Complications of chickenpox

Classification by etiology

In clinical practice, all adverse consequences of this infection are divided into two broad categories based on their mechanism of occurrence:

1. Specific complications. Caused by the direct damaging action of the pathogen itself. The most dangerous are central nervous system disorders—encephalitis and meningoencephalitis. Their key clinical feature is that neurological symptoms debut during the period when the elements dry out and crusts form. At the same time, the risk of developing encephalitis is completely unrelated to the overall severity of the disease. Viral nephritis and myocarditis are also classified as specific lesions.
2. Nonspecific complications. Occur due to the overlay of secondary bacterial microflora onto damaged skin and mucous membranes. Unlike viral lesions, bacterial superinfections can join at any stage of the pathological process.

Mechanisms of secondary infection development

To understand the causes of nonspecific complications, the nature of the exanthema must be considered. The rashes are subjectively accompanied by intense pruritus. Normally, the vesicle contains clear fluid with the active virus, which eventually becomes turbid due to the accumulation of fibrin, polymorphonuclear leukocytes, and degenerate cells.

When scratching the itchy areas, the vesicles rupture prematurely, creating ideal entry gates for bacteria. The localization of the exanthema covers the scalp, face, trunk, and extremities. Notably, the palms and soles are usually spared of lesions.

Mucosal involvement and the risk of stenosis

Involvement of mucous membranes is recorded in 10–30% of patients and is a risk factor for local complications. Elements may appear on the conjunctiva, oral mucosa, genitalia, and larynx. Such vesicles rupture extremely quickly, leaving erosions and small ulcers with a hyperemic rim (complete epithelialization occurs on days 3–5).

Localization of the rash in the larynx poses a particular danger. In this case, the patient may experience hoarseness, a harsh cough, and develop a life-threatening condition—laryngeal stenosis.

Risk factors and systemic manifestations

The development of skin manifestations occurs in waves. Each wave (the phenomenon of "successive crops") repeats every 1–2 days, accompanied by fever and increased itching. Because of this, false polymorphism forms on the skin—the simultaneous presence of macules, papules, vesicles, and crusts. The prolonged presence of fresh skin lesions makes the patient vulnerable to bacteria throughout the entire rash period.

To assess prognosis, physicians rely on severity criteria:

• Severity of the intoxication syndrome (in severe cases, temperature reaches 39.0–40.0°C).
• Intensity of the rash.
• Presence of hemorrhagic syndrome elements.
• Appearance of signs of encephalopathy.

In addition, the virus exerts a systemic effect. Moderate tachycardia, decreased blood pressure, and painless short-term enlargement of all lymph node groups are possible. When atypical forms (hemorrhagic, gangrenous, or visceral) develop, the risk of severe complications increases manifold.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Clinical picture of atypical forms (visceral, gangrenous, hemorrhagic)
• Evolution of exanthema and pathomorphology of vesicle formation
• Differential diagnosis of early rash in the prodromal period
• Criteria for assessing the severity of intoxication syndrome
• Mechanisms of lifelong immunity formation and risks in immunodeficiencies

Other topics in the "Respiratory Infections" section

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