تغذیه در بیمار سوختگی
ساعت ۸:٥٥ ‎ب.ظ روز ۱۳۸٩/٧/۱۱   کلمات کلیدی: parenteral nutrition ،burn patients
Do not Use Parenteral Nutrition, if at all Possible, in Burn Patients
Jeremy W. Pyle MD
James H. Holmes IV MD
Years of work and hundreds of studies have been performed to elucidate the best and most beneficial means of supplying nutrition to burn patients. Focus in the recent past has shifted from the overall importance of nutrition to a highly specialized and improved collection of recommendations. These include not only what and how much, but also where and when, why and how.
Burn wound pathophysiology and how it affects the body as a whole are fairly well understood, and the degree to which thermal injury alters nutrition requirements is directly related to the total body surface area (TBSA) of the burn. Burn wound derangements include grossly elevated local metabolic needs and increased systemic requirements. The battle to provide adequate nutrition in the face of this alteration has three fronts. First, a burn wound requires ramped-up repair efforts and immune support. Second, the body's response to the insult includes significant systemic derangements in neuroendocrine and cytokine-mediated processes. Finally, the gastrointestinal tract and its response to these changes are unique and important. Designing a nutrition regimen must address all three of these areas, paying special attention to the carbohydrate and protein requirements needed to avoid muscle and mucosal catabolism and avoiding a heavy reliance on lipids as a source of calories.
What not to Do
Postburn hypermetabolism has been shown to respond to a low-fat, high-protein enteral diet with fewer wound complications and a lower overall morbidity. Conversely, parenteral nutrition has consistently been linked to increased mortality in the burn patient. Burn wounds almost exclusively utilize glucose. This, coupled with the increased overall glucose requirements that come with thermal injury, means that glucose supply must be either increased in the diet or come from the catabolism of other tissues. For this reason, carbohydrates should serve as the major nonprotein source of nutrition. Doing so ensures not only that the wound will be better supplied with energy, but also that the rest of the body operates without quite so severe a demand for
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gluconeogenic substrates, and so protein stores can be preserved. If a patient is poorly fed, the end result of this demand in such a patient has an energy deficit that has been shown to develop very early postburn. Hence, early and aggressive feedings are recommended. They have been shown to positively affect protein requirements, energy deficiency, and insulin secretion. Because hyperglycemia and protein malnutrition are well known for their detrimental effects on wound healing, it seems reasonable to assume that increased insulin and a decreased need for endogenous gluconeogenic substrates provide a benefit. Ideal energy balance is met with 5 mg/kg/min of glucose.
The systemic effects of a burn wound, as mediated by cytokine release and neuroendocrine flux, are considerably more complex than the increased metabolism of a local wound. The altered interactions of glucagon and insulin affect blood glucose levels and protein metabolism while producing the hyperglycemia often seen in burns. Combining glucose and protein in enteral feeding provides a synergistic response that provides better nitrogen balance than either one alone. The effects of glucose are seen in decreased catabolism, and the effects of protein provide for the maintenance of amino acid stores. The importance of preburn protein levels has been delineated in studies looking at elderly patients who are protein deficient before burns, who have more complications postburn than matched, well-nourished patients. Current nutrition recommendations include 7 g/kg/day of glucose and about 2 g/kg/day of protein.
Once the basic components of nutrition are determined, attention is turned to the route and timing of administration. Research indicates that provision of enteral nutrition very early in the stay of a severely burned patient provides a benefit without sacrificing safety. Perhaps no organ benefits more from early enteral nutrition than the gut. Cell number, tissue mass, and the immunologic properties of the gastrointestinal tract are all improved by early enteral feeding, either intragastric or postpyloric. Manifestations of this benefit come in the form of fewer gastrointestinal bleeds and a decline in the incidence of the classic Curling ulcer. In fact, intragastric enteral feeding provides the equivalent of pharmacologic acid suppression. In the process of doing so, enteral feeding also increases splanchnic perfusion, thus providing better oxygen balance and decreased bacterial translocation. Preeminent among the reasons for enteral rather than parenteral nutrition is the protection that local maintenance of mucosal integrity provides against the perils of systemic infection, poor wound healing, and gut atrophy.
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What to Do
Immediate institution of total enteral nutrition should be maintained for as long as a patient is in the hospital and has nutritional requirements that cannot be met by the patient taking an oral diet. This includes constant feeding, up to and throughout intraoperative periods, because both intraoperative and perioperative total enteral nutrition have been proven to be safe if postpyloric. Efforts to ensure supranormal nutrition should continue well past the immediate postburn period. That children who sustain large burn injuries can have persistent growth delay for up to 2 years supports the fact that energy needs are elevated for months to years after a burn appears to be adequately healing. Patients with large total body surface area burns can have a resting metabolic rate of 120% of normal even 9 months after the injury.
Similarly, periodic evaluation of the requirements for and overall effects of total enteral nutrition is recommended. Indirect calorimetry provides a noninvasive means of evaluating energy expenditure and a useful means of garnering caloric requirements. Urine urea nitrogen (UUN), a representative measurement of protein catabolism, can be used to determine the protein-sparing effectiveness of a particular regimen, and feeding goals should include a consistently positive nitrogen balance. Use of the visceral proteins such as prealbumin and transferrin is most helpful when viewed as a part of a trend and not as a point in time.
Suggested Readings
Magnotti LJ, Deitch EA. Burns, bacterial translocation, gut barrier function, and failure. J Burn Care Rehabil 2005;26(5):383–391.
Pereira CT, Herndon DN. The pharmacologic modulation of the hypermetabolic response to burns. Adv Surg 2005;39:245–261.
Raff T, Hartmann B, Germann G. Early intragastric feeding of seriously burned and long-term ventilated patients: a review of 55 patients. Burns 1997;23:19.
Rettmer RL, Williamson JC, Labbe RF, Heimbach DM. Laboratory monitoring of nutritional status in burn patients. Clin Chem 1992;38:334.

Place Pregnant Patients with Right Side Elevated 15 Degrees
ساعت ۸:٥۳ ‎ب.ظ روز ۱۳۸٩/٧/۱۱   کلمات کلیدی: pregnant patients
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.
Suggested Readings
Kinsella SM, Lohman G. Supine hypotensive syndrome. Obstet Gynecol 1994;83:774.
Ueland K, Metcafe J. Circulatory changes in pregnancy. Clin Obstet Gynecol 1975;18:41.

در سکته قلبی حاد باید به شکل حاد در رفع انسداد ایجاد شده در عروق کرونری کوشید
ساعت ۳:٠٢ ‎ق.ظ روز ۱۳۸٩/٧/٦   کلمات کلیدی: acute mi ،reperfusion therapy
Be Aggressive in Considering Reperfusion Therapy in Acute Myocardial Infarction
Anthony D. Slonim MD, DrPH
Cardiovascular disease is a dominant cause of morbidity and mortality in the United States and acute myocardial infarction (MI) is one of the major underlying etiologies. Acute MI is a medical emergency that is precipitated when coronary occlusion leads to ischemia and then necrosis of cardiac myocytes. The necrosis will often precipitate a cardiac arrhythmia (e.g., ventricular fibrillation), which is a major cause of death for patients presenting in the acute phase. The diagnosis of an acute MI is based on the patient's history and diagnostic testing, including an electrocardiogram (ECG) and serum enzymes. The faster the diagnosis can be made and the occlusion reversed, the more likely the patient is to salvage myocardial tissue and benefit from improved outcomes.
Watch Out For
In nondiabetic patients, the major symptom of acute MI is pain. This pain is usually described as severe. It is located in a retrosternal area and may radiate to either the arms or neck. The characteristic quality of the pain is described as pressurelike or bandlike; however, other descriptions including burning, aching, and crushing have also been used. The pain usually lasts beyond 20 to 30 minutes and does not dissipate. Associated symptoms include nausea, vomiting, shortness of breath, dizziness, and diaphoresis.
In the setting of a possible acute MI, the ECG is a readily available, noninvasive, easy-to-obtain diagnostic test that has excellent sensitivity and specificity. The ECG provides information on the distribution of changes and the impact on cardiac rhythm. The pattern of ST-segment elevation representing a “current of injury” is usually associated with acute MI and implies a coronary occlusion. This is helpful for triaging for strategies of reperfusion.
In addition to the ECG, cardiac enzymes are particularly sensitive for detecting myocardial damage. These proteins are released from the myocardial cells that have sustained damage. Troponins are particularly important for the diagnosis of acute MI since under normal conditions, they are not found in the serum. These enzymes first
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become detectable from 2 to 4 hours after injury and persist for days. Creatine kinase (CK) and the MB subtype have for many years dominated the clinical arena as the major cardiac marker in the setting of acute MI now being supplanted by troponins. These tests are important early markers of myocardial necrosis but take longer to be detected and disappear from the serum more rapidly than troponins. It must be noted that in postoperative patients, creatine phosphokinase (CPK) and troponin have not been shown to be as sensitive markers for cardiac damage as they are in nonsurgical patients.
What to Do
The management of patients presenting with chest pain suggestive of acute MI should trigger a number of immediate events. The longest delay in therapy is usually related to the patient's delay in seeking care. Denial of the pain and the hope that it will go away are important underlying reasons for this phenomenon. When the patient presents to the emergency department with chest pain, a focused history, physical examination, and electrocardiogram should be obtained. If the appropriate clinical symptoms and ECG findings suggest an acute MI, aggressive management should include intravenous access, oxygen, sublingual nitroglycerin, morphine, and beta-blocker therapy. If the patient presents within 12 hours of symptoms, aggressive methods to achieve reperfusion should be considered.
The recommended strategy for achieving reperfusion is cardiac catheterization with angioplasty if the institution is capable of achieving a door-to-balloon time of <90 minutes. This strategy begins with the administration of glycoprotein IIb/IIIa inhibitors in addition to the more generic therapies described previously. This strategy has the advantage of achieving higher recanalization rates, reducing residual stenosis, and improving the outcomes in the setting of cardiogenic shock. When an institution is unable to provide primary angioplasty strategies, thrombolytic therapy can be attempted. A number of contraindications to thrombolytic therapy need to be considered before providing this intervention and include bleeding, a history of stroke, severe hypertension, recent trauma or surgery, pregnancy, aortic dissection, and intracranial or spinal cord neoplasms.
Suggested Readings
Goldman L, Ausiello D, eds. Cecil Textbook of Internal Medicine. 22d ed. Philadelphia: WB Saunders; 2004:410–424.
Keely EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction. A primary review of 23 randomized trials. Lancet. 2003;