Oral & Maxillofacial Surgery Review: A Study Guide
By Din Lam and Daniel Laskin
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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