Case Study

🧠 CLINICAL REASONING CYCLE: Sarah’s DKA Case Study

1⃣ CONSIDER THE PATIENT:

Sarah is a normally healthy 3.5-year-old who is now lethargic, dehydrated, has ketonuria, glucosuria, very high BSL (43.4 mmol/L), low BP, fever (38.5°C), and tachycardia.
Out of character behavior: lethargy, quietness.

2⃣ COLLECT CUES:

✅ Vital signs:

  • HR 125 (tachycardia)

  • RR 32 (tachypnoea)

  • BP 80/45 (hypotension)

  • Temp 38.5°C (fever)

  • SpO2 91% (mild hypoxia)

✅ Urine dipstick:

  • Ketonuria (ketones)

  • Glucosuria (glucose)

  • WBCs and protein present → infection possible

✅ Other:

  • Vomiting, abdominal pain, bedwetting, high fluid intake but dehydrated

✅ Bloods planned:

  • FBE, UECr, VBG, blood cultures

3⃣ INTERPRET INFORMATION:

✅ Most likely diagnosis:

  • Diabetic Ketoacidosis (DKA) likely secondary to new-onset Type 1 Diabetes Mellitus.

  • Infection (suggested by fever, WBCs in urine) may be a precipitating factor.

✅ Key problems:

  • Severe hyperglycaemia

  • Dehydration and electrolyte imbalances

  • Metabolic acidosis (due to ketones)

  • Risk of cerebral oedema (due to fluid shifts during treatment)

4⃣ Answering Specific Questions

🔵 What is the definition and pathophysiology of DKA?

✅

  • Definition: DKA is a life-threatening complication of diabetes caused by absolute insulin deficiency → high blood sugar, ketone production, and acidosis.

  • Pathophysiology:

    • No insulin → glucose can't enter cells → body burns fat for energy → fat breakdown produces ketones → ketones cause acidosis.

    • High glucose also causes osmotic diuresis → dehydration, electrolyte loss (potassium).

Rationale:

Insulin deficiency + stress = hyperglycaemia + ketone overproduction.

🔵 Why might Sarah have been at risk for developing DKA and why are paediatric patients more at risk?

✅

  • Sarah likely has new-onset Type 1 Diabetes (undiagnosed until now).

  • Fever and infection can worsen DKA development.

  • Children are more at risk because:

    • Higher metabolic rates

    • Faster dehydration

    • Harder to detect early symptoms

    • Smaller fluid reserves

🔵 Signs and Symptoms of DKA and why they occur:

✅

Sign/Symptom

Why It Happens

Polyuria, polydipsia

Osmotic diuresis from hyperglycaemia

Dehydration

Excessive urine loss

Vomiting, abdominal pain

Ketone irritation of GI tract

Kussmaul breathing (fast RR)

Body compensates for metabolic acidosis

Lethargy, confusion

Poor brain perfusion, acidosis

Fruity breath smell

Acetone (ketone) breath

Tachycardia, hypotension

Dehydration, low blood volume

🔵 Treatment Options for DKA

✅

  • IV fluids (0.9% NaCl) to correct dehydration

  • Insulin infusion (Actrapid) to reduce blood glucose and stop ketone production

  • Electrolyte replacement (especially potassium)

  • Antibiotics if infection is confirmed

  • Monitor blood glucose, ketones, electrolytes hourly

  • Supplemental oxygen for hypoxia

🔵 Nursing Care and Management for DKA

✅

  • Monitor vital signs closely (HR, BP, RR, SpO₂, temperature)

  • Cardiac monitoring (risk of arrhythmias due to potassium shifts)

  • Strict input/output monitoring (urine output)

  • Hourly blood glucose and ketone checks

  • Neurological assessments (for signs of cerebral oedema)

  • Maintain NBM until stable

  • Patient and family education

🔵 If Sarah develops cerebral oedema, what signs and symptoms would you expect to see and why do they occur?

✅
Signs/Symptoms of cerebral oedema:

  • Headache

  • Vomiting

  • Decreased level of consciousness (confusion, drowsiness)

  • Seizures

  • Unequal or sluggish pupils

  • Bradycardia and hypertension (late signs)

Why?

  • Rapid fluid shifts and correcting hyperglycaemia too fast → water enters brain cells → swelling.

✅ How can nurses prevent this?

  • Slow correction of blood glucose and fluid resuscitation

  • Monitor neuro observations closely

  • Immediate action if any signs appear

5⃣ Five Priority Nursing Problems (with Goals, Actions, Outcomes)

Problem

Goal

Actions

Outcome

Dehydration

Restore fluid balance

Start IV fluids, monitor input/output

Improved BP, HR, urine output

Hyperglycaemia

Reduce blood glucose safely

Start insulin infusion, monitor BSL hourly

Gradual decrease in BSL

Acidosis and Ketosis

Correct acid-base imbalance

Monitor VBGs, continue insulin therapy

Normal pH, reduced ketones

Risk of cerebral oedema

Prevent brain swelling

Careful fluid replacement, neuro checks

No signs of neurological decline

Risk of electrolyte imbalance

Maintain normal electrolytes

Monitor potassium, replace as needed

Normal electrolyte levels, no arrhythmias

6⃣ REFLECTION:

✅ What went well:

  • Early recognition of DKA signs (polyuria, vomiting, lethargy) and vital sign abnormalities.

✅ What could be improved:

  • Education for families on early signs of diabetes (polyuria, thirst, weight loss) to seek help sooner.

✅ What I learned:

  • In paediatric DKA, slow correction is vital to avoid cerebral oedema.

  • Hourly monitoring and teamwork (medical, nursing, pharmacy) is critical.

🏥 Quick Summary

  • Sarah likely has new-onset Type 1 Diabetes presenting with DKA.

  • Main priorities are rehydration, glucose control, electrolyte management, and monitoring for cerebral oedema.

  • Nursing vigilance can prevent life-threatening complications.