Guideline adherence for empirical treatment of pneumonia and patient outcome. Treating pneumonia in the Netherlands.

INTRODUCTION: According to the Dutch guidelines, severity of community acquired pneumonia (CAP) (mild, moderate-severe, severe) should be based on either PSI, CURB65 or a 'pragmatic' classification. In the last mentioned, the type of ward of admission, as decided by the treating physician, is used as classifier: no hospital admission is mild, admission to a general ward is moderate-severe and admission to an intensive care unit (ICU) is severe CAP. Empiric antibiotic recommendations for each severity class are uniform. We investigated, in 23 hospitals, which of the three classification systems empirical treatment of CAP best adhered to, and whether a too narrow spectrum coverage (according to each of the systems) was associated with a poor patient outcome (in-hospital mortality or need for ICU admission). PATIENTS AND METHODS: Prospective observational study in 23 hospitals. RESULTS: 271 (26%) of 1047 patients with CAP confirmed by X-ray were categorised in the same severity class with all three classification methods. Proportions of patients receiving guideline-adherent antibiotics were 62.9% (95% CI 60.0-65.8%) for the pragmatic, 43.1% (95% CI 40.1-46.1%) for PSI and 30.5% (95% CI 27.8-33.3%) for CURB65 classification. 'Under-treatment' based on the pragmatic classification was associated with a trend towards poor clinical outcome, but no such trend was apparent for the other two scoring systems. CONCLUSIONS: Concordance between three CAP severity classification systems was low, implying large heterogeneity in antibiotic treatment for CAP patients. Empirical treatment appeared most adherent to the pragmatic classification. Non-adherence to treatment recommendations based on the PSI and CURB65 was not associated with a poor clinical outcome.

Prognostic significance of the difference between mixed venous and jugular bulb oxygen saturation in comatose patients resuscitated from a cardiac arrest.

To determine the prognostic significance of the difference between mixed venous and jugular bulb oxygen saturation in survivors and non-survivors of a cardiac arrest, we studied 30 comatose patients (21 non-survivors and 9 survivors) resuscitated from a cardiac arrest. We measured mixed venous oxygen saturation (SmvO2) and jugular bulb oxygen saturation (SjO2) immediately after haemodynamic stabilisation (always within 6 h after cardiac arrest) and 6, 12 and 24 h later. In all patients the SjO2 was about 10% lower than the SmvO2 in the first measurement. In the survivors the SjO2 did not change and remained lower than SmvO2 in eight of nine survivors. However, in the non-survivors the SjO2 increased significantly and was finally higher than the SmvO2 in 12 of 20 patients 24 h after cardiac arrest suggesting a decrease in cerebral oxygen consumption due to extensive loss of functional brain tissue. The positive predictive value of (SmvO2-SjO2) < or = 0 for predicting irreversible brain damage at 24 h after cardiac arrest is 93% and the negative predictive value of (SmvO2-SjO2) > 0 is 53%. Sensitivity and specificity are 65 and 89%, respectively. In a previous study we concluded that early jugular bulb oximetry (within 4 h after cardiac arrest) cannot predict cerebral outcome in comatose patients after cardiac arrest. More studies are needed to clarify the role of prolonged monitoring in the prediction of cerebral outcome after cardiac arrest.

A comparison of near-infrared spectroscopy and jugular bulb oximetry in comatose patients resuscitated from a cardiac arrest.

One cause of cerebral damage in comatose patients resuscitated from a cardiac arrest is cerebral ischaemia occurring during the postresuscitation period. Near-infrared spectroscopy has been advocated as a useful monitor of brain oxygenation, but data on clinical use in comatose postarrest patients are not available. Therefore, we compared regional oxygen saturation measured with the INVOS 3100 with global oxygen saturation measured using jugular bulb oximetry in 10 comatose patients successfully resuscitated from an out-of-hospital cardiac arrest. Our data show that, in most patients, there is a significant difference between the two methods. The INVOS 3100 over-read at low jugular bulb saturations (< 60%) and under-read at high jugular bulb saturations (> or = 60%). During hypoventilation we found a significant increase in regional oxygen saturation. This increase was significantly correlated with the rise in cerebral blood flow and cardiac index, indicating that regional oxygen saturation is influenced by both cerebral and extracerebral components. We conclude that regional cerebral oxygen saturation measured with the INVOS 3100 cannot be compared with global cerebral oxygen saturation measured with jugular bulb oximetry in comatose patients resuscitated from a cardiac arrest. This may be due to characteristics of the INVOS 3100 or to the distribution of cerebral blood flow after cardiac arrest.

Cerebrovascular reactivity in comatose patients resuscitated from a cardiac arrest.

BACKGROUND AND PURPOSE: Cerebral blood flow after cardiac arrest is reduced during the delayed hypoperfusion phase, while cerebral metabolic rate of oxygen returns to baseline values. Hypocapnia can induce cerebral ischemia in neurosurgical patients who already have reduced cerebral blood flow. The purpose of the present study was to determine whether comatose patients resuscitated from a cardiac arrest have a normal cerebrovascular reactivity to changes in PaCO2 and whether hypocapnia causes cerebral ischemia. METHODS: We measured mean flow velocity (MFV) and pulsatility index (PI) in the middle cerebral artery, jugular bulb oxygen saturation (SjbO2), and arterial-jugular lactate difference (AJLD) during normo-, hypo-, and hyperventilation in 10 comatose patients resuscitated from a cardiac arrest. The first measurements were made within 6 hours after cardiac arrest and repeated 6, 12, and 24 hours later. RESULTS: During hypoventilation we observed a significant decrease in PI and an increase in MFV and SjbO2. During hyperventilation PI and MFV did not change, but SjbO2 showed a significant decrease. This was accompanied by an increase in AJLD, suggesting cerebral ischemia. In four patients the SjbO2 decreased below the ischemic threshold of 55%. CONCLUSIONS: The cerebrovascular reactivity to changes in arterial carbon dioxide tension is preserved in comatose patients resuscitated from a cardiac arrest. Hyperventilation may induce cerebral ischemia in the postresuscitation period.

Cerebral vasoconstriction in comatose patients resuscitated from a cardiac arrest?

OBJECTIVE: To determine the role of cerebral vasoconstriction in the delayed hypoperfusion phase in comatose patients after cardiac arrest. DESIGN: Prospective study. SETTING: Medical intensive care unit in a university hospital. PATIENTS: 10 comatose patients (Glasgow Coma Score +/- 6)successfully resuscitated from a cardiac arrest occurring outside the hospital. MEASUREMENTS: We measured the pulsatility index (PI) and mean blood flow velocity (MFV) of the middle cerebral artery, the cerebral oxygen extraction ratio and jugular bulb levels of endothelin, nitrate, and cGMP during the first 24 h after cardiac arrest. RESULTS: The PI decreased significantly from 1.86 +/- 1.02 to 1.05 +/- 0.22 (p = 0.03). The MFV increased significantly from 29 +/- 10 to 62 +/- 25 cm/s (p = 0.003). Cerebral oxygen extraction ratio decreased also from 0.39 +/- 0.13 to 0.24 +/- 0.11 (p = 0.015). Endothelin levels were high but did not change during the study period. Nitrate levels varied widely and showed a slight but significant decrease from 37.1 mumol/l (median; 25th-75th percentiles: 26.8-61.6) to 31.3 mumol/l (22.1-39.6) (p = 0.04). Cyclic guanosine monophosphate levels increased significantly from 2.95 mumol/l (median; 25th-75th percentiles: 2.48-5.43) to 7.5 mumol/l (6.20-14.0) (p = 0.02). CONCLUSIONS: We found evidence of increased cerebrovascular resistance during the first 24 h after cardiac arrest with persistent high endothelin levels, gradually decreasing nitrate levels, and gradually increasing cGMP levels, This suggests that active cerebral vasoconstriction due to an imbalance between local vasodilators and vasoconstrictors plays a role in the delayed hypoperfusion phase.

The influence of maternal exercise on the uteroplacental vascular bed resistance and the fetal heart rate during normal pregnancy.

The effects of maternal exercise were studied in 20 healthy women with uncomplicated pregnancies. A continuous-wave Doppler ultrasound system was used to record arterial flow velocity waveforms from the ascending vasculature downstream from the uterine artery. The fetal heart rate was monitored with a Doppler ultrasound cardiotocograph. No significant change was found in the uterine blood flow velocity waveform post-exercise, as expressed by the pulsatility index, suggesting absence of change in the uterine vascular bed resistance. The fetal heart rate significantly increased after exercise.