Case Discussion of Renal Failure Requiring CRRT/IHD

Question: Discuss about theCase Discussion of Renal Failure Requiring CRRT/IHD. Answer: Introduction Patients with kidney failure are faced with a situation where kidneys no longer functions. There might be several complications associated with such conditions as high blood pressure, anemia and heart diseases with symptoms as feeling tired or confusion or loss of appetite or leg swelling(Montague, 2008). Patient with impaired renal functions needs to be identified in cases of critical illness. Serum creatinine acts as a standard measure for measurement of renal functions and defining patients with chronic kidney disease. The current case analysis involves diagnosing a patient faced with renal failure whose blood tests are included along with a reflection on understanding relative to the case. Case Presentation The case is concerned with a 80 year old Chinese patient who was admitted to ICU for renal failure. The patient had Hyperkalemia (K 9.0 ) with decompensated metabolic acidosis (HCO3 13, pH 7.16) and fluid overload, hypertension - b/g ESRF, etiology unclear on HD 2/4/6 via L AVF. b/g ESRF, etiology unclear on HD 2/4/6 via LAVF - underwent emergent HD overnight, venous pressure high 400 (heparin-free dialysis) thus terminated HD 45 mins earlier, UF 2.3L (target was 2.5-3L) - post-dialysis weight 51.5kg on 14/10/17(DW 51.9kg acc to AMK FMC) - recheck K 5.9 2hours post dialysis, given resonium -started on CPAP EPAP 10, FiO2 30% for fluid overload, pt felt less SOB after, declined CPAP subsequently, weaned off from VM to RA - Trop I neg x 2 (48 62) - underwent 2nd session of dialysis (heparinsed) on 14/10/17, repeat RP post-dialysis: repeat K 4.7 2.Non-specific giddiness - ?Rhomberg's +ve, nil cerebellar signs - CT brain (14/10/17): Nonspecific left frontal subcortical white matter hypo density, may represent early chronic microvascular ischemic change or age-indeterminate infarct.Chronic infarcts. b/g Ca colon s/p primary resection 20years ago, moderately severe AR, HTN, HLD, Hepatic cysts/ erosive gastritis Above analysis for patient is undertaken and conducted using self-reflection. Analysis of pertinent findings from the patient in this case reflects renal failure required CRRT with IHD(Packham, 2015). All indications of the patient reflects that with failing IHD and dizziness, he requires IHD for overcoming his current conditions. Reflection In cases of this patient diagnosed with end-stage renal disease, hyperkalemia is considered to be a common condition(Lehnhardt, 2011). Chronic kidney disease (CKD) has been identified as a leading health challenge across the globe. With a number of growing elderly and patients of hypertensions health care practitioners will be faced with complex problems arising from renal failure. Such conditions affecting the patient has also led to effect on cardiac conductivity. Potassium content on an average person is expected to be at 3500 mmol where 98% are present in cells with only 2% being in extracellular compartments(Pannu, 2008). Changes in distribution amongst compartments of cells can change serum potassium concentration. While potassium is taken in, it is also excreted out. Excretion of potassium depends on renal activity and has no connection to intestinal excretions. It has been seen that maximum amount of oral potassium (approximately 90-95%) is excreted in urine and rest in stool . Excretion of oral potassium is a slow process and dietary potassium is absorbed first in extracellular fluid. Such dietary potassium excretion could easily lead to hyperkalemia in case it does not shifts from extracellular to intracellular compartments. Factors that might stimulate potassium shifts are insulin, metabolic alkalosis and catecholamine(Einhorn, The frequency of hyperkalemia and its significance in chronic kidney disease, 2009). As the patient in this case has end stage renal failure, kidneys that are responsible for excreting potassium cannot do so leading to hyperkalemia. The patient was visiting Nephrology Clinic as he was referred from Hepatology Clinic. He had been diagnosed with ESKD (End stage kidney failure) causes were unknown. The patient had been having HD treatment since July 2015. He had a history of colon cancer 20 years ago and hypertension with Dyslipidemia. He visited Hepatology Dr. Lee YM for erosive gastritis and hepatic cysts(Weisberg, 2008). He vomited and was feeling unwell with high BP which caused him to miss HD on 10th and 12th October. He also had lower limb weakness due to hyperkalemia which affects muscles. He had increasing dyspnea and orthopnea also in past few days reflecting that hyperkalemia had affected his heart. He had also been facing metabolic acidosis and fluid overload. Therefore, the patient was admitted to MICU for close up monitoring of cardiac activity. The patient has excess of potassium levels in extracellular compartments exceeding 5.5 (it is 9 in this case). But as seen in multiple cases hyperkalemia is seen in patients with excess intake of potassium through oral or intravenous supplementation. The case patient here has end-stage renal disease, skipping dialysis treatment (HD). It has been noted that drugs along with age have impaired urinary potassium excretion that have further aggravated hyperkalemia(Weir, Patiromer in patients with kidney disease and hyperkalemia receiving RAAS inhibitors, 2015). In cardiac tissues of the patient, hyperkalemia attacks cells with excitability making less capable to depolarize. The most feared clinical consequence faced by the patient is its effect on cardiac conductivity. The patient also suffers from hypertension, two sessions of HD had to be terminated and one session had to be stopped 45 minutes earlier as blood pressure rose immensely. There is peaked T-waves with prolonged PR intervals. The condition experienced by the patient is bound to affect his skeletal muscles rendering parasthesias and motor weakness. For treating the patient all life-threatening effects on cardiac conductivity has to be treated. Firstly, as patient feels dizzy intravenous infusion of calcium salts as calcium chloride or calcium gluconate has to be administered to change EKG(Smith, 2008). The threshold for cardiac muscles will help decrease excitability by increase administration of serum-calcium concentration. According to my learning and reflection, hemodialysis is the best therapy for severe hyperkalemia and patient with end stage renal disease. The patient needs to institute temporizing measures for lowering serum potassium accurately 2 hours before starting of hemodialysis. The therapy will help the patient to rapidly shift intracellular fluid compartments. It can be done using beta-2, bicarbonate and adrenergic agonists. Intravenous Insulin with combination of glucose will help in correction of hyperkalemia. The patient can develop hypoglycemia in this therapy, but Insulin with glucose is the most reliable drug. Intravenous Albuterol also can lower potassium in stable dialysis but it caused rise in seru m insulin levels. The patient had been given once cycle of IV calcium gluconate, insulin-dextrose given once. The patient is ESRD for treating of hyperkalemia removal of potassium either through gastrointestinal track (GI) or dialysis is undertaken. For this patient having hepatological factors referred to nephrological unit. Dialysis is the best treatment for severe hyperkalemia but in this case there are several factors related that might impact magnitude of removal of potassium, one such parameter being dialysate concentration of potassium, glucose and bicarbonate along with dialyzer blood flow. As most potassium removal happens during removal first 2 hours at times when potassium gradient between dialysate and blood is the highest(Sterns, 2010). For the patient hemodialysis is performed by use of 2-mm dialysate potassium concentration (2-K). By increasing potassium gradient in blood and dialysate lowering of dialysate potassium concentration can be done. But increasing potassium removal by lowering dialysate potassium concentration might impair dialysis adequacy. Low potassium dialysate increases potassium removal and is an effect treatment for acute hyperkalemia with ESRD. Such treatment might however reduce efficiency of urea clearance and aggravate ventricular arrhythmias(Khosla, 2009). Allon and Shanklin depicted that administering nebulized albuterol in patient 30 minutes before dialysis can lower potassium removal at the time of dialysis. There might be exaggerated rebound in serum potassium in case beta-adrenergic wears off post 4 to 6 hours. Preventing hyperkalemia in dialysis patient is of utmost importance. As kidney is the major source for excretion of dietary potassium, limiting such intake is critical for anephric dialysis patients. The patient need to be limited his daily dietary potassium to 2 to 3 grams by restricting potassium rich foods as beans, lentils, squash, chocolate, potatoes, salt substitutes, which are especially found in Chinese foods(Group., 2009). The patient is unable to intake much food due to vomiting and hepatic cysts. Due to suppr essed endogenous insulin secretion fasting hyperkalemia might be noted. As a result of net shift of potassium in intracellular compartments there might be decreased levels of plasma insulin. Dialysis patients lack adaptive measures or healthy controls hence they develop hyperkalemia. In various cases prolonged fasting leads to increase in serum potassium in dialysis patients with normal controls. In case dialysis patients are subjected to prolonged fasting there needs to monitoring for hyperkalemia. Acute renal failure (ARF) has claimed over 20-25% lives in ICU that has further risen leading to multi organ failure. However, the mortality of the diseases greatly depends upon underlying diseases and other risks factors in critically ill patients. Till date literature analysis had been focused on continuous renal replacement therapy (CRRT) and conventional intermittent haemodialysis (IHD). The time during which each one is applied greatly varies as CRRT has to be applied continuously and IHD is applied few hours during the day. IHD has to be an efficient therapy for fluid removal and toxins. IHD is performed by a low-flux dialysis member using diffusive therapies with high dialysate flow requiring dialysis monitor. CRRT modalities are low on efficiency hence a rather continuous technique is applied. CRRT is done using high-flux membrane with industry made substitution fluid in bags by convective therapy. CRRT demands less of technical expertise whereas IHD requires technical expert ise of dialysis team as well as nursing(Pavlakovi?, 2010). CRRT is found to be better technique as compared to IHD with mixed review of patients in both treatments. In case of CRRT haemodynamic stability of patient is greater as compared to IHD. In this case also CRRT would have yield better results as the patient had been suffering from hypertension with increased BP during IHD. IHD cannot deliver epuration in high catabolic ARF patient of ICU, but its was prescribed often for desired levels of metabolic control. There is still debate regarding biocompatibility of dialysis member with ARF patient. In case of biocompatible members outcomes were better with lower cases of sepsis as against cellulosic membranes. There are loss of amino acid and protein with use of high-flux polysulfone membranes as compared to low-flux cuprophane membranes. This can lead to inadequate nutrition management of patient. For treating lactic acidosis CRRT can be used as a modality for patients with multipl e organ failure. Extracorporal clearing of lactate is calculated to be low as against internal metabolisation hence metabolic acidosis cannot be effected by CRRT. CRRT can help in removing of mediators of inflammation, sepsis and cytokines. Molecules can be removed by membrane convection or adsorption, rate of synthesis of such molecules will not decrease their levels of plasma. Removal of anti-inflammatory cytokines with balance of anti and pro-inflammatory molecule plasma levels will be unchanged. CRRT is more expensive when compared to IHD as there is a need for large quantities of industry-prepared dialysate for artificial kidneys. Primary differences in IHD and CRRT arise from their weaknesses as IHD allows intermittent therapy that has haemodynamic intolerance. Conclusion Intermittent hemodialysis (IHD) involves steady renal replacement therapy for effective management of modalities. Hyperkalemia is an end stage renal disease that can be rectified with CRRT. For treatment purpose the patient may be administered with insulin and glucose, albuterol. Removal of potassium might also be suggested for patients as cation-exchange resins have not been used significantly. Across the world dialytic removing of potassium is the mostly used therapy. There can also be intervention with prevention of interdialytic hyperkalemia. Reference Lists Einhorn, L. M. (2009). The frequency of hyperkalemia and its significance in chronic kidney disease. Archives of internal medicine, 1156-1162. Group., E. T. (2009). Strict blood-pressure control and progression of renal failure in children. N Engl J Med, 2009, 1639-1650. Khosla, N. K. (2009). Predictors of hyperkalemia risk following hypertension control with aldosterone blockade. American journal of nephrology, 418-424. Lehnhardt, A. . (2011). Pathogenesis, diagnosis and management of hyperkalemia. Pediatric nephrology, 377-384. Montague, B. T. (2008). Retrospective review of the frequency of ECG changes in hyperkalemia. Clinical Journal of the American Society of Nephrology, 324-330. Packham, D. K.-S. (2015). Sodium zirconium cyclosilicate in hyperkalemia. New England Journal of Medicine, 222-231. Pannu, N. K. (2008). Renal replacement therapy in patients with acute renal failure: a systematic review. Jama, 793-805. Pavlakovi?, H. K. (2010). Hyperkalemia complicating propranolol treatment of an infantile hemangioma. Pediatrics, e1589-e1593. Smith, H. M. (2008). Cardiac arrests associated with hyperkalemia during red blood cell transfusion: a case series. Anesthesia Analgesia, 1062-1069. Sterns, R. H. (2010). Ion-exchange resins for the treatment of hyperkalemia: are they safe and effective? Journal of the American Society of Nephrology, 733-735. Weir, M. R. (2015). Patiromer in patients with kidney disease and hyperkalemia receiving RAAS inhibitors. New England Journal of Medicine, 211-221. Weir, M. R. (2015). Patiromer in patients with kidney disease and hyperkalemia receiving RAAS inhibitors. New England Journal of Medicine, 211-221. Weisberg, L. S. (2008). Management of severe hyperkalemia. Critical care medicine, 3246-3251.