Medically Compromised Patient (Anous) PDF

History and physical: SOAP note Subjective Intro MEDs, supp., Vit. C/o All, include reactions HPI SHx, tobacco, EtOH, rec. drugs P...

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. deficit 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 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 fistulas 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 fluid 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 List of medication that are used in the dental office and their dosage adjustment for renal failure patients 18 of 34 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 Classifications 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 Physiologic effect 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 & buffer 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 fluids (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 find 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 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 Significant 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 Difficulty 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 insufficiency, decreased blood flow & reduced oxygen tension leading to impair healing 21 of 34 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 deficiency 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 fluid 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  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 insufficiency 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 Thyroid Diseases A. Hashimoto’s Thyroiditis Autoimmune disorder that manifests most often as an asymptomatic diffuse goiter Lymphocytes replace functioning tissue leading to hypothyroidism B. Hypothyroidism Signs and symptoms: Dull expression dry brittle and coarse hair mental decline puffy 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 fibrillation 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 27 of 34 Pregnancy & Breastfeeding First trimester = organogenesis Fetus most susceptible to malformation Avoid treatment in the first trimester Patients may be insulin resistant (gestational DM) Breastfeeding: Most drugs prescribed will have little/no effect 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 benefit of use during pregnancy 28 of 34 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 inflammation Broken-down, non-restorable, non-functional, or partially erupted tooth with poor OH Patient lack of interest in saving teeth Inflammatory, infectious or malignant osseous disease associated with the tooth Chemotherapy Compromised immunity Kid. status Oral manifistations N/v (Nausea/ Vomiting) Bone marrow effect 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 MRONJ Definition 1. Current or previous treatment with antiresorptive or antangiogenic agents 2. Exposed bone or bone that can be probed through an intra/extra-oral fistula(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 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 defining 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 manifistations 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+