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Oral assessment necessitates viewing the oral cavity buy 100 mg quetiapine mastercard, so tongue depressors and torches are helpful (Jenkins 1989) buy 300mg quetiapine mastercard. As part of universal precautions (see Chapter 40) discount 300mg quetiapine with mastercard, protective gloves should be worn generic quetiapine 200 mg. Mouthcare 93 Lotions and potions Many mouthcare solutions and other aids have been marketed, most with little support beyond custom and practice. Few remove or prevent plaque, or provide other significant benefits, and many leave unpleasant tastes (nurses can understand patients’ experiences by tasting non-prescription products themselves). Lemon-flavoured swabs (introduced to stimulate salivary production) can decalcify teeth (Crosby 1989). Glycerine is hypertonic, so causes dehydration and reflex salivary gland exhaustion (Crosby 1989). Insufficient dilution of chemicals such as sodium bicarbonate and hydrogen peroxide can cause mucosal burns (Tombes & Galluci 1993); even chlorhexidine rinse can alter oral flora and stain teeth black. Some mouthwashes are antibacterial: pharmacists can advise which solution is best for each patient. Foam sticks can moisten mucosa between cleaning, but do not remove debris from surfaces or between teeth (Pritchard & Mallett 1992), and so plaque accumulation continues (Pearson 1996). As hard sticks cause oral trauma, they should be used carefully and (when possible) with good light. Toothbrush Toothbrushes (with or without toothpaste) remain the best way to clean patients’ teeth, loosening debris trapped between teeth and removing plaque from tooth surfaces (Pritchard & Mallett 1992). The technique reflects that of brushing one’s own teeth: brush away from the gums to remove, rather than impact, plaque from gingival crevices. Manipulating toothbrushes in other people’s mouths, especially when orally intubated, can be difficult; smallheaded multitufted toothbrushes, with soft, small, nylon heads and hollow-fibred bristles, are best for brushing the teeth of others (Pritchard & Mallett 1992; Jones 1998). Pritchard & Mallett (1992) and Jones (1998) recommend the ‘Bass’ method: placing the toothbrush at 44° to the gingival margin, using very small vibratory movements so bristles reach subgingivally to collect and remove plaque. With trismus (limited mouth opening), an interspace toothbrush will remove plaque (although not clean between teeth) (Pritchard & Mallett 1992). Gentle brushing of gums and tongue can also be useful with endentitious patients (Day 1993). Toothpaste should be removed with mouthwashes (Jenkins 1989) and gentle suction, as residual toothpaste can cause further drying of the mucosa. Vigorous brushing may cause bleeding, especially if patients have coagulopathies (e. Intensive care nursing 94 Lips Lips are highly vascular, with sensitive nerve endings, and are even more closely associated with communication (e. Lipcare can therefore prevent drying and cracking, while providing psychological comfort. Dental decay from plaque and debris occurs after one day (Pritchard & Mallett 1992), and so care should be performed at least daily (Treloar 1995; Burglass 1995), but comfort (e. Pressure sores Any body surface area is susceptible to pressure sore development (see Chapter 12). Endotracheal tubes and tracheostomies place pressure on various tissues, including the mouth and nose. Sores are especially likely when tubes rest on gingival surfaces rather than teeth (Liwu 1990); sides of lips are particularly susceptible to sores. The loosening and moving of tapes and tubes relieves prolonged pressure (Clarke 1993). Dentures Intubation and impaired consciousness normally necessitates removal of any dentures, but property should be checked on admission so that dentures are not lost. Nursing records should include whether patients normally wear partial or complete dentures, and relevant care. Like patients’ own teeth, dentures are easily damaged, warping easily, particularly if left dry or cleaned in hot water (Clarke 1993). As dentures containing metal may corrode, Jones (1998) suggests that they should be immersed for just 20 minutes, although this contradicts recommendations (Crosby 1989; Clarke 1993) that they should be left soaking in cold water. Room-temperature water is a medium for bacterial growth, and should be changed daily (Clarke 1993). If denture cleaners are available, these should be used; as toothpaste can damage denture surfaces (Clarke 1993), it should be avoided. Mouthcare 95 Implications for practice ■ mouthcare should be individually assessed, rather than following routine/rituals ■ toothbrushes (with or without toothpaste) are the best means for providing mouthcare ■ toothpaste should be removed with oral suction ■ mouthwashes or moist swabs can provide comfort, although are not on their own adequate for hygiene ■ if antibacterial washes are needed, consult pharmacists ■ find out whether patients wear dentures, recording where they are stored ■ lubricate lips (e. Clarke (1993) and Jones (1998) provide useful articles from wider nursing perspectives; Jones (1998) includes summaries of many available mouthwashes, although often relies on potentially dated sources. The Royal Marsden manual of clinical nursing procedures gives practical and substantiated advice; the 3rd edition (Pritchard & Mallet 1992) is more useful for mouthcare than the 4th edition (Mallett & Bailey 1996). Clinical scenario Pamela Merrell is 60 years old and employed as a television presenter. Computed tomographic scan revealed a large contused area to her frontal lobe leading to development of intracranial hypertension. Nursing interventions that could increase Pamela’s intracranial pressure are necessarily restricted. Consequently she has had minimal oral hygiene care and her teeth have not been brushed for at least 84 hours. However, suggestions necessarily remain tentative, substantial research being needed to develop evidence-based practice. Eye contact helps communication; nurses may feel squeamish about touching eyes, but ocular abnormalities often provoke anxiety among patients and relatives. Vision is, for most people, the most used sense, and so visual deficits contribute significantly to sensory imbalance. Intensive care nursing 98 Ocular damage The cornea, the outer surface of the eye, is vulnerable to trauma and lacerations (e. Blink reflexes and tear production, which normally protect and irrigate corneal surfaces, may be absent or weak (e. The cornea and lens are avascular, absorbing oxygen and nutrients from aqueous humour. Ocular trauma may remain unrecognised until patients regain full consciousness, finding their vision permanently impaired. Normal intraocular pressure is 12–20 mmHg (average 15 mmHg); impaired drainage of aqueous humour (e. Glasses and contact lenses are usually best removed (include in nursing records) for safety, although fully conscious patients often benefit from wearing them. Infection Fox (1989) suggests that most eye infections are caused by ■ Staphylococcus aureus ■ Haemophilus influenzae ■ Streptococcus spp. Eye infection from respiratory pathogens has necessitated corneal transplants with some patients (Ommeslag et al. If ocular infection is suspected, it should be reported and recorded; swabs may need to be taken and topical antibiotics prescribed.

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Traditional dietary management aims to compen-sate for electrolyte imbalances and reduce glomerular workload (and so damage) by restricting protein (a ‘renal’ diet) (Uldall 1988) 300 mg quetiapine amex, although this approach is now questioned buy generic quetiapine 300mg. When conservative measures fail buy generic quetiapine 50mg on line, some form of continuous renal replacement therapy (see Chapter 35) is needed cheap 100mg quetiapine mastercard. There are a number of possible new developments which may in time become established ways to manage renal failure, and these are discussed at the end of this chapter. Intensive care nursing 318 Diuretics Frusemide blocks sodium reabsorption in the ascending loop of Henle; as reabsorption of water is passive, retention of sodium in filtrate increases urine volume. Increased intraluminal flow may prevent or remove tubular obstruction from debris (Adam & Osborne 1997). Frusemide is ototoxic and so should be given slowly; with high-doses this necessitates continuous infusion. Mannitol, an osmotic diuretic, also vasodilates renal blood vessels (Joynes 1996). Reducing interstitial fluid reduces tubular swelling, while increasing intraluminal flow clears obstructing debris (Joynes 1996). McHugh (1997) suggests that high-dose mannitol can reduce duration of dialysis, although this remains to be established. Stimulation of dopamine receptors causes dilation, increasing glomerular blood flow, so increasing filtration volumes. Dopamine does increase urine volume, but animal studies suggest that dopamine- mediated vasodilation only occurs with normal perfusion, urine volumes being increased by dopamine inhibition of sodium reabsorption in distal tubules (which contain more dopamine receptors than juxtaglomerular apparatus) rather than increasing glomerular filtration (Ervine & Milroy 1997). Ervine and Milroy (1997) recommend dopexamine (at 2 mg/kg/min) to increase renal blood flow (this level exceeds recommended dose ranges). Currently, there is growing evidence that dopamine treats staff and fluid balance charts rather than patients; it may have a place in removing fluid overload and preventing tubular obstruction, but dobutamine and other inotropes are increasingly replacing renal dopamine. Renal rescue A protocol from Charing Cross Hospital (London) aims to achieve normo-volaemia, normotension and decreased ion pumping in the ascending loop of Henle by optimising fluid management (Palazzo & Bullingham 1994); this is effectively recognising and treating prerenal failure before it progresses. While management of multisystem-failure patients needs a holistic rather than a reductionist perspective, renal rescue protocols appear to be promising. Exogenous human atrial natriuretic peptide (extracted factor) can be given to improve creatinine clearance, reducing the need for dialysis and reducing mortality (Rahman et al. Urodilatin (a renal peptide, similar to atrial natriuretic factor) improves diuresis without causing systemic hypotension (Cedidi et al. Insulin-like growth factor Animal studies show that this hormone (also called somatomedin C) stimulates anabolism, protein synthesis and renal perfusion. Rhabdomyolysis Awareness of rhabdomyolysis (muscle necrosis) is poor, but improving, yet it causes up to one-quarter of all cases of acute renal failure (Cunningham 1997). The causes of muscle damage include ■ crush injuries ■ thermal injury ■ infection ■ prolonged immobilization. Myoglobin, the oxygen-carrying iron-containing pigment in skeletal muscle, is released; weighing 17 kDa, this is below renal threshold and so is filtered (colouring urine deep red or brown). While mortality from primary renal failure is encouragingly low, mortality from multisystem failure remains high. Renal failure is failure of renal function, and so it causes fluid overload, electrolyte imbalances, acid-base imbalances and other metabolic complications; these further complicate underlying pathologies. Further reading Most applied physiology texts include overviews of renal failure, although recent changes in practice limit the value of older texts. Among journal articles, McHugh (1997) gives a useful general perspective; Stewart and Barnett’s (1997) paediatric article is also useful. Uldall’s (1988) classic book on renal nursing is useful for basic principles, although its age necessitates cautious reading for changes in practice. Clinical scenario David Sinclair is a 58-year-old film critic who is known to suffer from hypertension, angina and gout. Mr Sinclair collapsed at home and was found by neighbours after lying on the floor for approximately 18 hours. A urinary catheter was inserted and Mr Sinclair produced less than 15 ml/h of dark cloudy urine. Examine his abnormal values and risk factors and give a rationale for Mr Sinclair having pre-, intra- or post-renal failure. As part of the multidisciplinary team, nurses should therefore understand how factors, such as likely extravasation, affect patients. Body fluid may be divided as: ■ extracellular ■ intracellular Extracellular fluid is further divided into ■ intravascular ■ interstitial Fluid balance is homeostasis of total body water. Although this chapter focuses on intravascular fluid resuscitation, these compartments are dynamic, not static, and problems with one compartment may compound other problems: critical illness is often complicated by both hypovolaemia and interstitial oedema. Therefore fluid management necessitates considering total body hydration and effects across all three compartments. Fluid management should depend on patient needs: ■ oxygen supply (haemoglobin, perfusion) ■ blood volume ■ other factors (electrolytes, clotting factors) Schierhout and Roberts’ (1998) meta-analysis concludes that colloids increase mortality, but this only reflects the debate that has persisted about the relative merits of colloids and crystalloids for fluid resuscitation. Individual metabolism, capillary leakage, renal/hepatic failure and haemofiltration all affect half-life, and so ranges vary. Manufacturers’ information often originates from animal and (usually) healthy volunteer studies, and information from clinical practice with critically ill patients can be sparse, especially with newer products. Fluids 323 Half-lives cited vary both among literature and between people; figures often derive from measurements on healthy volunteers; increased capillary permeability and other complications of critical illness frequently alter (usually shortening) half-lives. Fluid balance Total body water is approximately 600 ml/kg (Tonnesen 1994), although this varies with total body fat (fat repels water), which itself varies with ■ gender (women have more fat than men) ■ age (total body water reduces with age). Infants have proportionally less fat (and so more body water) than adults, but reach near- adult levels by 2 years of age. Fluid shifts between compartments are both passive (diffusion) and active (hydrostatic and oncotic pressure). Intravascular fluid regulates fluid gain and loss by ■ absorbing ingested fluid ■ osmoreceptor and baroreceptor regulation ■ production of urine and other body fluids from plasma ■ capillary oncotic pressure (normally 17 mmHg) Intravascular volume is also the compartment normally measured/monitored (cardiovascular monitoring, blood chemistry). Intensive care nursing 324 Inflammation enables antibodies and leucocytes (the largest blood cells) to migrate into infected tissue to destroy bacteria. Fluid exudation dilutes toxins, but causes oedema (which stimulates nociceptors, causing pain signals of tissue damage). Fluid management of critically ill patients necessitates the careful evaluation of benefits against disadvantages of each, and this is the focus of this chapter. Nursing observations and records can identify the likely causes of oedema to guide appropriate fluid management: compounding extravasation only prolongs hypovolaemia and pulmonary complications. Extravascular fluids create a counter osmotic pressure, aggravated by any extravasation/leak of low-weight ‘colloids’ from increased capillary permeability. Fluid balance in critical illness is complex, and so hypovolaemia necessitates careful fluid management. Webb (1997) identifies three options for treating hypotension: ■ crystalloids ■ colloids ■ inotropes Using inotropes before correcting hypovolaemia (‘dry drive’) causes unpredictable maldistribution of blood flow, tachycardia and increased oxygen demand (Webb 1997). Right ventricular stretching or displacement of the ventricular septum reduces left ventricular filling, which may limit fluid resuscitation (Robb 1997). A major factor in determining their effect is their molecular size (indicated by molecular weight, usually measured in daltons (Da) or kilodaltons (kDa); where ‘molecular weight’ is cited, this is a slightly different measurement, but approximates to daltons). Like any ‘normals’, exact figures vary between authors; as vascular permeability varies with pathologies (see Chapter 25), precise molecular weights are less important than ranges within which molecules are measured.

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If the signal reaches the terminal buttons generic quetiapine 100 mg on-line, they are signaled to emit chemicals known as neurotransmitters cheap quetiapine 300mg amex, which communicate with other neurons across the spaces between the cells quetiapine 200 mg on-line, known as synapses cheap quetiapine 100mg overnight delivery. Video Clip: The Electrochemical Action of the Neuron This video clip shows a model of the electrochemical action of the neuron and neurotransmitters. The electrical signal moves through the neuron as a result of changes in the electrical charge of the axon. Normally, the axon remains in the resting potential, a state in which the interior of the neuron contains a greater number of negatively charged ions than does the area outside the cell. When the segment of the axon that is closest to the cell body is stimulated by an electrical signal from the dendrites, and if this electrical signal is strong enough that it passes a certain level or threshold, the cell membrane in this first segment opens its gates, allowing positively charged sodium ions that were previously kept out to enter. This change in electrical charge that occurs in a neuron when a nerve impulse is transmitted is known as the action potential. Once the action potential occurs, the number of positive ions exceeds the number of negative ions in this segment, and the segment temporarily becomes positively charged. The electrical charge moves down the axon from segment to segment, in a set of small jumps, moving from node to node. When the action potential occurs in the first segment of the axon, it quickly creates a similar change in the next segment, which then stimulates the next segment, and so forth as the positive electrical impulse continues all the way down to the end of the axon. As each new segment becomes positive, the membrane in the prior segment closes up again, and the segment returns to its negative resting potential. In this way the action potential is transmitted along the axon, toward the terminal buttons. The entire response along the length of the axon is very fast—it can happen up to 1,000 times each second. An important aspect of the action potential is that it operates in an all or nothing manner. What this means is that the neuron either fires completely, such that the action potential moves all the way down the axon, or it does not fire at all. Thus neurons can provide more energy to the neurons down the line by firing faster but not by firing more strongly. Furthermore, the neuron is prevented from repeated firing by the presence of a refractory period—a brief time after the Attributed to Charles Stangor Saylor. Neurotransmitters: The Body’s Chemical Messengers Not only do the neural signals travel via electrical charges within the neuron, but they also travel via chemical transmission between the neurons. Neurons are separated by junction areas known as synapses, areas where the terminal buttons at the end of the axon of one neuron nearly, but don’t quite, touch the dendrites of another. The synapses provide a remarkable function because they allow each axon to communicate with many dendrites in neighboring cells. Because a neuron may have synaptic connections with thousands of other neurons, the communication links among the neurons in the nervous system allow for a highly sophisticated communication system. When the electrical impulse from the action potential reaches the end of the axon, it signals the terminal buttons to release neurotransmitters into the synapse. A neurotransmitter is a chemical that relays signals across the synapses between neurons. Neurotransmitters travel across the synaptic space between the terminal button of one neuron and the dendrites of other neurons, where they bind to the dendrites in the neighboring neurons. Furthermore, different terminal buttons release different neurotransmitters, and different dendrites are particularly sensitive to different neurotransmitters. The dendrites will admit the neurotransmitters only if they are the right shape to fit in the receptor sites on the receiving neuron. For this reason, the receptor sites and neurotransmitters are often compared to a lock and key (Figure 3. The neurotransmitters fit into receptors on the receiving dendrites in the manner of a lock and key. When neurotransmitters are accepted by the receptors on the receiving neurons their effect may be either excitatory (i. Furthermore, if the receiving neuron is able to accept more than one neurotransmitter, then it will be influenced by the excitatory and inhibitory processes of each. If the excitatory effects of the neurotransmitters are greater than the inhibitory influences of the neurotransmitters, the neuron moves closer to its firing threshold, and if it reaches the threshold, the action potential and the process of transferring information through the neuron begins. Neurotransmitters that are not accepted by the receptor sites must be removed from the synapse in order for the next potential stimulation of the neuron to happen. This process occurs in part through the breaking down of the neurotransmitters by enzymes, and in part through reuptake, a process in which neurotransmitters that are in the synapse are reabsorbed into the transmitting terminal buttons, ready to again be released after the neuron fires. More than 100 chemical substances produced in the body have been identified as neurotransmitters, and these substances have a wide and profound effect on emotion, cognition, and behavior. Neurotransmitters regulate our appetite, our memory, our emotions, as well as our muscle action and movement. Drugs that we might ingest—either for medical reasons or recreationally—can act like neurotransmitters to influence our thoughts, feelings, and behavior. Anagonist is a drug that has chemical properties similar to a particular neurotransmitter and thus mimics the effects of the neurotransmitter. When an agonist is ingested, it binds to the receptor sites in the dendrites to excite the neuron, acting as if more of the neurotransmitter had been present. An antagonist is a drug that reduces or stops the normal effects of a neurotransmitter. When an antagonist is ingested, it binds to the receptor sites in the dendrite, thereby blocking the neurotransmitter. As an example, the poison curare is an antagonist for the neurotransmitter acetylcholine. When the poison enters the brain, it binds to the dendrites, stops communication among the neurons, and usually causes death. Still other drugs work by blocking the reuptake of the neurotransmitter itself—when reuptake is reduced by the drug, more neurotransmitter remains in the synapse, increasing its action. It’s also Alzheimer’s disease is associated with an undersupply of used in the brain to regulate memory, acetylcholine. Involved in movement, motivation, and emotion, Dopamine produces feelings Schizophrenia is linked to increases in dopamine, of pleasure when released by the brain’s whereas Parkinson’s disease is linked to reductions in reward system, and it‘s also involved in dopamine (and dopamine agonists may be used to treat Dopamine learning. They are related to the compounds found in drugs such as opium, morphine, Released in response to behaviors such and heroin. The release of endorphins creates the as vigorous exercise, orgasm, and eating runner’s high that is experienced after intense physical Endorphins spicy foods. Imagine an action that you engage in every day and explain how neurons and neurotransmitters might work together to help you engage in that action. Describe the structures and function of the “old brain” and its influence on behavior. Explain the structure of the cerebral cortex (its hemispheres and lobes) and the function of each area of the cortex.

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