Gangrene Flashcards

1
Q

Define gangrene.

A

A complication of necrosis characterised by the decay of body tissues. There are two major categories: infectious gangrene (wet) and ischaemic gangrene (dry).

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2
Q

How is gangrene classified?

A

Infectious wet gangrene:

  • Type I (polymycrobial) necrotising fasciitis = e.g. Fournier’s gangrene or NF of the head and neck; commonly by Enterobacteriaceae
  • Type II (monomicrobial) necrotising fasciitis = e.g. Ludwig’s angina (submandibular/sublingual pain developing into NF)
  • Among drug abusers C perfringens, C sordellii, and C novyi are most commonly involved
  • Gas gangrene - usually clostridium species
  • Progressive bacterial (Meleney’s) synergistic gangrene - usually at abdo operative wound around ileostomy or colonostomy

Ischaemic dry gangrene:

  • Atherosclerosis
  • Thrombosis - vasculitis, trauma, drug abuse, malignancy
  • Vasospasm
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3
Q

What are the risk factors for infectious and ischaemic gangrene?

A

Ischaemic:

  • DM
  • atherosclerosis (ischaemic gangrene)
  • smoking (IG)
  • renal disease
  • drug abuse
  • malignancy
  • hypercoagulable states
  • prolonged application of tourniquets

Infectious:

  • trauma or abdominal surgery (infectious gangrene)
  • contaminated wounds (infectious gangrene)
  • DM
  • alcoholism
  • renal disease
  • malignancy
  • malnutrition
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4
Q

What are the types of gangrene? How do you treat each (briefly)?

A

Dry gangrene - necrosis in the absence of infection. Has a line of demarcation between living and dead tissue → restoration of blood supply +/- amputation

Wet gangrene - tissue death and infection (associated with discharge) occurring together → analgesia, broad spectrum IV antibiotics, surgical debridement +/- amputation

Gas gangrene - subset of necrotising myositis caused by spore forming clostridial species. Rapid onset of myonecrosis, muscle swelling, gas production, sepsis, and severe pain → remove all dead tissue +/ - amputation, give benzylpenicillin +/- clindamycin and hyperbaric O2.

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5
Q

What 4 features of diabetes make patients prone to limb threatening diabetic foot infections?

A
  • high blood glucose
  • inefficient immunological responses
  • peripheral neuropathy
  • peripheral arterial disease
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6
Q

What are the symptoms of gangrene?

A
  • Pain - but not always. Often burning pain in the ball of the foot and toes that is worse at night. Sudden onset of pain is usually the first symptoms of infectious gangrene.
  • Oedema
  • Skin discolouration - eschar, ecchymoses, purpura, skin blebs, haemorrhagic bullae
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7
Q

Whart are the signs of gangrene on examination?

A
  • Cold extremities, history of thrombosis, trophic skin changes
  • Ankle systolic of <50mmHg, toe systolic <30mmHg (but less reliable in DM patients)
  • ABPI 0.4 or less in critical limb ischaemia
  • Oedema and erythema
  • Crepitus (gas gangrene) on gentle palpation
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8
Q

What investigations would you do for gangrene?

A

Bloods:

  • FBC - Hb <135g/L; haemolytic anaemia common in gas gangrene; WCC >15 x 10^9/L common
  • Blood cultures
  • Metabolic panel - sodium <135 mmol/L present in nearly ALL; AKI, liver failure, or metabolic acidosis.
  • LDH/CRP - Elevated LDH levels in haemolytic anaemia

Imaging:

  • Plain XR - ?gas in soft tissues +/- osteomyelitis
  • CT/MRI of affected site - ?enhancement, oedema or thickening of fascia
  • Doppler USS- ?arterial/venous obstruction
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9
Q

Describe livedo reticularis.

A

Mottled reticulated vascular pattern that appears as a lace-like purplish discoloration of the skin. The discoloration is caused by swelling of the venules owing to obstruction of capillaries by small blood clots.

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10
Q

Describe eshar.

A

A slough or piece of dead tissue that is cast off from the surface of the skin, particularly after a burn injury, but also seen in gangrene, ulcer, fungal infections, etc

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11
Q

How can you clinically categorise the viability of an acutely ischaemic limb?

A

Viable:

  • no sensory loss or muscle weakness;
  • audible arterial and venous Doppler signals

Threatened marginally:

  • no or minimal (toe) sensory loss; no muscle weakness;
  • often inaudible arterial Doppler signals; audible venous Doppler signals.

Threatened immediately:

  • sensory loss of more than toes accompanied by rest pain;
  • mild to moderate muscle weakness;
  • usually inaudible arterial Doppler signals;
  • audible venous Doppler signals.

Irreversible/non-viable:

  • major tissue loss and/or permanent nerve damage;
  • profound anaesthesia;
  • profound paralysis (rigor);
  • inaudible arterial and venous Doppler signals.
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12
Q

Describe the presentation of necrotising cellulitis.

A
  • Dark wound drainage
  • Gas formation in the skin with sparing or fascia and deep muscles
  • Gradual onset with no pain,
  • Swelling and systemic toxicity
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13
Q

Describe the presentation of necrotising fasciitis (NF).

A
  • Deep infection of the subcutaenous tissue that results in progressive destruction of fascia and fat
  • Usually erythematous without sharp margins, swollen, warm, shiny and especially tender
  • Rapid progression over days with skin colour changes and bullae formation

Cutaneous gangrene observed within 3-5 days witha prodrome of anaesthesis before necrosis (helps distinguish NC from NF)

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14
Q

Describe the presentation of necrotising myositis.

A
  • Fever
  • Exquisite pain
  • Muscle swelling
  • Overlying skin erythema, warmth, petechia, bullae, vesicles, progression over several hours to involve contiguous muscle groups and soft tissue.
  • Septic shock (streptococcal toxic shock syndrome)
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15
Q

What is phlegmasia cerulea dolens? How does it present?

A

Rare condition associated with malignancy where there is a total or near-total obstruction of venous drainage.

  • Pain
  • Marked oedema
  • Cyanosis - usually preceded by white appearance of subcut oedema without venous congestion
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16
Q

What is the pathophysiology behind infectious gangrene?

A
  • Bacterial multiplication + production of exotoxins require low oxygen tension
  • Alpha-toxin (main) is a metalloenzyme which causes cell destruction by hydrolysis of cell membrane components (so can –> lysis of erythrocytes, leukocytes, platelets, fibroblasts + muscle cells)
  • Necrotic tissue e.g. wounds provides necessary environment for spore germination (tissue enzymes and low oxidation/reduction potential). This necrosis can spread and make the infection spread. Fermentation of glucose is probably the main mechanism of gas production.
17
Q

What is the pathophysiology behind ischaemic gangrene?

A
  1. Atherosclerosis
  2. Thombosis - hypercoagulable states, phlegmasia cerulea dolens (most caused by arterial obstruction but this is by venous)
  3. Vasospasm - Cocaine can cause severe vasospasm sufficient to produce gangrene.
18
Q

What is the management of infectious gangrene?

A

Surgical debridement -

  • Limb: guillotine amputation and later definitive amputation with wound closure
  • Perineal: wide excision of all necrotic tissue

Appropriate antibiotics - cover anaerobes + aerobes; change once culture results return

Intensive supportive care - massive amounts of fluids, pressors.

19
Q

What is the management of ischaemic gangrene?

A

IV heparin bolus followed by continuous heparin infusion

Assess viability of the limb - irreversible changes can occur within 4-6hrs

Surgery

Percutaneous transluminal angioplasty

Thrombolytic therapy - catheter based, intra-arterial or intravenous e.g. for phlegmasia cerulea dolens

Intensive supportive care- fluids, pressors.

20
Q

What are the complications of gangrene?

A
  • Sepsis
  • Shock
  • Acute renal failure
  • Haemolysis - especially in gas gangrene
  • Loss of limb
  • DIC
21
Q

What is the prognosis with gangrene?

A

Usually life and limb-threatening

NF mortality is 10-40% with surgery and abx

Ischaemic gangrene has amputation rates of 10-40%