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With normally aerated lung buy 20mg benicar with visa blood pressure under 50, ultrasonography is intensely reflected from the pleural surface buy cheap benicar 20 mg line hypertension patho, so that the air-filled lung is not visible as an identifiable structure benicar 10 mg with mastercard hypertension pamphlet. It is only when the interlobular septae or the alveolar compartment underlying the visceral pleura are diseased that they become visible to the examiner order 20 mg benicar mastercard pulse pressure compliance. This movement, seen as a shimmering mobile pleural line that moves in synchrony with the respiratory cycle, is called lung sliding (Chapter 11 Video 11. A related finding is lung pulse, whereby the pleural line moves with cardiophasic movement caused by transmitted cardiac pulsations (Chapter 11 Video 11. The identification of lung sliding or lung pulse excludes the presence of a pneumothorax at the site of transducer application with certainty [3]. When pleural air is interposed between the pleural surfaces, as that occurs with pneumothorax, the air acts as a barrier to ultrasound, so the movement of the underlying visceral pleura cannot be seen. As air within the pleural space usually distributes to the anterior thorax in the supine patient, the critically ill patient is ideally positioned to examine for pneumothorax. Multiple rib interspaces sites may be rapidly examined for sliding lung over both hemithoraces, so that the intensivist can promptly and confidently rule out a clinically significant pneumothorax with superior accuracy to chest radiography [3–5]. Although the presence of lung sliding rules out the presence of pneumothorax at the site being examined, the absence of lung sliding is not diagnostic of pneumothorax. Loss of lung sliding may occur in other processes that reduce the movement of the visceral pleura such as pleural symphysis from inflammatory, neoplastic, or therapeutic pleurodesis. In summary, the presence of lung sliding is a very useful sign, because it rules out the possibility of a pneumothorax being present. The absence of lung sliding is less useful, and always requires the clinician to consider whether there might be an alternative explanation for the lack of lung sliding. Lung Point When faced with the loss of lung sliding, identifying a lung point can confirm the presence of pneumothorax. The lung point represents the border of the pneumothorax, where the partially collapsed lung interfaces with the air-filled pneumothorax space. Some pneumothoraces are total, but most are partial with some remaining apposition of the visceral and parietal pleura at some point in the thorax, usually lateral or posterior depending on the size of the pneumothorax. A lung point is described as the intermittent respirophasic appearance of lung sliding from the edge of the screen (Chapter 11 Video 11. Although 100% specific for pneumothorax, lung point has only a 66% sensitivity for detection of pneumothorax [3]. The A line is a reverberation of the pleural line, caused by echoes which reflect off of the visceral pleura owing to the inability of ultrasound to penetrate aerated lung tissue. The reflected pulse returns to the probe face and is reflected off of its surface to be in turn reflected back from the pleural line. When this pulse returns to transducer, it is interpreted by the ultrasound machine as arising from an identical, but more distant tissue plane. This is known as a reverberation artifact and occurs when there is an air–tissue interface deep to the probe. When present without sliding lung, A lines represent either air between the visceral and parietal pleura (i. They move in synchrony with lung sliding (although mobility is not required, as in the case of B lines in the absence of lung sliding). B lines reflect the presence of a process that infiltrates or widens the interlobular septae of the lung, such as inflammation, neoplasm, or scarring; or that fills the alveolar space [6,7]. Depending on the disease process that is causing the B lines, they may be focal, scattered, or diffuse in distribution. More than two B lines in a single field are considered significant, with the exception that in normal individuals, several B lines may be present in the basilar-dependent rib interspaces. Z-lines are artifacts arising from the pleural line, but attenuate before the periphery and are not as discrete B lines. E Lines are vertical appearing artifacts that arise proximal to the pleural line from subcutaneous emphysema. Consolidation Consolidated lung yields a characteristic tissue density pattern on ultrasound examination (Chapter 11 Video 11. Consolidated lung has an echogenicity that is similar to liver (sonographic hepatization of the lung). If the bronchial structures that supply the affected consolidated lung are patent, the consolidated lung may have sonographic air bronchograms within it, appearing as small hyperechoic foci within the parenchyma. They may be mobile, reflecting movement of air within the bronchus owing to respiratory activity (Chapter 11 Video 11. All causes of airless lung, such as atelectasis (compressive, resorptive, or cicatricial), infiltrative processes (tumor, purulent material as in pneumonia), or severe pulmonary edema with complete filling of the alveolar compartment will yield the ultrasonographic finding of lung consolidation. When evaluating the patient with dyspnea and/or respiratory failure, the critical care clinician associates various profiles described below with the corresponding cause of respiratory failure compromise. This pattern rules out diseases that compromise the alveolar and/or interstitial compartment (pulmonary edema, pneumonia, fibrosis, etc. Identification of a normal aeration pattern of the dyspneic patient where pulmonary embolism is a concern requires the intensivist to perform a study for venous thromboembolism (see Chapter 92 on Venous Thromboembolism). A Lines, Absence of Lung Sliding, Presence of Lung Point When lung sliding is absent with A lines, pneumothorax is a possibility. If no lung point is identified, other methods are required to confirm if there is a pneumothorax, given the low sensitivity of lung point. The presence of lung pulse, B lines, or consolidation also rules out pneumothorax at the interspace being examined. Alveolar/Interstitial Disease: B Line Patterns Detection of profuse B lines at multiple symmetric points over the anterior chest indicates a high probability of an alveolar and/or interstitial process. For instance, when B lines are detected from subsegmental, segmental, lobar, or unilateral distribution, or involving one hemithorax with A line pattern for the rest of the lung, pneumonia is a prime consideration. It may appear as small multifocal areas of consolidation immediately below the pleural interface or in subsegmental, segmental, lobar, whole lung pattern with unifocal or multifocal distribution. The interface between the pleural surface and the consolidation is linear, whereas the interface between the consolidation and the adjacent aerated lung is irregular and often is associated with comet tail artifacts. Pneumonias often contain dynamic air bronchograms, which appear as mobile, branching, and hyperechoic within the parenchyma (Chapter 11 Video 11. Although suggestive of pneumonia, mobile air bronchograms may be found in association with non-pneumonia consolidation; a hypoechoic area with well-defined borders within an area of alveolar consolidation is consistent with necrosis or abscess (Chapter 11 Video 11. The mechanism of the atelectasis may differ (compressive, resorptive, or cicatricial), but there is a characteristic loss of lung volume in association with the alveolar consolidation. Mobile air bronchograms are uncommon, although static air bronchograms are often present, unless the cause for the atelectasis is complete endobronchial occlusion [11]. Compressive atelectasis from a pleural effusion causes the atelectatic lung to float within the effusion often in association with respirophasic or cardiophasic movement of the lung (Chapter 11 Video 11. The dual mechanism of compressive and resorptive atelectasis results in the airless lung that reinflates when the patient is successfully extubated. If the blockage is at the mainstem bronchial level, the affected lung undergoes major volume loss with associated marked ipsilateral shift of mediastinal and cardiac structures. This can occur rapidly if the patient is on a high FiO2 as is the case immediately following endotracheal intubation.

Enteral nutrition and resuscitation may begin on the day of injury with the caveat that patients in shock or requiring vasopressors can develop bowel ischemia and enteral feeds may increase the metabolic needs of the gut buy generic benicar 40 mg line blood pressure glucose levels, contributing to bowel ischemia and necrosis cheap benicar 40mg without a prescription ulterior motive. This risk can be minimized by initiating enteral rehydration and nutrition within 24 hours of the initial burn [18] buy 20mg benicar mastercard pulse pressure is quizlet. Patient’s not tolerating enteral feeds or those with abdominal hypertension (see Chapter 52) should be given total parenteral nutrition purchase benicar 20 mg free shipping blood pressure zoloft. Typically, by the third postburn day, the patient’s systemic inflammatory response has dampened and vascular integrity is returning, with decreased fluid requirements. After this point, it is reasonable to limit fluid replacement to maintenance levels and allow the patient to autodiurese or judiciously use diuretics in the elderly or cardiac- compromised patient [9]. Unfortunately, during the initial 4-to-24-hour postinjury period, even “adequate” volume repletion will not maintain baseline cardiac output, and decreased cardiac contractility and diastolic dysfunction prevail. This decrease in contractility is more pronounced among those with an inhalational injury and is related to both increased pulmonary vascular resistance and increased systemic nitric oxide production. This temporary and seemingly maladaptive cardiac dysfunction improves as time elapses from the initial injury and is followed by tachycardia, which is often maintained for weeks after burn [19,20]. Given this hyperdynamic response, the elderly and patients with preinjury cardiac compromise are more susceptible to heart failure in this period. Elevated troponins should not be used as an indication for emergent cardiac catheterization without other signs or symptoms of acute cardiac ischemia, such as electrocardiogram changes [19]. History of fire or explosion in a closed space and findings of singed facial structures, carbonaceous sputum, and respiratory distress often corroborate the diagnosis. Concurrent inhalational injury intensifies burn shock and may require up to 50% more fluid for adequate resuscitation. This component of the inhalational injury cascade appears to be driven by the sensory neuronal pathway, because the response can be truncated by sympathetic blockade in experimental animal models [21]. Clinically, in the acutely burned patient with an inhalational injury, airway management is paramount. The clinician should look for signs of upper airway obstruction secondary to edema, which often develops hours after initial injury. Stridorous patients should be intubated urgently; preferably with an 8-Fr endotracheal tube to allow for bronchoscopy and removal of respiratory tract secretions. Bronchoscopy is most useful to characterize the presence or absence of tracheobronchial inflammation and provide therapeutic pulmonary lavage [22]. Bronchial epithelium sloughs and combines with exudates and fibrin to form “plugs” that nurture bacterial growth and create mechanical airway obstructions. Aerosolized heparin in conjunction with N-acetyl-cysteine may prevent cast formation and has been shown to decrease lung injury scores and ventilator days and has been especially helpful for pediatric patients where narrow airways easily obstruct [24,25]. Although burn patients are at increased risk for pneumonia because of their immunocompromised state, immobility, and inability to clear secretions, prophylactic antibiotics are not recommended. Pneumonia and tracheobronchitis should be treated by culture-directed therapy, using Gram stain, culture of sputum, or bronchoscopy specimens and incorporate a hospital’s known bacterial sensitivities [26]. Patients’ overall condition and pulmonary performance by way of usual weaning parameters dictate extubation time [27]. The risk of upper airway obstruction before extubation should be assessed by deflating the balloon and audible appreciation of air leak. Protein catabolism, compounded by losses through the wound bed and the interstitium, results in severe hypoproteinemia, and the hypermetabolic response that occurs after a thermal injury is more than that observed after most other forms of trauma or sepsis. The loss of regulated vasomotor tone, possibly in an effort to provide maximal nutrient delivery and gas exchange to the wounded tissues, results in significant evaporative heat loss. Hypothermia from weeping wounds and dwindling energy supplies from the catabolic, muscle-wasting condition of burn shock is easily avoided with external warming. The ambient temperature in the patient’s room should be kept warm, 90°F to 100°F, in an effort to shunt calories away from being used in thermostasis. Muscle wasting, a difficult complication of the hypermetabolism associated with burn wounds, can be ameliorated through anabolic enhancement. The patient with a major thermal injury has a metabolism characterized by increased muscle proteolysis, lipolysis, and gluconeogenesis. Hyperglycemia is common with burn catabolism, may exacerbate muscle wasting, and should be tightly controlled with insulin. Nitrogen loss should also be supplemented to combat muscle wasting and to enhance the immune system [30]. Significant burn injuries require 2 g per kg protein, glucose should contribute 50% to 60% of the calories, and the calorie-to-nitrogen ratio should approach 150:1. All attempts should be made to feed the patient enterally, and, ideally, enteral nutrition should be initiated within 24 hours of admission. Prompt enteral feeding has been shown to decrease patient’s length of hospital stay as well as burn wound infection and is thought to maintain the integrity of the gastrointestinal track [14]. In addition to early enteral nutrition, supplementation with trace elements such as copper, zinc, and selenium is also important for helping decrease infectious complications [31]. However, primary treatment of infected burns remains surgical excision and tissue coverage with autograph or skin substitute (see “Early Excision and Grafting”). The signs of burn wound sepsis typically present as a greenish gray discoloration of the burn, purulent fluid from the wound, and eschar separation along with cellulitis in the surrounding unburned skin. Diagnosis can be confirmed by biopsy of the wound with quantitative culture but should not preclude total and urgent excision [32]. Systemic antibiotics are started if florid infection is suspected and tailored or stopped once burn biopsies for quantitative bacterial counts and blood culture results are obtained. The overall hypermetabolic state associated with severe burns can have significant effects on the pharmacokinetics and pharmacodynamics of many medications including anti-infectives. As one example, Mafenide acetate penetrates eschar and is most effective against Gram-negative organisms; however, Mafenide acetate is known to cause metabolic acidosis as a carbonic anhydrase inhibitor and may select for fungal overgrowth [26]. Immunity and Infection Significant burn injury that induces a systemic inflammatory response may also induce a compensatory anti-inflammatory response syndrome. As such, large surface area burn patients are at high risk for infection, which is often the precipitating cause of late deaths [33]. The pulmonary tree and the burn wound beds themselves are the most common sites and foci for fatal infection. Later, pseudomonas is a common and potentially lethal organism, although fungal infections may occur in the subacute period and are often ominous. A growing and considerable body of evidence links bacterial translocation from the gut as a source of unexplained bacteremia [26]. Once an area has been grafted with autologous tissue, shear forces must be minimized because the grafted skin initially lives by diffusion of nutrients from the underlying wound bed and imbibition until inosculation and neovascularization can take place. Using a combination of autografts on completely excised burns and xenografts on partial- thickness burns is also a means to facilitate timely healing.

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Urinary calcium excretion (normally 100 to 300 mg of calcium per day) depends on the glomerular filtration rate and the tubular sodium reabsorption generic benicar 40 mg mastercard high blood pressure medication toprol xl. Loop diuretics enhance urinary calcium excretion in conjunction with their effect on sodium excretion order 20 mg benicar fast delivery arteria hepatica propia. This results in bone resorption and dissolution of hydroxyapatite crystals resulting in the release of calcium and phosphate order benicar 10mg visa blood pressure chart 40 year old male. Clinically generic benicar 40mg online blood pressure medication starting with c, correction of the hypocalcemia can often only be achieved after correcting hypomagnesemia. Vitamin D Vitamin D is a steroid hormone that is essential for calcium balance and is also likely important in numerous other cellular functions [10]. Activation of vitamin D requires 25-hydroxylation in the liver and 1- hydroxylation in the kidney to form the active hormone 1,25 D. The effects of 1,25 D are exerted through interactions with nuclear receptors located in a variety of cells, including enterocytes, parathyroid chief cells, osteoblasts, and renal tubular cells. Medullary carcinoma of the thyroid is a malignant neoplasm of the C-cells and is characterized by elevated calcitonin levels. Also, patients can have undetectable levels of calcitonin after a thyroidectomy with no clear detrimental systemic effects. Despite the lack of clinical consequences from endogenous calcitonin excess or deficiency, exogenous calcitonin is a potent inhibitor of bone resorption. This phenomenon, possibly due to downregulation of calcitonin receptors, is of clinical importance when treating patients with hypercalcemia. The excellent short-term effects of calcitonin to lower serum calcium (within 12 to 48 hours) allows the institution of therapies that require several days to attain maximal effectiveness (e. The administration of a salmon calcitonin nasal spray has been shown to decrease markers of bone turnover, increase bone mineral density at the spine, and decrease the risk of vertebral fractures in postmenopausal women with osteoporosis [13]. The mental manifestations of hypercalcemia include stupor, obtundation, apathy, lethargy, confusion, disorientation, and coma. In general, for a given level of hypercalcemia, older patients exhibit more of the mental signs than younger patients. The neurologic and musculoskeletal effects of hypercalcemia are reduced muscle tone and strength, myalgias, and decreased deep tendon reflexes. Differential Diagnosis Elevated serum calcium measurements have been reported in approximately 1% of the general population [14]. The causes of hypercalcemia can be differentiated into two broad groups defined by whether or not the process is driven by abnormal parathyroid tissue. The malignancies most often associated with hypercalcemia include lung (35%), breast (25%), hematologic (myeloma and lymphoma [14%]), head and neck (6%), and renal (3%) [15]. Hypercalcemia occurs in 10% of patients, though hypercalciuria has been documented in as many as 20% [17]. Immobilization causes hypercalcemia as a result of decreased bone formation and persistent bone resorption. Hypercalcemia in the immobilized individual occurs most commonly among patients with high bone turnover (e. The routine measurement of serum calcium has altered the clinical presentation of hyperparathyroidism with most patients presenting with asymptomatic hypercalcemia. The latter occurs typically after chronic secondary hyperparathyroidism in the setting of end-stage renal failure. Hypercalcemia develops due to increased bone resorption, increased intestinal calcium absorption from stimulation of 1,25 D production, and increased renal tubular calcium reabsorption. In primary hyperparathyroidism, a single adenoma is present in 80% to 85% of cases, whereas four-gland hyperplasia occurs in 10% to 15% of cases [18]. Parathyroid cancer is present among less than 1% of these patients and typically presents with much higher serum calcium levels [19]. Hypercalcemia associated with the use of thiazide diuretics is often an indicator of underlying primary hyperparathyroidism. However, altered binding of calcium to proteins, as can occur with hypoalbuminemia or with abnormal proteins (e. Because of the interrelationships of calcium, magnesium, and phosphorus, the latter two minerals should be measured in all cases involving altered calcium metabolism. Because myeloma is characterized by bone resorption with little bone formation, the bone scan is usually negative, but a skeletal survey may find lytic lesions. The diagnosis would then be confirmed by urine immunoelectrophoresis, serum protein electrophoresis, and bone marrow examination. The diagnosis of milk-alkali syndrome is made by the patient’s history, often revealing large quantities of calcium carbonate ingestion. Thyrotoxicosis and Addison’s disease can be ruled out with thyroid function tests and a cosyntropin stimulation test, respectively (see Chapter 139 for a discussion about evaluating adrenal function in the critically ill). Vitamin D intoxication is quite rare, but the possibility can be eliminated by measuring 25-hydroxyvitamin D levels. General concepts in the management involve attempts to (a) increase renal calcium clearance, (b) decrease bone resorption, and (c) decrease intestinal calcium absorption. If, for example, the hypercalcemia in a patient with myeloma is due to a combination of increased bone resorption plus decreased renal calcium clearance, successful management of the hypercalcemia requires that both processes be treated. Saline hydration creates a diuresis that increases renal calcium excretion by decreasing calcium reabsorption in the proximal tubule. Hydration plays a critical role in the initial management of hypercalcemia because the onset of the therapeutic response is rapid. Because a potential complication of administration of this amount of saline is congestive heart failure, extreme care must be taken in treating the patient with underlying cardiac disease or renal insufficiency. The concomitant administration of a loop diuretic helps prevent volume overload and further increases renal calcium excretion by inhibiting distal tubular calcium reabsorption. Measurement of serum electrolytes, phosphorus, and magnesium is mandatory during saline hydration to replace adequately the quantities lost in the urine. If renal or cardiac failure precludes the use of saline hydration, dialysis with a calcium-free dialysate is an effective alternative. It also exerts transient effects to increase the renal excretion of calcium, along with sodium, potassium, magnesium, and phosphate. The benefits of calcitonin for the treatment of hypercalcemia include (a) rapid onset within 2 hours, (b) maximal effect within 24 to 48 hours, and (c) low toxicity [12]. It can be used safely in patients with renal failure, and its side effects are limited to transient nausea, facial flushing, and occasional hypersensitivity at the injection site. Usually calcitonin is effective for only 4 to 7 days [12], but it is still used for the rapid response, as bisphosphonates often require several days to attain maximal effectiveness. Bisphosphonates are synthetic analogues of pyrophosphate that are potent inhibitors of bone resorption through inhibition of osteoclastic activity and survival [16]. Because of the delay of reduction in serum calcium with bisphosphonates, these agents are often used in conjunction with other therapies. Zoledronic acid at a dose of 4 mg intravenously over not less than 15 minutes has been shown to be more effective at normalizing serum calcium in patients with hypercalcemia of malignancy [26].

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The central nervous system effects of H S toxicity may be exacerbated by2 hypoxemia secondary to severe pulmonary edema discount 20 mg benicar free shipping blood pressure low. In survivors discount 40 mg benicar amex pulse blood pressure chart, long- term neurologic sequelae purchase benicar 20mg overnight delivery arteria temporalis media, such as ataxia discount benicar 20mg with amex pulse pressure less than 10, intention tremor, sensorineural hearing loss, muscle spasticity, and memory impairment, have been reported [61]. Myocardial ischemia, arrhythmias, and dilated cardiomyopathy have all been reported after significant exposures [65,66]. As doses increase, loss of consciousness, cessation of brainstem function, and cardiopulmonary arrest will occur. Diagnosis and Management A high index of suspicion is the key to making the diagnosis of H S2 intoxication. Although blood levels of thiosulfate are helpful in confirming the diagnosis of H S poisoning [2 67], these tests are not readily available in most clinical laboratories. When available, atmospheric measures of H S concentration can be used to increase diagnostic2 suspicion and in classifying the expected the severity of exposure and intoxication. In the absence of specific exposure information, signs of ocular irritation, inflammation of mucosal membranes, and the smell of “rotten eggs” on the clothing or breath of a patient should suggest the diagnosis of H S intoxication. As a result, blood gas analyses typically show a PaO in the normal range and an2 elevated mixed venous oxygen tension (PvO ), typically in the range of 352 to 45 mm Hg. In addition, both methemoglobin and sulfhemoglobin are produced during the treatment of H S poisoning with sodium nitrite2 and amyl nitrite, as discussed later. A rapid decline2 in either PaO or SaO could indicate the development or progression of2 2 pulmonary edema. Serum lactate concentration is typically elevated as a result of the inhibition of aerobic metabolism. Sodium nitrite can be used as an antidote to generate methemoglobin by changing the normal ferrous state of iron in +2 +3 the heme molecule of hemoglobin (Fe ) to the ferric state (Fe ). The preferential binding of H S molecules to methemoglobin2 results in the formation of sulfhemoglobin that prevents circulating H S2 from entering cells and inhibiting cellular respiration. Basic supportive measures should not be forgotten and include irrigation of the eyes with sterile saline and the treatment of irritant-induced bronchospasm with inhaled β2-agonists. Consideration should be given to the administration of sodium bicarbonate for the treatment of severe metabolic acidosis in unconscious or hemodynamically unstable patients. If a benzodiazepine or barbiturate is given, patients should be carefully monitored for signs of respiratory insufficiency. The nature, location, and severity of respiratory tract injuries associated with the inhalation of an irritant gas depend on the physical and chemical properties of the gas, exposure dose, and host factors of exposed individuals. Exposure dose is determined by the concentration of the gas in the environment and the duration of exposure. Minute ventilation, age, and the presence of preexisting respiratory disease are the most important host factors (Table 178. Highly soluble gases, such as ammonia and sulfur dioxide, generally cause irritant damage to exposed mucous membranes, such as the eyes and upper airway (nose, lips, pharynx, and larynx), while sparing the lower airways. At high concentrations, however, a highly soluble irritant gas can overwhelm the upper respiratory tract, and significant amounts may reach the upper and lower airways, thereby producing both mucous membrane and airway injury. Irritant gases of intermediate solubility, such as chlorine, may produce significant upper airway injury, especially in the pharynx and larynx, but the mucous membrane irritation is usually not as intense as that caused by highly soluble gases. Because of its intermediate solubility, the irritant effects of chlorine will extend more distally at higher concentrations. Thus, high concentrations of inhaled chlorine can produce both upper and lower airway injuries, as well as pulmonary edema as a result of alveolar damage. The inhalation of low-solubility irritant gases, such as phosgene and oxides of nitrogen, typically produces minimal upper airway irritation but can cause intense lower airways and alveolar damage. As a result of lung tissue injury, the development of noncardiogenic pulmonary edema is more likely following inhalation of a low-solubility irritant gas or at high concentrations of gases with intermediate solubility. The inhalation of gases that are lipid soluble, but not water soluble, such as chloroform, ether, or other halogenated hydrocarbons, will produce central nervous system effects and little, if any, respiratory injury. Methylene chloride, found in paint remover and other solvents, is an exception to this rule in that high doses may cause pulmonary edema [71]. Direct cellular injury is commonly produced by irritant gases that possess either a highly acidic or a highly alkaline pH. Chlorine and phosgene, for example, produce hydrochloric acid when they come in contact with water in mucous membranes. Ammonia forms a strong alkali, ammonium hydroxide, when it comes in contact with water in mucous membranes and airways. Ammonium hydroxide causes liquefaction damage to cells and tissues on contact, with the severity of damage directly related to the hydroxyl ion concentration. Damage to respiratory tract cells and tissues can also be caused by irritant gases that generate the production of free radicals. Oxides of nitrogen, for example, cause the production of free radicals that cause cellular damage by lipid peroxidation. Both direct cell damage and cell damage secondary to free-radical formation result in the release of a variety of inflammatory mediators that elicit an inflammatory response, thereby causing further oxidant damage to respiratory tract cells. In the airways, the damage caused by irritant gases is manifested by mucosal edema, mucus production, increased smooth muscle contraction, and airway obstruction. At the alveolar level, damage of type 1 pneumocytes occurs followed by capillary leakage caused by epithelial cell damage, disruption of epithelial cell tight junctions, endothelial damage, and increased vascular permeability. Few individuals can tolerate a concentration greater than 100 ppm without experiencing nasal stuffiness and irritating cough. The voice is lost shortly after exposure, and patients typically experience sensations of choking and suffocation. Airway obstruction as a result of laryngeal edema, bronchial inflammation, bronchoconstriction, and plugs of sloughed epithelium may cause dyspnea, wheezing, and hypoxemia [74]. With exposure to high concentrations, alveolar damage and pulmonary edema can occur within 24 hours [74]. Industrial uses of Cl include the production of2 chemicals and bleaches, paper manufacturing, textile processing, and the production of polyvinyl chloride. Most Cl exposures result from2 accidental releases at industrial sites, from ruptured tanks during its transportation, or at swimming pools [76–78]. The relatively high density of Cl causes it to accumulate in low-lying areas, which should be avoided2 following its accidental release. Individuals exposed to low concentrations of Cl typically experience2 burning of the eyes and mucous membranes, as well as choking and coughing as a result of inflammation of the nasal–oral pharynx and upper airway. At higher concentrations, laryngeal edema, lower airway inflammation, bronchoconstriction, and pulmonary edema can develop. Although the majority presented with wheezing or rales, 17% and 11%, respectively, developed these symptoms later over the next 24 hours [2].

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