We describe the case of a patient with a hyperkalemic emergency (potassium >6.5 mmol/l with ECG alterations). The first step is the administration of iv calcium gluconate to counteract the cardiac toxicity of hyperkalemia (option 3 correct), giving us more time to initiate hypokalemic treatments (initially saline glucose with insulin, salbutamol, furosemide, and assessing dialysis if there is no good response).

We describe the case of a patient with a hyperkalemic emergency (potassium >6.5 mmol/l with ECG alterations). The first step is the administration of iv calcium gluconate to counteract the cardiac toxicity of hyperkalemia ([HIDDEN]), giving us more time to initiate hypokalemic treatments (initially saline glucose with insulin, salbutamol, furosemide, and assessing dialysis if there is no good response).

In a patient with known advanced chronic kidney disease (CKD G4, eGFR 20 ml/min) who comes to the emergency department for general weakness and is found to have severe hyperkalemia (K 7 mEq/l) with electrocardiographic abnormalities. What would be the first measure to take?

Administration of cation exchange resins.

Placement of a catheter to initiate dialysis.

Administration of intravenous calcium gluconate.

A case of advanced chronic kidney disease with severe hypocalcemia, how to safely manage and dialyze?

Patients often present with advanced chronic kidney disease (CKD) complicated with severe hypocalcemia that may be accompanied by electrocardiographic changes. The management of this kind of patients may require hemodialysis (HD). However, initiation of renal replacement therapy in this scenario needs special attention to avoid complications such as cardiac arrhythmias. A 22-year-old male presented to our emergency department with severe renal failure, hypocalcemia, hyperphosphatemia, severe acidosis, and QT prolongation on electrocardiography. The patient was kept in the emergency department under cardiac monitoring. He was started on IV calcium gluconate 1 g every 6 h aiming to increase his adjusted calcium level to 1.8 mmol/L. He subsequently received the first HD session with low blood flow, increased calcium, and decreased bicarbonate dialysate bath. There were no arrhythmias or hemodynamic instability. Intravenous calcium was discontinued; adjusted calcium improved progressively after dialysis and reached 1.9 mmol/L by the time of discharge and after receiving three sessions of HD. This case describes a not so infrequent presentation of advanced renal impairment with profound hypocalcemia, hyperphosphatemia in the setting of CKD-associated mineral bone disorder. Intravenous calcium administration may promote vascular and metastatic calcification, particularly with the coexistence of hyperphosphatemia, and hence, it is best avoided. There are no guidelines to direct initiating HD in this context. However, it appears that using a high calcium bath is prudent to minimize cardiovascular complications, particularly if there is the prolongation of the corrected QT interval on electrocardiography.

Electrocardiography is Unreliable to Detect Potential Lethal Hyperkalemia in Patients with Non-dialysis Chronic Kidney Disease.

Hemodialysis patients with hypercalcemia are less likely to manifest the usual electrocardiographic changes associated with hyperkalemia than in those with normal renal function. This study was conducted to determine whether electrocardiography (ECG) is a reliable indicator to detect severe life-threatening hyperkalemia in non-dialysis CKD patients. The study was conducted at three referral university hospitals between July 2017 and June 2018. Severe hyperkalemia was defined as serum potassium concentration ≥ 8.0 mEq/L. Serum potassium, sodium, bicarbonate, calcium, and creatinine concentrations were measured and simultaneous 12-lead ECG was obtained. Patients with end-stage renal disease receiving renal replacement therapy were excluded. Also excluded were patients with the usual ECG abnormalities to hyperkalemia. Of the 438 patients screened, 10 (2.3%) aged 2-14 years with severe hyperkalemia and normal ECG findings were identified. Median serum potassium level was 8.6 mEq/L (range 8.2-9.0). All had regular sinus rhythm. P, QRS, ST segment, T morphology, PR and QT interval, and QRS duration were all normal. Hyperkalemia was associated with CKD, metabolic acidosis, and hypercalcemia in all cases. Therapy with intravenous 0.9% saline, sodium bicarbonate, glucose, insulin, calcium, and salbutamol corrected the hyperkalemia in 7 patients. The remaining three patients evinced arrhythmias requiring hemodialysis. Although rare, non-dialysis CKD patients with hypercalcemia may not manifest the usual electrographic abnormalities associated with hyperkalemia. Thus, a normal ECG finding in non-dialysis CKD patients should be interpreted with caution.

Serum potassium in stage 5 CKD patients on their first presentation in a dialysis service of a county hospital in western Romania.

CKD patients present deficient elimination of potassium. Ambulatory treatment with hypotensors, mainly angiotensin-renin system inhibitors, can be associated in these patients with potassium retention and risk of hyperkalemia. In pre-dialysis stage-5 CKD patients, the use of medication accompanied by hyperkalemia increases risks of developing it. Using diuretics like spironolactone also increases this risk. Serum potassium can also increase in case of inappropriate consumption of potassium-rich food (bananas). Since ambulatory care does not always rigorously control hyperkalemia in CKD patients we consider it is useful to screen patients when they are referred to dialysis services. The screening can reflect the management of ambulatory CKD patients under treatment with ACE-I and ARB hypotensors. We remark that beta-blockers are attributed a (limited) role in increasing the values of serum K. We studied a group of 477 stage-5 CKD patients referred for dialysis to The Dialysis Centre of the Emergency County Hospital Timişoara. The average age of the patients was 57.41 +/- 14.26 years. 260 were males and 217 females. All were stage-5 CKD with GFR < 15 mL/min/1.73 m2, with a group average value of eGFR of 5.72 +/- 2.81 mL/min/1.73m2. Our investigations showed hypokalemia in 14 patients (2.93%). Hyperkalemia was found in 179 patients. Of these, 124 had mild hyperkalemia (5.5-6.4 mEq/L), 45 patients had medium hyperkalemia (6.5-7.5 mEq/L) and 10 (2.09%) had severe hyperkalemia (K > 7.5 mEq/L). Hyperkalemia was more frequent in patients who had been treated with blockers of the renin-angiotensin system than in patients who had used other hypotensors or who had not needed hypotensors and had not taken diuretics. Severe hyperkalemia (K > 7.5 mEq/L) was present both in patients treated with blockers of the renin-angiotensin system and in those treated with other hypotensors and in 1 case without hypotensor or diuretic treatment. 2 cases treated with blockers of the renin-angiotensin-aldosterone system with severe hyperpotassemia associated antialdosteronic diuretics, cumulating hyperpotassemic effects. Diuretic treatments with loop diuretics influenced the values of serum K of most patients. Hyperkalemia represents an important problem in nephrology because of the risks it induces in the treatment ofpre-dialysis CKD patients and it requires attentive monitoring.

Severe Persistent Hyperkalemia with Electrocardiogram Changes in a Patient with Hyperaldosteronism.

A 62-year-old female presented to the emergency department (ED) with fatigue and generalized body weakness for the last three days. Upon arrival, initial ECG showed wide complex tachycardia with sine waves and a heart rate (HR) ranging between 100-170 bpm. She was otherwise vitally stable. The patient had a past medical history of hyperaldosteronism, type 2 diabetes mellitus (DM), chronic kidney disease (CKD) with microalbuminuria, and hypertension. She also had a history of cerebrovascular accident (CVA) and residual left-sided weakness more pronounced in the upper limb. Initial venous blood gas (VBG) analysis showed a potassium level of more than 10 mmol/L, chloride 114 mmol/L, bicarbonate 9 mmol/L, sodium 135 mmol/L, and pH of 7.1. Treatment for hyperkalemia was started immediately with calcium gluconate 1 gm that effectively narrowed her QRS complex and normalized her ECG. Salbutamol nebulization, glucose/insulin infusion, and calcium polystyrene syrup were given. Later, she was started on 100 mg sodium bicarbonate infusion, and Foley's catheter was inserted to follow urine output (UOP) strictly. However, she did not show a decrease in serum potassium levels. Then the patient underwent hemodialysis for two hours. Her first potassium reading after hemodialysis was 5.2 mmol/L. The purpose of this case report is to emphasize the importance of hemodialysis in patients with persistent severe life-threatening hyperkalemia.

Therapeutic approach to hyperkalemia.

The foremost step in the initial clinical management of hyperkalemia is to decide whether a hyperkalemic patient requires immediate treatment to avoid a life-threatening situation (serum potassium concentration >6.0 mEq/l and EKG changes). When the decision for urgent treatment of hyperkalemia is based on EKG changes, an important caveat for clinicians is that absent or atypical EKG changes do not exclude the necessity for immediate intervention. Once an urgent situation has being handled with intravenous push of a 10% calcium salt, the initiation of short-term measures can be launched by either a single or combined regimen of the three agents that cause a transcellular shift of potassium - insulin with glucose, beta(2)-agonist (albuterol), and NaHCO(3). As the first choice among these available options, we favor an intravenous bolus of 10 units of insulin with 50 ml of 50% glucose alone or in combination with 10-20 mg of albuterol by nebulizer. These can be repeated as required until the institution of hemodialysis. The combination of insulin with glucose and NaHCO(3) as an another option needs further clarification for its additive effects. However, NaHCO(3) has lost its favor because of its poor efficacy as a potassium-lowering agent when used alone. The next step is to remove potassium from the body - diuretics (furosemide), cation exchange resin (kayexelate) with sorbitol, and dialysis (preferably hemodialysis). The final important step for the managements of hyperkalemia is a long-term plan to prevent its recurrence or worsening. In addition to every effort to elucidate underlying causes and pathophysiologic mechanisms for hyperkalemia, an extensive search must be made to uncover overt or sometimes covert medications that may have led to the development of hyperkalemia. Furthermore, one must obtain detailed dietary and medical history of hyperkalemic patients.

[The most frequent electrolyte disorders in the emergency department : what must be done immediately?].

Hyponatremia is the most common form of electrolyte disorder in the emergency room. The symptoms are unspecific and include nausea, dizziness and often falls. Typical symptoms of severe hypernatremia are vomiting, cerebral seizures, somnolence and even coma. The specific initial laboratory diagnostics include measurement of serum electrolytes, serum glucose, serum and urine osmolarity and sodium in urine. The main aim of the clinical examination is to estimate the volume status. If a patient has hypovolemia an infusion of isotonic sodium chloride solution (0.9 %) is the method of choice. If the patient is euvolemic the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or (neurotropic) drugs might be the cause. In these cases the primary measure is restriction of fluid intake. As a rapid correction of sodium levels can lead to pontine myelinolysis, the increase in sodium concentration must not be less than 10 mmol/l within the first 24 h and 18 mmol/l within the first 48 h. Clinical symptoms of hyperkalemia include neurological (e.g. muscle weakness, paresis, hyperreflexia, cramps and dysesthesia), gastrointestinal (e.g. nausea, vomiting and diarrhea) and cardiac symptoms (e.g. dysrhythmia and conductance disorders). Calcium injection stabilizes cardiac rhythm disorders immediately. For a rapid drop in potassium by shifting the potassium to the intracellular space, administration of glucose with insulin and high-dose inhalative administration of betamimetics can be used. Potassium elimination is achieved by infusion of isotonic sodium choride (0.9 %) with i.v. administration of furosemide, ion exchange resins and hemodialysis.

EMS Confined Space Care -- Issues of Concern -- Crush Injury and Crush Syndrome

Several electrolyte abnormalities may be present. Hypocalcemia should only be treated if the patient is symptomatic since the patient may later develop hypercalcemia. Start with 10 mL of intravenous calcium gluconate 10% or 5 mL of intravenous calcium chloride 10% over 2 minutes.  Hyperkalemia should be monitored and treated based on the potassium level and electrocardiographic changes.   The ECG may not change in some situations where the potassium level is dangerously elevated.  If there are severe or life-threatening electrocardiographic changes or arrhythmias such as the widening of the QRS to third-degree heart block or pulseless electrical activity, the intravenous calcium gluconate or chloride should be given immediately. It may be necessary to give several doses every 10 minutes to achieve the cardioprotective effects of calcium. If the patient is acidotic then sodium bicarbonate 1 meq/kg should be given immediately IV over several minutes.  To drive the potassium into the cells, 10 units of intravenous insulin, together with 1 to 2 ampules of D50, should be given.   The Beta agonist effect of albuterol inhalation treatments can also help transiently decrease potassium levels.  Kaexylate with sorbitol can be given orally at 25 to 50 gm, or it may be given as a retention enema.  Patients with life-threatening hyperkalemia need the potassium removed from their system.  The medications and treatments are temporizing measures to provide time for excretion of removal of potassium from the body.  The patient may require emergent dialysis.  Critiques of recent disaster responses were that there was an insufficient number of dialysis machines to treat those with renal failure secondary to crush injuries.  Blood products should be given as necessary and when indicated.

Hs and Ts

A common presentation of hyperkalemia is in the patient with end-stage renal disease who has missed a dialysis appointment and presents with weakness, nausea, and broad QRS complexes on the electrocardiogram. (Note however that patients with chronic kidney disease are often more tolerant of high potassium levels as their body often adapts to it.) Several medications, for example the antibiotic trimethoprim/sulfamethoxazole or an ACE inhibitor, can also lead to the development of significant hyperkalemia. The electrocardiogram will show tall, peaked T waves (often larger than the R wave) or can degenerate into a sine wave as the QRS complex widens. Immediate initial therapy is the administration of calcium, either as calcium gluconate or calcium chloride. This stabilizes the electrochemical potential of cardiac myocytes, thereby preventing the development of fatal arrhythmias. This is, however, only a temporizing measure. Other temporizing measures may include nebulized salbutamol,

Crush syndrome

Intravenous hydration of up to 1.5 L/h should continue to prevent hypotension. A urinary output of at least 300 mL/h should be maintained with IV fluids and mannitol, and hemodialysis considered if an increase in urine is not achieved. Use intravenous sodium bicarbonate to keep the urine pH at 6.5 or greater, to prevent myoglobin and uric acid deposition in kidneys. To prevent hyperkalemia/hypocalcemia, consider the following adult doses: calcium gluconate 10% 10 mL or calcium chloride 10% 5 mL IV over 2 minutes sodium bicarbonate 1 meq/kg IV slow push regular insulin 5–10 U 50% glucose 1–2 ampules IV bolus kayexalate 25–50 g with sorbitol 20% 100 mL by mouth or rectum. Even so, abnormal heart rhythms may develop; electrocardiographic monitoring is advised, and specific treatment begun promptly. References External links Life or Limb: What happens when your leg gets trapped under a building? Injuries Early complications of trauma Nephrology Syndromes

Hyperkalemia

Initial treatment in those with ECG changes is salts, such as calcium gluconate or calcium chloride. Other medications used to rapidly reduce blood potassium levels include insulin with dextrose, salbutamol, and sodium bicarbonate. Medications that might worsen the condition should be stopped and a low potassium diet should be started. Measures to remove potassium from the body include diuretics such as furosemide, potassium-binders such as polystyrene sulfonate and sodium zirconium cyclosilicate, and hemodialysis. Hemodialysis is the most effective method. Hyperkalemia is rare among those who are otherwise healthy. Among those who are hospitalized, rates are between 1% and 2.5%. It is associated with an increased mortality, whether due to hyperkalaemia itself or as a marker of severe illness, especially in those without chronic kidney disease. The word hyperkalemia comes from hyper- 'high' + kalium 'potassium' + -emia 'blood condition'.

Management of hyperkalemia in dialysis patients.

Hyperkalemia is common in patients with end-stage renal disease, and may result in serious electrocardiographic abnormalities. Dialysis is the definitive treatment of hyperkalemia in these patients. Intravenous calcium is used to stabilize the myocardium. Intravenous insulin and nebulized albuterol lower serum potassium acutely, by shifting it into the cells. Despite their widespread use, neither intravenous bicarbonate nor cation exchange resins are effective in lowering serum potassium acutely. Prevention of hyperkalemia currently rests largely upon dietary compliance and avoidance of medications that may promote hyperkalemia. Prolonged fasting may provoke hyperkalemia, which can be prevented by administration of intravenous dextrose.

InternalMed_Harrison

Intravenous bicarbonate has no role in the acute treatment of hyperkalemia, but may slowly attenuate hyperkalemia with sustained administration over several hours. It should not be given repeatedly as a hypertonic intravenous bolus of undiluted ampules, given the risk of associated hypernatremia, but should instead be infused in an isotonic or hypotonic fluid (e.g., 150 mEqu in 1 L of D5W). In patients with metabolic acidosis, a delayed drop in plasma K+ concentration can be seen after 4–6 h of isotonic bicarbonate infusion. 3. Removal of potassium. This is typically accomplished using cation exchange resins, diuretics, and/or dialysis. The cation exchange resin sodium polystyrene sulfonate (SPS) exchanges Na+ for K+ in the gastrointestinal tract and increases the fecal excretion of K+; alternative calcium-based resins, when available, may

Patiromer in a Patient with Severe Hyperkalemia on Incremental Hemodialysis with 1 Session per Week: A Case Report and Literature Review.

Hyperkalemia is common in patients with ESRD, undergoing hemodialysis (HD), and is associated with an increase in hospitalization and mortality. Residual kidney function in long-term dialysis patients is associated with lower morbidity and mortality in HD patients. Although the 2015 National Kidney Foundation-Kidney Disease Outcomes Quality Initiate (NKD-KDOQI) guidelines allow the reduction in the weekly HD dose for patients with a residual kidney urea clearance (Kur) >3 mL/min/1.73 m<sup2</sup, very few centers adjust the dialysis dose based on these criteria. In our center, the pattern of incremental hemodialysis (iHD) with once-a-week schedule (1 HD/W) has been an option for a group of patients showing very good results. This pattern is maintained as long as residual diuresis is >1,000 mL/24 h, Kur is >4 mL/min, and there is no presence of edema or volume overload, as well as no analytical parameters persistently outside the advisable range (serum phosphorus >6 mg/dL or potassium [K<sup+</sup] >6.5 mmol/L). Management of hyperkalemia in HD patients includes reduction of dietary intake, dosing of medications that contribute to hyperkalemia, and use of cation-exchange resins such as calcium or sodium polystyrene sulfonate. Two newer potassium binders, patiromer sorbitex calcium and sodium zirconium cyclosilicate, have been safely used for potassium imbalance treatment in patients with ESRD in HD with a conventional regimen of thrice weekly, but has not yet been studied in 1 HD/W schedules. We present the case of a 76-year-old woman in iHD (1 HD/W) treated with patiromer for severe HK and describe her clinical characteristics and outcomes. In addition, we review the corresponding literature. Based on these data, it can be anticipated that the use of patiromer may overcome the risk of hyperkalemia in patients with incident ESRD treated with less-frequent HD regimens.

[Electrolyte and acid-base balance disorders in advanced chronic kidney disease].

1. The kidneys are the key organs to maintain the balance of the different electrolytes in the body and the acid-base balance. Progressive loss of kidney function results in a number of adaptive and compensatory renal and extrarenal changes that allow homeostasis to be maintained with glomerular filtration rates in the range of 10-25 ml/min. With glomerular filtration rates below 10 ml/min, there are almost always abnormalites in the body's internal environment with clinical repercussions. 2. Water Balance Disorders: In advanced chronic kidney disease (CKD), the range of urine osmolality progressively approaches plasma osmolality and becomes isostenuric. This manifests clinically as symptoms of nocturia and polyuria, especially in tubulointerstitial kidney diseases. Water overload will result in hyponatremia and a decrease in water intake will lead to hypernatremia. Routine analyses of serum Na levels should be performed in all patients with advanced CKD (Strength of Recommendation C). Except in edematous states, a daily fluid intake of 1.5-2 liters should be recommended (Strength of Recommendation C). Hyponatremia does not usually occur with glomerular filtration rates above 10 ml/min (Strength of Recommendation B). If it occurs, an excessive intake of free water should be considered or nonosmotic release of vasopressin by stimuli such as pain, anesthetics, hypoxemia or hypovolemia, or the use of diuretics. Hypernatremia is less frequent than hyponatremia in CKD. It can occur because of the provision of hypertonic parenteral solutions, or more frequently as a consequence of osmotic diuresis due to inadequate water intake during intercurrent disease, or in some circumstance that limits access to water (obtundation, immobility). 3. Sodium Balance Disorders: In CKD, fractional excretion of sodium increases so that absolute sodium excretion is not modified until glomerular filtration rates below 15 ml/min (Strength of Recommendation B). Total body content of sodium is the main determinant of extracellular volume and therefore disturbances in sodium balance will lead to clinical situations of volume depletion or overload: Volume depletion due to renal sodium loss occurs in abrupt restrictions of salt intake in advanced CKD. It occurs more frequently in certain tubulointerstitial kidney diseases (salt losing nephropathies). Volume overload due to sodium retention can occur with glomerular filtration rates below 25 ml/min and leads to edema, arterial hypertension and heart failure. The use of diuretics in volume overload in CKD is useful to force natriuresis (Strength of Recommendation B). Thiazides have little effect in advanced CKD. Loop diuretics are effective and should be used in higher than normal doses (Strength of Recommendation B). The combination of thiazides and loop diuretics can be useful in refractory cases (Strength of Recommendation B). Weight and volume should be monitored regularly in the hospitalized patient with CKD (Strength of Recommendation C). 4. Potassium Balance Disorders: In CKD, the ability of the kidneys to excrete potassium decreases proportionally to the loss of glomerular filtration. Stimulation of aldosterone and the increase in intestinal excretion of potassium are the main adaptive mechanisms to maintain potassium homeostasis until glomerular filtration rates of 10 ml/min. The main causes of hyperkalemia in CKD are the following: Use of drugs that alter the ability of the kidneys to excrete potassium: ACEIs, ARBs, NSAIDs, aldosterone antagonists, nonselective beta-blockers, heparin, trimetoprim, calcineurin inhibitors. Determination of serum potassium two weeks after the initiation of treatment with ACEIs/ARBs is recommended (Strength of Recommendation C). Routine use of aldosterone antagonists in advanced CKD is not recommended (Strength of Recommendation C). Abrupt reduction in glomerular filtration rate: Constipation. Prolonged fasting. Metabolic acidosis. A low-potassium diet is recommended with GFR less than 20 ml/min, or GFR less than 50 ml/min if drugs that raise serum potassium are taken (Strength of Recommendation C). In the absence of symptoms or electrocardiographic abnormalities, review of medications, restriction of dietary potassium and use of oral ion exchange resins are usually sufficient therapeutic measures (Strength of Recommendation C). If symptoms and/or electrocardiographic abnormalities are present, the usual parenteral pharmacological measures should be used (10% calcium gluconate, insulin and glucose, salbutamol, resins, diuretics) (Strength of Recommendation A). Parenteral bicarbonate and ion exchange resins in enemas are not recommended as first-line treatment (Strength of Recommendation C). Hemodialysis should be considered in patients with glomerular filtration rates below 10 ml/min (Strength of Recommendation C). 5. Acid-Base Disorders in CKD: Moderate metabolic acidosis (Bic 16-20) mEq/L is common with glomerular filtration rates below 20 ml/min, and favors bone demineralization due to the release of calcium and phosphate from the bone, chronic hyperventilation, and muscular weakness and atrophy. Its treatment consists of administration of sodium bicarbonate, usually orally (0.5-1 mEq/kg/day), with the goal of achieving a serum bicarbonate level of 22-24 mmol/L (Strength of Recommendation C). Limitation of daily protein intake to less than 1 g/kg/day is also useful (Strength of Recommendation C). Use of sevelamer as a phosphate binder aggravates metabolic acidosis since it favors endogenous acid production and therefore acidosis should be monitored and corrected if it occurs (Strength of Recommendation C). Hypocalcemia should always be corrected before metabolic acidosis in CKD (Strength of Recommendation B). Metabolic acidosis is an infrequent disorder and requires exogenous alkali administration (bicarbonate, phosphate binders) or vomiting.

Assessment of kidney function

The severity of chronic kidney disease (CKD) is described by six stages; the most severe three are defined by the MDRD-eGFR value, and first three also depend on whether there is other evidence of kidney disease (e.g., proteinuria): 0) Normal kidney function – GFR above 90 (mL/min)/(1.73 m2) and no proteinuria 1) CKD1 – GFR above 90 (mL/min)/(1.73 m2) with evidence of kidney damage 2) CKD2 (mild) – GFR of 60 to 89 (mL/min)/(1.73 m2) with evidence of kidney damage 3) CKD3 (moderate) – GFR of 30 to 59 (mL/min)/(1.73 m2) 4) CKD4 (severe) – GFR of 15 to 29 (mL/min)/(1.73 m2) 5) CKD5 kidney failure – GFR less than 15 (mL/min)/(1.73 m2) Some people add CKD5D for those stage 5 patients requiring dialysis; many patients in CKD5 are not yet on dialysis. Note: others add a "T" to patients who have had a transplant regardless of stage.

Glomerular filtration rate

The severity of chronic kidney disease (CKD) is described by six stages; the most severe three are defined by the MDRD-eGFR value, and first three also depend on whether there is other evidence of kidney disease (e.g., proteinuria): 0) Normal kidney function – GFR above 90 mL/min/1.73 m2 and no proteinuria 1) CKD1 – GFR above 90 mL/min/1.73 m2 with evidence of kidney damage 2) CKD2 (mild) – GFR of 60 to 89 mL/min/1.73 m2 with evidence of kidney damage 3) CKD3 (moderate) – GFR of 30 to 59 mL/min/1.73 m2 4) CKD4 (severe) – GFR of 15 to 29 mL/min/1.73 m2 5) CKD5 kidney failure – GFR less than 15 mL/min/1.73 m2 Some people add CKD5D for those stage 5 patients requiring dialysis; many patients in CKD5 are not yet on dialysis. Note: others add a "T" to patients who have had a transplant regardless of stage.

[Hyperkalemic emergency: causes, diagnosis and therapy].

Eight patients with life threatening hyperkalemia were treated in the intensive care unit over a period of 2 years. Serum potassium at admission was 7.1-11.2. Two patients had to be resuscitated and 3 exhibited quadriplegia or paralyses but were alert. Seven showed marked ECG change: in 5 the QRS-complexes were extremely broadened and in one case an AV-rhythm was observed; the atrial wave was absent in all 7 patients. Renal failure was present in 7 of 8 patients. In 6 of these 8 cases drugs were also involved in the development of hyperkalemia. The following therapeutic procedure is recommended for hyperkalemia: (1) injection of calcium, (2) inhalation or injection of beta 2-mimetics (well documented in the literature; clinical experience limited), (3) insulin and glucose i.v., (4) sodium bicarbonate, but only in case of metabolic acidosis, (5) hemodialysis, (6) cation exchange resins or furosemide in non-acute situations.

Acute ascending muscle weakness secondary to medication-induced hyperkalemia.

Secondary hyperkalemic paralysis is an uncommon but potentially life-threatening consequence of drug-induced disease. We report a case of a 53-year-old female with history of chronic kidney disease presenting to the emergency department with a one-day history of upper and lower extremity weakness and paresthesias. Serum potassium concentration on admission was greater than 8 mEq/L, and serum creatinine was elevated above baseline. Electrocardiogram showed first-degree atrioventricular block with peaked T waves. The patient reported compliance with daily lisinopril 10 mg, spironolactone 25 mg, and 40 mEq twice daily of potassium chloride. Symptoms and electrocardiogram returned to baseline within 24 hours of presentation and serum potassium returned to 4.2 mEq/L at approximately 36 hours without the need for dialysis. This case emphasizes the importance of including such a condition in the differential diagnosis of patients with ascending paralysis and the importance of close monitoring of patients placed on potassium-elevating agents.

Renal Failure -- Treatment / Management -- Acute Renal Failure

The mainstay is treating the underlying cause and associated complications If the case of oliguria and no volume overload is noted, a fluid challenge may be appropriate with diligent monitoring for volume overload In the case of hyperkalemia with ECG changes, IV calcium, sodium bicarbonate, and glucose with insulin should be given. These measures drive potassium into cells and can be supplemented with polystyrene sulfonate, which removes potassium from the body. Hemodialysis is also an emergency method of removal. If acidosis is present, serum bicarbonate intravenous or oral versus emergency/urgent dialysis based on the clinical situation If obstructive etiology presents treat accordingly. Bladder outlet obstruction secondary to prostatic hypertrophy may benefit from Flomax or other selective alpha-blockers

Association of dyskalemias with short-term health care utilization in patients with advanced CKD.

<bBACKGROUND:</b Patients with advanced chronic kidney disease (CKD) are at high risk for dyskalemias, which may induce arrhythmias that require immediate emergent or hospital care. The association of dyskalemias with short-term hospital/emergency room (ER) visits in advanced CKD is understudied. <bOBJECTIVE:</b To assess the association of dyskalemias with short-term hospital/ER visits in an advanced CKD population. <bMETHODS:</b From among 102,477 US veterans transitioning to dialysis from 2007 to 2015, we identified 21,366 patients with 2 predialysis outpatient eGFR < 30 ml/min/1.73m<sup2</sup 90-365 days apart (with the second eGFR serving as the index date) and at least 1 potassium (K) in the baseline period (1 year before index) and 1 outpatient K (oK) in the follow-up (1 year after the index but before dialysis initiation). We examined the association of time-varying hypokalemia (K < 3.5 mEq/L) and hyperkalemia (K > 5.5 mEq/L) vs referent (3.5-5.5 mEq/L) with separate hospital and ER visits within 2 calendar days following each oK value over the 1-year follow-up period from the index. We used generalized estimating equations with binary distribution and logit link to model the exposure-outcome relationship adjusted for various confounders. We conducted various subgroup and sensitivity analyses to test the robustness of our results. <bRESULTS:</b Over the 1-year follow-up, 125,266 oK measurements were observed, of which 6.8% and 3.7% were classified as hyper- and hypokalemia, respectively. In the multivariable-adjusted model, hyperkalemia (adjusted odds ratio [aOR] = 2.04; 95% CI = 1.88-2.21) and hypokalemia (aOR = 1.66; 95% CI = 1.48-1.86) were associated with significantly higher odds of hospital visits. Similarly, hyperkalemia (aOR = 1.83; 95% CI = 1.65-2.03) and hypokalemia (aOR = 1.24; 95% CI = 1.07-1.44) were associated with significantly higher odds of ER visits. Results were robust to subgroups and sensitivity analyses. <bCONCLUSIONS:</b In patients with advanced CKD, dyskalemias are associated with higher risk of hospital/ER visits. Interventions targeted at lowering the risk of dyskalemias might help in reducing the health care utilization and associated economic burden among patients with advanced CKD experiencing dyskalemias. <bDISCLOSURES:</b This study was supported by grant 5U01DK102163 from the National Institute of Health (NIH) to Kamyar Kalantar-Zadeh and Csaba P. Kovesdy and by resources from the US Department of Veterans Affairs. The data reported here have been supplied in part by the United States Renal Data System (USRDS). Support for VA/CMS data were provided by the Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development, Health Services Research and Development, VA Information Resource Center (project numbers SDR 02-237 and 98-004). Opinions expressed in this article are those of the authors and do not necessarily represent the opinion of the Department of Veterans Affairs or the funding institution. Kovesdy has received honoraria from Akebia, Ardelyx, Astra Zeneca, Bayer, Boehringer-Ingelheim, Cara Therapeutics, Reata, and Tricida unrelated to this study. Kalantar-Zadeh has received honoraria and/or support from Abbott, Abbvie, ACI Clinical (Cara Therapeutics), Akebia, Alexion, Amgen, American Society of Nephrology, Astra-Zeneca, Aveo, BBraun, Chugai, Cytokinetics, Daiichi, DaVita, Fresenius, Genentech, Haymarket Media, Hofstra Medical School, International Federation of Kidney Foundations, International Society of Hemodialysis, International Society of Renal Nutrition & Metabolism, Japanese Society of Dialysis Therapy, Hospira, Kabi, Keryx, Kissei, Novartis, OPKO, National Institutes of Health, National Kidney Foundations, Pfizer, Regulus, Relypsa, Resverlogix, Dr Schaer, Sandoz, Sanofi, Shire, Veterans Affairs, Vifor, UpToDate, and ZS-Pharma, unrelated to this study. Gatwood has received research support from AstraZeneca, Merck & Co., and GlaxoSmithKline unrelated to this study. Obi has received research support from Relypsa/Vifor Pharma Inc. The remaining authors declare that they have no relevant financial interests.

[Successful resuscitation of intractable hyperkalemic cardiac arrest].

We report on a 42-year-old oliguric uremic man on regular hemodialysis who developed sudden cardiac arrest, secondary to severe hyperkalemia, with a plasma potassium concentration of 9.7 mEq x l(-1). The cardiac arrest persisted after the initiation of cardiopulmonary resuscitation and intensive treatment for marked hyperkalemia for an hour and 55 minutes. Therefore a portable percutaneous cardiopulmonary support (PCPS) system had to be instituted while the patient had very prolonged refractory ventricular fibrillation. His cardiac rhythm was restored immediately after application of PCPS and he recovered without neurological sequelae. We therefore suggest that PCPS should be considered as a therapeutic option during cardiopulmonary resuscitation for life-threatening cardiac arrest secondary to severe hyperkalemia.

Beating the odds--surviving extreme hyperkalemia.

Severe hyperkalemia (>7 mmol/L) is a medical emergency because of possible fatal arrhythmias. We here report the case of a 58-year-old woman surviving extreme hyperkalemia (>10 mmol/L). The patient with a history of congestive heart failure, a DDD pacemaker and mild chronic renal insufficiency was admitted with progressive weakness and sudden onset of hypotension and bradycardia in the absence of any pacemaker action. Laboratory tests revealed an extreme serum potassium level of 10.1 mmol/L, with a slightly elevated serum creatinine of 149 μmol/L. Treatment with norepinephrine, sodium bicarbonate, and insulin improved both the hemodynamic situation and the serum potassium with subsequent regaining pacemaker actions even before additional hemodialysis normalized the potassium level. A thorough investigation demonstrated that several mechanisms contributed to the extreme potassium level: urinalysis and a low transtubular potassium gradient in the presence of metabolic acidosis with normal anion gap pointed to preexisting interstitial nephritis, with renal tubular acidosis type IV as the predisposing factor, whereas several drugs and acute impairment of renal function contributed to the dangerous situation. Despite the odds for fatal outcome, the patient recovered completely, and long-term management was initiated to prevent recurrent hyperkalemia.

Recommendations for the management of hyperkalemia in the emergency department.

Hyperkalemia, a common electrolyte disorder, is seen often in emergency departments. Patient outcomes are impacted by proper management, which requires consideration of both clinical and laboratory findings in relation to kidney function, hydration, the acid-base balance, and heart involvement. Delicate decisions about the timing of potassium level correction must be tailored in each case. For these reasons the Spanish Society of Emergency Medicine (SEMES), the Spanish Society of Cardiology (SEC), and the Spanish Society of Nephrology (SEN) joined forces to come to a consensus on defining the problem and recommending treatments that improve hospital emergency department management of hyperkalemia. Intravenous calcium, insulin and glucose, and salbutamol continue to be used to treat acute hyperkalemia. Either loop or thiazide diuretics can help patients if volume is not depleted, and dialysis may be necessary if there is kidney failure. Ion-exchange resins are falling into disuse because of adverse effects and poor tolerance, whereas novel gastrointestinal cation-exchange resins are gaining ground and may even be of some use in managing acute cases. It is essential to adjust treatment rather than discontinue medications that, even if they favor the development of hyperkalemia, will improve a patient's long-term prognosis. Valid alternative treatment approaches must therefore be sought for each patient group, and close follow-up is imperative.

Association between Serum Potassium and Outcomes in Patients with Reduced Kidney Function.

Patients with CKD are more likely than others to have abnormalities in serum potassium (K(+)). Aside from severe hyperkalemia, the clinical significance of K(+) abnormalities is not known. We sought to examine the association of serum K(+) with mortality and hospitalization rates within narrow eGFR strata to understand how the burden of hyperkalemia varies by CKD severity. Associations were examined between serum K(+) and discontinuation of medications that block the renin-angiotensin-aldosterone system (RAAS), which are known to increase serum K(+). A cohort of patients with CKD (eGFR<60 ml/min per 1.73 m(2)) with serum K(+) data were studied (n=55,266) between January 1, 2009, and June 30, 2013 (study end). Serum K(+), eGFR, and covariates were considered on a time-updated basis. Mortality, major adverse cardiovascular events (MACE), hospitalization, and discontinuation of RAAS blockers were considered per time at risk. During the study, serum K(+) levels of 5.5-5.9 and ≥6.0 mEq/L were most prevalent at lower eGFR: they were present, respectively, in 1.7% and 0.2% of patient-time for eGFR of 50-59 ml/min per 1.73 m(2) versus 7.6% and 1.8% of patient-time for eGFR<30 ml/min per 1.73 m(2). Serum K(+) level <3.5 mEq/L was present in 1.2%-1.4% of patient-time across eGFR strata. The median follow-up time was 2.76 years. There was a U-shaped association between serum K(+) and mortality; pooled adjusted incidence rate ratios were 3.05 (95% confidence interval, 2.53 to 3.68) and 3.31 (95% confidence interval, 2.52 to 4.34) for K(+) levels <3.5 mEq/L and ≥6.0 mEq/L, respectively. Within eGFR strata, there were U-shaped associations of serum K(+) with rates of MACE, hospitalization, and discontinuation of RAAS blockers. Both hyperkalemia and hypokalemia were independently associated with higher rates of death, MACE, hospitalization, and discontinuation of RAAS blockers in patients with CKD who were not undergoing dialysis. Future studies are needed to determine whether interventions targeted at maintaining normal serum K(+) improve outcomes in this population.

Prevalence and correlates of hyperkalemia in a renal nutrition clinic.

Hyperkalemia (HK) is a frequent complication of chronic kidney disease (CKD). Vegetable-based renal diets are considered at risk due to the high potassium (K) content. The aim of this study was to describe the prevalence and correlates of chronic hyperkalemia (HK) in CKD patients on nutritional care, and in particular, the risk of HK in patients on plant-based versus animal-based low-protein diets. We recruited adult patients affected by CKD not on dialysis, afferent to our renal nutrition clinic from November 2014 to May 2019. We evaluated a total of 870 accesses in 219 patients (172 m, 47 f, age 67 ± 13 years). HK was defined as mild when K serum level was 5.1-5.9 mEq/l, moderate when K serum level was 6.0-6.9 mEq/l, and severe HK when K serum level was ≥ 7 mEq/l. Biochemical, anthropometric data and medications were recorded. The prevalence of HK in all the renal nutrition visits was 26.1%; all but six cases were mild HK, whereas no severe HK was observed. The prevalence of HK was associated with decreased eGFR, up to 36.5% for eGFR < 20 ml/min. Medications were similar in hyperkalemic and normokalemic patients, RAASi being present in up to 85% of patients. In a follow-up of 40 ± 14 months, no association was found between HK and mortality, whereas HK, at the start of follow-up, showed a trend to increased ESRD risk. Serum potassium levels and prevalence of HK were not different between patients on animal-based low-protein diet and plant-based low-protein diet. In conclusion, chronic HK is quite prevalent in a renal nutrition clinic, especially when eGFR falls down below 60 ml/min, thereby reaching the highest prevalence in CKD stage 4. Hyperkalemia is mostly mild, being moderate to severe HK quite infrequent. Hyperkalemia was not associated with higher risk of mortality, whereas a trend, although not statistically significant, was observed for lower ESRD-free survival. Plant-based low-protein diet is not associated with significant higher prevalence of HK with respect to animal-based LPD at the same residual kidney function.

Hyperkalemia in hospitalized patients: causes, adequacy of treatment, and results of an attempt to improve physician compliance with published therapy guidelines.

Hyperkalemia is a common, potentially life-threatening disorder. Electrocardiograms are considered to be sensitive indicators of the presence of hyperkalemia. Since the treatment of hyperkalemia involves relatively few maneuvers and because its success can be objectively scored, we investigated how physicians manage this disorder and how successful their prescribed therapy is. We also sought to determine whether treatment could be improved by providing the treating physicians with therapy guidelines on a real-time basis. Consecutive patients with hyperkalemia were identified by review of laboratory records. During the observation-only phase of the study, demographic data, contributing causes, electrocardiogram findings, treatments used, compliance with prescribing guidelines, and patient outcome were recorded. During the subsequent notification phase of the study, treatment recommendations were sent to the patient's ward when the elevated potassium value was noted. The same outcome data were collected. There were 127 episodes of hyperkalemia during the observation-only phase and 115 during the notification phase. No patients died or had life-threatening cardiac arrhythmias. Electrocardiographic abnormalities consistent with hyperkalemia were observed in only 14% of episodes. Renal failure (77%), drugs (63%), and hyperglycemia (49%) contributed to most episodes. Treatments used were exchange resin (51%), insulin (46%), calcium (36%), bicarbonate (34%), and albuterol (4%). The agents were equally efficacious. The time to first treatment was shorter in patients with potassium levels of 6.5 mmol/L or more than in patients with lower values (2.1 +/- 2.2 vs 2.8 +/- 2.4 hours; P<.05). Treatment was better in the intensive care unit than on regular wards. Only 39% of episodes during the observation-only period met the predetermined criteria for monitoring and diagnosis, initial treatment, and follow-up. During the notification period, physician performance was no better; only 42% of episodes met all criteria. The laboratory transmitted a copy of the guidelines to the patient's ward only 38% of the time. In a separate analysis of these episodes, there was no improvement in treatment. Physicians who did not receive the notification fulfilled all treatment criteria more often than physicians who did (50% vs 30%; P<.05). Although treatment of hyperkalemia was frequently suboptimal, no serious arrhythmias and no deaths complicated management of 242 episodes of severe hyperkalemia. A narrowly targeted effort to improve physician management of a disorder with discrete treatment options did not improve therapy.

Gynecology_Novak

Hyperkalemia is encountered infrequently in preoperative patients. It is usually associated with renal impairment but can be seen in patients who have adrenal insufficiency, are taking potassium-sparing diuretics, and have marked tissue breakdown such as that occurring with crush injuries, massive gastrointestinal bleeding, or hemolysis. The clinical manifestations are mainly cardiovascular. Marked hyperkalemia (potassium >7 mEq/L) can result in bradycardia, ventricular fibrillation, and cardiac arrest. The treatment chosen depends on the severity of the hyperkalemia and whether there are associated cardiac abnormalities detected with electrocardiography. Calcium gluconate (10 mL of a 10% solution), given intravenously, can offset the toxic effects of hyperkalemia on the heart. One ampule each of sodium bicarbonate and D5W, with or without insulin, will cause a rapid shift of potassium into cells. Over the longer term, cation exchange resins such as sodium polystyrene sulfate

Association of hyperkalemia with clinical outcomes in advanced chronic kidney disease.

Patients with advanced chronic kidney disease (CKD) are at greatest risk of hyperkalemia (HK). The relationship between HK and negative outcomes (mortality or progression of renal insufficiency) in non-dialysis dependent CKD patients is controversial. To determine the incidence, prevalence, and factors related with HK in a cohort of CKD patients, and its relationship with mortality, hospitalization rate, CKD progression, and dialysis initiation. A retrospective, observational study in an incident cohort of adult patients with stage 4 or 5 CKD not on dialysis. Inclusion criteria were: having at least three consecutive estimated glomerular filtration rate (eGFR) measurements in a follow-up period >3 months. Decline in renal function was estimated as the slope of the individual linear regression line of eGFR over follow-up time. HK was defined as serum K levels ≥5.5 meq/l. Associations of HK with outcomes were adjusted for major confounding variables in the multivariate analysis. The study group consisted of 1079 patients (574 males, mean age: 65±14 years) with mean baseline eGFR 14.8±4.5 ml/min/1,73 m<sup2</sup. Mean follow-up time was 15 months with a median of 7 serum sample determinations per patient. HK was observed at baseline in 26% of patients; in at least one serum sample during the individual follow-up period in 68%; or chronically (>50% of samples) in 33% of patients. By multivariate logistic regression, the best determinants of chronic HK were: male sex (OR = 1.529; 95% CI [1.154-2.025], p = .003), serum bicarbonate (OR = 0.863 [0.829-0.900], p <.0001), diuretic treatment (OR = 0.743 [0.556-0.992], p = .044), and angiotensin converting enzyme inhibitor and/or angiotensin receptor blockers (OR = 4.412 [2.915-6.678], p <.0001). Patients whose serum K levels were in the upper quartile showed a significantly faster CKD progression (-4.05±5.22 vs. -2.69±5.61 ml/min/1.73 m<sup2</sup/year, p <.0001), and more frequent dialysis initiation (63% vs. 57%, p = .115), though lower mortality (9% vs. 17%, p = .003) and hospitalization rates (2.68±5.94 vs. 3.16±6.77 days per year, p = .301) than the other study patients. However, in the multivariate analysis, average serum K levels were not independently associated with the clinical outcomes investigated. HK is a common biochemical finding in non-dialysis dependent CKD patients, mainly associated with prescribed medication. However, HK was not independently associated with major negative clinical outcomes.

[2 cases from the practice of intensive treatment].

Two cases from the intensive treatment practice are presented: Case I--a 43-year-old woman drawn out from a state of clinical death during chronic dialysis for chronic renal failure with importunate ultrafiltration to combat the severe pulmonary edema, which led to hypoxia and cardiac arrest with functionally affected hemodynamic parameters (central venous pressure), because of centrally placed a/v fistula. Case II--a 46-year-old woman with severe drug disease and extremely critical hypotonic hyperhydration and anasarca, treated also with ultrafiltration, enhanced sodium influx and intensive application of diuretics; for 24 hours a negative fluid balance was achieved (71191 ml) until finally a relative fluid-electrolyte equilibrium was reached.

Xipamide

Unlike with thiazides, only terminal kidney failure renders xipamide ineffective. Uses Xipamide is used for cardiac oedema caused by decompensation of heart failure renal oedema, chronic renal disease (but not with anuria) hepatic oedema caused by cirrhosis ascites lymphoedema hypertension in combination with chronic renal disease Pharmacokinetics After oral administration, 20 mg of xipamide are resorbed quickly and reach the peak plasma concentration of 3 mg/l within an hour. The diuretic effect starts about an hour after administration, reaches its peak between the third and sixth hour, and lasts for nearly 24 hours. One third of the dose is glucuronidized, the rest is excreted directly through the kidney (1/3) and the faeces (2/3). The total plasma clearance is 30-40 ml/min. Xipamide can be filtrated by haemodialysis but not by peritoneal dialysis. Dosage Initially 40 mg, it can be reduced to 10–20 mg to prevent a relapse.

Outcomes of severe hyperkalemia in cardiopulmonary resuscitation with concomitant hemodialysis.

To investigate the efficacy of hemodialysis during cardiopulmonary resuscitation as an effective adjunct to the treatment of severe hyperkalemia. A prospective study. In hospital dialysis units and intensive care units. Renal failure patients who developed hyperkalemia induced cardiac arrest and failed to recover from conventional cardiopulmonary resuscitation (CPR) were included. Three patients entered into this study: 2 patients with chronic renal failure maintained on regular hemodialysis and one with acute renal failure who suffered from severe hyperkalemia. All three patients developed asystolic cardiac arrest with unrecordable blood pressure due to severe hyperkalemia. Aggressive CPR together with intravenous epinephrine, sodium bicarbonate and calcium chloride were instituted. External cardiac massage with cardiac defibrillation was unable to restore spontaneous heart action. After lack or response to intensive resuscitation, hemodialysis was performed concomitant with CPR to eliminate the potassium load. Sinus rhythm and blood pressure were restored in all 3 patients but one of them eventually succumbed to her underlying disease. Hemodialysis during CPR is probably an effective adjunct to the treatment of severe hyperkalemia in patients with severe hemodynamic compromise and asystolic cardiac arrest.

Contrast-induced nephropathy

Decreased kidney function European guidelines classify a pre-existing decreased kidney function to be a risk factor of contrast-induced nephropathy in the following cases: Estimated glomerular filtration rate (eGFR) < 45 ml/min/1.73 m2 of body surface area before intra-arterial administration with first-pass renal exposure (not passing lungs or peripheral circulation before kidneys), or in the intensive care unit eGFR < 30 ml/min/1.73 m2 before intravenous administration or intra-arterial administration with second-pass renal exposure Known or suspected acute kidney injury To calculate estimated GFR from creatinine, European guidelines use the CKD-EPI formula in adults ≥ 18 years, and the revised Schwartz formula in children. Swedish guidelines recommends no specific formula in children because of lack of evidence, but on the other hand recommends GFR based on cystatin C rather than creatinine in those with abnormal muscle mass or liver failure or cirrhosis.