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I completed my medical school and background EM training from India (Christian Medical College, Vellore and Apollo Hospitals, Hyderabad) where I worked for 4 years. Following this, I devoted (with all my heart) about 1.5 years to do US Medical Licensing Exams. My stint towards an EM Residency in States did not work but it took me to places and it has been quite a journey. I then relocated to London, England to work as a Registrar (Non-Trainee) in A&E. This gave me an opportunity to better understand NHS, EM training pathways and more importantly the EM Mindsets in the United Kingdom. 

Currently, I am pursuing Higher Specialist Training in Emergency Medicine at South East Scotland Deanery where I have the honour and privilege of training under some of the most innovative brains in the field of Emergency Medicine. Over the past few years, I have realised that LEARNING and UNLEARNING (which can be challenging!) is equally important to deliver cutting edge care to our patients.And through this blog, I aspire to disseminate knowledge, assist trainees with exams and stay up to date with contemporary EM literature. I have always been an avid FOAMed supporter because FOAMed has always played an indispensable role during my training. 


Lakshay Chanana
ST4 EM Trainee 
Edinburgh, Scotland
drlakshayem@gmail.com

Monday, October 9, 2017

Hyperosmolar Hyperglycaemic State - HHS


HHS is a syndrome charcaterised by hyperglycemia and hyperosmolarity commonly precipitated by an illness (infection, infarction, any other illness or stress ). Classically, HHS is seen in frail elderly patients with poor thirst perception and uncontrolled diabetes mellitus. 




Pathophysiology
Relative Insulin Deficiency-->Hyperglycaemia-->Osmotic Diuresis-->Dehydration and electrolyte loss. There is lack of severe ketoacidosis in HHS possibly due to  higher levels of endogenous insulin and lower levels of counter-regulatory hormones. 




Changes in serum osmolality and Na explain mental status changes and coma. The normal serum osmolality ranges between 275 to 295 mOsm/kg. Values >320 mOsm are commonly associated with altered mental status. 

Diagnostic Criteria
  • Severe hyperglycemia with serum glucose usually >600 milligrams/dL (>33.3 mmol/L)
  • Elevated calculated plasma osmolality of >315 mOsm/kg
  • Serum bicarbonate >15 mEq/L (>15 mmol/L)
  • Arterial pH >7.3, with negative to mildly positive serum ketones 


Occasionally, it can be challenging to differentiate HHS from DKA. HHS may present with metabolic acidosis or ketonemia due to lactic acidosis, starvation ketosis, and renal failure in various combinations. Type 1 diabetics may present with HHS and Type 2 may are known to have DKA as well. It is important to recognize the mixed acid-base patterns in patients in these hyperglycaemic syndromes.
  


Management

  • Fluid Resuscitation to improvement of tissue perfusion (Average fluid deficit is 8-12 litres)
  • Insulin Drip (after initial fluid rests and ensuring normal K level)
  • Identify and treat the precipitating cause
  • Correct electrolyte abnormalities (HypoK, HypoMg)
  • Gradual correction of hyperglycaemia

Initial investigations include a complete metabolic profile, calculated and measured serum osmolality, coags, blood gas, CRP, Renal Function, serum ketones, FBC, blood and urine cultures should all be considered, Chest radiographs and electrocardiograms. Consider CT when suspecting a CNS infection or poor response to initial therapy.  

Management need to individualised with concurrent medical illnesses (CCF, CKD). Once serum glucose <300 milligrams/ dL (<16.6 mmol/L), switch to 5% dextrose in half normal saline, and reduce the insulin infusion to 0.02 to 0.05 unit/kg/h and glucose is maintained between 200 and 300 milligrams/dL (11.1–16.6 mmol/L). 


Take Home:
  • HHS develops over days and thus metabolic correction should be done gradually
  • Focus on fluids and electrolyte management 
  • Identify and Treat the precipitants


 Further  Reading:
  1. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN: Hyperglycemic crises in adult patients with diabetes. Diabetes Care 32: 1335, 2009. 
  2. Newton CA, Raskin P: Diabetic ketoacidosis in type 1 and type 2 diabetes mellitus: clinical and biochemical differences. Arch Intern Med 164: 1925, 2004. 
  3. Nyenwe E, Loganathan R, Blum S, et al: Admissions for diabetic ketoacidosis in ethnic minority groups in a city hospital. Metabolism 56: 172, 2007. 
  4. Umpierrez GE: Ketosis-prone type 2 diabetes: time to revise the classification of diabetes. Diabetes Care 29: 2755, 2006. 
  5. Kitabchi AE, Nyenwe EA: Hyperglycemic crises in diabetes mellitus: diabetic ketoacido- sis and hyperglycemic hyperosmotic state. Endocrinol Metab Clin North Am 35: 725, 2006. 
  6. KitabchiAE,UmpierrezG,FisherJN,metal:Thirty years of personal experience in hyper- glycemic crises: diabetic ketoacidosis and hyperglycemic hyperosmolar state. J Clin Endocrinol Metab 93: 1541, 2008. 
  7. www.ebmedicine.net

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     Lakshay Chanana
     
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine
     England

     @EMDidactic


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