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Acute renal failure due to acute diarrhoeal

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Article in The Journal of the Association of Physicians of India March 1990

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 ARTICLE 4
ACUTE RENAL FAILURE DUE TO ACUTE DIARRHOEAL
DISEASES
S. Shiva Kumar, R. Paramananthan, MA Muthusethupathi
SUMMARY
Fifty four patients with acute renal failure (ARF) due to acute
diarrhoeal diseases (ADD) were treated between August 1987 and May
1988. There were 39 males and 15 females. The mean age was 46.25
years. These patients were referred by general practitioners (GPs) and
private nursing homes during an epidemic of ADD in Madras city in
1987-88. Investigations revealed plasma urea (mean + SD) 129 + 52.8
mg/dl and plasma creatinine (mean + SD) 7.51 4.3 mg/dl. 42 patients
underwent peritoneal dialysis. 3 had haemodialysis. 29 patients died
(mortality 53.7%). The most significant factor for high mortality was
the time interval from onset of ADD to diagnosis of ARF which was
5.2 + 2.17 days in the patients who survived compared to 8.5 + 3.1
days in the patients who died (P<0.01). It is concluded that (a) GPs
had given inadequate fluid therapy before admission and (b) were
initially not aware of renal failure and so referred them late to hospital.
Key Words: Acute Diarrhoeal Diseases-Acute Renal Failure-Peritoneal
Dialysis
INTRODUCTION
Acute diarrhoeal diseases (ADD) are an important cause of acute
renal failure(ARF) in India.1 The mortality in cholera used to be greater
than 30% before 1963, due to hypovolaemic shock, renal failure and severe
metabolic acidosis.2 With the advent of rapid fluid therapy ( both oral and
intravenous), there has been a dramatic decline in mortality which is about

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30
1% at present.3 From July 1987 to Match 1988, there was an epidemic of
acute diarrhoeal diseases (cholera and non cholera) in Madras City. During
this period, many patients with ARF due to ADD were admitted at
Government General Hospital. Our experience with these patients is
discussed.
MATERIAL AND METHODS
ARF due to ADD was diagnosed by the following criteria:
1. Abrupt decline in glomerular filtration rate (GFR) as shown by
progressive elevation of plasma urea (Pu), ( >40mg/dl) and plasma
creatinine (P.Cr.) (> 2mg/dl)
2. Preceding history of acute diarrhoeal disease occurring within < 3
weeks.
3. Absence of other causes leading to ARF.
Once the diagnosis was established, the following data were noted:
(1) Therapy at onset of ADD (2) time-interval from onset of
ADD to diagnosis of ARF. (3) clinical features at
presentation of ARF.
Patients were started on conservative treatment including
correction and maintenance of fluid and electrolyte balance, provision of
high-calorie diet and protein restriction (0.6 g/Kg body wt/day). Patients
with severe renal failure (P.Cr. > 5mg/dl.) underwent peritoneal dialysis
(PD) Haemodialysis (HD) was done when (a) PD was contraindicated or
(b) when PD failed to control uraemic symptoms.
RESULTS
Of the fifty four patients with ARF due to ADD there were 39
males and 15 females. The mean age was 46.25 years. 41 of 54 patients
were seen between August 1987 and December 1987. Since most of these
patients were referred by general practitioners (GPs) and private nursing

JAPI 1990, Vol. 38, No.2 p 164 166

31
homes, data on therapy at onset of ADD could not be obtained as no
records were maintained. The age, sex distribution, biochemical
investigations, therapy and mortality are shown in table 1 and 2. Patients
presented with oliguria and in severe cases with fluid overload, uraemic
symptoms or metabolic acidosis. The mean time interval from onset of
ADD of ARF was 6.94 + 3.28 days. Seven patients recovered with
conservative treatment. Two patients died before dialysis could be started.
PD was done in 42 patients. Three patients underwent HD:29 of 54
patients died (53.7%).
Patients were divided into two groups (tables 1 & 2). Group I
consisted of 25 patients who survived. The mean time interval from onset
of ADD prior to diagnosis of ARF was 5.2 + 2.17 days, compared to Group
II which was 8.55 + 3.11 days. This was statistically significant (P < 0.01).
17 Patients underwent PD. Only one required HD. Seven patients
recovered with conservative treatment. Group II considered of 29 patients
who died. Twenty five patients underwent PD and 2 underwent HD. These
patients died during the procedure due to severe uraemia.
DISCUSSION
Acute diarrhoeal diseases are important cause of preventable ARF
in India. Inadequate or delayed restoration of diarrhoeal losses results in a
very high incidence of ARF4. In a preliminary study of 32 patients with
cholera, 21 (66%) developed plasma urea nitrogen of 60mg/dl. and five
died.5 Subsequently, a study conducted by Carpenter et al during a cholera
epidemic in 1963 in 58 patients has shown that volume deficit corrected
within 4 hours with 2:1 saline-lactate solution prevents development of
ARF.6 Patients treated in the traditional fashion received 600ml of 1.35 per
cent saline, 600ml of isotonic saline, 600ml of 5 per cent dextrose and
isotonic saline, and 200ml, of 20 per cent dextrose and 50ml of 7.5 per cent.

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32
Table 1: CLINICAL DATA AND MANAGEMENT OF PATIENTS
WITH ADD
Total Group I Group II Significance
Number 54 25 29 -
Male 39 17 22 -
Mean age 46.25 44.23 47.37 NS*
Time interval (days)
from onset of ADD to 6.94 + 3.28 5.2 + 2.17 8.55 + 3.1 (P < 0.01)
ARF (mean + SD)
Conservative treatment 9 7 (28%) 2 (6.9%) -
PD 42 17 25 -
HD 3 1 2 -

Table 2 : BIOCHEMICAL FEATURES OF PATIENTS WITH ADD

Total Group I Group II Signifi-
Cance
Plasma Urea mg/dl. 129 + 52.8 117 + 50.61 142.72 + 46.80 NS
S. Creatinine mg/dl. 7.51 + 4.3 6.02 + 2.82 8.11 + 2.88 NS
Pl. Na.Meq/L 132.56 + 6.9 132.41 + 8.38 132.8 + 5.15 NS
Pl. K. mEq/L 3.72 + 1.14 3.6 + 1.25 3.88 + 1.0 NS
PL HcO3 mEg/L 19.1 + 3.3 19.6 + 2.6 18.9 + 3.7 NS
NS Not Significant.

sodium bicarbonate during the first 4 hours. The average patient treated
with the aggressive regimen received approximately 4000ml fluid and 180
mEq of bicarbonate during the first 4 hours, whereas the patients treated
with the traditional regimen received an average of 2000ml and 44mEq of
bicarbonate. Every patient in the aggressively treated group was
normotensive and could stand unassisted, whereas half of the patients
treated by the traditional regimen remained hypotensive. All Patients in
both treatment groups survived, but plasma urea nitrogen rose to greater
than 60 mg/dl. In 50 per cent of the patients receiving traditional therapy
compared to none in the saline-lactate group. One hundred and forty

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33
consecutive hypotensive adult male cholera patients subsequently were
treated in a similar aggressive fashion, and plasma urea nitrogen rose to a
level greater than 60mg/dl in only one instance.6 These studies reveal that
rapid and effective restoration of ECF volume within four hours can
prevent ARF. Inspite of advances made in oral rehydration therapy, GPs
seem unaware of the principles of treatment and had given inadequate fluid
replacement before admission.
Fifty four patients with ARF were treated between August 1987
and Mat 1988. Mean time interval from onset of ADD to diagnosis of ARF
was 6.94 + 3.28 days. Forty seven patients had severe renal failure plasma
creatinine > 5mg/dl. Seven patients were treated conservatively. Forty two
patients underwent PD and 3 underwent HD. Mortality was 53.7% This
mortality was high compared to the average mortality of ARF at our
hospital. To analyse the cause of high mortality, the patients, were divided
into survived (Group I) and expired (Group II) patients. In Group I, 18 of
25 patients presented with severe renal failure and they recovered with
dialysis. Seven patients had mild renal failure (plasma creatinine <5
mg/dl.) which improved with conservative management. In Group II, all 29
patients had severe renal failure. Two patients died before they could be
shifted for dialysis. Twenty seven patients died during the procedure. The
mean serum creatinine was not statistically different in both groups as the
serum creatinine was more tham 5mg/dl Group I: creatinine 6.02 mg +
2.82; Group II: 8,11 + 2.88). The only significant factor was that patient in
Group II had come late (8.55 + 3.11 days) and therefore could not survive
therapy, while Group I patient came early (5.2 + 2.17 days). Hyperkalaemia
was not observed in either group.. It is difficult to interpret the severity of
acidosis as blood pH values were not available and plasma bicarbonate
values are not adequate to assess acidosis. In the various studies noted

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34
above, severe acidosis has contributed to the mortality due to losses in
stools and inadequate replacement of bicarbonate.5,6. The most crucial
aspect of management of severe ADD is the aggressive and adequate fluid
therapy in the initial stages of ADD. After renal failure has been
established, fluid therapy is dangerous and leads to fluid overload, which
has happened in these patients. This was probably because the GPs were
not aware that renal failure had occurred and had continued IV fluids. The
renal failure was detected late and the patients referred when they were
severely uraemic and in fluid overload.
Peritoneal dialysis, in our experience is an effective means of
dialysis and has several advantages like simplicity and convenience.7 The
high mortality in group II was not due to the procedure but to the fact that
they were critically ill due to late admission. Most of them died during the
procedure.
It is obvious from this study, that though the mortality on ADD has
been dramatically brought down due to advances in fluid therapy, primary
care physicians are not aware of the high incidence of ARF.

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35
REFERENCES
1. Muthusethupathi MA. Shiva Kumar S. Acute renal failure in South
India, J Assoc Physicians India, 1987: 35: 504 - 7.

2. Madias NE, Harrington JT. Postischemic acute renal failure In,

Brenner BM, Lazarus J (Eds.) Acute Renal Failure Philadelphia,
Saunders WB, 1983; PP 235-251.

3. Park JE, Park K, Cholera and acute diarrhoeal diseases. In Park JE

and Park K (Eds.) Text book of preventive and social medicine,
Jabalpur, Banarsidas Bhanot, 1986; Pp 191-203.

4. Carpenter CCJ. Cholera In. Weatherall DJ, Ledingham JGG, and

Warrell DA (Eds.) Oxford text book of medicine, Oxford, Oxford
University press, 1983; 195-8.

5. Carpenter CCJ, Mitra PP, Sach RB Clinical studies in Asiatic

Cholera I, Preliminary observations, November 1962 March 1963.
Bull Johns Hopkins Hosp, 1966; 118 ; 165-73.

6. Carpenter CCJ, Mondal A, Sack RB, et al, Clinical studies in Asiatic

cholera II. Development of 2:1 Saline Lactate regimen.
Comparison of this regimen with traditional methods of treatment
between April and May 1963. Bull Johns Hopkins Hosp, 1966; 1:8
174 - 96.
7. Muthusethupathi MA, Shivakumar, S, Domodarsn K, - Management
of renal failure in India. J Assoc Physicans India, 1985; 33 : 647-9.

JAPI 1990, Vol. 38, No.2 p 164 166

36
 Acute Renal Failure due to Acute Diarrhoeal Diseases:
To a question raised by a Doctor which reads as follows:

We read with interest the article on this subject. The

importance of fluid replacement and early recognition and management
of acute renal failure cannot be over emphasized. While the traditional
fashion of volume deficit correction has been elaborated, the aggressive
and more effective form of fluid replacement has not been elucidated in
the article. It will be useful if the authors explain the same.

REPLY FROM THE AUTHORS

We would like to outline the management of volume depletion

due to acute diarrhoeal diseases (ADD). On admission, the poatient
with ADD should be assessed for severity of volume depletion. Volume
depletion may be classified as (a) mild (<5% of body weight loss) which
clinically manifests as dry mouth, thirst, and normal skin elasticity; (b)
moderate (5 10% of body weight loss) manifesting as reduced skin
elasticity and mucosal dryness, restlessness and tachycardia; and (c)
severe (10% of body weight loss) in which hypotension is present in
addition to the above manifestations.
Intravenous infusion is usually required for the initial
rehydration of moderate and severely depleted patients who are in shock
or unable to drink. Ringers lactate solution is the best available
solution (Constitution Na+ 130, K+4, Ca++3, Cl023 109, lactate 28
meq/L). It supplies adequate concentrations of sodium, potassium, and
lactate yields bicarbonate for correction of acidosis. If it is not
available, isotonic saline may be used to which sodium bicarbonate is
added (40 ml/l of saline). Carpenter et al1, used 2.1 saline lactate
solutions (1000 ml of saline and 500 ml of isotonic sodium lactate).

JAPI 1991,VOL 39, NO.4 p.356

37
 The recommended doses of IV fluids in severe volume
depletion is 100 ml/Kg of body weight. The initial rehydration should
be fast, at the rate of 100 ml/min (1000 ml/10 15 minutes) until an
easily palpable pulse is felt. After infusing 1 2 litres, rehydration
should be carried out at a slower rate (1000 ml/30 45 min), until the
pulse and blood pressure return to normal. A 50 Kg individual may
need about 5 litres of fluid (10% of his body weight). The deficit
correction should be done within 4 hours.
When the patient can take oral fluids, IV fluids should be
replaced with oral fluids as recommended by the WHO. In mild volume
depletion, oral therapy may be given from the onset of diarrhea. After
the initial deficit correction, oral fluids should be used to replace
concurrent losses and for maintenance therapy.
The patient must be examined at intervals during the
rehydration. It is advisable to measure plasma urea, creatinine and
serum electrolytes and make appropriate modifications. The volume
depletion should be corrected within four hours and if urine output does
not improve after 24 hours, fluid intake must be restricted and the
patient must be managed as for acute renal failure (ARF). We
recommend that renal investigations must be done daily and once ARF
is detected, the patient should be referred immediately to a hospital
where facilities for dialysis are available.

MA Muthusethupathi, S Shivakumar

REFERENCE:
1. Carpenter CCJ, Mondal A, Sack RB, et al. Clinical studies in Asiatic
cholera II. Development of 2:1 saline lactate regimen.
Comparision of this regimen with traditional methods of treatment
between April and May 1963. Bull Johns Hopkins Hosp 1966,
188:174-96

JAPI 1991,VOL 39, NO.4 p.356

38

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