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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4518_Библиотеки_им_академика_М_И_Перельмана
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9 Sleep-Disordered Breathing andObstructive Sleep Apnea
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Sleep Disorders
Insomnia
• Recurrent difculty with sleep initiation, maintenance, consolidation, or quality
causing daytime dysfunction. May include non-restorative sleep or sleep of
poor quality
• Daytime symptoms must include at least one:
– Fatigue or malaise, cognitive impairment (attention, concentration, or mem-
ory), social/vocational difculty or poor school performance, mood impairment or irritability, daytime sleepiness, reduced motivation or energy,
tendency to be accident-prone, headache, muscle tension, gastrointestinal
upset, concerns about sleep itself
Sleep-related breathing disorders
• Central sleep apnea syndromes
– Primary central sleep apnea
– Central sleep apnea due to Cheyne-Stokes breathing pattern (increased
risk of CHF)
– Central sleep apnea due to high-altitude periodic breathing
– Central sleep apnea due to medical condition not Cheyne-Stokes
– Central sleep apnea due to drug or substance
– Primary sleep apnea of infancy
• Obstructive sleep apnea syndromes
– Obstructive sleep apnea, adult
– Obstructive sleep apnea, pediatric
Role of tonsillectomy:
CHAT trial: 464 children with mild-to-severe OSA were followed for 7
months. 80% normalized after. T&A vs 46% in the control nonsurgical group.
Self-reported behaviors improved after T&A, but objective measures
did not.
Preoperative PSG is indicated for obesity, Down syndrome, craniofacial
abnormalities, neuromuscular disorders, sickle cell disease, or
mucopolysaccharidoses.
PSG can also be obtained if the diagnosis is uncertain or history is discordant with exam.
Patients should be monitored overnight if they are younger than age 3
or have severe sleep apnea (AHI >10, O2 nadir <80%).
• Spectrum of sleep-related breathing disorders
– Snoring:
No apneas or sleep fragmentation
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E. C. Kinberg et al.
– Upper airway resistance syndrome:
– Respiratory events causing sleep fragmentation and daytime sleepiness
Minimal qualifying apneas or hypopneas
– Obstructive sleep apnea:
Upper airway obstruction with apneas or hypopneas associated with sleep
disturbance
– Obesity hypoventilation syndrome:
Triad of:
Obesity (BMI >30)
Sleep disordered breathing
Hypercapnia (increase of 10 mmHg PaCO2 during sleep)
Hypersomnias of central origin
• Subclasses:
– Narcolepsy
Mean sleep latency of <8min
Low CSF hypocretin-1 levels (1/3 of normalized mean)
– Kleine-Levin syndrome
Episodic hypersomnia with sleep time of 18 h daily, sometimes associated
with huge appetite and weight gain
Frequently associated with intense dreams
Hypersomnia episodes followed by period of insomnia
– Menstrual-related hypersomnia
May improve with oral contraceptives or carbamazepine
– Idiopathic hypersomnia
Affects adolescents and young adults
Persistent lethargy, difculty waking up
Requires a PSG and a sleep latency test
– Behaviorally induced insufcient sleep syndrome
– Hypersomnia due to medical condition
– Hypersomnia due to drug or substance
Circadian rhythm sleep disorders
– Advanced sleep phase syndrome
Recurrent pattern of early evening sleepiness and early morning awakening
– Delayed sleep phase syndrome
A person’s sleep cycle is delayed by 2 h beyond a conventional bedtime.
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Parasomnias
• Disorders of arousal
– Confusional arousals
Occurs mostly in infants and toddlers
Agitated behavior, appears alert but does not respond to interaction
– Sleepwalking
Semi-alert state, tends to stop by adolescence but can occur in adults
– Sleep terrors
Occurs in late childhood and adolescence.
Marked by loud screams and distress.
The episode is vaguely remembered but in less detail than a nightmare.
• Parasomnias usually associated with REM Sleep
– REM sleep behavior disorder (including parasomnia overlap disorder and sta-
tus dissociatus)
Mainly in older men
Pathologic preservation of muscle tone allowing dreams to be acted out
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– Recurrent isolated sleep paralysis
Sleep paralysis: REM sleep-based atonia combined with sconscious
awareness.
Isolated episodes occur in the absence of known disorders such as
narcolepsy.
– Nightmare disorder
Dysphoria most common in REM sleep at the last 1/3 of a night
Treatment: reassurance, cognitive-behavioral therapy, pharmacologic
intervention
• Other parasomnias
– Sleep-related dissociative disorders
– Sleep enuresis
– Sleep-related groaning (catathrenia)
Marked by end-inspiratory apnea (breath holding) and expiratory groaning
– Exploding head syndrome
The perception of abrupt loud noises when going to sleep or waking up
• Parasomnias associated with obstructive sleep apnea
– OSA-induced arousals from REM sleep
– OSA-induced arousals in NREM sleep
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– OSA-induced cerebral anoxic attacks or nocturnal seizures
– REM rebound from CPAP use leading to:
Confusional arousals
Sleepwalking
Sleep terrors
Sleep-related movement disorders
• Subclasses
– Restless leg syndrome
Rule out iron deciency.
Reduce caffeine intake.
Treat with a dopamine agonist (pramipexole).
Alternative is an alpha 2-delta agonist (gabapentin).
– Periodic limb movement disorder
Treatment: clonazepam and dopamine agonist therapy
– Sleep-related leg cramps
– Sleep-related bruxism
Bruxism is related to sleep arousals, so avoid alcohol, caffeine, and tobacco
before bedtime.
Mouth guards.
E. C. Kinberg et al.
– Sleep-related movement disorder, unspecied
– Sleep-related movement disorder due to drug or substance
– Sleep-related movement disorder due to medical condition
Isolated symptoms, apparently normal variants, and unresolved issues
• Subclasses
– Long sleeper
– Short sleeper
– Snoring
– Sleep talking
– Sleep starts (hypnic jerks)
– Benign sleep myoclonus of infancy
– Hypnagogic foot tremor and alternating leg muscle activation during sleep
– Propriospinal myoclonus at sleep onset
– Excessive fragmentary myoclonus
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Further Reading
1. 05.03 - Polysomnography - Unit 05 - Medicine: Overview of Sleep Medicine - Ronald
Chervin, M.D. - (Standard Track) | Coursera. https://www.coursera.org/lecture/sleep/05- 03-
polysomnography- PBYJm. Accessed 4 February 2020.
2. Marin JM, Agusti A, Villar I, etal. Association between treated and untreated obstructive
sleep apnea and risk of hypertension. JAMA. 2012;307(20):2169–76. https://doi.org/10.1001/
jama.2012.3418.
3. Patil RD, Patil YJ.Perioperative management of obstructive sleep apnea: a survey of veterans
affairs health care providers. Otolaryngol Head Neck Surg. 2012;146(1):156–61. https://doi.
org/10.1177/0194599811427251.
4. Lalwani A.Current diagnosis and treatment in otolaryngology: head and neck surgery. 3rd ed.
Philadelphia: Mosby/Elsevier; 2012.
5. Freedman N. Treatment of obstructive sleep apnea syndrome. Clin Chest Med.
2010;31(2):187–201. https://doi.org/10.1016/j.ccm.2010.02.012.
6. Holty J-EC, Guilleminault C.Surgical options for the treatment of obstructive sleep apnea.
Med Clin. 2010;94:479–515. https://doi.org/10.1016/j.mcna.2010.02.001.
7. Li HY, Lee LA, Wang PC, Chen NH, Lin Y, Fang TJ.Nasal surgery for snoring in patients
with obstructive sleep apnea. Laryngoscope. 2008;118(2):354–9. https://doi.org/10.1097/
MLG.0b013e318158f73f.
8. Friedman M, Ibrahim H, Joseph NJ. Staging of obstructive sleep apnea/hypopnea syndrome: a guide to appropriate treatment. Laryngoscope. 2004;114(3):454–9. https://doi.
org/10.1097/00005537- 200403000- 00013.
9. Flint P, Cummings C.Cummings otolaryngology: head and neck surgery. 5th ed. Philadelphia:
Mosby/Elsevier; 2010.
10. Nightmares and nightmare disorder in adults- UpToDate. https://www.uptodate.com/contents/
nightmares- and- nightmare- disorder- in- adults#H423383543. Accessed 4 February 2020.
11. Sharpless BA.A clinician’s guide to recurrent isolated sleep paralysis. Neuropsychiatr Dis
Treat. 2016;12:1761–7. https://doi.org/10.2147/NDT.S100307.
12. Drakatos P, Higgins S, Duncan I, etal. Catathrenia, a REM predominant disorder of arousal?
Sleep Med. 2017;32:222–6. https://doi.org/10.1016/j.sleep.2016.06.010.
13. Sharpless BA. Exploding head syndrome. Sleep Med Rev. 2014;18(6):489–93. https://doi.
org/10.1016/j.smrv.2014.03.001.
Chapter 10
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Fluids, Hemostasis, Nutrition,
andPulmonary Physiology
PeterFilip, AlexanderN.Goel, andFredY.Lin
Pearls
• Fluid and electrolyte optimization serves an integral role in the management of
the surgical patient.
• Electrolyte disturbances should be addressed promptly and may require medical
consultation particularly if there are symptoms.
• Routine preoperative coagulation studies and platelet counts may be unnecessary
and should be guided by patient history and the surgical bleeding risk that accompanies the proposed procedure.
• Alcohol abuse may be a co-contributor to nutritional deciencies in this patient
population.
Fluids and Electrolytes
• Fluid and electrolyte requirements
– Total body uid volume (liters) is at least half of body weight.
– Blood volume calculations become important when considering recussitation
and blood transfusions in the setting of substantial intraoperative blood loss,
particularly in pediatric patients.
P. Filip (*) · A. N. Goel · F. Y. Lin
Department of Otolaryngology- Head and Neck Surgery, Icahn School of Medicine at the
Mount Sinai Hospital, New York, NY, USA
e-mail: alexander.goel@mountsinai.org; fred.lin@mountsinai.org
© Springer Nature Switzerland AG 2023
F. Y. Lin, Z. M. Patel (eds.), ENT Board Prep,
https://doi.org/10.1007/978-3-031-26048-3_10
163
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P. Filip et al.
65 ml/kg in women
75 ml/kg in men
75–80 ml/kg in children
80 ml/kg in infants
– Fluid therapy by replacing water and electrolytes lost in normal physiologic
processes, i.e., respiratory tract, skin, stool, and urine
Can be given enterally or intravenously
Adults—4/2/1 rule
• 4 ml/kg for rst 10kg
• 2 ml/kg for next 10kg
• 1 ml/kg for anything over 20kg
– Fluid therapy replacing water and electrolytes lost in pathologic processes,
i.e., diarrhea, vomiting, trauma
If patient is in an unstable clinical condition, administer a bolus of isotonic
replacement uid such as 0.9% NS, Lactated Ringer’s, or Plasma-Lyte.
• Electrolyte homeostasis
– Sodium and water
Normal serum sodium 135–145 mEq/L.
Serum sodium disorders are due to changes in total body water balance or
distribution.
Hyponatremia (sodium <135 mEq/L).
• Pathophysiology: excess of water relative to sodium
• Treatment:
– Correction with 0.9% NS or 3% NS should be guided by calculating
the sodium decit. Increase serum sodium at rate of 0.5 mEq/L/h to
avoid central pontine myelinolysis.
– If CNS symptoms (seizures, cerebral edema, increased intracranial
pressure) are present, correct sodium rapidly with hypertonic saline
(3% NS). Increase serum sodium by 2 mEq/L/h until symptoms
resolve.
Hypernatremia (sodium >145 mEq/L).
• Pathophysiology: decit of water relative or sodium gain in the setting
of lack of access to free water or inability to concentrate urine
• Treatment:
– Correction of free water decits with hypotonic solution (D5W, 1/2
NS, 1/4 NS) should be guided by calculating the free water decit.
Decrease serum sodium at rate of 0.5 mEq/L/h to avoid cerebral edema.
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– Hypovolemic: First give 0.9% NS if hemodynamic instability.
Replace free water decit with hypotonic solution.
– Euvolemic: Central DI (seen in frequently in transphenoidal pitu-
itary resection)—dDAVP. Neurogenic DI—treat cause, thiazide
diuretic + sodium restriction.
– Hypervolemic: loop diuretic and D5W or PO ingestion of free water.
– Potassium
Normal serum potassium 3.5–5.0 mEq/L
Hypokalemia (potassium <3.5 mEq/L)
• Pathophysiology: due to transcellular shift or potassium depletion
• Clinical: nausea, vomiting, anorexia, ileus, weakness, muscle cramps,
polyuria, EKG changes—u waves, ventricular ectopy (PVCs), increased
QT interval
• Treatment:
– Patients can tolerate mild hypokalemia (serum potassium
3–3.5 mEq/L).
– Correct hypomagnesemia.
– Goal serum potassium = 4mEq/L for patients with underlying car-
diac disease (i.e., CAD, arrhythmias) or on digoxin.
– Oral—preferable, safer route.
– IV—consider if patient is NPO or life-threatening hypokalemia.
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Hyperkalemia (potassium >5.0 mEq/L)
• Pathophysiology: due to transcellular shift or renal dysfunction
• Clinical: weakness, nausea, paresthesias, palpitations
• EKG: peaked t waves, long PR interval, increased QRS width,
asystole/PEA
• Treatment: guided by the serum potassium level and if there are
EKG changes
– EKG changes or serum K ≥ 6.5 mEq/L: calcium gluconate or chlo-
ride (give rst), regular insulin/D50, albuterol, NaHCO
3
– No EKG changes: Kayexalate PO/rectal
– Renal insufciency: consider hemodialysis, loop diuretic
– Calcium
Normal serum total calcium 9–10 mg/dL, ionized calcium 1.1–1.3 mmol/L
99% of calcium is in the bone, remaining 1% in the serum is ionized (active
form) or complexed with anions or albumin (inactive form)
• Total serum calcium value affected by change in anions or albumin levels; Corrected calcium = [0.8 × (normal albumin − patient’s albumin)]
+ serum calcium level.
• Calcium balance is regulated by PTH and calcitriol (1,25 vitamin D).
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Hypocalcemia (serum total calcium <8.4 mg/dL, ionized calcium
<1 mmol/L)
• Pathophysiology: decreased PTH activity, vitamin D deciency
• Clinical: perioral or peripheral numbness, tingling, headaches, cramps,
Chvostek sign (facial nerve irritability), Trousseau sign (carpal spasm),
laryngospasm, growth failure, bone pain, osteomalacia, osteitis brosa
cystica, cardiovascular instability, ventricular ectopy
• Treatment: guided by cause and if there are symptoms
– Replete hypomagnesemia rst.
– Symptomatic: calcium gluconate or chloride 1–2 g IV, consider con-
tinuous infusion.
– Asymptomatic or chronic: calcium (1–3 g/day) + calcitriol PO.
– Total thyroidectomy and parathyroidectomy: patients are at risk for
hypocalcemia postoperatively; consult endocrinology to optimize
vitamin D preoperatively; ionized calcium should be measured at
least once every 6 h postoperatively and repleted accordingly.
Patients undergoing four gland surgery in the setting of end stage
renal disease are at higher risk for hypocalcemia and hungry bone
syndrome (rapid, profound, and prolonged hypocalcemia associated with hypophosphatemia and hypomagnesemia); consider
ICU admission.
Hypercalcemia (serum total calcium >10.6 mg/dL, ionized calcium
>1.3 mmol/L)
• Pathophysiology: Increased PTH, neoplasm, familial hypocalciuric
hypercalcemia, hypervitaminosis D
• Clinical: symptoms usually with total serum calcium >12 mg/dL or ionized calcium >3 mmol/L
• “Bones, stones, abdominal groans, and psychiatric moans”—nausea,
vomiting, ileus, constipation, pancreatitis, cardiovascular instability,
short QT interval, altered mental status, polyuria, nephrolithiasis, osteopenia, fractures
• Treatment: manage acutely if symptoms or serum calcium >12 mg/dL,
reverse underlying cause
– Correct hypovolemia with 0.9% NS.
– Furosemide.
– Bisphosphonates.
– Calcitonin.
– Malignancy—glucocorticoids.
– Parathyroidectomy (see head and neck chapter for details).
– Magnesium
Normal serum levels 1.6–2.5 mEq/dL.
Normal intake 20 mEq/day.
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No hormones affect magnesium balance.
Magnesium concentration affects renal excretion.
Hypomagnesemia (serum magnesium <1.4 mEq/dL):
• Etiology: impaired intestinal absorption (alcohol abuse, malnutrition,
NGT drainage, diarrhea), increased renal excretion (drugs, uncontrolled
diabetes), chelation from the serum (pancreatitis, hungry bone
syndrome)
• Clinical: altered mental status, fasiculations, tremor, seizure, electrolyte
abnormalities—hypocalcemia, hypokalemia, hypophosphatemia
• EKG changes—prolonged PR and QT interval, torsade de pointes
• Treatment:
– Caution with renal insufciency
– Symptomatic: magnesium sulfate 2 g bolus then infusion
– Asymptomatic: magnesium oral (associated with diarrhea)
Hypermagnesemia (serum magnesium >2.2 mEq/dL):
• Etiology: iatrogenic, renal insufciency, DKA, tumor lysis syndrome
• Clinical: hyporeexia, lethargy, weakness, paralysis, hypotension, bradycardia, arrhythmias
• Treatment:
– Symptomatic: supportive care, calcium gluconate 1 g IV bolus; con-
sider dialysis with renal insufciency.
– Asymptomatic: with normal renal function, magnesium levels will
return to normal; consider dialysis with renal insufciency.
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– Phosphorus
Normal serum levels 3.0–4.5 mg/dL
Phosphorus balance affected by PTH, phosphorus concentration, insulin
and calcitriol (1,25 vitamin D)
Hypophosphatemia (serum phosphorus <2.8 mg/dL)
• Etiology: impaired intestinal absorption (malabsorption, oral phosphate
binder use, alcoholism, vitamin D deciency), increased renal excretion
(hyperparathyroidism, DKA, sepsis), transcellular shift (refeeding syndrome in the setting of cancer cachexia, respiratory alkalosis).
• Clinical: symptoms occur due to decreased ATP and tissue oxygen
delivery—weakness, heart failure, impaired diaphragm function, paresthesia, altered mental status, hemolysis, platelet dysfunction.
• Treatment: serum phosphorus <1 mg/dl and/or symptoms: Replete with
IV phosphorus otherwise replete with oral phosphorus.
Hyperphosphatemia (serum magnesium >4.5 mg/dL)
• Etiology: transcellular shift (rhabdomyolysis, tumor lysis syndrome,
increased intake (Fleet enema, excess vitamin D), decreased renal
excretion (renal insufciency, hypoparathyroidism)
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