[The effect of needle type and immobilization on postspinal headache]. / Die Bedeutung von Nadeltyp und Immobilisation für den postspinalen Kopfschmerz.

UNLABELLED: Post-dural puncture headache (PDPH) is a significant complication of spinal anaesthesia. Diameter and tip of the needle as well as the patient's age have been proven to be important determinants. The question of whether post-operative recumbency can reduce the risk of PDPH has not been answered uniformly. And besides, some studies referring to this subject reveal methodical failures, for example, as to clear definition and exact documentation of post-operative immobilization. Furthermore, fine-gauge needles (26G or more) have not been investigated yet. The first aim of our study was therefore to examine the role of recumbency in the prevention of PDPH under controlled conditions using thin needles. Secondly, we wanted to confirm the reported prophylactic effect of needles with a modified, atraumatic tip (Whitacre and Atraucan) by comparing them to Quincke needles of identical diameter. Most of the former investigators compared Quincke with atraumatic needles of different size regardless of the known influence of the diameter on PDPH. PATIENTS AND METHODS: In a prospective study we included 481 consecutive patients undergoing a total of 500 orthopaedic operations under spinal anaesthesia. The latter was performed in a standardized manner (patient sitting, midline approach, needle with parallel bevel direction), using four different needles allocated randomly (26-gauge and 27-gauge needles with Quincke tip, 26-gauge Atraucan and 27-gauge Whitacre cannula). Half of the patients were instructed to stay in bed for 24 h (horizontal position without raising head), the others to get up as early as possible. An anaesthesiologist visited the patients on the fourth postoperative day or later and questioned them about headache and duration of recumbency. Additionally, the patients had to fill out a questionnaire 1 week after surgery. Any postural headache was considered as PDPH. RESULTS: The four groups of different needles had homogeneous demographic characteristics (see Table 1). A total of 47 patients (9.4%) developed PDPH. The incidence was highest after puncture with a 26-gauge Quincke cannula (17.6%) with a significant difference compared to the other needles (see Table 2). PDPH incidence correlated well with increasing age and number of dural punctures, but showed no relation to sex, patient's history of headache or experience of the anaesthesiologist. Only about half of the patients (60.5%) followed the instructions regarding mobilization or recumbency. The duration of strict bed rest did not influence the development of PDPH: The overall incidence was 9.4% in the recumbency group and 8.8% in the group of early ambulation. In all, 45 patients suffered from ordinary not posture-related headache. CONCLUSIONS: The significantly higher incidence of PDPH after spinal anaesthesia with 26-gauge Quincke needles compared to the 27-gauge Quincke and the 26-gauge Atraucan group confirmed the importance of both needle diameter and design of its tip. The Atraucan cannula has not been examined in a controlled study (in comparison with Quincke needle of the same diameter) before. In accordance with other investigators we found patient's age and number of puncture attempts as additional predictors of PDPH. Consequent bed rest, however, was not able to reduce its incidence. Our studies reveal the poor compliance of patients with regard to mobilization/immobilization, a problem which possibly has not been considered enough in former studies examining the influence of bed rest on PDPH. Based on the literature and the present findings, we recommend using thin needles with atraumatic tips for spinal anaesthesia if possible. Recumbency presents an avoidable stress for patients as well as medical staff and should no longer be ordered.

Continuous i.v. administration of the angiotensin-converting enzyme inhibitor enalaprilat in the critically ill: effects on regulators of circulatory homeostasis.

Several components are responsible for circulatory control at the central, regional, and microcirculatory level. Angiotensin-converting enzyme (ACE) inhibitors are known to act beneficially on circulation by various mechanisms. The influence of continuous i.v. administration of the ACE inhibitor enalaprilat on regulators of circulation was studied in 45 critically ill patients. According to a prospective randomized sequence, either 0.25 mg/h (group 1, n = 15) or 0.5 mg/h (group 2, n = 15) of enalaprilat or saline solution as placebo (control group, n = 15) were continuously given. Infusion was started on the day of admission to the intensive care unit (ICU) and continued for the next 5 days. From arterial blood samples, plasma levels of endothelin-1 (ET), atrial natriuretic peptide (ANP), renin, vasopressin, angiotensin-II, and catecholamines (epinephrine, norepinephrine) were measured. All measurements were carried out before infusion (= baseline values) and during the next 5 days. In both enalaprilat groups, mean arterial blood pressure (MAP) decreased similarly; heart rate (HR) and central venous pressure (CVP) did not change, and were without differences in comparison to the untreated control. Except for ET, plasma levels of all vasoactive substances exceeded normal range at baseline. Angiotensin-II plasma concentrations significantly decreased during enalaprilat infusion (0.25 mg/h: from 53.1 +/- 11.3 to 22.1 +/- 9.3 pg/ml; 0.50 mg/h: 62.1 +/- 14.4 to 17.9 +/- 7.9 pg/ml), but they remained significantly elevated in the untreated control patients. Vasopressin plasma level increased only in the control group (p < 0.01) and decreased in the patients in whom 0.50 mg/h of enalaprilat was infused.(ABSTRACT TRUNCATED AT 250 WORDS)

Do plasma levels of circulating soluble adhesion molecules differ between surviving and nonsurviving critically ill patients?

Adhesion molecules appear to play a central role in tissue damage secondary to inflammatory response. Besides various neutrophil- and endothelial-bound adhesion molecules, soluble forms of endothelial-derived adhesion molecules have been detected in the circulating blood in recent years. They seem to be good markers of endothelial damage, but their importance in the critically ill has not been definitely elucidated yet. Plasma levels of circulating (soluble) adhesion molecules (endothelial leucocyte adhesion molecules [sELAM-1], vascular cell adhesion molecule 1 [sVCAM-1], intercellular adhesion molecule 1 [sICAM-1]) were serially measured from arterial blood samples using enzyme-linked immunosorbent assays (ELISA) in 50 consecutive patients suffering from severe trauma (injury severity score [ISS] > 25 points) or postoperative complications. Measurements were carried out on the day of admission on the intensive care unit (ICU) ("baseline" value) and during the next 5 days. Survival was defined as survival throughout the study period. The survivor group (n = 30) consisted of more patients who had sustained trauma (53%), whereas in the nonsurvivors (n = 20) more patients with postoperative complications were found (65%). On admission to ICU, septic shock was more often seen in the nonsurvivors (30%) than in the survivors (13%) and the nonsurvivors showed a slightly higher APACHE II score at baseline. At baseline, plasma levels of all three adhesion molecules were elevated beyond normal range in both groups. The sICAM-1 and sELAM-1 plasma concentrations were significantly higher in the nonsurvivors than in the survivors already at baseline. The sELAM-1 and sICAM-1 values significantly decreased in the survivors without reaching normal values. At the end of the investigation period, sVCAM-1 plasma level was within normal range in the survivors. In the nonsurvivors, all three adhesion molecules increased significantly throughout the study period (sELAM-1, from 115 +/- 31 to 158 +/- 23 ng/mL; sICAM-1, from 830 +/- 210 to 1,536 +/- 199 ng/mL; sVCAM-1, from 861 +/- 168 to 1,249 +/- 151 ng/mL). None of the other hemodynamic or laboratory variables could be correlated with the time course of adhesion molecules, except for PaO2/Pao2 ratio, which was negatively correlated with plasma levels of soluble adhesion molecules in the nonsurvivors (analysis of covariance). It is concluded that plasma levels of soluble adhesion molecules were markedly higher in nonsurviving than in surviving critically ill patients. They may possibly serve as markers of the extent of inflammatory response, of the endothelial damage in patients at risk of multiple-organ failure or both.(ABSTRACT TRUNCATED AT 400 WORDS)

Cardiorespiratory response of intravenous angiotensin-converting enzyme inhibitor enalaprilat in hypertensive cardiac surgery patients.

Twenty-four patients undergoing elective coronary artery bypass surgery were studied. Either the angiotensin-converting enzyme (ACE) inhibitor enalaprilat, 0.06 mg/kg, (n = 12), or saline solution (= control group; n = 12), was randomly and blindly administered intravenously when the mean arterial blood pressure (MAP) increased to 90 mmHg after induction of anesthesia. Cardiorespiratory parameters were studied before injection, during the subsequent 30 minutes, precardiopulmonary bypass (CPB), post-CPB, and at the end of surgery. MAP was significantly reduced 5 minutes after administration of enalaprilat. The peak reduction of blood pressure was observed after 30 minutes (from 98 +/- 4 to 68 +/- 8 mmHg). Even immediately before CPB (112 +/- 12 minutes after injection of enalaprilat), MAP and systemic vascular resistance were significantly lower than baseline values. Heart rate remained almost unchanged in both groups. Cardiac index increased slightly in the enalaprilat patients (maximum: +0.75 L/min/m2 20 minutes after injection). Filling pressures (central venous pressure, pulmonary capillary wedge pressure) were also significantly reduced by enalaprilat. There were no differences from the control patients with regard to changes in right ventricular hemodynamics (right ventricular ejection fraction, right ventricular end-diastolic volume, right ventricular end-systolic volume), pulmonary gas exchange (PaO2), or intrapulmonary right-to-left shunting (Qs/Qt). VO2 increased only in the enalaprilat patients (from 179 +/- 28 to 230 +/- 30 mL/min) (p < 0.05). Cardiorespiratory parameters did not differ between the two groups post-CPB.(ABSTRACT TRUNCATED AT 250 WORDS)

Is continuous cardiac output measurement using thermodilution reliable in the critically ill patient?

OBJECTIVE: Evaluation of continuous cardiac output monitoring based on the thermodilution technique in the critically ill. DESIGN: Prospective clinical investigation. SETTING: A surgical intensive care unit of a university hospital. PATIENTS: Thirty-five critically ill patients (trauma and/or sepsis patients), who needed pulmonary artery catheterization. The patients were prospectively studied according to the following groups: a) patients with a heart rate of > 120 beats/min; b) those patients with a cardiac output of > 10 L/min; c) patients with a cardiac output of < 4.5 L/min; d) patients with a rectal temperature of > 39.0 degrees C; and e) patients with a pulmonary artery catheter inserted for > 4 days. INTERVENTIONS: Therapies were carried out according to modern intensive care medicine protocols by physicians who were not involved in the study. MEASUREMENTS: Cardiac output was monitored continuously using a new, modified pulmonary artery catheter. This catheter has a heating filament by which energy is transmitted to the circulating blood (modified thermodilution technique). A bedside microprocessor calculated cardiac output using a new algorithm. Standard bolus thermodilution technique (10 mL of ice-cold saline solution) was used to compare the continuous cardiac output measurement with the intermittent bolus cardiac output measurement. MAIN RESULTS: A total of 404 pairs of intermittent (bolus) cardiac output and continuous cardiac output measurements were obtained from the 35 patients. The bias (mean difference between bolus cardiac output measurement and continuous cardiac output measurement) of all measurements was 0.03 +/- 0.52 L/min and the 95% confidence limit (mean difference +/- 2 SD) was -1.01/1.06 L/min. Also, continuous cardiac output measurement agreed closely with bolus cardiac output measurement (bias was 0.16 +/- 0.57 L/min in the cardiac output of > 10 L/min group; bias was -0.17 +/- 0.50 L/min for the cardiac output of < 4.5 L/min group). Increased temperature and prolonged length of stay did not influence the agreement of continuous cardiac output measurement with bolus cardiac output measurement (bias was 0.09 +/- 0.51 L/min in the > 39 degrees C rectal temperature group). CONCLUSIONS: Continuous monitoring of cardiac output using a modified pulmonary artery catheter with a heated filament has proven to be accurate and precise in the critically ill patient when compared with the "standard" intermittent bolus thermodilution technique. The continuous monitoring technique enhances our armamentarium for more intensive monitoring of these patients under a variety of circumstances.

Platelet function in critically ill patients.

OBJECTIVE: The critically ill patient is at risk to develop coagulation abnormalities at different levels. Platelet dysfunction in these patients is of multifactorial origin, including drug interactions, hormonal response, and infection. The time course of platelet function in severely traumatized patients was studied. DESIGN: Prospective. SETTING: Clinical investigation, intensive care unit (ICU) of an university hospital. PATIENTS: Twenty-six consecutive, severely traumatized patients (injury severity score [ISS] > 30 points) were studied. The patients were divided into those who showed an uncomplicated course (n = 16) and those who developed sepsis during the investigation period ("complicated" trauma; n = 10). INTERVENTIONS: All therapy (parenteral feeding, antibiotics, volume therapy, ventilation) was comparable for all patients. MEASUREMENTS: Platelet function was assessed by aggregometry (inductors: adenosine diphosphate [ADP], 2.0 mumol/L; collagen, 4 micrograms/ml; epinephrine, 25 mumol/L; NaCl). Aggregometry was carried out from arterial blood samples within 24 h after admission to the ICU ("baseline") and the following 5 days. RESULTS: Standard coagulation variables (antithrombin III, fibrinogen, platelet count) showed no significant differences between the two groups. Platelet aggregation parameters were already reduced when the patients were admitted to ICU in all patients. In "uncomplicated" patients (without sepsis), aggregation increased during the following 5 days (maximal aggregation: ADP from 41 percent to 54 percent; collagen from 36 percent to 48 percent; epinephrine from 32 percent to 61 percent). Maximum gradient of platelet aggregation had a similar course. In the traumatized patients with sepsis, ADP- and collagen induced aggregation was significantly reduced within the investigation period. All patients with an ADP aggregation of less than 20 percent died. CONCLUSIONS: Platelet function in patients with isolated trauma recovered during the following 5 days. When sepsis complicated trauma, complex derangements in platelet function were present as seen by altered platelet aggregometry despite adequate platelet count.

Changes in regulators of circulation in patients undergoing continuous pump-driven veno-venous hemofiltration.

Continuous pump-driven veno-venous hemofiltration (CVVH) has become an established method for treatment of acute renal failure (ARF). Since severe disturbances of (micro-) circulation are intimately involved in the bad outcome of these patients, the profile of endocrinological regulators of circulation was prospectively and serially measured in patients undergoing pump-driven CVVH (n = 15). 15 patients with similar APACHE II score, but without ARF and without CVVH were also studied. Endothelin-1 (ET-1), atrial natriuretic peptide (ANP), vasopressin, renin, and catecholamine (epinephrine, norepinephrine) plasma levels were measured before start of CVVH (= "baseline") (in the non-CVVH patients: admission to intensive care unit) and during the next 5 days. Various hemodynamic parameters were additionally monitored. MAP, HR, PAP, CI, and right ventricular hemodynamics (RVEF, RVEDV, RVESV) remained almost unchanged in the CVVH patients and were without differences to the non-CVVH group within the entire investigation period. PCWP and RAP were higher in the CVVH patients already at baseline (RAP, 17.8 +/- 4.0 mmHg; PCWP, 22.1 +/- 4.5 mmHg) (p < .02) and remained elevated in the further course of the investigation. Renin plasma level was higher already at baseline in the CVVH patients (907 +/- 184 pg/ml) (p < .05) and further increased during CVVH (to 1453 +/- 186 pg/mL). Vasopressin increased only in the CVVH group (from 3.80 +/- .66 to 11.85 +/- 1.05 pg/mL) (p < .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Continuous hemofiltration and platelet function in critically ill patients.

OBJECTIVE: To evaluate platelet function in patients undergoing continuous pump-driven veno-venous hemofiltration. DESIGN: Prospective study. SETTING: Surgical intensive care unit of a university hospital. PATIENTS: Twenty consecutive, critically ill patients with acute renal failure (serum creatinine concentration > 3.0 mg/dL (> 265 mumol/L), serum urea > 200 mg/dL (> 33 mmol/L), urine output < 20 mL/hr) secondary to sepsis or trauma. A comparable group (n = 20) without renal failure and not undergoing hemofiltration served as a control group. INTERVENTIONS: Continuous pump-driven veno-venous hemofiltration was used in patients with renal insufficiency. Pump flow ranged from 60 to 100 mL/hr. MEASUREMENTS AND MAIN RESULTS: Platelet function was assessed by a turbidimetric technique using a double-channel aggregometer. Aggregation was induced by adenosine diphosphate (ADP) (2.0 mumol/L), collagen (4 micrograms/mL), epinephrine (25 mumol/L), and saline solution (control). Maximum aggregation was considered to be the maximum increase in light transmission after the addition of the aggregating agents. The maximum gradient of aggregation was considered to be the maximum increase per minute. Measurements were carried out before hemofiltration (baseline values) and during the following 5 days. In the control group, blood samples were taken at corresponding data points. Eight patients undergoing continuous hemofiltration survived during the investigation period; 16 patients in the control group survived. There were no significant differences among the two groups with respect to standard coagulation variables. Maximum platelet aggregation was lower than in normal patients after the addition of all three inductors (ADP, collagen, and epinephrine). In control patients, all aggregation variables remained almost stable during the entire investigation period. In the hemofiltered patients, maximum platelet aggregation was significantly reduced (ADP, decrease of 62 relative % from baseline values; collagen, decrease of 86 relative % from baseline values; epinephrine, decrease of 77 relative % from baseline values). Maximum platelet aggregation was also depressed in these patients (ADP, decrease of 40 relative % from baseline values; collagen, decrease of 88 relative % from baseline values; epinephrine, decrease of 85 relative % from baseline values). When platelet aggregation variables were reduced greater than a decrease of 60 relative % from baseline values (in all induction groups), the mortality rate was 100%. CONCLUSIONS: Continuous pump-driven veno-venous hemofiltration significantly changed platelet aggregability, which became obvious 2 to 3 days after the start of hemofiltration.

Cardiopulmonary actions of intravenously administered enalaprilat in trauma patients.

OBJECTIVE: To determine the cardiopulmonary actions of the intravenous administration of the angiotensin-converting enzyme inhibitor enalaprilat in hypertensive trauma patients. DESIGN: Prospective, before/after trial. SETTING: Intensive care unit (ICU) of a university hospital. PATIENTS: Twenty critically injured and hypertensive ICU patients. All patients were receiving continuous sedation (fentanyl and midazolam) for at least 2 days before the injection of enalaprilat and had a mean arterial pressure (MAP) of > 95 mm Hg. "Responders" were defined as having a decrease in MAP of > 15% within 30 mins after enalaprilat injection. INTERVENTIONS: Intravenous administration of 0.06 mg/kg of the angiotensin-converting enzyme inhibitor enalaprilat. Repeated doses were given when no sufficient response (decrease of MAP of > 15% within 30 mins after injection) was seen ("nonresponders"). MEASUREMENTS: In addition to standard hemodynamic monitoring, right ventricular hemodynamics and oximetric variables were also documented. Measurements were carried out before enalaprilat injection (during hemodynamic steady state [baseline values]) and at 1, 5, 10, 20, 30, 60, and 120 mins after enalaprilat administration. MAIN RESULTS: MAP was successfully controlled in 17 of 20 patients (maximum decrease -27 mm Hg [-26%]). In the three other patients, even reinjection of enalaprilat (0.06 mg/kg) did not sufficiently reduce MAP. In the 17 responders, heart rate did not increase, whereas central venous pressure, pulmonary arterial pressure, and pulmonary artery occlusion pressure decreased significantly after intravenous administration of enalaprilat. Cardiac index changed only slightly (mean maximum +0.70 L/min/m2 [+18%]). Right ventricular ejection fraction increased from 36% to 45% (p < .05); right ventricular end-diastolic and end-systolic volume index decreased significantly. Both systemic and pulmonary vascular resistance indices decreased within the investigation period (-31% and -16%, respectively). Pao2/FIO2, intrapulmonary right-to-left shunting, and oxygen extraction ratio were not altered. Oxygen delivery index (+17%) and oxygen consumption index (+20%) increased during the investigation period (p < .04). CONCLUSIONS: The intravenous administration of enalaprilat successfully decreased blood pressure in most of our patients. Mechanisms other than the renin-angiotensin system also appear to be involved in hypertensive, critically ill patients. Pulmonary function was not altered; right ventricular function, and both oxygen consumption and oxygen delivery improved in the enalaprilat responder group. Thus, the availability of intravenous enalaprilat seems to enlarge our armamentarium for treating hypertension in the critically ill patient.