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Compartment Syndrome

Posted on: Thursday, 30 December 2004, 03:00 CST

The silent danger related to patient positioning and surgery

Compartment syndrome affecting the limbs is a well-documented condition and there are cases where it has become evident following surgery undertaken with the patient in the Lloyd Davies position. This article explores the contributory factors and the devastating effect it can have on the patient, and questions whether we practise evidence-based care when patients are undergoing certain types of surgery. It also discusses factors related to abdominal compartment syndrome, a condition usually affecting the critically ill patient.

KEYWORDS Abdominal, Compartment syndrome, Lloyd Davies position

Introduction

As surgery becomes more complex and time-consuming, perioperative practitioners need to ensure that patients are safely prepared and positioned for their scheduled surgery. We should all be aware of the dangers of incorrect positioning of limbs to prevent nerve damage, and areas of the body particularly at risk during a specific operation. However, are we all aware of the factors that can cause a debilitating, occasionally fatal, consequence of both the surgery itself and the positioning for surgery - compartment syndrome?

This article discusses some of the causes and treatments of this condition and also discusses abdominal compartment syndrome, a term used when intra-abdominal pressures reach dangerously high levels.

What is compartment syndrome?

Compartment syndrome (CS) is a life-threatening condition observed when perfusion pressure falls below tissue pressure in a closed anatomic space or compartment. CS can occur wherever a compartment is present - within the hand, forearm and upper arm, buttock, legs and feet. Almost any injury can cause the condition.

CS develops through a combination of prolonged ischaemia and reperfusion of muscle within a tight osseofascial compartment (Turnbull et al 2002). Untreated CS can lead to tissue necrosis, functional impairment, possible renal failure and death (Maher et al 1994, Goldsmith & McCallum 1996, Boles 1999, Callum & Bradbury 2000, Paula 2002).

The human body has a number of areas in the limbs that function as closed compartments. Arteries and their subdivisions bring freshly oxygenated blood to the tissues, and the associated venous system returns deoxygenated blood to the venous circulation.

The long bones of the limbs are joined and surrounded by sheets of tough and relatively inelastic tissue called fascia which create comparatively inflexible boundaries. The placement of the fascia is such as to divide the leg, for instance, into a number of sections or compartments. These compartments contain muscles, arteries, veins and nerves and generally have a fairly constant volume, permitting only slight variation. If swelling occurs in these compartments the subsequent rise in compartment pressure can cause serious consequences.

The arterial blood system continues to bring blood into the compartment, but the low pressure system - that is the blood vessels with a low intra-luminal pressure (veins and their subdivisions) - is restricted. When this occurs it is further compounded by the release of fluid from the blood vessels, resulting in a further rise in compartment pressure and perpetuating the cycle.

Oedema within a closed compartment will increase the pressure within that compartment, eventually compromising the vascular supply. Such compromise will lead to further ischaemia and oedema formation, and a vicious cycle will be established as cells become deprived of oxygen.

Subsequent necrosis of muscle and loss of capillary wall integrity will lead to transudation, exudation and the development of massive oedema within the compartment (Lydon & Spielman 1984). The subsequent rhabdomyolysis leads to release of myoglobin with the potential for renal failure (Turnbull & Mills 2001).

Significant fluid losses into damaged tissues lead to hypovolaemia and metabolic acidosis, which not only act as potent pre-renal causes for renal impairment, but also enhance the nephrotic effect of myoglobin (Goldsmith & McCallum 1996, Callum & Bradbury 2000).

Severe metabolic complications may present after reperfusion when the damaged membranes continue to leak, aggravating oedema formation and increasing the pressure in the closed osteofascial compartment (Goldsmith & McCallum 1996).

If untreated, rhabdomyolysis may lead to myoglobinuria, permanent neurovascular damage, renal failure, sepsis and even death. Rhabdomyolysis is the dissolution, or breakdown, of striated muscle, which results in the production of myoglobin - a substance known to cause acute renal failure. This occurs as the myoglobin is released into the circulation where it can occlude the distal convoluted tubule and precipitate renal failure (Boles 1999).

Rhabdomyolysis is well-documented as the cause secondary to a range of conditions related to skeletal muscle injury (Boles 1999, Longmore et al 2001, Bocca et al 2002, Paula 2002). Causes of rhabdomyolysis (Tuckey 1996, Warrell et al 2003) include:

* CS

* direct injury

* severe burns

* severe physical exertion (eg: marathon running, intensive training, rave dancing)

* metabolic disturbances such as diabetes

* acute alcoholic binge

* hyperkalaemia

* infection

* hyperpyrexia

* grand mal seizures.

The history of CS

Damage to limbs, particularly the legs, related to nerve damage and unchecked intra-compartmental pressures were documented as long ago as 1872 by Richard von Volkmann. The combination of nerve- related damage and CS causing contracture related to a supracondylar fracture is still referred to as Volkmann contracture.

Observations and reports continued; damage caused by hypertension or ischaemia related to the limbs, and the association with rhabdomyolysis, were described by surgeons during World War II in patients who had sustained severe muscle injury (Tuckey 1996). They first reported the mechanisms and consequences of CS. Today CS following prolonged pelvic surgery is an uncommon, but well- documented complication.

Patient factors associated with CS

Although more commonly associated with trauma or surgery on the limbs, CS has been reported as a complication of some positions adopted for surgery, particularly the lithotomy (Leff & Shapiro 1979, Lydon & Spielman 1984, Alder et al 1990, Raza et al 2004) and knee-chest positions (Aschoff et al 1990).

Various papers identify serious complications following surgery, particularly during lithotomy or Lloyd Davies positions during urological surgery. It has even been reported as occurring in a 6- year-old patient (Bocca et al 2002). The consequences for the patient are devastating, often requiring multiple fasciotomies, with chronic pain and weakness the frequent result (Turnbull et al 2002).

The possibility of developing CS and rhabdomyolysis is especially high in the presence of other risk factors including obesity, peripheral vascular disease and prolonged duration of surgery (Bocca et al 2002). CS has also been described in instances of drug overdose where persons have remained in one position for several hours, with the force supplied by the weight of their body on the extremity being the causative mechanism for the syndrome developing (Lydon & Spielman 1984, Shaw et al 1994).

Figure 1

The Lloyd Davies position

Photos kindly supplied by Eschmann

Figure 2

Legs are supported on multi-jointed operating table leg supports

Risks in the perioperative environment

Within theatre, the success of many surgical procedures depends upon satisfactory exposure of the operative site, which often is achieved by placing patients in physiologically abnormal positions. With perceptive powers of the patient no longer intact, postural insults may occur that normally would not be tolerated in the awake state (Lydon & Spielman 1984).

Variations on the lithotomy position are used for many procedures. The Lloyd Davies position (Figure 1) and modified lithotomy Trendelenburg (with additional head-down tilt) provide optimal combination approaches (abdominal and perineal) for complex urological, colorectal and gynaecological surgical procedures.

This position allows the legs to be supported on multi-jointed operating table leg supports (Figure 2), rather than lithotomy pole stirrups, which reduce the degree of hip flexion and support the calves in semi-cylindrical padded cushions. The lower leg may be secured by soft straps or bandaging. While the theatre practitioner ensures that the patient is positioned safely and correctly to minimise joint strain and pressure points, there is very little done to prevent the possibility of compartment pressure increases.

It is difficult to prevent any increase in compartmental pressure by the very nature of the position. The patient may be wearing compression stockings (if these are too small the problem will be compounded) and will likely have intermittent compression devices attached to each lower leg. Turnbull & Mills (2001) question the use of these devices and recommend that their use is avoided when patients are to be placed in the Lloyd Davies position for surgery. The leg will still receive a degree of direct compression against the calf support, despite our care. It is essential to ensure that surgical assistants do not lean on the leg and provide additional compression.

Tuckey (1996) and Thorson (1999) question the prudence of using Lloyd Davies leg supports as they cause direct pressure on the c\alf muscles. Leff & Shapiro (1979) refer to experiments showing that the Trendelenburg tilt is the main factor in reducing limb perfusion rather than the lithotomy position itself. Should we return to using stirrups, as advocated by these writers, where the feet are supported and protected by padding for protracted surgical episodes and eliminate the pressure on the legs? We then have to ensure that the peroneal and tibial nerves are not subjected to undue pressure, which can in itself cause increased compartment pressures.

Figure 3

Measuring compartment pressures will confirm CS

Photo kindly supplied by Stryker

Reduced perfusion is inevitable. The elevation of the legs above the heart reduces limb perfusion that may be compounded by the head- down tilt. Other factors related to limb perfusion may be hypotension (induced by anaesthesia or sympathetic block) and surgically-induced pressure on major vessels during episodes of the procedure which may also affect venous return for short periods.

Pre-existing arterial disease may also be a contributory factor (Callum & Bradbury 2000). When surgery is prolonged, the risk of CS occurring is increased. Most literature refers to long surgical episodes (six hours or longer), but it is now thought that much shorter episodes can be responsible. Dua et al (2002) report an incidence occurring after 3.5 hours.

Signs and symptoms

CS usually presents after reperfusion of a limb, and pain and swelling may not occur immediately. The first signs usually occur after the patient has regained consciousness, undergone their post- anaesthetic care episode and returned to the ward. Often several hours are reported as uneventful before the first signs and symptoms are reported (Leff & Shapiro 1979, Lydon & Spielman 1984, Goldsmith & McCallum 1996, Tuckey 1996, Bocca et al 2002).

The first suspicions are usually aroused when a patient complains of severe pain in the lower legs when they have recovered consciousness or a few hours after surgery. Some patients have described pain despite postoperative epidural anaesthesia (Beerle & Rose 1993). The patient's leg(s) may appear tense and swollen. The level of pathological pain is found to be far greater than the ordinary postoperative pain to be expected from the surgical intervention (Garrett 2004).

The diagnosis of CS requires a high index of clinical suspicion and the typical presentation postoperatively includes leg pain out of proportion to clinical findings (Raza et al 2004). Attention should be paid to the patient who continues to complain of pain after receiving analgesia or states that the pain is continually increasing (Maher 1994).

Early diagnosis can affect outcome. It is possible that an initial diagnosis of deep vein thrombosis (DVT) may impede the correct one. The measurement of compartment pressures will confirm suspicions of CS (Figure 3), while venous Doppler studies will confirm a DVT.

There is no clear definition of a precise pressure/time limit for irreversible muscle and nerve damage. Normal limb intra-compartment pressure (ICP) at rest is on average less than 20mmHg. Goldsmith St McCallum (1996) discuss pressures above 45mmHg causing CS; other authors cite 30mmHg as a threshold. Matsen (1980) states that ICPs greater than 30mmHg generally are agreed to require intervention. It is important to compare compartment pressures against the patient's diastolic pressure - if it is elevated to within 10-30mmHg of the diastolic pressure, or 30-40mmHg of the mean arterial pressure, irreversible damage may occur. It is difficult to ascertain if one or all compartments of a limb are affected.

Prolonged delay may cause the nephrotoxic myoglobinuria (resulting from rhabdomyolysis) to affect the renal tubules. Diagnosis rests on clinical suspicion, dark urine testing strongly positive for blood on dipstick reagents, myoglobinuria and an increased serum creatine kinase (Goldsmith & McCallum 1996).

Treatment

Medical decompression may be instigated if CS is suspected and intra-compartment pressures are only marginally increased. A mannitol infusion has been reported as effecting a complete resolution (Daniels et al 1998, Raza et al 2002).

Surgical decompression is the standard treatment of established CS. Immediate surgical intervention is required to stop the rise in compartment pressures and damage by performing fasciotomies (surgical incisions of the affected compartments). As soon as the fascia is sectioned, or surgically split open by an incision through all the layers down to, and including, the fascia, the compartmental contents can bulge, thus allowing pressures to decline along with reinstitution of the normal circulatory pattern. When diagnosed and treated early, full recovery usually follows.

Fasciotomy must be undertaken promptly by a skilled surgeon, ensuring that all compartments (for instance all four of the lower leg) are accessed through a single lateral incision or double vertical whenever possible.

Pearse et al (2002) discuss the current recommendations for treatment, advocating prompt release of intra-compartment pressure by fasciotomy. Delays greater than eight hours may limit the efficacy of the treatment. Early diagnosis benefits from early treatment. Fasciotomies are not benign procedures - they may lead to chronic venous insufficiency due to impairment of the calf muscle pump.

During fasciotomy it is vital to identify and protect the peroneal nerve. Wounds are usually left open initially, being protected by suitable sterile dressings. Inspection of the wound after 48 hours may necessitate further necrotic tissue excision. Delayed skin closure or skin grafting may become treatment options. Adequate analgesia and antibiotic cover are essential for improving outcomes.

In cases where treatment and prophylaxis of renal failure associated with rhabdomyolysis is suspected or diagnosed, prompt fluid and metabolic correction is essential to re-establish a good urine output. Goldsmith & McCallum (1996) advocated that 'Early, aggressive fluid replacement, guided by CVP monitoring, is required and often large positive fluid balances are necessary. Mannitol has further beneficial actions in being a renal vasodilator and intravascular expander'.

Tuckey (1996), Goldhill & Withington (1997) and Bocca et al (2002) also support a mannitol infusion to induce an osmotic diuresis. However, others have disagreed in the past - Maher (1994) states that hypertonic mannitol has not been proven effective in clinical studies. Debate continues and actual treatment will depend on the individual clinician.

Dialysis may be necessary if these methods of treatment fail.

Summary

Current knowledge related to the risk of CS when operating in these positions (Lloyd Davies and Trendelenburg tilt) is such that it can be deemed negligent to keep patients in this position (with legs higher than the heart) when not absolutely necessary. If it means repositioning and redraping, thus adding a few extra minutes to the episode and costing a small amount in additional drapes, surely this is a small price to pay for excellent perioperative care?

If repositioning is impossible to execute, the headdown tilt position should be reversed every two hours, for a short period of time, to allow more natural perfusion of the lower limbs to occur. Raza et al (2004) recommend that if the anticipated procedure duration is beyond four hours, the legs should be removed from supports every two hours for a short period to prevent reperfusion injury. The use of Allen stirrups is preferred to calf supports or metal skids.

Turnbull & Mills (2001) suggest that we should certainly review our use of compression stockings and intermittent compression devices when operating on patients in the Lloyd Davies position.

It will be deemed negligent to misdiagnose (ie: mistake for a DVT) or delay treatment (by prolonged re-assessment) of CS postoperatively when patients have been subjected to prolonged surgery in these abnormal positions. Delayed or missed diagnosis may not only be limb-threatening (and cause a very protracted hospital stay) - it can be life-threatening. With today's current knowledge, surgeons undertaking prolonged surgery in abnormal positions must be aware of this, fortunately rare, complication.

Practice guidelines within perioperative care should reflect current knowledge and ensure that risk is minimised. Patients who take legal action if they have experienced this condition may be awarded substantial costs against negligence if lack of care can be proven or diagnosis has been delayed.

Abdominal compartment syndrome

Abdominal compartment syndrome (ACS) is a potentially fatal consequence of increased intra-abdominal pressure due to trauma or surgery. It has been recognised for years, but the term ACS was only introduced in the 1980s (Tal et al 2004). The risk of life- threatening elevation in intra-abdominal pressure is not limited to postoperative patients (Watson & Howdieshell 1998). Other causes that may cause raised ICP include haemorrhage, oedema, distended bowel, mesenteric venous obstruction, tense ascites, peritonitis and tumours (De Backer 1999, Tal et al 2004). Intra-abdominal packing as a means of creating a tamponade has also been described (Watson & Howdieshell 1998).

Pathophysiology

Various systems are involved in the development of ACS. An increase in intra-abdominal pressure is transmitted to the pleural space so lung compliance decreases. Hypoventilation and altered ventilation/perfusion distribution lead to hypoxaemia and hypercapnia. Very high inspiratory pressures may be required to deliver the tidal volume required during anaesthesia or artificial ventilation (De Backer 1999).

This increase in pressure directly affects the circulatory system by decreasing venous return and compressing the heart. This in turn affects the perfusion of intra-abdominal organs and may lead to oliguria and renal failure as compression \of renal veins and collecting systems occurs. Further organ failure or brain damage may occur if intracranial pressure is increased due to the decrease in cerebral venous return and increased venous pressure (De Backer 1999).

The intra-abdominal cavity is exposed to extremely low pressures almost bordering on the negative. Mechanical ventilation produces a positive intra-abdominal pressure close to the end expiratory pressure, with values of up to 10mmHg, considered normal. After abdominal surgery, pressures are typically 3-15mmHg (Nathens et al 1997). If pressures are allowed to escalate higher than 25mmHg compression can produce potentially fatal complications.

Elevated pressures are commonly found in post-operative surgical patients admitted to intensive care. Tal et al (2004) discuss the incidence as being as high as 33%, while in patients with renal impairment the incidence may be as high as 69%. It is thought that progressive visceral oedema may develop, which in turn can lead to ischaemia of the intestinal mucosa and sepsis, multi-organ failure and death.

Different authors discuss varying definitions of the effects of intra-abdominal pressures but agree that the complication of ACS is suspected when the pressure is above 35mmHg and one of the following signs of clinical deterioration is present (Watson & Howdieshell 1998, De Backer 1999, Johna et al 1999, Mayberry 1999, Walker & Griddle 2003, Tal et al 2004):

* Oliguria

* Raised pulmonary pressure

* Hypoxia

* Decreased cardiac output

* Hypotension

* Acidosis.

Diagnosis of this syndrome is difficult because it usually occurs in critically ill patients with other causes of circulatory or respiratory failure. Abdominal pressures can be measured and monitored via a two-way indwelling catheter in the bladder connected to a manometer or transducer. The bladder pressure is thought to closely relate to intra-abdominal pressure. Other methods have been conducted during research but as yet little else is as reliable or as non-invasive.

Diagnosis is confirmed when abdominal decompression results in improvement in the patient's condition. This decompression is achieved by re-opening the wound, also known as a decompressive celiotomy. (If ACS is anticipated during major surgery, primary closure of the abdomen may not be attempted.)

Sudden release of the pressure may lead to additional complications such as acidosis, vasodilatation, cardiac dysfunction and arrest. Careful assessment and treatment of hydration and electrolyte/acid-base balance is essential to avoid overcorrection (reperfusion syndrome). It may be necessary to preload the patient with crystalloid solution before such an attempt is made (De Backer 1999).

Modern advances in laparoscopic surgery have improved the postoperative morbidity for patients, nevertheless it induces a deliberate, although controlled, elevation in intra-abdominal pressure. Watson & Howdieshell (1998) cite studies where the pneumoperitoneum required for laparoscopic vision can induce intraoperative oliguria. They also refer to the term 'tension pneumoperitoneum' which has been applied to occasions where laparoscopic overdistension leads to serious pathologic consequences.

Conclusion

When the patient position required for these laparoscopic surgical procedures is Lloyd Davies with Trendelenburg the risk to the patient could be increased, the development of both ACS and limb CS are a possibility. Perhaps further reports in medical journals will report such consequences. Meanwhile, those involved in protracted surgical operations should ensure that the patient is not subjected to unnecessary risks by being positioned in unnatural positions for longer than is absolutely necessary.

Compartment syndrome has been reported as a complication of some positions adopted for surgery, particularly lithotomy

Suspicions are usually aroused when a patient complains of severe pain in the lower legs a few hours after surgery

The success of many surgical procedures depends upon exposure of the operative site

It can be deemed negligent to keep patients with legs higher than the heart when not necessary

References

Alder LM, Loughlin JS, Morin CJ, Haning RV 1990 Bilateral Compartment Syndrome Mer a Long Gynaecologic Operation in Lithotomy Position American Journal of Obstetrics and Gynecology 162 (5) 1271- 1272

Aschoff A, Steiner-Milz H, Steiner HH 1990 Lower Limb Compartment Syndrome Following Lumbar Discectomy in the Knee-chest Position Neurosurgical Review 13 (2) 155-159

Beerle BJ, Rose RJ 1993 Lower Extremity Compartment Syndrome from Prolonged Lithotomy Position not Masked by Epidural Bupivacaine and Fentanyl Regional Anesthesia 18 (3) 189-190

Bocca G, van Moorselaar J, Wout F, van der Staak F, Monnens L 2002 Compartment Syndrome, Rhabdomyolysis and Risk of Acute Renal Failure as Complications of the Lithotomy Position Journal of Nephrology 15 (2) 183-185

Boles JM 1999 Rhabdomyolysis and Compartment Syndrome. In Andrews et al (eds) Oxford Textbook of Critical Care Oxford, Oxford University Press

Bywaters EG, Beall D 1941 Crush Injuries with Impairment of Renal Function Journal of the American Society of Nephrology 9 (2) 322- 332

Callum K, Bradbury A 2000 ABC of Arterial and Venous Disease: acute limb ischaemia British Medical Journal 320 (7237) 764-767

Daniels M, Reichman J, Brezis M 1998 Mannitol Treatment for Acute Compartment Syndrome Nephron 79 (4) 492-493

De Backer D 1999 Abdominal Compartment Syndrome Critical Care 3 (6) 103-104

Dua RS, Bankes MJK, Dowd GSE, Lewis AAM 2002 Compartment Syndrome Following Pelvic Surgery in the Lithotomy Position Annals of the Royal College of Surgeons of England 84 (3) 170-171

Goldhill DR, Withington PS 1997 Textbook of Intensive Care London, Chapman & Hall Medical

Goldsmith AL, McCallum MID 1996 Compartment Syndrome as a Complication of the Prolonged Use of the Lloyd Davies Position Anaesthesia 51 (11) 1048-1052

Johna S, Taylor E, Brown C, Zimmerman G 1999 Abdominal Compartment Syndrome: does intra-cystic pressure reflect actual intra-abdominal pressure? A prospective study in surgical patients Critical Care 3 (5) 135-138

Leff RG, Shapiro SR 1979 Lower Extremity Complications of the Lithotomy Position: prevention and management Journal of Urology 122 (1) 138-139

Longmore M, Wilkinson I, Trk E 2001 Oxford Handbook of Clinical Medicine 5th ed, Oxford, Oxford University Press

Lydon JC, Spielman FJ 1984 Bilateral Compartment Syndrome Following Prolonged Surgery in the Lithotomy Position Anesthesiology 60 (3) 236-238

Maher A, Warner-Salmond S, Pellino T 1994 Orthopaedic Nursing London, WB Saunders

Matsen FA 1980 Compartment Syndrome New York, Grune and Stratton

Mayberry J 1999 Prevention of the Abdominal Compartment Syndrome The Lancet 354 (9192) 1749-1750

Nathens AB, Brenneman FD, Boulanger BR 1997 The Abdominal Compartment Syndrome Canadian Journal of Surgery 40 (4) 254-268

Paula R 2002 Compartment Syndrome, Extremity Available from: www.emedicine.com

Pearse M, Harry L, Nanchahal J 2002 Acute Compartment Syndrome of the Leg British Medical Journal 325 558-559

Raza A, Byrne D, Townell N 2004 Lower Limb (Well Leg) Compartment Syndrome After Urological Pelvic Surgery Journal of Urology 171 (1) 5-11

Shaw A, Sjolin S, McQueen M 1994 Crush Syndrome Following Unconsciousness: need for urgent orthopaedic referral British Medical Journal 309 (6958) 857-859

Tal A, Lask J, Keslin J, Livne PM 2004 Abdominal Compartment Syndrome: urological aspects British Journal Urology International 93 474-477

Thorson A 1999 Lloyd Davies Position with Trendelenburg - a disaster waiting to happen? Diseases of the Colon and Rectum 42 (7) 919-920

Tuckey J 1996 Bilateral Compartment Syndrome Complicating Prolonged Lithotomy Position British Journal of Anaesthesia 77 (4) 546-549

Turnbull D, Mills G 2001 Compartment Syndrome Associated with the Lloyd Davies Position Anaesthesia 56 (10) 980-987

Turnbull D, Farid A, Hutchinson S, Shorthouse A, Mills G 2002 Calf Compartment Pressures in the Lloyd Davies Position: a cause for concern? Anaesthesia 57 (9) 905-908

von Volkmann R 1872 Verletzungen und Krannkheiten der Bewwgungsorgane Handbuch der Allegemeinen und Speziellen Chirurgie (2) 234-920

Walker J, Criddle LM 2003 Pathophysiology and Management of Abdominal Compartment Syndrome American Journal of Critical Care 12 (4) 367-373

Warrell D, Cox T, Firth J, Benz E 2003 Oxford Textbook of Medicine 4th ed, Vol 3, Sections 18-33, p257, Oxford, Oxford University Press

Watson RA, Howdieshell TR 1998 Abdominal Compartment Syndrome Southern Medical Journal 91 (4) 326-362

Sarah Wilde, Senior Nurse,

Gynaecological Theatres,

Northampton General Hospital

NHS Trust, Northampton,

NN1 5BD

Copyright National Association of Theatre Nursing Dec 2004

Source: British Journal of Perioperative Nursing

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