Chronic Compartment Syndrome Secondary to Advanced Lower Limb Lymphedema: A Case Report

Chronic exertional compartment syndrome is diagnosed based on symptoms and elevated intramuscular pressure and often is treated with fasciotomy. However, what contributes to the increased intramuscular pressure remains unknown. We investigated whether the stiffness or thickness of the muscle fascia could help explain the raised intramuscular pressure and thus the associated chronic compartment syndrome symptoms. We performed plain radiography, bone scan, and intramuscular pressure measurement to diagnose chronic compartment syndrome and to exclude other disorders. Anterior tibialis muscle fascial biopsy specimens from six healthy individuals, 11 patients with chronic compartment syndrome, and 10 patients with diabetes mellitus and chronic compartment syndrome were obtained. Weight-normalized fascial stiffness was assessed mechanically in a microtensile machine, and fascial thickness was analyzed microscopically. Mean fascial stiffness did not differ between healthy individuals (0.120N/mg/mm; SD, 0.77N/mg/mm), patients with chronic compartment syndrome (0.070N/mg/mm; SD, 0.052N/mg/mm), and patients with chronic compartment syndrome and diabetes (0.097N/mg/mm; SD, 0.073N/mg/mm). Similarly, no differences in fascial thickness were present. There was a negative correlation between fascial stiffness and intramuscular pressure in the patients with chronic compartment syndrome and diabetes. The lack of difference in fascial thickness and stiffness in patients with chronic compartment syndrome and patients with chronic compartment syndrome and diabetes compared with healthy individuals suggests structural and mechanical properties are unlikely to explain chronic compartment syndrome. To prevent chronic exertional compartment syndrome, it is necessary to address aspects other than the muscle fascia. Level II, prognostic study. See the guidelines online for a complete description of level of evidence.

Patients with chronic compartment syndrome (CCS) experience pain during exercise. At cessation of exercise, pain subsides within minutes. Supposed aetiology is that exercise causes abnormal increase in intramuscular pressure, impairing local tissue perfusion, resulting in ischemia and pain. Besides clinical findings, diagnosis is confirmed through intra-compartmental pressure (ICP) post-exercise. With near infrared spectroscopy (NIRS) tissue oxygen saturation (StO2) can be measured in a noninvasive manner. Patients with chronic exertional compartment syndrome have shown greater deoxygenation. PURPOSE To determine a difference in StO2 between healthy volunteers and military men with suspected CCS. METHODS Those who met criteria for CCS at a first visit (ICP ≥ 35 mmHg post-exercise), completed a second visit after fasciotomy, volunteers had just one visit. Subjects performed a standardized exercise protocol at each visit. StO2 was monitored continuously in the tibialis anterior muscle of both legs throughout the exercise. StO2 data were compared between patients and volunteers. Pre- and post-fasciotomy StO2 was compared for patients RESULTS A significant difference between StO2 of volunteers compared with CCS was found for: peak exercise value (p = 0.0002), absolute (p = 0.0050) and percent change (p = 0.0011) between baseline and peak exercise StO2, and recovery StO2 as a percent of baseline (p = 0.0211). Average peak exercise value for volunteers was higher than for those with CCS. Healthy volunteers showed less change between baseline and peak exercise. The StO2 values in legs with confirmed CCS returned to the normal range post-fasciotomy. All changes differed significantly with pre-operative values. CONCLUSION StO2 was comparable to ICP in distinguishing healthy from diseased legs. This study provides compelling evidence supporting NIRS as a non-invasive, painless alternative in the diagnosis of CCS. Supported by Hutchinson Technology Inc. BioMeasurement Div., Hutchinson, MN USA

Compartment syndrome has been defined as “a condition in which increased pressure within a limited space compromises the circulation and function of the tissues within that space”.1 It is most commonly seen after injuries to the leg2-5 and forearm6-8 but may also occur in the arm,9 thigh,10 foot,11-13 buttock,14 hand15 and abdomen.16 It typically follows traumatic injury, but may also occur after ischaemic reperfusion injuries,17 burns,18 prolonged limb compression after drug overdose19 or poor positioning during surgery.20-24 Furthermore, subclinical compartment syndromes may explain the occurrence of a variety of postoperative disabilities which have been identified after the treatment of fractures of long bones using intramedullary nails.25 Approximately 40% of all acute compartment syndromes occur after fractures of the tibial shaft26 with an incidence in the range of 1% to 10%.26-30 A further 23% of compartment syndromes are caused by soft-tissue injuries with no fracture and fractures of the forearm account for 18%.26 Acute compartment syndrome is seen more commonly in younger patients, under 35 years of age31 and therefore leads to loss of function and long-term productivity in patients who would otherwise contribute to the country’s workforce for up to 40 years.

Background: There are few reports concerning chronic compartment syndrome producing symptoms in the forearm, although in the lower limb this is a well recognised condition. The objective was to demonstrate...

Bothrops atrox Snakebite: How a Bad Decision May Lead to a Chronic Disability: A Case Report

Background:The diagnostic gold standard for diagnosing chronic exertional compartment syndrome (CECS) is a dynamic intracompartmental pressure (ICP) measurement of the muscle. The potential role of a repeat ICP (re-ICP) measurement in patients with persistent lower leg symptoms after surgical decompression or with ongoing symptoms after an earlier normal ICP is unknown.Purpose:To study whether re-ICP measurements in patients with persistent CECS-like symptoms of the lower leg may contribute to the diagnosis of CECS after both surgical decompression and a previously normal ICP measurement.Study Design:Case series; Level of evidence, 4.Methods:Charts of patients who underwent re-ICP measurement of lower leg compartments (anterior [ant], deep posterior [dp], and/or lateral [lat] compartments) between 2001 and 2013 were retrospectively studied. CECS was diagnosed on the basis of generally accepted cutoff pressures for newly onset CECS (Pedowitz criteria: ICP at rest ≥15 mmHg, ≥30 mmHg after 1 minute, or ≥20 mmHg 5 minutes after a provocative test). Factors predicting recurrent CECS after surgery or after a previously normal ICP measurement were analyzed.Results:A total of 1714 ICP measurements were taken in 1513 patients with suspected CECS over a 13-year observation period. In all, 201 (12%) tests were re-ICP measurements for persistent lower leg symptoms. Based on the proposed ICP cutoff values, CECS recurrence was diagnosed in 16 of 62 previously operated compartments (recurrence rate, 26%; 53 patients [64% female]; median age, 24 years; age range, 15-78 years). Recurrence rates were not different among the 3 lower leg CECS compartments (ant-CECS, 17%; dp-CECS, 33%; lat-CECS, 30%; χ2 = 1.928, P = .381). Sex (χ2 = 0.058, P = .810), age (U = 378, z = 1.840, P = .066), bilaterality (χ2 = 0.019, P = .889), and prefasciotomy ICP did not predict recurrence. Re-ICP measurements evaluating 20 compartments with previously normal ICP measurements (15 patients [53% female]; mean age, 31 ± 10 years) detected CECS in 3 compartments (15%, all ant-CECS).Conclusion:Previous fasciotomy for lower leg CECS or previously normal muscle pressure (ICP) do not rule out CECS as a cause of persisting lower leg symptoms. Repeat ICP measurement may have a potential role in the evaluation of patients with persistent lower leg complaints. However, other reasons for lower leg exertional pain must always be considered prior to secondary surgery.

Assessment of Lymphovenous Anastomosis Patency: Technical Highlights.

Lymphœdèmes pénoscrotaux : étude rétrospective de 33 cas

A review of the literature is presented, including data on the incidence, pathophysiology, and clinical picture of patients with chronic compartment syndrome (CCS) of the lower extremities. Chronic exercise compartment syndrome (CECS) is characterized by pain with repetitive exertion and increased intracompartmental pressure affecting the lower extremities in physically active patients. In severe chronic venous insufficiency of the lower extremities, chronic venous compartment syndrome (CVCS) develops, which is fundamentally different from previously known clinical pictures. Progressive dermatolipofasciosclerosis and cicatricial destruction of the fascia of the leg in patients with C4b-C6 clinical classes according to CEAP affect the pressure in the muscle-fascial compartments at each step. In severe cases, this leads to significant changes in the muscles, accompanied by chronic ischemia associated with necrosis and glycogen deficiency. The analysis of various diagnostic methods, conservative treatment and methods for performing surgical decompression of the CCS was carried out. The lack of a clear pathophysiology for CECS and CVCS complicates the diagnosis and treatment of this condition. Diagnosis of calf CCS is still based on pressure testing in the musculofascial compartments of the calf using the Pedowitz criteria, however standard procedures for this, including patient position, static or dynamic movements, muscles and equipment tested, are not agreed upon. In patients with CCS, if conservative treatment is ineffective, fasciotomy of the affected parts of the lower leg is the method of choice. Various techniques for fasciotomy of the lower leg include the traditional open fasciotomy, the semi-closed technique with one or more incisions, the minimally invasive technique using endoscopic compartment release, and the use of ultrasound guidance. Fasciectomy of the lower leg to correct CVCS is performed mainly for recurrence of trophic ulcers after shave therapy, severe calcification of the lower leg tissues and for the treatment of deep transfascial necrosis. Randomized, blinded, controlled trials are needed to further expand our knowledge of the diagnosis and treatment of CCS.

Intramuscular pressure was recorded in 80 patients suspected of suffering from chronic anterior compartment syndrome in the lower leg; the diagnosis was verified in 22 of these patients. The history and clinical findings of the chronic compartment syndrome patients were compared with those of the 58 patients without the syndrome. Pain induced only by athletic activity and only in the anterior lower leg forcing the patient to interrupt running indicated chronic compartment syndrome. The history and clinical findings alone were found to be insufficient to establish the diagnosis. In relation to generally accepted pressure parameters at rest, the muscle relaxation pressure during exercise was found to be a reliable parameter for diagnosing chronic compartment syndrome, whereas mean muscle pressure and muscle contraction pressure were found to be unreliable.

Iliac vein compression is highly prevalent in the general population, which may lead to misdiagnosis of lower limb lymphedema as iliac vein compression syndrome and subsequent stent placement. This study retrospectively analyzed the treatment outcomes of 11 patients with secondary lymphedema who had previously been diagnosed with iliac vein compression by venography and underwent iliac vein stenting. Following iliac vein stent placement, six patients with Stage I and IIa lymphedema experienced partial relief of limb swelling; however, symptoms recurred and worsened within three months. The remaining patients showed no improvement in swelling after the stent was placed. Due to inadequate symptom relief following stent implantation, these patients underwent reevaluation and were subsequently diagnosed with lymphedema. Based on disease staging, they received appropriate interventions including complex decongestive therapy, lymphovenous anastomosis, or a combination of liposuction and lymphovenous anastomosis. Four patients with Stage I and IIa lymphedema underwent complex decongestive therapy, four patients with Stage I and IIa lymphedema received lymphovenous anastomosis, and the remaining three patients with Stage IIb lymphedema underwent liposuction combined with secondary lymphovenous anastomosis. Follow-up assessments were conducted at 3, 6, and 12 months post-treatment to evaluate limb morphology and functional outcomes using the Disability and Health Questionnaire for Lower Limb Lymphedema scores. Therapeutic outcomes analysis revealed that complex decongestive therapy, lymphovenous anastomosis, and liposuction demonstrated favorable efficacy in managing lymphedema cases with suboptimal response to prior iliac vein stenting.

ACUTE compartment syndrome (ACS) represents a limb-threatening condition. Delaying diagnosis and therapy may lead to irreversible neuromuscular ischemic damages with subsequent functional deficits.1 Diagnosis is primarily clinical and characterized by a pain level that quality exceeds the clinical situation. Diagnosis is assessed by invasive pressure monitoring within the suspected compartment. Once ACS has been confirmed it represents a surgical emergency with definitive treatment requiring immediate fasciotomy to relieve the pressure within the affected compartment. Irreversible tissue damage can occur within 4–6 h after the onset of symptoms. However, nerves are already seriously damaged after 2 h of increased compartment pressure.1,2 Concerns about masking pain as cardinal symptom and therefore leading to a delay in diagnosis and therapy have been raised in connection with regional anesthesia.3,4 Moreover, several case reports and case series have blamed different types of regional anesthesia4–11 and even the use of opioid patient-controlled analgesia12 for delaying diagnosis of ACS. Therefore, the use of regional anesthesia for trauma and orthopedic surgery remains controversial.4,6,13 A case involving continuous regional anesthesia of the upper extremity and the development of an ACS is presented.A 47-yr-old woman was scheduled for surgical treatment of a complex distal humerus fracture of her right dominant arm. Medical history was unremarkable except for obesity (body mass index 41.5), a metabolic syndrome (diabetes, obesity, and hyperlipidemia), and sulfazine treatment due to Crohn disease. The right arm showed classical signs of hematoma and swelling without any clinical sign for increased compartment pressure. All nerve functions were preserved. An open reposition of the fracture, osteosynthesis of the capitulum, trochlea humeri, and radial condylus were performed with postoperative placement of an open arm splint. The anesthetic management combined infraclavicular catheter, placed preoperatively but no local anesthetic was given until after the patient has been extubated, and general anesthesia performed with target-controlled infusion of propofol (Disoprivan®, AstraZeneca, Zug, Switzerland) and remifentanil (Ultiva®, GlaxoSmithKline, Münchenbuchsee, Switzerland). Infraclavicular catheter placement and general anesthesia were uneventful including stable patient’s hemodynamic parameters during the 150 min lasting surgical intervention. After extubation, the sensomotor function of the operated arm was checked by the surgeons and the infraclavicular catheter was started thereafter. An initial bolus of 30 ml ropivacaine 0.5% (Naropin®, AstraZeneca) was applied with intermittent aspiration, and block assessment indicated a successful block. The patient was transferred to the postoperative care unit for further observation and a patient-controlled regional analgesia infusion with ropivacaine 0.3% (Naropin®) was started with a continuous rate of 6 ml/h, an additional bolus of 5 ml with a lockout time of 20 min. Additionally, acetaminophen (Perfalgan®, Bristol-Myers Squibb, Baar, Switzerland) 4 × 1 g/day was prescribed.During the first 2 h in the postoperative care unit, the patient did not complain about pain, hemodynamic parameters remained within normal range, and peripheral pulses were present. The wound drainage showed 70 ml blood loss before discharge to ward and assessment of the infraclavicular catheter revealed a good function.Patient’s pain assessed on the visual analog scale was 10/100 during the first postoperative night without the need for additional analgesics. Fourteen hours after surgery she developed severe forearm pain (visual analog scale 90/100). The anesthesia resident on call found a sensory and motor block of all target territories/muscles in the hand but a preserved contraction of the biceps and coracobrachial muscles. Suspecting a not blocked musculocutaneous nerve being responsible for the increasing pain she administered an additional bolus of 20 ml ropivacaine 0.5%. The severe pain was still present 20 min after its administration despite the occurrence of a new complete motor and sensory block of all territories. The characteristics of the breakthrough pain alarmed the anesthesiologist who suspected an incipient ACS. The orthopedic surgeons were informed and observed an intense pain on the dorsolateral part of the right forearm in the area of the extensor compartment with a significant increase in pain with stretching of these muscles. The intracompartmental pressure was measured using the Stryker Intra-Compartmental Pressure Monitor System (Stryker®, Kalamazoo, MI). The pressure in this compartment was 40 mmHg. Emergency fasciotomy of the extensor compartment of the forearm was performed under general anesthesia within 1 h after assessment of intracompartmental pressure. Intraoperatively, the extensor compartment of the forearm was greatly swollen and very tense. Upon decompression, the muscles were edematous but viable. Further exploration of the wound revealed two hematomas which were evacuated but no other compartments (of the forearm or arm) were under tension. The fascia of the extensor compartment was left open but the skin could be closed without any problem. Therefore, primary wound closure was performed. The infraclavicular catheter was removed. The motor and sensory function returned to normal after 4 h. The patient made an uneventful recovery and was discharged 3 days later. The follow up at 3 months showed no sensory or motor disabilities of the operated arm.ACS is defined as an increase of pressure within a fixed osteofascial anatomic space, leading due to decreased local tissue perfusion to an impairment of cellular function and, when sustained, to irreversible changes like infarction of muscles and nerves in the compartment. Important variables affecting the outcome are the amount and the duration of pressurization and the extent and severity of soft tissue injury.14The different symptoms and signs describing ACS are reported in table 1. Although previous studies have reported that resting interstitial tissue pressures in the healthy vary between 0 and 8 mmHg for the dorsal and volar forearm compartments and less than 15 mmHg in the interosseous muscles of the hand15 pressure measurement is considered to be accurate. Interstitial tissue pressure measurement is measure point dependent in noninjured15 and injured extremities with higher pressures within 5 cm of the fracture.16Different absolute compartment pressures or calculated pressures (difference between systolic or mean arterial pressure and the compartment pressure) have been described in the literature.17,18 Although the mean arterial pressure for the difference calculation (mean arterial pressure—compartmental pressure) seems to be more accurate comparative, clinical trials are lacking. It must be emphasized that much of above work exclude children and was mainly carried out studying ACS of the lower extremity. Upper extremities might have other pressure thresholds but due to lacking evidence the established threshold of ΔP 30mmHg is retained. In children, the mean arterial pressure rather than the diastolic pressure has been suggested to calculate the ΔP as the diastolic blood pressure is often lower in children.19Data from the Royal Infirmary of Edinburgh show an average annual incidence of 3.1 per 100,000 people (7.3 per 100,000 men and 0.7 per 100,000 women).17The key element is the elevation of tissue pressure within encapsulated muscles. In the ACS, fluid shifts between the blood and the extra- and intracellular space due to an increased tissue pressure of the compartment leading to an increased extravascular venous pressure. Further pressure leads to a decrease of capillary blood flow and decrease in tissue Po2 ending in a metabolic deficit. The end stage is deficit muscle ischemia and necrosis. Tissue metabolism requires an oxygen tension of 5–7 mmHg. This tension is maintained by capillary perfusion pressure of 25 mmHg which is above the normal interstitial tissue pressure of 4–6 mmHg. The tissue perfusion pressure equals capillary perfusion pressure minus interstitial pressure. When tissue pressures reach 30–40 mmHg,20 the extraluminal pressure causes progressive arteriole collapse due to direct pressure effects and to interferences with critical closing pressures leading to local tissue hypoxia with secondary shunting to areas with less vascular resistance. Moreover, local tissue perfusion ceases when the interstitial tissue pressure equals the diastolic blood pressure. The rising tissue pressure causes collapse of the veins. Arterial flow increases the venous pressure reestablishing the flow, but the increased venous pressure adversely affects the arteriovenous gradient with consecutive ischemia21 (fig. 1).Two pathophysiology theories are the “arteriovenous gradient theory” and the “ischemia–reperfusion syndrome.”22 Both theories share the increasing tissue pressure, the consequently decreasing capillary blood flow, and the decrease of tissue Po2 resulting in a metabolic deficit. If the ACS is caused either by external pressure or by an increased internal pressure, first the arteriovenous gradient theory explains the reduced capillary blood flow with increasing venous pressure or increasing capillary resistance. In the case of additional injuries leading to hypovolemic shock, the “arteriovenous gradient theory” explains the diminished arterial pressure resulting in reduced capillary blood flow. In the case of reperfusion after revascularization or tourniquet release, the “ischemia–reperfusion mechanism” explains how different factors such as the release of oxygen-free radicals, massive accumulation of calcium in the ischemic muscles, and the infiltration of neutrophils into the reperfused vessels lead to an increase in compartment pressure. The hypoxic injury releases vasoactive substances, which increase the endothelial permeability. Subsequently, this mechanism leads capillary leakage into the extravascular space provoking additional edema and additional rise in compartment pressure. The falling pH and the degradation products contribute to a further increase in the tissue pressure, thereby reducing microperfusion as explained by the “arteriovenous gradient theory” leading to a self-perpetuating vicious circle. As a result of ischemia nerve conduction slows down.However, several authors have demonstrated that early decompression leads to a drop in extraluminal pressure, restoration of local blood flow, removal of anaerobic metabolites, and return of normal cellular function.23 Cells may become edematous and demonstrate histological evidence of injury after decompression, but the morphology and function of most of them will return to normal within some days.Pain is considered to be the main clinical symptom of a developing ACS. Pain exceeding clinical expectance, pain not responding to analgesics, palpable tenseness in the affected compartment and pain worsening with passive stretching of the muscles in the according compartment are the most accurate early indicators. Paresthesia, paresis, and pulselessness are in most circumstances late signs of an ACS and already indicating a potentially irreversible compartment and muscle damage. However, pain may not be useful in children or in adults with an altered level of consciousness.1Commonly used signs in clinical practice are neither reliable nor sufficiently specific or sensitive if there are not at least three signs.24 Pulselessness in fact is considered to be a late sign and is associated with bad prognosis.4,18 Even pain is unreliable if there is no breakthrough pain or increasing analgesic demand.4 In fact, the simple presence of pain was insufficient to prevent from delaying ACS diagnosis.25–27 Even the clinical palpation of the tense and swollen extremity has been shown to be strongly assessor dependent and unreliable with a sensitivity of 24% and specificity of 55%.28 Paresthesia and other altered sensations are also of questionable diagnostic value due to many confounders like central acting analgesics, alcohol, brain and spine injuries, altered level of sensation, other distracting injuries, extremes of age, language, and ethnical barriers.1 Despite these limitations arguments against regional anesthesia or even opioid patient-controlled analgesia focus on the possible interference of these techniques with the classical signs of ACS.2,3The reference method for diagnosis of ACS remains the measurement of interstitial tissue pressures. Different methods for measuring intracompartmental pressure have been described to directly, indirectly, or continuously measure compartment pressure29 (table 2). There are less invasive new technologies like laser doppler flowmetry and 99Tcm-methoxy-isobutryl isonitril scintigraphy. However, it is unclear how practical and cost-effective these methods are in clinical practice. An interesting development in the field of noninvasive measurement techniques was introduced by the near-infrared spectroscopy which detects changes and trends in relative oxygen saturation of hemoglobin. In the setting of ongoing ACS, near-infrared spectroscopy has been described to have a high sensitivity and specificity detecting and providing continuous monitoring of intracompartmental ischemia and hypoxia.30 However, more studies are warranted to define the correlation with critical pressure thresholds. Magnetic resonance imaging and scintigraphy are not sensitive enough to be recommended for ACS diagnosis.In the case of an incipient compartment syndrome, frequent clinical reevaluation must be completed and accurately documented.14 Casts and circumferential dressings must be removed and positioning with tension or distorsion must be avoided to not further compromise blood flow. Fluid therapy must be carefully evaluated, electrolytes, renal function, coagulation, and hemodynamic parameters must be monitored. Once the diagnosis of ACS has been established, surgical decompression of the affected osseofascial compartments is warranted.31The most outcome relevant factors are fasciotomy, timing of diagnosis and fasciotomy performance, and the concomitant injuries. However, for the ACS of the upper extremities controversial opinions exist. Good results are reported after early diagnosis and quick fasciotomy, poor results with delayed treatment. However, there is no prospective study documenting the benefit of early fasciotomy for upper extremity ACS.32Delaying fasciotomy for more than 12 h has been shown to significantly worsen outcome.16 According to Hayakawa et al.33 fasctiotomy performed by 6 h after diagnosis of ACS led to a satisfactory outcome in 88% of cases with an amputation rate of 3.2% and 2% deaths, whereas fasciotomy after 12 h showed satisfactory outcome in only 15% of cases with 14% amputations and 4.3% deaths. There is sparse data about the timeframe >6 h but <12 h, as residual deficits happen also if fasciotomy is performed only 2 h after ACS diagnosis.34Regional anesthesia in patients at risk for developing an ACS is a highly controversial topic discussed.2,3,35 However, there is no randomized trial comparing outcome after different anesthesia managements. Actual clinical practice is based only on case reports, retrospective case series, recommendations and reviews, and the belief that regional anesthesia completely blocks pain and alters sensory-motor response to impede diagnosis of ACS.4 Advances in regional anesthesia techniques, drugs, and concentrations which allow a goal-directed therapy of pain with spare of sensory-motor functions are ignored.This patient presents an ACS of the upper extremity involving regional anesthesia. Interestingly, some of the published case reports blame a peripheral nerve block (PNB) for masking an ACS in a territory not covered by the block. This challenges the sole responsibility of the PNB in masking the ACS.7,10 There is one recent case report blaming continuous perineural blocks for delaying diagnosis of ACS after distal femur and proximal tibia osteotomy.5 Additional to general anesthesia continuous sciatic and femoral nerve blocks were run with ropivacaine 0.2% after an initial bolus of 30 ml ropivacaine 0.5% through each catheter. Due to persistent breakthrough pain on postoperative day 2 the surgeon performed a clinical evaluation (dense swollen gastrocnemius muscle, excruciating upon passive plantar flexion, and dorsiflexion of the foot) and a compartment pressure measurement (30 mmHg). Despite these findings, a reevaluation was performed 2 h later showing the same findings. Finally, an emergent decompressive fasciotomy was performed. Once again, the breakthrough pain was ignored. This delay had serious consequences: tissue loss and functional deficits resulted. A second case report using continuous popliteal nerve block describes a patient who was sent home on postoperative day 1 with a popliteal catheter after foot surgery despite a dense motor and sensory block.11 Pain became worse overnight and presented to the emergency department on postoperative day 2. The cast was splinted but not removed, no compartment pressures were measured. Patient refused to have the continuous PNB removed and was managed through the telephone. On postoperative day 4 the catheter was removed uneventfully. Probably, this is not a case of ACS but of pressure pain induced by tight cast which could have led to an ACS. However, patient management in this case report is not according to common standard. The case described by Noorpuri et al.9 describes an ACS after an ankle block for a revisional forefoot arthroplasty. The patient developed increasing pain despite receiving supplementary analgesia, paresthesia, motor weakness and showed a tense swollen forefoot with a delayed capillary refill. No compartment pressure monitoring was performed and fasciotomy was performed due to increment clinical signs. Despite the neglect of typical clinical signs the authors blamed the ankle block for masking the ACS and delaying its diagnosis.None of the five currently published case reports blaming peripheral regional analgesia for delaying diagnosis or therapy of ACS can stand a thorough study of the case. Ignored increasing pain and typical clinical signs are present in all cases and in one regional anesthesia did not even block the area of interest.Our case shows the development of an ACS in a patient treated for analgesia using an infraclavicular catheter. As reported in section IV and in table 3 we suggest not to activate the perineural catheters in patients the surgeons consider to be at risk for either surgery associated nerve damage or compartment syndrome. This allows an immediate testing after surgery without delay in diagnosis. In the case of high risk for an ACS a delay in starting the catheter can be wise or the application of a very low concentration of local anesthetics preventing motor block might be suggested.In this case the ACS developed slowly and breakthrough pain was a symptom. The resident evaluated the pain as postsurgical due to the motor function of the biceps and coracobrachial muscles. The fingers were according to her first description not swollen. Interesting is the fact that despite 20 ml 0.5% ropivacaine after 20 min the pain was still present despite the occurrence of a new complete motor block. This and the measured compartment pressure were the only clinical signs. The swelling was only appreciated after removal of the splint. This further suggests, that at least for PNB, regional anesthesia does not mask the cardinal symptom of ACS: breakthrough pain. However, the typically used 0.5% concentration for the top up of the catheters should be reconsidered in patients at risk for ACS. What would happen with our patient if pain had improved by 50%? Moreover, the communication between anesthesiologist and surgeons remains to be of pivotal importance. ACS is a surgical diagnosis and therefore patients with unclear pain must be evaluated by both, anesthesiologist and surgeon.There is no single case report showing a delay in ACS diagnosis due to peripheral regional anesthesia, even considering continuous regional anesthesia. Almost all published cases including epidural analgesia (EDA) showed that patient complained of increasing pain despite regional anesthesia,10 loss of motor function despite reduction of local anesthetic concentration36 or increasing analgesic demand.4,5,11 Only in two cases was a dense motor block noted after EDA at time point of ACS diagnosis.26,37 Other cases even blamed a continuous PNB for an ACS in a territory the block did not cover.7,10 The other case reports did not give any details about documentation or patient management before start of symptoms/clinical signs.4 Therefore, regional anesthesia can only be considered to be associated but not the cause of the delay in diagnosis. Excluding both cases with dense motor block after EDA26,37 there was no evidence that regional anesthesia masked important symptoms of compartment syndrome.Despite this evidence, the use of regional anesthesia for patients at risk for ACS remains a topic of dispute between anesthetists and surgeons.3 As reported by Cascio et al.38 a good, standardized documentation improved the awareness of this complex diagnosis. However, in a retrospective study of preoperative medical records of 30 consecutive patients who underwent for ACS, documentation was in patient a high level of with postoperative clinical and if invasive monitoring are of must be at least in a in the case of new or findings, the of assessment must be The classical are of unreliable in the presence of regional anesthesia and should therefore be by the clinical signs and of As described by et increasing analgesia changes by an average of h However, in cases of compartment syndrome the average time to surgical decompression from the increase in analgesia was which were in our with the orthopedic surgeons are presented in table The of regional anesthesia is if there are general anesthesia or central blocks like anesthesia, to surgery time should be The of anesthesia in the of testing motor and sensory function after surgery and therefore to a for further clinical at high risk for general anesthesia and with a surgery time the duration time of and local anesthetics can benefit from a continuous anesthesia which as the of the local anesthetic can be to the surgery as to application should not be used for analgesia the level of the surgical block is more to If general anesthesia is a of EDA with anesthesia considering the described above are EDA should not be started until the surgeon has made the clinical low concentration of ropivacaine can be as the on motor function is must be considered from case to case. with or without is possible but not considered as a first As EDA is the most blamed in for delaying diagnosis of ACS its use should be and should be However, with EDA dense motor blocks must be avoided and if techniques are PNB are only recommended if postoperative pain is not a with low on motor function after surgery are are the to our In cases of high risk for an ACS, general anesthesia is combined with a continuous PNB which is placed but not started continuous before general anesthesia until postoperative evaluation is performed. Pain therapy is performed with low of in with remifentanil target infusion or even remifentanil until start of continuous This allows a timing with the surgeon but requires that catheters are placed without first local anesthetic through the The catheter should be started with a low concentration bolus of ml ropivacaine to initial motor function loss and with a continuous infusion patient-controlled using ropivacaine 0.2% ml/h, bolus out 0.3% has been shown not to motor to 0.2% for block and could be used in an for surgery under continuous However, according to our using a bolus of ropivacaine might lead to a motor block and should for be avoided in this wound infusion or are not even using ropivacaine pathophysiology of ischemic pain is highly complex and is by and acting on ischemia it is that and are some of the leading to ischemic pain. Tissue the pain acting on muscle resulting in pain and leading to a of with et who that compartment ischemia can lead to an regional anesthesia with 0.2% In our ropivacaine 0.3% was and breakthrough pain was still present even after a bolus with 0.5% It would be interesting to the concentration and for bolus application and continuous infusion to use regional anesthesia as an and early of increased muscle anesthetics on the The is the main for pain in the peripheral of this for the postoperative could be of for patients at risk for ACS and for continuous PNB motor outcome studies with the and of intracompartmental pressure monitoring and data on the diagnostic characteristics of intracompartmental pressure monitoring are Moreover, the critical ΔP for other of the and for children must be

IntroductionLymphoedema is an incurable, progressive condition, which results in the swelling of a limb or limbs and impairs mobility (Lymphatic Framework, 2006). The psychosocial impact of lower limb lymphoedema is also devastating as body image and quality of life are greatly affected (Lasinski et al, 2012). Although lymphoedema is a chronic condition, it is manageable through treatment modalities which include manual lymphatic drainage, compression bandaging, compression hosiery, skin care and exercise, otherwise known as Complex Decongestive Therapy (CDT) (Todd, 2012). The area of lower limb, non-cancer related, lymphoedema is poorly resourced and poorly researched, therefore this thesis proposes to explore treatment outcomes for patients with non-cancer related lower limb lymphoedema during the intensive and maintenance phases of CDT,examine their experiences of living with lymphoedema and the challenges of lifelong self-care maintenance.Research QuestionsThe research questions for the study were as follows;1. What is the impact of Complex Decongestive Therapy (CDT) as a treatment for primary and secondary lower limb lymphoedema during the intensive and maintenance phases of CDT, in relation to;a. Quality of life?b. Limb circumferential and volumatic changes?c. Self-efficacy in managing lymphoedema self care?2. What are the patients’ experiences of living with lymphoedema?3. What are the patients’ experiences of the four elements of CDT used during the intensive and maintenance phases of treatment?Aims & ObjectivesThe aims of this study were twofold;1. To examine the impact of Complex Decongestive Therapy (CDT) as a treatment for primary and secondary, non-cancer related, lower limb lymphoedema during the intensive and maintenance phases of CDT;2. To explore the experiences of patients with primary and secondary, non-cancer related lower limb lymphoedema during the intensive and maintenance phases of CDT.The objectives of the study are as follows:1. To determine the impact of CDT on limb circumference and quality of life.2. To explore the patients’ experience of living with lymphoedema.3. To investigate the patients’ reported experience of the four elements of CDT.4. To examine the patients’ reported maintenance regimen of self-care and its resulting effect on limb volume and quality of life.MethodsA mixed methodology, using both quantitative and qualitative data in a sequential manner was used. This study was divided into 3 parts,Part 1 a quantitative approach was used to measure;a) Limb volume changes.b) Quality of Life changesc) Self-efficacyPart 2 –A qualitative approach was used to analyse data from face to face, semi-structured interviews with 18 participants exploring the experiences of patients living with lymphoedema and their experiences of Complex Decongestive Therapy.Part 3 – Descriptive analysis of 18 participant diaries was used during maintenance self-care, over a 4-month period, to examine the participants’ experiences of lymphoedema self care.ResultsA purposive sample of 20 participants were recruited to this study All participants were diagnosesd with lower limb lymphoedema, 10 participants had primary lymphoedema and 10 participants had secondary, non-cancer related lymphoedema. The study setting was a lymphoedema clinic in the Midlands of Ireland, run by the researcher who is also a Tissue Viability Nurse and Manual Lymphatic Drainage Therapist.The findings included a reduction in limb volume from baseline to week 8 during intensive therapy and then a fluctuation of oedema for 6 of the participants during the 4-month self-maintenance period. Quality of life improved for all participants from baseline to week 24. Thematic analysis of the interviews identified themes of lack of knowledge, delayed diagnosis, physical, psychosocial and financial burden of lymphoedema and positive therapeutic effect of treatment. The diary analysis identified self-care challenges that were influenced by elevated body mass index and carer support.ConclusionPrimary and secondary, non-cancer related lower limb lymphoedema is an area of lymphoedema that is poorly researched. It is also true to say that there is a sparsity of research in the area of lymphoedema self maintenance care. The aims of this research study were twofold, to explore patient outcomes with regard to limb volume, quality of life and self-efficacy during the intensive and maintenance phases of CDT and to examine the experiences of the patients living with lymphoedema, during their treatment and following on into self maintenance. The findings included reduction in limb volume during therapy, an improvement in quality of life and a fluctuation in self-efficacy that was influenced by elevated body mass index. Thematic analysis of interviews concluded that living with lymphoedema poses many challenges resulting from poor knowledge within the health professions and a lack of referral pathways and services. The success of lymphoedema self maintenance is greatly influenced by the patients physical ability and support structures, especially in the case of the patient with an elevated body mass index.

Background Compartment syndrome commonly occurs in patients with forearm and lower leg fractures. Compartment syndromes of the gluteal and thigh muscles are less common. It is imperative that compartment syndrome be diagnosed and treated with fasciotomy as soon as possible. However, there are few reports on the diagnosis and treatment strategies for compartment syndromes that occur simultaneously in multiple anatomical regions or in the ipsilateral gluteal region and thigh. Case presentation: We report on a 76-year-old man who was obliquely crushed under a tree extending from the right forearm to the left groin. He was brought to our emergency room, where he was diagnosed with compartment syndrome of the right forearm and left lower leg, and crush syndrome. Emergency fasciotomy was performed. On the day after admission, swelling and tightness of the left gluteal thigh became apparent, and intracompartmental pressures were elevated, which led to an additional diagnosis of these compartment syndromes. A fasciotomy was performed, the gluteal skin incision was made according to the Kocher-Langenbeck approach (one of the posterior approaches for hip fractures), and the thigh was approached by extending the incision laterally. This surgical approach enabled the decompression of the compartments through a single incision and allowed for easier wound treatment and closure. Conclusion This case highlights the diagnosis and treatment of compartment syndrome in four anatomical regions. Extension of the Kocher-Langenbeck approach to the lateral thigh can be a useful surgical approach for ipsilateral gluteal and thigh compartment syndrome.

Lower extremity compartment syndrome after off-pump aortocoronary bypass