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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

5 4 3 2 1

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

Contents

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

Preface

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.

Contributors

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

Chapter 1

Medical Assessment

Alia Koch and Steven M. Roser

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)

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.

Valvular Disease

Arrythmias

CHADS2 scoring table

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

Stroke risk assessment

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.

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.)

 

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

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)

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.

Duke criteria for diagnosis

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.

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.

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

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

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 versus restrictive lung disease

 

Obstructive

Restrictive

FEV1

Decreased

Decreased

FVC

Normal

Decreased

FEV1/FVC

Decreased

Normal/increased

Lung volume

Increased

Decreased

Flow rates

Decreased

Decreased

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

 

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.

Medications for treatment of asthma

 

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.

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

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

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 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

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

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.

Contraindications to anticoagulation

Relative

Absolute

Thrombocytopenia

Prior hemorrhagic stroke

Recent internal bleeding

Active internal bleeding

Aortic dissection

Active hemorrhagic stroke

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

A

Acidosis

E

Electrolyte abnormality

I

Ingestion

O

Overload

U

Uremia

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

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

Severity of chronic renal disease based on albuminuria

Albuminuria stage

Albumin excretion rate (mg/day)

Albumin excretion

A1

< 30

Normal to increased

A2

30–300

Moderately increased

A3

> 300

Severely increased

Complications of CRF

 

Treatment

Anemia

Erythropoietin injections, iron

Renal osteodystrophy

Phosphate binder

Hyperkalemia

Dietary restriction, diuretic

Acidosis

Sodium bicarbonate

Pericarditis

Dialysis

Dialysis infections

Antibiotics, catheter removal

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.

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.

Secondary nephrotic syndrome

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

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

 

Pathology

Treatment

Subacute bacterial endocarditis

Crescent glomerulonephritis

Antibiotics

Post-streptococcal

Subepithelial humps

Resolves after treatment of streptococcal infection

Membranoproliferative

glomerulonephritis

Subendothelial deposits

Treat cryoglobulinemia

Pauci immune glomerulonephritis

 

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 Versus Nephritic Disease

 

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.

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 [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

Quick Guide to ABG Interpretation

Step one: Identify primary disorder

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

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

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

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

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

Acid-Base Disorders

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)

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 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

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

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

Gastrointestinal Disease

Irritable Bowel Syndrome

 

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

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)

Acute complications

Chronic complications

Stroke

Splenic infarct

Osteomyelitis

Retinopathy

Avascular necrosis of the hip

Chronic renal failure

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

Disease

Thrombosis

Factor V Leiden

Venous

Protein C/S deficiency

Arterial and venous

Heparin-induced thrombocytopenia (HIT)

Arterial and venous

Anticoagulation medications

 

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

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

 

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

Insulin types

Oral hypoglycemics

 

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

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

 

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.

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

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

Cushing syndrome

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

Pituitary Disorders

Hormones released from pituitary gland include: ACTH, thyroid-stimulating hormone (TSH), luteinizing hormone/follicle stimulating hormone (LH/FSH), growth hormone (GH), prolactin.

Hypopituitarism

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

Hyperpituitarism

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

Hypercalcemia

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

Hypocalcemia

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

Autoimmune Disease

Sarcoidosis

Definition: