PREDICTORS OF OUTCOME IN HOSPITALIZED PATIENTS: RESULTS

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Demographic and Clinical Characteristics of Study Patients

We found severe hyponatremia in 168 patients out of a total of 5994 patients with a diagnosis of hyponatremia at our facility over the study period, yielding an incidence of approximately 2.8%. Tables 1 and 2 summarize the demographic and clinical features of these patients.

The mean age (SD) of the 168 patients (96 men, 72 women) was 52.1 ± 17.4 years. The patients were predominantly black (92.8%), and 81.54% were admitted to the internal medicine floor service, while 18.45% were managed in the intensive care unit (ICU). One hundred thirty-eight patients (82.14%) had acute hyponatremia, 28 patients (16.67%) had chronic hyponatremia, and for two patients it could not be determined if hyponatremia was acute or chronic. Symptoms of hyponatremic encephalopathy were present in 89 patients (52.97%), while 79 patients (47.02%) had no documented symptoms. Of the symptomatic patients, altered sensorium was documented for 46 patients (51.7%); seizures for 20 patients (22.5%); nausea and vomiting for eight patients (4.8%); two patients were comatose ( 2.2%); dysarthric speech was noted in two patients (2.2%); while gaiet disturbance and frequent falls occurred with six patients (3.6%). Symptoms were present in nine patients with chronic hyponatremia (32.14%), and 80 patients with acute hyponatremia were symptomatic (89.9%).
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Figure 1. FLUID PRESCRIPTION TO CORRECT HYPONATREMIA IN OUR STUDY POPULATION

Diabetes Mellitus was the most common co-morbid condition present in 40 patients (23.8%), while 34 patients (20.2%) had human immunodeficiency virus infection (HIV). Hypoxia was documented in 28 patients (16.7%), while 16 patients (9.5%) had a diagnosis of sepsis.
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Table 1.

Demographic Characteristic		P Value
Age Mean-   SD	52.1-17.4	0.16
Sex (%)
Men	96	0.86
Women	72
Race(%)
Black	156	0.65
White	CO
Other	CO
Location:
ICU	31
Medical Floor	137
History of Alcoholism #(%)	40 (23.8%)	0.39
#Taking HCTZ	27 (16.7%)
Symptomatic	89 (52.97%)
Asymptomatic	79 (47.02%)
# of Patients who had Chest Radiograp	145(86%)
# of Patients with Cerebral Imaging	40(23.8%)

Hypovolemia was an etiologic factor of hyponatremia in 39 patients (23.21%), while 30 patients (17.9%), had a clinical picture compatible with the syndrome of inappropriate antiduretic hormone secretion (SIADH). Other factors causing hyponatremia in this study population included congestive heart failure (10.1%), use of thiazide diuretics (7%), cirrhosis (6%), psychogenic polydipsia in 2.3%, rapid administration of hypotonic fluids, along with use of morphine and non-steroidal anti-inflammatory drugs to treat sickle-cell pain crisis patients (5.95%). Endocrine causes contributed to hyponatremia in six patients (3.5%), two patients with hypothyroidism, three patients with adrenal insufficiency, and one patient with panhypopituitarism. Multiple factors contributed to hyponatremia in 18 patients (10.9%).
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Figure 2. HISTOGRAM SHOWING DISTRIBUTION OF PLASMA NA NADIR IN SURVIVORS AND DEATHS FROM SEVERE HYPONATREMIA

There was no association between the demographic variables, cause of hyponatremia, admission to ICU, or HIV status and outcome. Similarly, there was no relationship between serum sodium nadir (index of severity) and survival, as shown in Figure 2. Whether hyponatremia was acute vs. chronic did not affect mortality (p=0.297).

Table 2. CLINICAL VARIABLES AND COMORBIDITY

Mean plasma Sodium Nadir (mmol/L)	109 (5.5)
Mean Plasma Osmolarity Nadir (mosm/kg)	242.4 (26.1)
Acute hyponatremia	140 (83.3%)
Chronic hyponatremia (%)	28(16.7%)
Gl Bleed	5(2.9%)
Diabetes # (%)	40 (23.8%)
Congestive heart failure # (%)	20 (11.9%)
Renal Failure # (%)	15(8.9%)
Cirrhosis # (%)	12(7.14%)
Sepsis* (%)	16(9.5%)
COPD	9 (5.4%)
Hypoxia/or resp. failure # (%)	28 (16.7%)
Pulmonary Edema on Chest X-Ray	25 (14.8%)
Rate of correction in 1st 24 hours	0.869 (26.1)
Mean Na at 48 Hours	127.086 (7.913)
HIV #(%)	34(20.23%)

Correction of Hyponatremia and Outcome

Figure 1 summarizes fluid prescription to correct hyponatremia in our study population. The total of 137 patients (82%) received normal saline during correction of hyponatremia, while hypertonic (3%) saline was used in only 12 patients (7.14%). Restriction of hypotonic fluids was imposed on all but one patient. The mean hourly rate of correction in the first 24 hours was 0.8mmol/L. The mean absolute serum sodium concentration after 48 hours of therapy (available in 110 patients; 65.5%), was 120.02 ± 8.31 mmol/L. Overly rapid correction (>25mmol/L/48hours) occurred in 17 patients (15.5%). One of these patients developed a progressive encephalopathic illness from which she died six weeks later. However, her brain autopsy did not reveal any demyelinating lessions to suggest possible osmotic demyelination syndrome.
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Table 3. MULTIVARIATE ANALYSIS OF ASSOCIATION OF SELECTED FACTORS WITH MORTALITY

Variable	Mortality Odds Ratio (%)	p.
Hypoxia	13.457 (4.7-38.4)	<0.0001
Rate of Correction (hourly)	0.334 (0.126-0.883)	0.027
Sodium at 48 Hours	3.59	0.0012
Sepsis	8.623 (2.11-35.16)	0.002
Presence of Symptoms	3.038(1.08-8.5)	0.035

The overall mortality rate was high -20.2%, and there was a trend towards increasing mortality with a slower rate of correction. The amount of correction at 48 hours, as measured by the absolute serum sodium concentration (127.09 ± 7.91 in survivors vs. 118.83 ± 9.84 in non-survivors), was significantly associated with mortality (p=0.0016). The presence of hypoxia also was strongly associated with mortality in severe hyponatremia (p=0.0001). Other factors with significant association with short-term mortality include a co-morbid diagnosis of sepsis (p=0.0006) and the presence of symptoms (p=0.0032) (see Table 3). Neither the presence of hypokalemia nor a history of alcoholism affected mortality (p=0.948 and 0.392, respectively.)