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Fig. 37.14 Anterior ethmoidal artery (AEA) in the right eye in frontoethmoidal suture line, which is in line with the nasion

Fig. 37.15 A transconjunctival incision is made at least 2mm inferior to the tarsus

is provided to the medial orbit for intraconal and extraconal lesions such as cavernous haemangiomas. The precaruncular incision does not require closure. Chloromycetin ointment is placed in the medial canthus postoperatively.

Inferior Portal

Standing at the head of the patient, a transconjunctival incision is made at least 2mm inferior to the tarsus (Fig.37.15). The incision is directed to the inferior orbital rim and can then be extended medially or laterally depending on the indication for the surgery. A subperiosteal dissection must be carried out to avoid damaging the inferior oblique muscle that originates at the medial aspect of the orbital rim (Fig.37.16). The inferior orbital ssure forms the lateral limit, and medially the dissection can extend to the medial orbital wall/lamina papyracea.

D. Lubbe and N. Goncalves

Fig. 37.16 Left orbital oor exposed using inferior transconjunctival approach

The infraorbital nerve is found in the oor of the orbit and is usually covered by a layer of bone. The orbital oor can be resected, inferior orbital tumours removed or the infraorbital nerve followed back in malignant pathologies, according to the pathology that needs to be addressed.

The oor can be reconstructed with cartilage or polydioxanone sheeting for small defects and preformed bare titanium implants covered with

0.25-mm polydioxanone sheeting for larger defects. It is usually not necessary to close the incision. A temporary tarsorrhaphy suture can be placed in patients with chemosis.

Postoperative Management

Specic postoperative care is essential to ensure good outcomes and reduce recovery times. Local lubricant eye ointment is used to prevent dry eye. Ice packs are used directly over the eye for a few minutes every hour for 24h to reduce swelling and orbital ecchymosis.

A small suction drain is recommended to prevent a lateral orbital haematoma when using the superior lateral approach, unless a CSF leak has been repaired, when a suction drain is contraindicated [6].

Postoperative care of excessive chemosis (usually encountered preoperatively with proptosis) is treated with a suspension (Frost) suture. Postoperative antibiotic prophylaxis is given for 24h if both the orbit and nasal cavity are entered during the procedure. An ophthalmology clinical review is required postoperatively to assess vision.

37 Transorbital Endoscopic Surgery oftheParanasal Sinuses andSkull Base

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489

Complications

Only a few units perform regular transorbital surgery and few complications have thus far been reported. In the author’s experience, complications are only likely to occur due to the following:

– Too much retraction on the eye by the assis-

tant trying to provide a wider surgical corridor. It is important that the surgeon check the pupil regularly for changes in shape and size and relax the retraction every few minutes. Excessive retraction during the superior lateral approach can lead to a superior orbital ssure syndrome with CN III, IV and VI palsies and blindness if the optic nerve itself is damaged by a retractor.

– Upper eyelid retraction can lead to temporary

damage of the levator palpebrae muscle with ptosis. Dissection through the orbital septum can lead to permanent damage to the muscle that will require a blepharoplasty.

– CSF leaks can ensue if the anterior cranial

fossa is breached during the precaruncular or superior approach and the middle cranial fossa during the lateral approach.

– Enophthalmos can occur if reconstruction of

the oor or medial orbit is required post resection of these walls in patients without exophthalmic conditions (such as thyroid eye disease). The need for orbital wall reconstruction needs to be discussed and considered both preoperatively and intraoperatively.

– The lacrimal system can be injured if the dis-

section is too supercial during the precaruncular approach. Inserting probes into the canaliculi can prevent injury.

Areas ofControversy

Transorbital surgery for sphenoid wing meningiomas is a relatively new approach. There is no doubt that an optic nerve decompression prior to resection of the intracranial and lateral

orbital component enhances postoperative visual improvement [7, 8]. There is uncertainty whether complete surgical resection is possible with the transorbital route alone when compared to a pterional approach. Which patients should be offered transorbital surgery versus a craniotomy is not clear, and further studies with long-term outcomes need to be examined to ascertain the role of transorbital surgery for these lesions.

Access to the anterior and middle cranial fossa through the superior lateral approach is relatively easy, but whether neurosurgeons can utilize these portals to address pathology of the frontal and temporal lobes remains to be seen.

Key Learning Points

• Multidisciplinary input is essential if transor-

bital surgery is contemplated.

• Before embarking on transorbital surgery,

training is essential and special instruments/

retractors are required.

• Multiportal surgery allows resection of lesions

crossing surgical boundaries.

• A subperiosteal tissue plane preserves neuro-

vascular structures and orbital muscles.

• Suturing of the periosteum is important to

avoid ptosis and lateral canthal dystopia.

References

1. Lubbe D, Mustak H, Seayaroyh K, Goncalves N, Fagan J. Transorbital endoscopic surgery. Curr Otorhinolaryngol Rep. 2019;7(2):173–80.

2. Moe KS, Lubbe DE. Chapter 20: Transorbital neuroendoscopic surgery of the skull base and brain. In: Stamm AC, Mangussi-Gomes J, editors. Transnasal endoscopic skull base and brain surgery: surgical anatomy and its applications. 2nd ed. Thieme; 2019.

3. Lubbe DE, Moe KS. Chapter 16: Transorbital approaches to the sinuses, skull base, and intracranial space. In: Bleier BS, Freitag SK, Sacks R, editors. Endoscopic Surgery of the Orbit: Anatomy, Pathology, and Management. 1st ed. NewYork, NY: Thieme; 2019.

4. Kier EL, Mahajan A, Conlogue GJ. Sphenoidal artery: review of the literature and analysis of a dis-

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D. Lubbe and N. Goncalves

sected arterially injected fetal orbit. Surg Radiol Anat. 2021;43(3):405–11.

5. Cornelis MM, Lubbe DE.Precaruncular approach to the medial orbit and landmarks for anterior ethmoidal artery ligation: a cadaveric study. Clin Otolaryngol. 2016;41(6):777–81.

6. Moe KS, Kim LJ, Bergeron CM. Transorbital endoscopic repair of cerebrospinal uid leaks. Laryngoscope. 2011;121(1):13–30.

7. Lubbe D, Mustak H, Taylor A, Fagan J.Minimally invasive endo-orbital approach to sphenoid wing meningiomas improves visual outcomes—our experience with the rst seven cases. Clin Otolaryngol. 2017;42(4):876–80.

8. Lubbe D, Mustak H.Combined endoscopic endonasal and transorbital approach for orbital cranial tumors. In: Agarwal V, editor. Surgery of the orbit in neurooncology: indications, technique, and nuances. 1st ed. Cambridge University Press; 2022.

CSF Rhinorrhoea andtheAnterior

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Skull Base

HansRudolfBriner andAndrewC.Swift

CSF Physiology

Cerebrospinal uid (CSF) surrounds and protects the central nervous system (brain, spinal cord and adjacent nerves). The uid is unique and consists of 99% water and actively regulated balanced electrolytes and proteins (Fig.38.1) [1]. CSF not only provides hydromechanical protection but maintains an optimal neural microenvironment that supports the clearance of brain metabolites, creating a microenvironment essential for normal brain development, function and health.

The volume of CSF in adults is normally about 150mL, with about 75mL contained within the spinal subarachnoid space. CSF is produced mainly by the choroid plexus of the lateral ventricles and the tela choroidea of the third and fourth ventricle. The CSF is completely replaced about

Supplementary Information The online version contains supplementary material available at https://doi.

org/10.1007/978- 3- 031- 28690- 2_38.

three to four times per day, which equates to a volumetric production of about 400–600mL/day.

Following circulation, the CSF is resorbed via arachnoidal villi, which evaginate into the cerebral sinuses, mainly the superior sagittal sinus, but also via arachnoid villi in the spinal nerve roots. What is less well known is that a signicant part of CSF resorption takes place via extra- arachnoid pathways, such as the brain parenchyma, meningeal lymphatic vessels around the dural sinuses and the cribriform plate, and via perineural sheaths of the cranial nerves [2].

The pressure of CSF is variable and is dependent on several physiological factors such as posture, blood pressure in the carotid arteries, jugular venous pressure, respiration, intraabdominal pressure and physical activity. In an adult lying on the left side, the pressure of CSF is approximately 10–15 cmH2O [1].

H. R. Briner (*) Center for Otorhinolaryngology, Head and Neck Surgery, Hirslanden Clinic, Zurich, Switzerland e-mail: briner@orl-zentrum.com

A. C. Swift Liverpool Head and Neck Centre, Liverpool University Hospitals Foundation Trust, Liverpool, UK

https://doi.org/10.1007/978-3-031-28690-2_38

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H. R. Briner and A. C. Swift

Fig. 38.1 (a, b) MR image (T2 TSE sagittal (a), T2 space coronar (b)) that shows cerebrospinal uid (CSF) surround- ing the brain and spine (images by B.Schuknecht, MRI Institute, Zurich, Switzerland)

Table 38.1 Aetiological classication of CSF leaks

CSF leak Traumatic Non-traumatic

External trauma

Remarks Most

common

Surgery Anatomical Planned

opening of the dura in endoscopic skull base surgery

Repair part of the surgical plan

Inadvertently during endoscopic sinus surgery

Repair as soon as possible

malformation

Rare Common:

High intracranial pressure

idiopathic intracranial hypertension

Other causes (tumour, no cause identiable)

Rare

Classication ofCSF Leaks

CSF rhinorrhoea can be categorised into two main groups– traumatic leaks and non-traumatic leaks [3].

Traumatic leaks: These account for approximately 95% of all CSF leaks [4]. Traumatic leaks can further be divided in leaks caused by external trauma (e.g. head injury) and leaks caused by surgery. This surgical subgroup includes pituitary surgery, transnasal skull base surgery and complications of endoscopic sinus surgery.

Non-traumatic leaks: CSF leaks in this subgroup are less common and can be found in approximately 5% of patients with CSF rhinorrhoea. The aetiology of non-traumatic leaks includes rare congenital anatomical malforma-

tions, CSF rhinorrhoea with high intracranial pressure, skull base tumours and cases where no cause for the leak can be found (Table38.1).

CSF leaks can also be classied according to anatomical localisation, such as the posterior/ dorsal wall of the frontal sinus, the ethmoidal roof, the cribriform plate, the sphenoid or the skull base adjacent to the temporal bone (Table38.2).

The aetiological classication can be combined with the anatomical classication to facilitate a precise description for clinical practice. Figure 38.2 illustrates a clinical example of a ‘non-traumatic CSF leak of the left cribriform plate due to an arachnoid protrusion associated with idiopathic intracranial hypertension’ (Fig.38.2a–e).

38 CSF Rhinorrhoea andtheAnterior Skull Base

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Table 38.2 Anatomical classication of CSF leaks

CSF leak Anterior skull base Lateral skull base

Frontal sinus (dorsal wall)

Remarks Traumatic leaks Most common

Ethmoid roof Cribriform plate Sphenoid Temporal bone (mastoid,

middle ear)

location of inadvertent leaks during endoscopic sinus surgery

Common, traumatic and non-traumatic CSF leaks

Arachnoidal cysts in the lateral sphenoidal recess, associated with intracranial hypertension

CSF rhinorrhoea via Eustachian tube

493

Fig. 38.2 (a) Patient with spontaneous, non-traumatic CSF rhinorrhoea on the left side, provoked by bending the head forward. (b) Coronal CT scan of the same patient with a non-traumatic CSF leak of the left cribriform plate due to an arachnoid protrusion (arrow) into the left olfactory rim associated with idiopathic intracranial hypertension (image by B. Schuknecht, MRI Institute, Zurich, Switzerland). (c) Nasal endoscopy demonstrates CSF rhi- norrhoea originating from the left olfactory cleft. The CSF

is yellow due to intrathecal application of uorescein sodium by a lumbar puncture before endoscopy. (d) Endoscopic view of the non-traumatic CSF leak of the left cribriform plate during endoscopic repair. The arachnoidal protrusion appears yellow because of the intrathecal application of uorescein sodium. (e) Endoscopic view of the same lesion with the blue light lter. The CSF appears green due to uorescein sodium and the leakage is more obvious

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H. R. Briner and A. C. Swift

Fig. 38.2 (continued)

Complications ofCSF Leaks

The dura is a watertight anatomical layer that prevents CSF from leaking into the surrounding tissue. A dural defect will result in a CSF leak, and should this occur in the anterior skull base or travel along the Eustachian tube from a temporal bone defect, it will present as CSF rhinorrhoea.

A profuse loss of CSF will induce low intracranial pressure that presents with headache and non-specic neurological symptoms such as visual disturbances, hearing abnormalities or cognitive decits [5].

A breach in the dura can also act as a conduit for bacterial migration from the nasal cavity, paranasal sinuses or mastoid cells into the intradural space to cause meningitis. The incidence of meningitis depends on various factors such as the cause and the size of the dural defect and the duration of the leak. There is an ever-present cumulative risk of meningitis with an active CSF leak, irrespective of the site of the dural defect. Recurrent bacterial meningitis may occur over many years in the presence of a dural defect, and the latter may not be recognised as a cause of recurrent meningitis.

A dural defect may also allow air to enter the intracranial cavity and intradural space leading to

pneumocephalus. Risk factors for pneumocephalus include large dural defects, raised intranasal air pressure induced by nose blowing and a lumbar drain. Pneumocephalus frequently causes headaches and may lead to non-specic neurological symptoms such as an altered mental status. A tension pneumocephalus is a serious, potentially life-threatening complication associated with CSF rhinorrhoea caused by the dural defect acting as a valve [6].

Indication forCSF Leak Closure

Every persistent CSF leak must be closed to prevent development of severe, possibly lifethreatening complications, particularly where the CSF leak is profuse. Repair of large dural defects should be performed as soon as possible to prevent complications such as intracranial hypotension, meningitis and pneumocephalus.

A dural defect may cause minimal episodic, intermittent CSF rhinorrhoea, but such leaks are not so innocent and carry an inherent increased long-term cumulative risk of meningitis. The defect should be identied and repaired in all such cases.

The timing of closure depends on the clinical situation and the estimated risk of developing a complication.

Post-traumatic CSF rhinorrhoea after a skull base fracture may stop spontaneously, but exploration and dural repair remains a subject of debate. Spontaneous healing of small posttraumatic dural defects and the surrounding tissues is relatively common. However, there is still a potential long-term risk of meningitis, especially after fractures of the frontal skull base where spontaneous healing may not be as robust as in fractures of the temporal bone [4]. A healed skull base fracture may leave a bony dehiscence where the scar tissue may become tenuous and lead to dural herniation and a CSF leak many years after the initial head trauma.

38 CSF Rhinorrhoea andtheAnterior Skull Base

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Clinical Features ofCSF Leaks

CSF rhinorrhoea can present with a range of clinical feature, such as profuse positional rhinorrhoea following trauma to infrequent episodes of minimal rhinorrhoea where the diagnosis can be challenging. As a general principle, the diagnosis of CSF rhinorrhoea should ideally be proven and the site located prior to surgical exploration.

Careful assessment of the medical history is key in establishing the diagnosis of CSF rhinorrhoea. Typically, it presents as unilateral clear, watery rhinorrhoea, provoked by bending the head forward or by physical activity leading to increased intracranial pressure (Fig.38.2a). The rhinorrhoea can vary from infrequent episodes with minimal leakage to frequent profuse watery rhinorrhoea. CSF rhinorrhoea usually continues when the patient is asleep and may lead to visible ‘water stains’ or a halo sign on the pillow. Patients with profuse rhinorrhoea often describe a ‘salty taste’, but this symptom is non-specic.

Specic enquiry with leading questions should include the following: previous head trauma, even from many years ago; previous sinus surgery; and previous meningitis; especially if recurrent.

Non-traumatic spontaneous CSF rhinorrhoea may be associated with idiopathic intracranial hypertension in some patients and this should always be considered (IIH: vida infra).

Occasionally, patients will complain of nonspecic accompanying symptoms such as headache, visual disturbances, dizziness or tinnitus. These non-specic symptoms are mostly explained by other, mainly neurological conditions and not by a CSF leak. However, it is important to appreciate that non-specic symptoms may occasionally be associated with increased intracranial pressure in addition to a CSF leak.

norrhoea. The diagnosis can be easily conrmed by analysing the uid for beta-2 transferrin and/ or beta-trace protein.

CSF rhinorrhoea can also be mimicked by water collecting in the maxillary sinus after nasal rinsing or water sports, particularly after endoscopic surgery.

Occasionally, patients can present with episodic watery rhinorrhoea that is associated with exercise or eating. The nasal drip in these instances is physiological and more likely in more senior age groups. Head injury may, on rare occasions, cause watery rhinorrhoea induced by emotion or exercise. This condition is known as a pseudo-CSF leak and is the result of an altered autonomic response.

Clinical Examination

CSF rhinorrhoea may be demonstrated during clinical examination and its origin may be determined by nasal endoscopy. Endoscopy may reveal other causes of rhinorrhoea such as chronic rhinitis or rhinosinusitis, as well as assess operative access and anatomical anomalies of the septum and middle turbinates.

Otoscopy and microscopy should be performed with suspected CSF rhinorrhoea to exclude a temporal bone defect with CSF tracking along the Eustachian tube.

In patients with infrequent or minimal leaks, it is helpful to try to induce a leak by placing the patient prone on a couch, exed at the waist with the hands on the oor, in a head-down position.

Investigations

Beta-2 Transferrin andBeta-Trace Protein

Watery Rhinorrhoea That Mimics CSF Leaks

Severe allergic rhinitis can cause episodes of profuse rhinorrhoea that may be similar to CSF rhi-

In patients without an obvious CSF leak that can be localised with nasal endoscopy, a CSF leak should always be conrmed by identication and analysis of two CSF-specic proteins: beta-2 transferrin and beta-trace protein; both have high sensitivity and specicity for CSF [7–9].

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Beta-2 transferrin: This is a glycoprotein found in CSF, perilymph, aqueous and vitreous humour of the eye. The concentration in nasal secretion, tears and serum is normally very low, so detection of beta-2 transferrin in nasal liquid suggests the presence of CSF.Depending on the assay used, only small amounts (10 μL) of liquid are sufficient to detect the protein. Detection of beta-2 transferrin in the collected liquid is possible for up to 14days if it is stored in the refrigerator. A serum sample should be analysed alongside the nasal liquid as the serum concentration may occasionally be elevated and lead to a false- positive result, particularly in patients with chronic liver, kidney disease, alcoholism and rare glycoprotein metabolic disorders. False-negative results can occur when the amount of liquid is below the detection threshold of the assay or when there is bacterial contamination.

Beta-trace protein: This is prostaglandin D synthase produced in the choroid plexus and the meninges and has a high CSF to serum ratio. The assays for beta-trace protein are faster, cheaper and more automated than beta-2 transferrin assays and have a very high sensitivity and specicity in detection of CSF. Beta-trace protein is reported as an actual level that can be interpreted as either ‘unlikely, equivocal or denite’ presence of CSF in the collected sample. Small amounts (200μL) of liquid– which can be collected also by placing absorbent foam swabs within the nose– are sufcient for the detection of the protein. Renal insufciency and bacterial meningitis may lead to higher levels of betatrace protein in serum and lower levels in CSF, leading to false-positive results. As with beta-2 transferrin, the nasal liquid to serum beta-trace protein ratio should be measured to achieve higher reliability. Beta-trace protein and beta-2 transferrin tests can also be combined for further accuracy.

Historically, a glucose oxidase test was used to differentiate CSF from nasal secretion, but the sensitivity and specicity is low and the test is no longer recommended.

Imaging

The modern possibilities of imaging allow a detection and precise localisation of most CSF leaks. High-resolution computed tomography (HRCT) and magnetic resonance imaging (MRI) are the two principal examination methods that are complementary [8, 10, 11]. Imaging will help with preoperative planning and identify other pathologies such as signs of intracranial hypertension or other intracranial/sinonasal pathologies.

HRCT of the skull, anterior skull base, paranasal sinus system and the temporal bone is the prime examination in CSF rhinorrhoea. Multiplanar reconstruction with a bone window algorithm allows detection of even small bony defects associated with CSF leaks at almost every location (Fig.38.3a, b). Secondary signs of CSF rhinorrhoea such as intracranial air, mucosal reaction to CSF or liquid in adjacent sinuses can be of help in conrming the diagnosis.

MRI is superior to HRCT in differentiating soft tissue pathologies such as herniation of brain tissue in a meningoencephalocele, but not as good in detecting small bony skull base defects. Secondary signs of a CSF leak, such as liquid in the adjacent sinuses, are easy to detect (Fig.38.3c,

d). MRI may also show signs of increased intra-

cranial pressure, such as an ‘empty’ sella or widened optic nerve sheaths.

Modern technology offers the option of fusion of HRCT and MRI imaging (Fig. 38.4a, b). However, for this to be successful, the MRI has to be performed with the acquisition of ne detail to facilitate adequate image fusion, and it is advisable to let the radiologist know of the intent on how the images will be utilised.

CT cisternography with intrathecal application of contrast is an option if a leak is difcult to detect, but this has largely been replaced by less invasive MRI sequences such as MR cisternography with intrathecal gadolinium.

Historically, CSF rhinorrhoea was often conrmed by radionuclide cisternography after intrathecal injection of a radionuclide, but modern scanning techniques have made this technique defunct.

38 CSF Rhinorrhoea andtheAnterior Skull Base

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Fig. 38.3 (a) Patient with non-traumatic rhinorrhoea on the left side associated with increased intracranial pressure after irradiation of brain metastasis of a kidney cell carcinoma. HRCT (coronal, bone window) shows a small arachnoid herniation (arrow) at the lateral lamella of the left cribriform plate (image by Neuroradiology Hirslanden Clinic, Zurich, Switzerland). (b) On the axial scan, the small arachnoid herniation (arrow) at the lateral lamella of the left cribriform plate is visible with a slight thickening of the adjacent ‘soft tissue’, corresponding to liquid or mucosal thickening (image by Neuroradiology Hirslanden Clinic, Zurich, Switzerland). (c) Coronal MRI (T2, fat

suppressed) shows liquid with the same signal quality as CSF in an ethmoidal cell adjacent to the arachnoid herniation (arrow) in the lateral lamella. In addition to the arachnoid herniation, uid in the adjacent ethmoid cell (arrowhead) is an indirect sign of the CSF leak (image by Neuroradiology Hirslanden Clinic, Zurich, Switzerland). (d) Axial MRI (T2) is also able to demonstrate a uid level in the ethmoidal cell adjacent to the CSF leak (image

by Neuroradiology Hirslanden Clinic, Zurich, Switzerland). (e) Close endoscopic view of the arachnoi-

dal herniation at the lateral lamella of the left cribriform plate during endoscopic repair

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