Recent eLetters

Dear Editor,

We read with interest Vardy et al's “Audit of the safety and effectiveness of ketamine for procedural sedation in the emergency department” [1]. A point of concern was that 77% of patients in their sample received propofol, midazolam or ketamine at a dose that depressed their conscious level such that they were unresponsive to verbal stimulus (scoring "P" or "U" on the AVPU scale). Furthermore, 15.9% of all patients experienced some form of complication.

They concede a high complication rate but do not appear to consider that the level of "sedation" administered in the majority of all cases is equivalent to a general anaesthetic. The "P" of the AVPU scale is considered to correspond to a GCS of 8 [2], at which a patient is at risk of loss of airway reflexes. The recommendation put forward by the Intercollegiate Working Party on safe sedation practice considers deep sedation as a state where a patient does not respond to verbal or simple physical stimuli, with consensus that its supervision requires the same level of training and skill as general anaesthesia [3].

We therefore have to question whether the degree of depression of consciousness achieved in this cohort might adversely affect the level of care offered. It would be interesting to ascertain the level of anaesthetic and life support training undertaken by those staff performing the sedation for these procedures, given that a proportion of the SHO workforce will constitute FY2 doctors, and around 50% of those who are ACCS ST doctors will be ST1, neither group of which can be assumed to have achieved basic anaesthetic competencies [4].

There is a clear case for further regulating procedural sedation in the Emergency Department, rather than simply introducing new and alternative agents.

[1] Audit of the safety and effectiveness of ketamine for procedural sedation in the emergency department. Vardy, JM. Dignon, N. Mukherjee, N. Sami, DM. Balachandran, G. Taylor, S. Emergency Medicine Journal 2008;25:579-582 [2] Simple bedside assessment of level of consciousness: comparison of two simple assessment scales with the Glasgow Coma Scale. McNarry, AF. Goldhill, DR. Anaesthesia 2004;59:34-37 [3] Implementing and ensuring safe sedation practice for healthcare procedures in adults. Report of an Intercollegiate Working Party chaired by The Royal College of Anaesthetists; The Academy of Medical Royal Colleges, London, 2001 [4] Modernising Medical Careers: educational implications for the Emergency Department. McGowan, A. Emerg Med J 2006;23:644-646.

Competing Interests: None

Since the early 1930's there has been a mistaken belief concerning what happens when the refrigerant gas, R-22, also known as chlorodifluoromethane, is exposed to high temperature heat sources. Admittedly, several compounds, including hydrogen fluoride (which then forms hydrofluoric acid when it comes into contact with water vapor in the air), hydrogen chloride (which then forms hydrochloric acid when it comes into contact with water vapor in the air) are formed during thermal decomposition. However, the focus of all the literature and all of the training in the HVAC industry has been on the fact that a chemical compound called phosgene (carbonyl chloride) is formed when R-22 is heated. The reason for the focus on phosgene will become more evident as you read this article, but suffice it to say that phosgene has been used as a chemical weapon – it is highly toxic.

R-22 was one of several refrigerant gases, collectively referred to as CFC’s, that had been invented in the mid- to late 1920s to replace the highly toxic refrigerant gases then in use. Although it was widely accepted that the CFC’s were non-toxic while still performing well as refrigerants, Underwriter’s Laboratories conducted comprehensive testing of the CFC’s in the late 1920's and early 1930's. Because of the chemical makeup of CFC’s one concern of UL was what would happen if these gases were heated to high temperatures. In answering that question as to R-22, UL anticipated that phosgene might be one of the products formed. Subsequent testing by UL verified (incorrectly) this prediction.[1] Since that time, this belief that phosgene is formed when R-22 is heated has become an incontrovertible postulate in the HVAC industry.

Phosgene was a concern for three reasons. First, as mentioned, it was used as a war gas in World War I and is extremely harmful even in very low doses. Second, very low amounts of R-22 were thought to be needed to create toxic levels of phosgene. Third, there was one critically important, but quite unique aspect of phosgene. Every other product of R- 22 thermal decomposition is highly noxious and unpleasant. When these substances come into contact with mucous membranes in the eyes, mouth, nose and throat, they produce great discomfort and pain. The detection threshold is such these compounds are detected well before they reach harmful levels and the substantial discomfort that is caused upon hitting the detection threshold causes people to flee quickly...very quickly. On the other hand, phosgene is insidious. At levels which are dangerous to humans, phosgene smells something like new mown hay...sort of sweet and musty. It is not even an unpleasant smell much less a noxious one.

Given the evidence and universal belief that R-22 produces phosgene when it comes into contact with hot surfaces, its presence in the home is viewed as a potentially dangerous and perhaps even lethal situation. And, the fact that the damage may be done by phosgene before one even knows he’s been exposed, gives rise to all kinds of potential claims. Consequently, when a component of an HVAC unit leaks refrigerant gas into a home (or other inhabited location), lawsuits against the manufacturers of HVAC equipment claiming damage due to exposure to phosgene will result. While the great weight of historical information and documentary evidence actually supports such an argument, scientifically, we now know it is wrong.

In 2003, the authors herein acted as co-defense counsel for two separate defendants in a case where a family of four, we’ll call them the Smith family, made a “R-22 = phosgene” contention. There was no dispute that the evaporator coil of the Smith’s A/C system leaked R-22, and it was possible if not probable that a small amount of R-22 actually got from the unit located in the garage into their home. With evidence of heat sources from gas stove burners, pilot lights, toaster elements, curling irons, etc. the family was convinced that they had been exposed to phosgene. The Smith’s claimed to have experienced a wide variety of symptoms: some consistent with phosgene exposure and others that could not have possibly resulted from phosgene exposure. They claimed that the “phosgene contamination” damaged their health, and permanently and irreparably damaged their home and their personal property that was in the home. The only solution was to destroy all of their personal property, raze the house to bare land, and rebuild everything.

Notwithstanding a virtual mountain of evidence against them, defense counsel, using a toxicologist, a forensic organic chemist and an article which was written by a DuPont researcher who worked with Freon routinely, were able to systematically layout not only the reason phosgene could not be obtained from heating R-22 but were able to explain the UL testing errors that created the original mistaken belief as to this phosgene being produced from heating R-22. Unfortunately, the Smiths were so heavily invested in their belief and position, while they heard the same evidence the jury heard, the Smiths could not accept either the indisputable scientific evidence or the jury’s decision.

Unfortunately, there was nothing about the Smith decision which became known outside of the actual case itself. So, when the R-22-phosgene issue arose in another case, Johnson v. American Standard, Inc., the attorneys in that matter had no knowledge as to what had happened in the Smith case. Those defense attorneys clearly did not know about organic chemistry. They had no alternative but to use HVAC technicians as expert witnesses. Since virtually the entire world of HVAC technicians all believe the R-22-phosgene connection, the only information available to defense counsel was that when you heat R-22, you produce phosgene!

The Johnson matter wound its way through the court system for years, eventually being decided by the California Supreme Court. It was dismissed by the trial court using a somewhat new legal challenge called the “sophisticated user” doctrine. The Appellate Court upheld the trial court. Finally, the California Supreme Court was asked to review the decision of the lower court. This case was decided April 3, 2008. It began when an HVAC technician did work on a commercial A/C system which required doing some brazing work [2] on a component of the system. Using standard protocol, the technician removed the R-22 refrigerant gas from the system before he began brazing, however trace amounts remained. While brazing, he was hit with a very pungent, potent and unpleasant odor that he contended was phosgene. He alleged the highly toxic gas caused him permanent lung damage. Since California workers compensation law prevented him from suing his employer, his lawyer creatively sued the manufacturer of the A/C system (American Standard) claiming that it owed the plaintiff a duty to warn him about exposure to phosgene if he heated a part of the system that contained R-22.

The manufacturer defended the lawsuit with the sophisticated user doctrine. The plaintiff’s expert sought to establish that the plaintiff was exposed to phosgene which caused him lung damage. The defendant’s expert not only agreed with the plaintiff’s expert but attempted to also prove that phosgene was produced by heating R-22 AND that this was common knowledge among the HVAC technicians of the world. Thus, there was no need to warn Johnson of something he (and every other HVAC person) obviously knew or should have known! The court agreed with the defendants’s position, finding that everyone in the HVAC business knows about the R-22/phosgene connection. The problem is it simply isn’t true.

While the defendant’s position was legally sound it is scientifically wrong and dangerously so. The next time that American Standard has to deal with a phosgene case, it may not be a Johnson-type sophisticated used case, but a homeowner case. The difference will be that in the Smith case, notwithstanding the overwhelming evidence against our position, we were able to demonstrate to the jury that phosgene is not a thermal decomposition product of R-22. That will not be a viable option for American Standard (it admitted R-22 can create phosgene), or perhaps most other HVAC manufacturers. They will be stuck with American Standard’s position in the Johnson case and will not know how to challenge it. Furthermore, there is the implication that even the California Supreme Court has now validated the finding concerning the phosgene/R-22 connection.

Consider where this leaves us. There is a 75 year old mistake that appears to have no legitimate prospect for being corrected and even worse, seems to be gaining proponents and is being re-enforced, both in the HVAC trades and in the legal arena. In an already litigious society, this simply encourages more law suits. It also victimizes innocent people. When a homeowner is concerned about what he may have been exposed to when he is told his A/C unit had to be recharged with Freon by a technician performing routine maintenance on the system, he goes to the Internet and he can find a variety of horror stories about phosgene poisoning from a leaky A/C system. For example, see the following website: http://www.toxichome.net/the_real_story.htm. The family who has this website, the Veerkamps, were charged a large amount of money by lawyers and consultants to tilt at windmills.

Consider a nationally-known company who, on its website, makes the following statement:

“The most dangerous and most common cause of indoor air contamination comes from leaking refrigerants contacting a heat source that can convert the freon into deadly phosgene gas (mustard gas). Carbon sooting frequently evidences the presence of this reaction. Almost all air conditioners and many refrigerators leak freon. There are many sources of heat in the home (heat strips, pilot lights, electric range and oven, toasters, etc.), which are capable of converting the freon into phosgene gas.”

This company offers to “test” your home for these substances for fees ranging from $300 to $5,000. The entire general public who have either A/C units or refrigerators are at risk in the sense that they are told that ordinary household appliances may expose them to a horrible war gas and that they can have their homes tested for its presence by spending $5,000, when, in fact, none of the information quoted above is accurate, correct or truthful. This 75 year old mistake is causing people to spend substantial sums of money looking for the nonexistent while simultaneously creating the potential of creating the next area of mass tort litigation in the United States.

ENDNOTES

[1] It is not the intent of the authors to be critical of the UL investigators who made these findings. Based upon the then state of knowledge of electrochemical bonding energies and the unavailability of tools such as gas chromatographs and mass spectrometers routinely used by chemists of today, the UL investigators came to conclusions that were completely appropriate in the 1930s. It is only with the advantages of contemporary increases in knowledge and modern diagnostic devices which make our hindsight 20/20 enabling us to “see” and understand the mistake made by the original investigators.

[2] Brazing is a process that uses a propane or butane type torch and is more or less a process that lies between soldering and welding. Most significantly, it involves creating high temperatures of the objects being brazed.

Kent Seitzinger John Broghammer

We read with interest the article by Duncan et al (1) making us aware about the increasingly common household hazard of contact burns due to hair straighteners particularly in children. We would also like to share similar experience in our department of 2 cases who presented with contact burns from hair straighteners.

Case 1: 18 month old boy with superficial partial thickness burn over the palmar aspect of his left middle finger extending form the proximal interphalangeal crease till the pulp of the finger.

Case 2: 24 month old boy with superficial partial thickness burns over the palmar aspect of his left little finger from proximal interphalangeal crease till middle interphalangeal crease; ring finger from proximal interphalangeal crease till middle interphalangeal crease and hypothenar eminence of the same hand measuring 1cm× 1.2cm along with 2 large blisters.

In both the cases the mechanism was accidental contact and possibility of non-accidental injury was ruled out. Both of the cases were managed conservatively, the blisters were left intact (2) and the wounds were covered with chlorhexidine acetate 0.5% (Bactigrass®) dressing. The burns in both the cases healed spontaneously without any residual scarring.

We completely agree with the authors that hair straighteners are becoming increasingly common potential hazard as more and more of such cases are reported. This preventable cause of childhood morbidity has not been well recognised. Since these burns are potentially avoidable the public need to be made aware by education and the manufacturing companies should compulsorily add a word of caution to “keep away from children” by legislation.

References:

1) Duncan RA, Waterson S, Beattie TF, Stewart K. Contact burns from hair straighteners: a new hazard in the home. Emerg. Med. J 2006;23;e21

2) Swain, AH, Azadian, BS, Wakeley, CJ, Shakespeare, PG. Management of blisters in minor burns; British Medical Journal 1987;295(6591);181

We read with interest the article by Duncan et al (1) making us aware about the increasingly common household hazard of contact burns due to hair straighteners particularly in children. We would also like to share similar experience in our department of 2 cases who presented with contact burns from hair straighteners.

Case 1: 18 month old boy with superficial partial thickness burn over the palmar aspect of his left middle finger extending form the proximal interphalangeal crease till the pulp of the finger.

Case 2: 24 month old boy with superficial partial thickness burns over the palmar aspect of his left little finger from proximal interphalangeal crease till middle interphalangeal crease; ring finger from proximal interphalangeal crease till middle interphalangeal crease and hypothenar eminence of the same hand measuring 1cm× 1.2cm along with 2 large blisters.

In both the cases the mechanism was accidental contact and possibility of non-accidental injury was ruled out. Both of the cases were managed conservatively, the blisters were left intact (2) and the wounds were covered with chlorhexidine acetate 0.5% (Bactigrass?) dressing. The burns in both the cases healed spontaneously without any residual scarring.

We completely agree with the authors that hair straighteners are becoming increasingly common potential hazard as more and more of such cases are reported. This preventable cause of childhood morbidity has not been well recognised. Since these burns are potentially avoidable the public need to be made aware by education and the manufacturing companies should compulsorily add a word of caution to ?keep away from children? by legislation.

References:

1) Duncan RA, Waterson S, Beattie TF, Stewart K. Contact burns from hair straighteners: a new hazard in the home. Emerg. Med. J 2006;23;e21

2) Swain, AH, Azadian, BS, Wakeley, CJ, Shakespeare, PG. Management of blisters in minor burns; British Medical Journal 1987;295(6591);181

I read with interest Moharari et al study and their conclusion that intra-articular lidocaine produces the same pain relief as intravenous meperidine and diazepam and that is a suitable alternative to sedation-analgesia for closed reduction of anterior shoulder dislocation.

The authors achieved a very high rate of successful reduction with the traction counter-traction technique by two specifically trained operators. There were no failures in the 48 patients who had their dislocations reduced, 24 patients received 25 mg of meperidine and 5 mg of diazepam and 24 patients received 20 ml of 1% lidocaine intra-articularly.

The administered doses of analgesic in the study seem lower and that of sedative higher than those that most would normally use. The mean pain scores before reduction in both groups were 57.9 in the intravenous sedation-analgesia arm and 52.6 in the intra-articular lidocaine group, which is suggestive of insufficient analgesia in both groups and over sedation in the intravenous group, as 5 out of 24 patients had respiratory depression requiring bag mask ventilation.

Many would use more than one technique and most would administer the combination of a titrated dose of an intravenous opiate with a smaller dose of a short acting benzodiazepine such as Midazolam. Propofol with remifentanil 1 and etomidate alone 2 are recent additions to the multiple drug combinations available.

There must be very few situations in clinical practice where intra- articular lidocaine should be considered as first choice. Furthermore, the majority of those reducing dislocated shoulders do not have sufficient experience with its use, perhaps because it has failed to convince. Until more date is made available, intravenous sedation-analgesia in safe and effective doses should remain the first choice. Familiarity with a combination of techniques is an important advantage for successful reduction.

Emergency medicine physicians should become proficient with a number of techniques and medications in order to quickly and safely reduce shoulder dislocations.3

References

1. Dunn M, Mitchell R, Souza CD, et al. Evaluation of propofol and remifentanil for intravenous sedation for reducing shoulder dislocations in the emergency department. Emerg Med J., 2006; 23(1): 57-58 2. Burton JH, Bock AJ, Strout TD, et al. Etomidate and midazolam for reduction of anterior shoulder dislocation: a randomized controlled trial. Ann Emerg Med., 2002; 40: 496-504 3. Cunningham N J. Techniques for reduction of anteroinferior shoulder dislocation. Emerg Med Aus., 2005; 17: 463-471

We commend Dr. Baskerville for highlighted the important issue of ionising radiation dose in the trauma patient population. The detail of his commentary, however, could lead to a great deal of confusion. It seems that the decision to use milligray in this commentary has been one of expediency and not necessarily accuracy. Dr. Baskerville talks of the average radiation exposure of his trauma patients, but then quotes a unit that represents maximal tissue absorption of the radiation that the body is exposed to. To explain, a CT head dose of 70.42 mGy may well be true for the dose absorbed by the cornea (if the eyes are within the CT beam), but will not represent the average dose absorbed by the patients entire head. That same CT head represents an ionising radiation exposure of approximately 3 milli sievert (mSv). This is the amount of radiation generated by the CT scanner. To quote an equivalence for mSv and mGy is erroneus if there are tissues present in the beam that are more sensitive to ionising radiation.

Dear Editor,

We were interested to read Dr Oliphant et al’s paper on relocating temporomandibular joint dislocations (1). In our practice we prefer the Hippocratic method of reduction, but agree that this can be very worrying to the clinician as their thumbs are placed directly in line of the bite!

To solve this problem we apply mallet splints to the examiners thumbs. This acts as thumb protection, as illustrated in figure 1. Should the patient bite down following reduction of the dislocation, there is now a safeguard.

An additional tip is to place tape around the mallet splint, improving purchase on the teeth and preventing displacement of the splint into the oropharynx!

We hope this modification will reduce the anxiety associated with the Hippocratic technique, and perhaps save a few emergency physicians thumbs in the process!

Yours

Gemma Mullen ST1 ACCS (EM)

Simon Carley Consultant in Emergency Medicine

References:

1. R Oliphant, B Key, C Dawson, and D Chung. Bilateral temporomandibular joint dislocation following pulmonary function testing: a case report and review of closed reduction techniques. Emerg. Med. J Jul 2008; 25: 435 - 436.

Sir,

Sajith et al. 1 report a case of oesophagogastric injury and massive pneumoperitoneum after out of hospital intubation by paramedics. The patient had received 25 minutes cardiopulmonary resuscitation with chest compression by the LUCAS device prior to restoration of cardiac output.

We report 2 similar cases after use of the LUCAS device in elderly patients.

Case 1

A 64 year old woman had a cardiac arrest at home. The patient received 30 minutes out of hospital CPR with the LUCAS device by the paramedics. No attempt at intubation was made and the patient was ventilated via bag-valve mask on the way to hospital. On arrival in the ED it was noted that her abdomen was grossly distended. A Size 7.5 ETT was passed first time, copious vomit was noted in the upper airways. Ventilation was difficult due to the distended abdomen, even after placement of an NG-tube. Return of cardiac output occurred 55 minutes after the initial arrest. Unfortunately, she deteriorated again soon afterwards. After discussion with her relatives a joint decision was made to withdraw further resuscitation attempts. Further history from the family revealed that the patient had suffered from COAD. After withdrawal of care surgical emphysema was noted on the anterior chest wall as well as post-mortem abdominal distension. After discussion with all staff involved in pre-hospital and ED resuscitation we decided that the suction bell of the LUCAS device had been placed correctly onto the chest wall. The coroner’s post-mortem showed no viscus perforation, but copious gastric contents in both lungs. A post-mortem diagnosis of (Ia) coronary heart disease and (II) COPD was made.

Case 2

A 74 year old lady was found lifeless at home. 30 minute bystander CPR and CPR by paramedics with LUCAS device was carried out prior to arrival in the ED. On arrival the thin, frail patient was noted to have a grossly distended abdomen. An NG-tube was passed and an ET-tube inserted at first attempt without any problems. Spontaneous circulation did not recur, and all efforts to resuscitate were abandoned 60 minutes after first bystander CPR. On discontinuation of the LUCAS device, it was noted that the suction bell had been incorrectly applied (too low and not in contact with the chest during the whole cycle of CPR). Also, surgical emphysema and rib crepitus was noted over the anterior chest wall. A coroner’s post mortem showed a de Bakey type I / Stanford type A dissection of the thoraco-abdominal aorta as the main cause of death. In addition, a moderate pneumoperitoneum was found with no evidence of hollow viscus perforation. Moderate emphysema was present in the lungs with no evidence of pneumothorax and no mediastinal surgical emphysema.

Discussion

Unfortunately, in Sajith et al1 the circumstances of the initial oesophageal intubation are not described in detail. Both our cases bear striking similarities to the case reported by Sajith et al1. Both patients exhibited a grossly distended abdomen, but without any evidence of oesophageal intubation. Both patients had surgical emphysema in the chest wall. NG-tubes were placed in both patients without any obvious reduction in distension. No viscus perforation was demonstrated on either post-mortem. Both patients were elderly and likely to have suffered from COAD. There was no demonstrable pneumothorax in either patient on post mortem examination. Oesophageal, gastric or even laryngeal ruptures after oesophageal insertion of medical devices (ET-tube, ECHO-probe, Combitube, NG-tube) are recognized, but rare events 2-7. This is usually caused by physical injury from repeated blind insertion or difficult intubation attempts, rather than the inflation pressure or the cuff of the device. The maximal inflation pressure of an AMBU-bag® via an ET-tube is 45 cm H2O 8. The power exerted by a LUCAS device onto the chest is 530-600 N/m2 9 , a force likely to be a multiple of that exerted by a hand-operated bag- valve-mask. The force of chest compressions and their relation to chest injuries has been previously described 10, 11 . It seems likely that the pneumoperitoneum was a consequence of the compressions, especially given the extent of the internal injuries 1. Likewise, the raised Troponin can be explained by the chest compressions, rather than the initial oesophageal intubation by the paramedic crew. One possible cause is distension of the stomach during bag-valve-mask ventilation, but that does not explain the pneumoperitoneum and the fact that nasogastric tube placement had little or no effect on the amount of distension. Gastric overdistension alone as a cause for the trauma seems unlikely, given the force of the bag-valve-mask contrasted with the force of the ongoing LUCAS compressions at 100 per minute. A possible explanation for the intraabdominal air is rupture of a pulmonary bulla and subsequent tracking of air through the diaphragm, a process known as pneumatosis abdominis. The location of the oesophageal trauma in 1 appears consistent with intubation trauma, but does not explain the pneumoperitoneum much further distal to that site. Since there is no post-mortem report, we do not know if perforation had actually taken place in the patient reported by Sajith et al 1. Previous studies have shown that intubation by paramedics is both safe and effective, with unrecognized oesophageal intubation being a rare event 12-15. Given the unclear evidence of the LUCAS device for overall outcome and survival, these cases should further guard from its use, especially in the elderly. Heartlands Hospital ED has suspended the use of LUCAS pending an investigation by the Medicines and Healthcare products Regulatory Agency (MHRA) and further research into the effectiveness of the LUCAS device.

1 Sajith A, O’Donohue B et al.: CT scan findings in oesophagogastric perforation after out of hospital cardiopulmonary resuscitation. Emerg Med J 2008;25:115-6.

2 Keldahl M, Sen S, Gamelli-Richard L: Gastric rupture after cardiopulmonary resuscitation in a burn patient. J Burn Care Res 2006;27(5):757-9.

3 Koscielny S, Gottschall R: Die Perforation des Hypopharynx als seltene, lebensbedrohliche Komplikation der endotrachealen intubation. Der Anästhesist 2006;55(1), 45-52.

4 Offerman SR, Holmes JF, Wisner DH: Gastric rupture and massive pneumoperitoneum after bystander cardiopulmonary resuscitation. J Emerg Med 2001; 21(2): 137-9.

5 Richards CF: Piriform sinus perforation during esophageal-tracheal Combitube placement. J Emerg Med 1998;16(1): 37-9.

6 Ahmed A, Aggarwal M et al.: Esophageal perforation: a complication of nasogastric tube placement. Am J Emerg Med 1998;16(1): 64-6.

7 Miller JS, Itani KM et al.: Gastric rupture with tension pneumoperitoneum: a complication of a difficult endotracheal intubation. Ann Emerg Med 1997; 30(3): 343-6.

8 Mackway-Jones K., Molyneux E. et al.: Advanced Paediatric Life Support, 4th edition, BMJ books, 2005. Blackwell Publishing Group.

9 Personal communication, Medtronic Ltd, Watford (UK Distributors for Jolife AB, manufacturers of LUCAS, Lund, Sweden).

10 Tomlinson, AE et al.: Compression force - depth relationship during out of hospital cardiopulmonary resuscitation. Resuscitation 2006;72: 364-70.

11 Hoke RS, Chamberlain D: Skeletal chest injuries secondary to cardiopulmonary resuscitation. Resuscitation 2004 ;63: 327-38.

12 Davis DP, Fisher R et al.: Predictors of intubation success and therapeutic value of paramedic airway management in a large, urban EMS system. Prehosp Emerg Care 2006;10(3): 356-62.

13 Wang HE, Yealy DM: How many attempts are required to accomplish out-of-hospital endotracheal intubation? Acad Emerg Med 2006;13(4): 372-7.

14 Pratt JC, Hirschberg AJ: Endotracheal tube placement by EMT-Basics in a rural EMS system. Prehosp Emerg Care 2005;9(2): 172-5.

15 Rocca B, Crosby E et al.: An assessment of paramedic performance during invasive airway management. Prehosp Emerg Care 2000;4(2), 164-7

Dear Editor, We agree that audit of poisons centre enquiry records is important to update TOXBASE (1), however cases summaries requested from service users are more valuable. Callers often contact a poisons information service before it is possible to determine whether a patient has actually been exposed or absorbed a toxic dose, and before the full clinical effects and outcome are known. Case follow-up is therefore important for diagnostic confirmation and knowledge consolidation (2). It has been undertaken since the National Poisons Information Service (NPIS) began (3) and is the origin of a significant amount of information on TOXBASE. Although NPIS follow-up activity has recently expanded to include selected TOXBASE enquiries (4), NPIS needs to ensure that sufficient resources are allocated to improve collection and evaluation of case follow-ups.

We support the recommendation for greater interaction between NPIS and its users to improve service quality (1) but believe that the NPIS strategy to reduce access by telephone and promote TOXBASE as an alternative (4) will reduce interaction. Although there are benefits to making poisons databases accessible to healthcare professionals, nevertheless there is a risk of not only undermining poisons centres’ efforts to gather epidemiological data, but also of reducing interaction with poisons centre staff (5). Such interaction provides enquirers with advice and estimates of risk that take account of the nature of exposure and clinical information. Experienced poisons specialists can advise on treatment when the name of a chemical product or plant is unknown, or help to identify it. Telephone conversations are a valuable opportunity for poisons specialists to clarify information when they recognise the potential for error or misunderstanding, and provide information appropriate to enquirers’ differing knowledge and experience. Moreover, the expertise and judgement of poisons specialists are widely recognized as essential for development of toxicological surveillance systems (2).

REFERENCES

1 Thanacoody HKR, Good AM, Waring WS, Bateman DN. Survey of cases of paracetamol overdose in the UK referred to National Poisons Information Service (NPIS) consultants. Emerg Med J 2008; 25:140-143.

2. Waring WS, Palmer SR, Bateman DN. Alerting and Surveillance Using Poisons Information Systems (ASPIS): Outcomes from an international working group. Clin Toxicol 2007; 45: 543-548.

3. Braimbridge MV. Poisons Information Service. Lancet 1965 Mar 13; 1(7385): 592.

4. 6. National Poisons Information Service. National Poisons Information Service Annual Report 2006/7. Health Protection Agency, 2007 http://www.camr.org.uk/web/HPAweb&HPAwebStandard/HPAweb_C/1196942160030

5 Hoffman RS. Poison information centers and epidemiology. In Goldfrank LR, Flomenbaum NE, Lewin NA, Howland MA, Hoffman RS, Nelson LS (eds). Goldfrank’s Toxicologic Emergencies. 7th Edition, New York, McGraw Hill, 2002, 1747-1752.

Author’s reply:

The use of species-specific snake antivenom is more scientific, as suggested by Prof. Balasundaram, whenever correct species identification of the offender snake is possible. But species identification may not be possible in many cases of snakebites as observed in our study (65.5%). Species-specific antivenom is not freely available in India and the majority of centers use polyvalent antivenom for treating snakebite envenoming. Even in Malaysia, polyvalent antivenom is still in use, though specific antivenom is more commonly used.[1] The incidence of allergic reactions may be less common with specific antivenom, but the reactions are not unusual and even the rate of their occurrence may be species- specific.[2]

Species identification based only on symptoms and signs of envenoming and the known prevalence of type of snakes in the locality, without observing the offender snake may not be always correct because of the similarity of some of the symptoms of envenoming by different species. Use of polyvalent antivenom may be justified in such situations and also when species-specific antivenom is unavailable.

References:

[1] Jamaiah I, Rohela M, Ng TK, et al. Retrospective prevalence of snakebites from Hospital Kuala Lumpur (HKL) (1999-2003). Southeast Asian J Trop Med Public Health. 2006; 37: 200-5.

[2] Isbister GK, Brown SG, Macdonald E, White J, Currie BJ; The Australian Snakebite Project Investigators. Current use of Australian snake antivenoms and frequency of immediate-type hypersensitivity reactions and anaphylaxis. Med J Aust. 2008;188: 473-476.

Author’s reply:

The concept of door to needle time/ medical contact to needle time in the treatment snakebite envenoming proposed by Prof. J Francis is important. All the patients who reached the emergency department of our institution directly, with clinical and laboratory evidence of envenoming at the time of arrival, received antivenom as soon as the diagnosis of envenoming was made. Hence the medical contact to needle time could have been small and negligible. We could not estimate the medical contact to needle time in those cases referred to us from other institutions after receiving antivenom. The higher medical contact to needle time could be an important reason for the high snakebite-related complications and mortality rates in many states of India. Lack of adequate training in the management of envenoming and fears about complications related to envenoming and the high rates of allergic reactions to antivenom, prevent primary-care physicians to start antivenom even if it is available locally. [1] Attempts to lower the medical contact to needle time by proper training of the primary-care physicians and making antivenom available even in the rural settings should reduce the snakebite-related mortality rates and complications in India.

Though cardiac manifestations are not uncommon, ventricular tachycardia is rarely reported as a complication of snakebite envenoming as commented by Prof. Francis. The patient who developed ventricular tachycardia in our series had been a 32-year old male with viper envenoming. His ECG and echocardiography had been normal after the cure of envenoming. Electrophysiological studies had not been advised because of the absence of structural heart disease at baseline and the patient had been advised to follow up the cardiology clinic if he develops any cardiac symptoms later. The exact cause of ventricular tachycardia could not be found in this patient and we presume that his cardiac arrythmia had been a manifestation of envenoming. Even myocardial infarction in the absence of coronary artery disease had been reported as a complication of snakebite envenoming. [2]

Cardiac manifestations may be related to various properties of snake venom that cause damage to remote tissues and organs. Cobra cardiotoxins, a family of basic polypeptides having lipid- and heparin-binding capacities similar to the cell-penetrating peptides, had been shown to induce severe tissue necrosis and systolic heart arrest in snakebite victims. [3] Tumor necrosis factor alpha and xanthine oxidase had been proposed as potential mediators of tissue injury including cardiac damage caused by viper venom. [4] L-amino acid oxidases of snake venom had been shown to cause severe pneumorrhagia, pulmonary interstitial edema, fusion of pulmonary alveoli, cardiac interstitial edema and bleeding when injected intravenously in experimental animals. [5]

References:

[1] Simpson ID. Snakebite management in India, the first few hours: a guide for primary care physicians. J Indian Med Assoc. 2007; 105: 324, 326, 328.

[2] Saadeh AM. Case report: Acute myocardial infarction complicating a viper bite. Am J Trop Med Hyg. 2001; 64: 280-2.

[3] Wang CH, Liu JH, Lee SC, Hsiao CD, Wu WG. Glycosphingolipid- facilitated membrane insertion and internalization of cobra cardiotoxin. The sulfatide.cardiotoxin complex structure in a membrane-like environment suggests a lipid-dependent cell-penetrating mechanism for membrane binding polypeptides. J Biol Chem. 2006; 281: 656-67.

[4] Szold O, Weinbroum AA, Ben-Abraham R, Englender TE, Ovadia D, Sorkine P. Xanthine oxidase and tumor necrosis factor alpha: possible mediators of remote tissue injury after viper envenomation. Isr Med Assoc J. 2000; 2: 816-20.

[5] Wei XL, Wei JF, Li T, et al. Purification, characterization and potent lung lesion activity of an L-amino acid oxidase from Agkistrodon blomhoffii ussurensis snake venom. Toxicon. 2007; 50: 1126-39.

Dear Sir

Guy’s and St Thomas’ Poisons Unit (GTPU) has over 100 enquiries about aconite poisoning on its case database. There is a large amount of literature on the subject including toxicity from the plant itself and herbal preparations; however it is a relatively rare cause of poisoning in the UK. GTPU was consulted over a fatal case of intentional aconite poisoning in 1992. This patient had a cardiac arrest soon after arrival at A&E and could not be resuscitated. Like the patient in the report by McGregor et al., he also appeared to have an interest in horticulture. Aconite poisoning (presumably because of its toxicity and speed of action) was also suggested as one of the possible causes of the death of the Pakistan cricket coach, Bob Woolmer, in 2007(1).

In view of the number of published case reports it is disappointing that the National Poisons Information Service (NPIS) was reported as having little information on the subject. GTPU, in collaboration with The Royal Botanic Gardens Kew, produced a CD-ROM of the poisonous plants in Britain and Ireland including a monograph on aconite (2). There are no definitive treatment recommendations for aconite poisoning and management is supportive with attention to the treatment of arrhythmias. Several antiarrhythmic drugs have been used with varying success. Mexiletine has been used in a previous case (3), and was successful in an animal study at preventing aconite-induced dysrrhythmias 4).

Following the recent decision by the Health Protection Agency (HPA) not to reinstate a contract with Guy’s & St Thomas’ NHS Foundation Trust, GTPU will no longer be able to provide a 24 hour telephone service for human poisoning. The HPA’s decision will mean the loss of expertise, commitment and innovation from GTPU as well as the potential loss of collaboration between the NPIS and The Royal Botanic Gardens, Kew. The future long-term provision of poisons information in the UK, particularly in specialist areas such as plant poisoning needs to be reconsidered.

1. BBC News http://news.bbc.co.uk/1/hi/6658547.stm

2. Dauncey E, Rayner TGJ (botany), Shah-Smith DA (mycology), Bates NS and others (toxicity monographs) (editors). 2000 Poisonous Plants in Britain and Ireland. CD-ROM.

3. Poy JY, Racle JP, Benkhadra A, Colas A, Brenez M. [Aconitine intoxication. Cardiac arrhythmia successfully treated with mexiletine]. Cah Anesthesiol 1986 34(5):429-433.

4. Winslow E. Evaluation of antagonism of aconitine-induced dysrhythmias in mice as a method of detecting and assessing antidysrhythmic activity. Br J Pharmacol 1980 71(2):615-22.

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