Ketoacidosis (Nursing)

Pranita Ghimire; Amit S. Dhamoon; Chaddie Doerr.

Last Update: August 11, 2021.

Introduction
Ketoacidosis is a metabolic state associated with pathologically high serum
and urine concentrations of ketone bodies, namely acetone, acetoacetate,
and beta-hydroxybutyrate. During catabolic states, fatty acids are
metabolized to ketone bodies, which can be readily utilized for fuel by
individual cells in the body. Of the three major ketone bodies, acetoacetic
acid is the only true ketoacid chemically, while beta-hydroxybutyric acid is
a hydroxy acid, and acetone is a true ketone. Figure 1 shows the schematic
of ketogenesis where the fatty acids generated after lipolysis in the adipose
tissues enter the hepatocytes via the bloodstream and undergo beta-oxidation
to form the various ketone bodies. This biochemical cascade is stimulated
by the combination of low insulin levels and high glucagon levels (i.e., a low
insulin/glucagon ratio). Low insulin levels, most often secondary to absolute
or relative hypoglycemia as with fasting, activate hormone-sensitive lipase,
which is responsible for the breakdown of triglycerides to free fatty acid and
glycerol.
The clinically relevant ketoacidoses to be discussed include diabetic
ketoacidosis (DKA), alcoholic ketoacidosis (AKA), and starvation
ketoacidosis. DKA is a potentially life-threatening complication of
uncontrolled diabetes mellitus if not recognized and treated early. It typically
occurs in the setting of hyperglycemia with relative or absolute insulin
deficiency. The paucity of insulin causes unopposed lipolysis and oxidation
of free fatty acids, resulting in ketone body production and subsequent
increased anion gap metabolic acidosis. Alcoholic ketoacidosis occurs in
patients with chronic alcohol abuse, liver disease, and acute alcohol
ingestion. Starvation ketoacidosis occurs after the body is deprived of
glucose as the primary source of energy for a prolonged time, and fatty acids
replace glucose as the major metabolic fuel.

Nursing Diagnosis
 Nausea, vomiting
 Abdominal pain
 Excess thirst
 Dyspnea
 Malaise
 Excessive urination
 Confusion
 Elevated blood sugar levels
 Fruit scented breath
 High levels of ketones in the urine

Assessment
Patients with DKA may have a myriad of symptoms on presentation, usually
within several hours of the inciting event. Symptoms of hyperglycemia are
common, including polyuria, polydipsia, and sometimes more severe
presentations include unintentional weight loss, vomiting, weakness, and
mentation changes. Dehydration and metabolic abnormalities worsen with
progressive uncontrolled osmolar stress, which can lead to lethargy,
obtundation, and may even cause respiratory failure, coma, and death.
Abdominal pain is also a common complaint in DKA. AKA patients usually
present with abdominal pain and vomiting after abruptly stopping alcohol.
On physical exam, most of the patients with ketoacidoses present with
features of hypovolemia from gastrointestinal or renal fluid and electrolyte
losses. In severe cases, patients may be hypotensive and in frank shock. They
may have a rapid and deep respiratory effort as a compensatory mechanism,
known as Kussmaul breathing. They may have a distinct fruity odor to their
breath, mainly because of acetone production. There may be neurological
deficits in DKA, but less often in AKA. AKA patients may have signs of
withdrawal like hypertension and tachycardia. There are signs of muscle
wasting in patients with starvation ketoacidosis like poor muscle mass,
minimal body fat, obvious bony prominences, temporal wasting, tooth
decay, sparse, thin, dry hair and low blood pressure, pulse, and temperature.

Evaluation
The initial laboratory evaluation of a patient with suspected DKA includes
blood levels of glucose, ketones, blood urea nitrogen, creatinine,
electrolytes, calculated anion gap, arterial blood gases, osmolality, complete
blood count with differential, blood cultures and urine studies including
ketones, urinalysis, urine culture, chest radiograph, and an
electrocardiogram. Hyperglycemia is the typical finding at presentation with
DKA, but patients can present with a range of plasma glucose values.
Although ketone levels are generally elevated in DKA, a negative
measurement initially does not exclude the diagnosis because ketone
laboratory measurements often use the nitroprusside reaction, which only
estimates acetoacetate and acetone levels that may not be elevated initially
as beta-hydroxybutyrate is the major ketone that is elevated. The anion-gap
is elevated, as mentioned above because ketones are unmeasured anions.
Leukocytosis may indicate an infectious pathology as the trigger and
cultures are sent from blood, urine, or other samples as clinically indicated.
Serum sodium is usually relatively low because of shifts of solvent (water)
from the intracellular to extracellular spaces because of the osmotic pull of
hyperglycemia, and hence, normal or elevated serum sodium is indicative of
severe volume depletion. Serum potassium levels may be elevated due to
shifts from the intracellular compartment for exchange with acids in the
absence of insulin and normal or low potassium, indicating an overall
depleted body store and subsequent need for correction before initiation of
insulin therapy.
In AKA, transaminitis, and hyperbilirubinemia due to concurrent alcoholic
hepatitis may also be present. The alcohol level itself need not be elevated
as the more severe ketoacidosis is seen once the level falls, and the counter-
regulatory response begins and shunts the metabolism towards lipolysis.
Hypokalemia and increased anion-gap are usually seen with similar
mechanisms to those seen in DKA.
Hypomagnesemia and hypophosphatemia are common problems seen on lab
evaluation due to decreased dietary intake and increased losses. As
mentioned above, the direct measurement of serum beta-hydroxybutyrate is
more sensitive and specific than the measurement of urine ketones.
Starvation ketoacidoses patients may again have multiple electrolyte
abnormalities due to chronic malnutrition, along with vitamin deficiencies.
The pH may not be as low as in DKA or AKA, and the glucose levels may
be relatively normal.

Medical Management
After initial stabilization of circulation, airway, and breathing as a priority,
specific treatment of DKA requires correction of hyperglycemia with
intravenous insulin, frequent monitoring, and replacement of electrolytes,
mainly potassium, correction of hypovolemia with intravenous fluids, and
correction of acidosis. Given the potential severity and the need for frequent
monitoring for intravenous insulin therapy and possible arrhythmias,
patients may be admitted to the intensive care unit. Blood glucose levels and
electrolytes should be monitored on an hourly basis during the initial phase
of management.
Aggressive volume resuscitation with isotonic saline infusion is
recommended in the initial management of DKA. Volume expansion not
only corrects the hemodynamic instability but also improves insulin
sensitivity and reduces counter-regulatory hormone levels. After starting
with isotonic saline, the subsequent options can be decided on the serum
sodium levels that are corrected for the level of hyperglycemia. Normal or
high serum sodium levels warrant replacement with hypotonic saline, and
low sodium levels warrant continuation of the isotonic saline. This fluid has
to be supplemented with dextrose once the level reaches around 200 to 250
mg/dl. Along with fluids, an intravenous infusion of regular insulin has to
be initiated to maintain the blood glucose level between 150 to 200 mg/dl
and until the high anion-gap acidosis is resolved in DKA. Like mentioned
above, potassium levels are usually high because of the transcellular shifts
due to the acidosis and the lack of insulin. When the potassium levels are
low, this means that the total body potassium is low. Hence, insulin therapy
should be postponed until at least the level of serum potassium is greater
than 3.3 mEq/L. Otherwise, a further drop in levels would put the patient at
risk for cardiac arrhythmias. In the 3.3 to 5 mEq/L; range, supplementation
should be added in the maintenance fluids to target a steady 4.0 to 5.0 mEq/L
range, and if higher than that, insulin and intravenous fluids alone can be
started with just the frequent monitoring of the serum potassium level. The
treatment of the acidosis itself is more controversial. Treatment with sodium
bicarbonate therapy is controversial. It has been studied and found to provide
no added benefit when the arterial blood pH is greater than 6.9 and may be
associated with more harm.[5] A 2011 systematic review found that
bicarbonate administration worsened ketonemia. Several studies have found
higher potassium requirements in patients receiving bicarbonate. Studies in
children have observed a possible association between bicarbonate therapy
and cerebral edema.[6]
AKA typically responds to treatment with intravenous saline and
intravenous glucose, with rapid clearance of the associated ketones due to a
reduction in counter-regulatory hormones and the induction of endogenous
insulin. Like in DKA, this is the first step in management because of the
need for correction the hypovolemia/shock. Thiamine replacement is
important in alcohol-related presentations, including intoxication,
withdrawal, and ketoacidosis, and should be initially done parenterally and
after that maintained orally. Electrolyte replacement is critical. Potassium
losses that occur through gastrointestinal (GI) or renal losses should be
monitored and replaced closely as glucose in the replacement fluid induces
endogenous insulin, which in turn drives the extracellular potassium inside
the cells. Also of paramount importance is monitoring and replacing the
magnesium and phosphate levels, which are usually low in both chronic
alcoholism and prolonged dietary deprivation as in starvation.
The treatment of starvation ketoacidosis is similar to AKA. Patients need to
be monitored for refeeding syndrome, which is associated with electrolyte
abnormalities seen when aggressive feeding is started in an individual
starved for a prolonged time. The resultant insulin secreted causes
significant transcellular shifts, and hence, similar to AKA, monitoring and
replacing potassium, phosphate, and magnesium is very important.

Nursing Management
 Monitor vitals
  Check blood sugars and treat with insulin as ordered
 Start two large-bore IVs
 Administer fluids as recommended
 Check electrolytes as potassium levels will drop with insulin treatment
 Check renal function
 Assess mental status
 Look for signs of infection (a common cause of DKA)
 Educate the patient on the importance of compliance with diabetic
medications
 Educate the patient on the importance of follow up
 Check urine output
 Encourage patient to quit smoking and abstain from alcohol
 Encourage a healthy diet
 Ask the patient to wear an ID bracelet signifying that he or she has had
a DKA episode
 Check urine and blood cultures
 Listen to the lungs for rales and crackles

When To Seek Help

Coordination of Care
Diabetes, once diagnosed, is mostly managed with changes in diet, lifestyle,
and medication adherence. The goal is to prevent high glucose levels, which
helps prevent diabetic complications. The nurse practitioner, pharmacist,
primary care provider, and an endocrinologist should educate the patient on
glucose control at every opportunity.
Empowering the patient regarding management is hence of the utmost
importance. Diabetes self-management education (DSME) and diabetes
self-management support (DSMS) are recommended at the time of diagnosis
of prediabetes or diabetes and throughout the lifetime of the patient. DSMS
is an individualized plan that provides opportunities for educational and
motivational support for diabetes self-management. DSME and DSMS
jointly provide an opportunity for collaboration between the patient and
health care providers to assess educational needs and abilities, develop
personal treatment goals, learn self-management skills, and provide ongoing
psychosocial and clinical support. Improved outcomes and reduced costs
have been associated with DSME and DSMS.[7][8]

Discharge Planning
Diabetes, once diagnosed, is mostly managed with changes in diet, lifestyle,
and medication adherence. The goal is to prevent high glucose levels, which
helps prevent diabetic complications. To prevent the complications of
diabetes like ketoacidosis, the condition is best managed by an
interprofessional team that includes the nurse practitioner, pharmacist,
primary care provider, and an endocrinologist; all these clinicians should
educate the patient on glucose control at every opportunity.
The diabetic nurse should follow all outpatients to ensure medication
compliance, followup with clinicians, and adopting a positive lifestyle.
Further, the nurse should teach the patient how to monitor home blood
glucose and the importance of careful monitoring of blood sugars during
infection, stress, or trauma. The physical therapist should be involved in
educating the patient on exercise and the importance of maintaining healthy
body weight.
The social worker should be involved to ensure that the patient has the
support services and financial assistance to undergo treatment. The members
of the interprofessional team should communicate to ensure that the patient
is receiving the optimal standard of care.

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