{"title":"战壕足","authors":"Robert E. Burr FACP, FACEP","doi":"10.1580/0953-9859-4.4.348","DOIUrl":null,"url":null,"abstract":"Trench foot is the result of prolonged (many hours) cooling of the lower extremities to temperatures above freezing but below 60° F. Although trench foot is a significant cause of injury in military operations [1], it is rarely seen in civilian practice. Prolonged cooling of extremities produces direct injury to all the soft tissues, but primarily to peripheral nerves [2,3,4]. The injury is initially reversible, but becomes irreversible if cooling is sustained. Wet conditions increase the risk and accelerate the injury. In addition to environmental cooling, factors that reduce circulation to the extremities contribute to the injury. These factors include constrictive clothing and boots, prolonged immobility, hypothermia and cramped posture. When first seen, the injured part is pale, anesthetic, pulseless and immobile, but not frozen. The clinical hallmark of trench foot is the failure of these signs to change after warming. After several hours (occasionally 24-36 h), a vigorous hyperemia develops associated with severe burning pain and reappearance of sensation proximally, but not distally. Edema, often sanguineous, and bullae develop as perfusion increases. Skin that remains poorly perfused after hyperemia appears, is likely to slough as the injury evolves. Persistance of pulselessness after 48 hours suggests severe deep injury and high likelihood of substantial tissue loss. The hyperemia appears to be due to a vasomotor paralysis with passive engorgement of cutaneous vessels, characterized by pallor on elevation and rubor on dependency. The hyperemic phase lasts a few days to many weeks, depending on the severity of the injury. In the second week after injury, sharp intermittent 'lightning' pains develop. The injury evolves slowly, as befits its neuropathic component. Improved sensitivity to light touch and pin prick in the area of persistent anesthesia within 4-5 weeks suggests reversible nerve injury and less likelihood of persistent symptoms. Persistence of anesthesia to touch beyond six weeks suggests neuronal degeneration. Injury of that degree requires much longer to resolve and has a greater likelihood of persistent disabling symptoms. Hyperhidrosis is a common, prominent late feature of trench foot and seems to precede the recovery of sensation both in time and location. A distinct advancing hyperhidrotic 'zone' can develop [5] which is presumed to mark the point to which regenerating sudomotor sympathetic nerves have advanced. The excessive sweating may be permanent and can predispose to blistering, skin maceration and dermatophyte infection. Two schemes of classification have been used, based on clinical series from World War II. These two systems correlate well and provide useful prognostic information. Both systems recognize four degrees of severity.","PeriodicalId":81742,"journal":{"name":"Journal of wilderness medicine","volume":"4 4","pages":"Pages 348-352"},"PeriodicalIF":0.0000,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1580/0953-9859-4.4.348","citationCount":"1","resultStr":"{\"title\":\"Trench foot\",\"authors\":\"Robert E. Burr FACP, FACEP\",\"doi\":\"10.1580/0953-9859-4.4.348\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Trench foot is the result of prolonged (many hours) cooling of the lower extremities to temperatures above freezing but below 60° F. Although trench foot is a significant cause of injury in military operations [1], it is rarely seen in civilian practice. Prolonged cooling of extremities produces direct injury to all the soft tissues, but primarily to peripheral nerves [2,3,4]. The injury is initially reversible, but becomes irreversible if cooling is sustained. Wet conditions increase the risk and accelerate the injury. In addition to environmental cooling, factors that reduce circulation to the extremities contribute to the injury. These factors include constrictive clothing and boots, prolonged immobility, hypothermia and cramped posture. When first seen, the injured part is pale, anesthetic, pulseless and immobile, but not frozen. The clinical hallmark of trench foot is the failure of these signs to change after warming. After several hours (occasionally 24-36 h), a vigorous hyperemia develops associated with severe burning pain and reappearance of sensation proximally, but not distally. Edema, often sanguineous, and bullae develop as perfusion increases. Skin that remains poorly perfused after hyperemia appears, is likely to slough as the injury evolves. Persistance of pulselessness after 48 hours suggests severe deep injury and high likelihood of substantial tissue loss. The hyperemia appears to be due to a vasomotor paralysis with passive engorgement of cutaneous vessels, characterized by pallor on elevation and rubor on dependency. The hyperemic phase lasts a few days to many weeks, depending on the severity of the injury. In the second week after injury, sharp intermittent 'lightning' pains develop. The injury evolves slowly, as befits its neuropathic component. Improved sensitivity to light touch and pin prick in the area of persistent anesthesia within 4-5 weeks suggests reversible nerve injury and less likelihood of persistent symptoms. Persistence of anesthesia to touch beyond six weeks suggests neuronal degeneration. Injury of that degree requires much longer to resolve and has a greater likelihood of persistent disabling symptoms. Hyperhidrosis is a common, prominent late feature of trench foot and seems to precede the recovery of sensation both in time and location. A distinct advancing hyperhidrotic 'zone' can develop [5] which is presumed to mark the point to which regenerating sudomotor sympathetic nerves have advanced. The excessive sweating may be permanent and can predispose to blistering, skin maceration and dermatophyte infection. Two schemes of classification have been used, based on clinical series from World War II. These two systems correlate well and provide useful prognostic information. Both systems recognize four degrees of severity.\",\"PeriodicalId\":81742,\"journal\":{\"name\":\"Journal of wilderness medicine\",\"volume\":\"4 4\",\"pages\":\"Pages 348-352\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1993-11-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1580/0953-9859-4.4.348\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of wilderness medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0953985993712012\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of wilderness medicine","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0953985993712012","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Trench foot is the result of prolonged (many hours) cooling of the lower extremities to temperatures above freezing but below 60° F. Although trench foot is a significant cause of injury in military operations [1], it is rarely seen in civilian practice. Prolonged cooling of extremities produces direct injury to all the soft tissues, but primarily to peripheral nerves [2,3,4]. The injury is initially reversible, but becomes irreversible if cooling is sustained. Wet conditions increase the risk and accelerate the injury. In addition to environmental cooling, factors that reduce circulation to the extremities contribute to the injury. These factors include constrictive clothing and boots, prolonged immobility, hypothermia and cramped posture. When first seen, the injured part is pale, anesthetic, pulseless and immobile, but not frozen. The clinical hallmark of trench foot is the failure of these signs to change after warming. After several hours (occasionally 24-36 h), a vigorous hyperemia develops associated with severe burning pain and reappearance of sensation proximally, but not distally. Edema, often sanguineous, and bullae develop as perfusion increases. Skin that remains poorly perfused after hyperemia appears, is likely to slough as the injury evolves. Persistance of pulselessness after 48 hours suggests severe deep injury and high likelihood of substantial tissue loss. The hyperemia appears to be due to a vasomotor paralysis with passive engorgement of cutaneous vessels, characterized by pallor on elevation and rubor on dependency. The hyperemic phase lasts a few days to many weeks, depending on the severity of the injury. In the second week after injury, sharp intermittent 'lightning' pains develop. The injury evolves slowly, as befits its neuropathic component. Improved sensitivity to light touch and pin prick in the area of persistent anesthesia within 4-5 weeks suggests reversible nerve injury and less likelihood of persistent symptoms. Persistence of anesthesia to touch beyond six weeks suggests neuronal degeneration. Injury of that degree requires much longer to resolve and has a greater likelihood of persistent disabling symptoms. Hyperhidrosis is a common, prominent late feature of trench foot and seems to precede the recovery of sensation both in time and location. A distinct advancing hyperhidrotic 'zone' can develop [5] which is presumed to mark the point to which regenerating sudomotor sympathetic nerves have advanced. The excessive sweating may be permanent and can predispose to blistering, skin maceration and dermatophyte infection. Two schemes of classification have been used, based on clinical series from World War II. These two systems correlate well and provide useful prognostic information. Both systems recognize four degrees of severity.