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Published on: September 6, 2024
Evidence for increased intracranial pressure in high altitude pulmonary edema
Peter J Fagenholz1, Jonathan A Gutman, Alice F Murray
1Department of Surgery, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. pfagenholz@partners.org
We sought to determine if optic nerve sheath diameter (ONSD), a surrogate measure of ICP, is increased in high altitude pulmonary edema (HAPE). Five HAPE patients (one with a codiagnosis of high altitude cerebral edema [HACE]) treated at the Himalayan Rescue Association clinic in Pheriche, Nepal (4240 m), underwent optic nerve sheath ultrasonography (ONSU) at admission to determine ONSD. Results were compared to ONSD in 32 control subjects at the same altitude without evidence of altitude illness. Four of the five HAPE patients underwent repeat ONSU at discharge. All exams were read by two blinded observers. The mean ONSD for HAPE patients on presentation was 5.7 +/- 0.44 mm and for controls was 4.7 +/- 0.56 mm (p = 0.003). Excluding the patient with a coexistent clinical diagnosis of HACE, mean ONSD at presentation for the other four HAPE patients was 5.7 +/- 0.50 mm and was significantly different from controls (p = 0.007). In the four HAPE patients with repeat exams, ONSD decreased by 17% +/- 15% (95% CI 4-30%) between admission and discharge. We conclude that HAPE is associated with increased ONSD, a surrogate measure of increased ICP.
We sought to determine if optic nerve sheath diameter (ONSD), a surrogate measure of ICP, is increased in high altitude pulmonary edema (HAPE). Five HAPE patients (one with a codiagnosis of high altitude cerebral edema [HACE]) treated at the Himalayan Rescue Association clinic in Pheriche, Nepal (4240 m), underwent optic nerve sheath ultrasonography (ONSU) at admission to determine ONSD. Results were compared to ONSD in 32 control subjects at the same altitude without evidence of altitude illness. Four of the five HAPE patients underwent repeat ONSU at discharge. All exams were read by two blinded observers. The mean ONSD for HAPE patients on presentation was 5.7 +/- 0.44 mm and for controls was 4.7 +/- 0.56 mm (p = 0.003). Excluding the patient with a coexistent clinical diagnosis of HACE, mean ONSD at presentation for the other four HAPE patients was 5.7 +/- 0.50 mm and was significantly different from controls (p = 0.007). In the four HAPE patients with repeat exams, ONSD decreased by 17% +/- 15% (95% CI 4-30%) between admission and discharge. We conclude that HAPE is associated with increased ONSD, a surrogate measure of increased ICP.
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