Case report
Journal of the Intensive Care Society
Management of severe dehydration
Stephanie Ruth Strachan and Lucy Francesca Morris
Abstract
The presented case is one of severe dehydration and acute kidney injury with significant resultant complications that
required considerable fluid and electrolyte replacement. Approaches to fluid resuscitation in the context of hyperna-
traemia and the hyperosmolar state were considered and then judiciously combined to manage a complex case with a
successful outcome. Conflicting guidance in this domain is discussed with recommendations for a future management
strategy that is tailored to individual patients.
Keywords
Dehydration, fluid therapy, hypernatraemia, uraemia, water-electrolyte imbalance
Case presentation
A 68-year-old Caucasian man was transferred to our
specialist tertiary referral centre with an acute sub-
dural haematoma requiring emergency neurosurgery.
Investigation results pre-operatively were profoundly
deranged (Table 1) demonstrating a severe metabolic
disturbance but it was decided that, despite the high
risk of peri-operative mortality this presented, an
emergency evacuation of the SDH was in the patient’s
best interests.
The medical notes from his local district general
hospital revealed the patient had presented to them
4 days previously having been found collapsed at
home by neighbours with a 3-week history of diar-
rhoea and vomiting. He had a past medical history
of hypertension, for which he took candesartan. On
presentation there, he was confused and clinical
observations, in combination with test results, sug-
gested a profound dehydration (Table 2).
The initial working diagnosis made was an acute
kidney injury (AKI) secondary to diarrhoea and
vomiting, on a background of angiotensin-receptor
blocker use. He was transferred from the Emergency
Department to the High Dependency Unit for fluid
resuscitation and monitoring (Table 3).
On the third day of the admission, he developed a
right hemiplegia (1/5 power in both his right arm and
leg). An urgent CT head was performed and it demon-
strated a large subdural haemorrhage (SDH) with
subarachnoid extension; there was evidence of midline
shift and developing hydrocephalus (Figure 1).
At this point, neurosurgical advice was sought but
before transfer could be arranged his condition
2017, Vol. 18(3) 251–255
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deteriorated: his GCS fell to 8/15 and he developed
a fixed and dilated pupil. A decision was made to
provide end of life care, however, over the following
24 h the patient made a significant, spontaneous,
neurological recovery; he became alert, was obeying
commands and his pupils normalised but he remained
dysphasic with a right-sided weakness. Further discus-
sions with the neurosurgical team led to the patient
being transferred to our institution for urgent
neurosurgery.
Post-operatively, he was brought to our
Neurosurgical Critical Care Unit (NCCU) for man-
agement of his dehydration and recovery from evacu-
ation of sub-dural haematoma. He required
intubation for 5 days, during which time his fluid
status and biochemistry were carefully corrected; he
never required renal replacement therapy.
He was discharged to a neurosurgical ward on day
12 and on day 32 was repatriated to his local hospital.
He had, by this stage, made a dramatic neurological
recovery with no residual motor deficit or dysphasia,
although he remained mildly confused. He was
followed up in the neurosurgical outpatient clinic
6 months after repatriation and, by this stage, he
was living at home independently, suffering no obvi-
ous sequelae of these events. No cause was ever found
for the precipitating diarrhoea and vomiting.
Critical Care Department, King’s College Hospital, London, UK
Corresponding author:
Stephanie Ruth Strachan, Critical Care Department, King’s College
Hospital, London SE5 9RS, UK.
Email: stephanie.strachan@nhs.net
252 Journal of the Intensive Care Society 18(3)

Management of the severely

dehydrated patient
Appropriate management of the severely dehydrated
and uraemic patient is challenging and there is no
specific guidance in the literature. Clinicians must
use their judgement and discretion when tailoring
alternative available guidelines for use in individual
patient cases.
Since at least 1949, it has been understood that
the mainstays of treatment for uraemia included the
meticulous correction of water and electrolyte dis-
turbance, with water balance taking precedence over
electrolytes.1 Today’s clinician has a greater ability to
monitor, measure and modify fluid and electrolytes,
but this still must be done with caution and an aware-
ness of the potential risks.
There are, broadly, two theoretical approaches one
could take to correcting this patient’s severe dehydra-
tion and uraemia:
existing management of hypernatraemia guidelines
(e.g. Adrogué),2 or
2. Managing and correcting the hyperosmolar state,
but the only available guidance here is the hyper-
osmolar hyperglycaemic state (HHS) guideline
where the hyperosmolar state is secondary to an
elevated glucose (although these patients are add-
itionally profoundly dehydrated and may have an
elevated sodium too).3
Hypernatraemia approach (Adrogué)
Formulae hypothetically allow a clinician to calculate
a patient’s free water deficit by utilising the

1. Management of hypernatraemia by estimating and

correcting the fluid deficit according to serum
sodium levels and managing the patient as per

Table 1. Results pre-operatively on arrival at tertiary referral

centre.

Biochemistry

Sodium 169 mmol/L

Potassium 3.3 mmol/L
Urea 49.6 mmol/L
Creatinine 365 mmol/L
Glucose 12 mmol/L
Calculated osmolarity 399.6 mmol/L Figure 1. CT head scan.

Table 2. Clinical and laboratory data from time of initial hospital presentation.

Arterial blood gas

Observations (15 L/min oxygen) Haematology Biochemistry

RR 23/min pH 7.4 Hb 173 g/L Na 152 mmol/L

Temp 33.2 C pCO2 4.4 kPa WCC 15.4  109/L K 6.1 mmol/L
BP 80/50 mmHg pO2 54.2 kPa Platelets 226  109/L Urea 118.3 mmol/L
HR 150/min (AF) HCO3 22.3 mmol/L CRP 14.4 mg/L Creatinine 2491 mmol/L
SpO2 unrecordable BE 4.4 mmol/L INR 1.1 Glucose 6.4 mmol/L

Table 3. Patient results over the first few days at his local hospital.

Day 1
(presentation) Day 2 Day 3 Day 4

Sodium (mmol/L) 152 152 156 166

Urea (mmol/L) 118 107 85 47
Creatinine (mmol/L) 2491 1841 1100 349
Fluid balance – 4 L þve 250 mL þve ?
Strachan and Morris
extracellular sodium concentration as a surrogate
marker of hydration status. Hypotonic solutions
(5% dextrose in water, 0.2% sodium chloride in
5% dextrose in water and 0.45% sodium chloride
in water) are recommended as the intravenous
resuscitation fluids in the accompanying guidance
excepting in the presence of ‘frank circulatory com-
promise’, when ‘isotonic’ solutions such as 0.9%
sodium chloride are advised. The theory is that
dehydration culminating in a relative water deficit is
visible to the clinician via the measured sodium
concentration.
Applying the Adrogué formula to this case of
hypernatraemia, at the time of arrival to the NCCU,
with an estimated patient weight of 65 kg and a
plasma sodium concentration of 169 mmol/L:
Total body water ðTBWÞ
¼ weight ðkgÞ  correction factor for age and gender
Patient TBW ¼ 65 kg  0:6 ¼ 39 L
Change in serum Naþ ¼ ðinfusate Naþ  serum Naþ Þ
 ðTBW þ 1Þ
Change in serum Naþ with 1 L 5%dextrose fluid
administration : ð0  169Þ=ð39 þ 1Þ ¼ 4:2 mmol=L:
This suggests that after 1 L of 5% dextrose, the
expected measured sodium would be approximately
165 mmol/L and to normalise sodium (reference
range 135–145 mmol/L), 6 L of 5% dextrose would
be required.
Lindner et al. analysed four different formulae
designed to aid the correction and maintenance of
serum sodium in a critical care setting through
estimation of the free water deficit and found the
formulae were not able to accurately guide infu-
sion therapy in hypernatraemic states in the ICU
patient.4
The established and consistent guidance in the lit-
erature on managing chronic hypernatraemia (an ele-
vated sodium for >48 h) is of a maximum reduction in
sodium concentration of 10 mmol/L (equivalent to an
osmolarity of 20 mmol/L) in a 24-h period due to the
risks of fluid overload, cerebral oedema or central
pontine myelinolysis caused by fluid shifts due to
altered tonicity.5
Hyperosmolar state approach
For practical purposes, osmolality (mosmol/kg) and
osmolarity are interchangeable, with the latter being
calculable and measured in mmol/L. At the time of
presentation to the admitting hospital, our patient
had a calculated osmolarity of 428.7 mmol/L
(normal range 285–295 mmol/L). On arrival in our
253
NCCU, his calculated osmolarity was 399.6 mmol/L.
The equation we have used to calculate this is:


Osmolarity ¼ 2Naþ þ urea þ glucose:
The HHS guideline’s goals of treatment, which
make it potentially helpful in this case, are to:
. normalise the osmolality;
. replace fluid and electrolyte losses;
. (normalise blood glucose levels).3
It is important to note that the guideline is, of
course, designed to guide the rehydration of patients
who are hyperosmolar secondary to severe hypergly-
caemia. This is important to consider because whilst
sodium and glucose are both effective osmoles contri-
buting to tonicity, urea is not, as it may cross the cell
membrane freely.
The rate of decline of osmolarity suggested by the
HHS guideline is 3–8 mmol/L/h utilising 0.9% saline
as the preferred resuscitation fluid. However, the
reduction in osmolarity must be balanced against
the rate of change in serum sodium level (a maximum
change of 10 mmol/L in a 24-h period, as before), the
sodium being expected to rise in the first instance as
water moves intracellularly. The expected fluid
replacement required in the management of HHS is
6–13 L in a 60 kg patient, with 50% being given in the
first 12 h.
Our approach
On initial presentation at his local hospital, our
patient was moderately hypernatraemic (sodium
152 mmol/L), severely uraemic (urea 118 mmol/L) and
hyperosmolar (calculated osmolarity 428 mmol/L),
but his effective tonicity if urea is discounted as
being an ineffective osmole was not elevated (effective
osmolarity 310 mmol/L). He was given fluids (precise
details are unknown) and had an initial positive fluid
balance but close monitoring and fluid resuscitation
stopped when the patient was briefly palliated.
Four days after the initial presentation, on arrival
at our institution, he was severely hypernatraemic
(sodium 169 mmol/L), severely uraemic (49 mmol/L)
and hyperosmolar (calculated osmolality 399 mmol/L),
but due to the effectiveness of the components of
osmolality, he had a higher effective tonicity (effective
osmolarity 350 mmol/L) than on initial presentation
to hospital.
We felt it prudent to be somewhat cautious with
rehydration post-operatively as his initial period of
fluid administration was associated with development
of an SDH. We postulated that the SDH occurred
through a combination of uraemic platelet dysfunc-
tion, a known cause of intracranial haemorrhage,
and fluid shifts in less elastic tissue through
severe dehydration, in this patient with complex
254 Journal of the Intensive Care Society 18(3)

Table 4. Details of fluids administered during his post-operative recovery phase.

5 6 7 8 9 10 11 12

Day of hospital admission

Fluid input (ml) 6878 4391 4679 6494 3662 3246 5644 4975
Fluid balance (ml) 6090 2082 649 9 843 244 764 1680
Including the following quantities:
0.9% Saline (ml) 1050 0 0 0 0 0 0 0
Hartmann’s (ml) 4400 0 250 750 250 0 170 500
5% Dextrose (ml) 200 2400 2400 2660 0 0 0 0
Enteral water (ml) 0 0 150 550 0 200 1825 1310

Table 5. Biochemistry result normalisation during his post-operative recovery phase. Monitoring of biochemistry on fluid resusci-
tation took place multiple times during the initial post-operative period, but daily results are tabulated here.

Day of hospital admission

5 6 7 8 9 10 11 12

Sodium (mmol/L) 166 164 159 151 144 148 150 146
Urea (mmol/L) 48.1 43 31.1 18.1 12 11 8.3 5.9
Creatinine (mmol/L) 346 338 248 156 147 133 110 87
Calculated osmolarity (mmol/L) 386.1 377 355.1 326.1 306 313 314.3 303.9

Calculated osmolarity Sodium

Proposed change in osmolarity
450 175
430 170
410
165
Osmolarity mmol/L

390
Sodium mmol/L

370 160

350 155
330 150
310
145
290
270 140

250 135
1 2 3 4 5 6 7 8 9 10 11 12 13
Day of admission

Events log
Day 1: Presentaon to local hospital with dehydraon
Day 3: SDH development
Day 4: Transfer for SDH evacuaon and ICU admission
Day 12: Step down to ward

Figure 2. Changes in plasma sodium and osmolarity with rehydration.

pathophysiology.6 In addition, the rise in serum hospital) suggests there was perhaps a dilutional rela-
sodium, with a reduction in urea but more minimal tive hyponatraemia secondary to uraemia initially.
change in the calculated osmolarity following that Changes in plasma sodium may also have been influ-
first episode of fluid resuscitation (at the local enced by the consequent cerebral dysfunction.
Strachan and Morris
We elected to reduce the calculated serum osmo-
larity by 20 mmol/L each day, utilising the osmolar
effect of a 10 mmol/L sodium reduction as our refer-
ence point. We needed to correct, by this stage, a pro-
found hypernatraemia in addition to the uraemia and
raised tonicity. To achieve this, we used a combin-
ation of fluids together with regular monitoring, as
the patient’s salt and water deficit, the distribution
of salt and water across intracellular and extracellular
compartments, renal excretion, and response to fluid
resuscitation were, essentially, all unknowns (Tables 4
and 5). Figure 2 displays graphically the changes in
sodium and calculated osmolarity during the patient’s
hospital admission, from day 1 at the admitting hos-
pital, transfer to the tertiary service during day 4,
through to transfer to a neurosurgical ward on day 12.
Initially, large quantities of isotonic fluids were
used for rehydration with frequent blood sampling
targeting a daily reduction in calculated osmolarity
of 20 mmol/L. Following the initial rehydration,
hypotonic solutions were able to be utilised safely
and, once the biochemistry results were near reference
ranges, enteral water was used. Intravenous fluids
given are itemised, with the remainder of fluid input
comprising medications and nasogastric feed.
The patient required regular blood sampling to
assess the serum biochemical changes in response to
fluid type and volume, with close fluid balance moni-
toring. Normal sodium, urea and creatinine test
results were not seen until day 12 of admission, at
which point the patient had a cumulative positive
fluid balance of 16 L (40% estimated TBW).
Calculated osmolarity at this point was 303.9 mmol/L.
When comparing his actual cumulative fluid bal-
ance with the initial estimate of free water required
from the Adrogué calculation method (6 L), it can be
seen how inaccurate that method can be. The stand-
ard fluid quantities required to resuscitate a patient
with HHS, however are more suggestive of the quan-
tities of fluid that may be required (up to 13 L) in a
patient with hypernatraemia secondary to dehy-
dration through hyperglycaemia. Additionally, the
Adrogué method promotes the use of hypotonic solu-
tions and advises against isotonic solutions; in direct
conflict, the HHS guidelines advocate the use of
isotonic rather than hypotonic fluids, although both
caution against rapid changes in plasma sodium.
Conclusion
The presented case is one of severe dehydration and
AKI that required considerable fluid and electrolyte
replacement. Approaches to fluid resuscitation in the
context of hypernatraemia and the hyperosmolar state
were considered. These were judiciously combined to
manage a complex case of severe dehydration and
biochemical disarray with a successful outcome.
255
It may be that we were overly cautious in the speed
of correction of this patient’s biochemistry, but in
addition to estimating how much fluid may be
required to resuscitate a dehydrated patient, this
case also serves as a reminder of the potential conse-
quences of dehydration, including hyperviscosity,
AKI and uraemic platelet dysfunction; difficulties
prognosticating for individuals when the literature
provides information regarding cohorts; and the
amazing resilience of some patients.
We suggest a reconsideration of the approach to
correcting hypernatraemia in patients with chronic
hypernatraemia (>48 h) and dehydration, as attempt-
ing to calculate the free water deficit in critically ill
patients is highly inaccurate. We suggest individual-
isation of resuscitation regimes for patients based on
osmolarity, monitoring and reviewing the response to
fluid administration whilst maintaining the clear guid-
ance on safe parameters for changes in sodium con-
centrations. Our recommendation draws significant
parallels with the current guidance on the manage-
ment of HHS.
Consent
Published with the written consent of the patient.
Declaration of conflicting interests
The author(s) declared no potential conflicts of interest with
respect to the research, authorship, and/or publication of
this article.
Funding
The author(s) received no financial support for the research,
authorship, and/or publication of this article.
References
1. Joekes AM. The treatment of uraemia with special ref-
erence to acute renal failure. Postgrad Med J 1949; 25:
61–70.
2. Adrogué HJ, and Madias NE. Hypernatraemia. N Engl J
Med 2000; 342: 1493–1499.
3. Joint British Diabetes Societies Inpatient Care Group.
The management of hyperosmolar hyperglycaemic state
in adults with diabetes. Joint British Diabetes Societies
for Inpatient Care 06, www.diabetes.org.uk or www.dia
betologists-abcd.org.uk (2012, accessed 31 January
2017).
4. Lindner G, Schwarz C, Kneidinger N, et al. Can we
really predict the change in serum sodium levels?
An analysis of currently proposed formulae in hyperna-
traemic patients. Nephrol Dial Transplant 2008; 23:
3501–3508.
5. Martin RJ. Central pontine and extrapontine
myelinolysis: the osmotic demyelination syndromes.
J Neurol Neurosurg Psychiatry 2004; 75(Suppl 3):
iii22–iii28.
6. Salman S. Uremic bleeding: Pathophysiology, diagnosis
and management. Hosp Physician 2001; 37: 45–50, 76.