Hyperglycemic crises
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Hyperglycemic crises like diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are life-threatening complications of diabetes that require prompt treatment. DKA occurs when there is uncontrolled hyperglycemia, ketosis, and acidosis due to insulin deficiency. It is more common in type 1 diabetes but can occur in type 2 diabetes during stress. HHS involves severe hyperglycemia without significant ketosis and mainly affects elderly patients with type 2 diabetes. Both conditions require fluid resuscitation, electrolyte replacement, insulin therapy, and treatment of any underlying causes to prevent complications like hypoglycemia, electrolyte imbalances, and cerebral edema.
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Hyperglycemic crises
- 2. Definition DKA is a life-threatening complication in Pt. with DM DKA occurs mostly in type 1 DM frequently presented to hospitals with DKA for the first time at onset DKA is less common in type 2 DM, but it may occur in situations of physiologic stress. Search a cause?
- 3. PATHOGENESIS Glucose Ketones Hyperglycemia Ketoacidosis Glycosuria is a state of Acidosis uncontrolled catabolism associated with Osmotic insulin deficiency. Vomiting Diuresis Fluid & Electrolyte Depletion Renal Hypoperfusion Impaired Excretion of Ketones & Hydrogen ions
- 4. Pathophysiology  1. Hyperglycemia : gluconeogenesis, glycogenolysis ,â glucose uptake into cell (underutilization) 2. Ketosis (acidosis) : lipolysis, ketogenesis , â Peripheral tissue uptake ketone -- ketonemia 3. Hypertriglyceridemia : âfree fatty acid 4. Osmotic diuresis ,dehydration : hyperglycemia -- ) renal loss glucose, Na & K -- )electrolyte imbalance  5. Volume depletion : hyperglycemia,
- 5. CLINICAL FEATURES âą Polyuria leading to Oliguria âą Dehydration, Thirst âą Hypotension, Tachycardia, âą Peripheral circulatory failure âą Ketosis âą Hyperventilation âą Vomiting âą Abdominal pain (acute abdomen) âą Drowsiness, Coma
- 6. Lab  1. Glucose & ketone in serum & urine 2. Serum electrolyte, BUN, Cr, Ca, PO4,Mg 3. Blood gas : capillary or arterial blood gas ABG 4. EKG : hypo/ hyperkalemia
- 7. Diagnosis Severe Hyperglycemia 1. Serum glucose > ~300 mg/dl DD< euglycemic Ketosis> pregnancy, alcolhol drinking, stravation >
- 8. ASSESSMENT OF ABG 1. Acidosis : serum HCO3 < 15 mEq/ml or pH < 7.25 severity of DKA Mild : HCO3 > 15-18 mq/L & pH > 7.3 Alert 2. Moderate : HCO3 10-15 mq/L & pH 7.1-7.3 ~ 3. Severe : HCO3 < 10 mq/L & pH < 7.1 < wide anion gap: >15 mEq/L>
- 9. DKA 1. Ketone : positive ketone in urine and / or serum B hydroxybutyrate
- 10. Anion gap average anion gap for healthy adults is 8-12 mEq/L ïThe concentrations are expressed in units of milliequivalents/liter (mEq/L) or in millimoles/litre (mmol/L). ï[edit] With potassium ïIt is calculated by subtracting the serum concentrations of chloride and bicarbonate (anions) from the concentrations of sodium plus potassium (cations): ï = ( [Na+]+[K+] ) â ( [Clâ]+[HCO3â] ) ï[edit] Without potassium (Daily practice) ïHowever, the potassium is frequently ignored because potassium concentrations, being very low, usually have little effect on the calculated gap. This leaves the following equation: ï = ( [Na+] ) â ( [Clâ]+[HCO3â] )
- 11. DKA- Monitoring ïAdmission ? Observation, ?Home, ?Ward and ? ICU ï2 IVâs, Oxygen, cardiac monitor, continuous vitals, pulse ox ïFoley to monitor I &O ïInitially blood work every 1-2 hours ïIf pH is less that 6.9 be frightened ïNasogastric, Anticoagulant ïAntibiotic 13
- 12. DKA- Monitoring Standard blood work ïGlucose, lytes with calculated anion,ABG, Mag ïBun & creatinine, calculate GFR ïBeta-hydroxybutyrate or serum ketones ïUA ïCBC ïEKG ïInfection-cultures,chest xray ïCardiac status-cardiac enzymes 14
- 13. Diabetic Ketoacidosis: ïTreatment involves 5 key components: ïMonitoring ïFluid resuscitation / ï Electrolyte repletion ïInsulin ïTreating underlying cause 15
- 14. DKA- Fluids ïDeficits are typically 100 ml per kg ïFluid replacement will lower glucose ïInitial Tx usually fluid, fluid, fluid ïInitial resuscitation 15-20 ml/kg stat for severe dehydration with normal saline ï1l,1l,1l,then 500ml X4 hours, reassess/reassess ïOnce glucose below 250, switch to D5W/.45% N saline or D5W/.9% saline (separate or Mix) 16
- 15. Insulin Delay insulin if Hypokalemic until corrected ï??? 10 units R Insulin IV, .15 units/kg , Not Recommended Only if pharmacy delay infusion ïInsulin infusion pump, most protocols 5-7 units per hour, .1 units/kg/hr adjusted every 1 or 2 hours ïPatient to ICU ïStop insulin drip when sugar is less 17
- 18. Electrolytes- K ïWhole body potassium deficits exist. (3-5 mmol/kg) ïAcidosis increases K ïGlucose + Insulin lowers K ïStart K with K less than 5 mmol and adequate urine output ïIf initial K less than 3.3 mmol replete, and then start insulin when K above 3.3 mmol/L 20
- 19. Electrolytes- K ïCommonly under repleted ïResident mistakenly uses the replacement of potassium protocol, which vastly under repletes potassium ïWatch like a hawk!!!! ïReplace/repete/replace/repete ïHco3 potentiate electrolyte defecit not recommeded except in deep coma or severe acidosis ïPhosphate replaced with K as K phosphate of ~ effect 21
- 20. Bicarbonate ï Beneficial ONLY if patient is ï Hypokalemia severely acidotic or nearing ï Paradoxical acidosis of CSF cardiorespiratory collapse ï Adverse effects on oxyHb ï HCO3 + H = carbonic acid = dissociation curve: tissue H2O + CO2 in ECF hypoxia ï CO2 readily enters cells, where ï Overshoot alkalosis reverse reaction occurs, i.e., H is ï Acceleration of ketogenesis by produced intracellularly, raising pH leading to intracellular acidosis ï Cerebral edema ï Local necrosis
- 21. Electrolytes- Mg ïA serum deficit usually exists of .5-1 mmol per L ïConsider repleting if less than 1.8 mg/dL 23
- 24. Complication âąHypoglycemia âąElectrolyte imbalance âąHyperglycemia âąMetabolic acidosis âąCerebral edema âąHypoxemia,ARDS âąThrombotic events:CVA,MI
- 25. HHS ïMild Type 2 Diabetic ïOld age ïPolyurea from Hyperglycemia and from Impaired renal function ïSevere dehydration ïCNS Manifestation very evident (cellular dehydration) ïInsulin is enough to inhibit ketosis but not hyperglycemia ïCritical and prognosis is bad ïSame management as DKA
- 26. Dx Criteria for HHS ïGlucose > 600 ïArterial pH <7.30 ïSerum bicarb <15 mEq ïUrine and Serum ketones- small ïB-hydroxybutyrate- n or elevated ïAnion gap-variable ïPatient is stupor/coma ïOsmalality >320 mOsm/kg ïOsmolality = (2 x (Na + K)) + (BUN / 2.8) + (glucose / 18) Trachtenbarg David, Diabetic Ketoacidosis, American Family Physician, 29 2005;71:1705-1714
- 27. Lactic acidosis ïDiabetic type 2 receiving BIGUANIDE (metformin) ïSuffering from IHD,Chr resp impairement,heart failure,liver impairement,renal impairement and severe anemia (Metabolite accumulation &increase lactic acid) ïSame line of management of DKA
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- IAFP 2002 Clinical signs of OA Crepitus, a cracking or popping sensation, is produced when joint tissues rub against each other during movement. Coarse cracking felt with joint movement is produced by movement of uneven surfaces over one another and may indicate damage to or absence of articular cartilage. One or two cracks detected over the knee during joint movement may signify a loose body or torn meniscus. Examination of joint function may also have diagnostic value. In OA of the hip, internal rotation and abduction are initially restricted, followed by restriction of adduction, hyperextension, and external rotation. However, loss of flexion in the knee is not usually caused by OA, and may indicate a locking of the joint due to a loose body, or contracture due to immobilization. It is also important to test for abnormal passive movement of the joint, i.e., laxity. Such abnormalities are common in patients with OA of the knee and are due to laxity of the capsule and ligaments. Hard swelling of the joint are characteristic of OA, especially in the fingers and the knee, and may be palpable even before they are detectable in radiographs. Soft tissue swelling and palpable joint effusion may be present in finger joints and in the knee. Bony swellings may lead to joint deformity. Joints may be tender or warm, sometimes with effusion. Muscles may be weak or atrophied. Patients with OA of the load-bearing joints may limp while walking.
- IAFP 2002 Clinical signs of OA Crepitus, a cracking or popping sensation, is produced when joint tissues rub against each other during movement. Coarse cracking felt with joint movement is produced by movement of uneven surfaces over one another and may indicate damage to or absence of articular cartilage. One or two cracks detected over the knee during joint movement may signify a loose body or torn meniscus. Examination of joint function may also have diagnostic value. In OA of the hip, internal rotation and abduction are initially restricted, followed by restriction of adduction, hyperextension, and external rotation. However, loss of flexion in the knee is not usually caused by OA, and may indicate a locking of the joint due to a loose body, or contracture due to immobilization. It is also important to test for abnormal passive movement of the joint, i.e., laxity. Such abnormalities are common in patients with OA of the knee and are due to laxity of the capsule and ligaments. Hard swelling of the joint are characteristic of OA, especially in the fingers and the knee, and may be palpable even before they are detectable in radiographs. Soft tissue swelling and palpable joint effusion may be present in finger joints and in the knee. Bony swellings may lead to joint deformity. Joints may be tender or warm, sometimes with effusion. Muscles may be weak or atrophied. Patients with OA of the load-bearing joints may limp while walking.
- IAFP 2002 Risk factors: other Being overweight antedates the development of OA and increases the risk for disease progression. The increased risk for OA of the knee among overweight individuals is greater in women than in men. The relationship between increased body weight and hip OA is weaker than its association with knee OA [Felson 2000; Ann Intern Med 133:635]. Genetic factors are strongly associated with at least 50% of cases of OA of the hands and hips [Spector 1996; BMJ 312:940]. Factors that decrease joint stability (e.g. dysplasias, tears in menisci and ligaments) precede the development of OA in some individuals. Weakness of the quadriceps muscle is common in patients with knee OA. Sports activities that involve high-intensity, acute, direct joint impact increase the risk for developing OA. Repetitive impact and twisting of joints is correlated with joint deterioration as exemplified by the knees of soccer players and the elbows of baseball pitchers [Buckwalter 1997; Am J Sports Med 25:873]. In contrast, ordinary running and jogging involve little risk of developing OA [Lane 1993; J Rheum 20:461]. Jobs requiring kneeling, squatting, or heavy lifting are associated with high rates of knee and hip OA [Felson 1991; J. Rheum18:1587]. Female employees in textile mills whose jobs required repeated pinching motions of the thumb and fingers had a higher rate of OA in the distal interphalangeal joints than did other female workers [Hadler 1978; Arthr Rheum 21:210].
- IAFP 2002 Risk factors: other Being overweight antedates the development of OA and increases the risk for disease progression. The increased risk for OA of the knee among overweight individuals is greater in women than in men. The relationship between increased body weight and hip OA is weaker than its association with knee OA [Felson 2000; Ann Intern Med 133:635]. Genetic factors are strongly associated with at least 50% of cases of OA of the hands and hips [Spector 1996; BMJ 312:940]. Factors that decrease joint stability (e.g. dysplasias, tears in menisci and ligaments) precede the development of OA in some individuals. Weakness of the quadriceps muscle is common in patients with knee OA. Sports activities that involve high-intensity, acute, direct joint impact increase the risk for developing OA. Repetitive impact and twisting of joints is correlated with joint deterioration as exemplified by the knees of soccer players and the elbows of baseball pitchers [Buckwalter 1997; Am J Sports Med 25:873]. In contrast, ordinary running and jogging involve little risk of developing OA [Lane 1993; J Rheum 20:461]. Jobs requiring kneeling, squatting, or heavy lifting are associated with high rates of knee and hip OA [Felson 1991; J. Rheum18:1587]. Female employees in textile mills whose jobs required repeated pinching motions of the thumb and fingers had a higher rate of OA in the distal interphalangeal joints than did other female workers [Hadler 1978; Arthr Rheum 21:210].
- IAFP 2002 Osteoarthritis (OA): health and financial impact Osteoarthritis (OA) is the most common form of arthritis. [Felson 2000; Ann Intern Med 133:635] Formerly called degenerative joint disease, OA is characterized by progressive erosion of articular cartilage and formation of osteophytes. [Pinals 1996; Drugs 52 (Suppl 3):14] In the US, symptomatic OA of the knee occurs in approximately 6% of adults 30 years of age or older, and symptomatic OA of the hip in about 3% of this population. [Felson 1998;Arthr Rheum 41:1343] Due to the prevalence of OA and the disability that frequently accompanies OA of the knee and hip, OA accounts for more difficulty in walking and climbing stairs than any other illness. [Guccione 1994; Am J Public Health 84:351] OA is the most common reason for total hip and total knee replacement. [Felson 2000; Ann Intern Med 133:635] The economic impact of OA and other musculoskeletal disorders in the US was estimated to be $149 billion dollars in 1992, an amount equal to approximately 2.5% of the gross national product. [Yelin 1995;Arthr Rheum 38:1351]
- IAFP 2002 Risk factors: other Being overweight antedates the development of OA and increases the risk for disease progression. The increased risk for OA of the knee among overweight individuals is greater in women than in men. The relationship between increased body weight and hip OA is weaker than its association with knee OA [Felson 2000; Ann Intern Med 133:635]. Genetic factors are strongly associated with at least 50% of cases of OA of the hands and hips [Spector 1996; BMJ 312:940]. Factors that decrease joint stability (e.g. dysplasias, tears in menisci and ligaments) precede the development of OA in some individuals. Weakness of the quadriceps muscle is common in patients with knee OA. Sports activities that involve high-intensity, acute, direct joint impact increase the risk for developing OA. Repetitive impact and twisting of joints is correlated with joint deterioration as exemplified by the knees of soccer players and the elbows of baseball pitchers [Buckwalter 1997; Am J Sports Med 25:873]. In contrast, ordinary running and jogging involve little risk of developing OA [Lane 1993; J Rheum 20:461]. Jobs requiring kneeling, squatting, or heavy lifting are associated with high rates of knee and hip OA [Felson 1991; J. Rheum18:1587]. Female employees in textile mills whose jobs required repeated pinching motions of the thumb and fingers had a higher rate of OA in the distal interphalangeal joints than did other female workers [Hadler 1978; Arthr Rheum 21:210].
- IAFP 2002 Medical history questions When taking an OA medial history, it is important to ascertain the following: Are the pain and stiffness symptoms characteristic of OA or of another disease? Has OA been diagnosed in other family members? (Some forms of OA have been associated with genetic factors.) At what age did initial symptoms and signs occur? (Secondary OA attributable to trauma, joint laxity, dysplasia, or metabolic disease may occur at a younger age than idiopathic OA.) Were initial symptoms linked to trauma that produced tears in tendons, ligaments, menisci, or muscles? (Trauma can induce secondary OA.) Does the patientâs occupation or other activities involve repetitive joint stress? Does the patient have an underlying metabolic disease that could cause secondary OAâchondrocalcinosis, hemochromatosis, hyperparathyroidism, or Wilsonâs disease? Did the patient ever have a joint infection?
- IAFP 2002 History and physical examination During the physical examination, it is also important to determine whether the patientâs pain is experienced upon active or passive movement of the joint, what makes it better or worse, and its source. Limb swelling and deformities should be evaluated. Hard swelling of the joint are characteristic of OA, especially in the fingers and the knee. Palpation of crepitus may be of diagnostic significance. Fine crepitation felt throughout the entire range of joint movement usually originates in the joint capsule and frequently occurs in normal individuals. However, coarse cracking felt with joint movement may indicate damage to or absence of articular cartilage. Examination of joint function and tests for joint laxity may also have diagnostic value.
- IAFP 2002 History and physical examination During the physical examination, it is also important to determine whether the patientâs pain is experienced upon active or passive movement of the joint, what makes it better or worse, and its source. Limb swelling and deformities should be evaluated. Hard swelling of the joint are characteristic of OA, especially in the fingers and the knee. Palpation of crepitus may be of diagnostic significance. Fine crepitation felt throughout the entire range of joint movement usually originates in the joint capsule and frequently occurs in normal individuals. However, coarse cracking felt with joint movement may indicate damage to or absence of articular cartilage. Examination of joint function and tests for joint laxity may also have diagnostic value.
- IAFP 2002 History and physical examination During the physical examination, it is also important to determine whether the patientâs pain is experienced upon active or passive movement of the joint, what makes it better or worse, and its source. Limb swelling and deformities should be evaluated. Hard swelling of the joint are characteristic of OA, especially in the fingers and the knee. Palpation of crepitus may be of diagnostic significance. Fine crepitation felt throughout the entire range of joint movement usually originates in the joint capsule and frequently occurs in normal individuals. However, coarse cracking felt with joint movement may indicate damage to or absence of articular cartilage. Examination of joint function and tests for joint laxity may also have diagnostic value.
- IAFP 2002 Clinical signs of OA Crepitus, a cracking or popping sensation, is produced when joint tissues rub against each other during movement. Coarse cracking felt with joint movement is produced by movement of uneven surfaces over one another and may indicate damage to or absence of articular cartilage. One or two cracks detected over the knee during joint movement may signify a loose body or torn meniscus. Examination of joint function may also have diagnostic value. In OA of the hip, internal rotation and abduction are initially restricted, followed by restriction of adduction, hyperextension, and external rotation. However, loss of flexion in the knee is not usually caused by OA, and may indicate a locking of the joint due to a loose body, or contracture due to immobilization. It is also important to test for abnormal passive movement of the joint, i.e., laxity. Such abnormalities are common in patients with OA of the knee and are due to laxity of the capsule and ligaments. Hard swelling of the joint are characteristic of OA, especially in the fingers and the knee, and may be palpable even before they are detectable in radiographs. Soft tissue swelling and palpable joint effusion may be present in finger joints and in the knee. Bony swellings may lead to joint deformity. Joints may be tender or warm, sometimes with effusion. Muscles may be weak or atrophied. Patients with OA of the load-bearing joints may limp while walking.
- IAFP 2002 Clinical signs of OA Crepitus, a cracking or popping sensation, is produced when joint tissues rub against each other during movement. Coarse cracking felt with joint movement is produced by movement of uneven surfaces over one another and may indicate damage to or absence of articular cartilage. One or two cracks detected over the knee during joint movement may signify a loose body or torn meniscus. Examination of joint function may also have diagnostic value. In OA of the hip, internal rotation and abduction are initially restricted, followed by restriction of adduction, hyperextension, and external rotation. However, loss of flexion in the knee is not usually caused by OA, and may indicate a locking of the joint due to a loose body, or contracture due to immobilization. It is also important to test for abnormal passive movement of the joint, i.e., laxity. Such abnormalities are common in patients with OA of the knee and are due to laxity of the capsule and ligaments. Hard swelling of the joint are characteristic of OA, especially in the fingers and the knee, and may be palpable even before they are detectable in radiographs. Soft tissue swelling and palpable joint effusion may be present in finger joints and in the knee. Bony swellings may lead to joint deformity. Joints may be tender or warm, sometimes with effusion. Muscles may be weak or atrophied. Patients with OA of the load-bearing joints may limp while walking.