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Necrotising Fasciitis

Helen Parriss Band 5 Physiotherapist Burns and Plastics May - September 2010

Aims of the Presentation


To

develop knowledge of the condition. To identify best practice with treatment of this condition. To review a case study of a patient with necrotising fasciitis.

Definition

Necrotising soft tissue infections recognised by Hippocrates in the 5th century BC. Known as malignant ulcer, gangrenous ulcer and putrid ulcer in the18th century. In 1871Joseph Jones, a war surgeon, called it hospital gangrene. In 1924 Meleney called it hemolytic streptococcal gangrene. In 1952 Dr B Wilson called it necrotising fasciitis.
Fascia fibrous tissues that enclose and connect the muscles Necrosis death of a portion of tissue A rare, potentially life-threatening, progressive, rapidly spreading, inflammatory infection characterised by widespread necrosis of the skin, subcutaneous tissue down to the deep fascia. Primarily involves the superficial layers of the extremities (57.8%), abdomen or perineum.

Anatomical Structures Affected by Necrotising Fasciitis

Prevalence and Incidence


UK

incidence estimated to lie between 0.4 and 0.53 cases per 100,000 population. UK prevalence is approximately 500 cases per year.

70-100 caused by the bacterium group A streptococcus.

Male

: female ratio 2:1. Worldwide rates increased from mid-1980s to early1990s.

Types of necrotising fasciitis


Type

I : a polymicrobial flora.

A mixture of aerobic and anaerobic organisms, commonly


Pseudomonas Haemolyic saphylococcus Bacteroides Diphterioids Coliforms

Type

II : a monomicrobial flora.

Generally due to Group A -Streptococcus bacteria (most common case, approx 15% of cases).
Type

III : marine vibrio gram-negative rods.

Puncture wound from fish, cut or insect bite exposed to sea water, shellfish or fish in tropical water.

Causes of necrotising fasciitis


Primary

or idiopathic cause cause

Challenging in the absence of a known causative factor.


Secondary

Exposed to an individual with an opening in their skin. Direct contact with someone carrying the bacteria . The bacterium being carried by the person itself. Enter through weakened skin, as a contusion, a bruise, a blister, or even an abrasion. Sight of entrance can be as minor as a paper cut or a pin prick. Sometimes there is no obvious entry point.
Remember,

it can happen to anyone!!!!!!

Predisposing Factors
Diabetes

(leading predisposing factor) IV drug use Alcoholism Immuno-suppression eg HIV/AIDS, steroid usage, DM, major burns Invasive treatment procedures eg DM and kidney dialysis Trauma Recent surgery Atherosclerosis Chronic venous ulceration Severe illnesses: heart, lung, or liver disease Obesity

Signs and Symptoms


Three

stages of symptoms:

Early symptoms (usually within 24 hours) include:


Disproportionate and increasing pain. Small cut or scratch on the skin.
Sometimes there is no evidence of any trauma.

Flu-like symptoms, such as fever, nausea, confusion, dizziness, weakness and diarrhoea Thirst as the body becomes dehydrated.

Signs and Symptoms


Advanced symptoms (usually within 3-4 days) include:
Swelling of the painful area, accompanied by a rash. Large dark blotches developing into fluid filled blisters. A mottled, flaky appearance at the trauma site as tissue below the skin becomes necrotic. Diarrhoea and vomiting.

Critical symptoms (usually within 4-5 days) include:


Severe fall in blood pressure. Toxic shock from the poisons released by the bacteria. Unconsciousness as the body weakens and unable to fight off infection.

Investigations
Laboratory

tests:

leucocytosis raised urea and creatinine hypoalbuminaemia acidosis altered coagulation profile

Plain

radiography

helps identify soft tissue gas

Investigations
MRI/CT:

can show soft tissue gas can show soft tissue necrosis
Incisional

or excisional biopsy:

this can be done at the bedside but it is usually preferable for it to be done in theatre to permit adequate and thorough debridement of all necrotic tissues provides histological confirmation of the diagnosis and tissue culture to identify pathogens and sensitivities rapid frozen section may prove useful

Medical intervention
Necrotising

disease. Requires early recognition and treatment. IV resuscitation for systemic sepsis, eg tachycardia, oliguria, hypotension. Broad spectrum antibiotic combinations against anaerobes, gram-negative and gram-positive bacilli. Antibiotic combinations determined according to culture sensitivity and clinical course of patient. Debridement of area to healthy tissue, repeated as necessary. Amputation may be required. Reconstructive surgery following full bacteria eradication. Nutritional supplementation.

fasciitis is a challenging and potentially lethal

Prognostic Factors and Prognosis


Prognosis decreases sharply with time. Dependent on


Early recognition and intervention Extent of infection Delayed first debridement Multi-organ failure DM PVD Malnutrition Malignancy Immunosuppression Obesity IV drug abuse Chronic alcoholism

Overall mortality ranges from 6-76% in published literature, although more recent studies suggest up to 25% mortality.

Case Study

Social History
37 year old unemployed male. Mum died when patient 11 yrs old. Lives with long term partner and three children (two teenage and one 21yrs+).

Past Medical History


IVDU with 19 year history of heroin abuse. Began injecting into femoral vein over last year. Last injected mid July 2010. HIV -ve. ? Hep C +ve (presumptive diagnosis) - outstanding result on discharge
Approx. 50% IVDU patients are Hep C +ve.

Alcohol excess approx. 15 cans lager/day. Smokes approx. 20 cigarettes/day.

Case Study

Link with PMH


Skin and soft tissue bacterial infections are a common complication of intravenous drug use. This high rate, estimated at 25%, is due to: Injection of drugs into the fatty layer under the skin (skin popping)
Leakage of drugs out of veins during the injection (extravasation) Tissue death (necrosis) due to toxic materials in drugs Increased numbers of bacteria on the skin surface.

Heroin is cut with fillers eg caffeine, baking soda, flour, soil and faecal material. Injection of sclerosing adulterants and drugs produce tender and inflammatory plaques that ulcerate and heal resulting in ulceration and scar tissue to the epidermis, dermis and subcutaneous tissue.

Case Study
History

of Present Condition

Last injected into right femoral vein mid-July 2010. Admitted to Countess of Chester Hospital ICU 08/08/2010 with a 2/52 history of gross swelling of right lower limb with red pustules extending to the groin. Diagnosis made of cellulitis. Diagnosed with necrotising fasciitis 11/08/2010
IV antibiotics given
Flucloxacillin and benzylpenicillin then Ciprofloxacic and Clindamycin.

Blood cultures grew Streptococcus Anginosus


Metronidazole and Tigecycline.

Case Study
CXR 11/08/2010 showed LLL patchy consolidation. Intubated and sedated 11/08/2010. Theatre - three debridements on 12/08/2010, 13/08/2010 and 16/08/2010 due to spread of necrotising fasciitis. Right lower limb degloved down to muscle from groin to foot. Result - infection controlled, wound clear and antibiotics stopped. Pain relief on discharge from COCH
Zomorph (morphine sulphate) 60mg bd Oramorph 5mg four hourly

Patient transferred to Whiston Burns Unit 27/08/2010.

Case Study

On admission to Burns Unit received OOH chest physio. Sputum sample obtained 29/08/2010
e-coli - commenced on IV tacazin.

Theatre 31/08/2010 for right lower limb debridement and split skin graft. Donor site left lower limb and meshed 2:1. Achieved approx. 80-90% coverage of defect. Plan to have further surgery for residual raw area in approx. 1/52. CXR 01/09/2010 showed bibasal consolidation and diagnosed with LLL pneumonia, therefore, received continued chest physio. Referred to Dietician 01/09/2010 - advised high protein/high energy meals and snacks and additional supplementary drinks to promote wound healing and minimise weight loss.

Case Study

01/09/2010
Ankles - left PG; right 5degs PF. Knees - left 15-45degs flx; right 15-20degs flx. Passive and active assisted hip and knee movements. TA stretches.

02/09/2010
Ankles - as 01/09/2010. Knees - left 0-55degs flx; right 0-40degs flx. Active assisted hip and knee movements. TA stretches. Lie - sit over edge of bed with max AO2. Reluctant to flx knees B/L. Repositioned self on bed.

Case Study

03/09/2010
Ankles - left PG; right 10degs PF. Knees - left 0-55degs flx; right 40degs flx. CPM machine started
right lower limb 0-30degs flx up to 55degs flx. left lower limb 0-35degs flx up to 55degs flx.

Attempt to lie - sit but patient reluctant and became aggitated towards therapists. Fixing upper limbs with limited lower limb flx. Therefore, treatment stopped. Attempt to provide foot drop splints due to reduced ROM ankles B/L although patient declined.

04/09/2010
Received OOH physio by B&P team using CPM
Achieved 0-70degs knee flx B/L.

Case Study

06/09/2010
Achieved 0-70degs knee flx B/L. Foot drop splints provided.

07/09/2010
Theatre for further debridement and split skin graft of residual gluteal region right lower limb.

08/09/2010
Achieving approx. 30degs AROM hip/knee B/L. CPM used to achieve 0-95degs flx B/L.

Pain not been tolerated well up to this point


160mg MST/day and 200mg oramorph/day.

Case Study

09/09/2010
Lie - sit - stand with AO3. Step round tx with pilot frame bed to chair with AO3.

10/09/2010
Lie - sit - stand with AO2. Stood with pilot frame approx. 5 mins. Closed chain lower limb exercises
Left knee 0-80deg flx Right knee 0-40deg flx pain ++

11/09/2010
Received OOH physio by B&P team
Achieved AAROM 0-95degs knee flx B/L. AA hip/knee mvts using re-ed board. SQs and SLR left achieved; right unable to tolerate.

Case Study

13/09/2010
Left knee 0-95deg flx Right knee 0-40deg flx pain ++

Lie - sit over edge of bed with AO1. Independent sitting balance. Mobilisation with gutter frame with mod. AO2.

14/09/2010
Left knee 0-110deg flx Right knee 0-50deg flx

Lie - sit over edge of bed with min. AO1. Sit - stand with mod. AO2. Step round transfer with wheeled zimmer frame and mod. AO2.

15/09/2010
Mobilised approx. 25m with wheeled zimmer frame and AO2. Completed parallel bars for right foot facilitation.

Case Study

16/09/2010
Ankles - left PG; right 5degs PF. Knees - left 0-110degs flx; right 75degs flx. Sit - stand with min. AO1. Mobilised with wheeled zimmer frame independently. Home exercise programme provided. Discharge planning with patient Bed downstairs Family/friends to support ADLs Appropriate equipment

Case Study

17/09/2010
Home visit discharge Car transfer requiring min. AO1 - partner to assist. Limited mobilising area around living area as bed downstairs. Commode in situ. Partner to assist with PADLs and DADLs. Encouraged home exercise programme and regular mobility. Plan: Community therapy referral completed. Review in clinic 24/09/2010.

Post op picture

References and Useful Websites Health Protection Agency.


http://www.hpa.org.uk/Topics/InfectiousDiseases/InfectionsAZ/Ne Accessed on 16th September 2010. Angoules, A.G., et al (2007) Necrotising fasciitis of upper and lower limb: a systematic review. Injury, Int. J. Care Injured. 385; S18-S25. Chen, J., et al (2001) Necrotizing fasciitis associated with injection drug use. Clinical Infection Diseases. 33; 6-15. Hasham, 3S., et al (2005) Necrotising fasciitis. BMJ. 330; 830-833. Sarini, B., et al (2009) Necrotizing fasciitis: current concepts and review of the literature. The American College of Surgeons. 10:032; 279-288. Taviologlu, K., and Yanar, H., (2007) Necrotizing fasciitis: strategies for diagnosis and management. World Journal of Emergency Surgery. 2:19; 1-3.