February issue.indd

Percutaneous drainage of spontaneous subcapsular haematoma of the spleen complicating chronic pancreatitis

T.L.T. Siu
Division of Surgery, The Canberra Hospital, Yamba Drive, Garran, ACT 2605, Australia
Correspondence to: T.L.T. Siu, 24 McAuley Place, Waitara, NSW 2077, Australia
Email: siloti@tpg.com.au

Case report 1

Case report 2

Letters to the Editor

Keywords: Haematoma, spleen, chronic pancreatitis, complications, percutaneous drainage
Surg J R Coll Surg Edinb Irel., 2 February 2004, 52-55

Subcapsular haematoma of the spleen is a rare complication of chronic pancreatitis. In the literature only a handful of cases have been documented.^1-5 The exact aetiology and natural history of this complication remains speculative and its management controversial. A case of spontaneous subacute haematoma of the spleen in a patient with chronic relapsing alcohol-related pancreatitis was reported. A percutaneous drainage was performed with good outcome. A review of the literature has demonstrated only one previous similar report

INTRODUCTION
A 38 year-old man, with a known history of relapsing alcohol related pancreatitis (for 7 years) was admitted to hospital with a sudden onset of left upper quadrant abdominal pain. Prior to admission, he was well with no preceding events of note. He denied having rigor, chills or fever. He stated that he had abstained from alcohol for many months. On examination he was afebrile. Haemodynamic parameters were within the normal range. Abdominal examination demonstrated marked epigastric and left upper quadrant tenderness. No rebound tenderness or guarding was detected. Laboratory investigations revealed a leucocytosis (white cell count 12.1 × 109/L), mild anaemia (haemoglobin 129 g/L), elevated amylase (366 U/L) and lipase (1505 U/L) levels but normal liver function and coagulation profile. A computed tomographic (CT) scan of the abdomen demonstrated an irregular hypodense lesion within the body of the spleen measuring 10 × 20 × 35 mm (Figure 1). A small amount of subcapsular fluid was also noted in the region of the hilum. Multiple foci of pancreatic parenchymal calcifications, in keeping with chronic pancreatitis, were demonstrated. No pseudocyst was revealed. He was treated conservatively with nil by mouth, intravenous fluids and analgesia. His pain failed to resolve, however, in the ensuing week despite the implementation of patient controlled analgesia. A repeat CT scan at that stage revealed a marked progress of the splenic lesion into a large subcapsular collection measuring 8 × 5 × 13 cm. (Figure 2) A left sided pleural effusion had also developed but no pseudocyst was found. Over the same period his haemoglobin level had fallen to 96 g/L but his coagulation profile had remained normal. There was no history of injury over this period. A CT-guided percutaneous drainage of the haematoma was subsequently performed. Using the Seldinger technique, a 10F cope loop nephrostomy catheter was inserted into the haematoma. Approximately 600 mls of old liquefied blood was drained. Five thousand units of thrombin was introduced into the cavity and the catheter was removed at the end of the procedure with near complete drainage of the haematoma (Figure 3). The amylase level of the fluid was 7369 U/L. The patients pain resolved rapidly after the procedure and he was discharged home four days later without any complications. He remained pain free six months after the procedure.

Figure 1a (top): Axial abdominal CT images showing a small subcapsular collection and Figure 1b (bottom): A hypodense lesion in the hilar region of the spleen

Figures 2a (top) and 2b (bottom): Axial abdominal CT images demonstrating the evolution of the previous lesion into a large subcapsular haematoma of the spleen 11 days later

Figures 3a (top) and 3b (bottom): Axial abdominal CT images showing near complete drainage of the haematoma. The drainage catheter was in situ

DISCUSSION
Haemorrhagic complications of the spleen are one of the least common complications of chronic pancreatitis.^1-7 Although the actual incidence is not known, in a recent large series of 500 patients, an estimated prevalence of 0.4% was reported.⁵ In the past, the pathogenesis of these complications has principally been associated with pancreatic pseudocyst.¹ A number of case reports have demonstrated that dissection of the pancreatic pseudocyst into the splenic hilum can lead to infarction, haemorrhage and rupture of the spleen.¹ It is believed that the direct contiguity of the pancreatic tail and the hilum of spleen, in the absence of peritoneal division, provides a portal for inflammatory extension.^1,2

With close proximity of the splenic vessels, erosion into the splenic artery and congestion from splenic vein thrombosis added to the evolution of haemorrhagic complications.¹

In the absence of a pancreatic pseudocyst, as in the present case, splenic involvement in pancreatitis is generally considered very rare.^2,7 Only a handful of cases have been reported in the literature to date.^2,3,5 The exact aetiology is less defined but it is thought that, similar to the mechanism of dissection by pancreatic pseudocyst, spread of inflammation from the tail of the pancreas is implicated.² As demonstrated in the present report, the gradual progression of a small hilar lesion into a large subcapsular haematoma containing a high level of amylase supports the notion of a gradual erosion of the hilum by pancreatic exudates as a probable mechanism. In contrast, a propensity for trauma and clotting disorder did not seem to contribute to the formation of the haematoma in the present case.^1,10,11

The management of a subcapsular splenic haematoma in pancreatitis remains controversial. Some reports have advocated aggressive management with early splenectomy to avoid splenic rupture.^5,8 The persistence of a potential cavity within the spleen by drainage alone has also been postulated to contribute to recurrence.³ Malka et al. (1998) in their series of 500 patients with chronic pancreatitis showed that 7 out of a total of 11 patients with splenic complications had splenic vein occlusion.5 It was postulated that the prevalence of venous hypertension may preclude non-opearative therapeutic intervention when considering the resultant impaired haemostasis and the prospect of uncontrolled haemorrhage.

However, Vyborny et al.(1988) demonstrated for the first time successful non-operative management with ultrasound-guided catheter drainage.2 In a retrospective study of patients with splenic subcapsular collections from pancreatitis, Rypens et al. (1997) demonstrated that expectant management was feasible in 12 out of 16 patients and suggested that most of these complications could potentially regress and, therefore, be managed conservatively.¹³ This is the second documented case of successful percutaneous drainage of a subcapsular haematoma complicating chronic pancreatitis. The benefits of percutaneous drainage of a splenic haematoma include prompt relief of symptoms, short recovery time, avoidance of rupture and, most importantly, spleen preservation. In this institution, the interventional radiologist was able to perform immediate splenic embolisation should uncontrolled haemorrhage occur during the procedure. With available facilities and appropriate expertise, imaging-guided percutaneous drainage appears to be a feasible option for management of splenic haematoma complicating chronic pancreatitis.

REFERENCES
1. Warshaw AL, Chesney TM, Evans GW, McCarthy HF. Intrasplenic dissection by pancreatic pseudocysts. N Eng J Med 1972;287:72-75.
2. Vyborny CJ, Merrill TN, Reda J, Geurkink RE, Smith SJ. Subacute subcapsular hematoma of the spleen complicating pancreatitis: successful percutaneous drainage. Radiology 1988;169:161-2.
3. Agnifili A, Gianfelice F, Gola P, et al. Subcapsular splenic hematoma complicating chronic relapsing pancreatitis: case report. Eur J Surg 1991;157:63-65.
4. Kuramitsu T, Komatsu M, Ono T, et al. Ruptured subcapsular giant hematoma of the spleen as a complication of chronic pancreatitis. Intern Med 1995;34(6):564-8.
5. Malka D, Hammel P, Levy P, et al. Splenic complications in chronic pancreatitis: prevalence and risk factors in a medicalsurgical series of 500 patients. Br J Surg 1998;85:1645-1649.
6. Shafiroff BB, Berkowitz D, Li JK, Fletcher P. Splenic erosion and hemorrhage secondary to pancreatic pseudocyst. Am J Gastroenterol 1977; 68:145-153.
7. Sitzmann JV, Imbembo AL. Splenic complications of a pancreatic pseudocyst. Am J Surg 1984;147(2):191-6.
8. Greenstein A, DeMaio EF, Nabseth DC. Acute hemorrhage associated with pancreatic pseudocyst. Surgery 1971;69:56-62.
9. Lankisch PG. The spleen in inflammatory pancreatic disease. Gastroenterol 1990;98: 509-516.
10. Byrd BF Jr, Couch OA Jr. Pancreatitis with rupture of spleen and hemorrhagic pleural effusion. JAMA 1955;157:1112-1113.
11. Clave P, Guillaumes S, Blanco I, et al. Splenic hematoma in acute pancreatitis. Role of coagulation disorders. Z Gastronenterol 1992;30(8):538-42.
12. Thompson JE, Ashley SW. Subcapsular hematoma of the spleen associated with acute pancreatitis. Surgery 1997;121:231-233.
13. Rypens F, Deviere J, Zalcman M, et al. Splenic parenchymal complications of pancreatitis: CT findings and natural history. J Comput Assist Tomogr 1997;21:89-93.

Perforation of the terminal ileum: a possible complication of nicorandil therapy

P.M. King, S.A. Suttie, J.O. Jansen, A.J.M. Watson
Department of Surgery, Aberdeen Royal Infirmary, Foresterhill, Aberdeen, AB25 2ZN, U.K.

Correspondence to: P.M. King, Ward 49, Aberdeen Royal Infirmary, Foresterhill, Aberdeen, AB25 2ZN, U.K. Email: P.M.King@arh.grampian.scot.nhs.uk

Recent reports have implicated nicorandil as a possible causative agent in the pathogenesis of anal and oral ulceration. We report a case of ulceration and perforation of the terminal ileum in a patient taking nicorandil. The possibility of an association between nicorandil therapy and gastrointestinal ulceration is discussed

INTRODUCTION
Nicorandil, a potassium channel activator used in the treatment of severe ischaemic heart disease, has recently been implicated in the pathogenesis of anal and oral ulceration.^1-3 To our knowledge, there are no reports of nicorandil-associated ulceration at other gastrointestinal sites in humans. We report a case of terminal ileal ulceration and perforation which may be related to nicorandil usage.

CASE REPORT
A 53 year old female with ischaemic heart disease, peripheral vascular disease and chronic leg ulceration was admitted with generalised peritonitis. She had not experienced any gastro-intestinal symptoms prior to admission. Her regular cardiac medications included aspirin, glyceryl trinitrate, diltiazem, simvastatin and nicorandil (30mg twice daily). The aetiology of her leg ulcer was unclear, but previous biopsy and histological examination had revealed only chronic granulation tissue and failed to show evidence of infection, neoplasia, or vasculitis. A clinical diagnosis of pyoderma gangrenosum was made and in view of the chronicity of the lesions, the patient had been commenced on oral steroid therapy (prednisolone 30mg daily) three days prior to admission.

At laparotomy, the patient was found to have a perforated terminal ileum. A right hemicolectomy was performed, but on transecting the small bowel it became apparent that the ileal mucosa was extensively ulcerated (Figure 1), necessitating an extended small bowel resection. Intestinal continuity was restored by primary ileocolic anastomosis, and the patient made a full recovery.

Routine histological examination of the specimen confirmed a non-specific perforation of the terminal ileum, against a background of florid mucosal ulceration of the small and large bowel. The ulcers were sharply demarcated and associated with a brisk inflammatory response within the bowel wall. The intervening intact mucosa was architecturally unremarkable and contained no inflammatory infiltrate. The base of each ulcer contained a polymorphous inflammatory infiltrate comprising of plasma cells, eosinophils and lymphocytes. There was no evidence of a lymphomatous or other neoplastic infiltrate and blood vessels outwith the inflammatory process showed no evidence of intrinsic vasculitis.

DISCUSSION
The most common causes of small bowel ulceration are inflammatory bowel disease, neoplasms and infection. Less common causes include mesenteric vascular occlusion and vasculitides. There was no histological evidence of these conditions in this patient. Although it is possible that the appearances observed were the result of a regional reduction in perfusion, perhaps as a result of her advanced ischaemic heart disease, the presence of essentially normal mucosa in between ulcers renders this possibility unlikely.

Steroid administration is known to be associated with peptic ulcer disease, but there are few reports of ulceration at other sites. In contrast, a number of cases of anal and oral ulceration have recently been reported in patients taking high dose nicorandil, although the pathogenesis has yet to be elucidated. Putative mechanisms of oral and anal ulceration related to nicorandil include a “vascular steal” phenomenon, although neither the pharynx or the anus are areas of vascular watershed, and a direct local effect of either nicorandil itself or a metabolite.^3-5 The findings in this case raise the possibility of nicorandil, or one of its metabolites, being associated with small bowel ulceration and perforation.

CONCLUSION
A report of a single case, particularly when involving concomitant steroid therapy, is insufficient to establish a link between nicorandil therapy and small bowel ulceration or perforation. Surgeons and physicians, nevertheless, should be aware of the possibility of such an association when confronted with unusual patterns of gastrointestinal mucosal damage in patients receiving nicorandil.

REFERENCES
1. Agbo-Godeau S, Joly P, Lauret P, Szpirglas R, Szpirglas H. Association of major apthous ulcers and nicorandil. Lancet 1998; 352: 1598-9.
2. Scully C, Azul AM, Crighton A, Felix D, Field A, Porter SR. Nicorandil can induce severe oral ulceration. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001; 91:189-93.
3. Watson A, Al Ozairi O, Fraser A, Loudon M, O’Kelly T. Nicorandil associated anal ulceration. Lancet 2002; 360: 546-47.
4. Vella M, Molloy RG. Nicorandilassociated anal ulceration [Letter]. Lancet 2002; 360: 1979.
5. Gupta A, Morris G. Major aphthous ulcers induced by nicorandil. Age Ageing 2000; 29: 372-73.

CONTINUED PROFESSIONAL DEVELOPMENT
The ethos of continuing professional development (CPD) for surgeons, as with all health professionals, is changing rapidly, driven by both central pressures for accountability and for the professional’s need, and wish, to periodically review fitness to practice through appraisal and revalidation. The emphasis has moved from the acquisition to the application of learning, not just on an individual basis but as it impacts on the surgical team. The acceptance of evidencebased education, rather than prescriptive performance review as the benchmark of continuing professional competence is to be welcomed, and the input of journals both to the acquisition of knowledge and to its relevance to clinical practice is of prime importance.

As an aid to reading and reflection The Surgeon will, from 2004, request from each published contributor a number of questions relating to their article, this to allow the reader to assess their understanding of the topic. The answers will be available within the same issue, hence allowing the CPD loop to be closed without cost to the subscriber, and ensuring that the maximum benefit is obtained.

The Editorial Board welcomes discussion on how the process is implemented, and indeed how it may evolve.

Re: Myths of Whiplash. Ferrari R. Surg J R Coll Surg Edinb Irel 2003. 1; 2: 99-103

I read with interest the article by Dr Ferrari, Myths of whiplash, published in April 2003.

Although whiplash injury is not a spinal disorder, the whiplash injury pain is mainly felt by the patients on the lateral side of the neck, over the trapezius muscle, behind or between the shoulder blades; so this situation erroneously encourages members of the medical profession to think that the pain is spinal in origin.

In 1997 I reported that the pain in the neck and shoulder after whiplash injury arises from the median nerve at the wrist.¹ Recently, Ide et al. (2001) also described entrapment of the brachial plexus and of peripheral nerves including the median nerve at the carpal tunnel.² To follow our earlier observations, our more recent studies have demonstrated the management of chronic pain in the neck and shoulder in whiplash injury, by decompression of carpal tunnel and, therefore, we coined the term ‘atypical carpal tunnel syndrome’. Our aim in introducing this new terminology is to draw our colleagues’ attention to the fact that the pain in whiplash injury is felt away from the nerve lesion and neurophysiological studies are rarely abnormal in these patients. However, unconditional reverence for neurophysiological investigations is the biggest trap to the clinician, even if a patient elicits carpal tunnel symptoms, when neurophysiological studies are normal, the diagnosis is usually missed. In fact, we have reported that neurophysiological studies are rarely abnormal and cannot verify the diagnosis.¹ Further studies have reported that all patients had normal ECG and nerve conduction studies.^2,3 Through these findings we have shown that there is a definable pathology in the peripheral nerves. In acute cases 50 minutes after the accident, neurological symptoms are present. Fortunately, in a large number of patients the lesion heals. The commonest lesion is the median nerve-atypical carpal tunnel (95%) and atypical pronator teres syndrome (5%) of cases. Greater occipital neuralgia is another common nerve lesion (C2). The symptoms of whiplash injury are caused by stretching and rotational deformity of central nervous system, cranial and peripheral nerves. Patients’ main concern is pain and when they cannot obtain a reasonable explanation their anxiety increases.

Finally, I entirely disagree with Dr Ferrari that chronic whiplash has no definable pathology and is dependent on the cultural background for the population studied. His biased view and reliance on the much criticised Lithuanian study shows his conformist nature. The myth he did not mention in his article is ‘medicine changes everyday’. In fact, medicine changes very slowly, because members of the medical profession, like the clergy, are very resistant to change. The greatest barrier to the progress of medicine is our enforced conformity. On the other hand, progress depends on the sceptic, the person who does not wholly conform and thinks the unthinkable.

REFERENCES
1. Alpar EK. Whiplash injury and median nerve entrapment. Injury 1997; 28: 243.
2. Ide M, Ide J, Yamaza M. Symptoms and signs of irritation of the brachial plexus in whiplash injuries. J Bone and Joint Surg (Br). 2001; 83B: 226-29.
3. Alpar EK, Onusha G, Killainpalli VV. Management of chronic pain in whiplash injury. J Bone and Joint Surg (Br) 2002; 84B: 807-11.

‘Ye are forgers of lies, ye are all physicians of no value’.[Job 13(4)] I thank Dr. Alpar for expressing his varied philosophies, more than I or Horatio could have dreamt of. The review on the myths of whiplash was intended, in a lateral fashion, to make the readership ask the unthinkable: “Why do we physicians lie to our patients?” As Dr. Alpar and I are physicians I shall follow here the biblical call for introspection where neck pain and physicians are concerned: ‘O! that you could turn your eyes towards the napes of your necks, and make but an interior survey of your good selves’ William Shakespeare. (Coriolanus Act II, Scene 1).

We tell our patients about horrendous tears and calamitous inflammation we cannot see or measure, about nerve injuries that we cannot define or demonstrate, fantastical mechanisms of pain that we cannot reproduce or elucidate without invoking a great deal of faith, and making the “hard sell”. Perhaps “lie” is too strong a word - better terms are embellish, distort or skirt the truth, exercise our creativity, et cetera.

Most structures from the vertex of the skull to the coccyx have at one time or another been blamed for chronic pain, on each occasion with an expression of deep conviction from physicians, for they spoke only the truth. We have in the medical field, in particular, made syndromes our new religion. Our higher being is in the existence of a future technology which will reveal all and quiet the sceptics who once mocked. In this religion of syndromes we give ourselves purpose in a world that is increasingly telling physicians that we are too much possessed by technological and structural demons for explanations for human suffering. We have adopted proverbs: “Absence of evidence is not evidence of absence”. We also have our tautologies, as any worthy religion should have. We design our beliefs, for example, that our syndromes can always be diagnosed as matters of convenience and neither proved nor disproved. We have for example, “real carpal tunnel syndrome”, and in case we need it, we have “atypical carpal tunnel syndrome”. For parsimony, we might also have “subclinical carpal tunnel syndrome”. We can never be wrong, because carpal tunnel syndrome can be diagnosed when there are objective abnormalities, and according to Dr. Alpar, atypical carpal tunnel syndrome can be diagnosed when such evidence is lacking. Our religious fervour for syndromes also incorporates a form of original sin, wherein someone first committed the sin of blaming ailments on the nervous system without a speck of proof, but with a load of conviction, and we have since repeated that sin over and over. That is, Ferrari and Shorter (2003) have reviewed this history of recycling of nervous system irritation and inflammation as an explanation for the inexplicable patient and, thus, Dr. Alpar’s model of nerve injury has been seen before.1 The account provided by Ferrari and Shorter finishes with the telling of the current phase of blaming peripheral nervous events for the suffering of whiplash patients.¹ Physicians perhaps do not always lie, but we are simply unaware of our own history of lies.

So we, the readership, can ask ourselves the unthinkable. How many of us would honestly tell patients that studies have been done in Greece and Germany that show those whiplash victims recover quickly from whiplash injury while our patients do not? How many of us would honestly tell our patients that we do not know what injury the patient has because we cannot see into the neck, and have no way of detecting most whiplash injuries? We do not know what happened to them at the time of the collision or if there is any injury!

And what would be the price paid for telling them this truth? The price is that a great wall would crumble, so deafening that some would be too ‘gob-smacked’ to carry on. Instead, we must therefore brace this wall of falsehoods, like diligent soldiers. We actively go out of our way to conduct research to strengthen a collapsing wall, behind which a truth is hidden that we cannot dare let patients see.²

I suggest the myths of whiplash will come and go like the tides, and so too will physicians continue to police themselves:

We all have our faults ‘Thou censurest me, so have I done others, and may do thee..Go now, censure, criticise, scoff, and rail’.³

1. Ferrari R, Shorter E. From railway spine to whiplash - the recycling of nervous irritation. Med Sci Mon 2003; In press.
2. Kwan O, Ferrari R, Friel J. Tertiary gain and disability syndromes. Med Hypo 2001;57: 459-64.
3. Robert Burton [Democritus Junior]. The Anatomy of Melancholy. Chatto & Windus: London; 1898:8.

Re: Myths of Whiplash. Ferrari R. Surg J R Coll Surg Edinb Irel 2003. 1; 2: 99-103

I find it astonishing that a journal of the caliber of the JRCS Ed and Ire would publish a paper of such poor contents as Myths of Whiplash by R Ferrari in April 2003.

He supports the view of Schrader et al. that late symptoms of whiplash injury are a myth and merely a money-spinner for the whiplash industry which at present in the UK are dealing with 300,000 whiplash injuries per year, and paying out in the vicinity of £700,000,000 in compensation per annum.

This paper has been systematically discredited and destroyed repeatedly since its publication in the Lancet on 4th May 1996. I refer to:

1. Correspondence section of the Lancet 13th July 1996 - pages 124-126.
2. 1998 Whiplash Conference Documentation - (convenors Lyons Davidson). The epidemiology of late whiplash by Dr Michael D. Freeman - pages 170-180.
3. Whiplash Injuries - third edition 2002 - pages 412-414 by S.M. Foreman & Arthur Croft. Publisher - Llippincott William.

I recommend that your readers consult these three articles in full, and then conduct a straw poll amongst your readership to see how many of them adhere to the Schrader hypothesis and how many do not.

Karl Popper lives! I thank Mr. Price for reminding us all of Popper’s methodological rules known as Falsificationism, the idea that science advances by unjustified, exaggerated guesses followed by unstinting criticism.

We need to remember that physicians defend myths religiously for many reasons, and that the whiplash industry is one with many gains for the physician. Thus, one expects the reactionary tones of Mr. Price to continue to ring so long as research explores these myths. Further, however, Price draws attention to a phenomenon that may be a coping mechanism for clinicians embroiled in whiplash debates. That is, we often refer to coping mechanisms for chronic pain patients, but how do physicians, themselves, cope when something threatens their ideology? The soldiers of the “chronic injury” model of whiplash can utilise a simple mechanism to reduce anxiety levels when a study appears that threatens to shatter the wall of myths they defend: ignore Lithuania. For some, that is the easiest solution, both relieving anxiety and perhaps lessening the guilt of tertiary gain.

As Price remarks, in 1996, the Lancet published a study by Schrader et al.(1996), the first systematic and effective analysis of the outcome of the acute whiplash syndrome outside the medicolegal context.1 One of the co-authors of of this article is Dr. Obelieniene. Dr. Obelieniene may be, paradoxically, the world’s expert on chronic whiplash because of a lack of experience with the same. She practices as a neurologist in a country where she could not possibly make a living off seeing patients with chronic whiplash - they are not there. She did not, prior to 1993, know that chronic whiplash was or should be an issue anywhere in the world. When she met with a Norwegian neurologist Dr Harald Schrader at an international neurology conference, he spoke of an epidemic of chronic whiplash flooding his practice in Norway, Obelieniene was astounded. Thus, was born a collaboration that would bring the world a landmark study on the natural history of the acute whiplash injury in Lithuania.¹

In a later prospective controlled inception cohort study, 47 % of 210 victims of rear-end car collisions consecutively identified from the daily records of the traffic police, had initial pain. The symptoms disappeared in most cases after a few days. No subject reported collision-induced pain later than three weeks. After one year, there were no significant differences between the collision victim group and the control group concerning frequency and intensity of both neck pain and headache. As none of the collision victims seemed to have developed persistent and disabling symptoms due to the collision, the studies either evaluated alone or together have sufficient power to reject estimates of the incidence of the so-called chronic whiplash syndrome in previous, methodologically flawed studies and to question the validity of the condition as a chronic physical injury. Thus we learn from this study that while the acute whiplash injury may be universal, chronic whiplash is likely to be culturally-dependent.

As I stated in my article, the first Lithuanian study in 1996 was closely scrutinised, and critics conducted extensive power analyses, only to find that their power considerations were without much avail: the second Lithuania study was published in 1999.² Since then, the critics have coped by engaging silence. Critics have been unable to bend their criticisms around the impressive 1999 results, often publishing extensive and rambling diatribes on the subject, being bluntly critical of the 1996 study too, but ignoring the 1999 study altogether. One suspects these critics could not overcome the strengths of this study with their model, and it only takes one study to reject a model, so they have steered well clear of Lithuania II. Others have used similar or related coping mechanisms to maintain their chronic injury model, the details of which have been thoroughly reviewed elsewhere in a methodological critique of the whiplash literature.³

Unfortunately for Mr. Price and others of a similar jib, the outlook is growing even bleaker since the Lithuanian studies appeared, as now the Greeks and Germans have followed in the steps of the Lithuanian research and the results are equally startling - the acute whiplash injury exists in all countries where there are cars and collision, but the chronic whiplash syndrome is not readily permitted across certain cultural borders. The results of another Lithuanian prospective study (under review) may prove ever more anxiety-provoking, and further increase the stress levels of those faced with the challenge of defending the Myths of Whiplash. Alas, we all have our burdens. I applaud this esteemed journal for not only allowing the free exchange of ideas, but also for allowing individuals like Mr. Price to find some comfort in having expressed an opposing view. Such differences in opinion are welcome for the very reason Winston Churchill posited: ‘If the two of us thought alike, one of us would not be necessary.’

REFERENCES
1. Schrader H, Obelieniene D, Bovim G, Surkiene D, Mickeviciene D, Miseviciene I, et al. Natural evolution of late whiplash syndrome outside the medicolegal context. Lancet 1996, 347: 1207-11.
2. Obelieniene D, Schrader H, Bovirn G, Miseviciene I and Sand T. Pain after whiplash - a prospective controlled inception cohort study. J Neurol Neurosurg Psychiatry 1999; 66: 279-83.
3. Kwan O and Friel J. A review and methodologic critique of the literature supporting “chronic whiplash injury”. Parts I. Med Sci Monit 2003, 9: RA203-15.