Lucent metaphyseal bands are radiotransparent bands 2–15 mm wide on radiographs [3, 8]. They are caused by nutritional dysfunction that interferes with osteogenesis of the epiphyseal growth plate. These bands commonly occur at sites of rapid growth, such as the proximal tibia, proximal and distal femur, proximal humerus, and distal radius [2, 3] (Fig. 1). Histologically, trabeculae are reduced in both dimension and number [3]. The incidence has been reported to be 7.1–55% [2, 8, 9].

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Fig. 1 —4-year-old boy who presented to emergency department with left shoulder pain and was found to have acute lymphocytic lymphoma. Radiograph shows lucent metaphyseal bands (arrows) in right humerus.

Although not often seen in the early stag es of the disease and nonspecific in children younger than 2 years old, because they can be seen in systemic diseases and malnutrition, lucent metaphyseal bands are suggestive of leukemia in children older than 2 years [8]. The differential diagnosis includes normal variant of rapid growth; transplacental infections, including rubella, syphilis, herpes, toxoplasmosis, and cytomegalovirus; bone marrow metastases from nonhematologic malignancies, including metastatic neuroblastoma; trauma; and malnutrition [10].

Periosteal reaction describes periosteal elevation from the osseous cortex due to formation of new layers of bone. It occurs in 2–50% of patients with leukemia, most commonly in the tibial and fibular diaphysis [2]. Leukemic infiltration in the medullary cavity, which travels from the medullary canal through the haversian and Volkmann canals, reaches and lifts the periosteum from the cortex of the bone [2]. Leukemia and lymphoma can be associated with aggressive-appearing periosteal reaction, although thin or laminated periosteal reaction is common [11].

Periosteal reaction is not pathognomonic of leukemia. It can be caused by various physiologic, traumatic, aggressive, and non-aggressive pathologic etiologic factors. Examples include psoriatic and reactive arthritis, periosteal reaction of the neonate, pachydermoperiostosis, fractures, fluorosis, hypervitaminosis A, prostaglandin use, and osteomyelitis [11]. Its varied radiologic appearances depend on cause, patient age, and aggressiveness of the underlying process, ranging from smooth continuous duplication of the cortex to irregular patterns (Fig. 2).

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Fig. 2A —8-month-old girl with periosteal reaction due to acute myeloid leukemia. A, Anteroposterior (A) and lateral (B) radiographs of right femur show smooth periosteal reaction (arrows). Left femur (not shown) had similar appearance.

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Fig. 2B —8-month-old girl with periosteal reaction due to acute myeloid leukemia. B, Anteroposterior (A) and lateral (B) radiographs of right femur show smooth periosteal reaction (arrows). Left femur (not shown) had similar appearance.

Bone marrow is almost completely hematopoietic red marrow at birth and converts to predominantly fatty yellow marrow from peripheral to central bones. In long bones, conversion begins in the epiphysis then occurs in the mid diaphysis and is finally seen in the metaphysis [1]. Red marrow is composed of 40% water, 40% fat, and 20% protein. On T1-weighted MR images, red marrow appears slightly hyperintense to muscle and intervertebral disks [1]. Yellow marrow is composed of 80% fat, 15% water, and 5% protein and, given the higher fat content, appears more hyperintense to skeletal muscle on T1-weighted images than does red marrow [1]. Both red and yellow marrow are somewhat hyperintense and difficult to differentiate on T2-weighted or STIR images.

The overgrowth of leukemic cells in bone marrow interrupts normal hematopoiesis. On T1-weighted MR images, diseased marrow appears hypointense or isointense to intervertebral disks and skeletal muscle (Fig. 3). In young adults, this pattern can be difficult to differentiate from normal hematopoietic marrow. On T2-weighted fat-suppressed or STIR images, signal intensity is variably increased. Contrast-enhanced T1-weighted images show enhancement of the abnormal marrow [12]. Intervertebral disks appear darker than the enhancing vertebrae [13].

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Fig. 3 —3-year-old boy with leukemic infiltration of bone marrow due to acute lymphocytic leukemia. Sagittal T1-weighted MR image of spine shows T1 signal intensity is lower in vertebral body (arrow) than in intervertebral disks (arrowhead), consistent with leukemic bone marrow infiltration.

The differential diagnosis of leukemic infiltration includes anemia, abnormal calcium metabolism, hemochromatosis, myeloproliferative disorders, marrow-stimulating medications, exposure to high altitude, and cigarette smoking [14].

Pathologic fractures are defined as fractures through a focal neoplasm, either benign or malignant [15]. They have been reported as an initial presentation in 5.7–12% of pediatric patients with ALL [2, 9]. A pathologic fracture may be the first sign of underlying disease. The spine is most commonly affected [16]. Bone involvement can be either monostotic or polyostotic [17].

Differentiating pathologic and benign fractures can be challenging. Compared with images of stress fractures, radiographs and CT scans of pathologic fractures may show cortical destruction or endosteal scalloping, aggressive periosteal reaction, lytic or permeative marrow pattern, mineralized bony matrix, or an associated soft-tissue mass. MRI can help characterize marrow signal-intensity abnormalities. In benign fractures, abnormal T1 hypointensity represents acute edema and hemorrhage, so imaging may show indistinct margins and patchy intervening normal fatty marrow [15]. In pathologic fractures, abnormal T1 hypointensity is partially caused by the infiltrative tumor, resulting in more homogeneous abnormal T1 hypointensity with well-defined convex margins [15] (Fig. 4). Signal-intensity abnormalities on T2-weighted images are less specific [15].

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Fig. 4A —6-year-old boy with pathologic fractures due to acute lymphoblastic leukemia. A, Sagittal T1-weighted (A) and T2-weighted (B) MR images show diffuse low signal intensity and height loss in multiple vertebral bodies (most pronounced at arrows) consistent with compression fractures.

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Fig. 4B —6-year-old boy with pathologic fractures due to acute lymphoblastic leukemia. B, Sagittal T1-weighted (A) and T2-weighted (B) MR images show diffuse low signal intensity and height loss in multiple vertebral bodies (most pronounced at arrows) consistent with compression fractures.

The differential diagnosis of pathologic fractures includes benign and malignant conditions. Benign causes include osteomyelitis, osteogenesis imperfecta, benign bone tumors, radiation therapy, and long-term corticosteroid treatment. Malignant causes include neuroblastoma, malignant bone tumors, and metastatic tumors [17]. Biopsy may be necessary to determine the underlying pathologic entity and to guide therapy.

Primary bone lymphoma—Primary non-Hodgkin lymphoma of bone is a lymphoid neoplasm producing at least one mass in bone without involvement of supraregional lymph nodes or extranodal sites [18]. It is rare and accounts for approximately 7% of all bone malignancies [18] and approximately 2% of non-Hodgkin lymphomas in pediatric patients [19], presenting at a mean age of 11 years [19, 20].

The diagnosis of primary bone lymphoma is often challenging and delayed given the nonspecific clinical symptoms, such as pain without antecedent trauma [20], and variable radiologic appearances that overlap with the appearances of other osseous neoplasms and nonmalignant entities, such as osteomyelitis. Multiple radiographic patterns have been described, including lytic destructive, which may be permeative or moth-eaten most commonly; lytic with well-defined margins; mixed lytic sclerotic; and even normal findings [21]. At MRI, focal lesions of marrow replacement are best visualized as low marrow signal intensity on T1-weighted images (Fig. 5). T2 signal intensity is usually high because of edema; however, low signal intensity can be seen if fibrosis is present [21]. The lesions are enhancing with gadolinium and restrict diffusion. Diffusion restriction may be seen in early disease before other signal-intensity changes [22]. The lesions are FDG avid at PET/CT. The most common sites of involvement are the femoral metadiaphysis, pelvis, and spine, but lesions are often multifocal and involve an average of three sites [20, 21]. Unlike in the adult form of the tumor, soft-tissue masses are rare in pediatric primary non-Hodgkin lymphoma of bone [22], but soft-tissue masses, cortical breakthrough, and pathologic fractures suggest poorer prognosis [21].

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Fig. 5A —6-year-old girl with primary lymphoma of bone (B-lymphoblastic lymphoma) who presented with 2-month history of limb pain at different sites. Radiographs were normal (not shown). A, Coronal T1-weighted MR image of tibias shows heterogeneous decreased marrow signal intensity (arrows) relative to muscle.

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Fig. 5B —6-year-old girl with primary lymphoma of bone (B-lymphoblastic lymphoma) who presented with 2-month history of limb pain at different sites. Radiographs were normal (not shown). B, Fused PET/MR image (T2-weighted fat-suppressed) shows FDG uptake corresponding to areas of marrow replacement (red).

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Fig. 5C —6-year-old girl with primary lymphoma of bone (B-lymphoblastic lymphoma) who presented with 2-month history of limb pain at different sites. Radiographs were normal (not shown). C, Whole-body PET/MR image shows extent of multifocal FDG-avid lesions, including bilateral upper and lower extremities, sternum, and scapulae (arrows).

Imaging after treatment is often challenging because radiographic abnormalities may persist for years after clinical improvement owing to the slow remodeling and healing of bone [22]. PET/CT or PET/MRI most reliably shows treatment response and is usually performed 6–8 weeks after completion of treatment [22].

Granulocytic sarcoma—Granulocytic sarcoma, also known as myeloid sarcoma and chloroma, is a rare, extramedullary manifestation of AML [23]. The reported incidence is 2.5–9.1% [24, 25]. In as many as 35% of patients, granulocytic sarcoma is diagnosed without a primary AML diagnosis [23]. Patients found to have granulocytic sarcoma without known AML usually have AML within 2 years [26].

Granulocytic sarcomas are most commonly found in skin, lymph nodes, bone, peritoneum, soft tissues, and the gastrointestinal tract [24, 27–29]. Other documented sites include the CNS and genitourinary system [30–34]. Clinical presentation depends on tumor location, and symptoms are associated with either the mass itself or dysfunction of the associated organ [24, 28].

Cross-sectional imaging delineates tumor location and extent. Lesions in bone and adjacent muscles are usually hypointense to isointense on T1-weighted MR images and mildly hyperintense on T2-weighted images with intense enhancement [35] (Fig. 6A). Craniospinal lesions are usually hyperattenuating on unenhanced CT studies and homogeneously enhancing on contrast-enhanced CT studies. Lesions in the abdominal viscera and orbit are usually hypoattenuating and only mildly enhancing. Myeloid sarcomas can be differentiated from abscesses and hematomas, which also occur in AML, by means of CT and MRI [36]. At PET/CT, granulocytic sarcoma shows avid uptake [35, 37]. PET/CT is mostly used for planning radiation therapy and monitoring treatment response [38]. These imaging findings are nonspecific and cannot be used to differentiate granulocytic sarcoma from other malignancies [35].

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Fig. 6 —19-year-old woman with granulocytic sarcoma associated with relapsed B-lymphoblastic leukemia. Axial contrast-enhanced T1-weighted MR image shows enhancing mass (arrows) in lumbar soft tissues. Biopsy revealed B-lymphoblastic leukemia.

The diagnosis of myeloid sarcoma with known AML is fairly simple, but the diagnosis of primary myeloid sarcoma is more challenging [39]. The rate of pathologic misdiagnosis is 25–47% [40, 41]. Cases are commonly misdiagnosed as malignant lymphoproliferative disorders, including Hodgkin lymphoma, histiocytic lymphoma, mucosa-associated lymphoid tissue lymphoma, large cell lymphoma, Ewing sarcoma, thymoma, melanoma, round blue cell tumors, and poorly differentiated carcinoma [40–42]. Histologic analysis usually reveals infiltrating myeloid cells at various stages of granulocytic or monocytic maturation, similar to the findings in AML [43].

Granulocytic sarcomas frequently respond to systemic chemotherapy, generally resolving completely in less than 3 months, though they recur in approximately 23% of patients [36]. If urgent decompression is needed or if the lesion is refractory to systemic chemotherapy, surgical débridement or radiation therapy may be considered [38, 44].

In compartment syndrome, increased pressure within a confined fascial space causes venous outflow obstruction, eventually leading to arterial flow obstruction, ultimately causing ischemia and necrosis. Signs of compartment syndrome in children include anxiety, agitation, and increased need for analgesia. Pain, pallor, paresthesias, paralysis, and pulselessness are less reliable findings in children than in adults and are usually seen only after irreversible damage has occurred [45].

Compartment syndrome due to tumor cell infiltration or soft-tissue bleeding rarely occurs in pediatric patients with hematologic malignancies [46]. Rare cases of compartment syndrome have been reported in patients with hyperleukocytic acute leukemia (WBC count greater than 100,000/μL) and chronic myeloid leukemia [47, 48].

Imaging is not routinely used given that compartment syndrome is a clinical diagnosis. MRI can aid in diagnosis in clinically ambiguous cases and can delineate the affected compartments for planning of fasciotomy. Edema of the affected compartment is observed as T1 hypointensity and T2 hyperintensity at MRI. T1-weighted images show loss of normal muscle architecture. The affected compartment is strongly enhancing (Fig. 7). Nonenhancing areas of liquefaction may be present [49].

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Fig. 7 —19-year-old woman with compartment syndrome due to B-lymphoblastic leukemia who presented with painful swollen leg. Axial contrast-enhanced T1-weighted MR image shows fascial enhancement and convexity (arrows) of left lower anterior compartment, concerning for compartment syndrome. Patient underwent fasciotomy. Pathologic analysis showed diffuse leukemic infiltrate.

Permanent ischemic injury to nerves and muscles occurs as early as 6–8 hours after compartment syndrome develops. Treatment involves emergency fasciotomy within 6 hours [50].

Osteopenia and insufficiency fractures—Osteopenia is often a feature of ALL at presentation due to leukemic marrow infiltration. At the onset, osteopenia is observed radiographically in 13–40% of cases [51]. Osteopenia is also a complication of treatment [52]. Insufficiency fractures may arise secondary to the use of steroids, chemotherapy agents, and radiation therapy [15].

Radiation therapy impairs osteoblast function, causing decreased matrix production [53]. Osteopenia may develop within 1 year after initiation of radiation therapy. Immediately after the initiation of radiation, T1-weighted MRI shows decreased marrow signal intensity due to edema and necrosis [13]. The STIR sequence is more sensitive for depicting early postradiation changes within a few hours to days of treatment [54]. Bone repair and sclerosis occur within the following 2 years [1]. Vascular damage may contribute to late radiation changes, such as bone atrophy. Attempts to repair damaged bone result in deposition of new bone on ischemic trabeculae, and radiographs show heterogeneous bone density with punctate areas of increased density, osteopenia, and coarse trabeculation [53]. Methotrexate, often used to treat ALL, can cause methotrexate osteopathy, in which patients present with bone pain. Radiographs depict findings similar to those of scurvy, including osteopenia, dense provisional zones of calcification, pathologic fractures (most commonly metaphyseal), and sharply outlined epiphyses but without the subperiosteal hemorrhage seen in scurvy [52].

Avascular necrosis—Avascular necrosis is usually a late and secondary complication of leukemia treatment that can result in limb or joint destruction [2, 55]. Most cases affect the hips, shoulders, and knees [52], and more than one joint is often involved [55]. The cumulative incidence of symptomatic avascular necrosis at the end of leukemia therapy is 0.9–17.6%; asymptomatic avascular necrosis occurs in as many as 53.9% of patients [56]. Treatment-related risk factors for avascular necrosis include use of steroids, hematopoietic stem cell transplant, total body irradiation, and chronic graft versus host disease [57, 58].

Radiography, though not the most sensitive modality, may show a radiolucent subchondral crescent with prominent sclerosis and collapse of subchondral bone, occurring only as a late sign of osteonecrosis [52]. MRI shows serpentine alternating hypointense (sclerosis) and hyperintense (granulation tissue) lines on T2-weighted fat-suppressed images of long bones, known as the double line sign [52] (Fig. 8). Bone marrow edema is an early sign of progressive osteonecrosis and eventual bone collapse [59]. Bone scintigraphy depicts ischemic necrosis as a photopenic area or doughnut sign (a ring of increased activity around a photopenic center). Metaphyseal and diaphy-seal lesions (bone infarcts) occur in children with cancer but are usually asymptomatic. They are seen as well-demarcated often ring-shaped areas of decreased signal intensity on T1-weighted images and as areas of increased signal intensity on STIR images [52].

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Fig. 8A —16-year-old boy with bilateral ankle pain and history of avascular necrosis due to chemotherapy 3 years earlier for pre–B-cell acute lymphocytic leukemia. A, Radiograph shows left ankle without focal abnormality.

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Fig. 8B —16-year-old boy with bilateral ankle pain and history of avascular necrosis due to chemotherapy 3 years earlier for pre–B-cell acute lymphocytic leukemia. B, Sagittal T1-weighted MR image of left ankle shows high-signal-intensity lesions (arrows) with serpentine rim consistent with avascular necrosis.

Treatment options for avascular necrosis include analgesia, physical therapy, and surgery, including core decompression and joint replacement [51]. Newer procedures include vascularized bone grafting [60]. Bisphosphonates have been found to contribute to pain relief [61].

Osteomyelitis—Osteomyelitis is a rare complication of leukemia and its treatment. A case series [62] described nine cases of osteomyelitis in 637 children with leukemia. Staphylococcus species, Escherichia coli, Pseudomonas, and Salmonella organisms and fungi are reported causes in pediatric patients with leukemia [52, 62]. The pathogenesis involves hematogenous dissemination of infection in an immunocompromised host due to the underlying malignancy or the effect of chemotherapy. High-dose steroids can cause osteonecrosis, which increases the risk of bacterial seeding in the bone in patients with bacteremia [63].

Osteomyelitis, particularly when chronic, can be difficult to detect clinically. Although radiography has low sensitivity and specificity for detecting acute osteomyelitis and as many as 80% of patients who present in the first 2 weeks of infection have normal radio-graphic findings, radiography is the first-line imaging modality when osteomyelitis is suspected. Bone marrow edema is the earliest pathologic feature but is not visible on radio-graphs. Features of acute osteomyelitis that may be visible include periosteal reaction, a well-circumscribed bony lucency representing an intraosseous abscess, and soft-tissue swelling [64]. Bone destruction becomes apparent 7–10 days after the onset of symptoms [64]. In chronic osteomyelitis, a sequestrum may be visible on radiographs as a focal sclerotic lesion with a lucent rim. There may also be cortical destruction, a disorganized trabecular pattern, and ill-defined bony lucencies [64].

Nuclear medicine imaging with ¹¹¹In- or ^99mTc-labeled WBCs can depict osteomyelitis 10–14 days before changes are visible on radiographs; however, low specificity causes difficulty differentiating osteomyelitis from other conditions, such as fractures and neoplasms [65]. Scintigraphy can localize suspected but clinically occult infection [52]. Although CT depicts bony changes, such as cortical destruction and periosteal reaction, MRI has better marrow and soft-tissue contrast resolution, making it the modality of choice for diagnosing osteomyelitis [64]. T1-weighted imaging shows central hypointensity, and T2-weighted imaging shows central hyperintensity (Fig. 9). Contrast-enhanced imaging shows marrow enhancement and adjacent soft-tissue enhancement and possibly abscesses [64, 66].

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Fig. 9A —8-year-old girl with right shoulder and arm pain from osteomyelitis due to relapsed acute lymphocytic lymphoma after bone marrow transplant. A, Coronal STIR MR image of humerus shows increased signal intensity in bone marrow and adjacent soft tissues concerning for edema (arrowhead).

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Fig. 9B —8-year-old girl with right shoulder and arm pain from osteomyelitis due to relapsed acute lymphocytic lymphoma after bone marrow transplant. B, Sagittal unenhanced T1-weighted MR image shows abnormal low signal intensity in bone marrow of proximal metaphysis and diaphysis.

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Fig. 9C —8-year-old girl with right shoulder and arm pain from osteomyelitis due to relapsed acute lymphocytic lymphoma after bone marrow transplant. C, Sagittal T1-weighted fat-suppressed contrast-enhanced MR image shows peripheral contrast enhancement (arrows) and central absence of enhancement (asterisk) in proximal humeral bone marrow and adjacent soft tissues, consistent with osteomyelitis with abscess.

Posttreatment bone marrow changes—Marrow edema due to radiation therapy can be detected less than 2 weeks after radiation therapy in adults [54, 67, 68]. A mild transient increase in contrast enhancement can be detected at this time owing to increased vascular permeability. STIR images show increased signal intensity during this period, reflecting early marrow edema and necrosis (Fig. 10). After 3 weeks, a heterogeneous mottled appearance of marrow is seen. During weeks 3–6, marrow cellularity is replaced by central fat predominately surrounding the basivertebral veins. Focal areas of low signal intensity, especially in the pelvis, may be due to marrow fibrosis or necrosis [69] or hypocellularity, which can be caused by chemotherapy alone [52]. Fatty transformation correlates with increased signal intensity on T1-weighted images [52].

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Fig. 10A —11-year-old boy with bone marrow edema due to acute myeloid leukemia after 10-day course of radiation treatment of chloroma. A, STIR MR images show postradiation bone marrow edema 4 days after radiation therapy as increased heterogeneous signal intensity (arrow, A) in vertebral bodies compared with pretreatment appearance (B).

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Fig. 10B —11-year-old boy with bone marrow edema due to acute myeloid leukemia after 10-day course of radiation treatment of chloroma. B, STIR MR images show postradiation bone marrow edema 4 days after radiation therapy as increased heterogeneous signal intensity (arrow, A) in vertebral bodies compared with pretreatment appearance (B).

Marrow regeneration is more likely to occur in children than in adults and when a large volume of marrow is irradiated than when radiation therapy is localized [70]. Reconversion to red marrow may occur after marrow stress [71], especially in children who undergo treatment with hematopoietic growth factors [72, 73]. Marrow regeneration is typically symmetric in the extremities but can be asymmetric or unilateral [73], which can mimic leukemic infiltration or metastatic disease. Heterogeneous red marrow and red marrow hyperplasia should be differentiated from neoplastic replacement and expected posttreatment changes [74]. Leukemic infiltrate usually has higher signal intensity than reconverted red marrow on STIR images, but signal intensity characteristics alone may not always be adequate to exclude tumor. Bone marrow scintigraphy and three-phase bone scintigraphy may be helpful, but biopsy may be needed [75].

Pyomyositis, a purulent bacterial infection of muscle, is a rare complication. Case reports describe its occurrence soon after induction chemotherapy [76]. The exact pathophysiologic mechanism is unclear but is thought to be transient bacteremia in association with compromised muscle integrity. Staphylococcus aureus is the pathogen in more than 85% of cases [77].

The clinical presentation of pyomyositis is divided into three stages. The first, or invasive, stage occurs when the microorganism enters the muscle. It presents with a low-grade fever and dull cramping pain. The purulent stage occurs when a collection of pus has formed in the muscle. It is characterized by a high fever, severe pain, and muscle edema. Pyomyositis is most commonly diagnosed in this stage. If the condition is not treated, the late stage is characterized by spread of the abscess to involve the entire muscle, which can lead to septic shock and death [77].

Diagnosis of pyomyositis can be difficult because the condition arises deep within the muscle. Radiography should be used initially for screening, but few patients have findings suggestive of muscle inflammation or abscess formation, such as enlargement and loss of definition of the muscle, gas in the soft tissues, and reactive changes in adjacent bone. Ultrasound reveals a hypoechoic intramuscular collection without internal vascularity, occasionally with internal debris and air bubbles. MRI is the best modality for diagnosing pyomyositis because it clearly depicts muscle inflammation and abscess formation [78]. Fluid collections are visualized as localized hypointense areas on T1-weighted images and high signal intensity on T2-weighted images (Fig. 11). Contrast-enhanced imaging shows peripheral enhancement with lack of central enhancement [79]. Although MRI is favored, CT performed when MRI and ultrasound are contraindicated or unavailable may show asymmetric muscle enlargement with hypoattenuating intramuscular focus or gas formation and peripheral contrast enhancement [77]. CT, however, may not show inflammatory changes in early infection. The differential diagnosis includes trauma and extramedullary malignancy.

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Fig. 11A —12-year-old boy with leg pain and septic shock due to pyomyositis associated with chemotherapy treatment of B-cell acute lymphocytic leukemia diagnosed 3 months earlier. A, Coronal spectral attenuated inversion recovery MR image of right upper thigh shows adductor longus muscle edema (arrows) with focal small fluid collection (arrowhead).

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Fig. 11B —12-year-old boy with leg pain and septic shock due to pyomyositis associated with chemotherapy treatment of B-cell acute lymphocytic leukemia diagnosed 3 months earlier. B, Ultrasound image obtained 10 days after A shows hypoechoic complex collection (arrow) in medial right upper thigh consistent with intramuscular abscess. Incision and drainage yielded pus containing Staphylococcus aureus organisms.

If pyomyositis is diagnosed and treated early, complications occur in less than 5% of cases. Complications include osteomyelitis, septic arthritis, and meningitis from abscess dissemination. Treatment includes parenteral antibiotics, abscess drainage, and possible surgical débridement of necrotic tissue [77].