Intraoperative

Difficult Airway Algorithm

1. Assess the likelihood and clinical impact of basic management problems:
   1. Difficulty with patient cooperation or consent
   2. Difficult mask ventilation
   3. Difficult supraglottic airway placement
   4. Difficult laryngoscopy
   5. Difficulty intubation
   6. Difficult surgical airway access
2. Actively pursue opportunities to deliver supplemental oxygen throughout the process of difficult airway management.
3. Consider the relative merits and feasibility of basic management choices:
   1. Awake intubation vs. intubation after induction of general anesthesia
   2. Non-invasive techniques vs. invasive techniques for the initial approach to intubation
   3. Video-assisted laryngoscopy as an initial approach to intubation
   4. Preservation vs. ablation of spontaneous ventilation
4. Develop primary and alternative strategies:

Source: https://pubs.asahq.org/anesthesiology/article/118/2/251/13535/Practice-Guidelines-for-Management-of-the

Techniques for Difficult Intubation/Ventilation

Techniques for Difficult Intubation

• Awake intubation
• Blind intubation (oral or nasal)
• Fiberoptic intubation
• Intubating stylet or tube-changer
• Supraglottic airway as an intubating conduit
• Larygoscopy blades of varying design and size
• Light wand
• Videolaryngoscope

Techniques for Difficult Ventilation

• Intratracheal jet stylet
• Invasive airway access
• Supraglottic airway
• Oral and nasopharyngeal aiways
• Rigid ventilating bronchoscope
• Two-person mask ventilation

*These are commonly cited techniques. It is not a comprehensive list. The order of presentation is alphabetical and does not imply preference for a given technique or sequence of use. Combinations of techniques may be used. The technique chosen by the practitioner in a particular case will depend on specific needs, preferences, skills, and clinical contraints.

Source: https://pubs.asahq.org/anesthesiology/article/118/2/251/13535/Practice-Guidelines-for-Management-of-the

Cormac-Lehane Laryngoscopy Grades

• Grade I: Full view of vocal cords
• Grade IIA: Partial view of vocal cords
• Grade IIB: View of arytenoids and epiglottis
• Grade III: Only epiglottis visable
• Grade IV: Neither the epiglottis nor glottis seen

Hypoxia

Initial Response

• Increase to 100% FiO₂ high flow, look for other vitals
• Work from patient to machine (or vice versa):
  • Listen to lungc: atelectasis, bronchospasm, mucus plug, mainstem intubation, pneumothorax
  • Check ETT: kinked, patient biting tube, patient extubated, cuff leak
  • Check circuit: disconnect at ETT or at machine
  • Check machine: inspiratory and expiratory valves, bellows, FiO₂, MV
  • Check monitors: pulse ox waveform, EtCO₂, gas analyzer
• Hand ventilate: feel compliance or leaks, recruitment maneuver
• Suction ETT
• Call for HELP if worsening or no clear cause. Communicate to surgical team

Differential Diagnosis

• Hypoventilation
  • Low TV/RR or MV
  • High or low EtCO₂
  • High PIP
  • Circuit leaks
  • Kinked/obstructed ETT
  • Poor chest rise
  • Patient bucking ventilator
• Shunt/VQ mismatch
  • Mainstem intubation
  • Bronchospasm
  • Anaphylaxis
  • Mucus plug
  • Aspiration
• Diffusion impairment
  • Pulmonary edema, fibrosis, emphysema – usually chronic
• Low FiO₂
  • Hypoxic FiO₂ gas mixture; may have to go to alternative O₂ source (tank)
• Increased O₂ demand
  • MH
  • Thyrotoxicosis
  • Sepsis
• Artifact
  • Poor waveform: cold extremity, light interference, cautery, dyes, extremity movement

Depending on likely diagnosis, consider:

• Recruitment breaths
  • Caution if hypotensive
• Bronchodilators
  • Albuterol MDI
  • Volatile anesthetics (except for Desflurane)/Ketamine
• Increase FRC
  • Head up (if bp stable), desufflate abdomen
• Needle decompression
  • For pneumothorax

Source: http://web.stanford.edu/dept/anesthesia/em/semv3.1_digital.pdf

Suggested Algorithm for management of hypoxia

Reference: Pocket Anesthesia

Alveolar Gas Equation

Alveolar – arterial (A-a) Gradient:

A-a Gradient = P_AO₂ – P_aO₂

Hypercarbia

• Caused by inadequate ventilation or increased CO₂ production
• Can lead to respiratory acidosis, increased pulmonary artery pressure, and/or increased intracranial pressure

Differential Diagnosis

• Inadequate Ventilation
  • Central depression of medullary respiratory center
    • Opioids, barbiturates, benzodiazepines
  • Neuromuscular depression
    • Muscle relaxants
    • Phrenic nerve paralysis
  • Low minute ventilation
    • Inappropriate ventilator settings
    • Altered respiratory mechanics in spontaneously ventilated patients
  • Equipment problems
    • Ventilator malfunction
    • Leak in breathing circuit
  • Increased airway resistance
    • Bronchospasm
    • Severe COPD
    • Upper airway obstruction
    • Pneumoperitoneum with CO₂
  • ET tube issue
    • Kinked ETT
    • Endobronchial intubation
  • Rebreathing of exhaled gases
    • Exhausted CO₂ absorber
    • Inadequate fresh gas flows
• Increased CO₂ production
  • Exogenous CO₂
    • Insufflation during laparoscopy
  • Reperfusion
    • Release of tourniquet, removal of cross-clamps
  • Hypermetabolic states
    • Malignant hyperthermia
    • Sepsis
    • Thyrotoxicosis
    • Fever/shivering
  • Seizures
  • IV sodium bicarbonate administration

Investigations/Treatments

• Assess oxygenation and airway
• Ensure appropriate ventilator settings; increase minute ventilation; increase fresh gas flow
• Check CO₂ absorber
• Consider checking ABG to confirm capnography
• Ensure muscle relaxant reversal, residual narcotic/anesthetic effect (if increased CO₂ during emergence)
• Treat secondary causes, such as shivering, malignant hyperthermia, thyroid storm, etc.

Source: Freeman BS. Hypocarbia and Hypercarbia. Chapter 142. Anesthesiology Core Review. Part One: BASIC Exam.

Elevated PIP

Initial Response:

1. ABCs (100% FiO₂, switch to bag, hand ventilate, verify EtCO₂)
2. Address most common diagnoses, auscultate bilaterally (bronchospasm [wheezing], endobronchial intubation [check tube depth- neck flexion can increase tube depth by 2 cm], mucus plug)

If Unresolved:

1. Sweep from machine, circuit, ETT, lungs, chest wall
2. Suction ETT
3. Go through systematic differential of possible causes. Assess if plateau elevated or just PIP.

Static Compliance

Cstat = Vt / (Pplat – PEEP)

• Measured in the absence of gas flow
• Based on plateau pressure

Dynamic Compliance

Cdyn = Vt / (Ppeak – PEEP)

• Measured in the presence of gas flow
• Based on peak pressure

Increased PIP Normal Plateau

Things that increase airway resistance and peak pressure, so dynamic compliance curve shifts to the right and flattens. Plateau pressure and static compliance are unchanged.

• Mechanical
  • Kinked circuit
  • Faulty inspiratory valve
• Endotracheal tube
  • Kinked
  • Mucus plug
  • Depth
  • Esophageal
• Conducting airways
  • Bronchospasm

Increased PIP Elevated Plateau

Things that reduce lung compliance increase both peak and plateau pressure, so both static and dynamic compliance fall.

• Alveolus
  • Atelectasis
  • Edema
  • Aspiration
  • Restrictive lung disease
• Pleural space
  • Tension pneumothorax
  • Pleural effusion
• Chest wall
  • Obesity
  • Paralytic weaning off
  • Surgeon leaning on chest
  • Narcotic-induced rigidity

Peak Inspiratory Pressure

Pulmonary emboli do not change resistance or compliance, so both curves are unchanged.

Peak airway pressure made up from:

1. Alveolar pressure present at the beginning of the breath (PEEP)
2. Elastic recoil of the lung and chest wall (pulmonary compliance – static pressure)
3. Inspiratory flow resistance

Source: https://healthjade.net/peak-inspiratory-pressure/

Bronchospasm

Signs

• Increased PIP
• Wheezing
• Increased expiratory time
• Increased ETCO₂, upsloping ETCO₂ waveform

Management

• Assess oxygenation (FiO₂ 100%) and airway
• Initially switch to manual ventilation
• If put back on ventilator, appropriate settings
  • Lower RR (6-8/min), longer expiratory times (I:E 1:3 or 1:4)
  • VCV with TV 6 cc/kg, peak airway pressure < 40 cm H₂)
  • Minimal PEEP
• Deepen anesthetic (volatiles act as bronchodilator, exception is Desflurane)
• Ketamine (bronchodilator)
• Inhaled beta 2-agonist (albuterol)
• Consider IV Steroids (hydrocortisone 100 mg IV)
• Consider epinephrine if severe (start with 10 mcg IV)

Hypotension

Preload

Volume of blood at end of diastole.

Absolute hypovolemia

• Hemorrhage
• Diuresis
• Bowel prep
• NPO status

Relative hypovolemia

• Increased intra-abdominal pressure (insufflation)
• Increased thoracis pressure (pneumothorax)
• Surgical IVC compression
• Positional (Reverse Trendelenburg)

Afterload

Resistance the heart must overcome to eject blood.

• Vasodilation (sepsis, anaphylaxis)
• Drugs (anesthetics)
• Sympathectomy (spinal, epidural)

Contractility

• The heart’s force of pumping.
• Ischemia
• Arrythmias
• CHF
• Iatrogenic (beta-blockers)
• Anesthetic effect

Management

• Open IV fluids, place in Trendelenburg
• Room sweep
  • Confirm BP (examine cuff for fit, check other site for BP)
  • Check EtCO₂ (drop in EtCO₂ would support real drop in BP)
  • Check EKG
  • Check ventilator for increased PIP
  • Check surgical field: hemorrhage, CO₂ insufflation, retraction
• Consider fluid status examine arterial line (or pulse ox) waveform for variation
• Ensure IV site isn’t infiltrated
• Decrease anesthetic agents
• Vasopressors
  • Phenylephrine
  • Ephedrine
  • Vasopressin

Hypertension

Primary Hypertension

• Long-standing HTN (no known cause, 70%-95% of HTN)
• Specific disease processes
  • Preeclampsia
  • Kidney failure

Secondary Hypertension

• Pain/surgical stimulation (inadequate anesthesia; usually associated with tachycardia unless beta-blocked)
  • Incision
  • Distended bladder
  • Tourniquet pain
  • ETT stimulation
• Hypoxia, hypercarbia
• Intracranial pathology (increased ICP)
• Endocrine problems (pheochromocytoma, Cushing syndrome, hyperthyroidism)
• Alcohol withdrawal
• Malignant hyperthermia
• Inadvertent drug administration
• Illicit drug use (amphetamines, cocaine)

Management

Cuff Error

• Check size of cuff and placement
• Surgeon leaning on cuff?

Surgical Stimulation

• Increase depth of anesthesia
• Opioids

Full Bladder

• Check Foley

Improve Oxygenation/Ventilation

• Check FiO₂, EtCO₂

Medications

• Alpha/beta adrenergic-blocking agents (labetalol 5-10 mg IV)
• B-adrenergic-blocking agents (metoprolol 1-5 mg IV)
• Vasodilators (hydralazine 2.5-5 mg IV, NTG gtt at 30-50 ug/min IV)
• Ca channel blockers (diltiazem 5-10 mg IV)

Other Things to Consider

• Drug contamination (e.g., epi-soaked gauze in surgical field)
• Elevated ICP
• Malignant hyperthermia
• Hypervolemia

Bradycardia

Etiologies

• Hypoxia
• Acute MI (especially inferior wall)
• Sick sinus syndrome
• Drugs
  • Succinylcholine (especially in peds)
  • Anticholinesterases (neostigmine)
  • Beta blockers
  • Calcium channel blockers
  • Digoxin
  • Synthetic narcotics (fentanyl, remi, alfenta, sufenta)
  • Alpha-2 antagonists (dexmedetomidine)
• Increased vagal tone/reflexes
  • Visceral traction (spermatic cord)
  • Laparoscopic insufflation
  • Brainstem manipulation
  • Carotid body manipulation
  • Valsalva
  • Oculocardiac reflex
• Elevated ICP

Treatment

• Ensure adequate oxygenation and ventilation
• Stable vs. unstable? MAP decreased by >20%? EtCO₂ decreased? Weak or absent pulse?
• Stable: glyco (start 0.2 mg), ephedrine (5-10 mg)
• Unstable: atropine (0.5 mg) or epi (50 mcg); transcutaneous pacing for severe or refractory
• Remove offending stimulus! Desufflate abdomen, release ocular traction

Further Work-Up

• EKG: Sinus brady vs. heart block

Tachycardia

Stable vs. Unstable?

Unstable → ACLS guidelines

Stable → Check EKG, changes indicative of ischemia?

Differential Diagnosis

• Inadequate depth of anesthesia: Check that vaporizer is filled, IV is not infiltrated (if during TIVA)
• Inadequate analgesia
• Hypovolemia/hypotension: Check PPV, fluid responsiveness
• Hypoxemia/hypercarbia: FiO₂, EtCO₂
• Hyperthermia: Is warmer on too high?
• Drugs: Did patient miss beta blocker dose? Have you given glycopyrrolate, atropine, ephedrine, etc.? Epi soaked gauze on the field?
• Myocardial ischemia? Check EKG
• Endocrine: pheochromocytoma, thyrotoxicosis
• Hypermetabolic state: trauma patient, burn patient, malignant hyperthermia
• Unusual events: tension PTX, embolism, sepsis

Treatment

• If light anesthesia: anesthetics to deepen
• If inadequate analgesia: opioids
• Hypovolemia: fluids
• Can patient tolerate tachycardia? Does the patient need the tachycardia to maintain hemodynamic stability?
• Can administer B-blocking agents
  • Metoprolol 1-5 mg IV
  • Esmolol 5-10 mg IV
  • Labetalol 5-10 mg IV if HTN as well
• If stable, SVT/Afib
  • May start with beta blockade as above
  • Consider amiodarone 150 mg in 100-cc bag as loading dose (over 10 minutes) followed by 1 mg/min infusion

Anaphylaxis

Clinical Manifestations

• Cardiovascular: tachycardia, hypotension, dysrhythmias
• Respiratory: bronchospasm/wheezing, dyspnea, laryngeal edema, hypoxemia, pulmonary edema
• Dermatologic: rash, facial edema

Etiologies

• Muscle relaxants (succinylcholine, rocuronium, atracurium)
• Latex (gloves, tourniquets, Foley catheters)
• Antibiotics (penicillin, B-lactams)
• Hypnotics (propofol, thiopental)
• Colloids (dextran > albumin > HES)
• Opioids (morphine, meperidine)
• Other (sugammadex, chlorhexidine)

Treatment

• STOP OFFENDING AGENT
• Notify surgeon and your attending; call for help!
• 100% FiO₂
• Ensure adequate IV access
• Rapidly infuse IV fluid (10-30 mL/kg IV) to restore intravascular volume
• If hypotensive, turn off anesthetic agents; consider amnestic agents (ketamine, midazolam)
  • Inhaled anesthetics cause vasodilation
  • Narcotic infusions suppress sympathetic response

Drugs:

• Epinephrine (1-10 mcg/kg IV as needed) to restore BP and decrease mediator release
  • Epi gtt (0.02-0.2 mcg/kg/min) may be required to maintain BP
• Beta-agonists (albuterol) for bronchoconstriction
• Methylprednisolone (2 mg/kg IV, MAX 100 mg) to decrease mediator release
• Diphenhydramine (1 mg/kg IV, MAX 50 mg) to decrease histamine-related effects
• Famotidine (0.25 mg/kg IV) or ranitidine (1 mg/kg IV) to decrease effects of histamine

*If anaphylactic reaction requires laboratory confirmation, send mast cell tryptase level within 2 hours of event

Source: Previous Anesthesia Pocket Survival Guide, Dr. Shaik and Dr. Gonzalez

Source: Kim BA, Yang SW. Anaphylaxis. Chapter 105. Anesthesiology Core Review. Part One: BASIC Exam.

Hypothermia

Source of Heat Loss

• Redistribution: initial decrease in core temperature because of redistribution of heat to the peripheral compartment; most common etiology of hypothermia in the first hour after induction of anesthesia; not heat loss per se, just redistribution of heat
• Radiation: main mechanism of heat loss in the OR; vasodilation and cutaneous blood flow to body surfaces exposed to cold OR environment
• Conduction: dissipation of heat from warm to cool objects that are touching
• Convection: heat loss to airflow surrounding the patient
• Evaporation: heat loss through vaporization (gas exhalation, exposed viscera)

Prevention

• ASA standard: “Every patient receiving anesthesia shall have temperature monitored when clinically significant changes in body temperature are intended, anticipated, or suspected.”
• Skin surface warming (Bair Hugger) for 30 minutes prior to induction of anesthesia has been shown to prevent redistribution hypothermia
• Bair Hugger in OR (upper body ± lower body)
• Warm IV fluids
• Lower gas flows
• Ensure patient’s head is warm (via Bair Hugger, place warm blankets around head, etc.)
• Increase temperature of OR

Source: Patel R, Hawkins K. Hypothermia, Chapter 102. Anesthesiology Core Review. Part One: BASIC Exam.

Source: Sessler DI, Schroeder M, Merrifield B, Matsukawa T, Cheng C. Optimal duration and temperature of prewarming. Anesthesiology. 1995;82:674–81.

Hyperthermia

Etiology

• Drug reactions
  • Serotonin syndrome (SSRIs, MAOIs, amphetamines)
  • Neuroleptic malignant syndrome (antipsychotic medications)
  • Sympathomimetic toxicity (amphetamines, cocaine)
  • Anticholinergic syndrome (antihistamines, antipsychotics, TCAs)
• Transfusion reactions
• Infections
• Exogenous heating sources (forced air warming, fluid warming devices, cardiopulmonary bypass)
• Endocrine: pheochromocytoma, thyroid storm
• Pulmonary: atelectasis, PE, aspiration
• CNS: seizures

Treatment

• Remove external warming devices
• Active cooling strategies: forced air cooling, fluid infusions
• Focused treatment depending on diagnosis

Source: Edwards C. Nonmalignant Hyperthermia. Chapter 103. Anesthesiology Core Review. Part One: BASIC Exam.

Malignant Hyperthermia

MH Hotline: 1-800-644-9737 (1-800-MH-HYPER)

Signs

• Hypermetabolism: increased CO₂ production, increased O₂ consumption, metabolic acidosis
• Increased sympathetic activity: increased HR, increased BP, arrhythmias
• Muscle damage: masseter muscle rigidity, increased serum CK, increased K+, myoglobinemia
• Hyperthermia: fever, diaphoresis

*Nearly 50% of patients with MH have had prior uneventful anesthetic (where they were exposed to triggering agent)

Treatment

• Call for help
• Get Malignant Hyperthermia (MH) Kit
• Stop procedure if possible
• Stop volatile anesthetic. Transition to non-triggering anesthetic. Consider changing circuit and soda lime.
• Request chilled IV saline
• Hyperventilate patient to reduce CO₂: 2-4 times patient’s minute ventilation; 100% FiO₂
• Dantrolene 2.5 mg/kg IV every 5 minutes until symptoms resolve
  • Assign dedicated person to mix dantrolene (20 mg/vial) with 60 mL of sterile water
• Bicarbonate 1-2 mEq/kg IV for suspected metabolic acidosis; maintain pH >7.2
• Cool patient if temperature >39 °C
  • NG lavage with cold water
  • Apply ice externally
  • Infuse cold saline IV
  • Stop cooling if temperature <38 °C
• Hyperkalemia treatment
  • Ca gluconate 30 mg/kg IV or Ca chloride 10 mg/kg IV
  • Sodium bicarbonate 1-2 mEq/kg IV
  • Regular insulin 0.1 units/kg IV (MAX 10 units) and 0.5 g/kg dextrose (MAX 50 mL D50)
• Dysrhythmia treatment: standard antiarrhythmics; do NOT use calcium channel blocker
• Send labs: ABG or VBG, electrolytes, serum CK, serum/urine myoglobin, coagulation
• Place Foley to monitor urine output; ABG, central line
• Call ICU to arrange disposition

Source: Previous Anesthesiology Pocket Survival Guide, Dr. Shaik and Dr. Gonzalez.

Source: OpenAnesthesia keywords: MH Presentation, Malignant Hyperthermia, Malignant Hyperthermia – periop mgmt

Delayed Emergence

Management

Drug Effects

• Ensure anesthetic agents are OFF
• Reverse neuromuscular blockade as appropriate. Check for return of TOF/tetanus with peripheral nerve stimulator. Pseudocholinesterase deficiency?
• Consider narcotic reversal
  • 40 mcg naloxone IV repeat q2 mins up to 0.2 mg
• Too much midazolam?
  • Flumazenil 0.2 mg q1min up to 1 mg
• Excess cholinergics such as scopolamine. Physostigmine 1.25 mg IV can reverse cholinergic effects (e.g., scopolamine) and possibly anesthetic agents
• Alcohol or other drug intoxication

Metabolic Derangements

• Check blood glucose, ABG, and electrolytes
  • Hypo/hyperglycemia?
  • Hypoxia? Assess pulse ox
  • CO₂ narcosis from hypercarbia? Assess EtCO₂. Obtain ABG?
  • Electrolyte abnormalities? Hyponatremia?
  • Acidosis?
• Check patient’s temperature; actively warm if hypothermic Neurologic Disorder

Neurologic Disorder

• If no correctible abnormalities, concern for neurological event?
  • Postictal?
  • Consider head CT scan, neurology/neurosurgery consult to rule out possible CVA
  • Increased ICP?

Source: http://ether.stanford.edu/delayed_emergence.html

Source: https://www.cambridge.org/core/books/postanesthesia-care/signs-and-%20symptoms/B3160878057B599C56AE65B8A215DF30

Source: Open Anesthesia, Delayed emergence: differential diagnosis

Venous Air Embolism

Background

• At-risk surgeries: sitting position (crani, most commonly in surgery in the posterior fossa), C-sections  during uterine exteriorization, any surgery in which the operative field is above the heart
• Adult lethal volume of air entrained as acute bolus: 3-5 mL/kg in adults (~200-300 mL)

Signs

• If patient is awake (e.g., awake crani), first sign will be coughing
• Decreased EtCO₂
• Oxygen desaturation
• Altered mental status, wheezing

Sensitivity of Modalities for VAE detection (most to least sensitive)

• TEE (most sensitive)
• Doppler (L or R parasternal, between 2^nd and 3^rd rib, mill-wheel murmur)
• EtCO₂ and/or PA pressure
• Cardiac output and/or CVP
• Blood pressure, EKG (RV strain pattern, ST depression), stethoscope (least sensitive)

Treatment

• Prevention of further air entrainment: notify surgeon to flood/pack surgical field, lower surgical site if possible
• 100% FiO₂; ensure NO nitrous oxide
• Supportive treatment (pressors PRN)
• Aspiration of air from R atrium – intuitive solution, although this has very questionable success rates
• Hyperbaric oxygen therapy?

Source: http://www.openanesthesia.org/venous_air_embolism/

Source: Mirski MA et al. Diagnosis and Treatment of Vascular Air Embolism. Anesthesiology 2007; 106:164-77. http://www.sarasotaanesthesia.com/reading/monthlyarticles/Anes_Jan07_VenouseAir.pdf

Nonthrombotic Embolism

Fat Embolism

• Associated with traumatic fracture of the femur, pelvis, tibia, and after intramedullary nailing and femoral/knee arthroplasty.
• Bone marrow biopsy, bone marrow transplant, CPR, liposuction, median sternotomy

Signs

• Pulmonary dysfunction is earliest to manifest, 75% of patients; progresses to respiratory failure in 10%
• Nonpalpable petechial rash in chest, axilla, conjunctiva, and neck
• Other nonspecific findings: tachycardia, pyrexia, renal changes, jaundice

Diagnosis

Gurd’s and Wilson’s criteria

• One major and four minor criteria
  • Major criteria: petechial rash, respiratory insufficiency, cerebral involvement
  • Minor criteria: tachycardia, fever, retinal changes, jaundice, renal signs, thrombocytopenia, anemia, high ESR, fat macroglobinemia

Schonfeld’s criteria

• Need a score of 5 or greater
  • Petechiae = 5, X-ray chest diffuse infiltrates = 4, Hypoxemia = 3, Fever = 1, Tachycardia = 1, Tachypnea = 1, Confusion = 1

Treatment

Supportive care

• Management of ARDS
• Management of hemodynamic instability
• Transfusions/bronchodilators to improve oxygenation
• ECMO in severe cases
• Very high mortality in patients with sickle cell disease

Amniotic Fluid Embolism

• Currently pregnant or within 48 hours of delivery
• Multiparity, abruption, intrauterine fetal death, tumultuous labor, oxytocin or prostaglandin hyperstimulation, C-section, manual removal of the placenta

Signs

• Respiratory distress (51%), can lead to ARDS
• Hypotension (27%), can lead to cardiovascular collapse
• Coagulopathy (12%)
• Seizures
• Nausea

Diagnosis

Clinical diagnosis: classic triad: hemodynamic and respiratory compromise accompanied by DIC

• Currently pregnant or within 48 hours of delivery
• One or more of: hypotension, respiratory distress, DIC, or coma and/or seizures
• Absence of other medical explanations

Treatment

AOK treatment:

• Atropine: vagolysis
• Ondansetron: block serotonin receptors, vagolysis
• Ketorolac 30 mg: block thromboxane production

Treatment for coagulopathy: FFP, cryoprecipitate/fibrinogen concentrate, and antifibrinolytics

Source: Shaikh, N. Emergency management of fat embolism syndrome J Emerg Traum Shock. 2009 Jan- Apr; 2(1): 29-33.

Source: https://behindthedrape.wordpress.com/2016/11/21/clinical-update-on-amniotic-fluid-embolism/

Source: https://www.pulmonologyadvisor.com/home/decision-support-in-medicine/pulmonary-%20medicine/nonthrombotic-pulmonary-embolism-air-amniotic-fluid-fat-tumor/

Local Anesthetic Systemic Toxicity – LAST

Background

• Inadvertent IV injection, vascular uptake from local spread
• Bupivacaine is more lipophilic and has greater affinity for voltage-gated sodium channels; greatest cardiotoxic profile

Signs

• Perioral numbness, tinnitus, metallic taste, agitation dysarthria, confusion
• Seizures, coma
• CV derangements: HTN, tachycardia followed by bradycardia and hypotension→ ventricular arrhythmias and asystole
• The majority of adverse events occur within 1 minute after injection of LA

Risks

• Type and dose of LA; more lipophilic = increased risk of toxicity
• Site of injection. Absorption of LA highest to lowest: IV > tracheal > intercostal > caudal > paracervical > epidural > brachial plexus > sciatic
• Extremes of age
• Preexisting cardiac disease can make patients more prone to arrhythmogenic and myocardial depressant effects
• Liver/kidney failure, malnutrition or anything resulting in a decreased albumin

Treatment

• Stop local anesthetic injection
• Lipid emulsion resuscitation: 1.5 mL/kg bolus of 20% intralipid, infusion at 0.25 mL/kg/min (mac 0.5 mL/kg/min). May repeat loading dose × 3
• If pulseless, CPR, <1 mcg/kg epinephrine;  avoid vasopressin
• Treat seizures with benzodiazepines
• May require prolonged resuscitation

Source: https://www.nysora.com/local-anesthetic-systemic-toxicity-last/

Burn

1. Stop the Burning Process
2. Airway Management
   • Administer high flow oxygen/raise head as appropriate to decrease airway edema
   • If there is an airway involvement, early oral intubation is preferable with the largest ETT possible
3. Circulation
   • Secure large bore IV cannula in adequate vein or establish IO (required for patients with burns > 20%)
   • IV/IO may be placed through burned skin if access is needed
   • Two large bore peripheral IV lines preferred for burns > 30%
   • Remove restrictive jewelry/clothing if possible
   • Lactated Ringers (LR) is the fluid of choice; 0.9% Normal Saline (NS) may be used if LR unavailable
   • Initial management (adjust after TBSA calculated – see Step 5):
     • < 5 y/o: LR @ 125mL/hr
     • 6-13 y/o: LR @ 250mL/hr
     • >14 y/o: LR @ 500mL/hr
4. Physical Exam
   • Check for associated injuries
   • Calculate % TBSA using Rule of Nines (see image below) and only include partial and full thickness injuries in calculation
   • Obtain glucose on pediatric patients
   • Utilize cardiac monitor for electrical burn patients
5. Fluid Resuscitation (after TBSA calculated):
   • Deliver 1/2 over first 8 hours, and remaining 1/2 over next 16 hours
     • Adults: LR 2mL/kg/%TBSA
     • Children (<14 yrs or <40kg): LR 3mL/kg/%TBSA
     • Infants <10kg: Add D5LR at maintenance rate to IVF resuscitation (if approved within EMS system protocols)
     • Electrical burns: LR 4mL/kg/%TBSA

Source: Illinois Department of Public Health, Hospital Preparedness Program

Fluids

Transfusion Therapy

Available Blood Components

Suggested Platelet Transfusion Thresholds

<10,000 – Prophylaxis (based on studies in cancer pts N Engl J Med. 337[26]: 1870-1875)

<20,000 – Any bleeding or pre-procedure; pts with concurrent coagulation disorder/infection

<50,000 – Major bleeding or during surgery; prior to CNA or major eye surgery; bleeding with trauma; pretracheal bleeding; after prolonged cardiopulmonary bypass

*Give platelets for ITP with life-threatening bleeding from GI/GU tracts or from CNS; mucous membrane bleeding usually precedes fatal hemorrhage

Indications for FFP Transfusion

INR > 2.0 – Prophylactic transfusion prior to invasive procedures or for actively bleeding pts

INR 1.5 – 2.0 – FFP may be of value in actively bleeding pts; uncertain benefit as pre-procedure prophylaxis; unlikely to correct INR value without massive no. of units of FFP (Transfusion 2006;46:1279)

INR < 1.5 – FFP not indicated

Calculating Allowable Blood Loss

Estimated allowable blood loss = EBV × (H_initial – H_low)/H_initial

H_initial = initial Hct

H_low = final lowest acceptable Hct

Estimated blood volume (EBV) = weight (kg) × average blood volume

Average Blood Volume

• Premature neonates – 95 mL/kg
• Full-term neonates – 85 mL/kg
• Infants – 80 mL/kg
• Adult men – 75 mL/kg
• Adult women – 65 mL/kg

Estimating Blood Loss in Surgical Sponges

• 4×4 sponge – 10 mL fluid capacity
• Ray-tech sponge – 10 – 20 mL fluid capacity
• Lap sponge – 100 mL fluid capacity

Source: https://aneskey.com/electrolytes-transfusion-therapy/

Acid/Base

Acid-Base Disorders Worksheet

Adapted from Joshua Steinberg, M.D.

Acid-Base Guide by Dr. Gallagher

Acute

Chronic

Surgical Patient Changes

Metabolic Acidosis:

• Hypoperfusion – Lactic Acidosis
• Hyperchloremia
• Renal Tubular
• Ketoacidosis

Metabolic Alkalosis:

• GI Losses
• Hypochloremia
• Iatrogenic
• Blood – Large volume

To Solve Acid-Base Problem

1. Determine the pCO₂
2. Based on the pCO₂ determine what the HCO₃ should be
3. If actual HCO₃ is greater than determined HCO₃ – metabolic alkalosis
4. If actual HCO₃ is less than determined HCO₃ – metabolic acidosis

Pure Respiratory Acidosis/Alkalosis

Every pCO₂ changed of 10 torr changes pH by 0.08

• Example:
  • pCO₂ 50 – pH 7.32
  • pCO₂ 30 – pH 7.48

Henderson Equation

Used to validate numbers for acid-base determination.

1. If values calculated on right side of the equation are within 4-5 of the [H+], then probably correct
2. If values calculated on the right side of the equation are >5 from [H+], then probably wrong
3. Calculations of acid base work best the closer in time ABG and BMP are collected