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It is well known that hydration and infection operate in a vicious synergistic cycle: suboptimal hydration predisposes patients to infection and increases its severity, while infection facilitates fluid loss and sometimes prevents individuals from being able to replace their fluids.
It makes sense, then, that COVID-19, like other infectious diseases affecting the respiratory tract, commonly results in dehydration. But what do we know about how these mechanisms work, and what can be done to increase the comfort and safety of patients suffering from COVID?
One very old study reported that in well-hydrated rabbits injected with Vaccinia, the virus was localised and not able to infect the surrounding tissues.1 The mechanism behind this seemed to be a decreased permeability of the cells, but the authors also reported that inadequate hydration status compromised the body’s ability to mount an appropriate immune response.
Furthermore, respiratory viruses spread more efficiently in cold and dry climates, possibly due to the fact that people in colder surroundings spend more time indoors where humidity tends to be lower and overcrowding more likely. However, there is also some evidence which suggests that dry indoor air promotes the drying of mucosal barriers and results in a loss of physical protection against pathogens, leading to an increased rate of respiratory transmissions.
Lauc et al. suggest that fluid deficit may also prevent the appropriate rehydration of mucosal barriers, which may then lead to increased risk of respiratory infection in affected individuals.2 Another group of researchers hypothesised that chronic hypertonic dehydration not only increases the individual’s risk of becoming infected but may lead to a more exaggerated immune response.3
Despite these claims, there are currently no studies which have investigated this issue: assessing hydration status is difficult, as haematological and urinary biomarkers do not always reflect a patient’s actual state until severe dehydration develops. Mild dehydration may be missed, misdiagnosed, or misused – the latter is seen in older patients being admitted for social reasons.
Additionally, infection and dehydration often coexist at the time of diagnosis, making it difficult to establish which developed first. A number of studies have demonstrated that COVID-19 patients often present with dehydration or ‘hypernatremia’ (where an individual has too much sodium in their blood), sometimes in the absence of other symptoms. Fluid deficiency is a common cause of hypernatremia, and very young and very old patients are at the highest risk. Hypernatremia has been documented in paediatric4 and older COVID-19 patients5,6 as well as in other age groups.7,8 Studies also reported that hypernatremia at admission was a prognostic factor for increased morbidity and mortality.7,8
Dehydration can also develop later as the disease progresses. One retrospective point-prevalence survey of hypernatremia in 17 ICU patients with SARS-CoV-2-induced acute respiratory distress syndrome (ARDS), reported that nine people became hypernatremic following admission to ICU.9 The authors concluded that since urine osmolarity was in a normal range and patients were maintained on positive fluid balance, dehydration likely occurred as a result of insensible fluid losses via skin and breathing. This is not surprising in patients who were likely pyrexic.
Expert opinion differs, but some recommend as much as 500ml of additional fluid per one degree of fever. However, it could be argued that patients developed hypernatremia due to impaired kidney function resulting from infection. Kidneys have been reported to be disproportionally affected by the SARS-CoV-2 virus, and abnormal sodium reabsorption with increased urine output has also been described.10 However, the authors of the above survey also reported that urine osmolarity was normal and the sodium intake was comparable to other patients, thus confirming that hypernatremia was due to fluid deficit.9
Unfortunately, another feature of COVID-19 may be ‘hyponatremia’, the opposite of hypernatremia – low levels of sodium in the blood.
Some studies showed that in COVID-19 patients hyponatremia10 was more common than hypernatremia at admission and that it was significantly more prevalent at admission than in non-COVID-19 patients presenting with similar symptoms. Studies estimated that hyponatremia was also a risk factor for disease severity,7,10 and mortality10 when compared to COVID-19 patients with normal sodium levels. Faced with a high proportion of hyponatremic patients, clinicians may be reluctant to provide additional fluids to COVID-19 patients.
However, one study7 demonstrated that patients experienced a progressive rise in serum sodium levels after hospital admission and that some hyponatremic patients later turned hypernatremic. Authors also reported that these patients whose sodium levels increased after hospital admission were at higher risk of dying. Interestingly, they also reported that hyponatremia was not associated with increased mortality except in one group of patients who were also hypovolemic, thus suggesting that it is not the electrolyte imbalance but fluid deficit which is a risk factor for increased mortality.
During this year’s nutrition and hydration awareness week, we would like to highlight that COVID-19, as other infectious diseases affecting respiratory tract, commonly results in dehydration. This is probably due to sensible and insensible fluid losses as well as inability of some patients to replenish lost fluids. Fluid deficit seems to develop slowly in COVID-19 patients and may be present in individuals regardless of their electrolyte status. This makes it particularly challenging for clinicians to diagnose and manage, but doing so will undoubtedly save lives.
To find out more about Nutrition and Hydration Week 2021, head over to their website: https://nutritionandhydrationweek.co.uk/
1 Hickson M, Bulpitt C, Nunes M, Peters R, Cooke J, Nicholl C, et al. Does additional feeding support provided by health care assistants improve nutritional status and outcome in acutely ill older in-patients? A randomised control trial Clin Nutr, 2004;23(1):69-77.
2 Lauc A, Markotic A, Gornik I, Primorac D. Fighting COVID-19 with water. J Glob Health, 2020; 10(1): 010344
3 Stookey JD, Allu PKR, Chabas D, Pearce D, Lang F. Hypotheses about sub-optimal hydration in the weeks before coronavirus disease (COVID-19) as a risk factor for dying from COVID-19 Med Hypotheses, 2020; 144: 110237
4 Besharat M, Khorram PB. Fever and Dehydration as the First COVID-19 Presentation in a 2-Months Old Boy in Northeast of Iran Arch Pediatr Infect Dis, 2021; 9(1):e107308
5 Bavaroa DF, Diellaa L, Fabriziob C, Sulpassoa R, Bottalicoc IF, Calamod A et al. Peculiar clinical presentation of COVID-19 and predictors of mortality in the elderly: A multicentre retrospective cohort study Int J Infect Dis, 2021; 105:709-715
6 Clifford CT, Pour TR, Freeman R, Reich DL, Glicksberg BS, Levin MA et al. Association between COVID-19 diagnosis and presenting chief complaint from New York City triage data Am J Emerg Med, 2020; S0735-6757(20)30986-4
7 Tzoulis P, Waung JA, Bagkeris E, Hussein Z, Biddanda A, Cousins J et al. Dysnatremia is a predictor for morbidity and mortality in hospitalized patients with COVID-19 J Clin Endocrinol Metab, 2021; 106(6):1637-1648
8 Hirsch JS, Uppal NN, Sharma P, Khanin Y, Shah HH, Malieckal DA et al. Prevalence and outcomes of hyponatremia and hypernatremia in patients hospitalized with COVID-19 Nephrol Dial Transplant, 2021; 36: 1135–1138
9 Redant S, Vanderhulst J, Maillart E, Attou R, Gallerani A, Honoré PM et al. Significance of hypernatremia due to SARS-CoV-2 associated ARDS in critically ill patients J Transl Int Med, 2020; 8(4):255-260
10 Zimmer MA, Zink AK, Weißer CW, Vogt U, Michelsen A, Priebe H-J et al. Hypernatremia—A Manifestation of COVID-19: A Case Series A&A Practice. 2020;14(9):e01295
11 Atila C, Sailer CO, Bassetti S, Tschudin-Sutter S, Bingisser R, Siegemund M et al. Prevalence and outcome of dysnatremia in patients with COVID-19 compared to controls Eur J Endocrinol, 2021; 184(3): 409–418