Sunday, 24 February 2013
The Treatment for Catbite
Wednesday, 20 February 2013
The Treatment for snakebite
The Treatment for snakebite
First help
The aim of first help is to retard the systemic absorption of venom and prevent life-threatening complications by prompt transport to a medical facility. First help can be performed by victim himself/herself or by any person who happens to be nearby. Traditionally, first aid included making local incisions or "tattooing" at the site of the bite, attempts at suctioning venom out of the wound, use of tight bands (tourniquets) around the limb, and/or local application of ice packs. None of the traditional remedies have any proven medical benefit. They should be discouraged as they do more harm than good and delay transport to a medical facility. Incision, suction, electric shocks, cryotherapy, or washing the wound are contraindicated as any interference with the wound introduces infection, increases bleeding from the site, and hastens absorption of the venom.
The current guidelines for first help include the following:
Reassure the victim (70% of all snakebites are by nonvenomous snakes and 50% of bites by venomous species are dry bites )
Immobilize the affected limb (by bandage or clothes to hold splint, but tight arterial compression is not recommended)
quickly transfer of victim to hospital
Pressure immobilization method (PIM) was gathered by the Australian Venom Research Unit, university of Melbourne, Australia, for rapidly acting neurotoxic elapid snake venom. As per the PIM, immobilization and bandaging of the bitten part is a bit like that done in the case of a sprained ankle. Studies have shown that it's seldom applied properly in simulated environments and, moreover, mobilizing the limb for more than 10 min nullifies the benefits of even the correctly applied bandage.
In most instances, health care providers, general public, or community health workers are the first responders to come to the aid of the snakebite victim. If outcomes are to be improved, it's vital that they should all be made aware of the importance of immediate immobilization of the limb and transfer to the hospital at the earliest.
Hospital treatment Emergency care department
When the patient reaches the emergency department, evaluation should begin with the assessment of the airway, breathing, circulatory status, and consciousness.
Urgent resuscitation will be recommended in those in shock (cardiovascular toxicity), those with respiratory failure (neurotoxin), and in those who have had cardiac arrest (beacuse of hypoxia, cardiac toxicity, or hyperkalemia from rhabdomyolysis).
Oxygen should be administered to every envenomed patient and a large-bore intravenous catheter should be inserted. A bolus of normal saline or Ringer's lactate should be given to all patients with suspected envenomation. The patient may then be administered specific treatment after a precise history has been taken and thorough physical examination done.
History
Physical examination
During the initial evaluation, the bite site should be examined for signs of local envenomation (edema, petechiae, bullae, oozing from the wound, etc) and for the extent of swelling. The bite site and at the rather least two other, more proximal, locations should be marked and the circumference of the bitten limb should be measured every 15 min thereafter, until the swelling is no longer progressing. The extremity should be placed in a well-padded splint for at the very least 24 h. Serial measurement of circumference helps in estimating spread of venom and effect of antivenom. [9] Lymph nodes draining the limb should be palpated and the presence of lymphangitic lines noted.
Distal pulses should be checked and monitored if there's presence of gross swelling. The presence of a pulse does not rule out compartment syndrome however, and compartment pressure should be measured directly if there's concern that a compartment syndrome is developing. The diagnosis is established if the compartment pressure, measured directly by inserting a 22G IV cannula and connecting it with manometer, is raised above 55 cm water/saline. Direct measurement is required before resorting to fasciotomy since compartment syndrome is rare in snakebite victims and fasciotomy done without correction of hemostatic abnormality may cause the patient to bleed to death.
signals for severe snake envenomation should be sought. They consist of the following:
Snake identified is a very venomous one
Rapid early extension of local swelling from the site of the bite
Early tender enlargement of local lymph nodes, indicating spread of venom in the lymphatic systems
Early systemic symptoms
Early spontaneous systemic bleeding (particularly bleeding from the gums)
Passage of dark brown urine
Laboratory Investigations
Although lab tests are of little value in the diagnosis of snake envenomation, they're useful for prognosticating and for making decisions about specific interventions.
Specific investigations
(a) The 20-min whole blood clotting test (20 WBCT): The 20 WBCT is a simple bedside test of coagulopathy to diagnose viper envenomation and rule out elapid bite. It requires a new clean, dry test tube made up of simple glass that has not been washed with any detergent. A few milliliters of fresh venous blood is drawn and left undisturbed in the test tube for 20 min; the tube is then tilted gently. If the blood is still liquid after 20 min, it is evidence of coagulopathy and confirms that the patient has been bitten by a viper. Cobras or kraits dont cause antihemostatic symptoms.
(b) Enzyme linked immunosorbent assay (ELISA): ELISA tests are now available to identify the species involved, based on antigens in the venom. These tests, however, are expensive and not freely available and thus have limited value in diagnosis; at present, they find use mainly in epidemiological studies.
Other nonspecific tests include
Hemogram: The hemogram may show transient elevation of hemoglobin level due to hemoconcentration (because of the increased capillary leak) or may show anemia (due to hemolysis, especially in viper bites). Presence of neutrophilic leucocytosis signifies systemic absorption of venom. Thrombocytopenia may be a feature of viper envenomation.
Serum creatinine: This is necessary to rule out renal failure after viper and sea snake bite.
Serum amylase and creatinine phosphokinase (CPK): Elevated levels of these markers implies muscle damage (caution for renal damage).
Prothrombin time (PT) and set in motion partial thromboplastin time (aPTT): Prolongation may be present in viper bite.
Fibrinogen and fibrin degradation products (FDPs): Low fibrinogen with elevated FDP is present when venom interferes with the clotting mechanism.
Arterial blood gas and electrolyte determinations: These test are necessary for patients with systemic symptoms.
Urine examination: Can reveal hematuria, proteinuria, hemoglobinuria, or myoglobinuria. (Arterial blood gases and urine examination should be repeated at frequent intervals during the acute phase to assess progressive systemic toxicity).
Electrocardiogram (ECG): Nonspecific ECG changes such as bradycardia and atrioventricular block with ST-T changes may be seen.
Electroencephalogram (EEG): Recently, EEG changes have been noted in up to 96% of patients bitten by snakes. These changes start within hours of the bite but are not associated with any features of encephalopathy. Sixty-two% showed grade I changes, 31% cases manifested grade II changes (moderate to severe abnormality), and the remaining 4% showed severe abnormality (grade III). These abnormal EEG patterns were seen mainly in the temporal lobes.
The first blood drawn from the patient should be typed and cross-matched, as the effects of both venom and antivenom can interfere with later cross-matching.
Specific Therapy Anti-snake venom
Anti-snake venom (ASV) are immunoglobulins prepared by immunizing horses with the venom of poisonous snakes and subsequently extracting and purifying the horses' serum. they are the only effectual antidote for snake venom. Antivenoms may be species specific (monovalent/monospecific) or may be effective against multiple species (polyvalent/polyspecific). Antibodies raised against the venom of one species may have cross-neutralizing activity against other venoms, sometimes that from closely related species. This is known as paraspecific activity. As per the recommendations of WHO, the most effective treatment for snakebite is the administration of monospecific ASV ; however, this therapy is not always available to snakebite victims because of its high cost, frequent lack of availability, and the difficulty in properly identifying the snake.
WHO recommends that if an adequate cold chain is in place, antivenoms should be prepared in the liquid form, since this reduces production costs and avoids the potential adverse physicochemical alterations to the product often brought about by lyophilization. On the other hand, if the integrity of the cold chain cannot be guaranteed, antivenoms should be lyophilized to maintain stability.
several antivenom preparations are available internationally. In India, polyvalent antivenom prepared by Central Research Institute, Kasauli (HP) is effectual against the most common Indian species Antivenom produced at the Haffkine Corporation, Parel (Mumbai) is effective against the venom of even more species. lists ASV producers in India, both in the public along with the private sector.
ASV is supplied in dry powder form and has to be reconstituted by diluting in 10 ml of normal saline/D 5 W. Mixing is done by swirling and not by vigorous shaking.
Indications for ASV
the recommended use of antivenom is essential and requires an informed evaluation of the patient. Not every poisonous snakebite merits its use. Antivenom treatment carries a risk of severe adverse reactions and in most countries it is expensive and may be in limited supply. It should therefore be used only in patients in whom the benefits of antivenom treatment are considered to exceed the risks. Crotalidae polyvalent immune Fab (ovine) (CroFab; FabAV) has recently been approved for use in the United States. CroFab is a venom-specific Fab fragment of immunoglobulin G (IgG) that works by binding and neutralizing venom toxins, facilitating their redistribution away from target tissues and their elimination from the body. It has been demonstrated that these fragments are safe and effectual, with a low incidence of sequelae; however, allergic reactions can occur when any animal protein derivatives are administered to human subjects. The overall incidence of immediate and delayed allergic reactions to this product appears so far to be lower than that reported with classic whole-IgG antivenom. Antivenom is indicated whenever there are signs of systemic envenomation or presence of severe local swelling.
Antivenom therapy
Antivenom should be ideally administered within 4 h of the bite, but is effectual even if given within 24 h. The dosage needed varies with the degree of envenomation.
Dose of ASV
Despite widespread use of antivenom, there have been virtually no clinical trials to determine the right dose. The dosage has remained a matter of much debate. The classic dosing in our setup is based on the degree of envenomation
WHO/SEARO recommends the dose of antivenom to be the amount required to neutralize the average venom yield when captive snakes are milked of their venom. Published research has indicated that the Russell's viper injects, on average, 63 mg (SD: ± 7 mg) of venom in the first bite. As each vial of polyvalent ASV neutralizes 6 mg of Russell's viper venom, the initial dose should be 8-10 vials to ensure that the majority of the victims are covered by the initial dose; this will also aid keep the price of ASV down to acceptable levels. As snakes inject identical amount of venom into young people and adults, children should receive the same dose of antivenom as adults.
Response to infusion of antivenom is marked by normalization of blood pressure. Within 15-30min bleeding stops, though coagulation disturbances may take up to 6 h to normalize. Neurotoxicity begins to improve within the first 30 min, but patients may require 24-48 h for full recovery.
A repeat dose of ASV should be given when there is persistence of blood incoagulability even after 6 h or continued bleeding after 1-2 h of the initial dose. ASV should also be repeated when there are worsening neurotoxic or cardiovascular signs even after 1-2 h.
ASV administration
ASV can be administered either by slow intravenous injection at a rate of 2 ml/min or by intravenous infusion (antivenom diluted in 5-10 ml per kilogram body weight of normal saline or D 5 W and infused over 1 h). Slow intravenous injection has the advantage that a doctor or nurse is present during the injection period when there is a risk of some early reaction to the ASV. All patients should be strictly observed for an hour for growth of any anaphylactic reaction. Epinephrine should always be kept ready before administration of antivenom.
ASV should never be given locally at the site of the snakebite since it has not been shown to be efficient and, moreover, this route of administration is associated with very note worthy risks. For example, it's utterly painful and may increase intracompartmental pressure. Intramuscular injections are also not preferred since ASV is composed of large molecules (IgG or fragments) which are absorbed slowly via lymphatics, making the bioavailability by this route poor as compared to intravenous administration. Other disadvantages include pain on injection and risk of hematoma formation and sciatic nerve damage in patients with hemostatic abnormalities. Intramuscular injections should only be given in settings where intravenous access cannot be obtained and/or the victim cannot be transported to a hospital immediately.
ASV sensitivity testing
ASV sensitivity testing is no longer required as a lack of response does not predict the large majority of early (anaphylactic) or late (serum sickness type) reactions. Such testing could also presensitize the patient to the serum protein and, in addition, occassionally delays treatment.
ASV reaction
Approximately 20% patients treated with ASV develop either early or late reaction.
Early anaphylactic reactions occurs within 10-180 min of start of therapy and is characterized by itching, urticaria, dry cough, nausea and vomiting, abdominal colic, diarrhea, tachycardia, and fever. Some patients may develop severe life-threatening anaphylaxis characterized by hypotension, bronchospasm, and angioedema.
Pyrogenic reactions sometimes develop 1-2 h after treatment. Symptoms include chills and rigors, fever, and hypotension. These reactions are caused by contamination of the ASV with pyrogens during the manufacturing process.
Late (serum sickness-type) reactions develop 1-12 (mean 7) days after treatment. Clinical features include fever, nausea, vomiting, diarrhea, itching, recurrent urticaria, arthralgia, myalgia, lymphadenopathy, immune complex nephritis and, rarely, encephalopathy.
Treatment of ASV reaction
When the patient shows signs of a reaction, antivenom administration must be temporarily stopped and adrenaline (1 in 1000) given intramuscularly in an initial dose of 0.5 mg in adults or 0.01 mg/kg body weight in children. The dose can be repeated every 5-10 min if required.
After adrenaline, an anti-H1 antihistamine such as chlorpheniramine maleate (adult dose 10 mg, small people 0.2 mg/kg) should be given intravenously. it may be followed by intravenous hydrocortisone (adult dose one hundred mg, children 2 mg/kg).
Late (serum sickness-type) reactions occassionally respond to a 5-day course of oral antihistamine (e.g., chlorpheniramine 2 mg six hourly in adults and 0.25 mg/kg/day in divided doses in young people). Patients who fail to respond within 24-48 h should be given a 5-day course of prednisolone (5 mg six hourly in adults and 0.7 mg/kg/day in divided doses in young people).
Supportive Therapy
The patient should be moved to an appropriate area of the hospital. The ICU will be needed for patients with signs of severe envenomation (coma, respiratory paralysis, hypotension, pulmonary edema, and history of syncope). Patients with presence of fang marks, moderate pain, minimal local edema, erythema, ecchymosis, and no systemic reactions can be treated in the ward under close monitoring. Supportive therapy is required to buy time while the damaged organs recover. The varieties of supportive care that may be necessary is summarized below.
Coagulopathy with bleeding
Coagulopathy often reverses after ASV treatment. In incredible cases, when there is severe bleeding or when urgent surgery is needed, restoration of coagulability can be accelerated by giving fresh frozen plasma, cryoprecipitate (fibrinogen, factor VIII), fresh whole blood, or platelet concentrates.
Neurotoxic symptoms
Antivenom treatment alone cannot be relied upon to save the life of a patient with bulbar and respiratory paralysis. Once there's loss of the gag reflex, failure to cough, or respiratory distress, endotracheal intubation and initiation of mechanical ventilation is indicated. Tracheostomy and inclusion of a cuffed tracheostomy tube can be done whenever expertise for endotracheal intubation is not available. Since Elapid toxin result in pathophysiological changes resembling those of myasthenia gravis, anticholinesterase drugs can have a useful effect in patients with neurotoxic envenomation, particularly in those bitten by cobras. A trial of anticholinesterase should be performed in every patient with neurotoxic envenomation. Injection neostigmine can be given as 50-100 μg/kg 4 hourly or as a continuous infusion. Glycopyrrolate 0.2 mg can be given before neostigmine as, unlike atropine, glycopyrrolate does not cross the blood-brain barrier. Seneviratne and Dissanayake, in a prospective study on the neurological manifestations, disease course, and outcome in neurotoxic envenomation, demonstrated that neostigmine improved the muscle weakness. However, the number of cases in the study was too little for them to build an unequivocal recommendation. They were of the opinion that it would maybe be reasonable to offer anticholinesterase therapy to those who demonstrate a positive response to the tensilon test or a decremental response to repetitive nerve stimulation.
Care of bitten part
The appearance of an immobile, tensely-swollen, cold, and apparently pulseless snake-bitten limb may suggest to surgeons the possibility of increased intracompartmental pressure, especially if the digital pulp spaces or the anterior tibial compartment are involved. Swelling of envenomed muscle within such tight fascial compartments could result in an increase in tissue pressure above the venous pressure and result in ischemia. However, the classical signs of an intracompartmental pressure syndrome may be difficult to assess in snakebite victims. Fasciotomy should not be contemplated until hemostatic abnormalities have been corrected, otherwise the patient may bleed to death. It has also been reported that fasciotomy worsens the amount of myonecrosis in crotalid snake venom-injected tissue.
As most snakes harbor aerobic as well as anaerobic bacteria in their mouths, a prophylactic course of penicillin (or erythromycin for penicillin-hypersensitive patients) and a single dose of broad spectrum antibiotic course which will cover anaerobes together with a booster dose of tetanus toxoid is needed.
Snake Venom Chemical composition
Snake Venom Chemical composition
The normal function of snake venom is to immobilize the prey and to assist in digestion. The toxic component of snake venom can be classified into four broad categories: enzymes, polypeptides, glycoproteins, and compounds of low molecular weight. They can also be classified as protein (90-95%) and nonprotein (5-10%) compounds. provides the chemical composition of snake venom.
Toxic effects of snake venom
The toxic effect of snake venom results from both the protein and the nonprotein component. it is further sophisticated and elaborate by the inflammatory response of the victim's body.
Phospholipase A2 is present in the venom of all families of poisonous snakes and is the enzyme that has been most widely studied. Phospholipase A2 inhibits electron transfer at cytochrome C level and renders mitochondrial-bound enzymes soluble. It damages red blood cells, leukocytes, platelets, skeletal muscle, vascular endothelium, peripheral nerve endings, and the myoneural junction.
Hyaluronidase helps spread of venom through tissues, and proteolytic enzymes are sensible for the local edema, blistering, and necrosis.
α- Neurotoxins bind to acetylcholine receptors at the motor end-plate, whereas β- neurotoxins first cause release of acetylcholine at the nerve endings at the myoneural junction and then damage the endings, preventing further release of transmitter.All this leads to a flaccid paralysis of the victim.
Polypeptides, being smaller molecules, are rapidly absorbed into the systemic circulation and cause systemic toxicity in vessel-rich organs (e.g., heart, lung, kidneys, etc.) along with at pre- and postsynaptic membranes.
Clinical Features of Snakebite
Clinical Features of Snakebite
some people who are bitten by snakes (or suspect or imagine that they have been bitten) may develop quite striking symptoms and signs, even when no venom has been injected. This results from an understandable fear of the consequences of a real venomous bite. Anxious people may hyperventilate so that they develop pins-and-needles sensation in the extremities, spasm of their hands and feet, and dizziness. Others may develop vasovagal shock after the bite or suspected bite, with faintness and collapse with profound slowing of the heart. Others may become highly agitated and irrational and may manifest a wide range of misleading symptoms.
The clinical presentation of a snakebite victim varies with the age and size of the patient, the species of snake, the number and location of the bites, and the quantity and toxicity of the venom.
Morbidity and mortality depends rather much on the age and size of victim (young people receive larger envenomation relative to body size) along with comorbid conditions (elderly patients succumb more easily to snake venom). Other factors affecting severity and outcome are listed in. Factors not contributing to outcome are size of the snake and time of bite (day/evening).
Elapid bites
Bites by krait, coral snake, and some cobras are associated with minimal local changes; however, bite by the Indian cobra (Naja naja) results in tender local swelling, blistering, and necrosis. Local necrosis causes a picture of "wet gangrene" with a characteristic putrid smell due to the direct cytolytic action of the venom. "Skip lesions" are typical findings. Systemic absorption occurs through venous channels and result in neurotoxic symptoms. Nausea, vomiting, malaise, prostration, and abdominal pain are the usual initial systemic symptoms. Paralysis is heralded by ptosis, followed by ophthalmoplegia. Paralysis of facial, palatal, tongue, and neck muscles follow. Respiratory failure, precipitated by upper airway obstruction and paralysis of intercostals and diaphragm, is the usual cause of death.
Viper bites
Viper bite is primarily vasculotoxic. It causes rapidly developing bruising and growth of the bitten part. Local necrosis is mainly ischemic as thrombosis blocks the local blood vessels and causes a dry gangrene. Systemic absorption is slow; it occurs via the lymphatics and leads to lymphangitis. Hemostatic abnormalities are characteristic of viper bites and are the cause of the complications that lead to death. A persistent ooze from the bite mark and the site of the IV cannula is an indication of the altered clotting mechanism. Hemorrhage and increased capillary permeability leads to shock and pulmonary edema. Oliguria ensues, followed by loin pain due to renal ischemia. Renal failure is the common event before death.
Sea snake bite
The effects of a sea snake bite are both myotoxic and neurotoxic and result in clinical and pathological changes typical of segmental myopathic lesions in the skeletal muscles. Muscle pains may last for several months unless treated. Myoglobin and potassium released from damaged skeletal muscle can cause renal failure, while the hyperkalemia thus produced may lead to cardiac arrest.
The average fatal dose, LD50, in mice and the average time to fatality of various snakes poison is given in.
Management of Snakebite
WHO/SEARO has published guidelines, specific for the South East Asia region, for the clinical management of snakebites; these guidelines appeared in the supplementary issue of the South East Asian Journal of Tropical Medicine and Public Health.
Tuesday, 19 February 2013
Snake Epidemiology
Snake Epidemiology
Snakes are distributed throughout most of the earth's surface with some exceptions such as the Arctic, Antarctic, and many small islands. Snakes are poikilothermic carnivorous reptiles that have evolved the venomous apparatus for the purpose of procurement of food. [9] To a large extent the manifestation of snakebite depends upon the species of snake, and therefore identification of the type of snake is paramount. At times the bite mark might not be visible (e.g., in the case of krait). The killed snake brought as evidence helps in identification of snake, in which case species-specific monovalent Anti snake venom (ASV) can be administered. The clinical manifestations of the patient may not correlate with the species of snake brought as evidence. it is therefore advantageous to know the appearance of the snake so as to recognize the species.
The three major families of venomous snakes are the Elapidae, the Viperidae, and the Hydrophidae.
Elapidae
Elapidae (cobra, king cobra, krait, and coral snake): These snakes have heads that are of about identical width as their necks. The head is bathed in large scales but lack laureal shields. Their pupils are round and they are oviparous. These snakes have grooved fangs that are short, fixed, and covered by mucous membrane. They, therefore, cannot bite through clothes and sometimes deliver only a sublethal dose.
Viperidae
Viperidae (vipers): The head of a viper is triangular, wider than the neck, and has laureal shields. They have vertically elliptical pupils and are ovi-viviparous. Their fangs are long, movable, and canalized like hypodermic needles. they're further subdivided into pit viper and pitless viper subfamilies. The Crotalinae (pit vipers) have a special sense organ, the pit organ, to detect their warm-blooded prey. This is situated between the nostril and the eye. The rattlesnake belongs to the pit viper subfamily, while the Russell's viper and the saw-scaled viper belong to the pitless viper subfamily.
Hydrophidae
Hydrophidae (sea snake): Sea snakes are found in the vicinity of the seacoast. They have a tiny head and a flattened tail that helps them swim. Though venomous, they seldom bite.
In India, more than 200 species of snakes have been identified but only 52 are poisonous; the common krait (Bungarus caeruleus), Indian cobra (Naja naja), Russell's viper (Daboia russelii), and saw-scaled viper (Echis carinatus) are the most poisonous ("the big four"). In the Indian setting, nearly two-thirds of bites are attributed to saw-scaled vipers, about one-fourth to Russell's viper, and only a little proportion to cobras and kraits.
Host and environmental factors
Thorough statistical analysis of snakebite is difficult and the available data is not always complete because of the varied distribution (and because most bites occur in remote villages). Snakebite may be termed an occupational disease, as farmers, plantation workers, herdsmen, hunters, or workers on growth sites are mostly affected. Snakebites show a classical seasonal variation, being more common in summers and in the rainy season, when it's associated with agricultural activities. The majority of snakes dont bite without provocation; most bites are inflicted when the snakes are inadvertently trodden upon. Males are bitten almost twice as sometimes as females, with the majority of the bites being on the lower extremities. Fortunately, 50% of bites by venomous snakes are "dry bites" that result in negligible envenomation. The percentage of dry bites ranges from 10-80% for various poisonous snakes.
Conclusion
Snakes do not generally attack human beings unless provoked. However, once bitten, a wide spectrum of clinical manifestations may result. The emphasis should be on early and adequate medical management. Delayed medical management and lack of public awareness results in prolonged hospital and ICU stay of the patients. This can be decreased if regular public programs regarding prevention, prehospital management (first aid), and the importance of early transfer to hospital are conducted.
Overemphasis on reducing the load of snake venom in the victim during prehospital management can be dangerous because its role is debatable and too much valuable time is wasted in its administration. Most of the traditional methods for first aid treatment of snakebite, both western and "traditional/herbal," have been found to result in more harm than good. Identification of the species of snake sensible for the bite is very important for optimal clinical management. Antivenom is the only efficient antidote for snake venom. However, it's costly and sometimes in short supply and its use carries the risk of potentially dangerous reactions.
Friday, 15 February 2013
THE DANGERS OF AN INHABITABLE
ABSTRACT
of our generation we live to day it obvious that there are lot of Danger, which we as human has contributed to in one way or the other. This Danger will always be there because of our strive for wanting more from our environment (Energy, Medicine, Technological advancement etc.) since it difficult or impossible to eliminate Danger then we simply have to think of way to live with them and yet be safe.
Safety is what we as a people have to inculcate into whatever we do so as to protect our lives or properties even our environment, we simply have to have good safety practice in our place of work, where we live even as we go out it must be included in us, is only by doing this can we really reduce danger.
The Dangers of an Inhabitable
Danger is the possibility of suffering injury or harms to person society and state.
We cannot shy away from the fact that the environment that we live in greatly affects our health; you can't avoid it, but everywhere you turn there is exhaust from a car, factories emitting smokes from their smoke stacks, Earthquake, hurricanes, tornado, landslide, flooding and not to mention the fast food that is offered is so convenient and affordable that is makes it hard to turn away. Since these things are a part of our time we live in, how are they really affecting us? The effects may be greater than you think.
I will need to chat about the extreme situation that is cause by us as a result of quest for more energy to technological advancement and those that are cause by nature.
The extreme situations of danger are those that have the ability to cause very engrossing health problems can take lives damage to properties, example of extreme are group into three categories ,
1) Military conflicts, Technological failures
2) Technological failures, act of nature
3) Environmental contamination, flooding high water.
The extreme situation distribution can be of Local, regional, national and global characteristic.
The extreme situation can be long term or short term; it can be deliberate as an inadvertent character.
There are two main source of the extreme situation which are,
1) Anthropological
2) Natural.
Anthropocentric situation
This are situation that the danger is as a result of the gas that are being emitted into the environment that are leading to global warming, Exhaust and fumes from vehicles will never go away. Even in the wake of manufacturers creating new methods to give us cleaner air with better exhaust system we breathe this in every day. Research shown that diesel exhaust is more damaging than bio diesel which is a plant based fuel. A team of researches test the effects of diesel exhaust against the bio diesel exhaust. The diesel in fact murdered and damaged the cells while the bio diesel had very tiny effect at all.
The end result of these studies proves that the damage is what causes respiratory diseases of all kinds. Asthma is just one of those diseases, but it would be interesting to see if mesothelioma, a cancer that affects the lining of the lungs would also be caused by diesel fumes.
the same is also true of air pollution from factories and how it affects us. Studies have shown that this too causes respiratory illness. A study also show that liquid particles as well as what is called "particulate matter", float through the air and when you breath can attach themselves into the airway. The fine particles which are the strongest are the ones that come from paper mills, steel mills, and cement mills. These are the ones that tend to reveal the most destruction. All this combine the damage it cause to the environment,
Topological effect: high water flooding, river drying up, vase land becoming desert, and so on
Natural situation
These are dangers that are being imposed by natural disaster and they're not under our control. Natural disasters such as flood, fire, earthquake, tornado, hurricanes and windstorm affect thousands of people every year. Taking very many numbers of lives and causing large scale of devastating damage to property, thereby making a whole lot people homeless, I will take time to mention some of this catastrophic disaster:
Tashkent 1988. Central Asia’- 20,000 person where lost.
Indian Ocean earthquake 2004 -230,000 person where lost, $14 billion (2004 US$) in humanitarian aid
Hurricane Katrina 2005 at least 1,833 people passed away, total property damage was estimated at $81 billion (2005 US D)
MEASURE TO DOWNTURN THE DAMAGE
we simply have to get substantial about dealing with the man-made greenhouse-gas emissions that drive warming and industries should be environmentally friendly. We as a people must begging to do thing that will reduce danger, so that we and other living thing can be safe, but in case of natural disaster it is vital we recognizing an impending hazard and knowing what to do to protect yourself and your family will help us take effective steps to prepare beforehand and help recovery after the event.
Some of the things you can do to prepare for the unexpected, such as assembling a supply kit and developing a family emergency plan, are identical for all varieties of hazards. However each emergency is unique and knowing the actions to take for each threat will impact the specific decisions and preparations you make. By learning about these specific threats, you are preparing yourself to react in an emergency.
In general we should have a good safety practice which will aid to reduce damage to properties or loss of life, if have safety consciousness then we can recognize danger and know how to manage it.
CONCLUSION
Danger will always be around us know what will do we can’t eliminate it, but can reduce by the things we do and the way we do them, for that reason we must reduce anthropological profound solution to manage the natural danger as well, Safety should be our watch dog in other to keep us from danger.
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