- pain
- dehydration
- temperature
Practise exam
Case study 1 Adi: Adi is a 22 year old woman who was on holiday camping when she noticed a blister on her right ankle. She covered it with waterproof plaster so that she was able to swim in the lake. Over a two day period the blister became increasingly reddened and swollen. After becoming increasingly unwell Adi presents at the emergency department distressed, pale, shivering and clammy.
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1: discuss the clinical reasoning for white blood cell count.
White blood cells play an important role in the body’s defence system against infections. As a result, completing a white blood cell count for Adi will provide a good indication of the presence of infection. There are five types of white blood cells; neutrophils, basophils, lymphocytes, monocytes, and eosinophils. In particular, high white blood cell count known as leukocytosis is an indicator for infection (most commonly bacterial/viral). Although WBC count cannot determine the exact underlying cause, it can help diagnose infection or the inflammatory process.
2: what are the risks of Adi’s current health issues and the complications for them with rational.
3. Explain how Adi’s injury has led to her current status
Based on Adi’s presenting …show more content…
symptoms, the most probable explanation of her current status is sepsis. This process occurs after the entry of an organism in the bloodstream through the skin or the respiratory, genitourinary or GI tract. Organisms include bacteria, yeast, viruses and/or parasites. In Adi’s case, she had a blister on her right ankle which although she had covered with a waterproof plaster, had swum in a nearby lake and the wound had later then become infected. We can assume that some kind of bacteria from the lake had been exposed to the wound site and thus entered Adi’s bloodstream, triggering the infection and thus sepsis. Sepsis, is a complex syndrome characterised by simultaneous activation of the inflammatory response and coagulation in response to microbial insult in the body system. Although the body should naturally produce a non-specific defensive response to inflammation, sepsis produces an exaggerated, excessive inflammatory response throughout the body. A variety of mediators such as histamine, cytokines, and prostaglandins are released into the circulation. This causes widespread vasodilation causing blood pressure to plummet. Capillaries become more permeable, allowing fluid to leak out into interstitial spaces producing hypovolaemia (further lowering blood pressure). This reduced blood flow causes the pale and clammy appearance.
4. What nursing interventions would you provide for Adi’s current status
- administer appropriate medications such as a broad spectrum antibiotic within one hour of diagnosis to treat cause of the sepsis which is wound infection. Non-steroidal inflammatory medicine may also be helpful in decreasing swelling and pain or fever.
- clean and dress the wound to minimise infection and assist in wound healing. Complete a wound assessment to observe any wound exudate, wound depth etc. and at the same time complete a wound culture swab to determine what bacteria/organism Adi is dealing with. This will determine a specific antibiotic to treat the infection.
- Fluid replacement via administration of IV fluids— to reduce hypotension and prevent dehydration.
- Complete a blood test to determine extent of sepsis. For example, during sepsis, the coagulation system also becomes activated and small blood clots (microthrombi) form in small blood vessels. These interfere with blood flow to the tissues and organs, and in combination with hypotension and hypovolaemia, can lead to organ failure.
5. Give the rational for the appropriate interventions * Treating the underlying cause * Fluids and antibiotics – Volume resuscitation | Hypotension is caused by myocardial depression, pathological vasodilatation and extravascation of circulating volume due to widespread capillary leak. The initial resuscitative effort is to attempt to correct the absolute and relative hypovolemia by refilling the vascular tree. There is good evidence that early goal directed aggressive volume resuscitation improves outcomes in sepsis (1).Conventionally clear resuscitation fluids (crystalloids) such as normal saline or Ringer’s lactate are used (hypo-osmolar dextrose based fluids have no role). In this process, very large amounts of fluid may be required due to redistribution to extravascular “3rd” spaces (which sequester fluid), and the patient may become extremely edematous. Large volume saline resuscitation may be associated with acidemia, due to hyperchloremia (so called “dilutional acidosis”). Lactate cannot safely be given to patients with severely impaired liver function. Acetate buffered fluids (such as Normisol) have not yet gained widespread use. | * * Obtaining blood cultures –identify any micro-organisms which may be in the blood. A blood culture will also reveal lactic acid levels (lactic acid levels tend to be elevated during sepsis as the body releases this when tissues are not receiving enough oxygen—resulting in anaerobic metabolism), provide a full blood count (high white blood cell count may indicate infection), urea and electrolyte count (kidney functioning—high levels of urea and creatnine indicate impaired kidney function), glucose levels, liver functioning (ALT and GGT levels), and clotting screen.
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1: Adi is about to be discharged from the ward what planning would you (RN) do?
2: explain the developmental implications that could have an effect on Adi.
Oral contraceptive: Early/unexpected pregnancy is an increasing issues amongst young women. Nutrition depletion (folic acid, vitamin B, magnesium, zinc) immunosuppressed.
Risk taking: Developmental stages of late teens and early twenties — a time of life that is becoming commonly referred to as "emerging adulthood." It is the time of life when many young people are creating their identity, exploring sexual relationships, and deciding on future life goals. It is also a time in life when brain development changes dramatically. To understand why adolescents and emerging adults take risks, it is important to understand what is happening in their brain. As puberty begins, the prefrontal cortex also begins to develop at an amazing rate, paralleling brain growth in the first three years of life. The prefrontal cortex controls judgment, emotions, inhibition control, decision making, and abstraction. As adolescents mature, this part of the brain is rapidly expanding by creating new synapses between neurons that allow teens to think and respond on new levels. At the same time, the prefrontal cortex also goes through a pruning process in which neurons rarely used are discarded to increase efficiency in the brain. For adolescents and emerging adults, the cognitive changes in the prefrontal cortex are accompanied by changes in the socio-emotional networks of the brain. While the cognitive changes in the prefrontal cortex occur as teens mature and experience the world, the socio-emotional aspects of the brain change much more rapidly and become more assertive when stimulated. Within normal adolescent behavior, the socio-emotional aspects, impulse control and desire for risk, are controlled by the slowly increasing capabilities of the cognitive system.
Harmful use of substances: reduces self-control and encourages risky behaviour.
Malnutrition: Many youth are entering adulthood undernourished (eating unhealthy, fast food, etc) making them more vulnerable to disease etc. Obesity and being overweight is another form of malnutrition and can cause serious health consequences for people. Without proper nutritional intake, delayed wound healing and susceptibility to infection is inevitable.
Case study 2 Tom: Tom is an 80 year old man who fractured his right hip following a fall. He has a history of heart disease, hypertension and Alzheimers disease. You arrive on the pm shift and during handover you are informed that he has returned from theatre two hours ago following a total hip replacement. During your initial assessment you find that Tom is difficult to rouse.
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1: what are the implications for the following.
-pain:
-dehydration:
-temperature:
2: what is the nursing management for tom? with pathological rational.
3. Why would tom be difficult to rouse with pathological rational
1-hypoglaecamia (he had to be NBM for sure because elderly patients the risk of complications is too high so they wouldn't send him to surgery strait away, they would make sure that he will be able to cope with the surgery)
2-Fat emboli a process by which fat tissue passes into the bloodstream, lodge within a blood vessel and block it. 90% of the cases it happens following a trauma, fracture of a large bone and in surgery (knee and hi replacements) It is a result of the broken bone, the bone marrow fat scapes into the bloodstream.It is possible that he has start to develop that when he fell or during the surgery.
3- pulmonary embolism. the blockage usually is cause by a blood clot that travels to the lung from a vein in the leg (from large veins)
4-hypothermia (can be caused by low ambient temperature the patient become poikilothermic which is minimal ability to thermorregulate, and can be caused by infusion of cold fluid (IV used in theatre)
5- hypovolaemia can be caused by excessive loss of fluid during the surgery 6- hyponatraemia eletrolyte disturbance, decreased sodium level in the blood can be caused by loss of blood volume or excessive isotonic (IV infusion)
6- stroke due to blood clots and last prolonged drug action (opioid overdose) given pre-op, during surgery and after surgery because he is an elderly patient his drug metabolism is not as effective(any patient that present signs of opioid overdose should be treated with opioid antagonist drug called naloxene.
Alzheimer's medication wouldn't be the cause because if any interaction had happened the patient would be "hyperactive" and delirious. He said that after 2 hours post op patient should not be having difficult to rouse due anaethesia the anaesthetist knowing that the patient is elderly and all his co-morbidities would administer a lower dose of anaethesia, and also patients do not leave Pacu before they have awake and are safe to leave
4. What is the pathological rational for the following assessments
30min obs
GCS
Pain assessment check all vital signs inclusive BSL's + sodium serum level. and check wound site, if there is too much bleeding we should contact the surgeon asap because they might take the patient back to theater to stop the bleeding (cauterization or maybe suture it again)
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1: tom is about to be discharged from the ward what planning would you do?
2: Toms wife explains that she is finding it difficult to manage toms illness due to her own medical issues what would you do to support both tom and his wife.
Case study 3 jimmy: Jimmy is a 68 year old man with emphysema and hearing loss. He is able to do most things around the house but needs to pace himself and does not think his breathing problems are that bad. He is a smoker, uses his inhaler when absolutely necessary and is not oxygen dependent.
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1: discuss the clinical reasoning for O2 therapy.
2: discuss the pathological reason for jimmy being CO2 retaining.
CO2 retention is a pathophysiological process in which too little carbon dioxide is removed from the blood by the lungs. The end result is hypercapnia, an elevated level of carbon dioxide dissolved in the bloodstream.
The principal result of the increased amount of dissolved CO2 is acidosis (respiratory acidosis when caused by impaired lung function); other effects include tachycardia (rapid heart rate) seizures, coma, respiratory arrest and death.
CO2 retention is a problem in various respiratory diseases, particularly chronic obstructive pulmonary disease (COPD). Patients with COPD who receive excessive supplemental oxygen can develop CO2 retention, and subsequent hypercapnia. The mechanism that underlies this state is a matter of controversy. Some authorities point to a reduction in the hypoxic "drive", a condition called carbon dioxide narcosis. When carbon dioxide levels are chronically elevated, the respiratory center becomes less sensitive to CO2 as a stimulant of the respiratory drive, and the PaO2 provides the primary stimulus for respirations. Administering excess supplemental oxygen can potentially suppress the respiratory center. However, it is unclear whether such a hypoxic drive exists in the first place. An alternative explanation is that, in patients with COPD, the administration of oxygen leads to an increase in the degree to which diseased alveoli are perfused with blood relative to other, less-diseased alveoli. As a result, a larger fraction of blood passes through parts of the lung that are poorly-ventilated, with a resulting increase in the CO2 concentration of the blood leaving the lungs.
As CO2 levels increase, patients exhibit a reduction in overall level of consciousness as well as respiratory effort. Severe increases in CO2 levels can lead to respiratory arrest.
CO2 retention is the hallmark of type II respiratory failure. While in type I any degree of hypoxia is compensated for by hyperventilation (and a decrease in CO2), this mechanism fails in type II. Mechanical ventilation (through intubation, CPAP orBIPAP) may be indicated, or infusion of doxapram.
3. Jimmy’s ABG results return and show that he has increase PaCO2 what could this mean? Provide rational in your answer
Hypercapnia (high levels of carbon dioxide in the blood) means less oxygen is being delivered to tissues—possible hypoxia in body cells. One of the most common causes of high levels of carbon dioxide in the body is hypoventilation. This means that the person is not breathing fast enough to support the functions of the body. This occurs when the individual is experiencing diminished consciousness or if he or she has some sort of lung disease or infection. High levels of carbon dioxide in the blood can cause flushed skin, increased blood pressure, muscle twitches, reduced brain and nerve function, headaches, confusion and lethargy. In extreme cases, the patient will need to be given oxygen to breathe so that the balance of oxygen in the blood as also the level of carbon dioxide is brought back to a normal level. When an individual experience an increase of carbon dioxide in the blood, it is important that this is brought back to normal. Long periods of enduring such a condition can lead to damage to internal organs such as the brain.
4. How does jimmy’s smoking led to emphysema? constant exposure to irritants such as tar from smoking causes the alveoli to inflate inside the lungs. As a result they lose their elasticity, less oxygen is able to absorb, causing them to shrink and harden. These lung tissues involved in the exchange of oxygen and carbon dioxide are destroyed as a result. Smoking furthermore causes inflammation and irritation of the airways. This causes obstruction of the airflow within the lungs and thus makes it harder for Jimmy to breathe.
5. How does jimmy’s inhaler relieve his SOB?
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1: why would you (an RN) educate jimmy the importance of quitting smoking?
Emphysema cannot be cured. The goal of treatment is to help people with the disease live more comfortably and to prevent progression of the disease. Quitting smoking is the single most important step people can take toward treating their emphysema. Quitting smoking—even in the late stages of disease—is beneficial. The rate of breathing dysfunction in patients with emphysema slows after quitting, and even people with advanced disease in their sixties who have stopped smoking have been shown to live longer than people who continue to smoke.
A variety of options are available to help people stop smoking, such as nicotine-containing patches, gum and nasal spray and perhaps most important, support groups. Certain anti-depressants can also be helpful. Quitting smoking can be extremely difficult. Remember that concerned professionals and other people are available to help you through this tough change.
Emphysema is one of the most common forms of chronic obstructive pulmonary disease (COPD). Another common form of COPD is chronic bronchitis, which is an inflammation and swelling of the bronchial wall that obstruct airflow. Emphysema and bronchitis often occur together.
Emphysema lasts a lifetime. If caught in the early stages and treated properly, disease progression can be slowed. However, this requires lifestyle changes, including quitting smoking.
2: how would you plan a population based care service about the prevention of emphysema?
Avoiding air pollution and environmental contaminants is also beneficial.
Certain exercises and dietary supplements can be helpful. There are exercises that strengthen the diaphragm and abdominal muscles used in breathing. Learning how to control your breathing can also make you feel better. Establishing a general exercise regimen, such as a walking program, under your doctor’s supervision can help you build strength and improve your overall well-being.
A ten minute exercise called “pursed-lip breathing” can improve lung function, especially right before beginning an activity.
Lie flat on a bed with your head on a pillow and inhale through your nose, consciously moving your abdominal muscles so that your lungs fill with air. Then exhale through the mouth with the lips pursed, so that you make a hissing sound. The exhalation should last twice as long as the inhalation. Try to push all the air out of the lungs. You should feel pressure in your chest and windpipe. Repeat several times. Once you are accustomed to this exercise, you can perform it anytime you need more air, even while
standing.
Learning special positions for sleeping and lying down can help clear your lungs of mucus. A technique known as postural drainage may help some patients. It is usually taught by a physical therapist and can help to drain the upper, middle and lower portions of your lungs. Each position is help approximately 5 to 10 minutes. To drain the middle and lower sections, you should be positioned with your chest above your head. Placing pillows under your hips or using a tilt bed, if one is available, will enable you to achieve this position. To drain the upper lungs, sit up at a 45 degree angle. When you are in the proper postural drainage position, change your position in sequence: turn side to side, lay on your stomach and then lay on your back.
Dietary supplements can help you maintain your weight and nutritional balance if you are becoming too thin. Products such as Ensure (a nutritional drink) may help add calories to the daily intake. Starches and sugars do not need to be limited in stable patients.
Maintaining good hydration to keep secretions loose also assists in eliminating mucus. Try to drink eight glasses of water per day, unless instructed otherwise. Using a humidifier in your home may help as well.
Case study 4 Matthew: Matthew, a 7-year-old boy, is admitted to the children’s medical ward with rheumatic fever, painful swollen knee joints, fever and a history of recurrent nosebleeds. Matthew is pale and tired. He is normally fit and healthy apart from a sore throat that he had 3 weeks ago. Matthew has a lot of family support and lives at home with 5 older brothers, his parents and paternal grandparents
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1: discuss the reasoning for long term antibiotics
Patients who have had an attack of rheumatic fever and develop subsequent GAS pharyngitis are at high risk for a recurrent attack of rheumatic fever, with progression in severity of rheumatic heart disease from the initial episode. The most effective method to limit progression of rheumatic heart disease severity is prevention of recurrent GAS pharyngitis, especially since GAS infection need not be symptomatic to trigger a recurrent attack of rheumatic fever.
For these reasons, prevention of recurrent rheumatic fever (secondary prevention) requires continuous antimicrobial prophylaxis, rather than recognition and treatment of acute GAS pharyngitis episodes. Continuous prophylaxis is warranted for patients with well-documented history of rheumatic fever (including cases with Syndenham chorea as the sole manifestation) and those with definite evidence of rheumatic heart disease.
Prior to initiation of prophylaxis, a full therapeutic course of antibiotic therapy should be given to patients with acute rheumatic fever to eradicate residual GAS, even if a throat culture is negative.
Prophylactic antibiotics should be initiated immediately at the end of the therapeutic antibiotic course. During the course of prophylaxis, patients and their household contacts who develop acute episodes of group A streptococcal pharyngitis should be evaluated and treated promptly as outlined separately.
2: What is the process of rheumatic fever?
In response to a streptococcal A infection, the body’s immune system responds by producing antibodies 97-98% of the time, this process is effective in eradicating the infection. 2-3% of cases however results in the body’s antibodies attacking its own tissue. This is because some bacteria are very similar to the body’s own antigens. This results in an auto-immune response resulting in health effects on joints, cardio tissue, skin/subcutaneous tissue and the CNS.
3. Explain the nursing management for Matthew
Antibiotic therapy — Patients with acute rheumatic fever should be initiated on antibiotic therapy to eradicate GAS carriage. Treatment should proceed as delineated for management of streptococcal pharyngitis, whether or not pharyngitis is present at the time of diagnosis. In addition, household contacts should have throat cultures performed; those with positive results should also receive a full course of antibiotic therapy, even if asymptomatic.
Carditis — Patients with severe carditis (significant cardiomegaly, congestive heart failure, and/or third-degree heart block) should be treated with conventional therapy for heart failure.
Valve surgery may be necessary when heart failure due to regurgitant lesions cannot be managed with medical therapy alone. Surgical outcomes are generally better if valve surgery can be performed when carditis is quiescent. Valve repair, if feasible, is preferred over valve replacement since repair avoids the need for long-term anticoagulation associated with mechanical valves and the long-term risk of deterioration of a bioprosthesis.
Arthritis and rash — Anti-inflammatory agents are the mainstay of symptomatic management due to acute rheumatic fever [8]. Aspirin (80 to 100 mg/kg per day in children and 4 to 8 g/day in adults) is helpful for reducing discomfort related to arthritis and fever. Anti-inflammatory therapy should be continued until all symptoms have resolved. Normalization of inflammatory markers (erythrocyte sedimentation rate and C-reactive protein concentration) may be used as indicator of resolution. The rash associated with ARF is temporary and does not require specific treatment, although antihistamines may help to alleviate pruritus.
The natural history of the polyarthritis in ARF is altered by empiric treatment with nonsteroidal antiinflammatory drugs. In such cases arthritis subsides quickly in the joints affected and does not "migrate" to new joints. Arthritis in Children is treated by steroids and anti-inflammatory's , if shows no sign of effect the child goes on immunosuppressants such as methotrexate. From the reading i have done they do use aspirin in RF as it has shown the most success at reducing the inflammation and therefore preventing carditis and RHD. Aspirin is not usually used in kids because of the risk of Reyes syndrome but they take that risk in RF because of the risk vs benefit of taking it, although i do think that dose is way to high, I've read that they are giving low dose aspirin
4. Give the pathological rational for Matthews symptoms of painful swollen knee joints, fever and history of recurrent nose bleeds
The vasculitis occurring in nasal mucosa, associated with active Rhc disease, renders capillaries more susceptible to ordinary small traumas as nose blows etc. The altered fibrous tissue manifested by fibrinoid degeneration hinders platelets aggregation and the sealing of the ruptured capillaries. The defective aggregation hinders as well the release of coagulation factors notably factor 3 essential for thromboplastic generation.
- Other factors interfering with platelets activity, release of platelet factors and thromboplastic generation may be related to the lowered phospholipids in blood and platelets or to a suppressive
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1: why is Matthews family and living arrangement important to Matthews’s on-going care?
2: what arrangements should be made before Matthew is discharged?
Case study 5 Briana: Briana is a 4-year-old girl admitted with infected eczema and cellulitis of her right arm. She has a history of moderate to severe eczema, allergic rhinoconjunctivitis and asthma. She has eczema flares on her arms, chest, neck, behind her knees and ears. The areas on behind her knees and on her arms are very red and inflamed. Briana lives at home with her mother and two-week-old brother.
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1: explain the connection between Briana’s eczema, asthma and Rhinoconjunctivitus.
So Brianna's case study all the conditions are interrelated, they are all allergic reactions triggered by IgE antibodies these antibodies attach to mast cells and trigger the inflammatory process by releasing histamine and other inflammatory mediators to fight the allergen. Histamine causes vasodilation and increase vascular permeability-which makes blood vessels leaky- this causes increase of fluid in the extra-cellular space. Histamine also irritates nerve endings (they bind to the nerve endings known as C-fibers) nerve endings send a message to the brain and this message comes back as itch sensation. scratch damage the skin and direct release of inflammatory mediators that enhance or cause further itching. Therefore patients who have eczema have this constant cycle eventually skin get infected and if it is not treated can lead to cellulites. Furthermore, mast cells are also found in the respiratory mucosa, bronchial smooth muscles and in the nasal cavity. inflammatory response can then trigger rhinoconjuntivitis and asthma.
the allergy creates a massive IgE outbreak.. and then learn what this leads to (mast cells releasing histamine which cause inflam, permeability etc), and then how would manage it - antihistamines, steroid creams etc
majority of pts with AD progress into having hay fever, asthma and food allergy (cumulatively called the atopic diseases). Apart from impaired skin permeability and barrier functioning, they also tend to have more abundant IgE antibodies. These IgE bodies are attached to mast cells so when an antigen of an allergen binds to mast cell, it triggers the inflammatory response. Mast cells are also found in nasal cavities and somewhere else which i can't remember. Since people with AD are sensitized to a vast variety of antigens over time, when pollen triggers eczema, it usually triggers hayfever too. Then hayfever is known to exacerbate asthma. So i think she's likey to have all 3 together when eczema is flared
2: explain the pathological rational for the presence of cellulitis the epidermis is 15% water 85% lipids which contains ceremides....when the skin is sensitized by allergens then histamine is released which causes brianna to scratch her eczema...this reduces the amount of ceramides which causes the skin to become dry and itchy which causes brianna to itch more continuing the cycle until is is moisturised. Therefore patients who have eczema have this constant cycle eventually skin get infected and if it is not treated can lead to cellulites.
3. what nursing interventions would be appropriate for Briana’s developmental stage?
1. Acute pain related to irritation of the skin, impaired skin integrity, ischemic tissue. Severe cellulitis can be very painful, especially if it has spread throughout the system. A possible diagnosis is "acute pain related to skin infection as manifested by patient reporting extreme discomfort." Ask the patient to describe the type and intensity of the pain and monitor the effect of pain medication. If the medication isn't helping, contact the patient's doctor to determine if a higher dose needs to be given. Regularly assess vital signs, as pain can increase heart rate and blood pressure.
2. Impaired Skin Integrity related to the presence of gangrene in the extremities. Cellulitis makes skin susceptible to other damage, including bed sores. Even if there are no open sores from the infection, the swelling can weaken the skin and lead to problems. This can be expressed as "risk for impaired skin integrity related to edema." If sores are present, "impaired skin integrity related to edema as manifested by open wounds" is a likely diagnosis. Interventions include avoiding friction against the infected area, turning the patient regularly and keeping the area dry.
3. Anxiety related to lack of knowledge about the disease and activity. The patient's tolerance for activity can be affected by cellulitis. The related factor may include pain, fatigue due to medication or general weakness as expressed by the patient. For example, "activity intolerance related to side effects of medication as manifested by patient saying she feels weak." Encourage the patient to engage in as much physical activity as she feels possible, help her perform range of motion exercises and allow for adequate periods of rest and relaxation.
4. Imbalanced Nutrition Less Than Body Requirements related to poor food intake.
5. Sleep Pattern Disturbance related to pain in a leg wound.
6. Knowledge Deficit: the prevention of symptoms and treatment of conditions related to inadequate information. Cellulitis may be prevented by taking simple precautions, especially with wounds. A nursing diagnosis of "knowledge deficit related to wound care" should be followed up with interventions that teach the patient how to properly care for a wound. These include cleaning the wound, applying antibiotic cream, keeping it covered and watching for signs of infection.
7. Fever: Fever is a common symptom of cellulitis and could be expressed as "hyperthermia related to bacterial infection." The evidence may include elevated heart rate, flushing, warm skin or excessive sweating. Since fever can lead to dehydration, it is important to make sure your patient gets plenty of fluids. Fever can also be the cause of a diagnosis, such as "risk for deficient fluid volume." In this case, your interventions would involve keeping the patient free of fever by administering doctor-prescribed fever reducers and monitoring vital signs.
4. Explain how eczema occurs
It is generally agreed that the tendency to atopy is genetically inherited. People with eczematous dermatitis have a variety of abnormal immunologic findings which are probably related to more than one genetic defect. For example, such individuals tend to have elevated IgE antibody (immunoglobulin E) levels and have difficulty in fighting off certain viral, bacterial, and fungal infections.
Common triggers of atopic dermatitis include the following: Harsh soaps and detergents, Solvents, Low humidity, Lotions, Rough wool clothing, Sweating, Occlusive rubber or plastic gloves, Rubbing and Staphylococcal bacteria
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1: you enter Briana’s room and her mother is tearful and is upsetting Briana and her brother what would you do?
2: Briana’s mother tells you that she has very little support at home and isn’t coping. What do you do?
Case study 6 Tim: Tim is a 70 year old man who has undergone a below knee amputation for peripheral vascular disease. He has a history of diabetes mellitus type 2, renal impairment and coronary heart disease. Tim is now second day post-op.
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1: explain the process and relevant connections between diabetes, peripheral vascular disease, renal impairment, and CHD.
Persons with diabetes run a greater risk of developing cardiovascular problems, with the most common heart condition being coronary artery disease - also called hardening of the arteries or atherosclerosis. This condition consists of a build-up of plaque in the blood vessels that supply oxygen and nutrition to the heart and then on to other parts of the body like the brain. Plaque, which is made up of cholesterol and other fatty substances as well as fibrin and calcium, can block these vital blood vessels, causing them to rupture and prevent blood flow.
The build-up usually begins before the blood sugar level increases that occur in type 2 diabetes. In other words, heart disease has often established itself prior to a diagnosis of diabetes.
Studies have shown that hyperinsulinemia (high blood insulin levels) and hyperglycemia (high blood glucose levels) can lead to atherosclerosis. High levels of glucose cause proteins to become sticky and not function properly. This can occur in several areas, including the inner lining of the blood vessels where proteins travel in the blood.
These proteins with glucose stuck to them are called AGEs, or advanced glycosylation end products, which accumulate in the blood and become incorporated in the walls of the arteries to form atherotic plaques. Macrophages, or immune cells, play a big role in forming plaques. They absorb glycosylated proteins and LDL "bad" cholesterol particles, swell up to become foam cells and enter into the now-sticky arterial wall. This process causes the blood vessel to narrow and restrict blood flow.
PAD is a manifestation of atherosclerosis characterized by atherosclerotic occlusive disease of the lower extremities and is a marker for atherothrombotic disease in other vascular beds.
Diabetes, inflammation, and risk for PAD
Inflammation has been established as both a risk marker and perhaps a risk factor for atherothrombotic disease states, including PAD (11). Elevated levels of CRP are strongly associated with the development of PAD (12). In addition, levels of CRP are abnormally elevated in patients with impaired glucose regulation syndromes, including impaired glucose tolerance and diabetes.
In addition to being a marker of disease presence, elevation of CRP may also be a culprit in the causation or exacerbation of PAD. CRP has been found to bind to endothelial cell receptors promoting apoptosis and has been shown to colocalize with oxidized LDL in atherosclerotic plaques. CRP also stimulates endothelial production of procoagulant tissue factor, leukocyte adhesion molecules, and chemotactic substances and inhibits endothelial cell nitric oxide (NO) synthase (eNOS), resulting in abnormalities in the regulation of vascular tone. Finally, CRP may increase the local production of compounds impairing fibrinolysis, such as plasminogen activator inhibitor (PAI)-1.
Renal artery disease most often is related to peripheral artery disease (atherosclerosis in arteries outside the heart) or coronary artery disease.
There is an increased prevalence of cardiovascular disease- (CVD-) related mortality in patients with chronic kidney disease (CKD). Endothelial dysfunction is a primary event in the development of atherosclerosis and hypertension and likely contributes to the elevated cardiovascular risk in CKD. Endothelial dysfunction has been shown to occur in the peripheral vasculature of patients with both severe and moderate CKD.
Like the atherosclerosis that affects the arteries of the legs (peripheral artery disease), renal artery disease is caused by the buildup of plaque in the arteries that lead to the kidneys. Plaque is made up of fats and cholesterol, and as it accumulates in the renal arteries, it causes the arteries to stiffen and narrow, which blocks the flow of blood to the kidneys. Obstructions (blockages) in the renal arteries, known as renal artery stenoses, can cause poorly controlled high blood pressure, congestive heart failure, and kidney failure.
The kidneys play an important role in regulating blood pressure by secreting a hormone called renin. If the renal arteries are narrowed or blocked, the kidneys cannot work effectively to control blood pressure. Persistent or severe high blood pressure is a common symptom of renal artery stenosis.
2: why is it important to monitor tims surgical wound? it is not surprising to find that such patient risk factors can result in an array of wound-healing difficulties, thus prolonging debilitation and reducing quality of life. The UK's increasingly ageing population means that more elderly patients will be operated on in the future, thus giving rise to a growing trend in postoperative tissue viability problems where skin fragility and multiple pathologies such as diabetes and peripheral vascular disease co-exist.
In most instances, surgeons performing a lower limb amputation will use the primary closure technique, in which the edges of the wound are closely approximated, thus eliminating dead space and involving minimal formation of granulation tissue. There may be a drain in situ which will be removed on the first or second postoperative day. The drain is often not sutured in place to allow its removal without disturbing bandages or dressings.
It is advisable to assess amputation wounds regularly for evidence of problems such as offensive odour, haemorrhage or excessive exudate. In most cases surgical wounds are managed with a simple island dressing, orthopaedic wool padding and a light retention bandage. It could be argued that such low cost, traditional dressings are adequate for most surgical wounds. However, amputees with poor tissue integrity often require modern woundcare products that offer additional benefits, such as the low adherence offered by the soft silicone range. Indeed, dressing adherence as a result of dried blood products can cause trauma, pain and anxiety at dressing changes. Wound dressings also need to be robust enough to withstand movement and use of the stump; they should not limit or interfere with the patient's rehabilitation.
There is a lack of agreement surrounding the length of time a surgically closed wound should be covered. Some clinicians argue that the wound can be left exposed after 24 to 48 hours. However, others propose that exposure may contribute to wound pain, suggesting that the wound should remain covered until suture removal. In light of hospital-acquired infection rates, it would seem prudent to challenge regimens of the past and maximise the time a wound is covered. Moreover, the stump often requires additional protection from trauma, which can be experienced during transfer to and from the patient's wheelchair.
A correctly placed stump bandage can be used to mould the stump and allow early mobilisation so may be left in place for four to five days, only being changed if there is increasing stump pain, odour or pyrexia. Practice varies according to local protocols - rigid plaster dressings are fitted in some centres in the immediate postoperative period, with reports of quicker wound healing and earlier ambulation.
Stump oedema: Excessive and prolonged stump swelling or oedema is thought to be due to pre-existing venous insufficiency, generalised fluid retention (usually due to congestive cardiac failure) and chronic hypervascularity (often seen in patients with diabetes who do not have significantly impaired arterial blood flow). Deep vein thrombosis (DVT) can also be a cause of limb swelling. A diagnosis of DVT is frequently associated with the lower limb amputee. Other causes may include hypoproteinaemia, stump dependency and infection. It is essential to identify and, where possible, treat the underlying cause of stump oedema. Nutritional support may be required in the form of high protein supplementation.
A stump wound associated with excess oedema and resulting exudate is likely to heal slowly, if at all. It is now believed that, in some instances, components of wound exudate can be harmful to wound healing and the condition of the surrounding skin. Measures must be taken to achieve an acceptable balance of exudate. Excess wound drainage or exudate can be attributed to seroma/haematoma formation and infection. Postoperative oedema of the amputation site may be overcome by a strict regimen of limb elevation
Haematoma: A haematoma is a localised collection of blood which can form in an organ, space or tissue [14]. It acts as a focus for infection and can create dead space, weakening the suture line and thus increasing tension in the wound. In most cases they drain on their own, without the need for surgical intervention; however, large amounts of clotted blood may warrant prompt surgical debridement. Wounds with no drainage may be at risk of haematoma formation under the suture line, causing tension and oedema at the wound site, as well as providing ideal conditions for bacterial growth. Partridge believes that the increased tension under the suture line can lead to a disruption in blood supply, resulting in dehiscence and necrosis
Pain: It is thought that pain experienced after an amputation may scare and confuse patients and features in case reports as a difficulty for patients. Amputees can experience two different types of pain: incisional stump pain and phantom pain. Stump pain is localised to the area immediately around the stump and the amputation scar and is described by patients as 'pressing', 'throbbing', 'burning' and 'squeezing'. If unresolved, such pain is considered to negatively affect wound healing and to impact on quality of life
Successful relief of incisional stump pain can be achieved by the use of opiates, non-steroidal anti-inflammatory agents and local anaesthetics. Phantom limb pain may be relieved with anticonvulsants, tricyclic antidepressants, transcutaneous electrical nerve stimulation (TENS) and therapeutic touch and massage. If the patient's pain is worsening and becoming unmanageable, despite appropriate interventions, referral to an acute pain service may be indicated.
Infection: Infection can pose serious complications for the amputee. The authors of this report explain that high infection rates are likely to be related to underlying risk factors that affect wound healing and vulnerability to infection, such as poor limb perfusion and diabetes. On average, patients with diabetes are approximately five times more likely to have a post-surgical wound infection than non-diabetics.
One complication is cellulitis, which is characterised by swelling, pain, pus formation, erythema, heat, sometimes accompanied by fever, leading in severe cases to septicaemia. Even localised wound infection can be problematic, resulting in excess exudate and breakdown of the suture line. A severe infection can lead to wound dehiscence, significant tissue necrosis and result in the need for further surgery.
In addition to the use of systemic antibiotics, wound infection can also be addressed by enhancing the host defence mechanisms (for example controlling blood sugar levels), wound debridement, wound cleansing, increased frequency of dressing changes and use of topical antimicrobials such as silver or iodine dressings.
3. What is the nursing management for Tim now that he is 2 days post-op?
Assessment
1. Neurovascular status of involved extremity. 2. History to determine causative factors and health problems that can compromise recovery. 3. Client’s understanding of the extent of the surgery. 4. Client’s coping status. 5. Client’s support system.
Nursing Diagnosis * Body image disturbance * Constipation * Diversional activity deficit * Fear * Risk for injury * Impaired physical mobility * Self-care deficit * Risk for skin integrity * Situation low self-esteem
Nursing Interventions 1. Provide care preoperatively by initiating exercise to strengthen muscles of extremities in preparation for crutch walking. 2. Encourage coughing and deep breathing exercises. 3. Monitor vital signs and stump dressing for signs of hemorrhage. 4. Elevate stump for 12 to 24 hours to decrease edema. 5. Maintain elastic bandage to shrink and shape stump in preparation for prosthesis. 6. When wound is healed, wash stump daily, avoiding the use of oils which may cause maceration. 7. Apply pressure to the end of the stump with progressively firmer surfaces to toughen stump. 8. Encourage the client to move the stump. 9. Place the client with a lower extremity amputation in a prone position twice daily to stretch the flexor muscles and prevent hip flexion contractures. 10. Teach the client about phantom limb sensation. 11. Support the client through fitting, application, and utilization of prosthesis. 12. Encourage family to participate in care. 13. Allow the client to express emotional reactions.
Lo2
1: what method would you use to promote diabetes awareness to a population group?
2: what education would you supply to Tim?