1593
Interatrial shunts and decompression sickness in divers SIR,—In our letter (April 14, p 914) we discussed deficiencies in the design of Dr Wilmshurst and colleagues’ study (Dec 2, p 1302). Dr Wilmshurst’s accompanying reply confirms that the study was not adequately blinded; nor were attempts made to avoid selection bias. Our second point covered the intriguing area of the pathophysiological mechanisms implicated in neurological decompression sickness (DCS). We explained that the autochthonous bubble hypothesis is supported by the results of experiments in animals and that there are theoretical reasons for the proposition that this mechanism may explain the pathogenesis of rapid-onset spinal cord decompression sickness.1,2 We therefore disagree that the statistical association between fulminant neurological dysbarism and a patent foramen ovale shows that arterial gas embolism is a probable mechanism for the condition. The absence of information on more precise diagnostic subsets of neurological dysbarism further clouds this issue. We accept that the pathology associated with arterial gas
embolism may be different if the embolised tissue contains a raised partial pressure of inert gas. However, Wilmshurst’s hypothesis demands an explanation of how gas bubbles originating intravascularly can be found within myelin at histology 2-5 The Institute of Naval Medicine is not "in two minds" about the possibility of arterial gas emboli causing spinal cord decompression sickness. We maintain an open mind. Although we think that autochthonous bubbles are the most probable explanation for the mechanism of rapid-onset spinal cord DCS, they do not explain all cases-for example, those in which onset is delayed. In these cases, as with cerebral DCS, we think that arterial gas embolism is the most likely explanation of the mechanism.
Institute of Naval Medicine,
Undersea Medicine Department, Alverstoke, Gosport, Hampshire PO12 2DL, UK
D. J. SMITH T. J. R. FRANCIS M. HODGSON A. W. MURRISON J. J. W. SYKES
Sykes JJW, Yaffe L. Light and electron microsopic alterations in spinal cord myelin sheath after decompression sickness. Undersea Biomed Res 1985; 12: 251-58. 2. Francis TJR. The role of autochthonous bubbles in spinal cord decompression sickness. University of London: PhD thesis, 1990: 3. Burns BA, Hardman JM, Beckman EL. In-situ bubble formation in acute cerebral nervous system decompression sickness. J Neuropathol Exp Neurol 1988; 47: 371. 4. Francis TJR, Pezeshkpour GH, Lutka AJ. Arterial gas embolism as a pathophysiologic mechanism for spinal cord decompression sickness. Undersea 1.
Biomed Res 1989; 16: 439-51. 5. Francis TJR, Pezeshkpour GH, Dutka AJ, Hallenbeck JM, Flynn ET. Is there a role for the autochthonous bubble in pathogenesis of spinal cord decompression sickness? Neuropathol Exp Neurol 1988; 47: 475-87.
Splenectomy for chronic thrombotic thrombocytopenic purpura
of Internal Medicine, University of Tubingen, D-7400 Tubingen, West Germany
Department
H. J. LENZ
K. JASCHONEK
U. SCHULER G. EHNINGER
B. STEINKE H. D. WALLER
1. Bukowski RM. Thrombotic thrombocytopenic purpura: a review. In: Spaet T, ed. Progress in hemostasis and thrombosis. New York: Grune and Stratton, 1982: 6: 287-337. 2. Kwaan HC. Thrombotic microangiopathy Sem Hematol 1987; 14: 2-3. 3. Byrnes JJ, Moake JL. Thrombotic thrombocytopenic purpura and the hemolyticuraemic
syndrome: evolving concepts
of pathogenesis and
therapy. Clin Hematol
1985; 15: 413-42. 4. Lian EC, Mui PT,
et al. Inhibition of platelet aggregating activity in thrombotic thrombocytopenic purpura plasma by normal adult immunoglobulin.J Clin Invest 1984; 73: 548-55. 5. Wong P, Itoh K, et al. Treatment of thrombotic thrombocytopenic purpura with intravenous gammaglobulin. N Engl J Med 1986; 314: 385. 6. Viero P, Cortelazzo S, et al. Thrombotic thrombocytopenic purpura and high dose immunoglobulin treatment. Ann Intern Med 1986; 104: 282. 7. Schneider P, Rayner A, et al. The role of splenectomy in multimodality treatment of thrombotic thrombocytopenic purpura. Ann Surg 1985; 202: 318-21. 8. Cahalane SF, Horn RC. Thrombotic thrombocytopenic purpura of long duration. Am J Med 1959; 17: 333-41. 9. Cuttner J. Chronic thrombotic thrombocytopenic purpura: report of a case with five relapses and review of literature. Mount Sinai J Med 1978; 45: 418-25.
Late consequences of sprained ankle SIR,—Your June 2 editorial rightly points out that ankle sprains are among the most common presentations in accident departments and that some fractures might be missed on the initial radiographs. I believe that the frequency of residual symptoms can be decreased by the implementation of a good audit system whereby all radiographs reported as abnormal by the radiologists are returned to the accident and emergency consultant. Whether the abnormality has been noted by the junior doctor can then be checked.l We have reduced the number of missed radiological abnormalities to 73 (3-8%) of 1937 abnormalities in 6224 patients who were radiographed over 2 years for sprained ankles. 22 of the 73 mistakes were attributable to non-recognition of the clinical significance of soft-tissue swelling both malleoli. Patient education plays an important part in recovery after an ankle sprain. In a busy accident and emergency department the doctor’s explanation of the injury and its management are often hurried and the patient’s recall of instructions is poor. It is not unusual that patients limp or return days later with swelling of the foot and ankle, which is responsible for some of the long-term disability of this injury. We intend to issue information tailored to individual patients (including children), with the aid of our computer system.2 This will include a description of the injury, instructions for management, warnings of drug side-effects, the signs of more serious injury, and which doctor to ask for on re-attendance.
over one or
is
SIR,- Thrombotic thrombocytopenic purpura (TTP) by thrombotic, microangiopathic anaemia, thrombocytopenia, neurological dysfunction, and fever. In most patients the clinical course is short, and death occurs within 3 months in 80% of untreated cases.1 Treatment ofTTP is empirical, since the pathogenesis of the disease is not certain.2,3 Treatment with immunoglobulins4- or splenectomy has been successful in non-responders to plasmapheresis.’ We are aware of only a few patients with a chronic or relapsing course of the disease. Assumptions about primary manifestations often rely on patient history alone; a generally acceptable definition of chronic disease is therefore difficult. A chronic or relapsing course of the disease for more than 5 years has been reported in at least 15 patients, and for more than 10 years in 6.1,8,9 We present a 50-year-old woman with a 131 year history of signs and symptoms ofTTP, which responded to splenectomy. In February, 1974, she presented with signs of anaemia and thrombocytopenia, which were treated with steroids. In 1976 neurological abnormalities developed, which were regarded as characterised
transient ischaemic attacks. Renal function declined and by 1985 creatinine was 3-5 mg/dl. TTP was diagnosed and additional treatment with fresh frozen plasma (about 12 litres) and an antiplatelet agent (dipyridamole) was started. Platelet counts were over 100 000/µ1 for 6 months and there was no evidence of haemolysis. 14 months later paraesthesia developed, and she had petechial bleeding. Repeated plasmapheresis was done with only limited effect. Treatment with a prostacyclin derivative CG 4203, vincristine, prednisolone, and intravenous immunoglobulins (10 g for 5 days) had no effect on platelet counts. By 111 In-labelling of her platelets, the spleen was identified as the main site of sequestration. In August, 1987, she was prepared for splenectomy by daily plasmapheresis and the platelet count reached 73 000/µl; one week after operation this had risen to 427 000/µ1 and there was no evidence of neurological dysfunction. She has now been well for 3 years on maintenance with low-dose aspirin.
Accident and Emergency Department, Central Middlesex Hospital,
London NW10 7NS, UK
SAPAL TACHAKRA
SS, Beckett MW Why do casualty officers miss radiological abnormalities? Ann R Coll Surg Ed 1985; 30: 311-13. 2. Grout P, Hunt MT, Touquet R. The benefits of an accident and emergency computer system. Theor Surg 1989; 4: 1-9. 1. Tachakra
Interatrial shunts and decompression sickness in divers SIR,—In our letter (April 14, p 914) we discussed deficiencies in the design of Dr Wilmshurst and colleagues’ study (Dec 2, p 1302). Dr Wilmshurst’s accompanying reply confirms that the study was not adequately blinded; nor were attempts made to avoid selection bias. Our second point covered the intriguing area of the pathophysiological mechanisms implicated in neurological decompression sickness (DCS). We explained that the autochthonous bubble hypothesis is supported by the results of experiments in animals and that there are theoretical reasons for the proposition that this mechanism may explain the pathogenesis of rapid-onset spinal cord decompression sickness.1,2 We therefore disagree that the statistical association between fulminant neurological dysbarism and a patent foramen ovale shows that arterial gas embolism is a probable mechanism for the condition. The absence of information on more precise diagnostic subsets of neurological dysbarism further clouds this issue. We accept that the pathology associated with arterial gas
embolism may be different if the embolised tissue contains a raised partial pressure of inert gas. However, Wilmshurst’s hypothesis demands an explanation of how gas bubbles originating intravascularly can be found within myelin at histology 2-5 The Institute of Naval Medicine is not "in two minds" about the possibility of arterial gas emboli causing spinal cord decompression sickness. We maintain an open mind. Although we think that autochthonous bubbles are the most probable explanation for the mechanism of rapid-onset spinal cord DCS, they do not explain all cases-for example, those in which onset is delayed. In these cases, as with cerebral DCS, we think that arterial gas embolism is the most likely explanation of the mechanism.
Institute of Naval Medicine,
Undersea Medicine Department, Alverstoke, Gosport, Hampshire PO12 2DL, UK
D. J. SMITH T. J. R. FRANCIS M. HODGSON A. W. MURRISON J. J. W. SYKES
Sykes JJW, Yaffe L. Light and electron microsopic alterations in spinal cord myelin sheath after decompression sickness. Undersea Biomed Res 1985; 12: 251-58. 2. Francis TJR. The role of autochthonous bubbles in spinal cord decompression sickness. University of London: PhD thesis, 1990: 3. Burns BA, Hardman JM, Beckman EL. In-situ bubble formation in acute cerebral nervous system decompression sickness. J Neuropathol Exp Neurol 1988; 47: 371. 4. Francis TJR, Pezeshkpour GH, Lutka AJ. Arterial gas embolism as a pathophysiologic mechanism for spinal cord decompression sickness. Undersea 1.
Biomed Res 1989; 16: 439-51. 5. Francis TJR, Pezeshkpour GH, Dutka AJ, Hallenbeck JM, Flynn ET. Is there a role for the autochthonous bubble in pathogenesis of spinal cord decompression sickness? Neuropathol Exp Neurol 1988; 47: 475-87.
Splenectomy for chronic thrombotic thrombocytopenic purpura
of Internal Medicine, University of Tubingen, D-7400 Tubingen, West Germany
Department
H. J. LENZ
K. JASCHONEK
U. SCHULER G. EHNINGER
B. STEINKE H. D. WALLER
1. Bukowski RM. Thrombotic thrombocytopenic purpura: a review. In: Spaet T, ed. Progress in hemostasis and thrombosis. New York: Grune and Stratton, 1982: 6: 287-337. 2. Kwaan HC. Thrombotic microangiopathy Sem Hematol 1987; 14: 2-3. 3. Byrnes JJ, Moake JL. Thrombotic thrombocytopenic purpura and the hemolyticuraemic
syndrome: evolving concepts
of pathogenesis and
therapy. Clin Hematol
1985; 15: 413-42. 4. Lian EC, Mui PT,
et al. Inhibition of platelet aggregating activity in thrombotic thrombocytopenic purpura plasma by normal adult immunoglobulin.J Clin Invest 1984; 73: 548-55. 5. Wong P, Itoh K, et al. Treatment of thrombotic thrombocytopenic purpura with intravenous gammaglobulin. N Engl J Med 1986; 314: 385. 6. Viero P, Cortelazzo S, et al. Thrombotic thrombocytopenic purpura and high dose immunoglobulin treatment. Ann Intern Med 1986; 104: 282. 7. Schneider P, Rayner A, et al. The role of splenectomy in multimodality treatment of thrombotic thrombocytopenic purpura. Ann Surg 1985; 202: 318-21. 8. Cahalane SF, Horn RC. Thrombotic thrombocytopenic purpura of long duration. Am J Med 1959; 17: 333-41. 9. Cuttner J. Chronic thrombotic thrombocytopenic purpura: report of a case with five relapses and review of literature. Mount Sinai J Med 1978; 45: 418-25.
Late consequences of sprained ankle SIR,—Your June 2 editorial rightly points out that ankle sprains are among the most common presentations in accident departments and that some fractures might be missed on the initial radiographs. I believe that the frequency of residual symptoms can be decreased by the implementation of a good audit system whereby all radiographs reported as abnormal by the radiologists are returned to the accident and emergency consultant. Whether the abnormality has been noted by the junior doctor can then be checked.l We have reduced the number of missed radiological abnormalities to 73 (3-8%) of 1937 abnormalities in 6224 patients who were radiographed over 2 years for sprained ankles. 22 of the 73 mistakes were attributable to non-recognition of the clinical significance of soft-tissue swelling both malleoli. Patient education plays an important part in recovery after an ankle sprain. In a busy accident and emergency department the doctor’s explanation of the injury and its management are often hurried and the patient’s recall of instructions is poor. It is not unusual that patients limp or return days later with swelling of the foot and ankle, which is responsible for some of the long-term disability of this injury. We intend to issue information tailored to individual patients (including children), with the aid of our computer system.2 This will include a description of the injury, instructions for management, warnings of drug side-effects, the signs of more serious injury, and which doctor to ask for on re-attendance.
over one or
is
SIR,- Thrombotic thrombocytopenic purpura (TTP) by thrombotic, microangiopathic anaemia, thrombocytopenia, neurological dysfunction, and fever. In most patients the clinical course is short, and death occurs within 3 months in 80% of untreated cases.1 Treatment ofTTP is empirical, since the pathogenesis of the disease is not certain.2,3 Treatment with immunoglobulins4- or splenectomy has been successful in non-responders to plasmapheresis.’ We are aware of only a few patients with a chronic or relapsing course of the disease. Assumptions about primary manifestations often rely on patient history alone; a generally acceptable definition of chronic disease is therefore difficult. A chronic or relapsing course of the disease for more than 5 years has been reported in at least 15 patients, and for more than 10 years in 6.1,8,9 We present a 50-year-old woman with a 131 year history of signs and symptoms ofTTP, which responded to splenectomy. In February, 1974, she presented with signs of anaemia and thrombocytopenia, which were treated with steroids. In 1976 neurological abnormalities developed, which were regarded as characterised
transient ischaemic attacks. Renal function declined and by 1985 creatinine was 3-5 mg/dl. TTP was diagnosed and additional treatment with fresh frozen plasma (about 12 litres) and an antiplatelet agent (dipyridamole) was started. Platelet counts were over 100 000/µ1 for 6 months and there was no evidence of haemolysis. 14 months later paraesthesia developed, and she had petechial bleeding. Repeated plasmapheresis was done with only limited effect. Treatment with a prostacyclin derivative CG 4203, vincristine, prednisolone, and intravenous immunoglobulins (10 g for 5 days) had no effect on platelet counts. By 111 In-labelling of her platelets, the spleen was identified as the main site of sequestration. In August, 1987, she was prepared for splenectomy by daily plasmapheresis and the platelet count reached 73 000/µl; one week after operation this had risen to 427 000/µ1 and there was no evidence of neurological dysfunction. She has now been well for 3 years on maintenance with low-dose aspirin.
Accident and Emergency Department, Central Middlesex Hospital,
London NW10 7NS, UK
SAPAL TACHAKRA
SS, Beckett MW Why do casualty officers miss radiological abnormalities? Ann R Coll Surg Ed 1985; 30: 311-13. 2. Grout P, Hunt MT, Touquet R. The benefits of an accident and emergency computer system. Theor Surg 1989; 4: 1-9. 1. Tachakra
