End stage renal failure has increased significantly in the Australia in the last two decades. Approximately one in seven Australian adults over the age of 25 years is thought to be living with some degree of renal disease. It is well established that Aboriginal and Torres Strait Islander people’s incidence rate of End Stage Kidney Disease (ESKD) is significantly higher than non-Indigenous Australians. This essay will be discussing about a Haemodialysis patient, Kathy Gill (name changed for confidentiality and privacy purpose), an indigenous lady with End Stage Renal Failure, secondary to diabetic nephropathy. Kathy is on regular haemodialysis, three times per week.
Kathy is 47 year old indigenous lady from Khalkarinji community, who had to shift to Darwin permanently to start on Haemodialysis. Her End Stage Renal Failure is presumed to be secondary to diabetic nephropathy. She is a known case of Type 2 diabetes mellitus, which was diagnosed in the year 2008. She has a right brachiocephalic fistula as her vascular access for haemodialysis. She had some access issues, related to high venous pressure and prolonged bleeding after removal of the fistula needles. In addition to this, she has a past history of coronary artery disease and had coronary angiogram done in September 2011 which showed 80% of stenosis of the left anterior descending artery with minor circumflex disease. A metal stent was inserted in the left anterior descending artery on the same year. She was also an ex-smoker, stopped in 2009.
Kathy presented to Emergency Department with missed three dialysis session, Shortness of breath secondary to fluid overload and bilateral pitting oedema to both legs and hypertension, on physical examination a diabetic ulcer was noted in the left foot. The vital signs were recorded as Blood pressure of 198/110mm of hg, respiratory rate 28/minute and Saturation 98% with 4L oxygen via nasal prongs. Urgent Blood investigation was done for full blood count, C reactive protein (CRP), electrolyte urea creatinine (EUC) and a wound swab for culture and sensitivity was sent from the foot. Blood result showed Kathy was hyperkalemic with potassium of 6.8mmol/l, urea of 40.1mmol/l, bicarbonate of 19.0 with elevated CRP level with no ECG changes (The ideal range for potassium in a person on dialysis is 3.5-5.5 and bicarbonate tests the amount of total carbon dioxide in the blood. Bicarbonate enters and exits kidneys to keep the body’s electrolytes, such as salt, chlorine and potassium, in maintaining the PH, balance of acid in body (Manoj et al., 2016). As the kidney function fail, the level of acid can rise causing the bicarb level to drop so bicarb bag is secured to the dialysis machine. The sodium bicarbonate powder is automatically mixed with water making a saturated solution and it is then balanced with water and acid to attain the prescribed dialysate to correct the metabolic acidity. (Desai, 2015).
She was seen by the Renal Team and was advised for urgent Haemodialysis and was transferred to Dialysis Unit. As per the Missed dialysis Protocol for the Hospital, Kathy was given two hour of heparin free Treatment with 1.5 L of fluid removal. She was then transferred to Renal ward for further care.
She was referred to the Diabetic Foot clinic for further review for her foot ulcer. She received five daily dose of intravenous Tazocin as advised by the infectious diseases team. She had her missed dialysis protocol completed over three days which resolved her shortness of breath and bilateral foot oedema. She was reviewed by the high risk foot team for the ulcer and dressing was done as per their instruction which reduced the slough, clean edges, controlled the pain and wound healing with no evidence of surrounding cellulitis.
The primary reason of the patient’s current hospital admission is this client is missing three sessions of haemodialysis and the right foot ulcer.
Haemodialysis keeps the body in balance by removing waste products, salt and water from accumulating in the body. It also helps to control the blood pressure and regulates important chemicals such as sodium and potassium in the blood (Daugirdas & Blake, 2007). As mentioned in Denhaerynck et al. (2007), successful treatment of patients with ESRD is by strict diet, restricting fluid intake and by taking medicines regularly. Being non–compliant to haemodialysis treatments can result in serious life-threatening complications such as hyperkalaemia, electrolyte imbalances, fluid overload and overall increase the risk of mortality. Fluid non-adherence can be assessed by measuring intra-dialytic weight gain. Skipping one dialysis session is associated with 25-30% increase in the risk of death (Denhaerynck et al.2007). As for this client, her potassium was up to 6.8mmol/l and she has gained a huge amount of fluid by missing dialysis treatments.
Diabetic foot ulcer was the other reason
Diabetic foot ulcers are often preventable. The pathophysiology of diabetic foot ulcer includes various contributory factors such as peripheral neuropathy, peripheral vascular disease, and inflammatory cytokines and impaired resistance to infection (Alavi et al., 2014).
Neuropathy is a disease affecting nerves which may impair sensation, movement and other aspects of health depending on the nerve affected. Peripheral neuropathy is one of the major cause of diabetic foot ulcer. Metabolic abnormalities due to hyperglycaemia cause neuropathy. Neuropathy in diabetic patients is manifested in motor, autonomic and sensory divisions of the nervous system(Noor, Zubair, & Ahmad, 2015). When neuropathy affects motor nerves, it damages the motor nerves which adjusts ability of the body to co-ordinate activities and originates the formation of foot deformity. Motor neuropathy also causes atrophy in foot muscles adding alterations in the foot anatomy causing osteomyelitis. Sensory neuropathy can cause wreckage of sensory nerves present in extremities. Repetitive ulcers in foot are outcomes of sensory neuropathy and it damage the skin integrity. Loss of sensation in the feet leads to ulcers caused by ill-fitting shoes, exposures to heat, and hurt due to foreign bodies(Noor et al., 2015). The client had ill-fitting shoes for long time and her underlying history of diabetes mellitus might have led to her current foot problem. Autonomic neuropathy leads to deportation in functions of sweat and sebaceous glands in foot which leads to dry skin. As an outcome of natural moisturizing capability of foot is lost, the overlying skin becomes more vulnerable to breaks and development of infection. Therefore disturbances in motor, sensory and autonomic functions due to neuropathy leads to damage of skin integrity (Noor et al., 2015).
Peripheral Vascular disease
Peripheral vascular disease (PVD) is another contributing factor for diabetic foot. PVD defines as an atherosclerotic occlusive disease of lower extremity. Diabetes is one of the high-risk factors for peripheral vascular disease. Diabetic patients have a higher rate of atherosclerosis, thickening of basement membranes of capillaries and hardening of arteriolar walls. The hardening and narrowing of large and medium sized arteries leads to acute or chronic ischemia. Ischemia has been reported as a major contributing factor in diabetic patients undergoing amputation. Improper supply of blood to peripheries leads to poor wound healing as well. Peripheral vascular diseases are not measured as independent risk factors, it combines with neuropathy and becomes leading cause of diabetic ulcers (Noor et al., 2015).
Inflammatory cytokines and susceptibility to infection
Once an ulcer develops in patients with diabetes, susceptibility to infection exists because of a loss of essential barrier function. In chronic wounds, microorganisms aggregate together and develop within groups where they enclose themselves with in extracellular polymeric substances containing polysaccharides and lipids. This enclosed collection of microorganisms, identified as a biofilm, increases resistance to antimicrobial, immunologic, and chemical attacks. Bacterial biofilms give to an interruption in healing and the occurrence of chronic inflammation and repetitive infections. Once diabetic foot ulcer have developed, they are often slow to heal because of impaired cell migration(Alavi et al., 2014).
1. Aspirin 100mg daily with food.
Aspirin normally use as analgesic, antipyretic, anti-inflammatory and anti-platelet agents. It is a non-selective NSAID (non-steroidal anti-inflammatory drug), prevents the synthesis of prostaglandins by non-competitively inhibiting both forms of cyclo -oxygenase which in turn lead to anti-inflammatory, anti-platelet and analgesic actions (AMH online).Aspirin is used in end stage renal failure patients to improve the patency of their arteriovenous (AV) fistula and also to increase the blood flow by preventing any thrombus formation in AV fistula (Paraskevas, Mikhailidis, Roussas, & Giannoukas, 2012). Therefore, as Kathy is a haemodialysis patient with Left brachio-cephalic fistula and has a history of coronary artery disease, aspirin has been prescribed.
2. Injection Piperacillin/Tazobactum 4.5gram twice a day
Tazocin is an injectable antibacterial combination contains piperacillin 4g which is a penicillin type broad spectrum antibiotic and tazobactam 0.5g prevents beta –lactamase, which extends spectrum of activity of piperacillin with tazobactam to cover many beta-lactamase producing organisms (AMH online). In Kathy ’s case, Tazocin is used to treat her foot ulcer. Kathy received tazocin post dialysis in dialysis days because haemodialysis removes 31 – 39% of piperacillin and tazobactam from the body (Cervelli, M J. 2008).
3. Calcitriol 0.25 mcg daily per oral:
Calcitriolwhich is the active form of vitamin D to help the body absorb and balance calcium level and control the parathyroid hormone (PTH) level to keep bones healthy and strong. People with chronic kidney disease (CKD) and those on dialysis can experience loss of bone minerals, including calcium and phosphorus. The calcium and phosphorus can combine together, get hard and build up to form calcification in the small blood vessels of the feet, intestines and heart and this condition can lead to amputations, abdominal pain, gangrene of the intestines and heart failure. These complications are due to the combination of dietary calcium, phosphorus, vitamin D and a hormone called PTH (parathyroid hormone). The oral form of Active vitamin D can balance the calcium, phosphorus and PTH. Vitamin D that the body naturally gets from sunlight and food is inactive when renal failure occurs (Jean, 2017).
4. Gliclazide 120mg daily with meal:
Gliclazide helps to increase pancreatic insulin secretion and may decrease insulin resistance (AMH online). Gliclazide usually give with food, to avoid risk of hypoglycaemia. Kathy has Type 2 diabetes related with high blood sugar therefore Kathy is prescribed with gliclazide.
5. Calcium carbonate tablet 1250mg three times per day with meal.
Kidneys excrete excess amount of dietary phosphate, in renal failure phosphate accumulate in the body which cause hyperphosphataemia. The phosphate removal capacity of dialysis is limited. Kathy usually gets calcium carbonate 1250mg with each meal, it is generally help to bind phosphate in the gut lumen and reduce its absorption (AMH online).
6. Metoprolol 50mg per oral:
Metoprolol is a beta-blocker which competitively block beta receptors in most of the organs like kidney and heart. Beta-blockers reduce heart rate, blood pressure and cardiac contractility and also depress sinus node rate (AMH on line). Metoprolol is normally prescribed for hypertension, angina, MI (myocardial infarction) and chronic systolic heart failure. Kathy receives this drug due to her past history of coronary artery disease.
6. Clopidogrel 75mg oral per day: Clopidogrel is an antiplatelet drug and it prevent vascular ischaemia associated with atherothrombotic events. Clopidogrel is also prescribed to prevent the thromboembolism after placement of intracoronary stent (AMH online). Kathy has a history of coronary artery disease and a metal stent was inserted in the left anterior descending artery so she receives Clopidogrel 75mg oral per day.
7.Bactrim antibiotic: as a prophylaxis for melioidosis during the wet season October to April. Meliodosis, is an infection caused by environmental bacterium, which is widespread in the soil and surface water in Northern Territory and the organism is basically resistant to many antimicrobial agents.
8.Vitamin tablets as the dialysis process eliminates large quantities of water-soluble vitamins, such as vitamin C, B-complex vitamins and folic acid. While a kidney diet can typically keep up with these vitamin loss, many people on dialysis have poor appetite and vitamins helps to maintain the muscle, nerve and body function. Most nephrologists’ states that the use of a B-complex vitamin along with folic acid is a good protection when patients don’t have an appetite and it helps to prevent anaemia by working together with iron. (Clase, Ki &Holden, 2013).
9.Darbepoetin alfa injection 80mcg IV once weekly on dialysis
Kathy has the history of chronic anaemia and her latest haemoglobin on admission was 84g/L. Anaemia in ESRD is very common and it responds well to the erythropoiesis–stimulating agents (ESA). ESA has proven benefits in reducing blood transfusion and increasing quality of life (essay%201.docx#_ENREF_1">Agarwal, 2008).
For Clients receiving Darbepoetin, Haemoglobin should be monitored monthly to avoid overshooting the target and efficiency of the treatment. It also important to monitor the blood pressure before administration Darbepoetin as it can increase the blood pressure. Darbepoetin can increase the serum endothelin and can increase blood pressure (essay%201.docx#_ENREF_23">Kanbay et al., 2007).
CURRENT MEDICAL TREATMENT
- Kathy is on regular haemodialysis, three times per week as her renal replacement therapy. Kathy was admitted to the hospital with diabetic foot ulcer and missed three dialysis. On arrival to the hospital she was very unwell and her blood results showed hyperkalaemia, anaemia and uraemia and definite signs of infection by an elevated CRP. Kathy received emergency haemodialysis and was admitted in the renal ward for further dialysis and wound management.
- Treatment for hyperkalaemia: In the emergency department Kathy received treatment for hyperkalaemia as her serum potassium was 6.8mmol/l. Hyperkalaemia is actually a life threatening condition in which serum potassium exceeds 5.5mmol/l (Lehnhardt & Kemper, 2011). Kathy was given Calcium Resonium prior to emergency dialysis to treat her hyperkalaemia. Calcium Resonium helps to remove the excessive amounts of potassium from the blood (AMH online).
- Haemodialysis: Haemodialysis is one of the treatment options for a patients with End stage renal disease which helps to remove the excess fluid, waste products and in turn balances electrolytes in the body (Daugirdas & Blake 2007).Kathy was given emergency dialysis to stabilise her urea, creatinine and electrolytes. As she missed three dialysis sessions together, she underwent missed dialysis protocol as per hospital guidelines. According to Top End Renal guideline (2015), patient who has missed three or more consecutive dialysis treatments should be dialysed in the acute dialysis unit with three gentle dialysis using low pump speed and low flux dialyzer for two hours and subsequently increasing to three and then to four hours in the next consecutive days. Kathy underwent haemodialysis for three consecutive days to complete her missed dialysis protocol. Through the missed dialysis protocol more fluid was removed and had stabilised serum electrolyte levels. Kathy continued to have haemodialysis three times in a week after completing missed dialysis protocol.
- Wound swab: The wound swab was sent withno organism found.
- High risk foot team: High risk foot team service also reviewed Kathy and she had debridement on her right foot and was started on antibiotics.
- ECHOCARDIOGRAM: Kathy has history of coronary artery disease and hence an ECHO was performed as per cardiology team. It showed left ventricular (LV) normal in size with mild segmental systolic dysfunction and mild to moderate left ventricular hypertrophy (LVH).
Fluid volume excess related to missed dialysis manifested by Shortness of breath, Hypertension and oedema
Goal: To improve client’s level of comfort through the maintenance of Ideal Target body weight without excess fluid.
Renal disorder impairs Glomerular filtration that results to fluid overload and is defined as the increases isotonic fluid retention in the tissue spaces. (Allsopp,2011) Kathy was transferred to Renal unit for urgent haemodialysis. Pre dialysis assessment of the patient done by the Nurse which included vital signs, the assessment for peripheral oedema, measuring jugular venous pressure and auscultation of chest and lungs (Steddon, Chesser, Cunningham, & Ashman, 2014). After the initial assessment, the Nurse noticed Kathy as hypervolemic as evidenced by peripheral oedema and shortness of breath. Her jugular venous pressure was elevated. An elevated jugular venous pressure shows an abnormal right heart dynamics, mostly reflecting elevated pulmonary capillary wedge pressure and this usually indicates fluid overload (Chua Chiaco, Parikh, & Fergusson, 2013).The lungs were auscultated, and basal crackles were noted which is a sign of fluid overload.(Jarvis,2012). Kathy was 8.4kg above her estimated ideal body weight. After conducting pre-dialysis assessment, a haemodialysis plan was made as per missed dialysis protocol and Kathy had two hours of dialysis aiming for 1.5litres of fluid removal including isolated ultrafiltration (ISO UF).ISO UF helps to remove extra fluid from the body while avoiding disequilibrium syndrome for the initial one or two dialysis treatments in acutely uremic patients (Daugirdas et al., 2007). After completing her missed dialysis protocol Kathy was able to achieve her Ideal Body weight and was feeling much better.
Hyperkalaemia secondary to missed dialysis:
Goal: to maintain the potassium level within the normal range.
Kathy was hyperkalemic due to missing her dialysis session requiring urgent dialysis. Hyperkalemia cause substantially increased mortality rate in ESRD patients (essay%201.docx#_ENREF_35">Pani, Floris, Rosner, & Ronco, 2014). Dialysis is the definitive treatment of hyperkalemia. Treatment of acute hyperkalemia involves stabilizing of heart function, shifting potassium to the intracellular space (using a combination of IV insulin plus glucose, albuterol and sodium bicarbonate and removing potassium with potassium binders, diuretics, or dialysis. Kathy had daily dialysis for 3 days to achieve her IBW including potassium to be within the range.
Knowledge deficit regarding condition and treatment:
Goal: To provide knowledge regarding disease condition, fluid restriction, importance of dialysis.
The purpose of patient education is to promote, maintain and restore health.
Nurses got a vital role in providing knowledge to the clients regarding their disease condition as a way of providing nursing care to obtain the best outcomes for their patients.
Kathy is non-compliance with her dialysis treatment and medication, so family meeting was arranged with Multidisciplinary team including the Primary Renal Consultant, Social Worker, Dietician, Liaison Officer, and the Primary Nurse. The patient concerns and the family issues were considered during meeting. Kathy talked about her concerns and her family in the community. Explained her that missing treatment can lead to frequent hospital admission and death. As a Nurse ,
Author also tried to explain the importance of fluid restriction with the help of a dietician. Advised patient to drink only 500 ml to 1000 ml each day to control the fluid overload. Author provided her with a book to write the amount of food and fluid consumed each day to a track, which she really enjoyed after a while. Kathy showed willingness to learn more .She was given more education about the wound care by the Diabetic Nurse/Wound Nurse. And she was confident in doing wound care by herself. A new pair of footwear was provided to her by the Diabetic Care Unit to enhance wound healing.
This complex case study illustrates the history of the client with End Stage Renal Failure was presented in Emergency Department with missed Dialysis, hyperkalemia, fluid overload. She received an effective dialysis treatment over two weeks. She had her missed dialysis protocol for first three days then continued with three sessions per week. She received a complete dose of tazocin which helped her with the foot ulcer.
Providing information to the client was one the most important aspect noted here.
Agarwal, A. K. (2008). Darbepoetin alfa for anemia in chronic kidney disease. Expert review of clinical pharmacology, 1(3), 369-379. doi: 10.1586/175124188.8.131.529
Alavi, A., Sibbald, R. G., Mayer, D., Goodman, L., Botros, M., Armstrong, D. G., . . . Kirsner, R. S. (2014). Diabetic foot ulcers: Part I. Pathophysiology and prevention. Journal of the American Academy of Dermatology, 70(1), 1.e1-1.e18. doi: http://dx.doi.org/10.1016/j.jaad.2013.06.055
Allsopp, K. (2011, 2011/03//). Caring for patients with kidney failure: Karen Allsopp discusses dialysis, fluid management and pain relief in emergency department patients with chronic and end-stage renal disease. Emergency Nurse, 18, 12+.
Australian Medicines Handbook 2013, viewed on July 2014.
Booth, J., Pinney, J., & Davenport, A. (2011). Do Changes in Relative Blood Volume Monitoring Correlate to Hemodialysis-Associated Hypotension? Nephron Clinical Practice, 117(3), c179-c183. doi: 10.1159/000320196
Cervelli,m.(2008).The Renal Drug Reference guide,1st edn,Australia
Chua Chiaco, J. M. S., Parikh, N. I., & Fergusson, D. J. (2013). The jugular venous pressure revisited. Cleveland Clinic journal of medicine U6 – ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info:sid/summon.serialssolutions.com&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The+jugular+venous+pressure+revisited&rft.jtitle=Cleveland+Clinic+journal+of+medicine&rft.au=Chua+Chiaco%2C+John+Michael+S&rft.au=Parikh%2C+Nisha+I&rft.au=Fergusson%2C+David+J&rft.date=2013-10-01&rft.eissn=1939-2869&rft.volume=80&rft.issue=10&rft.spage=638&rft_id=info:pmid/24085809&rft.externalDocID=24085809¶mdict=en-US U7 – Journal Article U8 – FETCH-LOGICAL-p838-92ab6c9629abb3f04f43e08475c08ac18c1a6ddde135c9065de09e7be255f4b03, 80(10), 638.
Daugirdas,J,T.,Blake,P.G & Ing,T.S. (2007).Handbook of dialysis (4th edn).Lippincott Williams & Wilkins,Philadelphia USA
Denhaerynck,K.,Manhaeve,D.,Dobbels,F.,Garzoni,D.,Nolte,C.,De Geest,s. (2007).Prevalence and Consequences of Nonadherence to Hemodialysis Regimens, AM J Crit Care May 16:222-235 http://internal.health.nt.gov.au/PGC/DM/_layouts/wordviewer.aspx.
Jiang, Y., Xu, Z., & Fu, X. (2012). Healing Diabetic Foot Ulcers Step by Step. The International Journal of Lower Extremity Wounds, 11(4), 307-310.
Joubert, M., Fourmy, C., Henri, P., Ficheux, M., Lobbedez, T., & Reznik, Y. (2015). Effectiveness of continuous glucose monitoring in dialysis patients with diabetes: The DIALYDIAB pilot study. Diabetes Research and Clinical Practice, 107(3), 348-354. doi: http://dx.doi.org/10.1016/j.diabres.2015.01.026
Kanbay, M., Akcay, A., Delibasi, T., Uz, B., Kaya, A., Koca, C., . . . Yigitoglu, R. (2007). Comparison of effects of darbepoetin alfa and epoetin alfa on serum endothelin level and blood pressure. Advances in Therapy, 24(2), 346-352. doi: 10.1007/BF02849903
Noor, S., Zubair, M., & Ahmad, J. (2015). Diabetic foot ulcer—A review on pathophysiology, classification and microbial etiology. Diabetes & Metabolic Syndrome: Clinical Research & Reviews, 9(3), 192-199. doi: http://dx.doi.org/10.1016/j.dsx.2015.04.007
Paraskevas, K. I., Mikhailidis, D. P., Roussas, N., & Giannoukas, A. D. (2012). Effect of Antiplatelet Agents, Statins, and Other Drugs on Vascular Access Patency Rates. Angiology, 63(1), 5-8. doi: 10.1177/0003319711414177
Scott, L. (2013). Diabetic foot ulcers. Nursing standard (Royal College of Nursing (Great Britain) : 1987), 27(47), 59.