Medically compromisd Patient (Anous).pdf

Approaches to the Medically Compromised Patient Medical History - Consideration of systemic diseases is an essential step before treating patients and performing procedures. - All practitioners should ensure that the medical history is: Completed and/or reviewed at the start of treatment W...

Approaches to the Medically Compromised Patient Medical History - Consideration of systemic diseases is an essential step before treating patients and performing procedures. - All practitioners should ensure that the medical history is: Completed and/or reviewed at the start of treatment Well documented Regularly updated In general, all patients can be classi ed according to the American Society of Anesthesiologists (ASA) Physical Status Classi cation System: ASA I, II —> Outpatient Setting ASA III —> Outpatient at the discretion of the operator, with the appropriate precautions ASA IV —> Hospital Setting ASA V/VI —> Not applicable 1 of 34 fi fi  Cardiovascular Disease Hypertension De ned as sustained pressures equal or greater than 130/80 Approximately 1 in 4 people su er from high blood pressure People may live asymptomatically for years but eventually can experience symptomatic damage to the kidneys, heart, brain & eyes. (Silent killer) Primary (essential) hypertension (90%) —> idiopathic Secondary hypertension (10%) —> underlying cause/condition may be identi ed Sleep apnea Chronic steroid therapy or Cushing syndrome Drug-induced/related Pheochromocytoma Chronic kidney disease, primary Coarctation of the aorta aldosteronism, renovascular disease Thyroid/parathyroid disease Lifestyle plays an important role: obesity, excessive alcohol intake, excessive dietary sodium, physical inactivity are signi cant contributing factors Every increase in BP 20 mm Hg systolic and 10 mm Hg diastolic doubles the mortality related to ischemic heart disease and stroke Guidelines Systolic blood pressure (SBP) —> pressure at peak ventricular contraction Diastolic blood pressure (DBP) —> total resting resistance in the arterial system after passage of the pulsating force produced by contraction of the left ventricle Pulse pressure (PP) = SBP - DBP Mean arterial pressure (MAP )= DBP + (PP x 1/3) 15-20% of patients with untreated stage I hypertension have “white coat hypertension” Signs and Symptoms Early: Elevated blood pressure readings Narrowing & sclerosis of retinal arterioles Headache, dizziness, tinnitus Advanced: Rupture & hemorrhage of retinal arterioles. Papilledema Left ventricular hypertrophy, congestive heart failure, angina pectoris Renal failure, proteinuria Dementia, encephalopathy 2 of 34 fi fi ff fi  Hypertensive urgency: is a clinical situation in which blood pressure is very high (e.g., ≥180/≥110 mmHg) with minimal or no symptoms, & no signs or symptoms indicating acute organ damage. Hypertensive Emergency: severe elevation in BP with evidence of impending or progressive target organ dysfunction - (Hypertensive encephalopathy, intracerebral hemorrhage, acute MI, left ventricular failure with pulmonary edema, or unstable angina pectoris) Considerations: Identify patients with hypertension Diagnosed or undiagnosed, medications, compliance, presence of signs or symptoms Stress reduction —> Oral sedation, nitrous oxide Limit epinephrine use Intraoperative monitoring Antihypertensives including diuretics/Thiazides, Beta blockers, ACE inhibitors, ARBs, CCBs Watch for orthostatic hypotension, avoid prolonged use of NSAIDs 1. Risk imposed by the patient’s cardiovascular disease: Major Risk Factors: Unstable coronary syndromes (acute or recent MI, unstable angina), decompensated heart failure, signi cant arrhythmias, severe valvular disease Intermediate Risk Factors: History of IHD, history of compensated or previous heart failure, history of cerebrovascular disease, diabetes mellitus, renal insu ciency Minor Risk Factors: Advanced age (>70 years), abnormal ECG, rhythm other than sinus rhythm, uncontrolled systemic hypertension (>180/110 mm Hg) 2. Risk imposed by the procedure: High Risk (>5% risk): prolonged procedures, excessive blood loss, GA. Intermediate Risk ( new-onset pain, increasing in frequency/intensity, precipitation by less e ort than prior events, or pain that occurs at rest. Key feature = changing character of the angina episode Not relieved by rest Nitroglycerin If the pain is more severe, lasts longer than 15 minutes, the use of vasodilators or cessation of activity does not resolve symptoms —> likely an acute MI If acute MI suspected MONA Management of acute chest pain M orphine: 2 mg IV or 5 mg IM O xygen N itroglycerin: 0.3, 0.4 or 0.6 mg sublingual tablet, or 0.4 mg sublingual spray A SA: 325mg uncoated chewable 4 of 34 ff fl fl ff fi ff More info: - Oxygen, Use 4 L/min nasal cannula; titrate as needed to keep oxygen saturation to 94-99%. - ASA, if no allergy, give 160 to 325 mg ASA to chew. - Avoid coated ASA. - Ideally, baby aspirin is the aspirin of choice. - GTN, give 0.3 to 0.4 mg SL/spray x two doses at 3 to 5-minute intervals, Do not use if SBP Be aware of orthostatic hypotension Maybe of antiplatelets or anticoagulants Patients may be on Digoxin Avoid benzodiazepines —> serum levels of Digoxin may be increased Avoid excessive use of vasoconstrictors —> may precipitate arrhythmias Untreated/symptomatic heart failure increases the risk of MI, arrhythmias, acute heart failure or sudden death 6 of 34 fi fi fl fi fi  Duke Activity Status Index (DASI): 12-item questionnaire that uses self-reported physical work capacity to estimate peak metabolic equivalents (METs) Higher score = higher functional capacity More perimeters than the NYHA and thus suggested to be more precise 1 MET= 1 kcal/kg/hr 1 MET = 3.5 ml/kg/min —> oxygen consumption at rest Infective Endocarditis Microbial infection of the endothelial surface of the heart or heart valves Mortality rate in the US = 40% Classi cation by: Causative microorganism: Streptococcal candida endocarditis staphylococcal Type of valve e ected: Native valve endocarditis (NVE) Prosthetic valve endocarditis (PVE) Source of infection: Community-acquired/hospital-acquired intravenous drug use (IVDU) Di cult to treat so emphasis is on prevention Signs and Symptoms: Fever Heart murmur Positive blood cultures are classic ndings Peripheral manifestations – less common with the advent of antibiotics Osler’s nodes – subcutaneous nodules of digits Janeway lesions –petechiae of palms and soles Splinter hemorrhages in the nail beds Roth spots – oval retinal hemorrhages Splenomegaly Clubbing of the digits 7 of 34 ffi fi ff fi American Heart Association (AHA) Guidelines: Prosthetic cardiac valve OR prosthetic material used for valve repair Previous infective endocarditis Congenital heart disease (CHD): Unrepaired cyanotic CHD, including palliative shunts and conduits Truncus Arteriosis Tetralogy of Fallot Transposition of the Great Arteries Total Anomalous Tricuspid Valve Atresia Pulmonary Venous Return Completely repaired CHD with prosthetic material or device during the rst 6 months after the procedure (endothelialization of prosthetic material occurs within 6 months after the procedure) Repaired CHD with residual defects to the site of a prosthetic patch or prosthetic device Cardiac transplantation recipients who develop cardiac valvulopathy 8 of 34 fi  Pulmonary Disease A. Asthma “Wheezing” In ammatory chronic obstructive lung disease De ned as: chronic airway in ammation, temporary expiratory air ow obstruction and bronchial mucosal reactivity A ects approximately 7% of the population Overt attacks can be: provoked by allergens, Exercise Smoke Upper respiratory tract Cold air, Highly emotional states. infection Chemicals Certain medications (salicylates, NSAIDs, cholinergic drugs, beta blockers) Greatest risk factor is atopy – often seen in patients with eczema, urticaria and rhinitis Classi cation (mild, moderate, severe) based on: Frequency of symptoms Impairment of lung function Risk of attacks Mild —> symptoms once per week, FEV1 greater than 80% Moderate —> daily symptoms that a ect sleep or activity level, requiring occasional emergency care, FEV1 between 60-80% Severe —> ongoing symptoms that limit normal activity, FEV1 less than 60% Management: Control airway in ammation with steroids (inhaled or systemic), anti-leukotrienes, and theophylline Rescue relief during acute phases (beta-adrenergic agonists) Preoperative: Evaluation of poorly controlled disease (recent hospital visits, use of short- acting inhalers, recent need for oral corticosteroids) Auscultate lungs, look for use of accessory muscles (SCM, scalenes, pectoarlis major and minor, serratus posterior – superior and inferior) Continue all medications Considerations: Avoid drugs that induce histamine release, respiratory depression Natural Narcotics Succinylcholine NSAIDs/aspirin not advisable (small percentage (8-20%) of patients have precipitation of asthma attacks) Common in-o ce medications are safe Propofol = bronchodilator, ketamine = smooth muscle relaxation Consider low- ow supplemental O2 (2-3L/min) Chair positioning: Semi-supine or upright chair position may be better tolerated Instruct patient to bring the inhaler each visit & use prophylactically in moderate-severe cases In case of emergency: Tachypnea (>25 breaths/min), tachycardia, diaphoresis, accessory muscle usage Use fast-acting bronchodilator (repeat every 20 mins), O2, +/- epinephrine (1:1000) 0.3 - 0.5 ml SQ Activate EMS 9 of 34 ff fl fi fi ffi fl fl fl ff fl  B. Smoking Decreases O2 delivery to tissues (preferential binding of CO) Nicotine is a sympathomimetic and thus can elevate metabolism Cardiac e ects Risk factor for CVD CO decreases oxygen delivery and thus increases myocardial work Release of catecholamines resulting in coronary vasoconstriction Decreases exercise capacity Respiratory e ects Major risk factor for chronic obstructive pulmonary disease (COPD) Decrease in mucociliary activity Airways become hyperreactive Decrease in pulmonary immune function Surgical considerations: Compromise healing and causes complications Advisable to initiate smoking cessation 4 weeks prior to surgery Immediate cessation before surgery: Can increase: sputum production irritability sleep disturbances nicotine withdrawal restlessness anxiety However, can improve carboxyhemoglobin levels and improve oxygenation Electric Cigarettes: Major components: nicotine, propylene glycol, glycerol and avoring E-cigarettes shown to have no statistically signi cant di erence in ap Both cigarettes and e-cigarettes showed a signi cant increase in ap necrosis in comparison to the negative control group (non-smoking group) Decreased endothelial cell proliferation, cytotoxic to endothelial cells, reduced cutaneous blood ow, increases H2O2, decrease in epithelial, alveolar macrophage and neutrophil anti- microbial activity, upregulation of in ammatory markers. C. Chronic Obstructive Pulmonary Disease (COPD) Respiratory disease involving the conducting airways as well as the alveoli Strongly attributed to smoking 1/5 smokers will develop COPD (genetic susceptibility to the production of cytokines to cigarette smoke?), Smoking Accounts for 85-90% of COPD related deaths Chronic airway obstruction involving two distinct disease processes causing decreased air ow 1- Chronic bronchitis – in ammation/infection “Blue bloaters”:chronic productive cough, frequent respiratory infections Chronic hypoxemia causes respiratory acidosis, pulmonary hypertension, right sided heart failure, and secondary erythrocytosis 2- Emphysema – alveolar destruction “Pink pu ers”, distant breath sounds, hyperlucency on chest x-ray. Alveolar walls and pulmonary capillaries are destroyed – reduces oxygen di usion capacity but does not lead to pulmonary vasoconstriction & secondary e ects 10 of 34 fl ff ff ff fl fl fi fi ff fl ff fl fl ff fl  Medical Management Smoking cessation bronchodilators in uenza lifestyle changes pneumococcal vaccinations low ow O2 Examples: Anticholinergics (eg. Ipratropium): Reduce glandular mucous, relax smooth muscle by blocking Ach at muscarinic receptors B2- adrenergic bronchodilators: Relax smooth muscle by increasing cAMP levels Phosphodiesterase inhibitors (eg. Theophylline): Narrow therapeutic range Phosphodiesterase-4-selective inhibitors (eg. Cilomilast, ro umilast): Reduces exacerbations Considerations O2 at 2-3L/min with pulse oximeter monitoring Caution in patients with advanced disease – pts have adapted to hypercarbic state, rely on this for the respiratory drive (hypoxemic drive) —> patients may become bradypnic Avoid nitrous oxide - can accumulate in air spaces of the diseased lung Avoid narcotics – respiratory depression Avoid morning appointments: Increased coughing due to accumulated mucus overnight Chair positioning, reduce stress 11 of 34 fl fl fl  D: Obstructive Sleep Apnea Common disorder characterized by recurrent episodes of partial (hypopnea) and complete (apnea) upper airway obstructions Risk factors: Obesity, being male Age (>45 years old) Increased neck circumference Family history Narrowed airway Comorbidities: Hypertension Stroke Pulmonary hypertension Diabetes Heart failure Nutritional de ciencies Dysrhythmias Fatty liver in ltration MI Diagnosis done by —> sleep study, evaluation of the apnea-hypopnea index (AHI) along with questionnaires, & HPE It could be: Mild(≥5to30) Medical management: Behavior /medical modi cation Positive airway pressure Oral appliances and/or surgery Considerations: Di cult bag-mask ventilation Di cult intubations and desaturate more quickly due to decreased functional residual capacity Avoid opioids – respiratory events can occur even 1 week after anesthesia Consider admission overnight after general anesthesia 12 of 34 ffi ffi fi fi fi  Gastrointestinal Disease A. Gastroesophageal Re ux Disease (GERD) Decreased tone of the cardiac esophageal sphincter Gastric contents re ux into the esophagus causing retrosternal discomfort (heartburn) Management H2-antagonists (eg. Ranitidine) Proton-pump inhibitors (PPIs) (eg. Pantoprazole) Considerations: Avoid supine or Trendelenburg positions Advise to take medications the day of the procedures Avoid NSAIDs Patients on some H2-anatagonists or PPIs may: Reduce the absorption of ampicillin May increase the concentration of benzodiazepines, warfarin, and phenytoin Liver diseases Viral Hepatitis Alcohol fatty liver Autoimmune hepatitis Gallstones & cholecystitis Primary Biliary Cirrhosis Ascites Primary Sclerosing Cholangitis SBP (Spontaneous bacterial peritonitis) Hemochromatosis Hepatorenal Syndrome Wilsons Encephalopathy Liver Enzymes Liver function tests (LFTs) ALT (alanine transaminase) AST, also called (serum glutamic oxaloacetic transaminase, SGOT) Alkaline Phosphatase Bilirubin Chronic Liver Disease Chronic liver diseases are classi ed based on etiology: Viral hepatitis Autoimmune hepatitis Drug-induced Hepatitis,(e.g. Acetaminophen)hepatitis Alcoholic hepatitis... others Symptoms: Malaise, jaundice, ascites or cirrhosis Pruritus Fatigue Easy bleeding or bruising Nausea Hemorrhagic diathesis, Vomiting, Abdominal distension Hematemesis Altered mental status Patients with cirrhosis and end-stage liver diseases may have comorbidities: Hepatic encephalopathy, Hepatorenal syndrome, Pleural e usions, Portal hypertension Hepatopulmonary syndrome 13 of 34 ff fl fl fi CAUSES OF CIRRHOSIS Alcohol Primary Biliary Cirrhosis Alpha 1 antitrypsin de ciency Viral B/C Sclerosing Cholangitis Budd-Chiari dis. Cryptogenic Hemochromatosis Autoimmune Wilsons Stigmata of liver disease HANDS: Palmar Erythema Leuconychia Clubbing FLAPPING TREMOR (Asterxis) Dupytrens contracture HEENT/UPPER BODY Jaundice Gengivitis/periodontitis Spider Angiomata (nevai) Foetor hepaticus Parotdiitis Gynaecomastia & scant body hair Temporalis waste Scratch marks ABDOMEN Ascites Distended abdomen veins Small testes Hepatospleenomegally Esophgeal varices Caput Medusa Hemorrhoids on PR Oral Manifestations Nutritional def. result in glossitis & loss of tongue papillae, along with angular/labial cheilitis, which is complicated by concomitant candidal infection Spontaneous gingival bleeding, mucosal ecchymosis & petechiae. Sialadenosis of parotids Increase risk of squamous cell carcinoma Lichen planus associated with Hep. C Parotid lymphoma in HCV Sjogren's syndrome Complications ( Portal Hypertension) causing: 1. Variceal bleed (esp. lower esophygeal veins), blood drain via di. pathways avoiding the liver 2. Splenomegaly causing low platelets (thrombocytopenia) 3. Ascites 4. Encephalopathy 5. SBP (Spontaneous bacterial peritonitis) 6. Hepatorenal syndrome 14 of 34 fi ff Ascites Accumulation of free uid in peritoneum: Decrease plasma oncotic press. due to low Albumin Fluid retention due to dec. the liver metabolism to the aldosterone Portal HTN Assessment involves taking sample of uid & checking albumin content SAAG: Serum Ascites Albumin Gradient —> SAAG = Serum Albumin – Ascites Albumin Acne rosacea – (red pimples around the nose, cheeks and chin) Considerations: Decreased ability to metabolize drugs – lower requirement and longer half-life Benzodiazepines require a longer recovery Ketamine should be avoided (build-up of secondary metabolites, reduced elimination) Opioids–prolonged elimination half-lives and active metabolites, avoid in outpatient treatment Avoid acetaminophen and codeine in patients with End stage renal disease (ESLD) Avoid metronidazole, vancomycin Increased risk of bleeding – reductions in coagulation factors, thrombocytopenia May need vitamin K, platelet or clotting factor replacement If Hepatitis B &/ C risk of infection Risk assessment using the Child-Pugh score Contraindications to elective surgery in patients with liver disease: Acute alcoholic hepatitis Sudden hepatic failure Acute viral hepatitis Severe chronic hepatitis Child-Pugh class C cirrhosis Severe coagulopathy (prolongation of prothrombin time >3s despite vit K admin.) Severe extrahepatic complications Acute renal failure Cardiomyopathy, heartfailure Hypoxemia * Perioperative mortality rates signi cantly increase with increasing Child- Pugh classi cations The AAA (Abdominal Aortic Aneurysm) 1. Bleeding tendencies 2. Unpredictable metabolism of certain drugs 3. Increase tolerance to local anesthetics, sedative and hypnotic drugs, and general anesthesia. 4. Risk or spread of infection. 1. Impaired reticuloendothelial capacity. 2. Abx prophy is recommended. Pugh Class B or C. 15 of 34 fl fi fl fi History and physical: SOAP note Subjective Intro MEDs, supp., Vit. C/o All, include reactions HPI SHx, tobacco, EtOH, rec. drugs PMHx FHx PSHx, list Sx, anesth. ?comp. Signs and symptoms: Fever Rubor (redness) Chills Dolor (pain) Fatigue Calor (heat of site) Malaise Tumor (swelling) Night sweat Reveiw of systems CNS: HA, N/V, dizziness, focal neuro. de cit CVS: CP, SOB, exercise tolerance, palpatations Resp.: cough, dyspnea, phlegm, hemoptysis GI: Hematemesis, diarrhea, melena , hematochezia, cramps, ab pain GU: Hematouria, dysuria, polyuria Endo: thyroid, goitre, DM, MSK: Joint, mus. Pain., restrict ROM neck/back, weakness Skin lesions Objective On examination Vitalsigns BP RR HR O2 Sat TEMP Extra oral exam: signs of inf. (rubor, calor, dolor, tumor) Mus. of mastication Trismus TMJ Palpate for enlarged lymph nodes Intraoral: OH Dischrge Soft tissue teeth Sweliing Labs: CBC: ESR Electrolytes Blood culture BUN, Cr C&S CRP Radiographs: OPG, PA, CBCT 16 of 34 fi  Genitourinary Disease Chronic Kidney Disease Progressive loss of renal function GFR < 60 ml/min) for three months or longer Most caused by diabetic nephropathy, followed by hypertensive nephrosclerosis Once GFR drops below 15 ml/min – end-stage renal disease (ESRD) Stage V Check, Cr, BUN, GFR, lytes balance Manifestaions (Uremia Vs Azotemia): Hyperkalemia, hyperphosphatemia, hypocalcemia Metabolic acidosis Anemia (increased cardiac output) Uremic coagulopathy (increased bleeding time, platelet dysfunction) Neurologic changes Cardiovascular changes – CHF, dyslipidemia, HTN Renal osteodystrophy Pruritus Considerations: Patients with CKD often undergo dialysis 3x per week Treatment on non-dialysis days (preferably the day after) Be aware of AV stulas Use caution with benzodiazepines Metabolized by the liver but eliminated by the kidneys Diazepam – active metabolites, best to avoid Oral benzodiazepines for anxiolysis should be avoided due to inability to titrate Monitor uid administration (250 ml reasonable) Avoid Lactated Ringers (contains K+), D5 1⁄2 NS preferred Avoid use of NSAIDs & reno-toxic meds Medication doses may need to be adjusted depending on severity of CKD 17 of 34 fl fi List of medication that are used in the dental o ce and their dosage adjustment for renal failure patients 18 of 34 ffi  Endocrine & Metabolic Diseases Diabetes is a chronic disorder of: carbohydrate fat protein characterized by hyperglycemia & other metabolic derangements Caused by inadequate action of insulin on body tissues, due to either: reduce circulating levels of insulin or resistance of target tissues to its actions Insulin Function: Transfer glucose from blood to cells- dependent tissues Stimulate transfer of amino acids from blood to cells Stimulate triglyceride synthesis from fatty acids Inhibit breakdown of triglycerides for mobilization of fatty acids Classi cations A. Type I (IDDM): - 10% of diabetic patients - juvenile onset - polyuria, polydipsia, polyphagia, wt. loss & incontinence - Complete or almost complete absence of insulin - Without insulin —> ketoacidosis - Occurrence in children & young adults - Lean rather than obese Weak genetic component - HLA- D region involved in the susceptibility to type I diabetes - Environmental trigger —> virus = congenital rubella, CMV, mumps, hepatitis, coxsackie virus - Autoimmune response to beta cells of the pancreas B. Type II (NIDDM): adult onset - slight wt loss or gain, nocturnal awakenings to void - Some insulin is produced - Ketoacidosis does not occur - HHS (Hyperosmolar Hyperglycaemic State) more common - Insulin therapy in severe hyperglycemia - Occurrence in adults older than 40 years of age - Secondary diabetes: gestational, steroids, tumor, or pancreatic resection patients - Strong genetic component - Increased insulin resistance (precursor) - decreased post-receptor activity (major) - Decreased receptors (minor) - Decreased insulin secretion in later stage of the disease - Increased in alpha/ beta cell ratio —> excess glucagon secretion over insulin - Strong relationship to obesity 19 of 34 fi  Physiologic e ect of chronic uncontrolled DM Cortisol secretion- protein breakdown & loss in urine Body shifts to fat metabolism fatty acids metabolized through Kreb's cycle excess acetoacidic acid, beta-hydroxybutyric acid, excreted into the urine Respiratory, renal regulators & bu er systems fail —> patient becomes acidotic (ketoacidosis) Chronic complications of Type I Retinopathy - retinal hemorrhages (HTN) Neuropathy - stocking glove distribution Autonomic neuropathy - impotence, neurogenic bladder Nephropathy - account for 25% of all new cases of End stage renal disease (ESRD) Vascular disease - non-healing foot ulcers, lower extremity amputations Coronary disease - atherosclerosis, HTN Enteropathy - decreased GI motility Micro/Macro-angiopathy: Ketoacidosis (typeI) Hyperglycemia(>27),aniongap metabolic acidosis, & ketonemia Hyperosmolar hyperglycemic nonketotic coma (type II) Diabetic retinopathy - blindness Cataracts Diabetic nephropathy - renal failure Accelerated atherosclerosis Coronary heart disease Stroke Ulceration and gangrene of feet Diabetic neuropathy: Dysphagia impotence numbness Gastric distension muscle weakness tingling diarrhea cramps, deep burning pain Early death Managment of Diabetic ketoacidosis: IV FLUID Fluid replacement INSULIN Isotonic uids (normal saline or lactated Ringer's) at 1 liter/hr K+ (drops after insulin) 1⁄2 NS at 150-250 cc/hr Insulin Hco3 Insulin: Continuous IV infusion with frequent monitoring Potassium replacement Potassium replacement: initially K+ is high but drops with aggressive IV insulin treatment Bicarbonate: acidotic, as raise pH, then K+ decreases Physical exam to nd underlying cause Treatment Aggressive IV hydration —> Normal Saline until Infusion 0.14U/kg/hr – 10U/hr Potassium Replacement Bicarbonate therapy Severe acidosis Cardiac Instability Serum Glucose q1h Lytes/venous pH/osmolal. q2-4h 20 of 34 fl ff fi ff  Complication of DKA Management Hypoglycemia Arterial thrombosis Lactic acidosis Hypokalemia Cerebral edema Acetone breath / Keto acids Blood [Acetoacetic acid] Greatly increased in severe diabetics Converted to acetone Early diagnostic tool Keto acids Usually not produced in excessive amounts Severe insulin resistance / increased fat utilization Symptoms Of Diabetic ketoacidosis: Manifestations evolve rapidly over 24hr N/V Polyuria/dipsia Altered Mental Status Dehydration Kussmaul’s respiration HTN **When pH falls below 7.0 – acidotic coma & death can occur in hours Nonketotic hyperosmolar hyperglycemia As opposed to DKA, predom. Older DM II pts Same predisposing factors Higher mortality rate Symptoms: Severe dehydration & Neurological signs Signi cant hyperglycemia and serum osmolality No anion-gab metabolic acidosis/ketosis Treatment Aggressive rehydration with NS and potassium replacement Insulin bolus/infusion Oral complications Uncontrolled Diabetes Mellitus Xerostomia Poor healing Infection Burning mouth syndrome Increased incidence and severity of periodontal disease Oral fungal infections (Candida, mucormycosis) Enamel hypoplasia (mother diabetic) Infection & Wound Healing Di culty managing infections hyperglycemia reduces chemotaxis & phagocytic action of granulocytes hyperglycemia facilitates growth of certain microorganisms Impaired wound healing ketoacidosis inhibits migration of granulocytes vascular wall changes, vascular insu ciency, decreased blood ow & reduced oxygen tension leading to impair healing 21 of 34 ffi fi ffi fl Tissue that can utilize glucose without the help of Insulin Brain Intestinal mucosa Renal Cortex Lens RBC **Muscle, Fat & Liver require insulin to utilize glucose from the blood Rapid (humalog/novolog/novolin): covers insulin needs for meals eaten at same time as injection Regular(R) – humulin 3-8hr duration - for meals eaten within 30-60m Intermediate NPH (N) (neutral protamine Hagedorn) covers needs for about half the day or overnight Long – cover needs for one day. Like NPH, usually combined when needed with rapid/short acting (lantus / levemir) lantus – insulin is delivered at a steady state level Pre-mixed (either humulin/rapid) usually 70/30, 50/50 or 75/25 Diagnosis of Diabetes Mellitus Urinary Glucose —> Proportional to severity and carb intake Fasting Blood Glucose/Insulin 4.5-5.0 normal FBG 5.5-7.0 pre-diabetic state DMI: Low/undetectable insulin DMII: Severalfold higher baseline Increases to a greater extent after standard glucose load Diagnosis of Diabetes Mellitus Glucose Tolerance Test 1gm glucose/kg body weight Normal 5mmol/L —> 6.5-7.5 Should fall back to normal in 2 hours Diabetic Baseline: 6 - 7.5 -> much greater rise Fall after 4 - 6 hours Fails to fall below control level Treatment Insulin preparations Fast-acting – regular and semilente Intermediate – NPH and lente Prolonged – protamine and ultralente Often an exam question (hold fast acting forms the AM of surgery, consider 1/2 dose of prolonged forms the night prior) Lantus ( base line ) 22 of 34 Oral hypoglycemics Metformin (Glucophage) – decreased hepatic gluconeogenesis production and intestinal absorption Glyburide (sulfonylurea) – stimulates insulin release form beta cells Can delay wound healing by producing: Leukopenia Thrombocytopenia Increased bleeding Exacerbate wound infections Short acting agents held the day of surgery Long acting agents held the day before surgery OMFS Management Surgical risk assessment: Disease control (HgA1c) target is 6 hours (avoid hypoglycemia (ACC) Gastroparesis & risk of aspiration Early am appointment Surgical Management Diabetes Mellitus type II A. Controlled with an oral hypoglycemic: Discontinue the meds the day of surgery Long acting should stop the day before B. Pre, intra and post op. management: 1. Measurement of glucose ( pre & intra-operatively for long surgeries & after the procedure) 2. Hyperglycemia treated with short acting insulin SC 3. Sliding scale insulin if glucose exceed and remain above 13.5 mmol/l 4. Patient should consume some calorie by mouth within 3 hours after surgery is completed. 5. Once the patient tolerate PO intake restart the medications Hypoglycemic: Mild: Hunger Pallor Weakness Sweating Tachycardia Paraesthesis Severe (life threatening ) Unconsciousness Hypothermia Tonic or clonic movements Rapid thready pulse Hypotension Hypoglycemia ( Addison’s Disease Destruction of the adrenal cortex leading to de ciency of all of the adrenocortical hormones Lack of cortisol and aldosterone Impaired metabolism of glucose, fat, and protein, as well as hypotension, increased ACTH secretion, impaired uid excretion, excessive pigmentation and an inability to tolerate stress adults —> adrenal suppression is probable Secondary (More common) Consequence of hypothalamic or pituitary disease Critical illness or the administration of exogenous corticosteroids High levels of cortisol altering the proteins, carbohydrate and fat metabolism, 24 of 34 ffi ffi fl fi  Addison’s disease may undergo an adrenal crisis if challenged by stress: Sunken eyes cyanosis headache myalgias profuse sweating nausea dehydration arthralgia hypotension vomiting fever hyponatremia weak pulse weakness dyspnea eosinophilia If not treated rapidly, the patient may develop hypothermia, severe hypotension, hypoglycemia, confusion, and circulatory collapse that can lead to death. Adrenal crisis is less common in secondary adrenal insu ciency as aldosterone secretion is normal Thus, hypotension, dehydration and shock are rare Considerations: Stress reduction! Primary - supplemental glucocorticoids may be required pre-op/post-op Secondary – patients should receive only their usual daily dose of corticosteroid b/4 surgery Patients who take daily equivalent/lower doses of steroid (5-10 mg equivalents of prednisone daily) on a long term basis typically maintain adrenal function and do not experience adverse outcomes after surgery Intra-op BP monitoring Post-op pain control is crucial to avoid adrenal crisis Post-op monitoring for 24 hours Fluid balance, blood pressure Check-in 4 hours post-op to check for symptoms 25 of 34 ffi  Thyroid Diseases A. Hashimoto’s Thyroiditis Autoimmune disorder that manifests most often as an asymptomatic di use goiter Lymphocytes replace functioning tissue leading to hypothyroidism B. Hypothyroidism Signs and symptoms: Dull expression dry brittle and coarse hair mental decline pu y eyelids increase in tongue size dry and rough skin cold sensitivity Considerations: Untreated hypothyroidism – sensitive to the actions of narcotics, barbiturates, and tranquilizers Stressful situations (cold, operations, infections or trauma) can precipitate a hypothyroid (myxedema) coma —> severe myxedema, bradycardia, severe hypotension C. Hyperthyroidism (Graves’ Disease) Autoimmune disease in which thyroid stimulating Igs bind to activate thyrotrophic receptors which increase gland growth and thus increase synthesis of T3 and T4 Signs and symptoms Nervousness heat intolerance fatigue weight loss rapid heartbeat/palpitations Atrial brillation in 20% of older patients D. Thyroid Storm Precipitating factors – infection, trauma, surgical emergencies, operations Early S/S: extreme restlessness, N&V, abdominal pain Later S/S: fever, diaphoresis, tachycardia, arrhythmias, pulmonary edema, and congestive heart failure. Coma may follow. Severe hypotension develops and death may occur Treatment: Antithyroid drugs (propylthiouracil), potassium iodide, propranolol, hydrocortisone, dexamethasone, IV glucose, vitamin B complex, wet packs, fans and ice packs Considerations: Avoid epi in poorly controlled patients Monitor BP NSAIDs may increase the amount of circulating T4 (use appropriately) 26 of 34 ff fi ff 27 of 34 Pregnancy & Breastfeeding First trimester = organogenesis Fetus most susceptible to malformation Avoid treatment in the rst trimester Patients may be insulin resistant (gestational DM) Breastfeeding: Most drugs prescribed will have little/no e ect on milk supply or infant Considerations: Use lidocaine for local anesthetic (Avoid articaine, bupivacaine, mepivivaine) Avoid category C or D antibiotics Acetaminophen is the analgesic of choice Supine hypotensive syndrome Caused by impaired venous return due to compression of the inferior vena cava Sings and symptoms: Abrupt fall in BP nausea bradycardia weakness and air hunger in the supine sweating position Treatment: Roll patient to their left side Category A: Controlled studies in humans have failed to demonstrate a risk to the fetus, and the possibility of fetal harm appears remote. Category B: Animal studies have not indicated fetal risk, and human studies have not been conducted, or animal studies have shown a risk, but controlled human studies have not. Category C: Animal studies have shown a risk, but controlled human studies have not been conducted, or studies are not available in humans or animals. Category D: Positive evidence of human fetal risk exists, but in certain situations, the drug may be used despite its risk. Category X: Evidence of fetal abnormalities and fetal risk exists based on human experience, and the risk outweighs any possible bene t of use during pregnancy 28 of 34 fi fi ff 29 of 34  Oncologic Considerations A. Cancer – Radiation & Chemotherapy Goal is to reduce risk of infection or osteoradionecrosis (ORN) Risk of ORN is greatest in: posterior mandible In patients who have received radiation doses >65 Gy Those who continue to smoke Those who have undergone a traumatic (eg. Extraction) procedure Considerations: Avoid epinephrine (to minimize hypovascularity after radiotherapy) Consider hyperbaric oxygen (HBO) Prophylactic Abx use Avoid extractions during radiotherapy Guidelines for Tooth Extraction in Patients Scheduled to Receive H&N Irradiation or Chemotherapy: Indicators for Extraction An emergency is an emergency Pocket depths 6mm or greater, excessive mobility, purulence on probing Presence of periapical in ammation Broken-down, non-restorable, non-functional, or partially erupted tooth with poor OH Patient lack of interest in saving teeth In ammatory, infectious or malignant osseous disease associated with the tooth Chemotherapy Compromised immunity Kid. status Oral mani stations N/v (Nausea/ Vomiting) Bone marrow e ect on WBC, neutrophils & platelets Extraction Guidelines At least 2 weeks prior to initiation of radiation therapy At least 5 days (maxilla) or 7 days (mandible) before initiation of chemotherapy Eliminate sharp edges Obtain primary closure Avoid packing agents (gel foam) which can become a nidus for bacterial growth Transfuse if the platelet count is less than 50,000/mm3 Delay extraction if the WBC is less than 2000/um or if the absolute neutrophil count is less than 1000/um Prophylactic antibiotics may be used if the extraction is necessary Antimicrobial (CHX m.w.) 30 of 34 fl fi ff fl MRONJ De nition 1. Current or previous treatment with antiresorptive or antangiogenic agents 2. Exposed bone or bone that can be probed through an intra/extra-oral stula(e) in the maxillofacial region that has persisted for more than 8 weeks 3. No history of radiation therapy to the jaws or obvious metastatic disease to the jaws. Symptoms Pain Discomfort Teeth loss Burning sensation Stubborn Infection Halitosis Sensitivity Fistula/e formation BONE Avascular necrosis Discolored bone Loss of jaw/s Eroded soft tissue Bone shedding Creeping necrosis Exposed bone Sequestration Poor healing Management of MRONJ Prevention Vandore et al reported 50% dec. in ONJ in pts. Who were screened prior to drug therapy Necessary exos., denture adj., elective DA Sx Cessation of medication (drug holiday) Controversial AAOMS recommend Damm & Jones —> stop drug 2 months prior (level V evidence) 2009, 3m before & after or until osseous healing if O. BP >3ys Risk is higher after 4y No enough data to stop meds, need more studies. Pt. education O.BPs no alteration nor delay of DA Sx O.BPs drug holiday 2 months prior & not to be restarted until osseous healing occur O.BPs >4y +/- other meds —> drug holiday 2 months prior & not to be restarted until osseous healing occur *O.BP = Oral Bisphosphonates Case treatment sequence: Abs CHX OH optimize HBO (Hyperemic oxygen therapy dives) —> (total of 30 dives) Debridement Implant removal Daily irrigation 2nd debridement Daily irrigation Complete healing achieved in 2months 31 of 34 fi fi ORN (Osteoradionecrosis) Occur following surgical trauma to site or spontaneously Exposed bone fails to heal (6 months following RT) Endarteritis oblitrans —> Hypovascularity (hypocellular-hypovascular- hypoxia theory) R. MARX Soft tissue necrosis Bone necrosis Post. Mandible > Maxilla Due to less blood supp., dense cortical bone & more direct involvement of the mandible to RT Prevention & management 1. Appropriate dental check up 2wks prior to RT 2. Avoid exo. post RT (post. mandible more at risk) 3. Optimize oral hyg. (avoid aggressive brushing) 4. Ppx Abx, Pen. VK 2g 1hr pre-op, Cont. Pen VK 500mg p.o. qid X 1wk 5. Plain local anesthetic (no vasocon.) 6. HBO A. 20 pre-op dives B. 10 post-op dives 7. RCT when possible, avoid exo. Exo. should be as atrumatic as possible Avoid elevating the periosteum Limit exo to 2 teeth per appointment Irrigate with normal saline Primary closure No bony edges to be left 8. Post-op Hyg Mouth wash (warm salty water) CHX Fluoride gel No tobacco F/u q3m * Pen VK = Penicillin V Potassium * HPO (Hyperemic oxygen) 32 of 34  AIDS AIDS, stage 3 HIV infection CD4+ 200 cells/uL but have AIDS de ning condition (e.g. Candidiasis, CMV, EBV, Kaposi, Burkitt, Myco-infections TB.....) Treatment: ART: Antiviral therapy HAART: Highly Active Antiretroviral Therapy (HAART) Chemoprophylaxis, CD4+ multiple vaccines given Oral mani stations oral hairy leukoplakia candida HSV ANUG HZV NUP linear gingival erythema Management Universal precautions, transmission 0.3% An emergency is an emergency Any oral lesion should be diagnosed Care in prescribing meds as hepatotox may occur AIDS with stage 3 HIV infection CD4+