Indian Journal of Critical Care Medicine September 2014 Vol 18 Issue 9
infection.[2] In this context, we would like to suggest the probable mechanisms based on our earlier observations[3] and measures to tackle such situations.
3.
4.
Though the exact mechanism of subdural hemorrhage in this patient is not known, there is a possibility of rupture of small vessels plugged by infected red cells in combination with severe thrombocytopenia.[4] This hypothesis has been supported by histopathological studies disclosing widespread cerebral vasculopathy due to parasite-specific factors such as adhesion and sequestration of parasitized erythrocytes in vascular endothelium with increased endothelial permeability, perivascular infiltrations, and cerebral edema; capillaries and venules are also distended and packed with erythrocytes.[5]
5. 6.
S e n t h i l K u m a r a n S , B a l a m u r u g a n N , S u r e s h P, Thirumalaikolundusubramanian P. Extradural hematoma in Plasmodium vivax malaria: Are we alert to detect? J Neurosci Rural Pract 2013;4 Suppl S1:145-6. Anstey NM, Russell B, Yeo TW, Price RN. The pathophysiology of vivax malaria. Trends Parasitol 2009;25:220-7. Menezes RG, Pant S, Kharoshah MA, Senthilkumaran S, Arun M, Nagesh KR, et al. Autopsy discoveries of death from malaria. Leg Med (Tokyo) 2012;14:111-5. Price RN, Tjitra E, Guerra CA, Yeung S, White NJ, Anstey NM. Vivax malaria: Neglected and not benign. Am J Trop Med Hyg 2007;77 (6 Suppl):79-87.
Access this article online Quick Response Code: Website: www.ijccm.org
DOI: 10.4103/0972-5229.140157
In P. vivax infections, parasitemia seldom exceeds 2-5% of circulating RBCs, and high parasite indices are not attributed to the severity of the disease. However, cytokine production during P. vivax infections is higher than that during P. falciparum infections with similar degree of parasitemia.[6] By up-regulating endothelial adhesion molecules, TNF- may promote cerebral sequestration of platelets and red cells thus leading to hemorrhage. The serum TNF- level correlates well with the severity of disease. In addition, patient-specific factors such as oxidative stress, enhanced host inflammatory responses, and alterations in splenic functions might have played a pivotal role. Thus, patient susceptibility to develop vascular complications may be attributable to gene polymorphism.
Invasive pulmonary aspergillosis in an immunocompetent patient with severe dengue fever Sir, We read the article “invasive pulmonary aspergillosis in an immunocompetent patient with severe dengue fever” by Nasa et al.[1] with interest. The author reported a case of a 65-year-old female patient who was admitted with severe dengue fever and developed invasive pulmonary aspergillosis (IPA). We want to highlight certain issues regarding diagnosis of this patient.
This is common for all clinical conditions and not specific for plasmodium vivax complications.
Subramanian Senthilkumaran, Chidambaram Ananth1, Sandeep B. Gore2, Ponniah Thirumalaikolundusubramanian3
Department of Emergency and Critical Care Medicine, Sri Gokulam Hospital, Salem, Tamil Nadu, 1Departments of Anaesthesiology and 3Internal Medicine, Chennai Medical College and Research Center, Irungalur, Trichy, 2Department of Accident and Emergency Medicine, Fortis Hospital, Mulund, Mumbai, Maharashtra, India
The patient developed features of IPA on day 6 of admission and was thought to be “immunocompetent.” This patient did not have neutropenia, which is an important predisposing factor for IPA. But it is well known that abnormalities of T cell-mediated immunity predispose to systemic fungal infections.[2] Mathew et al.[3] had reported impaired T cell proliferation and cell-mediated responses with acute dengue infection. We believe that in this case the severe dengue might have caused T cell abnormality, which made the host susceptible to invasive aspergillosis. Again La Russa and Innis[4] had reported that severe dengue causes bone marrow suppression within 3-4 days of infection. Hence,
Correspondence: Dr. Subramanian Senthilkumaran, Head, Department of Emergency and Critical Care Medicine, Sri Gokulam Hospital, Salem, Tamil Nadu - 636 005, India. E-mail: [email protected]
References 1. 2.
Ghosh S. Curious association between Plasmodium vivax malaria and nontraumatic acute subdural hematoma. Indian J Crit Care Med 2014;18:335-6. Kochar DK, Das A, Kochar SK, Saxena V, Sirohi P, Garg S, et al. Severe Plasmodium vivax malaria: A report on serial cases from Bikaner in north western India. Am J Trop Med Hyg 2009;80:194-8. 93
637
Indian Journal of Critical Care Medicine September 2014 Vol 18 Issue 9
it would be better if the term “immunocompetent” is avoided for this patient.
CT may have been preferred over magnetic resonance imaging (MRI). However in a clinical scenario where cerebral invasion is suspected along with rhinosinusitis, MRI is preferred over CT scan. Contrast enhanced T1-weighed images are helpful in delineating intracranial spread and identifying invasion of cavernous portion of internal carotid artery.[2,3] The sensitivity of initial CT and MRI in detecting sinusitis is 97% and 100% respectively. However, initial MRI is more sensitive in detecting disease beyond sinuses like extension to orbits, cranium.[4] Since, she developed ophthalmoplegia at 72 h of admission, cavernous sinus thrombosis should be strongly suspected. Involvement of brain stem could not be ruled out as she had right facial palsy with left hemiparesis.
Birendra Pradhan, Atul Jindal
Department of Pediatrics, All India Institute of Medical Sciences, Raipur, Chhattisgarh, India
Correspondence: Dr. Atul Jindal, Department of Pediatrics, All India Institute of Medical Sciences, Raipur - 492 099, Chhattisgarh, India. E-mail: [email protected]
References 1. 2. 3. 4.
Nasa P, Yadav R, Nagrani SK, Raina S, Gupta A, Jain S. Invasive pulmonary aspergillosis in an immunocompetent patient with severe dengue fever. Indian J Crit Care Med 2014;18:323-5. Kliegman RM, Stanton BF, St. Geme JW III, Schor NF, Behrman RE. Nelson Textbook of Pediatrics. 19 th ed. Philadelphia: Elsevier Publication; 2011. p. 719. Mathew A, Kurane I, Green S, Vaughn DW, Kalayanarooj S, Suntayakorn S, et al. Impaired T cell proliferation in acute dengue infection. J Immunol 1999;162:5609-15. La Russa VF, Innis BL. Mechanisms of dengue virus-induced bone marrow suppression. Baillieres Clin Haematol 1995;8:249-70.
Authors have mentioned amphotericin B as the treatment of choice in mucormycosis, but the current literature suggests that combination antifungal therapy is better than monotherapy in mucormycosis. Reed et al. concluded from a retrospective study that combination of caspofungin-polyene therapy is superior to polyene monotherapy.[4] Addition of echinocandins to polyenes increases the efficiency of polyenes by following mechanisms: Disruption of glucan linking on the cell wall of Rhizopus resulting in better delivery of polyenes Altered virulence of fungus by stunting filamentation or altering cell wall contents Enhanced host response to the fungus.
Access this article online Quick Response Code: Website: www.ijccm.org
DOI: 10.4103/0972-5229.140158
Rhino-orbito-cerebral mucormycosis in a child with diabetic ketoacidosis
The authors have reported mortality of 40% and 10% in mucormycosis with and without cerebral involvement. However, a systematic review showed that children with cerebral, gastrointestinal, disseminated, and cutaneous mucormycosis had mortality of 100%, 100%, 88%, and 0% respectively.[5]
Snehamayee Nayak, Atul Jindal
Department of Pediatrics, All India Institute of Medical Sciences, Raipur, Chhattisgarh, India
Sir, We read the article “Rhino-orbito-cerebral mucormycosis in a child with diabetic ketoacidosis (DKA)” by Kumar et al.[1] with interest. The author reported a 9-year-old girl with DKA and rhino-orbito-cerebral mucormycosis. We want to highlight certain issues regarding diagnosis and management of this child.
Correspondence: Dr. Atul Jindal, Department of Pediatrics, All India Institute of Medical Sciences, Raipur - 492 099, Chhattisgarh, India. E-mail: [email protected]
References 1.
The child was diagnosed with rhino-orbital-cerebral mucormycosis after 48 h of admission. Her initial computed tomography (CT) brain was found to be normal. It is not clear whether the CT brain was plain or contrast enhanced. We can understand due to sickness of the child, 638
2. 3.
94
Kumar MM, Poovazhagi V, Anbalagan S, Devasena N. Rhino-orbito-cerebral mucormycosis in a child with diabetic ketoacidosis. Indian J Crit Care Med 2014;18:334-5. Herrera DA, Dublin AB, Ormsby EL, Aminpour S, Howell LP. Imaging findings of rhinocerebral mucormycosis. Skull Base 2009;19:117-25. Mohindra S, Mohindra S, Gupta R, Bakshi J, Gupta SK. Rhinocerebral mucormycosis: The disease spectrum in 27 patients. Mycoses 2007;50:290-6.
Copyright of Indian Journal of Critical Care Medicine is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
infection.[2] In this context, we would like to suggest the probable mechanisms based on our earlier observations[3] and measures to tackle such situations.
3.
4.
Though the exact mechanism of subdural hemorrhage in this patient is not known, there is a possibility of rupture of small vessels plugged by infected red cells in combination with severe thrombocytopenia.[4] This hypothesis has been supported by histopathological studies disclosing widespread cerebral vasculopathy due to parasite-specific factors such as adhesion and sequestration of parasitized erythrocytes in vascular endothelium with increased endothelial permeability, perivascular infiltrations, and cerebral edema; capillaries and venules are also distended and packed with erythrocytes.[5]
5. 6.
S e n t h i l K u m a r a n S , B a l a m u r u g a n N , S u r e s h P, Thirumalaikolundusubramanian P. Extradural hematoma in Plasmodium vivax malaria: Are we alert to detect? J Neurosci Rural Pract 2013;4 Suppl S1:145-6. Anstey NM, Russell B, Yeo TW, Price RN. The pathophysiology of vivax malaria. Trends Parasitol 2009;25:220-7. Menezes RG, Pant S, Kharoshah MA, Senthilkumaran S, Arun M, Nagesh KR, et al. Autopsy discoveries of death from malaria. Leg Med (Tokyo) 2012;14:111-5. Price RN, Tjitra E, Guerra CA, Yeung S, White NJ, Anstey NM. Vivax malaria: Neglected and not benign. Am J Trop Med Hyg 2007;77 (6 Suppl):79-87.
Access this article online Quick Response Code: Website: www.ijccm.org
DOI: 10.4103/0972-5229.140157
In P. vivax infections, parasitemia seldom exceeds 2-5% of circulating RBCs, and high parasite indices are not attributed to the severity of the disease. However, cytokine production during P. vivax infections is higher than that during P. falciparum infections with similar degree of parasitemia.[6] By up-regulating endothelial adhesion molecules, TNF- may promote cerebral sequestration of platelets and red cells thus leading to hemorrhage. The serum TNF- level correlates well with the severity of disease. In addition, patient-specific factors such as oxidative stress, enhanced host inflammatory responses, and alterations in splenic functions might have played a pivotal role. Thus, patient susceptibility to develop vascular complications may be attributable to gene polymorphism.
Invasive pulmonary aspergillosis in an immunocompetent patient with severe dengue fever Sir, We read the article “invasive pulmonary aspergillosis in an immunocompetent patient with severe dengue fever” by Nasa et al.[1] with interest. The author reported a case of a 65-year-old female patient who was admitted with severe dengue fever and developed invasive pulmonary aspergillosis (IPA). We want to highlight certain issues regarding diagnosis of this patient.
This is common for all clinical conditions and not specific for plasmodium vivax complications.
Subramanian Senthilkumaran, Chidambaram Ananth1, Sandeep B. Gore2, Ponniah Thirumalaikolundusubramanian3
Department of Emergency and Critical Care Medicine, Sri Gokulam Hospital, Salem, Tamil Nadu, 1Departments of Anaesthesiology and 3Internal Medicine, Chennai Medical College and Research Center, Irungalur, Trichy, 2Department of Accident and Emergency Medicine, Fortis Hospital, Mulund, Mumbai, Maharashtra, India
The patient developed features of IPA on day 6 of admission and was thought to be “immunocompetent.” This patient did not have neutropenia, which is an important predisposing factor for IPA. But it is well known that abnormalities of T cell-mediated immunity predispose to systemic fungal infections.[2] Mathew et al.[3] had reported impaired T cell proliferation and cell-mediated responses with acute dengue infection. We believe that in this case the severe dengue might have caused T cell abnormality, which made the host susceptible to invasive aspergillosis. Again La Russa and Innis[4] had reported that severe dengue causes bone marrow suppression within 3-4 days of infection. Hence,
Correspondence: Dr. Subramanian Senthilkumaran, Head, Department of Emergency and Critical Care Medicine, Sri Gokulam Hospital, Salem, Tamil Nadu - 636 005, India. E-mail: [email protected]
References 1. 2.
Ghosh S. Curious association between Plasmodium vivax malaria and nontraumatic acute subdural hematoma. Indian J Crit Care Med 2014;18:335-6. Kochar DK, Das A, Kochar SK, Saxena V, Sirohi P, Garg S, et al. Severe Plasmodium vivax malaria: A report on serial cases from Bikaner in north western India. Am J Trop Med Hyg 2009;80:194-8. 93
637
Indian Journal of Critical Care Medicine September 2014 Vol 18 Issue 9
it would be better if the term “immunocompetent” is avoided for this patient.
CT may have been preferred over magnetic resonance imaging (MRI). However in a clinical scenario where cerebral invasion is suspected along with rhinosinusitis, MRI is preferred over CT scan. Contrast enhanced T1-weighed images are helpful in delineating intracranial spread and identifying invasion of cavernous portion of internal carotid artery.[2,3] The sensitivity of initial CT and MRI in detecting sinusitis is 97% and 100% respectively. However, initial MRI is more sensitive in detecting disease beyond sinuses like extension to orbits, cranium.[4] Since, she developed ophthalmoplegia at 72 h of admission, cavernous sinus thrombosis should be strongly suspected. Involvement of brain stem could not be ruled out as she had right facial palsy with left hemiparesis.
Birendra Pradhan, Atul Jindal
Department of Pediatrics, All India Institute of Medical Sciences, Raipur, Chhattisgarh, India
Correspondence: Dr. Atul Jindal, Department of Pediatrics, All India Institute of Medical Sciences, Raipur - 492 099, Chhattisgarh, India. E-mail: [email protected]
References 1. 2. 3. 4.
Nasa P, Yadav R, Nagrani SK, Raina S, Gupta A, Jain S. Invasive pulmonary aspergillosis in an immunocompetent patient with severe dengue fever. Indian J Crit Care Med 2014;18:323-5. Kliegman RM, Stanton BF, St. Geme JW III, Schor NF, Behrman RE. Nelson Textbook of Pediatrics. 19 th ed. Philadelphia: Elsevier Publication; 2011. p. 719. Mathew A, Kurane I, Green S, Vaughn DW, Kalayanarooj S, Suntayakorn S, et al. Impaired T cell proliferation in acute dengue infection. J Immunol 1999;162:5609-15. La Russa VF, Innis BL. Mechanisms of dengue virus-induced bone marrow suppression. Baillieres Clin Haematol 1995;8:249-70.
Authors have mentioned amphotericin B as the treatment of choice in mucormycosis, but the current literature suggests that combination antifungal therapy is better than monotherapy in mucormycosis. Reed et al. concluded from a retrospective study that combination of caspofungin-polyene therapy is superior to polyene monotherapy.[4] Addition of echinocandins to polyenes increases the efficiency of polyenes by following mechanisms: Disruption of glucan linking on the cell wall of Rhizopus resulting in better delivery of polyenes Altered virulence of fungus by stunting filamentation or altering cell wall contents Enhanced host response to the fungus.
Access this article online Quick Response Code: Website: www.ijccm.org
DOI: 10.4103/0972-5229.140158
Rhino-orbito-cerebral mucormycosis in a child with diabetic ketoacidosis
The authors have reported mortality of 40% and 10% in mucormycosis with and without cerebral involvement. However, a systematic review showed that children with cerebral, gastrointestinal, disseminated, and cutaneous mucormycosis had mortality of 100%, 100%, 88%, and 0% respectively.[5]
Snehamayee Nayak, Atul Jindal
Department of Pediatrics, All India Institute of Medical Sciences, Raipur, Chhattisgarh, India
Sir, We read the article “Rhino-orbito-cerebral mucormycosis in a child with diabetic ketoacidosis (DKA)” by Kumar et al.[1] with interest. The author reported a 9-year-old girl with DKA and rhino-orbito-cerebral mucormycosis. We want to highlight certain issues regarding diagnosis and management of this child.
Correspondence: Dr. Atul Jindal, Department of Pediatrics, All India Institute of Medical Sciences, Raipur - 492 099, Chhattisgarh, India. E-mail: [email protected]
References 1.
The child was diagnosed with rhino-orbital-cerebral mucormycosis after 48 h of admission. Her initial computed tomography (CT) brain was found to be normal. It is not clear whether the CT brain was plain or contrast enhanced. We can understand due to sickness of the child, 638
2. 3.
94
Kumar MM, Poovazhagi V, Anbalagan S, Devasena N. Rhino-orbito-cerebral mucormycosis in a child with diabetic ketoacidosis. Indian J Crit Care Med 2014;18:334-5. Herrera DA, Dublin AB, Ormsby EL, Aminpour S, Howell LP. Imaging findings of rhinocerebral mucormycosis. Skull Base 2009;19:117-25. Mohindra S, Mohindra S, Gupta R, Bakshi J, Gupta SK. Rhinocerebral mucormycosis: The disease spectrum in 27 patients. Mycoses 2007;50:290-6.
Copyright of Indian Journal of Critical Care Medicine is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
