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Bite Wound Treatment

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1. Immediate Wound Management (All Bites)

1. Irrigation - Wash the wound thoroughly with soap and water, then irrigate under pressure with saline or sterile water. This is the single most effective step for reducing bacterial counts. Avoid blind high-pressure irrigation of puncture wounds.
2. Cleaning agent - Use 1% povidone-iodine or 1% benzalkonium chloride on the skin surface. Do not apply directly into deep wound tissue (toxic to exposed tissue).
3. Debridement - Remove superficial devitalized tissue and foreign material (including any retained teeth fragments).
4. Analgesia - Adequate pain control is needed before proper examination and wound care.
5. Examine thoroughly - Assess for tendon, joint capsule, nerve, and vascular damage. Use a blood pressure cuff inflated above systolic for a bloodless field. Extend puncture wound margins in high-risk areas (over joints/tendons) for better visualization.

Do NOT seal bite wounds with tissue adhesive at any age or appearance.

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2. Wound Closure

• Facial/scalp wounds <6 hours old from any species: may be sutured after preparation
• Puncture wounds, wounds >12 hours old, or infected wounds at presentation: do not suture
• Infected nonfacial wounds: delayed primary or secondary closure preferred

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3. Antibiotic Treatment

Prophylactic Antibiotics - When to Give

Antibiotic Regimens by Species

• Duration: 5-7 days prophylaxis; up to 14 days for established infection
• MRSA coverage: Consider empirically in high-risk situations while awaiting cultures
• Monotherapy failures: Erythromycin, clindamycin alone, and first-generation cephalosporins fail against Pasteurella - avoid as single agents

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4. Additional Assessments (All Bites)

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5. Human Bite - Special Considerations

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6. Snake Bite - Surgical Management

• Antivenom is the primary treatment - adequate early dosing prevents most tissue destruction
• Prophylactic antimicrobials: Penicillin or erythromycin; add gentamicin or cefuroxime if the wound was incised with unsterile instruments
• Tetanus booster should be given
• Fasciotomy: Consider only with confirmed intracompartmental syndrome (not routine)
• Debridement: Indicated at earliest signs of necrosis, followed by immediate split-skin grafting
• Blisters/bullae: Leave alone unless threatening to rupture - then aspirate with fine needle
• Do NOT: Apply occlusive dressings (conceal envenoming progression); early aggressive excision is not evidence-based

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Shoe Bite (Friction Blister) Treatment

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How It Forms

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Treatment by Stage

Stage 1 - Raw/Red Skin (No Blister Yet)

• Stop the friction immediately - remove the shoe or cover the area
• Apply a hydrocolloid blister pad (like Compeed) or moleskin directly over the sore spot
• Keep the area clean and dry

Stage 2 - Intact Blister (Unbroken)

• Clean gently with soap and water
• Cover with a sterile bandage or hydrocolloid dressing
• Avoid further pressure/rubbing on the site

1. Sterilize a needle with alcohol
2. Pierce the edge of the blister with a small puncture (make a small "window" in the roof)
3. Gently press out the fluid
4. Keep the roof intact - do not peel or cut away the skin; it acts as its own natural dressing
5. Apply antiseptic and cover with a clean bandage

Stage 3 - Ruptured Blister (Broken)

• Gently wash with soap and water, pat dry
• Try to keep the remaining roof in place over the wound
• Apply antiseptic ointment (e.g., mupirocin or povidone-iodine)
• Cover with a sterile bandage or non-stick dressing
• Change the dressing daily

Stage 4 - Signs of Infection (Seek Medical Attention)

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Topical Aids

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Prevention

• Correct shoe fit - the most important factor. No tight spots; heel should not slide up and down
• Wear socks - preferably acrylic fiber, moisture-wicking, or a double-sock system (thin polyester liner + thick wool outer). These are proven to significantly reduce blisters in runners and soldiers (Andrews' Diseases of the Skin, p. 1875)
• Break in new shoes gradually before long walks
• Pretreat high-risk areas with a lubricant (petroleum jelly/Vaseline) on friction-prone spots before activity
• Antiperspirant on feet - a 20% aluminum chloride hexahydrate solution applied for at least 3 days before prolonged activity significantly reduces foot blisters, though it can cause some skin irritation (Andrews' Diseases of the Skin, p. 1875)
• Cushioned insoles or low-friction PTFE insole patches reduce shear forces

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Special Warning - Diabetic Patients

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Medicines for Shoe Bite

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Stage 1 - Raw/Sore Skin (No Blister)

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Stage 2 - Intact or Drained Blister

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Stage 3 - Infected Blister (Spreading Redness, Pus, Swelling)

Do not self-prescribe oral antibiotics. Use them only if a doctor confirms infection.

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For Pain Relief

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Simple Home Medicines That Work

• Honey - raw honey has proven antibacterial and anti-inflammatory properties; apply a thin layer and cover with a bandage
• Petroleum jelly (Vaseline) - keeps the wound moist and prevents the dressing from sticking to the wound

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Quick Summary

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ABG vs VBG - Detailed Comparison

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1. What Are They?

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2. Normal Values Comparison

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3. Why Are They Different? (Physiology)

Lungs → Arterial blood (high O2, low CO2) 
             ↓
        Tissues extract O2, add CO2
             ↓
        Venous blood (low O2, high CO2, slightly lower pH)

• Tissues consume O2 → venous pO2 drops dramatically
• Tissues produce CO2 → venous pCO2 rises
• More CO2 in blood → more carbonic acid (H2CO3) → pH falls slightly
• Venous HCO3- is higher because venous blood carries CO2 as bicarbonate (the Haldane effect)

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4. Parameter-by-Parameter Clinical Analysis

pH

• VBG pH is reliably 0.03-0.04 less than ABG pH
• This relationship holds even in shock states and severe DKA
• Clinical rule: If VBG pH is normal → ABG pH will be normal
• Use: VBG pH is adequate to assess acid-base status in most ED/ICU scenarios
• Limitation: Confidence narrows when VBG pH is very abnormal (outside normal range)

pCO2

• Average difference is 5.7-8.6 mmHg (venous is higher)
• Most contested parameter - wide confidence intervals (-17.4 to +23.9 mmHg in some studies)
• Key screening rule: Venous pCO2 < 45 mmHg has 100% negative predictive value for hypercarbia (arterial will also be normal)
• Limitation: If you need a precise CO2 number (e.g., post-cardiac arrest, neuro-trauma, ventilator management), use ABG
• In circulatory failure, venous pCO2 can be 3-4x higher than arterial

pO2 / Oxygenation

• Cannot be used interchangeably - ever
• Venous pO2 is 30-40 mmHg vs arterial 80-100 mmHg
• VBG tells you nothing about lung oxygenation function
• For oxygenation assessment: use ABG or pulse oximetry (SpO2)

HCO3- (Bicarbonate)

• VBG HCO3- runs ~2-3 mEq/L higher than ABG
• Both are actually calculated values (from Henderson-Hasselbalch equation using pH + pCO2)
• Clinically, VBG HCO3- is adequate to assess metabolic acid-base status

Lactate

• Equivalent between arterial and venous samples
• VBG lactate is reliable for diagnosing lactic acidosis / shock

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5. Types of VBG

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6. When to Use ABG vs VBG

Use VBG When:

• Assessing acid-base status (DKA, metabolic acidosis, sepsis)
• Monitoring pH and HCO3- serially
• Screening for hypercarbia (if venous pCO2 < 45 → patient is not hypercarbic)
• Patient has difficult arterial access
• COPD on non-invasive ventilation (NIV/BiPAP) - trends are sufficient
• DKA management - VBG is sufficient; ABG changed management only 1% of the time in DKA studies
• Assessing undifferentiated dyspnea in the ED

Use ABG When:

• Assessing oxygenation (ARDS, pneumonia, respiratory failure, hypoxemia)
• Precise pCO2 is needed for clinical decisions:
  • Post-cardiac arrest (targeting normocapnia)
  • Traumatic brain injury (avoid hypercapnia/hypocapnia)
  • Ventilator management and titration
• Patient has poor peripheral perfusion (makes pulse oximetry unreliable)
• Severe hemodynamic instability (ABG-VBG correlation breaks down)
• Confirming an abnormal VBG before major clinical decisions

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7. Reliability of VBG in Specific Conditions

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8. Practical Conversion Formula

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9. Sample Collection Errors (Affect Both)

• Air exposure → decreases pCO2, raises pH, lowers CO2 content
• Saline/fluid dilution → lowers both pCO2 and HCO3- equally
• Delayed analysis → cells continue to metabolize → pH falls, pCO2 rises
• Temperature error → hypothermia: spuriously high pCO2, low pH, high pO2

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Summary in One Line Per Parameter

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What Findings Can We See on an ABG?

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Core ABG Parameters and Normal Values

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Finding 1 - Acid-Base Disorders

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Respiratory Acidosis (pH ↓, PaCO2 ↑)

• COPD, asthma exacerbation
• Sedation/opioids depressing respiratory drive
• Neuromuscular disease (myasthenia gravis, Guillain-Barré)
• Obesity hypoventilation
• Sleep apnea

Respiratory Alkalosis (pH ↑, PaCO2 ↓)

• Anxiety/panic attack
• Pulmonary embolism
• Sepsis (early)
• Altitude
• Mechanical ventilation (too fast)
• Salicylate toxicity (early)
• Pregnancy

Metabolic Acidosis (pH ↓, HCO3- ↓)

• M - Methanol
• U - Uraemia (renal failure)
• D - Diabetic ketoacidosis (DKA)
• P - Paraldehyde / Propylene glycol
• I - Isoniazid / Iron
• L - Lactic acidosis (most common)
• E - Ethylene glycol
• S - Salicylates

• Diarrhoea (GI bicarbonate loss)
• Renal tubular acidosis (RTA)
• Addison's disease
• Saline infusion (dilutional)

• Winter's formula: Expected PaCO2 = (1.5 × HCO3) + 8 ± 2

Metabolic Alkalosis (pH ↑, HCO3- ↑)

• Vomiting (loss of HCl)
• NG tube suctioning
• Diuretics (loop/thiazide - cause Cl- and K+ loss)
• Hyperaldosteronism
• Excess alkali/NaHCO3 intake

• Expected PaCO2 = 40 + 0.7 × (HCO3 - 24)

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Finding 2 - Compensation Assessment

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Finding 3 - Mixed Acid-Base Disorders

ΔΔ = Δ Anion Gap ÷ Δ HCO3-

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Finding 4 - Oxygenation Status

A-a Gradient (Alveolar-Arterial Oxygen Gradient)

PAO2 = (FiO2 × [Patm - PH2O]) - (PaCO2 / R) A-a gradient = PAO2 - PaO2

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Finding 5 - Ventilation Status

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Finding 6 - Respiratory Failure Classification

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The 6-Step Systematic ABG Interpretation Method

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Quick Reference Summary Card

pH < 7.35 = ACIDOSIS        pH > 7.45 = ALKALOSIS

↑ CO2 + ↓ pH = Respiratory Acidosis  
↓ CO2 + ↑ pH = Respiratory Alkalosis
↓ HCO3 + ↓ pH = Metabolic Acidosis   
↑ HCO3 + ↑ pH = Metabolic Alkalosis

PaO2 < 60 = Type 1 Respiratory Failure
PaCO2 > 45 = Type 2 Respiratory Failure (hypoventilation)

AG = Na - (Cl + HCO3)  [Normal: 9-15]
High AG → MUDPILES