Reducing the burden of brain tumor surgery.

BACKGROUND: Even though the need has been challenged, admitting patients to an intensive care or medium care unit (ICU/MCU) after adult supratentorial tumor craniotomy remains common practice. We have introduced a "no ICU, unless" policy for tumor craniotomy patients and evaluate costs, complications, and length of stay. METHODS: A prospective cohort study was performed comparing patients that underwent tumor craniotomy for supratentorial tumors during 2 years after introduction of the new policy with the year before. RESULTS: A reduction in ICU/MCU admittance from 88 to 23% of patients was found resulting in 13% cost reduction. Also, the new policy resulted in a 1.4-day shorter post-operative length of stay. Minor complications were reduced, while major complications remained the same. All major complications are reviewed. CONCLUSIONS: We show that routine post-operative ICU/MCU admittance after tumor craniotomy does not reduce complications, but actually interferes with recovery of our patients. Changing the paradigm results in earlier discharge and cost reduction.

Selective Intensive Care Unit Admission After Adult Supratentorial Tumor Craniotomy: Complications, Length of Stay, and Costs.

BACKGROUND: Admitting patients to an intensive care or medium care unit (ICU/MCU) after adult supratentorial tumor craniotomy remains common practice even though some studies have suggested lower level care is sufficient for selected patients. We have introduced a "no ICU, unless" policy for tumor craniotomy patients. OBJECTIVE: To provide a quieter postoperative environment for patients, reduce the burden on the ICU department, and to evaluate whether costs can be reduced. METHODS: A cohort study was performed comparing patients that underwent tumor craniotomy for supratentorial tumors during 1 yr after introduction (n = 109) of the new policy with the year before (n = 107). Rate of complications was evaluated, as was the length of stay and patient satisfaction using qualitative evaluation. Finally, costs were evaluated comparing the situation before and after implementation of the new protocol. RESULTS: A reduction in ICU/MCU admittance from 64% to 24% of patients was found resulting in 13.3% cost reduction (€1950 per case), without increasing the length of stay at the ward. The length of stay in the hospital was similar. Complications were significantly reduced after implementing the new policy (0.98 vs 0.53 per patient, P = .003). Patients that were interviewed after the new policy reported feeling safe and at ease at the ward. CONCLUSION: Changing our policy from "ICU, unless" to "no ICU, unless" reduced complication rates and length of stay in the hospital while keeping patients satisfied. Hospital costs related to the admission have been significantly reduced by the new policy.

Increased mitochondrial ATP production capacity in brain of healthy mice and a mouse model of isolated complex I deficiency after isoflurane anesthesia.

We reported before that the minimal alveolar concentration (MAC) of isoflurane is decreased in complex I-deficient mice lacking the NDUFS4 subunit of the respiratory chain (RC) (1.55 and 0.81% at postnatal (PN) 22-25 days and 1.68 and 0.65% at PN 31-34 days for wildtype (WT) and CI-deficient KO, respectively). A more severe respiratory depression was caused by 1.0 MAC isoflurane in KO mice (respiratory rate values of 86 and 45 at PN 22-25 days and 69 and 29 at PN 31-34 days for anesthetized WT and KO, respectively). Here, we address the idea that isoflurane anesthesia causes a much larger decrease in brain mitochondrial ATP production in KO mice thus explaining their increased sensitivity to this anesthetic. Brains from WT and KO mice of the above study were removed immediately after MAC determination at PN 31-34 days and a mitochondria-enriched fraction was prepared. Aliquots were used for measurement of maximal ATP production in the presence of pyruvate, malate, ADP and creatine and, after freeze-thawing, the maximal activity of the individual RC complexes in the presence of complex-specific substrates. CI activity was dramatically decreased in KO, whereas ATP production was decreased by only 26% (p < 0.05). The activities of CII, CIII, and CIV were the same for WT and KO. Isoflurane anesthesia decreased the activity of CI by 30% (p < 0.001) in WT. In sharp contrast, it increased the activity of CII by 37% (p < 0.001) and 50% (p < 0.001) and that of CIII by 37% (p < 0.001) and 40% (p < 0.001) in WT and KO, respectively, whereas it tended to increase that of CIV in both WT and KO. Isoflurane anesthesia increased ATP production by 52 and 69% in WT (p < 0.05) and KO (p < 0.01), respectively. Together these findings indicate that isoflurane anesthesia interferes positively rather than negatively with the ability of CI-deficient mice brain mitochondria to convert their main substrate pyruvate into ATP.

Isoflurane anesthetic hypersensitivity and progressive respiratory depression in a mouse model with isolated mitochondrial complex I deficiency.

BACKGROUND: Children with mitochondrial disorders are frequently anesthetized for a wide range of operations. These disorders may interfere with the response to surgery and anesthesia. We examined anesthetic sensitivity to and respiratory effects of isoflurane in the Ndufs4 knockout (KO) mouse model. These mice exhibit an isolated mitochondrial complex I (CI) deficiency of the respiratory chain, and they also display clinical signs and symptoms resembling those of patients with mitochondrial CI disease. METHODS: We investigated seven Ndufs4(-/-) knockout (KO), five Ndufs4(+/-) heterozygous (HZ) and five Ndufs4(+/+) wild type (WT) mice between 22 and 25 days and again between 31 and 34 days post-natal. Animals were placed inside an airtight box, breathing spontaneously while isoflurane was administered in increasing concentrations. Minimum alveolar concentration (MAC) was determined with the bracketing study design, using the response to electrical stimulation to the hind paw. RESULTS: MAC for isoflurane was significantly lower in KO mice than in HZ and WT mice: 0.81% ± 0.01 vs 1.55 ± 0.05% and 1.55 ± 0.13%, respectively, at 22-25 days, and 0.65 ± 0.05%, 1.65 ± 0.08% and 1.68 ± 0.08% at 31-34 days. The KO mice showed severe respiratory depression at lower isoflurane concentrations than the WT and HZ mice. CONCLUSION: We observed an increased isoflurane anesthetic sensitivity and severe respiratory depression in the KO mice. The respiratory depression during anesthesia was strongly progressive with age. Since the pathophysiological consequences from complex I deficiency are mainly reflected in the central nervous system and our mouse model involves progressive encephalopathy, further investigation of isoflurane effects on brain mitochondrial function is warranted.