Table of Contents  

Ahmad, Alrais, Elkhouly, Elkholy, Hadi, and Beniamein: Causes of hyponatraemia in traumatic brain injury patients in intensive care unit settings

Introduction

Hyponatraemia is the most common electrolyte abnormality seen in patients with traumatic brain injuries (TBIs) and other neurosurgical injuries.14 It usually develops between 2 and 7 days after the initial injury, and is associated with increased mortality and morbidity.5,6 Hyponatraemia is a common cause of secondary brain injury.7,8 It is defined by a serum sodium level less than 135 mmol/l.9,10 If it is not treated promptly in acute TBI patients, it can lead to serious complications, such as malignant brain oedema, which may lead to brain herniation and eventually death, thus affecting morbidity and mortality data.11,12 It is very important to understand the causes leading to hyponatraemia, before treatment is commenced, as the wrong diagnosis can lead to delayed correction and may affect the neurological outcome. There are various causes of hyponatraemia in TBI patients.9,10,1317 The most common are syndrome of inappropriate antidiuretic hormone secretion (SIADH) and cerebral salt wasting (CSW) disease.5,6 The difference between the two syndromes is extracellular fluid volume status; CSW is a volume-contracted state while SIADH is an euvolaemic state.1820 There are various other causes, for example dehydration on admission owing to poor intake as a result of poor neurological status,21 use of hypotonic fluids (5% dextrose water and 0.45% saline), use of diuretics and overuse of desmopressin acetate to treat diabetes insipidus. Use of desmopressin acetate is very common in severe traumatic injury patients and, if this is overlooked while treating hypernatraemia in these patients, iatrogenic hyponatraemia may result.16 Others causes, such as organ failure [heart failure, liver cirrhosis and chronic renal failure (CRF)] do also exist.1517 Some patients may develop dilutional hyponatraemia during the weaning phase of mechanical ventilation, as a result of increased fluid retention due to non-osmotic secretion of serum antidiuretic hormone (ADH),16,21 such as hypovolaemia, hypotension, pain, nausea, agitation or stress, which are very common findings in these patients once sedation is reduced or stopped for weaning. Some patients may develop postoperative dilutional hyponatraemia due to increased serum ADH activity. Dilutional hyponatraemia may develop in the postextubation phase from drinking excessive volumes of clear fluids.16 Other causes can be endocrinal failure with hypothyroidism, cortisol deficiency or pituitary insufficiency.2224 Many studies of the prevalence of SIADH and CSW in TBI patients have been carried out, but studies of other causes of hyponatraemia in these patients are scarce. This study was conducted in patients admitted to our intensive care unit (ICU) with the aim of understanding the various other causes of hyponatraemia, particularly in critically ill patients, which may be uncommon outside the ICU environment.

Material and methods

Ethics

Prior approval from the hospital ethics committee was sought before starting this study.

Study design

This was an observational analytical study.

Inclusion criteria

All patients diagnosed with acute TBIs admitted to the Surgical, Medical and Neurosurgical ICU, Rashid Hospital Trauma Centre, Dubai, United Arab Emirates, who developed hyponatraemia, including all age groups, were included in the study.

Data collection

Data were collected using a convenience sampling technique.

Patients and methods

A retrospective analysis of 442 patients with various TBIs who were admitted to the Surgical, Medical and Neurosurgical ICU from January 2010 to August 2013 was carried out. A total of 150 patients who developed hyponatraemia during their stay in ICU were analysed further and different causes of hyponatraemia were investigated. The incidence of hyponatraemia in TBI patients was calculated in our set-up. Data were collected in Microsoft Excel® (Microsoft Corporation, Redmond, WA, USA) and analysed using the online documentation system IntelliVue Clinical Information Portfolio (Philips, Amsterdam, the Netherlands), which is used in our department for the electronic documentation of patient data. Standard investigations, such as serum sodium, serum osmolality, urine osmolality, spot urine sodium concentration, blood glucose, serum urea, serum creatinine, serum cortisol and thyroid function tests, were carried out in our hospital laboratory in all hyponatraemic patients to investigate the definitive cause before starting treatment. Standard protocols and guidelines were followed to diagnose different causes of hyponatraemia, present in our hospital file net practical guidelines, diagnostic algorithm for hyponatraemia (Figure 1).

FIGURE 1

Diagnostic algorithm for hyponatraemia.

8-4-3-fig1.jpg

Data analysis

Data were analysed using Statistical Product and Service Solutions (SPSS) Statistics Base 21 (IBM Corporation, Armonk, NY, USA).

Results

The majority of the patients were male (87%). Out of a total of 150 patients, 129 were adults, but 21 (14%) belonged to the paediatric age group (≤ 12 years). Sixty per cent (90/150) of patients were admitted with severe TBI, while 29% and 31% had moderate and mild head injuries, respectively. TBI is categorized into severe, moderate and mild on the basis of the Glasgow Coma Scale (GCS) score on admission, whereby a GCS score of 3–8 is defined as severe TBI, a GCS score of 9–12 is defined as moderate TBI and a GCS score of 13–15 is defined as mild TBI. The predominant age groups were 25–36 years and 37–48 years (31% and 21%, respectively). Ten (7%) patients were in the 49–60 year age group and 13 (9%) were > 60 years. Fourteen per cent of patients were in the paediatric age group (≤ 12 years) and 18% were 13–24 years (Figure 2). The incidence of hyponatraemia was 34%. The mean time to onset of hyponatraemia after TBI and ICU admission was 7.74 days. Mean serum sodium before treatment started was 132.2 ± 2.9 mmol/l (standard deviation). Severe hyponatraemia was found in only four cases (serum sodium < 125 mmol/l), with the lowest value being 117 mmol/l. Twenty-six per cent of cases (39/150) fulfilled diagnostic criteria for SIADH and 21% (32/150) for CSW (Figure 3). Mean time to onset of hyponatraemia was 7.95 days post ICU admission in patients diagnosed with SIADH and 9 days with CSW.

FIGURE 2

Age groups.

8-4-3-fig2.jpg
FIGURE 3

Causes of hyponatraemia in TBI patients.

8-4-3-fig3.jpg

Other causes of hyponatraemia were found in 53% (79/150) of patients (Figure 4), mainly dehydration (8/150), overuse of fluids (15/150), use of hypotonic fluids (5/150), overtreatment with desmopressin acetate (8/150) and use of diuretics (10/150). In addition, 20 patients were found to have dilutional hyponatraemia during the weaning phase of mechanical ventilation, after reduction or complete stoppage of sedation (Figure 4), and 10 patients developed dilutional hyponatraemia during the postextubation phase as a result of increased oral intake of clear fluids (Figure 4). Hyponatraemia in three patients was caused by CRF. No cases of hyponatraemia as a result of endocrinal abnormality (adrenal, thyroid or pituitary) were recorded (Figure 4), the reason being that most of the patient sample were young and previously healthy without any previous comorbid conditions. While comorbid conditions, such as type 2 diabetes mellitus, hypertension, ischaemic heart disease, CRF, chronic alcoholism and bronchial asthma, were found in 10% of cases, all other (90%) were previously healthy. Ninety-five per cent of all patients (143/150) who developed hyponatraemia during their stay in ICU were discharged; however, seven patients died. The average length of stay in these patients was found to be 16.6 ± 9.8 (standard deviation) days (range 2–55 days).

FIGURE 4

Other causes of hyponatraemia.

8-4-3-fig4.jpg

Discussion

Our study was conducted on critically ill neurosurgical injury patients. All age groups were included, including the paediatric population, because the Rashid Hospital Trauma Centre is a solo centre for intensive management of these patients, and we receive a significant number of paediatric patients throughout the year. We calculated the incidence of hyponatraemia in these patients because this is a very common problem in the ICU. Our study found that younger patients are more likely to experience TBI and be admitted to the ICU, and that the majority of our patients were previously healthy, having no previous comorbid condition prior to ICU admission. We found that a significant number of patients developed hyponatraemia as a result of various causes other than those more commonly noted (CSW and SIADH). We found that a significant number of patients developed dilutional hyponatraemia during the weaning phase of mechanical ventilation, which explains non-osmotic secretion of serum ADH as a result of pain, stress and agitation once sedation is reduced or ceased. Some results from our study were comparable to internationally published data. The incidence of hyponatraemia was 34% and the mean time to onset of hyponatraemia after ICU admission was 7.74 days. These results are comparable to those obtained in a similar study carried out by Chitsazian et al.26 in August 2013, in which the incidence of hyponatraemia was 31.6% and the mean time to onset of hyponatraemia was 9.29 ± 6.8 days. However, the study population was significantly smaller than ours, a total of 95 patients compared with our 442 patients.

A similar study was conducted by Costa et al.27 in 2009, in which incidence of hyponatraemia was 34.6%, which is again quite similar to the incidence in our study. However, the sample was very small, only 26 patients, and hyponatraemia in these patients was attributed to CSW, while in our study only 21% of cases fulfilled the criteria for diagnosis of CSW. In 2009, Sherlock et al.25 conducted a similar study on a large number of patients (1698 in total). They found that the mean time to onset of hyponatraemia was 6.7 days post TBI and that the mean age of the study population was 41.7 years. In our study, the mean time to onset of hyponatraemia was 7.74 days and the most common age group was the 25–36 years group (31%). However, compared with the study carried out by Sherlock et al.,25 our sample size was quite small.

Born et al.,28 in a similar study conducted in head injury patients, found that SIADH was responsible for hyponatraemia in 33% of patients whereas we found that 26% of cases fulfilled the criteria for diagnosis of SIADH. Similarly, Fahimi et al.29 performed a comparative study on a paediatric age group, ranging in age from 1 to 14 years, on different intravenous fluid maintenance therapy and they found that 14 out of 108 patients developed hyponatraemia with hypotonic fluids. In our study, we found that only 5 out of 150 patients developed hyponatraemia as a result of hypotonic fluids administration. However, our study comprised all age groups, not only paediatric patients. Therefore, in our study, the incidence of hyponatraemia and time to onset of hyponatraemia were very similar to the results of a few international studies. However, we found significant causes of dilutional hyponatraemia, other than SIADH, which were not rigorously investigated in previous studies. However, there were some limitations in our study. We performed a retrospective analysis and it was asingle-centre observational study. In future, further studies may be needed for a prospective analysis of these patients and these should be carried out in a multicentre fashion.

Conclusion

The two most common causes of hyponatraemia in TBI patients are SIADH and CSW, but a significant number of other causes also exist, especially in the ICU. There are variety of causes of dilutional hyponatraemia other than SIADH due to non-osmotic secretion of serum ADH, especially in ICU settings.

Acknowledgements

I am very thankful for all the hard work carried out by my coauthors for the completion of this study. Special thanks are extended to Dr Zeyad Alrais, Head Intensivist, who critically reviewed and edited this article. Special regards to our medical secretary, Ms Rita, and biostatician, Ms Annie, for their technical support in formatting text and analysing the data. There was no financial compensation for their technical support. There was also no other financial requirement to complete this study.

References

1. 

Rabinstein AA, Wijdicks EF. Hyponatraemia in critically ill neurological patients. Neurologist 2003; 9:290–300. http://dx.doi.org/10.1097/01.nrl.0000095258.07720.89

2. 

Donati-Genet PC, Dubuis JM, Giradin E, Rimensberger PC. Acute symptomatic hyponatraemia and cerebral salt wasting after head injury: an important clinical entity. J Pediatr Surg 2001; 36:1094–7. http://dx.doi.org/10.1053/jpsu.2001.24770

3. 

Webster JB, Bell KR. Primary adrenal insufficiency following traumatic brain injury: a case report and review of the literature. Arch Phys Med Rehabil 1997; 78:314–18. http://dx.doi.org/10.1016/S0003-9993(97)90040-X

4. 

Zafonte RD, Mann NR. Cerebral salt wasting syndrome in brain injury patients: a potential cause of hyponatraemia. Arch Phys Med Rehabil 1997; 78:540–2. http://dx.doi.org/10.1016/S0003-9993(97)90173-8

5. 

Tisdall M, Crocker M, Watkiss J, Smith M. Disturbances of sodium in critically ill neurologic patients. J Neurosurg Anesthesiol 2006; 18:57–63. http://dx.doi.org/10.1097/01.ana.0000191280.05170.0f

6. 

Diringer MN, Zazulia AR. Hyponatraemia in neurologic patients: consequences and approaches to treatment. Neurologist 2006; 12:117–26. http://dx.doi.org/10.1097/01.nrl.0000215741.01699.77

7. 

Ke C, Poon WS, Ng HK, Tang NL, Chan Y, Wang JY, Hsiang JN. The impact of acute hyponatraemia on severe traumatic brain injury in rats. Acta Neurochir Suppl 2000; 76:405–8. http://dx.doi.org/10.1007/978-3-7091-6346-7_84

8. 

Haddad SH, Arabi YM. Critical care management of severe traumatic brain injury in adults. Scand J Trauma Resusc Emerg Med 2012; 20:12. http://dx.doi.org/10.1186/1757-7241-20-12

9. 

Spasovski G, Vanholder R, Allolio B, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Intensive Care Med 2014; 40:320–31. http://dx.doi.org/10.1007/s00134-014-3210-2

10. 

Adrogué HJ, Madias NE. Hyponatraemia. N Engl J Med 2000; 342:1581–9. http://dx.doi.org/10.1056/NEJM200005253422107

11. 

Mulloy AL, Caruana RJ. Hyponatraemic emergencies. Med Clin North Am 1995; 79:155–68.

12. 

Arieff Al. Hyponatraemia, convulsions, respiratory arrest, and permanent brain damage after elective surgery in healthy women. N Engl J Med 1986; 314:1529–35. http://dx.doi.org/10.1056/NEJM198606123142401

13. 

Arieff Al, Ayus JC, Fraser CL. Hyponatraemia and death or permanent brain damage in healthy children. BMJ 1992; 304:1218–22. http://dx.doi.org/10.1136/bmj.304.6836.1218

14. 

Kokko JP. Fluids and electrolytes. In: Goldman L, Ausiello D (eds.) Cecil Textbook of Medicine, 22nd edn. Philadelphia, PA, USA: Saunders; 2004, pp. 678–81.

15. 

Cho KC. Electrolytes and acid-base disorders. In: Papadakis MA, McPhee SJ, Rabow MW (eds.) Current Medical Diagnosis and Treatment, 52th edn. San Francisco, CA, USA: McGraw Hill; 2013, pp. 871–5.

16. 

Ahmad K, Alrais Z, Majeed S, et al. Causes of hyponatraemia in traumatic brain patients in ICU settings. ESICM Annual Congress; 2014. URL: www.esicm.org/news-article/ePosters-LIVES-2014-online-new-portals

17. 

Cole CD, Oren N, Gottfried MD, Liu JK, Couldwell WT. Hyponatraemia in the neurosurgical patient: diagnosis and management. Neurosurg Focus 2004; 16:4. http://dx.doi.org/10.3171/foc.2004.16.4.10

18. 

Carlotti AP, Bohn D, Rutka JT, et al. A method to estimate urinary electrolyte excretion in patients at risk for developing cerebral salt wasting. J Neurosurg 2001; 95:420–4. http://dx.doi.org/10.3171/jns.2001.95.3.0420

19. 

Harrigan MR. Cerebral salt wasting syndrome: a review. Neurosurgery 1996; 38:152–60. http://dx.doi.org/10.1097/00006123-199601000-00035

20. 

Palmer BF. Hyponatraemia in patients with central nervous system disease: SIADH versus CSW. Trends Endocrinol Metab 2003; 14:182–7. http://dx.doi.org/10.1016/S1043-2760(03)00048-1

21. 

Alejandro A, Rabinstein, Eelco FM, Wijdicks: Hyponatraemia in critically ill neurosurgical patients. The Neurologist 2003; 9:290–300. http://dx.doi.org/10.1097/01.nrl.0000095258.07720.89

22. 

Moses AM, Streeten DHP. Disorders of neurohypophysis. In: Isselbacher KJ, Braunwald E, Wilson JD, et al (eds.) Harrison’s Principles of Internal Medicine, 13th edn. New York, NY, USA: McGraw-Hill; 1994, pp. 1921–30.

23. 

Powner DJ, Boccalandro C, Alp MS, Vollmer DG. Endocrinal failure after traumatic brain injury. Neurocrit Care 2006; 5:61–70. http://dx.doi.org/10.1385/NCC:5:1:61

24. 

Claussen MS, Landercasper J, Cogbill TH. Acute adrenal insufficiency presenting as shock after trauma and surgery: three cases and review of literature. J Trauma 1992; 32:94–100. http://dx.doi.org/10.1097/00005373-199201000-00020

25. 

Sherlock M, O’Sullivan E, Agha A, et al. Incidence and pathophysiology of severe hyponatraemia in neurosurgical patients. Postgrad Med J 2009; 85:171–5. http://dx.doi.org/10.1136/pgmj.2008.072819

26. 

Chitsazian Z, Zamani B, Mohagheghfar M. Prevalence of hyponatraemia in intensive care unit patients with brain injury. Arch Trauma Res 2013; 2:91–4. http://dx.doi.org/10.5812/atr.9877

27. 

Costa KN, Nakamura HM, da Cruz LR, de Miranda LSVF, dos Santos-Neto RC, de Lavor Cosme S, Casulari LA. Hyponatraemia and brain injury. Arq Neuropsiquiatr 2009; 67:1037–44. http://dx.doi.org/10.1590/S0004-282X2009000600014

28. 

Born JD, Hans P, Smitz S, Legros JJ, Kay SS. Syndrome of inappropriate antidiuretic hormone secretion after severe head injury. Surg Neurol 1985; 23:383–7. http://dx.doi.org/10.1016/0090-3019(85)90212-5

29. 

Fahimi D, Delavar MA, Karahoudi M, Honarmand M, Eghbalkhah A. Comparison of two intravenous fluid maintenance therapy with different sodium concentration in hospitalized children. A randomized trial study. J Ped Nephrol 2014; 2:110–15.




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