Case 8-2006: A Woman with Crohn's Disease and Altered Mental Status
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《新英格兰医药杂志》
To the Editor: Podolsky et al. (March 16 issue)1 describe a woman admitted to the hospital with a brain mass and hyponatremia (serum sodium, 131 mmol per liter). The day after admission, she had a generalized tonic–clonic seizure and required tracheal intubation. The discussants did not address the reason for this acute neurologic deterioration. The clinical picture may have been attributable to acute hospital-acquired hyponatremia. This patient was at high risk for acute neurologic deterioration from hyponatremia for a variety of reasons, including being a woman2 and having a space-occupying lesion, vasogenic cerebral edema,3 and a hypoxic event.4 Hyponatremia can lead to cytotoxic cerebral edema, which expands brain tissue and can lead to herniation. No data were provided on either the composition of the intravenous fluid administered on admission or the serum sodium level at the time of the neurologic deterioration. The acute neurologic deterioration may have been precipitated by the administration of hypotonic fluids, which further lowered the serum sodium level. We have previously advocated the administration of isotonic saline as a prophylactic measure to prevent neurologic complications from hospital-acquired hyponatremia.5
Michael L. Moritz, M.D.
Children's Hospital of Pittsburgh
Pittsburgh, PA 15213
michael.moritz@chp.edu
Juan C. Ayus, M.D.
University of Texas Health Science Center at San Antonio
San Antonio, TX 78229
References
Case Records of the Massachusetts General Hospital (Case 8-2006). N Engl J Med 2006;354:1178-1184.
Ayus JC, Wheeler JM, Arieff AI. Postoperative hyponatremic encephalopathy in menstruant women. Ann Intern Med 1992;117:891-897.
McJunkin JE, de los Reyes EC, Irazuzta JE, et al. La Crosse encephalitis in children. N Engl J Med 2001;344:801-807.
Ayus JC, Armstrong D, Arieff AI. Hyponatremia with hypoxia: effects on brain adaptation, perfusion, and histology in rodents. Kidney Int 2006;69:1319-1325.
Moritz ML, Ayus JC. Prevention of hospital-acquired hyponatremia: a case for using isotonic saline. Pediatrics 2003;111:227-230.
Dr. Harris, editor of the Case Records, replies: Moritz and Ayus suggest that hospital-acquired hyponatremia played a role in the deterioration in this patient's neurologic condition. Since this is not the diagnostic issue that Dr. Podolsky was asked to address in the Clinicopathological Conference, physicians involved in the care of the patient provided the following assessment.
Fourteen hours before the seizure, the serum sodium level was 131 mmol per liter, and the glucose level was 212 mg per deciliter. After correction for the elevated glucose level, the effective serum sodium level was 133 mmol per liter.1 Twelve hours before the seizure, the patient vomited several times, and an infusion of half-normal saline was begun. Immediately after the seizure, the serum sodium level was 127 mmol per liter, and the blood glucose level was 492 mg per deciliter; the corrected sodium level thus remained 133 mmol per liter. After the seizure, boluses and an infusion of normal saline were administered, and the serum sodium level rose to 135 mmol per deciliter. During the remainder of the patient's hospital stay, the serum sodium level remained between 127 and 133 mmol per deciliter, despite infusions of normal saline and correction of blood glucose levels.
The patient's physicians agree that isotonic saline is appropriate fluid replacement for patients with brain edema. However, this patient's serum sodium level does not appear to have been low enough to cause a seizure. Cerebral edema attributable to the large B-cell lymphoma of the brain likely contributed to the seizure. A syndrome of inappropriate antidiuretic hormone secretion may have caused persistent mild hyponatremia.
Nancy Lee Harris, M.D.
Massachusetts General Hospital
Boston, MA 02114
References
Fried LF, Palevsky PM. Hyponatremia and hypernatremia. Med Clin North Am 1997;81:585-609.
Michael L. Moritz, M.D.
Children's Hospital of Pittsburgh
Pittsburgh, PA 15213
michael.moritz@chp.edu
Juan C. Ayus, M.D.
University of Texas Health Science Center at San Antonio
San Antonio, TX 78229
References
Case Records of the Massachusetts General Hospital (Case 8-2006). N Engl J Med 2006;354:1178-1184.
Ayus JC, Wheeler JM, Arieff AI. Postoperative hyponatremic encephalopathy in menstruant women. Ann Intern Med 1992;117:891-897.
McJunkin JE, de los Reyes EC, Irazuzta JE, et al. La Crosse encephalitis in children. N Engl J Med 2001;344:801-807.
Ayus JC, Armstrong D, Arieff AI. Hyponatremia with hypoxia: effects on brain adaptation, perfusion, and histology in rodents. Kidney Int 2006;69:1319-1325.
Moritz ML, Ayus JC. Prevention of hospital-acquired hyponatremia: a case for using isotonic saline. Pediatrics 2003;111:227-230.
Dr. Harris, editor of the Case Records, replies: Moritz and Ayus suggest that hospital-acquired hyponatremia played a role in the deterioration in this patient's neurologic condition. Since this is not the diagnostic issue that Dr. Podolsky was asked to address in the Clinicopathological Conference, physicians involved in the care of the patient provided the following assessment.
Fourteen hours before the seizure, the serum sodium level was 131 mmol per liter, and the glucose level was 212 mg per deciliter. After correction for the elevated glucose level, the effective serum sodium level was 133 mmol per liter.1 Twelve hours before the seizure, the patient vomited several times, and an infusion of half-normal saline was begun. Immediately after the seizure, the serum sodium level was 127 mmol per liter, and the blood glucose level was 492 mg per deciliter; the corrected sodium level thus remained 133 mmol per liter. After the seizure, boluses and an infusion of normal saline were administered, and the serum sodium level rose to 135 mmol per deciliter. During the remainder of the patient's hospital stay, the serum sodium level remained between 127 and 133 mmol per deciliter, despite infusions of normal saline and correction of blood glucose levels.
The patient's physicians agree that isotonic saline is appropriate fluid replacement for patients with brain edema. However, this patient's serum sodium level does not appear to have been low enough to cause a seizure. Cerebral edema attributable to the large B-cell lymphoma of the brain likely contributed to the seizure. A syndrome of inappropriate antidiuretic hormone secretion may have caused persistent mild hyponatremia.
Nancy Lee Harris, M.D.
Massachusetts General Hospital
Boston, MA 02114
References
Fried LF, Palevsky PM. Hyponatremia and hypernatremia. Med Clin North Am 1997;81:585-609.