[Spontaneous thrombosis of the superior longitudinal sinus in puerperium (so-called puerperal head)].
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Dural sinus thrombosis developed in two young women with paroxysmal nocturnal haemoglobinuria (PNH). The incidence, the clinical presentation, the radiologic findings, the therapy and the pathophysiology of haemolysis and thrombosis are discussed.
Complications and local extension of paranasal sinus infections most often involve the orbit and periorbita. Because of the widespread use of antibiotics since World War II, intracranial extension of maxillofacial sinusitis is rarely seen today. Nevertheless, the clinician must be aware of the potential for these complications, because late recognition of this condition and delays in treatment can increase morbidity and mortality rates. A comprehensive, current review of sinogenic intracranial complications is presented, with illustrative cases of brain abscess, subdural empyema, meningitis, cavernous sinus thrombosis, epidural abscess, and osteomyelitis. The mechanisms and potential for intracranial spread of infection from the frontal, sphenoid, and ethmoid sinuses are discussed in detail. The management of each type of complication is outlined, including the use of computed tomography and magnetic resonance imaging, and the role of surgical drainage.
The pathophysiology of cerebral venous infarctions is poorly understood, due partially to the lack of a suitable experimental model. Therefore, we developed a model in rats to study acute and long-term changes of brain function and morphology following thrombosis of the superior sagittal sinus. The superior sagittal sinus of rats was exposed, ligated, and injected with thrombogenic material. Thrombosis of the longitudinal sinus and ascending cortical veins was monitored by intravital fluorescence angiography. Histology was studied at 24 h and 4 weeks after thrombosis and changes in intracranial pressure, electroencephalogram (EEG), and tissue impedance were noted. Spontaneous locomotor activity was followed for 4 weeks after thrombosis. The effect of heparin treatment on tissue impedance was evaluated. Thrombosis of the superior sagittal sinus could be regularly induced, although pathological sequelae developed only if ascending veins were affected. Sinus and venous thrombosis was histologically characterized by bilateral, parasagittal infarctions. Thrombosis induction was followed by an increase in intracranial pressure from 4.7 +/- 1.6 to 12.8 +/- 2.4 mm Hg (n = 4) at 1 h after thrombosis, associated with an exponential rise in tissue impedance to 165 +/- 14% (n = 8) of the control. EEG changes were similar to those following global cerebral ischemia and remained pathological for up to 6 months after thrombosis (n = 6). As a permanent behavioral deficit spontaneous locomotor activity was reduced to 60 +/- 10% (n = 6) of the control. Finally, the administration of heparin (1 IU/g body weight) after thrombosis induction was found to reverse the pathological tissue impedance response of the brain. In conclusion, involvement of ascending cortical veins following sinus thrombosis appears to be critical for the development of irreversible tissue damage, such as infarction. Changes in intracranial pressure and tissue impedance suggest that the venous thrombosis was followed by brain edema of a predominantly cytotoxic nature. Venous thrombosis led to long-term changes of brain function, as demonstrated by persistent disturbances of the EEG or of the spontaneous locomoter drive. These deficits may be amenable to treatment with heparin.
Radiographic signs of cavernous sinus thrombosis were found in eight consecutive patients with an angiographic diagnosis of carotid-cavernous sinus fistula; six were of the dural type and the ninth case was of a shunt from a cerebral hemisphere vascular malformation. Diagnostic features consisted of filling defects within the cavernous sinus and its tributaries, an abnormal shape of the cavernous sinus, an atypical pattern of venous drainage, and venous stasis. Progression of thrombosis was demonstrated in five patients who underwent follow-up angiography. Because of a high incidence of spontaneous resolution, patients with dural-cavernous sinus fistulas who show signs of venous thrombosis at angiography should be followed conservatively.
The case is reported of a young man with Fusobacterium necrophorum septicemia who developed cavernous sinus thrombosis, meningitis, carotid artery stenosis and stroke. This article presents the only reported case of arterial stroke in Lemierre's syndrome. Clinical presentation, diagnostic difficulty and treatment are discussed.
Paroxysmal nocturnal haemoglobinuria may be complicated by life-threatening venous thrombosis. A patient who presented with the classical clinical picture of cerebral sinus thrombosis is described. Management of the condition is discussed.
We studied 30 patients with infectious sphenoid sinusitis (15 acute cases and 15 chronic cases) in an effort to characterize the clinical presentation, bacteriology, and associated complications of this frequently misdiagnosed infection. Severe frontal, temporal, or retro-orbital headache that radiated to the occipital regions or pain in the trigeminal (V1 to V3) distribution or both were the most prominent presenting symptoms. In acute cases, purulent exudate was frequently seen in the middle and superior nasal turbinates. Computerized axial tomography or sinus tomography and cannulation of the sphenoid sinus proved to be the most useful diagnostic studies. Organisms detected in acute cases included streptococci other than Streptococcus pneumoniae (41 per cent), Staphylococcus aureus (29 per cent), and Str. pneumoniae (17 per cent). In chronic infections, gram-negative bacilli (43 per cent) and staphylococcal species (24 per cent) were the predominant organisms. In acute disease, early diagnosis and aggressive therapy, including surgical drainage, were important. Delay in treatment was always associated with serious morbidity or mortality. Fatal complications included cavernous sinus thrombosis and bacterial meningitis.
Mucormycosis is an acute and often fatal infection caused by a fungus of the Mucorales order of the Zygomycetes class. There are various clinical types, usually associated with an underlying disorder. The rhinocerebral mucormycosis is usually seen in diabetics, especially in ketoacidosis, but may also appear in healthy people. We report three cases of mucormycosis diagnosed since april 1987 through january 2001 at the Dr. Domingo Luciani Hospital, Caracas, Venezuela. Two of them had diabetes and one was apparently healthy. The most common clinical presentation of mucormycosis was the rhinocerebral infection, seen in the two diabetic patients, both of them had cavernous sinus thrombosis one with involvement of the carotid artery. The other patient with sinus involvement had no predisposing factors. All patients were treated with amphotericin B and two of them had surgical debridement of involved tissue. We emphasize the importance of an early clinical diagnosis and treatment with surgical debridement of infected tissue combined with amphotericin B.
PURPOSE: We report a case of sagittal sinus thrombosis occurring after spinal analgesia for labour to highlight the difficulty of such diagnosis in the presence of postpartum atypical headache following regional anesthesia/analgesia. CLINICAL FEATURES: A previously healthy 21-yr-old, primiparous, preeclamptic parturient was admitted to the hospital at 37 weeks gestation for uterine contractions. Before pregnancy she was taking no medication other than oral contraceptives and was a non-smoker. Spinal analgesia was established on the first attempt at 8 cm of cervical dilation, in the setting of rapid progression of labour. Following an uneventful delivery, on the third day postpartum, the patient experienced gradual onset of an atypical headache with unclear postural character, followed by focal neurological signs five days later. Emergency neuroimaging revealed direct evidence of thrombosis in the posterior sagittal venous sinus. Anticoagulation was initiated with iv heparin (500 UI x kg(-1) x day(-1)). The patient's headache decreased progressively and full motor recovery was noted by day 14 postpartum. After 24 days, the patient was discharged without any neurological disability. Common inherited thrombophilic dispositions were absent, with the exception of a decrease in protein S level. CONCLUSION: Central venous thrombosis, while rare, is a recognized cause of puerperium stroke. The present case highlights the importance of considering the diagnosis in the presence of postpartum atypical headache following spinal anesthesia/analgesia. Early intervention with systemic heparinization is critical when the diagnosis is confirmed.
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BACKGROUND: Treatment of extensive intracranial venous sinus thrombosis with thrombolytic drugs is described, although the indications for and most efficacious technique for achieving thrombolysis remain uncertain. We report the successful lysis of superficial and deep venous system thrombosis by infusion of recombinant human tissue-type plasminogen activator (rt-PA) into the anterior superior sagittal sinus. CASE DESCRIPTION: A 34-year-old man presented with headaches followed by decreased level of consciousness and left hemiplegia. Angiography showed thrombosis of the superior sagittal and both transverse and straight sinuses with extension into the internal cerebral veins. The superior sagittal sinus was catheterized via a transfemoral route and rt-PA, 25 mg, was infused. There was no significant change in the thrombosis. The catheter was left in place and rt-PA was infused at 1 mg/minute for 19 hours. Repeat angiography showed resolution of the thrombosis. The patient was placed on heparin and then coumadin. He recovered completely. CONCLUSIONS: This report suggests that superselective infusion of thrombolytics into thrombosed intracranial venous sinuses can lyse intracranial venous sinus thrombosis. The thrombolytic agent must be infused for hours. The apparent successful lysis of clot in the deep venous system when infusion was into the superior sagittal sinus might be related to diffusion of rt-PA throughout the intracranial venous system or to improved venous outflow caused by lysis of clot in superficial dural sinuses.
Intracranial complications of paranasal sinusitis constitute true surgical and medical emergencies. The charts of all patients (n = 649) admitted for acute or chronic sinusitis to the University of Minnesota Hospital and to the University of Michigan Medical Center during a 13-year period (1975 to 1988) were retrospectively reviewed to determine the incidence of complications. The clinical presentation, bacteriology, involved sinuses, influencing host factors, white blood cell count on presentation, length of hospitalization, and postinterventional complications are presented. Twenty-four patients with intracranial complications from paranasal sinusitis are studied for an incidence of 3.7%. Aggressive medical and semi-emergent surgical intervention are required to prevent excessive morbidity and/or mortality. Intracranial complications included subdural empyema, frontal lobe abscesses, intrahemispheric abscesses, cavernous and superior sagittal sinus thrombosis, and osteomyelitis.
Similarities between benign intracranial hypertension and cerebral venous sinus thrombosis are well recognised and the importance of excluding the latter-especially sagittal sinus thrombosis-is understood. Some have suggested that all benign intracranial hypertension is caused by venous hypertension, mostly from stenoses or occlusions of the lateral sinuses. We describe a woman with refractory benign intracranial hypertension. With venography and manometry we showed partial obstruction of both transverse venous sinuses, with raised pressures proximal to the obstructions. Dilation of one of the sinuses with a stent reduced the pressure gradient, with striking symptomatic improvement. Investigation and treatment of benign intracranial hypertension should be revisited in view of these findings.
Several clinical cases of sinus thrombosis have been reported, but localized cerebral cortical venous thrombosis is a fairly rare clinical entity. We report a case of a 51-year-old woman who presented with right hemiparesis on admission. CT scan revealed subcortical hemorrhage with perifocal edema in the left front-parietal lobe. A T2W image revealed a large area of hyperintensity indicating edema, and coronal Gd enhanced T1 weighted image showed a reverse-triangle-shaped enhanced lesion. Left carotid angiogram showed cerebral cortical venous thrombosis in the left frontal lobe, but the superior sagittal sinus was not occluded. A month after admission, right hemiparesis had suddenly improved and the patient could walk without any support. Left carotid angiogram showed recanalization of thrombosed cortical veins and CT scan showed disappearance of any low density lesion indicative of edema. It is an important fact that neurological deficit improved quickly a month after onset, and it was suspected that, even without resorting to fibrinolytic therapy, recanalization of thrombosed cerebral veins would still eventually occur. We found the reverse-triangle-shaped enhanced lesion on MRI and we suspected that it was typical finding for cerebral cortical venous thrombosis.