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Many centres avoid using traction buy generic dilantin 100 mg symptoms stomach flu, but buy dilantin 100mg otc symptoms pregnancy, if used cheap dilantin 100 mg online medications 2, lifting weights should be avoided as tube movement may dislodge clots buy dilantin 100mg lowest price treatment of scabies. Since deflation can traumatise friable healing tissue, some centres avoid inflating oesophageal balloons, relying on occlusion of flow from inflation of gastric balloons to stop the haemorrhage. They can temporarily control haemorrhage for 28–70 per cent of patients, although up to one-third may re-bleed during treatment (Boyer & Henderson 1996); like tamponade, vasopressin can buy time for more definitive treatments. Vasopressin causes systemic vasoconstriction, and extravasation may cause necrosis, and so it should be given into central veins (Boyer & Henderson 1996). The hormone somatostatin inhibits gastrin secretion, reducing gastric acid secretion. Schoenfield and Butler (1998) claim that the longer-acting synthetic analogue octreotide is as effective as endoscopy, but anecdotal reports suggest it is ineffective. Cold water may also cause vagal stimulation, increasing gastric motility and irritation to ulcers. Treatment may be preventative (protecting against gastric acidity), supportive (replacing blood volume and clotting factors), medical (treating bacteria—see below) or surgical. Gastric mucus maintains wide pH differences between gastric acid (or alkaline bile) and epithelium. Mucosal failure may be caused by ■ excess acid production (from gastromas) ■ lack of neutralising factors (absence of enterai nutrition) ■ bile reflux ■ irritant drugs (e. The bacterium Helicobacter pylori is particularly associated with peptic ulceration. About one-half of the population harbour this gram negative bacterium, with colonisation often starting in childhood (MacConnachie 1997a). As it is found in water, enteric transmission seems likely (Cotterill 1996), and it is particularly prevalent when sanitation is poor. Most people colonised by Helicobacter pylori remain asymptomatic (Cotterill 1996), but most people with ulcers are infected by it (MacConnachie 1997a), and it appears to cause gastritis, ulcers and gastromas (Cotterill 1996). According to MacConnachie (1997a) it provokes: ■ local inflammatory responses (disrupting mucosal barriers) ■ systemic immune response and inhibits endogenous somatostatin release (so increasing acid production). Since Helicobacter pylori requires an alkaline environment, in stomach acid it produces urease to convert urea to ammonia (the alkaline environment it needs) and carbon dioxide (Cotterill 1996). Helicobacter pylori can be detected by carbon dioxide production on ingesting urea isotopes (carbon 13 or 14), but, being costly, tests are not often performed (Cotterill 1996). Urgent fluid resuscitation is usually required, especially with colloids, clotting factors and blood transfusions. Intensive care nursing 360 Gastrointestinal tract bacteria digest blood, releasing ammonia. Prevention Enteral feeding helps to protect against gastric ulceration; however, enterai feeding should include rest periods to enable gastric pH to fall (see Chapter 9). H2-blockers (cimetidine, ranitidine), once used to reduce gastric acid secretion, do not reduce incidence of bleeding (Sung 1997). Sucralfate, an aluminium salt, stimulates mucosal blood flow and mucus secretion, together with local prostaglandin production (Sung 1997), thus increasing endogenous defences. Sucralfate does not reduce gastric acidity so that gram negative colonisation is inhibited; it can also cause constipation, and aluminium toxicity can provoke renal failure (Sung 1997). Stools should be observed for frank blood; occult bleeding can be confirmed by testing. Observations should be recorded and reported; samples may be required for testing. Most bleeds are small, but if large bleeds do not resolve spontaneously, early surgery (e. McCaffrey (1991) gives a simplistic description of Sengstaken tubes, useful for those unfamiliar with using them. He smokes an average of 20 cigarettes each day and usually drinks several pints of beer after work during the week, with more at the weekends. Kevin has recently experienced epigastric pain for which he has taken oral antacids. A colleague accompanied Kevin to the Accident & Emergency Department (A & E) after he had vomited ‘dark fluid’ and collapsed in a business meeting. Include resources needed such as equipment, drugs, investigations and specialists. Kevin then has endoscopie banding ligation to obliterate the ruptured and bleeding vessels. His initial experience of haematemesis and speed of emergency interventions have made him highly anxious. Advice should include the reason for and practical strategies on: • Avoiding vigorous coughing and sneezing • Recognition of early signs and symptoms of re-bleeding • Relaxation techniques • Drug action affected by his condition and hepatic impairment, e. The pancreas normally secretes 1,500 ml of digestive juices each day as secretion is a reflex vagal response to acidic chyme in the duodenum. Pancreatic juice, which enters the duodenum at the sphincter of Oddi, is strongly alkaline (pH about 8. Phospholipidase A, released as an inactive proenzyme to prevent autodigestion, is normally activated in the duodenum by trypsin; activation in the pancreas or outside the gastrointestinal tract (via fistulae) causes autodigestion and fat necrosis. Congestion eventually ruptures the pancreatic ductules, releasing pancreatic juice directly into the gland. Pancreatic damage releases a cascade of vasoactive mediators, including ■ kinins ■ interleukins ■ platelet activating factor ■ free oxygen radicals (Gunning 1997). Intensive care nursing 364 Gross vasodilation causes hypotension and ischaemia and further release of mediators from ischaemic endothelium, often progressing to multisystem dysfunction. Gut ischaemia facilitates translocation of bacteria, and so prophylactic antibiotics are usually prescribed (Johnson 1998). Serum amylase levels usually increase up to tenfold (Reece-Smith 1997) within 6 hours, but may return to normal within 48 hours (Santamaria 1997). Chronic underlying pancreatic disease (from alcoholism) may prevent a rise in serum amylase (Johnson 1998) so that normal levels can not preclude diagnosis. Acute pancreatitis can progress to fulminant stages, most texts identifying these as acute oedematous or toxic pancreatitis, and necrotizing or fulminant pancreatitis. Tissue damage causes release of vasoactive mediators (see above), triggering massive extravasation of plasma, hypovolaemic shock and gross oedema. Disruption of vessels in and around the pancreas causes systemic release of enzymes and toxic chemicals, resulting in inflammation, haemorrhage and fat necrosis. The problems may not be apparent until patients relapse some weeks following apparent recovery from acute pancreatitis. Most pseudocysts resolve spontaneously (Venables 1991), but until resolution, surrounding tissues can be compressed and fistulae into surrounding tissue can develop, causing haemorrhage (especially hepatic or splenic) or infection (especially with bowel fistulae). Pseudocysts unresolved after six weeks should be drained percutaneously, under endoscopy, or removed surgically (Venables 1991). Pancreatitis 365 Symptoms Oedema and distension of the pancreatic capsule, biliary tree obstruction or chemical peritoneal burning (phospholipidase A) cause severe acute abdominal pain (Krumberger 1995), requiring opiate analgesia. Use of morphine is controversial; theoretically, morphine constricts the sphincter of Oddi, accentuating pain, but Krumberger (1995) suggests morphine has minimal effects on the sphincter of Oddi.

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Syndromes

  • Diarrhea, may be watery or bloody
  • Eaten foods such as turkey, turkey dressing, chicken, or eggs that have not been cooked well or stored properly
  • Having an abnormal urinary tract
  • Excessive bleeding
  • Put warm compresses on the ear to help relieve discomfort.
  • Avoiding operating motor vehicles or using dangerous equipment

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If FiO2 is increased manually buy dilantin 100mg otc symptoms 1dp5dt, it should be returned to baseline levels once PaO2 is restored order 100mg dilantin amex medications just for anxiety. Catheters Removing oral secretions is easiest and safest with Yankauer catheters; angling the head to enable drainage of secretions into the cheek avoids trauma to the delicate soft palate generic dilantin 100 mg without prescription 5 medications for hypertension. Endotracheal (soft) catheters should remove the maximum amount of secretions in the quickest possible time with minimal trauma discount dilantin 100 mg medications and mothers milk. The practice of reusing disposable catheters for more than one pass seems to be based on anecdotal evidence that infection risks are not increased. Without substantive evidence, nurses reusing catheters should consider their professional accountability, and the legal liabilities of reusing equipment labelled by manufacturers as single-use (de Jong 1996). Using clean (rather than sterile) gloves for suction similarly appears based on anecdotal claims that infection rates are not significantly increased. Gloves of any sort protect (universal precautions) nurses, and clean gloves are both quicker to put on and cheaper; with gloved hands not touching catheter tips, infection risks appear small, but any substantive evidence to support this is lacking (Odell et al. Ventilation continues during catheter insertion and so catheters should be advanced more carefully to reduce trauma (passes should not be slowed so much that patient discomfort is increased). Concerns that they create reservoirs for microbial colonisation appear to be unfounded (Adams et al. Nurses’ concerns that closed circuit catheters may be more difficult to manipulate (Graziano et al. Closed circuit systems can be cost effective if they replace sufficient numbers of disposable items. Most manufacturers recommend replacement after 24 hours; Quirke (1998) found 48-hour changes safe and suggests that further research may support weekly changes; however, staff should remember their legal liability if flouting manufacturer’s recommendations. Widespread practice of saline instillation to loosen secretions has little support beyond anecdotal literature. Mucus is not water soluble and so will not easily mix with saline; encrustations on dentures can be difficult to remove after soaking overnight, and a few seconds contact with saline seems unlikely to significantly loosen airway encrustations. Ackerman (1993) found saline instillation reduced PaO2, possibly from bronchospasm or creating a fluid barrier to gas perfusion. However Ackerman’s methodology alternated use and non-use of saline in the same patients, ignoring possible late complications of consolidation through inadequate removal of mucus. Temperature differentials between cold fluids and airways may trigger bronchospasm so that warming fluids (from hand heat) may reduce complications (Gunderson & Stoeckle 1995). There may be individual cases where saline is indicated, but what those indications currently are remains unclear. Substantial research evidence is needed before saline instillation can be recommended. Nebulisation produces smaller droplets which should reach distal bronchioles, but Asmundsson et al. Hyperinflation Hyperinflation (‘bagging’, to loosen secretions) can be achieved with manual (‘rebreathe’) bags or through most modern ventilators (e. Muscle recoil following hyperinflation mimics the cough reflex and so loosens secretions. It also potentially ■ removal raises intrathoracic pressure ■ removal reduces cardiac return ■ causes (mechanical) vagal stimulation (resulting in bradycardia) ■ causes barotrauma. Manual rebreathe bags are available in various sizes; adult systems should include ■ pressure escape valves ■ oxygen reservoirs if patients normally receive high concentration oxygen ■ 2-litre bags (ideal hyperinflation volume is 1. Relative merits of manual and mechanical hyperinflation remain debated (Robson 1998), but ventilator-controlled hyperinflation leaves nurses’ hands free while ensuring hyperinflation volume is both controlled and measured (limiting barotrauma). Children’s tracheas are smaller and so where 1 mm of oedema might cause slight hoarseness in adults, it would obstruct three-quarters of a child’s airway (Marley 1998). Despite the frequency and long history of mechanical ventilation, many dilemmas of nursing management remain unresolved, influenced more by tradition or small-scale (often inhouse) studies than substantial research and meta- analysis. No aspect of airway management should be considered routine; as with all other aspects of care, frequent assessment enables the individualisation of care in order to meet the patient’s needs. Overviews are usually best obtained from books, but many articles usefully pursue aspects in detail. Wood (1998) provides an extensive literature review on dilemmas of endotracheal suction. Reviewing literature for developing departmental guidelines, McKelvie (1998) gives a reliable overview. Identify those effects that you have observed in your own clinical practice and those from the literature. Lighter sedation ■ enables patients to remain semiconscious, thus reducing psychoses while promoting autonomy ■ reduces hypotensive and cardioinhibitory effects caused by most sedatives Light sedation is a narrow margin between over- and under-sedation. The focus is therefore a nursing one rather than pharmacological, although some widely used sedatives are described. Neuromuscular blockade, once a common adjunct of sedation therapy, is also mentioned. Shelly (1998) stresses that comfort (in its widest sense) can be achieved through sedation. Sedation is now usually only necessary for ventilation if patients have: ■ tachypnoea, which will cause exhaustion ■ discomfort from artificial ventilation (usually from oral endotracheal tubes; also for brief procedures such as cardioversion and bronchoscopy). There are some specific pathologies, such as intracranial hypertension, where sedation is therapeutic. Some authors suggest that potential line displacement justifies sedation (Shelly 1994). Amnesia prevents recall of often horrific procedures, but inability to recall experiences, however horrific, may cause greater psychological trauma (Perrins et al. Prolonged benzodiazepine use causes receptor growth and down-regulation (tolerance), necessitating higher doses (Eddleston et al. Endorphins (endogenous opiates) contribute to sedative effects of critical illness. Midazolam is largely hepatically metabolised and renally excreted, so failure of these organs may cause accumulation of active metabolites (especially with older people, who usually have reduced renal clearance); causing unpredictable increases in half-life with critical illness (Bion & Oh 1997). Being relatively cheap, midazolam is still used by many units for prolonged sedation. Flumazenil’s effect is far shorter than benzodiazepines (half-life under one hour (Armstrong et al. Opiates Most opiates have sedative effects; as analgesia is usually necessary, this ‘side effect’ can be beneficial, provided it is remembered when assessing sedation. Opiates may become Sedation 51 the most important part of sedative regimes (Bion & Oh 1997). Morphine remains one of the most powerful opiates, but newer drugs, such as fentanyl, achieve rapid sedation with strong respiratory depression (which facilitates ventilation). Propofol Propofol’s lipid emulsion facilitates transfer across the blood-brain barrier, achieving rapid sedation. Inactivity of metabolites (Sherry 1997) and rapid redistribution into fatty tissue (Eddleston et al.

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