Named after the soldiers who stood in the trenches of World War I, an infection of the feet develops from a combination of being constantly cold, wet, and dirty. Men suffered from standing for hours on end in waterlogged trenches without removing their wet socks or boots. During the winter of 1914 and 1915 more than 20,000 British soldiers were treated for trench foot. More recently, 14 percent of all the military casualties in the Falkland Island conflict were due to trench foot.

As trench foot begins its tissue-killing grip, the feet swell two or three times their normal size while slowly becoming completely numb, the skin changes from pink to white then to a red and/or blue color. One can almost cut their own foot off without a painkiller due to loss of normal afferent nerve tissue response.

If swelling happens to retreat, an intolerable pain of indescribable agony commences. Left untreated, trench foot will turn to a gangrene-like rotting requiring amputation.

One case-of-record, who presented severe bilateral trench foot, was observed in a man who lived in the out-of-doors 21 days without removing his boots. Non-operative management yielded no clinical improvement, resulting in bilateral below-knee amputation! Microscopic examination of this subject's tissues showed both skin and muscle cell death with secondary arterial blood clotting.[1]

Prevention, the only real remedy for trench foot, is accomplished by frequently drying out the feet and changing to dry socks several times a day. Covering the feet with a grease-like material may prolong this requirement, reducing the hypothermic effects from the dirty-wet and cold.

Nerve tissues in the lower extremities are last in line for blood flow. These tissues strongly object to this sort of confined yet prolonged exposure. At the first instance of the feet turning non-responsive or the least bit numb, a Code-3-siren-blaring medical emergency should be sounded and treated by warming your "dogs" up and drying them out.

Peripheral neuropathy is most likely to occur when the extremities are exposed to prolonged periods of wet conditions at temperatures just above freezing. Clinically, trench foot is characterized by a well-defined acute clinical picture and chronic sequelae.

Opinions vary as to the type of nerve fibers most susceptible to damage and proposed mechanisms of injury include direct axonal damage, swelling, ischaemia, and ischaemia/reperfusion. A series of investigations have been performed to clarify which nerve fibers are more susceptible to damage, and to identify this mechanism of nerve injury.

An in vivo rabbit hind limb model was subjected to 16 hours of cold immersion(1-2 degrees C), provided the basis of one study. Nerve specimens were examined by semi-thin sectioning for myelin fibre counts, by electron microscopy to assess the unmyelinated fibre population, and fine nerve terminals in the plantar surfaces or bottom of the "foot" were assessed immunohistochemically [micro-chemistry of cells and tissues].

"Myelinated" nerves are those that have a fat-like insulated sheath-covering. Trench foot typically presents large myelinated fiber damage, while small myelinated or unmyelinated fibers are initially and relatively spared.

Nerve damage was found to start proximal and extend distally in time. Serial temperature measurements identified a warm-cold interface in the upper tibial region of immersed limbs. As this was the initial site of injury, this suggests that a dynamic balance exists in the cold immersed limb between the protective effects of cooling and the damaging effects of deficient blood flow.

A non-invasive technique of near infrared spectroscopy measured changes in tissue oxygen supply and utilization and blood volume, supporting the hypothesis that an interface is created at the site of initial nerve damage[in the upper tibia, lower leg], where cyclical ischaemia-reperfusion injury occurs.[2]

[Ischaemia-reperfusion is blood flow return to a tissue site where flow was impaired and/or was severely deficient. Larger nerve fibers first affected makes most vulnerable the highly motivated Eco-athlete who pursues and pushes through the initial pain, then, when the feet go numb, continues to disregard them until a serious event-ending "Trench Foot" disorder occurs.

Generally when this happens both the large and small nerve fibers are traumatized, reducing the strongest-willed athlete to a first aid stretcher!

A clinical example conducted on a 40-year-old human subject who suffered from a severe non-freezing cold injury in both feet. Clinical sensory tests, including two-point discrimination and pressure, vibration and thermal thresholds, indicated damage to both large and small diameter nerves.

On immunohistochemical assessment, terminal cutaneous nerve fibers within the plantar skin stained much less than in a normal control whereas staining to von Willebrand factor pointed to increased vascularity in all areas. The results indicate that all nerve populations (myelinated and unmyelinated) were damaged, possibly from the typical cycle of loss of blood supply ischaemia] followed by a return of blood flow volume [reperfusion].[3]

Simply put, the most feared of deadly foes faced by the stalwarts in this year's world Eco-Challenge is not the myriad of creatures, bugs, slithering-deadly poisonous snakes, swarming bees, enraged elephants, other charging beasts of the jungle wilds, or even the likelihood of invading unseen microbial-infestations prevalent away from home.

The real Public Enemy Number One is the agony of "de feet," which may spell "defeat." Left untreated, it may progress in time to "NO FEET" at all, from the muddy grime and never-ending tropical wet of Sabah.

REFERENCE [1]-A case of bilateral trench foot. Parsons SL, Leach IH, Charnley RM, Injury 1993 Dec 24:10 680-1. [2]-Nature and mechanism of peripheral nerve damage in an experimental model of non-freezing cold injury. Irwin MS, Ann R Coll Surg Engl 1996 Jul 78:4 372-9. [3]-Neuropathy in non-freezing cold injury (trench foot). Irwin MS, Sanders R, Green CJ, Terenghi G, J R Soc Med 1997 Aug 90:8 433-8. You are hereby authorized permission to reprint the included document. We request the copyrighted material also include the author's home websites as emboldened below.