Purulent diseases of the hand

Causes and mechanism of development

Purulent processes in the hand are most commonly triggered by Staphylococcus (Staphylococcus), although other microflora are occasionally found. The entry gates for bacteria are imperceptible, "hidden" microtraumas: minor punctures, abrasions, or skin chafing.

The risk of inflammation is significantly increased by the presence of foreign bodies, such as splinters, metal shavings, or glass shards. The pathogenesis of the disease begins with the introduction of infection into the area of microtrauma or around the foreign body. First, edema and primary inflammatory infiltration develop in the tissues, which subsequently progress to the purulent stage.

The process can also develop primarily as a deep infection — this occurs with direct penetrating wounds when the infection is delivered directly into the joint cavity or tendon sheath.

Influence of anatomical structure

The specific nature of inflammation development directly depends on the complex anatomy of the hand, which is determined by the diversity of its functions.

A special role is played by the structure of the subcutaneous adipose tissue. On the palmar surface, there are dense vertical connective tissue septa. Because of these, the purulent exudate cannot spread freely across the plane under the skin. Instead, the inflammation rushes deep into the tissues — toward the tendons, joints, and bones. This explains why superficial infections often lead to the secondary development of deep forms (e.g., articular or tendinous felon).

The skin of the dorsal surface of the hand has a completely different structure. It is characterized by high elasticity and mobility, easily stretches and gathers into folds, and the subcutaneous tissue here is extremely poorly developed.

Pathogenesis of tendon lesions

Synovial tendon sheaths play a key role in the progression of purulent complications. It is important to note the topography of the sheaths of digits II, III, and IV: they begin at the level of the metacarpophalangeal joints, end at the base of the nail phalanges, and are completely isolated from each other.

The mechanism of tendon death during inflammation:

1. Accumulation of exudate. Inflammatory fluid begins to accumulate in a closed space between the visceral and parietal layers of the synovial sheath.
2. Compression. Increasing pressure leads to the compression of the tendon mesentery (mesotenon) and the blood vessels running inside it that nourish the tissues.
3. Necrosis. Due to acute disruption of blood supply, dry necrosis forms — the tendon dies.

The only way to prevent this process is timely surgical opening of the sheath. This is the only way to relieve vascular compression and preserve normal hand function.

Clinical presentation and diagnostics

The disease proceeds with a sequential change of stages: initial (serous-infiltrative) and purulent (purulent-necrotic). The clinical picture consists of general symptoms (fever) and classic local signs: edema, hyperemia, severe pain, and impaired hand function.

In severe, neglected cases, the inflammation can encompass absolutely all tissues of the digit — such a condition is called pandactylitis.

For differential diagnosis of the abscess location, surgeons use the method of determining the point of maximum tenderness using a blunt probe. The following characteristic zones are distinguished:

• Bone felon: sharp pain in the area of the distal phalanx.
• Articular felon: tenderness is projected strictly onto the interphalangeal joint.
• Subcutaneous felon: maximum pain on the palmar surface of the affected phalanx.
• Tendon felon (tenosynovitis): pain spreads linearly along the course of the tendon sheath.
• Palmar callosity abscess: pain is localized in the distal part of the palm, directly over the heads of the metacarpal bones.
• Tenosynovitis of digit I and the radial bursa: pain along the course of the flexor tendon of the thumb with transition to the thenar eminence.
• Tenosynovitis of digit V and the ulnar bursa: tenderness in the projection of the little finger flexor with transition to the hypothenar eminence.

Class and exam questions

What else to study on this topic

• Anatomy of the palmar surface: skin, fasciae, and fascial spaces
• Classification of purulent-inflammatory diseases of the hand
• Surgical tactics and rules for opening tendon sheaths
• Structural features and topography of the synovial bursae of digits I and V

Other topics from the section "CHAPTER 11. SURGICAL INFECTION (PURULENT-INFLAMMATORY DISEASES)"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.