Case report

Journal of the Intensive Care Society

2017, Vol. 18(3) 251–255
! The Intensive Care Society 2017
Management of severe dehydration Reprints and permissions:
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DOI: 10.1177/1751143717693859
Stephanie Ruth Strachan and Lucy Francesca Morris journals.sagepub.com/home/jics

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

deteriorated: his GCS fell to 8/15 and he developed

Case presentation a fixed and dilated pupil. A decision was made to
A 68-year-old Caucasian man was transferred to our provide end of life care, however, over the following
specialist tertiary referral centre with an acute sub- 24 h the patient made a significant, spontaneous,
dural haematoma requiring emergency neurosurgery. neurological recovery; he became alert, was obeying
Investigation results pre-operatively were profoundly commands and his pupils normalised but he remained
deranged (Table 1) demonstrating a severe metabolic dysphasic with a right-sided weakness. Further discus-
disturbance but it was decided that, despite the high sions with the neurosurgical team led to the patient
risk of peri-operative mortality this presented, an being transferred to our institution for urgent
emergency evacuation of the SDH was in the patient’s neurosurgery.
best interests. Post-operatively, he was brought to our
The medical notes from his local district general Neurosurgical Critical Care Unit (NCCU) for man-
hospital revealed the patient had presented to them agement of his dehydration and recovery from evacu-
4 days previously having been found collapsed at ation of sub-dural haematoma. He required
home by neighbours with a 3-week history of diar- intubation for 5 days, during which time his fluid
rhoea and vomiting. He had a past medical history status and biochemistry were carefully corrected; he
of hypertension, for which he took candesartan. On never required renal replacement therapy.
presentation there, he was confused and clinical He was discharged to a neurosurgical ward on day
observations, in combination with test results, sug- 12 and on day 32 was repatriated to his local hospital.
gested a profound dehydration (Table 2). He had, by this stage, made a dramatic neurological
The initial working diagnosis made was an acute recovery with no residual motor deficit or dysphasia,
kidney injury (AKI) secondary to diarrhoea and although he remained mildly confused. He was
vomiting, on a background of angiotensin-receptor followed up in the neurosurgical outpatient clinic
blocker use. He was transferred from the Emergency 6 months after repatriation and, by this stage, he
Department to the High Dependency Unit for fluid was living at home independently, suffering no obvi-
resuscitation and monitoring (Table 3). ous sequelae of these events. No cause was ever found
On the third day of the admission, he developed a for the precipitating diarrhoea and vomiting.
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 Critical Care Department, King’s College Hospital, London, UK
subarachnoid extension; there was evidence of midline
Corresponding author:
shift and developing hydrocephalus (Figure 1). Stephanie Ruth Strachan, Critical Care Department, King’s College
At this point, neurosurgical advice was sought but Hospital, London SE5 9RS, UK.
before transfer could be arranged his condition Email: [email protected]
252 Journal of the Intensive Care Society 18(3)

Management of the severely

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

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 253

extracellular sodium concentration as a surrogate NCCU, his calculated osmolarity was 399.6 mmol/L.
marker of hydration status. Hypotonic solutions The equation we have used to calculate this is:
(5% dextrose in water, 0.2% sodium chloride in

5% dextrose in water and 0.45% sodium chloride Osmolarity ¼ 2Naþ þ urea þ glucose:
in water) are recommended as the intravenous
resuscitation fluids in the accompanying guidance The HHS guideline’s goals of treatment, which
excepting in the presence of ‘frank circulatory com- make it potentially helpful in this case, are to:
promise’, when ‘isotonic’ solutions such as 0.9%
sodium chloride are advised. The theory is that . normalise the osmolality;
dehydration culminating in a relative water deficit is . replace fluid and electrolyte losses;
visible to the clinician via the measured sodium . (normalise blood glucose levels).3
concentration.
Applying the Adrogué formula to this case of It is important to note that the guideline is, of
hypernatraemia, at the time of arrival to the NCCU, course, designed to guide the rehydration of patients
with an estimated patient weight of 65 kg and a who are hyperosmolar secondary to severe hypergly-
plasma sodium concentration of 169 mmol/L: caemia. This is important to consider because whilst
sodium and glucose are both effective osmoles contri-
Total body water ðTBWÞ buting to tonicity, urea is not, as it may cross the cell
¼ weight ðkgÞ  correction factor for age and gender membrane freely.
The rate of decline of osmolarity suggested by the
Patient TBW ¼ 65 kg  0:6 ¼ 39 L
HHS guideline is 3–8 mmol/L/h utilising 0.9% saline
as the preferred resuscitation fluid. However, the
Change in serum Naþ ¼ ðinfusate Naþ  serum Naþ Þ reduction in osmolarity must be balanced against
 ðTBW þ 1Þ 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
Change in serum Naþ with 1 L 5%dextrose fluid water moves intracellularly. The expected fluid
administration : ð0  169Þ=ð39 þ 1Þ ¼ 4:2 mmol=L: 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.
This suggests that after 1 L of 5% dextrose, the
expected measured sodium would be approximately
165 mmol/L and to normalise sodium (reference
Our approach
range 135–145 mmol/L), 6 L of 5% dextrose would On initial presentation at his local hospital, our
be required. patient was moderately hypernatraemic (sodium
Lindner et al. analysed four different formulae 152 mmol/L), severely uraemic (urea 118 mmol/L) and
designed to aid the correction and maintenance of hyperosmolar (calculated osmolarity 428 mmol/L),
serum sodium in a critical care setting through but his effective tonicity if urea is discounted as
estimation of the free water deficit and found the being an ineffective osmole was not elevated (effective
formulae were not able to accurately guide infu- osmolarity 310 mmol/L). He was given fluids (precise
sion therapy in hypernatraemic states in the ICU details are unknown) and had an initial positive fluid
patient.4 balance but close monitoring and fluid resuscitation
The established and consistent guidance in the lit- stopped when the patient was briefly palliated.
erature on managing chronic hypernatraemia (an ele- Four days after the initial presentation, on arrival
vated sodium for >48 h) is of a maximum reduction in at our institution, he was severely hypernatraemic
sodium concentration of 10 mmol/L (equivalent to an (sodium 169 mmol/L), severely uraemic (49 mmol/L)
osmolarity of 20 mmol/L) in a 24-h period due to the and hyperosmolar (calculated osmolality 399 mmol/L),
risks of fluid overload, cerebral oedema or central but due to the effectiveness of the components of
pontine myelinolysis caused by fluid shifts due to osmolality, he had a higher effective tonicity (effective
altered tonicity.5 osmolarity 350 mmol/L) than on initial presentation
to hospital.
We felt it prudent to be somewhat cautious with
Hyperosmolar state approach
rehydration post-operatively as his initial period of
For practical purposes, osmolality (mosmol/kg) and fluid administration was associated with development
osmolarity are interchangeable, with the latter being of an SDH. We postulated that the SDH occurred
calculable and measured in mmol/L. At the time of through a combination of uraemic platelet dysfunc-
presentation to the admitting hospital, our patient tion, a known cause of intracranial haemorrhage,
had a calculated osmolarity of 428.7 mmol/L and fluid shifts in less elastic tissue through
(normal range 285–295 mmol/L). On arrival in our 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 255

We elected to reduce the calculated serum osmo- It may be that we were overly cautious in the speed
larity by 20 mmol/L each day, utilising the osmolar of correction of this patient’s biochemistry, but in
effect of a 10 mmol/L sodium reduction as our refer- addition to estimating how much fluid may be
ence point. We needed to correct, by this stage, a pro- required to resuscitate a dehydrated patient, this
found hypernatraemia in addition to the uraemia and case also serves as a reminder of the potential conse-
raised tonicity. To achieve this, we used a combin- quences of dehydration, including hyperviscosity,
ation of fluids together with regular monitoring, as AKI and uraemic platelet dysfunction; difficulties
the patient’s salt and water deficit, the distribution prognosticating for individuals when the literature
of salt and water across intracellular and extracellular provides information regarding cohorts; and the
compartments, renal excretion, and response to fluid amazing resilience of some patients.
resuscitation were, essentially, all unknowns (Tables 4 We suggest a reconsideration of the approach to
and 5). Figure 2 displays graphically the changes in correcting hypernatraemia in patients with chronic
sodium and calculated osmolarity during the patient’s hypernatraemia (>48 h) and dehydration, as attempt-
hospital admission, from day 1 at the admitting hos- ing to calculate the free water deficit in critically ill
pital, transfer to the tertiary service during day 4, patients is highly inaccurate. We suggest individual-
through to transfer to a neurosurgical ward on day 12. isation of resuscitation regimes for patients based on
Initially, large quantities of isotonic fluids were osmolarity, monitoring and reviewing the response to
used for rehydration with frequent blood sampling fluid administration whilst maintaining the clear guid-
targeting a daily reduction in calculated osmolarity ance on safe parameters for changes in sodium con-
of 20 mmol/L. Following the initial rehydration, centrations. Our recommendation draws significant
hypotonic solutions were able to be utilised safely parallels with the current guidance on the manage-
and, once the biochemistry results were near reference ment of HHS.
ranges, enteral water was used. Intravenous fluids
given are itemised, with the remainder of fluid input Consent
comprising medications and nasogastric feed. Published with the written consent of the patient.
The patient required regular blood sampling to
assess the serum biochemical changes in response to Declaration of conflicting interests
fluid type and volume, with close fluid balance moni- The author(s) declared no potential conflicts of interest with
toring. Normal sodium, urea and creatinine test respect to the research, authorship, and/or publication of
results were not seen until day 12 of admission, at this article.
which point the patient had a cumulative positive
fluid balance of 16 L (40% estimated TBW). Funding
Calculated osmolarity at this point was 303.9 mmol/L. The author(s) received no financial support for the research,
When comparing his actual cumulative fluid bal- authorship, and/or publication of this article.
ance with the initial estimate of free water required
from the Adrogué calculation method (6 L), it can be References
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