Acute Care Case Study
- Patient CM underwent both physical and laboratory tests. The two tests indicated different results, which suggest renal failure and associated fluid overload in patient CM. Physical observation showed that the patient has small crackles, rales, and wheezing. The small crackles and wheezes consist of sounds, which indicate the presence of fluids in the lungs of patient CM. The sound created vary in pitch as they occur as subtle, short, high-pitched, intermittently cracking sounds. The sounds occur when air passes the fluid present in the lungs. Yet, the wheezes indicate a severe problem in the patient CM’s body. The wheezes happened in the form of snoring, gurgling, and low-pitch moans, which mainly occur during exhalation due to the blockage, of main airways in the CM’s body, by fluids such as mucus and foreign bodies. In addition, the patient indicated lower extremity swelling and pitting edema, which indicate kidney failure in patient CM. These symptoms indicate the presence of fluids in CM’s body, resulting from renal failure.
The laboratory tests realized some results, which indicated a renal failure in patient CM. The laboratory results showed a high concentration of creatinine, which occurs due to the failure of the kidney that should excrete it. Second, the BUN test measures the level of urea. Patient CM results indicated test results of 23 moles per liter that indicate abnormal kidney function rather than the normal range, occurring between 7-20 mmol/l. The Hct ratio of 0.34 also indicated kidney failure as it lowered than the normal range of o.45 to 0.52 in CM. Additionally, the Blood gas test also indicated the incidence of renal failure as the pressure of Hydrogen Carbonate dropped to 18 away from the normal range of 22 to 28, which resulted from patients vomiting. Yet, low urine output of 300ml per 24hours indicates low kidney function. The laboratory results support the occurrence of the incidence of kidney failure as experienced by patient CM.
- Metabolic acidosis primarily occurs in patients who indicate chronic kidney disease. The metabolic acidosis has several causes, which consist of minimized tubular bicarbonate reabsorption, impaired ammonia removal, and inadequate kidney bicarbonate production in correlation with the number of acids that the body synthesis and ingests with food (Adamczak et al., 2018, p. 959). As a result, several metabolic disorders occur that may lead to dysfunction of numerous organs. According to Adamczak et al. (2018), patients indicating metabolic acidosis show faster development of kidney illness towards end-stage renal failure and by increased mortality (Adamczak et al., 2018, p. 959). The plasma concentration and value of pH in CKD patients rely on the acidic food supply, glomerular filtration, alkaline foods supply, and effectiveness of non-renal mechanisms such as bones that compensate metabolic acidosis.
Blood gas measurements determine the levels or amount of oxygen and carbon dioxide in human blood. In addition, the blood gasses indicate the pH levels in the body (Blaivas, 2018). Blood gasses allow health workers to evaluate several body ailments that occur in human beings. First, blood gasses influence the occurrence of respiratory disorders and conditions, which affect the lungs (Blaivas, 2018). Besides, blood gasses allow for effective oxygen therapy and, notably, provide needed information concerning the acid-base balance in the body (Blaivas, 2018). The acid-base balance provides vital information and clues of renal function and the overall body metabolic state. Normal blood gasses of partial oxygen pressure (PaO2) range from 75 to 100 mmHg (Blaivas, 2018). The partial pressure of carbon dioxide (PaCO2) occurs between 38 to 42 mmHg, and oxygen saturation indicates a percentage between 94 to100 (Blaivas, 2018). Normal conditions maintain the blood pH at the range of 7.38 and 7.42 (Blaivas, 2018. The Hydrogen Bicarbonate normal levels keep at 22 to 28 mill equivalents per liter (Blaivas, 2018). Abnormal laboratory results indicate kidney, lung, or metabolic disorders.
- The patient CM manifests the anemia of inflammation, also referred to as anemia of chronic disease (ACD). This type of anemia affects individuals who possess conditions, which influence inflammation. The influencers of inflammation consist of infections, autoimmune diseases, cancer, and notably, chronic kidney disease (CKD). Anemia refers to a condition in which an individual’s blood has fewer red blood cells than average (Nameth and Ganz, 2014). The red blood cells may indicate less hemoglobin than average. Hemoglobin – iron-rich protein – allows red blood cells to convey the red blood cells to the rest of the body from the lungs (Nameth and Ganz, 2014). The body requires sufficient oxygen to function properly. Thus, the lack of enough hemoglobin or reduced blood cells minimizes the oxygen accessed by the body. Additionally, the incidence of anemia of inflammation may indicate an average or increased amount of iron – stored in the body tissues, but show a low level of iron in the blood (Nameth and Ganz, 2014). Anemia of inflammation prevents patient CM from using stored iron to produce sufficient healthy red blood cells, which results in anemia as indicated by fatigue.
The anemia of inflammation has several signs and symptoms, with which some of them occur as depicted by patient CM. The anemia of inflammation develops slowly throughout the life of a patient (Nameth and Ganz, 2014). Yet, the anemia of inflammation may cause few or zero symptoms to the patients. At times patients only experience the signs of the significant causative disease of anemia and miss additional symptoms. The symptoms of anemia show similarity with those of other types of anemia and consist of fast heartbeat, body aches, fainting, feeling weak or tired, feeling tired quickly during or after physical activity (Nameth and Ganz, 2014). Other symptoms of the anemia of inflammation consist of pale skin and shortness of breath. Patient CM reports signs such as shortness of breath and fatigue, which supports the occurrence of anemia of inflammation.
- Renal disorders require early diagnosis, which prevents the patient from experiencing severe health consequences. Patient CM requires a well-structured and goal-affiliated therapy for treatment to aid in efficient recovery. According to Annigeri et al. (2017), the timely realization of patients exposed to risks or with acute kidney disorders remains an essential aspect of therapy (p. 559). Early recognition remains necessary as it minimizes further damage and indicates improved outcomes. Early management of patients who show symptoms of the renal disorder such as patient CM should consist of clinical assessment. Clinical evaluation presents the opportunity to realize reversible factors, which consist of fluid volume status, potential nephrotoxins, and analyzing the possible and underlying health disorders of the kidney.
Implementation of these assessments ensure early interventions that include enough fluid resuscitation while avoiding overload of the fluid, eradication of the nephrotoxins, and notably, the adjustment of more initial prescribed doses with regards to the level of renal disorder reached (Annigeri et al., 2017, p. 559). Medical care should prescribe diuretics to minimize fluid overload in patients who indicate exposure to cardiac disorders such as patient CM. Most importantly, the patient CM must adopt and observe a healthy and balanced diet. A balanced diet ensures that patient CM gets the required food supplements for stabilizing the renal disorder. Patient CM should continue with his previous medication of Lisinopril, ASA, and Rosuvastatin to increase blood flow and reduce the incidence of inflammatory fluids.
- Patient CM has a chronic post-renal failure, as seen from the symptoms under study. Severe post-renal failure indicates that the patient has already lived past the other two categories of chronic renal disorder, which consist of chronic pre-renal and chronic intrinsic renal failure. The pre-renal failure begins with a reduction of blood access to the kidney, which causes damage. Pre-renal failure occurs due to the inability of the kidney to maintain automated regulation of blood, leading to direct damage of the nephron. Severe chronic pre-renal failure results in chronic intrinsic renal failure, which results from the direct destruction of the nephron (Hamdi et al., 2012, p. e1032). Persistent chronic intrinsic renal failure leads to chronic post-renal disorder.
Increased mortality rate occurs during the chronic intrinsic renal failure, which can even result from the intake of medicine – medically induced effect (Hamdi et al., 2012, p. e1032). Severe renal failure occurs as a result of the blockage of the flow of urine flow. Urine blockage leads to back pressure towards the kidney, which causes severe damage to the nephrons (Hamdi et al., 2012, p. e1032). The action of nephron damage, obstructive nephropathy, may cause the acute renal disorder. Other common causes of obstructive nephropathy include urinary tract stones, and prostatic hypertrophy (Hamdi et al., 2012, p. e1032). Patient CM indicates reduced urine count, which indicates urinary contraction, a sign of the chronic renal disorder.
- Patient CM has experienced sepsis shock. Sepsis shock refers to a deregulated response from the body against an infection, which results from life-threatening organ failures. These types of shock get defined and quantified, as seen with the increase of the Sequential Organ Failure Assessment (SOFA) score by 2 points (Standi et al., 2018). The medical care team, in the emergency care environment, applies the SOFA test to screen patients (Standi et al., 2018). The test only requires a preliminary evaluation of the patient’s state of consciousness, blood pressure, and respiration rate.
Any realized alteration of the normal blood pressure 90mmHg, respiration rate of 22/min, and dull consciousness together with suspected infection to major body organs suggests sepsis shock (Standi et al., 2018). The septic shock requires treatment to influence the circulation of blocked fluids into the affected body parts (Standi et al., 2018). Additionally, the administration of vasopressors, inotropic, and eventually, organ replacement therapy could eradicate the occurrence of septic shock (Standi et al., 2018). Cause treatment should begin the moment the medical team receives the report from samples collected from the patient. Individuals should normalize going for medical tests in an attempt to prevent such acute diseases such as renal failure, which affects their body functioning slightly.
References
Adamczak, M., Masajtis-Zagajewska, A., Mazanowska, O., Madziarska, K., Stompór, T., & Więcek, A. (2018). Diagnosis and treatment of metabolic acidosis in patients with chronic kidney disease – Position statement of the working group of the Polish Society of Nephrology. Kidney and Blood Pressure Research, 43(3), 959-969. https://doi.org/10.1159/000490475
Annigeri, R. A., Ostermann, M., Tolwani, A., Vazquez-Rangel, A., Ponce, D., Bagga, A., Chakravarthi, R., & Mehta, R. L. (2017). Renal support for acute kidney injury in the developing world. Kidney International Reports, 2(4), 559-578. https://doi.org/10.1016/j.ekir.2017.04.006
Blaivas, A. J. (2018). Blood gases. U.S National Library of Medicine. https://medlineplus.gov/ency/article/003855.htm
Hamdi, A., Hajage, D., Van Glabeke, E., Belenfant, X., Vincent, F., Gonzalez, F., Ciroldi, M., Obadia, E., Chelha, R., Pallot, J., & Das, V. (2012). Severe post-renal acute kidney injury, post-obstructive diuresis, and renal recovery. BJU International, 110(11c), E1027-E1034. https://doi.org/10.1111/j.1464-410x.2012.11193.x
Nameth, E., & Ganz, T. (2014). Anemia of Inflammation. U.S National Library of Medicine. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4115203/
Standl, T., Annecke, T., Cascorbi, I., Heller, A. R., Sabashnikov, A., & Teske, W. (2018). The nomenclature, definition and distinction of types of shock. Deutsches Aerzteblatt Online. https://doi.org/10.3238/arztebl.2018.0757