​Kembara Xtra - Medicine - Hypokalemia

​Kembara Xtra - Medicine - Hypokalemia 
A serum potassium level of 3.5 mEq/L (normal range, 3.5 to 5.0 mEq/L) is considered hypokalemic.
Mild hypokalemia (3.0 to 3.5 mEq/L of serum potassium) 
Serum potassium levels of 2.5 to 3.0 mEq/L indicate moderate hypokalemia. 
Extremely low serum potassium levels (2.5 mEq/L) 

Epidemiology 
Males predominate over females.

Prevalence >20% of hospitalized patients (when defined as potassium 3.6 mEq/L) >10% of inpatients with alcoholism >80% of patients receiving diuretics >12-18% of patients with chronic kidney disease >Higher (5-20%) in people with eating disorders >Higher in people with AIDS >Associated risk following bariatric surgery 

Pathophysiology and Etiology 
Most typical reasons:
GI loss: vomiting, diarrhea, nasogastric tubes, laxative misuse, fistulas, colorectal tumor, bowel diversion, ureterosigmoidostomy, malabsorption, chemotherapy, radiation enteropathy, bulimia
Intoxications (theophylline, caffeine, barium, toluene), refeeding syndrome, excessive activity, metabolic alkalosis, excess insulin, excess -adrenergic catecholamines (acute stress, 2-agonists), hypokalemic periodic paralysis
Amphotericin B, aminoglycosides, antipseudomonal penicillins (carbenicillin), high-dose penicillin, and clay (bentonite) are some medications that might cause renal potassium loss. - Mineralocorticoid excess causes renovascular hypertension, secondary hyperaldosteronism, congestive heart failure, cirrhosis, nephrotic syndrome, malignant hypertension, and primary hyperaldosteronism (Conn syndrome). - Exogenous mineralocorticoids (such as carbenoxolone, nasal steroids, and the glycyrrhizic acid in licorice). - Osmotic diuresis, such as those caused by poorly managed diabetes
- Magnesium deficiency - Types I and II renal tubular acidosis - Excess glucocorticoids - Cushing syndrome - Exogenous steroids - Ectopic synthesis of adrenocorticotrophic hormone - Refeeding syndrome
Treatment of diabetic ketoacidosis (DKA) with inadequate or postponed potassium replenishment Genetics
There are a number of uncommon, familial conditions that can result in hypokalemia, including: 11-hydroxysteroid dehydrogenase deficiency; apparent mineralocorticoid excess; congenital adrenogenital syndromes; familial glucocorticoid resistance; familial hypokalemic periodic paralysis; familial interstitial nephritis; Fanconi syndrome; Geller syndrome; and sodium channel mutations: Bartter, 

Risk factors include: ACE; Thiazide/loop diuretic usage; higher systolic blood pressure

Low BMI and blood cholesterol, as well as a higher albumin-to-creatinine ratio. 

Prevention 

Check your potassium level before starting a diuretic.

Acute GI conditions that cause severe vomiting or diarrhea, an increased risk of cardiac arrhythmias, and a predictor of the onset of a severe alcohol withdrawal syndrome are all associated conditions.

Typically asymptomatic until serum potassium levels fall below 3.0 mEq/L, unless they do so quickly or the patient has a potentiating condition, such as a propensity for arrhythmia.
The neuromuscular, cardiovascular, renal, and endocrine systems are mostly involved in the signs and symptoms.


Presenting History: Polyuria, polydipsia, nocturia; hyperglycemia; alkalosis/acidosis; usage of diuretics; malnutrition; vomiting; diarrhea; easy fatigue; leg cramps; muscle weakness 

clinical assessment 
Neuromuscular—proximal > distal skeletal muscle weakening, ascending paralysis - Hypomobility of the GI smooth muscle
- Respiratory acidosis and respiratory arrest in the respiratory muscle

Cardiovascular: orthostasis, peripheral edema, hypotension; listen for rales and arrhythmias.
Chronic kidney disease (tubular interstitial nephritis, nephrogenic diabetes insipidus, renal cyst) and metabolic acidosis, rhabdomyolysis, and myoglobinuria are among the renal conditions.


Multiple Diagnoses 

Once laboratory error has been ruled out, the diagnosis of hypokalemia is a laboratory finding that does not need to be distinguished from other entities.

Laboratory Results: Serum potassium concentration of 3.5 mEq/L (3.5 mmol/L)
Disorders that could affect lab results include: Leukocytosis and leukemia
Initial examinations (lab, imaging)
If the history excludes GI or iatrogenic reasons, begin the workup with an ECG.
- The level of potassium in the serum and urine to assess the degree of hypokalemia Basic metabolic test (serum sodium, potassium, glucose, chloride, bicarbonate, BUN, and creatinine); serum magnesium, calcium, and/or phosphorus to rule out any associated electrolyte abnormalities, particularly if drunkenness is suspected - Urinalysis and urine pH to check for renal tubular acidosis; Spot urine electrolytes (potassium and chloride) to distinguish between renal and nonrenal causes; Arterial blood gas to check for metabolic acidosis or alkalosis; Serum digoxin level for patients taking digitalis
- Creatinine kinase in severe hypokalemia for rhabdomyolysis
- TSH in case of tachycardia or suspicion of hypokalemic periodic paralysis; urine/serum drug screen for amphetamines and other sympathomimetic drugs

Tests in the Future & Special Considerations
There are two main parts. - The excretion of potassium in the urine to differentiate renal loss from other causes 24-hour urine potassium excretion is the best approach for determining acid-base status. >15 mEq/day = inappropriate renal loss; in the absence of - A potassium-to-creatinine ratio of more than 13 mEq/g (1.5 mEq/mmol) in a single spot of urine may signify untimely renal loss; or Transtubular potassium gradient (TTKG) values greater than 4 can also indicate renal loss.
Metabolic acidosis plus low urinary excretion results in GI loss. TTKG = (urine K+/plasma K+) / (urine Osm/plasma Osm)
DKA, renal tubular acidosis type 1 or 2, metabolic alkalosis + low urinary excretion, usage of diuretics, metabolic acidosis + urine potassium wasting, metabolic alkalosis + urinary potassium wasting
Vomiting (low urine chloride), Gitelman-Bartter syndrome (normal urine chloride), and diuretics (Urine chloride varies with kinds) are examples of normotensive symptoms. - Hypertensive: glucocorticoid resistance, Liddle syndrome, Geller syndrome, and primary aldosteronism
To distinguish between adrenal and nonadrenal causes of hyperaldosteronism, measure plasma renin and aldosterone levels if there is excessive renal potassium loss (>20 mEq/day) and hypertension.

Imaging should be taken into consideration in situations with a high clinical index of suspicion.
- MRI of the pituitary gland to rule out Cushing syndrome; - MRI/CT of the adrenal gland with suspicion of mineralocorticoid, glucocorticoid, or catecholamine excess
- Abdominal CT for Interpretation of the VIPoma Test
ECG: T-wave flattening, ST-segment alterations, and U waves (a tiny, positive deflection that follows a T wave that is most prominent in the V2 and V3 intervals). - pac/pvc, paroxysmal atrial or junctional tachycardia, atrioventricular block, ventricular tachycardia, or fibrillation are a few examples of arrhythmias.

Management 

Reduce potassium loss and replenish potassium reserves.
Determine any probable toxicity.
Identify the cause.


General Actions 
Manage the underlying illness or get rid of the contributing condition.
- Stop using laxatives and switch to diuretics that are potassium-neutral or potassium-sparing.
– treat vomiting and diarrhea.
- If the patient is receiving nasogastric suction, use H2 blockers; - If glucosuria is present, control hyperglycemia.

Non-emergent situations (serum potassium > 2.5 mEq/L [> 2.5 mmol/L], no cardiac symptoms) are treated with medication. - Preference for oral therapy: split doses of 40 to 120 mEq/day (40 to 120 mmol/day) - Make sure to drink enough water (100 to 250 mL), preferably with or after a meal.
- Only administer IV potassium when oral delivery is impractical (e.g., when vomiting or in a postoperative state). To decrease burning and discomfort at the IV site and to prevent phlebitis, the rate should not exceed 10 mEq/hr and the concentration shouldn't exceed 40 mEq/L.
A central line is advised for rates greater than 10 mEq/hr; central access can safely administer up to 40 mEq in 100 mL.
For all types of hypokalemia, potassium chloride (KCl) is an effective treatment.
 In metabolic acidosis, potassium bicarbonate or its precursors (gluconate, acetate, or citrate) Potassium phosphate in DKA and phosphate deficiency
Emergencies (arrhythmias, serum potassium 2.5 mEq/L [2.5 mmol/L])
Standard IV replacement infusion rates are 10 mmol/hr and 20 mmol/hr, respectively. Central lines are preferable.
(2)[A] If the patient has hypomagnesemia
Give 4 mL of MgSO4 50% (8 mmol) in 10 mL of NaCl 0.9% over the course of 20 minutes, then start a 40 mmol KCl infusion before replacing the magnesium.
The danger of hyperkalemia exists with any potassium replacement therapy.
– The elderly, diabetic patients, and patients with renal failure are groups at higher risk and should have their serum potassium evaluated more frequently. In order to account for the intracellular shift in DKA patients taking insulin, more prompt and vigorous potassium replacement is needed (4)[A].
– Dietary potassium does not make up for potassium loss caused by chloride depletion (for as through diuretics or vomiting) since it is almost entirely related to phosphate rather than chloride.
Important potential interactions The risk of hyperkalemia is increased by concurrent administration of potassium-sparing diuretics (spironolactone, triamterene, amiloride, and ACE inhibitors).

Aspects of Geriatrics
Although senior patients acquire hypokalemia more quickly, younger patients have a larger prevalence of the condition.
Low serum potassium levels can result in myonecrosis, limb paralysis, and an increased risk of falling.

Referral 

Referrals to endocrinology or nephrology should be made for patients with unexplained hypokalemia, refractory hyperkalemia, or symptoms that point to a different diagnosis (such as aldosteronism or hypokalemic periodic paralysis).

Admission 

For asymptomatic patients receiving oral replacement therapy, outpatient follow-up is sufficient.
Patients who exhibit cardiac symptoms require IV replenishment and ongoing cardiac monitoring in a hospital environment.
ICU hospitalization is necessary for patients who have life-threatening complications including arrhythmias or respiratory failure.

Patient Follow-Up Monitoring
Patients getting IV therapy should have their blood potassium levels checked every 4-6 hours and have constant cardiac monitoring.
Serum potassium and magnesium levels for patients who need potassium supplements should be checked at intervals decided by clinical judgment and patient compliance.


Diet
Make sure you consume enough foods high in potassium, such as oranges, bananas, cantaloupes, prunes, raisins, dried beans, dried apricots, and squash.
Limit your salt consumption because a high-sodium diet might lead to potassium loss in the urine.


Patient education should emphasize the risks of not taking a potassium supplement as well as recommendations for a healthy diet.
Consumer Fact Sheet about Potassium. 

The majority of hypokalemia cases will improve with replacement within 24 to 72 hours.
If the underlying cause is treated, hypokalemia should go away without additional intervention.
Linked to increased morbidity and mortality from cardiac arrhythmias 

Complications include hyperkalemia while receiving medication, an increased risk of digoxin toxicity, and an increased risk of arrhythmias due to an increase in the resting potential of myocytes and, consequently, their refractory time.