Prevention of obstruction and respiratory failure
One of the most formidable manifestations of the disease is laryngeal involvement with the development of stenosis and subsequent acute respiratory failure. To prevent asphyxia, strict clinical monitoring of the patient is established.
Signs of deterioration and increasing stenosis:
- Onset of restlessness in the patient.
- Increased frequency and significant prolongation of suffocation attacks.
- Progressing pallor of the skin progressing to cyanosis.
- Pronounced tachycardia, hypercapnia, and hypoxemia.
For the purpose of conservative prevention of edema and to improve airway patency, corticosteroids and antihistamines are prescribed. If conservative measures are ineffective and the pharyngeal lumen is critically narrowed (especially with signs of the incipient rejection of the diphtheria membrane), there is a colossal risk of immediate and complete obstruction. In such a situation, to prevent a fatal outcome, emergency surgical intervention — conicotomy or tracheostomy — is indicated.
Prevention of systemic toxic effects
To relieve the toxic effect and prevent multiorgan failure, early initiation of specific therapy is critical. The main drug is diphtheria antitoxin serum (DAT).
The dosage is selected individually depending on the severity:
- For localized croup (respiratory diphtheria), 15,000 – 20,000 IU is administered intramuscularly.
- In severe combined toxic forms (grade III with laryngeal involvement), the dose is increased to 150,000 IU (exceeding the base dose due to the combined nature of the lesion).
- In cases of delayed therapy initiation (e.g., from the fifth day of illness), the course dose can reach 400,000 IU, although the effectiveness of preventing severe complications decreases accordingly.
In parallel, nonspecific detoxification is performed to correct hemostasis and metabolic shifts, and broad-spectrum antibiotics (semisynthetic penicillins, cephalosporins, or fluoroquinolones) are prescribed.
Prevention of late complications
Even after pathogen eradication and discharge from the hospital, the patient requires monitoring due to the persistent risk of developing severe delayed complications. The toxic effect of diphtheria exotoxin leads to the development of multiorgan pathology.
Main groups of complications:
- Cardiovascular: acute myocarditis manifested by arrhythmia, enlargement of heart borders, tachycardia, and muffled heart sounds.
- Renal: acute nephrosis and the development of renal failure.
- Neurological: encephalopathy (presumably of metabolic origin), as well as severe polyneuropathies. Neuritis of the IX, X, and VII cranial nerve pairs develops, which manifests as palatal paresis, aphonia, choking during swallowing (fluid leaks through the nose), and absence of the gag reflex. Subsequently, flaccid paresis of the spinal muscles and extremities may join.
Swallowing disorders and paresis in turn create a risk of aspiration, which requires the prevention of secondary bacterial pneumonias (accumulation of foul-smelling purulent discharge in the airways, moist rales, and pronounced mixed dyspnea).
Differential diagnosis
Careful differential diagnosis is required to correctly choose tactics and prevent medical errors.
Before performing laryngoscopy, laryngeal diphtheria should be differentiated from:
- Exacerbation of chronic laryngitis.
- Parainfluenza.
- Tumor processes of the larynx and mediastinum.
During laryngoscopy, evidence favoring diphtheria includes edema of the vocal fold and epiglottic mucosa (up to glottic narrowing), as well as the presence of characteristic membranes. Specific diagnostics include mandatory bacteriological examination of oro- and nasopharyngeal swabs. It may also be necessary to rule out a peritonsillar abscess (with pharyngeal asymmetry, fluctuation, trismus, and sharp pain), which can simulate the toxic form of diphtheria.
Briefly: answers to topical questions
What is the primary prevention of diphtheria (vaccination)?
The basis of specific diphtheria prevention is active routine immunization of the population with toxoids.
- The goal of vaccination is the formation of antitoxic immunity and the prevention of severe toxic forms of diphtheria and its consequences.
- Preparations — diphtheria toxoid (exotoxin detoxified with formaldehyde and adsorbed on aluminum hydroxide), which is part of combined vaccines (DTP, DT, DT-M, D-M).
- Schedule — primary vaccination of children is carried out at 3, 4, 5, and 6 months, the first revaccination at 18 months; subsequent ones at 6–7 years, 14 years, and then every 10 years throughout life for adults (using preparations with a reduced antigen content).
What nutrient media are used to inoculate throat and nasal swabs to confirm diphtheria?
Special elective and differential-diagnostic nutrient media are used to cultivate the diphtheria pathogen.
- Roux's elective medium — contains coagulated horse serum.
- Klauberg II medium — blood-tellurite medium.
- Tinsdale medium — serum agar with potassium tellurite and cystine.
Potassium tellurite in the media inhibits the growth of concomitant microflora, while the diphtheria pathogen is resistant to it.
What changes are detected during laryngoscopic examination in a patient with laryngeal diphtheria?
Laryngoscopic examination in a patient with laryngeal diphtheria reveals signs of true croup. These include:
- hyperemia and edema of the epiglottis and vocal fold mucosa;
- narrowing of the glottis;
- presence of fibrinous membranes (cast membranes) on the vocal folds, as well as in the lumen of the trachea and bronchi;
- obstruction of the airway lumen by cast membranes.
DAT — Diphtheria Antitoxin Serum: the main rule for preventing fatal outcomes is to administer it early and in an adequate dose.
Class and exam questions
What does specific diagnosis of diphtheria involve?
The main method is bacteriological examination of nasopharyngeal and oropharyngeal swabs.
What are the indications for emergency tracheostomy in diphtheria?
Progressing laryngeal stenosis, narrowing of the pharyngeal lumen, and signs of rejection of the diphtheria membrane, creating a risk of complete obstruction.
What neurological complications are typical during the convalescent period?
Development of cranial nerve neuritis (IX, X, VII pairs), flaccid paresis of the extremities and spinal muscles, leading to swallowing and breathing disorders.
What else to study on this topic
- Rationale for diphtheria antitoxin (DAT) dosages in various forms
- Mechanism of multiorgan failure development in toxic diphtheria
- Differential diagnosis of peritonsillar abscess and toxic oropharyngeal diphtheria
- Management of patients with bulbar disorders and paresis at home
- Instrumental and laboratory monitoring in the ICU (acid-base balance, blood gases, creatinine)
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