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ICU Grand Rounds August 8th, 2003. Dr. G Alvarez Dr. B. Cartwright. Hypo Na: Not SIADH!. Case Presentation. 29 y.o. Irish Tourist arrived Sydney 28/7/03 “cold” resolving over a week before flight dry cough, rhinorrhea, itchy eyes driving from airport, vomited twice
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ICU Grand RoundsAugust 8th, 2003 Dr. G Alvarez Dr. B. Cartwright
Case Presentation • 29 y.o. Irish Tourist arrived Sydney 28/7/03 • “cold” resolving over a week before flight • dry cough, rhinorrhea, itchy eyes • driving from airport, vomited twice • stayed @ home most of day and slept
Case Presentation • 29/7:walking around Opera house and gardens • slept on grass, anorexic, lethargy, light headed • saw MD @ Martin place, BP 95/60 • that evening, witnessed TC seizure for 2 min • Emergency • GCS 10, BP 97/66, P92 sinus, T 36 39C • delirious and combative
Case Presentation • Emergency • Given Ceftriaxone 2gm IV, NS @ 250/hr • CT head Normal • ABG: 7.44/34 co2 /84 o2 /23 ho3 • Toxic screen negative • hgb 122, wbc 2.86, plt 186, • Na 112, Cl 76. • LFT/Ca/Po4/glc/Cr/Coag/ESR N
Physical Exam Dehydrated Laboratory Exam Posm 262 Uosm 460 UNa 106 UrineK <10 What do You want now?
Case Presentation • 30/7 @ 0730 • Intubated b/c GCS 7, hypotensive • 30/7 @0900 • I thought she was dehydrated • volume and eventually Noradrenaline • correct Na to “safe” range 120mmol/L • correct 120 to 140 over 48hours • aim 10mmol/L first 24 hours • gave her 200mg hydrocortisone, then 100mg q6
Case Presentation • EEG • generalized delta wave slowing • minimal activity 2nd to sedation? • NO seizure activity • Lumbar puncture • Normal glucose and protein • No wbc or rbc seen • started on Ceftriaxone and Acyclovir
Case Presentation • PiCCO inserted • CI 5.05 • SVRI 1072 • ITBVI 695 NorAD @ 0.08ug/kg/min • EVWLI 10 • MAP 75 • FiO2 25%
SO, what do you think now? • I spoke with patient on medical floor • April/2000 admitted to Cairns Hospital with diagnosis of viral gastroenteritis • malaise, N/V, fever, arthralgias and myalgias • Cuts her vacation short and returns to Ireland
The 3 years before her return • Over the next year • crampy stomach pain, N/V and diarrhoea • anorexia, wt loss and weakness • postural dizziness and low BP • GI Physician: endoscopy showed reflux esophagitis, IBS and Rx PPI • “I craved salty foods like bacon and chips” • “people told me I really kept my tan a long time”
Back to the case • Random am Cortisol: 43! (155-599) • ACTH 536 (0-50) • Neurology involved, wanted MRI b/c poor pupils reflex and didn’t know what was going on? • Normal MRI
The rest of the tests • TSH, free T4 Normal • Troponin 0.5 • Procalcitonin 17.3 (I stopped Ab and acyclovir) • CSF viral PCR negative • Legionella, Chlamydia, Mycoplasma serology
The happy end of the story • Extubated the next day to room air • Still delirious but improved each day • Transferred to ward Day 3 • Switched to oral steroid and mineralcorticoid replacement • Discharged home august 8th, 2003
Lets talk Low Sodium • Figure out Volume status? • Order Urine Osm, electrolytes and Posm • Euvolemic Hyponatremia SIADH polydipsia (Uosm <80) post-surgical, narcotics or sedatives Endocrine: hypothyroid and hypoadrenal
Why does endocrine failure cause low Na? • HypoThyroid • Cardiac output and GFR • ADH secretion to hemodynamic stimulus • HypoAdrenal 1. ADH (a) indirectly 2nd volume depletion (b) directly b/c co-secreted with CRF 2. mineralcorticoids
Distributive Shock • Septic • Hyperdynamic not hypodynamic • Neurogenic • Anaphylaxis • Hypoadrenal • All characterised by low systemic vascular resistance and low filling pressures
Hypothalamic-pituitary-adrenal axis • copes with stresses such as infections, hypotension, and surgery • anterior pituitary amplifies requests from the hypothalamus • likewise the adrenal cortex responds to corticotropins to produce cortisol • negative feedback system
Cortisol • 5-10% free; rest bound to binding globulin • role in • metabolism CHO, protein • secretion of adrenal androgen/aldosterone • immune response • negative feedback control of: • corticotropin, CRH, ADH by glucocorticoid Rcs
Adrenal Insufficiency • Primary versus Secondary • Abrupt versus slow onset • Abrupt primary more likely to occur in the ICU setting such as adrenal haemorrhage or necrosis with sepsis
PRIMARY adrenal haemorrhage, necrosis or thrombosis occurs in sepsis, coagulopathy and antiphospholipid syndrome post-adrenal surgery for Cushing’s SECONDARY postpartum pituitary necrosis (Sheehan) bleed into pituitary adenoma head trauma with pituitary injury Differential diagnosis of adrenal insufficiency - ACUTE
Primary autoimmune TB adreno-myeloneuropathy systemic fungal infections AIDS metastatic carcinoma isolated deficiency Secondary pituitary tumour craniopharyngioma pituitary surgery lymphocytic hypophysitis empty sella syndrome hypothalamic syndrome long term steroids Differential diagnosis of adrenal insufficiency - CHRONIC
Addison’s disease • In 1855, Thomas Addison described the clinical syndrome of adrenal insufficiency • In his 43-page monograph, "On the Constitutional and Local Effects of Disease of the Suprarenal Capsules," Addison [15] described 10 cases marked by "anemia . . . feebleness of the heart action . . . a peculiar change of color in the skin occurring in connection with a diseased condition of the 'suprarenal capsules'."
Addison’s disease • rare, may occur at any age, and affects both sexes equally • Must involve >90% of adrenal glands • Previously caused by chronic granulomatous infections such as TB but majority now autoimmune related idiopathic atrophy • Some also have antibodies to thyroid, parathyroid, and/or gonadal tissue • increased incidence of chronic lymphocytic thyroiditis, premature ovarian failure, type 1 diabetes mellitus, and hypo- or hyperthyroidism • Two or more of above = polyglandular autoimmune syndrome
Primary adrenalinsufficiency • destruction of the adrenal cortex • medulla is usually spared • but synthesis of adrenaline in the adrenal medulla depends on the presence of high local cortisol concentrations
Primary adrenalinsufficiency • Presentation • tiredness, weakness, depression • Commonly misdiagnosed as chronic fatigue syndrome • anorexia, weight loss (parents thought Anorexia nervosa!) • dizziness, orthostatic hypotension • nausea, vomiting, diarrhoea • hyponatraemia, hyperkalaemia, hypoglycaemia, anaemia, lymphocytosis, eosinophilia • hyperpigmentation, vitiligo
Adrenal Insufficiency in ICU • Need to consider if vasopressor resistant shock with any other features on history or exam as given above • Especially if associated with abdominal pain, vomiting, confusion, hypotension, typical electrolyte changes and no apparent source of infection • A plasma cortisol of <25 is diagnostic but need to investigate further if <150mcg/dL
Further tests to investigate a low serum cortisol • ACTH, CRH levels • Adrenal antibody levels • Stimulation response tests • Will localise pathology along hypothalamic-pituitary-adrenal axis
Management in ICU • Identify cause • Replacement steroids: hydrocortisone 200-300mg over the course of the first 24hours • Correct hypovolaemia and hyponatraemia with isotonic saline • Supplemental glucose
Long term management • Symptomatic adrenal insufficiency: Glucocorticoid replacement in the morning, titrated to urinary cortisol levels to reduce side effect profile • Primary adrenal insufficiency: aldosterone replacement with fludrocortisone • MedicAlert bracelet + carry steroids for injury / stress / febrile illness
“Sepsis-induced adrenal deficiency syndrome” • Adrenal insufficiency in septic shock • Occurs but definition, prevalence and characteristics remain controversial • Mechanism = mix of: Corticotropin resistance versus reduced glucocorticoid synthesis • Studies have shown • a low serum cortisol response to ACTH is associated with a longer length of stay and more severe organ dysfunction • Nonsurvivors of severe sepsis had lower basal plasma cortisol concentrations
Steroid replacement • a short corticotropin test at presentation in septic patients can help identify those with relative adrenal insufficiency • low-dose glucocorticoids reduce mortality rates and the need for vasopressor agents. • Precisely which patients, how much steroid and other treatment/s is still unclear