A 10-year-old girl with refractory epilepsy is being evaluated for surgical intervention. MRI brain shows focal cortical dysplasia in the left frontal lobe. Video-EEG telemetry confirms seizure onset from this region, with semiology consistent with left frontal focus. Neuropsychological testing shows verbal IQ of 95 and performance IQ of 88. Functional MRI indicates language dominance in the left hemisphere. What is the most critical additional investigation before considering surgical resection?
Q32
A 13-year-old boy with type 1 diabetes for 6 years is commenced on an ACE inhibitor for persistent microalbuminuria. Three months later, his blood tests show: sodium 138 mmol/L, potassium 5.8 mmol/L, urea 8.2 mmol/L, creatinine 95 μmol/L. He is asymptomatic and his blood pressure is 118/72 mmHg. ECG shows normal sinus rhythm with peaked T waves. What is the most appropriate immediate management?
Q33
A 7-year-old boy with focal epilepsy has been taking carbamazepine 200 mg twice daily for 14 months with good seizure control. He now presents with a 5-day history of fever, sore throat, and lethargy. Examination reveals cervical lymphadenopathy and pharyngeal erythema. Blood tests show: Hb 68 g/L, WBC 1.8 × 10⁹/L (neutrophils 0.4 × 10⁹/L), platelets 42 × 10⁹/L. What is the most likely diagnosis?
Q34
A 12-year-old girl with type 1 diabetes for 5 years presents with a 6-week history of intermittent abdominal pain, bloating, and alternating constipation and diarrhoea. She has lost 2 kg in weight. Her HbA1c is 68 mmol/mol (8.4%). Examination reveals mild abdominal distension but is otherwise unremarkable. Coeliac serology shows tissue transglutaminase IgA antibody titre of 85 U/mL (normal <20) and total IgA is normal. What is the most appropriate next investigation?
Q35
What is the typical EEG finding characteristic of juvenile myoclonic epilepsy?
Q36
A 5-year-old girl is brought to the emergency department having had a witnessed tonic-clonic seizure lasting 8 minutes at home. On arrival, she is still seizing. She has no previous history of epilepsy. Initial management with buccal midazolam 7.5 mg has been given by the paramedics 5 minutes ago. She is now 13 minutes into the seizure. What is the most appropriate immediate next step?
Q37
A 14-year-old boy with type 1 diabetes for 7 years attends for routine screening. Fundoscopy reveals multiple cotton wool spots and flame haemorrhages in both eyes with venous beading and intraretinal microvascular abnormalities. Visual acuity is 6/9 bilaterally. His HbA1c is 76 mmol/mol (9.1%) and blood pressure is 138/86 mmHg. What stage of diabetic retinopathy is present?
Q38
A 6-year-old girl with childhood absence epilepsy has been treated with ethosuximide 250 mg twice daily for 8 months with good seizure control. Her mother reports no seizures for the past 6 months. However, the child has now developed three generalized tonic-clonic seizures over the past month. EEG shows 3 Hz spike-and-wave discharges. What is the most appropriate management?
Q39
A 9-year-old boy with type 1 diabetes mellitus presents to clinic for his annual review. His mother reports he has been experiencing nocturnal sweating and occasional nightmares over the past 3 months. His HbA1c today is 42 mmol/mol (6.0%). His insulin regimen consists of insulin glargine 18 units once daily at bedtime and insulin aspart with meals. Blood glucose monitoring shows pre-breakfast readings between 4.2-5.8 mmol/L. What is the most appropriate initial management?
Q40
An 11-year-old girl with newly diagnosed type 1 diabetes is being commenced on a basal-bolus insulin regimen. Her parents are being educated about 'sick day rules' for managing intercurrent illness. Which of the following statements represents the most important principle in sick day management?
Chronic Paediatric Conditions UK Medical PG Practice Questions and MCQs
Question 31: A 10-year-old girl with refractory epilepsy is being evaluated for surgical intervention. MRI brain shows focal cortical dysplasia in the left frontal lobe. Video-EEG telemetry confirms seizure onset from this region, with semiology consistent with left frontal focus. Neuropsychological testing shows verbal IQ of 95 and performance IQ of 88. Functional MRI indicates language dominance in the left hemisphere. What is the most critical additional investigation before considering surgical resection?
A. Wada test (intracarotid amobarbital procedure) (Correct Answer)
B. Magnetoencephalography (MEG)
C. PET scan with fluorodeoxyglucose
D. Repeat MRI with higher resolution sequences
E. Single-photon emission computed tomography (SPECT)
Explanation: ***Wada test (intracarotid amobarbital procedure)***
- Given the **left frontal seizure focus** and confirmed **left hemisphere language dominance**, the **Wada test** is critical to precisely map **language and memory functions** relative to the planned resection area.
- It assesses the functional capacity of the **contralateral (right) hemisphere**, thereby predicting the risk of **post-operative aphasia** or memory deficits by temporarily inactivating one side.
*Magnetoencephalography (MEG)*
- **MEG** is a non-invasive technique that localizes the **epileptogenic zone** by mapping magnetic fields produced by neuronal activity, offering high spatial resolution.
- However, the **seizure focus** is already well-defined by **MRI** and **video-EEG**, and MEG does not assess the **functional risk to eloquent cortex** or the language/memory reserve.
*PET scan with fluorodeoxyglucose*
- **FDG-PET** is primarily used to identify areas of **interictal hypometabolism** to help localize the **epileptogenic zone**, especially in MRI-negative cases.
- In this patient, the **focal cortical dysplasia** is clearly visible on MRI and confirmed by video-EEG, so further metabolic localization isn't the most critical next step for surgical planning related to language.
*Repeat MRI with higher resolution sequences*
- A repeat **MRI** with higher resolution aims to provide more detailed **anatomical information** about the **focal cortical dysplasia** lesion.
- While useful for surgical planning, the fundamental lesion and its relationship to the seizure focus are already established, and this investigation does not address the crucial question of **functional language lateralization**.
*Single-photon emission computed tomography (SPECT)*
- **Ictal SPECT** is used to localize the **seizure onset zone** by detecting increased cerebral blood flow during a seizure, typically in cases where other localization methods are inconclusive.
- This study is primarily a **localization tool** and does not provide the necessary **functional assessment of language and memory lateralization** vital for safely operating on a dominant frontal lobe.
Question 32: A 13-year-old boy with type 1 diabetes for 6 years is commenced on an ACE inhibitor for persistent microalbuminuria. Three months later, his blood tests show: sodium 138 mmol/L, potassium 5.8 mmol/L, urea 8.2 mmol/L, creatinine 95 μmol/L. He is asymptomatic and his blood pressure is 118/72 mmHg. ECG shows normal sinus rhythm with peaked T waves. What is the most appropriate immediate management?
A. Stop ACE inhibitor and repeat electrolytes in 1 week (Correct Answer)
B. Continue ACE inhibitor and add calcium resonium
C. Continue ACE inhibitor and repeat electrolytes in 3 months
D. Stop ACE inhibitor and arrange urgent haemodialysis
E. Stop ACE inhibitor and administer IV calcium gluconate
Explanation: ***Stop ACE inhibitor and repeat electrolytes in 1 week***- This patient has developed **moderate hyperkalaemia** (K+ 5.8 mmol/L) following the initiation of an **ACE inhibitor**, which inhibits aldosterone-mediated potassium excretion.- Given the potassium level and the presence of **peaked T waves** on ECG, the most appropriate immediate action is to **withdraw the offending agent** and monitor for resolution within a week.*Continue ACE inhibitor and add calcium resonium*- Continuing the **ACE inhibitor** would perpetuate or worsen the hyperkalaemia, posing a significant cardiac risk.- **Calcium resonium** (a potassium binder) is not the first-line treatment for drug-induced hyperkalaemia where the causative agent can be easily removed.*Continue ACE inhibitor and repeat electrolytes in 3 months*- Waiting three months to recheck electrolytes is dangerously long as **hyperkalaemia** can rapidly progress to severe cardiac arrhythmias or arrest.- Any potassium level above the normal range, especially when associated with ECG changes, warrants prompt intervention and closer monitoring.*Stop ACE inhibitor and arrange urgent haemodialysis*- **Haemodialysis** is an extreme measure reserved for **severe, refractory hyperkalaemia** (typically >6.5-7.0 mmol/L) or patients with **end-stage renal disease**.- The patient's potassium level (5.8 mmol/L) and creatinine (95 μmol/L) do not indicate the severity that would necessitate urgent dialysis.*Stop ACE inhibitor and administer IV calcium gluconate*- **IV calcium gluconate** is primarily used for **severe hyperkalaemia** (typically K+ >6.5 mmol/L) or with more pronounced cardiac toxicity (e.g., QRS widening, absent P waves) to stabilize myocardial membranes.- While peaked T waves are present, the potassium level of 5.8 mmol/L is better managed initially by **removing the precipitating factor** rather than immediate membrane stabilization.
Question 33: A 7-year-old boy with focal epilepsy has been taking carbamazepine 200 mg twice daily for 14 months with good seizure control. He now presents with a 5-day history of fever, sore throat, and lethargy. Examination reveals cervical lymphadenopathy and pharyngeal erythema. Blood tests show: Hb 68 g/L, WBC 1.8 × 10⁹/L (neutrophils 0.4 × 10⁹/L), platelets 42 × 10⁹/L. What is the most likely diagnosis?
A. Infectious mononucleosis
B. Acute lymphoblastic leukaemia
C. Carbamazepine-induced aplastic anaemia (Correct Answer)
D. Viral-induced bone marrow suppression
E. Immune thrombocytopenic purpura
Explanation: ***Carbamazepine-induced aplastic anaemia*** - **Carbamazepine** is a known cause of idiosyncratic bone marrow suppression, leading to **pancytopenia** (low Hb, WBC, and platelets) which matches the patient's blood test results. - The fever and sore throat are symptoms of severe **neutropenia** (0.4 × 10⁹/L), making the patient highly susceptible to infections. *Infectious mononucleosis* - While presenting with fever, sore throat, and **lymphadenopathy**, it typically causes **lymphocytosis** and atypical lymphocytes, not severe pancytopenia. - **Splenomegaly** is a common finding in mononucleosis, which is not mentioned in this patient's presentation. *Acute lymphoblastic leukaemia* - Can cause **pancytopenia** due to bone marrow infiltration, but often presents with a high **WBC count** due to circulating blasts. - The strong temporal association with long-term **carbamazepine therapy** makes drug-induced bone marrow failure a more direct and likely cause. *Viral-induced bone marrow suppression* - Viral infections can cause transient marrow suppression, but the severe and global **pancytopenia** (Hb 68 g/L, severe neutropenia, severe thrombocytopenia) is more consistent with severe **aplastic anaemia**. - **Carbamazepine** is a well-documented cause of severe aplastic anaemia, which would be the primary concern given the drug history. *Immune thrombocytopenic purpura* - This condition is characterized by **isolated thrombocytopenia**, often presenting with bruising or bleeding. - The patient's significant **anemia** and severe **neutropenia** exclude isolated thrombocytopenia as the diagnosis.
Question 34: A 12-year-old girl with type 1 diabetes for 5 years presents with a 6-week history of intermittent abdominal pain, bloating, and alternating constipation and diarrhoea. She has lost 2 kg in weight. Her HbA1c is 68 mmol/mol (8.4%). Examination reveals mild abdominal distension but is otherwise unremarkable. Coeliac serology shows tissue transglutaminase IgA antibody titre of 85 U/mL (normal <20) and total IgA is normal. What is the most appropriate next investigation?
A. Upper gastrointestinal endoscopy with duodenal biopsies (Correct Answer)
B. Faecal elastase measurement
C. Small bowel MRI
D. Colonoscopy with biopsies
E. Trial of gluten-free diet for 6 weeks
Explanation: ***Upper gastrointestinal endoscopy with duodenal biopsies***
- Histological confirmation is required to diagnose **Coeliac disease** in this patient, as her **tissue transglutaminase (tTG) IgA** titre is elevated but less than 10 times the upper limit of normal.
- Biopsies typically reveal **villous atrophy**, **crypt hyperplasia**, and increased **intraepithelial lymphocytes**, which are necessary to confirm the diagnosis before lifelong dietary changes.
*Faecal elastase measurement*
- This test is used to assess **exocrine pancreatic insufficiency**, which is not the primary suspicion given the positive **tTG antibodies**.
- While diabetes can have pancreatic associations, the clinical presentation and serology point specifically toward **Coeliac disease**.
*Small bowel MRI*
- **MRI enterography** is useful for assessing transmural inflammation in **Crohn's disease** but is not a diagnostic tool for Coeliac disease.
- It cannot provide the **mucosal histology** required to identify the microscopic changes of gluten-sensitive enteropathy.
*Colonoscopy with biopsies*
- This procedure visualizes the large bowel and terminal ileum, whereas Coeliac disease primarily affects the **duodenum** and **proximal jejunum**.
- It would be more appropriate if **Inflammatory Bowel Disease (IBD)** was the leading differential, but the serology here indicates a small bowel pathology.
*Trial of gluten-free diet for 6 weeks*
- A **gluten-free diet** should never be started before a definitive biopsy is performed, as it can lead to **mucosal healing** and false-negative results.
- Diagnostic guidelines require the patient to remain on a **gluten-containing diet** until all diagnostic investigations are complete.
Question 35: What is the typical EEG finding characteristic of juvenile myoclonic epilepsy?
A. 3 Hz spike-and-wave discharges
B. 4-6 Hz polyspike-and-wave discharges (Correct Answer)
C. Hypsarrhythmia
D. Centrotemporal spikes
E. Periodic lateralized epileptiform discharges
Explanation: ***4-6 Hz polyspike-and-wave discharges***- This generalized pattern is the hallmark of **Juvenile Myoclonic Epilepsy (JME)** and is often precipitated by **photic stimulation** or sleep deprivation.- The pattern correlates with clinical **myoclonic jerks** that typically occur shortly after awakening in adolescent patients.*3 Hz spike-and-wave discharges*- This finding is classic for **Childhood Absence Epilepsy**, which typically presents with brief staring spells rather than myoclonic jerks.- The frequency in JME is characteristically faster (**greater than 3 Hz**) and involves multiple spikes (polyspikes).*Hypsarrhythmia*- This chaotic, high-voltage pattern with multifocal spikes is diagnostic of **West Syndrome** (infantile spasms), which occurs in infants.- It is a much more disorganized background compared to the discrete discharges seen in **JME**.*Centrotemporal spikes*- These are characteristic of **Self-limited Epilepsy with Centrotemporal Spikes** (formerly Benign Rolandic Epilepsy), which presents in childhood.- These discharges are **focal** rather than generalized and are typically activated during sleep.*Periodic lateralized epileptiform discharges*- Also known as **PLEDs**, these suggest an acute focal structural brain injury such as **herpes simplex encephalitis** or a stroke.- They represent a localized cortical irritability rather than the **idiopathic generalized epilepsy** syndrome seen in JME.
Question 36: A 5-year-old girl is brought to the emergency department having had a witnessed tonic-clonic seizure lasting 8 minutes at home. On arrival, she is still seizing. She has no previous history of epilepsy. Initial management with buccal midazolam 7.5 mg has been given by the paramedics 5 minutes ago. She is now 13 minutes into the seizure. What is the most appropriate immediate next step?
A. Administer rectal diazepam 10 mg
B. Administer intravenous lorazepam 0.1 mg/kg (Correct Answer)
C. Administer intravenous phenytoin 20 mg/kg
D. Administer intravenous phenobarbital 20 mg/kg
E. Prepare for rapid sequence intubation
Explanation: ***Administer intravenous lorazepam 0.1 mg/kg***
- According to **APLS guidelines**, if a seizure continues 5–10 minutes after a first dose of a **benzodiazepine** (like buccal midazolam), a second dose should be administered using **IV lorazepam** if access is available.
- This patient is in **established status epilepticus** (seizure > 5 minutes) and requires the most effective and rapid-acting intravenous benzodiazepine to terminate the activity.
*Administer rectal diazepam 10 mg*
- **Rectal diazepam** is an alternative first or second-line treatment only if **intravenous access** cannot be established or in a community setting.
- Since the patient is in the **Emergency Department**, intravenous access should be prioritized to deliver more reliable titration of medication.
*Administer intravenous phenytoin 20 mg/kg*
- **Phenytoin** is considered a **second-stage/third-line agent** used for refractory status epilepticus after two doses of benzodiazepines have failed.
- Administering this now would be premature as the **benzodiazepine algorithm** has not yet been completed (only one dose given so far).
*Administer intravenous phenobarbital 20 mg/kg*
- **Phenobarbital** is typically reserved for **refractory status epilepticus** or specific scenarios like neonatal seizures.
- It is not the immediate next step after a single failed dose of **buccal midazolam** in a 5-year-old following standard protocols.
*Prepare for rapid sequence intubation*
- **Rapid sequence intubation (RSI)** is indicated in the **refractory stage** of status epilepticus if the seizure lasts beyond 30-60 minutes or if there is respiratory failure.
- At 13 minutes, the priority remains pharmacological termination of the seizure with **benzodiazepines** followed by anticonvulsant infusions before moving to anesthesia.
Question 37: A 14-year-old boy with type 1 diabetes for 7 years attends for routine screening. Fundoscopy reveals multiple cotton wool spots and flame haemorrhages in both eyes with venous beading and intraretinal microvascular abnormalities. Visual acuity is 6/9 bilaterally. His HbA1c is 76 mmol/mol (9.1%) and blood pressure is 138/86 mmHg. What stage of diabetic retinopathy is present?
A. Background diabetic retinopathy
B. Mild non-proliferative diabetic retinopathy
C. Moderate non-proliferative diabetic retinopathy
D. Severe non-proliferative diabetic retinopathy (Correct Answer)
E. Proliferative diabetic retinopathy
Explanation: ***Severe non-proliferative diabetic retinopathy***
- The presence of **venous beading** and **intraretinal microvascular abnormalities (IRMA)** in the fundoscopy findings are hallmarks of severe non-proliferative diabetic retinopathy.
- These specific signs, along with **cotton wool spots** and **flame hemorrhages**, indicate significant retinal ischemia and fulfill the criteria of the **4-2-1 rule** for high-risk progression.
*Background diabetic retinopathy*
- This stage typically only includes **microaneurysms** and occasional **dot/blot hemorrhages**.
- It lacks the more advanced signs of retinal ischemia such as **venous beading**, **IRMA**, or **cotton wool spots**.
*Mild non-proliferative diabetic retinopathy*
- Characterized by the presence of at least one **microaneurysm** and potentially some dot/blot hemorrhages.
- This stage does not feature the widespread **microvascular abnormalities** or **venous beading** observed in the patient.
*Moderate non-proliferative diabetic retinopathy*
- This stage includes more extensive **hemorrhages** and **microaneurysms** than mild NPDR, and may have **cotton wool spots**.
- However, it does not meet the specific criteria of the **4-2-1 rule**, such as **venous beading** in two or more quadrants or **IRMA** in at least one quadrant, which are present here.
*Proliferative diabetic retinopathy*
- The defining feature of this stage is the presence of **neovascularization** (new vessel growth) on the retina or optic disc, or **vitreous hemorrhage**.
- While the patient has severe ischemia, the absence of **new vessel formation** means the disease has not yet progressed to the proliferative stage.
Question 38: A 6-year-old girl with childhood absence epilepsy has been treated with ethosuximide 250 mg twice daily for 8 months with good seizure control. Her mother reports no seizures for the past 6 months. However, the child has now developed three generalized tonic-clonic seizures over the past month. EEG shows 3 Hz spike-and-wave discharges. What is the most appropriate management?
A. Continue ethosuximide and add lamotrigine
B. Switch from ethosuximide to carbamazepine
C. Continue ethosuximide and add phenytoin
D. Switch from ethosuximide to sodium valproate (Correct Answer)
E. Increase the dose of ethosuximide
Explanation: ***Switch from ethosuximide to sodium valproate***
- **Ethosuximide** is a narrow-spectrum anticonvulsant effective only for **absence seizures** and provides no protection against **generalized tonic-clonic seizures (GTCS)**.
- **Sodium valproate** is a **broad-spectrum anticonvulsant** and the drug of choice for patients presenting with both **absence seizures** and **GTCS**, as it effectively treats both seizure types.
*Continue ethosuximide and add lamotrigine*
- While **lamotrigine** has activity against both seizure types, **sodium valproate** is generally considered first-line for mixed absence and GTCS, prioritizing **monotherapy** over polytherapy.
- Using multiple antiepileptic drugs increases the risk of **drug-drug interactions** and adverse side effects in a pediatric patient.
*Switch from ethosuximide to carbamazepine*
- **Carbamazepine** is contraindicated in primary generalized epilepsies, as it can **exacerbate absence seizures** and worsen the characteristic **3 Hz spike-and-wave discharges** on EEG.
- It is primarily used for **focal seizures** and is unsuitable for generalized epilepsy syndromes like childhood absence epilepsy.
*Continue ethosuximide and add phenytoin*
- **Phenytoin**, similar to carbamazepine, can **aggravate absence seizures** and is not indicated for the management of generalized pediatric epilepsy syndromes.
- It also carries a significant side-effect profile, including **gingival hyperplasia** and hirsutism, making it an unfavorable choice for a young girl.
*Increase the dose of ethosuximide*
- Increasing the dose of **ethosuximide** will not address the new **generalized tonic-clonic seizures**, as its mechanism of action is specific to **T-type calcium channels** relevant only to absence pathology.
- The patient's absence seizures are already well-controlled; the clinical problem is the development of a **new seizure type** requiring broad-spectrum coverage.
Question 39: A 9-year-old boy with type 1 diabetes mellitus presents to clinic for his annual review. His mother reports he has been experiencing nocturnal sweating and occasional nightmares over the past 3 months. His HbA1c today is 42 mmol/mol (6.0%). His insulin regimen consists of insulin glargine 18 units once daily at bedtime and insulin aspart with meals. Blood glucose monitoring shows pre-breakfast readings between 4.2-5.8 mmol/L. What is the most appropriate initial management?
A. Reassure that nocturnal symptoms are normal at this age
B. Reduce the dose of bedtime insulin glargine
C. Increase the dose of bedtime insulin glargine
D. Perform 3am blood glucose monitoring (Correct Answer)
E. Switch from insulin glargine to NPH insulin
Explanation: ***Perform 3am blood glucose monitoring***
- The patient presents with symptoms highly suggestive of **nocturnal hypoglycemia** (sweating, nightmares) followed by a potential **Somogyi effect** (rebound glucose response).
- Monitoring glucose at **3 AM** is the critical first step to differentiate between the **Somogyi effect** and the **Dawn phenomenon** before making treatment adjustments.
*Reassure that nocturnal symptoms are normal at this age*
- Symptoms like **nocturnal sweating** and **nightmares** in a patient with **Type 1 Diabetes** should never be dismissed as normal variation.
- These are classic clinical signals of **counter-regulatory hormone** release in response to low blood sugar during sleep.
*Reduce the dose of bedtime insulin glargine*
- While reducing the **basal insulin** may ultimately be the treatment, it should not be done without **biochemical confirmation** of hypoglycemia.
- Making dosage changes based solely on subjective symptoms without **3 AM glucose data** may lead to suboptimal glycemic control.
*Increase the dose of bedtime insulin glargine*
- Increasing the **insulin glargine** dose is dangerous as it would significantly worsen the risk of **severe nocturnal hypoglycemia** and potential seizures.
- This action is only appropriate for the **Dawn phenomenon**, which must first be distinguished from the Somogyi effect via monitoring.
*Switch from insulin glargine to NPH insulin*
- **NPH insulin** has a more pronounced peak than **insulin glargine**, which often actually increases the risk of **nocturnal hypoglycemia**.
- Switching to a less stable basal insulin would be counterproductive and does not address the immediate need for **diagnostic clarity**.
Question 40: An 11-year-old girl with newly diagnosed type 1 diabetes is being commenced on a basal-bolus insulin regimen. Her parents are being educated about 'sick day rules' for managing intercurrent illness. Which of the following statements represents the most important principle in sick day management?
A. Stop all insulin during illness to prevent hypoglycaemia from reduced oral intake
B. Double all insulin doses during illness due to insulin resistance
C. Continue basal insulin at usual doses and adjust rapid-acting insulin based on blood glucose and ketone monitoring (Correct Answer)
D. Switch to a sliding scale insulin regimen during any intercurrent illness
E. Reduce basal insulin by 50% and give rapid-acting insulin only if blood glucose exceeds 15 mmol/L
Explanation: ***Continue basal insulin at usual doses and adjust rapid-acting insulin based on blood glucose and ketone monitoring***
- Insulin should **never be stopped** during illness even if oral intake is reduced, as stress hormones increase insulin resistance and stimulate **ketogenesis**.
- Maintaining **basal insulin** prevents metabolic decompensation, while frequent monitoring of blood glucose and **ketones** allows for safe, reactive dosing of rapid-acting insulin.
*Stop all insulin during illness to prevent hypoglycaemia from reduced oral intake*
- This is a dangerous misconception; stopping insulin can rapidly precipitate **Diabetic Ketoacidosis (DKA)** due to lack of suppression of fatty acid oxidation.
- Regardless of food intake, the body requires **basal insulin** to manage hepatic glucose production and prevent **ketone** buildup during stress.
*Double all insulin doses during illness due to insulin resistance*
- Indiscriminately doubling doses creates a significant risk of **hypoglycaemia**, as insulin requirements vary widely depending on the severity and type of illness.
- Dose adjustments must be tailored based on real-time **blood glucose** levels and the presence of **ketones** rather than a fixed multiplier.
*Switch to a sliding scale insulin regimen during any intercurrent illness*
- **Sliding scale** regimens are less effective than basal-bolus methods for maintaining stable glycemic control and are typically reserved for **inpatient settings**.
- Outpatient management focuses on preserving the physiological **basal-bolus** foundation while providing supplemental "correction" doses as needed.
*Reduce basal insulin by 50% and give rapid-acting insulin only if blood glucose exceeds 15 mmol/L*
- Reducing basal insulin significantly increases the risk of **ketosis**, even if blood glucose levels do not appear excessively high.
- Waiting until glucose reaches **15 mmol/L** is often too late to prevent metabolic distress; frequent proactive monitoring is the gold standard of **sick day management**.
