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Impacted Teeth
-impacted teeth are ones that don’t erupt into arch in expected time
-teeth become impacted b/c adjacent teeth, dense overlying bone, or excessive soft tissue prevents eruption
-inadequate arch length is most common reason teeth fail to erupt
-impacted teeth are retained for pt’s lifetime unless surgically removed
-most common impacted teeth are mand. 3rd molars, max. 3rd molars, and max. canines
-unerupted teeth include both impacted teeth and teeth in process of erupting
-embedded teeth is used interchangeably w/ impacted teeth (Embedded teeth = Impacted teeth)
-impacted max. 3rd molars can be displaced into:
1) infratemporal space -removed via hemostat
2) maxillary sinus -removed via Caldwell-Luc approach
-mand. 3rd molars can be displaced into:
1) submand. space (most likely)
2) IA canal
3) cancellous bone space
Caldwell-Luc Procedure
-opening made into max. sinus by incision into canine fossa above max. PM roots
-after tooth/root removal, figure-8 suture made, antibiotics, nasal spray, and decongestant given
-palatal root of max. 1st molar is most often dislodged into sinus
Complications of Extractions
1) Tearing of mucosal flap
2) Puncture wounds in palate, tongue, etc.
-control bleeding and allow healing by secondary intention
3) Oral-antral communication
-manage w/ figure 8 suture over socket, antibiotics, and nasal spray
-if very small, just let blood clot form
-if very large, then close w/ flap procedure
-complications: chronic oroantral fistula and max. sinusitis
4) Root fracture
5) Tooth displacement
a) max. molar into max. sinus (palatal root of max. 1st M most common)
b) max. 3rd molar into infratemporal fossa
c) mand. molar roots forced into submandibular space
d) tooth lost into oropharynx (may cause airway obstruction, should take to ER for chest x-rays)
6) Injury to adjacent teeth
7) Alveolar process fractures (max. tuberosity)
-if tuberosity fxs completely off, then smooth sharp edges of bone and suture soft tissue
-if fxns but still intact, then manually reposition and stabilize w/ sutures
-tuberosity fx most often occurs on lone-standing molars or extraction of last molar in arch
8) Trauma to inferior alveolar nerve (mand. 3rd molars)
9) Excessive bleeding
a) injury to IA artery
b) arteriolar bleed from elevating flap
c) pt’s hemostasis (warfarin, hemophilia, von Willebrand’s, chronic liver deficiency)
10) Infections (rare)
11) Dry socket (localized alveolar osteitis)
-occurs in 3% of mand. 3rd molar extractions
12) Air emphysema (from nonsurgical handpieces)
Dry Socket
-caused by increased fibrinolytic activity, causing loss of blood clot in extraction site
-smoking and oral contraceptives have been indicated, as well as rinsing, hot liquids
-most common in mandibular molars (most common complication seen after mand. molar extraction)
-signs: worsening throbbing pain, radiating pain, bad odor and taste, poor healing extraction site
-treatment: irrigation w/ saline, sedative dressing (eugenol) changed every 2 days until asymptomatic, and
analgesics (no antibiotics needed)
Extraction Tips
-sequence of extraction should be maxillary before mandibular and posterior to anterior
-first force applied should be apical
-B-L forces are less effective in mand. posterior teeth due to dense bone
-normal saline should be used for irrigation b/c it is isotonic
-distilled water is hypotonic and can cause cell lysis
Alveoloplasty
-indicated in any area that may cause difficulty in denture construction
Tori Removal
-only need to be removed for denture fabrication
-palatal tori removal:
1) make stent pre-op
2) double-Y incision made over midline of torus
3) osteotome used to remove in small portions
-should not remove en masse b/c can enter into nose by removing palatine bone
4) large bur used to smooth area
5) close wound w/ horizontal mattress suture and place stent to prevent hematoma
Sutures
-as suture diameter decreases, strength decreases
-size 0 suture is average size
-adding 0’s means they are getting smaller (4-0 smaller than 3-0)
-assigning positive numbers means suture size increases (2, 3, 5, etc)
-smallest diameter suture that is sufficient to keep wound closed should be used
-3-0 and 4-0 most common in dental surgery
-can be resorbable or nonresorbable
1) resorbable: gut, polyglactin (vicryl), polyglycolic acid (dexon), polydixanone
-plain gut made form sheep intestine and rapidly digested
-chromic gut is chromitized to be more resistant to proteolytic enzymes
2) nonresorbable: nylon, silk, polypropylene
-must be removed in 5-7 days
Dead Space
-any area that remains devoid of tissue after closure of wound
-created by removing tissues in depths of wound or not reapproximating tissue planes during closure
-dead space usually fills in w/ blood to form hematoma w/ high potential for infxn
-can eliminate dead space by:
1) closing wound in layers
2) apply pressure dressings
3) use drains
4) place packing into void until bleeding stops
Wound Healing
1) Primary intention: occurs in closely approximated wound edges
-lower risk of infxn and minimal scar formation
2) Secondary intention: occurs when large gap btw incision edges
-requires larger amt of epithelial migration, collagen deposition, contraction, and remodeling
-slower healing and more scar formation (granulation tissue)
-granulation tissue is weaker than original tissue
-factors that impair wound healing: foreign material, necrotic tissue, ischemia, tension, systemic conditions
Stages of Wound Healing
1) Inflammatory stage: from time of injury to 2-5 days
-hemostasis (vasoconstriction, clot formation) and inflammation (vasodilation, phagocytosis)
-neutrophils and lymphocytes predominate
2) Proliferative stage: 2 days to 3 weeks
-epithelialization, angiogenesis, granulation tissue formation, and collagen deposition
-fibroblasts predominate
3) Remodeling/Maturation stage: 3 weeks to 2 years
-collagen fibers increase tensile strength and contraction occurs
Stages of Hemostasis
1) Vascular phase: vasoconstriction
2) Platelet phase (Primary hemostasis): platelet and collagen interaction leading to platelet plug
3) Coagulation phase (Secondary hemostasis): cascade of coagulation factors
4) Repair process: growth of fibroblasts and smooth muscle, fibrinolysis of clot
Dental Implants
-factors that need to be considered:
1) Primary stability
2) Amount of bone
3) Anatomic structures (sinus, other teeth, IA nerve)
-loss of teeth for extended time can lead to ridge resorption (esp. mand.) and ridge augmentation may be
needed (bone grafting)
-common sites for autogenous bone grafts include:
1) iliac crest 3) anterior cortex of chin (small areas of bone)
2) rib 4) lateral cortex of ramus/external oblique ridge
-allogenic grafting also possible
-PAN and CT scan should be used in implant txt planning
-most popular type of implants used are root-form implants
Osseointegration
-direct adaptation of bone to dental implant
-defined histologically as being evident at light microscope level
-implant success criteria defined as:
1) implant immobile clinically
2) no peri-implant radiolucency present
3) mean vertical bone loss less than 0.2mm annually
4) no pain or infxn
5) implant placement doesn’t inhibit placement of crown/prosthesis
Facial Fractures
-facial fractures should always be considered after car accidents, fights, falls, or sports accidents
-signs of facial fracture include:
1) pain 5) abnormal mobility of bone 9) malocclusion
2) contour deformity 6) numbness (CN V-3) 10) step defect
3) ecchymosis 7) crepitation 11) mobility of mandible segments
4) laceration 8) hematoma/ecchymosis of FOM
-when there is lip laceration w/ fractured tooth, always take soft tissue radiograph to detect any broken
fragments of tooth material
-txt goals of maxillofacial fractures: control hemorrhage, restore occlusion, reduction and stabilization of
fractured segments
-fat embolism is most often a sequelae of fractures
-highest incidence of fractures occurs in males btw 15-24 yrs old from trauma
Midface Fractures
-midface fxs best evaluated w/ CT scans of face
-both axial and coronal orientations needed to fully evaluate fractures
-can involve maxilla, zygoma, nose, and orbits
-orbital floor fracture is termed “blowout fracture”
-zygomaticomaxillary complex (tripod) fractures are most common midface fx (40%)
-maxillary fractures classified as:
1) LeForte I (transverse maxillary): separation of maxilla only with intact nasofrontal complex
-signs: malocclusion (open bite), buccal vestibule ecchymosis (Guerin’s sign), epistaxis
2) LeForte II (pyramidal): separation of maxilla and nasal complex from cranial base (mobile
nasofrontal complex)
-signs: malocclusion (open bite), perioribtal edema, subconjunctival hemorrhage,
paresthesia of infraorbital nerve
3) LeForte III (craniofacial dysjxn): complete separation of midface at level of naso-orbital-
ethmoid complex (mobile nasofrontal and malar complexes)
-major sign is rhinorrhea from CSF leaking into nasal cavity
-also have restricted mand. movement
Maxillary Surgery
-referred to LeForte I osteotomies
-maxilla can be moved forward and down more easily than up or back
-maxilla can also be sectioned into two or three segments to better position the occlusion
Mandibular Surgery
-most often done using one of two osteotomies:
1) Sagittal split osteotomy: ramus is divided by horizontal osteotomy on medial aspect and vertical
osteotomy on lateral aspect
-lateral and medial aspects then separated and mand. advanced or set back
2) Vertical ramus osteotomy: ramus cut vertically and mand. positioned forward or back
-mandible can be moved anteriorly to correct retrognathia (class II) or posteriorly to correct prognathia
(class III)
-chin can be moved using a genial osteotomy (genioplasty) to correct macrogenia or microgenia
Distraction Osteogenesis
-involves cutting an osteotomy to separate segments of bone and application of an appliance that will
facilitate the gradual and incremental separation of bone segments which will fill in with new bone
Prescription:
-Tab Carbamazepine 200mg BID
-Tab Gabapentin 300mg TID
Postherpetic Neuralgia
-sequelae of herpes zoster infxn
-pain is burning, aching, or electric shock-like
-treatment: 1) anticonvulsants
2) antidepressants
3) sympathetic blocks
-Ramsay-Hunt syndrome: herpes zoster infxn of sensory and motor branches of CN VII and VIII, resulting
in facial paralysis, vertigo, deafness, and cutaneous eruption of external auditory canal
Neuromas
-can occur after a nerve injury
-proximal section of transected nerve forms sprouts filled w/ Schwann cells
-becomes very sensitive to stimuli and can cause chronic neuropathic pain
Burning Mouth Syndrome
-pts complain of pain, dryness, burning of mouth and tongue, and altered taste
-most common in postmenopausal females
-thought to be secondary to defect in pain modulation
-symptoms of 50% of pts resolve w/o txt in 2-yr period
-hormone therapy, anticonvulsants, and antidepressants NOT useful
Chronic Headaches
1) Migraine
a) Onset: acute
b) Location: unilateral
c) Symptoms: nausea, vomiting, photophobia, phonophobia
d) Pain: throbbing
e) Duration: prolonged
f) Diagnostic test: check for hx of symptoms
g) Prior hx of headaches: yes
2) Cluster
a) Onset: acute
b) Location: unilateral
c) Symptoms: rhinorrhea, lacrimation of ipsilateral side
d) Pain: sharp, stabbing
e) Duration: 30 mins to 2 hrs
f) Diagnostic test: history of symptoms
g) Prior hx of headaches yes
3) Tension
a) Onset: chronic
b) Location: global and unilateral
c) Symptoms: multisomatic complaints
d) Pain: aching
e) Duration: daily
f) Diagnostic test: none
g) Prior hx of headaches: yes
4) Temporal Arteritis
a) Onset: acute or chronic
b) Location: localized
c) Symptoms: weight loss, polymyalgia, fever, vision problems, jaw claudication
d) Pain: severe throbbing pain
e) Duration: prolonged
f) Diagnostic test: erythrocyte sedimentation rate test (ESR), tender temporal arteries
g) Prior hx of headaches: no
-can lead to blindness on affected side if not treated quickly
Nerve Injuries
1) Anesthesia: loss of sensation
2) Paresthesia: abnormal sensation (burning, tingling, etc.)
3) Hyperesthesia: increase in sensitivity
4) Dysesthesia: painful sensation to normal stimulus
5) Neurapraxia: mild injury w/ no axonal damage (spontaneous recovery within 4 weeks)
6) Axonotmesis: axonal damage but intact endoneural and perineural sheath
-Wallerian degeneration occurs distal to injury
-Potential for recovery in 1-3 months
7) Neurotmesis: complete severance of axon with a gap created
-no recovery expected w/o surgery
Part 5: Temporomandibular Disorders
TMJ
-classified as ginglymoarthrodial joint w/ both translational and rotational movement
-synovial joint
-anatomy:
1) TMJ: articulation btw condyle of mandible and squamous portion of temporal bone
2) Articular surface of temporal bone: fxnal aspect of TMJ made of dense fibrous CT
a) concave portion: articular fossa (glenoid/mandibular fossa)
b) convex portion: articular eminence (tubercle)
3) Articular disc: dense fibrocartilagenous CT (avascular and aneural)
-separates joint into inferior and superior joint spaces
-anterior/posterior bands: thick (post. band thicker and attached to retrodiscal tissues)
-intermediate zone: thin (center of disc)
4) Retrodiscal tissues: loose CT that is vascular and innervated
Ankylosis
-pt presents w/ severely restricted range of motion and limited interincisal opening w/ pain
-bony ankylosis results in more limitation of motion than fibrous ankylosis
-trauma is most common cause of ankylosis, but surgery, radiation therapy, and infxn can also cause it
Pathologic Mechanism
-highly virulent Strep species initiate infectious process in deep tissues
-cellulitis then occurs (aerobic), followed by proliferation of anaerobic organisms (form abscess)
-aerobic organisms consume the oxygen, making environment more favorable for anaerobes
-disease progresses by following path of least resistance, often through bone cortex and invading fascial
space (most often enter vestibular space)
-can drain spontaneously and result in asymptomatic, chronic draining fistula
Ludwig’s Angina
-bilateral infxn of submandibular, sublingual, and submental spaces
-can lead to blockage of airway
Osteomyelitis
-inflammation of medullary portion of bone
-osteomyelitis spreads via infxn, inflammation, and ischemia
-most common initiating causes are odontogenic infxns and trauma
-infxn begins in medullary space of cancellous bone, then spreads to cortical bone, periosteum, and soft
tissues
-occurs more often in immunocompromised and in mandible over maxilla
-causative agents are similar to odontogenic infxns (Strep, anaerobic cocci and gram- rods)
-treatment done by debridement and antibiotics
Necrotizing Fasciitis
-rapidly progressing infxn of skin and fascia w/ high mortality rate (30-50%)
-caused by group-A strep or C. perfringens
-treated w/ surgical debridement and antibiotics
Sinusitis
1) Acute (less than 1 month)
-S. pneumonia, H. influenzae, M. catarrhalis
2) Chronic (over 3 months)
-results from obstruction of sinus drainage
-diabetics may develop mucormycosis (fungal infxn)
3) Txt: amoxicillin or augmentin (amoxicillin+clavulanate), antihistamines, or surgery to establish drainage
4) Complications of sinusitis: orbital cellulitis, cavernous sinus thrombosis, meningitis, osteomyelitis
Animal Bite Infections
-caused by Pasteurella multicida
-txt w/ ampicillin or amoxicillin
Part 7: Biopsies
Biopsy Technique
-block anesthesia preferred b/c injection into lesion can distort the architecture and make diagnosis difficult
1) Suction: use low volume suction wrapped in gauze so not to aspirate the specimen
-hemostasis is impt so a high volume suction isn’t needed
2) Incision: use sharp scalpel to avoid excessive damage to tissue and achieve clearly defined margins
3) Laser: carbon dioxide laser in super-pulsed mode is acceptable if hemostasis concerns are significant
-a fine peripheral zone of necrosis does occur w/ laser
4) Handling/tagging: if suspect malignancy, a tissue tag should be used to help identify orientation
-tissue should be placed in 10% formalin in volume 20x that of specimen
5) Records: biopsy data sheet must be filled out including pt hx and clinical findings
Incisional Biopsy
1) Uses: when lesion is large (>1cm), polymorphic, suspicious for malignancy, or in high morbidity area
2) Method: portion of lesion is incised and must be obtained in a representative area of the lesion, avoiding
areas of necrosis and in adequate depth to make definitive histological diagnosis
Excisional Biopsy
1) Uses: for smaller lesions (<1cm) that appear benign or on small vascular and pigmented lesions
2) Method: entails removal of entire lesion and a perimeter of surrounding uninvolved tissue
Biopsying an Ulcer
-should wait 14 days (2 wks) to biopsy an oral ulcer, b/c they should heal within 14 days
Part 8: Surgical Management of Cysts and Tumors
Overview
-goals of surgical management are eradication of pathology and esthetic functional rehabilitation
-cysts can be classified as fissural and odontogenic
-odontogenic keratocysts tend to act more aggressively and have higher recurrence rates than
fissural cysts and cysts of odontogenic inflammatory origin
-cysts of jaw are treated w/ either:
1) Enucleation 3) Staged enucleation and marsupialization
2) Marsupialization 4) Enucleation and curettage
Enucleation
1) Description: shelling out lesion w/o rupture
2) Indications: used when it can safely be done w/o sacrificing adjacent structures
3) Pros: is a definitive txt and easier postop wound care
4) Cons: may weaken jaw and damage adjacent structures
Marsupialization
1) Description: surgical window made, followed by decompression and evacuation
2) Indications: done if enucleation would damage adjacent structures or it would be unsuccessful
3) Pros: simple and may spare vital structures
4) Cons: difficult wound care and some pathologic tissue may be left
Reconstruction
-optimally done before performing any definitive txt
-can range from no reconstruction w/ wound management and secondary healing to complex reconstruction
w/ placement of endosseous implants
Sialolithiasis
-salivary gland stones
-most often affects submandibular gland (85%)
-causes pain and swelling which worsens when saliva flow is stimulated
-gland can become infected, causing purulence, erythema, FOM edema, and lymphadenopathy
Part 9: Local Anesthesia
Local Anesthetics
-drugs which reversibly blocks the conduction of nerve impulses
-dental concern is sensory nerve block, but motor nerves can be blocked in high conc.
-local anesthetics block sodium channels
-all LAs are made of a lipophilic aromatic ring linked to a hydrophilic amino group
-bond is either an ester or amide bond which determines class of LA
Trismus
-caused by IA injxn directed into medial pterygoid muscle
-causes spasm of muscle
-management: apply hot, moist towels to site for 20 mins every hour, analgesics, and gradual
opening/closing of mouth
Vasoconstrictors
-vasoconstrictors increase the duration of LA action (primary)
-decrease systemic toxicity by decreasing rate of systemic absorption (secondary)
-reduces bleeding by decreasing blood flow into operative area (only infiltrations, not nerve
blocks)
-reduce rate of vascular absorption by causing vasoconstriction
-help make anesthesia more profound by increasing conc. of LA at nerve membrane
-vasoconstrictors act at alpha receptors to constrict arterioles
Drug Interactions w/ Vasoconstrictors
1) Antidepressants (tricyclic and polycyclic)
-increased sensitivity to Epi
2) Nonspecific beta-blockers (propranolol)
-enhance peripheral alpha-1 adrenergic effects (increased BP w/o tachycardia)
3) Max doses
a) healthy pt: 200 ug Epi
b) Cardiovascular pt: 40 ug Epi
Trigeminal Nerve
-CN V
-is both sensory and motor nerve
-originates in pons
-3 branches:
1) Opthalmic nerve (V1): nasociliary, supraorbital, lacrimal, frontal, supratrochlear, and
infratrochlear nerves
2) Maxillary nerve (V2): zygomatic, PSA, MSA, ASA, infraorbital, greater palatine, and
nasopalatine nerves
3) Mandibular nerve (V3): auriculotemporal, lingual, buccal, and IA/mental nerves
Needle Dimensions
1) Length
a) Short needle: 20mm
b) Long needle: 32mm
2) Diameter
a) 30 gauge: 0.3mm
b) 27 gauge: 0.4mm
c) 25 gauge: 0.5mm
-positive aspiration is directly correlated to needle gauge
-larger gauge needles don’t deflect as often
-larger gauge needles don’t break as often (97% of needle breaks involve 30 gauge needles)
-pts can’t tell the difference btw 25, 27, and 30 gauge needles
Nasopalatine Block
1) Area of anesthesia: palatal tissue from canine to canine (premaxilla area)
2) Technique: topical and pressure anesthesia initially, then insert needle tip 45 degrees to palatal soft tissue
at jxn of palate and incisive papilla at depth of bone
Neurolept Anesthesia
-combined administration of:
1) Neuroleptic agent (Droperidol)
2) Narcotic analgesic
3) Nitrous oxide
-has slow induction of anesthesia, but return to consciousness is quick after N2O removed
Inhalation Anesthetics
-inhalation anesthesia uptake dependent on:
1) Solubility
a) Blood solubility: decreased blood solubility=rapid induction and recovery time
b) Lipid solubility: increased lipid solubility=increased potency
2) Alveolar blood flow
3) Difference in partial pressure btw alveolar gas and venous blood
Malignant Hyperthermia
-inherited condition that most often occurs when exposed to inhalation anesthetics
-inhalation agents cause increased muscle metabolism which can lead to death
-treated w/ 100% oxygen, cooling procedures, and administration of dantrolene
Nitrous Oxide
-colorless, nonirritating gas w/ mild odor and taste
-is potent analgesic, but weak general anesthetic
-works on CNS (reticular activating system and limbic system)
-first symptom is tingling of hands
-requires minimum of 30% oxygen delivery
-no biotransformation
-excreted unchanged by lungs
-is inhalation anesthetic w/ fastest onset of action
-side effects: headache, nausea/vomiting (most common), lethargy, diffusion hypoxia
-N2O should be avoided in pts w/ COPD but is fine in asthmatic pts
Diffusion Hypoxia
-nitrous oxide from bloodstream diffuses into alveoli in lungs for elimination and mixes w/ inhaled room
air that contains 20% oxygen, resulting in hypoxia
-prevented by administering high conc. oxygen during recovery period of nitrous sedation
Barbiturates
-act as sedatives and hypnotics
-are potent anesthetics, but weak analgesics
-act by depressing CNS activity by decreasing rate of GABA dissociation at its receptor
-increases duration of chloride channel opening to decrease neuronal firing
-this prolongs the inhibitory effect of GABA in reticular activating system (RAS)
-are very lipid-soluble which results in very rapid onset of action; why they are used for induction of
anesthesia b/c produce unconsciousness in less than 30 seconds
-agents:
1) Thiopental (Pentothal): ultra-short acting agent
- has high lipid solubility so crosses BBB quickly
2) Methohexital: ultra-short acting
3) Phenobarbital: long-acting agent
Benzodiazepines
-act as anxiolytics, anticonvulsants, antispasmodics, sedatives, and amnesics
-act by enhancing binding of GABA to GABA receptors
-increases frequency of chloride channel opening to decrease neuronal firing
-available in oral and IV forms
-risk of respiratory depression and coma is less for benzos than barbiturates
-agents:
1) Short-acting: triazolam (Halcion) and midazolam (Versed)
2) Intermediate-acting: alprazolam (Xanax)
3) Long-acting: diazepam (Valium), lorazepam (Ativan), chlordiazepoxide (Librium)
-flumenazil is used to reverse effects of benzos by competing at GABA receptor (antagonist)
-effect lasts only 20 minutes, so beware of re-sedation
-presence of propylene glycol in IV mixture for benzos can cause phlebitis (irritation/inflammation of vein)
Propofol (Diprivan)
-IV sedative agent that is highly lipophilic
-good for outpatient anesthesia due to its rapid induction and recovery and low incidence of
nausea/vomiting
-nicknames “Milk of Amnesia”
Ketamine
-is NMDA receptor agonist and short-acting
-produces dissociative anesthesia (dissociation btw thalamus and limbic system)
-pt appears awake, but is unconscious and doesn’t feel pain
-is quick form of anesthesia good for short procedures
-is cardiovascular stimulant
-can cause postop disorientation and hallucinations
-often used in children and young adults
Chloral Hydrate
-CNS depressant used in children
-active metabolite is trichloroethanol
-has onset of 30 mins to 1 hr and lasts for 4-8 hours
-toxicity causes hypotension, resp. depression, hypothermia, cardiac arrhythmia, and coma
-contraindicated in hepatic and renal impaired pts
Opioids
-narcotics that act as agonists on mu, delta, kappa, and sigma receptors in CNS
-provide analgesia and euphoria
-available in oral and IV forms:
1) Fentanyl: IV, oral
2) Sufentanil: IV
3) Alfentanil: IV
4) Morphine: IV, oral
5) Codeine: oral
6) Meperidine (Demerol): IV, oral
-naloxone is mu-receptor agonist that reverses effect of opioids
Opioid Withdrawal
1) HTN 6) Restlessness
2) Piloerection, chills 7) Mydriasis
3) Sweating 8) Lacrimation and rhinorrhea
4) Nausea/vomiting 9) Insomnia
5) Abdominal cramping
-opioid withdrawal is not life-threatening like alcohol or benzo withdrawal is
Complications of Sedation
1) Malignant hyperthermia: prevents release of calcium from sarcoplasmic reticulum of skeletal muscle,
leading to persistent contraction
-rigidity, fever, tachycardia, hypoxia
-triggered by succinylcholine and Halothane
-treated w/ Dantrolene
2) Phlebitis: inflammation of superficial veins that can occur after insertion of IV
- pain, tenderness, induration, erythema
-treated w/ elevating limb, moist heat, NSAIDs
3) Laryngospasm: forceful, involuntary spasm of laryngeal muscles caused by oral fluids triggering
laryngeal reflex during lighter stages of anesthesia
-prevented by using pharyngeal barrier and tonsil suction
-treated w/ positive pressure oxygen-supplemented ventilation w/ facemask
-if still persists, use succinylcholine or last resort cricothyrotomy
-most common complication of office-based anesthesia is loss of airway
-most common dental emergency is syncope
Syncope
-transient loss of consciousness caused by transient cerebral hypoxia
-txt: 1) place pt in supine position w/ feet slightly elevated (Tendelenburg position)
2) Establish airway by chin left and administer 100% oxygen
3) Monitor vital signs
Vital Signs
1) Temperature: normal oral temp is 98.6 F or 37 C
2) Heart rate: normal range is 60-80 bpm
3) Blood pressure: normal is 120/80
4) Respiratory rate: normal range is 12-18 breaths/min
Shock
-syndrome in which there is inadequate cellular perfusion/oxygen for metabolic demands of tissues
-reduced cardiac output is main factor in all types of shock
-characterized by:
1) increased vascular resistance 4) myocardial ischemia
2) tachycardia (increased HR) 5) mental status change
3) adrenergic response (sweating)
Stages of Shock
1) Compensatory: compensatory mechanisms attempt to maintain perfusion to vital organs
-increased HR and peripheral resistance
2) Progressive: metabolic acidosis
3) Irreversible: organ damage occurs and survival not possible
Categories of Shock
1) Hypovolemic: produced by reduction in blood volume
-caused by hemorrhage, dehydration, vomiting, diarrhea, and fluid loss from burns
2) Cardiogenic: circulatory collapse from pump failure of left ventricle
-caused by massive myocardial infarction
3) Septic: due to severe infxn
-caused by gram- endotoxins
4) Neurogenic: results from severe injury/trauma to CNS
5) Anaphylactic: occurs w/ severe allergic rxn
Bleeding Times
1) Bleeding time: 1-9 minutes
2) Prothrombin time (PT): 11-16 seconds
3) Partial thromboplastin time (PTT): 32-46 seconds
-warfarin increases PT and PTT
Symptoms of Dehydration
1) Oliguria
2) Rise in body temp
3) Increase in HR and cardiac output
4) Decrease in blood pressure
5) Severe cell dysfxn
Breathing Terms
1) Apnea: transient cessation or absence of breathing
2) Hypercapnea: excess CO2 in arterial blood
3) Hypocapnea: below normal CO2 in arterial blood
4) Dyspnea: difficulty breathing
5) Respiratory arrest: permt cessation of breathing
5) Hyperapnea: abnormally deep and rapid breathing
6) Hyperventilation: increased pulmonary ventilation in excess of metabolic requirements
-results in loss of CO2 from blood
7) Hypoventilation: underventilation in relation to metabolic requirements
-results in increased levels of CO2 in blood
8) Atelectasis: occurs when mucus/foreign object obstructs airflow in bronchus, causing collapse of lung
tissue into airless state
-prolonged atelectasis leads to pneumonia
9) Pneumothorax: occurs when air leaks into pleural space causing lung to recoil from chest wall