Hepatic resection.pm

Tetramine poisoning
We report on two patients who presented with status epilepticus due
to ingestion of rat poison containing tetramine. Both had eaten the
same meal, subsequently presumed to be the source of the poison.
Physical examination and investigation were unremarkable and diag-
nosis was based on patient history. Seizures were ultimately control-
led with ketamine, after unsuccessful attempt of benzodiazepine and
sodium thiopentone. One week after poisoning, both patients
underwent one session of high-volume haemofiltration followed by
charcoal haemoperfusion to eliminate the toxin from the body. Plasma
tetramine levels then decreased from 0.95
µg/mL to 0.35 µg/mL and
from 0.53
µg/mL to 0.40 µg/mL, respectively.
Case reports
Key words:
Case 1
A 38-year-old construction worker was admitted with status epilepticus in January 2003. He had a history of epilepsy but had defaulted from follow-up and taken no anticonvulsant drugs for 3 months. While in the Accident and Emergency Department, he had a generalised tonic-clonic convulsion that lasted 30 minutes. His temperature was 37ΟC andGlasgow Coma Scale (GCS) score was 3/15. There was no neck rigidity and both pupils were dilated and reactive. There were no localising signs and no external evidence of head injury. Cardiovascular examination was unremarkable: pulse, 110 beats per minute regular; blood pressure, 180/100 mm Hg; electrocardiogram (ECG), normal. His chest was clear to auscultation and pulse oximeter read 95% on room air. The seizure remained uncontrolled following administration of lorazepam 8 mg,diazepam 10 mg, and phenytoin 750 mg. He was intubated and plain computed tomography of the brain revealed mild cerebral oedema.
Intensive Care Unit, North District
Results of laboratory investigations were shown in the Table. Osmolar Hospital, Sheung Shui, Hong Kong
gap, calcium, glucose, ammonia, and liver function tests were normal.
Intensive Care Unit, Pamela Youde
Nethersole Eastern Hospital, Chai Wan,

A further seizure occurred despite rapid escalation of anticonvulsant Hong Kong
therapy (midazolam 14 mg immediately followed by 10 mg/h, phenytoin 2 g, thiopentone 2 g loading followed by 375 mg/h). A ketamine infusion Department of Intensive Care Medicine,
Singapore General Hospital, Singapore

at a dose of 120 mg/h eventually brought the seizure under control.
Sodium thiopentone, midazolam, and ketamine infusion were graduallystopped after 16 hours of seizure-free activity on electroencephalography Correspondence to: Dr CM Chau
(e-mail: [email protected])

Hong Kong Med J Vol 11 No 6 December 2005 511 Table. Laboratory findings
prescribed blood flow rate of 200 mL/min. Tinzaparin was again used as anticoagulant. This time, plasma te- tramine level decreased from 0.53 µg/mL to 0.40 µg/mL, a reduction of 25%. Blood was taken 5 minutes after cessation of blood flow during both HVHF and HP.
The patient remained in the intensive care unit (ICU) for 16 days and was then discharged. He had normal mental function at 1-month follow-up.
Case 2
A 33-year-old woman, who shared the same meal with the patient in case 1, presented with vomiting that was successfully controlled with prochlorperazine. She refused admission but presented again the followingday with confusion and a generalised tonic-clonicconvulsion. Examination revealed a GCS score of15/15 but no focal signs. She was afebrile and Questioning of the patient’s wife revealed that cardiovascular and laboratory examinations were her husband’s colleague (patient in case 2), who unremarkable: blood pressure, 117/75 mm Hg; pulse, shared the same meal, had also had a convulsion.
85 beats per minute; pulse oximeter 95% on room air; A dog that ate the remains of the meal had convul- and ECG normal. Her GCS score decreased to 9/15 sions and was found dead the following day. Probable after a further seizure and she was intubated and given food or drug poisoning was suspected. Activated charcoal 50 g every 6 hours was commenced onadmission and continued for 2 days. Plasma cholineste- She was extubated 5 hours later. Tetramine was rase level was 6606 IU/L. Methaemoglobin level was detected in vomitus and blood (0.54 µg/mL) on day 7.
0.3%. Serum lead was normal (0.3 µmol/L) and the She was confused but experienced no further seizures.
arsenate level was negative. Blood and urine were She was discharged on day 10 having made a full negative for salicylate, paracetamol, and cannabinoids.
The patient was extubated on day 7. He remained Discussion
confused and exhibited frequent facial twitching.
Tetramine, the active component of a rat poison Tetramethylene disulphotetramine (TETS), commonly ‘dushuqiang’, was identified in vomitus 1 week after called tetramine, is an odourless and tasteless small admission. Intravenous pyridoxine 50 mg daily was molecule with MV 248. It binds to the gamma- prescribed for 5 days from day 7 onward. One session aminobutyric acid (GABA) receptor on the neuronal of high-volume haemofiltration (HVHF) followed cell membrane and blocks the chloride channels.1,2 by a session of charcoal haemoperfusion (HP) were Available pharmacokinetic data are incomplete and sometimes contradictory. Both reversible2 andirreversible binding3 to the GABA receptors have been described. The TETS can be absorbed through on-line haemofiltration system and a high-flux the gastro-intestinal tract and respiratory system.
polysulphone diafilter (APS900, Asahi dialyzer, Japan; Thereafter, it is rapidly distributed to various body 1.8 m2, removes molecules of up to 66 000 dalton).
tissues and organs. It has a high volume of distribution, Blood flow was set at 200 mL/min and ultrafiltration a slow metabolism, and is excreted unchanged in the flow at 200 mL/min. Predilution replacement fluid was urine and stool. It can remain in the body for up to 6 given at 200 mL/min for 10 hours. Tinzaparin was used months. The lethal dose 50% for humans is 0.1 mg/kg as anticoagulant. The plasma tetramine level decreased and there is no specific and effective antidote reported by 63% from 0.95 µg/mL to 0.35 µg/mL. The follow- in the literature at the time of writing.2,3 ing day the tetramine level increased to 0.53 µg/mL: a6-hour HP was performed with a cartridge containing The quoted toxic and lethal ranges for tetramine 300 g of activated charcoal (Adsorba 300C; Gambro are 0.002 to 0.369 µg/mL and 0.64 to 5.49 µg/mL, Lundia AB, Sweden) coated with cellulose and at a respectively.4 In mild-to-moderate poisoning, symp- 512 Hong Kong Med J Vol 11 No 6 December 2005 toms include headache, dizziness, nausea, vomiting, High-volume haemofiltration may be an alterna- abdominal pain, bradycardia, tachycardia, twitching, tive to HP since the charcoal cartridge for the latter is agitation, and visual and auditory hallucinations. In not readily available in most ICUs and its shell-life is severe cases, status epilepticus, coma, and multi- limited. Although the success of haemofiltration organ failure can occur. Electroencephalography has not been extensively evaluated, the number of suc- demonstrates generalised slow waves and spikes.
cessful case reports is increasing. Its use in tetramine Onset time is rapid and occurs within 30 minutes of exposure and may last up to 13 hours. A fatality rateas high as 3.67% has been reported.5 Diagnosis de- In the first patient reported here, the plasma pends principally on history and clinical presentation.
tetramine level was decreased by both HVHF and HP.
Detection of tetramine in blood or the excreta by gas The drop in plasma tetramine level was greater chromatography/mass spectroscopy is confirmatory.
following HVHF (63%) than charcoal HP (25%).
The increase in tetramine level from 0.35 µg/mL to 0.53 µg/mL 12 hours after HVHF was compatible with antidotal effect. Animal and human studies reveal the rebound phenomenon and redistribution of the toxin that it prolongs the latent period of convulsions and from tissue stores to plasma. The difference in plasma reduces convulsive time and mortality.6,7 Binding of level reduction following HVHF and HP may have GABA in the brain is also enhanced. The anticonvul- been due to different treatment durations and the sant effect is increased by high-dose vitamin B6 mechanisms involved. It is difficult to compare the and diazepam.7-9 Dimercaptopropanesulphonate is efficacy of toxin removal by HVHF and HP if the available in some major hospitals in Hong Kong.
amount of tetramine removed cannot be quantified.
Extracorporeal toxin removal has been frequently As there is limited immediate access to charcoal performed in China by plasma exchange, HP, and HP in most ICUs, HVHF can be considered an haemodialysis with variable results.2,4,10,11 Plasma alternative treatment for tetramine poisoning.
exchange is reported to be more successful in cases ofsevere intoxication. Haemoperfusion is nonetheless Conclusion
more common and is associated with less reboundphenomena and stable haemodynamics. Haemodialy- Early and adequate resuscitation combined with sis is least useful unless the patient is in renal failure.
seizure control are crucial to the management of acutetetramine poisoning. Ketamine and conventional The efficacy of ketamine in prolonged status anticonvulsant drugs may have synergistic and epilepticus has been demonstrated in both animal additive effects in the management of refractory models and humans.12,13 It decreases the excitatory status epilepticus. High-volume haemofiltration may effects of glutamate and other excitatory neurotrans- be an alternative to charcoal HP in tetramine poisoning.
mitters through blockade of the N-methyl-D-aspartate–gated calcium channel. Ketamine and conventional References
anticonvulsants may have synergistic or additiveeffects when prescribed together.
1. Centers for Disease Control and Prevention (CDC).
Poisoning by an illegally imported Chinese rodenticidecontaining tetramethylenedisulfotetramine—New York City, Haemoperfusion is the standard treatment in China 2002. MMWR Morb Mortal Wkly Rep 2003;52:199-201.
for severe tetramine poisoning. An intoxicated patient 2. Tang XJ, Kuang SR, Li LY. Dushuqiang (tetramine) and with plasma tetramine level of 70 µg/L excreted only treatment for poisoning [in Chinese]. Chin J Occup Med 60 µg after 24 hours and a total of 80 µg after 48 hours.14 Nonetheless one session of HP removed up to 3. Tetramine information. Chinese Psychology Online website: 1 mg of tetramine when the initial plasma level was www.zgxl.net/light/yjcs/zhongdu/dsq.htm. Accessed Jun 2002.
4. Feng Y. An analysis of tetramine and its distribution in human 100 µg/L.14 There was no demonstratable difference bodies. In: Essays on rat poison intoxication conference, Tian in plasma tetramine level before and after HP: this Jin [in Chinese]. Beijing: Centre for Physical Evidence was attributed to redistribution of tetramine from the body store.15 Abnormalities of EEG have been 5. Cheng YZ, Chen BZ. Study on the emergency treatment of reported to persist for up to 1 year in patients not 106 acute tetramine poisoning [in Chinese]. Zhongguo WeiZhong Bing Ji Jiu Yi Xue 2004;16:1-8.
receiving HP.15 Earlier resolution of EEG abnormali- 6. Wu JH. Clinical observation of tetramine poisoning treating ties has been observed in patients who receive more with dimercaptopropanesulphonate and vitamin B6 [in Chinese]. Chuan Bei Yi Xue Yuan Xue Bao 2004;3:26-7.
Hong Kong Med J Vol 11 No 6 December 2005 513 7. Li YF, Zhang BL, Guo AP. Therapeutic observation of 11. Croddy E. Rat poison and food security in the People’s treating severe tetramine poisoning with dimercapto- Republic of China: focus on tetramethylene disulfotetramine propanesulphonate: 20 cases [in Chinese]. Handan Yi Xue (tetramine). Arch Toxicol 2004;78:1-6.
Gao Den Jiao Ke Xue Xiao Xue Bao 2004;17:295.
12. Sheth RD, Gidal BE. Refractory status epilepticus: response 8. Zhao CH, Lu ZQ, Li HP, Li JR. Treatment with diazepam to ketamine. Neurology 1998;51:1765-6.
and dimercaptopropanesulfonate sodium for acute tetramine 13. Borris DJ, Bertram EH, Kapur J. Ketamine controls prolonged intoxication [in Chinese]. Zhonghua Lao Dong Wei Sheng Zhi status epilepticus. Epilepsy Res 2000;42:117-22.
14. Ge X, Li X, Guan L, Ma P, Wang H. Study on the effect 9. Qui Z, Lan H, Zhang S, Xia Y, Huang S. Antidotal effects of using hemoperfusion to treat poisoned patients [in Chinese].
vitamin B(6) and sodium dimercaptopropane sulfonate on Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi 2002;20: acute poisoning with tetramethylene disulphotetramine in animals [in Chinese]. Zhonghua Nei Ke Za Zhi 2002;41:186-8.
15. Cui FX, Cui J, Wang CD. Effect of hemoperfusion on 10. Meng XK. Advances in studies of poisoning by tetramine.
prognosis in dushuqiang (tetramine) poisoning [in Chinese].
Chinese Journal of Critical Care Emergency 2002;22:245-66.
Zhonghua Er Ke Za Zhi 2003;41:950-1.
514 Hong Kong Med J Vol 11 No 6 December 2005

Source: http://ww.dead-planet.net/chemical-terrorism/pdfs/hk_tetscase2.pdf

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