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http://projects.csail.mit.edu/courseware/?term=an-essay-on-entertainment an essay on entertainment 8,9 clinical presentation and diagnosis refer to the clinical presentation and diagnosis of stroke textbox for information on the signs and symptoms of stroke. It is important to note that hypertension is one of the major risk factors for both ischemic and hemorrhagic stroke. For ich specifically, hypertension has been shown to increase risk by a factor of 3. 68. 10 other risk factors for hemorrhagic stroke include trauma, cigarette smoking, cocaine use, heavy alcohol use, anticoagulant use, and cerebral aneurysm and avm rupture.

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http://cs.gmu.edu/~xzhou10/semester/honors-college-thesis-usf.html honors college thesis usf If there is extensive involvement, a "second look" operation may be done within 24 to 48 hours to determine whether any areas that appeared necrotic are actually viable. The length and areas of removed bowd are recorded. If large areas are resected, the length and position of the remaining bowd are noted, as this will affect the long-term outcome. In approximately 14% of infants with this condition, nec totalis (bowel necrosis from duodenum to rectum) is found. In these cases, mortality is almost certain. 5. In elbw infants (<1,000 g) and extremely unstable infants, peritoneal drainage under local anesthesia may be a management option. In many cases, this temporizes laparotomy until the infant is more stable, and in some cases, no further operative procedure is required. A recent multicenter cohort study comparing laparotomy versus peritoneal drainage in nec with perforation showed no significant differences in survival or need for long-term total pn between the two procedures. However, some studies have suggested worse long-term neurodevdopmental outcome in infants with nec treated with peritoneal drains alone, perhaps representing the infants who were too sick to undergo laparotomy. Optimal surgical therapy still remains controversial. C. Long-term management. Once the infant has been stabilized and effectively treated, feedings can be reintroduced. We generally begin this process after 2 weeks of treatment by stopping gastric decompression. If infants can tolerate their own secretions, feedings are begun very slowly while parenteral alimentation is gradually tapered. No conclusive data are available on the best method or type of feeding, but breast milk may be better tolerated and is preferred. The occurrence of strictures may complicate feeding plans. The incidence of recurrent nec is 4% and appears to be independent of type of management. Recurrent disease should be treated as before and will generally respond similarly. If surgical intervention was required and an ileostomy or colostomy was created, intestinal reanastomosis can be dectivdy undertaken after an adequate period of healing. If an infant tolerates enteral feedings, reanastomosis may be performed after a period of growth at home. However, earlier surgical intervention may be indicated in infants who cannot be advanced to full-volume or strength feedings because of malabsorption and intestinal dumping. Before reanastomosis, a contrast study of the distal bowel is obtained to establish the presence of a stricture that can be resected at the time of ostomy closure. Iv. Prognosis. Few detailed and accurate studies are available on prognosis. In uncomplicated cases of nec, the long-term prognosis may be comparable with that of other low birth weight infants. However, those with stage lib and stage iii nec have a higher incidence of mortality {of over 50%), growth delay (delay in growth of head circumference is of most concern), and poor neurodevelopmental outcome. Nec requiring surgical intervention may have more serious sequelae, including mortality secondary to infection, respiratory failure, pn-associated hepatic disease (see chap. 26), rickets, and significant developmental delay.

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http://projects.csail.mit.edu/courseware/?term=crucible-essay-question crucible essay question A. Sequelae of nec can be directly related to the disease process or to the longterm nicu management often necessary to treat it.

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how to be a good student essay The offending microorganisms colonize the skin surface and invade through abrasions, insect bites, or other small traumas viagra uk forum. The scabby, crusty eruption of impetigo ensues. These lesions may occur anywhere on the body, but are most common on the face and extremities. 10 clinical presentation and diagnosis impetigo lesions are numerous, well localized, and erythematous. They begin as small, thin-walled blisters that can quickly evolve into ruptured lesions, with the dried discharge forming a honey-colored crust reminiscent of cornflakes. 4 s. Aureus and β-hemolytic strep is most often implicated in impetigo. 4 the lesions of impetigo are rarely painful, but are pruritic.

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https://graduate.uofk.edu/user/diploma.php?sep=science-homework-help-com science homework help com Textbook of medical physiology, 8th ed. Philadelphia, pa. Saunders, 1991:275, with permission. ) table 13–2  hypovolemic shock manifestations on major organs heart • myocardial ischemia • dysrhythmias brain • restlessness, confusion, obtundation • global cerebral ischemia liver • release of liver enzymes • biliary stasis lungs • pulmonary edema • ards kidneys • oliguria • decreased glomerular filtration • acute kidney injury gi tract • stress-related mucosal disease • bacterial translocation hematologic • thrombocytopenia • coagulopathies ards, acute respiratory distress syndrome. Gi, gastrointestinal. Treatment desired outcomes referred to as the multiple organ dysfunction syndrome (mods). Involvement of the heart is particularly devastating considering the central role it plays in oxygen delivery and the potential for myocardial dysfunction to perpetuate the shock state. Preexisting organ dysfunction and buildup of inflammatory mediators can also exacerbate the effects of hypovolemic shock to the point of irreversibility. 5 for example, acute or chronic heart failure can lead to pulmonary edema, further aggravating gas exchange in the lungs and ultimately tissue hypoxia. Only about one-third of early-onset mods is quickly reversible (within 48 hours) with proper fluid resuscitation. Thus it is imperative that hypovolemic shock be treated quickly to avoid mods. 9 table 13–1  major hyopovolemic shock etiologies1,2 i.  Hemorrhagic  trauma   gi bleeding   abdominal aortic aneurysm ii. Nonhemorrhagic (dehydration)  vomiting  diarrhea   third spacing  burns  fistulae gi, gastrointestinal. The major goals in treating hypovolemic shock are to restore effective circulating blood volume, as well as manage its underlying cause. In achieving this goal, the downward spiral of events that can perpetuate severe or protracted hypovolemic shock is interrupted. This is accomplished through the delivery of adequate oxygen and metabolic substrates such as glucose and electrolytes to the tissues throughout the body that will optimally bring about a restoration of organ function and return to homeostasis. Evidence of the latter is a return to the patient’s baseline vital signs, relative normalization of laboratory test results, and alleviation of other signs and symptoms of hypovolemic shock previously discussed. Concurrent supportive therapies are also warranted to avoid exacerbation of organ dysfunction associated with the hypovolemic shock event. General approach to therapy securing an adequate airway and ventilation is imperative in hypovolemic shock patients consistent with the “vip rule” of resuscitation. Ventilate (oxygen administration), infuse (fluid resuscitation, and pump (administration of vasoactive agent). 2 any compromise in ventilation only accentuates the tissue hypoxia occurring secondary to inadequate perfusion. Thus, early sedation with tracheal intubation and mechanical ventilation typically occurs at this stage of resuscitation (figure 13–3). Intravenous (iv) access is also essential for administration of fluids and medications that can be facilitated through the placement of peripheral iv lines or catheterization with central venous lines if rapid or large volumes of resuscitative fluids are indicated. Placement of an arterial catheter is advantageous to allow for accurate and continual monitoring of bp, as well as 232  section 1  |  cardiovascular disorders clinical presentation and diagnosis of hypovolemic shock general patients will be in acute distress, although symptoms and signs will vary depending on the severity of the hypovolemia and whether the etiology is hemorrhagic versus nonhemorrhagic. Symptoms •• thirst •• weakness •• light-headedness signs •• hypotension, arterial sbp less than 90 mm hg or fall in sbp greater than 40 mm hg •• tachycardia •• tachypnea •• hypothermia •• oliguria •• dark, yellow-colored urine arterial blood gas (abg) sampling. A bladder catheter should be inserted for ongoing monitoring of urine output. Baseline laboratory tests that should be done immediately include complete blood cell count with differential, serum chemistry profile, liver enzymes, prothrombin and partial thromboplastin times, and serum lactate. A urinalysis and an abg should also be obtained, and ongoing electrocardiogram (ecg) monitoring should be performed.

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