Peritoneal dialysis in hyperosmolar coma
fusion. After 6 hours blood glucose levels raised to
1,388 mg/dl with pH 7.34, 170 mEq/l Na, 3.6 mEq/l
K, 410 mOsm/l osmolarity, 3.3 mmol/l lactate, 23
mmHg pCO2, 74 mmHg pO2, and an arterial pres-
sure of 85/48. However 11 hours later, blood glu-
cose dropped to 650 mg/dl with 180 mEq/l Na, 4.3
mEq/l K, 135 mEq/l Cl, 9.9 mmol/l lactate, 70 mg/dl
BUN and 1.8 mg/dl creatinine. The patient was olig-
uric (60 ml x 24 h).
bodies was not performed at the time of admission
to hospital 10 years ago.
DISCUSSION
To our knowledge this is the first report of hyperos-
molar coma in a neonate undergoing peritoneal dial-
ysis who survived such a condition without showing
late neurological or other consequences than Type 1
diabetes. At the presentation therapeutic measures
were taken as expected in a case like this. However,
despite infusion therapy with saline hypotonic solu-
tion first, followed by insulin infusion after, blood glu-
cose and sodium levels remained very high after 24
hours. The clinical situation got worse with the ap-
pearance of lactic acidosis and anuria. To compen-
sate for the severe dehydration, further administra-
tion of fluids and bicarbonate were carried out to
correct lactic acidosis. In a similar case reported in
literature, exanguinotransfusion was unsuccessful (6).
Persisting lactic acidosis and the appearance of
anuria prompted us to implement peritoneal dialysis.
This was carried out to maintain liquid in the ab-
domen for a short time to prevent high blood glu-
cose from causing a massive re-absorption of fluids
from the abdomen. A progressive reduction of blood
glucose, sodium levels and lactate with a normaliza-
tion of acid-base equilibrium was obtained 72 hours
later. Neurological manifestation observed two hours
after beginning peritoneal dialysis should have been
caused by hyperosmolarity and the unlikely throm-
bosis of cerebral arteries for vascular disseminated
coagulation, even though it was not detectable at
computerized tomography.
Given that anuria with lactic acidosis developed and
that hyperglycemia and hyperosmolarity persisted,
the patient was placed on peritoneal dialysis while
simultaneously administered insulin (0.25 IU/kg/h).
Briefly, intermittent peritoneal dialysis was per-
formed using a 14 diameter gauge positioned in
the right pelvic fossa. For the in and out flow of dial-
ysis fluid we used a Y system with a separate line
for each flow. Isotonic bags (Traverol) with low glu-
cose concentration (1.36%) were employed. The to-
tal quantity of fluids administered ranged between
100-150 ml, whereas fluids removed ranged be-
tween 66 and 165 ml. The total of peritoneal dial-
ysis lasted for 45 hours. Two and a half hours after
beginning dialysis, the patient experienced con-
vulsions with each crisis lasting between 2 and 3
minutes at various intervals of 20-35 minutes. The
dialysis was stopped during convulsion. A calcium
value of 6.8 mg/dl was reported. She was then
treated with benzodiazepine first and 10% calcium
gluconate soon after, intubated and transferred to
the Neonatal Intensive Care. Pulmonary ventilation
with positive pressure followed by intermittent pul-
monary ventilation (IPPV) were implemented.
Eleven hours after beginning IPPV, her breathing
became spontaneous. Subsequently, the oxymet-
ric values gradually set off normality, improvement
of sensorium, decrease of blood glucose up to near
normal values, progressive normalization of sodi-
um, lactate and base excess were observed. Lactate
became normal in 20 hours and diuresis returned
physiological 20 hours later.
Management of the hyperosmolar hyperglicemic
coma is not easy especially when other complica-
tions arise. The key for a successful outcome is a
prompt, rapid administration of crystalloid solution
that has tonicity appropriate to the level of hyper-
osmolarity (7). In the presence of renal failure treat-
ment becomes extremely difficult.
The patient was transferred to the ward; her neu-
rological examination at this stage was normal.
Meals consisted of adapted milk every 3 hours with
small insulin boluses. She was discharged from hos-
pital 60 days later without any neurological defects,
insulin being her sole therapy.
Today (2000) this girl is 10 years old, her metabol-
ic control with subcutaneous insulin is good,
weight-height development is above average (75°
centile), neurological defects are not present and
she regularly attends school succeeding in her stud-
ies. C-peptide levels in this patient are very low
(<0.3 ng/ml) clearly indicating that she is affected
by Type 1 diabetes. Measurement of islet cell anti-
We have no evidence to state that implementation
of peritoneal dialysis was the reason for the suc-
cessful outcome of this baby girl.
However, we were forced to adopt such a procedure
because of anuria and it might be possible that its
use has accelerated the clinical improvement, there-
fore limiting the time of exposure to high blood glu-
cose which could have caused brain damage.
In conclusion, implementation of peritoneal dialysis
seemed to be the variable which might have chan-
ged the course of hyperosmolar coma in this
neonate at least compared with other cases re-
ported in the literature (2). Such an approach, there-
fore, should be considered in similar cases to re-
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