Addisonian Crisis (Acute Adrenal Insufficiency)
Definition
Addisonian crisis, or acute adrenal insufficiency, is a relative or absolute deficiency of adrenal corticosteroid hormones resulting in hemodynamic or other compromise.
Etiology
Primary adrenal insufficiency (Addison disease)
Secondary adrenal insufficiency (pituitary disease)
Failure of hormone synthesis
Etomidate inhibits adrenal corticosteroid synthesis (should be used with caution in critically ill patients)
Typical Situations
Patients who have primary or secondary adrenal insufficiency
Abrupt termination of steroid therapy
Patients with a recent history of steroid therapy who are stressed by major surgery or perioperative infections
Septic patients unresponsive to vasopressor therapy
Prevention
Administer preoperative corticosteroids to any patient who has received adrenal suppressive doses of corticosteroids (more than 5 mg/day, for more than 3 weeks, of prednisone or equivalent) within the year prior to surgery
Major surgery or stress:
Hydrocortisone IV, 100 mg prior to induction of anesthesia, followed by 200 to 300 mg/day in divided doses
Minor surgery or stress:
Hydrocortisone IV, 50 mg prior to induction of anesthesia, followed by 100 to 200 mg/day in divided doses
Identify patients with primary or secondary adrenal insufficiency
Have a high index of suspicion for adrenal insufficiency in patients with significant systemic diseases that are often treated with corticosteroids (e.g., connective tissue diseases, asthma)
Careful communication with patients to identify steroid use before surgery
Manifestations
Onset may be acute or delayed to the postoperative period.
Hypotension or shock refractory to treatment with fluids and vasopressors
Hyponatremia, hyperkalemia, and hypoglycemia
Nausea and vomiting
Similar Events
Septic shock (see Event 13, The Septic Patient )
Anaphylaxis (see Event 16, Anaphylactic and Anaphylactoid Reactions )
Hypotension secondary to other etiologies (see Event 9, Hypotension )
Patients on antihypertensive medications (e.g., ACEI)
Management
If hypotension or cardiovascular collapse occurs in the patient at risk of adrenal insufficiency
Rapidly expand circulating fluid volume (crystalloid and/or colloid)
Administer hydrocortisone IV, 100 mg bolus, repeat q8 h
Replace Na + using normal saline (NS)
Replace K + if hypokalemic (see Event 42, Hypokalemia )
Administer dextrose to correct hypoglycemia if present (see Event 41, Hypoglycemia )
Hemodynamic support with vasopressors, inotropes as necessary
Ephedrine IV, 5 to 20 mg, escalate as necessary
Phenylephrine IV, 100 to 200 µg, escalate as necessary
Epinephrine IV, 5 to 20 µg, escalate as necessary
Identify and treat underlying causes of adrenal insufficiency if possible
Ensure that other more likely etiologies of hypotension and shock are not responsible for hypotension
Hypovolemia (see Event 1, Acute Hemorrhage , and Event 9, Hypotension )
Anesthetic or drug overdose (see Event 72, Volatile Anesthetic Overdose )
Primary cardiovascular impairment (see Event 15, Acute Coronary Syndrome , and Event 20, Pulmonary Edema )
High intrathoracic pressure (see Event 7, High Peak Inspiratory Pressure )
Anaphylaxis (see Event 16, Anaphylactic and Anaphylactoid Reactions )
If no response to hydrocortisone and IV fluid administration
TEE or TTE to assess myocardial filling and function
Laboratory studies
Plasma electrolytes and glucose
Baseline cortisol and adrenocorticotropic hormone (ACTH) levels (ideally draw before administering hydrocortisone, but if hypotension is life-threatening, do not delay therapy)
Suspect adrenal crisis in older patients who remain vasopressor dependent after surgical procedures despite adequate volume resuscitation
Complications
Refractory hypotension
Organ hypoperfusion/dysfunction
Cardiac arrest
Complications of steroid therapy (e.g., hyperglycemia)
Suggested Reading
Diabetic Ketoacidosis
Definition
Diabetic ketoacidosis (DKA) is a metabolic acidosis associated with hyperglycemia and high levels of ketoacids in the blood and urine of the diabetic patient.
Etiology
An absolute or relative deficiency of insulin, causing mobilization and oxidation of fatty acids with resulting production of ketoacids
Typical Situations
In patients with insulin-dependent diabetes mellitus
When an appropriate insulin dose has been administered but the patient’s insulin requirements are increased because of
Trauma
Concurrent infection
Excessive fluid losses or inadequate fluid intake
Increased catabolic stress
An absolute deficiency of insulin
Inadequate insulin dose administered
Delayed absorption of SC insulin due to poor peripheral perfusion
Prevention
Prevention of DKA, rather than prevention of hyperglycemia, is the primary aim of surgical care of the diabetic patient.
Identify insulin-dependent patients preoperatively and optimize therapy
The appropriate perioperative insulin regimen must be based on prior insulin requirements, the patient’s history, the timing of surgery, and frequent measurements of blood glucose
Most insulin-dependent patients should receive some insulin on the day of surgery
Maintain euglycemia or mild hyperglycemia during anesthesia and surgery; the goal is 100 to 180 mg/dL
Treat infections early and aggressively with antibiotics
Replace fluid losses or treat dehydration aggressively
Manifestations
The conscious patient may complain of nausea, vomiting, hunger, abdominal pain, sweating, or demonstrate confusion and/or altered level of consciousness
Hypovolemia
Hypotension
Tachycardia
Metabolic acidosis with increased anion gap
Hyperventilation (Kussmaul breathing) to compensate for metabolic acidosis
Polyuria or oliguria depending on the patient’s underlying fluid volume status
Similar Events
Other forms of metabolic acidosis (see Event 46, Metabolic Acidosis )
Hyperosmolar hyperglycemic nonketotic syndrome
Hypovolemia from other causes (see Event 9, Hypotension )
Abdominal pain from other causes
Hyperglycemia from other causes
Management
Confirm the diagnosis
Obtain blood and urine samples for
ABGs
Serum glucose
Serum ketoacids
Serum lactate
Serum electrolytes (including PO 4 3 − , Mg 2 + )
Serum creatinine and BUN
Plasma osmolality
CBC with differential
Urine ketoacids
Troponin
Blood cultures
Ensure adequate oxygenation and ventilation
Intubate the trachea if the patient is obtunded or if respiratory distress is present
Expand the circulating fluid volume
Administer 500 to 1000 mL of crystalloid
Additional fluid administration should be based on the patient’s response
Average fluid deficit is 3 to 6 L
If the patient has CAD, CHF, or renal failure, place an arterial line and consider a CVP catheter to assess/monitor filling pressures and fluid responsiveness, and to guide fluid management
Begin insulin therapy
Administer regular insulin IV, 10 units
Initiate an IV infusion of regular insulin at 5 to 10 units/hr
Avoid SC insulin administration as absorption through this route is variable
Administer NaHCO 3 only for profound acidosis (pH below 7.1) (see Event 46, Metabolic Acidosis )
Repeat measurements of serum glucose, electrolytes, and ABGs q1 – 2h until the values normalize
When blood glucose reaches 250 to 300 mg/dL
Consider adding glucose to IV solutions
Reduce insulin infusion rate, but continue infusion until anion gap normalizes
Replace K + deficit once urine output is ensured (see Event 42, Hypokalemia )
Most patients with DKA have a large total body K + deficit
Replace PO 4 3 − , Mg 2 + as indicated by laboratory measurements
Treat underlying etiology (infection, sepsis, MI, etc.)
Consult an internist or endocrinologist to assist in the patient’s perioperative management
Consider briefly delaying urgent surgery to adequately resuscitate the patient
Cancel elective procedure
Complications
Hypotension
Hypoglycemia
Hypokalemia
Hyperkalemia
Pulmonary edema
Thrombotic events
Suggested Reading
Hyperkalemia
Definition
Hyperkalemia is a serum K + level > 5.5 mEq/L.
Etiology
Excessive intake
Excessive parenteral or oral K + supplements
Massive blood transfusion
Administration of hyperkalemic cardioplegia solution
Inadequate excretion of K +
Renal failure
Adrenal insufficiency
K + -sparing diuretics
Administration of ACEIs (indirectly reduces the secretion of aldosterone)
Shift of K + from the tissues to the plasma
Extensive tissue damage (muscle crushing injury, hemolysis, internal bleeding)
Administration of succinylcholine (in patients with renal failure, acute SCI, upper motor neuron disorders, prolonged immobilization, or severe burn injury)
Respiratory or metabolic acidosis
Acute release of K + into the plasma from transplanted organs with a high K + content
Hyperkalemic periodic paralysis
MH
Pseudohyperkalemia usually secondary to mechanical trauma caused by venipuncture
Typical Situations
Major trauma
Aortic cross-clamp release
Cardiac and transplant surgery
During IV K + replacement
Renal failure patients, with or without ongoing renal dialysis
Burn victims
Patients receiving massive transfusion
Rarely in patients receiving epsilon-aminocaproic acid
Prevention
Use appropriate K + replacement protocols for at-risk patients
Avoid succinylcholine in patients susceptible to excessive K + release
Measure serum K + concentration frequently in patients at risk for hyperkalemia
Use continuous ECG monitoring
Administer K + supplements carefully; replace only to physiologic levels
Avoid metabolic or respiratory acidosis
Dialyze hyperkalemic renal failure patients preoperatively
Administer blood products via an appropriate blood-warming device to avoid hemolysis and hyperkalemia
Manifestations
ECG abnormalities and arrhythmias usually seen after serum K + is above 6.5 mEq/L
Tall, peaked T waves
Prolonged PR interval, loss of P waves, or atrial asystole
Complete heart block
Widened QRS complex
Sine wave-type ventricular arrhythmia
VF or asystole
If serum K + rises rapidly, the first sign may be VF or asystole
Skeletal muscle weakness
Similar Events
Sample handling error
Blood sample hemolysis with poor venipuncture technique
In vitro hemolysis in the laboratory
Patients with thrombocytosis or leukocytosis
Transient rise following succinylcholine administration
Management
If ECG changes after induction of anesthesia suggest hyperkalemia
Hyperventilate the patient
Administer CaCl 2 10% IV, 500 to 1000 mg
Stop administration of any K + containing solutions
IV K + replacement
LR IV solution (contains 4.0 mEq/L)
PRBCs
Confirm diagnosis by STAT serum K + measurement
If moderate or severe hyperkalemia (serum K + greater than 6.0 mEq/L)
Increase the blood pH
Hyperventilate the patient unless contraindicated
Administer NaHCO 3 IV, 50 to 150 mEq
Draw blood for an ABG measurement
Treat underlying metabolic acidosis, if present
Administer CaCl 2 10% IV, 500 to 1000 mg
Administer dextrose 50% IV, 50 g, and regular insulin IV, 10 units
Administer inhaled β2-agonist
Albuterol MDI, 6 to 10 puffs
Force a diuresis
Increase fluid administration
Administer loop diuretics IV (e.g., furosemide IV, 5 to 20 mg)
Patient may require a urinary catheter
Obtain emergent nephrologist or internist consultation to institute emergency peritoneal dialysis or hemodialysis
Mild hyperkalemia (serum K + less than 6.0 mEq/L)
Monitor trend in serum K + every 1 to 2 hours and treat aggressively if symptoms persist or levels increase
Administer cation exchange resins by rectal or oral routes
Complications
Arrhythmias
VF
Complications of therapy
Hypokalemia
Alkalosis
Hyperosmolality
Hypoglycemia or hyperglycemia
Dialysis-related problems (vascular access, heparin-related)
Suggested Reading
Hypoglycemia
Definition
Hypoglycemia is a blood glucose level of < 70 mg/dL.
Etiology
Underproduction of glucose
Overutilization of glucose
Impaired gluconeogenesis
Typical Situations
Patients who have inadequate glucose intake
Chronic starvation
Preoperative fasting
Discontinuation of hyperalimentation
Patients who have metabolic diseases
Hormone deficiencies
Enzyme deficiency in the glycogenic pathway
Acquired liver disease
Patients taking drugs that alter glucose metabolism
Oral hypoglycemic agents
Alcohol
Propranolol
Salicylates
Patients with excessive circulating insulin
Insulin administration
Insulinoma
Newborn infants of diabetic mothers
“Dumping syndrome” following upper GI surgery
Prevention
Identify and treat patients at risk of hypoglycemia preoperatively
Optimize the patient’s metabolic status prior to surgery
Measure serum glucose frequently in these patients
Establish a preoperative infusion of a glucose-containing solution in diabetic patients who are receiving insulin
Reduce the patient’s daily insulin dose on the day of surgery
Do not administer oral hypoglycemic agents on the morning of surgery
Continue hyperalimentation in the perioperative period or replace it with a 10% dextrose solution
Manifestations
Hypoglycemia can be masked by general anesthesia or β-blockade .
CNS
In the awake patient:
Altered mental status, irritability, tremulousness
Headache
Lethargy
Seizures
In the anesthetized patient:
Seizures
Failure to awaken from general anesthesia
Sympathetic nervous system stimulation
Hypertension
Sweating
Tachycardia
Cardiovascular collapse is a late sign of hypoglycemia
Similar Events
Light anesthesia
Hypoxemia (see Event 10, Hypoxemia )
TURP syndrome (see Event 43, Hyponatremia and Hypo-osmolality )
Seizures from other causes (see Event 57, Seizures )
Failure to awaken from general anesthesia due to other causes (see Event 55, Postoperative Alteration in Mental Status )
Management
Confirm the diagnosis
Measure blood glucose level STAT
Treat suspected or known hypoglycemia
Therapy for hypoglycemia carries little risk, whereas failure to treat hypoglycemia may be catastrophic
Administer dextrose 50% IV, 1 mL/kg bolus, while waiting for clinical laboratory results
Start a dextrose 10% IV infusion at 1 to 2 mL/kg/hr
Stop or reduce administration of insulin or other drugs that lower blood glucose levels
Monitor serum glucose frequently
Correct underlying metabolic problems
If there is no response to 50% dextrose IV, consider other etiologies for CNS manifestations
Complications
CNS injury
Cardiac arrest
Hyperglycemia and hyperosmolality from excessive glucose administration
Suggested Reading
Hypokalemia
Definition
Hypokalemia is a plasma K + concentration of < 3.0 mEq/L.
Etiology
GI deficiency or loss
Deficient dietary intake
NG suction
GI loss caused by diarrhea, iliostomy drainage, or vomiting
Renal loss
Diuretic therapy
Excess mineralocorticoid or glucocorticoid effect
Renal tubular diseases
Mg 2 + depletion
Cellular shifts
Metabolic or respiratory alkalosis
Insulin effect
Hypokalemic periodic paralysis
Hyperaldosteronism
β 2 -agonists and α-adrenergic antagonists enhance cellular K + entry
Typical Situations
Acute hypokalemia presents a greater threat to patient safety than chronic hypokalemia.
Patients with diarrhea, vomiting, or preparation for large bowel surgery
Patients receiving diuretics, particularly loop diuretics
Following cardiac surgery
Following treatment of hyperkalemia
Hyperventilation
Increased availability of insulin
Elevated β-adrenergic stimulation (e.g., after administration of albuterol and dobutamine)
Prevention
Replacement of K + for patients receiving K + -wasting diuretics
IV replacement of fluids and electrolytes during cathartic preparation for bowel surgery
Monitor serum K + and replace as necessary during and after CPB
Avoid hypomagnesemia
Avoid conditions that reduce serum K + acutely
Hyperventilation
Metabolic alkalosis
β 2 -adrenergic stimulation
Manifestations
Serum K + less than 3.0 mEq/L
Cardiac
ECG abnormalities (unusual until serum K + is less than 3.5 mEq/L)
PVCs
T-wave flattening or inversion
Increased U-wave amplitude
ST segment depression
Tachycardia
Digitalis toxicity may worsen significantly if combined with hypokalemia
AV arrhythmias
Cardiac conduction defects
Cardiac arrest
Neuromuscular
Increased sensitivity to neuromuscular blocking drugs
Skeletal muscle weakness causing
Respiratory failure
Paralysis
Decreased activity of the GI system, with paralytic ileus
Renal
Polyuria
Metabolic alkalosis
Similar Events
Laboratory error
Arrhythmias from other causes
Inadequate reversal of nondepolarizing muscle relaxants
Other causes of ST-T wave abnormalities (see Event 12, ST Segment Change )
Management
If serum K + is greater than 3.0 mEq/L and there are no ECG changes, carefully consider whether or not to proceed with elective surgery prior to K + replacement.
Postpone elective surgery and use oral K + replacement if serum K + is less than 3.0 mEq/L
Oral replacement 20 to 80 mEq/day
For urgent or emergent surgery, if serum K + is less than 3.0 mEq/L, or if the patient is symptomatic
Replace K + by the IV route to achieve a serum K + of at least 3.5 mEq/L before anesthesia induction
Monitor the ECG during the infusion (see Event 40, Hyperkalemia )
Administer through a CVP line, if possible
Infuse no faster than 10 mEq/30 min, except for treatment of life-threatening ventricular arrhythmias in a patient known to be severely hypokalemic
Prevent K + from accumulating in the IV tubing or blood-warming devices
Measure serum K + hourly during rapid administration of K +
In the hypokalemic patient
Be sure that muscle relaxants are fully reversed and that the patient has recovered appropriate neuromuscular function before the trachea is extubated
Measure ABGs if neuromuscular function is slow to recover following surgery
Complications
Residual neuromuscular blockade
Hyperkalemia, myocardial arrhythmias, or cardiac arrest from excessive K + replacement
Pain or thrombophlebitis at IV site from K + replacement through a peripheral IV
Suggested Reading
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