Pathology ( 2002 ), 34, December
7. Isbister GK. Data collection in clinical toxinology: Debunking myths and developing diagnostic algorithms. J Toxicol Clin Toxicol 2002; 40: 231–7. 8. Currie BJ. Snakebite in tropical Australia, Papua New Guinea and Irian Jaya. Emerg Med 2000; 12: 285– 94.
Coagulopathy from tiger snake envenoming and its treatment: authors’ reply Sir, The coagulation changes after snake envenomation is an area that is poorly understood because of differences amongst individual patients in the amount of venom inoculated, type of snake species encountered and duration of exposure before medical assistance is sought. Our paper details coagulation activation in three cases of envenomation from a particular species of tiger snake.1 It describes the complex and unique coagulation changes including the observation of the transient presence of an inhibitor and depletion of fibrinogen and clotting factor V. All of the published reports regarding options for clinical management rely on observations from case series that limit any certainty as to an appropriate treatment pathway. Death from cerebral haemorrhage has been reported in at least six published cases of tiger and brown snake envenomation. 2– 6 Apart from the profound coagulation abnormalities of defibrination and depletion of coagulation factors, it has also been suggested that the use of adrenaline and localised trauma after collapse are additional predisposing factors for excessive haemorrhage. The prevention of this serious complication is important to save lives after snakebite. There is no doubt that identification of the snake species and administration of appropriate antivenom is the mainstay of treatment. However the amount and duration of antivenom required to neutralise the circulating venom for a particular situation is uncertain. In the absence of other appropriate markers that indicate the complete reversal of all circulating venom, it is suggested that normalisation of the coagulation results after transfusion could act as an indicator for adequate antivenom treatment. It avoids the delay in awaiting natural replenishment of consumed clotting factors and, in our hands, reduces the severity of the transient coagulopathy that could be associated with cerebral haemorrhage and death. The theoretical increase in FDP exacerbating the bleeding problem should be minimised with appropriate venom neutralisation. We do not advocate using blood products without antivenom because of these concerns and the reports of unprovoked lower limb thrombosis due to rampant coagulation consumption. Like all blood products there is a rare risk of transmission of viral infection, but this risk is balanced against the potential for fatal and unpredictable haemorrhage. Our case series suggest that, should a clinical decision be made to treat the coagulopathy in western tiger snake envenomation, the appropriate products would be both fresh frozen plasma to correct the factor deficiency ( especially factor V) and cryoprecipitate for fibrinogen replacement. The implication of the profound coagulopathy and risk of haemorrhage needs to be balanced against fuelling the defibrination process from unneutralised venom. However the finding of coagulation correction after blood products quickly alerts the clinician of adequate
antivenom treatment. Clotting factor replacement also has the potential to reduce fatal bleeding events, but a definitive answer to this question will only be possible as further evidence accumulates. In response to the question of the identity of the snakes in our cases, in one case the identity of the snake was confirmed by the victim, a professional herpetologist. It was assumed on the basis of a snake venom detection kit in the others, there being only one species of tiger snake in Western Australia, and no other Western Australian snake is known to react as a tiger snake on the kit. Alan Morling
Department of Haematology Royal Perth Hospital Perth Western Australia 1. Ferguson LA, Morling A, Moraes C, Baker R. Investigation of coagulopathy in three cases of tiger snake ( Notechis ater occidentali s ) envenomation. Pathology 2002; 34: 157– 61. 2. Tibballs J, Henning RD, Sutherland SK, Kerr AR. Fatal cerebral haemorrhage after tiger snake ( Notechis scutatus ) envenomation. Med J Aust 1991; 154: 275– 6. 3. 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– 4. 4. Sutherland SK. Deaths from snakebite in Australia, 1981–1991. Med J Aust 1992; 157: 740– 6. 5. Sprivulis P, Jelinek GA. Fatal intracranial haematomas in two patients with brown snake envenomation. Med J Aust 1995; 162: 215– 6. 6. Midyett FA. Neuroradiologic findings in brown snake envenomation : computed tomography demonstration. Australas Radiol 1998; 42: 248– 9.
Pagetoid spread of melanocytes in Spitz naevi Sir, I have read with much interest the recent article regarding the difficulties in distinguishing Spitz naevi from spitzoid melanomas by light microscopy.1 The authors state that ‘features commonly found in Spitz naevi include . . . intraepidermal nests of melanocytes with some single cells’.1 I have always thought that clusters of two or three intraepidermal melanocytes can be seen in Spitz naevi, whereas single spread of melanocytes into the epidermis was more in favour of melanoma. In fact, Weedon2 states that the absence of pagetoid spread of single melanocytes into the epidermis is one of the major diagnostic criteria for Spitz naevi. I hope the authors can shed light on this apparent dichotomy of opinion. Gino R. Somers Royal Children’s Hospital Melbourne Victoria Australia 1. Crotty KA, Scolyer RA, Li LXL, Palmer AA, Wang L, McCarthy SW. Spitz naevus versus spitzoid melanoma: When and how can they be distinguished? Pathology 2002; 34: 6–12. 2. Weedon D. Skin Pathology. New York: Churchill Livingston, 1997; 681– 3.