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ABC of Intravenous Fluids, Electrolyte Disorders and AKI Management in Adults

MANAGEMENT OFHYPOKALAEMIA

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Hypokalaemia (HoK) is a serum potassium concentration (s[K]) ,3.5mmol/L. This is the commonest electrolyte disorder in hospitalised patients; most cases are mild. It can be life-threatening if severe[1–4].

HoK-related Symptoms and Signs (S/S)[1–7]

Often asymptomatic. S/S are prominent when the reduction in s[K] occurs rapidly or is large.

Muscle weakness – ascending, can involve respiratory muscles, ileus, rhabdomyolysis secondary to decreased muscle blood fl ow.

Cardiac: ECG changes – fl attening T, ST depression, increased amplitude U waves (V4–V6), prolonged QT, arrhythmias – Sinus Bradycardia, A/VEs, AVB, VT, and VF. The progression of ECG changes varies widely between patients; VF can be the fi rst presentation.

Glucose Intolerance; Metabolic Alkalosis; Polyurea

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S/S develop usually when s[K] is ,3 and resolvewith correction of HoK

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ABC of Intravenous Fluids32

Common Causes

The cause is usually clear from the history[1–6]

a. K depletion (the commonest cause): Renal loss: u[K].20mmol/L – diuretics, mineralocorticoid

excess, glucocorticoid therapy, Mg depletion, Renal Tubular Disease; also occurs secondary to GI fl uid loss and volume depletion

Extra-renal loss: u[K],20mmol/L – gastro-intestinal fl uid loss; skin

b. Intracellular shift (redistributive HoK): insulin or bicarbonate treatment, theophylline, β2 agonists, periodic paralysis, chloroquine intoxication, rapid blood cell proliferation –e.g. GCSF therapy

c. Reduced intake (rare): anorexia nervosa

Investigations[1–6,8]

It is fundamental to understand K distribution for a selective investigation approach

Immediate:

If s[K],3: check ECG, and s[Mg] Repeat urgent K on plasma sample (lithium heparin) as release of

K1 from cells during clotting may give a falsely higher level in serum FBC/glucose

Further, if cause unclear, select as clinically indicated: [Serum HCO3, Cl2, Mg21, PO4, Ca and Urine (paired spot sample with serum) K, Cl, PH (RTA), Ca (BS), P AR (CS, LS]

HCO3, if: 1. Normal: anorexia nervosa, laxatives 2. Metabolic acidosis in absence of diarrhoea: consider RTA,

refer to Renal team 3. Metabolic alkalosis: indicates chronic depletion (see table)

u[K]: if cause not obvious

Abbreviations: A/VEs5Atrial/Ventricular Ectopics; AVB5Atrio-Ventricular Block; VT5Ventricular Tachycardia; VF5Ventricular Fibrillation; u[K]5Urine Potassium concentration; s[Mg]5Serum Magnesium concentration; GCSF5Granulocyte Colony Stimulating Factor; RTA5Renal Tubular Acidosis; BS5Barter’s Syndrome;P AR5Plasma Aldosterone and Renin; CS5Cushing’s Syndrome; LS5Liddle’s Syndrome.

Treatment is shown on the next page.

Beware of blood taken from drip arm!If cause not obvious, refer to Renal or Endocrine Team

for further evaluation

HoK: many patients, up to 40%, are also Mg defi cient. Hypomagnesaemia can induce renal K wasting. Combined defi ciency may potentiate the risk of cardiac arrhythmias – both arepro-arrhythmic. Simultaneous repletion of the Mg stores will facilitate more rapid correction of hypokalaemia and is recommended in severe cases of hypokalaemia[4,8]


Management of Hypokalaemia33

Hypokalaemia (continuation)

K level (mmol/l) Treatment[1–4,6,8–11]

3.0–3.4(mild)

– In most patients– Usually

asymptomatic (including no ECG changes)

Prompt identifi cation and treatment of underlying cause

Potassium loss: gradual oral correction (over days to weeks[2]):

GI losses: vomiting/metabolic alkalosis – give KCl: Sando-K, 1–2 tabs tds (36–72mmol/d) with extra fl uids – alternatively KayCeeL 25ml od-tds (25–75mmol/d). [KHCO3 (KCitrate – 40mmol): if diarrhoea/metabolic acidosis]

Renal losses – e.g. CCF/diuretics: give a K-sparing diuretic after stabilisation, Amiloride is better tolerated.

Monitor s[K] daily to ascertain response and to avoid hyperkalaemia[2,3]. Continue treatment, around three days, until K is in normal range[11].

Rapid IV correction if on digoxin (HoK of any severity increases predisposition to arrhythmia[2]); or symptoms present – see below

Correct concomitant electrolytes defi cits: particularly hypomagnesaemia; patients can be refractory to potassium replacement alone

Concurrent metabolic acidosis: treat hypokalaemia before addressing acidosis

Prevent recurrence: address precipitating factors and ensure adequate dietary potassium intake[2,4].

Redistributive HoK: cautious correction if serious complications present or imminent – paralysis or arrhythmia.

Beware of rebound hyperkalaemia and fatal arrhythmias,particularly in HPP[3].

2.5–2.9 (moderate) + asymptomatic

Treatment measures stated above 1 Rapid oral correction:

Urgent ECG, s[Mg] – ask the lab to add it if not already done Replace with oral K1, choices as above, at higher doses: Sando-K – 2

tabs 6 hourly. IV route (see below) if oral or enteral route not possible – nil by

mouth or severe dyspepsia/diarrhoea Close daily clinical and biochemical monitoring



< 2.5 (severe)

Severe if:,2.5 and/orSymptomatic: Paralysis, arrhythmia -(or pre-existing cardiac disease e.g. ACS, Digoxin toxicity …)

Treatment measures stated above1IV correction:

Continuous ECG monitoring or telemetry Secure proper IV access: large veins, or CV line if access poor. Use

infusion pump to prevent overly rapid potassium administration. Give 1L NS 0.9%/40mmol KCl IV, over 4hrs. Do not use 5% Dextrose.

[Use 1L 0.45% saline/40mmol KCl in DKA/HHS] It is not recommended to exceed 2–3mmol K/kg/BWT/24hrs[11]. Monitor s[K] levels after every 40–80mmol K, and daily to ascertain

the response, as it is diffi cult to predict. Avoid volume overload. Close monitoring until S/S resolved and K level .3; then switch to

oral therapy as per the mild/moderate regime above.

If life threatening/intractable cardiac arrhythmia: double infusion rate, up to 40mmol/hr[3], and contact resuscitation team. If life threatening cardiac arrhythmia: add IV MgSO4, 10mmol over 30 minutes, even before the s[Mg] is known[4].

Renal impairment: cautious K replacement – risk of overcorrection (hyperkalaemia) – contact renal team if severe renal failure or patient on dialysis Use pre-mixed infusion fl uid. NEVER add KCl to infusion bags[9]

Abbreviations: CCF5Congestive Cardiac Failure; HPP5Hypokalaemic Periodic Paralysis; CV5Central Venous; DKA5Diabetic Ketoacidosis; HHS5Hyperosmolar Hyperglycaemic State; BWT5Body Weight; Hr(s)5Hour(s)

Hypokalaemia: further evaluation if the cause is unclear:

Hypokalaemia: further evaluation if the cause is unclear:[1–6]

Extra-renal loss: metabolic (M)acid-base status

Renal loss: metabolicacid-base status

Normal M Acidosis M Alkalosis M Alkalosis M Acidosis Variable

AN Laxative abuse

RTA, DKA MgDepletion



Metabolic Alkalosis

Low u[Cl]<10mmol/L (low u[K])

High u[Cl] (.10mmol/L) – (high u[K])

Normotensive Normotensive Hypertensive

Volumecontraction: due tosurreptitious vomiting

Diuretics use, BS, GS: (1/2 low Mg)

High (P)Aldosterone (A)

Normal (P)A and R

Low (P)A and R

a. Low R: Conn’s (CS)b. High R: RVD

Cushing’s – U Cortisol, LD-DST: refer to endocrine

AME – (liquorice ingestion),CAH, LS

Abbreviations: AN5anorexia nervosa; u[Cl]5urine chloride concentration; BS5Barter’s syndrome; GS5Gitleman’s syndrome; P5Plasma; R5Renin; LD-DST5low dose dexamethasone Suppression test; RVD5Reno-vascular Disease; AME5apparent mineralocorticoid excess; CAH5congenitaladrenal hyperplasia

CONCLUSION

Due concern and appropriate management should be given to patients’ with hypokalaemia as it can be fatal.



PRACTICAL EXERCISE

All units are in mmol/L unless stated otherwise

A 74-year-old male was admitted with fever, vomiting, diarrhoea and shortness of breath for three days. He was confused, with dry mucus membranes, reduced skin turgor, supine BP 95/55, 75/50mmHg on sitting up, tachycardia, tacchypnoea, fever and body weight 70Kg. s[Na] 158, s[K] 2.8, sCr 119μmol/L, sUrea 12mmol/L, s glucose 9mmol/L, s osmolality 333mOsm/Kg and a spot urine – u[Na] 7, u[K] 26, urine osmolality 846mOsm/Kg. A clinical diagnosis of acute confusion secondary to pneumonia was made.

Q1: What is the cause of hypokalaemia?

A1: Hypokalaemia is due to a combination of:

a. Vomiting: Main factor is the increased Distal Tubular (DT) renal potassium loss

due to increased bicarbonate delivery to DTs, in addition hypovolaemia stimulates aldosterone secretion.

Upper GI K loss/reduced intake b. Diarrhoea: Lower GI loss/reduced intake Increased DT renal K loss due to hypovolaemia-induced RAAS activation

Q 2. What is the cause of hypernatraemia?

A 2. Chronic hypernatraemia is due to:

a. Hypotonic sodium and potassium loss secondary to vomiting and diarrhoea b. Pure water loss secondary to fever and tacchypnoea

Q 3. How would you correct hypokalaemia, hypernatraemia and hypovolaemia?

A 3. Therapeutic approach:

a. The fi rst aim is to correct hypovolaemia. He became haemodynamically stable after receiving 1.5L of NS (120mmol KCl per litre) within three hours, the repeat s[Na] was 158, s[K] was 3.

b. The second aim is to correct hypokalaemia and gradual correction of hypernatraemia over 2–3 days.



Estimating fl uid replacement using Formula 2, see chapter on hyponatraemia, to correct hypokalaemia and hypernatraemia: the desired water replacement in the fi rst 24 hours to reduce s[Na] by~ 10mmol/L using (5% D10.18% saline110mmol KCl per L) is:

1L of (0.18% saline+10mmol KCl) will reduce s[Na] by 3.3mmol/l, obtained from the equation (formula 2): (402166)/(35 11). Therefore, the volume required to reduce s[Na] by 10mmol/l510/3.353L, Plus 1.5L to compensate for 24 hour obligatory water losses5Total of 4.5L over 24 hours. 3L were given IV at 125ml/hr, he became more lucid during the day and managed to take 1.5L orally.

Close monitoring: UOP; s[Na], s[K], and serum glucose every 2 hours.

REFERENCES

[1] Unwin, R.J., Luft, F.C. and Shirley, D.G. Pathophysiology and management of hypokalemia:a clinical perspective. Nature Reviews Nephrology (2011), Vol. 7, pp.75–84. doi:10.1038/nrneph.2010.175.

[2] Gennari, F.J. Hypokalemia. New England Journal of Medicine (1998), pp.339:451.

[3] Uptodate. Clinical manifestations and treatment of hypokalemia in adults (Accessed 04.2015).

[4] Alfonzo, A., Isles, C., Geddes, C. and Deighan, C.. Potassium disorders – clinical spectrum and emergency treatment. Resuscitation (2006), Vol. 70, pp.10–25.

[5] Rastegar, A. and Soleimani, M. Fluid, Electrolytes and Acid-Base Disturbances. Nephrology Self-Assessment Program, ASN, (2015), Vol. 14, No. 1.

[6] The British Medical Journal Best Practice. Assessment of Hypokalaemia. 08.2014. http://bestpractice.bmj.com/best-practice/monograph/59/diagnosis.html

[7] Moore, R. and Stuart, L.L. Hypokalaemia and Hyperkalaemia. Nephrology Secrets, 3rd Edition, 2012.

[8] Cohn, J.N., Kowey, P.R., Whelton, P.K. and Prisant, L.M. New guidelines for potassium replacement in clinical practice. Archives of Internal Medicine (2000), Vol. 160, pp.2429–36.

[9] NPSA Patient safety alert. Potassium chloride concentrates solution Alert 01. 2002. London: National Patient Safety Agency.

[10] Guideline for the management of hypokalaemia in adults. Produced by Medicines Information, CGH: August 2010 http://www.gloshospitals.nhs.uk/SharePoint110/Antibiotics%20Web%20Documents/ TG/Hypokalaemia%20Guidelines.pdf

[11] Guidelines for potassium replacement in hypokalaemia. Nottingham City Hospital NHS Trust. Update 05.2013b. https://www.nuh.nhs.uk/handlers/downloads.ashx?id=35682
