Iatrogenic forearm compartment syndrome

Abstract

Limb compartment syndrome may be sequelae of trauma, but in the context of critical care blood sampling, arterial damage may have profound consequences. We describe a series of three cases and their progress and discuss guidelines for prevention of this potentially devastating occurrence in critically ill patients.

Introduction

‘First Do No Harm’ is core to the Hippocratic Oath sworn by physicians, since the third Century AD. Acute compartment syndrome (ACS) is an orthopaedic emergency and is associated with poor outcomes when identified late. Common aetiologies, including lower limb trauma, can help predict or forewarn physicians allowing close observation and rapid management. However, rare causes can be easily misdiagnosed or dismissed until it is too late. This is a report of a case series of three intensive care unit (ICU) patients who developed ACS of the forearm. All three cases were found to have been caused iatrogenically after attempts at obtaining radial artery blood samples for blood gas analysis. All occurred between February and July 2013 within one hospital department. These cases highlight common risk factors and have resulted in education amongst our medical and surgical physicians with emphasis on prevention.

Case 1

A patient in their 60 s was admitted to hospital with sudden onset of calf pain followed by acute shortness of breath. A clinical diagnosis of pulmonary embolism (PE) was made, and the patient started on a therapeutic dose of low-molecular weight heparin. Subsequent computed tomography pulmonary angiography (CTPA) confirmed bilateral large PEs. The patient was transferred to the ICU, where a heparin infusion was started. Within 24 h, the patient was referred to the orthopaedic team for suspected compartment syndrome of the right forearm. On examination, they were alert, orientated and complaining of moderate pain in the right forearm; their observations were otherwise stable. Their forearm was tense and swollen. There was evidence of multiple attempts to obtain arterial blood samples from the right radial artery. This was shown as multiple needle punctures around the palpable area of the radial pulse at the wrist. The radial pulse was palpable and equal to the other side. Sensation was reduced in all finger tips of the right hand, and the capillary refill was less than 2 s. There was no pain on passive stretch of the flexor muscle group, but the patient was neither able to actively flex nor extend the fingers. The working diagnosis at this stage was ACS. The compartment pressure was measured using an arterial line set under aseptic technique. At this stage, the blood pressure was 110/42 mmHg. The anterior compartment pressure was 15 mmHg. The delta pressure (diastolic pressure less the intra-compartmental pressure) was 27 mmHg; the posterior compartment pressure was 17 mmHg (delta pressure 25 mmHg). These findings (delta pressures less than 30 mmHg) confirmed ACS. Emergency fasciotomy of the right forearm superficial and deep anterior compartments, extensor compartment and carpal tunnel decompression was performed. Intra-operative findings were consistent with ACS. There were superficial and deep haematomas in the anterior compartments. Muscles showed several dusky areas which were debrided and the wound left open. A further operative review at 48 h revealed necrotic muscles involving the flexor carpi radialis, radial half of the flexor digitorum superficialis, all of flexor digitorum profundus, pronator quadratus and flexor pollicis longus. All necrotic tissues were debrided and excised. At that stage, a vacuum dressing was applied. Five re-debridements of the necrotic tissues and re-applications of vacuum dressings were undertaken, until the wound was ready for closure. Neuro-vascular structures were preserved. However, most of the muscles in the anterior, superficial and deep compartment were excised. Final closure was performed six weeks later with plastic surgery input and the use of a small skin graft. At final follow-up (14 months after the first procedure), despite intensive physiotherapy, the patient continued to show poor hand function particularly wrist and finger flexion with impaired sensation of the median and ulnar nerve distributions in the hand.

Case 2

This patient was admitted to ICU with a PE which was confirmed with CTPA. The patient was on treatment dose anticoagulation and had thrombolytic therapy. Arterial access was required, and trials of obtaining arterial blood samples resulted in progressive forearm swelling and suspected development of ACS. At this stage, the patient was referred to the orthopaedic team. On examination, the patient was alert and orientated, complaining of right forearm swelling with altered sensation of the fingers. The forearm was tense and swollen with pain on passive finger extension. The radial pulse was palpable with capillary refill measured at less than 2 s. There was reduced sensation of all finger tips of the right hand. A clinical diagnosis of ACS was made. The patient underwent right forearm emergency fasciotomy and carpal tunnel decompression which involved releasing anterior (superficial and deep) and posterior compartments. Intra-operative findings were consistent with ACS, with haematomas and muscle necrosis. Necrotic tissues were debrided. The carpal tunnel incision was closed and the rest of the fasciotomy wound left open. This was followed by several intra-operative wound washouts and debridement, until the wound was ready for closure. Wound closure was performed without the need for a skin graft. At the last follow-up (nine months later), the patient had only partial improvement of the neurological symptoms (motor and sensory).

Case 3

This patient developed a deep vein thrombosis and PE during their ICU admission. The patient was on a heparin infusion and had an inferior vena cava filter in situ. Several attempts at arterial blood gas samples from the right radial artery were undertaken and subsequently the patient developed acute forearm swelling. The patient was referred to the orthopaedic team with a diagnosis of possible ACS. On examination, the forearm was very swollen and tense. The radial pulse was weak with a normal ulnar pulse; capillary refill was less than 2 s. Passive muscle stretching caused significant distress. Full neurological assessment could not be undertaken due to an altered level of consciousness. At that point, the working diagnosis was ACS. After discussion between the orthopaedic, ICU and anaesthetic consultants and on the basis that the patient’s prognosis was very poor, the decision was made to treat this patient non-operatively. The patient died after seven days.

Discussion

ACS is an orthopaedic emergency; ACS of the forearm following arterial blood sampling from the radial artery is a rare but potentially devastating complication. It was first described in 1978. ¹ It is characterised by raised pressure within the closed osteofascial compartment by 30 mmHg from diastolic pressure. ² This reduces tissue perfusion and eventually causes tissue ischaemia and necrosis. Skeletal muscles are more sensitive to ischaemia than other tissues. The degree of muscle injury is directly related to the severity and duration of ischaemia. ³ Prolonged ischaemia leads to muscle scarring and contractures (Volkmann’s ischaemic contracture). Cellular destruction may also lead to the release of myoglobin into the circulation, and later rhabdomyolysis, acute renal failure, and even death. ⁴

Recognised aetiologies are an increase in volume of the compartment contents (i.e. haemorrhage/oedema) and reduction in the size of the compartment. ⁵ Internal bleeding is usually traumatic (with or without fractures); however, patients with coagulopathy or on anticoagulant treatment are at much greater risk.^5–7

Our case series shares a common iatrogenic aetiology, which is internal compartment bleeding caused by attempted sampling from the radial artery. Several attempts to obtain arterial blood samples and/or to insert arterial catheter in patients who are on therapeutic anticoagulation or have received thrombolytic therapy led to internal bleeding which was significant enough to produce ACS.

In the ICU setting, patients may require regular arterial blood sampling or arterial catheter access. Such patients may well be on anticoagulant therapy, in either prophylactic or therapeutic doses. Such therapy increases the risk of causing iatrogenic injury and bleeding; however, little extra precautions had been taken to observe or prevent complications such as ACS in the event of difficult or unsuccessful arterial sampling or cannulation. This is particularly important when considering that many patients are unable to communicate pain due to heavy sedation or intubation which in turn can lead to a delayed diagnosis. Patients in ICU may not be fit for surgery (case 3) due to significant comorbidities or anaesthetic risk. This puts much more focus on the importance of prevention.

Our learning points since these index cases are as follows:

In high-risk patients who have coagulopathy or are receiving treatment for venous thromboembolism with anticoagulants, care should be taken while obtaining arterial samples or even performing venous cannulation. Samples should be obtained by trained members of staff or under supervision by a senior member of the team. If the first attempt is unsuccessful, we have advised the use of bedside ultrasound guidance, in line with increasing published evidence of its efficacy.^8,9 This evidence suggests there are higher initial success rates with ultrasound guidance, and given the seriousness of complications and the steep learning curve associated with ultrasound vascular access, future complications could be minimised by increased availability, education and utilisation of ultrasound in daily practice. Current research into the efficacy of ultrasound compares it against a standard of blind/landmark techniques. This has resulted in recommendations for ultrasound use in current national and international guidelines ¹⁰ and at least recent reference to it in national guidelines. ¹¹ In the event of unsuccessful cannulation, pressure should be applied for at least 2 min, or longer if anticoagulated, and the limb elevated for at least 10 min.

Following the procedure, the team is to have a high index of suspicion of ACS and to have a low threshold for early referral to the orthopaedic team. We believe that following these steps will reduce the patient’s risk and give the best possible outcome should ACS occur.