Anaesthesia, Pain, Intensive Care and Emergency - Part 8 pdf

Regional anaesthesia in the patient with pre-existing neurological dysfunction 329 accurately predicts clinical outcome, these studies illustrate the importance of minimising direct needle trauma during regional techniques, especially in patients at increased risk of neurological complications Neurological deficits after regional anaesthesia may be a direct result of local anaesthetic toxicity Clinical and laboratory findings indicate that anaesthetic solutions are potentially neurotoxic [10–14] It is generally agreed that local anaesthetics administered in clinically appropriate doses and concentrations not cause nerve damage [15] However, prolonged exposure to high concentrations of local anaesthetic solutions may result in permanent neurological deficits Patients with underlying nerve dysfunction may have a decreased requirement for local anaesthetic and a decreased threshold for neurotoxicity [12] Indeed, Yee et al [16] have demonstrated that the dose requirement for local anaesthetics is decreased and potency increased in aged animals This may have implications for the use of local anaesthetics in an ageing patient population Neural ischaemia may occur as a result of systemic or local vascular insufficiency Systemic hypotension with or without a spinal anaesthetic may produce spinal cord ischaemia in the watershed areas between radicular vessels, resulting in flaccid paralysis of the lower extremities (anterior spinal artery syndrome) The use of local anaesthetic solutions containing epinephrine or phenylephrine may theoretically result in local ischaemia, especially in patients with microvascular disease, but clinical data are lacking [11, 17] Furthermore, large clinical studies have failed to identify the use of vasopressors as a risk factor for neurological injury Most cases of presumed vasopressor-induced neurological deficits after spinal anaesthesia have been single case reports, often with several other risk factors involved [18] The neural double crush Patients with a pre-existing neurological condition may be at increased risk for regional-anaesthesia-related nerve injury on the basis of the “double crush”, which hypothesises that nerve fibres that are already compromised are also more vulnerable to injury at another site (Fig 1) All patients (N=360) who underwent ulnar nerve transposition at the Mayo Clinic from 1985 to 1999 were retrospectively studied to evaluate whether the performance of an axillary block in the presence of a pre-existing (ulnar) neuropathy [19] A general anaesthetic was performed in 260 (72%) patients The remaining 100 (28%) patients each received an axillary block, including 64 patients in whom an ulnar paraesthesia or nerve stimulator motor response was elicited at the time of block placement Patient characteristics, the severity of preoperative ulnar nerve dysfunction and surgical variables were similar in the two groups Anaesthetic technique did not affect neurological outcome (new or worsening pain, paraesthesias, numbness or motor weakness) immediately after surgery or at or weeks after surgery All patients in the axillary group who reported new or worsening neurological symptoms after surgery had received bupivacaine in combination with either an ulnar paraesthesia or motor response Although laboratory studies have identified multiple risk factors for the deve- 330 T.T Horlocker lopment of neurological injury after regional anaesthesia, clinical studies have not been performed to verify the results Even less information is available for the variables affecting neurological damage in patients with pre-existing neurological disease However, several disorders of the central and peripheral nerves require further mention Multiple sclerosis Multiple sclerosis is a degenerative disease of the CNS and is characterised by multiple sites of demyelination in the brain and spinal cord The peripheral nerves are not involved The course of the disease consists in exacerbations and remissions of symptoms, and the unpredictability in the patient’s changing neurological status must be appreciated when an anaesthetic technique has to be selected Stress, surgery and fatigue have been implicated in the exacerbation of multiple sclerosis Epidural and, more often, spinal anaesthesia have been implicated in the relapse of multiple sclerosis, although the evidence is not strong [20] The mechanism by which spinal anaesthesia may exacerbate multiple sclerosis is presumed to be direct local anaesthetic toxicity Epidural anaesthesia has been recommended in preference to spinal anaesthesia, because the concentration of local anaesthetic in the white matter of the spinal cord is one-fourth that after epidural administration [21] A dilute solution of local anaesthetic with spinal or epidural anaesthesia is also advised Because multiple sclerosis is a disorder of the CNS, peripheral nerve blocks not affect neurological function and are considered appropriate anaesthetic techniques The largest series of neuraxial anaesthesia in patients with pre-existing CNS conditions involved 139 patients [22] Post-polio syndrome and multiple sclerosis were the most common CNS disorders (Table 1) Table Central nervous system diagnoses a Neurological diagnosis Number of patients (N) Percentage (%) Post-poliomyelitis 79 56.4 Multiple sclerosis 35 25 Traumatic spinal cord injury 13 9.3 Amyotrophic lateral sclerosis 3.6 Guillain–Barré syndrome 2.1 Meningomyelocele 1.5 Cauda equina syndrome 0.7 Huntington’s chorea 0.7 Neurosyphilis with paraplegia 0.7 aOne patient had a diagnosis of both multiple sclerosis and prior poliomyelitis From [22] Twenty-five (18%) patients had a co-existing radiculopathy, peripheral sensorimotor neuropathy or spinal stenosis Gender distribution was 86 (62%) male and 53 (38%) female The mean age of these patients was 60±17 years CNS diagnoses had been known for a mean of 23±23 years The majority of patients had sensori- Regional anaesthesia in the patient with pre-existing neurological dysfunction 331 motor deficits at the time of block placement There were no patients with new or worsening postoperative neurological deficits compared with preoperative findings (0.0%; 95%CI 0.0–0.3%) Diabetes mellitus A substantial proportion of diabetic patients report clinical symptoms of a peripheral neuropathy However, a subclinical peripheral neuropathy may be present before the onset of pain, paraesthesia or sensory loss and may remain undetected without electrophysiological testing for slowing of nerve conduction velocity The presence of underlying nerve dysfunction suggests that patients with diabetes may have a decreased requirement for local anaesthetic The diabetes-associated microangiopathy of nerve blood vessels decreases the rate at which local anaesthetic uptake occurs from the site of administration, resulting in prolonged exposure to local anaesthetic solutions The combination of these two mechanisms may cause nerve injury with an otherwise safe dose of local anaesthetic in diabetic patients In a study examining the effect of local anaesthetics on nerve conduction block and injury in diabetic rats, Kalichman and Calcutt [12] reported that the local anaesthetic requirement is decreased and the risk of local anaesthetic-induced nerve injury is increased in diabetics These findings support the suggestions that diabetic patients may require less local anaesthetic to produce anaesthesia and that a reduction in dose may be necessary to prevent neural injury by doses considered safe in nondiabetic patients Similarly, Singelyn et al [23] reviewed block difficulty, success rate and neurological complications in a series of 1,342 patients undergoing popliteal fossa block using a nerve stimulator approach The 371 patients with a diagnosis of diabetes mellitus required more needle passes to obtain a satisfactory motor response, but also noted a higher success rate There were no neurological complications in any patient A recent retrospective review of 567 patients with a sensorimotor neuropathy or diabetic polyneuropathy who underwent neuraxial block evaluated the risk of neurological complications All patients had a single neurological diagnosis; there were no co-existing spinal canal or CNS disorders [22] The majority of patients had sensorimotor deficits at the time of surgery Two (0.4%; 95%CI 0.1–1.3%) patients experienced new or worsening postoperative neurological deficits compared with preoperative findings This frequency is consistent with previous investigations examining nondiabetic patients The investigators concluded that neuraxial blockade does not appear to increase the risk of neurological complications among patients with diabetic sensorimotor or polyneuropathy Epidural and spinal anaesthesia after major spinal surgery Previous spinal surgery has been considered to represent a relative contraindication to the use of regional anaesthesia Many of these patients experience chronic back pain and are reluctant to undergo epidural or spinal anaesthesia, fearing 332 T.T Horlocker exacerbation of their pre-existing back complaints Several postoperative anatomical changes make needle or catheter placement more difficult and complicated after major spinal surgery In a study 105 of 48 patients with chronic low back pain after spinal fusion, showed significant spinal stenosis on computed tomographic scans and required surgical decompression [24] The ligamentum flava may be injured during surgery, resulting in adhesions within or obliteration of the epidural space The spread of epidural local anaesthetic may be affected by adhesions, producing an incomplete or ‘patchy’ block Obliteration of the epidural space may increase the incidence of dural puncture and make subsequent placement of an epidural blood patch difficult Needle placement in an area of the spine that has undergone bone grafting and posterior fusion is not possible with midline or lateral approaches; needle insertion can be accomplished at unfused segments only The guidelines for epidural anaesthesia after spinal surgery are unclear Daley et al [25] reviewed the charts of 18 patients with previous Harrington rod instrumentation who underwent 21 attempts at epidural anaesthesia for obstetric analgesia Continuous lumbar epidural anaesthesia was successfully established in 20 of 21 attempts, but only 10 procedures were performed easily at the first attempt The remaining 11 patients required larger amounts of local anaesthetics or complained of a patchy block or both There was no correlation between the level of surgery and the easy of insertion or the quality of epidural anaesthesia There were no side-effects except for low back pain in two patients in whom multiple attempts at catheter placement had been necessary Crosby and Halpern [26] studied nine parturients with previous Harrington rod instrumentation who underwent epidural anaesthesia for analgesia during labour and delivery Five of the nine catheters were successfully placed at the first attempt Four of the nine procedures were complicated and involved multiple attempts before successful insertion, traumatic catheter placement requiring a second insertion, inadequate epidural analgesia with subsequent dural puncture on a repeated attempt or inability to locate the epidural space despite attempts at two levels Seven of the nine patients obtained satisfactory analgesia There were no adverse sequelae related to the epidural insertion Hubbert [27] described attempted epidural anaesthesia in 17 patients with Harrington rod instrumentation Four of five patients with fusions terminating above the interspace between L-3 and L-4 had successful epidural placement However, in 12 patients with fusions extending to the interspace between L-5 and S-1, attempts were unsuccessful, patients required multiple attempts, and patient had a dural puncture after multiple attempts at epidural placement before it was successfully achieved A false loss of resistance was reported to have occurred frequently Thus, historically it was concluded that epidural anaesthesia may be successfully performed in patients who have had previous spinal surgery, but successful catheter placement may be possible on the first attempt in only 50% of patients, even by an experienced anaesthesiologist Although adequate epidural anaesthesia is eventually produced in 40–95% of patients, there appears to be a higher incidence of traumatic needle placement, unintentional dural puncture and unsuccessful Regional anaesthesia in the patient with pre-existing neurological dysfunction 333 epidural needle or catheter placement, especially if spinal fusion extends to between L-5 and S-1 A more recent investigation examined the overall success and neurological complication rates among 937 patients with spinal stenosis or lumbar disc disease undergoing neuraxial block between 1988 and 2000 [22] Of these, 210 (22%) patients had a co-existing peripheral neuropathy in addition to their spinal cord pathology Gender distribution was 619 (66%) male and 318 (34%) female The mean age of these patients was 67±14 years Neurological diagnoses had been known for a mean of 5±6 years; 335 (51%) patients had active symptoms at the time of the block In addition, 207 (22%) patients had a history of prior spinal surgery before undergoing neuraxial block, although the majority were simple laminectomies or discectomies (Table 2) Table Outcomes of neuraxial blockade in patients with spinal stenosis of lumbar disc disease From [22] Patients without prior spine surgery (N=730) Block efficacy Satisfactory Unilateral Segmental No block Technical complications Unable to locate epidural or intrathecal space Traumatic (bloody) Paraesthesia “High” spinal Unable to advance catheter (epidural) Accidental dural puncture (epidural) Neurological complications Patients with prior spine surgery (N=207) N 709 12 (%) (97.1) (0.0) (1.2) (1.6) N 202 (%) (97.6) (0.5) (0.0) (1.9) 19 37 (0.8) (2.6) (5.1) (0.1) (0.0) (3.9) (4.4) (0.0) 14 (4.9) (4.1) (2.8) (1.0) (2.7) (1.4) Success rates did not differ between patients who had previous surgery and those who had undergone a spinal procedure Ten (1.1%; 95%CI 0.5–2.0%) patients experienced new or progressive neurological deficits compared with preoperative findings Although the majority of the deficits were related to surgical trauma or tourniquet ischaemia, the neuraxial block was the primary aetiology in patients The preliminary nature of these data warrants care in their interpretation However, overall, patients with spinal stenosis or lumbar disc disease may undergo successful neuraxial block without a significant increase in neurological complications Importantly, this includes patients who have undergone prior (minor) spinal surgery 334 T.T Horlocker Anaesthetic management of neurological disease Progressive neurological disease is considered by some to be a relative contraindication to regional anaesthesia, because of the difficulty in determining the cause of new neurological deficits that appear perioperatively There are no controlled clinical studies identifying regional anaesthesia as a significant factor in increased risk of neurological injury; only anecdotal reports are available The medicolegal issue, however, remains, and if regional anaesthesia is indicated for other pre-existing medical conditions or by patient request, the patient should be informed of the risk of neurological complications, including coincidental progression of preoperative deficits, associated with anaesthesia and surgery This discussion, along with preoperative neurological status, should be fully documented in the patient’s record Patients with preoperative neurological deficits may undergo further nerve damage more readily from needle or catheter placement, local anaesthetic systemic toxicity, and vasopressor-induced neural ischaemia Although the use of paraesthesia techniques is not contraindicated, care should be taken to minimise needle trauma and intraneuronal injection Dilute local anaesthetic solutions should be used whenever feasible to decrease the risk of local anaesthetic systemic toxicity The use of epinephrine-containing solutions is controversial The potential risk of vasopressor-induced nerve ischaemia must be weighed against the advantages of predicting local anaesthetic intravascular injections, improved quality of block, and decreased blood levels of local anaesthetics Because epinephrine also prolongs and block and therefore neural exposure to local anaesthetics, the appropriate concentration and dose of local anaesthetic solutions must be considered Patients with microvascular disease in combination with an underlying peripheral neuropathy, such as those with diabetes, may be most sensitive to the vasoconstrictive effects of epinephrine Efforts should also be made to decrease neural injury in the operating room through careful patient positioning Postoperatively, these patients must be followed closely to detect potentially treatable sources of neurological injury, including constrictive dressings, improperly applied casts and increased pressure on neurologically vulnerable sites New neurological deficits should be evaluated promptly by a neurologist for formal documentation of the patient’s evolving neurological status and the arrangement of further testing and long-term followup Regional anaesthesia in the patient with pre-existing neurological dysfunction 335 References Gower DJ, Baker EL, Bell WO et al (1987) Contraindications to lumbar puncture as defined by computed cranial tomography J Neurol Neurosurg Psychiatry 50:1071–1074 Wedel DJ, Mulroy MF (1983) Hemiparesis following dural puncture Anesthesiology 59:475–477 Sakabe T, Maekawa T, Ishikawa T, Takeshita H (1974) The effects of lidocaine on canine cerebral metabolism and circulation related to the electroencephalogram Anesthesiology 40:433–441 Usubiaga JE, Wikinski J, Ferrero R et al (1966) Local anesthetic-induced convulsions in man—an electroencephalographic study Anesth Analg 45:611–620 Perkins WJ, Jr, Lanier WL, Sharbrough FW (1988) Cerebral and hemodynamic effects of lidocaine accidentally injected into the carotid arteries of patients having carotid endarterectomy Anesthesiology 69:787–790 Phillips OC, Ebner H, Nelson AT, Black MH (1969) Neurologic complications following spinal anesthesia with lidocaine: a prospective review of 10,440 cases Anesthesiology 30:284–289 Selander D, Edshage S, Wolff T (1979) Paresthesiae or no paresthesiae? Nerve lesions after axillary blocks Acta Anaesthesiol Scand 23:27–33 Selander D, Dhuner KG, Lundborg G (1977) Peripheral nerve injury due to injection needles used for regional anesthesia An experimental study of the acute effects of needle point trauma Acta Anaesthesiol Scand 21:182–188 Rice AS, McMahon SB (1992) Peripheral nerve injury caused by injection needles used in regional anaesthesia: influence of bevel configuration, studied in a rat model Br J Anaesth 69:433–438 10 Schneider M, Ettlin T, Kaufmann M et al (1993) Transient neurologic toxicity after hyperbaric subarachnoid anesthesia with 5% lidocaine Anesth Analg 76:1154–1157 11 Myers RR, Heckman HM (1989) Effects of local anesthesia on nerve blood flow: studies using lidocaine with and without epinephrine Anesthesiology 71:757–762 12 Kalichman MW, Calcutt NA (1992) Local anesthetic-induced conduction block and nerve fiber injury in streptozotocin-diabetic rats Anesthesiology 77:941–947 13 Rigler ML, Drasner K, Krejcie TC et al (1991) Cauda equina syndrome after continuous spinal anesthesia Anesth Analg 72:275–281 14 Drasner K (1993) Models for local anesthetic toxicity from continuous spinal anesthesia Reg Anesth 18:434–438 15 Selander D (1993) Neurotoxicity of local anesthetics: animal data Reg Anesth 18:461–468 16 Yee TC, Kalichman MW (1997) Effects of aging on nerve conduction block induced by bupivacaine and procaine in rats J Periph Nerv System 2:175–179 17 Bromage PR (1976) Paraplegia following epidural analgesia: a misnomer Anaesthesia 31:947–949 18 Kane RE (1981) Neurologic deficits following epidural or spinal anesthesia Anesth Analg 60:150–161 19 Hebl JR, Horlocker TT, Sorenson EJ, Schroeder DR (2001) Regional anesthesia does not increase the risk of postoperative neuropathy in patients undergoing ulnar nerve transposition Anesth Analg 93:1606–1611 20 Crawford J, James FI, Nolte H (1981) Regional analgesia for patients with chronic neurological disease and similar conditions Anaesthesia 36:821 21 Warren TM, Datta S, Ostheimer GW (1982) Lumbar epidural anesthesia in a patient with multiple sclerosis Anesth Analg 61:1022–1023 336 T.T Horlocker 22 Hebl JR, Horlocker TT, Schroeder DR (2005) Neurologic complications after neuraxial anesthesia or analgesia in patients with pre-existing spinal stenosis or lumbar disc disease Reg Anesth Pain Med 29:A89 23 Singelyn FJ, Gerard C, Fuzier R (2005) The influence of diabetes mellitus on the success rate of posterior popliteal sciatic nerve blockade Anesthesiology A–1125 24 Laasonen EM, Soini J (1989) Low-back pain after lumbar fusion Surgical and computed tomographic analysis Spine 14:210–213 25 Daley MD, Rolbin SH, Hew EM et al (1990) Epidural anesthesia for obstetrics after spinal surgery Reg Anesth 15:280–284 26 Crosby ET, Halpern SH (1989) Obstetric epidural anaesthesia in patients with Harrington instrumentation Can J Anaesth 36:693–696 27 Hubbert CH (1985) Epidural anesthesia in patients with spinal fusion Anesth Analg 64:843 Chapter 30 Infectious complications of regional anaesthesia D.J WEDEL Infectious complications may occur after any regional anaesthetic technique, but are of greatest concern if the infection occurs near or within the central neuraxis Possible risk factors include underlying sepsis, diabetes, depressed immune status, steroid therapy, localised bacterial colonisation or infection, and chronic catheter maintenance Bacterial infection of the central neuraxis may present as meningitis or cord compression secondary to abscess formation The infectious source may be exogenous (e.g contaminated equipment or medication), or endogenous (a bacterial source in the patient seeding to the needle or catheter site) Microorganisms can also be transmitted via a break in aseptic technique, and indwelling catheters may be colonised from a superficial site (skin) and subsequently serve as a wick for spread of infection from the skin to the epidural or intrathecal space Although individual cases have been reported in the literature, serious central neuraxial infections such as arachnoiditis, meningitis, and abscess are rare following spinal or epidural anaesthesia In a combined series of more than 65,000 spinal anaesthetics, there were only cases of meningitis A similar review of approximately 50,000 epidural anaesthetics failed to disclose a single epidural or intrathecal infection [1] A more recent multicentre, prospective study including 40,640 spinal and 30,413 epidural anaesthetics reported no infectious complications [2] Few data suggest that spinal or epidural anaesthesia during bacteraemia is a risk factor for infection of the central neuraxis Although the authors of the large studies cited did not report how many patients were febrile during administration of the spinal or epidural anaesthetic, a significant number of the patients included in these studies underwent obstetric or urological procedures, and it is likely that some patients were bacteraemic after (and perhaps during) needle or catheter placement In a recent retrospective review of 4,767 consecutive spinal anaesthetics by Horlocker et al [3], two infectious complications were noted One patient, who developed a disc space infection following spinal anaesthesia, was noted to have had a recent untreated episode of urosepsis The second patient developed a paraspinal abscess 11 days after spinal anaesthesia performed after unsuccessful attempts at caudal blockade for treatment of a suspected rectal fistula Despite the apparently low risk of central nervous system infection following regional anaesthesia, anaesthesiologists have long considered sepsis to be a relative contraindication to the administration of spinal or epidural anaesthesia This impression is based largely on anecdotal reports and conflicting laboratory and clinical investigations 338 D.J Wedel The clinical presentation of infections of the central nervous system, the laboratory and clinical studies evaluating the association between meningitis and dural puncture in bacteraemic subjects, the risk of central neuraxial blockade in patients with herpes simplex and human immunodeficiency virus (HIV) and the clinical studies investigating the risk of infection during chronic epidural catheterisation in febrile and immunocompromised patients will be discussed An understanding of these concerns will assist clinicians in evaluation of the febrile patient for central neuraxial blockade Neuraxial anaesthesia and infection Dural puncture has been cited as a risk factor for meningitis in the septic patient The presumed mechanisms include introduction of blood into the intrathecal space during needle placement and disruption of the normal protective mechanisms provided by the blood–brain barrier but these have not been confirmed In 1919 Weed et al [4] demonstrated that dural puncture performed in septicaemic rats invariably resulted in fatal meningitis In the same year Wegeforth and Latham [5] described 93 patients suspected of having meningitis, all of whom underwent diagnostic lumbar puncture (LP) and blood cultures It was found that 38 patients had proven meningitis, while the other 55 (6 were bacteraemic at the time of LP) had normal CSF Of the patients with bacteraemia, subsequently developed meningitis These findings suggest that patients with bacteraemia are at risk The LPs in this study were performed during two epidemics of meningitis occurring at a military installation These two historical studies provided support for the claim that LP during bacteraemia was a risk factor for meningitis Subsequent clinical studies yielded conflicting results Pray [6] reported that the incidence of meningitis in children who underwent diagnostic LP during pneumococcal sepsis was no higher among patients who had normal CSF results than among those who did not undergo diagnostic LP Eng and Seligman [7] retrospectively reviewed the records of 1,089 bacteraemic patients, 200 of whom underwent LP There was no difference between the incidence of spontaneous and “LP-induced” meningitis Teele et al [8] reviewed the records of 277 children with bacteraemia from 1971 to 1980 Meningitis occurred in (15%) of 46 children in whom LP revealed normal CSF, but in only (1%) of 231 children who did not undergo LP This difference was statistically significant In addition, children receiving antibiotics at the time of LP were less likely to develop meningitis Carp and Bailey [9] supported the finding that treatment with antibiotics may prevent LP-induced meningitis Twelve of 40 bacteraemic rats subjected to cisternal puncture with a 26-G needle developed meningitis Neither bacteraemic animals not subjected to dural puncture nor animals undergoing dural puncture in the absence of bacteraemia developed meningitis In humans, antibiotic therapy is often deferred until after cultures are obtained There are several other limitations to this study While E coli is a common cause of bacteraemia, it is an uncommon cause of meningitis In addition, the authors knew of sensitivity to the bacteria 362 R.D White Manz M, Pfeiffer D, W J et al (1991) Intravenous treatment with magnesium in recurrent persistent ventricular tachycardia New Trends in Arrhythmias 7:437–442 Parham WA, Mehdirad AA, Biermann KM et al (2006) Hyperkalemia revisited Tex Heart Inst J 33:40–47 Tijunelis M, Herbert M (2005) Myth: intravenous amiodarone is safe in patients with atrial fibrillation and Wolff-Parkinson-White syndrome in the emergency department Can J Emerg Med 7:262–265 10 Exner DV, Muzyka T, Gillis AM (1995) Proarrhythmia in patients with the Wolff-Parkinson-White syndrome after standard doses of intravenous adenosine Ann Intern Med 122:351–352 11 Gupta AK, Shah CP, Maheshwari A et al (2002) Adenosine induced ventricular fibrillation in Wolff-Parkinson-White syndrome Pacing Clin Electrophysiol 25:477–480 12 Schutzenberger W, Leisch F, Kerschner K et al (1989) Clinical efficacy of intravenous amiodarone in the short term treatment of recurrent sustained ventricular tachycardia and ventricular fibrillation Br Heart J 62:367–371 13 Credner SC, Klingenheben T, Mauss O et al (1998) Electrical storm in patients with transvenous implantable cardioverter-defibrillators: incidence, management and prognostic implications J Am Coll Cardiol 32:1909–1915 14 Helmy I, Herre JM, Gee G et al (1988) Use of intravenous amiodarone for emergency treatment of life-threatening ventricular arrhythmias J Am Coll Cardiol 12:1015–1022 15 Gorgels AP, van den Dool A, Hofs A et al (1996) Comparison of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia Am J Cardiol 78:43–46 16 Marill KA, Greenberg GM, Kay D et al (1997) Analysis of the treatment of spontaneous sustained stable ventricular tachycardia Acad Emerg Med 4:1122–1128 17 Armengol RE, Graff J, Baerman JM et al (1989) Lack of effectiveness of lidocaine for sustained, wide QRS complex tachycardia Ann Emerg Med 18:254–257 18 Domanovits H, Paulis M, Nikfardjam M et al (1999) Sustained ventricular tachycardia in the emergency department Resuscitation 42:19–25 19 Ho DS, Zecchin RP, Richards DA et al (1994) Double-blind trial of lignocaine versus sotalol for acute termination of spontaneous sustained ventricular tachycardia Lancet 344:18–23 20 Wik L, Hansen TB, Fylling F et al (2003) Delaying defibrillation to give basic cardiopulmonary resuscitation to patients with out-of-hospital ventricular fibrillation: a randomized trial JAMA 289:1389–1395 21 Cobb LA, Fahrenbruch CE, Walsh TR et al (1999) Influence of cardiopulmonary resuscitation prior to defibrillation in patients with out-of-hospital ventricular fibrillation JAMA 281:1182–1188 OBSTETRICS AND PAEDIATRICS Chapter 33 Obstetrics at high risk R ALEXANDER, N VOLPE Why Mothers Die 2000-2002–Report on confidential enquiries into maternal deaths in the United Kingdom (http://www.cemach.org.uk/publications/WMD2000_2002/content.htm) During this triennium, 391 maternal deaths were reported to the Enquiry, a slight increase on the 378 cases reported in 1997–99 Of the 391 deaths, 106 were classified as Direct and 155 as Indirect deaths, representing 27% and 40% of reported cases, respectively (Table 1) Thirty-six (9%) were classified as Coincidental and 94 Table Number of maternal deaths reported to the Enquiry by cause; United Kindom 1985-2002 Chapter Cause 1985-87 1988-90 1991-93 1994-96 1997-99 2000-02* Direct deaths (occurring during pregnancy and up to and including 42 days inclusive after delivery Thrombosis and thromboembolism 032 033 35 048 035 130 Hypertensive disease of pregnancy 027 027 120 020 015 014 Haemorrhage 010 022 015 012 017 017 Amniotic fluid embolism 109 011 110 017 018 015 Death in early pregnancy total 022 024 18 015 017 015 Ectopic 016 015 08 012 013 011 Spontaneous miscarriage 105 016 013 012 012 011 Legal termination 011 013 015 011 012 013 Other 00 010 012 010 010 110 Genital tract sepsis 116** 017** 019** 014*** 014*** 011*** Other Direct total 027 017 014 017 017 018 Genital tract trauma 116 013 014 015 012 011 Fatty liver 116 015 012 012 014 013 Other 015 019 018 010 011 014 Anaesthetic 116 014 018 011 013 226 Total number of Direct deaths 139 145 128 134 106 106 Indirect deaths (up to and including 42 days after delivery) 10 Cardiac 122 018 11 Psychiatric N/A N/A 12 Other Indirect 162 075 13 Indirect malignancies N/A N/A Total number of Indirect deaths 184 093 14 Coincidental deaths 126 15 Late deaths (42-365 days after delivery) Direct Indirect Coincidental Total number of Late deaths N/A N/A N/A 016 037 N/A 063 N/A 100 039 019 086 N/A 134 035 015 075 011 136 244 016 090 005 1155 139 146 136 129 036 013 010 025 048 010 023 013 046 014 032 036 072 017 039 061 107 004 45 45 94 N/A = Not available deaths reported to the Enquiry only and excluding other deaths identified by ONS; ** Excluding early pregnancy deaths due to sepsis *** Including early pregnancy deaths due to sepsis * 366 R Alexander, N Volpe (24%) as Late The total number of Direct and Indirect maternal deaths reported to the Enquiry, 261, is higher than the 242 reported in the previous triennium As first seen in the last report, the number of Indirect deaths now exceeds the number of Direct deaths The overall maternal mortality rate for the United Kingdom for this triennium from deaths due to both Direct and Indirect causes is 13.1 maternal deaths per 100,000 maternities Table gives the actual numbers of deaths and Table shows the UK maternal death rates per million maternities by specific cause of death for the last six triennia Table Definitions of maternal deaths Term Maternal deaths* Definition Deaths of women while pregnant or within 42 days of the end of the pregnancy, from any cause related to or aggravated by the pregnancy or its management, but not from accidental or incidental causes Direct* Deaths resulting from obstetric complications of the pregnant state (pregnancy, labour and puerperium), from interventions, omissions, incorrect treatment or from a chain of events resuiting from any of the above Indirect* Deaths resulting from previous existing disease, or disease that developed during pregnancy and which was not due to direct obstetric causes, but which was aggravated by the physiologic effects of pregnancy Late* Deaths occurring between 42 days and year after abortion, miscarriage or delivery that are due to Direct or Indirect maternal causes Coincidental (Fortuitous)** Deaths from unrelated causes which happen to occur in pregnancy or the puerperium Pregnancy-related deaths** Deaths occurring in women while pregnant or within 42 days of termination of pregnancy, irrespective of the cause of the death * = ICD ICD 9/10 classifies these deaths as Fortuitous but the Enquiry prefers to use the term Coincidental as it a more accurate description The Enquiry also considers deaths from Late Coincidental causes *** = ICD 10 ** = Obstetrics at high risk 367 Table Mortality rates by major cause of maternal death per million maternities; United Kingdom 1985-2002 Chapter Rate per million maternities Cause 1985-87 14.1 11.9 4.4 4.0 7.9* 4.4 11.9 1988-90 14.0 11.4 19.3 4.7 7.6* 5.5 7.2 1991-93 1994-96 1997-99 2000-02 Thrombosis and thromboembolism 15.1 21.8 165 15.0 Hypertensive disease of pregnancy 8.6 9.1 7.1 7.0 Haemorrhage 6.5 5.5 3.3 8.5 Amniotic fluid embolism 4.3 7.7 3.8 2.5 Deaths in early pregnancy 5.2* 6.8 8.0 7.5 Genital tract sepsis 6.4 6.4* 6.6* 5.5* Total uterine trauma/other 6.0 3.2 3.3 4.0 Direct Genital tract trauma 2.6 1.3 1.7 2.3 1.0 0.5 Other Direct 9.3 5.9 4.3 0.9 2.3 3.5 Anaesthetic 2.6 1.7 3.5 0.5 1.4 3.0 10 Cardiac Indirect 9.7 7.6 15.9 17.7 16.5 22.0 11 Psychiatric Indirect** – – – 4.1 7.1 8.0 12 Other Indirect 27.3 31.0 27.0 39.1 35.3 45.6 13 Indirect malignancies – – – – 5.1 2.5 2-13 Total Direct and Indirect 98.3 100.1 98.1 121.9 114.0 131.1 14 Coincidental (Fortuitous) 11.3 16.5 19.9 16.4 10.8 18.0 15 Late 7.1 20.3 19.9 32.8 50.3 47.0 * Including sepsis in early pregnancy; ** until 1993-96 counted as Coincidental and note that these are only for suicides which occur during the first weeks A futher explanation od actual death rates from suicide can be found in the text This table excludes cases identified by ONs but not notified to the Enquiry The main causes of death in pregnancy and delivery are thromboebolism, hypertensive disease, cardiac disease and haemorrhage The first three will be discussed in further detail Thromboebolic disease Pregnant women and, in particular, those with a history of thromboembolic disease are at appreciable risk during pregnancy The reported incidence of deep vein thrombosis (DVT) and nonfatal pulmonary embolism varies considerably because of the peculiar diagnostic difficulties in pregnancy Real-time ultrasound scanning combined with Doppler studies, being noninvasive, are the first-line diagnostic techniques for DVT in pregnancy [1] The following are the recommendations of the American College of Obstetricians and Gynecologists: – Pregnant patients with a history of isolated venous thrombosis directly related to a transient, highly thrombogenic event (orthopaedic trauma, complicated surgery) in whom an underlying thrombophilia has been excluded may be offered heparin prophylaxis or no prophylaxis during the antepartum period However, they should be counselled that their risk of thromboembolism is likely to be higher than the normal population Prophylactic warfarin should be offered for weeks postpartum – Pregnant patients with a history of idiopathic thrombosis, thrombosis related to pregnancy or oral contraceptive use, or a history of thrombosis accompanied by an underlying thrombophilia other than homozygous for the factor V 368 R Alexander, N Volpe Leiden mutation, heterozygous for both the factor V Leiden and the prothrombin G20210A mutation, or antithrombin-III (AT-III) deficiency should be offered antepartum and postpartum low-dose heparin prophylaxis – Patients without a history of thrombosis but who have an underlying thrombophilia and have a strong family history of thrombosis also are candidates for antepartum and postpartum prophylaxis At the minimum, postpartum prophylaxis should be offered – Pregnant patients with a history of life-threatening thrombosis, with recent thrombosis, with recurrent thrombosis, receiving chronic anticoagulation, or patients with thrombosis found to be AT-III deficient, homozygous for the factor V Leiden mutation or prothrombin G20210A mutation, heterozygous for both the factor V Leiden and the prothrombin G20210A mutation should be given adjusted-dose heparin every hours to maintain the activated partial thromboplastin time (APTT) at least 1.5 times control throughout the dosing interval Low-molecular-weight heparin (LMWH) administered twice daily also is an alternative – Patients at risk for thrombosis should receive warfarin postpartum for weeks to achieve an international normalised ration (INR) of approximately 2.0 to 3.0 Heparin should be given immediately postpartum with warfarin for at least days until the INR is therapeutic – Patients with antiphospholipid syndrome and a history of thrombosis require adjusted-dose prophylactic anticoagulation – Patients who are candidates for either prophylactic or therapeutic heparin may be given enoxaparin or dalteparin during pregnancy However, because of the lack of data regarding adequate dosing during pregnancy, antifactor Xa levels may be monitored – The safety of epidural anaesthesia with twice-daily dosing of LMWH is of concern and should be withheld until 24 hours after the last injection – Epidural anaesthesia appears to be safe in women taking unfractionated low-dose heparin if the APTT is normal The major concerns with heparin use during pregnancy are not foetal but maternal and include heparin-induced osteoporosis and heparin-induced thrombocytopoenia (HIT) Bleeding is also an issue Warfarin derivatives cross the placenta A skeletal embryopathy resulting in stippled epiphyses and nasal and limb hypoplasia can occur when warfarin is given between and 12 weeks of gestation Midtrimester exposure may result in optic atrophy, microcephaly and developmental delay Bleeding can occur in the foetus at any time, resulting in a high foetal loss rate Management of hypertensive diseases of pregnancy Hypertensive diseases of pregnancy are one of the most common direct causes of maternal death in the developed world The largest single cause of death amongst women with pre-eclampsia and eclampsia in the United Kingdom is intracranial Obstetrics at high risk 369 haemorrhage, reflecting a failure of effective anti-hypertensive therapy HELLP syndrome associated with pre-eclampsia is another cause of death Gestational hypertension occurs after 20 weeks of gestation and returns to normal within months of delivery It has none of the other features of pre-eclampsia Eclampsia indicates the occurrence of seizures in a parturient who may have no underlying pathology Pre-eclampsia is a complex multi-system disorder that may sometimes precede eclampsia The classic diagnostic triad for pre-eclampsia of hypertension, proteinuria and oedema is no longer considered useful Oedema occurs in up to 80% of normotensive parturients and, conversely, pre-eclampsia can occur in the absence of proteinuria There are several definitions of pre-eclampsia, but they generally involve hypertension occurring after 20 weeks with the involvement of at least one other organ system, for instance headache or epigastric pain Hypertension in pregnancy is defined as a systolic pressure of 140 mmHg and /or a diastolic pressure of >90 mmHg Pathophysiology Hypertension affects 10% of all pregnancies, and pre-eclampsia complicates approximately 2–8% in the UK It also occurs more frequently in women who have previously suffered from pre-eclampsia Other risk factors include diabetes, obesity, advanced age, nulliparity and a family history of pre-eclampsia The presence of antiphospholipid antibodies and other autoimmune and chronic diseases increases the likelihood of pre-eclampsia Pre-eclamptic toxaemia (PET) is a multi-system disorder of endothelial dysfunction, characterised by widespread increased capillary permeability and generalised vasoconstricted hypovolaemic circulation with a lower cardiac output However, the haemodynamic findings in pre-eclampsia are complex and vary widely between studies Circulating catecholamines and administered vasoactive drugs may cause exaggerated responses A high index of suspicion must be maintained even when the classic signs and symptoms are mild [2] Patients with pre-eclampsia are at risk of developing pulmonary oedema Early in the disease process the hypercoagulable state of normal pregnancy may be enhanced Later on, both platelet activation and consumption are increased which can lead to significant thrombocytopenia (platelet count 140/90 Proteinuria >300 mg/24 h Cerebral involvement (headache, visual disturbances) Features of severe pre-eclampsia Blood pressure >160/110 mmHg Proteinuria >5 g/24 h Cerebral involvement (hyperreflexia, seizures) Oliguria