The scientific background to the intensive care of brain damage appears to be in the process of rapid evolution. Such a situation has resulted from the development of various monitoring methods and the establishment of standard therapeutic techniques, both of which have enabled reliable multi-institutional trials of new therapies to be conducted. As a representative example, the current changes in the intensive care of traumatic brain injury are reviewed. While the relevance of secondary ischemic insults to the traumatized brain has been recognized, several questions in the clinical setting remain to be answered. The development of various monitoring techniques including measurement of the jugular venous oxygen saturation, which is now widely adopted in the intensive care of traumatic brain injury, has yielded invaluable information for establishing a standard protocol of therapies. These changes have, in turn, provided and opportunity of perform multi-institutional trials of new therapies, such as mild hypothermia, more reliably. Basic studies employing reproducible animal models of traumatic brain injury have also played a vital role in developing new therapies. It appears that the scientific background to the intensive care of brain damage is now being established as an academic field in its own right.

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Adequate control of sedation and pain relief is of great importance in the treatment of patients in the ICU, particularly for those requiring artificial ventilation to reduce distress and to facilitate treatments. Since there is no single regimen acceptable for all critically ill patients, and since the condition of such patients may change rapidly, an individualized plan of pain treatment should be formulated by scoring the pain and sedation with an account to respiratory and hemodynamic conditions as well as to overall health, body size and individual sensitivity. In many ICUs, opioid (morphine, fentanyl) and benzodiazepine (diazepam, midazolam) combinations are the treatment of choice. However, metabolism of midazolam is impaired in critically ill patients with septic shock, resulting in unpredictable prolongation of its effects. Furthermore, resistance to opioids frequently occurs in those with septic shock. Epidural morphine is recommended for pain relief following hepatectomy, esophagectomy, or thoracic trauma. Midazolam and isoflurane are used to provide sedation for patients who require long-term mechanical ventilation. Neuromuscular blocking agents should be avoided. Proper use of currently available sedative and analgesic techniques not only provides patient comfort but can actually decrease morbidity.

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Neurologic deficits are a major source of serious morbidity in patients resuscitated from cardiac arrest. Recent evidences support the hypothesis that accumulation of excitatory amino acids and overstimulation of their receptors in the brain tissue contribute to ischemic neuronal damage. In the present study, we measured concentrations of amino acid neurotransmitters, including glutamate and aspartate, in human cerebrospinal fluid (CSF) following cardiopulmonary resuscitation (CPR) to clarify whether CSF levels of excitatory amino acids reflect the global ischemic insults during cardiac arrest. In 11 post-CPR patients without any evidence of intracranial causes of cardiac arrest (the CPR group), CSF was sampled 2 to 12 hours following CPR. After deproteinization and storage at-80°C, derivatization, elution, and analysis of amino acids in CSF samples were performed by high-performance liquid chromatography. Sixteen patients scheduled for spinal anesthesia and elective surgery were regarded as normal control (the control group).
The results showed that glutamate and aspartate in the CSF of the CPR group significantly increased 3.6 and 5.7-fold com pared with fhose the control group. Taurine and alanine also significantly increased. Thus, in the present clinical study, we demonstrated elevations of neurotoxic glutamate and aspartate in CSF following CPR, which might relate post-CPR neurologic deficits.

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The aim of this experiment was to determine the influence of pH on MRSA growth. MRSA growth wau suppressed in acidic medium, and the degree of suppression paralleled the degree of acidity. The results showed that MRSA hardly grew in the media with a pH below 4, few cultures were identified at pH 2 and 3. A bacteriocidal effect was noted in the media with a pH below 3. At pH 5, cultures were markedly inhibited, and even at pH 6, culture failed to yield certain strains of MRSA.
The usefulness of antibiotics can not be denied, but proper implementation of infection control should be excuted to avoid the outbreaks of resistant pathogens. Although treatment with dilute hydrochloric acid (pH 2) may only be applicable in superficial infections such as MRSA colitis, it seems to be promising as an attempt of antimicrobial therapy without any induction of resistant strains.

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New indicators, Oxygen Cost of Breathing (ΔV_O2), Work of Breathing (WOBp), intrapreural Pressure Time Product (PTP) and P_0.1 were clinically examined to determine which of these indicators is the most specific and sensitive for predicting the outcome of weaning from mechanical ventilation. Twenty-three weanings were attempted and divided into a successful weaning group (Group-S) and a failed weaning group (Group-F). There were significant differences in Minute Volume, ΔV_O2, ΔV_CO2, WOBp, P_0.1, PTP, Lung Compliance and Intrinsic PEEP between the groups. ΔV_O2 and P_0.1 in particular, were statsitically significantly different in the two groups (ΔV_O2: 14.4±11.7 in Group-F VS. -7.7±9.6% in Group-S P<0.005, P_0.1: 4.9±1.6 in Group-F VS. 2.5±1.3cmH₂O in Group-S P<0.01) and 5% in ΔV_O2 and 3.5cmH₂O in P_0.1 are the Cutt-Off values for prediction of the success or failure of weaning trials. WOBp greater than 9 Joule min^-1 and PTP above 200cmH₂O sec min^-1 suggested difficulty in weaning from the ventilator. ΔV_O2 and P_0.1 are considered to be the most sensitive indicators, because in the group-F these indicators exhibited significant increases in the early stage of weaning from the ventilator.

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A case of hypercitrullinemia is reported. A 52-year-old woman was admitted to our hospital because of eating and sleeping disturbailces due to chronic intractable pain.
When aminoacid-containing hyperalimentation fluid was administerd to the patient, she fell into deep coma. She returned to consciousness when the infusion was discontinued, however, subsequent aminoacid-free hyperalimentation induced hyperglycemia again followed by unconsciousness.
Although it has already been reported in the literature that coma is triggered by aminoacid infusions in patients with hypercitrullinemia, we obtained new evidence that aminoacid-free, glucose-rich solutions also cause unconsciousness.
In this report, we discuss the possible mechanism of plasma ammonia level elevation in response to the administration of amino acids and/or glucose, and concluded that a cautious nutrition therapy plan, with frequent measurement of blood pH, ammonia and glucose levels, is mandatory.

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A case of MOF following the fume inhalation is reported. The clinical course and high concentrations of cadmium measured in the blood and urine samples (but low concentrations of silver, cupper and zinc) strongly suggested acute cadmium poisoning. Following early toxic signs resembling those of a common cold, toxicity advanced to include the acute respiratory distress syndrome, renal failure and hepatic dysfunction. The patient was treated with various active therapies including mechanical ventilation, artificial hemofration (CVVHF), plasma exchange (PE), and steroid and CaNa₂EDTA administration, and subsequently left the ICU on the 52nd ICU day, with mild renal dysfunction. Although the patient was in a semicomatous state in the eary stage of the clinical course, the possibility that it resulted from acute cadmium poisoning is unclear.

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