ANAESTHESIA RELATED NEUROLOGICAL COMPLICATIONS

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1 SANDHU, Indian J. Anaesth. DASH :ANAESTHESIA 2004; 48 (6) : RELATED NEUROLOGICAL COMPLICATIONS 439 REVIEW ARTICLE ANAESTHESIA RELATED NEUROLOGICAL COMPLICATIONS SUMMARY Dr. K. Sandhu 1 Dr. H. H. Dash 2 Anaesthesia has made rapid strides in the past decades. However, the vexing problem of complications associated with anaesthesia persists. The spectrum is wide and this article attempts to address only the neurological aspect of these complications. These can range from permanent brain damage to minor neurological sequelae. Various factors are implicated, be it an anaesthetic agent, a faulty technique or a hereditary, familial or a pre-existing disease that predisposes to the development of these complications. As always, prevention is the best. Proper selection of the anaesthetic technique, meticulous intra-operative monitoring, careful positioning of the patients and good post-operative care can significantly reduce the incidence of these neurological complications. Keywords : Neurological, Complications, Anaesthesia. Introduction Modern anaesthesia has brought new challenges as well as benefits. Ironically, the promise to alleviate suffering has not come without a price. Anaesthetic complications may either culminate in a major catastrophe like death or permanent brain damage or minor neurological complications such as headache, backache or peripheral nerve injury. Although anaesthesia is now fairly safe, it is important to realize that death and complications can occur even in healthy patients. The complications may involve litigation or medico-legal problems for both anaesthesiologists and neurologists. 1-3 Death is the worst outcome from the medico-legal point of view but severe cerebral damage resulting from anaesthesia can be even more appalling. The relatives are subjected to the harrowing experience of seeing the patient in a vegetative state. Death or permanent brain damage associated with anaesthesia is defined as death or brain damage occurring during or within 24 hrs of anaesthesia, or after failure of a patient conscious before, to regain consciousness after anaesthesia. 4 Incidence Retrospective studies from advanced countries have shown that mortality solely related to anaesthesia varies from per 10,000 patients. 5-7 Pederson et al performed a series of studies in the late 1980 s to look into factors attributable to anaesthesia that led to significant morbidity and mortality. Up to 37% of anaesthesia related 1. M.D., Classified Specialist, Anaesthesiology 2. M.D., Prof. and Head, Department of Neuroanaesthesia Neurosciences Centre, A.I.I.M.S., New Delhi, India. Correspond to : Dr. (Lt Col) K Sandhu Department of Anaesthesiology, Army Hospital (RR) Delhi Cantt (Accepted for publication on ) morbidity was assessed to be preventable. 8 Accumulating data including a prospective study by Eichhorn clearly demonstrated that risk directly attributable to anaesthesia has declined over time and a death rate of 1/1,51,400 anaesthetics during has been curtailed to 0/2,44,000 by A more recent report was put forth by the Anaesthetic Mortality Committee of Western Australia in They too found that the deaths due to anaesthesia had come down from 1 in 20,000 during to 1 in 40,000 between It is hard to lay a finger on any one factor that causes neurological complications following anaesthesia. It could be an anaesthetic agent, a faulty technique or even a familial, hereditary or preexisting disease that may predispose to the development of neurological complications. Neurological complications associated with anaesthetics Premedicants like atropine and scopolamine have been reported to cause central anticholinergic syndrome and hyperpyrexia in paediatric patients. 11 Promethazine has often been blamed for producing extra pyramidal symptoms. Ketamine, a popular induction agent with good analgesic properties can cause hallucinations. The occurrence of myoclonic and seizure like motor activity has been observed clinically in non-epileptic patients after both intravenous and intramuscular ketamine. 12 Propofol, a newer intravenous inducing agent, is being extensively used as it has a short duration of action. A 1% incidence of neurological symptoms, which include twitching, myoclonic movements, opisthotonus and seizures, has been reported with use of this agent. 13 Delayed neuroexcitatory symptoms after uneventful anaesthesia have also been described. 14 Halothane often gives rise to intense shivering in the postoperative period, which is centrally mediated. Cognitive activity may be impaired for several days

2 440 INDIAN JOURNAL OF ANAESTHESIA, DECEMBER 2004 after halothane anaesthesia. Features include memory difficulties, reduced ability to concentrate and impairment of psychomotor tasks. 15 Bromide released during the metabolism of halothane is the probable culprit. 16 Many anaesthetic drugs and volatile agents have been reported to induce seizures clinically or produce epileptiform activity in the EEG. Etomidate is known to induce myoclonias 17 and methohexital can cause epileptiform activity. 11 Enflurane has been shown to cause epileptiform activity and grand mal seizure patterns. The ability of enflurane to produce seizures is influenced by both its concentration and the PaCO 2. Higher concentrations and lower PaCO 2 levels both contribute to increased epileptiform activity. 17 Isoflurane has also been implicated in producing seizure activity when administered along with nitrous oxide. 17 Terasko and Ishmi reported seizure like activity following sevoflurane anaesthesia. 18 Meperidine neurotoxicity is well known and is manifest clinically as shakiness, tremor, myoclonus and seizures. 19 This neuroexcitement is attributed to its N-demethylated metabolite normeperidine. 20 There have been reports too of grandmal seizure activity in patients after administration of fentanyl. 21 This phenomenon has also occurred after sufentanil and alfentanil administration. 22,23 Disorders associated with Neurological Complications There are several neurological diseases, which make the patient vulnerable to develop neurological complications during and following anaesthesia. An unexpected death during anaesthesia should raise the possibility of the patient suffering from a predisposition to malignant hyperpyrexia. Genetically susceptible subjects exhibit an abnormal response to anaesthesia particularly if halothane or suxamethonium have been administered. The response causes a rapid increase in body temperature associated with acidosis and intense muscle rigidity, as the calcium storage function of the sarcoplasmic reticulum is reduced in such patients. A multifactorial inheritance is probably responsible for production of this fulminant condition. Dantrolene 5-7 mgkg -1 IV in divided doses 48 hrs prior to anaesthesia and 3-5 mgkg -1 IV intraoperatively is recommended for prevention of muscle rigidity. The best option is to avoid halothane and suxamethonium during anaesthesia. Patients with atypical plasma cholinesterase are very sensitive to suxamethonium as in them the muscle relaxant property of suxamethonium is unduly prolonged. 24 Suxamethonium may aggravate myotonia in patients with dystrophia myotonica. Patients with lower motor/upper motor neuron or demyelinating diseases may develop cardiac arrest following administration of suxamethonium due to hyperkalemia. Altered response to suxamethonium has been reported in patients with Von Recklinghausen s disease and hypokalemic periodic paralysis. Patients with myasthenia gravis are very sensitive to hypnotics, sedatives, narcotics and particularly nondepolarising muscle relaxants. Muscle relaxants should also be used cautiously in patients with dermatomyositis. Cases of Lambert-Eaton syndrome too are sensitive to both depolarising and nondepolarising muscle relaxants. Barbiturates especially thiopentone can produce severe porphyric neuropathy and coma in cases of acute intermittent porphyria. Neurological complications associated with General Anaesthesia Adverse outcome associated with respiratory events constitute the single largest class of injury in the ASA closed claim study (34% of 1541 cases). 1 Death or brain damage occurred in 85% cases. While this may represent the most feared outcome following acute hypoxia, prolonged sub-acute hypoxia may lead to personality changes and intellectual impairment and headache and vomiting postoperatively. Majority of these events (72%) were considered preventable with better monitoring. An intriguing case of transient language disturbance following anaesthesia has been described wherein an English speaking patient started talking only Spanish, postoperatively. 25 Eichhorn and Tinker highlighted the fact that continuous use of EtCO 2 monitoring of ventilatory functions and SaO 2 for monitoring of circulatory functions is a boon for the modern anaesthesiologist. 9,26 Use of these sophisticated monitors is recommended to help avoid these mishaps. Delayed emergence following general anaesthesia, hypothermia, hyperpyrexia, convulsions and hypoxic encephalopathy along with raised intracranial pressure can be grouped under preventable neurological complications. Meticulous care during selection of drugs, dosages and anaesthetic technique with monitoring of core temperature, ventilatory and circulatory functions help in averting these neurological complications. A very distressing complication following balanced anaesthesia is awareness and recall of intraoperative events. This has the potential to cause adverse psychological sequelae. Even during seemingly adequate general anaesthesia, implicit memory may be retained along with the ability to subconsciously process auditory stimuli. 27 Lyons et al, studied 3000 obstetric patients who underwent general anaesthesia for caesarean section and reported an incidence of recall of 0.9% although no patient complained of pain. 28 Jones found the incidence of awareness with pain to be 1 in 10,000 cases. 29 For mitigation of this neurological complication the use of

3 SANDHU, DASH :ANAESTHESIA RELATED NEUROLOGICAL COMPLICATIONS 441 benzodiazepines and intermittent administration of inhalational anaesthetics has been recommended. It is also imperative to avoid a light plane of anaesthesia intraoperatively. Neurological complications of Local and Regional anaesthesia Headache and low backache are common following spinal or epidural anaesthesia. Horner s syndrome after high spinal, facial nerve palsy due to excessive CSF leak, adhesive arachnoiditis and meningitis has been reported. The spectre of paraplegia resulting from anaesthetic technique still haunts modern anaesthesiologists and the famous Woolley and Roe case of 1947 continues to serve as a stark reminder of the devastating effects of contaminated local anaesthetic solution on neural tissue. Severe neurological injury can occur from a variety of other causes after spinal or epidural anaesthesia (table 1). 30 Table - 1 : Causes of spinal cord and nerve root injury associated with neuraxial blockade (Sage et al, ) Cord compression Haematoma - Needle trauma - Tumor - Vascular anomaly - Bleeding disorders - Idiopathic Abscess Exogenous infection via a needle Haemotogenous Cord ischaemia Anterior spinal artery syndrome Cord trauma Needle damage Toxic injectate Intercurrent neurologic disease Hong and Lawrence have recently reported a case of anterior spinal artery syndrome following epidural anaesthesia for total hip replacement. 31 Mayall and Calder published a report of permanent paraparesis following needle puncture of the cord during placement of an epidural catheter. 32 The currently popular spinal or combined spinalepidural anaesthesia using atraumatic needles is not bereft of its own complications. Reynolds reports seven cases where damage to the conus medullaris occurred following use of these techniques. 33 The tip of the conus usually lies at L 1-2, although it may extend further in some patients. He therefore stresses the need for greater caution in selection of an appropriate lumbar interspace as the Tuffier s line is not always a reliable indication of the L 4-5 interspace. Besides this, cases of cauda equina syndrome following use of hyperbaric lignocaine have been cited and the incidence is quoted at 1: spinal anaesthetics. 34 The sacral nerve roots are poorly myelinated and particularly vulnerable to damage. Bilateral frontal haemorrhages following continuous spinal analgesia and an intracranial subdural haematoma following spinal anaesthesia have been reported recently. 35,36 The presumed mechanism is CSF leak causing low CSF pressure and traction on intracranial vessels following contraction of the subarachnoid space. A rupture of any of these vessels could result in an intracerebral bleed. 5 Within the last decade, the occurrence of transient neurological symptoms occurring after sub arachonoid anaesthesia has been a matter of concern. Although this bilateral paraesthesia is reversible, it contributes to a major cause of morbidity. Studies by various authors have quoted different incidence with various anaesthetics. A recent study by Keld et al places the incidence of transient neurological symptoms at 26% in patients anaesthetised with hyperbaric lignocaine as against 3% with hyperbaric bupivacaine. 37 Local anaesthetics used may themselves cause CNS complications. These are almost always due to overdose or inadvertent intravascular injections. Early CNS complications include restlessness, nervousness, slurred speech, tinnitus and sleepiness. Toxic reactions of CNS include stimulation of the cerebral cortex leading to excitement, disorientation, incoherent speech and seizures. Stimulation of the medulla can lead to vasomotor, respiratory and vomiting centers being affected and arrythmias along with hypotension and vomiting can ensue. Lignocaine has long been associated with generalised seizures. Bupivacaine, a predominantly cardiotoxic long acting agent, has been incriminated as the aetiological factor of generalized convulsions following caudal epidurals and also after local infiltration. 37,38 Nerve injuries Compression, inadvertent stretching, needle injury, direct injury and idiopathic causes are the major aetiological factors of peripheral nerve injuries following anaesthesia. Improper care during anaesthesia, induction and maintenance may damage the supraorbital, supratrochlear and facial nerves. Injury to the facial and lower cranial nerves can be encountered during posterior fossa surgery. Kroll et al in 1990 examined the ASA closed claim study database to define the role of nerve damage in the overall spectrum of anaesthesia related injury that leads to litigation. 2 A fresh analysis was carried out by Cheney

4 442 INDIAN JOURNAL OF ANAESTHESIA, DECEMBER 2004 et al. 39 While the proportion of claims for death following anaesthesia have decreased significantly in the 1990 s, the proportion of claims for nerve injury remain essentially constant. In the 1990 report, the proportion of nerve damage in 1541 total claims was 15% compared to 16% out of 4183 claims in The most frequent sites of injury were ulnar nerve (28%), brachial plexus (20%), lumbosacral nerve roots (16%) and spinal cord (13%). Majority of ulnar nerve injuries (85%) occurred in association with general anaesthesia whereas the other nerve injuries were found to be more likely following regional techniques (fig.1). The exact mechanism of injury remains unclear and was explicitly stated in only 9% of all cases. Anaesthetic care was judged as appropriate in 66% of all nerve injury claims. Addition of padding to the elbows was found to be present in 27% of all ulnar nerve injuries. The symptoms of ulnar neuropathy began few days after surgery while lower extremity neuropathies were noted soon after anaesthesia. 40,41 % of claims in group Ulnar (n=190) Brachial plexus (n=137) Fig. 1 : Incidence of general and regional anaesthesia in each category of nerve damage. P<0.5 compared to non-nerve damage 28 Males are probably more prone to ulnar nerve injury due to gender dependent differences in the anatomy of the ulnar nerve and related structures at the elbow. 40 In the lower limb neuropathies, prolonged positioning in the lithotomy position was cited as a major risk factor by Wainer et al. 41 Neurological complications during and following neuroanaesthetic procedures The neurological complications during and following neurosurgical operations differ depending on the surgical procedures and site of operation. The two most important complications are intracranial hypertension and deterioration of sensorium and aggravation of the neurological deficit. Focal and generalized seizures are common following anterior cranial fossa surgery as the motor cortex is located here. Convulsions up to a tune of 5% can occur following posterior fossa surgery also. Diabetes insipidus and inappropriate ADH secretion can result after pituitary surgery although improved surgical techniques have resulted in the decline of their incidence. Hypothermia and autonomic disturbances can follow Lumbosacral nerve root (n=105) Spinal cord (n=84) General Regional craniopharyngioma surgery or thalamic operations and pose problems for both the neuroanaesthesiologist and surgeon. Air embolism is a frequent complication during neurosurgery, especially in the sitting position. The incidence has been reported as 2-45% depending on the monitoring methods used for its detection (fig.2) Ultrasonic Doppler and EtCO 2 monitoring are advocated for its early detection as immediate management helps in salvaging the patients. 44 Tension pneumocephalus is another life threatening complication following posterior fossa surgery in the sitting position and there is a report of a similar occurrence during surgery in the supine position. 45,46 Air locked inside the cranial cavity after surgery may manifest as raised intracranial pressure culminating in seizures, neurological deficit or even cardiac arrest. Fluoroscopic imaging and CT scan are diagnostic. 47 Prompt evacuation of intracranial air is life saving in these patients. Quadriplegia can occur following posterior fossa surgery in the sitting position due to kinking of the anterior spinal arteries as a result of excessive neck flexion. Hence careful positioning of the head during surgery in the sitting position is of paramount importance. Fig. 2 : Incidence of venous air embolism as recorded by different monitoring aids Neurological complications in the postoperative period and ICU Hypoxaemia, fluid and electrolyte imbalance and aggravation of preoperative neurological problems are commonly encountered in the postoperative period. Severe hyponatremia (108 mmoll -1 ) may result in convulsions, coma, respiratory arrest and permanent brain damage. 48 Adequate administration of sodium containing fluids with 5% dextrose helps in averting this complication. Severe coma or seizures can be managed with a combination of hypertonic saline (3%), fluid restriction and frusemide. 49 It is important to remember that rapid treatment of hyponatremia can lead to central pontine myelinolysis and permanent brain damage. Increase in sodium levels more than 12 mmolday -1 may lead to neurologic sequelae. 50

5 SANDHU, DASH :ANAESTHESIA RELATED NEUROLOGICAL COMPLICATIONS 443 Postoperative abnormal psychiatric behaviour is commonly encountered in patients following open-heart surgery. The brain is most vulnerable to injury during extracorporeal circulation. Types of dysfunction cover a wide spectrum ranging from very subtle impairment (personality changes, memory loss, mild cognitive deficits and disorientation) through focal deficits (paraplegia, hemiplegia, visual defects and hearing loss) to coma and death. 51 Sensitive psychomotor tests in the early postoperative period reveal an incidence of dysfunction as high as 50-70%. 52 The aetiological factors are hypoperfusion, embolic phenomenon during cardiopulmonary bypass and the prolonged sojourn of patients in ICU. Improvement of surgical technique, shortening of perfusion time and use of membrane oxygenators during bypass goes a long way in minimising these complications. One of the key factors in good ICU care is appropriate analgesia and sedation. Under sedation causes agitation and discomfort with adverse psychological and physical effects. On the other hand, excessive sedation could lead to prolonged coma, respiratory depression and hypotension. During recovery from long periods of sedation, it is not uncommon for patients to experience confusion and sometimes exhibit frankly psychotic behaviour. Detriche et al, have put forward a simple Brussels sedation scale to help tackle this bugbear of optimum sedation. 53 Sleep plays an important part in the recovery of patients in ICU and chronic sleep deprivation has been associated with the development of psychosis, impaired tissue repair and cellular immune function. 54,55 These patients are frequently disoriented in time as their normal circardian rhythm is disrupted. 56 Alterations in the ICU environment such as reduced lighting, noise and interruptions at night may be more effective than overzealous use of sedatives. Neurological complications associated with pain management The management of chronic pain has always been a challenge for the anaesthesiologist. Nerve blocks are useful for both diagnostic and therapeutic management of painful conditions and can be associated with several potential neurological complications. A Gasserian ganglion block treats trigeminal neuralgia. Complications can result from injection of the drug into the subarachnoid space that surrounds the ganglion. Profound anaesthesia of the ipsilateral cranial nerves and loss of consciousness can result. Temporary or permanent loss of function associated with oculomotor, abducens, auditory, cochlear, vestibular and facial nerves have been reported Stellate ganglion block is given for reflex sympathetic dystrophy and painful conditions of the arm. Persistent relief can be obtained by administering a series of local anaesthetics. The cervical sympathetic chain is not closely confined within a fascial space and accidental injection into the vertebral artery or subarachnoid space can occur. Reports of bilateral superior laryngeal nerve block 60 and Horner s syndrome 61 after unilateral block provide support for concern. Coeliac plexus block is given for treatment of pain in intra abdominal malignancy. The most common neurological complication is somatic nerve injury, which has been documented as numbness or weakness in T 10 -L 1 dermatomes in 8% of patients in one large series. 62 A survey of pain clinics performing coeliac neurolysis in England and Wales during disclosed 4 cases of permanent paraplegia. 63 Radiological imaging was used in all cases, thereby making direct neuraxial injection less likely an explanation than indirect medullary injury. Lumbar sympathectomy can sometimes result in post sympathetic neuralgia. The incidence has been reported between 30-50%. 64 Parasthesias, paraplegia, and bilateral block are known to occur. Erickson in a series of 241 patients, reported a mortality of 2.1%. 65 It should be borne in mind before contemplating any neurolytic technique that there is a possibility of mortality. Techniques should be immaculate, injections should be slow and controlled and a precise dosage should be used. Conclusion Prevention is always better than cure. Hence prompt detection and immediate management of respiratory and circulatory inadequacies should be instituted at the earliest. Proper positioning of the patient must be accorded the attention it deserves. Meticulous administration of anaesthesia along with excellent postoperative care goes a long way in minimizing neurological complications. References 1. Caplan RA, Posner KL, Ward RJ et al. Adverse respiratory events in anaesthesia: A closed claim analysis. Anesthesiology 1990; 72: Kroll DA, Caplan RA, Posner K et al. Nerve injury associated with anaesthesia. Anesthesiology 1990; 73: Caplan RA, Ward RJ, Posner K et al. Unexpected cardiac arrest during spinal anaesthesia: A closed claim analysis of predisposing factors. Anesthesiology 1998; 68: Harrison GG. Death attributable to anaesthesia. A ten year survey ( ). Br J Anaesth 1978; 50: Bodlander EMS. Deaths associated with anaesthesia. Br J Anaesth 1975; 47:

6 444 INDIAN JOURNAL OF ANAESTHESIA, DECEMBER Utting JE, Gray TC, Shelly FC. Human misadventure in anaesthesia. Can Anaesth Soc J 1979; 26: Tiret L, Desmonts JM, Hatton F. Complications associated with anaesthesia. A prospective study in France. Can Anaesth Soc J 1986; 33: Pederson T, Eliasen K, Henriksen E. A prospective study of mortality associated with anaesthesia and surgery. Acta Anaesth Scand 1990; 34: Eichhorn JH. Prevention of intraoperative anaesthesia accidents and related severe injury through safety monitoring. Anesthesiology 1989; 70: Eagle CCP, Davis NJ. Report of Anaesthetic Mortality Committee of Western Australia Anaesth Intens Care 1997; 25: Modica PA, Tempelhoff R, White PF. Pro and anti- convulsants effects of anaesthetics (Part II). Anesth Analg 1990; 70: Torline RL. Extreme hyperpyrexia associated with central anti-cholinergic syndrome. Anesthesiology 1972; 76: Physician s desk reference, 52 nd ed. Montvale NJ, USA: Medical economics company Islander G, Vinge E. Severe neuroexcitatory symptoms after anaesthesia with focus on propofol anaesthesia. Acta Anaesth Scand 2000; 44: Storms LH, Stark AM, Calverley RK et al. Psychological functioning after halothane or enflurane anaesthesia. Anesth Analg 1980; 59: Tinker JH, Gandofi AJ, Van Dyke RE. Elevation of plasma bromide levels in patients following halothane anaesthesia: time correlation with total halothane dosage. Anesthesiology 1976; 44: Modica PA, Tempelhoff R, White PF. Pro and anti- convulsant effects of anaesthetics (Part I). Anesth Analg 1990; 70: Terasko K, Ishni S. Postoperative seizure like activity following sevoflurane anesthesia. Acta Anaesth Scand 1996; 40: Goething MG, Thirman MJ. Neurotoxicity of meperidine. Ann Emerg Med 1985; 14: Kaiko RF, Foley KM, Grabinski PY. Central nervous system excitatory effects of meperidine in cancer patients. Ann Neurol 1983; 13: Rao TLK, Mamuraneui N, El-Etr AA. Convulsions: an unusual response to intravenous fentanyl administration. Anaesth Analg 1982; 61: Molbegott LP, Flashburg MH, Karasic L et al. Probable seizures after sufentanil. Anesth Analg 1987; 66: Strong WE, Matson M. Probable seizure after alfentanil. Anesth Analg 1989; 68: Davis L, Britten JJ, Morgan M. Cholinesterase: Its significance in anaesthetic practice. Anaesthesia 1997; 52: Ward ME, Marshall JC. Speaking in tongues. Paradoxical fixation on a non-native language following anaesthesia. Anaesthesia 1999; 54: Tinker JH, Dull DL, Caplan et al. Role of monitoring devices in prevention of anaesthetic mishaps: A closed claim analysis. Anesthesiology 1989; 71: Bailey AR, Jones JG. Patient s memories of events during general anaesthesia. Anaesthesia 1997; 52: Lyons G, Macdonald R. Awareness during Caesarean section. Anaesthesia 1991; 46: Jones JG. Perception and memory during general anaesthesia. Br J Anaesth 1994; 73: Sage DJ. Major neurologic injury following regional anaesthesia. In : Complications of regional anaesthesia ed. Finncaine BT, Churchill Livingstone, New York 1999; Hong DK, Lawrence HM. Anterior spinal artery syndrome following total hip arthroplasty under epidural anaesthesia. Anaesth Intensive Care 2001; 29: Mayall MF, Calder I. Spinal cord injury following an attempted thoracic epidural. Anaesthesia 1999; 54: Reynolds F. Damage to the conus medullaris following spinal anaesthesia. Anaesthesia 2001; 56: Loo CC, Irestedt L. Cauda equina syndrome after spinal anaesthesia with hyperbaric 5% lignocaine: A review of six cases of cauda equina syndrome reported to the Swedish Pharmaceutical Insurance Acta Anaesthesiol Scand 1999; 43: Crofts TR, Monagle J, Buist M et al. Bilateral frontal haemorrhage associated with continuous spinal analgesia. Anaesth Intensive Care 2001; 29: Acharya R, Chhabra SS, Ratra M et al. Cranial subdural haematoma after spinal anaesthesia. Br J Anaesth 2001; 86(6): Keld DB, Hein L, Dalgaard M et al. The incidence of transient neurologic symptoms (TNS) after spinal anaesthesia in patients undergoing surgery in the supine position. Hyperbaric lignocaine 5% versus hyperbaric bupivacaine 0.5%. Acta Anaesthesiol Scand 2000; 44: Berde CB. Convulsions associated with paediatric regional anaesthesia. Anesth Analg 1992; 75: Cheney FW, Domino KB, Caplan RA et al. Nerve injuries associated with anaesthesia. A closed claim analysis. Anesthesiology 1999; 90: Wainer MA, Wainer DO, Matsumoto JY et al. Ulnar neuropathy in surgical patients. Anaesthesiology 1999; 99: Wainer MA, Wainer DO, Harper MC et al. Lower extremity neuropathies associated with lithotomy positions. Anesthesiology 2000; 93: Muley SS, Saini SS, Dash HH. End tidal monitoring for detection of venous air embolism. Ind J Med Res (B) 1990; 92: Black S, Ockert DB, Oliver WC Jr et al. Outcome following posterior fossa craniectomy in patients in sitting or horizontal positions. Anesthesiology 1988; 69:

7 SANDHU, DASH :ANAESTHESIA RELATED NEUROLOGICAL COMPLICATIONS Dash HH, Bithal PK, Joshi S, Saini SS. Airway pressure monitoring as an aid in the diagnosis of air embolism. J Neurosurg Anaesth 1993; 5: Dash HH, Bithal PK, Muley SS Vishnoi N Saini SS. Tension pneumocephalus following posterior fossa surgery in sitting position. J Anaesth Clin Pharmacol 1990; 6: Satapathy GC, Dash HH. Tension pneumocephalus after neurosurgery in the supine position. Br J Anaesth 2000; 84(1): Dash HH, Bithal PK, Muley SS. Fluoroscopic imaging for monitoring tension pneumocephalus. Anesthesiology 1989; 71: A Arieff AI. Hyponatremia, convulsions, respiratory arrest and permanent brain damage after elective surgery in healthy women. N Eng J Med 1986; 314: Sarnaik AP, Meert K, Hachbarth R et al. Management of hyponatremic seizures in children with hypertonic saline. A safe and effective strategy. Crit Care Med 1991; 19: Stern RH, Riggs JE, Schochet SS Jr. Osmotic demyelination syndrome following correction of hyponatremia. N Eng J Med 1986; 314: Scott J, Ream AK. Complications of extra corporeal circulation. In Gravenstien N, Kirby RR, editors, Complications in Anaesthesiology, Philadelphia 1996; Slogoff S, Girgis KL, Keats AS. Aetiologic factors in neuropsychiatric complications associated with cardiopulmonary bypass. Anesth Analg 1982; 61: Detriche O, Bene J, Massant J et al. The Brussels sedation scale. Use of simple clinical sedation scale can avoid excessive sedation in patients undergoing mechanical ventilation in ICU. Br J Anaesth 1999; 83: Novaes MAFP, Aronovich A, Ferraz MB et al. Stressors in I C U patient s evaluation. Intensive Care Med 1997; 23: Tung A, Rosenthal M. Patients requiring sedation. Crit Care Clin 1995; 11: Krachman S L, Alonzo GE, Criner GJ. Sleep in the I C U. Chest 1995; 107: Saini SS. Retrogasserian anhydrous glycerol injection therapy in trigeminal neuralgia. J Neurol Neurosurg Psychiatry 1987; 50: Dash HH, Bithal PK. Percutaneous anhydrous glycerol injection therapy in trigeminal neuralgia. Ind J Pain 1992; 6: Dash HH. Management of patients with trigeminal neuralgia. J Anaesth Clin Pharmacol. 1999; 15: Wallace MS, Millholland A V. Contralateral spread of local anaesthetic with stellate ganglion block. Reg Anesth 1993; 18: Smyth R J, Evans D, Shumka D. Bilateral Horner s syndrome following unilateral stellate ganglion block. Pain Digest 1992; 2: Black A, Dwyer B. Coeliac plexus block. Anaesth Intens Care 1973; 1: Davies DD. Incidence of major complications of neurolytic coeliac plexus block. J R Soc. Med 1993; 86: Mochus M B, Rutherford RB, Rosales C et al. Sympathectomy for causalgia. Arch Surg 1987; 122: Erickson HG. Lumbar sympathectomy in obliterative arteriosclerosis. Scand J Thorac Cardiovasc Surg 1979; 13: 333. Are you changing your address? If so please complete this form in block letters & mail to : i) Dr. J. Ranganathan, Secretary ISA (National) IMA Bulding, Near 5 Roads, Saradha College Road, Salem (T.N.) ii) This is very essential to ensure your copy of IJA. Name : I.S.A. NO. : Old Address : New Address (with Pin code) : Signature :

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