Compartment syndrome of the biceps brachii compartment following rupture of the long head of the biceps.
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HYPOTHESIS: Measuring intracompartmental pressure is a well accepted method in evaluating a compartment syndrome, which may occur after limb ischemia followed by reperfusion. As a compartment syndrome is paralleled by a decreased microcirculation it should be possible to evaluate a compartment syndrome also by measuring intramuscular pO2. METHODS: Anesthetized rats (spontaneous breathing via tracheotomy) were subjected to infrarenal ligation of the aorta. A pressure catheter was placed subfascial in the crural muscle group of one hind limb, whereas the contralateral side was prepared with a pO2 catheter. Besides a sham operated group, three experimental groups were subjected to either 2 hrs, 4 hrs or 6 hrs of ischemia followed by 4 hrs of reperfusion. One further group was also subjected to 4 hrs of ischemia and 4 hrs of reperfusion but received a fasciotomy at the time of reperfusion. Compartment pressure and intramuscular pO2 were recorded every 15 min. For histological examination muscle specimen were obtained after each experiment. RESULTS: Two hours of ischemia followed by 4 hrs of reperfusion did not result in any morphological changes and also not in any significant change in compartment pressure during both phases, whereas pO2 significantly dropped during ischemia (from 19.0 mmHg to 3.0-5.0 mmHg) and returned to normal during reperfusion. In prolonged ischemia (4hrs) morphologically a severe interstitial edema was evident, compartment pressure increased during reperfusion (from 2.0 mmHg to 8.8 mmHg) and pO2 dropped during ischemia down to 3.0 mmHg and did not return to normal during reperfusion (10.5 mmHg versus 19.0 mmHg normal). In case of 6 hrs ischemia, partial necrosis and only little interstitial edema were found morphologically. There was no significant change in compartment pressure throughout the study; and pO2 remained significantly decreased even during reperfusion (2.0-3.0 mmHg). DISCUSSION: Normal compartment pressure could mislead to false negative interpretation of compartment syndrome, whereas pO2 clearly identifies the microcirculatory state of the muscle. Thus, intramuscular pO2 monitoring presents a valuable method in evaluating compartment syndrome, especially in case of suspect clinical signs but normal compartment pressure.
PURPOSE OF THE STUDY: Compartment syndrome represents a clinical entity, whose diagnosis depends both on clinical findings as well as on measurement of the intracompartmental pressure. Physiopathology and clinical aspects of diagnosis and treatment of the acute compartment syndrome are discussed, based on the literature review and personal clinical experience. MATERIAL AND METHODS: We have based our experience on a series of 100 consecutive fractures of the leg, in which we studied mechanism of trauma, fractures localization, timing of surgery for fasciotomy and wound closure. RESULTS: The incidence of compartment syndrome was 8 per cent. Younger age (< 30 years), high energy trauma, or trauma occurring during physical activity appeared to increase the risk of occurrence. Localization of the fracture on the proximal, mid or distal thirds of the leg did not. DISCUSSION: The following aspects are discussed: 1) The perfusion pressure of a compartment is defined as the difference between the diastolic blood pressure and the intracompartmental pressure. 2) Fasciotomy is indicated whenever this value is inferior to 30 mmHg. 3) Failure to measure the pressure within 5 cm from the fracture site may cause underestimation of the compartment pressure. 4) Intramedullary nailing does not seem to increase the risk of compartment syndrome.
Measuring intracompartmental pressure is a well-accepted method in evaluating a compartment syndrome, which may occur after limb ischaemia followed by reperfusion. As a compartment syndrome is paralleled by a decreased microcirculation it should be possible also to evaluate a compartment syndrome by measuring intramuscular partial oxygen tension (PO2). In this study, anaesthetized rats (spontaneous breathing via tracheotomy) were subjected to infrarenal ligation of the aorta. A pressure catheter was placed subfascial in the crural muscle group of one hind limb, whereas the contralateral side was prepared with a PO2 catheter. Besides a sham operated group, three experimental groups were subjected to either 2, 4 or 6 h of ischaemia followed by 4 h of reperfusion. One further group was also subjected to 4 h of ischaemia and 4 h of reperfusion but received a fasciotomy at the time of reperfusion. Compartment pressure and intramuscular PO2 were recorded every 15 min. For histological examination muscle specimens were obtained after each experiment. Two hours of ischaemia followed by 4 h of reperfusion did not result in any morphological changes and also in no significant change in compartment pressure during both phases, whereas PO2 significantly dropped during ischaemia (from 19.0 mmHg to 3.0-5.0 mmHg) and returned to normal during reperfusion. In prolonged ischaemia (4 h) morphologically a severe interstitial oedema was evident, compartment pressure increased during reperfusion (from 2.0 mmHg to 8.8 mmHg) and PO2 dropped during ischaemia to 3.0 mmHg and did not return to normal during reperfusion (10.5 mmHg versus 19.0 mmHg normal). In the case of 6 h ischaemia, partial necrosis and no interstitial oedema was found morphologically. There was no significant change in compartment pressure throughout the study, and PO2 remained significantly decreased even during reperfusion (2.0-3.0 mmHg). Normal compartment pressure could mislead to false negative interpretation of microcirculatory disorders preceding or following compartment syndrome, whereas PO2 clearly identifies the microcirculatory state of the muscle. Thus, intramuscular PO2 monitoring presents a valuable method in evaluating compartment syndrome, especially where there are suspected clinical signs and risk of ischaemia but normal compartment pressure.
The reason for the described clinical variability of acute compartment syndrome of the thigh, with high morbidity and mortality in some patients and an uncomplicated clinical course in others, is not known. To better define the clinical spectrum and factors determining the clinical course of this rare clinical entity, we did a retrospective multicenter study of 28 patients with 29 thigh compartment syndromes. The leading cause of acute thigh compartment syndrome was blunt trauma from motor vehicle accidents (46%) or contusion (39%). Pain with passive motion was present in all patients who were conscious, followed by paresthesia (60%), and paralysis (42%). The anterior compartment was involved most frequently with mean compartment pressure of 58 +/- 3 mm Hg. Myonecrosis, sepsis, and need for skin grafting were observed more frequently in patients with ipsilateral femur fracture. Only 7% of patients with isolated thigh compartment syndromes had short-term complications compared with 57% of patients with ipsilateral femur fractures. The incidence of complications correlated with the time to fasciotomy. Mortality was limited to patients with high injury severity scores. The clinical spectrum of thigh compartment syndrome is comparable with that of other compartment syndromes and its clinical course is determined by its associated injuries.
To determine the possible relationship between outcome and fixation method for tibial fractures associated with compartment syndrome, the authors retrospectively reviewed the records of 96 patients (average age, 31.8 years) with this injury. Seventy-eight patients had multiple injuries (average Injury Severity Score, 22.37). There were 68 closed and 28 open fractures, including 3 gunshot wounds. Compartment syndrome was diagnosed by direct measurement or by clinical findings. The attending surgeon selected the type of fixation based on fracture pattern and associated injuries. Time to healing for the 96 fractures averaged 31.6 weeks. There was no significant difference in healing times between open and closed fractures or between methods of treatment. Healing time for closed fractures was significantly different from that reported for closed fractures not associated with compartment syndrome (30.2 compared with 17.3 weeks, respectively; open fracture healing times were not significantly different (35 compared with 29.3 weeks, respectively). The authors conclude that (1) compartment syndrome significantly lengthens the time to healing for closed tibial fractures but does not significantly affect the time to healing for open tibial fractures; (2) closed tibial fractures with compartment syndrome appear to act as open fractures; and (3) the method of fixation does not appear to affect time to healing for closed or open fractures associated with compartment syndrome.
In this study, the tolerance of skeletal muscle to tourniquet application (ischemia) and to acute compartment syndrome (ischemia and pressure) was compared. In five animals, the cuff of a pneumatic tourniquet was inflated to 350 millimeters of mercury at the level of the thigh for three hours. In five other animals, an acute experimental compartment syndrome was created in one anterolateral compartment by autologous plasma infusion. The compartment pressure (measured by wick catheter) was maintained at a level equal to the mean arterial pressure for three hours. At three hours, reperfusion was established in both groups, either by tourniquet release or by decompressive fasciotomy and epimysiotomy. During both the ischemic period and a two-hour recovery period immediately thereafter, the mean intracellular pH and high-energy phosphate profile (levels of adenosine triphosphate and phosphocreatine) of the muscles of the anterolateral compartment were monitored non-invasively by phosphorus nuclear magnetic-resonance spectroscopy. Muscle biopsies were done the following day to take specimens for electron microscopic analysis of ultrastructural cellular degeneration. During ischemia, the cellular levels of phosphocreatine decreased at an identical rate in both groups. In contrast, the levels of adenosine triphosphate diminished rapidly in the animals with the compartment syndrome, but remained unchanged in the tourniquet group. Ischemic muscle acidosis was more severe in dogs with the compartment syndrome. In the tourniquet group, the phosphocreatine, adenosine triphosphate, and pH were all normal within fifteen minutes after release of the tourniquet, but these values remained depressed even two hours after fasciotomy in the group with compartment syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
The chronic form of the anterior compartment syndrome can be overlooked if the symptoms of leg pain are attributed to shin splints. Herein is presented a case report which I feel represents an acute exacerbation of the chronic form of anterior compartment syndrome in a long-distance runner secondary to bleeding into the extensor digitorum longus muscle. Chronic anterior compartment syndrome can be a disabling injury which may require a fasciotomy, depending upon the severity and duration of the patient's symptoms and the intracompartmental pressures. The lay term "shin splints" should be separated from medical use, and a more reliable assessment of the etiology of the patient's symptoms should be made. The term shin splints should be utilized only for pain localized to the posterior medial border of the tibia at the origin of the posterior tibialis muscle.
Avulsion of the tibial tubercle is an uncommon physeal injury. Complications from this fracture are infrequent. Adolescent boys developed compartment syndrome after tibial tubercle avulsion. Injury to the soft tissue surrounding the tibial tubercle avulsion may be more extensive than is usually appreciated. The anatomy of the proximal tibia and the tibial tubercle with nearby branches of the anterior tibial recurrent artery suggest a predisposing factor for the development of compartment syndrome. Compartment syndrome should be added to the list of possible complications of tibial tubercle avulsion fractures.
Acute compartment syndrome has multiple causes: fractures, crush injury, vascular trauma and burns. Exertional compartment syndrome may be acute (progressive) or chronic (usually reversible). The acute form usually occurs after intensive exercise. Closed muscle rupture is an uncommon cause with few reports. We report two cases, in the peroneal compartment of the leg and the flexor compartment of the forearm, to show that a high index of suspicion, allowing prompt diagnosis and fasciotomy, will enable a full recovery without complications.
The aim of this study was to evaluate the use of MR imaging for diagnosis and therapy management of compartment syndromes. In total, 15 patients (5 with an imminent compartment syndrome and 10 with manifest compartment syndrome) underwent MR imaging with a variety of pulse sequences including fat suppression, magnetization transfer imaging, and intravenous gadopentetate dimeglumine (Gd-DTPA) administration. Early and late follow-up MR images were obtained. Manifest compartment syndromes showed swollen compartments with loss of normal muscle architecture on T1-weighted spin-echo images. T2-weighted spin-echo and magnetization transfer imaging showed bright areas, which enhanced after Gd-DTPA. Early follow-up showed changes in enhancement patterns; late follow-up showed fibrosis and cystic and fatty degenerations of the affected compartments. MR imaging can help make the diagnosis of a manifest compartment syndrome in clinically ambiguous cases. It points out the affected compartments and allows the surgeon to selectively split the fascial spaces.
Although the aetiology, pathophysiology and treatment of acute compartment syndrome have been well described in the literature, there is limited information on the long-term impact of compartment syndrome on quality of life. We reviewed the medical records and radiographs of all the patients treated with surgical decompression of compartment syndrome. Between 1993 and 1998, 42 cases were identified. There were 30 cases of tibial compartment syndrome and 12 cases involving other limbs. These 30 patients were recalled for a follow-up assessment during which they were asked to complete an EQ-5D (EuroQol), a standardised measure of health related quality of life based on five dimensions (self-care, pain/discomfort, mobility, usual activities and anxiety/depression). Patients were compared with EQ-5D age/sex norms derived from a randomly selected group of patients that had sustained isolated closed tibial shaft fractures. The minimum follow-up time was 12 months. Patients who stated that the appearance of the surgical site was a problem, reported significantly poorer health related quality of life than did patients who had no problem with the appearance. Patients with skin graft reported more problems with pain and discomfort than patients without skin graft. Patients with faster closure times of the wound showed significantly better self-rated health status than patients in whom the wound closure time was longer. Although the patients in this study reported significantly more problems on the dimensions of EQ-5D than were reported in the control group, their overall self-rated health was not statistically different. This study has demonstrated that compartment syndrome may be associated with long-term impact on health related quality of life.
Exercise-induced exertional compartment syndrome was first described by Vogt in 1945 as "march gangrene." The authors report a case of a 20-year-old United States Marine presenting with the florid findings of acute crural compartment syndrome. The patient's history of prior episodes of crural pain following long hikes led the authors to conclude that this patient had a chronic exertional compartment syndrome.
Only a small number of cases of compartment syndrome in the upper arm has been reported in the literature. The authors have reviewed 14 patients with 14 cases of compartment syndrome treated at their institution from 1980 to 1988. In the majority of cases in this series, compartment syndrome was caused by blunt, high-energy trauma. There were 9 patients with multiple trauma, 7 of whom were motor cyclists, and fracture of the upper arm was present in most of these. In 5 patients scapulothoracic dissociation with disruption of the neurovascular bundle of the upper extremity concerned was present. In this series, 2 patients died of their injuries and three arms had to be amputated. At final follow-up after an average of 45 months (range 11-91 months) the functional result was dependent mainly on the severity of the associated injuries. Patients with isolated compartment syndrome had full recovery of upper limb function.
Compartment syndromes in the thigh are rare and the diagnosis may be difficult in the light of subtle early physical findings in the patient with spinal cord injury. Clinical awareness of the impending compartment syndrome is important to provide timely proper treatment and avoid disabling deformities. A compartment syndrome should not be ignored in the paraplegic, because the potential for late fibrosis and contractures may limit the independence of such patients. Greater awareness and index of suspicion are needed to successfully recognize and promptly treat the compartment syndrome in this patient population.
We report a retrospective study in patients with compartment syndrome with the aim to analyse: 1) whether the level of rise in CK levels is a useful marker to the presence of compartment syndrome and; 2) whether an early fasciotomy assists in lowering of the elevated CK levels. The results of our study suggest that although raised CK levels are not diagnostic, they are a useful adjunct in making a diagnosis, and hence CK estimation should be done in all patients with suspected compartment syndrome. Moreover, an early fasciotomy (< 12 hours) has a statistically significant influence in lowering elevated CK levels, confirming the view that the earlier the decompression, the lesser the muscle damage.
This study examines the effect of delayed exposure to hyperbaric oxygen on muscle necrosis and edema development following compartment syndromes in the canine hindlimb. Compartment syndromes (100 mm Hg for 8 h) were generated in one anterolateral compartment of six anesthetized dogs. After a 2-h delay, three 1-h hyperbaric oxygen treatments (2 atm absolute pure oxygen) were given during the next 12 h. Two days later, technetium-99m stannous pyrophosphate (99mTc Sn-PYP) was injected intravenously; 3 h later, samples were obtained from the pressurized and contralateral control muscles, weighed for edema development, counted for 99mTC Sn-PYP uptake, and evaluated histologically. Hyperbaric oxygen treatments, even when delayed 2 h, reduced muscle necrosis and intramuscular edema to negligible levels (p less than 0.05) compared with untreated animals. In addition, muscle morphology remained essentially normal in all hyperbaric oxygen-treated animals. We conclude that even if hyperbaric oxygen treatments are delayed 2 h, edema and muscle necrosis are reduced significantly in a model compartment syndrome.
BACKGROUND: Intra-abdominal hypertension has been recognized as a source of morbidity and mortality in the traumatized patient following laparotomy. Multiple organ dysfunction attributable to intra-abdominal hypertension has been called the abdominal compartment syndrome. The epidemiology and characteristics of these processes remain poorly defined. METHODS: Intra-abdominal pressure was measured prospectively in all patients admitted to a trauma intensive care unit over 9 months. Data were gathered on all patients with intra-abdominal hypertension. RESULTS: Some 706 patients were evaluated. Fifteen (2 per cent) of 706 patients had intra-abdominal hypertension. Six of the 15 patients with intra-abdominal hypertension had abdominal compartment syndrome. Half of the patients with abdominal compartment syndrome died, as did two of the remaining nine patients with intra-abdominal hypertension. Patients with abdominal compartment syndrome had a mean intra-abdominal pressure of 42 mmHg compared with 26 mmHg in patients with intra-abdominal hypertension only (P < 0.05). CONCLUSION: The incidence of intra-abdominal hypertension and abdominal compartment syndrome was 2 and 1 per cent respectively. Intra-abdominal hypertension did not necessarily lead to abdominal compartment syndrome, and often resolved without clinical sequelae. Abdominal compartment syndrome did not occur in the absence of earlier laparotomy. Abdominal compartment syndrome was associated with a marked increase in intra-abdominal pressure (above 40 mmHg).