Volume 164 Issue 8

Limited adverse occurrence screening: using medical record review to reduce hospital adverse patient events Alan M Wolff Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - ©MJA1997 Abstract Objectives: To determine whether continuous detection of adverse patient occurrences followed by analysis and medical intervention can alter the rate of adverse occurrences. Design and participants: 15 912 patients discharged from one hospital were reviewed in two stages. Medical records were screened retrospectively by medical records staff for one or more of eight general patient outcome criteria. Those that screened positive for the criteria were reviewed by one of four doctors. If an adverse occurrence was confirmed, further analysis and recommendations for action to prevent its recurrence were made at meetings of the four doctors, and forwarded to a committee of visiting medical officers who decided on the appropriate course of action. Setting: A rural base hospital in Horsham, Victoria, between July 1991 and June 1994. Main outcome measures: The rate and severity of adverse patient occurrences in each year. Results: 1465 records were screened positive for one or more criteria, and an adverse patient occurrence was confirmed in 155. 88 cases were determined to be minor or not preventable and further action (mostly by changes to hospital policies) was recommended for the remaining 67. Over the three years, the number of adverse occurrences fell from 69 (1.35% of all patient discharges in the first year) to 33 (0.58% of all patient discharges in the third year) ( P < 0.0001) and there was no significant change in severity. Conclusions: The rate of adverse patient occurrences can be significantly reduced by their continuous detection using retrospective screening in conjunction with review, analysis and action to prevent recurrences. MJA 1996; 164: 458-461 Introduction The objective of medical quality assurance programs is to improve the quality of care provided to patients. However, "quality medical care" has proved difficult to define, leading some programs to attempt to detect "disquality", or events that should not happen under optimal conditions.1 Quality, then, may be defined as the absence or lowering of the rate of adverse patient events or occurrences. Many preventable adverse patient events occur in hospitals. The Quality in Australian Health Care Study, which reviewed over 14 000 patient admissions in 28 hospitals in New South Wales and South Australia, found 16.6% involved an adverse event; half of these were assessed as highly preventable.2 The Harvard Medical Practice Study, a review of over 30 000 inpatient medical records from 51 acute-care hospitals in the United States, showed that adverse events occurred in 3.7% of hospitalisations and that many of these were the result of substandard care.3 Both these studies used methods that required substantial resources in time and money to detect adverse patient events, and neither looked at the effect of intervention in preventing recurrence of an adverse event. Limited adverse occurrence screening is a continuous process of retrospective screening and review of inpatient medical records to detect adverse patient occurrences.4 It is referred to as "limited" because only eight general patient outcome criteria are used. When an adverse occurrence is found, appropriate action is taken to prevent its recurrence and the success of the action is determined by ongoing monitoring.4 Thus, the quality assurance feedback loop is securely closed. This study was designed to determine whether limited adverse occurrence screening could reduce the number and rate of adverse occurrences and therefore improve the quality of patient care. Methods The study was undertaken at Wimmera Base Hospital in Horsham, 300 km north-west of Melbourne. There are 11 specialists and 14 general practitioners on the medical staff who treat between 5000 and 6000 inpatients per year. Four doctors were chosen by the Hospital Medical Staff Group to be medical reviewers and to form a Patient Care Committee. All doctors held dual positions in the hospital and had postgraduate clinical qualifications. They were a physician (also Director of Intensive Care), a surgeon (also Chairman of the Medical Staff Group), a general practitioner (also Director of Postgraduate Education) and the Medical Director (also Director of the Accident and Emergency Department). The medical records for all inpatients discharged between 1 July 1991 and 30 June 1994 were screened by medical records staff using eight general patient outcome criteria (Box 1, below). An adverse patient occurrence analysis form was attached to any medical record that met one or more of the criteria. The record was reviewed by the doctor allocated to that criterion, who evaluated the care given to determine if an adverse patient occurrence had arisen before or during admission, and then completed the form. Adverse occurrences for which patients had had previous admissions were excluded. 1: General patient outcome criteria used for screening of medical records Death. Return to operating theatre within 7 days. Transfer from general ward to intensive care unit. Unplanned readmission within 28 days of discharge. Cardiac arrest. Transfer to another acute-care facility. Length of stay greater than 35 days (reduced to 21 days in 1993-1994). Theatre booking cancelled. An adverse patient occurrence was defined as "an untoward patient event which, under optimal conditions, is not a natural consequence of the patient's disease or treatment".1 I have described the limited adverse occurrence screening method in detail in an earlier paper.4 Medical care was evaluated using a six-point scale,5 to help the reviewer decide whether an adverse patient occurrence was caused by medical management: 1 = little or no evidence, 2 = slight evidence, 3 = not likely (less than 50:50 odds but a close call), 4 = more likely than not (greater than 50:50 odds but a close call), 5 = strong evidence, 6 = virtually certain. A score of four or more on this scale was regarded as an adverse patient occurrence. Severity of adverse occurrences was graded on a seven-point scale:1 0 = minor severity, 1 = minor temporary, 2 = minor permanent, 3 = major temporary, 4 = major permanent, 5 = potential major or major continuing, 6 = death. The medical reviewer wrote brief notes about the case for the Patient Care Committee. Adverse occurrences were discussed at the Committee's bimonthly meetings and recommendations for further action relating to patient care were made and forwarded to the Medical Staff Group, which consisted of all visiting medical officers in the hospital and the Director of Medical Services. All data from the adverse patient occurrence analysis forms were entered into a database program developed from the Clipper Dbase Compiler software package.6 A chi-squared test was used for statistical analysis, and confidence intervals were calculated for odds ratios using standard methods.7 Results A total of 15 912 inpatients were discharged between 1 July 1991 and 30 June 1994. Using the eight general patient outcome criteria, 1465 records (9.21%) were screened positive for one or more criteria by medical records staff. The commonest criteria among these were unplanned readmission of a patient within 28 days of discharge (3.4% of all records screened) and transfer of a patient to another acute-care facility (2.8% of all records screened) (Box 2). A medical record was most likely to be subsequently confirmed as containing an adverse patient occurrence when it was selected by the criterion "return to operating theatre within seven days" (odds ratio = 3.98; 95% confidence interval, 2.15-7.37) (Box 2). After medical review, 155 records (0.97% of all records screened) were found to contain an adverse patient occurrence using the six-point scale (Box 3). Of these adverse occurrences, 45 were minor and 110 were major (Box 4). Of the 155 adverse patient occurrences confirmed on medical review, no further action was recommended by the Patient Care Committee in 88 cases (56.8%) (i.e., the adverse occurrence was considered to be not preventable or of minor significance). Recommended action for the other cases included changing the relevant hospital policy; presenting the case at a postgraduate meeting; undertaking a quality assurance program to investigate the adverse occurrence in detail; discussion with, or counselling of, the doctor involved; and, rarely, review of the doctor's clinical privileges or reporting the case to the hospital's insurers. Over the three-year period of the study, 66 recommendations were made by the Patient Care Committee and almost all were accepted by the Medical Staff Group and became hospital policy. Changes in hospital policies were both clinical and administrative. Clinical policy changes included restricting some drug prescribing; revised protocols for reporting vital signs; eliminating use of multidose drug vials; formulating guidelines regarding fitness for general anaesthesia; and developing protocols for managing patients with alcohol withdrawal, haematemesis and melaena, and for patients who have had a cerebrovascular accident or who require analgesia. Administrative policy changes included sending copies of referral letters when patients were transferred to other hospitals; sending private antenatal notes to the obstetric ward before the patient's confinement; redesigning the preadmission form to allow consent for procedures to be obtained in the consultant's room; and routinely including a copy of the death certificate in the medical record (if the patient had died in hospital). (Examples of the types of adverse occurrences, more detailed recommendations for further action and their subsequent reduction in incidence are given in an earlier paper.4) The adverse patient occurrences were grouped by year to determine whether the actions instigated had any effect on the subsequent rate of adverse occurrences. The rate of adverse patient occurrences fell from 69 in the first year (1.35% of all patient discharges in that year) to 33 in the third year (0.58% of all patient discharges in that year) (Box 4). The proportion of adverse occurrences fell significantly with time (chi-squared = 17.11; df = 2; P = 0.0002) and this trend was linear (chi-squared = 16.87; df = 1; P< 0.0001). When the severity rating of adverse events was divided into minor (severity score 0-2) and major (severity score 3-6), there was no significant change in the severity of adverse patient occurrences between the first, second and third years of the study (Box 4). Also, the proportion of adverse patient occurrences detected in each year by screening did not alter significantly over time for patient age, sex or insurance status (Box 5). The commonest major diagnostic categories, using the ICD-9 classification,8 in which patients had adverse occurrences were injury and poisoning, followed by digestive and circulatory disorders (Box 6, below). Patient characteristics such as sex and age did not change significantly during the three years of the study, but the proportion of inpatients privately insured fell from 26.6% to 24.3% (chi-squared = 10.24; df = 2; P< 0.01). Discussion Limited adverse occurrence screening has been shown to be effective in detecting approximately 50% of adverse patient occurrences,9 a much higher proportion than found by traditional medical quality assurance programs. This study has shown that it is also possible to subsequently reduce the number of adverse occurrences by more than 50% over a three-year period. These results indicate that use of a more complex and expensive screening system is not required to achieve a significant reduction in adverse occurrences. Adverse occurrence screening has been shown to be valid and reliable, with a high level of agreement between reviewers as to whether a patient has had an adverse occurrence.10 Although in this study each medical record was reviewed by only one doctor, other studies using a similar methodology and rating scale have shown high agreement.5 Limited adverse occurrence screening is efficient as it requires the review of the medical records of slightly less than 10% of all patients discharged, costs only 0.1% of an acute-care hospital's total budget, and is fast and accurate (false positive rate, 2.0%; false negative rate, 0.4%).9 In this study, 9.21% of medical records were screened positive for one or more of the eight general patient outcome criteria and an adverse occurrence was confirmed in 0.97%. Little or no clinical judgement was required in the screening process. This compares with a rate of 8.4% (confirmed in 0.73%) in a study using similar screening criteria in a medium-sized New South Wales hospital.11 In the Quality in Australian Health Care Study, potential adverse events were detected in 43.7% of the medical records on initial screening (a much higher rate than in other studies) using 18 criteria, some of which required clinical judgement.2 Adverse events were confirmed in 16.6%, although, unlike in this study, 49% of these occurred before the sample admission. An average rate of potential adverse events of 13.2% was found in a study of 146 Veterans Affairs Medical Centers in the United States that used nine screening criteria.12 There was considerable variation between centres, with a 25th percentile of 8.6% (confirmed in 1.7% of records) and a 75th percentile of 27.2% (confirmed in 7.9% of records). In the Harvard Medical Practice Study, potential adverse events were detected on initial screening in 25.9% of medical records using 18 screening criteria.13 Adverse events were confirmed in 0.2% to 7.9%, depending on hospital complexity and location, with the rate in rural hospitals being 1%.13 Limited adverse occurrence screening can be adapted to all sizes of hospital. It has recently been introduced into 10 small hospitals in central western Victoria by the Division of General Practice in that area working with the Monash University Centre for Rural Health in Moe, Victoria. In larger hospitals, limited adverse occurrence screening could be introduced on a departmental basis. The program could be enhanced by combining its retrospective medical record review with prospective critical incident reporting. In the United States, adverse occurrence screening and incident reporting both detected a substantial number of adverse events; however, there was less than a 50% overlap in the adverse events detected by each method when used concurrently.14 Thus, a program that simultaneously uses both methods may detect the largest pool of adverse occurrences for analysis and development of preventive strategies. Acknowledgements I wish to thank Mr Ian Campbell, Dr David Leembruggen and Dr Grant Phelps for their enthusiastic participation in the Patient Care Committee; Mrs Cathy Dooling, Chief Medical Records Administrator, and her staff, for their support with the screening program; Mr Kieran Loughran, Computer Systems Officer, for assistance with data collection; and Mrs Naomi Uytdehaag for preparing the manuscript. References Craddick JW, Bader B. Medical management analysis: a systematic approach to quality assurance and risk management. Auburn (CA): Joyce W. Craddick, 1983. Wilson RM, Runciman WB, Gibberd RW, et al. The Quality in Australian Health Care Study. Med J Aust 1995; 163: 458-471. Brennan TA, Leape LL, Laird NM, et al. Incidence of adverse events and negligence in hospitalized patients. N Engl J Med 1991; 324: 370-376. Wolff A. Limited adverse occurrence screening: a medical quality control system for medium sized hospitals. Med J Aust 1992; 156: 449-452. Hiatt HH, Barnes BA, Brennan TA, et al. A study of medical injury and medical malpractice: an overview. N Engl J Med 1989; 321: 480-484. Clipper [computer program]. Version 5.0. Los Angeles: Nantucket Corporation, 1990. Daly LE, Bourke GJ, McGilbray J. Interpretation and uses of medical statistics. Oxford: Blackwell Scientific Publications, 1991: 398-424. US Department of Health and Human Services. The international classification of diseases. 9th revision. Clinical modification (ICD-9-CM). 3rd ed. Bethesda, Md: DHHS, 1989. Wolff A. Limited adverse occurrence screening: an effective and efficient method of medical quality control. J Qual Clin Pract 1995; 15: 221-233. Panniers TL, Newland J. The adverse patient occurrence inventory: validity, reliability and implications. Qual Rev Bull 1986; 12: 311-315. Britton S. A hospitalwide outcome study. Aust Clin Rev 1991; 11: 132-135. Goldman R, Walder DJ. An initial assessment of the Veterans Affairs Occurrence Screening Program. Qual Rev Bull 1992; 18: 327-332. 13. Brennan TA, Herbert LE, Laird NM, et al. Hospital characteristics associated with adverse events and substandard care. JAMA 1991; 265: 3265-3269. 14. O'Neil AC, Petersen LA, Cook EF, et al. Physician reporting compared with medical record review to identify adverse medical events. Ann Intern Med 1993; 119: 370-376. (Received 2 Sep 1995, accepted 2 Feb 1996) Authors' details Wimmera Base Hospital, Horsham, VIC. Alan M Wolff, FRACGP, MBA, Director of Medical Services, and Director of the Accident and Emergency Department. Reprints: Dr A M Wolff, Medical Administration, Wimmera Base Hospital, Baillie Street, Horsham, VIC 3400. ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Alan M wolff

Suspected snakebite in children: a study of 156 patients over 10 years Helen J Mead and George A Jelinek Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Results - Discusssion - References - Authors' details - - ©MJA1997 Abstract Objective: To describe the epidemiology and clinical features of children presenting to an emergency department with suspected snakebite. Design: A retrospective study of patient records. Setting: An emergency department of a children's teaching hospital (Princess Margaret Hospital) in Perth, Western Australia. Participants: All children attending the emergency department from 1984 to 1993 with suspected snakebite. Main outcome measure: Clinical and laboratory evidence of envenomation. Results: Over the decade studied, 156 children (mean age, six years and eight months) presented with suspected snakebite; over two-thirds (68%) were boys. In at least 31% of cases, no appropriate first aid had been applied. Only 14 children were envenomed according to clinical and laboratory criteria: 10 of these had coagulopathy; one of the 10 also had rhabdomyolysis. A Venom Detection Kit was used in 117 children. The test gave a positive result in 21 children (13%). Antivenom was given to 18 children, 14 of whom were definitely envenomed. Four of the envenomed children returned a negative result of Venom Detection Kit testing at all sites tested, and in five patients not clinically envenomed the urine specimen tested positive with the Venom Detection Kit (presumably a false positive result or subclinical envenomation). Of the 156 children, 130 were admitted to hospital, and 26 were discharged directly from the emergency department. All children recovered completely. Conclusions: (i) Many children did not receive appropriate first aid for snakebite; (ii) Most children with suspected snakebite presenting to the emergency department were not envenomed; (iii) Envenomation was best diagnosed by clinical features and laboratory investigations, with the Venom Detection Kit being used to determine the appropriate antivenom; (iv) Discharging children directly from the emergency department is not recommended. MJA 1996; 164: 467 Introduction Three major Australian studies of snakebite in children have been published.1-3 Two were from south-east Queensland1,2 and the third from Victoria.3 No similar studies have been reported from Western Australia, but one has been published on patterns of envenomation in 193 adults admitted to Perth teaching hospitals.4 There are also no published data on children presenting to Australian emergency departments with snakebite. Our aim was to describe the presenting features, treatment and outcome in children with suspected snakebite attending an emergency department. We also examined aspects of the use of the Venom Detection Kit, which was widely used as an adjunct in the diagnosis and management of these children. Methods We studied the records of all children presenting to Perth's Princess Margaret Hospital for Children with suspected or definite snakebite between 1 January 1984 and 31 December 1993. If parents or other carers had a reasonable suspicion that a child may have been bitten by a snake, this was classified as "suspected snakebite", and in "definite snakebite" a reliable history was available of a snake striking the child (whether or not envenomation occurred), or there was clinical and/or laboratory evidence of envenomation in circumstances consistent with snakebite. To ensure all records were found, multiple data sources were accessed, including hospital morbidity coding for inpatient admissions; intensive care unit records; and emergency department records. Data extracted from the records were entered onto a Microsoft Access 2.0 database to assist with analysis.5 To facilitate a comparison with the study in adults from Perth hospitals,4 data on patients' snakebite history and envenomation status were extracted and patients were grouped in the categories listed in the Perth study4 and shown in Box 1. Systemic envenomation was deemed present if there was clinical (vomiting, abdominal pain, or neurotoxic effects -- ptosis, convulsions, or difficulty with breathing or swallowing) or laboratory evidence (coagulopathy, haemolysis, rhabdomyolysis or renal failure). Results Over the 10 years, 160 children presented to the Emergency Department at Princess Margaret Hospital with suspected snakebite. Patient records were available for 156 children. The snake was brought in with the patient for identification on 16 occasions (on one occasion the snake was still alive!). Thirty-one children were admitted to the Intensive Care Unit, 87 to a general ward, 12 to the Emergency Department observation ward and 26 were discharged directly from the Emergency Department. Age and sex distribution The mean age of the children was six years and eight months (range, 15 months to 14 years 4 months), and over two-thirds (68%) were boys. Athough there was an even age distribution among children who were envenomed, there were 46 (29%) toddlers (less than three years) among the children presenting. Location Most snakebites occurred in the victims' garden (59 cases; 38%) or surrounding suburban bushland (51 cases; 33%). Eight (5%) occurred in a house or outbuilding and 26 (17%) children were bitten in open country. The location of the remaining 12 (7%) was not specified. Seasonal distribution Most children presented in the summer months, with very few presentations during winter; only three of the 14 children who were envenomed were bitten outside the months of October to April. Bite site Most children were bitten on a limb (lower limb: 103 cases, 66%; upper limb: 43 cases, 28%). There was one bite to the torso and one to the head, with the site not recorded in eight cases. Puncture marks were noted in 81 cases (52%). First aid It was often difficult to determine from the patient records whether first aid had been applied. However, in 39 cases it was clearly documented that no first aid was used, and inappropriate first aid (such as washing the site or use of an arterial tourniquet) was recorded in 10 cases (i.e., at least 49 children [31%] did not have effective first aid). The pressure- immobilisation first aid technique was used in 75 children (48%), although in some it was noted that the bandage had been applied only loosely or the limb was not fully immobilised. There was no record of whether first aid was applied in 32 children (21%). In some cases first aid measures were inappropriately left in place for a prolonged period after reaching hospital. Envenomation Fourteen children had systemic envenomation and 17 possible systemic envenomation according to the criteria used in this study (Box 1). The details of the clinical features, management and outcome of the 14 envenomed children are summarised in Box 2. In two children with possible envenomation, laboratory coagulation tests gave values just outside the normal range; both had an uneventful course and were not given antivenom. Four other child ren classified with possible envenomation received antivenom early for non-specific symptoms, without confirmatory laboratory evidence of envenomation. Venom detection Of the 117 cases in which the Venom Detection Kit was used, a positive result was obtained in 21 children (12 from wound swabs, 10 from urine, and four from blood). In nine of these child ren with no evidence of systemic envenomation, venom was detected in urine in five, and in skin swabs in the other four. In a child with borderline coagulopathy, the Venom Detection Kit gave a positive result in blood, but a negative one in urine. Another child treated for possible envenomation tested positive for venom at the "bite site", but tests of urine and blood gave a negative result with the Venom Detection Kit (Case D under "Use of antivenom"). The venom type detected by the Venom Detection Kit in envenomed patients is shown in Box 2. Use of antivenom Antivenom was given to 18 children (polyvalent in eight cases, brown snake in seven and tiger snake in five; two patients received more than one type of antivenom). Four children who were given antivenom may not have been envenomed. Case A: An eight-year-old boy with a witnessed bite received antivenom for regional lymphaden o pathy and headache. No venom was detected at the bite site, nor in blood or urine. Case B: A 10-year-old girl (no snake was seen) had a negative result of a Venom Detection Kit test of a bite site, and urine and coagulation studies showed no abnormality, but she was given antivenom because of symptoms of tiredness and non-specific weakness. Case C: A nine-month-old girl who was crying and vomiting and noted to have a mark on her arm was given polyvalent antivenom before transfer to Princess Margaret Hospital. No venom detection tests were undertaken. Her symptoms of fever and intermittent vomiting were subsequently thought to be due to a viral illness. Case D: A six-year-old girl had tiger snake venom detected at a possible bite site (but no venom detected in blood or urine). She was given tiger snake antivenom for symptoms of headache, fever, abdominal pain and nausea. A groin abscess was noted the next day, which may possibly have been the cause of her illness. Other supportive treatment Three children were administered fresh frozen plasma. No child required artificial ventilation. Outcome All children were discharged well from hospital; no permanent morbidity was recorded. Discusssion As in the previous epidemiological studies of snakebite in children in Australia,1-3 most of the children who presented to hospital with suspected snakebite were not envenomed (Box 3). In our study the over-representation of toddlers in the children presenting, despite an even age distribution of children with envenomation, probably reflected heightened parental concern and the difficulty obtaining a history from this age group. Patterns of envenomation and treatment for snakebite in Perth children were similar to those reported previously in adults.4 The sex distribution of victims, the seasonal pattern of envenomation and the site of bites were also similar. The venoms of the two snake genera responsible for most bites in Perth, Pseudonaja (brown snake) and Notechis (tiger snake), have powerful procoagulants, and coagulopathy was present in most (71%) of the envenomed patients. Among Perth snakes, only the tiger snake produces myolysis, and only one patient in this series had rhabdomyo lysis. Despite local differences in fauna, these findings are very similar to those in children with snakebite in Victoria.3 Despite continuing confirmation of the great efficacy of the pressure-immobilisation first aid technique in delaying venom spread,6,7 it is disturbing that this method is still not being used widely. In many cases it is also being applied incorrectly. More public education on first aid in snakebite is needed. The role of the Venom Detection Kit in patients with suspected snakebite attending emergency departments is discussed in Box 4. Although it appeared that no child came to harm after discharge from the Emergency Department, this practice is fraught with danger, as a case from 1973 illustrates. A two-year-old girl with restlessness and dry retching presented to hospital with an unclear history; the possibility of snakebite was raised by the parents. The examining medical officer concluded that she had been bitten by an insect, no investigations were ordered and she was discharged. The next morning she was found dead in bed, and it was later confirmed that tiger snake envenomation had been the cause of death. The Coroner found that there had been a lack of care on the part of the hospital, contributing to her death.10 In most children presenting to an emergency department there is no way of determining absolutely whether a venomous snakebite has occurred. There are special difficulties in obtaining a reliable history from young children and it may be tempting to use a negative result of a Venom Detection Kit to facilitate early discharge. Indeed, a number of children in this study were discharged from the Emergency Department without laboratory investigations, apart from use of the Venom Detection Kit. However, all children in whom snakebite is suspected, whether a snake was seen or not, should be admitted to hospital for observation and investigation (including coagulation profiles). In a number of cases of envenomation in our series, no snake bite was observed, and in two cases no snake was seen. Discharging children with suspected snakebite directly from emergency departments without a period of observation is not recommended. References Munro JGC, Pearn JH. Snake bite in children. A five year population study from South-East Queensland. Aust Paediatr J 1978; 14: 248-253. Jamieson R, Pearn J. An epidemiological and clinical study of snake-bites in childhood. Med J Aust 1989; 150: 698-702. Tibballs J. Diagnosis and treatment of confirmed and suspected snake bite. Implications from an analysis of 46 paediatric cases. Med J Aust 1992; 156: 270-274. Jelinek GA, Hamilton T, Hirsch RL. Admissions for suspected snake bite to the Perth adult teaching hospitals, 1979 to 1988. Med J Aust 1991; 155: 761-764. Microsoft Access [database]. Version 2.0. Redmond, WA: Microsoft Corporation, 1989-1994. Howarth DM, Southee AE, Whyte IM. Lymphatic flow rates and first-aid in simulated peripheral snake or spider envenomation. Med J Aust 1994; 161: 695-700. Sutherland SK. The pressure immobilisation technique. Med J Aust 1994; 161: 700-701. CSL Diagnostics. Snake venom detection kit. Product information leaflet. Melbourne: CSL Diagnostics, 1992. Wentworth B, Moisidis A, Jones S. Performance of the new snake venom detection kit at high and low concentrations [abstract]. Proceedings of the 22nd Annual Scientific Meeting of the Australasian Society of Immunology; 1992 Dec 2-4; Auckland. Parkville: Australasian Society of Immunology, 1992. Snake and lack of care killed girl. The West Australian 1973 19 Jun: 3 (col. 3, 4 and 5). (Received 6 Jul, accepted 20 Dec 1995) Authors' details Department of Emergency Medicine, Fremantle Hospital, Fremantle, WA. Helen J Mead, FRACP, FACEM, Staff Specialist; formerly, Senior Registrar, Intensive Care Unit, Princess Margaret Hospital for Children, Perth, WA; George A Jelinek, MD, FACEM, Assistant Director and Staff Specialist. No reprints will be available. Correspondence: Dr George A Jelinek, Department of Emergency Medicine, Fremantle Hospital, PO Box 480, Fremantle, WA 6160. ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Helen J Mead · George A Jelinek

For Debate Trauma in pregnancy and cerebral palsy: is there a link? The link between maternal trauma during pregnancy and cerebral palsy remains to be proven Marisa T Gilles, Eve Blair, Linda Watson, Nadia Badawi, Louisa Alessandri, Vivienne Dawes, Aileen J Plant and Fiona J Stanley MJA 1996; 164: 500-501 Introduction - Acknowledgements - References - Authors' details - - Articles on similar material Introduction Maternal trauma during pregnancy has been implicated in the aetiology of cerebral palsy in the surviving offspring.1,2 In 1991, a child with cerebral palsy received a settlement of three million dollars after it was alleged that the mother's negligent driving of a motor vehicle resulted in an accident which caused cerebral palsy in the child.1 The case rested on the testimony of an expert witness whose argument was based on a case series of six children with cerebral palsy born to mothers who had been involved in motor vehicle accidents. (Bergin AM, Stack JP, Stephenson JBP, King M. Cerebral palsy after motor accidents in pregnancy. Proceedings of the British Paediatric Neurology Association, Dublin, 1990 [unpublished data].) Possible mechanisms for the association between pregnancy trauma and cerebral palsy include reduced placental bloodflow, placental embolisation and placental abruption. To address the issue of trauma in pregnancy and subsequent cerebral palsy, we examined the Western Australian Cerebral Palsy Register3 (a subset of the Maternal and Child Health Research Database)4 which collects information on all children in the State who develop cerebral palsy (updated to the age of five years). We also examined the Hospital Morbidity Data System, which collects information on all acute hospital admissions. These two databases were selected in order to compare the rates of cerebral palsy in the offspring of women who, during their pregnancy, had trauma that required hospitalisation with the rates of cerebral palsy in the children of women who did not experience trauma. The Box outlines the methods and results of our study. Despite the fact that this was a population-based study over 11 years (1982-1992), the unadjusted relative risk of having a child with cerebral palsy after exposure to trauma was 1.4 (95% confidence interval, 0.34-5.77), which was not statistically significant. It was inappropriate to adjust for gestational age or low birth weight as they may have been factors in the aetiological pathway (e.g., trauma may induce a premature birth). Trauma occurs more commonly during the third trimester of pregnancy than at any other time in a woman's life.5 The incidence of trauma during pregnancy is reported to be about seven to eight per cent, but hospitalisation for trauma in pregnancy is rare. In the years of our study, only 0.3% of pregnant women were hospitalised. However, the severity of maternal trauma does not correlate well with the degree of fetal damage. Even minor trauma can cause fetal death and preterm labour,6-8 but few studies have considered the effect on long-term fetal outcome.2 Women who are not hospitalised (because of apparently minor trauma) may still have fetal compromise. In addition, women experiencing domestic violence may avoid medical attention, and hence such women may be under-represented in our study. Domestic violence during pregnancy, reported at rates between 8% and 17%, has been linked to fetal death, fetal distress and intrauterine growth retardation.9-11 The existence of one woman who was admitted to hospital for trauma at 28 weeks' gestation but had not been recorded as pregnant in the Hospital Morbidity Data System calls into question the validity of this data system in recording certain admission and discharge details relevant to our study. For example, in the presence of major trauma a pregnancy may be overlooked or not recorded, especially if the woman is in early pregnancy. This would lead to an underestimation of the number of women experiencing trauma during pregnancy who did not have a child with cerebral palsy, as only those women who were coded as being pregnant in the Hospital Morbidity Data System were included in the sample population. Our study has not resolved whether major trauma during pregnancy is associated with long term neurological problems in the child. In view of increasing litigation in this area, larger analytical studies into the outcomes following physical trauma during pregnancy are needed. This will best be achieved when better mechanisms for recording details of trauma during pregnancy, including domestic violence, are developed. Acknowledgements This study would not have been possible without the financial support of Healthway and PHRDC, who fund the Cerebral Palsy Register; data provided by the Health Department of WA; the expertise of Dr Richard Hockey, who carried out the linkage; and the editorial support generously supplied by Dr Ian Rouse and Dr Jennifer Kurinczuk. References Lynch v Lynch & Anor. Supreme Court of New South Wales (1991). Australian Tort Reports 81-117. Anquist KW, Parnes S, Cargill Y, Tawagi G. An unexpected fetal outcome following a severe maternal motor vehicle accident. Obstet Gynecol 1994; 84: 656-658. Stanley FJ, Watson L. Methodology of a cerebral palsy register. The Western Australian experience. Neuroepidemiology 1985; 4: 146-160. Stanley FJ, Croft ML, Gibbins J, Read AW. A population database for maternal and child health research in Western Australia using record linkage. Paediatr Perinat Epidemiol 1994; 8: 433-447. Patterson RM. Trauma in pregnancy. Clin Obstet Gynecol 1984; 27: 32-38. Williams JK, McClain L, Rosemurgy AS, Colorado NM. Evaluation of blunt abdominal trauma in the third trimester of pregnancy: Maternal and fetal considerations. Obstet Gynecol 1990; 75: 33-37. Farmer DL, Adzick S, Crombleholme WR, et al. Fetal trauma: relation to maternal injury. J Pediatr Surg 1990; 25: 711-714. Murdoch Eaton DG, Ahmed Y, Dubowitz LMS. Maternal trauma and cerebral lesions in preterm infants. Case reports. Br J Obstet Gynaecol 1991; 98: 1292-1294. Macfarlane J, Parker B, Soeken K, Bullock L. Assessing for abuse during pregnancy. Severity and frequency of injuries and associated entry into prenatal care. JAMA 1992; 267: 3176-3178. Dye TD, Tolliver NJ, Lee RV, Kenney CJ. Violence, pregnancy and birth outcome in Appalachia. Paediatr Perinat Epidemiol 1995; 9: 35-47. Webster J, Sweett S, Stolz TA. Domestic violence in pregnancy. A prevalence study. Med J Aust 1994; 161: 466-470. Stanley FJ, Watson L. Trends in perinatal mortality and cerebral palsy in Western Australia, 1967 to 1985. BMJ 1992; 304: 1658-1663. World Health Organization. International Classification of Diseases. 1975 revision, Vol 1. Geneva: Presses Centrales, 1977. Gee V. The 1991 Western Australian Birth Cohort. Statistical Series 34. Perth: Health Department of Western Australia, 1994: 5. Authors' details Health Statistics Branch, Health Department of Western Australia, Perth, WA. Marisa T Gilles, FAFPHM, Research Registrar; and Research Registrar, National Centre for Epidemiology and Population Health, Canberra. TVW Telethon Institute for Child Health Research, Perth, WA. Eve Blair, PhD, Senior Research Officer; Linda Watson, Research Assistant; Nadia Badawi, MSc, MRCPI, Paediatric Research Fellow; Louisa Alessandri, BSc(Hons), PhD, Research Officer; Fiona J Stanley, MD, FAFPHM, Professor of Paediatrics. Department of Public Health, The University of Western Australia, Perth, WA. Aileen J Plant, PhD, FAFPHM, Senior Lecturer. Women's Cancer Screening Service, Health Department of Western Australia, Perth, WA. Vivienne Dawes, FAFPHM, Medical Officer. No reprints will be available. Correspondence: Linda Watson, TVW Telethon Institute for Child Health Research, PO Box 855, West Perth, WA 6872. E-mail: Linda@ichr.uwa.edu.au Material trauma and cerebral palsy: a Western Australian population-based study, 1982-1992 Cerebral Palsy Register The study population was extracted from the Cerebral Palsy Register, a data subset of the Maternal and Child Health Research Database, and consisted of mothers of all children with cerebral palsy born between 1982 and 1992 inclusive, excluding those children who had a documented postnatal cause of cerebral palsy. A year-of-birth cohort of the Cerebral Palsy Register is only considered complete at the age of five years. Thus, by including the years 1990 to 1992 it is possible that as yet unregistered cases of cerebral palsy may have been misclassified as not having cerebral palsy. However, because cerebral palsy is rare (approximately 2 per 1000 live births),12 the effect of this error is very small. Hospital Morbidity Data System The sample population comprised all women between the ages of 14 to 50 with an ICD-9 external cause of injury (excluding poisons, drugs and medical misadventure)13 and the additional code for pregnancy in the Hospital Morbidity Data System. To validate the Hospital Morbidity Data System, a second method of identifying cases was used. The period of pregnancy was defined as the time between the second postmenstrual week and delivery, and the dates defining this period were identified for each pregnancy that resulted in a child with cerebral palsy. Database linkage Data from the Cerebral Palsy Register were linked with the births file, another subset of the Maternal and Child Health Research Database, to obtain identifying data for each mother in the study group, such as surname, maiden name, date of birth and address at the time of delivery. Using these identifying data, mothers were linked to the Hospital Morbidity Data System to determine exposure to trauma requiring hospitalisation during pregnancy. Statistical analysis Data were analysed using two-by-two contingency tables, and the relative risk was calculated with 95% confidence intervals. Results 529 children were born with cerebral palsy between 1982 and 1992, inclusive (extracted from the Cerebral Palsy Register). (See Box.) 770 pregnant women were hospitalised for trauma between 1982 and 1992 (extracted from the Hospital Morbidity Data System). The details of two of the mothers hospitalised for trauma during their pregnancy matched the details of two mothers of children with cerebral palsy. The incidence of cerebral palsy in children of women hospitalised for trauma during pregnancy was 2.6 per 1000 pregnant women. The incidence of cerebral palsy in children of women who did not experience trauma requiring hospitalisation during their pregnancy was 1.8 per 1000 pregnant women. A woman exposed to trauma requiring hospitalisation during pregnancy had 1.4 times the risk of having a child with cerebral palsy compared with a woman who had not had this experience (unadjusted relative risk, 1.4; 95% confidence interval, 0.34-5.77). The number of cases was small and this result was not statistically significant (Box). One mother who had a child with cerebral palsy and had been hospitalised for trauma during pregnancy was not recorded as being pregnant on the Hospital Morbidity Data System. Inclusion of this case in the two-by-two analysis increased the relative risk to 2.2 (95% confidence interval, 0.66-6.69), but only those women coded as being pregnant in the Hospital Morbidity Data System were included in the sample population (see text). Back to text

Marisa T Gilles · Eve Blair · Linda Watson · Nadia Badawi · Louisa Alessandri · Vivienne Dawes · Aileen J Plant · Fiona J Stanley