Medical Student Elective
Case of the Month
Submitted by: Courtney Yuhas, MS4, New York University School of Medicine
Chief ComplaintDizziness x 2 days
HPI35 y/o male, h/o HTN and on no medications, BIB EMS from his workplace for “dizziness.” Pt says his boss had called an ambulance for him without him even knowing, because a costumer had complained the pt looked “drunk on the job.” He had first noticed feeling “off” when he woke up two days ago. He describes his dizziness as an overall unsteady sensation, saying the world appears to be on a slant to him, and he has intermittently been seeing double over the past two days. The onset of this was gradual and it has never happened to him before.
PMHHypertension, no longer] treated with medication
Social HistoryPatient denies alcohol, tobacco, and illicit drug use.
Family HistoryNone relevant
MedsPreviously on amplodipine, discontinued several weeks ago
ROSPositive for lower back pain, which pt states is a chronic problem
PE (pertinent)Vitals: BP 132/90; HR 86; RR 16; O2 98%; FS 100, Oral temp. 99.5General: A&Ox3, NAD, well developed, lying in bed comfortableHead: autraumatic, normocephalic, no sinus pain or temporal painEars: L TM wnl, but R TM difficult to visualize due to cerumenEyes: EOMI, PERRL, sclera noninjected, nystagmus on vertical gaze; no visual field deficits, but when pt covers R eye, he states that he only sees examiner’s R eye (this was resolved on attending exam); denies diplopia during exam; visual acuity 20/20Nose: wnlThroat: oropharynx w/o erthema or lesions; uvula midlineNeck: supple, full ROM, no palpable LNs, no thyomegaly, no C-spine tendernessCV: RRR, no MRG, nl S1 and S2Resp: CTAB, no RRWChest: no deformities, nontenderAbdomen: soft, NT, ND, +BS, no massesBack: no CVA tenderness, no midline or paraspinal tendernessExtremities: no c/c/eSkin: no rashes, lesions, abrasionsNeuro: A&Ox3; CN II-XII intact; full strength in U&L extremities; full sensation; biceps and patellar reflexes wnl; NL speech, although somewhat slow; gait slow and unsteady with questionable broad base, pt seems to concentrate significantly to keep from falling, must lean on support to turn around; no pronator drift; vertical nystagmus; shin-to-knee test wnl; finger-to-nose test: pt moves slowly and overshoots finger several times; no dysdiadochokinesis on rapid, alternating movements
Recap35 y/o male, h/o htn, c/o 2 days of “dizziness”, noticed to act intoxicated at work, normal vitals but abnormal PE findings (unsteady gait, dysmetria, vertical nystagmus)
Differential DiagnosisVertigo (peripheral or central), stroke, mass lesion in brain, intracranial bleed, multiple sclerosis, intoxication, electrolyte imbalance, hydrocephalus, Wernicke’s encephalopathy, tertiary syphillis, hepatic encephalopathy
LabsCBC: Hbg 13.8, Hct 38.6, WBC 7.7, Plt 230Hepatic Panel: TP 7.8, Alb 5.0, Bili Tot 3.3, Alk Phos 59, AST 49, ALT 46, Bili Dir 1.5BMP: Na 123, K 4.2, Cl 77, HCO3 30, BUN 13, Cr 0.6, Glu 100Salicylate Level: <1mg/dLAlcohol (ethyl) Level: <10mg/dL
CT HeadPatient sent for an emergent non-contrast CT of the head. “No evidence of intracranial hemorrhage, mass lesion, or acute infarct
What is the most likely diagnosis for this patient?
Hypotonic Isovolemic Hyponatremia
CourseOn further questioning, it was discovered that the patient had been trying to lose weight and had gotten into the habit of drinking excessive amounts of water…about 5-6 liters per day! It was immediately decided to water-restrict the patient and begin slowly repleting his sodium with 1L of normal saline IV. The patient was later admitted to a medicine floor for further treatment, workup, and monitoring. It took three days to sufficiently correct his sodium.
BackgroundHyponatremia is the most common electrolyte disorder encountered in clinical medicine with up to 6.1 million people treated for it in the US annually. Twenty-five percent of these patients are initially treated in the emergency room. Several things can lead to hyponatremia, and management differs depending on the etiology behind it. One has to take into account a patient’s osmolality and volume status to tease out the potential cause of his or her low sodium level.Some examples of causes:
The dangers of hyponatremia arise as a result of fluid shifts: If sodium is low in the extracellular space, water flows intracellularly (from high water concentration to low water concentration), and cells may swell. This can lead to cerebral edema and its related sequelae. If untreated, brain herniation, obtundation, coma, seizure, and death may occur.In this case, the patient was diagnosed with psychogenic/primary polydipsia, a clinical disorder characterized by excessive water-drinking in the absence of a physiologic stimulus to drink. His hyponatremia was “chronic” (developed over more than 48 hours) and he was euvolemic, but he was symptomatic.
Guidelines for Treatment
Take Home Messages
SourcesBoscoe et al. Cost of illness of hyponatremia in the United States. Cost Effectiveness and Resource Allocation. 2006, 4:10.Craig et al. Hyponatremia in the Emergency Department. http://emedicine.medscape.com/article/767624-overview. April 2010.Dundas et al. Psychogenic polydipsia review: Etiology, Differential, and Treatment. Current Psychiatry Reports. 2007, 9:236-241.Ghali, Jalal. Mechanisms, Risks, and New Treatment Options for Hyponatremia. Cardiology. 2008, 111: 147-157.
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