Electrolyte derailments

In 1966, Desertenne, the first to describe the condition, suspected that it was caused by electrolyte disturbances in the form of hypokalemia or hypomagnesemia and that it had a bifocal etiology (Lüderitz 1993).

Electrolyte imbalance refers to salts that are dissolved, i.e., present in ionic form in the aqueous environment of the body, and whose quantity is outside the physiological concentration (Founder 2019).

Throughout the body, dissolved in extracellular and intracellular fluid, electrolytes are found. The most important electrolytes include:

01. Na +:

02. K +:

03. Ca 2 +:

04. Mg 2 +:

05. HPO 4 -:

06. CL -

07. HCO 3 -

08. SO 4 - (Halwachs- Baumann 2011)

09. Fe 2 +

10. Fe 3 + (Founder 2019)

The roles of electrolytes are:

- Triggering of action potentials

- Buffer function of the plasma

- Maintaining the balance in the acid-base household (Founder 2019).

For some electrolytes, the physiological concentration has only a small range of variation (Gründer 2019).

Classic emergency situations can be triggered by shifts in electrolytes due to, for example,:

- hyperkalemia

- hypercalcemia

- Hyponatremia (Menche 2020).

• 1. 1 Sodium deficiency see also hyponatremia:

In the case of hyponatremia, a so-called pseudohyponatremia must first be excluded. This is defined as a decrease in serum sodium caused by a decreased water content due to increased hyperlipoproteinemia or hyperproteinemia (Rabold 2013). Therefore, to exclude pseudohyponatremia, serum osmolality should always be determined in addition to serum sodium, which is < 280 mmol / l in the case of a real decrease in sodium, and > 280 mmol / l in the case of pseudohyponatremia (Pottgießer 2019).

In real hyponatremia, both fluid and sodium are reduced (Rabold 2013).

- Normal values: serum sodium: 135 - 145 mmol / l (Grabowaki 2013). Osmolality < 280 mosmol / kg (Pottgießer 2019). It is already called severe hyponatremia when the serum sodium value falls below 120 mmol / l (Rabold 2013).

- The cause of hyponatremia is a disturbance of renal water excretion and / or an increased intake of water as found, for example, in:

- severe vomiting

- diarrhea

- renal diseases

- diuretics (Menche 2020)

- after outpatient colonoscopy (Kluge 2010)

- peritonitis

- Adrenocortical insufficiency

- Diabetes mellitus (in the context of osmotic diuresis)

- pancreatitis (Rabold 2013)

- Symptoms may include:

In slowly developing hyponatremia: Asymptomatic.

In rapidly developing:

- Nausea

- malaise

- Neurological disorders such as headache, seizures, drowsiness and even coma (Schoenenberger 2009)

• 1. 2. sodium excess: see also hypernatremia

- Normal values: serum sodium: 135 - 145 mmol / l (Grabowaki 2013).

- Hypernatremia can be caused by, for example:

- diabetes insipidus

- fever

- heavy sweating (Menche 2020)

- in elderly patients, by a drop in GFR and simultaneous salt load (Mertz 2000)

Symptoms can be:

- apathy

- weakness

- seizures

- clouding of consciousness up to coma (Schoenenberger 2009)

• 2. 1 Potassium deficiency: see also hypokalemia

- Normal values: 3 .6 - 5.0 mmol / l (Herold 2022)

- Causes of hypokalemia can be, for example:

- vomiting

- diarrhea

- diuretics

- laxatives

- primary and secondary hyperaldosteronism

- primary polydipsia with polyuria (Schoenenberger 2009)

- Symptoms may include:

- fatigue

- apathy

- constipation

- rhabdomyolysis

- tetany

- muscle cramps

- Muscle weakness up to paralysis with respiratory paralysis (Schoenenberger 2009)

• 2. 2 Potassium excess: see also hyperkalemia

- Normal values: 3 .6 - 5.0 mmol / l (Herold 2022)

- Causes include:

- renal dysfunction (Menche 2020)

- strong cell decay

- drug-induced by e.g. potassium-sparing diuretics,beta- blockers, succinylcholine (Ziegenfuß 2014).

- insulin deficiency

- hyperglycemia

- digitalisin intoxication

- Hypoaldosteronism (Schoenenberger 2009).

- Symptoms may include:

- muscle weakness

- in polyradiculitis ascending paralysis

- furry feeling in the area of the tongue

- paresthesias perioral

- cardiac arrhythmias up to ventricular fibrillation and asystole (Schoenenberger 2009)

• 3.1 Calcium deficiency: see also hypocalcemia

- Normal values: total calcium 2.2 - 2.7 mmol / l (Herold 2022)

- Causes can be e.g.:

- parathormone deficiency

- Vit. D hormone deficiency

- hyperventilation

- Diuretics (Menche 2020)

- Tissue sequestration in rhabdomyolysis, tumor lysis, pancreatitis (Schoenenberger 2009)

- Symptoms can be:

- paresthesias in the acral and perioral area

- striated muscles may develop painful tonic contractions

- smooth muscles may react equivalently

- extrapyramidal symptoms with hypo- and hyperkinesias

- seizures

- panic attacks (Schoenenberger 2009)

• 3. 2 Calcium excess: see also hypercalcemia

- Normal values: total calcium 2.2 - 2.6 mmol / l (Herold 2022)

- Causes by e.g.:

- primary hyperparathyroidism

- in connection with malignancies, e.g. breast, prostate, bronchial carcinoma, multiple myeloma

- Vitamin D intoxication (Schoenenberger 2009)

- Symptoms can be:

- Apathy, somnolence up to coma

- vomiting

- fatigue

- muscle weakness

- polyuria

- arterial hypertension

- tachycardia (Schoenenberger 2009)

• 4. 1 Magnesium deficiency: see also hypomagnesemia.

Magnesium deficiency also inhibits the parathyroid hormone. Therefore, magnesium deficiency is often accompanied by hypocalcemia.

- Normal values serum magnesium: 0.75 - 1.0 mmol / l (Founder 2019).

- Possible causes of hypomagnesemia include:

- malnutrition

- during pregnancy (Menche 2020)

- Cardiac arrhythmias (Lüderitz 1993).

- Symptoms can be:

- fatigue, weakness

- anorexia

- cardiac arrhythmias

- neuromuscular disorders (Gerok 2007)

- hypocalcemia (due to parathyroid resistance and hypoparathyroidism)

- Hypokalemia (there is increased distal Na- supply in the kidney due to inhibition of reabsorption of sodium in the loop of Henle [Battegay 2017]).

• 4. 2 Magnesium excess: see also hypermagnesemia.

- Normal values serum magnesium: 0.75 - 1.0 mmol / l (Founder 2019).

- Possible causes can be:

- acute and chronic renal insufficiency (Menche 2020)

- increased intake by e.g. antacids, laxatives

- endocrine diseases such as

- hypothyroidism

- Addison's disease (Gerok 2007)

- Symptoms can be:

- nausea, vomiting

- constipation

- muscle weakness

- Vasodilatation with drop in blood pressure

- respiratory paralysis

- Cardiac arrest (Gerok 2007)

• 5. 1 Phosphate deficiency: see also hypophosphatemia

- Normal values serum phosphate: 0.84 - 1.45 mmol / l (Herold 2022)

- Caused by e.g.:

- malnutrition in alcoholics

- in the context of certain kidney diseases (Menche 2020)

- anorexia nervosa

- primary hyperparathyroidism

- paraneoplastic syndrome

- Z. n. kidney transplantation (Hartig 2004)

- Symptoms may include:

- signs of acute heart failure

- arrhythmias

- confusion

- epileptiform seizures

- paresthesias

- paralysis of the cranial nerves (Hartig 2004)

• 5. 2 Phosphate excess: see also hyperphophatemia

- Normal values serum phosphate: 0.84 - 1.45 mmol / l (Herold 2022)

- Caused by e.g:

- Renal insufficiency (main cause [Hartig 2004]).

- Hormonal disorders (Menche 2020)

- Hypoparathyroidism (PTH deficiency)

- acromegaly

- Vit. D intoxication (Hartig 2004)

- Symptoms can be:

- Hypocalcemia and extraosseous soft tissue calcification due to formation of poorly soluble calcium-phosphate bonds.

- Pain in the joints (Külpmann 2013)

The most frequent cause of emergency problems is a derailment of the potassium balance. Problems with calcium and magnesium balance can also cause life-threatening emergencies, but occur much less frequently (Ziegenfuß 2014).

The most common electrolyte disturbance in the elderly is hyponatremia. On hospital admission, this is found in less than 10%, but during hospitalization this figure rises to up to 30% (Rabold 2013).

The uneven distribution of electrolytes in the intracellular or extracellular space creates an electrical voltage, which is also referred to as an "electrical potential". The function of muscle and nerve cells is based on the generation of electrical potentials, as are the stimuli from sensory organs, which transmit electrical signals to the brain (Lauber 2017).

In addition to eliminating the precipitating cause of electrolyte imbalance, should be done in case of:

• 1. 1. sodium deficiency:

In the case of sodium deficiency, substitution should always be performed slowly, because if correction is too rapid, there is a risk of central pontine myelinolysis with demyelinating brainstem lesion. This risk is particularly high in the elderly and alcoholics (Rabold 2013).

• 1. 2. sodium excess:

Hypovolemic hypernatremia: Volume substitution with 5% glucose solution plus isotonic electrolyte solution, which should equal 1/3 of the fluid deficit (Herold 2022).

Hypervolemic hypernatremia: Do not supply isotonic solutions. If serum sodium > 160 mmol / l, 5% glucose solution and a loop diuretic such as furosemide should also be used (Schaps 2007). In renal failure , dialysis is indicated (Herold 2022).

• 2. 1. potassium deficiency:

Substitution of potassium with attention to pH. An extracellular deficit of serum potassium of 1 mmol / l corresponds to a deficiency of 100 mmol of potassium (Herold 2022).

• 2. 2 Excess potassium:

- Immediately stop potassium intake and avoid foods containing potassium such as bananas.

- Promote influx of potassium into cells by:

- Sodium bicarbonate (in metabolic acidosis): Dosage recommendation: 50 - 100 ml of an 8.4 % solution over 30 min i. v.; duration of action is about 2 h.

- Glucose and insulin: dosage recommendation: 50 ml of 40 % glucose solution plus 10 I. E. normal insulin i. v. over 30 min; duration of action between 4 - 6 h

- Calcium gluconate: dosage recommendation: 10 ml of 10 % calcium gluconate; duration of action is about 30 min; contraindication: additional hypercalcemia and digitized patients.

- Removal of potassium by:

- a forced diuresis with e.g. 0.9 % NaCl as infusion plus furosemide

- cation exchange resins such as Resonium A; duration of action 4 - 6 h; contraindication: arterial hypertension, hypernatremia

- Hemodialysis in e.g. chronic renal insufficiency or acute renal failure

(Herold 2022)

• 3. 1. calcium deficiency:

If tetany occurs, calcium should be substituted e.g. with calcium gluconate 10 % slow i. v. . Any magnesium deficiency that may exist in parallel should also be compensated.

As a long-term therapy, oral substitution of calcium (possibly together with vitamin D) is indicated (Herold 2022).

• 3. 2. calcium excess:

If the calcium excess is asymptomatic with values < 3.5 mmol / l, outpatient therapy is usually possible.

If, on the other hand, values > 3.5 mmol / l, inpatient treatment is required. This consists of:

- Stopping the calcium intake (calcium is contained e.g. in mineral waters)

- under constant control of the water and electrolyte balance, a forced diuresis with physiological saline solution 5 l / d or more and additional administration of furosemide should be carried out. Substitution of potassium may be necessary (Herold 2022).

- Bisphosphonates:

Especially in tumor-induced hypercalcemia, bisphosphonates are the drug of choice; dosage recommendation: e.g., pamidronic acid 15 - 90 mg over 2 h i. v. (Herold 2022).

- Calcitonin:

Up to 30% of patients do not respond to calcitonin. It is also relatively short acting (Herold 2022).

- Hemodialysis in renal insufficiency (Herold 2022).

• 4. 1. Magnesium deficiency:

If magnesium is deficient, it should be substituted orally. Dosage recommendation: 10 - 30 mmol / d (Herold 2022).

• 4. 2. magnesium excess:

If the cause of hypermagnesemia is terminal renal failure, dialysis is recommended.

If the cause is parenteral magnesium overdose, calcium i. v. may be used as an antidote (Herold 2022).

- 5. 1. phosphate deficiency:

Therapy should be relatively rapid as long as the deficiencies are still reversible.

If the deficiency is moderate, an increase in oral intake combined with vitamin D substitution is usually sufficient (Herold 2022).

Oral intake e.g.:

- Milk (1 mg phosphate / ml)

In cases of lactose intolerance, potassium or sodium phosphate 1 - 3 g / d can be administered orally (Herold 2022).

In severe phosphate deficiency, infusions of 4 - 8 mmol phosphate / h over 6 h are recommended, with a total amount between 24 - 48 mmol. Checks of calcium and phosphate levels are indicated every 6 - 8 h (Herold 2022).

- 5. 2. Phosphate excess:

Provided normal renal function is present, acute hyperphosphatemia may normalize within 6 - 12 h without therapy (Paumgartner 2003).

Symptomatic treatment consists of reducing phosphate intake (Herold 2022) to < than 600 mg / 24 h. This can be achieved, for example, by reducing dairy and meat products (Paumgartner 2003), Coca- Cola, food preservatives, etc. (Füsgen 2004).

Medication can be used:

- Carboanhydrase inhibitors such as acetazolamide 15 mg / kg bw p. o. every 3 - 4 h

- Increase of renal excretion of phosphate by e.g. 1,000 - 2,000 ml 0.9 % NaCl infusion over 2 h (Paumgartner 2003).

In chronic hyperphosphatemia, we recommend:

- Aluminum salts up to 3 g / 24 h

- Calcium salts up to 8 g / 24 h

- Magnesium salts between 2 - 3 g / 24 h

- Phosphate binders: Initially, 0.5 - 1 g of phosphate binders should be taken about 10 - 20 min before meals. The dose should be increased gradually until a normal value of phosphate is reached (Paumgartner 2003).

In severe cases, dialysis is recommended (Herold 2022).

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