Hypokalaemia Flashcards
What is hypokalaemia
Serum potassium (K+) level < 3.5 mEq/L Severe hypokalemia: K+ level < 2.5 mEq/L
What causes hypokalaemia
Magnesium deficiency
Insufficiency intake: alcohol abuse, anorexia, eating disorder, or not enough in IV fluids
GI Losses: Vomiting, diarrhoea, malabsorption, high output stoma, laxative abuse, poor oral intake/TPN or feed inadequate
Renal Losses: Genetic syndromes (CAH, Gitelman Bartter Liddle, CAH), Fancoin syndrome, renin secreting tumours, mineralocorticoid excess eg Conn’s or Cushing’s, Renal tubular acidosis Type I-III, Diuretics
Intercellular shift: alkalosis, insulin, adrenaline, beta2 agonists
Other: Alcohol withdrawal, phaeohromocytoma, Hypoosmolality, acute MI, head trauma, Familial periodic paralysis -intermittent weakness lasting up to 72h appears to be caused by K+ shifting from extra- to intracellular fluid, toxification, hypothermia
What drugs cause hypokalaemia
Diuretics: thiazides, loop Badrenergic agonists Corticosteroids Catecholamines Antibiotic Antifungals Theophylline Liquorice Sympathometic use
What can cause hypokalaemia with hypertension
• Cushing’s syndrome
• Conn’s syndrome (primary hyperaldosteronism)
• Renovascular disease and renin secreting tumour
• Liddle’s syndrome
• 11-beta hydroxylase deficiency*- 21-hydroxylase deficiency, which accounts for 90% of congenital adrenal hyperplasia cases, is not associated with hypertension
Carbenoxolone, an anti-ulcer drug, and liquorice excess can potentially cause hypokalaemia associated with hypertension
What can cause hypokalaemia with no hypertension
- Diuretics
- GI loss (e.g. Diarrhoea, vomiting)
- renal tubular acidosis (type 1 and 2**)
- Bartter’s syndrome
- Gitelman syndrome
- Magnesium deficiency
**type 4 renal tubular acidosis is associated with hyperkalaemia
What causes hypoklaemia with alkalosis
vomiting
thiazide and loop diuretics
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)
What causes hypokalaema with acidosis
○ diarrhoea
○ renal tubular acidosis
○ acetazolamide
partially treated diabetic ketoacidosis
What is the clinical manifestations
Leads to palpitations, light headdresses, arrythmias, constipation, and in patients who are susceptible it can lead to hepatic encephalopathy
Cardiovascular effects:
○ Symptoms of arrythmia’s e.g palpitations, irregular pulse, syncope
○ Hypotension
○ Can potentiate the unwanted effects of digoxin and drugs that prolong QT interval
Neurological effects:
○ Muscle cramps and spasm
○ Muscle weakness (leading to paralysis)
○ Respiratory failure secondary to paralysis of muscles
○ Rhabdomyolysis
○ Hypotonia, hyporeflexia
GI effects:
○ Nausea, vomiting
○ Constipation, ileus
○ Fatigue
Other manifestations: ○ Hyperglycaemia ○ Polyuria ○ Symptoms of the underlying disease: ○ Dehydration in gastroenteritis ○ Tachycardia and tremor in alcohol withdrawal ○ Symptoms of thyrotoxicosis Symptoms of digoxin toxicity in patients with digoxin
What is the ECG features of hypokalaemia
U have no Pot and no T, but a long PR and a long QT
• U waves • small or absent T waves (occasionally inversion) • prolong PR interval • ST depression • long QT The ECG below shows typical U waves. Note also the borderline PR interval.
What is a U wave
small (0.5 mm) deflection immediately following the T wave, usually in the same direction as the T wave
How do you investigate hypokalaemia
• History • Examination • Investigations ○ UE (especially looking at K+, Mg- magnesium low can cause refractory hypokalaemia) ○ ABG to look for metabolic alkalosis ○ Consider urinary potassium Other tests according to the cause
How do you manage hypokalaemia
• If possible, and if there is time, first treat the cause
• Replacement can be by mouth or by intravenous infusion
Oral replacement is preferable – it is certainly safest
○ Sando-K (12 mmol/tablet) is the first choice; Slow K (8 mmol/tablet) should be reserved for those unable to tolerate Sando-K. The usual dose is 40-120 mmol/day. The maximum daily dose is 300 mmol.
The dose depends on how profoundly hypokalaemic the patient is. Always put a stop date of 2-3 days for oral potassium replacement so the patient does not remain on it indefinitely. Here is a possible prescribing plan:
K 3.4: one tablet twice a day.
K 3.3: two tablets twice a day.
K 3.2: two tablets three times per day.
• Intravenous replacement should be reserved for those
○ i. with symptoms ( paralysis, arrhythmia, hepatic encephalopathy)
○ ii. in whom the K+ is below 2.5 mmol/
○ iii. intolerant of oral K+
Infuse potassium into a large vein at up to 20 mmol K+ /hr (not more than 200 mmol/day)
If plasma K+< 2 mmol/L with arrhythmia, 40 mmol K+ may be given over 1h.
When will potassium supplement by ineffective
Note that potassium supplement will be ineffective if there is concurrent hypomagnesium which is untreated
What is the maintenance requirement for K+
1 mmol/kg/day as above which will maintain (keep the value static) not replace. Therefore giving 60 mmol potassium to a 60 kg patient with a potassium of 2.9 may not be sufficient to increase it (depending on ongoing losses & how well the kidneys conserve it). That said if the patient is eating & drinking they will get their maintenance requirements through food so any IV preparations will supplement.
With this in mind, you really want to think about giving 40 mmol or more. IV potassium comes in pre-prepared preparations for nurses in 0.9% sodium chloride or dextrose – either 10, 20 or 40 mmol of potassium in 1L. You cannot add more potassium to other types of fluids eg Hartmann’s or Plasma-Lyte – which both only contain 5 mmol.
If the patient has profound hypokalaemia (e.g. less than 3) you might want to give oral (at max dose as above) & IV replacement. Some might not tolerate Sando-K as it can taste awful and in these patients you might consider IV replacement and depending on how low their potassium is you might wish to give lower amounts (i.e. less than 40 mmol) e.g. 0.9% sodium chloride with 20 mmol potassium.
How quickly should you give K+
Typical prescription is 40mmol in 1L of 0.9% sodium chloride or glucose over 8 hours.
The maximum rate at which you can give potassium on a ward is 10mmol/hour and if you need to give it faster than that, you will need cardiac monitoring and a central line (i.e. HDU environment).
Therefore if the patient requires fluid resuscitation & potassium replacement, consider administering fluid resuscitation in parallel to the bag containing potassium i.e. 500 ml 0.9% sodium chloride bolus at the same time as an 8 hour bag of IV 40mmol KCl in 1L 0.9% sodium chloride.
If the potassium is below 3 mmol or you’re concerned you need to give the infusion quicker than 10mmol/hour – involve your seniors so they can facilitate discussions with HDU & ITU.
