Hypernatremia in patients with traumatic brain injury: about 43 cases
Jawad Rochdi (jawadinou at hotmail dot com) #, Khalid Lahmadi, Abdelkader Laatiris, Saida Tellal
Laboratory of Biochimistry, Military Hospital of Instruction Mohammed V Rabat, Morocco
# : corresponding author
DOI
//dx.doi.org/10.13070/rs.en.2.1463
Date
2015-10-30
Cite as
Research 2015;2:1463
License
Abstract

Introduction: Traumatic brain injuries (TBI) are common diseases primarily affecting the young population. They generate some very serious consequences and may make it impossible to socio-economic reintegration of the patient. Hypernatremia is a common electrolyte disturbance in patients with TBI admitted to surgical intensive care units (SICU). Hospitalized patients with hypernatremia have a significantly higher mortality rate (40-60%) compared with patients without hypernatremia. Objectives: The aim of this study is to describe the prevalence and outcomes of hypernatremia in patients with head injury admitted to a surgical intensive care unit. Patients and Methods: We included 43 hospitalized cranial traumas in surgical ICU of HMIMV between January 2007 and November 2008. These patients were classified according to the severity of head injury based on the Glasgow Coma Score (GCS). Changes in serum sodium and plasma osmolarity were followed for a period of 22 days. Results: In our series, there were a total of 37 male and 6 female (sex ratio 6.17). The mean age was 39.26 ± 17 (15 to 85) years. Age groups of 20 to 39 dominate with 48.84℅. Accident public roads were the primary cause of head injuries 86.05 ℅. There were 12 cases of mild head injury (27.91%), 8 moderate head injury (18.6%) and 23 severe head injury (53.49%). 13 patients (30.2%) had hypernatremia during their stay in the SICU. There were 8 with severe head injury (34.8%), 3 with moderate (38.5%), and 2 with mild head injury (16.7%). Ten of hypernatremic patients died (76.9%) and 3 had a good evolution. The comparison of the installation time of hypernatremia in the "death" group and the "favorable" group showed a statistically significant difference (p = 0.001). Conclusion: hypernatremia is frequently encountered in patients with TBI and is associated with poor outcomes. Efforts should focus on the prevention of hypernatremia by regular monitoring and adequate correction.

Introduction

Head injuries are a major public health problem both because of their frequency as health costs they generate. They are the leading cause of death among those aged less than 40 years. Despite advances in neurocritical care, nearly a third of patients admitted with a severe traumatic brain injury die, and less than half have a favorable neurologic outcome [1-3].

Patients with severe TBI have a high risk of developing hypernatremia over the course of their ICU stay, due to the coexistence of predisposing conditions such as impaired sensorium, altered thirst, central diabetes insipidus (CDI) with polyuria, and increased insensible losses [4]. Moreover, these patients often receive mannitol or hypertonic saline solutions (HTS) with the aim of reducing cerebral edema and controlling intracranial pressure (ICP) [5]. Hospitalized patients with hypernatremia have a significantly higher mortality rate (40%-60%) compared with patients without hypernatremia [6-9]. In this clinical setting, it is not known, however, whether increased serum sodium (Na) is an independent risk factor for death, or is simply a surrogate marker of illness severity. Some authors have suggested that it could be used as an indicator of quality of care [10].

We proposed in this work to evaluate the prevalence and prognosis of hypernatremia in 43 TBI patients admitted to the surgical intensive care unit of the Military Hospital of Instruction Mohammed V.

Hypernatremia in patients with traumatic brain injury: about 43 cases figure 1
Figure 1. Distribution of patients according to the etiology of brain injury.
Patients and methods

This is a descriptive and analytical retrospective study of a series of cases over a period of 23 months from January 2007 to November 2008 conducted in surgical intensive care unit of the Military Hospital of Instruction Mohammed V in Rabat.

We included all TBI patients who stayed in the surgical intensive care unit for a period of at least 3 days. We excluded from this study cases that lacked data on laboratory tests. The clinical data, CT, biological and therapeutic was made from the hospital registry, medical record and prescription card. The patients were divided according to the severity of head injury based on the GCS. Changes in serum sodium were followed for a period of 22 days. Meanwhile, there were the values of serum potassium, blood sugar and blood urea. Osmolarity was calculated from these data. The determination of blood volume is based on the value of the central venous pressure (PVC). The therapeutic data represented by the infusion of plasma expanders (isotonic saline serum 0.9%; hypertonic saline serum); Mannitol 20%; and DDAVP (desmopressin).

Hypernatremia in patients with traumatic brain injury: about 43 cases figure 2
Figure 2. Distribution of hypernatremia depending on the severity of the head injury.
Results

We included in the study 43 TBI patients (mean age 39.26 ± 17 years). Age groups of 20 to 39 dominate with 48.84%. 37 males and 6 females (sex ratio was 6.17%). Accident public roads were the primary cause of head injuries 86.05% (figure 1). There were 12 cases of mild head injury (27.91%) and 8 moderate head injury (18.6%). Severe head injury was found in 23 (53.49%)

Hypernatremia was documented in 13 patients (30.2%), 11 men and 2 women. There were 8 with severe head injury (34.8%), 3 with moderate (38.5%), and 2 with mild head injury (16.7%) (figure 2). The median time to development of hypernatremia was 4 days. Ten of hypernatremic patients died (76.9%) and 3 had a good evolution. The comparison of the installation time of hypernatremia in the "death" group and the "favorable" group showed a statistically significant difference (p = 0.001) (Table I).

Time installation IC 95℅ p
Evolutiondeath3,000±0.707(1,614-4,386) 0.001
good10,860 ±1.111(8,684-13,037)
Table 1. Time installation hypernatremia and evolution.
Discussion

Hypernatremia is a frequent and potentially life-threatening electrolyte disturbance in hospitalized patients. About 7–9% of critically ill patients in the ICU develop hypernatremia [11, 12]. It is usually caused by progressive loss of water from the kidney or gastrointestinal tract and insensible perspiration, which is sometimes accompanied by insufficient fluid intake or inappropriate treatment with electrolyte solution. Patients with TBI have disordered consciousness, loss of sensation of thirst and concomitant fever, and are usually treated with diuretics to control intracranial pressure which results in loss of body fluid.

To our knowledge, very few studies have focused exclusively on head injuries, most were made of different services. In a 5-year study made by O’Donoghue et al, the incidence of hypernatremia was 7.7% in the general ICU [13]. Studying patients receiving mannitol for treatment for dehydration in the neurologic/ neurosurgical intensive care units, Aiyagari et al. found that the incidence of hypernatremia was 24.3% [14]. Maggiore et al. reported that the incidence of hypernatremia was as high as 51.5% in a cohort study of patients in the ICU [15]. Another study revealed an incidence of 28.8% among patients with TBI in the NICU [16].

Paiva et al, in prospective study conducted in 80 consecutive patients diagnosed with TBI who were managed in 1 year and were hospitalized in the surgical ICU, found 20 cases of hypernatremia (25%) [17]. In a multicenter study, 34.1% of patients hospitalized in intensive care units presented hypernatremia [18]. The incidence of hypernatremia in our study was 30.2%which is almost comparable to other reported studies.

The median time to development of hypernatremia was 4 days in this study, which is lesser than 5 days seen by Paiva et al. [17], but longer than the 3-days seen by O'Donoghue et al [13].

The mortality rates in head-injured patients with hypernatremia are higher than rates in such patients with normal sodium concentrations [19]. Once the serum sodium concentration is elevated, it can result in remarkable brain swelling. Since the amount of the infusion volume is controlled manually in head-injured patients, unexpected loss of free water as a result of excretion of hypotonic urine can induce hypernatremic dehydration. Furthermore, losses of water can decrease renal plasma flow and renal filtration rates, resulting in aggravation of the hypernatremia [17]. It has been reported that the mortality rate for patients with hypernatremia ranges from 32 to 66% in the ICU [10]. In the study by Li et al. the mortality rate for patients with sodium level of >150 mmol was 67.4% (180/267) [16] which is comparable to that reported in a study of Mandal et al. (66%) [20]. In our study, we found a higher mortality (76.9%) which is consistent with the other reported studies. The main cause found in our patients was septic shock in 5 cases (including nosocomial pneumonia), three patients died from neurological worsening and one patient died from bleeding disorder (pulmonary embolism). We found also that early installation of hypernatremia was associated with higher mortality (p = 0.001).

In the literature, hypernatremia in intensive care is a potential iatrogenic event [18]. The effects of mannitol and hypertonic saline on the osmolarity and electrolytes have been reported in a study conducted in Geneva [21]. It showed a significant change in serum sodium and osmolarity in patients receiving hypertonic solutions, with a significant difference between the group receiving isotonic NaCl and the two groups receiving hypertonic solutions. The difference between the two groups that received hypertonic solutions was also statistically significant.

In a retrospective study of over 4000 patients with brain damage, severe hypernatremia was an independent factor associated with increased mortality, frequently found in the most severe patients who received osmotherapy [14]. The management of hypernatremia in patients who have cerebral edema and elevated intracranial pressure is not so easy. These patients are often treated with osmotic diuretics such as mannitol, which cause a free water diuresis and often lead to hypernatremia. This hypernatremia might help in the treatment of cerebral edema by raising the serum osmolarity. On the other hand, evidence from medical-surgical literature suggests that hypernatremia leads to increased mortality. The dose, duration, and serum sodium target of the intervention remains unclear. Furthermore, hypertonic saline and mannitol have serious adverse effects on their own. Mannitol administration can lead to renal failure, metabolic derangements (hypochloremic alkalosis), and rebound increases in ICP; HTS can lead to volume expansion, heart failure, and hyperchloremic acidosis [14].

The hypernatremia can also be the result of the underlying disease; it is the case of central diabetes insipidus. In fact this type of diabetes may be at the origin of hypernatremia in patients with head injury. Post-traumatic diabetes insipidus represents 18% of all causes of diabetes insipidus [22]. A study of 130 cranial trauma patients showed that hypernatremia, present in 50% of patients, was independently associated risk death three times higher [15]. In this study, the occurrence of diabetes insipidus treated with desmopressin was an additional factor of death. Similarly to other studies, Maggiore et al found that CDI is associated with an increase in the severity of brain injury, and in the risk of death [23-25].

Our study has certain limitations. It is retrospective in nature, and as a result, we were unable to explore all the consequences of hypernatremia.

Conclusion

Hypernatremia is a common and largely preventable complication of TBI. It has various adverse physiologic consequences and is associated with poor outcomes. Efforts should focus on the prevention of hypernatremia by regular monitoring and adequate correction.

Declarations
Author Contributions

All the above mentioned authors have contributed to this article from data collection to final drafting work. All authors also declare to have read and approved the final manuscript.

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