphteriae, Salmonella,
Brucella, sterptococci, staph, Clostridium perfringes, N
Meningitidis, Borella burgdorferi
Fungi Aspergillus, Candida, Blastomyces, cryptococci,
coccidiodomyses
Protozoa Typanosoma, toxoplasma
Metazoa Trixhinella, Echinococcus

(Adapted from Cotran, Kumar & Robbins, 1991)

Pathological features of Myocarditis

Heart increase in weight and size with dilated chambers.

Pale discoloured myocardium.
Histopathological dx inflammatory cell infiltrate with
myocyte necrosis.
Inflammation varies from focal to widespread myocyte
necrosis with florid interstitial inflammatory infiltrates
composed of lymphocytes, eosinophils or neutrophils.
Others are myocyte hyperthrophy, interstitial fibrosis with
scarring, giant-cells in degenarating myocytes
The extent of myocaridal damage may occasionally be out
of proportion to the relatively unimpressive clinical
symptoms
Acute viral myocarditis

The interstitial
lymphocytic infiltrates
shown here are
characteristic for a viral
myocarditis, which is
probably the most
common type of
myocarditis. Many of
these cases are probably
subclinical. Some may be
a cause for sudden death
in young persons. There
is usually little necrosis.
The most common viral
agent is Coxsackie B.
 Rheumatic Fever
Rheumatic fever is a rec febrile illnes of childhood
characterized by SC nobules, wrthema marginatum,
chorea, migratory polyarthralgia and carditis.
Follows Group A streptococci immunologicalrxtn
between tissues and streptococci
Pathological features heart elarged with dilated
chambers, vegetations (bead like) along the valve leaflets.
Histological Aschoff Bodies round to oval nodules
with central fibrinoid degenarations and a surrounding rim
of cardiac histiocytes. Anitschkow cells oval vesicular
nuclei with centrally aggregated ribbons of chromatin.
 Endocarditis
Tend to occur as a complication of underlying
defects such as TOF, LV outflow obstructions or
ductus arteriosus with or without corrective
surgery..
Also occurs in children who have had rheumatic
fever.
Assoc with sepsis elsewhere or those with
indwelling vascular catheters.
Causes 70% Staph aureus or streptococcus
viridans
 Aortitis

Bacterial infection may involve the aorta in

areas of flow disturbance such as
coarctation of aorta.
Death usually from rupture of the eroded
vessel wall.
 Respiratory Conditions
Most common non infectious causes Upper
airway obstruction due to narrowness of the
airways in younger age grp eg choanal narrowing,
lingual thyroglossal duct cysts, choriostomas of
the upper airway & structural defects (eg laryngo-
tracheal malacia)
Asthma sudden death is a well recognized
complication, can be due to status asthmaticus,
arrtyhmias, hypokalaemia or asphyxia.
 Respiratory infections
Respiratory Retropharyngeal abscess, epiglottitis, Acute LTB,
bacterial tracheitis, diphtheria, Acute viral/bacterial pneumonia,
bronchiolitis
Retropharyngeal abscess following a penetrating injury to the
posterior pharyngeal wall, sequelae of pharyngitis or tonsillitis. Death
from Obstruction of the airway.
Acute epiglottitis death from upper airway obstruction. Autopsy
red, swollen edematous epiglottis, marked submucosal edema, acute
inflammation & surface ulceration. Blood C& S essential (50 75%
positive)
Acue LTB most cases in form of epidemic croup due to parinfluenza
& influenza viruses. Death from Upper Airway obstruction.
Occasionally secondary bacterial infections with staph. Aureus
producing thick pseudomembranes causing upper airway obstructions.
 Diphtheria Corynebacterium diphtheriae,
unvaccinated children, exotoxin causing
epithelial inflammation & necrosis with
formation of an inflammatory
pseudomembrane composed of necrotic
mucosal cells & debris. Death Acute
Airway Obstruction due to impaction of
dislodged pharyngeal pseudomembranes in
the lower airway or cardiac damage from
the exotoxin.
 Acute bacterial pneumonias
In children the most common serious lower respiratory
infection is acute lobar pneumonia due to Strep pneumoniae
(90%).
Lungs lobar or brochopneumonia
Lobar confluent areas of consolidation.
Bronchopneumonia mottled with scatttered areas of patchy
consolidation.
On cut section discrete, pale and firm areas of consolidation
through out the lungs.
Histological alveoli filled with neutrophils, fibrin & necrotic
debris. In bronchopneumonia the acute inflammatory infiltrate
is bronchocentric. In lobar pneumonia the stage if red
hepatization is marked microscopically by extravasation of
RBCs into confluent alveoli filled withpus. This progress to
the stage of grey hepatization as the inflammatory & RBCs
disintegrate. Tissue and Blood C&S essential, although
antibiotic rx may give negative result.
Acute bronchopneumonia in

At medium power
magnification, numerous
neutrophils fill the alveoli
in this case of acute
bronchopneumonia in a
patient with a high fever.
Pseudomonas aeruginosa
was cultured from sputum.
Note the dilated capillaries
in the alveolar walls from
vasodilation with the acute
inflammatory process.
Viral Pnuemonia in a child

Scattered giant cells with

a scant mononuclear
interstitial infiltrate are
seen. The pink, rounded
intracytoplasmic inclusion
in the giant cell of the
inset at the upper right is
typically seen with
respiratory syncytial virus
(RSV), a common cause
for pneumonia in infants
and children under 2
years of age.
 Central Nervous System Causes
CNS causes incl. epilpesy, ic Hges & tumours.
There are no pathognomonic features of epilepsy.
To dx Arnold Chiari Malformations req. special techniques
SC dissesction.
CNS meningitis, encephalitis, poliomyelitis
Meningitis Inflammation and pus in the meninges. PMN
cells infiltrate of the meninges and CSF cloudy. Bilateral
adrenal gland hges, Inflammation of the meninges may not
be apparent on inspection due to rapid onset of the clinical
course. CSF Cultures maybe negative with prior antibiotic
Rx. Death from septicaemia and/ meningitis.
 Encephalitis - Viruses may infect the
substance of the brain resulting in
inflammation, necrosis & edema.
Poliomyelitis death occur from respiratory
paralysis which may be sudden mimicking
SIDS. Autopsy usually non specific on
microscopy destruction of motor neurons
particularly of the anterior horns of the
spinal cord.
 GIT Causes
GIT usually infectious, rarely intestinal obstruction due to
intussuseption or volvolus. Late prsenting diaphragmatic hernias.
AGE Autopsy features are
Marked dehydration sunken eyes, depressed fontanelle in infants,
decreased skin turgor, dry mucous membranes & internal organs.
Depressed fontanelle more clearly seen by deflecting the scalp.
PM Vitreous fluid for Na (> 155mol/l), Cl ( > 135mmol/l) and
Urea (> 40 mmol/l).
Cause of sudden death may also be due to hyperkalaemic cardiac
arrythmia or cerebral he or infarction from venous thrombosis.
Botulism infantile botulism, sudden death due to neurotoxin that
interferes with respiration.
Primary peritonitis H/O diarrhea & vomiting, acute prostation
prior to sudden death. Purulent ascitic fluid with no demonstrable
focus of infection.
 Genitourinary Causes

Very rarely non infectious cause UT

obstruction, glomerulonephritis, Wilms
tumour embolism.
Pyelonephritis H/O Fever, loin pain.
Sudden death is rare and unusual, if present
may be parental inatention or
underestimation of severity by doctor.
 Other conditions
Metabolic Reye syndrome, Fatty acids oxidation defects ( eg
MCAD), carbohydrate disorders (eg galactosaemia), AA disorders (eg
homocystinuria), Ura cycle disorders, Organic acids disroders.
Endocrine congenital adrenal hyperplasia, Diabetes mellitus, Thyroid
disease.
Miscellaneous Connective tissue disorders (eg Marfan),
Chromosomal disroders (eg trisomy 21), skeletal disorders (eg
achondroplasia), Dermatological disorders ( eg hypohydrotic
ectodermal dysplasia), muscular conditions (eg malignant
hyperthermia), Immunological disorders (eg anaphylaxis).
Septicaemia usually secondary to other foci of infection. Autopsy,
focus of infection may be present. In the absent of history of
antemortem sepsis, the dx must be by positive blood cultures with
disseminated sepsis with isolation of organism from multiple
sites.Histological evidence include areas of localized acute
inflammation, he and intravascular fibrin thrombi from DIVC.
Endotoxaemia
Viraemia
Immunodeficiency states congenital or acquired
 Sudden Infant Death Syndrome
SDS sudden death in infant under 1 yr age which
remains unexplained after a thorough case ix,
includiing autopsy, death scene examination &
review of clinical history.
Difficult, important is dy/dx this condition where
no autopsy features from cases where death due to
oganic disease, or to accidental or inflicted injury.
Remains one of the major causes of unexpected
infant death in Western countries.
 Death scene to exclude accidental cause eg wedging and
full autopsy needed to rule our organic causes.
SIDS cannot be dx unless complete full autopsy has been
conducted.
Cases that have been dx as SIDS in the past may have to
be re evaluated if further evidence is forth coming
concerning eg dangerous sleeping position or faulty cot
that may result into accidental suffocation, unknown
diseases or adult who may later admitted to inflicting fatal
injury or further infant death in the family.
However in majority of cases the COD will not be found &
fatality will be attributed to SIDS.
But in our local situation often dx of SIDS cannot be made
because the above criteria cannot be fulfilled, in this
situation the COD will probably end up as Sudden Natural
death in infant with cause undetermined.