Diabetic ketoacidosis

Learning objectives

1. Define DKA and understand its pathophysiology.

2. Identify the common causes and risk factors.

3. Recognize clinical presentation and diagnostic criteria.

4. Outline the principles of emergency management.

5. Understand potential complications and preventive strategies.

Diabetic ketoacidosis (DKA) is a serious, acute metabolic
complication of diabetes, resulting from absolute insulin deficiency. It is
a medical emergency with potential complications such as
hypoglycaemia, hypokalaemia, pulmonary oedema, acute respiratory
distress syndrome, and cerebral oedema. Despite decreased mortality
rates in the UK over the past two decades, a single episode of DKA still
carries a 5% risk of death, which increases to around 25% in those with
recurrent episodes, especially in low- and middle-income countries.

The Gaza war has caused a catastrophic collapse of healthcare

systems, leaving diabetes patients without life-saving insulin,
monitoring tools, or functional cold chains for medication storage.

In Gaza, the combination of severe physical trauma, psychological

stress, and forced reliance on high-carbohydrate aid rations has led to
uncontrollable glucose levels and a surge in fatal complications
(AlSamhori et al., 2025.

Death usually results from the underlying trigger rather than the
metabolic imbalance itself. DKA is most often seen in individuals with
type 1 diabetes and may even be the first sign of the disease. It can
also occur in type 2 diabetes, particularly in those with long-standing
disease, significant β-cell dysfunction, or those misclassified as type 2
instead of type 1. In known diabetics, DKA is often triggered by illness
or physiological stress, with infections like pneumonia and urinary tract
infections being common causes, along with myocardial infarction,
stroke, and pancreatitis. Other triggers include surgery, trauma,
pregnancy, or insulin deficiency due to discontinuation, administration
errors, or insulin delivery failures. A patient’s medication or drug
history may reveal factors like glucocorticoid use, SGLT2 inhibitors, or
cocaine, which are linked to DKA. In younger individuals with repeated
DKA episodes, psychological issues or deliberate insulin omission are
frequent underlying causes.

Pathophysiology

DKA results from relative or absolute insulin deficiency combined with

counterregulatory hormone excess (gglucagon, catecholamines,
cortisol, and growth hormone). Both insulin deficiency and glucagon
excess, in particular, are necessary for DKA to develop. The decreased
ratio of insulin to glucagon promotes gluconeogenesis, glycogenolysis,
and ketone body formation in the liver, as well as increases in
substrate delivery from fat and muscle (free fatty acids, amino acids)
to the liver. Ketosis results from a marked increase in free fatty acid
release from adipocytes, with a resulting shift toward ketone body
synthesis in the liver. Reduced insulin levels, in combination with
elevations in catecholamines and growth hormone, also increase
lipolysis and the release of free fatty acids. Markers of inflammation
(cytokines, C-reactive protein) are elevated in both DKA and HHS.
Clinical features of diabetic kketoacidosis

Laboratory Abnormalities and Diagnosis

Core Diagnostic Features

DKA is primarily defined by a triad of metabolic disturbances:

 Hyperglycemia: Serum glucose usually >13.9 mmol/L (250

mg/dL).

Note: “Euglycemic DKA” (normal glucose) can occur, particularly in

patients taking SGLT2 inhibitors.

 Ketosis: Presence of serum ketones. While nitroprusside tests

primarily detect acetoacetate, \beta-hydroxybutyrate assays are
preferred for accuracy.
 Metabolic Acidosis: Serum bicarbonate <15–18 mmol/L with an
increased anion gap and an arterial pH typically between 6.8 and
7.3.

Electrolyte and Lab

The text highlights a discrepancy between serum levels and actual

body stores:
Potassium: Total-body stores are depleted, yet serum levels may
appear falsely elevated due to acidosis and dehydration.

Sodium: Serum sodium is typically low due to hyperglycemia. You can

calculate the “corrected” sodium by adding 1.6 mmol/L for every 5.6
mmol/L (100 mg/dL) increase in glucose. A “normal” sodium reading
actually suggests severe dehydration.

Kidney Function: Elevated BUN and creatinine reflect significant

volume depletion.

Pancreatitis Mimicry: Elevated amylase is common but often

originates from salivary glands; serum lipase is necessary to confirm
actual pancreatitis.

Key Clinical Considerations

 Ketonemia is the defining factor that distinguishes DKA from

simple hyperglycemia.
 False Positives: Medications like captopril or penicillamine can
cause false-positive urine ketone results.
 Differential Diagnosis: Clinicians must rule out starvation ketosis,
alcoholic ketoacidosis (where bicarbonate is usually higher), and
other anion-gap acidoses

Electrocardiograph (ECG)

Perform an early ECG to look for T-wave changes as a first indicator of

hyperkalaemia (tall and peaked) or hypokalaemia (flat or inverted), or
a clinically silent myocardial infarction (Ml) as a precipitant of HHS or
DKA.

Severity Classification of DKA

Parameter Mild Moderate Severe
Arterial pH 7.25–7.30 7.00–7.24 < 7.00
Serum Bicarbonate 15–18 mEq/L 10 to <15 mEq/L < 10 mEq/L
Anion Gap > 10 mEq/L > 12 mEq/L > 12 mEq/L
Mental Status Alert Alert/Drowsy Stupor/Coma
Plasma Glucose Usually >250 mg/dL Usually >250 mg/dL Usually >250 mg/dL
Serum Ketones Positive Positive Positive
Core Management Objectives
DKA is a medical emergency requiring hospitalization (ideally in a high-dependency
unit). The primary goals are:

 Restore Volume: Correct circulating fluid deficits.

 Balance Electrolytes: Replace lost minerals, particularly
potassium.
 Stop Ketogenesis: Use insulin to halt lipolysis and the
production of ketones.
 Address Triggers: Identify and treat the underlying cause while
preventing further complications.

The Three Pillars of Treatment

Management relies on evidence-based protocols centered on:

1. Intravenous Insulin.
2. Intravenous Fluids.
3. Potassium Replacement.

1. Fluid Replacement
The priority is restoring circulating volume using isotonic saline (0.9% NaCl).

 Initial Action: Commenced immediately upon diagnosis. If

systolic BP is <90 mmHg, a rapid bolus (10–15 mins) is required.
 Special Populations: Use a cautious approach for young adults,
elderly, pregnant patients, or those with heart/kidney failure.
 Transition to Glucose: When blood glucose falls below 14
mmol/L (252 mg/dL), introduce 10% glucose alongside the
0.9% saline. This prevents hypoglycemia while insulin continues
to suppress ketosis.

2. Insulin Replacement
An intravenous insulin infusion should be started within 60min of the patient’s arrival in
the ED.

Management relies on a Fixed-Rate Intravenous Insulin Infusion (FRIII).

 Dose: Typically 0.1 U/kg/hr.

  Monitoring: Blood ketones must be checked hourly. The goal is
a decrease of at least 0.5 mmol/L/hr. If this target isn't met,
increase the insulin rate.
 Long-acting Insulin: Continue the patient's usual subcutaneous
long-acting insulin during the IV infusion to prevent "rebound"
hyperglycemia when the IV is eventually stopped.
 Resolution Criteria: DKA is resolved when:
o Blood ketones <0.6 mmol/L
o Bicarbonate >15 mmol/L
o Venous pH >7.3

NURSING ALERT When mixing the insulin drip, it is important To

flush the insulin solution through the entire IV infusion set and to
Discard the first 50 mL of fluid. Insulin molecules adhere to the Inner
surface of IV infusion sets; thus, the initial fluid may contain a
Decreased concentration of insulin.

3. Potassium & Electrolytes

Potassium levels can fluctuate dangerously during treatment.

 Initial Step: Usually not added to the first liter of fluid.

 Replacement Protocol:
o K > 5.5 mmol/L: No potassium added.
o K 3.5 – 5.5 mmol/L: Add 40 mmol/L of potassium
chloride to fluids.
o K < 3.5 mmol/L: High risk. Start cardiac monitoring and
involve critical care; aggressive replacement is needed.

NEVER START INSULIN if serum potassium is < 3.3 mEq/L.

Insulin will shift potassium into cells, potentially causing fatal
arrhythmias or cardiac arrest.

NURSING ALERT Because the patient’s serum potassium level May

drop quickly due to rehydration and insulin treatment, potas- ! sium
replacement must begin once potassium levels drop to normal.

 Bicarbonate/Phosphate: Generally not recommended.

Bicarbonate is only considered if pH < 6.9, as it can
paradoxically worsen CSF acidosis and lead to cerebral edema.

4. Ongoing Management & Transition

 Switching to Subcutaneous (SC) Insulin: Only once the
patient is biochemically stable and eating/drinking.
DO NOT STOP THE IV INSULIN DRIP immediately after giving
the first dose of subcutaneous (SC) insulin. The IV infusion
must overlap with the SC dose for 30 to 60 minutes to prevent
a “gap” that could trigger a DKA relapse

 The Overlap Rule: Continue the IV insulin infusion for 30

minutes after the first SC mealtime insulin dose to ensure
coverage.
 Discharge & Prevention: * Review precipitating causes
(injection technique, pump failure, etc.).
o Provide "sick day rules," a blood ketone meter, and contact
info for the specialist team.
o Address psychological support if needed.
*Choice of Fluid in DKA – Summary:*
- No strong evidence favors one crystalloid over another.
- Normal saline (0.9% NaCl) is widely used despite risk of
hyperchloraemic acidosis.
- That acidosis risk is not considered clinically significant.
- Colloids are not recommended — they are less
physiological for replacing electrolyte losses.
Why Hartmann’s solution is controversial compared to Normal Saline in
DKA management?

The Controversy: Normal Saline vs. Hartmann’s

Hartmann’s Solution (Ringer's
Feature Normal Saline (0.9% NaCl)
Lactate)
Chloride High (154 mmol/L) — Much higher Physiological (109 mmol/L) —
Content than human blood (~100 mmol/L). Closely mimics human plasma.
Can cause Hyperchloremic Metabolic Potential (though rare) concern about
Risk
Acidosis. lactate metabolism.
Complex; adding Potassium is
Very Easy to add Potassium (KCl)
Ease of Use technically more difficult in some
supplements.
settings.
Current Standard of care in most Used by some centers to speed up
Status UK/International guidelines. "Anion Gap" closure.

1. The Problem with Normal Saline: Hyperchloremia

Normal Saline contains a high concentration of chloride. When given in the large
volumes required for DKA (3–6 liters), the excess chloride can cause a specific type of
acidosis called Hyperchloremic Acidosis.

 The Confusion: This can make it look like the DKA isn't
improving because the "Bicarbonate" stays low, even though the
"Ketones" are gone.
 The Solution: Measuring the Anion Gap or Chloride levels
helps distinguish if the lingering acidosis is from DKA or just from
the saline.
2. The Benefit of Hartmann’s Solution

Because Hartmann’s has a chloride level closer to human blood, patients often see a
faster normalization of their pH and bicarbonate levels. It avoids the "chloride overload"
seen with Normal Saline.

3. Why isn't Hartmann’s the Universal Gold Standard?

 Potassium Mixing: In many hospitals, "pre-mixed" bags of

Normal Saline with 20mEq or 40mEq of Potassium are standard.
Hartmann’s often requires manual addition of Potassium, which
increases the risk of medication errors.
 Compatibility: Some medications or high-dose potassium
infusions are less stable in the calcium-containing environment of
Hartmann's.

CLINICAL SUMMARY

If you see a patient whose Anion Gap has closed (meaning the ketones are gone) but
their Bicarbonate is still low, they likely have Hyperchloremic Acidosis from the
saline. At this stage, clinical indices of recovery are usually reassuring, and the kidneys
will eventually excrete the excess chloride.

DKA Management: Pitfalls and Difficult Situations

1. Diagnostic & Laboratory Pitfalls

Atypical Glucose: Plasma glucose is not always high, especially in

patients with significant vomiting or those with “Euglycemic DKA.”

Pseudo-Infection: A high White Cell Count (WCC) is common due to

stress/acidosis and does not always indicate an infection.

False Creatinine Elevation: Ketonemia can interfere with lab assays,

leading to falsely high creatinine levels.

Amylase vs. Pancreatitis: Amylase can be raised up to 10x with

abdominal pain without actual pancreatitis. If suspected, confirm with
Serum Lipase or imaging (US/CT).

Ketones vs. DKA: Ketonuria does not always mean DKA; in patients with
normal glucose, consider Alcoholic Ketoacidosis.
Sodium Fluctuations: Both hyponatremia and hypernatremia are
frequently encountered.

2. Fluid & Acid-Base Challenges

Bicarbonate Danger: Avoid bicarbonate therapy even if pH < 7.0. It

risks:

Severe sodium overload.

Paradoxical intracellular acidosis.

Cerebral Edema (due to respiratory depression from CSF alkalosis).

Note: It may only be considered in specific “Normal Anion Gap” cases

with senior consultation.

Hyperchloremic Acidosis: Aggressive resuscitation with 0.9% Saline

often causes high chloride levels 12–24 hours later. This keeps the
bicarbonate low even when the patient is recovering.

Saline vs. Hartmann’s: Hartmann’s solution may prevent

hyperchloremic acidosis but is not the standard in some guidelines (like
the UK) due to the complexity of adding potassium.

3. Respiratory & Monitoring Pitfalls

Mechanical Ventilation: If ventilation is necessary, the machine must

hyperventilate aggressively to maintain the patient’s physiological
compensation for metabolic acidosis. Monitor via ABGs closely.

Patient Comfort: Repeated Arterial Blood Gases (ABGs) are painful.

Venous Blood Gases (VBGs) are usually sufficient for monitoring and
improve the patient experience.

4. Electrolyte Issues

Hypomagnesemia: Commonly occurs during fluid and insulin therapy. It

is rarely severe and often resolves spontaneously once the patient
resumes eating and drinking.

Nursing Interventions for DKA:-

1. Fluid & Electrolyte Management

 Monitor Balance: Track strict intake and output (I&O) and
encourage oral fluids when safe.
  Administer Therapy: Give IV fluids and electrolytes exactly as
prescribed.
 Lab Surveillance: Closely monitor serum electrolytes, focusing
heavily on sodium and potassium levels.
 Frequent Assessment: Check vital signs hourly for dehydration
(tachycardia, hypotension) and assess breath sounds, mental
status, and cardiac rhythm (ECG).
2. Monitoring & Managing Complications
 Fluid Overload: Watch for signs of volume excess (edema,
crackles in lungs, venous distention) through frequent
hemodynamics and physical exams.
 Hypokalemia: Ensure adequate renal function before giving
potassium; monitor ECG and potassium levels continuously to
prevent cardiac arrhythmias.
 Cerebral Edema: Ensure a gradual decline in blood glucose;
use hourly flow sheets to track neurologic status and minimize
activities that increase intracranial pressure.
3. Diabetes Knowledge & Education
 Assess Adherence: Evaluate the patient’s understanding of
their current management plan and identify what triggered
the DKA (stress, illness, or omission of insulin).
 Address Barriers: Explore why medications might have been
missed (e.g., social or financial factors) to prevent future
readmissions.
 Survival Skills: Reteach core skills if forgotten, including how
to manage “sick days” and recognizing early DKA symptoms.
4. Teaching Self-Care & Follow-up
 Core Training: Teach diet, insulin administration, glucose
monitoring, and urine ketone testing.
 Prevention: Link specific lifestyle factors to DKA prevention
and emphasize the importance of blood glucose control.
 Continuity of Care: Arrange referrals to home health,
dietitians, or diabetes centers, and stress the importance of
attending follow-up appointments