This book updates the previous edition, while expanding its remit by approximately one-third embracing new topics and introducing fresh authorship. The book is divided into 11 sections, the first 10 representing an organ system and the last miscellaneous topics, incorporating 62 chapters. A predominant American authorship is preserved but with wider geographical experience than before. Three new chapters on acupuncture, perioperative analgesia, and electroconvulsive therapy embellish this edition. Despite this diversity, the editors have managed to preserve a thematic approach to each chapter throughout the book. Clinically orientated chapters provide an initial brief case presentation before progressing to expound sequentially four essential aspects of the disorder being considered. These are: (i) the medical disease under review and its differential diagnosis; (ii) preoperative assessment, investigation, evaluation, and preparation of the patient; (iii) intraoperative anaesthetic management; and (iv) postoperative anaesthetic care. Within each chapter, issues are addressed by posing a series of ‘relevant questions’, which are then answered and include some appropriate references. Predominantly, graphical illustrations appear in some chapters. The editors have also incorporated some cross referencing of subject matter to other chapters. This pedagogic approach will no doubt appeal to many readers but I found the repeated use of abbreviations without adjacent definition and the tendency to quote predominantly American literature an irritation. I would strongly recommend to the editors that the next edition includes a list of abbreviations and their meanings! In my opinion, the ‘problem orientated’ approach fails to deliver in a number of chapters. For example, the chapter on magnetic resonance imaging (MRI) concentrates on a restless 2-yr-old child. The author glosses over paramount checks pertaining to the environment, instead concentrates on the virtues of the laryngeal mask in paediatrics and does not incorporate specific issues about anaesthesia for an adult requiring MRI. There was an apparent error in my copy of the book as both sections 4 and 6 have been classified as covering the endocrine system in the index and the section headings, when it appears section 4 should read the nervous system. I think the anaesthetist who enjoys theoretical information, presented in the context of a clinical condition, may be drawn to this style of writing. There is no doubt that most authors have attempted to provide comprehensive cover of their subject matter, albeit constrained by the ‘problem-orientated’ framework, highlighting domains of controversy while concentrating heavily on areas where consensus opinion has now been reached, for example, in the definitions of acute lung injury or adult respiratory distress syndrome. Moreover, the indexing system allows the reader to find specific subtopics easily, although I found it necessary to backtrack to original clinical problem sections in order to fully understand context. The pharmacological scope of this book is constrained to US medication, for example, atropine is covered in depth whereas glycopyrollate hardly features and is not indexed. Overall, I found the book well written and organized. However, although many elements are useful, there are others of less value. For its price, this book represents excellent value for money and while it will doubtless appeal to US anaesthesiologists in training it could find favour with other anaesthetists who like this style of presentation. After careful scrutiny, I remain concerned, however, that although the reader may be enriched in knowledge of the ingredients of an ‘anaesthetic cake’, they will remain oblivious to the wisdom required to bake it!

This timely concise textbook, written by a largely American, protagonistic, multi-authorship, heralds resurgence of interest in therapeutic mild hypothermia for cerebral ischaemia in the USA. The book includes contributions from both editors and is written with a preface, list of contents, list of contributors, 10 referenced chapters, and an index. The book comprises an introductory overview, five chapters outlining explanatory and pragmatic experimental hypothermia research, three chapters critiquing pragmatic clinical research studies of brain hypothermia, and a concluding review of hypothermia in clinical practice. Despite the ‘inevitable’ overlap of subject matter found in multi-author, ‘current review’ style textbooks, I found this book well written, referenced and indexed, and adequately illustrated. The reader will find excellent sections outlining some of the history of brain hypothermia research, and the dilemmas faced when trying to carry forward results of pre-clinical, multi-species, multi-model research into the clinical domain. Throughout the book, key differences between studies of mild, moderate, and deep hypothermia are emphasized. The introductory chapter provides a useful and concise ‘state of the art’ overview of the place of hypothermia in brain ‘protection’ for anyone studying for examinations, with the caveat that the book has clearly been written for the US market and therefore retains bias in favour of the hypothermic technique currently prevalent in that domain. Readers lacking background knowledge of current biochemical, inflammatory, and histological markers of ischaemic damage and genomics and proteomics may find some sections of the next five chapters devoted to pre-clinical research ‘hard going’. While the authors are to be congratulated for condensing a vast literature on experimental hypothermia, detailed critique of the numerous pre-clinical models and markers is sadly lacking. Instead, chapters devoted to experimental focal and global ischaemia and brain trauma overlap to excess, with considerable text devoted to their authors’ current research. Concise editing to avoid repetition and devotion of space to explaining the relative merits of different experimental designs and their intended clinical analogues would have greatly enhanced this section of the book and provided firmer foundations for subsequent clinical considerations. In stark contrast, later chapters devoted to clinical aspects of hypothermia in intensive care and the operating theatre are easier to read and can stand alone as relevant pre-clinical experimental data are discussed. Dilemmas of when?, where?, how?, how much? and how long? are reasoned concisely and fairly, with repeated frank admission that clinical efficacy in brain ischaemia and brain trauma remains unproven. The implications of inconsistencies in clinical trial design and influences of inadequate adherence to trial protocols on trial results are intelligently aired. There is inevitably some overlap of cited literature, with an ‘American’ bias, but the authors retain clarity over its application to the particular clinical setting being discussed. Overall, I enjoyed this short textbook but I am unsure to whom it is primarily aimed. Those familiar with the field may find its contents too basic and rather biased in favour of hypothermia. Those with interest in pre-clinical hypothermia research will be cognizant with the hoard of endpoints cited but may desire more detail and a wider reference base to that provided. Clinicians involved in clinical research will immediately sense its ‘American’ perspective and may be disappointed with the rather superficial way ‘lessons for the future’ are handled. Frankly, there are better reviews on the failings of clinical trial design and protocol implementation in the literature. This book may be of some interest to European intensivists and anaesthetists occasionally working in the fields of brain trauma, subarachnoid haemorrhage, ischaemic stroke, and resuscitation who wish to update themselves on current thinking on hypothermia and brain ischaemia. However, given the recent publication of excellent reviews on this subject I could not recommend European readers to purchase this book because of its hefty price.

Objectives : To describe risk factors for the development of acute renal failure (ARF) in a population of intensive care unit (ICU) patients, and the association of ARF with multiple organ failure (MOF) and outcome using the sequential organ failure assessment (SOFA) score. Design : Prospective, multicenter, observational cohort analysis. Setting : Forty ICUs in 16 countries. Patients : All patients admitted to one of the participating ICUs in May 1995, except those who stayed in the ICU for less than 48 h after uncomplicated surgery, were included. After the exclusion of 38 patients with a history of chronic renal failure requiring renal replacement therapy, a total of 1411 patients were studied. Measurements and results : Of the patients, 348 (24.7 %) developed ARF, as diagnosed by a serum creatinine of 300 μmol/l (3.5 mg/dl) or more and/or a urine output of less than 500 ml/day. The most important risk factors for the development of ARF present on admission were acute circulatory or respiratory failure; age more than 65 years, presence of infection, past history of chronic heart failure (CHF), lymphoma or leukemia, or cirrhosis. ARF patients developed MOF earlier than non-ARF patients (median 24 vs 48 h after ICU admission, p < 0.05). ARF patients older than 65 years with a past history of CHF or with any organ failure on admission were most likely to develop MOF. ICU mortality was 3 times higher in ARF than in other patients (42.8 % vs 14.0 %, p < 0.01). Oliguric ARF was an independent risk factor for overall mortality as determined by a multivariate regression analysis (OR = 1.59 [CI 95 %: 1.23–2.06], p < 0.01). Infection increased the risk of death associated with all factors. Factors that increased the ICU mortality of ARF patients were a past history of hematologic malignancy, age more than 65 years, the number of failing organs on admission and the presence of acute cardiovascular failure. Conclusion : In ICU patients, the most important risk factors for ARF or mortality from ARF are often present on admission. During the ICU stay, other organ failures (especially cardiovascular) are important risk factors. Oliguric ARF was an independent risk factor for ICU mortality, and infection increased the contribution to mortality by other factors. The severity of circulatory shock was the most important factor influencing outcome in ARF patients.

The injured brain may be damaged by primary impact, secondary injury from secondary damage due to initiation of destructive inflammatory and biochemical cascades by the primary injury or secondary ischemic injury following secondary insults that initiate or augment these immunological and biochemical cascades. Cerebral ischemia will arise whenever delivery of oxygen and substrates to the brain fall below metabolic needs. Many factors lead to the development of secondary insults to the injured brain during initial resuscitation, transport, surgery, and subsequent intensive care. Continuous monitoring of cerebral oxygenation (jugular oximetry, brain tissue PO2) and cerebral blood flow velocity (transcranial Doppler ultrasonography) in patients with brain trauma reveals multiple episodes of transient hypoperfusion with an adverse relationship between incidence and outcome. Secondary brain insults arise through systemic or intracranial mechanisms that reduce cerebral blood flow from compromised CPP, vascular distortion or cerebrovascular narrowing or lower oxygen delivery from hypoxemia associated with airway obstruction, pulmonary pathology, or anemia. Secondary brain ischemia remains a common pathway to secondary brain damage in most critically ill neurosurgical patients. In the future prevention of secondary brain injury may well hinge on giving a cocktail of novel agents that modify destructive biochemical and inflammatory pathways, each having a potential therapeutic window possibly in a subgroup of patients. To date, phase 3 clinical trials of several agents including PEGSOD and tyrilizad mesylate have failed to show relevant efficacy after brain trauma or subarachnoid hemorrhage. The therapeutic role of calcium channel blockers in traumatic subarachnoid hemorrhage is currently under investigation following the results of subgroup metaanalysis. Several phase 3, NMDA receptor antagonist studies are underway in brain trauma with results expected soon. Although we know that secondary insults promote excitotoxic secondary brain damage there is currently no pharmacological intervention with proven efficacy and, therefore, detection and correction of secondary insults appear to offer the best therapeutic strategy. After brain trauma, systemic hypotension, compromised CPP, raised ICP, elevated temperature, hypoxemia, and jugular bulb venous desaturation are associated with poor prognosis. Clinical trials of moderate hypothermia following brain trauma are ongoing. Following adult brain trauma maintenance of CPP above at least 65 mmHg (probably > 40 mmHg in children below 8 years) seems important to improve outcome indicating the need for continuous ICP monitoring during intensive care of brain-injured patients.

BACKGROUND:Patients with symptomatic internal carotid artery (ICA) stenosis greater than 70 per cent in association with a contralateral ICA occlusion may have an increased risk of stroke following carotid endarterectomy. Such patients might benefit from the theoretically shorter ischaemic time offered by carotid angioplasty and stenting.METHODS:Nine patients who underwent carotid angioplasty and stenting were monitored using near-infrared spectroscopy, continuous jugular venous oximetry and transcranial Doppler ultrasonography to detect both haemodynamic ischaemia and embolic events.RESULTS:Significant ischaemia occurred in four of the nine patients once the stenosis had been crossed by the guidewire (spectroscopy and oximetry). Inflation of the angioplasty balloon resulted in a brief period of ischaemia and showers of emboli in all patients (ultrasonography) and this persisted for more than 3 min after balloon deflation in three patients. One patient had a major disabling stroke due to ICA thrombosis.CONCLUSION:Angioplasty and stenting in these high-risk patients may not confer any advantage over conventional surgery in terms of both haemodynamic ischaemia and embolization.

Objectives: To examine the effects of either regional (RA) or general (GA) anaesthesia upon parameters of cerebral metabolism (near infrared spectroscopy, continuous jugular venous oximetry) during carotid endarterectomy.Design: Prospective, non-randomised, observational study.Materials: Sixty-Jive consecutive patients (33 RA;32 GA) undergoing carotid endarterectomy.Methods: (i) Near infrared spectroscopy: measurement of concentrations of cerebral oxyhaemoglobin (HbO(2), deoxyhaemoglobin (HHb) and oxidised cytochrome oxidase (caa(3)). (ii) Continuous jugular venous oximetry: O-2 saturation of jugular venous blood (S)vO(2)). (iii) Stump pressure in internal carotid artery.Results: A reduction in SJvO(2) (XA: 13% (95% CI-3 to 29%) GA: 9% (95% CI-2 to 20%), p < 0.08) and a fall in caa(3) levels (RA vs. GA: 25/31 vs. 19/31, p = 0.2) was move likely in patients given a XA following application of the carotid clamps. When HbO(2) and caa(3) did fall however spontaneous recovery occurred more often (RA vs. GA;caa(3): 18/25 vs. 5/19, p<0.005; HbO(2): 30/31 vs. 4/28, p<0.001).Conclusions: Although GA may offer a degree of cerebral protection by reducing cerebral metabolic rate (lower falls in SJvO(2) and caa(3)) XA preserved cerebral autoregulation as judged by the spontaneous recovery in caa(3) and HbO(2) levels.

Summary Twenty-six patients requiring clipping of cerebral aneurysms were anaesthetized with propofol, alfentanil and atracurium infusions and their lungs ventilated mechanically to hypocapnia (3.4– 4.5 kPa). was measured continuously with an Oximetrix fibreoptic oximetry catheter. Normovolaemia was maintained by observing the response of mean arterial pressure (MAP) and central venous pressure (CVP) to fluid administration. The response of to increased MAP was noted and the lactate oxygen index (LOI) calculated at regular intervals. measurements indicated a critical MAP of between 80 and 110 mm Hg in nine patients, and one patient had a persistently low value despite an MAP of 110 mm Hg. An increase in MAP was associated with an increase in in 19 patients (P 0.001). When the effects of changes in were eliminated, this change was still significant (P 0.004) (n 9). Patients with an LOI 0.08 at any time during the procedure had a worse initial outcome (within the first day) (P 0.02) than patients who had a normal LOI throughout. Long-term outcome was similar to those with a normal LOI. Increasing MAP did not have a consistent effect on LOI. Jugular bulb cannulation to assess hypoperfusion in conjunction with lactate measurements and calculation of LOI provide useful information on which to base the intra- and postoperative management of patients with subarachnoid haemorrhage. (Br. J. Anaesth. 1995; 75: 527–530)

Twenty-six patients requiring clipping of cerebral aneurysms were anaesthetized with propofol, alfentanil and atracurium infusions and their lungs ventilated mechanically to hypocapnia (3.4-4.5 kPa). SjO2 was measured continuously with an Oximetrix fibreoptic oximetry catheter. Normovolaemia was maintained by observing the response of mean arterial pressure (MAP) and central venous pressure (CVP) to fluid administration. The response of SjO2 to increased MAP was noted and the lactate oxygen index (LOI) calculated at regular intervals. SjO2 measurements indicated a critical MAP of between 80 and 110 mm Hg in nine patients, and one patient had a persistently low SjO2 value despite an MAP of 110 mm Hg. An increase in MAP was associated with an increase in SjO2 in 19 patients (P < 0.001). When the effects of changes in PaCO2 were eliminated, this change was still significant (P = 0.004) (n = 9). Patients with an LOI > 0.08 at any time during the procedure had a worse initial outcome (within the first day) (P < 0.02) than patients who had a normal LOI throughout. Long-term outcome was similar to those with a normal LOI. Increasing MAP did not have a consistent effect on LOI. Jugular bulb cannulation to assess hypoperfusion in conjunction with lactate measurements and calculation of LOI provide useful information on which to base the intra- and postoperative management of patients with subarachnoid haemorrhage.

Primary traumatic brain damage may be compounded by secondary pathophysiological insults that can occur soon after trauma, during transfer to hospital or subsequent treatment of the head-injured patient. The aim of this prospective study was to quantify the burden of a wide range of secondary insults occurring after head injury and to relate these to 12-month outcome. In 124 adult head-injured patients studied during intensive care using a computerized data collection system, < or = 14 clinically indicated physiological variables were measured minute-by-minute. Verified values falling outside threshold limits for > or = 5 min, as defined by the Edinburgh University Secondary Insult Grading scheme, were analysed by insult grade and duration. A greater incidence of secondary insults was detected than previous studies have indicated. Insults were found in 91% of patients and occurred in all severities of head trauma, at all ages, and at every level of Injury Severity Score (ISS). The cumulative durations were much greater than previously recorded although 85% of the total time was at the least severe grade. Short duration insults were common. In 71 patients, in whom 8 insults could be assessed (intracranial pressure, arterial hypo- and hypertension, cerebral perfusion pressure, hypoxemia, pyrexia, brady- and tachycardia), outcome at 12 months was analysed using logistic regression to determine the relative influence of age, admission Glasgow Coma Sumscore, ISS, pupil response on admission, and insult duration on both mortality and morbidity. The most significant predictors of mortality in this patient set were durations of hypotensive (p = .0064), pyrexic (p = .0137), and hypoxemic (p = .0244) insults. When good versus poor outcome was considered, hypotensive insults (p = .0118) and pupil response on admission (p = .0226) were significant.

Previous studies have suggested that only a small proportion (< 15%) of comatose head-injured patients whose initial computerized tomography (CT) scan was normal or did not show a mass lesion, midline shift, or abnormal basal cisterns develop intracranial hypertension. The aim of the present study was to re-examine this finding against a background of more intensive monitoring and data acquisition. Eight severely head-injured patients with a Glasgow Coma Scale score of 8 or less, whose admission CT scan did not show a mass lesion, midline shift, or effaced basal cisterns, underwent minute-to-minute recordings of arterial blood pressure, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) derived from blood pressure minus ICP. Intracranial hypertension (ICP > or = 20 mm Hg lasting longer than 5 minutes) was recorded in seven of the eight patients; in five cases the rise was pronounced in terms of both magnitude (ICP > or = 30 mm Hg) and duration. Reduced CPP (< or = 60 mm Hg lasting longer than 5 minutes) was recorded in five patients. Severely head-injured (comatose) patients whose initial CT scan is normal or does not show a mass lesion, midline shift, or abnormal cisterns nevertheless remain at substantial risk of developing significant secondary cerebral insults due to elevated ICP and reduced CPP. The authors recommend continuous ICP and blood pressure monitoring with derivation of CPP in all comatose head-injured patients.

Transcranial doppler (TCD) allows repeated or continuous non-invasive measurement of blood flow velocity in major intracranial vessels [1]. Flow velocity is proportional to cerebral blood flow (CBF) and inversely related to cross-sectional area of the insonated vessel. Increased blood flow velocity may therefore occur in association with elevated CBF or reduced vessel diameter. Both situations are known to occur following brain injury [6, 7]. The present study aims to examine the relationship between increased blood flow velocity and subsequent development of ischaemic neurological complications following severe brain injury.

TRANSCRANIAL DOPPLER MEASUREMENTS of blood flow velocity in the middle cerebral artery were made during treatment of raised intracranial pressure (ICP) in 22 patients with severe brain injury. Twenty patients also had continuous measurement of arterial and jugular bulb venous oxygen saturation (SJO2). The transcranial Doppler parameters studied included both mean flow velocity and pulsatility index (PI). Successful treatment was defined as a reduction of ICP to less than 20 mm Hg with improvement or preservation of cerebral perfusion pressure (CPP) above 60 mm Hg. Successful therapy was associated with a significant rise in SJO2 and reduction of cerebral arteriovenous oxygen content difference (AVDO2) and PI only when the pretreatment CPP was less than 60 mm Hg. An increase in CPP beyond 70 mm Hg did not further improve cerebral oxygen delivery and PI, suggesting that autoregulation became a factor above this CPP threshold. Treatment failure during administration of hypnotic drugs resulted in a reduction in arterial pressure, CPP, SJO2, and mean velocity and in an increase in PI and AVDO2, despite a decrease in ICP. CPP is the most important parameter to monitor during ICP therapy. It should be maintained above 70 mm Hg in patients with severe brain injury.

During intensive care management of severely head injured patients undergoing IPPV sedation may be administered, to obtund paroxysmal ICP rises during therapeutic manoeuvres, and to treat persistently elevated ICP. The recently reintroduced intravenous anaesthetic, 2, 6 di-isopropyl phenol (Propofol), has attracted attention as a sedative in ICU both for general critical care patients and head injured patients [1, 3]. Propofol causes a decrease in CBF and CBV and is therefore of potential value in treatment of intracranial hypertension after severe head injury [6, 8]. However, there is concern that CBF is reduced more than CMR resulting in desaturation of cerebral venous blood [7, 8].

The Camino pressure transducer is accurate experimentally over a range of clinically relevant intracranial pressures (ICPs). Three clinical studies have shown that intraparenchymal pressure mirrors intraventricular pressure. In two a different type of transducer was used, and one was a mixed animal and human study [3, 4, 2]. This study compares intraparenchymal pressure, measured with a Camino fibre-optic transducer, with intraventricular pressure, using a fluid filled catheter, in unconscious head injured patients and evaluates the clinical efficacy of the Camino system.

Ischaemic brain damage is present in over 90% of patients suffering from fatal head injury. Early detection and treatment of ischaemia may improve outcome after head trauma. Monitoring of blood flow velocity of the middle cerebral artery by noninvasive transcranial doppler ultrasound provides an alternate means of identifying cerebral ischaemia.

Fibreoptic reflection oximetry allows continuous in-vivo estimation of jugular venous oxygen saturation. In combination with pulse oximetry the oxygen extraction ratio SaO2-SjO2/SaO2 can be derived enabling identification of states of global luxury perfusion, normal coupling of global cerebral blood flow with global cerebral metabolism, global cerebral hypoperfusion and global cerebral ischemia. Several technical difficulties may arise affecting the accuracy of SjO2 recordings which must be recognised by the clinician before medical intervention is contemplated.

After head-injury cerebral metabolic rate (CMRO2) is reduced [2]. Cerebral blood flow (CBF) may be increased, normal or decreased. According to the Fick Principle, the relationship between global CMRO2 and CBF can be described by measurements of the arterio-jugular venous oxygen content difference (AJDO2). Thus, AJDO2 = CMRO2/CBF. The AJDO2 = Haemoglobin × 1.39 × (Arterial oxygen saturation — Jugular bulb venous oxygen saturation)/ 100. It is now possible to monitor the Jugular bulb venous oxygen saturation (SjO2) continuously using the “Oximetrix 3” system with a fibre-optic catheter placed high in the jugular bulb [1, 3]. If arterial oxygen saturation (SaO2), haemoglobin concentration and the position of the haemoglobin dissociation curve remain constant, SjO2 is proportional to CBF/CMRO2 · SjO2 above 75% represents luxury perfusion, while below 54% increased oxygen extraction signifies hypoperfusion [4]. This study examines the effects of both hypnotic and osmotic treatments of raised intracranial pressure (ICP) on cerebral perfusion pressure (CPP) and SJO2 after severe head injury.

Uncontrolled intracranial hypertension remains an important cause of mortality and morbidity after severe brain injury. Controversies surrounding ICP treatment include the relative importance of lowering ICP or preserving CPP although the optimal level of CPP in severely brain injured patients is not known.