Lecture on acute specific infection in surgical practice

1. Acute specific
surgical infection
Professor Ruslan I Sydorchuk MD PhD

2. • Erysipelas
• Acute anaerobic infection.
Gas gangrene.
• Tetanus.
• Anthrax.
• Wound diphtheria.
ACUTE SPECIFIC SURGICAL INFECTION
classification

3. Erysipelas

4. Erysipelas (Greek ερυσίπελας – red skin)
(also known as "Holy fire", and
"St Anthony's fire) is an acute
streptococcus bacterial infection of the
dermis.
Characterized by fever, headache, vomiting,
and purplish raised lesions
Erysipelas

5. ETIOLOGY
Hemolytic Streptococci (S.hæmolyticus)
beta-hemolytic group A streptococci
Erysipelas

6. EPIDEMIOLOGY
• Carriers
• Sick persons (tonsillitis, erysipelas, scarlet
fever – scarlatina, rheumatism, several
cases of respiratory diseases)
Erysipelas

7. RISK FACTORS
• elderly, infants, and children
• immune deficiency, diabetes, alcoholism
• skin ulceration, fungal infections and impaired
lymphatic drainage
Erysipelas

8. STAGES:
– Prodromal (weakness, fatigue, ↑temps, chills,
intoxication, sweating, loss of appetite, vomiting) –
no local signs or itching;
– Fastigium (height of disease) – raised clinics;
– Reconvalescence (outcome, decrease of
symptoms).
Erysipelas

9. SIGNS AND SYMPTOMS:
– fevers, shaking, chills, fatigue, headaches, vomiting
(general symptoms)
– erythematous skin lesion which enlarges rapidly
and has a sharply demarcated raised edge (local)
– red, swollen, warm, hardened and painful rash,
similar in consistency to an orange peel (local)
Erysipelas

10. SIGNS AND SYMPTOMS:
– More severe infection can result in vesicles, bullae,
and petechiae, with possible skin necrosis. Lymph
nodes may be swollen, and lymphedema may
occur.
– Occasionally, a red streak extending to the lymph
node can be seen.
Erysipelas

11. LOCATION:
– face, arms, fingers, legs and toes
– tends to favor the extremities
Erysipelas

12. CLINICAL FORMS:
– erytematous
– bullaeous
– necrotic (necrotizing fascitis)
– phlegmonous
– combined
Erysipelas

13. Erysipelas

14. Erysipelas

15. TREATMENT:
– antibiotics, using beta lactams, clindamycin or
erythromycin
– physiotherapy e.g. UV-radiation
– NSAIDs, detoxication
– surgery
Erysipelas

16. COMPLICATIONS:
– septic shock
– septic arthritis and infective endocarditis
– recurrence of infection
– necrotizing fasciitis
– lymphatic damage (elephantiasis)
Erysipelas

17. Acute anaerobic infection
GAS GANGRENE

19. GAS GANGRENE
definition
A deadly bacterial infection caused by
certain Clostridium bacteria that
produces gas
within tissues in gangrene

20. GAS GANGRENE
the schematic view

21. GAS GANGRENE
the background

22. GAS GANGRENE
etiology
Clostridium perfringens
Clostridium haemolyticum
Clostridium novyi
Clostridium oedematiens
Vibrio septicum

23. GAS GANGRENE
etiology
Clostridia
Gram+, oblig. ANA

24. GAS GANGRENE
classification
Clinical forms
Toxic
Suppurative (phlegmonous)
Emphisematous (gas-forming), classic
Fulminant (septic)
Mixed

25. GAS GANGRENE
symptoms
Shaving (razor blade) symptom
Ligature symptom
Crepitating symptom
The Cork of Champagne symptom

26. GAS GANGRENE
symptoms

27. GAS GANGRENE
symptoms
Myonecrosis, gas production, and sepsis
Progression to toxemia and shock is often
very rapid.

28. GAS GANGRENE
symptoms
The site of infection becomes inflamed with
a pale to brownish-red and very painful
tissue swelling.
If pressed on the swollen tissue with fingers,
it may give a feel of gas as a crackly
sensation (crepitation).

29. GAS GANGRENE
symptoms
The edges of the infected area expand so
quickly that changes can be seen over a few
minutes. The involved tissue may be
completely destroyed.

30. GAS GANGRENE
symptoms
Air under the skin (subcutaneous
emphysema)
Blisters filled with brown-red fluid
Drainage from the tissues, foul-smelling
brown-red or bloody fluid (serosanguineous
discharge)
Increased heart rate (tachycardia)
Moderate to high fever

31. GAS GANGRENE
symptoms
Moderate to severe pain around a skin injury
Pale skin color, later becoming dusky and
changing to dark red or purple
Progressive swelling around a skin injury
Sweating
Vesicle formation, combining into large
blisters
Yellow color to the skin (jaundice)

32. GAS GANGRENE
symptoms
Symptoms usually begin
suddenly and quickly worsen!

33. GAS GANGRENE
diagnosis
Anaerobic tissue and fluid cultures may
reveal Clostridium species.
Blood culture may grow the bacteria causing
the infection.
Gram stain of fluid from the infected area
may show gram-positive rods (Clostridium
species) or other bacterial types.
X-ray, CT scan, or MRI of the area may
show gas in the tissues.

34. GAS GANGRENE
treatment
Start immediately!
Maximally intensive!
Comprehensive!

35. GAS GANGRENE
treatment

36. GAS GANGRENE
treatment
Surgery
Antibiotix-x
Detox-x
Immuno-x (Antitoxins, mono- +
polyvalent)
hyperbaric oxygen therapy (HBOT)
Supportive & symptomatic therapy

37. GAS GANGRENE
treatment

38. GAS GANGRENE
treatment
Surgery
Debridement
Wide, stripe like excisions (oxygen)
Amputation necessary in many cases

39. GAS GANGRENE
treatment
Surgery

40. GAS GANGRENE
treatment
Surgery

41. GAS GANGRENE
outcome

42. Diphtheria

43. Diphtheria
Nome, Alaska; the 1925 serum run to Nome
to deliver diphtheria antitoxin is now known
as the "Great Race of Mercy".

44. Definition
Diphtheria (Greek – διφθέρα (diphthera)
"pair of leather scrolls")
is an upper respiratory tract illness caused
by Corynebacterium diphtheriae,
a facultative anaerobic Gram-positive bacterium

45. Etiology
Corynebacterium diphtheriae
Klebs-Löffler bacillus
Gram stained Corynebacterium diphtheriae culture

46. Epidemiology
Disability-adjusted life year for diphtheria per 100,000 inhabitants

47. Epidemiology
Diphtheria Hotspots 2000 - present; cases reported to the WHO

48. Classification
Respiratory
Skin (wound diphtheria)
Probable: a clinically compatible case that is not laboratory-
confirmed and is not epidemiologically linked to a laboratory-
confirmed case
Confirmed: a clinically compatible case that is either
laboratory-confirmed or epidemiologically linked to a
laboratory-confirmed case

49. Spreading
Diphtheria is a highly contagious disease spread by
direct physical contact or breathing the aerosolized
secretions of infected individuals
Pathways:
1)Direct contact
2)Aerosol

50. Data & signs
The cutaneous form of diphtheria is often a
secondary infection of a preexisting skin disease.
Signs of cutaneous diphtheria infection develop an
average of seven days after the appearance of the
primary skin disease.

51. Data & signs
The respiratory form has an incubation period of 2–5
days. The onset of disease is usually gradual.
Symptoms include fatigue, fever, a mild sore throat
and problems swallowing.

52. Data & signs

53. Diagnosis
Is based on both laboratory and clinical criteria
Laboratory criteria
Isolation of Corynebacterium diphtheriae from a clinical
specimen, OR
Histopathologic diagnosis of diphtheria
Clinical criteria
Upper respiratory tract illness with sore throat
high-grade fever, and
An adherent pseudomembrane of the tonsil(s), pharynx, nose or
wound.

54. Treatment
*Patients MUST be put in a hospital intensive
care unit (ICU) and be given a diphtheria anti-
toxin. Since antitoxin does not neutralize toxin
that is already bound to tissues, delaying its
administration is associated with an increase in
mortality risk. Therefore, the decision to
administer diphtheria antitoxin is based on clinical
diagnosis, and should not await laboratory
confirmation

55. Treatment
*obstruction in the throat may require intubation or a
tracheotomy
*symptomatic treatment for:
-abnormal cardiac rhythms that can occur early in the course of
the illness or weeks later, and can lead to heart failure.
-diphtheria can also cause paralysis in the eye, neck, throat, or
respiratory muscles

56. Treatment
*Antibiotics are used in patients or carriers only to
eradicate C. diphtheriae and prevent its transmission to
others:
Erythromycin (orally or by injection) for 14 days (40 mg/kg per
day with a maximum of 2 g/d), OR
Penicillin. Patients with allergies to penicillin or erythromycin can
use rifampicin or clindamycin.

57. Anthrax
Anthrax
Black Death

58. Definition
Anthrax (Άνθραξ), the Greek word for coal is
an acute lethal infectious disease caused by
Bacillus anthracis.
This name comes from the charred
looking skin lesions.

59. Etiology
Gram stain of the Bacillus anthracis

60. Forms
intestinal (ingestion),
pulmonary (inhalation),
cutaneous (skin).
No live B. anthracis are transmittable, spores are

61. Forms
pulmonary form

62. Forms
cutaneous form
Cutaneous (on the skin) anthrax infection in humans
shows up as a boil-like skin lesion that eventually forms
an ulcer with a black center (eschar).
The black eschar often shows up as a large,
painless necrotic ulcer (beginning as an irritating
and itchy skin lesion or blister that is dark and usually
concentrated as a black dot, somewhat resembling bread
mold) at the site of infection.
Unlike bruises or most other lesions, cutaneous
anthrax infections normally do not cause pain.

63. Forms
cutaneous form

64. Treatment
Early antibiotic treatment of anthrax is essential
Large doses of intravenous and oral antibiotics,
such as fluoroquinolones, like ciprofloxacin (cipro),
doxycycline, erythromycin, vancomycin or penicillin.
Delays of only a few days may make the disease untreatable
and treatment should be started even without symptoms if
possible contamination or exposure is suspected.

65. TETANUS

66. • Tetanus was well known to ancient people
who recognized the relationship between
wounds and fatal muscle spasms.
• The word "tetanus" is derived from the
Greek τέτανος (tetanos) meaning "taut",
and τείνειν (teinein) to "stretch".
Tetanus

67. • In 1884, Arthur Nicolaier isolated the
strychnine-like toxin of tetanus from free-
living, anaerobic soil bacteria.
• The etiology of the disease was further
elucidated in 1884 by Antonio Carle and
Giorgio Rattone, who demonstrated the
transmissibility of tetanus for the first time.
Tetanus

68. Tetanus
a medical condition characterized by a
prolonged contraction of skeletal muscle
fibers.

69. Tetanus
Disability rates per 100.000 (WHO)

70. Tetanus
Incidence rates (WHO)

71. Tetanus
The primary symptoms are caused
by tetanospasmin, a neurotoxin
produced by the Gram-positive,
obligate anaerobic bacterium
Clostridium tetani. Infection
generally occurs through wound
contamination and often involves
a cut or deep puncture wound.
As the infection progresses,
muscle spasms develop in the jaw
(thus the name "lockjaw")
and elsewhere in the body.

72. Tetanus

73. prophylaxis/prevention

74. treatment
Specific (toxoid, antitoxin)
Sedatives, tranquillizers
Environment, avoidance of irritation and
stimuli
Surgery, local
Miorelaxants, spasmolytics
Artificial breathing
Symptomatic

75. Tetanus antitoxin
1) In bulk: 5500IU/ml
2) In amp: 1,500IU/amp, 3,000IU/amp, 5,000IU/amp

76. Tetanus toxoid
History of Adsorbed
Tetanus Toxoid
(Doses)
Clean, Minor
Wounds
All Other
Wounds
Td TIG Td TIG
Unknown or
< Three
Yes No Yes Yes
≥ Three No† No No§ No
† Yes, if > 10 years since last dose.
§ Yes, if > 5 years since last dose.
Tetanus and Diphtheria Toxoids Adsorbed For Adult Use (Td) 0.5 mL
Tetanus Immunoglobulin (TIG)