Dysphagia

DOI 10.1007/s00455-012-9414-0

ORIGINAL ARTICLE

Dysphagia, Nutrition, and Hydration in Ischemic Stroke Patients

at Admission and Discharge from Acute Care
Michael A. Crary Jamie L. Humphrey
Giselle Carnaby-Mann Raam Sambandam
Leslie Miller Scott Silliman

Received: 28 January 2012 / Accepted: 18 May 2012

Springer Science+Business Media, LLC 2012

Abstract Dysphagia may predispose stroke patients

toward undernutrition and hydration. These comorbidities
increase patient risks for reduced functional outcome and
short-term mortality. Despite this impact, available information on relationships among dysphagia, nutrition, and
hydration status in acute stroke is limited and conflicted.
This study evaluated nutrition and hydration status in
ischemic stroke patients with versus without clinically

Data Collection at Shands Hospital at Jacksonville. Data Analysis at

Swallowing Research Laboratory, University of Florida Health
ScienceCenter.
M. A. Crary (&)
J. L. Humphrey
G. Carnaby-Mann

R. Sambandam
L. Miller
S. Silliman
Swallowing Research Laboratory, University of Florida Health
Science Center, Box 100174, Gainesville, FL 32610-0174, USA
e-mail: mcrary@phhp.ufl.edu
M. A. Crary
Department of Speech, Language, and Hearing Sciences,
College of Public Health and Health Professions,
University of Florida, Gainesville, FL 32610, USA
J. L. Humphrey
Department of Geography, College of Arts and Sciences,
University of Colorado at Boulder, Boulder, CO 80309, USA
G. Carnaby-Mann
Department of Behavioral Science and Community Health,
College of Public Health and Health Professions,
University of Florida, Gainesville, FL 32610, USA
R. Sambandam
S. Silliman
Department of Neurology, University of Florida College
of Medicine, Jacksonville, FL 32209, USA
L. Miller
Rehabilitation Services, Shands Hospital Jacksonville,
Jacksonville, FL 32209, USA

significant dysphagia at admission and at discharge from

acute care. Sixty-seven patients admitted to the stroke unit
in a tertiary-care hospital provided data for this study. On
the day of hospital admission and upon discharge or at
7 days post admission, serum biochemical measures were
obtained for nutrition (prealbumin) and hydration status
(BUN/Cr). Clinical evaluation for dysphagia, nutrition
status, and stroke severity were completed an average of
1.4 days following hospital admission. Dysphagia was
identified in 37 % of the cohort. At admission 32 % of
patients demonstrated malnutrition based on prealbumin
levels and 53 % demonstrated evidence of dehydration
based on BUN/Cr levels. No differences in nutrition status
were attributed to dysphagia. Patients with dysphagia
demonstrated significantly higher BUN/Cr levels (greater
dehydration) than patients without dysphagia at admission
and at discharge. Dehydration at both admission and discharge was associated with dysphagia, clinical nutrition
status, and stroke severity. Results of this study support
prior results indicating that dysphagia is not associated
with poor nutrition status during the first week post stroke.
Dehydration status is associated with dysphagia during this
period. The results have implications for future confirmatory research and for clinical management of dysphagia in
the acute stroke period.
Keywords Dysphagia
Nutrition
Hydration

Acute stroke
Deglutition
Deglutition disorders

Dysphagia is highly prevalent in acute stroke, with some

estimates exceeding 50 % [1]. This limitation in the ability
to safely ingest adequate amounts of food and liquid places
the patient with acute stroke at risk for poor nutrition and
hydration and related complications [28]. Though the

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M. A. Crary et al.: Dysphagia, Nutrition, Hydration Following Stroke

consequences of dysphagia, specifically poor nutritional

and hydration status, can be severe, potential relationships
among this trilogy of stroke-related morbidities are poorly
understood [2, 913]. A better understanding of these relationships will contribute to better prevention and management of stroke-related complications, improve rehabilitation
strategies, and streamline health-care resource utilization for
patients with acute stroke [1420].
Relationships between poststroke dysphagia and nutritional status are variably depicted in available literature. A
systematic review on this topic, which included eight
studies [6, 9, 10, 2125], concluded that the odds of malnutrition were increased if dysphagia was present following
stroke [26]. However, only five of the eight studies included in the review reported significant associations between
dysphagia and malnutrition, and the pooled analysis
revealed a significant effect only for trials conducted several weeks following stroke. Thus, the relationship between
poststroke dysphagia and nutritional status, especially in
acute stroke, remains ambiguous. This relationship is likely
multifactorial and reported associations are influenced by
time of assessment and tools used to measure dysphagia
and nutritional status [26].
Relationships between poststroke dysphagia and hydration are even less studied than dysphagianutrition comparisons. One reason for this paucity of information may be
the absence of an accepted standard for assessing dehydration [27, 28], although the BUN/Cr ratio may be the best
indicator of dehydration commonly available [29]. BUN/Cr
levels are a common referent for hydration status, with
ratios above 20:1 typically indicated as evidence of under
hydration. However, Lin et al. [30, 31] reported that BUN/
Cr [15 significantly predicted poststroke deterioration
(stroke in evolution). Prior studies report a relatively high
prevalence (2945 %) of dehydration upon admission for
acute stroke [27, 2931]. Average BUN/Cr levels have
been reported to decrease during hospitalization for acute
stroke, though anecdotal evidence is offered that in patients
with dysphagia, these levels may increase, reflecting
greater dehydration [27]. Dehydration has been associated
with poststroke complications [32] and 3 month mortality
following stroke [33].
In a prior study we found no significant relationships
between dysphagia and clinically measured nutritional
status in patients within the first week following stroke. In
the present study we re-examined that finding using a fastreacting hepatic marker for nutritional change (prealbumin)
and we examined potential relationships between dysphagia and hydration status (BUN/Cr) and nutritional status
and hydration status in hospitalized patients within the first
week following ischemic stroke. We examined prevalence
of dysphagia, poor nutritional status, and poor hydration
status at admission and monitored change in nutrition and

123

hydration markers until discharge from acute care. Of

specific interest were differences in nutrition and hydration
values between patients with and without dysphagia. In
addition, we evaluated potential associations among dysphagia, poor nutritional status, poor hydration status, and
factors that may impact any association in a population of
patients with ischemic stroke.

Methods
Patients
Subjects included 67 consecutive ischemic stroke patients
meeting inclusion criteria who were recruited from a Joint
Commission-certified primary stroke center in a tertiary-care
academic hospital. All participants underwent brain-imaging
examinations [computed tomography (CT) or magnetic resonance imaging (MRI) or both] to confirm ischemic stroke
diagnosis. Brain-imaging results were later interpreted by a
neurologist with fellowship training in stroke and cerebrovascular diseases. Patients were excluded from the study if
they had a prestroke history of oropharyngeal dysphagia,
head/neck surgery or trauma, or concomitant neurologic disorder that would impact oropharyngeal swallowing ability.
Enrolled patients, or assigned legal guardians, gave informed
consent for the study protocol previously approved by the
local Institutional Review Board.
All participants received stroke, dysphagia, and nutrition
clinical examinations. Stroke-specific evaluations were
completed by qualified stroke neurologists. Dysphagia and
clinical nutrition evaluations were completed by a licensed
speech pathologist trained in the assessment procedures
used in this study. Serum biomarkers for nutrition and
hydration status were obtained on the day of hospital
admission and again on the day of discharge or at 7 days
post admission, whichever came first. Stroke neurologists
were blinded to the results of dysphagia and clinical
nutritional evaluations and the speech-language pathologist
was blinded to the results of stroke-specific examinations.
The speech-language pathologist was also blinded to serum
biomarker results. Stroke neurologists were blinded to
serum biomarker results unless they were required for
medical decisions regarding specific patients under their
care. Finally, time-interval measurements were taken
between hospital admission and completion of dysphagia,
clinical nutrition, and neurologic examinations.
Stroke Evaluation
Stroke subtype was classified by the Oxfordshire Community Stroke Project classification criteria [34]. Stroke

M. A. Crary et al.: Dysphagia, Nutrition, Hydration Following Stroke

severity was assessed using the National Institutes of

Health Stroke Scale (NIHSS) [35, 36]. Obtained scores
were used except when this measure was dichotomized. An
NIHSS cutoff score of 8 was used for dichotomized analyses. Although no cut point on this scale is universally
accepted, this value was chosen because a score of more
than 8 was used in the National Institute of Neurological
Disorders and Stroke recombinant tissue plasminogen
activator study to define a severe poststroke neurologic
deficit [37].
Stroke-related disability was measured using the modified Rankin Scale (mRS) [38, 39] and the Barthel index
(BI) [40, 41]. Dichotomized cutoff scores were 3 or greater
for the mRS and less than 75 for the BI [42].
Dysphagia Evaluation
Clinical evaluation of dysphagia was completed with the
Mann assessment of swallowing ability (MASA) [43].
This tool evaluates cognitive, communicative, and motor
aspects of a stroke patients abilities that may impact
swallowing ability. With this clinical tool, a score of 178 or
less identifies patients with clinical signs of dysphagia. The
scoring system and ability to detect dysphagia with this
clinical tool have been validated against instrumental
assessment of dysphagia by videofluoroscopy [1]. Ability
to consume food, liquid, or both by mouth was documented
with the functional oral intake scale (FOIS) [44]. This is a
7-point ordinal scale that describes the typical functional
oral intake of patients with stroke and dysphagia. When
this scale was dichotomized, a score below 6 of a maximum of 7 was used to indicate limitations in oral intake of
food and liquid.
Nutrition and Hydration Evaluations
Clinical nutrition status was evaluated with the mini
nutritional assessment (MNA) tool [45]. The MNA is a
standardized and validated clinical tool for evaluating
nutritional status. A score of less than 23.5 on the MNA
indicates patients at risk for malnutrition.
Prealbumin and BUN/Cr biomarkers were assessed from
blood samples obtained on the day of hospital admission
and again at 7 days post admission or on the day of discharge, whichever came first. Prealbumin is an accepted
and preferred predictor of nutritional outcomes [46] for
patients who are critically ill or living with chronic disease
[47]. In this study we used a cutoff point of \15 mg/dL to
identify inadequate nutrition based on prealbumin [48]. A
BUN/Cr ratio C20:1 is typically accepted as abnormal and
potentially indicative of poor hydration. However, a recent
study by Lin et al. [31] reported that a Bun/Cr ratio [15:1
was an independent risk factor for stroke-in-evolution.

Given this stroke-related observation, in the present study

we used BUN/Cr [15:1 as the indication for dehydration.
Statistical Analyses
Patient demographic variables were described by mean and
variance statistics for continuous variables and by prevalence statistics for categorical variables. Correlation analyses were used to examine potential relationships of
dysphagia and stroke variables with nutrition and hydration
status at admission and discharge. Subgroups were identified based on presence of dysphagia (MASA B 178) and v2
or t tests were used to examine differences between dysphagia subgroups. Dichotomized variables between dysphagia subgroups were then examined using relative risks
(RR) with 95 % confidence intervals (CI) to identify any
variable significantly associated with poor nutrition or poor
hydration as defined in this study.
Change in nutrition (prealbumin) and hydration (BUN/
Cr) was calculated between admission and discharge.
Paired-sample t tests (2-tailed) were used to evaluate significant change in nutrition or hydration status in each
dysphagia subgroup based on these biomarkers.

Results
Patients
Among the 67 patients in this stroke cohort, 37 % were
identified as dysphagic, 57 % female, and 54 % African
American (Table 1). The mean age at stroke onset was
65.7 years. Average length of hospital stay was 3.45 days;
however, mean length of hospital stay differed significantly
between patients with and without dysphagia (4.92 vs.
2.39 days, respectively; p \ 0.0001). The average time from
admission to the hospital to completion of all clinical evaluations was 1.4 days. The majority of the cohort experienced
partial anterior circulation infarcts (n = 30) or lacunar
infarcts (n = 18). Dysphagic patients presented with significantly greater stroke severity (NIHSS; p \ 0.0001),
stroke-related disability (BI; p \ 0.0001), and functional
swallowing impairment (FOIS; p \ 0.0001). No significant
difference was identified between the subgroups on clinical
nutrition status (MNA).
Nutrition and Hydration
Based on prealbumin \15 mg/dL, 32 % of subjects demonstrated poor nutrition at baseline and 33 % at discharge.
No dysphagia subgroup differences were detected in
nutrition levels (prealbumin) at baseline or discharge. On
average, both subgroups demonstrated reduced prealbumin

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M. A. Crary et al.: Dysphagia, Nutrition, Hydration Following Stroke

Table 1 Demographic and
clinical characteristics of acute
ischemic stroke patients

N or mean

Dysphagia

No dysphagia

p value

No. of patients [n (%)]

67

25 (37.3)

42 (62.7)

Female [n (%)]

38

15 (39.5)

23 (60.5)

ns

Male [n (%)]

29

Mean age (years) (SD)

65.7

Caucasian [n (%)]

10 (34.5)

19 (65.5)

ns

65.6 (13.0)

65.5 (13.4)

ns

29

15 (51.7)

14 (48.3)

ns

African American [n (%)]

36

9 (25.0)

27 (75.0)

0.003

Diabetes mellitus [n (%)]

19

7 (36.8)

12 (63.12)

ns

Hyperlipidemia [n (%)]

17

7 (43.8)

9 (56.2)

ns

Hypertension [n (%)]

46

17 (36.0)

29 (64.0)

ns

TACI [n (%)]

12

11 (91.7)

1 (8.3)

PACI [n (%)]

30

12 (40.0)

18 (60.0)

LACI [n (%)]

18

2 (11.8)

16 (88.2)

POCI [n (%)]

0 (0)

Oxford stroke classification

TACI total anterior circulation

infarct, PACI partial anterior
circulation infarct, LACI lacunar
infarct, POCI posterior
circulation infarct, MASA Mann
assessment of swallowing
ability; FOIS functional oral
intake scale, NIHSS National
Institutes of Health Stroke
Scale, BI Barthel index, MNA
mini nutritional assessment

Mean length of stay (days) (SD)

Mean dysphagia MASA (SD)

0.002

2.39 (1.87)
194.1 (5.62)

\0.0001
\0.0001

5.16 (2.37)

2.84 (2.08)

6.69 (0.72)

\0.001

Mean NIHSS (SD)

9.18 (7.29)

15.84 (5.78)

4.93 (4.47)

\0.0001

Mean BI (SD)

53.69 (38.40)

15.40 (23.06)

77.63 (23.15)

\0.0001

Mean MNA (SD)

23.30 (3.83)

22.94 (4.09)

23.38 (3.75)

ns

45

26

40

24

35

20

Admit
Discharge

18

BUN/Cr

28

30
25

Admit
Discharge

20

16

15

14

10

12

5
0

10
Total

Dysphagia

NO Dysphagia

Fig. 1 Change in nutritional status (prealbumin). Adequate prealbumin level is [15 mg/dL. Dotted line represents the cutoff point
(15 mg/dL) to dichotomize nutritional status

values from baseline to discharge; however, these changes

were not statistically significant (Fig. 1).
BUN/Cr [15:1 identified deficient hydration in 53 % of
patients at baseline and 66 % of patients at discharge.
Dysphagia vs. no-dysphagia subgroup differences were
identified in hydration levels (Bun/Cr ratio) at baseline
(t = -2.34, p = 0.0226) and at discharge (t = -2.53;
p = 0.0205). At both time points patients with dysphagia
had higher BUN/Cr values than patients without dysphagia
(Fig. 2). Average BUN/Cr values increased specifically in
the dysphagia subgroup (?5.78) from baseline to discharge. However, this difference was not statistically significant (Fig. 2). Given the difference between baseline and
discharge duration between patients with and without
dysphagia, we evaluated the impact of this time period on

123

4.92 (2.82)
125.6 (42.89)

ns

Mean FOIS (SD)

22

mg/dL

3.45 (2.36)
168.15 (42.68)

7 (100)

\.00001

Total

Dysphagia

NO Dysphagia

Fig. 2 Change in hydration (Bun/Cr ratio). Dotted line represents the

cutoff point (15:1) to dichotomize hydration status

change in BUN/Cr with an analysis of covariance. The

ANCOVA results indicated that the marginal means for
change in hydration status (BUN/Cr) over time in patients
with and without dysphagia were not significant after
accounting for the effect of assessment interval (F = 1.92,
p \ 0.175).
Correlations Among Dysphagia, Stroke, Nutrition, and
Hydration Markers
Both dysphagia measures (MASA and FOIS) were significantly correlated with stroke severity measures (NIHSS,
BI, and mRS). Clinical swallowing examination scores
(MASA) were not significantly correlated with nutrition or
hydration biomarker levels at admission or discharge.
However, functional oral intake levels (FOIS) were

M. A. Crary et al.: Dysphagia, Nutrition, Hydration Following Stroke

Table 2 Correlations among outcome measures for dysphagia, stroke severity, clinical nutritional status, and biomarkers for nutrition and
hydration at baseline and discharge
FOIS

MNA

PreAlb

Bun/Cr

BL
MASA
FOIS

0.904*

Age

DC

BL

DC

NIHSS

BI

mRS

0.052

0.147

0.248

-0.158

-0.263

0.121

-0.793*

0.792*

-0.630*

0.015

0.167

0.280

-0.247

-0.362*

-0.056

-0.762*

0.812*

-0.657*

0.257

0.347*
0.578*

-0.218
-0.070

-0.192
0.082

-0.181
-0.091

-0.029
-0.117

0.198
0.239

-0.060
-0.192

0.035

-0.150

-0.155

-0.314*

0.288

-0.196

0.021

0.235

-0.284*

0.215

0.126

0.378*

-0.454*

0.276

-0.070

0.199

MNA
PreAlb BL
PreAlb DC
Bun/Cr BL

0.304*

Bun/Cr DC
Age

00.019

NIHSS

-0.829*

0.783*

BI

-0.796*

* p \ 0.05
MASA Mann assessment of swallowing ability, FOIS functional oral intake scale, MNA mini nutritional assessment, PreALB BL prealbumin level
at baseline (admission), PreAlb DC prealbumin level at discharge, BUN/Cr BL BUN/Cr levels at baseline (admission), BUN/Cr DC BUN/Cr
levels at discharge, NIHSS National Institutes of Health Stroke Scale, BI Barthel index

significantly inversely correlated with hydration levels

(BUN/Cr) at discharge (Table 2).
Prealbumin levels at baseline did not correlate with any
dysphagia, stroke, or clinical nutrition variable. At discharge, however, prealbumin levels demonstrated a significant inverse correlation with stroke severity as measured
by the NIHSS and a significant positive correlation with
clinical nutritional status as measured by the MNA
(Table 2).
Bun/Cr levels at baseline demonstrated a significant
inverse correlation with stroke impairment (BI). At discharge, Bun/Cr values were significantly inversely correlated with FOIS and stroke impairment (BI), and
significantly positively correlated with stroke severity as
measured by the NIHSS (Table 2).

Fig. 3 Associations of stroke,

nutrition, dysphagia variables,
and dehydration at baseline (a)
and discharge (b). MNA mini
nutritional assessment, FOIS
functional oral intake scale,
MASA Mann assessment of
swallowing ability, mRS
modified Rankin scale, BI
Barthel index, NIHSS National
Institutes of Health Stroke
Scale, HTN hypertension,
HYPERLIPID hyperlipidemia

(a)

Relative Risk of Dehydration

Since hydration status differed based on dysphagia status at
baseline and at discharge and was significantly correlated
with FOIS at discharge, we focused on identification of risk
factors for poor hydration in this cohort (Fig. 3a, b). No
demographic patient variables were significantly associated
with hydration status. However, stroke and dysphagia
variables did reveal significant associations with hydration
status at baseline and at discharge. At baseline, stroke
severity (NIHSS: RR 1.76, 95 % CI 1.102.83), stroke
impairment (BI: RR 1.91, 95 % CI 1.153.16), clinical
nutrition status (MNA: RR 1.86, 95 % CI 1.182.93), and
dysphagia (MASA: RR 1.65, 95 % CI 1.042.62) demonstrated significant associations with poor hydration. At

(b)

MNA

MNA

FOIS

FOIS

MASA

MASA

mRS

mRS

BI

BI

NIHSS

NIHSS

HTN

HTN

HYPERLIPID

HYPERLIPID

DIABETES

DIABETES

RACE

RACE

SEX

SEX
0

RR and 95% CI

RR and 95% CI

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M. A. Crary et al.: Dysphagia, Nutrition, Hydration Following Stroke

discharge these same variables were significantly associated with poor hydration (NIHSS: RR 1.62, 95 % CI
1.1342.31; BI: RR 1.62, 95 % CI 1.022.58; MNA: RR
1.55, 95 % CI 1.052.28; MASA: RR 1.53, 95 % CI 1.01
2.32) in addition to BUN/Cr at baseline (RR 1.97, 95 % CI
1.153.37).

Discussion
In the present study dysphagia was not associated with
nutritional status measured clinically (MNA) or from prealbumin levels. However, measures of swallowing ability
(MASA and FOIS) were associated with hydration status at
admission and at discharge. Acute stroke patients with
dysphagia demonstrated significantly higher BUN/Cr levels than those without dysphagia.
The absence of significant association between dysphagia and nutritional status supports our prior report [9] based
on evaluation at the time of admission for ischemic stroke.
Extending the prior observation, we now note that this lack
of association is maintained through discharge from acute
care. This finding is consistent with the conclusions of a
systematic review by Foley et al. [26] who reported the
absence of an association between malnutrition and dysphagia in the first 7 days following hospital admission for
ischemic stroke. However, the lack of nutritional deterioration during the acute phase of stroke noted in the current
study is discrepant from at least two prior studies [5, 6].
Different metrics of dysphagia and nutritional status might
explain some of the discrepancies between these studies.
For example, Foley et al. [49] report that the wide range of
nutritional assessments, many of which are not validated,
may contribute to extensive variation in estimates of malnutrition. In the present (and prior) study we utilized the
MNA, which is considered a valid clinical assessment of
nutritional status [45]. Furthermore, in the present study we
employed prealbumin levels as a metric of nutritional
status which is considered a superior nutritional metric in
acute stroke [50]. Other differences might be related to the
nature of study outcomes. Some studies report increased
prevalence between assessment time points as evidence of
increased malnutrition [6]. In the present study, our focus
was on patients with versus without dysphagia and we
reported mean prealbumin values from these two subgroups. Though both subgroups of acute stroke patients
demonstrated a reduction in prealbumin levels between
admission and discharge, these changes were not statistically significant.
The prevalence of cases at risk for malnutrition based on
clinical nutrition examination (MNA) in the prior study [9]
was just over 26 %. In the present study, based on the
prealbumin level, the prevalence was 32 % at admission.

123

Thus, between one-quarter and one-third of ischemic stroke

patients demonstrated a degree of malnutrition upon hospital admission. This observation may be related to prestroke variables [7, 9] or possibly to stroke-related
metabolism changes [51]. However, in the current study,
consistent with our prior work [9], nutritional status was
not significantly associated with any stroke severity measure. The mechanism or mechanisms relating to poor
nutritional status upon admission for ischemic stroke are
likely complex and beyond the scope of the current study.
Based on a BUN/Cr level [15:1, the prevalence of
dehydration in this study was high at baseline (53 %) and
even higher at discharge (66 %). Beyond that result, the
degree of dehydration reflected in the BUN/Cr levels was
significantly greater in patients with dysphagia than in
those with no dysphagia at baseline and at discharge.
Furthermore, dehydration was associated with clinical
measures of dysphagia (MASA and FOIS) and clinical
nutrition status (MNA) at both baseline and discharge.
Finally, dehydration was associated with stroke severity
(NIHSS, BI) at both baseline and discharge. Given the
complexity of these univariate associations, it is difficult to
speculate about specific factors that contribute to dehydration in acute ischemic stroke. However, since patients
with dysphagia demonstrate dehydration at admission and
BUN/Cr levels increase (though not significantly) during
hospitalization, acute ischemic stroke patients with dysphagia should be considered at risk for dehydration upon
admission and monitored for adequate hydration during
hospitalization.
Variables not directly addressed in this study include
clinical management of patients with dysphagia at admission and the nature of dysphagia management in postadmission acute care specific to fluid intake. The care
pathway in this specific comprehensive stroke center is to
keep patients who fail initial dysphagia screening on nil per
os (NPO) status until they receive a dysphagia evaluation
by a speech-language pathologist. However, in the interim
these patients are administered intravenous hydration.
Furthermore, initial hydration assessment via BUN/Cr was
completed upon admission, minimizing any influence of
immediate care pathways on hydration status in stroke
patients with (or without) dysphagia. However, in postadmission acute care, a common practice is to use thickened
liquids in an attempt to reduce liquid aspiration. In some
instances this practice may contribute to under hydration
[4]. Given this concern, we note that BUN/Cr levels at
discharge were significantly inversely correlated with FOIS
levels. Thus, lower FOIS levels corresponding to more
restrictive oral food/liquid intake significantly correlated to
higher BUN/Cr levels, indicative of increased dehydration.
Though the present study cannot claim that dysphagia
management practices, specifically use of thickened

M. A. Crary et al.: Dysphagia, Nutrition, Hydration Following Stroke

liquids, contributed to increased dehydration during acute

hospitalization, current results suggest the need for future
studies investigating this potential relationship.
The current results should be interpreted cautiously.
Significant correlations and relative risk values were
modest. The observation that a substantial number of
patients demonstrated poor nutrition or hydration upon
admission might reflect prestroke lifestyle or health factors,
or perhaps biological changes occurring in the peristroke or
immediate poststroke period. Furthermore, dehydration
was maintained, if not increased, in some patients with
dysphagia following stroke. Thus, the impact of acute
stroke dysphagia management should be considered in
future studies.

Conclusions
Consistent with prior studies, this study did not identify any
significant relationship between dysphagia and nutritional
status in patients with acute ischemic stroke. However,
based on current results, ischemic stroke patients with
dysphagia are at risk for dehydration upon admission to the
hospital. In these patients, the degree of dehydration may
increase during the period of acute hospitalization. Given
the risk factors from dehydration in this population, further
research is warranted to identify patient and/or health-care
factors that contribute to poor hydration in this population.
Conflict of interest Michael A. Crary, Jamie L. Humphrey, Giselle
Carnaby-Mann, Raam Sambandam, Leslie Miller, and Scott Silliman
have no conflicts of interest to disclose.

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Michael A. Crary

PhD
MPH

Jamie L. Humphrey
Giselle Carnaby-Mann
Raam Sambandam
Leslie Miller
Scott Silliman

MA
MD

MD

PhD