Necrotising Fasciitis

Definition

Rare but very severe bacterial infection of deep fascia with secondary necrosis of soft tissue (e.g. muscle, skin).

Aetiology

Type I – Polymicrobial

· Mixed aerobic and anaerobic bacteria

Type II - Monomicrobial

· Group A Streptococcus (e.g. Streptococcus pyogenes)

· Staphylococcus aureus (commonly MRSA)

Pathogenesis

Trauma causing the breaking of skin (e.g. surgery, cut, scratch) allows bacteria to enter body. The bacteria colonises soft tissue and spreads in the fascial plane, releasing toxins which destroy the soft tissue. Certain toxins can cause systemic effects (e.g. renal failure, septic shock).

Signs and Symptoms

Symptoms start at site of infection – intense pain in excess of that expected with visual inspection. Signs of inflammation apparent – redness, swelling, heat. Spread of infection leads to a rapidly growing bronze- or purple-coloured patch. Within an hour, the skin may break open and exudation may occur.

Generalised signs and symptoms: malaise, fever, sweating, chills, nausea, dizziness, weakness, shock.

Without treatment, death can occur rapidly (73% untreated mortality rate).

Investigations

CT scan to view extent of necrosis.

Culture to confirm bacteria and determine antibiotic use.

Management

Before culture results, presumptive broad-spectrum aggressive intravenous antibiotic therapy. Intravenous donor antibodies. Targeted antibiotic therapy after identification of pathogenic bacteria.

Surgery to drain infected areas and debridement of necrotic tissue. Consider amputation if infection cannot be controlled. Skin grafting after infection cessation.

Hyperbaric oxygen therapy if bacteria is anaerobic.

Prognosis

Scarring and deformity common.

High death rate even with aggressive treatment.

Complications

Local progressive tissue damage, systemic infection (sepsis, shock), scarring and disfiguration, functional limb loss, death.

Prevention

Proper asepsis following penetrative trauma and surgical incisions.

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

Definition

Inappropriate secretion of ADH leading to water retention and hyponatraemia (normal 135 mmol/L)

Presentation

Plasma sodium <>

Plasma sodium <>

No oedema

Aetiology

Tumours – small cell lung carcinoma, prostate, thymus, pancreas, lymphomas

Pulmonary lesions – pneumonia, tuberculosis, lung abscess

CNS causes – meningitis, tumours, head injury, subdural haematoma, cerebral haematoma, SLE vasculitis

Metabolic causes – alcohol withdrawal, porphyria

Drugs – chlorpropamide, carbamazepine, cyclophosphamide, vincristine, phenothiazines

Diagnosis

Dilutional hyponatraemia due to excessive water retention

Low plasma osmolality with urine osmolality higher than that of plasma

Continued urinary sodium eexcretion > 30 mmol/L

No hypokalaemia (or hypotension)

Normal renal, adrenal and thyroid function

Treatment

Treat underlying cause where possible

Symptomatic relief:

1. Restrict fluid intake to 500-1000ml daily

2. Frequent measurement of plasma sodium and osmolality and bodyweight

3. If water restriction poorly tolerated or ineffective, demeclocycline may be given to inhibit action of ADH on kidney causing reversible nephrogenic diabetes insipidus

4. When syndrome very severe, rarely hypertonic saline (300 mmol/L slow i.v.) is given with furosemide – dangerous and used with extreme caution

Source: Kumar and Clark

Osmolarity vs Osmolality

Osmolality – measurement of number of osmoles of solute dissolved in each kilogram of water for a particular solution. A solution with 1 osmole of solute dissolved in 1kg of water has an osmolality of 1 osmole/kg (of water).

Osmolarity – measurement of number of osmoles of solute dissolved in each litre of a particular solution. A solution with 1 osmole of solute dissolved in water to make 1 litre of solution has an osmolarity of 1 osmole/L (of solution).

To determine osmotic pressure, osmolality is supposed to be used but for dilute solutions (e.g. body fluids) osmolarity can be used instead, as the difference is less than 1% and osmolarity is more readily measured.

Source: Guyton & Hall, Medical Physiology 11 ed.

Management of Chronic Renal Failure

1. Treat underlying cause(s)

2. Renoprotection

Goals of treatment

BP <>

Proteinuria <>

Treatment

Patients with chronic renal failure and proteinuria > 1 g/24 hours:

ACE inhibitor increasing to maximum dose

Add angiotensin receptor antagonist if goals are not achieved

Add diuretic to prevent hyperkalaemia and help to control BP

Add calcium-channel blocker (verapamil or diltiazem) if goals not achieved

Additional measures

Statins to lower cholesterol to <>

Stop smoking (threefold higher rate of deterioration in CRF)

Treat diabetes (HbA1c <>

Normal protein diet (0.8-1 g/kg bodyweight)

3. Correction of complications

Hyperkalaemia

Dietary restriction of potassium intake

Stop drugs causing potassium retention

Ion-exchange resins to remove potassium in gastrointestinal tract (e.g. Sodium polystyrene sulfonate)

Acidosis

Sodium bicarbonate supplements

Hypocalcaemia

Calcium carbonate supplements

Calcitrol or Vitamin D analogue (e.g. alfacalcidol)

Hyperphosphataemia

Oral calcium carbonate / acetate reduces absorption of dietary phosphate

Sevelamar used as gut phosphate binder

Nicotinamide to block intestinal sodium/phosphate cotransporter

Anaemia

Synthetic human erythropoietin

Male erectile dysfunction

Oral phosphodiesterase inhibitor (e.g. sildenafil, tadalafil, vardenafil)

4. Renal replacement therapy

Haemodialysis

Blood from patient pumped through array of semi-permeable membranes

Blood comes in close association with dialysate and substances are filtered down their concentration gradients

Approximately 4-5 hours’ treatment 3 times a week

All patients anticoagulated (e.g. heparin)

Haemofiltration

Removal of plasma water and dissolved constituents across semi-permeable membrane

Replacement with solution of desired biochemical composition

22L exchange 3 times a week

Peritoneal dialysis

Utilizes the peritoneal membrane as a semi-permeable membrane

Tube placed into peritoneal cavity and dialysate run into cavity

Dissolved substances pass into dialysate down concentration gradients

Fluid changed regularly to repeat process

Transplantation

Surgical anastomosis of human kidney on to iliac vessels of recipient

Donor ureter placed into recipient’s bladder

Immunosuppressive treatment needed (e.g. corticosterioids, azathioprine, ciclosporin)

Sources: Kumar and Clark, Clinical Medicine