[Accelerating consult letter time in inpatient psychiatric and psychotherapeutic care]. / Verkürzung der Ubermittlungsdauer von Arztbriefen stationär behandelter Patienten in der Psychiatrie und Psychotherapie.

Consult letters are the main way of relaying information between attending physicians involved in patient treatment at different levels of care and should therefore reach continuing care physicians with minimal delay. The quality assurance project described here was intended to reduce dispatch times for inpatient consult letters at our department of psychiatry and psychotherapy. To accomplish this, different measures were put to work at two levels of intervention. These included standardizing work flow, centralizing and optimizing work distribution in the secretaries' office, enabling faster access to typewritten consult letters by way of central data storage on the clinic's server, sending email notifications to all persons involved, using a central office for signing letters, and prompt monitoring and reporting of consult letter delays. These interventions helped reduce the average delay of dispatching consult letters from 29 days to 11. All in all, the project led to a high degree of workplace satisfaction for all persons involved and should be adaptable to other departments and units without difficulty. In our own department, ward-specific consult letter efficiency has become an important quality indicator.

Risk and predictors of early epileptic seizures in acute cerebral venous and sinus thrombosis.

We assessed the risk and determined predictors of early epileptic seizures (ES) in patients with acute cerebral venous and sinus thrombosis (CVST). A prospective series of 194 consecutive patients with acute CVST admitted to neurological wards in two German university hospitals was analysed for frequency of ES and in-hospital mortality. Demographic, clinical and radiological characteristics during the acute stage were retrospectively analysed for significant association with ES in univariate and multivariate analyses. During the acute stage, 19 patients (9.8%) died. Early symptomatic seizures were found in 86 patients (44.3%). Status epilepticus occurred in 11 patients (12.8%) of whom four died. Amongst patients with epileptic seizures, mortality was three times higher in those with status than in those without (36.4% and 12%, respectively). In multivariate logistic regression analysis, motor deficit [odds ratio (OR) 5.8; 95% CI 2.98-11.42; P < 0.001], intracranial haemorrhage (OR 2.8; 95% CI 1.46-5.56; P = 0.002) and cortical vein thrombosis (OR 2.9; 95% CI 1.43-5.96; P = 0.003) were independent predictors of early epileptic seizures. Status epilepticus was an important source of morbidity and early mortality in patients with CVST in this study. Patients with focal motor deficits, cortical vein thrombosis and intracranial haemorrhage carried the highest risk for ES. Prophylactic antiepileptic treatment may be an option for these patients.

Cerebral venous and sinus thrombosis.

Cerebral venous and sinus thrombosis (CVST) can present with a variety of clinical symptoms ranging from isolated headache to deep coma. Prognosis is better than previously thought and prospective studies have reported an independent survival of more than 80% of patients. Although it may be difficult to predict recovery in an individual patient, clinical presentation on hospital admission and the results of neuroimaging investigations are--apart from the underlying condition--the most important prognostic factors. Comatose patients with intracranial haemorrhage (ICH) on admission brain scan carry the highest risk of a fatal outcome. Available treatment data from controlled trials favour the use of anticoagulation (AC) as the first-line therapy of CVST because it may reduce the risk of a fatal outcome and severe disability and does not promote ICH. A few patients deteriorate despise adequate AC which may warrant the use of more aggressive treatment modalities such as local thrombolysis. The risk of recurrence is low (< 10%) and most relapses occur within the first 12 months. Analogous to patients with extracerebral venous thrombosis, oral AC is usually continued for 3 months after idiopathic CVST and for 6-12 months in patients with inherited or acquired thrombophilia but controlled data proving the benefit of long-term AC in patients with CVST are not available.

Cerebral venous and sinus thrombosis: patients with a fatal outcome during intravenous dose-adjusted heparin treatment.

INTRODUCTION: Although anticoagulation (AC) reduces the risk of a fatal outcome or severe disability in patients with cerebral venous and sinus thrombosis (CVST), prognosis of severe cases is still difficult to predict. The authors studied the clinical course of patients with CVST who died despite AC therapy to look for clinical features that might explain the lethal course of these patients. MATERIALS AND METHODS: Retrospective analysis of a series of 79 consecutive patients with CVST who were treated with a standard regimen of dose-adjusted iv heparin. Case histories of patients with a fatal outcome are presented. RESULTS: The authors identified eight patients with a fatal outcome. All patients were stuporous or comatose at the start of AC, and four patients showed markedly delayed intracranial circulation times, indicating extensive venous thrombosis. Two patients improved, but deteriorated secondarily after reduction or discontinuation of AC. Sufficient activated partial thromboplastin time levels were reached only after a delay in three patients, and critical deterioration occurred in two of them during this time. CONCLUSION: Although inadequate AC may have contributed to the fatal outcome, some patients with extensive venous thrombosis who are stuporous or comatose at the start of AC may carry an increased risk of death, despite heparin therapy. More aggressive treatment approaches, such as endovascular thrombolysis, may be needed for this subgroup of patients with CVST.

Risk of recurrence of cerebral venous and sinus thrombosis during subsequent pregnancy and puerperium.

OBJECTIVE: To assess the risk of recurrence of cerebral venous and sinus thrombosis (CVST) during subsequent pregnancy and puerperium in women with previous cerebral venous occlusive disease. METHODS: The authors retrospectively studied the relapse rate of CVST and the incidence of extracerebral venous thrombosis during subsequent pregnancies in 39 women (from 125 patients with CVST) who suffered a CVST at childbearing age. RESULTS: Mean follow up was 10.25 years (range 1 to 20). Twenty two pregnancies and 19 births were observed in 14 women without evidence of either recurrence of CVST or extracerebral venous thrombosis. One pregnancy occurred during oral anticoagulation and was interrupted and two pregnancies ended with spontaneous abortions. Low dose heparin had been given during five pregnancies. CONCLUSIONS: The risk of recurrence for CVST during pregnancy seems to be low and these data do not justify a negative advice on pregnancy in women with previous CVST. Further studies are needed to evaluate the need for a prophylactic anticoagulation during pregnancy and puerperium.

Heparin treatment in cerebral sinus and venous thrombosis: patients at risk of fatal outcome.

We performed a retrospective analysis of 79 patients with cerebral sinus venous thrombosis, who were treated with a fixed regimen of dose-adjusted intravenous heparin, to determine predictors of a fatal course. The parameters investigated were the state of consciousness and the presence of intracranial haemorrhage (ICH) at the start of heparin treatment, involvement of the internal venous system, mean delay from initial symptom to stupor or coma and from initial symptom to hospital admission, focal neurological deficits, mean intracranial circulation time (ICT) on conventional angiography, and age and sex distribution. Mortality rate was 10% in this series (8/79). There was a strong link between the outcome and the level of vigilance: 53% of the patients with stupor or coma at the start of the heparin therapy died (8/15), whereas all of the 64 patients with no more than mildly impaired vigilance survived (p < 0.00001). Furthermore, mean age and mean ICT were significantly higher in the group of patients who died. There was a statistical trend (p = 0.056) for ICH to be more frequent in cases with fatal outcome, but there was reason to assume that ICH represented an epiphenomenon of a severe course rather than an independent predictor. Other investigated parameters were not linked with a fatal outcome.

[Hereditary thrombophilia with ischemiC stroke and sinus thrombosis. Diagnosis, therapy and meta-analysis]. / Hereditäre Thrombophilien bei ischämischem Schlaganfall und Sinusvenenthrombosen. Diagnostik, Therapie und Meta-Analyse.

Hereditary thrombophilias are a heterogenous group of genetic coagulation disorders which, particularly in combination with acquired prothrombotic factors, induce a predisposition to thrombosis. After characterization of frequent thrombophilic syndromes like factor V-Leiden or the prothrombin 20210GA mutation, a number of case-control studies screened for the prevalence of these mutations in ischemic stroke and cerebral venous thrombosis (CVT). Our meta-analysis shows that factor V-Leiden and prothrombin are frequent and significantly associated with CVT (16.4% vs. 4.9% or 4.3, P < 0.001, and 12.1% vs. 1.9% or 5.8, P < 0.001). In ischemic stroke, only factor V-Leiden and not prothrombin is a weak but significant risk factor (5.9% vs. 2.6% or 1.6, P < 0.001, and 4.1% vs. 3.3% or 1.4, P = 0.1). The C677T homozygous point mutation in the MTHFR, a homocysteine-degrading enzyme, was also associated with arterial stroke (16% vs. 15% or 1.5, P < 0.001). For CVT, sufficient data are lacking. We therefore recommend screening for thrombophilia in CVT. In ischemic stroke, atrial premature complex (APC) resistance should be considered. As long as controlled studies are lacking, individual anticoagulant therapy must take hereditary and precipitating factors into account to assess potential thrombotic risk.

Monitoring of venous hemodynamics in patients with cerebral venous thrombosis by transcranial Doppler ultrasound.

OBJECTIVES: To test the assumption that transcranial Doppler ultrasound (TCD) is able to detect and to monitor intracranial venous blood flow velocities in patients with confirmed cerebral venous thrombosis (CVT). DESIGN: Prospective case study in 18 patients. SETTING: Inpatient neurologic service in a university hospital. SUBJECTS AND METHODS: Serial TCD examinations were performed in 18 consecutive patients with CVT (14 females, 4 males) aged 16 to 64 years (mean+/-SD, 36.8+/-13.1 years) during a mean follow-up ranging from 34 to 783 days (mean+/-SD, 201+/-185 days) between 1993 and 1997. Venous TCD was performed with a 2-MHz range-gated transducer. RESULTS: Venous blood flow velocities were successfully measured in all patients. The highest measured velocities in the monitored intracranial venous vessels ranged from 20 to 150 cm/s (mean+/-SD, 58.9+/-38.8 cm/s), and the lowest were from 9 to 84 cm/s (mean+/-SD, 27.9+/-17.0 cm/s). Fifteen patients (83%) showed a decrease of velocities-2 of them after a transient increase during cessation of heparin therapy. The percentage of velocity decrease ranged from 34% to 73% (mean+/-SD, 56.4%+/-10.9%). A plateau phase, defined as no further decrease in velocities, was reached in these patients within 4 to 314 days (mean+/-SD, 59.9+/-73.7 days). Three patients (17%) showed no changes in velocities as defined by a limit of velocity variation of 30% during the course of CVT. High venous velocities were significantly associated with altered consciousness (P = .001). A nonsignificant relationship was observed with affliction of the superior sagittal sinus. No correlations were noted for onset of disease, initial motor deficits, and presence of bleeding. No predictive value was gained from analyzing the outcome in relation to absolute velocities or their decrease. CONCLUSIONS: Serial TCD studies allow monitoring of venous hemodynamics and collateral pathways in patients with CVT. Normal venous velocities in serial measurements, however, do not exclude a diagnosis of CVT.

Increased rate of factor V Leiden mutation in patients with cerebral venous thrombosis.

We investigated the association between cerebral venous thrombosis and hereditary resistance to activated protein C (APC) in 12 consecutive German patients with non-fatal cerebral venous thrombosis and in 187 controls without a history of thrombotic disorder. Three patients (25%) had a mutation in the factor V Leiden gene against only one subject in the control group. This difference was significant (P < 0.05), with an odds ratio of 11.7 (1.5-87; 95% confidence interval). Two patients carrying the mutation had additional common risk factors for thrombosis, and 2 had a positive family history of thromboembolism. We conclude that inherited APC resistance by a mutation in factor V Leiden is an important risk factor in non-fatal cerebral venous thrombosis. We recommend testing for APC resistance and, if abnormal for factor V Leiden mutation in patients with cerebral venous thrombosis.

Assessment of normal flow velocity in basal cerebral veins. A transcranial doppler ultrasound study.

BACKGROUND AND PURPOSE: Transcranial Doppler ultrasound has not yet been applied systematically to the analysis of the venous system and cerebrovenous disorders. Assessment of the intracranial venous system, however, would contribute to the understanding of cerebral hemodynamics and thus allow new possibilities for clinical application of the Doppler technique. Therefore, we demonstrated the validity of the transcranial Doppler technique in analyzing the basal cerebral veins. METHODS: Venous transcranial Doppler ultrasound was performed with a range-gated 2-MHz transducer in 60 healthy volunteers in patients without central nervous disorders ranging in age from 10 to 71 years (mean +/- SD, 41.9 +/- 15 years). RESULTS: A venous signal away from the probe and adjacent to the posterior cerebral artery, considered to correspond to the basal vein of Rosenthal, was found in all subjects on at least one side. Mean blood flow velocity ranged from 4 to 17 cm/s (mean +/- SD, 10.1 +/- 2.3 cm/s). Analysis for age dependency revealed a trend of decreasing values with increasing age, exclusively caused by a significant reduction of velocity in men aged 40 years or older. No significant intraindividual side-to-side differences were found. A venous signal away from the probe and paralleling the middle cerebral artery, interpreted as corresponding to the deep middle cerebral vein, was found in 21.7% of the subjects with similar velocities. CONCLUSIONS: We have shown that transcranial Doppler methods can also be used for evaluation of the basal cerebral veins in both sexes, in differing age groups, and without major difficulty. The cerebral basal veins could be identified on the basis of their anatomic relation to specific arteries.

Pathophysiological aspects of cerebral sinus venous thrombosis (SVT).

In a series of 102 patients with angiographically proven cerebral sinus venous thrombosis (SVT) significant differences with arterial cerebrovascular disease were noted with respect to disease onset, reversibility of symptoms, occurrence of epileptic seizures and headache, cerebral blood flow under resting and stimulated conditions, occurrence of intracranial bleedings, and response to heparin therapy. From these findings pathophysiological differences are hypothesized: Whereas arterial cerebral ischemia usually is a monophasic abrupt thrombotic process and there is only a small penumbra, SVT is a continuing process of disequilibrium between prothrombotic and thrombolytic mechanisms; large areas of the brain are only functionally or metabolically disturbed but not irreversibly damaged. Intracranial bleeding in SVT is a consequence of increased venous and capillary pressure and thus occurs more frequently than in arterial thrombotic disease in which capillary pressure is reduced by the thrombosis and bleeding occurs during reperfusion of tissue damaged by ischemia. Heparin treatment in SVT is effective since it shifts the equilibrium away from the prothrombotic side and is able to save large areas of brain tissue that are only reversibly damaged. It improves venous outflow and thus decreases the risk of intracranial hemorrhage, in contrast with the arterial thrombotic disease where heparin increases the risk or at least the severity of intracranial bleedings.

Heparin treatment in sinus venous thrombosis.

Treatment of sinus venous thrombosis (SVT) is controversial. Although heparin has been used for this condition, many investigators have opposed its use because of the frequent occurrence of intracranial haemorrhage (ICH) and SVT. Therefore we have evaluated anticoagulation with adjusted-dose intravenous heparin for treatment of aseptic SVT in a randomised, blinded (patient and observer), placebo-controlled study in 20 patients (10 heparin, 10 placebo). The clinical course of the two groups, as judged by a newly designed SVT-severity scale, started to differ in favour of the heparin group after 3 days of treatment (p less than 0.05, Mann-Whitney U-test) and the difference remained significant (p less than 0.01) after 8 days of treatment. After 3 months, 8 of the heparin-treated patients had a complete clinical recovery and 2 had slight residual neurological deficits. In the placebo group, only 1 patient had a complete recovery, 6 patients had neurological deficits, and 3 patients died (p less than 0.01, modified Fisher's exact test). An additional retrospective study on the relation between heparin treatment and ICH in SVT patients was based on 102 patients, 43 of whom had an ICH. 27 of these patients were treated with dose-adjusted, intravenous heparin after the ICH. Of these 27 patients, 4 died (mortality 15%), and 14 patients completely recovered. Of the 13 patients that did not receive heparin after ICH, 9 died (mortality 69%) and only 3 patients completely recovered. We conclude that anticoagulation with dose-adjusted intravenous heparin is an effective treatment in patients with SVT and that ICH is not a contraindication to heparin treatment in these patients.