- Email: [email protected]
Kidney function in the extensive burn
Burns, 7. 361-364
361
PrintedinGreatBritain
Kidney function in the extensive Dino Barisoni
and Donatella
burn
Bertolini
Plastic Surgery Division and Regional Burns Centre, Verona, Italy Summary
The results obtained from a series of 48 major burn cases, as regards the impact of the bum wounds on renal function are described. These results show that burn shock and the onset of kidney function impairment can be avoided provided proper resuscitation and proper surgical treatment are applied as early and as extensively as possible. Special care should be dedicated to those cases who had pre-existing kidney problems or were not resuscitated properly in the acute phase. INTRODUCTION
tissue perfusion following the loss of fluids caused by burn injuries in excess of 15 per cent of total body area, sodium depletion (Moyer et al., 1965) and the myocardial muscle depressing factor released in the early post-burn phase (Rosenthal et al., 1972; Raffa and Trunkey, 1978) all lead eventually to the onset of shock. Hypovolemia reflects primarily upon kidney function which is dependent on a large share of cardiac output, but bum induced renal insufftciency may be presumed, in its early phase, to be a reversible functional response to renal ischemia (Ollstein and Burns, 1973). That urine output is markedly reduced immediately following burns, may be considered evidence, although a crude one, of impaired glomerular filtration secondary to poor renal perfusion. However, if the lost fluids are replaced as early as possible, the reversible phase due to hypovolemia does not evolve towards acute renal failure, which involves glomeruli and tubuli and is responsible for a INADEQUATE
high mortality
rate.
Paper presented at the 5th International Congress on Bum Injuries. Stockholm. Sweden, 1978.
On the other hand, factors besides fluid loss can play a role, in the later phase. in producing renal impairment or failure, such as toxins released from necrotic tissues or bacterial embolism during septic bouts (Rosenthal et al., 1972; Schoenenberg et al., 1974; MacMillan. 1975). Proper treatment of a burn case in excess of I5 per cent of total body area involves replacement of fluids and removal of necrotic tissues; surgical procedures should be started as soon as replacement of lost fluids has been taken care of. Many authors have studied renal function during the early post-burn period (Cameron, 1969: Eklund, 1970; Settle, 1974; Monafo, 1976). This study covers the acute phase and the later one, up to day 30 post burn, when most surgery had already been performed. The purpose of the study was, first, to make an early diagnosis of renal impairment, and second, to fmd a correlation with a specific cause or phase of the burn disease. MATERIALS
AND
METHODS
Samples of blood and urine were obtained from a group of 48 adult patients, hospitalized for second and third degree burns. which ranged from 25 to 80 per cent of total body area, the mean body area burned (BAB) being 42 per cent. Resuscitation was based on a modified Evans‘ formula [2 cc Ringer’s acetate soln. + (1 cc fresh human plasma O/o BAB-’ kg body weight) in the first 24 h; half the same dosage in the second 24 h]. This modified formula was in turn adjusted to the patient’s response; we often found the quantity of plasma to be inadequate for compensating the protein loss through the burned area. Over the later phase, intravenous treatment consisted of blood. electrolyte and
Burns Vol. ~/NO. 5
362 Tab/e/. Tests used to carry out evaluation of kidneys Urine output Urine specific gravity (USG) Blood urea nitrogen (BUN) Plasma osmolality (Posm) Urine osmolality (Uosm) Plasma creatinine (Per) Urine creatinine (Ucr) Urine sodium (UNa) Urine urea nitrogen (Uun) Tubular reabsorption of ‘free water’ (TcH,O)
amino acid solutions which varied broadly with individual needs. Surgery was started as early as day 4 post bum for bums not exceeding 30 per cent BAB and involving areas of cosmetic or functional interest, and not later than day 12 post burn in major wounds which would imply a high surgical risk when treated earlier. Every surgical procedure involved at least 20 per cent either by tangential excision or escharotomy. The evaluation was carried out according to the tests listed in Table I, which give a specific pattern of glomerular and tubular function and are easily performed on blood and urine samples; other traditional tests, technically difficult to perform in a bum case, were not taken into consideration. In the normal kidney, urea and creatinine are concentrated in the urine to 20 times their plasma concentration; urine osmolality is a parameter of urine concentration which will be impaired if the kidney is impaired; in this case the ratio between urine and plasma osmolality will be decreased. Urine sodium concentration is also of help in defining the extent of tubular impairment, because,in this case, sodium, which is normally reabsorbed in its greatest part, will be lost in the urine. Dividing the urine sodium concentration by the ratio between urine and plasma creatinine determines the filtering and excreting activity of the tubule; the failing kidney, losing sodium and not concentrating creatinine, will show a decrease in this ratio. T,H20 is the amount of ‘free’ water reabsorbed per minute by the distal tubule and is calculated by subtracting osmolar clearance from urine output per minute, osmolar clearance being the plasma volume filtered per minute through the tubule and purified from all osmotically active substances. RESULTS
Although
45 patients
did not show consistent
and significant abnormality in their tests, 3 of them had pathological results and these will be discussed separately. CASE REPORTS Case 1
A 24-year-old man who was a factory worker, sustained a 27 per cent bum in a fire and was admitted on day 5 post bum, having been satisfactorily resuscitated in another hospital. He had a medical record of glomerulonephritis in infancy which had apparently healed: the patient had no follow-up controls afterwards. He underwent surgery on the seventh day post bum and his hospitalization was uneventful. We think that the abnormal results shown in Figs. I- 4 could not depend only upon the bum injury, but also upon a pre-existing chronic glomerular and tubular imbalance. This young man showed a pattern ofglomerular and tubular impairment. The patient was dismissed on day 30 post bum and has been under treatment by a kidney specialist since then. Case 2 A 54-year-old man was admitted immediately after second- and third-degree bums (mostly third degree) inolving 52 per cent body area. He had a previous history of hypertension, dating back several years. He was resuscitated properly and his urine output was quite satisfactory, but, as shown by Figs. 5 and 6, his kidneys behaved as ifthey were not there. Considering the long term hypertension, we think we have good reason to suspect a pre-existing nephrosclerosis, which was the cause of acute glomerular and tubular failure, of the non oliguric kind. This brought the patient to his death on day 7 post bum. Case 3 A 40-year-old man sustained a 58 per cent thirddegree bum in a gas explosion. Six hours elapsed before he was brought to a small hospital where he received severely inadequate resuscitative treatment. He was transferred to our Bums Unit on the third day post bum and was in the reversible phase of shock. We had to administer enormous quantities of plasma and electrolyte solutions before a satisfactory urine output was re-established. Figs. 7-9 demonstrate a reversible renal insufficiency due to inadequate fluid replacement during the first 48 hours. His kidneys had barely survived on the small amount of fluids given the patient in the acute phase, and it took them weeks to return to normal. DISCUSSION
This series of48 burn patients demonstrates that bum shock, and consequently, acute renal failure are not necessarily connected with burn injury, even a major one, providing that the preburn renal condition is normal, and proper
Barisoni
and
Bertolini:
30 20
Kidney
Function
363
-
-
10 ty
r; _y’“;
*
10
But.4 hv. lo-20
mg%l
Fig. I. Case 1. Urine output quite satisfactory throughout hospitalization. BUN shows pathological levels on several occasions. Ratio between Uun and BUN is nearly always pathological.
Case I. Urine osmolality always below normal values. Ratio between urine and plasma osmolality constantly abnormal. EYg
3.
hv. SO
50 30
IP 1
2
7
13
l5
20
oayr
25
30
Fig. 2. Case I. Plasma creatinine quite above normal values, while ratio Ucr/Pcr sufficient. Ratio between urine sodium excretion and creatinine urine and plasma values quite above normal, thus demonstrating a tubular insufftciency in sodium reabsorption.
Fi,e. 4. Casr 1. Tubular reabsorption of free water pathological in the first two weeks and improving over the following weeks, without ever reaching normal values.
> 500,
ml/h
Urtne cwtwt
,n.v a 501
70
5
3
oavs 5
B”“.
mg % ml
I”.“. 10 - 201
600
/
6
1
,j
0 2
3
Davl
5
6
0
I
2
3
Dayl
5
6
) 500,
“mm ,” ”
I
-
0 1
2
3
Dayl
5
6
F/g. 5. C‘use 2. Notwithstanding a sufficient urine output, BUN and plasma creatinine increase steadily, while Uun and the ratios Ucr/Pcr and Uun/BUN show a pathological decrease. These data clearly demonstrate a tubular and glomerular failure.
Fi,q. 6. C‘a~r 2. Constantly pathological values of urine as well as plasma osmolality are evidence of tubular impairment. This fact is confirmed by the very low level of tubular reabsorption of free water and the ratio between urine sodium and creatinine.
is given. This fact is confirmed by the 45 patients that had no symptoms of kidney impairment throughout their hospitalization. We believe, in the light of these results, that
our formula of resuscitation is quite adequate to compensate for the loss of fluids in the acute post-burn phase. We also believe that early surgical treatment plays a very important role in
resuscitation
Burns Vol. ~/NO. 5
364
0
46
10
15 OWS
Fig. 7. Case 3. In spite of good urine output BUN level increase steadily until day 10 post burn. The ratio Uun/BUN confirms the insufficient glomerular filtration up to the tenth day.
21
0
24 I
46
10
15
21
24
Da”*
Fig. 8. Case 3. Creatinine blood levels show impaired glomerular filtration and tubular excretion. Pathological tubular function is demonstrated by the ratio between urine sodium and cretinine ratio.
patients closely watched, even in collaboration with nephrologists, so that the standard treatment might. be improved by the use of diuretic drugs or dialysis.
2.51
REFERENCES
0
4
6
10
15
21
24
OWS
0
4
6
10
15
21
24
Davr
Fig. 9. Case 3. The plasma osmolality, the ratio urine/plasma osmolality and the TCH,O levels show the insufftcient concentration of reabsorption of urine and water at least during the ftrst two weeks post bum.
by the renal impairment caused in the later phase, especially when it is applied as extensively as possible, so that the source of toxemia can be eliminated in the shortest possible interval. On the other hand, at least in our experience, early and extensive surgery, even with the many difftcult problems it provides, does not reflect on kidney function, as again demonstrated by the substantial normal group. The problem of patients with pre-existing renal diseases, with diseases that might involve the renal function, or those who received poor resuscitative treatment still remains. For this reason we think that medical records should be accurately collected and analysed, and these avoiding toxemia
Requesfs,for reprinrsshouldbe
Cameron J. S. (1969)Disturbances of renal function in burnt patients. Proc. R. Sot. Med. (Land) 62,49. Eklund J. (1970) Renal regulation of body osmolal balance in bums. A clinical and experimental study with special reference to hyperosmolality. Acta Chir. Scund. (Suppl.) 410. MacMillan B. G. (1975) Bum wound sepsis-a IO-year experience. Burns 2, 1. Monafo W. W. (1976) Renal function after thermal trauma: the effects on renal blood flow and sodium and water excretion. Surgery 79,342. Moyer C. A., Margraf H. W. and Monafo W. W. (1965) Bum shock and extravascular sodium deficiency. Treatment with Ringer’s solution with lactate. Arch. Surg. 90,799. Ollstein R. N. and Burns G. C. (1973) Renal consideration in the burned patient. In: Lynch J. B. and Lewis S. R. (eds.) Symposium on the Treatment of Burns. St Louis, Mosby, pp. 66-72. Raffa J. and Trunkey D. D. (1978) Myocardial depression in acute thermal injury. J. Trauma 18, 90. Rosenthal S. R., Hawley P. L. and Hawkin A. A. (1972) Purified bum toxic factor and its competition. Surgery71,527. Schoenenberger G. A., Cueni L. B., Hatt A. M. et al. (1974) Verbrennungskenheiten-Toxinwirkung oder Infektionsfolgez. Chirurgie45,20. Settle A. D. (1974) Urine output following severe burns. Burns 1, I. Paper accepted I5 January 1980.
addressed PJ; Dr D. Barisoni. Plastic Surgery Division and Regional Burns Centre. Verona, Italy.
361
PrintedinGreatBritain
Kidney function in the extensive Dino Barisoni
and Donatella
burn
Bertolini
Plastic Surgery Division and Regional Burns Centre, Verona, Italy Summary
The results obtained from a series of 48 major burn cases, as regards the impact of the bum wounds on renal function are described. These results show that burn shock and the onset of kidney function impairment can be avoided provided proper resuscitation and proper surgical treatment are applied as early and as extensively as possible. Special care should be dedicated to those cases who had pre-existing kidney problems or were not resuscitated properly in the acute phase. INTRODUCTION
tissue perfusion following the loss of fluids caused by burn injuries in excess of 15 per cent of total body area, sodium depletion (Moyer et al., 1965) and the myocardial muscle depressing factor released in the early post-burn phase (Rosenthal et al., 1972; Raffa and Trunkey, 1978) all lead eventually to the onset of shock. Hypovolemia reflects primarily upon kidney function which is dependent on a large share of cardiac output, but bum induced renal insufftciency may be presumed, in its early phase, to be a reversible functional response to renal ischemia (Ollstein and Burns, 1973). That urine output is markedly reduced immediately following burns, may be considered evidence, although a crude one, of impaired glomerular filtration secondary to poor renal perfusion. However, if the lost fluids are replaced as early as possible, the reversible phase due to hypovolemia does not evolve towards acute renal failure, which involves glomeruli and tubuli and is responsible for a INADEQUATE
high mortality
rate.
Paper presented at the 5th International Congress on Bum Injuries. Stockholm. Sweden, 1978.
On the other hand, factors besides fluid loss can play a role, in the later phase. in producing renal impairment or failure, such as toxins released from necrotic tissues or bacterial embolism during septic bouts (Rosenthal et al., 1972; Schoenenberg et al., 1974; MacMillan. 1975). Proper treatment of a burn case in excess of I5 per cent of total body area involves replacement of fluids and removal of necrotic tissues; surgical procedures should be started as soon as replacement of lost fluids has been taken care of. Many authors have studied renal function during the early post-burn period (Cameron, 1969: Eklund, 1970; Settle, 1974; Monafo, 1976). This study covers the acute phase and the later one, up to day 30 post burn, when most surgery had already been performed. The purpose of the study was, first, to make an early diagnosis of renal impairment, and second, to fmd a correlation with a specific cause or phase of the burn disease. MATERIALS
AND
METHODS
Samples of blood and urine were obtained from a group of 48 adult patients, hospitalized for second and third degree burns. which ranged from 25 to 80 per cent of total body area, the mean body area burned (BAB) being 42 per cent. Resuscitation was based on a modified Evans‘ formula [2 cc Ringer’s acetate soln. + (1 cc fresh human plasma O/o BAB-’ kg body weight) in the first 24 h; half the same dosage in the second 24 h]. This modified formula was in turn adjusted to the patient’s response; we often found the quantity of plasma to be inadequate for compensating the protein loss through the burned area. Over the later phase, intravenous treatment consisted of blood. electrolyte and
Burns Vol. ~/NO. 5
362 Tab/e/. Tests used to carry out evaluation of kidneys Urine output Urine specific gravity (USG) Blood urea nitrogen (BUN) Plasma osmolality (Posm) Urine osmolality (Uosm) Plasma creatinine (Per) Urine creatinine (Ucr) Urine sodium (UNa) Urine urea nitrogen (Uun) Tubular reabsorption of ‘free water’ (TcH,O)
amino acid solutions which varied broadly with individual needs. Surgery was started as early as day 4 post bum for bums not exceeding 30 per cent BAB and involving areas of cosmetic or functional interest, and not later than day 12 post burn in major wounds which would imply a high surgical risk when treated earlier. Every surgical procedure involved at least 20 per cent either by tangential excision or escharotomy. The evaluation was carried out according to the tests listed in Table I, which give a specific pattern of glomerular and tubular function and are easily performed on blood and urine samples; other traditional tests, technically difficult to perform in a bum case, were not taken into consideration. In the normal kidney, urea and creatinine are concentrated in the urine to 20 times their plasma concentration; urine osmolality is a parameter of urine concentration which will be impaired if the kidney is impaired; in this case the ratio between urine and plasma osmolality will be decreased. Urine sodium concentration is also of help in defining the extent of tubular impairment, because,in this case, sodium, which is normally reabsorbed in its greatest part, will be lost in the urine. Dividing the urine sodium concentration by the ratio between urine and plasma creatinine determines the filtering and excreting activity of the tubule; the failing kidney, losing sodium and not concentrating creatinine, will show a decrease in this ratio. T,H20 is the amount of ‘free’ water reabsorbed per minute by the distal tubule and is calculated by subtracting osmolar clearance from urine output per minute, osmolar clearance being the plasma volume filtered per minute through the tubule and purified from all osmotically active substances. RESULTS
Although
45 patients
did not show consistent
and significant abnormality in their tests, 3 of them had pathological results and these will be discussed separately. CASE REPORTS Case 1
A 24-year-old man who was a factory worker, sustained a 27 per cent bum in a fire and was admitted on day 5 post bum, having been satisfactorily resuscitated in another hospital. He had a medical record of glomerulonephritis in infancy which had apparently healed: the patient had no follow-up controls afterwards. He underwent surgery on the seventh day post bum and his hospitalization was uneventful. We think that the abnormal results shown in Figs. I- 4 could not depend only upon the bum injury, but also upon a pre-existing chronic glomerular and tubular imbalance. This young man showed a pattern ofglomerular and tubular impairment. The patient was dismissed on day 30 post bum and has been under treatment by a kidney specialist since then. Case 2 A 54-year-old man was admitted immediately after second- and third-degree bums (mostly third degree) inolving 52 per cent body area. He had a previous history of hypertension, dating back several years. He was resuscitated properly and his urine output was quite satisfactory, but, as shown by Figs. 5 and 6, his kidneys behaved as ifthey were not there. Considering the long term hypertension, we think we have good reason to suspect a pre-existing nephrosclerosis, which was the cause of acute glomerular and tubular failure, of the non oliguric kind. This brought the patient to his death on day 7 post bum. Case 3 A 40-year-old man sustained a 58 per cent thirddegree bum in a gas explosion. Six hours elapsed before he was brought to a small hospital where he received severely inadequate resuscitative treatment. He was transferred to our Bums Unit on the third day post bum and was in the reversible phase of shock. We had to administer enormous quantities of plasma and electrolyte solutions before a satisfactory urine output was re-established. Figs. 7-9 demonstrate a reversible renal insufficiency due to inadequate fluid replacement during the first 48 hours. His kidneys had barely survived on the small amount of fluids given the patient in the acute phase, and it took them weeks to return to normal. DISCUSSION
This series of48 burn patients demonstrates that bum shock, and consequently, acute renal failure are not necessarily connected with burn injury, even a major one, providing that the preburn renal condition is normal, and proper
Barisoni
and
Bertolini:
30 20
Kidney
Function
363
-
-
10 ty
r; _y’“;
*
10
But.4 hv. lo-20
mg%l
Fig. I. Case 1. Urine output quite satisfactory throughout hospitalization. BUN shows pathological levels on several occasions. Ratio between Uun and BUN is nearly always pathological.
Case I. Urine osmolality always below normal values. Ratio between urine and plasma osmolality constantly abnormal. EYg
3.
hv. SO
50 30
IP 1
2
7
13
l5
20
oayr
25
30
Fig. 2. Case I. Plasma creatinine quite above normal values, while ratio Ucr/Pcr sufficient. Ratio between urine sodium excretion and creatinine urine and plasma values quite above normal, thus demonstrating a tubular insufftciency in sodium reabsorption.
Fi,e. 4. Casr 1. Tubular reabsorption of free water pathological in the first two weeks and improving over the following weeks, without ever reaching normal values.
> 500,
ml/h
Urtne cwtwt
,n.v a 501
70
5
3
oavs 5
B”“.
mg % ml
I”.“. 10 - 201
600
/
6
1
,j
0 2
3
Davl
5
6
0
I
2
3
Dayl
5
6
) 500,
“mm ,” ”
I
-
0 1
2
3
Dayl
5
6
F/g. 5. C‘use 2. Notwithstanding a sufficient urine output, BUN and plasma creatinine increase steadily, while Uun and the ratios Ucr/Pcr and Uun/BUN show a pathological decrease. These data clearly demonstrate a tubular and glomerular failure.
Fi,q. 6. C‘a~r 2. Constantly pathological values of urine as well as plasma osmolality are evidence of tubular impairment. This fact is confirmed by the very low level of tubular reabsorption of free water and the ratio between urine sodium and creatinine.
is given. This fact is confirmed by the 45 patients that had no symptoms of kidney impairment throughout their hospitalization. We believe, in the light of these results, that
our formula of resuscitation is quite adequate to compensate for the loss of fluids in the acute post-burn phase. We also believe that early surgical treatment plays a very important role in
resuscitation
Burns Vol. ~/NO. 5
364
0
46
10
15 OWS
Fig. 7. Case 3. In spite of good urine output BUN level increase steadily until day 10 post burn. The ratio Uun/BUN confirms the insufficient glomerular filtration up to the tenth day.
21
0
24 I
46
10
15
21
24
Da”*
Fig. 8. Case 3. Creatinine blood levels show impaired glomerular filtration and tubular excretion. Pathological tubular function is demonstrated by the ratio between urine sodium and cretinine ratio.
patients closely watched, even in collaboration with nephrologists, so that the standard treatment might. be improved by the use of diuretic drugs or dialysis.
2.51
REFERENCES
0
4
6
10
15
21
24
OWS
0
4
6
10
15
21
24
Davr
Fig. 9. Case 3. The plasma osmolality, the ratio urine/plasma osmolality and the TCH,O levels show the insufftcient concentration of reabsorption of urine and water at least during the ftrst two weeks post bum.
by the renal impairment caused in the later phase, especially when it is applied as extensively as possible, so that the source of toxemia can be eliminated in the shortest possible interval. On the other hand, at least in our experience, early and extensive surgery, even with the many difftcult problems it provides, does not reflect on kidney function, as again demonstrated by the substantial normal group. The problem of patients with pre-existing renal diseases, with diseases that might involve the renal function, or those who received poor resuscitative treatment still remains. For this reason we think that medical records should be accurately collected and analysed, and these avoiding toxemia
Requesfs,for reprinrsshouldbe
Cameron J. S. (1969)Disturbances of renal function in burnt patients. Proc. R. Sot. Med. (Land) 62,49. Eklund J. (1970) Renal regulation of body osmolal balance in bums. A clinical and experimental study with special reference to hyperosmolality. Acta Chir. Scund. (Suppl.) 410. MacMillan B. G. (1975) Bum wound sepsis-a IO-year experience. Burns 2, 1. Monafo W. W. (1976) Renal function after thermal trauma: the effects on renal blood flow and sodium and water excretion. Surgery 79,342. Moyer C. A., Margraf H. W. and Monafo W. W. (1965) Bum shock and extravascular sodium deficiency. Treatment with Ringer’s solution with lactate. Arch. Surg. 90,799. Ollstein R. N. and Burns G. C. (1973) Renal consideration in the burned patient. In: Lynch J. B. and Lewis S. R. (eds.) Symposium on the Treatment of Burns. St Louis, Mosby, pp. 66-72. Raffa J. and Trunkey D. D. (1978) Myocardial depression in acute thermal injury. J. Trauma 18, 90. Rosenthal S. R., Hawley P. L. and Hawkin A. A. (1972) Purified bum toxic factor and its competition. Surgery71,527. Schoenenberger G. A., Cueni L. B., Hatt A. M. et al. (1974) Verbrennungskenheiten-Toxinwirkung oder Infektionsfolgez. Chirurgie45,20. Settle A. D. (1974) Urine output following severe burns. Burns 1, I. Paper accepted I5 January 1980.
addressed PJ; Dr D. Barisoni. Plastic Surgery Division and Regional Burns Centre. Verona, Italy.