You can beat the feeling • LITFL • Metabolic Muddle

aka Metabolic Muddle 006

It’s a busy night shift in the ED (as always) and one of the Interns comes to present a case to you. He’s seen a 23 yr old female who has presented with lethargy and weakness. While you’re listening to the Intern your phone rings — it’s the lab calling to tell you the patient’s potassium is 1.9 mmol/L.

Questions

Q1. What are the clinical features of hypokalaemia?

Answer and interpretation

The clinical features of hypokalaemia result from effects on multiple organ systems. They include:

Cardiovascular
— ECG changes when K < 2.7mmol/L: changes include P wave prominence, T wave flattening, and U waves
— Tachydysrhythmias
— Hypokalaemia also potentiates digoxin toxicity
Musculoskeletal
— Weakness progressing to paralysis
— Rhabdomyolysis
Gastrointestinal
— Ileus
Renal
— Nephrogenic diabetes insipidus
— Increased ammonia production

Learn more:

LITFL ECG Library — Hypokalemia

While hypokalaemia is easy to diagnose. The key question is ‘why is it low?’.

Q2. How would you proceed?

Answer and interpretation

There are a wide variety of causes of hypokalaemia including:

Decreased intake
GI Losses
— e.g. vomiting, NG losses, diarrhoea, fistula
Renal Losses
— e.g. drugs, aldosteronism (primary & secondary), renal tubular acidosis, diuresis
Transcellular Shifts
— e.g. alkalosis, hypokalaemic periodic paralysis, thyrotoxic periodic paralysis
Congenital
— e.g. Bartter Syndrome, Gitelman Syndrome , Liddle Syndrome
Drugs
— e.g. loop & thiazide diuretics, insulin, salbutamol, liquorice ingestion

On further questioning she states she drinks 4 litres of a popular brand cola beverage every day, and has done for the last few years.

Q3. How much cola needs to be drunk to result in hypokalemia?

Answer and interpretation

There are several case reports in the literature linking excessive cola consumption to severe hypokalaemia, the case series review by Tsimihodimos, et al (2009) being the largest.

All these reports involved chronic excessive consumption in the region of 2 – 9 litres per day over months to years.

The majority of cases responded well to treatment, but there have been cases of acute renal failure due to rhabdomyolysis, and deaths have been attributed to hypokalaemia secondary to cola.

Q4. How does cola consumption cause hypokalaemia?

Answer and interpretation

The mechanism/s of cola associated hypokalaemia as not fully understood but several mechanisms have been postulated including:

Osmotic diuresis
— due to large amounts of glucose in cola drinks
Hyperinsulinaemia
— secondary to large glucose load causing intra-cellular shift of potassium
Osmotic diarrhoea / GI loss
— from large unabsorbed fructose load passing through GI tract.
Caffeine mediated
— multifactorial involving respiratory alkalosis, intra-cellular K+ shift due to increased cAMP, increased renin release, and diuresis.

Treatment involves potassium replacement whilst ceasing excess cola consumption.

Q5. What are the other important complications of excessive soft drink ingestion?

Answer and interpretation

Aside from hypokalaemia and secondary rhabdomyolysis excess, cola consumption has also been liked to other health problems, including:

Obesity
Dental Disease
Increased risk of type 2 diabetes mellitus
Non-alcoholic fatty liver disease

On a much rarer note a case report from the Journal of Toxicology linked excessive consumption of a cola containing brominated vegetable oil to systemic bromism requiring dialysis. Cola can also cause acidification of the urine, which may lead to delayed excretion of some medications (e.g. methotrexate).

Whether chronic excessive cola consumption is linked to any form of cancer is uncertain. Finally, cola was also implicated in a out-break of epidemic illness in Belgium in 1999, later attributed to mass sociogenic illness following a food contamination scare.

References

LITFL

Journal articles and textbooks

Assy N, Nasser G, Kamayse I, Nseir W, Beniashvili Z, Djibre A, Grosovski M. Soft drink consumption linked with fatty liver in the absence of traditional risk factors. Can J Gastroenterol. 2008 Oct;22(10):811-6. PMID: 18925303
Dunn R, Dilley S, Brookes J, Leach D, Maclean A, Borland M. The Emergency Medicine Manual (5th Edition), Venom 2010.
Horowitz BZ. Bromism from excessive cola consumption. J Toxicol Clin Toxicol. 1997;35(3):315-20. PMID: 9140329
Malik VS, Popkin BM, Bray GA, Després JP, Willett WC, Hu FB. Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis. Diabetes Care. 2010 Nov;33(11):2477-83. PMID: 20693348
Nemery B, Fischler B, Boogaerts M, Lison D, Willems J. The Coca-Cola incident in Belgium, June 1999. Food Chem Toxicol. 2002 Nov;40(11):1657-67. PMID: 12176091
Santucci R, Levêque D, Herbrecht R. Cola beverage and delayed elimination of methotrexate. Br J Clin Pharmacol. 2010 Nov;70(5):762-4. doi: 10.1111/j.1365-2125.2010.03744.x. PubMed PMID: 21545633; PubMed Central PMCID: PMC2997317.
Tintinalli JE, Stapczynski JS, Ma OJ, Cline DM, Cydulka RK. Tintinalli’s Emergency Medicine (7th Edition), McGraw Hill 2011.
Tsimihodimos V, Kakaidi V, Elisaf M.Cola-induced hypokalaemia: pathophysiological mechanisms and clinical implications. Int J Clin Pract. 2009 Jun;63(6):900-2. PMID: 19490200