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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2010  |  Volume : 21  |  Issue : 1  |  Page : 113-117
Behavioural induced severe hypernatremia without neurological manifestations


1 Department of Accident and Emergency, King Khalid University Hospital, King Saud University, Riyadh, Saudi Arabia
2 Department of Critical Care and Emergency Medicine, King Khalid University Hospital, King Saud University, Riyadh, Saudi Arabia

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Date of Web Publication8-Jan-2010
 

   Abstract 

Hypernatremia is a relatively common entity and is more prevalent among the elderly and critically ill. A number of medical conditions are commonly associated with hypernatremia, and these differ substantially among children and adults. Severe hypernatremia is usually associated with central nervous system manifestations and carries a high mortality rate. We report a case of a female patient who presented to the emergency department of the King Khalid University Hospital, Riyadh, Saudi Arabia with severe hypernatremia and without any associated co-morbid conditions or neurological manifestations. We did not find any etiological background despite extensive eva­luation other than under hydration due to decreased fluid intake, which was secondary to beha­vioural causes.

How to cite this article:
Hassan HA, Al Aseri ZA, Suriya OM. Behavioural induced severe hypernatremia without neurological manifestations. Saudi J Kidney Dis Transpl 2010;21:113-7

How to cite this URL:
Hassan HA, Al Aseri ZA, Suriya OM. Behavioural induced severe hypernatremia without neurological manifestations. Saudi J Kidney Dis Transpl [serial online] 2010 [cited 2020 Jul 14];21:113-7. Available from: http://www.sjkdt.org/text.asp?2010/21/1/113/58784

   Introduction Top


The serum sodium concentration and thus, se­rum osmolality, are closely controlled by water homeostasis, which is mediated by thirst, ar­ginine vasopressin, and the kidneys. [1] A disrup­tion in the water balance is manifested as an abnormality in the serum sodium concentration in the form of hypernatremia or hyponatre­mia. [2],[3] Because sodium is functionally an imper­meable solute, hypernatremia contributes to hy­pertonic hyperosmolality leading to movement of water across the cell membrane causing cellular dehydration, at least transiently. The re­sultant morbidity may be inconsequential, se­rious, or even life-threatening, associated with mortality rates ranging from 42 to 60%. [4],[5],[6],[7] El­derly patients are believed to be at high-risk of severe hypernatremia, because with advancing age their renal response to dehydration alters and they have a poorer thirst response. [8],[9] Also, renal concentrating ability declines with age. [10] The principle serious clinical feature associated with hypernatremia is neurological involvement, which probably contributes to the high mortality rate. [11],[12],[13],[14]


   Case Report Top


A 45-year-old female patient, not known to have any prior medical illness, presented to the emergency room (ER) with two weeks history of decreased appetite, decreased fluid intake followed by lethargy, and four days history of constipation, decrease in urine frequency and volume. She denied history of diarrhea, nausea, vomiting, fever, and excessive sweating. She also denied history of visual symptoms, recent head trauma, or history suggesting tuberculosis (TB), sarcoidosis or any possible underlying cause. There was no history of taking any drug, which can cause hypernatremia. Initially, the patient was reluctant to talk with the attending physician but later she was convinced to talk. Detailed history did not reveal any clue to jus­tify her recent decrease in appetite, reduced fluid intake and behavioural change, but her atten­dant (son) was mainly concerned about fatigue, lethargy and recent behavioural change. On fur­ther questioning in the absence of her son, she gave some hints about her recent mental stress due to family matters, which were insignificant.

On physical examination, she looked dehydra­ted. Her body temperature was 36.8°C; heart rate, 90 beats/min; respiratory rate 18/min, blood pressure 113/78 mmHg with mild postural drop (10-15 mmHg difference) and O2 saturation was 96% at room air. Head and neck examination was normal, and the jugular veins were not dis­tended. Examination of the heart disclosed nor­mal sounds without gallop or murmurs. Her peri­pheral pulses were full and regular. Examination of the chest revealed bilateral equal vesicular breath sounds. Abdominal examination was ne­gative for organomegaly, masses or tenderness. There was no clubbing, cyanosis, edema, arthri­tis, lymphadenopathy, or rash. Neurological exa­mination showed normal orientation to time, place and person, normal cranial nerve exami­nation, normal power and tone of all muscle groups without any focal deficit; reflexes were brisk and plantars were flexor. Fundal exami­nation was unremarkable.

Initial lab work-up revealed blood urea of 42.2 mmol/L, serum creatinine of 179 ΅mol/L, so­dium (Na + ) of 191 mmol/L, potassium (K + ) of 4.0 mmol/L, chloride of 135 mmol/L, random blood sugar of 7.8 mmol/L and osmalility of 421 mosm/L. The white blood cell count (WBC) was 11,000/mm 3 , with normal differentials, red blood cell count was 5.6 Χ 10 5 , hemoglobin (Hgb) was 12.6 gm/dL with low MCV and MCH, mid stream urine showed Ketone 1 + , Blood 1 + , Hgb 1 + , WBC: 11, RBC: 45 and nitrites were ne­gative. Arterial blood gas analysis showed pH of 7.39, PaO 2 of 88.6 mmHg, PaCO 2 of 38.3 mmHg, bicarbonate (HCO 3 ) of 23.8 mmol/L and oxygen saturation of 94% at room air.

She underwent radiological exam including a chest x-ray [Figure 1] followed by computed tomography of brain [Figure 2] to rule out any space occupying lesion or edema; both were normal.

On the basis of the above findings, a preliminary diagnosis of pre-renal azotemia with severe hypernatremia possibly due to decreased fluid intake supposedly secondary to behavioural cha­nges, was made. Since the patient's weight was 51 kg at presentation, the total body water de­ficit calculated with standard protocol was ap­proximately 8500 mL. Therefore, treatment was started with 5% dextrose normal saline infusions administered at 200 mL/hour for six hours fo­llowed by 150 mL/hour; the urea and electro­lytes were monitored six-hourly. The following day, the patient was treated with slow replace­ment of fluid under the supervision of the neph­rologists. Subsequent serial lab results for urea and electrolytes showed satisfactory improve­ment [Table 1]. The patient was then encou­raged to take orally; although she was reluctant initially, the patient eventually agreed to take oral fluids.

The patient remained in the ER as a long stay patient; when she was declared to be free of any medical or nephrological problems, she was re­ferred to the psychiatrist for evaluation. Thorough review was inconclusive for major psychiatric disorder except mild depression. After two se­ssions with the psychotherapist, she started to take fluids orally and was quite stable from mood point of view. Finally, on day seven in the ER, all the lab parameters of the patient reached normal limits with serum Na of 140 mmol/L, K of 3.0 mmol/L, urea of 2.7 mmol/L and creatinine of 60.0 ΅mol/L.

She was then discharged with the advice to attend follow-up after one week with the psy­chiatrist.


   Discussion Top


Hypernatremia can be caused by derangement of the thirst response or the behavioural response thereto (primarily in infants, psychiatric patients, and elderly patients who are institutionalized) and by pathological process involving the renal concentrating mechanism such as diabetes insi­pidus (DI) either due to kidney pathology (neph­rogenic DI) or due to difficulty with the neuro­hormonal control of this concentrating mecha­nism (central DI). [6],[11],[12],[13],[14],[15],[16],[17],[18] It can also occur due to loss of free water from other sources including gastro intestinal losses, [19] administration of diu­retics such as mannitol, [20],[21] impaired thirst me­chanism due to hypothalamic involvement in granulamatous diseases like sarcoidosis, crohn's disease, Cushing's disease, tumours or vascular pathology. [22],[23] The main feature associated with hypernatremia is neurological involvement that begins with lethargy, weakness, irritability, twit­ching of muscles, and can progress to dis­orientation, delirium, seizures and if untreated, to coma. In severe cases, it has been reported that initial low Glasgow Coma Scale and Acute Physiology and Chronic Health Evaluation II (APACHE II) scores are associated with high mortality and poor outcome. [24],[25],[26] In the literature, some rare neurological manifestations of hyper­natremia described include hydrocephalus, [27] bila­teral choroid plexus haematomas and extensive destruction of choroid plexus due to diffuse intravascular coagulation.

The signs and symptoms of hypernatremia are variable and evidence suggests that higher the level of sodium worse the outcome, with a mor­tality of up to 40%. This is explained by the complex patho-physiological phenomenon ini­tiated by hypernatremia itself and the other co­existing conditions like metabolic acidosis, hy­perglycemias, etc. which eventually lead to cel­lular necrosis, demyelinating lesions and hypoxic ischemia of brain tissue.[26]

The most common cause of hypernatremia in elderly or institutionalized patients is lack of free water intake adequate to meet losses. As explained earlier, thirst is the body's main de­fence against increased serum tonicity. Most patients with an intact thirst mechanism and ac­cess to water can prevent the development of hypernatremia. Even patients with a defective renal concentrating mechanism such as those with DI generally can keep up with water losses (even up to 20 L/day) if they are allowed free access to water.

Some patients, however, cannot respond to their thirst drive. Infants and elderly patients who are debilitated depend on their caregivers to provide fluids. Similarly, institutionalized patients may have limited access to water se­condary to either external or internal constraints. Intrinsic water losses cannot be avoided, and some urine must be produced, even if it is ma­ximally concentrated. Without access to water, these patients develop a free water deficit, and their serum sodium level increases. It is defined as "adipsic hypernatremia" which could be of behavioural origin as seen in our patient.

In conclusion, since our patient recovered fully and no pathologic cause was identified, we speculate that the possible underlying cause of hypernatremia in our patient was behavioural neglect of fluid intake for more than two weeks.

 
   References Top

1.Genera FJ. Serum osmolality: Uses and limi­tations. N Engl J Med 1984;310:102-5.  Back to cited text no. 1      
2.Rose BD. New approach to disturbances in the plasma sodium concentration. Am J Med 1986; 81:1033-40.  Back to cited text no. 2      
3.Hyponatremia and hypernatremia. In: Adrogue HJ, Wesson DE. (Eds). Salt& water. Boston: Black-well Scientific 1994;205-84.  Back to cited text no. 3      
4.Himmelstein DU, Jones AA, Woolhandler S. Hypernatremic dehydration in nursing home patients: An indicator of neglect. J Am Geriatr Soc 1983;31:466-71. Mahowald JM, Himmelstein DU. Hypernatremia in the elderly: Relation to infection and morta­lity. J Am Geriatr Soc 1981; 29:177-80.  Back to cited text no. 4      
5.Synder NA, Feigal DW, Arieff AI. Hypernatremia in elderly patients: A heterogeneous, morbid, and iatrogenic entity. Ann Intern Med 1987; 107:309-19.  Back to cited text no. 5      
6.Long CA, Marin P, Bayer AG, Shetty HG, Pathy MS. Hypernatraemia in an adult in-patient population. Postgrad Med J 1991;67:643-5.  Back to cited text no. 6      
7.Silver AJ, Morley JE. Role of opioid system in the hypodipsia associated with ageing. J Am Geriat Soc1992;40:556-60.  Back to cited text no. 7      
8.Phillips PA, Rolls BJ, Ledingham JG, et al. Reduced thirst after water deprivation in healthy elderly men. N Engl J Med 1984;311:753.  Back to cited text no. 8      
9.Beck LH. Changes in renal function with aging. Clin Geriatr Med 1998;14:199-209.  Back to cited text no. 9      
10.Thompson CJ, Baylis PH. Thirst in diabetes insipidus: Clinical relevance of quantitative assessment. Q J Med 1987;65:853.  Back to cited text no. 10      
11.Sze L, Ulrich B, Brandle M. Severe hyperna­traemia due to nephrogenic diabetes insipidus: A life-threatening side effect of chronic lithium therapy. Exp Clin Endocrinol Diabetes 2006; 114:596.  Back to cited text no. 11      
12.Manganaro R, Mami C, Marrone T, et al. Inci­dence of dehydration and hypernatraemia in exclusively breast-fed infants. J Pediatr 2001; 139:673.  Back to cited text no. 12      
13.Oddie S, Richmond S, Coulthard M. Hyperna­traemic dehydration and breast feeding: A population study. Arch Dis Child 2001;85:318.  Back to cited text no. 13      
14.Adrogue HJ, Madias NE. Hypernatremia. N Engl J Med 2000;342:1493.  Back to cited text no. 14      
15.Lindner G, Funk GC, Schwarz C, et al. Hyper­natremia in the critically ill is an independent risk factor for mortality. Am J Kidney Dis 2007;50:952.  Back to cited text no. 15      
16.Palevsky PM, Bhagrath R, Greenberg A. Hyper­natremia in hospitalized patients. Ann Intern Med 1996;124:197.  Back to cited text no. 16      
17.Polderman KH, Schreuder WO, van Schijndel S, Thijs LG. Hypernatraemia in the intensive care unit: An indicator of quality of care? Crit Care Med 1999;27:1041.  Back to cited text no. 17      
18.Kovacs A, Chan L, Hotrakitya C, et al. Rota­virus gastroenteritis. Clinical and laboratory features and use of the Rotazyme test. Am J Dis Child 1987;141:161.  Back to cited text no. 18      
19.Gipstein RM, Boyle JD. Hypernatremia compli­cating prolonged mannitol diuresis. N Engl J Med 1965;272:1116.  Back to cited text no. 19      
20.Gault MH, Dixon ME, Doyle M, Cohen WM. Hypernatremia, azotemia, and dehydration due to high-protein tube feeding. Ann Intern Med 1968;68:778.  Back to cited text no. 20      
21.Phillips PA, Bretherton M, Johnston CI, Gray L. Reduced osmotic thirst in healthy elderly men. Am J Physiol 1991;261:R166.  Back to cited text no. 21      
22.Pathogenesis and management of hyperna­tremia. Curr Opin Crit Care 1996;2(6):418-23.  Back to cited text no. 22      
23.Moder KG, Hurley DL. Fatal hypernatremia from exogenous salt intake: Report of a case and review of the literature. Mayo Clin Proc 1990;65:1587.  Back to cited text no. 23      
24.van der Helm-van Mil AH, van Vugt JP, Lammers GJ, Harinck HI. Hypernatremia from a hunger strike as a cause of osmotic mye­linolysis. Neurology 2005;64:574.  Back to cited text no. 24      
25.Aiyagari V, Deibert E, Diringer MN. Hyperna­tremia in the neurologic intensive care unit: How high is too high? J Crit Care 2006;21(2): 163-72.  Back to cited text no. 25      
26.Franco-Saenz R, Wolffing BK, Rivers RJ. Hypodipsia and hypernatremia in congenital hydrocephalus. Am J Med Sci 1989;297(6):385­-86.  Back to cited text no. 26      
27.Roach ES, Angelo JN, Boyle RJ. Hypernatre­mia with choroid plexus hematomas and ele­vated CSF protein level. Southern Med J 1983; 76(8):1055-6.  Back to cited text no. 27      

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Correspondence Address:
Hossam A Hassan
Department of Accident and Emergency King Khalid University Hospital, Dept. 65 King Saud University, P.O. Box, 7805, Riyadh 11472
Saudi Arabia
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PMID: 20061704

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