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Bone marrow aplasia after high voltage electrical injury
184
Burns,10, 184-l 87
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GreatEritain
Bone marrow aplasia after high voltage electrical injury Korn6l Gab6
and Piroska VBr
Burn Center of the Central Hospital, Budapest Summary
This report describes a patient with severe high voltage electrical injury in whom bone marrow aplasia developed on post-bum day 3. In addition to bone marrow aplasia alterations suggesting disintegration of leucocytes and reduced nitro-blue tetrazolium reductase activity pointing to functional disorders have been
observed. Beyond the effect of the extensive burns to depress the bone marrow the possibility of an additional similar action of the high voltage electrical injury is raised. INTRODUCTION HAEMATOLOGICAL
involvement of bum injuries is a well-known phenomenon though its development is not yet fully understood. According to recent studies early leucocytosis is the consequence of the demargination of granulocytes and an increased release from the bone marrow granulocyte pool, as well as haemoconcentration (Eurenius, 1979). In fact, the total granulocyte reserve of the organism decreases due to inhibited myelopoiesis (Asko-Seljavaara, 1974) and increased peripheral consumption (Eriksson et al., 1979). Recent observations have revealed the frequent occurrence of leucopenia during toxaemia of bums elicited primarily by the inhibiting action of sulphonamide containing protective dressings (Fraser-Moodie and Nancarrow, 1976) as well as endotoxins. Leucopenia is rare in the early phase of thermal injury. Over a period of 3 years we have observed it in only 5 of 800 cases. This paper reports a detailed haematological examination of one patient. CASE HISTORY
While standing on the top of a railway coach a
19-year-old male patient suffered an arc burn from a 20 Kvolt high tension line. The entry wound was on the right parietal part ofthe skull, the exit wound on the proximal phalanx of the right big toe. The patient lost consciousness, fell from the coach, his clothes caught fire and he suffered flame injury on 75 per cent of the body surface (Fig. 1). Due to apnoea and asystoly, mouth-to-mouth resuscitation and closed cardiac massage was started immediately. On arrival of the ambulance, intubation and artificial respiration with Ambu-balloon, as well as fluid replacement were started. The patient was admitted in a deep coma; there was no spontaneous respiration. Intermittent positive endpressure ventilation was started immediately. The patient had a BP of 220/l 60 mmHg, a pulse rate of 120/min and temperature of 36.5 ’ C, with constricted pupils. There were no signs of neurological focal symptoms. Bone defect was seen at the entrance site on the skull. Shock
Fig. 1. Sketch of electrical injury circumstances extent of burn wound.
and
185
Szab6 and VBr: Bone marrow aplasia
0-m
HR
1
200
-X
BP mgklg
Temp “C
t
38
36
PB day
Fig. 2. Circulation
indices and rectal temperature. o-v-0
HCR
‘T’ mmol/l
c 0.6
0.2
t
PB day
Fig. 3. Haemoglobin
and haematocrit
treatment was started with hypertonic NaCIlactate solution and supplemented by glucose, K+ and insulin (Szabo et al., 1980) in addition to artificial respiration. ECG records showed transient incomplete RBBB. The circulation was unstable. Asystoly, atria1 extrasystoly, supraventricular, then ventricular tachycardia required targeted, occasional antiarrhythmic medication (isopropilone, oxprenolone, lignocaine). Hypothermia had been present throughout (Fig. 2). Diuresis was however found satisfactory, haemodilution during shock treatment occurred as
findings.
commonly observed (Fig. 3.). For the open wound treatment 2 per cent mercurochrome was used. On day 4 of shock treatment sinus impulse formation suddenly stopped, and transient ventricular automation of 40/min rate followed by asystoly developed. Repeated resuscitation remained unsuccessful. Autopsy revealed cerebral oedema and toxaemic parenchymatous alterations characteristic of burn injury. On post-burn day 2 leucocytosis was followed by severe leucopenia (1.8 g/l) with a granulocyte ratio of 54 per cent which reached later only 5
186
Burns Vol. 1 O/No. 3 ._‘ WBC
o-wPlatelet cell count
Cl/f 2o--x\
-200
15-
II
%
?? .
\.
*.
lo-
. .
?? \ *.
-100
\ ‘lx
5-
*.Ow%.__O \
0
Fig.
1 4.
2 PB day
.-=Ax 3
4
Leucocyte count and platelet number.
Fig. 5. Bone marrow smear (May-Griinwald-Giesma staining). A relatively cell-rich part of the aplastic bone marrow (x 103).
per cent (1.4 g/l). Nitro-blue tetrazolium reductase staining of blood smear (Szklenarik et al., 1977) showed a reduced (16 per cent) positive incidence in those granulocytes, which were present. Chemical determination of reduced nicotinamide adenine dinucleotide in the serum showed an increase. The findings suggested substantial granulocyte disintegration. The thrombocyte count was reduced to 75 and 49 g/l, respectively (Fig. 4). Acanthocytic lymphocytes, and occasionally impaired granulocytes were detected in the peripheral blood smear. Bone marrow examination showed total depression of myelopoiesis. Sporadic nucleated erythrocytes, myelocytes, and lymphoid cells (Fig. 5) may be seen. DISCUSSION
The origin of postburn leucopenia is not fully understood. Drug and chemical induced leuco-
penia, as well as neutropenia of sepsis, due to Gram-negative bacteria, mainly Pseudomonas aeruginosa, are well known. Leucopenia in burn injury develops commonly at a later period (Eurenius, 1979). In the present patient the haemopoietic complication developed at an unusually early stage and in a most severe form, i.e. with total bone marrow aplasia. Instead of the common myeloproliferative appearance (Bernat. 1971) total aplasia was present. In accordance with findings on a large series of patients (Heck et al., 1979; Ransjij et al., 1978) granulocyte function was reduced. Prior to the injury the patient had been healthy and did not take any drugs. During the few days oftreatment he received no bone marrow-impairing drugs. The total of 40 ml mercurochrome solution did not contain sufficient mercury to have been toxic by absorption. Mercury-induced aplasia reported in literature (Ryrie et al., 1970; Wilson, 1966) was a consequence of prolonged exposure to, and higher concentrations of mercury. There was neither clinical nor histological evidence of sepsis. Accordingly, bone marrow impairment in the present case could not be attributed to these factors. As the primary aetiological factor severe thermal injury may be considered. Bone marrow cellular changes are observed in the early phase of burns. In addition to the demargination of granulocytes into the circulation and cell impairment (Eurenius, 1979) experimental investigations have shown that cytotoxic substances released by burned tissue reduce bone marrow cell proliferation (Asko-Seljavaara et al., 1976). A similar mechanism might have been responsible for the early marrow depression observed in our patient.
Szab6 and VBr: Bona marrow aplasia
187
The causal effect of the high voltage electrical injury to produce the bone marrow aplasia remains an open question. Although the leucopenia inducing effect has been mentioned by Irinyi et al. (1967) the possible pathological mechanism is unknown. Reports discussing pathology and clinical course of electrical injuries rarely mention the possibility of haematological involvement. The biological effect of an electrical injury depends on heat energy release. It might be particularly strong in bones being highly resistant (Editorial, Lam-et 1978). In the present case the confirmed passage ofthe electrical current through the body might have produced a heat effect that impaired directly the bone marrow. It seems noteworthy that from the five burned patients in whom early leucopenia was observed an identical high voltage electrical injury had occurred in two additional, previously healthy persons and was most probable in the fourth case. The possibility of an electrical injury could be excluded merely in one patient. These data suggest that high voltage electrical injury may act, either directly or indirectly by an as yet unknown mechanism, to produce a bone marrow aplasia in some patients. REFERENCES Asko-Seljavaara S. (I 974) Inhibition cell proliferation in burned mice. Reconst. Surg 8, 192.
of
bone marrow
Stand.
Asko-Seljavaara S., Sundel B., RytGmaa T. (1976)The effect of early excision on bone marrow cell growth in burned mice. Burns 2, 140. Bernat I. (1971) AZ Cgisi anaemia pathogenesise. .4kadPmia. Budapest,
129.
Editorial (1978) High tension electrical injury. Lunc~~ 2,978. Eriksson E., Straube R. C., Robson M. C. (1979) White cell consumption in the microcirculation after a major burn. J. Trauma 19,94. Eurenius K. (1979) Hematologic changes in burns. In: Artz C. P., Moncrief J. A., Pruitt B. A. (ed.) Burns Philadelphia Saunders. Fraser-Moodie A., Nancarrow J. (1976) Neutropenia and thrombocytopenia in burns. Burns 3,235: Heck E. L.. Edear M. A.. Masters B. S. et al. f 19791 The role of
J. P&t.
Paper accepted 8 February 1983.
Burns,10, 184-l 87
Printedin
GreatEritain
Bone marrow aplasia after high voltage electrical injury Korn6l Gab6
and Piroska VBr
Burn Center of the Central Hospital, Budapest Summary
This report describes a patient with severe high voltage electrical injury in whom bone marrow aplasia developed on post-bum day 3. In addition to bone marrow aplasia alterations suggesting disintegration of leucocytes and reduced nitro-blue tetrazolium reductase activity pointing to functional disorders have been
observed. Beyond the effect of the extensive burns to depress the bone marrow the possibility of an additional similar action of the high voltage electrical injury is raised. INTRODUCTION HAEMATOLOGICAL
involvement of bum injuries is a well-known phenomenon though its development is not yet fully understood. According to recent studies early leucocytosis is the consequence of the demargination of granulocytes and an increased release from the bone marrow granulocyte pool, as well as haemoconcentration (Eurenius, 1979). In fact, the total granulocyte reserve of the organism decreases due to inhibited myelopoiesis (Asko-Seljavaara, 1974) and increased peripheral consumption (Eriksson et al., 1979). Recent observations have revealed the frequent occurrence of leucopenia during toxaemia of bums elicited primarily by the inhibiting action of sulphonamide containing protective dressings (Fraser-Moodie and Nancarrow, 1976) as well as endotoxins. Leucopenia is rare in the early phase of thermal injury. Over a period of 3 years we have observed it in only 5 of 800 cases. This paper reports a detailed haematological examination of one patient. CASE HISTORY
While standing on the top of a railway coach a
19-year-old male patient suffered an arc burn from a 20 Kvolt high tension line. The entry wound was on the right parietal part ofthe skull, the exit wound on the proximal phalanx of the right big toe. The patient lost consciousness, fell from the coach, his clothes caught fire and he suffered flame injury on 75 per cent of the body surface (Fig. 1). Due to apnoea and asystoly, mouth-to-mouth resuscitation and closed cardiac massage was started immediately. On arrival of the ambulance, intubation and artificial respiration with Ambu-balloon, as well as fluid replacement were started. The patient was admitted in a deep coma; there was no spontaneous respiration. Intermittent positive endpressure ventilation was started immediately. The patient had a BP of 220/l 60 mmHg, a pulse rate of 120/min and temperature of 36.5 ’ C, with constricted pupils. There were no signs of neurological focal symptoms. Bone defect was seen at the entrance site on the skull. Shock
Fig. 1. Sketch of electrical injury circumstances extent of burn wound.
and
185
Szab6 and VBr: Bone marrow aplasia
0-m
HR
1
200
-X
BP mgklg
Temp “C
t
38
36
PB day
Fig. 2. Circulation
indices and rectal temperature. o-v-0
HCR
‘T’ mmol/l
c 0.6
0.2
t
PB day
Fig. 3. Haemoglobin
and haematocrit
treatment was started with hypertonic NaCIlactate solution and supplemented by glucose, K+ and insulin (Szabo et al., 1980) in addition to artificial respiration. ECG records showed transient incomplete RBBB. The circulation was unstable. Asystoly, atria1 extrasystoly, supraventricular, then ventricular tachycardia required targeted, occasional antiarrhythmic medication (isopropilone, oxprenolone, lignocaine). Hypothermia had been present throughout (Fig. 2). Diuresis was however found satisfactory, haemodilution during shock treatment occurred as
findings.
commonly observed (Fig. 3.). For the open wound treatment 2 per cent mercurochrome was used. On day 4 of shock treatment sinus impulse formation suddenly stopped, and transient ventricular automation of 40/min rate followed by asystoly developed. Repeated resuscitation remained unsuccessful. Autopsy revealed cerebral oedema and toxaemic parenchymatous alterations characteristic of burn injury. On post-burn day 2 leucocytosis was followed by severe leucopenia (1.8 g/l) with a granulocyte ratio of 54 per cent which reached later only 5
186
Burns Vol. 1 O/No. 3 ._‘ WBC
o-wPlatelet cell count
Cl/f 2o--x\
-200
15-
II
%
?? .
\.
*.
lo-
. .
?? \ *.
-100
\ ‘lx
5-
*.Ow%.__O \
0
Fig.
1 4.
2 PB day
.-=Ax 3
4
Leucocyte count and platelet number.
Fig. 5. Bone marrow smear (May-Griinwald-Giesma staining). A relatively cell-rich part of the aplastic bone marrow (x 103).
per cent (1.4 g/l). Nitro-blue tetrazolium reductase staining of blood smear (Szklenarik et al., 1977) showed a reduced (16 per cent) positive incidence in those granulocytes, which were present. Chemical determination of reduced nicotinamide adenine dinucleotide in the serum showed an increase. The findings suggested substantial granulocyte disintegration. The thrombocyte count was reduced to 75 and 49 g/l, respectively (Fig. 4). Acanthocytic lymphocytes, and occasionally impaired granulocytes were detected in the peripheral blood smear. Bone marrow examination showed total depression of myelopoiesis. Sporadic nucleated erythrocytes, myelocytes, and lymphoid cells (Fig. 5) may be seen. DISCUSSION
The origin of postburn leucopenia is not fully understood. Drug and chemical induced leuco-
penia, as well as neutropenia of sepsis, due to Gram-negative bacteria, mainly Pseudomonas aeruginosa, are well known. Leucopenia in burn injury develops commonly at a later period (Eurenius, 1979). In the present patient the haemopoietic complication developed at an unusually early stage and in a most severe form, i.e. with total bone marrow aplasia. Instead of the common myeloproliferative appearance (Bernat. 1971) total aplasia was present. In accordance with findings on a large series of patients (Heck et al., 1979; Ransjij et al., 1978) granulocyte function was reduced. Prior to the injury the patient had been healthy and did not take any drugs. During the few days oftreatment he received no bone marrow-impairing drugs. The total of 40 ml mercurochrome solution did not contain sufficient mercury to have been toxic by absorption. Mercury-induced aplasia reported in literature (Ryrie et al., 1970; Wilson, 1966) was a consequence of prolonged exposure to, and higher concentrations of mercury. There was neither clinical nor histological evidence of sepsis. Accordingly, bone marrow impairment in the present case could not be attributed to these factors. As the primary aetiological factor severe thermal injury may be considered. Bone marrow cellular changes are observed in the early phase of burns. In addition to the demargination of granulocytes into the circulation and cell impairment (Eurenius, 1979) experimental investigations have shown that cytotoxic substances released by burned tissue reduce bone marrow cell proliferation (Asko-Seljavaara et al., 1976). A similar mechanism might have been responsible for the early marrow depression observed in our patient.
Szab6 and VBr: Bona marrow aplasia
187
The causal effect of the high voltage electrical injury to produce the bone marrow aplasia remains an open question. Although the leucopenia inducing effect has been mentioned by Irinyi et al. (1967) the possible pathological mechanism is unknown. Reports discussing pathology and clinical course of electrical injuries rarely mention the possibility of haematological involvement. The biological effect of an electrical injury depends on heat energy release. It might be particularly strong in bones being highly resistant (Editorial, Lam-et 1978). In the present case the confirmed passage ofthe electrical current through the body might have produced a heat effect that impaired directly the bone marrow. It seems noteworthy that from the five burned patients in whom early leucopenia was observed an identical high voltage electrical injury had occurred in two additional, previously healthy persons and was most probable in the fourth case. The possibility of an electrical injury could be excluded merely in one patient. These data suggest that high voltage electrical injury may act, either directly or indirectly by an as yet unknown mechanism, to produce a bone marrow aplasia in some patients. REFERENCES Asko-Seljavaara S. (I 974) Inhibition cell proliferation in burned mice. Reconst. Surg 8, 192.
of
bone marrow
Stand.
Asko-Seljavaara S., Sundel B., RytGmaa T. (1976)The effect of early excision on bone marrow cell growth in burned mice. Burns 2, 140. Bernat I. (1971) AZ Cgisi anaemia pathogenesise. .4kadPmia. Budapest,
129.
Editorial (1978) High tension electrical injury. Lunc~~ 2,978. Eriksson E., Straube R. C., Robson M. C. (1979) White cell consumption in the microcirculation after a major burn. J. Trauma 19,94. Eurenius K. (1979) Hematologic changes in burns. In: Artz C. P., Moncrief J. A., Pruitt B. A. (ed.) Burns Philadelphia Saunders. Fraser-Moodie A., Nancarrow J. (1976) Neutropenia and thrombocytopenia in burns. Burns 3,235: Heck E. L.. Edear M. A.. Masters B. S. et al. f 19791 The role of
J. P&t.
Paper accepted 8 February 1983.