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Biomedical subjects

B A Hansen

Publications and source records attributed to B A Hansen.

At least 37 records · Page 2Linked to original sources
PubMed1997

Haemodynamic changes after high-volume plasmapheresis in patients with chronic and acute liver failure.

OBJECTIVE: To evaluate the haemodynamic changes during treatment with high-volume plasmapheresis in patients with chronic liver failure compared to patients with acute liver failure. METHODS: Haemodynamic measurements were performed with a Swan-Ganz catheter and thermodilution technique. High-volume plasmapheresis (mean plasma exchange of 8.6 litres) was performed in 11 patients with chronic and 16 patients with acute liver failure. RESULTS: In patients with chronic liver failure, systemic vascular resistance index was unaltered: 1193 +/- 494 dynscm-5m2 before treatment versus 1180 +/- 399 dynscm-5m2 after. Mean arterial pressure increased from 69 +/- 11 mmHg to 78 +/- 13 mmHg (P < 0.05) and cardiac output increased from 8.1 +/- 2.4 l/min to 8.9 +/- 2.4 l/min (P < 0.05) during high-volume plasmapheresis. In patients with acute liver failure, systemic vascular resistance index increased from 1154 +/- 628 dynscm-5m2 to 1614 +/- 738 dynscm-5m2 (P < 0.001). In this group mean arterial pressure increased from 78 +/- 16 mmHg to 95 +/- 10 mmHg (P < 0.001) and cardiac output decreased from 9.6 +/- 3.7 l/min to 8.2 +/- 2.9 l/min (P < 0.01). CONCLUSION: The hyperkinetic circulation in chronic and acute patients was differently affected by high-volume plasmapheresis. We suggest that in chronic liver failure both portosystemic shunting and chronic peripheral vasodilation may contribute to the hyperkinetic syndrome, whereas in acute liver failure a humoral factor which can be removed by high-volume plasmapheresis is a main contributor.

Acute Disease↗
PubMed1996

Preservation of cerebral oxidative metabolism in fulminant hepatic failure: an autoregulation study.

Under normal conditions cerebral blood flow (CBF) is regulated to secure oxidative brain metabolism, but in patients with fulminant hepatic failure (FHF), insufficient CBF has been suggested to precede cerebral edema and intracranial hypertension. In order to determine if insufficient CBF and hypoxia are present in patients with FHF we increased the mean arterial pressure and measured cerebral metabolism. In six patients with FHF CBF determined by 133Xenon injection technique, transcranial Doppler mean flow velocity in the middle cerebral artery (Vmean) and cerebral metabolism were determined, before and after an increase in mean arterial pressure by norepinephrine infusion. Mean arterial pressure was measured in a radial artery, and blood samples from the radial artery and internal jugular vein allowed calculation of the cerebral arteriovenous oxygen (AVDO2), -glucose (AVDgl), and -lactate (AVDlac) differences. Cerebral metabolic rates (CMRO2,-gl,-lac) were calculated as AVDO2,-gl,-lac times CBF. Mean arterial pressure was raised from 70 (54-105) to 111 (93-128) mm Hg during intravenous infusion of norepinephrine. CBF increased from 34 (12-55) to 47 (27-81) mL . 100g-1. min-1 (p < 0.05) and Vmean from 53 (42-60) to 67 (61-79) cm.s-1 (p < 0.05), whereas CMRO2 (1.4 (0.9-2.4) mL . 100g-1 . min-1), CMRgl (11 (4.8-20) mumol 100g-1 . min-1), and CMRlac (3.2 (0-8.9) mumol . 100g-1 . min-1) remained unchanged. Our finding indicates that cerebral oxidative metabolism is preserved in patients with FHF. Cerebral autoregulation is absent, however, and neuroprotective critical care is suggested to be guided by internal jugular vein oxygen saturation to secure appropriate cerebral oxygenation.

Adolescent↗
PubMed1996

Interictal SPECT of rCBF is of clinical utility in the preoperative evaluation of patients with partial epilepsy.

Fifty-eight patients with drug-resistant partial epilepsy were studied preoperatively by interictal rCBF measurements using 99mTc-HMPAO and a dedicated brain SPECT camera (Tomomatic 64). Follow-up of seizure outcome, using the "Engel score", was at least 3 years. The data were analyzed in a blinded set-up, first visually and subsequently quantitatively by an automatic regional analysis. By visual analysis 95% of the patients were considered abnormal in one part of the brain, of whom 27% were abnormal on CT, 45% on MRI and 98% on scalp EEG. Using a quantitative regional analysis subdividing each hemisphere into 17 larger regions, 85% of the patients had an abnormal rCBF compared to an age-matched control population of healthy volunteers (using the Wilcoxon 2-sample test with Bonferroni's correction). The average number of abnormal regions of interest was 4.7. The percentage of patients with abnormal SPECT-CBF or the total number of abnormal regions of interest (ROIs) per patient showed no correlation to duration of epilepsy or seizure load (number of seizures per year x epilepsy duration) or seizure type. Neither were the rCBF changes prognostic for the outcome as measured by the Engel score. In 20 patients ictal SPECT of rCBF was additionally performed. In 2 cases it added further information to the patient evaluation.

Adolescent↗
PubMed1996

Cerebral blood flow, oxygen metabolism and transcranial Doppler sonography during high-volume plasmapheresis in fulminant hepatic failure.

OBJECTIVE: The effect of high-volume plasmapheresis on hepatic encephalopathy, cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) was investigated in patients with fulminant hepatic failure (FHF). METHODS: Twelve consecutive patients (8 women, 4 men, median age 34 years (range 19-51), were studied before and after high-volume plasmapheresis with 10-16 litres fresh frozen plasma, while PaCO2 and body temperature were maintained at 30 (23-34) mmHg and 37.6 degrees C (36.6-38.4), respectively. Blood samples from the internal jugular vein and a radial artery allowed calculation of the cerebral arteriovenous oxygen difference (AVDO2) and oxygen extraction (AVDO2 divided by arterial oxygen content). CBF was determined by a xenon-133 clearance method in eight patients and CMRO2 calculated as AVDO2 times CBF. Cerebral perfusion pressure (CPP) was determined as the difference between mean arterial and subdural pressures in eight patients. RESULTS: High-volume plasmapheresis was initiated 22 (6-168) h after the development of hepatic encephalopathy and 11 patients had grade 4 encephalopathy. Following high-volume plasmapheresis the grade of encephalopathy improved in four patients. The CBF increased from a median of 31 (16-86) to 45 (18-97) ml/100 g/min and as oxygen extraction remained unchanged (32 (9-41) vs. 29 (7-39)%), CMRO2 increased from 1.24 (0.96-1.82) to 1.86 (1.00-2.07) ml/100 g/min (P < 0.05). The CPP increased from 62 (19-76) to 92 (50-105) mmHg (P < 0.01), whereas the intracranial pressure remained unchanged (19 (3-45) vs. 11 (5-33) mmHg). No statistical difference was found between the relative changes in the above parameters in survivors compared to non-survivors. CONCLUSION: Although the clinical status did not improve in all patients, both CBF and CMRO2 increased after high-volume plasmapheresis. The alleviation of brain oxygen metabolism by high-volume plasmapheresis may reflect partial removal of neuroinhibitory plasma factors.

Adult↗
PubMed1995

[Paracetamol poisoning at a department of hepatology].

In this retrospective study we evaluated the frequency of complications in 108 patients with acetaminophen poisoning admitted to the Department of Hepatology, Rigshospitalet, Copenhagen from 1.10.1990-30.9.1993. Twenty-five patients (23%) developed hepatic encephalopathy grade II-IV, with a survival rate of 44%. In patients who developed grade IV encephalopathy the median time from intoxication to INR > 3.7 was 60 hours. At a median of only five hours later grade II encephalopathy was present, and grade IV at a median of a further 20 hours later. Ninety-three patients were re-evaluated according to the nomogram indicated by Prescott (6). If the initial position was in the "very severe" area the risk of developing encephalopathy was 34% (20-51%), if not the risk was 6% (1-16%). Serum creatinine above 200 microM at admission indicated a risk of hepatic encephalopathy of 64% (35-87%). INR > 1.54 was associated with a 35% risk of hepatic encephalopathy. Patients in the "very severe" area should be referred to a unit where liver transplantation is possible, even if other factors known to indicate poor prognosis are not present.

Acetaminophen↗
PubMed1995

[Fulminant liver failure before and after introduction of liver transplantation at Rikshospitalet].

The impact of liver transplantation on the survival in fulminant hepatic failure was evaluated in a retrospective study including 87 patients admitted to Rigshospitalet over a three and a half year period before and a three and a half year period after the Danish liver transplantation programme was started. The number of admissions increased by 178% in the second period. Fifty-two percent of the patients had acetaminophen induced liver failure, which over the last seven years has become the most common cause of severe acute liver disease in Denmark. In about half of the patients high volume plasmapheresis was used as liver-assist either alone or in combination with liver transplantation. Three patients in grade 4 hepatic coma (one with Hepatitis B, two with acetaminophen intoxication) were withdrawn from the waiting list for emergency liver transplantation after high volume plasmapheresis due to recovery. In patients with an estimated survival chance of less than 5-10% liver transplantation was performed with a survival rate of 60%. The survival rate for the non-liver transplanted patients was 49% in the same period compared to 30% in the three and a half year period before liver transplantation started.

Acetaminophen↗
PubMed1995

Functional loss of cerebral blood flow autoregulation in patients with fulminant hepatic failure.

In management of patients with fulminant hepatic failure, it is recommended that mean arterial pressure should be raised if cerebral perfusion pressure is lower than 50 mmHg, but the influence of such therapy on cerebral blood flow is unknown. We examined cerebral blood flow autoregulation in seven consecutive patients with fulminant hepatic failure during treatment of imminent insufficient cerebral perfusion pressure. Cerebral perfusion was evaluated by transcranial Doppler assessed mean flow velocity in the middle cerebral artery and by the arterio-venous difference for oxygen. Intracranial pressure was recorded by a subdural transducer and cerebral perfusion pressure calculated as the difference between mean arterial pressure and intracranial pressure. After 20 (range 10 to 43) min, mean arterial pressure was raised from 74 (43-80) to 94 (76-114) mmHg by i.v. noradrenaline, cerebral perfusion pressure increased from 49 (26-75) to 82 (50-108) mmHg (p < 0.01) as the intracranial pressure remained unchanged at 26 (3-35) mmHg. The mean flow veolocity increased from 68 (30-134) to 108 (48-168) cm s-1 and the arterio-venous difference for oxygen by 46 (10-82)% (p < 0.05). Both mean flow velocity (r = 0.63) and arterio-venous difference for oxygen (r = 0.71) were correlated to mean arterial pressure (p < 0.001), and a lower blood pressure limit of autoregulation could not be identified in any of the patients. These data suggest that the cerebral blood flow is not autoregulated in patients with fulminant hepatic failure and therefore cerebral blood flow should be "clamped" within the normal physiologic range by manipulation of arterial blood pressure in order to avoid cerebral hypoxia and/or hypertensive induced cerebral oedema.

Acute Disease↗
PubMed1995

Cerebral blood flow autoregulation and transcranial Doppler sonography in patients with cirrhosis.

Impairment of cerebral blood flow (CBF) autoregulation may have serious implications for patients with cirrhosis if arterial hypotension occurs during coma, anesthesia, bleeding, or sepsis. In this study, CBF autoregulation was investigated in patients with cirrhosis with no or mild encephalopathy. Ten patients (median age, 45 years; range, 30 to 61 years) and six healthy volunteers (median age, 30 years; range 21 to 61 years) were included. Catheters were placed in a radial artery and in the internal jugular veins. Baseline CBF was measured using single-photon emission computed tomography (SPECT) with concomitant measurements of cerebral arteriovenous oxygen content differences (AVDO2). CBF autoregulation was evaluated using the AVDO2 method and changes in mean flow velocity in the middle cerebral artery (Vmean) as determined by transcranial Doppler (TCD). Mean arterial pressure (MAP) was increased by 30 mm Hg by intravenous norepinephrine, and subsequently decreased by a combination of lower body negative pressure and ganglion blockade, whereas AVDO2 and Vmean were measured at each 5 mm Hg change in MAP. CBF was 61 (range, 45 to 78) mL 100 g-1 min-1 in patients with cirrhosis and 65 (range < 53 to 88) mL 100 g-1 min-1 in volunteers (not significant [NS]). There were no regional differences in CBF between the two groups. Arterial carbon dioxide tension was 31 (23 to 35) mm Hg in patients with cirrhosis and lower, compared with 36 (range, 34 to 47) mm Hg in the volunteers (P < .01). For evaluation of autoregulation, MAP was raised to 116 (range, 100 to 145) and then decreased to 39 (range, 34 to 50) mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Systemic vascular resistance during high-volume plasmapheresis in patients with fulminant hepatic failure: relationship with oxygen consumption.

BACKGROUND: In patients with fulminant hepatic failure, systemic vascular resistance and blood pressure are often reduced. OBJECTIVE: To determine whether systemic vascular resistance increases during high-volume plasmapheresis, which is assumed to eliminate endogenous vasodilatory substances from the bloodstream. DESIGN: A prospective study. PATIENTS AND METHODS: Ten patients [median age 48 (range 21-53) years] were admitted for liver transplantation. Systemic haemodynamic variables were determined using a catheter in a radial artery and a thermodilution catheter placed in a pulmonary artery. Ten (range 8-15) litres of fresh frozen plasma were exchanged, while body temperature [37.6 (range 36.6-38.4) degrees C], blood partial pressure of carbon dioxide [3.75 (range 3.30-4.50) kPa] and peak inspiratory ventilatory pressure [24 (range 20-26) mmHg] were kept constant. RESULTS: Mean arterial pressure increased from 74 (range 61-110) to 96 (range 68-103) mmHg and cardiac index decreased from 5.2 (range 3.6-7.5) to 4.2 (range 3.4-6.6) l/min/m2. The systemic vascular resistance index increased from 662 (range 430-1270) to 1060 (range 621-1520) dyn s/cm5/m2. In contrast, the pulmonary vascular resistance index [42 (range 20-110) dyn s/cm5/m2) remained constant. As cardiac index decreased, oxygen delivery decreased from 939 (range 680-1496) to 745 (range 601-1189) ml/min/m2 with no effect on oxygen consumption [171 (87-231) ml/min/m2], as the arteriovenous oxygen extraction ratio increased from 17 (range 9-22) to 25 (range 8-31)% (P < 0.02). CONCLUSION: In patients with fulminant hepatic failure, cardiac output, systemic vascular resistance and arterial blood pressure improved during high-volume plasmapheresis.

Acute Disease↗