Correspondence
Pulse oximetry: a n e w non-invasive assessment of peripheral arterial occlusive disease
Effect o f fibrin sealant on the healing colonic anastomosis
Sir We read with interest the article by Joyce ef al. ( B r J Surg 1990; 77: I 1 15-1 7) on the subject of pulse oximetry (Psa,02) in peripheral vascular disease. We assume that the patients and control groups are of comparable mean age, with similar smoking histories; no data are given on this point. More importantly, we find it difficult to understand why pulse oximetry. which reflects arterial oxygen saturation, should be influenced by arterial narrowing. Transcutaneous oximetry clearly mirrors the degree of oxygen utilization in the end-tissue - in other words, it is measuring a function of oxygenation at a level distal to the point at which oxygen is consumed. This is not the case with pulse oximetry. since measurements using this technique rely on the pulsatile nature of pre-capillary flow. Hence the saturation of the blood within the capillaries is not measurable by this method. Reduced P,,,O, readings in peripheral vascular disease may reflect diminished pulsatility in peripheral arterioles. Venous pulsation may therefore contribute a relatively greater proportion to the P,,,o, signal, leading to apparently lower arterial saturation. Thus the authors may in fact be exploiting a deficiency in the technique to reveal a difference between their control and disease groups which may well be spurious. We would be interested to hear the authors’ comments on these remarks.
We would like to endorse the findings of Dr van der Ham and colleagues that fibrin sealing of colonic anastomosis does not improve healing (Br JSurg 1991; 78:49-53). We examined theeffect of fibrin sealant (Tisseel. Immuno, Vienna) on a high risk anastomosis model (low anterior resection in mongrel dogs without bowel preparation). Twenty-five animals were randomized to anastomosis with and without fibrin sealant. All were killed on the ninth postoperative day. Anastomotic bursting pressure (ABP) measurement followed inspection of the anastomosis for dehiscence and careful removal of all perianastomotic tissue . Adhesion formation was graded as follows: 0, no adhesions; + , perianastomotic adhesions: , widespread adhesions. Two animals died postoperatively; one (fibrin sealant) from sepsis secondary to anastomotic dehiscence and the other (control) from hypovolaemia secondary to intra-abdominal haemorrhage. The results are summarized in the table:
Sir
T. R. Cheatie P. D. Coleridge Smith Depurlrnent of Surgery 1~tiir:er.sit~~ College and Middlesex School London W I N 8 A A
of
Medicine
L’K
++
Group -
-
Fibrin sealant Control
Number - _ _ ~ _
W. P. Joyce D. B. Gough T. F. Gorey J. M. Fitzpatrick Surgical Professorial Unir 4 7 Eci,les Streer Duhliti 7 Ireland
Br. J. Surg., Vol. 78, No. 7, July 1991
Adhesions
0
+
++
-
12
5
125(25)
0
4
8
12
6
129(22)
2
7
4
As no benefit was found with the fibrin sealant, we were concerned that this may have been due to a reaction to human fibrinogen. This now seems unlikely however as Dr van der Ham controlled for such a reaction by demonstrating similar results with both human and rat fibrin sealant in his rat model.
Author’s reply Sir We are indebted to Mr Cheatle and Mr Coleridge-Smith for their interest in our paper and for their informed comments on our study and its findings. Their letter raises some issues that we would like to address. Clearly our control group and patient group were not comparable either in respect ofage or smoking history. To match the former with the latter would have inevitably included a number of patients with sub-clinical vascular disease. Our intention was to utilize a group of healthy people to enable us to establish a baseline of information against which data from patients with peripheral vascular disease could be evaluated. We did not of course state that there was a direct and simple relationship between oxygen saturation, as measured by pulse oximetry, and arterial narrowing. The correlation between P,,,oi and angiographic score preoperatively and the maintenance of this relationship postoperatively does, however, suggest an indirect relationship which may very well reflect diminished pulsatility in arterial disease as Cheatle and Coleridge-Smith suggest. Their belief that venous pulsation makes a significant contribution to the P,,,o, signal is more putative. We would be genuinely interested in any data bearing on this aspect of pulse oximetry that they can provide. If their contention can be sustained then we shall need to re-evaluate the technique of pulse oximetry and the significance of its derived data. Nevertheless, our oximetry values, obtained by a conventional and current technique, are valid in as far as the technique is valid. The significance of the values obtained may ofcourse be subjected to different interpretations.
Dehiscence - __
ABP, mmHg mean(s.d.)
V. McAlister* P. J. O’Dwyer N. J. O’Higgins* Departnients of Surgery Utiitvrsitj’ of’ Glasgow Glasgow GI1 6 N T and *St. Vincent j. Hospital Duhliti 4 Ireland
Influence of methylprednisolone on the healing of intestinal anastomoses in rats Sir We read with interest Mastboom and colleagues’ recent paper (Br J Sury 1991 ; 7 8 : 5 4 7 ) examining the effect of steroid therapy on healing ileal and colonic anastomosis in the rat. Healing was assessed by the measurement of bursting pressure. There are, however, a number of points with which we take issue. At three days no difference could be detected between the bursting pressure of anastomosis in steroid treated and saline treated animals. This does not constitute evidence of a lack of effect of steroids on fibroplasia in the intestine. Any wound healing by first intention will have a lag phase during which no tissue bridges the wound space. This lag phase represents the period during which inflammatory cells infiltrate a wound space, capillary budding occurs and finally fibroblasts begin to appear that will deposit collagen and matrix to bridge the tissue gap. In fact the lag phase of linear gastric wounds has been shown to be somewhat longer than the usual 2-4 days seen in skin although subsequent gain of wound strength is much quicker’. Thus if the effects of steroids i n uiuo are to depress granulation tissue deposition we would only expect to see an effect on wound strength after this initial lag phase during which a wound has little intrinsic strength. At 7 days steroid treated colonic wounds had significantly increased
889
Pulse oximetry: a n e w non-invasive assessment of peripheral arterial occlusive disease
Effect o f fibrin sealant on the healing colonic anastomosis
Sir We read with interest the article by Joyce ef al. ( B r J Surg 1990; 77: I 1 15-1 7) on the subject of pulse oximetry (Psa,02) in peripheral vascular disease. We assume that the patients and control groups are of comparable mean age, with similar smoking histories; no data are given on this point. More importantly, we find it difficult to understand why pulse oximetry. which reflects arterial oxygen saturation, should be influenced by arterial narrowing. Transcutaneous oximetry clearly mirrors the degree of oxygen utilization in the end-tissue - in other words, it is measuring a function of oxygenation at a level distal to the point at which oxygen is consumed. This is not the case with pulse oximetry. since measurements using this technique rely on the pulsatile nature of pre-capillary flow. Hence the saturation of the blood within the capillaries is not measurable by this method. Reduced P,,,O, readings in peripheral vascular disease may reflect diminished pulsatility in peripheral arterioles. Venous pulsation may therefore contribute a relatively greater proportion to the P,,,o, signal, leading to apparently lower arterial saturation. Thus the authors may in fact be exploiting a deficiency in the technique to reveal a difference between their control and disease groups which may well be spurious. We would be interested to hear the authors’ comments on these remarks.
We would like to endorse the findings of Dr van der Ham and colleagues that fibrin sealing of colonic anastomosis does not improve healing (Br JSurg 1991; 78:49-53). We examined theeffect of fibrin sealant (Tisseel. Immuno, Vienna) on a high risk anastomosis model (low anterior resection in mongrel dogs without bowel preparation). Twenty-five animals were randomized to anastomosis with and without fibrin sealant. All were killed on the ninth postoperative day. Anastomotic bursting pressure (ABP) measurement followed inspection of the anastomosis for dehiscence and careful removal of all perianastomotic tissue . Adhesion formation was graded as follows: 0, no adhesions; + , perianastomotic adhesions: , widespread adhesions. Two animals died postoperatively; one (fibrin sealant) from sepsis secondary to anastomotic dehiscence and the other (control) from hypovolaemia secondary to intra-abdominal haemorrhage. The results are summarized in the table:
Sir
T. R. Cheatie P. D. Coleridge Smith Depurlrnent of Surgery 1~tiir:er.sit~~ College and Middlesex School London W I N 8 A A
of
Medicine
L’K
++
Group -
-
Fibrin sealant Control
Number - _ _ ~ _
W. P. Joyce D. B. Gough T. F. Gorey J. M. Fitzpatrick Surgical Professorial Unir 4 7 Eci,les Streer Duhliti 7 Ireland
Br. J. Surg., Vol. 78, No. 7, July 1991
Adhesions
0
+
++
-
12
5
125(25)
0
4
8
12
6
129(22)
2
7
4
As no benefit was found with the fibrin sealant, we were concerned that this may have been due to a reaction to human fibrinogen. This now seems unlikely however as Dr van der Ham controlled for such a reaction by demonstrating similar results with both human and rat fibrin sealant in his rat model.
Author’s reply Sir We are indebted to Mr Cheatle and Mr Coleridge-Smith for their interest in our paper and for their informed comments on our study and its findings. Their letter raises some issues that we would like to address. Clearly our control group and patient group were not comparable either in respect ofage or smoking history. To match the former with the latter would have inevitably included a number of patients with sub-clinical vascular disease. Our intention was to utilize a group of healthy people to enable us to establish a baseline of information against which data from patients with peripheral vascular disease could be evaluated. We did not of course state that there was a direct and simple relationship between oxygen saturation, as measured by pulse oximetry, and arterial narrowing. The correlation between P,,,oi and angiographic score preoperatively and the maintenance of this relationship postoperatively does, however, suggest an indirect relationship which may very well reflect diminished pulsatility in arterial disease as Cheatle and Coleridge-Smith suggest. Their belief that venous pulsation makes a significant contribution to the P,,,o, signal is more putative. We would be genuinely interested in any data bearing on this aspect of pulse oximetry that they can provide. If their contention can be sustained then we shall need to re-evaluate the technique of pulse oximetry and the significance of its derived data. Nevertheless, our oximetry values, obtained by a conventional and current technique, are valid in as far as the technique is valid. The significance of the values obtained may ofcourse be subjected to different interpretations.
Dehiscence - __
ABP, mmHg mean(s.d.)
V. McAlister* P. J. O’Dwyer N. J. O’Higgins* Departnients of Surgery Utiitvrsitj’ of’ Glasgow Glasgow GI1 6 N T and *St. Vincent j. Hospital Duhliti 4 Ireland
Influence of methylprednisolone on the healing of intestinal anastomoses in rats Sir We read with interest Mastboom and colleagues’ recent paper (Br J Sury 1991 ; 7 8 : 5 4 7 ) examining the effect of steroid therapy on healing ileal and colonic anastomosis in the rat. Healing was assessed by the measurement of bursting pressure. There are, however, a number of points with which we take issue. At three days no difference could be detected between the bursting pressure of anastomosis in steroid treated and saline treated animals. This does not constitute evidence of a lack of effect of steroids on fibroplasia in the intestine. Any wound healing by first intention will have a lag phase during which no tissue bridges the wound space. This lag phase represents the period during which inflammatory cells infiltrate a wound space, capillary budding occurs and finally fibroblasts begin to appear that will deposit collagen and matrix to bridge the tissue gap. In fact the lag phase of linear gastric wounds has been shown to be somewhat longer than the usual 2-4 days seen in skin although subsequent gain of wound strength is much quicker’. Thus if the effects of steroids i n uiuo are to depress granulation tissue deposition we would only expect to see an effect on wound strength after this initial lag phase during which a wound has little intrinsic strength. At 7 days steroid treated colonic wounds had significantly increased
889
