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Case Reports in Emergency Medicine
Volume 2017, Article ID 8692017, 3 pages
https://doi.org/10.1155/2017/8692017

Case Report
Cerebral Salt-Wasting Syndrome Caused by Minor Head Injury
Toshiki Fukuoka,1 Yuko Tsurumi,2 and Arihito Tsurumi2
1Department of Neurosurgery, Nagoya University Graduate School of Medicine, Nagoya, Japan
Department of Neurosurgery, Tsurumi Neurosurgery, Koga, Ibaraki, Japan

2Correspondence should be addressed to Toshiki Fukuoka; rugby104@gmail.com
Received 23 October 2016; Accepted 4 December 2016; Published 17 January 2017
Academic Editor: Vasileios Papadopoulos
Copyright © 2017 Toshiki Fukuoka et al. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.
A 34-year-old woman was admitted to hospital after sustaining a head injury in a motor vehicle accident (day 1). No signs ofneurological deficit, skull fracture, brain contusion, or intracranial bleeding were evident. She was discharged without symptoms on
day 4. However, headache and nausea worsened on day 8, at which time serum sodium level was noted to be 121 mEq/L. Treatment
with sodium chloride was initiated, but serum sodium decreased to 116 mEq/L on day 9. Body weight decreased in proportion to
the decrease in serum sodium. Cerebral salt-wasting syndrome was diagnosed. This case represents the first illustration of severe
hyponatremia related to cerebral salt-wasting syndrome caused by a minor head injury.

1. Introduction
Hyponatremia resulting from cerebral salt-wasting syndrome(CSWS) can occur after severe brain injury, severe cerebrovascular disease, or surgery [1–9]. Hyponatremia canresult in brain edema and secondary nausea, headache,altered consciousness, and sometimes death. Close monitoring of serum Na levels and immediate correction ofelectrolyte abnormalities are therefore necessary after severe
brain damage. If left untreated without correct diagnosis,
severe hyponatremia may result in seizures and worsening
cerebral edema [10].
However, no previous reports have described hyponatremia of CSWS occurring after minor head injury in theabsence of intracranial bleeding, skull fracture, or braincontusion. This report describes the case of a patient withminor head injury who developed severe hyponatremia dueto CSWS.

2. Case Report
A 34-year-old woman with no significant past medical history
sustained an injury to the right forehead in a motor vehicle
accident (day 1). She was not taking any regular medications.
Physical examination revealed no traumatic wounds otherthan a thin subcutaneous hematoma on the right forehead.

She presented with headache and nausea, and Glasgow coma
scale score was 14 (E3, V5, M6), but no obvious focal
neurological signs were present, including amnesia. Furthermore, computed tomography (CT) of the head revealed noskull fracture, intracranial hemorrhage, or brain contusion.
Complete blood cell (CBC) count and serum biochemistry
revealed no abnormalities, and serum Na concentration wasnormal (141 mEq/L). She was hospitalized for observation
under a diagnosis of brain concussion. By day 2, Glasgow
coma scale score had normalized and symptoms of headacheand nausea had almost resolved. On day 3, serum Na wasstill within the normal range but had decreased to 135 mEq/L.
CBC and serum biochemistry revealed no abnormalities, andthe patient was discharged without symptoms on day 4.
After discharge from hospital, she began to feel severe
and gradually worsening fatigue and nausea and finallypresented to the emergency department on day 8. Head CT
revealed no abnormal findings. Blood testing disclosed serum
Na of 121 mEq/L and serum Cl of 90 mEq/L, while serum
biochemistry showed no other abnormalities. Skin turgor wasslightly diminished, suggesting decreased circulating plasma
volume. She was therefore hospitalized for evaluation andmanagement of hyponatremia.
Treatment was initiated via intravenous saline and oraladministration of salt with frequent monitoring of serum Nalevels. Body weight was measured daily to help distinguish2Case Reports in Emergency Medicine
Oral ingestion of salt
Sodium chloride infusion
48150
145

47
46

135
130

45

125

44

Body weight (kg)

Sodium (mEq/L)

140

120
43115
110

1

Before the injury

42
8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23Date
3 months laterSodium
Body weight

Figure 1: Clinical course of treatment and examinations.

between the presence of CSWS, syndrome of inappropriate
secretion of antidiuretic hormone (SIADH), and other disorders. Blood testing on day 9 revealed serum Na of 116 mEq/Land serum osmolality of 251 mOsm/L (reference range: 275–285 mOsm/L). On day 10, blood testing showed serum
Na of 125 mEq/L (urine Na: 65 mEq/L), serum osmolalityof 251 mOsm/L (urine osmolality: 238 mOsm/L), a urine
acid level of 1.5 mg/dL (reference range: 2.3–7.0 mg/dL), anatrial natriuretic peptide (ANP) level of 114 pg/mL (referencerange: <43 pg/mL), a brain natriuretic peptide (BNP) levelof 142 pg/L (reference range: 0–18 pg/L), an antidiuretichormone (ADH) level of 0.79 pg/mL (reference range: 0.3–4.2 pg/mL), a plasma renin activity level of <2.0 pg/mL(reference range: 2.5–21.4 pg/mL), a thyroid-stimulating hormone (TSH) level of 2.734 𝜇g/mL (reference range: 0.350–4.940 𝜇g/mL), a free triiodothyronine level of 2.24 pg/mL(reference range: 1.71–3.71 pg/mL), a free thyroxine levelof 1.02 ng/dL (reference range: 0.70–1.48 ng/dL), a morning
fasting hydrocortisone level of 14.99 𝜇g/mL (reference range:6–20 𝜇g/mL), and an adrenocorticotropic hormone level of
30.2 pg/mL (reference range: 7.4–55.7 pg/mL). In addition,body weight decreased as serum Na decreased.
These results, the diminished skin turgor, and the decrease in body weight indicated a diagnosis of CSWS andthe absence of renal failure, thyroid dysfunction, and adrenalinsufficiency. Blood testing showed serum Na of 129 mEq/L
on day 11 (urine Na: 60 mEq/L) and serum Na of 136 mEq/L(urine Na: 55 mEq/L) on day 12. Serum Na subsequently
remained within the normal range. On day 16, intravenous
saline infusion was terminated. Fatigue and nausea resolved
as serum Na concentrations increased. After day 20, bodyweight started to improve towards baseline. She was discharged on day 24 without any subsequent recurrence ofhyponatremia. Serum BNP level on day 27 had completely
normalized to 10 pg/L (reference range: 0–18 pg/L). The
course of treatment is shown in Figure 1.

3. Discussion
CSWS is characterized by renal loss of sodium following
intracranial disorders, resulting in hyponatremia and hypovolemia [11–13]. CSWS ordinarily occurs after severe brain
injury, severe cerebrovascular disease, or surgery [1–9], andno previous reports have described CSWS after minor head
injury. Intriguingly, lightning injury [14] and therapeuticbarbiturate coma [15] may also cause CSWS. While manystudies have described aspects of CSWS, the pathogenesis ofrenal salt wasting derived from cerebral disease is not fully
understood. The most probable process involves disruptionof neural inputs to the kidney and/or central productionof a circulating natriuretic factor [6, 7, 11, 12, 16, 17]. In
addition, some authors have indicated that ANP and BNP
exert biologic effects that could lead to CSWS [3, 6, 7, 18–20]. The time from traumatic brain injury to development of
CSWS can vary from 2 days to 2 months [2, 3, 6, 18, 21, 22].
Regarding the severity of CSWS, highly invasive surgery andthe severity of findings on head CT are associated with theseverity of CSWS [9, 21]. In other words, CSWS is unlikely tooccur in the absence of severe brain damage.
Differentiating between CSWS and SIADH is criticalfor appropriate treatment of hyponatremia, because therapeutic strategies for the two syndromes differ markedly.
When hyponatremia is treated inappropriately, the patientis at increased risk of delayed ischemic deficits and/or
osmotic demyelination leading to disability and mortality[23]. The primary distinction between CSWS and SIADHis whether the circulating blood volume is decreased orincreased [6, 12, 24, 25]. Since some CSWS cases do notpresent with characteristic physical findings, comprehensive
judgment is frequently needed to reach a definitive diagnosis.
In the present case, serum Na concentrations, osmolality,ANP, BNP, ADH, diminished skin turgor, decreasing bodyweight, and prolonged natriuresis despite hyponatremia were

Case Reports in Emergency Medicine
consistent with the diagnosis of CSWS rather than SIADH. Asa matter of fact, serum Na levels and symptoms were greatly
improved with substantial hydration and NaCl administration.
CSWS is generally caused by severe brain injury or
severe cerebrovascular disease, and head CT and magnetic
resonance imaging typically reveal abnormal findings. In
the present case, head CT was notable for the absence of
intracranial bleeding and brain contusion. This case showsthat even minor head injuries can cause disruptions to theneural inputs to the kidney and/or central production ofcirculating natriuretic factors that eventually contribute toCSWS. Clinicians should be aware that even minor head
injury may result in CSWS, hyponatremia, and secondary
symptoms.

Competing Interests
The authors declare that they have no competing interests.

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