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Clinical Toxicity the severity and time to manifestation of arsine poisoning depend on the concentration and duration of the exposure generic 150mg irbesartan fast delivery diabetes insipidus ddavp. After an acute massive exposure trusted irbesartan 150mg diabetes diet create your healthy-eating plan, death may occur without the classic signs and symptoms of arsine poisoning generic 300 mg irbesartan visa diabetes awareness ribbon. However cheap irbesartan 300mg without a prescription diabete 2 sintomi, high concentrations of arsine may exceed the binding capacity of the erythrocytes, and the gas may directly damage vital organs. In cases in which signs and symptoms of arsine poisoning develop over time, the associated morbidity and mortality is partly related to the consequences of its hematologic and renal effects. In general, after a significant exposure to arsine, there is usually a delay of 2 to 24 hours before symptoms of arsine poisoning become apparent. Initial complaints include dizziness, malaise, weakness, dyspnea, nausea, vomiting, diarrhea, headache, and abdominal pain. Dark-red discoloration of the urine, hemoglobinuria, and/or hematuria frequently appear 4 to 12 hours after inhalation of arsine. Depending on the severity of the exposure, reddish staining of the conjunctiva and duskily bronzed skin may become apparent within 12 to 48 hours [15]. The triad of abdominal pain, hematuria, and bronze-tinted skin is recognized as a characteristic clinical feature of arsine poisoning [13]. In cases of acute and severe arsine poisoning, exchange transfusion or plasma exchange may be an efficient and effective means of management [13,16,17]. In situations in which there is evidence of renal insufficiency or failure, both exchange transfusion and hemodialysis may be required. Hemolysis due to arsine poisoning can be a dynamic process; there is one report of ongoing hemolysis for at least 4 days in patients not selected for exchange transfusion. Theoretic support for the use of exchange transfusion came from animal studies where a large proportion of the fixed arsenic in the blood of animals poisoned with arsine was in a nondialyzable form, and adequate removal of arsine and its associated toxic complexes would be a problem with hemodialysis alone. It has been suggested that with early diagnosis of arsine poisoning and prompt institution of exchange transfusion, the incidence of renal damage and long-term renal insufficiency may be reduced. However, for the past 20 years, environmental and occupational exposure to lead as well as the severity of lead poisoning have decreased because of government regulations and increased public health awareness of the problems associated with lead, especially at low-concentration exposures. Combustion of leaded gasoline by motor vehicles produced lead in automobile emissions, which is the main source of airborne lead. More than half of the older residential and commercial structures built before 1960 have been painted with lead- based paints. With time, flaking, chipping, peeling, and chalking of the paint occurs—a potential source of lead exposure. High-concentration exposure may result from renovation, sandblasting, torching, or demolition of older applications. Food may be contaminated with lead when it is harvested, transported, processed, packaged, and prepared. Lead exposure may occur from use of lead-glazed pottery or ceramic ware for cooking and eating as well as from the consumption of food from lead-soldered cans. Water from leaded pipes, soldered plumbing, and water coolers is also a potential source of lead exposure. Some traditional Hispanic, Asian, and Middle Eastern folk medicine has been shown to contain significant amounts of lead. Other names such as alarcon, coral, liga, Maria Luisa, and rueda have been given to these lead- containing folk remedies. In Asian communities, lead-containing folk remedies include bali goli, chuifong tokuwan, ghasard, knadu, pay-loo- ah, and Po Ying Tan. Children can ingest chips from lead- painted surfaces, or by mouthing items contaminated with lead from dust, soil, or paint. Another potential source of lead exposure in children is the preparation of infant formulas in vessels with lead solder. One source of lead exposure that is not often considered is retained lead bullets, especially those that are near synovial surfaces. Hobbies and related activities such as home remodeling, target shooting at indoor firing ranges, stained glass making, glazed pottery making, lead soldering, and making illicitly distilled whiskey (“moonshine”) can potentially subject adults and their families to high concentrations of lead. Pharmacology In adults, about 10% of an ingested dose is absorbed, whereas in children, up to 50% may be absorbed. These particles (when inhaled) are returned to the posterior pharynx through ciliary action and swallowed. Dermal absorption of lead is rapid and extensive for alkyl lead compounds, but minimal for inorganic lead. The half-life of lead in the soft tissues is about 40 days, whereas the half-life in bones is 20 to 30 years. The major depot for lead in the body is the skeletal system, which contains more than 90% in adults and more than 70% in children, in terms of the total-body lead burden. The primary sources of lead that cause clinical and subclinical symptoms are the blood and soft tissues. Lead that is deposited and incorporated into the matrix of bone can be mobilized during pregnancy, lactation, osteoporosis, and prolonged immobilization. The kidneys filter lead unchanged (with some active tubular transport at high concentrations), and the excretion rate depends on the glomerular filtration rate and renal blood flow. However, elimination of lead from the body is influenced by the relative concentration of lead in the various body compartments. The multisystemic toxicity of lead is mediated by at least two primary mechanisms: the inhibition of enzymatic processes, sometimes as a result of sulfhydryl group binding, and interaction with essential cations, in particular calcium, zinc, and ferrous iron. Pathologic alterations in cellular and mitochondrial membranes, neurotransmitter biosynthesis and function, heme biosynthesis, and nucleotide metabolism may also occur. One of the principal toxic effects of lead is inhibition of enzymes along the heme biosynthesis pathway. Lead also inhibits the nonenzymatic mobilization of iron stores, which further contributes to the effect of anemia. Impaired heme biosynthesis may have widespread effects because of its impact on the cytochrome systems. However, neither anemia nor basophilic stippling is a sensitive or specific indicator of lead intoxication. Lead-induced anemia results from either a prolonged exposure or a concentrated short-term exposure with a latent period of several weeks. Lead toxicity produces anatomic lesions in the proximal tubule and loops of Henle, which is characterized by round acidophilic intranuclear inclusion bodies. Most often, lead-induced renal injury is associated with prolonged exposure to large amounts of lead, resulting in progressive renal insufficiency. Peripheral nervous system toxicity is known as lead palsy and is due to the degenerative changes in the motoneurons and their axons, with secondary effects involving the myelin sheaths [20]. Clinical Toxicity Poisoning is usually the result of continued exposure to small amounts of lead rather than a single acute event. Usually, the clinical presentation of acute lead toxicity appears to be associated with a sharp incremental rise in the concentration of lead in various soft tissues, and this often occurs against the background of chronic lead poisoning. The multisystemic toxicity of lead presents a spectrum of clinical findings ranging from overt, life-threatening intoxication to subtle, subclinical deficits. Acute ingestion of very large quantities of lead (gram quantities) may cause abdominal pain, toxic hepatitis, and anemia (usually hemolytic).

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For patients in whom it is felt that surgical or endoscopic relief of the bowel obstruction is not feasible buy generic irbesartan 150 mg online type 2 diabetes definition dictionary com, it is reasonable to evaluate them for a percutaneous endoscopic gastrostomy tube placement for gastric drainage buy 300 mg irbesartan amex diabetes mellitus ogtt. Surgical decision-making becomes more challenging for end of life patients who are not stable and require a decision regarding an emergent operation generic 150mg irbesartan with mastercard diabetes prevention program youth. It may be argued that this is not a purely palliative surgery consult as the surgical intervention has the potential to rescue the patient from a life-threatening complication of their life-limiting illness generic 300 mg irbesartan free shipping diabetes type 1 rubber bracelets. On the other hand, it may also be considered palliative as it will not cure the patient of the underlying disease process. Needless to say, this is often an emotionally charged time, even for patients with long-standing illness such as advanced cancer, because they are now faced with the imminent risk of dying. Of the 376 patients who underwent emergency surgery for obstruction, the 30-day mortality rate was 18% with a 41% morbidity rate and 60% were discharged to an institution. While most patients will survive the initial operation, a substantial number will die soon after the surgery and many experience postoperative complications, reoperations, stays in nursing homes, or hospital readmissions. While these data are helpful for surgeons and caregivers to advise patients of the risks of surgery, set expectations for the postoperative experience, discharge location and overall survival, both at the time when the decisions is made for surgery and if complications occur, important data regarding whether the goals of the patients and families were met and whether or not they would make the same choice again are still severely lacking at this time. As with a lower intestinal obstruction, acute symptoms should be initially managed with nasogastric decompression, bowel rest, and intravenous resuscitation, including aggressive electrolyte repletion. Options for managing upper gastrointestinal obstructions include intraluminal stenting, surgical bypass, and decompression gastrostomy with possible feeding jejunostomy. Similar to colonic stenting, the potential benefits of duodenal stenting include immediate palliation of nausea and vomiting with a less invasive procedure than surgical bypass and earlier return to oral nutrition [20,21]. Stenting has been shown to provide a comparable survival outcome and equivalent morbidity and mortality to surgical bypass [22]. In a systematic review of the literature from 1990 to 2008 comparing endoscopic stenting with open surgical bypass, Ly et al. The major limiting factor for the endoscopic approach is being unable to pass the scope through the obstruction. The major complications reported are gastric ulceration, bowel perforation, biliary obstruction, stent dysfunction, and stent migration. Stent placement would be contraindicated in patients with multiple levels of intestinal obstruction and should be considered carefully for patients with peritoneal carcinomatosis who are at risk of more distal obstructions. For patients in whom stenting is not an option, surgical bypass can relieve both the symptoms of the obstruction and allow the patient to resume enteral nutrition. Surgical bypass, most commonly in the form of a gastrojejunostomy, can either be performed laparoscopically or through a relatively small upper midline incision. The estimated risk of morbidity and mortality from these procedures is 25% to 60% and 0% to 25%, respectively [22,23]. While surgical bypass is usually technically successful, patient selection with regard to preoperative nutritional status and life expectancy is imperative to the palliative success of this approach. For example, in addition to general surgical risks such as bleeding or infection, a patient with chronic gastric outlet or duodenal obstruction who is malnourished is at increased risk of a leak from the intestinal anastomosis. Other potential complications specific to gastric bypass include dumping syndrome, alkaline reflux gastritis, and delayed gastric emptying. Placement of a gastrostomy tube for decompression is another option for palliation of gastric outlet, duodenal and nonoperable small bowel obstruction or profound gastrointestinal dysmotility from carcinomatosis. Gastrostomy tubes can be placed either endoscopically, fluoroscopically, or surgically (either laparoscopic or open). Decompression gastrostomy tubes provide patients the ability to drain the stomach as for nausea and to avoid vomiting. Many endoscopists, surgeons, and interventional radiologists are leery of placing gastrostomy tubes in the setting of malignant ascites. They are concerned about the risk of infecting the ascites, intraperitoneal leakage from the stomach due to poor apposition to the anterior abdominal wall, as well as leakage of ascites from around the tube. There is a growing body of literature demonstrating the safety of placing gastrostomy tubes in patients with malignant ascites from a variety of tumors [24–26]. Also, consideration of placing a peritoneal drainage catheter at the time of gastrostomy may also help lower any risk associated with the ascites. As gastrostomy may be the only viable palliative option for these patients, all efforts to manage the ascites and increase the safety of gastrostomy placement are warranted. Unfortunately, while the symptom relief from a paracentesis or thoracentesis is immediately helpful, it is usually temporary. For patients requiring frequent drainage of either the peritoneal or pleural cavity, a tunneled intraperitoneal catheter that can be intermittently connected to a self-contained vacuum drainage system is a helpful option [27]. As there is often no cytoreductive surgery involved, this can be done laparoscopically, which, although less invasive, still does require general anesthesia. Similarly, an alternative treatment option for patients with recurrent malignant pleural effusion is pleurodesis. Pleurodesis can be performed using a number of different agents including talc, chemotherapy, or abrasion. The intent is to create an inflammatory reaction within the pleural cavity resulting in fusion of the visceral and parietal pleura, thereby obliterating the peritoneal space and the opportunity for fluid re- accumulation. Talc has been shown to be the most effective pleurodesis agent in randomized clinical trials with reported success rates of 60% to 90% [30]. However, although these procedures can be done at the bedside, they do require the placement of a larger bore chest tube and can be rather painful [31]. Unlike patients with a bowel obstruction, patients with a perforated viscus are more likely to have pain from peritonitis, adding another element of consideration to both the decision-making process and the emotional charge of the situation. Currently, there is a small, but growing body of literature supporting the use of nonsurgical management for bowel perforation in select (hemodynamically stable, non-peritonitic) patients. Some studies have reported a greater than 90% success rate in nonsurgical management of patients with perforated diverticulitis [32]. Unfortunately, for patients with advanced cancer, who are not stable or who have peritonitis, and who undergo emergent surgery, the outcomes are even worse than for those with a bowel obstruction. Independent preoperative predictors of death at 30 days included renal failure, septic shock, ascites, dyspnea at rest, and dependent functional status. Postoperative respiratory complications and advanced age (greater than 75 years) were also predictors of mortality. Similar to the patients who presented with a bowel obstruction, only 4% had a “do not resuscitate” order in place prior to surgery despite the advanced nature of their cancer. Again, while data from studies like this may help surgeons answer questions about the risks associated with surgical interventions and guide some patients in their decisions, in a society in which people are not prepared for dying, these data can often make things harder for the surgeon who is asked to operate in the face of such overwhelming odds. Professionalism demands that the surgeon make a sincere effort to understand and be understanding of the perspective of the patient and family—without realistic expectation of the same in return. This can be particularly challenging when the surgeon is busy or when these events occur in the middle of the night. In the name of “full disclosure and informed consent,” some surgeons paint as bleak a picture as possible for the patient and family, in an effort to dissuade the patient from choosing surgery.

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Broad-spectrum antibiotic coverage should be followed by pathogen-specific therapy after the causative organism has been identified buy irbesartan 300mg amex diabetes for kids. Failure to substantially improve within 3 days of intensive corticosteroid therapy and within 7 days of rescue therapies is indications for surgery [1 order irbesartan 300 mg with amex diabetic diet 2500 calories,13 generic irbesartan 300 mg with mastercard diabetes diet guidelines after your visit,25 order irbesartan 300mg diabetes symptoms vision,26]. Some physicians actually view early surgical management of toxic megacolon as the conservative approach, noting that delay of operative therapy may promote higher mortality [15,37]. Perforation is associated with severe complications, including peritonitis, extreme fluid and electrolyte imbalance, and hemodynamic instability. Other indications for emergent surgery precluding protracted medical management include signs of septic shock and imminent transverse colon rupture (diameter > 12 cm). Hypoalbuminemia, persistently elevated C-reactive protein or erythrocyte sedimentation rate, small bowel ileus, and deep colonic ulcers are poor prognostic factors for successful medical therapy [17]. Although the surgical management of fulminant colitis is similar to that of toxic megacolon, the absence of acute colonic dilatation may permit delay of surgical intervention. The type of operation performed for treatment of fulminant colitis or toxic megacolon depends on the clinical status of the patient and the experience of the surgeon [3,4,16]. A one-stage procedure that cures ulcerative colitis without the need for a second operation is appropriate for older patients or those not desiring restorative ileal pouch-anal anastomosis. Most surgeons prefer a limited abdominal colectomy with ileostomy, leaving the rectosigmoid as a mucous fistula or the rectum alone, using a Hartmann procedure [3,13]. This approach has the advantages of limiting the lengthy pelvic dissection in acutely ill patients while allowing for the option of a subsequent restorative, sphincter- saving procedure (ileoanal anastomosis) [40]. In patients with indeterminate colitis or Crohn disease, preservation of the rectum may provide the opportunity for an eventual ileorectal or ileoanal anastomosis to preserve anal continence after temporary diversion and pathologic review of the colectomy specimen. The type of operation selected depends on the clinical condition of the patient and the experience of the surgeon [3,37,41]. Regnault H, Bourrier A, Lalande V, et al: Prevalence and risk factors of Clostridium difficile infection in patients hospitalized for flare of inflammatory bowel disease: a retrospective assessment. Pola S, Patel D, Ramamoorthy S, et al: Strategies for the care of adults hospitalized for active ulcerative colitis. Moulin V, Dellon P, Laurent O, et al: Toxic megacolon in patients with severe acute colitis: computed tomographic features. Allez M, Lemann M, Bonnet J, et al: Long term outcome of patients with active Crohn’s disease exhibiting extensive and deep ulcerations at colonoscopy. Ra G, Thanabalan R, Ratneswaran S, et al: Predictors and safety of venous thromboembolism prophylaxis among hospitalized inflammatory bowel disease patients. Ulcerative colitis practice guidelines in adults: American College Of Gastroenterology, Practice Parameters Committee. D’Haens G, Lemmens L, Geboes K, et al: Intravenous cyclosporine versus intravenous corticosteroids as single therapy for severe attacks of ulcerative colitis. Van Assche G, D’Haens G, Noman M, et al: Randomized, double-blind comparison of 4 mg/kg versus 2 mg/kg intravenous cyclosporine in severe ulcerative colitis. Garcia-Lopez S, Gomollon-Garcia F, Perez-Gisbert J: Cyclosporine in the treatment of severe attack of ulcerative colitis: a systematic review. Brandse J, Wildenberg M, de Bruyn J, et al: Fecal loss of infliximab as a cause of lack of response in severe inflammatory bowel disease. Laharie D, Bourreille A, Branche J, et al: Ciclosporin versus infliximab in patients with severe ulcerative colitis refractory to intravenous steroids: a parallel, open-label randomised controlled trial. The rationale for nutrition support comes from the knowledge that critically ill patients are prone to developing malnutrition, which is known to be associated with serious complications such as sepsis and pneumonia, leading to poor outcomes and even death [1]. Early enteral nutrition, within 24 to 48 hours, was recommended for all patients determined to be at risk [3]. Traditional nutritional indicators or surrogate markers are no longer recommended because they have not been validated in critical care. Although guidelines continue to evolve, there are sufficient data on clinically proven principles and methods of nutrition support to permit practical and useful recommendations for the specific problems and questions confronted by the intensivist. Immune modulating enteral formulations should not be used routinely for critically ill patients but may be appropriate for postoperative patients. Antioxidant vitamins and trace minerals, specifically containing selenium, should be given to all critically ill patients receiving nutrition therapy. Protocols to promote moderately strict control of serum glucose levels (150–180 mg/dL) when providing nutrition support are recommended. This response to injury can lead to changes in substrate metabolism, causing alterations in body composition and nutrient deficiencies that become clinically evident [4]. During starvation, the body uses fat and muscle protein as a source of energy in order to preserve visceral protein [5]. Mobilization of fat for fuel is an important adaptive response for survival because glucose stores, in the form of glycogen, provide only 1,200 kcal in the first 24 hours of starvation. The body attempts to use muscle protein rather than visceral protein because visceral protein is essential for vital functions of the body. Because these changes are difficult to assess, intensivists have traditionally used a variety of tools such as clinical, anthropometric, chemical, and immunologic parameters that reflect altered body composition [7]. Nutritional Assessment It is not known how long a critically ill patient can tolerate lack of nutrient intake without adverse consequences, but because critical depletion of lean tissue can occur after 14 days of starvation among severely catabolic patients, it is recommended that nutrition support be instituted for patients who are not expected to resume oral feeding for 7 to 10 days [8]. The need for nutritional support is determined by the balance between endogenous energy reserves of the body and the severity of stress. The best clinical markers of stress are fever, leukocytosis, hypoalbuminemia, and a negative nitrogen balance. The purpose of nutritional assessment is to identify the type and degree of malnutrition to devise a rational approach to treatment. Percentage weight loss during the past 6 months, serum albumin level, and total lymphocyte count are readily available, commonly used measures to assess nutritional status. A 10% or 10-lb weight loss over the previous 12 months is an indicator of protein calorie malnutrition. Normal concentrations of albumin are unattainable for many critically ill patients because of large fluid shifts and inadequate synthesis to meet demands. Malnutrition is most effectively treated by nutrition support and treatment of the stresses that led to this severe catabolic condition. Weight loss of 10 lb or 10% of usual weight is considered clinically important, whereas weight loss of 20% to 30% suggests moderate protein calorie malnutrition and weight loss of greater than 30% suggests severe protein calorie malnutrition. Unfortunately, for many critically ill patients, total body weight is often an insensitive parameter because of progressive total body salt and water retention. Malnutrition is closely correlated with alterations of immune response as measured by skin test reactivity and total lymphocyte count. A total lymphocyte count less than 3 1,000 per mm is indicative of altered immune function and is associated with decreased skin test reactivity. Loss of delayed cutaneous hypersensitivity to common antigens is a measure of impaired cellular immunity, which has been consistently found to be associated with malnutrition [10].

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Safety of bedside percutaneous tracheostomy in the critically ill: Evaluation of more than 3 irbesartan 300 mg free shipping blood glucose quiz,000 procedures purchase 150 mg irbesartan otc signs gestational diabetes pregnancy. Percutaneous dilatational tracheostomy versus surgical tracheostomy in critically ill patients: a systematic review and meta-analysis generic irbesartan 150mg overnight delivery diabetic diet gluten free. Yarmus L buy irbesartan 300 mg visa diabetic diet 1600 calories, Pandian V, Gilbert C, et al: Safety and efficiency of interventional pulmonologists performing percutaneous tracheostomy. Alansari M, Alotais H, Al Aseri Z, et al: Use of ultrasound guidance to improve safety of percutaneous dilatational tracheostomy: a literature review. Guinot P-G, Zogheib E, Petiot S, et al: Ultrasound-guided percutaneous tracheostomy in critically ill obese patients. Belanger A, Akulian J: Interventional pulmonology in the intensive care unit: Percutaneous tracheostomy and gastrostomy. Yarmus L, Gilbert C, Lechtzi N, et al: Safety and feasibility of interventional pulmonologists performing bedside percutaneous endoscopic gastrostomy tube placement. Lichtenstein D, Hulot J-S, Rabiller A, et al: Feasibility and safety of ultrasound-aided thoracentesis in mechanically ventilated patients. In general, stages N1 and N2 are “lighter” than stage N3, which is also known as “slow wave” or “deep” sleep and is believed to play a key role in the body’s restorative processes. Circadian Rhythms Achieving a normal duration and pattern of sleep relies on individual factors such as age, comorbid conditions, intrinsic sleep–wake cycle, volitional control of sleep duration, and drugs, along with environmental factors such as ambient temperature, noise, and light [2]. The sleep– wake cycle is regulated through two complementary processes, the sleep homeostat and circadian pacemaker. As an opposing process, the circadian pacemaker, or process C, dictates wakefulness and is largely synchronized to environmental light– associated suppression of melatonin release from the pineal gland. Thermoregulation Sleep and circadian rhythms play an integral role in body temperature and thermoregulation. In healthy adults, body temperature peaks late in the day, falls during sleep, nadirs late in sleep, and rises before awakening. Respiratory Processes N1 sleep is characterized by decreased respiratory drive and muscle activity, irregular breathing, and increased upper airway collapsibility. This hypoventilation is believed to occur in the setting of decreased central ventilatory drive, upper airway muscle relaxation, and increased airway resistance [1]. Cardiovascular Processes Alterations of blood flow and electrical activity that occur during sleep can increase one’s risk of life-threatening cardiovascular events, especially in those with diminished cardiorespiratory reserve [4]. Alternatively, cortisol, a key hormone involved in glucose metabolism, stress, and wound healing, follows a diurnal cycle, rising in the morning and falling toward bedtime. Lines represent levels of melatonin, cortisol, growth hormone, prolactin, and thyroid- stimulating hormone across the sleep–wake cycle. Regardless of sedation or mechanical ventilation status, critically ill patients experience marked variability in sleep duration, with reported ranges of 3. In a notable study involving polysomnographic recordings from 22 critically ill patients, of whom 20 were mechanically ventilated, patients averaged 41 ± 28 episodes of sleep per 24-hour period, each averaging 15 ± 9 minutes, highlighting the profound level of sleep fragmentation in this population [12]. Actigraphy Actigraphy, which involves accelerometer-based sleep estimation using a wristwatch-like interface, is a well-established research instrument. Despite their low cost and ease of use, these instruments are potentially limited by recall bias, rater fatigue across repeated daily assessments, noncompliance, impaired patient cognition or consciousness, and lack of daytime sleep ratings. This study also noted that although staff conversations were loudest in the rooms of the sickest patients, they were often unrelated to patient care and held directly over patients under the assumption that sedation rendered patients unaware of their surroundings. When light levels falls below 100 lux (normal indoor light ~180 lux), melatonin is secreted from the pineal gland, promoting sleep. Independent of light levels, impaired melatonin secretion has been described in patients with sepsis [63] and delirium [64,65], suggesting that factors other than light influence circadian rhythms in the critically ill. Patient Care Interactions Although difficult to measure accurately, critically ill patients experience approximately 7. These interactions include care- related activities such as vital sign checks, blood draws, medication administration, radiographs, baths, wound care, respiratory care (e. Efforts to minimize patient care interactions should involve engagement of staff to evaluate the timing and necessity of interactions during patient sleep. When quantified, patients receiving mechanical ventilation average 20 to 63 sleep arousals per hour [8–12], which can be precipitated by issues related to patient-ventilator synchrony, or by noxious factors associated with mechanical ventilation, such as suctioning, repositioning, ventilator alarms, physical restraints, provider assessments, and discomfort from endotracheal, nasogastric, or orogastric tubes. As important limitations, the authors acknowledged the small sample size and single-site design of the included studies. Hence, until larger multisite trials are performed, practitioners should adopt an individualized approach to ventilator management during sleep, and consider use of less conventional ventilator modes to optimize patient- ventilator synchrony. Additionally, agents such as dexmedetomidine and propofol, which have gained popularity as less deliriogenic non-benzodiazepine sedative options [34,80–82], may also contribute to fragmented sleep [83] but are considered less disruptive to sleep than benzodiazepines and opioids [80,81,84,85]. Until research expands in this area, practitioners should aim to administer minimal or no sedation and perform daily interruptions of sedation, consistent with current guidelines [34], as a strategy to minimize sedation-related disruptions to sleep architecture. However, in critically ill patients with various types and degrees of shock, it is unclear to what extent these drugs penetrate the blood–brain barrier [79]. Abrupt discontinuation of prolonged, high-dose opioid and benzodiazepine infusions may precipitate sleep disruptions and insomnia, lending further support to strategies for sedation minimization, daily sedation interruption, and gradual tapering of prolonged sedation [79]. Finally, withdrawal from alcohol, nicotine, and illicit drugs such as cannabis and amphetamines can lead to profound insomnia and sleep disruption, and, in extreme cases, delirium [79]. Additionally, antihistamines such as diphenhydramine and doxylamine, commonly found in over-the-counter sleep preparations, can be oversedating and deliriogenic, particularly among the elderly. Although the sickest patients likely deserve and theoretically should experience the most restorative sleep, studies on the association of severity of illness and sleep architecture are limited. Nevertheless, critically ill patients with sepsis have demonstrated perturbed melatonin levels, suggesting poorer sleep quality in this population [63]. Finally, critically ill patients often experience pain, which has been shown to contribute to arousals, sleep fragmentation, and reduced total sleep time [7,8]. From a cardiovascular standpoint, during sleep deprivation, a surge in sympathetic tone and catecholamine release can lead to blood pressure, heart rate lability, and an elevated risk of myocardial ischemia [4]. Immunologic Consequences It is a popular belief that proper sleep is necessary to prevent and fight infection. At an extreme level, animal studies have demonstrated that profound sleep deprivation leads to an immunocompromised state, with decreased lymphocytes, leukocytes, and spleen weight, followed by septicemia and death [4]. Although studies in humans have fortunately not produced similar results, they have instead yielded some more complex ones. For example, although multiple studies have demonstrated that sleep-deprived individuals have an attenuated response to vaccination and alterations in markers and modulators of immunity, these data are inconsistent and are not supported by microbiologic studies [4]. Although notable, the mechanisms and implications surrounding these alterations are poorly understood and have not been studied in the critically ill. Finally, sleep restriction has been shown among healthy subjects to blunt insulin secretion, decrease sensitivity to insulin, and impair glucose regulation [4]. How these alterations impact the critically ill, who often develop hyperglycemia and suffer adverse consequences from it [95], is unclear, and represents another important area of investigation. Mobility-Related Consequences Prolonged immobilization is common during critical illness and contributes to short- and long-term physical, functional, and cognitive impairments, along with early death [96,97]. Delirium and Other Consequences Delirium affects up to 80% of critically ill patients and has been shown in numerous studies to be associated with devastating short- and long-term outcomes including prolonged mechanical ventilation and length of stay, cognitive and physical disability, and early death [104].

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