Letters to the Editor
was weaned from intubation. The patient was discharged on tapering doses of decadron. On outpatient follow‑up two weeks later, laboratory reports were completely normal, and there was a dramatic clinical improvement. The patient presented with characteristic drug hypersensitivity‑related febrile exanthema, and subsequently, developed cytopenias that are not usually part of this syndrome. It is suggested that cell destruction by cytotoxic antibodies[2] and a reversible depression of stem cell activity[3] with myeloid maturation blockade contribute to the pathophysiology of the cytopenias. Drug hypersensitivity results in hypercytokinemia, leading to uncontrolled activation of benign scavenger macrophages and development of hemophagocytosis in the reticuloendothelial system. [4] This entity is probably underdiagnosed because both syndromes share nonspecific symptoms, bone marrow biopsies are not usually part of the diagnostic work‑up in a classic drug hypersensitivity syndrome, and hemophagocytosis pathology can be missed on bone marrow aspiration.[5] This case illustrates the diagnostic and therapeutic importance of considering all possible underlying causes in a patient with HPS, including a drug‑induced etiology.
Address for correspondence: Dr. Hamid Shaaban, Department of Hematology and Oncology, St Joseph's Regional Medical Center, Paterson, New Jersey, USA. E-mail: [email protected]
REFERENCES 1. 2.
3. 4. 5.
Filipovich AH. Hemophagocytic lymphohistiocytosis and other hemophagocytic disorders. Immunol Allergy Clin North Am 2008;28:293‑313, viii. Kiefel V, Santoso S, Schmidt S, Salama A, Mueller‑Eckhardt C. Metabolite‑specific (IgG) and drug‑specific antibodies (IgG, IgM) in two cases of trimethoprim‑sulfamethoxazole‑induced immune thrombocytopenia. Transfusion 1987;27:262‑5. K e i s u M , W i h o l m B E , P a l m b l a d J . Tr i m e t h o p r i m ‑ sulphamethoxazole‑associated blood dyscrasias. Ten years’ experience of the Swedish spontaneous reporting system. J Intern Med 1990;228:353‑60. Tiab M, Mechinaud F, Hamidou M, Gaillard F, Raffi F, Harousseau JL. Hemophagocytic syndromes. A series of 23 cases. Ann Med Interne (Paris) 1996;147:138‑44. Lambotte O, Costedoat‑Chalumeau N, Amoura Z, Piette JC, Cacoub P. Drug‑induced hemophagocytosis. Am J Med 2002;112:592‑3. Access this article online
Website: www.ijciis.org
Quick Response Code:
DOI: 10.4103/2229-5151.152349
Dron Gauchan, Hamid Shaaban, Neil Parikh1, Nai-Lun Chang2, Zaid Altheeb1, Michael Maroules
Departments of Hematology and Oncology, 1Medicine, 2Pathology, St Joseph's Regional Medical Center, Paterson, New Jersey, USA
A letter in response to“Thoracostomy tubes: A comprehensive review of complications and related topics” Dear Editor, I read with interest the article titled “Thoracostomy tubes: A comprehensive review of complications and related topics”[1] in which the authors have meticulously reviewed the complications associated with tube thoracostomy. In addition to the mentioned complications I would like to add a few complications reported in relation to tube thoracostomy which though rare, still deserves special mention.
or due to inadvertent systemic absorption causing ataxia, arrhythmia etc[3] • Direct mechanical injury by the intercostal tube may result in phrenic nerve,[4,5] long thoracic nerve[6] or ulnar neuropathy.[7]
• Tension pneumothorax can complicate intercostal tube drainage insertion if Heimlich’s valve are improperly attached as reported by Mainini et al.,[2] as this will lead to progressive entry of air into the pleural space during inspiration while the flutter valve will prevent egress of the air during expiration • Toxicity due to the effects of local anesthetic may be encountered either due to large dose of administration
Address for correspondence: Dr. Animesh Ray, Department of Pulmonary Critical Care and Sleep Medicine, Vardhman Mahavir Medical College and Safdarjang Hospital, New Delhi ‑ 110 029, India. E‑mail: [email protected]
Animesh Ray
Department of Pulmonary Critical Care and Sleep Medicine, Vardhman Mahavir Medical College and Safdarjang Hospital, New Delhi, India
REFERENCES 1.
Kwiatt M, Tarbox A, Seamon MJ, Swaroop M, Cipolla J, Allen C, et al. Thoracostomy tubes: A comprehensive review of complications and related topics. Int J Crit Illn Inj Sci 2014;4:143‑55.
International Journal of Critical Illness and Injury Science | Vol. 5 | Issue 1 | Jan-Mar 2015
61
Letters to the Editor 2. 3. 4. 5. 6.
Mainini SE, Johnson FE. Tension pneumothorax complicating small‑caliber chest tube insertion. Chest 1990;97:759‑60. Porcel JM, Brieva L, Antoni Schoenenberger J. Acute transient ataxia caused by local lidocaine injection during insertion of a pleural catheter. Arch Bronconeumol 2009;45:472‑3. Hwang MS, Chu JJ, Su WJ. Diaphragmatic paralysis caused by malposition of chest tube placement after pediatric cardiac surgery. Int J Cardiol 2005;99:129‑31. Nahum E, Ben‑Ari J, Schonfeld T, Horev G. Acute diaphragmatic paralysis caused by chest‑tube trauma to phrenic nerve. Pediatr Radiol 2001;31:444‑6. Hassan WU, Keaney NP. Winging of the scapula: An unusual complication of chest tube placement. J Accid Emerg Med 1995;12:156‑7.
7.
Rosing JH, Lance S, Wong MS. Ulnar neuropathy after tube thoracostomy for pneumothorax. J Emerg Med 2012;43:e223‑5. Access this article online
Website: www.ijciis.org
Quick Response Code:
DOI: 10.4103/2229-5151.152350
Predictors of mortality in poisonous snake bite Dear Editor, Sir, we would like to discuss on the report on “Predictors of mortality in poisonous snake bite.[1]” Chaudhari et al., reported that “mortality in patients with snake bite can be predicted by simple variables like presence of bleeding tendencies, respiratory failure, and shock.[1]” In fact, there is a similar report on this topic from India by David et al.[2] In the study by David et al., another interesting factor that is not mentioned by Chaudhari et al., is the “pre‑hospital delay.[2]” In fact, as an acute disease, the early diagnosis and prompt treatment is the key principle for management of poisonous snake bite. Finally, it should be noted that the skill of medical care provider in management of poisonous snake bite is another possible factor to be addressed. According to a report from Thailand, a country with high incidence of poisonous snake bite, “ training programs on appropriate management of snakebites for the medical and paramedical[3]” was necessary to reduce the mortality.
Address for correspondence: Prof. Sim Sai Tin, Medical Center, Shantou, China. E‑mail: [email protected]
REFERENCES 1. 2. 3.
Chaudhari TS, Patil TB, Paithankar MM, Gulhane RV, Patil MB. Predictors of mortality in patients of poisonous snake bite: Experience from a tertiary care hospital in central India. Int J Crit Illn Inj Sci 2014;4:101‑7. David S, Matathia S, Christopher S. Mortality predictors of snake bite envenomation in southern India-a ten‑year retrospective audit of 533 patients. J Med Toxicol 2012;8:118‑23. Buranasin P. Snakebites at Maharat Nakhon Ratchasima Regional Hospital. S Asian J Trop Med Public Health 1993;24:186‑92. Access this article online
Website: www.ijciis.org
Quick Response Code:
DOI: 10.4103/2229-5151.152351
Sim Sai Tin, Viroj Wiwanitkit1
Medical Center Unit, Shantou, 1Department of Tropical Medicine, Hainan Medical University, Hainan, China
Guillain–Barré syndrome presenting as Bell’s palsy with crossed hemiparesis Dear Editor, The rare variants of Guillain–Barré syndrome (GBS) are Miller–Fisher and Bickerstaff’s brainstem encephalitis, and facial diplegia. [1] GBS can very rarely present as crossed hemiparesis, which occurred in our case. A 45‑year‑old female presented with left‑sided Bell’s palsy [Figure 1a] for 1 day with right‑sided hemiparesis. The reflexes were diminished bilaterally and plantars were mute. First possibility in this case was a posterior circulation stroke, but her MRI brain ruled out any infarct or hemorrhage. On 2 nd day, she developed quadriparesis with facial 62
diplegia [Figure 1b], dysphagia, and bulbar palsy. Now we could make a confident diagnosis of GBS and cerebrospinal fluid (CSF) examination also showed albumino‑cytological dissociation (proteins 259 mg/ dl and total leukocyte count of 4 cells/mm 3). She was treated with intravenous immunoglobulins and a month later she came back walking without support and facial diplegia was also improving [Figure 1c and d]. To conclude, GBS can very rarely present as Bell’s palsy with crossed hemiparesis. Vivek Chauhan, G Sharma, B S Rana, V Jearth, J Sandhu
International Journal of Critical Illness and Injury Science | Vol. 5 | Issue 1 | Jan-Mar 2015
Copyright of International Journal of Critical Illness & Injury Science 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.
was weaned from intubation. The patient was discharged on tapering doses of decadron. On outpatient follow‑up two weeks later, laboratory reports were completely normal, and there was a dramatic clinical improvement. The patient presented with characteristic drug hypersensitivity‑related febrile exanthema, and subsequently, developed cytopenias that are not usually part of this syndrome. It is suggested that cell destruction by cytotoxic antibodies[2] and a reversible depression of stem cell activity[3] with myeloid maturation blockade contribute to the pathophysiology of the cytopenias. Drug hypersensitivity results in hypercytokinemia, leading to uncontrolled activation of benign scavenger macrophages and development of hemophagocytosis in the reticuloendothelial system. [4] This entity is probably underdiagnosed because both syndromes share nonspecific symptoms, bone marrow biopsies are not usually part of the diagnostic work‑up in a classic drug hypersensitivity syndrome, and hemophagocytosis pathology can be missed on bone marrow aspiration.[5] This case illustrates the diagnostic and therapeutic importance of considering all possible underlying causes in a patient with HPS, including a drug‑induced etiology.
Address for correspondence: Dr. Hamid Shaaban, Department of Hematology and Oncology, St Joseph's Regional Medical Center, Paterson, New Jersey, USA. E-mail: [email protected]
REFERENCES 1. 2.
3. 4. 5.
Filipovich AH. Hemophagocytic lymphohistiocytosis and other hemophagocytic disorders. Immunol Allergy Clin North Am 2008;28:293‑313, viii. Kiefel V, Santoso S, Schmidt S, Salama A, Mueller‑Eckhardt C. Metabolite‑specific (IgG) and drug‑specific antibodies (IgG, IgM) in two cases of trimethoprim‑sulfamethoxazole‑induced immune thrombocytopenia. Transfusion 1987;27:262‑5. K e i s u M , W i h o l m B E , P a l m b l a d J . Tr i m e t h o p r i m ‑ sulphamethoxazole‑associated blood dyscrasias. Ten years’ experience of the Swedish spontaneous reporting system. J Intern Med 1990;228:353‑60. Tiab M, Mechinaud F, Hamidou M, Gaillard F, Raffi F, Harousseau JL. Hemophagocytic syndromes. A series of 23 cases. Ann Med Interne (Paris) 1996;147:138‑44. Lambotte O, Costedoat‑Chalumeau N, Amoura Z, Piette JC, Cacoub P. Drug‑induced hemophagocytosis. Am J Med 2002;112:592‑3. Access this article online
Website: www.ijciis.org
Quick Response Code:
DOI: 10.4103/2229-5151.152349
Dron Gauchan, Hamid Shaaban, Neil Parikh1, Nai-Lun Chang2, Zaid Altheeb1, Michael Maroules
Departments of Hematology and Oncology, 1Medicine, 2Pathology, St Joseph's Regional Medical Center, Paterson, New Jersey, USA
A letter in response to“Thoracostomy tubes: A comprehensive review of complications and related topics” Dear Editor, I read with interest the article titled “Thoracostomy tubes: A comprehensive review of complications and related topics”[1] in which the authors have meticulously reviewed the complications associated with tube thoracostomy. In addition to the mentioned complications I would like to add a few complications reported in relation to tube thoracostomy which though rare, still deserves special mention.
or due to inadvertent systemic absorption causing ataxia, arrhythmia etc[3] • Direct mechanical injury by the intercostal tube may result in phrenic nerve,[4,5] long thoracic nerve[6] or ulnar neuropathy.[7]
• Tension pneumothorax can complicate intercostal tube drainage insertion if Heimlich’s valve are improperly attached as reported by Mainini et al.,[2] as this will lead to progressive entry of air into the pleural space during inspiration while the flutter valve will prevent egress of the air during expiration • Toxicity due to the effects of local anesthetic may be encountered either due to large dose of administration
Address for correspondence: Dr. Animesh Ray, Department of Pulmonary Critical Care and Sleep Medicine, Vardhman Mahavir Medical College and Safdarjang Hospital, New Delhi ‑ 110 029, India. E‑mail: [email protected]
Animesh Ray
Department of Pulmonary Critical Care and Sleep Medicine, Vardhman Mahavir Medical College and Safdarjang Hospital, New Delhi, India
REFERENCES 1.
Kwiatt M, Tarbox A, Seamon MJ, Swaroop M, Cipolla J, Allen C, et al. Thoracostomy tubes: A comprehensive review of complications and related topics. Int J Crit Illn Inj Sci 2014;4:143‑55.
International Journal of Critical Illness and Injury Science | Vol. 5 | Issue 1 | Jan-Mar 2015
61
Letters to the Editor 2. 3. 4. 5. 6.
Mainini SE, Johnson FE. Tension pneumothorax complicating small‑caliber chest tube insertion. Chest 1990;97:759‑60. Porcel JM, Brieva L, Antoni Schoenenberger J. Acute transient ataxia caused by local lidocaine injection during insertion of a pleural catheter. Arch Bronconeumol 2009;45:472‑3. Hwang MS, Chu JJ, Su WJ. Diaphragmatic paralysis caused by malposition of chest tube placement after pediatric cardiac surgery. Int J Cardiol 2005;99:129‑31. Nahum E, Ben‑Ari J, Schonfeld T, Horev G. Acute diaphragmatic paralysis caused by chest‑tube trauma to phrenic nerve. Pediatr Radiol 2001;31:444‑6. Hassan WU, Keaney NP. Winging of the scapula: An unusual complication of chest tube placement. J Accid Emerg Med 1995;12:156‑7.
7.
Rosing JH, Lance S, Wong MS. Ulnar neuropathy after tube thoracostomy for pneumothorax. J Emerg Med 2012;43:e223‑5. Access this article online
Website: www.ijciis.org
Quick Response Code:
DOI: 10.4103/2229-5151.152350
Predictors of mortality in poisonous snake bite Dear Editor, Sir, we would like to discuss on the report on “Predictors of mortality in poisonous snake bite.[1]” Chaudhari et al., reported that “mortality in patients with snake bite can be predicted by simple variables like presence of bleeding tendencies, respiratory failure, and shock.[1]” In fact, there is a similar report on this topic from India by David et al.[2] In the study by David et al., another interesting factor that is not mentioned by Chaudhari et al., is the “pre‑hospital delay.[2]” In fact, as an acute disease, the early diagnosis and prompt treatment is the key principle for management of poisonous snake bite. Finally, it should be noted that the skill of medical care provider in management of poisonous snake bite is another possible factor to be addressed. According to a report from Thailand, a country with high incidence of poisonous snake bite, “ training programs on appropriate management of snakebites for the medical and paramedical[3]” was necessary to reduce the mortality.
Address for correspondence: Prof. Sim Sai Tin, Medical Center, Shantou, China. E‑mail: [email protected]
REFERENCES 1. 2. 3.
Chaudhari TS, Patil TB, Paithankar MM, Gulhane RV, Patil MB. Predictors of mortality in patients of poisonous snake bite: Experience from a tertiary care hospital in central India. Int J Crit Illn Inj Sci 2014;4:101‑7. David S, Matathia S, Christopher S. Mortality predictors of snake bite envenomation in southern India-a ten‑year retrospective audit of 533 patients. J Med Toxicol 2012;8:118‑23. Buranasin P. Snakebites at Maharat Nakhon Ratchasima Regional Hospital. S Asian J Trop Med Public Health 1993;24:186‑92. Access this article online
Website: www.ijciis.org
Quick Response Code:
DOI: 10.4103/2229-5151.152351
Sim Sai Tin, Viroj Wiwanitkit1
Medical Center Unit, Shantou, 1Department of Tropical Medicine, Hainan Medical University, Hainan, China
Guillain–Barré syndrome presenting as Bell’s palsy with crossed hemiparesis Dear Editor, The rare variants of Guillain–Barré syndrome (GBS) are Miller–Fisher and Bickerstaff’s brainstem encephalitis, and facial diplegia. [1] GBS can very rarely present as crossed hemiparesis, which occurred in our case. A 45‑year‑old female presented with left‑sided Bell’s palsy [Figure 1a] for 1 day with right‑sided hemiparesis. The reflexes were diminished bilaterally and plantars were mute. First possibility in this case was a posterior circulation stroke, but her MRI brain ruled out any infarct or hemorrhage. On 2 nd day, she developed quadriparesis with facial 62
diplegia [Figure 1b], dysphagia, and bulbar palsy. Now we could make a confident diagnosis of GBS and cerebrospinal fluid (CSF) examination also showed albumino‑cytological dissociation (proteins 259 mg/ dl and total leukocyte count of 4 cells/mm 3). She was treated with intravenous immunoglobulins and a month later she came back walking without support and facial diplegia was also improving [Figure 1c and d]. To conclude, GBS can very rarely present as Bell’s palsy with crossed hemiparesis. Vivek Chauhan, G Sharma, B S Rana, V Jearth, J Sandhu
International Journal of Critical Illness and Injury Science | Vol. 5 | Issue 1 | Jan-Mar 2015
Copyright of International Journal of Critical Illness & Injury Science 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.
