Collar Stud Abscess

Definition

Cervical tuberculous cold abscess (Bailey & Love, Fig. 6.34)

Pathogenesis

1. Primary deep infection - Suppuration begins at depth, often in a lymph node (e.g. cervical tuberculous lymphadenitis causing caseation and liquefaction).
2. Fascial erosion - Over weeks to months, the pus erodes through the overlying fascia at a single point, creating a narrow communication.
3. Superficial collection - Pus tracks through the defect and accumulates beneath the superficial fascia, forming the visible/palpable superficial lump.
4. Cross-fluctuation - Because the two cavities communicate, pressure on one transmits fluctuation to the other - this is a key clinical sign.
5. Progression - Without treatment, the superficial collection enlarges, may burst through skin, and forms a discharging sinus (in TB: a tuberculous sinus with watery discharge and undermined edges).

Classical Sites

Cervical Collar Stud Abscess

Palmar Collar Stud Abscess

Digital Collar Stud Abscess

Finger abscess types (Pye's Surgical Handicraft, Fig. 26.25): 1 = apical; 2 = pulp with collar-stud extension; 3 = subcutaneous; 4 = intracutaneous

Clinical Features

• The superficial component is the presenting feature - a painless or mildly tender fluctuant swelling
• In TB: the swelling is a cold abscess - no warmth, redness, or tenderness (no features of acute inflammation)
• Cross-fluctuation is demonstrable between the two components
• If asked to press the superficial swelling, pus is seen welling up from the deeper defect
• Untreated: progressive enlargement → skin breach → discharging sinus → tuberculous ulcer with undermined edges

Causative Organisms

• Mycobacterium tuberculosis - the classic cause in the neck
• Pyogenic organisms (Staphylococcus aureus, Streptococcus) - in hand/finger lesions

Investigations (for cervical TB type)

• FNAC / aspiration of cold abscess - pus for Ziehl-Neelsen stain for acid-fast bacilli and culture & sensitivity
• Excision biopsy if still in nodal phase (part sent fresh to lab)
• Raised ESR and CRP, low haemoglobin
• Chest X-ray - assess pulmonary TB
• Mantoux / tuberculin skin test - though now largely superseded
• Interferon-gamma release assay (IGRA / QuantiFERON-TB Gold) - more specific than Mantoux; not affected by prior BCG vaccination; measures T-cell IFN-γ response to M. tuberculosis-specific antigens
• HIV test where relevant (immunocompromised patients)
• Search for a primary focus: carious teeth, septic tonsils, spinal tuberculosis (Pott's disease)

Treatment

Surgical Drainage

1. General anaesthesia preferred
2. Incision along a skin crease over the superficial component
3. Superficial cavity is drained and the walls are rubbed out
4. Pus is seen welling up from the deeper collection through the fascial defect
5. Fascia is incised in the same line to access the deep collection
6. Deep collection or granulation tissue is dissected or curetted away
7. Swabs taken for culture (including caseous material)
8. Any clearly involved lymph node is excised for histology
9. Skin is lightly approximated with a few sutures around a corrugated rubber drain

1. Tourniquet control for a bloodless field
2. Superficial abscess is uncapped first
3. Deep connection is gently probed then enlarged by incision through the dermis
4. Pus and loose slough are evacuated; dead fat is excised
5. Skin edges are cut back with scissors to form a narrow diamond-shaped opening
6. No drains, no gauze wicks - dry dressing applied

Medical Treatment (for tuberculous type)

Key Pitfall

If only the superficial abscess is drained without addressing the deep component, the pathological process continues and a sinus will inevitably form.

DVT Prophylaxis for Major Surgical Procedures

Why It Matters

• Endothelial injury - from surgery or trauma
• Venous stasis - immobility, tourniquet, positioning
• Hypercoagulability - cancer, sepsis, obesity, estrogen, thrombophilia

Risk Stratification

Caprini Score (most widely used)

Rogers Score

Methods of Prophylaxis

A. Mechanical Methods

• Should commence just before surgery and continue postoperatively
• Standard of care when pharmacologic agents are contraindicated (active bleeding, coagulopathy, severe thrombocytopenia, intracranial hemorrhage)
• Used alone in low-risk settings; combined with pharmacologic agents in high-risk settings

• Acceptable in low-risk settings, less effective than IPC in high-risk settings

In major open surgery, a more aggressive regimen combining sequential compression devices and pharmacologic prophylaxis is recommended over either method alone.

B. Pharmacologic Methods

• LMWH advantages over UFH: once-daily dosing, lower risk of heparin-antibody formation (HIT), predictable pharmacokinetics, no routine lab monitoring
• Both LMWH and LDUH reduce symptomatic and asymptomatic VTE risk by 60-70%
• Fondaparinux vs. dalteparin in major abdominal surgery: comparable VTE prevention and bleeding; more effective than IPC alone but with higher bleeding rate

Timing of Initiation

Delays of over 24 hours in initiating pharmacologic VTE prophylaxis after major trauma/ICU admission are associated with a threefold increase in VTE.

Duration of Prophylaxis

VTE risk continues for at least 30 days after an operation. Despite early ambulation, patients remain at elevated risk.

Contraindications to Pharmacologic Prophylaxis

• Active bleeding
• Intracranial hemorrhage
• Coagulopathy (INR >1.5 in non-therapeutic setting)
• Severe thrombocytopenia (platelets <50,000)

• Recent GI bleeding
• Recent surgery (especially neurosurgery, ophthalmic, spinal)
• Moderate thrombocytopenia

In patients with absolute/relative contraindications: use mechanical prophylaxis alone until the bleeding risk subsides, then add pharmacologic prophylaxis.

Special Considerations

Cancer Surgery

• Combined LMWH + IPC intraoperatively and postoperatively
• Extended-duration LMWH post-discharge (4 weeks) - this is a strong recommendation from ACCP guidelines

Orthopaedic Surgery (Hip/Knee Arthroplasty)

• Mechanical compression devices are used alongside pharmacologic agents
• Duration: minimum 10 days; consider up to 35 days for hip arthroplasty
• Stop antiplatelet agents (aspirin, clopidogrel) approximately 1 week preoperatively

Neuraxial Anaesthesia

• Neuraxial (spinal/epidural) anaesthesia reduces intraoperative bleeding (but does not independently reduce VTE incidence)
• Timing of pharmacologic prophylaxis relative to neuraxial block is important: wait 12 hours after LMWH dose before performing neuraxial block

Heparin-Induced Thrombocytopenia (HIT)

• Occurs in 1-5% of patients exposed to heparin
• Caused by IgG antibodies to heparin-PF4 complex
• 4Ts score for diagnosis: Thrombocytopenia, Timing (days 5-10), Thrombosis, oTher causes
• If suspected: stop all heparin immediately, switch to direct thrombin inhibitor (argatroban or bivalirudin) or fondaparinux

IVC Filters

• Reserved for patients with proximal DVT who cannot receive anticoagulation or who have VTE despite adequate anticoagulation
• Do not use routinely - increased rate of recurrent DVT with filters
• FDA recommends removal within 29-54 days when no longer needed; prefer retrievable filters

Quick Summary Table

DVT Prophylaxis for Major Surgical Procedures

Risk Stratification (Caprini / Rogers Score)

Mechanical Methods

• IPC (Intermittent Pneumatic Compression) - start just before surgery; first-line when pharmacologic agents are contraindicated
• Graduated Compression Stockings (GCS) - adjunct; less effective alone in high-risk patients
• In major open surgery: always combine mechanical + pharmacologic for high-risk patients

Pharmacologic Agents

Timing

Delay >24h in starting pharmacologic prophylaxis after major trauma/surgery = 3× increased VTE risk

Duration

Contraindications to Pharmacologic Prophylaxis

• When contraindicated: use IPC alone until pharmacologic prophylaxis is safe to add

HIT (Heparin-Induced Thrombocytopenia)

• Occurs in 1-5% of patients on heparin
• Platelet drop >50%, typically days 5-10 after heparin exposure
• Diagnose with 4Ts score → confirm with serotonin release assay
• Management: stop all heparin immediately → switch to argatroban, bivalirudin, or fondaparinux

Special Populations

• Cancer patients: highest risk group - extended 4-week LMWH post-discharge is strongly recommended
• Orthopaedic (THA/TKA): add aspirin or DOAC options; mechanical devices mandatory; stop clopidogrel ~1 week pre-op
• Obese/septic/ICU patients: standard doses may fail; consider goal-directed LMWH dose titration

Filariasis

Definition & Epidemiology

Classification of Filarial Diseases

Life Cycle (Lymphatic Filariasis)

1. Mosquito bite - infective L3 larvae deposited into skin
2. Migration to lymphatics - larvae develop into adult male and female worms (takes ~1 year)
3. Adult worms colonise lymphatic channels and lymph nodes; mate and release microfilariae
4. Microfilariae enter the bloodstream - exhibit nocturnal periodicity (peak in peripheral blood at night, timed with night-biting habits of vector mosquitoes)
5. Mosquito ingests microfilariae during a blood meal → larvae develop in mosquito → cycle continues

Pathogenesis

1. Direct Mechanical Damage

2. Immune-Mediated Damage

• Th1-mediated response - granuloma formation around adult parasites in chronic lymphatic filariasis
• Th2-mediated response - IgE and eosinophils stimulated by IL-4 and IL-5; underlies tropical pulmonary eosinophilia
• Recurrent lymphangitis causes fibrosis of lymph channels → irreversible elephantiasis

Role of Wolbachia Bacteria

Immune Evasion Mechanisms

• Elastases and trypsin-like proteases (tissue invasion)
• Surface glycoproteins with antioxidant function (protect from reactive oxygen species)
• Cystatins (impair MHC class II antigen-processing)
• Serpins (inhibit neutrophil proteases)
• Homologues of TGF-β and macrophage migration inhibition factor (dampen host immune response)

Clinical Features

Spectrum of Disease

• Episodic fever with lymphadenitis and lymphangitis
• The characteristic lymphangitis spreads centrifugally (away from the lymph node, down the limb) - distinguishing it from bacterial lymphangitis which spreads centrally
• Adult worms may occasionally be palpable subcutaneously
• Males predominantly affected (females less exposed to mosquito bites due to clothing)

Left lower limb elephantiasis (Bailey & Love, Fig. 6.8)

Elephantiasis of the leg - massive edema with subcutaneous fibrosis and hyperkeratosis (Robbins Pathology, Fig. 8.62)

• Massive lower limb edema - obstruction of lymphatics
• Skin thickening resembling peau d'orange (orange peel) from cutaneous lymphatic obstruction
• Tough subcutaneous fibrosis with epithelial hyperkeratosis
• Secondary streptococcal infection is common and accelerates progression
• Histology: dilated dermal lymphatics, widespread lymphocytic infiltrates, focal cholesterol deposits, thickened hyperkeratotic epidermis

Scrotal and penile elephantiasis (Bailey & Love, Fig. 6.9)

• Bilateral lower limb filariasis commonly associated with scrotal and penile elephantiasis
• Hydrocele (early manifestation - fluid in tunica vaginalis; hydrocele fluid may contain cholesterol crystals, red cells, hemosiderin)
• Chronic infection can lead to thickening and calcification of the tunica vaginalis

• Chyluria - chylous (milky) urine from rupture of lymphatics into urinary tract
• Chylous ascites - lymphatic rupture into peritoneum
• Tropical Pulmonary Eosinophilia (TPE) - hypersensitivity to microfilariae in the lungs; nocturnal paroxysmal cough, wheeze, low-grade fever, very high eosinophilia and IgE; diffuse interstitial infiltrates on CXR; if untreated leads to chronic restrictive lung disease

Diagnosis

Blood Smear (Gold Standard)

• Nocturnal peripheral blood smear - Giemsa-stained thick smear collected between 10 PM and 2 AM (when microfilarial count is highest due to nocturnal periodicity)
• Characteristic microfilariae: 250-320 μm in length, with sheath
• Microfilariae may also be seen in chylous urine, ascites fluid, and hydrocele fluid

Other Investigations

• Rapid immunochromatographic card test - detects circulating W. bancrofti antigen (adult worm antigen, not microfilariae); advantage: can be collected at any time of day (no nocturnal restriction); no equivalent test for Brugia infections
• PCR - highly sensitive but available only as a research tool
• Serologic antifilarial antibody tests - limited value due to cross-reactivity with other nematodes; cannot distinguish active from past infection
• Eosinophilia - peripheral blood eosinophilia is common
• D-dimer - not helpful after surgery/injury
• Scrotal ultrasound - can visualise adult worms in spermatic cord lymphatics as the "filarial dance sign" (pathognomonic - worms in constant motion)
• CXR - in TPE: diffuse interstitial infiltrates or mottled opacities; elevated IgE and antifilarial antibodies

Treatment

Individual Patient Treatment

Practical Notes

• DEC is both microfilaricidal and partially macrofilaricidal - kills microfilariae rapidly; kills adult worms slowly and incompletely (all worms eliminated in <25% of patients with single course)
• Repeated courses every 6-12 months attempted to eliminate adult worms in non-endemic patients
• Antihistamines for first few days to limit allergic reactions; corticosteroids if severe reactions occur
• Lymphedema due to established filariasis is usually NOT reversible with DEC treatment - except in very early stages

Management of Established Lymphedema

• Meticulous hygiene - wash affected limb with soap/water; prevent/treat secondary bacterial and fungal infections promptly
• Limb elevation and physiotherapy
• Elastic compression stockings
• Intermittent pneumatic compression - helpful in early limb swelling; must be repeated over prolonged periods
• Surgical reduction of limb size - rarely performed, largely unsuccessful

Surgical Management

• Hydrocele - excision and eversion of the tunica vaginalis sac with excision of redundant scrotal skin (standard operation)
• Reduction surgery for grossly enlarged limbs - rarely done; value largely unproven

Mass Drug Administration (MDA) - WHO Global Programme

Chemoprophylaxis

• Bancroftian/Malayan filariasis: DEC 50 mg monthly
• Loiasis: DEC 300 mg weekly (or 300 mg × 3 consecutive days each month)

Prognosis

• Asymptomatic microfilaremia with subclinical lymphatic damage can be halted by early treatment
• Once chronic lymphedema is established, it is not reversible with drug treatment
• Progression can be limited by hygiene, secondary infection prevention, and physiotherapy
• Hydroceles recur unless surgically treated
• Elephantiasis causes permanent, severe disability

Summary Box (Bailey & Love)

• Caused by Wuchereria bancrofti, transmitted by mosquito
• Lymphatics mainly affected, resulting in gross limb swelling
• Eosinophilia present; microfilariae seen on nocturnal peripheral blood smear
• Early cases amenable to medical treatment with DEC
• Intermittent pneumatic compression gives some relief
• Surgical procedures largely unproven and rarely performed

Types of Body Fluid Changes

Body Fluid Compartments - Overview

• ICF: K⁺ is the principal cation; phosphate and protein are main anions
• ECF: Na⁺ is the principal cation; Cl⁻ and HCO₃⁻ are main anions

Classification of Body Fluid Changes

1. Volume changes - gain or loss of salt solution (isotonic)
2. Concentration changes - gain or loss of free water → changes in serum sodium
3. Composition changes - changes in electrolytes other than sodium (K⁺, Ca²⁺, Mg²⁺, phosphate) without major osmolality shift

1. VOLUME CHANGES

A. Extracellular Volume Deficit (Hypovolemia)

• Loss of GI fluids: vomiting, nasogastric suction, diarrhea, fistula
• Sequestration: soft tissue injury, burns, peritonitis, bowel obstruction, prolonged surgery ("third space loss")
• Hemorrhage
• Excessive diuresis

• Urine osmolality > serum osmolality
• Urine Na⁺ typically <20 mEq/L (kidneys conserving sodium)
• Serum sodium may be high, normal, or low (does not reliably reflect volume status)
• Acute deficit: cardiovascular and CNS signs predominate
• Chronic deficit: tissue signs (skin turgor, sunken eyes) also present

B. Extracellular Volume Excess (Hypervolemia)

• Iatrogenic (excessive IV fluid administration)
• Renal dysfunction
• Congestive heart failure
• Cirrhosis / hypoalbuminemia

• Well tolerated in fit patients
• Elderly and cardiac patients may rapidly develop congestive heart failure with even moderate excess

2. CONCENTRATION CHANGES (Sodium Disorders)

A. Hyponatremia (Serum Na⁺ < 135 mEq/L)

• Pseudohyponatremia - extreme elevations in plasma lipids or proteins; no true decrease in Na⁺ relative to water
• Hyperglycemia / mannitol - osmotic dilution; correct Na for glucose: for every 100 mg/dL rise in glucose above normal, Na⁺ falls by 1.6 mEq/L

• Headache, confusion
• Hyperactive or hypoactive deep tendon reflexes
• Muscle cramps/twitching, weakness, fatigue
• Anorexia, nausea, vomiting
• Seizures, coma, increased intracranial pressure (severe)
• Oliguria

• Urine Na <20 mEq/L → depletional (non-renal cause)
• Urine Na >20 mEq/L → renal sodium wasting (SIADH, renal disease)

B. Hypernatremia (Serum Na⁺ > 145 mEq/L)

• Restlessness, lethargy, irritability
• Ataxia, tonic spasms
• Delirium, seizures, coma
• Dry sticky mucous membranes, red swollen tongue
• Tachycardia, hypotension, syncope
• Fever
• Oliguria

3. COMPOSITION CHANGES (Electrolyte Disorders)

A. Potassium Disorders

B. Calcium, Magnesium, and Phosphate Disorders

Summary Framework

BODY FLUID CHANGES
├── VOLUME CHANGES (isotonic)
│   ├── Deficit (Hypovolemia) ← commonest surgical fluid disorder
│   └── Excess (Hypervolemia)
│
├── CONCENTRATION CHANGES (Na⁺ / osmolality)
│   ├── Hyponatremia (Na < 135) ← excess free water relative to Na
│   └── Hypernatremia (Na > 145) ← free water deficit or Na excess
│
└── COMPOSITION CHANGES (electrolytes, no major osmolality shift)
    ├── Potassium: hyperkalemia / hypokalemia
    ├── Calcium: hypercalcemia / hypocalcemia
    ├── Magnesium: hypermagnesemia / hypomagnesemia
    └── Phosphate: hyperphosphatemia / hypophosphatemia

Clinical pearl (Schwartz): "Serum concentration does not necessarily reflect volume status - it may be high, normal, or low when a volume deficit is present." Volume and concentration are independent disorders and must be assessed and corrected separately.