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The presumed effcacy of treatment with plasma buy trimox 250mg visa, fbrinogen buy 500mg trimox with visa, cryo- precipitate trimox 500 mg without prescription, or platelets is not based on randomized controlled trials but appears to be rational therapy in bleeding patients or in patients at risk for bleeding with a signifcant depletion of these hemostatic factors [37]. It may be required to use large volumes of plasma to restore normal concentrations of coagulation factors. Coagulation factor concentrates, such as prothrombin complex concentrate, may overcome this impediment, but these agents may lack important factors (e. Moreover, in older literature, caution is advocated with the use of prothrombin complex concentrates in systemic coagulation activation, as it may aggravate the coagulopathy due to small traces of activated factors in the concentrate. It is, how- ever, less likely that this is still the case for the concentrates that are currently in use. Specifc defciencies in coagulation factors, such as fbrinogen, may be corrected by administration of purifed coagulation factor concentrates [37]. Experimental studies have shown that heparin can at least partly inhibit the activation of coagulation in sepsis [78]. In addition, there are several studies showing that critically ill patients with sepsis need adequate prophylaxis for venous thromboembolism, usually with (low molecular weight) heparin [82, 83]. Therapeutic doses of heparin are indicated in patients with clinically overt thromboembolism or extensive fbrin deposition, like purpura fulminans or acral ischemia. Patients with sepsis may beneft from prophylaxis to prevent venous 4 The Coagulation System in Sepsis 53 thromboembolism, which may not be achieved with standard low-dose subcutane- ous heparin [84]. Restoration of the levels of physiological anticoagulants in sepsis may be a ratio- nal approach [85]. Based on successful preclinical studies, the use of antithrombin concentrates has been examined mainly in randomized controlled trials in patients with severe sepsis. All trials have shown some benefcial effect in terms of improve- ment of laboratory parameters, shortening of the duration of the coagulopathy, or even improvement in organ function. In several small clinical trials, the use of very high doses of antithrombin concentrate showed even a modest reduction in mortal- ity, however, without being statistically signifcant. A large-scale, multicenter, ran- domized controlled trial also showed no signifcant reduction in mortality of patients with sepsis [86]. Interestingly, post hoc subgroup analyses of this study indicated some beneft in patients who did not receive concomitant heparin and in those with the most severe coagulopathy [87]. Recent propensity-adjusted retrospective data from Japan demonstrated a signifcant beneft of antithrombin-treated patients with severe infection and sepsis [88, 89]. Of note, patients with the most severe coagulopathy benefted most from this treatment [73]. The most promising intervention at this moment is recombinant soluble throm- bomodulin. Several preclinical studies in experimental sepsis models have shown that soluble thrombomodulin is capable of improving the derangement of coagu- lation and may restore organ dysfunction [93]. Markers of coagulation activation were lower in the thrombomod- ulin group than in the placebo group. The promising results with recombinant soluble thrombomodulin are supported by retrospective data in large series of Japanese patients and are currently being evaluated in a large international multicenter trial [97, 98]. However, despite the fact that these interventions (such as recombinant human- activated protein C or antithrombin concentrate) have shown effcacy in reversing the coagulopathy, they have not resulted in an improvement on clinically relevant outcomes, such as survival or improvement of organ dysfunction [99]. One of the factors responsible for this may be that all these anticoagulants are clearly limited by the potential risk of major hemorrhage in critically ill patients. For example, non-anticoagulant heparin inhibits the expression and function of adhesion molecules, such as P-selectin and L-selectin. Non-anticoagulant heparin has a strong affnity for extracellular histones that result from cellular destruction during severe infammation and that are robustly associated with endothelial dysfunction, organ failure, and death during sepsis [100]. Binding of this non-anticoagulant heparin to histones strongly inhib- ited cytotoxic activity in vitro and translated to impaired infammation and improved survival in animal models of systemic infection and infammation. Similarly, recent experiments indicate a benefcial effect of activated protein C variants that have lost their anticoagulant properties [101]. Another interesting new target may the glycocalyx covering the endothelial sur- face of the vascular bed [102]. The endothelium of the capillary bed is the most important interface in which the interaction between infammation and coagulation takes place. All physiologic anticoagulant systems and various adhesion molecules that may modulate both infammation and coagulation are connected to the endothe- lium. Moreover, specifc disruption of the glycocalyx results in thrombin genera- tion and platelet adhesion within a few minutes. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Extrinsic coagu- lation blockade attenuates lung injury and proinfammatory cytokine release after intratracheal lipopolysaccharide. Multiple coagulative defects in a patient with the Waterhouse- Friderichsen syndrome. Vanderschueren S, De Weerdt A, Malbrain M, Vankersschaever D, Frans E, Wilmer A, et al. Thrombocytopenia in patients in the medical intensive care unit: bleeding prevalence, transfusion requirements, and outcome. Platelets release thrombopoietin (Tpo) upon activation: another regulatory loop in thrombocytopoiesis? Thrombocytopenia in the sepsis syndrome: role of hemophagocytosis and macrophage colony-stimulating factor. D-dimer correlates with pro- infammatory cytokine levels and outcomes in critically ill patients. Signifcant correlations between tissue factor and thrombin markers in trauma and septic patients with disseminated intravascular coagulation. Inhibition of endotoxin-induced activation of coagulation and fbrinolysis by pentoxifylline or by a mono- clonal anti-tissue factor antibody in chimpanzees. Increased tissue thromboplastin activity in monocytes of patients with meningococcal infection: related to an unfavourable prognosis. Induction of tissue factor expression in whole blood – lack of evidence for the presence of tissue factor expression on granulocytes. The platelet-activating factor signaling system and its regulators in syndromes of infammation and thrombosis. Plasminogen activator and plasminogen activator inhibitor I release during experimental endotoxaemia in chimpanzees: effect of interventions in the cytokine and coagulation cascades. Variation in plasminogen-activator-inhibitor-1 gene and risk of meningococcal septic shock.

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It is most often injured during dissections common in the typical maxillofacial practice cheap trimox 250 mg free shipping, and as such it at Level Ib buy trimox discount. It is located 1 cm anterior and inferior to the is important to understand the key anatomic landmarks in angle of the mandible at the mandibular notch order trimox american express, deep to the the neck. Control of the neck is one of the most important fascia of the submandibular gland (superfcial layer of deep aspects of the successful management of these particular cervical fascia) and superfcial to the adventitia of the facial pathologies. It is important to note that more than one branch is leagues regarding treatment and patient management man- often present, and during surgical procedures, the sensory dates an understanding of important anatomic sites. Te fascia of the head and neck is composed of loose fbrous masseter, is rhomboidal in shape, and is important in cos- connective tissue envelopes and may be divided into the metic surgery (such as lower [cervicofacial] facelifts), because superfcial and deep fascia. Between the fbers of the matrix dissection is bloodless and provides safety for all facial nerve 2 are interstices that are flled with tissue fuid or ground sub- branches, as they are located outside this plane. Te loose fbrous connective tissue that makes up the the platysma muscle that arises superiorly from the fascia fascia of the head and neck is found in varying degrees of over the zygomatic arch. Tese four subtypes are the fascial spaces of the superfcial temporal fascia superiorly, superfcial to the the face, suprahyoid fascial spaces, infrahyoid fascial spaces, parotideomasseteric fascia, and it connects to the fascial mus- and the fascial spaces of the neck. Location and anatomic identifcation of this layer are impor- 3 tant in surgical manipulation for both reconstructive and Fascial Space Subtype 4 cosmetic procedures. Fascial Space Subtype Components Fascial spaces of the Canine, buccal, parotid, face infratemporal, Deep Fascia masticatory spaces Te deep fascia begins at the anterior border of the masseter — Masseteric muscle, attaches to the superior temporal and nuchal lines, — Pterygomandibular and posterior and inferior to these margins it continues crani- — Temporal ally as the pericranium. Te deep facial fascia represents a Suprahyoid fascial Sublingual, submental, continuation of the deep cervical fascia cephalad into the face spaces submandibular, lateral and, more posterior, invests the muscles of mastication, the pharyngeal, peritonsillar surgical importance of which lies in the fact that the facial Infrahyoid fascial spaces Pretracheal 1 nerve branches within the cheek lie deep to this fascial layer. Fascial spaces of the Retropharyngeal, danger, neck carotid sheath Fascial Spaces of the Face Superfcial Fascia Te fascial spaces of the face are subdivided into fve spaces: the canine space, the buccal space, the masticatory space Te superfcial fascia of the head and neck lies just under the (further divided into the masseteric, pterygomandibular, and skin, as it does in the entire body, invests the superfcially temporal spaces), the parotid space, and the infratemporal situated mimetic muscles (platysma, orbicularis oculi, and space (Figure 8-1, A). Infection spreads to the deep fascia, which covers and invests the structures lying this space through the root apices of the maxillary teeth, deep to the skin while maintaining the movability of the skin, usually the canine. Direct surgical access is achieved through with the two layers allowing for separation during blunt incision through the maxillary vestibular mucosa above the dissection. Te areolar cleavage plane overlies the lower mucogingival junction (Figure 8-1, B). Te buccal and posterior directions, which permits the spread of pathol- space frequently communicates posteriorly with the mastica- ogy both to and from the buccal space. Surgical access to this space may be space and suspicion of malignancy, may require a preauricular achieved intraorally in the case of simple infections, but may or submandibular approach. Infection in this space may temporal line and passes inferiorly to the zygomatic arch. However, primary infection in this is rare extremely dense and frm fbrous connective tissue. Com- and is generally blood-borne or retrograde through the municating facial-zygomaticotemporal nerve branches pierc- parotid duct. Te fascia that forms the borders of the masseteric space is a well-defned fbrous tissue that surrounds the muscles of mastication and contains the internal maxillary artery and Suprahyoid Fascial Spaces the inferior alveolar nerve. It is bounded anteriorly by the mandible, posteriorly by the parotid gland, medially by the Sublingual Space lateral pharyngeal space, and superiorly by the temporal space. Te sublingual space is bounded between the mylohyoid Most masseteric space infections are of odontogenic origin muscle and the geniohyoid and genioglossus muscles. Te Periapical molar infections may perforate the lingual man- submasseteric space is bounded laterally by the masseter dible cortex above the mylohyoid line and spread to this muscle, medially by the mandible ramus, and posteriorly by space. Infections are mostly of odontogenic origin approach, but when other spaces are involved extraoral (usually a mandibular third molar) and are often misdiag- access may be utilized, usually through a submandibular nosed as a parotid abscesses or parotitis. Te submental space is bounded anteriorly by the symphysis of the mandible, laterally by the anterior bellies of digastric Pterygomandibular Space muscles, superiorly by the mylohyoid muscle, and inferiorly Te pterygomandibular space is bounded by the mandible by the superfcial fascia of the platysma muscle. No vital laterally and medially and inferiorly by the medial ptery- structures traverse the submental space. Te posterior border is formed by the parotid involved in odontogenic infections from the anterior man- gland as it curves medially around the posterior mandibular dibular teeth, as benign or malignant lesions in this area ramus and anteriorly by the pterygomandibular raphe, the are rare. Te inferior alveolar and lingual nerves, other struc- access through an extraoral incision below the chin. When tures in this space, are of particular importance in the infection has spread to this space, it represents one of the administration of local anesthesia, including the inferior components (along with bilateral submandibular and sublin- alveolar vessels, the sphenomandibular ligament, and the gual space involvement) of Ludwig’s angina. Te submandibular space extends from the hyoid bone to the Te buccopharyngeal gap is a potentially dangerous con- mucosa of the foor of the mouth and is bound anteriorly and nection between the submandibular and lateral pharyngeal laterally by the mandible and inferiorly by the superfcial layer spaces that is created by the styloglossus muscle as it passes of the deep cervical fascia. Te mylohyoid muscle separates between the middle and superior constrictors, which may it superiorly from the sublingual space, which communicates allow infection to spread directly to the lateral pharyngeal with it freely around the posterior border of the mylohyoid. Surgical access for drainage may be either intraoral or Te mylohyoid muscle also plays a key role in determining extraoral. When infection has spread to the bilateral subman- the direction of the spread of dental infections. It attaches dibular spaces, it represents one of the components (along to the mandible at an angle, leaving the apices of the second with submental and bilateral sublingual space involvement) and third molars below the mylohyoid line and the apex of of Ludwig’s angina. Periapical molar infections may almost always through multiple extraoral incisions. Te lateral pharyngeal space can riorly by the attachments of the infrahyoid muscles and their be divided into anterior (prestyloid) and posterior (retrosty- fascia to the thyroids cartilage and to the hyoid bone, and loid) compartments by the styloid process. Te anterior com- continues into the anterior portion of the superior mediasti- partment contains only fat, lymph nodes, and muscle, whereas num bounded inferiorly by the sternum and scalene fascia. Rotation of the neck away from the side and thyroid gland between the levels of the inferior thyroid of swelling causes severe pain from tension on the ipsilateral artery and the oblique line of the thyroid cartilage. As this space communicates may allow infection to spread into the superior mediastinum, with the other fascia spaces, spread of infection may also arise as these spaces communicate. Posterior space involvement may have more ominous Fascial Spaces of the Neck signs. Lemierre syndrome may result from pharyngitis or tonsillitis with bacterial spread to the lateral pharyngeal space Te fascial spaces of the neck all lie between the deep cervical that may involve internal jugular vein thrombosis with septic fascia surrounding the pharynx anteriorly and the spine pos- emboli and metastatic infections that most frequently involve teriorly. Te other fascial spaces of the neck bophlebitis and carotid artery erosion or thrombosis. Te intraoral approach cervical fascia, and connects posteriorly to the danger space. Tey may be complicated by the development Peritonsillar Space of supraglottic edema with airway obstruction, aspiration Te peritonsillar space is a potential space of loose areolar pneumonia due to rupture of the abscess, and acute medias- tissue that surrounds the tonsil and is bounded laterally by tinitis that may lead to empyema or pericardial efusions.

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A prospective randomized trial of biologic mesh versus synthetic mesh for the repair of com- plex ventral hernias purchase generic trimox from india. Multicentric prospective randomized study comparing technique of tension-free repair with placement of a bovine pericardium bioprosthesis (Tutopatch® and Tutomesh®) to current con- ventional surgical techniques in potentially contaminated hernia repair and abdominal wall reconstruction discount trimox 250mg amex. Clinical outcomes achieved and the staffng resources required were compared for 30 high-risk open abdominal surgery patients at two metropolitan hospitals cost of trimox. Both hospitals were simi- lar in preoperative morbidity, demographics, and operative characteristics. Development of clinically rele- vant outcome measures such as those described can provide objective data for guid- ing staffng, future service planning, and setting research priorities. Lately, the same group conducted a study aiming to determine if the addition of deep breathing exercises and secretion clearing techniques to a standardized physiotherapist-directed program of early mobilization improved clinical outcomes in patients undergoing open abdominal surgery. This study suggested that, in this clinical setting, the addition of deep breathing and coughing exercises to a physiotherapist-directed program of early mobilization does not signifcantly reduce the incidence of clinically signifcant postoperative pulmonary complications in high-risk open abdominal surgery subjects. This study found that, in this clinical setting, the addition of coached lateral basal expansion and secretion clearance techniques to a targeted program of physiotherapist- directed early mobilization conferred no additional beneft in reducing the incidence of postoperative pulmonary complications after open abdominal surgery in high-risk subjects. This study was signifcant in that, unlike previous randomized trials of physio- therapy after open abdominal surgery, it documented the actual type and dosage of physiotherapy interventions and used a sample of subjects from the population of open abdominal surgery patients who are most likely to beneft from physiotherapy, that is, those identifed as high risk of developing postoperative pulmonary complications. These results were obtained in a clinical setting where patient-controlled epi- dural analgesia was used extensively and the standardized early mobilization pro- gram was implemented and monitored by the physiotherapists. Due to the lack of literature in the rehabilitation after open abdomen procedures in emergency surgery, we can investigate other kinds of abdominal surgery to derive a rationale to apply in rehabilitation programs after and during open abdomen procedures. Many authors talk about surgery interventions that allow patients to conduct some preoperative physical activities in order to undergo surgery in the best physi- cal condition; as far as open abdomen surgery is concerned, this kind of prevention is not possible because it is often an emergency condition. Moreover, after surgery, patients experience tiredness, lethargy, changed emotional state, and a desire to sleep and rest, more commonly known as “postoperative fatigue. These interventions may include lung expansion exercises, secretion clearance techniques, limb exercises, progressive mobilization programs, and other tech- niques [2, 4]. Multiple fac- tors may be involved in diaphragmatic dysfunction, such as irritation and infamma- tion caused by trauma from manipulation close to the diaphragm, refex inhibition of afferent abdominal receptors, and postoperative pain. The incidence of postoperative pulmonary complications has been shown to be lower in open abdominal surgery patients who receive physiotherapy compared to those who receive none [2, 10, 11]. In some cases, such as low blood pressure, severe premorbid debility, patient refusal, pain, atrial fbrillation or other cardiac arrhythmia, nausea and vomiting, motor block from epidural, nurse concern, low hemoglobin, or others [12], physio- therapy should be delayed in order to permit patient’s clinical stabilization. Raised maximal oral temperature >38°C on more than one consecutive postop- erative day 3. Pulse oximetry oxygen saturation (SpO2) <90% on more than one consecutive postoperative day 4. An otherwise unexplained white cell count greater than 11 × 109/l or prescrip- tion of an antibiotic specifc for respiratory infection 7. New abnormal breath sounds on auscultation different to preoperative assessment 8. Since clinical decisions about patient management incorporate a wide range of factors, practical approaches are required to assist clinicians in making the optimal management decisions. Outcome measures most frequently used are temperature, expectoration, subjec- tive experiences and time to chest tube removal, postoperative complications, alveo- lar–arteriolar oxygen difference and cough, dyspnea, mobilization, pain, use of bronchodilators, antibiotics, oxygen, pulse rate, and pulmonary auscultation [13]. Decreased cognition also has been cited as a risk factor for pulmonary complica- tions due to the decreased ability to protect their airway [1, 14]. The primary modifable risk factors are shallow breathing, incision pain, and immo- bility. Breathing exercises and early mobilization are cornerstones of postoperative management. Early mobility following surgery is deemed crucial, since postoperative immobilization is widely held to contribute to cardiovascular instability, thromboem- bolic complications, and catabolism, in addition to pulmonary morbidity. Patients are included in standardized programs of physical therapy treatment which structured the model of patient care, focusing on the use of additional therapeutic resources [4, 15, 16], early sitting position, and ambulation (onset <48 h after surgery) [4, 17]. Physical therapy modalities are generally left to the discretion of the therapists, provided that they correspond with guidelines regarding abdominal strengthening and stabilization, abdominal myofascial release and scar mobilization/massage, core strengthening in neutral only (no crunches), balance training, hip mobilization, gluteus medius strengthening, lumbar strengthening, posture retraining, and upper back strengthening. Physical therapy is recommended—at least two sessions per week for 6 weeks—and encourages a return to independence with regard to mobil- ity and activities of daily living [19]. Sitting out of bed has been shown to be associated with an increase in postoperative func- tional residual capacity [20], and it has been suggested that a program of active enforced progressive mobilization can improve pulmonary function [21]. In the immediate frst period after surgery, it is important to encourage people to move in the right way in order to prevent fear of movement, pain, and lung volume reduction. Changes in body position and physiotherapy aimed to airways clearance are the most necessary interventions. In a second postoperative phase, when the patient has fnally reached stable clinical conditions, it is important to focus on physical activity in order to recover a complete independence in all daily living activities [1, 2, 7, 20, 23–25]. They found out that the sitting and semire- cumbent positions compared with the supine position in six of 12 studies improved postoperative pulmonary function. However, a change from the supine to lateral position in patients in the intensive care unit showed a limited effect on pulmonary function. The duration of the mobilization has not been considered, including repeated measurements over days. The physiologic effects of postoperative immo- bilization have never been thoroughly examined, but are widely supposed to add to thromboembolic and pulmonary complications as well as catabolism and cardiovas- cular instability [27]. Although most agree that postoperative immobilization should be avoided, standard care often includes physiological immobilization for several days [28]. The turning of patients from the supine to lateral position is a routine practice in the postoperative intensive care unit. Despite the lack of evidence of a substantial benefcial effect on pulmonary function revealed in this review, it is still recommended in respect to decubitus prophylaxis and prevention of atelectasis and deep vein thrombosis [27]. The criteria used to assess patient suitability for mobilization are: • Patient awake • Stable blood pressure • Stable heart rate • No dyspnea at rest Pain score <8 on visual analogue scale [2, 7, 24]. No further statistically sig- nifcant increases were observed in these parameters with walking on the spot for 1 min [26].

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Etomidate is also used for trauma patients who are hemodynamically unstable and are often hypovolemic buy trimox from india. It is widely believed that etomidate depresses airway reflexes less than propofol (unless co-administered with another sedative/analgesic agent) discount trimox 500 mg overnight delivery. Etomidate also relaxes the smooth musculature of the pulmonary vasculature system to a similar degree as propofol purchase trimox in india. Etomidate inhibits the activity of the enzyme 11β-hydroxylase and prevents the conversion of cholesterol to cortisol. It has been postulated that one dose is sufficient to transiently suppress the adrenocortical axis. Although35 many studies conclude that there are no direct adverse outcomes following a bolus of etomidate, even in the septic population, other studies propose the36 opposite. However, most practitioners, in an effort to limit this possibility,37 will not administer repeat doses or continuous infusions. Ketamine was discovered in the search for a phencyclidine derivative with similar anesthetic and analgesic properties, but with fewer psychomimmetic effects (Fig. Key features38 associated with ketamine administration included marked nystagmus, significant analgesia, and unconsciousness. Emergence from ketamine anesthesia was associated with emergence delirium, hallucinations, and alterations in mood and affect. The use of ketamine as an anesthetic has been limited by its cardiovascular stimulating properties and the disturbing emergence reactions. The effects of ketamine related to pain can be best described as antihyperalgesic, antiallodynic, or tolerance- protective. More recently, ketamine has gained interest in the treatment of39 major depression, however its clinical effects are of short duration. The S(+) enantiomer of ketamine is three to four times more potent than the R-enantiomer. The high lipid solubility and low protein binding (20%)42 allow for a rapid uptake of ketamine in the brain, as well as a fairly rapid redistribution. The onset of anesthesia after intravenous administration of ketamine is 30 to 60 seconds, with duration of 10 to 15 minutes. The liver extensively metabolizes ketamine by demethylation to its principal metabolite norketamine. Norketamine is biologically active but only has one-third to one-fifth the activity of racemic ketamine. However, ketamine also has clinical effects at opioid, noradrenergic, cholinergic, nicotinic, and muscarinic receptors. Volunteers who were subjected to painful heat stimulation showed a typical pattern of pain activation from the thalamus to the insula, to the cingulate, and ultimately to the prefrontal cortex. There was a dose-dependent reduction in these cerebral activation pathways when volunteers were given ketamine. Activity of the medial thalamic nuclei and medial reticular formation—important relays in nociceptive transmission between the spinal and supraspinal levels—are both depressed. Ketamine binds to μ, δ, and κ opioid receptors; however this does not account for its analgesic effects. The primary analgesic47 mechanism of ketamine is believed to be in the prevention of developing hyperalgesia. Ketamine’s effect on noradrenergic neurons is partly responsible for the hypnotic, psychic, and analgesic effects observed. Clinical Uses 1271 Anesthesia Ketamine administration has been described as causing a dissociative amnestic state. Patients are unconscious with eyes open, maintain spontaneous respiration, and do not react to painful or noxious stimuli. Despite this increased epileptiform activity, there is no clinical evidence of seizure activity or spread of the epileptiform activity to cortical areas. Ketamine anesthesia is associated with profound analgesia that occurs at subanesthetic levels. Induction doses of ketamine are 1 to 2 mg/kg, with an onset of 1 minute and a duration of 10 to 20 minutes. Ketamine administration is associated with an increase in heart rate and blood pressure. Ketamine is therefore a good choice for anesthetic induction in the hemodynamically unstable patient. Ketamine has been compared to etomidate in the unstable patient and has the advantage of not causing adrenal suppression. The increased blood pressure49 and heart rate associated with ketamine may make it unsuitable for some cardiac patients (critical coronary artery disease). Sedation Ketamine has been used to provide sedation to burn patients during wound care. Benefits of ketamine in this patient population include analgesia as well as maintenance of spontaneous respiration and airway reflexes. Ketamine can be administered via intramuscular injection and has been used to provide sedation or anesthesia in uncooperative or hostile patients. Ketamine has also been used in pediatric patients for painful procedures such as reduction and casting of bone fractures in the emergency department. Ketamine has been shown to lower pain scores and decrease opiate requirements in postoperative patients. Administration of both a ketamine bolus prior to surgical incision and a ketamine infusion postoperatively has been found to be the most effective use of ketamine for acute pain. The analgesic effects of ketamine are achieved at subanesthetic blood concentrations. Ketamine reduces opiate requirements for postsurgical pain, but it cannot replace opiates altogether. Ketamine is useful in patients who will require high doses of opiates, such as patients on chronic 1272 opiate therapy or patients with a history of opiate abuse.

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