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Mucormicosis en pacientes post covid 19
- 1. Blanca Núñez Millán Residente otorrinolaringología y cirugía de cabeza y cuello 4to año Hospital Civil Culiacán Mucormicosis en pacientes post COVID-19
- 2. Introducción Chakrabarti A, Denning DW, Ferguson B, et al. Fungal rhinosinusitis: a categorization and definitional schema addressing current controversies. Laryngoscope. 2009;119(9):1809–18. • Clasificación Invasión a tejido Invasión No invasión Granulomatosa Crónica Aguda fulminante Infestación saprófita RSFA Bola fúngica
- 3. Introducción • Las cigomicosis son infecciones causadas por hongos de la clase Zygomycetes • Formado por los órdenes: Mucorales - Mucormicosis Entomoftorales - Entomoftoromicosis Spellberg B, Edwards J, Ibrahim A. Novel perspectives on mucormycosis: pathophysiology, presentation, and management. Clin Microbiol Rev. 2005 Jul 1;18(3):556-69. #1 Familia Mucoracea #1 Especie Rhizopus oryzae
- 4. Patogénesis Spellberg B, Edwards J, Ibrahim A. Novel perspectives on mucormycosis: pathophysiology, presentation, and management. Clin Microbiol Rev. 2005 Jul 1;18(3):556-69. • Vasotropismo - angioinvasión - trombosis - necrosis isquémica • Proteínas que se unen al hierro (1) • Neutrófilos (2a) • Macrófagos tisulares (2b) • Células endoteliales (3)
- 5. Patogénesis Spellberg B, Edwards J, Ibrahim A. Novel perspectives on mucormycosis: pathophysiology, presentation, and management. Clin Microbiol Rev. 2005 Jul 1;18(3):556-69. • Factores de riesgo -Estados de neutropenia prolongada -Diabetes -CAD* -Uso de corticoesteroides*
- 6. Mucormicosis + COVID-19 Suwanwongse K, Shabarek N. Newly diagnosed diabetes mellitus, DKA, and COVID‐19: Causality or coincidence? A report of three cases. J Med Virol. 2021 Feb;93(2):1150-3. + Corticoesteroides
- 7. Patogénesis Spellberg B, Edwards J, Ibrahim A. Novel perspectives on mucormycosis: pathophysiology, presentation, and management. Clin Microbiol Rev. 2005 Jul 1;18(3):556-69. • Factores de riesgo para sitio de infección Factor predisponente Sitio de infección Cetroacidosis diabética Rinocerebral Corticosteroides Rinocerebral, pulmonar, diseminada Neutropenia Pulmonar, diseminada Desnutrición Gastrointestinal Trauma Cutánea, subcutánea
- 8. Epidemiología Prakash H, Chakrabarti A. Global epidemiology of mucormycosis. Journal of Fungi. 2019 Mar;5(1):26.
- 9. Epidemiología Corzo‐León DE, Armstrong‐James D, Denning DW. Burden of serious fungal infections in Mexico. Mycoses. 2015 Oct;58:34-44.
- 10. Presentación clínica Spellberg B, Edwards Jr J, Ibrahim A. Novel perspectives on mucormycosis: pathophysiology, presentation and management. Clin Microbiol Rev. 2005;18:556–69. • Clasificación: 1. Rinomaxilar
- 11. Presentación clínica Spellberg B, Edwards Jr J, Ibrahim A. Novel perspectives on mucormycosis: pathophysiology, presentation and management. Clin Microbiol Rev. 2005;18:556–69. • Clasificación: 2. Rinoorbital
- 12. Presentación clínica Spellberg B, Edwards Jr J, Ibrahim A. Novel perspectives on mucormycosis: pathophysiology, presentation and management. Clin Microbiol Rev. 2005;18:556–69. • Clasificación: 3. Rinoorbitacerebral
- 13. Presentación clínica • #1 Cavidad nasal • #1 Cornete medio • Obstrucción nasal • Descarga sanguinolenta • Escara indolora Mankekar, G. (Ed.). (2014). Invasive Fungal Rhinosinusitis.
- 14. Presentación clínica • Fiebre que no responde a AB • Edema facial y periorbitario • Síntomas oculares • Parálisis PC II, III, IV, V, VI, VII • Alteraciones SNC • Muerte ( aprox. 50-80%) Mankekar, G. (Ed.). (2014). Invasive Fungal Rhinosinusitis.
- 17. Diagnóstico Mankekar, G. (Ed.). (2014). Invasive Fungal Rhinosinusitis.
- 18. Diagnóstico • Criterios clínicos Mankekar, G. (Ed.). (2014). Invasive Fungal Rhinosinusitis. Menores Mayores • Secreción / congestión nasal • Ulceración / escara / • Inflamación periorbitaria • Alteración sensibilidad maxilar • Perforación / lesiones necróticas negras de paladar • Invasión radiológica de SPN, es decir, erosión de las paredes, extensión de la infección a las estructuras vecinas, destrucción extensa de la base del cráneo
- 19. Diagnóstico • Criterios diagnósticos DeShazo RD. Syndromes of invasive fungal sinusitis. Med Mycol. 2009;47(Suppl I):S 309–14. 1. Engrosamiento de la mucosa o niveles hidroaéreos compatibles con sinusitis en imágenes radiológicas 2. Evidencia histopatológica de hifas dentro de la mucosa sinusal, submucosa, vasos sanguíneos o hueso. Las tinciones concomitantes para micobacterias deben ser negativas
- 20. Diagnóstico Mankekar, G. (Ed.). (2014). Invasive Fungal Rhinosinusitis. Cultivo Sensibilidad <70% Biopsia Microscopia directa
- 21. Diagnóstico • Diagnóstico histopatológico • Demostrar elementos fúngicos • Identificar invasión tisular • Identificar tipo de reacción inflamatoria • PAS / Groccot • HE Mankekar, G. (Ed.). (2014). Invasive Fungal Rhinosinusitis.
- 22. Diagnóstico • Diagnóstico histopatológico • 10-15 μm de ancho • Hifas aseptadas en forma de cinta que se pliegan sobre sí mismas y se ramifican en ángulos rectos Mankekar, G. (Ed.). (2014). Invasive Fungal Rhinosinusitis.
- 23. Tratamiento Spellberg B, Edwards J, Ibrahim A. Novel perspectives on mucormycosis: pathophysiology, presentation, and management. Clin Microbiol Rev. 2005 Jul 1;18(3):556-69. Diagóstico temprano Revertir causa de fondo Debridamiento quirúrgico apropiado Terapia antifúngica apropiada
- 24. Tratamiento Spellberg B, Ibrahim AS, et al. Mucormycosis. In: Longo DL, editor. Harrison’s principles of internal medicine. 18th ed. London: The McGraw-Hill Companies, Inc.; 2012. p. 1663–6.
- 25. Tratamiento Cornely OA, Alastruey-Izquierdo A, Arenz D, Chen SC, Dannaoui E, Hochhegger B, Hoenigl M, Jensen HE, Lagrou K, Lewis RE, Mellinghoff SC. Global guideline for the diagnosis and management of mucormycosis: an initiative of the European Confederation of Medical Mycology in cooperation with the Mycoses Study Group Education and Research Consortium. The Lancet infectious diseases. 2019 Dec 1;19(12):e405-21.
- 26. Tratamiento Nithyanandam, S., M. S. Jacob, R. R. Battu, R. K. Thomas, M. A. Correa, and O. D’Souza. 2003. Rhino-orbito-cerebral mucormycosis. A retrospective analysis of clinical features and treatment outcomes. Indian J. Ophthalmol. 51:231–236. • Debridamiento quirúrgico con márgenes limpios * • Enucleación - 85% • 70% AnfoB vs 14% Cx + AnfoB • Anfotericina B + Cirugía
- 27. Tratamiento • Terapia adjuvante Mankekar, G. (Ed.). (2014). Invasive Fungal Rhinosinusitis. Oxígeno hiperbárico Quelantes de hierro Inhibidores de calcineurina Administración de citoquinas Estatinas Terapia antifúngica apropiada Colistina
- 28. Tratamiento • CAD + COVID-19 • Insulina - 4UI/kg/d - IV • SUSPENDER - Metformina e inhibidoress SGLT-2 • Parestesias ? • Disminución agudeza visual ?
- 29. Caso clínico • Masculino de 36 años con antecedente de DMII de 12 años de evolución en tratamiento con insulina, COVID-19 hace en mes tratado con AB no especificado y dexamentasona IM por 12 días . • Inicia padecimiento 2 semanas posteriores con parestesias faciales predominando en hemicara derecha • Presencia de tejido necrotico en pared lateral nasal derecha, abundante moco blanquecino • Se realiza tomografia y se envía biopsia a estudio histopatologíco por parte del departamento de micología
- 31. Caso clínico • Confirmación diagnóstica
- 32. Caso clínico • Tratamiento con debridacion quirúrgica endoscópica • Anfotericina B 1.5 mg/kg/día • Control glícemico • Egreso: Posaconazol 800mg/día • Seguimiento —->
- 33. Gracias
Notas del editor
- Las cigomicosis son infecciones causadas por hongos de la clase Zygomycetes, formado por los órdenes Mucorales y Entomophthorales. Los entomoftorales son causas poco frecuentes de infecciones subcutáneas y mucocutáneas conocidas como entomoftoromicosis, q ue afectan en gran medida a huéspedes inmunocompetentes en países en desarrollo. Por el contrario, los hongos del orden Mucorales son causas de mucormicosis, una infección por hongos potencialmente mortal afectando casi uniformemente a huéspedes inmunodeprimidos en países en desarrollo o industrializados. Los hongos pertenecientes al orden Mucorales se distribuyen en seis familias, todas las cuales pueden causar infecciones cutáneas y profundas (129). Las especies pertenecientes a la familia Mucoraceae son aislado con mayor frecuencia de pacientes con mucormicosis que cualquier otra familia. Entre las Mucoraceae, Rhizopus oryzae (Rhizopus arrhizus) es, con mucho, la causa más común de infección (129). Otras especies aisladas con menor frecuencia de la familia Mucoraceae que causan un espectro similar de infecciones incluyen Rhizopus microsporus var. rhizopodiformis, Absidia corymbifera, Apophysomyces elegans, especies de Mucor y Rhizomucor pusillus (61, 81, 129). También se ha informado de un aumento de casos de mucormicosis debido a la infección por Cunninghamella spp. (en la familia Cunninghamellaceae) (24, 78, 82,161). Hasta la fecha, los informes de casos raros han demostrado la capacidad de especies pertenecientes a las cuatro familias restantes para causar mucormicosis
- FIG. 1. Pathogenetic mechanisms of and host defense mechanisms against mucormycosis. To cause disease, the agents of mucormycosis must scavenge from the host sufficient iron for growth, must evade host phagocytic defense mechanisms, and must access vasculature to disseminate. A) In a normal host, primary defense mechanisms against mucormycosis include sequestration of iron in serum by specialized iron-binding proteins (1), phagocytes including circulating neutrophils (2a) and tissue macrophages (2b), and endothelial cells (3), which regulate vascular tone and permeability. Acting in concert, these mechanisms prevent establishment of infection in tissue and subsequent endovascular invasion. B) In susceptible hosts, normal defense mechanisms break down. For example, in diabetic ketoacidosis (DKA), the acidic pH of the serum causes dissociation of free iron from sequestering proteins (1). This release of free iron allows rapid fungal growth. Defects in phagocytic defense mechanisms (2), for example, deficiency in cell number (neutropenia) or functional defects caused by corticosteroids or the hyperglycemia and acidosis of diabetic ketoacidosis, allow proliferation of the fungus. Finally, adherence to and damage of endothelial cells by the fungus (3) allows fungal angioinvasion and vessel thrombosis and subsequent tissue necrosis and dissemination of the fungal infection. _ These species are vasotropic, they are characterized by being angioinvasive causing thrombosis of the blood vessels and as a consequence ischemic necrosis of the tissue, in turn this necrosis prevents the release of leukocytes and antifungal factors to the site of the injury, making the infection progress easily and this mechanism also contributes to hematogenous spread and to target organs. (3, 6)
- The main defense factor of the host against fungal infections are neutrophils, macrophages and monocytes and any condition that causes a numerical or functional deficiency of these will be a predisposing factor. (3) Patients with a prolonged neutropenic state are at higher risk, mainly in this group being diabetic patients and being treated with corticosteroids. (4) Ketoacidosis status is the main risk factor in diabetic patients. Low serum pH has been shown to decrease the phagocytic and chemotactic capacity of neutrophils. (5) In addition, the other important predisposing factors are serum levels of free iron, which are elevated in patients with diabetic ketoacidosis and favor the growth of the fungus. (6) Despite treatment with systemic antibiotics and surgical debrides, this condition has a high mortality rate of 70% to more than 80%. (7) Having diabetes mellitus has been associated as a risk factor for severe disease of Covid-19 and in turn there have been case reports of patients with diabetes mellitus that debut after Covid-19 infection, which raises the question of whether it is infection can cause endocrine abnormalities. (8)
- With the onset of the Covid-19 pandemic, cases have been reported in which DMII has been diagnosed debuting with diabetic ketoacidosis after Covid-19 infection. (9) Rubino et al. proposes that the mechanism by which Covid-19 causes ketosis is caused by the binding of the virus to ACE-2 receptors that are abundant in the beta cells of the pancreas and in adipose tissue, which leads to abnormalities in the metabolism of the glucose and destruction of pancreatic beta cells. (10) In addition to this, it is believed that the aberrant immune reaction caused by SARS-CoV-2 can cause autoimmune damage to the pancreatic islets causing deficiency in insulin production. (11) Reddy et al. They propose as a mechanism of ketoacidosis a dysregulation of the renin-angiotensin-aldosterone system due to SARS-CoV-2. ACE-2 expressed in the lung and pancreas would serve as an entry point for the virus, leading to pancreatic damage and a decrease in insulin production. Furthermore, as ACE-2 stimulates aldosterone secretion which increases the risk of hypokalemia which will result in a higher requirement for potassium replacement to break ketogenesis. (12) Pal et al. They found that the majority of their Covid-19 patients (77%) who had diabetic ketoacidosis had pre-existing DMII. (13) Another implicated mechanism that occurs is an increase in interleukin-6 (IL-6), an important cytokine in the pro-inflammatory state in patients with Covi-19 and that promotes ketogenesis. (13) Furthermore, IL-6 is highly involved in the maladaptive immune response to the SARS-Cov-2 virus. (14) Some authors have found an elevated mortality of up to 50% in patients with diabetic ketoacidosis and Covid-19. (17)
- Mucormycosis is less frequent than invasive Candida or Aspergillus infections, some series of autopsy cases vary from 1-5 cases per 10,000, which is 10-50 times less than invasive aspergillosis and candidiasis.
- Depending upon the progression of the infection, Spellberg et al. [6] classified it as: Stage 1: Rhinomaxillary (Fig. 1; Figs. 1, 2, 3 in Chapter “Radiology in Invasive Fungal Sinusitis”) Stage 2: Rhino-orbital (Fig 2; Figs. 4, 5, 6 in Chapter “Radiology in Invasive Fungal Sinusitis”) Stage 3: Rhino-orbito-cerebral (Fig. 3; Fig. 7 in Chapter “Radiology in Invasive Fungal Sinusitis”)
- Depending upon the progression of the infection, Spellberg et al. [6] classified it as: Stage 1: Rhinomaxillary (Fig. 1; Figs. 1, 2, 3 in Chapter “Radiology in Invasive Fungal Sinusitis”) Stage 2: Rhino-orbital (Fig 2; Figs. 4, 5, 6 in Chapter “Radiology in Invasive Fungal Sinusitis”) Stage 3: Rhino-orbito-cerebral (Fig. 3; Fig. 7 in Chapter “Radiology in Invasive Fungal Sinusitis”)
- Depending upon the progression of the infection, Spellberg et al. [6] classified it as: Stage 1: Rhinomaxillary (Fig. 1; Figs. 1, 2, 3 in Chapter “Radiology in Invasive Fungal Sinusitis”) Stage 2: Rhino-orbital (Fig 2; Figs. 4, 5, 6 in Chapter “Radiology in Invasive Fungal Sinusitis”) Stage 3: Rhino-orbito-cerebral (Fig. 3; Fig. 7 in Chapter “Radiology in Invasive Fungal Sinusitis”)
- It is the most lethal form of fungal sinusitis, and the incidence of reported mortality is 50–80 % [1]. It is usually seen in immunocompromised individuals but is also seen occasionally in immunocompetent persons. It is also postulated that the nasal cavity is the primary site of infection, with the middle turbinate being affected in two-thirds of the biopsy positive cases [2]. Initially patient may complain of nasal block with bloodstained or serosanguine- ous nasal discharge. There may be painless, necrotic nasal septal ulcer or eschar. There is rapid progression over a few days with angioinvasion and haematogenous dissemination with fungi invading the mucosa, submucosa, blood vessels and bony walls of the nose and paranasal sinuses. Hyperglycemia and acidosis provide ideal conditions for fungal growth and tissue invasion. Also ketoacidosis has been shown to adversely affect phagocytic activity [3]. There may be intracranial spread either through the cribriform plate or via the orbital apex or via septic emboli. Once the ophthalmic and other orbital arteries are involved, infection can further reach the cavernous sinus and carotid artery. Acute subdural hematoma, cavernous sinus thrombosis and internal carotid artery thrombosis may occur in rhinocerebral mucormycosis. Invasion of the carotid arteries can rapidly lead to cerebral ischemia and death
- • Fever with spikes, not responding to antibiotics. It is the most common present- ing feature [7]. • Persistent nasal blockage with bloodstained serosanguineous nasal discharge with cough. • With progression of the disease, there could be facial or periorbital swelling (Fig. 4), facial pain, numbness and headache. Orbital symptoms: Spread of disease to orbit may cause chemosis, proptosis, ptosis, blurring of vision, loss of vision and ophthalmoplegia. • Cranial nerve palsies especially 2nd, 3rd, 4th, 5th, 6th and 7th nerve due to cav- ernous sinus thrombosis or temporal lobe mycotic infarcts. • CNS symptoms such as altered consciousness, delirium, convulsions, hemipare- sis, hemiplegia or coma may be seen in patients with intracranial involvement.
- • Fever with spikes, not responding to antibiotics. It is the most common present- ing feature [7]. • Persistent nasal blockage with bloodstained serosanguineous nasal discharge with cough. • With progression of the disease, there could be facial or periorbital swelling (Fig. 4), facial pain, numbness and headache. Orbital symptoms: Spread of disease to orbit may cause chemosis, proptosis, ptosis, blurring of vision, loss of vision and ophthalmoplegia. • Cranial nerve palsies especially 2nd, 3rd, 4th, 5th, 6th and 7th nerve due to cav- ernous sinus thrombosis or temporal lobe mycotic infarcts. • CNS symptoms such as altered consciousness, delirium, convulsions, hemipare- sis, hemiplegia or coma may be seen in patients with intracranial involvement.
- • Fever with spikes, not responding to antibiotics. It is the most common present- ing feature [7]. • Persistent nasal blockage with bloodstained serosanguineous nasal discharge with cough. • With progression of the disease, there could be facial or periorbital swelling (Fig. 4), facial pain, numbness and headache. Orbital symptoms: Spread of disease to orbit may cause chemosis, proptosis, ptosis, blurring of vision, loss of vision and ophthalmoplegia. • Cranial nerve palsies especially 2nd, 3rd, 4th, 5th, 6th and 7th nerve due to cav- ernous sinus thrombosis or temporal lobe mycotic infarcts. • CNS symptoms such as altered consciousness, delirium, convulsions, hemipare- sis, hemiplegia or coma may be seen in patients with intracranial involvement.
- Histopathological diagnosis of invasive fungal diseases has three components, namely, (a) demonstration of fungal elements (b) identifying tissue invasiveness, and (c) identifying type of inflammatory reaction – on the basis of which further classification is made. In majority of the cases, fungal elements can be identified on hematoxylin and eosin (H&E)-stained sections. However, identification becomes easy with special staining techniques like periodic acid-Schiff (PAS) stain and Gomori’s (Grocott– Gomori’s) silver methenamine (GMS) preparation. Gomori methenamine has been described to be the most sensitive of the commonly used stains, and it has been recommended that a negative diagnosis should not be given unless a silver stain has been performe. (10-15 μm de ancho) hifas aseptadas de hongos en forma de cinta que se pliegan sobre sí mismas y se ramifican en ángulos rectos
- while Aspergillus species which also may cause acute invasive fulminant process (Figs. 8 and 9) appears as narrow (2–5 μm wide) septate acutely branching fungal hyphae
- Four factors are critical for eradicating mucormycosis: rapidity of diagnosis, reversal of the underlying predisposing factors (if possible), appropriate surgical debridement of infected tissue, and appropriate antifungal therapy.
- Given the rapidly progressive nature of rhinocerebral mucormycosis and the marked increase in mortality when the fungus penetrates the cranium, any diabetic patient with a headache and visual changes is a candidate for prompt evaluation with imaging studies and nasal endoscopy to rule out mucormycosis. performed on an urgent basis. In rhinocerebral mucormycosis, early surgical excision of the infected sinuses and appropriate debridement of the retroorbital space can often prevent the infection from extending into the eye, thereby obviating the need for enucleation and resulting in extremely high cure rates (85%) (107). Repeated surgical exploration of the sinuses and orbit may be necessary to ensure that all necrotic tissue has been debrided and the infection has not progressed. Published case series continue to support the need for surgical debridement to optimize outcomes. For example, in a case series totaling 49 patients with rhinocerebral mucormycosis, the mortality was 70% in cases treated with antifungal agents alone versus 14% in cases treated with antifungal agents plus surgery (75, 118).
- 1. Hyperbaric oxygen therapy has been found to be a beneficial adjunctive therapy for mucormycosis, particularly diabetic patients with rhinocerebral disease [9]. Specifically, the increased partial pressure of oxygen achieved with hyperbaric therapy seems to improve neutrophil activity and oxidative killing by amphoteri- cin B. In addition, high concentrations of oxygen can inhibit the growth of Mucorales in vitro and improve the rate of wound healing by increasing the release of tissue growth factors [10]. There are no clinical data to suggest appro- priate pressures and duration of therapy. It is usually started during the acute phase of the illness and not as salvage therapy at 2.4–3.0 ATA range of pressures, twice daily depending on the patient’s general condition and ability to tolerate the pressures. In some successful cases up to 30 treatments have been reported [11]. 2. Iron plays a pivotal role in the pathogenesis of mucormycosis, its proliferative and angioinvasive properties. The role of deferasirox, an iron chelator without xenosiderophore activity in Mucorales, was emphasised in a recent case series from our centre. Deferasirox starves the fungus of iron which is critical for its growth and pathogenicity [12]. 3. Immune augmentation strategies are also considered in patients with refractory mucormycosis, including administration of cytokines (e.g. granulocyte- macrophage colony-stimulating factor, interferon). In select neutropenic patients, granulocyte transfusion may be a useful bridge until neutrophil recovery, although the clinical benefit remains unproven; and serious adverse effects, including pulmonary toxicity and accelerated cavitation/bleeding, have been reported in patients with opportunistic lung mycoses [5]. Management of Invasive Fungal Sinusitis 69 4. Research reveals that both yeast and moulds have homologues of calcineurin and mTOR that play a significant part in fungal growth and proliferation. Hence, in addition to their immunosuppressive effects, the calcineurin inhibitors (tacroli- mus, cyclosporin) and mTOR inhibitors (sirolimus, everolimus) have been found to have antifungal activity against both yeast and moulds [5]. The potential clini- cal relevance of this development needs to be further explored as knowledge of interactions between antifungal agents and immunosuppressants could improve outcomes. 5. Another potential adjunctive agent currently under study is colistin which has been shown to exert fungicidal activity in vitro against R. oryzae by damaging cytoplasmic and vacuolar membranes, leading to the leakage of intracellular contents [13]. 6. Statins have been found to have fungicidal activity against Glomeromycota and act synergistically with other antifungal agents, such as voriconazole [14].
- There is still no consensus on the insulin dose required in patients with diabetic ketoacidosis and Covid-19, however it has been observed that these patients require a higher than usual insulin dose of up to 4IU / kg / d and it has been proposed that the standard method of administration for these patients is intravenous insulin. (15). It is important to take into account that the use of vasopressors and corticosteroids as part of the treatment against Covid-19 can alter insulin requirements. (14) In diabetic patients who are being treated with Metformin and SGLT-2 inhibitors, it is important to suspend them when presenting any symptoms suggestive of Covid-19 because they increase the risk of lactic acidosis and diabetic ketoacidosis respectively. (16) Los fármacos inhibidores del SGLT2 comercializados son: dapagliflozina, canagliflozina y empagliflozina
- Masculino de 36 años con antecedente de DMII de 12 años de evolución en tratamiento con insulina humalog 45 UI en la mañana y 20 UI en las noches, COVID-19 hace en mes tratado con AB no especificado y dexamentasona IM por 12 días . Inicia padecimiento 2 semanas posteriores con parestesias faciales predominando en hemicara derecha Presencia de tejido necrotico en pared lateral nasal derecha, abundante moco blanquecino Se realiza tomografia y se envía biopsia a estudio histopatologíco por parte del departamento de micología