Atormac
Neurology India
menu-bar5 Open access journal indexed with Index Medicus
  Users online: 4132  
 Home | Login 
About Editorial board Articlesmenu-bullet NSI Publicationsmenu-bullet Search Instructions Online Submission Subscribe Videos Etcetera Contact
  Navigate Here 
 Search
 
  
 Resource Links
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Article in PDF (610 KB)
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this Article
   References
   Article Figures

 Article Access Statistics
    Viewed1264    
    Printed25    
    Emailed0    
    PDF Downloaded40    
    Comments [Add]    

Recommend this journal

 


 
Table of Contents    
LETTER TO EDITOR
Year : 2014  |  Volume : 62  |  Issue : 6  |  Page : 690-691

First case report of caissons disease with pneumobilia


1 Department of Neurology, Sundaram Arulrhaj Hospitals, Tuticorin, India
2 Department of Physician, Sundaram Arulrhaj Hospitals, Tuticorin, India
3 Department of Radiologist, Sundaram Arulrhaj Hospitals, Tuticorin, India
4 Department of Neurologist, Appusami Hospital, Salem, Tamil Nadu, India

Date of Submission27-Nov-2014
Date of Decision06-Dec-2014
Date of Acceptance09-Dec-2014
Date of Web Publication16-Jan-2015

Correspondence Address:
Eswaradass Prasanna Venkatesan
Department of Neurologist, Appusami Hospital, Salem, Tamil Nadu
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.149413

Rights and Permissions



How to cite this article:
Kannan B, Kannan A, Saravanan C, Venkatesan EP. First case report of caissons disease with pneumobilia. Neurol India 2014;62:690-1

How to cite this URL:
Kannan B, Kannan A, Saravanan C, Venkatesan EP. First case report of caissons disease with pneumobilia. Neurol India [serial online] 2014 [cited 2019 Oct 22];62:690-1. Available from: http://www.neurologyindia.com/text.asp?2014/62/6/690/149413


Sir,

A 35-year-old male went for deep sea diving using self-contained underwater breathing apparatus (SCUBA) diving apparatus for collecting sea shells. At the end of two-and-half hours, he was rapidly pulled up to surface. He immediately developed severe back pain and neck pain, followed by severe myalgia. Within few minutes, he also had giddiness, abdominal pain, and vomiting. On arrival, he complained of bilateral hearing loss and weakness of both lower limbs. On examination, patient was irritable and agitated. Vitals at admission were: Pulse 120/min regular, blood pressure 100/70 mm Hg, respiratory rate 30/min, and oxygen saturation 80%. On neurologic examination, he had hypotonia of all the limbs, motor power 4/5 in upper limbs and 3/5 lower limbs which further worsened to 0/5, areflexia, and plantar responses were mute. Fundus showed few petechial hemorrhages. Abdomen examination showed guarding and right hypochondriac tenderness with distended bladder. The clinical diagnosis was acute decompression sickness (DCS).

Patient was intubated and given injection methyl prednisolone for 3 days. On day 5, he was extubated and started on nasogastric feeds. Blood biochemistry and complete blood picture were normal except for mild elevation of alkaline phosphatase (ALP) of 189 IU/L. Chest X-ray revealed bilateral hilar shadows [Figure 1]. X-ray abdomen erect was normal but ultrasonogram showed pneumobilia [Figure 2]. Magnetic resonance imaging (MRI) of brain showed T2 and fluid attenuated inversion recovery (FLAIR) hyperintensities in periventricular and parieto occipital grey matter [Figure 3]. MRI spine showed hyperintense signal involving central portion of spinal cord extending from C2 to C5, possibility of spinal cord infarct [Figure 4]. After 2 weeks, patient shows marked improvement with steroids, supportive measures, and active physiotherapy. At the time of discharge, his hearing had improved, his abdominal distension was relieved and was able to take orally and his power was 4/5 in upper limb and 2/5 in lower limb.
Figure 1: CXR shows bilateral perihilar shadows

Click here to view
Figure 2: USG abdomen shows pneumobilia

Click here to view
Figure 3: MRI brain shows FLAIR hyperintensities in periventricular and parieto occipital grey matter

Click here to view
Figure 4: MRI spine shows hyperintense signal involving central portion of spinal cord extending from C2 to C5

Click here to view


Tuticorin is a town situated in southern coastal Tamil Nadu. One of the occupations of people here is deep sea diving for collecting sea shells. SCUBA diving has become widely available for occupational and recreational activity. SCUBA enables the diver to breathe high pressure gas from a cylinder through a regulator which allows the diver to stay underwater for about 2 to 3 hours. [1] Acute DCS is rarely reported in India, the first case report was by Tripathy et al. in 1964. [2] When the diver ascends, the sum of the gas tensions in the tissue exceeds the ambient pressure causing inert gases (nitrogen), which were dissolved under higher pressure, to come out of physical solution and form gas bubbles which leads to multiorgan dysfunction. [3],[4]

The central nervous system (CNS) involvement in DCS has been studied in detail by Koshi et al. It is believed that arterialized bubbles passing through the lungs and heart involve the brain. MRI commonly shows multiple border zone infarcts. [5] Involvement of cortical gray matter and cerebellum are characteristic due to cerebral arterial gas embolism. Pneumobilia is accumulation of air in biliary tree. To best of our knowledge, pneumobilia in DCS has not been reported in literature. We propose that nitrogen air bubbles probably have accumulated in biliary tree producing pneumobilia.

Our divers need to be educated about DCS and its preventive measures. It can be prevented by formal training of divers and following safety measures like slow ascent of 9-10 meters/minute and ear plugs to prevent barotrauma. In our country where there is no formal training, incidence of DCS is likely to increase in future. Physician must have a strong clinical suspicion to diagnose DCS. Early diagnosis and treatment with steroids and hyperbaric oxygen is essential to prevent complications.

 
  References Top

1.
Melamed Y, Shupak A, Bitterman H. Medical problems associated with underwater diving. N Engl J Med 1992;326:30-5.  Back to cited text no. 1
    
2.
Tripathy BB, Satpathy SN, Misra KC. Decompression sickness (caisson disease). J Indian Med Assoc 1964;42:130-1.  Back to cited text no. 2
    
3.
Phatak UA, David EJ, Kulkarni PM. Decompression syndrome (Caisson disease) in an Indian diver. Ann Indian Acad Neurol 2010;13:202-3.  Back to cited text no. 3
[PUBMED]  Medknow Journal  
4.
Carturan D, Boussuges A, Vanuxem P, Bar-Hen A, Burnet H, Gardette B. Ascent rate, age, maximal oxygen uptake, adiposity, and circulating venous bubbles after diving. J Appl Physiol (1985) 2002;93:1349-56.  Back to cited text no. 4
    
5.
Kohshi K, Katoh T, Abe H, Wong RM. Central nervous system involvement in patients with decompression illness. Sangyo Eiseigaku Zasshi 2003;45:97-104.  Back to cited text no. 5
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

Top
Print this article  Email this article
   
Online since 20th March '04
Published by Wolters Kluwer - Medknow