Medicine Flashcards
What is the difference between moderate sedation and deep sedation
Moderate sedation allows purposeful responses to verbal or tactile stimulation with adequate spontaneous ventilation and no airway intervention, while deep sedation requires repeated or painful stimulation for a response, and airway intervention may be needed due to inadequate spontaneous ventilation. CV are maintained in both.
ASA Classifications
Class I: A healthy patient
Class II: mild systemic disease WITHOUT functional limitations
– Ex: current smoker, social alcohol drinker, pregnancy, obesity (BMI 30–40), well-controlled DM/HTN, mild lung disease.
* Class III: severe systemic disease that limits activity but is not incapacitating
– Ex: poorly controlled DM/HTN,COPD, morbid obesity (BMI ≥40), active hepatitis, ESRD with dialysis, history (>3 months) of MI, CVA, TIA, or CAD/ stents.
Class IV: severe systemic disease with constant threat to life.
– Ex: recent (< 3 months) MI, CVA,TIA, or CAD/stents, ongoing cardiac ischemia.
Class V: moribund patient who is not expected to survive without operation.
* Class VI: declared brain-dead patient whose organs are being removed for donor purposes.
BMI scales
- BMI Scale (m/kg2):
- Normal: 18.5–24.9
- Overweight: 25–29.9
- Obese: 30–39.9 ASA II
- Morbidly obese:
40–49.9 ASA III - Super obese: >50
Describe your airway examination?
I perform a head & neck exam, TMJ exam, I would measure thyromental distance , neck circumference , neck mobility, mandible size and position, MIO, intraoral and dental exam, mallampati score & tongue and tonsil sizes and I auscultate the heart and lungs.
Mallampati Score
Class I: soft palate, uvula, tonsillar pillars, and fauces are visible.
– Class II: superior 2/3 of uvula and soft palate are visible.
– Class III: <1/3rd of uvula and soft palate are visible.
– Class IV: soft palate not visible.
Describe the thyromental Distance?
The distance between the top of the thyroid cartilage and the menton of the mandible. It is an indicator of the ability to displace the tongue during direct laryngoscopy. A distance of <6.5 cm (three finger breadths) may indicate difficulty with intubation.
Describe the Neck Circumference?
if greater than 43 cm (17 inches), associated with difficulty for intubation, more predictive than BMI.
What Cormack-Lehane classification?
The Cormack-Lehane classification is used to describe the view of the vocal cords during laryngoscopy and assess airway difficulty.
Grade I:
Full view of the vocal cords.
Easiest for intubation.
Grade II:
Partial view of the vocal cords.
May require adjustments for intubation.
Grade III:
Only the epiglottis is visible.
Intubation is challenging;
Grade IV:
Neither the vocal cords nor the epiglottis are visible.
Intubation is very difficult;
What is the Fishbaugh classification for tonsillar hypertrophy?
Fishbaugh Classification for Tonsillar Hypertrophy is a system used to grade the size of the tonsils based on their relation to the space between the tonsillar pillars.
Grade 0:
Tonsils are absent (e.g., post-tonsillectomy).
Grade 1:
Tonsils occupy less than 25% of the oropharyngeal width.
Grade 2:
Tonsils occupy 25%–50% of the oropharyngeal width.
Grade 3:
Tonsils occupy 50%–75% of the oropharyngeal width.
Grade 4:
Tonsils occupy 75%–100% of the oropharyngeal width, often touching at the midline (“kissing tonsils”).
Describe the differences between adult and pediatric airway?
- Pediatric airway is smaller. Uncuffed ET size = age in years/4 +4
- Large occiput
- Large tongue and smaller mouth
- Obligatory nose breather
- Large tonsils and adenoids
- Larynx is higher and more anterior. At the level 2-3 cervical vertebrae, adult 6-7
- Epiglottis is floppy and project posteriorly.
- Cricoid rings are narrowest point of airway.
- Length of the trachea is smaller.
How do you determine the appropriate size and depth of an endotracheal tube (ETT) in pediatric patients, and what anatomical differences influence the choice of cuffed versus uncuffed tubes?
- Children younger than 8 have an anatomical narrowing at the cricoid ring that provides a natural “cuff.”
- Children who are 8 and older can tolerate a cuffed tube more easily.
- A cuffed tube is commonly used because of high volume/low pressure.
Several formulas are available:
1- Uncuffed tracheal tube size: [age (in years)/4]+4 = internal diameter (in millimeters).
2- Cuffed tracheal tube size: [age (in years)/4]+3 = internal diameter (in millimeters).
3- Depth of insertion: [age (in years)/2]+12 = depth of insertion (in centimeters).
What is Down syndrome?
Trisomy 21, genetic condition caused by the presence of an extra copy of chromosome 21 which affects the development of the body and brain.
What are some features of down syndrom?
- Intellectual disability
- Cardiac conditions: atrioventricular septal defect, patent ductus arteriosus, and tetralogy of Fallot.
- Dentofacial deformities: Flattened face, small head, short neck , slanting eyelid , macroglossia , short hand, small ear.
What is Tetralogy of Fallot (TOF) and what are the components?
Congenital heart defect affect blood flow and oxygenation.
It includes four main structural heart abnormalities:
1- Pulmonary stenosis
2- Right ventricular hypertrophy
3- Overriding aorta
4- Ventricular septal defect (VSD)
How do you work up down syndrom patient prior sedation.
- Communicate with the cardioligiest
- Ideally treat the patient in the hospital.
- Obtain CBC, BMP, EKG and Echo
- If the patient uncooperative premedicate with:
Oral Midazolam (Versed):
Dose:0.5 mg/kg(maximum 20 mg) given20–45 minutesprior to anesthesia.
Can be mixed with syrup or juice
Your patient is extremely anxious and combative, refusing IV placement. What premedication options can you consider to manage the situation effectively?
1- Oral Midazolam (Versed):
Dose:0.5 mg/kg(maximum 20 mg) given20–45 minutesprior to anesthesia.
Can be mixed with syrup or juice
2- IM Ketamin Dart 4mg/kg
onset of action is typically 2–4 minutes.
3- Intramuscular Ketamine Combination:
Dose:1.5 mg/kg ketamine
+0.1mg glycopyrrolate(to reduce secretions) +0.1 mg/kg midazolam.
Total IM dose should not exceed3 ccin the anterolateral thigh.
Follow with IV midazolam for anxiolysis and to minimize ketamine-related emergence delirium.
4- Oral Clonidine:
α2-agonist causing sedation, anxiolysis, and analgesia.
Dose based on weight:
≤50 lbs:0.1 mg (1 tablet).
51–75 lbs:1.5 tablets (0.15 mg).
75 lbs:2 tablets (0.2 mg).
Crush tablets and administer in-office under monitoring.
What is Sickle Cell Anemia (SCA) ?
- Autosomal recessive disorder causes the body to produce abnormal shape of RBC which fails to deliver O2 to the tissue.
Cause: mutation where valine is substituted for glutamic acid
What are some clinical finding of Sickle Cell Anemia (SCA) ?
- Key pathologic processes in SCA: severe hemolytic anemia and vasoocclusive crises
- Atrophy of lingual papilla
- Pallor and yellowish of oral mucosa
- Delay teeth eruption
- Delay wound healing.
- Acute chest pain
- Necrosis of hand and foot
- Increase risk of bacterial infections due to loss of functioning spleen tissue (Pneumococcal, Meningiococcal)
- Pain crises
- Stroke and splenic sequestration
How do you work up SCA/what is the anesthesia and surgical consideration?
- Communicate with hematologiest, check how sever is the disease.
- CBC: anemia , platelet and elevated WBC
- BMP: (creatinine, BUN) and electrolytes.
- LFt and PT/INR
- Medical clearance
- Consider Prophylactic Antibiotics
- Avoid Hypoxia and Hypercapnia
How is SCA managed?
- Fluid hydration
- Pain management (PO or IV)
- adequate oxygenation. Oxygen therapy (O2 < 92%)
- Minimize blood loss
- Steroids.
-Treatment:
- Hydroxyurea 15mg/kg/day for 12 weeks (increases HbF which prevents sickling)
- Bone marrow transplant.
- folic acid (↑ RBC)
SCA facts
Sickling is exacerbated by:
* Acidosis, hypoxia, dehydration, cold, and hypercarbia * Pain, and infection
Chronic anemia with Hct= 19-24
* * *
Shortened life span of RBCs
* Normal = 120 days
* Sickle Cell trait = 29 days
* Sickle Cell Dz = 17 days
Everything went well, the patient with SCA is in the recovery area and suddenly started to have severe chest pain, what is going on and how you are going to manage it?
Acute Chest Syndrome
Wheezing or cough, tachypnea
New infiltrate on chest X-ray
Chest pain, temp >38.5C,
Cause: Most are Fat emboli, Infectious or a Combination.
Treatment:
● Supportive: O2, fluid, abx,
● Transfusions,
● Bronchodilators and possibly NO (vasodilator, ↓ adhesion).
● It is the second-most common complication and it accounts for about 25% of deaths in patients with SCD, majority of cases present with vaso-occlusive crisis then they develop ACS.
Transfusion reaction
Cross-agglutination of blood by antibodies in plasma
S/S: fever, ↓ BP, sweats/chills,
hives, anaphylaxis/dyspnea, vomiting, flank pain, headache
Treatment of transfusion reaction
- Maintain BP & Renal perfusion
- IV fluids: NS, strict i/o’s
- Consult nephrology
- if no diuretic response ~ 2-3h,
assume ATN(acute tubular necrosis) , don’t give more IVF - Diurese w/ Lasix 40-80mg
(+2mg/kg) > 100 cc urine/h - Dialyze, watch electrolyes, give
benadryl
What is Leukemia?
- Leukemia:
Increase lifespan of myeloid or lymphoid cells. - Pathogenesis: Block in stem cells differentiation
What is AML?
AML:
- Increase number of immature myeloid cells.
- Occur in adult, more men
- Risk factor: Down syndrome, radiation, cisplatin and carboplatin
- Fatigue , dyspnea , dizziness, weight loss , fever, infection, gingivitis , easy bleeding.
- Work up: CBC (low wbc, anemia and thrombocytopenia), BMP, coagulation labs PT/PTT/INR
What is CML
-Malignant myeloproliferative disorder associated with Philadelphia chromosome.
- common in adult > 60 M
- CBC shows wbc between 50,000-200,000
- Tx: Tyrosin kinase inhibitor , chemo and bone marrow transplant
What is ALL?
- Malignancy by proliferation of immature lymphoid cells
- More common in children 80% and 20% in adult
- Fatigue , pallor , lymphadenopathy , mouth ulceration, oral bleeding and numb chin syndrome which is numbness along mental nerve distribution.
- Work up requires a CT of neck, chest, abdomen, and pelvis. CT/MRI head for those with neurological symptoms.
- They have anemia, thrombocytopenia, low and high WBC
- More responsive to treatment.
Define Schizophrenia?
- Psychiatric disorder characterized by chronic and recurrent psychosis.
- Positive symptoms:
- Hallucination, delusion, disorganized thought
- Negative symptoms:
- Apathy, flat affect, Aloofness
How Schizophrenia treated?
- First generation dopamine receptor blockade: works also on serotonin type 2 (5-HT2), alpha-1, histaminic
- Chlorpromazine
- Haloperidol Haldol.
- Fluphenazine
- Perphenazine - Second generation D2 blockade :
- Seroquel
- clozapine (agranulocytosis low level of WBC require serial CBC ), side effect hypotension , weight gain , glucose intolerance. - Side effect both drugs:
1- Tremor
2- Tardive dyskinesia (involuntary movement of perioral region and extremity)
3- Prolonged QT interval = can cause cardiac arrest
How would you evaluate Schizophrenia patient prior sedation?
- CBC (clozapine can cause (agranulocytos)
- BMP
- EKG to assess the QT interval = high risk of ventricular dysrthymia.
- Assess for substance abuse (50% of schizophrenic pts have substance abuse)
- Avoid ketamine = can worse the hallucination
- Obtain appropriate level of sedation.
Define Hemophilia A?
Hemophilia A: 80% common
- X linked recessive bleeding disorder characterized by congenital deficiency of factor VIII.
- M>F
- Dx:
- Genetic testing
- family hx
- PTT prolonged, PT is normal, platelet is normal
- Hem A factor 8 activity is below 40%
Define Hemophilia B?
Hemophilia B: 20% common
- X linked recessive bleeding disorder characterized by congenital deficiency of factor IX.
- M>F
- Genetic testing
- family hx
- PTT prolonged, PT is normal, platelet is normal
- Hem B factor 9 activity is below 40%
What is the classification of hemophilia A & B?
Classification of hemophilia A & B:
- Mild disease: factor level greater than 5-40%
- Moderate disease: factor activity 1-5%
- Sever: factor level below 1%
What are the Symptoms of hemophilia A & B?
- Spontaneous bleeding
- Prolong bleeding.
- Gingival bleeding.
- Hemarthrosis
- Intracranial hemorrhage
- GI bleeding
- Muscle bleeding
How would you evaluate Hem A, B patients prior surgery?
- I will contact the hematologist to discuss and get more details about the severity of the condition and to appropriately co-manage the patient.
- Obtain labs CBC, BMP, PT, PTT and coagus
- Avoid NSAID and aspirin.
- I will give recombinant factor concentrates of factor VIII or IX.
- Goal is to raise the levels 80–100% prior to surgery and maintain 50% 1–2 weeks postoperatively. The factor should be giving 20-minute prior surgery due to short half-life.
- I will use hemostatic adjunct
What are some hemostatic adjunct can be use with hem A,b pts?
- Tranexamic acid:
Antifibrinolytic agent, inhibits conversion of plasminogen into plasmin.
Dosage: - 25mg/kg PO qid
- 5% mouth wash with 10ml
- 10mg/kg IV. All for 5-7 days.
- Amicar:
Antifibrinolytic agent, inhibits conversion of plasminogen into plasmin - Dosage:
- 6g PO QID, can be giving preop 5g 30-minute prior
- Desmopressin:
Synthetic analog vasopressin Causes release of stored vWF and factor 8 from endothelial cells. - Dosgae:
- IV 0.3 μg/kg over 20 minutes.
- Intranasal 150 μg spray to each nostril. Monitor free water intake as there is a risk of hyponatremia and seizures.
Define vWD?
- Congenital platelet bleeding disorder due to a deficiency or dysfunction of von Willebrand factor (vWF).
- vWF is responsible for mediating platelet adhesion and prevent factor 8 degradation.
- Can be inheritance or acquired due to autoimmune disorders such as SLE OR hypothyroidism.
What are the types of vWD and describe the symptoms?
1- Partial quantitative, most common. AD 85%
2- Partial qualitative, 2A, 2B, 2N,2M. AD 15%
3- Total quantitative autosomal recessive
- Symptoms:
- mucous membrane bleeding
- Gingiva bleeding.
- Menorrhagia.
- Epistaxis.
- GI bleeding.
- Type III can result in more severe symptoms including joint bleeding.
What you expect to see in vWD labs?
- CBC, PT, PTT are normal.
- Factor 8 decrease
- vWF antigen decrease.
What is the treatment of vWD?
- Type 1:
- Desmopressin (DDAVP)
Synthetic analog vasopressin Causes release of stored vWF and factor 8 from endothelial cells.
- Dosgae:
- IV 0.3 μg/kg over 20 minutes.
- Intranasal 150 μg spray to each nostril. Monitor free water intake as there is a risk of hyponatremia and seizures.
- Type 2 and 3:
- Cryoprecipitate can be used to treat all types of vWD.
- Is portion of the plasma that Contains Factors 8, 9, vWF, fibrinogen, and fibronectin.
- Peds 1-2 unit per 10kg
- adult 1 unit per 10kg.
- Both will increase the fibrinogen 100mg/dl
- Humate-P (vWF/Factor VIII) concentrate: It is a blood clotting factor replacement therapy used in the treatment of hemophilia A and von Willebrand disease. Loading dose 40-60 IU/kg then taper the dose.
What is lymphoma?
Malignancy of lymphocyte that arise usually in lymph node.
- Two main types:
- Hodgkin lymphoma (HL)
- Non Hodgkin lymphoma (HL)
Define Hodgkin lymphoma (HL)?
- Malignancy of lymphocyte that arise in lymph node.
- Present as painless lymphadenopathy usually supraclavicular 75% in the neck
- Spleen involved in 20%
- Male age 15-35 years
**- B symptoms: **
- Night sweats, fever and weight loss
- Characterized by the presence of Reed- Sternberg malignant cells that are seen on histopathology (binucleated cells with owl eye nuclei).
-Work up:
-Biopsy
- CT and PET scan for staging
- CBC, BMP to look for anemia, leukocytosis, thrombocytosis, and hypoalbuminemia.
**-Tx: **
- Radiation 20G
- chemotherapy (bleomycin…)
What is albumin?
- Albumin is protein produced by the liver and is a major component of blood plasma.
Normal value 3.5 to 5.0 g/dL.
Define Non- Hodgkin lymphoma?
- Malignant lymphoproliferative lesions that are not Hodgkin lymphoma.
- 85% are of B cell origin.
- Express CD20 marker
- B symptoms: night sweats, fever and weight loss
- Virus may play role: EBV (Burkitt’s lymphoma, HIV and Hep B)
- Can also see extranodal involvement – bone marrow, lungs, liver, bone.
- Work up:
- Biopsy, CT and PET scan for staging, CBC, BMP to look for anemia, leukocytosis, thrombocytosis, and hypoalbuminemia.
- Tx:
- Radiation 20G
- chemotherapy (Rituximab anti CD20…)
Define Multiple Myeloma?
- Malignant of plasma cells causing osteolytic lesion, hypercalcemia, osteopenia and pathologic fracture.
- Affect more male, 60-70.
Clinical presentation:
- Jaw lesion in 30%
- bone pain
- Hypercalcemia
- Anemia
- Petechiae due to platelet dysfunction
- Amyloidosis in soft tissue
- Renal failure from Bence-Jones protein (Amyloid is nephrotoxic)
- Radiograph:
Punched out radiolucency without sclerotic border in skull
How would you work up patient with MM?
- Clinical exam
- Protein electrophoresis to detect monoclonal protein
- serum and urine M protein
- bone marrow biopsy
- CBC, anemia , platelet dysfunc
- BMP
- CT and PET scan
- Peripheral smear shows Rouleaux formation (stacked RBCs resembling coins)
How would you manage patient with MM?
- CBC, BMP , coagus and type and screen
- Consult hematologist.
- Transfuse if necessary.
- Maximize hydration.
- Pre and post op abx
- Avoid steroid, can precipitate tumor lysis.
- Consider risk of MRONJ , avoid IAN if bleeding concerns.
What is Duchenne Muscular Dystrophy (DMD)
Neuromuscular disease caused by mutation of dystrophin gene leads to progressive necrosis of the muscle fiber.
Epidemiology: 1 in 3,600 boys.
Onset: Early childhood with motor delays, learning disabilities, attention issues.
Progression: Wheelchair-bound; life expectancy ~20 years (respiratory failure, heart failure, arrhythmias, pneumonia).
What is clinical presentation of Duchenne Muscular Dystrophy (DMD)
Muscle: Calf/tongue pseudohypertrophy, long bone fractures, kyphoscoliosis (↓ respiratory function).
Weakness of Pharyngeal muscles causing aspiration, nasal regurgitation, nasal speech.
Cardiac:
Mitral valve regurgitation tachycardia (tall R wave)
arrhythmias.
How DMD diagnosed?
Labs:
↑ Serum CK.
EMG: Myopathic pattern.
Biopsy: Muscle atrophy and hypertrophy.
DNA: Dystrophin gene mutation.
How do you manage DMD?
Pre-op:
- Steroid supplementation
- assess for ACE inhibitors, beta blockers, digoxin (toxicity: N/V, visual changes).
Pre-op Workup: EKG, echo, chest X-ray.
Anesthesia:
- TIVA preferred; avoid volatile agents (risk: malignant hyperthermia).
- No succinylcholine (risk: rhabdomyolysis, hyperkalemia).
- Use desflurane if needed.
- NPO: Longer duration (gastroparesis).
- Pre-induction: H2 agonist + metoclopramide.
- Avoid narcotics
- monitor TMJ subluxation,
- ↓ pulmonary reserve → ICU post-op if required.
Myasthenia Gravis
Autoimmune disorder features by autoantibodies affecting postsynaptic neuromuscular nicotinic ACH receptor
It is characterized by weakness and fatigue of the skeletal muscles with improvement with rest.
Clinical features of MG
- Fatigue of voluntary muscles most commonly eyelid ptosis
- Generalized weakness
- Thymoma in 15% of patients
- Slow speech, jaw claudication, swallowing difficulty
- Respiratory weakness
- Peek sign: patient closes eyes and after a short time scleral show begins due to orbicularis oculi weakness.
Diagnosis of MG
- Anti-acetylcholine receptor antibody test is the confirmatory diagnostic test of choice.
- Edrophonium chloride (Tensilon) test. Patient is injected with anticholinesterase with improved strength.
- Treatment:
- Pyridostigmine (anticholinesterase) first line of treatment.
- IV immunoglobulin
Work up and anesthesia concerns in MG?
- Consider reduced or avoidance of sedatives or opioids in those with reduced respiratory reserve.
- Short-acting opioids such as remifentanil are preferred.
- Warn patient of possible need for prolonged ventilatory support.
- Usually resistant to succinylcholine and sensitive to non-depolarizing muscle relaxants.
- Rapid sequence intubation, succinylcholine should be adjusted to 1.5–2 mg/kg
- Nitrous oxide is safe.
- Avoid aminoglycosides (e.g., gentamycin) as they are known to impair neuromuscular transmission. Erythromycin, azithromycin, fluoroquinolones, and tetracycline have reports of increased myasthenic weakness.
- Inhalational agents such as sevoflurane, isoflurane, and halothane are known to reduce neuromuscular transmission and may be exacerbated in the myasthenic patient.
- Reports of adverse effects with ketamine and etomidate.
- Propofol is safe in these patients.
- Controversial on reversal of neuromuscular blockage due to concern postoperative weakness due to cholinergic crisis or inadequate muscular transmission.
- Cholinergic crisis, excess of acetylcholine. Normally due to administration of excess anticholinesterase drugs resulting in involuntary twitches and fasciculation and muscle weakness.
- Differentiate from myasthenic crisis by administration of the edrophonium test. In myasthenic crisis, pupils will be dilated as well.
Multiple Sclerosis ?
Demyelinating disease of the central nervous system (CNS) marked by relapses, followed by periods of remission.
Pathogenesis – demyelination in the periventricular areas of the brain.
Symptoms:
visual disturbances, gait disturbances, ascending paresis
What is the surgical/anesthesia concerns for pts with MS
- Rule out cardiovascular or respiratory issues in those MS with advance disease.
- Surgical stresses can exacerbate the symptoms.
- Provide adequate anxiolysis and pain management to avoid exacerbations.
- No elective surgery during periods of relapse.
- The informed consent discussion should include the possibility of worsening MS symptoms.
- Consider stress-dosing the patient who is on long-term steroids.
- Patients taking interferon should have a CBC to exclude anemia, neutropenia, and thrombocytopenia.
- Avoid succinylcholine in patients with paralysis or paresis because of the potential for hyperkalemia.
COPD
Irreversible disease that causes airway obstruction by either chronic bronchitis and/or emphysema.
- Risk factors include smoking (most common), respiratory infection, occupational exposure.
What are the sign and symptoms of COPD?
wheezing
chronic cough
productive cough
hyperinflation of chest
hypertrophy of the accessory muscles
weight loss
fatigue
dyspnea on exertion
pulmonary hypertension leading to neck vein distention and peripheral edema.
Classification of COPD
COPD patients typically exhibit hypercarbia and hypoxemia. Advanced disease can lead to pulmonary hypertension and cor pulmonale.
I Mild:
FEV1 > 80%
Short acting bronchodilator
II Moderate:
FEV1 > 50-79%
Long acting bronchodilator
III Sever:
FEV1 > 30-49%
Inhaled steroid
IV very sever:
FEV1 < 30%
Oxygen, pulmonary rehab
Chronic bronchitis (“blue bloaters”)
Emphysema
* Chronic bronchitis (“blue bloaters”):
chronic hypersecretion of mucus in the bronchi resulting in airway obstruction.
* Emphysema (“pink puffers”) enlargement of the airway due to destruction of the airway walls leading to loss of elasticity/recoil of the bronchioles.
Diagnosis of COPD
- Pulmonary function tests including spirometry
- Bronchitis diagnosis is based on a history of a productive cough for at least 2 consecutive years.
- Chest radiographs look for lung nodules, bullae, hyperinflated lungs, masses, or fibrotic changes.
- Blood labs may show hypercarbia, polycythemia and leukopenia.
What is the surgical/anesthesia concerns/management for pts with COPD
- Consult with a pulmonologist and optimize prior surgery.
- Smoking cessation for 6 weeks
- EKG to rule out right-sided heart disease and ischemic heart disease.
- Chest X-ray warranted if concern for respiratory infection or occult malignancy.
- No sedation because patients have limited ability to tolerate hypoventilation as they have a diminished response to hypercarbia.
- Presence of extensive bullae translates to a higher risk pneumothorax.
- Delay surgery if any signs of active infection purulent sputum, or worsening cough.
- Nitrous oxide has the potential to expand and possible rupture pulmonary bullae.
- Consider β-2 agonist and an antimuscarinic (e.g., robinul) to increase airway patency.
- Maintain oxygen saturation between 88% and 92%.
- Opioids diminish the respiratory drive and predispose the patient to apnea (use opioids judiciously).
- Local anesthesia is preferred.
Eating Disorders
Psychiatric disorder characterized by abnormal eating habits with psychological implications and excessive concern about body weight.
Bulimia Nervosa
Binge eating disorder followed by purging at least once a week for 3 months.
Patients have strong negative views on their personal shape and weight
Anorexia Nervosa
Eating disorder characterized by intentional restricted caloric intake leading to low body weight BMI (less than 18.5 kg/m2)
Signs/Symptoms of patients with eating disorders.
- Low body mass index.
- Dehydration.
- Delayed gastric emptying.
- Resting bradycardia.
- Hypertrophic salivary glands.
- Hypokalemia, hypocalcemia, hyponatremia, and hypoproteinemia.
- Amenorrhea and atrophy of breasts in females.
- Seizures.
- Hypothermia.
- Anxiety.
- Dry skin (normally scaly, yellow, and erythematous patches) and hair loss (alopecia).
- Lethargy.
- Hypokalemic hypochloremic metabolic alkalosis may occur secondary to excessive vomiting.
- Russell sign – callus on dorsal surface of index and long finger due to induced vomiting (seen in bulimia).
You are sedating patient with eating disorders, what is your anesthesia concerns?
- Fluid rehydration – patients are commonly dehydrated leading to hypotension.
- EKG – preoperative EKG should be monitored for Bradycardia, dysrhythmias including PVCs, T wave inversions, and heart blocks.
- CBC – review white blood cell, platelet, and preoperative hemoglobin. This may be severely reduced due to malnutrition.
BMP: evaluate for hydration based on BUN/creatinine ratio elevation. Rule out unsafe levels of electrolytes
LFTs – hypoproteinemia and reduced liver function may make patients more susceptible to bleeding and may decrease wound healing.
NPO period – increase of NPO time due to delay in gastric emptying.
Slowly titrate medications because these patients have amplified response to the medication due to low body fat level and low protein plasma which increase bioavailability
Patients may require an extended time to emerge from anesthesia
What are the physiological changes that occurs during pregnancy?
- Cardiovascular: Increase HR, CO by 30%, benign systolic murmur S3 d/t relative anemia, DVT 2/2 uterine compression of inferior vena cava.
- Hematology: Hemodilution anemia, hypercoagulable state risk for PE&DVT, leukocytosis, suppression of immune system due to decrease chemotaxis.
- Respiratory: decrease residual volume, decrease FRC, respiratory alkalosis 2/2 increase in minute ventilation and rapid desaturation.
- Genitourinary: increase GFR, renal blood flow, Cr, bladder capacity decreases due to pressure which increase risk of UTI due to stasis, decrease lower esophageal sphincter tone, increase gastric pressure heart burn and reflux and hypoglycemia.
Oral manifestation in pregnant patients?
Chronic gingivitis, 5% develop pyogenic granuloma.
Definition of preeclampsia, eclampsia
- Preeclampsia:
Abnormal placental implantation results in hypertension and proteinuria that occurs after 20 weeks of gestation. - Eclampsia: Form of severe preeclampsia characterized by seizures or coma.
- HELLP Syndrome: Syndrome characterized by hemolysis, elevated liver enzymes, and low platelet counts.
- Gestational Hypertension Elevated blood pressure without proteinuria. SBP ≥140 mm Hg and/ or DBP ≥90 mm Hg
Do not use during pregnancy
- Aspirin: Cause intrauterine growth restriction and intra cranial brain bleeds.
- NSAID: Avoid third trimester, may close PDA.
- Gentamicin: ototoxicity in fetus.
- Tetracycline: Cause tooth staining and decrease bone development.
- Benzodiazepine and barbiturates: risk for fetal craniofacial anomalies, cleft lip/palate
How would you manage pregnant patient?
- No elective care in the first trimester, urgent treatment only.
- Second trimester is the safest and most ideal.
- If the patient develop supine hypotension roll the patient to the left side. This occurs secondary to compression of the inferior vena cava.
- Patients are more prone to emesis due to relaxation of the lower esophageal sphincter and longer gastric emptying times.
- Pregnant patients are more sensitive to local anesthesia and have reduce onset time.
- Consultation with the patient’s obstetrician should be considered to determine the need for intraoperative fetal monitoring.
- Perioperative antibiotics may be indicated in the setting of gestational diabetes and reduced immune capability.
- N2O is controversial, as evidence of use without scavenging unit in dental assistants has shown increase in spontaneous abortion.
What is the risk of fetus exposure to radiation? Can the pregnant patient get pano, ICAT?
Yes, pano , ICAT and PA are ok
It is estimated that a radiation dose of >10 Gy (5 Gy first trimester) can cause congenital fetal anomalies.
- A standard full mouth series, orthopantogram, or cone beam radiation exposure to the fetus is estimated 0.01-0.00001 Gy.
What is the Pregnancy and Lactation Labeling Rule (PLLR)?
The Pregnancy and Lactation Labeling Rule (PLLR) replaces the old FDA pregnancy letter categories (A, B, C, D, X)
Provides risk summary, clinical considerations, and data on medication use during pregnancy.
- P1/L1, safest, data available
- P2/L2, safe, limited data
- P3/L3, probably safe, no data
- P4/L, probably hazardous, human trials suggest risk
- P5/L, hazardous, major risk likely to exceed benefits
What about IV Sedation for pregnant patients?
“The effects of catecholamine surge with resulting impaired uteroplacental perfusion are dangerous to fetus.”
Do not sedate pregnant patients!
Bone Morphogenetic Protein and 5FU in pregnancy
BMP: Concerns include carcinogenicity and teratogenic effects
5FU:
- Use in 1st trimester can cause congenital abnormalities and miscarriage
- Use during 2nd and 3rd trimester can cause growth restriction and stillbirth.
Inpatient Perioperative Management for pregnant patients.
- OB consult
- Consider fetal monitoring:
- Fetal monitoring monitors heart rate and uterine tone to avoid uteroplacental insufficiency.
- Left lateral position using bump under right hip
- Moves uterus off inferior vena cava and aorta
- Position slowly (changes in maternal position can have profound hemodynamic effects)
. Rapid sequence induction and extubate fully awake d/t risk of aspiration - Avoid hypotension, hypoxia, hypercarbia, hypoglycemia and hypothermia
- If these factors are controlled, there is no increased risk of fetal anomalies, miscarriage, or preterm labor.
What is Chronic renal disease (CRD)?
Long-term kidney damage to the glomerulus or tubules, leading to irreversible complications over months to years.
CRD occurs when the GFR is reduced to 50 mL/ min.
What is the manifestation of CRD?
Cardiovascular: dyslipidemia, CHF, left ventricular hypertrophy, HTN.
Anemia, platelet dysfunction
GI issues nausea and vomiting, risk of aspiration
Risk of infection due to impaired phagocytosis , neutrophil
Acid base disturbance and hyperkalemia.
Oral manifestation: halitosis, stomatitis, gingival bleeding, osteolytic changes
What is your CKD work up prior sedation?
CBC: Anemia , platelet dysfunction
BMP: check the electrolyte and Hyperkalemia
EKG, Echo
What is your anesthesia concerns for CKD patients?
- DC diuretics, ARB and ACE the day of surgery
- antiemetic due to risk of aspiration
- Avoid sevo, has compound A
- Avoid Succ cause hyperkalemia
- Avoid NSAID
- consider abx prophy.
- Propofol is safe – metabolize by liver.
- Fentanyl is safe = lipid soluble
- Benzo uses with caution.
What is the stages of CRD
Stage I : slight renal damage GFR>90
Stage 2 : mild damage GFR 60-89
Stage 3 : Moderate damage 30-59
Stage 4 : Sever damage 15-29
Stage 5 : ESRD GFR <15
What is Sevofluorane?
fluorinated volatile anesthetic agent with a low blood/gas partition coefficient, therefore a rapid onset and recovery from anesthesia. The MAC is 1.71.
What is MAC, pertaining to volatile anesthetics?
The concentration of an inhaled anesthetic, at 1ATM, that prevents skeletal muscle movement in response to a painful stimulus (skin incision) in 50% of patients. A MAC of 1.3 prevents movement in approximately 95% of individuals undergoing surgery.
During the case, the anesthetist complains of increasing airway pressures. What could be the cause?
Circuit or ETT obstruction (kinking), airway secretions or mucous plugging, bronchospasm.
How should potential bronchospasm be treated intraoperatively, in intubated patient?
1- Suction ETT and trachea with suction catheter.
2- Albuterol MDI 8-10 puffs into endotracheal tube on inspiration, through chamber, or a 60cc syringe connected to the anesthesia circuit close to the ETT.
3- If this doesn’t work, then epinephrine 0.3mg SC.
Near the end of the case, the anesthetist is now complaining that the ETCO2 is abnormally high, and non-responsive to increasing the ventilatory rate. The patient has also become mildly tachycardic. The CRNA asks you what you think is going on?
Malignant Hyperthermia.
- Hypermetabolic state that occurs on exposure to volatile anesthetics agents (except nitrous oxide) and succinylcholine. Due to a genetic mutation in the ryanodine receptor
- lowers the threshold of calcium release channel activation. Elevated calcium levels lead to sustained muscle contraction.
- Testing includes:
1- caffeine-halothane contracture test
2- muscle biopsy
3- RYR1 gene testing.
How do you recognize and treat Malignant Hyperthermia?
- History (and family history)
- 70% of MH-susceptible patients have increases of resting concentrations of creatine kinase.
- The earliest clinical signs of MH include unexplained sustained elevation in ETCO2
- Tachycardia.
- Arterial hypoxemia
- Metabolic and respiratory acidosis
- Increase in body temperature (late finding).
- Dysrhythmias, peaked T waves on EKG due to hyperkalemia
- Masseter spasm
How do you treat MM
- Activate EMS
- Stopping the triggering agent
- Changing the anesthesia circuit
- Hyperventilating with 100% O2
- IV fluids to maintain urine output to 2 mL/ kg/h.
- Administering 2.5mg/kg Dantrolene Sodium IVP and repeat every 10-15 minutes as needed (up to 10mg/kg)
- Initiate active cooling (cold IV saline
- Gastric lavage with cold saline
- Diuresis 1 mg/kg IV.
- Correct metabolic acidosis with sodium bicarbonate 1–2 mEq/kg IV as guided by arterial pH
- Hyperkalemia treated with calcium chloride 5–10 mg/kg IV or regular insulin 0.15 U/kg in 1 mL/kg of 50% dextrose.
- The patient must be transported to and managed in an ICU setting at the appropriate time.
How do you prep the dantrolene?
Administering 2.5mg/kg Dantrolene Sodium IVP and repeat every 10-15 minutes as needed (up to 10mg/kg)
Preparation of Dantrolene:
20 mg dantrolene bottle mixed with 60 mL sterile water and 3 g of mannitol.
Ryanodex (Concentrated Formulation):
Each vial contains 250 mg of dantrolene sodium and requires minimal preparation.
Add 5 mL of sterile water to the vial. Shake the vial vigorously for 10 seconds
Each mL delivers 50 mg/mL of dantrolene.
Define Alzheimer’s disease ?
- Neurodegenerative disease characterized by the progressive loss of cortical neurons.
- AD is the most common neurodegenerative disease and the most common cause of dementia in persons older than 65 years of age.
- Hallmarks of the disease include impaired memory, judgment, and decision-making, and emotional lability.
What is the Classification of Alzheimer’s disease?
- Classification:
- **Familial form (early-onset AD) **
o Rare.
o Early onset, usually before age 60.
**- Sporadic form **
o More common.
o Typically occurs after 60 years of age.
- **Familial form (early-onset AD) **
How you diagnose Alzheimer’s disease?
- The clinical diagnosis of AD is by exclusion.
- Definitive diagnosis is usually made on post- mortem examination via autopsy (presence of accumulation of amyloid plaques and neurofibrillary tangles).
- MRI imaging is preferred in diagnosis of AD. Will demonstrate marked cortical atrophy with ventricular enlargement.
What is the treatment of Alzheimer’s disease?
- There is no cure for AD and treatment focuses on control of symptoms. Even with treatment, prognosis is poor.
- The pharmacological agents for AD include cholinesterase inhibitors (tacrine, donepezil, rivastigmine, and galantamine), and the glutamate antagonist, memantine.
What is preop or anesthesia concern for Alzheimer’s disease?
- Patients with AD are often confused and can be uncooperative. While some patients may tolerate a procedure with local anesthesia, many may need some sort of procedural sedation.
- Inquire who makes health care decisions for the patient if the patient does not possess capacity (power of attorney/health care advocate).
- Doses of sedative-hypnotics should be reduced by 30% due to increased sensitivity and slower distribution and reduction in clearance.
- Preferred medications include short-acting sedative-hypnotics, anesthetic agents, and narcotics since they allow a more rapid recovery.
- Centrally acting anticholinergics, such as atropine and scopolamine, may contribute to post- operative cognitive dysfunction and should be avoided if possible.
- Glycopyrrolate, which does not cross the blood–brain barrier, is the preferred agent when an anticholinergic is needed.
- Have the patient continue their AD medications preoperatively.
Parkinson’s Disease
- Neurodegenerative disease characterized by the classic triad of bradykinesia, rigidity, facial immobility, and resting (pill-rolling) tremor.
- It is caused by the progressive loss of dopaminergic neurons in the pars compacta in the basal ganglia
Workup and Diagnosis of Parkinson ?
- The diagnosis of PD is made according to the clinical signs of tremor, bradykinesia, muscular rigidity, and postural instability.
Treatment of Parkinson?
Treatment:
- The goal is to increase the concentration of dopamine in the basal ganglia.
1- Carbidopa-levodopa (Sinemet®) is the main- stay of treatment of PD.
- Levodopa is a dopamine precursor combined with carbidopa and prevent conversion of levodopa to dopamine, thereby optimizing the amount of levodopa entering the CNS.
2- Selegiline and rasagiline are type B mono- amine oxidase (MAO-B) inhibitors that help control PD symptoms by inhibiting the catabolism of dopamine in the CNS.
3- Surgical tx: Thalamotomy, deep brain stimulator.
Management and anesthesia consideration in Parkinson disease?
- Continue medication preop.
- Nausea/vomiting are side effects of levodopa and may be treated with ondansetron, dexamethasone, and transdermal scopolamine.
- Avoid phenothiazines (promethazine), butyrophenones (droperidol), and metoclopramide because their antidopaminergic activity can exacerbate symptoms.
- Diphenhydramine may be used for patients with tremor.
- Propofol is relatively safe.
- Opioids should be used judiciously as patients with PD have a higher incidence of chest wall rigidity.
- Be mindful of serotonin syndrome risk on patients taking MAOI (hypertension, tachycardia, hyperthermia, diaphoresis, confusion and agitation).
- Ketamine may be relatively contraindicated due to elevated blood pressure.
What is Seizure?
Sudden onset of abnormal, highly discharges of neurons.
Define Epilepsy?
Chronic disorder defined as recurrent seizures, two separate unprovoked seizures are required to make the diagnosis of epilepsy.
Seizures classification
Seizures classification:
**- Partial focal seizure: **affect single area of the brain.
- simple partial with intact consciousness
- complex with impaired consciousness
- Generalized seizures- **Diffuse. Affect most of the brain.
- Absence (petit mal) most commonly in children. Brief loss of awareness+ blank stare
- Tonic Clonic (Grand mal): stiffening and movement
- Myoclonic: quick, repetitive movement
Etiology and presentation of seizure
Etiology:
- Syncope is most common cause in OMFS office then seizure
- Anesthesia / drugs
- Alcohol
- Brain tumor
- CNS disease
- Head trauma
- CVA
- Other metabolic changes that produce seizure activity include hypoglycemia, hypernatremia, hyponatremia and hypomagnesemia.
- Presentation:
- LOC
- Confusion
- Abnormal movement
- Tongue /lip biting
- Incontinence
How do you diagnosed seizure?
Work up:
-MRI, EEG , electrocorticography
Preop and anesthesia consideration for patient with seizure disorders?
- Consult neurologist.
- Ask about how bad is the seizure, frequency and medication.
- Propofol and benzo are good.
- Nitrous is safe.
- Sevo lowering seizure threshold
- Avoid ketamine, tramadol, methohexital and flumazenil. (lowering seizure threshold)
- Alfentanil is contraindicated due to excessive impact on EEG activity.
- Continue meds
- Get a CBC as some meds cause bone marrow suppression
- Be aware of any hepatically metabolized meds you use as their effect could be prolonged due to the use of antiepileptic drugs
What are common meds for seizure patients?
- Phenytoin, aka “Dilantin”
1.300mg po daily
2.Stabilizes inactive state of voltage gated Na+ channels 3.Levels need to b between 2-20
4.Metabolized in liver
5.Causes blood dyscrasias so get CBC and LFT’s - Keppra, aka “Levitiracetem”
- 1.500mg BID
2.Inhibits Ca++ channels - Valproic Acid, “Depakote”
1.Works on Na+ and Ca++ channels
2.Produces thrombocytopenia and GI symptoms - Topiramate, aka “Topamax” 1.GABA, Na+, Ca++ channels 2.Used for migraines also
- Tegretol, “Carbamazepine”
1.Produces n/v and somnolence 2.Works on voltage gated Na+ channels
Status Epilepticus
seizure lasting more than 30 min or multiple seizures in a row.
Treat as status epilepticus after 5 min of seizing
Treatment of status epilepticus:
- Activate EMS/911 if no self-resolution in 5 minutes.
- Airway Breathing Circulations (ABCs), vitals, ECG. Patient may require airway protection with endotracheal intubation.
- Supplemental oxygen.
- Establish venous access – consider administering benzodiazepines.
- Consider drawing labs for electrolytes, toxicology, anticonvulsant drug levels, and hematology.
- Midazolam: 10 mg for >40 kg, 5 mg for 13–40 kg.
- Lorazepam: 0.1 mg/kg/dose, max: 4 mg/dose.
- Diazepam 0.15–0.2 mg/kg/dose, max: 10 mg/dose.
- Rule out hypoglycemia and treat as needed (50 mL of 50% dextrose).
- Routine glucose administration is not indicated because hyperglycemia can exacerbate brain injury.
- Arterial blood gas draws to monitor for metabolic acidosis and to assess ventilation.
- Hyperthermia frequently occurs and requires active cooling.
- If seizure continues, consider second-line therapy such as phenobarbital (10–15 mg/ kg at 100 mg/min) or phenytoin (15–18 mg/ kg T 50 mg/min) or anesthetic dose of propofol.
What is a cerebrovascular accident (CVA)?
A sudden onset of neurological deficits that occurs secondary to cerebral ischemia or cerebral hemorrhage.
Also known as stroke.
Define transient ischemic attack (TIA).
Sudden onset of focal neurological deficits that resolve within 24 hours.
TIA is often considered a warning sign for future strokes.
What characterizes a reversible ischemic neurological deficit (RIND)?
Neurological deficit that lasts more than 24 hours but resolves in less than 3 weeks.
RIND indicates a temporary but significant disruption in blood flow.
What is the majority cause of ischemic strokes?
- Thrombotic, caused by atherosclerotic plaques.
- Embolic origin is mostly from the atrium of the right heart as seen in atrial fibrillation or left ventricle from an MI.
Embolic strokes mostly originate from the heart, particularly in conditions like atrial fibrillation.
Where do most hemorrhagic strokes occur?
Mostly intracerebral, with the remaining being subarachnoid.
These types of strokes are due to bleeding into the brain or surrounding areas.
What is the hallmark of ischemic or hemorrhagic stroke?
Contralateral deficits of motor and sensory nerves of the cerebral hemisphere involved.
This means that if one side of the brain is affected, the opposite side of the body will show deficits.
What are the risk factors for strokes?
Hypertension, smoking, atrial fibrillation, diabetes, ischemic heart disease, peripheral vascular disease, increased homocysteine levels, excessive alcohol consumption.
What are common symptoms of strokes?
Hemiplegia, aphasia, dysarthria, hemineglect, seizures, and gait disturbances.
What symptoms are common in hemorrhagic strokes?
Headache, loss of consciousness, nausea, and vomiting.
How do symptoms manifest in strokes?
Symptoms manifest clinically based on the anatomical area of neurological involvement (e.g., hemiplegia due to cortico-spinal tract involvement).
What are craniomaxillofacial manifestations of strokes?
Facial droop, ptosis, ocular muscle weakness, weakened parapharyngeal muscles (weakened gag and swallowing reflex), anosmia, visual field deficits, and disturbances in tongue movement.
Diagnosis and work up of stroke
- CT scan w/o contrast
- Echo to rule out of emboli.
- CTA/MRA and carotid doppler
- Coagulopathy: CBC, BMP, coags , pregnancy test, cardiac enzyme.
What is the role of statin in stroke patient?
- Statins reduce risk of stroke even in the absence of hyperlipidemia.
Treatment of Ischemic Stroke
- IV tissue plasminogen activator (tPA) converts plasminogen into plasmin, in patients who meet criteria and in whom treatment can begin within 3–4.5 hours from initial symptom.
- Inclusion criteria:
- 18 years or older, ischemic stroke with neuro deficit, time within 3 hours
- Exclusion criteria:
- Intracranial bleeding, hx of brain bleed, uncontrolled HTN >185/110, known AV malformation, neoplasm, or aneurysm.
Treatment of Hemorrhagic Stroke
- DC and reverse all anticoagulation.
- Consider fresh frozen plasma.
- Neurosurgery consult for possible placement of EVD.
- If pt intubated, mechanical hyperventilation help reduce ICP
- Elevated ICP can be managed with IV mannitol 3g/kg, or hypertonic saline, avoid hypotonic.
- Monitor blood glucose.
Management of stroke patient prior sedation:
- Identify high-risk patients (e.g., risk factors and recent CVA).
- The patient should be considered ASA class II if patient had a CVA >6 months earlier and has no evidence of residual neurologic deficit.
- The patient should be considered ASA class III if patient had a CVA >6 months earlier and has some evidence of residual neurologic deficit.
- The patient should be considered ASA IV if patient had a CVA <6 months earlier or if substantial residual deficit remains.
- Maintain adequate oxygenation.
- Monitor EKG
- Discuss drug holiday with physician.
- Avoid ketamine.
- Maintain adequate blood pressure.
- Can do elective cases within 6 months after stroke if the pt is stable.
Pre-hospital assessment for stroke
Cincinnati Prehospital Stroke Scale
Cincinnati Prehospital Stroke Scale
- Facial droop: Have the patient smile or show teeth.
- Arm drift: close eyes, extend your arm straight out with palm up for 10 seconds.
- Speech: Have the pt say “You can’t teach an old dog new tricks “
- Time to act.
- FAST
Time is brain – Critical time goals:
- Immediate assessment within 10 minutes of arrival
- Neurologic assessment, CT scan within 25 minute
- Interpretation of CT scan within 45 minutes
- Initiation of tPA within 3 hours
Cystic Fibrosis
- disease affecting lungs, pancreas 2/2 defect in CFTR protein
- 1:3000
- Dx = genetic test, sweat test
- Tx: Supplement with vitamins:
ADEK, dornase alpha, inhaled
cortico, chest PT - Chronic infxns: P. aeruginosa…
- Tx: levofloxacin inhaled
Subacute bacterial endocarditis
infection of the heart’s inner lining or valves 2/2 S. viridans
* Can be fatal 6 wks-1 year
* S/S: fever, cough, SoB, joint
pain, diarrhea, flank pain + Murmur
* Osler nodes - raised tender
lumps on fingers/toes
* Janeway lesions - palms, soles
* Splinter hemorrages
Hyperthyroidism
- Production of ↑TH r/i ↑metabolic
state, tremors, ↑ reflexes - Causes: Graves’, goiter, tumors,
overdose of TH meds - Dx: TFTs showing ↑T4–>T3
- Tx: propylthiouracil/methimazole
inhibit TH
Anesthesia concerns:
- delay case until controlled
- avoid sympathomimetics
- be aware of potential for thyroid storm
- Tx: propanolol, cooling, IVF
Hypothyroidism
- Hypometabolic state ↓TH 2/2
autoimmune disease,
throidectomy, iodine ↓ - S/S: ↑ weight, cold intolerance,
fatigue, lethargy, dull - Dx: ↓ T4
- Tx = replace TH
- Anesthesia: slow recovery
Beta-thalassemia:
Decrease in the synthesis of the beta-globin chain of Hgb.
Autosomal recessive
More commonly found in mediterranean populations, middle east, Africans, Greeks.
Beta-thalassemia variants
- Minor: mild microcytic anemia due to DNA splicing defect, decreased HbA, increase in RBC count, HbA2 and ferritin production, usually no treatment
- Major: severe hemolytic anemia due to a nonsense mutation of a stop codon, no production of HbA, increased HbA2 and HbF
Patients have a lifelong danger of iron overload and lifelong need for transfusions
Beta-Thalassemia: Anesthesia and Surgery Considerations for Extraction Under Sedation
- Check hemoglobin, manage anemia (transfuse if needed), and assess for iron overload, cardiac, and liver function.
- Ensure oxygenation, avoid hypoxia and acidosis, and monitor bleeding risk.
- Maintain hydration and provide careful pain management.
Consult hematology or cardiology if complications are present.
HTN
- What is the HTN?
- Systemic vascular disease characterized by persistently elevated arterial blood pressure of 130/80 mmHg or higher.
- What is the essential HTN?
- HTN with no identifiable cause 90% of HTN pts
- What is secondary HTN:
- HTN with identifiable cause like renal artery stenosis, Cushing syndrome, pheochromocytoma, pregnancy.
- How do you diagnose HTN:
- Diagnosed by 2 elevated readings of at least 130/80 mmHg on 2 or more visits.
Tell me the different stages or classifications of HTN?
- The JNC 7 Classification:
– Normotension <120/80 mmHg
– Elevated 120–129/<80 mmHg
– Stage I 130–139/80–89 mmHg
– Stage II >140/90 mmHg
What is your cutt off of HTN in your office?
For me a blood pressure over 160/100 I will start to get more concerned about uncontrolled HTN
How dose smoking contributes to HTN?
- Smoking release nicotine, which can cause blood vessels to constrict or narrow.
- Nicotine stimulates the release of adrenaline which lead to increase HR and eventually increase BP.
- Smoking increase the inflammation on the blood vessels and interfere with their ability to regulate the BP.
- What are some sequalae of untreated HTN:
- Left ventricular hypertrophy
- CHF
- Stroke
- Renal disease
- What are some factors that can cause HTN?
- Obesity
- Diabetes
- Alcohol
- Aging
- Smoking
- OSA
- Family history
- Ethnicity (African American)
- Sex (Males have higher rates of HTN)
What monitors you put in your patient?
- Standard ASA monitors, BP cuff, puls ox , end tidal CO2, three lead EKG and temperature measure will be readily available.
What staff with you in the room?
Myself and two ancillary staff that are BLS certified.
- How do you judge your level of sedation?
A combination of checking response to stimuli, airway, spontaneous ventilation, vital signs and Verrill sign which is ptosis when the upper eyelid cover the upper half of the pupil.
Treatment of HTN:
- Calcium channel blocker: decrease the influx of Ca ions resulting in vasodilation. Example: amlodipine, verapamil, diltiazem, felodipine
- ACE inhibitors: Block the conversion of angiotensin I to angiotensin II. Angiotensin II responsible for vasoconstriction (e.g., lisinopril, fosinopril, enalapril, captopril, ramipril).
- Angiotensin II (AII) receptor blockers (ARBs) – block the effects of AII through antagonism of AII receptors leading to decreasing vasoconstriction and aldosterone secretion. (e.g., losartan, valsartan, Olmesartan, telmisartan).
- β-blockers – block β-adrenergic receptors resulting in a decrease in myocardial contractility, decrease in renin production, and relaxation of smooth muscles (e.g., metoprolol, atenolol, esmolol, carvedilol, labetalol).
- Thiazide diuretics – block the reabsorption of NaCl in the distal convoluted tubule of the nephron leading to a contracted intravascular volume (e.g., hydrochlorothiazide, chlorthalidone).
- Vasodilators – work by decreasing vascular smooth muscle tone (e.g., hydralazine, sodium nitroprusside).
- Alpha-2 adrenergic agonist – works on central adrenergic receptors leading to decreased norepinephrine release (e.g., clonidine).
- Direct renin inhibitor – prevents renal release of renin with a subsequent decrease in AII production (e.g., aliskiren).
HTN Patient management prior sedation:
- Get CBC, BMP and EKG
- Monitor EKG for sign of myocardial ischemia.
- Defer elective cases if BP > 180/120 and refer to PCP if they are asymptomatic, if they have symptoms send the pt to the ER.
- Amide LA metabolism can be reduced in patient taking B blocker.
- Continue antihypertension meds.
- Look for hypokalemia in patients using ACE and ARBs.
- patients using ACE and ARBs more prone to anesthesia induced hypotension.
- LA with vasoconstriction 0.04mg with epi that’s the limit.
- Avoid ketamine
- Contact EMS for evidence of a hypertensive crisis (BP 180/120 with signs/symptoms of myocardial ischemia, bradycardia, hypertensive encephalopathy, dyspnea, chest pain, confusion, nausea/vomiting, headache, seizures, and pulmonary edema).
- Who recovers your patient?
Typically, I have nurse in my office who will recover the patient, they will stay in the room for 15 minutes after the anesthetics, and will take some vital sings, we use modified Aldrete score.
Assigns a score of 0–2 to the following categories:
activity, breathing, circulation, consciousness, and oxygen saturation.
A score of 9 out of 10 is required for discharge from the facility/PACU.
Atherosclerosis
- Atherosclerosis:
- Hardening of the arteries due to lipid accumulation within the arterial wall.
- Risk factor: Genetic, dyslipidemia 240mg/dl increase chance CAD, elevated LDL, elevated HDL is good is protective from CAD, tobacco, HTN, DM.
- Pathophysiology:
- Damage to endothelium, then leukocytes accumulated, smooth muscles secrete matrix that traps the lipid and form a bulk, matrix also form cap, as lesion increase in size the cape rupture and thrombus form.
Congestive Heart Failure (CHF):
Inability of the heart to pump enough blood to meet the metabolic demands of the body.
Systolic failure
- Due to impaired contractility of the heart or high afterload (chronic volume overload from mitral and aortic regurgitation, dilated cardiomyopathies, HTN, aortic stenosis).
- Ejection fraction <40%. HFrEF
Diastolic failure
- Due to impaired diastolic relaxation or ventricular failing of the heart (caused by left ventricular hypertrophy, restrictive cardiomyopathy, myocardial fibrosis, myocardial infarction).
- Can have preservation of the ejection fraction (>50%). HFpEF
CHF Risk factor
- Risk Factors
o Ischemic heart disease.
o Hypertension.
o Myocardial infarction.
o Valvular diseases.
o Congenital heart disease.
o Cardiomyopathies.
Left-Sided Heart Failure
Signs and Symptoms
o Dyspnea.
o Paroxysmal nocturnal dyspnea.
o Orthopnea.
o Pulmonary congestion.
o Clinically can appreciate a third heart sound (S3) and pulmonary rales. S4 sound with diastolic failure.
Right-Sided Heart Failure
Signs and Symptoms
- Most common cause is left-sided heart failure.
- Abdominal discomfort.
- Anorexia.
- Hepatomegaly.
- Peripheral edema.
- Jugular venous distension.
New York Heart Association Classification of CHF
- CLASS I – heart disease with no symptoms or limitation of physical activity.
- CLASS II – No symptoms at rest and slight limitation with ordinary activity.
- CLASS III – Marked limitation of activity with minimal exertion.
- CLASS IV – Symptoms at rest. Severe limitation of activity.
CHF Workup:
CHF Workup:
- EKG
- ECHO
- Chest xray
- CBC to evaluate for anemia.
- BMP- Look for hypokalemia.
- LFTs to evaluate hepatic function and congestion.
- Fasting glucose level to assess for diabetes.
- Clinical exam- auscultation for sign of volume overload rales and S3, JVD, pedal edema and hepatomegaly.
- Test: Normal BNP BELOW 100pg/ml
- Brain natriuretic peptide BNP, BNP>35 diagnostic for non-acute onset CHF, BNP >100pg/ml for acute onset CHF.
Treatment of CHF:
Treatment of CHF:
- Diuretics (Lasix): treat systemic and pulmonary congestion.
- Beta Blocker: decrease myocardial oxygen consumption.
- Digoxin: increase cardiac contractility.
- Signs and symptoms of digitalis toxicity which include xanthopsia (vision deficiency leading to predominance of yellow vision) nausea, vomiting, confusion, paresthesias, ventricular tachycardia, premature ventricular contractions, heart block, bigeminy, trigeminy.
- Narrow therapeutic range. 0.5– 0.9 ng/ml.
Marfan Syndrome
- Autosomal dominant connective tissue disorder affecting cardiac, skeletal, and ocular tissue.
- The pt will be tall, thin, has an outward displacement of ribs, micrognathia, malar hypoplasia, high arched palate, glaucoma, myopia aortic dissection, MVR.
- What is your anesthesia plan for Marfan syndrom?
- Versed/ Propofol, I will avoid fentanyl in this patient, control BP, fluids, ventilatory pressure should be reduced to prevent barotrauma.
Describe your work up for Mrafan?
- AHA does not recommend abx , cardiology consult for evaluation of valvular function, monitor EKG , ECHO, control BP, pulmonary function evaluation since these patients exhibits restrictive lung disease , chest x ray
How do you tell if MVP is regurgitant?
- Clinical evaluation A systolic murmur heard over the apex of the heart, ECHO, MRI
- What else about Marfan’s concerns you?
- CHF, continue BP meds to prevent and control BP to prevent sharing force on the vessels and TMJ dislocation
Patient takes Zoloft. What concerns do you have about Zoloft, Prozac, lexapro?
- Zoloft (sertraline) or any other selective serotonin reuptake inhibitor (SSRI), concern of bleeding this medication can affect platelet function, it can affect the clearance and metabolism of fentanyl causing serotonin syndrome which increase serotonin activity in the central nervous system.
- Prozac = Fluoxetine SSRI
- Lexapro SSRI
Serotonin Syndrome
- An adverse drug reaction producing excess serotonergic effects of the central nervous system.
- Serotonin syndrome typically occurs shortly after an increase in the dose of a serotonin agonist (a MAOI or an SSRI inhibitor) and meperidine, fentanyl and tramadol) and ondansetron
- Onset of the reaction can be within minutes of drug administration or over the course of several hours. Fortunately, most reactions are mild and resolve within several hour
- Clinical diagnosis. No labs
- Symptoms include hypertension, diarrhea, tachycardia, hyperthermia, hyperkalemia, diaphoresis, ataxia, myoclonus, mydriasis, hallucinations, and confusion.
- Concern for rhabdomyolysis, ventricular arrhythmia, respiratory arrest, and coma.
- Some can be severe and life-threatening mimicking malignant hyperthermia.
Treatment of Serotonin Syndrome
- Activate 911 to transfer for definitive treatment.
- Chilled IV fluids and ice until EMS transfer.
- If intubation is indicated, avoid succinylcholine, which can cause additional hyperkalemia.
- Lorazepam 1–2 mg IV push for agitation. 0.1mg/kg for pediatric
- Methysergide 2–6 mg to counteract serotonin.
- Labetalol or propranolol for HTN and tachycardia.
- Cyproheptadine histamine-1 receptor antagonist 4 mg po to counteract serotonin. Comes only oral. DO NOT GIVE PREGNANT PATIENT cause congenital deformity.
- Dantrolene for severe cases: hyperthermia, rhabdomyolysis, hyperkalemia and DIC.
Patient Management Serotonin Syndrome
- Avoid drugs that may trigger serotonin syndrome (fentanyl, tramadol, ondansetron).
- Look for signs of serotonin syndrome.
- EKG monitoring for lithium-induced dysrhythmias.
- Patients on MAOIs are at risk for orthostatic hypotension.
- Careful use of sympathomimetic agents – vasoconstrictors may have exaggerated effects, especially in patients on TCAs.
- Ephedrine should be avoided in patients with MAOIs. Ketamine use should be carefully considered due to sympathetic effects.
- CYP450 inhibitors such as macrolide antibiotics may lead to toxic levels of TCAs.
Ehler Danlos syndrome:
- Genetic connective tissue disorders characterized by defects in fibrillar collagen production leading to changes in skin, tendons, blood vessels, and viscera.
- 80% of cases fall under the classical and hypermobile (most frequent) types.
- There are six major subtypes based on the Villefranche nosology.
- Vascular EDS subtype is life threatening due to spontaneous rupture of small and large arteries.
Classical Features of EDS
- Joint hypermobility with subluxation.
- Skin hyperelasticity.
- Easily bruised.
- Gorlin sign – ability to touch tongue to tip of nose
- Abnormal scarring.
- Extremely soft skin.
- Hernias are common.
Anesthesia and surgery concerns in EDS
- CBC, BMP , EKG and Echo
- Cardiac evaluation to monitor risk of aortic root dilatation and mitral valve prolapse, usually non-significant.
- 26% of patients have platelet aggregation defects. Consider discussion with hematologist for plan of action (commonly desmopressin) . Additionally, use of prophylactic tranexamic acid should be considered.
- Individuals can be resistant to local anesthetic, most commonly seen in hypermobility subtype.
- Be cognizant of TMJ subluxation during intubation and neck extension instability (occipitoatlantoaxial)
- Reduce airway pressures due to pneumothorax risk.
- Postural orthostatic tachycardia syndrome prevalent in hypermobile variant, ensure adequate hydration.
- Consider avoiding NSAIDs for pain control due to bruising risk.
- Commonly have dental issues with poor periodontal health due to fragility of periodontium, especially in vascular subtype.
- Subtypes with vascular fragility should have type and cross match.
- Skin tape placement should be minimized
What is DM?
A metabolic disorder, which results in a defect in insulin secretion, action, or both, resulting in hyperglycemia.
What are the different types of DM?
Type 1 diabetes mellitus is due to impaired production of insulin and occurs early in life. Type 2 diabetes mellitus is characterized by insulin resistance.
What is the function of insulin?
The functions of insulin are to increase glycogen synthesis, decrease gluconeogenesis, increase potassium uptake, and increase lipid synthesis.
How do you diagnose DM?
Fasting glucose of >126 mg/dl on 2 or more occasions, glucose tolerance test (readings >200 mg/dl 2 hours after a 75-gram glucose load), HgB A1C of 6.5 or greater, non-fasting plasma glucose ≥200 mg/dl and symptoms of DM.
Which drug is typically prescribed first for a patient with DMII on insulin and metformin?
Metformin.
What is the mechanism of action of metformin?
Decrease hepatic gluconeogenesis and decrease intestinal glucose absorption.
What is your concern about DM?
I want to know how well the DM is controlled, the regimen, and check the HgB A1C for glycemic control. DM patients can develop silent ischemia and are at risk of infection.
What are the pre-surgical recommendations for a patient with diabetes?
- NPO 12 hours for IDDM
- early morning appointments
- pre and post op finger stick to assess glucose
- obtain recent HbA1c
- give fluids 100-200ml of 5% dextrose solution hourly, avoid LR
- stop oral hypoglycemics on day of surgery.
- Omit short-acting insulin on morning of procedure.
- Take between 1⁄2 - 2/3 total morning dose of intermediate acting glucose.
- If the pt blood glucose < 100mg/dl , consider D5W with 0.45% NS and consider NS if blood glucose >130.
What is a concern about long-standing DMII?
Long-standing DMII can lead to peripheral neuropathy, CAD, silent ischemic episodes, diabetic retinopathy, and nephropathy.
What concerns do you have for a patient with type I DM before surgery?
Rapid development of diabetic ketoacidosis, infection risk, managing blood glucose levels, and adjusting insulin doses preoperatively.
What concerns do you have for a patient with DM on an oral hypoglycemic regimen before surgery?
Oral regimens should be discontinued, glucose levels should be measured, and metformin should be stopped due to lactic acidosis risk.
Discontinuation of sulfonylureas is due to its association with hypoglycemia and increased risk of perioperative myocardial ischemia and infarction.
How would you handle a call from a diabetic patient complaining of nausea and vomiting after sedation?
I will ask the patient to come in and examine her.
What is DKA?
DKA is a metabolic condition that occurs secondary to an insulin shortage that results in hyperglycemia, ketonemia, and an anion gap metabolic acidosis.
What are some signs and symptoms of DKA?
Vomiting, confusion, polydipsia, polyuria, dehydration, abdominal pain, Kussmaul breathing, hyperglycemia, hyperkalemia, ketotic ‘fruity’ breath, dry mucous membranes, and hypotension.
What triggers DKA to occur?
CVA, MI, UTI, stress, cocaine usage, and inadequate insulin.
How are ketones generated in someone with DKA?
Result of the breakdown of fatty acids through the ketogenesis cycle.
What is the management of DKA in ICU?
ABG, IV fluids 0.9% NS, IV regular insulin, replace K, correct pH with bicarb if <7.
Why would we give potassium to a DKA patient?
Because insulin drives K into the cell, causing hypokalemia.
How does DMII contribute to HTN?
Insulin resistance increases sympathetic nervous system activity and contributes to endothelial dysfunction.
Why are diabetics more prone to infections?
Due to impaired chemotaxis and phagocytosis 2/2 glycosylation of the neutrophils.
