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Biomedical subjects

M Vermeulen

Publications and source records attributed to M Vermeulen.

At least 199 records · Page 11Linked to original sources
PubMed1985

Plasma and gamma-globulin infusion in chronic inflammatory polyneuropathy.

We treated 17 patients with chronic inflammatory polyneuropathy (CIP) with infusions of fresh-frozen plasma (FFP). Thirteen patients had a beneficial response: 12 improved considerably and one moderately. The first signs of improvement were seen within 8 days of the onset of treatment. None of these patients had had spontaneous remissions for 2 months prior to treatment, and none had received immunosuppressive medication during the plasma infusions. The treatment effect was short-lasting in 9 patients. Re-institution of the FFP infusions was always followed by improvement. The same effect could be achieved by intravenous gamma-globulin. We conclude that infusions with FFP, of which the IgG fraction is the effective part, may induce a rapid and clinically important improvement in patients with CIP.

Adolescent↗
PubMed1985

Perimesencephalic hemorrhage: a nonaneurysmal and benign form of subarachnoid hemorrhage.

We studied 28 patients with subarachnoid hemorrhage and normal angiograms. On early CT (within 5 days) in 13 cases, blood was seen mainly or only in the cisterns around the midbrain. This pattern of hemorrhage was found in only 1 of 92 patients with a ruptured aneurysm. None of the unexplained perimesencephalic hemorrhages was associated with intracerebral hematoma or intraventricular hemorrhage. The clinical features also differed from those of aneurysmal hemorrhage; loss of consciousness was rare, and after 3 months, all 13 patients had returned to normal life. The cause of this benign disorder remains elusive, but a venous or capillary source seems likely.

Humans↗
PubMed1985

Acute hydrocephalus after aneurysmal subarachnoid hemorrhage.

Hydrocephalus, defined as a bicaudate index above the 95th percentile for age, was found in 34 (20%) of 174 prospectively studied patients with subarachnoid hemorrhage (SAH) who survived the first 24 hours and who underwent computerized tomography (CT) scanning within 72 hours. The occurrence of acute hydrocephalus was related to the presence of intraventricular blood, and not to the extent of cisternal hemorrhage. The level of consciousness was depressed in 30 of the 34 patients. Characteristic clinical features were present in 19 patients, including a gradual obtundation after the initial hemorrhage in 16 patients and small nonreactive pupils in nine patients (all with a Glasgow Coma Scale score of 7 or less). In the remaining 15 patients (44%), the diagnosis could be made only by CT scanning. After 1 month, 20 of the 34 patients had died: six from rebleeding (four after shunting), 11 from cerebral infarction (eight after an initial improvement), and three from other or mixed causes. Only one of nine patients in whom a shunt was placed survived, despite rapid improvement in all immediately after shunting. The mortality rate among patients with acute hydrocephalus was significantly higher than in those without, with the higher incidence caused by cerebral infarction (11 of 34 versus 12 of 140 cases, respectively; p less than 0.001). Death from infarction could not be attributed to the extent of cisternal hemorrhage, the use of antifibrinolytic drugs, or failure to apply surgical drainage, but could often be explained by the development of hyponatremia, probably accompanied by hypovolemia.

Acute Disease↗
PubMed1985

Source of fibrin/fibrinogen degradation products in the CSF after subarachnoid hemorrhage.

In 48 patients with a subarachnoid hemorrhage, levels of fibrin/fibrinogen degradation products (FDP's), total protein, and plasminogen were measured in the cerebrospinal fluid (CSF) between Days 9 and 15 after the bleed. Of these 48 patients, 22 received tranexamic acid. Despite a significant reduction in the incidence of rebleeding in patients taking tranexamic acid, no difference in FDP levels was found between patients receiving tranexamic acid and a control group of patients who were not; nor was any relationship evident between FDP levels and rebleeding. In patients with detectable levels of FDP's, CSF protein and plasminogen values were also increased, and FDP's were found more frequently in the CSF of patients with an impaired level of consciousness or with a neurological deficit. These findings suggest that in the 2nd week after subarachnoid hemorrhage, the presence of FDP's in the CSF reflects a damaged blood-CSF barrier rather than ongoing local fibrinolysis in the subarachnoid space. A finding of FDP's in the CSF is, therefore, an unreliable monitor of antifibrinolytic treatment in subarachnoid hemorrhage and cannot be used for selecting patients at high risk of rebleeding.

Blood Physiological Phenomena↗
PubMed1984

Antifibrinolytic treatment in subarachnoid hemorrhage.

We enrolled 479 patients with subarachnoid hemorrhage in a multicenter, randomized, double-blind, placebo-controlled trial to determine whether treatment with the antifibrinolytic agent tranexamic acid improves outcome by preventing rebleeding. At three months there was no statistical difference between the outcomes in the tranexamic acid group and the control group. Of the 173 patients who died, 84 had received tranexamic acid and 89 placebo (95 per cent confidence interval for the difference in mortality rate, -6 to 11 per cent). Similarly, when analysis was restricted to patients with an angiographically demonstrated aneurysm, there was no significant difference between the groups. This absence of effect was not due to a lack of antifibrinolytic action, since the rate of rebleeding was reduced from 24 per cent in the control group to 9 per cent in the tranexamic acid-treated group (chi-square = 18.07, P less than 0.001), but resulted from a concurrent increase in the incidence of ischemic complications (15 per cent in the control group and 24 per cent in the tranexamic acid group; chi-square = 8.07, P less than 0.01). We conclude that until some method can be found to minimize ischemic complications, tranexamic acid is of no benefit in patients with subarachnoid hemorrhage.

Cerebral Angiography↗
PubMed1984

Respiratory arrest in subarachnoid hemorrhage.

Sudden loss of consciousness and cardiorespiratory disorders occurred in 43 of 254 patients with subarachnoid hemorrhage. Two patients had ventricular fibrillation, 37 had one or more episodes with a disturbance of respiratory rhythm that required assisted ventilation, and 4 died suddenly without recorded vital signs. Sixteen patients recovered after resuscitation. The outcome could not be predicted at an early stage from the anatomic type of hemorrhage on CT, the initial presence or absence of brainstem reflexes, or the type of cardiorespiratory disorder. Spontaneous respiration and responsiveness returned within 1 hour in all patients who recovered.

Arrhythmias, Cardiac↗
PubMed1984

Causes of acute deterioration in patients with a ruptured intracranial aneurysm. A prospective study with serial CT scanning.

The authors studied the acute neurological deterioration in 150 patients with aneurysmal hemorrhage. These patients were closely observed for a 4-week period or until death or operation. Forty-six patients suffered a total of 62 episodes of deterioration that developed within 5 minutes after aneurysm rupture; 59 of these episodes consisted of severe impairment of consciousness. Computerized tomography (CT) was performed within a few hours of the event. Serial scans were obtained at least weekly after admission. Rebleeding was diagnosed as the cause of 42 episodes (68%), including six patients who died rapidly without a repeat CT scan. The final diagnosis of the cause in other acute episodes was epilepsy (in six), acute onset of ischemia (in three), and ventricular fibrillation (in one). Ten unexplained events occurred in nine patients. Rebleeding could be excluded with confidence in nine of these events, because the residual clots had disappeared or markedly decreased on CT. It is concluded that a purely clinical diagnosis of rebleeding will be incorrect in about every third patient, even if these patients are under close observation.

Cerebral Hemorrhage↗
PubMed1983

Ataxic tetraparesis from lacunar infarction in the pons.

A 45-year-old woman with hypertension suffered four episodes of right hemiparesis and two attacks of left hemiparesis, within seven months. On examination she showed weakness and cerebellar ataxia of all four limbs. Computed tomography demonstrated a radiolucent area in the base of the pons, consistent with lacunar infarction.

Cerebellar Ataxia↗
PubMed1983

Spectrophotometric analysis of CSF after subarachnoid hemorrhage: limitations in the diagnosis of rebleeding.

We studied the course of CSF xanthochromia after subarachnoid hemorrhage by serial spectrophotometric analysis of lumbar CSF in 15 patients without clinical or CT evidence of rebleeding. The xanthochromic index rose in some patients up to the seventeenth day, and the proportion of oxyhemoglobin or the absolute concentration of hemoglobin often fluctuated. Therefore, rebleeding can be demonstrated in lumbar CSF only by increased xanthochromia, if previous samples had shown a decrease. These criteria could be applied in only 6 of 17 consecutive patients with rebleeding as demonstrated by CT, and they were met in 5.

Bilirubin↗
PubMedDate not supplied

On the mechanism of high-dose intravenous immunoglobulin treatment of patients with chronic inflammatory demyelinating polyneuropathy.

A proportion of patients with a chronic inflammatory demyelinating polyneuropathy (CIDP) improves after polyvalent intravenous immunoglobulin (IVIg) treatment. When anti-neuroblastoma cell line (NBL) antibodies are present, they decrease or disappear after IVIg treatment. Purified IgM anti-NBL antibodies from a CIDP patient were inhibited by F(ab')2 of IVIg and by F(ab')2 of a patient recovered from Guillain-Barré syndrome (GBS). Inhibition of anti-NBL antibodies was also found among sera from normal individuals. This suggests that the self-limiting character of GBS and the therapeutic effect of IVIg in CIDP are dependent on suppression of auto-antibodies. This suppression may be mediated by anti-idiotypes present in recovered GBS patients and in the normal donor population contributing to IVIg.

Adolescent↗
PubMedDate not supplied

Long-term survival and vascular event risk after transient ischaemic attack or minor ischaemic stroke: a cohort study.

BACKGROUND: Determinants of survival and of risk of vascular events after transient ischaemic attack (TIA) or minor ischaemic stroke are not well defined in the long term. We aimed to restudy these risks in a prospective cohort of patients after TIA or minor ischaemic stroke (Rankin grade< or =3), after 10 years or more. METHODS: We assessed the survival status and occurrence of vascular events in 2473 participants of the Dutch TIA Trial (recruitment in 1986-89; arterial cause of cerebral ischaemia). We included 24 hospitals in the Netherlands that recruited at least 50 patients. Primary outcomes were all-cause mortality and the composite event of death from all vascular causes, non-fatal stroke, and non-fatal myocardial infarction. We assessed cumulative risks by Kaplan-Meier analysis and prognostic factors with Cox univariate and multivariate analysis. FINDINGS: Follow-up was complete in 2447 (99%) patients. After a mean follow-up of 10.1 years, 1489 (60%) patients had died and 1336 (54%) had had at least one vascular event. 10-year risk of death was 42.7% (95% CI 40.8-44.7). Age and sex-adjusted hazard ratios were 3.33 (2.97-3.73) for age over 65 years, 2.10 (1.79-2.48) for diabetes, 1.77 (1.45-2.15) for claudication, 1.94 (1.42-2.65) for previous peripheral vascular surgery, and 1.50 (1.31-1.71) for pathological Q waves on baseline electrocardiogram. 10-year risk of a vascular event was 44.1% (42.0-46.1). After falling in the first 3 years, yearly risk of a vascular event increased over time. Predictive factors for risk of vascular events were similar to those for risk of death. INTERPRETATION: Long-term secondary prevention in patients with cerebral ischaemia still has room for further improvement.

Aged↗
PubMedDate not supplied

Conversion rates for prehospital paroxysmal supraventricular tachycardia (PSVT) with the addition of adenosine: a before-and-after trial.

OBJECTIVE: To determine whether the prehospital administration of adenosine to adults with stable and unstable paroxysmal supraventricular tachycardia (PSVT) influences conversion rate (CR) to sinus rhythm, scene time, use of synchronized electrical cardioversion (SEC), and accuracy of rhythm strip interpretation by paramedics. METHODS: This before-and-after study compared a retrospective control group (CG) prior to the introduction of adenosine with a prospective treatment group (TG) following the addition of adenosine to the PSVT treatment protocol in a large urban advanced life support emergency medical services system. The population represented patients > or = 18 years of age with PSVT diagnosed by the paramedic (defined as spontaneous onset of a regular narrow-complex tachycardia between 140 and 250 beats/minute). RESULTS: The CG comprised 74 calls and the TG 137 calls. The overall CR was higher in the TG (59% vs 32%, p < 0.001). The SEC and spontaneous conversion rates remained unchanged. The proportion of untreated patients with PSVT decreased from 26% CG to 12% TG (p < 0.01). Scene times were longer in the TG (26 vs 19 minutes, p < 0.001). Agreement between paramedic and physician rhythm strip interpretations was fair to moderate (CG kappa 0.43 [95% CI: 0.14, 0.72]; TG kappa 0.37 [95% CI: 0.13, 0.61]). CONCLUSIONS: The introduction of adenosine was associated with a significant increase in the prehospital CR of stable and unstable PSVT, while the SEC and spontaneous conversion rates were similar in each group; however, scene times were longer in the TG and paramedic accuracy in rhythm strip interpretation remained fair to moderate.

Adenosine↗