Patients with craniocerebral trauma are in a high catabolic and high metabolic state, and partially or completely lose the ability to actively take in nutrients. Early, reasonable and sufficient nutritional support is the basis for the successful recovery of patients with craniocerebral trauma. However, many clinicians have not paid enough attention to this. There are still many patients with craniocerebral trauma who are fasting for a long time and only rely on a small amount of intravenous nutrition to maintain. Therefore, we call on neurosurgeons to pay attention to the nutritional problems of patients with craniocerebral trauma. “Food is the God of the people” (Han Shu – Li Eating Biography) reflects that diet is the fundamental to maintain health. Healthy people need to consume certain kinds and quantities of nutrients every day to meet the needs of human metabolism. Nutrients needed by the human body include protein, fat, carbohydrates, vitamins, inorganic salts, water and fiber. When the environment and the condition of the body change, the supply of nutrients should be adjusted accordingly to avoid insufficient or excessive supply of nutrients. After craniocerebral trauma, the patient’s early stress response leads to increased body temperature, increased respiration and heart rate, and the repair and regeneration of traumatized tissues, all of which increase the body’s energy demand. However, reduced or even inability to eat due to the patient’s impaired consciousness, nausea and vomiting due to increased intracranial pressure, perioperative fasting, as well as insufficient and/or untimely energy supplementation can lead to a significant decrease in exogenous energy intake by the body. The contradiction between energy demand and energy acquisition makes the organism rely on the mobilization of endogenous nutrients to satisfy the body’s needs, which is manifested by the massive depletion of blood glucose and the accelerated decomposition of hepatic glycogen and myoglycogen. Due to the body’s limited glycogen reserves, further energy demand mainly comes from the gluconeogenesis of protein and fat. Prolonged gluconeogenesis leads to fat loss and muscle breakdown in the body, which in turn causes wasting and fatigue. Long-term negative nitrogen balance leads to hypoproteinemia, which will aggravate cerebral edema; delay the recovery of brain tissue and wound healing; reduce the production of antibodies in the body, the body’s immune function decreases, and the incidence of infection increases; affect the lung function; and affect the function of the whole body organs. Therefore, nutritional support for patients with craniocerebral trauma is very important. Early nutritional support should be given after craniocerebral trauma. After craniocerebral trauma, the timing of nutritional support has a great impact on prognosis. Studies have shown that the mortality rate of patients without nutritional support 5 days after injury increases twofold; the mortality rate of patients without nutritional support 7 days after injury increases fourfold. Therefore, the Clinical Guidelines for the Treatment of Craniocerebral Trauma clearly suggest that early nutritional support is recommended for patients with severe craniocerebral trauma. Nutritional support treatment is usually started within 24-72 hours after injury. The route and preparation of nutritional support after craniocerebral trauma should be reasonable. The structure and function of the gastrointestinal tract change after craniocerebral trauma. After craniocerebral trauma, the body’s stress response causes blood to prioritize to ensure cardiac and cerebral supply, and the gastrointestinal tract is hypoperfused, resulting in gastric mucosal ischemia, mucosal epithelial edema and necrosis. Therefore, after craniocerebral trauma, the gastrointestinal tract digestion and absorption function decreases; poor gastrointestinal dynamics, manifested as gastric retention, abdominal distension; stress ulcers; and impaired gastrointestinal mucosal barrier function. The above pathophysiologic changes in the gastrointestinal tract after craniocerebral trauma seem to support early parenteral nutrition (PN) support. However, long-term PN can show degradation of gastrointestinal function such as atrophy of intestinal mucosa and reduction of intestinal peristalsis, and it is also prone to complications such as water and electrolyte disorders, and acid-base balance imbalance. Early enteral nutrition (EN), especially the application of nasoenteric tube, not only has a similar nutritional support effect to PN, but also helps to recover and maintain the structure and function of the gastrointestinal tract, avoiding the complications associated with PN. Therefore, EN is preferred for patients with craniocerebral trauma as long as the gastrointestinal function is permitted, and when the gastrointestinal function is not suitable for EN, PN can be chosen first; after the gastrointestinal function is recovered, the transition from PN to EN will be made in a timely manner. The formula of PN includes the application of glucose and fat to supply energy, and the application of amino acids to supply nitrogen. There are also essential vitamins and trace elements. The formula of EN not only considers the supply of energy and nitrogen, but also considers the absorption capacity of the gastrointestinal tract. In the early post-injury period, short peptide formulas that are easily digested and absorbed can be given first, and after the gastrointestinal function is restored, the whole protein formula can be applied. That is, “sequential EN treatment”. In addition, for patients with stress hyperglycemia, low-sugar formulations or preparations containing slow-release starch can be used. For patients with limited fluid intake, a high-calorie, high-protein formula may be preferred. Caloric and nitrogen supplementation for nutritional support after craniocerebral trauma should be adequate. Patients with craniocerebral trauma have significantly increased caloric and nitrogen requirements. In this regard, the formula for calculating caloric requirements is: caloric requirements = resting metabolic expenditure (RME) × resting metabolic rate (%RME). Where: male RME (kJ) = 4.18 × [66 + 13.7 × body weight (kg) + 5 × height (cm) – 6.8 × age in years]; female RME (kJ) = 4.18 × [65 + 9.6 × body weight (kg) + 1.8 × height (cm) – 4.7 × age in years]; resting metabolic rate (%RME) was calculated as follows: the average for ambulatory patients was 140% and 100% on average for ambulatory patients. The resting metabolic rate of unsedated patients with craniocerebral trauma can reach 140% to 200% of the normal value. With sedation, the resting metabolic rate decreases from 160% to 100% to 120%. Simple calculation: the total calorie requirement of ambulatory patients is about 30kcal/kg body weight/day; the total calorie requirement of ambulatory patients is about 25kcal/kg body weight/day. The body of patients after craniocerebral trauma is in a state of negative nitrogen balance, and protein supplementation is very important. The daily urea nitrogen excretion of medium-sized craniocerebral trauma is 10~15 grams, equivalent to 50~100 grams of protein. The daily urea nitrogen excretion of heavy craniocerebral trauma is 20~30 grams, equivalent to 150~200 grams of protein. The peak of urea nitrogen excretion after craniocerebral trauma is 10~14 days after the injury, and the negative nitrogen balance lasts for 2~3 weeks. Protein should generally be supplemented with 1.25~2.0g/kg body weight/day. In the case of patients with fever, other parts of the injury, etc., the caloric requirement and protein requirement should be increased as needed. Nutritional treatment of craniocerebral trauma. In Chinese medicine, it has been said since ancient times that “dietary supplementation is better than medicinal supplementation”. Nutritional support is to supplement the nutritional needs of patients with craniocerebral trauma. Nutritional therapy is the application of nutritional formulas to treat craniocerebral trauma and its complications. The ketogenic diet (ketogenic diet) is a diet that is high in fat, low in carbohydrates, and appropriate protein. This therapy has been used for decades in the treatment of refractory epilepsy in children, and although its antiepileptic mechanism is currently unknown, its effectiveness and safety have been recognized. Recently, our experimental study showed that the ketogenic diet had a protective effect against craniocerebral trauma in young rats, suggesting that the ketogenic diet could be used in the treatment of craniocerebral trauma in children. In summary, nutritional support after craniocerebral trauma should be early in time, reasonable in route and preparation, and adequate in dose. Nutritional therapy for craniocerebral trauma has a broad prospect.