ISCHÆMIC FOREARM BLOCK
1
850 against coronary-artery disease in about 13,000 males, 50-59 years of age. This latter study has been organised by a research committee, and the first results will probably be available next spring. P. A. OWREN A. HELLEM A. ØDEGAARD. University Hospital (Rikshospitalet), Oslo, Norway. ADENOSINE AND PLATELET ADHESIVENESS SIR,-Dr. Philp and Dr. Payling Wright (July 31) deter- mined, in normal fasting subjects, platelet-counts and platelet adhesiveness, which decreased and increased respectively dur- ing alimentary lipxmia. The addition of adenosine decreased platelet adhesiveness in fasting blood; this effect was greatly diminished during lipxmia. Lillehei and I 1 2 have shown that the phosphatases are the prime movers in the activation of profibrinolysin to fibrinolysin (with coenzymes). Quick 3 tried to determine the mode of action, in relation to the coagulation mechanism, of A.T.P. (adenosine triphosphate) which, in vitro, showed activity at the same level as that at which it is present physiologically in normal blood. He stated that " the results obtained with the thrombin time clearly indicate that the action is on fibrinogen ". Nevertheless, Quick himself clearly demonstrated that the action of A.T.P. was due to the digestion of fibrin. Although he labelled A.T.P. as an anticoagulant, its primary action is that of fibrinolysis-thus secondarily becoming an anticoagulant in the maintenance of blood-fluidity. On my own,4.; and with Shafiroff, I have shown that A.T.P. is an activator of the fibrinolytic mechanism. Hence the decreased adhesiveness of platelets is due to A.T.P.’s activation of the fibrinolytic mechanism. Lipaemia inhibits this mechanism, thus causing decreased platelet-counts and increased adhesiveness. A.T.P. is the main factor which maintains the blood-fluidity in man within physiological levels. 4 New York, 23, New York. Y. I. MISIRLIOGLU. Y. I. MISIRLIOGLU. ISCHÆMIC FOREARM BLOCK SIR,-One of the commonest complications of ischxmic arm block is reaction to systemic release of large quantities of local anxsthetic on release of the tourniquet. This is most easily prevented by reducing the amount of local anxsthetic used, but below a certain quantity satisfactory anaesthesia is not obtained except by reducing the volume of tissue to be anxsthetised. In operations confined to the hand, which account for many of the procedures suitable for ischaemic block, the volume of tissue requiring anaesthesia can be reduced by carrying out a forearm block. This differs from the method described by Holmes only in that the tourniquet is applied to the upper forearm instead of above the elbow and consequently a smaller quantity of local anaesthetic is used. Full anxsthesia can be obtained by injecting 10-14 ml. of 0’5% lignocaine into a vein on the dorsum of the hand. This technique has been applied to about 50 cases in the accident department of the Auckland Hospital, and previously in the septic hand clinic at St. George’s Hospital, London. No adverse reactions have occurred on releasing the tourniquet; irregularities and changes in the rate of the pulse have not occurred, and no patient has reported dizziness or faintness on direct questioning. No complications, either immediate or late, have occurred from having a tourniquet round the forearm. For procedures lasting more than 10 minutes the double- tourniquet method can be used with one tourniquet above and one below the elbow, the lower tourniquet being inflated and the upper one deflated when analgesia is obtained, in about 2 to 5 minutes. This method requires 14-20 ml. of0’5°o lignocaine for adequate anxsthesia. Larger quantities have proved 1. Misirlioglu, Y. I., Lillehei, C. W. Angiology, 1962, 13, 185. 2. Misirlioglu, Y. I., Lillehei, C. W. J. Am. med. Ass. 1963, 184, 211. 3. Quick, A. J. Nature, Lond. 1963, 200, 469. 4. Misirlioglu, Y. I. Lecture given at the Unity Hospital, Brooklyn, New York, on July 18, 1964. 5. Misirlioglu, Y. I. Summary, 1964, 16, 67. 6. Misirlioglu, Y. I., Shafiroff, B. G. Circulation, 1964, 30, suppl. 3, p. 20. 7. Holmes, C. McK. Lancet, 1963, i, 245. unnecessary except where there has been technical failure such as perivenous injection or deflation of a faulty cuff; and the maximum volumes mentioned have been used only on large men. These volumes are comparable with those named by van Niekerk and Coetzee for intra-arterial ischxmic block without the problems associated with arterial injection. These techniques of course do not provide full muscle relaxation since the proximal parts of the forearm muscles are above the tourniquet. This is no disadvantage, as the patient can position his hand and move it when requested. D. S. ROBERTSON. Auckland Hospital, Park Road, Auckland, C.3, New Zealand. AMITRIPTYLINE AND IMIPRAMINE POISONING SIR,-Amitriptyline and imipramine are absorbed quickly from the intestinal tract, and they are largely bound to plasma- proteins. They accumulate rapidly in various tissues; so that the serum-concentration can never be high. After medium toxic doses the tissue concentration is 10-30 times that of the serum-concentration. After demethylation and glucuronisation in the liver they are excreted in the urine, and hydroxylation takes place.in the liver and tissues. This happens quickly, and no drug can be found in the tissues 24 hours after administra- tion of medium toxic doses. Only small and unimportant amounts of free drug can be found in the urine after administra- tion of high doses. Blood-clearing methods, such as dialysis and peritoneal dialysis,9 10 are theoretically and practically of no value. Clinically my colleagues and I found forced diuresis to be of no therapeutic help, although we did not measure the excretion quantitatively. Rabbits who received 50 mg. per kg. of ami- triptyline intraperitoneally were treated with mannitol, and urinary excretion of the drug was found to be below 2 The forced diureses reported by Dr. Stark and Dr. Bethune (Aug. 21) we feel were effective as treatment of the poisoning caused by amylobarbitone only. This view is supported by the fact that the patient was unconscious for 5 days. In our experience the course of poisoning with the thymoleptic group of drugs is rapid; the life-threatening symptoms, cerebral excitation, and heart-damage occur within 24 hours, and the period of unconsciousness is of almost the same duration. Since 1959 we have treated in this department 38 cases of amitriptyline poisoning (the largest ingested amount was about 3 g., in a patient who died) and 29 cases of imipramine poison- ing (the largest ingested amount was 4700 mg., and 1 patient died). Many clinical findings suggest an atropine-like effect of the thymoleptic group of drugs. Pyridostigmine in small doses (about 0-010 mg. per kg.) has been reported to reduce the fatality-rate in mice who received L.D’100 of amitriptyline to 25 %12. Rabbits who received 50 mg. per kg. of amitriptyline intraperitoneally developed severe atrioventricular bundle- branch block corresponding to the results in man where they lead to forward cardiac failure. Pyridostigmine has some effect in restoring these findings to normal.11 We treat convulsions with phenobarbitone as a prophylactic basic narcotic, and use pentobarbitone for further narcosis as required. Our present principles in treatment, which we have applied in only 1 patient, are best illustrated by the case we report here. An otherwise healthy 41-year-old man, with no history of previous disease or disposition to disease, was admitted to hospital at least 2 hours after the ingestion of 4700 mg. of imipramine. On admission he was unconscious, and after a few minutes he developed tonic convulsions for 30 seconds. The blood-pressure was 70/50 mm. Hg, pulse-rate 84, and heart- 8. van Niekerk, J. P. de V., Coetzee, T. ibid. 1965, i, 1353. 9. Sunshine, P., Yaffe, S. J., Alto, P. Am. J. Dis. Child. 1963, 106, 501. 10. Harthorne, J. W., Marcus, A. M., Kaye, M. New Engl. J. Med. 1963, 268, 33. 11. Rasmussen, J., Nymark, M. Unpublished. 12. Scharer, K. Schweiz. med. Wschr. 1965, 95, 173.
Transcript of ISCHÆMIC FOREARM BLOCK
850
against coronary-artery disease in about 13,000 males, 50-59years of age. This latter study has been organised by a researchcommittee, and the first results will probably be available nextspring.
P. A. OWRENA. HELLEMA. ØDEGAARD.
University Hospital (Rikshospitalet),Oslo, Norway.
ADENOSINE AND PLATELET ADHESIVENESSSIR,-Dr. Philp and Dr. Payling Wright (July 31) deter-
mined, in normal fasting subjects, platelet-counts and plateletadhesiveness, which decreased and increased respectively dur-ing alimentary lipxmia. The addition of adenosine decreasedplatelet adhesiveness in fasting blood; this effect was greatlydiminished during lipxmia.
Lillehei and I 1 2 have shown that the phosphatases are theprime movers in the activation of profibrinolysin to fibrinolysin(with coenzymes).Quick 3 tried to determine the mode of action, in relation to
the coagulation mechanism, of A.T.P. (adenosine triphosphate)which, in vitro, showed activity at the same level as that atwhich it is present physiologically in normal blood. He statedthat " the results obtained with the thrombin time clearlyindicate that the action is on fibrinogen ". Nevertheless, Quickhimself clearly demonstrated that the action of A.T.P. was dueto the digestion of fibrin. Although he labelled A.T.P. as ananticoagulant, its primary action is that of fibrinolysis-thussecondarily becoming an anticoagulant in the maintenance ofblood-fluidity. On my own,4.; and with Shafiroff, I haveshown that A.T.P. is an activator of the fibrinolytic mechanism.Hence the decreased adhesiveness of platelets is due to
A.T.P.’s activation of the fibrinolytic mechanism. Lipaemiainhibits this mechanism, thus causing decreased platelet-countsand increased adhesiveness. A.T.P. is the main factor whichmaintains the blood-fluidity in man within physiological levels. 4
New York, 23, New York. Y. I. MISIRLIOGLU.Y. I. MISIRLIOGLU.
ISCHÆMIC FOREARM BLOCK
SIR,-One of the commonest complications of ischxmic armblock is reaction to systemic release of large quantities of localanxsthetic on release of the tourniquet. This is most easilyprevented by reducing the amount of local anxsthetic used, butbelow a certain quantity satisfactory anaesthesia is not obtainedexcept by reducing the volume of tissue to be anxsthetised.
In operations confined to the hand, which account for manyof the procedures suitable for ischaemic block, the volume oftissue requiring anaesthesia can be reduced by carrying outa forearm block. This differs from the method described byHolmes only in that the tourniquet is applied to the upperforearm instead of above the elbow and consequently a smallerquantity of local anaesthetic is used. Full anxsthesia can beobtained by injecting 10-14 ml. of 0’5% lignocaine into a veinon the dorsum of the hand. This technique has been appliedto about 50 cases in the accident department of the AucklandHospital, and previously in the septic hand clinic at St. George’sHospital, London.No adverse reactions have occurred on releasing the
tourniquet; irregularities and changes in the rate of the pulsehave not occurred, and no patient has reported dizziness orfaintness on direct questioning. No complications, eitherimmediate or late, have occurred from having a tourniquetround the forearm.For procedures lasting more than 10 minutes the double-
tourniquet method can be used with one tourniquet above andone below the elbow, the lower tourniquet being inflated andthe upper one deflated when analgesia is obtained, in about 2 to5 minutes. This method requires 14-20 ml. of0’5°o lignocainefor adequate anxsthesia. Larger quantities have proved1. Misirlioglu, Y. I., Lillehei, C. W. Angiology, 1962, 13, 185.2. Misirlioglu, Y. I., Lillehei, C. W. J. Am. med. Ass. 1963, 184, 211.3. Quick, A. J. Nature, Lond. 1963, 200, 469.4. Misirlioglu, Y. I. Lecture given at the Unity Hospital, Brooklyn, New
York, on July 18, 1964.5. Misirlioglu, Y. I. Summary, 1964, 16, 67.6. Misirlioglu, Y. I., Shafiroff, B. G. Circulation, 1964, 30, suppl. 3, p. 20.7. Holmes, C. McK. Lancet, 1963, i, 245.
unnecessary except where there has been technical failure suchas perivenous injection or deflation of a faulty cuff; and themaximum volumes mentioned have been used only on largemen. These volumes are comparable with those named byvan Niekerk and Coetzee for intra-arterial ischxmic blockwithout the problems associated with arterial injection.These techniques of course do not provide full muscle
relaxation since the proximal parts of the forearm muscles areabove the tourniquet. This is no disadvantage, as the patientcan position his hand and move it when requested.
D. S. ROBERTSON.
Auckland Hospital,Park Road,
Auckland, C.3,New Zealand.
AMITRIPTYLINE AND IMIPRAMINE POISONING
SIR,-Amitriptyline and imipramine are absorbed quicklyfrom the intestinal tract, and they are largely bound to plasma-proteins. They accumulate rapidly in various tissues; so thatthe serum-concentration can never be high. After mediumtoxic doses the tissue concentration is 10-30 times that of theserum-concentration. After demethylation and glucuronisationin the liver they are excreted in the urine, and hydroxylationtakes place.in the liver and tissues. This happens quickly, andno drug can be found in the tissues 24 hours after administra-tion of medium toxic doses. Only small and unimportantamounts of free drug can be found in the urine after administra-tion of high doses.
Blood-clearing methods, such as dialysis and peritonealdialysis,9 10 are theoretically and practically of no value.
Clinically my colleagues and I found forced diuresis to be of notherapeutic help, although we did not measure the excretionquantitatively. Rabbits who received 50 mg. per kg. of ami-triptyline intraperitoneally were treated with mannitol, andurinary excretion of the drug was found to be below 2 Theforced diureses reported by Dr. Stark and Dr. Bethune
(Aug. 21) we feel were effective as treatment of the poisoningcaused by amylobarbitone only. This view is supported by thefact that the patient was unconscious for 5 days. In our
experience the course of poisoning with the thymolepticgroup of drugs is rapid; the life-threatening symptoms,cerebral excitation, and heart-damage occur within 24 hours,and the period of unconsciousness is of almost the sameduration.
Since 1959 we have treated in this department 38 cases ofamitriptyline poisoning (the largest ingested amount was about3 g., in a patient who died) and 29 cases of imipramine poison-ing (the largest ingested amount was 4700 mg., and 1 patientdied).Many clinical findings suggest an atropine-like effect of the
thymoleptic group of drugs. Pyridostigmine in small doses(about 0-010 mg. per kg.) has been reported to reduce thefatality-rate in mice who received L.D’100 of amitriptyline to25 %12. Rabbits who received 50 mg. per kg. of amitriptylineintraperitoneally developed severe atrioventricular bundle-branch block corresponding to the results in man where theylead to forward cardiac failure. Pyridostigmine has some effectin restoring these findings to normal.11We treat convulsions with phenobarbitone as a prophylactic
basic narcotic, and use pentobarbitone for further narcosis asrequired. Our present principles in treatment, which we haveapplied in only 1 patient, are best illustrated by the case wereport here.
An otherwise healthy 41-year-old man, with no history ofprevious disease or disposition to disease, was admitted tohospital at least 2 hours after the ingestion of 4700 mg. ofimipramine. On admission he was unconscious, and after a fewminutes he developed tonic convulsions for 30 seconds. The
blood-pressure was 70/50 mm. Hg, pulse-rate 84, and heart-8. van Niekerk, J. P. de V., Coetzee, T. ibid. 1965, i, 1353.9. Sunshine, P., Yaffe, S. J., Alto, P. Am. J. Dis. Child. 1963, 106, 501.
10. Harthorne, J. W., Marcus, A. M., Kaye, M. New Engl. J. Med. 1963,268, 33.
11. Rasmussen, J., Nymark, M. Unpublished.12. Scharer, K. Schweiz. med. Wschr. 1965, 95, 173.
