Complications of Diabetes Mellitus
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Complications of Diabetes Mellitus

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Complications of Diabetes Mellitus

Complications of Diabetes Mellitus

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  • 1. COMPLICATIONS OFDIABETES MELLITUS
  • 2. Alterations in blood sugars: hyperglycemia and hypoglycemiaMacrocirculation (large blood vessels) Atherosclerosis occurs more frequently, earlier in diabetics Involves coronary, peripheral, and cerebral arteriesMicrocirculation (small blood vessels) Affects basement membrane of small blood vessels and capillaries Involves tissues affecting eyes and kidneys
  • 3. HYPERGLYCEMIA high blood sugar DKA HHKS Dawn phenomenon:  rise in blood sugar between 4 am and 8 am  not associated with hypoglycemia (associated with Diabetes Type 1 and 2) Somogyi effect:  combination of hypoglycemia during night with a rebound morning hyperglycemia that may lead to insulin resistance for 12 to 48 hours
  • 4. THREE BLOOD GLUCOSE PHENOMENA IN DIABETIC CLIENTS
  • 5. ACUTE COMPLICATIONS
  • 6. ACUTE COMPLICATIONS OF DMHypoglycemiaDiabetic KetoacidosisHyperglycemic, Hyperosmotic Non Ketotic Coma
  • 7. HYPOGLYCEMIA
  • 8. HYPOGLYCEMIASerum glucose level < 55 mg/100ml brain damage develops when the brain is deprived of needed glucose after a dramatic drop in blood sugar i nsulin reaction, insulin shock, “the lows”Mismatch between insulin dose, carbohydrate availability and exercise
  • 9.  Causes:  Excess or overdose of insulin or OHA (oral hypoglycemic agents)  Skip meal or omitting a meal  Overexertion/ stress  Under-eating  Eating late  Unplanned exercise
  • 10. HYPOGLYCEMIA: SIGNS & SYMPTOMS Mild  Diaphoresis  Pallor  Paresthesia ANS/Adrenal Medulla  Palpitations  Tremors  AnxietyNote: Clients taking medications, such as beta-adrenergicblockers may not experience manifestations associated withautonomic nervous system
  • 11. HYPOGLYCEMIA: SIGNS & SYMPTOMSModerate: Severe  Confusion/  Seizures disorientation  Loss of Consciousness  Behavioral Changes  Shallow respirations  Severe hypoglycemia cold clammy can result in death extremities, yawning, tremors, blurred vision
  • 12. HYPOGLYCEMIA: DIAGNOSIS Signs & Symptoms SMBG FSBG or FSBS
  • 13. MANAGEMENT: MILD Simple Sugars p.o (15 gm of rapid-acting sugar)  8 oz fruit juice  8 oz of skim milk  3 glucose tablets  3-4oz regular soft drink  3-4 pieces hard candy ( life savers)  1 tbsp sugar  5 ml pure honey
  • 14. RULES TO REMEMBERDo not add sugar to OJRecheck FSBS/CBG q 15 min until WNLAvoid high fat  slows absorption of glucoseInstruct: carry fast sugarIf meal is >1 hr away, follow with a protein and complex carbohydrateNPO if “unconscious” or confused
  • 15. 15/15 rule: wait 15 minutes and monitor blood glucose; if still low (BG<80), client should eat another 15 gm of sugarContinue until blood glucose level has returned to normalClient should contact medical care provider if hypoglycemia occurs more than 2 or 3 times per week
  • 16. PROTEIN SOURCES1 Tbsp peanut butter1 oz cheese1 oz meat
  • 17. HYPOGLYCEMIA TREATMENT UNCONSCIOUSGlucagon 1 mg Subq, IM, IV; follow with oral or intravenous carbohydrate Action: (hormone)  raises BS levels Onset:10 minutes Duration 25 minutes S/E: N/VPosition: side lying
  • 18. HYPOGLYCEMIA TREATMENT UNCONSCIOUSOr give 25mL of D50 as IV pushfollowed by infusion of 5% dextrose in water
  • 19. HYPOGLYCEMIA GERONTOLOGICAL CONSIDERATIONCognitive deficits   not recognize S&SDecreased renal function   oral hypoglycemic meds stay in body longerMore likely to _________a meal  SkipVision problems   inaccurate insulin draws
  • 20. HYPOGLYCEMIA NURSING MEASURESFollow protocolTeach Carry simple sugar at all times S&S or hypoglycemia How to prevent Hypoglycemia Check FSBS if you suspect  NOW!
  • 21. HYPOGLYCEMIA NURSING MEASURESEncourage to wear ID braceletTeach family that belligerence is sign of hypoglycemia
  • 22. DIABETIC KETOACIDOSIS (DKA)
  • 23. DKASerious complication of hyperglycemia due to lack of insulinUsually occurs with type I DM(> 250mg/dl)
  • 24. DKAResults from breakdown of fat and overproduction of ketones by the liver and loss of bicarbonate
  • 25. DKA: ETIOLOGY#1 cause: illness, infection, stress (physical or emotional stress)surgery, trauma, pregnancyabsence or inadequate insulin taking too little insulin omitting doses of insulinknown diabetic has increased energy needs,Initial or undiagnosed diabetesdeveloping insulin resistance
  • 26. DKA: 4 MAIN CLINICAL FEATURES1. Hyperglycemia2. Dehydration3. Electrolyte loss4. Metabolic Acidosis
  • 27. PATHOPHYSIOLOGY DKANo Insulin h fat metabolismGlucose stays in Muscle not blood - getting energy Increased ketone in bloodHyperglycemia Metabolic AcidosisOsmotic diuresis Polyuria Electrolyte loss i serum pH Polydipsia h respiratory rateDehydration
  • 28. Environment, infection, emotional stress Lack of insulinBreakdown of fats in Breakdown of Decreased Proteincells glycogen to use of breakdown glucose glucoseFree fatty acids toliver Hyperglycemia Gluconeo- IncreasedFormation of ketone Osmotic diuresis genesis BUNbodies Dehydration ElectrolyteKetones in urine imbalanceand blood Hyperosmolality and Hemoconcentration Acidosis COMA
  • 29. S&S OF DKAHyperglycemia ↑blood glucose Tired Polyphagia Decreased attention, confusion N/V, abdominal pain Blurred vision
  • 30. S&S OF DKADehydration Polydipsia Polyuria Dry/flushed skin Orthostatic hypotension Tachycardia Headaches Decreased Na+ and K+ levels
  • 31. S&S OF DKAAcidosis ↑Resp. rate  Kussmaul’s Fruity breath, acetone breath Serum pH  Decreased  Normal Serum pH 7.35 – 7.45  i pH = acidic / acidosis  h pH = alkaline/ alkalosis
  • 32. DKA: DIAGNOSISBlood  pH  Serum Osmolality i  less than 7.3  h  thick  sugar levels  Ketones  Elevated  greater than 250 mg/dL +  bicarbonate  BUN Blood Urea i Nitrate  less than 15 mEq/L  increased = dehydration
  • 33. DKA: DIAGNOSISUrine  Ketones +  Glucose +  Specific gravity of urine i
  • 34. DKA: DIAGNOSISHemoglobin Normal  Female : 12-16 g/dL  Male: 14-18 g/dL Elevated  Dehydration  COPD Decreased  Anemia, hemorrhaging, over-hydration
  • 35. DKA: DIAGNOSISHematocrit Normal  Female: 37-47%  Male 42-52% Elevated  Dehydration & COPD Decreased  Anemia, leukemia
  • 36. DKA: DIAGNOSISSerum Potassium levels Normal levels  3.5-5.5 mEq/L  Increased K + levels = Hyperkalemia  Decreased K + levels = Hypokalemia Purpose of K +  Skeletal & cardiac muscle activity DKA  decreased K + levels
  • 37. HYPOKALEMIA S&SFatigueAnorexia N/VMuscle weaknessLeg crampsDysrhythmias↑sensitivity to digitalis
  • 38. MANAGEMENT OF DKAFocus on the four main clinical features Hyperglycemia Dehydration Electrolyte loss Acidosis
  • 39. MANAGEMENT OF DKAHyperglycemia Give insulin  IV
  • 40. MANAGEMENT OF DKADehydration Rehydrate  IV, push fluids  I&O  Check vital signs  Check Lung sounds  Monitor lab values
  • 41. MANAGEMENT OF DKAElectrolyte loss  Polyuria  loss of K +  Treatment of DKA dehydration  drop in K+5 K / 1 ml serum 5 K / 2 ml serum 5.0 mEq/L 2.5 mEq/L KKKKK KKKKK
  • 42. MANAGEMENT OF DKAElectrolyte loss Replace K+ Monitor lab values closely
  • 43. MANAGEMENT OF DKAAcidosis Reversed with insulin  Insulin   glucose enters muscles   i fat metabolism   i in Ketones   acidosis reversed
  • 44. PREVENTION OF DKA#1 cause of DKA? IllnessSick Day Rules
  • 45. SICK DAY PROTOCOL/RULESNever omit insulinIf you are unable to eat normally, DO NOT stop taking insulinSliding scaleTest blood sugar every 3-4 hoursTest urine for ketones every 3-4 hoursTake liquid/fluids q hour
  • 46. SICK DAY PROTOCOL/RULESIf you can not eat your usual meal, substitute soft foodsHave “sick day” food in houseIf vomiting, diarrhea or fever persists, take liquids q half hourIf miss or replace 4 meals with fluids, call MD
  • 47. SICK DAY PROTOCOL/RULESGo to bed and keep warmFriends: good to have someone around who understands and knows about insulin reactions and diabetes
  • 48. HYPERGLYCEMIA HYPEROSMOLAR NONKETONICSYNDROME (HHNK)
  • 49. HHNKoccurs when there is insufficient insulin to prevent hyperglycemia, but there is enough insulin to prevent KetoacidosisOccurs in all types of diabetes Esp Diabetes Type 2
  • 50. Life threatening medical emergency, high mortality rateCharacterized by Plasma osmolarity 340 mOsm/L or greater (normal: 280 -300) Blood glucose severely elevated, 600 - 1000 or 2000 (normal 70-110) Altered level of consciousness
  • 51. HHNKSextreme hyperglycemia (800- 2000mg/dl)undetectable ketonuriaabsence of acidosismajor difference from diabetic ketoacidosis is the lack of ketonuria because there is some residual ability to secrete insulin in NIDDM.
  • 52. PRECIPITATING FACTORS Infection (most common) Therapeutic agent or procedure Acute or chronic illness Overeating Stress Too little insulin
  • 53. Environment, infection, emotional stress Lack of insulinBreakdown of fats in Breakdown of Decreased Proteincells glycogen to use of breakdown glucose glucoseFree fatty acids toliver Hyperglycemia Gluconeo- IncreasedFormation of ketone Osmotic diuresis genesis BUNbodies Dehydration ElectrolyteKetones in urine imbalanceand blood Hyperosmolality and Hemoconcentration Acidosis COMA
  • 54. Extracellular Dehydration Renal insufficiency Hypovolemia Severe hyperosmolality ShockIntracellular dehydration Tissue hypoxia COMA COMA
  • 55. S&S OF HHNK SYNDROME Altered level of consciousness (lethargy to coma) Neurological deficits: hyperthermia, motor and sensory impairment, seizures Dehydration: dry skin and mucous membranes, extreme thirst
  • 56. MANAGEMENT Usually admitted to intensive care unit of hospital for care since client is in life-threatening condition: unresponsive, may be on ventilator, has nasogastric suction vigorous fluid replacement give insulin IV  Lower glucose with regular insulin until glucose level drops to 250 mg/dL potassium, sodium chloride given IV dextrose is given when blood sugar reaches around 250mg/100ml to prevent hypoglycemia Treat precipitating factors
  • 57. NURSING RESPONSIBILIT YSame as with DKA Insulin Hydration Electrolyte replacement and monitoring Treat underlying cause
  • 58. SUMMARYAcute complications of DM Hypoglycemia Diabetic Ketoacidosis Hyperglycemia Hyperosmolar Non-ketonic Syndrome
  • 59. CHRONICCOMPLICATIONS
  • 60. COMPLICATIONSMacrovascular complications Microvascular complications  Arteriosclerosis  Characterized by basement  Characterized by membrane thickening thickening and loss of elasticity of the arterial  Effects smallest blood walls “hardening of the vessels arteries”.  Due to hyperglycemia  Coronary Artery Disease  Cerebrovascular Disease  Peripheral vascular disease
  • 61. CARDIOVASCULAR DISEASEmajor source of mortality in patients with type 2 DM.Approximately two thirds of people with diabetes die of heart disease or stroke.Men with diabetes face a 2-fold increased risk for CHD, and women have a 3- to 4-fold increased riskDiabetics more likely to develop MI, Congestive Heart Failure
  • 62. ATHEROSCLEROSISAbout two out of three people with diabetes die of heart diseasetwo to four times higher risk for stroke.
  • 63. HYPERTENSIONAffects 20 – 60 % of all diabeticsIncreases risk for retinopathy, nephropathy
  • 64. PERIPHERAL VASCULAR DISEASEIncreased risk for Types 1 and 2 diabeticsDevelopment of arterial occlusion and thrombosis resulting in gangreneGangrene from diabetes most common cause of non-traumatic lower limb amputation
  • 65. DIABETIC NEPHROPATHY
  • 66. DIABETIC NEPHROPATHYDiabetes is the leading cause of kidney failure, accounting for 44% of new cases in 2008.Most common cause of end-stage renal failure in U.S.
  • 67. DIABETIC NEPHROPATHYglomerular changes in kidneys of diabetics leading to impaired renal function
  • 68. DIABETIC NEPHROPATHYAka: Kimmelstiel-Wilson syndrome is a kidney condition associated with long- standing diabetes glomerulosclerosis associated with diabetesFirst indicator: microalbuminuria
  • 69. DIABETIC NEPHROPATHYDiabetics without treatment go on to develop hypertension, edema, progressive renal insufficiency In type 1 diabetics, 10 – 15 years May occur soon after diagnosis with type 2 diabetes since many are undiagnosed for years
  • 70. Damage to the tiny h glucose levels blood vessels within  Stress kidney’s the kidney. filtration mechanismDue to Blood protein leaks  Hyperglycemia into urine Pressure in blood vessel of kidney h Kidney failure
  • 71. NEPHROPATHY: PATHOPHYSIOLOGYNormallyKidneys filter bloodSmall molecules & waste squeeze through kidneys  urineBig stuff (I.e. protein, RBC), stay in blood where they belong
  • 72. NEPHROPATHY: PATHOPHYSIOLOGY Diabetes damages the system Filters start to leak Protein and RBC lost in urine  Microalbuminuria  Macroalbuminuria  Proteinuria Filters collapse Lose of filtering ability  Kidney failure  ESRF / ENRD Waste products build up in blood
  • 73. S&S / DX Proteinuria / albuminuria i urine output Edema BUN & Creatinine ↑ h BP
  • 74. NEPHROPATHY: MANAGEMENTTight glucose controlAnti-hypertensives  Calcium-channel blockers  Alpha blockers  ACE inhibitorDialysisTransplant
  • 75. PREVENTIONControl BGControl HTNTx UTINo nephrotoxic substancesi Nai Protein
  • 76. DIABETIC RETINOPATHY
  • 77. DIABETIC RETINOPATHYRetinal changes related to diabetesDM is the major cause of blindness in adults aged 20-74 years in USaccounts for 12,000-24,000 newly blind persons every year.Affects almost all Type 1 diabetics after 20 yearsAffects 60 % of Type 2 diabetics
  • 78. Diabetics also have increased risk for cataract development
  • 79. DIABETIC RETINOPATHYdue to hyperglycemiaDamage to the tiny blood vessels that supply the eye Small hemorrhages occurLeads to retinal ischemia and breakdown of blood-retinal barrier
  • 80. DIABETIC RETINOPATHYprogressive, Pools of blood, or irreversible vision hemorrhages, on the loss. retina of an eye are visible in this image.
  • 81. PREVENTIONControl Diabetics should be  Glucose screened for  BP retinopathy No straining Use laxatives Avoid lowering head Avoid lifting above shoulders
  • 82. DIABETIC RETINOPATHY
  • 83. RETINOPATHY Medical Management Nursing Considerations Photocoagulation  Expected “laser” treatment  Odds are good Control hypertension  Frequent eye exams Control blood glucose  Bilateral but uneven No smoking
  • 84. OTHER OPTIC COMPLICATIONSCataractsLens ChangesExtraocular muscle palsyGlaucoma
  • 85. DIABETIC NEUROPATHY
  • 86.  Damage to the Nerves due to hyperglycemia Most common complication Various Types of Neuropathies…  Sensory-Motor Polyneuropathy  Autonomic neuropathy
  • 87. DIABETIC NEUROPATHY
  • 88. SENSORY-MOTOR POLYNEUROPATHY s/s AKA peripheral neuropathy Paresthesias: primarily lower extremities i deep tendon reflexes Numb feet i proprioception i sensation Unsteady gait h risk foot injury
  • 89. AUTONOMIC NEUROPATHY  Uri n a r y Autonomic NS  Retention Can af fect almost any  Neurogenic bladder  Re pro duc t i ve system  Male impotence  Cardiovascular  Adre n a l G l a n d  “Hypoglycemic Unawareness ”  Tachycardia  Adrenal Medulla  Adrenergic symptoms  Orthostatic hypotension  No longer feel S&S  MI  Strict BG control & frequent monitoring  Sudo m oto r n e uro pa t hy  Gastro-intestinal  No sweating  Delayed gastric emptying  Anhidrosis   dr y feet  Constipation   foot ulcers  Diarrhea
  • 90. MANAGEMENTControl serum glucose levelsPain control  Analgesics (non-narcotic)  Tri-cyclic antidepressants  Anticonvulsants
  • 91. OTHER COMPLICATIONS FROM DIABETES
  • 92. DIABETES MELLITUSIncreased susceptibility to infection  Predisposition is combined effect of other complications  Normal inflammatory response is diminished  Slower than normal healingPeriodontal diseaseFoot ulcers and infections: predisposition is combined effect of other complications
  • 93. INFECTIONS
  • 94. High risk of foot  Peripheral vascular disease infections  Circulation  Neuropathy i  Pain sensation  WBC i i  Pressure sensation  Oxygen i i  wound healing  Dryness  Poor h  Antibiotics  Fissures i h  Gangrene
  • 95. Immuno- Once they occur  compromised difficult to treat  WBC + hyperglycemia  Poor circulation = sluggish WBC’s  Antibiotic not get there  Sluggish WBC’s  Unknown wounds Particular concern  Foot infections/wounds
  • 96. HIGH RISK FOR FOOT INFECTIONSDuration of diabetes Progression ofh Age eventsSmoking  Soft tissue injury   Injury not sensed i Peripheral pulses  Infection i Sensation  Drainage, swelling,Deformities/pressur redness  e areas  Gangrene Hx of foot ulcers
  • 97. Boils: Cellulites AKA: "furuncles" noncontagious inflammation of the round, pus-filled connective tissue of bumps on the skin the skin, D/T: D/T bacterial Staphylococcus infection aureus bacteria Treatment  Antibiotics  Analgesics
  • 98. INFECTIONS OF CONCERNUTI’s GangreneYeast Infections term to describe thePeriodontal disease decay or death of an organ or tissue d/t i blood supply.
  • 99. MANAGEMENT OF INFECTIONSBed rest Teach foot careAntibiotics  prevention  Topic vs. IV Teach wound careDebridementControl Glucose levels? Amputation
  • 100. CANCERpeople with type 2 diabetes are at an increased risk for many types of cancer 2010 Consensus Report from a panel of experts chosen jointly by the American Diabetes Association and the American Cancer Society
  • 101. PREVENTION OF COMPLICATIONS1. Managing diabetes2. Lowering risk factors for conditions3. Routine screening for complications4. Implementing early treatment