Burns and sudden death

Burns and sudden death

1. BURNS and
sudden
death
MOHAMMAD TAILAKH

2. Definition
Burns are a result of the effects of thermal
injury on the skin and other tissues
Human skin can tolerate temperatures up to
42-44
0
C (107-111
0
F) but above these, the
higher the temperature the more severe the
tissue destruction
Below 45
0
C (113
0
F), resulting changes are
reversible but >45
0
C, protein damage
exceeds the capacity of the cell to repair

3. Classification According to Depth
First-degree Burns (mild): epidermis
Pain, erythema & slight swelling, no blisters
Tissue damage usually minimal, no scarring
Pain resolves in 48-72 hours
Superficial Second-degree Burns: entire epidermis &
variable dermis
Vesicles and blisters characteristic
Extremely painful due to exposed nerve endings
Heal in 7-14 days if without infection
Midlevel to Deep Second-degree Burns:
Few dermal appendages left
There are some fluid & metabolic effects
Full-thickness or Third-Degree: entire epidermis and
dermis, no residual epidermis
Painless, extensive fluid & metabolic deficits
Heal only by wound contraction, if small, or if big,
by skin grafting or coverage by a skin flap

4. Burn Photos
Mild Burn
2
nd
degree Burn 1 hr
2
nd
degree Burn 1 day
2
nd
degree Burn 2 days

5. Extent of Burns

6. Classification According to Extent
Mild: 10%
Moderate:
10-30%
Severe: > 30%
•Hospitalization
for > 10% of
body surface area
Anatomic
structure
Surface
area
Head 18%
Anterior Torso 18%
Posterior Torso 18%
Each Leg 14%
Each Arm 9%
Perineum 1%
Infant Rule of Nines
(for quick assessment of
total body surface area
affected by burns)

7. Kinds of Burns
Scald Burn: most frequent in home injuries; hot
water, liquids and foods are most common causes;
above 65
o
C, cell death
Flame Burn: due to gasoline, kerosene, liquified
petroleum gas (LPG) or burning houses
Chemical Burn: common in industries and
laboratories but may also occur at home; acid is
more common than alkali
Electrical Burn: worse than the other types; with
entrance and exit wounds; may stop the heart and
depress the respiratory center; may cause
thrombosis and cataracts
Radiation Burn: from X-ray, radioactive radiation
and nuclear bomb explosions

8. Burn Photos
Scald Burns Flame Burns

9. Burn Photos
Chemical (Acid) Burns
Radiation (Flash) Burns

10. Burn Photos
Electrical Burns
Entrance Wounds
Electrical Burns
Exit Wounds
Entrance wound of electrical
burns from an overheated tool
Severe swelling
peaks 24-72 hrs after
Electrical burns mummified
1
st
2 fingers later removed

11. Pathologic Features
Zone of coagulation (necrosis): Superficial area of
coagulation necrosis and cell death on exposure to
temperatures >45
0
(primary injury)
Zone of stasis (vascular thrombosis): Local capillary
circulation is sluggish, depending on the adequacy of the
resuscitation, can either remain viable or proceed to cell
death (secondary injury)
Zone of hyperemia (increased capillary permeability)

16. Burn Pathophysiology: Edema
Injured tissue  Increased permeability of entire
vascular tree  loss of water, electrolytes and
proteins from the vascular compartment  severe
hemoconcentration
Protein leakage  resultant hypoproteinemia,
increased osmotic pressure in the interstitial space
Decreased cell membrane potential cause inward
shift of Na
+
and H
2
O  cellular swelling
In the injured skin, effect maximal 30 min after the
burn but capillary integrity not restored until 8-12
hours after, usually resolved by 3-5 days
In non-injured tissues, only mild and transient
leaks even for burns >40% BSA

17. Burn Pathophysiology: Cardiac
Cardiac output decreases due to:
1)Decreased preload induced by fluid shifts
2)Increased systemic vascular resistance caused
by both hypovolemia and systemic
catecholamine release
3)A myocardial depressant factor has been
described that impairs cardiac function
Cardiac output normal within 12-18 hours, with
successful resuscitation
After 24 hours, it may increase up to 2 ½
times the normal and remain elevated until
several months after the burn is closed

18. Burn Pathophysiology: Renal
Renal blood flow and GFR decrease soon after
due to hypovolemia, decreased cardiac output,
and elevated systemic vascular  oliguria and
antidiuresis develops during 1
st
12-24 hours
Followed by a usually modest diuresis as the
capillary leaks seal, plasma volume normalizes,
and cardiac output increases after successful
resuscitation and coinciding with onset of the
postburn hypermetabolic state, and
hyperdynamic circulation

19. Burn Pathophysiology: Immunologic
Mechanical barrier to infection is impaired because
of skin destruction
Immunoglobulin levels decreased as part of general
leak and leukocyte chemotaxis, phagocytosis, and
cytotoxic activity impaired
The reticuloendothelial system's depressed bacterial
clearance is due to decreases in opsonic function
These changes, together with a non-perfused,
bacterially-colonized eschar overlying a wound full
of proteinaceous fluid, put the patient in a
significant risk for infection

20. First Aid Measures in Burns
1.Extinguish flames by rolling in the ground, cover
child with blanket, coat or carpet
2.After determining airway is patent, remove
smoldering clothes and constricting accessories
during edema phase in the 1
st
24-72 hours after
3.Brush off remaining chemical if powdered or solid
then wash or irrigate abundantly with water
4.Cover burn wounds with clean, dry sheet and
apply cold (not iced) wet compresses to small
injuries; significant burns (>15-20% BSA)
decreases body temperature which
contraindicates use of cold compress dressings
5.If burn caused by hot tar, mineral oil to remove it

21. Outpatient Management
For 1
st
and 2
nd
degree burns less than 10% BSA
Blisters should be left intact and dressed with silver
sulfadiazine cream
Dressings should be changed daily washing with lukewarm
water to remove any cream left

22. Recommendations for Hospitalization
1.Total burns >10% BSA or >2% full
thickness, halved for <2 or >40 yr
2.Hands, face, feet or genitalia involved
3.Evidence or suspicion of inhalation injury
4.Associated injuries present
5.Suspicion that burn inflicted
6.Burn is infected
7.Burn circumferential
8.History of prior medical illness
9.Patient is comatose
10.Patient or family unable to cope with
situation

23. Hospital Management
1.General assessment and
cardiopulmonary stabilization
2.Resuscitation
3.Establishment of IV lines and blood
studies
4.Wound care and infection control
5.Pain relief and psychological support
6.Nutritional support
7.Physical Therapy/Occupational
Therapy

24. Airway compromise?
Respiratory distress?
Circulatory compromise?
Intubation, 100% O
2

IV access, fluids
Multiple trauma?
Yes No
Evaluate & treat
injuries
Burns >15% or
complicated burns?
Yes
No
Burn care, tetanus prophylaxis,
analgesia
IV access;
fluid replacement
Circumferential full
thickness burns?
Escharotomy
Yes
Yes
No
No

25. Initial Procedures
Fluid infusion must be started immediately
NGT insertion to prevent gastric dilatation,
vomiting and aspiration
Urinary catheter to measure urine output
Weight important and has to be taken daily
Local treatment delayed till respiratory
distress and shock controlled
Hematocrit and bacterial cultures necessary

26. Fluid Resuscitation
For most, Parkland formula a suitable starting
guide (4 ml Ringer’s Lactate/kg body weight/%
BSA burned), ½ to be given over 1
st
8 hr from
time of onset while remaining over the next 16 hr
During 2
nd
24 hr, ½ of 1
st
day fluid requirement to
be infused as D5LR
Oral supplementation may start 48 hr after as
homogenized milk or soy-based products given
by bolus or constant infusion via NGT
Albumin 5% may be used to maintain serum
albumin levels at 2 g/dl
Packed RBC recommended if hematocrit falls
below 24% (Hgb <8 g/dl)
Sodium supplementation may be needed if burns
greater than 20% BSA

27. Inhalation Injury
Three syndromes:
1.Early CO poisoning, airway obstruction &
pulmonary edema major concerns
2.ARDS usually at 24-48 hrs or much later
3.Pneumonia and pulmonary emboli as late
complications (days to weeks)
Assessment:
1.Observation (swelling or carbonaceous material
in nasal passages
2.Laboratory determination of
carboxyhemoglobin and ABGs
Treatment:
1.Maintain patent airway by early ET intubation,
adequate ventilation and oxygenation
2.Aggressive pulmonary toilet and chest
physiotherapy

28. Infection Control
Tetanus prophylaxis: 250-500 IU TIG or 3000
units equine ATS ANST IM; Toxoid also
Antibiotic of choice is one that will include
Pseudomonas in its spectrum; most frequent
pathogens in burns are Staphylococcus aureus,
Pseudomonas aeruginosa and the Klebsiella-
Enterobacter species
Topical therapy:
0.5% Silver nitrate dressing
Mafenide acetate or Sulfacetamide acetate
cream
Silver sulfadiazine cream
Povidone-iodine ointment
Gentamicin cream or ointment

29. Pain Relief and Adjustment
Important to provide adequate
analgesia, anxiolytics and
psychological support to:
a)Reduce early metabolic stress
b)Decrease potential for posttraumatic stress
syndrome
c)Allow future stabilization and rehabilitation
Family support patient through
grieving process and help accept
long-term changes in appearance

30. Nutritional Support
Shriners Burn Institute at Galveston,
Texas Guidelines for Caloric Intake
Infants
1000 kcal/m
2
BSA burned +
2100 kcal/m
2
total BSA
2-15 years
1300 kcal/m
2
BSA burned +
1800 kcal/m
2
total BSA
Adolescents
1500 kcal/m
2
BSA burned +
1500 kcal/m
2
total BSA

31. Complications of Burns
Burn Shock
Pulmonary complications due to
inhalation injury
Acute Renal Failure
Infections and Sepsis
Curling’s ulcer in large burns over
30% usually after 9
th
day
Extensive and disabling scarring
Psychological trauma
Cancer called Marjolin’s ulcer, may
take 21 years to develop

32. Sudden death
Definition :
Unexpectedly death within 24 hrs from onset of symptoms
with or without known preexisting conditions.
In forensic view most of cases occur within minutes or even
seconds from onset of symptoms .
There are no obvious criminal or accidental causes, and
becomes of some concern to the forensic pathologist
simply because of the difficulty or even impossibility to
furnish a certifiable cause of death.
The numerous causes of sudden natural death may
conveniently be classified according to the different
anatomical systems of the body.

33. Causes of sudden death
Cardiovascular System
Respiratory System
Gastrointestinal System
Gynecological conditions
Central Nervous System
Other

34. Heart
•The heart of an adult Indian
–Male 275-300 g
–Female 225-250g
•Thickness
–Atrial wall 1-2 mm
–Right ventricle 3-5 mm
–Left ventricle 10-15 mm
•Layers of the heart
–Outer epicardium
–Middle myocardium
–Inner endocardium
•Heart enclosed by visceral and parietal pericardium

35. Heart
The Left Coronary Artery: originating from the left
aortic sinus, after a short course, bifurcates into:
–Left anterior descending which runs in the
anterior inter-ventricular groove, provides blood
to anterior left ventricle, the adjacent anterior
right ventricle and anterior two thirds of the inter-
ventricular septum
–Left circumflex branch, which runs in left atrio-
ventricular groove, supplies the lateral wall of the
left ventricle

36. Heart
The Right Coronary Artery runs in the right atrio-
ventricular groove. It usually nourishes the
remainder of the right ventricle and the postero-
septal region of the left ventricle, including the
posterior third of the inter-ventricular septum.

37. The localization of
atheroma or thrombus
Left anterior descending (left anterior inter-
venrticular) (45-64%)
•Right main coronary (45-46%)
•Left circumflex coronary (3-10%)
•Left main coronary (0-10%)

38. Heart causes of sudden
death
Ischemic heart disease :the most common cause.
Coronory atherosclerosis .
HTN
Aortic valve disease.
Cardiomyopathies.
Death in old ages.

39. Bridging
Frequent cause of sudden death
Presence of coronary blood vessels deep in
myocardium (normally : epicardium).
Myocardial contraction compromises the
coronary blood flow .

40. RESPIRATORY SYSTEM
Pulmonary Embolism
massive haemorrhage in the air passages
Pneumothorax
asthma
Chest infections :H.influanza: fulminating epiglottis
in pediatric ,
Diptheria: laryngeal obstruction.

41. GIT causes
Bleeding:
esophageal verices
PUD
CA in stomach or esopheus.
Mesenteric infraction .
Strangulated hernia.
Fulminating peritonitis.

42. GUT
Mostly related to pregnancy
Ectopic pregnancy .
Induced abortions: hemorrhage, air embolus,
tract perforation.

43. Epilepsy
Epileptic sufferers may die during a prolonged
single seizure or more usually during a series of
repeated seizures termed status epilepticus
Death is due to asphyxia if the epileptic ceases to
breathe or aspirates regurgitated vomit, or has an
airway obstructed by the tongue.