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The Roles of Solute Loading and Water Diuresis

Table of Contents

Introduction.

Discussion.

Assessment of data identification.

Assessment data interpretation.

Critical analysis of the interpretation.

The rationale for clinical intervention and impact analysis.

Reference list

Introduction to Polyuria Evaluation

Providence of clinical support for the critical patient demands most efficacy of the nurse. In this case, a female patient of age 59 years has been admitted to the state hospital with the complication of DKA (diabetic ketoacidosis). For the last 2 to 3 months the patient suddenly found her less energetic to perform her regular work and was getting obsessed. However, for the last 30 hours, the condition started deteriorating heavily with severe abdominal pain, nausea. The patient has vomited twice (once at night and in the morning). The patient has a history of hypothyroidism and has to take Thyronorm 50 mg regularly and have diabetes. The decision of insulin therapy and potassium replacement has been decided to manage the acute condition of DKA. The purpose of the study is to analyse the effectiveness and safety of the selected clinical intervention for this patient with acute DKA.

Discussion on Polyuria Evaluation

Assessment of Data Identification

In the introductory segment of this study, the basic medical history has been provided. The age of the female patient is 59 and she has the complication of hypothyroidism and type-II diabetes. As per the viewpoint of Talwalkar et al., (2019), obesity, hypothyroidism and hyperglycaemia (diabetes) are very much interrelated and are noticed collectively for the major patients and the occurrence is tagged with a metabolic disorder. In this case, also the same thing has been identified. The low level of thyroid hormone in blood initiates the issue of diabetes-type 2. This may be true for this patient as she has the issue of diabetes. The pathological test has been conducted for the patient. It has been identified that the patient has the issue of polyuria. As per the words of Bhasin & Velez (2016), polyuria is the excessive flow of urine or the enhancement of the renal output of an individual which can occur for multiple reasons. In this case, the patient has the renal output of two litres per day. During testing, a fruity smell like acetone has been identified in the urine. In this case, the renal output of the patient is about 2400 ml per day.

The blood glucose level has also been analysed which has shown a high range of about 540 mg/dL. The patient is suffering from excessive thirst and has unidentified confusion and drowsiness with cognition issues. Confusion regarding place and time has been identified while communicating with the caregiver and some irrelevant answers have been provided by the patient to the nurse. The valuation of the patient consciousness has been done with the support of the Glasgow Coma Scale (GCS). The valuation of 12 out of 15 has been identified which a little is alarming. The HR of the patient is about 120 bpm which is a little bit alarming but the blood pressure is about 85/60 in the mercury column. The CVP (central venous pressure) of the patient is about 2cmm Hg. Routine blood tests have also been performed for the patient and it has been identified that the blood is a little acidic in pH. The PH value of the blood is 7.1 for the patient. The anion gap has also been analysed for the patient which is about16 mmol/Litre. Hence, all these values are needed to be analysed thoroughly to identify the clinical condition of the patient. The creatinine level of the patient’s serum is about 450 micromole/litre and standard bicarbonate value is 13.4 mmol per litre. The potassium level has been noted as 3.2 micromoles per litre.

Assessment Data Interpretation

The overproduction of the hepatic glucose and increase in the absorption of splanchnic glucose along with low utilisation of glucose leading to deposition in blood and mucus is triggered with abnormal functionality of thyroid hormone (Chaker et al., 2016). In the case of this patient, there is an acute probability of this thing which has triggered the occurrence of DKA. However, the analysis of the other signs and symptoms along with the parameters of the blood tests should be analysed to identify the clinical condition of the patient. It has been noticed that the patient has been admitted with the issue of severing thirst and frequent urge of urination. As per the viewpoint of Goldenberg et al., (2016), the frequent urge of urination and abnormal increase in renal output is one of the major signs of DKA. Additionally, while providing the initial support to the pats, the caregiver has identified a fruity and sweet smell in the breadth of the patient. Kim (2015) has researched the deadly issue of DKA and has mentioned that the fruity and sweet smell in the breadth of a patient with diabetes indicates the development of DKA in the body. Additionally, in the previous section, it has been mentioned that the urine test of the patient, a smell of acetone has been identified. This has triggered the attention to perform the tests to identify DKA. As per the idea of Kumar & Gill (2018), Rothera’s test helps in the identification of the presence of ketone body in the urine of an individual. This is a confirmatory test to identify the presence of acetone in the urine sample with ammonium sulphate and sodium nitroprusside (Jain et al., 2020). A purple colouration has been identified in the sample. On the other hand, Gardhard’s test has also been performed to identify the presence acetone with nitric acid which has initially confirmed the presence acetone. Hence, this has helped to identify the issue of ketonuria for the patient. The patients have type -2 diabetes and regularly take metformin to support the condition. However, insulin has not ever been charged to manage this situation. The medical report has revealed that the blood glucose level of the patient is quite high about 540mg/dL. As per the idea of Piero et al., (2015) the normal blood glucose range is within 140 mg/dL and this is between 140 to 199 mg/dL for the pre-diabetic patients. Hence, from this angle, it can be mentioned that the patient is highly diabetic. The association of diabetes with ketonuria indicates the occurrence of DKA for the patient.

Additionally, the patient has been identified with polyuria and urine volume of the patient is about 2400 ml per day. As per the research of Fayfman et al., (2017), the normal range of real output or urine volume of a healthy individual is 800 to 2000 ml per day. This is another factor which is tagged with the symptoms of DKA and has confirmed the occurrence of the same for the patient. Misra & Oliver (2015) has mentioned that disorientation and less consciousness along with fatigue and high thirst are the indications of DKA. These have also been noticed for this patient.

However, the issue of hypovolemic shock has imparted crisis to the condition of the patient. As per the idea of Yadav et al., (2020), the loss of high quality of fluid through urine creates hypovolemic shock. In this case, the low pressure of the patient with high pulse and poor capillary refill indicates the hypovolemic shock to the patient, which needs to be managed with the supply of fluid to the body.

Critical Analysis of The Interpretation

The normal ketone level of blood of a healthy individual is about less than 0.06 mmol/litre. However, in this case, the blood ketone level of the patient has been identified as 4.4 mmol/litre, which indicate that she has a high level of ketosis in the body. Her blood PH is 7.1 which further indicates that she has acidosis in the body. Hence, the issue of ketoacidosis has been pinpointed in the body of the patient. As per the viewpoint of Wolfsdorf et al., (2018), DKA is tagged with ketoacidosis which is a life-threatening condition for an individual. The pathophysiology of the disease indicates that the long-chain free fatty acid structure of the substrate of ketone body helps its uptake by the liver after getting released from the adipose tissue (Patoulias et al., 2018). The liver keeps the reserve of the same in the form of triglyceride (fat). The liver utilises the fat for energy generation in the time of urgency of the body like prolonged starvation hypoglycaemia or more. However, in the case of low insulin level in the blood, the blood sugar cannot be metabolised to take an entry into the cell for energy generation. This triggers the depletion of fat at a very high rate to generate energy for the body in the form of ketones. The pathophysiology of this disease can indicate the seriousness and life-threatening aspect of this clinical condition. Lin (2018) has researched and mentioned that the synthesis of energy from fatty acid takes place at a very high rate in the body and the rapid ketone build up in the blood turns the blood acidic which is considered as a toxic condition for the human body. Hence, from this angle, it can be mentioned that immediate clinical intervention is needed for the patient. Farsani et al., (2017) has stated that DKA commonly occurs for the pats with type-1 diabetes or juvenile diabetes, which is considered as insulin-dependent diabetes. However, in this case, the patient has a type -II diabetes. The enquiry to the patient associates has revealed that the patient has not visited for endocrinological consultation for the last two years and has not updated her dosage of metformin and Thyronorm for the same period. This negligence has triggered such deadly clinical conditions. The PH of the patient has touched to 7.1 which indicate the initiation of acidosis in the body of the patient and this can be justified with the pathophysiology of the disease.

The serum creatinine level of the patient has been analysed higher than that of the normal range. As per the viewpoint of Jang et al., (2015), osmotic polyuria induced by the blood glucose level of the patient is noticed for the patient with ketoacidosis and this invokes acute kidney injury. However, malfunctioning of the kidney often creates creatinine build up in the body. This is found in the case of this patient as the creatinine level is about 450 micromole/litre which should be within 55 to 125 micromole per litre. Hence, from this angle, it can be mentioned that the kidney functioning of the patient is also getting disrupted for the ketone build-up in the blood.

The issue of a hypovolemic shock for the patient is also common as polyuria develops due to DKA. However, the valuation of standard bicarbonate and sodium is lower than that of the normal range. The sodium level valuation has been pointed out as 128 mmol/litre which should be within 134 to 145 mmol per litre and the standard bicarbonate value is 13.4 mmol per litre. Jang et al., (2015) has commented that 22-30 mmol per litre should be the normal range of standard bicarbonate in the blood of an individual. Hence, from this angle, it can be stated that the condition of the patient is quite acute. As per the research paper of Viera & Wouk (2015), with the issue of acidosis, the level standard bicarbonate in the body decreases. This is the indication regarding the blood toxicity for the body of a DKA patient.

The loss of fluid from the body initiates the loss of balance in the sodium-potassium level this invokes major problems like unconsciousness, confusion, lack of cognition and improper response to the verbal cues. The initiation of the same thing has been noticed for this patient as she has shown the value of 12 out of 15 in the Glasgow coma scale. The confusion regarding time and place has been identified in the patient along with the loss of capability to move. The low level of sodium, potassium and BP is the major factor which is needed to be managed along with the hypovolemic shock. The application of potassium replacement therapy can be done along with insulin administration to manage the acute condition of the patient.

The Rationale for Clinical Intervention and Impact Analysis

It has been stated by the majority of the researchers that immediate action is critically essential for the patient with the issue of ketoacidosis. The sugar level of the patient is 540 mg/dL which needs to be checked immediately to manage the condition of hyperglycaemia. As per the viewpoint of Davis et al., (2016), ketoacidosis develops in the body when the sugar molecule cannot be metabolised and utilised as the source of energy. In this case, this glucose build up in the body has happened due to the lack of adequate insulin level in the blood of the patient. Hence, insulin therapy is initially needed to metabolise the glucose level of the blood. With the administration of insulin therapy, the body of the patient will uptake glucose as the source of energy and fat metabolism will get stopped. As per the viewpoint of Dhatariya & Umpierrez (2017), with the administration of insulin in the body, the fat metabolism gets restricted which simultaneously helps to stop ketone generation in the body. Hence, the acidosis due to ketone generation can be restricted with active insulin therapy for the patients of DKA. This helps in the management of toxicity of blood triggered by acidosis for DKA. Hence, this is the major rationale, to modulate the acute condition of DKA to this patient it has been identified that the patient has the clinical issue of hypothyroidism and obesity, for which she regularly takes thyronorm 50. However, insulin has no interaction and adverse reaction with thyronorm (Islam et al.,, 2018). Hence there is no risk in such clinical intervention associated with insulin therapy. The administration of IV in the initial stage is needed to manage the hypovolemic shock that has happed for polyuria. As per the idea of Myles et al., (2017), isotonic solution (crystalloid) should be administered for the patient with hypovolemic shock with 0.45% salinity and 5% dextrose content. Hence, by following this guideline, the colloidal solution should not be administered in the IV of the patient as she has the deficit of free water in the body circulation. The fluid resuscitation will help the patient to regain the normal fluid volume of the body. Additionally, it has been identified that the patient has serious low blood pressure. This needs to be enhanced to prevent the patient from deteriorating. The application of epinephrine in low dosage should be provided to enhance the blood pressure along with the cardiac output of the patient. However, as per the instruction of Long et al., (2018), the cardiac condition of the patient should be analysed first to identify the safety aspect of the administration of epinephrine. It has been identified that epinephrine often invokes hyperglycaemia which is serious for this type of patient. However, insulin therapy may help to manage such side effects of this drug.

On the other hand, the application of Potassium Replacement therapy should be implemented to manage the condition of this patient. As per the viewpoint of Davis et al., (2016), acute hypokalaemia is one of the most noted side effects of the treatment of DKA with insulin therapy. Initially, the potassium level of the patient has been identified as lower than the normal range. As per the idea of the normal range of potassium in the body in between 3.6 to 5 micromoles per litre in the case of this patient the potassium level is 3.2 micromole per litre which is lower than that of the normal range. This will get further deteriorated with the administration of insulin therapy. Jang et al., (2015) has researched and mentioned that the administration of insulin initiates hypokalemia as transportation of potassium from urine to the cell is disrupted with a high level of insulin present in the body. Antinatriuretic impact of insulin helps in the heightening of the pressure of the past by conserving sodium from being excreted out. However, in the case of potassium, the active transport gets disrupted which induces hypokalemia.

Potassium replacement is actively needed for this patient to help in the management of potassium balance in the body. The administration should be done in the concentration of potassium chloride 20-40 mEq/L and IV administration is the best option for potassium replacement therapy in the management of DKA patients. In the management of the patient the mentioned concentration should be continued until the potassium level reaches to 5.5 mEq/L. This will helps the patient to get back the normal cognition level and to be more active as well.

Additionally, ACE inhibitors may be implemented with potassium replacement therapy for the management of potassium level to the long term. As per the idea of Viera & Wouk (2015), ACE inhibitor interferes within the renin-angiotensin-aldosterone system of insulin and turns down the hypothalamic response of insulin. The major advantage of this therapy is that the sensitivity of the body towards insulin in and the response of the body to the insulin therapy is not unaltered with the administration of ACE inhibitor. Hence, the hyperglycaemic condition can be managed with insulin therapy; potassium level can be managed with the administration of ACE inhibitor. However, to manage the initial crisis the application of potassium replacement therapy will be the best option.

Conclusion on Polyuria Evaluation

At the end of the study it can be concluded that specifically for the patients of diabetic ketoacidosis (DKA), there are multiple complications associated with the management of the acute condition of the patient. However, the care plan should be developed for the long term as it is also considered as a chronic disease. In this case, the acute condition of a female patient with 59 years ago has been managed with the implementation of the clinical intervention of potassium replacement and insulin therapy. It has been noticed that the patient has high creatinine, blood glucose and ketone level in the body. Additionally, the standard bicarbonate and sodium value have got lowered down which indicates the acidosis in the blood of the patient. This is the major factor for which potassium replacement therapy has been selected for the patient. The insulin therapy create hyperkalemia which needed to be managed with the implementation of potassium replacement therapy

Reference List for Polyuria Evaluation

Bhasin, B., & Velez, J. C. Q. (2016). Evaluation of polyuria: the roles of solute loading and water diuresis. American Journal of Kidney Diseases67(3), 507-511. https://doi.org/10.1053/j.ajkd.2015.10.021

Chaker, L., Ligthart, S., Korevaar, T. I., Hofman, A., Franco, O. H., Peeters, R. P., & Dehghan, A. (2016). Thyroid function and risk of type 2 diabetes: a population-based prospective cohort study. BMC medicine14(1), 1-8. https://doi.org/10.1186/s12916-016-0693-4

Davis, S. M., Maddux, A. B., Alonso, G. T., Okada, C. R., Mourani, P. M., & Maahs, D. M. (2016). Profound hypokalemia associated with severe diabetic ketoacidosis. Pediatric diabetes17(1), 61-65. . https://doi.org/10.1111/pedi.12246

Dhatariya, K. K., & Umpierrez, G. E. (2017). Guidelines for management of diabetic ketoacidosis: time to revise?. The Lancet Diabetes & Endocrinology5(5), 321-323. http://dx.doi.org/10.1016/

Farsani, S. F., Brodovicz, K., Soleymanlou, N., Marquard, J., Wissinger, E., & Maiese, B. A. (2017). Incidence and prevalence of diabetic ketoacidosis (DKA) among adults with type 1 diabetes mellitus (T1D): a systematic literature review. BMJ open7(7), 224-227. http://doi.org/10.1136/bmjopen-2017-016587

Fayfman, M., Pasquel, F. J., & Umpierrez, G. E. (2017). Management of hyperglycemic crises: diabetic ketoacidosis and hyperglycemic hyperosmolar state. Medical Clinics101(3), 587-606. https://doi.org/10.1016/j.mcna.2016.12.011

Goldenberg, R. M., Berard, L. D., Cheng, A. Y., Gilbert, J. D., Verma, S., Woo, V. C., & Yale, J. F. (2016). SGLT2 inhibitor–associated diabetic ketoacidosis: clinical review and recommendations for prevention and diagnosis. Clinical Therapeutics38(12), 2654-2664. http://dx.doi.org/10.1016/j.clinthera.2016.11.002

Islam, T., Sherani, K., Surani, S., & Vakil, A. (2018). Guidelines and controversies in the management of diabetic ketoacidosis–A mini-review. World Journal of Diabetes9(12), 226. https://doi.org/10.4239/wjd.v9.i12.226

Jain, A., Jain, R., & Jain, S. (2020). Qualitative Analysis of Urine for Abnormal Constituents. In Basic Techniques in Biochemistry, Microbiology and Molecular Biology (pp. 191-200). Humana, New York, NY. https://doi.org/10.1007/978-1-4939-9861-6_45

Jang, T. B., Chauhan, V., Morchi, R., Najand, H., Naunheim, R., & Kaji, A. H. (2015). Hypokalemia in diabetic ketoacidosis is less common than previously reported. Internal and emergency medicine10(2), 177-180. https://doi.org/10.1007/s11739-014-1146-8

Kim, S. Y. (2015). Endocrine and metabolic emergencies in children: hypocalcemia, hypoglycemia, adrenal insufficiency, and metabolic acidosis including diabetic ketoacidosis. Annals of Pediatric Endocrinology & Metabolism20(4), 179. https://doi.org/10.6065/apem.2015.20.4.179

Kumar, V., & Gill, K. D. (2018). Qualitative analysis of ketone bodies in urine. In Basic Concepts in Clinical Biochemistry: A Practical Guide (pp. 119-122). Springer, Singapore. https://doi.org/10.1007/978-981-10-

Lin, Y. H. (2018). Sodium-glucose cotransporter-2 inhibitors induced eu-glycemic diabetic ketoacidosis: The first report in a type 2 diabetic (T2D) Taiwanese and literature review of possible pathophysiology and contributing factors. Journal of the Formosan Medical Association117(9), 849-854. https://doi.org/10.1016/j.jfma.2018.02.004

Long, L. R. P., Gardner, L. S. M., Burgert, J., Koeller, L. C. A., O'Sullivan, L. J., Blouin, D., & Johnson, C. D. (2018). Humerus intraosseous administration of epinephrine in normovolemic and hypovolemic porcine model. American journal of disaster medicine13(2), 97-106. https://doi.org/10.5055/ajdm.2018.0291

Misra, S., & Oliver, N. S. (2015). Diabetic ketoacidosis in adults. Bmj351. : https://doi.org/10.1136/bmj.h5660

Myles, P. S., Andrews, S., Nicholson, J., Lobo, D. N., & Mythen, M. (2017). Contemporary approaches to perioperative IV fluid therapy. World journal of surgery41(10), 2457-2463. https://doi.org/10.1007/s00268-017-4055-y

Patoulias, D., Manafis, A., Mitas, C., Avranas, K., Lales, G., Zografou, I., ... & Karagiannis, A. (2018). Sodium-glucose cotransporter 2 inhibitors and the risk of diabetic ketoacidosis; from pathophysiology to clinical practice. Cardiovascular & Haematological Disorders-Drug Targets (Formerly Current Drug Targets-Cardiovascular & Hematological Disorders)18(2), 139-146. https://doi.org/10.2174/1871529X18666180206123149

Piero, M. N., Nzaro, G. M., & Njagi, J. M. (2015). Diabetes mellitus-a devastating metabolic disorder. Asian journal of biomedical and pharmaceutical sciences5(40), 1. : https://doi.org/10.15272/ajbps.v4i40.645

Talwalkar, P., Deshmukh, V., & Bhole, M. (2019). Prevalence of hypothyroidism in patients with type 2 diabetes mellitus and hypertension in India: a cross-sectional observational study. Diabetes, metabolic syndrome and obesity: targets and therapy12, 369. https://doi.org/10.2147/DMSO.S181470

Viera, A. J., & Wouk, N. (2015). Potassium disorders: hypokalemia and hyperkalemia. American family physician92(6), 487-495. https://www.aafp.org/afp/2015/0915/p487.html

Wolfsdorf, J. I., Glaser, N., Agus, M., Fritsch, M., Hanas, R., Rewers, A., ... & Codner, E. (2018). ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and the hyperglycemic hyperosmolar state. Pediatric diabetes19, 155-177. . https://doi.org/10.1111/pedi.12701

Yadav, P., Kumar, A., Mathur, R., Garg, P., Gopalakrishnan, M., & Garg, M. K. (2020). Tubelight Adrenals in Diabetic Ketoacidosis. Clinical Practice and Cases in Emergency Medicine4(3), 482. https://doi.org/10.5811/cpcem.2020.6.47617

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