[e-drug] Management of hypokalaemia

[Valeria Frighi <valeria.frighi@dtu.ox.ac.uk>]

E-drug: Management of hypokalaemia
---------------------------------------------

Challenges in managing profound hypokalaemia
was published in BMJ 2002;324:269-270 ( 2 February)
The full text can be viewed at
http://www.bmj.com:80/cgi/content/full/324/7332/269?eaf--

In case you have difficulty in accessing the website, the text 
(without table) is also below.

Dr. Valeria Frighi
Diabetes Trials Unit
Radcliffe Infirmary
Woodstock Road
Oxford OX2 6HE
UK

tel. -44-1865-228422
fax -44-1865-224584
e-mail valeria.frighi@dtu.ox.ac.uk


BMJ 2002;324:269-270 ( 2 February )

Papers

Challenges in managing profound hypokalaemia

William Welfare, medical student a, Phillip Sasi, research fellow
b, Mike English, research paediatrician
  b. a University of Edinburgh Medical School, Edinburgh EH8 9AG,
  b Centre for Geographic Medicine Research, Coast, KEMRI/Wellcome 
Trust Research Laboratories, PO
Box 230, Kilifi, Kenya

Correspondence to: M English menglish@kilifi.mimcom.net

Potentially life threatening profound hypokalaemia with metabolic
acidosis may not be adequately dealt with by current treatment recommendations

Abnormalities of serum potassium are associated with well described
clinical features: lassitude when potassium <3.5 mmol/l,
possible muscle necrosis at < 2.5 mmol/l, and a flaccid paralysis with
respiratory compromise at <2 mmol/l.1 World wide,
hypokalaemia is most often caused by diarrhoea, although specific
treatment of hypokalaemia is not mentioned in international
guidelines for managing gastroenteritis.2 Furthermore, a recent case
made us concerned that the potassium replacement
recommended in medical texts (a maximum rate of infusion of 0.3-0.5
mmol/kg/hour and a maximum daily replacement of
3-5 mmol/kg) may be inadequate for profound hypokalaemia (1.5 mmol/l).

Patients, methods, and results

The patient (case 1, table) was an 8 month old child with 
gastroenteritis who was too weak to respond appropriately to pain, 
with reduced respiratory effort, metabolic acidosis, intermittent 
sinoatrial block, and an inappropriately low heart rate (72 
beats/min) given the
degree of dehydration. The risk of inadequate treatment seemed to 
outweigh the risk of aggressive fluid and potassium replacement as 
mechanical ventilation and inotropic support were not available. The 
maximum recommended administration rate and total daily dose for 
intravenous potassium were therefore exceeded by at least 4 and 3 
fold respectively without adverse effects.

  View this table:
      [in this window]
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  Characteristics of cases identified as profoundly hypokalaemic on 
admission and response to treatment

We identified further cases with potassium concentrations 1.5 mmol/l
(614 Na+/K+ Analyser, Chiron Diagnostics) from paediatric admissions 
to the high dependency unit of Kilifi District Hospital in1993-2000. 
Data were extracted from the case records and examined for blood gas 
and potassium values at 4-8 hours and 18-30 hours after admission 
(early and late
resuscitation phases). The maximum and average hourly rates and total of
potassium infusion during resuscitation were calculated.

Thirteen patients, seven of whom died, were identified (table). In four
death was too rapid to allow evaluation, and in one survivor data 
were inadequate. Strikingly, nine out of 11 patients with data on 
blood gases on admission were markedly acidotic. Although acidosis 
was persistent (possibly confounding potassium measurements) and 
continued stool losses could not be measured, there was a significant 
correlation between the late phase change in potassium and the 
average rate of potassium
replacement over 24 hours (Spearman's  0.78, P=0.02). The only child
developing a potassium value>5.6 mmol/l during admission was a child 
with a Gram negative septicaemia (case 8): potassium rose to 6.6 
mmol/l (pH 6.99, base excess -23.9 mmol) at 48 hours, shortly before 
death.

Comment
Current guidelines for potassium replacement may not deal adequately
with the rare but life threatening situation of profound hypokalaemia 
(1.5 mmol/l) associated with metabolic acidosis seen in our 
developing country setting. Furthermore, recent prospective data 
suggest that half the children admitted with gastroenteritis have a 
base excess -10 mmol and 7% a potassium <2 mmol/l (PS, unpublished 
data) even though acidosis would normally be expected to increase 
potassium concentrations (due to efflux of
intracellular potassium in exchange for extracellular hydrogen). About
500 children with gastroenteritis and 300 with severe malnutrition 
are admitted to our hospital annually, so the problem of hypokalaemia 
with acidosis is important.

Globally, lack of resources makes it likely that such hypokalaemia is 
rarely recognised. Paradoxically, therefore, children with severe 
gastroenteritis, perhaps at highest risk of hypokalaemia, may receive 
intravenous fluids2 with little or no potassium (0.9% saline, 
Ringer's lactate, or Hartmann's). In fact by ameliorating any 
associated acidosis through correcting hypovolaemia or direct 
alkalinisation (by lactate) cells may import potassium in exchange 
for intracellular hydrogen ions, further lowering serum
potassium with possibly disastrous consequences.3 Further research on
potassium replacement in severe gastroenteritis is required, 
particularly in potentially life threatening, profound hypokalaemia.

Acknowledgments
We gratefully acknowledge the help of the clinical and laboratory staff
of Kilifi District Hospital and the KEMRI/Wellcome Trust Research 
Laboratories. ME is supported by a Wellcome Trust Career Development 
Fellowship. This paper is published with the permission of the 
director of KEMRI.

Contributors: ME conceived the study and contributed to data collection,
analysis, and drafting the manuscript. WW undertook
data collection and analysis and was involved in drafting the
manuscript. PS helped in data collection and interpreting and
drafting the manuscript.

  Footnotes
Funding: ME is supported by a Wellcome Trust career development
fellowship.

Competing interests: None declared.

  References
1.  Gennari FJ. Hypokalemia. N Engl J Med 1998; 339: 451-458[Full Text].

2.  World Health Organization. Management of the child with a serious
infection or severe malnutrition. Geneva: World Health Organization, 2000.

3.  Heyman S, Nehama H, Horovitz J, Sofer S, Orbach J, Amir Y, et al.
Sudden death from fluid resuscitation: lesson from Ruanda. Lancet 
1994; 344: 1509-1510[Medline].
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