History of Endodontics aae/abe



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Tooth with necrotic pulp and an immature apex (Kling/Cvek AF = 1.1-5 mm)

  • Pulp space not needed for post/core, final restoration

  • No known allergies to antibiotics if intended for use

  • Compliant patient (parent/guardian)




    Informed Consent

    • Two (or more) appointments

    • Use of antimicrobial(s)

    • Possible adverse effects: staining of crown/root, lack of response to treatment, pain/infection

    • Alternatives: MTA apexification, no treatment, extraction (when deemed non-salvageable)

    • Permission to enter information into AAE database (optional)



    Regenerative Endodontic Procedures

    First Appointment

    • Local anesthesia, rubber dam isolation, access

    • Copious, gentle irrigation with 20ml 1.5% NaOCl using an irrigation system that minimizes the possibility of extrusion of irrigants into the periapical space (e.g., needle with closed end and side-vents, or EndoVac). The lower concentrations of NaOCl are advised, to minimize cytotoxicity to stem cells in the apical tissues. (Essner/Eleazer)

    • Dry canals

    • Place antibiotic paste or calcium hydroxide:

    • Ca(OH)2 is antimicrobial at concentrations that do not induce stem cell toxicity and is widely available

    • As an alternative, if the triple antibiotic paste is used:

      • consider sealing pulp chamber with a dentin bonding agent (to minimize risk of staining)

      • mix 1:1:1 ciprofloxacin:metronidazole:minocycline in a lower concentration (0.01-0.1 mg/ml) to avoid stem cell toxicity; these lower concentrations appear as a liquid form and are no longer a paste (Ruparel)

      • 1:1 Cipro:Metro also eliminates the staining from minocycline.

    • Deliver into canal system via Lentulo spiral, MAP system or syringe

    • If triple antibiotic is used, ensure that it remains below CEJ (minimize crown staining). As an alternative, Ca(OH)2 does not cause staining.

    • Seal with 3-4mm Cavit, followed by IRM, glass ionomer cement or another temporary material

    • Dismiss patient for 3-4 weeks



    Kakoli – infection of dentinal tubules is deeper and affects more tubules in young patients vs older patients … possible complication to disinfection protocol

    Regenerative Endodontic Procedures

    Second Appointment

    • Assess initial treatment: If signs/symptoms of persistent infection, consider additional treatment with the antimicrobial, or an alternative antimicrobial. Recall the patient in about 3-4 weeks as before.

    • Anesthesia: 3% mepivacaine without vasoconstrictor, rubber dam

    • Copious, slow irrigation: 20ml 17% EDTA, followed by normal saline, using a similar closed end needle.

    • Dry with paper points

    • Create bleeding into canal system by over-instrumenting (endo file, endo explorer, or 17% EDTA dipped endo explorer)

    • Stop bleeding 3mm from CEJ and place CollaPlug/Collacote (Petrino)

    • Place 3-4 mm of MTA and reinforced glass ionomer and place permanent restoration. Glass ionomer may be an alternative to MTA in cases where discoloration of the crown is a potential concern (Giesler)



    Regenerative Endodontic Procedures

    Triple Antibiotic Paste:



    1. Hoshino –1:1:1 Ciprofloxacin, Metronidazole, Minocycline

    • Effective for eradicating bacterial infection from infected dentin

    • Creating environment for ingrowth of vascularity and regenerative cells

    1. Windley/Tropedog study, infected canals, 1.25% NaOCl irrigation = 10% teeth bacteria free, 2 wks triple antibiotic paste = 70% teeth bacteria free

    2. Law 2013 (review) – 2-4 weeks for TAP medicament interappt

    Irrigation: 1.25% NaOCl (1st appt), 17% EDTA (2nd appt), NO CHX

    1. Essner/EleazerHigher conc. of NaOCl are cytotoxic to stem cells, tested .04% - .33% NaOCl

    2. Martin 2012 – Higher conc. of NaOCl  DSPP capacity to induce SCAP differentiation

    3. Trevino 201117% EDTA best supported SCAP cell survival, protocols with 2% CHX lacked any viable stem cells

    Regenerative Endodontic Procedures
    Triple Antibiotic Paste vs. CaOH2: Balance of antibacterial effects and stem cell survival


    1. Chueh - CaOH2 as intracanal medicament, no staining

    2. Bose/Hargreaves – Case series,TAP > CaOH2 for root wall width growth

    3. Law 2013 – TAP (0.01-0.1 mg/mL) or CaOH2; consider eliminating Minocycline or use Dentin bonding agent (Kim) to avoid staining

    4. Ruparel 2012 – TAP, DAP, and Augmentin at currently used clinical concentrations (thick slurry pastes >0.1 mg/mL) are cytotoxic to SCAP cells. CaOH2 supported SCAP survival at all concentrations

    Anesthetic: 3% Mepivicaine w/o epinephrine



    1. Petrino 2010 – Use 3% Mepivicaine w/o vasoconstrictor – the use of a vasconstrictor may impede the ability to induce bleeding in the canal, the crucial step for attaining a scaffold and delivery of stem cells

    Regenerative Endodontic Procedures
    Irrigation: 17% EDTA (2nd appt), NO CHX

    1. Trevino 2011 – 17% EDTA best supported SCAP cell survival, protocols with 2% CHX lacked any viable stem cells

    2. Ring/Murray – Irrigants effect stem cell adherence to dentin

    3. Galler – EDTA promotes exposure of growth factors in dentin, differentiation of stem cells into odontoblast like cells and adhesion of those cells to dentin

    Collagen matrix for MTA placement:



    1. Petrino 2010– Collagen matrix (Collagplug or Collacote) may be used as a matrix barrier for MTA placement

    MTA Barrier: (3-4 mm) – (4 mm seal: Al-Kahtani; Lawley)



    1. Holland; Nair – MTA promotes complete hard tissue barrier w/no infl.

    2. Torabinejad/Parirokh–MTA is biocompatible, osteoconductive/inductive

    Regeneration Success

    Hargreaves 2012, Law 2013

    Clinical criteria: No pain/swelling, no pain to percussion/palpation, no sinus tracts Radiographic criteria: Healing of AP, Continued radiographic root development: Increased root width, Increased root length

    Recall time: 12-18 months (Cheuh, Bose/Hargreaves, Law)

    1. Bose/Hargreaves 2009Retrospective, compared differences in root lengthening and root wall thickening for various intracanal medicaments (TAP, CaOH2, and Formocresol). Root Length: TAP = CaOH2 >> Controls (NSRCT or MTA apexification), Root Width: TAP >> CaOH2 >> Controls. 12-18 month recall.




    1. Jeeruphan/Hargreaves 2012Retrospective, 61 teeth, Pulpal regeneration vs. MTA apexification vs. CaOH2 apexification, Immature necrotic teeth. Findings Root length: Revasc>MTA>CaOH2; Root width: Revasc>CaOH2>MTA; Survival: Revasc (100%) >MTA (95%)>CaOH2 (77%) – >6 months (avg 14 months) recall

    Regeneration Outcomes – Histological Evaluation


    1. Wang/Thibodeau/Trope JOE 2010 – Histological characterization of regenerated tissues in canal space following revascularization procedures in immature dogs teeth: Cementum-like, Bone-like, and PDL-like tissues within the canal space




    1. Torabinejad/Faras JOE 2012 – Histological evaluation of canal contents of immature human premolar treated with regenerative endodontic procedure and PRP scaffold: Vital Pulp-like connective tissues




    1. Shimizu JOE 2013 – Histological evaluation of immature human maxillary incisor treated with revascularization procedure (26 months): Cementum-like and Bone-like tissues within canal space. No pulp-like connective tissues observed. Need new regenerative protocols to promote regeneration of pulp tissues within canal space


    Medically Compromised

    What is Sickle cell anemia, how does it effect the root canal?
    Kaya IEJ 2004 – SCA is a genetic and systemic disease which may cause pulp necrosis without necessarily having an identifiable etiology. SCA causes radiographically observable differences in jaw structure, especially in the mandible. The clinical problem is directly associated with the defective RBC. The patients are prone to infection because the macrophages are involved in the phagocytosis of the RBC and not available for destroying bacteria. The distorted cells may also occlude the Microvasculature and impede blood flow to an area. This mechanism is suspected by Ingle & Taintor 1985 to be the cause of pulpal necrosis and repeated episodes of pain as described by Andrews/England 1983 in sickle cell patients
    Costa JOE 20138.33x higher incidence of PN with Sickle Cell patients
    Radiographic observation- “stepladder” appearance of the widening trabeculation due to increased marrow space (increased hematopoiesis/RBCs)

    What are characteristics of Vit D resistant rickets ?
    Bender & Naidorf 1985 JOE –


    1. Pulp horn extension into the DEJ is pathognomonic for Vit. D resistant rickets




    1. Clinically: frontal bossing, bowing of legs, short enlarged wrists and ankles




    1. Dental: hypoplastic/hypocalcified enamel, draining sinus tract, gingival swelling, apical abscesses




    1. Radiographic: enlarged pulp chambers, wide root canals, and loss of lamina dura, shortened roots



    What are the characteristics of hyperparathyroidism ?

    Primary – caused by adenoma (80%), carcinoma of the parathyroid or PTH release from ectopic malignant tumor.

    Treatment – surgical removal of parathyroid


    Secondary – caused by Chronic kidney disease, Vit D deficiency, Calcium malabsorption states ( Ca,  phosphate, K)

    Treatment – renal dialysis or transplant


    Classic signs = stones, bones, groans

    1. Ectopic calcifications – kidney stones

    2. Bone lesions

      1. Lytic lesions (brown tumors = central giant cell granuloma)

      2. Ground glass appearance with decreased trabeculation

      3. Loss of lamina dura

    3. Vague abdominal pain, bone pain, fatigue, weakness

    4. Emotional liability, psychoses

    Diabetes

    Bender 2003 JOE – Inherent factors of the disease:

    1. Prone to bacterial or opportunistic infections (see below)

    2. Vulnerability caused by a generalized circulatory disorder (peripheral microvascular collapse)

    3. Blood vessels are damaged by the accumulation of atheromatous deposits (macrovascular disease)

    4. Capillaries develop a thickened basement membrane (microvascular diesease)

    5. Impaired leukocyte chemotaxis and immune cell delivery

    6. Decreased PMN microbicidal ability

    7. Due to limited pulpal/periapical circulation, patients are more prone to infection and impaired healing!!


    Fouad et al 2003 JADAPreoperative periradicular lesions and a history of diabetes have a significant reduction in successful outcome for endodontic treatment. PARL + Diabetes = Success of NSRCT (impaired healing)

    Segura 2005; Marota/Siqueira 2012 – Type 2 Diabetics have an increased prevalence for AP (prone to infection)

    Diabetes

    1. Types:

    1. Type Iloss of insulin producing beta cells of the islets of Langerhans in pancreas leading to insulin deficiency; immune-mediated – T cell attack; Prevalence: 10%; Sudden onset; Childhood; Ketoacidosis common

    2. Type IIinsulin resistance +/- reduced insulin secretion (insulin receptor); unknown defect; Prevalence: 90%; Gradual onset; Adult; Ketoacidosis uncommon

    1. Other types: Gestational, Prediabetes, LADA

    2. Signs/Symptoms: (Cardinal) Polyuria, Polydipsia, Polyphagia, Wt loss

    3. Complications: Diabetic retinopathy, Diabetic nephropathy, atherosclerosis/ischemic heart disease, peripheral vascular disease

    4. Testing: HbA1c (Glycosolated hemoglobin: measures 2-3 month prior glucose levels): <6% Normal, <7% Well controlled diabetic

    5. Diagnostic criteria: Fasting glucose: >126 mg/dL, 2 hr glucose: >200 mg/dL, HbA1c: >6.5%

    Coronary Heart Disease/Coronary Atherosclerosis/Ischemic HD

    Symptomatic Coronary Atherosclerosis aka Ischemic Heart Disease:

    • Angina, possible MI

    • Oxygen deprivation due to reduced blood flow to myocardium

    Stable Angina:

    • Predictable, reproducible, ppt by physical effort, relieved by cessation of exercise/rest/Nitro. Limit EPI, short appts, stress reduction, N2O2, vitals

    Unstable Angina:

    • New, Increasing in frequency/intensty, ppt at rest, not relieved by Nitro

    • Changing pattern, poorer prognosis, MI likely

    • Avoid elective care, consult phys.,monitor ECG/Pulse ox/BP, N2O2, Nitro

    -Avoid NSAIDs (excluding Aspirin) with hx of MI or Stroke (Olson)

    -Avoid EPI in Unstable Angina/recent MI, Limit 2 carps in Stable Angina

    Frisk – No significant association between coronary heart disease (CHD) and RCT treated teeth or teeth with AP

    Rodriguez JOE 2014 – Suggests association between coronary heart disease and teeth with AP

    HTN

    Classifications of BP:

    1. Normal: <120, <80

    2. Pre-Hypertensive: 120-139, 80-89

    3. Stage 1 HTN: 140-159, 90-99

    4. Stage 2 HTN:  160,  100 – If Symptomatic: Emer tx only, Refer immed.

    Systolic = Arterial pressure at peak ventricular contraction (more sign. >50 yrs)

    Diastolic = Resting Arterial pressure



    Treatment Considerations:

    -Avoid long term (>2 wks) NSAIDs in pts taking anti-hypertensive medications (ACEIs, Beta blockers, Diuretics, Alpha/Beta blockers)

    -Limit Epi to 2 carps w/ Non-selective Beta blockers (Propranolol, Coreg): Block Beta 2 which maintains normal peripheral vasodilatory toneUnopposed alpha stimulation (peripheral vasoconstriction,  BP,  HR)

    -Avoid EPI in Uncontrolled HTN, limit 2 carps in controlled HTN

    -Defer elective dental tx if >180/110

    -Orthostatic Hypotension: Temporary in BP, Dizziness/light-headed/Fainting



    Medications

    HTN/CAD/Angina/Arrythmias/CHF:

    1. ACE Inhibitors (“PRILs”): Enalapril, Lisinopril

    MOA: Acts on Renin/Angiotensin/Aldosterone system; Prevents Angiotensin I  II =  arteriolar resistance, cardiac output,  Na/H2O excretion,  HTN


    1. ARBs (“SARTANs”): Losartan, Valsartan, Olemsaran (Benicar)

    MOA: Blocks activation of Angiotensin II receptor = Vasodilation,  HTN


    1. Beta Blockers (“LOLs”):

    Selective (1 only): Metoprolol, Atenolol, Acebutolol, Bisoprolol

    Non-Selective (1 + 2): Propranolol, Carvedilol (Coreg)

    MOA: Block action of epi/norepi (sympathetic) on  adrenergic receptors; 1-heart, kidneys; 2-lungs, gi, vascular smooth muscle, skeletal muscle

    1: Cardiac output/contractility, Renin release (kidneys)

    2: Smooth muscle relaxation/Peripheral Vasodilation, Bronchodilation



    Medications

    HTN/CAD/Angina/Arrythmias/CHF:


    1. Calcium Channel Blockers (“VD-PINEs”): Amlodipine (Norvasc), Nifedipine, Verapamil, Diltiazem

    MOA: Blocks calcium channels within vascular smooth muscle, cardiac muscle = Vasodilation,  contractility (ionotropic),  HR (chronotropic)


    1. Diuretics: (“IDES”)

    Loop (ascending loop): Furosemide

    Potassium Sparing (collecting duct): Triamterine, Spironolactone

    Thiazide (distal convoluted tubule): Hydrochlorothiazide

    MOA: Prevent kidney resabsorption of Na, Cl, K, H2O = Inc fluid excretion




    1. Combo Drugs:

    Lotrel (Amlodipine/Benazepril) = Ca channel blocker + ACE inhibitor

    Azor (Amlodipine/Olemasartan) = Ca channel blocker + ARB

    Medications

    Anti-Platelet – Prevention of thromboemboli (dislodged thrombus)

    1. Aspirin: AcetylSalicylic Acid (ASA)

    • NSAID but more selective for Cox-1 and irreversibly inhibits Cox enzyme =TXA2(Platelet aggreg./production); Avoid <19 y.o. (Reye’s)

    1. NSAIDs: Ibuprofen, Naproxen, Indomethacin, Ketorolac, Diclofenac, Meloxicam, Celebrex (Cox-2 selective)

    • Analgesic ( PGs), Antipyretic ( PGs), Anti-platelet (Thromboxane A2), Anti-inflammatory; reversibly inhibits Cox enzyme (AA  PGH2)

    1. Plavix (Clopidogrel)

    • Alters Platelet fx through irreversible inhibition of ADP chemoreceptor on platelet surface

    Anti-Coagulant – Prevention of thromboemboli – stroke, MI

    1. Coumadin (Warfarin) – Inhibits Vit K-dep. (liver) synthesis of clotting factors (II, VII, IX, X). INR(PT-extrinsic factor VII) 2.0–3.0 = normal range

    2. Heparin (pulmonary emobli)– Activates Anti-thrombin, prothromthrom

    3. Pradaxa (Dabigatran) Direct thrombin (Factor II) inhibitor , A Fib

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    macintosh hd:users:matt:downloads:1000px-coagulation_full.svg.png

    Cardiac Arrythmias

    **Avoid elective dental care in with patients with severe arrythmias: High grade AV blocks, Symptomatic Ventricular arrythmias, Supraventricular arrythmias

    **Avoid Epi in patients taking Digoxin

    Digoxin Toxicity: Hypersalivation, Nausea/Vomiting, Drowsiness, Visual disturbance - YELLOW or GREEN appearance

    **Avoid Epi in patients with severe arrythmias, limit to 2 carps in others

    MED CONSULT, Nitrous oxide, Oxygen and Nitro should be used

    Atrial Fibrillation – Pradaxa (anti-coagulant/direct thrombin inhib. = factor II) – check aPTT (intrinsic/common pathways), use local hemostatic measures



    **Antibiotics not recommended for Pacemakers/Atrial defibrillators

    RoedigIn vitro, Electromagnetic interference with pacemakers – battery powered Curing Light and Magnetostrictive Ultrasonic units

    Wilson/BaumgartnerIn vivo, No Electromagnetic interference with pacemakers/cardio-defibrillators – 2 EALs (Root ZX), 1 EPT

    GomezIn vitro, No Electromagnetic interference with pacemaker/defibrillators – Piezoelectric Ultrasonic units

    Congestive Heart Failure

    CHF = complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood

    1. Etiology: CAD/CHD, HTN, Cardiomyopathy, etc

    2. Sequelae: MI/Cardiac arrest… peripheral edema, fluid retention, pulm. HTN

    3. Avoid: NSAIDs, EPI (also for Digoxin)

    4. Dental Tx: MED CONSULT

      1. Without limitations: Elective Tx

      2. With limitations/but ok at rest: Elective Tx with Med Consult

      3. Symptoms at Rest: No Elective Tx, Hospital based Tx for emergencies

    5. Medical Consultation: Physical status, Lab values, Control of condition, Stability, Meds/Recommendations

    6. Nitrous Oxide: Ok to use

    7. Semisupine/upright position, short/stress free appts/monitor vitals/pulse ox/N2O2 (stress reduction!)

    Pulmonary Disorders

    COPD: Chronic Bronchitis & Emphysema

    1. Chronic Bronchitis (“Blue bloaters”): cyanotic w/chronic cough

    1. Excessive trachobronchial mucus production

    2. Chronic cough with sputum production

    3. At least 3 months for 2 consecutive years

    1. Emphysema (“Pink puffers”): barrel chested w/exertional dyspnea

    1. Permanent enlargement of the airways distal to terminal bronchioles

    2. Destruction of the alveolar walls or septa without fibrosis

    Defer Tx: Shortness of Breath at rest, Productive cough, URI, O2 Sat < 91%

    Avoid: Respiratory depressants (Sedatives – Benzos/Flexaril, Narcotics, Barbituates), Nitrous Oxide (Severe COPD only)

    Dental Tx: Semisupine position, Pulse Ox monitoring, O2 (2-3L/min) <95%



    *Theophylline:

    1. MOA: inhibits TNF, Leukotrienes; relaxes bronchial smooth muscle,  HR, Contractility, BP (non-selective beta agonist)

    2. Toxicity: Nausea/Diarrhea (2),  HR, Arrhythmias (1), CNS Exc/Seizures

    3. Adverse Drug Interactions: Ciprofloxacin, Macrolides (CMT)

    Pulmonary Disorders

    Asthma

    • Reversible episodes of airway hyperresponsivness

    • Recurrent episodes of wheezing, coughing, and dyspnea

    • Extrinsic (smoke, seasonal), Intrinsic (drugs, foods), Exercise, Stress

    Avoid:

    • NSAIDs/AspirinBronchoconstriction in 10% (40% w/pansinusitis, nasal polyps – triad asthmaticus) due to build up of AALeukotrienes

    • EPI - Sulfates in LA w/ EPI – build up of sulfur dioxide – acute attack

    • Respiratory Depressants–Barbituates, Narcotics, Benzos, Flexaril

    Nitrous Oxide: Okay to use, not a respiratory depressant or irritant

    If Attack occurs in office:



    • Short acting beta2 agonist (bronchodilator): Albuterol q20 mins

    • Subcutaneous injection – 0.3-0.5 mL 1:1000 epi

    • Oxygen admin, Monitor Vitals, Pulse Ox, EMS

    Treatment: Short acting Beta2 Agonists (albuterol), Long acting Beta2 Agonists, Corticosteroids (Advair), Corticosteroids (oral)

    G.I. Disorders (PUD/CUD)

    1. Peptic Ulcer Disease

    • Ulceration of the stomach lining or first part of the small intestine (duodenum), acid related, H. pylori major factor

    • Severe abdominal pain, bloating, nausea, vomiting, loss of apetite

    1. Crohn’s Disease

    • IBD, inflammatory ulceration of any part of the G.I. tract (mouth – anus)

    • Autoimmune mediated, mucosal ulcerations

    • Symptoms: Abdominal pain, diarrhea, fever, wt. loss, anemia, skin rash

    • No cure, Steroids, Immunosuppresants, Biologics, Methotrexate, Sx

    1. Ulcerative Colitis

    • IBD, similar to Crohn’s Disease, intermittent ulcerations of the intestinal tract lining. Marked by diarrhea, anemia. Mucosal ulcerations.

    • Unlike Crohn’s only affects the large intestine (colon)

    • Treatment: Steroids, Biologics (Humira), Colectomy

    **AVOID: NSAIDs/Aspirin, Clindamycin (C. dif assoc. pseudomem. colitis), steroids

    **Caution: Antacids, Proton pump inhibitors “ZOLEs” – ie Omeprazole (H+ pump of gastric parietal cells) interact with certain antibiotics, benzodiazepines, methotrexate



    Liver Disease

    Hepatitis:



    • Inflammation of the liver, may be acute (<6 months) or chronic

    • Symptoms: Often asymptomatic, jaundice, poor apetitie, malaise

    • Self limiting or leading to fibrosis/cirrhosis, poss. Hepatocellular carcinoma

    • Causes: Viral (Hepatitis A, B, C, D, E), alcohol, medications, autoimmune

    • Diagnosis: CBC, Liver enzymes (ALT/AST, ALP, Bilirubin), PT time

    • Chronic can have compromised: liver fx, drug metabolism, hemostasis

    Dental Tx:

    • Acute hepatitis: Emergency only, Hospital based, Avoid drugs metabolized in liver (LAs, Pain meds), check bleeding/PT timeExtrinisic pathway (VII)

    • Bleeding issues (Vit K dep clotting factors – Prothrombin(2), 7, 9, 10) – chk CBC, PT, Platelets (thrombocytopenia), Med Consult prior to Surgery!

    • Higher tolerance to drugs: LAs, sedatives, GA, AVOID Tylenol, NSAIDs

    HCV needlestick: Blood to Blood transmission

    • Baseline testing of patient – HCV antibody enzyme immunoassay (ELISA)

    • Baseline and follow up (6 months) – HCV antibody and liver enzyme activity

    • HCV antibody ELISA postive results confirmed with HCV qPCR or RBIA

    Chronic Kidney (Renal) Disease

    Definition: Progressive loss in renal function,  fluid/K/Cl/Na/H2O excretion

    Signs/Symptoms:


    • HTN/CHF (fluid retention/overload)

    • Hyperkalemia, Hyperphosphatemia, Hypocalcemia (Vit D3 deficiency)

    • Metabolic Acidosis (accumulation of sulfates, phosphates, uric acid)

    • Iron Deficiency Anemia (weakness/pallor/ cardiac output)

    • Accelerated atherosclerosis

    Causes: Diabetes Mellitus, HTN, Chronic Glomerulonephritis, PKD

    Diagnosis: Creatinine ( levels), urinalysis, adbominal ultrasound, GFR

    Staging: CKD = <60 mL/min (3 months), >90/90-60/60-30/30-15/<15 mL/min

    Stage 5 (End Stage Renal Disease) = < 15 mL/min

    ESRD Hematologic Abnormalities:



    • Anemia: erythropoeitin/RBC production (weakness/pallor/breathless)

    • Leukocyte dysfunction - risk of infection, leukopenia

    • Platelet dysfunction: Abnormal platelet aggregation, thrombocytopenia

    • Coagulopathy: Atherosclerosis, HTN/CHF

    Chronic Kidney (Renal) Disease

    ESRD Renal Osteodystrophy & Secondary Hyperparathyroidism:



    •  Vit D3 production   Calcium absorption (gastric mucosa)

    •  Renal excretion of Phosphate and Potassium (binds free Ca+2)

    •  Serum Calcium   Parathyroid Hormone (PTH) secretion

    PTH Secretion  Secondary Hyperparathyroidism:

    • Inhibits tubular reabsorption of Phosphate

    • Stimulates renal production of Vit D3 for calcium absorption

    • Sustained levels of PTH  Bone remodeling, Calcium mobilization from bones, Renal and metastic calcifcations:

      • Ostomalacia – increased bone matrix

      • Osteitis fibrosa – lytic lesions of bone, marrow fibrosis

      • Osteosclerosis – enhanced bone density

    • STONEs (kidney stones), BONEs (lytic lesions), GROANs (pain)

    • Radiographic Changes: Loss of Lamina Dura, Demineralized bone (Ground Glass), RL jaw lesions (CGCGs/Brown’s tumors), Widened Trabeculations, Metastatic calcifications within the skull

    Hemodialysis

    • Every 2-3 days (4-6 hrs), Heparin admin IV to prevent coagulation

    • Antibiotic prophylaxis NOT needed for AV fistula for routine dental care but is necessary for I&D Abscess (leukopenia)

    • Best day to Tx: Day after hemodialysis

    • Avoid Tx within 4-6 hours of hemodialysis due to Heparin

    • Avoid BP cuff or IV meds on arm with AV Shunt


    ESRD

    • Dental Tx: Med consult, Hospital based treatment w/comorbid conditions, Aggressive management of orofacial infections (leukocyte dysfunction)

    • Surgery: Med consult, Screening for Platelets, PT, aPTT, TT, bleeding time, assess need for Antibiotics (leukocyte dysfunction)

    • Medications/Drugs:

      • Reduce dosageseliminated slower/reach toxic levels faster

      • Avoid most pain meds, antibioticsTylenol, Clindamycin OK (liver)

    Diabetes

    1. Types:

    1. Type Iloss of insulin producing beta cells of the islets of Langerhans in pancreas leading to insulin deficiency; immune-mediated – T cell attack; Prevalence: 10%; Sudden onset; Childhood; Ketoacidosis common

    2. Type IIinsulin resistance +/- reduced insulin secretion (insulin receptor); unknown defect; Prevalence: 90%; Gradual onset; Adult; Ketoacidosis uncommon

    1. Signs/Symptoms: (Cardinal) Polyuria, Polydipsia, Polyphagia, Wt loss

    2. Complications: Diabetic retinopathy, Diabetic nephropathy (microvascular) atherosclerosis/ischemic heart disease, peripheral vascular disease

    3. Testing: HbA1c (Glycosolated hemoglobin: 2-3 months prior glucose levels): <6% Normal, <7% Well controlled diabetic

    4. Diagnostic criteria: Fasting glucose: >126 mg/dL, 2 hr glucose: >200 mg/dL, HbA1C: >6.5%

    5. Risk of Infection: Tx aggressively!! I&D, Antibiotics (esp >200 mg/dL)

    Diabetes

    1. Drug Interactions:

      1. Sulfonylureas (ie: Glypizide, Glyburide) and ASA/NSAIDs -  Hypoglycemic effect of drug – Avoid ASA/NSAIDs




    1. Insulin Shock/Hypoglycemic Shock (Fast onset):

      1. Mild: Hunger, Weakness, Tachycardia, Pallor, Sweating

      2. Moderate: Incoherent, Uncooperative, Beligerent, Poor orientation

      3. Severe: Unconsciousness, Tonic/Clonic movements, Hypotensive

      4. Tx: Oral glycemic (juice, cake icing) or IV glucose, glucagon, epi




    1. Hyperglyemic Crisis (Slow onset):

      1. Diabetic Ketoacidosis (DKA) – Insulin insuffiency, Excessive blood glucose, and Dehydration. Cells break down Fatty acids into ketone bodies/keto acids, blood pH drops, and excessive excretion of fluids/glucose.

      2. Symptoms: confusion, hunger, dehydration, “fruity” smell breathe

    Diabetes

    Bender 2003 JOE – Inherent factors of the disease:

    1. Prone to bacterial or opportunistic infections (see below)

    2. Vulnerability caused by a generalized circulatory disorder (peripheral microvascular collapse)

    3. Blood vessels are damaged by the accumulation of atheromatous deposits (macrovascular disease)

    4. Capillaries develop a thickened basement membrane (microvascular diesease)

    5. Impaired leukocyte chemotaxis and immune cell delivery

    6. Decreased PMN microbicidal ability

    7. Due to limited pulpal/periapical circulation, patients are more prone to infection and impaired healing!!


    Fouad et al 2003 JADAPreoperative periradicular lesions and a history of diabetes have a significant reduction in successful outcome for endodontic treatment. PARL + Diabetes = Success of NSRCT (impaired healing)

    Segura 2005; Marota/Siqueira 2012 – Type 2 Diabetics have an increased prevalence for AP (prone to infection)

    Adrenal Insufficiency


    1. Primary Adrenal Insufficiency: Addison’s disease (Autoimmune)

      1. Insufficent production of cortisol and/or aldosterone

      2. Symptoms: Hypoglycemia, dehydration, wt loss, disorientation, abdominal pains, vomiting, fatigue, depression, hypotension, kidney failure and shock (adrenal crisis)

      3. Treatment: Hydrocortisone, Prednisone

    2. Adrenal Crisis: (initial symptoms similar to Insulin shock)

      1. Insufficient levels of cortisol to respond to stressful stiuation (SITS = Stress Infection Trauma Surgery)

      2. Symptoms: Sweating, hypotension, weak pulse, lethargy, confusion/pyschosis, convulsions, loss of consciousness

      3. Untreated may lead rapidly to: Hypothermia, Severe Hypotension, Hypoglycemia, and Circulatory Collapse

      4. Treatment: IV Hydrocortisone (SoluCortef), Fluids

      5. Diagnosis: ACTH stimulation test, Cortisol level, Blood sugar

    Adrenal Insufficiency


    1. Secondary Adrenal Insufficiency:

      1. Steroid-induced – most commonly

      2. Pituitary Adenoma – results in ACTH

      3. Rare to have Adrenal Crisis with 2 Adrenal Insufficiency

      4. Long term Steroids: Insomnia, Gastric Ulceration, Delayed wound healing

    2. Supplemental Steroids & Surgery:

      1. Only Addison’s disease requires supplemental steroid therapy

      2. Minor Sx: 25 mg/day hydrocortisone prior to Surgery

      3. Moderate Sx: 50-75 mg/day hydrocortisone prior to Sx and 1 day post Surgery

      4. Major Sx: 100 mg/day hydrocortisone prior to Sx (or GA procedure) and 2-3 days post Surgery

      5. 2 Adrenal Insufficiency receive normal daily dose of steroids within 2 hours of Surgery

    Hyperadrenalism


    1. Cushing’s Syndrome (opposite of Addison’s)

      1. Prolonged exposure to inappropriately high levels of cortisol

      2. Causes: Exogenous glucocorticoids (ie: Prednisone), Pituitary Adenoma (secondary hypercortisolism aka “Cushing’s Disease”,  ACTH), or Adrenal tumor

      3. Symptoms:

        1. Rapid wt gain – buffalo hump, moon facies

        2. Irritability, insomnia

        3. Muscle/Bone weakness

        4. Memory/Attention dysfunction

        5. Osteoporosis

        6. Diabetes Mellitus/Hyperglycemia

        7. Hypertension

        8. Hirsutism – excessive hair growth (females), Acne

      4. Treatment: Taper off steroids, Removal of Tumor

    Thyroid Disease


    1. Hyperthyroid

    1. Definition: Overproduction of thyroid hormones (T3, T4), aka thyrotoxicosis (hypermetabolic condition), leading to overstimulation of metabolism and exacerbates the sympathetic nervous system effects

    2. Symptoms:

    1. Weight loss

    2. Anxiety, Irritability

    3. Heat intolerance, Sweating

    4. Weakness/Fatigue

    5. Exopthalmus

    6. Tremors – Epi/NorEpi Symp.

    7. Heart palpitations/Arrythmias – Epi/NorEpi Symp.




    1. Causes: Grave’s Disease (autoimmune), Thyroid adenoma

    2. Testing: Labs – TSH (low), T4 (high); Normal T4:T3 ratio = 20:1

    3. Treatment: Anti-thyroidics, Surgical removal, Radioiodine tx

    Thyroid Disease


    1. Thyroid Storm/Thyrotoxic Crisis

    1. Definition: Rare but life threatening form of hyperthyroid

    2. Precipitating Factors: (similar to Adrenal Crisis) - SITS

    1. Stress

    2. Infection

    3. Trauma

    4. Surgical Procedure

    1. Clinical Manifestations: Restlessness, Fever, Pain, Delirium, Psychosis, Tachycardia, Arrythmia, Pulmonary edema, Coma, Heart failure

    2. Treatment: Call EMS, Cool patient with cold towels, Injection of 100-300 mg hydrocortisone

    NOTE: Avoid EPI and ASA/NSAIDs in patients with Uncontrolled Hyperthyroidism


    Thyroid Disease


    1. Hypothyroid

    1. Definition: Underproduction of thryoid hormones (T3, T4) – Understimulation of metabolism and Underexaggeration of Sympathetic Nervous System effects

    2. Symptoms (opposite of Hyperthyroid):

      1. Fatigue

      2. Cold Feeling

      3. Bradycardia

      4. Weight gain

      5. Poor memory/concentration

    3. Causes: Hashimoto’s Thyroiditis (autoimmune), iodine, Thyroidectomy

    4. Testing: TSH (high), T4 (low)

    5. Treatment: Levothryoxine (synthetic replacement) – LIMIT EPI



    Thyroid Disease


    1. Myxedematous Coma

    1. Definition: Stressful event (SITS) in hypothyroidic patient (typically elderly) precipitates myxedma coma

    2. Precipitating Factors: (same as Thyroid Storm + CNS depressants)

      1. Infection

      2. Trauma

      3. Surgical Procedure

      4. Stress

      5. CNS/Respiratory depressants – Narcotics, Benzos, Flexaril

    3. Symptoms (Similar to Adrenal Crisis, Hypoglycemic Shock): Hypothermia, Bradycardia, Hypotension, Seizures, Hypoxia

    4. Treatment: Call EMS, Heat patient with blankets, Injection of 100-300 mg hydrocortisone, IV injections: T4, T3, levothyroxine


    NOTE: Avoid CNS/Respiratory depressants in Uncontrolled Hypothyroidism

    Pregnancy

    Treatment Considerations:



    1. Dental Tx: 2nd trimester or 1st half of 3rd trimester (weeks 14-32)

    2. Analgesic: Acetominophen (B), Ibuprofen (B, D3constriction of ductus arteriosus, post-partum hemorrhage, delayed labor)

    3. Local Anesthesia: Lidocaine (B) or Etidocaine (B), Mepivicaine (C)

    4. Antibiotics: Amoxicillin, Penicillin, Clindamycin, Metronidazole all class B

    5. Narcotics/Anxiolytics: AVOID – Hydrocodone (C/D3), Triazolam (X)

    6. Radiation exposure:

      1. Danforth9 in 1 billion chance of birth defect from FMX

    7. Risk Classifications:

      1. Human studies – no risk

      2. Animal studies – no risk or Animal – risk/Human – no risk

      3. Animal studies – risk/Human studies – no studies or Animal/Human – no studies

      4. Human studies – risk, drug may be used despite risk (situational)

    X. Human studies - Fetal harm outweighs possible benefit

    Pregnancy

    1. Nitrous Oxide (pregnant patient): 50% O2, <30 mins admin.

    2. Nitrous Oxide (pregnant employee):

      1. Rowland – Nitrous oxide exposure without scavenger (3 hour/week or more) increases the risk of spontaneous abortion

    3. Maximum radiation exposure for pregnant worker = 5 mSv/year


    Inferior Vena Cava Syndrome

    1. Definition:

      1. Prolonged supine position in late pregnancy places pressure on the inferior vena cava and drops blood return

    2. Symptoms:

      1. Intense pain on the R side, Muscle twitching, drop of blood pressure, and fluid retention

    3. Treatment:

      1. Turn patient on L side, monitor BP

    HIV/AIDS

    HIV: Human immunodeficiency virus, AIDS: Acquired immunodeficiency syndrome



    1. HIV: enveloped RNA retrovirus, infects most commonly CD4+ cells (TH, macrophages), entry-reverse transcription RNA-DNA-integration into host

    2. Transmission: Exchange of infected bodily fluids (blood, seminal/vaginal fluids, tears, breast milk, CSF, urine

    3. Stages:

      1. Stage 1: Acute seroconversion syndrome: 1-3 wks post-exp, symptoms: fever, nausea/vomiting, lymphadenopathy, CD4+ 500.

      2. Stage 2: Latent period: 8-10 years, asymptomatic, lymphadenopathy, steady decline in CD4+ 200-499 cells/L

      3. Stage 2: Early symptomatic stage: 1-3 years, Herpes Zoster, Oral hairy leukoplakia, Fungal infections. Signs/Symptoms increase as CD4+ count declines/approaches 200 cells/L, Platelet count 

      4. Stage 3: AIDS: opportunistic infections – Kaposis’s sarcoma, lymphoma, cancer. High viral load. CD4+ count <200/L

    HIV/AIDS

    1. Laboratory Counts:

      1. Stage 1 (acute seroconversion): CD4+ T cell count: 500 cells/L

      2. Stage 2 (latent/early sym): CD4+ T cell count: 200-499 cells/L

      3. Stage 3 (AIDS): CD4+ T cell count: <200 cells/L

    2. Dental Treatment:

      1. Stage 1: No modifications, Monitor CD4+ and viral load

      2. Stage 2: No modifications, Labs: CD4+, viral load, WBC/ CBC (est. immune status)

      3. Stage 3: Antibiotic coverage for surgical/invasive treatment (neutrophil count <500 cells/L), Emergency care only

      4. Avoid NSAIDs/ASA w/Thrombocytopenia

    3. Occupational Exposure:

      1. Risk: 0.3% (3 in 1000 sticks or sharps exposure)

      2. PEP: 4 weeks of 2 or 3-drug regimen ARTs

      3. Testing: baseline, 3 months, 6 months, 12 months

    4. Effect of HIV on NSRCT:

      1. Succhina; ShettyNo difference in success of NSRCT

    Allergies & Anaphylaxis

    Type 1: IgE Mediated – Anaphylactic:

    • Immediate response – Mast cells, Bradykinin (Vasodilation, Inc vas. Permeability)

    • Antigens: Allergens – dust, pollen, food, drugs

    • Symptoms: Anaphylaxis - Asthma, Urticaria (hives), Angioedema (face, throat)

    Type 2: Cytotoxic – IgG, IgM:

    • Antibody mediated – cytotoxic hypersensitivity

    • Ab bind to host cells recognized as foreign

    • Examples: Mismatch transfusions, Rh incompatibility

    Type 3: Immune complex mediated:

    • Immune complexes (Ab-Ag) lodge in vessel walls, incite inflammatory rxn, PMNs/macrophages, Complement activation

    • Examples: SLE, Erythema multiforme

    Type 4: Cell-mediated – Delayed Type:

    • T lymphocytes, No antibodies

    • Delayed response – 2 days after exposure

    • Examples: Contact dermatitis, Graft Rxn, Tb, Drug hypersensitivity

    Treatment: Call EMS, Supine positiion, 0.3-0.5 mL 1:1000 EPI IM or SC, IV Diphenhydramine (Benedryl – Antihistamine) 50-100 mg, Oxygen

    If angioedema/hives, w/ no throat or tongue swelling–50 mg Diphenhydramine oral 4x/day



    Rheumatological & Connective Tissue Disorders

    1. Rheumatoid Arthritis

      1. Autoimmune disease resulting in chronic systemic inflammation of the synovial joint spaces, destruction of the articular cartilage, and fusion of the joints, leading to severe loss of function/mobility

      2. Treatments: Methotrexate (anti-folate), Biologic agents (TNF- blockers, IL-1 blockers), NSAIDs, Steroids

      3. Lab tests: RF, Imaging of hands/feet

      4. Possible anemia, thrombocytopenia, secondary adrenal insufficiency

    2. Giant Cell Arteritis

      1. Inflammatory disease of the arterial wall, T cells/macrophages form granulomatous lesion within vascular wall

      2. Affects the External Carotid or Superficial Temporal artery

      3. Signs/Symptoms: Jaw pain, Fever, Throbbing Headache (unilateral/back of head), Scalp Sensitivity, Blurred/loss of vision

      4. Diagnosed by Biopsy/Histopathology (gold standard)

      5. Lab Tests: Sedimentation rate, C-reactive protein, ALP (liver)

    Giant Cell Arteritis

    **Commonly misdiagnosed as TMD!

    macintosh hd:users:matt:downloads:800px-cerebral_giant-cell_vasculitis.jpg

    Rheumatological & Connective Tissue Disorders


    1. Systemic Lupus Erythematosus

      1. Systemic autoimmune disease that attacks connective tissues throughout the body with a Type III Hypersensitivity rxn

      2. Involved organs: heart, lungs, skin, joints, blood vessels, liver, kidneys, CNS, may lead to athersclerosis and CAD

      3. Signs/Symptoms: Butterfly rash, Polyarthritis, Malaise, Fever

      4. Treatment: Immunosuppressants – cyclophosphamide, corticosteroids, DMARDs

      5. Lab tests: ANA, Immunofluorescence, Liver/Kidney enzymes, CBC

      6. Dental considerations:

        1. Leukopenia/corticosteroids – post op antibiotics

        2. Secondary adrenal insufficiency – corticosteroids

        3. Thrombocytopenia – platelet count; Anemia

        4. Possible cardiac, liver, and kidney impairment

    Prosthetic Joint Replacement


    1. Cover high-risk patients with prosthetic joints for invasive dental tx:

      1. Immunocompromised/Immunosuppresed with inflammatory arthropathies:

        1. Rheumatoid arthritis

        2. SLE

        3. MG

      2. Disease, drug, or radiation induced immunosuppresion

      3. Insulin dependent Type I Diabetes

      4. Hemophilia

      5. < 2 years post-joint replacement

      6. Previous prosthetic joint infection

    2. Antibiotic regimen:

      1. No allergy to Penicillins: Amox, Cephalex 2 g 30-60 mins prior

      2. Allergy to Penicillins: Clindamycin 600 mg 30-60 mins prior

      3. IV meds only: Ampicillin 2 g IM/IV or Clinda 600 mg IM/IV

    Organ & Bone Marrow Transplantation


    1. Medical Consulation Pre-Surgery:

      1. Patient status

      2. Need for Antibiotic prophylaxis

      3. Need for modification of drugs, anesthetics dosages

      4. Bleeding precautions

      5. CBC (platelets, WBC), INR/PT, aPTT, bleeding time

    2. Post-Transplantation Surgery:

      1. Defer elective tx for 6 months

      2. Medical consultation:

        1. Antibiotic prophylaxis

        2. Modification of dosages of drugs, anesthetics

        3. Bleeding: INR, PT, aPTT, CBC (WBC, RBC, …)

        4. Supplemental Steroids

    3. Heart transplant:

      1. Cover SBE for heart transplant with cardiac valvulopathy

    Red Blood Cell Disorders


    1. Sickle Cell Anemia

      1. Autosomal recessive (singe nucleotide mutation of -globin gene) inherited blood disorder resulting in abnormal sickling shape of RBCs (HbS) which have decreased elasticity and are susceptible to breakdown within capillaries




      1. Trait vs. Disease:

        1. Trait (carrier - HbS) = 1 allele (heterozygous), symptomatic only in oxygen deprivation/severe dehydration

        2. Disease (SCA - HbSS) = 2 alleles (homozygous), Anemic, intermittent vaso-occlusive crises




      1. Pathophysiology: low-oxygen tension, repeated sickling of RBCs, decreased elasticity, inability to deform in capillaries, leading to vaso-occlusion and ischemia (pain, necrosis – tissues, pulps)

    Red Blood Cell Disorders


      1. Lab Tests: Sickledex test (Initial test - detects HgS), hemoglobin electrophoresis (differentiates trait from disease); CBC, High reticulocyte count ( RBC production to compensate)



      1. Aplastic Crisis: (H.A.D.I.)

        1. Signs/Symptoms: 5-7 days, severe anemia  pallor, fatigue, tachycardia, reticulocytopenia

        2. Provoked by: Hypoxia, Acidosis, Dehydration, Infection

        3. Treatment: Blood transfusions




      1. Vaso-occlusive Crisis:

        1. Signs/Symptoms: Obstructed capillaries  ischemia, pain, necrosis, organ damage

        2. Provoked by: Hypoxia, Acidosis, Dehydration, Infection

        3. Treatment: NSAIDs, hospitalization

    Red Blood Cell Disorders

      1. Dental Considerations:

        1. Medical consultation for status

        2. Drug modifications:

          1. Monitor O2 Saturation: Want >95%

          2. Nitrous oxide: Okay, provide 50% O2

          3. Avoid Epi (non-surgical) – vasoconstrict/hypoxia

          4. Limit Epi (2 carps) – Surgery

          5. Avoid Narcotics, Barbiturates, Benzos, Flexaril (Respiratory Depression) – Hypoxia = crisis

          6. Avoid ASA/NSAIDs – Acidosis = crisis

        3. Aggressive management of infections (prevent crisis):

          1. I&D

          2. Antibiotics

          3. Endo, Ext

    NOTE: Prophylactic Abs for Sx – prone to infections, macrophages phagocytizing abnormal RBCs



    Red Blood Cell Disorders


    1. Aplastic Anemia

      1. Disease of bone marrow stem cells resulting in a deficiency of RBCs, WBCs, and platelets aka Pancytopenia (anemia, leukopenia, & thrombocytopenia)




      1. Diagnosis: Bone marrow biopsy




      1. Treatment: Immunosupression (corticosteroids, cyclosporine), Stem cell transplantation




      1. Dental Management: Med Consult, Severe pancytopenia – Emergency care only, Aggressive management for oral infections (antibiotics, supportive tx)



    White Blood Cell Disorders


    1. Leukemia

      1. Group of Tumors developing from malignant immature abnormal leukocytes

      2. Types: AML, ALL, CML, CLL; Lymphocytic (B cell lineage), Myeloid (undifferentiated lineage – RBC, WBC, or platelet)

      3. Complications: Crowding of immature leukocytes impairs development of RBCs, WBCs, and Platelets. This leads to the following:

        1. Anemia, Pallor (anemia)

        2. Susceptible to infections (neutropenia/leukopenia)

        3. Bleeding/clotting dysfunction (thrombocytopenia)

        4. Fever/Flu-like symptoms

        5. Splenomegaly, Hepatomegaly

      4. Diagnosis: CBC, Bone marrow biopsy

      5. Treatment: Chemotherapy, Radiation, Bone marrow transplant

    White Blood Cell Disorders


    1. Lymphoma

      1. Group of tumors developing from malignant Lymphocytes (B, T, NK cell), often times originating in lymph nodes, bone marrow, or spleen

      2. Major Types: Hodgkin’s, Non-Hodgkins, Multiple Myeloma

      3. Symptoms: Lymphadenopathy, Night Sweats, Fever, Fatigue, Weight Loss

      4. Diagnosis: Lymph node biopsy

      5. Histopathology: Reed Sternberg cells – “owls eyes” (HL only)

      6. Prognosis: HL (85%) > NHL (69%)

      7. Treatment: Chemotherapy, Radiation, Surgery

    White Blood Cell Disorders


    1. Multiple Myeloma

      1. Tumors developing from malignant Plasma cells (precursors to Abs), accumlate in the bone marrow and interfere with normal production of RBCs, WBCs, and platelets

      2. Signs/Symptoms: “CRAB” = Calcium (elevated), Renal Failure, Anemia (RBCs), and Bone pain; Infection (WBCs), Bleeding ( Platelets)

      3. Diagnosis: Serum electrophoresis, Bone marrow biopsy, Bence-Jones proteins (Urinalysis)

      4. Histopathology: Plasmacytoma

      5. Radiographic: “Punched Out” resorptive bony lesions (similar to 2 HPT/ESRD) throughout skeletal system (overexpression of RANKL in bone marrow)

      6. Treatment: Protease Inhibitors, Bisphosponates, Chemotherapy, Bone marrow transplant

    White Blood Cell Disorders
    Dental Management of WBC Disorders:

    • MED CONSULT: Immune status, Bleeding/Clotting Issues

    • Antibiotics: Pen VK 2g 1 hr prior + 500 mg 4x/day, 7 days

      • WBC < 2000 cells/L

      • Neutrophil count < 500 cells/L

      • 6 months post splenectomy (lymphoma patients)

    • Platelet transfusion:

      • Platelets <50,000 cells/L

    • Emergency care ONLY for advanced WBC disorders

    • Routine care for stable disease progression or state of remission

    Bleeding and Hypercoagulable Disorders

    AVOID ASA/NSAIDs in all bleeding/clotting disorders!



    1. Thrombocytopenia

    1. Definition: Abnormal decrease in platelet count <50,000 cells/L

    2. Clinical Signs/Symptoms:

    • Petechia, Purpura, Ecchymosis

    • Bleeding – nose bleeds, gingival bleeding

    • Malaise, Fatigue, Weakness

    1. Causes:

    •  Production: Vitamin B12 def. leukemias, AA, liver disease

    •  Destruction: SLE, HIV, Thrombotic Purpura

    • Medication Induced: Valproic Acid, Methotrexate, H2/PP inhibitors

    1. Lab Testing: Platelet count

    2. Dental Considerations:

    • Counts: Surgery >50,000, NSRCT >30,000

    • Avoid NSAIDs/Aspirin -  Bleeding due to  Thromboxane A2

    • Local hemostatic measures: Gelfoam/Collagen, Thrombin, Amicar

    Bleeding and Hypercoagulable Disorders


    1. Coumadin and Anti-coagulants

    1. Drugs: Coumadin/Warfarin, Heparin, Pradaxa

    2. MOA:

    • Coumadin: Inhibits liver synthesis of Vit K-dependent clotting factors: Factors 2 (Prothrombin), 7, 9, 10

    • Heparain, Pradaxa: Anti-Thrombin (II), Direct thrombin inhibitor

    1. Lab Values: INR (Coumadin only), PT time (Ext/Common)

    2. Dental Considerations:

    • INR (within 48 hours): < 3.0 (surgery), < 3.5 (NSRCT)

    • Med consult: bleeding control, INR, comorbid conditions

    • Delay treatment 2-3 days for  anti-coagulant

    • Avoid: Aspirin/NSAIDs, Metronidazole, Macrolides, Tetracyclines (CMT = Coumadin avoid Metro/Macro, Tetra)

    • Local hemostatic measures: Gauze, gelfoam, Collagen (plug/tape), Thrombin, Amicar, Tranexamic acid

    Bleeding and Hypercoagulable Disorders


    1. Hemophilia

    1. Hemophilia A (Factor VIII)

    • X linked recessive trait, Males predominately

    • Dysfunctional or  Production of Factor VIII

    • Signs/Symptoms: Spontaneous or prolonged bleeding episodes, bruising/ecchymosis, internal bleeding

    • Tests: Prolonged aPTT, Normal PT/TT/Platelets

    • Treatment: IV infusion Factor VIII, Desmopressin ( VWF/VIII)




    1. Hemophilia B (Factor IX/Christmas)

    • X linked recessive trait, Males predominately

    • Deficiency of Factor IX gene due to mutation

    • Signs/Symptoms: Same as Factor VIII defiicency

    • Tests: Same as Factor VIII, Prolonged aPTT/Normal PT/TT/Platelets

    • Treatment: IV Infusion Factor IX only, NO Desmopressin!

    macintosh hd:users:matt:downloads:350px-classical_blood_coagulation_pathway.png
    Bleeding and Hypercoagulable Disorders


    1. Von Willebrand’s Disease (vWD)

    1. Definition: Most Common inherited coagulaopathy (1 in 100), qualitative or quantitative deficiency in the vWF. Most Asymptomatic.

    2. vWF: Large glycoprotein that binds Factor VIII and Platelets, promotes platelet adhesion to vascular endothelium at the site of injury

    3. Types: 3 Forms: Hereditary, Acquired, Psuedo. 3 Types of Hereditary VWD: Type I (most common, 60-80%), II, and III with mulitple subtypes (II A, B, N, M)

    4. Clinical Signs/Symptoms: Prolonged bleeding, Bruising

    5. Lab Tests: vWF antigen assay - Type I (vWF 10-45 IUs), Factor VIII assay, aPTT time (elevated due to VIII def.), CBC, PT

    6. Treatment: Desmopressin (DDAVP = Syn. analog of ADH Vasopressin) – Type I, IIA only -  vWF/VIII (Intranasal/IV), Infusion Factor VIII, Blood transfusions (correct anemia and hypotension)


    Dental Considerations with Hemophilia and vWD


    • Medical Consultation!

    • Lab Values: aPTT, Factor VIII, IX, vWF assays, CBC, bleeding time

    • Avoid Aspirin/NSAIDs! -  Bleeding due to  Cox/Thromboxane A2

    • Pre-op Clotting Aids:

      • Desmopressin – Factor VIII, vWF only – releases vWF/VIII from vascular endothelium

      • Amicar, Transexamic acid – clotting stimulators

      • Factor VIII, IX, and vWF IV infusions

    • Avoid infiltrations/block injections for patients not on desmopression and/or IV Factor concentratesinternal bleeding risk

    • Local hemostatic measures – Collagen, gauze, Thrombin, Amicar

    • vWF Type I and some Type II may be managed in-office with Desmopressin. May require Infusions - Factor VIII/vWF




    Laboratory findings in various platelet and coagulation disorders (V - T)

    Condition

    Prothrombin time

    (PT)

    Activated Partial thromboplastin time

    (aPTT)

    Bleeding time

    Platelet count

    Vitamin K deficiency or warfarin

    Prolonged

    Normal or mildly prolonged

    Unaffected

    Unaffected

    Disseminated intravascular coagulation

    Prolonged

    Prolonged

    Prolonged

    Decreased

    Von Willebrand’s disease

    Unaffected

    Prolonged or unaffected

    Prolonged

    Unaffected

    Hemophilia

    Unaffected

    Prolonged

    Prolonged

    Unaffected

    Aspirin

    Unaffected

    Unaffected

    Prolonged

    Unaffected

    Thrombocytopenia

    Unaffected

    Unaffected

    Prolonged

    Decreased

    Liver failure, early

    Prolonged

    Unaffected

    Unaffected

    Unaffected

    Liver failure, end-stage

    Prolonged

    Prolonged

    Prolonged

    Decreased
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