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1
Weinhouse, Gerald L., and John W. Devlin, eds. Sleep in Critical Illness. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-06447-0.
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C, Parsons Lynn, Lehman Cheryl, and Prevost Suzanne S, eds. Rehabilitation after critical illness. Philadelphia: W.B. Saunders, 2001.
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Galley, Helen F. Cardiology in critical illness. Edited by NetLibrary Inc and Intensive Care Society of the United Kingdom. London: BMJ Books, 2001.
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W, Ryan David, ed. Current practice in critical illness. London: Chapman & Hall, 1996.
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Rombeau, J. L., and J. Takala, eds. Gut Dysfunction in Critical Illness. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80224-9.
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Stevens, Robert D., Tarek Sharshar, and E. Wesley Ely, eds. Brain Disorders in Critical Illness. Cambridge: Cambridge University Press, 2013. http://dx.doi.org/10.1017/cbo9781139248822.
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Wijdicks, Eelco F. M., 1954-, ed. Neurologic complications of critical illness. 2nd ed. Oxford: Oxford University Press, 2002.
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L, Rombeau John, and Takala J. 1953-, eds. Gut dysfunction in critical illness. Berlin: Springer, 1996.
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A, Cynober Luc, and Moore Frederick A. 1953-, eds. Nutrition and critical care. Basel: Karger, 2003.
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S, Wheeler Derek, Wong Hector R. 1963-, and SpringerLink (Online service), eds. Cardiovascular Pediatric Critical Illness and Injury. London: Springer-Verlag London, 2009.
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Wise, Matt, and Paul Frost. Critical illness. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0147.
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Critical illness can be considered to be any disease process which causes physiological instability that leads to disability or death within minutes or hours. Fortunately, physiological instability associated with critical illness is easily detected by perturbations of simple clinical observations such as blood pressure, heart rate, respiratory rate, oxygen saturations, level of consciousness, and urine output. Individual abnormalities in these observations are sensitive for the presence of critical illness but non-specific. Specificity for critical illness improves as the number of abnormal clinical observations increases. Over recent years, a greater appreciation of the importance of deviations in simple clinical observations as a method of detecting critical illness has led to the development of a number of ‘early warning’ or ‘track and trigger’ systems. These systems attribute a score according to the magnitude and number of abnormal observations that are present, and a high score prompts immediate medical review. Although intuitively sensible, the evidence that these systems are effective in ameliorating or preventing critical illness is currently lacking. This chapter looks at the approach to diagnosis of critical illness, including the pitfalls in diagnosis.
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Current Practice in Critical Illness: Volume II (Current Practice in Critical Illness). A Hodder Arnold Publication, 1997.
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Current Practice in Critical Illness: Volume III (Current Practice in Critical Illness). A Hodder Arnold Publication, 1999.
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Ryan, D. W. Current Practice in Critical Illness. Hodder Education Group, 2001.
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Hough, Catherine L. Chronic critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0377.
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Chronic critical illness (CCI) is common and describes a state of prolonged critical illness, in which patients have persisting organ failures requiring treatment in an intensive care setting. There are many different definitions of CCI, with most including prolonged (> 96 hours) mechanical ventilation. Advanced age, higher severity of illness, and poor functional status prior to critical illness are all important risk factors, but prediction of CCI is imperfect. Although requirement for mechanical ventilation is the hallmark, CCI encompasses much more than the respiratory system, with effects on metabolism, skin, brain, and neuromuscular function. During CCI, patients have a high burden of symptoms and impaired capacity to communicate their needs. Mortality and quality of life are generally poor, but highly variable, with 1-year mortality over 50% and most survivors suffering permanent cognitive impairment and functional dependence. Patients at highest and lowest risk for mortality can be identified using a simple prediction rule. Caring for the chronically critically ill is a substantial burden both to patients’ families and to the health care system as a whole. Further research is needed in order to improve care and outcomes for CCI patients and their families.
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Critical illness cover. London: Mintel International Group Limited., 2002.
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Mulryan, Chris. Acute Illness Management. SAGE Publications, Limited, 2011.
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Mulryan, Chris. Acute Illness Management. SAGE Publications, Incorporated, 2011.
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19
Fullerton, James N., and Mervyn Singer. Oxygen in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0032.
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Oxygen therapy is primarily administered to alleviate arterial hypoxaemia and tissue hypoxia, and to facilitate aerobic cellular respiration. Hypoxaemia (PaO2 < 8 kPa [60 mmHg], SaO2 <92%) is associated with end-organ damage and adverse clinical outcomes, serving as a proxy measure for reduced intracellular PO2. Increasing the fraction of inspired oxygen should form part of an overall strategy to maximize tissue oxygen delivery. Permissive hypoxaemia represents a valid treatment strategy in a selected patient cohort. Oxygen is a drug and oxygen therapy is not benign, and oxygen administration at high, sustained doses (FiO2 >0.5, >12 hours) may cause oxygen toxicity. Observational studies in both mechanically-ventilated patients and survivors of non-traumatic cardiac arrest indicate an independent association between increasing hyperoxaemia and mortality. Oxygen therapy may additionally precipitate hypercapnic ventilatory failure in those at risk and oxygen should be administered to achieve a prescribed target SaO2 or PaO2 range, via adjustment of dose and delivery device. If no monitoring is available, hypoxaemia should be avoided by giving high-flow oxygen to achieve a FiO2 of near 1.0 with subsequent titration once oxygenation status is established.
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Dhand, Rajiv, and Michael McCormack. Bronchodilators in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0033.
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Inhaled beta-agonists and anticholinergic agents, as well as systemically administered methylxanthines, are frequently employed to achieve bronchodilation in critically-ill patients. Inhaled agents are given by pressurized metered dose inhaler (pMDI), nebulizer, or dry powder inhaler. In ventilator-supported patients, aerosolized agents are generally only administered by pMDI or nebulizer. The ventilator circuit, artificial airway, and circuit humidity complicate the delivery of aerosolized agents, and there is a wide variability in drug delivery efficiency with various bench models of mechanical ventilation. Aerosolized drug by pMDI is affected by the use of spacer devices, synchronization of pMDI actuation and ventilator breath delivery, and appropriate priming of the pMDI device. The efficiency of aerosolized drug delivery by jet nebulization is also affected by device placement in the circuit, as well as by a number of other factors. Several investigators have demonstrated comparable efficiency of aerosol delivery with mechanically-ventilated and ambulatory patients when careful attention is given to the technique of administration. Appropriate administration of aerosolized bronchodilators in patients receiving invasive or non-invasive positive pressure ventilation produces significant therapeutic effects.
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De Backer, Daniel, and Patrick Biston. Vasopressors in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0034.
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Vasopressors are used in various shock states to correct hypotension, aiming at restoring or improving organ and tissue perfusion. Vasopressor therapy may be associated with excessive vasoconstriction, but also metabolic and other side-effects. Hence, the ideal target for arterial pressure remains undetermined. Adrenergic agents remain the most commonly used vasopressor agents. Adrenergic agents increase arterial pressure through stimulation of alpha-adrenergic receptors. The effects of the different adrenergic agents differ mostly due to variable associated beta-adrenergic effects. Epinephrine and norepinephrine are strong and equipotent vasopressor agents. Their impact on outcome is as yet unanswered, but there is no sign that epinephrine might be associated with better outcomes. Accordingly, norepinephrine is the adrenergic agent of choice, especially in patients with cardiogenic shock. Vasopressin is a non-adrenergic vasopressor acting via V1 receptor stimulation, with weak vasopressor effects in normal conditions, but markedly increased vascular tone in shock states, especially in septic shock. Splanchnic vasoconstriction may occur. Arginine vasopressin at low doses appears to be a promising alternative to adrenergic agents, but its exact place is not yet well defined.
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Groeneveld, A. B. J., and Alexandre Lima. Vasodilators in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0035.
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Vasodilators are commonly used in the intensive care unit (ICU) to control arterial blood pressure, unload the left or the right heart, control pulmonary artery pressure, and improve microcirculatory blood flow. Vasodilator refers to drugs acting directly on the smooth muscles of peripheral vessel walls and drugs are usually classified based on their mechanism (acting directly or indirectly) or site of action (arterial or venous vasodilator). Drugs that have a predominant effect on resistance vessels are arterial dilators and drugs that primarily affect venous capacitance vessels are venous dilators. Drugs that interfere with sympathetic nervous system, block renin-angiotensin system, phosphodiesterase inhibitors, and nitrates are some examples of drugs with indirect effect. Vasodilator drugs play a major therapeutic role in hypertensive emergencies, primary and secondary pulmonary hypertension, acute left heart, and circulatory shock. This review discusses the main types of vasodilators drugs commonly used in the ICU.
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Patel, Mayur B., and Pratik P. Pandharipande. Analgesics in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0043.
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Analgesia is a critical component of intensive care unit (ICU) care. Accordingly, understanding the mechanism, physiological consequences, and assessment of pain is important when caring for the ICU patient. Non-pharmacological approaches should be attempted before supplementing analgesia with pharmacological agents. Pharmacologically-based therapies are divided into regional and systemic therapies. Regional analgesic therapies target specific areas of the body while limiting the systemic effects of intravenous analgesics, but at the risk of invasiveness, local anaesthetic toxicity, and infection of in-dwelling catheters. Systemic analgesic therapy is comprised of two main categories—non-opioids and opioids. Typically, non-opioid analgesics are used as adjunctive therapies and consist of agents such as non-steroidal anti-inflammatory drugs, gabapentinoids, ketamine, or α2 agonists. Opioid analgesia in the ICU is commonly infusion-based using fentanyl, hydromorphone, morphine, or recently, remifentanil.
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Beach, Scott R., and Theodore A. Stern. Antidepressants in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0044.
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Selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs), and atypical antidepressants are considered first-line agents for depression in the intensive care unit (ICU) setting, and are preferred over older antidepressants due to their more benign side effect profile and tolerability. This chapter reviews the literature on the use of antidepressants in the ICU. Common side effects of SSRIs include insomnia and gastrointestinal discomfort, while citalopram may uniquely cause prolongation of the QTc interval. All SSRIs carry a risk for the development of serotonin syndrome following overdose. SNRIs are similar to SSRIs in their side effect profile, although they are more likely to cause hypertension. Mirtazapine is strongly associated with sedation and weight gain. Stimulants may also be used to treat depression in the medically ill, and can be particularly effective in treating apathy, low energy, and loss of appetite. Monotherapy is typically the initial treatment strategy and low doses are generally recommended in the ICU setting. Efficacy may not be apparent for up to 8 weeks. Patients who have been taking an antidepressant prior to their arrival in the ICU should continue on the medication so as to prevent discontinuation syndrome. Delirium may warrant cessation of the antidepressant and potentially dangerous medication interactions also need to be evaluated. At present, there is no evidence to suggest that an antidepressant should be initiated after a significant physical or emotional trauma.
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Keh, Didier. Steroids in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0054.
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The benefit of prolonged application of moderate-dose corticosteroids in systemic inflammatory diseases remains controversial. In critical illness, the endogenous cortisol effect may become insufficient due to adrenal dysfunction and corticosteroid resistance to counterbalance an exaggerated and protracted inflammatory response, which has been termed ‘critical illness-related corticosteroid insufficiency’ (CIRCI). There is evidence that moderate-dose hydrocortisone (200–300 mg/day) significantly fastens shock reversal in patients with septic shock, but may improve survival probably only in patients with high risk of death. Thus, therapy should be considered only in refractory shock with poor response to fluid administration and vasopressor therapy. The indication should be based on clinical judgement and not on cortisol measurement. The application prolonged of moderate-dose methylprednisolone (1 mg/kg/day) was found to be most effective in early acute respiratory distress syndrome, and associated with improved lung function, reduction of mechanical ventilation, and faster discharge from the ICU, but a survival benefit was found only in pooled data, including cohort studies. A continuous infusion and weaning of corticosteroids may be preferable to bolus applications and abrupt withdrawal to avoid side effects such as rebound of inflammation and shock, glucose variability, or respiratory failure. There is currently no evidence that prolonged application of moderate-dose corticosteroids increase the risk of secondary infections or muscle weakness, but infection surveillance should be implemented and combination with muscle relaxants be avoided.
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Volk, Hans-Dieter, and Levent Akyüz. Immunotherapy in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0055.
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Immunotherapy in critically-ill patients is only feasible at clinical experimental level; no therapy has been approved so far. To develop a potential therapeutic strategy we need to know the pathogen, immune status of the patient, and interaction between the particular pathogen and immune cells to readjust the patient´s individually imbalanced immunological responsiveness. Giving the right treatment at the right time is crucial for a better outcome and the best economic use of resources. The process starts by matching the therapeutic selection to the clinical need. Personalized immunotherapy, highly dependent on the available biomarker, is required. Future studies on new immunotherapeutic approaches in critically-ill patients can only be interpreted in combination with immunological biomarker analyses. Immune modulation is a promising approach despite many disappointing results and there is a clear need for immunological stratification of critically-ill patients for improved efficacy. The search continues for new clinical endpoints in surviving patients with medical and health-economical impact.
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Webb, Andrew. Colloids in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0056.
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Colloid solutions are homogenous mixtures of large molecules suspended in a crystalloid solution. The efficacy of colloids as volume substitutes or expanders, and length of effect are determined by their physicochemical properties. Smaller volumes of colloid than crystalloid are required for resuscitation. The primary use of colloids is in the correction of circulating volume. Rather than using fixed haemodynamic endpoints, fluid can be given in small aliquots with assessment of the dynamic haemodynamic response to each aliquot. The aim of a fluid challenge is to produce a small, but significant (200 mL) and rapid increase in plasma volume with changes in central venous pressure or stroke volume used to judge fluid responsiveness. Colloid fluids give a reliable increase in plasma volume to judge fluid responsiveness.
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Raghunathan, Karthik, and Andrew Shaw. Crystalloids in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0057.
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‘Crystalloid’ refers to solutions of crystalline substances that can pass through a semipermeable membrane and are distributed widely in body fluid compartments. The conventional Starling model predicts transvascular exchange based on the net balance of opposing hydrostatic and oncotic forces. Based on this model, colloids might be considered superior resuscitative fluids. However, observations of fluid behaviour during critical illness are not consistent with such predictions. Large randomized controlled studies have consistently found that colloids offer no survival advantage relative to crystalloids in critically-ill patients. A revised Starling model describes a central role for the endothelial glycocalyx in determining fluid disposition. This model supports crystalloid utilization in most critical care settings where the endothelial surface layer is disrupted and lower capillary pressures (hypovolaemia) make volume expansion with crystalloids effective, since transvascular filtration decreases, intravascular retention increases and clearance is significantly reduced. There are important negative consequences of both inadequate and excessive crystalloid resuscitation. Precise dosing may be titrated based on functional measures of preload responsiveness like pulse pressure variation or responses to manoeuvres such as passive leg raising. Crystalloids have variable electrolyte concentrations, volumes of distribution, and, consequently variable effects on plasma pH. Choosing balanced crystalloid solutions for resuscitation may be potentially advantageous versus ‘normal’ (isotonic, 0.9%) saline solutions. When used as the primary fluid for resuscitation, saline solutions may have adverse effects in critically-ill patients secondary to a reduction in the strong ion difference and hyperchloraemic, metabolic acidosis. Significant negative effects on immune and renal function may result as well.
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Ostermann, Marlies, and Ruth Y. Y. Wan. Diuretics in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0058.
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Fluid overload and chronic hypertension are the most common indications for diuretics. The diuretic response varies between different types and depends on underlying renal function. In patients with congestive heart failure, diuretics appear to reduce the risk of death and worsening heart failure compared with placebo, but their use in acute decompensated heart failure is questionable. Diuretics are also widely used in chronic kidney disease to prevent or control fluid overload, and treat hypertension. In acute kidney injury, there is no evidence that they improve renal function, speed up recovery, or change mortality. In patients with chronic liver disease and large volume ascites, paracentesis is more effective and associated with fewer adverse events than diuretic therapy, but maintenance treatment with diuretics is indicated to prevent recurrence of ascites. Mannitol has a role in liver patients with cerebral oedema and normal renal function. The use of diuretics in rhabdomyolysis is controversial and restricted to patients who are not fluid deplete. In conditions associated with resistant oedema (chronic kidney disease, congestive heart failure, chronic liver disease), combinations of diuretics with different modes of action may be necessary. Diuresis is easier to achieve with a continuous furosemide infusion compared with intermittent boluses, but there is no evidence of better outcomes. The role of combination therapy with albumin in patients with fluid overload and severe hypoalbuminaemia is uncertain with conflicting data.
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Baldwin, Matthew, and Hannah Wunsch. Mortality after Critical Illness. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0003.
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Many critically ill patients now survive what were previously fatal illnesses, but long-term mortality after critical illness remains high. While study populations vary by country, age, intervention, or specific diagnosis, investigations demonstrate that the majority of additional deaths occur in the first 6 to 12 months after hospital discharge. Patients with diagnoses of cancer, respiratory failure, and neurological disorders leading to the need for intensive care have the highest long-term mortality, while those with trauma and cardiovascular diseases have much lower long-term mortality. Use of mechanical ventilation, older age, and a need for care in a facility after the acute hospitalization are associated with particularly high 1-year mortality among survivors of critical illnesses. Due to challenges of follow-up, less is known about causes of delayed mortality following critical illness. Longitudinal studies of survivors of pneumonia, stroke, and patients who require prolonged mechanical ventilation suggest that most debilitated survivors die from recurrent infections and sepsis. Potential biologic mechanisms for increased risk of death after a critical illness include sepsis-induced immunoparalysis, intensive care unit-acquired weakness, neuroendocrine changes, poor nutrition, and genetic variance. Studies are needed to fully understand how the severity of the acute critical illness interacts with comorbid disease, pre-illness disability, and pre-existing and acquired frailty to affect long-term mortality. Such studies will be fundamental to improve targeting of rehabilitative, therapeutic, and palliative interventions to improve both survival and quality of life after critical illness.
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Allison, Teresa A., Karen Berger, Kathleen A. Bledsoe, Jennifer Bushwitz, Amber Castle, Katleen Chester, Aaron M. Cook, et al. Neuropharmacotherapy in Critical Illness. Edited by Gretchen Brophy. Rutgers University Press, 2017. http://dx.doi.org/10.36019/9780813584706.
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Berger, Karen, Gretchen Brophy, Teresa A. Allison, Kathleen A. Bledsoe, and Jennifer Bushwitz. Neuropharmacotherapy in Critical Illness. Rutgers University Press, 2018.
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Neuropharmacotherapy in Critical Illness. Rutgers University Press, 2018.
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Berger, Karen, Gretchen Brophy, Teresa A. Allison, Kathleen A. Bledsoe, and Jennifer Bushwitz. Neuropharmacotherapy in Critical Illness. Rutgers University Press, 2018.
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Neurology of critical illness. Philadelphia: F.A. Davis, 1995.
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Acute Illness Management. SAGE Publications, Limited, 2011.
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Acute Illness Management. SAGE Publications, Limited, 2011.
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Endocrinology of Critical Illness, Critical Care Clinics. Saunders, 2006.
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Colebourn, Claire, and Jim Newton. Valve disease in critical illness. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757160.003.0005.
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This chapter describes the pathophysiology and methods of assessment of valve lesions affecting the aortic and mitral valves. It describes the management of these valve lesions in the critical care setting and guides decision-making about the impact of the valve lesion on the critical illness. The diagnosis and management of infective endocarditis are described in detail.
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Fowler, Robert, and Abhijit Duggal. Management of pandemic critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0009.
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Adequate and appropriate provision of critical care services during pandemics may dramatically alter vital outcomes of patients who develop acute respiratory distress syndrome and critical illness. Specific anti-viral therapy, antibiotics directed towards probable secondary infections, supportive ventilation and oxygenation, and adherence to multisystem critical care ‘best practices’ can prevent substantial mortality and morbidity, and lessen the pandemic’s impact on global health. However, severe acute respiratory syndrome and the 2009 H1N1 pandemic also highlighted the limited capacity for increased provision of critical care, even in well-resourced settings, and the potential for dramatic differences in mortality in under-resourced settings. Pandemic preparedness hinges on the development of appropriately-trained staff with well-defined roles, and the ability to manage surge in the number of patients. A rigorous infection control programme, and triage protocols based on equitable distribution of resources and ethical principles of justice, beneficence and non-maleficence. Research preparedness, with approved protocols, electronic case report forms and harmonized clinical trials is necessary.
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Fayssoil, Abdallah, and Djillali Annane. Inotropic agents in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0036.
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Inotropes are drugs commonly used in the intensive care unit. This class of agents includes a broad variety of molecules that improve cardiac index by increasing intracellular concentrations of cyclic AMP, or sensitivity to intracellular calcium, or by inhibiting the sodium/potassium pump. The main inotropic agents available are digoxin, catecholamines, and non-catecholergic drugs, e.g. phosphodiesterase inhibitors and levosimendan. In practice, dobutamine, a beta1 and beta2 agonist, is the inotrope of choice in patients with acute heart failure, or in patients with severe sepsis and evidence for left ventricle dysfunction. Levosimendan may be an alternative choice in patients with severe heart failure, particularly for those previously treated with beta-blockers. The main serious adverse events related to any inotrope are life-threatening arrhythmias.
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LeMaitre, John, and Jan Kornder. Anti-arrhythmics in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0038.
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Anti-arrhythmic drugs (AADs) are an important component of the pharmacological arsenal used in the management of the critically-ill patient. The benefits of AADs, as well as their potential disadvantageous side effects, largely depend on their effects upon the cardiac action potential. AADs can be broadly grouped according to their cellular actions, upon which their clinical effects depend. However, there is substantial cross-over amongst the groups in terms of these actions and efficacy for particular arrhythmias, and also for side effects. Amiodarone exhibits a broad spectrum of antiarrhythmic activity and is often the most useful AAD for the critically-ill patient where short-term use reduces concerns relating to toxic side effects associated with chronic administration. However, each of the other available AADs have their uses for particular scenarios in the critically-ill patient, although attention needs to be paid to comorbidities to attenuate the risk of adverse response. AADs are pro-arryhthmic in 5-10% of patients with potential lethal consequences, and the use of AADs in the critically-ill patient should be considered very carefully as correction of the underlying substrate may be sufficient in some circumstances to resolve the index arryhthmia.
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Chousterman, Benjamin, and Didier Payen. Pulmonary vasodilators in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0039.
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Pulmonary vasodilators (PV) are commonly used in the intensive care unit (ICU) to treat pulmonary hypertension and/or hypoxaemia. The choice of drug is based on its pharmacokinetic and pharmacodynamic properties. The inhaled route of administration is preferred to treat hypoxaemia as it improves the ventilation/perfusion ratio. Systemic administration of PVs can lead to a decrease of mean arterial pressure and a worsening of hypoxaemia. Despite their beneficial effects, PVs have not shown improvement in mortality in acute respiratory distress syndrome patients. Rebound of hypoxaemia and/or pulmonary arterial hypertension should be prevented during PV treatment discontinuation with a slow de-escalation protocol. This chapter reviews the use of the main PV available for use in the ICU.
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Pollandt, Sebastian, and Lori Shutter. Antiseizure agents in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0045.
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Seizures are a common problem in intensive care units (ICU) and the advent of continuous electroencephalography is demonstrating that the incidence of seizures is still underestimated. Many patients considered encephalopathic from any cause are now found to be in non-convulsive status epilepticus. While the significance of non-convulsive seizures remains unclear, there is little disagreement that these seizures should be treated with antiseizure agents and prevention of any type of seizure is a reasonable therapeutic goal. Many antiseizure agents have been studied in ICU populations and extensive experience exists with drugs such as phenytoin, valproate, or pentobarbital. Since the previous edition of this textbook, several new antiseizure agents have been introduced. Levetiracetam, topiramate, and lacosamide have been established as reasonable pharmacologic options, in particular for treatment of status epilepticus. Patients with seizures in the ICU often present with challenging clinical scenarios, which influence the choice of antiseizure agents. For example, reduced liver or renal function, especially if needing continuous renal replacement therapy or intermittent haemodialysis, has an impact on drug level variability and susceptibility to seizure development. ICU patients will typically require a multitude of pharmacological agents for their specific clinical situation and drug–drug interactions must be considered. Additionally, many medications used in ICUs are associated with seizures, in particular, certain antibiotics. Overall, the development of new drugs and better monitoring methods will undoubtedly improve our ability to control seizures in ICU patients, but currently no treatment has been shown to be universally effective for challenges, such as refractory status epilepticus.
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Pollard, Brian J. Muscle relaxants in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0047.
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The place of neuromuscular blocking agents in the intensive care unit (ICU) has changed markedly over the last 20 years. Originally regarded as a mainstay of the process of ‘sedation’, they are now only used for specific indications. The principal disadvantage is probably the difficulty in neurological assessment when a muscle relaxant is used coupled with the increased risk of awareness, because inadequate sedation will be masked. Of the available agents, the intermediate acting ones are the most popular. The degree of relaxation can be readily controlled and they have few side effects. In the presence of renal and/or hepatic disease atracurium or cisatracurium are preferred. Succinylcholine is only used for securing the airway due to its very rapid onset of action. Rocuronium given in a higher dose also possesses a rapid onset in situations when succinylcholine might be contraindicated. When using a muscle relaxant, its effect should always be monitored with a simple train of four pattern of stimulation from a hand-held nerve stimulator. This will ensure that an adequate and not excessive block is secured. If a more rapid reversal is required then a dose of neostigmine with glycopyrrolate may be used. Alternatively, if rocuronium is the relaxant in use then the new agent sugammadex is effective.
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Perrott, Jerrold L., and Steven C. Reynolds. Neuroprotective agents in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0048.
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The prevention and reduction of secondary injury following primary CNS insult is an important goal in critically-ill patients. Numerous pharmacological therapies have been studied as potential neuroprotective agents with few translating from research to clinical benefit. These are nimodipine and statins in aneurysmal subarachnoid haemorrhage and phenytoin in traumatic brain injury. Additionally, in traumatic brain injury, clinical studies have identified that corticosteroids and albumin colloid resuscitation are associated with increased risk of mortality, and as such should be avoided. Future research into new pharmacological neuroprotective strategies is warranted.
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Cooper, Mark S. Hormone therapies in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0049.
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A range of hormonal manipulations have been proposed as adjunctive therapy during critical care. These therapies might be used to treat a pre-existing or acquired hormonal disorder. Additionally, hormonal manipulation has been suggested to alter the long-term outcome of critical illness, even in patients without structural abnormalities of endocrine glands. Currently, the effectiveness of these anabolic therapies has not been established and they might be harmful in some patient groups. Recently, it has been recognized that many critically-ill patients have low levels of vitamin D and this is associated with an adverse outcome. It is still unclear whether replacement of vitamin D will be effective in improving outcome. This chapter will also highlight the importance of recognizing and addressing hormonal deficiency in patients with known pituitary disease and with traumatic brain injury (TBI). TBI is associated with a high prevalence of acute and long-term pituitary dysfunction. The management of the rare, but important thyroid disorders requiring critical care, thyroid storm, and myxoedema coma, will also be discussed.
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Hunt, Beverley J. Haemostatic agents in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0052.
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Antifibrinolytics can prevent excessive bleeding during surgery and are also used to reduce established bleeding. By blocking the effects of plasmin, they prevent premature clot breakdown and enhance clot stability. The CRASH-2 trial showed that use of tranexamic acid in those with or at high risk of traumatic haemorrhage reduced mortality by 9%. Importantly for a drug that affects haemostasis, there appears to be no increased risk of either arterial or venous thromboembolism. Aprotinin while an excellent agent in reducing bleeding disproves previous assumption that reducing bleeding improves outcome, for the BART study demonstrated an increased mortality compared with tranexamic acid and EACA. It is still used occasionally in very high risk cardiac surgery patients. DDAVP (desmopressin) stimulates platelet function and is of use in patients with uraemia, although needs to be given with an antifibrinolytics, because it does also stimulate fibrinolytic activity. Off-license use of rVIIa is waning, clinical trials have as yet failed to show major benefit. Moreover, there is a high rate of arterial thrombosis after using rVIIA.
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Wilson, A. P. R., and Preet Panesar. Antimicrobial drugs in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0053.
Full textAbstract:
The pharmacokinetics of antimicrobials are altered in critically-ill patients, particularly in the presence of renal or hepatic failure. Maintaining a choice or diversity of antibiotics is important due to the emergence of resistance. Antibiotic use should also be kept to the minimum and local protocols need to be established. For community-acquired infection, co-amoxiclav or a parenteral cephalosporin can be used, while for hospital-acquired infection, piperacillin/tazobactam, ciprofloxacin, or ceftazidime are recommended. For suspected vascular catheter infection or methicillin-resistant Staphylococcus aureus (MRSA) infection, teicoplanin or vancomycin should be used, with meropenem or imipenem reserved for second line treatment. Prophylactic antibiotics should not be continued once a surgical patient has returned from the theatre. Patients with febrile neutropenia receive piptazobactam, meropenem, ceftazidime or ciprofloxacin and a glycopeptide. Antifungals, usually caspofungin or liposomal amphotericin, are used if fungal infection is suspected, especially after failed antibacterial treatment. Cephalosporin use has declined as they have been linked with emergence of MRSA and Clostridium difficile. However, this reflects overuse and they still have a place as part of a diverse choice of antibiotics. Vancomycin and teicoplanin use has increased greatly in order to treat MRSA and line infections, but resistance remains unusual. Carbapenem use has increased rapidly with the emergence of extended spectrum beta-lactamase producing Gram-negative bacteria.
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Carlucci, Annalisa, and Paolo Navalesi. Weaning failure in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0103.
Full textAbstract:
Weaning failure has been defined as failure to discontinue mechanical ventilation, as assessed by the spontaneous breathing trial, or need for re-intubation after extubation, so-called extubation failure. Both events represent major clinical and economic burdens, and are associated with high morbidity and mortality. The most important mechanism leading to discontinuation failure is an unfavourable balance between respiratory muscle capacity and the load they must face. Beyond specific diseases leading to loss of muscle force-generating capacity, other factors may impair respiratory muscle function, including prolonged mechanical ventilation, sedation, and ICU-acquired neuromuscular dysfunction, potentially consequent to multiple factors. The load depends on the mechanical properties of the respiratory system. An increased load is consequent to any condition leading to increased resistance, reduced compliance, and/or occurrence of intrinsic positive-end-expiratory pressure. Noteworthy, the load can significantly increase throughout the spontaneous breathing trial. Cardiac, cerebral, and neuropsychiatric disorders are also causes of discontinuation failure. Extubation failure may depend, on the one hand, on a deteriorated force-load balance occurring after removal of the endotracheal tube and, on the other hand, on specific problems. Careful patient evaluation, avoidance and treatment of all the potential determinants of failure are crucial to achieve successful discontinuation and extubation.