Nsg Dx
Ineffective breathing pattern
related to acidosis as evidenced
by DKA
Fluid volume deficit r/t
electrolyte imbalances
Rationale
Lack of glucose in cells results in
catabolism of fats and proteins,
leading to excessive amounts of
fatty acids and their metabolites
known as ketones or ketoacids, in
the blood. Excessive ketones in
the blood cause ketoacidosis.
Ketone bodies are acids; their
accumulation in the circulation
due to lack of insulin leads to
metabolic acidosis. However, as
dehydration develops, the
glomerular filtration rate in the
kidney is decreased, and excretion
of acids becomes more limited.
Ketoacidosis leads to Kussmauls’
respirations. Kussmaul
respirations represent the body’s
attempt to decrease the acidosis,
counteraffecting the effect of the
ketone build-up.
Though the patient doesn’t
manifest polydispsia and polyuria,
emesis occurs. Emesis could lead
to dehydration because
Nsg Interventions
1. Administer oxygen as
ordered.
2. Monitor oxygen saturation
levels and assess depth or
rhythm of respirations every
hour.
3. Elevate head of the bed.
4. Encourage adequate rest
periods between activities.
5. Review environmental
factors.
6. Assess LOC by evaluating
neurological responses and
patient’s ability to effectively
answer questions every hour.
1. Measure and record urine
output hourly; report urine
output less than 30ml for 2
consecutive hours.
Rationale
Airway and breathing remain the
first priority. Oxygen
administration may help alleviate
the patient tachypnea.
Detects
respiratory compensation during
a time of the respiratory crisis of
Kussmaul breathing (caused by
the
DKA).
Gravity pulls the diaphragm
downward, allowing greater chest
expansion and lung ventilation.
To limit fatigue.
May require
avoidance/modification of
lifestyle or environment to limit
impact on client’s breathing.
Provides constant monitoring of
neurological status
.
Fluid volume deficit reduces
glomerular filtration and renal
blood flow causing oliguria.  The
patient in DKA may also be
electrolytes were loss. Emesis
occurs for the reason that it is one
of the signs and symptoms of
metabolic acidosis due to the
reason that there are increased
ketone bodies in circulation.
Ketone bodies were formed
because there is insulin deficiency
there will be breakdown of fats
(lipolysis) takes place. Lipolysis
will lead to increased fatty acids
and glycerol. The free fatty acids
are converted into ketone bodies
in the liver. So thus, increased
ketone bodies will leads to
metabolic acidosis. Accumulation
of ketones is reflected in urine
and blood.
undergoing osmotic diuresis and
have excessive outputs.
2. Weigh patient daily. Changes in weight can provide
information on fluid balance and
the adequacy of volume
replacement.  1lb = 2.2kg.
3. Assess neurological status. Alterations in mental status can
occur from severe volume
depletion and altered sodium
levels, patients are also at risk for
seizures.
4. Initiate and administer Insulin Insulin is necessary to correct the
therapy: ketoacidosis. Insulin has an
 IV bolus dose of affinity to the tubing.  With the
regular insulin is administration of insulin, the
followed by potassium re-enters the cells
continuous along with the glucose.
infusion. 50ml must be primed through the
 Prime the line by tubing, to allow the mixture to
wasting 50ml of coat the tubing and make sure the
the mixture. patient is receiving the true dose.
5. Initiate and administer IV Initial goal is to correct circulatory
therapy volume deficit. Hypotonic saline
 Half-strength solution may be used for patients
normal saline with high blood pressure. IV
(0.45%) solution. therapy may be needed to replace
fluid losses caused by vomiting.
Fluid therapy causes expansion of
plasma volumes, and a return of
normal renal function, which is

6. Monitor for effects of IV
therapy.
7. Administer potassium IV as
ordered: typically 20 to 30
mEq/L.
8. Promote comfortable
environment. Cover patient
with light sheets.
9. Maintain fluid intake of at
least 2500 mL/day within
cardiac tolerance when oral
essential.
Volume replacement is necessary
to provide adequate circulation,
perfusion and oxygenation of the
tissues.  Replacement is adequate
when vital signs are back to
baseline.
Potassium is added to Iv infusions
once renal function has been
established and serum potassium
levels are below 5.5 mEq/L. As
hydration progresses, laboratory
values will change as the
electrolytes move from
compartment to fluid
compartment. Potassium
replacement becomes more
crucial with the administration of
insulin. Insulin causes potassium
to move into the intracellular
compartment at the time acidosis
is corrected.
Avoids overheating, which could
promote further fluid loss.
Maintains hydration/circulating
volume.

Imbalanced Nutrition: less than
body requirement related to
catabolism of fats and proteins
for fuels.
Insulin deficiency leads to
breakdown of fats and proteins.
Catabolism of fats and proteins
occurs because the transport of
glucose and amino acids into cells
is impaired, as well as the
synthesis of protein and glycogen.
In turn, these metabolic
abnormalities affect lipid
metabolism.
intake is resumed.
1. Weigh daily or as indicated.
2. Ascertain patient’s dietary
program and usual pattern;
compare with recent intake.
3. Auscultate bowel sounds.
Note reports of abdominal
pain/bloating, nausea,
vomiting of undigested food.
4. Provide small and frequent
feeding.
5. Perform fingerstick glucose
testing.
Assesses adequacy of nutritional
intake (absorption and
utilization).
Identifies deficits and deviations
from therapeutic needs.
Hyperglycemia and fluid and
electrolyte disturbances can
decrease gastric motility/function
(distension or ileus), affecting
choice of interventions. Note:
Long-term difficulties with
decreased gastric emptying and
poor intestinal motility suggest
autonomic neuropathies affecting
the GI tract and requiring
symptomatic treatment.
Bedside analysis of serum glucose
is more accurate (displays current
levels) than monitoring urine
sugar, which is not sensitive
enough to detect fluctuations in
serum levels and can be affected

6. Administer regular insulin by
intermittent or continuous IV
method, e.g., IV bolus
followed by a continuous drip
via pump of approximately 5–
10 U/hr so that glucose is
reduced by 50 mg/dL/hr.
7. Provide diet of approximately
60% carbohydrates, 20%
proteins, 20% fats in
designated number of
meals/snacks.
by patient’s individual renal
threshold or the presence of
urinary retention/renal failure.
Note: Some studies have found
that a urine glucose of 20% may
be correlated to a blood glucose
of 140–360 mg/dL.
Regular insulin has a rapid onset
and thus quickly helps move
glucose into cells. The IV route is
the initial route of choice because
absorption from subcutaneous
tissues may be erratic. Many
believe the continuous method is
the optimal way to facilitate
transition to carbohydrate
metabolism and reduce incidence
of hypoglycemia.
Complex carbohydrates decrease
glucose levels/insulin needs,
reduce serum cholesterol levels,
and promote satiation. Food
intake is scheduled according to
specific insulin characteristics
(e.g., peak effect) and individual
patient response. Note:A snack at
bedtime (hs) of complex
carbohydrates is especially
important (if insulin is given in
divided doses) to prevent
hypoglycemia during sleep and
potential Somogyi response.
Fatigue related to metabolic
acidosis and Decreased
metabolic energy production
Insulin functions are to transports 1. Discuss with patient the need  Education may provide
and metabolize glucose for for activity. Plan schedule motivation to increase activity
energy. Since there is insulin with patient and identify level even though patient may
deficiency, there will be activities that lead to fatigue. feel too weak initially.
weakness. In addition to,
metabolic acidosis develops as 2. Alternate activity with periods Prevents excessive fatigue.
ketoacids bind with bicarbonate of rest/uninterrupted sleep.
ions in the buffer, leading to
decreased serum bicarbonate 3. Monitor pulse, respiratory Indicates physiological levels of
levels and decreased serum pH. rate, and BP before/after tolerance.
As dehydration progresses, renal activity.
compensation are reduced,
acidosis becomes
decompensated, and serum pH
falls, resulting in loss of
consciousness. So thus, Lethargy
and weakness causes fatigue to
the patient.