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Treatment with sodium bicarbonate

StudyPopulationInterventionOutcomesResultsCommentsDesignEL
Morris et al, 198651521 adults with severe diabetic ketoacidosis (pH 6.9–7.14)
Mean age bicarbonate group 34 ± 5, control group 28 ± 4 years
USA
Inclusion criteria: plasma glucose level ≥ 250 mg/dl, serum testing acetone positive at > 1:2 dilution, serum bicarbonate level ≤ 15 mEq/l, arterial pH 6.9–7.14, age ≥ 15 years
Intravenous bicarbonate infused over 30 min (133.8 mEq for arterial pH of 6.9–6.99, or 89.2 mEq for arterial pH 7.1–7.14), repeated every 2 hours until pH was 7.15 or more
versus
no bicarbonate therapy
Treatment regimen for all patients to treat diabetic ketoacidosis (irrespective of adjunct bicarbonate therapy):
Insulin 0.30 units/kg body weight, half IV bolus, 1.2 units IM injection, then hourly injections of 7 units IM
Intravenous fluid as 0.9% saline or 0.45% saline at 250–1000 ml/hour depending on patient’s state of hydration
Primary outcome: overall rate of recovery from diabetic ketoacidosis
Secondary outcome: number of concomitant complications during treatment
Comparison of patients before and after bicarbonate therapy: At randomisation there was no difference in the biochemical profile between the two groups. No significant differences were seen in the rate of change of pH, ketone bodies, bicarbonate levels or plasma lactate levels
No significant differences were noted in the recovery time between the 2 groups in terms of the number of hours required for glucose levels to reach 250 mg/dl (13.9 mmol/l) (4.9 ± 1.3 vs. 4.2 ± 1.0 hours) or for bicarbonate to reach 15 mEq/l (21 ± 4.3 vs. 21 ± 4.0 hours)
Various chemical components of cerebrospinal fluid also showed no statistically significant differences in glucose, bicarbonate, pH, lactate and ketones at three time points (0, 6–8, 10–12 hours)
There was no effect on mental status. Initially there appeared to be a greater decline in blood glucose levels in the control group compared with the bicarbonate group, although this was not statistically significant
Frequency of hypokalaemia (potassium < 3.3 mEq/l) measured by decline in serum potassium over time showed no significant difference with or without bicarbonate
Episodes of hypoglycaemia: (0 vs. 1 episode) and total insulin administered for complete control (124 ± 22 vs. 92 ± 11 u) did not significantly differ between the two groups
Intravenous fluid therapy over 8 hours did not significantly differ in the amount of sodium (33 ± 31 vs. 451 ± 74 mEq), chloride (333 ± 31 vs. 451 ± 74 mEq), potassium (67 ± 21 vs. 70 ± 17 mEq) or glucose (36 ± 11 vs. 40 ± 8 g) administered in the bicarbonate or no bicarbonate groups
Similarly, no differences were seen in electrolyte supplementation over 24 hours of therapy, or the amount of intravenous fluid administered in the bicarbonate or no bicarbonate groups either at 8 hours (7.2 ± 0.96 vs. 9.4 ± 1.3 ml/kg/hour) or 24 hours (4.8 ± 0.5 vs. 5.9 ± 0.6 ml/kg/hour)
No description of how randomisation took place
No description of selection of patients
RCTIb
Gamba et al, 199151420 adult patients with severe diabetic ketoacidosis admitted to an emergency room
Mean age bicarbonate group 29 ± 2.0, placebo group 28 ± 5.6 years
Mexico
Diabetic ketoacidosis: arterial pH < 7.15, arterial bicarbonate < 15 mEq/l, positive urine ketone test >++
Randomisation of patients in groups of 4, stratified according to arterial pH, into 2 intervention groups:
  1. sodium bicarbonate (44.8 mEq in 50 ml for arterial pH 7.10–7.14, 89 mEq in 100 ml for arterial pH 7.00–7.09, 133.5 mEq in 150 ml for arterial pH 6.90–6.99)
  2. 0.9% saline solution
Dose was given over 30 min and repeated after 2 hours if the increment in pH was < 0.05
Additional therapy in all patients: IV bolus of 5 units insulin/hour until blood glucose < 250 mg/dl and ketone urine <++ or negative. On admission all patients received 1000 ml of 0.9% saline solution with 20 mEq potassium chloride for 1 hour. Further treatment was given as necessary over the next 24 hours. 5% glucose was instigated when blood glucose < 250 mg/dl
Recovery rate of arterial pHNo significant differences were seen between groups in patient age, weight, duration of diabetes and clinical parameters
At 2 hours, arterial pH was significantly higher in the bicarbonate-treated group, compared with the non- bicarbonate-treated group (7.24 ± 0.04 vs. 7.11 ± 0.09, p < 0.02 95% CI 0.06 to 0.19). At 2 hours, arterial bicarbonate was also higher in the bicarbonate than the non-bicarbonate-treated group (6.1 ± 1.56 vs. 3.6 ± 2.0 mEq/l, difference between means 95% CI 0.8 to 4.2, p < 0.01). Changes in arterial pH and bicarbonate were also higher in the treatment group compared with the non-bicarbonate-treated group over the first 2 hours (0.17 ± 0.09 vs. 0.07 ± 0.05, difference betweens means 95% CI 0.03 to 0.16, p < 0.01, and 3.2 ± 1.2 vs. 1.1 ± 1.7 mEq/l, difference between means 95% CI 0.7 to 3.5, p < 0.01, respectively)
No significant differences were seen in pCO2 or blood glucose levels between the groups at any point throughout the study. pO2 fell equally in both groups with no significant difference at 2 hours (−5.2 ± 12.2 vs. −7.2 ± 18.7, p < 0.05, 95% CI −13 to 17) or at 24 hours (−9.9 ± 12.4 vs. −10.3 ± 15.2, p > 0.05, 95% CI −12.9 to 13.7)
Heart rates, respiratory rates, mental status, plasma sodium, urea and mean arterial pressure did not differ between the groups
Significantly higher levels of serum potassium were seen in the non-bicarbonate-treated group at 24 hours (3.64 ± 0.62 vs. 2.92 ± 0.45 mEq/l, p < 0.05, 95% CI 0.16 to 1.31), but at no other time points throughout the study
There were no differences in the amount of insulin solution or potassium received by each group in the first 2 hours. The amount of insulin required to decrease blood glucose to < 250 mg/dl and reduce ketosis did not differ between the two groups. More potassium was given in the non- bicarbonate-treated group than the bicarbonate group, but this was not significant (p > 0.10)
There were no deaths in either group throughout the study
All patients in the bicarbonate group developed hypokalaemia, possibly due to the differences in potassium administration. Mean sodium bicarbonate received by the bicarbonate group was 84 ± 34 mEq
No description of how randomisation took place
No value given for blood glucose inclusion criterion
RCT double blindIb

From: Evidence tables

Cover of Type 1 Diabetes
Type 1 Diabetes: Diagnosis and Management of Type 1 Diabetes in Children and Young People.
NICE Clinical Guidelines, No. 15.2.
National Collaborating Centre for Women's and Children's Health (UK).
London: RCOG Press; 2004 Sep.
Copyright © 2004, National Collaborating Centre for Women’s and Children’s Health.

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