Downloaded 16 times
![5- Other important laboratory
findings
A.Anion Gab
useful to assess severity of acidosis and to follow
progress of therapy
Anion Gab = [Na]- [Cl] + [HCO3]
Normal values are 8- 16](https://image.slidesharecdn.com/metabolicendocrineemergencies2-190805173147/75/Metabolic-amp-endocrine-emergencies-2-17-2048.jpg)
![5- Other important laboratory
findings
B- serum osmolality:
= 1.86[Na]+(glucose/18)+(BUN/2.8)
osmolality values above 340 mOsm/kg usually result in
mental status changes.
Below this value, other causes for lethargy or coma
should be investigated.
This value may also be used to diagnose hyperosmolar
hyperglycemic state (HHS) and ingestions of ethanol,
ethylene glycol, or other alcohols.](https://image.slidesharecdn.com/metabolicendocrineemergencies2-190805173147/75/Metabolic-amp-endocrine-emergencies-2-18-2048.jpg)
Uploaded byBe a Good Doctor Ali Dirie
Metabolic & endocrine emergencies 2
1. The document discusses disorders of carbohydrate metabolism, focusing on diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). 2. DKA is characterized by high blood glucose, low pH, and ketones in the blood or urine. HHS involves extremely high blood glucose without acidosis or significant ketones. 3. Treatment for both involves fluid resuscitation, insulin administration, electrolyte replacement, and monitoring for complications. Careful attention must be paid to fluid balance, electrolyte levels, and glucose control during resuscitation.
More Related Content
Similar to Metabolic & endocrine emergencies 2
More from Be a Good Doctor Ali Dirie
Metabolic & endocrine emergencies 2
- 1. ADNAN ALI MBBS, MD EMERGRNCYSPECIALIST Disorders of Carbohydrate Metabolism.
- 2. Disorders of Carbohydrate Metabolism. -INCLUDES - Diabetic ketoacidosis - Hyperosmolar Hyperglycemic state(HHS) - Hyperglycemia - Hypoglycemia - Lactic acidosis - Alcoholic ketoacidosis
- 3. Most CHmetabolism disorders related to Diabetes mellitus a broad spectrum of Emer. conditions Toxin ingestion, Cardiovascular diseases, multisystem trauma, CV diseases, my mimic or exacerbate these conditions. Clinical appearance variation From significant mental disorders to well appearance while at edge of metabolic decompensation.
- 4. Most common acutelife threatening complication of Diabetes. Commonly type 1 DM, may occur in type 2 Diabetic ketoacidosis
- 5.
- 7. Criteria for diagnosis Patients who Arterial PH < 7,3 Serum Glucose >250 mg/ dL Serum Bicarbonate =/< 15 mEq/L Ketoneuria or ketonemia an anion gap >10
- 8. Causes diabetic ketoacidosis Omission or reduced daily insulin injections Dislodgement/occlusion of insulin pump catheter Recent or current infection of any type (most common) Pregnancy Hyperthyroidism Medications: steroids, thiazides, antipsychotics, sympathomimetics Heat-related illness Cerebrovascular accident GI hemorrhage Pulmonary embolism Acute or acute-on-chronic pancreatitis Major trauma Surgery Acute coronary syndrome or myocardial infarction Ethanol or drug abuse/ Gastroenteritis
- 9.
- 10. Typical findings include: general fatigue and weakness abdominal pain( pseudoperitonitis) Kussmaul's respirations (rapid deep respirations attempting to compensate for acidosis). fruity or acetone-like odor polyuria, polydipsia and polyphagia nausea and vomiting are found in up to 25% of patients Mental status changes ranging from mild
- 11. Investigation Routine lab CBC RFT RBG UG ABG Radiological imaging CXR Other ECG Coagulation profile
- 12. 1- Key findings serum glucose ≥ 250 mg/ dL serum ketones or ketonuria serum bicarbonate ≤ 15 mEq/L and arterial pH < 7.3 (Arterial blood gas determination can be limited to patients with an uncertain diagnosis or respiratory concerns. Venous blood is an acceptable alternative. The pH value is usually 0.03 lower than that of arterial blood. This is especially useful for repeated pH determinations.
- 13. 2- Serum Potassium initial serum potassium is unpredictable of real potassium status Acidosis drives potassium out of the cells causing a relatively higher serum potassium level despite total body deficits that may be as much as 3-5 mEq/kg. the determination of serum potassium should precede insulin therapy.
- 14. Serum potassium Ifserum potassium is initially low, insulin administration will exacerbate the situation by facilitating the cellular entry of potassium. The rapid development of severe hypokalemia may cause lethal arrhythmia
- 15. 3- Serum sodium Significant diuresis and emesis frequently lower serum sodium Osmotic pressure from glucose also dilutes the serum and fictitiously lowers the reported sodium value. Sodium deficits may approach 7-10 mEq/kg; however, rapid correction with increasing osmolality may precipitate cerebral edema,
- 16. 4- Serum phosphate Serum phosphate values may be normal or elevated Routine phosphate repletion does not improve outcome in DKA hypophosphatemia (<1 mg/dL), however, may cause skeletal, cardiac, and respiratory muscle depression Phosphate should be replaced in this circumstance. This can be done by using potassium phosphate as 1/3 of potassium
- 17. 5- Other importantlaboratory findings A.Anion Gab useful to assess severity of acidosis and to follow progress of therapy Anion Gab = [Na]- [Cl] + [HCO3] Normal values are 8- 16
- 18. 5- Other importantlaboratory findings B- serum osmolality: = 1.86[Na]+(glucose/18)+(BUN/2.8) osmolality values above 340 mOsm/kg usually result in mental status changes. Below this value, other causes for lethargy or coma should be investigated. This value may also be used to diagnose hyperosmolar hyperglycemic state (HHS) and ingestions of ethanol, ethylene glycol, or other alcohols.
- 19. 5- Other importantlaboratory findings C serum ketones: The laboratory determination of serum ketones is not always reliable as a diagnostic test The primary ketone body formed in DKA initially is β- hydroxybutyrate. However, standard ketone assays measure only acetoacetate
- 20. 5- Other importantlaboratory findings D- Blood urea nitrogen and creatinine Their levels may be elevated because of severe dehydration, acute tubular necrosis, or renal failure. In these circumstances, establish urine output prior to initiating potassium repletion
- 21.
- 22. ESSENTIALS OF DIAGNOSIS Most symptoms relate to severe dehydration Absence of acidosis, small or absent serum ketones, and hyperglycemia usually ≥ 600 mg/dL Kussmaul's respirations and abdominal pain are unusual findings
- 23. General Considerations patientswith HHS have sufficient insulin activity to prevent lipolysis and ketogenesis HHS results from gradual diuresis, resulting in severe dehydration and electrolyte depletion without significant early symptoms. This leads to profound electrolyte deficiencies and eventually mental status changes.
- 24. General Considerations HHSis most commonly seen in older patients and oftenly caused by physiologic stressors such as infection myocardial infarction cerebrovascular accident trauma decreased access to water and drug effects or interactions
- 25. History Risk factors; Age> 65 years change in diabetes regimen addition of medications that may elevate glucose levels (e.g., corticosteroids, thiazides, anticonvulsants, sympathomimetics) recent or current infection, and dementia.
- 26. Symptoms and Signs polydipsia, polyuria, or polyphagia; generalized weakness; altered mental status (clouded thinking to confusion to lethargy or coma); dry mucous membranes; poor skin turgor; and delayed capillary refill. Abdominal pain is not a typical finding in HHS (in contrast to DKA);
- 27. Laboratory Findings Keylaboratory findings—Key findings to diagnose HHS and differentiate it from DKA are as follows:
- 28. Laboratory Findings Serumglucose ≥ 600 mg/dL. Urine or serum ketones are small or absent (a small amount of ketone may be detected secondary to starvation.) Glucosuria is prominent. Serum bicarbonate is usually > 15 mEq/L. pH is usually > 7.30. The anion gap may be variable depending on precipitating cause but is usually ≤ 10. Serum osmolality is ≥ 320 mOsm/kg.
- 29. Serum sodium Inthe early stages of HHS, serum sodium findings are similar to those in patients with DKA. Urinary losses and fluid shifts out of the cell and into the extracellular compartment create hyponatremia usually 125-130 mg/dL. Correction for hyperglycemia with the addition of 1.8 mg/dL sodium per 100 mg/dL of glucose represents a more accurate value.
- 30. Serum potassium Serumpotassium levels will most commonly be normal or low, unless renal failure is present. Total body deficits are often 4-6 mEq/Kg or as much as 500 mEq total.
- 31. Blood urea nitrogenand creatinine Blood urea nitrogen (BUN) is often markedly elevated. Gastrointestinal bleeding may also elevate BUN and is a possible precipitating cause of HHS in elderly patients
- 32.
- 33. Treatment ofDKA and HHS is very similar Continuous monitoring of vital signs, mental status, and laboratory parameters is essential. A flow sheet may be helpful during resuscitation due to the complexity of treatment and need for frequent therapeutic changes
- 34. Resuscitation Issues Standardairway management is indicated Hypoxia should trigger an investigation for aspiration, pneumonia, or pulmonary edema. Oxygen therapy is indicated for all DKA or HHS patients via techniques adequate to maintain oxygen saturation above 96% or Po2 ≥70 mm
- 35. Fluid Therapy Adequatefluid replacement is the most important initial treatment of DKA and HHS. Fluid therapy is dictated by three parameters: vital signs, corrected serum sodium, and serum glucose Overall fluid deficits approach 6-10 L in most patients. Large-bore (≥18-gauge) intravenous lines are essential. Central venous access may be indicated. Hypotension should prompt a bolus of 1-2 L of
- 36. Fluid Therapy Caution:Cardiogenic shock and renal failure complicate crystalloid resuscitation. Reassess patients frequently for adequate urine output and signs of pulmonary edema or congestive heart failure. Invasive hemodynamic monitoring is indicated in very select cases to facilitate fluid management if cardiogenic shock is present. During fluid Therapy Serum electrolytes including potassium, bicarbonate, and sodium should be monitored every 1-2 hours along with hourly glucose determination. The calculated serum osmolality should not decrease
- 37. Fluid Therapy Usually1-1.5 L of 0.9% saline is infused over the first hour while initial laboratory values are determined. Subsequent infusion can be decreased to 500 mL/h, then 250-500 mL/h, then 150-300 mL/h as the hydration status improves. If the serum sodium is high normal or high, 0.45% saline is recommended after initial fluid boluses to avoid severe hypernatremia. If serum sodium is low or low normal, 0.9% saline should be continued. Once serum glucose reaches approximately 250 mg/dL, 5% dextrose in 0.45% NaCl is the fluid of choice at a rate of 250 mL/h; alternatively use 5% dextrose in normal saline if the corrected serum sodium remains low. The clinical relevance of the urine output is unreliable while glucose levels remain high due to osmotic diuresis. Once glucose levels approach normal, urine output may be used to guide therapy; 30-50 cc/h is considered adequate.
- 38. Potassium: Potassium repletionmay begin once urine output is confirmed and an initial potassium level is determined. With target levels of 4.0-5.0 mEq/L the following algorithm is usefull If the serum potassium is 3.3 mEq/L or less, withhold insulin therapy and give potassium replacement. If the serum potassium is 5.0 mEq/L or more, hold potassium repletion and recheck the serum potassium in 1-2 hours. If levels are significantly elevated (above 6 mEq/L) or ECG changes are noted, a regular insulin bolus of 8-12 units can be given along with other standard treatments for hyperkalemia Assume a deficit of about 100 mEq potassium for each 1
- 39. Insulin Therapy Insulintherapy should be delayed if the potassium level is less than 3.3 mEq/L until the potassium level is rising continuous infusion of regular insulin at 0.1 Unit/kg body weight per hour is the treatment of choice. After the serum potassium determination, a bolus of 0.1-0.15 Unit/kg body weight of regular insulin may be considered (not recommended in pediatric patients). If glucose is not decreasing by at least 50-70 mg/dL/h, the insulin dosage should be doubled until this rate of decline is achieved. Decrease insulin infusion by 25-75% if the decline in serum glucose is more than 100 mg/dL/h since this results in rapid
- 40. Sodium bicarbonate therapy Sodium bicarbonate therapy is generally not indicated except for unstable patients with severe acidosis such as an arterial pH < 6.9. Bicarbonate therapy is rarely indicated for HHS patients NaHCO3 (50 mmol) is diluted in 200 mL sterile water and infused at 200 mL/h. This may be repeated every 2 hours until the venous pH is greater than 7.
- 41. Treatment of Precipitants Infection is the most common pathological precipitant of DKA and HHS. The patient's entire skin surface should be examined for wounds and cellulitis. Analysis and cultures of all appropriate body fluids (blood, sputum, urine, cerebrospinal fluid) should be obtained. The empiric administration of broad-spectrum antibiotics should be considered until culture
- 42. Timeline for thetypical adult patient with suspected diabetic ketoacidosis.
- 43. Timeline for thetypical adult patient with suspected diabetic ketoacidosis.
- 44. Timeline for thetypical adult patient with suspected diabetic ketoacidosis
- 45. Complications Related to Therapy Major complications related to therapy of DKA include hypoglycemia hypokalemia, hypophosphatemia, adult respiratory distress syndrome cerebral edema. A gradual return to normal metabolic balance will diminish the likelihood of such outcomes.
- 46.
- 47. Cerebral edema occurin children, between 4 and 12 hours after the start of therapy, or as late as 48 hours afterward. often seen when the patient appears to be improving clinically and biochemically, and carries a high mortality. Subclinical brain swelling has been reported in asymptomatic children during treatment of DKA.16 There are no specific presentation or treatment variables that predict or contribute to the development of cerebral edema. There is no evidence demonstrating an association between the volume or sodium content of IV fluids or rate of change in serum glucose and risk for cerebral edema. Gradual replacement of water and sodium deficits and slow correction of hyperglycemia may lessen the risk. Young age and new-onset diabetes are the only identified potential risk factors. Excessive initial fluid administration of >4 L/m2 of body surface area per day has been associated with cerebral edema in
- 48. Disposition Patients withall but very mild cases of DKA and all patients with HHS should have cardiac monitoring and a higher level of nursing care for at least 24 hours. Whether the patient goes to an intermediate care, telemetry unit, or the intensive care unit is based on severity of the case and response to initial therapy as judged by the treating physician
- 49.