ubp_set_3_extra_topics_copy_20190502182336 Flashcards

1
Q

What are the systemic manifestations of rheumatoid arthritis (RA)?

A

The systemic manifestations of RA are thought to be due to –

  • a vasculitis that develops secondary to the deposition of immune complexes.

Cardiac manifestations include –

  • pericardial thickening,
  • effusion,
  • pericarditis,
  • myocarditis,
  • aortitis,
  • cardiac valve fibrosis,
  • myocardial ischemia,
  • diastolic dysfunction,
  • pulmonary hypertension, and
  • formation of rheumatoid nodules in the conduction system leading to cardiac dysrhythmias.

Other systemic manifestations include –

  • pleural effusions,
  • pulmonary fibrosis,
  • interstitial lung disease,
  • peripheral neuropathy (i.e. carpal tunnel syndrome),
  • liver dysfunction,
  • kidney dysfunction, and
  • mild anemia.

Joint involvement with the potential to affect laryngoscopy typically includes –

  • the cervical spine,
  • temporomandibular joint, and
  • the crico-arytenoid joints making intubation difficult.
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2
Q

What pharmacologic treatment is this patient potentially receiving and how would this change your anesthetic management?

A

The goals of pharmacotherapy for rheumatoid arthritis (RA) include –

  • providing analgesia,
  • reducing inflammation,
  • producing immunosuppression, and
  • inducing remission.

The three groups of drugs commonly used to achieve these goals include:

  1. NSAIDs, to provide analgesia and reduce inflammation and swelling;
  2. disease modifying antirheumatic drugs (DMARDs) = (methotrexate, sulfasalazine, leflunomide, azathioprine, D-penicillamine, etc.), to slow or halt the progression of the disease; and
  3. corticosteroids, to rapidly decrease inflammation until the much slower acting DMARDs begin to bring the illness under better control (usually 2-6 months).

If the patient were taking aspirin or an NSAID, I would evaluate the patient for –

  • gastrointestinal complications (gastric ulcers),
  • renal complications (renal insufficiency), and
  • platelet dysfunction;

adjusting my anesthetic plan based on my findings (drug selection, drug dosing, regional vs. general anesthesia).

If the patient was receiving corticosteroid therapy, I would consider administering perioperative exogenous steroids to compensate for increased perioperative requirements (related to the stress of surgery) and reduce the risk of life-threatening perioperative adrenal insufficiency.

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3
Q

Assume that this patient is receiving a DMARD, which potentially increases the risk of infection.

Would you provide supplemental steroids and further increase this risk in a patient who is about to have a total knee replacement?

A

Given the life-threatening risk of inadequate adrenal function (addisonian crisis),

I would provide perioperative supplementation to anyone who has received the equivalent of 5 mg of prednisone per day (long term suppression of the hypothalamic-pituitary-adrenal axis is unlikely with smaller doses) in the last year

(even topical application of steroids has been demonstrated to potentially depress adrenal function for as long as 9 months to a year).

While there is a real risk of infection with chronic steroid therapy, it is unclear as to whether this risk is further increased with perioperative supplementation.

Moreover, other complications associated with perioperative steroid administration, such as impaired wound healing (although the evidence is inconclusive), hypertension, fluid retention, stress ulcers, and psychiatric disturbances, are rare and/or unproven.

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4
Q

How would you evaluate this airway?

A

Rheumatoid involvement of –

  • the cervical spine (atlantoaxial subluxation, limited neck movement),
  • temporomandibular joint (limited mandibular movement and mouth opening), and
  • crico-arytenoid joints (limited vocal cord movement with narrowed glottic opening, increased risk of crico-arytenoid dislocation),

can lead to difficult airway management.

Therefore, in addition to the normal airway exam, I would perform a focused history and physical examination to identify any signs of involvement in these areas, such as –

  • neurologic deficits,
  • neck and upper extremity pain,
  • headaches,
  • limited range of motion in the cervical spine or temporomandibular joint, and
  • crunching sounds with neck movement.

As always, I would evaluate the patient’s mouth opening, thyromental distance, tongue size, dentition, and Mallampati score.

If there were evidence of possible cervical spine involvement, placing the patient at increased risk of atlantoaxial subluxation –

(anterior subluxation of C1 on C2 could potentially lead to displacement of the odontoid process into the cervical spine, medulla, and vertebral arteries, precipitating quadriparesis, spinal shock, and death),

I would order anteroposterior and lateral cervical spine radiographs, with flexion, extension, and open-mouth odontoid views.

If the separation of the anterior margin of the odontoid process from the posterior margin of the anterior arch of the atlas exceeded 3 mm, I would consult a neurosurgeon and consider proceeding with regional anesthesia.

If general anesthesia were Required for some reason, I would perform an awake fiberoptic intubation with a cervical collar in place (assuming the consulting neurosurgeon agreed to this course of action).

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5
Q

Following surgery the patient complains of bilateral eye irritation and a gritty sensation with blinking.

What do you think is the cause?

A

Bilateral eye irritation with a gritty sensation when blinking is consistent with –
keratoconjunctivitis,

which occurs with impaired lacrimal gland function and subsequent inadequate tear formation.

This condition, along with xerostomia (from impaired salivary gland function),

is a manifestation of Sjogren syndrome (a condition associated with rheumatoid arthritis) and may lead to drying of the eyes and increased risk for perioperative corneal abrasion.

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6
Q

What is your definition of conscious sedation?

(You are asked to write a “conscious sedation” policy for the new endoscopy suite in your hospital.)

A

According to the ASA statement on the definition of general anesthesia and the levels of sedation/analgesia (amended Oct 21, 2009),

moderate sedation/analgesia (“Conscious Sedation”) is a drug-induced depression of consciousness during which patients respond purposefully to verbal commands, either alone or accompanied by light tactile stimulation.

No interventions are required to maintain a patent airway, and spontaneous ventilation is adequate.

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7
Q

What training and supervision would you recommend for non-anesthesia sedation providers?

(You are asked to write a “conscious sedation” policy for the new endoscopy suite in your hospital.)

A

Only physicians, dentists or podiatrists who are qualified by education, training, and licensure to administer moderate sedation should supervise the administration of moderate sedation.

Non-anesthesiologist sedation practitioners may directly supervise patient monitoring and the administration of sedative and analgesic medications by a supervised sedation professional.

The supervised sedation professional who is granted privileges to administer sedative and analgesic drugs under supervision of a non-anesthesiologist sedation practitioner or anesthesiologist and to monitor patients during moderate sedation, can be a registered nurse who has graduated from a qualified school of nursing or a physician assistant who has graduated from an accredited physician assistant program.

They may only administer sedative and analgesic medications on the order of an anesthesiologist or non-anesthesiologist sedation practitioner.

They should have satisfactorily completed a formal training program in –

  1. the safe administration of sedative and analgesic drugs used to establish a level of moderate sedation,
  2. use of reversal agents for opioids and benzodiazepines,
  3. monitoring of patients’ physiologic parameters during sedation, and
  4. recognition of abnormalities in monitored variables that require intervention by the non-anesthesiologist sedation practitioner or anesthesiologist.
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8
Q

What equipment would you require be immediately available?

(You are asked to write a “conscious sedation” policy for the new endoscopy suite in your hospital.)

A

The ASA has set standards for non-operating room anesthetizing locations.

(Statement on non-operating room anesthetizing locations Oct 22, 2008)

At minimum I would require –

  • 2 sources of oxygen,
  • ASA standard monitors,
  • airway equipment,
  • emergency medications,
  • crash cart,
  • a battery powered flashlight, and
  • personnel trained in cardiopulmonary resuscitation.
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9
Q

How would you plan to recover patients following endoscopy?

(You are asked to write a “conscious sedation” policy for the new endoscopy suite in your hospital.)

A

The ASA standards for post anesthetic care apply to all locations and all patients who have received general anesthesia, regional anesthesia, or monitored anesthesia care.

In general, the standards include transfer of the patient to a designated PACU or equivalent area by a member of the anesthesia team, a verbal report of the patient given to the PACU nurse, continual evaluation, and monitoring in the immediate post-operative period.

General medical supervision, coordination of patient care, and discharge from the PACU should be the responsibility of an anesthesiologist.

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10
Q

How would you react to this information?

(Your partner has been acting strange the last several weeks. He is always volunteering to give breaks and take extra weekend call. The pharmacy administrator confides in you that he has been administering inappropriately large doses of narcotics for the procedures being performed and is concerned that he may be diverting narcotics for personal use.)

A

This pattern of behavior is concerning due to risk that drug abuse poses to the health and well-being of the using physician and his patients, as well as exposure of the hospital, staff, and anesthesia department to significant liability.

Therefore, I would immediately share my concern with the head of the anesthesia department and medical staff committee.

Ideally, there would already be policies and procedures in place to help potentially addicted physicians.

A good hospital policy would involve an intervention with my partner to encourage him to undergo a multidisciplinary medical evaluation by a team of experts at an experienced inpatient or residential treatment program.

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11
Q

What is the difference between narcotic abuse, addiction, and dependence?

(Your partner has been acting strange the last several weeks. He is always volunteering to give breaks and take extra weekend call. The pharmacy administrator confides in you that he has been administering inappropriately large doses of narcotics for the procedures being performed and is concerned that he may be diverting narcotics for personal use.)

A

Narcotic abuse is defined as = the use of a psychoactive substance in a manner detrimental to the individual or society but not meeting the criteria for dependence.

Addiction is = a medical disease manifested by compulsive use of an addictive drug with loss of control and irrepressible craving.

Dependence = is a physiological state of adaptation to a specific psychoactive substance characterized by the emergence of a withdrawal syndrome during abstinence.

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12
Q

What is the incidence of substance abuse among anesthesiologists?

(Your partner has been acting strange the last several weeks. He is always volunteering to give breaks and take extra weekend call. The pharmacy administrator confides in you that he has been administering inappropriately large doses of narcotics for the procedures being performed and is concerned that he may be diverting narcotics for personal use.)

A

In 1994-95 the reported incidence among anesthesia residents was 0.40 percent with faculty incidence at 0.10 percent.

Opioids are the drug of choice for anesthesiologists, with fentanyl and sufentanil being the most commonly used, followed by meperidine and morphine.

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13
Q

Is substance abuse more common among anesthesiologists compared to other physicians?

(Your partner has been acting strange the last several weeks. He is always volunteering to give breaks and take extra weekend call. The pharmacy administrator confides in you that he has been administering inappropriately large doses of narcotics for the procedures being performed and is concerned that he may be diverting narcotics for personal use.)

A

Anesthesiologists are over-represented in addiction treatment programs at a rate about three times higher (12-15 percent of physicians in treatment programs) than would be expected based on the percentage of U.S. anesthesiologists.

This may be due to easy access to drugs, being accustomed to giving large doses of mood-altering parenteral substances with immediate results, or because there is more awareness in anesthesiology.

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14
Q

What are the signs, symptoms, and/or behaviors associated with opioid addiction?

(Your partner has been acting strange the last several weeks. He is always volunteering to give breaks and take extra weekend call. The pharmacy administrator confides in you that he has been administering inappropriately large doses of narcotics for the procedures being performed and is concerned that he may be diverting narcotics for personal use.)

A

The signs and symptoms of opioid addiction include:

  1. unusual changes in behavior,
  2. signing out increasing quantities of narcotics,
  3. frequent breakage of narcotic vials,
  4. a desire to work alone,
  5. volunteering for extra cases,
  6. frequent bathroom breaks,
  7. pinpoint pupils,
  8. charting irregularities, and
  9. signs and symptoms of withdrawal, such as diaphoresis, tremors, mydriasis, rhinorrhea, myalgia, nausea, and vomiting.
  10. Other signs of opioid abuse/addiction include – the apparent administration of inappropriately high doses of narcotics for the specific procedures being performed, and
  11. an excessive number of post-operative patients experiencing pain that is disproportionate to charted narcotic dosing.
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15
Q

How can you reduce the risk of substance abuse in your anesthesia department?

(Your partner has been acting strange the last several weeks. He is always volunteering to give breaks and take extra weekend call. The pharmacy administrator confides in you that he has been administering inappropriately large doses of narcotics for the procedures being performed and is concerned that he may be diverting narcotics for personal use.)

A

The incidence, morbidity, and mortality of substance abuse may be reduced by policies that promote physician emotional and physical health, and facilitate the early identification of physicians at risk.

Specifically, each department should –

provide at least one designated, educated member to whom anyone can go for help or information;

ensure physician accountability by monitoring narcotic check-out, utilization, and waste;

aid physicians in stress management; and

provide better addiction-related education to physicians, residents, and medical students.

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16
Q

Type and cross-matched blood is not yet available.

What will you transfuse?

A

If typed and cross-matched blood products were not available and urgent transfusion was needed,

I would transfuse type-O Rh-negative pRBCs and change to type specific pRBC’s when they became available.

Contrary to previous thought, many transfusion specialists consider it safe to convert to type specific blood even when the patient has received 10 or more units of type-O pRBCs.

  • The concern is that the administration of large amounts of type-O blood may result in an accumulation of anti-A and anti-B antibodies leading to an incompatibility reaction when the patient’s own blood type is subsequently administered.
  • However, this concern is probably more justified following the use of whole type-O blood, which contains a significant amount of plasma, rather than pRBCs, which contain only a very minimal amount of plasma.
17
Q

What is the difference between type & screened blood and type & cross-matched blood?

A

Type and screened blood mixes recipient plasma with a panel of commercial RBCs to detect the presence of various known antibodies, and carries the advantage of identifying rare antibodies.

Type and cross-matching takes it a step further, and mixes the recipient plasma with donor RBCs to detect incompatibility with a specific unit to be administered.

The risk of hemolytic reaction is 2/1000 for type-specific blood, 6/10,000 for type and screened blood, and 5/10,000 for type and cross-matched blood.

18
Q

Fifteen minutes after you start transfusing the patient with type specific pRBCs, the patient develops hypotension, tachycardia, and hematuria.

What do you think is happening?

A

The occurrence of hematuria, hypotension, and tachycardia shortly after the administration of non-screened or non-crossmatched blood is consistent with

a hemolytic transfusion reaction,

which is often difficult to detect in patients under general anesthesia.

Given this possibility, I would –

  • stop the transfusion,
  • treat hypotension with fluids and vasopressors,
  • recheck the unit number and patient ID, and
  • obtain appropriate lab work to confirm a hemolytic reaction.

I would then consider administering mannitol, furosemide, and NaHCO3 to preven renal injury.

19
Q

What is the cause of hemolytic transfusion reactions?

A

Hemolytic transfusion reactions are most often due to –

ABO incompatibility secondary to clerical error, and usually result from the binding of anti-A or anti-B IgM antibodies to RBC membranes, causing complement mediated hemolysis.

Other, less common causes of intravascular hemolysis include –

mismatched liver, kidney, or bone marrow transplantations, and incompatible platelets containing anti-A antibodies.

20
Q

What is the pathogenesis of acute porphyrias?

(A 38-year-old female with a history of acute intermittent porphyria presents for an excision of a left breast mass.)

A

The porphyrias result when one of the enzymes in the heme biosynthetic pathway is deficient, resulting in overproduction of porphyrias.

The accumulation of these precursors is responsible for the clinical manifestations of the various forms of porphyria.

The type of porphyria that develops depends on the specific enzyme deficiency, as deficiencies at different points in the pathway lead to the accumulation of different precursors

(there is an accumulation of the chemicals in the heme biosynthetic pathway that immediately precede the enzymatic block).

Only the acute forms of porphyria are “inducible” by exposure to various drugs, potentially resulting in a life-threatening condition characterized by –

severe abdominal pain, nausea, vomiting, psychiatric disturbance, autonomic nervous system instability, electrolyte disturbances, hypovolemia, seizures, skeletal muscle weakness, quadriparesis, and respiratory failure (bulbar paralysis).

Clinical Notes:

  • The combination of autonomic neuropathy, hypovolemia, and CNS involvement may result in cardiovascular instability
    • (usually tachycardia and hypertension, but sometimes hypotension).
  • The most abundant form of porphyrin in the human body is found in the form of – heme, which is bound to proteins to form hemoglobin and cytochrome-P450 proteins.
    • Production of heme is controlled by the activity of the enzyme aminolevulinic acid (ALA) synthetase.
    • In patients susceptible to porphyria, any increase in heme requirements such as anemia or cytochrome-P450 metabolism (since heme is inserted into newly produced cytochrome P450 proteins, the demand for heme is increased with induction of the cytochrome P450 system) may trigger an acute attack of porphyria by reducing the feedback inhibition of ALA synthetase (resulting in increased activation of ALA synthetase).
  • Types of Porphyria:
    • Acute Porphyrias include:
      • Plumboporphyria (aminolevulinic acid dehydratase porphyria)
      • Acute Intermittent Porphyria
      • Hereditary Coproporphyria
      • Variegate Porphyria
    • Other Porphyrias:
      • Congenital Erythropoietic Porphyria
      • Porphyria Cutanea Tarda
      • Erythropoietic Uroporphyria
      • Erythropoietic Protoporphyria
21
Q

How would you evaluate this patient preoperatively?

(A 38-year-old female with a history of acute intermittent porphyria presents for an excision of a left breast mass.)

A

I would focus my preoperative evaluation on the severity and susceptibility of porphyria in this patient.

Therefore, I would perform a careful history and physical to determine –

  • the last time she experienced an acute attack,
  • the precipitating factor,
  • the subsequent treatment, and
  • the presence of any current symptomatology.

Specifically, I would evaluate the patient for the presence of –

  • peripheral neuropathy,
  • autonomic nervous system instability (hypertension and tachycardia),
  • skeletal muscle weakness,
  • cranial nerve dysfunction,
  • fluid imbalance, and
  • electrolyte abnormalities.

Clinical Notes:

  • When the family history suggests possible porphyria susceptibility, a thorough physical exam should be performed to identify –
    • any skin lesions,
    • peripheral neuropathy,
    • autonomic nervous system instability,
    • skeletal muscle weakness, or
    • cranial nerve dysfunction.
      • The most appropriate screening test is a determination of erythrocyte porphobilinogen activity.
  • When there are signs of an acute exacerbation in the preoperative period:
    • Elective surgery should be postponed.
    • An assessment of skeletal muscle strength and cranial nerve function should be performed
      • (cranial nerve dysfunction and diminished skeletal muscle strength are associated with an increased risk of aspiration and impending respiratory failure).
    • Tachycardia, hypertension, hypovolemia, and electrolyte disturbances should be identified and treated/corrected.
22
Q

What steps would you take to reduce the risk of triggering a porphyric crisis?

(A 38-year-old female with a history of acute intermittent porphyria presents for an excision of a left breast mass.)

A

To reduce the risk, I would attempt to – AVOID and/or MINIMIZE factors that can lead to hormonal fluctuations suspected of potentially inducing a porphyric crisis, such as – fasting, dehydration, stress, and infection.

Therefore, I would ensure – adequate hydration, administer versed for anxiolysis, and consider administering 10% glucose in saline to provide a source of carbohydrates, which have been shown to suppress porphyrin synthesis.

I would also avoid drugs suspected to have porphyrinogenic potential (drugs that induce the activity of ALA synthetase or interfere with negative feedback control – (i.e. drugs that require P-450 for their metabolism), such as Thiopental, Thiamylal, Methohexital, Etomidate, Ketorolac, Phenacetin, and Nifedipine.

I would also keep in mind that the administration of multiple potential enzyme-inducing drugs is more dangerous than exposure to any one drug and remember that repeated or prolonged use of one of these drugs may further increase the risk of inducing a crisis.

Clinical Notes:

  • Lists of “safe” and “unsafe” anesthetic drugs are unreliable because they are based on animal or cell culture experiments.
    • Moreover, it is difficult to attribute an acute perioperative exacerbation to any given drug because there are a number of other factors that could potentially precipitate an event such as stress, fasting, or sepsis.
  • Anesthetic agents that are “likely safe” include – propofol, ketamine, nitrous oxide, volatile agents, most analgesics (except ketorolac), and neuromuscular blocking drugs.
  • Regional anesthesia has been safely utilized in porphyric patients, however:
    • It should probably be avoided during an acute exacerbation of acute intermittent porphyria due to the hemodynamic instability, porphyria-related neuropathy, and mental confusion often associated with an acute attack.
    • A prior neurologic exam should be performed in order to reduce the risk in that an exacerbation of a neuropathy will be inappropriately attributed to the regional anesthetic.
23
Q

The post-op nurse calls you and reports that the patient is experiencing nausea, vomiting, and abdominal pain.

What would you do?

(A 38-year-old female with a history of acute intermittent porphyria presents for an excision of a left breast mass.)

A

This patient’s symptomatology is consistent with a porphyric crisis.

Therefore, I would:

  1. discontinue any porphyrinogenic drugs;
  2. ensure adequate ventilation, oxygenation, hydration, analgesia, and anxiolysis;
  3. administer carbohydrates (initiate an infusion of 10% glucose in saline);
  4. treat any nausea and vomiting with an antiemetic;
  5. control any tachycardia and/or hypertension with B-blockers;
  6. correct any electrolyte disturbances; and
  7. treat the development of any seizure activity with a benzodiazepine or propofol (traditional anticonvulsants are considered unsafe). If she showed no improvement after 1-2 days of conservative therapy, I would –
  8. administer hematin to supplement the intracellular pool of heme, thereby suppressing ALA synthetase activity (3 to 4 mg/kg IV over 20 minutes).
24
Q

What ventilator settings would you order for this patient?

(You are transferring a critically ill patient with chronic obstructive pulmonary disease (COPD), who failed to meet extubation criteria, to the ICU for postoperative mechanical ventilation.)

A

Keeping in mind that this is a critically ill patient with COPD, I would employ ventilator settings that minimize the risk of cardiovascular compromise or additional lung injury.

First, recognizing that the delivery of supraphysiologic tidal volumes ( >/= 8 mL/kg) to this critically ill patient with COPD could potentially lead to cardiovascular compromise (reduced venous return with increasing intrathoracic pressures), barotrauma, and ventilator-associated lung injury (VALI), I would set his initial tidal volumes at 6 mL/kg (ideal body weight should be used rather than actual body weight, since lung volumes more closely correlate with height than weight).

Given the risk of auto-PEEP (air trapping) associated with COPD secondary to limited expiratory flow (auto-PEEP increases the risk of barotrauma, pneumothorax, cardiovascular compromise, and VALI), and recognizing the increased morbidity and mortality associated with the development of auto-PEEP in COPD patients,

I would provide adequate sedation and attempt to prolong the expiratory time by employing low tidal volumes, a low rate of ventilation (8-12 breaths/minute), and a reduced inspiratory time.

25
Q

Wouldn’t this strategy result in increased peak airway pressures and risk the development of respiratory acidosis?

Does this concern you?

(You are transferring a critically ill patient with chronic obstructive pulmonary disease (COPD), who failed to meet extubation criteria, to the ICU for postoperative mechanical ventilation.)

A

A reduced inspiratory time does necessarily result in increased inspiratory flow rate and, subsequently, increased peak airway pressures.

However, most of the peak pressure is dissipated as gas flows through the endotracheal tube and large airways, making this an acceptable trade for an increased expiratory time, which can significantly reduce ventilator-associated complications in COPD patients.

Moreover, the increased expiratory time leads to a reduction in end-expiratory, static or plateau, and mean airway pressures, despite the increased inspiratory flow rate.

Finally, while hypercapnia and respiratory acidosis are not desirable, the benefits of avoiding significant auto-PEEP most likely outweigh the potential detrimental effects of respiratory acidosis in this patient.

26
Q

How would you wean this patient from mechanical ventilation?

(You are transferring a critically ill patient with chronic obstructive pulmonary disease (COPD), who failed to meet extubation criteria, to the ICU for postoperative mechanical ventilation.)

A

There are several options for weaning a patient from mechanically supported ventilation such as:

  1. a progressive reduction in the number of mandatory breaths/minute while employing synchronized intermittent mandatory ventilation,
  2. the incremental reduction of pressure-support ventilation, and
  3. trials of total separation of the patient from mechanical ventilation (“T-piece trials”).

However, the most important component of separating the patient from mechanical ventilation is the resolution of the underlying condition responsible for the needed respiratory support.

Therefore, I would treat the underlying condition and employ daily T-piece trials once the inciting condition improved, the patient was hemodynamically stable, and his oxygenation was adequate.

27
Q

When would you extubate him?

(You are transferring a critically ill patient with chronic obstructive pulmonary disease (COPD), who failed to meet extubation criteria, to the ICU for postoperative mechanical ventilation.)

A

I would consider extubation when

he was awake and alert,

demonstrating active laryngeal reflexes,

generating an effective cough and clearing secretions, and

when he was able to comfortably breathe without ventilatory support for 2 hours without experiencing a deterioration of his cardiac function, mental status, or arterial blood gases.

Moreover, I would take into consideration other proposed extubation criteria such as:

  1. a Pao2 above 60 mmHg with a Fio2 < 50%,
  2. a PaCo2 less than 50 mmHg,
  3. an arterial pH > 7.30,
  4. a vital capacity > 15 mL/kg, and
  5. required < 5 cm H2O.

Clinical Notes:

  • Modes of Ventilation: Mechanical ventilators are typically volume or pressure cycled, although some newer models combine features of both.
    • Volume-cycled ventilation includes assist-control (A/C), Continuous mandatory ventilation (CMV), and synchronized intermittent mandatory ventilation (SIMV). This mode of ventilation delivers a set tidal volume, with airway pressures varying according to lung compliance and the selected flow rate.
      • A/C - This mode is the simplest and most effective means of providing full mechanical ventilation. In this mode, each inspiratory effort beyond the set sensitivity threshold triggers delivery of a fixed tidal volume. In order to ensure a desired minimum respiratory rate, a mandatory respiratory rate is established.
      • CMV - In this mode, the ventilator provides mechanical breaths according to a preset rate and volume, ignoring any patient respiratory effort. This mode of ventilation is uncomfortable, usually requiring patient sedation.
      • SIMV - Like CMV, this mode of ventilation delivers breaths at a preset rate and volume. However, in this mode, the breaths are synchronized to the patient’s efforts. Moreover, in contrast to A/C ventilation, patient efforts above the set respiratory rate are unassisted.
    • Pressure-cycled ventilation includes continuous positive airway pressure (CPAP), pressure control ventilation (PCV), pressure support ventilation (PSV), airway pressure-release ventilation (APRV), and several noninvasive modalities. With all of these modes, the ventilator delivers a set inspiratory pressure, with tidal volume varying according to lung compliance. Unfortunately, changes in respiratory system mechanics can result in unrecognized changes in minute ventilation.
      • CPAP - provides a continuous level of elevated pressure to maintain adequate oxygenation, and decrease the work of breathing. No cycling of ventilator pressures occurs and the patient must initiate all breaths. CPAP may be used invasively through an endotracheal tube or tracheostomy or non-invasively with a face mask or nasal prongs.
      • Pressure control ventilation - is similar to A/C ventilation, except that each inspiratory effort beyond the set sensitivity threshold delivers a set amount of pressure support rather than a set tidal volume. This mode of ventilation is set to maintain a minimum respiratory rate and the preset pressure is maintained for a fixed inspiratory time.
      • Pressure support ventilation - provides ventilation support only when triggered by the patient. Pressure is typically cut off when backpressure causes flow to drop below a certain point. Thus, a longer or deep inspiratory effort by the patient results in a larger tidal volume. This mode is commonly used to liberate patients from mechanical ventilation by letting them assume more of the work of breathing. However, there is not sufficient evidence to indicate that this approach is more successful.
      • APRV - This mode of ventilation cycles between two different levels of CPAP - an upper pressure level (inspiratory) and a lower pressure level (expiratory). The bi-level positive airway pressure allows gas movement in and out of the lung, while maintaining continuous positive pressure. It is important to understand that the baseline airway pressure is the upper CPAP level, and that this baseline pressure is intermittently “released” (decreased) to a lower level in order to eliminate waste gas.
    • Some of the newest modes integrate volume- and pressure-targeted concepts as in SIMV + PS, in which the mandatory (SIMV) breaths deliver a target volume during inspiration and the patient’s spontaneous breaths are supported with a target pressure.
28
Q

What possible complications would you anticipate?

(A 6-year-old female is scheduled for laser treatment of laryngeal polyps.)

A

In this case, I would anticipate the possibility of difficult intubation, difficult mask ventilation, airway obstruction, airway fire, bronchospasm, laryngospasm, and corneal or tissue burns.

Additionally, if a jet ventilation technique is employed, there is increased risk of barotrauma and/or distribution of the papilloma virus into lower airways.

Finally, operating personnel are at risk of inhaling vaporized debris and eye injury, necessitating the use of special surgical masks and laser-specific eye goggles.

Therefore, to minimize the risk of complications, I would ensure the presence of adequate airway equipment, laser protective wear, skilled personnel, and emergency medications.

I would also take precautions to avoid and/or address an airway fire, such as –

using a laser-resistant ETT, having a syringe of normal saline available (to douse an airway fire), delivering no more than 30% oxygen during laser use, and preparing a plan of action to deal with an airway fire.

29
Q

The ETT ignites during laser treatment.

What would you do?

(A 6-year-old female is scheduled for laser treatment of laryngeal polyps.)

A

I would alert the surgical team, stop ventilation, disconnect the oxygen supply from the airway, and remove the endotracheal tube.

If the flame persists, I would flood the surgical field with saline.

Once the fire has been extinguished, I would ventilate with 100% oxygen, reintubate the patient, and perform bronchoscopy to rule out foreign bodies and assess the extent of lower airway damage and edema.

Depending on the extent of the injury, I would consult a pulmonologist and monitor the patient with serial chest x-rays and continuous pulse oximetry.

30
Q

Could this have been prevented?

  • (The ETT ignites during laser treatment.)*
  • (A 6-year-old female is scheduled for laser treatment of laryngeal polyps.)*
A

Not necessarily, but there are multiple steps that can be taken to reduce the risk of airway fire, including –

using a laser-resistant endotracheal tube, decreasing the concentration of gases that support combustion, filling the ETT cuff with saline, and limiting the intensity and duration of laser treatment.

Other options include –

employing an apneic anesthetic technique without an endotracheal tube, or utilizing a jet ventilator to avoid the need of an endotracheal tube in the oropharynx during laser use.

31
Q

What does Laser stand for?

(A 6-year-old female is scheduled for laser treatment of laryngeal polyps.)

A

The word laser is an acronym for light amplification by stimulated emission of radiation.

Laser energy rapidly increases the temperature of tissue water, denatures proteins, and results in vaporization of the target tissue.

32
Q

How would you manage the care of this neonate?

(You are called to be available during the vaginal delivery of a term neonate. The mother has refused an epidural for labor and thick meconium was noted following artificial rupture of maternal membranes. Moreover, she is a diabetic patient with preeclampsia.)

A

Prior to delivery

I would ensure that the appropriate support personnel and equipment were available for neonatal resuscitation

(i.e. a self-inflating bag attached to 100% oxygen, a neonatal oxygen mask, wall suction, a radiant warmer or other heat source, warmed linens, appropriately sized laryngoscopy blade and ETTs, resuscitation medications, and blow by oxygen capabilities).

My intervention following delivery would depend on the condition of the neonate.

If the neonate was vigorous, with strong respiratory effort, good muscle tone, and a heart rate > 100 beats/minute, I would dry and stimulate the baby, provide warmth, position and clear the airway as necessary, and continue to evaluate respirations, color, and heart rate.

If, however, the baby was not vigorous, I would – repeatedly suction the trachea until only a small amount of meconium was recovered (usually with an endotracheal tube attached to a meconium aspirator which is attached to a regulated suction source), or until it was necessary to proceed with additional resuscitative measures.

Further resuscitative efforts would be based on a continual assessment of respirations, heart rate, and color.

Clinical Note:

  • Current recommendations NO longer support routine intrapartum oropharyngeal suctioning (i.e. bulb suction when following delivery of the head and prior to delivery of the shoulders) of neonates born to mothers with meconium staining of the amniotic fluid.
  • This is due to the fact that large multicenter studies have not demonstrated any benefit to this practice, combined with the potential for inducing bradycardia in the neonate with vigorous oropharyngeal stimulation.
  • Also, the decision to perform endotracheal suctioning is no longer based on the density of meconium staining (“thick” or “thin”).
  • Rather, the recommendation is to base your decision on whether the baby is vigorous or not (tracheal suctioning should be performed if the baby does not demonstrate strong respiratory effort, good muscle tone, and a heart rate > 100 beats/minute).
33
Q

Immediately following delivery, the baby is making no respiratory effort, grimaces with stimulation, demonstrates flaccid muscle tone, is acrocyanotic, and has a heart rate of 80 bpm.

What is this infant’s APGAR score?

(You are called to be available during the vaginal delivery of a term neonate. The mother has refused an epidural for labor and thick meconium was noted following artificial rupture of maternal membranes. Moreover, she is a diabetic patient with preeclampsia.)

A

Since the baby grimaces with stimulation (+1), is flaccid (+0), demonstrates no respiratory effort (+0), is acrocyanotic (+1), and has a herart rate < 100 bpm (+1),

he would be assigned an APGAR score of three.

The APGAR score, which was developed to aid in the rapid assessment of the newborn, is calculated by summing the assigned score (ranging from 0-2 points) for 5 different categories, consisting of the following:

  • Appearance (skin color),
  • Pulse (heart rate),
  • Grimace (reflex irritability),
  • Activity (muscle tone),
  • Respirations (breathing rate and effort).

The score is assessed at both 1 and 5 minutes following delivery, with a score of 8-10 indicating a normal clinical status; a score of 4-7 indicating moderate impairment; and a score of 0-3 indicating a need for immediate resuscitation.

  • Clinical Note:*
  • (see Apgar score figure attached)*
34
Q

How would you treat this infant?

(You are called to be available during the vaginal delivery of a term neonate. The mother has refused an epidural for labor and thick meconium was noted following artificial rupture of maternal membranes. Moreover, she is a diabetic patient with preeclampsia.)

A

After suctioning the trachea until only a small amount of meconium was recovered, I would dry and stimulate the baby, provide warmth, position and clear the airway as necessary, and continue to evaluate his respirations and heart rate.

If after following these initial steps the baby’s heart rate was still below 100, he remained apneic, or he was gasping, I would provide positive mask ventilation with air, or an air/oxygen mixture, and consider applying a pulse oximeter.

If after 30 seconds of positive mask ventilation the HR was less than 60, then I would intubate, increase the oxygen concentration to 100%, begin chest compressions (3 compressions to 1 breath for a total of 120 events/minute), and establish venous (umbilical vein catheterization) or intraosseous access (risks include tibial fracture and osteomyelitis).

If after another 30 seconds there were still no improvement, I would administer 0.01-0.03 mg/kg of epinephrine via the umbilical vein or established intraosseous access, and consider volume expansion.

Hypoglycemia, magnesium toxicity, and narcosis should also be considered in this particular case given the mother’s diabetes, probably treatment with magnesium sulfate (due to her preeclampsia), and pain control with intravenous narcotics.

If magnesium toxicity were confirmed, I would administer calcium (100 mg/kg of calcium gluconate or 30 mg/kg of CaCl2), recognizing that calcium therapy has been associated with cerebral calcification and decreased survival in stressed newborns (therefore, it should only be administered to reverse the effects of magnesium toxicity).

In the case of hypoglycemia (glucose < 35 mg/dL), glucose should be administered (8 mg/kg/minute of 10% solution).

While placental transfer of maternally administered narcotics could potentially be exacerbating this neonate’s condition, I would not administer naloxone unless all other resuscitative efforts had failed;

as this drug is no longer recommended during the initial resuscitation in the delivery room (can worsen the neurologic damage caused by asphyxia).

If I felt that the administration of naloxone was necessary, I would first ensure the restoration of the neonate’s heart rate and color with supported ventilation and then give 0.1 mg/kg by either the intravenous or intramuscular route (endotracheal administration is no longer recommended).

Given the relatively short duration of action of naloxone when compared to many narcotics, I would plan to monitor the neonate for an extended period of time to avoid recurrent respiratory depression.

  • Clinical Notes:*
  • Naloxone administration should be avoided when the neonate’s mother is suspected of long-term opioid abuse, because it has been associated with seizures and intraventricular hemorrhage under these circumstances.
35
Q

When would you consider placing a pulse oximeter and where would you place it?

(You are called to be available during the vaginal delivery of a term neonate. The mother has refused an epidural for labor and thick meconium was noted following artificial rupture of maternal membranes. Moreover, she is a diabetic patient with preeclampsia.)

A

I would consider utilizing oximetry –

  • when I anticipated the need for resuscitation,
  • when positive pressure ventilation was required for more than a few breaths,
  • when supplemental oxygen was necessary, or
  • when cyanosis was persistent.

I would place the oximeter on the right upper extremity (finger, wrist, or medial palmar surface) in order to monitor pre-ductal blood flow, which provides a better assessment of central nervous system oxygenation.

Unfortunately, it often takes 1-2 minutes to place and obtain reliable readings from the pulse oximeter.