Renal disorders and their dental management

PRESENTED BY:

DR DIVYA RANA

PG 2nd YEAR

MGDCH

Bones can break, muscles can atrophy, glands can loaf, even the brain can go to sleep without immediate danger to survival. But -- should kidneys fail.... neither bone, muscle, nor brain could carry on.

Homer Smith, Ph.D.

Renal circulation receives 20 - 25 % of cardiac output under normal physiologic conditions.

The bodies blood volume circulates through the kidney every 6 minutes (12 times/hour).

Renin secretion and the regulation of volume and composition of extracellular fluid.

Excretion Blood pressure control

Vitamin D activation Acid-base balance

regulation. Erythropoietin

production Urine formation

Renin is important in the regulation of blood pressure.

It is released from the granular cells of the efferent arteriole in response to decreased arteriole blood pressure, renal ischemia, extracellular fluid depletion, increased norepinephrine, and increased urinary Na+ concentration.

4 mechanisms are involved Volume control Aldosterone effect Renin-angiotensin-aldosterone Renal prostaglandin

Prostoglandins (PGs)- synthesized by most body tissues. In the kidney, PGs are synthesized in the medulla and have a vasodilating action and promote Na+ excretion. PGs counteract the vasoconstrictor effect of angiotensin and norepinephrine. Renal PGs systemically lower blood pressure by decreasing systemic vascular resistance.

Acquired by the body through diet or through synthesis by ultraviolet radiation on the cholesterol in the skin.

The liver and the kidney make the vitamin active in the body.

Erythropoietin is produced and released by the kidneys in response to decreased oxygen tension in the renal blood supply that is created by the loss of red blood cells.

Erythropoietin stimulates the production of RBCs in the bone marrow.

Erythropoietin deficiency leads to anemia in renal failure.

Kidney secrete Erythropoietin, it stimulates the bone marrow to produce RBC’s

in oxygen delivery simulates release in response the RBC count rises in 3 - 5 days speeds the maturation of RBC’s

Kidneys regulate acid-base balance by stabilizing body fluid volume & flow rate to enhance the reabsorption or excretion of bicarbonate & hydrogen ions

Sodium Potassium Calcium Need to Know: Phosphate Normal Values Magnesium Functions Chloride Factors affect

Over 200 waste products excreted Only 2 are used for clinical assessment

BUN Creatinine

Over 200 waste products excreted Only 2 are used for clinical assessment

BUN Creatinine

Normal 8 - 20 mg/dl Nitrogenous waste product of protein

metabolism Unreliable in measurement of renal function

Relevance is assessed in conjunction with Creatinine

Urine flow low renal perfusion Volume depletion Metabolic rate Protein metabolism Drugs

A waste product of muscle metabolism Normal value 0.6 - 1.2 mg/dl 2 times normal = 50% damage 8 times normal = 75% damage 10 times normal = 90% damage Exception - severe muscular disease can

greatly Creatinine levels

Blood TestsBUN elevated (norm 10-20)Creatinine elevated (norm 0.6 - 1.2)K elevatedPO4 elevatedCa decreased

UrinalysisSpecific gravityProteinCreatinine clearance

Biopsy Ultrasound X-Rays

Sudden onset - hours to days Often reversible Severe - 50% mortality rate overall; generally

related to infection.

Homeostatic functions affected most Electrolyte imbalances Volume regulation Blood pressure control

Endocrine functions affected lease Require time to evolve

Renal size is preserved Evidence of acute illness or insult exists

Sudden fall in glomerular filtration rate (GFR) Retention of nitrogenous (BUN and creatinine)

and other wastes Hours to days

About 5% of all hospitalizations About 20% of ICU admissions

Mortality 50 – 80% Independent risk factor for death – 5x

increase risk

Slow progressive renal disorder related to nephron loss, occurring over months to years

Culminates in End Stage Renal Disease

Cause & onset often unknown Loss of function precedes lab abnormalities Lab abnormalities precede symptoms Symptoms (usually) evolve in orderly

sequence Renal size is usually decreased

Diabetes Hypertension Glomerulonephritis Cystic disorders Developmental - Congenital Infectious Disease

Neoplasms Obstructive disorders Autoimmune diseases

Lupus Hepatorenal failure Scleroderma Amyloidosis Drug toxicity

24 hour urine for creatinine clearance

Can estimate creatinine clearance by:140 – {age x weight (kg)} 72 x serum creatinine

Reduced Renal Reserve

Renal Insufficiency

End Stage Renal Disease (ESRD)

Stage 1: GFR > 90 ml/min despite kidney damage

Stage 2: Mild reduction (GFR 60 – 89 ml/min)

1. GFR of 60 may represent 50% loss in function.2. Parathyroid hormones starts to increase.

No symptoms

Serum creatinine doubles

Up to 50% nephron loss

Stage 3: Moderate reduction (GFR 30 – 59 ml/min)1. Calcium absorption decreases2. Malnutrition onset3. Anemia secondary to Erythropoietin deficiency4. Left ventricular hypertrophy

Stage 4: Sever reduction (GFR 15 – 29 ml/min)1. Serum triglycerides increase2. Hyperphosphatemia3. Metabolic acidosis4. Hyperkalemia

Signs and symptoms worsen if kidneys are stressed

Decreased ability to maintain homeostasis

75% nephron loss Decreased: glomerular filtration rate, solute

clearance, ability to concentrate urine and hormone secretion

Symptoms: elevated BUN & Creatinine, mild azotemia, anemia

Stage 5: Kidney failure (GFR < 15 ml/min)1. Azotemia

Residual function < 15% of normal Excretory, regulatory and hormonal functions

severely impaired. metabolic acidosis Marked increase in: BUN, Creatinine,

Phosphorous Marked decrease in: Hemoglobin,

Hematocrit, Calcium Fluid overload

Uremic syndrome develops affecting all body systems can be diminished with early diagnosis &

treatment

Last stage of progressive CRF Fatal if no treatment

Mood swings Impaired judgment Inability to concentrate and perform simple

math functions Tremors, twitching, convulsions Peripheral Neuropathy

restless legs foot drop

Pale, grayish-bronze color Dry scaly Severe itching Bruise easily Uremic frost

Visual blurring Occasional blindness

Volume expansion and fluid overload Metabolic Acidosis Electrolyte Imbalances

Hyperkalemia

Uremic fetor Anorexia, nausea, vomiting GI bleeding

Anemia Platelet dysfunction

Muscle cramps Soft tissue calcifications Weakness Related to calcium phosphorous imbalances

Hypertension Congestive heart failure Pericarditis Pulmonary edema Pleural effusions

Erythropoietin production decreased Hypothyroidism Insulin resistance Growth hormone decreased Gonadal dysfunction Parathyroid hormone and Vitamin D3

Hyperlipidemia

Oral manifestations Enlarged (asymptomatic) salivary glands Decreased salivary flow Dry mouth Odor of urea on breath Metallic taste Increased calculus formation Low caries rate Enamel hypoplasia Dark brown stains on crowns Extrinsic (secondary to liquid ferrous sulfate therapy) Intrinsic (secondary to tetracycline staining)

Dental malocclusions Pale mucosa with diminished color demarcation between

attached gingiva and alveolar mucosa Low-grade gingival inflammation Petechiae and ecchymosis Bleeding from gingiva Prolonged bleeding Candidal infections Burning and tenderness of mucosa Erosive glossitis Tooth erosion (secondary to regurgitation associated with

dialysis) Dehiscence of wounds

Radiographic manifestations Demineralization of bone Loss of bony trabeculation Ground-glass appearance Loss of lamina dura Giant cell lesions, “brown tumors” Socket sclerosis Pulpal narrowing and calcification Tooth mobility Arterial and oral calcifications

Hemodialysis Peritoneal Dialysis Transplant

Removal of soluble substances and water from the blood by diffusion through a semi-permeable membrane.

Blood removed from patient into the extracorporeal circuit.

Diffusion and ultrafiltration take place in the dialyzer.

Cleaned blood returned to patient.

Arterio-venous shunt (Scribner External Shunt)

Arterio-venous (AV) Fistula PTFE Graft Temporary catheters “Permanent” catheters

External- one end into artery, one into vein.

Advantagesplace at bedsideuse immediately

Disadvantages infectionskin erosionaccidental separation limits use of extremity

Patients own artery and vein surgically anastomosed.

Advantagespatients own veinlongevitylow infection and thrombosis rates

Disadvantageslong time to mature, 1- 6 months“steal” syndromerequires needle sticks

Synthetic “vessel” anastomosed into an artery and vein.

Advantages for people with inadequate vesselscan be used in 7-14 daysprominent vessels

Disadvantagesclots easily“steal” syndrome more frequentrequires needle sticks infection may necessitate removal of graft

Dual lumen catheter placed into a central vein-subclavian, jugular or femoral.

Advantagesimmediate useno needle sticks

Disadvantageshigh incidence of infectionsubclavian vein stenosispoor flow-inadequate dialysisclotting

NO BP’s, needle sticks to arm with vascular access. This includes finger sticks.

Place ID bands on other arm whenever possible.

Palpate thrill and listen for bruit. Teach patient nothing constrictive, feel for

thrill.

During dialysisFluid and electrolyte related

hypotensionCardiovascular

arrythmiasAssociated with the extracorporeal circuit

exsanguinationNeurologic

seizuresother

fever

Between treatments Hypertension/Hypotension Edema Pulmonary edema Hyperkalemia Bleeding Clotting of access

Long termMetabolic

hyperparathyroidism diabetic complications

Cardiovascular CHF AV access failure

Respiratory pulmonary edema

Neuromuscular neuropathy

Long term cont’d Hematologic

anemia GI

bleeding dermatologic

calcium phosphorous deposits Rheumatologic

amyloid deposits

Long term cont’d Genitourinary

infection sexual dysfunction

Psychiatric depression

Infection bloodborne pathogens

Fluid restrictions Phosphorous restrictions Potassium restrictions Sodium restrictions Protein to maintain nitrogen balance

too high - waste products too low - decreased albumin, increased mortality

Calories to maintain or reach ideal weight

Removal of soluble substances and water from the blood by diffusion through a semi-permeable membrane that is intracorporeal (inside the body).

CAPD: Continuous ambulatory peritoneal dialysis

CCPD: Continuous cycling peritoneal dialysis IPD: Intermittent peritoneal dialysis

Catheter into peritoneal cavity Exchanges 4 - 5 times per day Treatment 24 hours; 7 days a week Solution remains in peritoneal cavity except

during drain time Independent treatment

Fill: fluid infused into peritoneal cavity Dwell: time fluid remains in peritoneal cavity Drain: time fluid drains from peritoneal

cavity

Infectionperitonitistunnel infectionscatheter exit site

Hypervolemiahypertensionpulmonary edema

Hypovolemiahypotension

Hyperglycemia Malnutrition

Obesity Hypokalemia Hernia Cuff erosion

Independence for patient No needle sticks Better blood pressure control Some diabetics add insulin to solution Fewer dietary restrictions

protein loses in dialysate generally need increased potassium less fluid restrictions

Vitamins - water soluble Phosphate binder - (Phoslo, Renagel,

Calcium, Aluminum hydroxide) Give with meals

Iron Supplements - don’t give with phosphate binder or calcium

Antihypertensives - hold prior to dialysis

Erythropoietin Calcium Supplements - Between meals, not

with iron Activated Vitamin D3 - aids in calcium

absorption Antibiotics - hold dose prior to dialysis if it

dialyzes out

Many drugs or their metabolites are excreted by the kidney

Dosages - many change when used in renal failure patients

Dialyzability - many removed by dialysis varies between HD and PD

Alleviate fear Dialysis process Fistula/catheter care Diet and fluid restrictions Medication Diabetic teaching

Restoration of “normal” renal function Freedom from dialysis Return to “normal” life

Life long medications Multiple side effects from medication Increased risk of tumor Increased risk of infection Major surgery

Major surgery with general anesthesia Assessment of renal function Assessment of fluid and electrolyte balance Prevention of infection Prevention and management of rejection

ATN? (acute tubular necrosis) 50% experience

Urine output >100 <500 cc/hr BUN, creatinine, creatinine clearance Fluid Balance Ultrasound Renal scans Renal biopsy

Accurate I & OCRITICAL TO AVOID DEHYDRATIONOutput normal - >100 <500 cc/hr, could be

1-2 L/hrPotential for volume overload/deficit

Daily weights Hyper/Hypokalemia potential Hyponatremia Hyperglycemia

Major complication of transplantation due to immunosuppression

HANDWASHING Crowds, Kids Patient Education

Hyperacute - preformed antibodies to donor antigen function ceases within 24 hours Rx = removal

Accelerated - same as hyperacute but slower, 1st week to month Rx = removal

Acute - generally after 1st 10 days to end of 2nd month 50% experience must differentiate between rejection and

cyclosporine toxicity Rx = steroids, monoclonal (OKT3), or polyclonal

(HTG) antibodies

Chronic - gradual process of graft dysfunction Repeated rejection episodes that have not been

completely resolved with treatment Rx = return to dialysis or re-transplantation

Prednisone Prevents infiltration of T lymphocytes

Side effects cushnoid changes Avascular Necrosis GI disturbances Diabetes infection risk of tumor

Azathioprine (Imuran) Prevents rapid growing lymphocytes

Side Effects bone marrow toxicity hepatotoxicity hair loss infection risk of tumor

Cyclosporin Interferes with production of interleukin 2 which

is necessary for growth and activation of T lymphocytes.

• Side Effects– Nephrotoxicity– HTN– Hepatotoxicity– Gingival hyperplasia– Infection

Cytoxan - in place of Imuran less toxic FK506 - 100 x more potent than Cyclosporin Prograf Cellcept

OKT3 - monoclonal antibody used to treat rejection or induce immunosuppressiondecreases CD3 cells within 1 hour

Side effectsanaphylaxis fever/chillspulmonary edemarisk of infectiontumors

1st dose reaction expected & wanted, pre-treat with Benadryl, Tylenol, Solumedrol

Atgam - polyclonal antibody used to treat rejection or induce immunosuppressiondecreased number of T lymphocytes

Side effectsanaphylaxisfever chillsleukopeniathrombocytopeniarisk of infectiontumor

Signs of infection Prevention of infection Signs of rejection

decreased urine output increased weight gain tenderness over kidney fever > 100 degrees F

Medications time, dose, side effects

Indication Drug Magnesium content Antacids (Maalox, milk of

magnesia) Laxatives

Potassium content IV fluids Salt substitutes Massive penicillin therapy (1.7

mEq/million U)

Sodium content Carbenicillin (4.7 mEq/g) Alka Seltzer (23 mEq tablet) IV fluid

Acidifying effects Ascorbic acid Ammonium chloride (in cough syrup) Nonsteroidal anti-inflammatory

agents

Catabolic effects Tetracyclines

Steroids

Nephrotoxicity Phenacetin Ketorolac

Cephalosporins*

Alkalosis effect Absorbed antacids

Carbenicillin (large doses

Penicillin (large doses

Before treatment

Determine dialysis schedule and treat on day after dialysis. Consult with patient’s nephrologist for recent laboratory tests and discussion of antibiotic prophylaxis. Identify arm with vascular access and type; notate in chart and avoid taking blood pressure measurement/injection of medication on this arm. Evaluate patient for hypertension/hypotension. Institute preoperative hemostatic aids (DDAVP, conjugated estrogen) when appropriate. Determine underlying cause of renal failure (underlying disease may affect provision of care). Obtain routine annual dental radiographs to establish presence and follow manifestations of renal osteodystrophy. Consider routine serology for HBV, HCV, and HIV antibody. Consider antibiotic prophylaxis when appropriate. Consider sedative premedication for patients with hypertension

During treatment

Perform a thorough history and physical examination for presence of oral

manifestations. Aggressively eliminate potential sources of infection/bacteremia. Use adjunctive hemostatic aids during oral/periodontal surgical

procedures. Maintain patient in a comfortable uncramped position in the

dental chair. Allow patient to walk or stand intermittently during long

procedures

After treatment

Use postsurgical hemostatic agents. Encourage meticulous home care. Institute therapy for xerostomia when appropriate. Consider use of postoperative antibiotics for traumatic

procedures. Avoid use of respiratory-depressant drugs in presence of severe

anemia. Adjust dosages of postoperative medications according to extent

of renal failure. Ensure routine recall maintenance.

Recurrent herpes labialis in an immunocompromised patient

Recurrent herpes labialis

Recurrent intraoral herpes in a cardiac transplant recipient.

Chronic herpes simplex in a chronically immunosuppressed transplant recipient

Pseudomembranous candidiasisHyperplastic candidiasis in a kidney transplant recipient. This infection did not respond to fluconazole

Graft-versus-host disease in a patient who had undergone HCT. Note the clinical resemblance to erosive lichen planus

Pre-transplantation considerations

Significantly ill patient with end-organ damage Medical consultation required Consider postponing elective treatment Dental consultation prior to anticipated transplant: Rule out dental infectious sources, definitively Perform necessary treatment; this will require consultation with

transplantation physician to determine medical risk-to-benefit ratio Obtain laboratory information/supplemental information as

needed Become acquainted with specific management issues (eg, blood

products, prophylactic antibiotics) that may need to be employed if

treatment is rendered.

Post-transplantation considerations Immediate post-transplantation period No elective dental treatment performed Emergency treatment only with medical consultation and consideration of specific management needs Stable post-transplantation period Elective treatment may be performed after medical consultation with the transplantation physician Issues of immunosuppression must be recognized Oral mucosal disease must be diagnosed and treated Supplemental corticosteroids (steroid boost) may be necessary Consideration of antibiotic prophylaxis needed Consideration of specific management needs Post-transplantation chronic rejection period Only emergency treatment Patients are very ill as they are immunosuppressed and have organ failure

Thank you.