ASSIGNMENT FOR FSIC 312 Wounds and its Medico -

Legal Aspects

SUBMITTED BY: SUBMITTED TO :

Simran Singh Dr. Amarnath Mishra
Enrollment No. A5905914022 Asst.Professor
B.Sc (Hons) Forensic Science
Group 1
Semester 6
AIFS
2014-2017
 INJURIES DUE TO HEAT OR HYPERTHERMIC INJURIES
Hyperthermia can cause systemic as well as localized injuries to the body. A delicate balance
between heat loss and heat dissipation maintains thermal homeostasis. To maintain it both
environmental and internal heat of the body are involved. Internal heat is generated by the
oxidation of heat produced during rest that is the basal metabolism of the body.
Environmental heat comes from the sun and its effects are influenced by:
i. Moisture content of the air
ii. By its wavelength
iii. Spectral distribution
iv. Absorption by ozone and dust
v. Reflection and absorption by skin
vi. Clothing worn by the individual
Both the internal and environmental heat is measured in calories. A calorie represents the
quantity of heat needed to raise a kilogram of water from 0 C to 1C.
Exogenous or No Febrile Hyperthermia
The human body reacts to an environmental elevation of temperature by reducing thermo
genesis and by increasing heat dispersion. Thermo genesis is decreased by reduction of
metabolic rate to the minimal required for the vital functions and thermo dispersion is
achieved by:
(i) peripheral vasodilatation
(ii) profuse sweating
(iii) evaporation converting sweat to water vapour.
All these factors are affected by the high humidity and lack of air movement. The diseased
states due to the effect of excessive heat are divided in to four categories in progressive
order of severity:
Heat cramps
Heat exhaustion
Thermogenic anhydrous
Heat stroke.
Heat Cramps (Boilers room, Miners cane cutters)
The painful spasm of the voluntary muscles especially of the extremities and abdominal wall
is produced during or after physical activity in a hot environment. The predisposing factors
such as ill health and intake of alcohol result in depletion of salt that are the main causes of
heat cramps.
The cramps are severe, paroxysmal and affect the muscles of legs, arms and abdominal wall.
Flushing of face and dilatation of pupil occurs. Administration of physiologic saline brings
about dramatic relief. Prophylactically, salt tablets can be used to combat heat cramps.
Heat Syncope
Heat syncope is a circulatory phenomenon induced by posture and/or exercises.
Heat Exhaustion
Heat exhaustion results from dehydration and salt depletion producing the following
symptoms:
(i) intense thirst
(ii) nausea, vomiting and headache.
(iii) mental fogginess
(iv) dizziness
(v) irritability
(vi) incapability to work
(vii) fainting
(viii) peripheral vascular collapse
(ix) sweating
(x) temperature may or may not rise
(xi) skin is not dry
(xii) oliguria
(xiii) death results from heart failure.
Thermogenic Anhydrous
Thermogenic anhydrous is also known as Desert syndrome or Anhydrite heat exhaustion. It
occurred in some soldiers who were separated during the summer in American desert. The
features are most likely that of heat exhaustion.
After profuse generalised sweating for several days perspiration ceases suddenly in all parts
of the body below the neck region and persists in face and neck. Eruption of prickly heat
rash is seen known as miliria profunda. The condition is not uncommon in Bengali children,
tanker personnel reforming from Persian Gulf. There is no suitable explanation for this.
There is hyperkeratotic plugging of sweat glands leading to functional failure of sweat
apparatus or a combination of both.
Heat Stroke
In heat stroke, there is complete absence of sweating and the body temperature is raised to
106F or 41C. In the environmental heat stress, absence of any other cause of pyrexia
constitutes heat hyperpyrexia. Several workers have pointed out that heat stroke can occur
at lower temperatures also. At a temperature of 32 C with 100%, humidity may lead to
heat stroke. The features of heat stroke include hot and dry skin, increased depth of
respiration, pulse is raised to 160-180/ min and there is severe asthenia. Cerebral deficit
produces convulsions, delirium, stupor and coma.
When there is hypotension, increased urea concentration and raised potassium levels then
prognosis is bad. Urine shows proteins and casts. Serum iron and bilirubin levels are raised
due to liver damage. SGOT is raised due to liver and muscle damage. The first 24 hours are
critical and death usually occurs within a week.
Autopsy Findings of Hyperthermic Deaths
1. The autopsy findings in hyperthermic deaths are similar to those in cardiac failure.
2. Visceral haemorrhages and congestion in heart, liver, lungs and kidneys are present due
to thrombocytopenia, decreased plasma fibrinogen concentration and decreased
prothrombin levels causing hepatic damage.
3. Haemorrhage also occurs due to increased capillary fragility due to anoxia and circulatory
collapse.
4. Patients who survive for more than 24 hours show lobar pneumonia, acute tubular
necrosis, centrilobular necrosis, adrenal necrosis and haemorrhages.
5. Heart shows subendocardial haemorrhages, changes in the muscle fibers and the
chambers are dilated.
6. Brain is congested and oedematous; convolutions are flattened and scattered patches are
found in the walls of the third ventricle and floor of the fourth ventricle.
7. The cerebellar changes are more rapid and in the form of oedema of purkinje layer and
swelling, degeneration and reduction of purkinje cells.
8. Those who survive longer show rarefaction of granular layer along with oedema of
hypothalamic nuclei.
9. In the brain, the heat dissipation center (preoptic and supra-optic area) and the heat
conservation and production center (occipitolateral portion of hypothalamus) are usually
affected.
Medicolegal Aspects of hyperthermia
1. All hyperthermic deaths are accidental
2. Autopsy examination is done to rule out any other cause of death or contributory cause
of death.