Vascular/Renal/Psychiatry Flashcards
Abdominal Aortic Aneurysm (AAA) Open Repair
Considerations
Goals
Conflicts
Abdominal Aortic Aneurysm (AAA) Open Repair
Considerations
Potential for hemorrhage, large fluid shifts & hypothermia
Cross-clamp level & cross-clamp/unclamp physiology
Associated comorbid disease (coronary disease, hypertension, diabetes, renal failure, COPD, smoking)
Perioperative organ dysfunction (cardiac, renal, visceral, spinal cord ischemia) & complication (MI/renal failure/heart failure/paralysis/death)
Postoperative pain control & monitoring in high acuity unit/ICU
For ruptured AAA, add the following:
Full stomach, limited time to optimize
Emergency procedure requiring immediate OR
Need for extra help, second anesthesiologist
Hemorrhagic shock with high mortality (85%)
Goals
Adequate resuscitation of massive hemorrhage to goal end points
Management of comorbidities
Minimize hemodynamic changes associated with aortic cross clamping & unclamping
Conflicts
Hemodynamic instability vs. full stomach and need for RSI
Requirement for immediate OR vs. resuscitation
Carotid Endarterectomy
Considerations
Anaesthetic goals
Anaesthetic options
Carotid Endarterectomy
Considerations
Shared airway
Significant hemodynamic fluctuations:
X-clamp: hypertension, tachycardia, increased myocardial O2 demands
Carotid sinus manipulation: bradycardia, hypotension
Coexisting disease (CAD, DM, HTN, PVD, CKD, CVD, smoking, advanced age)
Neuromonitoring (usually EEG, cerebral oximetry, TCD, stump pressure)
Complications:
CNS: CVA (ischemic/embolic), hyperperfusion syndrome, CN dysfunction
Cardiovascular: MI, labile BP (hypertension/hypotension)
Airway: hematoma, airway obstruction/loss, RLN injury
Perioperative medication management (ASA, plavix, antihypertensives, statins)
Anesthetic Goals
Maintain stable hemodynamics
Optimize cerebral perfusion & protect myocardium
Crisp emergence with awake patient ready for neurological exam
Smooth emergence to minimize risk of bleeding
Anesthetic Options
GA vs. regional (superficial cervical plexus block) vs. local
Carotid artery stenting also an option if patient unsuitable for an anesthetic
Acute Kidney Injury (AKI)
Considerations
Conflicts
Management
Acute Kidney Injury (AKI)
Considerations
Higher risk of peri-operative morbidity & mortality
Altered pharmacology
Dysregulation of volume status, acid-base (metabolic acidosis), & electrolytes
Management
Consult nephrology
Avoid further renal insults:
Maintain euvolemia
Maintain adequate renal perfusion: MAP > 65
Avoid nephrotoxins: contrast dye, NSAIDs, aminoglycoside antibiotics
Identify & treat underlying cause:
Replace intravascular volume
Optimize cardiac output & blood pressure
Correct any outflow obstruction (e.g., BPH)
Stop nephrotoxic medications
Know indications for hemodialysis:
Acidosis
Electrolyte disturbances (↑ K)
Intoxication (e.g. methanol, ethylene glycol)
Volume overload
Uremia
Conflicts
RSI with succinylcholine vs. high K+
Need for contrast vs. AKI
Need for surgery vs. AKI
Chronic Renal Failure
Considerations
Conflicts
Goals
Chronic Renal Failure
Considerations
Gastroparesis & risk of aspiration
Dysregulation of volume status, acid-base (metabolic acidosis), & electrolytes (↑ K, ↓ Na, ↓ Ca, ↑ PO4, ↓ glucose, ↑ triglycerides)
Coexisting diseases & end-organ complications:
Autonomic dysfunction with hemodynamic instability
Pulmonary: pulmonary edema from low albumin, ↓ forced vital capacity, atelectasis
Cardiac: LV dysfunction, hypertension, coronary disease, heart failure, pericarditis, pericardial effusion, arrythmias
Hematologic: anemia/thrombocytopenia
Altered pharmacokinetics due to ↓ elimination, acidosis, hypoalbuminemia
Potential difficult IV access
Cr > 200 independent risk factor for cardiac complications & mortality
Conflicts
Hyperkalemia vs. need for emergency surgery/RSI
Hemodynamic instability vs. RSI
Goals
Optimize electrolytes, volume status, comorbidities
Avoid worsening renal failure (avoid nephrotoxins, maintain adequate volume status)
Coordinate perioperative dialysis if on hemodialysis
If on peritoneal dialysis: consider draining it to optimize respiratory function
Avoid compromising dialysis access (AV fistulas, indwelling IV lines, PD ports)
TURP & TURP Syndrome
Considerations
Goals & Conflicts
TURP Syndrome
Presentation
Prevention
Treatment
Correction of hypoNa
TURP & TURP Syndrome
Considerations
Coexisting disease common in this population
Coronary disease, acute kidney injury, elderly
Considerations of intraoperative complications:
TURP syndrome ~2%
Fluid overload/pulmonary edema; electrolyte abnormalities; dysrhythmias hyperglycinemia (blindness), hyperammonemia (encephalopathy), hypothermia
Concealed hemorrhage
Bladder perforation ~ 1%
Septicemia (usually gram negative)
DIC (rare complication associated with prostate cancer)
Positioning: lithotomy with nerve injury; hemodynamic & respiratory effects of trendelenberg position
Choice of anesthetic: GA or spinal
Goals & Conflicts
Optimization of co-existing diseases
Prevention or early recognition of TURP syndrome
Attention to blood loss & appropriate replacement
Conflict: preference for neuraxial technique to monitor CNS symptoms vs. any contraindications to neuraxial
Problems in PAR include: post-op delirium, hypotension, respiratory distress (need to consider comorbidities)
TURP Syndrome
Presentation: due to fluid overload & hyponatremia:
Classic triad: hypertension, bradycardia, & mental status changes
Pulmonary: pulmonary edema, ↑ JVP
Cardiovascular: arrhythmias, hypertension
CNS: pupillary reflex sluggish or absent with glycine toxicity but intact with cerebral edema
Prevention:
Appropriate irrigation agent, minimize resection time, hemostasis, avoid high irrigating pressures (limit bag height to 30-40cm, frequent drainage), avoid hypotonic IV fluids, check electrolytes in patients with renal failure (metabolic abnormalities, hyponatremia)
Treatment:
Inform surgeon to terminate procedure ASAP
Oxygenation & circulatory support
Consider invasive monitoring if hemodynamically unstable (arterial line, CVP)
Blood work (electrolytes, creatinine, glucose, CBC, ABG)
12 lead ECG
Correction of hyponatremia:
Near-normal serum osmolality & asymptomatic: no interventions to correct serum sodium are recommended even in the presence of hyponatremia
Mild symptoms (serum Na > 120 mEq/L): fluid restriction & loop diuretic (furosemide 40-120 mg)
Symptomatic, life-threatening hypoosmolality & serum Na < 120 mEq/L (rare with modern techniques) can be treated with hypertonic saline (rarely necessary):
Start @ 100cc bolus & assess for resolution of symptoms or Na > 120 mEq/L
Can give 2 more boluses
Start at rate of 50-100 cc/h (do not exceed correction of > 1.5 mEq/L/h because rapid correction of serum sodium is associated with central pontine myelinolysis (osmotic demyelination syndrome) & cerebral edema
Diuresis with furosemide & fluid restriction:
Stop 3% saline once symptoms subside or serum Na > 120 mEq/L: treat remaining hyponatremia with diuresis & normal saline or fluid restriction
Seizure treatment as necessary
Transfer to ICU for ongoing care in severe cases
q1h blood work (Na, K)
Frequent CNS assessment
Electroconvulsive Therapy (ECT)
Considerations
Goals
Conflicts
Pregnancy Considerations
Electroconvulsive Therapy (ECT)
Considerations
Unprotected airway & remote location
Significant physiological changes:
CNS: ↑ cerebral blood flow & O2 consumption, ↑ICP
Cardiovascular:
Initial phase (parasympathetic): bradycardia, hypotension
Later phase (sympathetic): tachycardia, dysrhythmia, HTN, ↑ systemic & myocardial O2 consumption
↑ IOP, ↑ intragastric pressure
Transient apnea/hypoventilation
Contraindications:
Absolute: Pheochromocytoma, MI <3 months, Recent CVA <1 month
Relative: ↑ICP, Severe cardiac disease (conduction defects, poorly controlled CHF/IHD), Aortic & cerebral aneurysms, High-risk pregnancy
Co-morbid disease in patients with mental illness; often elderly
Use of concurrent medications (TCAs, MAOIs, etc)
Need for brief motor relaxation to prevent physical harm to patient
Goals
Amnesia
Prevention of physical injury
Control of hemodynamic changes
Rapid recovery
Minimal interference with seizure activity:
If available, methohexital superior to propofol
If propofol interfering with seizure activity: consider reducing dose, adding remifentanil or etomidate
Conflicts
“Full stomach”: use NDMR to intubate & reverse
Hx pseudocholinesterase deficiency/MH: use NDMR & reverse
Pregnancy Considerations
NOT contraindicated
Obtain obstetrical consultation & plan for fetal monitoring
Aspiration prophylaxis & consider intubation if >20 weeks GA
Resources readily accessible in event of neonatal or obstetrical emergency
MAOI (Monoamine Oxidase Inhibitors) Therapy
Background
Considerations
MAOI (Monoamine Oxidase Inhibitors) Therapy
Background
Inhibit breakdown of norepinephrine & serotonin, & also inhibit hepatic microsomal enzymes. These may result in:
Risk of hypertensive crisis with norepinephrine release
CNS ‘type I’ reaction: risk of serotonin syndrome under certain conditions resulting in agitation, headache, fever, seizures, coma, & death
CNS ‘type II’ reaction: ↓ hepatic opioid metabolism & thus opioid build-up causing sedation, respiratory depression, & cardiovascular collapse
Considerations
Indication for MAOIs: depression, anxiety, psychosis, hypotension, narcolepsy, headache
Continuation vs discontinuation of MAOI pre-op:
May need to consult prescribing physician (psychiatry, neurology)
If possible, try to discontinue 2 weeks pre-op with a tapering regimen
If cannot discontinue: be mindful of systemic effects below & avoid inpatient diets containing high amounts of tyramine
Risk of severe hypertension if sympathetic stimulation or sympathomimetic drugs:
Avoid light anesthesia
Avoid ketamine, pancuronium
Avoid indirect acting vasopressors such as ephedrine
Avoid foods contaning high amounts of tyramine (cheese, wine)
Risk of CNS adverse reactions:
Type I reaction leading to serotonin syndrome: avoid anticholinergics & meperidine
Type II reaction from accumulation of opioids: need to monitor closely for adverse events, opioid use not necessarily contraindicated & have been safely used
Altered response to anesthetic agents:
↑ MAC due to ↑ concentrations of CNS norepinephrine
Possible prolonged succinylcholine effect
Exaggerated hypotension with neuraxial techniques
Direct acting vasopressors only, consider ↓ doses
Neuroleptic Malignant Syndrome (NMS)
Background
Considerations
Management
Neuroleptic Malignant Syndrome (NMS)
Background
Rare, potentially fatal condition due to antipsychotic drug therapy
May reflect dopamine depletion in the CNS
Can occur anytime during the course of antipsychotic treatment but often is manifest during the first few weeks of therapy or following an ↑ in drug dosage.
Clinical manifestations usually develop over 24-72 hours, remember the mnemonic FEVERS:
F ever
E ncephalopathy
V ital signs unstable
E levated labs
R igidity (vs myoclonus in serotonin syndrome)
S weating
Considerations
Emergency situation, full stomach
Potentially life-threatening situation with high mortality:
↓ LOC: coma which may mandate airway management
Autonomic instability: tachycardia, hypertension, cardiac dysrhythmias (most likely cause of death)
Hypermetabolic state: fever, severe muscular rigidity, volume depletion
Tachypnea & potential respiratory insufficiency from hypoventilation/rigidity
Rhabdomyolysis, renal failure, acidosis
Psychiatric patient, potentially uncooperative
Management
Resuscitation & ICU monitoring following trigger
Stop offending agents
Supportive treatment: cooling, treat acidosis/electrolyte abnormalities, hemodynamic support
Pharmacologic (case reports, no strong evidence):
Bromocriptine: PO/NG 2.5 mg q8-12 hrs
Dantrolene: IV 2.5mg/kg bolus, up to 10mg/kg/day
Amantadine: initial dose is 100 mg PO/NG & titrated upward as needed to a maximum dose of 200 mg q12h
Benzodiazepines
Rule out other high risk conditions on differential diagnosis
“Trigger free” anesthetic in patients with history of NMS (controversial)
Serotonin Syndrome
Background
Considerations
Anaesthetic management
Serotonin Syndrome
Background
A potentially life-threatening adverse drug reaction due to ↑ CNS serotoninergic activity, characterized by the mnemonic MAD HOT:
M yoclonus
A utonomic instability
D elirium, D iarrhea,
HOT (fever)
It is seen with therapeutic medication use, drug interactions, & self-poisoning
Considerations
Multisystem effects of serotonin excess:
CNS: seizure, altered LOC
CVS: tachycardia & HTN, autonomic instability, arrhythmia
MSK: rigidity, rhabdomyolysis, hyperkalemia & renal failure
Hyperthermia; DIC
Psychiatric patient: co-operation, informed consent/substitute decision maker
Anesthetic Management
Stop offending agent
Admit to ICU/HAU
Supportive care & sedation:
Benzodiazepines very useful for sedation
Support ventilation & oxygenation
Fluid resuscitation
Treat hyperthermia
Autonomic instability:
Hypotension: use direct acting vasopressors, reduced doses initially
Hypertension: use phentolamine, nitroprusside, esmolol
Specific antidote is cyproheptadine (potent antihistamine & serotonin antagonist):
Initial: 12 mg followed by 2 mg every 2 hours or 4-8 mg every 6 hours
DO NOT use bromocriptine (a serotonin agonist, may exacerbate serotonin syndrome), dantrolene (no evidence)
Rule out other differential diagnosis (e.g., MH, NMS, thyrotoxicosis)
