Paramedics were called to a campus party after a 911 call was placed with a report that a 19-year-old male suddenly “passed out.”
Paramedics were called to a campus party after a 911 call was placed with a report that a 19-year-old male suddenly “passed out.” The paramedics who brought him to the emergency department (ED) by ambulance were told that he is a college student at a nearby university. The patient is not accompanied by anyone. When first-responders arrived, no one at the party was able to give a consistent history of what had happened.
A few students at the party said he suddenly passed out but no one admitted to being with him when he lost consciousness. Further, nobody was able to recall exactly what time he started to become unwell or to display any unusual symptoms before he was found to be unconscious. It is unclear who found him and where exactly he was when he passed out, but the students concurred that he had attended the party. Witnesses denied that the young man was drinking or using drugs or that there was any alcohol or illegal substances at the event. Most of the students were in the process of leaving at the time the ambulance arrived.
The patient's parents were called when he arrived at the hospital. On their three-hour trip way to the ED, the parents provided his medical history, stating that there is no significant medical illness in the family. They also reported that he has no allergies and he does not take any medications except for topical over-the-counter acne cream.
Vital Signs. Pulse is 135, his blood pressure is 90/45, and respiratory rate is 32 breaths per minute. The patient is conscious, but he does not seem to be aware of his surroundings. He is too lethargic to answer questions or follow commands. He opens his eyes briefly in response to sounds. He does not appear to have any involuntary movements and he is not combative.
Skin appears normal with no rashes, wounds, bruises, or discoloration. The patient has had involuntarily loss of bladder control twice after arriving to the ED. Heart rate is regular. Pulses are weak throughout bilateral upper and lower extremities and he does not have carotid bruits. Breathing is shallow and rapid, with clear breath sounds. The abdomen is soft and non-distended with no tenderness.
Neurological examination. The face is symmetric with pupils slightly dilated, equal, round, and reactive to light. Extra ocular movements appear intact without nystagmus. Reflexes are brisk on both the upper and lower extremities without asymmetry and bilateral downgoing response of the toes. Muscle tone is normal in the left upper and lower extremities. In the right upper and lower extremities, muscle tone is diminished and the right leg is flaccid. There is no response to sensory stimuli of his extremities.
Laboratory tests. Blood alcohol level was 0.281%. CBC and electrolyte tests were unremarkable with the exception of serum Na level that was found to be 132 mEq/L (normal range is 135 and 145 milliequivalents per liter [mEq/L]).
Computed tomography. Brain CT scan was normal.
Diagnosis: central pontine myelinolysis
Central pontine myelinolysis (CPM) (also known osmotic demyelination syndrome, or ODS), is a rare demyelinating syndrome that can occur as the result of rapid changes in fluid and electrolyte balance, particularly with changes in sodium level. It is primarily a concern in the inpatient hospital setting and may occur with rapid correction of electrolyte abnormalities. Patients with liver disease, kidney disease, diabetes, or who are recent organ transplant recipients are most prone to osmotic imbalance and to adverse responses to electrolyte and fluid correction.1
Deliberate polydipsia is a rare cause of the syndrome but can occur for a number of reasons.2 Patients who have psychiatric disorders have been noted to drink excessive volumes of water, often without a clear explanation. Young patients who drink too much alcohol rapidly, either to become intoxicated or as part of a game or a dare may also experience rapid electrolyte shifts. In addition, patients who drink excessive fluids as part of a “health cleanse” may not consume enough nutrients to balance electrolyte levels. Any of these scenarios can induce hyponatremia and early signs of central pontine myelinolysis.
The clinical presentation can vary, but early symptoms almost always involve impairment of consciousness, while focal neurological deficits develop later. The time course of demyelination is rapid and may vary from hours to days. Brain CT scan would not be expected to show changes, and brain MRI, which provides a clearer view of the brainstem, can show demyelinating changes in the pons, although these changes may not become apparent until days after irreversible damage has taken place.
Slow and careful correction of electrolyte alterations are key the prevention of CPM. In the above case, the patient needed IV fluid and electrolyte replacement with 0.3% hypertonic saline solution and close monitoring of his sodium level. Additionally, vasopressin receptor antagonists promote excretion of water without altered sodium or potassium loss.3
If CPM has already taken place, some patients experience an improvement of symptoms without permanent disability, but there are no clear prognostic indicators. Steroids have been used in an attempt to reverse pontine damage, but there is no evidence that this approach is effective.
Take home points
• When there is an unclear history of events leading to loss of consciousness, rapid diagnostic testing is necessary
• CPM is a rare condition, but it should be considered in the differential diagnosis when a patient has a change in mental status
• Rapid consumption of alcohol can cause hyponatremia or other electrolyte and fluid imbalances
1. Singh TD, Fugate JE, Rabinstein AA. Central pontine and extrapontine myelinolysis: a systematic review. Eur J Neurol. 2014;21:1443-1450.
2. Penders TM, Stanciu CN, Ganpat P, Ingersoll JA. Psychogenic polydipsia, hyponatremia and osmotic myelinolysis. BMJ Case Rep. 2015; Jan 27.
3. Sterns RH, Silver S, Kleinschmidt-DeMasters BK, Rojiani AM. Current perspectives in the management of hyponatremia: prevention of CPM. Expert Rev Neurother. 2007;7:1791-1797.