Posts by ciberweb

    Preop:


    Additional studies:

    • CT scan: location, size, shape of the lesion
    • Pulmonary function test: none needed it
    • Cardiovascular Test : EKG and echo
      • Chronic airway instruction:
        • EKG:
          • Right atrial hypertrophy: P waves in leads II, III and aVF
          • Right ventricular hypertrophy: right axis deviation and partial or complete right bundle branch block
    • Airway bleeding, airway fire, obstruction of the surgical field, seeding of the papillomas into the distant airways, failure to pass the ETT as a result of the airway obstruction, increase airway resistance, and further airway is scarring from repeated airway manipulation and surgeries.

    Premedications: versed


    IV placement: in preop if patient comfortable otherwise will do it in the OR


    Intraop:


    If the patient doesn’t have an IV, I will perform as slow inhalation induction with sevoflurane and 100% oxygen and maintain a spontaneous respirations.


    If the patient have a IV in place, I would induce with lidocaine, glycopyrrolate, midazolam and Ketamine.


    In either case, I would have emergency airway equipment in the room and a ENT doctor in a standby for an amazing tracheostomy if the airway is lost.


    Problems with intubation:



    Precautions while using a carbon dioxide laser:


    Flammable surgical drapes should be minimize and wet towels should cover the face, neck, shoulder to absorb laser energy. The eyes should be protected with shield or moist gauze pads. Safety glasses should be worn by operating room personnel. Fio2 should be as low posible and nitrous oxide must not be used.


    Laser safety ETT with saline filled cuff, fire extinguisher, smoke evacuator, especially masks to prevent the spread of virus upon vaporization


    Airway Fire


    Call for help, stop the flow of oxygen, disconnect the ETT from the gas source, and immediately extubate, ensuring that the entire ETT has been removed. A chest x-ray and a bronchoscopy should be performed to determine the extent of injury.


    Postop:


    If mild edema:


    After resecuring the airway with a smaller size ETT, I would continue with conservative measures by monitoring and giving humidified oxygen, steroids, and racemic epinephrine

    This is a disease of motor weakness that is often characterized by proximal weakness, especially of the lower extremities. It is caused by autoantibodies to the voltage gated calcium channels of the presynaptic membrane. Calcium is not able to enter the nerve ending and to allow acetylcholine release.


    Weakness typically improves with repetitive use as these allow to build up calcium.


    Patients are sensitive to both the depolarizing and nondepolarizing muscle relaxants and patient may need postoperative ventilatory support.


    It is often seen as a paraneoplastic syndrome related to a small cell cancer of the lung. It may also be seen with sarcoidosis, other malignancies, thyroiditis, and collagen vascular disease

    Corticosteroids suppress the immune system and attenuate the production of this abnormal antibodies to acetylcholine receptor at the motor endplate.


    Treatment start with cholinesterase inhibitor . In more advances cases corticosteroids and thymectomy are used. In more severe cases, immunosuppressant (such as azathioprine or cyclosporine)and plasmapheresis are used. Intravenous immunoglobulins is used for myasthenic crisis.

    Recommended the use the same day of surgery to avoid any possible respiratory difficulty before surgery.


    The disadvantage of continuing cholinesterase inhibitor is the possibility of prolonged motor block with succinylcholine, and the possibility of developing cholinergic crisis

    It is an autoimmune disorder involving antibodies the subunit alpha of the postsynaptic nicotinic acetylcholine receptor at the neuromuscular junction leading to a decrease number of functional receptors.


    With repeated simulation and decrease acetylcholine release, fatigue occurs.


    The extent of involvement can be limited to ocular muscles, but muscles of respiration and swallowing can also be involved, causing distressed or aspiration


    MG is associated with thymus hyperplasia, thymomas, or autoimmune disease such as thyroid disease, pernicious anemia and rheumatoid arthritis. MH also occurs in women’s with certain HLA types.


    Unstable vital signs: hypoxia, hypotension, malignant arrhythmia


    Anesthesia - induced causes: residual anesthesia, narcotic overdose or reaction


    Possible delirium tremens from withdrawal from a previously unknown substance abuse agent


    Potential metabolic end endocrinological causes: hyponatremia, hypokalemia, hypoglycemia, hyperglycemia, hypothermia, hypothyroidism, and Addison’s disease


    Neurological causes: include postictal state, cerebral edema, and stroke


    As soon the event occurred:


    Go to the patient:

    • Check the monitor: signs of hypoxia, changes in the blood pressure, malignant arrhythmia
    • Perform a focused history and physical:
      • History: check the anesthesia record, I check the nurses notes, for medications, when the symptoms started, are they getting better or worse, and severity
      • Physical: check breast sounds, look for neurological signs, including pupillary size, and any focal neurological deficit
    • Stat labs: Arterial blood gases, electrolytes and glucose, CBC.
    • If a stroke is suspected a CT scan should be realized.

    PCA ( patient controlled analgesia)


    Can provide relief without risking overdosing as the patient must be aware and alert in order to administrate the medicine


    PCEA ( patient controlled epidural analgesia)


    Less opioid medication is used because of the local anesthesia can also be delivered epidurally.

    Impaired immune response will increased risk of infection


    Impaired wound healing


    Dehydration


    Electrolyte disturbances secondary to the osmotic diuretic effect of high serum glucose levels


    The diabetic patient who takes oral hypoglycemic medication is at risk for developing potentially fatal nonketotic hyperosmolar coma

    Respiratory parameters for extubation:


    RR: 10-30 B/min


    Sat: >95%


    VC: >10 ml/kg of IBW


    TV: >5 ml/kg of IBW


    Have an emergency airway equipment on standby


    Patient is sitting position to optimize the pulmonary mechanics


    Reversed the paralytics


    Patient is spontaneously breathing


    As soon the patient respond to commands and is able to protect his airway, we will extubate

    Based on the information provided, management of the patient and airway may be difficult, so to follow we need to do an fiber optic awake intubation


    step one: we pre-oxygenate with 100% oxygen


    step two: topicalize the airway with 1%-2% lidocaine spray or nebulize and perform a superior laryngeal nerve block and a transtracheal recurrent nerve block

    Preoperably:

    • history and physical to assess comorbid conditions
    • limited use of sedatives: because increases sensitivity in obstructive sleep apnea
      • ketamine
      • Sodium citrate
      • Metoclopramide
    • airway exam, because possible difficult airway

    Intraoperatively:

    • Preoxygenation: prone to desaturation because decrease FRC
    • if the airway is difficult, have the difficult airway card in the room , for an awake intubation
    • Multimodal pain management
      • IV NSAIDS
      • IV Tylenol
      • Rectus Sheath block
      • Local wound infiltration

    Monitors

    • Standard American Society of Anesthesiologists monitors
      • pulse oximeter
      • 5 lead EKG
      • Non invasive blood pressure
      • Temperature probe
      • Capnograft
    • Foley catheter
    • Intravenous access is difficult, would place a centerline



    Postoperatively:

    • Extubate in the head of position to improve pulmonary mechanics an extubate only after the patient is fully awake.
    • Have a CPAP machine in the post anesthesia care unit and continue to monitor the patient close in the PACU for any episodes of apnea and desaturation

    OSA: no airflow x 10 seconds, more than five times per hour



    The Pickwickian syndrome


    chronic hypoventilation that is worse during sleep, resulting in an elevation partial pressure of carbon dioxide levels.


    A diagnosis of PS


    Bmi>30


    Paco2 >44


    no alternative explanation for hypoventilation

    Cardiac: patient usually have hypertension and left ventricular hypertrophy. Pulmonary hypertension may also present.


    Pulmonary: there is increased ventilation/perfusion mismatch from decreased functional residual capacity


    Gastrointestinal: often the stomach is dispensed upward because of the extra abdominal, placing them at risk for good


    Renal: the patient may have hypertensive nephropathy


    Neurological: hyper somnolence is frequently observed with increased sensitivity to aesthetic agents