بهترین پوزیشن در زن حامله در شرایط بحرانی چیست:
ساعت ۱٠:٠٥ ‎ق.ظ روز ۱۳٩٠/۱۱/۱۱   کلمات کلیدی:

پوزیشن خوابیده به پشت و متمایل به سمت چپ توصیه شده است چرا؟

Place Pregnant Patients with Right Side Elevated 15 Degrees
Glen Tinkoff MD
A woman in the third trimester of pregnancy is predisposed to hypotension while in the supine or sitting position due to the hemodynamic and anatomic changes of pregnancy. The large uterus of late pregnancy can compress the inferior vena cava (IVC) such that venous return is significantly reduced. This decreased preload can lead to decreased cardiac filling and hence decreased cardiac output and hypotension. This can be especially deleterious in the usual setting of increased cardiac demand in pregnancy.
Of normovolemic pregnant patients, only 8% to 10% display supine hypotension due to adequate physiologic compensation; however, when faced with blood or other fluid losses such as in trauma or critical illness, supine hypotension of late pregnancy is more prevalent. In these instances, simple repositioning can be life saving. Establishing left uterine displacement by elevating the patient's right side greater than 15 degrees allows the uterus to be displaced off the inferior vena cava. After a traumatic injury, before this maneuver is performed assessment of the stability of the patient's spinal cord must be undertaken, and if uncertainly exists, the patient should not be moved without using formal spinal precautions.

رابدومیلوزیس در آی سی یو و خروجی ادرار بیمار:
ساعت ۱٠:٠٢ ‎ق.ظ روز ۱۳٩٠/۱۱/۱۱   کلمات کلیدی:
Aim for 2 Milliliters Per Kilogram Per Hour of Urine Output in Rhabdomyolysis
Awori J. Hayanga MD
Elliott R. Haut MD
Rhabdomyolysis is a syndrome characterized by muscle necrosis and the release of intracellular muscle constituents into the circulation. The severity of illness ranges from asymptomatic elevations of serum muscle enzymes to life-threatening cases associated with severe electrolyte imbalances, acute renal failure, disseminated intravascular coagulation, and death.
The classic presentation of rhabdomyolysis includes myalgias, pigmenturia due to myoglobinuria, and elevated serum muscle enzymes. The most commonly measured enzyme is serum creatinine kinase (CK), which is typically greater than 10,000 IU/L. It should be noted that serum CK levels may remain elevated in the absence of myoglobinuria since myoglobin is cleared from the serum more rapidly than CK. Since serum and/or urine myoglobin levels often take at least hours (if not days) to obtain results, these should not be relied upon to make the diagnosis. Rhabdomyolysis can be reliably diagnosed with the combination of the urine dipstick that is positive for heme (because of urine myoglobin) and urine microscopy showing an absence of red blood cells. Other abnormal electrolyte findings include hyperkalemia, hyperphosphatemia, hypocalcemia, and metabolic acidosis.
Rhabdomyolysis has many varied etiologies, which are difficult to categorize. Direct mechanical injury resulting in rhabdomyolysis can be caused by trauma, electrocutions, prolonged immobilization, ischemic limb injury, and crush injuries. Other cases can be caused by heatstroke and exertional rhabdomyolysis following vigorous exercise (e.g., strong-man triathlons). In addition, rhabdomyolysis can be caused by drugs and toxins, which can exert either direct myotoxicity (e.g., statins) or cause indirect muscle damage (e.g., alcohol or cocaine). Infections, inflammatory disorders, endocrine, and metabolic etiologies are also included in the long list of differential diagnoses. Genetic causes must be considered if no other cause is readily apparent.
The most important goal of treatment in rhabdomyolysis is preservation of renal function. Plasma volume expansion with intravenous isotonic saline should be given as soon as possible, even while trying to establish the cause of the rhabdomyolysis. As an example, saline
 

infusion may be started before reperfusion of the trapped body part in the case of severe crush injury. The time to adequate fluid volume restoration directly influences the rate of renal failure. Massive amounts of fluids (well over 10 L) are often required to compensate for the amount of fluid sequestered by necrotic muscle. Urine output is the most important early marker of adequate hydration and many experienced physicians aim for 2 mL/kg/h.
Controversy still exists about the use of mannitol and alkalinization of the urine as additional possible therapies to help prevent renal failure. While some physicians have very strong beliefs regarding the utility of these maneuvers, most agree that neither approach should be used in patients with oliguria. There is no clear evidence that alkalinization is beneficial and there is a risk that alkalinization may worsen hypocalcemia. Likewise, there is no good evidence of the benefit of mannitol use. Saline diuresis seems to be the primary therapeutic action. Monitoring with serial measurements of serum potassium, calcium, phosphate, and creatinine is recommended. It should be noted that hypocalcemia should not be corrected unless the patient is symptomatic to avoid worsening the common rebound hypercalcemia seen during the recovery phase.
Acute renal failure secondary to rhabdomyolysis is managed expectantly and renal replacement therapy begun to control hyperkalemia and/or volume overload. Rhabdomyolysis-induced renal failure behaves somewhat differently than renal failure from other causes. Serum creatinine rises to a higher level more quickly, yet the patients have a better prognosis for recovery of renal function.
Suggested Readings
Melli G, Chaudhry V, Cornblath DR. Rhabdomyolysis: an evaluation of 475 hospitalized patients. Medicine (Baltimore). 2005;84(6):377–385.
Sauret JM, Marinides G, Wang GK. Rhabdomyolysis. Am Fam Phys. 2002;65(5):907–912.

عوارض تغذیه بیش از حد در بیماران بخش ویژه:
ساعت ٩:٥٤ ‎ق.ظ روز ۱۳٩٠/۱۱/۱۱   کلمات کلیدی:

گاهی فکر می کنیم تغذیه بیش از حد و پر کالری به درمان بیماری های جسمی و تنفسی کمک می کند در حالیکه داستان به این سادگی ها نیست:

Be Alert for Overfeeding
Jason Sperry MD
Heidi L. Frankel MD
Providing inadequate caloric supplementation during times of critical illness is associated with negative effects. Equally as detrimental is the administration of excessive calories, or overfeeding. Overfeeding is associated with significant metabolic disorders including hyperglycemia, elevated serum triglycerides, and subsequent hepatic steatosis. In addition, overfeeding may cause a significant increase in CO2 production that can be deleterious to those with respiratory insufficiency and may make ventilator weaning challenging (or impossible).
What to Do
To avoid overfeeding, accurate estimates of energy and caloric requirements of critically ill patients are required. Critically ill patients typically undergo a period of catabolism, which can be associated with significant body protein loss, depending on the severity of critical illness and the length of the catabolic process. Calculation of nitrogen balance can quantify the extent of catabolism and evaluate the efficacy of supplemental nutrition in these patients. Nitrogen balance is calculated by subtracting total nitrogen losses (urine, stool, insensible losses) from nitrogen intake (1 g nitrogen per 6.25 g of protein). The primary mode of nitrogen excretion is urinary, and 24-hour urine collection for urinary urea nitrogen (UUN) is the most common means of measurement. Fecal and insensible losses are typically small but estimated. UUN can be a poor estimate of overall nitrogen losses in burn patients, when urine output is low (<1L/d), in patients with acute or chronic renal failure and in patients with enteric fistulas where exceedingly high losses occur in the fistulae output.
Alternatively, nutritional assessment can be accomplished via indirect calorimetry, where O2 consumption and CO2 production are measured and a respiratory quotient (RQ) is calculated at the patient's bedside. An RQ of 0.7 is typical of fat oxidation and an RQ of <0.7 suggests ketosis, lipolysis, and underfeeding. An RQ ≥1.0 exemplifies primary carbohydrate metabolism and possible overfeeding. Because of the accuracy of measurements required for indirect calorimetry, it is generally limited to those who are on ventilatory support. Since changes in minute ventilation, cardiac output, fraction of inspired
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oxygen, and acid-base status can affect CO2 production and O2 uptake, indirect calorimetry must also be performed, with the patient at a relative steady state for maximal accuracy.
Suggested Readings
Brandi LS, Bertolini R, Santini L, et al. Effects of ventilator resetting on indirect calorimetry measurement in the critically ill surgical patient. Crit Care Med. 1999;27(3):531–539.
Dickerson RN, Tidwell AC, Minard G, et al. Predicting total urinary nitrogen excretion from urinary urea nitrogen excretion in multiple-trauma patients receiving specialized nutritional support. Nutrition. 2005;21(3):332–338.
Hunter DC, Jaksic T, Lewis D, et al. Resting energy expenditure in the critically ill: estimations versus measurement. Br J Surg. 1988;75(9):875–878.
Long CL, Schaffel N, Geiger JW, et al. Metabolic response to injury and illness: estimation of energy and protein needs from indirect calorimetry and nitrogen balance. J Parenter Enteral Nutr. 1979;3(6):452–456.
Mann S, Westenskow DR, Houtchens BA. Measured and predicted caloric expenditure in the acutely ill. Crit Care Med. 1985;13(3):173–177.

اشتباهات شایع در بخش ای سی یو: شروع یا عدم شروع تغذیه برای بیمار، چرا؟
ساعت ٩:٥۱ ‎ق.ظ روز ۱۳٩٠/۱۱/۱۱   کلمات کلیدی:
 
این مطلب به تغذیه زودرس و دلایل آن برای بیماران تأکید دارد:
Consider Early Enteral Feeding
Bryan A. Cotton MD
If the gut works, use it!
As with other basic principles in patient care, this simple maxim of nutrition has sometimes been inexplicably ignored as our technological and pharmacological advances have exponentially increased over the past several decades. However, to ignore this simple idea is often to the detriment of the patient. Numerous studies have demonstrated a correlation with poor nutritional status and poor postoperative outcome. The current literature supports the preferential use of enteral feeding over parenteral nutrition (total parenteral nutrition, TPN) in intensive care unit (ICU) patients whenever possible. The reasons for this include not only the beneficial effects of enteral support but also the detrimental effects of TPN.
Beneficial Effects of Enteral Feeding
Several recent studies have demonstrated that gut mucosal dysfunction, in the form of increased permeability and villous sloughing, occurs early in the absence of enteral feedings. In the critically injured patient, several authors have demonstrated improvements in the catabolic state, specifically through improved nitrogen balance, when enteral nutrition is utilized instead of TPN. Physiological advantages of enteral nutrition over TPN include its stimulation of gallbladder emptying and release of pancreatic secretions, as well as maintenance of gut-associated lymphoid tissue (GALT) and mucosal immune function. The improved gut mucosal integrity noted with enteral feedings is likely responsible for the decreased bowel perforation rate, improved intestinal anastomotic healing, and decreased septic complications. In addition, enteral feeding is significantly less expensive (even when excluding the costs associated with TPN complications) than parenteral formulations.
Detrimental Effects of Parenteral Nutrition
The intestinal mucosa and submucosa is an area of intense metabolic and immunologic activity, especially in the critically ill and severely injured patient. Utilization of TPN in these patients further
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compromises an already tenuous situation, with loss of mucosal mass and weight, increased villous sloughing, and disturbed mucosal enzyme activity. TPN use has been shown to decrease IgA in the gut, as well as in upper respiratory secretions. From a metabolic standpoint, TPN causes metabolic acidosis, hyperglycemia, hyperlipidemia, and significant electrolyte disturbances. In addition, TPN has been associated with hepatic steatosis and cellular injury leading to liver dysfunction and failure. Systemically, the effects of TPN include impairment of leukocyte chemotaxis, impaired phagocytosis, and an attenuated inflammatory response. Other authors, however, have shown TPN associated alterations may actually potentiate the systemic inflammatory state by allowing increased bacterial translocation and increasing free-radical formation. Some studies have demonstrated higher mortality, especially among the critically ill, in those receiving parenteral nutrition compared with enteral feeding, with TPN almost doubling the risk of dying. Of note, the risks of TPN toxicity can be reduced by the addition of low-rate (sometimes referred to as trophic) tube feedings (10 to 30 mL/h).
When and How to Give Enteral Feedings
Several authors have investigated the impact and timing of early enteral nutrition. In the trauma and burn setting, delays of as little as 24 hours have been demonstrated to impact morbidities and outcomes. In fact, no evidence exists to support withholding enteral feedings in those patients with an open abdomen. Among the emergency surgery population, enteral feedings should be utilized early in the postoperative period. Although tube feedings are routinely held because of concerns of bowel-wall edema and nonperistalsis, this is not supported by the literature. With the exception of bowel obstruction and proximal enteric fistulae, early enteral nutrition has been demonstrated to be tolerated and of benefit even among those presenting with significant peritonitis and premorbid malnutrition. Early enteral support is also recommended following surgery for gastrointestinal malignancies and even in cases of severe pancreatitis, with evidence of attenuated organ dysfunction and improved outcomes.
When possible, the postpyloric position should be utilized for enteral feeding, with the nasojejunal location preferred in pancreatitis. Although many patients experience gastroparesis and some evidence suggests increased risk for aspiration, numerous studies support safety and tolerance of the gastric route. Most importantly, aggressive attention to placing enteral access (whether surgical or nasal route) should
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be considered prior to completion of the operative procedure. It is at this time that placement is most likely to be successful from a technical standpoint and best tolerated with regard to patient comfort.
One final note is that some experienced clinicians who believe in early and aggressive enteral feedings do not support the use of high volume enteral feedings during the initial phase of active resuscitation from shock or sepsis or in high-dose pressor use.
Suggested Readings
Jabbar A, McClave SA. Pre-pyloric versus post-pyloric feeding. Clin Nutr. 2005;24:719–726.
Kaur N, Gupta MK, Minocha VR. Early enteral feeding by nasoenteric tubes in patients with perforation peritonitis. World J Surg. 2005;29:1023–1027.
Marik PE, Pinsky M. Death by parenteral nutrition. Intens Care Med. 2003;29:867–869.
Simpson F, Doig GS. Parenteral vs. enteral nutrition in the critically ill patient: a meta-analysis of trials using the intention to treat principle. Intens Care Med. 2005;31:12– 23.

اشتباهات شایع در بخش آی سی یو: فنی توئین و تداخل غذایی
ساعت ٩:٤٧ ‎ق.ظ روز ۱۳٩٠/۱۱/۱۱   کلمات کلیدی:

فنی توئین از داروهایی است که در بخش ویژه کاربردهای بسیاری دارد. آیا تا کنون به تداخلات غذایی آن فکر کرده ایم؟

مطلب زیر را بخوانید:

Be Aware that Enteral Feeds can Lower Phenytoin Levels
Timothy M. Moore MD, PHD
Faramarz Zarfeshanfard RPH
Phenytoin (Dilantin) is an anticonvulsant drug, which can be useful in the treatment of seizures and epilepsy. The primary site of action appears to be the motor cortex where spread of seizure activity is inhibited, possibly by promoting sodium efflux from neurons and stabilizing the threshold against hyperexcitability caused by excessive stimulation or environmental changes capable of reducing membrane sodium gradient. Loss of posttetanic potentiation prevents cortical seizure foci from detonating adjacent cortical areas. Phenytoin reduces the maximal activity of brain-stem centers responsible for the tonic phase of tonic-clonic (grand mal) seizures.
Phenytoin exhibits nonlinear, dose-dependent, Michaelis-Menten pharmacokinetics. At therapeutic levels, phenytoin enzyme hepatic metabolism reaches its capacity and its pharmacokinetics changes from first order to zero order, at which time a small increase in the daily dose will result in a disproportionately higher level. Because of its capacity-limited metabolism, phenytoin half-life and time to reach steady state are concentration dependent. The higher the concentration, the longer the half-life and the longer the time it takes to reach steady state. The plasma half-life in humans after oral administration of phenytoin averages 22 hours, with a range of 7 to 42 hours. After intravenous (IV) administration, the half-life ranges between 11 and 15 hours. The difference in half-life is due to slower absorption and varying bioavailability of phenytoin formulations. Drug interactions may increase or decrease phenytoin half-life. Estimation of time to reach steady state cannot be based on half-life. Serum level determinations should be obtained after treatment initiation, dosage change, or addition or subtraction of an interacting food or drug to the regimen. Trough levels provide information about clinically effective serum level range and are obtained just prior to the patient's next scheduled dose. Peak levels indicate an individual's threshold for emergence of dose-related side effects and are obtained at the time of expected peak concentration. For Dilantin capsules, peak serum levels occur 4 to 12 hours after administration. For Dilantin Infatabs and Dilantin suspension, peak serum levels occur 1.5 to 3 hours after administration. The timing of levels is dependent on the clinical situation as well
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as route of administration and dosage form. In the acute setting, it is advisable to check non-steady-state phenytoin levels to avoid subtherapeutic or toxic levels prior to reaching steady state. Suggested sampling time after oral load is in 24 hours. Because of slow absorption of oral formulations, timing is not critical for level monitoring, but trough levels are suggested. Suggested sampling time for IV maintenance is also a trough level (or just prior to the next dose). Though beyond the scope of this review, detailed pharmacokinetic equations are available to help dose and monitor phenytoin treatment. (See suggested readings.)
Optimum control without clinical signs of toxicity occurs more often with total serum levels between 10 and 20 µg/mL and free levels of between 1 and 2 µg/mL, although some mild cases of tonic-clonic (grand mal) epilepsy may be controlled with lower serum levels of phenytoin. In most patients maintained at a steady dosage, stable phenytoin serum levels are achieved. There may be wide inter-patient variability in phenytoin serum levels with equivalent dosages. The patient with large variations in phenytoin plasma levels, despite standard doses, presents a difficult clinical problem. Unusually high levels result from liver disease, congenital enzyme deficiency, or drug interactions resulting in metabolic interference. Plasma protein binding is decreased in renal failure and hypoalbuminemia. Patients with unusually low levels may be noncompliant or hypermetabolizers of phenytoin. However, in the ICU setting in patients receiving enteral feeds, unusually or persistently low serum phenytoin levels may actually be attributable to a known interaction with enteral feeding.
Although it has been widely reported that serum phenytoin levels are lowered in patients receiving concomitant enteral feeding, the exact mechanism underlying this interaction is unknown. The majority of studies have suggested that there is some physical incompatibility between phenytoin and certain components in enteral feeding formulas causing decreased bioavailability of the drug. Other proposed mechanisms include binding of phenytoin to the feeding tube lumen, pH interaction of feeds and drug, increased metabolism or clearance of the drug after prolonged use of enteral feeds, and interaction of phenytoin and other drugs being administered via the enteric tube. A small number of studies have refuted the existence of an interaction between phenytoin and enteral feeding altogether. Interestingly, these studies were prospective but were also performed in healthy volunteers rather than in an ICU patient population. Ethical and logistic considerations limit the ability to perform prospective, controlled, randomized trials in appropriate patients.
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The predominantly recommended method for reducing this interaction between enteral feedings and phenytoin is to stagger phenytoin administration with feeding time. When continuous feeds are required, it has been recommended to hold feeds 1 to 2 hours prior to phenytoin dosing, flush the feeding tube with at least 20 cm3 free water or saline before and after administration, and resume feeding 1 to 2 hours after dosing. It should be noted that there is no clear evidence that this strategy increases absorption. Other strategies to achieve and maintain seizure control in the tube-fed patient include simply adjusting the phenytoin dosage while on continuous feeds without interrupting the feeds regimen, changing phenytoin administration to intravenous, changing the antiseizure medication regimen, and changing the enteral feeding formula. An alternative strategy is to use the injectable product down the feeding tube. This strategy has been shown to increase the rate of absorption but not the extent of absorption. It is important to note that implementation of any or all of these recommendations should be made only upon careful consideration of the overall clinical condition of the critically ill patient. It is also especially important to remember that if a correction is made to increase serum phenytoin levels in the patient receiving enteral feeds, a correction must likely also be made during weaning off feeds to limit the possibility of phenytoin toxicity secondary to overdose.
Suggested Readings
Au Yeung SCS, Ensom MH. Phenytoin and enteral feedings: does evidence support an interaction? Ann Pharmacother. 2000;34:896–905.
Dipiro JT, Spruill WJ, Blouin RA, et al. Concepts in Clinical Pharmacokinetics. 4th ed. Bethesda, MD: The American Society of Health-System Pharmacists; 2005.
Doak KK, Haas CE, Dunnigan KJ, et al. Bioavailability of phenytoin sodium with enteral feedings. Pharmacotherapy. 1998;18(3):637–645.
Gilbert SJ, Hatton J, Magnuson B. How to minimize interaction between phenytoin and enteral feedings: two approaches—a strategic approach. Nutr Clin Pract. 1996;11:28–30.
Kitchen D, Smith D. Problems with phenytoin administration in neurology/ neurosurgery ITU patients receiving enteral feeding. Seizure. 2001;10:265– 268.
Levy RH, Mattson RH, Meldrum BS, Perucca E, eds. Antiepileptic Drugs. 5th ed. Philadelphia: Lippincott Williams & Wilkins; 2002.
Murphy JE, ed. Clinical Pharmacokinetics Pocket Reference. 2nd ed. Bethesda, MD: The American Society of Health-System Pharmacists; 2000.
Winters ME. Basic Clinical Pharmacokinetics. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2003.

لینک های جالب آموزشی برای پرستاران و پزشکان عمومی:
ساعت ٩:٢۸ ‎ق.ظ روز ۱۳٩٠/۱۱/۱۱   کلمات کلیدی:

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دیابت نوع 1:

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دیابت نوع 2:

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تغذیه و دیابت:

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ایدز و بیماری های آمیزشی:

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مالاریا:

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پوزش از تأخیر بروز رسانی
ساعت ٩:٢٢ ‎ق.ظ روز ۱۳٩٠/۱۱/۱۱   کلمات کلیدی:

دوستان،

علت تأخیر دفاع از پایان نامه کارشناسی ارشد بود که بالاخره با تمام مشکلات گفتنی و ناگفتنی به خیر گذشت. و اکنون به تهیه مقالات مربوط به ان مشغل هستم.

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