Hypokalemia Periodic Paralysis
Hypokalemia Periodic Paralysis
Hypokalemia Periodic Paralysis
I. PATIENT’S PROFILE
Weight: 55kg.
Gender: Female
Birthplace: Marikina
Occupation: N/A
Chief complaint upon history taking: “masakit ang puson dahil naiihi”
Source of information: Ms. Dianne Bona (patient) and Aida Bona (Mother)
II. HISTORY
A history of a 23 year old Female with hypokalemic periodic paralysis presented to the
emergency room with a sudden onset of paralysis.
College years (2015) 4 years PTA, the patient’s first experienced paralysis or unable to move
her left thumb first and within a few hours, the paralysis had resolved itself completely.
Then, 7 days later, again,she had a second attack on the right thumb and gone after a few
hours. She noticed that attack normally happens during cold weather. Episodes of legs
2016/2017 PTA- she went to see a doctor for consultation regarding frequency/duration of
urination she experienced although it is not painful but it took longer to urinate. negative of
Urinary Tract Infection as per her information
1 month PTA, patient experienced excessive thirst accompanied with frequent urination,
after a few days she complained of unable to move her left lower extremitieswith pain that
feels likes bone her bones are being crushed from distal to proximal then gone and after a
few hours right lower extremities would paralyzed too, lower back pain occured as well.
Patient didn’t take any medicine for pain reliever and as always would call a “manghihilot”to
help her relieved the paralysis. Aside from the fact that seeing a physician was not possible
due to limited funds.
1 day PTA, she suffered from diarrhea for 3 cafter taking a bath patient felt untollerable pain
and unable to move her lower extremities. The weakness was bilateral and involved both
muscles of the lower extremities from distal to proximal. She had no respiratory of
swallowing difficulty and was able to move her neck and facial muscles.
C. FAMILY HISTORY
She denied use of alcohol, smoking or drugs, or significant changes in diet or activity levels.
A. GENERAL SURVEY
A 23 year old woman, with a blood pressure was 90/60 mmHg, patient was half asleep and
restless due to unable to urinate as per the doctors advice prior to her scheduled KUB UTZ
B. INTERGUMENTARY
(-) lesion
C. NEURO
D. CARDIO
E. GASTRO
“Masakit ang puson ko at gusto ko ng umihi, pero hindi p pde” as per the drs. Advice prior to
KUB UTZ scheduled for that day
F. URINARY
G. MUSCULO
H. ENDOCRINE
Skin fair, warm, dry and elastic.No lesions noted. Hair black, below shoulder length, messy and
oily,Normal distribution of hair on scalp and perineum. No hair legs. Nail beds pink without
clubbing. Cuticles smooth, no detachment of nailplate.
Head symmetrically round, hard, and smooth without lesions or bumps. Face oval, smooth, and
symmetrical. Temporal artery elastic and nontender. Temporo mandibular joint palpated with
full range of motion without tenderness. Neck symmetric with centered head position and no
bulging masses. C7 is visible and palpable with neck flexion. Has smooth, controlled, full range
of motion of neck. Thyroid gland nonvisible but palpable when swallowing. Trachea in
midline. Lymph nodes nonpalpable.
Lips slightly pink, smooth, and moist without lesions. Buccal mucosa pink, moist, and without
exudates. Lack missing tooth in front but gums pink without redness or swelling.tongue in
midline, slightly pink with small visible veins present.Frenulum in midline. Soft palate smooth
and pink. Tonsillar pillars pink and symmetric.
Nose somewhat large but smooth and symmetric. Able to sniff through each nostril, no
obstruction of airflow. No purulent drainage noted.
Respirations 20/minute, relaxed and even. Chest expansion symmetric. No retraction or bulging
of interspaces. No pain or tenderness on palpation.
Patient received sleeping in bed, I introduced myself to the mother of the patient.was able to have
a short talk with my patient’s mother since D.B. still sleeping, she was able to answer some of my
questions and shared a little information about her daughter and the reason of her admission. By
the time my patient woke up, I didn’t get a chance to ask her more , She is scheduled for her KUB
UTZ around 10:00am, and shes a bit restless during that time because she keeps on saying on
how much she needed to urinate and it felt uncomfortable already. KUB UTZ full bladder. I
ended up asking questions with the mother since patient D.B. Doesnt want to speak much that
time.
While waiting for the patient from her UTZ we were given a chance to read the Patients chart so
as to be aware of their diagnosis and other patients information that we might need.
Patient received awake, Ma’m D.B. Were in a good mood today, after my brief introduction and
greetings i took her Vital Sign BP of 90/60, T: 37.5, PR:93,RR:21.before i start my NPI for that
day. Hospital linen were changed so, as assist the patient to do her morning care, she just rejected
the idea of taking a full bath but approved of half bath because for her she need to have an
adequate sleep before she can take a bath. Clothes changed, hair tied up.
Hypokalemia (below 3.5 mEq/L [3.5 mmol/L]) usually indicates a deficit in total potassium
stores. However, it may occur in patients with normal potassium stores: When alkalosis is
present, a temporary shift of serum potassium into the cells occurs.
Pathophysiology
Potassium-losing diuretics, such as the thiazides and loop diuretics, can induce hypokalemia
(Baumberger-Henry, 2008). Other medications that can lead to hypokalemia include
corticosteroids, sodium penicillin, carbenicillin, and amphotericin B. GI loss of potassium is
another common cause of potassium depletion. Vomiting and gastric suction frequently lead
to hypokalemia, partly because potassium is actually lost when gastric fluid is lost and
because potassium is lost through the kidneys in response to metabolic alkalosis. Because
relatively large amounts of potassium are contained in intestinal fluids, potassium deficit
occurs frequently with diarrhea, which 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 potassium-rich
mucus). Alterations in acid–base balance have a significant effect on potassium distribution
due to shifts of hydrogen and potassium ions between the cells and the ECF. Respiratory or
metabolic alkalosis promotes the transcellular shift of potassium and can have a variable and
unpredictable effect on serum potassium (O’Neill, 2007). 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 (see later discussion of 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, or
malignant hypertension (Heitz & Horne, 2005). 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 nutrition.
Patients who do not eat a normal diet for a prolonged period are at risk for hypokalemia.
This may occur in debilitated elderly people, patients with alcoholism, and patients with
anorexia nervosa. In addition to poor intake, people with bulimia frequently suffer increased
potassium loss through self-induced vomiting, misuse of laxatives, diuretics, and enemas.
Magnesium depletion causes renal potassium loss and must be corrected first; otherwise,
urine loss of potassium will continue.
Clinical Manifestations
In hypokalemia, the serum potassium concentration is less than the lower limit of normal.
Electrocardiographic (ECG) changes can include flat T waves or inverted T waves or both,
suggesting ischemia, and depressed ST segments (Fig. 14-5). 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 (Her, 2007). This is discussed further in the section on acid–base disturbances
in this chapter. The source of the potassium loss is usually evident from a careful history.
However, if the cause of the loss is unclear, a 24-hour urinary potassium excretion test can
be performed to distinguish between renal and extra renal loss. Urinary potassium excretion
exceeding 20 mEq/day with hypokalemia suggests that renal potassium loss is the cause.
Medical Management
If oral administration of potassium is not feasible, the IV route is indicated. The IV route is
mandatory for patients with severe hypokalemia (eg, serum level of 2 mEq/L). Although
potassium chloride is usually used to correct potassium deficits, potassium acetate or
potassium phosphate may be prescribed.
Nursing Management
Because hypokalemia can be life-threatening, the nurse needs to monitor for its early
presence in patients who are 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.
Prevention may involve encouraging the patient at risk to eat foods rich in potassium (when
the diet allows). Sources of potassium include fruit juices and bananas, melon, citrus fruits,
fresh and frozen vegetables, fresh meats, milk, and processed foods. If the hypokalemia is
caused by 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 that are
amenable to prevention through education. Careful monitoring of fluid I&O 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
The oral route is ideal to treat a mild to moderate hypokalemia because oral potassium
supplements are absorbed well. 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. In addition, because of the physiologic loss of
renal function with advancing years, potassium may be retained more readily in older than in
younger people.
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; when oliguria occurs, potassium administration can cause the serum
potassium concentration to rise dangerously (Hayes, 2007b).
Each health care facility has its own standard of care for the administration of potassium,
which should be consulted; however, the maximum concentration of potassium that should
be administered on a medical-surgical unit through a peripheral IV line is 20 mEq/100 mL
and the rate no faster than 10 to 20 mEq/h. Concentrations of potassium greater than 20
mEq/100 mL should be administered through a central IV catheter using an infusion pump
with the patient monitored by ECG. Caution must be used when selecting the correct
premixed solution of IV fluid containing potassium chloride as the concentrations range
from 10 to 40 mEq/100 mL. Renal function should be monitored through BUN and
creatinine levels and urine output if the patient is receiving potassium replacement. During
potassium replacement, smooth muscle hyperactivity can lead to hyperactive bowel sounds,
a sign of hyperkalemia (Hayes, 2007b).
VII. PATHOPHYSIOLOGY
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