Diabetic Complications PDF

Diabetic Complications Dr Miray Hasan  Diabetic Ketoacidosis DKA is an acute, major, life-threatening complication of diabetes characterized by hyperglycemia, ketoacidosis, and ketonuria. It occurs when absolute or relative insulin deficiency inhibits the ability of gl...

Diabetic Complications Dr Miray Hasan  Diabetic Ketoacidosis DKA is an acute, major, life-threatening complication of diabetes characterized by hyperglycemia, ketoacidosis, and ketonuria. It occurs when absolute or relative insulin deficiency inhibits the ability of glucose to enter cells for utilization as metabolic fuel, the result being that the liver rapidly breaks down fat into ketones to employ as a fuel source. The overproduction of ketones ensues, causing them to accumulate in the blood and urine and turn the blood acidic. DKA occurs mainly in patients with type 1 diabetes The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria The following are other signs and symptoms of DKA: Malaise, generalized weakness, and fatigability Nausea and vomiting; may be associated with diffuse abdominal pain and anorexia  Rapid weight loss in patients newly diagnosed with type 1 diabetes History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons Altered consciousness On examination, general findings of DKA may include the following: Ill appearance, Dry skin, Dry mucous membranes, Decreased skin turgor, Decreased reflexes, Characteristic acetone (ketotic) breath, Tachycardia, Hypotension, Tachypnea, Hypothermia. Search for signs of infection is mandatory in all cases.  Laboratory studies for patients with DKA include the following: Serum glucose levels Serum electrolyte levels (eg, potassium, sodium, chloride, magnesium, calcium, phosphorus) Bicarbonate levels  Urine dipstick Ketone levels ABG measurements Complete blood count (CBC) BUN and creatinine levels Urine and blood cultures if intercurrent infection is suspected Electrocardiogram CXR CT /MRI Brain Diabetic ketoacidosis is typically characterized by hyperglycemia over 250 mg/dL, a bicarbonate level less than 15 mEq/L, and a pH less than 7.30, with ketonemia and ketonuria.  Management Treatment of ketoacidosis should aim for the following: Fluid resuscitation Reversal of the acidosis and ketosis Reduction in the plasma glucose concentration to normal Replenishment of electrolyte and volume losses Identification of the underlying cause Pharmacotherapy: Medications used in the management of DKA include the following: Rapid-acting insulins (eg, insulin aspart, insulin lispro) Short-acting insulins (eg, regular insulin) Electrolyte supplements (eg, potassium chloride) Sodium bicarbonate  Fluid Resuscitation: Initial correction of fluid loss is either by isotonic sodium chloride solution or by lactated Ringer solution. The recommended schedule for restoring fluids is as follows: Administer 1-3 L during the first hour. Administer 1 L during the second hour. Administer 1 L during the following 2 hours Administer 1 L every 4 hours, depending on the degree of dehydration and central venous pressure readings Isotonic saline should be administered at a rate appropriate to maintain adequate blood pressure and pulse, urinary output, and mental status. When blood sugar decreases to less than 180 mg/dL, isotonic sodium chloride solution is replaced with 5-10% dextrose with half isotonic sodium chloride solution.  Insulin Therapy: Insulin should be started about an hour after IV fluid replacement is started Only short-acting insulin is used for correction of hyperglycemia. The initial insulin dose is a continuous IV insulin infusion at a rate of 0.1 U/kg/h until the blood glucose level drops to less than 180 mg/dL; the rate of infusion is then decreased until the ketoacidotic state abates. Do not allow the blood glucose level to fall below 200 mg/dL during the first 4-5 hours of treatment. Hypoglycemia may develop rapidly with correction of ketoacidosis due to improved insulin sensitivity. Rapid correction of hyperglycemia and hyperosmolarity may shift water rapidly to the hyperosmolar intracellular space and may induce cerebral edema.  Electrolyte correction: Potassium replacement should be started with initial fluid replacement if potassium levels are normal or low. Add 20-40 mEq/L of potassium chloride to each liter of fluid once the potassium level is less than 5.5 mEq/L.  Correction of Acid-Base Balance Bicarbonate typically is not replaced as acidosis will improve with the above treatments alone. Sodium bicarbonate only is infused if decompensated acidosis starts to threaten the patient's life, especially when associated with either sepsis or lactic acidosis. HYPEROSMOLAR HYPERGLYCEMIC STATE (HHS) It is a life-threatening emergency that has a much higher mortality rate. HHS is most commonly seen in patients with type 2 DM who have some concomitant illness that leads to reduced fluid intake. Infection is the most common preceding illness, but many other conditions, such as stroke or myocardial infarction, can  SIGNS & SYMPTOMS Physical exam findings and signs related to HHS include the following: Tachycardia, Orthostatic decrease in blood pressure, Hypotension, Tachypnea, Hyperthermia, if infection is present, Altered mental status, confusion, Lethargy, Dry mucous membranes, Sunken eyes, Decreased skin turgor, Poor capillary refill, Decreased urine output, Coma  Workup in Hyperosmolar Hyperglycemic State Diagnostic features of HHS include: Plasma glucose level of 600 mg/dL or greater Effective serum osmolality of 320 mOsm/kg or greater (Normal serum osmolality ranges from 280 to 290 mOsm/kg) Serum pH greater than 7.30 Bicarbonate concentration greater than 15 mEq/L Small ketonuria and low to absent ketonemia Profound dehydration, up to an average of 9L Some alteration in consciousness  Management The main goals in the treatment of HHS are as follows: To vigorously rehydrate the patient while maintaining electrolyte homeostasis To correct hyperglycemia To treat underlying diseases To monitor and assist cardiovascular, pulmonary, renal, and CNS function Airway management is the top priority.  Fluid resuscitation: Aggressive fluid resuscitation is key in the treatment of HHS. This is to avoid cardiovascular collapse and to perfuse vital organs. Fluid resuscitation with 0.9% saline at the rate of 15-20 mL/kg/h or greater (about 1-1.5 L) is indicated to expand the extracellular volume quickly in the first hour.  When the blood glucose concentration, initially checked hourly, reaches 250 mg/dL, change the infusion to 5% dextrose in 0.45% normal saline. Patients with persistent hypotension may require pressor support in the ICU while rehydration is being accomplished.  Insulin Therapy for Correction of Hyperglycemia: All patients with HHS require IV insulin therapy If hypokalemia (K < 3.3mEq/L) has been excluded, an IV bolus of regular insulin of 0.10 U/kg/h should be administered. Begin a continuous insulin infusion of 0.1 U/kg/h. Monitor blood glucose by means of bedside testing every hour Once blood glucose concentration reaches 300 mg/dL, decrease the insulin infusion rate by 0.5-1.0 U/h. Add dextrose to the IV fluids.  Do not discontinue the insulin drip. Continue IV insulin at a goal glucose level of 250-300 mg/dL until the patient becomes more alert and hyperosmolarity has resolved.  Electrolyte Replacement: Potassium may be added to the infusion fluid and should be started at a level of 3.5 mEq/L or less and with adequate urine output. The goal is to keep a potassium level of between 4 and 5 mEq. A patient who is symptomatic with tetany requires replacement therapy for calcium.  Hypoglycemia Hypoglycemia is characterized by a reduction in plasma glucose concentration to a level that may induce symptoms or signs such as altered mental status and/or sympathetic nervous system stimulation. This condition typically arises from abnormalities in the mechanisms involved in glucose homeostasis. The most common cause of hypoglycemia in patients with diabetes is injecting a shot of insulin and skipping a meal or overdosing insulin. The glucose level at which an individual becomes symptomatic is highly variable (threshold generally at < 50 mg/dL). Carefully review the patient's medication history for potential causes of hypoglycemia (eg, new medications, insulin usage or ingestion of an oral hypoglycemic agent). Review patient’s medical and/or social history for Diabetes mellitus, renal insufficiency/failure, alcoholism, hepatic cirrhosis/failure, nutritional deficiencies, other endocrine diseases, or recent surgery, Weight reduction, nausea and vomiting  Neurogenic or neuroglycopenic symptoms of hypoglycemia may be categorized as follows: Neurogenic (adrenergic) (sympathoadrenal activation) symptoms: Sweating, shakiness, tachycardia, anxiety, and a sensation of hunger Neuroglycopenic symptoms: Weakness, tiredness, or dizziness; inappropriate behavior, difficulty with concentration; confusion; blurred vision; and, in extreme cases, coma and death Reactive hypoglycemia includes the following features: More common in overweight and obese people who are insulin- resistant May be a frequent precursor to type 2 diabetes Possible higher risk in patients with a family history of type 2 diabetes or insulin-resistance syndrome True loss of consciousness is highly suggestive of an etiology other than reactive hypoglycemia.  Diagnosis of Hypoglycemia The Whipple triad is characteristically present: documentation of low blood sugar, presence of symptoms, and reversal of these symptoms when the blood glucose level is restored to normal. Laboratory studies that should be obtained include the following: Glucose and electrolyte levels 72-hour fasting plasma glucose Complete blood count Blood cultures, Urinalysis Serum insulin, cortisol levels, and thyroid hormone levels C-peptide levels, Proinsulin Imaging modalities to evaluate insulinomas may include the following: CT scanning/ MRI Octreotide scanning  Management of Hypoglycemia  Pharmacotherapy: The mainstay of therapy for hypoglycemia is glucose. Medications used in the treatment of hypoglycemia include the following: Glucose supplements (e.g. dextrose) Glucose-elevating agents (e.g. glucagon, glucagon intranasal) Inhibitors of insulin secretion (e.g. diazoxide, octreotide) Antineoplastic agents (e.g. streptozocin)  Other therapies: Fasting hypoglycemia: Dietary therapy (frequent meals/snacks preferred, especially at night, with complex carbohydrates); IV glucose infusion; IV octreotide Reactive hypoglycemia: Dietary therapy (restriction of refined carbohydrates, avoidance of simple sugars, increased meal frequency, increased protein and fiber); alpha-glucosidase inhibitors  Surgery: Definitive treatment for fasting hypoglycemia caused by islet cell tumor is surgical resection.  Diabetic Retinopathy Patients with diabetes often develop ophthalmic complications, such as corneal abnormalities, glaucoma, iris neovascularization, cataracts, and neuropathies. The most common and potentially most blinding of these complications, however, is diabetic retinopathy Diabetic renal disease is an excellent predictor of retinopathy; both conditions are caused by DM-related microangiopathies, and the presence and severity of one reflects that of the other. Aggressive treatment of the nephropathy may slow progression of diabetic retinopathy and neovascular glaucoma.  Signs and Symptoms of Diabetic Retinopathy In the initial stages of diabetic retinopathy, patients are generally asymptomatic; in the more advanced stages of the disease, however, patients may experience symptoms that include floaters, blurred vision, distortion, and progressive visual acuity loss. Signs of diabetic retinopathy include the following: Microaneurysms: The earliest clinical sign of diabetic retinopathy; they appear as small, red dots in the superficial retinal layers Dot and blot hemorrhages: they occur as microaneurysms rupture in the deeper layers of the retina Flame-shaped hemorrhages: Splinter hemorrhages that occur in the more superficial nerve fiber layer Retinal edema and hard exudates: Caused by the breakdown of the blood-retina barrier, allowing leakage of serum proteins, lipids, and protein from the vessels  Cotton-wool spots: Nerve fiber layer infarctions from occlusion of precapillary arterioles; they are frequently bordered by microaneurysms and vascular hyperpermeability Macular edema: Leading cause of visual impairment in patients with diabetes  Nonproliferative diabetic retinopathy: Mild NPDR is indicated by the presence of at least 1 microaneurysm. Moderate NDPR includes the presence of hemorrhages, microaneurysms, and hard exudates. Severe NPDR (4-2-1) is characterized by hemorrhages and microaneurysms in 4 quadrants, with venous beading in at least 2 quadrants and intraretinal microvascular abnormalities (IRMA) in at least 1 quadrant.  Proliferative diabetic retinopathy Neovascularization: Hallmark of PDR Preretinal hemorrhages Hemorrhage into the vitreous Traction retinal detachments Macular edema  Management Pharmacologic therapy: Triamcinolone: Administered intravitreally; corticosteroid used in the treatment of diabetic macular edema Anti–vascular endothelial growth factor therapy or anti- VEGF therapy, is the use of medications that block vascular endothelial growth factor. These include: Bevacizumab: Administered intravitreally; monoclonal antibody that can help to reduce diabetic macular edema and neovascularization of the disc or retina Ranibizumab: Administered intravitreally; monoclonal antibody that can help to reduce diabetic macular edema and neovascularization of the disc or retina Glucose control: Intensive glucose control in patients with diabetes decreased the incidence and progression of diabetic retinopathy.  Laser photocoagulation: This involves directing a high- focused beam of light energy to create a coagulative response in the target tissue. In nonproliferative diabetic retinopathy, laser photocoagulation is indicated in the treatment of clinically significant macular edema. Pan retinal Laser photocoagulation (PRP) is used in the treatment of PDR. It involves applying laser burns over the entire retina, sparing the central macular area. Vitrectomy: This procedure can be used in PDR in cases of long-standing vitreous hemorrhage & tractional retinal detachment Cryotherapy: When laser photocoagulation in PDR is precluded in the presence of an opaque media, such as in cases of cataracts or vitreous hemorrhage, cryotherapy may be applied instead. Thank You