Endocrine Flashcards
Acromegaly
Consideration
Goals
Conflicts
Crises
Acromegaly
Considerations
Difficult airway:
Macroglossia & enlarged epiglottis, resulting in difficult bag-mask ventilation & direct laryngoscopy
Recurrent laryngeal nerve palsy, narrow glottic opening, subglottic narrowing (stridor)
Nasal turbinate enlargement; caution with nasal intubation & consider smaller ETT
Multisystem disease:
Cardiovascular:
Hypertension, left ventricular hypertrophy, diastolic dysfunction
Arrhythmias
Coronary artery disease, cardiomyopathy
Respiratory:
Obstructive sleep apnea
Pulmonary hypertension, right ventricular dysfunction
CNS:
Pituitary dysfunction
Potential for raised ICP
Peripheral neuropathies common
Endocrine:
Diabetes mellitus/hyperglycemia
Difficult patient positioning, access, monitoring, regional anesthesia
Radial arterial line contraindicated due to poor collateral circulation
Goals
Safely secure difficult airway: consider awake fiberoptic intubation with stridor & voice changes
Thorough cardiopulmonary examination, including volume status assessment
Conflicts
Avoidance of CPAP following trans-sphenoidal surgery
Post-operative pain vs. enhanced sedation/respiratory depression
Crises
Post-operative stridor (subglottic edema, vocal cord paralysis)
Endocrine emergencies
Diabetes insipidus, SIADH
Adrenocortical Insufficiency (Addisonian crisis)
Background
Considerations
Goals
Medications
Adrenocortical Insufficiency (Addisonian crisis)
Background
Primary Addisonian crisis commonly due to autoimmune destruction of adrenal gland; mineralocorticoid activity also lost
Secondary Addisonian crisis caused by ↓ ACTH production either from hypothalamic pituitary disease or from adrenal suppression from chronic steroids, mineralocorticoid activity usually preserved
Considerations
Potential life-threatening situation: shock, dehydration, hypotension
Physiologic abnormalities:
Cardiovascular:
Impaired myocardial contractility
Arrhythmias secondary to hyperkalemia
Volume status: dehydration can occur (2-3 L)
Electrolyte imbalance
Hyperkalemia
Hyponatremia (↓ level of consciousness, seizures)
Hypoglycemia (↓ level of consciousness, seizures)
Stress dosing of steroids pre-operatively:
Hydrocortisone 100mg IV q6-8h
Fludrocortisone if 1° adrenal insufficiency
Pharmacologic concerns:
↓ circulating catecholamines (consider vasopressin for hypotension)
Succinylcholine-induced hyperkalemia
Goals
Prevent perioperative cardiovascular collapse:
Steroid supplementation
Volume resuscitation
Correction of electrolyte abnormalities
Medications
Hydrocortisone 100mg IV q6-8h for 24h then taper to maintenance of 15-20mg PO qAM & 5-10mg PO qPM
Add maintenance fludrocortisone 0.05-0.2mg PO daily if aldosterone-deficient (1° adrenal insufficiency) when tapering hydrocortisone
Alcoholism
Considerations
Multisystem disease:
Alcohol Withdrawal & Syndromes
Alcoholism
Considerations
Multisystem disease:
CNS: peripheral neuropathy, Wernicke-Korsakoff syndrome (ocular, ataxia, confusion), cerebral atrophy/dementia
Cardiovascular: cardiomyopathy, palpitations, arrhythmias
GI: liver dysfunction/cirrhosis, esophagitis, gastritis, pancreatitis, malnutrition
Heme: pancytopenia
Endocrine/metabolic: hypoglycemia, hypoalbuminemia, electrolyte abnormalities (hypokalemia, hypomagnesemia)
MSK: myopathies, osteoporosis
Other addictions
Altered pharmacology:
Induction of liver enzymes
↑ MAC
Alcohol withdrawal syndromes & need for CIWA protocol (tremors, autonomic hyperactivity, DTs)
Alcohol Withdrawal & Syndromes
Earliest & most common:
Generalized tremors that may be accompanied by perceptual disturbances (nightmares, hallucinations), autonomic nervous system hyperactivity (tachycardia, hypertension, cardiac dysrhythmias), nausea, vomiting, insomnia, & mild confusional states with agitation
Symptoms usually begin within 6 to 8 hours after a substantial ↓ in blood alcohol concentration & are typically most pronounced at 24 to 36 hours
These withdrawal symptoms can be suppressed by the resumption of alcohol ingestion or by administration of benzodiazepines
Delirium tremens:
Occurs in ~5% of those experiencing withdrawal
Symptoms begin 2-4 days after alcohol cessation
Manifests as hallucinations, combativeness, hyperthermia, tachycardia, hypertension or hypotension, & grand mal seizures
Treatment:
First line = benzodiazepines (titrated to effect without loss of respiration)
Beta blockers to reduce tachycardia & hypertension
Fix metabolic abnormalities (potassium, magnesium, & thiamine)
Severe cases will need ICU admission & propofol infusion/dexmedetomidine & possible intubation
Mortality = 10% (usually due to hypotension, dysrhythmias, or seizures)
Wernicke-Korsakoff syndrome:
Wernicke’s encephalopathy:
Loss of neurons in the cerebellum
Acute syndrome requiring emergent treatment to prevent death & neurologic morbidity
Korsakoff’s psychosis:
Chronic neurologic condition
Loss of memory resulting from the lack of thiamine (vitamin B1), which is required for the intermediary metabolism of carbohydrates
Anorexia Nervosa
Considerations
Goals/Optimization
Anorexia Nervosa
Considerations
↓ gastric empyting & aspiration risk
Metabolic & electrolyte abnormalities:
↓Na, ↓K, ↓Mg, ↓PO4
Hypoglycemia
Osteoporosis
Metabolic alkalosis from vomiting
Cardiovascular dysfunction:
Hypovolemia
Cardiomyopathy (LV failure)
Mitral valve prolapse
Arrhythmias: ↑QTc, bradycardia
Autonomic dysfunction
Malnutrition:
Anemia
Thrombocytopenia
Osteoporosis, fracture risk
Risk of re-feeding syndrome
Coexisting psychiatric disease:
Possibly uncooperative
Medications
Goals/Optimization
Minimize aspiration risk: fasted, aspiration prophylaxis
Rule out cardiomyopathy & underlying arrhythmias
Assess functional capacity/ECG/echocardiogram
Fix underlying electrolyte abnormalities
Very careful with glucose management (risk of refeeding syndrome & electrolyte shifts with replacement)
Avoid hypothermia
Careful positioning with osteoporosis
Multidisciplinary management including consultation with internal medicine, endocrinology, psychiatry
Carcinoid
Background
Consideration
Goals
Conflicts
Carcinoid
Background
Carcinoid syndrome presents in approximately 20% of patients with carcinoid tumours, usually with hepatic metastases
“Carcinoid triad”:
Carcinoid heart
Diarrhea
Flushing
Implicated malignancies: neuroendocrine tumors in GI tract (midgut), bronchial tumors
Considerations
Tumor: mass effect, metabolic derangements, medications, & metastases:
Mass effect: hemoptysis, bowel obstruction
Metabolic derangements: flushing, diarrhea, hemodynamic instability, bronchospasm (serotonin-related)
Medications: octreotide
Metastases: liver dysfunction, raised ICP if brain metastases
Cardiovascular dysfunction (20-40%):
Right-sided valvular lesions (10% present with left-sided lesions)
Right ventricular dysfunction
Dysrhythmias (eg. SVT)
Constrictive pericarditis
Preparation & treatment of perioperative carcinoid crisis:
Symptoms include flushing, diarrhea, hypotension, hyperglycemia, bronchospasm
Carcinoid tumors can also secrete GH (acromegaly) & ACTH (Cushing’s)
Goals
Prevent, recognize & treat perioperative carcinoid crises
Triggers include:
Histamine-releasing drugs, vasoactive drugs, succinylcholine
Tumour manipulation
Hypovolemia, hypoxia, hypothermia, hypercarbia
Treatment of perioperative bronchospasm:
Avoid beta agonists, theophylline, epinephrine
Responds to:
Octreotide
Steroids
Histamine blockade (diphenhydramine)
Atrovent
Prevention & treatment of carcinoid crisis:
Must prophylax with octreotide 300-500mcg IV
During crisis: octreotide 100mcg IV boluses titrated to effect, or an infusion
H1 antagonists (diphenhydramine 25-50 mg IV)
Refractory hypotension:
Give fluids
USE: octreotide, phenylephrine, vasopressin
AVOID: epinephrine, norepinephrine, ephedrine
Conflicts
RSI (bowel obstruction) vs. titrated induction
RSI vs. need to avoid succinylcholine
Need for deep anesthesia vs. cardiovascular dysfunction
Bronchospasm vs. need to avoid adrenergic agents
Cushing’s syndrome
Considerations
Cushing’s syndrome
Considerations
Possible difficult airway: obesity, obstructive sleep apnea (OSA)
Cardiovascular:
Left ventricular hypertrophy, pulmonary hypertension/right ventricular failure, systolic & diastolic dysfunction
Hypertension, volume overload (↑ renin & glucocorticoid vascular reactivity)
Respiratory: possible OSA
Metabolic:
Hypokalemic metabolic alkalosis: mineralcorticoid effect of glucocorticoids
Diabetes: insulin deficiency
Osteoporosis: need for careful positioning
CNS: possible psychosis
Pharmacologic considerations:
Perioperative steroid replacement (stress dose & post-operative replacement)
Sensitivity to neuromuscular blockers (due to possible muscle weakness, hypokalemia, catecholamines)
Cancer considerations (mass effect, metabolic derangements, metastases, medications) if primary Cushing’s (adrenal adenoma)
Diabetes Insipidus (DI)
Background
Considerations
Treatment
Potential conflicts
Diabetes Insipidus (DI)
Background
Central DI:
↓ secretion ADH
Most often idiopathic or induced by trauma, pituitary surgery, or hypoxic or ischemic encephalopathy
Nephrogenic DI:
Normal ADH secretion but kidneys are resistant to its water-retaining effect
Diagnosis:
Dilute urine (<150 mOsm/L)
Hypernatremia (Na>150)
Hyper-osmolality (>290)
Considerations
Hypernatremia:
Altered level of consciousness, seizures, coma, hyperreflexia
Risk of intracranial hemorrhage with acute, severe hypernatremia
↑ MAC requirements
Volume depletion:
Resuscitate with normal saline initially
Associated conditions:
Neurogenic (pituitary surgery, traumatic brain injury, tumor, idiopathic)
Nephrogenic (chronic renal failure, lithium toxicity, hypercalcemia, hypokalemia, congenital, fluoride toxicity)
Treatment
Consultation with nephrology may be valuable
Treat hypernatremia by estimating water deficit & replacing with free water:
Water deficit = total body water x (Serum Na [ ]/140-1)
Central DI: desmopressin 1-2 mcg IV BID
Nephrogenic DI: hydrochlorothiazide/amiloride
Complications of treatment:
Avoid rapid overcorrection if chronic hypernatremia (goal = <10 mEq/day)
Cerebral edema, water intoxication, volume overload
Potential conflicts
Emergency surgery vs. need for optimization of electrolytes/volume status
Diabetes Mellitus
Considerations
Goals
Crises
Special Populations
Diabetes Mellitus
Considerations
Potential difficult airway (↓TMJ mobility, obesity)
Aspiration risk with gastroparesis
End organ disease:
Hypertension, coronary artery disease, left ventricular hypertrophy & cardiomyopathy
Peripheral vascular disease
Chronic kidney disease
Neuropathy
Autonomic instability
Chronic pain
Perioperative complications & management of blood glucose & medications:
Related to severity of disease & control of blood glucose (hypoglycemia)
DKA or HONK
Hypoglycemia
Related to end organ disease
Goals
Evaluate severity of end organ dysfunction
Perioperative management of elevated blood glucose: Canadian Diabetes Association guidelines suggests 5-10 mmol/L
If only on PO hypoglycemics at home: start IV insulin infusion at 1-2 units/hr
If on insulin at home, divide 24 hr dose by 24 & give 1/2 to 2/3 that per hour as an IV insulin infusion
Consider bolusing a few units up front
Preoperatively (see SAMBA guidelines below):
Type II diabetes, diet controlled: fast, check blood glucose
Type II diabetes, on oral hypoglycemics: fast, hold pills morning of surgery, check blood glucose
Type II diabetes, on insulin: fast, insulin dose depends on type (see below), start D5W infusion
Crises
Hyperglycemia (DKA, HONK)
Hypoglycemia
Special populations
Pregnancy:
↑ risk of DKA, HONK, pregnancy-induced hypertension, difficult airway, aspiration, pre-term labor, cesarean section, polyhydramnios, postoperative infection
For fetus:
Macrosomia (birth trauma, shoulder dystocia, cesarean section, postpartum hemorrhage)
Euglycemic DKA
Background
Considerations
Prevention
Euglycemic DKA
Background
Major adverse event in T2DM (rarely T1) taking SGLT2 inhibitors
Triggered by:
intercurrent illness, surgery, fasting, reduced carbohydrate intake
SGLT2 inhibitors:
Lowers blood glucose by inhibiting renal glucose reabsorption
e.g. canagliflozin, dapagliflozin, empagliflozin
Considerations
Timing: few hours to 6 wks post-op
Risk factors:
Reduced carb intake, volume depletion, concurrent illness, ↑ surgical stress, insulin being held, bariatric surgery, pregnancy
High degree of suspicion for serum/urine ketones
Signs:
Normoglycemia / moderate hyperglycemia
Metabolic acidosis with high anion gap
decreased serum HCO3
Ketonemia &/or ketonuria
Symptoms:
Excessive thirst / urination
Vomiting / dehydration / other sx of hypotension
Altered LOC
Weakness / tiredness / fatigue
Kussmaul respiration (deep, rapid)
Need to hold SGLT2i at least 24 hrs pre-op
Resume >24hrs post-operatively only when adequate PO intake
Prevention
Avoid dexamethasone
Hold SGLT2i at least 24-48 hr pre-op
Resume 24-48hrs post-op assuming normal PO intake
Good post-op pain control
Maintain euvolemia
Hyponatremia
Considerations
Management
Hyponatremia
Considerations
Acute vs. chronic hyponatremia
Central pontine myelinolysis from rapid overcorrection
Physiologic manifestations (severe = neurologic symptoms or < 120 mEq/L):
CNS: ↓ LOC, seizures, cerebral edema, central pontine myelinolysis
Hyper- or hypovolemia
Respiratory arrest
↓ MAC
Etiology:
Hypervolemia:
Congestive heart failure
Hypoalbuminemia (cirrhosis, nephrotic syndrome)
Renal failure
TURP syndrome
Euvolemia:
SIADH (stress, pain, post neurosurgery)
Psychogenic
Hypovolemia:
Cerebral salt wasting
Hemorrhage
Addison’s disease
Peritonitis
Edema from burns
Diarrhea
Diuretics
Management
Correct severe hyponatremia before surgery
Restore volume deficit
Normal saline 20mL/kg IV bolus prn
Restore plasma sodium concentration
Acute:
Generally restrict free water (500mL-1L/day) +/- diuretic
Severe hyponatremia (< 120mEq/L or presence of neurologic symptoms)
Hypertonic saline 3% 1-2 ml/kg/hr until Na>125
Loop diuretics
Sodium bicarbonate (1 mEq/ml) to terminate seizures: 0.5-1mL/kg boluses prn
Chronic: avoid rapid overcorrection (0.5-1 mEq/hr, < 8 in mEq in 24hrs)
SIADH: treat underlying cause & fluid restriction
Identify & treat mineralocorticoid deficiency
Hyperaldosteronism
Considerations
Optimization
Hyperaldosteronism
Considerations
Hypertension & end-organ dysfunction:
Cardiomyopathy
Cerebrovascular disease
Chronic kidney disease
Fluid & electrolyte abnormalities:
Hypokalemia (weakness, potentiates non-depolarizing muscle relaxants)
Metabolic alkalosis
Volume depletion
Hypomagnesemia
Associated endocrine disorders:
Acromegaly
Pheochromocytoma
Primary hyperparathyroidism
Medications such as spironolactone
Adrenalectomy:
Bilateral? Need steroids
Laparascopic vs. open (pain & disposition)
Optimization
Antihypertensive therapy
Correction of electrolyte abnormalities
Hyperkalemia
Considerations
Management
ECG changes
Hyperkalemia
Considerations
Emergency situation with potential for life threatening arrhythmias, cardiac arrest
Etiology:
Shift:
Metabolic or respiratory acidosis, diabetic ketoacidosis
Digoxin toxicity
Total body excess:
Rhabdomyolysis (malignant hyperthermia, crush injuries, burns)
Post cardiopulmonary bypass
Iatrogenic (IV or oral)
Hemolysis
Tumor lysis
Transfusion (massive transfusion, old packed red blood cells)
Renal failure
Hypoaldosteronism
Addison’s
Drugs (succinylcholine, ACE inhibitors, beta blockers, spironolactone, NSAIDs, cyclosporin)
Systemic effects
Arrhythmias
Muscle weakness
Drug interactions
Succinylcholine contraindicated
Non-depolarizer muscle relaxants: resistance
Management
Stabilize myocardium:
Calcium gluconate 100 mg/kg
Shift potassium intracellularly:
Insulin 0.1 units/kg + Glucose 0.5-1 g/kg (25 g for every 10 U insulin)
Sodium bicarbonate 1 mEq/kg
Ventolin 5-10 mg via nebulizer or 5 mcg/kg IV
Hyperventilation
Epinephrine
Eliminate potassium:
Furosemide 20-40mg IV
Kayexalate 30 g PR or PO
Dialysis
ECG changes
Mild (5.5-6.5 mEq/L): peaked T waves, prolonged PR interval (1st degree AV block)
Moderate (6.5-8 mEq/L): loss of P wave, prolonged QRS, ST segment elevation, ectopic beats/escape rhythms
Severe (>8.0 mEq/L): progressive widening of QRS, bundle branch blocks, fascicular blocks, sine wave, ventricular fibrillation, asystole
Diabetic Ketoacidosis
Diagnosis
Considerations
Conflicts
Crises
Management
Goals
Complications
Diabetic Ketoacidosis
Diagnosis
Glucose > 14
HCO3 < 18
pH < 7.3
+ ketones in urine/blood
Considerations
Life threatening anion gap metabolic acidosis (ketoacidosis)
CNS: ↓ LOC (hypovolemia, cerebral edema)
Cardiovascular: cardiac arrythmias, congestive heart failure
Hyperventilation (very high minute ventilation, caution with intubation & positive pressure ventilation)
Hypovolemia:
Osmotic diuresis (hyperglycemia)
Crystalloid volume replacement
Electrolyte abnormalities:
Depletion of potassium, phosphorus, magnesium
Hyponatremia (factitious hyponatremia)
Consequences of therapy:
Electrolyte abnormalities
Hypo/hyperkalemia, hypomagnesemia, hypophosphatemia
Hypoglycemia
Cerebral edema, central pontine myelinolysis
Address underlying cause:
Infection, trauma, intoxication (cocaine), pancreatitis, acute coronary syndrome
Medication noncompliance (insulin)
Conflicts
Resuscitation vs. emergency surgery
Severe metabolic acidosis vs. intubation/ventilation
Hypovolemia vs. aspiration risk (RSI)
Crises
Electrolyte abnormalities (hyper/hypokalemia, hypomagnesemia, hyponatremia)
Hypoglycemia
Cerebral edema (glucose correction without correcting hyponatremia)
Central pontine myelinolysis (rapid serum sodium correction)
Management
Treat as per hospital protocol in consultation with endocrinology
For example, see BC Children’s Hospital’s DKA protocol:
Goals
Normal anion gap (AG)
pH > 7.2
Potassium > 3.5
Bicarbonate > 20
Glucose < 13
Urine output 1 ml/kg/hr
Volume replacement:
Normal saline to correct hypovolemia (3-5L deficit)
Then slow to maintenance (up to 500ml/hr)
Change to D5NS when glucose < 14
Add potassium to IV fluids once < 4.5 & urinating
Insulin R
Start infusion at 0.14 u/kg/hr (10units/hr in 70kg male) OR give 0.1 u/kg bolus followed by infusion 0.1 u/kg/hr
DO NOT start insulin if potassium <3.3
Glucose goal 10-15 mmol/L
When glucose <11: add D5W to solution
Potassium management
If < 3.3: DO NOT start insulin, give 20-30 meq/hr of potassium until K > 3.3
If > 3.3 & < 5.3: give potassium 20meq/L of fluid
If > 5.3: Do NOT give potassium
Frequent monitoring: ABG, electrolytes (AG), BUN, creatinine, osmolality, plasma & urinary ketones, magnesium, phosphate, lactate
Consider sodium bicarbonate if pH < 7 & myocardial dysfunction or vasodilation or life-threatening hyperkalemia
Complications
Cerebral edema
Pulmonary edema
Hyperthyroidism / Thyroid storm
Considerations
Optimization
Conflicts
Thyroid Storm
Hyperthyroidism / Thyroid storm
Considerations
Potential difficult airway if goitre present (airway compression, anterior mediastinal mass)
End organ effects of chronic hyperthyroidism:
Hypermetabolic state (↑ VO2, VCO2)
Cardiovascular: hypertension, tachycardia, myocardial ischemia, cardiomyopathy, arrhythmias
CNS: anxiety, psychiatric disorders
Muscle weakness
Risk of thyroid storm
Interactions with anesthetics:
↑ anesthetic requirements to control BP & HR. MAC requirement is NOT increased
Avoid sympathetic stimulants (ketamine, cocaine, epinephrine, etc)
Thyroidectomy:
Shared airway
Airway obstruction (tracheomalacia, recurrent laryngeal nerve injury, neck hematoma, hypocalcemia)
Optimization
Optimize thyroid function & limit end organ effects: heart rate <90, normal TSH
Identify difficult airway or anterior mediastinal mass
Identify & manage thyroid storm
Conflicts
Difficult airway/hemodynamic instability & sympathetic stimulants (cocaine, epinephrine, glycopyrrolate)
Hemodynamic instability & RSI
Thyroid storm
Emergency situation (mortality= 20%), consider endocrinology consult
IV fluids
Cool (blankets, IV solution, acetaminophen)
Control hemodynamics:
Esmolol 0.25-0.5 mg/kg bolus or 50-200 mcg/kg/min infusion
Propranolol 10-40 mg PO or up to 1 mg/min IV
Stop conversion of T4 to T3:
PTU 200-400 mg PO/NG/PR q6h
Hydrocortisone 100-200 mg IV q8h
Stop synthesis & release of new hormone:
Potassium iodide 5 gtts PO/NG q6h or sodium iodide 0.25 g IV q6h (1 hr after PTU)
Look for & treat complications:
CVA, loss of consciousness
Myocardial infarction, atrial fibrillation (avoid amiodarone because of iodide content; use digoxin instead) or congestive heart failure
Hypoventilation & hypercarbia
Electrolyte abnormalities
Consider differential diagnosis for hypermetabolic state
Consider last ditch treatments: plasmapheresis, dantrolene, lithium, neuraxial blockade to T4
Hyperparathyroidism
Background
Considerations
Optimization
Conflicts
Hyperparathyroidism
Background
Primary hyperparathyroidism: parathyroid adenoma or carcinoma
Secondary hyperparathyroidism: an appropriate compensatory response of the parathyroid glands to counteract a disease process that produces hypocalcemia
Ectopic hyperparathyroidism: due to secretion of parathyroid hormone (or a substance with similar endocrine effects) by tissues other than the parathyroid glands
Considerations
Potential difficult airway:
Mass effect (goitre)
Osteopenic bone (pathologic fractures of mandible & vertebral bodies)
Physiologic changes of hypercalcemia:
CNS: ↓LOC, hallucinations, psychosis
Cardiovascular: hypertension, hypovolemia, conduction blockade
Hypercalcemia ECG: ↑PR interval, ↓QTc
Respiratory: potential respiratory muscle weakness, poor clearance of secretions
Renal: renal failure, nephrolithiasis (70%)
GI: ↑ aspiration risk, nausea/vomiting, abdominal pain, pancreatitis
MSK: weakness (titrate neuromuscular blockers to effect), pathologic fractures (careful positioning)
Hematologic: anemia
Underlying etiology:
Parathyroid tumour, PTH-producing tumour
Chronic renal failure (usually associated with hypocalcemia, hyperphosphatemia)
Considerations of cancer & associated syndromes (MEN 1):
MEN 1: hyperparathyroid, pancreatic islet cell tumors, pituitary hyperplasia or tumor
MEN 2A: hyperparathyroid, medullary thyroid carcinoma, pheochromocytoma
Post-op airway obstruction after parathyroidectomy:
Hematoma, laryngospasm, hypocalcemia, recurrent laryngeal nerve injury, tracheomalacia
Mandibular fracture
Optimization
Management of hypercalcemia:
IV rehydration
Furosemide after IV hydration → goal is 3-5 L urine output/day
If severe, add:
Bisphosphonate (etidronate 7.5mg/kg IV OD or 20mg/kg PO OD)
Calcitonin 200 IU nasal spray/day
IV steroids
Phosphate repletion
Hemodialysis if life threatening hypercalcemia or acute renal failure
Monitor EKG & calcium concentrations perioperatively
Prevent pathological fractures (careful positioning)
Airway vigilance postoperatively
Conflicts
Hypovolemia vs. RSI (ESWL or percutaneous drainage for nephrolithiasis)
Renal failure vs. succinylcholine for RSI
Hypothyroidism
Considerations
Optimization
Conflicts
Myxoedema Coma
Hypothyroidism
Considerations
Possible difficult airway:
Enlarged goiter: anatomical deviation/obstruction
Anterior mediastinal mass
Recurrent laryngeal nerve involvement
Prior neck radiation
Aspiration risk
Physiologic manifestations:
Cardiovascular: congestive heart failure, ↓ CO (↓ contractility/rate), hypotension, pericardial effusion, autonomic instability, hypovolemia
Respiratory: hypoventilation, ↓ response to hypoxemia/hypercarbia
Electrolytes: hyponatremia
Endocrine: hypoglycemia, adrenal insufficiency (cortical atrophy)
Hypothermia
↓ metabolic rate
Interactions with anesthetic:
↓ MAC
Delayed emergence
Sensitivity to respiratory depressents
Perioperative endocrine supplementation (thyroid, steroids)
Potential for myxedema coma
Thyroid surgery:
Shared airway
Post-operative airway obstruction (recurrent laryngeal nerve injury, tracheomalacia, hematoma, hypocalcemia)
Optimization
Euthyroid patient preoperatively
Optimize volume status, give steroids, & manage glucose & sodium
Conflicts
Thyroid replacement & coronary artery disease (can precipitate myocardial ischemia)
Potential for over-sedation vs. difficult airway (post-operative analgesia)
Myxedema Coma
Life-threatening form of hypothyroidism (mortality > 50%) precipitated by stress
Exaggerated features of hypothyroidism:
↓ LOC
Risk of aspiration
↑ sensitivity to neuromuscular blockers & sedatives
↓ cardiac output/heart rate, congestive heart failure, pulmonary edema
Respiratory depression
Hypothermia
Metabolic: SIADH, hypoglycemia, adrenal suppression
High risk for delayed emergence & need for post-operative ventilation
Treatment:
IV thyroxine
IV T3 0.2mcg/kg q6h (onset 6-24 hrs)
T4 200-300mcg IV over 5-10 mins then 100mcg IV q24
Risk of precipitation of myocardial ischemia with IV T3/T4 supplementation in those with CAD
Hydrocortisone 100mg IV then 25mg q6h (common association with adrenal suppression)
Passive rewarming with blankets
Post-operative ventilation, fluids, pressors, inotropes
ICU & endocrinology consult
Obesity
Definitions (WHO, NIH)
Considerations
Anaestehtic goals
Potential conflicts
Obesity
Definitions (WHO, NIH)
Overweight: BMI ≥25.0 to 29.9
Obesity: BMI ≥30
Obesity class I: BMI of 30.0 to 34.9
Obesity class II: BMI of 35.0 to 39.9
Obesity class III (severe obesity, massive obesity): BMI ≥40
Considerations
Potentially difficult airway
Physiologic changes of obesity:
↓ FRC → fast desaturation
↑ cardiac demand & output with limited reserve
↑ gastric volume & abdominal pressure → ↑ aspiration risk
↑ postoperative morbidity & mortality (respiratory failure, wound infections, thromboembolism risk)
Co-morbid diseases:
Airway: OSA
Respiratory: obesity hypoventilation syndrome (OHS), pickwickian syndrome, pulmonary hypertension, restrictive lung disease
Cardiac: hypertension, coronary artery disease, left ventricular hypertrophy, biventricular failure
Endocrine: diabetes
GI: reflux, non-alcoholic fatty liver disease
Altered pharmacology:
Implications for loading vs. steady state infusions (IBW vs TBW)
Sensitivity to sedatives & opioids
↓ neuraxial dose may be needed
Potential technical difficulties:
Vascular access
Monitoring (NIBP)
Regional
Anesthetic Goals
Safe airway management; avoid hypoxemia & aspiration
Evaluate physiologic impact of obesity on patient
Establish whether regional technique is feasible
Minimize perioperative complications:
Minimize postoperative airway obstruction/hypoventilation (ensure no residual anesthetic, extubate & nurse semi-recumbent, continuous oxygen saturation monitoring postoperatively & effective postoperative analgesia)
Avoid thrombotic complications
Avoid peripheral nerve injury
Potential Conflicts
Difficult airway vs. aspiration risk (RSI)
OSA vs. opioid requirements postoperatively & difficulty with regional procedures
Panhypopituitarism
Background
Considerations
Panhypopituitarism
Background
Deficiency of anterior pituitary hormones
ACTH → cortisol deficiency (2° adrenal insufficiency)
Tx w/ Hydrocortisone (note: mineralocorticoid replacement not necessary)
TSH → hypothyroidism
Gonadotropins (LH/FSH) → anovulation, perimenopausal symptoms in females, testicular hypofunction in males
Growth hormone (GH) → short stature in children, Δ in body composition in adults
Prolactin → inability to lactate
Causes:
Hypothalamus: tumors (ex craniopharyngiomas), RTX, infiltrative lesions (ex sarcoidosis), infxn (ex meningitis), TBI, stroke (ischemic, hemorrhagic)
can also lead to ↓ vasopressin –> diabetes insipidus
Pituitary gland: mass lesion (ex pituitary adenoma), pituitary surgery, pituitary infarction (ex Sheehan syndrome after postpartum hemorrhage), RTX, pituitary apoplexy (sudden hemorrhage into pituitary gland), congenital dz, hypophysitis, hemochromatosis
Considerations
Adrenocortical insufficiency can be life-threatening w/ complete vascular collapse → tx w/ IV hydrocortisone, IV fluids, +/- glucose
Need for stress dose steroids
Hypothyroidism
Diabetes Insipidus
May present for Pituitary Surgery
Perioperative Steroids
Risk Stratification
Dosing
Perioperative Steroids
Risk Stratification
Definitely suppressed hypothalamic-pituitary-adrenal (HPA) axis → supplement
those on prednisone > 20mg/day for >3 weeks in last year
Definitely non-suppressed HPA axis → no need for supplementation
those on prednisone < 5mg/day for any duration
those on steroids < 3weeks in last year
inhaled/topicals rarely cause suppression (although they can)
Intermediate risk patients → consider HPA testing or base on patient status
> 5mg/day but < 20mg/day
Dosing
Moderate risk surgery: hydrocortisone 50mg IV q8h X 3 doses
High risk surgery: hydrocortisone 100mg IV q8h X 3 doses
Porphyria
Considerations
Goals
Complications
Pregnancy
Drugs to avoid
Porphyria
Considerations
Risk of perioperative porphyric crisis
The need to avoid certain anesthetic drugs, including:
Barbiturates/etomidate
Ropivacaine (caution in regional anesthesia), lidocaine & bupivacaine are OK
Ketorolac
Anti-seizure medications: phenytoin, barbiturates
Acute intermittent porphyria (AIP) attacks last days to weeks & are multi-systemic:
Risk of aspiration (bulbar dysfunction)
CNS: seizures, peripheral neuropathy, quadriplegia, altered LOC
Respiratory: respiratory failure from respiratory muscle weakness
Cardiovascular: autonomic instability, tachycardia, hypertension
Electrolyte imbalances: especially hyponatremia but also hypomagnesemia and hypokalemia
GI: severe abdominal pain
Psych: anxiety, restlessness, agitation, hallucinations, hysteria, disorientation, delirium, apathy, depression, phobias and altered consciousness, ranging from somnolence to coma
Chronic effects:
Usually symptom-free between attacks
But, some have persistent hypertension & develop kidney disease, chronic pain, depression/anxiety/suicidality
Goals
Minimize risk of aspiration
Optimization:
Ensure consultation with hematology before procedure
Avoid prolonged fasting
Give pre-operative glucose load (e.g., maintain on D10NS IV prior to surgery)
Correct anemia
Manage pain & anxiety
Avoid triggers of porphyric crisis:
Drugs: sodium thiopental, etomidate, chlordiazepoxide, ropivacaine, diazepam, steroids, ergots, ketorolac and diclofenac, cephalosporins, sulphonamides
Physiologic: fasting/hypoglycemia, anemia, stress, estrogen, progesterone, infection
Substance abuse: alcohol, smoking, marijuana, cocaine, ecstasy, amphetamines
Prepare to treat crisis:
Hydration, glucose, electrolyte replacement, analgesia, hematin, cimetidine, somatostatin, plasmapheresis
Seizures: use midazolam, propofol
Complications
Aspiration
Muscle weakness, neuropathy, paraplegia:
Postoperative ventilation requirements
Confusion with respect to neuropraxia and complications after regional
Acute porphyric crisis:
Symptoms:
CNS: changes, seizures, sensory loss, pain, quadriplegia, upper motor neuron signs, cranial nerve lesions
Cardiovascular: autonomic instability (tachycardia, hypertension, hypotension)
Respiratory: respiratory paralysis/failure
GI: abdominal pain, vomiting, constipation, diarrhea
Treatment:
Eliminate drug/triggering factor
Hydration
Glucose 20g/hr infusion (D10W)
Hematin 3-4 mg/kg IV over 20 min (specific therapy)
Beta blockers for hypertension/tachycardia
Octreotide
Analgesia
Propofol and midazolam for seizures
Seizure attack:
Use propofol, benzodiazepenes
AVOID phenytoin, barbiturates
Porphyria in pregnancy
No evidence to choose between general anesthesia vs. neuraxial technique
Epidural definitely OK
Propofol/succinylcholine OK for RSI
Ergotamine is CONTRAINDICATED! Use oxytocin, hemabate for postpartum hemorrhage
Some key drugs to avoid
Barbiturates
Etomidate
Ergotamine
Antiepileptics (phenytoin)
Corticosteroids
Hydralazine
Pheochromocytoma
Considerations
Goals
Pregnancy considerations
Background
Pheochromocytoma
Considerations
Preoperative optimization:
Alpha & beta blockade
Restore intravascular volume
Hemodynamic lability & potential for pheochromocytoma crises:
Hypertension, tachycardia, arrhythmia, myocardial ischemia
Need for invasive hemodynamic monitoring
Avoidance of sympathetic stimulation, histamine-releasing drugs and unopposed alpha stimulation
End organ dyfunction:
Relative hypovolemia
Left ventricular hypertrophy and cardiomyopathy, ischemic heart disease, MI, arrhythmia
Hypertensive encephalopathy & CVA
Renal failure
Associated conditions:
MEN 2A: hyperparathyroidism, medullary thyroid carcinoma, pheochromocytoma
MEN 2B: medullary thyroid carcinoma, pheochromocytoma, mucosal neuromas
Neurofibromatosis
Von Hippel Lindau syndrome (cerebellar hemangiomas, renal cell carcinoma)
Postoperative complications:
Hypotension
Hypertension
Hypoglycemia
Hypoadrenalism
Goals
Adequate pre-op optimization:
Start with alpha blockade: phenoxybenzamine used classically; alternatively: terazosin, prazosin, doxazosin
Once alpha blocked, may start beta blockade
Fix hypovolemia
Prevent and manage pheochromocytoma crises:
Invasive monitoring and tight hemodynamic control
Avoid SNS surges (anxiolysis, deep induction, epidural)
Avoid histamine releasing drugs (precipitates catecholamine release from tumour)
Anticipate and prepare for hypotension following tumour vein ligation (volume +/- pressors/inotropes)
Conflicts:
Deep anesthesia vs. hypovolemia
Pregnancy Considerations
Caution with hemodynamic agents that cross placenta (esmolol, propanolol)
Same optimization with alpha blockade followed by beta blockade applies but some suggest having hemodynamic goals even lower than Roizen criteria (e.g. upper limit 150/80mmHg but avoid orthostatic hypotension to prevent uteroplacental malperfusion)
Pregnancy specific management:
Controversial, based on case reports:
If gestational age <24 weeks: may undergo open or laparascopic resection of pheochromocytoma
If gestational age >24 weeks: medical management, & may wait until fetal maturity & do combined cesarean section & tumor resection (the problem is that gravid uterus >24 weeks obstructs access to tumor resection)
Cesarean section is preferred as abdominal squeeze during labour can precipitate a hypertensive crisis
General anesthesia or epidural anesthesia > spinal anesthesia
probably best NOT TO ALLOW LABOR
Increased incidence of intrauterine fetal demise, growth restriction, abruption
Often misdiagnosed as pre-eclampsia
Background
Roizen criteria:
No in-hospital blood pressure reading higher than 165/90 mmHg should be evident for 48 hours before surgery. We often measure arterial blood pressure every minute for 1 hour in a stressful environment (eg. postanesthesia care unit). If no reading is greater than 165/90mmHg, this criterion is considered satisfied.
Orthostatic hypotension should be present, but blood pressure on standing should not be lower than 80/45mmHg.
ECG should be free of ST-T changes that are not permanent
No more than one PVC should occur every 5 minutes
Anti-hypertensive agents:
Use short acting agents only!
Sodium nitroprusside (50mg in 250mL NS = 200mcg/mL): run at 25-200mcg/min or 0.3-3mcg/kg/min
prepare syringe of 100mcg/mL for bolusing
Esmolol (10mg/mL as per ampule): run at 50-250 mcg/kg/min
Phentolamine (10mg ampule): administer 1-2mg boluses; may increase to 5mg/dose; onset/offset immediate
MgSO4: 4-6g at induction over 30 minutes then 1-2g/hr
Anti-hypotensive agents:
Norepinephrine (4mg in 250mL NS = 16 mcg/mL): run at 1-20mcg/min
bolus 20-30mcg/dose
Vasopressin: run at 0.01-0.04 U/min and boluses 4U/dose for hypotension refractory to norepinephrine
Consider calcium if magnesium used intraoperatively
SIADH
Considerations
Treatment
Goals
Management
SIADH
Considerations
Hyponatremia:
Cerebral edema
Seizures
Coma
Respiratory arrest
Associated conditions:
Tumours (lung, pancreas, prostate, lymphoma)
CNS insult (trauma, subarachnoid hemorrhage, tumour, infection)
Pulmonary (infection, cystic fibrosis, positive pressure ventilation)
Medications (opiates, oxytocin, chlorpropamide, vincristine)
Postoperative ADH secretion
Idiopathic
Iatrogenic (hypotonic IV solutions)
Treatment
Free water restriction
Eliminate underlying cause
Caution with rapid correction of serum sodium (central pontine myelinolysis)
Goals
Preoperative correction of serum electrolytes when possible to target sodium >125
Avoid overcorrection or overly rapid correction resulting in central pontine myelinolysis
Correct underlying reversible etiologies (infection, tumour, medications, iatrogenic)
Management
Restore sodium concentration
Generally restrict free water (500mL-1L/day)
+/- loop diuretic
Acute:
Severe hyponatremia (<120mEq/L or neuro symptoms)
Hypertonic saline 3% 1-2 ml/kg/hr until sodium >125
Furosemide
Sodium bicarbonate (1 mEq/ml) to terminate seizures: 0.5-1mL/kg boluses prn
Chronic:
Avoid rapid overcorrection (0.5-1 mEq/hr, <8 in mEq in 24hrs)
Demeclocycline 300-600 mg PO bid (antagonizes ADH at collecting duct)
Conivaptan = vasopressin receptor antagonist
