Glyxambi
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 
  • Users Online: 3469
  • Home
  • Print this page
  • Email this page


 
   Table of Contents      
BRIEF REPORT
Year : 1999  |  Volume : 47  |  Issue : 3  |  Page : 192-193

Lipaemia retinalis in a case of Juvenile diabetic ketoacidosis


Department of Ophthalmology, Lokmanya Tilak Municipal Medical College, Mumbai, India

Correspondence Address:
S S Jain
Department of Ophthalmology, Lokmanya Tilak Municipal Medical College, Mumbai
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


PMID: 10858777

Rights and PermissionsRights and Permissions

How to cite this article:
Jain S S, Thomas S, Motwane S A, Seth A. Lipaemia retinalis in a case of Juvenile diabetic ketoacidosis. Indian J Ophthalmol 1999;47:192-3

How to cite this URL:
Jain S S, Thomas S, Motwane S A, Seth A. Lipaemia retinalis in a case of Juvenile diabetic ketoacidosis. Indian J Ophthalmol [serial online] 1999 [cited 2019 Sep 17];47:192-3. Available from: http://www.ijo.in/text.asp?1999/47/3/192/14916

A rare case of diabetic retinal lipaemia is described in a 5-year-old child.

We report a rare case of diabetic retinal lipaemia which is the most common pathological type of transportation hyperlipaemia.[1] Originally described by Heyl in 1880, it mainly affects young male diabetics[1] who present in coma with a high degree of ketoacidosis. Visual function is not affected.[2] The condition is rarely detected, and in this case, its remarkable, unmistakable and pathognomonic[1] appearance assisted us in the medical management of the clinical condition.


  Case Report Top


A 5-year-old-girl with breathlessness and altered sensorium for 4 hours, fever and discharge from ears since one week and weight loss since one month was admitted to the paediatric intensive care unit. On systemic examination, she had cold extremities, weak peripheral pulses, heart rate of 148/min, and respiratory rate of 50/min. Her systolic blood pressure was recorded as 80 mmHg. She also showed signs of dehydration and prolonged capillary refill time. An ophthalmologist's opinion was sought. On ophthalmologic examination, the vision could not be recorded, and the pupils were mid-dilated, reacting to light. The intraocular pressure of both eyes by Schiotz tonometry was 13.4 mm Hg. Fundoscopy of both eyes revealed pale retinae and optic discs with milky-white, uniformly appearing arteries and veins. The choroidal pattern could not be appreciated. There were perivascular yellowish-white stripes[1] [Figure - 1], probably due to permeation of fat into the perivascular area. On admission blood drawn for investigations appeared creamy pink and blood sugars were 315 mg%. The arterial blood gases estimation indicated severe uncompensated metabolic acidosis.[3] Blood Urea Nitrogen (BUN), serum electrolytes, and lipid levels could not be measured due to the milky serum. Urine analysis revealed glucose 3+ and ketones 2+. History suggestive of polyphagia, polydypsia and polyuria since 1 month was elicited retrospectively. On the fourth day of admission serum triglycerides (2340 mg%) and serum cholesterol (495 mg%) could be measured, indicating severe hyperlipidemia.

The patient was managed[3] with correction of the fluid-electrolyte imbalance and acidosis and administration of intravenous insulin therapy. Within 6-8 hours of treatment, her sensorium improved and respiratory distress settled. Thirty six hours later, a planned diet and subcutaneous insulin therapy was initiated. A week after insulin therapy, serum triglyceride (378 mg%) and serum cholesterol (320 mg%) reduced significantly. Resolution of lipaemia retinalis was noted [Figure - 2], i.e, vessels near the disc appeared salmon pink while the peculiar colour lingered longer at periphery. The patient was discharged on subcutaneous insulin and a planned diet. On follow up 6 weeks later, her urine and blood sugar were under control. Her fundus appeared normal and vision of both eyes was 6/6, N5.


  Discussion Top


Diabetic ketoacidosis[3] results following insulin deficiency and excessive counter-regulatory hormones leading to hyperglycemia, hyperketonemia and ensuing osmotic diuresis, dehydration and urinary loss of serum electrolytes, which is life threatening. The predisposing conditions are infections and insulin deficiency in insulin-dependent diabetes mellitus (IDDM). Acidosis correlates with disease severity and is compensated by hyperventilation. When the content of neutral triglycerides is raised sufficiently (>1000 - 2500 mg%) the serum is milky in appearance. This is also noticed ophthalmoscopically in retinal circulation, and lipaemia retinalis is diagnosed. To produce lactescence it is necessary for fat to be emulsified into chylomicra greater than 0.1μ in diameter to be rendered visible. In making correlations between lipaemia retinalis and serum triglycerides, three factors[4] are essential: the periphery of fundus be carefully examined, since this is where grade-1 lipaemia retinalis is seen; the blood specimen must be taken after 12-16 hours of fasting, since triglyceride elevations after a fatty meal are rapidly transient and give falsely elevated plasma triglyceride levels; and fundus must be examined at approximately the time blood sample is drawn, since degree of lipaemia retinalis may change from day to day as the triglyceride level changes with treatment. If there is any doubt as to whether the patient has early peripheral signs of lipaemia retinalis, one may centrifuge chelated blood. If the plasma is clear or only slightly turbid, lipaemia retinalis is absent. On pathological examination retina is normal, but plasma is loaded with fat which permeates into perivascular area. More than one episode of lipaemia may occur in the same patient. Probably it occurs more frequently[1] than the scant literature indicates, but the eyes are not routinely examined in a comatose diabetic patient. The retinal lipaemia is also likely to disappear following correction of ketoacidosis[5].

 
  References Top

1.
Duke-Elder S, Dobres JH. Retinopathies associated with general diseases. In : Duke-Elder S, editor. System of Ophthalmology. St.Louis: CV Mosby Company; 1973. Vol.10, p 452-55.  Back to cited text no. 1
    
2.
Scheie HG, Albert DM. Medical Ophthalmology-Endocrine diseases. In: Textbook of Ophthalmology. 9th ed. Philadelphia:W.B. Saunders Company; 1977. p 426-39.  Back to cited text no. 2
    
3.
Niffenegger JH, Fong D, Cavallerano J, Aiello LM. Diabetes Mellitus. In : Albert DM, Jakobiec FA, editors. Principles and Practice of Ophthalmology: Clinical Practice. Philadephia: WB Saunders Company; 1994. Vol.5, p 2925-36.  Back to cited text no. 3
    
4.
Vinger PF, Sachs BA. Ocular manifestations of hyperlipoproteinemia. Am J Ophthalmol 1970;70:563-73.  Back to cited text no. 4
[PUBMED]    
5.
Bron AJ, Williams HP. Lipaemia of limbal vessels. Br J Ophthalmol 1972;56:343-46.  Back to cited text no. 5
    


    Figures

  [Figure - 1], [Figure - 2]



 

Top
 
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
Case Report
Discussion
References
Article Figures

 Article Access Statistics
    Viewed3550    
    Printed102    
    Emailed4    
    PDF Downloaded8    
    Comments [Add]    

Recommend this journal