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Acute complications of Diabetes اعضای گروه 1. ارشیا زمانی 2. شمیم داداشی 3. آینور خرمالی 4. باسط زیتونلی 5. محمدمهدی منوچهری 6. مهدی فرهمند 7. سینا مظلومی 8. امیرحسین بابایی
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Main Topics Introduction Complications Diabetic ketoacidosis Hyperglycemic hyperosmolar state
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Introduction Individuals with type 1 or type 2 DM and severe hyperglycemia (>13.9 mmol/L [250 mg/dL]) should be assessed for clinical stability, including mentation and hydration. Ketones, an indicator of DKA, should be measured in individuals with type 1 DM when the plasma glucose is >13.9 mmol/L (250 mg/dL), during a concurrent illness, or with symptoms such as nausea, vomiting, or abdominal pain. Blood measurement of β-hydroxybutyrate is preferred over urine testing with nitroprusside based assays that measure only acetoacetate and acetone. DKA and HHS are acute, severe disorders directly related to both types of diabetes(formerly considered a hallmark of type 1 DM/individuals with type 2 DM who can sometimes subsequently be treated with oral glucose-lowering agents).
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Diabetic ketoacidosis (DKA)
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Clinical Features *usually develop over 24 h.
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Clinical Features Nausea and vomiting are often prominent. Abdominal pain may be severe and can resemble acute pancreatitis or ruptured viscus. Hyperglycemia leads to glucosuria, volume depletion, and tachycardia. Hypotension can occur because of volume depletion in combination with peripheral vasodilatation. Kussmaul respirations and a fruity odor on the patient’s breath are classic signs of the disorder Lethargy and central nervous system depression may evolve into coma with severe DKA but should also prompt evaluation for other reasons for altered mental status (e.g., infection, hypoxemia). Cerebral edema, is seen most frequently in children. precipitating factors: Signs of infection (even in the absence of fever), issue ischemia (heart, brain), Omission of insulin (because of an eating disorder, mental health disorders, or an unstable psychosocial environment)
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Pathophysiology DKA results from relative or absolute insulin deficiency combined with counterregulatory hormone excess. The decreased ratio of insulin to glucagon promotes gluconeogenesis, glycogenolysis, and ketone body formation in the liver, as well as increases in substrate delivery from fat and muscle (free fatty acids, amino acids) to the liver. Markers of inflammation (cytokines, C-reactive protein) are elevated in both DKA and HHS. The combination of insulin deficiency and hyperglycemia reduces the hepatic level of fructose-2,6-bisphosphate, which alters the activity of phosphofructokinase and fructose-1,6-bisphosphatase. Glucagon excess decreases the activity of pyruvate kinase, whereas insulin deficiency increases the activity of phosphoenolpyruvate carboxykinase. These changes shift the handling of pyruvate toward glucose synthesis and away from glycolysis. Insulin deficiency also reduces levels of the GLUT4 glucose transporter, which impairs glucose uptake into skeletal muscle and fat and reduces intracellular glucose metabolism.
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Pathophysiology Ketosis results from a marked increase in free fatty acid release from adipocytes, with a resulting shift toward ketone body synthesis in the liver. Normally, these free fatty acids are converted to VLDL in the liver. However, in DKA, hyperglucagonemia alters hepatic metabolism to favor ketone body formation, through activation of the enzyme carnitine palmitoyltransferase I (crucial for regulating fatty acid transport into the mitochondria). The increased free fatty acids increase VLDL-triglyceride production. VLDL clearance is also reduced because the activity of insulin-sensitive lipoprotein lipase in muscle and fat is decreased.
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Diagnosis characterized by hyperglycemia (serum glucose > 13.9 mmol/L[250 mg/dL], ketosis, and metabolic acidosis (serum bicarbonate <15 mmol/L with increased anion gap) along with a number of secondary metabolic derangements. the serum glucose is only minimally elevated, and may even be normal (euglycemic DKA/in individuals treated with SGLT2 inhibitors). Arterial pH ranges between 6.8 and 7.3 (depending on the severity) Despite a total-body potassium deficit, the serum potassium at presentation may be mildly elevated, secondary to the acidosis and volume depletion. Total-body stores of sodium, chloride, phosphorus, and magnesium are also reduced in DKA but are not accurately reflected by their levels in the serum because of hypovolemia and hyperglycemia. Elevated BUN and serum creatinine levels reflect intravascular volume depletion. Leukocytosis, hypertriglyceridemia, and hyperlipoproteinemia are commonly found as well. *Hyperamylasemia may suggest a diagnosis of pancreatitis, especially when accompanied by abdominal pain. However, in DKA the amylase is usually of salivary origin and thus is not diagnostic of pancreatitis. Serum lipase should be obtained if pancreatitis is suspected.
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Diagnosis * 1.6-mmol/L [1.6-meq] reduction in serum sodium for each 5.6-mmol/L [100-mg/dL] rise in the serum glucose. Serum ketones are present at significant levels (usually positive at serum dilution of ≥1:8). The nitroprusside tablet, or stick, is often used to detect urine ketones; certain medications such as captopril or penicillamine may cause false-positive reactions. Serum or plasma assays for β-hydroxybutyrate are preferred because they moreaccurately reflect the true ketone body level. Ketonemia is a consistent finding in DKA and distinguishes it from simple hyperglycemia. The differential diagnosis of DKA includes starvation ketosis, alcoholic ketoacidosis (bicarbonate usually >15 meq/L), and other forms of increased anion-gap acidosis
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Treatment After initiating IV fluid replacement and insulin therapy, the agent or event that precipitated the episode of DKA should be sought and aggressively treated. If the patient is vomiting or has altered mental status, a nasogastric tube should be inserted to prevent aspiration of gastric contents. After the initial bolus of normal saline, replacement of the sodium and free water deficit is carried out over the next 24 h (fluid deficit is often 3–5 L). When hemodynamic stability and adequate urine output are achieved, IV fluids should be switched to 0.45% saline depending on the calculated volume deficit. *Alternatively, initial use of lactated Ringer’s IV solution may reduce the hyperchloremia that commonly occurs with normal saline. bolus of IV (0.1 units/kg) short-acting regular insulin is usually administered immediately, and subsequent treatment should provide continuous and adequate levels of circulating insulin. IV administration is usually preferred (0.1 units/kg of regular insulin per hour) because it ensures rapid distribution and allows adjustment of the infusion rate as the patient responds to therapy.
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Treatment DKA can also be treated with SC short-acting insulin analogues. IV regular insulin should be continued until the acidosis resolves and the patient is metabolically stable. As the acidosis and insulin resistance associated with DKA resolve, the insulin infusion rate can be decreased (to 0.02–0.1 units/kg per hour). Long-acting insulin, in combination with SC short-acting insulin, should be administered as soon as the patient resumes eating, because this facilitates transition to an outpatient insulin regimen and reduces length of hospital stay. Hyperglycemia usually improves at a rate of 4.2–5.6 mmol/L (50–100 mg/dL) per hour as a result of insulin-mediated glucose disposal, reduced hepatic glucose release, and rehydration. The latter reduces catecholamines, increases urinary glucose loss, and expands the intravascular volume. When the plasma glucose reaches 11.1–13.9 mmol/L (200–250 mg/dL), glucose should be added to the 0.45% saline infusion to maintain the plasma glucose in the 8.3–11.1 mmol/L (150–200 mg/dL) range, and the insulin infusion should be continued at a lower rate to inhibit ketogenesis.
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Treatment Ketoacidosis begins to resolve as insulin reduces lipolysis, increases peripheral ketone body use, suppresses hepatic ketone body formation, and promotes bicarbonate regeneration. *However, the acidosis and ketosis resolve more slowly than hyperglycemia. As ketoacidosis improves, β-hydroxybutyrate is converted to acetoacetate. Ketone body levels may appear to increase if measured by laboratory assays that use the nitroprusside reaction, which only detects acetoacetate and acetone. A hyperchloremic acidosis (serum bicarbonate of 15–18 mmol/L [15–18 meq/L]) often follows successful treatment and gradually resolves as the kidneys regenerate bicarbonate and excrete chloride.
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Treatment Potassium stores are depleted in DKA (estimated deficit 3–5 mmol/kg [3–5 meq/kg]) factors contribute to the development of hypokalemia: insulin-mediated potassium transport into cells, resolution of the acidosis (which also promotes potassium entry into cells), and urinary loss of potassium salts of organic acids If the initial serum potassium level is elevated, then potassium repletion should be delayed until the potassium falls into the normal range. Inclusion of 20–40 meq of potassium in each liter of IV fluid is reasonable, but additional potassium supplements may also be required. To reduce the amount of chloride administered, potassium phosphate or acetate can be substituted for the chloride salt. The goal is to maintain the serum potassium at >3.5 mmol/L (3.5 meq/L).
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Treatment Despite a bicarbonate deficit, bicarbonate replacement is not usually necessary. In fact, theoretical arguments suggest that bicarbonate administration and rapid reversal of acidosis may impair cardiac function, reduce tissue oxygenation, and promote hypokalemia. in the presence of severe acidosis (arterial pH <7.0), the ADA advises bicarbonate (50 mmol [meq/L] of sodium bicarbonate in 200 mL of sterile water with 10 meq/L KCl per hour for 2 h until the pH is >7.0). Hypophosphatemia may result from increased glucose usage. If the serum phosphate is <0.32 mmol/L (1 mg/dL), then phosphate supplement should be considered and the serum calcium monitored. Hypomagnesemia may develop during DKA therapy and may also require sup lementation.
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Treatment With appropriate therapy, the mortality rate of DKA is low (<1%) and is related more to the underlying or precipitating event, such as infection or myocardial infarction. Venous thrombosis, upper GI bleeding, and acute respiratory distress syndrome occasionally complicate DKA. The major nonmetabolic complication of DKA therapy is cerebral edema, which most often develops in children as DKA is resolving. The etiology of and optimal therapy for cerebral edema are not well established, but overreplacement of free water and rapid normalization of serum glucose should be avoided. During illness or when oral intake is compromised, patients should (1) frequently measure the capillary blood glucose; (2) measure urinary ketones when the serum glucose is >13.7 mmol/L (250 mg/dL); (3) drink fluids to maintain hydration; (4) continue or increase insulin; and (5) seek medical attention if dehydration, persistent vomiting, or uncontrolled hyperglycemia develop.
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Treatment
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Hyperglycemic hyperosmolar state (HSS)
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Clinical Features The prototypical patient with HHS is an elderly individual with type 2 DM, with a several-week history of polyuria, weight loss, and diminished oral intake that culminates in mental confusion, lethargy, or coma. The physical examination reflects profound dehydration and hyperosmolality and reveals hypotension, tachycardia, and altered mental status. *Notably absent are symptoms of nausea, vomiting, and abdominal pain and the Kussmaul respirations characteristic of DKA. HHS is often precipitated by a serious, concurrent illness such as myocardial infarction or stroke. Sepsis, pneumonia, and other serious infections are frequent precipitants and should be sought. In addition, a debilitating condition (prior stroke or dementia) or social situation that compromises water intake usually contributes to the development of the disorder.
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Pathophysiology Relative insulin deficiency and inadequate fluid intake are the underlying causes of HHS. Insulin deficiency increases hepatic glucose production (through glycogenolysis and gluconeogenesis) and impairs glucose utilization in skeletal muscle (see above discussion of DKA). Hyperglycemia induces an osmotic diuresis that leads to intravascular volume depletion, which is exacerbated by inadequate fluid replacement. The absence of ketosis in HHS is not understood. Presumably, the insulin deficiency is only relative and less severe than in DKA. Lower levels of counterregulatory hormones and free fatty acids have been found in HHS than in DKA in some studies. It is also possible that the liver is less capable of ketone body synthesis or that the insulin/glucagon ratio does not favor ketogenesis.
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Diagnosis Most notable are the marked hyperglycemia (plasma glucose may be >55.5 mmol/L [1000 mg/dL]), hyperosmolality (>350 mosmol/L), and prerenal azotemia. The measured serum sodium may be normal or slightly low despite the marked hyperglycemia. The corrected serum sodium is usually increased (add 1.6 meq to measured sodium for each 5.6-mmol/L [100-mg/dL] rise in the serum glucose). In contrast to DKA, acidosis and ketonemia are absent or mild. A small anion-gap metabolic acidosis may be present secondary to increased lactic acid. Moderate ketonuria, if present, is secondary to starvation.
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Treatment Volume depletion and hyperglycemia are prominent features of both HHS and DKA. Consequently, therapy of these disorders shares several elements. In both disorders, careful monitoring of the patient’s fluid status, laboratory values, and insulin infusion rate is crucial. Underlying or precipitating problems should be aggressively sought and treated. In HHS, fluid losses and dehydration are usually more pronounced than in DKA due to the longer duration of the illness. The patient with HHS is usually older, more likely to have mental status changes, and more likely to have a lifethreatening precipitating event with accompanying comorbidities. Even with proper treatment, HHS has a substantially higher mortality rate than DKA (up to 15% in some clinical series).
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Treatment Fluid replacement should initially stabilize the hemodynamic status of the patient (1–3 L of 0.9% normal saline over the first 2–3 h). Because the fluid deficit in HHS is accumulated over a period of days to weeks, the rapidity of reversal of the hyperosmolar state must balance the need for free water repletion with the risk that too rapid a reversal may worsen neurologic function. If the serum sodium is >150 mmol/L (150 meq/L), 0.45% saline should be used. After hemodynamic stability is achieved, the IV fluid administration is directed at reversing the free water deficit using hypotonic fluids (0.45% saline initially, then 5% dextrose in water [D5W]). The calculated free water deficit (which averages 9–10 L) should be reversed over the next 1–2 days (infusion rates of 200–300 mL/h of hypotonic solution). Potassium repletion is usually necessary and should be dictated by repeated measurements of the serum potassium. In patients taking diuretics, the potassium deficit can be quite large and may be accompanied by magnesium deficiency. Hypophosphatemia may occur during therapy and can be improved by using KPO4 and beginning nutrition.
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Treatment As in DKA, rehydration and volume expansion lower the plasma glucose initially, but insulin is also required. A reasonable regimen for HHS begins with an IV insulin bolus of 0.1 unit/kg followed by IV insulin at a constant infusion rate of 0.1 unit/kg per hour. If the serum glucose does not fall, increase the insulin infusion rate by twofold. As in DKA, glucose should be added to IV fluid when the plasma glucose falls to 11.1–13.9 mmol/L (200–250 mg/dL), and the insulin infusion rate should be decreased to 0.02–0.1 unit/kg per hour. The insulin infusion should be continued until the patient has resumed eating and can be transferred to a SC insulin regimen. The patient should be discharged from the hospital on insulin, although some patients can later switch to oral glucose-lowering agents.
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Summary
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Thanks for your attention The End
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Question 1 سوال: پسر ۱۷ ساله‌ای با تشخیص کتواسیدوز دیابتی بستری شده‌است. پس از ۱۰ ساعت درمان، وضعیت هوشیاری طبیعی و استفراغ برطرف شده‌است. نتیجه آزمایشات به شرح زیر است: قند خون ۲۰۰ میلی‌گرم در صد، PH خون=۷.۳۶، بی‌کربنات=۱۶ میلی‌‌اکی‌والان در لیتر، کتون سرم منفی و کتون ادرار ۱+ است. کدام توصیه شما برای درمان ارحج است؟ الف) قطع انسولین وریدی و شروع انسولین NPH و ساده زیرپوستی ب) قطع انسولین وریدی، اندازه‌گیری قند پلاسما هر ۶ ساعت و تجویز انسولین ساده بر اساس سطح قندخون ج) ادامه انسولین وریدی تا طبیعی‌شدن بی‌کربنات و PH خون د) ادامه انسولین وریدی و شروع انسولین زیرپوستی NPH و ساده جواب: د
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Question 2 سوال: مرد ۲۲ ساله با علائم خواب‌آلودگی، درد شکم و دیسترس تنفسی به اورژانس آورده می‌شود. علائم پرادراری، پرنوشی و کاهش وزن را در ۳ هفته اخیر ذکر می‌کند. در معاینه مخاطات خشک، تاکی‌پنه، بوی کتون +، BP: 80/50، در آزمایشات انجام‌شده؛ PH=6.9, BS=600 mg/dl, HCO3:4, Cr:1.5, PR:110, T:36.5, Na:145, K:3, RR:30 کدامیک از اقدامات درمانی زیر اولین اقدام مناسب است؟ الف) تجویز انسولین رگولار ۶ واحد در ساعت به صورت انفوزیون وریدی ب) تجویز ۲ ویال بیکربنات + ۴۰۰ سی‌سی نرمال‌سالین در عرض ۲ ساعت ج) تجویز مایعات متناسب با وضعیت همودینامیک بیمار + KClوریدی د) تجویز مایعات متناسب با وضعیت همودینامیک بیمار و انسولین رگولار وریدی جواب: ج
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Question 3 سوال: پسر ۱۸ ساله با وزن ۷۰ کیلوگرم بدون سابقه بیماری در گذشته، با پرنوشی و پرادراری از ۳ روز قبل مراجعه کرده است. در معاینه، درد شکم و تندرنس خفیف پری‌امبلیکال دارد. علائم حیاتی به قرار زیر است: BP=120/80, RR=20, PR=90 و آزمایشات: BS=300mg/dl, K=3.1, PH=7.1, HCO3=10meq/L, Na=140 تمام اقدامات درمانی زیر صحیح است بجز؛ الف) تجویز سرم نرمال‌سالین یک لیتر بولوس ب) تجویز انسولین رگولار ۷ واحد بولوس وریدی و ادامه با ۷ واحد در ساعت ج) تجویز KCl با دوز ۸۰-۴۰ meq در هر لیتر سرم د) تعبیه سوند فولی و کنترل I/O جواب: ب
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Question 4 سوال: خانم ۲۰ ساله‌ای با تشخیص DKA چهار ساعت تحت درمان می‌باشد و ساعتی ۱۰ واحد انسولین رگولار به صورت انفوزیون وریدی و محلول نمکی ۰.۴۵٪ با ۲۰ میلی‌اکی‌والان پتاسیم دریافت می‌کند. آزمایشات به قرار زیر است: PH=7.2, Glucose=190 mg/dl, K=4meq/dl, Bicarbonate=10, Serum keton=4+ مناسب‌ترین اقدام بعدی کدام است؟ الف) تبدیل انسولین وریدی به زیرجلدی ب) اضافه‌کردن گلوکز به محلول سالین ۰.۴۵٪ ج) قطع پتاسیم وریدی د) تجویز ۲ ویال بی‌کربنات جواب: ب
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Question 5 سوال: در بیمار مبتلا به کتواسیدوز با Na=127meq/l و BS=600mg/dl میزان واقعی سدیم چند میلی‌اکی‌والان در لیتر می‌باشد؟ الف) ۱۴۰ ب) ۱۳۰ ج) ۱۴۵ د) ۱۳۵ جواب: د
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Question 6 سوال: آقای ۳۴ساله مبتلا به دیابت نوع۱ از ۱۴ سالگی، با تشخیص DKA بستری شده‌است. ابتدا ساعتی ۱۵۰ میلی‌لیتر نرمال‌سالین و ۱۰ واحد انسولین رگولار دریافت می‌کند. بعد از چهار ساعت، ساعتی ۱۵۰ میلی‌لیتر نرمال‌سالین، ۱۵۰ میلی‌لیتر محلول دکستروز، ۶ واحد انسولین و ۲۰ میلی‌اکی‌والان پتاسیم دریافت می‌کند. پس از ۱۰ ساعت درمان، حال عمومی بیمار خوب بوده و آزمایش‌های وی به شرح زیر است: Glucose=200mg/dl, Na=138meq/L, K=4.6meq/L, PH=7.37, HCO3=15meq/L, PCO2=23, Chloride=116meq/L, Serum keton=Negative بهترین توجیه برای نتیجه‌ آزمایش‌های گازهای خون بیمار کدام است؟ الف) بتا هیدروکسی بوتیرات اسیدوزیس ب) اضافه‌شدن لاکتیک اسید ج) مصرف متانول د) اسیدوز هیپرکلرمیک بعد از درمان DKA جواب: د
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Question 7 سوال: پسر بچه ۱۰ ساله با سابقه دیابت نوع 1 به علت درد شکم و تهوع بستری شده‌است. در آزمایشات قند 350mg/dl، کتون ادرار +۲، پتاسیم 4mg/dl، سدیم 132mg/dl، بی‌کربنات ۱۶ و pH=7.25 گزارش گردیده است. تب ندارد و فشارخون 90/60mmHg و نبض ۱۱۰ بار در دقیقه دارد. تجویز کدامیک از موارد زیر در رابطه با این بیمار صحیح است؟ الف) انسولین + سرم نرمال سالین + پتاسیم ب) کلرید سدیم هیپرتونیک + انسولین + پتاسیم ج) سرم نرمال سالین + بی‌کربنات + انسولین د) کلرید سدیم هیپرتونیک + بیکربنات + پتاسیم جواب: الف
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Question 8 سوال: زن ۶۵ ساله‌ای کیس شناخته‌شده دیابت و تحت درمان با داروهای خوراکی پایین آوردنده قند بوده‌است که با کاهش سطح هوشیاری در حد لتارژی به اورژانس آورده شده‌است. در معاینه تب‌دار و تاکی‌کارد می‌باشد و دهیدره است. معاینات نکته مثبتی ندارد. آزمایشات به قرار زیر است: K:3.8meq/L (3.5-5), Na:145meq/L (136-146), BS:780mg/dl, HCO3:20, WBC:1200, Hb:11, U/A: WBC=20-30, Cr:2, Urea:120, ABG: pH=7.3 از بین تشخیص‌های زیر محتمل‌ترین علت برای کاهش سطح هوشیاری بیمارکدام است؟ الف) کتواسیدوز دیابتی ب) کومای هیپراسمولار ج) سکته مغزی د) نارسایی کلیه جواب: ب
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Question 9 سوال: خانم ۷۰ ساله مبتلا به دیابت نوع۲ از ۵ سال قبل تحت درمان با داروهای خوراکی بوده و کنترل مناسب داشته است از ۲ روز قبل دچار تب و خواب‌آلودگی شده و به اورژانس بیمارستان منتقل شده‌است. یافته فوکال نورولوژیک ندارد، تب دارد و دهیدراته است، رال ریه راست دارد. از سوند فولی جریان ادرار برقرار است: T:39, PR=100/min, BP=110/60 و آزمایشات به قرار زیر می‌باشند: BS=900mg/dl, Na=158meq/dl, K=2.4meq/dl, Cr=2mg/dl و ECG نرمال است. پس از انجام اقدامات تشخیصی ضروری، مناسب‌ترین اقدام درمانی در ساعت اول کدام است؟ الف) تجویز نرمال‌سالین ۰.۹٪ یک لیتر در یک ساعت ب) تجویز نرمال‌سالین ۰.۹٪ یک لیتر + ۲۰ سی‌سی KCl در یک ساعت ج) انسولین رگولار و تجویز سالین ۰.۴۵٪ به همراه ۷ واحد بولوس وریدی انسولین رگولار د) تجویز سالین ۰.۴۵٪ یک لیتر + ۲۰ سی‌سی KCl در یک ساعت جواب: د
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Question 10 سوال: خانم ۷۴ ساله با دیابت تیپ ۲ به علت هیپرگلیسمی و کاهش سطح هوشیاری و بی‌اختیاری ادرار بستری شده‌است. در معاینه، خواب‌آلود است و BP:110/60 mmHg و PR:92 دارد. مخاطات خشک است. سایر معاینات: W:84kg, Na:134meq/L, K:5.3meq/L, Cl:106meq/L, PH:7.35, HCO3:18, BUN:79, Cr:1.9mg/dl, BS:961mg/dl, Urin keton:1+ اقدام اولیه درمانی مناسب برای ایشان کدام است؟ الف) ۱.۵ لیتر سالین هیپرتونیک + انسولین رگولار U/h ۸ ب) ۱.۵ لیتر سالین ایزوتونیک + انسولین رگولار U/h ۸ ج) ۱.۵ لیتر سالین ایزوتونیک + انسولین رگولار U/h ۴ د) ۱.۵ لیتر سالین نیم‌نرمال + انسولین رگولار U/h ۸ جواب: ب