Acute Injury

In animals it is clear that both endogenous and exogenous ROS can produce acute injury to pulmonary cells in vitro and in vivo, and that a variety of antioxidant substances can reduce such damage. However, although... 

The cornerstone of nonpharmacologic therapy for acute injury in the first 48 to 72 hours is known by the acronym RICE rest, ice, compression, and elevation. 

Heat should not be applied during the acute injury phase (the first 48 hours) because it promotes swelling and inflammation. 

The musculoskeletal system consists of the muscles, bones, joints, tendons, and ligaments. Disorders related to the musculoskeletal system often are classified by etiology. Acute soft-tissue injuries include strains and sprains of muscles and ligaments. Repeated movements in sports, exercise, work, or activities of daily living may lead to repetitive strain injury, where cumulative damage occurs to the muscles, ligaments, or tendons.1-3 While tendonitis and bursitis can arise from acute injury, more commonly these conditions occur as a result of chronic stress.3,4 Other forms of chronic musculoskeletal pain, such as pain from rheumatoid arthritis (see Chap. 54) or osteoarthritis (see Chap. 55), are discussed elsewhere in this text. 

Musculoskeletal disorders owing to acute injury may be associated with other signs of the injury such as abrasion. 

Treatment of musculoskeletal disorders involves three phases (1) therapy of an acute injury using the RICE principle, (2) pain relief using oral or topical agents, and (3) lifestyle and behavioral modifications for rehabilitation and to prevent recurrent injury or chronic pain (Fig. 57-3). 

In addition to minimizing the acute inflammatory response, rest prevents additional injury to the affected area.13 The properties of the muscle-tendon unit are altered during the acute injury, with limitations on the ability of the muscles and tendons to stretch. Early activity predisposes a patient to further injury, but prolonged inactivity can lengthen recovery times. 

NSAIDs are used commonly for musculoskeletal pain because of their availability without a prescription and anti-inflammatory effects.30,31 NSAIDs are a preferred choice over acetaminophen in musculoskeletal disorders where inflammation is evident.27 However, there is some controversy because the inflammatory response may be necessary for healing.13 Nevertheless, most experts recommend the use of NSAIDs early after acute injury to control inflammation and the range -of-motion limitations that may accompany swelling.27... 

If pain from acute injury does not decrease greatly within... 

Develop a plan to assess effectiveness of pharmacologic therapy. If pain is from an acute injury, assess effectiveness within 7 to 10 days. For chronic pain treated with capsaicin, begin to assess pain control in 2 weeks. 

Chronic pain can be nociceptive, neuropathic/functional, or both (e.g., pain that persists after the healing of the acute injury, pain related to a chronic disease, pain without an identifiable cause, and pain associated with cancer). 

Acute injuries or CNS insults that cause extensor or flexor posturing... 

Inflammation is the normal host response to infection or injury that mediates immune elimination of pathogens and tissue repair. Inflammatory processes include increased production of cytokines, chemokines, nitric oxide, and eicosanoids by the innate immune system in conjunction with altered leukocyte homing, all of which greatly impact acquired immunity. Aberrant inflammatory responses evoke both acute injury such... 

It is widely believed that vegetation growing in the humid eastern United States would be severely injured if oxidant concentrations reached the daily peak concentrations (0.20-0.40 ppm) commonly experienced in the less humid sections of California. An air pollution episode that occurred on July 27-30, 1970, in the Washington, D.C., area is indicative of what may happen. During this 4-day period, the peak oxidant concentrations ranged from 0.14 to 0.22 ppm and were accompanied by a low concentration of sulfur dioxide (0.04 ppm). Oxidant injury was observed on 31 tree, 15 shrub, and 18 herbaceous species in an area of 72 mi (about 187 km ). Increased emisskm of the precursors of photochemical-oxidant formation could result in repeated episodes of acute injury or even chronic injury to eastern vegetation. 

Petunia, tomato, romaine lettuce, others 0.015-0.02 4 Acute injury 457... 

Most direct toxins entering the alveoli primarily affect Type I cells and their associated capillary endothelial cells. After acute injury, the epithelium and/or underlying capillary endothelial cells may swell and disrupt, distort, or lose their connections with others, leaving large areas of basement membrane uncovered. This allows fluid to move into the alveolar lumen from capillaries, with subsequent pulmonary edema. 

The sequel to acute injury depends on the potency and concentration of the toxic agent and the duration of exposure. Potent gases produce a severe vascular reaction and alveolar flooding. The fluid prevents gaseous exchange, and death of the human or animal ensues. After acute mild nonlethal damage, excess fluid is removed and the resistant Type II cells proliferate and reline the alveoli. The cells subsequently differentiate into Type I cells. 

Noa, M., S. Mendoza, R. Mas, and N. Mendoza. Effect of D-003, a mixture of high molecular weight primary acids from sugar cane wax, on CL4C-in-duced liver acute injury in rats. Drugs Exp Clin Res 2002 28(5) 177-183. 

Acute injuries of the eyes, primarily from effects of blast and missiles, may occur from tear-gas weapons, such as pen guns. The lnmeulate effects of these Injuries include swelling and edema of the lids, with penetration of skin, conjunctiva, cornea, sclera, or globe by gunpowder and CN conjunctival ischemia and chemosls corneal edema, erosion, Inflammation, or ulceration and focal hemorrhage. 13,20... 

Morphine blocks the deep, aching perception of chronic pain, without interrupting the fast signals sent by an acute injury. As pain signals rise through the spinal cord to reach the brain, morphine interrupts them at a relay station within the core of the brain, called the thalamus. Morphine also blocks pain messages as they enter the spinal cord. 

Acute symptoms of injury from various pollutants in different horticultural and agronomic groups are visible on the affected plant. Symptom expressions produced include chlorosis, necrosis, abscission of plant parts, and effects on pigment systems. Major pollutants which produce these injuries include sulfur dioxide, peroxyacetyl nitrate (PAN), fluorides, chlorides, nitrogen dioxide, ozone, and particulate matter minor pollutants are ethylene, chlorine, ammonia, and hydrogen chloride. Symptoms of acute injury are often used to identify pollutant source and to estimate agricultural damage. 

Tisible symptoms of acute injury have been the principal means of identifying the effect of air pollutants on plants for well over a century. They have served as major factors in assessing the impact of man s activities on the total environment and have served as the basis for numerous estimates of economic damage to agricultural crops. Such estimates are admittedly crude because the total effect of air pollutants on growth and development is not indicated by symptoms of acute injury. Nevertheless, such evaluations are essential since adequate controls historically develop only after economic pollutant damage is well documented. 

Leaves with symptoms of acute injury usually drop prematurely. Abscission layer development may be stimulated by a rapid reaction of leaves to a high concentration of toxicant, resulting in heavy defoliation without detectable necrosis or chlorosis. Exposure to very high concentrations of nitrogen dioxide, chlorine, or hydrogen chloride may cause extensive defoliation within a few hours. Much lower concentrations may cause gradual development of typical symptoms of senescence, followed by premature dropping of affected leaves. 

Descriptions of acute injury produced by individual air pollutants are abundant in the literature (2, 3, 4, 5, 6, 7, 8, 9), and several review articles provide excellent summaries of these descriptions (6, 10, 11, 12, 13, 14). Color prints of symptom expressions considered to be typical for a particular toxicant have been included in several of the publications (5, 6, 9, 10, 11, 14). This paper is not an exhaustive review of the literature or a detailed description of all possible acute symptoms produced by the various pollutants. It is a synoptic report of acute pollutant injury on plants. 

Sulfur Dioxide. S02 injury on plants has received much attention, particularly during the past half century, and the toxic effects are well known. Symptoms of acute injury to specific crops have been described by investigators in several countries (2, 3, 4, 6, 7, 8, 15). Acute necrosis results from rapid absorption of S02. Once S02 enters the mesophyll tissue, it reacts with water to produce the sulfite ion which has strong phytotoxic properties. When lethal concentrations accumulate in the most susceptible areas of the leaf, a dark green, water-soaked discoloration develops. The affected area soon becomes flaccid, and upon drying becomes white to ivory on most plants. In some instances the dead tissue may turn red, brown, or almost black. 

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