Critical states in surgical patients: acute respiratory distress syndrome, abdominal cavity syndrome, collapse.
Acute respiratory distress syndrome (ARDS), also known as respiratory distress syndrome (RDS) or adult respiratory distress syndrome (in contrast with IRDS) is a serious reaction to various forms of injuries to the lung.
ARDS is a severe lung disease caused by a variety of direct and indirect issues. It is characterized by inflammation of the lung parenchyma leading to impaired gas exchange with concomitant systemic release of inflammatory mediators causing inflammation, hypoxemia and frequently resulting in multiple organ failure. This condition is often fatal, usually requiring mechanical ventilation and admission to an intensive care unit. A less severe form is called acute lung injury (ALI).
ACUTE RESPIRATORY DISTRESS SYNDROME
Historical Perspective and Definitions
The first description of acute respiratory distress syndrome appeared in 1967, when Ashbaugh and colleagues described 12 patients with acute respiratory distress, cyanosis refractory to oxygen therapy, decreased lung compliance, and diffuse infiltrates evident on the chest radiograph. Initially called the adult respiratory distress syndrome, this entity is now termed the acute respiratory distress syndrome, since it does occur in children. Because the initial definition lacks specific criteria that could be used to identify patients systematically, there was controversy over the incidence and natural history of the syndrome and the mortality associated with it. In 1988, an expanded definition was proposed that quantified the physiologic respiratory impairment through the use of a four-point lung-injury scoring system that was based on the level of positive end-expiratory pressure, the ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen, the static lung compliance, and the degree of infiltration evident on chest radiographs. Other factors included in the assessment were the inciting clinical disorder and the presence or absence of nonpulmonary organ dysfunction
Although the lung-injury scoring system has been widely used to quantify the severity of lung injury in both clinical research and clinical trials, it cannot be used to predict the outcome during the first 24 to 72 hours after the onset of the acute respiratory distress syndrome and thus has limited clinical usefulness. When the scoring system is used four to seven days after the onset of the syndrome, scores of 2.5 or higher may be predictive of a complicated course with the need for prolonged mechanical ventilation.
In
Epidemiology
Incidence
An accurate estimation of the incidence of acute lung injury and the acute respiratory distress syndrome has been hindered by the lack of a uniform definition and the heterogeneity of the causes and clinical manifestations. An early estimate by the National Institutes of Health (NIH) suggested that the annual incidence in the
ARDS Causes
•Direct Lung Injury:
a) PNA and aspiration of gastric contents
or other causes of chemical pneumonitis
b) pulmonary contusion, penetrating lung injury
c) fat emboli
d) near drowning
e) inhalation injury
f) reperfusion pulm edema after lung transplant
•Indirect lung injury
a) sepsis
b) severe trauma w/ shock hypoperfusion
c) drug over dose
d) cardiopulmonary bypass
e) acute pancreatitis
f) transfusion of multp blood products
ARDS was defined as the ratio of arterial partial oxygen tension (PaO2) as fraction of inspired oxygen (FiO2) below 200 mmHg in the presence of bilateral alveolar infiltrates on the chest x-ray. These infiltrates may appear similar to those of left ventricular failure, but the cardiac silhouette appears normal in ARDS. Also, the pulmonary capillary wedge pressure is normal (less than 18 mmHg) in ARDS, but raised in left ventricular failure.
A PaO2/FiO2 ratio less than 300 mmHg with bilateral infiltrates indicates acute lung injury (ALI). Although formally considered different from ARDS, ALI is usually just a precursor to ARDS. (Consensus after 1967 and 1994)
ARDS is characterized by
Acute onset
Bilateral infiltrates on chest radiograph sparing costophrenic angles
Pulmonary artery wedge pressure < 18 mmHg (obtained by pulmonary artery catheterization), if this information is available; if unavailable, then lack of clinical evidence of left ventricular failure suffices:
if PaO2:FiO2 < 300 mmHg (40 kPa) acute lung injury (ALI) is considered to be present
if PaO2:FiO2 < 200 mmHg (26.7 kPa) acute respiratory distress syndrome (ARDS) is considered to be present
To summarize and simplify, ARDS is an acute (rapid onset) syndrome (collection of symptoms) that affects the lungs widely and results in a severe oxygenation defect, but is not heart failure.
ARDS Symptoms
- Severe difficulty in breathing
- Agitation
Clinical, Pathological, and Radiographic Features
The definitions discussed above identify patients early in the course of acute lung injury and the acute respiratory distress syndrome. However, the syndrome is often progressive, characterized by distinct stages with different clinical, histopathological, and radiographic manifestations. The acute, or exudative, phase is manifested by the rapid onset of respiratory failure in a patient with a risk factor for the condition. Arterial hypoxemia that is refractory to treatment with supplemental oxygen is a characteristic feature.
An arterial blood gas analysis and chest X-ray allow formal diagnosis by the aforementioned criteria. Although severe hypoxemia is generally included, the appropriate threshold defining abnormal PaO2 has never been systematically studied. Note though, that a severe oxygenation defect is not synonymous with ventilatory support. Any PaO2 below 100 (generally saturation less than 100%) on a supplemental oxygen fraction of 50% meets criteria for ARDS. This can easily be achieved by high flow oxygen supplementation without ventilatory support.
Any cardiogenic cause of pulmonary edema should be excluded. This can be done by placing a pulmonary artery catheter for measuring the pulmonary artery wedge pressure. However, this is not necessary and is now rarely done as abundant evidence has emerged demonstrating that the use of pulmonary artery catheters does not lead to improved patient outcomes in critical illness including ARDS.
Plain Chest X-rays are sufficient to document bilateral alveolar infiltrates in the majority of cases. While CT scanning leads to more accurate images of the pulmonary parenchyma in ARDS, it has little utility in the clinical management of patients with ARDS, and remains largely a research tool.
Radiographically, the findings are indistinguishable from those of cardiogenic pulmonary edema. Bilateral infiltrates may be patchy or asymmetric and may include pleural effusions. Computed tomographic scanning has demonstrated that alveolar filling, consolidation, and atelectasis occur predominantly in dependent lung zones, whereas other areas may be relatively spared. However, bronchoalveolar-lavage studies indicate that even radiographically spared, nondependent areas may have substantial inflammation. Pathological findings include diffuse alveolar damage, with neutrophils, macrophages, erythrocytes, hyaline membranes, and protein-rich edema fluid in the alveolar spaces, capillary injury, and disruption of the alveolar epithelium.
Although acute lung injury and the acute respiratory distress syndrome may resolve completely in some patients after the acute phase, in others it progresses to fibrosing alveolitis with persistent hypoxemia, increased alveolar dead space, and a further decrease in pulmonary compliance. Pulmonary hypertension, owing to obliteration of the pulmonary-capillary bed, may be severe and may lead to right ventricular failure. Chest radiographs show linear opacities, consistent with the presence of evolving fibrosis. Pneumothorax may occur, but the incidence is only 10 to 13 percent and is not clearly related to airway pressures or the level of positive end-expiratory pressure. Computed tomography of the chest shows diffuse interstitial opacities and bullae. Histologically, there is fibrosis along with acute and chronic inflammatory cells and partial resolution of the pulmonary edema
The recovery phase is characterized by the gradual resolution of hypoxemia and improved lung compliance. Typically, the radiographic abnormalities resolve completely. The degree of histologic resolution of fibrosis has not been well characterized, although in many patients pulmonary function returns to normal.
Clinical Disorders and Risk Factors
The ability to identify patients at risk for acute lung injury and the acute respiratory distress syndrome is important if therapies are to be developed to prevent the disorder. The commonly associated clinical disorders can be divided into those associated with direct injury to the lung and those that cause indirect lung injury in the setting of a systemic process.
Overall, sepsis is associated with the highest risk of progression to acute lung injury or the acute respiratory distress syndrome, approximately 40 percent. The presence of multiple predisposing disorders substantially increases the risk, as does the presence of secondary factors including chronic alcohol abuse, chronic lung disease, and a low serum pH.
Outcomes
Until recently, most studies of acute lung injury and the acute respiratory distress syndrome have reported a mortality rate of 40 to 60 percent. The majority of deaths are attributable to sepsis or multiorgan dysfunction rather than primary respiratory causes, although the recent therapeutic success of ventilation with low tidal volumes indicates that in some cases death is directly related to lung injury. Two reports suggest that mortality from this disease may be decreasing. The first, from a large county hospital in
Factors whose presence can be used to predict the risk of death at the time of diagnosis of acute lung injury and the acute respiratory distress syndrome include chronic liver disease, nonpulmonary organ dysfunction, sepsis, and advanced age. Surprisingly, initial indexes of oxygenation and ventilation, including the ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen and the lung-injury score, do not predict outcome. In three large studies, the mortality rate among patients with an initial ratio of partial pressure of arterial oxygen to fraction of inspired oxygen of 300 or less was similar to that among patients with a ratio of 200 or less. However, the failure of pulmonary function to improve during the first week of treatment is a negative prognostic factor.
In most patients who survive, pulmonary function returns nearly to normal within 6 to 12 months, despite the severe injury to the lung. Residual impairment of pulmonary mechanics may include mild restriction, obstruction, impairment of the diffusing capacity for carbon monoxide, or gas-exchange abnormalities with exercise, but these abnormalities are usually asymptomatic. Severe disease and prolonged mechanical ventilation identify patients at highest risk for persistent abnormalities of pulmonary function. Those who survive the illness have a reduced health-related quality of life as well as pulmonary-disease–specific health-related quality of life.
Pathogenesis
Stages of ARDS
1. Exudative (acute) phase – 0- 4 days
2. Proliferative phase – 4- 8 days
3. Fibrotic phase – >8 days
4. Recovery
Endothelial and Epithelial Injury
Two separate barriers form the alveolar–capillary barrier, the microvascular endothelium and the alveolar epithelium. The acute phase of acute lung injury and the acute respiratory distress syndrome is characterized by the influx of protein-rich edema fluid into the air spaces as a consequence of increased permeability of the alveolar–capillary barrier. The importance of endothelial injury and increased vascular permeability to the formation of pulmonary edema in this disorder has been well established.
The critical importance of epithelial injury to both the development of and recovery from the disorder has become better recognized. The degree of alveolar epithelial injury is an important predictor of the outcome. The normal alveolar epithelium is composed of two types of cells. Flat type I cells make up 90 percent of the alveolar surface area and are easily injured. Cuboidal type II cells make up the remaining 10 percent of the alveolar surface area and are more resistant to injury; their functions include surfactant production, ion transport, and proliferation and differentiation to type I cells after injury.
The loss of epithelial integrity in acute lung injury and the acute respiratory distress syndrome has a number of consequences. First, under normal conditions, the epithelial barrier is much less permeable than the endothelial barrier. Thus, epithelial injury can contribute to alveolar flooding. Second, the loss of epithelial integrity and injury to type II cells disrupt normal epithelial fluid transport, impairing the removal of edema fluid from the alveolar space. Third, injury to type II cells reduces the production and turnover of surfactant, contributing to the characteristic surfactant abnormalities. Fourth, loss of the epithelial barrier can lead to septic shock in patients with bacterial pneumonia. Finally, if injury to the alveolar epithelium is severe, disorganized or insufficient epithelial repair may lead to fibrosis.
Neutrophil-Dependent Lung Injury
Clinical and experimental studies have provided circumstantial evidence of the occurrence of neutrophil-mediated injury in acute lung injury and the acute respiratory distress syndrome. Histologic studies of lung specimens obtained early in the course of the disorder show a marked accumulation of neutrophils. Neutrophils predominate in the pulmonary edema fluid and bronchoalveolar-lavage fluid obtained from affected patients, and many animal models of acute lung injury are neutrophil-dependent. Some of the mechanisms of the sequestration and activation of neutrophils and of neutrophil-mediated lung injury are summarized in.
New evidence raises the question of whether neutrophilic inflammation is the cause or the result of lung injury. Acute lung injury and the acute respiratory distress syndrome may develop in patients with profound neutropenia, and some animal models of acute lung injury are neutrophil-independent. In clinical trials in which patients with severe pneumonia received granulocyte colony-stimulating factor in order to increase the number of circulating neutrophils, the incidence or severity of lung injury did not increase. The neutrophil has a critical role in host defense in this disorder, a factor that may explain, in part, why antiinflammatory strategies have largely been unsuccessful.
Other Proinflammatory Mechanisms
Inflammation
Inflammation alone, as in sepsis, causes endothelial dysfunction, fluid extravasation from the capillaries and impaired drainage of fluid from the lungs. Dysfunction of type II pulmonary epithelial cells may also be present, with a concomitant reduction in surfactant production. Elevated inspired oxygen concentration often becomes necessary at this stage, and they may facilitate a ‘respiratory burst’ in immune cells.
In a secondary phase, endothelial dysfunction causes cells and inflammatory exudate to enter the alveoli. This pulmonary edema increases the thickness of the alveolo-capillary space, increasing the distance the oxygen must diffuse to reach blood. This impairs gas exchange leading to hypoxia, increases the work of breathing, eventually induces fibrosis of the airspace.
Moreover, edema and decreased surfactant production by type II pneumocytes may cause whole alveoli to collapse, or to completely flood. This loss of aeration contributes further to the right-to-left shunt in ARDS. As the alveoli contain progressively less gas, more blood flows through them without being oxygenated resulting in massive intrapulmonary shunting.
Collapsed alveoli (and small bronchi) do not allow gas exchange. It is not uncommon to see patients with a PaO2 of 60 mmHg (8.0 kPa) despite mechanical ventilation with 100% inspired oxygen.
The loss of aeration may follow different patterns according to the nature of the underlying disease, and other factors. In pneumonia-induced ARDS, for example, large, more commonly causes relatively compact areas of alveolar infiltrates. These are usually distributed to the lower lobes, in their posterior segments, and they roughly correspond to the initial infected area.
In sepsis or trauma-induced ARDS, infiltrates are usually more patchy and diffuse. The posterior and basal segments are always more affected, but the distribution is even less homogeneous.
Loss of aeration also causes important changes in lung mechanical properties. These alterations are fundamental in the process of inflammation amplification and progression to ARDS in mechanically ventilated patients.
Cytokines
A complex network of cytokines and other proinflammatory compounds initiate and amplify the inflammatory response in acute lung injury and the acute respiratory distress syndrome. Proinflammatory cytokines may be produced locally in the lung by inflammatory cells, lung epithelial cells, or fibroblasts. The regulation of cytokine production by extrapulmonary factors has also been described. Macrophage inhibitory factor is a regulatory cytokine produced by the anterior pituitary that is found in high concentrations in the bronchoalveolar-lavage fluid of patients with the syndrome. This cytokine increases production of the proinflammatory cytokines interleukin-8 and tumor necrosis factor α and can override glucocorticoid-mediated inhibition of cytokine secretion.
New evidence indicates that it is not only the production of proinflammatory cytokines that is important, but also the balance between proinflammatory and antiinflammatory mediators. Several endogenous inhibitors of proinflammatory cytokines have been described, including interleukin-1–receptor antagonist, soluble tumor necrosis factor receptor, autoantibodies against interleukin-8, and antiinflammatory cytokines such as interleukin-10 and 11. Better understanding of the role of cytokines in acute lung injury and the acute respiratory distress syndrome will be gained through studies of the biologic activity of specific cytokines, rather than by an assessment of static levels by immunologic methods.
Ventilator-Induced Lung Injury
Mechanical ventilation is an essential part of the treatment of ARDS. As loss of aeration (and the underlying disease) progress, the work of breathing (WOB) eventually grows to a level incompatible with life. Thus, mechanical ventilation is initiated to relieve respiratory muscles of their work, and to protect the usually obtunded patient’s airways.
Older studies focused on the potential toxic effects of high fractions of inspired oxygen, but experimental evidence indicates that mechanical ventilation at high volumes and pressures can injure the lung, causing increased permeability pulmonary edema in the uninjured lung and enhanced edema in the injured lung. Initial theories formulated to explain these deleterious effects focused on capillary stress failure due to alveolar overdistention. More recently, cyclic opening and closing of atelectatic alveoli during mechanical ventilation have been shown to cause lung injury independently of alveolar overdistention. Alveolar overdistention coupled with the repeated collapse and reopening of alveoli can initiate a cascade of proinflammatory cytokines.
However, mechanical ventilation may constitute a risk factor for the development, or the worsening, of ARDS.
Aside from the infectious complications arising from invasive ventilation with tracheal intubation, positive-pressure ventilation directly alters lung mechanics during ARDS. The result is higher mortality, i.e. through baro-trauma, when these techniques are used.
In 1998, Amato et al. published a paper showing substantial improvement in the outcome of patients ventilated with lower tidal volumes (Vt) (6 mL·kg-1).This result was confirmed in a 2000 study sponsored by the NIH.Although both these studies were widely criticized for several reasons, and although the authors were not the first to experiment lower-volume ventilation, they shed new light on the relationship between mechanical ventilation and ARDS.
One opinion is that the forces applied to the lung by the ventilator may work as a lever to induce further damage to lung parenchyma. It appears that shear stress at the interface between collapsed and aerated units may result in the breakdown of aerated units, which inflate asymmetrically due to the ‘stickiness’ of surrounding flooded alveoli. The fewer such interfaces around an alveolus, the lesser the stress.
Indeed, even relatively low stress forces may induce signal transduction systems at the cellular level, thus inducing the release of inflammatory mediators.
This form of stress is thought to be applied by the transpulmonary pressure (gradient) (Pl) generated by the ventilator or, better, its cyclical variations. The better outcome obtained in patients ventilated with lower Vt may be interpreted as a beneficial effect of the lower Pl. Transpulmonary pressure, is an indirect function of the Vt setting on the ventilator, and only trial patients with plateau pressures (a surrogate for the actual Pl) were less than 32 cmH2O (3.1 kPa) had improved survival.
The way Pl is applied on alveolar surface determines the shear stress to which lung units are exposed. ARDS is characterized by a usually inhomogeneous reduction of the airspace, and thus by a tendency towards higher Pl at the same Vt, and towards higher stress on less diseased units.
The inhomogeneity of alveoli at different stages of disease is further increased by the gravitational gradient to which they are exposed, and the different perfusion pressures at which blood flows through them. Finally, abdominal pressure exerts an additional pressure on inferoposterior lung segments, favoring compression and collapse of those units.
The different mechanical properties of alveoli in ARDS may be interpreted as having varying time constants (the product of alveolar compliance × resistance). A long time constant indicates an alveolus which opens slowly during tidal inflation, as a consequence of contrasting pressure around it, or altered water-air interface inside it (loss of surfactant, flooding).
Slow alveoli are said to be ‘kept open’ using positive end-expiratory pressure, a feature of modern ventilators which maintains a positive airway pressure throughout the whole respiratory cycle. A higher mean pressure cycle-wide slows the collapse of diseased units, but it has to be weighed against the corresponding elevation in Pl/plateau pressure. Newer ventilatory approaches attempt to maximize mean airway pressure for its ability to ‘recruit’ collapsed lung units while minimizing the shear stress caused by frequent openings and closings of aerated units.
The prone position also reduces the inhomogeneity in alveolar time constants induced by gravity and edema. If clinically appropriate, mobilization of the ventilated patient can assist in achieving the same goal.
In patients with acute lung injury and the acute respiratory distress syndrome, ventilation at traditional tidal volumes (10 to 15 ml per kilogram of predicted body weight) may overdistend uninjured alveoli, perhaps promoting further lung injury, inhibiting resolution of the disorder, and contributing to multiorgan failure. The failure of traditional ventilatory strategies to prevent end-expiratory closure of atelectatic alveoli may also contribute to lung injury. These issues have led to a number of clinical trials of protective ventilatory strategies to reduce alveolar overdistention and increase the recruitment of atelectatic alveoli. Interestingly, a recent study found that a strategy of protective ventilation could reduce both the pulmonary and the systemic cytokine response.
Other Mechanisms of Injury
Like any form of inflammation, acute lung injury and the acute respiratory distress syndrome represent a complex process in which multiple pathways can propagate or inhibit lung injury. For example, abnormalities of the coagulation system often develop, leading to platelet–fibrin thrombi in small vessels and impaired fibrinolysis within the distal air spaces of the injured lung. Also, abnormalities in the production, composition, and function of surfactant probably contribute to alveolar collapse and gas-exchange abnormalities.
Fibrosing Alveolitis
After the acute phase of acute lung injury and the acute respiratory distress syndrome, some patients have an uncomplicated course and rapid resolution of the disorder. Others have progression to fibrotic lung injury, and such injury can be observed histologically as early as five to seven days after the onset of the disorder. The alveolar space becomes filled with mesenchymal cells and their products, along with new blood vessels. The finding of fibrosing alveolitis on histologic analysis correlates with an increased risk of death, and patients who die of the condition have a marked accumulation of collagen and fibronectin in the lung at autopsy.
The process of fibrosing alveolitis apparently begins early in the course of the disorder and may be promoted by early proinflammatory mediators such as interleukin-1. Levels of procollagen III peptide, a precursor of collagen synthesis, are elevated in the alveolar compartment very early in the course of the illness, even at the time of intubation and the initiation of mechanical ventilation. Furthermore, the early appearance of procollagen III in the alveolar space is associated with an increased risk of death.
Resolution
Strategies that hasten the resolution of the illness may ultimately be as important as those that attenuate early inflammatory lung injury. Alveolar edema is resolved by the active transport of sodium and perhaps chloride from the distal air spaces into the lung interstitium. Water follows passively, probably through transcellular water channels, the aquaporins, located primarily on type I cells. In clinical studies, clearance of alveolar fluid can occur surprisingly early and is often apparent within the first few hours after intubation and the initiation of mechanical ventilation. Maintenance of the ability to remove alveolar fluid is associated with improved oxygenation, a shorter duration of mechanical ventilation, and an increased likelihood of survival.
A considerable quantity of both soluble and insoluble protein must also be removed from the air spaces. The removal of insoluble protein is particularly important, since hyaline membranes provide a framework for the growth of fibrous tissue. Soluble protein appears to be removed primarily by diffusion between alveolar epithelial cells. Insoluble protein may be removed by endocytosis and transcytosis by alveolar epithelial cells and by phagocytosis by macrophages
The alveolar epithelial type II cell is the progenitor for reepithelialization of a denuded alveolar epithelium. Type II cells proliferate to cover the denuded basement membrane and then differentiate into type I cells, restoring the normal alveolar architecture and increasing the fluid-transport capacity of the alveolar epithelium. This proliferation is controlled by epithelial growth factors, including keratinocyte and hepatocyte growth factors.
The mechanisms underlying the resolution of the inflammatory-cell infiltrate and fibrosis are unclear. Apoptosis (programmed cell death) is thought to be a major mechanism for the clearance of neutrophils from sites of inflammation and may be important in the clearance of neutrophils from the injured lung. However, in one study of bronchoalveolar-lavage fluid from patients with acute lung injury and the acute respiratory distress syndrome, the numbers of apoptotic neutrophils were low, perhaps because of the presence of antiapoptotic factors such as granulocyte colony-stimulating factor and granulocyte–macrophage colony-stimulating factor. Nevertheless, high concentrations of the markers of apoptosis are present in the pulmonary edema fluid of patients, and exposure in vitro to bronchoalveolar-lavage fluids from these patients can promote epithelial-cell apoptosis. These are potentially important observations, since the mechanisms that alter epithelial integrity need to be identified. The role of proapoptotic and antiapoptotic mechanisms in both the injury and repair of the alveolar epithelium and the lung endothelium is an important area for future research.
Exams and Tests for ARDS
- Arterial blood gas analysis reveals hypoxemia (reduced levels of oxygen in the blood).
- A complete blood count may be taken. The number of white blood cells is increased in sepsis.
- Chest x-ray will show the presence of fluid in the lungs.
- CT scan of the chest may be required only in some situations (routine chest x-ray is sufficient in most cases).
- Echocardiogram (an ultrasound of the heart) may help exclude any heart problems that can cause fluid build-up in the lung.
- Monitoring with a pulmonary artery catheter may be done to exclude a cardiac cause for the difficulty in breathing.
- Bronchoscopy (a procedure used to look inside the windpipe and large airways of the lung) may be considered to evaluate the possibility of lung infection.
Treatment
Approach to Treatment
Improvement in the supportive care of patients with acute lung injury and the acute respiratory distress syndrome may have contributed to the recent decline in the mortality rate. There should be a careful search for the underlying cause, with particular attention paid to the possibility of treatable infections such as sepsis or pneumonia. Abdominal infections should be treated promptly with antimicrobial agents or surgery. Prevention or early treatment of nosocomial infections is critical, since patients frequently die of uncontrolled infection. Adequate nutrition through the use of enteral feeding is preferred to parenteral nutrition since this route does not carry the serious risk of catheter-induced sepsis. Prevention of gastrointestinal bleeding and thromboembolism is also important.
An improved understanding of the pathogenesis of acute lung injury and the acute respiratory distress syndrome has led to the assessment of several novel treatment strategies. Although many specific therapies have not proved beneficial, it is encouraging that the quality of clinical trials is improving. An important advance has been the establishment of a network supported by the NIH that includes 10 centers, 24 hospitals, and 75 intensive care units and that provides the infrastructure for well-designed, multicenter, randomized trials of potential new therapies.
General
Acute respiratory distress syndrome is usually treated with mechanical ventilation in the Intensive Care Unit. Ventilation is usually delivered through oro-tracheal intubation, or tracheostomy whenever prolonged ventilation (≥2 weeks) is deemed inevitable.
The possibilities of non-invasive ventilation are limited to the very early period of the disease or, better, to prevention in individuals at risk for the development of the disease (atypical pneumonias, pulmonary contusion, major surgery patients).
Treatment of the underlying cause is imperative, as it tends to maintain the ARDS picture.
Appropriate antibiotic therapy must be administered as soon as microbiological culture results are available. Empirical therapy may be appropriate if local microbiological surveillance is efficient. More than 60% ARDS patients experience a (nosocomial) pulmonary infection either before or after the onset of lung injury.
The origin of infection, when surgically treatable, must be operated on. When sepsis is diagnosed, appropriate local protocols should be enacted.
Commonly used supportive therapy includes particular techniques of mechanical ventilation and pharmacological agents whose effectiveness with respect to the outcome has not yet been proven. It is now debated whether mechanical ventilation is to be considered mere supportive therapy or actual treatment, since it may substantially affect survival.
Mechanical Ventilation
The most appropriate method of mechanical ventilation in the acute respiratory distress syndrome has been controversial since the syndrome was first described. Although the tidal volume iormal persons at rest is 6 to 7 ml per kilogram, historically a volume of 12 to 15 ml per kilogram was recommended in patients with acute lung injury and the acute respiratory distress syndrome. This comparatively high tidal volume may cause further lung injury. Interestingly, the possibility of ventilator-associated lung injury was first considered in the 1970s, leading to a study of extracorporeal membrane oxygenation in which the tidal volume was reduced to 8 to 9 ml per kilogram. However, this strategy, like extracorporeal removal of carbon dioxide in a subsequent study, failed to decrease mortality.
As described in this issue of the Journal, the NIH Acute Respiratory Distress Syndrome Network compared a traditional tidal volume (12 ml per kilogram of predicted body weight) with a lower tidal volume (6 ml per kilogram of predicted body weight) in 861 patients. In the group receiving lower tidal volumes, plateau pressure (airway pressure measured after a 0.5-second pause at the end of inspiration) could not exceed
The positive results of this trial differed from those of two previous studies of low tidal volumes, a Canadian study of 120 patients and a European study of 116 patients. There are several possible explanations for the discrepant results. First, the NIH study had the lowest tidal volume when the tidal volumes were compared with the use of the same calculation of ideal body weight. Thus, the NIH study may have been better able to show a difference between the treatment groups. Second, the study treated respiratory acidosis associated with alveolar hypoventilation and hypercapnia by allowing the respiratory rate to increase to 35 breaths per minute and by the administration of sodium bicarbonate. Conceivably, respiratory acidosis could have had deleterious effects in the groups treated with low tidal volumes in the other two studies. Finally, the other studies had many fewer patients, thus reducing the statistical power to find a treatment effect.
APRV (Airway Pressure Release Ventilation) and ARDS / ALI
No particular ventilator mode is known to improve mortality in ARDS. The landmark ARDSNet trial used a volume controlled mode and showed decrease mortality with smaller volumes. However, other modes of ventilation have not been directly compared to volume controlled ventilation.
Some practitioners favor airway pressure release ventilation (APRV). Advantages to APRV ventilation include: decreased airway pressures, decreased minute ventilation, decreased dead-space ventilation, promotion of spontaneous breathing, almost 24 hour a day alveolar recruitment, decreased use of sedation, near elimination of neuromuscular blockade, optimized arterial blood gas results, mechanical restoration of FRC (functional residual capacity), a positive effect on cardiac output (due to the negative inflection from the elevated baseline with each spontaneous breath), increased organ and tissue perfusion, potential for increased urine output secondary to increased renal perfusion.
A patient with ARDS on average spends 8 to 11 days on a mechanical ventilator; APRV may reduce this time significantly and conserve valuable resources.
A study is needed to evaluate whether APRV will reduce patient mortality when compared to the ARDSNet protocol. However, there seems to be little political will, within the medical community, to address the need for this study, in spite of the clinical successes seen with APRV.
Positive end-expiratory pressure
There has also been considerable interest in the optimal level of positive end-expiratory pressure in patients with acute lung injury and the acute respiratory distress syndrome. It was noted early on that the use of positive end-expiratory pressure could improve oxygenation in these patients, allowing the fraction of inspired oxygen to be reduced. The best-documented effect of positive end-expiratory pressure on lung function is an increase in functional residual capacity, probably as a result of the recruitment of collapsed alveoli. Although lung injury was prevented in rats by the prophylactic use of positive end-expiratory pressure, the prophylactic use of a positive end-expiratory pressure of
Recently, Amato et al. used an “open-lung” approach to mechanical ventilation in patients with acute lung injury and the acute respiratory distress syndrome. In addition to a low tidal volume and pressure-controlled inverse-ratio ventilation, the protocol included raising the level of positive end-expiratory pressure above the lower inflection point on a pressure–volume curve for each patient in an attempt to ensure adequate recruitment of atelectatic lung. With this approach, mortality was reduced. However, the adoption of this approach cannot yet be recommended for several reasons. First, this study was small, involving only 53 patients and only a single center. Second, mortality in the group treated with conventional ventilation was unusually high (71 percent), suggesting that the high tidal volume used may have been especially injurious. Furthermore, the difference in mortality between the two groups was only apparent at 28 days; the rates of survival until hospital discharge were not significantly different between the two groups. Third, a reliable measurement of the lower inflection point of the pressure–volume curve is technically difficult and usually requires sedation and paralysis of the patient.
Positive end-expiratory pressure (PEEP) is used in mechanically-ventilated patients with ARDS to improve oxygenation. In ARDS, three populations of alveoli can be distinguished. There are normal alveoli which are always inflated and engaging in gas exchange, flooded alveoli which caever, under any ventilatory regime, be used for gas enchange, and atelectatic or partially flooded alveoli that can be “recruited” to participate in gas exchange under certain ventilatory regimes. The recruitable aveoli represent a continuous population, some of which can be recruited with minimal PEEP, and others which can only be recruited with high levels of PEEP. An additional complication is that some or perhaps most alveoli can only be opened with higher airway pressures than are needed to keep them open. Hence the justification for maneuvers where PEEP is increased to very high levels for seconds to minutes before dropping the PEEP to a lower level. Finally, PEEP can be harmful. High PEEP necessarily increases mean airway pressure and alveolar pressure. This in turn can damage normal alveoli by overdistension resulting in DAD.
The ‘best PEEP’ used to be defined as ‘some’ cmH2O above the lower inflection point (LIP) in the sigmoidal pressure-volume relationship curve of the lung. Recent research has shown that the LIP-point pressure is no better than any pressure above it, as recruitment of collapsed alveoli, and more importantly the overdistension of aerated units, occur throughout the whole inflation. Despite the awkwardness of most procedures used to trace the pressure-volume curve, it is still used by some to define the minimum PEEP to be applied to their patients. Some of the newest ventilators have the ability to automatically plot a pressure-volume curve. The possibility of having an ‘instantaneous’ tracing trigger might produce renewed interest in this analysis.
PEEP may also be set empirically. Some authors suggest performing a ‘recruiting maneuver’ (i.e., a short time at a very high continuous positive airway pressure, such as 50 cmH2O (4.9 kPa), to recruit, or open, collapsed units with a high distending pressure) before restoring previous ventilation. The final PEEP level should be the one just before the drop in PaO2 (or peripheral blood oxygen saturation) during a step-down trial.
Intrinsic PEEP (iPEEP), or auto-PEEP, first described by John Marini of St. Paul Regions Hospital, is a potentially unrecognized contributor to PEEP in patients. When ventilating at high frequencies, its contribution can be substantial, particularly in patients with obstructive lung disease. iPEEP has been measured in very few formal studies on ventilation in ARDS patients, and its contribution is largely unknown. Its measurement is recommended in the treatment of ARDS patients, especially when using high-frequency (oscillatory/jet) ventilation.
A compromise between the beneficial and adverse effects of PEEP is inevitable.
In spite of these issues, the study by Amato et al. raises the possibility that improved alveolar recruitment with the use of higher levels of positive end-expiratory pressure than were used in the NIH study might further reduce ventilator-associated lung injury. This possibility is currently being tested in a new NIH Acute Respiratory Distress Syndrome Network ventilation trial. A number of alternative approaches to conventional mechanical ventilation have also been proposed, including prone positioning of the patient during ventilation, but have not yet been proved to be beneficial.
Prone position
Distribution of lung infiltrates in acute respiratory distress syndrome is non-uniform. Repositioning into the prone position (face down) might improve oxygenation by relieving atelectasis and improving perfusion. However, although the hypoxemia is overcome there seems to be no effect on overall survival.
Fluid and Hemodynamic Management
The rationale for restricting fluids in patients with acute lung injury and the acute respiratory distress syndrome is to decrease pulmonary edema. Studies in animals with acute lung injury indicated that the degree of edema was reduced if left atrial pressure was lowered. Some clinical studies have supported this hypothesis. Soon, a randomized trial of fluid management designed to compare restricted with liberal fluid management based on monitoring hemodynamics with either a pulmonary-artery catheter or a central venous catheter will be carried out by the NIH Acute Respiratory Distress Syndrome Network. While we await these results, a reasonable objective is to maintain the intravascular volume at the lowest level that is consistent with adequate systemic perfusion, as assessed by metabolic acid–base balance and renal function. If systemic perfusion cannot be maintained after the restoration of intravascular volume, as is the case in patients with septic shock, treatment with vasopressors is indicated to restore end-organ perfusion and normalize oxygen delivery. However, on the basis of the negative results of clinical trials, the use of supranormal levels of oxygen delivery cannot be recommended.
Surfactant Therapy
Because of the success of surfactant-replacement therapy in infants with the neonatal respiratory distress syndrome, surfactant replacement has been proposed as a treatment for patients with acute lung injury and the acute respiratory distress syndrome. However, in one study, treatment with a synthetic surfactant had no effect on oxygenation, the duration of mechanical ventilation, or survival. There are several possible explanations for the negative results. First, the surfactant was delivered as an aerosol, and less than 5 percent may have reached the distal air spaces. Also, the product used, a protein-free phospholipid preparation, may not be the most effective for patients with acute lung injury and the acute respiratory distress syndrome. Newer preparations of surfactant that contain recombinant surfactant proteins and new approaches to their instillation, including tracheal instillation and bronchoalveolar lavage, are being evaluated in clinical trials.
Inhaled Nitric Oxide and Other Vasodilators
Nitric oxide is a potent vasodilator that can be delivered to the pulmonary vasculature by inhalation without causing systemic vasodilation. Although observational studies suggested that inhaled nitric oxide might be beneficial in patients with acute lung injury and the acute respiratory distress syndrome, the results of randomized, double-blind studies have been discouraging. In a phase 2 study, inhaled nitric oxide did not reduce mortality or reduce the duration of mechanical ventilation. The improvements in oxygenation with this treatment were small and were not sustained, and pulmonary-artery pressure decreased very little, and only on the first day of treatment. Also, a recent phase 3 study of inhaled nitric oxide showed that it had no effect on either mortality or the duration of mechanical ventilation. Thus, inhaled nitric oxide cannot be recommended for the routine treatment of acute lung injury and the acute respiratory distress syndrome, but it may be useful as a rescue therapy in patients with refractory hypoxemia. Treatment with several less selective vasodilators, including sodium nitroprusside, hydralazine, alprostadil (prostaglandin E1), and epoprostenol (prostacyclin), has also not been shown to be beneficial.
Glucocorticoids and Other Antiinflammatory Agents
Recognition of the inflammatory nature of the lung injury in acute lung injury and the acute respiratory distress syndrome prompted interest in antiinflammatory treatments, particularly glucocorticoids. However, glucocorticoids had no benefit when they were given before the onset of the disease or early in its course. More recently, glucocorticoids have been used to treat the later, fibrosing-alveolitis phase of the disease. Encouraging results were reported in preliminary studies and in a small randomized trial of 24 patients. A larger randomized, multicenter
A short course of high-dose glucocorticoids could be considered as rescue therapy in patients with severe disease that is not resolving. In addition to glucocorticoids, other antiinflammatory agents designed to interrupt the process of acute lung injury have been investigated but have proved unsuccessful. The failure may reflect the complexity and redundancy of the inflammation in acute lung injury or the inability to deliver these agents early enough in the course of the illness.
Acceleration of Resolution
Recognition of the importance of the resolution phase of acute lung injury and the acute respiratory distress syndrome has stimulated interest in strategies to hasten patients’ recovery from lung injury. Experimentally, removal of pulmonary edema fluid from the alveolar space can be enhanced by both catecholamine-dependent and catecholamine-independent mechanisms, including those increased by inhaled and systemic beta-agonists. Beta-agonists are appealing candidates because they are already in wide clinical use and have no serious side effects, even in critically ill patients. Treatment with beta-agonists may also increase the secretion of surfactant and perhaps exert an antiinflammatory effect, thus helping to restore vascular permeability of the lung.
Since acute injury to epithelial type I cells causes denudation of the alveolar epithelium, an additional approach to hastening the resolution of acute lung injury and the acute respiratory distress syndrome is to accelerate reepithelialization of the alveolar barrier. The proliferation of alveolar epithelial type II cells is controlled by a number of epithelial growth factors, including keratinocyte growth factor. Experimentally, administration of keratinocyte growth factor protects against lung injury, probably in part by increasing the proliferation of alveolar type II cells and the clearance rate of alveolar fluid and by inducing antioxidant effects, and perhaps by reducing lung endothelial injury. These findings raise the possibility that an epithelium-specific growth factor could be used to accelerate the resolution of the syndrome. Overall, strategies directed at restoring the function of alveolar epithelium deserve careful evaluation.
Conclusions
In conclusion, substantial progress has been made in the understanding of acute lung injury and the acute respiratory distress syndrome. More information regarding epidemiology and pathogenesis has become available, and the importance of the resolution phase of the illness has been recognized, opening up new avenues for therapeutic intervention. Although progress in specific treatments has lagged behind basic research, the formation of the NIH Acute Respiratory Distress Syndrome Network led to a clinical trial of a ventilation strategy involving low tidal volumes, which reduced mortality by 22 percent. Large, prospective, randomized trials of new ventilatory and pharmacologic strategies may further reduce mortality from this common clinical syndrome.
General Principles of Emergency Care
General Principles of Emergency Care
Splint injured parts in the position they are found Prevent chilling, but do not add excessive heat Do not remove penetrating objects Do not try to give anything by mouth to an unconscious person or one with serious injuries Stay with the injured person until medical care or transportation arrives
Physical Examination :
The first priority: ABCs Airway, breathing, and circulation Watch chest for rhythmic breathing; listeear mouth and nose for air movement Palpate the carotid and peripheral pulses Once respiration and circulation established, assess for uncontrolled bleeding and shock If none, assess systematic head-to-toe
Evaluation of Accident and Emergency Patients :
Primary survey (ABCDE): Airway Breathing Circulation/hemorrhage Disability or defibrillation Exposure Secondary survey (head-to-toe): Head, face, neck, neurologic status Chest Abdomen/genitourinary system Limbs Log roll
Systematic Head-to-Toe Assessment
Evaluate comprehension: ask patient to follow simple commands, such as opening and closing the eyes Inspect eyes to assess pupil size, equality, and reaction to light Ask about neck pain or stiffness and the ability to swallow Inspect for chest wall movement symmetry
Systematic Head-to-Toe Assessment :
Systematic Head-to-Toe Assessment Assess breathing, dyspnea, and abnormal sounds associated with respirations Examine contour of abdomen for distention Light palpation to detect pain or tenderness Inspect the extremities for deformity or injury, and evaluate movement Assess peripheral pulses and warmth and sensation in the extremities
Cardiopulmonary Arrest :
Cardiopulmonary Arrest Absence of a heartbeat and respirations Causes Myocardial infarction, heart failure, electrocution, drowning, drug overdose, anaphylaxis, and asphyxiation Signs and symptoms Collapse and quickly lose consciousness No pulse or respiration
Cardiopulmonary Arrest :
Cardiopulmonary Arrest Interventions Determine responsiveness Open airway Check for breathing (look, listen, feel) If nonresponsive and not breathing, palpate for a pulse If no pulse in 10 seconds, begin compression:ventilation cycles of 30:2 If a pulse, deliver 10-12 rescue breaths per minute Io advanced airway, continue the 30:2 ratio With advanced airway, compressions of 100 per minute without pausing for ventilations which are done at a rate of 8-10 per minute
Figure: Airway :
Cardiopulmonary Arrest :
Cardiopulmonary Arrest Two-rescuer CPR One rescuer compresses the chest at a rate of 100 per minute without pausing for ventilations Second rescuer ventilates with 8-10 breaths/minute Swap roles about every 2 minutes to avoid tiring Recovery position Unresponsive victim who is breathing should be log-rolled to one side if no cervical trauma is suspected
Choking or Airway Obstruction :
Choking or Airway Obstruction Assessment Universal sign of choking is grabbing the throat with one or both hands First determine if airway completely blocked If victim is able to speak, breathe, or cough with good air exchange, do nothing If unable to speak, breathe, or cough with good air exchange, act quickly to prevent suffocation
Choking or Airway Obstruction :
Choking or Airway Obstruction Victim is conscious Perform the Heimlich maneuver If effective, air expels foreign body from the airway If not, repeat maneuver until the object is expelled or victim loses consciousness
Choking or Airway Obstruction :
Choking or Airway Obstruction Victim unconscious/loses consciousness Lift the jaw and sweep a finger through the mouth to try to remove the object Tilt the head back, lift the chin, pinch the nostrils, try to ventilate If the airway is still obstructed, attempts at ventilation will fail Reposition the head and attempt once more to ventilate If unsuccessful, proceed to the next step Straddle the victim’s thighs, place one hand on top of the other, and deliver up to five abdominal thrusts Repeat these three steps until the airway is clear
Straddle the victim’s thighs, place one hand on top of the other, and deliver up to five abdominal thrusts Repeat these three steps until the airway is clear
Shock :
Shock Results from acute circulatory failure caused by inadequate blood volume, heart failure, overwhelming infection, severe allergic reactions, or extreme pain or fright
Hemorrhage :
Hemorrhage The loss of a large amount of blood Loss of more than
Exsanguination :
Exsanguination To Bleed Out all the Blood from the body
Hemorrhage :
Hemorrhage Apply direct, continuous pressure Elevate and immobilize the injured part (unless fracture is suspected) After bleeding stops, secure a large dressing, if available, over the wound Reinforce the dressing but do not change it If direct wound pressure and elevation fail to control bleeding, apply indirect pressure to the main artery that supplies the area
Hemorrhage Epistaxis Blood from anterior or posterior portion of the nose Most anterior nosebleeds respond to pressure Instruct the patient to sit down and lean the head forward Pinch the nostrils shut for at least 10 minutes Advise patient not to blow or pick at nose for several hours Continued bleeding or bleeding from the posterior area of the nose requires medical treatment
Fracture :
Fracture A break in a bone Simple (closed) fracture Does not break the skin Compound (open) fracture Broken bone protrudes through the skin Complete fracture Broken ends are separated Incomplete fracture Bone ends are not separated
Fracture :
Fracture Assessment Primary symptom is pain Numbness/tingling from nerve injury and blood vessels Signs: deformity, swelling, discoloration, decreased function, and bone fragments protruding through the skin
Strains and Sprains :
Strains and Sprains Strains Injuries to muscles or tendons, or both Sprains Injuries to ligaments These injuries are painful; may be swelling Emergency treatment is: RICE- (rest, ice, compression, elevation) Victim to see physician for further evaluation
Head Injury :
Head Injury Suspected with any type of blow to the head or any unexplained loss of consciousness Assessment Inspection and palpation of the head Evaluate for signs and symptoms of increased intracranial pressure Be alert for the leakage of cerebrospinal fluid that occurs with basilar skull fractures
Head Injury :
Head Injury Must be assessed by a physician as soon as possible Immobilize neck and keep victim flat with proper alignment of the neck and head Backboard used for transporting victim
Neck and Spinal Injuries :
Neck and Spinal Injuries Assessment Assess breathing and circulation and then begin resuscitation if needed Remember to use the jaw-thrust method to open the airway! Assess movement and sensation in all extremities
Neck and Spinal Injuries Immediately summon expert emergency team In remote or life-threatening settings, the victim may have to be moved A rolled towel or article of clothing can be used as a collar to support the neck The victim can then be moved by log-rolling to one side and then rolling back onto a board, keeping the spine as straight as possible Throughout the movement, one rescuer supports the head while two others support the shoulders, hips, and legs
Eye Injury :
Eye Injury Assessment Inspect eyelid for trauma and the eye for redness, foreign bodies, or penetrating objects To inspect for foreign bodies, evert the eyelids
Ear Trauma :
Ear Trauma Assessment Assess extent of injury; note if any tissue is fully separated and severity of bleeding Apply direct pressure to injury to control bleeding
Ear Trauma :
Ear Trauma If injured part is actually separated, reattachment may be possible Retrieve the tissue, wrap it in plastic, keep it cool, and transport it with the victim
Chest Injury :
Chest Injury Critical injuries: open pneumothorax, flail chest, massive hemothorax, and cardiac tamponade
Pneumothorax
Cardiac Tamponade
Assessment of Pt with Chest Injuries rate and character of respirations, skin color, pulse rate and rhythm symmetry of the chest wall movement presence of any apparent injuries to the chest Signs and symptoms of chest injuries Dyspnea Tachycardia Restlessness Cyanosis asymmetric or other abnormal chest wall movement, abnormal sounds of breathing Note mental state and level of consciousness
Abdominal Injury: Assessment :
Abdominal Injury: Assessment Assess abdomen for evidence of injury Nausea/ Vomiting Inspect Suspect internal abdominal injuries if victim complains of abdominal pain or abdomen shows evidence of trauma or distention Protrusion of internal organs through a wound is called evisceration
Abdominal Injury :
Abdominal Injury Cullen’s Sign- Bluish tinge around umbilicus may indicates abdominal hemorrhage
Abdominal Injury: Interventions :
Abdominal Injury: Interventions Require medical evaluation Give nothing by mouth in preparing for transport Do not attempt to replace eviscerated organs in the abdomen; this may cause additional harm Cover organs with material, such as plastic wrap or foil, to conserve moisture and warmth A saline-soaked sterile dressing is ideal but is not likely to be available on the scene of an accident Cover wound with clean cloth; transport to hospital
Traumatic Amputation :
Traumatic Amputation If partially/completely detached, reattachment possible Clean the wound surfaces with sterile water or saline and place the tissue in its normal position A body part that is completely detached should ideally be wrapped in sterile gauze moistened with sterile saline, placed in a watertight container such as a resealable plastic bag, and placed in an iced saline bath The tissue should not be frozen or placed in contact with ice Amputated extremities may be healthy enough for reattachment for 4-6 hours; digits as long as 8 hours
Amputated Hand :
Amputated Hand
:
Shark Bite Amputation
Burns: Assessment :
Burns: Assessment Determine the type of burn If patient has a flame burn or was in a closed, smoke-filled area, assess respirations first Determine the extent and depth of the burns Inspect skin for color, blisters, tissue destruction Superficial burns: typically pink or red and painful Deeper burns: red, white, or black; may destroy not only the skin but also the underlying tissues Electrical: difficult to assess; full extent of tissue damage may not be apparent for several days Chemical: immediately remove any remaining chemical
Burns: Interventions :
Burns: Interventions Ensure a patent airway and respirations for burn victims Rescue breathing, if needed
Hyperthermia :
Hyperthermia Body temperature >37.2° C (99° F) Heat edema and heat cramps are mild degrees of hyperthermia Can be treated by moving individual into cool place and providing fluids with electrolytes Heat exhaustion and heat stroke more serious See Table 16-5, p. 236
Hypothermia :
Hypothermia Decrease in body core temperature to <36° C (95° F) Caused by prolonged exposure to cold, extremely cold temperatures, or immersion in cold water Causes depression of vital functions, and if not corrected, death results from cardiac dysrhythmias
Hypothermia :
Hypothermia Mild stage Patient shivers in an effort to generate body heat Blood vessels in the extremities are constricted, and performing complex motor tasks is impaired Moderate hypothermia Appears dazed, poor motor coordination, slurred speech, and violent shivering May behave irrationally Severe hypothermia Waves of shivering, rigid muscles, and pale skin Pulse rate is slow and the pupils are dilated
Hypothermia
Frost Bite and Frost Nip :
Frost Bite and Frost Nip Frost nip: mild tissue damage caused by cold Frost bite: More serious cold injury Blood vessels constrict when exposed to extreme cold. Blood clots form and circulation is impaired Tissues die as a result Pain is the first sign, followed by tingling, and numbness
Treatment for Frostbite :
Treatment for Frostbite Mild- rapid re-warming More serious- Do not attempt to thaw tissue unless warmth maintained Re-warm in heated 100-105* water-Do not rub or massage area Feet should be defrosted only if the person doesn’t need to walk
Carbon Monoxide Poisoning :
Carbon Monoxide Poisoning Assessment Early signs and symptoms: headache and shortness of breath with mild exertion Then dizziness, nausea, vomiting, and mental changes As carbon monoxide in bloodstream rises, victim loses consciousness and develops cardiac and respiratory irregularities Cherry-red skin clear indicator of carbon monoxide poisoning, but skin color often found to be pale or bluish with reddish mucous membranes
Nursing Diagnosis, Goal, and Outcome Criteria :
Nursing Diagnosis, Goal, and Outcome Criteria Impaired gas exchange related to carbon monoxide poisoning The goal of nursing care for the emergency treatment of the victim of carbon monoxide poisoning is normal oxygenation
Interventions :
Interventions Immediately move the victim to fresh air If persoot breathing, start rescue breathing Seek emergency medical assistance immediately Give oxygen as soon as it is available At the hospital the patient may be placed in a hyperbaric oxygen chamber
Prevention :
Prevention Keep gas furnaces and stoves in proper repair Burners that use gas must be vented to the outside Don’t use charcoal or wood-burning devices in closed area Never let automobile engine run in closed garage Install carbon monoxide detector alarm
Drug or Chemical Poisoning :
Drug or Chemical Poisoning Assessment History: data about relevant signs and symptoms Name of drug or chemical. If the victim cannot provide the information, look for clues and save the container Amount consumed Length of time since substance was taken Last food consumed: amount, time Signs and symptoms that may be caused by poisons Victim’s age and approximate weight Other medications, drugs, or alcohol ingested
Drug or Chemical Poisoning :
Drug or Chemical Poisoning Interventions Immediately call your poison center Some poisonings can be treated at home, others require a physician or a hospital Treatment of poisoning in an emergency facility may be with activated charcoal, total bowel lavage, and/or cathartics
Food Poisoning :
Food Poisoning Assessment Symptoms: nausea, vomiting, abdominal cramps, and diarrhea Botulism caused by Clostridium botulinum has neurotoxic effects: difficulty breathing, seeing, and swallowing Clue that food poisoning is causing victim’s symptoms is that all who consumed a certain food become ill To assist in identifying poisons, collect samples of stool or vomited materials for possible lab analysis
Food Poisoning :
Food Poisoning Ptomaine poisoning Bacterial or chemical Cleanliness, good personal hygiene, and proper preparation and handling of foods Symptoms and treatment (Also refer to Health Promotion Points 44-2.)
Multistate Outbreak of E. coli O157:H7 Infections Linked to Eating Raw Refrigerated, Prepackaged Cookie Dough Multistate Outbreak of E. coli O157:H7 Infections Associated with Beef from JBS Swift Beef Company
Healthy People 2010 Food Safety :
Healthy People 2010 Food Safety Focus area # 10: Food Safety. To reduce food-borne illnesses.
Food Poisoning: Interventions :
Food Poisoning: Interventions Medical care necessary if symptoms are severe or persistent The physician may order antiemetics and antidiarrheals Intravenous fluids may be prescribed with severe vomiting and diarrhea
Bites and Stings :
Bites and Stings Assessment Try to determine the type of bite Inspect bite to identify characteristics of bite site and any changes in surrounding tissue Ask about any symptoms that developed after the bite: pain, edema, numbness, tingling, nausea, fever, dizziness, and dyspnea Interventions: see Table 16-7, p. 239
Animal Bites :
Animal Bites Animal bites and Animal Control Agency: Wash area with warm soapy water for 5-10 minutes Rabies immunization or 5 IM injections given over a period of 3 weeks
Copperhead Snake :
Snakebite: :
Snakebite: Poisonous snakes and venomous snakebite Treatment Wash area Immobilize Apply suction Go to hospital Give antivenin
Insect Bites and Stings :
Remove Stinger
Health Promotion Points : Anaphylaxis Kit Individuals who have known allergies to insect bites or other common environmental allergens should carry an anaphylaxis kit. Family and friends should know how to use the contents in case the individual is unable to treat herself.
Coral Snake
Snakebite: :
Snakebite: Poisonous snakes and venomous snakebite Treatment Wash area Immobilize Apply suction Go to hospital Give antivenin
Insect Bites and Stings :
Insect Bites and Stings
Remove Stinger
Health Promotion Points : Anaphylaxis Kit :
Health Promotion Points : Anaphylaxis Kit Individuals who have known allergies to insect bites or other common environmental allergens should carry an anaphylaxis kit. Family and friends should know how to use the contents in case the individual is unable to treat herself.
Administering Epi Pen :
Signs and Symptoms of Anaphylaxis :
Signs and Symptoms of Anaphylaxis Hives Swelling Generalized weakness Chest tightness Abdominal cramps Constriction of throat Loss of consciousness
Safety Alert : Lightning :
Safety Alert : Lightning If outdoors when lightning occurs, avoid water, high ground, open spaces, and metal objects. Do not seek shelter under canopies, small picnic or rain shelters, or trees.
Acts of Bioterrorism Deliberate release of pathogens to kill people Anthrax, botulism, plague, smallpox, tularemia: most common biologic agents in terrorist attack Easily spread; potential to cause many deaths Health care providers must know how to protect themselves and others Staff should know where to obtain personal protective equipment and what types of precautions (i.e., patient isolation) should be taken
Disaster Planning :
Disaster Planning A challenge for the health care system is to be ready for natural disasters that often occur with short warning American Red Cross and the Salvation Army are experienced in handling these situations and quickly move in to help A call for nurse volunteers usually follows Regardless of the area of clinical expertise, there is certain to be a way each nurse can contribute
Psychological Emergencies :
Psychological Emergencies Combative patient Domestic violence/abuse Child abuse Elder abuse Psychological trauma
Legal Aspects of Emergency Care Emergency doctrine In emergencies, person may be unable to consent to care Treatment can be provided under the assumption that the patient would have consented if able Good Samaritan laws Limit liability and provide protection against malpractice claims when health care providers render first aid at the scene of an emergency These laws do not protect the nurse in the event of gross negligence or willful misconduct
Source Information
From the Cardiovascular Research Institute (L.B.W., M.A.M.) and the Departments of Medicine (L.B.W., M.A.M.) and Anesthesia (M.A.M.),
Address reprint requests to Dr. Matthay at CVRI,
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Підготував Доброродній А.В.
