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Oral & Maxillofacial Surgery Review: A Study Guide
Oral & Maxillofacial Surgery Review: A Study Guide
Oral & Maxillofacial Surgery Review: A Study Guide
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Oral & Maxillofacial Surgery Review: A Study Guide

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This comprehensive text, prepared by experts in their field, provides a quick and effective way for both residents and busy clinicians to review important information and published literature in dentoalveolar surgery and implantology, anesthesiology, medicine, pathology, orthognathic surgery, craniofacial and reconstructive surgery, cosmetic surgery, and TMJ disorders and facial pain, as well as to gain new knowledge in these areas. The content is organized in bullet-point format and complemented by numerous illustrations, tables, and algorithms, making the material easy to remember. This is an excellent resource for board preparation as well as recertification. 187 illus.
LanguageEnglish
Release dateMar 19, 2020
ISBN9780867157031
Oral & Maxillofacial Surgery Review: A Study Guide

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    Oral & Maxillofacial Surgery Review - Din Lam

    Chapter 1

    Medical Assessment

    Alia Koch and Steven M. Roser

    Cardiovascular Disease

    Respiratory Disease

    Renal Disease

    Acid-Base Disorders

    Gastrointestinal Disease

    Hematologic Disease

    Endocrine Disease

    Autoimmune Disease

    Neurologic Disorders

    Perioperative Management

    Cardiovascular Disease

    Acute Coronary Syndrome

    Major blood vessels supplying the heart are damaged/diseased by cholesterol plaques, which cause the vessels to narrow. In turn, less blood reaches the myocardium, leading to an acute coronary syndrome.

    •Symptoms: Dull substernal pain and pain radiating to left arm and jaw; associated with diaphoresis, dyspnea

    •Diagnosis: electrocardiogram (ECG), cardiac enzymes

    –ST segment elevation myocardial infarction (STEMI)

    ∘Treatment: Immediate reperfusion (angioplasty or thrombolytic therapy) within 12 hours of onset of chest pain

    –Non-ST segment elevation myocardial infarction (NSTEMI)

    ∘Treatment: Medical therapy (aspirin, beta blockade, angiotensin-converting enzyme [ACE] inhibitor)

    –Unstable angina

    ∘Treatment: Medical therapy (same as NSTEMI)

    Congestive Heart Failure

    •Systolic heart failure: Reduced ejection fraction (< 40%), S3 murmur, dilated left ventricle

    •Diastolic heart failure: Preserved ejection fraction (> 50%), S4 murmur, left ventricle hypertrophy

    •Symptoms: Chest pain, shortness of breath, orthopnea, extremity swelling, jugular vein distention

    •Diagnosis

    –Echocardiogram: Evaluate heart motion, ejection fraction

    –ECG: Evaluate changes in ECG, heart strain

    –Stress test: Evaluate coronary artery disease

    –Brain natriuretic peptide: Normal value rules out acute heart failure

    –Chest radiograph: Evaluate heart size, fluid in the intrathoracic cavity

    Classification of congestive heart failure (CHF)

    Valvular Disease

    Arrythmias

    CHADS2 scoring table

    Stroke risk assessment in atrial fibrillation to determine necessity of anticoagulation or antiplatelet treatment.

    Stroke risk assessment

    Heart block (Fig 1-1)

    Fig 1-1 Heart block ECG strips. (a) First degree. (b) Second degree, type 1. (c) Second degree, type 2. (d) Third degree. P waves indicated by a red vertical line. (Reprinted with permission from EKG-Uptodate 2013.)

    Hypertension

    •Primary hypertension: No identifiable cause

    •Secondary hypertension: Identifiable cause, some listed below

    –Renal artery stenosis

    –Diabetic nephropathy

    –Thyroid disease

    –Cocaine use

    –Pheochromocytoma

    –Obstructive sleep apnea

    •Diagnosis: At least two elevated BP readings on at least two different occasions

    –Prehypertension: Systolic blood pressure (SBP) from 120 to 130 mm Hg, diastolic blood pressure (DBP) from 80 to 89 mm Hg

    –Stage 1: SBP from 140 to 159 mm Hg, DBP from 90 to 99 mm Hg

    –Stage 2: SBP ≥ 160 mm Hg, DBP ≥ 100 mm Hg

    •Etiology: Obesity, familial, smoking, diabetes, kidney disease, Cushing syndrome, catecholamines, obstructive sleep apnea

    •Treatment: Diet, weight reduction, aerobic activity, sodium restriction, medications

    Medications

    Hypertensive emergencies

    Infective Endocarditis (IE)

    Duke criteria for diagnosis

    •Definite IE: 2 major; 1 major and 3 minor; 5 minor

    •Possible IE: 1 major and 1 minor; 3 minor

    Treatment

    •Native valve endocarditis: Vancomycin and gentamicin

    •Prosthetic valve endocarditis: Vancomycin, rifampin, and gentamicin

    •Culture positive: Treat organism

    Surgical Management of Patients on Cardiovascular Medications

    Preoperative treatment decision algorithm

    1. Urgent surgery, nonurgent surgery with unstable/active cardiac condition

    •Medical consult/discussion with surgeon

    2. Nonurgent surgery

    •Surgical procedure risk ( Box 1-1 )

    –Low risk: Medical consult preoperatively

    –Moderate/high risk: Go to step 3

    3. Evaluate patient’s functional capacity ( Box 1-2 )

    •> 4 METs: Statin therapy and beta blocker preoperatively

    •≤ 4 METs: Go to step 4

    4. Evaluate risk of surgical procedure (see Box 1-1 )

    •Moderate risk: Statin, beta blocker, ECG, possible ACE inhibitor

    •High risk: Go to step 5

    5. Evaluate cardiac risk factors ( Box 1-3 )

    •≤ 2: Preoperative statin, beta blocker, possible ACE inhibitor

    •> 2: Noninvasive testing, discuss anesthesia technique, consider changing surgical management

    MET, metabolic equivalent of task.

    Respiratory Disease

    Normal Lung Volumes (Figs 1-2 and 1-3)

    Fig 1-2 Lung volumes and capacities. IRV, inspirational reserve capacity; TV, tidal volume; ERV, expiratory reserve volume; RV, residual volume; IC, inspirational capacity; FRC, functional residual capacity; TLC, total lung capacity; VC, vital capacity.

    Fig 1-3 Flow volume curves. (Reprinted with permission from Levitzky MG. Pulmonary Physiology, 7 ed. New York: McGraw-Hill, 2007.)

    Common abbreviations

    •Residual volume (RV): Air left after maximal expiration

    •Tidal volume (TV): Entering air during normal inspiration

    •Expiratory reserve volume (ERV): Air that can still be expired after normal expiration

    •Functional residual capacity (FRC): RV + ERV

    Abbreviations associated with pulmonary function tests (PFTs)

    •Forced expiratory volume in 1 second (FEV1): Air that can be expired in 1 second

    •Forced vital capacity (FVC): Maximum volume of air that can be forcefully exhaled

    •Total lung capacity (TLC): FVC + RV

    Common types of pulmonary disease

    Obstructive versus restrictive lung disease

    Chronic Respiratory Diseases

    Asthma

    •Definition: Chronic obstructive reversible disorder of airway hyper-reactivity causing dyspnea, cough, wheezing, and chest tightness

    •Diagnosis: Diagnosed by showing reversible obstructive lung disease with normal diffusing capacity

    •Exam will show expiratory wheezing during acute exacerbations, with a prolonged expiratory phase

    •Severe attacks will have pulsus paradoxus, accessory muscle use, and silent chest

    Medications for treatment of asthma

    Chronic Obstructive Pulmonary Disease (COPD)

    •Definition: Nonreversible chronic airway restriction

    •Symptoms: Worsening dyspnea, increasing cough and change in sputum, hyperinflation, prolonged expiration, wheezing

    •Chronic bronchitis: Chronic productive cough for 3 months in 2 consecutive years; blue bloater

    •Emphysema: Enlargement of airways and wall destruction distal to bronchioles; pink puffer; pursed-lip breathing

    •Diagnosis:

    –PFTs to evaluate FEV1, FEV1/FVC, and postbronchodilator values

    –Arterial blood gas (ABG) analysis will show hypercarbia, hypoxemia

    –Evaluate for alpha 1 antitrypsin deficiency in emphysema patients

    –Chest radiograph

    Classification of COPD

    Acute Pulmonary Diseases

    Acute respiratory distress syndrome (ARDS)

    •Definition: Acute, hypoxemic respiratory failure associated with bilateral lung infiltrates

    •Etiology: Pneumonia, aspiration, trauma, acute pancreatitis, inhalational injury, reperfusion injury

    •Symptoms: Rapid onset of dyspnea, tachypnea, diffuse lung crackles

    •Diagnosis: Bilateral infiltrates on chest radiograph, ratio of PaO 2 to FiO 2 < 200

    •Treatment

    –Treat underlying cause

    –Use mechanical ventilation with low tidal volumes of 6 cc/kg

    –Positive end-expiratory pressure (PEEP)

    –Conservative fluid management

    Pulmonary embolus (PE)

    •Risk factors: Prior PE, pregnancy, malignancy, obesity, immobility, stroke, tobacco use, recent surgery, trauma

    •Symptoms: Dyspnea, hemoptysis, fever, cough, tachypnea, tachycardia

    •Diagnosis

    –Modified Wells criteria (see table below)

    –D-dimer test: Only helpful to exclude PE in low-risk patients (Wells score ≤ 4)

    –Computed tomography angiography (CTA): Multidetector-row CTA (MDCTA) is standard pulmonary angiography when CTA is not available

    –ECG: New right heart strain; nonspecific anterior T wave inversions; sinus tachycardia; large S wave in lead I, a large Q wave in lead III, and an inverted T wave in lead III (S1Q3T3)

    –ABG analysis: Respiratory alkalosis with increased alveolar arterial gradient

    –V/Q scan: Ventilation without perfusion suggests PE

    •Treatment

    –Heparin as bridge to coumadin to maintain INR of 2 to 3 for at least 3 to 6 months

    –Inferior vena cava filter if anticoagulation is contraindicated

    –Direct thrombin inhibitors for patients with heparin-induced thrombocytopenia (HIT)

    –Thrombolysis for massive PE

    –Thrombectomy

    Modified Wells criteria

    To determine likelihood of PE.

    •≤ 4 = Unlikely PE

    •> 4 = Likely PE

    Contraindications to anticoagulation

    Renal Disease

    Acute Renal Failure

    •Increase in serum creatinine ≥ 0.3 mg/dL over baseline

    •Urine output less than 0.5 cc/kg/hour for more than 6 to 12 hours

    Prerenal

    •Etiology: Volume depletion, severe liver disease, severe CHF

    •Diagnosis: Fractional excretion of sodium (FENa) < 1%; ratio of blood urea nitrogen (BUN) to creatinine, 10–15:1; high urinary osmolarity

    •Treatment: Fluids (rapid improvement with fluids)

    Renal

    •Etiology: Tubular injury, acute tubular necrosis, interstitial disease, glomerular disorder

    •Diagnosis: FENa >1%; BUN-to-creatinine ratio, 10–15:1; muddy brown casts

    •Treatment: Remove underlying agent, treat underlying cause

    Postrenal

    •Etiology: Urinary tract obstruction

    •Diagnosis: FENa < 1%, oliguria/anuria

    •Treatment: Remove obstruction

    Need for emergent dialysis

    Chronic Renal Failure (CRF)

    •Permanent loss of renal function for at least 3 months

    •Etiology: Hypertension, diabetes, renal artery stenosis, polycystic kidney disease

    •Diagnosis: Glomerular filtration rate (GFR) < 15 mL/minute, albuminuria > 30 mg/day

    •Treatment: Management of hypertension with ACE inhibitors and angiotensin receptor blockers, low density lipoproteins < 100 mg/dL

    •Predictor of disease progression: Proteinuria

    Severity of chronic renal disease based on GFR

    Severity of chronic renal disease based on albuminuria

    Complications of CRF

    Urinalysis interpretation

    Nephrotic Disease

    •Symptoms: Peripheral edema, hypoalbuminemia, hyperlipidemia, increased proteinuria

    •Diagnosis: Urinalysis shows oval fat bodies, proteinuria, and 24-hour urine protein > 3.5 g/day

    Primary nephrotic syndrome

    Direct damage to glomeruli causing massive proteinuria.

    Secondary nephrotic syndrome

    Damage of glomeruli secondary to systemic disease.

    Nephritic Disease

    Inflammatory disorder in the glomeruli.

    •Glomerulonephritis: RBCs in urine with or without cellular casts and varying degrees of proteinuria

    •Symptoms: Hypertension, edema, oliguria, hematuria

    •Diagnosis: Red blood cell (RBC) casts in urine, renal biopsy

    •Types of glomerulonephritis

    –Immune complex: Decreased complement levels

    –Pauci immune: Normal complement levels

    Immune complex glomerulonephritis

    Pauci immune glomerulonephritis

    Nephrotic Versus Nephritic Disease

    Acid-Base Disorders

    Arterial Blood Gas (ABG) Versus Venous Blood Gas (VBG)

    •ABG: The gold standard to evaluate acid-base disorders

    –Invasive procedure

    –Serial examinations necessary

    –Risk of hematoma and nerve injury

    •VBG

    –Easier to obtain and less injury to patients

    –Data (pH, bicarbonate [HCO 3 ], lactate, and base excess) are similar to those found in ABG

    –Partial pressure of carbon dioxide (PaCO 2 ) is also well correlated except in patients with severe shock or when PaCO 2 > 45 mm Hg

    Quick Guide to ABG Interpretation

    Step one: Identify primary disorder

    •Evaluate pH and PaCO 2 :

    –If change in same direction → metabolic disorder

    –If change in different direction → respiratory disorder

    Step two: Check for compensation if disorder has a primary origin

    •Metabolic disorder: Calculate the expected PaCO 2

    •Respiratory disorder: Calculate the expected pH

    •If the actual value is different from the calculated value (pH or PaCO 2 ), expect an additional acid-base disorder

    Step three: Calculate the anion gap if metabolic acidosis or mixed disorder is detected

    •Anion gap (AG): Na – (Cl + HCO 3 ) ≤ 12

    •If AG < 12, acidosis is due to loss of bicarbonate (ie, diarrhea)

    •If AG > 12, acidosis is due to increase of nonvolatile acids (ie, lactic acidosis)

    •AG can be influenced by an abnormal albumin level

    Acid-Base Disorders

    Sodium Disorders

    •Normal sodium concentration in the body is 135 to 145 mEq/L

    •To determine the cause of sodium disorder, measure

    –Plasma osmolality (290 mOsm/kg H 2 O)

    ∘(2 × Plasma Na+) + Glucose/18

    –Extracellular volume

    ∘Clinical examination (eg, peripheral edema, orthostatic hypotension, and skin turgor)

    ∘Not the most reliable method but is readily available

    ∘Invasive monitoring (cardiac filling pressures and cardiac output)

    Potassium Disorders

    •Normal potassium level is between 3.5 mEq/L and 5 mEq/L

    •Work-up should include:

    –Urine potassium and chloride level

    –Serum magnesium level

    –ABG as needed

    Gastrointestinal Disease

    Irritable Bowel Syndrome

    Hepatitis

    Hepatitis B serology

    Gastroesophageal Reflux Disease

    •Etiology: Lower esophageal sphincter relaxation

    •Symptoms: Retrosternal burning, regurgitation, excessive salivation, bitter test, throat fullness, halitosis

    •Diagnosis: Treat empirically; if no success, upper endoscopy with biopsy, esophageal pH monitoring

    •Treatment: Elevate head of bed, stop tobacco and alcohol use, dietary modification, antacids, histamine blockers, proton pump inhibitors

    •Complications: Barrett esophagus, adenocarcinoma, upper gastrointestinal bleeding, cough, asthma

    End Stage Liver Disease (ESLD)

    •Etiology: Chronic hepatocellular injury leads to fibrosis of liver

    •Symptoms: Fatigue, anorexia, impotence, melena, spider nevi, gynecomastia, jaundice, testicular atrophy, coarse hand tremor, caput medusae, spider telangiectasia, Dupuytren contractures

    •Diagnosis: Liver function tests, liver biopsy; monitor disease with Child-Turcotte-Pugh score or model for end stage liver disease (MELD) score

    •Treatment: Avoid alcohol and medications metabolized by the liver, treat underlying disease process, screen for hepatocellular carcinoma, monitor for complications

    •Complications: Esophageal varices, ascites, increase in bleeding risk, portal hypertension, hepatic encephalopathy

    Child-Turcotte-Pugh score

    •5 to 6 points: Class A, 90% 3-year survival rate

    •7 to 9 points: Class B, 50% to 60% 3-year survival rate

    •> 9 points: Class C, 30% 3-year survival rate

    Hematologic Disease

    Anemia

    Hypoproliferative (low reticular cell count)

    Hyperproliferative (high reticular cell count)

    Sickle Cell Disease

    Homozygous defect in gene for beta-globulin that produces hemoglobin S.

    •Triggers: Dehydration, acidosis, hypoxia

    •Diagnosis: Target cells, sickle cells, Howell Jolly bodies, hemoglobin S on smear

    •Symptoms: Acute chest pain, stroke, autosplenectomy

    •Treatment: Folate, hydroxyurea, aggressive hydration, analgesia, oxygen, transfuse for major surgery (9 to 10 g hemoglobin)

    Bleeding Disorders

    Disseminated Intravascular Coagulation (DIC)

    Consumptive coagulopathy associated with serious illness.

    •Symptoms: Thrombocytopenia, excessive bleeding or clotting

    •Diagnosis: Decreased fibrinogen, platelets; increased prothrombin time (PT)/ partial thromboplastin time (PTT), d-dimer test; schistocytes present

    •Treatment: Treat underlying cause; platelets and cryoprecipitate for bleeding, low-dose heparin for clotting

    Hypercoagulable State

    •Risk factors: Prior embolus, pregnancy, surgery, tobacco use, prolonged immobilization, hospitalization, malignancy

    •Diagnosis: History and physical examination, complete blood count, PTT

    •Treatment: Postoperative patients should be treated for 3 months at an INR of 2 to 3, all others for 3 to 6 months

    •Exceptions

    –Active cancer: Treat for duration of disease

    –Mechanical heart valves: INR goal is 3 to 4

    Specific thrombophilic disorders

    Anticoagulation medications

    Endocrine Disease

    Diabetes Mellitus (DM)

    Diagnosis

    •Random glucose > 200 mg/dL

    •Fasting glucose > 126 mg/dL

    •Two-hour glucose > 200 mg/dL (75 gm)

    •Hemoglobin A1c (HbA1c) > 6.5

    Insulin types

    Oral hypoglycemics

    Goals of treatment

    •BP < 130/85 mm Hg

    •Low-density lipoprotein < 100 mg/dL, total glycerides < 150 mg/dL, high-density lipoprotein > 40 mg/dL

    •Smoking cessation

    •Glycemic control for HbA1c < 7

    Monitoring glycemic control in DM

    •HbA1c >10 is poor control

    •HbA1c between 8.5 and 10 is fair control

    •HbA1c between 7 and 8.5 is good control

    •Fasting glucose < 130 mg/dL

    •Peak postprandial glucose < 180 mg/dL

    Diabetic Ketoacidosis

    An insulin deficiency and glucagon excess that causes severe hyperglycemia and ketogenesis. Severe hyperglycemia causes an osmotic diuresis leading to dehydration and volume depletion.

    •Symptoms: Abdominal pain, nausea, vomiting, Kussmaul respirations, ketone breath, anion gap metabolic acidosis, marked dehydration, tachycardia, polydipsia, polyuria, weakness, altered consciousness

    •Diagnosis: Serum glucose > 250 mg/dL, metabolic acidosis (pH > 7.3 and serum bicarbonate < 15 mEq/L), increased anion gap, ketonuria, ketonemia; check chemistry panel for hyperkalemia and hyponatremia

    •Treatment:

    –IV insulin dose at 0.1 units/kg, then start drip at 0.1 units/kg/hour (check potassium prior to starting insulin); drip should run with normal saline replacement

    –Once anion gap has closed and acidosis is resolved, start to decrease the insulin and switch to subcutaneous insulin

    –Add dextrose to IV fluids when glucose is below 250 mg/dL

    –Manage sodium, potassium, and magnesium levels very closely

    Thyroid Disorders

    Adrenal Disorders (Fig 1-4)

    Fig 1-4 Diagnostic algorithm for adrenal disorders. Na, sodium; K, potassium; Ca, calcium; AM, morning; ACTH, adrenocorticotropic hormone.

    Complications: Adrenal crisis—shock, nausea, vomiting, confusion, fever; can be fatal

    Addison disease (primary adrenal insufficiency)

    •Etiology: Autoimmune adrenalitis, malignancy, infection

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