​Kembara Xtra - Medicine - Hyperkalemia

​Kembara Xtra - Medicine - Hyperkalemia 
An electrolyte disease known as hyperkalemia is characterized by a plasma potassium (K) concentration that is greater than 5.5 mEq/L (or 5 mmol/L).

Hyperkalemia slows down the heart's ability to beat and can cause deadly arrhythmias.
Normal K regulation occurs when ingested K reaches the portal circulation and the pancreas responds by releasing insulin. K entrance into cells is facilitated by insulin. Angiotensin I is activated by K in the renal circulation, which promotes renin release from juxtaglomerular cells. Angiotensin I is then converted to angiotensin II in the lungs. Aldosterone secretion is stimulated by angiotensin II's action in the adrenal zona glomerulosa. At the renal collecting ducts, aldosterone causes sodium to be retained while K is expelled.
● four main factors
- Increased load: exogenous from a high intake or endogenous from tissue release, frequently accompanied by a decrease in excretion – Reduced excretion: caused by a lower glomerular filtration rate or a problem with aldosterone secretion – Cellular redistribution: changes from intracellular to extracellular space (the majority of K is intracellular); pseudohyperkalemia: associated with red cell lysis during blood sample collection or transport; thrombocytosis; or leukocytosis Geriatric Considerations
comorbid diseases, decreased renin and aldosterone, and an increased risk of hyperkalemia

Prevention Incidence
Patients with older ages, male sex, worse renal function, comorbidities, and usage of renin-angiotensin-aldosterone system inhibitors have greater incidence rates.
Prevalence can reach 50% in individuals with chronic kidney disease, compared to 1%–10% of hospitalized patients and 2%–3% of the general population.

Pathophysiology and Etiology 
Hemolysis of red blood cells in a phlebotomy tube, a symptom of pseudohyperkalemia (most frequently bogus result) Leukocytosis (reverse pseudohyperkalemia) with thrombolysis
Thrombocytosis, Hereditary Spherocytosis, Infectious Mononucleosis, Traumatic Venipuncture, and Clenching of the Fists During Phlebotomy (Spurious Result) Pseudohyperkalemia in families
Increasing K intake - Giving chronic renal disease patients salt replacements - Eating more bananas, potatoes, melons, citrus juice, and avocados
- Consuming ignite match heads and clay
Transcellular redistribution (shift) insulin shortage, metabolic acidosis, and hyperglycemia (also known as diabetic ketoacidosis or hyperosmolar hyperglycemia condition) - Impaired K excretion - Tissue injury (rhabdomyolysis, burns, trauma), cocaine addiction, high sweating during exercise, and renal insufficiency or failure
- Addison's illness
- Primary hyporeninemia and primary hypoaldosteronism - Type IV renal tubular acidosis (hyporeninemic hypoaldosteronism) - Mineralocorticoid deficiency - Cirrhosis - Obstructive uropathy - Congestive heart failure
Medication-induced (many) Genetics Sickle cell disease Amyloidosis Gordon syndrome Systemic lupus erythematosus
Familial hyperkalemic periodic paralysis and congenital adrenal hyperplasia are linked to various inherited diseases and disorders. 

Acidemia, massive cell lysis (rhabdomyolysis, burns, trauma), use of K-sparing diuretics, excessive K supplementation, and comorbid illnesses such chronic kidney disease, diabetes, heart failure, and liver disease are risk factors. 

Prevention Low K diet compliance and use of oral supplements in persons at risk


Chronic kidney illness, end-stage renal disease, congestive heart failure, myocardial infarction, rhabdomyolysis, liver disease, and the use of drugs like ACE inhibitors or angiotensin II receptor blockers are all associated conditions.

Serum K levels above the normal range (3.5 to 5.0 mEq/L) is the diagnosis. 

Presenting History Abdominal pain Palpitations Numbness Neuromuscular cramps, myalgias, muscle weakness, or paralysis

Clinical examination findings include: Weakness or flaccid paralysis of the extremities; decreased deep tendon reflexes; and 

Laboratory Results 

Renal function: BUN and creatinine Serum electrolytes
K, creatinine, and osmoles in urine (to determine fractional excretion of K and transtubular K gradient, all of which evaluate renal processing of K)
Conditions that could affect lab results K moves from the intracellular to extracellular area during acidemia.
Cortisol, aldosterone, and renin levels to test for mineralocorticoid deficit after other explanations have been checked out include: - Insulin deficiency - Hemolysis of sample When K 7 mEq/L, diagnostic procedures and other ECG abnormalities typically occur.
Lengthening of PR interval, loss of P wave, widened QRS Sine wave at very high K Can eventually result in arrhythmias such as bradycardia, ventricular fibrillation, and asystole. Peaked T wave with shortened QT interval in precordial leads (most common, typically earliest ECG change; however, neither sensitive nor specific).

Management 
Stabilize myocardial membranes with calcium gluconate IV 1,000 mg (10 mL of 10% solution) over 2 to 3 minutes; with continuous cardiac monitoring; repeat if necessary after 5 minutes; effect starts to take effect within minutes but only lasts 30 to 60 minutes; should be used in conjunction with definitive therapies. - Calcium chloride can also be used, albeit it requires central or deep vein infusion to prevent tissue necrosis.
Get extracellular K into the cells.
- Nebulized albuterol and other -agonists had an additive effect with insulin and glucose (at 10 to 20 mg/4 mL saline for >10 minutes—4 to 8 times bronchodilation dose) (5)[B].
- Close monitoring is required, especially for the first hour or two after injection. - Dextrose 50% 1 amp (if plasma glucose 250 mg/dL) and insulin 10 U IV may drive K intracellularly but do not lower total body K. This combination may cause hypoglycemia.
- Although sodium bicarbonate isn't typically advised, it may be beneficial in cases of severe metabolic acidosis.
Remove any extra K from your body.
When dialysis is not easily available, cation exchange resins are a definite therapeutic option but need to be administered in multiple doses.Kayexalate (sodium polystyrene sulfonate), patiromer calcium (Veltassa), and zirconium cyclosilicate are cation exchangers in the gastrointestinal system that bind K.
In particular, patiromer is preferred because it increases tolerance and reduces side effects in both acute and chronic contexts.
- Patiromer calcium (Veltassa): 8.4 g PO per day (study doses range from 4.2 to 16.8 g BID). This takes between 7 and 24 hours to reduce K. If more time is needed, repeat this every 12 hours.
- Kayexalate (sodium polystyrene sulfonate): 15 g PO or 30 g rectally; this lowers K in 1 to 4 hours.
If need, repeat this every six hours.
Enema has a quicker impact than PO.
Furosemide 40 mg IV every 12 hours or as a continuous infusion
- When other treatments are ineffective, hemodialysis is the only option. When situations like digitalis toxicity, rhabdomyolysis, end-stage renal illness, severe chronic kidney disease, or acute kidney injury are present, this may be necessary. One should also keep an eye out for postdialysis rebound– Although there is little clinical evidence, diuretics (loop and thiazides) can be used to manage persistent hyperkalemia.
Treatment for chronic hyperkalemia involves reviewing medications and stopping any that may be causing the condition.
- Advice on eating foods high in K.
- Thiazide and loop diuretic medication for diuretic therapy.


Caution: Kayexalate, which contains sodium polystyrene sulfonate, may make patients who already have fluid overload due to renal or cardiac failure worse.
Due to the significant risk of intestinal necrosis, sodium polystyrene sulfonate should not be used in individuals who are postoperative, have a bowel blockage, or have ileus.
Rapid calcium injection may cause a deadly dysrhythmia in people who have digitalis poisoning. With considerable caution, calcium should be infused slowly over 20 to 30 minutes in 5% dextrose. Digoxin-specific antibody fragment treatment is favored.

Furthermore Treated 

Replaced mineralocorticoids 
Consider a trial of fludrocortisone 0.1 mg daily for 3 to 5 days (in patients with moderately advanced chronic kidney disease, consider maintaining or increasing diuretics in tandem with the assistance of a nephrology consulting service) if the patient does not have a contraindication (greater than stage 1 HTN, volume overload, history of heart failure).

Admission 

If hyperkalemia is severe, treat it first before doing any diagnostic tests.
Intravenous calcium to stabilize the myocardium (use caution if digoxin toxicity or digoxin-induced hyperkalemia exists; this medication can result in heart block). 
Insulin (10 U IV, typically given with 50 mL of 50% glucose [if serum glucose 250 mg/dL] to prevent hypoglycemia]); repeat if elevation persists.
Inhaled 2-agonist (albuterol nebulized)
Stop using any medications (such as exogenous K and K-sparing diuretics) that could raise K levels.
If there are ECG changes or if K is greater than 6 mEq/L (6 mmol/L), you should be admitted for cardiac monitoring.

Patient Follow-Up Monitoring
Serum Until the patient has stabilized and recurrent hyperkalemia is no longer a danger, K levels should be monitored again every 2 to 4 hours.
The recommended daily intake of potassium is 80 mEq (80 mmol). A lot of foods contain K. Bananas, orange juice, other citrus fruits and juices, figs, molasses, seaweed, dried fruits, almonds, avocados, lima beans, bran, tomatoes, tomato juice, cantaloupe, honeydew melon, peaches, potatoes, and salt alternatives are some foods that are exceptionally high in K (>6.4 mEq/serving). Alfalfa, dandelion, horsetail nettle, milkweed, hawthorn berries, toad skin, oleander, foxglove, and ginseng are just a few of the herbal remedies that can raise K levels.


Discuss a low-K diet with a dietician.

Prognosis Associated with poor prognosis in patients with chronic kidney disease and heart failure Associated with poor prognosis in emergency medicine, with trauma, tissue necrosis, K+ supplementation, metabolic acidosis, if calcium gluconate is used to treat hyperkalemia, if AKI, or if hyperkalemia lasts for an extended period of time

 Potential side effects of using ion-exchange resins to treat hyperkalemia include volume overload and intestinal necrosis. Complications Life-threatening heart arrhythmias