589742
research-article2015
CPJXXX10.1177/0009922815589742Clinical PediatricsMetropulos and Antoon
Resident Rounds
Primary Polydipsia in a Child
Clinical Pediatrics 1–3 © The Author(s) 2015 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/0009922815589742 cpj.sagepub.com
Diana Metropulos, MD1, and James W. Antoon, MD, PhD2
Case Report A 4-year-old Caucasian boy was admitted for evaluation of polyuria. The patient and family reported increasingly worsening polyuria and polydipsia over the previous 6 months. The polyuria had been intermittent but worsening in frequency and volume over the past 2 months, including development of intermittent nocturnal enuresis 3 to 4 times a week over this time. The patient’s nutritional intake was highly variable and he preferred beverages included water, milk, or soda. He had no fever, abdominal pain, vomiting, diarrhea, fatigue, upper respiratory symptoms, headache, vision changes, weight changes, or other symptoms. He had received the recommended routine immunizations and was taking no medications prior to the onset of his symptoms. Family history was significant for paternal aunt with panhypopituitarism and nystagmus, paternal grandparents with diabetes and maternal uncle with delayed puberty. The patient recently moved from an army base in South Korea 1 month prior to evaluation. The patient was born at 33 weeks gestation and previous magnetic resonance imaging (MRI) performed in Korea, presumably due to prematurity, showed a mass believed to be a Rathke’s cleft cyst. His vital signs on admission were a temperature of 36.9°C, heart rate of 102 beats/min, blood pressure of 103/71 mm Hg, respiratory rate of 20 breaths/min, and weight of 17.45 kg. On physical examination, patient was well appearing and interactive. Pupils were equal round and reactive to light and extraocular muscles were intact. No palpable lymphadenopathy was present. Respiratory, cardiovascular, and abdominal exams were unremarkable. Neurologic examination was within normal limits for age, including normal cranial nerve exam, gait and reflexes. Initial laboratory values were as follows: sodium 141 mmol/L, potassium 4.4 mmol/L, chloride 106 mmol/L, bicarbonate 22 mmol/L, blood urea nitrogen 16 mg/dL, creatinine 0.4 mg/dL, glucose 112 mg/dL, white blood cells 6.7/mm3, hemoglobin 11.1 gm/dL, hematocrit 33.7 gm/dL, platelets 337, anemia profile consistent with iron deficiency, prolactin 10 ng/mL, free T4 1.32 ng/dL. Urinalysis was significant for a specific gravity of 1.003 and otherwise normal.
The patient was admitted for further workup. Repeat MRI scan was negative for any masses or lesions. Results of water deprivation test are depicted in Table 1. Given the patient’s normal exam, laboratory testing and lack of clinical symptoms other than polyuria and polydipsia a diagnosis was made and patient was discharged home without medications.
Final Diagnosis Primary polydipsia.
Discussion The case above highlights the difficulty in working up and diagnosing primary polydipsia. The differential diagnosis of polyuria and polydipsia in a child is broad and includes common and uncommon systemic disorders, including those of the endocrine, renal and neurologic systems.1-4 The causes of excessive water intake are varied and include psychiatric (eg, posttraumatic stress disorder, schizophrenia, behavioral), neurologic (hypothalamic lesions), autoimmune (including sarcoidosis), pharmacologic (phenothiazine, anticholinergics), and iatrogenic.1,2,5-9 Primary polydipsia (also known as psychogenic polydipsia, behavioral polydipsia, habitual polydipsia, or excessive water intake) is a rare but known cause of polyuria and polydipsia in childhood. It is most often associated with behavioral/habitual intake in infancy or early childhood.1 In children without signs or laboratory symptoms of diabetes, primary polydipsia (PP) is most often confused with diabetes insidious (DI), as demonstrated in the case of above. Primary polydipsia can cause physiologic suppression of serum antidiuretic hormone (ADH) resulting 1
Feinberg School of Medicine, Northwestern University, Chicago, IL, USA 2 Children’s Hospital, University of Illinois Hospital & Health Sciences System, Chicago, IL, USA. Corresponding Author: James W. Antoon, Department of Pediatrics, University of Illinois at Chicago, 840 S. Wood Street, Chicago, IL 60612, USA. Email: [email protected]
Downloaded from cpj.sagepub.com at University of Sussex Library on July 26, 2015
2
Clinical Pediatrics
Table 1. Water Deprivation Test. Laboratory Serum sodium Serum osmolality Urine pH Urine specific gravity Urine osmolality
Normal Values 135-145 mmol/L 275-295 mOsm/kg 1.003-1.030 5.0-9.0 Variable mOsm/kg
0h
1h
2h
3h
4h
5h
6h
7h
140 295 6.5 1.003 174
141 297 6.0 1.003 207
139 289 7.0 1.009 484
139 293 7.5 1.009 502
139 295 7.0 1.013 641
141 298 6.5 1.015 694
139 293 7.0 1.015 710
140 293 7.0 1.015 714
Table 2. Laboratory Values Associated With Polyuria Differential Diagnosis. After Water Deprivation
Baseline Normal Central DI Nephrogenic DI (cortex)
Serum ADH Normal Decreased
Normal or increased Nephrogenic DI (medullary) Normal or increased Primary polydipsia Decreased
Serum Sodium
Serum Osmolality
Normal Normal to increased Increased
Normal Normal to increased Increased
Increased Normal
Urine Urine Osmolality Serum ADH Osmolality
After ADH Urine Osmolality
50-1500
research-article2015
CPJXXX10.1177/0009922815589742Clinical PediatricsMetropulos and Antoon
Resident Rounds
Primary Polydipsia in a Child
Clinical Pediatrics 1–3 © The Author(s) 2015 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/0009922815589742 cpj.sagepub.com
Diana Metropulos, MD1, and James W. Antoon, MD, PhD2
Case Report A 4-year-old Caucasian boy was admitted for evaluation of polyuria. The patient and family reported increasingly worsening polyuria and polydipsia over the previous 6 months. The polyuria had been intermittent but worsening in frequency and volume over the past 2 months, including development of intermittent nocturnal enuresis 3 to 4 times a week over this time. The patient’s nutritional intake was highly variable and he preferred beverages included water, milk, or soda. He had no fever, abdominal pain, vomiting, diarrhea, fatigue, upper respiratory symptoms, headache, vision changes, weight changes, or other symptoms. He had received the recommended routine immunizations and was taking no medications prior to the onset of his symptoms. Family history was significant for paternal aunt with panhypopituitarism and nystagmus, paternal grandparents with diabetes and maternal uncle with delayed puberty. The patient recently moved from an army base in South Korea 1 month prior to evaluation. The patient was born at 33 weeks gestation and previous magnetic resonance imaging (MRI) performed in Korea, presumably due to prematurity, showed a mass believed to be a Rathke’s cleft cyst. His vital signs on admission were a temperature of 36.9°C, heart rate of 102 beats/min, blood pressure of 103/71 mm Hg, respiratory rate of 20 breaths/min, and weight of 17.45 kg. On physical examination, patient was well appearing and interactive. Pupils were equal round and reactive to light and extraocular muscles were intact. No palpable lymphadenopathy was present. Respiratory, cardiovascular, and abdominal exams were unremarkable. Neurologic examination was within normal limits for age, including normal cranial nerve exam, gait and reflexes. Initial laboratory values were as follows: sodium 141 mmol/L, potassium 4.4 mmol/L, chloride 106 mmol/L, bicarbonate 22 mmol/L, blood urea nitrogen 16 mg/dL, creatinine 0.4 mg/dL, glucose 112 mg/dL, white blood cells 6.7/mm3, hemoglobin 11.1 gm/dL, hematocrit 33.7 gm/dL, platelets 337, anemia profile consistent with iron deficiency, prolactin 10 ng/mL, free T4 1.32 ng/dL. Urinalysis was significant for a specific gravity of 1.003 and otherwise normal.
The patient was admitted for further workup. Repeat MRI scan was negative for any masses or lesions. Results of water deprivation test are depicted in Table 1. Given the patient’s normal exam, laboratory testing and lack of clinical symptoms other than polyuria and polydipsia a diagnosis was made and patient was discharged home without medications.
Final Diagnosis Primary polydipsia.
Discussion The case above highlights the difficulty in working up and diagnosing primary polydipsia. The differential diagnosis of polyuria and polydipsia in a child is broad and includes common and uncommon systemic disorders, including those of the endocrine, renal and neurologic systems.1-4 The causes of excessive water intake are varied and include psychiatric (eg, posttraumatic stress disorder, schizophrenia, behavioral), neurologic (hypothalamic lesions), autoimmune (including sarcoidosis), pharmacologic (phenothiazine, anticholinergics), and iatrogenic.1,2,5-9 Primary polydipsia (also known as psychogenic polydipsia, behavioral polydipsia, habitual polydipsia, or excessive water intake) is a rare but known cause of polyuria and polydipsia in childhood. It is most often associated with behavioral/habitual intake in infancy or early childhood.1 In children without signs or laboratory symptoms of diabetes, primary polydipsia (PP) is most often confused with diabetes insidious (DI), as demonstrated in the case of above. Primary polydipsia can cause physiologic suppression of serum antidiuretic hormone (ADH) resulting 1
Feinberg School of Medicine, Northwestern University, Chicago, IL, USA 2 Children’s Hospital, University of Illinois Hospital & Health Sciences System, Chicago, IL, USA. Corresponding Author: James W. Antoon, Department of Pediatrics, University of Illinois at Chicago, 840 S. Wood Street, Chicago, IL 60612, USA. Email: [email protected]
Downloaded from cpj.sagepub.com at University of Sussex Library on July 26, 2015
2
Clinical Pediatrics
Table 1. Water Deprivation Test. Laboratory Serum sodium Serum osmolality Urine pH Urine specific gravity Urine osmolality
Normal Values 135-145 mmol/L 275-295 mOsm/kg 1.003-1.030 5.0-9.0 Variable mOsm/kg
0h
1h
2h
3h
4h
5h
6h
7h
140 295 6.5 1.003 174
141 297 6.0 1.003 207
139 289 7.0 1.009 484
139 293 7.5 1.009 502
139 295 7.0 1.013 641
141 298 6.5 1.015 694
139 293 7.0 1.015 710
140 293 7.0 1.015 714
Table 2. Laboratory Values Associated With Polyuria Differential Diagnosis. After Water Deprivation
Baseline Normal Central DI Nephrogenic DI (cortex)
Serum ADH Normal Decreased
Normal or increased Nephrogenic DI (medullary) Normal or increased Primary polydipsia Decreased
Serum Sodium
Serum Osmolality
Normal Normal to increased Increased
Normal Normal to increased Increased
Increased Normal
Urine Urine Osmolality Serum ADH Osmolality
After ADH Urine Osmolality
50-1500
