The management of major injuries
Ashley W. Blom, David Warwick, Michael R. Whitehouse in Apley and Solomon’s System of Orthopaedics and Trauma, 2017
Awarenes’ Electrical burns are caused when an individual makes contact between an electrical source and the earth, and severe, non-lethal electrical injuries constitute 3–5% of admissions to burns units in the USA. Current flows through the skin and variably through different tissues from the point of electrical contact to the ground contact, causing burns and necrosis along its path. The physiological effects of an electric shock are related to the amount, duration, type (AC or DC), and path of current flow. Severe electrical skin burns are associated with high-voltage shocks, whereas most domestic, low-voltage shocks are not associated with skin burns even though they may cause death from ventricular fibrillation. Alternating current (AC) shocks produce tetanic muscle spasm, which can cause the victim’s hand to clutch onto the electrical source, and the respiratory muscles can be paralyzed, resulting in respiratory arrest. Electrical muscle damage can result in rhabdomyoly-sis and renal failure, with hugely raised serum, cre-atine kinase levels.
Mitochondrial Dysfunction Affecting the Peripheral Nervous System in Diabetic Neuropathy and Avenues for Therapy
Shamim I. Ahmad in Handbook of Mitochondrial Dysfunction, 2019
DPN has been defined as a “length-dependent, symmetrical sensorimotor polyneuropathy that is attributable to metabolic and micro-vessel alterations, resulting from chronic hyperglycemia exposure (diabetes) and cardiovascular risk covariates” (6). The sensory symptoms spread in a ‘stocking-glove’ distribution, starting in the toes and moving over time to reach the knees, and then moving to the upper limbs. A variety of symptoms may be present that includes prickling and tingling sensations (paresthesias), electric shocks, burning feeling, or pain insensitivity. Hyperalgesia, an increased sensitivity to pain, or allodynia, a painful response to otherwise painless stimuli, are other notable DPN symptoms that are mediated through neuropathy of the small fibers. Of individuals with DPN, 20–30% will suffer from neuropathic pain (5,6,19,24), and this is typically observed to be worse at night. Notably however, the stronger painful symptoms do not appear to directly correlate with severity of damage to axons (4).
Diagnosis and Management of Electrical Injury
Mark V. Boswell, B. Eliot Cole in Weiner's Pain Management, 2005
Most victims of electrical shock experience transient numbness and weakness, followed by pain. The pain usually subsides over time, particularly with adequate medical help. However, some patients have persistent symptoms. The factors that determine whether the pain resolves remain to be determined. As mentioned previously, heavily myelinated fibers are more susceptible to electroporation than unmyelinated fibers, whereas there should be no difference in their relative susceptibility to heat injury. Figure 39.4 shows a plot of the second action potential as a function of the time interval between the second stimulus and the left (top) and right (bottom) ulnar nerves of an electrical injury survivor. The survivor experienced the shock in the right upper extremity. Note that the faster myelinated fibers are not functioning in the electrically injured extremity. This pattern of abnormality is quite common (Abramov et al., 1996).
Effect of hydroalcoholic Echium amoenum extract on scopolamine-induced learning and memory impairment in rats
Published in Pharmaceutical Biology, 2018
Zahra Rabiei, Mahbubeh Setorki
Passive avoidance memory was measured by shuttle box. This apparatus has a bright chamber connected to a dark chamber by a guillotine door. Electric shocks are exerted to a conductive metal grid on the floor of the apparatus by a separate stimulus. This test was performed on each rat for four consecutive days. On the first two days, rats were individually allowed to freely explore the apparatus for 5 min. On the third day, an acquisition test was conducted. Rats were left in the bright chamber and, after 2 min acclimatization, the guillotine door was opened and after the animal entry into the dark chamber, it was closed and an electrical shock (1 mA/s) was exerted to it and the latency to enter the dark chamber was recorded as initial latency. Twenty-four hours later, each rat was placed in the bright chamber and latency to enter the dark chamber was measured as secondary latency (up to 60 s) (Rabiei et al. 2015).
Reframing chronic pain as a disease, not a symptom: rationale and implications for pain management
Published in Postgraduate Medicine, 2019
Daniel J. Clauw, Margaret Noyes Essex, Verne Pitman, Kim D. Jones
Neuropathic pain is the direct result of lesions or diseases of the somatosensory nervous system [1]. Damage to sensory nerves may cause cell death or altered and disordered neural processing of afferent input in the peripheral or central nervous system [32,33]. Changes in ion channels, the balance between excitatory and inhibitory neurotransmitter signaling, and modulation of pain messages in the CNS have been implicated [33]. Patients with neuropathic pain typically experience electric shock-like, lancinating, aching, numbing, burning, or tingling sensations that are distinct from nociceptive pain symptoms [34]. Conditions associated with peripheral neuropathic pain include post-herpetic neuralgia, diabetic neuropathy, Lyme disease, radiculopathy, and trigeminal neuralgia, whereas those associated with central neuropathic pain include multiple sclerosis, Parkinson’s disease, spinal cord injury, tumors, and ischemic stroke [33]. Injury or trauma from surgery may also trigger this type of pain. When pathophysiologic changes in peripheral and central nervous systems persist independent of the inciting condition or injury, the neuropathic pain may become a chronic disease state. Neuropathic or neuropathic-like pain may also occur with other pain types, including with nociceptive chronic pain conditions such as CLBP [35], OA [36], and failed back surgery syndrome [37].
Uncontrollable chronic stress affects eating behavior in rats
Published in Stress, 2019
Marina Liliana González-Torres, Cristiano Valerio dos Santos
Dyads of rats were formed taking one subject of the controllable group and another of the uncontrollable group, resulting in eight dyads. The rats were placed in the Plexiglas chamber described in the apparatus section. Electric shock sessions lasted approximately 10 min and were conducted between 6 and 8 pm. Ten electric shocks were scheduled on average once every 60 s, with an intensity of 0.6 mA and a maximum duration of 10 s. When the “controllable” subject spun the wheel two or more times, the electric shock was switched off both for itself and for the “uncontrollable” rat yoked to it. The rats were returned to the home cages at the end of the shock sessions. When the average latency of the escape response in a session was less than 4 s, the minimum response requirement was increased by one turn. The rats of the third group received the same amount of shocks, but with a fixed duration of 5 s (the mean duration for the other groups). The rats in the control group also were placed in the foot-shock cage for the same period but received no foot-shock.
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