Frostbite Injuries Introduction

Frostbite is a localized cold-induced injury as a result of improper protection of oneself from the harshness of a cold environment. The first official report of the effects of cold injury was published in 1805 (Wilson and Goldman, 1970). However, these injuries have existed as far back as ancient times, including numerous accounts of soldiers perishing in various wars (Lange and Loewe, 1946; Nakagomi etal, 1985; Orr and Fainer, 1951; Sarhadi etal, 1995; Shelton, 1991; Somboonwong etal, 2000). Some of the signs, symptoms, and sequelae were even described by Hippocrates during his time (Lange and Loewe, 1946; Robson etal, 1982).

Soldiers in military campaigns staged during cold winters have a high propensity to develop frostbite and mountain climbers and explorers are also prone to frostbite injuries (Boswick etal, 1979; Grindlay and Reynolds, 1986; Kulka, 1961; Lange and Loewe, 1946; McCauley etal., 1990). As alluded to earlier, frostbite injury, unlike thermal injury, is more common in people who do not cover themselves appropriately. With the appropriate clothing and accessories, these injuries can be prevented. Some of the risk factors described in the literature include impairment as a result of alcohol, drugs, or other substances, (Klein and Penneys, 1988; Knize, 1977), thereby making the individual unable to clothe themselves adequately. Mental instability has also led to cold-related injury (Klein and Penneys, 1988). Military studies, in addition, have shown that darker colored soldiers are more likely to suffer cold injury in comparison to their white counterparts in similar conditions (Whayne and DeBakey, 1958). Also, individuals from warmer climates are more prone to cold injuries than people from colder climates (Weatherly-White etal, 1964). This observation makes sense, in light of the fact that people from colder climates are accustomed to dressing for colder weather and are physiologically adapted to tolerate such weathers. Furthermore, disease states, such as atherosclerosis, that alter blood flow to vital organs, such as the skin, predispose one to frostbite (Larrey, 1814; Porter etal, 1976). With the advent of proper cold weather clothing and accessories, in addition to sports gear designed for cold weather sports such as skiing and mountain climbing, the incidence of frostbite has decreased compared to historic times.

Anatomy and pathophysiology of frostbite injury

Frostbite injury does not only depend on the ambient temperature and duration of exposure, but also on factors such as: humidity, wind chill, wetness, and the overall physical condition of the individual (Mills, 1973).

Clinically and anatomically, frostbite is divided into four degrees of injury based on the extent of physical injury after freezing and subsequent rewarming.

1 1st degree frostbite: Involves the superficial skin with the loss of sensation and erythema. There are firm whitish or yellowish plaques. Even though edema is common, there is no tissue loss.

2 2nd degree frostbite: Involves the superficial skin but is a little deeper than 1st degree injuries. There are skin vesiculations with milky or clear fluid within them. Erythema and edema normally surround these blisters (Figure 11.3, Figure 11.4 A—D).

3 3rd degree frostbite: Involves the reticular dermis and the dermal vascular plexus. The blisters are deeper, unlike 2nd degree injuries. These blisters frequently contain blood and are red to purplish in color (Figure 11.4 A—D).

4 4th degree frostbite: Involves the deeper dermis and adnexal structures. The avascular subcuticular tissue is also affected causing mummification with the involvement of tissues like muscle and bone.

Predicting the extent of injury can be difficult at times, but with good physical examination, the physician should be able to classify the extent of a frostbite injury according to the four historic classifications (Bourne etal, 1986; Knize, 1977; Knize etal, 1969; Kulka, 1956, 1964; Mallonee etal, 1996; Mills, 1964, 1976). A two-division classification system postulated by Mills makes these injuries simpler to classify. Mills'

Fourth Degree Frostbite
Figure 11.3 Vesiculation of right ear (arrow) with clear fluid characteristic of second-degree frostbite (by permission, Auerbach, 2001, Wilderness Medicine, 4th edn. St. Louis, Missouri: Mosby Publishers).

classification is divided into mild and severe (Mills, 1976). The mild injuries are without tissue loss while the severe injuries are associated with tissue loss. Comparing the historic classification to the Mills classification, the 1st and 2nd degree injuries correspond to Mills' mild category, whereas 3rd and 4th degree injuries fall under the severe category. Note, some 3rd degrees can be classified as mild depending on the presentation. Therefore, it is essential to perform a good clinical inspection in order to categorize an injury as mild or severe.

Classically, the frostbite injury has been divided into four phases that may overlap from time to time (Bourne etal, 1986; Kulka, 1956, 1964). These pathologic phases are the pre-freeze phase, free-thaw phase, vascular stasis phase, and late ischemic phase (Kulka, 1956).

1 Pre-freeze phase: The temperature of the pre-freeze phase ranges from 3 °C to 10 °C. This phase follows the initial chilling and is before the formation of ice crystals. The changes associated with this phase are a result of the spasm of the capillary vessels, along with the leakage of plasma from the vasculature.

2 Freeze-thaw phase: The temperature of this phase is generally below -15 °C during which tissue temperatures reach freezing point. There is actually formation of ice

Figure 11.4 A-D A. Acute frostbite with clear fluid in superficial blisters. B. Blisters before treatment but after debridement. C. After 48 hours of therapy with topical Aloe vera gel (Dermaide Aloe). D. Sixteen days after injury (by permission, Auerbach, 2001, Wilderness Medicine, 4th edn. St. Louis, Missouri: Mosby Publishers).

Figure 11.4 A-D A. Acute frostbite with clear fluid in superficial blisters. B. Blisters before treatment but after debridement. C. After 48 hours of therapy with topical Aloe vera gel (Dermaide Aloe). D. Sixteen days after injury (by permission, Auerbach, 2001, Wilderness Medicine, 4th edn. St. Louis, Missouri: Mosby Publishers).

crystals during this phase causing a severe impairment in circulation and tissue perfusion. This in turn may lead to a precipitous drop in skin temperature at a rate of 1 °C every two minutes.

3 Vascular stasis phase: This phase involves the loss of plasma through the vasculature. In addition, there is capillary spasm and dilatation along with the shunting of blood and coagulation due to stasis. This phase is of utmost importance when it comes to the treatment of frostbite with anti-inflammatory agents.

4 Late ischemic phase: In this phase, there is ischemic damage and gangrene as a result of thrombosis and arteriovenous shunting. Autonomic dysfunction can ensue as a result. This phase may result in long-term complications and sequelae. In addition, reversibility may be difficult to achieve.

The characteristics of each phase changes with the extent and duration of the injury and also with the velocity of freezing. These injuries are the result of direct and indirect cellular injury (Bulkley, 1983; Herndon etal., 1987; Visuthikosol etal., 1995; Zacarian, 1985). The direct injuries cause changes including extracellular and intracellular ice formation, cell dehydration and shrinking, abnormal intracellular electrolyte concentration, thermal shock, and lipid-protein complex denaturation (Zacarian, 1985). The indirect injuries, in comparison to the direct injuries, are frequently more severe (Visuthikosol etal., 1995). The direct injuries cause more or less progressive dermal ischemia as seen in burns, ultimately leading to tissue loss and subsequent death of the affected extremity or organ (Bulkley, 1983). Robson etal, have determined that the ischemia in frostbite injuries might be due to the same inflammatory mediators that are responsible for the progressive dermal ischemia seen in thermal injuries (Robson etal., 1980). PGE2, PGF2a, and TxA2 are elevated in frostbite injuries as well as in other eicosanoids, making eicosanoid inhibitors useful in the treatment of frostbite injuries (Robson etal, 1980).

Management of thermal and frostbite injuries

For these injuries to be successfully managed, first we have to understand the anatomy and pathophysiology of the injury. This has already been dealt with. Second, we have to be able to better clinically assess the injury before formulating and undertaking a treatment plan. Clinical judgement is the best available method when it comes to assessing these injuries.

For a thermal injury, the depth of the wound, the size, and the anatomical site of injury should all be determined before any attempts to manage the wound are ensued. Clinical wound inspection, in addition to pinpricking the wound, will help determine the depth of the wound. As discussed previously, the depth of the wound is associated with different qualities such as color and pain. The size of burns are widely estimated using different methods such as:

1 Wallace's 'Rule of Nines'-useful for rapid estimation (Figure 11.5).

2 Lund and Browder Chart-more precise estimation (Figure 11.6).

3 Patient Palm Method (The palm is approximately 1% of the body surface area). Useful in pediatric burns and smaller burns.

Figure 11.5 Wallace's estimation of burn size 'The Rule of Nines' (Wolf and Herndon, 1999 Vademecum in Burn Care. Austin, Texas: Landes Bioscience).

Burn Chart Adult
in Burn Care. Austin, Texas: Landes Bioscience).

It is important to examine anatomical sites because certain areas need paramount attention, such as important functional and aesthetic areas including hands, feet, face, eyelids, perineum, genitalia, and joints. Special attention is given to these areas to prevent cosmetic and functional problems as a result of hypertrophic scarring.

For a frostbite injury, the clinical appearance may be deceiving. Most of the time the extremities involved show a frozen appearance. Rapid rewarming almost always produces instant hyperemia, regardless of the severity of the injury (Herndon etal, 1987). Sensation improves after thawing. Assessment of the injury following this initial rewarming phase is imperative. Diagnostic techniques, such as radioisotope scanning using technetium-99m methylene diphosphonate (99mTc MDP), technetium-99m stannous pyrophosphate, xenon- 133 (133Xe), iodine-131 labelled human serum albumin (131I-RISA), angiography, digital plethysmography, and routine x-rays can aid in the estimation of the extent of these injuries. These modalities are also successful in predicting tissue loss and also for estimating the vascular response to vasodilators and identifying tissue boundaries for surgical intervention.

The initial management of these injuries is preceded by the usual initial trauma protocols: airway maintenance, breathing, and circulatory support (Committee on trauma, 1999). Also resuscitation and smoke inhalation injury support are paramount © 2004 by CRC Press LLC

when it comes to thermal injuries. In frostbite injuries, systemic hypothermia support is important to address after the initial resuscitation efforts are carried out. The core temperature should be brought back to at least 34 °C before any further management is undertaken. Unlike thermal injuries, fluid abnormalities are frequently not a problem in frostbite injuries, and thus time should not be wasted in attempts to correct such abnormalities.

After assessing the injury, it is paramount to initiate first aid, by removing the source, which in so doing limits tissue damage. Edema and protein extravasation can also be minimized as a result. Blister management is controversial in both thermal and frostbite injury. In thermal injuries, many experts believe in leaving small blisters thus creating a biological dressing, whereas large blisters are usually removed. In frostbite injuries, the clear and white blisters are debrided just as in burns, whereas the hemorrhagic ones are left intact but should be aspirated to decrease inflammatory agents. Escharatomies are employed in both types of injuries. In thermal injuries, they are reserved for circumferential full thickness burns of the chest, limbs, and digits. Many agents have been used to date in the management of these injuries. Some of the notable agents used to treat burn injuries range from anti-catabolic agents to wound healing agents, such as silvadene, and the potent anti-inflammatory, 'Aloe vera' (Alexander, 1981; Boswick, 1987; Heggersetal, 1987; Reus etal, 1984; Robson etal, 1979; Snider and Porter, 1975; Vaughn, 1980; Zacarian etal, 1970). The same agent, Aloe vera gel, is also useful in the treatment of frostbite injuries because of similar pathophysiology in terms of progressive dermal ischemia (Bulkley, 1983; Robson and Heggers, 1981; Zacarian etal., 1970). Some of the other agents that have been used in frostbite injuries include thromboxane inhibitors, like aspirin and ibuprofen, sympathetic blockers, and sympathectomy, as well as IV dextran and intraarterial reserpine, reserving amputation for gangrene (Bouwman etal, 1980; Engrav etal, 1983; Fujita etal, 1976; Kyosola, 1974; Marzella etal, 1989; Muller etal, 1996; Orr and Fainer, 1951; Robson etal, 1982; Simeone, 1960; Visuthikosol etal, 1995).

The use of aloes dates back to as far as 1750 B.C. in Mesopotamia, where clay tablets showed evidence of writings that Aloe vera was being used for medicinal purposes. (Coats and Ahola, 1979; Schechter and Sarot, 1968). Books from Egypt in 550 B.C. make mention of aloes in the treatment of skin infection. Discordes, a Greek physician, wrote a book in 74 A.D. in which he wrote that aloes could treat wounds and heal infections of the skin (Coats and Ahola, 1979; Schechter and Sarot, 1968). There are many historical citations about aloes, although much of the information was unproven until recently. Many admit to using Aloe vera gel from a houseplant leaf in self-treating small burns and cuts (Coats and Ahola, 1979). The evidence of the successful use of aloes in the treatment of burns is overwhelming. Heggers and others have studied this miraculous plant in much detail with convincing evidence about its beneficial effects (Robson and Heggers, 1981).

The therapeutic properties of aloes are many (Cera etal., 1980; Gottshall etal., 1950; Heggers etal, 1987; Robson etal, 1979; Snider and Porter, 1975). It is important to mention that there are some unforeseen properties and benefits making this miraculous succulent -'the herb of herbs'- a force to be reckoned with. Some of the known and proven properties include:

1 The ability to penetrate the burn wound.

2 The ability to anesthetize the wound thereby providing analgesia, as well as a soothing effect.

3 The bactericidal, viridical, and fungicidal properties.

4 The ability to act as a potent anti-inflammatory agent.

5 The vasodilatory properties, with the ability to dilate capillaries, thereby increasing blood supply to the burn areas.

Many of the beneficial effects of aloes are comparable to those of the well studied and tested eicasanoid inhibitors, which have proven over time to have therapeutic benefit in the prevention of progressive dermal ischemia, after thermal injury, frostbite, and drug injuries (Heggers etal., 1987; Heggers etal., 1993; Lawrence etal., 1994; Muller etal., 1996; Reus etal., 1984; Robson and Heggers, 1981; Robson etal, 1979).

The chemical constituents in aloes that provides its potent therapeutic properties include lignin, lectins, saponin, and gibberellin (Danhof and McAnally, 1983; Gottshall etal., 1950; Schechter and Sarot, 1968). Lignin, a polyphenolic compound, gives aloes their ability to penetrate skin. Lectin, a hemagglutination protein, binds to glycoproteins thereby decreasing inflammation. Gibberellin also acts to decrease inflammation. It acts as a growth hormone in plants but stimulates protein synthesis, unlike steroids (Danhof and McAnally, 1983). Saponin, acts to provide antisepsis, thereby decreasing the microbial load (See Chapter 9).

Overwhelming evidence exists that shows Aloe vera to be a potent antimicrobial (Benigni, 1950; Zimmerman and Simms, 1969). Aloes have been effective against deadly bacteria such as Mycobacterium tuberculosis, Bacillus subtilis, Staphylococcus aureus, Streptococcus pyogenes, Salmonella paratyphi, Streptococcus agalactiae, Klebsiella pneumonae, Pseudomonas aeroginosa, Serratia marcescens, Enterobacter cloacae, and many more (Benigni, 1950; Bruce, 1967; Golding etal, 1963; Lehr etal, 1991; Zawacki, 1974). In this capacity, it exerts either bactericidal or bacteriostatic effects. The mechanism of the antimicrobial properties of aloes is not well established, but saponin, one of the chemicals of aloe, is credited for these actions.

Many investigators have tried to establish a rationale for the potent anti-inflammatory properties for Aloe vera. Robson and Heggers (1981) have shown that salicylate is a by-product of Aloe vera, thus contributing to its anti-inflammatory properties. Fujita and colleagues have found a bradykinin-inactivating carboxypeptidase in Aloe arborescens, also culminating in its anti-inflammatory properties (Fuhrman and Crissman, 1947; Fujita etal, 1979). Also, magnesium lactate found in aloes is a known inhibitor of the enzyme histidine decarboxylase that catalyzes histamine formation in mast cells from histidine (Kemp and Sibert, 1997). These three postulates best serve to elucidate the anti-inflammatory properties of aloes.

This elucidated anti-inflammatory property explains its benefits in the treatment of thermal injuries, frostbites, and drug injuries which all share a common pathophysiology in terms of the production of inflammatory agents. All three injuries share a common pathway as alluded to earlier, and the end result is the progressive dermal ischemia and eventual loss of tissue (Cera etal., 1982; Heggers etal., 1987; Heggers etal., 1993; Lawrence etal, 1994; Reus etal, 1984; Robson and Heggers, 1981). This loss of tissue is mediated by Thromboxane A2 (TxA2), a potent vasoconstrictor. Aloe vera gel inhibits TxA2 synthetase, and also maintains equilibrium between PGE2 and PGF2a, thereby exercising its vasodilatory properties, and eventually causing tissue perfusion and prevention of tissue loss (Cera etal., 1982; Cera etal., 1980; Heggers etal., 1993; Lawrence etal., 1994; Reus etal, 1984; Robson and Heggers, 1981; Vaughn, 1980).

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Aloe and Your Health

Aloe and Your Health

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