Christer Carlsson

A New Diagnostic Approach to the Patient with Severe Pneumonia

36 patients with severe community-acquired pneumonia, treated in an intensive care unit (ICU), were examined in a prospective study using a comprehensive diagnostic program to establish an early etiological diagnosis. The resulting prompt and adequate antimicrobial therapy may have decreased the number of fatal cases. Special emphasis was placed on the use of a method incorporating fiberoptic bronchoscopy, together with protected brush sampling and bronchial lavage. An etiological diagnosis was established in 81% (29/36) of the cases. This etiological diagnosis was established within 48-72 h in 53% (19/36) of the patients, S. pneumoniae being the most frequent agent found (12 patients). This information, however, was poorly utilized since in only 11/19 of these patients was the antimicrobial therapy changed from a broad-spectrum antibiotic to a more specific narrow spectrum agent. The overall mortality rate was 22% (8/36). 7/8 patients who died had compromising factors. Most deaths in community-acquired pneumonia are still associated with pneumococcal infection. We conclude that fiberoptic bronchoscopy with brush samples via a plugged double lumen catheter provides the least misleading information concerning the etiological agent in pneumonia; sampling should be done as soon as possible after admission to the hospital, ideally before the need for ICU treatment; factors other than prompt antimicrobial therapy may influence the outcome of severe community-acquired pneumonia.

Pneumonia: A Deadly Disease despite Intensive Care Treatment

In a retrospective study of 30 patients with pneumonia treated in the intensive care unit, it was found that cultures from sputum and bronchial secretions did poorly correspond with blood cultures or serological tests. In only 15 of the patients a reliable etiological diagnosis was ever established. Mechanical ventilation was used in 22 patients, usually with a high oxygen need. At the start of this ventilation a significant blood pressure fall and a further pulmonary deterioration was observed. In fatal cases this pulmonary dysfunction was progressive. The overall mortality was 47%. When an FI02 above 0.6 was needed in the ventilator the mortality was 13/14 (93%).

Thrombosis following percutaneous radial artery cannulation

A prospective study of the arterial supply of the hand was carried out in 100 ICU patients after cannulation of the radial artery. Patency of the radial artery was checked using a reversed Allens test and Doppler ultrasonic technique. Furthermore, radial artery angiography was carried out in 15 patients with suspect thrombosis, and the artery was examined by microscopy in four patients at autopsy. Signs of thrombosis, Allens test and Doppler technique, were found in 33/100 patients. In 10/15 angiograms a thrombosis was visualized, and in 3/4 patients at autopsy a thrombosis was found. The incidence of thrombosis was not correlated to sex, age, size of artery (judged by wrist circumference), cannulation technique or the presence of hypotension. It did, however, correlate to the presence of haematoma at the puncture site. After removal of the cannula recanalisation occurred soon in the majority of cases.

Methylmethacrylate monomer produces direct relaxation of vascular smooth muscle in vitro

Methylmethacrylate bone cement is associated with severe hypotensive reactions during surgery and anesthesia. The purpose of this in vitro study was to determine if methylmethacrylate monomer could produce hypotension by acting directly on vascular smooth muscle.

The effects of N-methyl-D-aspartate agonists and antagonists on isolated bovine cerebral arteries

This pharmacologic study examines the direct cerebrovascular effects of N-methyl-D-aspartate (NMDA) receptor agonists and antagonists to determine whether large cerebral arteries have NMDA receptors. Bovine middle cerebral arteries were cut into rings to measure isometric tension development in vitro. Two competitive agonists, L-glutamate and NMDA, each had negligible effects on ring tension in the absence of exogenous vasoconstrictors. L-glutamate (in high concentrations) produced direct relaxation of potassium (K+)-constricted arteries, but the relaxation was not selective for L-glutamate, D-glutamate, or mannitol. Relaxation with L-glutamate was abolished when it was isosmotically substituted in the K+-rich medium. NMDA (in the absence or presence of glycine) and two competitive antagonists, 2-amino-5-phosphopentanoic acid (AP5) and (+/-)-3-(s-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), each had little effect on the tone of arteries preconstricted with potassium or the stable thromboxane A2 analog U-46,619. Three noncompetitive antagonists (S(+)-ketamine, dizocilpine, and dextrorphan) and their stereoisomers (R(-)-ketamine, (-)MK-801, and levorphanol) each produced dose-dependent relaxation of K+- or U-46,619-constricted arteries; relaxation was not selective for the (+) or (-) stereoisomers. These results suggest that large cerebral arteries lack NMDA receptors mediating constriction or relaxation. All noncompetitive antagonists dilated cerebral arteries, but by mechanisms that were not stereospecific. (Anesth Analg 1996;82:264-8)

Ketamine directly dilates bovine cerebral arteries by acting as a calcium entry blocker.

This in vitro study was performed to determine the role of calcium in ketamine-induced cerebral vasodilation. Isolated bovine middle cerebral arteries were cut into rings to measure isometric tension development or into strips to measure radioactive 45Calcium (45Ca) uptake. Ketamine produced direct relaxation of arterial rings; the relaxation was attenuated in Ca(2+)-deficient media. Ketamine produced dose-related relaxation of arteries preconstricted with potassium, a stable thromboxane A2 analogue, or endothelin. Endothelial stripping with Triton X-100 had no effect on subsequent ketamine-induced relaxation. In Ca(2+)-deficient media containing potassium or the stable thromboxane A2 analogue, ketamine produced competitive inhibition of subsequent Ca(2+)-induced constriction. Ketamine blocked potassium- and thromboxane A2-stimulated 45Ca uptake in a dose-dependent manner, but had no effect on basal 45Ca uptake, the externally bound 45Ca content, or the volume of the 3H-sorbitol space. These results indicate that ketamine can directly dilate cerebral arteries by acting as a calcium channel antagonist; ketamine inhibits 45Ca uptake through both potential-operated (potassium) and receptor-operated (thromboxane A2) channels in cerebrovascular smooth muscle.

Cryoprecipitate infusion fails to improve organ function in septic shock.

Plasma fibronectin may be of critical importance for the septic patient through its proposed function as the major opsonin for macrophage clearance of circulating, noncellular debris. As a rule, critically ill, septic patients are depleted of fibronectin. In earlier uncontrolled studies, infusion of fibronectin-rich cryoprecipitate had resulted in improved renal and pulmonary functions and changes in peripheral hemodynamics. In this controlled study, 32 septic ICU patients (mean initial fibronectin level = 60% of normal) received cryoprecipitate or control infusions. Although the fibronectin level was significantly elevated to the normal range in the cryoprecipitate group, no effects were seen in hemodynamics, oxygen metabolism, or lung and kidney functions. Our results indicate that this form of fibronectin therapy does not influence the impaired organ function in septic shock.

Diagnostic obturator nerve block for inguinal and back pain : a recovered opinion

&NA; Peripheral nerve blocks are very useful in diagnosing certain pain conditions. We report a case of chronic inguinal and back pain secondary to hip arthropathy. An obturator nerve block was used to help determine the origin of the pain.

N-methyl-D-aspartate (NMDA) antagonists--S(+)-ketamine, dextrorphan, and dextromethorphan--act as calcium antagonists on bovine cerebral arteries.

Ketamine, an intravenous anesthetic and a major drug of abuse, is a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist. Ketamines enantiomer, S(+)-ketamine, acts stereoselectively on neuronal NMDA receptors. The purpose of this in vitro study was to compare the direct effects of S(+)-ketamine, 2 other noncompetitive NMDA receptor antagonists (dextrorphan and dextromethorphan), and the calcium entry blocker nimodipine on the cerebral vasculature, using bovine middle cerebral arteries as an experimental model. Arterial rings were mounted in isolated tissue chambers equipped with isometric tension transducers to obtain pharmacologic dose-response curves. In the absence of exogenous vasoconstrictors, the NMDA antagonists or nimodipine had negligible effects on cerebral arterial tone. When rings were preconstricted with either potassium or the stable thromboxane A2 mimetic U46619, the NMDA antagonists and nimodipine each produced dose-dependent relaxation. Prior endothelial stripping had no effect on subsequent drug-induced relaxation of K+-constricted rings. In Ca2+-deficient media containing either potassium or U46619, the NMDA antagonists and nimodipine each produced competitive inhibition of subsequent Ca2+induced constriction. In additional experiments, arterial strips were mounted in isolated tissue chambers to directly measure calcium uptake, using 45calcium (45Ca) as a radioactive tracer. The NMDA antagonists and nimodipine each blocked potassium-stimulated or U46619-stimulated 45Ca uptake into arterial strips. These results indicate that S(+)-ketamine, dextrorphan, and dextromethorphan, like nimodipine, directly dilate cerebral arteries by acting as calcium antagonists; they all inhibit 45Ca uptake through both potential-operated (potassium) and receptor-operated (U46619) channels in cerebrovascular smooth muscle.

Vascular effects of etomidate administered for electroencephalographic burst suppression in humans.

Although its status as a neuroprotectant is controversial, etomidate is often employed for pharmacologic cerebral protection in aneurysm surgery. One purported advantage of etomidate over thiopental is its hemodynamic stability. This study examined the cardiovascular effects of etomidate given for electroencephalographic (EEG) burst suppression during cerebral aneurysm clipping in humans and the direct effects of etomidate on arteries in vitro. The charts of intracranial aneurysm surgery patients were retrospectively reviewed to determine the dose of etomidate employed, the frequency of concurrent vaspressor administration, and whether hemodynamic changes were associated with etomidate use. Against a background of balanced anesthesia, the dose of etomidate to induce burst suppression was 0.73 +/- 0.49 mg/kg (mean +/- SD) and the maintenance dose was 48 +/- 30 microg/kg/min. Etomidate produced an immediate decrease in mean arterial pressure that was sustained in patients who did not receive vasopressor support. During etomidate administration, 48% of patients (10 of 21) received some form of vasopressor support such as phenylephrine or ephedrine, and 62% of patients (13 of 21) receiving isoflurane had the anesthetic discontinued or its inspired concentration decreased. Etomidate in vitro produced dose-dependent relaxation of human internal mammary arterial rings that had been preconstricted by potassium or norepinephrine. Etomidate, in EEG burst suppression doses, decreases mean arterial pressure in anesthetized patients undergoing cerebral aneurysm surgery. One mechanism of etomidate-induced hypotension may be direct relaxation of vascular smooth muscle, because etomidate directly dilates preconstricted human arteries in vitro.