Complications of Diabetes Mellitus


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Complications of Diabetes Mellitus

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Complications of Diabetes Mellitus

  2. 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. 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
  6. 6. ACUTE COMPLICATIONS OF DMHypoglycemiaDiabetic KetoacidosisHyperglycemic, Hyperosmotic Non Ketotic Coma
  8. 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. 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. 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. 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. 12. HYPOGLYCEMIA: DIAGNOSIS Signs & Symptoms SMBG FSBG or FSBS
  13. 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. 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. 15/15 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. 16. PROTEIN SOURCES1 Tbsp peanut butter1 oz cheese1 oz meat
  17. 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. 18. HYPOGLYCEMIA TREATMENT UNCONSCIOUSOr give 25mL of D50 as IV pushfollowed by infusion of 5% dextrose in water
  19. 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. 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. 21. HYPOGLYCEMIA NURSING MEASURESEncourage to wear ID braceletTeach family that belligerence is sign of hypoglycemia
  23. 23. DKASerious complication of hyperglycemia due to lack of insulinUsually occurs with type I DM(> 250mg/dl)
  24. 24. DKAResults from breakdown of fat and overproduction of ketones by the liver and loss of bicarbonate
  25. 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. 26. DKA: 4 MAIN CLINICAL FEATURES1. Hyperglycemia2. Dehydration3. Electrolyte loss4. Metabolic Acidosis
  27. 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. 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. 29. S&S OF DKAHyperglycemia ↑blood glucose Tired Polyphagia Decreased attention, confusion N/V, abdominal pain Blurred vision
  30. 30. S&S OF DKADehydration Polydipsia Polyuria Dry/flushed skin Orthostatic hypotension Tachycardia Headaches Decreased Na+ and K+ levels
  31. 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. 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. 33. DKA: DIAGNOSISUrine  Ketones +  Glucose +  Specific gravity of urine i
  34. 34. DKA: DIAGNOSISHemoglobin Normal  Female : 12-16 g/dL  Male: 14-18 g/dL Elevated  Dehydration  COPD Decreased  Anemia, hemorrhaging, over-hydration
  35. 35. DKA: DIAGNOSISHematocrit Normal  Female: 37-47%  Male 42-52% Elevated  Dehydration & COPD Decreased  Anemia, leukemia
  36. 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. 37. HYPOKALEMIA S&SFatigueAnorexia N/VMuscle weaknessLeg crampsDysrhythmias↑sensitivity to digitalis
  38. 38. MANAGEMENT OF DKAFocus on the four main clinical features Hyperglycemia Dehydration Electrolyte loss Acidosis
  39. 39. MANAGEMENT OF DKAHyperglycemia Give insulin  IV
  40. 40. MANAGEMENT OF DKADehydration Rehydrate  IV, push fluids  I&O  Check vital signs  Check Lung sounds  Monitor lab values
  41. 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. 42. MANAGEMENT OF DKAElectrolyte loss Replace K+ Monitor lab values closely
  43. 43. MANAGEMENT OF DKAAcidosis Reversed with insulin  Insulin   glucose enters muscles   i fat metabolism   i in Ketones   acidosis reversed
  44. 44. PREVENTION OF DKA#1 cause of DKA? IllnessSick Day Rules
  45. 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. 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. 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
  49. 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. 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. 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. 52. PRECIPITATING FACTORS Infection (most common) Therapeutic agent or procedure Acute or chronic illness Overeating Stress Too little insulin
  53. 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. 54. Extracellular Dehydration Renal insufficiency Hypovolemia Severe hyperosmolality ShockIntracellular dehydration Tissue hypoxia COMA COMA
  55. 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. 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. 57. NURSING RESPONSIBILIT YSame as with DKA Insulin Hydration Electrolyte replacement and monitoring Treat underlying cause
  58. 58. SUMMARYAcute complications of DM Hypoglycemia Diabetic Ketoacidosis Hyperglycemia Hyperosmolar Non-ketonic Syndrome
  60. 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. 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. 62. ATHEROSCLEROSISAbout two out of three people with diabetes die of heart diseasetwo to four times higher risk for stroke.
  63. 63. HYPERTENSIONAffects 20 – 60 % of all diabeticsIncreases risk for retinopathy, nephropathy
  64. 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
  66. 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. 67. DIABETIC NEPHROPATHYglomerular changes in kidneys of diabetics leading to impaired renal function
  68. 68. DIABETIC NEPHROPATHYAka: Kimmelstiel-Wilson syndrome is a kidney condition associated with long- standing diabetes glomerulosclerosis associated with diabetesFirst indicator: microalbuminuria
  69. 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. 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. 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. 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. 73. S&S / DX Proteinuria / albuminuria i urine output Edema BUN & Creatinine ↑ h BP
  74. 74. NEPHROPATHY: MANAGEMENTTight glucose controlAnti-hypertensives  Calcium-channel blockers  Alpha blockers  ACE inhibitorDialysisTransplant
  75. 75. PREVENTIONControl BGControl HTNTx UTINo nephrotoxic substancesi Nai Protein
  77. 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. 78. Diabetics also have increased risk for cataract development
  79. 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. 80. DIABETIC RETINOPATHYprogressive, Pools of blood, or irreversible vision hemorrhages, on the loss. retina of an eye are visible in this image.
  81. 81. PREVENTIONControl Diabetics should be  Glucose screened for  BP retinopathy No straining Use laxatives Avoid lowering head Avoid lifting above shoulders
  83. 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. 84. OTHER OPTIC COMPLICATIONSCataractsLens ChangesExtraocular muscle palsyGlaucoma
  86. 86.  Damage to the Nerves due to hyperglycemia Most common complication Various Types of Neuropathies…  Sensory-Motor Polyneuropathy  Autonomic neuropathy
  88. 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. 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. 90. MANAGEMENTControl serum glucose levelsPain control  Analgesics (non-narcotic)  Tri-cyclic antidepressants  Anticonvulsants
  92. 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. 93. INFECTIONS
  94. 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. 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. 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. 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. 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. 99. MANAGEMENT OF INFECTIONSBed rest Teach foot careAntibiotics  prevention  Topic vs. IV Teach wound careDebridementControl Glucose levels? Amputation
  100. 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. 101. PREVENTION OF COMPLICATIONS1. Managing diabetes2. Lowering risk factors for conditions3. Routine screening for complications4. Implementing early treatment
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