Isolated Hyponatremic Dehydration in the Setting of COVID-19–Associated Gastroenteritis in a Toddler

**Background:** The COVID-19 pandemic has generally affected children less severely than adults, with most pediatric cases being mild or asymptomatic. Common symptoms include low-grade fever, dry cough, and fatigue, but gastrointestinal (GI) symptoms such as nausea, vomiting, and diarrhea have also been reported. A post-COVID-19 multisystem inflammatory syndrome in children (MIS-C) has emerged, but acute presentations with isolated hyponatremic dehydration due to COVID-19-associated gastroenteritis have not been previously described. This case report presents the first such instance in a toddler.

**Methods:** This is a single case report of a 15-month-old male who presented to the pediatric emergency department (ED) with a history of recent hospitalization for gastroenteritis requiring intravenous rehydration. Three days after discharge, he continued to have intermittent nonbloody, nonbilous emesis, tactile fevers, and nonbloody diarrhea for 4 days. He represented to the ED after >24 hours of anuria. On arrival, he was afebrile (98.6°F), tachycardic (129 bpm), with normal respiratory rate (28) and oxygen saturation (98%). Physical exam showed fatigue, poor skin turgor, delayed capillary refill >2 seconds, and no rashes or abdominal abnormalities. Laboratory findings included: white blood cell count 7/nL with lymphopenia (20%), hemoglobin/hematocrit 12.1 g/dL and 36%, platelets 381/nL, sodium (Na) 124 mEq/L, chloride 76 mEq/L, anion gap 28 mEq/L (metabolic acidosis), blood urea nitrogen/creatinine 14 mg/dL/0.4 mg/dL, and serum osmolality 258 mOsm/L. Hepatic panel was normal. A nasogastric tube was placed and a 20 mL/kg normal saline bolus (320 mL total) was given. He was admitted with hyponatremic dehydration. On the pediatric floor, he was afebrile (98°F), tachycardic (123 bpm), normotensive (111/70 mm Hg), with a 1.7-kg weight loss since prior admission. Further labs: phosphorus 3.7 mg/dL, magnesium 2 mg/dL, C-reactive protein 2.2 mg/L, urinary electrolytes with <20 mEq/L of Na and chloride. Reducing substances, occult blood, and stool cultures were negative. A COVID-19 nasal swab PCR was positive. Fluid deficit was estimated at 20% (1560 mL) and Na deficit at 80 mEq. Repletion over 24 hours used D5 normal saline at 195 mL/hr for first 8 hours, then 120 mL/hr for 16 hours, equating to Na repletion rates of 5 and 2.5 mEq/h, respectively. A repeat basic metabolic panel at 12 hours showed Na 125 mEq/L and bicarbonate 10.2 mEq/L, prompting addition of 10 mEq/L sodium bicarbonate. Na normalized to 140 mEq/L by hospital day 3, diarrhea resolved by day 4. He never developed respiratory symptoms or required oxygen. A baseline chest radiograph showed bilateral perihilar interstitial markers. By hospital day 4 (day 17 of illness), he tolerated regular diet/fluids, returned to baseline mental status, and was discharged. A televisit 3 days later reported an asymptomatic well-child.

**Key Results:** The patient presented with severe hyponatremic dehydration (Na 124 mEq/L) and metabolic acidosis (anion gap 28 mEq/L) in the setting of COVID-19-associated gastroenteritis, without any respiratory symptoms. He required aggressive fluid and electrolyte repletion over 3 days. His inflammatory markers were normal (CRP 2.2 mg/L), and he did not meet criteria for MIS-C. Urinary electrolytes showed low Na (<20 mEq/L) and chloride, consistent with hypovolemic hyponatremia from extrarenal losses, not SIADH. Stool studies were negative for other pathogens. The patient recovered fully.

**Clinical Implications:** This case demonstrates that COVID-19 in children can present with isolated GI symptoms leading to severe hyponatremic dehydration, even in the absence of respiratory involvement. Clinicians should maintain a high index of suspicion for COVID-19 in children with prolonged GI symptoms and electrolyte abnormalities, especially during the pandemic. Early recognition and appropriate fluid and electrolyte management are crucial to prevent complications. This presentation is distinct from MIS-C, which involves multisystem inflammation and fever. The pathophysiology may involve angiotensin-converting enzyme 2 receptor expression in the GI tract, leading to viral entry and GI symptoms without villous atrophy, possibly due to protein dysregulation or toxin production. Hyponatremia in COVID-19 may also be due to SIADH, but in this case, hypovolemic hyponatremia from GI losses was more likely. This case expands the spectrum of pediatric COVID-19 presentations and underscores the need for testing in children with nonpulmonary manifestations.