- Email: [email protected]
Do Jungle Boots Stop Jungle Rot?
Wilderness and Environmental Medicine, 15, 230 233 (2004)
Letters to the Editor Do Jungle Boots Stop Jungle Rot? To the Editor: Increasing numbers of people leave the UK each year on expeditions to tropical regions, sporting a variety of gear purchased on the advice gained from numerous sources. During their time in the jungle environment, they are at risk of suffering from tropical foot disorders that are capable of rendering its victims immobile, thus adversely affecting both the individuals affected and the expedition. This letter describes the incidence of foot problems in 26 adults during a 2-month expedition to Borneo in relation to the type of footwear worn. Until the 1960s, foot problems associated with the jungle environment were widely defined and given names such as ‘‘immersion foot,’’ ‘‘tropical jungle foot,’’ and ‘‘jungle rot.’’ These covered a multitude of symptoms, from dermatomyositis and pyoderma to abrasions.1 During the Vietnam War, research led to the more accurate terms warm water immersion foot, in which the soles become painful, white, and wrinkled, and tropical immersion foot, in which the ankles and dorsa of the feet become swollen and tender. This occurred after soldiers’ feet had been exposed to warm water (22⬚C–32⬚C) for more than 72 hours.2 While on a 2-month expedition in Sabah, Borneo, several expedition members succumbed to either warm water immersion foot or tropical immersion foot. All expedition members were subject to the same climatic conditions. Temperatures ranged between 29⬚C and 38⬚C, with humidity between 65% and 100%. Activities consisted of carrying loads weighing approximately 20 kg across primary and secondary jungle terrain. Small tributaries were frequently crossed, and the only time feet were dry was at night, while persons were asleep in hammocks.
Incidence of foot problems No Mild Moderate Severe problems problem problem problem Jungle Boots Other boots
9 1
5 5
0 3
0 3
Of the 26 members of the expedition, 14 wore army issue jungle combat boots, while 12 chose regular 2- to 3-season hill walking boots. The Table shows the incidence of foot problems in relation to the type of footwear worn. Expedition members developed mild, moderate, and severe forms of warm water immersion foot and tropical immersion foot. The severity of the problem was measured in terms of clinical appearance, treatment administered, and level of physical incapacity and thus is partially subjective. Chi-square tests showed a significantly reduced chance of developing any type of foot problem if jungle boots were worn (P ⫽ .004). In addition, not wearing jungle boots significantly increased the risk of a moderate or severe foot problem (P ⫽ .003, chi-square test). Although the author recognizes limitations regarding group size and clinical assessment, this remains an interesting observation that does not appear to have been previously reported in the medical literature. Army issue jungle boots are of single-layered leather/ canvas construction, with built-in drainage vents, compared with 2- to 3-season hill walking boots, which are multilayered and designed to keep water out. The construction of hill walking boots means that once water is inside, it is prevented from draining. While on expedition, those with hill walking boots found it almost impossible to prevent their footwear from being waterlogged most of the time, and they had to keep their feet immersed in a ‘‘jacket’’ of warm water: a feature that has previously been described as ‘‘moon-boot foot syndrome.’’3,4 Although the feet of those wearing jungle boots were wet, proper drainage prevented this ‘‘jacket effect,’’ and when it was possible to keep feet dry for a day or two, their boots dried more quickly. In light of this observation and given the lack of available data regarding foot disease prevention,5 consideration should be given to a randomized study with greater scientific validity. In the meantime, however, expeditions to jungle environments would benefit from a strong recommendation in favor of jungle boots to reduce the risk of foot disease, suffering, and incapacity. James K. Moore, RN, FRGS Bristol, UK Acknowledgment The author thanks Jonathan Benger, MD, FRCS, FFAEM, for assistance with statistical analysis.
Letters to the Editor References 1. Whayne TF, DeBakey ME. Cold injury, ground type, in World War II. In: Adnot J, Lewis CW, eds. Immersion Foot Syndromes. Military Dermatology. Falls Church, VA: US Department of the Army; 1994:55–88. Available at: http://www.vnh.org/MilitaryDerm/Ch4.pdf. Accessed February 29, 2004. 2. Allen AM, Taplin D. Tropical immersion foot. Lancet. 1973;2:1185–1189. 3. Blogg H. Moon-boot foot syndrome. Br Med J. 1982;285: 1774–1775. 4. Phillip R. Moon-boot foot syndrome. Br Med J. 1983;286: 562. 5. Adnot J, Lewis CW, eds. Immersion Foot Syndromes. Military Dermatology. Falls Church, VA: US Department of the Army; 1994. Available at: http://www.vnh.org/ MilitaryDerm/Ch4.pdf. Accessed February 29, 2004.
Ascorbate, Blood-Brain Barrier Function and Acute Mountain Sickness: A Radical Hypothesis To the Editor: I read with keen interest a recent publication examining the effects of oral medroxyprogesterone against acute mountain sickness (AMS).1 The scientific basis for chemoprophylaxis relates principally to the drug’s ability to increase chemosensitivity with attendant improvements in peripheral oxygen diffusion. However, its ability to suppress nuclear factor kappa B and meningeal release of substance P inhibiting the development of neurogenic edema and neurovascular headache2 may prove equally important from a mechanistic perspective. Despite expected improvements in arterial oxygenation, medroxyprogesterone did not influence the incidence or severity of AMS in a high-risk setting, although analyses were to some extent constrained by limited statistical power. However, as indicated by the authors, a noticeable trend was observed toward selectively lower AMS scores in the active drug trial, leading to the suggestion that a more sensitive scoring system may have essentially resurrected their statistically negative findings. My interpretation is somewhat different because I would like to contend that the choice of placebo may have proven the critical limiting factor that may have tempered any potential drug effect. Recent evidence suggests that the neurological sequelae ubiquitous to AMS may have a free radical basis with selective increases observed in molecular footprints of free radical–mediated lipid peroxidation and sarcolemmal membrane permeability.3 Oral administration of a potent cocktail of aqueous and lipid-phase antioxidant vitamins (250 mg of L-ascorbic acid, 100 IU of dl-␣-
231 tocopherol acetate, and 150 mg of ␣-lipoic acid bolus dose, 4 times daily) was subsequently shown to be an effective prophylactic4 adding some conviction to what is emerging as the ‘‘neuro-oxidative’’ hypothesis to AMS.3 In the published study, the incorporation of L-ascorbic acid as the placebo treatment cannot therefore be considered pharmacologically inert, thus questioning its role as an effective comparator. Supplementation incorporated a daily bolus dose of 300 mg equivalent to 5 times the recommended daily allowance, which, over the duration of the experimental period, resulted in a cumulative intake of 2.1 g. This regimen would have been sufficient to saturate the intracellular concentration of ascorbate (achieved at 200 mg), although a larger dose would have been required to satisfy plasma saturation (1000 mg).5 Ascorbate is a thermodynamically ideal terminal chain-breaking antioxidant capable of scavenging almost every oxidizing species generated in a biological system. This can be achieved both directly and indirectly. Direct scavenging involves the one electron oxidation of ascorbate to yield the ascorbate-free radical (A•⫺), a relatively unreactive intermediate that can donate an electron to other oxidizing species thereby preventing chain propagation of potentially damaging downstream redox reactions. Indirectly, ascorbate can reduce the oxidized form of Vitamin E (tocopheroxyl radical) back to its original form so that it can continue to function as the primary lipid-soluble chain-breaking antioxidant acting at the membrane-water interface. Because the therapeutic benefits of medroxyprogesterone were measured relative to this redox-active control, it is eminently plausible that the prophylactic benefits of the active drug were, at least to some extent, underestimated. To address this possibility, albeit from a pharmokinetic perspective, I have examined how a similar dosing regime with ascorbic acid would have influenced the redox status of human blood using the only molecular technique available for the direct measurement of free radicals—electron paramagnetic resonance (EPR) spectroscopy.3 Incorporating a double-blinded design and after ethical approval, peripheral venous blood was obtained from a resting 35-year-old man before and 1.5 hours after an oral bolus dose of L-ascorbic acid (6 ⫻ 50 mg). This procedure was repeated after 7 days supplementation with L-ascorbic acid (6 ⫻ 50 mg/d). Venous blood was mixed ex-vivo with the spin-trap ␣-phenyl-tert-butylnitrone (PBN) to extend the lifetime of biological radicals and thus facilitate EPR detection as previously described.3 Separate samples of blood were mixed with a molar excess of dimethylsulfoxide (DMSO) to promote one-electron reversible oxidation of
Letters to the Editor Do Jungle Boots Stop Jungle Rot? To the Editor: Increasing numbers of people leave the UK each year on expeditions to tropical regions, sporting a variety of gear purchased on the advice gained from numerous sources. During their time in the jungle environment, they are at risk of suffering from tropical foot disorders that are capable of rendering its victims immobile, thus adversely affecting both the individuals affected and the expedition. This letter describes the incidence of foot problems in 26 adults during a 2-month expedition to Borneo in relation to the type of footwear worn. Until the 1960s, foot problems associated with the jungle environment were widely defined and given names such as ‘‘immersion foot,’’ ‘‘tropical jungle foot,’’ and ‘‘jungle rot.’’ These covered a multitude of symptoms, from dermatomyositis and pyoderma to abrasions.1 During the Vietnam War, research led to the more accurate terms warm water immersion foot, in which the soles become painful, white, and wrinkled, and tropical immersion foot, in which the ankles and dorsa of the feet become swollen and tender. This occurred after soldiers’ feet had been exposed to warm water (22⬚C–32⬚C) for more than 72 hours.2 While on a 2-month expedition in Sabah, Borneo, several expedition members succumbed to either warm water immersion foot or tropical immersion foot. All expedition members were subject to the same climatic conditions. Temperatures ranged between 29⬚C and 38⬚C, with humidity between 65% and 100%. Activities consisted of carrying loads weighing approximately 20 kg across primary and secondary jungle terrain. Small tributaries were frequently crossed, and the only time feet were dry was at night, while persons were asleep in hammocks.
Incidence of foot problems No Mild Moderate Severe problems problem problem problem Jungle Boots Other boots
9 1
5 5
0 3
0 3
Of the 26 members of the expedition, 14 wore army issue jungle combat boots, while 12 chose regular 2- to 3-season hill walking boots. The Table shows the incidence of foot problems in relation to the type of footwear worn. Expedition members developed mild, moderate, and severe forms of warm water immersion foot and tropical immersion foot. The severity of the problem was measured in terms of clinical appearance, treatment administered, and level of physical incapacity and thus is partially subjective. Chi-square tests showed a significantly reduced chance of developing any type of foot problem if jungle boots were worn (P ⫽ .004). In addition, not wearing jungle boots significantly increased the risk of a moderate or severe foot problem (P ⫽ .003, chi-square test). Although the author recognizes limitations regarding group size and clinical assessment, this remains an interesting observation that does not appear to have been previously reported in the medical literature. Army issue jungle boots are of single-layered leather/ canvas construction, with built-in drainage vents, compared with 2- to 3-season hill walking boots, which are multilayered and designed to keep water out. The construction of hill walking boots means that once water is inside, it is prevented from draining. While on expedition, those with hill walking boots found it almost impossible to prevent their footwear from being waterlogged most of the time, and they had to keep their feet immersed in a ‘‘jacket’’ of warm water: a feature that has previously been described as ‘‘moon-boot foot syndrome.’’3,4 Although the feet of those wearing jungle boots were wet, proper drainage prevented this ‘‘jacket effect,’’ and when it was possible to keep feet dry for a day or two, their boots dried more quickly. In light of this observation and given the lack of available data regarding foot disease prevention,5 consideration should be given to a randomized study with greater scientific validity. In the meantime, however, expeditions to jungle environments would benefit from a strong recommendation in favor of jungle boots to reduce the risk of foot disease, suffering, and incapacity. James K. Moore, RN, FRGS Bristol, UK Acknowledgment The author thanks Jonathan Benger, MD, FRCS, FFAEM, for assistance with statistical analysis.
Letters to the Editor References 1. Whayne TF, DeBakey ME. Cold injury, ground type, in World War II. In: Adnot J, Lewis CW, eds. Immersion Foot Syndromes. Military Dermatology. Falls Church, VA: US Department of the Army; 1994:55–88. Available at: http://www.vnh.org/MilitaryDerm/Ch4.pdf. Accessed February 29, 2004. 2. Allen AM, Taplin D. Tropical immersion foot. Lancet. 1973;2:1185–1189. 3. Blogg H. Moon-boot foot syndrome. Br Med J. 1982;285: 1774–1775. 4. Phillip R. Moon-boot foot syndrome. Br Med J. 1983;286: 562. 5. Adnot J, Lewis CW, eds. Immersion Foot Syndromes. Military Dermatology. Falls Church, VA: US Department of the Army; 1994. Available at: http://www.vnh.org/ MilitaryDerm/Ch4.pdf. Accessed February 29, 2004.
Ascorbate, Blood-Brain Barrier Function and Acute Mountain Sickness: A Radical Hypothesis To the Editor: I read with keen interest a recent publication examining the effects of oral medroxyprogesterone against acute mountain sickness (AMS).1 The scientific basis for chemoprophylaxis relates principally to the drug’s ability to increase chemosensitivity with attendant improvements in peripheral oxygen diffusion. However, its ability to suppress nuclear factor kappa B and meningeal release of substance P inhibiting the development of neurogenic edema and neurovascular headache2 may prove equally important from a mechanistic perspective. Despite expected improvements in arterial oxygenation, medroxyprogesterone did not influence the incidence or severity of AMS in a high-risk setting, although analyses were to some extent constrained by limited statistical power. However, as indicated by the authors, a noticeable trend was observed toward selectively lower AMS scores in the active drug trial, leading to the suggestion that a more sensitive scoring system may have essentially resurrected their statistically negative findings. My interpretation is somewhat different because I would like to contend that the choice of placebo may have proven the critical limiting factor that may have tempered any potential drug effect. Recent evidence suggests that the neurological sequelae ubiquitous to AMS may have a free radical basis with selective increases observed in molecular footprints of free radical–mediated lipid peroxidation and sarcolemmal membrane permeability.3 Oral administration of a potent cocktail of aqueous and lipid-phase antioxidant vitamins (250 mg of L-ascorbic acid, 100 IU of dl-␣-
231 tocopherol acetate, and 150 mg of ␣-lipoic acid bolus dose, 4 times daily) was subsequently shown to be an effective prophylactic4 adding some conviction to what is emerging as the ‘‘neuro-oxidative’’ hypothesis to AMS.3 In the published study, the incorporation of L-ascorbic acid as the placebo treatment cannot therefore be considered pharmacologically inert, thus questioning its role as an effective comparator. Supplementation incorporated a daily bolus dose of 300 mg equivalent to 5 times the recommended daily allowance, which, over the duration of the experimental period, resulted in a cumulative intake of 2.1 g. This regimen would have been sufficient to saturate the intracellular concentration of ascorbate (achieved at 200 mg), although a larger dose would have been required to satisfy plasma saturation (1000 mg).5 Ascorbate is a thermodynamically ideal terminal chain-breaking antioxidant capable of scavenging almost every oxidizing species generated in a biological system. This can be achieved both directly and indirectly. Direct scavenging involves the one electron oxidation of ascorbate to yield the ascorbate-free radical (A•⫺), a relatively unreactive intermediate that can donate an electron to other oxidizing species thereby preventing chain propagation of potentially damaging downstream redox reactions. Indirectly, ascorbate can reduce the oxidized form of Vitamin E (tocopheroxyl radical) back to its original form so that it can continue to function as the primary lipid-soluble chain-breaking antioxidant acting at the membrane-water interface. Because the therapeutic benefits of medroxyprogesterone were measured relative to this redox-active control, it is eminently plausible that the prophylactic benefits of the active drug were, at least to some extent, underestimated. To address this possibility, albeit from a pharmokinetic perspective, I have examined how a similar dosing regime with ascorbic acid would have influenced the redox status of human blood using the only molecular technique available for the direct measurement of free radicals—electron paramagnetic resonance (EPR) spectroscopy.3 Incorporating a double-blinded design and after ethical approval, peripheral venous blood was obtained from a resting 35-year-old man before and 1.5 hours after an oral bolus dose of L-ascorbic acid (6 ⫻ 50 mg). This procedure was repeated after 7 days supplementation with L-ascorbic acid (6 ⫻ 50 mg/d). Venous blood was mixed ex-vivo with the spin-trap ␣-phenyl-tert-butylnitrone (PBN) to extend the lifetime of biological radicals and thus facilitate EPR detection as previously described.3 Separate samples of blood were mixed with a molar excess of dimethylsulfoxide (DMSO) to promote one-electron reversible oxidation of