- Email: [email protected]
High altitude cerebral oedema
CMRP-171; No. of Pages 3 current medicine research and practice xxx (2016) xxx–xxx
Available online at www.sciencedirect.com
ScienceDirect journal homepage: www.elsevier.com/locate/cmrp
Case Report
High altitude cerebral oedema K.V.S. Hari Kumar a,*, K.P. Shijith b, Dalbara Singh b a b
Department of Endocrinology, Command Hospital, Chandimandir 134107, India Department of Radiology, Command Hospital, Chandimandir 134107, India
article info
abstract
Article history:
Soldiers who work in extremes of altitude are at risk for medical disorders resulting from the
Received 22 November 2015
altered physiology and environment. Cerebral oedema and pulmonary oedema are the two
Accepted 17 March 2016
major life-threatening complications seen amongst soldiers working in high altitude areas.
Available online xxx
Acclimatization plays an essential role in the prevention of these complications in high altitude areas. We report a young soldier, who presented with high altitude cerebral oedema
Keywords:
despite adequate acclimatization. The patient had characteristic neuroimaging findings and
HACO
recovered completely without any neurological disability. In this report, we discuss the
HAPO
pathogenic mechanisms and treatment options of high altitude cerebral oedema.
High altitude
# 2016 Sir Ganga Ram Hospital. Published by Elsevier, a division of Reed Elsevier India, Pvt. Ltd. All rights reserved.
Corpus callosum
1.
Introduction
High altitude cerebral oedema (HACO) is a potentially lifethreatening condition seen in soldiers working at altitudes above 10,000 feet. The disease is also observed in mountaineers and in people with poor acclimatization.1 The disease is often preceded by the acute mountain sickness and coexists with the high altitude pulmonary oedema. Acute mountain sickness is a constellation of non-specific symptoms observed immediately after ascent to altitudes in excess of 7000 feet. It is characterized by the headache, nausea, vomiting, easy fatigability, altered sleep hygiene and loss of appetite.2 AMS may progress to the life-threatening HACO with further ascent and absence of therapy. High altitude pulmonary oedema (HAPO) is usually seen after 2–3 days after arrival in these areas.3 HAPO is characterized by the presence of cough, pink frothy sputum, breathlessness
and easy fatigability. HAPO and HACO coexist together in 15– 25% of the patients and the underlying pathogenesis remains the same between these two emergencies.4 Early identification and treatment is essential to prevent the mortality associated with these emergency disorders. In this report, we present a young soldier who developed HACO plus HAPO, despite adequate acclimatization.
2.
Case report
A 32-year-old soldier, with no comorbidities, posted at an altitude of 10,000 feet for over a year was included in a mountaineering expedition. The team consisted of eight members with all of them having stayed at altitudes ranging between 9000 and 17,000 feet. The patient did not have any comorbidity and had no prior experience of altitudes in excess of 15,000 feet. The team ascended to an altitude of 17,000 feet
* Corresponding author. Tel.: +91 814 6141700; fax: +91 172 2851058. E-mail address: [email protected] (K.V.S. Hari Kumar). http://dx.doi.org/10.1016/j.cmrp.2016.03.008 2352-0817/# 2016 Sir Ganga Ram Hospital. Published by Elsevier, a division of Reed Elsevier India, Pvt. Ltd. All rights reserved.
Please cite this article in press as: Kumar KVSH, et al. High altitude cerebral oedema, Curr Med Res Pract. (2016), http://dx.doi.org/10.1016/j. cmrp.2016.03.008
CMRP-171; No. of Pages 3
2
current medicine research and practice xxx (2016) xxx–xxx
Fig. 1 – Splenium of the corpus callosum is hyperintense on FLAIR (A) and diffusion weighted images (B) along with an apparent diffusion coefficient map (C) confirming the restricted diffusion.
over 3 days by foot. On the morning after the 4th day, at an altitude of 17,000 feet, the patient developed breathlessness, cough, headache, vomiting and giddiness. The paramedical person accompanying the team suspected that to be a case of pulmonary oedema and acute mountain sickness. He was managed there with complete bed rest, acetazolamide, oxygen inhalation and intravenous dexamethasone. The patient was evacuated immediately within 4 h by air to our centre (at sea level) for further management. At admission, the patient had tachypnea, tachycardia, hypotension, hypoxaemia and bilateral lung crackles. Neurological examination revealed confused, disoriented individual with no long tract signs and normal fundus examination. He was managed with oxygen inhalation, intravenous dexamethasone and other supportive therapy. Acetazolamide was discontinued and serial monitoring revealed oxygen saturation above 98%. His haematological and biochemical parameters were normal and MRI brain revealed hyperintensity of the splenium of corpus callosum on T2 weighted and FLAIR images (Fig. 1). Restricted diffusion was noted on the apparent diffusion coefficient (ADC) map confirming the classical presentation of the HACO. Chest radiograph revealed resolving pulmonary oedema and the patient improved gradually over next 5 days. He was discharged on the 7th day of admission and was advised no further adventure activities in high altitude areas.
3.
Discussion
Our patient is unique in multiple ways pertaining to his presentation. They include occurrence of HACO despite adequate acclimatization, lack of symptoms of AMS preceding the HACO, coexistence of HACO and HAPO and the characteristic neuroimaging findings. The rapidity of the descent helped in the early recovery of the patient with no residual disability. This is the most effective intervention to be done in all suspected cases of HACO or HAPO.5 The incidence of HACO varies between 0.5 and 5%, depending on the case series and the altitude in consideration. The disease is most often preceded by the symptoms of AMS. The risk factors for the HACO and HAPO include smoking, rapid ascent, extremes of age and the presence of chronic
obstructive pulmonary disease.6 Our patient had none of the risk factors and was acclimatized adequately prior to proceeding on the mountaineering expedition. The pathogenesis of cerebral oedema in patients with HACO is unclear with equal contribution from the vasogenic and cytotoxic mechanisms.7 The pathophysiological mechanisms of vasogenic oedema include hypoxia mediated cerebral vasodilatation coupled with loss of cerebral autoregulation and disruption of the blood brain barrier by the release of toxic mediators, including VEGF (vascular endothelial growth factor) and CGRP (calcitonin gene related peptide). Exaggerated sympathetic activity leads to increased secretion of ADH and enhanced salt and water retention. Hypoxia also leads to release of vasodilatory factors like nitric oxide (NO) leading to increased perfusion of the brain capillary bed. This results in the cytotoxic damage of the microvasculature and leakage of the fluid leading to the cerebral oedema. The disruption of the blood–brain barrier also results in the multiple microhemorrhages and deposition of toxic metabolites in the brain substance. All these mechanisms contribute towards the cause of HACO. The imaging characteristics of HACO include involvement of the splenium of the corpus callosum with complete recovery on follow-up.8 The lesion appears hyperintense on T2 weighted and FLAIR images. Diffusion weighted imaging (DWI) shows the areas of restricted diffusion, which appear dark on the ADC mapping. Our patient demonstrated all the characteristic imaging patterns of the HACO. The preferential involvement of white matter without significant grey matter also gives an additional clue for the underlying vasogenic oedema. Irreversible changes are seen occasionally and occur are due to the underlying gliotic changes. Few authors have suggested that the imaging findings also help in the prognostication of the case beyond the diagnosis.9 FLAIR images help in the diagnosis of a patient, even after significant clinical improvement and DWI and ADC mapping helps in the prognostication of the case. HACO is a life-threatening condition and requires urgent evacuation to the sea level. Other supportive therapy includes oxygen, ventilator support and a short course of intravenous dexamethasone.10 The recovery is often complete without any neurologic sequelae as observed in our patient.
Please cite this article in press as: Kumar KVSH, et al. High altitude cerebral oedema, Curr Med Res Pract. (2016), http://dx.doi.org/10.1016/j. cmrp.2016.03.008
CMRP-171; No. of Pages 3 current medicine research and practice xxx (2016) xxx–xxx
4.
Conclusion
To conclude, we report a case of HACO and HAPO in a soldier despite acclimatization, who recovered completely without any sequelae. Our report highlights the need for extra vigil about these complications, even in acclimatized persons.
Conflicts of interest The authors have none to declare.
references
1. Hackett PH, Roach RC. High altitude cerebral edema. High Alt Med Biol. 2004;5:136–146. 2. Luo Y, Wang Y, Lu H, Gao Y. 'Ome' on the range: update on high-altitude acclimatization/adaptation and disease. Mol Biosyst. 2014;10:2748–2755.
3. Gabry AL, Ledoux X, Mozziconacci M, Martin C. High-altitude pulmonary edema at moderate altitude (<2,400 m; 7,870 feet): a series of 52 patients. Chest. 2003;123:49–53. 4. Basnyat B. High altitude cerebral and pulmonary edema. Travel Med Infect Dis. 2005;3(November (4)):199–211. 5. Luks AM, McIntosh SE, Grissom CK, et al. Wilderness Medical Society practice guidelines for the prevention and treatment of acute altitude illness: 2014 update. Wilderness Environ Med. 2014;25(December (4 suppl)):S4–S14. 6. Basnyat B, Murdoch DR. High-altitude illness. Lancet. 2003;361:1967–1974. 7. Hackett PH, Yarnell PR, Hill R, Reynard K, Heit J, McCormick J. High-altitude cerebral edema evaluated with magnetic resonance imaging: clinical correlation and pathophysiology. JAMA. 1998;280:1920–1925. 8. Venkata Nagesh I, Manoj G, Gurdarshdeep M. High altitude cerebral edema-serial MRI findings. Wilderness Environ Med. 2015;26(June (2)):278–280. 9. Wong SH, Turner N, Birchall D, Walls TJ, English P, Schmid ML. Reversible abnormalities of DWI in high altitude cerebral edema. Neurology. 2004;62:335–336. 10. Luks AM. Physiology in medicine: a physiologic approach to prevention and treatment of acute high-altitude illnesses. J Appl Physiol (1985). 2015;118:509–519.
Please cite this article in press as: Kumar KVSH, et al. High altitude cerebral oedema, Curr Med Res Pract. (2016), http://dx.doi.org/10.1016/j. cmrp.2016.03.008
3
Available online at www.sciencedirect.com
ScienceDirect journal homepage: www.elsevier.com/locate/cmrp
Case Report
High altitude cerebral oedema K.V.S. Hari Kumar a,*, K.P. Shijith b, Dalbara Singh b a b
Department of Endocrinology, Command Hospital, Chandimandir 134107, India Department of Radiology, Command Hospital, Chandimandir 134107, India
article info
abstract
Article history:
Soldiers who work in extremes of altitude are at risk for medical disorders resulting from the
Received 22 November 2015
altered physiology and environment. Cerebral oedema and pulmonary oedema are the two
Accepted 17 March 2016
major life-threatening complications seen amongst soldiers working in high altitude areas.
Available online xxx
Acclimatization plays an essential role in the prevention of these complications in high altitude areas. We report a young soldier, who presented with high altitude cerebral oedema
Keywords:
despite adequate acclimatization. The patient had characteristic neuroimaging findings and
HACO
recovered completely without any neurological disability. In this report, we discuss the
HAPO
pathogenic mechanisms and treatment options of high altitude cerebral oedema.
High altitude
# 2016 Sir Ganga Ram Hospital. Published by Elsevier, a division of Reed Elsevier India, Pvt. Ltd. All rights reserved.
Corpus callosum
1.
Introduction
High altitude cerebral oedema (HACO) is a potentially lifethreatening condition seen in soldiers working at altitudes above 10,000 feet. The disease is also observed in mountaineers and in people with poor acclimatization.1 The disease is often preceded by the acute mountain sickness and coexists with the high altitude pulmonary oedema. Acute mountain sickness is a constellation of non-specific symptoms observed immediately after ascent to altitudes in excess of 7000 feet. It is characterized by the headache, nausea, vomiting, easy fatigability, altered sleep hygiene and loss of appetite.2 AMS may progress to the life-threatening HACO with further ascent and absence of therapy. High altitude pulmonary oedema (HAPO) is usually seen after 2–3 days after arrival in these areas.3 HAPO is characterized by the presence of cough, pink frothy sputum, breathlessness
and easy fatigability. HAPO and HACO coexist together in 15– 25% of the patients and the underlying pathogenesis remains the same between these two emergencies.4 Early identification and treatment is essential to prevent the mortality associated with these emergency disorders. In this report, we present a young soldier who developed HACO plus HAPO, despite adequate acclimatization.
2.
Case report
A 32-year-old soldier, with no comorbidities, posted at an altitude of 10,000 feet for over a year was included in a mountaineering expedition. The team consisted of eight members with all of them having stayed at altitudes ranging between 9000 and 17,000 feet. The patient did not have any comorbidity and had no prior experience of altitudes in excess of 15,000 feet. The team ascended to an altitude of 17,000 feet
* Corresponding author. Tel.: +91 814 6141700; fax: +91 172 2851058. E-mail address: [email protected] (K.V.S. Hari Kumar). http://dx.doi.org/10.1016/j.cmrp.2016.03.008 2352-0817/# 2016 Sir Ganga Ram Hospital. Published by Elsevier, a division of Reed Elsevier India, Pvt. Ltd. All rights reserved.
Please cite this article in press as: Kumar KVSH, et al. High altitude cerebral oedema, Curr Med Res Pract. (2016), http://dx.doi.org/10.1016/j. cmrp.2016.03.008
CMRP-171; No. of Pages 3
2
current medicine research and practice xxx (2016) xxx–xxx
Fig. 1 – Splenium of the corpus callosum is hyperintense on FLAIR (A) and diffusion weighted images (B) along with an apparent diffusion coefficient map (C) confirming the restricted diffusion.
over 3 days by foot. On the morning after the 4th day, at an altitude of 17,000 feet, the patient developed breathlessness, cough, headache, vomiting and giddiness. The paramedical person accompanying the team suspected that to be a case of pulmonary oedema and acute mountain sickness. He was managed there with complete bed rest, acetazolamide, oxygen inhalation and intravenous dexamethasone. The patient was evacuated immediately within 4 h by air to our centre (at sea level) for further management. At admission, the patient had tachypnea, tachycardia, hypotension, hypoxaemia and bilateral lung crackles. Neurological examination revealed confused, disoriented individual with no long tract signs and normal fundus examination. He was managed with oxygen inhalation, intravenous dexamethasone and other supportive therapy. Acetazolamide was discontinued and serial monitoring revealed oxygen saturation above 98%. His haematological and biochemical parameters were normal and MRI brain revealed hyperintensity of the splenium of corpus callosum on T2 weighted and FLAIR images (Fig. 1). Restricted diffusion was noted on the apparent diffusion coefficient (ADC) map confirming the classical presentation of the HACO. Chest radiograph revealed resolving pulmonary oedema and the patient improved gradually over next 5 days. He was discharged on the 7th day of admission and was advised no further adventure activities in high altitude areas.
3.
Discussion
Our patient is unique in multiple ways pertaining to his presentation. They include occurrence of HACO despite adequate acclimatization, lack of symptoms of AMS preceding the HACO, coexistence of HACO and HAPO and the characteristic neuroimaging findings. The rapidity of the descent helped in the early recovery of the patient with no residual disability. This is the most effective intervention to be done in all suspected cases of HACO or HAPO.5 The incidence of HACO varies between 0.5 and 5%, depending on the case series and the altitude in consideration. The disease is most often preceded by the symptoms of AMS. The risk factors for the HACO and HAPO include smoking, rapid ascent, extremes of age and the presence of chronic
obstructive pulmonary disease.6 Our patient had none of the risk factors and was acclimatized adequately prior to proceeding on the mountaineering expedition. The pathogenesis of cerebral oedema in patients with HACO is unclear with equal contribution from the vasogenic and cytotoxic mechanisms.7 The pathophysiological mechanisms of vasogenic oedema include hypoxia mediated cerebral vasodilatation coupled with loss of cerebral autoregulation and disruption of the blood brain barrier by the release of toxic mediators, including VEGF (vascular endothelial growth factor) and CGRP (calcitonin gene related peptide). Exaggerated sympathetic activity leads to increased secretion of ADH and enhanced salt and water retention. Hypoxia also leads to release of vasodilatory factors like nitric oxide (NO) leading to increased perfusion of the brain capillary bed. This results in the cytotoxic damage of the microvasculature and leakage of the fluid leading to the cerebral oedema. The disruption of the blood–brain barrier also results in the multiple microhemorrhages and deposition of toxic metabolites in the brain substance. All these mechanisms contribute towards the cause of HACO. The imaging characteristics of HACO include involvement of the splenium of the corpus callosum with complete recovery on follow-up.8 The lesion appears hyperintense on T2 weighted and FLAIR images. Diffusion weighted imaging (DWI) shows the areas of restricted diffusion, which appear dark on the ADC mapping. Our patient demonstrated all the characteristic imaging patterns of the HACO. The preferential involvement of white matter without significant grey matter also gives an additional clue for the underlying vasogenic oedema. Irreversible changes are seen occasionally and occur are due to the underlying gliotic changes. Few authors have suggested that the imaging findings also help in the prognostication of the case beyond the diagnosis.9 FLAIR images help in the diagnosis of a patient, even after significant clinical improvement and DWI and ADC mapping helps in the prognostication of the case. HACO is a life-threatening condition and requires urgent evacuation to the sea level. Other supportive therapy includes oxygen, ventilator support and a short course of intravenous dexamethasone.10 The recovery is often complete without any neurologic sequelae as observed in our patient.
Please cite this article in press as: Kumar KVSH, et al. High altitude cerebral oedema, Curr Med Res Pract. (2016), http://dx.doi.org/10.1016/j. cmrp.2016.03.008
CMRP-171; No. of Pages 3 current medicine research and practice xxx (2016) xxx–xxx
4.
Conclusion
To conclude, we report a case of HACO and HAPO in a soldier despite acclimatization, who recovered completely without any sequelae. Our report highlights the need for extra vigil about these complications, even in acclimatized persons.
Conflicts of interest The authors have none to declare.
references
1. Hackett PH, Roach RC. High altitude cerebral edema. High Alt Med Biol. 2004;5:136–146. 2. Luo Y, Wang Y, Lu H, Gao Y. 'Ome' on the range: update on high-altitude acclimatization/adaptation and disease. Mol Biosyst. 2014;10:2748–2755.
3. Gabry AL, Ledoux X, Mozziconacci M, Martin C. High-altitude pulmonary edema at moderate altitude (<2,400 m; 7,870 feet): a series of 52 patients. Chest. 2003;123:49–53. 4. Basnyat B. High altitude cerebral and pulmonary edema. Travel Med Infect Dis. 2005;3(November (4)):199–211. 5. Luks AM, McIntosh SE, Grissom CK, et al. Wilderness Medical Society practice guidelines for the prevention and treatment of acute altitude illness: 2014 update. Wilderness Environ Med. 2014;25(December (4 suppl)):S4–S14. 6. Basnyat B, Murdoch DR. High-altitude illness. Lancet. 2003;361:1967–1974. 7. Hackett PH, Yarnell PR, Hill R, Reynard K, Heit J, McCormick J. High-altitude cerebral edema evaluated with magnetic resonance imaging: clinical correlation and pathophysiology. JAMA. 1998;280:1920–1925. 8. Venkata Nagesh I, Manoj G, Gurdarshdeep M. High altitude cerebral edema-serial MRI findings. Wilderness Environ Med. 2015;26(June (2)):278–280. 9. Wong SH, Turner N, Birchall D, Walls TJ, English P, Schmid ML. Reversible abnormalities of DWI in high altitude cerebral edema. Neurology. 2004;62:335–336. 10. Luks AM. Physiology in medicine: a physiologic approach to prevention and treatment of acute high-altitude illnesses. J Appl Physiol (1985). 2015;118:509–519.
Please cite this article in press as: Kumar KVSH, et al. High altitude cerebral oedema, Curr Med Res Pract. (2016), http://dx.doi.org/10.1016/j. cmrp.2016.03.008
3