Tea and Toast Syndrome: A Case Report

Abstract

Hyponatremia, characterized by serum sodium <135 mEq/L, poses a significant health concern, particularly among the elderly. This case report explores chronic hyponatremia, with a focus on the Tea and Toast Syndrome, prevalent in individuals with atypical dietary habits. We present a 69-year-old female presenting with chronic hyponatremia, revealing dietary factors as key contributors. Thorough diagnostic workup ruled out common causes, emphasizing the importance of meticulous approaches. The patient’s adherence to recommended dietary changes resulted in significant improvement, showcasing the pivotal role of targeted nutritional interventions. Pathogenetic mechanisms, such as reduced water-excretory capacity and solute excretion, were explored, with differentiation between AVP-mediated and non-AVP-mediated hyponatremia highlighted. The case underscores the intricate interplay between dietary habits, aging, and chronic hyponatremia, emphasizing the need for adjusted interventions in this vulnerable population. Addressing the nutritional aspects of chronic hyponatremia emerges as a crucial aspect, offering an opportunity for targeted management and improved patient care, especially in the aging demographic.

Introduction

Hyponatremia is given by serum sodium (Na+) concentration <135 mEq/L and can be classified as mild, moderate, and severe depending on sodium plasma levels, with values <135–130, 129–125, and <125 mEq/L, respectively (Buffington & Abreo, 2016). Another approach to classification of hyponatremia is by serum osmolarity (sOsm), which is calculated with the formula sOsm (mmol/kg) = (2 × Serum [Na]) + (serum [glucose]/18) + (blood urea nitrogen/2.8). Hypotonic, also called true hyponatremia, with low serum osmolality (<280 mosm/kg), Isotonic with normal osmolality (280–295 mosm/kg) and Hypertonic with high serum osmolality (>295 mosm/kg) (Filippatos et al., 2017).

Hyponatremia is the most recurring electrolyte disorder in both hospitalized patients as well as ambulatory patients. The same applies to elderly individuals who might be at an increased risk of developing adverse effects from this medical condition and its treatment, in this population the prevalence of hyponatremia ranges from 8% to 12%, being much higher in patients >75-year-olds and patients in nursing homes (Gosch, 2022; Heybeli et al., 2021). Additionally, the symptomatology of chronic hyponatremia, such as fatigue, cognitive impairment, mobility issues, falls, and adverse effects on bone health (such as osteoporosis) and fractures, are more prevalent and severe in the elderly population. Research also indicates that hyponatremia significantly worsens the prognosis for older adults, as it is independently associated with an increased risk of mortality, as well as numerous morbidities (Filippatos et al., 2017; Heybeli et al., 2021).

As regards to the pathogenetic mechanisms of elderly’s heightened susceptibility to hyponatremia, it can be attributed primarily to their reduced water-excretory capacity due to the natural decline in bodily functions with aging, mainly attributed to the reduction of glomerular filtration rate (GFR), the frequent use of medications that can disturb electrolyte balance, and the presence of illnesses linked to hyponatremia (Filippatos et al., 2017).

Moreover, one of the mechanisms that lead to hyponatremia is excessive free water supply, caused by an excessive intake of free water like psychogenic polydipsia and liquid-rich diet (such as Tea and toast syndrome), and a low-salt diet, all these causes hyponatremia by dilution or hypotonic, often observed in elderly patients (Kylies & Wenzel, 2020). We recently faced a typical case of chronic moderate hypotonic hyponatremia in an older adult patient due to high water and carbohydrate diet consistent with tea and toast syndrome.

Case Presentation

Clinical History and Initial Laboratory Data

A 69-year-old female patient with a medical history notable for Hypertension, Embolization due to an aneurysm in the Middle Cerebral Artery (MCA), Exocrine Pancreatic Insufficiency (pancreatic atrophy without signs of chronic pancreatitis), Gastroesophageal Reflux Disease, and irritable bowel syndrome was referred from the gastroenterology department to the outpatient nephrology service due to the incidental finding of hyponatremia. Her primary complaint revolved around a one-year history of asymptomatic moderate hyponatremia, with serum sodium levels consistently measuring at 124 mg/dl and later at 125 mg/dl. On admission, her vital signs and physical examination were unremarkable, and it was essential to investigate the underlying cause of her hyponatremia.

Additional Investigations

To determine the etiology of the patient’s chronic hyponatremia, an extensive workup was initiated. This investigation encompassed a thorough review of her medical history, medication profile, and a comprehensive set of laboratory tests. These tests ruled out pseudohyponatremia as a cause, as her hemogram, renal function, potassium, and chloride levels were all within the normal range. Additionally, her glucose and lipid profiles were unremarkable. Notably, there was no recent history of surgery, hyperproteinemia, or exposure to contrast media or mannitol. This ruled out pseudohyponatremia and left us with the suspicion that her chronic hyponatremia might be related to medications, particularly thiazides, even though she had discontinued Hydrochlorothiazide with no improvement. Other drugs that could potentially cause hyponatremia were considered but ultimately excluded since the patient had not used any of them.

Diagnosis

The patient’s hyponatremia was ultimately classified as true hypotonic hyponatremia, as her serum osmolality measured 256 mOsm/KgH₂O, falling below the 275 mOsm/KgH₂O threshold. While it was important to consider if antidiuretic hormone (ADH) played a role in her condition, further discussions with the patient revealed her dietary habits. She had a significantly low protein intake with an estimated osmolar load of 350 mmol/day, considerably less than the appropriate 510 mmol/day for her weight. Moreover, she was consuming an excessive amount of water, averaging 5 to 6 L daily. These findings shifted the focus from ADH secretion to her dietary behaviors and established the diagnosis of the “Tea and Toast Syndrome.”

Clinical Follow-Up

Subsequent clinical follow-up appointments were instrumental in monitoring the patient’s progress. She adhered to the recommended dietary changes, which included halving her daily water consumption to approximately 3 L and increasing her protein intake. By the third nephrology follow-up, 90 days after the initial diagnosis, the patient exhibited significant improvement, evident in her sodium levels and osmolar load, which was calculated using the formula Osmolar Load = (Urinary BUN/2.8) + 2 × (Urinary Na + Urinary K), yielding a result of 529 mmol/day. As the follow-ups continued, the patient showed consistent improvement, emphasizing the importance of addressing specific forms of chronic hyponatremia through targeted nutritional interventions, particularly in older adults with atypical dietary habits. Continuous monitoring remains a crucial aspect of ensuring her sustained progress and condition stability.

Discussion

We present an interesting case of “Tea and Toast” syndrome in an elderly patient with chronic undiagnosed hyponatremia. This syndrome is a form of malnutrition commonly experienced by elderly people who are unable to prepare meals and tend to themselves. It is characterized by a diet that is low in essential nutrients, leading to deficiencies in vitamins, minerals, and other nutrients (Baez et al., 2023).

According to Edelman’s formula (Serum [Na]) + (serum [K]/Total Body water) hyponatremia is always an indicator of total body water excess, which may be due to excess in free water intake (as in the case of primary polydipsia) or due to decrease in free water excretion (Edelman et al., 1958). The last one being the most common physiopatological explanation of hyponatremia, and it can be explained by five mechanisms: (1) Reduction of glomerular filtration rate (Acute kidney injury, chronic advance kidney disease); (2) Increase in proximal tubular reabsorption (congestive heart failure, cirrhosis); (3) Decrease in tubular dilution capacity (diuretics); (4) Decrease in solute excretion (potomania, tea, and toast syndrome); and (5) Increase in vasopressin (ADH) activity, which may be due to a normal physiological respond to hypovolemia or due to an increase antidiuretic activity in presence of normovolemia as in the case of inappropriate antidiuretic hormone ADH release syndrome (SIADH) or in glucocorticoid deficiency (Seay et al., 2020).

After confirming that we are facing a genuinely hyponatremic and hypotonic patient, an initial approach to hyponatremia relies in the differentiation among AVP (Arginine Vasopressin) mediated Vs Non AVP mediated hyponatremia and the assessment of extracellular volume (Seay et al., 2020). Plasma Copeptin has been used to aid in this differentiation, however related to some limitations regarding its role as an acute phase reactant, and limited availability throughout middle to low-income countries (Morgenthaler et al., 2008). In our case, urinary osmolarity >100 mOsm/KgH₂O was an initial indicator of a possible AVP mediated mechanism of hyponatremia. Euvolemia was established, glucocorticoid deficiency was ruled out clinically, previous thyroid hormones levels workup were normal, and exercise associated hyponatremia was non consistent with patients’ history. Inappropriate antidiuretic hormone ADH release syndrome (SIADH) was taken into account; however, further discussions with the patient revealed a significantly low daily protein intake and an excessive amount of water intake, averaging 5 to 6 L daily (due to “healthy recommendations”).

Normal daily osmolar load is estimated between 600 and 900 mmol/day, usually 10 mmol/kg/day (700 mmol/day in a 70 kg adult). It can be calculated using two methods: One method is to calculate the caloric distribution by weight in grams of each food consumed. The second method consists in calculating osmolar load by the equation (Urinary BUN/2.8) + 2 × (Urinary Na + Urinary K). Solutes intake and osmotic daily load have an important role in water excretion (Berl, 2008). Urinary volume is directly related to the total osmoles excreted per day (approximately 10 mmol/kg/day). Solutes like sodium, potassium, urea, glucose and mannitol are involved and responsible for water excretion (Najem et al., 2022). Therefore, we can conclude that low dietary osmolar load is directly related to a decrease in renal free water excretion. In this case, the patient had an estimated osmolar load of 350 mmol/day, considerably less than the appropriate 510 mmol/day for her weight. These findings shifted the focus from ADH secretion to her dietary behaviors, and a decrease in solute excretion as the main physiopatological explanation of her hyponatremia.

Furthermore, the volume (minimum and maximum) necessary to excrete these solutes is determined by our renal capacity to dilute and concentrate urine. Therefore the volume necessary for solute excretion is explained by the following equation: Osmolar load/renal maximum diluting and concentration capacity (40 a 1,200 mOsm/KgH₂O) (Lorenzo, 2014). This explains the crucial role of renal senescence in the development of hyponatremia in the elderly with “Tea and Toast syndrome.” In renal senescence approximately 20% of maximum dilution and concentration capacity is lost. With age, as the GFR decreases, the capacity for water excretion decreases and it has been estimated that in patients with GFR <25 mL/min maximum urinary dilution increases up to 200 mOsm/KgH₂O. This explains the generation of hyponatremia with lesser quantities of daily water intake as related to younger patients with intact maximum diluting renal capacity (Workeneh et al., 2023).

In this case the patient’s daily osmolar load was first estimated in 350 mmol/day using the caloric distribution by weight in grams of each food consumed method. On the follow up consultations, after dietary recommendations were made to increase protein intake and reduce daily water intake to 2 to 3 L maximum, osmolar load was calculated by the equation (Urinary BUN/2.8) + 2 × (Urinary Na + Urinary K) with a result of 529 mmol/day, which reflects the patient’s adherence to recommendations. Also, the increase in serum sodium in follow up consultations: Serum [Na] 131 mmol/L with 194 mOsm/KgH₂O urinary osmolarity and Serum [Na] 137 mmol/L with 346 mOsm/KgH₂O urinary osmolarity in one month follow up confirmed the significant improvement with dietary recommendations. On the other hand, it is important to mention that if our patient have had an inappropriate antidiuretic hormone ADH release syndrome (SIADH), water restriction would have needed to be much more strict in order to evidence improvement in serum sodium and urine osmolarity, as estimated by free water clearance formula.

This fascinating case highlights the importance of a judicious clinical history and the important role of estimating daily solute consumption in the routine workup of hyponatremia. Also, it highlights the importance of further studies in patients with chronic asymptomatic hyponatremia (which is related to high morbidity and mortality), and the crucial role of health workers as educators regarding the adequate recommendations of daily fluid intake; especially in our modern society with a “one size fits all” recommendation of high daily fluid intake, in despite of patients age or metabolic requirements.