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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

Monday, February 12, 2018

HypoAdrenal Shock

HypoAdrenal Shock is life-threatening exacerbation of adrenal insufficiency (AI) when an increased hormone demand fails to increase the supply. AI is specifically deficiency of adrenal gland hormone production in the cortex

The adrenal gland is made up of the cortex and medulla producing steroid hormones and catecholamines respectively. The adrenal cortex produces three categories of steroids: 

  • Glucocorticoids (cortisol) from zone fasciculate (Under Hypothalamus/Pitiutary control)
  • Mineralocorticoids (aldosterone) from zona glomerulosa (Under control of RAAS)
  • Gonadocorticoids (sex hormones) from zone reticular (Under Hypothalamus/Pitiutary control)
  • Catecholamines (adrenaline, noradrenaline and dopamine) from adrenal medulla 
Functions of steroid hormones:
GlucocorticoidsCortisol secretion is under control of hypothalmaic-pitiutary axis. Daily cortisol requirement is about 20 mg of hydrocortisone.  Cortisol facilitates (Permissive action of glucocorticoids) the stress response by affecting the heart, vascular bed, water excretion, electrolyte balance, potentiation of catecholamine action, and control of water distribution. It affects metabolism by stimulating glycogenolysis and glyconeogenesis. It is also involved in immunologic/inflammatory responses. 

Mineralocorticoids : Aldosterone secretion is controlled primarily by the renin-angio- tensin system (unlike cortisol) and serum potassium concentration. Aldosterone maintains sodium and potassium plasma concentrations. It regulates extracellular volume and controls sodium and water balance.

Gonadocorticoids: Promote the development of sex characteristics such as axillary and pubic hair and libido.

There are two types of Adrenal deficiency syndromes:

Primary AI (Addison’s disease) i.e. intrinsic adrenal gland dysfunction that results in decreased Glucocorticoids (cortisol), Mineralocorticoids (aldosterone), and sex hormones production. Fortunately, primary AI is a rare disease. Approximately 90% of the gland must be destroyed to manifest symptoms. Autoimmune disorders and infections such as tuberculosis are responsible for most cases of primary adrenal insufficiency. Infiltrative diseases such as amyloidosis, hemosiderosis, Thrombosis and/or haemorrhage (anticoagulation therapy, sepsis, DIC, meningococcemia i.e. Waterhouse-Friderichsen syndrome, APLA) and bilateral metastasis from cancer may also cause primary AI.  

Secondary AI occurs as a result of depressed adrenocorticotropic hormone (ACTH) secretion leading to diminished cortisol production. Aldosterone levels remain normal because of preserved stimulation by both the renin-angiotensin axis and potassium.  Secondary AI results in cortisol deficiency only. Adrenal sex hormone production is also preserved. Intracranial disorders such as brain tumor, pituitary disease, postpartum pituitary necrosis, or major head trauma may affect the hypothalamic-pituitary function may lead to secondary AI. However, the most common cause of secondary adrenal insufficiency is long-term therapy with pharmacologic doses of glucocorticoids. 

Clinical Features 
Primary adrenal insufficiency presents with symptoms of diminished cortisol, aldosterone, and gonadocorticoids, and elevated ACTH, which causes skin hyper pigmentation. Aldosterone deficiency symptoms include dehydration, syncope, salt craving, and hypotension. Gonadocorticoid deficiency symptoms are decreased axillary and pubic hair and decreased libido. Typical Primary AI presents with HypoNa, HyperK, Hypoglycemia, Hypotension.

Secondary adrenal insufficiency presents with symptoms of diminished cortisol (weight loss, lethargy, weakness, confusion, anorexia, GI distress, abdominal pain). Typically secondary AI presents as Hypoglycemia, Hypo/HyperNa, Hypokalemia, Hypotension.

In both primary and secondary AI, cortisol deficiency are seen

Initial set of bloods should include CBC, Basic metabolic panel, renal function and blood cultures. Serum Cortisol sample can also be drawn before administering steroids.  

Serum cortisol >18 mcg/dL generally rules out adrenal insufficiency. 
Serum adrenocorticotropic hormone (ACTH) level measurement also helps differentiate between primary and secondary adrenal insufficiency. A high ACTH level is seen in primary adrenal insufficiency, but ACTH is low in secondary adrenal insufficiency.

  • ABCs
  • IV Fluid Resuscitation (May need dextrose if hypoglycaemic)
  • IV Steroids once circulation is filled (Hydrocortisone 100mg IV)
  • Vasopressors
  • Manage Electrolytes (HyperK, Hypo/HyperNa)
  • Find and treat the underlying ethology
For primary AI, abdominal CT scan may be performed to evaluate the adrenal glands and CXR to assess for lower respiratory tract infections. For secondary adrenal insufficiency, a head CT or MRI, as well as blood tests of pituitary hormones, may be required for further evaluation. 

Take Home:
  • Consider adrenal crisis in situations of unexplained hypotension, especially in patients with a history of glucocorticoid therapy.
  • For a minor illness or injury, triple the daily glucocorticoid dose for 24 to 48 hours until symptoms improve.

Posted by:

     Lakshay Chanana
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine



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