Post on 05-Apr-2015
CASE ABSTRACT Mr. A.K.A, male aged 34, single, residing at
Queensrow Subdivision, Las Pinas city was rushed to the Las Pinas Medical City in Emergency Department (ER) last April 26, 2010 at around 7:05 am. Patient reported of numbness of lower extremities with initial vital signs of BP- 150/100 mmhg, T-36c, PR-84bpm, R-20cpm. Seen and examined by the attending physician Dr. Rafael Tecson with the diagnosis of T/C Hypokalemia. Intravenous Fluid (IVF) was hooked incorporated by Potassium Chloride and given Kalium durule 1tablet per orem. (PO) .
OBJECTIVES General Objectives
This Analysis aims to convey familiarity with the imbalance of electrolyte particularly potassium and provide effective nursing care and management with the patient suffering Hypokalemia.
Specific Objectives. To discuss the Anatomy and Physiology,
Pathophysiology of the Patient’s condition. To have knowledge of the patient’s medication
and be familiar to that medication. To formulate a workable nursing care plan on
the subjective and objective cues gathered and risks.
PHYSICAL ASSESSMENT A. Biographical Data
Name: A.K.A Gender: Male Age: 34 Civil Status: Single Birth date: October 26, 1975 Birthplace: Manila Address: Queensrow subdivision, Bacoor Cavite Religious Preferences: Roman Catholic Date of Consultant: April 26, 2010 Time: 7:05 am Chief Complaint: Numbness of lower
extremities Diagnosis: T/C Hypokalemia Attending physician: Dr. Rafael Tecson
B. Chief Complaint Patient reported Nubness of lower Extremities.
C. Vital signs T- 36 c P- 84 bpm R-20 cpm BP- 150/100 mmhg
D. Nursing History 1 day prior to admission patient feel cramps and
weakness on his right and lower extremities. He doesn’t have fever, colds, and doesn’t experienced diarrhea and vomiting.
E. Nursing assessment -The patient is Conscious and coherent. -His peripheral pulses on lower extremities
is symmetrical and weak. -Nails and nail beds is pallor, inflammation
is not present and capillary refill is not delayed.
-The patient cannot move his right and left leg, and do not respond to pain.
LABORATORY FINDINGS LABORATORY EXAMINATION:
Hematology:
Potassium = 3.5-5.5 mEq/L
Actual result = 2.0 mEq/L
Result of low K: ventricular arrhythmias
Characteristic of ECG changes in Hypokalemia:
Flattened T wavesDevelopment of U wavesDepressed ST segment
POTASSIUM The most abundant cation in the ICF Potassium is the major intracellular electrolyte;
in fact, 98% of the body’s potassium is inside the cells.
The remaining 2% is in the ECF; it is this 2% that is all-important in neuromuscular function.
Potassium is constantly moving in and out of cells according to the body’s needs, under the influence of the sodium-potassium pump.
Normal range in the blood is 3.5-5 mEq/L
Normal renal function is necessary for maintenance of potassium balance, because 80-90% of the potassium is excreted daily from the body by way of the kidneys. The other less than 20% is lost through the bowel and sweat glands.
Major electrolyte maintaining ICF balance Sources- Diet, vegetables, fruits, IVF,
medications
Functions: Maintains ICF Osmolality Important for nerve conduction and muscle
contraction Maintains acid-base balance Needed for metabolism of carbohydrates,
fats and proteins Potassium influences both skeletal and
cardiac muscle activity. For example, alterations in its
concentration change myocardial irritability and rhythm.
Regulations: renal secretion and excretion, Aldosterone promotes renal excretion acidosis promotes K exchange for hydrogen
Imbalances:Hypokalemia= <3.5 mEq/LHyperkalemia=> 5.0 mEq/L
INTRODUCTION OF HYPOKALEMIA Hypokalemia refers to the condition in
which the concentration of potassium (K+) in the blood is low. The prefix hypo- means low (contrast with hyper-, meaning high). Kal refers to kalium, theNeo-Latin for potassium, and -emia means "in the blood."
Normal serum potassium levels are between 3.5 to 5.0 mEq/L at least 95% of the body's potassium is found inside cells, with the remainder in the blood. This concentration gradient is maintained principally by the Na+/K+ pump.
Condition when the serum concentration of potassium is less than 3.5 mEq/L
PathophysiologyEtiology
Gastro-intestinal loss of potassium such as diarrhea and fistula
Vomiting and gastric suctioningMetabolic alkalosisDiaphoresis and renal disordersIleostomy
Other factor/sHyperaldosteronismHeart failureNephrotic syndromeUse of potassium-losing diuretics Insulin therapyStarvationAlcoholics and elderly
Decreased potassium in the body impaired nerve excitation and transmission signs/symptoms such as weakness, cardiac dysrhythmias etc.
NURSING PROCESS IN HYPOKALEMIA
Clinical ManifestationsPotassium deficiency can result in
widespread derangements in physiologic functions and especially nerve conduction.
Most important, severe hypokalemia can result in death through cardiac or respiratory arrest.
Clinical signs rarely develop before the serum potassium level has fallen below 3 mEq/L (51: 3 mmol/L) unless the rate of fall has been rapid.
If prolonged, hypokalemia can lead to impaired renal concentrating ability, causing dilute urine, polyuria, nocturia, and polydipsia
Manifestations of hypokalemia include fatigue, anorexia, nausea, vomiting, muscle weakness, decreased bowel motility, paresthesias, dysrhythmias, and increased sensitivity to digitalis.
ASSESSMENT
Physical examinationMuscle weaknessDecreased bowel motility and abdominal
distentionParesthesiasDysrhythmias Increased sensitivity to digitalis
Subjective cuesNausea , anorexia and vomitingFatigue, muscles crampsExcessive thirst, if severe
Laboratory findingsSerum potassium is less than 3.5 mEq/LECG: FLAT “T” waves, or inverted T waves,
depressed ST segment and presence of the “U” wave and prolonged PR interval.
Metabolic alkalosis
IMPLEMENTATION ASSIST IN THE MEDICAL INTERVENTION
Provide oral or IV replacement of potassium
Infuse parenteral potassium supplement. Always dilute the K in the IVF solution and administer with a pump. IVF with potassium should be given no faster than 10-20-mEq/ hour!
NEVER administer K by IV bolus or IM
NURSING MANAGEMENT Continuously monitor the patient by assessing
the cardiac status, ECG monitoring, and digitalis precaution
Prevent hypokalemia by encouraging the patient to eat potassium rich foods like orange juice, bananas, cantaloupe, peaches, potatoes, dates and apricots.
Correct hypokalemia by administering prescribed IV potassium replacement. The nurse must ensure that the kidney is functioning properly!
Administer IV potassium no faster than 20 mEq/hour and hook the patient on a cardiac monitor. To EMPHASIZE: Potassium should NEVER be given IV bolus or IM!!
A concentration greater than 60 mEq/L is not advisable for peripheral veins.
SIGNS AND SYMPTOMS
Mild hypokalaemia is often without symptoms, although it may cause a small elevation of blood pressure, and can occasionally provoke cardiac arrhythmias. Moderate hypokalaemia, with serum potassium concentrations of 2.5-3 mEq/L, may cause muscular weakness, myalgia, and muscle cramps (owing to disturbed function of the skeletal muscles), and constipation (from disturbed function of smooth muscles).
With more severe hypokalemia, flaccid paralysis, hyporeflexia, and tetany may result. There are reports of rhabdomyolysis occurring with profound hypokalaemia with serum potassium levels less than 2 mEq/L. Respiratory depression from severe impairment of skeletal muscle function is found in many patients.
Some electrocardiographic (ECG) findings associated with hypokalaemia are flattened or inverted T waves, a U wave, and prolongation of the QT interval. The prolonged QT interval may lead to arrhythmias.
CAUSES
Inadequate potassium intake: Perhaps the most obvious cause is insufficient
consumption of potassium (that is, a low-potassium diet). However, without excessive potassium loss from the body, this is a rare cause of hypokalaemia.
Gastrointestinal/integument loss A more common cause is excessive loss of
potassium, often associated with heavy fluid losses that "flush" potassium out of the body. Typically, this is a consequence of diarrhea, excessive perspiration, or losses associated with surgical procedures. Vomiting can also cause hypokalaemia, although not much potassium is lost from the vomitus. Rather, there are heavy urinary losses of K+ in the setting of post-emetic bicarbonaturia that force urinary potassium excretion
Urinary loss Certain medications can cause excess potassium
loss in the urine. Diuretics, including thiazide diuretics (e.g. hydrochlorothiazide) and loop diuretics (e.g. furosemide) are a common cause of hypokalemia. Other medications such as the antifungal, amphotericin B, or the cancer drug, cisplatin, can also cause long-term hypokalaemia.
A special case of potassium loss occurs with diabetic ketoacidosis. In addition to urinary losses from polyuria and volume contraction, there is also obligate loss of potassium from kidney tubules as a cationic partner to the negatively charged ketone,
Hypomagnesemia can cause hypokalemia. Magnesium is required for adequate processing of potassium. This may become evident when hypokalaemia persists despite potassium supplementation. Other electrolyte abnormalities may also be present.
Alkalosis can cause transient hypokalemia by two mechanisms. First, the alkalosis causes a shift of potassium from the plasma and interstitial fluids into cells; perhaps mediated by stimulation of Na+-H+ exchange and a subsequent activation of Na+/K+-ATPase activity. Second, an acute rise of plasma HCO3
- concentration (caused by vomiting, for example) will exceed the capacity of the renal proximal tubule to reabsorb this anion, and potassium will be excreted as an obligate cation partner to the bicarbonate. It should be noted that metabolic alkalosis is often present in states of volume depletion, so potassium is also lost via aldosterone-mediated mechanisms.
Rare hereditary defects of renal salt transporters, such as Bartter syndrome or Gitelman syndrome, can cause hypokalemia, in a manner similar to that of diuretics. As opposed to disease states of primary excesses of aldosterone, blood pressure is either normal or low in Bartter's or Gitelman's.
TREATMENT The most important treatment in severe
hypokalemia is addressing the cause, such as improving the diet, treating diarrhea or stopping an offending medication. Patients without a significant source of potassium loss and who show no symptoms of hypokalaemia may not require treatment.
Mild hypokalemia (>3.0 mEq/L) may be treated with oral potassium chloride supplements (Klor-Con, Sando-K, Slow-K). As this is often part of a poor nutritional intake, potassium-containing foods may be recommended, such as leafy green vegetables, tomatoes, citrusfruits, oranges or bananas. Both dietary and pharmaceutical supplements are used for people taking diuretic medications
Severe hypokalaemia (<3.0 mEq/L) may require intravenous supplementation. Typically, saline is used, with 20-40 mEq KCl per liter over 3-4 hours. Giving intravenous potassium at faster rates (20-25 mEq/hr) may predispose to ventricular tachycardias and requires intensive monitoring. A generally safe rate is 10 mEq/hr.
Difficult or resistant cases of hypokalemia may be amenable to a potassium-sparing diuretic such as amiloride, triamterene, or spironolactone. In contrast to the more commonly used diuretics like hydrochlorothiazide and furosemidethese potassium-sparing diuretics actually reduce the kidney's excretion of potassium.
When replacing potassium intravenously, infusion via central line is encouraged to avoid the frequent occurrence of a burning sensation at the site of a peripheral IV, or the rare occurrence of damage to the vein. When peripheral infusions are necessary, the burning can be reduced by diluting the potassium in larger amounts of IV fluid, or mixing 3 ml of 1% lidocaine to each 10 meq of kcl per 50 ml of IV fluid. The practice of adding lidocaine, however, raises the likelihood of serious medical errors.
ASSESSMENT DIAGNOSIS PLANNING INTERVENTION RATIONALE EVALUATION
S>”Namamanhid ang binti ko”as verbalized by the patientO>(+)Numbness of the lower extremities(+)Leg cramps(+)Cough(+)Vomiting(+)DiarrheaV/ST:36.6RR:20PR:84BP:150/100
FLUID VOLUME DEFICIT RELATED TO ACTIVE FLUID VOLUME LOSS
After 1 hour of nursing intervention the patient will, Stabilize fluid volume as evidenced by balanced I/O, vital signs within normal limits, stable weight, and free of signs of edema.
INDEPENDENT>Note presence of medical conditions/ situations that potentiate fluid excess.>Auscultate breath sounds.>Measures abdominal girth.DEPENDENT>Administer medication as ordered.COLLABORATIVE>Restrict sodium and fluid intake.
>To assess causative/ precipitating factors.>For presence of crackles/ congestion>For changes that may indicate increasing fluid retention.>To promote mobilization/elimination of excess fluid>To promote mobilization/elimination of excess fluid
After 1 hour of nursing intervention the patient was able to stabilize fluid volume as evidenced by balanced I/O, vital signs within normal limits, stable weight, and free signs of edema.
NURSING CARE PLAN
Name of Drug Classification Dose/ Frequency
Route Mechanism of Action
Indication Nursing Responsibilities
Generic Name:Potassium chloride
Brand Name:Kalium Durules
electrolytic and water balance
agent, replacement
solutions
1 Tab.40 mEq
P.O. Prevent and treat potassium deficit secondary to diuretic or corticosteroid therapy. When K+ is depleted by severe Vomiting, diarrhea; intestinal drainage, fistulas or malabsorption, prolonged diuresis, diabetic acidosis.
K+ sparing diuretics, angiothensinconverting enzyme (ACE) inhibitors may cause hyperkalemia
Tablet carcass may appear in stool, do not be alarmed. Sustained release tablet utilized a wax matix as carrier for KCl crystals that passes through the digestive system
Learn about sources of K+ with special reference to foods and OTC drugs
Avoid licorice, large amounts cause both hypokalemia and Na+ retention
Do not use salt substitute unless specifically ordered by Dr. these contain substantial amount of K+, and electrolytes other than Na+
Notify Dr of persistent vomiting because losses of K+ can occur
Report weakness, fatigue, polyuria, polydipsia: could be signs of K+ deficit
DRUG STUDY