CITY OF MANILA

UNIVERSIDAD DE MANILA
(Formerly City College of Manila)
Mehan Gardens, Manila
College of Nursing

In partial Fulfillment for the requirements

on the Related Learning Experience

(Medicine Ward)

MUSCLE PARESIS SECONDARY TO

ELECTROLYTE IMBALANCE

(HYPOKALEMIA)

Submitted by:

Costales, Butch

NR-32

November 26, 2010

Date Submitted
Muscle Paresis

Muscle Paresis is a general term referring to a mild to moderate degree of muscular

weakness, occasionally used as a synonym for Paralysis (severe or complete loss of motor
function). In the older literature, paresis often referred specifically to paretic Neurosyphilis.
"General paresis" and "general paralysis" may still carry that connotation. Bilateral lower
extremity paresis is referred to as Paraparesis.

POTASSIUM DEFICIT (HYPOKALEMIA)

Hypokalemia (below-normal serum potassium concentration) usually indicates an actual
deficit in total potassium stores. Hypokalemia may occur in patients with normal potassium
stores; however, when alkalosis is present, a temporary shift of serum potassium into the cells
occurs (see discussion of alkalosis later in this chapter).
As stated earlier, hypokalemia is a common imbalance (Gennari, 1998). GI loss of
potassium is probably the most common cause of potassium depletion. Vomiting and gastric
suction frequently leads to hypokalemia, partly because potassium is actually lost when gastric
fluid is lost, but more so because potassium is lost through the kidneys in association with
metabolic alkalosis. Because relatively large amounts of potassium are contained in intestinal
fluids, potassium deficit occurs frequently with diarrhea. Intestinal fluid may contain as much
potassium as 30 mEq/L. Potassium deficit also occurs from prolonged intestinal suctioning,
recent ileostomy, and villous adenoma (a tumor of the intestinal tract characterized by excretion
of potassiumrich mucus).
Alterations in acid–base balance have a significant effect on potassium distribution. The
mechanism involves shifts of hydrogen and potassium ions between the cells and the ECF.
Hypokalemia can cause alkalosis, and in turn alkalosis can cause hypokalemia. For example,
hydrogen ions move out of the cells in alkalotic states to help correct the high pH, and potassium
ions move in to maintain an electrically neutral state. (This is discussed further in the section on
acid–base balance.)
Hyperaldosteronism increases renal potassium wasting and can lead to severe potassium
depletion. Primary hyperaldosteronism is seen in patients with adrenal adenomas. Secondary
hyperaldosteronism occurs in patients with cirrhosis, nephrotic syndrome, heart failure, and
malignant hypertension (Wilcox, 1999).
 Potassium-losing diuretics, such as the thiazides (eg, chlorothiazide [Diuril] and
polythiazide [Renese]), can induce hypokalemia, particularly when administered in large doses
to patients with inadequate potassium intake. Other medications that can lead to hypokalemia
include corticosteroids, sodium penicillin, carbenicillin, and amphotericin B (Cohn et al., 2000;
Gennari, 1998).
Because insulin promotes the entry of potassium into skeletal muscle and hepatic cells,
patients with persistent insulin hypersecretion may experience hypokalemia, which is often the
case in patients receiving high-carbohydrate parenteral fluids (as in parenteral nutrition).
Patients who are unable or unwilling to eat a normal diet for a prolonged period are at
risk for hypokalemia. This may occur in debilitated elderly people, alcoholics, and patients with
anorexia nervosa. In addition to poor intake, people with bulimia frequently suffer increased
potassium loss through self-induced vomiting and laxative and diuretic abuse.
Magnesium depletion causes renal potassium loss and must be corrected first; otherwise,
urine loss of potassium will continue. Penicillins may produce renal potassium loss by acting as
poorly reabsorbable anions and thus increasing distal sodium delivery and sodium-potassium
loss.

Clinical Manifestations
Potassium deficiency can result in widespread derangements in physiologic function.
Severe hypokalemia can cause death through cardiac or respiratory arrest. Clinical signs rarely
develop before the serum potassium level has fallen below 3 mEq/L (3 mmol/L) unless the rate
of fall has been rapid. Manifestations of hypokalemia include fatigue, anorexia, nausea,
vomiting, muscle weakness, leg cramps, decreased bowel motility, paresthesias (numbness and
tingling), dysrhythmias, and increased sensitivity to digitalis (Gennari, 1998). If prolonged,
hypokalemia can lead to an inability of the kidneys to concentrate urine, causing dilute urine
(resulting in polyuria, nocturia) and excessive thirst. Potassium depletion depresses the release of
insulin and results in glucose intolerance.

Assessment and Diagnostic Findings

In hypokalemia, the serum potassium concentration is less than the lower limit of normal.
Electrocardiographic (ECG) changes can include flat T waves and/or inverted T waves,
suggesting ischemia, and depressed ST segments. An elevated U wave is specific to
hypokalemia. Hypokalemia increases sensitivity to digitalis, predisposing the patient to digitalis
toxicity at lower digitalis levels. Metabolic alkalosis is commonly associated with hypokalemia.
This is discussed further in the section on acid–base disturbances.
The source of the potassium loss is usually evident from a careful history. When this is
not the case, however, and the etiology of the loss is unclear, a 24-hour urinary potassium
excretion test can be performed to distinguish between renal and extrarenal loss. Urinary
potassium excretion exceeding 20 mEq/24 h with hypokalemia suggests that renal potassium loss
is the cause.

Medical Management

If hypokalemia cannot be prevented by conventional measures such as increased intake in

the daily diet, it is treated with oral or IV replacement therapy (Gennari, 1998). Potassium loss
must be corrected daily; administration of 40 to 80 mEq/day of potassium is adequate in the adult
if there are no abnormal losses of potassium.
For patients at risk for hypokalemia, a diet containing sufficient potassium should be
provided. Dietary intake of potassium in the average adult is 50 to 100 mEq/day. Foods high in
potassium include fruits (especially raisins, bananas, apricots, and oranges), vegetables, legumes,
whole grains, milk, and meat. When dietary intake is inadequate for any reason, the physician
may prescribe oral or IV potassium supplements (Gennari, 1998). Many salt substitutes contain
50 to 60 mEq of potassium per teaspoon and may be sufficient to prevent hypokalemia. When
oral administration of potassium is not feasible, the IV route is indicated. The IV route is
mandatory for patients with severe hypokalemia (eg, a serum level of 2 mEq/L). Although
potassium chloride is usually used to correct potassium deficits, the physician may prescribe
potassium acetate or potassium phosphate.

Nursing Management
Because hypokalemia can be life-threatening, the nurse needs to monitor for its early
presence in patients at risk. Fatigue, anorexia, muscle weakness, decreased bowel motility,
paresthesias, and dysrhythmias are signals that warrant assessing the serum potassium
concentration. When available, the ECG may provide useful information. For example, patients
receiving digitalis who are at risk for potassium deficiency should be monitored closely for signs
of digitalis toxicity, because hypokalemia potentiates the action of digitalis. Physicians usually
prefer to keep the serum potassium level above 3.5 mEq/L (3.5 mmol/L) in patients receiving
digitalis medications such as digoxin.

PREVENTING HYPOKALEMIA
Measures are taken to prevent hypokalemia when possible (Gennari, 1998). Prevention
may involve encouraging the patient at risk to eat foods rich in potassium (when the diet allows).
Sources of potassium include fruit and fruit juices (bananas, melon, citrus fruit), fresh and frozen
vegetables, fresh meats, and processed foods. When hypokalemia is due to abuse of laxatives or
diuretics, patient education may help alleviate the problem. Part of the health history and
assessment should be directed at identifying problems amenable to prevention through education.
Careful monitoring of fluid intake and output is necessary because 40 mEq of potassium is lost
for every liter of urine output. The ECG is monitored for changes, and arterial blood gas values
are checked for elevated bicarbonate and pH levels.

CORRECTING HYPOKALEMIA
Great care should be exercised when administering potassium, particularly in older
adults, who have lower lean body mass and total body potassium levels and therefore lower
potassium requirements. Additionally, with the physiologic loss of renal function with advancing
years, potassium may be retained more readily in older than in younger people.

ADMINISTERING IV POTASSIUM
Potassium should be administered only after adequate urine flow has been established. A
decrease in urine volume to less than 20 mL/h for 2 consecutive hours is an indication to stop the
potassium infusion until the situation is evaluated. Potassium is primarily excreted by the
kidneys; therefore, when oliguria occurs, potassium administration can cause the serum
potassium concentration to rise dangerously.

NONDRUG CAUSES DUE TO TRANSCELLULAR SHIFTS

Severe hypokalemia (serum potassium, <3.0 mmol per liter) can occur, although rarely,
in association with hyperthyroidism, resulting in a clinical syndrome characterized by the sudden
onset of severe muscle weakness and paralysis. This presentation has a predilection for people of
Asian origin, occurring in 2 to 8 percent of patients with hyperthyroidism in Asian countries.
Signs and symptoms of hyperthyroidism usually accompany these acute episodes of muscle
weakness and paralysis, but they may be subtle, and the misdiagnosis of familial periodic
paralysis may be made (see below). As in the case of familial periodic paralysis, the symptoms
respond rapidly to the administration of potassium.

Familial hypokalemic periodic paralysis is a rare autosomal dominant disease that has
been associated with mutations of the gene encoding the dihydropyridine receptor, a voltage-
gated calcium channel. The disorder is characterized by sudden attacks of muscle paralysis
associated with a decrease in serum potassium to low concentrations, often less than 2.5 mmol
per liter. Attacks can be provoked by high intake of carbohydrates or sodium or by exertion and
usually subside spontaneously in less than 24 hours. Although the hypokalemia is caused by a
shift of potassium into cells, the administration of potassium can be lifesaving and should be
given to treat acute attacks. Various approaches have been used to prevent recurrences with
varying degrees of success, including the administration of spironolactone, triamterene, and
acetazolamide.
 Serum potassium decreases abruptly in patients with delirium tremens, by 1.0 mmol per
liter on average. The severity of hypokalemia in this disorder is correlated with the plasma
epinephrine concentration, and the presumption is that the reduction in potassium is due to b-
adrenergic stimulation, which causes a shift of potassium into cells.

Accidental ingestion of barium compounds causes hypokalemia by blocking the exit of

potassium from cells, and in severe cases it can lead to muscle weaness, paralysis, and
rhabdomyolysis. Barium also causes vomiting and diarrhea, both of which exacerbate
hypokalemia by causing loss of potassium. Treatment with intravenous potassium should be
initiated rapidly.

Treatment of severe pernicious anemia (hematocrit, <20 percent) with vitamin B12
causes an acute reduction in serum potassium because of a rapid uptake of potassium by the new
cells that are formed. Hypokalemia can also occur after the transfusion of previously frozen
washed red cells, presumably because of the uptake of potassium by these cells.

NONDRUG CAUSES DUE TO INADEQUATE DIETARY INTAKE

When the dietary intake of potassium is reduced to less than 1 g per day (25 mmol per
day), depletion of potassium and hypokalemia result because the renal excretion of potassium
fails to decrease promptly. An isolated reduction of this magnitude in the dietary intake of
potassium requires a specially prepared diet, and therefore, hypokalemia is rarely the result of
decreased intake. With starvation or near-starvation, body potassium stores become depleted but
the breakdown of tissues releases potassium into the extracellular compartment, mitigating the
hypokalemia.

NONDRUG CAUSES DUE TO ABNORMALLOSSES OF POTASSIUM

Losses in Stool
The concentration of potassium in stool is 80 to 90 mmol per liter, but because of the low
volume of water in normal stool, only about 10 mmol is usually lost each day. In diarrheal states,
the potassium concentration in stool decreases, but large quantities of potassium can nonetheless
be lost as the volume of stool increases. Anything that increases stool volume, from infectious
diarrhea to cancer chemotherapy, can result in clinically significant potassium depletion and
hypokalemia.

Loss through the Kidney

Large amounts of potassium are lost through the kidney in patients with a variety of
disorders. For ease of diagnosis, these disorders are categorized according to acid–base status.
Metabolic Alkalosis
Hypokalemia is an almost invariable consequence of metabolic alkalosis. In the most
common form of this disorder, induced by selective chloride depletion due to vomiting or
nasogastric drainage, hypokalemia develops during the induction of alkalosis as a result of
increased renal potassium loss.
In the chloride-sensitive form of metabolic alkalosis, the administration of chloride
corrects the alkalosis and allows the repletion of body stores of potassium if potassium intake is
adequate. More rarely, metabolic alkalosis occurs independently of chloride depletion, as a result
of systemic or intrarenal abnormalities that augment sodium reabsorption in the distal nephron.
The most common of these abnormalities is primary hyperaldosteronism, a disorder often
heralded by severe hypokalemia (serum potassium, <3.0 mmol per liter). In the few affected
patients who do not have hypokalemia, the serum potassium concentration is virtually always
below 4.0 mmol per liter.

Hypokalemia can also develop in patients with Cushing’s syndrome, but it is usually
milder than in patients with hyperaldosteronism. Genetic abnormalities that influence the activity
of renal ion transporters are rare causes of metabolic alkalosis and hypokalemia. Two of these
disorders (Liddle’s syndrome and 11 b-hydroxysteroid dehydrogenase deficiency) stimulate
reabsorption of sodium by collecting-duct cells and cause the syndrome of apparent
mineralocorticoid excess, so named because this transport abnormality results in hypertension
and hypokalemia, but serum aldosterone concentrations are low rather than high. In two other
disorders, genetic mutations inactivate or impede the activity of chloride-associated sodium
transporters in the loop of Henle (Bartter’s syndrome) and early distal tubule (Gitelman’s
syndrome), causing metabolic alkalosis and hypokalemia without hypertension.

Metabolic Acidosis
Hypokalemia is a cardinal feature of type I or classic distal renal tubular acidosis. The
degree of hypokalemia in this disorder is not directly correlated to the degree of acidosis but
more likely reflects dietary sodium and potassium intake and serum aldosterone concentrations.
Life-threatening hypokalemia (serum potassium, <2.0 mmol per liter) can occur in patients with
untreated distal renal tubular acidosis. The administration of sodium bicarbonate ameliorates the
hypokalemia, but potassium supplementation is usually required on a long-term basis to manage
this disorder. In cases of type II or proximal renal tubular acidosis, hypokalemia only
occasionally occurs in untreated patients but often develops when sodium bicarbonate is
administered.

IMPLICATION:
Hypokalemia tends to lower the potassium level in the blood serum; thus, gradually
decreasing the amount of Sodium-Potassium exchange in the body. Potassium plays an important
role to the functional muscle. Muscle would not work properly if there is an imbalance in its
essential constituents needed to suffice breakdown of ATP to have adequate energy for muscle
contractions and muscle expansions. Consequently, electrolyte imbalance will cause muscle
paresis.