Overview
Definition:
New-onset Type 1 Diabetes Mellitus (T1DM) in children typically presents as either severe hyperglycemia with or without ketosis, or frank diabetic ketoacidosis (DKA)
T1DM is an autoimmune disease characterized by the destruction of pancreatic beta cells, leading to absolute insulin deficiency.
Epidemiology:
T1DM is the most common form of diabetes in children, with an incidence increasing globally
Peak onset is observed in early adolescence, but it can occur at any age
DKA is a common initial presentation, occurring in 15-60% of new-onset T1DM cases
Genetic predisposition and environmental triggers are implicated.
Clinical Significance:
Accurate and timely differentiation between DKA and simple hyperglycemia is crucial for appropriate management, preventing life-threatening complications of DKA such as cerebral edema, and ensuring optimal glycemic control and long-term outcomes
This distinction is vital for pediatric residents preparing for high-stakes examinations like DNB and NEET SS.
Clinical Presentation
Symptoms:
Classic symptoms of hyperglycemia: Polyuria
Polydipsia
Polyphagia
Unexplained weight loss
Fatigue
Blurred vision
Symptoms of DKA: Nausea and vomiting
Abdominal pain
Rapid, deep breathing (Kussmaul respiration)
Fruity breath odor
Lethargy or altered mental status.
Signs:
Vital sign abnormalities in DKA: Tachycardia
Hypotension
Tachypnea
Fever may be present
Physical examination findings: Dehydration (dry mucous membranes, decreased skin turgor)
Abdominal tenderness
Decreased level of consciousness
Signs of hypoperfusion.
Diagnostic Criteria:
DKA is diagnosed by the presence of hyperglycemia (blood glucose >200 mg/dL or 11.1 mmol/L), metabolic acidosis (serum bicarbonate <18 mEq/L or pH <7.3), and ketosis (ketonuria or moderate to large ketonemia)
Hyperglycemia without significant acidosis or ketosis defines severe hyperglycemia.
Diagnostic Approach
History Taking:
Detailed history of presenting symptoms: onset, duration, severity
Fluid intake and output
Vomiting or abdominal pain characteristics
Family history of diabetes
Recent infections or illnesses
Medication history
Red flags: rapid deterioration, altered consciousness, persistent vomiting.
Physical Examination:
Comprehensive assessment of hydration status
Neurological examination to assess mental status and rule out cerebral edema
Cardiopulmonary examination
Abdominal examination for tenderness
Vital signs including temperature, heart rate, blood pressure, and respiratory rate.
Investigations:
Initial laboratory tests: Blood glucose (capillary or venous)
Serum electrolytes (Na, K, Cl, HCO3)
Blood urea nitrogen (BUN) and creatinine
Arterial or venous blood gas analysis
Serum ketones or urinalysis for ketones
Complete blood count (CBC) with differential
Osmolality
Further tests: Complete lipid profile
HbA1c
Autoantibodies (GAD, IA-2, IAA).
Differential Diagnosis:
Other causes of abdominal pain and vomiting in children: Appendicitis
Gastroenteritis
Intussusception
Other causes of metabolic acidosis: Sepsis
Inborn errors of metabolism
Salicylate toxicity
Dehydration without DKA or significant hyperglycemia.
Management
Initial Management:
Immediate stabilization in a monitored setting (pediatric ICU for DKA)
Intravenous fluid resuscitation: Isotonic saline (0.9% NaCl) at 10-20 mL/kg over 1-2 hours
Correction of dehydration and electrolyte imbalances
Careful glucose monitoring.
Medical Management:
Insulin therapy: Continuous intravenous infusion of regular insulin at 0.1 U/kg/hour after initial fluid bolus and confirmation of no significant hypokalemia
Potassium replacement: Administer potassium chloride once serum potassium is >3.3 mEq/L
Bicarbonate therapy: Generally avoided, reserved for severe acidosis (pH < 6.9) or hemodynamic instability
Sodium bicarbonate 1-2 mEq/kg IV over 1-2 hours.
Supportive Care:
Close monitoring of vital signs, neurological status, fluid balance, and laboratory parameters (glucose, electrolytes, blood gases) every 1-2 hours
Gradual transition to subcutaneous insulin therapy once DKA resolves and patient is eating
Nutritional support: Oral or nasogastric feeding as tolerated
Education of patient and family on diabetes self-management.
Complications
Early Complications:
Cerebral edema: Most feared complication, presenting as headache, altered mental status, seizures, and potentially death
Hypoglycemia
Hypokalemia
Hyperchloremic metabolic acidosis
Recurrent DKA.
Late Complications:
Long-term complications of poorly controlled diabetes: Microvascular (retinopathy, nephropathy, neuropathy)
Macrovascular (cardiovascular disease)
Gastroparesis
Infections.
Prevention Strategies:
Aggressive management of hyperglycemia and ketosis
Gradual correction of fluid and electrolyte deficits
Careful titration of insulin therapy
Close monitoring for signs of cerebral edema
Education on sick day management and recognizing early symptoms of DKA
Regular follow-up with a multidisciplinary diabetes care team.
Prognosis
Factors Affecting Prognosis:
Severity of initial DKA
Presence and severity of cerebral edema
Timeliness and appropriateness of management
Adherence to long-term treatment and follow-up
Presence of comorbidities.
Outcomes:
With optimal management, most children with new-onset T1DM and DKA can recover fully without long-term sequelae
Long-term prognosis depends on achieving and maintaining good glycemic control to prevent chronic diabetic complications.
Follow Up:
Regular follow-up with pediatric endocrinologist and diabetes educator
Frequent blood glucose monitoring and HbA1c testing
Annual screening for microvascular complications
Ongoing education and support for self-management and psychological adjustment to living with diabetes.
Key Points
Exam Focus:
DKA diagnostic criteria: glucose >200, HCO3 <18, ketosis
DKA management: fluids, insulin infusion (0.1 U/kg/hr), potassium repletion
Cerebral edema prevention and recognition: slow fluid correction, mannitol if suspected
Difference between DKA and simple hyperglycemia.
Clinical Pearls:
Always check potassium before starting insulin infusion in DKA
Monitor neurological status vigilantly for cerebral edema
Avoid rapid correction of hyperglycemia and osmolality
Transition to subcutaneous insulin only when patient is hemodynamically stable and eating
Educate families thoroughly on sick day rules.
Common Mistakes:
Delayed diagnosis and management of DKA
Overly rapid fluid resuscitation leading to cerebral edema
Incorrect timing or dosing of potassium replacement
Unnecessary use of bicarbonate
Inadequate follow-up and education.