Prophylaxis of warm-water-immersion foot.
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We report a case of "green foot" in a child with a plaster cast applied for a fractured metatarsal who subsequently re-presented with circulatory compromise. The foot was green and smelly and profuse Pseudomonas aeruginosa was cultured. The infection cleared with simple exposure to air. Perhaps this diagnosis should be considered in patients presenting with circulatory compromise in a cast as severe infection can result in amputation.
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Male subjects comprised of six Inuit from Igloolik, N.W.T., and five Orientals and six Caucasians from Toronto, Ont., volunteered for tests to determine the effect of localized cold stress on peripheral temperatures. In each subject, skin temperatures of the right index finger, the arm, and the cheek, as well as blood pressure and heart rate, were measured before, during, and after foot immersion in water of 10 degrees C temperature for 10 min. There was an immediate decrease in finger temperature on foot immersion in all three subject groups; however, the Inuit finger temperatures recovered very quickly to control values, the Caucasian finger temperatures began to increase after decreasing for 7.5 min, and the Oriental finger temperatures decreased continuously during the foot immersion and remained cool even 10 min after the removal of the cold stimulus. The cold stimulus did not affect the cheek or arm temperatures of any of the groups. In all subjects, systolic and diastolic blood pressures and heart rates increased on foot immersion, gradually returning towards normal values. No intergroup differences were seen in these parameters.
The purposes of the present study were to compare the cardiovascular response patterns evoked by three versions of the cold pressor test (either forehead stimulation or hand or foot immersion) and to determine the reproducibility of the responses over a 2-week interval. Blood pressure, heart rate, stroke volume, cardiac output, total peripheral resistance, and systolic time intervals were obtained during rest and during the cold pressor test in 42 young men. Across conditions, the pressor response was supported by peripheral resistance increases with concomitant stroke volume decreases. Although the response patterns were generally similar across sites, exceptions were apparent for heart rate. Forehead stimulation was characterized by no significant change in heart rate, whereas limb (hand or foot) immersion was associated with significant heart rate acceleration. The responses elicited by the three cold pressor test conditions were reliable and showed little evidence of attenuation over the test-retest interval.
BACKGROUND: The genetic association between blood pressure (BP) at rest and during the cold pressor test (CPT) is not well characterized. The purpose of this study was to examine the genetic architecture of BP during the CPT, and to determine whether BP at rest and during the CPT share common genetic influences. METHODS: In 419 individuals distributed across four large families, variance components methods were used to estimate heritabilities of resting BP and CPT BP, along with genetic correlations among BP traits. The CPT consisted of immersion of the left foot in 4 degrees C water while the participant was supine. Blood pressure reactivity (DeltaBP) was defined as BP at 15 to 30 sec and 45 to 60 sec of foot immersion minus resting BP. RESULTS: Significant (P < .05) heritabilities were found for supine BP (h(2)(SBP) = 0.35), CPT BP (h(2)(SBP) = 0.27 and 0.33, h(2)(DBP) = 0.18 and 0.30), and DeltaSBP (h(2)(SBP) = 0.12 and 0.37) but not for DeltaDBP. Bivariate analyses detected significant (P < .05) genetic correlations between resting SBP and CPT SBP that were different from 0 and 1. Genetic correlations between resting DBP and CPT DBP were not significantly different from 1. Genetic correlations between resting SBP and DeltaSBP were not significant. CONCLUSIONS: Measures of BP at rest and during cold immersion are significantly influenced by additive genetic effects. These genetic influences are only partially shared between SBP at rest and SBP during cold immersion, suggesting that a somewhat different set of genes may influence SBP during cold immersion. Unique sets of genes also appear to influence DeltaSBP independent of those influencing resting SBP.
Six subjects performed a breathholding maneuver during facial cooling and immersed their foot in cold water, without drugs and after the intravenous administration of propranolol plus atropine (P + A). Cardiac interval (INT), mean interval for longest consecutive 5 cycles (L5INT/5); systolic time intervals including electromechanical systole (EMS), left ventricular ejection time (LVET), pre-ejection period (PEP), and PEP/LVET; and systolic (SP) and diastolic pressures (DP) were monitored during supine rest, during apnea with a plastic bag of ice water on the face, and from 16-30th and 46-60th sec of 1-min periods of foot immersion in 4 degrees C water. P+A administration induced reduction in INT, L5INT/5, and LVET and increase in PEP, PEP/LVET, and DP. INT, L5INT/5, PEP, SP, and DP increased during facial cooling without drugs. Only the increases in INT and L5INT/5 were abolished by P+A and thus considered to result from reflexes mediated by vagal or sympathetic outflow to the heart. Reductions in INT, L5INT/5, EMS, PEP, and PEP/LVET at 16-30 sec of foot immersion without drugs were not observed after P+A; 46-60 sec responses neared resting values, however, with and without P+A. These results indicate an initial cardiac reflex response to foot immersion may be overpowered by the ventricular afterload and the foot immersion may be overpowered by the ventricular afterload and the baroreceptor response due to the increased arterial pressure.
The hormone testosterone (T) is involved in the control of aggressive behavior in male vertebrates. T enhances the frequency and intensity of aggressive behaviors during competitive interactions among males. By promoting high-intensity aggression, T also increases the risk of injury and presumably the perception of painful stimuli. However, perception of painful stimuli during fights could counteract the expression of further aggressive behavior. We therefore hypothesize that one function of T during aggressive interactions is to reduce nociception (pain sensitivity). Here, we experimentally document that T indeed reduces behavioral responsiveness to a thermal painful stimulus in captive male house sparrows (Passer domesticus). Skin nociception was quantified by foot immersion into a hot water bath, a benign thermal stimulus. Males treated with exogenous testosterone left their foot longer in hot water than control birds. Conversely, males in which the physiological actions of testosterone were pharmacologically blocked withdrew their foot faster than control birds. Testosterone might exert its effects on pain sensitivity through conversion into estradiol in the dorsal horn of the spinal cord. Decreased nociception during aggressive encounters may promote the immediate and future willingness of males to engage in high-intensity fights.
Intravenous opioids cause analgesia and increase release of ACh in spinal cord dorsal horn in animals, and these effects are enhanced by intrathecal neostigmine injection. The purpose of the current study was to test whether intrathecal neostigmine enhanced analgesia and increased cerebrospinal fluid concentrations of ACh over those induced by i.v. alfentanil in volunteers, and also to test whether neostigmine enhanced alfentanil-induced side effects. After human studies committee approval, 40 healthy volunteers received an intrathecal injection of saline or neostigmine (50, 100 or 200 microg) followed in 60 min by a computer-controlled, stepped i.v. infusion of alfentanil to escalating targeted plasma concentrations. Pain report to hand and foot immersion in ice water, sedation, nausea, weakness, vital signs, end-tidal CO2 and oxyhemoglobin saturation were measured 60 min after spinal injection and at the end of each 20-min alfentanil infusion. Cerebrospinal fluid was sampled once after drug administration. Intrathecal neostigmine alone caused analgesia in the foot but not in the hand, and was accompanied by leg weakness, whereas IV alfentanil alone caused equivalent analgesia in both the hand and the foot and was accompanied by nausea, sedation, increased end-tidal CO2 and decreased oxyhemoglobin saturation. Neostigmine enhanced analgesia but not respiratory effects induced by i.v. alfentanil; it also enhanced nausea and sedation. Intravenous alfentanil increased cerebrospinal fluid ACh concentration, and neostigmine enhanced this change. These data in humans are consistent with a spinal cholinergic mechanism of i.v. opioid analgesia. Because neostigmine enhances both analgesia and side effects induced by i.v. alfentanil, the clinical utility of their use in combination will depend on the relative strength of these interactions.
We have previously shown that irritable bowel syndrome (IBS) patients have both visceral and cutaneous hyperalgesia. The neural mechanisms of these forms of hyperalgesia were further characterized by comparing cortical processing of both rectal distension (35, 55mmHg) and cutaneous heat nociceptive stimuli (foot immersion in 45 and 47 degrees C water bath) in IBS patients and in a group of healthy age/sex-matched controls. Our approach relied on functional magnetic resonance imaging neuroimaging analyses in which brain activation in age/sex-matched control subjects was subtracted from that found in IBS patients. These analyses revealed that both rectal distension and cutaneous heat stimuli evoked greater neural activity in several brain regions of IBS patients in comparison to age/sex-matched control subjects. These include those related to early stages of somatosensory processing (e.g. thalamus, somatosensory cortex) as well as those more related to cognitive and affective processing (insular, anterior cingulate, posterior cingulate, prefrontal cortex). Thus, our results support the hypothesis that hyperalgesia of IBS is manifested by increased somatosensory processing at all cortical levels. This was found to be the case not only for visceral hyperalgesia but also for cutaneous heat hyperalgesia, a likely form of secondary hyperalgesia. Furthermore, visceral and heat hyperalgesia were accompanied by increased neural activity within the same brain structures. These results support the hypothesis that visceral and cutaneous hyperalgesia in IBS patients is related to increased afferent processing in pathways ascending to the brain rather than to selectively increased activity at higher cortical levels (e.g. limbic and frontal cortical areas).
OBJECTIVES: Our study objectives were as follows: (1) to determine whether urinary excretion of potassium is lower in black than in white children, (2) to determine whether cardiovascular reactivity (CVR) varies inversely with dietary intake of potassium, and (3) to confirm that CVR is greater in black than in white children, and in children with a family history of hypertension than in those without such a history. STUDY DESIGN: Baseline measurements included 24-hour urinary sodium, potassium, and creatinine levels and food intake (by questionnaire). Resting and stress blood pressure were measured during blood sampling, cold water foot immersion, and a video game before and after 1 week each of supplementation with potassium citrate, 1.5 mmol/kg per day, and placebo administered in random order. RESULTS: Thirty-nine children aged 7 to 15 years were studied. White subjects had higher baseline excretion of potassium than black subjects (p < 0.001) and higher vegetable intake (p < 0.01), which were positively correlated (r = 0.53, p < 0.001). At baseline, the 24-hour urinary potassium/creatinine ratio varied inversely with diastolic CVR to the video game stressor in white children (r = -0.55, p = 0.02). Cardiovascular reactivity was not attenuated measurably by potassium supplementation compared with placebo. The CVR was greater in children with a family history of hypertension than in those without, but was not greater in black children than in white children. CONCLUSIONS: The urinary potassium/creatinine ratio is higher in white than black children because their intake of vegetables is greater; dietary potassium intake may modulate CVR, particularly in white children with a family history of hypertension, but may need to be supplemented for more than 1 week to demonstrate attenuation of CVR; and a family history of hypertension may be a stronger predictor of enhanced CVR than is race.