Ultrastructural modifications of muscle in three types of compartment syndrome

Hoffmeyer, Pierre; Cox, Jennifer; Fritschy, Daniel

doi:10.1007/bf00266058

Cited by 8 publications

(3 citation statements)

References 20 publications

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“…In all cases, the diagnosis of ACS was confirmed at the time of fasciotomy. Marked edema is usually present even in the early stage of the condition, 31 compartments are described as having a "woody" feeling, 22 and the muscle belly bulges out of its fascia at the time of fasciotomy. Patients who underwent fasciotomy for reasons other than ACS were excluded from the analysis.…”

Section: Methodsmentioning

confidence: 99%

Acute compartment syndrome: How long before muscle necrosis occurs?

Vaillancourt

Shrier

Vandal

et al. 2004

CJEM

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Objectives: Acute compartment syndrome (ACS) is a limb-threatening condition often first diagnosed by emergency physicians. Little is known about the rapidity with which permanent damage may occur. Our objective was to estimate the time to muscle necrosis in patients with ACS. Methods: This historical cohort analysis of all patients who had a fasciotomy for ACS was conducted in 4 large teaching hospitals. Diagnosis was confirmed clinically or by needle measurement of compartment pressure. Muscle necrosis was determined using pathology reports and surgeons' operative protocols. We used descriptive statistics and estimated tissue survival probability using the Vertex exchange method for interval-censored data. Results: Between 1989 and 1997 there were 76 cases of ACS. Most cases occurred in young men (median age 32) as a result of a traumatic incident (82%). Forty-nine percent (37/76) of all patients suffered some level of muscle necrosis, and 30% (11/37) of those with necrosis lost more than 25% of the muscle belly. Necrosis occurred in 2 of 4 cases in which the patient had been operated on within 3 hours of the injury, and our exploratory survival analysis estimates that 37% (95% confidence interval, 13%-51%) of all cases of ACS may develop muscle necrosis within 3 hours of the injury. Conclusions: This is the largest cohort of ACS and the first clinical estimation of time to muscle necrosis ever published. Ischemia from ACS can cause muscle necrosis before the 3-hour period post-trauma that is traditionally considered safe. Further research to identify risk factors associated with the development of early necrosis is necessary. RÉSUMÉObjectifs : Le syndrome de loge aigu est une atteinte menaçant l'intégrité des membres qui est souvent diagnostiqué par les médecins d'urgence. On sait peu de choses au sujet de la rapidité à laquelle des lésions permanentes peuvent subvenir. Notre objectif était d'estimer le délai d'instal-

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Section: Methodsmentioning

confidence: 99%

Acute compartment syndrome: How long before muscle necrosis occurs?

Vaillancourt

Shrier

Vandal

et al. 2004

CJEM

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“…The capillary perfusion decreases below a level necessary for tissue viability [7] compromising the circulation and function of the tissues leading to muscle and nerve ischaemia with muscle infarction and nerve damage. In the early stage of ACS Hoffmeyer et al [8] found marked perifascicular and intrafascicular oedema with dissociation of the muscle fibres and necrosis in the tissue sections. In the late stages atrophy and hypertrophy of muscle fibres with lipid globules appear in the tissue examined.…”

Section: Discussionmentioning

confidence: 97%

Acute compartment syndrome in children: a case series in 24 patients and review of the literature

Erdös

Dlaska

Szatmary

et al. 2010

International Orthopaedics (SICOT)

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Trauma-associated acute compartment syndrome (ACS) of the extremities is a well-known complication in adults. There are only a handful of articles that describe the symptoms, the diagnostic procedure and treatment of ACS in children. The aim of this study was to analyse the diagnostic procedures in children compared to adolescents with ACS to obtain evidence for the diagnosis, treatment and outcome of children with ACS. Twenty-four children and adolescents with ACS have been treated at the

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“…4). [19][20][21] The usual causes of the syndrome are trauma (bone fracture or the crush syndrome) and an exercise-induced increase in muscle volume; a less common cause is infection, as in this case. These tissue-destructive group A beta- hemolytic streptococci infections may elicit little or no inflammatory response, despite a high concentration of streptococci in the muscle (Stevens DL: personal communication).…”

Section: P Athological Discussionmentioning

confidence: 93%

Case 21-1995

Barza¹,

Brennick²

1995

N Engl J Med

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A 33-year-old man was admitted to the hospital because of fever and increasing pain in the right leg.The patient had been well until 11 days earlier, when a sore throat developed while he was attending a meeting in Texas. No other symptoms occurred, and he was aware of only low-grade fever. During the next week the sore throat gradually improved. Three days before admission the sore throat was barely noticeable, although fatigue was present. Late in the afternoon he had a shaking chill that lasted more than an hour. The temperature was 38.3ºC and rose to 39.7ºC 30 minutes later. A physician found that his throat was clear. A single tender left submandibular lymph node, less than 1 cm in diameter, was palpated. The hematocrit was 46.6 percent, the white-cell count was 16,700 per cubic millimeter, and the platelet count was 175,000 per cubic millimeter. Radiographs of the chest were normal. A viral syndrome was suspected, and acetaminophen was prescribed. On the next day he felt better, except for a mild headache and anorexia; the temperature was 38.3ºC. One day before admission the headache resolved, but the temperature again ranged as high as 38.3ºC. That evening pain developed above the right medial malleolus and worsened progressively. Early the next day he could not walk because of increasing pain and was brought to the hospital by ambulance.The patient was a physician who performed research on neuromuscular problems; he had no exposure to animals or pathogenic microorganisms. There was a history of hives after treatment with penicillin at 10 years of age. Gilbert's syndrome was first noted three years before admission. There was no history of leg trauma, risk factors for infection with the human immunodeficiency virus, nausea, vomiting, diarrhea, cough, dyspnea, thoracic or abdominal pain, pain in joints other than the ankle, dysuria, urinary frequency, urethral discharge, rash, or nuchal rigidity.The temperature was 37.3ºC, the pulse was 100, and the respirations were 18. The blood pressure was 120/80 mm Hg.On physical examination the patient appeared lethargic and acutely ill. There was diffuse erythema over the chest that blanched on pressure; no lymphadenopathy or cutaneous signs of sepsis were found. The conjunctivae were injected; the head was normal in other respects, and the neck was supple. The lungs, heart, and abdomen were normal. The right calf was slightly swollen, with a circumference of 37 cm, as compared with 35 cm on the left side. Poorly defined erythematous streaks were observed over the medial malleolus. There was tenderness on deep palpation of the right calf, and Homans' sign was present. No tender cord was palpated. The peripheral pulses were full and equal. No joint swelling or limitation of movement was detected at the ankles or other joints, and no peripheral edema was present. Neurologic examination was normal.The prothrombin and partial-thromboplastin times were normal, as were the values for urea nitrogen, creatinine, protein (albumin and globulin), magnesium, calcium, phosphorus,...

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Ultrastructural modifications of muscle in three types of compartment syndrome

Cited by 8 publications

References 20 publications

Acute compartment syndrome: How long before muscle necrosis occurs?

Acute compartment syndrome: How long before muscle necrosis occurs?

Acute compartment syndrome in children: a case series in 24 patients and review of the literature

Case 21-1995

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