[Compartment syndrome].
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In the past 5 years, a great deal of time and effort has been expended in an effort to better define clinical, anatomic, and laboratory parameters of CECS. It is now a well-recognized entity and one that can be readily resolved with fasciotomy. But the reasons for predisposition and the pathophysiologic mechanisms remain obscure. It appears, however, that basing the decisions for fasciotomy on clinical characteristics alone leads to overdiagnosis and excessive surgery. In this series, almost 50% of the referred subjects failed to demonstrate adequate laboratory criterion for the diagnosis of CECS. Fasciotomy in these patients may have effected a cure, but the reasons may be unrelated to increased intracompartmental pressure. Furthermore, in the laboratory diagnosis of CECS, the rate of return to resting compartment pressure following exercise seems more accurate than reliance on resting pressure alone. 31P-NMR has proved valuable in the dynamic assessment of muscle ischemia as reflected by relative PCr concentrations. Finally, although a mechanism explaining the source of pain has not been established by this study, it appears that ischemia is not a significant factor.
I studied the results of fasciotomy of the affected muscle compartment in eight patients with chronic anterior-compartment syndrome (involvement of the anterior tibial compartment) and in nine patients with medial tibial syndrome (involvement of the deep posterior compartment), all of whom had pain with exercise. In the patients with chronic anterior-compartment syndrome, the preoperative intramuscular pressure in the anterior tibial compartment, as measured by the wick-catheter method, was increased ten minutes after exercise to 52 +/- 36 millimeters of mercury. After fasciotomy this pressure was significantly lowered to 4 +/- 6 millimeters of mercury (p less than 0.01). In the patients with medial tibial syndrome, the preoperative intramuscular pressure in the deep posterior compartment was normal ten minutes after exercise (8 +/- 4 millimeters of mercury) and did not significantly change after the fasciotomy (5 +/- 6 millimeters of mercury). The clinical results after fasciotomy were good in both groups of patients. There was complete relief of pain in all of the patients with chronic anterior-compartment syndrome and in five of the nine patients with medial tibial syndrome. The other four patients considered their condition to be improved in spite of some remaining symptoms.
Acute exertional compartment syndrome of the superficial posterior compartment of the leg secondary to minor soft tissue injury is rare. This case series highlights the risk of misdiagnosis as deep venous thrombosis, followed by inadvertent anticoagulation. The delay in management did fortunately not lead to catastrophic consequences. Clinicians must not dismiss the possibility of an acute exertional compartment syndrome in the absence of direct trauma or after minor closed soft tissue injury.
Chronic exertional compartment syndrome is one cause of pain in the lower extremity, a common disability in athletes. The significance of intracompartmental pressures in the diagnosis of chronic exertional compartment syndrome is somewhat controversial. The goal of this study was to review the compartment pressure tests in a group of patients that underwent fasciotomy for refractory exertional compartment syndrome and to compare these pressures with an asymptomatic control group. The results are presented and compared with those of previous studies.
Compartment syndromes of the lower extremity can cause significant mobidity when appropriate treatment is not rendered. Paramount to the management of a compartment syndrome is a timely diagnosis. The physician must be intimately familiar with the anatomy as well as the signs and symptoms that a compartment syndrome presents. This familiarity can provide the opportunity for early diagnosis and treatment to prevent debilitating sequalae.
BACKGROUND: Abdominal compartment syndrome has been reported to occur after fluid resuscitation in injured patients, even in the absence of intra-abdominal injuries. This report describes a set of patients who developed the secondary extremity compartment syndrome (SECS) in uninjured extremities after resuscitation for other injuries. METHODS: This study was a retrospective chart review of all trauma patients developing SECS at a Level I trauma center. Data are mean +/- SD. RESULTS: From 1996 to 2001, 10 patients (8 men, age 31 +/- 13 years, Injury Severity Score of 29 +/- 17, and 3 with penetrating trauma) from a series of 11,996 trauma admissions developed SECS after resuscitation for other injuries. The mean number of extremities developing the SECS per patient was 3.1. This included compartment syndromes in 10 upper extremities and in 12 lower extremities that did not have any apparent injuries (i.e., contusions, fractures, or vascular injuries). After evaluation by the trauma team, abdominal silos were needed in 7 of the 10 patients also, and the mortality in patients with the SECS was 70%. CONCLUSION: SECS is a rare complication of the postresuscitation systemic inflammatory response syndrome, is associated with significant morbidity, and may be a marker for mortality. SECS should be ruled out by measurement of compartment pressures in uninjured and injured extremities in patients with severe diffuse edema after resuscitation for injury.
Chronic exertional compartment syndrome (CECS) is currently diagnosed using invasive pressure measurements. We report the use of 99Tcm-methoxyisobutyl isonitrile (99Tcm-MIBI) scintigraphy as a new non-invasive method of diagnosis. Forty-six patients with suspected chronic compartment syndrome underwent graded treadmill exercise to reproduce the presenting symptoms. At peak exercise, 300 MBq of 99Tcm-MIBI were injected intravenously. Subsequent cross-sectional imaging provided by emission tomography demonstrated regional abnormalities in muscle perfusion in the calf. A repeat study was performed at rest the following day. All patients in whom there was a strong clinical suspicion of CECS were considered for invasive pressure measurements. Statistical analysis of the results for investigation of CECS using 99Tcm-MIBI versus pressure studies gave P = 0.06. A comparison of 99Tcm-MIBI versus outcome gave P < 0.0001. The sensitivity was 80% and the specificity 97% for 99Tcm-MIBI studies based on outcome. The positive predictive value was 89% and the negative predictive value 94%. Thus 99Tcm-MIBI can detect compartment syndromes with good positive and negative predictive values. It is relatively simple, cheap and less invasive than pressure measurements. This technique shows promise in the diagnosis of CECS.
Acute Extremity Compartment Syndrome is a disorder, which can cause loss of limb if left untreated. Compartment syndrome develops when pressures within the fascial compartments become elevated, resulting in decreased perfusion to muscles and nerves. Left untreated, tissue death occurs. Rapid identification of clinical signs can decrease severity of symptoms. Diligent nursing assessment and monitoring of clinical signs, with communication to the physician, will facilitate rapid treatment by the physician. The primary treatment option is early identification and intervention through performance of a fasciotomy.
Compartment syndrome, if not identified and acted upon early, will result in irreversible damage to neuromuscular soft tissues. Therefore, orthopaedic nurses must be aware of the risks, signs and symptoms, unusual circumstances, and appropriate medical and nursing interventions with this syndrome. Usually compartment syndrome is considered to occur with fractures of the tibia, the forearm, or in vascular injuries or burns where there is significant edema. Not as common are compartment syndromes that occur after intramedullary nailing, in the thigh or upper arm, or in the presence of fracture blisters. These unexpected compartment syndromes each occurred only once in the author's many years as an orthopaedic clinical nurse specialist at a major trauma center. However, in each case, the situation and actions were significant. Compartment syndrome will be reviewed with supporting current literature. Each scenario will then be analyzed in terms of the particular considerations surrounding the diagnosis, treatment and nursing implications with the compartment syndrome.
Various forms of compartment syndrome can now be distinguished. Acute compartment syndrome is the result of a discrepancy between the volume of the compartment and its contents. This leads to increased pressure at rest and during load, which cuts off the micro-circulation and hence destroys the intracompartmental structures. Chronic compartment syndrome had only been seen in athletes and soldiers up to now. The disease mainly affects the anterior compartment and the fibular muscle group, and only rarely the lateral muscle compartment. In the course of severe venous diseases, a chronic venous compartment syndrome develops which is fundamentally different from the clinical pictures previously known. The cicatricial destruction of the crural fascia exerts an effect on the intracompartmental pressure with every step the patient takes. In severe cases, this results in considerable changes in the muscles involving chronic ischaemia associated with necrosis and glycogen deficiency. Further investigations are necessary in order to define the clinical picture, particularly by measuring the intracompartmental pressure under dynamic and standardised conditions. We suggest also making a verbal distinction between the two forms: a chronic exertional compartmental syndrome and a chronic venous compartmental syndrome.
Increases in compartment pressure associated with chronic compartment syndrome (CCS) may be due to changes in the mechanical properties and/or thickness of fascia (4,22). To explore this possibility, we compared the mechanical and biochemical characteristics (stiffness, thickness, time-dependent response, collagen content, and collagen crosslinking) of fascia from patients with symptomatic anterior compartment syndrome to fascia from adjacent collateral compartments. We tested 43 specimens harvested from 20 individuals during surgical fasciectomy. Properties of normal (lateral)-compartment (NC) and pathological (anterior)-compartment (PC) fascia were mechanically tested in the axial and transverse directions forming four groups. An external control group (EX) of six specimens of anterior and lateral-compartment fascia harvested from amputated legs was also included in the study. PC fascia was found to be thicker and structurally stiffer (elastic modulus times thickness) in the axial direction than was NC fascia (p < or = 0.05). No significant differences were found between NC and PC time-dependent response, although significant differences between percent relaxation in the pooled axial and transverse direction specimens were observed. No differences were found in the collagen content, as measured by hydroxyproline (Hyp) concentration, between NC and PC fascia. PC fascia was found to have less collagen crosslinking by hydroxylyslpyridinoline (HP) concentration. In conclusion, although this study does not elucidate etiological factors in CCS, the changes found in PC fascia suggest that fascial mechanical properties contribute to the pathology.
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Acute Atraumatic Compartment Syndrome (AACS) can be a potentially life and limb threatening complication of either drug abuse or medication injection. Prompt recognition followed by emergency fasciotomy is required to avoid permanent disability. A better understanding of the different clinical presentations may lead to improved outcomes through more expedient diagnosis and treatment. We describe five new cases of AACS caused by illicit drug abuse within the McGill University Hospitals, with a review of all 102 similar patients previously documented in the literature between January 1970 and May 1997. The average age for all cases was 29 years, with 74% being male. The presence of edema, pain, tension, and skin changes were the most frequent symptoms and signs reported. There appear to be two distinct mechanisms of poisoning-induced AACS: (1) direct vasotoxicity and (2) limb compression caused by prolonged comatose state. Direct vasotoxicity is more likely to lead to eventual amputation, whereas prolonged limb compression is more likely to progress to systemic complications such as azotemia, hypotension, cardiac arrhythmia, and renal failure (Crush Syndrome). Long-term sequelae of motor loss, sensory disruption, and development of contracture were common in AACS of both causes. Because Compartment Syndrome is a surgical emergency, primary care and emergency physicians must have a high index of suspicion to promptly recognize and treat this problem.
Chronic exertional compartment syndrome is an often overlooked and uncommon cause of pain in the extremities of individuals who engage in repetitive physical activity. A thorough history, a careful physical examination, and compartment pressure testing are essential to establish the diagnosis. Catheter measurements can provide useful information on baseline resting compartment pressures as well as compartment pressures after exercise or trauma. Patients with chronic exertional compartment syndrome usually do not respond to nonsurgical therapy other than completely ceasing the activities that cause the symptoms. Surgical intervention entails fasciotomies of the involved compartments. Although obtaining accurate compartment pressure measurements can be difficult and fascial releases must be done carefully, patients typically have satisfactory functional results and are able to return to their usual physical activities after fasciotomy.
The abdominal compartment is limited by the abdominal wall, Mm. Psoas, vertebral column, diaphragm and the pelvis. Thus the retroperitoneum is included. Elevated intraabdominal pressure may profoundly impair the function of the entire gastrointestinal tract, the cardiovascular, respiratory, and renal system. Reduction of increased intraabdominal pressure may reverse all these adverse effects. The most common causes of elevated intraabdominal pressure are abdominal operations, abdominal trauma, diffuse peritonitis, ascites and peritoneal edema following resuscitation. Excessively increased intraabdominal pressure may result in a total loss of function and may lead to death. Such a condition is called an abdominal compartment syndrome. It usually requires operative decompression. According to animal experiments and clinical experiences suggestions for treatment are given. Diagnostic suspicion of elevated intraabdominal pressure may be confirmed with objective measurements. Since bedside manometry using a Foley catheter provides a valuable estimate of intraabdominal pressure and is easy to perform, intraabdominal pressure values may contribute to medical decision making. At this time there is a great need of controlled clinical trials to point out the importance of increased intraabdominal pressure and the abdominal compartment syndrome.
Compartment syndrome can be classed as imminent, with moderate disturbances of muscular perfusion, no neurological symptoms and increasing tissue pressure, and manifest, with compromised circulation and loss of tissue function in the space and pathologic tissue pressure. When compartment syndrome is suspected, the most important immediate measure is wide splitting of any constricting dressings that have been applied. For decompression, the only adequate therapy, in imminent compartment syndrome, subcutaneous fasciotomy is required. The skin incision can be closed. Manifest compartment syndrome necessitates therapeutic fasciotomy, which means long incisions of skin and fascia, splitting of retinacula, excision of necrotic tissues, evacuation of hematoma and, if possible, rigid fixation of fractures. Skin closure is not permitted because of postoperative swelling, which can produce a rebound compartment syndrome. After 4-8 days edema decreases and the wound is closed by delayed sutures or a mesh graft. In the same session a second look operation for re-debridement of the tissues is done. Special problems arise in complex lesions of the foot, because of the thin layer of soft tissue coverage and the diminished blood supply to the bones of the foot. In the foot, decompression requires not only that the compartments of the short pedal muscles be opened, but also that the skin be adequately released.
The acute compartment syndrome is a condition in which increased pressure within a limited space compromises the circulation and function of the tissues therein, resulting in tissue ischaemia, necrosis and nerve damage. This rise in tissue pressure originates in a decrease of the compartment size or increase of the intracompartmental volume by oedema and/or haemorrhage. Following the arterio-venous gradient theory, capillary blood flow may be impaired through increased venous pressure, decreased arterial pressure and increased peripheral vascular resistance. Often, compartment syndromes develop during reperfusion following a period of ischaemia. During ischaemia, there is a gradual depletion of intracellular stores of high energy phosphate bonds and glycogen stores. There is a buildup of products of glycolysis, particularly lactic acid, with accompanying hydrogen ion accumulation as well as an increase in intracellular reducing agents. Reperfusion may, instead of restoring normal muscle metabolic activity, cause harmful effects by washing out necessary precursors for adenine nucleotide resynthesis. Production of oxygen free radicals occurs with ensuing lipid peroxidation, and calcium influx occurs upon reoxygenation with resultant disruption of oxidative rephosphorylation in the mitochondria. Furthermore, several lines of evidence suggest that white blood cells are important in the pathogenesis of reperfusion injury. Upregulation of both neutrophil receptors and endothelial leucocyte adhesion molecules leads to the sequestration of white blood cells in the muscle with prolongation of the reperfusion injury. This subsequently results in damage to remote organs such as lungs, liver, heart and kidneys.