SODIUM IMBALANCES

HYPONATREMIA (SODIUM <135 mEq/L

 OCCURS WHEN THERE IS IMBALANCE IN WATER

 LOW SODIUM IN URINE (VOMITING, DIARRHEA, SWEATING).
 DILUTIONAL HYPERNATREMIA-ECF INCREASE WITHOUT EDEMA.
CLINICAL MANIFESTATIONS

 POOR SKIN TURGOR

 DRY MUCOSA
 HEADACHE
 DECREASE SALIVA PRODUCTION
 ORTHOSTATIC HYPOTENSION
 NAUSEA/VOMITING
 ABDOMINAL CRAMPING
NEUROLOGIC CHANGES

 ALTERED MENTAL STATUS

 STATUS EPILEPTICUS-seizure more than 5 minutes
 COMA
 BRAIN HERNIATION(TISSUE,BLOOD, CSF SHIFTS FROM NORMAL POSITION)
AND COMPRESSION OF MIDBRAIN STRUCTURE CAN CAUSE ACUTE
HYPONATREMIA (DEVELOP IN LESS THAN 48 HRS) MORE DEADLY THAN
THE CHRONIC.
<115 mEq/L of sodium.

 INCREASE INTRACRANIAL PRESSURE

 LETHARGY
 CONFUSION
 MUSCLE TWITCHING
 FOCAL WEAKNESS
 HEMIPARESIS-weakness of one entire part of the body
 PAPILLEDEMA-optic nerve at the back of the eye becomes swollen.
 SEIZURES
 DEATH
ASSESSMENT/DIAGNOSIS

 HISTORY AND PHYSICAL EXAMINATION

 IF DUE TO SODIUM LOSS
 URINE SODIUM IS LESS THAN 20 mEq/L AND USG OF 1.002-1.004 (LOW).
 GREATER THAN 20 IF DUE TO SIADH AND HIGH (GREATER THAN 1.012).
 PITTING EDEMA IF HYPONATREMIA (SIADH)
MEDICAL MANAGEMENT

 SODIUM BY MOUTH, NSG TUBE, PARENTERAL TUBE

 0.9 NaCl (WHO CANNOT DO ORAL THERAPY).
 SERUM SODIUM MUST NOT INCREASE MORE THAN (12 mEq/L IN 12 HRS-
CAN CAUSE DEMYLINATION(DAMAGE OF THE MYELIN-protective coating of
nerves).)
 100 mEq/L per day (in adults)
 Normal Fluid Excess Volume (fluid restriction)
 If neurologic symptoms are severe (small volumes of hypertonic solution).
PHARMACOLOGIC THERAPY

 AVP RECEPTOR ANTAGONISTS

 IV (VAPRISOL)-contraindicated to patients with seizures, delirium or coma.
 TOLVAPTAN (SAMSCA)- ORAL MEDS
NURSING MANAGEMENT

 IDENTIFY AT RISK FOR HYPERNATREMIA, MONITOR I&O, BODY WEIGHT.

 DECREASED RENAL FUNCTION AND CONFUSION IN ADULTS.
 NEUROLOGIC SIGNS (VERY LOW SODIUM LEVELS)
 WATER RETENTION (RESTRICT FLUIDS
 HYPERTONIC SOLUTIONS (ALLEVIATE NEUROLOGIC SYMPTOMS
 ADMINISTRATION OF SODIUM IN CLIENTS
(NORMOVOLEMIA,HYPERVOLEMIA)-CAUSES FLUID OVERLOAD.
HYPERNATREMIA-145 mEq/L

 OCCURS WITH PATIENT (FVD OR FVE).

 LOSSES MORE WATER THAN SODIUM.
 CLIENT MAYBE INGESTS MORE SODIUM THAN WATER.
PATHOPHYSIOLOGY

 HYPERNATREMIA(FLUID DEPRIVATION).
 AFFECTS VERY OLD, VERY YOUNG, AND COGNITIVELY IMPAIRED.
 DIABETES INSIPIDUS AND DIARRHEA CAUSES HYPERNATREMIA
CLINICAL MANIFESTATIONS

 DEHYDRATION
 SLIGHT FEVER
 THIRST
ASSESSMENT AND DIAGNOSTIC
FINDINGS

 INCREASE SODIUM LEVELS IN ECF

 USG AND URINE OSMOLALITY INCREASES.
MEDICAL MANAGEMENT

 GRADUAL LOWERING OF SODIUM LEVELL

 HYPOTONIC SOLUTIONS
 RAPID REDUCTION OF SODIUM CAN CAUSE CEREBRAL EDEMA.
 DIURETICS
 REDUCE SODIUM AT 0.5 TO 1 MEQ/L/H
NURSING MANAGEMENT

 ASSESS FOR ABNORMAL LOSSES OF WATER

 ASSESS FOR LARGE GAINS OF SODIUM (TAKING OTC DRUGS-CATION).
 NOTES PATIENTS THIRST OR ELEVATED BODY TEMPERATURE.
 MONITOR CLOSELY FOR CHANGES IN BEHAVIOR
 RESTLESNESS
 DISORIENTATION
 LETHARGY
PREVENTING HYPERNATREMIA

 PROVIDE ORAL FLUIDS AT REGULAR INTERVAL

 IF UNCONSCIOUS (ENTERAL OR PARENTERAL ROUTE).
POTASSIUM IMBALANCES

 98 %-ICF 2%-ECF.
 IMPORTANT FUNCTION IN NEUROMUSCULAR.
HYPOKALEMIA <3.5

 ALKALOSIS (ONE CONTRIBUTING FACTOR).

 HYPERALDOSTERONISM- INCREASES RENAL POTASSIUM WASTING.
 SEEN IN PATIENTS WITH ADRENAL ADENOMAS.
 INSULIN HYPERSECRETION CAUSES HYPOKALEMIA ALSO WITH PATIENTS
RECEIVING HIGH CARBS PARENTERAL NUTRITION.
 OLDER ADULTS AND PATIENT WITH ALCOHOLISM
 OR ANOREXIA NERVOSA-self starvation
 BULIMIA-LOSS OF CONTROL OVER EATING.
 MAGNESIUM DEPLETION ALSO CAUSE POTASSIUM LOSS.
CLINICAL MANIFESTATION

 FATIGUE
 ANOREXIA
 NAUSEA/VOMITING
 MUSCLE WEAKNESS
 DECREASED BOWEL MOTILITY
 VENTRICULAR SYSTOLE
 PARESTHESIAS
 LEG CRAMPS
ASSESSMENT

 POTASSIUM CONCENTRATION IS LESS.

 FLAT T WAVES AND ST DEPRESSION
 INCREASE SENSIVITITY TO DIGITALIS
 METABOLIC ALKALOSIS
 URINARY POTASSIUM GREATER THAN 20 MEQ/DAY (RENAL POTASSIUM LOSS
IS THE CAUSE).
MEDICAL MANAGEMENT

 ORAL THERAPHY FOR DEFICIENCIES AND TREATED CAUTIOUSLY WITH IV

REPLACEMENT THERAPY.
 40-80 mEq/day FOR ADULTS IF THERE ARE NO ABNORMAL LOSSES OF K+.
 AVERAGE ADULT- 50 TO 100 mEq/day.
 FOODS LIKE: FRUITS AND VEGETABLES, LEGUMES, WHOLE GRAINS, MILK
AND MEAR.
NURSING MANAGEMENT

 EAT FOODS RICH IN POTASSIUM (BANANAS, MELON, CITRUS FRUITS, FRESH

AND FROZEN VEGETABLES, LEAN MEATS, MILK, WHOLE GRAINS.
 ADMINISTER IV POTASSIUM
 SHOULD BE GIVEN AFTER ADEQUATE URINE OUTPUT HAS BEEN ESTABLISHED.
 <2 ML PER HOUR OF URINE FOR 2 HRS INDICATE THE NEED TO STOP
POTASSIUM INFUSION.
 RENAL FUNCTION IS MONITORED THROUGH BUN AND CREATININE.
HYPERKALEMIA

 INCREASED RISK FOR OLDER ADULTS DUE TO DECREASE OF RENIN AND

ALDOSTERONE.
 MORE DANGEROUS THAN HYPOKALEMIA.
CAUSES

 DECREASED RENAL EXCRETION OF POTASSIUM

 RAPID ADMIN OF POTASSIUM
 COMMON IN PT. WHO HAS RENAL INJURY
 ADDISON DISEASE(HYPOALDOSTERONISM)
 MEDICATIONS SUCH AS KCL, HEPARIN, ACE inhibitors, NSAIDs, beta blockers,
cyclosporine and potassium sparring diuretics.
 IMPROPER USE OF POTASSIUM SUPPLEMENTS (ESPECIALLY IF SALT
SUBSTITUTES ARE USED).
 ACIDOSIS-HYPERKALEMIA.
CLINICAL MANIFESTATIONS

 CARDIAC EFFECT IF (ABOVE 8 MEQ/L OF POTASSIUM).

 PROFOUND MUSCLE WEAKNESS, TACHYCARDIA TO BRADYCARDIA.
 DYSRYTHMIAS, FLACCID PARALYSIS
 PARESTHESIAS, INTESTINAL COLIC
 IRRITABILITY
 HYPERACTIVE BOWEL SOUND, DIARRHEA
 DECREASE DTR
ASSESSMENT

 METABOLIC AND RESPI ACIDOSIS FOR HYPERKALEMIA

MEDICAL MANAGEMENT

 ECG TO DETECT CHANGES (ELEVATION)

 POTASSIUM SHOULD BE OBTAIN FROM A VEIN WITHOUT IV SOLUTION.
 NONACUTE-RESTRICTIONS OF POTASSIUM
 KAYEXALATE-RETENTION ENEMA (CAUTION: CAN CAUSE SODIUM
RETENTION AND FLUID OVERLOAD. CONTRAINDICATED TO PT. WITH
HEART FAILURE.
 IV CALCIUM GLUCONATE-FOR EMERGENCY- ANTAGONISTS THE ACTION
OF HYPERKALEMIA IN THE HEART.
 DETECT HYPOTENSION (FROM INFUSION OF IV CG.