Rathke's cleft cyst surgery

The Rathke's fissure cyst is a congenital cyst derived from the residual epithelial cells of the embryonic craniopharyngioma. At 4 weeks of embryos, the outer embryonic layer cells above the original mouth bulged upward to form a Rathke sac, which closed into the craniopharynx tube 7 weeks before the embryo, and the anterior wall formed a pituitary pit, which later developed into the anterior pituitary; Less developed into the middle pituitary. Shanklin (1949) found 22 cases of residual cavities between the two tissues in 100 normal autopsies. Of these, 13 formed small cysts with cystic fluid without clinical symptoms, which was called Rathke's fissure. Since then, some authors have discovered that the cyst formed by this fissure can gradually increase, causing compression of the surrounding structure and clinical symptoms, which is called symptomatic Rathke's fissure cyst. E1-Mahdy (1998) reported 28 cases, in which single-layer columnar or cubic epithelium accounted for 71.4%, pseudostratified squamous epithelium accounted for 17%, mixed epithelial cells accounted for 7%; intracapsular liquid transparent yellowish accounted for 21.4%, sticky It is 60.7% thick and turbid or mucous, and its color varies from green to brown. In addition, some authors report that their contents resemble epithelioid cysts. 1, the incidence According to literature statistics, in routine autopsy, the incidence rate is 12% to 13%. These patients have no clinical symptoms before death, only when they increase, oppressing the surrounding structures to produce clinical symptoms, called symptomatic Rathke's fissure cyst. Before the 1980s, CT and MRI were not widely used, and the diagnosis was very difficult. Only case reports were reported. Yoshida (1997) statistics only reported 34 cases in the past literature. Later, due to the application of CT and MRI, the incidence increased significantly. Voelker (1991) reported 155 cases. E1-Mahdy (1998) reported 400 cases of pituitary lesions in operation, and 28 cases were symptomatic Rathke cysts, accounting for 7 cases. %. According to the report, these cysts are generally located between the anterior and middle lobe of the pituitary gland. Larger cysts can reach the saddle and the stalk and the funnel. Individual cysts contain substantial tumor mass, or with the difficult pituitary gland. Tumor or craniopharyngioma grows together and sometimes protrudes upward into the third ventricle. 2, clinical manifestations Symptomatic Rathke cysts can be seen at various ages, but occur mostly between the ages of 40 and 50. The course of the disease is slow, with an average of 3 to 4 years, but it can also occur rapidly due to pituitary apoplexy. The general clinical symptoms are headache, visual impairment and endocrine changes. The most common in endocrine changes are generalized weakness, sexual dysfunction, developmental delay, diabetes collapse, and obesity. Some lesions develop upwards, causing the pressure of the pituitary stalk to be twisted, which increases blood prolactin; in female patients, amenorrhea and lactation, and male patients show impotence. Blood tests have increased levels of prolactin, and other levels of pituitary hormones such as adrenocorticotropic hormone, gonadotropin, and thyroid stimulating hormone are reduced. Upward development of cysts can also cause vision and visual field changes. Individual cases report aseptic meningitis, secondary empty sella, or abscess formation in the cyst. Thomas (1998) reported that there were 9 cases of Rathke's fissure cyst combined with intracranial infection. In addition, there have been cases of sudden deterioration of the condition, hypopituitarism or adrenal insufficiency, and pituitary apoplexy. Therefore, I believe that the disease should be treated in time. There are also cases where the cyst can grow together with a pituitary tumor or a craniopharyngioma. 3, imaging examination CT and MRI showed that the Rathke cyst was a cystic space-occupying lesion in the saddle or in the saddle-saddle. It was rarely a saddle-occupying lesion, and it was required for cystic pituitary tumor, non-calcified craniopharyngioma, and saddle. Area epithelioid cysts and arachnoid cysts were identified. CT findings: According to E1-Mahdy (1998), 73.3% were low-density cysts; 26.7% were mixed-density shadows, the latter often represented a substantial pituitary mass or stroke in the cyst; 7.1% visible cyst wall Calcification. MRI is different, and the intracavitary signal is related to the cyst content. According to E1-Mahdy (1998), the T1 weighted image is 54.5% for high signals, 36.4% for low signals, and 9% for mixed signals. The T2 weighted image is 54.5% for the equal signal, 31.8% for the high signal, 4.5% for the low signal, and 9% for the mixed signal. Surgery sees its wall thickness or calcification, inflammatory reaction, cystic fluid green or brown viscous, denatured hemoglobin, accounting for 18.1%. The above imaging changes are sometimes difficult to distinguish from craniopharyngioma, so Landolt (1992) pointed out that the diagnosis of Rathke cysts is sometimes difficult. Only careful analysis of medical history and imaging data such as CT and MRI, combined with surgery and pathology. See to be able to determine the diagnosis. In general surgery, the cyst wall is smooth and calcified. The capsule is yellow thin or viscous liquid, no substantial tumor mass, and more support for Rathke cyst. Treatment of diseases: craniopharyngioma pituitary tumor Indication Because the disease is clinically and imagingly similar to the cystic pituitary tumor or craniopharyngioma that develops in the sella or slightly above the saddle, the surgical indications are the same as the upper two tumors in the site. Occasionally found that small asymptomatic people can not surgery. Contraindications 1. Nasal infection or chronic sinusitis, mucosal edema and congestion, prone to intracranial infection after surgery. 2. If the adult or sphenoid sinus is not well-formed, if the transsphenoidal approach is necessary, the bone in front of the sella should be ground with a micro-drill under the X-ray TV fluoroscopy. 3. The sphenoid sinus is over-vaporized, and the optic nerve and internal carotid artery can be exposed to the sphenoid sinus mucosa, which is easy to cause damage during operation. 4. Coronal CT scan showed that the tumor mass in the saddle and the sella was dumbbell-shaped, indicating that the saddle septum was small, and the transsphenoidal surgery was not easy to reach the saddle, and the saddle tumor was not easy to be seen after the saddle tumor was removed. Drop into the saddle during intracranial compression. 5. The tumor on the saddle is larger or extends to the anterior, middle, and posterior fossa. 6. The upper part of the tumor is larger, and the visual field of view is seriously damaged. The transsphenoidal surgery can not perform full optic nerve decompression, and the postoperative visual field recovery is not as good as transcranial microsurgery. Preoperative preparation 1. Endocrine examination: including a comprehensive determination of various endocrine hormones in the pituitary gland. 2. Imaging examination: In addition to the normal and multi-trajectory tomograms of the sella, thin-slice CT and MRI scans of the sella should be performed where possible. 3. Drug preparation: those with obvious hypopituitarism should be treated with appropriate replacement therapy before surgery, generally given dexamethasone or prednisone for 2 to 3 days. 4. Repeat the intranasal rinsing of the patient several days before the operation, or periodically add antibiotic solution. The nose hair was cut off 1 day before the operation, and washed, and the antibiotic solution was added dropwise. Surgical procedure 1. The earliest literature reports mostly use transcranial approach, and gradually enter the sphenoid sinus approach. Almost all of E1-Mahdy's (1998) and other large-scale case reports use transsphenoidal approach. 2. Most of the lesions seen during the operation were cystic lesions in the sella, and the cyst wall was partially removed after the cyst fluid was removed. Most authors advocate transsphenoidal approach to open the saddle dura mater and bone window, do not fill the fascia with fascia or fat, do not repair the saddle bottom, so that the cystic fluid continues to secrete into the sphenoid sinus, so as to avoid recurrence; It is necessary to keep the arachnoid membrane intact during the operation. If the membrane is ruptured, it is necessary to fill the saddle with fascia or fat to avoid cerebrospinal fluid leakage after operation. However, this treatment will inevitably lead to recurrence of the disease.