Key Clinical Message
Eating disorders and distal renal tubular acidosis are risk of refeeding
sydrome. Frequent measurement of serum phosphorus levels at the
initiation of nutrition and rapid administration of phosphate
preparations are required to prevent organ failure.
Introduction
Refeeding syndrome (RFS) is caused by electrolyte and fluid movement
upon resuming nutrition either orally, enterally, or parenterally, in
severely undernourished patients.1 Distal renal
tubular acidosis (dRTA) is caused by decreased acid excretion from the
distal tubules despite metabolic acidosis and a normal or mildly reduced
glomerular filtration rate. We encountered a case of RFS in a patient
with an underlying eating disorder and dRTA.
Case History
A 12-year-old girl visited the emergency department after vomiting for 3
days and experiencing generalized muscle weakness owing to vomiting. Her
father had ulcerative colitis. She had neither growth retardation nor
previous episodes of muscle weakness, although she had one previous
episode of frequent vomiting. However, she had restricted her diet due
to bullying at school 6 months earlier and had observed a 3.4 kg weight
loss. As her serum potassium level was 1.3 mEq/L, she was hospitalized
with an initial diagnosis of hypokalemic quadriplegia. Her blood
pressure was 125/88 mmHg without diminished cutaneous turgor. Her body
mass index (BMI) was 13.5 kg/m2 (height, 140.3 cm;
weight, 26.7 kg). Blood gas analysis upon admission revealed metabolic
acidosis at pH 7.181, with a base excess of -16.3 mmol/L and a normal
anion gap (14.7 mEq/L). After admission, treatment was initiated with
potassium infusion of up to 0.2 mEq/kg/h and total calorie intake of 300
kcal/day by parenteral nutrition. The patient’s vomiting and generalized
muscle weakness resolved and there was improvement in hypokalemia and
metabolic acidosis. However, on Day 3, her serum phosphorus and creatine
kinase (CK) levels decreased to 1.4 mg/dL and increased to 7726 U/L,
respectively (Fig. 1). Therefore, we diagnosed RFS with rhabdomyolysis.
To treat RFS, oral phosphate administration (900 mg/day of dibasic
sodium phosphate anhydrous) was initiated. The serum phosphorus levels
normalized on Day 6. Serum CK peaked on Day 4 (12,439 U/L) but
normalized on Day 7. Potassium correction continued until Day 7, with
oral phosphate preparation continued for an additional 3 days. She was
discharged after 31 days in hospital with no observed organ failure. In
this case, the patient’s metabolic acidosis had a normal anion gap, her
urinary beta 2-microglobulin level was high (64,567 μg/L), and her blood
pH was lower than 7.30. The patient’s urine pH did not fall below 5.5.
Moreover, we found that her HCO3- excretion fraction with sodium
bicarbonate load was 2.16% (normal: <3%). Her condition was
complicated with dRTA. At the last follow up, neither nephrocalcinosis
nor sensorineural hearing loss had been observed. Furthermore, her
anti-SS-A antibody titer increased to 65.7 U/mL, which was considered to
be dRTA caused by Sjogren’s syndrome, rather than primary dRTA. She has
continued oral administration of sodium bicarbonate and potassium
preparations. The patient and her patients agreed to the publication of
this case report.
Discussion
In general, when sugar is rapidly supplied to an undernourished patient,
insulin is simultaneously released with phosphate, potassium, and
magnesium which are taken into the cell, resulting in
hypophosphatemia.1 As a result, 2,3-diphosphoglycerate
levels in erythrocytes are reduced and the oxygen affinity of hemoglobin
is lowered, leading to reduced oxygen supply to peripheral
tissues.1 RFS reportedly occurs in 10-40% of
undernourished patients.2 Complications associated
with RFS include heart, respiratory and/or renal failures, and evidence
of skeletal muscle, nervous system, endocrine, and/or blood
disorders.3
In this case, hypokalemia was observed due to an underlying eating
disorder beginning from 6 months prior to admission, and latent dRTA.
Hypokalemia and low BMI have been previously reported as high-risk
factors for RFS development.3 To prevent RFS,
healthcare professionals must recognize the possibility of a patient to
develop RFS and understand the risk factors from the introduction of
nutrition therapy. Patients must be monitored frequently, and in case of
low serum phosphorus levels, phosphoric acid preparations must be
administered promptly.4
At the beginning of treatment, oral intake was difficult for our patient
due to nausea; therefore, parenteral nutrition was initiated with a
total caloric value of 300 kcal/day (approximately 11.5 kcal/kg/day).
This was in line with the recommended dose for patients at high-risk for
RFS at the start of nutrition, which is 5-15
kcal/kg/day.5 The patient’s calorie intake was
carefully increased, but RFS developed, nonetheless. However, no severe
organ failure related to RFS was observed due to the early recognition
of hypophosphatemia and the prompt initiation of orally administered
phosphate preparations.
In conclusion, to the best of our knowledge, this is the first reported
case of a patient with RFS complicated by dRTA. Patients with a low BMI
may be more likely to develop RFS when there is an underlying disease,
such as dRTA. Therefore, frequent measurement of serum phosphorus levels
at the initiation of nutrition and rapid administration of phosphate
preparations are required to prevent RFS-related organ failure.
Author Contributions:
YS wrote the manuscript. YA performed in-hospital care for this case. HK
critically reviewed the manuscript. All authors read and approved the
final manuscript.
Conflicts of interest
None declared
Abstract
We experienced refeeding syndrome (RFS) with an eating disorder and
distal renal tubular acidosis (dRTA). A low body mass is high-risk
factors for RFS development. Therefore, frequently measurement of serum
phosphorus levels at the initiation of nutrition and rapid
administration of phosphate preparations are required to prevent
RFS-related organ failure.
References
1. Crook, M. A. 2014. Refeeding syndrome: problems with definition and
management. Nutrition 30:1448-1455.
2. Walmsley, R. S. 2013. Refeeding syndrome: screening, incidence, and
treatment during parenteral nutrition. J Gastroenterol Hepatol
4:113-117.
3. National Collaborating Center for Acute Care. 2006. Nutrition Support
for Adults: Oral Nutrition Support, Enteral Tube Feeding and Parenteral
Nutrition. Clinical Guideline CG32, London.
4. Afzal, N. A., Addai, S., Fagbemi, A., Murch, S., Thomson, M., and
Heuschkel, R. 2002. Refeeding syndrome with enteral nutrition in
children: a case report, literature review and clinical guidelines. Clin
Nutr 21:515-520.
5. Reber, E., Friedli, N., Vasiloglou, M. F., Schuetz, P., and Stanga,
Z. 2019. Management of refeeding syndrome in medical inpatients. J Clin
Med 8:2202.
Figure Legend
Fig. 1 Clinical course in a 12-year-old girl
serum K - serum potassium, serum P - serum phosphorus, CIV continuous
intravenous infusion