Tag Archives: stroke

London Trauma Conference Day 2

London Trauma Conference 2013 – Day 2  by Dr Louisa Chan
So I find myself torn today: do I join the the main track with a Major incident theme or the Cardiac Masterclass? I never liked the thought of missing out on anything so I went to a bit of both.
Cardiac Masterclass
A lot of people probably think that managing cardiac arrest isn’t challenging and a bit dull because the patient is dead. But the Cardiac Masterclass would inspire you to think of a bright future for cardiac arrest management.
Mark Whitbread reminded us of how important dispatch is in the chain of survival. How much focus do we put on improving bystander CPR rates? Dispatcher assisted CPR has been shown to improve outcomes and needs to be skilfully done.
Ajay Jain pushes for all OHCA patients to be taken to a Cardiac Arrest centre for PCI. Why? Because the results he has from his centre for PCI in OHCA patients results in 77% (101/132) patients surviving to hosp discharge, 65% neurologically intact.
He also tells us that the ECG post arrest is a very poor predictor of PCI findings (although STEMI predicts a positive result) so they all should have PCI.
More data from TOPCAT shows us that non survivors of OHCA are easy to cool.
And maybe we should be cooling DURING cardiac arrest to minimise the reperfusion injury.
For persistent VF Prof Redwood says revascularisation is the key; when that doesn’t work then reducing LV volume may help so aspiration or an Impella may work. Failing that – ECMO.
Major Incidents
Major Incidents by their nature do not happen every day, so experience in these incidents is limited. The challenge then is how can we learn from incidents?
A standardised reporting system for a major incident database would be a good idea – www.majorincidentreporting.org – is where you will find the standard report form and open access database.
And then all I can suggest is that you need to come to the LTC and listen to the accounts of those who have been there. We heard about the Tokyo Sarin attack, Mumbai, and a very compelling story of multiple drownings from Steen Barnung.
Lessons from Tokyo – Sarin attack:

It will happen again
It will be chaos
Crowds cannot be controlled
Comms will fail
Clinical diagnosis – need a senior clinician
Treatment must be immediately available – 3min to absorb sarin
Decontamination – get naked, 90% decon with clothes removal.
Stream casualties
Empower the man on the ground.

LTC-MSUThe great thing about the London Trauma Conference is that it’s not just about the content of the tracks, there’s the networking and the opportunity to see new pieces of equipment.
The Norwegians won on the equipment front with their Mobile Stroke Unit. It’s due to go on line in 2014.
So TTFN and more from me on Day 3 of #LTC2013

Early surgery for intracerebral haemorrhage

ICHgraphicIconTo operate or not to operate on patients with an intracerebral haematoma? Deep ones can be tricky and risk damage to surrounding brain, so superficial ones may be more likely to benefit.
These patients with superficial lesions were assessed in STICH II, an international prospective randomised controlled trial comparing early surgery with conservative treatment.
Inclusion criteria were strict:

  • spontaneous lobar intracerebral haemorrhage on CT scan (≤1 cm from the cortical surface of the brain) with a volume of between 10 mL and 100 mL
  • within 48 h of onset
  • had a best motor score on the Glasgow Coma Score (GCS) of 5 or 6, and had a best eye score of 2 or more (ie, were conscious at randomisation).

The primary outcome was a Glasgow Outcome Scale-based evaluation of recovery (‘favourable’ vs ‘unfavourable’), which did not significantly differ between groups.
A predefined subgroup of patients with a poorer prognosis (using a score based on age, haematoma size and GCS) may have a better outcome with surgery. Some patients randomised to conservative therapy subsequently underwent delayed surgery. Thanks to appropriate intention-to-treat analysis they would have remained in the conservative treatment group which may have contributed to an underestimation of the benefit of surgery.
So, overall a negative trial, and patients with small lesions and higher GCS scores won’t benefit from surgery. Patients in poorer prognostic groups might benefit, but that remains unproven.
Some other ICH trials to be aware of are Clear III and MISTIE III, which are investigating thrombolytic agents in combination with clot removal, including with minimally invasive techniques.
Early surgery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (STICH II): a randomised trial
Lancet. 2013 Aug 3;382(9890):397-408
[EXPAND Abstract]

BACKGROUND: The balance of risk and benefit from early neurosurgical intervention for conscious patients with superficial lobar intracerebral haemorrhage of 10-100 mL and no intraventricular haemorrhage admitted within 48 h of ictus is unclear. We therefore tested the hypothesis that early surgery compared with initial conservative treatment could improve outcome in these patients.

METHODS: In this international, parallel-group trial undertaken in 78 centres in 27 countries, we compared early surgical haematoma evacuation within 12 h of randomisation plus medical treatment with initial medical treatment alone (later evacuation was allowed if judged necessary). An automatic telephone and internet-based randomisation service was used to assign patients to surgery and initial conservative treatment in a 1:1 ratio. The trial was not masked. The primary outcome was a prognosis-based dichotomised (favourable or unfavourable) outcome of the 8 point Extended Glasgow Outcome Scale (GOSE) obtained by questionnaires posted to patients at 6 months. Analysis was by intention to treat. This trial is registered, number ISRCTN22153967.

FINDINGS: 307 of 601 patients were randomly assigned to early surgery and 294 to initial conservative treatment; 298 and 291 were followed up at 6 months, respectively; and 297 and 286 were included in the analysis, respectively. 174 (59%) of 297 patients in the early surgery group had an unfavourable outcome versus 178 (62%) of 286 patients in the initial conservative treatment group (absolute difference 3·7% [95% CI -4·3 to 11·6], odds ratio 0·86 [0·62 to 1·20]; p=0·367).

INTERPRETATION: The STICH II results confirm that early surgery does not increase the rate of death or disability at 6 months and might have a small but clinically relevant survival advantage for patients with spontaneous superficial intracerebral haemorrhage without intraventricular haemorrhage.


Lowering the BP rapidly in ICH

ICH-iconIn our retrieval service case reviews, one thing that is that sure to generate discussion is what to do about the blood pressure in patients who present with intracranial haemorrhage and hypertension. We don’t want the bleeding to be worsened by higher blood pressure, but we don’t want to decrease cerebral perfusion pressure in patients who have raised intracranial pressure. Consensus guidelines exist for spontaneous intracerebral haemorrhage and subarachnoid haemorrhage, but they’re not based on strong data.
Here’s a study that attempted to provide more information. Intensive lowering to a target systolic of 140 mmHg within 1 hour was compared with lowering to a target of 180 mmHg. There was no significant reduction in the rate of the primary outcome of death or severe disability. The skeptic in me is disappointed there was no placebo arm. An ordinal analysis of modified Rankin scores favoured the intensive BP-lowering intervention, which means this study can be used by both those for and against intensive BP lowering to support their views.
As explained in an accompanying editorial, a number of factors may limit generalisability to Western practice, such as the predominant use of the alpha-blocking agent urapadil in the large numbers of Asian patients, a drug not available in the United States. Future publication of the ATACH-II trial using intravenous nicardipine will shed more light on this topic.
1. Rapid Blood-Pressure Lowering in Patients with Acute Intracerebral Hemorrhage
N Engl J Med. 2013 Jun 20;368(25):2355-65
[EXPAND Abstract]

BACKGROUND: Whether rapid lowering of elevated blood pressure would improve the outcome in patients with intracerebral hemorrhage is not known.

METHODS: We randomly assigned 2839 patients who had had a spontaneous intracerebral hemorrhage within the previous 6 hours and who had elevated systolic blood pressure to receive intensive treatment to lower their blood pressure (with a target systolic level of <140 mm Hg within 1 hour) or guideline-recommended treatment (with a target systolic level of <180 mm Hg) with the use of agents of the physician’s choosing. The primary outcome was death or major disability, which was defined as a score of 3 to 6 on the modified Rankin scale (in which a score of 0 indicates no symptoms, a score of 5 indicates severe disability, and a score of 6 indicates death) at 90 days. A prespecified ordinal analysis of the modified Rankin score was also performed. The rate of serious adverse events was compared between the two groups.

RESULTS: Among the 2794 participants for whom the primary outcome could be determined, 719 of 1382 participants (52.0%) receiving intensive treatment, as compared with 785 of 1412 (55.6%) receiving guideline-recommended treatment, had a primary outcome event (odds ratio with intensive treatment, 0.87; 95% confidence interval [CI], 0.75 to 1.01; P=0.06). The ordinal analysis showed significantly lower modified Rankin scores with intensive treatment (odds ratio for greater disability, 0.87; 95% CI, 0.77 to 1.00; P=0.04). Mortality was 11.9% in the group receiving intensive treatment and 12.0% in the group receiving guideline-recommended treatment. Nonfatal serious adverse events occurred in 23.3% and 23.6% of the patients in the two groups, respectively.

CONCLUSIONS: In patients with intracerebral hemorrhage, intensive lowering of blood pressure did not result in a significant reduction in the rate of the primary outcome of death or severe disability. An ordinal analysis of modified Rankin scores indicated improved functional outcomes with intensive lowering of blood pressure.

2. Blood pressure in intracerebral hemorrhage–how low should we go?
N Engl J Med. 2013 Jun 20;368(25):2426-7

Clopidogrel and aspirin for TIA

A large Chinese trial compared aspirin alone with combination aspirin / clopidogrel in patients who had had a TIA in the previous 24 hours. 90-day stroke outcome was reduced in the combination therapy group without an apparent increase in haemorrhage.
Clopidogrel with Aspirin in Acute Minor Stroke or Transient Ischemic Attack
N Engl J Med. 2013 Jul 4;369(1):11-19
[EXPAND Abstract]

Background Stroke is common during the first few weeks after a transient ischemic attack (TIA) or minor ischemic stroke. Combination therapy with clopidogrel and aspirin may provide greater protection against subsequent stroke than aspirin alone.

Methods In a randomized, double-blind, placebo-controlled trial conducted at 114 centers in China, we randomly assigned 5170 patients within 24 hours after the onset of minor ischemic stroke or high-risk TIA to combination therapy with clopidogrel and aspirin (clopidogrel at an initial dose of 300 mg, followed by 75 mg per day for 90 days, plus aspirin at a dose of 75 mg per day for the first 21 days) or to placebo plus aspirin (75 mg per day for 90 days). All participants received open-label aspirin at a clinician-determined dose of 75 to 300 mg on day 1. The primary outcome was stroke (ischemic or hemorrhagic) during 90 days of follow-up in an intention-to-treat analysis. Treatment differences were assessed with the use of a Cox proportional-hazards model, with study center as a random effect.

Results Stroke occurred in 8.2% of patients in the clopidogrel-aspirin group, as compared with 11.7% of those in the aspirin group (hazard ratio, 0.68; 95% confidence interval, 0.57 to 0.81; P<0.001). Moderate or severe hemorrhage occurred in seven patients (0.3%) in the clopidogrel-aspirin group and in eight (0.3%) in the aspirin group (P=0.73); the rate of hemorrhagic stroke was 0.3% in each group.

Conclusions Among patients with TIA or minor stroke who can be treated within 24 hours after the onset of symptoms, the combination of clopidogrel and aspirin is superior to aspirin alone for reducing the risk of stroke in the first 90 days and does not increase the risk of hemorrhage.


Stroke thrombolysis outcomes from registry

Data from a large national stroke registry are reported to show that in patients who received tPA, outcomes were worse the later it was given. From a registry of over a million patients, the study group included 58353 patients from 1395 sites treated after emergency department arrival with IV tPA within 4.5 hours of symptom onset. Reported odds ratios were small but statistically significant in this large sample size. There was a 4.9% rate of intracranial haemorrhage.
As there is no comparison with patients who did not receive tPA, one cannot conclude from this study that tPA is either beneficial or harmful. It may however be used as an argument that if you’re working in a centre where the patients are going to get the tPA, it’s advisable not to delay it.
Time to treatment with intravenous tissue plasminogen activator and outcome from acute ischemic stroke
JAMA. 2013 Jun 19;309(23):2480-8
[EXPAND Abstract]

IMPORTANCE: Randomized clinical trials suggest the benefit of intravenous tissue-type plasminogen activator (tPA) in acute ischemic stroke is time dependent. However, modest sample sizes have limited characterization of the extent to which onset to treatment (OTT) time influences outcome; and the generalizability of findings to clinical practice is uncertain.

OBJECTIVE: To evaluate the degree to which OTT time is associated with outcome among patients with acute ischemic stroke treated with intraveneous tPA.

DESIGN, SETTING, AND PATIENTS: Data were analyzed from 58,353 patients with acute ischemic stroke treated with tPA within 4.5 hours of symptom onset in 1395 hospitals participating in the Get With The Guidelines-Stroke Program, April 2003 to March 2012.

MAIN OUTCOMES AND MEASURES: Relationship between OTT time and in-hospital mortality, symptomatic intracranial hemorrhage, ambulatory status at discharge, and discharge destination.

RESULTS: Among the 58,353 tPA-treated patients, median age was 72 years, 50.3% were women, median OTT time was 144 minutes (interquartile range, 115-170), 9.3% (5404) had OTT time of 0 to 90 minutes, 77.2% (45,029) had OTT time of 91 to 180 minutes, and 13.6% (7920) had OTT time of 181 to 270 minutes. Median pretreatment National Institutes of Health Stroke Scale documented in 87.7% of patients was 11 (interquartile range, 6-17). Patient factors most strongly associated with shorter OTT included greater stroke severity (odds ratio [OR], 2.8; 95% CI, 2.5-3.1 per 5-point increase), arrival by ambulance (OR, 5.9; 95% CI, 4.5-7.3), and arrival during regular hours (OR, 4.6; 95% CI, 3.8-5.4). Overall, there were 5142 (8.8%) in-hospital deaths, 2873 (4.9%) patients had intracranial hemorrhage, 19,491 (33.4%) patients achieved independent ambulation at hospital discharge, and 22,541 (38.6%) patients were discharged to home. Faster OTT, in 15-minute increments, was associated with reduced in-hospital mortality (OR, 0.96; 95% CI, 0.95-0.98; P < .001), reduced symptomatic intracranial hemorrhage (OR, 0.96; 95% CI, 0.95-0.98; P < .001), increased achievement of independent ambulation at discharge (OR, 1.04; 95% CI, 1.03-1.05; P < .001), and increased discharge to home (OR, 1.03; 95% CI, 1.02-1.04; P < .001).
CONCLUSIONS AND RELEVANCE: In a registry representing US clinical practice, earlier thrombolytic treatment was associated with reduced mortality and symptomatic intracranial hemorrhage, and higher rates of independent ambulation at discharge and discharge to home following acute ischemic stroke. These findings support intensive efforts to accelerate hospital presentation and thrombolytic treatment in patients with stroke.


Endovascular stroke treatment

Two randomised controlled trials have been published which compare endovascular stroke treatments with intravenous tPA. Both the American Interventional Management of Stroke (IMS) III trial (1) and the Italian SYNTHESIS Expansion trial (2) had Modified Rankin Scores as their primary endpoint. No significant differences in this outcome or in mortality or intracranial haemorrhage rates were found in either trial, and IMS III was terminated early due to futility.
A third trial, from North America, called MR RESCUE, randomised patients within 8 hours after the onset of large vessel, anterior-circulation strokes to undergo mechanical embolectomy or receive standard care(3). No clinical outcome differences were demonstrated.
An accompanying editorial (4) draws the following conclusion:

“The IMS III and SYNTHESIS Expansion studies show that intravenous thrombolysis should continue to be the first-line treatment for patients with acute ischemic stroke within 4.5 hours after stroke onset, even if imaging shows an occluded major intracranial artery. Beyond 4.5 hours, the MR RESCUE trial does not provide data supporting the use of endovascular treatment in patients with an ischemic penumbra of any size.”

Many might argue that showing endovascular treatment is equivalent to thrombolysis just means endovascular treatment doesn’t work, because a significant proportion of the emergency medicine community views this as the correct interpretation of a thorough analysis of the stroke thrombolysis literature.
1. Endovascular Therapy after Intravenous t-PA versus t-PA Alone for Stroke
NEJM Feb 8, 2013 Full Text Link
2. Endovascular Treatment for Acute Ischemic Stroke
NEJM Feb 8, 2013 Full Text Link
3. A Trial of Imaging Selection and Endovascular Treatment for Ischemic Stroke
NEJM Feb 8, 2013 Full Text Link
4.Endovascular Treatment for Acute Ischemic Stroke — Still Unproven
NEJM Feb 8, 2013 Full Text Link

Magnesium doesn't improve SAH outcome

A multicentre RCT showed intravenous magnesium sulphate does not improve clinical outcome after aneurysmal subarachnoid haemorrhage, therefore routine administration of magnesium cannot be recommended.
Magnesium for aneurysmal subarachnoid haemorrhage (MASH-2): a randomised placebo-controlled trial
Lancet 2012 July 7; 380(9836): 44–49 Free full text
[EXPAND Click to read abstract]

Background Magnesium sulphate is a neuroprotective agent that might improve outcome after aneurysmal subarachnoid haemorrhage by reducing the occurrence or improving the outcome of delayed cerebral ischaemia. We did a trial to test whether magnesium therapy improves outcome after aneurysmal subarachnoid haemorrhage.

Methods We did this phase 3 randomised, placebo-controlled trial in eight centres in Europe and South America. We randomly assigned (with computer-generated random numbers, with permuted blocks of four, stratified by centre) patients aged 18 years or older with an aneurysmal pattern of subarachnoid haemorrhage on brain imaging who were admitted to hospital within 4 days of haemorrhage, to receive intravenous magnesium sulphate, 64 mmol/day, or placebo. We excluded patients with renal failure or bodyweight lower than 50 kg. Patients, treating physicians, and investigators assessing outcomes and analysing data were masked to the allocation. The primary outcome was poor outcome—defined as a score of 4–5 on the modified Rankin Scale—3 months after subarachnoid haemorrhage, or death. We analysed results by intention to treat. We also updated a previous meta-analysis of trials of magnesium treatment for aneurysmal subarachnoid haemorrhage. This study is registered with controlled-trials.com (ISRCTN 68742385) and the EU Clinical Trials Register (EudraCT 2006-003523-36).

Findings 1204 patients were enrolled, one of whom had his treatment allocation lost. 606 patients were assigned to the magnesium group (two lost to follow-up), 597 to the placebo (one lost to follow-up). 158 patients (26·2%) had poor outcome in the magnesium group compared with 151 (25·3%) in the placebo group (risk ratio [RR] 1·03, 95% CI 0·85–1·25). Our updated meta-analysis of seven randomised trials involving 2047 patients shows that magnesium is not superior to placebo for reduction of poor outcome after aneurysmal subarachnoid haemorrhage (RR 0·96, 95% CI 0·86–1·08).

Interpretation Intravenous magnesium sulphate does not improve clinical outcome after aneurysmal subarachnoid haemorrhage, therefore routine administration of magnesium cannot be recommended.


Emergency physicians providing stroke 'lysis in the UK

Although the worldwide emergency medicine community is split in its support for stroke thrombolysis, those who work in centres where it is provided might be interested in systems to optimise its effectiveness.
A study from the UK showed that emergency physicians can provide the majority of the service, with outcomes similar to the SITS-MOST data.
Interestingly there was only one (suspected) major intracranial haemorrhage case.
The best resource for reducing door-to-tPA time in ischaemic stroke, with heaps of related discussion, is here at EMCrit

Image from EMJ Open Access. Click for PubMed image source

BACKGROUND: Stroke thrombolysis is strongly supported as an effective therapy for selected cases of early stroke. The absence of 24 h stroke specialists in district general hospitals (DGHs) has led to the suggestion that regional hyper-acute stroke centres should be developed. This paper describes a cooperative model that uses the skills already present in a DGH to deliver a thrombolysis service initiated in the emergency department by the emergency physicians, and describes the outcomes of that service in comparison with the SITS-MOST trial.

METHOD: The outcomes of all stroke patients thrombolysed at Scarborough DGH from 2004 to January 2009 were reviewed. Outcome was defined using a three-part scale. Data at Scarborough DGH were compared with data from the SITS-MOST European-wide study of stroke thrombolysis.

RESULTS: Data were available for 98 of 110 patients thrombolysed during the study period. Fifty (51%) had a good outcome, seven (8%) had partial resolution of their symptoms, and 41 (42%) showed no improvement or deterioration. These outcomes were comparable to those in the European database.

CONCLUSION: Stroke thrombolysis can be effectively delivered in a non-specialist (a non-hyper-acute stroke centre) DGH in the UK. An audit of cases completed describes complications seen.

An analysis of outcomes of emergency physician/department-based thrombolysis for stroke
Emerg Med J. 2012 Aug;29(8):640-3
Free Full Text

Early CT may rule out subarachnoid haemorrhage

A multicentre Canadian study challenges the practice of routine lumbar puncture after negative CT in patients with suspected subarachnoid haemorrhage. CT scanning within six hours was highly sensitive, although a few cases of initially misinterpreted CTs “illustrate the importance of having a qualified radiologist with a high level of skill interpreting the head scans in a timely manner“.

Nearly 2% of patients were lost to all follow-up; the authors point out that even if a quarter of these patients could have experienced a subarachnoid haemorrhage, the corresponding negative likelihood ratio for a computed tomography performed within six hours rises to only 0.024 (0.007 to 0.07). They assert:

Such a likelihood ratio could be incorporated into the informed discussion surrounding the risks and benefits of lumbar puncture after negative results on computed tomography for this diagnosis

They point out that when CT imaging is obtained more than six hours after headache onset, clinicians should continue to be cautious because of the decreasing sensitivity for subarachnoid haemorrhage beyond this time.

Objective To measure the sensitivity of modern third generation computed tomography in emergency patients being evaluated for possible subarachnoid haemorrhage, especially when carried out within six hours of headache onset.

Design Prospective cohort study. Setting 11 tertiary care emergency departments across Canada, 2000-9.

Participants Neurologically intact adults with a new acute headache peaking in intensity within one hour of onset in whom a computed tomography was ordered by the treating physician to rule out subarachnoid haemorrhage.

Main outcome measures Subarachnoid haemorrhage was defined by any of subarachnoid blood on computed tomography, xanthochromia in cerebrospinal fluid, or any red blood cells in final tube of cerebrospinal fluid collected with positive results on cerebral angiography.

Results Of the 3132 patients enrolled (mean age 45.1, 2571 (82.1%) with worst headache ever), 240 had subarachnoid haemorrhage (7.7%). The sensitivity of computed tomography overall for subarachnoid
haemorrhage was 92.9% (95% confidence interval 89.0% to 95.5%), the specificity was 100% (99.9% to 100%), the negative predictive value was 99.4% (99.1% to 99.6%), and the positive predictive value was 100% (98.3% to 100%). For the 953 patients scanned within six hours of headache onset, all 121 patients with subarachnoid haemorrhage were identified by computed tomography, yielding a sensitivity of 100% (97.0% to 100.0%), specificity of 100% (99.5% to 100%), negative predictive value of 100% (99.5% to 100%), and positive predictive value of 100% (96.9% to 100%).

Conclusion Modern third generation computed tomography is extremely sensitive in identifying subarachnoid haemorrhage when it is carried out within six hours of headache onset and interpreted by a qualified radiologist

Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study
BMJ. 2011 Jul 18;343:d4277

CVT guideline

Thanks to neuro-icu.com for highlighting this one: The American Heart Association and American Stroke Association have produced guidelines for the diagnosis and management of cerebral venous thrombosis. Here is a summary of their recommendations. The full text of the guidelines is available via the link at the bottom.
Routine Blood Work

  • In patients with suspected CVT, routine blood studies consisting of a complete blood count, chemistry panel, prothrombin time, and activated partial thromboplastin time should be performed (Class I; Level of Evidence C).
  • Screening for potential prothrombotic conditions that may predispose a person to CVT (eg, use of contraceptives, underlying inflammatory disease, infectious process) is recommended in the initial clinical assessment (specific recommendations for testing for thrombophilia are found in the long-term management section of this document) (Class I; Level of Evidence C).
  • A normal D-dimer level according to a sensitive immunoassay or rapid enzyme-linked immunosorbent assay (ELISA) may be considered to help identify patients with low probability of CVT (Class IIb; Level of Evidence B). If there is a strong clinical suspicion of CVT, a normal D-dimer level should not preclude further evaluation.

Common Pitfalls in the Diagnosis of CVT

  • In patients with lobar ICH of otherwise unclear origin or with cerebral infarction that crosses typical arterial boundaries, imaging of the cerebral venous system should be performed (Class I; Level of Evidence C).
  • In patients with the clinical features of idiopathic intracranial hypertension, imaging of the cerebral venous system is recommended to exclude CVT (Class I; Level of Evidence C).
  • In patients with headache associated with atypical features, imaging of the cerebral venous system is reasonable to exclude CVT (Class IIa; Level of Evidence C).

Imaging in the Diagnosis of CVT

  • Although a plain CT or MRI is useful in the initial evaluation of patients with suspected CVT, a negative plain CT or MRI does not rule out CVT. A venographic study (either CTV or MRV) should be performed in suspected CVT if the plain CT or MRI is negative or to define the extent of CVT if the plain CT or MRI suggests CVT (Class I; Level of Evidence C).
  • An early follow-up CTV or MRV is recommended in CVT patients with persistent or evolving symptoms despite medical treatment or with symptoms suggestive of propagation of thrombus (Class I; Level of Evidence C).
  • In patients with previous CVT who present with recurrent symptoms suggestive of CVT, repeat CTV or MRV is recommended (Class I; Level of Evidence C).
  • Gradient echo T2 susceptibility-weighted images combined with magnetic resonance can be useful to improve the accuracy of CVT diagnosis (Class IIa; Level of Evidence B).
  • Catheter cerebral angiography can be useful in patients with inconclusive CTV or MRV in whom a clinical suspicion for CVT remains high (Class IIa; Level of Evidence C).
  • A follow-up CTV or MRV at 3 to 6 months after diagnosis is reasonable to assess for recanalization of the occluded cortical vein/sinuses in stable patients (Class IIa; Level of Evidence C).

Management and Treatment

  • Patients with CVT and a suspected bacterial infection should receive appropriate antibiotics and surgical drainage of purulent collections of infectious sources associated with CVT when appropriate (Class I; Level of Evidence C).
  • In patients with CVT and increased intracranial pressure, monitoring for progressive visual loss is recommended, and when this is observed, increased intracranial pressure should be treated urgently (Class I; Level of Evidence C).
  • In patients with CVT and a single seizure with parenchymal lesions, early initiation of antiepileptic drugs for a defined duration is recommended to prevent further seizures (Class I; Level of Evidence B).
  • In patients with CVT and a single seizure without parenchymal lesions, early initiation of antiepileptic drugs for a defined duration is probably recommended to prevent further seizures (Class IIa; Level of Evidence C).
  • In the absence of seizures, the routine use of antiepileptic drugs in patients with CVT is not recommended (Class III; Level of Evidence C).
  • For patients with CVT, initial anticoagulation with adjusted-dose UFH or weight-based LMWH in full anticoagulant doses is reasonable, followed by vitamin K antagonists, regardless of the presence of ICH (Class IIa; Level of Evidence B).
  • Admission to a stroke unit is reasonable for treatment and for prevention of clinical complications of patients with CVT (Class IIa; Level of Evidence C).
  • In patients with CVT and increased intracranial pressure, it is reasonable to initiate treatment with acetazolamide. Other therapies (lumbar puncture, optic nerve decompression, or shunts) can be effective if there is progressive visual loss. (Class IIa; Level of Evidence C).
  • Endovascular intervention may be considered if deterioration occurs despite intensive anticoagulation treatment (Class IIb; Level of Evidence C). In patients with neurological deterioration due to severe mass effect or intracranial hemorrhage causing intractable intracranial hypertension, decompressive hemicraniectomy may be considered (Class IIb; Level of Evidence C).
  • For patients with CVT, steroid medications are not recommended, even in the presence of parenchymal brain lesions on CT/MRI, unless needed for another underlying disease (Class III; Level of Evidence B).

Long-Term Management and Recurrence of CVT

  • Testing for prothrombotic conditions, including protein C, protein S, antithrombin deficiency, antiphospholipid syndrome, prothrombin G20210A mutation, and factor V Leiden, can be beneficial for the management of patients with CVT. Testing for protein C, protein S, and antithrombin deficiency is generally indicated 2 to 4 weeks after completion of anticoagulation. There is a very limited value of testing in the acute setting or in patients taking warfarin. (Class IIa; Level of Evidence B).
  • In patients with provoked CVT (associated with a transient risk factor), vitamin K antagonists may be continued for 3 to 6 months, with a target INR of 2.0 to 3.0 (Table 3) (Class IIb; Level of Evidence C).
  • In patients with unprovoked CVT, vitamin K antagonists may be continued for 6 to 12 months, with a target INR of 2.0 to 3.0 (Class IIb; Level of Evidence C).
  • For patients with recurrent CVT, VTE after CVT, or first CVT with severe thrombophilia (ie, homozygous prothrombin G20210A; homozygous factor V Leiden; deficiencies of protein C, protein S, or antithrombin; combined thrombophilia defects; or antiphospholipid syndrome), indefinite anticoagulation may be considered, with a target INR of 2.0 to 3.0 (Class IIb; Level of Evidence C).
  • Consultation with a physician with expertise in thrombosis may be considered to assist in the pro- thrombotic testing and care of patients with CVT (Class IIb; Level of Evidence C).

Management of Late Complications (Other Than Recurrent VTE)

  • In patients with a history of CVT who complain of new, persisting, or severe headache, evaluation for CVT recurrence and intracranial hypertension should be considered (Class I; Level of Evidence C)

CVT in pregnancy

  • For women with CVT during pregnancy, LMWH in full anticoagulant doses should be continued throughout pregnancy, and LMWH or vitamin K antagonist with a target INR of 2.0 to 3.0 should be continued for at least 6 weeks postpartum (for a total minimum duration of therapy of 6 months) (Class I; Level of Evidence C).
  • It is reasonable to advise women with a history of CVT that future pregnancy is not contraindicated. Further investigations regarding the underlying cause and a formal consultation with a hematologist and/or maternal fetal medicine specialist are reasonable. (Class IIa; Level of Evidence B).
  • It is reasonable to treat acute CVT during pregnancy with full-dose LMWH rather than UFH (Class IIa; Level of Evidence C).
  • For women with a history of CVT, prophylaxis with LMWH during future pregnancies and the postpartum period is probably recommended (Class IIa; Level of Evidence C).


  • Supportive measures for children with CVT should include appropriate hydration, control of epileptic seizures, and treatment of elevated intracranial pressure (Class I; Level of Evidence C).
  • Given the potential for visual loss owing to severe or long-standing increased intracranial pressure in children with CVT, periodic assessments of the visual fields and visual acuity should be performed, and appropriate measures to control elevated intracranial pressure and its complications should be instituted (Class I; Level of Evidence C).
  • In all pediatric patients, if initial anticoagulation treatment is withheld, repeat neuroimaging including venous imaging in the first week after diagnosis is recommended to monitor for propagation of the initial thrombus or new infarcts or hemorrhage (Class I; Level of Evidence C).
  • In children with acute CVT diagnosed beyond the first 28 days of life, it is reasonable to treat with full-dose LMWH even in the presence of intracra- nial hemorrhage (Class IIa; Level of Evidence C).
  • In children with acute CVT diagnosed beyond the first 28 days of life, it is reasonable to continue LMWH or oral vitamin K antagonists for 3 to 6 months (Class IIa; Level of Evidence C).
  • In all pediatric patients with acute CVT, if initial anticoagulation is started, it is reasonable to perform a head CT or MRI scan in the initial week after treatment to monitor for additional hemor- rhage (Class IIa; Level of Evidence C).
  • Children with CVT may benefit from thrombophilia testing to identify underlying coagulation defects, some of which could affect the risk of subsequent rethromboses and influence therapeutic decisions (Class IIb; Level of Evidence B).
  • Children with CVT may benefit from investigation for underlying infections with blood cultures and sinus radiographs (Class IIb; Level of Evidence B).
  • In neonates with acute CVT, treatment with LMWH or UFH may be considered (Class IIb; Level of Evidence B).
  • Given the frequency of epileptic seizures in children with an acute CVT, continuous electroencephalography monitoring may be considered for individuals who are unconscious or mechanically ventilated (Class IIb; Level of Evidence C).
  • In neonates with acute CVT, continuation of LMWH for 6 weeks to 3 months may be considered (Class IIb; Level of Evidence C).
  • The usefulness and safety of endovascular intervention are uncertain in pediatric patients, and its use may only be considered in carefully selected patients with progressive neurological deterioration despite intensive and therapeutic levels of anticoagulant treatment (Class IIb; Level of Evidence C).

Diagnosis and Management of Cerebral Venous Thrombosis: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association
Stroke. 2011 Feb 3. [Epub ahead of print] Full Text