Non-freezing Cold Injury Research Articles

Interventions for non-freezing cold injuries

Interventions for non-freezing cold injuries

Nonfreezing Cold Injury in a Pediatric Hiker

AbstractNonfreezing cold injury has been primarily described in military populations as a result of prolonged exposure to wet environments and cold, but not freezing, temperatures. This type of injury occurs less commonly in the civilian population and in children, but poses a risk for short-term debilitating extremity pain, tissue damage, and infection and for long-term chronic neuropathic pain and temperature intolerance. We describe a case of nonfreezing cold injury in a pediatric hiker.

Previous recreational cold exposure does not alter endothelial function or sensory thermal thresholds in the hands or feet.

What is the central question of this study? Does recreational cold exposure result in cold sensitivity and is this associated with endothelial dysfunction and impaired sensory thermal thresholds? What is the main finding and its importance? Previous cold exposure was correlated with cold sensitivity of the foot, which might indicate the development of a subclinical non-freezing cold injury. Endothelial function and thermal detection were not impaired in cold-sensitive individuals; therefore, further research is required to understand the pathophysiology of subclinical and clinical forms of non-freezing cold injury. In this study, we investigated whether cold-sensitive (CS) individuals, who rewarm more slowly after a mild cold challenge, have impaired endothelial function and sensory thermal thresholds (STTs) and whether this is related to reported cold exposure. Twenty-seven participants with varying previous cold exposure undertook three tests: an STT test, i.e. determination of warm and cold STTs of the fingers and dorsal foot; an endothelial function test, i.e. measurement of cutaneous vascular conductance (CVC) during iontophoresis of ACh on the forearm, finger and foot; and a CS test, involving immersion of a foot for 2min in water at 15°C followed by 10min of rewarming in air at 30°C. Toe skin temperature (Tsk ) measured during the CS test was used to form a CS group (<32°C before and 5min after immersion) and an otherwise closely matched control group [Tsk >32°C; n=9 (four women) for both groups]. A moderate relationship was found between cold exposure ranking and Tsk rewarming (r=0.408, P=0.035, n=27) but not STT or endothelial function. The Tsk and blood flow were lower in CS compared with control subjects before and after foot immersion [Tsk , mean (SD): 30.3(0.9) versus 34.8(0.8) and 27.9(0.8) versus 34.3(0.8)°C, P<0.001; and CVC: 1.08(0.79) versus 3.82(1.21) and 0.79(0.52) versus 3.45(1.07)fluxmmHg-1 , n=9, P<0.001, respectively]. However, no physiologically significant differences were observed between groups for endothelial function or STT. A moderate correlation between previous cold exposure and toe Tsk rewarming after foot immersion was observed; however, CS was not associated with impaired endothelial function or reduced thermal detection.

Nonfreezing Cold Injuries Among Long-Distance Polar Rowers

Nonfreezing cold injury (NFCI) is a peripheral cold injury that occurs when the extremities are exposed to cold temperatures, at or near the freezing point, for sustained periods of time (48-96 h at temperatures of usually around 0 to 6°C with associated wind chill). Although NFCI often goes unreported and may be underdiagnosed, it is a cause of significant morbidity in those working in cold conditions, particularly those in the military. Thus, further research into the prevention, recognition, and treatment of NFCI is warranted. The height, body weight, and body composition of 6 rowers taking part in 1 or 2 legs of the 2017 Polar Row expedition were measured. The weather conditions of the 2 legs of the journey were recorded, and symptoms relating to NFCI were documented. All incidences of NFCI occurred during Leg 2 of the expedition, which was colder and wetter. Of the Leg 2 rowers, those who developed NFCI had a trend toward higher pre-row body weight and body mass index and a trends toward losing more weight and body water relative to those who did not. The main factor contributing to the incidence of NFCI appeared to be weather; NFCI only occurred during the colder and wetter leg of the expedition. We also tentatively suggest that nutrition and dehydration may be linked to the incidence of NFCI as predisposing factors. More work, with sample sizes greater than those reported here, is required to investigate these associations to further characterize risk factors.

Erythromelalgia: skin redness and pain

Erythromelalgia is a rare disease that is associated with hemato-oncological diseases or after taking certain drugs and toxins, but it can also occur as an independent clinical picture, for example, due to mutations in the sodium channel NaV1.7. Clinically, there is a characteristic triad of attack-like burning pain and skin redness in the area of the distal extremities, which can be alleviated by excessive cooling. The attacks are triggered by heat, exertion, and stress. The diagnosis is primarily made clinically and can be confirmed by genetic testing if a sodium channel NaV1.7 mutation is present. Important differential diagnoses are complex regional pain syndrome, the non-freezing cold injury, and small fiber neuropathies. Therapy is multidisciplinary and has to be planned individually and include physical therapy and psychotherapy as well as drug therapy as integral components.

A review of trench foot: a disease of the past in the present.

From the French Invasion of Russia in 1812, to Glastonbury festival in 2007, trench foot has been reported, yet the exact nature of the condition remains unclear. This review explores the pathogenesis and treatment of trench foot. Trench foot is considered to be a nonfreezing cold injuryoften complicated by infection, in which exposure to cold temperatures just above freezing, combined with moisture, results in a peripheral vasoneuropathy. The presence of physical trauma, bacterial or fungal infections, malnutrition, venous hypertension and lymphoedema mean that some individuals are at greater risk of trench foot. Trench foot may be prevented by warming the feet, changing socks, staying active, rubbing the skin with oil and regularly inspecting the feet. Avoiding risk factors may help prevent the condition. The management of trench foot is less clear. Vasodilators such as iloprost and nicotinyl tartrate or sympathectomy may help. Trench foot may lead to necrosis, cellulitis, sepsis and amputation. It remains a poorly understood condition.

A 4-year follow-up of non-freezing cold injury with cold allodynia and neuropathy in 26 naval soldiers.

Background and aims Non-freezing cold injuries (NFCI), which typically may occur in military personnel, may result from exposure to cold, at temperatures around 0 °C or above, and worsened by wind and moisture. The injury is due to cooling but not freezing of tissue like in frostbite. NFCI may result in in chronic neuropathy and cold hypersensitivity. A recent retrospective study of small-and large fibres has suggested that NFCI results in neuropathic pain due to a sensory neuropathy and question a longitudinal study to verify a possible observation of improvement of NFCI over time. The present study is a 4-year follow-up investigation of large - and small-fibre function in 26 naval cadets and officers who were exposed to cold injury during the same military expedition. Methods The 26 soldiers were investigated clinically (with investigation of motor function, reflexes, sensibility), with nerve conduction studies (NCS) of major nerves in upper- and lower extremity, small fibre testing (QST, measurement of thermal thresholds), measurements of subcutaneous fat tissue and maximal O2 uptake. Investigations found place 2 months following the actual military expedition, with follow-up investigations of affected soldiers at 6-12 months and up to 3-4 years. In order to elucidate possible mechanisms (disinhibition of cold pain by myelinated nerve fibres) of cold allodynia, cold pain thresholds were measured following an ischemic block of conduction of large and small myelinated nerve fibres. Results Of 26 soldiers, 19 complained of numbness in feet and a large majority of 16 of cold hypersensitivity 2 months following injury. There were significant alterations of both large- and small-fibre function, indicating a general large- and small-fibre neuropathy. The most prominent finding was a pronounced cold allodynia, inversely correlated with the amount of subcutaneous fat. During the first year, results of NCS and thermal testing gradually normalized in most. Seven soldiers developed chronic symptoms in the form of cold hypersensitivity and with findings of cold allodynia, which was not further enhanced, but abolished following block of conduction of myelinated nerve fibres. Seven soldiers were free of symptoms from that start of the investigation, probably because they had been more eager to keep their legs moving during the exposure to cold. Conclusions Of a total of 26 soldiers, only seven developed chronic symptoms of cold hypersensitivity, corresponding to the finding of cold allodynia by thermal testing. The cold allodynia may not be explained by disinhibition of cold pain by myelinated fibres as in healthy subjects. A large majority recovered from an initial large-and small fibre neuropathy, demonstrating that recovery from NFCI may occur. Implications Although large-and small fibre neuropathy may be restored following cold injury, there is a risk of a permanent and disabling cold hypersensitivity, corresponding to the findings of cold allodynia. It is of uttermost importance to secure military personnel from the risk of cold injuries. It seems important to avoid immobilisation of extremities during exposure to cold.

Case series of non-freezing cold injury: the modern clinical syndrome

BackgroundNon-freezing cold injury (NFCI) occurs when peripheral tissue is damaged by cold exposure but not to the extent of freezing. Historically, the phenotype of NFCIs sustained was severe, whereas today...

20 Armoured Infantry Brigade downgrade study: epidemiology of principal conditions and plugging leaks in the rehabilitation pipeline

IntroductionIn April 2017, 22% of Army Full-time Trade Trained Strength was downgraded, reducing fully deployable strength to 60 546, against a target of 82 000. In June 2017, Commander 20...

Case series of non-freezing cold injury: epidemiology and risk factors

BackgroundNon-freezing cold injury (NFCI) occurs when the peripheral tissue is cooled sufficiently that damage occurs, but not to the point of tissue freezing. Historically, the phenotype of the injuries studied...

Distal limb pathologic conditions in horses treated with sleeve-style digital cryotherapy (285 cases)

Digital cryotherapy (DC) is frequently used as laminitis prophylaxis for horses. While DC with ice-water slurries is reported to be safe for up to 48 h, the safety of sleeve-style digital cryotherapy (SSDC) with ice in direct contact with the distal limb has not been evaluated. Our objective was to determine the incidence of distal limb pathologic conditions (DLPC) among horses treated with SSDC. A retrospective study of cases from 2011 to 2015 identified 285 horses treated with SSDC for a minimum of 12 h. Data collected from medical records included demographic, treatment, diagnostic, and SSDC treatment parameters. Bivariate statistics and a generalized linear regression model were created to evaluate risk factors associated with increased incidence of DLPC. Among horses treated with SSDC, 7% had tissue injury of the distal limb. Increasing duration of SSDC was associated with increased incidence of DLPC. Lesions observed included dermatitis, cellulitis, alopecia, coronitis, tissue necrosis, and distal limb edema. These lesions were similar to frostbite, non-freezing cold injury, and prolonged water immersion injuries seen in other species. While the incidence of DLPC was low, the authors recommend that horses undergoing SSDC with ice in direct contact with the skin should be monitored closely for injury when prolonged cryotherapy is clinically indicated. Further studies to improve safety, efficacy, and convenience of alternative methods of DC for horses are warranted.

Using a human thermoregulation model as a tool for design and refurbishment of industrial spaces for human occupancy

Requirements for industrial work conditions are determined by human occupancy, building construction and production processes and they should ensure the prevention and removal of heat and noxious substances from the working space. Till now costly and time-consuming experimental methods in existing buildings and fast but less reliable simulation methods at the design stage were used, which both treat the human factor as minor. In the present study we propose a user-centered methodology which combined the versatility of the thermo-physiological modeling and the reliability of in-situ measurements based on an example of a typical industrial hall.Based on the results we observed insufficient operative temperature for winter and summer months due to the missing HVAC system in the hall. As a consequence, sweat excretion, thermal sensation and skin wettedness exceeded their limits for physiological strain and thermal comfort during the summer months, and skin temperature decreased distinctly at the face and hands but was still above the limit for pain or non-freezing cold injury in the winter months.This methodology can be used for a wide range of thermal environments, activities and clothing. It eliminates the need for the exposure of human beings and provides information on physiological data, which are difficult or impractical to measure in a field study (e.g. sweat excretion, skin and core temperatures, thermal sensation). The methodology can be useful to reveal zones with distractive effect or are inappropriate for human exposition. Finally, this approach also allows using a single method and providing continuous output information for a variety of environments without needing to change approach and type of output data.

Field recognition and management of freezing and non-freezing cold injuries

AbstractPeripheral cold injuries have disabled entire armies in the past and, as recently as the Falklands conflict of 1982, jeopardised the success of an entire military operation. They can be divided into those that involve freezing of the peripheral tissue and those that do not, termed Freezing Cold Injury (FCI) and Non-Freezing Cold Injury (NFCI) respectively.This article focuses on the recognition and management of cold injuries in the field. It draws from the current literature, briefly outlining the pathophysiological basis of the two injuries, then focuses on the challenges of field recognition of cold injuries, especially NFCI, which is characterised by a lack of overt physical signs. A framework for field management of these injuries is then outlined, with an emphasis on the contrasting re-warming strategies for FCI and NFCI, and the pharmacological therapies used in each condition.The article is pertinent to those who may train or deploy to an area with temperatures lower than 20° Celsius, the generally accepted temperature below which peripheral cold injuries may occur. It is hoped that improved awareness of the risks coupled with better field recognition and management may reduce the incidence of cold injury, especially in light of recent observations that re-exposure to cold in those with NFCI can cause more significant morbidity, highlighting the importance of getting the diagnosis and management right in the field.

Field recognition and management of freezing and non-freezing cold injuries

Field recognition and management of freezing and non-freezing cold injuries

Trench Foot or Non-Freezing Cold Injury As a Painful Vaso-Neuropathy: Clinical and Skin Biopsy Assessments.

Trench foot, or non-freezing cold injury (NFCI), results from cold exposure of sufficient severity and duration above freezing point, with consequent sensory and vascular abnormalities which may persist for years. Based on observations of Trench foot in World War II, the condition was described as a vaso-neuropathy. While some reports have documented nerve damage after extreme cold exposure, sensory nerve fibres and vasculature have not been assessed with recent techniques in NFCI. To assess patients with chronic sensory symptoms following cold exposure, in order to diagnose any underlying small fibre neuropathy, and provide insight into mechanisms of the persistent pain and cold hypersensitivity. Thirty soldiers with cold exposure and persistent sensory symptoms (>4 months) were assessed with quantitative sensory testing, nerve conduction studies, and skin biopsies. Immunohistochemistry was used to assess intraepidermal (IENF) and subepidermal (SENF) nerve fibres with a range of markers, including the pan-neuronal marker protein gene product 9.5 (PGP 9.5), regenerating fibres with growth-associated protein 43 (GAP43), and nociceptor fibres with transient receptor potential cation channel subfamily V member 1 (TRPV1), sensory neuron-specific receptor (SNSR), and calcitonin gene-related peptide (CGRP). von Willebrand factor (vWF), endothelial nitric oxide synthase (eNOS), and vascular endothelial growth factor (VEGF) were used for assessing blood vessels, and transient receptor potential cation channel, subfamily A member 1 (TRPA1) and P2X purinoceptor 7 (P2X7) for keratinocytes, which regulate nociceptors via release of nerve growth factor. Clinical examination showed pinprick sensation was abnormal in the feet of 20 patients (67%), and between 67 and 83% had abnormalities of thermal thresholds to the different modalities. 7 patients (23%) showed reduced sensory action potential amplitude of plantar nerves. 27 patients (90%) had decreased calf skin PGP 9.5 IENF (p < 0.0001), the remaining 3 patients had decreased nerve markers in subepidermis or foot skin. There were marked increases of all vascular markers (for vWF in calf skin, p < 0.0001), and increased sensory or regenerating SENF (for calf skin, GAP43, p = 0.002). TRPA1 (p = 0.0012) and P2X7 (p < 0.0001) were increased in basal keratinocytes. A range of skin biopsy markers and plantar nerve conduction studies are useful objective assessments for the diagnosis of peripheral neuropathy in NFCI. Our results suggest that an increase in blood vessels following tissue ischaemia/hypoxia could be associated with disproportionate and abnormal nerve fibres (irritable nociceptors), and may lead to NFCI as a "painful vaso-neuropathy."

Chronic non-freezing cold injury results in neuropathic pain due to a sensory neuropathy.

Non-freezing cold injury develops after sustained exposure to cold temperatures, resulting in tissue cooling but not freezing. This can result in persistent sensory disturbance of the hands and feet including numbness, paraesthesia and chronic pain. Both vascular and neurological aetiologies of this pain have been suggested but remain unproven. We prospectively approached patients referred for clinical assessment of chronic pain following non-freezing cold injury between 12 February 2014 and 30 November 2016. Of 47 patients approached, 42 consented to undergo detailed neurological evaluations including: questionnaires to detail pain location and characteristics, structured neurological examination, quantitative sensory testing, nerve conduction studies and skin biopsy for intraepidermal nerve fibre assessment. Of the 42 study participants, all had experienced non-freezing cold injury while serving in the UK armed services and the majority were of African descent (76.2%) and male (95.2%). Many participants reported multiple exposures to cold. The median time between initial injury and referral was 3.72 years. Pain was principally localized to the hands and the feet, neuropathic in nature and in all study participants associated with cold hypersensitivity. Clinical examination and quantitative sensory testing were consistent with a sensory neuropathy. In all cases, large fibre nerve conduction studies were normal. The intraepidermal nerve fibre density was markedly reduced with 90.5% of participants having a count at or below the 0.05 centile of published normative controls. Using the Neuropathic Pain Special Interest Group of the International Association for the Study of Pain grading for neuropathic pain, 100% had probable and 95.2% definite neuropathic pain. Chronic non-freezing cold injury is a disabling neuropathic pain disorder due to a sensory neuropathy. Why some individuals develop an acute painful sensory neuropathy on sustained cold exposure is not yet known, but individuals of African descent appear vulnerable. Screening tools, such as the DN4 questionnaire, and treatment algorithms for neuropathic pain should now be used in the management of these patients.

Talk to the Hand: U.S. Army Biophysical Testing.

Many people are unaware of the science underlying the biophysical properties of Soldier clothing and personal protective equipment, yet there is a well-refined biomedical methodology initiated by Army physiologists in World War II. This involves a methodical progression of systematic material testing technologies, computer modeling, and human testing that enables more efficient development and rapid evaluation of new concepts for Soldier health and performance. Sophisticated manikins that sweat and move are a central part of this testing continuum. This report briefly summarizes the evolution and use of one specialized form of the manikin technologies, the thermal hand model, and its use in research on Soldier hand-wear items that sustain dexterity and protect the hand in extreme environments. Thermal manikin testing methodologies were developed to provide an efficient and consistent analytical tool for the rapid evaluation of new clothing concepts. These methods have been upgraded since the original World War II and Korean War eras to include articulation and sweating capabilities, as characterized and illustrated in this article. The earlier "retired" versions of thermal hand models have now been transferred to the National Museum of Health and Science. The biophysical values from manikin testing are critical inputs to the U.S. Army Research Institute of Environmental Medicine mathematical models that provide predictions of soldier comfort, duration of exposure before loss of manual dexterity, and time to significant risk of freezing (skin temperature <-1°C) and nonfreezing cold injuries (skin temperature <5°C). The greater thickness of better insulated handwear reduces dexterity and also increases surface area which makes added insulation increasingly less effective in retaining heat. Measurements of both thermal resistance (insulation) and evaporative resistance (permeability) collectively characterize the biophysical properties and enable mathematical modeling of the human thermophysiological responses. This information can help guide the hand-wear development and selection process which often requires trade-offs between factors such as material, cost, and sizing. Soldier hands provide fine motor dexterity in tactical functions, ranging from pulling a trigger to pulling a parachute ripcord; thus, protecting hand function is critical to soldier readiness. Also, the importance of protection against nonbattle cold injuries was highlighted during World War II in northern Europe, in the Aleutian Islands, and later in Korea. The U.S. Army has been on the forefront of the biophysical analysis of clothing including gloves since environmental research was established at the Armored Medical Research Laboratory and Climatic Research Laboratory during World War II. U.S. Army Research Institute of Environmental Medicine does not make the equipment but works with their Natick Soldier Research, Development, and Engineering Center partners to make the equipment better.

Wilderness cold-exposure injuries: An African perspective

Cold injuries may be systemic (hypothermia) or local (frostbite or non-freezing cold injury). Hypothermia (core temperature of <35°C) is very common in South Africa, particularly in trauma patients, and conditions suitable for the development of local cold injuries frequently occur. Despite this, cold injuries are underdiagnosed, and many practitioners lack insight into the modern management of frostbite. Risk factors include low ambient temperatures, increased duration of exposure, trauma, immobility, intoxication or mental illness, lack of protective clothing or equipment, immersion, level of fitness, extremes of age, and ethnicity. Core temperature measurement should be obtained using an oesophageal probe in intubated patients, or a rectal thermometer in those who are conscious. Field management involves prevention of further heat loss by insulation and vapour barriers, and moving the patient to shelter. Rewarming strategies depend on the severity of hypothermia, and include core rewarming with heat packs, warm blankets and warm fluids (orally or intravenously). Unconscious victims of severe hypothermia require careful handling, advanced airway management and invasive rewarming, which may include extracorporeal means. Local cold injuries should be protected and rewarmed in a warm-water bath as soon as they are no longer at a risk of refreezing. Warming should be completed before grading and prognostication. Surgery should be deferred in almost all cases. Intra-arterial thrombolysis and prostacyclin-analogue infusions are novel therapies which may prevent tissue loss.

Role of cyclooxygenase in the vascular responses to extremity cooling in Caucasian and African males.

What is the central question of this study? Compared with Caucasians, African individuals are more susceptible to non-freezing cold injury and experience greater cutaneous vasoconstriction and cooler finger skin temperatures upon hand cooling. We investigated whether the enzyme cyclooxygenase is, in part, responsible for the exaggerated response to local cooling. What is the main finding and its importance? During local hand cooling, individuals of African descent experienced significantly lower finger skin blood flow and skin temperature compared with Caucasians irrespective of cyclooxygenase inhibition. These data suggest that in young African males the cyclooxygenase pathway appears not to be the primary reason for the increased susceptibility to non-freezing cold injury. Individuals of African descent (AFD) are more susceptible to non-freezing cold injury (NFCI) and experience an exaggerated cutaneous vasoconstrictor response to hand cooling compared with Caucasians (CAU). Using a placebo-controlled, cross-over design, this study tested the hypothesis that cyclooxygenase (COX) may, in part, be responsible for the exaggerated vasoconstrictor response to local cooling in AFD. Twelve AFD and 12 CAU young healthy men completed foot cooling and hand cooling (separately, in 8°C water for 30min) with spontaneous rewarming in 30°C air after placebo or aspirin (COX inhibition) treatment. Skin blood flow, expressed as cutaneous vascular conductance (as flux per millimetre of mercury), and skin temperature were measured throughout. Irrespective of COX inhibition, the responses to foot cooling, but not hand cooling, were similar between ethnicities. Specifically, during hand cooling after placebo, AFD experienced a lower minimal skin blood flow [mean (SD): 0.5 (0.1) versus 0.8 (0.2) fluxmmHg-1 , P<0.001] and a lower minimal finger skin temperature [9.5 (1.4) versus 10.7 (1.3)°C, P=0.039] compared with CAU. During spontaneous rewarming, average skin blood flow was also lower in AFD than in CAU [2.8 (1.6) versus 4.3 (1.0) fluxmmHg-1 , P<0.001]. These data provide further support that AFD experience an exaggerated response to hand cooling on reflection this appears to overstate findings; however, the results demonstrate that the COX pathway is not the primary reason for the exaggerated responses in AFD and increased susceptibility to NFCI.

Role of cyclooxygenase in the vascular response to locally delivered acetylcholine in Caucasian and African descent individuals

IntroductionIndividuals of African descent (AFD) are more susceptible to non-freezing cold injury (NFCI) compared with Caucasian individuals (CAU). Vasodilatation to acetylcholine (ACh) is lower in AFD compared with CAU in the non-glabrous foot and finger skin sites; the reason for this is unknown. Prostanoids are responsible, in part, for the vasodilator response to ACh, however it is not known whether the contribution differs between ethnicities. Methods12 CAU and 12 AFD males received iontophoresis of ACh (1 w/v%) on non-glabrous foot and finger skin sites following placebo and then aspirin (600mg, single blinded). Aspirin was utilised to inhibit prostanoid production by inhibiting the cyclooxygenase (COX) enzyme. Laser Doppler flowmetry was utilised to measure changes in skin blood flow. ResultsNot all participants could receive iontophoresis charge due to high skin resistance; these participants were therefore excluded from the analyses.Foot: ACh elicited greater maximal vasodilatation in CAU than AFD following placebo (P=0.003) and COX inhibition (COXib) (P<0.001). COXib did not affect blood flow responses in AFD, but caused a reduction in the area under the curve for CAU (P=0.031).Finger: ACh elicited a greater maximal vasodilatation in CAU than AFD following placebo (P=0.013) and COXib (P=0.001). COXib tended to reduce the area under the curve in AFD (P=0.053), but did not affect CAU. ConclusionsCAU have a greater endothelial reactivity than AFD in both foot and finger skin sites irrespective of COXib. It is concluded that the lower ACh-induced vasodilatation in AFD is not due to a compromised COX pathway.