Decompressive craniectomy (DC) continues to be used as a life-saving treatment in patients with intractable intracranial hypertension. Although Cooper et al. reported that DC was not clinically effective in patients with mildly increased intracranial pressure (ICP) after traumatic brain injury (TBI), the flaws in their study have been questioned by scholars; some studies have confirmed that in patients with intractable intracranial hypertension, DC can effectively reduce ICP, and many patients achieve good outcomes. Although DC is technically uncomplicated, many scholars believe that postoperative complications can affect patient outcomes. Reviewing the literature, the following is a review of the progress in the diagnosis and treatment of hydrocephalus after DC surgery. Chibbaro et al. reported the results of 48 cases of heavy TBI with intractable intracranial hypertension treated with DC, and only 1 case of hydrocephalus occurred at a mean follow-up of 14 months. Huang et al. reported 3 cases of hydrocephalus (8%) at 6 months follow-up in 38 patients with hemorrhagic cerebral contusion foci treated with DC. Aarabi et al. reported 68 survivors at 48 months in 104 heavy TBI treated with DC, 13 cases (19%) had hydrocephalus and underwent V-P shunt. Honeybul [20] reported 4 cases (11%) of hydrocephalus at 18 months after DC in 41 cases of heavy TBI. De Bonis et al [21] summarized the results of 41 cases of heavy closed TBI, and hydrocephalus occurred in 9 (35%) of the 26 cases surviving after 1 month of DC. Kaen et al [22] reported that hydrocephalus occurred in 20 (27%) of 73 cases of heavy TBI treated with DC at a follow-up of more than 6 months. Among the 159 cases surviving for more than six months after surgery, 72 cases (45%) showed imaging ventricular enlargement, and 26 of them (36%) had symptoms of hydrocephalus and underwent V-P shunt. Chen Lei et al. reported that the incidence of hydrocephalus in 35 cases of heavy TBI treated with DC was 37% at 6-month follow-up. 2. mechanism of occurrence and associated factors The underlying factor for the occurrence of hydrocephalus is the impaired dynamic balance between cerebrospinal fluid production and absorption. rekate [25] concluded that hydrocephalus is obstructive at different sites, except for choroid plexus papilloma because of excessive cerebrospinal fluid production. there is a lack of agreement on the mechanism and risk factors for the occurrence of hydrocephalus in people with TBI after treatment with DC. 2.1 Mechanical obstruction theory Many scholars believe that traumatic subarachnoidal hemorrhage (SAH), intraventricular hemorrhage, and postoperative intracranial infection can easily cause impaired cerebrospinal fluid absorption due to mechanical blockage of arachnoid granules. the operation of DC itself, can increase the chance of scar formation and tissue debris leading to obstruction of cerebrospinal fluid reabsorption . 2.2 Theory of brain tissue displacement and altered cerebrospinal fluid dynamics Kaen et al [22] reported the results of a study on the correlation between interhemispheric subdural fluid and hydrocephalus after DC for heavy TBI. Of the 73 cases of heavy TBI in this group treated with DC, 20 (27%) developed hydrocephalus, of which 18 (90%) had subdural effusion; while of the 53 cases without hydrocephalus, only 18 (34%) had postoperative subdural effusion (P < 0.001). of the 17 cases with interhemispheric subdural effusion, 15 (88%) had hydrocephalus, and only 2 (12%) No hydrocephalus occurred (P < 0.01). Statistical analysis showed that interhemispheric subdural fluid was the only independent predictor of hydrocephalus and had the sensitivity and specificity to predict the occurrence of hydrocephalus. They concluded that the occurrence of interhemispheric subdural fluid and hydrocephalus after DC for heavy TBI is a result of two consecutive processes: (1) rebound phase: in patients with heavy TBI, the occupying lesion causes acute ICP increase and brain tissue shifts to the contralateral side; after DC, brain tissue shifts again but to the operative side, and the resulting suction effect increases the interhemispheric gap. At this stage, there may be a mechanical/inflammatory subarachnoid blockage that increases the resistance to cerebrospinal fluid uptake. This concept may explain why interhemispheric fluid accumulation is visible in the 1st d after DC; (2) hydrodynamic phase: the function of the arachnoid granules, which are pressure-dependent and unidirectional from the subarachnoid space-draining venous sinus, is impaired by cerebrospinal fluid pulsatile dynamics after cranial opening, making cerebrospinal fluid reflux The impaired cerebrospinal fluid pulsation kinetics after cranial opening causes the formation of hydrocephalus. Licata et al. also suggested that subdural effusion may be the initial sign of hydrocephalus. However, not all patients with hydrocephalus after DC have a process of interhemispheric fluid accumulation; on the contrary, not all those with interhemispheric fluid accumulation after DC develop hydrocephalus. In addition Aarabi et al [13] reported no correlation between subdural effusion and hydrocephalus occurrence after DC. In this group of 104 cases with heavy TBI who survived 48 months of follow-up after DC treatment, 13 (19%) had hydrocephalus, of which 6 (46%) had subdural effusion; 33 (60%) of 55 cases without hydrocephalus had subdural effusion. 2.3 Imbalance of extracellular fluid production and absorption theory De Bonis et al. reported that the upper boundary of the DC decompression window was too close to the midline (<25 mm) as an independent risk factor for the development of postoperative hydrocephalus (P = 0.01). They concluded that the development of hydrocephalus is determined by two main factors: the ICP pulsatile pressure originating from the choroid plexus and the asymmetric response of brain tissue to its pressure changes. The latter is represented by the non-linear manifestation of venous blood flow from the pontine veins through the lateral sulci (lacunae laterales) to the dural venous sinuses. This anatomical-functional complex, acting as a Starling resistor, determines the precise balance of extracellular fluid production and absorption in each cardiac circulation. Extracellular fluid is produced during systole and absorbed during diastole, and the imbalance resulting from increased absorption causes volume reduction in brain tissue, with the resultant enlargement of the ventricles to form hydrocephalus. the upper boundary of the decompression zone in DC is too close to the midline, causing a decrease in the external pressure acting on the veins during diastole and an increase in venous return, which further causes increased absorption of extracellular fluid and a decrease in brain parenchymal volume, resulting in enlargement of the ventricles. They attributed the 88% incidence of hydrocephalus in patients with cerebral infarction treated with DC reported by Waziri et al. to the fact that the upper boundary of the decompression zone in this group was within 2 cm of the midline. However, this doctrine does not explain why hydrocephalus persists and requires shunt surgery in some patients after cranial repair. waziri et al. suggest that it may be the persistence of the pathological mechanism of hydrocephalus occurrence after surgery that makes hydrocephalus an irreversible state. In contrast, Czosnyka et al. suggested that cranial repair may aggravate the obstruction of the subarachnoid space on the surface of the cerebral hemispheres, making the cerebrospinal fluid return resistance increase and leading to hydrocephalus formation. 2.4 Other risk factors Mazzini et al. reported older age (P < 0.05) and longer duration of coma (P < 0.01) in the hydrocephalus group. However, Kaen et al. reported that patient's age, gender, mechanism of injury, type of DC, preoperative GCS and pupillary changes, as well as basal pool changes on preoperative cranial CT scan, SAH and intraventricular hemorrhage, were not correlated with the development of hydrocephalus.Poca et al. reported that patient's age, initial GCS, SAH and type of brain injury were also not correlated with post-traumatic ventricular enlargement.Honeybul et al. reported Unilateral DC and ventriculitis were high risk factors for hydrocephalus requiring V-P shunt, but there was no statistical difference; there was no correlation between the distance of the superior border of the bone flap from the midline, SAH, time to skull repair and extraventricular drainage and the need for V-P shunt. However, multifactorial analysis showed that the highest ICP before decompression (P < 0.01), subdural effusion (P < 0.05) and low GCS at admission (P < 0.01) were independent factors for the development of hydrocephalus. They concluded that primary brain injury and impairment of cerebrospinal fluid return pathways were determinants of hydrocephalus occurrence after the use of DC for heavy TBI. 3. diagnostic criteria and differential diagnosis There is a lack of consistent criteria for the diagnosis of hydrocephalus after DC. aarabi et al. proposed the diagnostic criteria of enlarged temporal horn of the superior ventricle, bulbous dilatation of the third ventricle and enlarged lateral ventricles on cranial CT scan, or manifestation of CSF exudation around the ventricles. honeybul et al [11] reported the diagnostic criteria of enlarged ventricles with typical clinical manifestations, requiring shunt De Bonis et al. proposed the definition of traumatic hydrocephalus as progressive ventricular enlargement on imaging (Evans index > 0.3) and narrowing of the cerebrospinal fluid gap in the convex surface of the brain on CT scan; the patient’s early postoperative improvement in clinical status followed by worsening of consciousness or worsening of neurological status (excluding the presence of factors of infection or other disorders) can be used as clinical indicators to confirm the diagnosis of hydrocephalus. The diagnostic criteria for traumatic hydrocephalus proposed by Kaen et al. are: (1) modified frontal horn index >33%; (2) the cranial CT scans are in accordance with Gudeman’s criteria (distensible enlargement of the frontal horn of the lateral ventricle, enlargement of the temporal horn and third ventricle, and normal or absent sulci). The manifestation of periventricular exudate can be used as a basis for the diagnosis of hydrocephalus.The diagnostic criteria for traumatic ventricular enlargement reported by Honeybul et al [23] was ventricular enlargement on imaging 6 months after injury (Evans index >0.3). In contrast, the diagnostic criteria for traumatic hydrocephalus were progressive ventricular enlargement on imaging with periventricular exudate, along with (1) clinical manifestations of exacerbation or prolonged absence of improvement in neurological status, and (2) clinical improvement after V-P shunt. Combined with the above literature, the diagnosis of hydrocephalus in people with heavy TBI treated with DC currently relies mainly on the imaging manifestations. Progressive enlargement of the superior ventricular system on cranial CT scan, manifested by enlarged frontal angle of the lateral ventricles (Evans index >0.3), temporal angle ≥2 mm and rounding of the third ventricle, is necessary for the diagnosis of hydrocephalus. In contrast, periventricular hypodense exudate and narrowing or disappearance of the cerebral sulcus on the convex side of the brain are auxiliary conditions for the diagnosis. In patients who are comatose, most scholars have not yet included their clinical manifestations in the diagnostic criteria, but the presence of hydrocephalus should be evaluated in patients with exacerbation outside the decompression window, worsening after a once-improved neurological status, and the presence of other intracranial and extracranial underlying disorders discharged; and in postoperative awake patients with typical manifestations of mental retardation, gait instability and urinary incontinence, along with typical imaging signs, the diagnosis of hydrocephalus should be confirmed. To date, ICP measurement has not been used as a criterion for the diagnosis of hydrocephalus. The differential diagnosis requires differentiation from compensatory enlargement of the ventricular system after cerebral atrophy. The latter is commonly seen after diffuse axonal injury, with the typical imaging presentation of enlargement of the ventricular system accompanied by widening of the sulcus and no manifestation of periventricular hypodense exudate. Temporally, traumatic hydrocephalus tends to occur within 3 months after injury, whereas cortical atrophy ventricular enlargement tends to occur after 6 months after injury. The lumbar puncture drainage test is useful to identify hydrocephalus and compensatory ventricular enlargement, as well as to assess the preoperative outcome. Mazzini et al. concluded that single photon emission computed tomography (SPECT) is helpful in identifying ventricular enlargement and hydrocephalus after brain atrophy. Those with hydrocephalus showed significant temporal lobe hypoperfusion (P < 0.01) and frontal lobe hypoperfusion (P < 0.05) on SPECT, whereas parietal, occipital, thalamus and brainstem showed no hypoperfusion and there was no difference between the left and right cerebral hemispheres. However, the hypoperfusion manifestation on SPECT in those with cortical atrophy was diffuse (P < 0.01). They concluded that compared with CT and MRI, which show structural changes, SPECT shows the functional state of brain tissue and has a higher sensitivity for the diagnosis of hydrocephalus. However, those with heavy TBI treated with DC will have varying degrees of temporal and/or frontal lobe cerebral contusions present, and the sensitivity and specificity of SPECT in diagnosing hydrocephalus after DC needs to be confirmed by studies. 4. Prevention and control strategies and prognosis 4.1 Prevention Preventive measures should focus on reducing and minimizing risk factors. Intraoperatively, bleeding should be removed and flushed out as much as possible, and early postoperative drainage of bloody cerebrospinal fluid should be performed to reduce adhesions and blockage of the reflux pathway; intraoperative aseptic operation and reduction of dural sutures as much as possible should be emphasized to reduce blockage caused by inflammatory adhesions; the recommendation of De Bonis et al. that the upper border of DC should be more than 25 mm from the midline has yet to be confirmed by clinical studies. Chibbaro et al. reported 147 cases cranial repair within an average of 12 weeks after DC, and no hydrocephalus occurred. They concluded that early cranial repair to restore the kinetic state of cerebral blood flow and cerebrospinal fluid contributes to the prevention of hydrocephalus. 4.2 Treatment 4.2.1 Cerebrospinal fluid shunt modality: To date, for the treatment of hydrocephalus after TBI, cerebrospinal fluid shunts are still the main modality. Among them, V-P shunts account for the majority, L-P shunts have increased in recent years, while V-A shunts have gradually decreased. 4.2.2 Timing of surgery: There is no unanimous opinion, but those with typical signs on imaging, those with clinical worsening of consciousness or neurological status once improved and then worsened, and those with persistent external expansion of the decompression window aggravated, should be treated by surgery as early as possible. There are different views on whether cranial repair and shunt surgery should be performed in stage I. Advocates of staged surgery believe that it helps to reduce the post-shunt flap invagination syndrome, avoid the risk of postoperative paradoxical herniation, and reduce the burden of staged surgery. In contrast, advocates of staged surgery believe that the prolonged duration of stage I surgery and the 2 implants may increase the risk of postoperative infection. Honeybul et al. reported a case of death in a person with hydrocephalus after DC, who underwent cranial repair in stage II after V-P bypass. It is uncertain whether death can be avoided by stage I surgery. 4.2.3 Selection of shunts: Currently, it is considered that adjustable pressure shunts are the first choice for hydrocephalus shunts, and the set pressure can be adjusted to avoid excessive shunts or insufficient shunts after surgery according to clinical and imaging findings. There is a lack of credible conclusions on whether to choose antibacterial shunts and anti-siphon devices. 4.2.4 Others: Tzerakis et al [35] reported the use of V-P shunts for three cases of hydrocephalus combined with subdural effusion, and they concluded that in such patients, the effusion disappears with improvement of hydrocephalus. The differential diagnosis with chronic subdural hematoma and subdural hydrocephalus was also emphasized. The authors used a small subxiphoid incision to place the abdominal end of the shunt, and relying on intestinal peristalsis, the distal end of the shunt descended into the pelvic cavity in the vast majority of cases 1 d postoperatively. It is important to distinguish between symptomatic hydrocephalus and post-atrophic ventricular enlargement before surgery to avoid unnecessary shunt placement. 4.3 Prognosis Most authors report that hydrocephalus after DC is a risk factor that increases the poor prognosis of patients. 95% of the hydrocephalus group and 70% of the no hydrocephalus group were reported by Kaen et al. (P < 0.01), but the mortality rates of the two groups were 20% and 18.8%, respectively (P > 0.05). （Mazzini et al [30] also concluded that traumatic hydrocephalus not only affects the functional and behavioral prognosis of patients, but also correlates with post-injury epilepsy. A multicenter randomized controlled study was conducted to develop diagnostic criteria and diagnostic procedures for traumatic hydrocephalus, differential diagnosis methods for secondary ventricular enlargement after posttraumatic brain atrophy, and standardized operational guidelines for hydrocephalic shunts to avoid excessive shunts, reduce surgical complications, and improve efficacy and patient survival quality, which are directions for future basic and clinical research.