Chronic Paediatric Conditions — MCQs
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A 11-year-old boy with type 1 diabetes for 4 years presents to clinic. His insulin doses have remained stable over the past 6 months despite normal growth velocity. His HbA1c has improved from 72 mmol/mol to 54 mmol/mol. His mother reports he has had no hypoglycaemic episodes. On examination, he appears well with normal vital signs. Urinalysis shows glucose +++. What is the most likely explanation for his improved HbA1c?
A 8-year-old girl presents with episodes where she suddenly stops activity, drops objects from her hands, and appears briefly dazed for about 10 seconds before resuming normal activity with no recollection of the event. These occur multiple times daily. Her teacher reports she seems to be daydreaming frequently. An EEG is performed during hyperventilation. What is the most likely EEG finding?
A 13-year-old boy with type 1 diabetes presents with a 4-week history of persistent tingling and numbness in both feet, which is worse at night. On examination, he has reduced sensation to light touch and pinprick in a stocking distribution, and absent ankle reflexes. His recent HbA1c is 89 mmol/mol. What is the most likely diagnosis?
A 7-year-old boy with focal epilepsy has been seizure-free for 18 months on lamotrigine monotherapy. His parents enquire about stopping the medication. His EEG 6 months ago showed persistent focal epileptiform discharges. His neurological examination is normal and he has no learning difficulties. What advice should be given regarding antiepileptic drug withdrawal?
A 10-year-old girl with type 1 diabetes mellitus is found to have an albumin:creatinine ratio (ACR) of 3.8 mg/mmol on routine screening. A repeat sample 3 months later shows ACR of 4.2 mg/mmol, and a third sample confirms ACR of 4.5 mg/mmol. Her blood pressure is on the 60th centile for age. Her HbA1c is 68 mmol/mol. What is the most appropriate management?
A 14-year-old girl with type 1 diabetes for 6 years presents to clinic with her parents. Her HbA1c has risen from 58 mmol/mol to 76 mmol/mol over the past year. She admits to occasionally missing insulin doses and not checking her blood glucose regularly. She appears withdrawn and her mother reports she has been spending more time alone in her room. What is the most appropriate initial approach?
What is the typical age range for onset of childhood absence epilepsy?
A 12-year-old boy with type 1 diabetes mellitus for 5 years has been experiencing recurrent early morning hyperglycaemia despite increasing his bedtime insulin dose. His continuous glucose monitor shows blood glucose dropping to 3.2 mmol/L at 02:00 hours before rising to 14.8 mmol/L by 07:00 hours. What is the most appropriate management adjustment?
A 9-year-old boy with recently diagnosed focal epilepsy is started on carbamazepine. Three weeks later, he develops a widespread erythematous rash with mucosal involvement, fever, and facial swelling. Blood tests show eosinophilia and deranged liver function tests. What is the most likely diagnosis?
A 6-year-old girl with type 1 diabetes mellitus attends the emergency department with a 2-day history of vomiting and abdominal pain. Her mother reports she has been unwell with a viral illness. On examination, she is lethargic, has deep sighing respirations, and appears dehydrated. Capillary blood glucose is 24.3 mmol/L. Blood gas shows pH 7.18, bicarbonate 9 mmol/L, and base excess -18. What is the most appropriate initial fluid resuscitation strategy?
Chronic Paediatric Conditions UK Medical PG Practice Questions and MCQs
Question 111: A 11-year-old boy with type 1 diabetes for 4 years presents to clinic. His insulin doses have remained stable over the past 6 months despite normal growth velocity. His HbA1c has improved from 72 mmol/mol to 54 mmol/mol. His mother reports he has had no hypoglycaemic episodes. On examination, he appears well with normal vital signs. Urinalysis shows glucose +++. What is the most likely explanation for his improved HbA1c?
- A. Honeymoon phase with partial pancreatic beta-cell recovery
- B. Improved compliance with diabetes management
- C. Development of renal glucosuria reducing blood glucose
- D. Omission of insulin doses with fabrication of blood glucose records (Correct Answer)
- E. Reduced insulin requirements due to improved dietary control
Explanation: ***Omission of insulin doses with fabrication of blood glucose records*** - The combination of an **improved HbA1c** (suggesting better control) with **stable insulin doses** despite growth, and significant **+++ glucosuria** (indicating persistent hyperglycemia) is highly suspicious for insulin omission. - Adolescents with diabetes may **fabricate blood glucose records** to avoid parental or clinical scrutiny, leading to this paradoxical presentation of 'good' HbA1c but evidence of hyperglycemia. *Honeymoon phase with partial pancreatic beta-cell recovery* - The **honeymoon phase** typically occurs in the initial months after Type 1 Diabetes diagnosis, not **four years** into the disease. - While it reduces insulin requirements, the patient's insulin doses have been stable, and a significant improvement in HbA1c would usually require adjustment, not stable doses, particularly with growth. *Improved compliance with diabetes management* - Genuine **improved compliance** leading to a better HbA1c would generally require an *increase* in insulin doses to match an 11-year-old's growth, not stable doses. - The presence of **glucose +++** on urinalysis strongly contradicts the notion of truly improved and sustained glycemic control. *Development of renal glucosuria reducing blood glucose* - **Renal glucosuria** is characterized by glucose in the urine despite normal or near-normal blood glucose levels and would not significantly lower the **HbA1c** in a Type 1 Diabetic. - This rare condition does not explain the discrepancy of stable insulin doses, normal growth, improved HbA1c, and simultaneously high urinary glucose in a patient with Type 1 Diabetes. *Reduced insulin requirements due to improved dietary control* - While **dietary control** is crucial, it is unlikely to lead to stable insulin doses and a significant HbA1c improvement in a growing child with Type 1 Diabetes without any dose adjustments. - Effective dietary control, leading to lower blood glucose, would result in negative or trace **glucosuria**, not **+++ glucosuria**.
Question 112: A 8-year-old girl presents with episodes where she suddenly stops activity, drops objects from her hands, and appears briefly dazed for about 10 seconds before resuming normal activity with no recollection of the event. These occur multiple times daily. Her teacher reports she seems to be daydreaming frequently. An EEG is performed during hyperventilation. What is the most likely EEG finding?
- A. 3 Hz spike-and-wave discharges (Correct Answer)
- B. Hypsarrhythmia
- C. Focal sharp waves in the temporal region
- D. 4-6 Hz polyspike-and-wave complexes
- E. Centrotemporal spikes
Explanation: ***3 Hz spike-and-wave discharges***- This presentation is classic for **childhood absence epilepsy**, characterized by brief staring spells, abrupt impairment of consciousness, and immediate recovery without postictal confusion.- The pathognomonic EEG finding is generalized **3 Hz spike-and-wave discharges**, which are frequently provoked by **hyperventilation**.*Hypsarrhythmia*- This disorganized, high-amplitude EEG pattern is the hallmark of **West syndrome** (infantile spasms), not absence seizures.- It is typically seen in infants aged 3 to 12 months and is associated with **flexor or extensor spasms**.*Focal sharp waves in the temporal region*- These findings indicate **focal epilepsy** originating in the temporal lobe, which often presents with **complex partial seizures**.- Unlike absence seizures, focal impaired awareness seizures usually last longer and are often followed by a **postictal state**.*4-6 Hz polyspike-and-wave complexes*- This EEG pattern is highly suggestive of **Juvenile Myoclonic Epilepsy (JME)**, which typically presents in adolescence.- JME is characterized by **myoclonic jerks** occurring shortly after awakening, rather than brief staring spells.*Centrotemporal spikes*- These are characteristic of **Self-limited Epilepsy with Centrotemporal Spikes** (formerly Benign Rolandic Epilepsy).- This condition typically presents with nocturnal seizures involving **orofacial muscles** and drooling, usually occurring during sleep or upon awakening.
Question 113: A 13-year-old boy with type 1 diabetes presents with a 4-week history of persistent tingling and numbness in both feet, which is worse at night. On examination, he has reduced sensation to light touch and pinprick in a stocking distribution, and absent ankle reflexes. His recent HbA1c is 89 mmol/mol. What is the most likely diagnosis?
- A. Diabetic peripheral neuropathy (Correct Answer)
- B. Guillain-Barré syndrome
- C. Chronic inflammatory demyelinating polyneuropathy (CIDP)
- D. Vitamin B12 deficiency neuropathy
- E. Charcot-Marie-Tooth disease
Explanation: ***Diabetic peripheral neuropathy*** - This patient presents with classic features of **distal symmetric polyneuropathy**, including **persistent tingling and numbness** in both feet, which is worse at night, **reduced sensation in a stocking distribution**, and **absent ankle reflexes**. - The strong association with **type 1 diabetes** and a highly elevated **HbA1c of 89 mmol/mol** indicates poor glycemic control, the primary driver of this complication, even in adolescents. *Guillain-Barré syndrome* - Typically presents as an **acute, rapidly progressive** ascending paralysis or weakness, often following an infection. - While it features absent reflexes, it is primarily a **motor-dominant** condition, and the chronicity (4 weeks) and sensory-predominant presentation do not fit. *Chronic inflammatory demyelinating polyneuropathy (CIDP)* - Requires a symptom duration of at least **8 weeks** for diagnosis, whereas this patient has only had symptoms for 4 weeks. - Usually involves significant **proximal and distal muscle weakness** in addition to sensory symptoms, which is not the primary presentation here. *Vitamin B12 deficiency neuropathy* - Often presents with **subacute combined degeneration** of the spinal cord, leading to loss of **vibration and proprioception**, and can cause paresthesia. - While a cause of neuropathy, it is not directly linked to **poor glycemic control** and does not explain the specific stocking distribution of sensory loss in the context of diabetes. *Charcot-Marie-Tooth disease* - This is a group of **hereditary neuropathies** characterized by **slowly progressive distal muscle weakness** and sensory loss, often with **foot deformities** (e.g., pes cavus). - Its presentation is typically lifelong and gradually progressive, not acutely related to recent glycemic control, and lacks the typical rapid onset of symptoms described.
Question 114: A 7-year-old boy with focal epilepsy has been seizure-free for 18 months on lamotrigine monotherapy. His parents enquire about stopping the medication. His EEG 6 months ago showed persistent focal epileptiform discharges. His neurological examination is normal and he has no learning difficulties. What advice should be given regarding antiepileptic drug withdrawal?
- A. Withdraw medication immediately as he has been seizure-free for over 1 year
- B. Continue medication for at least 2 years seizure-freedom before considering withdrawal (Correct Answer)
- C. The abnormal EEG is an absolute contraindication to drug withdrawal
- D. Withdraw medication only if a repeat EEG is normal
- E. Continue medication indefinitely as focal epilepsy always requires lifelong treatment
Explanation: ***Continue medication for at least 2 years seizure-freedom before considering withdrawal*** - Current guidelines generally recommend a minimum period of **2 years of seizure freedom** before attempting to taper antiepileptic drugs in children. - Although this child has been seizure-free for 18 months, premature withdrawal increases the risk of **seizure recurrence**, especially with persistent EEG abnormalities. *Withdraw medication immediately as he has been seizure-free for over 1 year* - Immediate withdrawal is unsafe; medications must be **tapered gradually** over several months to prevent withdrawal seizures. - The recommended clinical milestone for withdrawal in the pediatric population is **24 months**, not 12 months. *The abnormal EEG is an absolute contraindication to drug withdrawal* - While persistent **focal epileptiform discharges** represent a higher risk for recurrence, they are not an **absolute contraindication** to withdrawal. - Clinical decision-making balances the **EEG findings** with the child's seizure-free duration and the parents' preferences. *Withdraw medication only if a repeat EEG is normal* - A **normal EEG** is a favorable prognostic marker but is not a mandatory prerequisite for attempting medication withdrawal. - Management should be individualized, as some children remain seizure-free even if **interictal abnormalities** persist on EEG. *Continue medication indefinitely as focal epilepsy always requires lifelong treatment* - Many forms of **pediatric focal epilepsy** have a good prognosis and may resolve as the brain matures. - The decision to stop treatment is based on the **seizure-free interval** rather than the initial epilepsy classification alone.
Question 115: A 10-year-old girl with type 1 diabetes mellitus is found to have an albumin:creatinine ratio (ACR) of 3.8 mg/mmol on routine screening. A repeat sample 3 months later shows ACR of 4.2 mg/mmol, and a third sample confirms ACR of 4.5 mg/mmol. Her blood pressure is on the 60th centile for age. Her HbA1c is 68 mmol/mol. What is the most appropriate management?
- A. Commence ACE inhibitor therapy immediately
- B. Optimize glycaemic control and recheck ACR in 6 months (Correct Answer)
- C. Refer to paediatric nephrology for renal biopsy
- D. Commence angiotensin receptor blocker therapy
- E. Commence statin therapy for cardiovascular protection
Explanation: ***Optimize glycaemic control and recheck ACR in 6 months***- The patient has confirmed **microalbuminuria** (ACR 3–30 mg/mmol), but her **HbA1c** is elevated, indicating that optimizing metabolic management is the first-line intervention.- In pediatric patients, microalbuminuria can be **transient** or reversible with improved glucose control, especially when **blood pressure** remains within the normal range (60th centile).*Commence ACE inhibitor therapy immediately*- **ACE inhibitors** are typically reserved for children who remain microalbuminuric after optimizing glycaemic control or those with **hypertension**.- Initiating medication is premature here as the patient is **normotensive** and has clear room for improvement in diabetes management.*Refer to paediatric nephrology for renal biopsy*- A **renal biopsy** is not indicated for isolated microalbuminuria in the context of Type 1 Diabetes; it is typically reserved for atypical presentations like **macroscopic hematuria**.- The diagnosis of early **diabetic nephropathy** is clinical and does not require histological confirmation at this stage.*Commence angiotensin receptor blocker therapy*- **ARBs** function similarly to ACE inhibitors in protecting the kidneys, but they are not the first-line choice for a **normotensive** child with poor glycaemic control.- Conservative management focusing on **HbA1c reduction** should be prioritized before identifying a permanent need for renin-angiotensin system blockade.*Commence statin therapy for cardiovascular protection*- **Statins** are not indicated based solely on microalbuminuria in a 10-year-old; they are considered for older adolescents or those with **dyslipidemia**.- While diabetes increases cardiovascular risk, the immediate priority for managing kidney health in this child is **glycaemic optimization**.
Question 116: A 14-year-old girl with type 1 diabetes for 6 years presents to clinic with her parents. Her HbA1c has risen from 58 mmol/mol to 76 mmol/mol over the past year. She admits to occasionally missing insulin doses and not checking her blood glucose regularly. She appears withdrawn and her mother reports she has been spending more time alone in her room. What is the most appropriate initial approach?
- A. Arrange urgent psychiatric assessment for depression
- B. Switch to an insulin pump to improve compliance
- C. Speak to the young person alone to explore psychosocial factors and provide support (Correct Answer)
- D. Increase the frequency of clinic appointments to weekly reviews
- E. Refer to social services for safeguarding concerns
Explanation: ***Speak to the young person alone to explore psychosocial factors and provide support***- Adolescence is a critical period where **diabetes distress**, peer pressure, and body image issues often lead to **poor compliance**; speaking alone fosters trust and honest communication.- Establishing a **supportive, non-judgmental environment** is the first step according to NICE guidelines to identify underlying barriers before escalating to formal mental health or medical interventions.*Arrange urgent psychiatric assessment for depression*- While the patient shows signs of being **withdrawn**, an initial exploratory assessment by her usual diabetes team is required before declaring a **psychiatric emergency**.- Deteriorating glucose control in isolation does not qualify for **urgent psychiatric referral** unless there is immediate risk of self-harm or severe clinical depression.*Switch to an insulin pump to improve compliance*- Transitioning to an **insulin pump (CSII)** requires a high level of patient engagement and regular **blood glucose monitoring**, which this patient is currently failing to maintain.- Escalating technology without addressing the **psychosocial foundation** is unlikely to succeed and may increase the risk of **diabetic ketoacidosis** if the device is neglected.*Increase the frequency of clinic appointments to weekly reviews*- Overloading an adolescent with clinical visits can be **counterproductive**, increasing the sense of being controlled and potentially causing the patient to **disengage** further.- The priority is the **quality of the consultation** and the therapeutic relationship rather than the mere frequency of appointments.*Refer to social services for safeguarding concerns*- There is no evidence of **abuse or neglect** in the clinical history; the parents are actively involved and brought the child to the clinic for help.- Deteriorating chronic disease management in adolescence is common and should be managed as a **clinical and psychosocial challenge** rather than a legal safeguarding issue.
Question 117: What is the typical age range for onset of childhood absence epilepsy?
- A. 2-4 years
- B. 4-8 years (Correct Answer)
- C. 6-12 years
- D. 10-16 years
- E. 12-18 years
Explanation: ***4-8 years*** - **Childhood absence epilepsy (CAE)** typically presents in school-aged children with a peak incidence between **5-7 years** of age. - It is characterized by frequent **brief episodes of impaired consciousness** and a classic **3 Hz spike-and-wave** pattern on EEG. *2-4 years* - Onset at this age is considered **unusually early** for CAE and would necessitate consideration of other early-childhood epilepsy syndromes. - Seizures appearing in this range are more likely to be associated with **Glucose transporter type 1 (GLUT1) deficiency** or other metabolic etiologies. *6-12 years* - While there is some overlap, the **peak onset** for CAE starts earlier than 6 years, typically around age 4 or 5. - This range leans more towards the transition into **Juvenile Absence Epilepsy (JAE)**, which is distinguished by a later age of onset. *10-16 years* - This age range is characteristic of **Juvenile Absence Epilepsy (JAE)** or **Juvenile Myoclonic Epilepsy (JME)**. - Patients in this group are less likely to experience the high frequency of daily absences seen in the **childhood form**. *12-18 years* - This encompasses the **adolescent period** where CAE typically reaches **remission** rather than initial onset. - Seizures appearing first in this age group are strongly indicative of **idiopathic generalized epilepsies** like JME, often featuring generalized tonic-clonic or myoclonic seizures.
Question 118: A 12-year-old boy with type 1 diabetes mellitus for 5 years has been experiencing recurrent early morning hyperglycaemia despite increasing his bedtime insulin dose. His continuous glucose monitor shows blood glucose dropping to 3.2 mmol/L at 02:00 hours before rising to 14.8 mmol/L by 07:00 hours. What is the most appropriate management adjustment?
- A. Further increase the bedtime long-acting insulin dose
- B. Add metformin to improve insulin sensitivity
- C. Reduce the bedtime long-acting insulin dose (Correct Answer)
- D. Give additional rapid-acting insulin at bedtime
- E. Switch to an insulin pump therapy
Explanation: ***Reduce the bedtime long-acting insulin dose***- The patient is experiencing the **Somogyi phenomenon**, where nocturnal **hypoglycaemia** (3.2 mmol/L at 02:00) triggers the release of counter-regulatory hormones, leading to rebound morning **hyperglycaemia**.- Reducing the **bedtime insulin** prevents the initial drop in glucose levels, thereby stopping the subsequent hormonal surge and correcting the morning high.*Further increase the bedtime long-acting insulin dose*- Increasing the dose would exacerbate the **02:00 hours hypoglycaemia**, potentially making the rebound hyperglycaemia worse or causing severe nocturnal seizures.- This approach is only appropriate for the **Dawn phenomenon**, which lacks the preceding nocturnal hypoglycaemic dip.*Add metformin to improve insulin sensitivity*- **Metformin** is primarily used in **Type 2 DM** and is not the standard treatment for managing acute nocturnal glucose fluctuations in Type 1 DM.- It does not address the underlying issue of **insulin-induced** rebound hyperglycaemia described in this scenario.*Give additional rapid-acting insulin at bedtime*- Administering **rapid-acting insulin** at bedtime would cause an even sharper drop in blood glucose levels during the early night, increasing the risk of **life-threatening hypoglycaemia**.- This would further stimulate **counter-regulatory hormones** like glucagon and adrenaline, worsening the morning glucose profile.*Switch to an insulin pump therapy*- While **insulin pump therapy (CSII)** provides more precise basal rate delivery, the immediate clinical priority is to fix the current dose-related **nocturnal hypoglycaemia**.- Adjusting the **MDI (Multiple Daily Injection)** regimen is the first-line corrective step before considering a total change in delivery technology.
Question 119: A 9-year-old boy with recently diagnosed focal epilepsy is started on carbamazepine. Three weeks later, he develops a widespread erythematous rash with mucosal involvement, fever, and facial swelling. Blood tests show eosinophilia and deranged liver function tests. What is the most likely diagnosis?
- A. Stevens-Johnson syndrome/toxic epidermal necrolysis (Correct Answer)
- B. Simple viral exanthem
- C. Urticaria secondary to carbamazepine allergy
- D. Erythema multiforme minor
- E. Scarlet fever
Explanation: ***Stevens-Johnson syndrome/toxic epidermal necrolysis*** - This is a severe cutaneous adverse reaction typically occurring 1-4 weeks after starting **carbamazepine**, characterized by **mucosal involvement**, systemic symptoms, and potential skin sloughing. - The presence of **fever**, **facial swelling**, **eosinophilia**, and **multiorgan involvement** (deranged LFTs) following high-risk medication exposure marks this as a medical emergency. *Simple viral exanthem* - Usually presents as a **morbilliform rash** following a prodromal viral illness, without the severe **mucosal involvement** or systemic organ dysfunction seen here. - **Eosinophilia** and deranged liver enzymes are not typical features of simple childhood viral infections. *Urticaria secondary to carbamazepine allergy* - Characterized by transient, itchy **wheals** that fluctuate in position and usually appear within hours of drug exposure rather than weeks. - Does not present with **fever**, **mucosal ulceration**, or laboratory abnormalities like **eosinophilia** and liver failure. *Erythema multiforme minor* - Typically presents with localized **target lesions** on the extremities and is most commonly triggered by **Herpes Simplex Virus (HSV)**. - It lacks the widespread distribution, **systemic toxicity**, and significant **mucosal involvement** associated with SJS/TEN. *Scarlet fever* - Caused by **Group A Streptococcus** and presents with a distinctive **sandpaper-like rash**, strawberry tongue, and circumoral pallor. - While it involves fever, it is treated with antibiotics and does not cause **eosinophilia** or liver dysfunction related to anticonvulsant therapy.
Question 120: A 6-year-old girl with type 1 diabetes mellitus attends the emergency department with a 2-day history of vomiting and abdominal pain. Her mother reports she has been unwell with a viral illness. On examination, she is lethargic, has deep sighing respirations, and appears dehydrated. Capillary blood glucose is 24.3 mmol/L. Blood gas shows pH 7.18, bicarbonate 9 mmol/L, and base excess -18. What is the most appropriate initial fluid resuscitation strategy?
- A. 0.9% sodium chloride 10 mL/kg bolus over 1 hour, then maintenance fluids with added insulin (Correct Answer)
- B. 0.9% sodium chloride 20 mL/kg bolus over 30 minutes, then reassess
- C. 0.45% sodium chloride with 5% dextrose at twice maintenance rate
- D. 0.9% sodium chloride at 1.5 times maintenance rate without initial bolus
- E. Colloid bolus 20 mL/kg followed by 0.9% sodium chloride maintenance
Explanation: ***0.9% sodium chloride 10 mL/kg bolus over 1 hour, then maintenance fluids with added insulin*** - This patient presents with **Diabetic Ketoacidosis (DKA)**, indicated by hyperglycemia, metabolic acidosis, and ketosis. Current guidelines recommend a cautious **10 mL/kg bolus of 0.9% sodium chloride** over 30-60 minutes to manage initial dehydration and restore perfusion without rapid osmotic shifts that could precipitate **cerebral edema**. - Following the initial bolus and reassessment, the next steps involve calculating fluid deficit, providing maintenance fluids (usually 0.9% NaCl initially, then adjusting), and initiating a fixed-rate **insulin infusion** (0.05-0.1 units/kg/hour) to suppress ketogenesis and lower glucose gradually. *0.9% sodium chloride 20 mL/kg bolus over 30 minutes, then reassess* - While a **20 mL/kg bolus** is common for general pediatric shock or severe dehydration, in **DKA**, such a rapid and large volume of fluid is associated with an increased risk of **cerebral edema**, particularly in children. - The primary goal in DKA fluid resuscitation is slow, careful rehydration to prevent rapid changes in **serum osmolality**, which can lead to shifts of water into brain cells. *0.45% sodium chloride with 5% dextrose at twice maintenance rate* - Hypotonic solutions like **0.45% sodium chloride** are contraindicated for initial resuscitation in DKA as they can rapidly lower **serum osmolality**, exacerbating the risk of **cerebral edema**. - **Dextrose** should only be added to IV fluids once the blood glucose level falls to around **14-17 mmol/L** (250-300 mg/dL) to prevent hypoglycemia while continuing the insulin infusion. *0.9% sodium chloride at 1.5 times maintenance rate without initial bolus* - This patient exhibits clinical signs of significant **dehydration** (lethargy, deep sighing respirations) and metabolic derangement, necessitating an initial fluid bolus to restore **circulating volume** and improve perfusion. - Delaying an initial bolus in a dehydrated DKA patient can lead to inadequate tissue perfusion, worsen **acidosis**, and potentially contribute to further clinical deterioration or **acute kidney injury**. *Colloid bolus 20 mL/kg followed by 0.9% sodium chloride maintenance* - **Crystalloids** (0.9% NaCl) are the recommended first-line fluids for resuscitation in DKA due to their effectiveness and safety profile; **colloids** offer no proven advantage and are not typically part of standard DKA management protocols. - Large volumes of colloid can interfere with laboratory monitoring and do not specifically address the complex **osmotic and electrolyte imbalances** inherent in DKA.
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