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Infectious Diseases · Respiratory Infections

Complications of diphtheria

Specific complications of diphtheria are caused by the systemic action of the exotoxin on target organs and local inflammatory reactions. The most formidable conditions requiring emergency intervention are infectious-toxic shock, severe myocarditis, polyneuropathy, and mechanical asphyxia against the background of airway edema.

MyocarditisThe first signs of cardiac involvement require the immediate prescription of strict bed rest.
StenosisDevelops due to tissue edema and fibrin accumulation in toxic forms and croup.
ITSHShock therapy requires the mandatory administration of antitoxic serum and high doses of hormones.
Serum sicknessPossible in case of unjustified overstatement of dosages of foreign horse serum.
4 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Septic shock

Shock develops as a result of pronounced microcirculatory disorders. They are provoked by the action of the diphtheria toxin itself on tissues, as well as inflammatory mediators and cell breakdown products. The main task of intensive therapy is to neutralize the circulating toxin and eliminate tissue hypoxia.

  • Specific therapy: Based on the intravenous administration of antitoxic diphtheria serum (ADS). Strict rule: before starting the infusion, the patient must receive prednisolone at a dose of 90–120 mg intravenously.
  • Hormonal support: Subsequently, high doses of glucocorticoids are prescribed (prednisolone at the rate of 5–20 mg/kg or hydrocortisone 20–75 mg/kg per day).
  • Hemodynamic correction: Includes the administration of colloidal and crystalloid solutions, the use of catecholamines (dopamine, norepinephrine, adrenaline, dobutamine), as well as oxygen therapy.
  • Combating DIC syndrome: Fresh frozen plasma, heparin, protease inhibitors, and activated protein C are used.

For nonspecific detoxification in severe toxic forms, plasmapheresis with the replacement of 70–100% of the plasma volume with cryogenic donor plasma can be used.

Diphtheritic myocarditis

Heart muscle damage requires the patient's immediate transfer to strict bed rest. The duration of bed rest depends on the severity of the disease and in toxic forms can reach 30–45 days. Treatment is aimed at restoring coronary blood flow, stopping arrhythmias, and improving myocardial metabolism.

Comprehensive therapy includes:

  1. Infusion of a polarizing mixture (glucose, potassium, insulin).
  2. Preparations to improve myocardial metabolism (ATP, riboxin, cocarboxylase, cytochrome C, antioxidants).
  3. Anticoagulants and antiplatelet agents to improve microcirculation.
  4. Glucocorticoids and nonsteroidal anti-inflammatory drugs.
  5. Symptomatic pain relief for attacks associated with myocardial ischemia.
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Respiratory failure and laryngeal stenosis

Acute respiratory failure often accompanies laryngeal diphtheria (croup) or severe toxic forms of oropharyngeal diphtheria. In the latter case, the pharyngeal lumen narrows due to massive soft tissue edema and the accumulation of dense fibrinous membranes.

  • Catarrhal stage: Steam inhalations with soda or herbal decoctions, aerosol and systemic glucocorticoids, antihistamines, diuretics, and aminophylline are prescribed.
  • Stenosis stage: The patient needs strict dynamic monitoring. With increasing hypoxemia, more frequent and prolonged suffocation attacks, the appearance of motor agitation, pronounced cyanosis, and tachycardia, emergency instrumental or surgical intervention (intubation, tracheostomy, or conicotomy) is indicated.

Polyneuropathy and iatrogenic complications

Severe polyneuropathy is another absolute indication for the immediate prescription of strict bed rest. When nerves regulating the act of swallowing are involved in the process, the patient loses the ability to feed independently — during this period, mandatory tube feeding is indicated.

A separate group consists of immune complications arising from irrational treatment. Unjustified overestimation of the dose or frequency of administration of horse antitoxic diphtheria serum provokes allergic reactions, up to serum sickness. This not only paradoxically aggravates the course of the diphtheria infection itself, but also significantly increases the risk of a fatal outcome.

Briefly: answers to topical questions

What ECG signs are characteristic of diphtheritic myocarditis?

Characteristic ECG signs of diphtheritic myocarditis:

  • prolongation of the PR interval;
  • changes in the ST–T complex;
  • rhythm and conduction disturbances, including blocks of various degrees.

What are the timings for the development of myocarditis in toxic diphtheria?

The timing of myocarditis development determines the severity of the course of toxic diphtheria.

Type of myocarditisOnset timing
EarlyFrom the 4th day of the disease; a prognostically unfavorable option is development as early as the 1st week of the disease
LateTypical course — 2–3rd week of the disease; the timing of development can stretch to 3–4 weeks

According to pathological anatomy data, diphtheritic myocarditis develops at the end of the 1st — beginning of the 2nd week of toxic diphtheria.

Which nerves are most often affected in diphtheria polyneuropathy, besides those regulating the act of swallowing?

In addition to the nerves involved in the act of swallowing, the sources indicate damage to other cranial nerves, peripheral nerves, and autonomic ganglia in diphtheria:

  • ciliary nerve (n. ciliaris) — accommodation paralysis, development of farsightedness;
  • abducens nerve (n. abducens) — strabismus, ptosis, asymmetry;
  • sympathetic and phrenic nerves;
  • III cervical sympathetic and nodose ganglia.

The sources also indicate that demyelination first affects the cranial nerves, then the rest.

Class and exam questions

Is a positive test for horse protein a contraindication to the administration of serum?

In localized forms, administration is canceled. However, in severe forms (toxic diphtheria, croup), the serum is administered for vital indications intravenously, but strictly under the cover of high doses of glucocorticoids in an intensive care unit.

In what cases with diphtheria is the patient transferred to tube feeding?

Tube feeding is necessary when specific polyneuropathy develops, which is accompanied by muscle paresis and persistent disturbance of the act of swallowing.

What clinical signs indicate the need for emergency tracheostomy or intubation?

Intervention is required for signs of decompensated stenosis: increasing cyanosis, changes in respiratory rhythm, pronounced tachycardia, motor agitation, and prolonged suffocation attacks.

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What else to study on this topic

  • Technique for conducting skin allergy tests for horse protein
  • Principles of serum dosing depending on the form of diphtheria
  • Extracorporeal detoxification and plasmapheresis in severe forms
  • Stages of diet therapy during the convalescence period (tables No. 4, 13, 15)

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