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1
Phillips, Lynn Dianne. Manual of intravenous therapeutics. Philadelphia: F.A. Davis, 1993.
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2
Hahn, Robert G. Intravenous fluids in anaesthetic practice. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0020.
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Infusion fluids may be regarded as drugs in the perioperative setting. The therapeutic effects of crystalloid solutions are strongly related to the administered volume, while fluids of the colloid type may also improve microcirculation and have anti-inflammatory properties. The anaesthetist should be able to handle all available infusion fluids and be aware of their benefits, limitations, and risks. Fluid administration programmes for surgery are traditionally based on a balance method in which perceived and measured losses are continuously replaced. Two outcome-guided approaches—restrictive and goal-directed fluid therapy—have been added in recent years. The latter places all patients on the top of the Frank–Starling curve by titrating repeated bolus infusions of colloid fluid while observing the stroke volume response. Areas where special consideration should be given to fluid therapy include burn injury, children, day surgery, endoscopic surgery, neurosurgery, induction of spinal and epidural anaesthesia, and in septic and trauma-related shock. As volume is the key component of infusion fluids, kinetic analysis of their disposition is based on their dilution effect on components already present in the blood, usually haemoglobin.
3
Wijdicks, Eelco F. M., and Sarah L. Clark. Fluid Therapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190684747.003.0014.
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Administration of intravenous fluids for maintenance and the more consequential fluid resuscitation are common therapeutic interventions in the neurosciences intensive care unit. Intravenous fluids are provided to ensure adequate hydration because acutely ill neurologic patients often cannot swallow safely. There is a reason to use certain types of fluids and certain measures to maintain an adequate fluid balance specifically in patients admitted to the neurosciences ICU. This chapter covers the regulation of fluid status and the effect of certain fluids on intravascular volume. Daily fluid requirements and the best methods of resuscitation are discussed. The chapter also outlines fluid solutions and the infusion rate associated with different techniques. The side effects of large-volume resuscitation are emphasized.
4
Inc, Medical Data International, ed. U.S. market for drug & i.v. fluid delivery devices & supplies. Irvine, Calif. (2 Park Plaza, Suite 750, Irvine 92714): Medical Data International, 1995.
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6
(Editor), Ann Corrigan, Gloria Pelletier (Editor), and Mary Alexander (Editor), eds. Core Curriculum for Intravenous Nursing (Books). 2nd ed. Lippincott Williams & Wilkins, 1999.
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7
J, Turner, and National Co-ordinating Centre for HTA (Great Britain), eds. A Randomised controlled trial of prehospital intravenous fluid replacement therapy in serious trauma. Alton: Core Research on behalf of the NCCHTA, 2000.
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8
Company, Market Intelligence Research, ed. Technological developments lead fluid and drug delivery systems market. Mountain View, CA, USA (2525 Charleston Rd., Mountain View 94043): Market Intelligence Research Co., 1990.
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9
Inc, Medical Data International, ed. U.S. markets for I.V. fluid and drug delivery devices. Irvine, Calif. (2 Park Plaza, Suite 1200, Irvine 92614): Medical Data International, 1998.
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10
Hahn, Robert G. Fluid and electrolyte physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0003.
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The maintenance of body fluid homeostasis is an essential task in perioperative care. Body fluid volumes are tightly controlled by the nervous system, by hormones, and by the kidneys. All these systems are affected by anaesthesia and surgery in ways that must be appreciated by the anaesthetist. Administration of infusion fluids is the key tool to prevent major derangements of the body fluid volumes during before, during, and after surgery. By varying its composition, an infusion fluid can be made to selectively expand or shrink a body fluid compartment. The total osmolality determines whether the infused volume distributes over the total body water or over the extracellular fluid volume, or even attracts fluid from intracellular space. Infusion fluid is the first-line tool in the management of the vasodilation that is induced by both general and regional anaesthesia. Fluids are also an essential component in the treatment of haemorrhage, in which a reduction in arterial pressure implies that 20% of the blood volume has been lost. Capillary refill restores the blood volume, but too slowly to prevent haemorrhagic shock. In this situation, prompt intravenous fluid therapy is life-saving. Electrolyte derangements may be induced by disease and/or medication. The most essential ones to consider during anaesthesia are sodium, potassium, calcium, and bicarbonate.
11
Bohn, Desmond. Fluids and Electrolytes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199918027.003.0011.
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This chapter provides essential information on the distribution of body water and key electrolytes (sodium and potassium) in children, including the extracellular and intracellular components of total body water. Guidelines are provided for the composition and volume of fluids needed to maintain homeostasis, including maintenance intravenous fluids and fluids needed for specific circumstances, such as postoperatively. Water and electrolyte compositions of commonly used intravenous fluids and electrolytes in body fluids are provided in table format. Approaches are also given for disorders of fluid and electrolyte balance, including etiology and treatment of those related to antidiuretic hormone secretion, hyponatremia, hypernatremia, hypokalemia, and hyperkalemia.
12
Company, Market Intelligence Research, ed. Fluid and drug delivery systems markets: How new technological advances impact market growth. Mountain View, CA, USA: Market Intelligence Research Co., 1988.
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13
Frost & Sullivan., ed. U.S. fluid and drug delivery system markets: Annual update identifies market hot spots. Mountain View, Calif: Frost & Sullivan, 1994.
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14
Plumer's Principles and Practice of Intravenous Therapy (8th Edition). 8th ed. Lippincott Williams & Wilkins, 2006.
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15
Staitieh, Bashar S., and Greg S. Martin. Therapeutic goals of fluid resuscitation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0070.
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Optimizing tissue perfusion by administering intravenous fluids presents a special challenge to the intensive care unit (ICU) clinician. Recent studies have drastically altered how we assess a patient’s fluid responsiveness, particularly with regard to upstream surrogates of tissue perfusion. Central venous pressure and pulmonary capillary wedge pressure have been found to be inaccurate markers of fluid responsiveness and have given way to methods such as cardiac output as assessed by echocardiography and the various forms of arterial waveform analysis. These newer techniques, such as stroke volume variation, systolic pressure variation, and pulse pressure variation, have been found to better delineate which patients will respond to a fluid challenge with an increase in cardiac output, and which will not. In addition, traditional methods of assessing the consequences of excessive fluid administration, such as pulmonary oedema and the non-anion gap acidosis of saline administration, have given way to more sophisticated measurements of extravascular lung water, now available at the bedside. Downstream markers of tissue perfusion, such as base deficit, central venous oxygen saturations, and lactic acid, continue to be useful in particular clinical settings, but are all relatively non-specific markers, and are therefore difficult to use as resuscitation targets for ICU patients in general. Finally, recent data on septic shock and ARDS have demonstrated the importance of conservative fluid strategies, while data in surgical populations have emphasized the need for judicious fluid administration and attention to the balance of blood products used in resuscitation efforts.
16
Corporation, Market Intelligence Research, and Frost & Sullivan., eds. European fluid and drug delivery systems market: Extensive forecasts document country differences and usage trends. Mountain View, CA: Market Intelligence, 1992.
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17
Learning, Delmar Thomson, and Allegra. Nursing Ce: Fluid and Electrolyte Fundamentals of Intravenous Infusion Therapy (Online Continuing Education (Ce) Courses for Nurses on the W). Delmar Thomson Learning, 2001.
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18
Holder, Helen. Nutrition and hydration. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642663.003.0010.
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On admission, patients should have nutritional screening and assessment, in order to plan effective peri-operative nutritional care and prevent surgical complications associated with a poor nutritional status. The malnourished patient may require enteral nutrition in the form of oral nutritional supplements or enteral tube feeding. The surgical patient is at risk of peri-operative and/or electrolyte disturbances which can lead to dehydration, fluid overload, and cardiac arrhythmias. Accurate fluid balance monitoring will enable the nurse to identify fluid disturbances, assess the effectiveness of interventions, and prevent complications associated with fluid and electrolyte disturbances. This chapter covers nutritional screening and assessment, fluid balance, intravenous fluid regimes, nutritional goals, and enteral and parenteral nutrition.
19
Infusion Nursing: An Evidence-Based Approach. Elsevier - Health Sciences Division, 2018.
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20
1955-, Alexander Mary, Corrigan Ann 1948-, and Infusion Nurses Society, eds. Infusion nursing: An evidence-based approach. 3rd ed. St. Louis, Mo: Saunders/Elsevier, 2010.
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21
Sevransky, Jon. Management of sepsis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0296.
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Sepsis is triggered by an infection, and treatment of sepsis requires timely identification of the patient, and rapid treatment with antibiotics, source control, and fluids. The site of infection, patient’s phenotype, and location of the patient will help drive decisions about initial antibiotic therapy. Patients with sepsis should be treated to ensure adequate cardiac output and organ perfusion, which usually requires infusion of intravenous fluids. In addition to haemodynamic and fluid support, some patients require infection source control. Many sepsis patients require additional supportive therapy with vasoactive agents, mechanical ventilation, renal replacement therapy, and nutritional therapy.. When using these supportive therapies, the clinician should attempt to minimize the complications of the therapies, including withdrawal of therapies that are no longer necessary.. Patients who do not respond to initial therapy should be evaluated for resistant organisms, persistent sources, or alternate diagnoses.
22
Corporation, Springhouse, ed. Medications and I.V.s. Springhouse, Pa: Springhouse Corp., 1987.
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23
Plumers Principles Practice Of Infusion Therapy. Lippincott Williams and Wilkins, 2014.
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24
Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 48-Year-Old with Progressive Weakness and Pain. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0005.
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Guillain-Barré syndrome may present in several ways, although predominant proximal weakness is a common feature of the disease to recognize. The differential diagnosis may be extensive and can include infection, vasculitis, toxin exposure, and malignancy. A lumbar puncture must be done with minimal delay to evaluate for cerebrospinal fluid (CSF) albuminocytological dissociation, however results may be normal early in the course of the disease. EMG/NCS are helpful to support the diagnosis, and early treatment with intravenous immunoglobulin (IVIG) is essential. This chapter discusses the clinical features and diagnostic considerations of this important condition.
25
Spevetz, Antoinette, and Joseph E. Parrillo. Diagnosis and management of shock in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0150.
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Sepsis is triggered by an infection and treatment of sepsis requires timely identification of the patient, and rapid treatment with antibiotics, source control, and fluids. In the absence of a true biomarker for sepsis, the clinician needs to recognize which patients are at risk, as well as the common signs and symptoms of infection. The site of infection, the patient’s phenotype, and the location of the patient will help drive decisions about initial antibiotic therapy. Patients with sepsis should be treated to ensure adequate cardiac output and organ perfusion, which usually requires infusion of intravenous fluids. Crystalloid fluids are most frequently infused, and patients will often require large doses in the first 6–24 hours of treatment. In addition to haemodynamic and fluid support, some patients require infection source control. Many sepsis patients require additional supportive therapy with vasoactive agents, mechanical ventilation, renal replacement therapy, and nutritional therapy. The use of these supportive therapies allows for a patients host defence system to work in conjunction with antibiotics to fight off the infection. When using these supportive therapies, the clinician should attempt to minimize the complications of the therapies and the causative infection. Once a patient starts to clinically improve, it is essential that therapies that are no longer necessary are withdrawn. Patients who do not respond to initial therapy should be evaluated for either resistant organisms, persistent sources, or alternate diagnoses.
26
Practical Applications Of Intravenous Fluids In Surgical Patients. Jaypee Brothers Medical Publishers, 2013.
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27
Kamat, Shaila. Practical Applications of Intravenous Fluids in Surgical Patients. Jaypee Brothers Medical Publishers (P) Ltd., 2013. http://dx.doi.org/10.5005/jp/books/11902.
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28
Venkatesh, Bala, and Jeremy Cohen. Pathophysiology and management of adrenal disorders in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0261.
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The existence of the syndromes of relative adrenal insufficiency, or critical illness corticosteroid insufficiency, are debatable. In sepsis, there are alterations in plasma cortisol profiles, and corticotropin responsiveness with marked variability in responses between patients. It is probable that the spectrum of plasma and tissue glucocorticoid changes may represent a ‘sick euadrenal state’ analogous to the sick euthyroid state and may not reflect adrenocortical insufficiency. Treatment of acute adrenal crisis should not be delayed for the results of adrenal testing, and should consist of immediate supportive measures, fluid resuscitation, and high-dose intravenous glucocorticoid therapy. Admission to intensive care with a primary diagnosis of hyperadrenalism is uncommon. Patients usually present uncontrolled hypertension, electrolyte abnormalities or encephalopathy.
29
Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghan. Polyuria. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0057.
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Polyuria describes the passage of more than 3 l of urine a day. This is an arbitrary definition, and the term is commonly applied to patients who are complaining of passing larger than normal volumes of urine. As water excretion is tightly regulated by the body to maintain normal osmolality, water excretion varies greatly depending on intake. Polyuria may be physiological or pathological. A patient with polyuria often presents with nocturia, urination overnight that disturbs sleep. It is usually accompanied by polydipsia (to maintain normal fluid balance). In hospital the commonest causes of polyuria are diuretic therapy and recovery from an acute renal injury (e.g. acute tubular necrosis or obstruction). This polyuric phase can result in an impressive diuresis (8–10 l/day) before tubular cells recover their ability to concentrate urine. During this period, patients are vulnerable to dehydration and may require intravenous fluid replacement. Following pituitary surgery, the urine output should be closely monitored for evidence of new diabetes insipidus. This chapter covers the approach to diagnosis, diagnostic tests, therapy, and prognosis.
30
McGregor, Laura, Monica N. Gupta, and Max Field. Septic arthritis in adults. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0098.
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Septic arthritis (SA) is a medical emergency with mortality of around 15%. Presentation is usually monoarticular but in more than 10% SA affects two or more joints. Symptoms include rapid-onset joint inflammation with systemic inflammatory responses but fever and leucocytosis may be absent at presentation. Treatment according to British Society of Rheumatology/British Orthopaedic Association (BSR/BOA) guidelines should be commenced if there is a suspicion of SA. At-risk patients include those with primary joint disease, previous SA, recent intra-articular surgery, exogenous sources of infection (leg ulceration, respiratory and urinary tract), and immunosupression because of medical disorders, intravenous drug use or therapy including tumour necrosis factor (TNF) inhibitors. Synovial fluid should be examined for organisms and crystals with repeat aspiration as required. Most SA results from haematogenous spread-sources of infection should be sought and blood and appropriate cultures taken prior to antibiotic treatment. Causative organisms include staphylococcus (including meticillin-resistant Staphylococcus aureus, MRSA), streptococcus, and Gram-negative organisms (in elderly patients), but no organism is identified in 43%, often after antibiotic use before diagnosis. Antibiotics should be prescribed according to local protocols, but BSR/BOA guidelines suggest initial intravenous and subsequent oral therapy. Medical treatment may be as effective as surgical in uncomplicated native SA, and can be cost-effective, but orthopaedic advice should be sought if necessary and always in cases of infected joint prostheses. In addition to high mortality, around 40% of survivors following SA develop limitation of joint function. Guidelines provide physicians with treatment advice aiming to limit mortality and morbidity and assist future research.
31
Paech, Michael J., and Patchareya Nivatpumin. Postdural puncture headache. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0027.
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Postdural puncture headache (PDPH) may follow either deliberate or unintentional (accidental) penetration of the interdigitating meninges, the dura and arachnoid mater. It is one of the most common and clinically important complications of regional anaesthesia and analgesia in the obstetric population. The headache develops as a consequence of cerebrospinal fluid loss, low intracranial pressure and cerebrovascular changes in the upright position and can prove debilitating. The diagnosis is clinical, making thorough assessment and regular review all the more important, to revise treatment plans, exclude rare serious pathology such as subdural haematoma, and avoid misdiagnosis. This chapter reviews the pathophysiology, incidence, risk factors (needle, technical and patient related), features, natural history, diagnosis, and management of PDPH. High level evidence supports prevention by using small gauge, non-cutting spinal needles, but other preventative strategies against either unintentional dural puncture or PDPH are poorly supported. The absent or poor efficacy of measures such as bed rest, hydration, cerebral vasoconstrictor therapy, epidural or intrathecal saline injection, intrathecal catheter placement or prophylactic epidural blood patch, is noted. Validation of better evidence supporting epidural morphine or intravenous cosyntropin is required. Symptomatic treatment of PDPH is also unreliable. Very limited evidence that requires substantiation supports a modest benefit from caffeine, gabapentinoids or intravenous hydrocortisone. The intervention of epidural blood patch is highly likely to relieve post-spinal PDPH, but only completely resolves epidural needle-induced PDPH in 30–50% of cases. Much detail about EBP remains undetermined, but delayed intervention and injection of approximately 20 mL of autologous blood appear appropriate.
32
Lippincott Williams & Wilkins., ed. Portable fluids & electrolytes. Philadelphia: Lippincott Williams & Wilkins, 2008.
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33
Mueller, Dana. Malaria and Dengue Fever. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0052.
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Malaria is a vector-borne parasitic illness characterized by acute fever, headache, chills, and vomiting. Medications must target both the parasite’s active and inactive forms. During pregnancy, treatment regimens should consist of quinine and clindamycin. Person-to-person transmission can occur via sharing of blood products or during pregnancy. It is possible to contract malaria even while on prophylactic medications because resistance is widespread. Country-specific recommendations for prophylaxis can be found in the CDC’s annual Health Information for International Travel Protection against mosquito bites. Dengue Fever is a vector-borne viral infection that causes a flu-like illness with occasional lethal complications. It occurs primarily in tropical and subtropical regions. All treatment is supportive, ranging from oral rehydration to intravenous fluid administration and vasopressor support. Aspirin and NSAIDs are contraindicated in this population. Person-to-person transmission can occur via sharing of blood products or during pregnancy, although vertical transmission is rare.
34
Rajendram, Rajkumar. Management of acute pancreatitis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0191.
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The major causes of morbidity and mortality in acute pancreatitis are organ dysfunction and infection of necrotic tissue. Management should aim to prevent, or to diagnose and treat, the complications of pancreatic inflammation, and any predisposing factors to avoid recurrence. Medical management is essentially supportive with oxygen, intravenous fluids, analgesia, enteral or parenteral nutrition, and correction of metabolic abnormalities. Patients with severe acute pancreatitis are unlikely to resume prompt oral intake so nutritional support is also required. Post-pyloric feeding is not required if nasogastric feeding is tolerated. However, enteral nutrition, whether oral, gastric, or post-pyloric, can cause pain, recurrence of pancreatitis or an increase in fluid collections, so parenteral nutrition may be necessary. The necrotic pancreas becomes infected in a third of patients with severe acute pancreatitis. Treatment of infection includes systemic antimicrobials, enteral nutrition, percutaneous aspiration, and necrosectomy. However, compared with open necrosectomy, a minimally invasive step-up approach consisting of percutaneous drainage followed, if necessary, by open necrosectomy, reduces morbidity and mortality. The aetiology of the pancreatitis must also be treated to prevent recurrence and the complications of pancreatic failure. Gallstones are the most common cause of pancreatitis that requires specific treatment. Endoscopic or surgical removal of stones may reduce the severity of pancreatitis. Patients should also have cholecystectomy after recovery from gallstone pancreatitis. Effective management of acute pancreatitis requires multidisciplinary engagement. The mainstay of management involves supportive prevention and treatment of complications, infection, and organ failure to avoid or delay surgery.
36
Clinical effectiveness and cost-effectiveness of prehospital intravenous fluids in trauma patients. Tunbridge Wells: Gray Publishing on behalf of NCCHTA, 2004.
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37
Society, Infusion Nurses, Mary Alexander, and Ann M. Corrigan. Core Curriculum for Infusion Nursing (Core Curriculum Series). 3rd ed. Lippincott Williams & Wilkins, 2003.
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38
1948-, Corrigan Ann, Alexander Mary 1955-, and Infusion Nurses Society, eds. Core curriculum for infusion nursing. 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2004.
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39
Gorski, Lisa A., Mary Alexander, Lynn Phillips, Ann M. Corrigan, and Infusion Nurses Society Staff. Core Curriculum for Infusion Nursing. Lippincott Williams & Wilkins, 2013.
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40
Debaveye, Yves, Dieter Mesotten, and Greet Van den Berghe. Hyperglycaemia, diabetes, and other endocrine emergencies. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0069.
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Although endocrine pathology is usually treated in outpatient clinic, intensive care may be required when endocrinopathies are associated with other medical illnesses or reach a state of decompensation. Although endocrine emergencies are quite rare, they are potentially life-threatening, if not recognized promptly and managed effectively. Therefore, every clinician should always be attentive to a possible diagnosis of these complex disorders. The three major diabetic emergencies comprise diabetic ketoacidosis, hyperglycaemic hyperosmolar state, and prolonged hypoglycaemia. Hyperglycaemic crises are characterized by hypovolaemia, electrolyte disturbances, and potentially life-threatening triggers. Hence, airway-breathing-circulation securement, diagnosis and treatment of the underlying condition, and fluid resuscitation are the cornerstones of acute diabetic ketoacidosis/hyperglycaemic hyperosmolar state management. Subsequently, monitoring and correction of electrolyte disturbances and insulin treatment are initiated. Profound hypoglycaemia should be suspected in every coma patient with an indistinct history or treated with insulin or sulfonylurea/meglitinide. This condition warrants an immediate and a sufficiently long administration of glucose, under blood glucose monitoring. Alternatively, glucagon may be injected subcutaneously, or preferably intramuscularly. Hyperglycaemia in intensive care unit patients is associated with adverse outcome which can be prevented via the implementation of glucose control with intravenous insulin. One should hereby target glucose levels to be as close to normal as possible, without evoking unacceptable glucose fluctuations and hypoglycaemia. The classical non-diabetic endocrine emergencies comprise thyroid storm, myxoedema coma, acute adrenal crisis, and phaeochromocytoma. They all pose diagnostic and therapeutic challenges and require specific treatment such as endocrine replacement or blockage therapy. It is important to note that they are occasionally the presenting manifestation in undiagnosed patients. This chapter also briefly discusses amiodarone-induced thyroid dysfunction.
41
Springhouse. Just the Facts: Fluids and Electrolytes (Just the Facts Series). Lippincott Williams & Wilkins, 2004.
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42
Arroyo, Vicente, Mónica Guevara, and Javier Fernández. Renal failure in cirrhosis. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0247.
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A major event in liver cirrhosis is the development of a progressive deterioration of circulatory function due to splanchnic arterial vasodilation and impairment in cardiac function. This feature determines a homeostatic activation of the renin–angiotensin–aldosterone system, sympathetic nervous system, and antidiuretic hormone. The splanchnic microcirculation is resistant to the vasoconstrictor effect of these systems. Therefore, the homeostasis of arterial pressure in cirrhosis occurs in the extrasplanchnic, mainly renal circulation. The activation of these systems produces renal fluid retention, which accumulates as ascites, and water retention and dilutional hyponatraemia. In the latest phase of cirrhosis, when circulatory dysfunction is severe, renal vasoconstriction is intense and patients develop type 2 hepatorenal syndrome (HRS) and refractory ascites.Type 1 HRS is an acute and rapidly progressive renal failure that occurs in the setting of a precipitating event, commonly an infection. Patients with type 1 HRS also present with rapid deterioration of liver function (encephalopathy, jaundice) and relative adrenal insufficiency. The mechanism of this multiorgan failure is an acute deterioration in circulatory function due to both an accentuation of arterial vasodilation and of cardiac dysfunction.There is no specific test for the diagnosis of HRS. The most accepted diagnostic criteria are those proposed by the International Ascites Club which are based on the exclusion of other types of renal failure. The course of renal failure following treatment of the precipitating event of HRS is another important diagnostic feature.The treatment of choice of tense ascites in cirrhosis is paracentesis associated with intravenous albumin infusion. Moderate sodium restriction and diuretics (spironolactone alone or associated with furosemide) are subsequently given to prevent re-accumulation of ascites. Diuretics are the treatment of choice in patients with moderate ascites. Patients with type 2 HRS and refractory ascites (not responding to diuretics) could be treated by frequent paracentesis or by the insertion of a transjugular intrahepatic portosystemic shunt (TIPS).Terlipressin plus albumin is the treatment of choice in type 1 HRS
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Ferrari, Lynne R. Sickle Cell Disease. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0051.
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Sickle cell anemia is a disease that combines molecular biology, clinical features, biochemistry, pathology, natural selection, population genetics, gene expression, and genomics and is the world’s most common life-threatening monogenic disorder. Clinical features include anemia; painful crisis especially in fingers, chest, and long bones; hemolysis; splenic infarction resulting in functional asplenia; and microinfarction leading to neurologic and renal impairment. The maintenance of adequate body temperature with active warming devices and warmed intravenous fluids, monitoring hydration and urine output, providing supplemental oxygen, and limiting surgical and anesthesia times to reduce pulmonary complications constitute the best management for patients with sickle cell disease.
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Peake, Sandra L., and Matthew J. Maiden. Management of septic shock in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0298.
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The management of septic shock is a medical emergency. Following prompt recognition, treatment priorities are haemodynamic resuscitation, empirical antimicrobials, urgent control of the source of infection and monitoring the response to therapy. Haemodynamic resuscitation is focused on maintaining an adequate macrocirculation, while also ensuring adequacy of microcirculatory blood flow to the cells. Intravenous fluids and catecholamines have been the mainstay of therapy. However, the amount and type of fluids, choice of vasoactive medications, and the appropriate resuscitation endpoints have been questioned. Greater awareness of the importance of resuscitating the microcirculation and cell function have led to endpoints such as venous O2 saturation and changes in lactate levels becoming resuscitation targets. Urgent definitive treatment of the infection is also crucial. This requires prompt broad-spectrum empirical antimicrobial therapy, draining infected collections and removing infected medical devices. Despite extensive research, no new therapies have improved survival from septic shock.
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Mesotten, Dieter, and Sophie Van Cromphaut. Management of diabetic emergencies in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0260.
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The three major diabetic emergencies comprise diabetic ketoacidosis (DKA), hyperglycaemic hyperosmolar state (HHS), and prolonged hypoglycaemia. These complications are preventable, treatable, and rather infrequently lead to prolonged intensive care (ICU) admission. Hyperglycaemic crises, whether DKA in type 1 diabetics, or HHS in type 2 diabetics, are characterized by moderate to severe hypovolaemia, electrolyte disturbances and a potentially life-threatening trigger. Hence, airway–breathing–circulation securement, diagnosis, and treatment of the underlying condition, as well as fluid resuscitation are the cornerstones of the acute management of DKA and HHS. Currently, a continuous, low (physiological) dose insulin scheme intravenously with omission of the priming bolus is advocated to avoid hypoglycaemia. An evidence-based treatment protocol, and reliable blood glucose and electrolyte measurements are compulsory to safely manage these crises until resolution of ketoacidosis or the hyperosmolar state. Profound hypoglycaemia should be suspected in every coma patient with an indistinct history or on a known regimen of insulin or sulphonylurea/meglitinide. This condition warrants immediate and sufficiently long administration of glucose orally or intravenously, as well as repeated monitoring of blood glucose levels. Alternatively, the counter-regulatory hormone glucagon may be injected intramuscularly in the emergency setting.
46
Felberg, Mary A. Mitochondrial Disease and Anesthesia. Edited by Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel, and Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0042.
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Mitochondrial disease is a genetically, biochemically, and clinically heterogeneous group of disorders that arise from defects in cellular oxidative phosphorylation, most commonly within the electron transport chain. All mitochondrial diseases involve disruption in energy production; clinical symptoms usually manifest in tissues with high energy demands although all organs may be affected. The extent of disease depends not only on the mitochondrial defect but on the numbers of dysfunctional mitochondria present in each tissue. Despite in vitro evidence that almost every anesthetic agent studied has been shown to decrease mitochondrial function, all anesthetic agents have been used safely. Discussion of the implications of mitochondrial disease for anesthetic management includes preoperative preparation, volatile and intravenous anesthetic agents, avoidance of succinylcholine, risk of malignant hyperthermia, perioperative fluids, and postoperative management.
47
Tobar, Ximena, and Shannon B. Putman. Viral Gastroenteritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0030.
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Viral gastroenteritis is a diarrheal disease associated with nausea, vomiting, headache, abdominal cramping, myalgias, and low-grade fever. Stools are often described as watery, with bouts of diarrhea and emesis that can occur on an hourly basis. Blood or mucus in the stool is suggestive of a bacterial or parasitic process. Additionally, the presence of fecal leukocytes excludes viral infection, as it is suggestive of colonic inflammation. Treatment is mainly supportive with appropriate hydration, including oral rehydration and/or intravenous fluids, being the key intervention. Specific antiviral agents are not available. Prevention and control of spread are important issues for viral gastroenteritis. Hand washing alone may reduce the spread of infection. The use of alcohol-based hand sanitizers and daily disinfection of surfaces with quaternary ammonium wipes has reduced the spread of Norovirus and was found superior to handwashing alone.
48
Beattie, R. Mark, Anil Dhawan, and John W.L. Puntis. Necrotizing enterocolitis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0005.
Full textAbstract:
Necrotizing enterocolitis 46Necrotizing enterocolitis (NEC) is the most common gastroenterological emergency in the neonatal intensive care unit (NICU) and the major cause of death for all newborns undergoing surgery. The mortality is greater than that from all the congenital disorders of the gastrointestinal tract combined. Survivors may be left with short-bowel syndrome as well as other long-term gastrointestinal, growth and neurodevelopmental sequelae. NEC frequently presents as feed intolerance with bile-stained gastric residuals, abdominal distension, blood in the stools, apnoea, and acidosis. It may develop insidiously, or be a rapidly progressive illness culminating in shock followed by death. The characteristic finding on abdominal radiograph is intramural gas (pneumatosis), produced by bacteria that have invaded the bowel wall. Other radiographic findings include portal gas, persistently dilated loops of bowel and pneumoperitoneum. Immediate management involves stopping enteral feeding, and giving intravenous fluids with broad-spectrum antibiotics. Blood and platelet transfusion may be required. Hypotheses regarding aetiology include the possibility that enteric bacteria ferment maldigested carbohyhdrate creating an acidic intraluminal environment that adversely affects mucosal blood flow. Immaturity of gastrointestinal motor function, digestion, immunity, and circulation are all implicated in the pathogenesis....
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Bellomo, Rinaldo, and John R. Prowle. Pathophysiology of oliguria and acute kidney injury. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0211.
Full textAbstract:
Oliguria and acute kidney injury (AKI) are common in critically-ill patients with studies reporting AKI affecting more than 50% of critically-ill patients. AKI is independently associated with increased mortality and is a potentially modifiable aspect of critical illness. The pathogenesis of AKI is complex and varies according to aetiology. The most common trigger in ICU patients is sepsis—the pathophysiology of septic AKI is poorly understood and probably involves intrarenal haemodynamic and inflammatory processes. In the setting of septic AKI, the classic acute tubular necrosis described in experimental models does not occur and histological changes are only minor. Activation of neurohormonal mechanisms is also important, particularly in the hepatorenal syndrome, where activation of the remain-angiotensin system appears to play a major role. The treatment of oliguria and AKI in ICU patients has traditionally relied on the administration of intravenous fluids. While such therapy is warranted in patients with a clear history, and physical examination suggestive of intravascular and extravascular volume depletion, its usefulness in other patients (e.g. septic patients) remains controversial. Removal of nephrotoxins, rapid treatment of the triggering factors, and attention to cardiac output and mean arterial pressure remain the cornerstones of the prevention and treatment of AKI in ICU.
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Bleck, Thomas P. Assessment and management of seizures in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0232.
Full textAbstract:
In previously conscious patients seizures are usually easily detected. Critically-ill patients are frequently sedated and a proportion are paralysed with neuromuscular blocking agents, in such patients it may be hard or impossible to detect seizures clinically. An urgent electroencephalogram (EEG) should be obtained whenever seizures are witness or suspected, especially if the patient does not rapidly return to baseline, when non-convulsive status epilepticus must be excluded. Unless the cause of the seizure activity is already known, an urgent CT, or MRI is indicated. If central nervous system infection is suspected a lumbar puncture may be needed. Status epilepticus is diagnosed when there is recurrent or continued seizure activity without intervening recovery. Most seizures are self-limiting and stop after 1–2 minutes, seizures that continue for more than 5 minutes should be treated. Treatment priorities for any seizure are to stop the patient hurting either themselves or anyone else. General supportive measures include attention to the airway, breathing, circulation, exclusion of hypoglycaemia and an EEG to exclude non-convulsive status epilepticus. A variety of drugs can be used to terminate seizures; parenteral benzodiazepines are the most commonly used agents although propofol and barbiturates are alternatives. Emergent endotracheal intubation may well be necessary, hypotension can be expected and may need treatment with intravenous fluids and vasopressors.