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  Marine/Human Environmental Health       Compiled and edited by Jim Larson (Naui 10346L)

Basic facts about sharks

Approximately 350 different species of sharks inhabit the oceans of the world; they are found in both temperate and tropical waters, essentially everywhere except Antartica. They are found at both shallow and deep depths, with some species known to live only at depths of thousands of feet. Some species are also known to inhabit freshwater lakes and rivers.
As a species, sharks are characterized by marked diversity and exquisite adaptation to their marine environment. When fully grown, they range in size from less then 6" to more than 60'long. Some species are fierce predators (e.g., great whites),while others are unobtrusive filter feeders (e.g., whale sharks). Most species are poikilotherms, but some species are at least semiwarmblooded (e.g., makos).
    Sharks reproduce in several ways, being oviparous (e.g. horn sharks), viviparous (e.g., hammerheads), and ovovivparous (e.g. nurse sharks). They have also developed a variety of special adaptations. For example, some species are bioluminescent, while others have perfected electroreception as a keen special sense, which may explain why great whites sometimes attack boats. And, some species seem to have at least rudimentary color vision. Similarly, they have perfected osmoregulation to an extreme degree, and they control their buoyancy via their large livers, since they have no swim bladders.
    Sharks also have some unique characteristics that are currently the subject of a number of studies that may have relevance to various human conditions. For example, sharks are not known to develop cancer, and studies are now focusing on a special protein found in shark cartilage that inhibits neovascularization and may have usefulness as an antineoplastic agent. Similarly, some species unexplainedly never stop growing.
    Sharks have very few natural enemies; mainly larger sharks and parasites, especially tapeworms. In recent decades, man has emerged as their primary enemy. At times, this is for reasons of alleged sport, while at other times it is because of their utilitarian value. For example, sharks are increasingly being used as a marketable fish (in addition to their long-standing use as the fish in english fish-and-chips and shark-fin soup in the orient), and their hides are still in demand to make leather goods. However, they are no longer harvested for their livers, as was done prior to the global laboratory synthesis of vitamin a.

Shark attacks

    Shark attacks on humans are quite rare. Only about 50 shark attacks have occurred in more than 100 years in Hawaii, one of the most heavily used marine environments in the world. Likewise, less than 60 shark attacks have occurred along the California coast in as many years, despite there being a sizable endemic population of great white sharks off the California coast and these waters being widely used for surfing, scuba diving, and other marine sports. (Interestingly, though, the frequency of shark attacks along the northern California coast has substantially risen in recent years, most likely as a result of partially restoring the native elephant seal population.) Overall, less than 100 shark attacks occur throughout the world annually, and most of these are the result of people being where they should not be or doing something that is known to increase the risk of an attack.
    Some perspective on the relative risk of sharks attacking man vs. humans attacking sharks can be gained by the following extrapolation. In 1976, the United Nations' food and agriculture organization reported that more than 300 metric tons of sharks were harvested. If we assume an average human body weight of 70 kg, and extrapolate a comparable figure for what this would have meant if the tables had been turned and sharks were attacking humans, it would translate into sharks killing about 4.5 million people. Clearly, sharks have more to fear from man than vice versa.
    About 20% of shark species are at least potentially dangerous to man, thirty-two species have been definitely identified in attacks on humans, and some 35 species are considered potentially dangerous. Nonetheless, the majority of shark attacks are accounted for by a handful of species- great whites, tigers, makos, hammerheads, and various types of bull and reef sharks.
    When sharks attack humans, there are two attack kinds: feeding or agonistic. Agonistic attacks are poorly understood, but seem to be defensive or, possibly, involve some type of territorial behavior. An especially good demonstration of this is provided by the pacific gray reef shark, in which a pre-attack threat posture has been identified. In contrast, most sharks attacks along the California coast probably have been feeding attacks involving cases of mistaken identity-that is, a surfer or diver dressed in a wet suit and fins is mistaked by the shark for an elephant seal or sea lion. However, in many of these cases, it appears that the shark very rapidly realizes that it has made a mistake, breaks off the attack, and swims away.
    Despite the statistics, shark attacks remain a much-discussed topic among marine enthusiasts. And, even though most of these people intellectually understand that the risk of being attacked by a shark is exceedingly small, this seems to be one of those subjects that is, more often than not, addressed on a visceral, rather than cerebral, level.

Management of shark attacks

Victims of shark attack can be properly cared for by utilizing standard prehospital and emergency medical procedures for trauma. Of course, the best management of shark attacks is prevention: avoiding those circumstances known to increase the risk of attack, which includes keeping clear of known dangerous areas( i.e., areas known to harbor great white, tiger, hammerhead, and other man-eating species) and not doing things that are known to attract or aggravate sharks.
When dealing with a shark attack victim, it is important to remember that shark bites usually result in deep, complex wounds involving injury to skin, muscle, major blood vessels, nerves, tendons and bones. They are similar to other types of major integumentary trauma, e.g.,as might occur in motor vehicle accidents or in motorboat propeller or chainsaw injuries. The most immediate danger is from bleeding and, indeed, most fatalities from shark bites are due to massive blood loss and hemorrhagic shock. If bleeding can be controlled, then most victims will survive.
    Application of direct pressure to the wound will generally be sufficient to control hemorrhage, although use of arterial pressure points and tourniquets occasionally may be needed (e.g.,in cases of extremity amputation). In addition to controlling hemorrhage and treating shock, several additional points should be stressed with regard to the prehospital care of shark attack victims:
Because of the novel and often dramatic nature of these injuries, there is sometimes a tendency to voice comments that would not be expressed in other more commonly encountered types of trauma. Such comments may be particularly problematic for the victim, who typically has suffered a significant psychological injury, as well as physical trauma. Thus, be attuned to the emotional component of these injuries, and be especially careful about flip comments. Similarly, it is important to give frequent reassurance to the victim.
    Remember, too, that immersion casualties are often hypothermic, especially if their cardiovascular status is compromised, so protect the victim from further heat loss and begin rewarming as necessary.
    As with other shock victims, the Trendelenberg's position and m.a.s.t. Should be used in accordance with established protocol. Likewise, isotonic intravenous fluids and blood should be administered as they would be used in hemorrhagic shock due to other causes. Supplemental oxygen also should be administered.
(Ed. note: The Trendelenberg position is in the process of being deleted from rescue diver training. 12/90)
    Only essential treatment measures should be initiated in the field, since shark attack injuries are surgical problems that are generally best treated in the operating room. Time should not be wasted with nonessential interventions. The same applies to the emergency department, although, as with other types of major trauma, basic resuscitative, diagnostic, and preoperative measures should be undertaken in the ER. This includes baseline laboratory and essential radiographic studies, type and crossmatch for blood, and tetanus immunoprophylaxis, as needed.
   When managing shark bites, it is important to remember that,in addition to being complex wounds, these injuries are usually also highly contaminated - typically containing sand, algae, shark-tooth fragments, and other foreign matter. Marine water also contains a variety of pathogenic bacteria. Not surprisingly, wounds often become infected. Unfortunately, very ittle work has been done to characterize the organisms causing these infections, although a recent study has underscored the probable role of vibrio species and the relative resistance of these organisms to a wide variety of antimicrobial agents. Thus, it is imperative to thoroughly debride these wounds and,generally, it is prudent to delay their primary closure for several days, until it is known whether infection will occur.

||||||||||Understanding marine envenomations

    Encounters with marine animals are usually accidental. Indeed, most marine animals are docile and sting only when provoked. As with most other venoms, marine venoms are complex, large molecular weight mixtures of proteins and various low molecular weight compounds (such as indoles, histamines, and kinins). Their effects are numerous and include denaturation of cell membranes, degranulation of mast cells, release of histamine, activation of bradykinin, interruption of cellular metabolism, and interference with neuronal transmission. Because of their largely protein nature, most marine venoms are heatlabile. Not surprisingly, envenomated patients may develop numerous clinical manifestations.
    It is easiest to discuss marine envenomations by classifying the envenomating creatures as vertebrates and invertebrates. Due to space constraints, this review will primarily address envenomations likely to be seen by physicians practicing in North America, as well as some more lethal injuries usually seen in the Pacific and Indian oceans.

Envenomating invertebrate organisms

Invertebrate denizens of the deep may be primitive, but they can nonetheless cause injuries that run the clinical gamut from minor misery to death. The most common envenomating invertebrates include sea sponges, coelenterates, corals, cone shells, otopuses, sea urchins, and sea cucumbers.

SEA SPONGE contact often produces allergic and/or irritant reactions. Sponges, constructed of rugged, but elastic skeletons of "spongin," are sedentary creatures found attached to the ocean bottom. They are frequently colonized by coelenterates, crustaceans, echinoderms, and other marine life, which also may be potentially harmful to divers. The brilliant yellow-orange- vermillion "fire sponge" (tedania ignis), found in large numbers off Hawaii and the Florida keys, is one of the most common offenders.
Sponge contact dermatitis occurs when toxin is introduced into the skin - particularly of the hands - from spicule induced abrasions. Initial local itching and burning may progress to joint swelling. Those with severe reactions sometimes develop erythema multiforme (which can occur as late as 7-14 days after envenomation) and, rarely, may develop manifestations of anaphy- laxis.
    Even if the patient has delayed seeking treatment by several days, decontamination of the site will help to alleviate symptoms. Dilute acetic acid soaks-common household vinegar is fine-applied immediately and several times daily until symptoms resolve - both clean the site and provide symptomatic relief.Isopropyl alcohol is reportedly less effective.
    Frequent follow-up wound checks are important, since patients may develop infection or secondary inflammation. It is usually impossible to differentiate the toxic reaction from a possible infection in the acute phase. Do not begin antibiotics until obtaining wound cultures and sensitivities. Preliminary work shows that vibrio species are under-recognized as a cause of infections that follow wounds incurred in the aquatic environment. For outpatient management of soft-tissue infections, a course of trimethothoprim sulfamethoxazole (bactrim, septra) or tetracycline is usually adequate. Patients with more serious soft tissue infections may require treatment with a third generation cephalosporin and/or an aminoglycoside, such as gentamicin (garamycin).
    If secondary inflammation develops, topical steroid lotions are sometimes beneficial. Patients with marked hypersensitivity reactions may require systemic corticosteroids. Delayed desquamation of the surface epithelium often occurs anywhere from ten days to two months later.

COELENTERATE envenomation is quite common in warm areas of the Atlantic and Pacific oceans and the Mediterranean sea. Over 9000 species of coelenterates exist and, of these, the portugese man-of-war, (hydrozoans), the true jellyfish (schyphozoans), anemones, and soft corals possess venom-inducing stinging cells or nematocysts. Nematocyst venom contains a number of identified compounds, but they are still not well characterized. The severity of envenomation depends on the species, the number of nematocysts discharged (a single man-of-war envenomation may involve several hundred thousand nematocysts), and the victim's prior state of health. Many "jellyfish" stings are relatively minor, whereas chironex fleckeri (the box jellyfish or sea wasp) is reputedly the sea's most venomous inhabitant.
    Both toxic and allergic manifestations follow envenomation. Victims most commonly suffer only symptoms of an irritant dermatitis, including stinging, burning paresthesias, and pruritus. Reddish-brown skin discolorations occur in a whip-like pattern that corresponds to "tentacle prints." A more severe envenomation produces local edema, desquamation, and subepithelial hemorrhage. Rarely, life-threatening multisystem collapse occurs. In particular, victims stung by sea anemones or box-jellyfish often develop neuromuscular spasm, cardiac arrhythmias, and a host of other systemic symptoms that may progress to cardiorespiratory arrest.
    Treatment ideally begins at the scene of the injury, but should be initiated even when delayed. Immediately rinse the wound with sea water, normal saline, or other isotonic fluid (fresh water activates nematocysts, causing intensification of symptoms and increasing the likelihood of a serious reaction). Follow with a copious irrigation of household vinegar or isopropyl alcohol. Alcohol appears to increase nematocyst discharge in vitro, but most physicians experienced in treating nematocyst envenomations find it effective, particulary if applied as a paste of alcohol-meat tenderizer.

    Taking care to avoid self-contamination, remove any large tentacle fragments with forceps, apply shaving cream, and gently shave the affected area to remove minute fragments. Scraping the affected area with a credit card or similarly-edged device suffices if a razor is not available. Then, reapply vinegar or alcohol until the patient's pain abates. 0.5-1% Hydrocortisone lotion or cream may also help alleviate symptoms.
    In severely injured patients, life support must proceed simultaneously with decontamination. Monitor and treat patients for impending cardiovascular and respiratory collapse or anaphylaxis. Other symptomatic measures may also be necessary, depending on the organ systems affected. Patients with muscle spasm should receive intravenous calcium gluconate or methocarbamol. Parenteral narcotics are often necessary to relieve pain.
    In Australia, patients who have suffered a chironex envenomation may require administration of antivenin. Administer an initial dose of 20,000 units intravenously over five minutes. The risk of reaction to the antivenin, a sheep product, is the same as for equine hyperimmune globulin preparations. Appropriate precautions, including a careful history of allergies, skin testing, and administering the pretest and antivenin in a critical care environment, help reduce the risk of anaphylaxis.

CORALS can inflict vicious lacerations - usually in the extremities - with their razor-edged calcereous outer skeletons. They are found in warm waters (20 degrees c or greater) at depths of up to 30 meters. Victims usually notice only a scrape or cut.
    Management consists of vigorous cleansing to remove all foreign material (coral fragments or "dust") and devitalized tissue. Irrigate the laceration copiously with saline, followed with hydrogen peroxide irrigation to "bubble" out minute particles. Following the initial cleansing, the most practical method of wound care consists of sterile wet-to-dry dressings, using saline or dilute povidone-iodine (ideally 1%). Clinicians should anticipate secondary infections from poorly characterized, fastidious organisms, such as vibrio, pseudomonas, or acinetobacter. If mild, these infections usually respond to trimethoprim sulfamethoxazole or tetracycline or, if serious, to a third-generation cephalosporin or aminoglycoside.

CONE SHELLS are beautiful but potentially deadly gastropods that possess a sophisticated venom apparatus. They live predominantly in the Indian and Pacific oceans, are nocturnal feeders, pose a particular hazard to night divers who are attracted to their intricate shell markings, their venom inhibits neuromuscular transmission and has a curariform effect.
    Depending on the severity of the envenomation, the victim may experience anything from minor discomfort to full-blown neurologic deterioration. Mild envenomations, which are the most common kind, resemble wasp stings. But even if initial symptoms are minor, clinicians must observe patients for progressive local ischemia, cyanosis, and numbness, severe envenomation may cause progressive parasthesias, generalized muscular paralysis, and respiratory failure. Other neurologic signs of severe envenomation include dysphagia, dysphonia, weakness, and dyplopia, in rare cases, dissenimated intravascular coagulation, coma, and cardiovascular collapse may occur, death can follow a sting within two hours, underscoring the need for scrupulous observation and readiness, for life support efforts.
    Whether the victim's reaction is mild or severe, clinicians should provide supportive care. Treat for pain by first immersing the wound in water as hot as the patient can tolerate (about 113 degrees f). Local anesthetics injected directly into the wound or nerve blocks also afford relief of pain, but should be used only as a last resort. Since no antivenin exists for cone shell envenomations, the development of neurologic symptoms necessitates vigorous symptomatic treatment and preparation for a full life-support effort.

OCTOPUSES are shy cephalopods that usually inhabit the warm, shallow waters off australia. Fatalities have been documented from the bites of the australian spotted and blue-ringed octopuses(h. Maculosus and h. Lunulatus, respectively), tiny and timid creatures that rarely exceed 20 cm. In length. Unprovoked, the blue-ringed octopus is covered with poorly visible, blue rings that turn an iridescent peacock blue when it is angered. Most wounds occur when the unwary swimmer picks up the apparently harmless creature. Venom is injected painlessly, but under considerable pressure, and spreads immediately through the dermis and inside the muscle fascia. The powerful toxin blocks conduction in central and peripheral nerves (presumably by altering sodium conduction).
    Victims are often unaware that they have been bitten until signs and symptoms appear about five to ten minutes later. Two small puncture wounds that are initially numb, but begin to "burn" or "throb" with central radiation, are classic. Local urticaria is variable, but local bleeding occurs frequently and may portend coagulation abnormalities. Within 30 minutes, most victims have marked local erythema, swelling, pruritus, and pain. Those with severe envenomations may experience neurologic symptoms similar to manifestations of cone shell envenomation, which may progress rapidly to flaccid paralysis and apnea.
    No antivenin exists, making therapy for octopus bites largely supportive. Early and intensive support of respiratory function is crucial. Some experts recommend immediate excision of the wound site, but no clinical trials exist to support the efficacy of such measures. If not excised, the wound should be treated like any other puncture wound.

CERTAIN SEA URCHINS, slow-moving, radially symmetric animals found on rocky botttoms or burrowed in sand- produce potent neurotoxins and, thus, painful and potentially dangerous injuries. They are globlular or flattened creatures that are covered by regularly arranged spines and whose vital organs are encased in a hard shell. Some species also have delicate, triple-jawed seizing organs (pedicellariae). Both the spines and pedicellariae may cause injury. Following puncture, the distal fraet of the spines may remain embedded in the skin and cause a foreign body reaction along with the toxin reaction, most truly poisonous sea urchins live in the Indian or Pacific oceans or in the Red Sea.
    Sea urchin envenomation causes a painful reaction, but one that generally does not threaten life. Victims experience immediate burning pain, bleeding, and marked local tissue reaction that may last weeks. Sometimes local tissue swelling and discomfort reoccurs periodically for a year or more after the injury. Irretrievable spines may fragment under the skin, leaving a telltale purple spot due to spine dye discoloration. Spines may be difficult to locate without radiographs. Systemic reactions, including numbness, paralysis, and bronchospasm may occur, but are rare.
    Therapy is largely supportive, consisting of removal of spines, pain relief and, if necessary, life support. Hot water soaks and analgesics may provide relief of pain. Embedded spines are more difficult to extract, as they are easily fractured. If incompletely removed, they may produce a foreign- body, sarcoid-like granulomatous local reaction. Spines that have penetrated joints or are aligned close to neurovascular structures are particularly problematic and may require removal by a surgeon under an operating microscope. No justification exists for blindly probing into these wounds or pounding the affected area to "break up" the spines.

SEA CUCUMBERS are free-living, worm-like echinoderms that appear on the ocean floor. They are an infrequent cause of marine envenomation. Sea cucumbers produce a visceral liquid toxin (holothurin) that is excreted anally when the animal is threatened. Because some sea cucumbers feed on nematocysts, holothurin may be accompanied by the coelenterate venom. Signs and symptoms of envenomation are similar to portugese man-of-war stings and other types of contact dermatitis and may also include intense corneal inflammation.
    Initial treatment of a cucumber sting consists of application of vinegar or isopropyl alcohol. If the eye is involved, physicians should limit initial therapy to irrigation with copious amounts of saline.

Envenomating vertebrated marine life

Common envenomating vertebrate marine animals include the stingrays, catfish, scorpionfish, weeverfish, and sea snakes. Stingrays are a relatively frequent cause of injuries to swimmers and divers in tropical and subtropical waters. In the United States, they occur most commonly in the southeast,
particularly in the waters of the gulf coast and off bermuda.
    Stingrays are round, diamond, or kite-shaped animals with wide wing- like pectoral fins. They are peaceful bottom feeders that generally lie submerged in the sand with only the eyes, spiracles, and parts of the tail exposed. Most injuries occur when an unsuspecting swimmer steps on the fish, which stimulates an upward and forward thrust of the tail and drives the spine into the victim's foot or leg. As the spine is withdrawn, serious damage may result to the underlying structures if fragments of the intefumentary sheath may be left in the wound.

Stingray envenomation victims usually experience immediate, sharp, excruciating pain and bleeding. The pain rapidly radiates to involve the entire extremity and may be described as "shooting" or "throbbing." It peaks in about 90 minutes without treatment, but most victims will be symptomatic for several days. Physicians may note either a cyanotic, edematous puncture wound or a laceration that has jagged edges and bleeds freely. Systemic manifestations, including nausea, vomiting, and syncope, are variably present. Despite the toxicity of stingray venom, mortality following stingray injuries is very low and usually occurs due to direct damage of vital structures.
    Emergency management ideally begins immediately after the envenomation and focuses on inactivating the venom, symptomatic measures, and preventing infection. One should immediately immerse the wound in hot water (up to 113 degrees f), which helps to inactivate the heat-labile venom and relieve pain. After soaking, copiously irrigate the wound, and explore it to remove any obvious retained integumentary sheath. Administer tetanus prophylaxis, if needed, and analgesics as necessary for pain relief. Systemic manifestitions are rare, but should be treated symptomatically. A substantial number of stingray injuries become secondarily infected, but there is no justification for giving prophylatic antibiotics unless there will be a delay of more than twelve hours prior to proper debridement and irrigation.
    Catfish inhabit both fresh and salt waters and account for numerous piscine stings. These creatures are named for their well- developed, sensory barbels ("whiskers") that surround the mouth. Marine catfish typically travel in large schools and are bottom feeders. Their venom apparatus consists of exquisitely sharp dorsal and pectoral fin spines that contain venom glands. Their venom is similar to, although milder than, stingray venom.
Catfish stings usually involve the upper extremity and typically occur in fishermen when they remove the fish from the hook or attempt to clean them. The victim usually suffers an instantaneous stinging or scalding sensation that may radiate throughout the extremity, if untreated, pain usually subsides over a few hours, but may persist for up to 48 hours in severe envenomations.
    Management of catfish envenomation is symptomatic, with relief of pain, cleansing the wound, and tetanus prophylaxis of top priority. Their venom is also heat-labile, so hot soaks have a role here, too. Sequelae are rare, but secondary infection and necrosis may occur. Scorpionfish. Most aquatic experts consider the family scorpaenidae to be the most dangerous of the venomous bony fishes, their envenomations are common, horribly painful and, depending on the species, potentially deadly. The approximately 300 species of scorpaenidae are typified by the three genera pterois (lionfish, zebrafish, turkeyfish), scorpaena scorpaenidae are distributed throughout the world's tropical waters, but are especially prevalent in the red sea and the indian and pacific oceans. Private and commercial fish handlers import many thousands of lionfish - and less numbers of scorpionfish - into the u.s. Each year, making them also at risk for envenomation, however, since this fish is only indigenous to the indo-pacific region.
    Envenomation usually occurs when the unsuspecting diver accidentally handles the well-camouflaged creature, which erects spines on its dorsal, anal, or pelvic fins. Pain occurs immediately after envenomation and is sharp, throbbing, and intense. The wound and surrounding area typically become cyanotic, and patients may report anesthesia or paresthesias.
Severe envenomation may result in localized tissue sloughing and cellulitis. More serious systemic manifestations are infrequent. Stonefish envenomations are usually more severe and have been associated with a number of deaths.
    According to a recent clinical study, simple hot water immersion is extremely effective in relieving the pain associated with scorpaenidae envenomation. 45 Of the 51 patients in this study (80%0 experienced complete resolution of pain with this method, and 14% described partial relief). Alleviation of pain occurs due to breakdown of the venom, whose principal toxin is heat-labile. Patients unresponsive to this regimen may require narcotics, but soaking is obviously the preferred and more specific treatment. Other non-specific supportive measures - similar to those for stingray envenomation - should be employed as necessary. Antivenin is indicated only for the more serious stonefish envenomation or for the very rare patient with life-threatening systematic symptoms.

    Weeverfish inflict one of the most dreaded and painful envenomations known to humans. These are extremely venomous fish that dwell in the eastern atlantic ocean, the mediterranean sea, and european coastal waters. They normally bury themselves in the soft sandy or muddy bottom. Typically, envenomation results when a swimmer or fisherman steps on them (the majority of stings occur in professional fishermen). Their dorsal and opercular dentinal spines, associated with venom-producing glands, can penetrate a leather boot.
    The pain of a weeverfish sting is immediate and severe. Patients describe it as "burning" or "sticking," and it may radiate into the thorax and mimic symptoms of a myocardial infarction. If untreated, the pain's intensity peaks in the first few minutes and resolves within 24 hours, but occasionally, the unfortunate victim suffers for days. When examining a patient for a weeverfish sting, look for a round puncture wound that usually does not bleed and may be ischemic and edematous. The entire limb sometimes becomes edematous, and myonecrosis and cellulitis can eventually ensue. Systemic signs and symptoms most frequently include disorientation, dyspnea with a choking sensation, cyanosis, and cardiac arrhythmias. Occasionally, syncope and seizures occur and, more rarely, shock. Emergency management of weeverfish stings is largely supportive and resembles that of stingray envenomation. Pain is usually more difficult to control, however, and warrants use of narcotics. Immersion in hot water may help to alleviate pain.
    Sea snakes. Fortunately, most american physicians will never see a sea snake envenomation. The greatest number of these injuries occur along the coast of southeast asia, in the persian gulf, and in the maylay archipelago. There are no sea snakes in the atlantic ocean or caribbean sea, but rare sightings of sea snakes have been reported from hawaii. Native fishermen, the accidental shake handler, or the unwary swimmer are the ones who most frequently suffer bites. The venom is more toxic than terrestrial snake venom and contains neurotoxic, hemolytic, and myotoxic fractions.
Most snake bites do not cause pain or other symptoms initially; rather, symptoms of envenomation usually evolve over six to eight hours. Initial complaints include restlessness, malaise, or euphoria. Neurologic deterioration is heralded by myalgias, stiffness, and difficulty in speaking. Ascending flaccid or spastic paralysis follows, with dysphagia, aphonia, and hyperreflexia that progresses to hyporeflexia. Untreated victims may lose their vision and develop respiratory distress, seizures, and/or lapse into coma. Myoglobinuria, frequently accompanied by albuminuria and hemoglobinuria, may appear three to six hours after the bite.
Rapidly transporting the victim to medical care is the highest priority. Incision and suction are of no value if delayed for longer than a few minutes after envenomation. Immobilize the affected limb, and keep it in a dependent position. Do not apply tourniquets. In australia, pressure immobilization with an elastic wrap is recommended.
    Antivenin is specific and absolutely indicated in all severe cases of envenomation. Clinicians must observe all victims for at least eight hours and be prepared to administer antivenin if any clinical indication of envenomation becomes evident, since supportive therapy often fails to maintain the victim.

An ounce of prevention

Marine envenomation patients are no longer limited to coastal and resort areas. When these patients seek care, clinicians must know how to identify the offending creature and provide treatment as specific as is available. In cases of chironex, stonefish, and sea snake envenomations, antivenin may be lifesaving and help prevent complications. Many other, more common envenomations can be treated by hot water immersion, which inactivates the protein venom. A better approach, obviously, is prevention. Knowing - and avoiding - local envenomating fish is common sense.

||||||||||Near-drowning

This series is heavily weighted toward cold water submersion cases (less than 70 degrees f). The data is difficult to analyze because of the many hospitals contributing cases, and the lack of standardization of parameters, e.g., temperature correction of blood gases, inconsistent reports from the field, differences in cpr skills, lack of uniform vital sign data, and the different circumstances of each near-drowning episode.

Prognosis for survival

The following are listed in order of importance with the highest values at the top of the list:

1. The age of the patient
The younger> infants and toddlers are more resuscitatable with the mean age of survivors being 11! In the teens and early 20's these patients are "over the hill" so to speak and unless other factors are apparent to a high degree they are not as likely to survive.

2. Submersion time
The shorter the submersion time the better. Given the water is cold as defined above, submersion times up to one hour are considered survivable under favorable circumstances as below, and rescue and resuscitation should be considered rather than a body recovery.

3. Water temperature
The colder the water the better the survival statistics. Resuscitations of 20-25 year olds in 28 degree water in alaska were common.
4. Struggle
The victims that struggled the least were eminently resuscitatable! That includes infants and toddlers who have frequently been reported to fall in the water and suddenly remain prone, floating, and apparently incapacitated. This also includes those who are heavily alcohol intoxicated. They struggle little and cool quickly as they are vasodilated.

5. Injuries, illnesses, etiology of near-drowning any burns,
Major fractures, crush injuries very negatively affect the survival of the cold immersion victim. This circumstance is much worse than either injury alone. The end result is not additive.

6. Quality of cpr
The quality of cpr was rated in many of cases using the witnesses as historians. Looking at credentials, experience factor, obvious errors, environmental circumstances, to decide if the cpr was appropriately done. Where it was either delayed, done incorrectly, or discontinuously, the results were uniformly poor.

7. Cleanliness of water
Water quality was looked at, e.g., swampy, muddy, brackish, salt vs. Fresh, and other liquids not water. There was no difference in salt vs. Fresh in the cold water survival series. Patients did better in cleaner water.

At this point if you can tell the age, water temperature, length of submersion, whether cpr is/was done promptly and correctly, presence of any other injuries, the body of water, and a little of the circumstances of the near-drowning, a good projection of the eventual survivability can be made.
For general interest other extraneous (perhaps) factors found of no help are;
Heimlich maneuver sex
Swimming ability race
Eating a meal (the great salt vs. Fresh water
Cramp theory) intercurrent illnesses
One factor which is confusing is that 10% of patients in this study had a history of prior seizure disorder. This compares with 0.5% of the people walking in the street.

||||||||||Hypothermia

    Emergency medical personnel have become increasingly skilled at managing accidental hypothermia. Furthermore, recent agreement among clinicians dealing with hypothermic patients has led to simplified treatment recommendations for managing this emergency. This series presents a basic summary of pertinent hypothermia signs, symptoms, and pre-hospital treatment measures.
    Hypothermia is simply a lowering of the body's normal core temperature. Significant hypothermia begins at core temperatures below 35 degrees c and severe hypothermia occurs at temperatures below about 31 degrees c. Nearly all physiologic functions are slowed in severe hypothermia, including heart rate, respiratory rate, metabolic rate, mentation and reflexes. A severely hypothermic patient is similar to a victim of multiple trauma, but one in which all organ systems are affected. The most important signs and symptoms are readily observed and/or measured by emergency medical services (ems) personnel:
Bradycardia
Bradypnea
Altered mental status (slurred speech, staggered gait, diminished response to pain or verbal stimuli, or unconsciousness)
Cold skin
Low core temperature

Severely hypothermic patients may have other pathophysiologic changes that rescuers cannot so easily detect but which may adversely affect the patient's outcome. These are:
Serum electrolyte abnormalities
Alterations in blood gases
Dysrhythmias
Dehydration
Temperature gradients between deep and superficial tissues

The primary goals for ems personnel in treating and handling of hypothermia patients in the field are to prevent cardiopulmonary arrest, to stabilize core temperature ( as opposed to rewarming the patient). And to transport the patient to a site of definitive medical care. These goals may be summarized simply as (rescue. Examine. Insulate. And transport).

Rescue
In moving the patient from cold environment, maintain as horizontal a posture as possible. This will minimize the risk of orthostatic hypotension and will facilitate cerebral profusion.This posture is particularly important for patients recovered from cold water. The hydrostatic pressure of the surrounding water on the patient's body acts to a degree like anti-shock trousers. When the patient is recovered from the water, particularly if it is done in a vertical posture, the hydrostatic pressure is removed (like suddenly deflating anti- shock trousers) and hypotension may result. This phenomenon has been suspected as a cause of post-rescue death among hypothermia victims. If the victim cannot be rescued in a horizontal posture, place the
Patient supine as quickly as possible after removal from the cold environment.

Examination
Abc's (airway, breathing, circulation) ensure an open airway, adequate ventilation, and circulation. If the patient is severely hypothermic, respirations and pulse may both be slow, shallow and hard to detect. Therefore, take up to a*********** to measure these vital signs.
Commence cpr, if necessary; mouth-to-mouth or mouth-to-mask ventilations are preferable to mechanical ventilations because both provide heated humidified gas to the patient during cpr. If available 100% heated humidified oxygen would be even better. Hypothermia patients with any measurable pulse or respirations do not require cpr, even though they may have extreme bradycardia and marked hypotension. In severe hypothermia, oxygen requirements are drastically diminished; the reduced levels of systolic pressure and heart rate are usually adequate to meet tissue metabolic needs. Inappropriate cpr in a severely hypothermic patient may precipitate ventricular fibrillation in the cold, irritable myocardium. If so the pulse and respirations are absent or immeasurable after one minute, commence cpr. If the patient is found floating face-down in water, assume he is a victim of cold-water near-drowning and commence cpr immediately in the normal manner. In this case, hypoxia needs to be corrected as soon as possible; hypothermia is only of secondary importance.
Do not apply the usual protocols for advanced cardiac life support (acls); defibrillation and drug treatments are not useful in managing the severely hypothermic patient in cardiac arrest whose temperature is below 30 degrees c, since the cold myocardium does not respond in the same manner as a normothermic heart. Worse, it can be damaged by repeated defibrillatory shocks. Most studies have shown that core temperature must reach approximately 30 degrees c before defibrillation will be effective. Furthermore, administered drugs will not be metabolized or cleared normally by a hypothermic liver and kidneys. Instead they may accumulate and become active as the body rewarms.
Note mental status; evaluate the patient's level of consciousness, pupillary size and light reflex, response to pain or verbal stimuli, ability to walk and think clearly. If any of these signs and symptoms are abnormal, consider hypothermia in your differential diagnosis.
Check closely for other possible injuries. Look especially for frostbite, soft tissue injuries, fractures, etc. Hypothermic patients's ability to feel and respond to pain are diminished, so his subjective response to injury may be absent.
Measure vital signs: pulse, respiratory rate, blood pressure, and temperature. Core temperature measurements are essential (e.g., rectal or esophageal temperature). If these cannot be obtained, take an oral or axillary temperature. Although not as accurate as rectal temperature, these more superficial sites will at least indicate that the patient's real core temperature is no lower than the thermometer reading in the mouth or axilla. In all temperature measurements, a low-reading
thermometer (down to 20 degrees c) is essential. A normal clinical thermometer is not appropriate since it reads only to 34 degrees c.
Control hemorrhage in the usual manner. Control shock, but elevate the patient carefully before applying anti-shock trousers. Inflation of the trousers may create a sudden bolus of cold, acidotic venous return from the lower extremities. Sudden temperature and/or ph changes have been shown to produce ventricular fibrillation in a cold myocardium. Anti-shock trousers should only be used if the hypotension is definitely known to be secondary to fluid depletion or blood loss. Hypothermia itself can cause hypotension without massive fluid loss.
Handle the patient very gently. Excessive mechanical stimulation of the cold myocardium has been another suspected cause of cardiac arrest and post-rescue death in the severely hypothermic patient.

Insulation
Prevent further heat loss. This is one of the primary goals in the pre-hospital management of hypothermia. Remove wet clothing. Do not expose the patient's skin to cold air, wind or spray, especially the down-wash created by helicopter rotor blades. If the patient requires helicopter transportation, wrap well in blankets, a sleeping bag, etc. And be sure to insulate his head as well.

Gently add heat. The intent is not to rewarm the patient but rather to stabilize the core temperature and prevent further heat loss. Active rewarming is frequently complicated by dysrhythmias, electrolyte and blood gas changes, etc., and should only be attempted in a hospital setting. Useful techniques for ems personnel are:
Administration of heated, humidified oxygen or air by endo- or nasotracheal tube or by mask at a temperature of approximately 40-42 degrees c. This will prevent further respiratory heat losses, which are significant in hypothermia patients, and will help stabilize heart, lung, and brain temperatures.
Application of external heat ( hot packs, heating pads, etc.) to the head, neck, trunk, and groin. These sources of external heat must be well insulated from direct contact with the patient's skin in order to prevent severe thermal burns. Hypothermic skin is very sensitive to heat and is easily injured. Third-degree burns have resulted from the application of a lukewarm hot water bottle.
Donation of a rescuer's body heat to the patient. When wrapped together in a blanket or sleeping bag, a rescuer can donate his body heat to a hypothermic patient. This technique is not without risk, since slow external warming in this manner may potentiate the venous return of cold, acidotic blood. Body-to-body rewarming should only be used when there will be a long delay in getting the patient to a site of definitive medical care and when more appropriate methods of adding heat are unavailable.
In no case should hot showers or hot baths be used in the
Field, these methods are associated with a high probability of producing rapid changes in blood gases and serum electrolytes, which may potentiate ventricular fibrillation.
Avoid the administration of oral fluids or food until the patient has recovered an adequate cough and gag reflex. Hot drinks are ineffective in warming a severely hypothermic victim, but they may be useful in raising the morale of mildly hypothermic survivors. Alcoholic beverages are contraindicated in all cases.
Administer warm intravenous fluids; d5w, d5n, or ns are preferable to lactated ringer's since a hypothermic liver may be unable to metabolize lactate normally. Most hypothermic patients are dehydrated, so the rapid administration of 300-500 cc's (for an adult male) followed by 75-100cc's/hr are indicated. Avoid the administration of cold fluids. Plastic I.v. Bottles can be easily carried inside a rescuer's clothing preferably next to the skin to keep the fluids warm.

Transportation
When transport times are less than 15 minutes, adding heat and administering I.v. Fluids are unnecessary. These treatments should, however, be used during longer transport times. The receiving facility should be selected on the basis of knowledge and experience in managing hypothermic patients. In the same manner that victims of multiple trauma are most appropriately managed in trauma centers, severely hypothermic patients are best managed in hospitals equipped to handle potential complications and provide core-rewarming therapy.

||||||||||The demand valve resuscitator
& Positive pressure oxygen systems

At one time pressure-cycled automatic resuscitators were standard pieces of equipment for ambulances, rescue squads, police emergency units, lifeguard stations and other emergency medical service installations. When cpr techniques were developed, however, it was found that external cardiac compressions would terminate the inflation cycle. Thus the patient was poorly ventilated, or worse yet, not ventilated at all. Technology then produced the manually triggered, oxygen- powered ventilating unit that is generally called the demand valve resuscitator. These units can either assist or control ventilation.
The pushbutton that controls oxygen flow is placed on top of the valve unit to which the facepiece is attached. Thus the operator can control oxygen flow while holding the mask firmly in place with both hands. Flow occurs in two ways. When the operator depresses the control button, oxygen flows through the face maskat a high rate (greater than 150 liters/minute in some models) and inflates the lungs until a preset pressure is reached: in some units this pressure is 40mm hg. The ability to provide oxygen until the preset pressure is reached or the control button is released makes the demand valve resuscitator not only useful, but also desirable in cpr efforts.
Flow also occurs in a demand valve resuscitator when a patient inhales through the face mask and continues until exhalation starts.
Since manually triggered, demand valve resusitators are oxygen powered, 100% oxygen is available to the patient. A proper seal must be maintained between the face mask and the patient's face at all times, however, to prevent loss of oxygen and pressure.

||||||||||Bacteriology of the freshwater environment:
Implications for clinical therapy

Wounds acquired in the aquatic environment are contaminated with water and often with mud or bottom sediment. To compound the hazard for infection, penetration of the skin by spines, teeth,baited fishhooks, or contaminated metal can result in inoculation of pathogenic organisms into a wound. Investigation of freshwater pathogens parallels the previous study of marine bact- eria, which indicated that bacteria found in marine water and on animals are not typical of terrestrial flora that cause soft tissue wound infections. There are diverse bacterial species present in fresh water and therefore in infected wounds of natural freshwater origin. Recognition of the potential for infection with uncommon organisms should alert the clinician to consider appropriate antibiotic therapy.
Aeromonas hydrophilia is a facultative anaerobic, motile, asporogenous, polarly-flagellated, and gram-negative bacillus of the vibrionaceae family that is often isolated from fresh water and occasionally from marine water. Several species of aeromonas are pathogenic to fish, frogs, and reptiles as well as to man. It is not generally considered to be a fecal contaminant, but rather a commensal found in water with a high content of nonfecal organic substances. The organism survives in water temperatures that range from 0 to 45 c, tolerates a wide range of ph, and has been cultured from both swimming pools and tap water. Infections in human beings are generally noted in the immunocompromised host or following a documented environmental exposure, such as alligator bite, water-skiing injury, or pulmonary aspiration associated with an episode of near-drowning. Both soft tissue and gastroenteritic human infections occur predominately during the period from may to november.
A commentary on cases reviewed from literature notes that the common clinical picture is that of a compromised host, often with underlying illness such as leukemia, carcinoma, hepatobiliary disease, renal failure, or drug-induced immunosup- pression, who developed a syndrome suggestive of gram-negative bacteremia. In this regard, aeromonas hydrophilia infection ap- pears to pose a similar hazard to ambulatory victims of freshwater acquired injuries as do vibrio species in the marine environment. During infections in the normal host, aeromonas is nearly always cultured from a local wound, with rare bacteremia. A wound, commonly a puncture, may become cellulitic within eight to 24 hours, with erythema, edema, and a purulent discharge. The appearance may be indistinguishable from streptococcal cel- lulitis, with localized pain, lymphangitis, fever, and chills. Left untreated or managed with antibiotics to which the organism is not susceptible, this may progress to a severe gas-forming soft tissue infection with bullae formation, necrotizing myositis or osteomyelitis.
Aermonas can be misidentified with routine microbiological tests because of its morphological and biochemical similarities to the enterobacteriaceae, including serratia and escherichia coli. When there is clinical concern, the laboratory should be alerted to the possibility of aeromonas hydrophilia, as they will

Need to inoculated special media, such as " xdca", for isolation of this pathogen. Cultural characteristics of aeromonas hydrophilia include oxidase (+); macconkey agar (+); hemolysis (sheep blood) (+); growth at 42 c; motility(+); cetrimide agar(- ); growth at ph 5.6; indole(+); gelatin(+); methyl red(+); nit- rate to nitrite(-); kligler iron agar, slant/butt (alkaline/acid and gas); arginine dihydrolase(+); lysine decarboxylase(+/-); malonate(-); o-nitrophenyl b-d-galactopyranoside(+); 10% lac- tose(+); glucose(+); gas glucose(+); starch(+); and lecithinase(+).
The antimicrobial susceptibility of aeromonas hydrophilia is not unlike that noted previously. The beta-lactamase elaborated by aeromonas may account for the inefficacy of the penicillins and first- generation cephalosporins. There has been no isolating bacterium violaceum from our specimens. This is not surprising considering that fewer than 15 cases have been reported in the united states. The organism is generally sensitive to piperacil- lin, carbenicillin, chloramphenicol, gentamicin, kanamycin, tob- ramycin, trimethoprim-sulfamethoxazole, and tetracycline, and resistant to ampicillin and cephalothin, which does not lead to altering forthcoming recommendations for antibiotic administration.
The identification of vibrio parahaemolyticus in a freshwater sample suggests that what has heretofore been considered a halophilic organism may adapt to a more hypotonic environment.
These laboratory data have clinical application. Management of freshwater-acquired infections should generally include therapy against aeromonas species. First-generation cephalosporins provide poor coverage against growth of freshwater bacteria. Third-generation cephalosporins provide excellent cov- erage, while second-generation products are less effective. Ciprofloxacin, imipenim, ceftazidime, gentamincin, and trimetho- prim-sulfamethoxazole are effective against gram-negative micro- organisms. It is noteworthy that trimethoprim alone is markedly ineffacious, as is ampicillin. Gram-positive organisms display predictable sensitivities.
The question of whether to begin antimicrobial therapy prior to development of a wound infection has not been answered. Pending a prospective evaluation of prophylactic antibiotics in freshwater-acquired wounds, these are the recommendations on the potentially serious nature of soft tissue infections caused by aeromonas species.
Minor abrasions or lacerations do not require the administration of prophylactic antibiotics in the normal host. Persons who are chronically ill (eg., diabetes, hemophilia, thalassemia), immunologically impaired (eg., leukemia, acquired immunodeficiency syndrome, undergoing chemotherapy or long-term corticosteroid in>
liver disease (eg., hepatitis, cirrhosis, hemochromatosis), particularly those with elevated serum iron levels, should be placed immediately on oral trimethoprim-sulfamethoxazole (1st choice) or tetracycline (2nd choice), as these persons appear to have an increased risk for serious wound infection and bacteremia. Although not tested in this series, doxycycline may be an acceptable alternative to tetracycline. Penicillin, ampi- cillin, erythromycin, and trimethoprim do not appear to be accep- table alternatives. Of course, the development of an infection indicates the need for promt debridement and early antibiotic therapy.
    Serious injuries include large lacerations, severe burns, deep puncture wounds, or a retained foreign body. All such wounds acquired in a natural freshwater setting (or land-acquired and immersed into natural fresh water) should be irrigated vigorously with normal saline to remove debris and as many bacteria as possible. All crushed or devitalized tissue should be sharply debrided. All major penetrating injuries, such as propeller lacerations or wounds with exposed tendons or bones, should be explored, cleaned, and debrided in the operating room. Whenever possible, large wounds should be closed around drains or left unsutured in preparation for delayed primary closure. Antitetanus prophylaxis is standard. If the victim requires surgery and hospitalization for wound management, recommended antibiotics include ciprofloxacin, imipenem-cilastatin, ceftazidime, gentamicin, or trimethoprim-sulfamethoxazole. If the victim is to be managed as an outpatient, the oral drugs of choice are trimthoprim-sulfamethoxazole or tetracycline. It is a clinical decision whether oral therapy should be preceded by a single iv or intramuscular loading dose of a similar or different antibiotic, commonly an aminoglycoside.
Infected wounds should be cultured. Pending culture and sensitivity results, the patient should be managed with antibiotics as outlined above. Persons who develop fever, rapidly progressive cellulitis characterized by bullae, and large areas of necrosis should be suspected of suffering from aeromonas hydrophila infection. Milder aeromonas infections may have the appearance of streptococcal cellulitis.

Conclusion Indigenous bacterial pathogens in the freshwater aquatic environment are not identical to those found on land. Culture and sensitivity data gathered in an investigation of common freshwater sources yield a unique array of microbes, including aeromonas, pseudomonas, and vibrio species. Antibiotics that are effective against the majority of gram-negative microorganisms include ciprofloxacin, imipenim, cefrazidime, and trimethoprim- sulfamethoxazole.

||||||||||Bacteriology of the marine environment:
Implications for clinical therapy

Wounds acquired in the marine environment are soaked in sea water and occasionally are contaminated with bottom sediment. To compound the hazard of a marine bacterial infection, penetration of the epidermis or dermis by the spines or teeth of marine animals, the razor-sharp edges of coral or shellfish, and the nematocysts of toxic pelagic coelenterates may inoculate pathogenic organisms into a wound.
Investigation indicates that the bacteria that may be found in wounds associated with marine water and animals are not ident- ical to the typical terrestrial wound contaminants that cause soft tissue wound infections. Others have established the presence of diverse bacterial species in sea water, marine animals, and infected wounds of marine origin. While some of these organisms are likely to be terrestrial wound contaminants, others clearly originate from the aquatic environment.
In a recent report, the teeth of a great white shark (carcharodon carcharis) were swabbed and yielded isolates that included v alginolyticus, v fluvialis, and v parahaemolyticus. The leopard and mako sharks cultured in this investigation yielded three additional vibrio species: v damsela, v furnisii, and v splendidus I. During the last decade, vibrio species other than v cholerae have been recognized as agents of serious infectious disease, and these bacteria have been found to cover a wide geographical range that only recently has been appreciated. Vibrio species are halophilic gram-negative rods that are facultative anaerobes. They are part of the normal flora of coastal waters not only in the united states, but in many exotic locations frequented by recreational and industrial divers and seafarers. Mesophilic organisms, vibrio species grow best at water temperatures of 24 c to 40 c, and are rarely found in water colder than 8 c.
In most studies reported to date, infections seem to cluster in the united states and european coastal regions in the summer months. However, this may be more closely related to increased numbers of people at the seashore in the summer months than to the concentration of bacterial in the water. Vibrio species are ubiquitous in tropical waters year round.
Gastrointestinal illness has been associated with v cholerae o group1, non 0 1, v parahaemolyticus, v fluvialis, v mimicus, v hollisae, v furnissii, and v vulnificus. Wound infections have been documented to yield v cholerae o group 1 and non 0 1, v parahaemolyticus, v vulnificus, v alginolyticus, and v damsela. Septicemia, with or without an obvious source, has been attributed to infections with v cholerae non 0 1, v parahaemolyticus, v hollisae, v alginolyticus, v vulnificus, and v metschnikovii.
The clinical appearance of a serious wound infection following inoculation with vibrio vulnificus is similar to that caused by v parahaemolyticus, with marked soft tissue edema and necrosis that may progress rapidly to septicemia. Wound infections due to v parahaemolyticus have been noted in previously healthy individuals. Rapidly progressive cellulitis, fulminant myositis, and septicemia generally have occurred in immunosuppressed of chronically ill persons, particularly those who suffer from liver disease. Extracellular proteases elaborated by the organism, which include a potent collagenase, probably contribute to the rapid invasion of healthy issue. There have not been enough reported cases to determine whether the hemorrhagic skin vesiculation seen with v parahaemolyticus septicemia is also a constant feature of v vulnificus and v damsela infections. V vulnificus previously was classified by the centers for disease control as a "lactose-positive" (able to ferment lactose) vibrio.
The identification of marine organisms requires special consierations in the clinical microbiology laboratory. Although plating on standard laboratory media may detect no more than 0.1% to 1% of the total number of microorganisms found in seawater or marine sediment, most marine bacteria that are pathogenic to human beings can be readily recovered on a standard media. In culture, marine bacteria may grow at a slower rate than do terrestrial bacteria, which delays identification. Pleomorphism in culture has been attrivuted to adaptation to small concentration of nutrients in seawater.
The clinician should alert the laboratory that marine- acquired organisms may be present. Although vibrio species known to be pathogenic can grow on conventional blood agar media, other marine bacteria may require saline-supplemented media and incubation at 25 c instead of the standard 35 c to 37 c. The pathogenic capacity of these bacteria is not known. If a labora- tory does not have the time or resources to perform a complete identification, the bacteria may be sent to a reference labora- tory.
Under investigation, 10% of the 67 isolates that were ident- ified were not capable of growth on the standard blood agar media used in clinical microbiology laboratories. All of these isolates were members of the genus alteromonas, which to date is not known to include any pathogenic species. Therefore, conventional cult- uring techniques should be adequate for initial isolation of most pathogenic marine organisms.
Standard media used for antimicrobial susceptibility testing may need to be supplemented with sodium chloride in order to permit the growth of marine bacteria. Most vibrio species isolated from clinical specimens are able to grow in unsupplemented mueller-hinton broth. Among marine isolates, sup- plementation of mueller-hinton broth with sodium chloride was necessary in most cases to achieve adequate growth. Four (6%) of isolates would not grow even with the additional salinity. Three of these isolates were identified as v splendidus I, which is not known to be pathogenic. The one remaining isolate was not identi- fied.
The antibiotic susceptibility of vibrio species is not un- like a previous evaluation of pseudomonas putrefaciens and five vibrio strains isolated from the teeth of a great white shark, carcharodon carcharias. In that report, gentamicin, moxalactam, sulfamthoxazole, tetracycline, chloramphenicol, amikacin, tobra- mycin, and cefoxitin were uniformly inhibitory. The susceptibil- ity to cefoperazone and cefotoaxime was variable. Antibiotics

With no appreciable effect included cephalothin, penicillin, ampicillin, and piperacillin. Gentamicin, tetracycline, and cef- oxitin to be effective against only 50% to 90% of these isolates, and cefoperazone, cefotaxime, and peperacillin to effective against more than 90% of the isolates. Human case reports and brief series corroborate these findings.
With regard to antibiotics, these in vitro data suggest that management of marine-acquired infections should include therapy against vibrio species. Imipenem is uniformly efficacious against gram-negative marine bacteria, as is azlocillin, mezlocillin, piperacillin, cefoperazone, cefotaxime, ceftazidime, and moxalactam. Notable is the apparent inefficacy of cefsulodin, another third-generation cephalosporin. Non-ferment- ative bacteria (alteromonas, pseudomonas, and deleya species) were susceptible to nearly all of the antibiotics tested. This series may contain the first in vitro demonstration of efficacy of imipenem (n-formimidoyl thienamycin) against vibrio species.
The issue of whether to begin antimicrobial therapy prior to establishment of a wound infection is controversial. There appears to be no advantage to quantitative wound culture prior to the appearance of a wound infection. Pending a well designed prospective evaluation of prophylactic antibiotics in marine wounds, the following recommendations on the often indolent nature of aquatic-acquired lisions and malignant potential of soft tissue infections caused by vibrio species.
Minor abrasions or lacerations (eg, coral cuts or superficial sea urchin puncture wounds) probably do not require the administration of prophylactic antibiotics in the normal host. Persons who are chronically ill, immunologically impaired, undergoing chemotherapy or long- term corticosteroid ingestion, or who suffer from serious liver disease should be placed immediately on oral trimethoprim-sulfamethoxazole or tetracycline. Penicillin, ampicillin, and erythromycin do not appear to be acceptable alternatives.
Serious injuries include large lacerations, major burns deep puncture wounds, or a retained foreign body. All significant wounds acquired in a marine setting ( or a land-acquired wound immersed in sea water) should be vigorously irrigated with sterile normal saline or water; crushed or devitalized tissue should be sharply debrided; and major penetrating injuries should be explored, cleaned, and debrided in the operating room. If the victim requires hospitalization, recommended parenteral antibiotics prior to culture and sensitivity results include gentamicin, tobramycin, or amikacin; cefoperazone, cefotaxime, or deftazidime, or chloramphenicol.
Infected wounds should be cultured for aerobes and anaerobes. Pending culture and sensitivity results, the patient should be managed with antibiotics. Imipenem is efficacious and , while not recommended as a prophylactic antibiotic, may prove extremely valuable for established infections. Persons who have been wounded in a marine environment and who develop rapidly progressive cellulitis and/or myositis with large hemorrhagic bullae should be suspected of suffering from vibrio parahaemolyticus or v vulnificus infection, particularly in the presence of chronic liver disease. Clostridium perfringens would be a less likely pathogen. If a wound infection is minor and has the appearance of a classic erysipeloid reaction (most commonly on the hand of a seafood handler), penicillin or erythromycin should be added to the therapeutic regimen in order to treat an infection caused by ersipelothrix rhusopathiae.
Other situations in which infection commonly complicates a marine accident include near-drowning, middle ear hemorrhage associated with ruptured tympanic membrane, and otitis externa. The microbiological considerations are the same, and the clinician and laboratory personnel should be alert to the presence of uncommon organisms. Similarly, sepsis following the ingestion of raw seafood should lead the clinician to suspect vibrio bacteremia.
These clinical recommendations are based on in vitro data. The management of a specific wound and choice of antibiotic(s) should be guided by this new information and the clinical judge- ment of the treating physician.

|||||||||||History of hyperbaric medicine

Nowak, in 1884, published a summary of medical aspects of raised atmospheric pressures in caissons, and in 1907, the british admiralty appointed a deep diving committee on which j.b.s.haldane was the physiological member. As a result of his investigations, haldane recommended the "stage" method of decompression, which was adopted by the committee, and with which the admiralty set the limit for diving operations at 64 meters.
Following the work of haldane and others, events progressed quite rapidly in both areas of pressure medicine. Diving operations were getting deeper and more complex, more clinical chambers were being installed in hospitals worldwide, and more research was being performed.
Orville cunningham, in 1920, built a large chamber in kansas and claimed cures for patients with diabetes, syphillis and cancer. In the 1930's, the timkens, of roller bearing fame, built the "ball" chamber. This chamber was several stories high and boasted libraries, sitting rooms and various other creature comforts. At this time, the american medical association questioned the effectiveness of hyperbaric oxygenation, and the field went into dormancy. The ball chamber was cut up for scrap during world war ii. However dr.albert behnke, while working with u.s. Navy divers during the 1930's, advanced the theories that the increased partial pressures of oxygen might be of benefit in the treatment of certain conditions, including decompression sickness. While the clinical applications of hyperbaric medicine lay generally dormant during ww ii, the development of more effective means of decompression and the treatment of decomp- pression sickness advanced due to the basic work done by behnke and others.
In 1960, borema, in holland, published his classic paper "life without blood." The paper described the ability of a laboratory animal to survive after investigators exchanged its blood for plasma and subjected it to a hyperbaric environment. This demonstrated the efficacy of increased partial pressures of oxygen (hyperbaric oxygen) in the treatment of gas gangrene and anemic states. The medical community had great expectations for hbo therapy, and unsubstantiated claims became prevalant for its usefulness, including curing senility, baldness, and sexual dysfunction. Because of this, hbo underwent another decade of decline.

||||||||||Flying after diving

There are many guidelines, recommendations, and rules concerning flying after diving, but little scientific research has been done to date in the area. Most authorities recommend a 4 - 12 hour wait after dives without decompression stops, with a 24 hour minimum wait after decompression stop dives. Prudence dictates use of these "surface times" as a minimum, but avoidance of long or deep dives in the time period just prior to flight should also be a part of dive/travel plans. Other ancillary measures that should be taken include avoidance of heavy exercise and alcohol prior to flight, as these factors are associated with an increased risk for development of dcs. Fluid loading (water, sorry) and the taking of 1 aspirin prior to flight may also lessen the risk of developing dcs by decreasing the likelihood of untoward platelet interactions with bubble surfaces (asa inhibits thromboxane a/2 secondary platelet aggregation). Although most airlines theoretically run cabin pressures of about 8000 feet agl equivalent for a 30,000 foot agl flight, you must check with the pilot to ensure that airplane's pressurization capability to be sure, or to determine if it is capable of higher pressures.

||||||||||Treatment and transport of dcs/air embolism cases

If you think a symptom may be dcs, treat it as dcs! Resolution of symptoms at pressure is often both diagnosis and cure for dcs, and there is no substitute to rapid and judicious application of hyperbaric treatment. Help at the dan facility (919-684-8111) or the usaf brooks afb hyperbaric unit (512-leo-fast) may be of aid. Although prevention is by far the best measure, the other guy may not adhere to guidelines and may suffer a dcs hit preflight or in flight. If so, give:

1. Oxygen - administer the highest percentage oxygen possible to aid offgassing of nitrogen.
2. Fluids - administer fluids via the preferred intravenous (normal saline or ringers) or oral routes to expand the intravascular volume. Ensure airway protection prior to oral fluids or hold if in doubt. 3. Maximum pressure available asap - a monoplace chamber nearby with a 2.8 maximum pressure is preferrable to a 6 ata, multiplace chamber far away. Positive effects of hb treatment may also be seen many hours after the injury, so always pursue treatment even if it takes a while to provide. If transport via air is necessary, travel at the highest possible pressure/lowest altitude within safety limits. An ambulance/car transport is preferrable if travel distances are short. Avoid in-water treatment if at all possible. Portable chambers capable of 2.8 ata treatment and transport are available in some locations.
4. 1 Aspirin - although the effects may be mostly theoretical, it is a "can't hurt" that may also alleviate some pain. Avoid higher doses that may interfere with vascular wall anti-clotting prostaglindins.
5. Bubble protection - position the patient head down, on their left side to protect them from the possibility of passage of venous bubble to the arterial side through a patent foramen ovale (17-20% of us have one).
6. Pain medication and supportive treatment - avoid exercise or straining the patient further if possible. Some practitioners use a blood pressure cuff over the pain site to try to alleviate pain.

||||||||||'Taravana' is the South Pacific native term for the condition they develop from a long day of free diving. It is similar to decompression illness in just about every respect. This also has considerable significance to the scuba diver!

||||||||||I had a heart attack 1 yr ago & I have a stent implant as a result . I'm on Lipitor but no other medications. My age is 32. My flying doc. said that I should have no problem w\diving . Do you have any comment . (My club members are a bit weary).
:
Points to consider seriously:
-a delay of at least a year post angioplasty
-no symptoms of angina pectoris, ischemia or arrhythmias at rest and during exercise (annual test until 13 METS), which normal blood pressure response
-no history of arrhythmias (24-hour Holter monitoring)
-good left ventricular function (echocardiography)
-life style and risk-factor control
-no use of drugs which alter the cardiovascular response to exercise, such as beta- blockers. (aspirin and Zocor are allowed)
-realize that there is a risk of drowning and risk to diving buddies should a cardiac event occur underwater

-dive only with experienced and informed divers
-dive more conservatively and avoid risky situations
-avoid excess of cardiovascular stress in diving (such as drifts, cold
water, weight-lifting...)
-dive in sheltered water

||||||||||Deep diving on air
Peter Bennett, Ph.D., Director of DAN, writing in Bove's Diving Medicine (pp.117-121) gives the following scenario regarding the changes that take place with nitrogen narcosis(excerpted and summarized):
Signs and symptoms start to be noticed at 100 ft., becoming increasingly more severe as depth increases. There is slowing of mental activity with decrease in powers of association and perception made especially dangerous due to the presence of overconfidence. Short term memory is impaired, intellectual capacities are severely limited, and at depths greater than 180 feet, "no trust should be placed in human performance or efficiency".

At depths greater than 300 feet, unconsciousness is usual. The narcosis is more severe on arrival at depth, improving shortly afterward followed by a relatively stable level of narcosis felt by the diver - but objective tests show no improvement. On return to the surface, there is amnesia of the events that occurred during the narcotic state. Subjectively, there is improvement with experience and frequency of exposure seems to result in some adaptation but there is no parallel mprovement
in objective performance.

Of course, nitrogen narcosis probably had little to do with the death of this teenager - but one still doubts the wisdom of this sort of diving activity in an inadequately prepared diver.

Breathing compressed air (a mixture of gases) at depth for specified times allows the absorption of gases according to strict parameters governed by the law of partial pressures. The proportion of the total pressure at depth exerted by a single gas such as nitrogen is called the 'partial pressure' of nitrogen and is in direct proportion to its percentage in the gas being breathed, no matter how much is breathed. In compressed air this would be 79.1%; in nitrox it would be a lesser percentage of nitrogen, the oxygen fraction being increased selectively. This is the advantage that is provided by nitrox diving in decreasing DCS.

Here is a short physics review:
Partial Pressure Physics
Dalton's Law (PT = (P1+P2+P3) - Pn)

Partial pressure of a gas:

--Is determined by the concentration of the gas and ambient pressure
--Reflects the increasing pressure and compression of the gas, the concentration remains the same the concentration of O2 in air is about 21%, and the partial ressure of O2 in air at surface (1 atm abs) is about 0.21 atm.
--at 2 atm abs, the number of O2 molecules per unit volume is twice what it is at the surface, and the partial pressure is double --The physiologic effects of gases
-----are related to their partial pressure
-----change according to depth.
-----Are related to rate of absorption due to blood flow to a particular tissue.

With this information in mind, the answer to your question would be no, it makes no difference how much air your use since the partial pressure of the mixture would be the same and the degree of nitrogen taken up by the tissues would be the same (depending upon the blood flow) - and consequently the same chance of  decompression sickness.
 
 
 

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8/15/06