October ’12

Medical Student Elective

Case of the Month
Submitted by: Courtney Yuhas, MS4, New York University School of Medicine

Chief Complaint
Dizziness x 2 days

35 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.

Pertinent Negatives

  • Denies headache
  • Denies eye pain, blurry vision, photophobia
  • Denies hearing deficits, tinnitus
  • Denies recent head trauma
  • Denies LOC
  • Denies nausea, vomiting, diarrhea
  • Denies fevers, chills
  • Denies chest pain, SOB
  • Denies personal or family h/o stroke, brain tumors, aneurysms, seizures

Hypertension, no longer] treated with medication

Social History
Patient denies alcohol, tobacco, and illicit drug use.

Family History
None relevant

Previously on amplodipine, discontinued several weeks ago

Shellfish, NKDA

Positive 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. 99.5
General: A&Ox3, NAD, well developed, lying in bed comfortable
Head: autraumatic, normocephalic, no sinus pain or temporal pain
Ears: L TM wnl, but R TM difficult to visualize due to cerumen
Eyes: 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 20/20
Nose: wnl
Throat: oropharynx w/o erthema or lesions; uvula midline
Neck: supple, full ROM, no palpable LNs, no thyomegaly, no C-spine tenderness
CV: RRR, no MRG, nl S1 and S2
Resp: CTAB, no RRW
Chest: no deformities, nontender
Abdomen: soft, NT, ND, +BS, no masses
Back: no CVA tenderness, no midline or paraspinal tenderness
Extremities: no c/c/e
Skin: no rashes, lesions, abrasions
Neuro: 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

35 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 Diagnosis
Vertigo (peripheral or central), stroke, mass lesion in brain, intracranial bleed, multiple sclerosis, intoxication, electrolyte imbalance, hydrocephalus, Wernicke’s encephalopathy, tertiary syphillis, hepatic encephalopathy

CBC: Hbg 13.8, Hct 38.6, WBC 7.7, Plt 230
Hepatic Panel: TP 7.8, Alb 5.0, Bili Tot 3.3, Alk Phos 59, AST 49, ALT 46, Bili Dir 1.5
BMP: Na 123, K 4.2, Cl 77, HCO3 30, BUN 13, Cr 0.6, Glu 100
Salicylate Level: <1mg/dL
Alcohol (ethyl) Level: <10mg/dL

CT Head
Patient 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

On 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.

Hyponatremia 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:

  • For hypertonic hyponatremia: hyperglycemia, mannitol, ethylene glycol, toluene
  • For isotonic hyponatremia: hyperlipidemia, hyperproteinemia
  • For hypotonic hypovolemic hyponatremia: vomiting, diarrhea, burns, pancreatitis, diuretics, aldosterone deficiency
  • For hypotonic hypervolemic hyponatremia: cirrhosis, CHF, acute renal failure, nephrotic syndrome
  • For hypotonic isovolemic hyponatremia: SIADH (lung cancer, hypothyroidism, sarcoidosis), primary polydipsia

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

  • Fluid restriction of 0.8 to 1.5 L/d
  • Correct [Na+] by 1-2 mEq/L for the first few hours with 0.9% NaCl.
  • Administration of furosemide, 20-40mg IV, may also be considered.
  • Rapid correction with hypertonic saline (3%) should be infused at a rate of 1-6 mL/kg if seizures and/or coma are present.
  • To prevent central pontine myelinolysis it is recommended that correction be less than 12 mEq/L the first day and less than 6 mEq/L/d for every day thereafter
  • Aggressive correction can be slowed or discontinued at serum sodium levels of 130 to 135 mmol/L.

Take Home Messages

  • Hyponatremia is the most common electrolyte disturbance in clinical medicine.
  • There are several classes of hyponatremia based on tonicity and volume status.
  • Symptomatic hyponatremia can present with many nonspecific findings, such as nausea, vomiting, lethargy, altered mental status, neurologic deficits, and seizures.
  • Question patients’ eating and drinking habits→ polydipsia is relatively common in certain patient populations, such as among those with psychiatric history.
  • Responsibly raise [Na+] levels according to the afore-mentioned guidelines in all symptomatic patients.

Boscoe 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.

Every month during director’s rounds, our students present interesting and educational cases. This is a synopsis of the case voted to be the best by the students and directors at the end of director’s rounds along with an interesting image.


Medical Student Program Directors

Jamie Edelstein, MD and Chen He, MD


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