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Introduction: The pandemic of COVID-19 in association with mucormycosis would be a deadly fungal infection with high level of mortality and morbidity. Our aim is to evaluate the surgical outcome of patients with rhino-orbito-cerebral mucormycosis to suggest better management strategies. Method(s): A total of 62 cases of COVID-19-associated rhino-orbito-cerebral mucormycosis were admitted to the ear, nose, throat department in Mashhad, Iran, from August 1 to October 15, 2021. All data were analyzed using SPSS version 27.0. Descriptive analysis was used for demographic and clinical characteristics. Result(s): Main predisposing conditions were diabetes mellitus (90%) followed by hypertension (41%). Main symptoms were headache (75%), periorbital or retro-orbital pain (61%), visual loss (45%), and facial numbness (41%). Mucosal and ocular findings showed necrosis (67%), blindness (n=35), ptosis (n=31), proptosis (n=27), ophthalmoplegia (n=25), and chemosis (n=20). Neurologic loss of consciousness (19%) and palsies of cranial nerves (53%) were observed. Endoscopy findings showed necrosis (70%), discharge (61%), and crusting (54%). Imaging enhancement revealed mucosal thickening (69%), opacification of sinus (69%), bony destruction of sinus (35%), and orbital involvement (25%). Debridement surgery was necessary in nearly all patients (96%), dominated by ethmoid sinus (90%), maxillary sinus (87%), middle turbinate (80%), and sphenoid sinus (79%). Based on our follow-up, 25 patients died (42%). Those who survived will suffer from no light perception (35%), cranial nerve palsy (12%), and cerebral vascular accident (1.6%). Conclusion(s): Mucormycosis is an aggressive fungal infection. Diabetes mellitus, COVID-19 complication, inappropriate use of corticosteroids, and delayed vaccination had significantly increased its incidence. As there is an urgent need to address this public health concern, we present our data set from Iran.
ABSTRACT
Objective: Adulthood retroclival hematomas (RCHs) are a rare condition characterized by intracranial bleeding along the posterior aspect of the clivus. There are few reports in the literature that describe these hematomas. There is no agreement on how to treat these hematomas. Methods: An extensive literature review was performed, and the data was classified and analyzed on this topic from January 2000 to January 2022. A systematic review was carried out in accordance with the PRISMA and CARE Guidelines. Results were analyzed and potential clinical links were extracted. Results: Twenty-seven RCHs in adulthood were reported in twenty high-quality articles. 12/27 RCHs in adults were spontaneous. Epidural retroclival hematomas were present in 12/27 patients, while subdural hematomas were present in 13/27 patients. 15 of 22 adult RCHs observed were small in size. Epidural hematomas are typically associated with trauma (9/15 traumatic RCHs), whereas subdural hematomas are more frequently associated with spontaneous bleeding (8/12 spontaneous RCHs). There was one case of hydrocephalus, six cases of cranial nerve palsies (five of which were traumatic), and thirteen cases of intraspinal extension of the hematoma. Seven individuals exhibited craniovertebral instability (100 percent traumatic). Most hematomas were conservatively treated (77.8 percent). 21 hematomas had favorable clinical outcomes. Conclusions: There is a lack of agreement on management protocols for RCHs in adulthood. These hematomas occur almost equally in both the extradural and the subdural spaces, and they are typically small in size. When an RCH occurs in the epidural space, it is more likely to result in cranial nerve palsies and craniospinal instability. Associated craniovertebral anomalies must be thoroughly analyzed in trauma patients. Only patients with a significant mass effect on the brainstem are candidates for surgical hematoma evacuation. It is imperative that future studies on this rare entity adhere to strict publication guidelines.
ABSTRACT
Aim and background: The novel coronavirus-2019 (COVID-19) pandemic is raging all across the world. As we are delving more into the management of COVID-19, many new challenges are emerging, which may pose additional threats. One of these is the emergence or re-activation of concomitant viral infections owing to lymphopenia, use of immunosuppressants, underlying comorbidities, and immune dysregulation. Although we have come across the threat of fungal infections and resistant bacterial infections, experience regarding reactivation or co-infection with other viral infections is still limited. We hereby describe a case of COVID-19 disease with cytomegalovirus (CMV) co-infection. Case summary: COVID-19 with Cytomegalovirus (CMV) Co-infection. A 55-year-old male, COVID unvaccinated, chronic smoker, overweight, and hypertensive patient was admitted to our ICU with a 1-week history of fever, cough, and breathlessness. SARSCoV- 2 reverse transcriptase-polymerase chain reaction (RT-PCR) test was positive. At admission, he had hypoxaemia (SpO2 86% on room air), respiratory rate (RR) 35-40/minute, and ground-glass opacities in chest X-ray involving 50% of bilateral lung parenchyma suggestive of severe COVID-19 pneumonia. He was managed with lung-protective invasive mechanical ventilation, restrictive fluid strategy, 16-18 hour/day proning sessions (4-5), intravenous (IV) remdesivir, IV dexamethasone 6 mg 12 hourly, and enoxaparin thromboprophylaxis. After 2 weeks of ICU stay, weaning was attempted but the weaning attempts failed due to underlying neuromuscular weakness. On examination, bilateral (B/L) cranial nerve palsies, areflexia, and motor power 0/5 in bilateral upper and lower limbs were noticed. A possibility of Guillain-Barre Syndrome (GBS) was kept and IV immunoglobulin therapy was empirically administered for 5 days with some improvement in power up to 1/5 in upper limbs. On day 35 of hospitalization, he developed pancytopenia along with features of deranged liver function and gut dysfunction (in the form of paralytic ileus and abdominal distension). In evaluation, polymerase chain reaction (PCR) for CMV turned out to be positive in blood with a very high viral load.Bone marrow aspiration and biopsy showed hemopoiesis with viral inclusion bodies and haemophagocytosis (HLH). Histological evidence of CMV inclusion bodies was present in the bone marrow besides viremia (detected by PCR for CMV), which confirmed the diagnosis of CMV co-infection. IV ganciclovir was initiated along with steroids in view of HLH. There was a decrease in CMV viral load after initiation of IV gancyclovir with subtle clinical recovery. However, the patient continued to deteriorate and succumbed to his illness in the 8th week of the ICU stay.
ABSTRACT
Introduction: COVID-19 pandemic has affected the whole world. Besides COVID, other viral infections may emerge during the course of the disease owing to lymphopenia, use of immunosuppressants, underlying comorbidities, and immune dysregulation, which may pose additional threats.1 We hereby describe two cases of COVID- 19 with viral co-infections belonging to the Herpesviridae family with undulating clinical course. Case 1: Cytomegalovirus (CMV) Co-infection: A 55-year-old male, COVID unvaccinated, chronic smoker, overweight and hypertensive was admitted to our ICU with a 1-week history of fever, cough, and breathlessness. SARSCoV- 2 reverse transcriptase-polymerase chain reaction (RT-PCR) test was positive. At admission, he had hypoxaemia (SpO2 86%on room air), respiratory rate 35-40/minute, and ground-glass opacities in chest X-ray involving 50% of bilateral lung parenchyma suggestive of severe COVID-19 pneumonia. He was managed with lung-protective invasive mechanical ventilation, restrictive fluid strategy, 16-18 hour/day proning sessions (4-5), intravenous (IV) remdesivir, IV dexamethasone 6 mg 12 hourly, and enoxaparin thromboprophylaxis. After 2 weeks of ICU stay, weaning was attempted but the weaning attempts failed due to underlying neuromuscular weakness. On examination, bilateral (B/L) cranial nerve palsies, areflexia, and motor power 0/5 in bilateral upper and lower limbs were noticed. possibility of Guillain-Barre syndrome (GBS) was kept and IV immunoglobulin therapy was empirically administered for 5 days with some improvement in power up to 1/5 in upper limbs. On day 35 of hospitalization, he developed pancytopenia along with features of deranged liver function and gut dysfunction. In evaluation, PCR for CMV turned out to be positive in blood. Bone marrow aspiration and biopsy showed hemopoiesis with viral inclusion bodies and hemophagocytosis (HLH) [Figs 1 and 2]. A diagnosis of secondary HLH related to CMV was contemplated and IV ganciclovir was initiated along with steroids. Histological evidence of CMV co-infection was present and moreover, the quantitative viral load of CMV showed a decreasing trend after initiating IV gancyclovir. However, the patient continued to deteriorate and succumbed to his illness in the 8th week of the ICU stay. Case 2: Herpes Simplex Virus (HSV) Co-infection: Twenty-three years postpartum female with no comorbidities and uneventful obstetric history was referred to our hospital two weeks after a full-term normal vaginal delivery. She developed generalized status epilepticus on the 10th day of delivery, which was managed with anti-epileptic drugs (AEDs). During the hospital stay, RTPCR for COVID-19 turned out to be positive but she remained asymptomatic and seizures were well-controlled on AEDs. On admission to our hospital, she was fully conscious and alert with no neurological deficits. Notable findings were pancytopenia with megaloblastic features, B/L pedal edema, and hepatosplenomegaly. NCCT brain revealed mild subarachnoid hemorrhage (SAH) along the bilateral parietooccipital region for which conservative management was planned. 2D echocardiography was normal. Ultrasonography of the abdomen showed gross splenomegaly and mild hepatomegaly with mesenteric lymphadenopathy. NCCT thorax and abdomen were unremarkable apart from hepatosplenomegaly. In pancytopenia workup, IgM anti-HSV-1 antibodies turned out to be positive in blood. In addition, tropical workup was suggestive of Leptospirosis (IgM antibodies positive). Serological evidence was suggestive of acute HSV-1 infection (based on antibody titers). Bone marrow workup had features of trilineage hematopoiesis with micronormoblastic maturation consistent with iron deficiency anemia without any evidence of hemophagocytosis. IV acyclovir, IV doxycycline, and iron replacement were added, after which she improved clinically and was discharged in stable condition. Tables 1 and 2 show a detailed description of these cases. Discussion: Herpesviridae family is the most important group of viruses responsible for persistent vi al infections in humans, of which CMV contributes to 60-90% of infections in adults, especially in developing countries.2 In healthy individuals, these viruses are kept dormant by the body's immune mechanisms but in an immunocompromised population, reactivation from the latent state can occur. SARS-CoV-2 infection predisposes patients to concomitant viral co-infections, owing to T-cell lymphopenia, decreased NK cell number, and use of immunosuppressive medications.3,4 The first case of CMV co-infection was first reported by D'Ardes and co-workers in 2020.5 Since then, many studies have been emerging in this area. In an observational study from France, 38 COVID-19 patients on >7 days of MV were studied for HSV and CMV pulmonary co-infections (by quantitative real-time PCR in tracheal samples) out of which 47% of patients had one of these infections (24% HSV, 5% CMV, 18% both).6 Another study looking for HSV-1 in patients on invasive MV found HSV-1 reactivation between days 11 and 40, which correlated with immunological markers of decreased innate immunity.7 A case series looking for CMV infection (by PCR in plasma or BAL) in COVID-19, also found CMV reactivation between day 7 and 45 of illness. Most of these patients were above 60 years of age and immunosuppressed (HIV, diabetes mellitus, medications).8 Although immunocompromised individuals are more vulnerable, healthy immunocompetent adults who are critically ill or on prolonged MV may also be susceptible to these infections.9-12 This may be explained by a state of immunoparalysis inherent to prolonged critical illness. In case 1, an ICU stay of around 9 weeks complicated with recurrent nosocomial infections, multiple blood product transfusions, and steroid usage could have the likely triggers. Whether viral co-infections are merely bystanders or truly pathogenic is difficult to comment but timely management is essential to avoid end-organ damage (EOD) which may occur directly (by enhanced viral load secondary to compromised host immunity) or indirectly (by inflammatory changes consequent to prolonged cell-mediated immunity required to maintain viral dormancy).2-4,13 It also seems imperative to study if a viral co-infection has a proclivity to develop more severe hematological anomalies (besides the inherent risk of HLH with COVID) as was seen in case 1, in which the patient had a downward spiral of illness with multiorgan dysfunction.14-15 Limitations: Dynamics of PCR trends and virology studies of samples from trachea, gut, and urine could not be analysed in our patients. Conclusion: Viral co-infections can occur in COVID-19 disease as these patients are often immunocompromised and critically ill. A high index of suspicion and prompt management is needed to improve the outcome of patients. Patients with organ dysfunctions especially hematologic abnormalities with bone marrow involvement should be worked up in detail to look for concomitant viral co-infections. In the future, large-scale research is needed to better elucidate the relationship between SARS-CoV-2 and other viral co-infections.
ABSTRACT
CASE: A 44-year-old male with past medical history of type II insulindependent diabetes mellitus (DM) and end stage liver disease (ESLD) due to alcohol use and nonalcoholic fatty liver disease (NAFLD) presented with one week of left-sided retroorbital headache and diplopia. Two weeks prior, the patient tested positive for COVID-19 and initially his severe headache was attributed to this diagnosis. On hospital presentation the patient was found to have ophthalmoplegia, ptosis and diminished sensation in the CN V1 distribution on the left. The patient was in diabetic ketoacidosis (DKA) with glucose of 686, venous blood gas of 7.32/29/15 and serum anion gap of 17. Contrasted orbital and maxillofacial CT showed complete opacification of the left sphenoid sinus and CT angiography/venography of the head were negative for venous sinus thrombosis. MRI of the brain showed left optic nerve ischemia and left frontal lobe cerebritis without abscess. Bedside nasal endoscopy with ENT showed purulent, fuzzy white debris bilaterally concerning for fungal sinusitis. He was taken urgently to the operating room and was found to have angioinvasive fungal sinusitis with cultures growing Lichthemia corymbifera, a fungus in the Mucor family. In addition to treatment with IV insulin and fluids for DKA, the patient was given amphotericin B and posaconazole;however, surgical intervention was deemed too high risk and futile in the setting of patient's comorbidities. IMPACT/DISCUSSION: Mucormycosis is a fungal infection that typically involves the sinuses, orbits and the central nervous system (CNS). Infection of the sinuses manifests with fever, sinus congestion/pain and headache, but can rapidly progress to involve the orbits, leading to vision changes, and the CNS, leading to encephalopathy. Other structures that can be involved include the cavernous sinus, leading to palsies of cranial nerves III-VI. Known risk factors for mucormycosis include DM, especially in patients with DKA, glucocorticoid treatment, immunosuppression and deferoxamine use. Urgent histopathologic diagnosis, initiation of intravenous antifungal agents (amphotericin B) and surgical intervention with ENT, ideally prior to extension beyond the sinuses, are fundamental to decreasing mortality, which is as high as 62%. There have been numerous case reports of mucormycosis in patients with COVID-19, particularly from India. Many of these patients were prescribed glucocorticoids as part of the COVID-19 treatment pathway or had underlying DM. Additional research is needed into the association between COVID-19 and invasive mucormycosis. CONCLUSION: In patients with poorly controlled DM or immunosuppression presenting with severe headache, sinus pain, and/or neurologic changes, mucormycosis must be considered, as it is a fatal entity requiring urgent surgical intervention and initiation of antifungal agents. Patients with COVID-19 infection may be at increased risk for mucormycosis, especially in those with underlying DM or on glucocorticoids.
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CASE: Patient is a 60-year-old woman who works at a local hospital in billing department. She has a history of rheumatic fever, non ST elevation MI, osteoarthritis, Crohn's disease. Her husband was diagnosed with COVID-19 infection in November 2020. A Week later, patient developed myalgias, diarrhea and subsequent testing confirmed COVID-19 infection. Overall, her symptoms were mild and required no treatment or hospitalization. Six weeks following the infection she woke up one morning with diplopia and a large left pupil. She tried to manage this by covering one eye initially, but later visited with a neurologist, ophthalmologist, neuro-ophthalmologist. She was found to have fixed, dilated left pupil and horizontal diplopia with some diagonal component. There were no other neurological signs or meningismus. Laboratory tests showed hemoglobin of 12.5, White cell count 5.7, platelets 405. Electrolytes, kidney function, liver function tests were normal. ACH receptor antibodies were negative. Imaging studies included a negative CTA head, negative brain MRI, face, orbits and optic nerves. She was diagnosed with left third cranial nerve palsy possibly as a complication of COVID-19 infection. She was prescribed oral prednisone 60 mg with a slow taper. Her pupil size and vision gradually improved over the ensuing weeks and the recovery of the third cranial nerve was nearly complete. IMPACT/DISCUSSION: The third cranial nerve supplies the levator muscle of the eyelid, medial rectus, superior rectus, inferior rectus, and inferior oblique;constricts the pupil through its parasympathetic fibers. Patients with oculomotor cranial nerve palsy develop diplopia and droopy eyelid. Etiology for third cranial nerve palsy include many pathologies such as a structural lesion, infectious or inflammatory conditions, cerebrovascular disease and trauma. Our patient developed acute 3rd cranial nerve palsy 6 weeks following the COVID-19 infection. The workup was negative for any structural lesions, CVA or other known causes. This raised the possibility that her symptoms are possibly complications of COVID-19 infection. Neurological complications of COVID-19 infection have been well documented. These include encephalopathy, stroke, dysgeusia and anosmia. There were two case reports of oculomotor nerve palsy that occurred during the acute phase of COVID-19 infection. These were thought to be from direct invasion of the virus. Our patient however, had developed symptoms 6 weeks following the infection raising the possibility of immune mediated complication. She made near complete recovery with oral glucocorticoid treatment. However, it is not known whether the improvement is the result of the treatment. CONCLUSION: 1. Oculomotor cranial nerve palsy is potentially associated with COVID-19 infection. 2. Oculomotor cranial nerve palsy could present several weeks after the acute COVID-19 infection. 3. In patients presenting with 3rd cranial nerve palsy, it is important to obtain the history of past COVID-19 infection.
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Objective: To report a series of patients with clinical and imaging findings suggestive of central nervous system (CNS) Tuberculosis (TB) and active or recent SARS-CoV-2 infection presenting to a single tertiary care center within a two-month period. Background: A presumptive diagnosis of CNS TB is made in the setting of relevant clinical and epidemiologic factors together with typical radiographic findings. Immunosuppression is clearly associated with reactivation or re-infection of TB, although triggers leading to a reactivation are unclear. It is postulated that the SARS-CoV-2 infection suppresses the host innate and adaptive immunity. Design/Methods: NA Results: Three patients with suspected and one with confirmed CNS TB were identified. Patient one presented with a history of fever and altered sensorium for one-week. Concurrent SARS-CoV-2 infection was confirmed. CT-brain showed an obstructive hydrocephalus and an External Ventricular Drain was placed. Cerebrospinal fluid (CSF) nucleic acid amplification test (NAAT) for TB was positive. Patients 2-4 were diabetic and had SARS-CoV-2 infection identified concurrently or in the preceding two weeks. They presented with a history of headache & diplopia of two weeks duration. Examination revealed multiple cranial nerve palsies. The common MRI features were contrast enhancement & soft tissue thickening in the cavernous sinus wall. Patient two had multiple tuberculomas, patient three had orbital apex involvement and patient four had Meckel's cave thickening. CSF analysis revealed elevated proteins without cells and NAAT for TB was negative. All patients were started on anti-TB chemoprophylaxis with corticosteroids. Conclusions: Given the potential immunomodulatory role of SARS-CoV-2, we hypothesize that the viral infection acted as a trigger for the reactivation of TB in the CNS. In addition, three out of four of our patients had cavernous sinus wall involvement which is an unusual finding in CNS TB.
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Introduction: The novel coronavirus 2019 (COVID-19) pandemic started in Wuhan city, China in December 2019 and now the infection has a high prevalence worldwide and the pandemic is still ongoing. Symptomatic patients with COVID-19 typically complain of fever and respiratory, as well as gastrointestinal symptoms. It is known that human coronaviruses and particularly severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) are neuroinvasive and neurotropic. There is growing evidence of various neurological complications and manifestations of COVID-19 infection. Neurological symptoms may range from mild, non-specific pre-sentations such as headache to severe complications both in the central or peripheral nervous system. Even rare neurological disorders can occur during or after this infection. Case presentation: We report a case of a 65-year-old female with COVID-19 infection, who also developed left ophthalmoparesis with two cranial nerve palsies, which further was concluded to be a probable Tolosa-Hunt syndrome, an association not yet been described in the literature. The decision was made to treat with glucocorticosteroids, followed by dramatic relief of pain (which also speaks in favor of the diagnosis). Conclusion This report describes an interesting case of probable Tolosa-Hunt syndrome, a rare peripheral nervous system involvement syndrome, co-occurred with COVID-19 infection. Whether this was just a co-occurrence or the inflammation was triggered by a SARS-CoV-2 in-fection, is still a question to be discussed. The possible causal link between these two conditions may help to understand both conditions better.