Acute Endocrinology in Critical Care: A Comprehensive Review for Residents
Abstract
Endocrine emergencies represent a significant proportion of
critical illness presentations in intensive care units (ICUs) and require
prompt recognition and management to prevent adverse outcomes. This review
provides critical care residents with an evidence-based approach to the
diagnosis and management of common acute endocrine disorders encountered in the
ICU setting. We discuss diabetic emergencies, thyroid crises, adrenal
insufficiency, pituitary disorders, and electrolyte abnormalities with a focus
on practical management strategies informed by recent literature and clinical
guidelines.
Introduction
Endocrine emergencies constitute a diverse group of
conditions that can precipitate or complicate critical illness. The stress
response to critical illness itself often leads to significant alterations in
endocrine function, creating a complex interplay between primary endocrine
disorders and adaptive or maladaptive responses to severe illness. Critical
care physicians must be adept at recognizing these conditions, understanding
their pathophysiology, and implementing timely interventions to optimize
outcomes.
This review aims to provide a practical framework for the
diagnosis and management of acute endocrine emergencies in the ICU setting,
with a focus on the most commonly encountered conditions and recent
evidence-based approaches to their management.
Diabetic Emergencies
Diabetic Ketoacidosis
(DKA)
Diabetic ketoacidosis remains a common and potentially
life-threatening complication of diabetes mellitus, particularly in type 1
diabetes. While mortality has decreased significantly over the past decades, it
remains an important cause of morbidity and ICU admission.
Pathophysiology
DKA results from absolute or relative insulin deficiency
coupled with increased counterregulatory hormones (glucagon, catecholamines,
cortisol, and growth hormone), leading to hyperglycemia, ketogenesis, and
metabolic acidosis. Critical illness can precipitate DKA through stress-induced
counterregulatory hormone release and inflammatory cytokines that enhance
insulin resistance.
Diagnosis
The diagnostic criteria for DKA include:
- Hyperglycemia (glucose >250 mg/dL, though
"euglycemic DKA" can occur with lower glucose levels, particularly in
patients on SGLT2 inhibitors)
- Metabolic acidosis (pH <7.3, bicarbonate <18 mEq/L)
- Ketonemia or ketonuria
Laboratory assessments should include:
- Complete blood count (CBC)
- Comprehensive metabolic panel
- Blood glucose
- Serum ketones (β-hydroxybutyrate is preferred over
acetoacetate)
- Arterial blood gas
- Urinalysis
- Cultures and imaging as indicated to identify
precipitating causes
Management
The cornerstone of DKA management follows these principles:
- Potassium:
Replete when serum potassium <5.2 mEq/L to maintain levels between 4-5 mEq/L
- Phosphate:
Consider replacement for severe hypophosphatemia (<1.0 mg/dL)
- Magnesium:
Maintain normal levels
Hyperosmolar
Hyperglycemic State (HHS)
HHS typically affects elderly patients with type 2 diabetes
and is characterized by severe hyperglycemia, hyperosmolality, and severe
dehydration without significant ketoacidosis.
Diagnosis
Diagnostic criteria include:
- Plasma glucose >600 mg/dL
- Serum osmolality >320 mOsm/kg
- Absence of significant ketosis/ketoacidosis
- Profound dehydration
Management
Management principles are similar to DKA but with several
important distinctions:
1. Fluid Resuscitation: More aggressive fluid replacement is
often required due to more severe dehydration. Initial crystalloid selection
should be guided by serum sodium (corrected for hyperglycemia).
2. Insulin Therapy: Lower insulin doses are typically needed
compared to DKA. Starting at 0.05-0.1 units/kg/hr is appropriate, with a focus
on gradual glucose reduction (50-75 mg/dL/hr) to avoid rapid osmolar shifts and
cerebral edema.
3. Thromboprophylaxis: HHS carries a high risk of thrombotic
complications; early initiation of prophylactic anticoagulation is recommended
unless contraindicated.
Hypoglycemia in the
ICU
Iatrogenic hypoglycemia remains a significant concern in critically
ill patients, particularly during intensive insulin therapy. Hypoglycemia is
independently associated with increased mortality in ICU patients.
Management
Treatment principles include:
- IV dextrose 50% (25g) for severe hypoglycemia
- Continuous glucose infusion may be required for prolonged
hypoglycemia, particularly with long-acting insulin or sulfonylurea overdose
- Octreotide may be useful in sulfonylurea-induced
hypoglycemia
Current guidelines recommend targeting blood glucose levels
between 140-180 mg/dL in most critically ill patients, as this range balances
the risks of hyperglycemia with those of hypoglycemia.
Thyroid Emergencies
Thyroid Storm
Thyroid storm represents the extreme manifestation of
thyrotoxicosis and is associated with significant mortality (10-30%) even with
optimal treatment.
Diagnosis
Clinical diagnosis is based on the presence of severe
thyrotoxicosis with evidence of systemic decompensation:
- Hyperthermia
- Tachycardia out of proportion to fever
- Central nervous system effects (agitation, delirium,
psychosis, coma)
- Gastrointestinal dysfunction (nausea, vomiting, diarrhea)
- Cardiovascular dysfunction (heart failure, hypotension)
The Burch-Wartofsky Point Scale can help assess the
probability of thyroid storm.
Management
Treatment must be initiated based on clinical suspicion
without waiting for laboratory confirmation:
1. Anti-thyroid drugs: Thionamides block new hormone
synthesis.
- Propylthiouracil
(PTU): 600-1000 mg loading dose, then 200-250 mg every 4 hours
- Methimazole:
60-80 mg loading dose, then 20-30 mg every 6 hours
- PTU is preferred
initially due to additional inhibition of peripheral T4 to T3 conversion
2. Iodine solutions: Inhibit thyroid hormone release
(Wolff-Chaikoff effect)
- Start 1 hour
after thionamides to prevent iodine utilization for increased hormone synthesis
- Lugol's solution
(8 drops q6h) or potassium iodide (5 drops q6h)
3. Beta-blockers: Control adrenergic symptoms
- Propranolol 60-80
mg orally every 4-6 hours or 1-2 mg IV q4h
- Esmolol infusion
is an alternative for better titration in hemodynamically unstable patients
4. Glucocorticoids: Inhibit peripheral conversion of T4 to
T3 and treat potential relative adrenal insufficiency
- Hydrocortisone
100 mg IV q8h or dexamethasone 2-4 mg IV q6h
5. Supportive care:
- Aggressive
cooling for hyperthermia
- Fluid
resuscitation
- Nutritional
support
- Treatment of
precipitating cause
Plasma exchange or plasmapheresis may be considered in
refractory cases unresponsive to conventional therapy.
Myxedema Coma
Myxedema coma is a rare but life-threatening manifestation
of severe hypothyroidism with mortality rates of 20-50%.
Diagnosis
Clinical features include:
- Altered mental status
- Hypothermia
- Bradycardia
- Hypoventilation
- Non-pitting edema
- Delayed relaxation of deep tendon reflexes
Laboratory findings typically show:
- Elevated TSH (except in secondary hypothyroidism)
- Low free T4 and T3
- Hyponatremia
- Hypoglycemia
- Hypercapnia
Management
1. Thyroid hormone replacement:
- Levothyroxine
(T4): 300-500 μg IV loading dose, followed by 50-100 μg IV daily
- Consider adding
liothyronine (T3) in patients with cardiovascular compromise: 5-20 μg IV q8h
2. Glucocorticoids:
- Hydrocortisone
100 mg IV q8h until coexisting adrenal insufficiency is ruled out
3. Supportive care:
- Passive rewarming
(aggressive rewarming can cause vasodilation and cardiovascular collapse)
- Cautious fluid
resuscitation
- Correction of
electrolyte abnormalities
- Ventilatory
support as needed
- Treatment of
precipitating factors
Adrenal Emergencies
Adrenal Crisis
Adrenal crisis is a life-threatening emergency characterized
by circulatory collapse and electrolyte abnormalities resulting from glucocorticoid
deficiency.
Diagnosis
Clinical features include:
- Hypotension refractory to fluids
- Abdominal pain, nausea, vomiting
- Fever
- Altered mental status
- Hyperpigmentation (in primary adrenal insufficiency)
Laboratory findings:
- Hyponatremia
- Hyperkalemia (primarily in primary adrenal insufficiency)
- Hypoglycemia
- Eosinophilia
- Elevated BUN/creatinine
Diagnosis is confirmed with random cortisol and ACTH levels,
followed by ACTH stimulation test once the patient is stabilized. However, treatment
should not be delayed pending test results.
Management
1. Glucocorticoid replacement:
- Hydrocortisone
100 mg IV bolus, followed by 50-100 mg IV q6-8h or continuous infusion of
200-300 mg/24h
- Transition to
oral replacement when patient is stable
2. Fluid resuscitation:
- Normal saline 1-2
L in the first hour, followed by continuous infusion guided by hemodynamic
parameters
3. Vasopressors:
- May be required
despite adequate fluid and steroid replacement
- Norepinephrine is
generally preferred
4. Electrolyte management:
- Correct
hypoglycemia with dextrose
- Monitor and
correct electrolyte abnormalities
5. Mineralocorticoid replacement:
- Generally not needed
during acute crisis management (high-dose hydrocortisone provides sufficient
mineralocorticoid effect)
- Add
fludrocortisone 0.1 mg daily once hydrocortisone doses are below 50 mg/day in
primary adrenal insufficiency
Critical
Illness-Related Corticosteroid Insufficiency (CIRCI)
CIRCI refers to inadequate corticosteroid activity relative
to the severity of a patient's illness, resulting from dysfunction at any level
of the hypothalamic-pituitary-adrenal (HPA) axis.
Diagnosis
The diagnosis remains challenging due to:
- Variable cortisol cutoffs in different studies
- Effects of hypoalbuminemia on total cortisol measurements
- Variable cortisol response in different critical illnesses
The 2017 guidelines of the Society of Critical Care Medicine
(SCCM) and European Society of Intensive Care Medicine (ESICM) suggest:
- Delta cortisol <9 μg/dL after cosyntropin 250 μg AND
- Random total cortisol <10 μg/dL
However, these criteria remain controversial, and clinical
judgment is essential.
Management
The use of corticosteroids in CIRCI remains controversial
and should be guided by specific clinical scenarios:
1. Septic shock:
- Consider
hydrocortisone 200-300 mg/day in divided doses or continuous infusion for
patients with refractory shock despite adequate fluid resuscitation and
vasopressor support
- Continue for 7
days or until vasopressors are discontinued
2. ARDS:
- Consider
methylprednisolone in moderate to severe ARDS
- Initial dose 1
mg/kg/day, followed by gradual taper
3. Post-cardiac surgery vasoplegic shock:
- Hydrocortisone
may reduce vasopressor requirements and ICU length of stay
The ADRENAL trial (2018) showed no mortality benefit but
faster shock resolution with hydrocortisone in septic shock, while the
APROCCHSS trial (2018) demonstrated reduced mortality with the combination of
hydrocortisone and fludrocortisone.
Pituitary Emergencies
Pituitary Apoplexy
Pituitary apoplexy is a medical emergency resulting from
sudden hemorrhage or infarction of the pituitary gland, often within a
pre-existing adenoma.
Diagnosis
Clinical features include:
- Sudden onset of severe headache
- Visual disturbances (visual field defects, reduced acuity,
ophthalmoplegia)
- Altered mental status
- Signs of meningeal irritation
- Features of hypopituitarism
Diagnosis is confirmed with urgent MRI showing hemorrhage or
infarction in the pituitary gland.
Management
1. Hormonal replacement:
- Hydrocortisone
100 mg IV q6-8h (priority - adrenal crisis can be life-threatening)
- Thyroid hormone
replacement if secondary hypothyroidism is present
2. Neurosurgical evaluation:
- Urgent
decompression may be needed for severe visual impairment or declining
consciousness
3. Supportive care:
- Fluid and
electrolyte management
- Correction of
other hormonal deficiencies once stabilized
Syndrome of
Inappropriate ADH Secretion (SIADH)
SIADH is a common cause of hyponatremia in critically ill
patients and is characterized by inappropriate release of vasopressin leading
to water retention.
Diagnosis
Diagnostic criteria include:
- Hypotonic hyponatremia (serum Na⁺ <135 mEq/L)
- Decreased serum osmolality (<275 mOsm/kg)
- Inappropriate urine concentration (urine osmolality
>100 mOsm/kg)
- Elevated urine sodium (>30 mEq/L with normal salt
intake)
- Normal adrenal, thyroid, and kidney function
- Absence of diuretic use or significant hypovolemia
Management
1. Mild asymptomatic hyponatremia (Na⁺ >125 mEq/L):
- Fluid restriction
(800-1000 mL/day)
2. Moderate symptomatic hyponatremia (Na⁺ 120-125 mEq/L):
- Fluid restriction
- Consider
vasopressin receptor antagonists (vaptans) in chronic cases
3. Severe symptomatic hyponatremia (Na⁺ <120 mEq/L) or
neurological symptoms:
- Hypertonic saline
(3%) 100-150 mL over 10-20 minutes, may repeat 2-3 times
- Target correction
rate: 4-6 mEq/L in first 24 hours to avoid osmotic demyelination syndrome
- Consider
continuous infusion with frequent electrolyte monitoring
4. Treat underlying cause when identified
Electrolyte Disorders
in Endocrine Emergencies
Hypercalcemia
Severe hypercalcemia (Ca²⁺ >14 mg/dL) represents a
medical emergency requiring ICU admission. Common causes in the ICU include
malignancy, primary hyperparathyroidism, and medication effects.
Management
1. Aggressive hydration:
- Normal saline
200-300 mL/hr initially, then adjusted based on volume status
- Enhances
calciuresis
2. Loop diuretics:
- Once adequately
hydrated, furosemide 20-40 mg IV q2-4h
- Increases renal
calcium excretion
3. Bisphosphonates:
- Zoledronic acid 4
mg IV over 15-30 minutes
- Onset of action
within 24-48 hours
4. Calcitonin:
- 4 IU/kg SC/IM
q12h
- Rapid but
temporary effect (48-72 hours)
- Useful as bridge
therapy
5. Glucocorticoids:
- Effective
primarily in vitamin D-mediated or granulomatous causes
- Hydrocortisone
200-300 mg/day or equivalent
6. Dialysis:
- Consider in
refractory cases or renal failure
Hyponatremia
Hyponatremia is the most common electrolyte disorder in
hospitalized patients and is associated with increased mortality.
Management
Management depends on the etiology, severity, and
chronicity:
1. Severe symptomatic hyponatremia (Na⁺ <120 mEq/L with
neurological symptoms):
- Hypertonic saline
(3%) boluses: 100 mL over 10 minutes, repeat up to 3 times as needed
- Target increase:
4-6 mEq/L in first 24 hours
- Maximum
correction rate: 8-10 mEq/L in 24 hours and 18 mEq/L in 48 hours
- Frequent
monitoring (every 2-4 hours)
2. Chronic hyponatremia (>48 hours):
- More conservative
correction to avoid osmotic demyelination syndrome
- Target increase:
<8 mEq/L in 24 hours
3. Hypervolemic hyponatremia:
- Fluid restriction
- Diuretics
- Treatment of
underlying cause (heart failure, cirrhosis)
- Consider vaptans
in appropriate patients
4. Hypovolemic hyponatremia:
- Isotonic saline
to restore volume status
- Treatment of
underlying cause
Glucose Control in
the ICU
Glycemic management remains a cornerstone of critical care.
Following the publication of the NICE-SUGAR trial, which demonstrated increased
mortality with intensive glucose control (81-108 mg/dL) compared to
conventional control (<180 mg/dL), most guidelines now recommend targeting
blood glucose levels between 140-180 mg/dL in critically ill patients.
Insulin Protocols
- Computer-guided or nurse-driven protocols based on
frequent monitoring improve glycemic control
- Subcutaneous insulin regimens are appropriate for stable
patients tolerating enteral nutrition
- Continuous insulin infusions are preferred for:
- Diabetic
emergencies
- NPO status or
variable nutritional intake
- Hemodynamic
instability
- Liver failure
- Significant
insulin resistance
Special
Considerations
1. Enteral nutrition interruptions:
- Reduce insulin
doses by 50-80% when feeds are interrupted
- Consider dextrose
infusion during prolonged interruptions
2. Steroid therapy:
- Significant
hyperglycemia may develop even in non-diabetic patients
- Insulin
requirements often increase dramatically
- Consider separate
"steroid-specific" insulin dosing
3. Continuous Renal Replacement Therapy (CRRT):
- May reduce
insulin requirements due to clearance of counterregulatory hormones
-
Dextrose-containing replacement fluids may increase glucose levels
Conclusion
Endocrine emergencies in critical care require prompt
recognition and management to optimize outcomes. A systematic approach to
diagnosis and treatment, coupled with awareness of recent evidence and
guidelines, allows critical care physicians to effectively manage these complex
conditions. Future research focusing on individualized approaches to hormone
replacement and targeted therapies holds promise for further improving outcomes
in critically ill patients with endocrine disorders.
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