Stroke of uncommon origin
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SPREAD V Ed. | |
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Paediatric and juvenile stroke - Stroke of uncommon origin |
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| S 17-1 | In paediatric and
juvenile age, non-conventional risk factors should be sought by
accurate clinical evaluation and extended instrumental work-up. Anamnesis
should be accurate and recent cranial and cervical trauma, fevers of unknown
origin or recent infections (especially by Varicella Zoster virus) should be
examined as well as congenital heart diseases, familiarity for thrombotic
metabolic diseases, history of migraine and use of abuse drugs and
oestroprogestinic agents. In children with sickle cell disease, any new neurological sign or symptom should be considered as expression of a possible cerebrovascular event. |
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| S 17-2 | There are no randomised trials that investigate the efficacy of preventive therapies or therapies for the acute phase of paediatric stroke. The recommendations are therefore in part derived from those relevant to stroke in general. As for the adult, the treatment encompasses organizational aspects, general support measures and antithrombotic treatments. | ||||||||||||||||||||||||||||||
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R 17.1 *GPP |
Therapy and rehabilitation should be performed in an environment appropriate to the age and development of the child, by a multi-disciplinary team focused on the child's and family's health, social and emotional needs. Such needs should be systematically evaluated also when planning for the follow-up. Whenever possible, the child should be involved in the decisional process. | ||||||||||||||||||||||||||||||
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R 17.2 *GPP |
All children with acute stroke should be treated under the supervision of a paediatrician expert in cerebrovascular diseases. | ||||||||||||||||||||||||||||||
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R 17.3 Grade D |
The therapeutic
recommendations for the acute phase in paediatric age are extrapolated from
those for the adults, in absence of specific data. As in any medical
emergency, the ABC (Airways, Breathing, Circulation) rule
should be applied. Fever, hypoxia, hypo- and hyper-glycaemia should be treated promptly. |
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R 17.4 Grade D |
In case epileptic seizures occur in a paediatric stroke, the early administration of antiepileptic agents is recommended, to prevent further occurrences and minimize the ischaemic damage attending repeated epileptic seizures. | ||||||||||||||||||||||||||||||
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R 17.5 Grade D |
In the event of an acute stroke in a child, while waiting a pathogenic classification, ASA at the dose of 5 mg/kg per day should be administered, except in patients with sickle cell disease. In these latter, other therapies are a priority, such as transfusion of red blood cells. | ||||||||||||||||||||||||||||||
| R 17.6 | In children with acute ischaemic stroke, the therapy with heparin should be considered in case of: | ||||||||||||||||||||||||||||||
| a. *GPP | ischaemic stroke due to dissection of extracranial arteries; | ||||||||||||||||||||||||||||||
| b. Grade C | cerebral venous thrombosis; | ||||||||||||||||||||||||||||||
| c. Grade C | cardioembolic diseases at high risk of early re-embolization, after discussing the case with the cardiologist. | ||||||||||||||||||||||||||||||
| S 17-3 | The intravenous thrombolysis is, to date, not approved in the paediatric age segment. Information on its use is limited and heterogeneous. There is no information on the potential benefit-risk ratio in these patients. | ||||||||||||||||||||||||||||||
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R 17.7 *GPP |
The long-term management of a child with stroke should be co-ordinated by a paediatric neuropsychiatrist in collaboration with an experienced neurologist. | ||||||||||||||||||||||||||||||
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R 17.8 Grade D |
In children with ischaemic stroke, after having excluded epi-aortic vessels dissection, moyamoya disease, heart diseases at high embolic risk and sickle cells disease, it is recommended to continue the treatment with ASA at the dose of 1-3mg/kg per day. | ||||||||||||||||||||||||||||||
| S 17-4 | Cardioembolic stroke represents one of the most important mechanisms of stroke in paediatric and juvenile age. In comparison with the adult, however, the range of the cardioembolic conditions is different, since rhythm disorders and valvular diseases are less relevant, while congenital heart diseases and interatrial septum defects assume a greater importance. | ||||||||||||||||||||||||||||||
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R 17.9 Grade D |
 In case of cryptogenic
stroke in paediatric and juvenile age, the presence of patent foramen ovale
should be investigated. This may not have a
pathogenic relevance, unless all other possible causes, in particular
dissections of the epiaortic vessels, are carefully excluded. |
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R 17.10 Grade D |
Trans-oesophageal echocardiography is indicated in all patients with cryptogenic stroke in the paediatric and juvenile age segments. | ||||||||||||||||||||||||||||||
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*GPP |
In the paediatric age, the indication for trans-oesophageal echocardiography should be carefully evaluated, in view of the invasivity of the technique and of the discomfort it brings to the young patients. | ||||||||||||||||||||||||||||||
| S 17-5 | In a juvenile patient with TIA or cryptogenic stroke, the presence of Fabry disease should be considered. The clinical hypothesis is supported in presence of one or more of: ischaemic lesions of the posterior circulation, dolicoectasia of the vertebrobasilar territory, proteinuria, cornea verticillata, hypertrophic cardiomyopathy, cutaneous angiokeratomata, neurosensorial hypoacousia, polyneuropathy, gastrointestinal disorders. The diagnsosis is confirmed by the measurement of alpha-galactosidase A in the leukocytes in males, and by the genetic tests in the females. | ||||||||||||||||||||||||||||||
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R 17.11 Grade D |
The enzyme replacement therapy is indicated in the patients with Fabry disease, to decrease renal and cardiac complications, but there are no data on the decrease of cerebrovascular complications. | ||||||||||||||||||||||||||||||
| S 17-6 | In patients of the paediatric and juvenile age segments with TIA, stroke or cerebral venous thrombosis with high plasma homocysteine levels (>100 mcMol/L), homocystinuria should be considered. The clinical hypothesis is supported in presence of mental underdevelopment, marfanoid habitus, early osteoporosis and dislocation of the crystalline lens. | ||||||||||||||||||||||||||||||
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R 17.12 Grade D |
Pyridoxine at high doses, folates, vitamin B12 and betain are indicated to decrease the homocysteine levels in homocystinuria. | ||||||||||||||||||||||||||||||
| S 17-7 | In patients with encephalopathy or stroke events, who exhibit metabolic acidosis and hyperammoniaemia, one should consider metilmalonic aciduria and deficit of ornitine transcarbamylase. | ||||||||||||||||||||||||||||||
| S 17-8 | In patients with
ischaemic cerebral events, particularly if associated with migraine-like
headache, epileptic seizures and the presence at neuroimaging of cortical
lesions in the posterior brain area, one should consider the diagnosis of
MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like
episodes). The clinical hypothesis is supported by the presence of one or more among:
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| S 17-9 |
The
antiphospholipid antibody syndrome is an acquired coagulation disorder,
responsible for venous and arterial thrombotic events and recurrent
abortions. It may be primary or associated with autoimmune collagen
disorders, within the frame of which it represent the main pathogenic
mechanism of cerebrovascular complications. |
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| S 17-10 | In juvenile patients
with cryptogenic stroke or cerebral venous thrombosis, in particular in presence of symptoms and signs of an autoimmune collagen disorder or when
the laboratory tests point out an unexplained prolongation of aPTT, one
should consider the possibility of an antiphospholipid antibody syndrome. The diagnosis is confirmed by positive lupus anticoagulant factor or by the presence of antibodies anti-cardiolipin or anti-beta2-glycoprotein of IgG and/or IgM type at medium-high titre in two or more tests performed at 12-week intervals. |
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R 17.13 Grade D |
A prophylactic anticoagulant treatment in asymptomatic patients with occasional findings of anti-cardiolipin antibodies is not recommended, unless the patient is concurrently exposed to other risk factors. | ||||||||||||||||||||||||||||||
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R 17.14 Grade D |
In patient with cryptogenic stroke or TIA and positive for antiphospholipid antibodies without the criteria for the antiphospholipid antibody syndrome, the therapy with antiplatelet agents is recommended. | ||||||||||||||||||||||||||||||
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R 17.15 Grade D |
In patients with stroke or TIA who exhibit the criteria for the antiphospholipid antibody syndrome with venous or arterial thrombotic events in different organs, or recurrent abortions, the anticoagulant therapy is recommended with target INR of 2-3. | ||||||||||||||||||||||||||||||
| S 17-11 | The sickle cell disease in the homozygous form is one of the commonest causes of stroke in the paediatric age and is the most frequent risk factor for stroke in black children. The children with sickle cell disease have a 200-400 times greater risk of stroke in comparison with controls. In this disease the steno-occlusive lesions occur principally in the proximal segment of the medial cerebral artery and in the distal segment of the external carotid. | ||||||||||||||||||||||||||||||
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R 17.16 Grade D |
Transcranial Doppler is recommended for children with sickle cell disease, since it may predict the risk of cerebrovascular events. If the mean velocity at the medial cerebral artery is greater than 200 cm/sec, the yearly risk increases from 1% to 10%. The transcranial Doppler should be performed every year starting from the age of 2 and, in the subjects with velocity between 170 and 199 cm/sec, every 3 to 6 months. | ||||||||||||||||||||||||||||||
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R 17.17 Grade C |
Children of more than 2 years of age with sickle cell disease in homozygous form and with mean velocity at the medial cerebral artery greater than 200 cm/sec at the transcranial Doppler, should receive blood transfusions every 3-6 weeks, with the objective of keeping haemoglobin S <30% and the concentration of haemoglobin between 10 and12,5g/dL. | ||||||||||||||||||||||||||||||
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R 17.18 Grade D |
Patient with sickle cell disease should continue the transfusional therapy even after the normalization of parameters at the transcranial Doppler. The risks of the adverse events of such treatment when continued for prolonged periods should, however, be taken into account. | ||||||||||||||||||||||||||||||
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R 17.19 Grade D |
In patients with sickle
cell disease and ischaemic stroke, an urgent exsanguinotransfusion
is recommended to decrease the proportion
of HbS to below 30% and keep haemoglobin between 10 and 12,5 mg/dL. Patients with severe anaemia (due to splenic sequestration or aplastic crisis) or when exsanguinotransfusion cannot be performed within 4 hour, should receive transfusions of concentrated red blood cells. |
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R 17.20 *GPP |
In the adults with sickle cell disease who experience TIA or stroke, in addition to the control of the concurrent risk factors and the antiplatelet treatment, the transfusional treatment should be considered with the objective of decreasing the S-haemoglobin proportion to between 30% and 50%. | ||||||||||||||||||||||||||||||
| S 17-12 | The term "connective tissue disorders" encompasses some diseases attending the structural or morphofunctional alterations of the proteins constituting the extracellular matrix of the connective tissue. Such disorders are responsible for alterations affecting the skin, the osteoarticular system, some visceral organs and the vascular system. They can predispose to intracranial stenoses, dissections and aneurysms responsible of cerebrovascular complications of ischaemic and haemorrhagic nature. | ||||||||||||||||||||||||||||||
| S 17-13 |
Autosomal
dominant polycystic kidney disease is a connective tissue disorder that
becomes evident in the adulthood with development of multiple renal and
hepatic cysts and aggravating kidney failure. Approximately 8% of patients
exhibit intracranial aneurysms, which are frequently multiple, small and at
high risk of rupture. |
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R 17.21 Grade D |
All subjects with familiarity for polycystic kidney disease should be submitted already in juvenile age to an angio MRI examination to exclude the presence of aneurysms. If a first test is negative, a follow-up of at least 10 years is recommended in subjects with familial history of subarachnoid haemorrhage. A yearly follow-up is instead recommended for patients with polycystic kidney and intracranial aneurysms at a first angio MRI examination. | ||||||||||||||||||||||||||||||
| S 17-14 | Marfan's syndrome is a dominant autosomal connective disorder characterized by skeletal dysmorphisms, ocular abnormalities, dilatation of the aortic root with or without valvular insufficiency and asymptomatic dilatation of the dural sac. The patients with Marfan's syndrome exhibit and increased risk of dissection of the aorta and of the epiaortic vessels, while the association with intracranial aneurysms remains controversial. A dissection of the supra-aortic vessels should be considered in each patient with ischaemic stroke or TIA, who exhibits Marfan's syndrome or a marfanoid habitus. | ||||||||||||||||||||||||||||||
| S 17-15 | The Ehler-Danlos syndrome encompasses a group of inherited collagen disorders characterised by hyperelastic skin, joint hypermobility and vascular alterations. Type-IV is the one most predisposed to vascular complications caused by rupture of large and mean size arterial vessels. This diagnosis should be hypothesized in patients with aneurysms of the internal carotid, carotid-cavernous fistulae or dissection of the epiaortic vessels. The clinical hypothesis is supported in presence of joint and skin hyperlaxity and in presence of familiarity for complications by arterial, intestinal or uterine rupture. | ||||||||||||||||||||||||||||||
| S 17-16 | Pseudoxanthoma elasticum is a multi-system disorder of the elastic tissue, affecting skin, eyes, heart and vessels. In young patients with TIA/lacunar stroke, dissection or dolicoectasia of the epiaortic vessels, who exhibit retinal neoangioid striae or yellow-orange papulae in the flexor areas, Pseudoxanthoma elasticum should be suspected. The diagnosis is based on skin biopsy and genetic analysis. | ||||||||||||||||||||||||||||||
| S 17-17 | Neurofibromatosis type I is a dominant autosomal inherited neurocutaneous syndrome, characterized by neurofibromas and coffee-milk skin stains, iris amartomas, central nervous system tumours, pheochromocytomas, skeletal deformities and arterial vascular alterations affecting multiple districts. At the cerebral level, these are constituted of steno-occlusive as well as dilatative type, responsible of ischaemic as well as of haemorrhagic strokes, including subarachnoid haemorrhage. In patients with fibromatosis type I, it is appropriate to exclude the presence of cerebrovascular lesions with brain MRI and angio MRI of the extra- and intracranial vessels. | ||||||||||||||||||||||||||||||
| S 17-18 | Osteogenesis imperfecta is a dominant autosomal inherited disease, characterised by bone fragility, easy fractures and skeletal abnormalities. It is associated with teeth malformations, blue sclerae, hyperlaxity of the connective tissue and deafness. In patients with osteogenesis imperfecta, it is suggested to investigate the presence of vascular lesions, such as carotid-cavernous fistulae, of arterial diseases of moyamoya type and of intracranial aneurysms. | ||||||||||||||||||||||||||||||
| S 17-19 | In patients with TIA or stroke preceded since hours or days by cervical pain and ipsilateral headache, one should hypothesise a dissection of the epiaortic vessels. The clinical hypothesis is supported by the presence of major trauma or repeated microtraumas in the days prior to the cerebrovascular episode and, in case of dissection of the internal carotid, by the presence of the Horner's syndrome or cranial nerve palsy. | ||||||||||||||||||||||||||||||
| S 17-20 | In case of epiaortic vessels dissection, echo-Doppler of supra-aortic vessels may monitor a restriction of the lumen or a reduced flow distal to the carotid bifurcation and, rarely, the paradigmatic "double lumen". With the echo-Doppler it may, instead, be difficult to diagnose a vertebral dissection. For the diagnostic definition, it is appropriate to early recur to non-invasive angiographic techniques, such as angio-CT or angio MRI of the epiaortic vessels, with contrast bolus; to the MRI of the neck and, in selected cases or in case of doubts, to the conventional angiography. | ||||||||||||||||||||||||||||||
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R 17.22 Grade D |
In patients with TIA or stroke due to extracranial dissection of the epiaortic vessels, the treatment with heparin at anticoagulant doses is recommended, to be followed by oral anticoagulants in the following three months. If the dissection extends intracranially, this therapy is not recommended because of the risk of subarachnoid haemorrhage. | ||||||||||||||||||||||||||||||
| S 17-21 | The most frequent manifestations of moyamoya disease are ischaemic in children and haemorrhagic in adults. The clinical hypothesis is supported by the evidence of a marked stenosis or a bilateral occlusion of the intracranial internal carotid and of the vessels of Willis circulation. The diagnostic confirmation is obtained by conventional angiography, which points out the typical circulatory neoformations at the base of the encephalon. Angiographic patterns similar to those of moyamoya have been reported also in other clinical conditions, such as neonatal anoxia, neurofibromatosis, fibromuscular dysplasia, polyarteritis nodosa, aortic coarctation, Marfan's and Down's syndromes, and intracranial radiotherapy. | ||||||||||||||||||||||||||||||
| S 17-22 |
Fibromuscular
dysplasia is a rare segmental angiopathy of the large and medium size
vessels, which can exhibit ischaemic TIA or stroke, artery dissections and
subarachnoid haemorrhage. The clinical hypothesis should be made if
angiographic examination brings to evidence morpho-structural alterations of
the epiaortic vessels, with multiple concentric irregularities separated by
normal or dilated arterial segments, tubular stenosis with regular narrowing
of the vessel lumen or focal segmental stenosis of the vessel with the
appearance of a divericulum-like pouch. |
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| S 17-23 | In paediatric and juvenile patients with TIA or stroke, a vasculitis should be excluded as pathogenic determinant, since they respond to specific immunosuppressive therapies. The clinical hypothesis is supported by concurrent symptoms pointing to the dysfunction of other organs, or diffused encephalopathy, including headache. In the isolated vasculitis of the central nervous system, the systemic symptoms are, by definition, absent. | ||||||||||||||||||||||||||||||
| S 17-24 | In paediatric and juvenile patients with TIA or stroke, in presence of a clinical hypothesis of vasculitic origin, it is appropriate to proceed to immunological tests, which are useful for a correct classification. The diagnosis is confirmed by biopsy of a sample of tissue from an involved organ, exhibiting the typical inflammatory findings. | ||||||||||||||||||||||||||||||
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R 17.23 Grade D |
Patients with TIA or stroke in whom the clinical profile and the diagnostic work-up indicate a vasculitic aetiology, the prompt administration of steroids, alone or associated with cyclophosphamide, is recommended. The response to such treatment represents and additional supporting element for the diagnosis of vasculitis. | ||||||||||||||||||||||||||||||
| S 17-25 | In patients with ocular or hemispheric TIA preceded by important and persistent headache and with elevated inflammation markers, one should consider the presence of a Horton's arteritis and promptly perform the biopsy of the temporal artery, starting at the same time an appropriate steroid treatment while awaiting the bioptic confirmation. | ||||||||||||||||||||||||||||||
| S 17-26 | In patients who develop episodes of TIA or ischaemic stroke within 1-3 months from a varicella infection, the hypothesis of a post-varicella vasculitis should be made. The clinical hypothesis is supported if steno-occlusive alterations of the intracranial carotid and of the initial segments of the medial cerebral artery and of the anterior cerebral artery are found, and confirmed by finding the viral DNA in serum and liquor. | ||||||||||||||||||||||||||||||
| S 17-27 | In patients who develop a stroke after a trigeminal herpes zoster, a post-zoster arteritis should be hypothesised. The hypothesis is supported by the presence of steno-occlusive alterations of the intracranial vessels and by inflammatory abnormalities of the liquor. | ||||||||||||||||||||||||||||||
| S 17-28 | Patients with HIV infection exhibit an increased risk of ischaemic and haemorrhagic stroke. In subjects with TIA or stroke, ischaemic or haemorrhagic, in paediatric and juvenile age, it is appropriate to investigate the presence of an HIV infection. | ||||||||||||||||||||||||||||||
| S 17-29 | Cerebrovascular complications are one of the main causes of morbidity and mortality attending the acute and chronic abuse of opioids, amphetamines and cocaine. It is appropriate to accurately monitor the abuse of such substances and their urinary metabolites, in patients with cryptogenic ischaemic and haemorrhagic stroke. | ||||||||||||||||||||||||||||||
| S 17-30 | Among heroin users who exhibit a TIA or an ischaemic or haemorrhagic stroke, the presence of a bacterial endocarditis should be considered. | ||||||||||||||||||||||||||||||
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R 17.24 a Grade C |
In drug-addict patients with bacterial endocarditis, a prompt and prolonged antibiotic treatment is recommended, since it may reduce the risk of cerebrovascular complications. | ||||||||||||||||||||||||||||||
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R 17.24 b Grade D |
In patients with bacterial endocarditis on a native valve who exhibit a TIA or an ischaemic stroke, the oral anticoagulant treatment in the acute phase is not recommended, since it increases the risk of haemorrhagic cerebral complications. | ||||||||||||||||||||||||||||||
| S 17-31 | The patients with bacterial endocarditis and mechanical prosthetic valves who exhibit a TIA or an ischaemic stroke represent a complex and delicate case. The interruption of the anticoagulant, that the patient is already taking, may be a risk for the thromboembolic events and the valvular dysfunction. These patients are, at the same time, at risk of haemorrhagic cerebral complications. | ||||||||||||||||||||||||||||||
| S 17-32 |
Sneddon's
syndrome should be considered in young-adult patients with TIA, stroke and
vascular dementia, who exhibit skin alterations in the form of livedo
racemosa. The clinical hypothesis is supported by the presence of
steno-occlusive alterations of the small and medium size intracranial
arteries at the cerebral angiography, and by skin biopsy. This should be
performed in the pale central area of the livedo. |
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| S 17-33 | Susac's syndrome should be suspected in young patients, especially if female, with episodes of encephalopathy with or without focal deficits, deafness and retinopathy. The clinical hypothesis is supported by the presence of multiple lacunar-like subcortical lesions at the MRI, hypoacousia for the medium-low frequencies at the audiometry, and by bilateral alterations of the retinal arteries at fluoroangiography. | ||||||||||||||||||||||||||||||
| S 17-34 | A significant association between migraine with aura and cerebrovascular risk was demonstrated in female subjects. This risk is significantly increased if associated with cigarette smoking and oestroprogestinic intake. | ||||||||||||||||||||||||||||||
| S 17-35 | A greater incidence of large patent foramen ovale was found among patients with migraine with aura. It is, however, unknown whether in migraine sufferers the presence of patent foramen ovale implies a high cerebrovascular risk and there are no evidences on the efficacy of foramen ovale closure as primary or secondary cerebrovascular prevention among patients with migraine. | ||||||||||||||||||||||||||||||
| S 17-36 | Migraine aura should be carefully differentiated from the transient ischaemic attacks. It may be complex – including sensibility deficits, strength deficits, aphasia, up to coma-like conditions and symptoms mimicking a cerebral trunk lesion – last for more than 60 minutes, may not be followed by headache or be followed by headache without the characteristics of migraine without aura. | ||||||||||||||||||||||||||||||
| S 17-37 | Migraine infarct is defined by the presence of one or more symptoms typical or migraine aura but with duration of more than 60 minutes and the demonstration of a congruent ischaemic lesion, in absence of other documented causes of stroke. | ||||||||||||||||||||||||||||||
| S 17-38 | Patients with migraine exhibit alterations of the white matter at brain MRI, the value of which as possible risk factors for cerebral ischaemic events of clinical relevance is still undefined. | ||||||||||||||||||||||||||||||
| S 17-39 | The aetiology of cerebral venous thromboses includes a wide range of factors and is often multi-factorial. In women, the genetic thrombophilias associated with the use of oestroprogestinics represent the major risk factor. | ||||||||||||||||||||||||||||||
| S 17-40 | The clinical
presentation of the cerebral sinus and vein thromboses is multiform and
misleading. Headache represents the main symptoms at onset and during the course of the illness. It does not exhibit specific characteristics. It may have an acute, subacute or chronic onset, may be the only manifestation at onset, or be associated with signs of endocranial hypertension, focal neurological deficits and epileptic seizures. |
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| S 17-41 | Brain MRI (T1, T2, FLAIR and T2-star) combined with angio MRI to study the cerebral venous sinuses, represent the optimal techniques to diagnose and follow-up the patients with cerebral vein thrombosis. If uncertainty persists or in doubtful cases, catheter angiography may be justified. | ||||||||||||||||||||||||||||||
| S 17-42 | If a cerebral vein thrombosis with parenchymal lesions is suspected, the value of the D-dimer is increased in almost all cases and it possesses therefore a high negative predictive value. In patients with cerebral vein thrombosis with headache as sole symptom and without evidence of parenchymal lesions, the values of the D-dimer are instead normal in more than one-quarter of cases. The D-dimer is not validated in the paediatric age. | ||||||||||||||||||||||||||||||
|
R 17.25 a Grade D |
In patients with cerebral vein thrombosis without contraindications to heparin, the treatment with subcutaneous low-molecular weight heparins or intravenous unfractionated heparin is recommended, with aPTT monitoring. The intraparenchymal haemorrhage concurrent with the cerebral vein thrombosis is not a contraindication to the treatment with heparin. | ||||||||||||||||||||||||||||||
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R 17.25 b Grade D |
In patients with cerebral vein thrombosis of possibly infectious aetiology, in addition to the anticoagulant therapy, a prompt broad-range antibiotic therapy is recommended, to be started even before the results of cultures and susceptibility tests are available. The antibiotic treatment should be continued for at least two weeks after the local signs of infection have disappeared. | ||||||||||||||||||||||||||||||
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R 17.25 c Grade D |
In patients with
cerebral vein thrombosis and isolated endocranial hypertension, papilloedema
and loss of visus (pseudotumor cerebri), the possibility to perform one or
more evacuative lumbar punctures should be
considered. In this case, the therapy with heparin should preferably be
initiated at least 24 hours after the last lumbar puncture. In those cases in whom, in spite of these measures, the vision impairs, it is recommended to consider invasive measures, such as the ventricular-peritoneal shunt and the defenestration of the optical nerve, in addition to the normal measured to manage the endocranial hypertension. |
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R 17.25 d Grade D |
The locoregional thrombolysis is recommended in selected cases of cerebral vein thrombosis when, in spite of the heparin therapy, the clinical conditions impair in absence of other causes, or when a rapid re-canalization of the thrombotic sinus is needed. Dose and mode of application of the thrombolytic are still not standardized. |
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