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Year : 2019  |  Volume : 24  |  Issue : 2  |  Page : 151-153

Refeeding syndrome in catatonic schizophrenia

1 Department of Psychiatry, Subharti Medical College, Meerut, Uttar Pradesh, India
2 Department of Medicine, Subharti Medical College, Meerut, Uttar Pradesh, India

Date of Web Publication22-Jul-2020

Correspondence Address:
Supriya Agarwal
Subharti Medical College, Meerut, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jmhhb.jmhhb_3_19

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Refeeding syndrome is an uncommon but potentially fatal condition. It occurs in a patient who consumes a large amount of calories over a brief period of time after a sustained period of starvation. This syndrome is characterized by a high risk of cardiovascular collapse secondary to electrolyte imbalance if left untreated or if there is a delay in the management. Psychiatric patients with a diagnosis of schizophrenia or severe depression are known to refuse food for a prolonged period of time, thus creating a malnourished or starved metabolic state. The purpose of this article is to bring an acute awareness and sensitize the fellow psychiatrists about refeeding syndrome, a likely fatal possibility in a starved or malnourished patient on refeeding. Prompt recognition and management in collaboration with medical colleagues can save the life of these patients.

Keywords: Catatonia, refeeding syndrome, schizophrenia

How to cite this article:
Agarwal S, Biswas RK, Gupta A, Choudhary S. Refeeding syndrome in catatonic schizophrenia. J Mental Health Hum Behav 2019;24:151-3

How to cite this URL:
Agarwal S, Biswas RK, Gupta A, Choudhary S. Refeeding syndrome in catatonic schizophrenia. J Mental Health Hum Behav [serial online] 2019 [cited 2023 Jun 4];24:151-3. Available from: https://www.jmhhb.org/text.asp?2019/24/2/151/290511

  Introduction Top

Refeeding syndrome is well recognized in the literature for over 50 years and occurs after introduction of feeding following prolonged starvation or fasting, resulting in a series of metabolic and biochemical changes in the body.[1] This unfavorable metabolic response causes nonimmune-mediated harm to the body. It can be mild moderate or severe in intensity. With food in abundance, carbohydrates are the main sources of energy in an individual. Excess glucose promotes glycogenesis and increases cellular uptake of potassium. Starvation leads to fall in glucose levels within 24–72 h, resulting in release of peptide hormone glucagon and also reduction in insulin secretion.[2] Glucose levels are maintained by glycogenolysis, but glycogen stores rarely the last >72 h.[3] The demands for glucose are met by the process of gluconeogenesis, i.e., noncarbohydrate sources are metabolized to glucose, resulting in loss of body fat and protein and depletion of potassium, phosphate, and magnesium.[4],[5] The reintroduction of nutrition to a starved individual results in a rapid increase of serum insulin which pushes the extracellular potassium, phosphate, and magnesium to the intracellular compartment, leading to the fall of these extracellular ions.[2],[6],[7],[8] Formation of phosphorylated carbohydrate compound in the liver and skeletal muscles depletes intracellular Adenosine Triphosphate (ATP) and 2,3-diphosphoglycerate in the red blood cell. This leads to cellular dysfunction and inadequate oxygen delivery to the body's organs such as heart, resulting in cardiac decompensation. Fatal cardiac complications including arrhythmia and cardiac arrest could be the sequela of cardiac decompensation.

Patients with schizophrenia presenting with catatonia (19%–15%) can develop extreme psychomotor retardation and self-neglect leading to a catabolic state and are prone to develop refeeding syndrome.[9] We present a case of a patient with catatonic schizophrenia who developed refeeding syndrome.

  Case Report Top

Mr. A, a 36-year-old male patient with a diagnosis of schizophrenia, was admitted in the department. Written and informed consent was obtained. The chief complaints were of worsened self-care and poor food intake for the past 2 months. His family mentioned that the patient had developed persecutory beliefs and social withdrawal for >8 months. He had been losing weight gradually since the past few months. Mental status examination revealed catatonic features including stupor, negativism, and mutism in the patient. Bush–Francis Catatonia Rating Scale score was 18. The baseline body weight during assessment was 50 kg. Complete neurological examination and physical examination were normal. His neuroimaging was planned but was refused by attendants. The baseline electrolyte levels were within the normal limits (potassium: 3.1 mEq/L; calcium: 9 mg/dL; and sodium 135 mEq/L), and hemoglobin was 13.3 g/dL [Table 1]. Phosphate levels are not routinely checked in patients in our ward and were not evaluated at the baseline in this patient. On admission, the patient received 2 mg of lorazepam in injectable form. Further treatment was planned to start 4 mg of lorazepam in divided doses and 2 mg of risperidone for psychotic symptoms from day 1. After receiving 2 mg of injectable lorazepam, the patient showed significant improvement in his catatonic symptoms. His Bush–Francis Catatonia Rating Scale score was 1. The patient resumed consuming food within an hour of improvement in catatonic symptoms, and as documented, he consumed 12 chapatis, 2 bowls of dal, and some fruits as well as 5–6 glasses of water within a time frame of a couple of hours. Six hours postresolution of catatonic symptoms, he developed fall in blood pressure which reached 80 mmHg systolic and 60 mmHg diastolic. He developed bradycardia with an irregular pulse. The patient was immediately shifted to the intensive care unit; his antipsychotic medications were on hold. His investigations were repeated and vitals were stabilized. His hemoglobin was 13.3 g/dL. He developed hypocalcemia (7.3 mg/dL). His potassium was 3 mEq/L and sodium was 131 mEq/L. He appeared to be weak and lethargic. No other physical signs and symptoms were seen in the patient. All possible causes of delirium including brain etiology were ruled out through detail history and thorough neurological examination. After consultations with the physician and neurologist, the diagnosis of refeeding syndrome was suspected and management was started on similar lines. Possible factors weighing in favor of refeeding syndrome were poor nutritional and catatonic features at the outset in the patient, consumption of large amount calories over very short span of time, rapid onset of instability of vitals including hypotension, irregular heart rhythm, lethargy, weakness, fall in the levels of serum electrolytes, absence of any other possible cause of cardiac instability, or neurological deficit. Unfortunately, after 2 days of the treatment, the family refused to continue treatment for the patient despite no improvement in condition. The patient had to be discharged against medical advice, and the patient was henceforth lost to follow-up. The patient on discharge had deranged cardiac parameters with complaints of lethargy and weakness and generalized swelling.
Table 1: Biochemical parameters before and after refeeding

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  Discussion Top

Refeeding syndrome is often and mostly discussed in psychiatric disorders in the context of anorexia nervosa. There are a number of case reports substantiating the evidence of the risk of metabolic complications and fatal outcomes seen in patient of anorexia, on rapid reinstitution of calories. However, it has been less frequently recognized in patients of other psychiatric conditions. Patients who are starved or malnourished such as in catatonic presentation of schizophrenia or other catabolic states are also prone to develop refeeding syndrome because of similar metabolic changes. As mental health professionals, we are often not sensitized to possibility of medical emergency in the form of refeeding syndrome, of which our patients are vulnerable to develop. Only one similar case report of a patient with catatonic schizophrenia developing refeeding syndrome has been reported by Wei-Hao and Po-Han in 2014.[10] In contrast to our case, this patient developed symptoms of refeeding syndrome on the 7th day of hospitalization and was receiving feeding through a nasogastric tube. However, in our case, the patient improved dramatically from his catatonic state and developed symptoms of metabolic disturbance on the very 1st day after consuming a large amount of calories in a very short span of time. This medical complication could have been anticipated in our patient with increased awareness and adequate vigilance. Early features of refeeding syndrome are nonspecific and may go unrecognized, especially in the setting of psychiatric hospitalization where the index of suspicion regarding this critical medical emergency is low. Therefore, awareness among psychiatric fraternity of this syndrome and a high index of clinical suspicion are mandated for early and effective management of this potentially life-threatening condition in liaison with the medical colleagues.

  Conclusion Top

Awareness and anticipation of early sign and symptoms of refeeding syndrome in chronically malnourished or starved patients of psychiatric disorders can prompt early recognition and timely management of this fatal metabolic condition.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Crook MA, Hally V, Panteli JV. The importance of the refeeding syndrome. Nutrition 2001;17:632-7.  Back to cited text no. 1
Allison SP. Effect of insulin on metabolic response to injury. JPEN J Parenter Enteral Nutr 1980;4:175-9.  Back to cited text no. 2
Ekberg K, Landau BR, Wajngot A, Chandramouli V, Efendic S, Brunengraber H, et al. Contributions by kidney and liver to glucose production in the postabsorptive state and after 60 h of fasting. Diabetes 1999;48:292-8.  Back to cited text no. 3
Hill GL, Bradley JA, Smith RC, Smith AH, McCarthy ID, Oxby CB, et al. Changes in body weight and body protein with intravenous nutrition. JPEN J Parenter Enteral Nutr 1979;3:215-8.  Back to cited text no. 4
Nordenström J, Carpentier YA, Askanazi J, Robin AP, Elwyn DH, Hensle TW, et al. Free fatty acid mobilization and oxidation during total parenteral nutrition in trauma and infection. Ann Surg 1983;198:725-35.  Back to cited text no. 5
Klein CJ, Stanek GS, Wiles CE 3rd. Overfeeding macronutrients to critically ill adults: Metabolic complications. J Am Diet Assoc 1998;98:795-806.  Back to cited text no. 6
John HL. Metabolic Consequences of Starvation. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Thomas R. Ziegler, editors. Modern Nutrition in Health and Disease. 11th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2014. p. 660-77.  Back to cited text no. 7
Solomon SM, Kirby DF. The refeeding syndrome: A review. JPEN J Parenter Enteral Nutr 1990;14:90-7.  Back to cited text no. 8
Taylor MA, Fink M. Catatonia in psychiatric classification: A home of its own. Am J Psychiatry 2003;160:1233-41.  Back to cited text no. 9
Wei-Hao L, Po-Han C. Letter-to-the editor refeeding syndrome in schizophrenia. Taiwan J Psychiatry 2014;28:268-70.  Back to cited text no. 10


  [Table 1]


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