PATH-202Death of AnimalSnake Venom, Drowning, Lightning, Electric CurrentSubmitted To: Dr Imtiaz AhmadSubmitted By: Waqas Nawaz11-Arid-975DVM 4thSemester
Snake VenomThere are ~420 venomous species of snakes living on the earth. Their venoms, each unique, canaffect multiple organ systems. The venoms have a predilection for the peripheral nervous systemwhere the neuromuscular junction is a favorite target. Those venoms affecting the release ofacetylcholine from the presynaptic membrane are called β-neurotoxins and those affecting thepostsynaptic 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 around5 million snakebites occur worldwide each year, causing ~125,000 deaths. Snakebites are morecommon in tropical regions and in agricultural areas where there is a high likelihood ofcontact with snakesSnake venoms are colorless to dark amber liquids that contain complex mixtures of smallpeptides with diverse pharmacological properties. Venom is a modified form of saliva andprobably evolved to aid in capture of prey, assist in chemical digestion, and defense againstpredators. Snakes use glands to inject venom, which are actually modified salivary glands thatare situated below the eyes. During envenomation, the venom passes from the venom glandthrough a duct into the snakes fangs and ultimately into prey. The amount of venom injected perbite depends on species of the snake, the elapsed time since the last bite, and the degree of threatthe snake feels as well as the size of the prey.The numerous toxins present in snake venoms result in injury to several organ systems includingmuscles, kidneys, and blood coagulation disturbances. The most important constituents insnake venom are neurotoxins. They are responsible for the neuromuscular weakness andparalysis 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 therespiratory muscles, and ultimately death if prompt treatment is not initiated.Effects of neurotoxins are manifested as interference of neuromuscular signal transmission andcan 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 orboth. Most snake venoms contain toxins that affect both.Envenomation with β-neurotoxins results in severe and prolonged paralysis that is very difficultto manage.
DrowningDrowning is defined as the entry or aspiration of fluid through the nose and mouth into therespiratory 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 andpreventing the absorption of oxygen leading to cerebral hypoxia and myocardial infarction.Submersion is followed by struggle which subsides with exhaustion and drowning begins. Whenthe breath can be held no longer, water is inhaled, with associated coughing and vomiting, and israpidly followed by loss of consciousness with death some minutes later.Mechanism of death in wet drowning Mechanism of death in dry drowning
Froth is expressed around the mouth and nostrils in a typical “wetdrowning”. Froth can bewashed away by the action of water before body retrieval, disappear after the body has been inthe open, or removed before transfer of the body for autopsy. Froth may be not seen byinvestigators 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 andscrapes the bottom.LightningLightning injury is almost always a dramatic and unexpected event. Lightning is so sudden andits course so rapid and variable that the human eye cannot record it accurately. Witnesses oftencatch only a glimpse of the event, often at the edge of their visual field.Mechanism PercentDirect strike 3-5%Contact strike 3-5%Side splash/flash 30-35%Ground current 50-55%Upward streamer 10-15%Blunt injury UnknownLightning strikes may cause skull fractures and cervical spine injury from associated blunttrauma. Tympanic membrane rupture is commonly found in lightning victims and may besecondary to the shock wave, a direct burn, or a basilar skull fracture. Injuries to the eyes includecorneal lesions, uveitis, iridocyclitis, hyphema, vitreous hemorrhage, optic atrophy, retinaldetachment, 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 transientvasospasm so severe that the extremities appear cold, blue, mottled, and pulseless. This usuallyresolves within a few hours and rarely requires vascular imaging or surgical intervention.Pulmonary contusion and hemorrhage are reported with lightning injury. Blunt abdominalinjuries occur rarely. Gallbladder necrosis or mesenteric thrombosis are seen with lightninginjury.Complications of lightning injury fall into three areas: (1) those that could be reasonablypredicted from the presenting signs and can be treated routinely, such as hearing loss fromtympanic membrane rupture or paresthesias and paresis from neurologic damage, (2) long-termneurologic deficits similar to those suffered with blunt head injury and chronic pain syndromes,and (3) iatrogenic complications that are secondary to overaggressive management.
Electric CurrentMuch has been written on the effects of electric shock on the body. However, in those cases inwhich victims become pulseless and therefore die suddenly, the underlying event has assuredlybeen ventricular fibrillation. In this condition of the heart, all of the muscle fibers of theventricles, 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 exhibitburns 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.36Although cataracts may be present initially or develop shortly after the accident, they moretypically appear months after the injury.Cardiac arrest, either from asystole or ventricular fibrillation, is a common presenting conditionin electrical accidents.Other than cardiac arrest, the most devastating injuries that accompany an electrical injury areburns, 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 skininjury, 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 asignificant concomitant head injury.Injury to the lungs may occur because of associated blunt trauma but is rare from electricalcurrent, perhaps because air is a poor conductor. Injury to solidvisceral organs also is rare, but damage to the pancreas and liver is reported.