Skip to main content
Download PDF
Download ePub

Mechanisms of hyponatremia and diabetes insipidus after acute spinal cord injury: a critical review

Chinese Neurosurgical Journal volume 9, Article number: 32 (2023) Cite this article

Abstract

The incidence of hyponatremia after spinal cord injury was reported to be between 25 and 80%. Hyponatremia can lead to a variety of clinical symptoms, from mild to severe and even life-threatening. Hyponatremia is often associated with diabetes insipidus, which refers to insufficient arginine vasopressin (AVP) secretion or defective renal response to AVP, with clinical manifestations of syndromes such as hypoosmolality, polydipsia, and polydipsia. Recent mechanistic studies on hyponatremia and diabetes insipidus after acute spinal cord injury have been performed in isolation, without integrating the above two symptoms into different pathological manifestations that occur in the same injury state and without considering the acute spinal cord injury patient’s condition as a whole. The therapeutic principles of CSWS and SIADH are in opposition to one another. It is not easy to identify the mechanism of hyponatremia in clinical practice, which makes selecting the treatment difficult. According to the existing theories, treatments for hyponatremia and diabetes insipidus together are contraindicated, whether the mechanism of hyponatremia is thought to be CSWS or SIADH. In this paper, we review the mechanism of these two pathological manifestations and suggest that our current understanding of the mechanisms of hyponatremia and diabetes insipidus after high acute cervical SCI is insufficient, and it is likely that there are other undetected pathogenetic mechanisms.

Background

Spinal cord injury (SCI) often leads to impaired somatosensory, motor, and autonomic nervous system function below the level of the injury. Though many neurorestorative treatments have been applied to restore damaged neurological functions and/or structures for patients with SCI, a variety of complications can still occur, the most common of which is hyponatremia [1]. Hyponatremia is defined as a serum sodium concentration < 135 mmol/L, and it occurs in up to 15 to 20% of patients admitted to the emergency department and in more than 20% of critically ill patients [2]. The incidence of hyponatremia after SCI was reported to be between 25 and 80% [3,4,5]. Hyponatremia can lead to a variety of clinical symptoms, from mild to severe and even life-threatening [6]. Hyponatremia can aggravate secondary SCI and affect patient rehabilitation, and early detection and correction of hyponatremia is essential to improve patient outcomes [7].

Hyponatremia is often associated with diabetes insipidus, which refers to insufficient arginine vasopressin (AVP) secretion or defective renal response to AVP, with clinical manifestations of syndromes such hypoosmolality, polydipsia, and polydipsia [8]. AVP is a neurohypophysial hormone synthesized within hypothalamus and transported to multiple areas, acting as a neurotransmitter/neuromodulator. Lin reported 17 patients with hyponatremia after SCI and 10 patients (58.82%) with diabetes insipidus [9]. Sun et al. reported 15 patients with complete SCI from C3 to C5 who developed hyponatremia and diabetes insipidus within day 5 to 12 after injury. After treatment, 13 patients showed improvement and two patients died [10]. If early treatment is improper in patients with hyponatremia complicated with diabetes insipidus after acute SCI, the patient’s condition can be aggravated, which may endanger their life and negatively affect their rehabilitation [11, 12].

Studies have found that the degree of blood sodium reduction in patients with acute cervical SCI and hyponatremia is related to the segment and degree of the SCI. The more severe the level of SCI, the lower the blood sodium concentration, and the more likely the patient is to have a worse level of polyuria [13, 14]. Recent mechanistic studies on hyponatremia and diabetes insipidus after acute SCI have been performed in isolation. In this paper, we reviewed the mechanism of these two pathological manifestations and tried to find out the intrinsic correlation of the pathological mechanisms for these two conditions.

Mechanism of hyponatremia after acute SCI

The mechanism of hyponatremia after SCI is complex and unclear. In addition to poor diet, application of diuretics and dehydrating agents, and combined craniocerebral trauma in early patients, hyponatremia after SCI is generally considered to be related to central nervous system dysfunction, including the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and cerebral salt wasting syndrome (CSWS) [15, 16]. Both SIADH and CSWS are clinically characterized by hyponatremia, low plasma osmolality, and the accompanying neurological symptoms, but their blood volume, sodium metabolism, and treatment are different. SIADH refers to hypervolemic hyponatremia that is caused by abnormally increased AVP secretion, which promotes renal water retention and sodium excretion and results in increased urinary sodium and water retention. CSWS refers to hypovolemic hyponatremia, which is caused by excessive renal sodium excretion that results from hypothalamic endocrine dysfunction (Fig. 1) [5].

Fig. 1
figure 1

A flowchart to illustrate hyponatremia mechanisms

Full size image

The origin of the two conflicting theories

These two theories for hyponatremia, SIADH and CSWS, are contradictory as follows: SIADH is hypervolemic hyponatremia that is caused by water retention, while CSWS is hypovolemic hyponatremia that is caused by excessive sodium excretion; SIADH is the hypersecretion of antidiuretic hormone which also known as arginine vasopressin (AVP), while CSWS is the hyposecretion of AVP; and SIADH requires water restriction and CSWS requires fluid replacement therapeutically. There are two opposite mechanisms to explain the same pathological manifestation after acute SCI.

With the invention of the flame photometer, it became possible to determine serum sodium concentration. In 1950, Peters found that in patients with central nervous system diseases, urinary sodium loss remained in the presence of hyponatremia and a low-salt diet. They proposed the theory of CSWS, which is characterized by polyuria, increased urinary sodium, and dehydration [17]. In 1957, Schwartz et al. found that patients with lung cancer developed unexplained hyponatremia and their clinical features were similar to those of patients who had been taking pituitrin extract, which was considered to be the antidiuretic effect that was produced by AVP in pituitrin extract. This was the origin of the SIADH theory, which suggests that hyponatremia is caused by impaired renal drainage that results from the action of AVP [18]. In 1981, Nelson et al. investigated 12 patients who met the SIADH criteria and found that these patients also had significantly reduced blood volume, which was attributed to the mechanism of hyponatremia that was characterized by this hypovolemia that resulted from CSWS. They attributed the cause of hyponatremia to CSWS, characterized by elevated natriuretic peptide levels, a negative sodium balance, and decreased central venous pressure [19].

In summary, SIADH and CSWS were historically artificially divided on the basis of their theoretical hyponatremia mechanisms. Although these conditions are different theoretically, they are not easily distinguished from each other in clinical practice, especially in patients with high-level SCI, the sympathetic nervous system is completely interrupted. Because these patients have hypotension and bradycardia, which makes it more difficult to differentiate SIADH from CSWS.

Difficulties in clinically differentiating between SIADH and CSWS

After 2016, Misra et al. [20] and Cui et al. [21] successively proposed the diagnostic criteria for CSWS and SIADH. The diagnostic criteria for CSWS are as follows: clinical manifestations of hypovolemia, such as hypotension, dry mucosa, tachycardia, or orthostatic hypotension; laboratory evidence of dehydration, such as elevated hematocrit, hemoglobin, serum albumin, or blood urea nitrogen; negative fluid balance; and central venous pressure (CVP, which describes the pressure of pressure of the right atrium and upper and lower vena cava thoracic segments) < 6 cmH2O. The diagnostic criteria for SIADH are as follows: no signs of hypovolemia; no laboratory evidence of dehydration; normal or positive fluid balance without weight loss; and CVP > 6 cmH2O [20, 21].

Changes in blood volume are a key factor in distinguishing CSWS from SIADH. Among the methods for assessing blood volume, the radioisotope dilution technique is the gold standard and commonly used methods include 51-chromium-labeled red blood cells and iodine-131 or iodine-125 labeled human serum albumin. These methods are currently only used for laboratory studies because of their high cost and the complex methods required for their use [22]. The method of clinically assessing blood volume is influenced by many factors, and subjective judgment can be erroneous when the difference is not obvious.

Plasma AVP and natriuretic peptide concentrations were once used to identify SIADH and CSWS. Both SIADH and CSWS have been implicated in the abnormal impermeable release of AVP; thus, measuring the concentration of AVP and its surrogate markers in serum to make a differential diagnosis has a limited role [23, 24]. In SIADH, natriuretic peptide levels increase when there is too much water in the arterial circulation [25]. However, the natriuretic peptide test index has a short half-life and is greatly affected by other factors, such as head injury, pulmonary infection, and advanced age, which cannot be used to distinguish SIADH from CSWS [21, 26].

In cases where laboratory test results cannot easily distinguish between CSWS and SIADH, diagnostic treatment was once considered to be an alternative. Water restriction is recommended to treat hyponatremia caused by simple SIADH [2], but this may cause cerebral vasospasm and cerebral hypoperfusion [27]; therefore, diagnostic water restriction is not a safe and feasible method to identify the type of hyponatremia.

Unclear mechanism of diabetes insipidus after SCI

Diabetes insipidus after SCI is common in patients with cervical and upper thoracic cord injury and rare in patients with lower thoracic and lumbar cord injury [28]. The current studies explain the mechanism of diabetes insipidus after SCI: sympathetic nerve interruption, loss of sympathetic innervation of the cardiovascular system, decreased blood pressure, and decreased heart rate. These factors cause decreased AVP secretion, resulting in polyuria (Fig. 2) [9,10,11,12]. This description is not compatible with a mechanism for regulating AVP production and secretion.

Fig. 2
figure 2

A flowchart to illustrate diabetes insipidus mechanism

Full size image

AVP secretion by the posterior pituitary is triggered by changes in plasma osmolality and effective circulating blood volume, which activate osmoreceptors [29] and baroreceptors [30], respectively. When serum sodium levels rise above 145 mmol/L, osmoreceptors in the hypothalamus are activated, which signals the supraoptic and paraventricular nuclei to secrete AVP into the blood via the posterior pituitary [31, 32]. Changes in thalamic magnocellular osmolality activate nonselective cation channels, increase the action potential firing rate, and trigger AVP release from axonal terminals [33, 34]. Elevated plasma AVP causes the kidney to reabsorb water, which dilutes the hypertonic sodium ions in the organism to reduce osmolality [28, 33]. Conversely, the decrease in osmotic pressure in vivo inhibits in vivo AVP secretion and promotes water excretion [35]. Changes in blood volume when blood pressure decreases, particularly when there is a decrease in effective circulating blood volume, can activate baroreceptors such that tonic inhibition of vagal afferent pathways is eliminated, which increases the non-osmotic release of AVP [32, 36]. Therefore, the decreased blood pressure does not decrease AVP secretion, and there must be another mechanism.

Some authors attributed diabetes insipidus after acute SCI to posterior pituitary dysfunction with a combined traumatic brain injury, resulting in AVP deficiency and thus diabetes insipidus [37, 38]. However, there was a lack of clinical evidence to support this claim. So the real mechanism of diabetes insipidus after SCI remains unclear.

Existing theories cannot guide the treatment of hyponatremia and diabetes insipidus after acute SCI

The therapeutic principles of CSWS and SIADH are in opposition to one another. It is not easy to identify the mechanism of hyponatremia in clinical practice, which makes selecting the treatment difficult. The principles of treating CSWS are volume expansion, sodium supplementation, and, in severe cases, hormone replacement therapy [2, 39, 40]. The principle of treating SIADH is to limit fluid replacement and, in severe cases, to administer vasopressin V2 receptor antagonists [1, 41, 42].

According to the existing theories, treatments for both hyponatremia and diabetes insipidus are contraindicated, whether the mechanism of hyponatremia is thought to be CSWS or SIADH. Treatment of diabetes insipidus involves limiting fluid intake and supplementing AVP or its analogs to improve symptoms such as polyuria and thirst [8]. If hyponatremia is considered to be CSWS, volume expansion to treat CSWS is the opposite of fluid restriction, which is required to treat diabetes insipidus. If hyponatremia is considered to be SIADH, an AVP receptor antagonist should be administered to treat SIADH, but AVP should be administered to treat diabetes insipidus, which are opposite treatments.

Future research direction

The serum AVP concentration sharply increased 15 min after spinal cord injury in an animal model. The differences were significantly observed compared to the control group [43]. However, the high secretion phase did not maintain such a long time. At 24 h after SCI, the urine output in the animal model significantly increased, and the concentration of serum AVP measured at 2 weeks after SCI significantly decreased [44, 45]. Research on the impact of SCI model in rats found that extensive activation of microglia occurred in the brain after SCI. It induced neuronal loss to a greater extent in the cortex, thalamus, and hippocampus at 12 weeks after SCI, which demonstrated that SCI would cause immune damage in the brain [46]. The immune damage of hypothalamic tissue after SCI may be a future research direction.

Conclusions

In summary, the results can be summarized as follows: (1) hyponatremia and diabetes insipidus often occur together after high acute SCI, and they are still regarded as two different pathological manifestations with different mechanisms and not as a single condition; (2) the mechanisms of hyponatremia are explained as SIADH and CSWS, respectively, on the basis of historical factors; (3) SIADH and CSWS mechanisms are contradictory; (4) SIADH and CSWS mechanisms are difficult to differentiate clinically; (5) the pathogenesis of diabetes insipidus remains unclear, and interpretation of some studies is not consistent with the physiological mechanism; and (6) existing theories cannot guide clinical treatment, and dividing hyponatremia into CSWS and SIADH is contradictory to the treatment of diabetes insipidus. Thus, these findings suggest that our current understanding of the mechanisms of hyponatremia and diabetes insipidus after high acute cervical SCI is insufficient, and it is likely that there are other undetected pathogenetic mechanisms.

Availability of data and materials

Not applicable.

Abbreviations

SCI:

Spinal cord injury

AVP:

Arginine vasopressin

SIADH:

Syndrome of inappropriate antidiuretic hormone secretion

CSWS:

Cerebral salt wasting syndrome

References

  1. Sharma HS, Chopp M, Chen L, Sarnowska A, Xue MZ, Ao Q, et al. The 2021 yearbook of neurorestoratology. J Neurorestoratology. 2022;10:612–32. https://doi.org/10.1016/j.jnrt.2022.100008.

    Article  CAS  Google Scholar 

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

    Article  PubMed  Google Scholar 

  3. Peruzzi WT, Shapiro BA, Meyer PR, Krumlovsky F, Seo BW. Hyponatremia in acute spinal cord injury. Crit Care Med. 1994;22:252–8. https://doi.org/10.1097/00003246-199402000-00016.

    Article  CAS  PubMed  Google Scholar 

  4. Nakao Y, Suda K, Shimokawa N, Fu Y. Risk factor analysis for low blood pressure and hyponatremia in acutely and subacutely spinal cord injured patients. Spinal Cord. 2012;50:285–8. https://doi.org/10.1038/sc.2011.142.

    Article  CAS  PubMed  Google Scholar 

  5. Kriz J, Schuck O, Horackova M. Hyponatremia in spinal cord injury patients: new insight into differentiating between the dilution and depletion forms. Spinal Cord. 2015;53:291–6. https://doi.org/10.1038/sc.2014.240.

    Article  CAS  PubMed  Google Scholar 

  6. Leng YX, Nie CY, Yao ZY, Zhu X. Analysis of the risk factors for early death in acute severe traumatic cervical spinal cord injury. Chin Critical Care Med. 2013;5:294–7. https://doi.org/10.3760/cma.j.issn.2095-4352.2013.05.014.

    Article  Google Scholar 

  7. Kogawa R, Kinoshita K, Tanjoh K. Increase in urinary sodium excretion in spinal cord injury patients in the emergency department. Eur J Trauma Emerg Surg. 2016;42:61–6. https://doi.org/10.1007/s00068-015-0503-2.

    Article  CAS  PubMed  Google Scholar 

  8. Refardt J, Winzeler B, Christ-Crain M. Diabetes insipidus: an update. Endocrinol Metab Clin North Am. 2020;49:517–31. https://doi.org/10.1016/j.ecl.2020.05.012.

    Article  PubMed  Google Scholar 

  9. Lin KX. Analysis of hyponatremia after cervical spinal cord injury (a report of 17 cases). Ortho J Chin. 2007;15:1425–7. https://doi.org/10.3969/j.issn.1005-8478.2007.18.023.

    Article  CAS  Google Scholar 

  10. Sun XJ, Dong BH, Zhao X, Zhang J, Xiao L. Clinical analysis of 15 cases of diabetes insipidus and hyponatremia caused by severe cervical spinal cord injury. J Trauma Surg. 2009;11:560. https://doi.org/10.3969/j.issn.1009-4237.2009.06.029.

    Article  Google Scholar 

  11. Li SB, Lu HX. Clinical analysis on diabetes insipidus and hyponatremia caused by cervical spinal cord injury. Sichuan J Anat. 2008;16:22–4. https://doi.org/10.3969/j.issn.1005-1457.2008.02.009.

    Article  CAS  Google Scholar 

  12. Huang ZZ. Clinical analysis of 22 cases of diabetes insipidus caused by cervical spinal cord injury. Chongqing Med. 2011;4:375–6. https://doi.org/10.3969/j.issn.1671-8348.2011.04.029.

    Article  Google Scholar 

  13. Han LL, Wang FY, Sun QZ, Xu LH, Li LY, Deng JH. Retrospective analysis of hyponatremia secondary to acute cervical spinal cord injury. Chin J Spine Spinal Cord. 2009;19:19–21. https://doi.org/10.3969/j.issn.1004-406X.2009.01.004.

    Article  CAS  Google Scholar 

  14. Frisbie JH. Salt wasting, hypotension, polydipsia, and hyponatremia and the level of spinal cord injury. Spinal Cord. 2007;45:563–8. https://doi.org/10.1038/sj.sc.3102144.

    Article  CAS  PubMed  Google Scholar 

  15. Ohbe H, Koakutsu T, Kushimoto S. Analysis of risk factors for hyponatremia in patients with acute spinal cord injury: a retrospective single-institution study in Japan. Spinal Cord. 2019;57:240–6. https://doi.org/10.1038/s41393-018-0208-6.

    Article  PubMed  Google Scholar 

  16. Silver JR. A study of predictors for hyponatraemia in patients with cervical spinal cord injury. Spinal Cord. 2018;56:621–2. https://doi.org/10.1038/sc.2017.103.

    Article  CAS  PubMed  Google Scholar 

  17. Peters JP, Welt LG, Sims EA, Orloff J, Needham J. A salt-wasting syndrome associated with cerebral disease. Trans Assoc Am Physicians. 1950;63:57–64. PMID: 14855556.

    CAS  PubMed  Google Scholar 

  18. Schwartz WB, Bennett W, Curelop S, Bartter FC. A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone. Am J Med. 1957;23:529–42. https://doi.org/10.1016/0002-9343(57)90224-3.

    Article  CAS  PubMed  Google Scholar 

  19. Nelson PB, Seif SM, Maroon JC, Robinson AG. Hyponatremia in intracranial disease: perhaps not the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). J Neurosurg. 1981;55:938–41. https://doi.org/10.3171/jns.1981.55.6.0938.

    Article  CAS  PubMed  Google Scholar 

  20. Misra UK, Kalita J, Bhoi SK, Singh RK. A study of hyponatremia in tuberculous meningitis. J Neurol Sci. 2016;367:152–7. https://doi.org/10.1016/j.jns.2016.06.004.

    Article  CAS  PubMed  Google Scholar 

  21. Cui H, He G, Yang S, Lv Y, Jiang ZM, Gang XK, et al. Inappropriate antidiuretic hormone secretion and cerebral salt-wasting syndromes in neurological patients. Front Neurosci. 2019;13:1170. https://doi.org/10.3389/fnins.2019.01170.

    Article  PubMed  PubMed Central  Google Scholar 

  22. Bartoli WP, Davis JM, Pate RR, Ward DS, Watson PD. Weekly variability in total body water using 2H2O dilution in college-age males. Med Sci Sports Exerc. 1993;25:1422–8.

    Article  CAS  PubMed  Google Scholar 

  23. Nigro N, Winzeler B, Suter-Widmer I, Schuetz P, Arici B, Bally M, et al. Evaluation of copeptin and commonly used laboratory parameters for the differential diagnosis of profound hyponatraemia in hospitalized patients: “The Co-MED Study.” Clin Endocrinol (Oxf). 2017;86:456–62. https://doi.org/10.1111/cen.13243.

    Article  CAS  PubMed  Google Scholar 

  24. Fenske W, Störk S, Blechschmidt A, Maier SG, Morgenthaler NG, Allolio B. Copeptin in the differential diagnosis of hyponatremia. J Clin Endocrinol Metab. 2009;94:123–9. https://doi.org/10.1210/jc.2008-1426.

    Article  CAS  PubMed  Google Scholar 

  25. Tobin G, Chacko AG, Simon R. Evaluation of NT-ProBNP as a marker of the volume status of neurosurgical patients developing hyponatremia and natriuresis: a pilot study. Neurol India. 2018;66:1383–8. https://doi.org/10.4103/0028-3886.241401.

    Article  PubMed  Google Scholar 

  26. Das SR, Drazner MH, Dries DL, Vega GL, Stanek HG, Abdullah SM, et al. Impact of body mass and body composition on circulating levels of natriuretic peptides: results from the Dallas Heart Study. Circulation. 2005;112:2163–8. https://doi.org/10.1161/CIRCULATIONAHA.105.555573.

    Article  CAS  PubMed  Google Scholar 

  27. Upadhyay UM, Gormley WB. Etiology and management of hyponatremia in neurosurgical patients. J Intensive Care Med. 2012;27:139–44. https://doi.org/10.1177/0885066610395489.

    Article  PubMed  Google Scholar 

  28. Daia C, Munteanu C, Andone I, Spinu A, Popescu C, Toader C, et al. Polydipsia-polyuria syndrome associated with traumatic spinal cord injury. Signa Vitae. 2021;17:74–81. https://doi.org/10.22514/sv.2021.104.

    Article  CAS  Google Scholar 

  29. Bourque CW, Oliet SH, Richard D. Osmoreceptors, osmoreception, and osmoregulation. Front Neuroendocrinol. 1994;15:231–74. https://doi.org/10.1006/frne.1994.1010.

    Article  CAS  PubMed  Google Scholar 

  30. McKinley MJ, Mathai ML, McAllen RM, McClear RC, Miselis RR, Pennington GL, et al. Vasopressin secretion: osmotic and hormonal regulation by the lamina terminalis. J Neuroendocrinol. 2004;16:340–7. https://doi.org/10.1111/j.0953-8194.2004.01184.x.

    Article  CAS  PubMed  Google Scholar 

  31. Kim SW. Hypernatemia : successful treatment. Electrolyte Blood Press. 2006;4:66–71. https://doi.org/10.5049/EBP.2006.4.2.66.

    Article  PubMed  PubMed Central  Google Scholar 

  32. Boone M, Deen PM. Physiology and pathophysiology of the vasopressin-regulated renal water reabsorption. Pflugers Arch. 2008;456:1005–24. https://doi.org/10.1007/s00424-008-0498-1.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  33. Bichet DG. Central vasopressin: dendritic and axonal secretion and renal actions. Clin Kidney J. 2014;7:242–7. https://doi.org/10.1093/ckj/sfu050.

    Article  PubMed  PubMed Central  Google Scholar 

  34. van Gastel MDA. Polycystic kidney disease and the vasopressin pathway. Ann Nutr Metab. 2017;70(Suppl):43–50. https://doi.org/10.1159/000463063.

    Article  PubMed  Google Scholar 

  35. Koshimizu TA, Nakamura K, Egashira N, Hiroyama M, Nonoguchi H, Tanoue A. Vasopressin V1a and V1b receptors: from molecules to physiological systems. Physiol Rev. 2012;92:1813–64. https://doi.org/10.1152/physrev.00035.2011.

    Article  CAS  PubMed  Google Scholar 

  36. Ishikawa SE. Hyponatremia associated with heart failure: pathological role of vasopressin-dependent impaired water excretion. J Clin Med. 2015;4:933–47. https://doi.org/10.3390/jcm4050933.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  37. Leroy C, Karrouz W, Douillard C, Cao CD, Cortet C, Wémeau JL, et al. Diabetes insipidus. Ann Endocrinol (Paris). 2013;74:496–507. https://doi.org/10.1016/j.ando.2013.10.002.

    Article  PubMed  Google Scholar 

  38. Macciocchi S, Seel RT, Thompson N, Byams R, Bowman B. Spinal cord injury and co-occurring traumatic brain injury: assessment and incidence. Arch Phys Med Rehabil. 2008;89:1350–7. https://doi.org/10.1016/j.apmr.2007.11.055.

    Article  PubMed  Google Scholar 

  39. Edate S, Albanese A. Management of electrolyte and fluid disorders after brain surgery for pituitary/suprasellar tumours. Horm Res Paediatr. 2015;83:293–301. https://doi.org/10.1159/000370065.

    Article  CAS  PubMed  Google Scholar 

  40. Zomp A, Alexander E. Syndrome of inappropriate antidiuretic hormone and cerebral salt wasting in critically ill patients. AACN Adv Crit Care. 2012;23:233–9. https://doi.org/10.1097/NCI.0b013e31824ebd1b. quiz 240–31.

    Article  PubMed  Google Scholar 

  41. Cuesta M, Thompson CJ. The syndrome of inappropriate antidiuresis (SIAD). Best Pract Res Clin Endocrinol Metab. 2016;30:175–87. https://doi.org/10.1016/j.beem.2016.02.009.

    Article  CAS  PubMed  Google Scholar 

  42. Thajudeen B, Salahudeen AK. Role of tolvaptan in the management of hyponatremia in patients with lung and other cancers: current data and future perspectives. Cancer Manag Res. 2016;8:105–14. https://doi.org/10.2147/CMAR.S90169.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  43. Zahra M, Samdani A, Piggott K, Gonzalez-Brito M, Solano J, Santo RDL, et al. Acute changes in systemic hemodynamics and serum vasopressin after complete cervical spinal cord injury in piglets. Neurocrit Care. 2010;13:132–40. https://doi.org/10.1007/s12028-010-9364-z.

    Article  PubMed  Google Scholar 

  44. Gumbel JH, Yang CB, Hubscher CH. Timeline of changes in biomarkers associated with spinal cord injury-induced polyuria. Neurotrauma Rep. 2021;2:462–75. https://doi.org/10.1089/neur.2021.0046.

    Article  PubMed  PubMed Central  Google Scholar 

  45. Montgomery LR, Hubscher CH. Altered vasopressin and natriuretic peptide levels in a rat model of spinal cord injury: implications for the development of polyuria. Am J Physiol Renal Physiol. 2018;314:F58–66. https://doi.org/10.1152/ajprenal.00229.2017.

    Article  CAS  PubMed  Google Scholar 

  46. Wu J, Zhao Z, Sabirzhanov B, Stoica BA, Kumar A, Luo T, et al. Spinal cord injury causes brain inflammation associated with cognitive and affective changes: role of cell cycle pathways. J Neurosci. 2014;34:10989–1006. https://doi.org/10.1523/JNEUROSCI.5110-13.2014.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

Download references

Acknowledgements

Not applicable.

Funding

Not applicable.

Author information

Authors and Affiliations

  1. Department of Orthopedics, the Fourth Medical Center of PLA General Hospital, Beijing, China

    Lianhua Li, Yanhui Guo, Chen Chen, Zhonghe Wang & Zhi Liu

Authors
  1. Lianhua Li
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Yanhui Guo
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Chen Chen
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Zhonghe Wang
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Zhi Liu
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

The authors confirm that their contributions to the paper are as follows. LHL designed the study and wrote the original draft. YHG and ZHW provided the research materials. ZL revised the manuscript. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Lianhua Li.

Ethics declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

Not applicable.

Competing interests

The authors declare that they have no competing interests.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Li, L., Guo, Y., Chen, C. et al. Mechanisms of hyponatremia and diabetes insipidus after acute spinal cord injury: a critical review. Chin Neurosurg Jl 9, 32 (2023). https://doi.org/10.1186/s41016-023-00347-y

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s41016-023-00347-y

Keywords

Chinese Neurosurgical Journal

ISSN: 2057-4967

Contact us