Hyperkalemia

Causes of Hyperkalemia
Renal failure, Acidosis
Decreased K+ secretion
Impaired Na+ reabsorption
Primary hypoaldosteronism: adrenal insufficiency, adrenal enzyme deficiency (21-hydroxylase,
3-hydroxysteroid dehydrogenase, corticosterone methyl oxidase)
Secondary hypoaldosteronism: hyporeninemia
Resistance to aldosterone: pseudohypoaldosteronism.
Drugs (K+-sparing diuretics, trimethoprim, pentamidine), drugs (ACE inhibitors, NSAIDs,
heparin)
Enhanced Cl- reabsorption (chloride shunt)
Gordon's syndrome
Cyclosporine
Clinical Features
Malaise, muscle weakness, which may progress to flaccid paralysis and hypoventilation if the
respiratory muscles are involved.
Cardiac toxicity: Arrhythmia, palpitation, sudden death
ECG:
a. The earliest electrocardiographic changes is peaked T waves.
b. More severe degrees of hyperkalemia result in a prolonged PR interval and QRS duration.
c. Atrioventricular conduction abnormality.
d. Loss of P waves.
e. Progressive widening of the QRS complex (sine wave pattern).
f. The terminal event is usually ventricular fibrillation or asystole.
Treatment of Acute hyperkalemia
Severe hyperkalemia requires emergent treatment directed at
minimizing membrane depolarization,
shifting K+ into cells, and promoting K+ loss.
Administration of calcium gluconate decreases membrane excitability, but it does not reduce S.
potassium level.
Insulin with glucose causes K+ to shift into cells. It is the fastest, earliest & the best way to
reduce S. potassium level.
When administered parenterally or in nebulized form, 2-adrenergic agonists promote cellular
uptake of K+
There is no role of NaHCO3 in the treatment of hyperkalemia. (Ref: Harrison, 19th edition. Page-
312)
Treatment of Chronic hyperkalemia
Removal of K+ can be achieved using diuretics, cation-exchange resin, or dialysis.
Hypokalemia
Causes of Hypokalemia
Decreased intake
Redistribution into cells
Acid-base - Metabolic alkalosis
Hormonal
a. Insulin
b. Beta2- agonists
c. Alpha antagonists
Anabolic state
a. Vitamin B12 therapy
b. Total parenteral nutrition
Other:
a. Pseudo-hypokalemia
b. Hypothermia
c. Barium toxicity
Increased loss
1. Nonrenal:
a. Diarrhea
b. Sweat
2. Renal
a. Increased distal flow: diuretics, osmotic diuresis, salt-wasting nephropathies
b. Increased secretion of potassium
Mineralocorticoid excess
Primary & Secondary hyperaldosteronism,
Apparent mineralocorticoid excess (licorice, chewing tobacco, carbenoxolone),
Congenital adrenal hyperplasia,
Cushing's syndrome,
Bartter's syndrome
Distal delivery of non-reabsorbed anions: vomiting, proximal (type 2) renal tubular acidosis,
Glue-sniffing
Other: Amphotericin B, Liddle's syndrome, Hypomagnesemia
Clinical Features
Muscle Weakness
Fatigue, myalgia, and muscular weakness of the lower extremities
Hypoventilation (due to respiratory muscle involvement), and eventually complete paralysis.
Impaired muscle metabolism and the blunted hyperemic response to exercise associated with
profound K+ depletion increase the risk of rhabdomyolysis.
Smooth-muscle function may also be affected and manifest as paralytic ileus.
Cardiac arrhythmia
Polyuria
ECG.
a. Flattening or inversion of the T wave,
b. Prominent U wave,
c. ST-segment depression,
d. Prolonged QT interval.
e. Prolonged PR interval,
f. Increased risk of ventricular arrhythmias
Hypokalemia: Treatment = Potassium supplementation. Slow I/V infusion, 10-20 mmol//l/hr
(AIIMS May 13)
SIADH
Causes
Carcinomas: Lung, Duodenum, Pancreas, Ovary, Bladder, ureter
Head trauma (closed and penetrating)
Infections: Pneumonia, bacterial or viral, Abscess, lung or brain, Tuberculosis, lung or brain,
Meningitis, bacterial or viral, AIDS
Vascular: . CVA (SAH)
Neurologic: Guillain - Barre- syndrome, Multiple sclerosis
Metabolic: Acute intermittent porphyrias
Drugs (MCQ):
a. Vasopressin or desmopressin,
b. Chlorpropamide,
c. Oxytocin,
d. Vincristine,
e. Carbamazepine,
f. Nicotine,
g. Phenothiazine,
h. Cyclophosphamide,
i. Tricyclic antidepressants,
j. MAOI
k. Serotonin reuptake inhibitor
Clinical features of SIADH
They are due to hyponatremia which are related to osmotic water shift. It lead to increase intra
cellular fluid volume in the brain cell causing swelling of the brain cell which lead to cerebral
edema. Patient may be asymptomatic, or may have convulsion (LQ 2012), Coma or death.
Laboratory features of SIADH
Hyponatremia (serum sodium < 135 mEq/L)
Inappropriately elevated urine osmolality (> 100 mosm/kg)
Decreased serum osmolality (< 280 mosm/kg)
B.U.N. and serum uric acid tends to fall because of plasma dilution and increased excretion of
nitrogenous products.
Serum potassium and Bicarbonate levels are normal in SIADH.
Increase urinary sodium (More than 30 meq/lil
Water loading test is done
Extra Edge Water loading test
In SIADH there is an abnormal water load test (i.e. inability to excrete at least 90% of a 20 ml/kg
water load in 4 h and/or failure to dilute urine osmolality <100 mosm/kg), and there is plasma
ADH levels inappropriately elevated relative to plasma osmolality.
Treatment of SIADH:
Acute SIADH
Standard first line therapy is water restriction.
If more rapid correction of hyponatremia is desired, the fluid restriction can be supplemented
with i. v. infusion of hypertonic saline (3%).
Important Points
A rapid correction will produce central pontine myelinolysis which is an acute potentially fatal
neurological syndrome characterized by quadriparesis, ataxia and abnormal extraocular
movements.
To prevent this complication the hypertonic saline should be infused very slowly.
Treatment of Chronic SIADH:
1. Hyponatremia can be corrected by with ◊ a. Demeclocycline b. Conivaptan
Recent Advances Conivaptan is a new drug. It is a treatment option for hyponatremia in place of
Demeclocycline.
Conivaptan
It is a non-peptide inhibitor ofantidiuretic hormone(vasopressin receptor antagonist).
It is forhyponatremia(low bloodsodiumlevels) caused bysyndrome of inappropriate antidiuretic
hormone(SIADH)
Conivaptan inhibits two of the three subtypes of thevasopressin receptor(V1aandV2).
Effectively, it causesiatrogenicnephrogenicdiabetes insipidus.
Pseudohyponatremia
Certain conditions that interfere with laboratory tests of serum sodium concentration (may lead to
an erroneously lowmeasurementof sodium. This is called pseudohyponatremia).
Hyperlipidemia
Hyper paraproteinemia (Multiple myeloma)
Severe hyperglycemia (DKA, NKHOC)
Cerebral salt-wasting syndrome (CSWS)
Hyponatremia dehydration
Due to hypersecretion of ANP, seen in mainly in CNS condition. In response to trauma/injury or
the presence of tumors in or surrounding thebrain.
This form of hyponatremia is due to excessive renal sodium excretion resulting from a centrally
mediated process.
Symptoms
Polyuriadue to inadequate sodium retention in the body,
Polydipsiadue to polyuria,
Extremesaltcravings,
Dysautonomia,
Dehydration.
Patients often "self-medicate" by naturally gravitating toward a high-sodium diet and by
dramatically increasing their water intake.
Advanced symptoms includemuscle cramps, lightheadedness, dizziness orvertigo, feelings of
anxiety or panic,tachycardia orbradycardia,hypotensionandorthostatic hypotensionsometimes
resulting insyncope.
Symptoms associated with dysautonomia include:headaches,pallor,malaise, facial
flushing,constipationordiarrhea,nausea, visual disturbances, numbness, loss of consciousness
andseizures.
Causes and Diagnosis
CSWS is usually caused by brain injury/trauma or cerebral lesion, tumor, or hematoma.
CSWS is a diagnosis of exclusion and may be difficult to distinguish from the SIADH, which
develops under similar circumstances and also presents with hyponatremia. The main clinical
difference is that of total fluid status of the patient:
CSWS leads to a relative or overt hypovolemiawhereas SIADH is consistent with a normal to
hypervolemic range.
Random urine sodium concentrations tend to be more than 150 mEq/L in CSWS and in (SIADH
>100).
If blood-sodium levels increase when fluids are restricted, SIADH is more likely.
Treatment
While CSWS usually appears within the first week after brain injury and spontaneously resolves
in 2–4 weeks,
It can sometimes last for months or years.
While fluid restriction is used to treat SIADH, CSWS requires aggressive hydration and
correction of the low sodium levels using sodium chloride tablets. (volume for volume) (Ref.
Nelson. 18th ed., Pg- 2302)
Sometimes,fludrocortisone(amineralocorticoid) improves the hyponatremia.
Extra Edge
Normal serum osmolality 500 – 800 mosmol/kg
Normal urine sodium 100 – 260 meq/day or >20 meq /l
Adipsic Hypernatremia
Clinical Characteristics
A defect in the thirst mechanism results in adipsic hypernatremia, a syndrome characterized by
chronic or recurrent hypertonic dehydration.
The hypernatremia varies widely in severity and usually is associated with signs of hypovolemia
such as tachycardia, postural hypotension, azotemia, hyperuricemia, and hypokalemia.
Muscle weakness, pain, rhabdomyolysis, hyperglycemia, hyperlipidemia, and acute renal failure
may also occur.
DI usually does not exist at presentation but may develop during rehydration.
Treatment: Adipsic hypernatremia should be treated by administering water orally if the patient is
alert and cooperative or by using hypotonic fluids (0.45% saline or 5% dextrose and water) via IV
if the patient is not.