Diagnosis: Type 1 Diabetes Mellitus with Infected Diabetic Foot Ulcer
This 28-year-old female presents with classic Type 1 diabetes mellitus (T1DM) manifesting as hyperglycemia with polyuria, polydipsia, weight loss, and blurred vision, complicated by an infected right leg wound—a presentation requiring immediate insulin therapy and aggressive wound management. 1
Primary Diagnosis: Type 1 Diabetes Mellitus
The clinical presentation strongly indicates new-onset T1DM rather than Type 2 diabetes based on several key features:
- Age and body habitus: 28 years old with BMI 17.24 (underweight), inconsistent with typical Type 2 diabetes presentation 1
- Classic triad: Polyuria, polydipsia, and significant weight loss indicate absolute insulin deficiency 1
- Acute symptom onset: Rapid development of symptoms suggests autoimmune β-cell destruction 1
- Inadequate response to oral agent: Currently on Gliclazide (a sulfonylurea) which is inappropriate for T1DM and explains poor glycemic control 2
The patient requires immediate transition from Gliclazide to insulin therapy as sulfonylureas are ineffective in absolute insulin deficiency and may delay appropriate treatment. 2
Secondary Diagnosis: Infected Diabetic Foot Ulcer
The infected right leg represents a diabetic foot infection requiring urgent classification and treatment:
Infection Severity Assessment
Based on clinical presentation, classify the infection severity 3:
- Mild infection: If only purulence/erythema present with cellulitis <2 cm, limited to skin/subcutaneous tissue, patient systemically well 3
- Moderate infection: If cellulitis extends >2 cm, lymphangitic streaking present, or involves deeper structures (fascia, muscle, tendon, bone) but patient metabolically stable 3
- Severe infection: If systemic toxicity present (fever, tachycardia, confusion, vomiting, severe hyperglycemia, acidosis) 3
Given the severe hyperglycemia and metabolic instability, this likely represents at minimum a moderate-to-severe infection. 3
Critical Evaluation Steps
Immediately assess 3:
- Vital signs: Temperature, heart rate, blood pressure to detect systemic toxicity 3
- Metabolic status: Check for diabetic ketoacidosis (DKA) given T1DM presentation—measure serum bicarbonate, ketones, arterial pH 3
- Wound characteristics: Debride and probe wound to determine depth, presence of purulence, involvement of bone (probe-to-bone test positive suggests osteomyelitis) 3
- Vascular assessment: Palpate dorsalis pedis and posterior tibial pulses; absent pulses indicate critical ischemia requiring urgent vascular consultation 3
- Laboratory markers: Elevated C-reactive protein >2 SD above normal, leukocytosis, severe hyperglycemia suggest serious infection 3
Management Priorities
Immediate Actions (First 24-48 Hours)
1. Hospitalization is mandatory given severe hyperglycemia, metabolic instability, and infected wound 3
2. Rule out hyperglycemic crisis 3:
- Check blood gas for acidosis (pH <7.3 suggests DKA)
- Measure serum/urine ketones
- Assess serum osmolality (>320 mOsm/kg suggests hyperosmolar state)
- Monitor for altered mental status, Kussmaul respirations
3. Metabolic stabilization 3:
- Aggressive IV fluid resuscitation for volume depletion from osmotic diuresis 3
- Correct electrolyte abnormalities, particularly hypokalemia (insulin drives potassium intracellularly) 2
- Initiate IV insulin infusion if DKA present; transition to subcutaneous basal-bolus regimen once stable 2
- Monitor blood glucose hourly initially, then every 2-4 hours 2
4. Infection management 3:
- Do NOT delay antibiotics for culture results in moderate-severe infection 3
- Obtain wound cultures via deep tissue biopsy or curettage after debridement (not superficial swab) 3
- Empiric broad-spectrum IV antibiotics covering Staphylococcus aureus (including MRSA if risk factors present), β-hemolytic streptococci, and gram-negative organisms 3
- Surgical debridement of necrotic tissue within 24-48 hours if present 3
- Plain radiographs (two views) to assess for osteomyelitis, gas in soft tissues 3
Common Pitfalls to Avoid
- Never continue sulfonylureas in suspected T1DM—this delays appropriate insulin therapy and worsens outcomes 2
- Never treat hyperglycemia before adequate fluid resuscitation—rapid glucose correction without volume repletion risks hypovolemic shock 2
- Never prescribe antibiotics for uninfected ulcers—but this wound is clearly infected based on clinical description 3
- Never assume adequate perfusion without pulse examination—ischemia dramatically worsens infection prognosis and may necessitate urgent revascularization 3
Hyperglycemia and Infection Relationship
Severe hyperglycemia directly impairs immune function, creating a vicious cycle 4:
- Decreased polymorphonuclear leukocyte chemotaxis and phagocytosis 4
- Impaired wound healing 3
- Increased infection-related mortality 4
Tight glycemic control (80-110 mg/dL in ICU setting) reduces infection complications and mortality, though targets may be liberalized to 140-180 mg/dL in non-ICU settings to reduce hypoglycemia risk 4
Long-term Diabetes Management
Once acute crisis resolved 1:
- Confirm T1DM diagnosis with autoantibodies (GAD, IA-2, ZnT8) and C-peptide level
- Initiate basal-bolus insulin regimen or insulin pump therapy
- Diabetes education on carbohydrate counting, insulin dosing, hypoglycemia recognition
- Screen for other autoimmune conditions (thyroid disease, celiac disease)
- Establish multidisciplinary foot care to prevent recurrent ulceration