Long-term follow-up There would seem to be little point undertaking longer term follow-up o f ICU patients unless appropriate help can be offered where needed. For many patients, the simple provision of advice about the speed of recovery combined with a stepped care approac h to assessment and care plan- ning is suf \201 cient to meet their needs. Physical recove ry after discharge from the ICU is, on the whole, excellent. However, for some patients, pa rticularly those aged >50yrs and those staying longer in ICU, physical recovery from critic al illness is prolonged, in some cases taking >1yr. Loss of lean body mass, mainly skeletal muscle, occurs in the catabolic phase of illness, leading to profound muscle weakness; the diaphragm and other skeletal muscle of the respiratory system are not protected from this. Rebuilding of lost muscle occurs slowly and requires both physical activity and good nutri tion. In addition, some patients may develop critical illness polyneuropathy (CIP), which i s characterized by axonal degeneration of motor nerves. Longer stay patients often report d if \201 culty climbing the stairs even 2 months after ICU discharge. They may have dif \201 culty walking outdoors and often tend to continue using a wheel- chair. Poor muscle st rength and easy fatigability account for some of the dif \201 culty in getting up if they fall. This can lead to a feeling of vulnerability and fear of falling. Psychological issues during recovery The psychological sequelae of critical illness have on ly just begun to be recognized. There may be profound long- term psychological and psychoso cial effects. An early questionnaire study of 3655 patients found a high incidence of psych osocial dysfunction, particularly in younger individuals. High levels of anxiety, depressio n, and post- traumatic stress disorder (PTSD) have also been reported. Such problems can ha ve a signi \201 cant long-term detrimental impact on both the patients \200\231 and their family \200\231s quality of life. Many patients are amnesic for parts of their time in ICU, as well as regarding events prior to admission. A delusional memory of hallucinations, nig htmares or paranoid delu- sions recalled from the time in ICU may be the traumatic event th at precipitates the development of PTSD. Recall of delusional memories may be increased in patients who have a previous history of psychological problems before admission to ICU. Cognitive de \201 cits following critical illness It has been shown that signi \201 cant cognitive de \201 cits may remain after critical illness. At present, it is unclear whethe r these cognitive de \201 cits are permanent, due to neurological 587 CHAPTER 33.18 Critical care follow-up ICU diaries The patients \200\231 amnesia for the time in the ICU can hinder their recovery , as many patients do not understand how ill they have been and consequently the length of time it will take them to get back to normal. ICU diaries have become increasingly popular. These diaries are a day by day record of the patient \200\231s stay in ICU, written in eve ryday language by the ICU staff and the patient \200\231s family. It also includes photogra phs taken at points of change in the patient \200\231s illness. These diaries are popular w ith patients and seem to help them rebuild a memory of their illness. Where the patient has periods of agitation, confusion or seemed to be hallucinating, this is recorded in the dia ry and seems to help the patient to identify the point at which delusional memories may hav e occurred. An example of this is a patient whose memory for ICU was being in a \201 re a nd having to be rescued by \201 remen. This memory kept replay- ing as a \202 ashback a nd hindering her recovery. When she read her diary she discovered she had gone to theater u rgently and she decided that this was where her delu- sional memory had come from. Each tim e she had a \202 ash- back of this memory she read her diary to put it in context. An ICU diary is a simple therapy that has the potential to reduce the psychological impact of suc h memories, and is undergoing further research to examine its impact on PTSD symptoms. PTSS-14 (see www.i-canuk.org.uk for copies of ques- tionnaires). However, it is important t hat staff have some training in PTSD assessment and can recognize how the patient is coping . Some individuals will be able to cope with quite high levels of symptoms, and feel that t hey can manage on their own. These individuals can be reassessed after 1 month. The provis ion of counseling, psychotherapy or psychology services targeted at post-ICU patients is al most non- existent in the UK. The growth of counseling services for patients diagnosed with cancer has arisen from the recog- nition of the psychological impact of such a severe illn ess. Perhaps critical care providers need to think along similar lines because of the high risk of psychological effects for both patients and families following an illness in ICU. T he correlation between high levels of PTSD-related symptoms in patients and their families points to the need for family therapy. Conclusion The physical, psychological and cognitive sequelae of critical illness can be an enormous burden on both patients and their families. Care must continue long after dischar ge from the ICU, and a prolonged recovery time can be expected. The pathway of care offered to patients after such a severe illness needs to be improved to ensure that patients reach their full recovery potential. ICU physicians, nurses, physiotherapists and other professi onals have important roles to play in the management of patients after discharge. Treating PTSD Patients can be overwhelmed by their PTSD symptoms and unable to engage with further medical care or return to their normal life. They usually do not seek help because of the overwhelming nature of their symptoms, and there is an onus on staff following-up th ese patients to recognize and refer patients for treatment. Although the incidence of PTSD amongst ICU patients varies considerably in different studies, possibly due to differences in case mix, and may have been exaggerated in some studies due to the tools used, it has a major impact on quality of life after critical ill- ness. Two recent sets of treatment guid elines emphasize the need to screen individuals after a traumatic event and refer those wit h high levels of symptoms for further professional help. Where patients have moderate sympt oms which they are coping with, \200\230watchful waiting \200\231 is recommended, as many patients will \201 nd their own way of working through their traumatic memories. Where PT SD symptom levels are very high or the patient is not coping, then they should be referred for professional help. Treatment guidelines pub- lished by the UK NICE make clear that indi viduals suffering from PTSD should be given information on common reac- tions to traumatic events, including the symptoms of PTSD, its course and treatment. ICU patients should be sc reened for PTSD, and to facilitate this there may be a role for the use of PTSD screening t ools, such as the Impact of Event Scale, the PTSS-10 or Further reading B ckman CG, Walther SM. Use of a personal diary written on the ICU during critical illness. Intensive Care Med 2001; 27: 426 \200\2239. Hopkins RO, Weaver LK, Collin gridge D, et al. Two-year cognitive, emotional, and quality-of-life outcomes in acute respi ratory distress syndrome. Am J Respir Crit Care Med 2005; 171: 340 \200\2237. Jones C, Back man C, Capuzzo M, et al. Precipitants of post- traumatic stress disorder following intensiv e care: a hypothesis generating study of diversity in care. Intensive Care Med 2007; 33: 97 8 \200\22385. Jones C, Griffiths RD. Identifying post intensive care patients who may need physical rehab ilitation. Clin Intensive Care 2000; 11: 35 \200\2238. Jones C, Skirrow P, Grif \201 ths RD, et al. Rehabilitation after critical illness: a rand omized, controlled trial. Crit Care Med 2003; 31: 2456 \200\22361. National Institute for Health and Clinical Excellence (NICE). Post- Traumatic stress disord er (PTSD): the management of PTSD in adults and children in primary and secondary care. Cli nical Guideline 26. London: NICE, 2005. Available at: www.nice. org.uk/CG026NICEguideline 588 J CARLET Managing antibiotic resistance Acquisition of resistant strains in the ICU: mechanisms Many factors explain that hospitals , in particular ICUs, are experimental factories for creating and amplifying resistance: wi despread usage of broad-spectrum antibiotics, often in combination, in the presence of extr emely sick patients who would have died 10 or 20yrs ago, with very severe underlying diseas es or prolonged ICU stay, and/or very high and permanent risk for cross-transmission of the microorganisms via either the hands of the healthcare providers, frequent transportation t o the X-ray depart- ment or the operating rooms, and the environment. The shorter the lengt h of stay, the lower the incidence of noso- comial infections and antibiotic resistance. It has been demonstrated that there is an \200\230inoculum \200\231 effect in ICUs regarding antibiotic-resistant microorganisms. When colonization pressure with resistant strains is above a certain level, then the risk of cross-transmission becomes extremely high and very dif \201 cult to overcome. Thus, in countries with a high endemic level of resistance, in particular for MRSA, Acinetobacter or Pseudomonas spp., there is a real risk of antibiotic \200\230spiral \200\231. A very strong and sustained program is mandatory to overcome this problem. Several countries, such as Denmark have been successful in slowly decreasing resi stance levels. Resistance to antibiotics is an international concern and has been an increasing problem ov er years. Nowadays reistance is so high in several countries that some infec- tions are bec oming almost impossible to treat. The threat of returning to the pre-antibiotic area is gre ater than ever. The issue is even more critical in the intensive care setting. More than 60 % of ICU patients receive antibiotics at some time during their stay, and cross-transmissio n of resistant microorganisms is dif \201 cult to prevent when patients are extremely sick and stay for long periods of time. When quality of care becomes suboptimal, in particular when ICU worker ratios are too low, the risk is considerably higher. Septic shock may be du e to resistant strains, and mortality is heavily in \202 uenced by the delay in providing appropriate antibiotic therapy. Multi-resistance to antibiotics in the ICU setting: epidemiology Resistance to antibiotics is extremely high in the ICUs of many countries. This is the case for both Gram-positive co cci such as MRSA and Gram-negative bacteria. A serious concern is represented by community- acquired MRSA, highly prevalent in many countries, including the USA, as well as glycopepti de-intermediate Staphylococcus aureus (GISA) and VRE. This is also true for Gram-negative b acte- ria such as E. coli and other enterobacteriacae harboring extended spectrum lactamase s, or Acinetobacter or Pseudomonas spp. sometimes resistant to almost every antibiotic exce pt colimycin. However, it is it of great interest, although imperfectly understood, that se veral countries, such as The Netherlands or the Scandinavian countries and to a lesser exte nt Switzerland and Canada, have been successful to date in maintaining very low levels of r esistance, even in the ICU. MRSA remains very rare in those countries. It seems, however, t hat even in those few and \200\230happy \200\231 or clever countries some resistant strain s, coming from outside, have been able to induce epidemic outbreaks and that the global lev el of resistance is increas- ing slowly. The attributable mortality of resistance to antibi otics in the ICU remains a very controversial issue. It is, however, widely accepted that i nappropriate initial antibiotic therapy is responsible for a dramatic overmortality. This s upports the concept discussed further here that both optimizing the empiric antibiotic ther apy and reassessing this therapy at day 2 or 3, when bacteriological data are back (some- t imes called \200\230de-escalation \200\231 or \200\230streamlining \200\231), is of para- mount importance . Surveillance of resistance in the ICU is more than ever a public health priority, and indicators should be decided in each hospital according to local epidemiolog y. MRSA is considered as the main public enemy in many countries. The increasing descriptio n of virulent MRSA strains in the community, carrying the Panton \200\223Valentine leucocid in toxin, and the presence of \201 ve strains of S. aureus fully resistant to glycopeptid es are strong arguments for screening for MRSA at ICU admission and for implementing isolat ion procedures in a systematic way. The topic remains highly controversial, however, and Eu ropean projects such as MOSAR are underway. Therapy for multi-resistant bacteria infections in the ICU Treating infections due to multi -resistant bacteria is very dif \201 cult, and a strong cooperation with microbiologists o r infectious disease specialists is key. A combination therapy is often helpful to widen th e target of the chosen antibiot- ics. It is important to be active against both resistant m icro- organisms and sensitive ones. For example, it has been shown that vancomycin therapy was suboptimal to treat susceptible S. aureus infections. A combination of vancomy- cin and nafcillin could be necessary in those settings. The dosage of antibiotics must be carefull y chosen. In general, initial doses must be high enough to provide appropriate serum and ti ssue levels. Regular assessments of plasma levels are often mandatory, for glycopeptides or aminogly- cosides, but also for cephalosporins, quinolones, penicillins or penems in the m ost severe cases. In some infections due to pan-resistant Gram-negative microorganisms resp onsible for recent epidemics in sev- eral countries, we have often come back to \200\230ol d \200\231 antibiotics such as colistin. This drug, as well as aminoglycosides, has been us ed in aerosols with promising results. There are very few new compounds active against very resistant Gram-negative bacteria, and this is very worrying. However, the real drama is th at we have very few antibiotics in the \200\230pipeline \200\231 active against resistant Gram-negative organisms. If clinicians decide to use carbapenems to treat commu- nity-acqui red infections due to E. coli because of the threat of ESBL strains, we will be left with n othing to treat nosocomial and resistant infections. Auditing the antibiotic usage in the I CU must be performed on a routine basis and should be used as a quality indicator. Can we prevent resistance to antibiotics? Two complementary programs have to be conducted s imultaneously: prudent and rational use of antibiotics and 589 CHAPTER 33.19 Managing antibiotic resistance monotony and pressure. We do not know for now if those antibiotics, in particular those whi ch belong to the new classes, will exert less resistance than \200\230old \200\230compoun ds, over the short and long term. Unfortunately as mentioned above, we have very few new co mpounds to treat infections due to multi-resistant Gram-negative microorganisms, and it is more than likely that resistance to carbapenems, or even colistin will increase in the next few years. Antimicrobials involved with innate immunity, such as defensins, either systemi cally or locally, need to be tested, as well as vegetable compounds such as compo- nents of green tea which exert a marked antimicrobial effect. prevention of cross-transmission of resistant strains. This will be a real challenge for th e next decades. The program should be hospital wide and not only localized in the ICU, beca use microorganisms have no boundaries. Guidelines are important but, even if inter- nationa l ones are sometimes useful, most of the time they should be tailored according to local ep idemiology. It is a key element not only to optimize therapy but also to minimize useless a ntibiotic therapies and help people in reassessing and stopping therapy. Educational progra ms and audit are important . The way people that diagnose infections in critically ill pati ents can probably have a profound impact upon antibi- otic usage and pressure. Any usage of useless antibiotics in the ICU setting can be considered as a non-quality indica- tor, as emphazised in the recent Surviving Sepsis Campaign Guidelines. In the same way, duration of antibiotic therapy is very porbably a key component of resistance pressure, and everything must be done to keep therapy as short as clini- cally and scienti \201 cally possible. Da ta are still scarce in this respect, and new studies should be encouraged. New diagnostic t echniques, such as real-time PCR (or microarrays) might dramatically improve the time neede d for diagnosis and thus the appropriateness of initial thera- pies, and might positively i n \202 uence antibiotic usage in the very near future. Cycling or rotation of antibiotics has been the subject of an extensive and controversial literature in the past few years. Re cent papers indicate the ef \201 cacy of this strategy on the incidence of nosocomial infe ctions and resistance to antibiotics in the short term, either in the ICU or even in non-IC U wards. Most people, at least in Europe, prefer treating patients \200\230 la carte \200\231, according to many factors such as pre-existing diseases (COPD), severity of illne ss, use of antibiotics in the past few days or weeks, length of stay in the hospital, long- term care facilities or the ICU, before the occurrence of infection. We must both provide t he best antibiotic up-front, in particular to the most severe cases, and minimize antibioti c resistance. The two objectives are not mutually exclusive and we can consider that qualit y of antibiotic therapy is a \200\230two-step contract \200\231. The \201 rst contract i s with the patient, the second with the ecology and with society. It is extremely urgent to implement the de-escalation strategy worldwide, and European or international professional societies have a special responsability to help in this respect. Conclusion Therapy of severe infections due to multi-resistant infec- tions remain a real c hallenge. Resistance to antibiotics in the hospital, particularly in the ICU, is a growing concern everywhere. Some countries have been able to maintain a very low level both in the community and in hospitals. In order to be successful, a strong and patient program combini ng a prudent and intelligent usage of antibiotics and an \200\230obsessional \200\231 prev en- tion of cross-transmission, in particular using hand decon- tamination with hand rub al coholic solutions, is needed. Some controversies persist regarding MRSA screening. Regular symposia should be organized, and knowledge should be disseminated. Since resistance is now an inter- national concern, a strong cooperation between countries is needed. We do not kn ow if the availability of new compounds will help in overcoming this important public healt h problem. Initial empiric antibiotic therapy must be efficient. Combination therapy remain s controversial. A systematic de-escalation strategy must be implemented in every hospital, and national or European professional societies have a special responsibility in promoting those programs. Further reading Borg MA. Bed occupancy and overcrowding as determinant factors in the incid ence of MRSA infections within general ward settings. J Hosp Infect 2003; 54: 316 \200\2238 . Chambers HF. Community-associated MRSA \200\224resistance and virulence converge. N Engl J Med 2005; 352: 1485 \200\2237. Cunningham R, Jenks P, Northwood J, et al. Effect of MRSA trans- mission of rapid PCR testi ng of patients to critical care. J Hosp Infect 2007; 65: 24 \200\2238. Gillet Y, Issartel B, Vanhems P, et al. Association between Staphylococcus aureus strains c arrying gene for Panton \200\223Valentine leukocidin and highly lethal necrotising pneumoni a in young immunocompetent patients. Lancet 2002; 359: 753 \200\22359. Could the use of new antibiotics reduce antibiotic resistance in the hospitals? Antibiotic \200\230monotony \200\231 has probably been an important factor in the increase in resista nce, in particular regarding the extensive international usage of glycopeptides, both syste mically and locally, and of quinolones. The widespread usage of third-generation cephalospo rins has been accused of promoting VRE as well as MRSA, or resistant enterobac- teriaecae. Hopefully, we have now a few new antibiotics to treat Gram-positive infections such as line zolid, synercid, ketolides, new penems and tigecycline. and several others will be introduc ed. Thus, the armamentarium of effective drugs will be somewhat broader for therapy of resi stant Gram-positive infections , and this, in principle, could decrease antibiotic Huskins WC, O \200\231Grady NP, Samore M. Design and methodology of the Strategies to Reduc e Trasmission Antimicrobial Resistant Bacteria in Intensive Care care Units (STAR-ICU) tria l. Infect Control Hosp Epidemiol 2007; 28: 245 \200\2236. Meyer E, Schwab F, Gastmeier P, et al. Stenotrophomonas maltophilia and antibiotic use in G erman intensive care units: data from Project SARI (Sur veillance of Antimicrobial Use and Antimiocrobial Resistance in German Intensive Care Units). J Hosp Infect 2006; 64: 238 \200 \22343. Peres-Bota D, Rodriguez H, Dimopoulos G. Are infections due to resistant pathogens associat ed with a worse outcome in critically ill patients? J Infect 2003; 47: 307 \200\2231. Vincent JL, Bihari DJ, Suter PM, et al. The prevalence of nosocomial infection in intensive care units in Europe. Results of the European Prevalence of Infection in Intensive Care (E PIC) Study. EPIC International Advisory Committee. JAMA 1995; 274: 639 \200\22344. This page intentionally left blank 591 Appendix Respiratory physiology 592 592 APPENDIX Respiratory physiology The symbols used in respiratory physiology are important in de \201 ning what they are des cribing. Please be aware that the literature is not as consistent as it might be in using t hese symbols. 1. Symbols. Primary/large capitals for physical amounts/quantities C Content of gas in blood D Diffusing capacity F Fractional concentration in dry gas F Frequency of r espiration (breaths/min) P Pressure or partial pressure \231Q Volume of blood \231V Volum e of blood per unit time R Respiratory exchange ratio S Saturation of hemoglobin with O2 3. Criteria for acute lung injury; 1. Acute onset of impaired oxygenation 2. Severe hypoxaemia de \201 ned; PaO2 to FIO2 ratio of \211 40 ( using kPa ) or \211 300 (in mmHg) 3. Bilateral diffuse in \201 ltrates on chest Xray 4. Pulmonary wedge pressure \211 18 m mHg to exclude a cardiogenic cause. 4. Bohr \200\231s equation de \201 nes physiological dead space. PaCo2 \200\223 P ECO2 PaCO2 VD = VT 5. Alveolar PO2 in its simplest form is PaCo2 R = PIO2 \200\223 PAO2 Secondary/ smaller capital ( gas phase) is usually location and quantity A Alveolar B Barom etric D Dead space I Inspired E Expired T Tidal Examples. Arterial oxygen saturation SaO2 . Alveolar par- tial pressure of oxygen PAO2. Fractional inspired oxygen FIO2 Secondary symb ols for blood phase a arterial c capillary c end-capillary i ideal v venous mixed venou s \200\223 above any symbol denotes a mean value . above any symbol denotes a value per un it time f frequency Examples. Arterial oxygen saturation SaO2. Alveolar par- tial pressure of oxygen PAO2. Fractional inspired oxygen FIO2 2. Lung volumes Adult values where R is the respiratory quotient usually around 0.8. From this the alveolar arterial gra dient ( A-a gradient) can be derived if te arterial oxygen is known. 6. Poiseuille equation ; laminar \202 ow through a tube. \231V \227 8l \227 \200r4 \227 980 P = Where P = pressure drop, \231V = volume per unit time, l is length, r radius, viscosity 7. Minute ventilation This comprises alveolar and dead space ventilation. \231VE = \231VA + \231VD Tidal volume 6 ml/kg ( 420 ml) Functional residual capacity 2.4 litres Residual volume 1.2 litres Total lung capacity 6.0 litres Vital capacity 4.8 litres Peak expiratory \202 ow r ate : 450 \200\223700 l/min (males) Or 300 \200\223500 l/min (females) Forced expiratory vo lume in 1 sec (FEV1) 70 \200\22383% of vital capacity 3.5 litres 593593 Index N.B. \200\230f \200\231 following a locator indicates a \201 gure and \200\230t \200 \231 indicates a table. A ABCDE resuscitation 482 \200\2233 abciximab 185, 294, 297 abdomin al compartment syndrome 336, 342, airway obstruction 162, 248 \200\2239, 272 airway pressure in mechanical resistance to 228 \200\2239, 474, 588 \200\2239 SDD 474 for variceal bleeding 326 ventilation 8, 9, 13 see also barotrauma; positive end-expiratory anticholinergic drugs 154 \200\2235, 196, 291 anticholinesterase drugs 375 anticoagulants 2 20 \200\2233, 236 \200\2237 pressure (PEEP) 344 \200\2235, 495 airway pressure release ventilation (APRV) 11 airway resistance (Raw) 90 alanine aminotrans ferase (ALT) 356 albumin 356, 423 albumin solution for \202 uid therapy 144, 244 alcohol abuse abdominal complications 514 \200\22315 abdominal hypertension 344 \200\2235, 515 abdominal surgery 512 \200\22313 abdominal trauma 482 \200\2233, 490 \200\2231 Abiomed BVS5000/AB5000 cardiac assist in extracorporeal circuits 32, 64, 69 in MI 294, 297 monitoring 406 in PE 275 in pre-eclamp sia 519 reversal 220, 221, 222, 367, 388, 389 in spinal injury 487 in stroke 370 devices 58 bleeding disorders 389 ketoacidosis (AKA) 420 liver failure 354, 355, 389 withdrawal 361 abscesses 277, 339, 472 accident analysis 565f ACE (angiotensin-converting enzyme) anticonvulsants 212 \200\22313, 242, 362 \200\2233, 520 antidepressants 207, 361 inhibitors 171, 284, 294 alfentanil 206 ALI see acute lung injury alkaline phosphatase 356 alkalosis 422 \200\2234 A llen \200\231s test 102 allergy (anaphylactic shock) 166, 456 \200\2237 1-adrenergic rece ptor agonists 174 \200\2235 2-adrenergic receptor agonists 208 \200\2239, 361 -adrenerg ic receptor antagonists 171 acetaminophen (paracetamol) 508 overdose 442 \200\2233 overdose 234, 351, 442 antidiarrhoeal drugs 200 \200\2231 antidiuretic hormone (ADH) (vasopressin) 175, 450 \200 \2231 acetazolamide 187, 423 acetyl salicylate (aspirin) 184, 185, 294, 370 overdose 147, 442 antidopaminergic drugs 196, 198, 208, 319 antiemetic drugs 196 \200\2237, 318 anti \201 br inolytic drugs 226, 525 antifungal drugs 230 \200\2231, 401 antihistamines 196 antihyperten sives see vasodilators antioxidants 86 acid \200\223base balance bicarbonate 146 \200\2238 drowning 501 metabolic acidosis 146 \200\2237, 357, 418 \200\2232 1, mixed and (labetolol) 171, 182, 287, 518 428 \200\2239 ALS (advanced life support) 240 \200\2231 alternative therapies 207 ambulances 577 amilorid e 187 aminophylline 168, 255 amiodarone 177, 180 amlodipine 183 ammonia 203, 357 amniotic \202 uid embolism 526 \200\2237 amphetamines 385, 441 amphotericin B 230, 467 amrinone 169 amylase 328 amyloidosis 389 anemia 392 \200\2233, 406 haemolytic 396 \200\2237 sickle cell 394 \200\2235 metabolic alkalosis 422 \200\2234 respiratory failure 6 mucolytics 158 paracetamol overdose 234, 351, 442 renal failure 312 \200\22313 Acinetobacter baumannii, MDR 229, 588 ACTH (adrenocorticotrophic hormone) 437 activated cha rcoal 440 activated partial thromboplastin time antiplatelet drugs 184 \200\2235, 294, 297, 370, 388 antipsychotic drugs 208, 360 \200\2231 , 385 antiretroviral drugs 466 antithrombin 220, 406 antithyroid drugs 432 \200\2233 antivi ral drugs 232 \200\2233, 466 anti-Xa 406 anxiolytics 208 \200\2239, 361 aortic dissection 1 14, 285 aortic rupture 488 aortic valve dysfunction 113 APACHE (Acute Physiology and Chroni c (aPTT) 150, 220, 406 acute acalculous cholecystitis (AAC) 340 \200\2231, 477, 515 acute chest syndrome 395 acute coronary syndrome see myocardial infarction acute heart failure 190 \200\2231, 300 \200\2236 acute liver failure 234, 350 \200\2231, 35 2 acute lung injury (ALI) 256t pharmacotherapy 156, 160 \200\2231 ventilatory support 22, 28 see also acute respiratory di stress Health Evaluation) score 569 APC (activated protein C) 236 \200\2237, 463 apnoea testing 53 0 apoptosis 463 aprepitant 197 aprotinin 226 aPTT (activated partial thromboplastin anesthetics for asthma 265 syndrome (ARDS) for cerebroprotection 132, 136, 214, 352 acute promyelocytic leukemia 389 acute renal failure 312 \200\22315, 351, 420, 468, 503 for sedation 208, 209 for status epilepticus 213, 362 dialysis for 64, 65, 71 analgesics 206 \200\2237, 394, 508 \200\2239 anaphylactic shock 166, 456 \200\2237 ANCA (an tineutrophil cytoplasmic acute respiratory distress syndrome (ARDS) diagnosis 256 \200\2237 nutrition 87, 258 pharmacotherapy 160 \200\2231, 234, 258 ventilato ry support 19, 22, 26, 31, 260 \200\2231 see also acute lung injury (ALI) time) 150, 220, 406 AQMS (acute quadriplegic myopathy syndrome) (also critical illness neuromyopathy) 139, 211, 376 \200\2237 antibody) 470 aneurysms, cerebral 368 \200\2239 angina 182 \200\2233, 184, 234, 292 angiodysplasia 332 an giography, cerebral 366, 368 angioplasty 184, 295, 296 \200\2237, 453 angiotensin II recept or blockers ARBs (angiotensin II receptor blockers) 284, acute respiratory failure (ARF) see respiratory 294 failure acyclovir 232 Addison \200\231s disease 436 \200\2237 adenosine 176 adrenal disorde rs 351, 436 \200\2237 sepsis and 354 \200\2235, 478 \200\2239 ARDS see acute respiratory distress syndrome argatroban 222 arginine 86 arginine vasopressin (AVP) 175, 450 \200\2231 artemisin in 468 arterial blood gasses, sampling for 393 arterial blood pressure monitoring 102 \200 \2233 arterial puncture, accidental 106 arterial waveform 56f, 103f arti \201 cial hearts 59 ascites 186, 355 aspartate aminotransferase (AST) 356 aspergillosis 230, 401 aspirin 184 , 185, 294, 370 (ARBs) 284, 294 angiotensin-converting enzyme (ACE) inhibitors 171, 284, 294 anidulafungin 231 anion gap 418, 440 antianginal drugs 182 \200\2233, 294 antiarrhythmic dr ugs 176 \200\22380, 291 antibiotics 228 \200\2239 for COPD 255 for diarrhea 323 for empyema 269 for endocarditis 308 \200\2239 guidelines on usage 228, 464, 472 for meningitis 365 fo r neutropenic sepsis 400 for pneumonia 276, 279 adrenaline (epinephrine) 166, 178 for asthma 265 for bradyarrhythmia 291 in cardiac arrest 241 for shock 450, 453t, 456 \200 \2237 advanced life support (ALS) 240 \200\2231 advanced trauma life support (ATLS) 482 \200\2233 aeromedical evacuation 267, 580 \200\2231 agitation 360 \200\2231 AIDS 234, 365, 466 \200 \2237 air embolism 488 air travel 267, 580 \200\2231 overdose 147, 442 assist volume/pressure control ventilation 10 assisted suicide 562 594 INDEX cardiac arrest stroke 366 \200\2239 assisted ventilation see ventilatory support asthma in drowning 500 \200\2231 organ donation and 538 \200\2239 post-resuscitation care 93, 242 \200\2233 resuscitation 52 \200\2233, 175, 240 \200\2231 bleeding disorders (coagulopathies) 388 \200\22390, 398, 535 diagnosis 262, 263t pharmacotherapy 154 \200\2235, 262 \200\2233, 265 ventilatory support 2 3, 31, 264 \200\2235 bleeding time 406 blood \200\223brain barrier (BBB) 216 blood \202 ow imaging see Doppler ultrasound blood gasses, sampling for 393 blood pressure cardiac arrhythmias \200\230at-risk \200\231 patients, outreach 582 \200\2235 atelectasis 252 \200\2233 atenol ol 182 ATLS (advanced trauma life support) 482 \200\2233 atracurium 210 atrial \201 brill ation (AF) 53, 99, 176, 288 atrial \202 utter 53, 99 \200\223100, 288 atrial natriuretic peptide (ANP) 312 atrial (supraventricular) tachycardia 53, de \201 brillation 52 \200\2233, 240 ECG results 99 \200\223100, 288t heart block 99, 290, 291 pacing 54 \200\2235, 180, 291 pharmacotherapy 176 \200\22380, 288, 289, 291 see also s peci \201 c patterns cardiac assist devices 58 \200\2239 cardiac contusion 489 cardiac fai lure 49f, 182 acute 190 \200\2231, 300 \200\2236 levosimendan 190 \200\2231 nitric oxide 15 6 ventilatory support and 6, 22, 304 \200\2235 cardiac ischaemia 99, 182 \200\2233, 184, 23 4, 292 arterial pressure monitoring 102 \200\2233 high see hypertension; vasodilators low see hypo tension blood transfusions 150 in anemia 392 \200\2233, 394 \200\2235 dilutional coagulopathy 388 in hematological maligna ncies 401 incompatible 396 in postpartum hemorrhage 524 bone marrow transplants 401, 404 bo tulinum toxin, pyloric injection 199, 319 botulism 380 \200\2231 bowels 99, 176, 288 atrioventricular (AV) node block 99, 290 atropine 178, 200, 291 audit 570 \200\2231, 584 \200\2235 autoantibodies 374, 389, 396, 470 automatic tube compensation (ATC) 11 autonomic hyper-re \202 exia 487 autonomy 542, 544, 562 autotriggering 9 see also myocardial infarction cardiac monitoring anastomosis 512 \200\22313 colitis 322, 328, 329, 334 \200\2235, 514 decontamination 474 \200\2235 irrigation 440 ischaemia 323, 342 \200\2233, 515 lower GI bleeding 332 \200\2233, 335, 514 obstruction/pseudo-obstruction 323, 330 \200\2231, ECG 98 \200\223100, 274, 288t, 292, 498f echo/Doppler 112 \200\22319, 122, 124, 127, 293, 303 B babies electric impedance 122 partial CO2 rebreathing 93, 122 pulmonary artery catheters 108 \200 \22311, 110f pulse pressure algorithms 120 \200\2231, 126 infant botulism 380 oxygen toxicity 4 respiratory distress/failure 156, 161 514 \200\22315 perforation 328 \200\2239 bradycardia 99, 290 \200\2231 brain monitoring 130 \200\2239 brai n natriuretic peptide (BNP) 302 \200\2233, 312 brainstem death 136, 530 \200\2231, 534 \200 \2236 breathing exercises 44 bronchial artery embolization 271 bronchiectasis 158 broncho-p ulmonary dysplasia 4 bronchodilators 154 \200\2235, 255, 262 \200\2233 bronchoscopy 42 \200 \2233 cardiac output differential diagnosis of shock 446, 447 low, as contraindication to vasopressor baclofen 197 balloon pumps, intra-aortic 56 \200\2237, 453 balloon tamponade for oesophagea l use 174 cardiac pacing 54 \200\2235, 180, 291 cardiac physiology 48 \200\2239, 56, 126 \200\2237 ca rdiac preload 48, 116 \200\22317, 124 \200\2235 \202 uid responsiveness 126 \200\2237, 24 4 varices 326 barbiturates for ICP reduction 132, 136, 352 for seizures 213, 362 cardiac shunt 6, 297 cardiac surgery pacing 54, 291 pharmacotherapy 167, 168, 184, 226, 389 barotrauma 7, 14 \200\22315 barrier nursing 465, 546 bedside rationing 544 bedside services 546 \200\2237 bendro \202 uazide 187 bene \201 cence 532 \200\2233, 544 benzoate 353 ben zodiazepines 208, 209t in burns patients 494 in haemoptysis 270 \200\2231 in pulmonary collapse 253 in tracheostom y placement 35 in upper airway obstruction 248 \200\2239 cardiac tamponade 117, 489 cardiac valves 113, 290, 308 \200\2239 cardiogenic pulmonary oed ema 24, 31 cardiogenic shock 167, 301, 447, 452 \200\2234 cardiopulmonary bypass 32 \200 \2233, 389 cardiopulmonary resuscitation (CPR) 52, burns 273, 492 \200\2235, 576 overdose 442 for pain management 508 for seizures 212, 362, 363 see also smoke inhalation buspirone 197 240, 241 CardioQ Doppler device 122 cardiovascular drugs 166 \200\22391 best interests 532 \200\2233, 543 -adrenergic agonists C C-reactive protein (CRP) 476 Cesarean sections 519, 522 calcium 411 \200\22312, 503 calci um channel blockers 170 \200\2231, 176, 179, 183, see also individual drugs or classes of drug for ARDS 258 as bronchodilators 154, 263, 265 cardiovascular uses 166 \200\2237, 178, 241, 291 for shock 450, 453t, 456 \200\2237 cardiovascular effects abdominal hypertension 344 brainstem death 534 burns 493 drowning 501 hypothermia 498f live r failure 350 \200\2231, 355 cardioversion 52 \200\2233, 240 carvedilol 171, 182 caspofungi n 231 catheterization arterial 102 in burns patients 492 central venous lines 104 \200\2237 , 492 infected lines 107, 402, 464, 473, 477 PCI 184, 295, 296 \200\2237, 453 pulmonary art ery 108 \200\22311, 110f urinary 464 -adrenergic antagonists ( -blockers) 284, 369 for angina/MI 182 \200\2233, 294, 296 for arrhythmias 176 \200\2237, 179 for hypertension 1 71, 287, 518 for thyroid storm 432 calcium sensitizers (levosimendan) 190 \200\2231, 453t candidiasis 230, 231, 401, 477 canna binoid CB1 receptor agonists 197 cannulation bicarbonate 146 \200\2238, 429, 440, 503 bilevel ventilation (BiPAP) 11 biliary disorders arterial 102 in burns patients 492 central venous lines 104 \200\2237, 492 infected lines 1 07, 402, 464, 473, 477 pulmonary artery 108 \200\22311, 110f cholecystitis 340 \200\2231, 477, 515 cholestasis 348, 349 bilirubin 95, 348, 356 bivalirud in 222 black ethnic groups 284 bladder injury 491 bladder pressure 342 bleach 441 bleeding canrenone 187 CAP (community-acquired pneumonia) 276 \200\2237 capacity for giving consent 542 \200\2233 CAPD (continuous ambulatory peritoneal central venous catheterization 104 \200\2237, 492 central venous pressure (CVP) 124, 493 ce phalosporins 229, 365 cerebellar infarction 371 cerebral blood \202 ow dialysis) 70 \200\2231 capnography 35, 92 \200\2233, 122 capnometry 92 carbapenems 229 carbimazole 432 carbon diox ide during bronchoscopy 43 gastrointestinal, lower 332 \200\2233, 335, 514 gastrointestinal, up per see gastrointestinal after cardiac arrest 242 hypertensive encephalopathy 286 monitoring 132 \200\2233, 138, 485 PEEP and 23 see also cerebroprotection bleeding, upper GI tract haemoptysis 270 \200\2231 haemorrhagic shock 450, 482 \200\2233 haemostatic therapy 150 \200\2231, 226, 326, 367, capnography/capnometry 35, 92 \200\2233, 122 cerebral blood \202 ow and 132 hypercapnia 1 3, 30 removal from blood 18, 32 \200\2233 525, 536 cerebral function monitors (CFMs)/cerebral function analyzing monitors (CFAMs) 134 intra-abdominal 512 in major trauma 482 \200\2233, 488, 490 \200\2231 postpartum 524 \200 \2235 carbon monoxide poisoning 94, 273, 441, 494 carboprost 525 cerebral malaria 468 595 INDEX colloids 144 \200\2235, 244 \200\2235 cryoprecipitate 151 cryptococcal meningitis 365, 466 \200\2237 crystalloids see saline CT s cans cerebral oedema 286, 352, 431 avoidance in burns patients 492 \200\2233 see also \202 uid therapy treatment 216 \200\22317 cerebral venous sinus thrombosis 371 cerebroprotection 60 \200\2231, 175, 214 \200\22315 colon see bowels color \202 ow mapping (CFM) 112, 113 coma, survival post-cardiac arrest 243 communication, aids to 383, 554 community-acquired pneumonia (CAP) 276 \200\2237 compar tment syndrome alveolar recruitment 26 cerebral hemorrhage 366, 368 haemoptysis 270 pneumothorax 14 CURB-6 5 score 276 Curling \200\231s ulcers 321 Cushing \200\231s ulcers 321 CVVH (continuous veno venous post-cardiac arrest 242 \200\2233 post-head injury 485 post-SAH 369 cerebrovascular accident see stroke cervical spinal injury 486 chemotherapy, complications and side abdominal 336, 342, 344 \200\2235, 495 in rhabdomyolysis 503 effects 197, 400 \200\2232, 514 chest drains 38 \200\2239, 267, 269 chest physiotherapy 25, 44 \200\2235, 253, 255 chest trauma 482, 483f, 488 \200\2239 chest X-rays see radiography, chest children