Metabolic Events




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





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





  • 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


  • 1. Schwartz J.J., Akhtar S., Rosenbaum S.H.: Endocrine function. Barash P.G. Cullen B.F. Stoelting R.K. Calahan M. Stock M.C. Clinical anesthesia . 2009. Lippincott Williams & Wilkins Philadelphia: pp. 1289-1291.
  • 2. Coursin D.B., Wood K.E.: Corticosteroid supplementation for adrenal insufficiency. JAMA 2002; 287: pp. 236-240.
  • 3. Jung C., Inder W.J.: Management of adrenal insufficiency during the stress of medical illness and surgery. Med J Aust 2008; 188: pp. 409-413.
  • 4. Connery L.E., Coursin D.B.: Assessment and therapy of selected endocrine disorders. Anesthesiol Clin North Am 2004; 22: pp. 93-123.



  • 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





    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


  • 1. Schwartz J.J., Akhtar S., Rosenbaum S.H.: Endocrine function. Barash P.G. Cullen B.F. Stoelting R.K. Calahan M. Stock M.C. Clinical anesthesia . 2009. Lippincott Williams & Wilkins Philadelphia: pp. 1300.
  • 2. Kitabchi A.E., Umpierrez G.E., Miles J.M., Fisher J.N.: Hyperglycemic crises in adult patients with diabetes. Diabetes Care 2009; 32: pp. 1335-1343.
  • 3. Dagogo-Jack S., George M.M., Alberti K.: Management of diabetes mellitus in surgical patients. Diabetes Spectrum 2002; 15: pp. 44-48.



  • 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


  • 1. Prough D.S., Funston J.S., Svensen C.H., Wolf S.W.: Fluids, electrolytes and acid–base physiology. Barash P.G. Cullen B.F. Stoelting R.K. Calahan M. Stock M.C. Clinical anesthesia . 2009. Lippincott Williams & Wilkins Philadelphia: pp. 313-314.
  • 2. Strom S.: Hyperkalemia. Roizen M.F. Fleisher L.A. Essence of anesthesia practice . 2010. Saunders Philadelphia: pp. 190.
  • 3. Elliott M.J., Ronksley P.E., Clase C.M., Ahmed S.B., Hemmelgarn B.R.: Management of patients with acute hyperkalemia. CMAJ 2010; 182: pp. 1631-1635.
  • 4. Weisberg L.S.: Management of severe hyperkalemia. Crit Care Med 2008; 36: pp. 3246-3251.



  • 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





    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


  • 1. Schwartz J.J., Akhtar S., Rosenbaum S.H.: Endocrine function. Barash P.G. Cullen B.F. Stoelting R.K. Calahan M. Stock M.C. Clinical anesthesia . 2009. Lippincott Williams & Wilkins Philadelphia: pp. 1300.
  • 2. Smiley D.D., Umpierrez G.E.: Perioperative glucose control in the diabetic or nondiabetic patient. South Med J 2006; 99: pp. 580-589.
  • 3. Lipshutz A.K.M., Gropper M.A.: Perioperative glycemic control: an evidence-based review. Anesthesiology 2009; 110: pp. 408-421.



  • 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


  • 1. Prough D.S., Funston J.S., Svensen C.H., Wolf S.W.: Fluids, electrolytes and acid–base physiology. Barash P.G. Cullen B.F. Stoelting R.K. Calahan M. Stock M.C. Clinical anesthesia . 2009. Lippincott Williams & Wilkins Philadelphia: pp. 311-313.
  • 2. Gennari F.J.: Hypokalemia. N Engl J Med 1998; 339: pp. 451-458.
  • 3. Sladen R.N.: Anesthetic considerations for the patient with renal failure. Anesthesiol Clin North America 2000; 18: pp. 863-882.
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    Feb 22, 2019 | Posted by in ANESTHESIA | Comments Off on Metabolic Events
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