Tag Archives: neurology


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).

Children

  • 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

TIA workup renders ABCD2 unhelpful

ABCD2 is recommended to stratify the risk of stroke in patients presenting to the ED with TIA symptoms. In some centres this is used to differentiate those that need to be admitted for further evaluation and treatment from those that can be followed up in the outpatient setting. A recent study showed that if a detailed work up was done in the ED on all TIA patients (followed by appropriate intervention), the ABCD2 score did not predict adverse outcomes, which were lower in this cohort than in the original ABCD2 cohort.

STUDY OBJECTIVE: We study the incremental value of the ABCD2 score in predicting short-term risk of ischemic stroke after thorough emergency department (ED) evaluation of transient ischemic attack.

METHODS: This was a prospective observational study of consecutive patients presenting to the ED with a transient ischemic attack. Patients underwent a full ED evaluation, including central nervous system and carotid artery imaging, after which ABCD2 scores and risk category were assigned. We evaluated correlations between risk categories and occurrence of subsequent ischemic stroke at 7 and 90 days.

RESULTS: The cohort consisted of 637 patients (47% women; mean age 73 years; SD 13 years). There were 15 strokes within 90 days after the index transient ischemic attack. At 7 days, the rate of stroke according to ABCD2 category in our cohort was 1.1% in the low-risk group, 0.3% in the intermediate-risk group, and 2.7% in the high-risk group. At 90 days, the rate of stroke in our ED cohort was 2.1% in the low-risk group, 2.1% in the intermediate-risk group, and 3.6% in the high-risk group. There was no relationship between ABCD2 score at presentation and subsequent stroke after transient ischemic attack at 7 or 90 days.

CONCLUSION: The ABCD2 score did not add incremental value beyond an ED evaluation that includes central nervous system and carotid artery imaging in the ability to risk-stratify patients with transient ischemic attack in our cohort. Practice approaches that include brain and carotid artery imaging do not benefit by the incremental addition of the ABCD2 score. In this population of transient ischemic attack patients, selected by emergency physicians for a rapid ED-based outpatient protocol that included early carotid imaging and treatment when appropriate, the rate of stroke was independent of ABCD2 stratification.

An Assessment of the Incremental Value of the ABCD2 Score in the Emergency Department Evaluation of Transient Ischemic Attack
Ann Emerg Med. 2011 Jan;57(1):46-51

GCS in intubated patients

We use the Glasgow Coma Score to describe conscious level, derived from eye opening, verbal response, and motor response.

One problem is that if your patient is intubated, there can’t be a verbal response. There are some ways round this. Imagine your intubated patient opens eys to a painful stimulus and withdraws his limb from one:

  • Just give him the lowest score (1) for the verbal component – E2M4V1
  • Write ‘V’ (ventilated) or ‘T’ (tube), eg. E2M4VT
  • Make it up, based on what you would expect the V score to be based on the E and M scores.

Weird as it sounds, there is a model for this, demonstrated in the paper abstracted below. The Derived Verbal Score = -0.3756 + Motor Score * (0.5713) + Eye Score * (0.4233).

Don’t worry…if you really want to use this, you don’t have to memorise that equation; there is an online calculator for it here and if you try it you’ll see this patient gets a derived verbal score of 2.3, and therefore a GCS of 7.3! Your decision now whether to round up or down. (In the meantime, I’ve given the patient a V of 1 and called it GCS E2M4VT=7.)

Alternatively, of course, you could try a better validated score that gives more information, the FOUR score, as validated here. The problem is, most people won’t know what you’re talking about.

The conundrum of the Glasgow Coma Scale in intubated patients: a linear regression prediction of the Glasgow verbal score from the Glasgow eye and motor scores.
Meredith W, Rutledge R, Fakhry SM, Emery S, Kromhout-Schiro S.

BACKGROUND: The Glasgow Coma Scale (GCS), which is the foundation of the Trauma Score, Trauma and Injury Severity Score, and the Acute Physiology and Chronic Health Evaluation scoring systems, requires a verbal response. In some series, up to 50% of injured patients must be excluded from analysis because of lack of a verbal component for the GCS. The present study extends previous work evaluating derivation of the verbal score from the eye and motor components of the GCS.

METHODS: Data were obtained from a state trauma registry for 24,565 unintubated patients. The eye and motor scores were used in a previously published regression model to predict the verbal score: Derived Verbal Score = -0.3756 + Motor Score * (0.5713) + Eye Score * (0.4233). The correlation of the actual and derived verbal and GCS scales were assessed. In addition the ability of the actual and derived GCS to predict patient survival in a logistic regression model were analyzed using the PC SAS system for statistical analysis. The predictive power of the actual and the predicted GCS were compared using the area under the receiver operator characteristic curve and Hosmer-Lemeshow goodness-of-fit testing.

RESULTS: A total of 24,085 patients were available for analysis. The mean actual verbal score was 4.4 +/- 1.3 versus a predicted verbal score of 4.3 +/- 1.2 (r = 0.90, p = 0.0001). The actual GCS was 13.6 + 3.5 versus a predicted GCS of 13.7 +/- 3.4 (r = 0.97, p = 0.0001). The results of the comparison of the prediction of survival in patients based on the actual GCS and the derived GCS show that the mean actual GCS was 13.5 + 3.5 versus 13.7 + 3.4 in the regression predicted model. The area under the receiver operator characteristic curve for predicting survival of the two values was similar at 0.868 for the actual GCS compared with 0.850 for the predicted GCS.

CONCLUSIONS: The previously derived method of calculating the verbal score from the eye and motor scores is an excellent predictor of the actual verbal score. Furthermore, the derived GCS performed better than the actual GCS by several measures. The present study confirms previous work that a very accurate GCS can be derived in the absence of the verbal component.

The conundrum of the Glasgow Coma Scale in intubated patients: a linear regression prediction of the Glasgow verbal score from the Glasgow eye and motor scores.
J Trauma. 1998 May;44(5):839-44 (if you have full text access to Journal of Trauma the best bit about this article is the discussion on pages 844-5 in which surgeons wrestle with the meaning of the word ‘conundrum’ and the spelling of ‘Glasgow’).

Hole in the head? Don’t waste the window!

Zampieri and colleagues from Brazil report the use of brain ultrasound in two ICU patients who had had hemicraniectomies.

One of the patients had a subarachnoid haemorrhage with hydrocephalus and an infarct due to vasospasm requiring hemicraniectomy, who subsequently deteriorated with decreasing ventricular catheter drainage, raising suspicion of acute hydrocephalus. Brain ultrasonography confirmed moderate hydrocephalus which was seen to improve after catheter desobstruction.

a Ultrasonography showing moderate hydrocephalus with the catheter tip inside lateral ventricle (white arrow). b Image after catheter cleaning showing the decompressed lateral ventricle

The authors note: ‘standard ultrasonography can be performed through a hemicraniectomy field and may be helpful in a small group of patients. Since decompressive hemicraniectomy is increasingly being used in critical care medicine, bedside evaluation of the brain using the hemicraniectomy as an insonation window could be useful as a noninvasive triage tool and reduce the need for patient transport to the imaging center.’

Use of ultrasonography in hemicraniectomized patients: a report of two cases
Intensive Care Med. 2010 Dec;36(12):2161-2

Not got a hole in the skull? Could try a bony ultrasound window – compare the clear scans above with this scan of an extradural haematoma

Isoflurane in refractory status epilepticus

One infrequently used option for refractory status epilepticus is isoflurane anaesthesia. A report of two cases demonstrates progressive MRI changes suggestive of neurotoxicity, that improved after discontinuation of isoflurane. Impossible to prove cause and effect here, since the both patients had status for weeks and were on multiple anticonvulsant medications, for example lorazepam, fosphenytoin, levetiracetam, valproate, and subsequent infusions of midazolam, pentobarbital, and ketamine. Neither patient recovered beyond a minimally conscious state. This article serves as a reminder that:

  1. Persistent status epilepticus may be associated with a poor neurologic outcome
  2. Some cases are extremely refractory to treatment
  3. Isoflurane is one of many options to try when standard anticonvulsant regimens are failing


Prolonged High-Dose Isoflurane for Refractory Status Epilepticus: Is It Safe?
Anesth Analg. 2010 Dec;111(6):1520-4

RCT of 7.5% saline in head injury

Over a thousand patients in North America with blunt traumatic head injury and coma who did not have hypovolaemic shock were randomised to different fluids pre-hospital. 250 ml Hypertonic (7.5%) saline was compared with normal (0.9%) saline and hypertonic saline dextran (7.5% saline/6% dextran 70). There was no difference in 6-month neurologic outcome or survival.

Out-of-Hospital Hypertonic Resuscitation Following Severe Traumatic Brain Injury
JAMA. 2010;304(13):1455-1464.

Brain tumours in kids

When might you suspect a brain tumour in a child who presents with, say, nausea and vomiting, or behavioural disturbance? A guideline has been produced which might prompt one to think of this important but often delayed diagnosis.

The diagnosis of brain tumours in children: a guideline to assist healthcare professionals in the assessment of children who may have a brain tumour Arch Dis Child. 2010 Jul;95(7):534-9