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Table of Contents    
CASE REPORT
Year : 2020  |  Volume : 68  |  Issue : 5  |  Page : 1224-1225

Approach to a Patient with Stroke After Flying


1 Aeromedical Research and Training Center, Eskisehir, Turkey
2 Van Military Hospital, Van, Turkey

Date of Web Publication27-Oct-2020

Correspondence Address:
Dr. Nazim Ata
USAEM Baskanligi, Eski Hava Hastanesi, Odunpazari, Eskisehir
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.299138

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 » Abstract 


Arriving at a definitive diagnosis in case of a patient with neurological symptoms after a low altitude flight is very critical, while at the same time presenting a dilemma in aeromedical decision making. Symptoms of stroke can closely mimic those of neurologic manifestations of decompression sickness. This paper discusses the approach to a case of a 28-year-old male helicopter passenger who developed left-sided numbness of the body after a 1.5 h flight at 13,000 feet altitude and was hospitalized with the diagnosis of transient ischemic attack.


Keywords: Altitude, decompression sickness, stroke
Key Message: In patients suffering from stroke after altitude exposure, arriving at a definitive diagnosis might be difficult. Altitude-induced decompression sickness can be easily confused with more common stroke etiologies. Under these conditions, in addition to standard medical treatment, hyperbaric oxygen treatment should also be considered as a supportive treatment modality.


How to cite this article:
Ata N, Cevık E. Approach to a Patient with Stroke After Flying. Neurol India 2020;68:1224-5

How to cite this URL:
Ata N, Cevık E. Approach to a Patient with Stroke After Flying. Neurol India [serial online] 2020 [cited 2020 Dec 5];68:1224-5. Available from: https://www.neurologyindia.com/text.asp?2020/68/5/1224/299138




Arterial gas embolism is rare in altitude exposure. Cerebral symptoms occurring after altitude exposure are usually attributed to decompression sickness (DCS).[1] DCS is a relatively rare entity in both military and civil aviation. It is caused by the formation of gas bubbles in blood or body tissues during or after rapid reduction of the ambient pressure. The symptoms of DCS range from mild, such as pain, to serious ones like neurological manifestations.[2] Altitude-induced DCS is usually seen at altitudes in excess of 18,000 feet as a consequence of loss of cabin pressure. DCS may also be encountered in some nonpressurized aircraft that are approved for flight above 20,000 feet.[3] Rarely, some individuals can develop this problem at lower altitudes. Usually, there are one or more risk factors for DCS in these rare cases.[4] Vascular obstruction causing stroke-like signs and symptoms can also mimic the neurological manifestations of DCS.[5] Hence, diagnosis of altitude-induced neurological DCS can pose a challenge, since it can be easily confused with other stroke etiologies. Signs of deep vein thrombosis (DVT) on Doppler ultrasonography or a right to left shunt on echocardiography support the transient ischemic attack (TIA) diagnosis. History of exposure to altitude supports the DCS diagnosis. The purpose of this paper is to underline the importance of a methodical approach and definitive diagnosis in a patient who develops symptoms similar to those of stroke after a low-altitude flight.


 » Case History Top


A 28-year-old male (height, 175 cm; weight, 98.4 kg; body mass index; 32.13 kg/m2) was admitted to the emergency room with a numbness on the left side of body after a 90 min flight in a helicopter at 13,000 feet altitude. Emergency medicine specialist and neurologist reviews revealed a blood pressure of 150/90 mmHg, heart rate of 70 beats/min, and respiratory rate of 15 breaths/min with saturation of 98% on room air. Left hemi-hypoesthesia was observed during neurological examination. His mental status, cranial nerves, motor system, reflexes, and coordination were normal. The patient claimed to have been sitting throughout the flight and did not give any history of hard exercise before or during the flight. There were no complaints of chest pain, joint pain, shortness of breath, or skin rash. Complete blood count and routine blood tests and electrocardiography were also normal. The patient was a heavy smoker (three packs per day) and had a history of hypertension for the last 3 years. His initial presentation was consistent with a diagnosis of stroke, and hence, he was hospitalized with the initial diagnosis of TIA. He was started on antiplatelet drugs, calcium channel blockers, and peripheral vasodilators. The physicians who treated the patient overlooked DCS at first because they were not flight surgeons. They performed tests to determine the etiology of stroke. Bilateral lower extremity arterial-venous and carotid-vertebral artery color Doppler ultrasonography and echocardiography were performed as part of the search for an etiologic factor. Patent foramen ovale, DVT, and other pathologies were ruled out. The patient's symptoms resolved completely within the first 24 h. There was no evidence of acute ischemia or presence of gas in the cerebral arteries on diffusion MRI scanning. Aerospace medicine specialist who is in charge in hyperbaric oxygen treatment facility in another city was asked for consultation. Hyperbaric oxygen therapy (HBOT) was not recommended in this case, since the patient's symptoms had resolved completely. The patient's recovery was uneventful and he was discharged after 5 days with a final diagnosis of TIA.


 » Discussion Top


Symptoms and signs of stroke can closely mimic those of neurologic DCS. Hence, neurological DCS should also have been considered in the differential diagnosis in this case; especially since the patient had a history of exposure to altitude before developing the symptoms.

Altitude-induced DCS can be easily confused with more common stroke etiologies. A neurological examination is generally inadequate to distinguish between different stroke etiologies. A definitive diagnosis is made primarily by the patient's anamnesis.[5] However, in many patients, even this proves to be inadequate.

The presence of risk factors such as heavy smoking and hypertension may suggest a thromboembolic disease. Although the patient's symptoms and his subsequent recovery were suggestive of TIA, the diagnosis of DCS should also have been considered in this case. The patient's age, absence of any signs of DVT on Doppler ultrasonography or a right to left shunt on echocardiography go against this diagnosis. A review of existing literature suggests that DVT can occur after 10 or more flight hours, which could have led to the TIA. Moreover, only 6% of patients with DVT have stroke.[6] Altitude-induced DCS should have been considered as a diagnosis for this patient, keeping in view the history of exposure to altitude. However, a diagnosis of altitude-induced DCS could also be argued against, since the exposure to altitude was below 18,000 ft and any specific DCS risk factors like a history of diving or dehydration were absent.

Typically, 18,000 feet is generally considered the threshold for occurrence of altitude-induced DCS symptoms. However clinically insignificant gas bubbles have been documented at lower altitudes as well.[7] A study by Butler on 111 cases of DCS below 18,000 feet altitude revealed that 35% of these cases were seen in the real flight, whereas the rest were observed in altitude chamber flights. In total, 75% of these cases had a history of physical exercise and prior exposure to altitude.[8] The most common symptom of DCS was pain only; neurological manifestations were present in only 18% of patients.[7]

The most common predisposing factors for DCS are high altitude, prolonged exposure to altitude, low temperature, physical exercise, injury, dehydration, diving before flying, alcohol consumption, hypoxia, obesity, smoking, and advanced age.[7],[9] The patient was a heavy smoker and obese; however, any other predisposing factors for low-altitude were absent.

In patients suffering from stroke after flight or altitude exposure, arriving at a definitive diagnosis (TIA or DCS) might be difficult. Under these conditions, in addition to standard medical treatment, HBOT should also be considered as a supportive treatment modality. Prompt treatment in accordance with US Navy Treatment can be beneficial in such cases. Diagnostic tests for ischemic cerebrovascular diseases should be performed concurrently. Resolution of symptoms after HBOT would confirm the diagnosis of DCS. Hence, HBOT would act as both a therapeutic and diagnostic measure.

In the absence of predisposing factors and lack of training in HBOT for physicians, the diagnosis of DCS can remain elusive. An awareness and strong suspicion are essential for the diagnosis and management of DCS. An early diagnosis and prompt referral for treatment would go a long way in decreasing the morbidity and mortality.[10]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
 » References Top

1.
Vann RD, Butler FK, Mitchell SJ, Moon RE. Decompression illness. Lancet 2011;377:153-64.  Back to cited text no. 1
    
2.
Rudge FW. Decompression sickness presenting as a viral syndrome. Aviat Space Environ Med 1991;62:60-1.  Back to cited text no. 2
    
3.
Black WR, DeHart RL. Decompression sickness: An increasing risk for the private pilot. Aviat Space Environ Med 1992;63:200-2.  Back to cited text no. 3
    
4.
Rudge FW. A case of decompression sickness at 2,437 meters (8,000 feet). Aviat Space Environ Med 1990;61:1026-7.  Back to cited text no. 4
    
5.
Weenink RP, Hollmann MW, van Hulst RA. Acute neurological symptoms during hypobaric exposure: Consider cerebral air embolism. Aviat Space Environ Med 2012;83:1084-91.  Back to cited text no. 5
    
6.
Belvís R, Masjuan J, García-Barragán N, Cocho D, Martí-Fàbregas J, Santamaría A, et al. Stroke and pulmonary thromboembolism after a long flight. Eur J Neurol 2005;12:732-4.  Back to cited text no. 6
    
7.
Fabian BG. Case report: Inflight decompression sickness affecting the temporomandibular joint. Aviat Space Environ Med 1998;69:517-8.  Back to cited text no. 7
    
8.
Butler W, Webb J. Decompression sickness below 18.000 feet: A large case series. Aviat Space Environ Med 2013;84:293.  Back to cited text no. 8
    
9.
Voge VM. Probable bends at 14,000 feet: A case report. Aviat Space Environ Med 1989;60:1102-3.  Back to cited text no. 9
    
10.
Auten JD, Kuhne MA, Walker HM, Porter HO. Neurologic decompression sickness following cabin pressure fluctuations at high altitude. Aviat Space Environ Med 2010;81:427-30.  Back to cited text no. 10
    




 

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