What is sagittal sinus thrombosis?
Q: My friend, 27 years old, pregnant with her first baby went to the hospital complaining of severe pain in her hand and neck. When examined, she was told that there was no problem and when the baby was examined, he was found dead due to diabetes. An abortion was done but she did not wake up after the surgery. She was diagnosed with sagittal sinus thrombosis. I need to know about this disease?
A:Here is some information about sagittal sinus thrombosis. Venous Sinus Thrombosis Thrombosis of cerebral veins or sinuses may occur in the absence of a demonstrable cause, but it also may occur in the setting of haematologic disorders or coagulation abnormalities or may result from local or contiguous infectious processes. Venous drainage from the brain begins with venules and veins that drain into the great venous sinuses. The venous sinus system itself lacks valves, thereby permitting retrograde propagation of clots or infections that emanate from structures such as those located in the central portion of the face or the middle ear. Septic Cavernous Sinus Thrombosis The cavernous sinuses comprise the most caudal dural venous chambers at the base of the skull. The paired structures lie on either side of the pituitary fossa, immediately above the midline sphenoid sinus. The cavernous sinus encloses the cavernous portion of the internal carotid artery; the third, fourth, and sixth cranial nerves en route to the apex of the orbit; and the ophthalmic and maxillary branches of the trigeminal nerve, which supply sensation to the forehead, periocular regions, cornea, and malar area of the face. Presenting symptoms are headache or lateralised facial pain, followed in a few days to weeks by fever, and involvement of the orbit, producing proptosis and chemosis secondary to obstruction of the ophthalmic vein. Paralysis of oculomotor nerves follows rapidly. Sensory dysfunction in the first and second divisions of the trigeminal nerve and a decrease in the corneal reflex are less obvious. Further involvement of the contiguous orbital contents follows, with mild papilloedema and decreased visual acuity, sometimes progressing to blindness. Increased intracranial pressure secondary to impaired venous drainage or extension to the opposite cavernous sinus or to other intracranial sinuses with cerebral infarction can result in stupor, coma, and death. Treatment relies on early diagnosis and consists of the prompt drainage of infected paranasal sinuses as well as specific antistaphylococcal agents, such as nafcillin (or oxacillin), given intravenously usually in combination with a third generation cephalosporin such as ceftriaxone or cefotaxime. Heparin anticoagulation may reduce morbidity from associated brain ischaemia, but this treatment remains controversial in the presence of documented infection. Septic Sagittal Sinus Thrombosis Septic sagittal sinus thrombosis is an uncommon condition that occurs as a consequence of purulent meningitis, infections of the ethmoid or maxillary sinuses spreading via venous channels, compound infected skull fractures, or, rarely, neurosurgical wound infections. Symptoms are primarily related to the elevated intracranial pressure (headache, nausea, and vomiting) and can evolve rapidly to stupor and coma. Seizures and haemiparesis may result from cortical infarction. The rate of progression, severity of symptoms, and prognosis are all related to the location of thrombosis. When only the anterior third of the sinus is obstructed, symptoms are less intense and evolve more slowly. If the thrombosis progresses to involve the middle and posterior thirds of the sinus, deterioration progresses more rapidly and outlook for recovery declines. CSF abnormalities accompany well over half the cases. The opening pressure is increased in proportion to the extent of the sagittal sinus involvement, and an increased cell count usually reflects the association of a meningeal or parameningeal process. Radiologically, septic sagittal sinus thrombosis may be excluded by visualisation of the normal sagittal sinus during the venous phase of cerebral angiography; the diagnosis can usually also be made by MRI, which demonstrates an abnormal increase in signal intensity (absent flow void) within the affected venous sinus. Contrast-enhanced CT scanning may reveal a contrast void lying at the junction of the transverse and sagittal sinuses (the region of the torcular); this so-called delta sign is an intraluminal clot surrounded by contrast material. Treatment Intravenous antibiotics should be directed at organisms recovered from the meningeal process or the meningeal site. S. aureus (including the methicillin-resistant strains), haemolytic streptococci, S. pneumoniae, and gram-negative aerobes such as Klebsiella spp. are the most common organisms. Initial antibiotic treatment should include nafcillin and a third-generation cephalosporin. Vancomycin can be used for antistaphylococcal coverage in patients with significant beta-lactam allergy or in whom methicillin-resistant strains are suspected. Associated paranasal sinusitis should be drained surgically. Heparin use has been little tested in septic venous thrombosis, but experience with noninfected sinus thrombosis has shown it to reduce both morbidity and mortality rates appreciably.