Dr. Waqas Nawaz PMAS Arid agriculture university rawalpindi, Pakistan

1. PATH-202
Death of Animal
Snake Venom, Drowning, Lightning, Electric Current
Submitted To: Dr Imtiaz Ahmad
Submitted By: Waqas Nawaz
11-Arid-975
DVM 4th
Semester

2. Snake Venom
There are ~420 venomous species of snakes living on the earth. Their venoms, each unique, can
affect multiple organ systems. The venoms have a predilection for the peripheral nervous system
where the neuromuscular junction is a favorite target. Those venoms affecting the release of
acetylcholine from the presynaptic membrane are called β-neurotoxins and those affecting the
postsynaptic membrane are called α-neurotoxins.
There are ~2340 species of snakes living on the earth and more than 420 species are venomous.
Venomous snakes are found on all continents except Antarctica. It has been reported that around
5 million snakebites occur worldwide each year, causing ~125,000 deaths. Snakebites are more
common in tropical regions and in agricultural areas where there is a high likelihood of
contact with snakes
Snake venoms are colorless to dark amber liquids that contain complex mixtures of small
peptides with diverse pharmacological properties. Venom is a modified form of saliva and
probably evolved to aid in capture of prey, assist in chemical digestion, and defense against
predators. Snakes use glands to inject venom, which are actually modified salivary glands that
are situated below the eyes. During envenomation, the venom passes from the venom gland
through a duct into the snake's fangs and ultimately into prey. The amount of venom injected per
bite depends on species of the snake, the elapsed time since the last bite, and the degree of threat
the snake feels as well as the size of the prey.
The numerous toxins present in snake venoms result in injury to several organ systems including
muscles, kidneys, and blood coagulation disturbances. The most important constituents in
snake venom are neurotoxins. They are responsible for the neuromuscular weakness and
paralysis that ensues after sustaining a bite from a venomous snake. Following envenomation,
the cranial nerves are usually affected first, which results in ptosis, ophthalmoplegia, dysarthria,
dysphagia, and drooling. This progresses to weakness of limb muscles, paralysis of the
respiratory muscles, and ultimately death if prompt treatment is not initiated.
Effects of neurotoxins are manifested as interference of neuromuscular signal transmission and
can vary from subtle alterations of neurotransmitter release to complete neuromuscular block.
The activity of neurotoxins can be exerted at the presynaptic elements, post-synaptic elements or
both. Most snake venoms contain toxins that affect both.
Envenomation with β-neurotoxins results in severe and prolonged paralysis that is very difficult
to manage.

3. Drowning
Drowning is defined as the entry or aspiration of fluid through the nose and mouth into the
respiratory tract. The definition excludes aspiration of vomit, blood, saliva, bile, or meconium.
Drowning is death from suffocation (asphyxia) caused by a liquid entering the lungs and
preventing the absorption of oxygen leading to cerebral hypoxia and myocardial infarction.
Submersion is followed by struggle which subsides with exhaustion and drowning begins. When
the breath can be held no longer, water is inhaled, with associated coughing and vomiting, and is
rapidly followed by loss of consciousness with death some minutes later.
Mechanism of death in wet drowning Mechanism of death in dry drowning

4. Froth is expressed around the mouth and nostrils in a typical “wetdrowning”. Froth can be
washed away by the action of water before body retrieval, disappear after the body has been in
the open, or removed before transfer of the body for autopsy. Froth may be not seen by
investigators at the scene. In one study, external foam was observed in only 19% of cases.
Facial or scalp blunt trauma means ruling out underlying cranial and cervical spine trauma;
however,cutaneous injuries are possible when the victim assumes a head-down position and
scrapes the bottom.
Lightning
Lightning injury is almost always a dramatic and unexpected event. Lightning is so sudden and
its course so rapid and variable that the human eye cannot record it accurately. Witnesses often
catch only a glimpse of the event, often at the edge of their visual field.
Mechanism Percent
Direct strike 3-5%
Contact strike 3-5%
Side splash/flash 30-35%
Ground current 50-55%
Upward streamer 10-15%
Blunt injury Unknown
Lightning strikes may cause skull fractures and cervical spine injury from associated blunt
trauma. Tympanic membrane rupture is commonly found in lightning victims and may be
secondary to the shock wave, a direct burn, or a basilar skull fracture. Injuries to the eyes include
corneal lesions, uveitis, iridocyclitis, hyphema, vitreous hemorrhage, optic atrophy, retinal
detachment, and choroidoretinitis.
Cardiac damage or arrest may be caused by either the electrical shock or induced vascular spasm.
Deep burns occur in fewer than 5% of lightning injuries. Lightning injury may cause transient
vasospasm so severe that the extremities appear cold, blue, mottled, and pulseless. This usually
resolves within a few hours and rarely requires vascular imaging or surgical intervention.
Pulmonary contusion and hemorrhage are reported with lightning injury. Blunt abdominal
injuries occur rarely. Gallbladder necrosis or mesenteric thrombosis are seen with lightning
injury.
Complications of lightning injury fall into three areas: (1) those that could be reasonably
predicted from the presenting signs and can be treated routinely, such as hearing loss from
tympanic membrane rupture or paresthesias and paresis from neurologic damage, (2) long-term
neurologic deficits similar to those suffered with blunt head injury and chronic pain syndromes,
and (3) iatrogenic complications that are secondary to overaggressive management.

5. Electric Current
Much has been written on the effects of electric shock on the body. However, in those cases in
which victims become pulseless and therefore die suddenly, the underlying event has assuredly
been ventricular fibrillation. In this condition of the heart, all of the muscle fibers of the
ventricles, the main pumping chambers, contract and relax randomly and pump no blood.
The head is a common point of contact for high-voltage injuries, and the patient may exhibit
burns as well as neurologic damage. Cataracts develop in approximately 6% of cases of high-
voltage injuries, especially whenever electrical injury occurs in the vicinity of the head.36
Although cataracts may be present initially or develop shortly after the accident, they more
typically appear months after the injury.
Cardiac arrest, either from asystole or ventricular fibrillation, is a common presenting condition
in electrical accidents.
Other than cardiac arrest, the most devastating injuries that accompany an electrical injury are
burns, which are most severe at the source and ground contact points.
In high-voltage injuries, muscle necrosis can extend to sites distant from the observed skin
injury, and compartment syndromes occur as a result of vascular ischemia and muscle edema.
In high-voltage injuries, loss of consciousness may occur but is usually transient unless there is a
significant concomitant head injury.
Injury to the lungs may occur because of associated blunt trauma but is rare from electrical
current, perhaps because air is a poor conductor. Injury to solid
visceral organs also is rare, but damage to the pancreas and liver is reported.