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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 - PowerPoint PPT Presentation
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ICU Grand RoundsAugust 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– 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
What do You want now?
• Physical Exam
Dehydrated
• Laboratory Exam
– Posm 262
– Uosm 460
– UNa 106
– UrineK <10
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 HyponatremiaSIADH
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
• HypoAdrenal1. 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
Differential diagnosis of adrenal insufficiency - ACUTE
• 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 - CHRONIC
• 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
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