Anxiety and lack of sleep. Increased sympathetic activity contributing to an increased meta bolic demand and adrenergic stress. The capacity of the circulation and respiratory system to meet this increase in metabolic demand may not be adequate. Myocardial ischaemia is a si gni \201 cant risk. The endocrine response to injury is exaggerated with consequent salt a nd water retention. Physiological attempts to limit pain may include immobility and muscle splinting, and consequent reductions in ventilatory function and cough. \200 Pain perception The degree of tissue damage is related to the magnitude of the pain stim- u lus. The site of injury is also important; thoracic and upper abdominal injury is more pain ful than injury elsewhere. However, the perception of pain is dependent on other factors, e .g. simultanous sensory input, per- sonality, cultural background, and previous experiences of pain. Management of pain Systemic analgesia \200 \200 Opioid analgesics form the mainstay of analgesic drug treatment. Small, frequent IV doses, or a continuous infusion provide the most stable blood levels. Since the degree of analgesi a is dependent on blood levels, it is important that they are maintained. Higher doses are required to treat rather than prevent pain. The dose of drug required for a particular indi vidual depends on their perception of pain and whether tolerance has built up to previous a nalgesic use. The use of non-opioid drugs may avoid the need for or reduce the dose require d of opioid drugs. This includes paracetamol and non- steroidals, ketamine, and A2-agonists such as clonidine. \200 Regional analgesia \200 Regional techniques reduce respiratory depression, but require experience to ensure procedu res are performed safely. Epidural analgesia may be with local anesthetic agents or opioids . Opioids avoid the vasodilatation and hypotension associated with local anesthetic agents, but do not produce as profound analgesia. The combination of opioid and local anesthetic i s synergistic. Intravenous opioids should be avoided or close monitoring should continue fo r 24h after cessation of epidural opioids due to the potential for late respiratory failure . Sample regimens are shown opposite. Local anesthetic agents may be used to block super \201 cial nerves, e.g. intercostal nerve block with 3 \200\2235mL 0.5% bupivacaine plus adr enaline. \200 \200 Non-pharmacological techniques Adequate explanation, positioning and physical techniques ma y all reduce drug requirements. PAIN 619 Regimens for epidural analgesia Lumbar 10 \200\22315mL 0.5% bupivacaine, followed by an infusion of 5 \200\22320mL/h 0.125% bupiva caine Thoracic 4 \200\2236mL 0.5% bupivacaine followed by an infusion of 6 \200\22310mL/h 0.125% bupivacai ne Opioid 5mg morphine gives up to 12h analgesia. Combined An infusion of 3 \200\2234mL/h 0.125% bupivacaine with 0.3 \200\2230.4mg/h morphine or 25 \200\22350mcg/h fentanyl See also: Non-opioid analgesics, p302; Opioid analgesics, p304; Epidural analgesia, p306; M ultiple trauma (2), p584; Blast injury, p596; Post-operative critical care, p620; Pain and comfort, p624. 620 CHAPTER 34 Pain and post-operative critical care Post-operative critical care Patients may be admitted to critical care after surgery, eithe r electively (see table opposite) or after unexpected peri-operative complications. General care \200 Ensure surgical and anesthetic plan has been agreed, e.g. overnight ventilation, special pr ecautions (e.g. wire cutters if mandible wired), movement restriction, haemodynamic targets , etc. Provide adequate analgesia. Ensure adequate rewarming. Maintain euglycaemia. Provide appropriate thrombosis prophylaxis. Blood gas, electrolyte, and hemoglobin monitoring. \200 \200 \200 \200 Post-operative respiratory problems Common in those with pre-existing respiratory disease, especially with a reduced vital capacity or peak \202 ow rate. Problems include: \200 \200 \200 \200 \200 Exacerbation of chronic chest disease. Retained secretions. Basal atelectasis. Pneumonia. U pper airway problems, e.g. laryngeal oedema. Anesthesia and surgery (especially upper abdominal surgery) reduce functional residual capa city, thoracic compliance, and cough. There is reduced macrophage function and systemic in \202 ammatory activation with infection and acute lung injury as possible consequences. Therapeutic aims Preoperative preparation may help avoid some of the problems: \200 \200 \200 \200 \200 Cessation of smoking for >1 week. Bronchodilatation. Respiratory muscle training. Chest phy siotherapy. Avoidance of hypovolaemia in the nil-by-mouth period. Post-operative clearance of secretions and maintenance of basal lung expansion are very imp ortant. These require effective analgesia and chest physiotherapy. Mechanical ventilation a ssists basal expansion and secre- tion clearance where anesthetic recovery is expected to b e prolonged or surgery 9 pre-existing disease increases the risk of secretion retention and atelectasis. Ensure a patent airway prior to extubation. Post-operative circulatory proble ms \200 Prevention of hypovolaemia is crucial in avoiding in \202 ammatory activation and, therefo re, many post-operative complications. Hemorrhage is usually obvious and managed by resusci tation, correction of coagulation disturbance, and surgery. Sub-clinical hypovolaemia is co mmon. Hypothermia and high catecholamine levels help to maintain CVP and BP despite continu ing hypovolaemia. Avoiding a reduced stroke volume, metabolic acidosis, and a low ScvO2 are the best indicators of adequate resuscitation. Fluid challenges with colloid should be use d to con \201 rm and treat hypovolaemia where there is any circulatory disturbance, metabo lic acidosis, or oliguria. POST-OPERATIVE CRITICAL CARE 621 Reasons for elective critical care admission \200 \200 Airway monitoring, e.g. major oral, head, and neck surgery. Respiratory monitoring, e.g. ca rdiothoracic surgery, upper abdominal surgery, prolonged anesthesia, previous respiratory d isease. Cardiovascular monitoring, e.g. cardiac surgery, vascular surgery, major abdominal surgery, prolonged anesthesia, previous cardiovascular disease. Neurological monitoring, e. g. neurosurgery, cardiac surgery with circulatory arrest, spinal surgery. Flap monitoring, e.g. major plastic, and head and neck surgical procedures. Elective ventilation, e.g. cardi ac surgery, major abdominal surgery, prolonged anesthesia, previous respiratory disease. See also: Critical Care Unit admission criteria, p10; Oxygen therapy, p38; Airway maintenan ce, p40; Ventilatory support \200\224indications, p44; Continuous positive airway pressure, p70; Non-invasive respiratory support, p76; Chest physiotherapy, p90; Blood transfusion, p 248; Fluid challenge, p342; Airway obstruction, p348; Respiratory failure, p350; Atelectasi s and pulmonary collapse, p352; Hypotension, p380; Oliguria, p398; Vomiting/gastric stasis, p406; Abdominal sepsis, p422; Bleeding disorders, p468; Electrolyte management, p482; Infe ction control \200\224general principles, p544; Pyrexia \200\224causes, p602; Pain, p618. This page intentionally left blank 623 Chapter 35 Oncological critical care Pain and comfort 624 Effects of chemo- and radiotherapy 626 Neutropaenia and infection 628 Leukemia/lymphoma 630 624 CHAPTER 35 Oncological critical care Pain and comfort Patients with oncological disease may complain of pain or discomfort relat ed to the neoplasm itself or as a consequence or complication of the treatment. Approximate ly 90% of patients with advanced cancer experi- ence severe pain that is often under-treate d. Pain management may be further complicated by a chronic dependency on analgesia, necessi tating high doses for managing acutely painful episodes. Patients may complain of persistent or continuous pain and/or break- through pain (brief, r apid-onset \202 are-ups of severe pain that can occur despite regular pain medication). A personalized approach is essential as effective strategies will vary between patients and some will be more affected by side effects, e.g. excessive drowsiness from opiates. Advice should be sought from palliative care or pain teams who are highly experi- enced in dealing with all aspects of cancer pain. Cancer pain/discomfort may arise from: Post-operative pain. Organomegaly with stretching of the capsule and pressure discomfort (e.g. splenomegaly). Occluded blood vessels causing di stal tissue ischaemia. Bone fracture(s) from metastases. Infection. In \202 ammation (e.g. pleurisy, peritonitis). Side effects from cancer therapy (e.g. chemo- or radiotherapy). Ne uropathy (compression, in \201 ltration, chemotherapy-related). Psychological or emotional problems. \200 \200 \200 \200 \200 \200 \200 Analgesia Post-operative pain should be managed in standard fashion, i.e. oral analgesics 9 dermal patches graduating to IV infusions/boluses of opiates and/or NSAIDS, epidurals, and patient-controlled analgesia. In addition to opiate and non-opioid treatment, speci \201 c conditions may warrant direct ed adjunctive therapy. For example, neuropathic pain may respond to antidepressants, antico nvulsants, oral or cutaneous lidocaine, and/or corticosteroids. Local or regional nerve blo cks may be useful for somatic or visceral pain. Transcutaneous electric nerve stimulation ( TENS) may block pain transmission by low-level stimulation of nerve endings. Alternative medicine therapies (e.g. acupuncture, therapeutic massage, homeopathy) may also prove effective in some patients. Psychological support Many psychological and emotional factors can contribute to suffering. These vary between individuals, and re \202 ect underlying personality and degree of fami ly support. Many patients manifest signs of clinical depres- sion, especially those at adva nced stages of the disease. Admission to critical care may be very frightening for mentally competent patients. Psychotherapy is an important part of cancer pain management. Provisio n of emotional support and stability can help patients to cope. Assistance can be sought fr om oncology and palliative care teams. Treatments such as hypnosis and relaxation technique s may prove useful. Adequate provi- sion of information regarding critical care management and prognosis is an important means of allaying anxiety for both patient and family. Care m ust be taken not to distress the patient further. PAIN AND COMFORT 625 See also: Communication, p18; Non-opioid analgesics, p302; Opioid analgesics, p304; Epidura l analgesia, p306; Anticonvulsants, p312; Corticosteroids, p328. 626 CHAPTER 35 Oncological critical care Effects of chemo- and radiotherapy Bone marrow suppression Neutropaenia, thrombocytopaenia, and anemia can be expected with most therapeutic regimens. The patient is at increased ris k of infection from bacterial, fungal, viral, and atypical infections, and from bleeding th at may be relatively minor (e.g. petechiae, cannula sites) or catastrophic (e.g. cerebral h emorrhage). Low platelet counts are generally well tolerated; transfusions are given to keep counts >10 x 109/L though higher levels will be targeted for active bleeding, for elective procedures , and in the presence of sepsis. Frequent platelet transfusions greatly increase the risk o f antiplatelet antibody formation with consequent risk of adverse reactions and a failure t o incre- ment the platelet count adequately. Excess transfusion should thus be avoided, if possible. Single donor pools may also be used to increase the increment. Anemia is generally managed by red cell transfusion. In general, hemoglobin levels \211 7g /dL are acceptable though higher levels may be needed for active bleeding or cardiorespirat ory impairment. Supplementation of haematinics such as folate and B12 should not be overloo ked. Impaired gas exchange The lung is often compromised by infection (pneumonia, pneumonitis), non-infective pneumonitis, pleural effusion, high or low pressure pulmo- nary oedema (i.e. ARDS or left heart failure), hemorrhage, bronchiolitis obliterans with organizing pneumonia (BOOP), or \201 brosis (especially after busulphan or radiotherapy). Fluid overload is c ommon following renal dys- function and/or large \202 uid volumes used for chemotherapy a nd multiple antibiotics. \200 Treat the underlying cause, e.g antibiotics for infection, steroids for pneumonitis, and BO OP. High FIO2 should be avoided with suspected \200\230busulfan lung \200\231. Aim for PaO 2 90 \200\22392%. Avoid \202 uid overload as excess capillary leak will worsen gas exchan ge. Mortality is high (>60%) if mechanical ventilation is necessary. CPAP and BiPAP can pro ve highly effective in avoiding the need for intubation, especially if used early to avoid fatiguing the patient. \200 Cardiomyopathy Certain chemotherapeutic agents (e.g. doxorubicin, mitoxantrone) can cause c ardiomyopathy. Secondary sepsis can also cause myocardial depres- sion. This may be dose-re lated or idiosyncratic. Treatment is based on standard heart failure regimens. Fluid overlo ad should be avoided. Heart failure should be considered if such patients fail to wean. Renal dysfunction Tumor lysis syndrome (hyperkalaemia, hyperuricaemia, and acute renal fail ure) may follow rapid destruction of a large white cell mass. Prevent with good hydration, a maintained diuresis, and rasburicase (recombinant urate oxidase) or allopurinol. Once est ablished, haemo(dia) \201 ltration and other measures to lower serum potassium levels may be necessary. EFFECTS OF CHEMO- AND RADIOTHERAPY 627 See also: Continuous positive airway pressure, p70; Non-invasive respiratory support, p76; Dyspnoea, p346; Respiratory failure, p350; Acute chest infection (1), p356; Acute chest inf ection (2), p358; Acute respiratory distress syndrome (1), p360; Acute respiratory distress syndrome (2), p362; Heart failure \200\224assessment, p392; Heart failure \200\224manageme nt, p394; Bleeding disorders, p468; Anemia, p472; Platelet disorders, p478; Infection \200 \224diagnosis, p552; Neutropaenia, p628. 628 CHAPTER 35 Oncological critical care Neutropaenia and infection Though de \201 ned as a neutrophil count <2 x 109/L, neutropaen ic patients are not generally placed in protective isolation until counts fall <0.5 \200 \2231 x 109/L. Adequate functionality is not guaranteed even despite restoration of a \200 \230normal \200\231 count. Many studies show equivalent outcomes between neutro- paenic and non-neutropaenic hematological oncology patients admitted to critical care. The patient is usually asymptomatic until infection super- venes, but they may deteriorate very rapidly. Causes in the oncology patient \200 The neoplasm itself (e.g. leukemia, myeloma) or as a consequence of chemotherapy or radiati on causing marrow suppression. Systemic in \202 ammation, infection, and sepsis. Nutrition al de \201 ciencies, e.g. folate, vitamin B12, malnutrition. Adverse drug reaction, e.g. s ulphonamides. Part of an aplastic anemia, e.g. idiopathic, drugs, infection. Hypersplenism. \200 \200 \200 \200 Infections \200 Initial infections are with common bacterial organisms such as pneumococci, staphylococci, and coliforms. With recurrent infections or after repeated courses of antibiotics, more unu sual and/or multi-resistant organisms may be responsible, e.g. fungi (NB. Candida spp.), Pn eumocystis jiroveci, CMV, TB. Management 1. In the absence of chemotherapy, any implicated drug should be dis- continued. 2. If the neutrophil count is low, consider protective isolation, ideally in a cubicle equipped with laminar \202 ow air conditioning. 3. Adopt strict infection control procedures. 4. Minimize invasive procedures and avoid PR examination. 5. Maintain good oral hygiene. Apply topical treatment as necessary, e.g. nystatin mouthwashes for oral fungal infection. 6. Clotrimazole cream for fungal skin infection. 7. For suspected sepsis, start parenteral antibiotics within 2h of fever \211 38*C (broad-spectrum if no organism has been isolated) . Seek cause, including CT scan and bronchoalveolar lavage, as indicated. Hematology units have their own regimens, frequently escalating antibacterial cover with antifungals 9 antiv irals 9 treatment of atypicals (e.g. Pneumocystis jiroveci). A balance must be reached betw een adequate treatment of infection versus problems related to resistance, bacterial overgr owth (e.g. C. dif \201 cile), liver, renal and gut toxicity, and \202 uid over- load. Th e pyrexia may be due to the antibiotic treatment itself. 8. Remove vascular catheters, if possibly implicated, including Hickman- type catheters. 9. Avoid uncooked foods (Pseudomonas risk) and bottled pepper (Aspergillus). 10. Granulocyte-colony stimulating factor (G-CSF) is frequently given to stimulate a bone marrow response. 11. Neutrophil infusions are short-lived, expensive, and often induce a pyrexial response. Their role remains controversial. NEUTROPAENIA AND INFECTION 629 See also: Full blood count, p220; Bacteriology, p224; Virology, serology, and assays, p226; Antimicrobials, p326; Infection control \200\224general principles, p544; Infection \200 \224diagnosis, p552; Infection \200\224treatment, p554; Pyrexia \200\224causes, p602; Effec ts of chemo- and radiotherapy, p626. 630 CHAPTER 35 Oncological critical care Leukemia/lymphoma Such patients may present acutely to critical care with complications ari sing from either the disease or the therapy. Complications arising from the disease \200 \200 Decreased resistance to infection. Hyperviscosity syndrome \200\224drowsiness, coma, focal neurological defects. Anemia, thrombocytopaenia, bleeding tendency, DIC. Weight loss, letha rgy, fever, night sweats. Central nervous system involvement. \200 \200 Management 1. The raised white cell mass may be reduced rapidly by leucophoresis if a hyperviscosity syndrome is present. 2. Frequent blood transfusions to maintain Hb levels >7g/dL. 3. Platelet transfusions if co unts remain <10 x 109/L, or if <50 x 109/L and remaining symptomatic, or undergoing an invasive procedure. 4. Fresh frozen plasma and other blood products as needed. 5. Neutropaenia management, incl uding protective isolation, appropriate antibiotic therapy 9 granulocyte-colony stimulating factor. 6. Psychological support for both patient and family is vital. Graft versus host disease (GVHD) An immune response following allogenic stem cell transplan tation. Features include mucositis, pneumonitis, hepatitis, jaundice, diarrhea, abdominal p ain, rash, and blistering. Treatment includes steroids 9 ciclosporin, tacrolimus, alemtuzumab, in \202 iximab, rituxi mab, anti-lymphocytic, or anti-thymocytic globulin and symptomatic relief. Parenteral nutri tion may be needed if diarrhea is severe. Grades of GVHD Grade Skin Liver Gut 1 Rash <25% body Bilirubin 35 \200\22350 mol/L Diarrhea <1L/d 2 Rash 25 \200\22350% body Bilirubin 51 \200\223100 mol/L Diarrhea 1 \200\2231.5L/d 3 Rash >50% body Bilirubin 101 \200\223250 mol/L Diarrhea >1.5L/d 4 Desquamation or bullae Bilirubin >250 mol/L Pain or ileus leukemia/LYMPHOMA 631 See also: Blood transfusion, p248; Blood products, p250; Corticosteroids, p328; Rituximab, p334; Bleeding disorders, p468; Anemia, p472; Platelet diorders, p478; Effects of chemo- an d radiotherapy, p626; Neutropaenia, p628. This page intentionally left blank 633 Chapter 36 Obstetric emergencies Pre-eclampsia and eclampsia 634 HELLP syndrome 636 Post-partum hemorrhage 638 Amniotic \202 uid embolus 640 634 CHAPTER 36 Obstetric emergencies Pre-eclampsia and eclampsia The hallmark of pre-eclampsia is hypertension with proteinuria. It is con- sidered mild if proteinuria is 0.25 \200\2232g/L and severe if >2g/L. Eclampsia is the same condition associated with seizures, but this only affects 1 in 100 pre-eclampt ics. Both are associated with cerebral oedema and, in some cases, hemorrhage. A reduced pla sma volume, raised peripheral resis- tance, and disseminated intravascular coagulation all impair tissue perfu- sion, with possible renal and hepatic failure. Pulmonary oedema may oc cur secondary to increased peripheral resistance and low colloid osmotic pressure. Pre-ecla mpsia and eclampsia are responsible for a \201 fth of deaths in pregnant women. Management Hypertensive crises and convulsions may continue for 48h post-partum, during whi ch time close monitoring in a high dependency or intensive care area is essential. Circulatory management \200 High blood pressure in (pre-)eclampsia is due to arteriolar vasospasm and reduced plasma vo lume so controlled plasma volume expansion is essential as the \201 rst-line treatment. A standard \202 uid challenge regimen carries little risk of \202 uid overload. Oliguria often coexists with reduced plasma volume; controlled volume expansion is usually more app ropriate than diuretic therapy. If plasma volume expansion fails to control hypertension, a nti- hypertensives such as labetalol, nifedipine, or hydralazine may be used. \200 Seizures \200 \200 Seizures are best avoided by good blood pressure control. Initial seizure control may be ac hieved with small doses of benzodiazepines. Magnesium sulfate is the treatment of choice fo r eclamptic seizures. Magnesium levels should be monitored and kept between 2.5 \200\2233.7 5mmol/L. Above 3.75mmol/L, toxicity with possible cardiorespiratory arrest may be seen. Pro phylactic anticonvulsant therapy with magnesium is often given in severe pre-eclampsia, and may be considerd in mild to moderate cases. Excess sedation should be avoided due to the r isk of aspiration although continued seizures may require elective intubation, mechanical h yperventilation, and further anticonvulsant therapy. Early fetal delivery The de \201 nitive treatment for (pre-)eclampsia is fetal delivery, b ut the needs of the fetus must be balanced against those of the mother. The mother \200\231 s life takes priority. If fetal maturity has been reached, immediate delivery after control of seizures and hypertension is necessary. PRE-ECLAMPSIA AND ECLAMPSIA 635 Drug dosages Labetalol Start at 2mg/min IV or quicker if a rapid response is required. Labetalol is usually effect ive once 200mg has been given after which a maintenance infusion of 5 \200\22350mg/h may be continued. Nifedipine 10mg SL is an often effective alternative, given every 20min if necessary. Hydralazine 5 \200\22310mg by slow IV bolus, repeat after 20 \200\22330min. Alternatively, by infusion starting at 200 \200\223300mcg/min and reducing to 50 \200\223150mcg/min. Magnesium 4g over 20 min, followed by 1 \200\2231.5g/h by intravenous infusion until seizures have st opped for 24h. Key papers Magpie Trial Collaboration Group. Do women with pre-eclampsia, and their babies, bene \201 t from magnesium sulfate? (2002) The Magpie Trial: a randomized placebo-control led trial. Lancet 359: 1877 \200\22390. Which anticonvulsant for women with eclampsia? (1995) Evidence from the Collaborative Eclam psia Trial. Lancet 345: 1455 \200\22363. See also: Blood pressure monitoring, p164; Hypotensive agents, p270; Hypertension, p382; Ge neralized seizures, p444; Raised intracranial pressure, p454. 636 CHAPTER 36 Obstetric emergencies HELLP syndrome HELLP syndrome is a pregnancy-related disorder associated with haemol- ysis, elevated liver function tests, and low platelets. \200 Microangiopathic haemolysis results from destruction of red cells as they pass through dama ged small vessels. Hepatic dysfunction is characterized by periportal necrosis and hyaline deposits in the sinusoids. In some cases, hepatic necrosis may proceed to hepatic hemorrhag e or rupture. Thrombocytopaenia results from increased platelet consumption, although proth rombin time and activated partial thromboplastin time are normal, unlike DIC. It rarely fal ls below 20x109/L. Nearly 10% of women with severe pre-eclampsia and 30 \200\22350% of eclamp- tics are affect ed though the exact relationship is unknown. Approximately half have complete HELLP (all co mponents present) while half have incomplete HELLP (1 \200\2232 components present). The ma ternal mortality is 1%, resulting from ruptured subcapsular liver haematoma, hemorrhage, an d stroke. Major hemorrhage is uncommon, but wound site oozing or subcutaneous haematoma may occur. Clinical features \200 \200 \200 \200 Epigastric or right upper quadrant pain with malaise. Nausea and vomiting, headache. Genera lized oedema is usual though 15% have diastolic BP <90 mmHg. Presentation may not occur unt il post-partum. The lowest platelet count usually occurs at 24 \200\22348h post-partum. Criteria for diagnosis of HELLP syndrome Haemolysis Abnormal blood \201 lm Hyperbilirubinaemia LDH >600U/L AST >70U/L Platelets <100 x 109/L Elevated liver enzymes Thrombocytopaenia Management \200 Priorities for management include basic resuscitation and exclusion of hepatic hemorrhage o r ruptured liver. In the latter case, an early Cesarean section and de \201 nitive urgent surgical repair are required. Magnesium prophylaxis is given to prevent seizures. Microangi opathic haemolysis and thrombocytopaenia may respond to plasma exchange and fresh frozen pl asma infusion. Platelet transfusions should be avoided unless there is active bleeding. Cor ticosteroids increase platelet count but do not affect outcomes. \200 \200 HELLP SYNDROME 637 Key paper Fonseca JE, Mendez F, Catano C, Arias F. (2005) Dexamethasone treatment does not improve the outcome of women with HELLP syndrome: a double-blind, placebo-controlled, rando mized clinical trial. Am J Obstet Gynecol 193: 1591 \200\2238. See also: Liver function tests, p218; Full blood count, p220; Jaundice, p428; Haemolysis, p 476; Platelet disorders, p478. 638 CHAPTER 36 Obstetric emergencies Post-partum hemorrhage Usually due to incomplete uterine contraction after delivery, but ma y be due to retained products. The magnitude of hemorrhage may be severe and life-threateni ng. It is the leading cause of maternal mortality. Resuscitation The principles of resuscitation are the same of those applying to any haem- o rrhagic condition. Blood transfusion requirements may be massive and therefore, there may b e a need to replace coagulation factors. There may be signi \201 cant retroplacental bleed ing which may lead to underestimation of blood volume loss. Large bore intravenous access m ust be established. It is safer to manage major \202 uid and blood replacement with haemo dy- namic monitoring. Stimulated uterine contraction Begin fundal massage and administer uterotonic drugs such as oxytocin (5U IV bolus or 10 \200\22320U in 1L of normal saline infused quickly). Prostagla ndin F2A, injected locally into the uterus or IM, is an effective method of stimu- lating u terine contraction and may avoid the need for surgery. Aortic compression Temporary reduction of hemorrhage may be achieved by compressing the aor ta with a \201 st pushed \201 rmly above the umbilicus, using the pres- sure between th e \201 st and vertebral column to achieve compression. This maneuver may buy time while d e \201 nitive surgical repair is organized. Arterial occlusion Angiographic embolisation or internal iliac artery ligation may avoid th e need for hysterectomy in some cases. The disadvantages of these proce- dures include a si gni \201 cant delay in organization and, in the latter case, a high failure rate. POST-PARTUM hemorrhage 639 See also: Full blood count, p220; Blood transfusion, p248; Blood products, p250; Basic resu scitation, p338. 640 CHAPTER 36 Obstetric emergencies Amniotic \202 uid embolus \200 An uncommon, but dangerous, complication of childbirth that presents with a precipitous ons et of hypoxaemic respiratory failure, disseminated intravascular coagulation, and shock, or even cardiac arrest. Tonic clonic seizures are seen in 50% of cases. High early mortality is associated with acute pulmonary hypertension. The initial response of the pulmonary vasc ulature to the presence of amniotic \202 uid is intense vasospasm, resulting in severe pu lmonary hypertension and hypoxaemia. Right heart function is initially compromised severely , but returns to normal with a secondary phase during which there is severe left heart fail ure and pulmonary oedema. Amniotic \202 uid contains lipid-rich particulate material whic h stimulates a systemic in \202 ammatory reaction. In this respect, the progress of the co ndition is similar to other causes of multiple organ failure with associated capillary leak and disseminated intravascular coagulation. Diagnosis is usually based on clinical feature s alone. It may be supported by amniotic \202 uid and fetal cells in pulmonary artery blo od and urine, though this \201 nding is not speci \201 c for embolus. \200 Management Management is entirely supportive. If amniotic \202 uid embolism occurs prior to delivery, perform urgent Cesarean section to prevent further embolisation. Respiratory support Provide oxygen to maintain SaO2 of 92 \200\22398%. CPAP or mechanical v entila- tion may be required. Cardiovascular support Standard resuscitation principles apply with controlled \202 uid l oading and inotropic support being started as required. Hematological management Management of the coagulopathy requires blood product therapy guid ed by laboratory assessment of coagulation times. In addition, some cases improve after tre atment with cryoprecipitate, possibly due to the effects of \201 bronectin replacement. AMNIOTIC FLUID EMBOLUS 641 See also: Ventilatory support \200\224indications, p44; Continuous positive airway pressure , p70; Coagulation monitoring, p222; Blood products, p250; Basic resuscitation, p338; Fluid challenge, p342; Systemic in \202 ammation/multi-organ failure \200\224causes, p556; Syst emic in \202 ammation/multi-organ failure \200\224 management, p558. This page intentionally left blank 643 Chapter 37 Transportation of the critically ill Intra-hospital transportation 644 Inter-hospital transportation \200\224road 646 Inter-hosp ital transportation \200\224air 648 644 CHAPTER 37 Transportation of the critically ill Intra-hospital transportation Critically ill patients frequently have to be moved out of th e Critical Care Unit for investigation or operative procedures. Although much of the equipm ent used in the Critical Care Unit has battery back-up power supply, many items are too lar ge to consider moving safely with the patient. Therefore, transportation within hospital re quires provision of suitably portable equipment. A hospital critical care trolley should be of \201 xed height with an equipment shelf and other \201 xed anchorage points below t he level of the patient to enable such equipment to be clamped for safe transportation. Speci \201 cation of transportation equipment The critical care transportation trolley mus t accommodate: \200 \200 \200 Portable ventilator. Oxygen cylinder. Monitor including ECG, NIBP, facility for direct BP, SpO2, ETCO2, temperature, FIO2. Syringe drivers. Volumetric pumps. Suction. Back-up batteri es. Anchorage for a 5-point patient harness. \200 \200 \200 \200 Patient preparation for intra-hospital transportation In addition to the usual requirements for provision of bedside critical care medicine, the following are required: \200 \200 \200 \200 \200 Assessment of the risk:bene \201 t ratio for the move. Assessment of degree of stabilizati on required before movement. Assessment of security equipment and tubes. Safe storage and s towage of equipment on the transportation trolley. Transfer is associated with an increased likelihood of arrhythmias so PaO2 should ideally be normalized. Required competencies of accompanying staff Accompanying staff must be competent in the fol lowing: \200 \200 \200 \200 \200 \200 \200 \200 Airway device insertion and management. Chest drain insertion and management. Cardiovascula r monitoring. Sedation/paralysis. Mechanical ventilation with transportation ventilators. L ifting and handling. Managing access in con \201 ned spaces. Management during imaging, e. g. special issues relating to ventilation during MRI. INTRA-HOSPITAL transportation 645 See also: Endotracheal intubation, p42; Pulse oximetry, p144; CO2 monitoring, p146; ECG mon itoring, p162; Blood pressure monitoring, p164; Inter-hospital transportation \200\224road, p646; Inter-hospital transportation \200\224air, p648. 646 CHAPTER 37 Transportation of the critically ill Inter-hospital transportation \200\224road Many critically ill patients are transported bet ween hospitals on a daily basis, mainly by ambulance. Staff may be unfamiliar with the ambu lance environment and may suffer from motion sickness. There should be at least two attenda nts, one of whom should be a critical care medical prac- titioner, ideally with previous ex perience of transportation in a supernumerary capacity. They must be familiar with the tran sportation equipment and commu- nication systems. Transportation services should be organiz ed and co-ordinated to deliver safe, ef \201 cient, and timely inter-hospital transfer. Patient preparation The steps in preparation for transportation are Assessment, Control, Co mmunication, Evaluation, Preparation and Packaging, and Transportation (ACCEPT). The decision to move a patient between hospitals must be taken jointly by the most senior c linicians available at the referring and receiving hospitals. Evaluate the risk:bene \201 t ratio of transportation, staf \201 ng, and equip- ment needs based on the nature of the illness, urgency, vehicle availability, geographical factors, traf \201 c and weather cond itions. Patients should be properly resuscitated and stabilized prior to transportation. Hy povolaemia is poorly tolerated. Intubate if GCS \211 8. Intubated patients should normally be paralyzed and sedated. Chest drains can be placed on Heimlich-type valves. Patients sho uld be covered in an insulating blanket. Required staff competencies for road transportation In addition to the competencies require d for intra-hospital transportation: \200 \200 \200 \200 \200 \200 \200 \200 Ability to assess patients remotely. Understanding the limitations of resource and power in an ambulance. Understanding physiological effects of acceleration and deceleration. Famili arity with chains of communication and command. Use of diverse modes of communication and a ssociated protocols. Handling emergencies on the road; when to stop and when to divert. Und erstanding ambulance emergency drills. Understanding the law relating to blue light use etc . Vehicle design Guidance covering design, speci \201 cation, and equipment requirements for road ambulances are contained within European Committee for Standardization CEN 1789. A ty pe C ambulance is a mobile ICU designed and equipped for transportation, advanced treatment , and monitoring of patients. To ensure that critical care can be continued throughout the journey, these vehicles need to have a 240V AC generator capable of pro- viding 2.2kVA, wit h a back-up inverter \201 tted. There should be six 240V outlets, positioned to allow equ ipment in use to be safely connected without creating trip hazards. The vehicles should als o have three 12V jack sockets, a pair of 12V switched screw terminals, and one 12V cigar-li ghter size socket. The vehicle should provide secure, CEN-compliant anchorage \201 xings for essential equipment, e.g. a portable ventilator, up to 6 syringe drivers, volumetric pu mps, gas cylinders etc. There must be CEN com- pliant provision for the \201 xing of crit ical care trolleys of different design. The vehicles must carry a minimum of two HX oxygen cylinders and have storage for D size spares for the stretcher trolley. INTER-HOSPITAL transportation \200\224ROAD 647 Transportation preparation (ACCEPT) Assessment Be aware of the full patient history and current problems. Control Identify the leader and allocate tasks. Communication Make sure all communication is clear, source identi \201 ed, and involves all staff involv ed with patient dispatch and receipt. Evaluation Assess risks and bene \201 ts of transportation, equipment needed, and urgency. Preparation and packaging Prepare patient, equipment, and staff. Transportation Having identi \201 ed the mode of transportation and completed the preparation, transporta tion the patient. See also: Endotracheal intubation, p42; Pulse oximetry, p144; CO2 monitoring, p146; ECG mon itoring, p162; Blood pressure monitoring, p164; Sedatives and tranquilisers, p308; Muscle r elaxants, p310; Intra- hospital transportation, p644; Inter-hospital transportation \200 \224air, p648. 648 CHAPTER 37 Transportation of the critically ill Inter-hospital transportation \200\224air Aircraft are preferred for longer distance transf ers with \201 xed wing aircraft preferred for distances >150 miles. Time to organize air transportation should be taken into account when judging any advantage of speed over longer distances. Helicopters are generally less comfortable, and provide a more cramped environm ent than either ambulance or \201 xed wing aircraft. Particular problems of air transportation A lower barometric pressure reduces alveolar part ial pressure of oxygen (leading to hypoxaemia) and increases the volume of gas \201 lled cavities. Noise and vibration may increase pain and discomfort or contribute to nausea. Patient preparation Patient assessment to calculate risk:bene \201 t ratio of air transpor tation and staf \201 ng and equipment needs based on the nature of the illness, urgency of transfer, availability of transportation, mobilization times, geographical factors, traf \201 c and weather conditions. An increased FIO2 is mandatory for all aeromedical transfers where the cabin is not pressur ized to sea level barometric pressure. Pneumothoraces must be drained. Nasogastric tubes sh ould be inserted and placed on free drainage. Pneumoperitoneum and intracranial air are rel ative contraindi- cations to air transportation. Tissues may also swell and plaster casts s hould be split. Nausea and pain must be adequately controlled. Required staff competencies for air transportation In addition to the competencies required for road transportation the following are required: \200 \200 Understanding the limitations of resource and power in aircraft. Understanding the effects of altitude, vibration, and noise on physiology and monitoring. Understanding emergency dri lls for helicopters and \201 xed wing aircraft. INTER-HOSPITAL transportation \200\224AIR 649 See also: Endotracheal intubation, p42; Chest drain insertion, p84; Enteral feeding and dra inage tubes, p122; Pulse oximetry, p144; CO2 monitoring, p146; ECG monitoring, p162; Blood pressure monitoring, p308; Sedatives and tranquilisers, p310; Muscle relaxants, p312; Intra hospital transportation, p644; Interhospital transportation \200\224road, p646. This page intentionally left blank 651 Chapter 38 Death and the dying patient Brain stem death 652 Withdrawal and withholding treatment 654 Care of the potential organ/t issue donor 656 652 CHAPTER 38 Death and the dying patient Brain stem death \200 