Patients with hyponatremia complicated by craniocerebral trauma are more common clinically, and the main factors of hyponatremia caused by clinical craniocerebral trauma are cerebral salt wasting syndrome (CSWS) and syndrome of inappropriatr antidiuretic hormone secretion hormone secretion (SIADH), both with hyponatremia as the main clinical manifestation, but their clinical manifestations are usually masked by craniocerebral injury and hyponatremia, which is easily missed and is one of the main factors causing clinical disability and/or death in patients with craniocerebral trauma. Now, the causes, diagnosis, differential diagnosis and treatment of craniocerebral trauma are briefly described for clinical reference. I. Causes of hyponatremia combined with heavy craniocerebral trauma The causes of hyponatremia complicated by craniocerebral trauma are mainly: (1) CSWS: CSWS refers to a group of syndromes of hyponatremia, hypernatremia and hypovolemia due to the progressive sodium loss from urine and excessive water carried away by the kidneys in the process of intracranial diseases. The pathogenesis of CSWS is still unclear, but it is believed that direct or indirect damage to the hypothalamus causes edema and ischemia, resulting in increased plasma brain natriuretic peptide (BNP) and cardiac natriuretic peptide (ANP), both of which are strong natriuretic factors. This causes hypovolemic hyponatremia, and sodium deficiency is more important than water deficiency. The hyponatremia caused by this cause is often combined with central urinary collapse, and this hyponatremia is not easily corrected quickly. (2) SIADH: SIADH is caused by hypothalamic-pituitary dysfunction due to craniocerebral trauma, and can appear at any time within 2 weeks after trauma. The main reason is that craniocerebral trauma causes direct or indirect damage to the hypothalamic osmolar hyperreceptors and pituitary gland, causing the pituitary gland to develop continuous secretion of AHD unrelated to osmolarity, and through its antidiuretic effect, fluid retention and lowering of plasma osmotic concentration, thus causing central hyponatremia. Subarachnoid hemorrhage (SAH) is the most important and common cause of SIADH after craniocerebral trauma. The hyponatremia caused by this cause should appear in the early post-injury period according to the theory, but due to the effect of early application of high-dose dehydrating agents, the blood sodium in laboratory tests is often normal. (3) Diabetes insipidus (DI) caused by reduced secretion of antidiuretic hormone: DI refers to a group of syndromes characterized by severe or partial deficiency of ADH (central DI), or renal insensitivity to ADH (renal DI), resulting in dysfunction of water absorption by renal tubules, thus causing polyuria, irritable thirst with low density urine and hypotonic urine. DI after craniocerebral trauma belongs to secondary central DI, which occurs mainly due to trauma-induced damage to hypothalamus or pituitary gland, resulting in impaired secretion or release of ADH, leading to a decrease in ADH. It occurs mostly in people with skull base fractures and brain base contusions. After urinary collapse, due to the obvious increase in urine volume and sodium excretion than normal, it is very easy to have electrolyte metabolism disorder, which can be manifested as hyponatremia, hypernatremia or normal. (4) Large application of dehydrating drugs and insufficient sodium intake Such as fasting, vomiting, infusion without sodium ions or too little, dehydrating drug use, etc. The total amount of sodium lost in adults is about 4.5g per day, but the increase in sodium due to the application of dehydrating drugs in the acute phase of traumatic brain injury may actually be much higher than l0.0g. In order to avoid aggravating cerebral edema in neurosurgery treatment, not giving 0.9% NaCl solution or only infusing glucose water during infusion are the causes of sodium deficiency. Second, the effect of hyponatremia on craniocerebral trauma The decrease of blood sodium concentration, the hypotonicity of blood extracellular fluid, the transfer of water from extracellular to intracellular, resulting in intracellular edema, and for brain tissue, it is brain cell edema and increased intracranial pressure, and the most common and serious secondary injury of craniocerebral trauma is cerebral edema, if combined with hyponatremia, cerebral edema is aggravated, leading to the aggravation of the disease, and the long-term serious hyponatremia leads to serious diffuse brain The difference between SIADH, CSWS and other types of hyponatremia in terms of recovery time and cure rate is not statistically significant, while the prognosis is closely related to the severity of the disease, the more severe the disease, i.e., the lower the Glassgow coma scale (GCS) score, the higher the incidence of hyponatremia, the The more severe the hyponatremia, the higher the death rate. Diagnosis and differential diagnosis SIADH diagnostic criteria: blood sodium <130 mmol/L; plasma osmolality <270 mmol/L; ratio of urine osmolality to plasma osmolality >1; urine sodium >20 mmol/L or >80 mmol/24h; no abnormalities of heart, liver, kidney, adrenal and thyroid functions; no clinical signs such as skin edema or ascites, decreased blood pressure and dehydration. Signs of reduced blood volume. Diagnostic criteria for CSWS: hyponatremia with blood sodium <130 mmol/L under normal salt intake or repletion; blood volume <70 ml/kg body weight; urinary sodium >20 mmol/L or >80 mmol/24h; increased plasma ANP; normal liver, kidney, thyroid and adrenal functions. According to clinical manifestations and laboratory tests, CSWS and SIADH have many similarities in diagnostic criteria, such as both have high urinary sodium and urinary osmotic concentration > plasma osmotic concentration; plasma cardiac natriuretic hormone and antidiuretic hormone can be increased in patients with CSWS and SIADH, so endocrine hormone determination is of little significance in differential diagnosis, and blood sodium and urinary sodium levels alone cannot be distinguished. The differentiation between CSWS and SIADH after craniocerebral trauma lies in the amount of extracellular volume and the positive and negative balance of sodium metabolism. in patients with CSWS, sodium excretion is accompanied by increased water excretion in the body. Therefore, patients with CSWS tend to show a decrease in body fluid, such as a decrease in central venous pressure, while in SIADH, patients tend to show an excess of body fluid, such as an increase in central venous pressure. However, we must realize that on the one hand, due to the application of large amount of dehydrating agents after craniocerebral trauma, SIADH can also present with reduced central venous pressure, and the monitoring of central venous pressure is limited by clinical conditions; on the other hand, patients with SIADH can also present with negative nitrogen balance. If the conditions are limited, rehydration or fluid restriction treatment can be used to differentiate, and those whose symptoms improve after sodium supplementation and those whose symptoms worsen after fluid restriction are considered to be CSWS type; conversely, they are SIADH type. IV. Treatment of hyponatremia All hyponatremia is treated on the basis of treatment of the primary disease: the main method of SIADH treatment is to eliminate excessive water by restricting fluid intake. Since SIADH is not a real sodium deficiency, but due to dilutive hyponatremia, it is characterized by balanced or slightly positive balance of sodium metabolism and normal or increased blood volume. Sodium supplementation not only fails to correct hyponatremia, but also stimulates the release of ADH and aggravates hyponatremia. Therefore, the principle of SIADH treatment is water restriction, and the amount of water restriction depends on the blood sodium level. capsulari et al. showed that: for blood sodium between 130 and 134 mmol/L, the daily water restriction is <1200 ml; for blood sodium between 126 and 130 mmol/L, the daily water restriction is <800 ml; for blood sodium <125 mmol/L, the daily water restriction is <600 ml. when the blood sodium is < 128 mmol/L, furosemide is the drug of choice for SIADH, but it should be noted that its use can cause hypokalemia and other electrolyte metabolic imbalances. For severe hyponatremia with CNS symptoms and manifestations of intracranial hypertension (blood sodium < 120 mmol/L = need for intravenous supplementation with 3% NaCl solution, expected supplemental sodium deficiency (mmol/L): [normal blood sodium value (125) - measured sodium value] x body mass (kg) x 0.6, then 17 mmol/L of sodium equals lg NaCl to convert the amount of saline. In the process of sodium supplementation, electrolytes should be checked promptly, and if the clinical symptoms improve and the blood sodium is 125-130 mmol/L or more, the supplementation of hypertonic saline should be stopped, and ACTH 25 mg intramuscular injection should be given 3 times a day to adjust the imbalance of ADH/ACTH. Treatment of CSWS should be adequately sodium and water rehydration, and the amount of sodium rehydration depends on the degree of sodium deficiency. Since sodium deficiency is often accompanied by blood volume deficiency, it is necessary to quickly replenish blood volume and increase plasma osmolality to improve microcirculation. The total sodium (mmol) to be replenished is calculated according to the formula: [normal blood sodium value 142 (mmol/L)] - [measured blood sodium value (mmol/L)] × body weight (kg) × 0.6 (0.5 for women), 2/3 sodium deficiency (mmol) + total 24h urine sodium (mmol) of the previous 1d] on the first day, and 1 The next day was given 1 /3 sodium deficit (mmol) + [total 24h urine sodium (mmol) on the first day], converted by 17 mmol of sodium equivalent to l g NaCl, combined with total sodium, urine sodium concentration, total fluid intake with 3%-5% NaCl hypertonic solution and/or isotonic solution in 2-6 times of daily supplementation; blood sodium, urine sodium and 24h urine volume were closely monitored daily during the treatment, and after blood sodium and urine sodium were The use of salt corticosteroids with adequate sodium supplementation can facilitate the recovery of sodium concentration. In the case of hyponatremia, care should be taken to prevent rapid normalization of blood sodium during sodium supplementation, as there is a risk of inducing central pontine myelinolysis with too rapid correction of blood sodium. Some authors recommend a smaller dose correction: a maximum rise of 12 mmol/L at 24 h, 18 mmol/L at 48 h or 0.7 mmol/L per hour. In patients at high risk of disruption (e.g., patients with malnutrition or alcoholism), the 24-h rise in blood sodium should not exceed 8 mmol/L. When it is clear that hyponatremia is due to DI, sodium and water should be supplemented promptly to maintain the balance of water and electrolyte metabolism, and hormone replacement therapy with posterior pituitary hormone should be applied to control urine output. Patients diagnosed with DI are given posterior pituitary hormone 1 to 3 U/h (0.9% NaCl 250 mL + posterior pituitary hormone 24 U, slow intravenous drip, adjusting the drip rate with urine volume, usually 4-10 drops/min) to control urine volume, and appropriate sodium supplementation (hyponatremia) or sodium restriction (hypernatremia). Hyponatremia is a serious complication of heavy craniocerebral trauma, and untimely treatment may bring serious consequences. Water and electrolyte metabolic balance should be maintained in the treatment of craniocerebral trauma, and blood electrolytes, plasma osmolality, urinary routine and other routine checks should be closely monitored, and central venous pressure monitoring is feasible in hospitals with conditions, which provides a reliable guarantee for early diagnosis and timely treatment of central hyponatremia, and not only corrects hyponatremia The research results show that early detection and timely treatment of hyponatremia is an important link in the successful treatment of heavy craniocerebral trauma. In the process of correcting hyponatremia, too fast should be avoided, and electrolytes, urine sodium and 24h urine volume should be closely monitored daily during the treatment. V. Summary The diagnosis of the cause of hyponatremia is difficult and is often a combination of various causes. Insufficient sodium intake and massive dehydration are often accompanied by endocrine abnormalities, while hyponatremia caused by different reasons are contradictory in treatment, which brings some difficulties to clinical treatment. For patients with hyponatremia after craniocerebral trauma, some scholars believe that hyponatremic patients should be treated with water restriction and sodium restriction at the initial stage, and if the symptoms are not relieved and the blood sodium value is still below the normal level, then change to measures such as massive infusion and supplementation of isotonic saline; while some other scholars believe that both CSWS and SIADH should be supplemented with hypertonic saline; most domestic scholars advocate that in order not to aggravate the disease and facilitate the differentiation of hyponatremic Most scholars in China advocate that in order not to aggravate the disease and to help distinguish the cause of hyponatremia, patients with hyponatremia should first be treated with sodium supplementation according to true salt loss, and the efficacy should be observed for the purpose of identification. Moreover, the first choice of sodium supplementation is also a safer and more reliable treatment method. Firstly, hyponatremia is more common in patients with craniocerebral trauma due to the use of larger doses of dehydrating drugs in the early post-injury period. Secondly, sodium supplementation, especially hypertonic sodium supplementation, can prevent further decrease of blood sodium level, especially for patients with severe hyponatremia, which can avoid serious consequences such as cerebral edema caused by severe hyponatremia. If the blood sodium level does not rise significantly or continues to fall after 2-3 days of sodium supplementation, SIADH-induced hyponatremia can be considered, and further water restriction measures can be taken along with sodium supplementation to achieve the treatment purpose. If the urine volume still does not decrease, treatment with neuropituitary hormone or ellagitannin can be added, and the diagnosis of DI can be made effectively.