Lecture Pearls by: Faith Armstrong, MD CCM Fellow
The most important thing is to identify these disorders which can potentially be fatal.
Thyroid
- Thyroid Storm
- Stimulated by stressful stimuli (such as being critically ill)
- Presents with delirium, tachycardia, vomiting/diarrhea, fever, dehydration (much like many other illnesses in ICU)
- High mortality
- Multiple etiologies: Graves’, Toxic Nodular Goiters, Thyroiditis (especially post-partum), rarely thyroid malignancies
- Can lead to multiple problems in pregnancy including placental abruption, preeclampsia, preterm delivery, IUGR, stillbirth, fetal goiters, and fetal thyroid dysfunction
- Treatment (be aware of side effect profiles)
- Antithyroid drugs (inhibit synthesis): PTU, methimazole, carbimazole
- B- adrenergic-antagonists (block action of thyroid hormone): e.g. propranolol
- Iodine-containing agents (inhibit release): e.g. Potassium iodide
- Misc (inhibit iodine transport, actions on tissues): e.g. Potassium perchlorate, lithium, steroids
- Myxedema Coma
- Extreme hypothyroidism + precipitating factor (such as critical illness, infection, just about anything including general inflammatory process)
- Disease of progressive MSOF with cardinal sign of progressive mental deterioration
- VERY HIGH MORTALITY (30-60%)
- Incidence of
hypothyroidism during pregnancy is 0.5% (2-3% subclinical)
- At risk for miscarriage, placental abruption, preeclampsia, preterm birth
- Treatment up front is essential
- Can often present with extreme weakness, failure to wean from ventilator
- Other physical findings: Hypotension/bradycardia (late), ileus, hypothermia, hypoventilation, myxedematous face, non-pitting edema
- Treatment: T4 (initially 100-500mcg IV followed by 75-100mcg IV daily until PO therapy), IVF resuscitation, aggressive electrolyte replacement
- Postpartum thyroiditis
- Abnormal TSH within first 12 months postpartum
- 43% present HYPO, 32% present HYPER
- Be aware that in this time period there is a risk for the above thyroid disorders
Glucose-Related Disorders
- DKA
- Severe hyperglycemia, ketosis, hypovolemia (osmotic diuresis), electrolyte abnormalities
- Presentation (may be difficult to identify in the intubated, non-verbal patient): thirst, polyuria, high anion gap, respiratory alkalosis (compensatory), tachypnea, possible complete cardiovascular collapse
- Treatment: ABCs, IV hydration, insulin infusion, electrolyte replacement
- Mortality is age related: <5% in patients younger than 40, as high as 20% in elderly
- Occurs in 1 per 80 months of treatment in insulin pump users
- 2-3% in pregnancy with 10-20% risk of fetal death
- Stress-induced
hyperglycemia
- Leads to impaired wound healing, neuromyopathy, progression to sepsis
- Issues at cellular and molecular level
- Glucose Regulation in
ICU
- NICE-SUGAR Study
- Intensive therapy (glucose levels 81-108 mg/dL)
- May increase mortality, higher incidence
of hypoglycemia
- Association of moderate (41-60 mg/dL) & severe (<41 mg/dL) hypoglycemia with death (not a causal relationship)
- No overall survival benefit with intensive glucose-control
- May increase mortality, higher incidence
of hypoglycemia
- Conventional therapy (recommended) are glucose levels <180 mg/dL
- Intensive therapy (glucose levels 81-108 mg/dL)
- NICE-SUGAR Study
Pituitary Disorders
- Adrenal Insufficiency
- Etiology: Decreased CRH/ACTH or cortisol, dysfunctional receptors, adrenal damage, tissue resistance
- Cortisol effects
- Endocrine: increases blood glucose, inhibits glucose uptake by periphery, increased lipolysis
- Cardiovascular: increased smooth muscle sensitivity to vasopressors
- Immune: anti-inflammatory, reduction in immune cells
- 90% cortisol is bound to CBG with <10% free/active
with short half-life to bind receptors and activate transcription (20% of
genome, inflammatory response)
- When critically ill, decreased CBG levels by 50% lead to increased free cortisol, influx of receptors, and subsequent increased transcription of inflammatory proteins (NF-kB, cytokines, heat shock proteins)
- 10-20% of critically ill affected, up to 60% of those in septic shock
- Usually failure of the HPA axis is reversible
- Recommendation from ACCCM
Task Force
- Change in cortisol after ACTH stim <9ug/dL, random total cortisol <10ug/dL suggestive of AI
- Free cortisol should not be routinely used
- ACTH stim test should not be used in septic shock or ARDS
- Overall, HC treatment in septic shock is favored
- 28 day survival favors treatment with HC in septic shock poorly responsive to IVF/vasopressors
- Vent-free at 28 days in ARDS patients favors treatment
with methylprednisolone (1mg/kg/d)
- Considered before day 14 in those with unresolving ARDS
- Recommendation (2B) is 200mg hydrocortisone/day
- Patients with chronic inflammatory diseases (SLE, RA, UC, COPD) develop systemic inflammation-associated GC resistance
- Pituitary and Pregnancy
(Obstetric patients in the ICU in general have a mortality rate of 10-20%, most maternal deaths were due to a delay in recognition or delay in transfer to ICU)
- Prolactinoma
- Autonomous production of prolactin
- Usually benign
- Increased estrogen can lead to increased size (leading to neurologic issues)
- Tx- dopamine agonist
- Sheehan’s Syndrome
- Ischemia secondary to hypotension associated with 90% infarction of pituitary gland
- Potentially lethal
- HA, nausea/vomiting, vision changes, hemodynamic instability/hypotension, severe hypoglycemia/hyponatremia
- Pituitary apoplexy
- Acute bleeding into gland
- Tx: transphenoidal decompression
- Surviving Sepsis
Campaign Review
- Goals
- MAP >65
- Identify source
- EARLY IV antibiotics
- Resuscitation to normalize lactate (not strong evidence, but some)
- Provide hemodynamic
support
- Crystalloid for initial resuscitation
- Norepinephrine first line pressor (weak evidence for preferred second line pressor)
- Steroids (HC 200mg/day in divided doses)
- Glucose <180mg/dL
- Do not use dopamine for “renal protection”
- Goals
