Oral and Maxillofacial Surgery Review: A Study Guide
Library of Congress Cataloging-in-Publication Data
Oral and maxillofacial surgery review : a study guide / edited by Din
Lam, Daniel Laskin.
p. ; cm.
ISBN 978-0-86715-674-4 (softcover)
I. Lam, Din, editor. II. Laskin, Daniel M., 1924- , editor.
[DNLM: 1. Oral Surgical Procedures--methods. WU 600]
RK529
617.5’22--dc23
2015002883
© 2015 Quintessence Publishing Co, Inc
Quintessence Publishing Co Inc
4350 Chandler Drive
Hanover Park, IL 60133
www.quintpub.com
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All rights reserved. This book or any part thereof may not be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, or otherwise, without prior written permission of the publisher.
Editor: Bryn Grisham
Design and production: Kaye Clemens
Cover design: Ted Pereda
Printed in the USA
Preface
Contributors
1 Medical Assessment
Alia Koch and Steven M. Roser
2 Anesthesia
Jason Jamali and Stuart Lieblich
3 Dentoalveolar Surgery
Esther S. Oh and George Blakey
4 Dental Implantology
Christopher Choi and Daniel Spagnoli
5 Orthognathic Surgery
David Alfi and Jaime Gateno
6 Trauma
Daniel E. Perez and Edward Ellis III
7 PathologyDin Lam and Eric R. Carlson
8 Maxillofacial Reconstruction
Din Lam and Andrew Salama
9 Orofacial Pain
David W. Lui and Daniel M. Laskin
10 The TMJ
David W. Lui and Daniel M. Laskin
11 Craniofacial Surgery
Jennifer Woerner and Ghali E. Ghali
12 Cosmetic Surgery
David E. Webb and Peter D. Waite
Index
When faced with a board or recertification examination, or just wanting to update your knowledge in oral and maxillofacial surgery, there is always the dilemma of where to begin and what and how much to study. This review book is designed to help you with this process. The format involves a detailed outline of the important items of didactic and clinical information in the 12 major areas of oral and maxillofacial surgery combined with numerous tables, summary charts, and useful mnemonics and surgical tips. Each chapter is also supplemented with many clinical photographs, diagrams, and photomicrographs, where appropriate.
The various chapters were each developed by two authors: (1) a young oral and maxillofacial surgeon who was board certified in recent years and is therefore very familiar with the process and the content, and (2) a more senior surgeon who has been a board examiner and/or involved in the recertification process and is therefore knowledgeable and experienced in the essential clinical aspects of the specialty.
To use this book as a review or study guide, it is suggested that you first read each chapter to determine what information is already familiar to you, what is new and needs to be learned, and what are the areas in which you desire more information from other sources such as the list of recommended reading at the end of each chapter. The last material should then be annotated where indicated in the various chapters. The book now becomes your study manual as well as a quick and easy way to review the material again just prior to the examination and a handy reference source during clinical practice.
We would like to express our deep appreciation and thanks to all of the contributing authors who gave so freely of their time and knowledge and who helped make this book a reality. Finally, we would like to thank Lisa Bywaters and Bryn Grisham of Quintessence Publishing for their expertise and guidance during the editorial process. Their concern for the success of this book was no less than ours.
David Alfi, DDS, MD
Attending Oral and Maxillofacial Surgeon
Department of Oral and Maxillofacial Surgery
Houston Methodist Hospital
Houston, Texas
Assistant Professor of Clinical Surgery
Weill Cornell Medical College
Cornell University
New York, New York
George Blakey, DDS
Director of Oral and Maxillofacial Surgery Residency Program
Distinguished Associate Professor
Department of Oral and Maxillofacial Surgery
School of Dentistry
University of North Carolina
Chapel Hill, North Carolina
Eric R. Carlson, DMD, MD
Professor and Kelly L. Krahwinkel Chair
Department of Oral and Maxillofacial Surgery
Director of Oral and Maxillofacial Surgery Residency Program
University of Tennessee Graduate School of Medicine
Director of Oral/Head and Neck Oncologic Surgery Fellowship Program
Cancer Institute
University of Tennessee Medical Center
Knoxville, Tennessee
Christopher Choi, DDS, MD
Private Practice Limited to Oral and Maxillofacial Surgery
Rancho Cucamonga, California
Assistant Professor
Department of Oral and Maxillofacial Surgery
School of Dentistry
Loma Linda University
Loma Linda, California
Edward Ellis III, DDS, MS
Professor and Chair
Department of Oral and Maxillofacial Surgery
School of Dentistry
University of Texas Health Science Center at San Antonio
San Antonio, Texas
Jaime Gateno, DMD, MD
Chair, Department of Oral and Maxillofacial Surgery
Houston Methodist Hospital
Houston, Texas
Professor of Clinical Surgery
Weill Cornell Medical College
Cornell University
New York, New York
Ghali E. Ghali, DDS, MD
Professor and Chairman
The Jack W. Gamble Chair
Department of Oral and Maxillofacial Surgery
Louisiana State University Health Sciences Center—Shreveport
Shreveport, Louisiana
Jason Jamali, DDS, MD
Clinical Assistant Professor
Department of Oral and Maxillofacial Surgery
College of Dentistry
University of Illinois at Chicago
Chicago, Illinois
Alia Koch, DDS, MD
Assistant Professor
Department of Oral and Maxillofacial Surgery
College of Dental Medicine
Columbia University
New York, New York
Attending Oral and Maxillofacial Surgeon
New York Presbyterian Hospital
Columbia University Medical Center
New York, New York
Din Lam, DMD, MD
Adjunct Assistant Professor
Department of Oral and Maxillofacial Surgery
School of Dentistry
Virginia Commonwealth University
Richmond, Virginia
Daniel M. Laskin, DDS, MS
Professor and Chairman Emeritus
Department of Oral and Maxillofacial Surgery
School of Dentistry
Virginia Commonwealth University
Richmond, Virginia
Stuart Lieblich, DMD
Clinical Professor
Department of Oral and Maxillofacial Surgery
School of Dental Medicine
University of Connecticut
Farmington, Connecticut
Private Practice Limited to Oral and Maxillofacial Surgery
Avon, Connecticut
David W. Lui, DMD, MD
Assistant Professor
Department of Oral and Maxillofacial Surgery
School of Dentistry
Virginia Commonwealth University
Richmond, Virginia
Esther S. Oh, DDS, MD
Clinical Assistant Professor
Department of Oral and Maxillofacial Surgery
College of Dentistry
University of Florida
Gainesville, Florida
Daniel E. Perez, DDS
Associate Professor
Department of Oral and Maxillofacial Surgery
School of Dentistry
University of Texas Health Science Center at San Antonio
San Antonio, Texas
Steven M. Roser, DMD, MD
DeLos Hill Professor and Chief
Division of Oral and Maxillofacial Surgery
Department of Surgery
Emory University School of Medicine
Atlanta, Georgia
Andrew Salama, DMD, MD
Assistant Professor, Department of Oral and Maxillofacial Surgery
Director, Advanced Specialty Education Program in Oral and Maxillofacial Surgery
Henry M. Goldman School of Dental Medicine
Boston University
Boston, Massachusetts
Daniel Spagnoli, DDS, MS, PhD
Associate Professor and Chairman
Department of Oral and Maxillofacial Surgery
School of Dentistry
Louisiana State University Health Sciences Center—New Orleans
New Orleans, Louisiana
Peter D. Waite, DDS, MD, MPH
Professor and Chairman
Department of Oral and Maxillofacial Surgery
School of Dentistry
University of Alabama at Birmingham
Birmingham, Alabama
David E. Webb, Maj. USAF, DC
Attending Oral and Maxillofacial/Head and Neck Surgeon
Department of Oral and Maxillofacial Surgery
David Grant USAF Medical Center
Travis AFB, California
Jennifer Woerner, DMD, MD
Assistant Professor and Fellowship Director
Craniofacial and Cleft Surgery
Department of Oral and Maxillofacial Surgery
Louisiana State University Health Sciences Center—Shreveport
Shreveport, Louisiana
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)
• 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
Stage |
Definition |
Treatment |
A |
Risk of HF due to comorbidities only |
Treat underlying condition |
B |
No symptoms but structural abnormality predisposes patient to HF |
ACE inhibitor, beta blocker |
C |
Structural disease with HF symptoms |
ACE inhibitor, beta blocker, diuretic, salt restriction |
D |
HF symptoms at rest |
Medical therapy with mechanical support |
HF, heart failure. |
Stroke risk assessment in atrial fibrillation to determine necessity of anticoagulation or antiplatelet treatment.
Condition |
Points |
|
C |
Congestive heart failure |
1 |
H |
Hypertension: Blood pressure consistently above 140/90 mm Hg (or treated hypertension with medication) |
1 |
A |
Age ≥ 75 years |
1 |
D |
Diabetes mellitus |
1 |
S2 |
Prior stroke or transient ischemic attack (TIA) or thromboembolism |
2 |
Score |
Risk |
Treatment |
0 |
Low |
Aspirin or none |
1 |
Moderate |
Aspirin or coumadin to INR of 2-3 |
2 or more |
Moderate/high |
Coumadin to INR of 2 to 3 |
INR, international normalized ratio. |
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.)
ECG finding |
Treatment |
|
Type 1 |
Increased PR Interval |
None |
Type 2A |
Increasing PR interval until dropped QRS |
Pacemaker for symptomatic patients only |
Type 2B |
Regularly dropped QRS with constant PR interval |
Search for cause/pacemaker |
Type 3 |
Complete dissociation of P waves and QRS complexes |
Search for cause/pacemaker |
• 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
Type |
Cause |
IV drug use |
Staphylococcus aureus |
Native valve |
Viridans streptococci, S aureus, enterococci |
Prosthetic valve |
Staphylococcus epidermidis, S aureus |
Culture negative |
HACEK organism (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella corrodens, Kingella), Candida, Aspergillus |
IV, intravenous. |
• Definite IE: 2 major; 1 major and 3 minor; 5 minor
• Possible IE: 1 major and 1 minor; 3 minor
Major criteria |
Minor criteria |
• Positive blood culture • Echocardiogram with evidence of endocardial involvement |
• Predisposition to IE (IV drug use, indwelling catheter, diabetes) • Fever • Vascular phenomena (Janeway lesions, arterial emboli, intracranial hemorrhage, splinter hemorrhage) • Microbiologic evidence • Immunologic phenomena (Osler nodes, Roth spots) |
IV, intravenous. |
• Native valve endocarditis: Vancomycin and gentamicin
• Prosthetic valve endocarditis: Vancomycin, rifampin, and gentamicin
• Culture positive: Treat organism
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.
Box 1-1 Risk of surgical procedures |
||
Low risk |
Intermediate risk |
High risk |
Dental Eye Gynecologic Breast Minor genitourinary |
Head and neck Transplant Major genitourinary Intraperitoneal Intrathoracic |
Open heart Vascular |
Box 1-2 Assessment of functional capacity |
Metabolic equivalents of task (METs) are a physiologic measurement that expresses the energy associated with physical activities. 1 MET • Can you take care of yourself? • Can you walk indoors? • Can you feed yourself? • Can you dress yourself? • Can you walk 1 to 2 blocks? 4 METs • Can you climb a flight of stairs? • Can you do heavy housework? • Can you participate in moderate recreational activities? > 10 METs • Can you participate in strenuous sports? |
Box 1-3 Cardiac risk factors |
• History of angina • History of myocardial infarction • History of heart failure • History of stroke • Diabetes mellitus • Renal failure |
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.)
• 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
• 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
Obstructive |
Restrictive |
Extraparenchymal restrictive |
• Asthma • Cystic fibrosis • Chronic obstructive pulmonary disease (COPD) |
• Sarcoidosis • Interstitial lung disease • Collagen disorder |
• Obesity • Scoliosis • Myasthenia gravis • Diaphragmatic weakness • Cervical spine injury |
Obstructive |
Restrictive |
|
FEV1 |
Decreased |
Decreased |
FVC |
Normal |
Decreased |
FEV1/FVC |
Decreased |
Normal/increased |
Lung volume |
Increased |
Decreased |
Flow rates |
Decreased |
Decreased |
• 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
Definition |
Treatment |
|
Mild intermittent |
< 2 days/week with PEF > 80% |
Bronchodilator as needed |
Mild persistent |
> 2 days/week but < 1 time/day with PEF > 80% |
Low-dose inhaled steroids |
Moderate persistent |
Daily symptoms with PEF between 60% and 80% |
Inhaled steroids and long-acting beta 2 agonist |
Severe persistent |
Continuous symptoms with PEF < 60% |
Add oral steroids |
PEF, peak expiratory flow. |
Mechanism of action |
Example |
|
Beta 2 agonist |
Beta 2 agonism causes an increase in cAMP formation leading to relaxation of bronchial muscle |
Albuterol, salmeterol |
Corticosteroids |
Suppresses inflammatory response and decreases mucosal edema |
Fluticasone, hydrocortisone, prednisolone |
Leukotriene modifier |
Leukotriene receptor antagonist decreases bronchoconstriction |
Montelukast |
5-Lipoxygenase |
Inhibits leukotriene formation |
Zileuton |
Anticholinergic |
Blocks cholinergic constriction causing bronchodilation |
Ipratropium bromide |
cAMP, cyclic adenosine monophosphate. |
• 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
Stage |
FEV1 |
Treatment |
1 |
> 80 |
Short-acting bronchodilator (albuterol) |
2 |
50–79 |
Long-acting B2 agonist (salmeterol) and anticholinergic bronchodilator (ipratropium) |
3 |
30–49 |
Inhaled steroid |
4 |
< 30 |
Oxygen, pulmonary rehabilitation, consider transplant in worst cases |
• 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 PaO2 to FiO2 < 200
• Treatment
– Treat underlying cause
– Use mechanical ventilation with low tidal volumes of 6 cc/kg
– Positive end-expiratory pressure (PEEP)
– Conservative fluid management
• 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
To determine likelihood of PE.
• ≤ 4 = Unlikely PE
• > 4 = Likely PE
Criteria |
Points |
Clinical signs and symptoms of DVT |
3 |
PE is primary diagnosis |
3 |
Heart rate > 100 bpm |
1.5 |
Immobilized for at least 3 days or surgery in previous 4 weeks |
1.5 |
Previous objectively diagnosed PE or DVT |
1.5 |
Malignancy with treatment within 6 months or palliation |
1 |
Hemoptysis |
1 |
DVT, deep vein thrombosis. |
Relative |
Absolute |
• Thrombocytopenia • Prior hemorrhagic stroke • Recent internal bleeding |
• Active internal bleeding • Aortic dissection • Active hemorrhagic stroke |
• 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
• 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)
• 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
• Etiology: Urinary tract obstruction
• Diagnosis: FENa < 1%, oliguria/anuria
• Treatment: Remove obstruction
A |
Acidosis |
E |
Electrolyte abnormality |
I |
Ingestion |
O |
Overload |
U |
Uremia |
• 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
GFR stage |
GFR (mL/min/1.73 m2) |
Kidney function |
G1 |
> 90 |
Normal |
G2 |
60–89 |
Mildly decreased |
G3a |
45–59 |
Mild to moderately decreased |
G3b |
30–44 |
Moderately to severely decreased |
G4 |
15–29 |
Severely decreased |
G5 |
< 15 |
Kidney failure |
G5D |
< 15 |
Kidney failure treated with dialysis |
Albuminuria stage |
Albumin excretion rate (mg/day) |
Albumin excretion |
A1 |
< 30 |
Normal to increased |
A2 |
30–300 |
Moderately increased |
A3 |
> 300 |
Severely increased |
Treatment |
|
Anemia |
Erythropoietin injections, iron |
Renal osteodystrophy |
Phosphate binder |
Hyperkalemia |
Dietary restriction, diuretic |
Acidosis |
Sodium bicarbonate |
Pericarditis |
Dialysis |
Dialysis infections |
Antibiotics, catheter removal |
• Symptoms: Peripheral edema, hypoalbuminemia, hyperlipidemia, increased proteinuria
• Diagnosis: Urinalysis shows oval fat bodies, proteinuria, and 24-hour urine protein > 3.5 g/day
Direct damage to glomeruli causing massive proteinuria.
Primary disease |
Pathology |
Treatment |
Membranous nephropathy |
Thickening of capillary loops with subepithelial deposits |
ACE inhibitor, steroid |
Focal segmental glomerulosclerosis |
Glomerulosclerosis |
Steroids, cyclosporine |
Goodpasture syndrome |
Linear IgG deposition along glomerular basement membrane |
Steroids, cyclophosphamide, plasmapheresis |
Minimal change disease |
Epithelial foot process loss |
Steroids |
IgG, immunoglobulin G. |
Damage of glomeruli secondary to systemic disease.
Pathology |
Treatment |
|
Diabetes mellitus |
Kimmelstiel-Wilson lesion |
Glucose, lipid, blood pressure control, ACE inhibitor, angiotensin receptor blocker |
Multiple myeloma |
Light chain involvement with positive Congo red stain |
Treatment of systemic disease |
Amyloidosis |
Amyloid deposition with positive Congo red stain |
Treatment of systemic 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
Pathology |
Treatment |
|
Subacute bacterial endocarditis |
Crescent glomerulonephritis |
Antibiotics |
Post-streptococcal |
Subepithelial humps |
Resolves after treatment of streptococcal infection |
Membranoproliferative glomerulonephritis |
Subendothelial deposits |
Treat cryoglobulinemia |
Pathology |
Treatment |
|
IgA nephropathy |
IgA deposits in mesangium |
ACE inhibitor/angiotensin receptor blocker, steroids |
Wegener granulomatosis |
Necrotizing crescent disease |
Steroids, cyclophosphamide |
Churg-Strauss syndrome |
Necrotizing crescent disease |
Steroids, cyclophosphamide |
IgA, immunoglobulin A. |
Nephrotic |
Nephritic |
|
Protein |
Very large amount |
Small amount |
Urinalysis |
No casts but will find lipid-laden macrophages and free lipid |
Abundant RBCs and RBC casts; no lipids seen |
BP |
Mildly elevated or normal |
Severely elevated |
GFR |
Normal |
Elevated |
BP, blood pressure. |
• 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 [HCO3], lactate, and base excess) are similar to those found in ABG
– Partial pressure of carbon dioxide (PaCO2) is also well correlated except in patients with severe shock or when PaCO2 > 45 mm Hg
• Evaluate pH and PaCO2:
– If change in same direction → metabolic disorder
– If change in different direction → respiratory disorder
Primary disorder |
Primary change |
Compensatory change |
Metabolic acidosis |
Decreased HCO3 |
Decreased PaCO2 |
Metabolic alkalosis |
Increased HCO3 |
Increased PaCO2 |
Respiratory acidosis |
Increased PaCO2 |
Increased HCO3 |
Respiratory alkalosis |
Decreased PaCO2 |
Decreased HCO3 |
• Metabolic disorder: Calculate the expected PaCO2
• Respiratory disorder: Calculate the expected pH
• If the actual value is different from the calculated value (pH or PaCO2), expect an additional acid-base disorder
• Anion gap (AG): Na – (Cl + HCO3) ≤ 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
Metabolic acidosis |
Decreased blood pH with decreased bicarbonate Etiology: Two types • AG > 12: “MUDPILES” – Methanol ingestion – Uremia – Diabetic ketoacidosis – Paraldehyde Ingestion – Isoniazid ingestion – Lactic acidosis – Ethylene glycol ingestion – Salicylate ingestion • Non-AG – Gastrointestinal losses: Diarrhea, small bowel fistula, pancreatic fistula – Renal loss: Renal tubular acidosis Signs/Symptoms • Hyperventilation (compensatory mechanism) • Decreased tissue perfusion • Decreased cardiac output • Altered mental status • Arrhythmias • Hyperkalemia Treatment • Treat underlying cause – Most of the time acidosis is not harmful – Cause of death in these patients due to underlying condition rather than acidemia • Sodium bicarbonate – Has shown to be ineffective therapy in management of acidosis – Only use in patients who are deteriorating rapidly |
Metabolic alkalosis |
Increased blood pH with increased bicarbonate Etiology • Extracellular fluid expansion – Adrenal disorders causing increased mineralocorticoid secretion; increased reabsorption of bicarbonate and sodium and secretion of chloride • Extracellular fluid contraction – Vomiting, nasogastric suction causing hydrochloric acid and bicarbonate loss – Excessive use of diuretics Signs/Symptoms • Hypokalemia • Elevated bicarbonate • Elevated pH • Hypoventilation • Arrhythmias • Decrease in cerebral blood flow Treatment • Treat underlying cause • Volume-depleted patient requires normal saline with potassium replacement • In the volume-overloaded patient, consider spironolactone |
Respiratory acidosis |
Alveolar hypoventilation: Decreased blood pH with arterial PaCO2 > 40 • Acute: No renal compensation • Chronic: Renal compensation with increase in plasma bicarbonate Etiology • Chronic obstructive pulmonary disease • Brainstem injury • Respiratory muscle fatigue • Drug overdose causing hypoventilation Signs/Symptoms • Confusion • Headaches • Fatigue • Central nervous system (CNS) depression Treatment • Supplemental oxygen • Treat underlying disorder • Consider mechanical ventilation with severe acidosis, deteriorating mental status, and impending respiratory failure |
Respiratory alkalosis |
Alveolar hyperventilation: Increased blood pH with decrease in PaCO2 • Acute renal compensation: For every 10 mm Hg decrease in PaCO2, bicarbonate will decrease by 2 • Chronic renal compensation: For every 10 mm Hg decrease in PaCO2, bicarbonate will decrease by 5 Etiology • Anxiety • Sepsis • Pregnancy • Liver disease • Pulmonary embolism • Asthma Signs/Symptoms • Decreased cerebral blood flow • Lightheadedness • Anxiety • Perioral numbness • Arrhythmias Treatment • Treat underlying disorder • Inhale CO2 (breathing into a paper bag) |
• 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 H2O)
∘ (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)
Hyponatremia |
Symptoms • Lethargy, seizures, nausea/vomiting, confusion Diagnosis/Etiology • Measure serum osmolality – Normal: Isotonic hyponatremia (pseudohyponatremia) ∘ Hyperlipidemia ∘ Hyperproteinemia – High: Hypertonic hyponatremia; hyperglycemia – Low: Hypotonic hyponatremia; measure volume status ∘ Hypovolemic –Extrarenal salt loss: Urine sodium low ∼10 mEq/L; diarrhea/vomiting –Renal salt loss: Urine sodium high ∼20 mEq/L; acute tubular necrosis or excessive diuretic use ∘ Euvolemic –Syndrome of inappropriate antidiuretic hormone secretion (SIADH): < 20 mEq/L urine sodium, < 100 mOsm/kg H2O urine osmolality –Psychogenic polydipsia: > 10 mEq/L urine sodium, > 100 mOsm/kg H2O urine osmolality –Hypothyroid disease ∘ Hypervolemic –CHF/liver disease: > 20 mEq/L urine sodium –Renal failure: < 20 mEq/L urine sodium Treatment • Based on volume status and neurologic symptoms • Rapid normalization of sodium level can lead to demyelinating encephalopathy – Plasma rise should not exceed 0.5 mEq/L per hour • Amount of replacement can be guided by calculation of sodium deficit – Sodium deficit = normal total body water × (130 – current plasma sodium) • Hypotonic – Hypovolemia: Hypertonic saline (3% NaCl) in symptomatic patients; isotonic saline in asymptomatic patients – Euvolemia: Combined furosemide diuresis and infusion of hypotonic saline in symptomatic patients; isotonic saline in asymptomatic patients – Hypervolemia: Diuretics with addition of hypertonic saline only in symptomatic patients |
Hypernatremia |
Symptoms • Lethargy, weakness, irritability, seizure, polyuria Diagnosis/Etiology • Measure volume status – Hypovolemic: More water loss than sodium loss ∘ Renal loss –Renal failure –Diuretics –Non–ketotic hyperglycemia (NKH): plasma glucose usually > 1,000 mg/dL ∘ Nonrenal loss –Diarrhea –Respiratory loss – Euvolemic: Loss of water only ∘ Diabetes insipidus: Central versus neurogenic – Hypervolemic: More sodium gain than water gain ∘ Excess of mineralocorticoids ∘ Cushing syndrome Treatment • Calculate the free water deficit and replace with isotonic fluid • Treat underlying causes – Central diabetes insipitus: Treat with vasopressin 2 to 5 units subcutaneously every 4 to 6 hours |
• 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
Hypokalemia |
Hypokalemia is better tolerated than hyperkalemia Etiology • Nonrenal: Urine potassium < 30 mEq/L; diarrhea • Renal loss: Urine potassium > 30 mEq/L – High urine chloride (> 25 mEq/L) ∘ Magnesium depletion ∘ Diuretic – Low urine chloride (< 25 mEq/L) ∘ Nasogastric suctioning ∘ Alkalosis Symptoms • Mild hypokalemia (2.5 to 3.5); can be asymptomatic • Severe hypokalemia (< 2.5 mEq/L); diffuse muscle weakness • Abnormal ECG; prominent U waves, flattening and inversion of T waves, and QT prolongation • Only occurs in 50% of cases Treatment • Treat underlying cause • Magnesium replacement • Potassium (KCl) replacement should be done gradually – Oral replacement in mild cases – Intravenous (IV) replacement in cases with arrhythmia; increase no greater than 20 mEq/L |
Hyperkalemia |
Poorly tolerated, especially when level is above 5.5 mEq/L; a patient with chronic renal disease may normally have an elevated potassium level Etiology • Nonrenal (transcellular shift) – Acidosis – Rhabdomyolysis • Impaired renal excretion – Adrenal insufficiency – Drug (eg, potassium-sparing diuretics) – Renal insufficiency Symptoms • ECG changes – Begins to change when potassium reaches 6 mEq/L – Stages ∘ 1st stage: Peaked T waves (V2 and V3) ∘ 2nd stage: Flattened P waves and PR interval lengthening ∘ 3rd stage: Disappearance of P waves and QRS prolongation ∘ Final: Ventricular asystole • Respiratory failure • Nausea/vomiting • Muscle weakness Treatment • ECG changes: IV calcium gluconate to decrease cardiac excitability • Shift potassium from extracellular to intracellular with insulin and dextrose • Diuretics, exchange resins (kayexalate), dialysis to remove potassium |
Crohn disease |
Ulcerative colitis |
|
Definition |
Chronic disease with patchy transmural inflammation |
Chronic disease with diffuse and continuous mucosal inflammation |
Symptoms |
Nonbloody diarrhea, low-grade fever, pain, malaise, weight loss |
Bloody diarrhea, fecal urgency, fever, uveitis, erythema nodosum, anklyosing spondylitis |
Location |
Anywhere in the gastrointestinal tract with propensity for the ileum |
Colon to the rectum |
Diagnosis |
Colonoscopy with biopsy |
Colonoscopy with biopsy, stool studies, abdominal radiograph showing lead pipe appearance of colon with loss of haustrations |
Malignancy potential |
Questionable increased malignancy risk |
Increased malignancy risk |
Treatment |
Steroid, immunomodulatory drugs, 5-aminosalicylic acid |
Mesalamine, steroid, surgery |
• 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
• 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
• 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
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)
Acute complications |
Chronic complications |
• Stroke • Splenic infarct • Osteomyelitis |
• Retinopathy • Avascular necrosis of the hip • Chronic renal failure |
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
• 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
Disease |
Thrombosis |
Factor V Leiden |
Venous |
Protein C/S deficiency |
Arterial and venous |
Heparin-induced thrombocytopenia (HIT) |
Arterial and venous |
Laboratory check |
Reversibility |
|
Warfarin |
INR |
Fresh frozen plasma, vitamin K |
Heparin |
PTT and platelet count (monitor for HIT) |
Protamine |
Low-molecular-weight heparin |
Antifactor Xa |
No |
Fondaparinux (factor Xa inhibitors) |
No monitoring |
No |
Dabigatran (direct thrombin inhibitors) |
PTT |
No |
• Random glucose > 200 mg/dL
• Fasting glucose > 126 mg/dL
• Two-hour glucose > 200 mg/dL (75 gm)
• Hemoglobin A1c (HbA1c) > 6.5
Type 1 DM |
Type 2 DM |
|
Symptoms |
Polyuria, polydipsia, polyphagia |
Mild or none |
Stature |
Skinny |
Obese |
Etiology |
Autoimmune islet cell destruction |
Insulin resistance associated with obesity |
Treatment |
Insulin therapy, glycemic control, lifestyle management |
Oral hypoglycemic, glycemic control, lifestyle management |
Complication |
Diabetic ketoacidosis |
Hyperosmolar nonketotic coma |
Chronic complications |
Retinopathy, neuropathy, nephropathy, infections, myocardial infarction, cardiovascular disease, stroke |
Mechanism |
Notes |
|
Biguanide (metformin) |
Decreases insulin resistance and glucose production |
Can cause lactic acidosis, gastrointestinal upset |
Sulfonylurea (glyburide) |
Stimulates insulin release |
Can cause hypoglycemia |
Meglitinide (repaglinide) |
Stimulates pancreas to release insulin |
Can cause weight gain |
Thiazolidinedione (pioglitazone) |
Decreases insulin resistance peripherally |
Causes retention of fluid |
• 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
• 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
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
Hypothyroid |
Hyperthyroid |
|
Diagnosis |
Elevated TSH and decreased T4 |
Decreased TSH and increased T4 |
Symptoms |
Fatigue, weight gain, cold intolerance, depression |
Palpitations, heat intolerance, sweating, anxiety |
Examples |
Hashimoto thyroiditis, subacute thyroiditis, iodine deficiency |
Graves disease, toxic nodule, goiter |
Treatment |
Synthroid |
Ablation surgery, propylthiouracil, methimazole |
Complications |
Myxedema coma with hypercapnia, hypoventilation, hypothermia |
Atrial fibrillation, thyroid storm |
TSH, thyroid-stimulating hormone; T4, thyroxine. |
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
• Etiology: Autoimmune adrenalitis, malignancy, infection
• Symptoms: Hyperpigmentation of the oral mucosa, dehydration, hypotension, fatigue, anorexia, nausea, vomiting, diarrhea, abdominal pain, salt craving, hyponatremia, hyperkalemia
• Diagnosis: Check chemistry panel for electrolyte abnormalities, low cortisol, high adrenocorticotropic hormone (ACTH)
• Treatment: Mineralocorticoid and glucocorticoid replacement
• Etiology: Exogenous steroids, pituitary adenoma, ectopic ACTH, adrenal hyperplasia
• Symptoms: Moon facies, “buffalo hump,” hypertension, truncal obesity, depression, striae, diabetes, osteopenia, hypokalemia, metabolic acidosis
• Diagnosis: Check chemistry panel for acidosis and abnormalities of electrolytes; conduct dexamethasone suppression test or 24-hour urine free cortisol level
• Treatment: For Cushing syndrome, adenoma resection; if ectopic ACTH release, treat underlying neoplasm
Hormones released from pituitary gland include: ACTH, thyroid-stimulating hormone (TSH), luteinizing hormone/follicle stimulating hormone (LH/FSH), growth hormone (GH), prolactin.
• Etiology: Invasive disease, infiltrative disease, infarction, head trauma, iatrogenic infection
• Symptoms: Depends on the hormone deficiency; GH, LH/FSH, TSH, ACTH, antidiuretic hormone
• Diagnosis: Blood test for specific hormones suspected in hypopituitarism
• Treatment: Treat the underlying cause and correct hormone deficiencies with appropriate oral/nasal hormonal medications
• Etiology: Adenoma, prolactinoma
• Symptoms: Headache, vision changes, additional symptoms specific to hormone released from pituitary gland
– Prolactinoma has additional symptoms: Galactorrhea, amenorrhea, impotence
• Diagnosis: MRI, visual field testing for bitemporal hemianopsia (other defects may occur with larger lesions)
• Treatment: Surgical removal of adenoma, dopamine agonists for prolactinomas
• Symptoms
– “Moans” (stupor, depression, psychosis)
– “Groans” (nausea, vomiting, constipation)
– “Stones” (kidney stones, nephrogenic diabetes insipidus)
– “Bones” (arthritis, fractures)
– Other symptoms: Weakness, hypertonia, bradycardia
• Etiology: Malignancy (parathyroid hormone-related protein [PTHrP], local osteolysis), granulomatous disorders, Paget disease
• Diagnosis: Check parathyroid hormone, ionized calcium
• Treatment: Normal saline infusion for urinary excretion
– If calcium is still elevated after normal saline infusion, consider diuretics to inhibit calcium reabsorption and bisphosphonates or calcitonin when hypercalcemia is secondary to malignancy
– Glucocorticoids may be used to treat hypercalcemia in patients with multiple myeloma
• Symptoms: Neuromuscular excitability (seizures, tetany), Chvostek sign, Trousseau sign, prolonged QT interval
• Etiology: Hypoparathyroidism, parathyroid hormone resistance, vitamin D deficiency
• Diagnosis: Check ionized calcium, parathyroid hormone values, renal function
• Treatment: Intravenous calcium drip acutely, oral calcium (calcitriol, if needed) chronically
• Definition: